Abdominal Pain - Key Features

1. Given a patient with abdominal pain, paying particular attention to its location and
chronicity:

a) Distinguish between acute and chronic pain.

Arbitrary number cannot be used to distinguish between acute and chronic pain. Pain of less than
a few days duration that has worsened progressively until the time of presentation may be
classified as acute. Pain that has remained unchanged for months or years may be classified as
chronic. Pain that does not clearly fit either category might be called subacute and requires
consideration of the differential diagnoses for both acute and chronic pain.

b) Generate a complete differential diagnosis (ddx).

GI tract:

Inflammatory: gastroenteritis, appendicitis, gastritis, esophagitis, diverticulitis, Crohn's

disease, ulcerative colitis, microscopic colitis
Obstruction: hernia, intussusception, volvulus, post-surgical adhesions, tumours, superior
mesenteric artery syndrome, severe constipation, hemorrhoids
Vascular: embolism, thrombosis, hemorrhage, sickle cell disease, abdominal angina,
blood vessel compression (such as celiac artery compression syndrome)
Digestive: peptic ulcer, lactose intolerance, coeliac disease, food allergies

Bile system:

Inflammatory: cholecystitis, cholangitis

Obstruction: cholelithiasis, tumours

Liver:

Inflammatory: hepatitis, liver abscess

Pancreatic:

Inflammatory: pancreatitis

Renal and urological:

Inflammation: pyelonephritis, bladder infection

Obstruction (kidney stones, urolithiasis)
Urinary retention, tumours
Vascular (left renal vein entrapment)

Gynaecological or obstetric:

Inflammatory: pelvic inflammatory disease

Mechanical: ovarian torsion
Endocrinological: menstruation, Mittelschmerz

1
 Tumors: endometriosis, fibroids, ovarian cyst, ovarian cancer
Pregnancy: ruptured ectopic pregnancy, threatened abortion

Abdominal wall:

muscle strain or trauma

neurogenic pain: herpes zoster, radiculitis in Lyme disease, abdominal cutaneous nerve
entrapment syndrome (ACNES)

Referred pain from the thorax:

pneumonia, pulmonary embolism, ischemic heart disease, pericarditis

from the spine:
from the genitals: testicular torsion

Metabolic disturbance:

uremia, diabetic ketoacidosis, porphyria, adrenal insufficiency, narcotic withdrawal

Blood vessels:

aortic dissection, abdominal aortic aneurysm

Immune system

sarcoidosis, vasculitis

Idiopathic

irritable bowel syndrome (affecting up to 20% of the population, IBS is the most
common cause of recurrent, intermittent abdominal pain)

c) Investigate in an appropriate and timely fashion.

Initial diagnostic testing - may consider following investigations

Complete blood count with differential, Electrolytes, BUN, creatinine, and glucose,
Aminotransferases, alkaline phosphatase, and bilirubin, Lipase, Urinalysis, Ferritin, Anti-
tissue transglutaminase, Pregnancy test in women of childbearing potential
Plain film 3 views of abdomen/CT (gas pattern, free air), Ultrasound (gallbladder disease,
gynecological problems)
Gastroscopy/colonoscopy (AAA, appendicitis)

2
2. In a patient with diagnosed abdominal pain (e.g., gastroesophageal reflux disease, peptic
ulcer disease, ulcerative colitis, Crohn’s disease), manage specific pathology appropriately
(e.g., with. medication, lifestyle modifications).

GERD

Lifestyle modifications, Head of bed elevation, avoidance of reflux-inducing foods (fatty

foods, chocolate, peppermint, and excessive alcohol,

Weight loss, avoidance of meals before bedtime

Medications
Proton pump inhibitors
H2 Antagonist (Ranitidine, Cimetidine, Famotidine, Nizatidine )
Prokinetic agents (bethanechol, metoclopramide)

PUD

Eradication of H. pylori
Antisecretory therapy after H. pylori eradication with Proton pump inhibitors and H2
Antagonist

Inflammatory Bowel Disease

5-aminosalicylate (5-ASA) Sulfasalazine , mesalamine, olsalazine, balsalazide

Prednisone
Cyclosporine
Hydrocortisone (100 mg IV q8h)
antibiotics in colitis flare - metronidazole , ciprofloxacin
anti-TNF - Infliximab

3. In a woman with abdominal pain:

a) Always rule out pregnancy if she is of reproductive age.
b) Suspect gynecologic etiology for abdominal pain.
c) Do a pelvic examination, if appropriate.

Ectopic Pregnancy, Adnexal Masses, Corpus luteum hematoma, Ruptured ovarian cyst, Ovarian
torsion, Acute Pelvic Inflammatory Disease, Endometriosis, Primary Dysmenorrhea, Secondary
Dysmenorrhea, Adhesions Interstitial Cystitis

4. In a patient with acute abdominal pain, differentiate between a surgical and a non-surgical
abdomen.
Obstruction - pain, anorexia, bloating, nausea, vomiting (bilious or feculent) and obstipation,
distension, high-pitched or absent bowel sounds
Peritonitis - abdominal wall rigidity, percussion/rebound tenderness, involuntary guarding,
diminished bowel sounds

3
5. In specific patient groups (e.g., children, pregnant women, the elderly), include group-
specific surgical causes of acute abdominal pain in the ddx.

Trauma - hemorrhage from solid organ laceration or fluid loss, organ ischemia from vascular
injury, and infection from perforated hollow viscus

In neonates - volvulus (as a complication of malrotation) and necrotizing enterocolitis.

Intussusception (invagination of a part of the intestine into itself, causing obstruction.

Among children of all ages, appendicitis can cause peritoneal irritation and focal tenderness.
Obstruction as the result of adhesions from previous surgery or inflammation, complications of
Hirschsprung disease, perforated ulcer, and primary bacterial peritonitis (usually as a
complication of nephrotic syndrome.

Incarcerated inguinal hernia diabetic ketoacidosis, hemolytic uremic syndrome, ruptured ectopic
pregnancy.

Ischemic bowel, aortic dissection, rupture of AAA

6. Given a patient with a life-threatening cause of acute abdominal pain (e.g., a ruptured
abdominal aortic aneurysm or a ruptured ectopic pregnancy):
a) Recognize the life-threatening situation.
b) Make the diagnosis.
c) Stabilize the patient.
d) Promptly refer the patient for definitive treatment.
Conventional angiography: Angiography remains the criterion standard for the diagnosis of AAA

Computed tomography: Preoperative CT scanning helps more clearly define the anatomy of the
aneurysm and other intra-abdominal pathologies. Nonenhanced CT scanning is used to size
aneurysms.

Diagnostic Tests for Detecting Ectopic Pregnancy

Sensitivity
Diagnostic test Specificity %)
(%)
Transvaginal ultrasonography with beta-hCG level greater than 100 (virtual
67 to 100
1,500 mIU per mL (1,500 IU per L) certainty)
Beta-hCG levels do not increase appropriately 36 63 to 71
Single progesterone level to distinguish ectopic pregnancy from
15 > 90
nonectopic pregnancy
Single progesterone level to distinguish pregnancy failure from
95 40
viable intrauterine pregnancy

7. In a patient with chronic or recurrent abdominal pain:

a) Ensure adequate follow-up to monitor new or changing symptoms or signs.

b) Manage symptomatically with medication and lifestyle modification (e.g., for irritable bowel
syndrome).

4
Dietary modification - lactose free diet , Exclusion of gas-producing foods , (beans, onions,
celery, carrots, raisins, bananas, apricots, prunes, brussel sprouts, wheat germ, pretzels, and
bagels) Food allergies, Gluten sensitivity, Carbohydrate malabsorption, increase in the intake of
fiber

Psychosocial therapies

Medications - Antispasmodic agents (hyoscine, cimetropium, pinaverium, dicyclomine)

Antidepressants (amitriptyline, imipramine, nortriptyline, and desipramine Paroxetine, fluoxetine,
sertraline), 5- serotonin 3 receptor antagonists (alosetron, cilansetron, ondansetron and
granisetron)

c) Always consider cancer in a patient at risk.

Risk factors for colorectal cancer: Hereditary CRC syndromes, Familial adenomatous polyposis,
MYH-associated polyposis, Lynch syndrome, Alcohol, Obesity, Age, Inflammatory bowel
disease

8. Given a patient with a diagnosis of inflammatory bowel disease (IBD) recognize any extra
intestinal manifestation.

Musculoskeletal: Peripheral arthritis, Sacroiliitis, Ankylosing spondylitis, Osteoporosis

Dermatologic: Erythema nodosum, Pyoderma gangrenosum, Aphthous stomatitis
Ocular: Uveitis, Scleritis, Episcleritis
Hepatobiliary Disease: Primary sclerosing cholangitis
Vascular: Thromboembolic events
Renal: Nephrolithiasis

Advanced Cardiac Life Support - Key Features

1. Keep up to date with advanced cardiac life support (ACLS) recommendations (i.e., maintain
your knowledge base).
PLEASE SEE LINK for 2010 Guidelines

2. Promptly defibrillate a patient with ventricular fibrillation (V fib), or pulseless or

symptomatic ventricular tachycardia (V tach).

5
ACLS Cardiac Arrest Algorithm

ACLS Cardiac Arrest Circular Algorithm

3. Diagnose serious arrhythmias (V tach, V fib, supraventricular tachycardia, atrial

fibrillation, or second- or third-degree heart block), and treat according to ACLS protocols.

-Ventricular tachycardia occurs when electrical impulses originating from the ventricles cause

6
rapid ventricular depolarization (140-250 beats per minute) – tx- see algorithm above
-Ventricular fibrillation occurs when parts of the ventricles depolarize repeatedly in an erratic,
uncoordinated manner. The EKG in ventricular fibrillation shows random, apparently unrelated
waves. Usually, there is no recognizable QRS complex . tx see algorithm above

Supraventricular tachycardia - A narrow QRS complex (<120 msec) reflects rapid activation of
the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia
originates above or within the atrioventricular (AV) node (ie, a supraventricular tachycardia). The
site of origin may be in the sinus node, the atria, the atrioventricular node, the His bundle, or
some combination of these sites. The Ddx: atrial fib, atrial flutter, and a variety of paroxysmal
SVTs, most commonly atrial tachycardias, AVNRT, and AVRT Tx- see ACLS adult tachycardia
algorithm below

7
Atrial Fibrillation: - Tx- see ACLS A fib algorithm below

2nd degree Heart Block:

Type 1 (Wenckebach) -progressively increasing PR interval culminating in a dropped beat
Tx: if asymptomatic- no tx, if symptomatic –ie bradycardia- tx= permanent pacemaker (reversible
causes should be excluded- MI, increased vagal tone, and meds)
Type 2 (Mobitz): PR interval remains unchanged prior to a P wave that suddenly fails to conduct
to the ventricles.
Tx: permanent pacemaker-(reversible causes should be excluded- MI, increased vagal tone, and
meds)

3rd degree HB: There is complete dissociation of atria and ventricles.

Tx: permanent pacemaker-(reversible causes should be excluded- MI, increased vagal tone, and
meds)
Atropine- may be effective by reversing the decrease in AV nodal conduction induced by vagal

8
tone in the emergent setting

Bradycardia Algorithm

4. Suspect and promptly treat reversible causes of arrhythmias (e.g., hyperkalemia, digoxin
toxicity, cocaine intoxication) before confirmation of the diagnosis.

Hyperkalemia- clinically weak and ECG shows tall peaked T waves, increased PR interval, and
wide QRS, progressing to sine wave pattern and PEA

Tx: r/o pseudohyperkalemia (hemolysis)

Acute management: calcium gluconate 2 amps IV, reg. insulin 10U with 1-2 amps D50W,
Salbutamol 10 to 20 mg by neb over 10mins
Tx to eliminate total body K+: Kayexalate 30-90gms PO/PR, diuretics e.g. furosemide 40mg IV,
or hemodialysis

9
Hypokalemia- clinically nausea, vomiting, weakness, muscle cramps, ST depression, flattened T,
prominent U wave, prolonged QT (Tx with KCL 10-20meq/hr IV if urgent or 40meq PO 4-6 hrs
for non urgent)

Digoxin toxicity - ST scooped-like depression, mild PR prolongation

if clinically significant manifestations (ventricular tach; ventricular fib; asystole; complete heart
block; Mobitz II heart block; symptomatic bradycardia) OR Evidence of end-organ dysfunction
(eg, renal failure, altered mental status) OR Hyperkalemia (serum potassium >5 to 5.5 meq/L .
Tx : digoxin-specific antibody (Fab) fragments aka ‘Digibind’ - if Fab fragments are not
immediately available, tx: bradycardia with atropine (0.5 mg IV in adults; 0.02 mg/kg IV in
children, minimum dose 0.1 mg) and hypotension with IV boluses

HYPERcalcemia- bones (pain), stones (renal/biliary) , groans (abd pain/nausea/vomiting),

psychic moans (dep/anxiety) , thrones (sit on the throne – polyuria), dehydration, change in
mental status, vomiting, pancreatitis, decreased reflexes, short QT TX: IVNS 4-6L/day,
furosemide IV q6hrs, pamidronate 60-80mg IV x 1 dose, ( calcitonin and glucocorticoids=
questionable evidence)

HYPOcalcemia- perioral paresthesias, depression, psychosis, seizures, chvostek’s sign (tap facial
nerve and contraction of facial muscles on ipsilatarel side), trousseau’s (inflate BP cuff and get
carpal spasm), prolonged QT TX: symptomatic: calcium gluconate 1-2gIV over 20mins +
calcitriol +/-Mg 50-100mEq.day, asymptomatic oral calcium 1-3g/d (calcium gluconate 500-
1000mg PO bid-qid and vit. D -ergocalciferol 50000IUpo/wkx6-8wks, in chronic hyoparathryoid
need to give calcitriol)

Cocaine intoxication mydriasis, euphoria, agitation, elevated HR and BP, sweating, tremors,
confusion, seizure, HTN, arterial vasoconstriction (eg, coronary arteries), thrombus formation,
psychomotor agitation (neurologic effects can range from agitation to seizures to intracranial
hemorrhage), severe hyperthermia, dyspnea (from pneumothorax, pulmonary infarction or other
pulmonary injury), and ischemic bowel. TX: stabilize vitals (ABC),
Airway management- Succinylcholine relatively contraindicated in rapid sequence intubation;
consider rocuronium (1 mg/kg IV) or other nondepolarizing agent as alternative
Psychomotor agitation-diazepam 5 to 10 mg IV every 3 to 5 min
Severe or symptomatic hypertension-diazepam (5 mg IV) or lorazepam (1 mg IV); may repeat q 5
minutes until sedated, Phentolamine (1 to 5 mg IV); repeat as necessary, DO NOT
ADMINISTER BETA-BLOCKERS, INCLUDING LABETALOL
Cocaine-associated myocardial ischemia- EKG, diazepam (5 mg IV) or lorazepam (1 mg IV) for
agitation or hypertension, Aspirin 325 mg PO, Nitroglycerin 0.4 mg SL with or without
continuous infusion, Phentolamine 1 to 5 mg IV, repeat as necessary; hold for SBP <100, DO
NOT ADMINISTER BETA-BLOCKERS, INCLUDING LABETALOL. Beta-blockade is
contraindicated in acute cocaine toxicity.
QRS widening on ECG (rare; suggests profound toxicity)- sodium bicarbonate, 1 to 2 mEq/kg IV
push

Hyperthermia- initiate cooling, if elevated CK (rabdomyolosis) IV fluids.

5. Ensure adequate ventilation (i.e., with a bag valve mask), and secure the airway in a timely
manner.

Bag-Mask Ventilation: All healthcare providers should be familiar with the use of the bag-mask
device for support of oxygenation and ventilation. Bag-mask ventilation is particularly helpful

10
during the first few minutes of resuscitation or when placement of an advanced airway is delayed
or unsuccessful. Effective bagmask ventilation requires adequate training and frequent practice.
When using a bagmask device (ie, no advanced airway is in place), the rescuer should deliver a
tidal volume sufficient to produce chest rise (approximately 6 to 7 mL/kg or 500 to 600 mL) over
1 second. This volume of ventilation minimizes the risk of gastric inflation. The rescuer should be
sure to open the airway adequately with a chin lift, lifting the jaw against the mask and holding
the mask against the face, creating a tight seal. During CPR, give 2 breaths during a brief (about 3
to 4 seconds) pause after every 30 chest compressions. When an advanced airway (eg,
endotracheal tube, esophageal-tracheal combitube [Combitube], or laryngeal mask airway
[LMA]) replaces the face mask, rescuers should deliver 8 to 10 breaths per minute during CPR.
Deliver each breath over about 1 second while chest compressions are delivered at a rate of 100
per minute, and do not attempt to synchronize the compressions with the ventilations.

6. In patients requiring resuscitation, assess their circumstances (e.g., asystole, long code
times, poor pre-code prognosis, living wills) to help you decide when to stop. (Avoid
inappropriate resuscitation.)

BLS- Termination of resuscitation rule for adult out of hospital cardiac arrest

ALS- Termination of resuscitation rule for adult out of hospital cardiac arrest

Terminating Cardiac Arrest Resuscitative Efforts in Adult In Hospital Cardiac Arrest

In the hospital the decision to terminate resuscitative efforts rests with the treating physician and
is based on consideration of many factors, including witnessed versus unwitnessed arrest, time to
CPR, initial arrest rhythm, time to defibrillation, comor- bid disease, prearrest state, and whether
there is ROSC at some point during the resuscitative efforts. Clinical decision rules for in-hospital
termination of resuscitation may be helpful in reduc- ing variability in decision making; however,
the evidence for their reliability is limited, and rules should be prospectively validated before
adoption.

7. In patients with serious medical problems or end-stage disease, discuss code status and end-
of-life decisions (e.g., resuscitation, feeding tubes, levels of treatment), and readdress these
issues periodically.

What is an advance directive? An advance directive is a mechanism whereby competent people

give instructions about what is to be done if they should subsequently lose the capacity to decide
or to communicate. It covers decisions about medical treatment, particularly the treatment which

11
might be provided as the patient approaches death. Also states legally appointed decision makers
who would make decisions according to patient’s wishes outlined in advance directive. Only used
if patient becomes incapable of making decisions. Drafting an advance statement is recommended
be done with medical advice and counseling as part of a continuing doctor-patient dialogue.
A living will may be referred to as a “medical directive” or “declaration” or “directive to
physicians,” and it provides written direction to healthcare providers about the care that the
individual approves should he or she become terminally ill and be unable to make decisions. A
living will constitutes evidence of the individual’s wishes, and in most areas it can be legally
enforced.
A durable power of attorney for health care is a legal document that appoints an authorized
person to make healthcare decisions (not limited to end-of-life decisions). Simply put, a living
will affects the care received, and a durable power of attorney accounts for unforeseen
circumstances. The latter decisions may be in conflict with the living will or advance directive; at
the time of the unforeseen circumstances they are considered to be valid expressions of the
patient’s best interests.

-Levels of treatment: comfort care, limited care (e.g. antibiotics/IV fluids/O2 for pneumonia),
surgical care, intensive care
-Feeding- basic feeding, supplemental feeding (e.g. vitamins, supplements), intravenous feeding,
tube feeding
-DNR vs. CPR
-can make changes to advance directive while competent

8. Attend to family members (e.g., with counseling, presence in the code room) during and
after resuscitating a patient.

Offering select family members the opportunity to be present during a resuscitation is reasonable
and desirable (assuming that the patient, if an adult, has not raised a prior objection) . Parents and
other family members seldom ask if they can be present unless they are encouraged to do so by
healthcare providers. Resuscitation team members should be sensitive to the presence of family
members during resuscitative efforts, assigning a team member to remain with the family to
answer questions, clarify information, and otherwise offer comfort.

9. In a pediatric resuscitation, use appropriate resources ( e.g., Braeslow tape, the patient’s
weight) to determine the correct drug doses and tube sizes.

In compensated shock, blood pressure remains normal; it is low in decompensated shock.

Hypotension is a systolic blood pressure less than the 5th percentile of normal for age, namely:

● <60 mm Hg in term neonates (0 to 28 days)

● <70 mm Hg in infants (1 month to 12 months)
● <70mmHg+(2 x age in years) in children 1 to 10 years
● <90 mm Hg in children ≥10 years of age

Uncuffed endotracheal tube size (mmID)= (age/4) + 4

Cuffed endotracheal tube size (mmID)= (age/4) + 3
(Endotracheal tube size is more reliably based on a child’s body length.)
(Adult women- 7.5-8.0 cuffed, Adult males- 8-8.5 cuffed )

12
Braeslow tape - which is used during pediatric emergencies to quickly estimate a child's weight,
determine weight-based drug doses, and select the correct size emergency or resuscitation
equipment.

Allergy - Key Features

1. In all patients, always inquire about any allergy and clearly document it in the chart. Re-
evaluate this periodically.
It is important to determine both the allergen, type of reaction, when the reaction occurred and
whether there has been exposure since the initial reaction without repeat reaction.

2. Clarify the manifestations of a reaction in order to try to diagnose a true allergic reaction
(e.g., do not misdiagnose viral rashes as antibiotic allergy, or medication intolerance as true
allergy).

Intolerance vs true allergy: An allergy is IgE mediated. It happens acutely (within 20min) with
every exposure and is NOT dose dependant. Allergic symptoms include: urticaria, angioedema,
flushing, rhinitis, stridor, vomiting etc. Intolerance IS dose dependant and may not happen with
small amounts of exposure. Patients should avoid things they are intolerant or allergic to however
the distinction is vital because intolerance does NOT cause anaphylaxis.

3. In a patient reporting allergy (e.g., to food, to medications, environmental), ensure that the
patient has the appropriate medication to control symptoms (e.g., antihistamines,
bronchodilators, steroids, an EpiPen).
For details of treatment see point 7.

4. Prescribe an EpiPen to every patient who has a history of, or is at risk for, anaphylaxis.
EpiPen training kits can be obtained from the manufacture for patients and family members to
learn how to use it. EpiPen’s expire after 1 year. For more information and resources
www.epipen.ca.

13
5. Educate appropriate patients with allergy (e.g., to food, medications, insect stings) and their
families about the symptoms of anaphylaxis and the self-administration of the EpiPen, and
advise them to return for immediate reassessment and treatment if those symptoms develop or
if the EpiPen has been used.
An EpiPen is meant to give a patient enough time to get to an ER where they can then be fully
treated and monitored for anaphylaxis. It does NOT replace emergency medical attention.

6. Advise patients with any known drug allergy or previous major allergic reaction to get a
MedicAlert bracelet.

7. In a patient presenting with an anaphylactic reaction:

a) Recognize the symptoms and signs.
Anaphylaxis is defined as "a severe allergic reaction to any stimulus, having sudden onset,
involving one or more body systems (oral, cutaneous, GI, cardio, resp) with multiple symptoms."
The two most common manifestations of anaphylaxis are urticaria and angioedema.

Other symptoms include:

Swelling of the throat, lips, tongue
Difficulty breathing or swallowing
Metallic taste or itching in the mouth
Generalized flushing, itching, or redness of the skin
Stomach cramps, nausea, vomiting, or diarrhea
Dysrhythmia
Plunging blood pressure
Paleness
Sudden feeling of weakness
Anxiety or an overwhelming sense of doom

b) Treat immediately and aggressively.

Adrenaline (Epi) should be given to all patients with respiratory difficulty and hypotension
Mild Rxn:

- Diphenhydramine 50-100mg PO/IM (peds 1-2mg/kg) then q4-6h PRN +/- ranitidine IV
(50mg q8h) or PO (150mg q12h) for puritis
- Epinephrine SC 0.3-0.5ml 1:1000

Mod Rxn:

- Epinephrine SC 0.3-0.5ml 1:1000 solution followed by hydrocortisone 200mg IM or

slow IV. May repeat epi q5-20 min x 3 PRN
- IV, O2 by mask, Ventolin neb PRN
- ECG monitor, ABGs, lytes
- Consider for ICU for 24 hours

Severe Rxn:

- Maintain airway (consider intubation), O2 by mask, IV, foley

- If pt is in shock run 0.9% NaCl through IV wide open
- Epinephrine 1:10 000 solution (1mg/10ml) 0.5-1.0ml IV q1min up to total of 1-2mg
(10-20cc) /hr. (Peds 0.01mg/kg 1/10 000 solution q5min x 1 PRN)

14
 - IF no IV access give SL or endotracheally (use IV doses). If no response consider
Dopamine at 2mcg/kg/min titrated to effect
- Solucortef 500mg IV (peds 5-10mg/kg) q6hr
- Diphenhydramine 50mg IV over 3min +/- Ranitidine 50mg IV
- Ventolin nebs PRN
- ECG monitor, ABGs, lytes
- Consider ICU admission

c) Prevent a delayed hypersensitivity reaction through observation and adequate treatment

(e.g., with steroids).
Biphasic reactions are common and a patient should remain under observation at least 4 hours
after being treated for anaphylaxis.

8. In patients with anaphylaxis of unclear etiology refer to an allergist for clarification of the
cause.

9. In the particular case of a child with an anaphylactic reaction to food:

a) Prescribe an EpiPen for the house, car, school, and daycare.
b) Advise the family to educate the child, teachers, and caretakers about signs and symptoms of
anaphylaxis, and about when and how to use the EpiPen.

10. In a patient with unexplained recurrent respiratory symptoms, include allergy (e.g., sick
building syndrome, seasonal allergy) in the differential diagnosis.

Anemia - Key Features

• Reduction in [Hb] more than 2 standard deviations below the mean, adjusted for sex and age
• Men <135g/L, Women <120g/L
• Normals may differ for certain populations
• High altitude, smokers, exposure to carbon monoxide, African Americans
• Associated with increased risk of hospitalization, death in older adults living in the community

15
Signs and symptoms of anemia

Underlying Causes
• Hemorrhage
• Hemolysis
• Defects in haemoglobin, RBC membrane
• Suppression of bone marrow
• Alcohol use
• Dietary deficiencies
• Chronic kidney disease
• Hypothyroid, hypogonadism
• Leukemia
• Myelodysplastic syndrome
• Infiltrative diseases (cancer, sarcoidosis)

History and Physical

• Bleeding
• FHx of anemia
• Medication use
• Alcohol intake
• Comorbid conditions
• GI symptoms
• Menorrhagia
• Glossitis, angular cheilitis, koilonychias, paresthesias

16
Algorithms for Microcytic, Normocytic, and Macrocytic Anemia

17
Treatment of Common Anemias
Iron Deficiency Anemia

• Assess underlying cause of anemia

• Rule out occult GI bleeding
• Menorrhagia must be convincing before being accepted as sole cause of iron deficiency
• If not obvious GI blood loss, consider screening for celiac disease
• If Hb fails to respond as anticipated, consider ongoing blood loss, medications that
impair iron absorption, different / concurrent cause of anemia, impaired erythropoietic
response

18
 • To increase adherence to oral supplements: slowly increase dose, start with a tablet after
meals, then change timing to before meals
• Avoid enteric-coated products -> poor absorption
• Treat until iron stores replenished
Nonpharmacologic Pharmacologic
• Oral iron salts: variety of forms with varying
concentration of elemental iron
• Diet: foods rich in heme iron (liver, lean o Absorption enhanced when given on
red meats, seafood: oysters, clams, tuna, empty stomach, but side effects (nausea,
salmon, sardines, shrimp) epigastric pain) more common this way
o Target dose = 105-200 mg/d of elemental
iron, in divided doses
• Parenteral iron: for patients with malabsorption or
• Takes longer to replete iron stores than true intolerance to oral iron, or if ongoing losses
supplements exceed capacity of GI tract to absorb oral iron
o Low risk of anaphylaxis
• Ascorbic acid (vitamin C) enhances • Reticulocyte response should be evident w/in 1
absorption of non-heme iron week, Hb expected to increase by 10g/L every 7-10d
• Polyphenols and phytates (found in tea /
coffee) can inhibit non-heme iron absorption

Megaloblastic Anemia

• Due to impaired DNA synthesis caused by deficiencies of vitamin B12 or folate, or due
to impaired DNA / RNA metabolism (drugs, myelodysplasia)
• Characterized by hypersegmented neutrophils on blood film
• Reticulocyte response evident in 3-4d, Hb improves by day 10, full resolution in 2
months
• Neurologic deficits may take 6 months or more to resolve, some may persist
• Risk of hypokalemia in older patients on diuretics for heart failure (obtain baseline
potassium, monitor, and supplement as needed)

• Vitamin B12 deficiency: can present with anemia, macrocytosis, pancytopenia,

neurologic complications e.g. dementia, weakness, sensory neuropathy, paresthesias
o Low-normal or normal serum vitamin B12 may be seen when deficient and responds to
supplements
o Need high index of suspicion, especially in older adults
o Meat and dairy are the only diet sources
o Strict vegans at risk
o Vegetarians may be at risk during high demand (e.g. pregnancy)
o Most common cause of deficiency is malabsorption due to pernicious anemia,
gastrectomy, gastritis, ileal resecrtion, Crohn’s, pancreatic insufficiency, certain drugs
(e.g. metformin, PPIs)

• Folate deficiency
o Most commonly caused by dietary deficiency and alcoholism
o Increased requirements in pregnancy, haemolytic anemia, and with use of certain
medications (e.g. methotrexate, phenytoin, trimethoprim)

• Nonpharmacologic Choices: normal dietary intake of vitamin B12 and folate

19
 o In case of neurologic deficits due to B12 deficiency -> need pharmacologic treatment
o Abstinence from alcohol may be necessary

Pharmacologic Choices

Vitamin B12 Folic Acid

• Treat with either cyanocobalamin or hydroxocobalamin
• Daily requirement: 6-9 mcg
• Doses > 100 mcg/d not absorbed but not tocity • Replacement doses: 1-5 mg/d
• Tend to give more than less, especially if neurological • Give only for confirmed folate
deficits deficiency or in situations of
• High dose oral vitamin B12 effective, but limited by increased demand
compliance and need for monitoring • Ensure patients do not have
• Approach: parenteral vitamin B12 until neurologic and concomitant vitamin B12 deficiency
hematologic findings resolve, maintenance route based on
patient’s circumstances

Anemias Responsive to Erythropoiesis Stimulation

• Chronic renal failure, HIV patients on ARVs, chronic Hep C patients on ribavirin,
chemotherapy patients (for non-hematologic cancers), surgery patients, low-risk myelodysplasia
• Select patients to treat based on endogenous EPO levels
• Ensure adequate iron supply along with EPO use
• Choices: Epoetin (Eprex) given 3x/wk, Darbepoetin (Aranesp) given once per 1-4 weeks
• Significant potential for toxicity
• Rapid/excessive correction of anemia can lead to HTN, seizures (monitor HTN 3x/wk initially,
then after each dose)
• Erythrocytosis can predispose to thrombosis
• Risk of pure red cell aplasia -> profound anemia

Key Features
1. Assess the risk of decompensation of anemic patients (e.g., volume status, the presence of
congestive heart failure [CHF], angina, or other disease states) to decide if prompt transfusion
or volume replacement is necessary.

2. In a patient with anemia, classify the anemia as microcytic, normocytic, or macrocytic by

using the MCV (mean corpuscular value) or smear test result, to direct further assessment and
treatment.

3. In all patients with anemia, determine the iron status before initiating treatment.

4. In a patient with iron deficiency, investigate further to find the cause.

5. Consider and look for anemia in appropriate patients (e.g., those at risk for blood loss [those
receiving anticoagulation, elderly patients taking a nonsteroidal anti-inflammatory drug]) or in
patients with hemolysis (mechanical valves), whether they are symptomatic or not, and in those
with new or worsening symptoms of angina or CHF.

20
6. In patients with macrocytic anemia:
a) Consider the possibility of vitamin B12 deficiency.
b) Look for other manifestations of the deficiency (e.g., neurologic symptoms) in order to make
the diagnosis of pernicious anemia when it is present.

7. As part of well-baby care, consider anemia in high-risk populations (e.g., those living in
poverty) or in high-risk patients (e.g., those who are pale or have a low-iron diet or poor weight
gain).

8. When a patient is discovered to have a slightly low hemoglobin level, look carefully for a
cause (e.g., hemoglobinopathies, menorrhagia, occult bleeding, previously undiagnosed
chronic disease), as one cannot assume that this is normal for them.

9. In anemic patients with menorrhagia, determine the need to look for other causes of the
anemia.

Antibiotics - Key Features

1. In patients requiring antibiotic therapy, make rational choices (i.e., first-line therapies,
knowledge of local resistance patterns, patient’s medical and drug history, patient’s context).

Otitis media

- Etiology – viral, Strep pneumonia, H. Influenza, M.catarrhalis

o If perforation or tubes consider staph aureus, Pseudomonas aeruginosa or virridans
strep
- Consider watchful waiting or delayed antibiotics
- Antibiotics SHOULD be given if <6 months, > 39 fever, immunodeficient, craniofacial
abnormalities, heart or lung disease, history of otitis media complications and Down’s
syndrome
- Amoxicillin first line treatment 75-90 mg/kg/day po divided q12h.
o Clarithromycin alternate for Betalactam allergy

Chronic Rhinosinusitis

- Bacterial more likely if symptoms lasting longer than 10 days or symptoms worsening
more than 5 days
- Etiology - >90% start as viral then Strep pneumonia, H. Influenza, M catarrhalis. If
chronic – Staph aureus, Grp A strep, enterobacteriacea, anaerobes
- 70% will resolve spontaneously – resever antibiotics for severe symptoms or moderate
symptoms that don’t improve in 7-10 days or get worse
- Amoxicillin first line treatment. Amox-clav for chronic sinusitis

21
 o TMP/SMX or doxycycline for betalactam allergy

Soft tissue infections

Impetigo
- Staph aureus, Grp A Strep
- Give systemic antibiotics if multiple, extensive or recurrent lesions, fever, constitutional
symptoms, lymphadenopathy, immunocompromised, valvular heart disease
- Mild symptoms - topical Mupirocin 2% or Fusidic acid 2%
- Systemic antibiotics – Cloxacillin or Cephalexin
o For betalactam allergy – erythromycin or clindamycin
Folliculitic or Furuncles
- Usually self-limited not requiring antibiotic treatment. Treat with systemic antibiotics if
on scalp
- If recurrences treat carrier state with mupirocin 2% topically to nares for 3-5 days
- Hot tub folliculitis may be due to Pseudomonas which is also usually self-limiting but if
severe can be treated with Ciprofloxacin
Cellulitis
- Do thorough history to rule out bites, dermatitis, foreign body, tinea, vascular causes
- Mild – cloxacillin or cephalexin
- Severe non-facial – cefazolin or clindamycin
- Severe facial – Cefazolin or cetriaxone
- Alternate for Betalactam allergy is clindamycin
Pharyngitis
- >90% viral and do not require antibiotics. Antibiotic treatment can be delayed while
waiting for swab
- Conjunctivitis, cough, hoarseness, rhinorrhea and diarrhea suggest viral etiology
- If bacterial – Group A strep, all other causes are rare
- Goals of antibacterial treatment are to prevent rheumatic fever, shorten course by 1 day
and prevent transmission
- Amoxicillin first line
o Erythromycin for betalactam allergy

Urinary Tract Infections

Acute cystitis
- First line
• SMP/TMX (be aware of local resistance patterns)
• Nutrofurantoin – not if CrCl <40
Recurrent cystitis < 1month
- Do cultures
- First line SMP/TMX or Nitrofurantoin
In pregnancy
- Do follow up cultures
- First line
o Amoxicillin
o Nitrofurantoin <36 weeks
Complicated UTI
- Men, obstruction, chronic catheter structural abnormalities, spinal cord injuries
- First line SMP/TMX or IV amp and gent

22
 - Consider culture and sensitivities
Pyelonephritis
- First line cipro for outpatient, IV amp and gent for inpatients
Prostatitis
- First line SMP/TMX or Cipro or IV amp and gent

Pneumonia

- Most common mycoplasma pneumonia, chlamydophylia pneumonia and strep

penumoniae
- First line Amoxicilin or macrolide (erythromycin, azithromycin or clarithromycin),
second line Doxycycline.
- IF comorbidities (COPD, diabetes, malignancy, renal failure, heart failure, alcoholism
etc.) but NO antibiotics or po steroids in past 3 months –
o All above etiologies plus H. Influenzae, M. Catarrhalis
o First line Azithromycin, clarithromycin or Doxycycline
- IF comorbidities AND antibiotics or po steroied in past 3 months –
o Above etiologies plus M. Catarrhalis, legionella pneumophilia
o Use
• Amox or amox/clav PLUS macrolide or doxy
• OR Respiratory fluroquinolone (levofloxacin, moxifloxacin)
- Nursing home residents
o chlamydophylia pneumonia, strep penumoniae, H. Influenzae, staph aureus, gram
negative rods, aspiration pneumonia
o Use
• Amox or amox/clav PLUS macrolide or doxy
• OR Respiratory fluroquinolone (levofloxacin, moxifloxacin)
- In hospitalized patients – treatment within 4 hours can decrease mortality
- In patients with antibiotic usage in the past 3 months, select an antibiotic from a
different class
- If pneumonia onset is >5 days from admission to hospital resistant organisms are more
likely to be present
- If at risk for MRSA
o Consider in athletes, military, inmates, very young, aboriginal, IVDU
o Add SMP/TMX, clindamycin, vancomycin or linezolid
- Aspiration pneumonia
o Oral anaerobes
o Consider if loss of consciousness, seizures, alcohol or drug overdose
o First line amox/clav or cefuroxime
• Second line clindamycin OR metronidazole PLUS fluoroquinolone
- Pseudomonas pneumonia
o Consider if in ICU, cystic fibrosis, HIV, structural lung disease, bronchiectasis
o First line Ciprofloxacin OR levofloxacin PLUS one of imipenem, meropenem,
cefrazidime, cefepime or pip-tazo

2. In patients with a clinical presentation suggestive of a viral infection, avoid prescribing

antibiotics.

3. In a patient with a purported antibiotic allergy, rule out other causes (e.g., intolerance to
side effects, non-allergic rash) before accepting the diagnosis.

23
- Approximately 85-90% of patients with reported penicillin allergies who undergo skin testing
do not have positive skin tests and are able to tolerate penicillins
- Differentiate between types of reactions as Type 1 carries risk of anaphylaxis if patient re-
exposed
- Do thorough history of reaction including time since last reaction (penicillin IgE Ab decrease
over time)
- Referral to allergy specialist is recommended
- Delayed cutaneous reactions more common if concurrent viral infection esp EBV
- Patients with history of Stevens-Johnson syndrome, toxic epidermal necrolysis, hypersentivity
syndrome or other exfoliative dermatoses should not be re-exposed under any circumstance

4. Use a selective approach in ordering cultures before initiating antibiotic therapy.

Usually do not order cultures in uncomplicated cellulitis, pneumonia, urinary tract infections, and
abscesses. For elderly patients – do not culture urine if not symptomatic. Do order cultures for
assessing community resistance patterns, in patients with systemic symptoms, and in
immunocompromised patients

5. In urgent situations (e.g., cases of meningitis, septic shock, febrile neutropenia), do not delay
administration of antibiotic therapy (i.e., do not wait for confirmation of the diagnosis).

Suspected
Empiric treatment Other considerations
condition
<1 month: Amp +cefotaxime
1-24 months: Vanco + ceftriaxone or
cefotaxime
Meningitis
2-50 years: Vanco + ceftriaxone or cefotaxime
>50 year: Vanco + ceftriaxone or cefotaxime +
amp
Septic shock Obtain cultures Assess for risk of pseudomonal
infection

24
 Empiric therapy

- Vancomycin PLUS one of

cefriaxone, cefotaxime, pip-tazo,
imipenem, meropenem
Initiate anti-pseudomonal beta-lactam ie:
cefepime, meropenem, pip-tazo Consider addition of an anti-
Febrile
Add other antibiotics in patients with focal fungal drug after 4-7 days in high
neutropenia
findings, complicated presentations or risk patients
demonstrated antimicrobial resistance

Anxiety - Key Features

1. Do not attribute acute symptoms of panic (e.g., shortness of breath, palpitations,

hyperventilation) to anxiety without first excluding serious medical pathology (e.g., pulmonary
embolism, myocardial infarction ) from the differential diagnosis (especially in patients with
established anxiety disorder).

2. When working up a patient with symptoms of anxiety, and before making the diagnosis of an
anxiety disorder:
a) Exclude serious medical pathology.
b) Identify:
- other co-morbid psychiatric conditions
- abuse.
- substance abuse.
c) Assess the risk of suicide.

3. In patients with known anxiety disorders, do not assume all new symptoms are attributable
to the anxiety disorder.

4. Offer appropriate treatment for anxiety:

- benzodiazepines (eg. deal with fear of them, avoid doses that are too low or too high, consider
dependence, other anxiolytics).
- non-pharmacologic treatment.

5. In a patient with symptoms of anxiety, take and interpret an appropriate history to

differentiate clearly between agoraphobia, social phobia, generalized anxiety disorder, and
panic disorder.

Physical causes: (always rule these out before making diagnosis)

• Cardiovascular: angina, arrythmias, CHF, HTN, hypovolemia, MI, syncope

• Dietary: caffeine, MSG, vitamin-deficiency diseases
• Drug-related: akathisia (2nd antipsychotic Rx), anticholinergic toxicity, digitalis
toxicity, hallucinogens, hypotensive agents, stimulants, withdrawal symptoms,
bronchodilators
• Immunologic: anaphylaxis, SLE

25
 • Metabolic:Cushing’s disease, hyperkalemia, hyperthermia, hyper/hypothyroidism,
hypocalcemia,hypoglycemia, hyponatremia
• Neurologic: encephalopathies, essential tremor, intracranial mass lesions, post-
concussive syndrome, seizure disorders, vertigo
• Respiratory: asthma, COPD, pneumonia, pneumothorax, pulm edema, PE
• Secreting tumors: carcinoid, insulinoma, pheochromocytoma

Drugs that can cause anxiety like symptoms:

• Stimulants (amphetamine, caffeine, cocaine, etc)

• Sympathomimetics (ephedrine, epinephrin, pseudoephedrine)
• Anticholinergics (cogentin, benadryl, demerol, TCA’s etc)
• Dopaminergics (sinimet, metoclopramide, neuroleptics, levodopa, etc)
• Miscellaneous (baclofen, cycloserine, hallucinogens, indomethacin)
• Drug withdrawal (barbitruates, benzos, narotics, alcohol, sedatives)

Be aware of risk of suicide in anxiety patients:

Risk Factors: “SAD PERSONS”

• Sex-male
• Age >60
• Depression
• Previous attempts
• Etoh
• Rational thinking loss (nuts-o)
• Suicide in family
• Organized plan
• No spouse/supports
• Serious illness

Patients with 0-2 of the above RF’s can be sent home. Those with 3-4 should be followed closely,
and hospitalization should be considered. Those with 5-6 should be strongly considered for
hospitalizations.

Risk Factors:
Family Hx of GAD, stressful life events, Hx of childhood emotional/ physical abuse/witnessing
trauma

GAD
Excessive worry & anxiety that are difficult to control, cause significant distress and impairment,
occurs in most days of at least 6 months period. 3 or more of:

• Restlessness
• Easy fatigability
• Difficulty concentrating
• Irritability
• Muscle tension

Management:

26
 Medications:
1. SSRIs: Paroxetine (20mg), Sertraline(50mg), Citalopram( 20mg),escitalopram(10mg),
Fluxetine(20mg),Fluvoxamine(50-100mg)
2. SNRIs: Venlafaxine XR 75-225 mg/day, Duloxetine
3. TCAs: Imipramine
4. BNZ: Alprazolam, lorazepam, oxazepam,chlordiazepoxide, diazepam,Clonazepam,
alprazolam
5. Other: Buspirone 10-20 mg tid (same effect of oxazepam w/o risk of dependence),
Pregabaline, Mirtazepine (refractory anxiety and insomnia), Quetiapine, Herbals
CBT
Combination of CBT & Meds

SSRI and SNRI are the 1st line meds, all meds take up to 4 weeks to effect, can use BNZ
meanwhile until 1st line meds take effect, continue Tx for 12 months
Always look for physical and drug causes before starting on anxiety medications

Panic Attack/Disorder
A discrete period of intense fear or discomfort in which ≥4 of following develops suddenly,
reaches to peak in 10 min, lasts usually <1hour

•Palpitation, pounding heart, ↑HR

•Sweating
•Trembling/shaking
•Feeling of choking
•Chest pain or discomfort
•Nausea/ Abdo distress
•Dizziness/lightheadedness/fainting
•Derealization/Depersonalization
•Fears of loosing control/getting crazy
•Fear of dying
•Chills/Hot flashes
•Paresthesia/numbness

Mnemonic: STUDENTS fear of 3Cs

Sweating, trembling, unsteadiness, deralizaition/depersonalization, excess Temp/HR, Nausea,
Tingling, syncope, fear of dying, chest pain, chills, choking
Panic disorder: Recurrent panic attacks with ≥1 of: Fear/worry of future attacks, Change in
behavior due to fear of attacks, phobic avoidance of situation that can trigger the attack
Management:

1. SSRIs:all SSRIs are effective equally

2. SNRIs
3. TCAs: Clomipramine, Imipramine, Nortriptyline
4. BNZ: Clonazepam(0.5-4mg), Alprazolam(0.5-6mg), Lorazepam(0.5-6mg)
5. MOAIs: Phenelezine, Meclobemide
6. CBT: very effective

Continue Tx for 1 year then reassess

27
Agoraphobia
Anxiety about or avoidance of certain situations where help may not be available or it would be
embarrassing or difficult to leave the situation if panic Sx happens. Situations are like waiting in
lines, crowds, grocery stores, shopping malls, movies, driving, flying, public transport,
doctors/dentist appointments, away from home
Management:

CBT
Antidepressants
BNZ short term

Specific Phobia
Significant anxiety associated with a specific object or situation that typically leads to avoidance
behavior
Like:Animals, insects, flying, height, water, closed spaces
Management: Exposure therapy (CBT), Systematic Desentisitization (CBT), Relaxation/breathing
therapy, Meds are 2nd line: BNZ(Lorazepam 0.5-2mg 30 minutes before exposure), Cycloserine

Social Anxiety Disorder (SAD) /Social Phobia

Excessive fears of scrutiny, embarrassment and humiliation in social or performance situations,
leading to significant distress and/or impairment in functioning
Types: generalized social fears, in most interpersonal and performance situations, and SAD with
discrete fears in only to 1- few situation
Management: generalized SAD( all meds for GAD), Specific SAD(Propranolol 20-60mg, 30 min
before situation, Lorazepam ), CBT

SSRIs side effects:

Serotonin syndrome (lethal, agitation, delirium,↑HR, HTN,↑T, tremor, GI distress, myoclonus,
hyperreflexia: D/C SSRI, BNZ, Cyproheptadine), sexual dysfunction, Wt gain, drowsiness, dry
mouth, blurred vision, constipation, nausea

Table 1. Diagnostic Criteria for CG*

Note: Patients must meet all 3 criteria to be diagnosed with CG.

Criteria Description
Yearning and heartache for the deceased at least daily or to the extent that it
significantly distresses individuals and/or disrupts their functioning.
Criterion
A
Do you feel yourself yearning/longing frequently for the person who has gone?
How is this impacting your life?
Criterion The person must experience 4 of the following 8 symptoms at least several times a day
B or to a distressing or disruptive degree:

1. Difficulty accepting the death. Are you having trouble accepting the loss of ____?
2. Difficulty trusting others. Has it been hard for you to trust other people since the
loss of ___?
3. Difficulty moving on with one’s life. Do you feel that moving on (for example,
making new friends) would be difficult?
4. Excessive bitterness or anger about the death. Do you feel angry about the loss of

28
 ____?
5. Numbness/detachment from others. Do you feel emotionally numb or detached from
others since the loss of ____?
6. Life is empty or meaningless without the deceased. Do you feel that life is empty or
meaningless without ____?
7. Lack of hope for the future. Do you feel that the future holds no meaning, hope or
possibility for fulfilment without ____?
8. Agitation. Do you feel jumpy or on edge since ____ died?
Criterion The above symptoms cause marked, persistent dysfunction in multiple domains (e.g.,
C social, occupational).
 Note: These diagnostic criteria do not appear in the Diagnostic and Statistical Manual of
Mental Disorders, Fourth Edition (DSM-IV). To date, CG has not been categorized as a
mental disorder.

DIAGNOSIS
14. Although people experiencing uncomplicated grief may initially exhibit some of the
symptoms of CG, by six months post-loss, their distressing feelings will have diminished in
intensity. They begin to accept the loss and to re-establish a balance in their lives.2;3
a. Those patients exhibiting symptoms (Table 1) for more than six consecutive months can be
diagnosed with CG.3
b. A diagnosis can be made regardless of when the six-month period of symptoms occurs in
relation to the loss. For most people diagnosed with CG, however, there is no delay in symptom
onset. More commonly, “their grief has been intense and unrelenting since the death.”4
15. There is some diagnostic overlap between CG and other psychiatric disorders including: 20
• major depressive disorder (MDD): sadness, loss of interest, loss of self esteem, guilt
• post-traumatic stress disorder (PTSD): triggered by a traumatic event or a shock; may be
manifested by feelings of helplessness, visualization of intrusive images and avoidance behaviour

16. Research has found, however, that CG is both “distinctive and distinguishable” from MDD
and PTSD.21-23 Careful assessment can help to distinguish between these disorders.
• For example, CG-related guilt is usually limited to the death of a loved one; thoughts of death
are related to a desire to be reunited. MDD, on the other hand, “is associated with more global
feelings of worthlessness and thoughts of death with suicide.”24
• The diagnosis of MDD and PTSD can be made before the typical six-month period required for
CG.
17. Co-morbidities are common in CG. In one U.S. study of 206 patients diagnosed with CG,
75% had some psychiatric co-morbidity, the most prevalent being MDD (55%) and PTSD
(48%).25 This finding is consistent with other studies using referral populations.17 Standard
practice guidelines can guide the diagnosis and treatment of MDD and PTSD

Asthma - Key Features

1. In patients of all ages with respiratory symptoms (acute, chronic, recurrent):

a) Include asthma in the differential diagnosis
b) Confirm the diagnosis of asthma by appropriate use of: history, physical examination,
spirometry

CLINICAL FEATURES: Recurrent:

29
 Symptoms Signs Airway Obstruction
Frequent episodes breathlessness Wheezing
Chest tightness Tachypnea
Wheezing (Worse at night or early am) Decreased breath sounds
Cough (Worse at night or early am) Accessory muscle use
Triggers: URTI, aeroallergens, irritants, exercise Supraclavicular/intercostal in-drawing
Improve w/ bronchodilators, ICS Nasal flaring

DIAGNOSIS: Suspect from clinical features, objective measures of airflow obstruction

for Dx:

Pulmonary Function
Children (>6yrs) Adults
Measurement
Spirometry (preferred)
<Normal lower limits (<0.8- <Normal lower limits (<0.75-
Reduced FEV1/FVC
0.9) 0.8)
AND
AND AND
Increase FEV1 with Tx*
≥ 12% ≥ 12% (& min ≥200 mL)
Peak Expiratory Flow (alternative)
60L/min (minimum ≥ 20%)
Increase w/ Tx*
≥ 20%
OR
OR >8% based on BID readings
Not recommended
Diurnal Variation >20% based on multi day
readings
Positive Challenge Test (alternative)
PC20<4mg/mL (4-16 mg/mL = borderline, >16 mg/mL is
Methacholine challenge
negative)
OR
OR
Exercise challenge
≥10-15% decrease in FEV1 post-exercise
 Treatment = after bronchodilators or course of controller therapy

2. In a child with acute respiratory distress, distinguish asthma or bronchiolitis from croup and
foreign body aspiration by taking an appropriate history and doing a physical examination.

• FB: Hx, asymmetric, monophonic wheeze (only 1 tone), unilateral hyperinflation or FB on CXR
• Croup: swelling of vocal cords → barking cough, causes: 1)viral (75% parainfluenza)
2)bacterial (diphtheria) 3)allergies/inhaled irritants 4)GERD. URTI, + nighttime, typically 5-6d

3. In a known asthmatic, presenting with an acute exacerbation or for ongoing care,

objectively determine the severity of the condition (e.g. with history, including pattern of
medication use, PE, Spirometry). Don’t underestimate severity.

Asthma Severity (Method of Canadian Consensus)

30
Severity Mild Moderate Severe
FEV1/PEF >80% 60-80% <60%
SABA use <Q8h Q4-8h Q2-4h
Near fatal episode - - +
Hospital admission - - +
Nighttime symptoms -/+ + +++
Daily activity limitations -/+ +/++ +++

SABA=short acting β-agonist, FEV=forced exp volume, PEF=peak exp flow Symptom
not reported -, reported +, reported more often ++ and +++

Asthma Control Criteria

Characteristic Frequency or Value
Daytime symptoms <4 days/week
Nighttime symptoms <1 night/week
Physical activity Normal
Exacerbations Mild, infrequent
Work/school agonist None
β-agonist <4 doses/week
FEV1 or PEF ≥90% personal best
PEF diurnal variation <10-15%

4. In a known asthmatic with an acute exacerbation:

a) Treat the acute episode (e.g. β-agonists repeatedly and early steroids, and avoid under-
treatment).
b) Rule out co-morbid disease (e.g. CHF, COPD).
c) Determine the need for hospitalization or D/C (basing the decision on the risk of recurrence
or complications, and on the patient’s expectations and resources).

5. For the ongoing (chronic) treatment of an asthmatic propose a stepwise management plan
including:

31
a) self-monitoring
b) self-adjustment of medication
c) when to consult back
• Create an Asthma Action Plan

6. For a known asthmatic patient, who has ongoing or recurrent symptoms:

a) Assess severity & compliance with med regimens
b) Recommend lifestyle adjustments (e.g. avoiding irritants, triggers) for less recurrence &
better control

Atrial Fibrillation - Key Features

1. In a patient who presents with new onset atrial fibrillation, look for an underlying cause
(e.g., ischemic heart disease, acute myocardial infarction, congestive heart failure,
cardiomyopathy, pulmonary embolus, hyperthyroidism, alcohol, etc.)

2. In a patient presenting with atrial fibrillation,

a) Look for hemodynamic instability,
b) Intervene rapidly and appropriately to stabilize the patient.

3. In an individual presenting with chronic or paroxysmal atrial fibrillation,

a) Explore the need for anticoagulation based on the risk of stroke with the patient,
b) Periodically reassess the need for anticoagulation.

4. In patients with atrial fibrillation, when the decision has been made to use anticoagulation,
institute the appropriate therapy and patient education, with a comprehensive follow-up plan.

5. In a stable patient with atrial fibrillation, identify the need for rate control.

6. In a stable patient with atrial fibrillation, arrange for rhythm correction when appropriate.

32
AF is the most common cardiac arrhythmia in adults; prevalence increases with age Pts with
untreated AF are at a 5-fold increase for complications including: Thromboembolism, Stroke,
Myocardial Ishcemia/Infarction, Heart Failure

Patients may be asymptomatic, have mild symptoms (e.g., palpitations, weariness, and reduced
exercise capacity), or may have more severe symptoms (e.g., syncope, hear t failure or angina).
Dyspnea, chest pain and palpitations are the most common presenting symptoms in emergency
admissions.

AF can present with or without an associated underlying condition. A predisposing condition

(both cardiac and non-cardiac) exists in > 90% of cases. Associated cardiac conditions are usually
much more common (up to 80%).

Definitions:
Proxysmal AF – terminates spontaneously in <7 days
Persistent AF - >7days; not self-terminating
Permanent AF – cardioversion failed

Management:
Initial management strategies depend on the patient’s presentation
Acutely unwell patients (rapid AF with hypotension, syncope, chest pain, dyspnea, heart failure
or neurological symptoms) require urgent rate control and possibly emergency cardioversion in a
hospital setting. Stable patients require medication to slow heart rate and prevent emboli.

Long term management will include rate and/or rhythm control strategies. As well, all patients
with AF should be stratified using a predictive index for stroke (e.g. CHADS) and for the risk of
bleeding (e.g. HAS-BLED), and most patients should receive antithrombotic therapy.

Several RCTs and meta-analyses have concluded there are no differences between rate and
rhythm control strategies in terms of mortality, cardiovascular events or stroke.

1. Rate Control:
Beta blocker is the preferred rate control drug, compared to a calcium channel blocker, in patients
with angina, previous MI, or left ventricular systolic dysfunction. Digoxin, a second-line choice,
is reserved for rate control in patients who are sedentary or who have left ventricular systolic
dysfunction and it may be useful as an adjunct to beta blockers and calcium channel blockers in
patients whose heart rate remains uncontrolled.

2010 Canadian guidelines recommend aiming for a “resting heart rate of less than 100 bpm”.

2. Rhythm Control:
Anit-arrhythmics are recommended for patients with AF who remain symptomatic with rate
control therapy or in whom rate control therapy is unlikely to control symptoms. Anti-arrhythmic
drugs should be avoided in patients with AF who have advanced sinus or AV nodal disease,
unless the patient has a pacemaker/ implantable defibrillator.

3. Cardioversion:
Direct-current and pharmacologic cardioversion impose similar risk of thromboembolism,
particularly if the arrhythmia has been present for more than 48 hours. Therefore, anticoagulation
prophylaxis must be initiated before the procedure.

33
Pharmacologic cardioversion raises the risk of torsades de pointes and other serious arrhythmias.
Pharmacologic cardioversion is most effective within seven days of AF onset.

Direct-current cardioversion is more effective than pharmacologic cardioversion when biphasic

shocks are used.

When urgent cardioversion is needed, recommendations include a screening transesophageal

echocardiograph and immediate anticoagulation with either unfractionated IV heparin or low-
molecular- weight heparin, prior to cardioversion.

If no thrombus is seen on TEE, convert to oral anticoagulation after cardioversion and

continue for at least four weeks — even if sinus rhythm is maintained.
If a thrombus is seen on TEE, cardioversion should be postponed and anticoagulation
should be continued indefinitely.

For patients with AF of 48-hours or longer (or when the duration of AF is unknown), full
anticoagulation is recommended for at least three weeks before and four weeks after
cardioversion, regardless of the whether electrical or pharmacological cardioversion is used.

4. Rhythm Maintenance:
Sinus rhythm will be maintained in approximately 20–30% of patients without the need for long-
term antiarrhythmic drug therapy. However, despite treatment, approximately 50–85% of patients
relapse to AF by 12 months.

Choice of agent is based on left ventricular function. When function is normal, preferred agents
are: dronedarone, flecainide, propafenone, or sotalol. However, flecainide and propafenone
should not be used if CAD is present. When left ventricular function is abnormal (EF < 35%),
amiodarone would be the preferred agent.

Overall, most patients converted to sinus rhythm from AF should not be placed on long-term
rhythm maintenance therapy, as the risks of antiarrhythmic drugs outweigh the benefits.

5. Ablation Therapy:
Catheter ablation is recommended for AF in patients who remain symptomatic following
adequate trials of anti-arrhythmic drug therapy. Catheter ablation is superior to antiarrhythmic
drug therapy in preventing recurrences and reducing symptoms.

6. Antithrombotic Therapy:
Stroke is the major complication of AF, and the strokes related to AF tend to be more severe than
strokes from other causes.

Decisions about antithrombotic therapy for individual patients are best informed by stratifying
each patient with AF using a predictive index for risk of stroke (e.g. CHADS ) and for risk of
bleeding (e.g. HAS-BLED).

Anticoagulation with dabigatran or warfarin reduces the risk of stroke by 50–68% Aspirin
reduces the risk of stroke by about 22–36%.

ofIt is recommended that most patients with a CHADS2 >1 receive anticoagulant therapy, either
warfarin or dabigatran.

34
For patients who are at increased risk for stroke but cannot or will not take warfarin or
dabigatran, the addition of clopidogrel to ASA may remain as an option.

Aspirin should not be added to an oral anticoagulant for AF patients without compelling
indications for antiplatelet therapy (such as the presence of CAD), even for patients with AF who
suffer an ischemic stroke or TIA despite therapeutic anticoagulation.

Bad News - Key Features

Always remember that giving bad news is any news that drastically and negatively alters the
patient’s view of his/her future. This is not always a terminal diagnosis (ie. DMT2).

1. When giving bad news, ensure that the setting is appropriate and ensure patient’s
confidentiality.

Setting up the interview – find a private, quiet and comfortable location to meet with the
patient. Ensure a safe, neutral environment. Prior to meeting, review with patient who
they would like to be present in the interview (ie. spouse, family member, friend). Make
sure to have your pager and phone turned off so you will not be interrupted. Prior to
meeting, review clinical information, mentally rehearse (ie. words/phrases) and prepare
yourself emotionally.

Position – make sure to introduce yourself to all individuals present. Maintain appropriate
body language through the interview. Sit at equal height to the patient, keep an open
posture and make eye contact as comfortable. Use touch as appropriate.

Patient perception – invite the patient to share their own knowledge and ideas about their
illness. Open-ended questions facilitate discussion ie. “What is your understanding as to
why we performed the MRI?”

Invitation – determine what and how much information the patient is hoping to gain ie.
“How many details would you like to know about your condition?”

Knowledge – offer information to the depth that they would like to know and attempt to
deliver in fashion aligning with their own perceptions. Avoid medical jargon.

Emotion/empathy – demonstrate compassion, allow for emotional expression and give

time for silence.

Summary/strategy – summarize discussion and devise a clear future plan. Although there
may not be a cure, always focus on small goals. Ask permission to have discussion
regarding future treatment option (ie. analgesia for pain control). Make sure patient and
others attending meeting have contact information for yourself, in case they have further
questions, as well as for support services (ie. social worker) for ongoing care.

2. Give bad news:

• In an empathetic, compassionate manner
– demonstrate sympathy and understanding throughout your communication.
• Allowing enough time
– make sure to set aside adequate time for meeting and make sure you will not be interrupted

35
(turn off pager and cell phone). Proceed at the patient’s pace.
• Providing translation, as necessary
– if language barrier present make sure to have professional translator (not a family member).
Avoid use of medical jargon.

3. Obtain patient consent before involving the family.

• Speak with patient privately about whom they would like to involve (if anyone) and to what
capacity they would like them to participate in the sharing of information.
• It is very important that the patient decides on their own, without influence what significant
others they would like to be present at the meeting.
• Emphasize patient confidentiality.

4. After giving bad news, arrange definitive follow-up opportunities to assess impact and
understanding.
• Explore what the news means to the patient.
• Arrange follow-up appointment to check in with patient and address any further questions that
may arise.
• Connect patient and family with social worker for ongoing support if given permission.
• Inform of any additional services in the community such as support groups for both patient and
significant others (interdisciplinary resources).
• Address your own needs (debriefing may be appropriate).

Behavioural Problems - Key Features

1. Because behavioural problems in children are often multifactorial, maintain a broad

differential diagnosis and assess all factors when concern has been raised about a child’s
behaviour:
• Look for medical conditions (e.g., hearing impairment, depression, other psychiatric
diagnoses, other medical problems).
• Look for psychosocial factors (e.g., abuse, substance use, family chaos, peer issues, parental
expectations).
• Recognize when the cause is not attention deficit disorder (ADD) (e.g., learning disorders,
autism spectrum disorder, conduct disorder).

Medical Conditions:

Medical evaluation consists of history review and physical exam to discern presence of biologic
risks (eg. prenatal or perinatal insults) or medical problems associated with behavioural problems
(eg. hypothyroidism, lead poisoning, etc). Please see Table 1 below for aspects of the history that
particularly relate to development and behaviour. Aspects of the physical exam that particularly
relate to behavioural problems are highlighted in Table 2.

The University of Utah provides a video for guidance in conducting a pediatric

neurodevelopment exam (available at:
library.med.utah.edu/pedineurologicexam/html/home_exam.html):

- Head circumference should be monitored for microcephaly, macrocephaly, and

increased or decreased growth velocity.
- Weight and height should be monitored for growth deficiency.

36
 - The child should be assessed for dysmorphology, including both minor (eg,
hypertelorism, micrognathia) and major congenital anomalies (eg, spina bifida, midline
defects).
- The eyes should be examined for acuity, poor tracking, strabismus, or cataracts.
- The ears should be evaluated for unusual shape or placement, recurrent acute otitis
media, or chronic otitis media with effusion; hearing acuity should also be assessed.
- The abdomen should be examined for hepatosplenomegaly, which may be a sign of
metabolic disease.
- The skin should be evaluated for neurocutaneous lesions.
- The neurologic examination should include assessment of primitive and protective
reflexes, symmetry, tone, muscle strength, and deep tendon reflexes.

Laboratory investigations should include evaluation for iron deficiency and lead poisoning.

Psychosocial Factors:

Psychosocial risk factors often are better predictors of developmental and behavioural disabilities
than are medical issues. Psychosocial risk factors focus on the parents’ challenges, including:

• Having less than a high school education

• Being single
• Being unemployed
• Mental health problems (of which depression or anxiety are particularly common)
• Housing/food instability
• Three or more children in the home
• Limited facility with the English language
• Limited literacy in any language
• Belonging to an ethnic minority
• Having a problematic parenting style (eg, not interested in teaching or conversing with
their children)

Psychosocial risks can be objectively evaluated using a measure such as the Family Psychosocial
Screen (FPS available online through Bright Futures). The FPS takes approximately 15 minutes
to administer and interpret (if an interview is required). It can be used as a clinic intake form so
that each patient receives only a single administration, although repeat administrations (often of
selected items, such as the two-item parental depression screen) are needed when family
circumstances change and to check on family well-being, especially in the first two years of life.
The FPS identifies risk factors for developmental and behavioral problems related to parents'
educational status, income, marital status, number of children in the home, parental mental health
problems, parents' history of abuse as a child, domestic violence, frequency of household moves,
etc. The presence of four or more such risk factors is associated with developmental delay. The
FPS also screens for maternal depression and substance abuse. Using larger inventories as the
gold standard, the FPS has a sensitivity and specificity of 90 percent in the detection of various
psychosocial risk factors.

Protective (sometimes called resilience) factors also tend to focus on parents, particularly on
positive parenting styles. Resilience is likely when parents actively (and age-appropriately) teach
children new things, label objects of interest, talk with children at meals, share books with their
children, perceive their child as able to be soothed, and are interested in conversing with their
children (including back-and-forth sound play in infancy, playing peek-a-boo, etc).

37
Other psychosocial risk factors as predictors of behavioural problems in children and adolescents
include substance use, abuse, unstable family life, peer issues and parental expectations.

Recognize when the cause is not ADHD

ADHD is a syndrome composed of three categories of symptoms: hyperactivity, impulsivity, and

inattention.

Consensus criteria for the diagnosis of ADHD have been defined by the American Psychiatric
Association and published in the Diagnostic and Statistical Manual of Mental Disorders-IV.
Several features of the DSM-IV criteria deserve emphasis:

• The symptoms must be present in more than one setting (eg, school and home)
• The symptoms must persist for at least six months
• The symptoms must be present before the age of seven years
• The symptoms must impair function in academic, social, or occupational activities
• The symptoms must be excessive for the developmental level of the child
• Other mental disorders that could account for the symptoms must be excluded

The symptoms of ADHD overlap with those of learning disabilities and behavioral and emotional
problems such as depression, bipolar disease, anxiety, or post traumatic stress disorder. These
disorders frequently coexist with ADHD and may or may not be responsible for the symptoms.
As an example, children who have learning disabilities may develop inattention as a result of
inability to understand new information. The use of broadband behavior scales and psychometric
testing may help to differentiate these problems from ADHD.

Other conditions to consider in children with symptoms of inattention, hyperactivity, and

impulsivity include (Table 3):

• Cognitive problems (intellectual disability [mental retardation], fragile X syndrome)

• Environmental factors (eg, stressful home environment, inappropriate educational
setting)
• Various medical conditions such as hearing or visual impairment, lead poisoning,
asthma, fetal alcohol syndrome, thyroid abnormalities, sleep disorder, and seizure
disorder (see appropriate topic reviews)

These conditions usually can be differentiated from ADHD because their symptoms fluctuate
with the course of disease. In contrast, the symptoms in ADHD are persistent and pervasive.

Table 1: Medical history in developmental surveillance

Prenatal Risk Factors

History of prenatal illness/infectious disease

Maternal drug/alcohol/tobacco use

Toxemia
Previous miscarriage or stillbirth
Maternal medications

38
 Perinatal Risk Factors
Prematurity, particularly gestational age ≤30 weeks

Very low birth weight (<1500 g)

Hypoxia
Seizures
Intraventricular hemorrhage
Meningitis
Sepsis
Severe hyperbilirubinemia
Failed newborn hearing screen
Pertinent past medical history
History of recurrent or chronic otitis media

Poor growth
Seizures
Vision and hearing concerns and assessment
Previous hospitalizations
Chronic illness (eg, asthma)
History of head trauma
Developmental and Behavioral History
Timeliness of acquisition of previous milestones

Sleep patterns and duration (eg, trouble falling asleep or staying asleep; symptoms of obstructive
sleep apnea)
Play interests

Table 2: Important aspects of the medical evaluation when assessing

behaviour/development

Physical examination Looking for:

Head circumference Microcephaly, macrocephaly, altered growth velocity
Weight and height Growth deficiency (failure to thrive, short stature), Overgrowth
General appearance Dysmorphic features
Eyes Visual acuity, tracking, strabismus, cataracts
Unusual shape or placement, signs of recurrent otitis media or chronic
Ears
otitis media with effusion, hearing acuity
Abdomen Hepatosplenomegaly
Skin Neurocutaneous lesions and vascular markings
Persistent primitive reflexes; abnormalities of symmetry, tone, strength,
Neurologic examination
deep tendon reflexes, protective reflexes
Laboratory
Looking for:
evaluation*
Hemoglobin/hematocrit Anemia
Blood lead level Lead poisoning

39
  Additional evaluation may be warranted for some children with historical or examination
findings suggestive of a medical etiology. The evaluation should be tailored to the
clinical findings and may include thyroid function testing, genetic testing, metabolic
screening, and/or neuroimaging or encephalography.

Table 3: Differential diagnosis for attention deficit hyperactivity disorder

Developmental
Normal variation

Mental retardation
Giftedness
Learning disability
Perceptual processing disorder
Language disorder
Pervasive developmental disorder
Emotional/Behavioral
Depression or mood disorder

Anxiety disorder
Oppositional defiant disorder
Conduct disorder
Obsessive compulsive disorder
Post-traumatic stress disorder
Adjustment disorder
Environmental
Child abuse or neglect

Stressful home environment

Inadequate or punitive parenting
Parental psychopathology
Sociocultural differences
Inappropriate educational setting
Frequent school absence
Medical
Sensory impairments

Seizure disorder
Sequelae of CNS infection/trauma
Fetal alcohol syndrome
Fragile X syndrome
Lead poisoning
Iron deficiency anemia
Neurodegenerative disorder
Tourette syndrome
Thyroid disorder
Diabetes mellitus
Substance abuse
Medication side effects (eg, bronchodilators, corticosteroids, isoniazid, neuroleptics)

40
Undernutrition
Sleep disorder
Enuresis/encopresis
Motor coordination disorder
Stereotypic movement disorder

Data from: Miller, KJ, Wender, EH. Attention deficit/hyperactivity disorder. In: Primary
Pediatric Care, 4th ed, Hoekelman, RA (Ed), Mosby, St. Louis 2001. p.756. Attention-deficit and
disruptive behavior disorders. In: Diagnostic and Statistical Manual of Mental Disorders, 4th ed,
Text Revision, American Psychiatric Association 2000.

2. When obtaining a history about behavioural problems in a child:

• Ask the child about her or his perception of the situation.
• - Use multiple sources of information (e.g., school, daycare).

Screening for behavioural problems may facilitate the detection of developmental, as well as
behavioural problems. Behavioural screening tests may be broadly or narrowly focused. Broadly
focused screens rely on parent-, teacher-, or child-completed questionnaires that, when socred,
have subsets that include multiple mental health cateories to screen for a broad range of possible
diagnoses (Table 4). Narrowly focused screens are directed toward a specific diagnosis (eg.
autism, ADD) (Table 5). For screening purposes, broad-band screening should precede narrow-
band screening.

Table 4: Selected broad-band behavioural screens

Time
Test/age range Purchasing information
frame*
Paul H. Brookes Publishing, Inc.
Ages and Stages
Questionnaire: P.O. Box 10624 About 10
Baltimore, MD 21285 minutes (if
Social-Emotional Phone: 800.638.3775 interview
(ASQ-SE) www.pbrookes.com needed)
3 to 66 months Cost of purchasing a specimen set: $149 (includes reproducible
questionnaires and users guide).
Pearson Assessments
Brief-Infant-
Toddler Social-
19500 Bulverde Road About 6
Emotional
San Antonio, TX 78259 minutes (if
Phone: 800.211.8378 interview
Assessment
www.pearsonassessments.com needed)
(BITSEA) (2006)
Cost of purchasing a specimen set: $105 (includes manual, 25
12 to 36 months
BITSEA parent forms, and 25 BITSEA teacher forms).
Conners Rating Pearson Assessments About 20
Scale-Revised minutes
Phone: 800.627.7271

41
 www.pearsonassessments.com
3 to 17 years Cost of purchasing a specimen set: $276 (includes manual and
25 quick score forms of various versions).
Eyberg Child
Psychological Assessment Resources
Behavior
Inventory/Sutter-
P.O. Box 998 About 5
Odessa, FL 33556 minutes (if
Eyberg Student
Phone: 800.331.8378 interview
Behavior Inventory-
www.parinc.com needed)
Revised
Cost of purchasing a specimen set: $120 (includes professional
(ECBI/SESBI-R)
manual, 50 ECBI and 50 SESBI-R test sheets).
2 to 16
PEDSTest.com, LLC

Parents' Evaluations 1013 Austin Court

of Developmental Nolensville, TN 37135
Phone: 615.776.4121 About 2
Status (PEDS) Fax: 615.776.4119 minutes
(2010) www.pedstest.com
Birth to 8 years Cost of purchasing a specimen set: $30 (includes 50 response
forms, 50 score and interpretation forms, and one brief
administration and scoring guide).
Pediatric Symptom
Checklist (PSC) and
Can be downloaded for free at:
About 3
Pictorial Pediatric minutes
www2.massgeneral.org/allpsych/psc/psc_forms.htm
Symptom Checklist
4 to 16 years
 Does not include score time.

Frances Page Glascoe, 2011, Nolensville, TN: PEDSTest.com, LLC, www.pedstest.com. Adapted
with permission.

Table 5: Selected narrow-band behavioural screens

Test/age range Purchasing information Time frame*

Conners Rating Scale- Pearson Assessments, Inc.
Revised (CRS-R)
Phone: 800.627.7271
(Subscales for Attention www.pearsonassessments.com About 20 minutes
Deficit Hyperactivity Cost of purchasing a specimen set: $276 (includes
Disorder) manual and 25 quick score forms of various
3 to 17 years versions).
Modified Checklist for Download for free at the First Signs Web site About 5 minutes
Autism www.firstsigns.org/downloads/m-chat.PDF (excluding follow-up
on any failed items)
in Toddlers (M-CHAT)
(1999)

42
16 to 48 months

3. When treating behavioural problems in children for whom medication is indicated, do not
limit treatment to medication; address other dimensions (e.g., do not just use amphetamines to
treat ADD, but add social skills teaching, time management, etc.).

Treatment for ADHD and other behavioural problems may involve medication,
behavioral/psychologic interventions, or educational interventions, alone or in combination.
Decisions regarding the choice of therapy should involve the patient and his or her parents, who,
in conjunction with the treating clinician, must weigh the risks and benefits to determine their
preferred management strategy. Some authors advocate a trial of behavioral interventions before
medical therapy is initiated. Others recommend a multimodal approach including medication,
counseling, and behavioral management, particularly for children with comorbid conditions.

Current guidelines recommend a management approach (pharmacotherapy and/or behaviour

therapy) that is designed to improve target symptoms and takes into account individual
circumstances and family preferences.

Behavioural problems requiring medication and/or behavioural therapy (eg. ADHD) should be
managed in a manner similar to other chronic conditions of childhood. In addition to regularly
monitoring the effectiveness of therapeutic interventions, primary care providers should provide
information to the family and child about the problem, help the family set specific treatment
goals, and offer information regarding support groups if they are available.

If the selected management strategy does not result in attainment of the target outcome, the
original diagnosis, comorbid conditions, and adherence to management plan should be
reevaluated.

Parent-child behavior therapy teaches parents how to use appropriate discipline strategies (eg,
setting specific goals and providing consistent rewards and consequences depending upon
whether the goals are met). For example, parents can help to shape the behavior of a child who
has ADHD by:

• Maintaining a daily schedule

• Keeping distractions to a minimum
• Providing specific and logical places for the child to keep his schoolwork, toys, and
clothes
• Setting small, reachable goals
• Rewarding positive behavior
• Using charts and checklists to help the child stay "on task"
• Limiting choices
• Finding activities in which the child can be successful (eg, hobbies, sports)
• Using calm discipline (eg, time out, distraction, removing the child from the situation)

Note – Managing Disruptive Behaviour: Strongest Families BC is a resource to support families

with consistent child behavioural problems. Please see links below.

43
http://www.gpscbc.ca/system/files/STRONGEST%20FAMILIES%20Physician%20Introductory
%20Letter.pdf

http://www.cmha.bc.ca/files/SF_ReferralForm.pdf

4. In assessing behavioural problems in adolescents, use a systematic, structured approach to

make an appropriate diagnosis:
• Specifically look for substance abuse, peer issues, and other stressors.
• Look for medical problems (bipolar disorder, schizophrenia).
• Do not say the problem is “just adolescence”.

As outlined above, a full history and physical exam should be obtained as well as relevant
investigations. A mental status examination is useful to determine if there is underlying
psychiatric illness contributing to the beahvioural problems.

Adolescents should be advised about the potential dangers of drugs, such as alcohol and tobacco,
which are legal (though not for their age group), as well as illegal substances. It may be helpful,
when interviewing an adolescent, to begin by asking whether illicit drugs are available at school,
whether the patient has close friends who use drugs, and whether the patient has access to drugs.

Drug abuse is more prevalent in patients who are depressed, anxious, or have any other
psychiatric comorbidity (including personality disorders), and in those who smoke tobacco and
who abuse alcohol.

5. In elderly patients known to have dementia, do not attribute behavioural problems to

dementia without assessing for other possible factors (e.g., medication side effects or
interactions, treatable medical conditions such as sepsis or depression).

Behavioural symptoms in Alzheimer disease (AD) and other types of dementia are extremely
common and often much more troubling than amnestic symptoms (eg. agitation, aggression,
delusions, hallucinations, wandering, depression and sleep disturbances). One or more of these
symptoms is observed in 61-92% of patients with dementia; the prevalence increases with disease
severity.

A concomitant medical illness (particularly urinary tract infection or pneumonia) or medication

toxicity (particularly anticholinergic side effects of drugs used to treat other illnesses) and other
causes of delirium must be considered whenever new behavioural disturbances arise, particularly
in the setting of an acute worsening in cognition (Table 6). Most behavioural symptoms have
precipitants. These possibilities should be ruled out prior to initiation of any treatment.

Table 6: Common causes of delirium and confusional states

Drug and toxins

Prescription medications (eg, opioids, sedative-hypnotics, antipsychotics, lithium, skeletal muscle
relaxers, polypharmacy)

Non-prescription medications (eg, antihistamines)

Drugs of abuse (eg, ethanol, heroin, hallucinogens, nonmedicinal use of prescription medications)

44
Withdrawal states (eg, ethanol, benzodiazepines)
Medication side effects (eg, hyperammonemia from valproic acid, confusion from quinolones,
serotonin syndrome)
Poisons:

Atypical alcohols (ethylene glycol, methanol)

Inhaled toxins (carbon monoxide, cyanide, hydrogen sulfide)
Plant-derived (eg, Jimson weed, salvia)

Infections
Sepsis

Systemic infections; fever-related delirium

Metabolic derangements
Electrolyte disturbance (elevated or depressed): sodium, calcium, magnesium, phosphate

Endocrine disturbance (depressed or increased): thyroid, parathyroid, pancreas, pituitary, adrenal

Hypercarbia
Hyperglycemia and hypoglycemia
Hyperosmolar and hypoosmolar states
Hypoxemia
Inborn errors of metabolism: porphyria, Wilson's disease, etc.
Nutritional: Wernicke's encephalopathy, vitamin B12 deficiency, possibly folate and niacin
deficiencies
Brain disorders
CNS infections: encephalitis, meningitis, brain or epidural abscess

Epileptic seizures, especially nonconvulsive status epilepticus*

Head injury*
Hypertensive encephalopathy
Psychiatric disorders*
Systemic organ failure
Cardiac failure

Hematologic: thrombocytosis, hypereosinophilia, leukemic blast cell crisis, polycythemia

Liver failure: acute, chronic
Pulmonary disease, including hypercarbia and hypoxemia
Renal failure: acute, chronic
Physical disorders
Burns

Electrocution
Hyperthermia
Hypothermia
Trauma: with systemic inflammatory response syndrome, *head injury, fat embolism
 Disorders that, while not truly systemic or "medical", may produce the clinical picture of
delirium or confusional state in all other aspects.

45
Breast Lump - Key Features

1. Given a well woman with concerns about breast disease, during a clinical encounter (annual
or not):
a) Identify high-risk patients by assessing modifiable and non-modifiable risk factors
b) Advise regarding screening (mammography, breast self- examination) and its limitations.
c) Advise concerning the woman’s role in preventing or detecting breast disease (breast self-
examination, lifestyle changes).

2. Given a woman presenting with a breast lump (i.e., clinical features):

a) Use the history, features of the lump, and the patient’s age to determine (interpret) if
aggressive work-up or watchful waiting is indicated.
b) Ensure adequate support throughout investigation of the breast lump by availability of a
contact resource.
c) Use diagnostic tools (e.g., needle aspiration, imaging, core biopsy , referral) in an
appropriate manner (i.e., avoid over- or under-investigation, misuse) for managing the breast
lump.

3. In a woman who presents with a malignant breast lump and knows the diagnosis:
a) Recognize and manage immediate and long-term complications of breast cancer.
b) Consider and diagnose metastatic disease in the follow- up care of a breast cancer patient by
appropriate history and investigation.
c) Appropriately direct (provide a link to) the patient to community resources able to provide
adequate support (psychosocial support).

RF’s:

o Female
o Increases with age
o +Fhx: 1st degree relative =2x risk, 3rd degree=4x
o Personal or +FHx breast or ovarian Ca esp before age 40
o Previous breast bx
o High breast density
o Nullparity; 1st preg>30y.o
o Radiation exposure
o >5yrs HRT
o Breast cancer risk assessment calculator available at http://www.cancer.gov/bcrisktool/

Protective factors

o Pregnancy before age 30

o Fewer years menstruating
o Lactation

Note promotion of overall healthy lifestyle and women’s health promotion; obesity, alcohol

46
Red Flags

o Unilateral non-cyclical pain

o Unilateral nipple discharge; watery, serous, serosanguineous, single duct
o Breast mass: unilateral, hard, immobile, noncystic, skin retraction, dimpling or edema
(peau d’orange)
o Hx: postmenopausal, previous hx cancer, fhx breast ca

Screening

o Genetic screening
• BRCA1/2 if +breast AND ovarian ca
• Strong fhx of br and ovarian ca (Ashkenazi Jew)
• Fhx male br ca
• <35y/o
o Mammography q1-2yrs-new guideline age 50-69 rather than 40-79
• Start 10yrs earlier of first age of Br Ca in first degree relative
o Breast self-exam no longer routinely advised

Investigation of breast cancer

o U/S→cystic vs solid
o MRI-high sensitivity poor specificity
o Galactogram/ductogram for nipple d/c – ductal lesions
o Metastatic work up as indicated – bone scan, abdo u/s, cxr, head CT (or CT
chest/abdo/pelvis)
o Diagnostic mammogram always indicated even if <50y/o

Diagnosis

o Needle aspiration if palpable, cystic; send for cytology if blood or cyst doesn’t
completely resolve
o U/S or mammography guided core needle bx (most common)
o Fine needle aspiration (FNA) for palpable solid masses, need experienced practioner
o Excisional bx- only as 2nd choice to core needle bx

DDx for breast mass:

o Benign
• Non proliferative: fibrocystic change, cystic mastitis, mammary dysplasia
• Proliferative - no atypia
• Fibroadenoma, intraductal papilloma, ductal hyperplasia without atypia
• Proliferative – with atypic
• Atypical hyperplasias
• Others - Fat necrosis, mammary duct ectasia, Montgomery tubercle, abscess,
galactocoele, silicone implant, Granulomatous mastitis (TB, Wegners, sarcoidosis)
o Breast Cancer
• Non-invasive: ductal in-situ, lobular in-situ
• Invasive: ductal, lobular, Paget’s disease, inflammatory ca, male br ca, sarcomas,
lymphomas, others (papillary, medullary, mucinous)

47
Complications of breast cancer

o Mets: bone>lungs>pleura>liver>brain
o Biopsychosocial
o Treatment or surgical S/E, body changes, fertility, family inheritance implications
o Bone health

Resources and support for patient

Provide contact info for patient while undergoing diagnosis and treatment
Supportive care for patient throughout experience

Cancer - Key Features

1. In all patients, be opportunistic in giving cancer prevention advice (e.g., stop smoking,
reduce unprotected sexual intercourse, prevent human papillomavirus infection), even when it
is not the primary reason for the encounter.

2. In all patients, provide the indicated evidence-based screening (according to age group, risk
factors, etc.) to detect cancer at an early stage (e.g., with Pap tests, mammography,
colonoscopy, digital rectal examinations, prostate-specific antigen testing).

3. In patients diagnosed with cancer, offer ongoing follow-up and support and remain involved
in the treatment plan, in collaboration with the specialist cancer treatment system. (Don’t lose
track of your patient during cancer care.)

4. In a patient diagnosed with cancer, actively inquire, with compassion and empathy, about
the personal and social consequences of the illness (e.g., family issues, loss of job), and the
patient’s ability to cope with these consequences.

5. In a patient treated for cancer, actively inquire about side effects or expected complications
of treatment (e.g., diarrhea, feet paresthesias), as the patient may not volunteer this
information.

6. In patients with a distant history of cancer who present with new symptoms (e.g., shortness
of breath, neurologic symptoms), include recurrence or metastatic disease in the differential
diagnosis.

7. In a patient diagnosed with cancer, be realistic and honest when discussing prognosis. (Say
when you don’t know.)
Note: For pain control, see the key features on chronic disease and palliative care. See also the
key feature on depression.

Approach to Cancer

Identifying populations at risk

48
 o This may include demographic features such as age or sex, or may be risk factors such
as smoking, other exposures, or family history.
o Screening guidelines are readily available from multiple sources online.
o Key historical questions: family history of malignancies (and age at diagnosis);
radiation/sun/toxin exposure; smoking; alcohol.

Choosing a screening method

o Multiple screening options mean approach needs to be tailored to individual. For

example, screening for colon cancer with FOB + DRE vs colonoscopy.

Further testing

o A positive screening test does not constitute a diagnosis of cancer; in nearly all cases,
further testing is required.
o For example; an abnormality on breast exam and screening mammography would
require a diagnostic mammogram and/or ultrasound. The abnormality may be a benign
finding.

Pursuing a tissue diagnosis

o Whenever a diagnosis of cancer is entertained, the aim of further testing should be to

obtain a tissue diagnosis. This will guide any possible surgical, chemotherapeutic, or
radiation interventions.
o For example, a patient with a history of smoking is found to have a nodule on CXR that
is further characterized on CT. The next step would be to obtain a biopsy, whether
through bronchoscopy, CT-guided biopsy, or excisional biopsy by a thoracic surgeon.

Awareness of context/goals of care/advance care planning

o Not all cancers need to be treated. Ideally, the time to discuss what a patient might want
to have done about a potential cancer is when any investigation for it is ordered.
o Clarifying what the next step would be if a positive screening result is returned helps to
unify patient and physician expectations and can alleviate anxiety regarding the direction
of care.

Treating symptoms

o Patients undergoing treatment for cancer also require special attention to pain,
gastrointestinal symptoms including nausea and bowel habits, mental health, and other

49
 symptoms in the context of their malignancy. Treatments aimed at the cancer itself are
only a small part of the overall therapeutic effort.

Chest Pain - Key Features

1. Given a patient with undefined chest pain, take an adequate history to make a specific
diagnosis (e.g., determine risk factors, whether the pain is pleuritic or sharp, pressure, etc.).

History: OPQRST
Onset

- Acute onset with greatest intensity pain at onset = pneumothorax, PE or aortic

dissection
- Gradual onset = ischemic event or esophageal disease.
- Vague onset = “Functional” or musculo-skeletal chest pain

P1 - Provocation - Aggravating factors may include:

- Post-prandial = GI or cardiac
- Exertion = Ischemic
- Swallowing = Esophageal
- Respiration/Pleuritic pain = PE, pneumothorax, viral/idiopathic pleurisy, pneumonia or
pleuropericarditis

P2 - Palliation - Alleviating factors may include:

- Antacids/Food = Likely GI
- Sublingual nitroglycerin - NOT helpful in distinguishing ischemic vs. non-ischemic
- GI cocktail (“Pink Lady/White Knight”) - NOT helpful in distinguishing
- Rest = Ischemic
- Sitting up/leaning forward = Pericarditis

Quality

- “Squeezing”/ “Tight” / “Pressure” = Ischemic

- “Ripping”/ “Tearing” = Aortic dissection
- Pleuritic = PE, pericarditis/myocarditis
- Levine sign (fist over their sternum to describe pain) = ischemia

Radiation

- Ischemic = Neck, lower jaw, shoulder, teeth, throat, arms

- Aortic dissection = between scapulae
- Acute cholecystitis = R shoulder
- Pericarditis = one or both trapezius ridges

Severity

50
 - not a useful predictor of pathology, but use 0- 10 scale to determine if patient’s
symptoms are worsening or improving.

Timing/Duration

- Lasting seconds or consistent over weeks = NOT ischemic

- Years w/out progression = Functional
- Minutes to hours = Possibly ischemia/infarction

Risk Factors for Coronary Artery Disease and Acute Coronary Syndrome

- Past medical history of CAD/stroke/MI

- Diabetes
- Hyperlipidemia
- HTN
- Smoking
- FHx (Positive family history is: first degree relative with MI, M<55, F<65)
- LVH
- Cocaine use
- Recent infection
- Recent chest trauma

Associated Symptoms of ACS:

- Diaphoresis
- N/V
- Shortness of breath
- Syncope
- Palpitations
- Psychiatric symptoms - Panic attacks, anxiety, depression, somatization

2. Given a clinical scenario suggestive of life-threatening conditions (e.g., pulmonary

embolism, tamponade, dissection, pneumothorax), begin timely treatment (before the diagnosis
is confirmed, while doing an appropriate work-up).

Pulmonary Embolism
Clinical Features - Acute onset dyspnea, pleuritic chest pain, cough, hemoptysis, tachycardia,
tachypnea, signs of DVT, orthopnea, jugular venous distention

Acute Treatment -

- Respiratory support: Supplemental oxygen +/- intubation and mechanical ventilation

- Hemodynamic support: IV Fluids, Vasopressors
- Anticoagulation: If no contra-indications start IV UFH or SC LMWH

51
 - Thrombolysis: If persistent hypotension despite adequate resuscitation

Work-up -

- Labs: CBC, ABG, Troponin, D-dimer

- ECG (S1Q3T3)
- CXR
- Imaging: V/Q scan, Angiography, Spiral CT

Tamponade
Clinical Features - Beck’s Triad (Hypotension, Elevated JVP, Muffled Heart Sounds), Sinus
tachycardia, Pulsus paradoxus, Pericardial rub.
Acute Treatment - In the setting of hemodynamic instability a patient may require urgent removal
of pericardial fluid by needle pericardiocentesis, open surgical drainage or video-assisted
thoracoscopic pericardiectomy.

Work-up -

- ECG: sinus tachycardia w/ low voltages

- CXR: enlarged cardiac silhouette
- Echocardiography: 2D and Doppler can assess hemodynamic stability
- CT: Not necessary if echo available

Aortic Dissection
Clinical Features - Acute onset “tearing” chest pain radiating to mid back between scapulae +/-
syncope, pulse deficit.
Acute Treatment -

- Lower SBP to 100-120 mmHg: 1st line is IV beta blockers (propranolol, labetalol), 2nd
line is IV nitroprusside, verapamil, or diltiazem.
- Pain control w/ IV morphine
- If hemodynamically unstable may require intubation

Work-up -

- ECG: Normal, non-specific ST changes, LVH/strain patterns w/ HTN, ischemic

changes
- CXR: widening of the aorta
- CT/TEE/MRI

Pneumothorax
Clinical Features - Sudden onset dyspnea and pleuritic chest pain w/ decreased excursion of chest
wall on affected side, diminished breath sounds, and hyper-resonant percussion. Hemodynamic
compromise indicates possible tension pneumothorax requiring immediate decompression.

Acute Treatment -

52
 - Supplemental oxygen
- Needle Decompression
- Chest tube insertion

Work-up -

- CXR: separation of visceral pleural line from parietal pleural line

- CT: more sensitive than CXR
- US: can be done at bedside in emergent situations

3. In a patient with unexplained chest pain, rule out ischemic heart disease.

Step 1: Hx and Physical

Step 2: If ACS suspected give ASA 162 mg PO chewed and swallowed, supplemental oxygen,
SL Nitroglycerin 0.4 mg/spray q 5 min x 3 (as needed), and/or morphine IV to treat the pain.
**This may precede Step 1 if strong suspicion of ACS.
Step 3: ECG, CXR, Cardiac blood work (CBC, Lytes, BUN, Creatinine, Troponin, Glucose)
Step 4: If the initial ECG is not diagnostic but the patient remains symptomatic and clinical
suspicion for ACS remains high, the ECG should be repeated at least every 20-30 minutes.
Step 5: Repeat troponin 6 hours after first drawn.

In a patient with no ECG changes and two consecutive negative serum troponins drawn at least 6
hours apart ACS can be ruled out.

4. Given an appropriate history of chest pain suggestive of herpes zoster infection, hiatal
hernia, reflux, esophageal spasm, infections, or peptic ulcer disease:
a) Propose the diagnosis.
b) Do an appropriate work-up/follow-up to confirm the suspected diagnosis.

Herpes Zoster Infection

history

o previous primary infection with chickenpox

o unilateral and dermatomal eruption typically occurring day 3-5 after pain and
paresthesia of a dermatome begins (although symptoms may precede rash by weeks)
• thoracic and lumbar dermatomes most common
o rash begins as maculopapular but quickly progresses to vesicular (identical to lesions of
chickenpox)
o time course typically 2 weeks but may persist for a month
o pain and paresthesia can last months to > 1 year with post-herpetic neuralgia

risk factors

o old age
o immunosuppression
o occasionally associated with dermatologic malignancy

diagnosis

53
 o almost invariably clinical
o may need additional diagnostic information if
• atypical rash in an immunocompromised host
• possible disseminated disease in an immunosuppressed host without cutaneous lesions
• methods include
• viral culture
• direct immunofluorescence testing
• polymerase chain reaction assay (most sensitive)

Hiatal hernia
types

o 4 types but ~95% are type I (both stomach and LES herniate above diaphragm)

history

o majority are asymptomatic

o symptoms of GERD
• epigastric or substernal pain, postprandial fullness, substernal fullness, nausea, and
retching; all usually 1-3 hrs post-prandial
• relief with standing, water, antacids

risk factors

o previous diaphragmatic surgery

o age (over 50)
o weakening of myofascial structure
o increased intraabdominal pressure (pregnancy, obesity)

diagnosis

o majority are found incidentally

o when dx suspected
• upper GI series or barium swallow
• Esophagogastroduodenoscopy (EGD) with biopsy
• If worried about Barett’s/CA/Esophagitis
• Document type and extent of tissue damage

Reflux
history

o waterbrash (sudden hypersalivation)

o heartburn (retrosternal burning radiating to mouth)
o non-specific chest pain
o dysphagia (abnormal motility or esophagitis, reflux-induced stricture)
o pharyngitis, laryngitis (with hoarseness)
o respiratory (chronic cough, asthma, aspiration pneumonia, wheezing)
o symptoms aggravated by
• position (lying or bending)

54
 • increase in intra-abdominal pressure (pregnancy or lifting)
• agents that decrease LES pressure (caffeine, fatty foods, alcohol, peppermint, cigarettes,
nitrates, beta-adrenergic agonists, calcium channel blockers (CCB’s), theophylline,
benzodiazepines, anticholinergics, morphine)
• foods that delay gastric emptying (alcohol, coffee, chocolate)

diagnosis

o practical approach is to observe for resolution with PPI

o 24-hour pH monitoring
• Gold standard for determining if reflux is present
o endoscopy
• determines if reflux has damaged the esophagus
o barium swallow
• determines if stricture present

Esophageal spasm
history

o intense substernal pain increased by swallowing

o decreased by NTG or CCB
o diagnosis of exclusion when unexplained chest pain and dysphagia occur

diagnosis

o barium swallow
• Corkscrew pattern/”rosary bead” esophagus
• Tertiary waves
o manometry

Infections (pneumonia)
history

o depends on infectious organism but generally speaking, includes some combination of

• fever
• dyspnea
• cough
• pleuritic chest pain
• sputum production

diagnosis

o chest xray +/-

• pulse ox, cbc, renal fn, blood cultures, sputum cultures, ABG if ill-appearing
• sputum gram stain rarely changes therapy
• consider CT scan or bronchoscopy if failing to respond to appropriate therapy

55
Peptic ulcer disease
history

o history not reliable in establishing diagnosis but duodenal ulcer is supposed to have 6
classical features:
• epigastric location
• burning
• develops 1-3 hours after meals
• relieved by eating and antacids
• interrupts sleep
• periodicity (tends to occur in clusters over weeks with subsequent periods of remission)
o gastric ulcers have more atypical symptoms (always require biopsy to exclude
malignancy)
• may present with complications
• bleeding 10% (especially severe if from gastroduodenal artery)
• perforation 2% (usually anterior ulcers)
• gastric outlet obstruction 2%
• penetration (posterior) 2% - may also cause pancreatitis

risk factors

o NSAID use
o smoking
o COPD, renal failure, cirrhosis

diagnosis

o consider H. Pylori testing first (present in approx 80% of gastric and 95% of duodenal
ulcers)
o upper GI series or EGD for definitive diagnosis

5. Given a suspected diagnosis of pulmonary embolism:

a) Do not rule out the diagnosis solely on the basis of a test with low sensitivity and specificity.
b) Begin appropriate treatment immediately.

Pulmonary Embolism
• ALWAYS determine pretest probability of PE in patients with suspected diagnosis
• pretest probability can be subjectively determined by clinician (though accuracy requires
clinical experience) or by using clinical score systems and decision rules (eg. Well’s criteria and
Well’s modified criteria, PERC score) that incorporate symptoms, signs and risk factors to
stratify patients into different categories of overall risk
diagnostic tests

o pulmonary angiography
• “gold standard”

56
 • not commonly used anymore as invasive and has morbidity and mortality rate of 1 to
5%
o D-dimer
• sensitivity depends on type of assay but anywhere from ~85-96%
• low specificity
• most published research restricts use of D-dimer to patients with low pretest probability
• positive d-dimer must be followed by confirmatory testing for PE (pulmonary
angiography, CT-PA or V/Q scanning)
o CT-PA (CT with pulmonary angiography, aka “spiral CT”)
• sensitivity anywhere between 70-90%
• specificity ~ 90%
• has emerged in most centers as imaging test of choice for evaluation of PE (as it often
detects alternative pulmonary abnormalities that explain patient’s symptoms)
o V/Q scan
• traditionally used as first imaging modality used in dx of PE
• problem is that it is often inconclusive
• may be useful in people who have an allergy to iodinated contrast or in pregnancy due
to lower radiation exposure than CT, or in centers with no CT-PA

Do not use ECG or ABG alone in diagnosis of PE!

Deciding what test to use:

• If you are in a CT-PA capable centre:

57
• If you only have V/Q available:

58
PERC rule: Should use first to determine if any further testing is warranted
Acute PE can probably be excluded without further diagnostic testing if the patient meets all
PERC criteria AND there is a low clinical suspicion for PE, according to either the Wells criteria
or a low gestalt probability determined by the clinician prior to diagnostic testing for PE.

1) Age less than 50 years

2) Heart rate less than 100 bpm
3) Oxyhemoglobin saturation ≥95 percent
4) No hemoptysis
5) No estrogen use
6) No prior DVT or PE
7) No unilateral leg swelling
8) No surgery or trauma requiring hospitalization within the past four weeks

Chronic Disease - Key Features

59
1. In a patient with a diagnosed chronic disease who presents with acute symptoms, diagnose:
- acute complications of the chronic disease (e.g., diabetic ketoacidosis)
- acute exacerbations of the disease (e.g., asthma exacerbation, acute arthritis)
- a new, unrelated condition

2. Regularly reassess adherence (compliance) to the treatment plan (including medications).

‘’’’’

3. In patients with chronic disease:

a) Actively inquire about pain.
b) Treat appropriately by:

- titrating medication to the patient’s pain

- taking into account other treatments and conditions (e.g., watching for interactions)
- considering non-pharmacologic treatment and adjuvant therapies
Massage, physio, exercise, CBT, counselling, mindful meditation, reframing, OT home
assessment (accommodate needs within limitations of pain/Dx)

4. In patients with chronic disease, actively inquire about: - the psychological impact of
diagnosis and treatment. - functional impairment
- underlying depression or risk of suicide
- underlying substance abuse

5. Given a non-compliant patient, explore the reasons why, with a view to improving future
adherence to the treatment plan.

Chronic Disease Risk Factors: What are the Primary Risk Factors?
According to the World Health Report 2002, the major risk factors include:

■ tobacco
■ alcohol
■ blood pressure
■ physical inactivity
■ cholesterol
■ overweight
■ unhealthy diet

Smoking
Leading preventable cause of premature death in Canada.

Prevalence of smoking among adult men and women (>20 yo) is ↑ in northern/rural regions, and ↓
in British Columbia and most major urban centres.
Prevalence decreased from 1994 to 2005.
Highest among people aged 20-24.
Alcohol

60
High-risk alcohol use associated with ↑ risks of > 60 chronic conditions including cancer, GI d/o,
neuro d/o, & cardiovascular disease (especially stroke).

↑ 1995 – 2005, 17% consume alcohol in hazardous manner. 28% youth aged 12-19 and 30% men
& 12% women > 20 years reported drinking heavily.
20-24 yo highest prevalence of heavy drinking (consuming >5 drinks/occasion) - 56% among men
and 33% of women. The prevalence ↓ with ↑’ing age.

Nutrition
Diet influences risk of developing cancer, coronary heart disease, stroke, HTN, DM and obesity
→ related to the risk of other chronic diseases.

Low consumption of fruits and vegetables (< 5 servings/day) was associated with lower income,
and other unhealthy behaviours such as cigarette smoking.

Physical Inactivity
Physical inactivity impacts physical and mental health and well-being and is considered to be a
primary risk factor for obesity.

Less than half of the Canadian population participates in the minimal amount of leisure time
physical activity required to obtain the health benefits, including a lower risk of developing
chronic disease, of a physically active lifestyle.
Levels of physical inactivity increase with age, particularly for ages >75. Women are more
physically inactive (50%) than men (45%)

Obesity
Obesity contributes to the development and exacerbation of major chronic diseases in Canada,
including heart disease, type 2 diabetes, some cancers (e.g., colon cancer) and osteoarthritis. The
self-reported prevalence of obesity in 2005 for Canada was 17% for men and 15% for women.
The longer one is obese, the greater the health risks and the greater the likelihood of premature
death.

The prevalence of obesity has nearly doubled in adults and tripled in children and youth over the
past 25 years.

In individuals, we can classify the risks factors as follows:

■Background risk factors, such as age, sex, level of education and genetic composition;
■Behavioural risk factors, such as smoking, unhealthy diet and physical inactivity; and
■Intermediate risk factors, such as serum cholesterol levels, diabetes, hypertension and
obesity/overweight

In Communities, the main factors that can impact health include:

■Social and economic conditions, such as poverty, employment, family composition;

■Environment, such as climate, air pollution;

61
 ■Culture, such as practices, norms and values; and
■Urbanization, which influences housing, access to products and services.

As Primary Care Physicians Responsible for:

• Annual review of chronic disease progression

o Identify any target organ damage including: cerebrovascular disease, coronary heart
disease (CHD), left ventricular hypertrophy (LVH), chronic kidney disease (CKD),
peripheral vascular disease, neuropathy, and retinopathy.
• Monitoring BW and investigations
• Ensuring annual follow-up referrals are tracked and booked appropriately
• Annual CPX and immunizations are up to date (flu, pneumovax, shingles, Hep A/B,
tetanus)

COPD - Key Features

1. In all patients presenting with symptoms of prolonged or recurrent cough, dyspnea, or

decreased exercise tolerance, especially those who also have a significant smoking history,
suspect the diagnosis of COPD.

Risk Factors DDX of COPD

Environmental
 Tobbaco Smoke ** Primary RF**
 Chemicals
 Fumes
 Dust
 Asthma
Genetics
 CHF
 α-1 Antitrypsinn deficiency  TB
 First degree relatives  Obliterative Bronchiolitis
 Bronchiectasis
Demographics  Diffuse panbronchiolitis

 Low BMI
 Male
 Hx of pediatric resp Infections
 Low socioeconomic Status

NOTE : Asthma may be a risk factor but evidence is not conclusive.

2. When the diagnosis of COPD is suspected, seek confirmation with PFTs (e.g. FEV1).

Chest X-ray is usually done to exclude co-morbidities (A chest X-ray may suggest COPD, but the
definitive diagnosis of COPD requires spirometry)
As per guidelines…. the Diagonosis of COPD is:

62
 o postbronchodilator, FEV1/FVC <0.7

FEV1 assists with staging/severity.

New guidelines do not focus on the difference between Chronic Bronchitis and Emphysema as
treatment does not differ…but just in case:

o Chronic Bronchitis: obstruction due to airway lumen narrowing by mucosal thickening,

excess mucous
 PFTs: normal TLC, normal or increased Dco
o Emphysema: dilation, destruction of airspaces distal to terminal bronchiole without
obvious fibrosis; decreased elastic recoil
 PFTs: increased lung volume, decreased Dco

3. In patients with COPD, use pulmonary function tests periodically to document disease
progression.

Disease management is based largely on symptomatolog y but serial PFTs is clearly indicated.

COPD Stage Spirometry (post-bronchodilator)

Mild FEV1 ≥ 80% predicted, FEV1/FVC <0.7
Moderate FEV1 50 – 79% predicted, FEV1/FVC <0.7
Severe FEV1 30 – 49% predicted, FEV1/FVC <0.7
Very Severe FEV1 < 30% predicted, FEV1/FVC <0.7
COPD Stage Symptoms
Mild SOB from COPD when hurrying on the level or walking up a slight hill
SOB from COPD causing the patient to stop after walking approximately 100m on
Moderate
the level
SOB from COPD resulting
 in the patient being too breathless to leave the house
Severe  breathlessness when dressing or undressing
 presence of chronic resp failure
 clinical signs of right heart failure

4. Encourage smoking cessation in all patients diagnosed with COPD.

This is KEY!!!
Total pack years = (cigarettes/day ÷20) x years of smoking

o A Hx of >10 pack years should raise the index of suspicion for COPD
o Smoking > 40 pack years increases likelihood ratio to 8.3

See Smoking Cessation key features

63
5. Offer appropriate vaccinations to patients diagnosed with COPD (e.g.
influenza/pneumococcal vaccination).

Annual influenza vaccine; Pneumovax (initially and a booster in 5 years)

6. In an apparently stable patient with COPD, offer appropriate inhaled medication for
treatment (eg. anticholinergics/bronchodilators if condition is reversible, steroid trial).

Goals of treatment:

o Prevent progression
o Relieve symptoms
o Minimize S/E of medications
o Prevent exacerbations

Lifestyle considerations

o Exercise training programs improve Sx

o Education
• Smoking cessation
• Coping skills – strategies to avoid dyspnea
• Self-management
• COPD action plan
o Pulmonary Rehab – see below
Mild Moderate Severe
SABD PRN
LAAC or LABA + SABA prn
LAAC + ICS/LABA + SABA prn
LAAC + SABA
Persistent Sx: LAAC + LABA + SABA
prn Persistent Sx: LAAC + ICS/LABA +
prn
OR SABA prn
Persistent Sx: LAAC + ICS/LABA +
LABA + SABD ± Theophylline
SABA prn
prn

SABD – short-acting bronchodilator, SABA – short-acting beta agonist, LABA- long acting beta
agonist, LAAC- long-acting anticholinergic , ICS- inhaled corticosteroid

If patient is having frequent Acute exacerbation >1 per year – treat as severe.

Consideration for O2:

o Severe Hypoxemia PaO2 ≤60mmHg

o Bilat. Ankle Edema
o Cor pulmonale
o Hematocrit > 56%

64
  Summary of Treatment

7. Refer appropriate patients with COPD to other health professionals (e.g. a respiratory
technician or pulmonary rehabilitation personnel) to enhance quality of life.

Indicated when

o Onset at early age

o Sx are severe or progress rapidly
o Exacerbations are severe or recurrent
o Response to standard therapy inadequate
o Consideration being given to
• pulmonary rehab
• O2
• Surgery

Pulmonary Rehab

Indication Benefits
 Reduces Dyspnea
 Restore Exercise Capacity
 Improves Exercise Capacity
 Meds are not effective  Improves quality of life
 Reduces number and length of hospital admissions

8. When treating patients with acute exacerbations of COPD, rule out co-morbidities (e.g. MI,
CHF, systemic infections, anemia).

Acute exacerbation: episode of increased dyspnea, coughing, change in sputum

65
volume/purulence

Etiology:

Common DON'T MISS

MI
Viral URTI 25 – 50%
PE
Bacterial
CHF

Management: ABCs; consider assisted ventilation if decreasing LOC/poor ABGs

- Supplemental O2 (controlled FiO2): target 88-92% SaO2 for CO2 retainers

- Neb bronchodilators: salbutamol + ipratropium bromide x 3 back to back
- Systemic corticosteroids:
• IV solumedrol 1-2 mg/kg q6-12 hrs IV x 3 days
• Prednisone 30-40 mg qd x 7-10 days, not necessary to taper
- Antibiotics: indicated if 2/3 – 1) increased SOB 2) increased sputum vol or 3) purulence
• Duration: 3-7 days
Group Sx and RF Pathogen 1st Choice
H. Influ, Macrolide (azithromycin, clarithromycin)
Increased sputum and
Simple Strep. Pneumo 2nd or 3rd gen Cephalosporin (i.e.
SOB
cefuroxime)
Moraxella Doxycycline Septra
Simple plus:
Klebsiella
Moxifloxacin
FEV1 <50%
Complex
>3 exacerbations/yr Gram –ve
Amoxicillin/Clavulanate
IHD Pseudomonas
Home O2

- ICU admission:
• for life-threatening exacerbations
• vent support: non-invasive (NIPPV, CPAP, BiPAP), conventional mech vent

9. In patients with end-stage COPD, especially those who are currently stable, discuss,
document, and periodically re-evaluate wishes about aggressive treatment interventions.

Natural progression of COPD:

- 40s – chronic productive cough

- 50s – first acute chest illness

66
 - 60s – dyspnea on exertion, increasing sputum production; more frequent acute
exacerbations
- Late Stage – hypoxemia with cyanosis, polycythemia, hypercapnia (morning headache),
hypoxemia, cor pulmonale

Prognostic Factors: severity of airflow limitation (FEV1) single best predictor

- 5-year survival: FEV1 < 1 L = 50%, < 0.75 L = 33%

Contraception - Key Features

1. With all patients, especially adolescents, young men, postpartum women, and
perimenopausal women, advise about adequate contraception when opportunities arise.

2. In patients using specific contraceptives, advise of specific factors that may reduce efficacy
(e.g., delayed initiation of method, illness, medications, specific lubricants).

3. In aiding decision-making to ensure adequate contraception:

a) Look for and identify risks (relative and absolute contraindications).
b) Assess (look for) sexually transmitted disease exposure.
c) Identify barriers to specific methods (e.g., cost, cultural concerns).
d) Advise of efficacy and side effects, especially short-term side effects that may result in
discontinuation.

4. In patients using hormonal contraceptives, manage side effects appropriately (i.e.,

recommend an appropriate length of trial, discuss estrogens in medroxyprogesterone acetate
[Depo– Provera]).

5. In all patients, especially those using barrier methods or when efficacy of hormonal methods
is decreased, advise about post- coital contraception.

6. In a patient who has had unprotected sex or a failure of the chosen contraceptive method,
inform about time limits in post- coital contraception (emergency contraceptive pill,
intrauterine device).

Combined Hormonal Contraception

→ Contains both estrogen and progesterone (oral pill, transdermal patch, vaginal ring available in
Canada)
→ With perfect use combined OC is 99.9% effective at preventing pregnancy; however typical
failure rate is between 3-8%
→ Effect on body weight on effectiveness of combined OC is controversial
→ Mechanism of action:

67
 • inhibits ovulationSuppress gonadotropin secretion
• Development of endometrial atrophy, making endometrial unresponsive to implantation
• Production of viscous cervical mucous that impedes sperm transport

→ Fertility is restored within 1-3 months after stopping combined OC

Absolute Contraindications:
→ < 6w postpartum if breast feeding
→ Smoker > age 35 (>15 cigarettes/day)
→ Hypertension (systolic >160, diastolic >100)
→ Current/past hx of venous thromboembolism or known thrombophilia
→ Ischemic heart disease
→ Hx of CVA
→ Complicated valvular heart disease (pulmonary htn, a fib, hx of subacute bacterial
endocarditis)
→ Migraine headache with focal neurological symptoms
→ Current breast cancer
→ Diabetes with retinopathy/nephropathy/neuropathy
→ Severe cirrhosis, liver tumour (adenoma/hepatoma)

Relative Contraindications
→ Smoker over the age of 35 (<15 cigarettes/day)
→ Adequately controlled hypertension (systolic 140-159, diastolic 90-99)
→ Migraine headache over the age of 35
→ Currently symptomatic gall bladder disease
→ Mild cirrhosis
→ Hx of combined OC-related cholestasis
→ Users of medications that may interfere with combined OC metabolism

Side Effects
→ Most common reasons for non-compliance of combined OC
→ Irregular bleeding – (10-30% in first month of use) – greatest pts should belikelihood during
first 3 cycles then usually subsides counselled to continue the combined OC and should review
other causes of irregular bleeding if continues
→ Breast tenderness and nausea – usually improves with time;less likely forcombined OC (↓)
containing lower amounts of estrogen
→ Possible: Weight gain and Mood changes– placebo controlled trials failed to show any
association
→ Rare: Chloasma:switching to a different pill will not help, and hyperpigmentation may never
completely disappear

Risks
→ Venous thromboembolism – 3-4x higher in users of combined OC than non-users – 1 –
1.5/10,000 users/year of use
→ MI – in women taking combined OC containing >50 mcg ethinyl estradiol, MI rates increase
3x, no shown risk with combined OC with <50 mcg
→ Stroke – specifically combined OC users with hypertension are at higher risk
→ potential increase risk of gall stone formationGall bladder disease – increases secretion of
cholic acid in bile

68
→ Breast cancer – controversial
→ Cervical cancer – controversial

Counselling Prior to Starting Any Contraception

→ Instructions on how to take combined OC

o Conventionally combined OC is started during first 5 days of menstrual cycle, or on the

first Sunday after menses begin (a backup method is not required for prevention of
pregnancy provided no pills have been missed.)
o Quick start method – start right away, after ruling out a pregnancy (back up method of
contraception should be used for the first improves complianceweek)
o f/u visit should be organized to review experience, satisfaction and compliance
o If using the patch, it should be started on the first day of menses (this will be the patch
change day)

→ Info on potential side effects

→ Non-contraceptive benefits of combined OC
→ Addressing common myths and misconceptions
→ Option for “continuous” use
→ Discussing risks and warning signs – including when to seek medical care

o Especially amenorrhea – can occur in 2-3% of combined OC users

o must r/o pregnancy

→ Discussing what to do if pills are missed

o Missing pills at beginning or end of 21 day cycle lengthens hormone-free period,

increasing the risk of ovulation. Forgetting tablets in second or third week of 21 day cycle
is unlikely to increase risk of ovulation as long as hormone-free interval doesn’t exceed 7
days

→ Emphasizing dual protection (use of condom to prevent STIs and HIV infections)
→ Information about emergency contraception in the event of a missed pill

Instructions Regarding Missed Pills

• If you miss 1 pill, take it as soon as you remember

• If you miss 2 pills in a row during the first 2 weeks of the pack, take 2 pills on the day
you remember and 2 on the following day. Use a backup method of contraception if you
have sex in the 7 days after you miss the pills. If you have had unprotected intercourse
after missing a pill, use emergency contraception.
• If you miss 2 pills in a row in the third week of the pack, throw out the remainder of the
pack and start a new pack on the day you remember. You may not have a period this
month. If you had unprotected intercourse after missing a pill, use emergency
contraception.
• If you miss 3 pills in a row, throw out the remainder of the pack and start a new pack on
the day you remember.
• If you had unprotected intercourse after missing a pill, use emergency contraception.
Use a backup method of contraception if you have intercourse in the first 7 days of the
new pack. You may not have a period this month.

69
Drug Interactions
→ Anti-convulsants - pt’s require combined OC with higher dose estrogen (50 mcg ethinyl
estradiol)
→ Antibiotics - controversial - rifampicin and griseofulvin have been shown to interact.

Progestin-Only Hormonal Contraception

→ Injectable, oral or as an intrauterine device
→ Depot medroxyprogesterone acetate (DMPA) – injectable. Failure rate of <0.3%/year
→ Oral progestin only pill (POP) – failure rate of 0.5% when used perfectly, typical failure rate
5-10%

• suppresses or partially suppresses ovulationInhibits secretion of pituitary

gonadotropins
• Increases the viscosity of cervical mucus8 and induces endometrial atrophy

→ Useful for women who have contraindications to combined OC

→ Absolute contraindications (WHO): known or suspected pregnancy, unexplained vaginal
bleeding, current diagnosis of breast cancer
→ Relative contraindications (WHO): severe cirrhosis, active viral hepatitis, benign hepatic
adenoma

Side Effects
→ Irregular bleeding or unwanted amenorrhea - common in first few months, then ↓

o If irregular bleeding persists after first 6 months, underlying causes of abnormal vaginal
bleeding should be r/o
o Once this is done management options include:
• Increasing DMPA dose to between 225 and 300 mg for 2-3 injections
• Decreasing interval between doses
• Supplemental estrogen therapy such as 0.625 mg of conjugated equine estrogen orally x
28 days
• NSAID agents, such as ibuprofen 400-800 mg BID x 10 days
• Adding combined OC pill for 1-3 months

→ Hormonal side effects such as headache, acne, decreased libido, nausea, breast tenderness
→ controversial; counsel regarding healthy eating/exerciseWeight gain
→ studies do not demonstrate increase in depressive symptomsMood effects

Risks
→ DMPA: Delayed return of fertility - average 9 month delay before restoration of full fertility
→ DMPA: ↓bone mineral density, some studies suggest there is an improvement in BMD after
DMPA is discontinued
→ VTE, CVD, Stroke - when used in standard contraceptive doses, DMPA does not appear to
increase risk

Starting DMPA and POP

→ DMPA Should be started within first 5 days of menses; if switching from combined OC to
DMPA, DMPA should be given within first 5 days of stopping combined OC
→ If given within first 5 days of menstrual cycle, contraceptive effect is achieved within 24
hours, but can be given at any time during menstrual cycle if pregnancy is ruled out

70
→ If given after first 5 days of menstrual cycle, back up method should be used for at least 1
week
→ Given as 150 mg IM injection Q12Weeks
→ POP is usually started on first day of menstrual cycle, but can be started at any time as long as
pregnancy is excluded – there is no pill free interval, and back up method should be used for first
7 days

Late/Missed Injections
→ If it has been <14 weeks since last injection, then next injection can be given
→ If it has been >14 weeks, but no intercourse within last 10 days and serum bHCG is negative
then injection can be given, and back up method should be used x2 weeks
→ If it has been >14 weeks, but pt has had intercourse in last 10 days, serum bHCG must be done
(and negative) and injection can be given, but back up method required x2 weeks, and repeat
bHCG should be done in 2 weeks

Instructions Regarding Missed Pills

• If a pill is missed, it should be taken as soon as possible.

• If the pill use is delayed by more than 3 hours, a backup method of birth control should
be used for the next 48 hour
• If 2 or more pills in a row have been missed, then the individual must take 2 pills per
day for 2 days and use a backup method of birth control for 48 hours.
• In the event of a missed or late pill, the use of emergency contraception may be
considered if appropriate

INTRAUTERINE DEVICES

Types and Statistics

IUD TYPES Failure Duration Ectopic

Copper 1.26/100 WY 5 yrs (lit. says 30mos) 0.25/100 WY
Mirena 0.9/100 WY 5 yrs 0.02/100 WY
 100WY is 100 woman years assuming regular intercourse.
 The overall ectopic rate is lower than for persons using other forms of contraception.

MOA
(1) Copper IUD

- A foreign body reaction inhibits fertilisation by changing the biochemical and

morphological characteristics of the endometrium.
- Cu ions inhibit sperm motility
- NO inhibition of ovulation

(2) Mirena IUD

71
 - Levonorgestral released very slowly from vertical arm results in thickened mucous
which decreases sperm penetration.
- Some women become anovulatory
- Foreign body reaction inhibits fertilisation (endometrial decidualization and gland
atrophy)

Indications
- Long-term protection
- Adjunct to breast feeding
- Unreliable use of other contraception
- Mennorhagia/dysmenorrhea

Contraindications
- Pregnancy
- Post Septic abortion
- Cancer (Endo/CVX)
- STI/PID (current/common or in 3 mod)
- Puerperal sepsis
- Abnormal Uterus (bicornate, fibroids...)
- Abnormal Vag. bleeding
- Copper allergy
- Breast Cancer (CI toward mirena only)

Relative Contraindications
- HIV (high risk or Test positive)
- Benign Trophoblastic Disease
- Between 48hrs and 4weeks Postpartum
- Ovarian Cancer
- High risk for STI (recurrent, sex trade...)

Non-Contraceptive Benefits
- Copper: decreased endometrial cancer secondary to unknown MOA
- Mirena: Decrease menorrhagia (in 74 - 97%) AND decrease endometrial hyperplasia while on
Tamoxifen

Side Effects
Copper:

- 65% have increased bleeding. Approx 12 days of spotting in the first month
- Pain is a common consequence which is often caused by FB reaction; however,
malposition, infection and pregnancy must be ruled out. So, do a detailed Vag. Exam,
BHCG, CBC, STI testing and consider an US to confirm placement.

Mirena

72
 - Bleeding is often increased in the first 1-3 months with irregular spotting; however, 74-
97% will have decreased bleeding.
- Amenorrhea is seen in 16-35% at 1 year. If a pt is amenorrheic check BHCG. If there is
no pregnancy then no need to worry.
- Pain is the same as for the the copper IUD.
- Functional Ovarian Cysts occur in 30% of women. most will resolve spontaneously and
require no investigation.
- Hormonal symptoms (Breast tenderness, Acne) are uncommon and are maximal at 3
months with gradual decline thereafter.

Risks
- Uterine perforation (0.1%)
- Expulsion (2-10%)... RF = previous, Nullip, <4-6wks post partum
- Ectopic Pregnancy (lower than normal rate, but increased risk if you do get pregnant)
- Pregnancy Loss (75% will abort if IUD left in with intrauterine pregnancy.... If this occurs
attempt GENTLE extraction)
- STI (RR = 3.8); not due to IUD itselfIf bacterial infection occurs treat with ABX. IUD can be
left in situ unless PID develops)

Lost IUD
- It has either gone up or fallen out.
- Detailed vaginal exam... it is often still there if it has fallen out
- If not found -> US (? intrauterine) -> AXR (?intra abdominal)

EMERGENCY CONTRACEPTION

There are only THREE forms of emergency contraception available in canada

1) Plan B

- Two 750mcg doses of levonorgestral given either 12 hours apart or as a 1.5mg single
dose
- 89% of pregnancies that would have occurred are prevented; Effective in the first
72hours, but efficacy decreases after 12 hours
- Safe in pregnancy

2) Yuzpe

- Two doses of 0.1mg estradiol and 0.5mg levonorgestral given 12 hours apart.
- Any similar regime from conventional OCP can be used. (see Appendix)
- 75% of pregnancies that would have occurred are prevented; Effective in the first
72hours, but efficacy decreases after 12 hours
- Safe in pregnancy

3) IUD insertion

- Should only be completed with the COPPER IUD

- Can be inserted up to 5 days post-coitus
- 98.7% of pregnancies that would have occurred are prevented

73
NOTE Mifepristone is not available in Canada at this point in time.

Hormonal EC
- MOA: Not completely understood, but there are many theories. Overall consensus is that it
inhibits ovulation.
- CI: Essentially none (allergy)
- FU: BHCG if no menses in 21 days. MOST women will have return of normal cycle in 21 days
- Side Effects : Nausea, Vomitting, Dizziness, Fatigue (All more common with Yuzep method)

IUD EC
- MOA: Inhibits ovulation
- CI: Pregnancy, Copper allergy, current STI
- FU: BHCG if no menses in 21 days.
- Side Effects: Pain, bleeding, PID, perforation, Expulsion

Cough - Key Features

1. In patients presenting with an acute cough:

a) Include serious causes (e.g. pneumothorax, pulmonary embolism [PE]) in the differential
diagnosis.

Consider life-threatening conditions: pneumothorax, PE, heart failure, exacerbation of asthma or

COPD, pneumonia

Approach to cough:

Divide patient population Divide cough

Pediatric: less than 15 yr. Acute: less than 3 weeks

Adult: older than 15 yr. Subacute: 3-8 weeks

Special populations: smoker, immunosuppression, Chronic: more than 8 weeks, more than 4
chronic (lung) disease weeks in children

For subacute cough: if history of infection treat as post-infectious until cough becomes chronic
(i.e. lasts longer than 8 weeks), if no history of infection, treat as chronic
In children with acute cough, consider croup, bronchiolitis, pertussis and treat

b) Diagnose a viral infection clinically, principally by taking an appropriate history.

No one sign, symptom or test rules out bacterial infection or rules in viral
However, if no red flag symptoms present, no CXR or further investigation is warranted
until the cough persists into chronic phase.

History Red Flag Symptom

Age Sudden fever - Suggestive of influenza,
pneumonia, SARS

74
 Shortness of Breath, chest pain – r/o life
Details of cough: Duration, ?productive, impact on threatening causes
function, other symptoms (fever, congestion, Recent surgical procedure – increases
muscle aches, SOB, chest pain) likelihood of PE, aspiration, atypical infection
Other medical conditions: asthma, COPD, Heart Other health problems – ?exacerbation of
Disease, cancer, HIV, immune-suppressed lung disease (COPD, asthma), risk of atypical
Recent surgery or hospitalization infection (immune suppression, IVDU)
Smoking status Smoker: get more infections, tend to persist
Medications, recent use of antibiotics longer
Infectious contacts, vaccination status Contact with infected person (influenza,
Occupation (infectious contacts, irritants, allergens) SARS)
Travel Recent travel – increases likelihood of
atypical infection
Physical Exam Red Flag Signs
Unusually ill, abnormal vitals
Vitals, weight
Shortness of breath, respiratory distress
Listen for cough in office, judge frequency, severity
High fever
H&N
Reduced air entry, signs of consolidation,
Cardiac – including volume status, signs of heart
restricted air entry
failure
Other signs of DVT
Chest
Weight loss, weight gain (if fluid overload)

c) Do not treat viral infections with antibiotics. (Consider antiviral therapy if appropriate.)

Acute bronchitis commonly lasts 7 to 10 days; up to 1 month in 25% of patients

Controversial, but may consider Abx if cough lasts >14 d
Abx do not increase/speed up resolution; but decreases “time feeling ill” by 0.5 days
Most people just want the cough to stop: Cough management options

Non-pharma (possibly more effective) Pharma (expert consensus only)

Decrease or quit smoking Beta agonists (only if wheezing)

Fluids (keep mucus thin) Codeine, Dextromethapham

Moist/humid air 1st gen antihistamines

2. In pediatric patients with a persistent (or recurrent) cough, generate a broad differential
diagnosis (e.g., gastroesophageal reflux disease [GERD], asthma, rhinitis, presence of a
foreign body, pertussis)

In children, divide chronic cough into specific (dx recognizable from description of
cough and/or other findings on hx or exam) and non-specific
Specific cough (Table 2)

Type of cough Diagnosis

75
Barking or brassy cough Croup, tracheomalacia, habit cough

Honking Psychogenic
Paroxysmal (+/- inspiratory “whoop”) Pertussis and parapertussis
Staccato Chlamydia in infants
Sign/Symptom Suggested etiology
Auscultatory findings (wheeze, crackles, Asthma, bronchitis, congenital lung disease,
differential breath sounds) foreign body aspiration, airway abnormality

Cough characteristics (eg, cough with choking, Congenital lung abnormalities

cough quality, cough starting from birth) Any cardiac illness
Cardiac abnormalities (including murmurs) Asthma, functional, pleuritis
Chest pain Any chronic lung disease
Chest wall deformity Chronic bronchitis, suppurative lung disease
Daily moist or productive cough Compromised lung function, immunodeficiency,
Failure to thrive cystic fibrosis
Feeding difficulties (including Compromised lung function, primary aspiration
choking/vomiting) Immune deficiency
Atypical and typical respiratory infections Primary or secondary aspiration
Neurodevelopmental abnormality Immunodeficiency, congenital lung problem,
Recurrent pneumonia airway abnormality

See ACCP Algorithm at end of document.

3. In patients with a persistent (e.g., for weeks) cough:

a) Consider non‐pulmonary causes (e.g., GERD, congestive heart failure, rhinitis), as well as
other serious causes (e.g. cancer, PE) in the differential diagnosis. (Do not assume that the
child has viral bronchitis).

Wide differential, often with multiple causes in the same person.

Start with hx and p/e as for acute cough, plus CXR. Be wary for constitutional symptoms
suggestive of cancer or TB infection.
Three most common causes in adults: Post-nasal drip, asthma, GERD

b) Investigate appropriately.

76
AAFP Algorithm

4. Do not ascribe a persistent cough to an adverse drug effect (e.g. from an angiotensin ‐
converting enzyme inhibitor) without first considering other causes.

If cough caused by ACEi, expect resolution within 2 weeks of stopping.

5. In smokers with persistent cough, assess for chronic bronchitis (chronic obstructive
pulmonary disease) and make a positive diagnosis when it is present. (Do not just diagnose a
smoker’s cough.)

See COPD topic

77
ACCP Guidelines. Table 2 show above.

Figure 3

Counselling - Key Features

1. In patients with mental health concerns, explore the role of counselling in treating their
problems. (Intervention is not just about medication use.)

Family physicians provide a significant amount of mental health care. Time is one of the major
obstacles to providing counseling in primary care. Counseling approaches developed specifically
for ambulatory patients and traditional psychotherapies modified for primary care are efficient
first-line treatments. Patients with psychiatric conditions and acute psychosocial stressors will
likely respond to problem-solving therapy or the BATHE (background, affect, troubles, handling,

78
empathy) technique. Although brief primary care counseling has been effective, patients who do
not fully respond to the initial intervention should receive multimodal therapy or be referred to a
mental health professional.

Approaches to Counseling in the Primary Care Setting

Counseling approach Problem type Patient characteristics

Highly responsive to medical authority; benefits
Five A’s Health risk behavior
from education alone with concrete plan
Requires objective evidence to consider change;
FRAMES Health risk behavior benefits from emotional support and recognition
of personal strengths
Stages of change May be at various stages with respect to
Specific behavior
(transtheoretical readiness for change; needs to consider pros and
(positive or negative)
model) cons of changing
Applies to specific Highly ambivalent, at best, about change; core
Motivational
behavior; however, range values and behavior often are inconsistent;
interviewing
of behavior is broad responds to empathy
Able to view life issues from an intellectual
EAnything that can be
Problem-solving perspective; not overwhelmed by emotional
formulated as a
therapy expression; able to process information
“problem”
sequentially and brainstorm
Reasonable verbal skills; able to meaningfully
Any type of psychosocial
BATHE* respond to questions; benefits from emotional
problem
support

BATHE = background, affect, troubles, handling, empathy; five A’s = ask, advise, assess, assist,
arrange; FRAMES = feedback about personal risk, responsibility of patient, advice to change,
menu of strategies, empathetic style, promote self-efficacy.

 — Developed specifically for family physicians.

Problem-Solving Therapy
Problem-solving therapy is a four-step approach (problem definition, generating alternative
solutions, decision making, solution verification and implementation). Its systematic framework
begins with the physician asking questions to specifically define the problem using factual,
concrete information. This method is particularly useful for patients exhibiting catastrophization,
a cognitive and emotional escalation process in which life difficulties are exaggerated. Diffusing
concerns and targeting a specific, potentially modifiable feature is particularly important when
addressing psychosocial crises.

While brainstorming for alternative solutions, the patient may indicate that the problem would be
readily solved if someone else would change. When this occurs, physicians should redirect the
patient to solutions that the patient can control to facilitate decision making and evaluation of
possible consequences for each possible solution.

Principles of Problem-Solving Therapy

79
 Component Description Examples of physician statements
Obtain factual, concrete “What part of this situation is most
information; clarify nature of the distressing for you?”
Problem definition
problem; describe the problem
objectively and succinctly “It sounds like the key difficulty is…”
“What options have you considered?”
Encourage the patient to
Generating Any others?” If the patient cannot
brainstorm and generate several
alternative solutions provide options, the physician may
possible solutions
suggest several possibilities and then
encourage the patient to generate options.
“Which of the options that we’ve talked
Evaluate possible solutions;
about seem better to you?”
Decision making predict possible consequences of
the selected solutions
“Of those, which one seems best?”
“At this point, your plan is…”
Restate the behavior plan; review
Solution verification “Is there anything that could get in the
any obstacles and develop a plan
and implementation way?”
for each
“What could you do about that specific
challenge?”

After the patient makes a decision, the physician verifies the solution by restating the plan and
addressing any obstacles that might interfere with its execution. Lastly, the physician addresses
the practical implementation of the plan. Research in health care settings supports the
effectiveness of problem-solving therapy for a range of clinical problems, including major
depressive disorder and nonadherence to a diabetes regimen.

"BATHE"
The BATHE (background, affect, troubles, handling, empathy) technique, developed specifically
for family physicians, is helpful for patients exhibiting psychiatric syndromes or a broad range of
psychosocial problems. The initial open-ended background question is a reminder to listen to the
patient’s presenting narrative. Although the hesitancy with open-ended questions is that they will
lead to overly long answers, most patients complete their answers in less than one minute, with
90 percent completing their answer in less than two minutes. If the patient takes longer than a few
minutes, keep the interview moving by politely interrupting and asking how the patient feels
about his or her concerns.

"BATHE Technique for Addressing Psychosocial Problems"

Component Examples of physician statements

“What’s going on in your life?”
Background
“What has happened since I last saw you?”
Affect “How do you feel about (a situation that has happened to the patient)?”

“Many people in that situation report feeling…”

80
 Suggest descriptors, then ask: “Do any of those words seem to fit how you’re
feeling?”
Troubles “What bothers/troubles you most about the situation?”
Handling “How are you coping with/handling the situation?”
Empathy “It sounds very frightening/frustrating/sad.”

Although the physician may briefly summarize the patient’s answer to the background question,
the physician should quickly proceed to the “affect” question. Some patients have difficulty
articulating feelings and continue to describe the problem, or they are simply unaware of their
emotions. In response, the physician may repeat the question or suggest descriptors.

The “troubles” question provides a useful focus, particularly when the problem seems
overwhelming. Although the physician may believe that he or she knows what is most upsetting,
the assumption may be incorrect. It may be tempting to recommend solutions, but handling the
problem is the patient’s responsibility. However, the patient’s attempted solutions often cause
more upheaval than the problem itself - a point that the physician may reflect back to the patient.
By focusing and labeling key dimensions, the physician’s questions facilitate the patient’s ability
to generate realistic coping strategies.

Communicating empathy creates a physician-patient partnership and indicates that the physician
is actively listening to the patient. If the visit is a follow-up, the opening question should target
events in the time interval from the last visit. Most BATHE interviews can be conducted in less
than five minutes.

2. When making the decision about whether to offer or refer a patient for counselling:
a) Allow adequate time to assess the patient.
b) Identify the patient’s context and understanding of her or his problem/situation.
c) Evaluate your own skills. (Does the problem exceed the limits of your abilities?)
d) Recognize when your beliefs may interfere with counselling.

3. When counselling a patient, allow adequate time.

4. When counselling a patient, recognize when you are approaching or exceeding boundaries
(e.g., transference, counter-transference) or limits (the problem is more complex than you
originally thought), as this should prompt you to re- evaluate your role.

Transference: Transference is the unconscious displacement onto the clinician of feelings,

thoughts, wishes, and qualities associated with an important individual from the patient’s past
(e.g., parent figure). It represents the unconscious re-creation of a past relationship in the present.
The clinician’s behavior also influences how the patient responds to him/her. Transference to the
clinician is thus based partly upon individuals from the patient’s past and partly upon the real
characteristics of the clinician.

Counter-transference: Countertransference is the clinician’s conscious and unconscious feelings

and thoughts about the patient. It consists of:

The clinician’s feelings and thoughts about an individual from a previous relationship
that are displaced onto the patient

81
 Feelings and thoughts induced in the clinician by the patient’s behavior

Recognizing countertransference provides data that help the clinician to discern problems that the
patient encounters in relationships outside the therapy. Other people probably respond to the
patient in a manner similar to the clinician.

In mental health settings, most evidence-based psychotherapies require a minimum of 10 to 15

sessions and approximately 50 percent of patients do not complete the treatment course.
Evidence-based reviews of primary care counseling indicate that brief approaches may lead to
short-term reductions in psychosocial distress and longer-term reductions in alcohol use and
depressive symptoms. The models presented above may be implemented in approximately five to
10 minutes and can be integrated into most office visits. These strategies make up the first stage
of a stepped-care approach in which brief interventions, including providing patients with
screening information, are the initial treatments. There are typically two options for patients who
fail or incompletely respond to the initial intervention. For highly symptomatic patients or those
with multiple high-risk behaviors, referral to a mental health specialist may be the next step.
Alternatively, in less severe situations, the physician may add a second intervention, such as
pharmacotherapy, more intensive education, or an additional counseling strategy. If problems
persist, referral to a mental health or substance abuse specialist is recommended.

Crisis - Key Features

1. Take the necessary time to assist patients in crisis, as they often present unexpectedly.

Reassure that you are available to help. Commend them for seeking help and validate their
experience. Establish rapport and use active-listening skills.

2. Identify your patient’s personal resources for support (e.g., family, friends) as part of your
management of patients facing crisis.

3. Offer appropriate community resources (e.g., counselor) as part of your ongoing

management of patients with a crisis.

4. Assess suicidality in patients facing crisis.

5. Use psychoactive medication rationally to assist patients in crisis.

6. Inquire about unhealthy coping methods (e.g., drugs, alcohol, eating, gambling, violence,
sloth) in your patients facing crisis.

7. Ask your patient if there are others needing help as a consequence of the crisis.

8. Negotiate a follow-up plan with patients facing crisis.

9. Be careful not to cross boundaries when treating patients in crisis (e.g., lending money,
appointments outside regular hours).

10. Prepare your practice environment for possible crisis or disaster and include colleagues

82
and staff in the planning for both medical and non-medical crises.

11. When dealing with an unanticipated medical crisis (e.g., seizure, shoulder dystocia),
a) Assess the environment for needed resources (people, material).
b) Be calm and methodical. c) Ask for the help you need.

Overview
a. Initial supportive assessment and safe environment, validate experience focus on rapport, open
communication
b. Evaluate medical (nutrition, injury related pain) needs and then psychiatric care (suicide,
homicide)
c. History taking: detailed history of events and previous traumatic events. Screen for comorbid
depression and anxiety
d. Develop action plan: include emotional stability and personal feelings of control of situation,
have list of resources (personal and community)
e. Follow-up to assess progress. Resources for support can include internal ones (e.g., exploration
of effective coping mechanisms and constructive thinking patterns.)

Preparation
Prepare your practice environment for possible crisis or disaster and include colleagues and staff
in the planning for both medical and non-medical crises.
Establish office policies for managing agitated/dangerous patients
Prepare for common emergencies encountered in the office setting (e.g. in general, asthma,
anaphylaxis, shock, seizures, and cardiac arrest).
Purchase equipment / medications for anticipated emergencies
Familiarize all staff with equipment and local protocols When dealing with an unanticipated
medical crisis (e.g., seizure, shoulder dystocia):

Assess the environment for needed resources (people, material).

Assign roles / delegate
Anticipate equipment needs.

Management
Be calm and methodical.
ABC’s, vitals, etc.
Reassess frequently
Communicate your assessments and thought process to team
Use closed-loop communication when giving orders
Ask for the help you need. Offer appropriate community resources (e.g., counselor) as part of
your ongoing management of patients with a crisis.
If mental and psychiatric statuses are not stable, this may include psychiatric referral,
hospitalization, or involuntary commitment.
Enquire about unhealthy coping methods (e.g., drugs, alcohol, eating, gambling, violence, sloth)
in your patients facing crisis.
Ask your patient if there are others needing help as a consequence of the crisis.
Assess suicidality in patients facing crisis:

See priority topic Suicide

83
 Thought of death, degree of intention, lethality of methods
Availability of means (firearms)
Prep attempts, nature, and family hex of suicide
Response to crisis may be self-harming behaviors

Homicidality?

Legally mandated duty to warn if there is a clear risk to identifiable person(s) that could
cause serious and imminent harm.

Suspected child abuse?

Statutory requirement to report to public authorities

Victim of abuse?

Encourage them to remove themselves (and others) from dangerous situations.

"Medications:"
Use psychoactive medication rationally to assist patients in crisis.
Provide rx for physical pain or for sleep
Take into account previous medications and responses to medications in the past and comorbid
illnesses
No evidence in acute setting 0-72hrs
Assessment of duration of crisis (once, cumulative or ongoing)
Goal of medication is to

1. Decrease symptoms of re-experiencing, avoidance/numbness or hyper-arousal

2. Help with comorbid illness
3. Reduce suicidal, impulsive and aggressive behavior

First Line:

SSRI for 8-12 weeks, first week reduction in anger/irritability, 2-4wk for rx effect,
fluoxetine has been studied, fluvoxamine may have better sleep related improvements
TCA- some studies of effectiveness of amitriptyline in male combat veterans
Benzodiazepines-help with anxiety and sleep, addictive potential
Beta-blockers- propranolol acutely may reduce later symptoms of post-traumatic stress
disorder

Follow-up
Reassess status/safety, reinforce positive efforts Immediacy should fit clinical scenario
(seriousness of crisis, reliability of patient). Higher level of care indicated if failure to improve
with current treatment.

84
"Things to Avoid"
Take care not to cross boundaries when treating patients in crisis
Exchanging gifts, services, and money may cause feelings of obligation or imply a dual
relationship.
Appointments outside of regular hours (especially unchaperoned) are associated with additional
boundary violations and cases of misconduct.
Excessive self-disclosure can strain rapport.
Physical contact (e.g. hugs, kisses, arm stroking, etc.) can be misinterpreted and blur relationship
boundaries.

Croup - Key Features

1. In patients with croup:

a) Identify the need for respiratory assistance (e.g., assess ABCs, fatigue, somnolence,
paradoxical breathing, in drawing)
b) Provide that assistance when indicated.

Respiratory compromise evaluation

- Appearance

o Hypoxia: restless or anxious

o somnolent
o Tone - decreased muscle tone, appear limp, weak.
o Interactiveness - does not respond to a caregiver or appropriately resist examination.
o Consolability
o Look/gaze - unresponsive stare suggests an altered mental status.
o Speech/cry - weak cry, a hoarse or muffled voice suggests upper airway obstruction
o Drooling, dysphagia –oropharyngeal or laryngotracheal obstruction.

- Breathing

o increased work of breathing

• Decreased work of breathing may indicate progression toward respiratory failure
o Airway sounds - stridor, snoring, grunting, wheezing
o Positioning - "sniffing position" , tripod position
o Accessory muscle use: supraclavicular, intercostal, and/or substernal groups
• Head bobbing (extension of the head on inhalation and forward movement on
exhalation)
• nasal flaring
o Vitals

- Circulation

o Pallor or cyanosis
o Poor capillary refill or cool skin
o Pulsus paradoxus –an exaggeration (greater than 10 mmHg) of the normal decrease in
blood pressure during inspiration
• correlates with degree of airway obstruction

85
Management
- Complete upper airway obstruction: Needle cricothyrotomy
- Foreign body

o Maneuvers should only be used for patients who are unable to phonate
o Back blows/chest thrusts (<1 year of age)
o Abdominal thrusts (≥1 year of age)
o Manual removal with finger sweep
o Laryngoscopy

- Laryngospasm: Positive pressure with a ventilation bag and tight fitting mask
- Soft tissue upper airway obstruction

o Head tilt/chin lift

o Jaw thrust: for patients who may have cervical spine injury
o Nasopharyngeal airway: May be tolerated by a conscious patient
o Oropharyngeal airway: in an unconscious patient

- Respiratory failure

o Bag-mask ventilation
o Endotracheal intubation

- Tension pneumothorax

o Needle thoracentesis
o chest tube placement following emergent decompression

- Cardiac tamponade: Pericardiocentesis

2. Before attributing stridor to croup, consider other possible causes (e.g., anaphylaxis, foreign
body (airway or esophagus), retropharyngeal abcess, epiglottitis).

Stridor DDx
- Congenital

o Nasal deformities: Choanal atresia or agenesis, septum deformities, turbinate

hypertrophy, vestibular atresia or stenosis.
o Pharynx
• Craniofacial anomalies: Crouzon's, Pierre Robin, Apert's Syndrome.
• Tongue Macroglossia and glossoptosis
o Larynx
• Laryngomalacia: Most common chronic stridor
• Laryngeal webs
• Laryngeal cysts
• Subglottic hemangioma
• Subglottic stenosis
o Trachea

86
 • Tracheal stenosis
• Tracheomalacia

- Bacterial tracheitis

o 6 mo to 8 yo
o S. aureus, Strep pyogenes, S. pneumonia, H. influenzae
o Initially similar to croup (hoarseness, barking cough, stridor)
o High fever, toxic, poor response to epinephrine
o IV antibiotics
o Intubation

- Epiglottitis

o Hemophilus influenza (rare since vaccination)

o 1-8 year old
o High fever, no barky cough, dysphagia, drooling, anxious appearance, sitting forward
in sniffing position
o Secure airway

- Laryngeal diphtheria

o Any age
o Gradual onset (2-3 days)
o Hoarseness, barking cough, dysphagia, fever
o Grayish-brown membrane on tonsils
o Inquire about vaccination

- Retropharyngeal abscess

o < 6 yo
o May be preceded by trauma, FB aspiration, URI
o Sore throat, dysphagia, drooling
o Neck pain, stiffness

- Foreign body

3. In any patient presenting with respiratory symptoms, look specifically for the signs and
symptoms that differentiate upper from lower respiratory disease (e.g., stridor vs. wheeze vs.
whoop).

Stridor

- Caused by the oscillation of a narrowed airway

- Suggests significant obstruction of large airways
- Stridor from extrathoracic area is more pronounced during inspiration
- Stridor caused by obstruction at the glottis (vocal cords) may occur during inspiration
only, or during both inspiration and expiration
- Originates in the intrathoracic airways more pronounced on exhalation

87
Wheeze

- Occur during inspiration or expiration

- Can originate from airways of any size
- Stridor refers to a monophonic wheeze that is loudest over the central airways

4. In a child presenting with a clear history and physical examination compatible with mild to
moderate croup, make the clinical diagnosis without further testing (e.g., do not routinely X-
ray).

Definition
- Aka laryngotracheobronchitis
- Parainfluenza
- Most commonly 6 mo to 3 years
- Autumn/winter months generally
- Abrupt onset of barmy cough
- Inspiratory stridor, hoarseness, respiratory distress
- Severity

o Mild: occasional barky cough, no stridor at rest, no to mild suprasternal/intercostal

indrawing
o Moderate: frequent barky cough, stridor, suprasternal/sternal wall retraction at rest, no
or little distress or agitation
o Severe: occasional expiratory stridor, marked sternal wall retractions, significant
distress and agitation
o Impending respiratory failure: lethargy, or decr LOC, dusky appearance on RA

History
- With or without antecedent upper respiratory symptoms of cough, rhinorrhea and fever
- Symptoms occur in evening
- Seal like barmy cough
- Inspiratory stridor
- Hoarseness
- No to moderate fever
- Symptoms fluctuate worse when child agitated
- Majority symptoms resolve within 48 hrs
- Resolution of croup symptoms, children may have typical URTI like symptoms

Physical
- Febrile, tachy, tachypnea
- O2 sats in severe cases
- Seal like barmy cough
- Hoarse voice
- Stridor (mostly inspiratory)
- Intercostal retractions
- No drooling

88
- Nontoxic
- Impending respiratory failure

o Change in mental status

o Pallor
o Dusky
o Decreased retractions
o Decreased breath sounds, decreasing stridor

5. In patients with a diagnosis of croup, use steroids (do not under treat mild-to-moderate cases
of croup)

Treatment
- Comfortable
- Do not agitate
- Oxygen if respiratory distress/hypoxia (<92%)

o Blow by : hose with end open held near nose/mouth

- Epinephrine

o Severe respiratory distress (sternal wall indrawing and agitation)

• Improvement occurs within minutes
• Wears off after 1 hr
o Racemic 0.5mL of 2.25% soln diluted into 3mL of NS or sterile H2O via nebulizer
o L Epinephrine 1:1000 sol’n via nebulizer
o May be repeated as necessary

- Dexamethasone

o For all children, regardless of severity

o Improvement after 2-3 hrs
o Persist 24-48 hrs
o Single dose - No evidence to support multiple doses
o 0.6 mg/kg po/IM
o Po is well absorbed, reaches peak serum levels as rapidly as IM
• Both equivalent results
o Reduces
• Rate/duration of intubation
• Rate/duration of hospitalization
• Rate of return to medical care
• Duration of symptoms in children with mild, moderate, severe symptoms

- Admission

o Respiratory compromise after >4 hrs with corticosteroids

o Relative
• Patient living long distance away or inadequate transportation

89
 • Inadequate observation or f/u
• Significant parental anxiety
• Recurrent ED visits within 24 hrs

- Discharge from ED

o Mild symptoms
o 2 hrs after epinephrine

6. In a patient presenting with croup, address parental concerns (e.g., not minimizing the
symptoms and their impact on the parents), acknowledging fluctuating course of the disease,
providing a plan anticipating recurrence of the symptoms.

- Symptoms worse at night

- Discharge instructions

o Provide humidified air, Steamed bathroom environment

o Avoid irritants (Smoke)
o Return if signs of Respiratory distress
o Symptoms lasts 3-5 days, up to 10 days

Deep Venous Thrombosis - Key Features

1. In patients complaining of leg pain and/or swelling, evaluate the likelihood of deep venous
thrombosis (DVT) as investigation and treatment should differ according to the risk.

2. In patients with high probability for thrombotic disease (e.g., extensive leg clot, suspected
pulmonary embolism) start anticoagulant therapy if tests will be delayed.

3. Identify patients likely to benefit from DVT prophylaxis.

4. Utilize investigations for DVT allowing for their limitations (e.g., Ultrasound and D-dimer).

5. In patients with established DVT use oral anticoagulation appropriately, (e.g., start
promptly, watch for drug interactions, monitor lab values and adjust dose when appropriate,
stop warfarin when appropriate,provide patient teaching).

6. Consider the possibility of an underlying coagulopathy in patients with DVT, especially

when unexpected.

7. Use compression stockings in appropriate patients, to prevent and treat post-phlebitic

syndrome.

Introduction
Risk factors= acronym THROMBOSIS

90
 Trauma,hypercoag.,OCP,malignancy,birth control,obesity,surgery,immobility,sickness

Most important sequale is venous insufficiency pulmonary embolism in 50%of proximal

thrombosis

Etiology =Virchow’s triad

Endothelial injury, stasis & hypercoagulability
Hypercoag may be inherited or idiopathic & acquired like age(60), trauma, surgery, neoplasm,
hyperhomocystinemia (TT folic acid 5mg daily), antiphospholipid antibodies (APLA), blood
dyscriasis, hormones & immobilization

Clinical picture:
Homan’s sign is calf pain on dorsifection of the foot (classic sign but not specific or sensitive)
Tenderness of affected leg and palpable cord like structure are also classic symptoms
Unilateral leg edema is the most sensitive indicator of DVT

91
92
Wells Criteria

Differential Diagnosis

Ruptured Baker’s cyst

Cellulitis
Ruptured Achilles tendon
Lymphedema
Superficial phlebitis

93
Algorithm for the Initial Work-up of Suspected DVT

D-dimer (fibrin degradation product) is usually increased in thromboembolic disease

Sensitivity of about 80% for DVT but Specificity of 30% [i.e. not the greatest test]
Real utility is its negative predicative value of over 90% [useful only if the test is negative]
Many studies show that low pre-test probability by Wells criteria and negative d-dimer rules out
DVT

There is about 1% false negative rate with negative US and negative D-dimer

Doppler (95% sensitive for proximal DVT, 75% for distal calf DVT)
Distinction between proximal and distal DVT is important because calf only DVT rarely leads to
PE
Prevention of pulmonary embolism is the reason for treating patients with DVT

Initial treatment
Unfractionated heparin =bolus 7500-10.000 IU followed by infusion of 1000-1500 IU\H or
weight based monogram

Reversible by protamine
Need to monitor aPT(level=2xnormal)

LMWH: subcutaneous as effective as heparin

94
 No monitor
Lower risk of HIT
Renal clearance & need adjustment

HIT patients = need hirudin, fondaparinux

If life threatening thrombosis we can use thrombolytic drugs like TPA, streptokinase

Long term treatment

Warfarin with target INR
LMWH in cancer patients

 DVT 1st episode=duration 3 months

 1st episode with ongoing risk like cancer, APLA consider indefinite period of treatment.
 1st episode with single inherit risk 6-9 months or indefinite
 Recurrent DVT=indefinite period.
 IVC filters if anticoagulant contraindications, with recurrent PE, pulmonary HTN, or pt
require urgent surgery.
 Pregnancy=use LMWH then warfarin 4-6 weeks postpartum. Total duration 3-6 M.

Initiation of warfarin
10 mg dose= shorter time to get target INR than start with 5mg without increase of side effects.
Overlap 4-5 days of heparin & warfarin required
Heparin antagonist vitamin K should be discontinued once harm stopped otherwise increase VTE.

Prophylaxis=BID 5000 IU if low risk, TID if high risk

 Risk of bleeding from heparin 7%

 Absolute contraindications of heparin: Include blood dyscrasias, recent ocular,
intracranial surg., recent ICH, active bleeding
 DVT initial u\s should be followed by another u\s in a week to for extension to proximal
veins

Dehydration - Key Features

1. When assessing the acutely ill patient, look for signs and symptoms of dehydration. (e.g.,
look for dehydration in the patient with a debilitating pneumonia).

Do this.

95
2. In the dehydrated patient, assess the degree of dehydration using reliable indicators (e.g.,
vital signs) as some patients' hydration status may be more difficult to assess (e.g., elderly, very
young, pregnant).

In patients with unstable vital signs or decreased level of consciousness, the possibility of severe
dehydration should be considered. Although change in weight is the most accurate way to
determine the degree of dehydration , this is often not practical and physical signs may be helpful.

The Degree of dehydration in children may be assessed as follows (1):

Degree of Mild (5-7% body Moderate (7-9% body Severe (>10% body
dehydration weight) weight) weight)
Fontanelle Slightly sunken Very sunken Very sunken
Mucous membranes Slightly sticky Dry Very dry
Skin turgor Normal Slightly decreased Markedly decreased
Capillary refill time Normal (<3 seconds) Normal (<3 seconds) Delayed (≥3 seconds)
Urine output Normal Slightly decreased Decreased or absent
Mental status Normal Slightly fussy Irritable or lethargic

The degree of dehydration in adults is less quantifiable, but signs of dehydration include the
following(2):
• Pulse rate >90
• Postural hypotension
• Decreased Urine Output
• Supine hypotension and absence of palpable pulse
• Dry tongue
• Sunken eyeballs
• Skin pinch
• Change in mental Status

Signs and symptoms of dehydration in the frail elderly are non specific such as: change in mental
status or falls. Orthostatic hypotension and dry mucous membranes may only be present with
profound dehydration(3).

3. In a dehydrated patient,
a) determine the appropriate volume of fluid for replacement of deficiency and ongoing needs.

In children using oral rehydration therapy, the fluid deficit (mild 5-7%; mod 7-9%) can be
corrected over 3-4 hours with appropriate oral rehydration formulas. Fluid deficits treated with
isotonic IV preparations should be corrected more slowly with boluses of 10 to 20mg/kg as
needed(1). Maintenance fluids can be calculated using the 4, 2, 1 rule and ongoing losses should
also be replaced. One can estimate a loss of 60-120 ml per diarrheal stool or vomiting episode(2).
Similar principles apply to adults.

b) use the appropriate route (oral if the patient is able; IV when necessary).

Oral rehydration therapy works well and is the first choice for mild to moderate dehydration(1).

96
4. When treating severe dehydration, use objective measures (e.g., lab values) to direct ongoing
management.

In severe dehydration, serum electrolytes, bicarbonate, blood urea nitrogen, creatinine, and serum
glucose levels should be obtained(4). This should not delay care.

5. In a dehydrated patient,
a) identify the precipitating illness or cause, especially looking for non-gastro-intestinal,
including drug-related, causes.

For instance, cognitive impairment, impaired thirst mechanisms, sepsis and diuretics may all
cause dehydration(3).

b) Treat the precipitating illness concurrently.

Nephrologists should only look at the dehydration, while decisions about the diuretics should be
left to the cardiologist, and no antibiotics should be prescribed without an ID consult.

6. Treat the dehydrated pregnant patient aggressively, as there are additional risks of
dehydration in pregnancy.

During pregnancy, decreased systemic vascular resistance, increased venous pooling, changes in
respiratory physiology and the presence of two rather than one patients makes the prompt
treatment of dehydration imperative(5).

Dementia - Key Features

1. In patients with early, non-specific signs of cognitive impairment:

a) Suspect dementia as a diagnosis.
b) Use the Mini-Mental State Examination and other measures of impaired cognitive function,
as well as a careful history and physical examination, to make an early positive diagnosis.

2. In patients with obvious cognitive impairment, select proper laboratory investigations and
neuroimaging techniques to complement the history and physical findings and to distinguish
between dementia, delirium, and depression.

3. In patients with dementia, distinguish Alzheimer’s disease from other dementias, as

treatment and prognosis differ.

4. In patients with dementia who exhibit worsening function, look for other diagnoses (i.e.,
don’t assume the dementia is worsening). These diagnoses may include depression or
infection.

5. Disclose the diagnosis of dementia compassionately, and respect the patient’s right to
autonomy, confidentiality, and safety.

6. In patients with dementia, assess competency. (Do not judge clearly competent patients as
incompetent and vice versa.)

7. In following patients diagnosed with dementia:

97
a) Assess function and cognitive impairment on an ongoing basis.
b) Assist with and plan for appropriate interventions (e.g., deal with medication issues,
behavioural disturbance management, safety issues, caregiver issues, comprehensive care
plans, driving safety, and placement).

8. Assess the needs of and supports for caregivers of patients with dementia.

9. Report to the appropriate authorities patients with dementia who you suspect should not be
driving.

10. In patients with dementia, look for possible genetic factors to provide preventive
opportunities to other family members, and to aid in appropriate decision-making (e.g., family
planning).

Note: Specific cognition-enhancing pharmacotherapy (initiation/discontinuation) may be

assessed later, as controversy on indications diminishes.

Recognition: no general population screening, cognitive impairment suspected with a Hx

of decline in occupational, social or daily functional status, may be reported by pt, family
member, friend and/or caregiver.

History
Complete Hx: (important to get collateral Hx)

• Review medications, OTC

• Alcohol dependence, drug Hx
• Symptoms:

• Onset gradual, abrupt, stepwise? Dramatic fluctuations in cognition?

• Needs new information repeated or asks same question repeatedly?
• Disorientation to time of day or place, ex. Gets lost when away from home?
• Difficulty with problem solving, sequencing, multi-tasking, mental flexibility?
(Executive Function)
• Aphasia: Difficulty understanding or finding words and expressing oneself?
• Apraxia: Difficulty with complex learned motor behaviors, ex: tying shoes, dressing,
playing instrument, knitting
• Agnosia: Difficulty recognizing faces or recognizing objects and knowing what they are
used for?
• Behavioral and psychological symptoms of dementia, ex: agitation, delusions,
hallucinations, apathy, depression, social withdrawal, unaccustomed anger or irritability?
• Other: hx of falls, poor balance, urinary incontinence?
Physical Exam Diagnostic Tests
• General physical • CBC • Neuroimaging not routinely indicated
exam
• Lytes/Ca/glucose • CT/MRI of brain may be useful, ex: age <60,
• Gait and balance • TSH abrupt or rapid progression, atypical or Dx
• Parkinsonian features • Serum B12 uncertain, Hx of CA, recent head injury, CNS
• Other tests based on signs, Vasc dementia suspected, pt on
• AbN neurological clinical suspicion: HIV, anticoagulants, new deterioration in gait, onset
signs, esp. lateralizing RPR, renal/liver function incontinence

98
or localizing signs
• Carotid bruits,
vasculature
Functional Status Objective Tests of Cognition
IADLs
• Meal
prep/housewor • Standardized Mini Mental State Exam
ADLs
k (SMMSE)
•
• Managing
Bathing/personal
finances/meds • Clock drawing test
hygiene/toileting
• Shopping • Montreal Cognitive Assessment (MoCA) for
• Dressing
• Driving, suspected Mild Cognitive Impairment (MCI)
• Walking
access to • Record for baseline and F/U
transportation
• Telephone

A new presentation of cognitive decline or confusion, rule out acute or treatable causes,
distinguish between dementia, delirium and depression

Feature DEMENTIA DELIRIUM DEPRESSION

Gradual; may coincide with life
Onset Insidious Acute
changes
Hours to < one month, At least 2 weeks, but can be
Duration Months to years
seldom longer several months to years
Stable and Progressive
Fluctuates: worse at night
Diurnal: usually worse in am,
Course
Vasc Dementia: Usually improves as day goes on
Lucid periods
stepwise
Fluctuates lethargic or
Alertness Generally N N
hyper-vigilant
May be N but often
Always impaired:
Orientation impaired for time/later in Usually N
time/place/person
the dz, place
Impaired recent and Recent memory may be
Memory sometimes remote Global memory failure impaired, long term memory
memory intact
Disorganized, distorted,
Slowed; reduced interests Usually slowed, preoccupied by
fragmented
sad and hopeless thoughts;
Thoughts Makes poor judgments somatic preoccupation
Bizarre ideas and topics
Words difficult to find
such as paranoid
Perseverates Mood congruent delusions
grandiose
Perception N Distorted (visual and Intact
auditory)
Hallucinations (often Hallucinations absent except in

99
 visual) Hallucinations common psychotic depression
Flat, unresponsive or sad and
Shallow, apathetic, labile
Irritable, aggressive, fearful
Emotions
fearful
Irritable
May be irritable
Often disturbed, nocturnal
wandering common
Sleep Nocturnal confusion Early morning awakening
Nocturnal confusion
Other physical dz may Past Hx of mood d/o
Poor insight into deficits
Other not be obvious
features Poor effort on cognitive testing;
Careless
Inattentive gives up easily
Comprehensive
Standard Confusion Assessment Geriatric Depression Scale
assessment (hx, Cpx, lab,
Tests Method (CAM) (GDS)
SMMSE)

Diagnosis:
Multiple cognitive deficits manifested by both:

Memory impairment and ≥ 1cognitive deficits:

• Aphasia (language disturbance)
• Apraxia (impaired ability to carry out purposeful movement)
• Agnosia (failure to recognize objects),
• Disturbance in executive functioning (planning, organizing, abstract thinking).

Associated with a decline in social/occupational functioning

Not explained by other neurological, medical or Psychiatric disorders

IF not all criteria met consider Mild Cognitive impairment: subjective memory impairment and
objective impairment with other cognitive abilities preserved, with no medical, neurological or
psychiatric d/o.
• May progress to dementia, F/U q6mos and counsel prn

Distinguish Alzheimer’s dz from other Dementia’s (often Mixed Dementia: Alzheimer and
Vascular Dementia):

Vascular Dementia with Lewy Fronto-temporal

Probable AD Other examples:
Dementia Bodies Dementia
• Gradual • Abrupt onset • Dementia present • Insidious onset and • Normal pressure
progression and stepwise gradual progression Hydrocephalus
decline • At least 2 of marked
• Negative fluctuation in cognition, • Early impairment in • Dementia of late
CNS exam • Temporal visual hallucinations, control of personal, stage Parkinson’s

100
 connection b/w social and
dementia and interpersonal conduct Dz or HIV
• No early gait
CVD • Dementia
involvement Parkinsonism
• CVD by focal • Emotional blunting, associated with
Prognosis:
signs and loss of insight alcohol dependence
imaging • Language deficits

In patients with dementia who exhibit worsening function, look for other Dx, don’t assume the
dementia is worsening. These dx’s may include depression or infection.

Disclose the diagnosis compassionately and respect the patient’s right to autonomy,
confidentiality and safety.
• At disclosure visit, Ask if the caregiver/family member can be in attendance (yes in most
situations)
• Consider timing/extent of info and pt/caregiver readiness for coping with the diagnosis
• Use open-ended Q’s ex: What do you think is causing the change in your memory and thinking?

• Establish a relationship – pt/caregiver input is valued and integral to goal setting and care
planning
• Discuss anticipated prognosis in a sensitive manner and indicate commitment to F/U care
• Provide written info about dementia care and around support and resources as appropriate

In patients with dementia, assess competency. (Do not judge clearly competent pt’s as
incompetent and vice versa)

Develop an on-going care plan/clinical action plan:

• Identify and modify potential safety issues with pt and caregiver ex: driving, nutrition, med
mgmt., kitchen safety, hygiene and wandering
• Support pt functioning and decision making to maximize independence ex: socialization,
financial and legal planning, neglect and abuse, end of life care
• Treat co-morbid conditions ex: HTN, depression, delirium, DM
• Refer pt and caregiver to Home and community care for adult day care, home care, respite care,
assisted living, long term care services as appropriate
• Refer pt and caregiver to the Alzheimer society
• F/U at least every 6 months

Assess the needs of and supports for caregivers of pt’s with dementia.

Report to the appropriate authorities patients with dementia who you suspect should not be
driving.
• Enter into discussion with the patient early about eventual driving cessation
• Get collateral hx of driving habits from observers
• On cognitive testing, visuospatial abilities and judgment may be predictors of driving risk
• In doubt recommend a performance based eval, ex: road test by ICBC, DriveAble or a driver
fitness review through the office of the superintendent of motor vehicles

101
In pt’s with dementia, look for possible genetic factors to provide preventative opportunities to
other family members and to aid in appropriate decision-making (ex: Family planning).
• Minority of AD cases are familial, autosomal dominant (5-10%), there are four genes that affect
disease development
• With ≥2 Family members with early onset Dementia <60, referral for genetic counseling and
testing offered
• If gene identified: referral for 1st degree relatives offered

Quick note on Pharmacotherapy (note: not a key feature):

AChEI’s are approved for symptomatic Rx of mild to moderate Alzheimer’s type dementia

o VaD or mixed dementia: Treat vascular risk factors. Possible role (AChEIs)
o Mixed dementias: Treat both pathologies
o DLB: Many patients respond to AChEIs

• Starting dose/usual effective max dose

o Donepezil (Aricept) 5mg daily/10mg daily

o Rivastigamine (Exelon) 1.5mg BID/3-6mg BID
o Galantamine (Reminyl) 8mg ER daily/16mg-24mg ER daily

• AChEI Relative CI’s: PUD, hepatic or renal dz, significant bradycardia or AV block, significant
bronchospastic dz, obstructive urinary dz, epilepsy or hx of seizure

Behavioral and psychological symptoms of Dementia (BPSD):

• 1st line: Environmental and behavioral modifications

• Pharmacological interventions (1st line: atypical antipsychotic agents, cautions around
increased risk of CV events, stroke, and mortality) for BPSD are only recommended
when:
o Alternate therapies are inadequate on their own
o There is an identifiable risk of harm to the patient and others
o Symptoms are severe enough to cause suffering and distress
• Use of antipsychotics in patients with DLB is associated with an increased risk of
extrapyramidal side effects and should be used with extreme caution

Depression - Key Features

1. In a patient with a diagnosis of depression:

a) Assess the patient for the risk of suicide.
b) Decide on appropriate management (i.e., hospitalization or close follow-up, which will
depend, for example, on severity of symptoms, psychotic features, and suicide risk).

2. Screen for depression and diagnose it in high-risk groups (e.g., certain socio-economic
groups, those who suffer from substance abuse, postpartum women, people with chronic pain).

3. In a patient presenting with multiple somatic complaints for which no organic cause is
found after appropriate investigations, consider the diagnosis of depression and explore this
possibility with the patient.

102
4. After a diagnosis of depression is made, look for and diagnose other co-morbid psychiatric
conditions (e.g., anxiety, bipolar disorder, personality disorder).
5. In a patient diagnosed with depression, treat appropriately:
- drugs, psychotherapy.
- monitor response to therapy.
- active modification (e.g., augmentation, dose changes, drug changes).
- referral as necessary.

6. In a patient presenting with symptoms consistent with depression, consider and rule out
serious organic pathology, using a targeted history, physical examination, and investigations
(especially in elderly or difficult patients).

7. In patients presenting with depression, inquire about abuse: - sexual, physical, and
emotional abuse (past and current, witnessed or inflicted). - substance abuse.

8. In a patient with depression, differentiate major depression from adjustment disorder,

dysthymia, and a grief reaction.

9. Following failure of an appropriate treatment in a patient with depression, consider other

diagnoses (e.g., bipolar disorder, schizoaffective disorder, organic disease).

10. In the very young and elderly presenting with changes in behaviour, consider the diagnosis
of depression (as they may not present with classic features).

Background:
1. A type of mood disorder (includes: depressive, bipolar, and secondary to general medical
condition (GMC))
2. Must distinguish between normal sadness i.e. bereavement
3. Prevalence rate of 3 to 5% in general population in Canada
4. Runs a chronic or recurrent course with high risk of mortality and morbidity
5. Neurotransmitter dysfunction at level of synapse (decreased activity of serotonin,
norepinepherine, dopamine)
6. Mean onset ~30 year, M:F 1:2

History:
Depression: MSIGECAPS

M: Depressed Mood
S: Increase/decreased Sleep
I: Decreased Interest
G: Guilt
E: Decreased Energy
C: decreased Concentration
A: Increased/decreased Appetite
P: Psychomotor retardation
S: Suicidal ideation

Mania: GST PAID

G: Grandiosity

103
 S: Sleep, decrease need
T: Talkative
P: Pleasure and pain
A: Activity
I: Inattention
D: Distractibility

Psychotic features: up to 20% of MDD patients can exhibit psychotic features of hallucination or
delusions

Medical Workup for Mood Disorder:

Routine screening

• Physical examination (to rule out general medical condition)

• CBC-d, electrolytes, liver panel, glucose, urea, creatinine, folate (metabolic
disturbance), Vit B12
• Thyroid function test
• Electrolytes
• Urinalysis, urine drug screen
• ECG
• Ethanol level (intoxication or withdrawal)

Major Depressive D/O

1. 5 (or more) symptoms that affect function for >2 weeks and represent a change in function.
(See DSM IV)
2. Not due to physiological effects of a general medical condition or substance abuse

Differential:
Dysthymia, Bipolar Disorder, Substance Induced Mood Disorder

Treatment:
1. Emergent: admit to hospital for high suicide risk or danger to self or others. May require
certification.
2. Treatment Options:

a) Medication (SSRI, SNRI, Bupropion, Mirtazipine, TCA, and MAOI) If patient is

started on medication they must be monitored weekly for suicidal ideation for 4 to 6
weeks. Note: anxiety and depression often co-exist so treatment of depression can
unmask anxiety disorder and unresponsive anxious patients should be screened for bi-
polar
b) Psychotherapy (interpersonal, cognitive, behavioural, supportive, psychodynamic)
c) Social: Education, regular exercise program, establish therapeutic alliance

3. Follow up: close follow up for response and safety assessment

4. Referral: refer to psychiatry if treatment resistant, psychotic features, thought disorder or
unsure of diagnosis.

104
Diabetes - Key Features

1. Given a symptomatic or asymptomatic patient at high risk for diabetes (e.g., patients with
gestational diabetes (GDM), obese, certain ethnic groups, and those with a strong family
history), screen at appropriate intervals with the right tests to confirm the diagnosis.

Risk factors for type 2 diabetes:

- Age ≥ 40 years
- T2DM in a first degree relative
- High risk population (Aboriginal, Hispanic, South Asian, Asian, African descent)
- History of impaired glucose tolerance or impaired fasting glucose
- Presence of complications associated with diabetes
- Vascular disease
- History gestational diabetes
- History of delivery of a macrosomic infant
- Hypertension
- Dyslipidemia
- Overweight
- Abdominal obesity
- Polysyctic Ovarian Syndrome
- Acanthosis nigricans
- Schizophrenia
- Other (see Canadian Diabetes Association 2008 Clinical Practice Guidelines – Appendix 1)

Screening recommendations:
- No screening for type 1 diabetes - no evidence for interventions to prevent or delay disease
- For all adults ≥ 40 years, perform fasting plasma glucose (FPG) every 3 years
- Consider testing more often and/or earlier in those with risk factors.
- FPG of 6.1 to 6.9 → 75g oral glucose tolerance test (OGTT)
- FPG of 5.6 to 6.0 + risk factors →75g OGTT
- Patients with GDM should have a 75g OGTT at 6 weeks to 6 months postpartum
- Those diagnosed with GDM are considered high risk, consider screening earlier/more often and
screen prior to subsequent pregnancy.

 See flow diagram on page S15 of the Canadian Diabetes Association 2008 Clinical
Practice Guidelines or BC Clinical Practice Guidelines on Diabetes Care – Appendix A

2. Given a patient diagnosed with diabetes, either new-onset or established, treat and modify
treatment according to disease status (e.g., use oral hypoglycemic agents, insulin, diet, and/or
lifestyle changes).

Optimal diabetes care ultimately depends on the daily commitment of the individual to self
manage, with support from a multidisciplinary team. High importance placed on self management
education and individualized treatment. In addition to diet, nutrition and exercise, smoking
cessation should be encouraged and supported.

Diet: Should be referred to a dietician.

- Follow Eating well with Canada’s Food Guide.

105
- Meal and carbohydrate regularity and spacing is important
- Carbohydrate 45-60% of energy and choose complex carbohydrates
- Protein 15-20% of energy
- Fat <15% of energy
- Alcohol has risk of delayed hypoglycaemia if using insulin or insulin secretagogues. Limit to 1-
2 drinks per day (≤ 12 per week for men, ≤9 per week for women)
- See page S43 of Canadian Diabetes Association 2008 Clinical Practice Guidelines

Exercise:
- Those who have been previously sedentary should be screen appropriately prior to engaging in
any activity more strenuous than a brisk walk. Exercise should be started slowly, even with 5-10
mins per day. Several short sessions per day may be easier than one extended session
- Goal = moderate to vigorous aerobic exercise for at least 150 mins per week, divided in at least
3 session, with never more than 2 days off at a time.
- Goal = resistance exercise at least 3 times per week, even in the elderly
- See page S38 Canadian Diabetes Association 2008 Clinical Practice Guidelines for definitions
and examples of appropriate aerobic and resistance exercise.

Pharmacologic management of Type 2 Diabetes:

- Treatment and targets should be individualized. General guidelines follow.
- HgA1c <9% at time of diagnosis → 2-3 month trial of lifestyle management → add anti-
hyperglycemic pharmacotherapy if not at target after that time.
- HgA1c ≥9% at time of diagnosis → lifestyle management + anti-hyperglycemics at same time,
consider initiating combination therapy with 2 oral agents or starting insulin.
- Goal is to attain HgA1c target within 6 to 12 months. Lag period before adding another agent
should be kept to a minimum.
- Metformin should be the initial drug used – for both overweight and non-overweight patients
- Add additional agents from different classes if needed
- Insulin may be added as a single injection of intermediate or long acting insulin at bedtime
initially. As type 2 diabetes progresses, insulin doses may need to be increased and additional
basal doses or prandial doses of short/rapid insulin may be needed.
- Insulin may also be used temporarily during illness, pregnancy, stress or for a medical
procedure or surgery.
- HgA1c should be checked every 3 months, with ongoing adjustments to management
throughout a patient’s life and the disease process.
- Full descriptions of oral anti-hyperglycemic agents can be found on pages S54-S56 of Canadian
Diabetes Association 2008 Clinical Practice Guidelines.

Insulin in Type 1 Diabetes:

- Basal-prandial regimens of either multiple daily injections or continuous subcutaneous insulin
infusions (CSII) are the insulin regimens of choice for adults – attempt to duplicate normal
pancreatic insulin production.
- Basal insulin (intermediate or long acting) is given once or twice a day.
- Prandial or bolus insulin (short or rapid acting) is given at each meal – takes into account
amount and glycemic index of carbohydrate consumed and exercise around meals; can be used to
correct hyperglycaemia. Choose rapid (aspart, lispro) over regular insulin to improve A1C and
postprandial targets, while minimizing hypoglycaemia. Rapid insulin is used with CSII
- Insulin induced HYPOGLYCEMIA COUNSELLING – risks, prevention, monitoring, and
treatment – for everyone.
- Details on insulin types, with duration, onset and peak of action can be found on page S47 of
Canadian Diabetes Association 2008 Clinical Practice Guidelines.

106
3. Given a patient with established diabetes, advise about signs and treatment of hypoglycemia/
hyperglycemia during an acute illness or stress (i.e., gastroenteritis, physiologic stress,
decreased intake.

Sick Day Guidelines from Fraser Health

Type I Diabetes:

Type 2 Diabetes:

Acute illness:
- Hypoglycemia: May occur due to nausea, vomiting, and anorexia/poor oral intake.
- Hyperglycemia: May occur due to increased peripheral insulin resistance, stress of illness,
failure to take insulin or other diabetic medications, dehydration or excess intake of sweet liquids.
Result can be DKA or hyperosmolar hyperglycemias state.
- Increase frequency of blood glucose monitoring
- Basal insulin and oral medications should be continued, although dosage may need adjustment.
Insulin must never be omitted because hyperglycemia and diabetic ketoacidosis can develop
without basal insulin.
- Frequent blood glucose monitoring is mandatory- q4h
- If blood glucose ≥14 for more than 8 hours, test for ketones – urine or serum.
- Use a sick day sliding scale if extra insulin needed for hyperglycemia.
- Seek medical attention if: elevated blood glucose for more than 8 hours, with moderate to large
urine ketones or serum ketones ≥1.5mmol/hr; unable to eat or drink and you take insulin and/or
diabetic medication; diarrhea lasting >24hours.

Hypoglycemia:
1) Symptoms. 2) Plasma glucose <4.0mmol/L. 3) Responds to carbohydrate.

Hypoglycemia symptoms:

Neurogenic (autonomic) Neurogenic

o Difficulty concentrating
o Trembling
o Confusion
o Palpitations o Weakness
o Sweating o Drowsiness
o Anxiety o Vision changes
o Nausea o Difficulty speaking
o Tingling o Headache
o Dizziness

Hypoglycemia Treatment:
- Mild to moderate hypoglycaemia: 15g carbohydrate to produce increase in plasma glucose of
2.1mmol/L at 20 mins with adequate symptom relief for most people → wait 15 mins and re-test
→ if remain <4mmol/L repeat 15g carbohydrate dose.

o 15g in form of glucose tablets

107
 o 15ml/3tsp or 3 packets of table sugar in water
o 175ml/ ¾ cup juice or pop
o 6 lifesavers (1=2.5g carbohydrate)
o 15ml/1tbsp honey

- Severe hypoglycaemia + conscious: 20g carbohydrate → wait 15 mins and re-test → if remain
<4mmol/L retreat with 15g carbohydrate.
- Severe hypoglycaemia + unconscious + >5 yrs old (at home): 1mg glucagon SC or IM (should
have trained support person) → call EMS
- To prevent repeated episodes, have usual meal/snack for that time of day. If meal >1hr away,
have snack with 15g carbohydrate + protein.
- Patients taking alpha-glucosidase inhibitors must use glucose/dextrose tablets, milk, or honey to
treat hypoglycaemia.

Hyperglycemia (in acute illness):

- There is no specific number or length of time at which symptoms of hyperglycemia may
develop. It varies between individuals.
- Symptoms experienced may be due to hyperglycemia alone ( hyperosmolar hyperglycaemic
state)or a combination of hyperglycemia and acidosis (DKA)
- See following questions for diagnosis and treatment.

Hyperglycemia symptoms:
o Polyphagia
o Polydipsia
o Headache
o fatigue
o Decreased concentration
o Blurred vision
o Weight loss

Hyperglycemia treatment:
- Take medications and insulin as prescribed
- Used sick day sliding scale
- See questions below for DKA and HHS treatment

4. In a patient with poorly controlled diabetes, use effective educational techniques to advise
about the importance of optimal glycemic control through compliance, lifestyle modifications,
and appropriate follow-up and treatment.

- Non-adherence with diabetic treatment is a problem in primary care → disease control is highly
dependent on self management, supported by an integrated diabetes healthcare team, including:

o Community based diabetes education

o Family physician
o Diabetic educators
o Nurses
o Dietitian
o …most importantly…the patient

108
- Interventions focusing on modifying the behaviour of people living with diabetes have better
outcomes than those focusing on modifying clinician's behaviour.
- Comprehensive interventions combining cognitive, behavioural, and educational components
(didactic and nondidactic) are more effective than single-focus interventions.
- Diabetes education must support self-management through informed, independent decisions
relating to the individual’s diabetes management.

o Use open questions (What do you know about...? What do you think about...?) when
addressing issues (treatment, prevention of complications, blood glucose monitoring,
diet, physical activity, foot care).
o Include problem-solving, goal-setting and active participation of patients in decision-
making. This includes support in interpreting and acting on the results of self-monitoring
of blood glucose or making informed decisions about insulin.
o Share with your patients his or her goals of care, e.g. “Ms. Dale, you have agreed to
lose some weight. Tell me how much weight you would like to lose by our next visit, and
then together we can discuss some strategies for achieving your goal.”
o Discuss patients’ expectations and try to identify specific problems related to diabetes
management.

- Self-management programs must be individualized, considering the type of diabetes, current

control, treatment recommendations, learning ability, ability to change, resources and motivation.
- Education should be offered in a timely and needs-based manner. Interventions that include
face-to-face delivery and practical application content are more likely to improve glycemic
control.
- Family support is beneficial for people with diabetes →involve family if possible.

5. In patients with established diabetes: a) look for complications. b) refer as necessary to deal
with complications.

Diabetic Retinopathy:
- Prevalence in diabetic adults in the US is 40%; prevalence sight-threatening retinopathy is ~8%.

- Most have no symptoms until very late stages (too late for effective treatment).
- Types:

o macular edema: diffuse or focal vascular leakage at the macula;

o nonproliferative: progressive accumulation of blood vessel change, including
microaneurysms, intraretinal hemorrhage, vascular tortuosity and vascular malformation
o proliferative: abnormal vessel growth;
o retinal capillary closure

- Treatment: retinal photocoagulation (laser therapy) and vitreoretinal surgery.

- Initial screening: Refer to an experienced ophthalmologist or optometrist
- In T1DM, those ≥15 yrs old should be screened q1yr, starting 5 years after diabetes onset.
- In T2DM, screen at the time of diagnosis, with follow-up tailored to the severity of retinopathy.
If no or minimal retinopathy, screen q1-2yrs.

Chronic Kidney Disease (CKD):

- Found in 50% of people with diabetes

109
- CKD associated with diabetes is the leading cause of kidney failure in Canada.
- The degree of proteinuria is characterized as either:

o microalbuminuria (urinary albumin 30 to 300 mg/day)

o overt nephropathy (urinary albumin >300 mg/day)

- Screen for microalbuminuria with a random urine albumin to creatinine ratio (ACR). Transient
microalbuminuria unrelated to diabetic nephropathy can occur, so at least 2 to 3 postive ACRs,
over a period of about 2 months, should be demonstrated before the diagnosis of
microalbuminuria is made.
- 24-h urine collections are not routinely recommended, BUT can be useful if in doubt about
eGFR accuracy, when screening for non-albumin urinary proteins (e.g. multiple myeloma) or
when estimating daily sodium intake in an individual with refractory edema or hypertension.
- Serum creatinine (Cr) is the most commonly used measure of renal function; however, Cr may
falsely indicate function is normal.

o May lose up to 50% of renal function before serum Cr becomes abnormal

o eGFR is more sensitive in identifying low kidney function in diabetes. In Canada,
eGFR is most often calculated using the abbreviated Modification of Diet in Renal
Disease (MDRD) equation, which takes into account the person’s serum creatinine, age
and sex.

- Please refer to the diagram below for CKD screening:

- Consider referral to a nephrologist or internist if:

o chronic, progressive loss of kidney function;

o eGFR is <30 mL/min;
o ACR is persistently >60 mg/mmol;
o unable to achieve BP targets
o Unable to tolerate renal-protective therapies → hyperkalemia, >30% increase in serum
Cr within 3 months of starting an ACE-I or ARB.

110
These include: Extreme proteinuria (>6 g/day), persistent hematuria (microscopic or
macroscopic) or active urinary sediment, fapidly falling eGFR, Low eGFR with little or no
proteinuria, other complications of diabetes not present or relatively not as severe, known
duration of diabetes less than 5 years, family history of nondiabetic renal disease (eg. Polycystic
kidney disease) or signs and symptoms of systemic disease.

Foot Complications:
- Major cause of morbidity and mortality in diabetes
- Contribute to increased healthcare costs
- With neuropathy or peripheral vascular disease, minor trauma to the foot can lead to skin
ulceration, infection and gangrene, often resulting in amputation.
- Foot examination by the patient and healthcare providers is integral to decrease the risk of foot
lesions and amputations, and should be performed at least annually, but more frequently in those
at high risk.
- Assessment by healthcare providers should include structural abnormalities (ankle and toe
ROM, callus pattern, bony deformities, skin temperatures), evaluation for neuropathy and
peripheral arterial disease, ulceration and evidence of infection.
- People at high risk of foot ulceration and amputation should receive foot care education
(including counseling to avoid foot trauma), professionally fitted footwear, smoking cessation
strategies and early referrals to a foot care professionals for arising issues.

111
- Management of foot ulceration requires an interdisciplinary approach that addresses glycemic
control, infection, lower-extremity vascular status and local wound care – to manage and prevent
amputation and recurrent problems.

Erectile Dysfunction (ED):

- 34 to 45% of men with diabetes
- Negatively impacts quality of life across all ages
- May be the earliest sign of cardiovascular disease.
- Regularly screen all adult men with DM for ED with a sexual function history.
- Validated questionnaires (e.g. International Index of Erectile Function or Sexual Health
Inventory for Men) have been shown to be both sensitive and specific in determining the presence
of ED and assessing response to therapy.
- Treatment: PDE5 inhibitors, reported to have a major impact on erectile function, quality of life,
and should be offered as first-line therapy to men with diabetes wishing treatment for ED.
- Referral to a specialist in ED should be offered to men who:

o do not respond to PDE5 inhibitors

o have contraindications to PDE5 inhibitors
o Are interested in 2nd-line therapies (e.g. vacuum constriction devices, intracorporal
injection therapy) or 3rd-line therapy (penile prosthesis)

Diabetic Neuropathy:
- Under-diagnosed in primary care, which impedes the benefits of early identification and
management necessary to prevent neuropathy-related sequelae.

o Detectable sensorimotor polyneuropathy will develop within 10 years of diabetes onset

in 40 to 50% of people with type 1 or type 2 diabetes

- The most frequently encountered neuropathies include:

o distal symmetric polyneuropathy;

o autonomic neuropathy;
o thoracic and lumbar nerve root disease, causing polyradiculopathies;
o individual cranial and peripheral nerve involvement (mononeuropathies, especially
affecting the oculomotor and the median nerve).

- Peripheral neuropathy screening: T2DM → should begin at the time of diagnosis and occur
annually. T1DM → annual screening after 5 years’ post-pubertal diabetes. Conducted with 10g
monofilament or sensitivity to vibration at the dorsum of the great toe.
- Intensive glycemic control is effective for primary or secondary prevention in T1DM. In T2DM,
lower blood glucose levels are associated with reduced frequency of neuropathy.
- Multiple medications are available for neuropathic pain management:

o Antidepressants, anticonvulsants, opioid analgesics and topical isosorbide dinitrate

should be considered alone or in combination

- Refer if there are significant early progressive symptoms of neuropathy or clinical suspicion of
non-diabetic neuropathy.

112
- Significant symptomatic autonomic neuropathy may require assessment by a specialist in the
affected system.

Coronary Artery Disease:

- Those with diabetes (especially women) are at higher risk of developing heart disease, and at an
earlier age.

o Often asymptomatic before either a fatal or nonfatal myocardial infarction (MI).

o It is helpful identify patients at high risk for vascular events.

- In addition to CAD risk assessment, do a baseline resting ECG if:

o >40 years of age;

o duration of diabetes more than 15 years;
o ALL (regardless of age) with HTN, proteinuria, reduced pulses or vascular bruits
o Repeat resting ECG every 2 years in people considered at high risk for CV events.

- Investigate for CAD by exercise stress testing as the initial test if:

o Typical or atypical cardiac symptoms (e.g. unexplained dyspnea, chest discomfort)

o Resting abnormalities on ECG (e.g. Q waves)
o Peripheral arterial disease (abnormal ankle-brachial ratio)
o Carotid bruits
o Transient ischemic attack
o Stroke

- Pharmacologic stress echocardiography or nuclear imaging should be done if resting ECG

abnormalities preclude the use of exercise ECG stress testing (e.g. LBBB or ST-T abnormalities)
or if unable to exercise.
- Those who demonstrate ischemia at low exercise capacity (<5 metabolic equivalents [METs])
on stress testing should be referred to a cardiac specialist.

6. In the acutely ill diabetic patient, diagnose the underlying cause of the illness and investigate
for diabetic ketoacidosis and hyperglycemia.

- Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) should always be
suspected in ill patients with diabetes. If either DKA or HHS is diagnosed, precipitating factors
must be sought and treated.
- DKA risk factors: inadequate or inappropriate insulin therapy, infection, myocardial infarction,
abdominal crisis, trauma.
- DKA:

o Triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia. Metabolic

acidosis is often the major finding.
o Clinical presentation: symptoms of hyperglycemia, Kussmaul respiration, acetone-
odoured breath, ECFV contraction, nausea, vomiting and abdominal pain. ± a decreased
level of consciousness.
o Ketoacidosis occurs as a result of elevated glucagon and absolute insulin deficiency.

- HHS :

113
 o Main features: extracellular fluid volume (ECFV) depletion and hyperosmolarity.
o Little or no ketones, with serum glucose usually more than 33 mmol/L → more
prolonged duration of relative insulin insufficiency and inadequate fluid intake (or high
glucose intake) results in higher glucose levels
o Hyperglycemia causes urinary losses of water and electrolytes (sodium, potassium,
chloride) and the resultant ECFV depletion.
o High catecholamine levels suppress insulin release.
o Often more profound ECFV contraction and decreased level of consciousness
compared to DKA.
o Can be a variety of neurological presentations that may resolve once osmolality returns
to normal.
o Neurologic complications (stupor, seizures or stroke-like state) related to higher
glucose levels and serum osmolality are more common in HHS.
o greater ECFV contraction, but minimal acid-base disturbance.

- To make the diagnosis and determine the severity of DKA or HHS, assess:

o Serum electrolytes (and anion gap), glucose, creatinine, osmolality and

betahydroxybutyric acid (beta-OHB) (if available), blood gases, serum and urine ketones.
o Anion gap gives an estimate of the quantity of unmeasured anions in the serum
(ketoacids) : anion gap = sodium - (chloride + bicarbonate)

- There are no definitive criteria for the diagnosis of DKA. Typically:

o arterial pH <7.3, serum bicarbonate <15 mmol/L, anion gap >12 mmol/L, positive
serum and/or urine ketones.
• Plasma glucose usually > 14.0 mmol/L, but can be lower.
o It is therefore important to measure ketones in both the serum and urine.
o If there is an elevated anion gap, and serum ketones are negative, beta-hydroxybutyrate
levels should be measured.
o Measurement of serum lactate should be considered in hypoxic states.

7. Given a patient with DKA, manage the problem appropriately and advise about preventing
future episodes.

- DKA and HHS is best managed in ICU or a step-down unit with specialist care.
- Volume status (including fluid intake and output), vital signs, neurologic status, plasma
concentrations of electrolytes, anion gap, osmolality and glucose need to be monitored closely,
initially as often as every 2 hours.
- Monitor serum glucose every hour
- Precipitating factors must be diagnosed and treated.
- IV fluid:

o The initial goal is to restore tissue perfusion. In DKA, 0.9% sodium chloride (NS)
should be administered by IV at 500 mL/hour for 4 hours, then 250 mL/hour for 4 hours.
o Higher initial rate of NS (1–2 L/hour) should be given in the presence of shock.

- Insulin:

114
 o Must correct hypokalemia prior to giving insulin.
o Continuous IV infusion of regular insulin at 0.1U/kg/hr is the treatment of choice.
o IV bolus of regular insulin (0.1 U/kg) is recommended in some reviews.
o When serum glucose reaches 11.1 mmol/L, switch NS to D5W. It may be possible to
decrease the insulin infusion rate to 0.02 to 0.05 U/kg per hour, but DO NOT STOP
INSULIN INFUSION until there is correction of Serum pH and the anion gap.

- Potassium:

o Typical recommendations suggest that potassium should be started for plasma

potassium <5.3 mmol/L, once diuresis has been established.
o If the patient at presentation is normo-or hypokalemic, potassium should be given
immediately, at concentrations in the IV fluid between 10 and 40 mmol/L.
o For potassium ≤ 3.3 mmol/L, withhold insulin until potassium replacement at 40
mmol/hour has restored plasma potassium to >3.3 mmol/L.

- Sodium bicarbonate therapy is controversial → considered only in adult patients in shock or

with arterial pH <7.0.
- Hypophosphatemia:

o Hypophosphatemia has been associated with rhabdomyolysis.

o Administration of potassium phosphate in cases of severe hypophosphatemia could be
considered for the purpose of trying to prevent rhabdomyolysis.

- Prevention:

o The most common precipitating factor to DKA is poor adherence to diabetes treatment.
Patients may discontinue diabetes monitoring for many reasons (cost, poor understanding
of the disease, psychological disorders such as depression and eating disorders).
o Instructions should clearly indicate when to consult the physician: any symptoms that
may signal DKA or dehydration → dizziness, trouble breathing, fruity breath, or dry and
cracked lips or tongue.
o Establish sick-day protocol (see previous question)

Diarrhea - Key Features

1. In all patients with diarrhea,

a) Determine hydration status:

-heart rate, BP, orthostatic vital signs, mucous membranes, skin turgor, urine output, capillary
refill time, eyes, fontanelle (peds), production tears (peds)

b) Treat dehydration appropriately.

-mild-moderate dehydration: trial of PO rehydration

-Severe or failure of PO rehdration: IV fluid therapy – NS or RL bolus

2. In patients with acute diarrhea, use history to establish the possible aetiology (e.g., infectious
contacts, travel, recent antibiotic or other medication use, common eating place for multiple ill
patients).

115
Note: acute diarrhea is < 14days duration

Infectious etiology:
• Bacterial: shigella, salmonella, campylobacter, yersinia, ecoli, clostridium, vibrio, staph aureus,
bacillus cereus
• Viral: norovirus, rotavirus, adenovirus, CMV, HSV
• Parasitic: cryptosporidium, microsporidia, entamoeba histolytica, giardia lamblia, cyclospora

Medications: Antibiotics, colchicine, laxatives, magnesium containing antacids

Food Intolerance: Lactose, fructose in soft drinks, sorbital, coffee

Intestinal Diseases (acute episodes): Celiac, inflammatory bowel dz

Clues from hx regarding specific cause:

• presence of fever, bloody diarrhea and tenesmes suggest inflammatory diarrhea (eg.
Shigella, salmonella, campylobacter, c diff colitis or IBD)
• Consider norovirus with classic history of nausea, vomiting, intense cramping, and
watery diarrhea that usually lasts 48-72 hrs
• Travelers diarrhea is most commonly caused by enterotoxogenic E. Coli, but still
consider other causes of diarrhea and specific organisms based on area of travel
• Exposure to contaminated water or camping think of parasites (giardia, cryptosporidium
and entamoeba)
• Exposure to animals: Young cats/dogs → campylobacter; Turtles → Salmonella
• Organisms that cause food poisonings:
o Dairy food -Campylobacter and Salmonella species; Eggs -Salmonella species
o Ground beef - Enterohemorrhagic E coli
o Poultry -Campylobacter species
o Pork -C perfringens, Y enterocolitica
o Seafood - Astrovirus and Aeromonas, Plesiomonas, and Vibrio species
o Oysters - Calicivirus and Plesiomonas and Vibrio species
o Vegetables -Aeromonas species and C perfringens

3. In patients with acute diarrhea who have had recent hospitalization or recent antibiotic use,
look for clostridium difficile.

• Suspect if antibiotic use within the last 2 months or discharge from hospital within last 72 hours;
can happen with almost all antibiotics (although clinda is the classical example). Presents with
watery diarrhea that is rarely bloody, crampy abdo pain, malaise, fever, anorexia.
• Can lead to fulminant colitis and toxic megacolon

4. In patients with acute diarrhea, counsel about the timing of return to work/school (re: the
likelihood of infectivity).

• No return to work until no diarrhea for at least 48 hours

116
• Food handlers/daycare workers/health care workers may require negative stool samples on 2
occasions at least 24 hrs apart prior to returning to work to prevent outbreaks

5. Pursue investigation, in a timely manner, of elderly with unexplained diarrhea, as they are
more likely to have pathology.

• Any change in bowel habit should raise possibility of colorectal cancer

• Also consider other pathology such as diverticulitis, inflammatory bowel disease, etc.

6. In a young person with chronic or recurrent diarrhea, with no red flag symptoms or signs,
use established clinical criteria to make a positive diagnosis of irritable bowel syndrome (do not
over investigate).

• Red flags: fevers/chills, weight loss, bloody stool, mucousy stool, nocturnal diarrhea, large
volume stool, greasy stool, FHx of IBD or cancer, anemia, persistent daily diarrhea or
constipation, severe pain

• Rome III criteria:

o Recurrent abdominal pain or discomfort for at least 3 days per month in the last 3
months associated with 2 or more of the following:
• Improvement with defecation
• Onset associated with a change in frequency of stool
• Onset associated with a change in form (appearance of stool)
o criteria fulfilled for the last 3 mths with sx onset at least 6 mths prior to dx
o Supportive sxs that are not part of the diagnostic criteria include:
• a) <3 BM/week, b) >3BM/day or abnormal stool form c) lumpy/hard stool d)
loose/watery stool e) defecation straining f) urgency or feeling of incomplete bowel
movement, passing mucus or bloating
o in the absence of structural or metabolic abnormalities to explain the sxs
o “discomfort” means an uncomfortable sensation not described as pain

7. In patients with chronic or recurrent diarrhea, look for both gastro-intestinal and non-
gastro-intestinal symptoms and signs suggestive of specific diseases

• Malabsorption Syndrome:

o Stool tend to be pale, greasy, voluminous, and foul-smelling

o Patients typically have weight loss despite adequate food intake
o Common disorders with malabsorption include: Lactose intolerance, chronic
pancreatitis, Celiac disease, Bacterial overgrowth of the small intestine

• Cholecystecomy:

o Reported in 5-12% of patients following cholecystectomy, due to excessive bile salts

entering the colon
o Usually resolves spontaneously over the course of weeks to months
o Can be treated with cholestryamine

117
• Inflammatory Bowel Disease: crohn’s and ulcerative colitis

o Age on onset typically between 15 and 40, but may have a second peak between 50 to
80
o Extraintestinal manifestions: iritis/uveitis, arthritis, skin changes, aphthous stomatitis,
nail changes, pericholangitis, and sclerosing cholangitis
o Need to monitor for cancerous changes in colon
o Crohn’s:
• present with abdo pain, diarrhea, weight loss and fever; hemoccult positive stools are
common, macroscopic bleeding less common
• Can get inflammation anywhere along GI tract (“from gums to bum”) in discontinuous
fashion
• Inflammation is transmural therefore commonly get fistula formation
o Ulcerative colitis:
• Only involves colon, always starting distally and ascends in continuous manner
• Variable presentation depending on extent of disease, typically presents with bloody
diarrhea, fever, weight loss

Difficult Patient - Key Features

1. When physician-patient interaction is deemed difficult, diagnose personality disorder when it

is present in patients.

RECOGNIZING PERSONALITY DISORDERS — The clinician may feel angry, threatened,

defensive, or incompetent, or may find it difficult to feel any emotional connection with the
patient. Alternatively, the clinician may find him or herself preoccupied with the patient without
any specific event or attribute that would reasonably induce such involvement. These clinician
reactions may provide some evidence toward the consideration of a personality disorder, although
they are certainly not pathognomonic for this diagnosis.

The consistent presence of certain behaviors and traits, with onset in middle to late adolescence
and continuing throughout adult life, are particularly suggestive of a personality disorder [22]:
• Frequent mood swings
• Angry outbursts
• Anxiety sufficient to cause difficulty making friends
• Need to be the center of attention
• Feeling of being widely cheated or taken advantage of
• Difficulty delaying gratification
• Not feeling there is anything wrong with their behavior (ego-syntonic symptoms)
• Externalizing and blaming the world for their behaviors and feelings

DSM-IV General Diagnostic criteria for personality disorder:

A. An enduring pattern of inner experience and behaviour that deviated markedly from the
expectations of the individual’s culture. This pattern is manifested in tow (or more) of the
following areas:

a. Cognition (ie. ways of perceiving and interpreting self, other people and events)
b. Affectivity (ie. the range, intensity, lability and appropriateness of emotional response)
c. Interpersonal functioning

118
 d. Impulse Control

B. The enduring pattern is inflexible and pervasive across a broad range of personal and social
situations
C. The enduring pattern leads to clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The pattern is stable and of long duration and its onset can be traced back at least to
adolescence or early adulthood.
E. The enduring pattern is not better accounted for as a manifestation or consequence of another
mental disorder.
F. The enduring pattern is not due to the direct physiological effects of a substance (ie. a drug of
abuse, a medication) or a general medical condition (ie. head trauma)

Cluster A characteristics: individuals may appear odd and eccentric

• Paranoid
• Schizoid
• Schizotypal

Cluster B characteristics: individuals often appear dramatic, emotional, or erratic in their

emotions and behaviour
• Histrionic
• Narcissistic
• Borderline
• Antisocial

Cluster C characteristics: Individuals often appear anxious or fearful

• Avoidant
• Dependent
• Obsessive-compulsive

See DSM-IV, or uptodate article, ‘Personality Disorders’ for full summary of diagnostic criteria
for specific personality disorders.

2. When confronted with difficult patient interactions, seek out and update, when necessary,
information about the patient’s life circumstances, current context, and functional status.

3. In a patient with chronic illness, expect difficult interactions from time to time. Be especially
compassionate and sensitive at those times.

4. With difficult patients remain vigilant for new symptoms and physical findings to be sure
they receive adequate attention (e.g., psychiatric patients, patients with chronic pain).

5. When confronted with difficult patient interactions, identify your own attitudes and your
contribution to the situation.

6. When dealing with difficult patients, set clear boundaries.

7. Take steps to end the physician-patient relationship when it is in the patient’s best interests.

119
8. With a difficult patient, safely establish common ground to determine the patient’s needs (eg.
threatening or demanding patients).

Disability - Key Features

1. Determine whether a specific decline in functioning (e.g., social, physical, emotional) is a

disability for that specific patient.

2. Screen elderly patients for disability risks (e.g., falls, cognitive impairment, immobilization,
decreased vision) on an ongoing basis.

3. In patients with chronic physical problems (e.g., arthritis, multiple sclerosis) or mental
problems (e.g., depression), assess for and diagnose disability when it is present.

4. In a disabled patient, assess all spheres of function (emotional, physical, and social, the last
of which includes finances, employment, and family).

5. For disabled patients, offer a multi-faceted approach (e.g., orthotics, lifestyle modification,
time off work, community support) to minimize the impact of the disability and prevent further
functional deterioration.

6. In patients at risk for disability (e.g., those who do manual labour, the elderly, those with
mental illness), recommend primary prevention strategies (e.g., exercises, braces, counseling,
work modification).

7. Do not limit treatment of disabling conditions to a short-term disability leave (i.e., time off is
only part of the plan).

What is Disability:
“because of disability” means for the reason that the person has or has had, or is believed to have
or have had,

(a) any degree of physical disability, infirmity, malformation or disfigurement that is

caused by bodily injury, birth defect or illness and, without limiting the generality of the
foregoing, includes diabetes mellitus, epilepsy, a brain injury, any degree of paralysis,
amputation, lack of physical co-ordination, blindness or visual impediment, deafness or
hearing impediment, muteness or speech impediment, or physical reliance on a guide dog
or other animal or on a wheelchair or other remedial appliance or device,
(b) a condition of mental impairment or a developmental disability,
(c) a learning disability, or a dysfunction in one or more of the processes involved in
understanding or using symbols or spoken language,
(d) a mental disorder, or
(e) an injury or disability for which benefits were claimed or received under the insurance
plan established under the Workplace Safety and Insurance

Based on Ontario Human Rights Commission

A. History
HPI:

120
MSIGECAPS
DIMS FU ==

Drugs (intox or withdrawal)

Infection (chest, GU, skin/soft tissue)
Metabolic (endocrinopathy [DM, TSH], electrolytes (Na, K, Ca), renal or liver failure
Structural (stroke, hemorrhage, seizure, neoplasm)
Fecal impaction
Urinary retention

SOC Hx:
Smoking/EtOH/Street Drugs/Caffeine
Check for ADLs (DEATH == Dressing, Eating, Ambulating, Toileting, and Hygiene)
Check for IADLs (SHAFT == Shopping, Housework, Accounting, Food Prep, Transportation)
Financial Support
Family Support
Employment or Social Outlet
± Advanced Directive

ROS:
Falls in the elderly: affected by the following:
• orthostatic hypotension,
• meds,
• environmental hazards, and
• medical conditions affecting gait, balance, vision, strength, and proprioception.

 The single best predictor of a fall is a prior fall* -> 50% of seniors will go on to another
fall within 12 months of their first fall

B Physical:
Visual Acuity (typically done in CPX), sometimes annually with Ophthalmologist
Weight and Height (typically done in CPX) (> 2 cm drop indicates vertebral fracture)
PHQ-9 (or Geriatric Depression Scale – GDS) scores to assess decline in emotional aspects of life

MMSE for monitoring dementia

Postural Vitals: Lying, Sitting, and Standing (waiting after five minutes to detect orthostatic
changes); Temperature
H&N: Cataracts, CN-exam, LAD, Thyroid
Resp: Symptoms of COPD
CV: New murmurs, bruits, collateral circulation
Abdomen: DRE (with sphincter tone)
GU: rectocele, vesicocele
Neuro: gait, balance
MSK: joint ROM, atrophy, weakness, some focus on feet (callus, corns, abnormal nails)
Skin: Suspicious Mass

121
(Timed) Get-up-and-Go Test (for mobility and falls assessment):
Person stands from a seated position and walks a distance of 3m (10 ft), turns, and walks back to
the chair and sits down.
< 10 sec is mobile, no impairment
> 30 sec is significant impairment

C Diagnosis

Refer to What is Disability section.

D Treatment and Interventions:

For Disabled Patients: (the key is a multi-faceted approach)

Conservative:

• Those who are employed will need time off work.

• Impaired mood will need counseling (eg CBT) and community programs.
• Pain will need to be controlled using the WHO Pain Ladder
• Mobility needs to include orthotic, walker, or wheelchair (O/T)
• Appropriate exercises to prevent further decline (P/T)

Non-conservative:

• Medications, injections, dialysis etc

• Surgery, ECT

For at risk for disability:

(targeted preventative maneuvers are not as effective as multi-faceted approaches)

• Influenza and Pneumococcal Vaccine for seniors

• Reducing or eliminating offending medications
• Improving visual acuity
• Improving footwear, or referral to podiatry
• Use of adaptive devices, such as arm supports, protective rails, walking aids
• Balance exercises, coupled with moderate physical activities -> careful with
recommending too much physical activity as this may increase the risk for disability);
Core stabilization.
• Socialization
• Hip protectors for the frail elderly -> but best to avoid the fall, rather than the impact of
the fall
• Improve the home environment: better lighting, fixing damaged floors, etc.

Dizziness - Key Features

122
1. In patients complaining of dizziness, rule out serious cardiovascular, cerebrovascular, and
other neurologic disease (e.g., arrhythmia, myocardial infarction [MI], stroke, multiple
sclerosis).

2. In patients complaining of dizziness, take a careful history to distinguish vertigo,

presyncope, and syncope.

3. In patients complaining of dizziness, measure postural vital signs.

4. Examine patients with dizziness closely for neurologic signs.

5. In hypotensive dizzy patients, exclude serious conditions (e.g., MI, abdominal aortic
aneurysm, sepsis, gastrointestinal bleeding) as the cause.

6. In patients with chronic dizziness, who present with a change in baseline symptoms, reassess
to rule out serious causes.

7. In a dizzy patient, review medications (including prescription and over-the-counter

medications) for possible reversible causes of the dizziness.

8. Investigate further those patients complaining of dizziness who have:

- signs or symptoms of central vertigo.
- a history of trauma.
- signs, symptoms, or other reasons (e.g., anticoagulation) to suspect a possible serious
underlying cause.

Population: 3rd most common complaint among all outpatients and the single most common
complaint among patients older than 75 years (in the US)
Incidence: 20 % of patients >60 yrs have dizziness severe enough to affect daily activities
Risk factors: In the elderly, 7 characteristics associated with dizziness:

- Anxiety trait
- Depressive symptoms
- Impaired balance (path deviation and time to turn circle greater than four seconds)
- Past myocardial infarction
- Postural hypotension (mean decrease in blood pressure 20 %)
- 5 or more medications
- Impaired hearing

History: – Ask open-ended questions

Clarify description of dizziness, i.e.: vertigo → out sensation of spinning - “whirling”,

"tilting," or "moving." Vague dizziness, imbalance, or disorientation; presyncope →
feeling faint like they’re going to pass out; disequilibrium → feeling of imbalance when
standing/walking
Cardiac Sxs: chest pain, palpitations, dyspnea
History of cardiac disease, including cardiac dysrhythmias (tachycardias or
bradyarrhythmias), coronary heart disease, congestive heart failure

123
 Ask about psychiatric symptoms, often they don’t volunteer these symptoms
Time course – vertigo is usually not continuous even when caused by central lesion
(vertigo that is continuous is often psychogenic); chronic dizziness needs re-evaluation to
detect changes or need for further investigations
Provoking factors – i.e.: positional or postural changes
Aggravating factors – vertigo is almost always made worse with head movement
Associated Sx – nausea, vomiting, hearing loss, headache, photophobia, diplopia,
dysarthria, dysphagia, weakness, or numbness (vertigo due to stroke almost always
associated with these)
Drugs – i.e. antidepressants, calcium channel or beta-blockers

Cause of Dizziness varies with age - in elderly, higher incidence of central vestibular causes of
vertigo (approx 20 %) most often stroke; psychiatric conditions and presyncope more so in young
people
Common cause of presyncope/syncope: Orthostatic hypotension, cardiac arrhythmias, and
vasovagal attacks (lack of spinning sensation cannot be used to exclude vestibular
disease); disequilibrium – a musculoskeletal disorder interfering with gait, vestibular
disorder, and/or cervical spondylosis; visual impairment can make the problem worse

Signs of Peripheral Cause of Vertigo Signs of Central Cause of Vertigo

Sometimes reverses direction when
Unidirectional, fast toward the normal
patient looks in the direction of the slow
ear, never reverses direction
phase
Nystagmus
Horizontal with a torsional component,
Can be any direction (vertical, horizontal
never purely torsional or vertical
or torsional)
Suppressed effect of visual fixation
No suppression of visual fixation
Severe instability, patient often falls
Neuro signs? No other neurologic signs
when walking
Hearing/tinnitus Deafness or tinnitus may be present No deafness or tinnitus

Periperhal causes of Vertigo Central Causes of Vertigo

Benign paroxysmal positional vertigo Migrainous vertigo

Vestibular neuritis Brainstem ischemia

Herpes zoster oticus (Ramsay Hunt syndrome) Cerebellar infarction and hemorrhage

Meniere's disease Chiari malformation

Labyrinthine concussion Multiple sclerosis
Perilymphatic fistula Episodic ataxia type 2
Semicircular canal dehiscence syndrome
Cogan's syndrome
Recurrent vestibulopathy
Acoustic neuroma
Aminoglycoside toxicity

124
Otitis media

Differentiating possible central causes of vertigo

Migraine
Recurrent headache
episodes, Central or accompanying
Migrainous History of Usually All tests are
last several peripheral or following
vertigo migraine none normal
minutes to characteristics vertigo, positive
hours visual
phenomena
Single or
recurrent Older patient, MRI + DWI
episodes vascular risk Usually other may
Vertebrobasilar Central
lasting factors, and or brainstem None demonstrate
TIA characteristics
several cervical symptoms vascular
minutes to trauma lesion.
hours
Sudden Usually other
onset, brainstem
MRI will
Brainstem persistent Central symptoms,
As above None demonstrate
infarction symptoms characteristics especially
lesion
over days lateral
to weeks medullary signs
Sudden Gait impairment
Older patient,
onset, is prominent. Urgent MRI,
Cerebellar vascular risk
persistent Central Headache, limb CT will
infarction or factors, None
symptoms characteristics dysmetria, demonstrate
hemorrhage especially
over days dysphagia may lesion
hypertension
to weeks occur

Treatment of Vertigo of peripheral cause (3 categories):

1. Specific to the underlying vestibular disease

2. Alleviating the acute symptoms of vertigo
anticholinergics (scopolamine patch behind ear q3days),
antihistamines (meclizine, dimenhydrinate, diphenhydramine)
Phenothiazine antiemetics (prochlorperazine, promethazine, metoclopramide,
domperidone, ondansetron)
Benzodiazepines
3. Promoting recovery, i.e.: vestibular rehab – exercises such as moving head up and
down, then side to side daily for several mins daily.

125
 Cause SX Treatment
Avoidance of caffeine/alcohol
Meniere’s Vertigo lasting hours-days, hearing loss,
disease tinnitus, aural fullness Low-dose HCTZ, anti-emetics
Serc
Vertigo lasting days, associated hearing loss,
Acute Rest, antiemetics, antibiotics if
usually after URTI in which there is a middle
labyrinthitis middle ear fluid is infected
ear effusion
Vertigo lasting days
Vestibular
No hearing loss, no ear pain Rest, reassurance, antiemetics
neuritis
Maybe after URTI
No other Sx
Vertigo lasting seconds
Benign Positional
Associated with rolling head left or right or
Vertigo
looking up || Reassurance, exercises – Dix
Hallpike
Non – cardiovascular Cardiovascular
Reflex mechanisms

Vasovagal and vasodepressor syncope

(neurocardiogenic syncope)
Micturition
Deglutition Cardiovascular disease
Cough
Orthostatic hypotension Arrhythmic causes
Dysautonomias AV block with bradycardia (structural changes, drugs)
Fluid depletion Sinus pauses/bradycardia (vagal causes, sick sinus
Illness, bed rest, reconditioning syndrome, negative chronotropic drugs such as beta
Drugs - antidepressants, sympathetic blockers and calcium channel blockers)
blockers Ventricular tachycardia due to structural heart disease
Psychogenic Nonarrhythmic causes
Hysterical Hypertrophic cardiomyopathy
Panic disorder Aortic stenosis
Anxiety disorder Syncope of unknown origin
Undiagnosed seizures About 50 percent of patients presenting to the hospital
Improperly diagnosed syncope -
confusional states, e.g., due to
hypoglycemia, stroke
Drug-induced loss of consciousness
(consider alcohol, illicit drugs)

Look for common causes of syncope if indicated by History

Major uncommon causes of syncope

Arrhythmic causes - SVT, Long QT, Idiopathic VTach, MI causing bradycardias and
tachycardias, Right ventricular dysplasia

126
Nonarrhythmic causes - PE, Pulmonary hypertension, Dissecting aortic aneurysm, Subclavian
steal, Atrial myxoma, Cardiac tamponade, Noncardiovascular disease,
Reflexes - Defecation, Glossopharyngeal, Postprandial, Carotid sinus hypersensitivity,
Hyperventilation
Other - Migraine, Carcinoid syndrome, Systemic mastocytosis, Metabolic, Hypoglycemia,
Hypoxia, Multivessel obstructive cerebrovascular disease

Domestic Violence - Key Features

1. In a patient with new, obvious risks for domestic violence, take advantage of opportunities in
pertinent encounters to screen for domestic violence (e.g., periodic annual exam, visits for
anxiety/depression, ER visits).

2. In a patient in a suspected or confirmed situation of domestic violence:

a. Assess the level of risk and the safety of children (i.e., the need for youth protection).
b. Advise about the escalating nature of domestic violence.

3. In a situation of suspected or confirmed domestic violence, develop, in collaboration with the

patient, an appropriate emergency plan to ensure the safety of the patient and other household
members.

4. In a patient living with domestic violence, counsel about the cycle of domestic violence and
feelings associated with it (e.g., helplessness, guilt), and its impact on children.

DEFINITION: intentional controlling or violent behaviour by a person the victim is/was

intimately related. Controlling behaviour may include physical, emotional, sexual, or economic.
Includes elder abuse.

Primary pattern of domestic violence is episodic, unpredictable outbursts. They tend to start as
emotional and verbal, but eventually lead to physical. Victims live in constant state of fear.
Violence frequently escalates.

15% prevalence, only pick-up < 5% so we need to screen in high risk groups.

- Female trauma victims

- Women with chronic headaches and abdominal pain
- Pregnant women (especially with injuries)
- Women with STIs
- Women with a history of childhood abuse
- Elders with signs of neglect or with injuries
- Elders with increasing chronic pain, depression and the number of health conditions
- Don’t forget about men (15% of abuse victims)

Pregnancy: classic medical teaching is that domestic violence starts (or escalates) in pregnancy
and in the post-partum period (so watch for it on the exam).

- 20% prevalence (higher than pre-eclampsia and gestational diabetes)

- Higher in unintended pregnancy
- Higher in those who seek late prenatal care
- Higher incidence of low birth weight, pyelonephritis, preterm labour

127
When to suspect domestic violence:

- Inconsistent explanation of injuries

- Delay in seeking treatment for injuries
- Increased somatic complaints such as headaches, abdo pain, fatigue, chronic pelvic pain
- Strange injures: breasts, abdomen, genitals, head and neck, forearms
- Many bruises at different stages of healing

Consequences of abuse:

- Social isolation, economic dependence

- Anxiety, depression, somatization

How to screen: 1 question method

“At any time, has your partner hit, kicked or otherwise hurt or threatened you?”

S.A.F.E. questionnaire method (outline for the entire encounter)

- “Do you feel safe in your relationship?”

- “Have you ever felt threatened or afraid?”
- “Is your family aware you have been hurt? Could you go to the for support?”
- “Do you have a safe place to go in an emergency?”

Treatment:

1) Assess level of violence

- Has the violence increased in severity or frequency over the past year?
- Has your partner threatened to kill you, your children, or himself?
- Are there weapons in the house?
- Does your partner know you are planning to leave?

2) If previous murder threats, or guns in the house (or you just feel it is VERY unsafe):
- Suggest immediate referral to mental health, social work, women’s shelter
2b) Lower risk domestic violence:
- Most victims not ready to leave abuser because of fear of retaliation, economic
dependence, hopes that violence might stop
- Involve counseling, social workers: improves a victim’s self worth, assess the degree of
danger, help to develop safety plan

3) Safety plan:
- Safe place to go, how to get there, having money, clothes, keys, medications, important
documents, taking the children
- Define where they will go: relative, emergency department, calling domestic violence
hotline (give number)
- See patient frequently in follow-up
- Re-visit idea of counseling/support if there is resistance

4) Documentation:
- State the diagnosis of domestic violence, use specifics in notes
- Injuries should be described and photographed

128
 - Mandatory reporting for abuse of minors (<18 years old) and those in imminent danger
- Domestic violence not reportable without women’s permission

Dyspepsia - Key Features

1. In a patient presenting with dyspepsia, include cardiovascular disease in the differential

diagnosis.

2. Attempt to differentiate, by history and physical examination, between conditions presenting

with dyspepsia (e.g., gastroesophageal reflux disease, gastritis, ulcer, cancer), as plans for
investigation and management may be very different.

3. In a patient presenting with dyspepsia, ask about and examine the patient for worrisome
signs/symptoms (e.g., gastrointestinal bleeding, weight loss, dysphagia).

Definition

• Chronic or recurrent pain or discomfort centered in the upper abdomen, “indigestion”

• Associated with bloating, early satiety, nausea, vomiting
• Can be intermittent, continuous, and may or may not be related to meals
• Prevalence: 25-50% in Western countries

Approach to Dyspepsia

129
Differential Diagnoses (Table 2, AFP)

• Functional (idiopathic, non-ulcer) (up to 70%)

• Peptic ulcer disease (gastroduodenal) (15-25%)

130
 • Reflux esophagitis (5-15%)
• Gastric or esophageal cancer (<2%)
• Other differential diagnoses are rare:
• Abdominal cancer (esp pancreatic)
• Biliary tract disease
• CHO malabsorption
• Gastroparesis
• Hepatoma, etc.

Risk Factors

• Medications: ASA, NSAIDs (Table 3, AFP)

• EtOH and tobacco are potential triggers
• Emotional stress frequently associated with functional dyspepsia

Gastroesophageal Reflux Disease

• Most common condition to affect the esophagus

• Can range from heartburn with endoscopy-negative reflux disease to ulcers, stricture,
Barrett's
• Everyone has some degree of GE reflux → Pathological when there are sx +
complications

Pathophysiology
Reflux of gastric contents into the esophagus, can occur with and without hiatus hernia
Factors:
LES function, intra-abdominal pressure
Peristalsis, salivation, Mucosal defense

Clinical Features
Heartburn, acid regurgitation after eating certain foods or following various postural
maneuvers
Waterbrash, angina-like chest pain, dysphagia, respiratory symptoms, odynophagia rare
Common in pregnancy (↑intra-abdominal pressure and LES relaxant effect of
progesterone)
If severe, stricture formation → wt loss (↓intake)
Aspiration: consolidation, bronchospasm, fibrosis

Diagnosis mostly via history and physical

Investigations reserved to answer following:

Amount of reflux abnormal?
Symptoms due to reflux?
Mucosal damage or other complications?
Patients with long-standing GERD → endoscopy
5-10% will have Barrett's (if > 5y of symptoms)
If young, typical and infrequent symptoms → empiric therapy

131
 Treatment
Lifestyle Modifications
Elevate head of bed, Quit smoking, Avoid recumbency for 3h after eating
Avoid trigger foods/drinks, Losing weight
Acid suppression: antacids, alginates, H2RA, PPI
Refractory Symptoms → endoscopy
Pregnancy: antacids, alginates, cimetidine

Oral Acid Suppressants

Helicobacter pylori Infection

• Most common gastric bacterial infection worldwide, Prevalence: 20-30% in Western

world
• Most H. pylori-infected individuals have associated gastritis, although many have no
symptoms
• Associated with increasing risk of PUD, gastric cancer, gastric MALT lymphoma
• Antral gastritis → atrophic gastritis + intestinal metaplasia → gastric cancer
• Risk factors: Immigration from a developing country, low SES, family overcrowding

Testing

* Serology: unable to differentiate active from past infection. Will remain positive for several
years following successful treatment.
** UBT, endoscopic gastric biopsy, fecal antigen testing may be affected by medications such as
antibiotics and acid lowering agents → hold bismuth and antibiotics x 28d and PPI for 7-14d
prior to testing.

H. pylori Eradication

132
 • Small but statistically significant improvement in functional dyspepsia symptoms
• Decreases risk of PUD and its complications
• NNT=15 for relief of symptoms
• Cost-effectiveness unknown

Prokinetics for Functional Dyspepsia

• Target patients with predominant symptoms of bloating, early satiation, nausea, and
vomiting
• Aim: improve GI motility
• Domperidone, metoclopramide, erythromycin, peppermint
• Evidence poor

Dysuria - Key Features

1. In a patient presenting with dysuria, use history and dipstick urinalysis to determine if the
patient has an uncomplicated UTI.

Most common clinical triad for an acute uncomplicated cystitis is: dysuria, frequency, and
urgency (in an immunocompetent woman of childbearing age who has no comorbidities or
urologic abnormalities).

Negative macroscopic-screened urines (dipsticks) do not routinely require microscopic

examination of urine, unless:
a) Dipstick analysis is positive for any of:
- leukocyte esterase or
- nitrite
- may be heme positive (blood)
- turbidity
- glucose >55mmol/l; protein (greater than trace)
- **Nitrites and leukocyte esterase are the most accurate indicators of acute uncomplicated
cystitis in symptomatic woman. Mid-stream urine is best.

Urine culture:
- Urine culture only recommended for patients with suspected acute pyelonephritis; pts with
symptoms that do not resolve or that recur within 2-4 weeks after completion of tx; and pts who
present with atypical symptoms.
- A CFU >103/ml of a uropathogen is diagnostic

b) Special case: pts presenting with a condition where clinical record justifies further
investigation such as:
- diabetes
- established kidney disease/transplant
- pregnancy
- recent urological sx/cystoscopy
- genitourinary problems
- neurogenic bladder

133
- requests by consultants for investigation of UT problems
- spinal cord injury or disease

2. When a dx of uncomplicated UTI is made, treat promptly without waiting for a culture
result.

- Choose antibiotic based on agent’s effectiveness, risks of adverse effects, resistance rates, and
propensity to cause collateral damage (ie. ecologic effects of AB therapy on normal body flora).
Pts should notice relief within 36 hours.
- Commonly used are septra DS 1 tab bid x 3-5 days, nitrofurantoin 100 mg po bid 5-7 days;
fluoroquinolones are reserved for exceptional cases (ie., allergies, etc) as there is a high rate of
resistance

3. Consider non-UTI related etiologies of dysuria (e.g., prostatitis, vaginitis, STI, chemical
irritation) and look for them when appropriate.

- If pts report vaginal discharge/irritation: vaginitis or cervicitis more likely

- Acute pyelonephritis should be suspected in ill-appearing pts, who are uncomfortable, and also
have fever/tachycardia/CVA tenderness.

In Men consider:
- urethritis: commonly in young sexually active men
- UTI’s: commonly in older men with prostatic hypertrophy
- gonorrhea
- acute/chronic prostatitis: in young/middle age men
- epididymitis: irritative voiding symptoms (dysuria, frequency, urgency) and pain in one testicle.
Often high fever and rigours.

In Women consider:
- urethritis: hx of unprotected sexual exposure
- gonorrhea/chlamydia
- Vaginitis: candidal, trichomonas, genital herpes
- Atrophic vaginitis: urine comes in contact with sensitive atrophied mucosal tissue
- Interstitial cystitis: often middle age, longstanding symptoms with negative cultures
- Pelvic Inflammatory Disease

4. When assessing patients with dysuria, identify those at higher risk of complicated UTI (e.g,
pregnancy, children, diabetes, urolitiasis).

Characteristics of Pts with Uncomplicated and Complicated UTIs

Uncomplicated Complicated
- hx of childhood UTIs
- Immunocompetent
- immunocompromised
- no comorbidities - preadolescent or postmenopausal
- no known urologic - pregnant
abnormalities - underlying metabolic disorder (ex. DM)
- non pregnant - Urologic abnormalities (ex. stones, stents, indwelling catheters,
- premenopausal neurogenic bladder, PCKD)
- *UTIs in men are usually complicated

134
5. In patients with recurrent dysuria, look for a specific underlying cause (e.g., post-coital UTI,
atrophic vaginitis, retention).

Recurrent UTI: >2 uncomplicated UTIs in 6 months, or commonly as >3 positive cultures within
preceding 12 months. About 25% of women affected by this
Risk Factors:

Premen Women: inc. freq. of sex inter, use of spermicide, new sex partners, anatomical
abnormalities
Postmen Women: Lactobacilli is natural pathogen against E.Coli. With vaginal atrophy,
decreased lactobacilli. Incontinence, pelvic floor prolapse, and increased post-void
residuals are at increased risk.

With recurrent infections, structural abnormalities should be considered. Especially if organisms

such as Proteus, Pseudomonas, Enterobacter, and Klebsiella are found (associated with anatomy
abnormalities or renal calculi).

Earache - Key Features

1. Make the diagnosis of otitis media (OM) only after good visualization of the eardrum (i.e.,
wax must be removed), and when sufficient changes are present in the eardrum, such as
bulging or distorted light reflex (i.e., not all red eardrums indicate OM).

2. Include pain referred from other sources in the differential diagnosis of an earache (eg.
Tooth abscess, trigeminal Neuralgia, TMJ dysfunction, pharyngitis, etc.).

3. Consider serious causes in the differential diagnosis of an earache (eg. tumors, temporal
arteritis, mastoiditis).

4. In the treatment of otitis media, explore the possibility of not giving antibiotics, thereby
limiting their use (e.g., through proper patient selection and patient education because most
otitis Media is of viral origin), and by ensuring good follow-up (e.g., reassessment in 48 hours).

5. Make rational drug choices when selecting antibiotic therapy for the treatment of otitis
media. (Use first-line agents unless given a specific indication not to.)

6. In patients with earache (especially those with otitis media), recommend appropriate pain
control (oral analgesics).

7. In a child with a fever and a red eardrum, look for other possible causes of the fever (i.e., do
not assume that the red ear is causing the fever).*

8. Test children with recurrent ear infections for hearing loss.

Note: *See the key features on Fever.

1. Diagnosis
- must meet all of the below criteria for certain diagnosis:

135
 i). abrupt onset of symptoms
ii). Presence of middle ear effusion (MEE) indicated by any of
a). bulging TM
b). limited/absent mobility of TM
c). air fluid level behind TM
d). otorrhea
iii). Signs of symptoms of middle ear inflammation as indicated by either
a). erythema of TM
b). distinct otalgia clearly referable to the ear (tugging at ear)

- A red TM is common but is not reliable for diagnosis without MEE (erythema alone has a PPV
of 15% for AOM)
- MEE with no inflammation is otitis media with effusion (OME)

** if febrile, any other cause for fever should be considered before concluding AOM

2. Risks
- bottle feeding, day care, passive smoking, craniofacial abnormalities, Aboriginal ethnicity.

3. Etiology (in order of frequency)

Viral, S. pneumoniae, H. influenza, M. catarrhalis

4. Differential Diagnosis
- the main DDx is between AOM and OME in children
- other causes of ear pain are otitis externa, malignant OE, foreign body, TMJ disorders,
pharyngitis, cerumen impaction, tooth abscess, trigeminal neuralgia.

5. Serious causes of earache

- in general tumors, temporal arteritis, mastoiditis and malignant OE must be excluded based on
history and physical.

6. Treatment
- Observation: oral analgesia with acetaminophen and ibuprofen with follow up in 48-72 hours to
reassess

Criteria for Antibacterial treatment

Age Certain Diagnosis Uncertain Diagnosis

<6 mo Antibiotics Antibiotics
Severe – antibiotics
6mo-2yr Antibiotics
Nonsevere – observe
Severe – antibiotics Severe – observe
≥2yr
Nonsevere - observe Nonsevere – observe

*Severe disease: fever ≥ 39 oC or moderate/severe otalgia

136
Nonsevere – Amoxicillin 80-90mg/kg/day BID → 1st line

Penicillin allergy: cefuroxime, azithromycin, clarithromycin

Severe – Amoxicillin/Clavulinic acid → 1st line

Penicillin allergy: ceftriaxone 1 or 3 days

Treatment failure – increase coverage to Amox/Clav or ceftriaxone; clindamycin if those fail.

7. Recurrent AOM or OME

- Refer if

a). hearing threshold < 20dB

b). MEE >3 months
c). 3 episodes in 6 months or 4 in 12 months

Elderly - Key Features

1. In the elderly patient taking multiple medications, avoid polypharmacy by:

- monitoring side effects.
- periodically reviewing medication (e.g., is the medication still indicated, is the dosage
appropriate).
- monitoring for interactions.

2. In the elderly patient, actively inquire about non-prescription medication use (e.g., herbal
medicines, cough drops, over-the- counter drugs, vitamins).

n.b.: combined response to 1 & 2:

Assessment of inappropriate drug prescribing: use STOPP criteria (more sensitive than Revised
BEERS criteria) which is a list of 65 drugs and when to avoid them (available online at
http://www.biomedcentral.com/content/supplementary/1471-2318-9-5-S1.doc)

Assessing Care of Vulnerable Elders (ACOVE-3) recommendations:

- Maintain a list of Rx
- Include OTC Rx and herbals in that list
- Annually review medication
- Assess for duplication
- Assess for interactions (including drug-drug, or drug-disease)
- Assess for adherence & affordability
- Assess for specific classes of Rx assoc with common adverse events:

warfarin
analgesic esp. narcoids & anti-HTN esp. ace and diureticsNSAIDs
psychotropics insulin and hypoglycemic agents 

137
- Minimize/avoid anticholinergic use

STOPP Age Ageing 2008; 37:673.

J Am Geriatr Soc 2007; 55 Suppl 2:S373.

3. In the elderly patient, screen for modifiable risk factors (e.g., visual disturbance, impaired
hearing) to promote safety and prolong independence.

138
139
140
141
142
143
144
4. In the elderly patient, assess functional status to:
- anticipate and discuss the eventual need for changes in the living environment.
- ensure that social support is adequate.

COMPLETE FUNCTIONAL ASSESSMENT

- does living environment need to change?
- is social support adequate?
- hearing aid, denture, glasses, walker?

145
1. ADLs
- Mnemonic: DEAT2H

- Dressing
- eating and EtOH (CAGE)
- ambulating (falls?)
- toileting (non-judgemental questions)
- transferring
- hygiene/bathing

- Communication (Vision/ hearing)

- Caregiver
- Depression (ask!)
- Dementia (memory/MMSE/MOCA/clock)
- Social/living situation
- Don’t miss Abuse/neglect

2. IADLs - Mnemonic:SHAFT-TT

- Shopping
- Housework
- Accounting
- Food prep
- Telephone
- Transportation
- Taking Rx

- weight loss? dentures fitting?

3. Assessment for Alzheimer’s:

Mnemonic: CURE FROM IRAN
Ask patient about CURE = staging – modified from Brief Cognitive Rating Scale

C – Current Events (mild)

U – USA president (moderate)
R – Relatives – children / spouse names forgotten(severe)
E – Everything forgotten (severe)

Ask caregiver about FROM IRAN (Modified from Functional Assessment Staging Tool FAST)

F – Function
R – Repetitive Questioning
O – Onset (Acute vs. Slowly progressing) M – Memory
I – IADL impaired (mild)
R – Repetitive dressing (moderate)
A – ADLs impaired (severe)
N – Non-ambulatory, non-verbal (very severe)

146
5. In older patients with diseases prone to atypical presentation, do not exclude these diseases
without a thorough assessment (e.g., pneumonia, appendicitis, depression).

- Most commonly missed diagnoses are cancer, pulmonary embolus, coronary disease,
aneurysms, appendicitis (J Am Board Fam Med 2012;25:87–97)
- Depression can present atypically with somatic complaints, cognitive, functional, or sleep
problems as well as complaints of fatigue or low energy. However, serious organic pathology can
present as depression; rule it out using a targeted history, physical examination, and
investigations

Specific statements in the Priority Topics & Key Features:

Anemia Consider anemia in elderly on NSAIDs
Dementia do not attribute behavioural problems to dementia without assessing for other possible
factors (e.g., medication side effects or interactions, treatable medical conditions such as sepsis or
depression).
Dehydration is difficult to assess clinically; use reliable signs ie. vitals
Diarrhea: In elderly with unexplained diarrhea, pursue investigation sooner as they are more
likely to have pathology
Fever: In elderly, there is no correlation between presence/absence of fever and presence/absence
of serious pathology.
Fracture: if XR neg, may need bone scan / CT.
Depression can present atypically with somatic complaints, cognitive, functional, or sleep
problems as well as complaints of fatigue or low energy. However, serious organic pathology can
present as depression; rule it out using a targeted history, physical examination, and
investigations
Infection: Look for infection as cause of ill- defined problems in elderly
Parkinsonism: Look for Parkinsonism in elderly with deterioration in functional status
Thyroid: Elderly are at higher risk
UTI: BPH is high-risk feature in elderly male. Suspect UTI in elderly with non-specific
presentation (abdo pain, fever, delirium)

*Addendum FYI: Elderly patients are mentioned in a number of other topics in the Priority
Topics and Key Features document, including:
Abdo pain: Include group-specific surgical causes of acute abdo pain in the elderly
Disability: Screen elderly patients for disability risks (e.g., falls, cognitive impairment,
immobilization, decreased vision) on an ongoing basis. In elderly, recommend primary
prevention strategies (e.g., exercises, braces, counselling, work modification). See #3 above.
Grief: Recognize atypical reactions ie. behaviour change
Immunization and Pneumonia: Elderly, nursing home, hospitalized patients benefit from
immunization ie. pneumococcus, flu, ribavirine. See #3 above.
Osteoporosis: Older men need osteoporosis counselling too.

Epistaxis - Key Features

1. Through history and/or physical examination, assess the hemodynamic stability of patients
with epistaxis.

Initial assessment:
Remember your ABC’s; your evaluation should always start with ensuring that there is an
adequate airway and hemodynamic stability.

147
Vital Signs
CVS: Pallor, tachycardia, weak thready pulse, hypotension, depressed JVP, dry mucous
membranes.
Resp: Tachypnea
Extremities: cool, clammy, mottled, prolonged cap refill, shut down.
CNS: Mental status changes, agitation, anxiety, confusion, combativeness, lethargy, coma.
GU: decreased urine output.
Systemic: Hypothermia

History: Quantify blood loss, duration, bleeding disorders, anticoagulation, CAD or other
comorbid conditions.

2. While attending to active nose bleeds, recognize and manage excessive anxiety in the patient
and accompanying family.

Patients often present with marked anxiety. Comfort, educate assess need for anxiolytics.

3. In a patient with an active or recent nosebleed, obtain a focused history to identify possible
etiologies (e.g., recent trauma, recent respiratory tract infection, medications).

History: Duration, severity, frequency, quantity of blood loss, laterality. Contributing or inciting
factors: trauma, nose picking, sinusitis, meds, drug use, environmental triggers. Nasal
obstruction. Personal or family history of bleeding disorders, or easy bruising.

Common Causes of Epistaxis

Local: Chronic sinusitis, Epistaxis digitorum (nose picking), foreign bodies, intranasal
neoplasm or polyps, irritants (e.g., smoking), medications (e.g., topical coticosteroids or
antihistamines), rhinitis, septal deviation, septal perforation, trauma, illicit drug use,
vascular malformations or talangectasia (e.g., Hereditary hemorrhagic telangectasia)
Systemic: Hemophilia, HTN (controversial), Leukemia, Liver disease, Renal disease,
Platelet dysfunction, Thrombocytopenia, Medications (e.g., ASA, anticoagulants, Plavix,
NSAIDS), alternative therapies (e.g., garlic, ginko, ginseng).

4. In a patient with an active or recent nosebleed:

a) Look for and identify anterior bleeding sites

More than 90% of bleeds occur along the anterior nasal septum at Kiesselbach’s area.

148
Blood supply: External carotid through the superior labial branch of the facial artery and the
terminal branch of the spenopalantine artery. Internal carotid through the anterior and posterior
ethmoidal arteries.

Utilize universal precautions, gown, gloves, face shield. Ensure adequate lighting, head lamp,
Frazier suction. Clear clots, have patient blow nose, may require use of forceps/suction. Examine
nares utilizing nasal speculum. Try to identify the bleeding point. Bleeding may have to be better
controlled to allow visualization: direct pressure/ice pack 15mins, gauze soaked with 4% cocaine
or 4% lidocaine + oxymetalazoline.

b) Stop the bleeding with appropriate methods.

Consider need for IV. Apply direct pressure pinching anterior aspect of nose while leaning
forward x 15 min. Place pledgets soaked in topical vasoconstrictors (oxymetazoline, cocaine) in
the anterior nares. If vessel is identified cauterize using silver nitrate or electric cautery (cauterize
only one side at once to prevent septal perforation). If refractory apply anterior nasal packing:
petroleum jelly soaked gauze, a sponge composed of hydroxylated polyvinyl acetate that expands
when wet (Merocel, Medtronic), an inflatable pack coated with hydrocolloid (Rapid Rhino,
Arthrocare). Packs are left in place 1-3 days prior to removal. A variety of absorbable or
degradable material that does not require formal removal is available and may be useful in
individuals with coagulopathy. These include Sugicel, Gel foam, Avitene, Suriflo, FloSeal. These
agents typically increase clot formation and provide some degree of tamponde. They form a
slurry which is injected into the nares with a syringe. Complications of nasal packing include
septal hematomas and abscesses, sinusitis, neurogenic syncope, pressure necrosis, and toxic
shock syndrome. For prolonged packing consider the use of antistaphylococcal antibiotic
ointment on packing materials.

5. In a patient with ongoing or recurrent bleeding in spite of treatment, consider a posterior

bleeding site.

10% of bleeds occur posteriorly, along the nasal septum or lateral nasal wall. Blood supply:
external carotid through the sphenopalantine branch of the internal maxillary artery.

Often treated by Otolaryngologist. Inflatable balloon such as epistat and foley catheter widely
used for posterior packing. Traditional posterior gauze packs, introduced through the mouth and
retracted back into the nasopharynx can also be used. The pack is retracted anteriorly and must
provide tamponade in the area of the choanae and the sphenopalantine foramen. The anterior end
is secured at the ala to ensure countertraction. When conservative measures fail embolization or
surgical ligation of the offending vessel may be necessary.

6. In a patient with a nosebleed, obtain lab work only for specific indications (e.g., unstable
patient, suspicion of a bleeding diathesis, use of anticoagulation).

Most patients will not require any blood work. Based on severity of presentation, use of
anticoagulation etc. consider obtaining CBC, PTT/INR, Blood type, cross match, may also
consider obtaining renal fxn and LFT’s.

7. In a patient with a nose bleed, provide thorough aftercare instructions (e.g., how to stop a
subsequent nose bleed, when to return, humidification, etc.)

149
How to stop the bleed: lean forward and spit out blood. Apply pressure by squeezing the soft part
of the nose not he boney segment. Hold for 10-15 minutes. Avoid packing as will likely rebleed
on removal. If bleeding persists after 20 mins of direct pressure seek medical attention.

Prevention: Don’t pick your nose, don’t use cocaine, quit smoking. Identify specific triggers such
as nasal spray, alternative therapies. Apply petroleum jelly to nares BID to relieve dryness and
irritation. Consider use of a humidifier at night. Avoid forceful nose blowing.

Family Issues - Key Features

1. Routinely ask about family issues to understand their impact on the patient’s illness and the
impact of the illness on the family.

2. Explore family issues:

- periodically
- at important life-cycle points (eg. When children move out, after the birth of a baby, etc)
- when faced with problems not resolving in spite of appropriate therapeutic interventions (eg.
Mediation compliance, fibromyalgia, hypertension)

Family can mean more than the traditional nuclear family to some patients. It is important to
enquire who your patient’s primary supports are and who they consider family. These are the
people who will have the greatest impact to them. Some people may not identify with having any
close family/friends, and it may be important to then enquire about work colleagues,
spiritual/faith groups, other regular activities they might attend and the people involved. Never
forget to inquire about pets … some people are as close to their pets as they would be family!!

Gain an understanding of the importance of different roles each family member has. For example,
in some families/cultural groups, the men are valued more than the women or there is one
decision maker who has the final say for the entire family. It is important to uncover these
hierarchical frameworks to most effectively take care of your families.

We usually only see people individually, but don’t forget to ask about the web of people that
shape their lives!

Fatigue - Key Features

1. In all patients complaining of fatigue, include depression in the differential diagnosis.

2. Ask about other constitutional symptoms as part of a systematic approach to rule out
underlying medical causes in all patients complaining of fatigue.

3. Exclude adverse effects of medication as the cause in all patients complaining of fatigue.

4. Avoid early, routine investigations in patients with fatigue unless specific indications for
such investigations are present.

5. Given patients with fatigue in whom other underlying disorders have been ruled out, assist
them to place, in a therapeutic sense, the role of their life circumstances in their fatigue.

150
6. In patients whose fatigue has become chronic, manage supportively, while remaining
vigilant for new diseases and illnesses.

Time Course of fatigue determines approach:

1-Recent Fatigue (less than 1 month)

-Key: screen for depression. Ask about life stressors

-Key: Laboratory evaluations in the absence of a positive history or physical examination
are of little diagnostic utility in the evaluation of the fatigued patient
-Key: screen for constitutional symptoms
-Key: go through list of meds to see if there are any meds (hypnotics, antihypertensives,
antidepressant meds, drug abuse, drug withdrawal)

2-Prolonged Fatigue (1 month to 6 months)

3-Chronic (over 6 months):

-Key: support these patients, but don’t write off all new symptoms as due to the same
fatigue syndrome!
-Key: help patients figure out if lifestyle, life stressors are contributing

Clinical fatigue incorporates three components, present to variable degrees in individual patients:
inability to initiate activity (perception of generalized weakness, in the absence of objective
findings); reduced capacity to maintain activity (easy fatiguability); and difficulty with
concentration, memory, and emotional stability (mental fatigue). Fatigue should be distinguished
from somnolence, dyspnea, and muscle weakness, although these symptoms may also be
associated with fatigue.

Hx: Onset, duration, course, impact on daily life, screen for psych dx, constitutional sx, organic
dx, sleep pattern, meds (b-blockers, antihistamines, opioids), rec drugs
Px: General appearance, lymphadenopathy, thyroid exam, CVS/Resp (CHF, COPD), Neuro exam
(muscle tone, bulk, strength, DTR, sensory, CN exam)
Labs:

CBC with differential

ESR
Chemistry screen (including electrolytes, glucose, renal and liver function tests)
Thyroid stimulating hormone (TSH)
Creatine kinase (CK), if pain or muscle weakness present

Major Causes of Chronic Fatigue:

V: CHF, COPD, Sleep apnea

I: Endocarditis, TB, Mono, Hepatitis, Parasites, HIV, and CMV
N: Occult malignancy, and severe anemia
D: Hypnotics, Antihypertensives, Antidepressant meds, Drug abuse and drug withdrawal
I: (dx of exclusion): Chronic fatigue syndrome (1-9%), Nonspecific Chronic Fatigue
(Fatigue for which no medical or psychiatric explanation can be found is seen in 8.5 to 34
percent )

151
 A: Rheumatic Disease,
T: Post-concussion syndrome
E: DM, Hypothyroidism, Chronic Renal Failure, Liver failure, Hypercalcemia, Adrenal
insufficiency
Psychiatric: most common: present in 60- 80 % of patients with chronic fatigue.
Depression (50%), Panic Disorder (14%), Anxiety Somatization (10%), Disturbed sleep

Chronic Fatigue Syndrome:

If you are interested in checking out Canadian Guidelines on Chronic Fatigue Syndrome
(AKA Myalgic Encephalomyelitis) go to
http://www.mefmaction.net/documents/me_overview.pdf

A diagnosis of exclusion—i.e.—you ruled out the above. However, dx is made mostly on

history.
Investigations: CBC, lytes, BUN Cr, TSH, ESR, and any other test for which there is a
HIGH pre-test probability.

Presentation:
-VERY common. Often in young to middle aged, 2x more in women with fibromyalgia
(70% of w CFS have fibromyalgia trigger points) and moderate to high socioeconomic
status
Hx-Relatively sudden onset of fatigue often associated with a typical infection such as an
upper respiratory infection or true mononucleosis.
- Patient is left with overwhelming fatigue and a number of additional symptoms,
especially altered sleep and cognition.
- Excessive physical activity characteristically exacerbates the symptoms.
****The pre-CFS medical history of the patient is not one of multiple somatic problems
such as chronic backache or chronic headache. Affected patients are typically highly
functioning individuals, some w psych hx, who are "struck down" with this disease****

Definition of Chronic Fatigue:

A-New onset fatigue that is persistent or relapsing, is not relieved by rest, is exacerbated
by physical activity and has led to substantial reduction in activity
And
B-Four or more of the following symptoms during 6 or more consecutive months that do
not predate the fatigue:
-Impairment short-term memory
-Muscle pain
-Sore throat
-New multi-joint pain without redness or swelling
-New headaches
-Tender axillary or cervical lymph nodes
-unrefreshing sleep
-Post-exertional malaise lasting over 24 hours.

Many patients with chronic fatigue syndrome are partially or totally disabled by its
manifestations. Their outward, healthy appearance belies the internal sense of ill health. It is

152
common for relatives and colleagues to accuse them of malingering. A vicious cycle of
frustration, anger, and depression commonly ensues.

Treatment:
1-Support and Trust: The patient has to believe that YOU believe that they have a real illness or
you can’t help them. Most of them feel guilty as it is.
2-Graded exercise program to prevent deconditioning and further fatigue/weakness
3-CBT

Fever - Key Features

1. In febrile infants 0-3 months old:

a) Recognize the risk of occult bacteria.
b) Investigate thoroughly (e.g., blood cultures, urine, lumbar puncture +/- chest X-ray).

CPS has an interesting guideline on measurement of fever. The summary is that rectal
temperature >38 remains the gold standard for children under 5, and oral temperature >38 for
children above 5 years old. Axillary temperature is reasonable for screening, but is not diagnostic.
Tympanic remains controversial, in terms of accuracy.

Treatment based on age, as most fevers in children are viral and the risk of occult serious
bacterial infection decreases with increasing age. There is significant debate over how to treat
febrile children at present, due to increased vaccination and falling infection rates.

Serious bacterial infection (SBI) is a heterogenous category: meningitis, sepsis, osteomyelitis,

septic arthritis, UTI, pneumonia, enteritis all crop up on the list.

You will see a lot of approaches break neonates down into <30 days, versus 30-90 days, versus 3-
36 months. The evidence in this realm is changing pretty rapidly, and I could not find any current
Canadian guidelines (the most recent CPS guideline I could find is from 1996, which is clearly
insane to study from).

Causative organisms by age

AGE LIKELY ORGANISMS POSSIBLE EMPIRIC ANTIBIOTICS

Neonate GBS, E .coli, S. aureus, Gr negs Amp + gent or amp + cefotaxime, consider acyclovir
Ceftriaxone 50-100mg/kg (or cefotaxime) +/-
1-3 mod Same as above and below
ampicillin, cloxacillin
Ceftriaxone 50mg/kg IM/IV (100mg/kg if suspect
meningitis).
3-36 S. pnemococcus, H. influenza,
mod meningococcus
Alternatives: clinda, macrolide. Consider vanco if a
lot of S. pneumo resistance

A few notes on this table: Ampicillin is added to cover Listeria - probably necessary up to 6-8
weeks. Vancomycin should also be considered if the source is thought to be skin/soft tissue, given
MRSA rates. Acyclovir shouldn’t be given to every febrile neonate, but in the setting of maternal
HSV, suspicious lesions, seizures, or a toxic/encephalopathic appearing child.

153
I TOXIC CHILD OF ANY AGE
These ones are easy - they all need aggressive investigation and management.

1. Admit
2. Do full septic workup
3. Empiric IV antibiotics based on age and local resistance patterns (see table) until
cultures back

II NONTOXIC CHILD

NONTOXIC NEONATES (0-1 MONTHS)

These ones are also easy - they all need aggressive investigation and management.
- Greatest risk of SBI (12-13% of febrile neonates) and least likely to appear toxic
- These children all need to be aggressively cultured regardless of WBC count etc.
- Most often have UTI>bacteremia>meningitis>gastro>other
- Obvious viral URTI does not decrease the risk of a concomitant SBI (unlike in older
children)
- Admit all, full septic workup including LP and possible HSV testing
- Empiric antibiotics +/- acyclovir until cultures back

What about the child who had a fever at home, but not in the ER? Check out this article if
interested - http://www.cjem-online.ca/v6/n5/p343. In summary, a measured (not tactile)
fever at home but not in-hospital is still associated with a pretty significant risk for
infection in the 0-30 day age group.

NONTOXIC FEBRILE INFANTS (1-3 MONTHS)

These ones are tricky - they may not need as aggressive treatment as was previously
recommended but guidelines are in evolution. There are no Canadian guidelines, for this
age group, more recent than 1996 that I could find.

These children are less likely to have SBI than the <1mo age group and there are a
variety of risk stratification criteria (Rochester, Baker etc.) Realistically speaking in
practice, I expect most of us would manage this age group in consultation with a
pediatrician.

I’m not going to regurgitate the Up To Date article for you. The current thinking is that,
in the absence of evidence to the contrary, these children should still be broadly cultured
and have a CBC and CXR. The need to do an LP, is controversial. The need for
admission, is controversial. Giving a dose of ceftriaxone for empiric coverage and
discharging, is controversial. Given how the topic is worded, I think your safest bet
would be to answer questions on the side of conservative investigation and management
in this age group -- ie, pan-cultures, admission, and broad spectrum antibiotics. Just be
aware that this may not necessarily be the case out in the real world.

NONTOXIC FEBRILE CHILDREN, 3-36 MONTHS

These children are your “normal” office patients. They are much less likely to have SBI
or occult bacteremia, if well-looking.

154
 There is a big role for clinical judgement in this age group as opposed to guidelines.
Sorry!! I’m not going to insult y’all by saying things like “common sources for infection
in this age group are acute otitis media, pneumonia etc. etc. bla bla bla.” Anyways the 99
topic question as I can tell isn’t so focused on this age group.

2. In a febrile patient with a viral infection, do NOT prescribe antibiotics.

Almost all of the “typical” family medicine infections are viral. Sinusitis - >98%. Sore throat -
>90% in the under 5 and over 18 age group, and about 70% in the 5-18 age group. Bronchitis -
>98% (COPD patients are an exception here, they warrant antibiotic treatment). Have a look at
the ARI series in Canadian Family Physician, they are really brief articles, 1 page each, on
common URIs. UTIs on the other hand, are almost always bacterial.

3. In a febrile patient requiring antibiotic therapy, prescribe the appropriate antibiotic(s)

according to likely causative organism(s) and local resistance patterns.

I think by now everybody probably has their list of antibiotics for the common stuff we see. I will
give you my list, which I try very hard to have be evidence-based - ie, appropriate for the bug, but
not overkill.

Coverage for common URI bugs: Amoxicillin, 40mg/kg/day in kids, the current American
Academy of Pediatrics guideline for AOM calls for high dose at 80mg/kg/day for improved inner
ear penetration and activity against resistant strains. Macrolides, Septra, and 3rd gen
cephalosporins are reasonable second line choices (though I tend to think that giving cefuroxime
for otitis media falls into the “overkill” category, personally)

Coverage for pneumonia - first line for outpatients is a macrolide or doxycycline if they are
otherwise healthy. First line for inpatients is a respiratory quinolone. The Canadian Thoracic
Society guidelines can be found at http://www.respiratoryguidelines.ca/sites/all/files/Community-
acquired-Pneumonia-Guidelines-2000.pdf, knock yourself out. The algorithm on risk stratifying
patients for admission versus discharge is interesting and educational but I won’t reproduce it
here.

Coverage for UTI - Septra and Macrobid are first-line. Cipro provides renal coverage, which
Macrobid does not and Septra does not very well, I believe.

Hopefully the more esoteric stuff will come up in other people’s topics.

4. Investigate patients with fever of unknown origin appropriately (e.g., with blood cultures,
echocardiography, bone scans).

5. In febrile patients, consider life-threatening infectious causes (e.g., endocarditis,

meningitis).

6. Aggressively and immediately treat patients who have fever resulting from serious causes
before confirming the diagnosis, whether these are infectious (e.g., febrile neutropenia, septic
shock, meningitis) or non-infectious (e.g., heat stroke, drug reaction, malignant neuroleptic
syndrome).

155
Keep in mind that there is fever without source (what we usually see, a toddler with a fever but
it’s not obvious where it’s coming from), versus fever of unknown origin. FUO is fever lasting
for 3 weeks without obvious source; the differential here is autoimmune, neoplastic, infectious,
and “miscellaneous” (drug-induced, hepatitis, other rare zebras). Check out the comprehensive
review. I think the key is that there is a broad differential with some “can’t miss” diagnoses, such
as TB, HIV, osteomyelitis, endocarditis, lymphoma, malignancy, RA, etc. The suggested initial
workup from the above AFP article suggests CBC, electrolytes, LFTs, blood cultures, urine
cultures, CXR, TB skin test, CXR, and ESR with further investigation depending on results.

I believe topic #5 and most of #6 is fairly self-explanatory. If you need to familiarize yourself
with early goal directed therapy for sepsis here is the Surviving Sepsis Campaign pocket guide.
The full guideline is on their website, but it’s pretty wordy and this gives you the basics.

There is an entire topic on meningitis so I am not going to cover that.

A brief word on a few other topics they mentioned:

Endocarditis - patients with abnormal heart structure are at high risk (congential defects, valvular
defects, prosthetic valves, cardiomyopathy). Other high risk patients are injection drug users and
those with prior endocarditis. Most cases caused by gram positive cocci specifically Strep
viridans, Staph aureus, Staph epidermidis. You may hear about HACEK - these are gram negative
infections responsible for 5-10% of endocarditis. Don’t make me name the bugs I promise you
you won’t remember.

There are detailed diagnostic criteria for endocarditis but fortunately the letters after my name are
not going to be FRCP(C) so I’m not going to go over them here. Just remember that the
presentation is nonspecific but can include anything on a spectrum from acute toxic illness with
high fever, to vague and nonspecific symptoms such as weakness, arthralgia, fatigue, malaise,
anorexia. Your physical exam should identify all the classic heavily pimped signs named after
physicians from the 1800s. Labs may or may not show anemia, elevated WBC, elevated CRP.
Blood cultures may or may not be positive, but you should get 2 sets 12 hours apart. TTE may or
may not show vegetations, TEE is still the gold standard if you are suspicious and the TTE is
negative. These people need long, long courses of antibiotics (6 weeks at a bare minimum).

Febrile Neutropenia - here’s a great guideline, from Alberta Health Services

In summary, Fever >38.3 degrees, ever, or >38 degrees for one hour (ie, 38-38.3 degrees) PLUS
ANC <0.5 in a patient who has received chemo in the last month is febrile neutropenia. You need
to identify the site of infection with CBC, LFTs, electrolytes and renal function, blood cultures,
urine cultures, CXR, sputum culture. LP does not need to be done routinely. Do not do a rectal
exam. I believe in an exam setting you would be safe so long as you identified an appropriate
broad spectrum antibiotic such as ceftazidime, imipenem, meropenem, pip-tazo. Vancomycin is
probably not empirically necessary but circumstances may suggest its use.

7. In the febrile patient, consider causes of hyperthermia other than infection (e.g., heat stroke,
drug reaction, malignant neuroleptic syndrome).

Hyperthermia - a nonphysiologic response which overrides the set point (remember, fever tends
to be a result of a raised hypothalamic set point).

Heat stroke - core body temperature >40.5ºC with associated CNS dysfunction in the setting of a
large environmental heat load that cannot be dissipated. Complications include ARDS, DIC, renal
or hepatic failure, hypoglycemia, rhabdomyolysis, and seizures. Mortality up to 20%.

156
There are two types of heat stroke:

Classic (nonexertional) heat stroke: in individuals with underlying chronic medical

conditions that either impair thermoregulation or prevent removal from a heat e.g.
cardiovascular disease, neurologic or psychiatric disorders, obesity, anhidrosis, extremes
of age, and use of drugs such as anticholinergic agents or diuretics
Exertional heat stroke: generally occurs in young, otherwise healthy individuals (e.g.
athletes, military recruits) who engage in heavy exercise in high ambient temperature and
humidity without access to salt and water. May be the first sign of increased
susceptibility to malignant hyperthermia.
Related problems: Heat cramps – muscle cramps after exercise in heat secondary to salt
loss and ingestion of hypotonic fluids. Temp is normal, skin is moist and cool. Rx: rest,
oral rehydration with salt solution, rarely IV NS.
Heat exhaustion: results from salt and water losses, minimal increase in core temp.
Present with N+V, headache, diaphoresis, cramps. Rx: rest in cool place, cooling and
rehydration. Avoid strenuous exercise for 2-3 days.

Malignant hyperthermia (MH) is a rare genetic disorder that manifests following treatment with
anesthetic agents, most commonly succinylcholine and inhaled anaesthetics. Early findings are
muscle rigidity , sinus tachy, increased CO2 production, and skin cyanosis with mottling.
Hyperthermia up to 45ºC occurs minutes to hours later; core temp rises 1ºC every 5 to 60 min.
Hypotension, dysrhythmias, rhabdomyolysis, electrolyte abnormalities, DIC, and mixed acidosis
are common.

Neuroleptic malignant syndrome (NMS) is an idiosyncratic reaction to antipsychotic agents. In

addition to hyperthermia, NMS is also characterized by "lead pipe" muscle rigidity, altered
mental status, choreoathetosis, tremors, and evidence of autonomic dysfunction, such as
diaphoresis, labile blood pressure, and dysrhythmias.

Serotonin syndrome may be confused with NMS, but is a distinct entity that includes agitation,
confusion, hyperthermia, diaphoresis, tachycardia and rigidity. Seen with SSRIs, but also L-
tryptophan, LSD, lithium, L-dopa and the MAOIs.

Treatment of hyperthermia
Antipyretics don’t help because they affect hypothalamic set-point, which isn’t the problem.
ABCs
Cooling to 39.5C rectal with ice packs, bath, fans, even cold peritoneal lavage. Do not use ETOH
rubs because a toxic amount can be absorbed cutaneously.
Inhibit shivering with benzos or chlorpromazine (don’t use this in NMS).
Labs – CBC, LFTs, INR, PTT, renal function, CK for rhabdo etc.
Mostly supportive Rx and specific Rx for MH (dantrolene) and NMS (stop neuroleptic, try
bromocriptine etc.)

8. In an elderly patient, be aware that no good correlation exists between the presence or
absence of fever and the presence or absence of serious pathology.

Fractures - Key Features

157
1. In a patient with multiple injuries, stabilize the patient (e.g., airway, breathing, and
circulation, and life-threatening injuries) before dealing with any fractures.

2. When examining patients with a fracture, assess neurovascular status and examine the joint
above and below the injury.

3. In patients with suspected fractures that are prone to have normal X-ray findings (e.g.,
scaphoid fractures in wrist injuries, elbow fracture, growth plate fracture in children, stress
fractures), manage according to your clinical suspicion, even if X-ray

4. In assessing elderly patients with an acute change in mobility (i.e., those who can no longer
walk) and equivocal X-ray findings (e.g., no obvious fracture), investigate appropriately (e.g.,
with bone scans, computed tomography) before excluding a fracture.

5. Identify and manage limb injuries that require urgent immobilization and/or reduction in a
timely manner.

6. In assessing patients with suspected fractures, provide analgesia that is timely (i.e., before X-
rays) and adequate (e.g., narcotic) analgesia.

7. In patients presenting with a fracture, look for and diagnose high-risk complications (e.g.,
an open fracture, unstable cervical spine, compartment syndrome).

8. Use clinical decision rules (e.g., Ottawa ankle rules, C-spine rules, and knee rules) to guide
the use of X-ray examinations.

Note: These key features do not include technical and or psychomotor skills such as casting,
reduction of dislocations, etc. See Procedural Skills.

GENERAL PRINCIPLES
-Stabilize ABCs, and rule out life-threatening injuries.
-History should include:

-Mechanism of injury
-Significant past injuries or surgeries in the affected area
-Concomitant injuries ("Did you injure any other part of your body?")
-Chronic medical conditions and medications. Most recent Tetanus.
-Allergies
-Last meal (in case an injury requiring urgent surgery is identified)

-On physical:

-Evaluate neurovascular function

-Look for open fracture – breaks in skin and signs of soft tissue damage.
-Palpate the entire area around the fracture site, including the entire bone in question,
adjacent bones, and at least one joint above and below.

-Basic principles when obtaining imaging:

-Obtain multiple and orthogonal views (at least two orthogonal).

158
 -Include the entire bone or joint in question.
-Obtain advanced imaging if clinical findings suggest # but plain x-rays are unrevealing.

-Fracture immobilization usually required if:

-Reduction was required, in order to maintain it.

-Two adjacent bone are involved (eg, fracture of radius and ulna)
-Segmental or spiral fractures
-Fracture dislocations
-Fractures where muscles exert strong forces that may cause displacement

-Provide adequate analgesia. Fracture immobilization, ice, elevation, and analgesic medications
all reduce pain.
-Provide clear instructions for injury care and monitoring, including cast or splint care, and a
follow-up plan. For uncomplicated fractures, a return visit within 3-7 days.

FRACTURES PRONE TO NORMAL X-RAYS

A. SCAPHOID #
-Most common carpal bone #. Typically occur from a FOOSH with the wrist in dorsiflexion.
Suspect a scaphoid fracture in any patient with wrist pain following a fall.
-Plain radiographs soon after injury may not reveal #. Order advanced imaging if an immediate
Dx is needed or immobilize and repeat imaging with a bone scan (after 3-5 days) or x-rays (after
7-10 days). Check x-rays for concomitant injury of the scapholunate ligament.
-The scaphoid has a tenuous blood supply leading to the possibility of nonunion or osteonecrosis
with # of the proximal pole.
-All # that are displaced (>1 mm) and those with a significantly ↑ or ↓ scapholunate angle should
be immobilized in a thumb spica splint and referred to ortho.
-Non-displaced # (≤1 mm) of the distal scaphoid → short-arm thumb spica cast for 6-10 weeks.
Non-displaced # at the wrist or proximal third of the scaphoid → long-arm thumb spica cast for
six weeks, followed by a short-arm cast until healing documented. These # require a longer
period of immobilization.
-If prolonged immobilization cannot be tolerated, refer the patient for operative fixation. Athletes
and workers engaged in heavy labor must continue to wear protection (rigid splint) for two
months after radiographic healing is noted.

B. ELBOW #
-Suspect # of the prox radius in all pts with lateral elbow pain following FOOSH.
-Immediate orth evaluation if: open #, neurovascular compromise, or # dislocation.
-Immediate reduction critical if there is a radial head or neck # and elbow dislocation. The longer
the joint remains dislocated, the more difficult the reduction and the greater the risk of avascular
necrosis.
-Isolated nondisplaced # (Mason I) can be managed by posterior splint for 1-2days or sling for
comfort for 1-2d.
-Obtain AP and lateral xray in all patients where a # about the elbow is suspected. If no # is
evident, a radiocapitellar (Greenspan) view may better characterize the radiocapitellar joint.
-Elevated anterior or posterior fat pads may be the only indication of a radial head #; can be
treated in the acute setting with either a posterior splint or sling.
-Assessing range of motion of both flexion-extension and pronation-supination is vital in patients
with Mason Type I radial head #s. If deficits are identified, further evaluation is needed following

159
hemarthrosis aspiration and local anesthetic injection. Early mobilization is paramount in
obtaining good short-term and long-term results.

C. GROWTH PLATE #.

Salter #.

D. STRESS #
-# that occurs when a bone breaks after being subjected to repeated tensile or compressive
stresses, in a person who is not known to have an underlying disease that would be expected to
cause abn bone fragility.
-High-risk stress # are those at greater risk for displacement, nonunion, or # propagation
-Important risk factors for stress # include a hx of prior stress #, low physical fitness, a sudden ↑
in the volume and intensity of physical activity, female gender and menstrual irregularity, a diet
poor in calcium and vit D, poor bone health, and poor biomechanics.
-Early Dx of stress # is essential to avoid Cx. In most cases, the history and physical provide
sufficient info to Dx and manage low-risk stress # without imaging studies.
-Many patients with stress # describe the insidious onset of localized pain within days to weeks of
beginning a strenuous activity. Examination → focal tenderness at the # site.
-X-ray when high-risk stress # are suspected → neg → MRI or bone scan.
-The ddx for stress # includes tendinopathy, muscle strain, joint sprain, nerve entrapment,
exertional compartment syndrome, neoplasm, and infection.
-Stress # at low-risk sites are managed conservatively with the following interventions:

– Acute pain control

– Protection of the fracture site with reduced weightbearing or splinting
– Reduction or modification of activities such that pain is not present
– Gradual resumption of activities if pain-free
– Rehabilitative exercise to promote optimal biomechanics
– Risk factor reduction

-Ortho consultation for pts with high risk #; if lengthy rehabilitation process interferes with return
to work; or some high-level athletes.

HIGH RISK COMPLICATIONS

-Life threatening conditions: severe hemorrhage as with femur or pelvic #; conditions associated
with hip # in elderly such as pneumonia, PE, or rhamdomyolitis secondary to immobilization; or
pulmonary contusion with rib #.
-Thromboembolic disease.
-Fat embolism: associated with closed long bone fractures of the lower extremity and pelvis. FE
typically manifests 24 to 72 hours after injury with dyspnea, tachypnea, and hypoxemia.
Neurologic abnormalities and a petechial rash may be present. Severe respiratory distress and
death can occur.
-Arterial injury
-Nerve injury
-Compartment syndrome: Acute compartment syndrome (ACS) occurs when increased pressure
within a compartment compromises the circulation and function of tissues within that space. With

160
#s, bleeding or swelling within a fascial compartment creates the increased pressure. Long bone
#s → most commonly associated with ACS, particularly #s of the tibia, distal radius,
supracondylar area of the humerus, and femur. ACS can also be caused by casts or bandaging that
limits the space available for soft tissue swelling.

Early S&S: pain out of proportion to the apparent injury, persistent deep ache or burning
pain, paresthesias, and pain with passive stretching of muscles in the affected
compartment.
Early recognition of ACS and immediate fasciotomy may be limb sparing.

-Open #: treat with immobilization, tetanus prophylaxis as needed, surgical irrigation and
debridement, and antibiotics. Rx of Posttraumatic osteomyelitis → Cefuroxime +/- Vancomycin
for 48 to 72 hours total or for 24 hours after wound closure.

Hallmarks of posttraumatic osteomyelitis are nonunion of the # site and poor wound
healing after wound closure. Other symptoms: fever and local wound drainage, erythema,
warmth swelling and pain. The tibia is the bone most frequently involved by
posttraumatic osteomyelitis.

-Osteomyelitis: open fractures are at greatest risk. The extent of soft tissue injury at presentation
appears to be the most significant risk factor.
-Nonunion and malunion: Incomplete healing of a fracture where the cortices of the bone
fragments do not reconnect is called a nonunion. When a fracture heals with a deformity (eg,
angulation, rotation, incongruent joint surface), this is called a malunion. Nonunions commonly
present with persistent pain, swelling, or instability beyond the time when healing should
normally have occurred. In most cases, symptomatic nonunions are treated with open reduction
and fixation.
-Complex regional pain syndrome: a complex disorder of the extremities characterized by
localized pain, swelling, limited range of motion, vasomotor instability, skin changes, and bone
demineralization. Fractures, with or without a nerve injury, are a common inciting event. Early
recognition and initiation of therapy is important for successful treatment.
-Post-traumatic arthritis

CLINICAL DECISION RULES

THE CANADIAN C-SPINE RULES involves the following steps:

Condition One: Perform radiography in patients with any of the following:

1) Age 65 years or older
2) Dangerous mechanism of injury: fall from 1 m (3 ft) or 5 stairs; axial load to the head,
eg diving accident; motor vehicle crash at high speed (>100 km/hour [>62 mph]);
motorized recreational vehicle accident; ejection from a vehicle; bicycle collision with an
immovable object, such as tree or parked car
3) Paresthesias in the extremities
Condition Two: In patients with none of the high risk characteristics listed in Condition
One above, assess for any low-risk factor that allows for safe assessment of neck range of
motion:
1) Simple rear end motor vehicle accident; excludes: pushed into oncoming traffic; hit by
bus or large truck; rollover; hit by high speed (>100 km/hour [>62 mph]) vehicle
2) Sitting position in emergency department

161
 3 )Ambulatory at any time
4) Delayed onset of neck pain
5) Absence of midline cervical spine tenderness
If no low-risk factors → NOT suitable for ROM testing and must be assessed with xray.
If low-risk factors → ROM testing, as below.
Condition Three: Test active ROM. Perform xray in pts who are not able to rotate their
neck actively 45˚ both L and R. Pts able to rotate their neck, regardless of pain, do not
require imaging.

OTTAWA ANKLE RULES

Ankle Xrays indicated if: pain in malleolar zone and any of: 1) tenderness at the posterior edge or
tip of either the medial or lateral malleolus extending 6cm prox, 2) inability to weight bear
immediately and in the ER.

Foot Xrays indicated if: pain in mid-foot zone and any of: 1) bone tenderness over the navicular
or the base of 5th metatarsal, 2) inability to wt bear immediately and in the ER.

OTTAWA KNEE RULES

Xray indicated if any of: 1) age >55, 2) inability to wt bear immediately and in the ER, 3) isolated
tenderness of the patella, 4) tenderness over head of the fibula, 5) inability to flex to 90 degrees.

HIP #
-Substantially ↑ risk of death and major morbidity in the elderly.
-Hip # are classified by anatomic location and fracture type. The general categories include
intracapsular (femoral neck and head) and extracapsular (intertrochanteric and subtrochanteric).
Intracapsular # have higher rates of nonunion, malunion, and avascular necrosis of femoral head.
-Initial management: analgesia and consult ortho. Obtain blood for type and crossmatch in pts
with any 2 of: age over 75 years, initial Hg ˂120, and a peritrochanteric fracture.
-Provide prophylaxis against thromboembolism and infection.
-Obtain an AP view of hip with max internal rotation, lateral view, and AP pelvis. If plain x-rays
neg but pain ++ or clinical suspicion is high, MRI is best, but CT 2nd line.
-In elderly patients, determine the reason for any fall (eg, syncope, stroke), and assess for
additional orthopedic and internal injuries (eg, intracranial hemorrhage, cervical spine fracture).
-Femoral neck # are intracapsular and have a tenuous blood supply. ↑ risk of Cx. Fracture-
dislocations have greatest risk. A displaced hip # → significant groin pain; the leg → externally
rotated and shortened. Typically little bruising. With insufficiency #, there may be no obvious
history of trauma and the patient may complain of vague knee, buttock, groin, or thigh pain.
-Intertrochanteric # are extracapsular. Lower risk for Cx. Significant ecchymosis may be present.
A large amount of blood can be lost into the thigh → closely monitor hemodynamic status.
-Assess the patient's ambulation, overall functional status, and medical comorbidities. Aside from
those in severely debilitated patients, most hip fractures are treated surgically.
-Isolated fractures of the greater and lesser trochanters are typically avulsion fractures caused by
forceful muscle contraction in active young adults. In the elderly, such injuries can occur from
direct trauma (eg, fall), but have also been associated with pathologic fractures.

Gastro-intestinal Bleed - Key Features

1. In a patient with blood in the stools who is hemodynamically stable, use history to
differentiate upper vs. lower GI bleed as the investigation differs 2. In a patient with

162
suspected blood in the stool, explore other possible causes (e.g., beet ingestion, iron,
Pepto-Bismol) before doing extensive investigation 3. Look for patients at higher risk for
GI bleed (e.g. previous bleed, ICU admission, NSAIDs, alcohol) so as to modify
treatment to reduce risk of GI bleed (e.g. cytoprotection) 4. In a patient with obvious GI
bleeding, identify patients who may require timely treatment even though they are not yet
in shock 5. In a stable patient with lower GI bleeding, look for serious cause (e.g.,
malignancy, inflammatory bowel disease, ulcer, varices) even when there is an apparent
obvious cause for the bleeding (e.g., do not attribute a rectal bleed to hemorrhoids or to
oral anticoagulation). 6. In a patient with an upper GI bleed; a. Include variceal bleeding
in your differential, b. Use the history and physical exam to assess the likelihood of a
variceal bleed as its management differs.

Lower GI Bleed Upper GI bleed

Proximal to ligament of treitz
Anatomy Distal to ligament of treitz
(75% of GI bleeds)
Etiology & • Diverticular disease • Above GE junction
History/Clinical o Usually painless but may o Epistaxis
presentation c/o of cramping as bleeding o Esophageal varices
causes irritation and the (10-30%)
bowel to spasm • hx of liver
o Presentation varies disease/portal
depending on amount of hypertension (ask about
volume loss, but often EtOH, IV drug use, etc)
bleeding is brisk • Often presents as major
o If bleeding is brisk pt may bleed with shock but may
be hemodynamically also present with coffee
unstable ground emesis
o Self-limited in 70-80% o Esophagitis
• Hx of GERD,
• Angiodysplasia (arteriovenous dysphagia, odynophagia
malformations) • May also result from
infectious causes:
o Usually painless and self- Candida most common
limited hematochezia or organism followed by
melena Herpes and CMV
o Tends to cause slow and o Esophageal cancer –
repeated bleeds so may constitutional
present with + FOBT, iron- symptoms,, progressive
deficiency anemia and dysphagia
syncope/pre-syncope o Mallory Weiss tear
(10%) – Hx of retching
• Colitis resulting in hematemesis
+/- melena
o Ischemic
• Can be insidious, • Stomach
presenting with pain and
rectal bleeding over several o Gastric ulcer -20%
weeks o Gastritis (e.g. H. pylori,
• May also be fulminant with NSAID, EtOH, post

163
 acute abdo pain, rectal
bleeding and hypotension
• Tends to affect older with
cardiovascular co-
morbidities
o Inflammatory
• UC>CD
• Depends on severity
• Can present as severe
bloody diarrhea +/-pus or
have minimal symptoms
• Fever, abdo pain, extra-
intestinal findings
o Infectious
surgery, infectious,
• Hx of exposure, abdo pain,
systemic) -20%
fever, diarrhea (may be
o Gastric cancer – early
watery +/- bloody depending
satiety, weight loss, abdo
on organism), dehydration
pain
• patients may be quite ill,
however blood loss is
usually mild • Duodenum
o radiation induced colitis
o Ulcer in bulb (25%)
• Neoplasm o Aortoenteric fistula
(usually only if previous
aortic graft)
o Right-sided: melena or
maroon colored stools, iron-
deficiency anemia • Coagulopathy
o Left-sided: bright red
blood per rectum. o Drugs, renal disease,
• Note that cecal bleeding liver disease)
can also present as melena
o Recall some colon cancers • Vascular malformation
may not bleed at all • Also, r/o dietary causes of black
stool such as iron
• Anorectal disease supplementation, Pepto-Bismol

o History of hemorrhoids,
blood on toilet paper.
Usually painless bleeding on
history unless strangulated.
Purititis also common
o Anal fissures – pain with
passing stool, blood on toilet
paper

• Need to rule out upper GI source

and dietary causes of red stool such
as beets
Management/Approach • History as above to determine if • 80% of upper GI bleeds stop

164
 upper or lower

• Initial management
spontaneously or only need
supportive therapy
o stabilize patient (ABC’s, 2
large bore IVs and IV fluids,
• Risk factors for mortality: co-
Monitors, Cross, Type and
existent illness,
screen)
hemodynamically unstable, age
o placing a NG tube to help
>60, anti-coagulation
localize bleed
• Initial management
o endoscopy to r/o UGIB
o colonoscopy to determine
site of bleed, etiology and o stabilize patient
potentially treat (e.g. (ABC’s, 2 large bore IVs
coagulation) and IV fluids, Monitors,
o May need to transfuse if Cross, Type and screen)
hemodynamically unstable o NG tube to help
o may require surgical differentiate between
intervention depending on UGIB and LGIB (except
etiology in variceal bleeds)

• Bedside tests • Endoscopy to visualize and

potentially treat
• PPI (IV omeprazole) for non-
o DRE
variceal bleeds
• For variceal bleeds, octreotide
• Massive GI bleed
• Ensure all potential causative
agents are stopped (e.g. NSAIDs,
o Systolic BP <90 mmHg EtOH)
o Hb <60 • May need to transfuse if
o Risk Factors hemodynamically unstable
• >65 years
• multiple medical co-
morbidities

Gender Specific Issues - Key Features

1. In the assessment of clinical problems that might present differently in men and women,
maintain an inclusive differential diagnosis that allows for these differences (e.g., women with
coronary artery disease, depression in males).

The patient's gender is an important factor in the consideration of nearly every clinical
presentation. While some concerns are anatomically sex-specific and present distinctly (ex.
menopause vs andropause, testicular vs ovarian torsion), others are more frequent in women (ex.
breast cancer, eating disorders) and may be more easily overlooked when they occur in men, and

165
vice-versa.

Depression: Women are historically diagnosed with depression twice as often as men, however
completed suicide rates are higher in men than women. Men tend to present less frequently to
medical attention and tend not to disclose emotionally distress to their physicians. Physicians may
require a higher index of suspicion in screening for depression in men, and recognize that
extreme conformity to masculine norms has been associated with higher rates of depression(1).
Depression in men may also be masked by substance use(2).

CAD: Cardiovascular mortality is much greater in men than women, however the prevalence of
angina is higher in women worldwide(3). Cardiac chest pain is more likely to be atypical in
women.

COPD: COPD tends to be under-diagnosed in women, however the impact on women in terms of
associated anxiety and quality of life is greater when COPD is diagnosed(4).

Many other gender-specific issues should be covered in more detail within each topic review.

2. As part of caring for women with health concerns, assess the possible contribution of
domestic violence.

See section on domestic violence for details.

3. When men and women present with stress-related health concerns, assess the possible
contribution of role-balancing issues (e.g., work-life balance or between partners).

Sociologic studies have indicated that work-life imbalance in men is predicted by “longer work
hours, wives who work fewer hours, perceived unfairness in sharing housework, marital
unhappiness, and tradeoffs made at work for family and at home for work. For women, only
marital unhappiness and sacrifices at home are imbalancing, and for women who are employed
full-time, young children are.”(5) These factors should be assessed in patients presenting with
stress-related concerns.

4. Establish office policies and practices to ensure patient comfort and choice, especially with
sensitive examinations (e.g., positioning for Pap, chaperones for genital/rectal exams).

5. Interpret and apply research evidence for your patients in light of gender bias present in
clinical studies (e.g., ASA use in women).

See individual topic reviews for details. Clinical studies have traditionally used men as a
prototype for all humans, however research increasingly suggests significant differences in the
presentation, epidemiology and management of many illnesses. Caution must be applied when
applying results from clinical trials in which results are not stratified by gender, or in which one
gender was under-represented. Clinical evidence is lacking for most health conditions for people
who are transgendered.

Particular attention has recently been paid to the use of statins and ASA in cardiovascular
protection in women. Whereas there is evidence that statins contribute to a reduction in all-cause
mortality when use for primary prevention in men, the same may not be true of women. Sex-
specific data has shown reductions in CHD events for women using statins, but not in decreasing

166
all-cause mortality(6). While newer evidence has made ASA less popular than it has been
previously for primary prevention, its potential for cardiovascular benefit in men relates to a
reduction in the incidence of MI, whereas in women the cardiovascular benefit of ASA relates to
reduction of CVA(7).

Optional reading: Some interesting facts from the Partnership for Gender-Specific Medicine at
Columbia University:
Brain/Nervous System
- Males are more likely than females to identify binge eating as normal.
- Women are more likely than men to recover their speech after a stroke.
- Parts of the hypothalamus are larger in heterosexual males than in transgender and homosexual
males.
- Women experience more pain from pressure and electrical stimulation than men.
- Men have larger brains; women have more brain cells.
- Because of the later maturation in males of the part of the brain that weighs risks and moderates
impulsive behavior, adolescent boys are more likely than girls to take life-threatening risks,
commit suicide and die violently than girls of the same age.

Heart
- Men who are diagnosed with heart disease are typically ten years younger than women.
- When a woman reaches menopause, her risk for cardiovascular disease increases four-fold.
- In general, coronary artery disease strikes men almost two decades earlier than it does women;
most men with coronary artery disease are dead by the time they are 65.
- Sudden cardiac death is more common in males.
- Men have larger hearts; women’s hearts beat faster.

Lungs
- It is more dangerous for women to smoke than for men. For the same number of cigarettes
smoked, women are 20 to 70 percent more likely than men to develop lung cancer.
- Women are less prone to hiccups than men.
- Even when corrected for body size, men’s lungs are bigger than women’s.
- A man takes 12 breaths per minute while a woman takes only nine breaths per minute on
average.

Immune System
- Because they have more active immune systems, women have the ability to fight off viral
infections better than men.
- Men are more susceptible to parasitic infestations than women because of their higher levels of
testosterone, which promotes parasite breeding rates.

Digestive System
- Boys between 11 and 15 are more likely than their sisters to have iron deficiency anemias
because girls absorb iron more easily from their gastrointestinal tracts than boys at that age.
- Women are more likely than men to feel overly full after eating and have more problems with
bloating and gas immediately following a meal.
- The composition of bile is different between the sexes; some of the breakdown products of bile
increase women's risk for colon cancer and may also explain the twice-higher incidence of
inflammatory bowel disease in women.
- Food takes twice as long to pass through the digestive system of women compared with that of
men. Food leaves a man's stomach a third faster than a woman's, and liquids twice as quickly.

167
Skeletal System
- Eighty percent of hip fractures occur in women.

Medications
- Women clear several medications faster than men, including erythromycin, prednisolone and
diazepam.
- There are sex-specific differences in the absorption and metabolism of pain killers and
anesthetics.

Mortality
- Life expectancy in men is six years shorter than in womenthan women when they die.

Cancer
- Pancreatic cancer occurs three times more frequently in men than in women. Estrogen and
progesterone appear to protect women from pancreatic cancer. Women develop melanoma on
different areas of the body than men. Skin cancer occurs more frequently on the ears and necks of
men and on the legs of women probably due to the shorter hairstyles of men and the exposed legs
of women, since they are almost always caused by exposure to the sun.
- A typical colon cancer is located 10 to 20 percent higher up in the colon in women than in men.

Grief - Key Features

1. In patients who have undergone a loss, prepare them for the types of reactions (e.g.,
emotional, physical) that they may experience.

2. In all grieving patients, especially those with a prolonged or abnormal grief reaction, inquire
about depression or suicidal ideation.

3. Recognize atypical grief reactions in the very young or the elderly (e.g., behavioral changes).

4. In patients with a presentation suggestive of a grief reaction without an obvious trigger, look
for triggers that may be unique to the patient (e.g., death of a pet, loss of a job)

Grief - subjective feeling precipitated by loss of loved one

Mourning - process by which grief is resolved
Bereavement - state of being deprived of loved one and in mourning
Death is the most powerful stressor in everyday life.

NORMAL GRIEF
Stage One - Shock

Duration: first couple of weeks

Characteristics: Numbness, sense of unreality, denial, disbelief, “going through motions”,
crying, sighing, abdominal emptiness, throat tightness.

Stage Two - Preoccupation with the deceased

168
 Duration: intense grief resolves by 1-2 months (person is able to sleep and eat, return to
work) and most symptoms resolve by 6 months, but may last for years in attenuated form.
Signs and symptoms: Intense yearning, anger, sadness, insomnia, anorexia, weakness,
fatigue, restlessness, guilt, dreams of deceased, thoughts of deceased, anhedonia,
introversion.
“Searching behaviours”: visual and auditory hallucinations, illusions of deceased’s
presence, but person is aware they are not real (i.e. not psychosis).

Stage 3 - Resolution

Duration: happens around 6 month to one year.

Characteristics: reorganization, return to life, able to think about past with joy, interest in
pleasurable activities, able to form new relationship.

Anniversary reactions
Anniversaries, etc. provoke waves of sadness, the amplitude of which diminishes over time, but
the grief may never fully go away.

Wide range of emotions and behaviours depending on cultural norms (e.g. intense display of
emotions vs. stoicism) and circumstances (e.g. unexpected vs. expected loss, child vs. adult).
Loss of newborn and miscarriage are not usually recognized as major losses, but can precipitate
prolonged grief.
Suicide or other socially disapproved death may lead to isolation and increased risk of suicide in
bereaved.

ANTICIPATORY GRIEF
Grieving begins when person is aware of impending death and ends with the occurrence of loss.
May take form of anxiety, sadness, reconciliation attempts, and caretaking behaviour. If loss is
delayed anticipatory grief may be expended and the bereaved may show few signs of acute grief.
Once anticipatory grief had been expanded it may be difficult to reestablish previous relationship
(e.g. persons returning from war, concentration camps).

GRIEVING CHILD
Resembles separation process: protest, despair, and detachment.
Protest - desire for caregiver, crying. Despair - child loses hope about caregiver’s return,
intermittent crying, withdrawal, apathy. Detachment - child relinquishes some emotional
attachment and exhibits interest in surroundings.
Child needs to find a substitute for the lost parent and they may transfer attachment to several
adults. If there is no consistent person available, severe psychological damage may occur, so that
the child no longer looks for, or expects, intimacy in any relationship. There is evidence that
depression and suicide attempts are more common in adults who experience the death of a parent
as a child. It is probably best for children to attend the funeral to prevent the ritual becoming a
frightening mystery, unless the child is reluctant or refuses.

DEATH OF A CHILD
Parental reaction to death of child or birth of very sick infant goes through the five stages of
terminal illness: shock, denial, anger, bargaining, depression and acceptance. Often a more
intense experience than death of an adult, with overwhelming feeling of guilt, blame of one
parent (e.g. in hereditary illnesses) helplessness, failing to protect the child. The grief may last a

169
lifetime. Unexpected death is often more traumatic as parents do not have anticipatory grief nor a
chance to overprotect the child or shower them with gifts etc.. Up to 50% of marriages in which a
child dies or is born with a major malformation end in divorce.

ABNORMAL BEREAVEMENT
Risk factors

Poor social supports, past psych. history, history of childhood separation anxiety or
abuse/neglect, high initial distress, unanticipated death, other major concurrent stresses
and losses, aversiveness to lifestyle change, highly dependent relationship with deceased,
death of a child).

Complicated grief
Defined as persistence, for at least 6 months, of disruptive emotional reactions including yearning
and four of:

- Difficulty moving on, numbness/detachment, bitterness, feeling life is empty without

deceased, trouble accepting death, future holds no meaning without deceased, being on
edge or agitated, difficulty trusting others.

May also exhibit social withdrawal and difficulty reengaging.

Complicate grief at 6 months is highly predictive of impairment at 12 and 24 months post loss
and may be at increased risk of cancer, HTN, heart disease, substance abuse, disability etc..
Sequelae of abnormal bereavement
Psychological: depression in 15-35% (4-9x higher than general population), suicide (especially in
older men in the first year)
Physical: higher rates of mortality (esp. older men), morbidity, consumption of EtOH, tobacco,
utilization of health care system, worsening of chronic medical conditions (esp. CHF, HTN).

GRIEF VERSUS DEPRESSION

Many patients with complicated grief meet criteria for MDD or GAD, but only < 20% get treated.
Criteria: depressive symptoms for two weeks, 6-8 weeks after a major loss should be treated with
psychotherapy +/- antidepressants. Antidepressants ameliorate depression, but not grief.

Grief vs. depression

Common features: sadness, tearfulness, anorexia, insomnia, anhedonia.
Differences:

Mood disturbance: constant in MDD, fluctuating in grief (“waves” of grief), able to have
moments of lighheartedness, happy memories, dysphoria triggered by thoughts of
deceased.
Shame and guilt: in depression due to distorted belief that one is wicked or worthless, in
grief related to not having done enough for deceased etc.
Hope: absent for many with MDD (will never feel better), bereaved realise grief is time
limited.
Suicide: in MDD threaten to suicide more often, unusual in grief except in physically
dependent older persons.
Timing: MDD can start at any time and can be chronic, in bereavement mood
disturbances start within 2 months of death and last less than 2 months.

170
ROLE OF THE PHYSICIAN
Before the death

Ensure a “good death” (means different things for different families).

Pay attention to family members, be available to them before the death. Consider
referring relatives with poor coping skills for psychosocial supports before the death.
Provide guidance, clear information and reassurance to family regarding difficult
decisions e.g. discontinuing life support.

After the death

Contact family members not at bedside if family wishes to answer questions etc.. Attend
funeral or memorial if family would like that. Call bereaved persons (e.g. spouse) to
check on them or offer an appointment, offer support groups.
Encourage bereaved to maintain normal patterns of activity, sleep, exercise and meals, as
these routines enhance adaptation during bereavement.
If sleep disruption is a problem, can offer a mild, short-term anxiolytic or hypnotic.
Anxiolytics can retard and inhibit grieving process, which the person has to go through to
come to a resolution.
Complicate grief can lead to prolonged dysfunction - need psychiatry referral for
complicated grief therapy (CGT). Some evidence the paroxetine may reduce some
symptoms (by 53%).
Bereavement related depression is treated with psychotherapy and antidepressants.

Headache - Key Features

1. Given a patient with a new-onset headache, differentiate benign from serious pathology
through history and physical examination.

2. Given a patient with worrisome headache suggestive of serious pathology (e.g., meningitis,
tumour, temporal arteritis, subarachnoid bleed):
a) Do the appropriate work-up (e.g., biopsy, computed tomography [CT], lumbar puncture
[LP], erythrocyte sedimentation rate).
b) Make the diagnosis.
c) Begin timely appropriate treatment (i.e., treat before a diagnosis of temporal arteritis or
meningitis is confirmed).
d) Do not assume that relief of symptoms with treatment excludes serious pathology.

3. Given a patient with a history of chronic and/or relapsing headache (e.g., tension, migraine,
cluster, narcotic-induced, medication-induced), treat appropriately, and avoid narcotic,
barbiturate dependence.

4. In a patient with a history of suspected subarachnoid bleed and a negative CT scan, do a

lumbar puncture.

5. In a patient suffering from acute migraine headache:

a) Treat the episode.
b) Assess the ongoing treatment plan. (referral when necessary, take a stepwise approach).

171
APPROACH TO PRIMARY HEADACHE DISORDERS

MIGRAINE
Classification: POUND pneumonic - 4/5 features has LR = 24 for migraine

• Pulsatile
• 4-72 hOurs
• Unilateral pain
• Nausea
• Disabling intensity

• *photophobia and phonophobia are also often present

• visual auras assʼd with migraine = bilateral, coloured, and tunnel-vision Sxs, other auras
include: disequilibrium/vertigo (common cause of vertigo in younger popʼn)
Triggers: Emotional stress, Hormones therapy, Not eating, Weather, Sleep disturbances, Odors,
Neck pain, Lights, Alcohol, Smoke, Heat, Food, Exercise, Sexual activity
Rx:

• Tylenol/NSAIDS 1st line

• 2nd line: Triptans - oral, SL, SC, intranasal preparations available, tend to work best if
taken early to abort migraine, theoretically faster-acting preparations best
avoid in HTN/CVD
• Status Migranous/ER Presentation
• 1L bolus NS
• Maxeran 10mg or Stemetil 5-10mg in mini bag over 15 mins +/- benadryl or
benztropine to prevent akathesia
• consider single dose Dexamethasone 10-15mg to prevent rebound headache

TENSION-TYPE HEADACHE (TTH)

Most common headache, but most common seen in office = migraine since most TTH is mild
and doesnʼt present to clinic
Classification:

• infrequent episodic <1d/month

• frequent episodic 1-14d
• chronic TTH 15+ days/month

Rx:

• Tylenol/NSAIDS 1st line

• combos with caffeine more effective but SEʼs, risk of Medication overuse headache
(see below)
• if pt responds to triptans, likely migraine component
• muscle relaxants have NO evidence and are NOT recommended

172
Table 1. International Classification of Headache Disorders II: Criteria for Diagnosis of
Tension-type Headache and Migraine(1)

Criteria Tension-type Headache Migraine

Number of
At least 10 episodes At least 5 previous attacks
Episodes
Duration 40 minutes to 7 days 4 to 72 hours (may be shorter in children)
At least two of the following: At least two of the following pain
characteristics:
Pressing or tightening, non-
pulsating quality Pulsating
Pain
Mild-to-moderate intensity, but does Moderate-to-severe intensity
Characteristics
not preclude activity Unilateral (may be bilateral in children)
Bilateral Aggravated by routine physical activity,
Not aggravated by routine physical or causing avoidance of routine physical
activity activity
Both of the following:
At least one of the following:
Associated No nausea or vomiting
Nausea and/or vomiting (often more
Features No photophobia or phonophobia or
prominent in children)
only one of photophobia or phono
Photophobia and phonophobia
phobia
Underlying
Not caused by another disorder. Not caused by another disorder
Conditions

(copied from McMaster module on headaches)

migraine and TTH can co-exist! similar triggers for both

Other Rx/prevention for both TTH and Migraine:

• non-pharmachologic options:
• heat/ice, massage, rest, biofeedback, meditation, exercise (relieve stress)
• prevention:
• good evidence for TCAs (amitryptilline most studied, nortriptylline less SEʼs)
• start at 10mg qhs, titrate up (q1-2 wks) to therapeutic effect (max 100mg/day) or SEʼs

CLUSTER HEADACHE:
Criteria:

• At least 5 attacks with severe unilat Sxs orbital or temporal,15-180 min untreated, freq
q2d - 8/d
• Accompanied by 1 of the following autonomic Sxs (conjunctival injection/lacrimation,
rhinorrhea, eyelid edema, facial sweating, miosis or ptosis, sense of agitation)

Classification:

173
 • episodic - 2+ cluster periods for 7d-1y with pain-free intervals > 1/12
• chronic - last > 1y without remission (or remission < 1 month)
• probably cluster headache - fulfills all but 1 of above criteria

Acute Rx = oxygen (non rebreather, 12L/min+, 15min duration) + sumatriptan SC or intranasal

• 2nd line agents - octreotide, lidocaine intranasal, ergots

Prevention: Verapamil start 240mg/day BID or TID depending on prep, titrate up by 80mg/d q
10-14d until desired prophylaxis

• use with onset of clusters or continuously (depends on freq of episodes), attempt to

wean slowly
• 2nd line prevention = high dose prednisone 5 days min +/- taper
• Topiramate may be useful adjunct with verapamil

• limitations = COPD (O2), triptans cause non-ischemic chest pain and distal paresthesias, use
caution in CAD

MEDICATION OVERUSE HEADACHE:

• co-exists with chronic daily headache
• Hx of prn use of analgesics for headache >2-3d/week for > 3 months
• all meds used to treat acute headaches have potential to cause this but some higher risk (in
order):

• highest with opioids, butalbital-containing combos, aspirin/acetaminophen/caffeine

combos
• intermed-high with triptans, tylenol
• lowest with NSAIDS

• often presents on awakening, only temporary relief with analgesics

• Rx is discontinuation - withdrawal Sxs 2-10 days (avg 3.5), include withdrawal headache, N&V,
hypotension, tachycardia, insomnia, anxiety

• NB: taper opioids/barbituates over 1 month, others can be abruptly stopped

• need to do this to accurately Dx headache condition and treat appropriately
• Withdrawal prevention: may consider TCA or prednisone during acute med withdrawal

“Sinus Headache” - overdx, most likely Sxs of congestion, sinus pressure, etc DUE TO
migraine!

SERIOUS CAUSES OF HEADACHE:

• Lesions on CT Scan (pus, blood, tumour):

• Blood - SAH, subdural, stroke, cerebral venous thrombosis

• Pus - Meningitis, encephalitis
• Tumor - primary vs metastatic, benign vs. malignant

174
• Non-Intracranial pathology:

• Cervical A dissection (carotid or vertebral)

• Hypertensive encephalopathy
• Pre-eclampsia/eclampsia
• Idiopathic intracranial hypertension
• Glaucoma

• Temporal Arteritis

• Meds/toxins (ie CO poisoning)

• RED FLAGS: New headache at age >50, sudden onset/maximal at onset, trauma, fever, vision
loss, severe neck pain, morning emesis, significant worsening freq/intensity, constitutional Sxs,
focal neuro findings, etc

Hepatitis - Key Features

1. In a patient presenting with hepatitis symptoms and/or abnormal liver function tests, take a
focused history to assist in establishing the etiology (e.g., new drugs, alcohol, blood or body
fluid exposure, viral hepatitis).

Hx: Medications (OTC, Rx, herbal), EtOH, IVDU, sexual partners/practices, tattoos, needle stick
injuries, transfusions, recent travel
Additional symptoms: jaundice, arthralgias, myalgias, rash, anorexia, weight loss, abdominal
pain, fever, pruritus, and changes in the urine and stool

2. In a patient with abnormal liver enzyme tests interpret the results to distinguish between
obstructive and hepatocellular causes for hepatitis as the subsequent investigation differs.

Obstructive picture: GGT and ALP elevated

Hepatocellular cause: AST and ALT increased
(EtOH = ratio of AST to ALT ratio of >=2:1 +/- 2-fold elevation in GGT)

3. In a patient where an obstructive pattern has been identified,

a) Promptly arrange for imaging,

Ultrasound, then CT if indicated

b) Refer for more definitive management in a timely manner.

Referral to surgery is cholecystitis (elevated WBC, RUQ pain, febrile)

Referral to oncology if cholangiocarcinoma (dx by CT)

4. In patients positive for Hepatitis B and/or C,

a) Assess their infectiousness,
If a person is Hep B antigen positive (particularly HBeAg) then they are infectious. HBsAg can
indicate an acute or chronic infection. The presence of HBeAg is associated with high levels of
HBV DNA and higher rates of transmission of HBV infection, which is why we predominantly

175
look at HBeAg to determine infectiousness.

from Uptodate

Hep C infectiousness depends on whether the patient has cleared the virus – so if there is
persistent HCV-RNA, then they are still infectious.

b) Determine human immunodeficiency virus status.

5. In patients who are Hepatitis C antibody positive determine those patients who are
chronically infected with Hepatitis C, because they are at greater risk for cirrhosis and
hepatocellular cancer.

80% people infected with Hep C won’t clear it.

Test for Anti-HCV Ab as initial screening test.
NB: Immunocompromised individuals, including those with HIV infection, patients on dialysis,
and transplant recipients, anti-HCV may not be detectable despite the presence of HCV infection.
Then test for HCV-RNA – if positive they have a chronic Hep C infection
If Anti-HCV Ab positive but HCV-RNA is negative, retest HCV-RNA in 6 months (there are a
high number of false negatives).

6. In patients who are chronically infected with Hepatitis C, refer for further assessment and
possible treatment.

Further treatment includes referral to specialist, liver biopsy – to determine genotype [genotype 1
is worst, then -4-3-2] and potential antiviral treatment.
No hepatotoxic meds
HIV and Hep B testing

7. In patients who are at risk for Hepatitis B and/or Hepatitis C exposure,

a) Counsel about harm reduction strategies, risk of other blood borne diseases,
b) Vaccinate accordingly.

Prevent Transmission = disclosure of carrier status and barrier protection for sex, not sharing
needles for IVDU or other drug paraphernalia, safe tattooing, no blood donation, don’t breastfeed
if cracked nipples, no shared razors, etc.
Health promotion = lose weight (especially if abdominal obesity), decrease EtOH intake (<2

176
drinks/week), stop smoking
Vaccination = Hepatitis A & B, annual influenza vaccine

8. Offer post-exposure prophylaxis to patients who are exposed or possibly exposed to Hepatitis
A or B.

In exposure with insufficient or unknown immunization history, give Hepatitis B

Immunoglobulin (HBIG) in less than 12 hours from exposure and start the regular vaccine (i.e. 0,
1, 6 months) schedule at the same time. HBIG must be given at a different site from the vaccine
so as not to diminish its effect. The same is true of neonates, and this is important, as 95% of
vertical transmission occurs in the perinatal period. There is also Hep A Ig, which is given once
only.

9. Periodically look for complications (e.g., cirrhosis, hepatocellular cancer) in patients with
chronic viral hepatitis, especially hepatitis C infection.

In cirrhosis, do an abdominal ultrasound for hepatocellular carcinoma every six months.

Monitor bloodwork – first sign can often be a decrease in platelets. Look at liver function INR,
albumin, as well as liver enzymes

Hyperlipidemia - Key Features

1. Screen appropriate patients for hyperlipidemia

Adults at any age with the following risk

Standard: Children:
factors:
Women ≥ 50 or post Evidence of FMHx -
Diabetes
menopausal atherosclerosis hypercholesterolemia
FMHx -
Men ≥ 40 Smoking Rheumatoid Arthritis
Chylomicronemia
HTN Systemic Lupus
minimum q 5 yrs for all Obesity (BMI >27) Psoriasis
FMHx: premature
HIV on HAART
CAD
Erectile dysfunction eGFR <60
Clinical signs (xanthelasmas, xanthomas, arcus
senilis/cornealis)

2. In all patients whose cardiovascular risk is being evaluated, include the assessment of lipid
status

Order a fasting (10-12h ideally with no alcohol for 24-48h) lipid profile on the people who fit into
the above categories. Include TC, HDL-C, triglycerides, fasting blood glucose. Also order TSH
(to uncover hypothyroid-induced hyperlipidemia) and ALT, AST, Cr, CK (for baseline, as you
will monitor these later if you start pharmacotherapy). Consider hs-CRP. No evidence that ApoB
is superior to other markers. “Despite an increasing number of new potential markers of risk, the

177
traditional CVD risk factors remain the priorities for screening and treatment as appropriate.” –
2009 CDN CVS guidelines

3. When hyperlipidemia is present, take an appropriate history, and examine and test the
patient for modifiable causes (e.g., alcohol abuse, thyroid disease)

Ask about all the risk factors listed in #1 above, and do tests listed in #2 above.
Assess: age (most important factor); family history of premature CVD (<60 years); obesity
(especially abdominal obesity); assess for metabolic syndrome [visceral adipose tissue mass (i.e.
toxic waist), dyslipidemia (elevated triglycerides and low HDL-C), elevated blood pressure and
elevated serum glucose – see Table 2 on page 2 of 2009 CDN CVS guidelines for more details];
level of cardiometabolic fitness; alcohol use (CAGE screen).

Consider tests for subclinical atherosclerosis:

- High sensitivity C-reactive protein (hs-CRP) (class I evidence for benefit of statin
therapy in those with intermediate risk Framingham score, and hs-CRP >2.0 mg/L)
- Anklebrachial index (class II, level C) - <0.90 = index for PVD, high likelihood of CVD
- Carotid ultrasound (class IIa, level C)
- Graded exercise testing (class IIa, level C)
- EKG (class IIb, level C)

4. Ensure that patients diagnosed with hyperlipidemia receive appropriate lifestyle and dietary
advice. Periodically reassess compliance with this advice (especially in patients at overall low
or moderate CV risk)

-Smoking cessation
-Diet (reduced saturated fats and refined sugars, low sodium, lots of fruits and vegetables;
for patients with hypertriglyceridemia reduce alcohol intake and increase omega-3 & -6
intake)
-Weight reduction and maintenance
-Exercise guidelines (with caveat that more is better for everyone):

Age 5 - 17 Adults Age >65

60 mins/day with 3 sessions >150 minutes/week, at least 10 Same as adults + exercise
vigorous activity/week, strengthen mins per session, strengthen bone to improve balance/prevent
bone and muscle 3 days/week and muscle 2 days/week falls

-Stress management

5. In treating hyperlipidemic patients, establish target lipid levels based on overall CV risk

Determine risk using the Framingham risk score (link provided below) modified for family
history (double the cardiovascular disease risk percentage if any cardiovascular disease is present
in a first-degree relative before 60 years of age). In men older than 50 years or women older than
60 years of age, of intermediate risk whose low-density lipoprotein cholesterol does not already
suggest treatment, high-sensitivity C-reactive protein can be used for risk stratification.

178
apoB Apolipoprotein B; CAD Coronary artery disease; FRS Framingham risk score; HDL-C
High-density lipoprotein cholesterol; hs-CRP Highsensitivity C-reactive protein; PVD Peripheral
vascular disease; RRS Reynolds Risk Score; TC Total cholesterol

Surprisingly, pharmacotherapy is NOT in the guidelines; see 2009 CDN CVS guidelines page 9
for summary, but basically most people do fine on statin monotherapy. Initiate Tx in all High
Risk pts, Moderate Risk patients with LDL >3.5 or TC/HDL >5, and in Low Risk patients with
LDL >5 or TC/HDL >6.

6. In patients receiving medication for hyperlipidemia, periodically assess compliance with and
side effects of treatment

Most lipid-lowering medications are well tolerated. Serum transaminases and creatine kinase
should be followed regularly (every 6 to 12 months) or when symptoms develop. Follow-up is
not required if levels are consistently normal and the patient has no symptoms.
Most common side effects for statins are:

-Mylagia (5%, though similar rates seen in placebo) – dull muscle ache worse with
exercise – diagnosis based on drug cessation and re-challenge.
-Myositis also involves muscle discomfort and CK >3x upper limit of normal.
-Rhabdomyolysis (rare <1:100 000) – severe muscle pain, acute renal failure,
myogolobinuria, CK >10000; stop statins and hospitalize for supportive care until stable.
-ALT >3 times upper limit of normal – usually dose related

179
 -CI in pregnancy

Most common side effects for niacin are:

-Increase in ALT (measure at baseline and at 1-3 months after starting niacin)
-Increase in serum glucose (check fasting glucose and HgbA1C q6-12 months, d/c if they
deteriorate)
-Check uric acid levels
-Flushing, itchy skin (Pg mediated, so take ASA first)

Most common side effects of fibrate-treated patients:

-Increase in plasma creatinine; start with low doses, re-evaluate kidney function ; Nx,
cramping
-Increases effect of warfarin (both fibrates & warfarin are albumin-bound)
-Increase gallstones risk (b/c increased cholesterol secretion in bile)

Hypertension - Key Features

1. Screen for hypertension

Check blood pressure in all patients over 18 yo at routine visits, and/or "all visits where
appropriate"

2. Use correct technique or equipment to measure blood pressure

Proper technique: patients should be seated quietly for at least 5 minutes in a chair (rather than on
an exam table), with feet on the floor, and arm supported at heart level. An appropriate-sized cuff
(cuff bladder encircling at least 80 percent of the arm) should be used to ensure accuracy. At least
two measurements should be made. SBP is the point at which the first of two or more sounds is
heard, and DBP is the point before the disappearance of sounds.

3. Make the diagnosis of hypertension only after multiple BP readings (ie. At different times
and during different visits)

Guidelines for diagnosis of hypertension (as per CHEP 2011)

CHEP 2011 provides excellent info describing how to diagnose HTN in multiple visits.

The bottom line: dx of HTN should be made on an average of at least 2 BP readings per visit
taken on 2 or more separate occasions. The timeframe to confirm HTN is controversial and
depends on the severity of HTN, presence of target organ damage, existing risk factors and
clinical findings at presentation.

Exclude and identify other causes of HTN: white coat HTN, drug induced, secondary causes
(including sleep apnea), anxiety disorders, ETOH intake, pregnancy

Classification of BP
Optimal SBP< 120 and/or DBP< 80

180
Normal SBP< 130 and/or DBP< 85
High Normal SBP 130-139 and/or DBP 85-89
Grade 1 HTN SBP 140-159 and/or DBP 90-99
Grade 2 HTN SBP 160-179 and/or DBP 100-109
Grade 3 HTN >= 180 and/or DBP >=110
Isolated systolic HTN SBP >= 140 and/or DBP<90

Optimal BP if Chronic Kidney Disease or DM is SBP < 130 and DBP < 80

4. In patients with established diagnosis of hypertension, assess and re-evaluate periodically

the overall cardiovascular risk and end-organ complications
a) take an appropriate history
b) do the appropriate physical exam
c) arrange appropriate laboratory investigations

History: Cardiovascular Risk Factors

Age>= 55, Male, Fhx of premature CVD (Men < 55, Women < 65), Sedentary lifestyle, Poor
diet, Obesity, Smoking, IGT or DM, Dyslipidemia, Stress, ethnicity (black african and black
carribean), familial hypercholesterolemai or other inherited dyslipidemia

• Ask about target end organ damage:

H/a? Visual changes? Altered LOC? Hematuria? Oligouria? Angina? Previous MI?
Previous revascularization? Previous CHF? Previous TIA? Previous stroke?
Claudication?
• Also consider asking about causes of secondary HTN, see below

Physical Exam:
Fundoscopy, Full cardiac exam (PMI for LVH, Renal bruits, Peripheral pulses, JVP, Peripheral
edema, Differing BP in each arm).

Routine Investigations:
CBC, Urinalysis, Fasting Glucose, Electrolytes, Urea, Creatinine, eGFR, Fasting Lipids, ECG
(assess for LVH or past MI)

Target Organ Damage Investigations:

Urinalysis, urine ACR (there are no good guidelines to suggest when you should do a urine ACR,
CHEP is not currently recommending it annually)

5. In appropriate patients with hypertension (eg. Young patients requiring multiple

medications, patients with an abdominal bruit, patients with hypokalemia in the absence of
diuretics) suspect secondary hypertension, investigate appropriately.

Causes of secondary HTN:

(this is a big topic i can't go into all of it here, but the big ones are sleep apnea, renovascular
disease, primary hyperaldosteronism and iatrogenic (drugs). Other less common are Cushings
(central obesity, moon facies, supraclavicular fat pads, humpback, OP, striae, psychological
changes) hyperthyroid, hypothyroid, hyperparathyroid (high calcium & high PTH)
pheochromocytoma, coarctation of the aorta (radio-femoral delay). (Drugs include OCP,
stimulants, MAOIs, SSRIs, licorice root!, EPO, NSAIDs, decongestants, anabolic steroids,
withdrawal of BBs or clonidine, Vanco, Carbamazepine, Levodopa, anticholinesterase eye drops)

181
-Suspect renovascular HTN if:

Sudden onset or worsening of HTN age >55 or <30 years, presence of abdo bruit, HTN
resistant to 3 txs, other atherosclerotic vascular disease, recurrent pulmonary edema
associated with hypertensive surges

-The following tests are recommended, when available to screen for renal vascular disease:

• captopril-enhanced radioisotope renal scan (this is recommended for those with GFRs
<60 mL/min)
• doppler sonography
• magnetic resonance angiography
• CT-angiography (for those with normal renal function)

-Hyperaldosteronism should be considered for patients with the following:

spontaneous hypokalemia (<3.5 mmol/L)

profound diurietic induced hypokalemia (<3.0 mmol/L)
hypertension refractory to treatment with 3 or more drugs
incidental adrenal adenomas

-Screening for hyperaldosteronism should include plasma aldosterone concentration (PAC) and
plasmin renin activity (PRA), aldosterone: renin ratio >25 suggestive or hyperaldosteronism
(PAC/PRA)

• aldosterone should be measured in morning samples

• (aldosterone antagonists, ARBs, beta blockers and clonidine should be discontinued
prior to testing)

-Consider pheo if paroxysmal and or severe sustained HTN refractory to usual antihypertesnive
therapy, HTN and symptoms suggestive of catecholamine excess (headaches, palpitations,
sweating etc)
Pheo HTN may be triggered by BBs, MAOIs, micturition or changes in abdo pressure
Think of multiple endocrine neoplasia (MEN 2A or 2B)
To test include 24 hour urine for metanephrines and catecholamines, assessmentof urinary VMA
is inadequate.
A normal pasma metanephrine level can be used to exclude pheochromoytoma in low risk
patients but the test is performed in few labs

-83% of refractory hypertensives have sleep apnea! Do sleep studies.

-Dexamethasone suppression test for Cushing’s syndrome

6. Suggest individualized lifestyle modifications to patients with HTN (eg. Weight loss,
exercise, limit alcohol comsumption, dietary changes)

182
• Recommend weight loss to BMI 18.5 - 24.9 kg/meter squared
• Recommend alcohol intake <2 drinks per day for men = 14 drinks per week, <1 drink per day
for women = 7 drinks per week
• Recommend waist circumference <102 cm for men, < 88 cm for women
• DIET: DASH diet (rich in fruits, veggies, low fat dairy, soluble fibre, whole grains, protein from
plant sources, reduced saturated fat and cholesterol
• Sodium intake --> the guidelines are getting more and more strict!!! <1500 mg sodium for
anyone 50 yo or less, 51-70 = <1300 mg, > yo = <1200 mg. Note sodium and 'salt' are not the
same thing, salt is NaCl, thus 5 grams of salt may only be 3 grams of sodium.

http://www.hypertension.ca/lifestyle-management

7. In a patient diagnosed with HTN, treat the HTN with appropriate pharmacologic therapy
(eg. Consider the patient's age, concomitant disorders, other CVD risk factors).

How do you choose the appropriate drugs?

The basics of this are that you should choose a drug based on other co-morbidities. Ie) diabetes or
microalbuminuria, use an ACEI/ARB.
If no comorbidities, choose a thiazide as first line (the ALLHAT trial showed thiazides are great,
cheap and work well when compared head to head with the others)
If BP is more than 20/10 ideal, it is considered acceptable to start with 2 drugs.
2/3 of patients will need 2 drugs to control their HTN, 2/3 of DM will need 3 drugs.

A good summary chart of what drugs to choose for certain comorbidities is found on the CHEP
website.

8. Given a patient with the signs and symptoms of hypertensive urgency or crisis, make the
diagnosis and treat promptly.

Hypertensive urgency – BP >=180/120 with NO symptoms except maybe some h/a

Hypertensive emergency – BP>=180/120 with symptoms (h/a, visual changes (retinal
hemorrhages/exudates, papilledema), malignant nephrosclerosis (hematuria, proteinuria, ARF),
cerebral edema, SAH, ICH (h/a, nausea, vomiting, altered LOC, seizures, coma)

Treat hypertensive crisis appropriately

Hypertensive Urgency – Usually BP is treated over hours to days. Can use oral agent to bring BP
down then start a long acting agent once BP is shown to have stabilized on the initial oral agent.
Clonidine, captoporil, hydralazine, nifedipine (used to be used a lot more, now is contraversial)

Hypertensive Emergency – Usually BP treated in 2 to 6 hours

Parenteral agents allow for better BP titration and for faster onset and are therefore used in this
situation (although there are a few oral meds that can be used if limited access to parenteral
medication).
Nitroprusside infusion at 0.25mcg/kg/minute
Nicardipine infusion at 5-15 mg/hour
Labetalol bolus of 20mg, followed by 20-80 mg boluses q 10 minutes to a maximum of 300mg.
Labetalol infusion 0.5-2mg/minute

9. In all patients diagnosed with HTN, assess response to treatment, medication compliance,
and side effects at follow up visits.

183
Adverse Effects
- CCBs - peripheral edema, headache, dizziness, flushing
- Beta blockers - fatigue, dizziness, syncope, weight gain, sexual dysfunction, negative
chronotropic effects, orthostatic drop
- ACEI - hyperkalemia, cough, angioedema, hypotension
- Thiazide diuretics - hypokalemia, hyponatremia

ASSESS COMPLIANCE AT EVERY VISIT! CHEP EMPHASIZES THIS!

Immigrants - Key Features

1. As part of the periodic health assessment of newly arrived immigrants:

a) Assess vaccination status (may not be up to date)
b) Provide the necessary vaccinations to update their status

All immigrants are required to undergo a medical examination before immigrating. These
medical examinations can be carried out in any country, but must be carried out by specific
doctors working “under the authority” of Health Canada. The exam includes physical exam and
vision screen, CXR (for TB), syphilis screen, urinalysis and HIV testing (age 15 and older).
These reports are not likely to be followed-up on except TB, syphilis and HIV. Reviewing and
updating immunizations is not included in this mandatory medical examination. These designated
doctors are not allowed to give patients the results of their tests (they are considered property of
the Canadian government). The applicant will only receive a letter if there is a problem with their
medical examination.

There is no official list of diseases that will make an applicant medically inadmissible. Each
applicant is considered individually particularly with respect to any disease or condition that 1) is
a danger to the health or safety of Canadians or 2) would cause excessive demand on the health
care system (i.e. dialysis) or social services.

Vaccination schedules for children not vaccinated in early infancy, children > 7 years of age and
adults can be found in the Canadian Immunization Guide at www.phac-aspc.gc.ca/publicat/cig-
gci/index.html. Many immigrants are susceptible to vaccine-preventable diseases upon arrival.
For example, 30-50% of new immigrants are susceptible to tetanus and 32-54% are susceptible to
measles, mumps or rubella. Recommendations and evidence for each vaccination for new
immigrants and refugees can be found in the Summary for evidence based recommendations for
immigrant and refugee health.

2. As part of the ongoing care of immigrants, modify your approach (when possible) as
required by their cultural context (i.e. history given only by husband, may refuse examination
by male physician, language barriers)

Other issues to consider when caring for immigrants and refugees:

• Previously limited screening for breast and cervical cancer (may not know what a pap test is and
require explanation of the procedure and purpose).

o All sexually active women should be screened by Papanicolaou test

184
• Mental and emotional issues:

o Loss of personal or cultural identity

o Separation from family – ask about family members remaining in home country
o Change in family roles and norms
o Isolation – especially in women who may not be able to access ESL as readily due to
child care responsibilities
o Uncertainty about community resources
o Unemployment or underemployment

• Diet changes – ask about diet since arriving in Canada, have they found grocery stores, counsel
about the prevalence of fatty/sugary foods available here and the need to maintain a healthy diet.
• Sex inequality and domestic violence – be alert for signs and symptoms of intimate partner
violence.
• Genital mutilation
• Contraception – screen immigrant women of reproductive age for unmet contraceptive needs.
Provide culturally sensitive patient-centered contraceptive counselling to decrease unintended
pregnancy and promote patient satisfaction

3. When dealing with a language barrier, make an effort to obtain the history with the help of a
medial interpreter and recognize the limitations of all interpreters (i.e. different agendas, lack
of medical knowledge, something to hide).

4. As part of the ongoing care of all immigrants (particularly those who appear not to be
coping):
a) Screen for depression (at higher risk and frequently isolated)
b) Inquire about a past history of abuse or torture
c) Assess patients for availability of resources for support (family, community organizations)

Depression – may need to ask specifically about sleep, concentration, worry and ‘nerves’ to begin
to assess depression. Also, multiple somatic complaints (stomach pain, body aches, headaches,
etc.) - once organic causes are ruled out - may be the presenting feature of an underlying
depression. Some cultures don’t easily have words or ways to describe their mental health.

PTSD – very common in refugees, must inquire sensitively.

• Be alert for signs and symptoms of PTSD – especially in the context of unexplained somatic
symptoms, sleep disorders, history of trauma.
• No evidence that routine screening for PTSD in well-functioning individuals results in more
harm than good, but should screen in those with any symptoms/complaints.
• But be alert and screen in patients not seeming to adjust well or with multiple clinic visits for
various somatic concerns.
• Hyperarousal symptoms:

o Sleep – is it hard to fall asleep, insomnia, awakening and nightmares, sleeping with
lights on, caffeine intake
o Startle response – how do loud noises or sirens affect you
o Memory and concentration, irritability and outbursts of anger – how is this affecting
you, relationships, work, ability to learn English.

• Intrusive recollection (and panic disorder)

185
 o Morbid rumination – how many hours a day do you read news from your home
country? Do you think all the time? What about?
o Nightmares and flashbacks
o Panic Disorder
o Somatization – frequent pains, headaches

• Avoidance and numbing

o Avoidance of triggers of bad memories, avoidance of people/isolation.

o Avoidance of feelings/restricted affect

5. In immigrants presenting with a new or ongoing medical condition, consider in the

differential diagnosis infectious disease acquired before immigration (e.g. malaria, parasitic
disease, TB)

Hepatitis B – 20-80% of immigrants who come from countries where chronic hepatitis B virus
infection is prevalent are not immune and have not been immunized. Immigrants from countries
with high prevalence of chronic hepatitis B (>2% HBsAg positive) should be screened and
treated to prevent hepatitis and HCC (i.e. from Africa, Asia, Eastern Europe and parts of South
America). Those susceptible (negative HBsAg, anti-HBc and anti-HBs) should be vaccinated.

Tuberculosis – Screen children, adolescents <20y and refugees between 20-50y from countries
with high TB incidence as soon as possible after arrival with tuberculin skin test. If tests are
positive rule out active TB and treat latent TB.

HIV – screen for HIV with informed consent all adolescents and adults from countries where HIV
prevalence is greater than 1% (sub-Saharan Africa, parts of Caribbean and Thailand).

Hep C – screen for antibody to HCV in all immigrants and refugees from regions with prevalence
of disease >3% (excludes South Asia, Western Europe, North America, Central America and
Sound America).

Intestinal parasites:

• Strongyloidiasis – screen refugees from Southeast Asia and Africa using serologic tests
(rather than stool tests). If positive treat with Ivermectin (first line) or albendazole (if
contraindications to Ivermectin)
• Schistosomiasis – Screen refugees from Africa with serologic tests for Schistosoma and
if positive treat with Praziquantel.

Malaria – do not routinely screen for malaria. Be alert for symptomatic malaria in migrants who
have lived or travelled in malaria-endemic regions in previous 3 months.

6. As part of the ongoing care of all immigrants, inquire about the use of alternative healers,
practices, and/or medications (e.g. natural or herbal medicines, spiritual healers, medications
from different countries, moxibustion).

186
Immunization - Key Features

1. Do not delay immunizations unnecessarily (e.g., vaccinate a child even if he or she has a
runny nose).

When to delay immunizations?

If patient has moderate to severe acute illness with or without fever.
For example, a cold is not a reason to delay immunization.

True contraindications to vaccination

1. Anaphylaxis upon administration of previous dose of a particular vaccine

2. Anaphylactic reaction or other serious reaction to a component of a vaccine (ex. Eggs,
thimerosal preservative)
3. Pregnant or immunocompromised should not receive live attenuated vaccines
4. Moderate to Severe acute illness
5. Avoid DPTp and Td if neurologic disease, uncontrolled epilepsy, encephalopathy
(current or within 7 days of administration of previous dose), or infantile spasms.

When to immunize?

1. In infancy
2. Before pregnancy
3. Before traveling
4. When new to the country if not previously immunized

2. With parents who are hesitant to vaccinate their children, explore the reasons, and counsel
them about the risks of deciding against routine immunization of their children.

Exploring fears and myths about immunizations

1. Side effects – Most common side effects are mild fever and sore extremity. Serious
reactions such as death, and encephalopathy are so rare that their incidence cannot be
calculated.
2. Autism – Concern regarding risk of vaccines causing autism. This was originally
associated with a preservative agent called thimerosal. The original paper in the Lancet
publishing this association was recently withdrawn and there have been no definitive
cases to support this claim. The only vaccines in Canada that are given to children and
contain thimerosal are the multidose influenza vaccine and Hepatitis B. Both these
vaccinations are available in formulations that do not contain thimerosal (ex. Vaxigrip for
children and pregnant mothers). The only true contraindication to thimerosal is
anaphylaxis.
3. Vaccines don’t work – No vaccine is entirely effective. If a vaccine-preventable
disease outbreak does occur, some vaccinated individuals will contract the disease.
However the proportion of unvaccinated individuals who contract the disease will be
much higher than the proportion of vaccinated individuals.

187
 4. Vaccine-preventable diseases no longer exist in Canada – Certainly some vaccine-
preventable diseases are rarely, if ever, seen in Canada and herd immunity for
unvaccinated individuals does occur. However, unvaccinated individuals may still be
exposed in their lifetime given the immigrant population that may not have been
vaccinated or if the unvaccinated chooses to travel later in life.

Why to immunize yourself or your child?

1. To protect yourself from common (HiB, Influenza, Varicella) or serious (Tetanus,

Hepatitis, Meningococcemia) preventable infectious diseases.
2. To protect individuals in society who are unable to receive vaccinations for true
contraindications from common or serious preventable infectious diseases.

3. Identify patients who will specifically benefit from immunization

Special Vaccinations

1. Age > 65 – yearly influenza vaccine and once-in-a-lifetime pneumococcal vaccine.

2. Age < 65 with a high-risk medical condition likely to result in severe consequence of
getting preventable illness – yearly influenza vaccine and once-in-a-lifetime
pneumococcal vaccine.
3. HPV – quadravalent vaccine against HPV strains. Currently indicated for girls and
women age 9 to 26. Not covered.. 3 doses 0,2,6 months required.
4. Varicella – routinely administered to children now, but consider vaccinating adults
who are susceptible.
5 Zoster - given to 50 years and older SC in upper arm single dose –contraindicated in
pregnancy ,active TB and HIV with CD4 less than 200
6. Palivizamab – to prevent RSV in children born at < 32 weeks gestational age who will
be younger than 6 months during RSV season and for children < 2 years of age with BPD
who required oxygen in the 6 months before the RSV season (Nov – Apr).
7. BCG – given to all children in some provinces (ex. NWT).
8. Hep A vaccine - 2 doses 4-6 months a part .immunoglobulin can be given to
immunocompromised children for short term prophylaxis.
9 quadrivalent meningococcal vaccine - protects from C,A,W-135 and Y.tp patients with
a splenia,Hajj travelers,lab. Workers and military recruits.
10. Rotavirus(RotaTeq) - protect from gastroenteritis 3 doses given at age 6-12 weeks not
covered.
11. Rabies - inactivated given IM only deltoid, 0,3,7,14 Ds with immunoglobulin day 0
post exposure to animal bite.

4. Clearly document immunizations given to your patients.

5. In patients presenting with a suspected infectious disease, assess immunization status, as the
differential diagnosis and consequent treatment in unvaccinated patients is different.

188
6. In patients presenting with a suspected infectious disease, do not assume that a history of
vaccination has provided protection against disease (e.g., pertussis, rubella, diseases acquired
while travelling).

Immunizations to avoid in pregnancy

1. MMR
2. Varicella
3. BCG (bacilli Calmette-Guerin vaccine)
4. Smallpox
5. Zoster

Immunizations with either unknown safety in pregnancy or to avoid unless benefit outweighs the
risk

1. Yellow fever
2. Typhoid
3. Meningococcal
4. Japanese encephalitis
5. BCG
6. Anthrax
7. Polio
8. Pneumococcal
9. HPV
10. Hepatitis A

Administration of the vaccine

Less than 1 year =anterolateral thigh
After 1 year =deltoid muscle
If 2 live attenuated vaccines – give at same visit simultaneously or 28 a part

National Guidelines for Childhood Immunization Practices

(Explanations of each [ http://www.phac-aspc.gc.ca/im/is-cv/index-eng.php#a immunization
guideline] found on above website)

1. Immunization services should be readily available.

2. There should be no barriers or unnecessary prerequisites to the receipt of vaccines.
3. Providers should use all clinical encounters to screen for needed vaccines and, when
indicated, vaccinate children.
4. Providers should educate parents in general terms about immunization.
5. Providers should inform parents in specific terms about the risk and benefits of
vaccines their child is to receive.
6. Providers should recommend deferral or withholding of vaccines for true
contraindications only.
7. Providers should administer all vaccine doses for which a child is eligible at the time
of each visit.
8. Providers should ensure that all vaccinations are accurately and completely recorded.

189
 9. Providers should maintain easily retrievable summaries of the vaccination records to
facilitate age-appropriate vaccination.
10. Providers should report clinically significant adverse events following vaccination –
promptly, accurately, and completely.
11. Providers should report all cases of vaccine-preventable disease as required under
provincial and territorial legislation.
12. Providers should adhere to appropriate procedures for vaccine management.
13. Providers should maintain up-to-date, easily retrievable protocols at all locations
where vaccinations are administered.
14. Providers should be properly trained and maintain ongoing education regarding
current immunization recommendations.
15. Providers should operate a tracking system (to generate reminders of upcoming
vaccinations).
16. Audits should be conducted in all immunization clinics to assess the quality of
immunization records and assess immunization coverage levels.

**Please note that travel vaccinations have not been addressed in this document.

Copies of the standard immunization schedule and the schedule to follow in individuals not
immunized in infancy can be found at www.phac-aspc.gc.ca/im/is-cv/index-eng.php#a

Infections - Key Features

1. In patients with a suspected infection,

a) Determine the correct tools (e.g., swabs, culture/transport medium), techniques, and
protocols for cultures,
b) Culture when appropriate (e.g., throat swabs/sore throat guidelines).

Swabs/cultures:
1) Throat

a. Main objective in diagnosis is to rule out Group A Strep (GAS)

b. Clinical Decision Criteria (Centor Criteria):
i. Tonsillar Exudates
ii. Tender anterior cervical adenopathy
iii. Fever by history
iv. Absence of cough
Absence of 3/4 above criteria has negative predictive value of 80%
c. Throat culture specimen obtained by vigorous scrubbing of both tonsils and posterior
pharynx. Over 90% sensitive and specific with proper technique.
d. Advise lab if N. gonorrhea is suspected (different plating method)
e. Rapid test lacks sensitivity but if + is diagnostic, provides a “same visit result”. ELISA
technique used.
f. Consider serology for EBV mononucleosis with persisting symptoms and systemic
involvement

2) Urine

190
 a. No need to culture in symptomatic young women if uncomplicated UTI suspected w/
obvious sx of dysuria and frequency and pyuria on urinalysis.
b. Culture in young women if complicated infection, atypical sx, failed therapy,
recurrence < 1mo post treatment.
c. A dipstick positive test (nitrites and/or leuks with blood) is a reliable indicator of
significant bacteriuria but a negative test does not r/o bacteriuria. If sxs indicate, send for
culture.
d. Nitrite positive indicates presence of Enterobacteriaceae (e.g. gram negative rods such
as E.Coli or Klebsiella)
e. Keep urine sample in fridge if not sending to lab immediately.
f. Culture in ALL children, pregnant women, elderly and men. In men, consider ddx of
prostatitis.

3) LP

a. Suspected CNS infection, subarachnoid hemorrhage, other weird things (NPH,

tuberculosis, CNS vasculitis etc)
b. No absolute contraindications but relative include: overlying infection, suspected
epidural abscess, thrombocytopenia, raised ICP - must do head CT before proceeding!

4) Skin

a. Cultures now should be routine for abscess drainage due to prevalence of MRSA, only
swab pus from abscess, not wound.
b. Patients with abscess >5cm, multiple lesions, extensive surrounding cellulitis,
immunosuppresion, systemic signs of infection or lack of response to I&D suggested to
use antibiotics.

5) Sputum

a. No role in acute bronchitis in otherwise healthy individuals

b. Also no role in initial diagnosis of acute exacerbations of COPD
c. While a positive blood or pleural fluid culture definitively identifies the pathogen, an
organism growing from a respiratory specimen is not definitive proof that it is the
etiologic agent. Many bacterial species are normal flora or colonizers of the respiratory
tract, and although present in respiratory secretions, they may not be responsible for the
clinical illness in an individual patient with pneumonia due to another cause.
d. May play important role in aiding diagnosis of inpatient illness because bronchoscopy
samples more reliable at isolating organisms.

6) Eye

a. Cultures are not necessary for the initial diagnosis and therapy of conjunctivitis, except
in neonates
b. The exception is patients with symptoms of hyperacute conjunctivitis at risk for
Neisseria gonorrhoeae.

191
7) Stool

a. Indications for stool culture include:

- diarrhea after possible pathogen exposure (e.g. recent travel)
- prolonged diarrhea (>5 days)
- diarrhea containing blood or mucous
- abdominal pain, cramping, nausea, vomiting, fever
- diarrhea with recent antibiotic therapy (C. difficile toxin test)

Enteric Bacterial Pathogens (send for stool C&S)

• Campylobacter jejuni
• Salmonella spp.
• Verotoxin producing E. coli (e.g., E. coli O157:H7)
• Shigella spp.
• Aeromonas spp. (toxin producing strains)
• Clostridium difficile
• Yersinia enterocolitica
• Pleisiomonas shigelloides

Enteric Protozoan Pathogens (send for stool O&P)

• Giardia lamblia (intestinalis)

• Cryptosporidium spp.
• Entamoeba histolytica
• Dientamoeba fragilis
• Microsporidium spp.
• Blastocystis hominis
• Cyclospora spp.
• Isospora belli

Enteric Viral Pathogens (usually reserved for pediatrics patients)

• Adenovirus 40/41
• Rotavirus
• Caliciviruses
• Astroviruses
• Norwalk virus

Vaginal swabs covered in Vaginitis Key Feature

2. When considering treatment of an infection with an antibiotic, do so

a) Judiciously (e.g., delayed treatment in otitis media, with comorbid illness in acute
bronchitis),

192
b) Rationally (e.g., cost, guidelines, comorbidity, local resistance patterns).

For one of those handy charts for antibiotic spectra, here’s a massive one:
http://drugtopics.modernmedicine.com/drugtopics/data/articlestandard//drugtopics/
362005/177776/article.pdf

List of Reportable Diseases (Consistent with National Guidelines but Toronto’s is up to date for
2011) www.toronto.ca/health/cdc/communicable_disease_surveillance/monitoring/pdf/
reportablediseases.pdf

Otitis Media
Further otitis media information in Earache Key Feature
From CPS Guideline 2009
-Watchful waiting appropriate for children older than 6 months of age without severe symptoms
(appear toxic, severe otalgia and/or high fever (greater than 39C orally))
-Parents must be capable of recognizing signs of worsening illness and be willing and able to
readily access medical care.

First-line therapy for child with no beta-lactam allergery = amoxicillin 75-90 mg/kg/day
For allergic, consider macrolide (clarithromycin, azithromycin)
5 days as effective as 10 days in children older than two years of age with uncomplicated AOM.

Acute Bronchitis
- Self-limiting inflammation of the bronchi due to upper airway infection - present with cough
and sputum production for 1-3 weeks.
- One of the most common conditions associated with antibiotic misuse
- Most commonly caused by virus (influenza A and B, parainfluenza, coronavirus, rhinovirus,
RS, metapneumonvirus) but still 60-90% of patients presenting with cough + sputum are given
anbx!
- Cough disappears by day 14 in 75% of patients with acute viral bronchitis.
- Suspect Pertussis (even adults) with cough lasting longer than two weeks (partial immunity
from prior immunizations) and send NPS swab.
- Sputum purulence does not signify bacterial infection
- If febrile, get CXR to r/o pneumonia
- DDx includes:

a. Chronic Bronchitis - cough + sputum for 3 months, 2 years in a row

b. Pneumonia
c. Postnasal drip
d. GERD
e. Asthma

Treat with antibiotics if:

1. At high risk of serious complications because of preexisting comorbidity (heart, lung,

renal, liver, neuromuscular disease, or immunosuppression)
2. Patients over 65 years of age with acute cough and two or more of the following, or
patients over 80 years of age with one or more of the following:
- Admission to hospital in the previous year
- Type 1 or type 2 diabetes

193
 - History of congestive heart failure
- Current use of oral glucocorticoids

Common Antibiotics in Primary Care and their Estimated Cost to Patient for a 10 day Rx
(Rx Files 8th edition - 2010)

From least to most expensive:

Pen- V - $10
Metronidazole (Flagyl) - $11
Cotrimoxazole (Septra) DS - $10-12 for both peds and adult suspensions and tabs
Amoxicillin - $15 for peds suspensions, $17-27 for adult capsules
Azithromycin (Zithromax) - $21 for peds suspensions, $28 for adult tabs
Nitrofurantoin (Macrobid) - $23
Cephalexin (Keflex) - $25 for both peds and adult suspensions and tabs
Cefixime (Suprax) - $26 for peds suspensions, $49 for adult tabs
Minocycline (Minocin) - $31
Ciprofloxacin - $43
Clarithromycin (Biaxin) - $37-67 for adult tabs
Clindamycin (Dalacin) - $50
Moxifloxacin (Avelox) - $74

3. Treat infections empirically when appropriate (e.g., in life threatening sepsis without culture
report or confirmed diagnosis, candida vaginitis post-antibiotic use).

Rationale for antibiotic treatment with Group A strep pharyngitis:

1. To prevent post streptococcal sequelae — anbx treatment can reduce incidence of

acute rheumatic fever by 75%. No firm evidence to suggest that antibiotic therapy
reduces incidence of poststreptococcal glomerulonephritis.
2. To prevent suppurative complications —Peritonsillar abscess, sinusitis, and
retropharyngeal abscess. Peritonsillar abscess typically occurs in adolescents and young
adults. Retropharyngeal abscess occurs most commonly in the first few years of life and
sinusitis is a very rare complication of GAS pharyngitis.
3. To reduce symptoms — There is a modest (approximately one day) reduction in
symptoms with early antibiotic treatment. A meta-analysis found that throat soreness and
fever was reduced by about one-half at day three for patients treated with antibiotics,
compared to those given placebo. For patients with GAS and severe symptoms (≥3
Centor criteria), symptoms resolved 2.5 days earlier with antibiotic therapy in one
randomized trial.
4. To prevent transmission — While this is important in pediatrics, due to extensive
exposures, it is considered far less important in adults.

Sepsis briefly:
SIRS Criteria:

194
 - Temp less than 36°C or greater than 38°C
- HR greater than 90 bpm
- RR greater than 20 or PaCO2 less than 32mmHg
- WBC less than 4 or greater than 12, or presence of 10% bands

1. Sepsis = SIRS + probable source

2. Severe Sepsis = above plus evidence of end organ dysfunction (renal failure, hypotension,
altered MS, ARDS, mottling etc
3. Septic Shock = above + MAP < 60 without pressers

Identify source: CXR, Urine, Blood Cultures x 2, sputum (usually if intubated); if sx indicate can
order: throat swab, LP, wound/fluid culture, stool culture.

Time to abx < 1 hr, choices include Vanco +:

a) cephalosporin 3rd or 4th gen

b) Beta-lactam/beta-lactamase inhibitor (pip/taz, ticar/clav)
c) Carbapenem (imi/mero)
d) If pseudomonas suspected then 2 antipseudomonals used.

Use Early Goal Directed Therapy:

1. ABCs, if necessary intubate

2. ++ fluid boluses, til CVP 8-12, ScvO2 > 70%, urine o/p >0.5cc/kg/hr - crystalloid (NS,
RL preferred as initial fluid therapy)
3. Pressors to MAP > 60, start with norepinephrine, then vasopressin
4. transfusion to HCT >0.3
5. Additional therapies: activated protein C, corticosteroids, insulin therapy etc

4. Look for infection as a possible cause in a patient with an ill-defined problem (e.g.,
confusion in the elderly, failure to thrive, unexplained pain [necrotizing fasciitis, abdominal
pain in children with pneumonia]).

5. When a patient returns after an original diagnosis of a simple infection and is deteriorating
or not responding to treatment, think about and look for more complex infection. (i.e., When a
patient returns complaining they are not getting better, don’t assume the infection is just slow
to resolve).

6. When treating infections with antibiotics use other therapies when appropriate (e.g.,
aggressive fluid resuscitation in septic shock, incision and drainage of abscess, pain relief).

Infertility - Key Features

1. When a patient consults you with concerns about difficulties becoming pregnant:
a) Take an appropriate history (e.g., ask how long they have been trying, assess menstrual
history, determine coital frequency and timing) before providing reassurance or investigating

195
further.
b) Ensure follow-up at an appropriate time (e.g., after one to two years of trying; in general, do
not investigate infertility too early).

Definition:
Inability to conceive after 12 months of intercourse without contraception.

History:
Remember to interview and investigate both the male and the female.
Age? Is it primary or secondary infertility? How often are they having intercourse? How long
have they been trying? Form of birth control before trying to conceive? Erectile dysfunction?
Ejaculation problems? Menstrual history (menarche, regularity, length of cycle, moliminal
symptoms, endometriosis?) Past medical history (Uterine surgery, Pelvic surgery, STIs, PID,
previous ectopic, previous tubo-ovarian abscess?) Intrauterine DES exposure? Symptoms of
PCOS? Hyperprolactinemia? Hypo or Hyperthyroidism? Family history of infertility, birth
defects, or mental retardation? Social history (smoking, EtOH, drugs, occupation, exercise).

2. In patients with fertility concerns, provide advice that accurately describes the likelihood of
fertility.

Epidemiology:
50% of women conceive in 3 months, 72% in 6 months and 85% in 12 months.
Male infertility 23% (other sources state closer to 50%)
Ovulatory dysfunction 18%
Tubal damage 14%
Endometriosis 9%
Coital problems 5%
Cervical factors 3%
Unexplained 28%
Likelihood of not conceiving in 12 months if couple is normally fertile is 7%

3. With older couples who have fertility concerns, refer earlier for investigation and treatment,
as their likelihood of infertility is higher.

If the woman is older than 35, start investigations and referral after 6 months of trying to
conceive. (SOGC 2011 Guidelines on Advanced Reproductive Age and Infertility).

4. When choosing to investigate primary or secondary infertility, ensure that both partners are
assessed.

Investigations
1) Is it male infertility?

Semen analysis with respect to concentration (>48x106/mL), motility (>63%) and

morphology (>12%). Should be collected after 2-7 days of abstinence, and submitted to
lab within one hour of collection.

2) Is the woman ovulating?

196
 -Regular periods with moliminal symptoms (breast tenderness, ovulatory pain, bloating)
implies ovulation.
-Serum progesterone level one week before expected menses (ie: day 21 of 28 day cycle)
-Basal body temperature [T increases by .5 to 1.0 degree F (0.25 to 0.5 degrees Celsius)
in luteal phase secondary to progesterone production by corpus luteum].
-Urinary testing (detects LH surge which occurs 38 hours before ovulation).
-Day 3 FSH level to test ovarian reserve (women with a reduced pool of follicles provide
insufficient inhibition of FSH secretion, so FSH inappropriately rises early in cycle).

3) If she is ovulating…

Consider luteal phase defect in which the corpus luteum does not adequately produce
progesterone or the progesterone has a diminished effect on the endometrium or the
endometrium lacks integrin adhesion molecule.
Endometrial biopsy to determine adequacy of luteal phase hormones on the endometrium
(done 10 days after ovulation).

4) If she is not ovulating…

TSH, prolactin, FSH, LH, progesterone, estradiol, free testosterone. looking for thyroid
issues, hyperprolactinemia, PCOS, ovarian failure.

5) Is it her uterus?

Hysterosalpingogram to examine for uterine fibroids, polyps, synechia, or other

anomalies
Hysteroscopy if hysterosalpingography demonstrates uterine concern.

5) Is it her tubes?

Hysterosalpingography to examine for obstruction as initial test (sometimes therapeutic

as well as diagnostic)
Consider laparoscopy as initial test if history of PID, intrabdominal infection,
endometriosis, previous surgery.

6) Is it the cervix?

Post-coital test to examine interaction between sperm and mucus. Done 1-3 days before
ovulation. Sample of mucus taken 2-12 hours post-coitus to look for >5cm spinnbarkeit
and >5 motile sperm/hpf. Some debate as to usefulness of this test.

WHO Classification of Anovulation

I - Hypogonadotropic hypogonadal anovulation (problem with FSH/LH therefore no ovarian
response)
II - Normogonadotropic normoestrogenic anovulation (no good reason for an ovulation)
III - Hypergonadotropic hypoestrogenic anovulation (ovaries not responding)

197
5. In couples who are likely infertile, discuss adoption when the time is right. (Remember that
adoption often takes a long time)

Treatment of Infertility

Lifestyle modifications – Gain or lose weight, smoking cessation, decrease ETOH and
caffeine intake, increase frequency of coitus.
Adoption – Must find appropriate time to discuss this.
Azoospermia or Oligospermia – Donor sperm
Uterus – Surgery (leiomyomas). Surrogacy (synechia/septa or congenital anomalies).
Laparoscopic cautery (endometriosis).
Cervix – Consider intrauterine implantation of sperm or IVF to bypass cervix.
Tubes – Hysterosalpingography (flush the tubes). Surgery [tubal reconstruction,
adhesiolysis, salpingectomy (for hydrosalpinges that may secrete embryotoxic
substance)]. Consider IVF.
Anovulation – Class II anovulation responds to treatment.
Medication - Clomiphene or other SERMs (to stimulate ovulation), Metformin +/-
clomiphene (PCOS), Gonadotropins (to stimulate ovulation in non-PCOS), Dopamine
(hyperprolactinemia).
Surgery – Wedge resection or drilling of ovary (PCOS).
IVF +/- oocyte donation

6. In evaluating female patients with fertility concerns and menstrual abnormalities, look for
specific signs and symptoms of certain conditions (e.g., polycystic ovarian syndrome,
hyperprolactinemia, thyroid disease) to direct further investigations (e.g., prolactin, thyroid-
stimulating hormone, and luteal phase progesterone testing).

PCOS signs and symptoms: Amenorrhea/oligomenorrhea, obesity (often, but not always),
hirsutism, acne, infertility, and bilaterally enlarged polycystic ovaries.
Family hx: 40% of sisters and 20% of mothers of affected women with PCOS also have it

Hyperprolactinemia signs and symptoms: Galactorrhea, amenorrhea. If resulting from pituitary

tumour, may experience headaches, visual disturbances.

Hypothyroid signs and symptoms: fatigue, weight gain, cold intolerance, constipation, myalgia,
oligomenorrhea or menorrhagia, anemia

Hyperthyroid signs and symptoms: anxiety, tremor, palpitations, weight loss, heat intolerance,
increased appetite, oligomenorrhea or amenorrhea

Insomnia - Key Features

1. In patients presenting with sleep complaints, take a careful history to:

- distinguish insomnia from other sleep-related complaints that require more specific treatment
(e.g., sleep apnea or other sleep disorders, including periodic limb movements, restless legs
syndrome, sleepwalking, or sleep talking).
- assess the contribution of drugs (prescription, over-the- counter-, recreational), caffeine, and
alcohol.

198
- make a sspecific psychiatric diagnosis if one is present.

2. When assessing patients with sleep complaints, obtain a collateral history from the bed
partner, if possible.

3. In all patients with insomnia, provide advice about sleep hygiene (e.g., limiting caffeine,
limiting naps, restricting bedroom activities to sleep and sex, using an alarm clock to get up at
the same time each day).

4. In appropriate patients with insomnia, use hypnotic medication judiciously (e.g., prescribe it
when there is a severe impact on function, but do not prescribe it without a clear indication).

Definition
Insomnia is a symptom, not a disease. Insomnia describes inadequate quality and/or quantity of
sleep that results in difficulty in daytime functioning. Can be transient/short term (< 3 weeks) or
chronic (> 3 weeks).

Epidemiology
One-third of adults will experience insomnia in their lifetime. Persistent insomnia occurs in 10%
of the population. The incidence increases with age and it is more common in women. There is
increased incidence in lower socioeconomic class, divorced, widowed, separated individuals and
increased with recent stress, ETOH abuse, drug abuse and depression.

1. Acute Insomnia: Duration of 4 weeks or less.

2. Chronic Insomnia: Duration of 4 weeks or more.
3. Primary Sleep Disorder: A primary or intrinsic sleep disorder is one that arises out of the
physiological processes of sleep.
4. Secondary Insomnia: Secondary insomnia refers to difficulty initiating and/ or maintaining
sleep that occurs as a result of or co-morbidly in conjunction with a medical, psychiatric or
psychological process.
5. Primary Insomnia: A disorder of somatized tension and learned sleep preventing associations
that results in a complaint of insomnia and consequent daytime impairment.
6. Daytime Impairment: The daytime consequences of insomnia include dysphoric states such as
irritability, impaired cognition such as poor concentration and memory, and daytime fatigue.

Criteria
One of:

Difficulty initiating sleep (initial insomnia)

Difficulty maintaining sleep (middle insomnia)
Waking too early
Feeling of insufficient or non-restorative sleep

Occurs despite adequate opportunity and circumstance for sleep

Impaired daytime function

Etiology of Transient Insomnia

1. Change in environment
2. Jet lag

199
 3. Shift work
4. Excessive noise
5. Uncomfortable room temperature
6. Stressful events
7. Acute medical or surgical illness
8. Stimulant medications

Sleep history Remember to take history from both patient and patient’s bed partner.
Onset, frequency, duration, severity, alleviating/aggravating factors.
Drug use, ETOH use, Medications, PMH (pain issues, neurological disorders), psychiatric
history, depression screening, snoring, irregular breathing, limb movement or jerking, talking in
sleep, nightmares, sleepwalking.
Consider having patient complete a sleep log for 2 weeks. Record bedtime, time to falling asleep,
number of times up in the night, rising time, how rested they felt, number of naps etc…

Investigations
Polysomnography, Actigraphy, Multiple Sleep Latency Test, Neuroimaging-mostly unnecessary.

Red Flags
- Major depressive episode
- Generalized anxiety or panic disorder
- Excessive daytime sleepiness (unexpected or irresistible sleepiness) resulting in imminent risk
to the patient and/or society
- Substance abuse

Risk Factors
Age: Older age
Gender: females are 1.2 to 1.5 times more likely to report insomnia than males.
Socioeconomic Status: Unemployed people and those with less education are at higher risk for
insomnia.
Other: People who are separated or divorced, the medically ill and those with depression, anxiety,
or substance abuse problems are also reported to have a higher prevalence of insomnia
relationship between insomnia, major depression, generalized anxiety disorder and substance
abuse

Primary Sleep Disorders

-Obstructive sleep apnea/sleep disordered breathing; common symptoms of sleep apnea are loud
snoring, choking or gasping episodes during sleep, and excessive daytime sleepiness that the
patient may attribute to poor sleep.
- Movement disorders in sleep- Periodic limb movements in sleep (PLMS)
- Restless legs syndrome- Periodic leg movement disorder commonly coexists with restless legs
syndrome. Iron deficiency, renal failure, pregnancy, and SSRI antidepressants are commonly
associated with restless legs syndrome.
- Circadian rhythm disorders- Delayed and advanced sleep phase, shift work sleep disorder and
jet lag are the most common circadian rhythm sleep disorders.

200
Secondary/Co-morbid Insomnia
• Psychiatric Disorders,
• Medical disorders

- Chronic Pain Syndromes

- Menopause
- Gastroesophageal Reflux and Peptic Ulcer Disease
- COPD/Asthma
- Benign Prostatic Hyperplasia

• Medications

- Nicotine, nicotine patches

- Caffeine, caffeine containing medications (e.g. Anacin)
- Antidepressants (SSRIs, SNRIs, bupropion, opiates)
- Corticosteroids
- Central nervous system stimulants and related drugs
· dextroamphetamine
· methylphenidate
· atomoxetine
- Bronchodilators
- Pseudoephedrine

• Alcohol

Treatment

Non-pharmacologic
Non-pharmacologic therapies are effective in the management of primary insomnia
especially when behavioural and cognitive techniques are used in combination.
Behavioural techniques include sleep hygiene, sleep consolidation, stimulus control, and
relaxation therapies. Cognitive techniques include cognitive behavioural therapy (CBT).

Behavioural Therapies
Sleep hygiene
Avoid caffeine after lunch and alcohol within 6 hours of bedtime
• Avoid nicotine close to bedtime or during the night
• Engage in moderate physical activity but avoid heavy exercise within 3 hours of
bedtime
• Avoid consuming excessive liquids or a heavy evening meal before bedtime
• Maintain a quiet, dark, safe, and comfortable sleep environment. Minimize noise and
light
• Avoid a bedroom that is too hot or too cold
• Avoid watching/checking the clock

Sleep consolidation

201
 Devise a “sleep prescription” with the patient: a fixed bedtime and wake time
• Determine the average total sleep time
• Prescribe the time in bed to current total sleep time plus 30 minutes
• The minimum sleep time should be no less than 5 hours.
• Set a consistent wake time (firmly fixed 7 days/week)
• The bed time is determined by counting backwards from the fixed wake time (For
example: a patient estimates the total sleep time to be 5-6 hours/night, the total time in
bed is 8 hours/night for a sleep efficiency of 5.5/8 = 68%. The prescribed total sleep time
would be 6.5-7 hours/night, if the wake time is 6AM then the prescribed bedtime is 11-
11:30 PM)
• For the first 2-4 weeks these times should remain consistent and the clinician should
monitor the patients adherence to the program with sleep logs (see sleep log attachment)
• Advise the patient that napping will reduce the depth and restorative quality of sleep the
following night
• Once the patient is sleeping for >85 to 90 percent of the time spent in bed for two
consecutive weeks, then the amount of time spent in bed is slowly increased by 15- 30
minute every week. If sleep efficiency of 90 percent is maintained, then therapy is
successful.

The average total sleep time for most people is between 6 and 8 hours a night.

Stimulus control
• Eliminate non-sleep activities in the bedroom. Remove the TV and computer from the
bedroom
• Use the bed and bedroom only for sleep and sex
• Go to bed only when sleepy, even if later than prescribed sleep schedule
• Get out of bed if not able to sleep within 15-20 minutes - go to another room and relax.
Return to bed only when sleepy
• Set alarm for agreed upon wake time
• Avoid excessive napping during the day - a brief nap (15-30 minutes) during the
midafternoon can be refreshing and is unlikely to disrupt nocturnal sleep

Anxiety Reducing Strategies and Relaxation therapies

• Avoid arousing activities before bed (late night phone calls, work, watching TV
• Designate at least one hour before bedtime to help unwind from the day’s stresses – dim
light exposure and engage in relaxing activities
• Relaxation techniques such as deep breathing, light exercise, stretching, yoga and
relaxation CDs can help promote sleep
• Stress management skills training and relaxation therapies such as progressive muscle
relaxation, biofeedback, hypnosis, meditation, imagery training, are usually provided by a
trained professional (through books, videos, or face-to-face sessions)
• Techniques for managing worry can be useful for some patients. This may include
keeping a worry journal, scheduling worry time, challenging worried thinking, or seeking
professional help

Pharmacotherapy Principles of Treatment

202
 Pharmacotherapy is generally recommended at the lowest effective dose as short-term
treatment lasting less than 7 days
1st line- Zopiclone 3.75-7.5 mg
2nd line- Trazodone 25-50 mg
Variable evidence- L’Tryptophan, valerian, melatonin

Ischemic Heart Disease - Key Features

1. Given a specific clinical scenario in the office or emergency setting, diagnose presentations
of ischemic heart disease (IHD) that are:
- classic
- atypical (e.g., in women, those with diabetes, the young, those at no risk).

IHD refers to a variable degrees of myocardial ischemia from an imbalance between oxygen
supply and demand resulting from narrowing of vessels. In stable angina, predictably exertion
and emotional changes where demand increases or eating where supply decreases lead to
presentation of angina symptoms. Once the increased demand is mitigated by stopping activity or
an increase in supply is provided by nitrates, symptoms resolve. Classically patients will
complain of retrosternal chest pain, discomfort, tightness, pressure, squeezing, or fullness which
may radiate into the arms, neck, jaw, shoulder or back and associated with nausea, fatigue, SOB,
sweating, or dizziness. Others, particularly women, diabetics, elderly, those with dementia,
hypercholesterolemia and no family history of heart disease, may present with atypical symptoms.
Atypical symptoms are those that are not typical, can be sharp chest pain, may only be associated
symptoms or discomfort not located in the chest (i.e., arms, epigastrium, shoulder, neck). In one
study, 65% of women presented with atypical symptoms. Elderly, obese, and diabetics also
present with atypical symptoms at higher frequencies.

2. In a patient with modifiable risk factors for ischemic heart disease (e.g., smoking, diabetes
control, obesity), develop a plan in collaboration with the patient to reduce her or his risk of
developing the disease.

203
Modifiable risk factors for IHD include obesity, smoking, hyperlipidemia, diabetes, poor
glycemic control, hypertension/ uncontrolled HTN and sedentary lifestyle. Plan patients about
their risk and assessment of RF as above to calculate a Framingham score. Early diagnosis and
treatment of HTN and diabetes is highly beneficial. Effect of blood lipid control in primary
prevention remains controversial, especially as it pertains to women and the elderly.

Smoking cessation: Educate, evaluate , medical interventions. Refer to QuitNow.

Physical activity: Give Rx, 30min OD at intensity no sing but talk, 15min resistance 3/wk.
Weight reduction: BMI below 27 is recommended Weight loss.
Dietary recommendations: fish, fruits, fiber, fresh vegetables, low-fat

3. In a patient presenting with symptoms suggestive of ischemic heart disease but in whom the
diagnosis may not be obvious, do not eliminate the diagnosis solely because of tests with limited
specificity and sensitivity (e.g., electrocardiography, exercise stress testing, normal enzyme
results).

In majority of cases, dx of IHD can be made on Hx and Px but objective test should be used to
add or subtract from the pretest probability. Testing should begin with calculation of pretest
probability of disease, and then appropriate test designated.

ECG- minimal diagnostic value

Resting ECG must be done on all patients but it has no utility for ruling out IHD. However, a
previous MI, LBBB, PRWP, T wave changes, or axis deviation may add to pretest probability but
by no means is it diagnostic. ECG during pain episodes may however show ST changes
supporting IHD diagnosis. Also presence of BBB or WPW disqualifies patients for stress ECG
testing.

204
Stress ECG testing- ideal for patients with intermediate pretest probability.
Sensitivity for IHD is 68% and specificity is 77%, therefore not ideal for ruling out disease. In
patients with high pretest probability this is not ideal diagnostic choice since high false negative
may lead to ignoring of the clinical findings. However, this test may be done for prognostication.
Angiography is warranted if there is severe stable angina with a high pre-test probability of
disease In low probability group, controversy remains. A negative test decreases the probability
but a positive test will then require further testing.


The sensitivity and specificity of non-invasive stress ECG is even poorer in women. However, no
consensus on whether directly advancing to imaging techniques with higher sensitivity and
specificity exists.If contraindications to stress ECG or dx still in doubt, exercise echo or MIBI
which provide higher sensitivity and specificity should be undertaken.

4. In a patient with stable ischemic heart disease manage changes in symptoms with self-
initiated adjustment of medication (e.g., nitroglycerin) and appropriate physician contact (e.g.,
office visits, phone calls, emergency department visits), depending on the nature an severity of
symptoms.

All patients should be given sublingual or spray NTG or chewable nifedipine and instructed in its
use. Anginal discomfort that lasts >2 or 3 minutes should prompt the patient to discontinue the
activity or remove himself or herself from the stressful event. If pain does not subside
immediately, the patient should be instructed to take NTG. If the first tablet or spray does not
provide relief within 5 minutes, then a second dose, at 5-minute intervals, should be taken. Pain
that lasts >15 to 20 minutes or persistent pain despite 2 NTG doses should prompt the patient to
seek immediate medical attention by calling 9-1-1 and going to the nearest hospital ED,

205
preferably by ambulance or the quickest available alternative. If the pattern of anginal symptoms
changes (eg, pain that is more frequent or severe, is precipitated by less effort, or now occurs at
rest), the patient should contact his or her physician to determine the need for additional treatment
or testing.

5. In the regular follow-up care of patients with established ischemic heart disease, specifically
verify the following to detect complications and suboptimal control:
- symptom control.
- medication adherence.
- impact on daily activities.
- lifestyle modification.
- clinical screening (i.e., symptoms and signs of complications).

6. In a person with diagnosed acute coronary syndrome (e.g., cardiogenic shock, arrhythmia,
pulmonary edema, acute myocardial infarction, unstable angina), manage the condition in an
appropriate and timely manner.

Patients presenting with prolonged (> 10 minutes) acute chest pain suggestive of ACS require a
history and physical examination. If a patient presents in a physician’s office or walk-in clinic
and no alternative cause can be found with certainty, referral of the patient to the Emergency
Department (ED) for further evaluation and observation is essential. If a previous
electrocardiogram (ECG) is available, send it with the patientAdmit and immediately treat
patients with a history and ECG (without ST segment elevation) compatible with ischemia, plus
either elevated cardiac biomarkers (>99th percentile) or hemodynamic compromise (hypotension
or electrical instability), for acute myocardial ischemia or patients with new ST segment elevation
or new LBBB and a history compatible with ACS, with the intent of re-establishing perfusion.

Management of patients with possible ACS

It is recommended that patients with a compatible history and a non-diagnostic initial ECG and
cardiac biomarkers, be observed in the ED and be re-assessed at six or more hours after the initial
testing with an ECG and cardiac biomarkers and exam for hemodynamic changes.For low-risk
patients without an obvious alternative explanation for the chest pain an out-patient stress test
within 72 hours and out- patient physician follow-up is recommended. For Intermediate-risk
patients a stress test prior to discharge is recommended.

Joint Disorder - Key Features

1. In a patient presenting with joint pain, distinguish benign from serious pathology (i.e.
sarcoma, septic joint):
(a) by taking pertinent history
(b) investigating in a timely and appropriate manner (i.e. aspirate, blood work, Xray).

• History: OPQRST, course, characteristics of joint involvement (pain, swelling, loss of function
of joint), pattern of joint involvement (symmetrical? Mono vs poly vs non-articular? Axial vs
peripheral), extra-articular features (skin, eyes, lungs, pulmonary, GI, psychiatric), ADL
limitations, general health (including fever, infection, family hx, constitutional symptoms, sexual
history), treatments attempted

• Investigations:
-BLOODWORK: CBC, BUN, Cr, acute phase reactants (ESR, complement C3 and C4,

206
fibrinogen, CRP, ferritin, albumin); serology: autoantibodies (RF present in 80% of RA/50% of
Sjogren’s; ANA present in 98% of SLE; anti-ds DNA in 50-70% of SLE; c-ANCA present in
>90% of Wegener’s;
-URINALYSIS to detect disease complications (active sediment, proteinuria)
-SYNOVIAL FLUID ANALYSIS: 3 C’s: cell count and differential; culture and gram stain
(bacterial, mycobacteria, fungal); crystal examination
-RADIOLOGY: plain film for bone pathology; CT for SI joints/ankle joints/spinal canal; MRI for
tendons/bursae/ligaments; US for tendons/bursae/effusions

2. In a patient presenting with non-specific MSK pain, make a specific rheumatologic

diagnosis when one is evident through hx, phys, and investigations (i.e. gout, fibromyalgia,
monoarthropathy vs. polyarthropathy). (note: chart contains key words/phrases, and is not
comprehensive)

Disease History Physical Investigations

-Acute attacks of
mono or oligo -Joint aspirate: >90%
-Red, swollen, tender joint
arthritis (esp. knee, aspirates show monosodium
ankle, 1st MTP); urate crystals (negative
Gout subside within days -Joint mobility may be limited birefringence)
(if cellulitis, joint mobility
preserved)
-Males >45yrs old; -punched-out/’holes in
-Tophi
EtOH and dietary bones’ on xray
excess
-Chronic (at least 3
mos), diffuse pain
with characteristic -Laboratory exams normal
-11/18 tender points with 4kg
tender points
force
Fibromyalgia -Workup includes TSH,
-F>M; ages 25-45 ESR, laboratory sleep
-Joint examination normal
-Ass’d with fatigue, assessment
hyperalgesia,
paresthesias
-Insidious onset,
gradually
progressive, -CBC, ESR normal
-Joint line tenderness
intermittent flare-ups
-RF, ANA negative
-Bony enlargement at affected
-Signs and -Synovial fluid=non-
joints (Bouchard’s=osteophytes
symptoms localized inflammatory
OA at PIP; Heberden’s= at DIP)
to affected joints (not -Xray: asymmetric joint
-1st CMC involved
systemic) space narrowing,
-Limited ROM; crepitus on
-Joint pain with subchondral sclerosis,
passive ROM
motion; relieved intraosseous cysts,
-Mild inflammation, if any
with rest; <1/2hr osteophytes
stiffness after
immobility
RA -Symmetrical joint -Joint effusions -Positive serology: RF+ in
involvement; 80%
polyarthritis (3 or

207
 more joints) for -Tenosynovitis
-Increased ESR in 50-60%
>6wks -Nodules
-Platelets increased
-Deformities: Boutonniere, swan
-Hgb and WBC decreased
neck, claw toe, hammer toe,
-Morning stiffness -Synovial fluid:
mallet toe, flexion contractures,
>30min, improving leukocytosis
ulnar deviation of MCP, radial
with use -Xray: demineralization,
deviation of wrist
-Constitutional sx symmetric joint space
-Bone-on-bone crepitus
i.e. myalgia, wt loss narrowing, erosions of
-No 1st CMC involvement
subchondral bone
-Rheumatoid nodules
-ANA+ in 98%
-Multisystemic
-Anti-DS DNA+ in 50-70%
-Anti-SM+ in 30%
-Photosensitivity,
-Decreased C3, C4
Raynaud’s, CNS -Malar rash, alopecia, cardiac
-Synovial fluid: mild
SLE symptoms and pulmonary serositis,
inflammation if +ANA
(headache, seizures, oral/nasal ulcers
-Urinalysis: proteinuria,
psychosis,
cellular casts
neuropathy)
-Xray:
->1hr AM stiffness
non-destructive/nonerosive;
may have osteoporosis
-Mid and low back
-Xray: SI joint =
stiffness
‘pseudowidening’ of joint
-Restricted ROM (decreased
due to erosion with joint
-Pain at rest Schober test)
sclerosis; late change =
-Persistent buttock bony fusion
Ankylosing
pain -Decreased chest wall expansion
Spondylitis
-Painful SI joint
-MRI/CT can detect
-Asymmetric large -Acute anterior uveitis
inflammation if no changes
joint peripheral -Aortic regurg, pericarditis
on xray and clinically
arthritis, mostly
suspect Ank Spond
lower limb

DDx Monoarthropathy: infectious, inflammatory, crystal-induced (gout/CPPD), hemarthrosis,

neoplasm, degenerative
DDx Polyarthropathy: infectious (lyme disease, viral ie. EBV/parvo, bacterial endocarditis,
septicemia, gonococcus), post-infectious (rheumatic fever, reactive arthritis, enteric infections) ,
inflammatory (seropositive/seronegative)

3. In a patient presenting with a monoarthropathy, rule out infectious causes (i.e. STDs).

• N. Gonorrheae accounts for 75% of septic arthritis in young sexually active adults; S. aureus:
all ages; Gram negatives: affect immunocompromised pts; S. Pneumonia: children; H. influenzae:
infants, esp if not immunized
• Investigations: blood and urine cultures; if high index of suspicion for gonococcal infection,
also C&S of endocervical/urethral/rectal/oropharyngeal; synovial fluid for CBC and diff, gram
stain, culture, crystals

208
4. In pts presenting with MSK pain, include referred and visceral sources of pain in the
differential dx (i.e. angina, slipped capital epiphysis presenting as knee pain, neuropathic
pain).

• especially in children and elderly people, examine and consider imaging the HIP when
presentation includes medial knee pain

5. Clinically diagnose ligamentous injuries. DO NOT do an Xray examination.

6. In a patient presenting with joint pain, include systemic conditions in the differential (i.e.
Wegener’s granulomatosis, lupus, ulcerative colitis).

• Also consider SLE, antiphospholipid syndrome, scleroderma, Sjogren’s, polyarteritis nodosa,

inflammatory bowel disease

7. In patients with a diagnosed rheumatologic condition:

a) actively inquire about pre-existing co-morbid conditions that may modify the treatment plan
b) choose the appropriate treatment plan (i.e. no NSAIDS in patients with renal failure or
peptic ulcer disease)

• Considerations in addition to the above: renal impairment, liver disease, EtOH abuse, allergies,
use of warfarin or anticoagulants, pregnancy

8. In assessing patients with a diagnosed rheumatologic condition, search for disease-related

complications (i.e. iritis)

• Review of systems key; do ENT, lungs, cardiac, pulmonary, GI, GU, neurologic, psychiatric
screening

9. In patients experiencing MSK pain:

a) actively inquire about the impact of the pain on daily life
b) treat with appropriate doses of analgesics
c) arrange for community resources and aids (cane/splints) if necessary.

• Analgesics for OA:

-Acetaminophen 4g/day, NSAIDS (oral and topical), cox-2 inhibitors, tramadol

-Corticosteroids: intra-articular injections
-intra-articular hyaluronic acid, capsaicin cream, glucosamine sulfate/chondroitin

• Arthritis Society excellent resource

10. In patients with RA, start treatment with DMARDs within an appropriate time interval.

• Early intervention has greatest impact on outcome. Analgesics, NSAIDs, and steroids do not
alter the course of RA; however, they should be used for symptomatic relief. Consider early
referral to rheumatologist.
• In mild and early disease: DMARDs for all patients whose disease does not remit after 2 to 3
months with use of NSAIDs alone. First lines: hydroxychloroquine (200mg BID, adjusted if
weight <61kg) or sulfasalazine (1000mg BID to TID). If after 6mos suboptimal, then consider

209
other DMARDs
• Moderate to severe disease: Immediate treatment with DMARDs. Consider methotrexate or
leflunomide; consider combination therapy; consider Remicade or Eternacept.
• DMARDs have a delayed onset of action (8-12wks)

Guidelines/Treatment for Specific Entities

1) Osteoarthritis
Diagnosis: Clinical, as per above chart
Management:
Non-pharmacologic: Patient education, Self-management programs (e.g., Arthritis
Foundation Self-Management Program), Weight loss (if overweight), Aerobic exercise
programs especially water-based, acupuncture, Physical therapy, Range-of-motion
exercises, Muscle-strengthening exercises, Assistive devices for ambulation, Patellar
taping, Appropriate footwear, Lateral-wedged insoles (for genu varum), Bracing,
Occupational therapy, Joint protection (ie. hip protectors) and energy conservation,
Assistive devices for activities of daily living
Pharmacologic: see item #9 above
Guidelines: BC Guidelines http://www.bcguidelines.ca/guideline_osteoarthritis.html

2) Rheumatoid Arthritis
Diagnostic Criteria: RA diagnosed if 4 or more of the following 7 criteria present
(American Rheumatism Association, 1987)
1. Morning stiffness Joint stiffness>1hour for >6 weeks
2. Arthritis of three or more joint areas At least 3active joints for >6 weeks; commonly
involved joints are PIp, MCp, wrist. elbow, knee, ankle, MTP
3. Arthritis of hand joints At least one active joint in wrist, MCP or PIP for >6 weeks
4. Symmetric arthritis Bilateral involvement of PIp, MCp, or MTP for >6 weeks
5. Rheumatoid nodules Subcutaneous nodules over bony prominences, extensor surfaces
or in juxta·articular regions
6. Serum RF Found in 60-80% of RA patients
7. Radiographic changes Erosions or periarticular osteopenia, likely to see earliest
changes at ulnar styloid, 2nd and 3rd MCP and PIP joints
Management: early stages with hydroxychloroquine/sulfasalazine; mod-severe:
methotrexate, leflunomide, azathioprine, gold; severe: anti-TNF drugs, cyclosporine
-if confident of diagnosis, do baseline bloodwork (CBC, liver/renal Ix, screen Hep B,
Hep C, HIV) and start sulfasalazine + MTX (provided patient not pregnant and doesn’t
have other contraindications), add prednisone while awaiting specialist consult for severe
symptoms
-need to do CXR to monitor for latent TB if starting anti-TNF drugs (if fail
MTX/leflunomide/etc.)
-surgery for multiple DMARD failure, intractable pain, structural joint damage (can
include joint replacement, fusion; surgery truly a last resort in RA patients)
Guidelines: http://www.bcguidelines.ca/guideline_ra.html;
http://rheum.ca/en/publications/treatment_recommendations_for_ra

210
3) Gout
Management of acute attack: NSAIDs plus/minus colchicine 0.6mg po up to tid (as
tolerated by GI side effects). If can’t tolerate NSAIDS (ie. renal failure/GI ulcer), can
substitute oral steroid for NSAID.
Long term Management (prevention of recurrence): if repeated attacks, measure serum
uric acid and, if elevated, Rx Allopurinol (or new uric acid-lowering drug Febuxostat).
Combine first 3-6 months of uric acid-lowering med (allopurinol/febuxostat) with
colchicine 0.6mg po od and then d/c colchicine. (Colchicine prevents recurrences while
on initial months of uric acid-lowering drug.)
Guidelines: Laubsher T, Dumont Z, Regier L, Jensen B. Taking the stress out of
managing gout. Canadian Family Physician 2009;55(12): 1209-1212.

4) SLE
Diagnostic Criteria: Diagnostic Criteria of SLE: 4 or more of 11 must be present serially
or simultaneously (American College of Rheumatology, 1997 update)
Clinical (7 criteria)
Malar rash - Classic "butterfly rash; sparing of nasolabial folds, no scarring
Discoid rash – May cause scarring due to invasion of basement membrane
Photosensitivity - Skin rash in reaction to sunlight
Oral/nasal ulcers - Usually painless
Arthritis - Symmetric, involving <2 small or large peripheral joints, non-erosive
Serositis - Pleuritis or pericarditis
Neurologic disorder - Seizures or psychosis
Laboratory (4 criteria)
Renal disorder - Proteinuria 1>0,5 g/day or 3+; cellular casts (RBC, Hb, granular,
tubular, mixed)
Hematologic disorder- Hemolytic anemia, leukopenia, lymphopenia, thromboctyopenia
Immunologic disorder - Anti-dsDNA Ab, anti-Sm Ab, Antiphospholipid antibodies based
on the finding of serum anticardiolipin Ab, lupus anticoagulant, or false positive VDRL
Antinuclear antibody lANA) Most sensitive test (98%)
Management: treatment directed at symptoms ie. NSAIDs for arthritis, topical steroids
for rash, high dose oral/IV steroids for serositis/nephritis, hydroxychloroquine for
MSK/derm involvement; MTX/anti-TNF drugs, cyclophosphamide for severe organ
involvement
-avoid sulfonamides, estrogens (can exacerbate symptoms); smoking cessation
Guidelines: none available
5) Ankylosing Spondylitis
Diagnosis: see above chart
Management: NSAIDS, exercises → opioids if needed → anti-TNF-alpha drugs or
sulfasalzine (only DMARD of use in ank spond)
Guidelines: none available

6) Fibromyalgia
Diagnostic Criteria (2):
(1) 3 months widespread pain (ie. pain in both sides of the body; pain above and below
the waist; axial skeletal pain such as cervical spine, anterior chest, thoracic spine or low
back) and
(2) pain in 11/18 tender points
Management:

211
 Non pharmacologic: Physical therapy, exercise and fitness program, stress-relief methods
(including massage/relaxation techniques), cognitive behavioural therapy, well-balanced
diet, avoid caffeine, sleep hygiene, acupressure/acupuncture
Pharmacologic: antidepressent esp SNRI (duloxetine), anticonvulsants (ie.
gabapentin/pregabalin), muscle relaxants, NSAIDs, sleep aids
Guidelines: http://fm-cfs.ca/resources-p.html

Lacerations - Key Features

1. When managing a laceration, identify those that are more complicated and may require
special skills for repair (e.g., a second- versus third-degree perineal tear, lip or eyelid
lacerations involving margins, arterial lacerations).

2. When managing a laceration, look for complications (e.g., flexor tendon lacerations, open
fractures, bites to hands or face, neurovascular injury, foreign bodies) requiring more than
simple suturing.

3. Given a deep or contaminated laceration, thoroughly clean with copious irrigation and
debride when appropriate, before closing.

4. Identify wounds at high risk of infection (e.g., puncture wounds, some bites, some
contaminated wounds), and do not close them.

Generally, do not close:

• Crush injuries
• Puncture wounds
• Bites involving the hands and feet
• Wounds more than 12 hours old (24 hours old on face)
• Cat or human bites, except those to the face
• Bite wounds in compromised hosts (eg, immunocompromised, absent spleen or splenic
dysfunction, venous stasis, diabetes mellitus [adults])

Similarly, consider antibiotic prophylaxis in the following cases:

• Animal bite wounds at high risk for infection
• Deep puncture wounds, especially cat bites
• Moderate to severe wounds with associated crush injury
• Wounds in areas of underlying venous and/or lymphatic compromise
• Wounds on the hand(s) or in close proximity to a bone or joint
• Wounds requiring surgical repair
• Wounds in immunocompromised hosts

5. When repairing lacerations in children, ensure appropriate analgesia (e.g., topical

anesthesia) and/or sedation (e.g., procedural sedation) to avoid physical restraints.

6. When repairing a laceration, allow for and take adequate time to use techniques that will
achieve good cosmetic results (e.g., layer closure, revision if necessary, use of regional rather
than local anesthesia).

7. In treating a patient with a laceration:

a) Ask about immunization status for tetanus.

212
b) Immunize the patient appropriately.

Source: Up to date

Learning - Key Features

Patients:
1. As part of ongoing care of children, ask parents about their children’s functioning in school
to identify learning difficulties.

• Often presents with parental concerns, usually when the child fails to achieve academic
milestones alongside his/her peers (report cards, etc)
• Can be first identified by teachers who initiate referrals to special education teams or for formal
psychometric testing and diagnosis
• Early identification = better outcomes, therefore ask routinely about child’s performance in
school
• Consider a learning disorder with any of the following concerns: academic, behavioral,
attention, or social interaction problems
• Have a low threshold for considering a learning disorder in children at risk, which includes:

o Family history of learning disorders

o Poverty
o Understimulating environment
o Premature
o Developmental or mental health disorders (ADHD, autism, anxiety, depression, etc)
o Neurologic disorders (seizures, neurofibromatosis, Tourette syndrome)
o Chromosomal disorders (Fragile X, Turner, etc)
o Chronic medical conditions (diabetes, etc)
o Traumatic brain injury
o CNS infection or radiation

2. In children with school problems, take a thorough history to assist in making a specific
diagnosis of the problem (eg mental health problem, learning disability, hearing)

• Evaluation requires complete history and physical to identify potential medical, neurologic
and/or behavioral conditions that may be related to the learning disorder

213
• Ask about education and learning (general questions about functioning in school)
• Ask about onset of the problem, whether it is improving or worsening, factors that improve or
aggravate the problem
• Ask about hearing, vision, motor skills, attention and task completion skills, language skills,
social skills
• Ask about school attendance
• Ask about developmental milestones, especially language
• Formal diagnosis requires psychometric testing (administered by psychologist or educator)

Note: lab work is not usually necessary, and physical examination is often normal

3. When caring for a child with a learning disability, regularly assess the impact of the
learning disability on the child and the family.

• Self-explanatory: use FIFE when interviewing

o Feelings
o Ideas
o Function
o Expectations

4. When caring for a child with a learning disability, ensure the patient and family have access
to available community resources to assist them.

• Will vary based on community, but are often available through the school system
• Some online resources include:

o www.kidsource.com/kidsource/content3/ada.idea.html (Provides information and

advice about LD and ADHD for parents, teachers, and other professionals)
o www.fape.org (Provides information and advocacy for children with special needs)
o www.cps.ca (Canadian Pediatric Society: online general information)

5. To maximize the patient’s understanding and management of their condition,

a) Determine their willingness to receive information
b) Match the complexity and amount of information provided with the patient’s ability to
understand.

• Self-explanatory: use SPIKES for sharing bad news

o SETTING up the interview,

o Assessing the patient’s PERCEPTION
o Obtaining the patient’s INVITATION,
o Giving KNOWLEDGE
o Addressing the patient’s EMOTIONS with EMPATHIC responses

Self-Learning:
6. Continuously assess your learning needs.

214
7. Effectively address your learning needs.
8. Incorporate your new knowledge into your practice.

Lifestyle - Key Features

1. In the ongoing care of patients, ask about behaviours that, if changed, can improve health
(diet, exercise, alcohol use, substance use, safer sex and injury prevention (e.g., seatbelts and
helmets).

• Canadian Task force for preventive health care recommends routine screening of the following
during periodic health exams of men and women:

o Good Evidence: smoking cessation; nicotine replacement therapy; fall prevention;

brushing/flossing teeth; fluoride (in toothpaste or supplemental); hearing protection;
noise control/ hearing protection.
o Fair Evidence: nutritional counseling, esp fruits and leafy greens (consider dietician
referral if high risk); regular moderate physical activity; avoid sun exposure; safe sex
practices; decrease alcohol consumption; seat belts.

2. Before making recommendations about lifestyle modification, explore a patient’s readiness

to change, as it may alter advice.

• Stages of change model:

o Pre contemplation goal is to get patient thinking about change

"What would have to happen for you to know that this is a problem?"
"What warning signs would let you know that this is a problem?"
"Have you tried to change in the past?"
o Contemplation goal is to examine benefits and barriers to change
"Why do you want to change at this time?"
"What are the barriers today that keep you from change?"
"What might help you with that aspect?"
"What things (people, programs and behaviours) have helped in the past?"
o Preparation = ask about successes and failures
Identify and assist in problem solving re: obstacles
Help patient identify social support
Encourage small initial steps
o Action = lots of praise
Focus on restructuring cues and social support
Bolster self-efficacy for dealing with obstacles
Combat feelings of loss and reiterate long-term benefits
o Maintenance
Plan for follow-up support
Reinforce internal rewards
Discuss coping with relapse

215
3. Explore a person’s context (i.e. poverty) before making recommendations about lifestyle
modification (i.e. healthy eating choices, exercise suggestions) so as to avoid making
recommendations incompatible with the patient’s context.

• In addition, be aware of various social programs available in your community – many

communities have programs that subsidize physical activity programs for adults and youth, or
provide nutritional support

4. In the ongoing care of patients, periodically review their behaviours, recognizing these may
change.

5. In the ongoing care of a patient, regularly reinforce advice about lifestyle modification,
whether or not the patient has instituted a change in behaviour.

Nutritional counseling:

- decrease fat and increase fiber

- if at increased risk consider referral to a clinical nutritionist
- calcium 1000-1500 mg/d (three or more servings of dairy, consider supplementation)
- Vit D (400-1000 IU if low risk, >50 1000 IU)

Exercise:

- moderate intensity for accumulated time of at least 30 min most days of the week

Obesity counseling:

- In Canada, 36% of adults are overweight, and 23% are in one of the obese categories
- Behaviour modification techniques, CBT, activity enhancement and dietary counseling
are effective
- Reduce calorie intake by 500-1000 kcal/day
- Initiate 30 min of moderate intensity exercise 3-5 x per week
- Increase exercise to more then 60 min on most days with endurance training
- Target weight loss of 5-10% of body weight or 0.5-1 kg/wk for 6 months

Smoking Counseling (A evidence):

- effective to reduce the proportion of smokers

- offer nicotine replacement or other smoking cessation meds (BC new Smoking
cessation program offers free smoking cessation meds and nicotine replacement to all
residents for up to 12 consecutive weeks each year).

Alcohol counseling and screening for problem drinking:

- Q1. Do you sometimes drink beer, wine or other alcoholic beverages?

- Q2 How many times in the past year have you had?

* At-risk drinking: Men - 5 or more drinks on one or more days in the last year, Women - 4 or
more drinks on one or more days in the last year.

216
 - CAGE questions, counseling on problem drinking, support program referral.
- Research has shown brief counseling results in a 40-50 % decrease in alcohol
consumption, 42% drop in ER visits, 55% decrease in MVAs.

Loss of Consciousness - Key Features

1. In an unconscious patient, assess ABC’s and resuscitate as needed.

2 As part of the assessment of a patient who has lost consciousness, obtain focused history
from the patient or witnesses that would include duration, trauma, preexisting conditions,
drugs, toxins, medications and seizure activity.

3 Examine unconscious patients for localizing and diagnostic signs (e.g., ketone smell, liver
flap, focal neurologic signs).

4 In patients with a loss of consciousness and a history of head trauma, rule out intracranial
bleeding.

5 In patients with a loss of consciousness who are anticoagulated, rule out intracranial
bleeding.

6 Assess and treat unconscious patients urgently for reversible conditions (e.g., shock, hypoxia,
hypoglycemia, hyperglycemia, and narcotic overdose).

7 When following up patients who have lost consciousness, assess and advise regarding return
to work, sporting, driving and recreational activities to minimize the possibility of injury to self
or others in the event of a recurrence.

8 In patients who have had a loss of consciousness without a clear diagnosis, pursue
investigations (e.g., rule out transient arythmia, seizure).

9 When following up patients who have lost consciousness and where there is potential for
recurrent episodes, discuss specific preventive and protective measures (e.g., position changes
with orthostatic pressure changes).

10 In patients with loss of consciousness following head trauma, treat and follow up according
to current concussion guidelines.

11 Advise authorities about appropriate patients with loss of consciousness (e.g., regarding
driving status).

1. Initial Assessment:

Airway - place prone, assess for trauma, breath sounds, place O2 and intubate as needed
(GCS < 8)
Breathing - equal breath sounds, SpO2
Circulation - general appearance, warmth, pulses, get ECG leads in place, assess for
arrythmias/shockable rhythm, get 2 X large bore IV access

217
Coma Cocktail (Empiric mgmt): IV Bolus: D50W 50 cc, thiamine 100 mg, narcan 0.2-0.4 mg

2. Differential dx
Most cases of stupor and coma presenting to an emergency department are due to trauma,
cerebrovascular disease, intoxications, and metabolic derangements (UTD)

Structural: trauma, bleed, clot, fat emboli, vasculitis, MS (very long list of other differential),
Cardiac (arrythmia) can be included in this category

ASK: hx of trauma, onset of symptoms (ie, abrupt R/O SA hemorrhage), preceding symptoms (ie,
visual change suggests ischemia in posterior circulation)

Non-structural:

Drugs: Sedatives, Barbiturates, Other hypnotics, Tranquilizers, Bromides, Alcohol,

Opiates, Paraldehyde, Salicylate, Psychotropics, Anticholinergics, Amphetamines,
Lithium, Phencylidine Monoamine oxidase inhibitors

Toxins: Lead, Thallium, Mushrooms, Cyanide, Methanol, Ethylene glycol, Carbon

monoxide
ASK: Medication use, compliance, substance history, access to substances, ability to use
meds appropriately,

Infection: Bacterial meningitis Viral encephalitis Postinfectious encephalomyelitis

Syphilis Sepsis Typhoid fever Malaria
ASK: prodromal illness, fever, neck stiffness, travel, sick contacts, headache

218
 Metabolic: Hypoxia Hypercapnia Hypernatremia* Hypoglycemia* Hypergylcemic
nonketotic coma Diabetic ketoacidosis Lactic acidosis Hypercalcemia Hypocalcemia
Hypermagnesemia Hyperthermia Hypothermia Reye's encephalopathy Aminoacidemia
Wernicke's encephalopathy Porphyria Hepatic encephalopathy* Uremia Dialysis
encephalopathy Addisonian crisis Hypothyroidism

Psychiatric: Catatonia, pseudo-seizure

Other: seizure with post-ictal period, non-convulsive status epilepticus, hypotension

**Consider also for ddx: Neuro vs Non-neuro**

3. Physical Exam
Vitals, pupil size & reactivity (usually spared in metabolic coma) EOM, fundi, corneal reflexes,
motor reflexes, respiratory patterns. Waxing and waning LOC typical of metabolic coma

Infection: fever, meningismus, septic signs

Herniation: hypertension with bradycardia

Resp: hyperventilation often due to metabolic acidosis (methanol, salicylates, DKA, uremia,
lactic) or resp alkalosis (sepsis, hepatic failure, heart failure)

Cheyne-Stokes respirations (a pattern of periodic waxing then waning hyperpnea, followed by

brief apnea) may occur with either impaired cardiac output or bicerebral dysfunction, and also in
elderly patients during sleep.

Toxidromes:
TCA overdose: hypotension, tachycardia, wide QRS, anticholinergic SE’s.
benzos overdose: *unlikely to alter VS unless co-ingestion* usually CNS changes with N vitals
anticholinergic: red, hot, dry, CNS disturbed, vis disturbance
amphetamine: *more likely agitated than obtunded* tachycardia, hypertension, agitation
opioid: decreased resp rate, pinpoint pupils

4. Investigations
BW: CBC, lytes, BS, Bun, Creat, lactate, LFTs, ABGs, cultures, Ca, Albumin, INR, PTT,
capillary bld sugar, drug screen (based on clinical setting)
ECG, CT head (see below), consider LP based on findings
*For trauma/post concussion see Canadian CT Head Rules *

5. Treatment
Sepsis: Early fluids, empiric antibiotics, locate source

Overdose treatments:

hypoglycemia: 1 amp D50W, may need IV D5W infusion following

219
 hyperglycemia: fluids followed by insulin (see DKA protocols)
benzos: flumazenil
acetaminophen: NAC (use normogram to assess need)
TCA: sodium bicarb infusion (for widened QRS), vasopressors if necessary following
Opiate: naloxone (Narcan) 0.2-0.4 mg to start- titrate with clinical benefit- watch for
withdrawal
beta blocker or Ca channel blocker: calcium and glucagon

CNS infection: get LP first if possible, however if IV empiric indicated: IV ceftriaxone

Head Trauma: elevate head of bed (20-30 degrees, helps increase venous outflow and decrease
ICP, hyperventilate, prevent hypotension (fluids), blood type & screen
Consider C-spine injury and C-spine precautions!

6. Follow up
Head Trauma: See www.thinkfirst.ca

Concussion assessment/mgmt (after brief LOC):

Signs of a structural brain injury could include: increasing headaches, decreasing LOC,
increasing tiredness and confusion, any lateralizing weakness, seizure temporally remote from the
injury, persistent vomiting.
Remember to examine neck, jaw, facial structures- blow to these areas can cause concussion. Full
neurologic assessment, tests of memory, orientation, concentration
Return to work/sport: Being “asymptomatic” refers to physical, cognitive, and emotional
manifestations of concussion. Any time symptoms reoccur, patients should take a step back from
activity

Seizure: Driving guidelines: http://www.cmaj.ca/content/168/4/441/T4.expansion.html

Loss of Weight - Key Features

1. Pursue an underlying cause in a patient with unexplained weight loss through history,
physical examination (including weight) and appropriate investigations.

2. Maintain an ongoing record of patients’ weights so as to accurately determine when true

weight loss has occurred.

3. In patients with persistent weight loss of undiagnosed cause, follow-up and reevaluate in a
timely manner in order to decide whether anything needs to be done.

Look out!! Involuntary weight loss, either with decreased or increased appetite, is nearly always a
sign of a serious medical or psychiatric illness

History: magnitude of the loss of weight loss?

- Clinically significant weight loss is 10 lbs or more, or 5 % of baseline body weight over
6-12 months
- Get their past history – from family members, i.e.: changes in eating habits, old growth
charts,

220
 - Previous variations in weight during adult life?
- Voluntary or involuntary weight loss?
- Appetite ↑ or ↓?
- Time course of weight loss?
- Diabetic - weight loss and increased appetite indicator of poor diabetic control
- Type 1 diabetes (ask especially in young patients) may purposely decrease their insulin
dose in an attempt to lose weight
- Recent changes to medications
- Herbal products

Differential Diagnosis
Involuntary weight loss with ↑’d appetite

- Hyperthyroidism, uncontrolled diabetes mellitus, malabsorption syndromes,

pheochromocytoma,
- Marked ↑ in physical activity (relatively fewer causes of weight loss with ↑’d appetite –
it’s either increase caloric expenditure or loss via the gut/kidneys)
- Hyperthyroid elderly patients may manifest anorexia (apathetic hyperthyroidism) rather
than ↑’d appetite

Involuntary weight loss with ↓’d appetite

- Medical disorders, malignancy, endocrinopathies, chronic illness, COPD, GI disease,

psych d/o (depression, manic phase, etc.), chronic drug use, alcohol, opiates,
amphetamines/cocaine, other meds topiramate and zonisamide, SSRI, levodopa, digoxin,
metformin, NSAID’s drugs, anticancer drugs)
- Cancer anorexia-cachexia syndrome – weight loss due to cancer occasionally is the only
manifestation of cancer
- HIV infection - Muscle wasting and weight loss are common in patients with HIV
- Endocrinopathies – Hyperthyroidism
- Adrenal insufficiency
- Hypercalcemia
- Diabetes
- Cardiac cachexia – weight loss in a patient with advanced congestive heart failure and
COPD
- GI diseases - weight loss with loss of appetite occurs either directly or indirectly by:
• Dysphagia
• Sensation of satiety
• Vomiting and regurgitation
• Abdominal pain or discomfort
• Chronic inflammation
• Malabsorption
• Spontaneous and surgical fistulas and bypasses
- Herbal products

Voluntary weight loss/ intentional ↓’d food intake

221
 - Treatment of obesity, intentional use of anorexic drugs – amphetamines and derivatives,
anorexia nervosa and bulimia, distance runners, models, ballet dancers, gymnasts
- Psych: bipolar illness during manic phase, depression, Munchausen syndrome – as a
mechanism for getting attention, delusional/paranoid disorders – ideations about food,
neuroleptic withdrawal cachexia (chlorpromazine, thioridazine, haloperidol), cannabis
withdrawal syndrome (sudden discontinuation of the “munchies”)

Possible CCFP Key Features:

1. Involuntary weight loss often indication of a serious underlying medical/psychiatric condition
(i.e. cancer).
2. Determining if there is an increase or decreased appetite can help differentiate a cause.
3. Various chronic diseases (Cardiac, Endocrine, GI, Pulmonary, Infectious, Psych) can often
lead to weight loss by different mechanisms.
4. A review of medications is essential since the use of some medications or the withdrawal of
others can cause involuntary weight loss.
5. There are relatively fewer causes of involuntary weight loss with ↑’d appetite compared to ↓’d
appetite. Appetite increases when either there is an increase in caloric expenditure or there’s a
loss, i.e. via GI/kidneys
6. Obese patients may exaggerate weight loss and patients with underlying organic cause may try
to minimize the weight loss.

Low-back Pain - Key Features

1. In a patient with undefined acute low-back pain (LBP):

a) Rule out serious causes (e.g., cauda equina syndrome, pyelonephritis, ruptured abdominal
aortic aneurysm, cancer) through appropriate history and physical examination.
b) Make a positive diagnosis of musculoskeletal pain (not a diagnosis of exclusion) through an
appropriate history and physical examination.

2. In a patient with confirmed mechanical low back pain:

a) Do not over-investigate in the acute phase.
b) Advise the patient:
- that symptoms can evolve, and ensure adequate follow-up care.
- that the prognosis is positive (i.e., the overwhelming majority of cases will get better).

3. In a patient with mechanical low back pain, whether it is acute or chronic, give appropriate
analgesia and titrate it to the patient’s pain.

4. Advise the patient with mechanical low back pain to return if new or progressive neurologic
symptoms develop.

5. In all patients with mechanical low back pain, discuss exercises and posture strategies to
prevent recurrences.

Differential Diagnosis of Acute Low Back Pain

Table 1 –

Disease/Condition Patient Location of Quality of Aggravating or Signs

222
 age
pain pain relieving factors
(years)
Low back,
Increased with
buttock, Local tenderness,
Back strain 20 to 40 Ache, spasm activity or
posterior limited spinal motion
bending
thigh
Sharp,
Decreased with
shooting or Positive straight leg
Acute disc Low back to standing;
30 to 50 burning pain, raise test, weakness,
herniation lower leg increased with
paresthesia in asymmetric reflexes
bending or sitting
leg
Ache, Increased with Mild decrease in
Low back to
shooting pain, walking, extension of spine;
Osteoarthritis or lower leg;
>50 “pins & especially up an may have weakness
spinal stenosis often
needles” incline; decreased or asymmetric
bilateral
sensation with sitting reflexes
Exaggeration of the
lumbar curve,
Back, Increased with
palpable “step off”
Spondylolisthesis Any age posterior Ache activity or
(defect between
thigh bending
spinous processes),
tight hamstrings
Sacroiliac
Decreased back
Ankylosing joints,
15 to 40 Ache Morning stiffness motion, tenderness
Spondylitis lumbar
over sacroiliac joints
spine
Fever, percussive
Lumbar tenderness; may have
Sharp pain,
Infection Any age spine, Varies neurologic
ache
sacrum abnormalities or
decreased motion
Dull ache, May have localized
Increased with
Affected throbbing tenderness,
Malignancy >50 recumbency or
bone(s) pain, slowly neurologic signs or
cough
progressive fever
Other diagnoses to consider:

• Abdominal aortic aneurysm (AAA): Sudden; severe; constant back/flank/abdominal/groin pain,

syncope, hypotension, shock (cyanosis, ↓ LOC, ↑HR, ). Past hx of: peripheral vascular disease,
smoking, COPD, HTN. FamHx of AAA. Pulsatile abdominal mass (<50% of cases). Abdominal
bruit.
• Cauda equine syndrome: Compression of lower spinal cord, typically caused by a tumour or
massive midline disc herniation. Bowel incontinence, bladder incontinence/retention, saddle
anaesthesia, bilateral sciatica, leg weakness.

History
1) Characterize the pain (OPQRST)

223
2) Ask about Red Flags to identify potentially serious problems requiring immediate diagnostic
testing.
mnemonic BACK PAIN
B – Bowel/bladder dysfunction
A – Anaesthesia (Saddle)
C – Constitutional symptoms (wt loss, fevers, chills, nt sweats, ↓energy)
K – Chronic disease, including history of malignancy, osteroporosis,
P – Parasthesias
A – Age > 50
I – IV drug use, Immunosuppression (e.g. corticosteroid use)
N – Neuro deficit, night-time pain or pain worse/unrelieved when lying down

Patients that should be seen on an urgent basis are the following:

a) Those with features of Cauda Equina Syndrome: loss of bladder/bowel control, widespread
progressive neurological symptoms or signs in lower limbs (leg weakness or gait abnormalities),
saddle area anesthesia or lax anal sphincter
b) Fever (38 C or 100.4 F that persists longer than 48 hours)
c) Severe unrelenting pain at rest or at night

3) Ask about Yellow Flags to identify potential barriers to resuming or increasing activity (i.e.
risk factors for chronicity).
a) Fear of movement/ re-injury → avoidance behaviour
b) Pain catastrophizing (misinterpreting any pain as a sign of underlying catastrophic cause)
c) Pain beliefs (including increased bodily awareness and pain “hypervigilence”)
d) Depression
Patients with yellow flags require constant reassurance and counseling by their family physician,
especially within 4-6 weeks of onset, before the back pain becomes chronic.

4) Consider the following Risk Factors for developing back pain: Smoking, obesity, age, female
gender, strenuous work / sedentary work / psychologically strenuous, low education, job
dissatisfaction and psychiatric problems.

Physical Examination
• Inspection – posture, gait, scoliosis, kyphosis, pain behaviour
• Back examination

o Palpation – Tenderness of bone / soft tissue

o ROM and painful arc
o Mobility (test by having patient, sit, lie down and stand up)

• Neurological exam

o Sensory:
L3 – Medial knee
L4 – Medial ankle
L5 – Middle foot / web space big toe
S1 – Lateral foot / posterior calf
o Motor:
L3 – Extend knee

224
 L4 – dorsiflex ankle
L5 – extend big toe
S1 – plantar flex ankle
o Reflexes
L4 – Knee jerk
S1 – Ankle jerk

• Straight leg raise – For radiculopathy (impingement of nerve root)

o Positive if Sciatica reproduced b/w 10-60 deg

• Crossed straight leg – lift other leg and pain is reproduced in affected leg
• Seated straight leg – seated position, extend leg to 90 deg → pain
• Pedal pulses
• +/- Hepatosplenomegaly, lymphadenopathy, DRE

Waddell’s Signs – Non-organic signs indicating the presence of a functional component of back
pain.
• Superficial, non-anatomic tenderness
• Pain with simulated testing (e.g. axial loading or pelvic rotation)
• Inconsistent response with distraction (e.g. straight leg raises while the patient is sitting)
• Nonorganic regional disturbances (e.g. non-dermatomal sensory loss)
• Overreaction

Investigations
• CBC, ESR/CRP, PSA, alkaline phosphatase, calcium, particularly to evaluate for infection and
malignancy
• Imaging is usually unnecessary in first 4-6 weeks as demonstrated by two large retrospective
studies, unless one of the following indications is present.
• Indications for radiographs in patients with acute low back pain:

o History of significant trauma

o Neurologic deficits
o Systemic symptoms
o Temperature greater than 38°C (100.4°F)
o Unexplained weight loss
o Medical history of cancer, corticosteroid use, drug or alcohol abuse
o Ankylosing spondylitis suspected

• If there is minimal improvement in pain and function by 4-6 weeks, consider spine x-ray. CT
scan or MRI imaging may be subsequently necessary, however, they have been found to
demonstrate abnormalities in “normal” asymptomatic” people which may not correlate with
clinical symptoms.
• Consider bone scan if normal radiographs but high suspicion of osteomyelitis, bony neoplasm or
occult fracture.
• Consider needle electromyography and nerve conduction studies to differentiate peripheral
neuropathy from radiculopathy and myopathy.

Management
NON-PHARMACOLOGIC

225
 1) Activity
a. Exercise – Aerobic activity (e.g. walking, biking, swimming) that minimally stress the
back, with gradual increase in daily recommended levels. Core muscle strengthening
exercises (e.g. oblique abdominal and spinal extensor muscles) should be included in the
physical therapy exercise regimen.
b. Activity restriction to avoid the painful arcs of motion. Caution with activities such as
long distance driving, heavy lifting, sitting for prolonged periods, repetitive twisting and
reaching.
c. The current recommendation is 2 to 3 days of bedrest in the supine position for patients
with acute radiculopathy, as sitting increases intradiscal pressures and can worsen
herniation and pain. Bedrest has not been shown to be beneficial and may be harmful in
other causes of back pain.
2) Physical therapy modalities – Superficial heat or cold packs, massage therapy and
ultrasound (deep heat) are useful for symptom relief in the acute phase and there use
should be limited to the first 2-4 weeks after the injury.
3) No convincing evidence has been demonstrated for lumbar traction, transcutaneous
electrical stimulation (TENS) or corsets.

PHARMACOLOGIC

1) Analgesics in the acute phase should be used on a time-contingent basis (e.g. QID)
rather than a pain-contingent basis.
a. NSAIDS are the mainstay of treatment. A 2-4 week course is recommended. If there is
a history of peptic ulcer disease, H2-antagonist or Misoprostol should be prescribed for
gastrointestinal prophylaxis.
• Ibuprofen 600 mg QID, or
• Naproxen 500 mg BID, or
• Diclofenac 50mg BID
b. Acetaminophen and/or Acetaminophen with codeine can be added as an adjuvant
(<4000mg per day).
c. Muscle relaxants (Cyclobenzaprine, Methocarbamol, Baclofen) are no more effective
than NSAIDS.
d. Short-term course of narcotics can be used in the acute phase, if necessary.
• Tramadol 50-100 mg QID
• Tylenol #3 1-2 tabs q4h PRN
• Dilaudid (hydromorphone) 2-4mg q4h PRN
• Oxycodone (Oxycontin) 2.5-5 mg q6h PRN
• Oxymorphone – 5-10 mg q6h PRN
• Morphine
e. Chronic pain, consider Gabapentin or Pregabalin
f. Corticosteroid injections

SURGICAL

Indications for immediate surgical consultation – suspected cauda equine lesion,

worsening neurological deficits or intractable pain resistant to conservative treatment.

FOLLOW-UP

1) In 2 weeks if the patient is not finding any improvement.

226
 2) At follow-up visit, update history and physical exam. Reassess for red flags and
neurological deficits.

Approach

Meningitis - Key Features

1. In the patient with a non-specific febrile illness, look for meningitis, especially in patients at
higher risk (e.g., immuno- compromised individuals, alcoholism, recent neurosurgery, head
injury, recent abdominal surgery, neonates, aboriginal groups, students living in residence).

2. When meningitis is suspected ensure a timely lumbar puncture.

3. In the differentiation between viral and bacterial meningitis, adjust the interpretation of the

227
data in light of recent antibiotic use.

4. For suspected bacterial meningitis, initiate urgent empiric IV antibiotic therapy (i.e., even
before investigations are complete).

5. Contact public health to ensure appropriate prophylaxis for family, friends and other
contacts of each person with meningitis.

Risk factors

- Extremes of age, specifically neonates & elderly

- “close contacts” => those living in dormitorities
- Immunocompromised => alcoholics, HIV, diabetics, hepatic / renal dysfunction
- Any exposure of meninges to “outside world” => neurosurgery, CSF shunts, basal skull
fractures, penetrating head trauma

Pathogenic Causes

- Aseptic
o Viral: Enterovirus, HSV, Varicella, HIV
o Others: syphilis (Treponema pallidum), M. pneumonia, Rocky mountain spotted fever
- Bacterial
o Infants: Gp B Strep, E Coli, Listeria
o Children / Adults: H Influenzae, N meningitidis, S penumoniae
o Elderly / immunocompromised / alcoholics: Same as above in adults + aerobic Gm neg
bacilli
o Penetrating trauma, post neurosurgery, CSF shunts: S aureus, coagulase neg staph,
aerobic Gm neg bacilli (including pseudomonas)

Clinical Findings of bacterial meningitis

- Fever, neck stiffness, altered mental status & headache (2 of the prev = 95% sensitivity)
- Photophobia
- Petechial rash
- Seizure
- Focal neurologic signs
- Papilledema
- Meningismus (Brudzinski / Kernig)

When to do CT before LP

- Adult with new onset seizures

- Focal neurological findings
- Mod to severe impaired level of consciousness
- Papilledema
- Known CNS diseases including CSF shunts, hydrocephalus, trauma, recent
neurosurgery, immunocompromised

228
 - Delay in ability to perform LP

** if need to delay LP for CT, obtain blood cultures and start empiric antibiotics. If
suspicious for bacterial meningitis, start dexamethasone 20 mins before antibiotics.

Typical CSF Findings in Meningitis

Pathogen WBC (per mcL) Glucose Protein (G/L)

Bacterial >500 (mostly neutrophils) Low >100
Partially treated bacterial >100 Normal >70
Aseptic, often viral 10-1000 (mostly lymphocytes) Normal <200

Empiric Antibiotic Therapy

- Neonates: ampicillin + cefotaxime

- Adults: vancomycin + ceftriaxone
- Immunocompromised adults (age > 50 yo, altered cellular immunity, alcoholics):
ampicillin + vancomycin + ceftriaxone
- Basilar skull fracture or cochlear implant: vancomycin + ceftriaxone
- Neurosurgery + CSF shunt + penetrating trauma: vancomycin + cefepime

Prevention

- H. influenza type B vaccine

- Conjugate meningococcal vaccine
- Conjugate pneumococcal vaccine

Prophylaxis

- Prescribe antibiotics for the following close contacts

o Anybody in close contact with pt x 8 hrs
o Contact oral secretions
o Living in household with 1 or more unvaccinated or incompletely vaccinated children

Menopause - Key Features

1. In any woman of menopausal age, screen for symptoms of menopause (e.g., hot flashes,
changes in libido, vaginal dryness, incontinence, and psychological changes).

Perimenopause
• Begins 5-10 yrs prior to menopause
• Irregular menses (usually shorter cycle)
• Vasomotor symptoms
• Still fertile!!! High rate of unintended pregnancies in women age 40-44.

Menopause (Marked ↓ in circulating estrogen)

229
• 12 months after final menses (typically age 50-51)
• Continuation of vasomotor symptoms
• Urogenital symptoms (vaginal dryness, dyspareunia)

RFs for early menopause

• Smoking
• Hysterectomy
• Chemotherapy / radiation

Symptoms
• Hot flashes
• Insomnia/sleep disturbances
• Weight gain/bloating
• Mood changes/irritability
• Painful breasts
• Headaches
• Fatigue/poor concentration
• ↓Libido
• Thinning of vaginal wall
• ↓ Uterus/ovary size
• Loss of pelvic tone (prolapse, incontinence)
• Loss of skin tone
• Loss of bone density
• Loss of dense breast tissue

2. In a patient with typical symptoms suggestive of menopause, make the diagnosis without
ordering any tests. (This diagnosis is clinical and tests are not required.)

CLINICAL DIAGNOSIS!! (No need for lab tests – unless atypical symptoms)

3. In a patient with atypical symptoms of menopause (e.g., weight loss, blood in stools), rule out
serious pathology through the history and selective use of tests, before diagnosing menopause.

Atypical symptoms
• Weight loss
• Blood in stools
• Drenching Night Sweats or atypical hot flashes
→In history R/O: hyperthyroid, meds, carcinoid syndrome, prolactinoma, and other
malignancies.
→R/O serious disease pathology with appropriate tests based on history (Always include: CBC,
Ferritin, TSH, and serum prolactin)

4. In a patient who presents with symptoms of menopause but whose test results may not
support the diagnosis, do not eliminate the possibility of menopause solely because of these
results.

5. When a patient has contraindications to hormone-replacement therapy (HRT), or chooses

not to take HRT: Explore other therapeutic options and recommend some appropriate choices

a) Conservative Management: Address in all women:

• Stress Management

230
• Sleep Hygiene
• Healthy Diet (Soy foods and Isoflavone supplements have shown no proven benefit)
• Smoking cessation
• Regular Exercise
• Reduction in Alcohol and Caffeine consumption

b) SSRIs and gabapentin often result in 30% improvement of hot flashes

c) Other alternatives include Clonidine and bellergal (Belladonna + Ergotamine – phenobarbital).

6. In menopausal or perimenopausal women:

a) Specifically inquire about the use of natural or herbal products.
b) Advise about potential effects and dangers (i.e., benefits and problems) of natural or herbal
products and interactions.

Without good evidence for effectiveness, and in the face of minimal data on safety, these
approaches should be advised with caution. Most have not been rigorously tested for the
treatment of moderate to severe hot flashes, and many lack evidence of efficacy and safety.
For specific herbals see pg 72-73 of Canadian Consensus Guidelines on Menopause 2006 Update

7. In a menopausal or perimenopausal women, provide counseling about preventive health

measures (e.g., osteoporosis testing, mammography).

Screening
• Osteoporosis –Do not treat with HRT (despite the fact that HRT has demonstrated a beneficial
effect in osteoporosis prevention there is no data available on reduction of fracture risk)
• Breast Cancer – Mammography @ starting at age 40
• Pap Test
• CV risk profile
• Colon ca screening
• Flu shot
• Mood Screen

8. Establish by history a patient’s hormone-replacement therapy risk/benefit status.

ESTROGEN THERAPY
• The only reason for using estrogen therapy in post menopausal women is to provide relief from
vasomotor symptoms
• Secondary benefits include improved libido, skin and mood.
• Other benefits include birth control, control regularity of menses, preserve BMD
• Peril: When using HRT for hot flashes, use continuously not cyclically as the hot flashes
reoccur during the pill free days
• Taper dose when stopping therapy
• If only sx are vaginal dryness and/or dyspurina, use topical estrogen (no progesterone required)

Adverse Effects
• Bloating
• Breast pain
• Vaginal bleeding
• Headaches

231
Absolute Contraindications
• Undiagnosed vaginal bleeding
• Severe/Acute liver disease
• Pregnancy
• Thromboembolic Event

Relative
• PMHx or strong FMHx of Breast ca (Conflicting data on the effects of estrogen therapy on
breast ca)
• Caution in patients with CVD and hyperlipidemia (There is some evidence that HRT increases
the risk of a CV event in woman >60 or >5 years of therapy)

Mental Competency - Key Features

1. In a patient with subtle symptoms or signs of cognitive decline (e.g., family concerns,
medication errors, repetitive questions, decline in personal hygiene),

a) Initiate assessment of mental competency, including use of a standardized tool,

b) Refer for further assessment when necessary.

2. In a patient with a diagnosis that may predict cognitive impairment, (e.g., dementia, recent
stroke, severe mental illness) identify those who require more careful assessment of decision-
making capability.

3. When a patient is making decisions (e.g., surgery/no surgery, resuscitation status) think
about the need to assess their mental competency.

4. In a patient with cognitive impairment, identify intact decision- making abilities, as many
may be retained.

Cognitive impairment should be suspected when there is a history that suggests a decline in
occupational, social or day-to-day functional status. This might be directly observed or reported
by the patient, concerned family members, friends and/or caregivers.

General population screening in asymptomatic individuals is not recommended

D/D
depression,
delerium,
dementia,
medications,
systemic diseases i.e vit B deficiency thyroid, Hypercalcemia

a) Delirium:
transient, usually reversible, cause of cerebral dysfunction and manifests clinically with a wide
range of neuropsychiatric abnormalities. The clinical hallmarks are decreased attention span and a
waxing and waning type of confusion.

232
I WATCH DEATH
•I nfections (Pneumonia, Urinary Tract Infections)
•W ithdrawal (Ethanol,opiate)
•A cute metabolic (acidosis, renal failure, imbalances, alkalosis)
•T rauma
•C NS pathology (epilepsy, cerebral haemorrhage)
•H ypoxia
•D eficiencies (vitamin B12, thiamine)
•E ndocrinopathies (thyroid, parathyroid, hypopituitarism, hyper/hypoglycemia, Cushing's)
•A cute vascular (Stroke, MI, PE, heart failure)
•T oxins or drugs (prescribed - Tramadol, recreational)
•H eavy metals

b) Depression:
MSIGECAPS

c) Dementia:
D/D

1) Alzheimer’s dementia
Slow progressive onset
Multiple cognitive deficits manifested by both:
• Memory impairment
• One or more additional cognitive deficits such as aphasia, apraxia, agnosia, disturbance
in executive functioning
Associated significant functional decline

2) Vascular Dementia
abrupt onset, step-wise decline
associated with cerebrovascular disease
Clinical and neuroimaging evidence supports the diagnosis

3) Mixed Dementia:
The degenerative changes of AD and the vascular changes of VaD commonly co-exist.
Presentation more commonly of AD pattern with significant vascular risk factors +/-
small vascular events

4) Dementia with Lewy body DLB

Fluctuating cognition with pronounced variation in attention and alertness
hallucinations, Dellusions, vivid dreams
Parkinsonism (DLB should occur before or concurrently with onset of PD)
Repeated falls/Syncope or transient loss of consciousness
Hypersensitivity to antipsychotics (typical and atypical)
reduced response to L-dopa compared to idiopathic PDD

233
 5) Parkinson associated Dementia
The cognitive features may appear similar to DLB Parkinsonian symptoms that typically
are present many years before the onset of the dementia for PDD **

6) Fronto-temporal dementia:
Insidious onset and gradual progression
middle-aged patients
Character & Behavioural changes
Relatively preserved memory, perception, spatial skills and praxis
Prominent language changes
Normal Pressure Hydrocephlus NPH
Gait
Dementia
Urinary incontinence

HISTORY
Ask about onset, duration, Course (fluctuating? Progressive? Step-wise) alertness,memory
loss( global? Recent? Emote?) perception (delusions, hallucinations) Sleep, Emotions, gait,
features of systemic diseaseses i.e PD, Thyroid, Peripheral neuropathy
Chronic vascular disease i.e CVA, DM, CAD, HTN

Assess
Basic ADLs (DEATH )

• Dressing
• Eating
• Ambolating
• Toileting
• hygiene

Instrumental ADLs (SHAFT)

• Shopping
• Housekeeping
• Accounting
• Food prepration
• Transportation

Advanced ADLs

• Going out to symphony

P/E
Identify medical conditions contributing to cognitive decline, and Identify neurologic
abnormalities including localizing signs, extrapyramidal signs, ataxia.

234
Mild Cognitive Impairment (MCI)
A diagnosis of MCI is made when other causes of impaired cognition (e.g., anxiety, depression,
delirium or substance abuse) have been excluded and the patient does not meet the criteria for a
diagnosis of dementia either because they lack a second sphere of cognitive impairment or
because their deficits are not significantly affecting their daily living.

LABORATORY TESTS
The following tests are recommended in the initial work up of suspected MCI or dementia:

• CBC
• Lytes also Serum calcium
• Glucose
• TSH
• B12*

SHORT COGNITIVE ASSESSMENT

• Say 3 words ask the repeat. Then recall items in 1 min

• Clock drawing test (“Ten after eleven”)
• If abnormal → do better test next time, send to OT

Better screening tests/ monitoring

• MMSE – commonly used screening and monitoring (takes 5 min, Affected by

age/educational level/language skills/hearing)
>24 no dementia, ** needs to be taken in context with above
• 3MS: Modified mini mental screening as well as monitoring has highly validity then
SMMSE
• MoCA: Montreal Cognitive Assessment: a 10-minute cognitive screening tool for
detection of mild cognitive impairment (MCI), a clinical state that often progresses to
dementia. In cases where there is a suspicion of cognitive impairment or concern about
the patient’s cognitive status, and the SMMSE score is in normal range (24-30) MoCA is
recommended

Competency of person

o Must be able to understand and remember sufficiently to support decision making

o Must be able to appreciate risks and benefits
o Insight and judgement

MANAGEMENT:
A CDM approach establish a disease register and recall patients for review with a planned visits
dedicated solely to the care of dementia
Involve family members in care
Involve allied health professionals( e.g. Home and Community Care case managers, mental
health teams etc.
Driving
After early cognitive deficits are first diagnosed, consider entering into a discussion with the

235
affected patient about eventual driving cessation.
Assist the affected driver to make the necessary lifestyle changes early and to cease driving by
choice rather than by compulsion.
Encourage patient to register with HandyDart, HandyPASS and TaxiSavers
When doubt exists about a patient’s driving competence Re road test by Insurance Corporations
i.e., ICBC
** Always document in the chart If pt unsafe to drive
If pt continues to drive physician is required to notify the Superintendent of Motor Vehicles

Self-Neglect, Neglect and Abuse

Refer to Home and Community Care or geriatric outreach teams

Financial

• Do MMSE/cognitive assessment then...

• Assets – property, vehicles, investments, banks
• Debts
• Income - where and how much?
• Expenses
• Power of attorney – only financial decisions
o Trusted family member/friend
o Can use joint bank accounts...
o Careful of family disagreements/strangers, etc

Testimonial Capacity

• Must know approx what pt owns

• Must know who would be the beneficiary
• Must be unbiased!!!

Drinking and Driving

• Comprehensive Trail making test

• Drive Able or Road test

Multiple Medical Problems - Key Features

1. In all patients presenting with multiple medical concerns (e.g., complaints, problems,
diagnoses), take an appropriate history to determine the primary reason for the consultation.

2. In all patients presenting with multiple medical concerns, prioritize problems appropriately
to develop an agenda that both you and the patient can agree upon (i.e., determine common
ground).

3. In a patient with multiple medical complaints (and/or visits), consider underlying depression,
anxiety, or abuse (e.g., physical, medication, or drug abuse) as the cause of the symptoms,
while continuing to search for other organic pathology.

236
4. Given a patient with multiple defined medical conditions, periodically assess for secondary
depression, as they are particularly at risk for it.

5. Periodically re-address and re-evaluate the management of patients with multiple medical
problems in order to:
- simplify their management (pharmacologic and other). - limit polypharmacy.
- minimize possible drug interactions.
- update therapeutic choices (e.g., because of changing guidelines or the patient’s situation).

6. In patients with multiple medical problems and recurrent visits for unchanging symptoms,
set limits for consultations when appropriate (e.g., limit the duration and frequency of visits).

Somatization disorder (reference [http://www.uptodate.com/index Uptodate)

-Multiple physical symptoms involving several organ systems, but are not explained by any
known diagnosable medical illness.
-onset of symptoms before 30 yo
-complaints must include pain, at least two gastrointestinal symptoms, a sexual or reproductive
issue, and at least one complaint related to the neurological system.
-symptoms must result in seeking medical treatment, must impair functioning, and must have no
known medical cause. These symptoms cause real distress, patient is not ‘faking’
-screen for depression, anxiety, and substance use disorders

-Some keys to management of patients with somatoform disorders:

-nonjudgmental care
-consistent physician
-regularly scheduled appointments every one to two months, with brief focused visits to
evaluate new complaints.
-psychoeducation includes cognitive behavior therapy and behavioral therapy utilizing a
basic reward system for health promotion and avoiding increased attention during periods
of escalating somatic complaints

-Other somatoform disorders:

-conversion disorder
-pain disorder
-hypochondriasis
-body dysmorphic disorder

Neck Pain - Key Features

1. In patients with non-traumatic neck pain, use a focused history, physical examination and
appropriate investigations to distinguish serious, non-musculoskeletal causes (e.g., lymphoma,
carotid dissection), including those referred to the neck (e.g., myocardial infarction,
pseudotumour cerebri) from other non-serious causes.

2. In patients with non-traumatic neck pain, distinguish by history and physical examination,
those attributable to nerve or spinal cord compression from those due to other mechanical

237
causes (e.g., muscular).

3. Use a multi-modal (e.g., physiotherapy, chiropractic, acupuncture, massage) approach to

treatment of patients with chronic neck pain (e.g., degenerative disc disease +/- soft neuro
signs).

4. In patients with neck pain following injury, distinguish by history and physical examination,
those requiring an X-ray to rule out a fracture from those who do not require an X-ray (e.g.,
current guideline/C-spine rules).

5. When reviewing neck X-rays of patients with traumatic neck pain, be sure all vertebrae are
visualized adequately.

Most common etiology: Degenerative changes

10% of population at any given time has neck pain
Majority of injuries/degeneration occurs C4-C7

Symptoms Suggesting Major Pathology:

• Hx of recent fall/major trauma (Need immobilization and ER assessment)
• Wt loss/Fevers/chills/sweats/hx of CA/Immunsuppression/IVDU/Chronic steroid use
(Tumour/Infection)
• Clumsiness, gait problems, bowel/bladder dysfx, babinksi sign (Cervical Myelopathy)
• H/A, shoulder/hip gurdle pain/visual symptoms (GCA)
• Shock like parasthesias (Lhertmitte’s phenom.) with neck flexion (MS, midline disk herniation)
• Anterior neck pain (Usually non-spinal aetiology)

Axial Neck Pain Disorders

Cervical Strain
Injury to paraspinal muscles/ligaments with assoc spasm of neck muscles
• Acute neck and trapezius pain
• No neurologic dysfx
• Pain, stiffness, tightness x 4-6 wks; **If lasting > 6 wks consider new dx and
imaging**
• Causes: Physical stresses, poor posture, poor sleeping habits, etc

Cervical Spondylosis
• Degenerative changes of cervical spine (soft tissue, disc, bone)
• X-rays:↓ disc height, osteophytes, Δ facet joints BUT correlation w presence/severity of
pain poor

Cervical Discogenic pain

• Distortion of intervertebral disc that results in mechanical neck pain
• Unable to distribute pressures b/w disc/vertebral endplated/facet joints
• Axial neck pain +/- extremity pain

238
 • Pain with neck held in one position for a long time (driving, working at computer,
reading)
• Assoc muscle tightness, spasm
• O/E: ↓ROM, no neuro signs

Cervical Facet syndrome

• Most common cause whiplash-related neck pain
• Pain is midline or slightly off to one side.
• Referred pain to shoulders, scapula, occiput, upper arm
• Axial pain > extremity pain
• Intra-articular inj with lidocaine (relief = diagnostic)→ No Dx w PEx /Imaging
'Whiplash – Abrupt flexion/extension injury
• Severe pain, muscle spasm, ↓ ROM, occipital headache
• Multiple injuries (soft tissue, spinal nerve, disc, ligaments, facet joints, bone
• Can become chronic (months, years)

Cervical Myofascial Pain

•Less generalized variant of fibromyalgia
•Regional pain assoc with trigger points, tight bands, pressure sensitivity
• Assoc with depression, insomnia

DISH (Diffuse Skeletal Hyperostosis)

• Inappropriate calcification @ insertion of ligament/tendon
• Dx on X-rays – specific changes
• Stiffness, loss of mobility

Tx Axial Neck Pain:

• Acute (<6 wks): Acetaminophen, NSAIDS, mild opioids (eg.tramadol), muscle
relaxants (cyclobenzaprine 5mg TID, benzos); Home exercises: Gentle stretching
exercises incl shoulder rolls and neck stretches (heat neck prior)
• Persistent (>6wks): Physical Tx, TCA’s (amitryptyline/nortryptyline 10-30 mg QHS),
duloxetine/venlafaxine esp w depression/anxiety/fibromyalgia

Extremity Pain/Neurologic Deficit Disorders

Cervical Spondylotic Myelopathy – Narrowing of the spinal canal → SC

injury/dysfunction
• Sx: Weakness, stiffness in L/E, poor coordination / gait imbalance, bowel/bladder dysfx
(rare), sexual dysfx.
• Signs: atrophy of hands, hyperreflexia, Lhermitte’s sign, sensory loss

239
 • DDx: MS, tumour, epidural abscess, ALS, syringomyelia
**Needs surgical decompression***

Cervical Radiculopathy – Dysfunction of spinal nerve root

• Pain, weakness, sensory changes, reflex changes along particular nerve root
• DDx: Degenerative/foraminal stenosis/herniated disc >> Shingles, DM radiculopathy
• Tx: analgesics, ?prednisone short course?

Non Spinal Causes

• Thoracic Outlet Syndrome – Triad:1)Numbness, 2)weakness, 3)sensation of swelling in

upper limb
• Shingles – unilateral pain followed by typical rash
• Diabetic Neuropathy
• Vascular: vertebral artery/carotid artery dissection
• CVS: angina, MI
• INfxn: pharyngeal abscess, meningitis, HZV, Lyme D.
• Rheum: RA, PMR, fibromyalgia, spondyloarthritis
• Neuro: cervical dystonia, tension H/A

Physical Exam
Inspection
ROM
Palpate paraspinal & trapezius
Neuro exam: motor, sensory, reflexes, gait
UMN signs? - ↑ Reflexes, ↑ tone/spasticity, ↑babinski
Special Tests

Spurling’s (Neck Compression Test) – For ? radicular pain

• Head in neutral position → press down on top of head
• Head rotated to affected side and hyper extended → neck compression
• Reproduction of sx beyond shoulder is +ve test
• C/I in RA, cervical malformations, metastatic

Upper Limb Tension Test – For ? radicular pain

•Head turned contralaterally, ipsilateral arm abducted, external rot, wrist ext
•Reproduction of arm sx is +ve test, used as tx?

Manual Neck Distraction Test

240
 Hoffman Sign – indicates myelopathy
Shoulder Abduction relief test – indicates herniation/nerve root imping, and therapeutic

Imaging
X-ray (odontoid, lateral, PA, both obliques)

• Hx of neck trauma
• New symptoms in patients >50y

CT/MRI

• Neurologic impairment
• Constitutional sx (fevers, chills, wght loss)
• Dramatic bony tenderness with impaired mobility
• Persistent symptoms after 6 weeks of conservative care

EMG

• Pain, dysesthesias more prominent in extremities

• not very useful for CSM, may help differentiate radiculopathy from peripheral nerve
entrapment

Trauma
Immobilization, neurological assessment, spinal palpation, radiographic studies

Clearing C-spine:

Clinical
• No C-spine tenderness
• No evidence of intoxication
• Alert and oriented (GCS=15)
• No focal neurological deficit
• No painful distracting injury

Lateral
Alignment
Anterior longitudinal line
Posterior longitudinal line
Spinolaminal line
Spinous processes

241
Ligamentous injury / instability

Bone (evaluate each vertebrae - ?Fracture, inc/dec density)

• Cortex – no discontinuity, angulation, step-off, bowing
• Dens – Difficult to see on lateral view. Atlanto-occipital dislocation

Cartilage / connective tissue

• Joint spaces

Soft Tissue
• Predental space should be <3 mm in adult, <5 mm in children
• Pre-vertebral space should be no more than 1/3 the diameter of the vertebral body

Newborn - Key Features

1. When examining a newborn, systematically look for subtle congenital anomalies (e.g., ear
abnormalities, sacral dimple) as they may be associated with other anomalies and genetic
syndromes.

2. In a newborn, where a concern has been raised by a caregiver (parent, nurse),

a) Think about sepsis, and
b) Look for signs of sepsis, as the presentation can be subtle (i.e. not the same as in adults,
non-specific, feeding difficulties, respiratory changes)
c) Make a provisional diagnosis of sepsis.

3. Resuscitate newborns according to current guidelines.

4. Maintain neonatal resuscitation skills if appropriate for your practice.

5. When a parent elects to bottle feed, support their decision in a non-judgemental manner.

6. In caring for a newborn ensure repeat evaluations for abnormalities that may become
apparent over time (e.g., hips, heart, hearing).

7. When discharging a newborn from hospital,

a) Advise parent(s) of warning signs of serious or impending illness, and
b) Develop a plan with them to access appropriate care should a concern arise.

History:
Review of current prenatal and delivery history:

Pregnancy - planned/not, prenatal care, results of routine tests (ABO blood type, Rh
antibody, Hemoglobin, TSH [if done], Urinalysis and urine culture, Chlamydia and
Gonorrhea screen) maternal infection screen, prenatal genetic screening, gestational DM,
GBS swab result
Labour - length of labour, duration of ROM, presence of meconium
Delivery - mode of delivery, Apgars, need for resuscitation

242
Review of mother’s previous OB history:
History of congenital abnormalities, stillbirths, genetic/syndromic conditions
Mother and father’s medical and genetic history - e.g., maternal lupus, pre-eclampsia

Sepsis Risk Factors:

• GBS+
• Intrapartum fever ≥38ºC (100.4ºF)
• Membrane rupture ≥18 hours
• Delivery at <37 weeks gestation
• Chorioamnionitis
• 5 minute Apgar <6
• Fetal distress during labour

Check if maternal intrapartum antibiotics received (at least 2 doses for GBS+)

Physical Exam:
General Appearance:

• Body position at rest - posture often reflects the position the fetus was in in utero
• Body Movement - check symmetry
• Nutritional state - subcutaneous fat in anterior thigh, gluteal region; amount of
Wharton’s jelly in umbilical cord
• Colour - pale, ruddy, jaundiced
• Respiratory effort - increased RR, nasal flaring, accessory muscle use, indrawing,
grunting

Measurements:

• Head circumference: avg. 35 cm at 40 weeks, may change over first few days because
of moulding, edema
• Length: avg. 51 cm at 40 weeks
• Weight: avg. 3.6 kg for males, 3.5 kg for females at 40 weeks
• Vital signs (axillary temp 36.1 to 37ºC (97.0 to 98.6ºF) in an open crib; RR
40-60/minute, count over full minute; HR 120-160 bpm)

Organ system:

• Skin
o Possible underlying disorder beneath abnormal pigmentation, macular stains,
congenital nevi, or hemangiomas
o Benign conditions include milia (white papules resulting from collection of keratin and
sebaceous material, often on nose and cheeks); transient pustular melanosis (superficial
pustules on top of hyperpigmented macules, mostly in African-American neonates);
erythema toxicum (white pustules on erythematous base); Mongolian spots (congenital
bluish-grey or brown pigmented macules, iindefinite borders, especially in African-
American or Asian babies); nevus simplex (i.e., macular stain, angel kiss, or stork bite);
nevus flammeus (i.e., port wine stain, may or may not be benign)

243
• Head - check shape and size; presence of abnormal hair; unusual lesions or
protuberances; lacerations, abrasions or contusions; scalp defects
o Fontanelles - normal is soft and flat with infant sitting. Tense or bulging fontanelles -
suspect increased ICP (e.g. bacterial meningitis, subdural hematoma)
o Sutures - often have moulding with transit through birth canal, but asymmetric skull
that persists for longer than 2-3 days after birth or a persistent palpable ridge along the
suture line may suggest craniosynostosis; consider increased ICP due to hydrocephalus
with widely split sutures with full fontanelle
o Bleeding: caput succedaneum (edema over presenting part of head, common, crosses
suture line, resolves within days); cephalohematoma (fluctuant mass, does not cross
suture line, takes weeks - months to resolve); subgaleal hemorrhages (blood between
aponeurosis of scalp and periosteum, extend across suture lines, feel fluctuant and firm,
can get ++bleeding, can be life-threatening)
• Face – check symmetry
o Facial palsies (increased risk if have forceps delivery or prolonged labour and delivery
in mother with prominent sacral promontory) should resolve within days to weeks;
ensure baby can feed prior to discharge; persistent facial palsy may be due to central
lesion
o Asymmetric Crying Facies due to inadequate depressor anguli oris muscle, causes
mouth asymmetry when crying; may be associated with cardiovascular anomalies
• Eyes
o Spacing (hypertelorism [wide interpupillary distance] associated with numerous
syndromes
o Symmetry: epicanthal folds, globe size, ptosis, extra-ocular movements
o Palpebral fissures: may be widened or narrow; could be normal variant or part of
syndrome; upward slanting from inner canthus seen in Down syndrome
o Sclera: normally white, clear; may be light blue in premature infants; consider
osteogenesis imperfecta if dark blue
o Conjunctiva: check for hemorrhage, inflammation, purulent discharge
o Cornea: consider glaucoma if enlarged (>12 mm), photophobia, increased tearing,
corneal haze
o Pupils: check shape, reactivity to light
o Iris: check for defects (e.g. coloboma), which may be part of syndrome
o Red reflex: abnormalities may be caused by cataracts, retinoblastoma, or persistent fetal
vasculature
• Ears: check position, size, and appearance
o Position – helix should be along horizontal line from outer canthus of eye and
perpendicular to vertical axis of head
o Malformations – check for sinuses, preauricular skin tags or pits, or dysplastic features;
may indicate anomalies of inner ear and associated hearing loss; may be part of
syndrome, esp. renal.
o Hearing – may need to repeat
• Nose: check shape (abnormal if extremely thin or broad or depressed nasal bridge) and
patency (rule out septal deviation, choanal atresia)
• Mouth: check size and shape; small jaw may be associated with Robin sequence; check
for cleft lip and palate; check tongue for tongue tie; assess gingival, palate, uvula; natal
teeth may be associated with syndrome
• Neck: check for masses (e.g., branchial cleft cyst, cystic hygroma, lymphangioma,
hematoma, thyroglossal duct cyst, thyromegaly, lymphadenopathy), decreased mobility
(torticollis), redundant skin (may be associated with syndrome, e.g. Turner), and clavicles
• Cardio: auscultate, palpate chest and pulses

244
 o Murmur: worrisome murmur: Grade III or higher, harsh quality, pansystolic, loudest
LUSB, abnormal S2, decreased femoral pulses, other abnormalities; patent ductus
murmur – continuous, harsh; some murmurs develop in few days, so auscultation needs
to be repeated prior to discharge and in outpatient visit
o Pulses: decreased femoral in coarctation; increased pulse pressure in PDA
• Resp: check size, symmetry, structure of chest, chest wall movement, and resp effort
• Breast: check size and nipple position (>25% of chest circumference = wide-spaced,
may occur in genetic syndromes, like Turner syndrome)
• Abdo: check size, overall appearance, normally slightly protuberant; look for distension
(e.g. with organomegaly, bowel obstruction, or ascites) or scaphoid appearance (e.g. with
diaphragmatic hernia), and abdo wall defects (umbilical hernia, omphalocele, or
gastroschisis). Palpate while infants’ legs are flexed, check liver edge (normal 1-3 cm
below R. costal margin), palpate for spleen (not usually palpable) and kidneys; check for
masses; inspect umbilical cord for signs of infection, number of vessels (single umbilical
artery associated with higher number of chromosomal and congenital abnormalities)
• Genitalia: confirm sex.
o Female: check labia, clitoris, meatus, and vaginal opening; labia minora and clitoris
more prominent in preterm infants
o Male: check testes (descent), penis, scrotum, position of urethral opening
o Ambiguous genitalia: may indicate sexual differentiation problem or congenital adrenal
hyperplasia (can get salt-wasting crisis)
o Anus: check location, patency; imperforate anus may be part of syndrome (e.g.
VACTERAL association)
• Hands and feet: check digits (fused or extra digits may be normal variant or part of
syndrome), palmar crease (single crease more common in Down syndrome), movement
of all 4 limbs (may have brachial plexus injury or palsies, like Erb’s palsy, which is
damage to C5 and C6 nerve roots)
• Hips: check for developmental dysplasia (risk factors: female, breech position, family
hx), needs to be repeated at outpatient follow-up visits
• Spine: visualize and palpate, check for neural tube defect (NTD), soft tissue masses
(lipomas, mylomeningoceles), sacral cleft or dimple (more worrisome if deep, big > 0.5
cm, above gluteal crease, skin changes associated with NTD). May have underlying
spinal cord abnormality if have tuft of hair, discolouration, or hemangioma over
sacrococcygeal region
• Neuro: check alertness, spontaneous motor movement, strength, tone, primitive reflexes

Exam for sepsis:

May have subtle, non-specific signs: temperature instability, respiratory distress, anorexia,
vomiting, jaundice, hepatomegaly, lethargy, cyanosis, irritability, apnea, abdo distension, diarrhea

245
Newborn Resuscitation Guidelines:

Follow-up:
Ensure newborn able to feed, void, stool; advise parents to seek immediate advice with physician
if baby lethargic or febrile; seek prompt help if other signs of sepsis. Should have follow-up
within first week for 1st newborn visit, esp. to check weight, feeding pattern, voiding/stooling,
address parental concerns

Obesity - Key Features

Definition
-obesity: BMI >30kg/m2
-overweight: BMI 25-29.9 kg/m2
-waist circumference >35 inches (88 cm) in women and 40 inches (102 cm) in men associated w/
increased health risk problems (DM II, HTN, dyslipidemia, metabolic syndrome, CVS disease)
(note that these values do differ pending on ethnic origin)
-waist to hip ratio >0.83 in men, >0.9 in women predictive of MI (better than BMI and waist
circumference)
-underweight: BMI <18.50 kg/m2

246
** note also that BMI does NOT take into account muscle mass, so often very fit people will have
a high BMI.

Incidence:
-23% of Canadians obese, another 59% overweight

-increase of 5 in BMI higher than 21 kg/m2 associated with corresponding 10% increase
in risk of mortality for women (regardless of risk factors).

Risk Factors:
-sedentary lifestyle
-diet: intake of energy dense foods, sugar sweetened soft drinks,
-low socio-economic status
-childhood obesity

Adverse Medical Consequences

-hypertenision-CAD-DM II-gallbladder disease-sleep apnea-respiratory problems: cough,
wheezing-cancers of endometrium, breast, prostate, colon, pancreas-OA-CHF-ischemic stroke-
non-alcoholic steatohepatitis-low back pain-increased total mortality-complications in pregnancy
(gestational DM, primary ovulatory infertility, perinatal mortality and increased neural tube
defects)-emotional distress, discrimination and social stigmatization-stress incontinence

Physical exam:
-BMI/WC (consider waist to hip ratio-BP) **canadian guidelines only do BMI if they
demonstrate a risk factor of obesity (see above). International guidelines recommend everyone on
their periodic health exam**

-secondary causes:

**rare!
-hypothyroidism, PCOS, Cushings
-Meds: atypical antispsychotics, lithium, TCAs, glucocorticoids, Depo-Provera,
sulfonyrureas, insulin
-very rare: hypothalamic disorders, insulinoma, Prader willi

Diagnosis
-as above guidelines
-pts over 65 yrs have wider low risk BMI range: 22-29 kg/m2
-WHO suggests 27 kg/m2 in asian race
-Metabolic Syndrome

-dyslipidemia (high triglycerides, low HDL)

-HTN
-hyperinsulinemia

Treatment:
-goal is to reduce wt by 10% from baseline
-0.5-1 kg/wk over 6 month period

247
1. lifestyle modification
-exercise:
-90min of daily moderate intensity activity (brisk walking).
-30-45 min of daily vigorous activity (fast cycling, aerobics).
-use pedometer to increase steps by 1000 per month.
-active obese have lower morbidity than inactive obese.

-diet: no diet superior than any other.

-all work by limiting total calories.
-low carb diets better in short term 6 months but not after 2yrs
**exercise without caloric restriction largely ineffective in initiating wt loss, but
important in the maintenance phase of wt loss**
-Mediterranean Diet: high in fruit, veggies, legumes, whole grains, fish, nuts, low fat
dairy, does not restrict fats but replace w/ vegetable oils
-shown to reduce total mortality as well as mortality from heart disease and cancer

2. Intensive Counselling/Behavior Modifications

-ask pt if she/he would be comfortable discussing wt and how it impacts health
-ask about pt’s wt hx and how excess wt has affected her/his life
-express your concerns about the health risks associated w/ excess wt and how this might
affect pt
-review relationships b/w pts BMI, waist circumference and health risks
-Behavior: regular eating schedule, focus on meal and eat slowly, use smaller plates,
avoiding second helpings, avoid distractions while eating

3. Pharmacotherapy
-considered only when 6-month regimen of diet exercise and behavior therapy fails.
-offered to pts w/ BMI >30 or BMI >27 who have obesity related disease (CAD, HTN,
hyperlipidemia, sleep apnea)
-Orlistat modestly effective in promoting wt loss
-wt gain recurs when tx stopped
- ** of note, as of 2010 Sibutramine (appetite suppressant) off the market. Only orlistat is
approved in Canada. Others are approved in the states**
-responders likely to continue to respond, non responders not likely to respond even w/
higher dose
-if pt does not lose 2kg in first 4wks, not likely to have long term response

Lipase Inhibitors
Orlistat (Xenical) 120 mg tid
Prevents absorption of dietary fat
Wt loss probably d/t avoidance of dietary fat to minimize GI effects
Hx of breast cancer: ? increased breast cancer

248
 GI: Fatty/oily stool, Fecal urgency, Oily spotting, Diarrhea
High attrition rate

4. Surgery
-if BMI >40 or >35 w/ evidence of obesity related co-morbidities (CAD, HTN,
hyperlipidemia, sleep apnea)
-long term wt loss possible
-61% of excess body wt lost on average
-recovery from chronic diseases: DMII (77%), HTN (62%), hypertrigyceridemia (46%),
OSA (62%), Urinary stress incontinence (47%)
-may cause long term nutrient deficiencies
-monitor fat specific Vits (ADEK)
Side Effects:
Less than 1% mortality rate from the procedure. But complication rate as high as 20%!

Answers from BC Guidelines Overweight and Obese Adults

1. In patients who appear to be obese, make the diagnosis of obesity using a clear definition
(i.e., currently body mass index) and inform them of the diagnosis.

Children/Youth
• Normal - BMI < 85th percentile
• Overweight- BMI > 85th percentile
• Obese > 95th percentile

Adults
• BMI ≥25 overweight
• BMI >27 overweight and increased risk of hypertension, diabetes and CVD
• BMI ≥ 30 obese, higher risk of complications

Adult Waist Circumference

Increased risk: female: ≥ 80 cm male ≥ 94 cm
High risk: female: ≥ 88 cm male ≥ 102 cm

2. In all obese patients, assess for treatable co-morbidities such as hypertension, diabetes,
coronary artery disease, sleep apnea, and osteoarthritis, as these are more likely to be present.

Hypertension:

-BP > 140/90 on at least 3 visits over 6 months or with evidence of end organ damage or
>160/90 on at least 2 visits

Diabetes

-FPG at or above 7.0 mmol/L

-two-hour value in an OGTT at or above 11.1 mmol/L
-random plasma glucose concentration 11.1 mmol/L in the presence of sx
-must be confirmed on a subsequent day by measuring any one of the three criteria.

249
Coronary artery disease

-angina, documented bruits, PMHx of MI

Sleep apnea

-poor unrestful sleep, daily headaches, HTN, sleepiness, Hx of snoring

Osteoarthritis

-pain in wt bearing joints worse w/ activity

3. In patients diagnosed with obesity who have confirmed normal thyroid function, avoid
repeated thyroid-stimulating hormone testing.

Further diagnostic assessment should be individualized based on risk factors and family history.
Extensive laboratory assessment of overweight, obese and physically inactive patients in the
absence of obvious risk factors or physical findings is rarely fruitful.

4. In obese patients, inquire about the effect of obesity on the patient’s personal and social life
to better understand its impact on the patient.

Depression Asthma Being bullied Learning difficulties Type 2 diabetes poverty

unemployment/employment education level workplace and home stresses current or previous
abuse

5. In a patient diagnosed with obesity, establish the patient’s readiness to make changes
necessary to lose weight, as advice will differ, and reassess this readiness periodically.

Educate adults about the risks of excess weight and the benefits of moderate weight loss and
increased activity. Reinforce the message that even modest weight loss and increased activity can
confer significant health benefits.
Increases in physical activity in a stable, overweight person likely confer greater health
advantages than diet in a physically inactive person.
Assess readiness to change: Ask the following questions:

• Are you considering trying to lose weight or increase activity?

• Are you currently trying to lose weight or increase activity?
• Would you like some information to help you?

6. Advise the obese patient seeking treatment that effective management will require
appropriate diet, adequate exercise, and support (independent of any medical or surgical
treatment), and facilitate the patient’s access to these as needed and as possible.

Help the patient who is ready to change to set realistic goals:

250
 • Emphasize gradual change in lifestyle over time
• Recommend increased physical activity (e.g. walking 30 minutes/day)
• Recommend some level of caloric restriction
• Provide self-help materials
• Praise success

Using the questions below, determine and record diet quality/dietary habits

1. Do you usually eat breakfast?

2. Do you usually* eat 5 or more servings of fruit and vegetables/day
3. Do you usually* choose whole grain products?
4. Do you usually* choose low fat or reduced fat alternatives at home and when eating
out?
5. How many boxes, cups or cans of fruit juice or pop do you usually drink per day?
6. What do you drink when you are thirsty?
More than one “no” answer and more than one serving of sweetened beverage per day
indicates the need for nutritional advice from the physician or referral to a registered
dietitian or Dial-A-Dietitian (1 800 667-3438)
*indicate to the patient that “usually” means 5 or more days of the week, most weeks.

7. As part of preventing childhood obesity, advise parents of healthy activity levels for their
children.

Activity level – determine and record

Children/youth Adults
Inactive <30 min/day <30 min/day
Moderately active 30-90 min/day 30-60 min/day
Very active >90 min/day >60 min/day
Inactive: no appreciable exercise

Moderately increased heart rate active: e.g.: walking

Very active: e.g.: Running, cycling, swimming lengths

8. In managing childhood obesity, challenge parents to make appropriate family-wide changes

in diet and exercise, and to avoid counterproductive interventions (e.g., berating or singling out
the obese child).

The below recommendations were derived from the following GAC endorsed guideline: National
Institutes of Health: National Heart, Lung, and Blood Institute (1998, September) Clinical
guidelines on the identification, evaluation, and treatment of overweight and obesity in adults:
The evidence report.

GOOD EVIDENCE
Weight loss is recommended to lower elevated blood pressure in overweight and obese persons

251
with high blood pressure.
Weight loss is recommended to lower elevated levels of total cholesterol, low-density lipoprotein
cholesterol, and triglycerides and to raise low levels of high-density lipoprotein cholesterol in
overweight and obese persons with dyslipidemia.
Weight loss is recommended to lower elevated blood glucose levels in overweight and obese
persons with Type 2 diabetes.
The initial goal of weight loss therapy should be to reduce body weight by approximately 10
percent from baseline. With success, further weight loss can be attempted.
Low-calorie diets are recommended for weight loss.
Reducing dietary fat alone without reducing calories is not sufficient for weight loss. Physical
activity is recommended as part of a comprehensive weight loss therapy and weight maintenance
program.
Weight loss and weight maintenance therapy should employ the combination of low-calorie diets,
increased physical activity, and behaviour therapy.

FAIR EVIDENCE
Weight loss should be about one to two lbs/week for a period of six months.
Initially, moderate levels of physical activity for 30 to 45 minutes, three to five days per week
should be encouraged. All adults should set a long-term goal to accumulate at least 30 minutes or
more of moderate-intensity physical activity on most, and preferably all, days of the week.
Behaviour therapy is a useful adjunct when incorporated into treatment for weight loss and
weight maintenance.
After the first six months of weight loss therapy, a weight maintenance program – consisting of
dietary therapy, physical activity, and behaviour therapy – should be a priority.
Various health professionals with different areas of expertise are available and helpful to
practitioners who would like assistance in helping their patients maintain weight loss.
In selected patients with clinical severe obesity (BMI of 40 or more, or BMI of 35 or more along
with comorbid conditions), weight loss surgery is an option when less invasive methods of weight
loss have failed and the patient is at high risk for obesity-associated morbidity or mortality.
Practitioners should use the body mass index (BMI) to assess overweight and obesity. Body
weight alone can be used to follow weight loss, and to determine efficacy of therapy.
The BMI should be used to classify overweight and obesity and to estimate relative risk for
disease compared to normal weight.
For adult patients with a BMI of 25 to 34.9 kg/m2, sex-specific waist circumference cutoffs
should be used in conjunction with BMI to identify increased disease risks.
The literature suggests that weight loss and weight maintenance therapies which provide a greater
frequency of contacts between the patient and the practitioner, and which are offered over a
longer rather than shorter term, should be put in place. This can lead to more successful weight
loss and weight maintenance.

Osteoporosis - Key Features

1. Assess osteoporosis risk of all adult patients as part of their periodic health examination.

2. Use bone mineral density testing judiciously (e.g., don’t test everybody, follow a guideline).

3. Counsel all patients about primary prevention of osteoporosis (i.e., dietary calcium, physical
activity, smoking cessation), especially those at higher risk (e.g., young female athletes,
patients with eating disorders).

4. In menopausal or peri-menopausal women, provide advice about fracture prevention that

252
includes improving their physical fitness, reducing alcohol, smoking cessation, risks of
physical abuse, and environmental factors that may contribute to falls (e.g., don’t stop at
suggesting calcium and vitamin D).

5. In patients with osteoporosis, avoid prescribing medications that may increase the risk of
falls.

6. Provide advice and counseling about fracture prevention to older men, as they too are at risk
for osteoporosis.

7. Treat patients with established osteoporosis regardless of their gender (e.g., use
bisphosphonates in men).

A condition characterized by decreased bone mass and microarchitectural deterioration of bone

tissue causing increased bone fragility and susceptibility to fracture.

Etiology
- Primary Osteoporosis - Due to post-menopausal decline in estrogen and/or increased age
- Secondary Osteoporosis

- GI - malabsorption (previous gastric surgery, IBD, celiac ds), poor nutrition, chronic
liver and renal disease
- Bone - multiple myeloma, lymphoma, leukemia, immobilization
- Endocrine - Cushing’s, hyperthyroidism, hyperparathyroidism, DM, acromegaly,
estrogen deficiency (hypogonadism, premature ovarian failure)
- Inflammatory: rheumatoid arthritis, SLE
- Drugs – corticosteroids(#2 reason to cause OP), phenytoin, heparin, androgen
deprivation Rx
- Psych – Anorexia nervosa, alcohol abuse

Screening
- *Canadian clinical practice guideline focuses on prevention of fragility # and their
consequences, rather than treating low BMD
- All patients over 50 years of age should be screened for osteoporosis and fracture risk factors
AND fall risk at their periodic health examination
- Assess 10 yr fracture risk with FRAX or CAROC
- Hx – prior fragility #, parental hip #, glucocorticoid use, smoking, high EtOH intake,
rheumatoid arthritis, falls in past year, gait and balance
- PE – weight, height (historical loss >6cm or prospective loss >2cm), rib to pelvis distance < 2
fingers breadth, occiput to wall distance > 5cm, fall risk – Get-Up-and-Go Test
- Based on Hx and Px, look at indications for a Bone Mineral Density (BMD). Wide-spread BMD
screening for those under 65 is not recommended.

Indications for measuring BMD

- All patients aged 65 yrs
- If age 50-64 yrs and

- Fragility fracture after age 40

- Prolonged use of corticosteroids*

253
 - Use of other high risk meds **
- Parenteral hip fracture
- Vertebral fracture or osteopenia seen on Xray
- Current smoking
- High EtOH intake
- Low body weight (< 60 kg) or major weight loss (> 10% of body weight)
- Rheumatoid Arthritis
- Other disorders strongly asst’d with OP

- If age < 50 yrs and

- Fragility Fracture
- Prolonged use of corticosteroids*
- Use of other high risk meds**
- Hypogonadism or premature menopause
- Malabsorption syndrome
- Primary hyperparathyroidism
- Other disorder strongly associated with rapid bone loss and/or fracture

* corticosteroid >7.5mg prednisone ODx3months

** aromatase inhibitor, androgen deprivation therapy

Clinical Features
- Commonly asymptomatic
- May have pain, especially back
- Height loss or thoracic kyphosis
- Fractures – hip, vertebrae, humerus and wrist are most common

Investigations
- Usually have normal Ca, PO4, ALP
- Check CBC, Cr, TSH, vit D, SPEP/UPEP, 24 hr urinary Ca excretion, PTH.
- Lateral thoracic and lumbar spine X-rays if clinical suggestion of vertebral #

Bone Mineral Density: - Dual-energy X-ray densitometry (DEXA) is gold standard

- Measure density at lumbar spine and femur, then compared to gender and ethnicity-matched
controls

BMD 1.0 - 2.5 SD below mean = Osteopenia

BMD > 2.5 below mean = Osteoporosis

Management
- Council all patients about primary prevention of osteoporosis

- Weight bearing endurance exercise (20-60 min 4-7 x/wk), balance & strengthening (2-
4x/wk) exercises
- Smoking cessation
- Caffeine and EtOH reduction
- Dietary or supplemental calcium (1200mg/d) and vitamin D (400-2000 IU/day)

254
- Institute a fall prevention program for those at risk

- Address mobility and sensory impairments, dizziness, urinary frequency, hazards in the
home
- Consider hip protectors if high risk and residing in long term care

- Prevent prescribing meds that increase fall risk

- Oral hypoglycemic agents, diuretics, anti-cholinergic, anti-hypertensive, psychotropic

meds etc

- Correct a reversible cause if there is one

- Discontinue osteoporosis-inducing medication if possible

Treatment
Pharmacotherapy reduces risk of vertebral fracture by 30-70%
Canadian guidelines recommend treatment based on FRAX or CAROC 10 yr fracture risk:

- High Risk (>20%) or >50yrs with fragility fracture of hip/vertebra or >1 fragility
fracture = pharmacological treatment
- Mod Risk (10-20%) – decision to treat with pharmacotherapy based on patient
preference and additional risk factors (additional vertebral #, prev wrist # if >65 and T-
score < -2.5, T-score lumbar spine <<femoral neck, rapid bone loss, men on androgen-
deprivation therapy for prostate CA, women on aromatase inhib therapy for breast CA,
long term/repeated systemic steroid use, >2 falls in past year, other d/o strongly
associated with osteoporosis, rapid bone loss/#’s)
- Low Risk (<10%) – lifestyle measures are sufficient

For menopausal women,

- Bisphosponates (alendronate or risendronate) - prevents hip, nonvertebral and vertebral

fractures
- Selective estrogen-receptor modulator SERM (raloxifene) - prevents hip fractures
- HRT – if woman has vasomotor Sx – prevents hip, nonvertebral and vertebral fractures
- If intolerant of first line therapies – calcitonin or etidronate – prevents vertebral
fractures
- PTH or calcitonin – if has had previous fracture

For men,

- Bisphosphonates
- Testosterone not recommended

Palliative Care - Key Features

1. In all patients with terminal illnesses (e.g., end-stage congestive heart failure or renal
disease), use the principles of palliative care to address symptoms (i.e.., do not limit the use of
palliative care to cancer patients).

255
- Guidelines for end-of-life care have been published by the American College of Physicians.
They recommend regular patient assessment and treatment for pain, dyspnea, and depression, and
obtaining advanced directives from patients with serious illness.
- 6 major components of attributes of a "good death":

(1) adequate pain & symptom management;

(2) patient participation in decision making;
(3) greater preparation for the end of life;
(4) a feeling of meaningfulness at the end of life;
(5) the ability to contribute to the well-being of others;
(6) and affirming the patient as a unique and whole person.

- 5 basic principles of palliative care:

(1) respecting the goals, preferences, and choices of the dying person;
(2) caring for the person's medical, emotional, social, and spiritual needs;
(3) supporting the needs of family members;
(4) helping with access to needed medical healthcare; and
(5) providing excellent care at the end of life.

2. In patients requiring palliative care, provide support through self, other related disciplines,
or community agencies, depending on patient needs (i.e.., use a team approach when
necessary).

-Communication is critical for ongoing patient and family support. It is important that physicians
ask about how caregivers are doing, and about psychological distress and the need for support.
-Families usually suffer emotionally, spiritually, and financially since they care for the patient.
Asking & providing information on financial aid or access to social workers can be instrumental
in easing these concerns.
-Families and caregivers often need outside help, respite care, or assistance with making
arrangements for the body after death. Hospice, social workers, and home health aides can offer
great assistance to patients & families in addressing these needs.

3. In patients approaching the end of life:

a) Identify the individual issues important to the patient, including physical issues (e.g.,
dyspnea, pain, constipation, nausea), emotional issues, social issues (e.g., guardianship, wills,
finances), and spiritual issues.
b) Attempt to address the issues identified as important to the patient.

Table: Assessment should include the following (From BMJ Clinical Practice)

Review the patient's disease course, including the primary illness and pertinent
History of illness
secondary diagnoses. Summarize the previous treatments and patient's response.
Physical assessment is best organized by symptoms and functional activities,
Physical rather than by organ system. The physical examination can be used to confirm
symptoms findings from the history. Occasionally, diagnostic tests are helpful if they
change the care plan and are in line with the patient's goals of care.
Psychological Inquire re mood/affect, emotions, fears, cognitive state, coping mechanisms,

256
symptoms unresolved issues.
Decision-making Evaluate global and decision-specific capacity. Begin advance-care planning
capacity discussions.
Social Evaluate the family, community, financial, and environmental circumstances
assessment that are affecting the patient.
Spiritual Inquire about personal meaning and value of the patient's life and illness, faith,
assessment religious denomination, and desired pastor services.
Determine caregiver, dependent, domestic, and residential needs, and how these
Practical needs
will change as the patient's illness progresses.
Determine caregiver, dependent, domestic, and residential needs, and how these
Death planning
will change as the patient's illness progresses.

Table: Options for the Management of Common Problems at the End of Life. (From
Essential Evidence, 2011 December)

Nonpharmacologic
Problem Prevalence Pharmacologic Options
Options
Nonopioids (eg, acetaminophen 4 g/d,
Massage, positioning, ibuprofen 1600 mg/d), advanced to
transcutaneous electrical mild opioids (eg, codeine 30 mg every
nerve stimulation, 4 hours or hydrocodone 5 mg every 4
Pain 35%-96% physical therapy, hours), or stronger opioids (eg,
chiropractic therapy, morphine 5-10 mg every 4 hours), as
acupuncture, hypnosis, needed; calcitonin; antidepressants;
spiritual practices, prayer anticonvulsants; nerve blocks;
radiotherapy; radiofrequency ablation
Stool softeners (eg, sodium docusate
300-600 mg/d oral); stimulant laxatives
(eg, prune juice 1/2-1 glass/d, senna 2-
Increasing fiber and
Constipation 15%-90% 4 tablet/d, bisacodyl 5-15 mg/d orally
fluids; increasing activity
or per rectum); osmotic laxatives (eg,
lactulose 15-30 mL every 4 to 8 hours,
magnesium hydroxide 15-30 mL/d)
Opioids (eg, codeine 30 mg every 4
hours, morphine 5-10 mg every 4
Dyspnea > 60% Pulmonary rehabilitation hours); anxiolytics (eg, lorazepam 0.5-
2 mg oral/sublingual/IV, diazepam 5-
10 mg oral/IV)
Decreasing or increasing Glucocorticoids (eg, dexamethasone 2-
activity; discontinuing or 4 mg per day); stimulants (eg,
Fatigue 40%-75% changing medications; dextroamphetamine 5-10 mg oral up
reducing sleep 20 mg); modafinil 100-200 mg up to
disturbances; acupuncture 400 mg/day
Depression 5%-26% Counseling; exercise; Antidepressants (eg, fluoxetine 10
music therapy mg/d and increase as needed);
psychostimulants (eg,
dextroamphetamine or
methylphenidate 2.5-5 mg twice daily)

257
 if rapid onset of action needed
Neuroleptic (eg, haloperidol 0.5-5 mg
Gentle reassurance;
oral/subcutaneous/IM/IV q1-4h,
reorientation; safety
risperidone 1-3 mg every 12 hours);
Delirium 20%-30% precautions; aide
anxiolytic (eg, lorazepam 0.5-2 mg
presence; reducing
oral/IM/IV); anesthetic (propofol 0.3-2
medications
mg/hour continuous infusion)
Progestogens for cancer patients (eg,
Eating with family
megestrol acetate 400-800 mg);
Anorexia/cachexia 70% members; taste of food
corticosteroids (eg, dexamethasone up
helpful
to 4 mg/day)
Offer ice chips and small
Hypodermoclysis (subcutaneous
Dehydration 62% amounts of fluid as
infusion of fluids)
tolerated; lubricate lips
Metoclopramide 20 mg or 0.5 mg/kg
orally; scopolamine patch every 72
hours; promethazine 25 mg oral or
rectal every 4-6 hours or 12.5-25 mg
Nausea and High protein meals with
IV/IM every 4-6 hours;
vomiting (late 13%-68% ginger; acupuncture point
diphenhydramine 25-50 mg oral/IM/IV
stage) stimulation wristband
every 4-6 hours; 5-HT3 blockers (eg,
ondansetron 8 mg or 0.15 mg/kg IV
once, prechemotherapy & 16-24 mg
orally once, prechemotherapy);

4. In patients with pain, manage it (e.g., adjust dosages, change analgesics) proactively
through:
- frequent reassessments.
- monitoring of drug side effects (e.g., nausea, constipation, cognitive impairment).

Approximately 71% to 100% of patients can achieve pain control by following the WHO
ladder guidelines. The ladder starts with the use of non-opioid analgesics for mild pain --
> weak opioids for moderate pain --> strong opioids for severe pain.

Table: Pain Management (from 2007 Clinical Practice Guidelines, VCH Community
Palliative Care)

If uncontrolled, r/a
Evaluation
daily.
Titration -Consider for all pts Timing of when to titrate depends on type of regular med in
experiencing use: (*BTD = breakthrough doses
uncontrolled pain. Short-acting Regular Titrate q24h, if >2-3 BTD* used in
Dose the last 24h
-Best to titrate with IR Long-acting Regular Titrate q48h, if >2-3 BTD per day
meds when possible. dose used in the last 48h
Fentanyl patches Titrate q48-72h, if >2-3 BTD per

258
 day used in the last 48-72h
Once pain is well-
Note: switching from an opioid-->methadone is complex &
Conversion controlled, covert to a
requires specialist consultation
long acting formula
Equianalgesic Dose Table
Oral Parenteral
Reasons for switching: Drug Examples
dose Dose
2x T3's approx =
- lack of efficacy Codeine 200mg n/a
morphine 10mg PO
- intolerable side effects
oxycodone 10mg po
Oxycodone 10mg n/a
= morphine 20mg PO
Switching - change in patient
morphine 10mg PO =
status Morphine 20mg 10mg
hydromorph 2mg PO
- practical
considerations (pt hydromorph 1mg PO
Hydromorphone 4mg 2mg
preference, route of = morphine 5mg PO
admin) Use as per
Fentanyl patch manufacturer's
guidelines

(from pre-existing CCFP document):

Opioid Dosage adjustment Opioid Rotation

-calculate daily dose by adding regular + -for escalating pain despite escalating dose
breakthrough doses
-for opioid neurotoxicity (delerium, myoclonus,
-adjust dose by 10-25% of daily dose (not difficult for pt to locate pain)
possible at low doses) -Conversion: determine equianalgesic dose of the 2
-typical dose adjustment program, mg opioids
morphine: Day 1: full dose old opioid, no new opioid
Day 2: lower old opioid by 1/3, add 1/3 dosc new
- 5-10-20-30-40-50-60-80-100-120- opioid
150-180-220 Day 3: lower old opioid by 2/3, add 2/3 dose new
opioid
- re-assess dose change efficacy q12-24hrs Day 4: no more old opioid, add full dose new opioid

5. In patients diagnosed with a terminal illness, identify and repeatedly clarify wishes about
end-of-life issues (e.g., wishes for treatment of infections, intubation, dying at home)

Table: Assessment should include the following (from Medical Care of the Dying, per
pre-existing CCFP document):

Advanced Directives Home Death

- which person you want to make - clarify well ahead with pt/family, whether or not pt intends
health care decisions for you when to die at home
you can’t

259
 -if home death intended: use advanced directives which
- the kind of medical treatment you
clearly states DNR, and ensure both physician & pt signs
want/don’t want
-ensure both family and any on-call physicians do not call for
- how comfortable you want to be
ambulance
- how you want people to treat you
-involved physician or nurse should proceed immediately to
- what you want your loved ones to
the home when notified, to pronounce death and assist family
know
with further arrangements

Parkinsonism - Key Features

1 In patients with suspected Parkinson’s disease, accurately distinguish idiopathic Parkinson’s

disease from atypical Parkinson’s disease (e.g., disease at a young age, drug-related disease),
as treatment differs.

2 In the care of all patients with Parkinson’s disease, involve other health care professionals to
enhance the patient’s functional status.

3 In an elderly patient with a deterioration in functional status, look for and recognize
Parkinson’s disease when it is present, as it is a potentially reversible contribution to the
deterioration.

4 In a patient with a tremor, do an appropriate physical examination (e.g., observation, use of

techniques to enhance the tremor) to distinguish the resting tremor of parkinsonism from other
(e.g., essential) tremors.

5 As part of the management of patients with Parkinson’s disease, identify anticipated side
effects of medications, especially those with which you are unfamiliar.

6 As part of the ongoing follow-up care of patients with Parkinson’s disease:

- Assess functional status.
- Monitor them for medication side effects.
- Look for other problems (e.g., depression, dementia, falls, constipation), as they are more
common

Presentation
• TRAP - any 2 of Tremor, Rigidity, Akinesia/bradykinesia, Postural instability
• Parkinsonʼs Disease

• Clinical Diagnosis
• Cardinal S&S: Distal Resting Tremor (3-6Hz, pill-rolling); Rigidity; Bradykinesia;
Asymmetrical onset
• Additional S&S: Difficulty turning over in bed, opening jars, rising from a chair; Poor
heel-to-toe gait; Shuffling gait; Loss of balance; Micrographia; Loss of olfaction
• Therapeutic Challenge: adequate response to levodopa trial

Differential Diagnosis
• Symptoms Suggesting Alternate Diagnosis: Lack

260
of Levodopa response, hallucinations, prominent/early dementia, early postural instability, severe
& early autonomic dysfunction, upward gaze paralysis, involuntary mvmts (other than tremor)

Investigations
• Physical Examination of Tremor
• Resting Tremor - seen w hand resting in lap
• Need to distinguish from Kinetic Tremor (occurs w mvmts) & Postural Tremor (limb is held
against gravity)
• LOOK: Observe (1) Hands in lap/arms at sides, (2) Extend arms to do finger-to-nose test, (3)
Perform tasks (drink from glass, write/draw)

• Classify: Involved body part (arms, head), When tremor present (rest, intention),
Frequency (fast/slow), Amplitude (fine/coarse)
• (4) Stand & Walk - difficulty initiating mvmt, dec arm swing, shuffling gate

• FEEL/MOVE: Rigidty & Bradykinesia - flex/ext arms, cog wheeling?

261
• CT or MRI - if diagnosis of idiopathic PD is uncertain and other diagnoses are being considered

Management
• Goal: maximize ptnt autonomy & QOL; Initiate therapy at onset of functional impairment
• United Parkinsonʼs Disease Rating Scale (UPDRS) - standardized assessment tool; Measures
(1) mental effects, (2) ADL limitations, (3) motor impairment, (4) treatment/disease
complications (see below).
• Assessing Functional Status

262
263
Periodic Health Assessment/Screening - Key Features

1. Do a periodic health assessment in a proactive or opportunistic manner (i.e., address health

maintenance even when patients present with unrelated concerns).

2. In any given patient, selectively adapt the periodic health examination to that patient’s
specific circumstances (i.e., adhere to inclusion and exclusion criteria of each

264
manoeuvre/intervention, such as the criteria for mammography and prostate-specific antigen
[PSA] testing).

General Population [by grade of evidence] Specific Population

Dental hygiene (fluoridation, brushing,
flossing) [A]

Noise control and hearing protection

Peds: developmental milestones [B]
Smokers: counsel on cessation,
home visit for high risk family [A]
provide: NRT, referral to smoking
Adolescents: counsel on sex and
cessation program, dietary advice on
contraception [B], counsel to prevent
leafy green veggie and fruits [A]
Discussion smoking initiaton
Perimenopausal women: osteoporosis
Seat belt use [B] & risks/benefits of HRT [B]
Injury prevention, smoke detectors, bike Adults >65: cognitive impairment,
helmets [B] Multi-disciplinary post-fall assessment
Moderate Physical Activity [B] [A]
Sun exposure, protection [B]
Problem drinking [B]
STI prevention counseling [B]
Dietary advise on fat and Cholesterol [B]
Peds: repeat hips, eyes, hearing (esp
in first year) [A]
Serial heights, weight, and HC
[B]
Clinical breast exam (women 50-69) [B]: no Visual acuity after age 2 [B]
longer recommended 2011
PE Adults>65: Visual acuity [B]
BP measurement [B]
BMI measurement in obese [B] Hearing testing (otoscope,
whisper test, inquire) [B]

1st Degree Relative with Melanoma:

full body skin exam
Colon cancer screening
Stool Occult blood (FIT preferred) q1-
2 yrs (50-74 yrs, no known risk factor):
sensitivity 5%
Flexible sigmoidoscopy: > 50 yr, Not to screen > 74 yrs old unless
Tests
average risk, or combined with FOBT specific indications
Air contrast barium: no role
Colonoscope: 50-74yr high risk factor
q 5-10 yrs [B] -strong fx:one 1st
degree relative
Tests Women: mammography (50-74)q 2-3 yrs [A] Peds: hgb for high risk infants [B]
Blood lead screening for high
Pap smear: all girls > 9 yr should have HPV risk infants [B]
vaccines. 20 – 69 yrs, annually 3, every 2 yrs if

265
 Diabetics: fundsocopy [B]

Urine micro alb (annual)

normal x 3 yrs. Hgb AIC (q 3 month)
Blood Chol for men >40 or post-menopausal
women TB high risk: mantouz skin test [A]
Serum Glucose q 3yrs or more frequent if risk- STI high risk: voluntary HIV screen
factors [A]
Bone mineral density: screen if 1 major or 2
minor risk factors Gonorrhea screen [A]
PSA screening not established. But if fx of P ca Chlamydia screen [B]
or African descent, start ageg 40 yr
FAP: sigmoidoscopy and genetic
testing [B]
HNPCC: colonoscopy [B]
Peds: routine immunz [A]

Folic acid supplementation for women of child Hep B immuniz [A]

bearing age [A] Influenza high-risk or >65: immuniz
[A] now for all 2011
Varicella vax for children 1-12 [A] Pneumonia high-risk or >65:
Therapy Rubella vax for all non-pregos of child-bearing pneumoncoccal vax [A]
age [B] TB high-risk: INH prophylaxis for
Tetanus vaccine q 10 yrs household contacts/skin test
Pertussis booster once during adulthood. Can converters [B]
be given as dTap.
INH prophylaxis for high-risk
sub-groups

3. In a patient requesting a test (e.g., PSA testing, mammography) that may or may not be
recommended:
a) Inform the patient about limitations of the screening test (i.e., sensitivity and specificity).
b) Counsel the patient about the implications of proceeding with the test.

PSA – sensitivity is ~80% & Specificity is ~70% at cut off of 4.0 (SN increased with higher cut
off, serial testing and in conjunction with DRE)

Mammography – sensitivity 75-90% and specificity 90-95% over age of 50. Very high false
positive rate in women under age 50. The NNS to prevent one death from breast cancer for
women aged 40–49 years is 2108, as compared with 721 for women aged 50–69 years. In
addition, the risk of a false-positive result from mammography is higher for women younger than
50 years. Thus, screening about 2100 women aged 40–49 years once every 2–3 years for about 11
years would prevent a single death from breast cancer, but it would also result in about 690
women having a false-positive result on a mammogram, leading to unnecessary follow-up testing,
and 75 women having an unnecessary biopsy of their breast

Pap smear: False negative 10-40% for single test, false positive 5-10 %.

266
Stool occult blood: Sensitivity of FOBT has been shown to range from 12% (any neoplasia) to
36% (high grade neoplasia). The positive predictive value (probability that a person with a
positive test has neoplasia) was 54% for any neoplasia, and 40% for advanced neoplasia; the
negative predictive value (probability that a person with a negative test does not have neoplasia)
was 64% and 88% respectively.

HPV: prevent up to 70% of cervical cancer

4. Keep up to date with new recommendations for the periodic health examination, and
critically evaluate their usefulness and application to your practice.

See Periodic Assessment form from CFPC website below. Dec 2010 updated

Personality Disorder - Key Features

1. Clearly establish and maintain limits in dealing with patients with identified personality
disorders. For example, set limits for:
- appointment length.
- drug prescribing.
- accessibility.

2. In a patient with a personality disorder, look for medical and psychiatric diagnoses when the
patient presents for assessment of new or changed symptoms. (Patients with personality
disorders develop medical and psychiatric conditions, too.)

3. Look for and attempt to limit the impact of your personal feelings (e.g., anger, frustration)
when dealing with patients with personality disorders (e.g.,stay focused, do not ignore the
patient’s complaint).

4. In a patient with a personality disorder, limit the use of benzodiazepines but use them
judiciously when necessary.

5. When seeing a patient whom others have previously identified as having a personality
disorder, evaluate the person yourself because the diagnosis may be wrong and the label has
significant repercussions.

DSM-IV-TR Definition
o An enduring pattern of inner experience and behaviour that deviates markedly from the
expectations of the individuals culture. Manifested in 2 or more of the following areas:

• Cognition
• Affectivity
• Interpersonal functioning
• Impulse control

o Enduring pattern is inflexible across a broad range of personal and social situations
o Leads to clinically significant distress or impairment in social, occupational or other important

267
areas of functioning
o Pattern is stable and of long duration and can be traced back at least to adolescence or early
adulthood
o Not better accounted for by another mental disorder, general medical condition or substance
effect.
Coded on Axis II.
Patients often lack insight regarding the connection between their behaviors and interpersonal
difficulties
More common in males, the young, poorly educated, and unemployed
Highly comorbid with Axis I disorders

Personality disorders are divided into 3 clusters

o Cluster A: Appears odd and eccentric – “mad”

• Paranoid
• Suspects others are exploiting, harming or deceiving them, doubts trustworthiness of
others, interprets benign remarks as demeaning, bears grudge, concerned of partners
fidelity
• Treatment - psychotherapy
• Schizoid
• Neither desires nor enjoys close relationships, isolated, chooses solitary activities;
indifferent to praise or criticism, emotional detachment
• Treatment - psychotherapy
• Schizotypal
• Odd beliefs/thinking/speech pattern, eccentric behavior, unusual perceptual experience
• Treatment - psychotherapy, social skills training, low-dose anti-psychotics

o Cluster B: Dramatic, emotional, and erratic – “bad”

• Borderline
• Frantic efforts to avoid abandonment, unstable relationships, impulsivity, affective and
emotional instability, self-harm/suicidal behaviour, chronic feelings of emptiness
• Use of Splitting as defense mechanism
• Treatment - psychotherapy, group psychotherapy, CB, dialectical behavioural therapy,
low dose anti-psychotics/anti-depressants
• Antisocial
• Criminal, aggressive, irresponsible behavior, lack of remorse, symptoms of conduct
disorder before age 15
• Treatment – Support groups, behaviour control, control of substance abuse
• Narcissistic
• Exaggerated sense of self-importance, believes they are special, preoccupied with
fantasies of unlimited success, power, beauty, love
• Treatment - psychotherapy
• Histrionic
• Not comfortable unless center of attention, dramatic/exaggerated expression of
emotions, inappropriately sexually seductive
• Treatment - psychotherapy

268
o Cluster C: Anxiety, fearfulness, constricted affect – “sad”

• Avoidant
• Avoids activities and interpersonal contact due to fear of criticism or rejection, views
self as inferior.
• Treatment – psychotherapy, CBT, systematic desensitization, assertiveness training
• Dependent
• Needs others to assume responsibility for most areas of life and decision-making
• Treatment – psychotherapy, CBT, group therapy, assertiveness training, social skills
training
• Obsessive-Compulsive
• Perfectionism interferes with task completion, pre-occupied with details, inflexible
morals, reluctant to delegate, excessively devoted to work.
o In OCPD symptoms are ego-syntonic (person is unaware of abnormal traits and
consistent with their way of thinking.
o In OCD symptoms are ego-dystonic (realizes the obsessions are not-reasonable).
• Treatment – psychotherapy, group therapy, CBT

General Management for PD

o Develop a treatment plan early on
o Treatment may involve combination of:

• Individual therapy
• Group therapy
• Self-education
• Substance abuse treatment
• Medication
• Hospitalization at times of crisis

o Compliance with treatment plans is often an issue

o Clearly establish and set limits in dealing with patients with identified personality disorder eg.

• Appointment length
• Drug prescribing
• Accessibility

o Look for medical and psychiatric diagnoses when the patient presents for assessment of new or
changed symptoms (patients with PD develop medical and psychiatric conditions too).
o Limit the use of benzodiazepines, but use them judiciously when necessary.
o When seeing a patient whom others have previously identified as having PD, evaluate the
person yourself because the diagnosis may be wrong and the label has significant repercussions.
o Be aware of counter-transference in doctor-patient relationship

Pneumonia - Key Features

Community-Acquired Pneumonia (CAP) – pneumonia contracted in the community, specifically

not in a hospital or a long-term care facility.

269
Healthcare-Associated Pneumonia (HAP) (hospital-acquired pneumonia) – pneumonia
contracted by a patient meeting any of the following criteria:

• admitted to a hospital for ≥2 days in the preceding 3 months

• living in a long-term care facility
• treated with IV antibiotics, dialysis, chemotherapy or wound care in the preceding
month
• has a family member infected with a multidrug-resistant pathogen

1. In a patient who presents without the classic respiratory signs and symptoms (e.g.
deterioration, delirium, abdominal pain), include pneumonia in the differential diagnosis.

In otherwise healthy adults, the classic symptoms of pneumonia include new onset cough
(productive or non-productive, pathogen-dependent), fever/chills/rigours, dyspnea, and pleuritic
chest pain. The classic physical exam findings (tachypnea, respiratory crackles, bronchial breath
sounds, dullness to percussion, and increased vocal fremitus) are definitely suggestive of a focal
pneumonia but are neither sensitive nor specific. While the absence of fever or
crackles/consolidation findings on physical exam makes a significant lobar pneumonia unlikely,
their absence does not rule out bronchopneumonia or small focal pneumonias. No combination of
signs and symptoms has been found to rule in or out pneumonia with any certainty.

Non-classic symptoms of pneumonia can include new onset mental confusion (especially in the
elderly), GI upset (nausea, vomiting and diarrhea), headache, fatigue, and myalgias. The elderly
are more likely to present with non-classic symptoms, and often do not mount a fever or elevated
WBC count in response to infection. In addition, it is not uncommon for children with pneumonia
to present with predominantly GI symptoms.

2. In a patient with signs and symptoms of pneumonia, do not rule out the diagnosis of a
normal chest X-ray film (e.g., consider dehydration, neutropenia, human immunodeficiency
virus [HIV] infection).

Chest X-ray remains the gold standard for diagnosing pneumonia in both adults and children.
There is level II evidence recommending that all adult patients in whom pneumonia is suspected
should have a chest X-ray to confirm the diagnosis. However, it is often argues that only children
in respiratory distress necessitate a confirmatory chest X-ray.

False negative chest X-rays can occur, especially in patients with dehydration, severe
neutropenia, PCP pneumonia, HIV, or in the first 24 hours of infection, false negative chest X-
rays are possible.

3. In a patient with a diagnosis of pneumonia, assess the risks for unusual pathogens (e.g., a
history of tuberculosis, exposure to birds, travel, HIV infection, aspiration).

The most common pathogen for community-acquired pneumonia in adults is Streptococcus

pneumonia (>50% of bacterial pneumonia cases). Haemophilus influenza, Mycoplasma and
Chlamydia pneumoniaes are not uncommon causes of CAP. Note, however, that the specific
bacterial pathogen is identified in <50% of cases.

270
Healthcare-associated pneumonia (or hospital-acquired pneumonia) may be caused by multiple
varying pathogens and polymicrobial infections are not uncommon. The most common HAP
pathogens are Staph aureus, Strep pneumonia, Klebsiella, Acinetobacter, and Pseudomonas. In
addition, these patients are at increased risk of multidrug resistant infection, most commonly
MRSA and drug-resistant Strep pneumoniae (DRSP).

In children, age is the best predictor of bacterial pneumonia pathogen though as with adults, the
responsible pathogen is not identified in 40 – 60% of cases. Viruses are the most common cause
of pneumonia in children under 2 years of age, while in school-aged children, pneumonia is
mostly commonly due to Strep and Mycoplasma pneumoniaes.

Elderly patients are at increased risk of having tuberculosis (especially those living in long-term
care facilities), multi-drug resistant and gram negative organisms (especially elderly patients with
decreased functional status and/or with multiple comorbid conditions). Patients with decreased
level of consciousness for any reason are at risk of aspirating and thereby developing aspiration
pneumonia (usually anaerobic pathogens) and/or chemical pneumonitis.

It is important to inquire about the patient’s travel history (e.g. possible risk of tuberculosis,
fungal infection, etc) and living/working environment (e.g. risk of Legionella pneumophila in
patients exposed to contaminated air conditioning, hot tubs, humidifiers, etc. or risk of Coxiella
burneii in patients exposed to infected farm animals). Past medical history is also very important
to consider as specific co-morbidities make patients susceptible to more uncommon pneumonia
pathogens (e.g. patients with HIV are at increased risk of PCP pneumonia, COPD increases the
risk for Haemophilus influenzae and Moraxella catarrhalis, and bronchiectasis increases the risk
for Pseudomonas aeruginosa infection.

Finally, in addition to HAP, numerous factors increase a patient’s risk of infection with multi-
drug resistant bacteria. Risk factors for MRSA infection include

• homelessness
• incarceration
• IV drug abuse
• First Nations persons living on reserves
• healthcare workers
• recent hospitalization (even admissions that don’t meet criteria for HAP)

Risk factors for DRSP include

• age >65 years

• antibiotic use within the preceding 3 months
• exposure to children attending daycare facilities
• co-morbid conditions including (but not limited to) pulmonary, cardiac, renal or liver
disease; alcoholism; diabetes; malignancy; immunosupression; etc.

4. In patients with pre-existing medical problems (e.g., asthma, diabetes, congestive heart
failure) and a new diagnosis of pneumonia:
a) Treat both problems concurrently (e.g., with prednisone plus antibiotics).

271
It is important to consider the effect the pre-existing condition may have on the pneumonia and
the effect the pneumonia may have on the pre-existing condition. For example, asthma and
COPD increase the risk of developing pneumonia and may prolong the course or worsen the
severity of pneumonia. On the other hand, infection and the resulting cough both act to inflame
the airways, thereby worsening the patient’s asthma/COPD symptoms. Thus, successful treatment
of the pneumonia (with antibiotics) necessitates effective treatment of the asthma flare (usually
with steroids).

b) Adjust the treatment plan for pneumonia, taking into account the concomitant medical
problems (e.g., be aware of any drug interactions, such as that between warfarin [Coumadin]
and antibiotics).

Antibiotics used in the treatment of pneumonia (macrolides, penicillins, and fluoroquinolones)

can enhance the anticoagulant effects of warfarin. It is recommended that patients on warfarin
undergo increased INR/PT monitoring when starting on or changing the dose of these antibiotics.

Macrolides and fluoroquinolones must not be given to patients on QTc-prolonging medications as

there is moderate to severe increased risk of QTc-prolongation and/or serious arrhythmias in
these patients. Both antibiotic families also decrease the absorption of typhoid vaccine (thereby
diminishing its therapeutic effect) and thus concomitant use should be avoided.

Amoxicillin and several common medications interact to increase or decrease serum

concentrations of one or both medications, increasing the risk of either toxic effects and/or
diminishing the therapeutic effectiveness of these medications. Examples of medications that can
diminish the therapeutic effectiveness of amoxicillin include fusidic acid and tetracycline
derivatives while Probenecid increases amoxicillin serum concentrations. Amoxicillin is known
to increase serum concentrations of methotrexate and vitamin K antagonists (warfarin) while it
decreases the serum concentrations of estrogen contraceptives (minor), mycophenolate, and
typhoid vaccines.

(*Please note, the above lists are in no way exhaustive.*)

5. Identify patients, through history-taking, physical examination, and testing, who are at high
risk for a complicated course of pneumonia and would benefit from hospitalization, even
though clinically they may appear stable.

There is no substitute for physician impression and judgement, and a decision whether or not to
hospitalize a patient must take into account subjective factors such as a patient’s living
conditions, availability of support, compliance with medications, and ability to return for follow-
up care. That being said, several severity-of-illness tools are available to assist physicians in
deciding on whether to hospitalize a patient or treating them as an outpatient. Many of these
tools/calculators require several lab test results which are often not immediately available in the
GP’s office [ex. the Pneumonia Severity Index (available at
http://pda.ahrq.gov/clinic/psi/psicalc.asp) and the CURB-65 tool). A reliable severity tool that
does not require immediate lab results is the modified CURB-65 tool. The Confusion, Respiratory
rate, Blood pressure, age >65 years (CRB-65) tool has been validated in the primary care setting.
The following table (from the May 2009 McMaster Module, “Pneumonia in Adults”, © The
Foundation of Medical Practice Education, www.fmpe.org) explains the tool.

272
Thus, hospitalization should be considered for any patient with a CRB-65 score of ≥1.
Hospitalization is indicated in patients with a score ≥3, are unable to take oral medications and/or
are hypoxic (Sp02 <90%).

6. In the patient with pneumonia and early signs of respiratory distress, assess, and reassess
periodically, the need for respiratory support (bilevel positive airway pressure, continuous
positive airway pressure, intubation) (i.e., look for the need before decompensation occurs).

There are several major and minor criteria that help to identify the patient who is at increased risk
of requiring respiratory support and/or ICU admission. These criteria are as follows:
Major Criteria

• invasive mechanical ventilation

• septic shock requiring vasopressors

Minor Criteria

• respiratory rate ≥30

• temperature <36⁰C
• hypotension requiring aggressive fluids or vasopressors
• new-onset confusion or disorientation
• multilobar infiltrates
• PaO2/FiO2 ≤250
• urea >7 mmol/L
• WBC <4
• platelets <100

Patients with 1 major or ≥3 minor criteria likely require ICU admission. Respiratory support
(including BiPAP, CPAP, and intubation) should be considered whenever a patient is in
respiratory distressed or hypoxic (Sp02 <90) and respiratory support should be initiated
(wherever possible) before decompensation occurs.

7. For a patient with a confirmed diagnosis of pneumonia, make rational antibiotic choices
(e.g., outpatient + healthy = first-line antibiotics; avoid the routine use of “big guns”).

273
A. As Strep pneumoniae is the single most common cause of pneumonia in adults, approach to
treatment is determined by a patient’s risk for -resistant Strep pneumoniae (DRSP).

Adults with Community-Acquired Pneumonia (Outpatient Treatment):

• For otherwise healthy adults who are at low risk of multi-drug resistant infection should
be treated with a macrolide (clarithromycin, azithromycin, or erythromycin). Patients
who cannot tolerate a macrolide should be treated with doxycycline or a respiratory
fluoroquinolone (moxifloxacin, levofloxacin, or gemifloxacin).
• Adults who are at increased risk for drug-resistant DRSP should be treated with either a
respiratory fluoroquinolone or combined therapy with a ß-lactam (amoxicillin or
amoxicillin/clavulanate) AND a macrolide.
• Patients at high risk for MRSA should have vancomycin or linezolid in addition to the
above antibiotic regime.

Adults with Community or Healthcare-Acquired Pneumonia (Inpatient Treatment):

• Hospitalized patients at low risk for DRSP or MRSA should receive monotherapy or
either a respiratory fluoroquinolone or the combination of a ß-lactam (in this case
ampicillin, ceftriaxone or cefotaxime) AND a macrolide.
• Hospitalized patients who are at increased risk for DRSP should receive combination
therapy of
1) a ß-lactam (in this case piperacillin-tazobactam) or an antipseudomonal cephalosporin
(cefepime or ceftazidime) or an antipseudomonal carbapenem (imipenem or meropenem)
AND
2) an antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin) or both
azithromycin and an aminoglycoside.
• Patients at high risk for MRSA, in addition to the above regime, should receive
3) vancomycin or linezolid

Adults with Inpatient ICU-Treated Pneumonia:

• Patients at low risk for DRSP should receive combination therapy with
1) a ß-lactam (in this case ceftriaxone or cefotaxime) AND
2) azithromycin or a respiratory fluoroquinolone
• Patients who are at high risk for DRSP should receive combination therapy with
1) a ß-lactam (in this case piperacillin-tazobactam) or an antipseudomonal cephalosporin
or an antipseudomonal carbepenem AND
2) an antipseudomonal fluoroquinolone or both azithromycin and an aminoglycoside
• Patients at high risk for MRSA, in addition to the above regime, should receive
3) vancomycin or linezolid
• Penicillin-allergic patients who are at low risk for DRSP should be treated with a
respiratory fluoroquinolone AND an aminoglycoside (as well as vancomycin or linezolid
if they are at increased risk for MRSA)

274
B. Since the most common pathogens in pediatric pneumonia change with a child’s age, the
approach to treatment also changes with the child’s age.
Children with Community-Acquired Pneumonia (Outpatient Treated):

• 3 months – 5 years:
o amoxicillin or
o a macrolide (if ß-lactam allergic)
• >5 years:
o a macrolide or
o doxycycline (if >8 years)

Children with Community or Hospital-Acquired Pneumonia (Inpatient Treated):

• 1 – 3 months (pneumonitis syndrome)

o a macrolide
• 1 – 3 months (bacterial pneumonia – consider referral)
o cefuroxime
• 3 months to 5 years
o cefuroxime
• >5 years
o cefuroxime and
o a macrolide (azithromycin or erythromycin only)

Critically Ill Children with Pneumonia: (*consider referral*)

• 1 – 3 months (pneumonitis syndrome)

o a macrolide (azithromycin or erythromycin only)
• 1 – 3 months (bacterial pneumonia)
o cefuroxime or
o cefotaxime and cloxacillin
• 3 months – 5 years
o cefuroxime and erythromycin or
o cefotaxime and cloxacillin
• >5 years
o azithromycin or
o cefuroxime and erythromycin

8. In a patient who is receiving treatment for pneumonia and is not responding:

a) Revise the diagnosis (e.g., identify other or contributing causes, such as cancer, chronic
obstructive pulmonary disease, or bronchospasm), consider atypical pathogens (e.g.,
Pneumocystis carinii,TB, and diagnose complications (e.g., empyema, pneumothorax).

Most patients are expected to improve clinically within the first 3 days of starting appropriate
antibiotic therapy. If a patient deteriorates or shows no improvement within 72 hours of treatment
initiation, it is important to consider the following possibilities:

275
 • incomplete antibiotic coverage
o atypical pathogen (TB, fungal infection, etc.)
• antibiotic-resistant organism
• parapneumonic effusion
• empyema
• pneumothorax
• undiagnosed underlying condition (e.g. in children, cystic fibrosis; in adults,
malignancy)
• incorrect diagnosis
o pulmonary embolus
o congestive heart failure
o foreign body aspiration
o chest wall pathology, etc.

b) Modify the therapy appropriately (e.g., change antibiotics).

Consider expanding the spectrum of antibiotic coverage, repeating the chest X-ray, investigating
further (e.g. blood and/or sputum cultures for atypical organisms), etc.

9. Identify patients (e.g., the elderly, nursing home residents, debilitated patients) who would
benefit from immunization or other treatments (e.g., flu vaccine, Pneumovax, ribavarine) to
reduce the incidence of pneumonia.

PNEUMOCOCCAL VACCINE:
The Public Health Agency of Canada currently recommends the pneumococcal vaccine in the
following situations:
Children

• all children age ≤23 months

• children age ≥24 months who have not previously received the vaccine and who have
any of the following risk factors for invasive pneumococcal disease:
o functional or anatomic asplenia
o sickle cell disease
o HIV
o primary immunodeficiency
o malignancy
o immunosuppressive therapy
o solid organ transplant
o nephritic syndrome
o chronic cardiac, renal, hepatic, or pulmonary disease
o bronchopulmonary dysplasia
o diabetes
o CSF leak
o First Nations children
o children attending daycare facilities

Adults

276
 • age ≥65 years
• current smokers
• cirrhosis
• alcoholism
• unknown immunization history
• any of the risk factors for IPD listed above (for children ≥5 years)

INFLUENZA VACCINE:
As influenza complications (including secondary bacterial pneumonia) are a significant cause of
morbidity and mortality, the Public Health Agency of Canada currently recommends a yearly
influenza vaccine to people who meet any of the following criteria:

• adults age ≥65 years

• healthy children age 6 – 23 months
• residents of long-term care facilities
• health care workers
• household contacts of
o children <6 months of age
o people at increased risk of influenza complications or IPD
• people with chronic medical conditions requiring regular medical care

All patients should be counselled on the importance of hand washing to prevent the spread of
viral infections that can predispose to pneumonia. As smoking is the strongest independent risk
factor for IPD, counselling and support for smoking cessation and avoidance of second-hand
smoke are critical for pneumonia prevention.

10. In patients with a diagnosis of pneumonia, ensure appropriate follow-up care (e.g., patient
education, repeat chest X-ray examination, instructions to return if the condition worsens).

Patients must be counselled on signs and symptoms of illness progression and when to return to
clinic and/or go proceed to the local emergency department. Patients should be seen in follow-up
in any of the following is true:

• illness progression despite antibiotic therapy

• no improvement within 72 hours of antibiotic initiation
• patients nearing the end of their antibiotic course who have not achieved at least two of
the following sings of clinical stability:
o temperature ≤37.8oC for at least 48 – 72 hours
o heart rate <100
o respiratory rate ≤24
o systolic blood pressure ≤90
o arterial oxygen saturation ≥90% or PO2 ≥60mmHg on room air
o ability to tolerate oral intake
o return to baseline mental status

277
11. In patients with a confirmed diagnosis of pneumonia, arrange contact tracing when
appropriate (e.g., in those with TB, nursing home residents, those with legionnaires’ disease).

All confirmed cases of the following infections are nationally-reportable:

• Tuberculosis
• Legionella
• invasive Group A Strep (Strep pyogenes)
• laboratory-confirmed Influenza
• Hantavirus Pulmonary Syndrome
• Severe Acute Respiratory Syndrome (SARS)

In addition, contact tracing for either close monitoring and/or prophylactic treatment should be
done for all patients with pneumonia confirmed to be caused by any of the above pathogens.
Contacts include anyone who has been exposed to the patient in the time period from one week
prior to the patient’s symptom onset to 24 hours after the patient has started appropriate
antimicrobial therapy and who has any of the following relationships with the patient:

• co-residents of long-term care facilities

• co-attendants of child care centres,
• IV drug users who have shared needles with the patient
• sexual partners or share the same bed with the patient
• household contacts who have spent an average of >4 hours/day with the patient
• anyone who has had direct mucous membrane contact with the oral or nasal secretions
or direct contact with an open skin lesion of the patient.

Poisoning - Key Features

1. As part of well-child care, discuss preventing and treating poisoning with parents (e.g.,
“child-proofing”, poison control number).

• Keep items locked and out of reach/sight. Don’t refer to medicine as “candy”. Keep meds in
their original containers with safety lids, don’t put them in food containers. Don’t take meds in
view of children. More danger of children getting poisoned away from home (ie friends/family).
• Most commonly ingested substances are personal care products, analgesics, and cleaning
products. Most commonly causing fatalities are analgesics, batteries, hydrocarbons, and plants.
• Highly hazardous medications include iron supplements, TCAs, Cardio meds, methyl saliclyate,
hydrocarbons, pesticides, sulfonylureas, CCBs, toxic alcohols, clonidine, and opioids.

2. In intentional poisonings (overdose) think about multi-toxin ingestion.

• Remember, patient’s history is often unreliable – use collateral sources (paramedics, police,
family, friends, pharmacist)
• Remember to ask about OTC meds, family/friends medications that might be in the house.
• Regularly screen over dose patients for presence of Acetaminophen, Salicylates with blood
work
• Urine drug screen

278
3. When assessing a patient with a potentially toxic ingestion, take a careful history about the
timing and nature of the ingestion.

• Remember, patient’s history is often unreliable – use collateral sources.

• GI decontamination has greatest benefit within 1 hour of ingestion, however, history often
unreliable. Risk outweighs benefit if truly delayed presentation.
• Ask about past history, chronic meds.
• Assume “worst case scenario”

4. When assessing a patient with a potential poisoning, do a focused physical examination to

look for the signs of toxidromes.

• Focus on vital signs, mental status, pupils (miosis, mydriasis, or nystagmus). Track pulse
oximetry, cardiac monitoring, and ECG findings. Obtain IV access, C-spine stabilization if
trauma suspected. Intubation may be required if patient unable to protect their airway, follow
ACLS protocols. O2 PRN, IV fluids.
• Physiological excitation: mydriasis, tachycardia, hypertension, tachypnea, hyperthermia (caused
by anticholinergics, sympathomimetics, hallucinogens, or drug withdrawl).
• Pysiological depression: miosis, depressed mental status, hypotension, bradycardia, shallow
breathing, hypothermia (caused by cholinergic, sympatholytic, opiates, alcohols, or sedative-
hypnotics.
• Mixed – think polydrug, hypoglycemics, toxic alcohols, heavy metals, antiarrhythmics, TCAs.
• Raised anion gap (Na – (Cl + HCO3) – MUDPILES – Methanol/Metformin, Uremia,
Diabetic/Starvation/Alcoholic Ketoacidosis, Paraldehyde/Poisons, Iron/Isoniazid, Lactic Acidosis
(cyanide, carbon monoxide, sulfides), Ethylene glycol, Salicylates/Sympathomimetics.

5. When assessing a patient exposed (contact or ingestion) to a substance, clarify the

consequences of the exposure (e.g., don’t assume it is non-toxic, call poison control).

6. When managing a toxic ingestion, utilize poison control protocols that are current.

• O2, Naloxone, Thiamine and Glucose for altered LOC. (note, doesn’t matter order of
thiamine/glucose).
• All patients should have Lytes, BUN, Creatinine, Urinalysis, Acetaminophen, Salicylates, and
glucose. Sick patients should add serum osmolality, ketones, creatine kinase, liver function tests,
amylase, calcium, and magnesium. BHCG in sick women of childbearing age. Depending on
patient, can also add ABGs, urine crystals, etc.
• Irrigate with water/saline for topical exposures.
• Activated charcoal for decontamination (1g/kg mixed with water as a slurry). Activated
charcoal superior to ipecac or gastric lavage. Contraindicated in patients with bowel obstruction,
perforated bowel, decreased LOC (until intubated). Hydrocarbons not bound by AC, risks
• Hemodialysis (esp. for salicylates, ethylene glycol, methanol, lithium, acidosis or
hyperkalemia).
• Most patients with toxic ingestions should be observed for 6 hours in the ED. Pts with moderate
to severe toxicity should go to the ICU.
• All patients with overdose require psych risk assessment
• Antidotes:

o Naloxone for opioids

o Flumazenil for benzos

279
 o N-Acetylcystine for Tylenol (based on 4 hour or greater nomogram) Almost 100%
effective if given within first 8-10 hours.
o Urine alkylinization, glucose for ASA, Phenobarbital
o Fomipazole/Ethanol, folic acid, +/- pyridoxine for toxic alcohols

7. When managing a patient with a poisoning,

a) Assess ABC's,
b) Manage ABC's,
c) Regularly reassess the patient’s ABC’s (i.e., do not focus on antidotes and decontamination
while ignoring the effect of the poisoning on the patient).

Pregnancy - Key Features

1. In a patient who is considering pregnancy:

a) Identify risk factors for complications.
b) Recommend appropriate changes (e.g. folic acid, smoking cessation, medication changes)

Risk Modification:

• Advise all women of childbearing age to supplement diet with 0.4mg/day of Folic acid.
(materna has 1 mg/day)
• Iron supplement if anemic, prenatal vitamins
• EtOH, smoking and drug cessation. Review meds/OTC meds.
• Discuss cessation of current form of birth control
• Avoidance of cats/litter/rodents, soft cheeses (listeria)
• Inquire about safety, domestic violence, genetic disease, maternal age, birth defects,
multiple gestation, PmHX (heart conditions, past uterine/cervical procedures, STI's)
• Genetic screening of high risk groups (tay-sachs, sickle cell, thalessemia)

2. In a female or male patient who is sexually active, who is considering sexual activity, or who
has the potential to conceive or engender a pregnancy, use available encounters to educate
about fertility.

Discuss STI's, appropriate forms of contraception, and emergency contraception.

3. In a patient with suspected or confirmed pregnancy, establish the desirability of the

pregnancy.

4. In a patient presenting with a confirmed pregnancy for the first encounter:

a) Assess maternal risk factors (medical and social)
b) Establish accurate dates
c) Advise the patient about ongoing care.

Definitions:
First Trimester = 0-12 wks, Second = 12-28 wks, Third = 28-40wks, Term = 37-42
Gravity = # pregnancies of any gestation, T = # of term infants, P = # premature, A = # of
abortions, L = # of living Children

280
Pre-natal Screening:

• Initial visit: (within 12 weeks of LMP) full Hx, Med review, FMHx, Social Hx, Urine
R+M plus culture, Hgb, Blood type, gestational age, P/E with pelvic and pap, swabs for
GC and Chlamydia, HIV, Hep B & C (if at risk), Syphilis, Rubella titre, toxoplasmosis
(optional), CMV, TB, TSH(optional)
• SIPS vs. IPS (SIPS + NT): Depending on the age(risk) of your patients and their desire
for screening after informed consent. Amniocentisis may be offered after age 40 with no
prior screening (BC Prenatal Genetic Screening Program)
• Gestational DM: screen with glucose tolerance test at 24-28 weeks (2 hour 75g ogtt)
• Group B Strep: screening recto-vaginal swab at 35-37 weeks.
• Third trimester Hgb: screening for anemia, especially if low normal first trimester hgb.

Other:

• Nagele’s rule = 1st day of LMP + 7days – 3 months.

• Most accurate dating is early first trimester U/S (recommended if available)
• Repeat visits q4weeks until 28, q2weeks until 36, qweekly until delivery.
• Inquire about financial concerns, living situation, paternity, abuse, stresses/supports
(don’t forget to FIFE the patient).
• Discuss items in question 1.
• Exercise, work (type/duration), intercourse, weight gain (for pre-pregnancy BMI)

5. In pregnant patients:
a) Identify those at high risk (e.g. teens, domestic violence victims, single parents, drug users,
impoverished women)
b) Refer these high-risk patients to appropriate resources throughout the antepartum and
postpartum periods.

6. In at-risk pregnant patients (e.g. HIV positive women, intravenous drug users, diabetic and
epileptic women), modify antenatal care appropriately.

Diabetes: Insulin for type 1, or type II uncontrolled by diet alone. Diet usually adequate for
GDM. Oral hypoglycemics (especially glyburide) are controversial. Multi-disciplinary approach
with diabetes educators, dieticians, and maternity care provider.

HIV: Fetus at risk of IUGR, pre-term labor or PROM. May deliver vaginally. Combined
retroviral for antepartum decrease risk of transmission to <1%. Discuss risk of transmission with
breast feeding.

Epileptics: For planning a pregnancy, switch to the safest effective anti-convulsant at lowest
dose(avoid valproic acid). If already pregnant, continue with same anti-convulsant meds. Folate
supplementation. Vit K supplementation in final month with enzyme inducing meds. Monitor
drug levels.

IVDU: Arrange supports, encourage cessation, surveilance for HIV/Hep B/C during pregnancy.

281
7. In a patient presenting with features of an antenatal complication (e.g. premature rupture of
membranes, hypertension, bleeding):
a) Establish the diagnosis
b) Manage the complication appropriately

PPROM: ROM prior to labour at any gestational age. Associated with trauma, smoking,
infection, multiple gestations, previous hx of same, or incompetent cervix. Perform sterile
speculum exam, pH paper, and ferning, repeat cultures. If PROM is confirmed admit and
monitor, Induce and deliver > 34-36weeks. Need antibiotic coverage if PROM < 34 weeks.
Betamethasome for fetal lung maturity < 34 weeks.

UTI: treat with Amoxicillin

Pregnancy Induced Hypertension: Hypertension associated with proteinuria at greater than

20weeks gest., diagnose if >140/90. Check for proteinuria, CBC, lytes, renal function, LFTs,
INR/PTT, U/S fetus, uric acid, LDH.

• Tx: mild – bed rest in LLDP, normal salt and protein intake, close monitoring for
symptoms or complications. Severe – Check for HELLP syndrome, deliver when safe,
MgSO4 (4g bolus, then 2g/hr until 24hrs following delivery), antihypertensives prn –
Hydralazine 5-10 mg IV q15-30 mins, or Labetalol 50-100 mg po BID, or 20-80mg Iv
q10min.

Third Trimester Bleeding: ddx- bloody show (most common), placenta previa, abruption, vasa
previa, cervical lesion, trauma or neoplasm, uterine rupture. Perform U/S and NST, large bore IV,
Rhogam (if mom Rh-). If 36 weeks and profuse bleeding – stabilize, C section.

8. In a patient presenting with dystocia (prolonged dilatation, failure of descent):

a) Diagnose the problem
b) Intervene appropriately

First stage: latent phase characterized by infrequent and irregular contractions, slow, cervical
effacement, usually 3-4cm dilatation. Active phase characterized by rapid cervical dilatation,
maximal slope of friedman curve, contractions approx q2-3mins

• Arrest of labour is no dilatation for >2hrs (or no further dilation past >4cm despite
adequate contractions).
• Difficult to define protracted 1st stage: Much variability, many definitions.
• Consider Oxytocin augmentation: requires IV, fetal monitor, and consider epidural
anesthesia.

Second Stage: full cervical dilatation until delivery

• Arrest of descent is no progress for >1hr

• Prolonged if > 2 hrs (nuliparity), or >3hrs with epidural. For multips, this is >1hr and
>2hrs(epidural). No intervention strictly necessary with prolonged descent, if no fetal
distress.
• look for Cephlo-pelvic-disproportion, change position, fetal monitor and consider C/S if
distress.

282
Third Stage: Delivery of placenta

• Administer Oxytocin routinely, prolonged if >30mins.

• If prolonged, may require manual extraction.

Fourth Stage: First hour post-partum.

9. In a patient presenting with clinical evidence of complications in labour (e.g. abruption,

uterine rupture, shoulder dystocia, non-reassuring fetal monitoring):
a) Diagnose the complication
b) Manage the complication accordingly

Fetal Heart-Rate Monitoring: Can be obtained via external Doppler device, or fetal scalp
monitor. Accelerations are >15bpm acceleration lasting >15sec, in response to fetal movement or
uterine contraction. Reassuring strips contain >2 accels in 20mins. Normal baseline 120-160bpm.

• Early decelerations – due to vagal response to head compression against cervix. Benign.
• Variable Deceleration – due to cord compression. Benign unless repetitive with slow
recovery (or <60bpm, <60bpm below baseline, or for >60 secs)
• Late Deceleration – Concerning, and a sign of uteroplacental insufficiency. Must see 3
or more with same shape to define.
o Approach: Change position of mother, give 100% O2, hold oxytocin, consider fetal
scalp electrode for beat to beat monitoring. Immediate delivery if recurrant prolonged
bradycardia.

Shoulder dystocia: Impaction of anterior shoulder of fetus against symphysis pubus after head has
been delivered. Watch for macrosomic babies, GDM moms, Obesity, prolonged gestation. May
observe “turtle” sign.

• Approach: Get help -> McRobert’s Manouver -> Supra-pubic pressure -> Wood’s
screw (+/- episiotomy) -> Release posterior Shoulder -> Remove posterior arm -> all
fours position ->fracture clavicle -> symphysectomy/Zavanelli

Uterine Rupture: Painful hemhorrage, shocky, tender uterus with palpable fetal parts. Regression
of dilation/station.

• History of uterine scar, oxytocin, trauma, CPD, Grand-multiparity.

• ABC's, STAT OR.

Abruption: Painful hemhorrage, with abdominal tenderness +/- uterine tetany. 20% are concealed,
with no bleeding. These may present as tetanic contractions, fetal distress, coagulopathy. May see
shock out of proportion to bleeding.

• Risk factors: previous abruption, DM, HTN, preeclamsia, renal disease, trauma, cocain
use, shock from other cause.

283
 • Do CBC, type and screen, DIC panel (abruption puts at risk for this), Ultrasound.
ABC's, and consider C section if severe and vaginal delivery not imminent. If mild, may
manage expectantly with serial ultrasounds/increased surveillance.

10. In a patient presenting with clinical evidence of a post-partum complication (e.g. delayed or
immediate bleeding, infection):
a) Diagnose the problem (e.g. unrecognized placental products, endometritis, cervical
laceration).
b) Manage the problem appropriately

Post-partum hemorrhage: Tone (uterine atony), Tissue (retained placenta), Trauma,

Thrombophilia

• Manage accordingly. Large bore IV, CBC and Type/cross match 4 units, treat cause,
may use oxytocin/misoprostol/hemabate. Hysterectomy as last resort.

Multiple other post-partum complications to review:

• Endometritis vs. Septic Pelvic Thrombophlebitis vs Wound Infection vs. Pelvic Abcess
• Breast Engorgement vs. Plugged ducts vs. Mastitis vs. Breast Abscess vs. Thrush
• Delayed onset Pre-Eclampsia

11. In pregnant or post-partum patients, identify post-partum depression by screening for risk
factors, monitoring patients at risk, and distinguishing post-partum depression from the
“blues”)

Blues: 85% of new mothers, onset day 3-10, extension of normal hormonal changes and
adjustment to new baby. Self limited and resolves by 2 weeks.

Depression: Major depression occurring in women within 6 months of delivery. 10-20%. Screen
all moms – if present higher risk for suicide or infanticide. Treatment: Antidepressants, ECT if
severe or rapid response required. Avoid TCA’s. It is generally suggested that women not breast
feed while using any psychotropic meds, but not absolutely contra-indicated. Closely monitor
moms during initial 2 weeks of medication as suicide risk is elevated.

12. In a breast-feeding woman, screen for and characterize dysfunctional breast-feeding (e.g.
poor latch, poor production, poor let-down.

Consider referral to lactation consultant if unfamiliar. Avoid live vaccines such as MMR.
Monitor infant weight in hospital, ensure good feeding prior to D/C.
Domperidone (10 mg po QID) trial reasonable for limited production.

Prostate - Key Features

284
1. Appropriately identify patients requiring prostate cancer screening.

Initiation

o CMA
• Offer screening to all men age 50 or older who have a life expectancy greater than 10
years (CMA 2011)
• Offer at age 40-45 for those at higher risk (1st degree with Pca, BRCA1or African
American ancestry) (CMA and US Task Force)
• Some trials demonstrated a benefit of establishing a baseline PSA for all men 40-49 yrs
but this is not widespread practice yet (CMA 2011)
o Canadian Task Force
• The PSA test should be excluded from the periodic health examination for
asymptomatic men over 50yrs of age (Grade D recommendation: fair evidence against
screening, Level 3-4 evidence)
• If screening is requested, the patient should be fully informed of the potential risks and
benefits (see below)

Frequency

o CMA: Annual screening is standard but two trials demonstrate 2-4 year intervals is OK
too
o CTF: You guessed it. Never screen asymptomatic men.

2. In a patient suitable for prostate cancer screening, use and interpret tests (e.g., prostate-
specific antigen testing, digital rectal examination [DRE], ultrasonography) in an
individualized/sequential manner to identify potential cases.

History is the simplest screening tool

o Usually asymptomatic
o Locally advanced disease
• Obstructive and irritative LUTS- hesitancy, increased frequency, dribbling, difficulty
with stream,dysuria, hematuria… (uncommon w/o spread)
o Metastatic disease
• Bony metastasis to axial skeleton is very common (osteoblastic)
• Also liver, lung and adrenal metastases
• Sx: B symptoms, Leg pain and edema with nodal metastasis, obstructing lymphatic and
venous drainage

DRE and PSA

o This is super controversial and I break it down a bit below

PSA Screening

285
 • PSA is specific to the prostate, but is NOT specific for prostate cancer
• PSA alone in screening asymptomatic men for cancer has not been shown to decrease
mortality
o PSA, DRE and TRUS must be used in conjunction for screening and investigation
o DRE cannot reach anterior aspect of prostate (miss ~ 40% of ca)

PSA may also be increased with:

• BPH
• Prostatitis
• Prostatic ischemia/infarction
• Acute urinary retention
• Manipulation of lower urinary tract (cystoscopy, bx, foley)
• Ejaculation (minor transient increase) wait for 2 days
• DRE does not increase PSA
• PSA is not an ideal tumour marker:
o Combining PSA with DRE improves screening effectiveness
Abnormal PSA Abnormal DRE Combined (PSA/DRE)
Sensitivity 35% 27% 38%
Specificity 75% 33% 92%
PPV 28% 18% 56%

Strategies to increase specificity of PSA test:

Age-Related Norms have been suggested

Normal PSA Value by Age Group

Age Range (yrs) Serum PSA Concentration (g/L)

40-49 <2.5

50-59 <3.5
60-69 <4.5
70-79 <6.5

Free-to-Total PSA Ratio

o Complexed PSA increases in prostate cancer, decreasing the percentage of the free
fraction
o Think “free and easy”: increased free/total ratio suggests benign cause of PSA elevation
o <10% free PSA suggestive of cancer
o >20% free PSA suggests benign cause

286
 PSA velocity
o Change of >0.75ng/mL (20%) per yr assoc with ↑ risk of cancer

PSA density
o PSA divided by prostate volume as found on TRUS
o >0.15ng/ml/g assoc w/ incr risk of cancer

Explaining Sensitivity and Specificity of PSA to pt

• Out of 100 men who have a PSA test done

o 90 will have a negative result- of the 90
• 1 patient will have undiagnosed prostate cancer
o 10 men with have a positive result – of those 10
• 7 will NOT have prostate cancer
• 3 will have prostate cancer

Digital Rectal Examination

• Findings increasing the risk of malignancy

o hard irregular nodule or diffuse dense induration involving one or both lobes
• Canadian Task Force
o Poor evidence exists to include or exclude digital rectal examination from the PHE of
men > 50 years of age [C].
o Insufficient evidence exists to have physicians who presently do the procedure change
their behavior. (Digital rectal examination can be done for other reasons other than to
detect prostate cancer.)

Investigations to Rule Out Suspected Prostate Cancer

• Family Physician
o TRUS (transrectal ultrasound) - assesses size and local staging (ask for prostate
volume, views of kidneys and bladder with post-void residual before referring to urology)
• Specialist
o TRUS-guided needle biopsy
o Bone scan -may be omitted in untreated prostatic ca with PSA <10
o Lymphangiogram and abdo/pelvic CT scanning to assess metastases

Gleason Tumour Grading

1-4 = well differentiated
5-7 = moderately differentiated
8-10 = poorly differentiated

287
3. In patients with prostate cancer, actively search out the psychological impact of the
diagnosis and treatment modality

FIFE away, young Jedi.

4. In patients with prostate cancer, considering a specific treatment option (e.g., surgery,
radiotherapy, chemotherapy, hormonal treatment, no treatment):
a) Advise about the risks and benefits of treatment.

Management:
Depends on:

• Overall health status

• Life expectancy
• Quality of life
• Patient preference

Staging
T1 (not palpable, not seen on imaging, found by ↑PSA or TURP)

o If young consider radical prostatectomy, brachytherapy or radiation

o Follow in older population (cancer death rate up to 10%)

T2 (palpable, confined to prostate)

o Radical prostatectomy or radiation (70-85% survival at 10yrs) or brachytherapy

T3 (tumour extends through prostate capsule),

T4 (tumour invades adjacent structures, besides seminal vesicles)

o Staging lymphadenectomy and radiation or hormonal treatment

N>0 (spread to regional lymph nodes) or M>0 (distant metastasis)

o Requires hormonal therapy/palliative radiotherapy to metastases

o Bilateral orchiectomy – removes 90% of testosterone
o LHRH agonists (ex. leuprolide (Lupron), goserelin (Zoladex))
o Estrogens (ex. diethylstilbestrol (DES))
o Antiandrogens
• Greater androgen blockage can be achieved by combining an antiandrogen with LHRH
agonist or orchiectomy
• Local irradiation of painful secondaries or half-body irradiation
o Chemotherapy regimen that incl docetaxel may improve survival in advanced disease
no longer responsive to hormone therapy

288
Risk Stratification

+ - low risk

++ - intermediate risk T1-T2 T3-T4

+++ - high risk

PSA <= 10 PSA 10.1 – 20.0 PSA>=20.1
Gleason <=6 <T2a (+) ++ +++ +++
Gleason = 7 ++ ++ +++ +++
Gleason >=8 +++ +++ +++ +++

Low risk/intermediate risk

• Radical prostatectomy, EBRT, or brachy

• Watchful waiting

High risk

• Curative –
o Neoadjuvant, concurrent and ongoing Androgen deprivation therapy
o Radical Prostatectomy, EBRT
• Palliative
o ADT and or radiation

Risks/Benefits of Treatment Options

• Watchful waiting – well differentiated (low Gleason 2-5), do well few die of prostate ca even
after f/u 10-15yrs, most differentiated (Gleason 8-10) die of prostate ca, therefore appropriate
with low-risk cancer and w/ shorter life expectancies
• Surgery (Radical prostatectomy)

o Risks: erectile dysfunction, urinary incontinence, urethral stricture, bowel damage, and
complications arising from anesthesia and major surgery, including death.
o Benefits: decreased metastasis, decreased mortality

• Radiotherapy

o External beam radiation therapy and brachytherapy

o Risks: genitourinary sx, GI sx (diarrhea, tenesmus), erectile dysfunction, dry ejaculate,
incontinence, urethral stricture, bowel damage

• Hormonal (ie. androgen ablation)

o Used for T3 and T4 stages

o LH-RH agonists ex. leuprolide (Lupron) or

289
Antiandrogens ex. cyproterone acetate

o Risks: loss of libido, erectile dysfunction, hot flashes, gynecomastia, fatigue à after
many yrs: loss of muscle mass, osteoporosis, adverse lipid profiles, glucose intolerance
o Benefit: 80% respond, median disease-free survival is 2-3yrs

• Chemo – ineffective at prolonging life with hormone-refractory ca

Prognosis
• Stage T1-T2: excellent, comparable with normal life expectancy
• Stage T3-T4: 40-70% survival at 10yrs
• Stage N+ and/or M+: 40% survival at 5yrs
• Prognostic factors: tumour stage, tumour grade, PSA value

b) Monitor patients for complications following treatment.

After Radical Prostatectomy (side effects)

o Pelvic pain is common, esp. among younger men after RP

• For 14 days post op men require catheter that may cause

• Swelling
• Pain
• Urine leak past
• Bladder spasms
• Rectal pain

o Incontinence will occur in the post op period

• Occurs days- years post op b/c of strictures and nerve damage

o Erectile functioning might return slowly over years

• Depends on age, erectile function before symptoms, size of the gland, and surgical
technique
• Improvement seen up to 5 years

o PDE5 inhibitors help only 50% of the time

• Both Nerve bundles spared

• age< 55 – 80% chance of response
• age 56-65- 45% chance of response
• age 66 + - 33% chance of response
• One nerve bundle spared
• Age <55 -44%
• No nerve bundles spared
• No response regardless of age

o Penile Shortening or fibrosis can occur

290
 • 70% of men

o PSA velocity is more reliable indicator of recurrence than PSA alone

• Cut point -0.2-0.4

• Velocity (doubling/tripling time) – should be assessed

After Radiation Therapy

o Bladder irritation is common

• Frequency/dysuria are main symptoms

• Treat with alpha blockers

o Bowel Complications might occur in long term

• Proctitis (rectal pain/irritation)-45% (EBRT)

• Diarrhea
• Rectal bleeding (brachytherapy)
• Rectal Ca (EBRT)

o Later onset of erectile dysfunction

• Later onset compared with surgery

• Brachy better than EBRT for sexual outcomes
• Use of PDE5 inhibitors soon after tx preserve erectile function

5. In patients with prostate cancer, actively ask about symptoms of local recurrence or distant
spread

Monitoring for Cancer Recurrence

• Recurrence depends on: Tumor size, Grade, Stage, LN involvement
• F/U at 6 wks à 3, 6, 9, 12 months semi-annually 2nd to 5th year, then annually x 5-10yr
• At each visit

o Ask about local symptoms (i.e.; LUTS obst/irritative ) and ask about –potential mets
symptoms, (GI sx, and bone pain)
o Test PSA.
• An increasing PSA level after curative therapy is termed a biochemical recurrence
(BCR). Occurs in 30-50% of pts during the course of their follow-up, regardless of
modality of treatment
• The significance of a BCR is in itself unclear. In one study, fewer than 1/3 of pts with
BCR after RP developed systemic recurrence. In those patients who progress, BCR
usually predates metastatic disease progression by an avg. of 7 yrs and prostate-cancer
mortality by 15 yrs
• Recent studies have shown that the speed at which PSA rises, or the PSA doubling time
(PSADT), is one of the strongest predictors of clinical progression and cancer mortality.

291
 If PSA doubles slowly (> 12 m), then recurrence is likely local. When PSA doubling time
is shorter than 6 m, it is more consistent with disseminated disease.

Factors that suggest BCR – local vs. distant

Factor Local Distant Recurrence

Gleason <7, positive surgical Gleason>7, extra-prostatic involvement,
Initial pathology
margins, no nodes nodal involvement
Time to BCR
>1-2 yr <1 yr
after tx
Pre treatment
<10 >10
PSA
PSA doubling
>12 mo <6 -12mo
time

• Annually

o DRE (not necessary)- nodules may be confused with scar tissue

• If on anti androgen therapy

o BMD q2-3 years

Following Patients with Prostate Cancer

PSA (usually check q3 months)
• If EBRT/Brachy used – PSA >0.4 or Nadir +2 = BCR- Refer for treatment and Bone Scan if
>20 or pt symptomatic
• If Radical Prostatectomy – PSA >0.4 = BCR – Refer for treatment and bone scan if >20 or
symptomatic
• If watchful waiting – PSA >10 or PSADT< 6 mo or symptomatic

o If currently using watchful waiting only – than begin ADT

o If currently using ADT – than hormone refractory disease – referral for chemo,
palliative radiation, or consider secondary hormonal therapy

Visit q 6 mo
• Assess treatment, clinical assessment, PSA
• DRE optional
• Bone scan if PSA >20 or symptomatic

6. Given a suspicion of benign prostatic hypertrophy, diagnose it using appropriate history,

physical examination, and investigations.

292
Benign Prostatic Hypertrophy
Hx:
• prior and current illnesses, prior surgery and trauma
• current meds include OTC
• Symptoms of BPH

Irritative
Obstructive symptoms Late complications
symptoms
• Hesitancy (difficulty starting urine flow)
• Hydronephrosis
• Urgency
• Straining
• Loss of renal concentrating ability
• Diminution in size and force or urinary
• Frequency
stream
• Nocturia • Systemic acidosis
• Stream interruption (double voiding)
• Hematuria • Renal failure
• Urinary retention (sensation of
• Urge
incomplete voiding)
incontinence -fatigue, anorexia, nausea,
• Post-void dribbling
malaise
• Overflow incontinence

• Assess the severity of symptoms – according to AUA

P/E:
• Palpate abdomen, groin LNs, CVA tenderness, testes, scrotum
• DRE for prostate size, symmetry, nodularity, tenderness and texture

-BPH: smooth, rubbery, nontender, symmetrically enlarged prostate

Diagnostic Tests
• PSA: normal <4 ng/mL

o Uncertain how to deal with values between 4-10

o If >10 can dx prostate pathology
o Do not test PSA immediately after DRE as level may be falsely elevated

• Cr, BUN
• Urinalysis for hematuria to r/o UTI
• Post-void residual volume by U/S
• Urodynamics – pressure/flow studies
• Not routinely recommended

o Cystourethroscopy
o IVP
o U/S

Referral to urologist if symptoms other than mild

293
7. In patients presenting with specific or non-specific urinary symptoms:
a) Identify the possibility of prostatitis.

Prostatitis
• Most common urologic dx in men <50yrs
• Very uncommon in men to develop UTI (unless abnormality in structure), therefore most LUTS
are due to prostatitis as opposed to Lower UTI

Clinical features
• Irritative LUTS- dysuria, hematuria, increased frequency, urgency
• Rectal, low back and perineal pain
• Systemic symptoms: fever, malaise, myalgia, arthralgia
• Hematuria

b) Interpret investigations (e.g., urinalysis, urine culture-and-sensitivity testing, Digital Rectal

Exam, swab testing, reverse transcription-polymerase chain reaction assay) appropriately.

Investigations
• Rectal exam

o Enlarged, tender, warm prostate

o Prostatic massage is not recommended d/t extreme tenderness and risk of inducing
sepsis, abscess or epididymo-orchitis

• Urine R&M, C&S – can do Initial void culture (urethritis) and mid stream culture (cystitis)
• Blood CBC, C&S

Diagnosis
• Based on a combination of clinical symptoms and tender prostate on exam – culture to dictate
what organisms involved

Rape/Sexual Assault - Key Features

1. Provide comprehensive care to all patients who have been sexually assaulted, regardless of
their decision to proceed with evidence collection or not.

General Management Principles:

Assessment and follow up of sexual assault victims should be carried out with great sensitivity
and in conjunction with local teams or services experienced in the management of victims of
sexual assault.

ABCs
Ensure pt not left alone, ongoing emotional support
Sexual assault kit (when available)
Obtain consent: physical exam, treatment, collection of evidence
Do not report to police unless victim requests or consents to this- if patient unsure whether she/he
wants to report to police at time of presentation, offer to collect forensic evidence for
storage/future use.
Legally required to report child abuse of any kind (in BC age <19yrs)
Offer community crisis resources (see below)

294
Documentation of Hx, Px and specimen collection is key

Non-disclosure and pre-contemplative pts:

Respect their decision, inform pt of options/resources, encourage pt to return for medical follow
up, express your availability as a resource, ensure confidentiality, re-address at future visits.

2. Apply the same principles of managing sexual assault in the acute setting to other
ambulatory settings (i.e. medical assessment, pregnancy prevention, STI
screening/treatment/prophylaxis, counseling).

History:
-Date/time/place, perpetrator info (known/unknown/HIV+/IVDU)? How many assailants? When?
Where did penetration occur/condom use? What happened? Any weapons or phys assault? -Post-
assault activities (urination, defecation, change of clothes, shower, etc)
-PMHx: OB/Gyn hx: GTPAL, LMP, contraception, last voluntary intercourse (sperm mobile 6-12
h in vagina, 5 d in cervix), Meds, Immunizations
-Available support systems to pt

Physical Exam:
-Injuries requiring immediate attention take precedence over rest of exam
-Pt should be asked to disrobe completely, & if forensic specimens to be collected, disrobe while
standing to collect all evidence (all clothing should also be collected)
-Examine for bruises, lacerations, vaginal/anal trauma, petechial hemorrhages on palate if Hx
forced oral penetration
-All injuries should be accurately documented on body-map diagrams
-Most forensic kits do not include tests for STIs or blood-borne pathogens, should offer baseline
testing in addition to forensic kit (including speculum exam with pt consent, urine test/blind
vaginal sampling alternative option)
* NB: colposcopy and photography rarely useful, may produce unnecessary distress

Investigations:
Syphilis: RPR/VDRL, TP-PA (confirmatory test)- rpt at 3 and 6 months if neg
Serum B-hCG
ABO, Rh type, baseline serology for HIV/HBV/HCV, rpt HIV 6wks/3mos/6mos
Cervical swabs GC/Chlamydia, vag swab for Trichomonas

Management:

1. Medical: suture lacerations, tetanus prophylaxis, Gyne consult (foreign body, complex
lacerations)

2. STIs:
-Offer Tx prophlyaxis for GC/Chlamydia: Azithromycin 1 g PO x 1 dose (or
Doxycycline 100 mg po BID x 7 d) and Cefixime 400 mg PO x 1 dose
-Prophylaxis for HIV – call local HIV/ID specialists for advice re: risk assessment and
need for PEP. If unknown assailant then no HIV PEP needed because low risk. PEP
generally recommended when assailant known HIV+, otherwise case-by-case basis
(known IVDU, mult. assailants, significant injury, etc.)

295
 -Hep B prophylaxis: if pt not immune- HBIG 1 dose IM (400 IU) as soon as possible
after exposure (up to 14d after exposure) AND Hep B vaccine at 0, 1, 6 mo

3. Pregnancy prophylaxis:
-Plan B (Levonorgestrel only) 1.5mg po x 1 dose or 0.75mg BID x 2 doses (if 1 dose not
likely to be tolerated) within 72 h of intercourse
-Gravol can be given 30min prior to second dose for anti-emetic, if vomiting within 1hr
first dose, give anti-emetics and rpt initial dose
-contraindicated if pregnancy established

4. Other Issues: If pt consents, appropriate referral as available/necessary (e.g. sexual

assault teams, local police/RCMP, psychological support (high incidence of
PTSD/anxiety), local victim support organizations, etc.).
-Become familiar with provincial requirements/procedures re: child abuse (age
requirements, etc), advise local agencies/ministries as required

3. Limit documentation in sexual assault patients to observations and other necessary medical
information (i.e., avoid recording hearsay information).

Record only objective info regarding pt’s own injuries and pt’s mental status, use pt’s own words,
note when an explanation is inconsistent with injury assessment, document injuries as accurately
as possible on body-map diagrams, describe stages of healing, reassess injuries at 24-48 h as
indicated.

4. In addition to other post-exposure prophylactic measures taken, assess the need for human
immunodeficiency virus and hepatitis B prophylaxis in patients who have been sexually
assaulted.

See management section above

5. Offer counseling to all patients affected by sexual assault, whether they are victims, family
members, friends, or partners; do not discount the impact of sexual assault on all of these
people.

See resources below

6. Revisit the need for counseling in patients affected by sexual assault.

Be aware that not all pts will be interested in counseling initially after assault, follow up
necessary with ongoing support and offer for referral to support resources.

7. Enquire about undisclosed sexual assault when seeing patients who have symptoms such as
depression, anxiety, and somatization.

296
As a FP, recognize that depression, anxiety, PTSD and somatization disorders are common
sequelae of assault.

Red Eye - Key Features

The common culprits: Assessment of red eye courtesy of Uptodate

1. In addressing eye complaints, always assess visual acuity using history, physical
examination, or the Snellen chart, as appropriate.

History (general eye questions):

297
 - Monocular vs binocular
- Transient (amaurosis fugax) vs acute vs gradual
- Painless vs painful
- Foreign body sensation – suggests active corneal process, objective FB sensation when
patient resistant to opening eye; “scratchy” or “gritty” more suggestive of conjunctivitis.
No FB sensation with iritis/glaucoma.
- Photophobia – corneal process or iritis
- Trauma
- Contact lens wearer – increases suspicion of keratitis
- Associated symptoms – eg. URTI with viral conjunctivitis.

Physical Exam

- General observation: ? opening eyes, in pain/distress, dark glasses, tearing/discharge.

- Visual acuity: always check best corrected visual acuity, use pinhole occlude to help
improve vision if refractive error present. Acuity testing: Snellen chart at 20 feet. Near:
Rosembaum/pocket vision at 14 inches. Gross testing: reading vision vs form perception
vs light perception only.
- Penlight exam
o lid, palpebral and bulbar conjunctiva, cornea (foreign body, corneal opacity)
o pattern of redness (affecting both p/b conjunctiva suggests conjunctivitis, vs ciliary
flush around limbus suggests iritis, infectious keratitis, acute angle closure glaucoma),
hemorrhagic pattern suggests subconjunctival hemorrhage.
o Fluorescein dye with cobalt blue light - ? corneal process
o Hypopyon (white cells in anterior chamber) and hyphema

2. In a patient with a red eye, distinguish between serious causes (e.g., keratitis, glaucoma,
perforation, temporal arteritis) and non-serious causes (i.e., do not assume all red eyes are
caused by conjunctivitis)
a) Take an appropriate history (e.g., photophobia, changes in vision, history of trauma)

See above.

b) Do a focused physical examination (e.g., pupil size, and visual acuity, slit lamp, fluorescein).

Pain

- While blinking (corneal abrasions / foreign bodies / keratitis)

- With eye movement (optic neuritis)
- With headache / nausea (acute angle-closure glaucoma)
- With brow or temporal pain (temporal arteritis)
- Photophobia (inflammation of iris & middle layer of eye, corneal irritation)
- “gritty sensation” (conjunctivitis, corneal abrasion)
- History of trauma (corneal abrasion)

Change in vision

298
 - normal vision reassuring (lid disorder, conjunctival process, corneal abrasion, foreign
body)
- red eye with decreased vision – infectious keratitis, iritis, acute angle glaucoma
- NB the causes of vision loss that are not common “red eye” culprits: retinal vascular
occlusion, papilloedema, retinal detachment, cortical blindness etc.

Photophobia

- corneal process, iritis

Keratitis – inflammation of cornea (photophobia, FB sensation)

- UV keratitis: eg welding or sunlamp, appears 6-10 hrs after exposure, bilateral redness,
photophobia, tearing. Fluorescein staining shows superficial punctuate keratitis.
- Viral keratitis – often herpes, can be other (eg adenovirus) – FB sensation, photophobia,
watery discharge. Herpes simplex: eyelid edema, can have decreased vision. Gray,
branching opacity with dentrite seen with fluorescein.
- Bacterial keratitis – FB sensation, difficulty opening eye, photophobia, mucopurulent
discharge, white spot on cornea that stains with flurescein. High risk with contact
wearing.

Acute Angle Closure Glaucoma

- Abrupt onset of severe pain, may be frontal or supraorbital headache, redness with
ciliary flush, photophobia, decreased/blurred vision, nausea/vomiting, fixed midposition
pupil, hazy (cloudy) cornea, elevated IOP (normal 10-20 mmHg, disease 60-80mmHg)
NO FB sensation!

Perforation

- History! Mechanism of injury (projectile, laceration of eyelid or periorbital area, corneal

abrasions occurring when hammering metal on metal, etc). Eye pain, acuity may be
affected.
- If you suspect, don’t press on globe! And never measure IOP!
- Slit lamp exam with fluorescein to check for abrasion, laceration, FB, hyphema, iritis,
lens dislocation.
- Signs: flat anterior chamber, pupil asymmetry or irregularity, extrusion of humor etc.

Temporal arteritis

- Head ache, jaw claudication, myalgia, fever, anorexia, temporal artery tenderness,
TIA/stroke, rapid/profound visual loss (unilaterally initially), afferent papillary defect.

299
c) Do appropriate investigations (e.g., erythrocyte sedimentation rate measurement,
tonometry).

- Bacterial keratitis or conjunctivitis – swab discharge for C&S

- Acute angle closure glaucoma – tonometry (dx 60-80 mmHg)
- Perforation – slit lamp with fluorescein, palpation around orbital rim, check extra ocular
movements (NB blowout fractures with trauma).
- Temporal arteritis – ESR or CRP, start prednisone and refer for biopsy of temporal artery if
highly suspicious

d) Refer the patient appropriately (if unsure of the diagnosis or if further work-up is needed).

REFER:

- Acute angle closure glaucoma – emergent – begin treatment to lower IOP – by reducing
acqueous humor (topical BB, alpha-adrenergic agonists, carbonic anhydrase inhibitors),
facilitating outflow of aqueous humor (parasympathomimetic miotic agents), reducint
volume of vitreous humor (IV mannitol)
- Perforation – emergent (normal acuity and ocular anatomy can f/u as outpatient within
48 hrs)
- Hyphema and hypopyon emergently
- Iritis – urgent
- Infectious keratitis (bacterial emergent, viral is urgent)
- Temporal arteritis

PRIMARY CARE:

- Stye (hordeoleum), chalazion, blepharitis, subconjunctival hemorrhage

- Conjunctivitis (bacterial, viral, allergic)
- Dry eye syndrome
- Episcleritis
- Corneal abrasion, corneal FB, contact lens overwear – Refer if not better within 24-48
hrs.

3. In patients presenting with an ocular foreign body sensation, correctly diagnose an

intraocular foreign body by clarifying the mechanism of injury (e.g., high speed, metal on
metal, no glasses) and investigating (e.g., with computed tomography, X-ray examination)
when necessary.

- Conjunctival abrasions/lacerations – c/o scratchy FB sensation, mild pain, tearing, and rarely
photophobia. Vision preserved unless full-thickness conjunctival laceration. Inspect for and
remove foreign particles.
- Corneal abrasions/lacerations – c/o FB sensation, photophobia, tearing. Mechanism of injury
important. Exam reveals conjunctival injection, tearing, lid swelling. Relief of pain with topical
anesthesia diagnostic of corneal abrasion. Photophobia may be present. Slit lamp exam with
fluorescein. If suspicious of penetrating injury, CT of orbit to assess changes in globe anatomy or
contour of FB within globe. Consult optho.
- Consider procedural sedation to examine children properly.

300
4. In patients presenting with an ocular foreign body sensation, evert the eyelids to rule out the
presence of a conjunctival foreign body.

- Have patient look down, use q-tip to help evert upper lid. Inspect tarsal conjunctiva. Remove FB
with moist cotton bud. May need penlight or magnification. Have patient look up and eyelid with
return to normal position.

5. In neonates with conjunctivitis (not just blocked lacrimal glands or ‘‘gunky’’ eyes), look for
a systemic cause and treat it appropriately (i.e., with antibiotics).

- Ophthalmia neonatorum = conjunctivitis in neonates up to 30 days old

- 5 main categories: chemical, gonococcal, chlamydial, other bacterial
(nongonococcal/nonchlamydial), and viral

- Chemical: watchful waiting as resolves within 48 hrs

- Gonococcal: can cause blindness! Prophylaxis with erythromycin ointment at birth.
Presents 2-7 days of life. Intense bilateral bulbar conjunctival erythema, chemosis, &
copious purulent discharge. Gram stain of discharge: gram negative diplococcic. All
infants require admission and evaluation for disseminated disease (i.e., blood, urine,
CSF). Tx: single dose of Ceftriaxone 50 mg/kg IV (if no hyperbilirubinemia);
Cefotaxime 50 mg/kg IV q8h
- Chlamydial: Presents 5-14 days of age. Unilateral or bilateral purulent d/c with intense
erythema of palpebral conjunctiva. Associated with chlamydial pneumonia. Tx: Systemic
erythromycin Base or Ethylsuccinate x 14 days.
- Other bacterial: Presents within 2 wks of birth; much less common. Hyperemia,
purulent discharge, and edema. Usual bugs: S. aueus, nontypeable H. influenza, and S.
pneumonia. Tx with topical bacitracin, polymyxin, or neomycin
- Viral: Herpes simplex types I and II. Presents 6-14 days of life. Bilateral lid edema &
conjunctival erythema. Suspicious if associated with mucocutaneous lesions & maternal
hx of herpes. Fluorescein exam shows keratitis or corneal dendrites. Requires hospital
admission, full sepsis work-up (esp CSF analysis). Tx: Acyclovir 20 mg/kg IV q8h x 14-
21 days & topical antivirals (trifluridine 1%, iododeoxyuridine 0.1%, vidarabine 3%)

6. In patients with conjunctivitis, distinguish by history and physical examination between

allergic and infectious causes (viral or bacterial)

Allergic conjunctivitis:

- Symptoms: watery discharge, redness, and itching. Signs: erythematous swollen eyelids,
injected & edematous conjunctiva with papillae on inferior conjunctival fornix

Infectious conjunctivitis:

- Bacterial:
- Symptoms: painless, unilateral, or bilateral mucopurulent discharge causing eyelids to
“stick” on awakening; injected conjunctiva; clear cornea. Signs: chemosis (edema of
conjunctiva). NB: preauricular lymph nodes absent, except for gonococcal infections.
- Viral:

301
 - Etiology: adenovirus (most common); measles, influenza, mumps; herpes simples /
herpes zoster. Symptoms: usually preceded by upper respiratory tract infections, “red
eye”, mild to moderate watery discharge; painless; initially unilateral then bilateral.
Signs: unilateral or bilateral conjunctival injection, occasional chemosis, and small
subconjunctival hemorrhages, and preauricular LA. On slit lamp, follicles on inferior
palpebral conjunctiva.

7. In patients who have bacterial conjunctivitis and use contact lenses, provide treatment with
antibiotics that cover for Pseudomonas

- Soft contact lenses prone Pseudomonas infection

- Tx: Fluoroquinolone (Ciloxan, Ocuflox) or AMG (Tobrex).

8. Use steroid treatment only when indicated (e.g., to treat iritis; avoid with keratitis and
conjunctivitis).

- Do not use ocular steroids in conjunctivitis due to occult herpetic infection. Should only use on
ophthalmologist recommendation
- Treatment of iritis includes blocking pupillary sphincter & ciliary body with long-acting
cycloplegic agents (homatropine or tropicamide). Ophthalmologic referral needed in 24-48 hrs!
Can add prednisone to reduce inflammation.

9. In patients with iritis, consider and look for underlying systemic causes (e.g., Crohn’s
disease, lupus, ankylosing spondylitis).

- Iritis = anterior uveitis.

- Uveitis may be divided into four major subsets based upon the etiology of inflammation:

i. Infections: bacterial, viral, fungal, parasitic (lyme disease, syphilis, TB, EBV, CMV,
HSV, HIV, candida etc)
ii. Systemic immune-mediated disease: Ankylosing spondylitis, Behcets, Crohn’s, UC,
vasculitis, MS, reactive arthritis etc.
iii. Syndromes confined primarily to the eye: eg trauma
iv. Masquerade syndromes: ischemia, leukemia, giant retinal tear, retinoblastoma.

- Symptoms: unilateral pain, maybe bilateral with systemic disease; red eye (conjunctival);
photophobia; and decreased vision. No discharge.
- Signs: perilimbal flush (injection greatest around limbus) or diffuse conjunctival injection, no
discharge, miotic pupil poorly reactive
- Systemic symptoms can include: arthritis, urethritis, and recurrent GI symptoms. Look for past
medical history of exposure to TB, history of genital herpes, history of previous symptoms. Also
ask about recent trauma or exposure to welding without goggles.

Schizophrenia - Key Features

1. In adolescents presenting with problem behaviours, consider schizophrenia in the

differential diagnosis.

302
2. In “apparently” stable patients with schizophrenia (e.g., those who are not floridly
psychotic), provide regular or periodic assessment in a structured fashion e.g., positive and
negative symptoms, ther performance of activities of daily living, and the level of social
functioning at each visit:
- seeking collateral information from family members and other caregivers to develope a more
complete assessment of symptoms and functional status;
- competency to accept or refuse treatement, and document specifically;
- suicidal and homicidal ideation, as well as the risk for violence;
- medication compliance and side effects.

3. In all patients presenting with psychotic symptoms, inquire about substance use and abuse.

4. Consider the possibility of substance abuse and look for it in patients with schizophrenia, as
this is a population at risk.

5. In patients with schizophrenia, assess and treat substance abuse appropriately.

6. In decompensating patients with schizophrenia, determine:

- if substance abuse is contributory.
- the role of medication compliance and side-effect problems.
- if psychosocial supports have changed.

7. Diagnose and treat serious complications/side effects of antipsychotic medications (e.g.,

neuroleptic malignant syndrome, tardive dyskinesia).

8. Include psychosocial supports (e.g., housing, family support, disability issues, vocational
rehabilitation) as part of the treatment plan for patients with schizophrenia.

Description:

• Schizophrenia is a chronic, severe disabling psychiatric disorder

• Major psychiatric disorder with prodrome, active and residual disturbances in
appearance, speech (loosened associations), behavior (grossly disorganized) , perception
(hallucinations), or thinking (delusions) that last for equal or more than 6 months.
• There are 5 types of schizophrenia: paranoid, disorganized, catatonic, undifferentiated,
and residual.

Prevalence:

• Lifetime risk is 0.2-0.7%. Highest prevalence in lower socioeconomic classes

• More prevalent in males than females. 1.4 to 1.
• Age of onset is usually from late teens to mid thirties.

Diagnosis:
DSM-IV diagnostic criteria for schizophrenia

303
 A Characteristic symptoms: Two or more of the following, each present for a significant
portion of time during a one-month period:
• delusions
• hallucinations
• disorganized speech (eg, frequent derailment or incoherence)
• grossly disorganized or catatonic behavior
• Negative symptoms (i.e., affective flattening, alogia, or avolition).

Note Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist
of a voice keeping up a running commentary on the person's behavior or thoughts, or two or more
voices conversing with each other.

B Social/occupational dysfunction: Since the onset of the disturbance, one or more major
areas of functioning, such as work, interpersonal relations, or self-care, are markedly
below the level previously achieved.
C Duration: Continuous signs of the disturbance persist for at least six months. This six-
month period must include at least one month of symptoms (or less if successfully
treated) that meet Criterion A.
D Exclusion of schizoaffective disorder and mood disorder with psychotic features.
E Substance/general medical condition exclusion: the disturbance is not due to the direct
physiological effects of a substance (eg, a drug of abuse, a medication) or a general
medical condition.
F Relationship to a pervasive developmental disorder: If there is a history of autistic
disorder or another pervasive development disorder, the diagnosis of schizophrenia is
made only if prominent delusions or hallucinations are also present for at least a month
(or less if successfully treated).

Treatment:

• 2 main groups of antipsychotics:

Conventional: Chlorpromazine, fluphenazine, Trifluoperazine, Perohenazine,
Thioridiazine, Haloperidol, and Thiothixene.
Atypical: Risperidone, Clozapine, Olanzapine, Quetiapine, Ziprasidone, Aripiprazole,
Paliperidone, Iloperidone, Asenapine.
• Medication choice is based on clinical and subjective response and side effects.
For Sensitivity to EPS: Atypical.
For tardive dyskinesia: clozapine.
For poor compliance: Injectable long antipsychotics such as fluphenazine.
For acute dystonic reaction/EPS give benztropine 1-4 mg Po/IM.

Seizures - Key Features

1. In a patient having a seizure:

a) Ensure proper airway control (OPA, nasal trumpet, lateral decubitus to prevent aspiration).
b) Use drugs (e.g. benzos, phenytoin) promptly to stop the seizure, even before the diagnosis is
known

304
→ ABCs, O2, 1 amp DW50 IV and thiamine 100 mg IM.
→ Meds to stop seizure, continue to next step if seizure doesn’t respond:

→ Lorazepam 2-4 mg (max 0.1 mg/kg) IV/IM OR diazepam 5-10 mg IV q2-3 min until
seizure stops. Can use diazepam PR if no IV access.
→ Phenytoin 20 mg/kg IV at no faster than 50 mg/min (use different IV tubing as benzos
and phenytoin are not compatable)
→ Consult neurology
→ Phenobarbital 20 mg/kg IV at 50-75 mg/min or Midazolam 10mg IV bolus then 0.01-
0.4mg/kg/hr
→ If the above fails, RSI—Induction amount of propofol
→ Emergency EEG if not response after 15-20 min
→ ICU admission

If pregnant:
→ MgSO4 4-6 g IV then 1-2 g IV per hour

If a child:
→ Lorazepam 0.05 to 0.1mg/kg IV at rate of 2mg/min. Can be repeated in 5 to 10 min (up to max
of 10mg over 10 min)
→ Then Fosphenytoin at 20PE (phenytoin equivalents)/kg.

c) Rule out reversible metabolic causes in a timely fashion (hypoglycemia, hypoxia, heat
stroke, and electrolyte abnormalities)

• Vitals
• BW: CBC, lytes, glucose, BUN, Cr, Ca2+, Mg2+, albumin, tox screen, ABG, anticonvulsant
level, blood cultures
• Imaging: c-spine Xray if (post trauma or caused trauma), CXR (r/o malignancy) EEG, CT (if
focal findings or pre-LP), MRI (1st seizure), EKG, LP (if febrile, concerned about infxn, or
leptomeningeal disease, or R/O SAH)

2. In a patient presenting with an ill-defined episode (fits, spells), take a history to distinguish a
seizure from other events

DDx: sleep disorder, migraine, TIA, transient global amnesia, syncope, pseudoseizure
HPI: circumstances leading up to seizure, ictal state, post-ictal state, previous seizures, febrile
seizures, similar episodes not labeled as seizures. Time of onset (day or night), position (any),
speed of onset (sudden or brief), aura, colour (N or cyanotic), timing (brief or prolonged), urinary
incontinence, tongue biting (side in seizure, tip in syncope) post ictal sx (w/ tonic-clonic or
complex partial), Todd paralysis, injuries (# or dislocations), triggers
Partial: (simple (no LOC), complex (LOC), partial evolving to generalized)
Generalized: (tonic-clonic, absence, myoclonic)
PMHx: head injury, stroke, Alzheimer's disease, history of intracranial infection, alcohol or drug
abuse
Meds: especially responsible for generalized tonic-clonic sz
FHx: esp absence or myoclonic
SHx: ETOH, drugs, driving, employment.

305
3. In a patient presenting with a seizure, take an appropriate history to direct the investigation
(e.g., do not over investigate; a stable known disorder may require only a drug-level
measurement, while new or changing seizures may require an extensive work-up).

As above

4. In all patients presenting with a seizure, examine carefully for focal neurologic findings.

Usually have normal physical exam with epileptic seizures. Especially look for signs of NE
infection or bleed; i.e. meningismus, Kernig’s/Brudzinski’s, lateralizing signs, hyperreflexia, +
Babinski, weakness… anything that points to a lesion.

5. In a patient with a previously known seizure disorder, who presents with a seizure or a
change in the pattern of seizures:
a) Assess by history the factors that may affect the primary seizure disorder (e.g., medication
compliance, alcohol use, lifestyle, and recent changes in medications [not just antiepileptic
medications], other illnesses).

• As above
• Top five drug induced eitologies- isoniazide, theophylline, oral hypoglycelmics carbon
monoxide, and bupropion.

b) Include other causes of seizure in the differential diagnosis. (Not all seizures are caused by
epilepsy.)

• Seizures are not synonymous with epilepsy. Acute symptomatic seizures/provoked make up
about 40% of all non febrile seizures and result from acutre brain insults. They resolve when the
provoking factor is treated and they do not require long term teratment with anti-epileptic drugs.
• Drugs: withdrawal (anti-epileptics below therapeutic level, ETOH, benzos, barbituates), toxicity
(demerol on penicillin, theophylline, lidocaine infusion, isoniazid, lithium, neuroleptics, cocaine,
amphetamine).
• CNS: tumor, previous CVA (most common reason for people >35 to have a seizure),
meningitis, encephalitis, CNS vasculitis, idiopathic, HIV giving mass lesions, encephalopathy or
meningitis
• Endo: hypocalcemia, hyponatremia, glucose, Mg2+, hypoxia, uremia, hypercarbia
• Misc: pseudoseizures
• Epilepsies are agroup of condition in which an underlying neurologic disorder results in a
chronic tendancy to have recurrent, unprovoked seizures. The occurency of two more more of
these siezures establishes the diagnosis of epilepsy.

6. In the ongoing care of a patient with a stable seizure disorder:

a) Regularly inquire about compliance (with medication and lifestyle measures), side effects of
anticonvulsant medication, and the impact of the disorder and its treatment on the patient’s life
(e.g., on driving, when seizures occur at work or with friends).

• A single, unprovoked seizure before diagnosis = no driving for at least 3 mo plus NE

assessment including EEG and CT
• After epilepsy diagnosis = may drive if 12 mos of seizure free, medicated time, physician
believes pt will remain compliant, and pt warned against ETOH, fatigue, etc…

306
b) Monitor for complications of the anticonvulsant medication (e.g., hematologic
complications, osteoporosis).

• Carbamazepine (Tegretol): agranulocytosis, aplastic anemia, thrombocytopenia, SJS/TEN,

SIADH
• VPA: blood dyscrasias, ↑ LFTs, thrombocytopenia, prolonged coagulation times,
hyperammonemia giving encephalopathy
• Topiramate (Topamax): acute closed angle glaucoma, osteoporosis, increased suicidality
• Phenytoin (Dilantin): macrocytic anemia, increased suicidality, drug induced lupus, SJS/TEN

c) Modify management of other health issues taking into account the anticonvulsant
medication (e.g. in prescribing antibiotics, pregnancy).

• No anticonvulsant has been shown to be more teratogenic than any other (risk is 4-8% as
opposed to 1-3%). Women should take 4-5 mg of folic acid per day to prevent NTD. Goal for
monotherapy at lowest possible dose during pregnancy.
• Many anticonvulsants increase estrogen and progesterone metabolism, thereby reducing their
concentrations. Women on OCP need to increase dose of estradiol for 35 to 50 mcg
• Anticonvulsants interact with many other drugs, including benzos, clarithromycin,
erythromycin, warfarin, antacids.

Sex - Key Features

1. In patients, specifically pregnant women, adolescents, and perimenopausal women:

a) Inquire about sexuality (e.g. normal sexuality, safe sex, contraception, sexual orientation,
and sexual dysfunction)

Sexual history: age of first intercourse, perceived gender of self, gender of partners, current
relationship status, current sexual activity, pain or bleeding with intercourse, type of sexual
activity, satisfaction (desire, arousal, orgasm), assault/abuse, contraception methods and use
thereof, review safer sex practices

b) Counsel the patient on sexuality (e.g. normal sexuality, safe sex, contraception, sexual
orientation, sexual dysfunction)

Useful website: sexualityandu.ca (www.sexualityandu.ca has lots of resources for pts and
professionals).

2. Screen high-risk patients (e.g., post-myocardial infarction patients, diabetic patients, patients
with chronic disease) for sexual dysfunction, and screen other patients when appropriate (e.g.,
during the periodic health examination).

High risk populations:

Antihypertensives (thiazide, ACEI, CCB, spironolactone), anticonvulsants,

opioids, benzos, H2 receptor blockers (ranitidine), antineoplastics, antipsychotics,
Medications
antidepressants, anticholinergics, anti-emetics (haldol, maxeran, prochlorperazine,
dimenhydrinate), chemotherapy, ketoconazole
Cancer Surgical disfigurement, alopecia, weight changes, hormonal changes, fatigues,
depression/anxiety, fungating wounds, fistulas, alteration in physical perceptions,

307
 brain metastases, RT, effect of sx medications
Neuro MS, CVA, spinal cord injury
Hypo/hyperthyroidism, diabetes, menopause, andropause, hypogonadism,
Endocrine
hyperprolactinemia
Vascular HTN, CAD, PVD
Urology/Gyne Anatomic abnormality, menopause, vestibulitis, STI
Depression, anxiety, PTSD, psychosis, sexual orientation issues, developmental
Psychiatric
issues
ETOH, smoking, mood altering drugs, marijuana, LSD, cocaine

Psychosocial Relationship changes, new couple, infertility, miscarriage, post-partum,

parenthood, teen, empty nest, loss of spouse, affairs, different sexual expectations
Social stressors (job, money, work, etc..)

3. In pts presenting with sexual dysfunction, identify features that suggest organic and non-
organic causes

SD Common in both men and women

Types of sexual dysfunction:

• Desire phase: hypo/hyperactive sexual desire, sexual aversion disorder

• Arousal phase: female sexual arousal disorder, vaginismus, dyspareunia, decreased
lubrication, ED
• Orgasm phase: female orgasmic disorder, premature ejaculation, delayed ejaculation

APA criteria for diagnosing the major female sexual disorders

• Hypoactive sexual desire disorder — deficient (or absent) sexual fantasies and desire
for sexual activity
• Female sexual arousal disorder — inability to attain, or to maintain until completion of
the sexual activity, an adequate lubrication-swelling response of sexual excitement
• Female orgasmic disorder — delay in, or absence of, orgasm following a normal sexual
excitement phase
• Dyspareunia — genital pain that is associated with sexual intercourse
• Vaginismus — involuntary contraction of the perineal muscles surrounding the outer
third of the vagina when vaginal penetration with penis, finger, tampon, or speculum is
attempted

Approach to organic, versus non-organic sexual dysfunction:

• Sexual history, INCLUDING PARTNER HISTORY

• Discontinue/switch possibly offending medications
• Physical exam (emphasis on endocrine, vascular, and uro/gyne)
• Psychiatric disorder screen (e.g. MDD, anxiety, PTSD, psychotic D/O)
• Nocturnal penile tumescence testing

308
 • Duplex Doppler imaging
• Blood work: free testosterone, total testosterone, prolactin, TSH, CBC
• Transvaginal ultrasound, cervical swabs for chlamydia and gonorrhea.

(Routine measurement of serum testosterone to detect hypogonadism in ED continues to be

debated, however Uptodate suggests measuring testosterone levels in men to detect
hypogonadism). Testosterone, FSH, LH level measurements not recommended in women with
sexual dysfunction.

Features that suggest a non-organic cause:

• Abrupt onset
• No history of trauma
• No new meds
• Ongoing nocturnal erections

4. In pts who have sexual dysfunction with an identifiable cause, manage the dysfunction
appropriately

Cause Treatment
Estrogen creams equivalent to Replens for vaginal dryness
Post-menopause
See below for details
Surgically-
induced Testosterone
menopause
Vaginismus Vaginal dilators, counseling, PT, awareness,
Primary: books, counselling
Female
Anorgasmia Secondary: change meds, sildenafil, vibrators if increase stimulation needs
Low libido: if from relationship, treat reason
Vulvar: skin conditions, vulvitis, vulvar vestibulitis, poorly repaired
Female episiotomy
Dyspareunia
Vaginal: lubrication, imperforate hymen, infections, vaginismus
(treat the cause) Pelvic: endometriosis, pelvic varicosities, ovary in cul-de-sac, tumor,
adhesions, UTI, interstitial cystitis, constipation, proctitis
Male decrease
History, possibly counseling
libido
Sildenafil (NO NITRATES), yohimibine or trazodone for psychological to
Erectile
increase libido, intraurethral alprostadil (MUSE), intracavernosal injections
dysfunction
(Caverject), vacuum assisted erection device, penile prosthesis
Ejaculatory
Couple sex therapy, SSRI
disorder

309
Constructive psychological and lifestyle change—balanced healthy diet, increasing physical
exercise, decreasing alcohol and tobacco use—positively impact sexual health by enhancing well-
being, self-worth, and body image and increasing overall stamina.

For postmenopausal women with hypoactive sexual desire disorder in whom non-pharmacologic
therapy has been unsuccessful, we suggest a trial of testosterone (Grade 2B). • For premenopausal
women with sexual dysfunction, recommendation is against androgen therapy (Grade 1B).

5. In pts with identified sexual dysfunction, inquire about partner relationship issues.

As above.

Barriers to effective diagnosis:

• Difficult or embarrassing to discuss.

• Persisting cultural and religious taboos about sex, self-blame about negative sexual
experiences or sexual dissatisfaction—even when related to pain—can lead women to
refrain from discussing
• Attribute to the normal effects of aging.
• May opt to discontinue sexual intercourse altogether.

Treatment of Vaginal atrophy

Nonhormonal treatments (useful for mild symptoms) - OTC vaginal moisturizing agents - do not
reverse atrophic vaginal changes.
Increasing sexual activity play an important role in improving vaginal function. (“use it or lose it
phenomenon”)
Vaginal Estrogen Therapy (VET) - Most effective treatment for moderate to severe symptoms of
VA, provided there are no CI’s (eg. estrogen-dependent tumors). Cream, tablet, or ring form

Low dose VET- solely for VA symptoms (≤50 mcg estradiol or ≤0.3 mg conjugated
estrogens/≤0.5 g cream. A preparation containing only 10 micrograms of estradiol
(Vagifem) is effective).
VET more effective than Systemic estrogen therapy for VA
Progestin not necessary to protect against endometrial hyperplasia or cancer in women
treated for VA with the low dose ring/cream or tablet

Sexually Transmitted Infections - Key Features

Based on the updated PHAC (Jan 2010) Canadian Guidelines on STI

1. In a patient who is sexually active or considering sexual activity, take advantage of

opportunities to advise about prevention, screening and complications of STI’s

Risk factors: Sexual contact has a known STI, under 25, more than 2 partners in the last year,
serial monogamy, no contraception, IDU, other substance use, unsafe techniques (sharing toys,
S&M, unprotected oral), sex work, survival sex, homelessness, anonymous partnering (internet
etc), sexual assault, previous STI
Prevention: Be open to discussing low/lower risk sexual activity (mutual masturbation, oral sex,
toys, etc); buying condoms in advance; limiting alcohol/drugs; harm reduction approaches

310
(making condoms and lube available to those practicing sex work); testing prior to mutual
monogamy

Discuss that condoms quite effective for HIV, Hep B, Chlamydia and Gonorrhea,
incomplete (~ 50% reduction of transmission) for HPV, HSV
Use caution with spermicides in lube – can increase transmission of HIV/STI’s by
causing disruptions and lesions in anal/vaginal mucosa

Key visits: contraception initiation or renewal, atypical symps (dysuria, vaginal infections,
inguinal nodes), Pap/well woman or man exam

2. In a patient with symptoms that are atypical or non-specific for STI’s (dysuria, recurrent
vaginal infections):
a) Consider STIs in the differential.
b) Investigate appropriately.

Common symptoms for women: dysuria, vaginal bleeding/discharge, vulvar or perineal lesion,
pelvic pain, dyspareunia
Common symptoms for men: dysuria, urethral d/c, testicular swelling or pain, genital or perineal
lesion, urethral “awareness” (very common symp of Chlamydia in males)
Other: mucocutaneous lesions/pharyngitis (gonorrhea more common), anorectal pain/discharge,
anorectal abscess
Systemic simps: Fever, weight loss, lymphadenopathy, malaise, flu-like illness, generalized rash

3. In high-risk patients who are asymptomatic, screen and advise about prevention.

It’s important to highlight that we don’t routinely test for all STI’s (ie HPV, HSV)
Women (asymp): Vaginal swab (BV, trich, yeast); cervical NAAT (GC/CT), HIV, RPR
Men (asymp): Urine NAAT (GC/CT), HIV, RPR
MSM or women who have regular receptive rectal sex (asymp): Anoscope, rectal C&S

4. In high-risk patients who are symptomatic for STI’s, provide treatment before confirmation
by laboratory results.

If very typical for HSV lesion, can treat with anti-viral (Acyclovir or Valacyclovir) after taking
swab to decrease symptoms and risk of transmission

High-risk for bacterial STI’s with typical symptoms, treat for both Gonorrhea/Chlamydia -
Cefixime 400 mg PO x1; Doxycycline 100 mg PO BID x 7 days OR Azithromycin 1g PO x1

5. In a patient requesting STI testing:

a) Identify the reasons for testing.
b) Assess patient’s risk.
c) Provide counseling appropriate to risk (i.e., human immunodeficiency virus [HIV] infection
risk, non-HIV risk)

Elements of pre-test counseling for HIV: assess risk, discuss window period (95% produce
antibodies within 3 months, 99% within 6 months), nominal vs. nominal testing, reportability,
risks of false positive, assess supports in case of positive result, obtain consent, make a plan for
obtaining results (usually 7 days).

311
6. In a patient with a confirmed STI, initiate:
- treatment of partner(s).
- contact tracing through a public health or community agency.

Key to complete full course of treatment and abstain from sex until 7 days after treatment of both
partners for bacterial STI’s and trichomonas. No need to repeat dose if vomiting occurs >1 hour
after dose is taken. Free treatment delivered to the partner from index case is available in some
provinces, but generally speaking, all contacts should be seen and assessed whenever possible.
Arrange follow up.

Contact tracing: has public health benefits as well as at the individual level.
Several strategies: Notification done by index case to partners, partners notified by health care
professional (never naming index case), tracing and notification done by public health services
(never naming index case)
Trace back period is 60 days (ie notify all sexual contacts from the past two months) for bacterial
STI’s, 3 months for primary syphilis, 6 months secondary syphilis, 1 year early latent syphilis,
variable for all others.
Reportable: Chlamydia, Gonorrhea, Syphilis, Acute/Chronic Hep B, HIV

7. Use appropriate techniques for collecting specimens.

Ensure universal precautions, labeling, appropriate amounts, etc etc. Self-collection looking
promising, but we are not there yet.

Urethral swab: warn re discomfort, best if no void for 2 hours, introduce 3-4cm and rotate slowly
Cervical swab: remove secretions first, 1-2 cm into canal, rotate 180 deg, not in pre-pubertal girls
Pharyngeal swab: swab post. pharynx and tonsilar crypts
Anorectal swab: blindly, inserting 2-3 cm into anus, or using anoscope (better if symps), culture
better than NAAT for rectal specimens
Vesicular lesion: de-roof and swab, or swab the base. Be sure to use viral culture/swab.
Chancroid lesion: If dark field microscopy available (in BC only at BCCDC), need to wash with
saline and collect fluid, for DFA/IFA, can press a glass slide firmly against lesion and send to lab

8. Given a clinical scenario that is strongly suspicious for an STI and a negative test result, do
not exclude the diagnosis of an STI (i.e., because of sensitivity and specificity problems or
other test limitations).

NAAT most sensitive and specific for both GC/CT; sens/spec of cultures depends on quality of
collection method, transport and culture medium; gram stain for GC has a sens/spec of 95% for
urethral samples in males, much lower in females; NAAT of fluid for HSV approaches 100%;
immunologic serologies for syphilis, HIV, Hep B generally quite good – all depend on window
periods.

Skin Disorder - Key Features

1. In dealing with a persistent skin problem that is not responding to treatment as expected:
a) Reconsider the diagnosis (e.g., “eczema” may really be a fungal infection).
b) Investigate or modify treatment (e.g., for acne).

Common Diagnoses

312
Eczema (Atopic Dermatitis)
• Hereditary relapsing immunologic hypersensitivity of skin producing pruritis (the rash is always
itchy and itching makes it worse!)
(1) Often have personal and family hx of atopy (asthma, hay fever, eczema)
- Usually presents in infancy on cheeks/scalp/extensor surfaces, kids in flexor creases/neck,
adults on hands/flexor surfaces/eyelids
- O/E: dry flaky red areas with indistinct borders. Can have itchy papules, crusts, signs of 2º
infxn, scales, excoriation, lichenification
- Dx: largely clinical, if not responding then consider serum IgE (usu high), patch/skin prick
allergy testing for contact/envir allergens
- Variants: Asteatotic (d/t dry skin, esp in elderly during fall/winter), Dyshidrotic
(papulovesicular lesions on hands/feet then cracks/fissures, Nummular (annular coin-shaped
patches similar to tinea!), Contact (usually irritant: sharp borders on palms, rarely allergic:
dorsum of hand, needs patch testing), Stasis (brown/red pigmentation, dry/scaling on lower legs
assoc with venous insuff)
(2) DDx: tinea, contact dermatitis, seborrheic dermatitis, drug reactions, psoriasis
- Tx: prevention: Glaxal base cream >3x/day esp after bathing. Avoid triggers eg. itching, foods,
washing ++, stress, enviro allergens
- Tx: Mild-moderate steroids OD-BID for flares: Hctz 1-2.5%, Betamethasone 0.05-0.1%.
Consider referral if not effective. At that point consider topical calcineurin inhibitors BID:
Tacrolimus (Protopic) 0.1% adults, 0.03% kids; Pimecrolimus (Elidel) 1%, b/c don’t cause
atrophy. But have incr risk of Ca in animal models.
- Tx: PO antihistamines to control itch eg. Claritin/Reactine/Allegra (non-drowsy), Camphor
(0.5%) and Menthol (0.5%) compounded in Rx cream also help soothe

Seborrheic Dermatitis
• Greasy red or yellow non-pruritic scaling plaques in areas rich in sebaceous glands (scalp, face,
presternal area, body folds)
• Malassezia furfur and Pityrosporum ovale thought to play a role in pathogenesis
• O/E: infants: cradle cap, kids: scalp/flexor creases, adults: scalp, eyebrows/lashes, beard, face,
behind ears, nasolabial folds, sternum. DDx: as for eczema (above.)
• Tx: face/body: Nizoral (Ketoconazole 2%) face/bodywash or cream OD + mild steroid cream
OD-BID; scalp/body: Nizoral shampoo (or Steiprox, or Selsun Blue or Head & Shoulders) OD
+/- Betamethasone 0.1% lotion OD; cradle cap: soak scale in any oil O/N, then brush out flakes,
then wash with warm water and SUNLIGHT soap, if persists use Nizoral cream/shampoo or Hctz
1-2% cream.

Psoriasis
• Plaque psoriasis is m/c; variants: guttate, pustular, erythrodermic, psoriatic arthritis
• Multifactorial inheritance, with 2 peaks of onset: late teens/early 20’s, and 50-60’s
• Chronic/recurrent condition, exacerbated by: trauma, stress, winter, drugs (B-blockers, ACEi,
indomethacin, lithium, antimalarials)
• Koebner phenomenon: induction of a new lesion d/t injury
• Auspitz sign: tiny dots of bleeding when scale is removed
• O/E: symmetrically distributed plaques on scalp, elbows, knees, and back. Plaques are
erythematous with sharply defined margins that are raised above surrounding normal skin. Usu
thick silvery scale, but recent bathing may remove it.
• Dx: largely clinical, punch bx helpful if dx is unclear/lesions not responding to tx
• DDx: atopic dermatitis, seborrheic dermatitis, tinea, cutaneous T-cell lymphoma
• Tx:

313
 • Avoid triggers, topical tx is 1st line (if 5-10% body surface affected), if >10% affected
or topical not effective use systemic tx)
• Topical tx: options are OD-BID mid-high potency corticosteroids, vit D analogue
calcipotrol (Dovonex), and retinoid tazarotene (Tazorac). Lotions or gels can be used for
scalp lesions. Combo tx best eg. calcipotriol + betameth (Dovobet).
• Systemic tx: UVB phototx with topicals, PUVA (Psolarens and long wave UVA
phototx), methotrexate, cyclosporine
• 3rd line tx is with biological agents eg. Remicade, Humira

• Guttate: discrete scattered plaques often following Strep pharyngitis, Tx: throat swab (tx with
Pen if GAS), topicals, UVB, time
• Pustular: sudden onset of red papules that turn into pustules, generalized or just palms/soles,
painful, Tx: topicals, UVB
• Psoriatic arthritis: presents in 5 different patterns, commonly in DIPs

Tinea (fungal infection)

- Infection of skin/hair/nails by dermatophytes results in digestion of keratin causing scaly
skin/broken hairs/crumbling nails
- Tinea captious: infection of scalp/eyelashes/brows, usually in kids, round scaly patches of
alopecia, a boggy kerion may form
- Tinea corporis (ringworm): itchy scaly round/oval plaque with red margin and central clearing
on trunk/limbs/face
- Tinea cruris (jock itch): itchy scaly patch with well-defined curved border and central clearing
on medial thigh (not scrotum)
- Tinea pedis (athletes foot): itchy scaling soles +/- maceration of web spaces, esp 4th
- Tinea unguium (onychomycosis): crumbling distally dystrophic nails, yellowish, opaque with
subungal hyperkeratotic debris
- Dx: skin scrapings, hair/nail clippings analyzed with KOH prep to look for Hyphae
- DDx: atopic dermatitis, seb dermatitis, psoriasis, cutaneous T-cell lymphoma
- Tx:

- Topical tx is 1st line for tinea corporis/cruris/pedis/manuum: clotrimazole (Canesten-

topical), ketoconazole (Nizoral), miconazole (Monistat-derm), terbinafine (Lamisil), or
ciclopirox (Loprox) cream OD-BID 2-4wks (at least 1 wk after resolution); ciclopirox
(Penlac) can be used for nails but not very effective, don’t use nystatin (only effective for
Candidiasis)
- Systemic tx for onychomycosis or tinea capitus: terbinafine (Lamisil) is a CYP 2D6
inhibitor → liver toxicity so no EtOH, itraconazole (Sporanox) is a CYP 3A4 inhibitor so
watch for interactions

Ulcers
- Assoc with venous insuff: commonly over medial malleolus
- Assoc with DM/peripheral neuropathy: at pressure points, painless, m/c at 1st MTP
- Assoc with arterial insuff: usually at tips of toes, painful, deep punched out appearance, feet are
cold/pale with claudication/gangrene/decr pulses, ABI <0.9
- Often secondary bacterial infection
- Dx: physical exam, +/- swab if open, XR or bone scan if ?osteomyelitis
- Tx: prevention (rest/elevate legs, 30 mmHg support stockings, proper footware), antibiotics for
infection (Cephalexin or Cloxacillin PO or may need IV abx), wound dressings, surgery may be

314
indicated

Acne Vulgaris
- Inflammation of the pilosebaceous unit characterized by presence of comedones. In areas of
increased sebum production eg. face/neck/chest/upper back/buttocks
- Onset usually 9-13 yo, due to corresponding rise in androgens, affects most teens
- Dx: clinical, classification depends on type and severity of lesions
- Mild: mostly comedones, may be a few inflammatory lesions, no scars
- Moderate: more papules and pustules, no deep cysts, few/no macroscopic scars
- Severe: cysts and/or nodules, or significant scarring
- Tx:

- Gentle cleansing using mild products eg. Spectro gel or Cetaphil

- Avoid exacerbating factors (eg. cosmetics, excoriating, stress)
- Mild acne: topical retinoic acid cream is best for comedones, benzoyl peroxide or
topical abx (eg. Clindamycin) best for papules, combo even better eg. Benzaclin (start tx
with lower concentration then increase or it will be too drying for skin)
- Moderate acne: add systemic tx to above topicals (eg. Minocycline or Doxycycline),
consider OCP for females (eg. Yaz, Yasmin, Alesse, Diane 35), consider systemic
retinoic acid Isotretinoin (Accutane) x5-6mos in refractory cases
- Severe acne: always use Accutane (0.5-1mg/kg/day divided BID) unless
contraindicated. Complete remission in most pts for yrs but may need one repeat course.
Must do Fasting lipids, LFTs, CBC, 2x neg preg test prior to initiating therapy. Two
forms of contraception (1month pre, during, 1 month post). S/E: Teratogenic, transient
dyslipidemia, increased transaminases, myalgias, often very drying to skin, rarely
precipitates depression/SI.

Rosacea - Chronic inflammatory acneiform disorder of facial pilosebaceous units, coupled with
increased capillary reactivity
- Very common, affecting ~10% fair-skinned people. Onset 30-50yo, females (3:1)
- O/E: papulopustular lesions (NO comedones) with prominent facial flushing and telangiectasias,
symmetrically distributed on central face (chin/forehead/nose/malar skin), can occur on
neck/chest /back/scalp. Sebaceous hyperplasia and fibrosis in late stage dz (eg. rhinophyma). Can
have ocular sx (eg. conjunctivitis, keratitis)
- DDx: acne, perioral dermatitis, folliculitis, seborrheic dermatitis, steroid acne, SLE
- Tx:

- Avoid exacerbators (hot food/drinks, EtOH, sun, wind, hot envir, cosmetics)
- Metronidazole gel/cream (0.75% BID or 1% OD), consider oral abx (eg. minocycline,
doxycycline), Accutane if refractory, laser ablation for telangiectasias

2. In a patient presenting with a skin lesion, distinguish benign from serious pathology (e.g.,
melanoma, pemphigus, cutaneous T-cell lymphoma) by physical examination and appropriate
investigations (e.g., biopsy or excision).

SERIOUS DIAGNOSES (DO NOT MISS)

Basal Cell Ca (BCC)

315
- RFs: exposure to UV light (especially as child), radiation tx, immunosuppression
- Nodular: m/c, usu on face, well-circ pearly/translucent papule, telangiec, ulceration
- Sclerosing: yellow or whitish shiny plaque with less distinct margins
- Superficial: red/pink scaly plaque with slightly rolled border, often on back/chest
- Dx: punch, shave or excisional biopsy
- DDx: intradermal nevus, sebaceous hyperplasia, SCC, melanoma
- Tx: electrodessication/curettage, cryotx, excision +/- Mohs, radiation, Aldara
- Prognosis: 95% cure if <2cm lesion, slow growing with <0.1% mets, yearly f/u

Squamous Cell Ca (SCC)

• RFs: chronic exposure to UV light, radiation tx, immunosuppression, PUVA
• Actinic keratosis: (precursor lesion) well-circ pink scaly plaques, sun-exposed areas
• O/E: hyperkeratotic red nodule/plaque with scale/crust and eventual ulceration
• Dx: punch or excisional bx
• DDx: BCC, melanoma, psoriasis, nummular eczema, Bowen’s dz (SCC in situ)
• Tx: cryotx, Aldara (Imiquimod), Efudex (5-FU) for AKs
• Tx: excision +/- skin grafting for SCC, radiation only if surgery not feasible
• Prognosis: 75% control over 5 yrs, better if neg margins/small lesions, 5-10% mets

Malignant Melanoma
• RFs: fair skin types, multiple common or atypical nevi, immunosuppression, xeroderma,
familial dysplastic mole syndrome, FmHx of melanoma
• O/E: Solitary lesions, usually in hard to see areas. M/c sites back (M), calves (F), but must
check skin/nails/muc membr/eyes. Often found through ABCDE’s (asymmetry, irreg borders,
colour variegation, diameter >6mm, enlargement). May also note bleeding, crusting, sensory
change
• Superficial spreading: (60%) irregular red/white/blue enlarging plaques/papules
• Nodular: (30%) black/blue well-defined ulcerated nodule
• Lentigo maligna: (10%) flat light brown patch then turns dark brown/black/blue
• Acrolentiginous: (5%) dark brown/blue/black macule on palms/soles/subungal area
• Dx: excisional bx and exam of skin/LNs/liver/spleen with ROS for metastatic dz
• DDx: atypical nevus, BCC, SCC
• Tx: wide local excision +/- LN dissec, chemotx if stage II(deep) or stage III (LNs)
• Prognosis: often spreads to LNs (primary RF for recurrence/survival is sentinel node status),
mets to lungs/liver/brain, needs regular self + clinical exams. Stage I (superficial) 90% 5yr
survival, stage II 70%, stage II 40%, stage IV(mets) 10%.

Cutaneous T-cell Lymphoma (Mycosis fungoides)

• T cell lymphoma 1st manifested in skin, usually >50 yo
• DDx: often misdiagnosed as eczema, psoriasis, or tinea
• Premycotic and patch phase: red itchy, often scaly, patches anywhere on body
• Infiltrative plaque phase: patches become raised, thicker, darker, denser. Develop into
horseshoe or bizarre patterns.
• Tumor phase: large mushroom-like lesions/ulceration, spread to LNs/liver/spleen
• Sezary Synd: pruritis, LAD, erythroderma, hair loss, WBC>20 with Sezary cells
• Dx: incisional bx, CBC/smear for Sezary cells, CXR ?hilar LAD, exam for LAD
• DDx: often misdiagnosed as nummular eczema or psoriasis
• Tx: PUVA/narrow band UVB, nitrogen mustard oint, electron beam RT, chemotx
• Prognosis: 5-15yr survival, only 2-3yr if tumors/LAD/extensive dz/erythroderma

Pemphigus

316
• Rare, acute or chronic autoimmune potentially fatal vesiculobullous diseases of the mucous
membr and skin with flaccid non-pruritic epidermal bullae/vesicles on an erythematosus or
normal skin base, many variants (some more serious than others)
• M/c in 40-60yo Asian/Jewish/Mediterranean, assoc with malignancy/MG/thymoma
• Vulgaris (PV): usu starts in mouth, spreads to face/scalp/axillae/groin, painful denuded, blisters
+/- 2º infxn
• Foliaceosus (PF): more superficial blistering with red/scaling/crusting. Starts on face and scalp,
spreads to back/chest, often more limited dz
• Dx: punch bx or shave bx, serum anti-desmoglein IgG Ab
• DDx: Bullous pemphigoid (pruritic with deeper bullae that don’t easily rupture)
• Nikolsky sign: lateral pressure applied to edge of bulla extends bulla laterally, suggesting
epidermis detachment
• Tx:

• Refer derm, if limited PF can try topical steroids first, usu req high dose prednisone 2-3
mg/kg/d until no new blisters, then 1-1.5 until clear, then taper.
• Often concomitant immsuppr agents eg. MTX, cyclophosphamide, azathioprine
• If widespread dz then monitor fluids/lytes, can also apply wet dressings

• Prognosis: usually progresses from mouth to generalized over 6-12mos, lesions heal with
hyperpigmentation but no scar, often fatal if no immunosuppressive tx

3. In a patient presenting with a cutaneous manifestation of a systemic disease or condition

(e.g., Wegener’s granulomatosis, lupus, a drug reaction), consider the diagnosis of systemic
disease and confirm it through history, physical examination, and appropriate investigations.

Systemic Lupus Erythematous

• AI disease affecting connective tissues and blood vessels
• Skin lesions in 85% of SLE

o Malar/Butterfly rash: facial erythematous rash, spares nasolabial folds

o Discoid plaques: raised erythematous patches with keratotic scaling and follicular
plugging
o Generalized erythematous papular/urticarial rash on face/dorsum of hands: spares skin
overlying joints, typically on tips of fingers
o Photosensitivity
o Palpable purpura (vasculitic)
o Palmar erythema
o Alopecia
o Mucous membrane ulcers: 80% on palate

• Tx: sunscreen, steroids (topical or oral), immunosuppressants (azathioprine, methotrexate,

cyclophosphaminde), thalidomide, antimalarials (hydroxychloroquine)

Wegener’s Granulomatosis
• Systemic vasculitis that affects upper airways, lungs, kidneys
• Skin lesions in 50%

o Ulcers: jagged, irregular, undermined borders

o Palpable purpura

317
 o Mucous membrane ulcers
o Eyes: conjunctivitis, episcleritis, scleritis

• Tx: cyclophosphamide, prednisone, +/-rituximab, +/- antibiotics

Thyroid Disorders
Hyperthyroidism/Graves disease
• Skin lesions:

o Pretibial myxedema: pink/skin colored, firm, asymmetrical, nonpitting nodules and

plaques progresses to confluent, smooth, “orange-peel” and possibly verrucous
appearance.

Hypothyroidism
• Skin lesions:

o Myxedema: dull, expressionless face with puffy eyes. Skin is swollen, cool, waxy,
course, pale
o Carotinemia: yellow-orange discoloration of palms/soles
o Alopecia

• Tx: regulate thyroid function

Sarcoidosis
• Granulomatous disease primarily affecting the lungs
• Skin lesions (can have almost any type of skin lesion):

o Papules: mostly on face, small skin-colored lesions, may have central depression of
papules
o Nodules: superficial or subcutaneous, 1-2cm, flesh-colored or hyperpigmented, mildly
tender or asymptomatic
o Plaques: brown/purple infiltrative plaques surrounding orifices on face (nose, mouth)
o Lupus pernio: diffuse violacious soft doughy infiltrations on nose, cheeks earlobes
causing gross enlargement
o Maculopapular rash
o Scars: lesions localize around scars
o Erythema nodosum: painful nodules anterior surface of legs

Scleroderma
• Inflammatory, vascular and sclerotic changes of the skin and other organs (lungs, heart, go)
• Skin lesions:

o Raynaud phenomenon: triphasic color changes with cold. Can be painful.

o Skin sclerosis: shiny, tight, stretched skin with loss of normal facial lines. Distal
anhidrosis (loss of swear glands) and loss of hair on distal extremities
o Rat bite necrosis: painful ulcerations at fingertips
o Sclerodactyly: tapering of fingers
o Beak nose
o Telangectasia: on face

318
 o Hyperpigmentation
o Cutaneous calcifications (aka calcinosis cutis)
o Mucous membranes

• Crest syndrome (calcinosis cutis + Reynauds + esophageal dysfunction + sclerodactyly +

telangectasia)

Inflammatory Bowel Disease

Crohn’s disease/Ulcerative Colitis
• Skin lesions:

o Pyoderma gangrenosum: neutrophilic infiltration of skin and destruction of tissue

causing a superficial, painful hemorrhagic pustule surrounded by erythematous halo.
Proceeds to ulceration.
o Erythema Nodosum: inflammatory/immunologic process causing painful nodules on
the anterior surface of the legs.
o Mucous membrane ulcers

Reiter Syndrome (reactive arthritis)

• Post infectious reactive arthritis
• Conjunctivitis, Urethritis, Arthritis (can’t see, can’t pee, can’t climb a tree)
• Skin lesions:

o Keratoderma blennorrhagicum: brown/red papules/vesicles and pustules with central

erosions and peripheral crusting/scaling (look like mollusk shells) on feet
o Circinate balanitis: shallow pustular erosions on penis
o Eyes: conjunctivitis, uveitis
o Mucous membrane: mouth ulcers

Drug Reaction
• Can mimic any dermatological morphology (usually morbilliform or urticarial)
• Usually within 2 weeks of beginning a new drug
• Rash usually resolves within 7-14 days

319
• Tx: antihistamines, topical steroids, topical antipruritics
• Airway control and epinephrine for anaphylaxis

4. When prompted by a patient with a concern about a localized skin lesion or when screening
for mucocutaneous lesions, inspect all areas of the skin (e.g., nails, scalp, oral cavity,
perineum, soles of the feet, back of the neck).

5. Diagnose and promptly treat suspected life-threatening dermatologic emergencies (e.g.,

Stevens-Johnson syndrome, invasive cellulitis, chemical or non-chemical burns).

Steven-Johnson Syndrome/Toxic Epidermal Necrolysis

- Mucocutaneous cytotoxic immune (T-lymphocyte) reaction characterized by extensive necrosis
and detachment of the epidermis. Usually drug induced (allopurinol, antibiotics, antipsychotics,
antiepileptics, NSAIDs) but can also be caused by chemicals, infections, systemic diseases,
immunizations or idiopathic.
- SJS = <10% body surface, SJS/TEN overlap = 10-30%, TEN = >30% body surface
- Dx: clinical. usually occurs 1-3 weeks after introduction of new drug
- Often febrile prodrome followed by rash
- O/E: starts with target lesions +/-purpura or diffuse erythema and progresses to necrosis
- +mucous membrane/genital/conjunctival involvement
- DDx: erythema multiforme, toxic shock syndrome, erythematous drug reaction, scarlet fever,
phototoxic eruption, GVDH, SSSS, exfoliative dermatitis, Kawasaki disease, paraneoplastic
pemphigus
- Tx: stop offending drug, fluid/electrolyte replacement, burn unit/ICU, steroids controversial
(generally only in adults with SJS, not in kids or TEN), IVIG controversial (generally beneficial),
ophthalmology if eye involvement, monitor for infxn/sepsis, plasmapheresis controversial
- Prognosis: mortality rate 30% TEN, <5% SJS
- associated with shock, electrolyte abn, ATN, GI/RESP sloughing

320
- SCORTEN prognostic scoring system

Cellulitis
- RFs: disruption of skin barrier, inflammation (radiation/eczema), preexisting derm condition,
edema/venous insufficiency
- Cellulitis affects deep dermis and subcut fat (vs. Erysipelas = superficial dermis and lymphatics,
well demarcated, raised)
- Pathogens: usually beta-hemolytic strep (A,B, C, G, F) and MSSA/MRSA(especially if
purulent) but other pathogens in immunocompromised/diabetic (pseudomonas)/neonatal (GBS)
patients
- DDx: nec fasc, gas gangrene, TSS, bursitis, OM, HZV, abscess, dermatitis, DVT, gout,
stings/bites, malignancy
- Cultures: only if anticipate atypical pathogens (diabetics, animal bites, water related injury,
recurrent/persistent infection)
- Tx: elevation, compression, diuretics, antibiotics: oral if systemically well, IV if unwell or
rapidly progressing

Necrotizing Cellulitis
• Clostridial cellulitis: clostridium perfringens – local trauma/recent surgery
• Crepitus in skin
• CK/CT/MRI can help differentiate from clostridial myonecrosis (involving muscle)
• Tx: IV antibiotics and surgical debridement

Necrotizing Fasciitis
• Infxn causing necrosis of subcutaneous fat/fascia but may spare skin.
• Type 1: mixed aerobic/anaerobic bacteria, mostly in diabetic/PVD patients or post-op

o Cervical nec fasc: usually from dental origin, can cause ludwig’s angina
o Fournier’s gangrene: perianal
o Surgical wound infxn

• Type 2: monomicrobial, usually group A strep, case reports of MRSA

• Tx: IV antibiotics and surgical debridement

Chemical burns
• Continue to cause damage as long as active component is in wound
• Acids cause coagulation necrosis, alkalines cause saponification of phospholipids membranes
and cell death
• Eye exposure: irrigate with Morgan lens, r/o globe rupture, optho
• Tx: ABCs, Remove offending agent, brush off dry chemicals, copious water irrigation until
neutral ph achieved (15-30 min for acid, >2h for alkali), fluid resuscitation, topical antibiotics
• Do not irrigate the following with water: lime, phenols, hydrochloric acid, sulfuric acid,
elemental metals
• Specific antidote: hydrochloric acid – calcium gluconate gel

Thermal Burns
• Classification

o Superficial (sunburn): red, blanches, painful

o Superficial partial thickness (scald): blisters, red, weeping, blanches, painful

321
 o Deep partial thickness (flame/oil/grease/scald): friable blisters, wet or waxy, does not
blanche, not painful, only sensitive to pressure
o Full thickness (flame/steam/oil/grease/chemical/electrical/immersion):
waxy/leathery/charred, dry, inelastic, does not blanche

• When to admit/transfer?

• ABCs/ATLS
• Respiratory: early intubation and oxygen for any smoke inhalation (consider CXR, ABG,
carboxyhemoglobin levels), many develop ARDS
• Fluids: (half of volume given over 8 h, then second half over following 16 h)

o Parkland formula: Ringers Lactate at 4mL/kg x % body burned

o Modified Brooke formula: 2mL/kg x % body burned – may reduce complications of
over resuscitation without causing harm
o Peds: Galveston formula: 5000 mL/m2 x % body burned. Add 2000 mL/m2 per day for
maintenance requirements

• Analgesia: opiates/benzos
• Tetanus prophylaxis
• Complications: infection, mesenteric constriction/ulcers/aspiration, scarring may require
escharotomy
• Tx: wound care, topical antibiotics, fluid resuscitation, infection control, transfer to burn unit for
major burns

6. In high-risk patients (diabetics, bed or chair bound, peripheral vascular disease):

a) Examine the skin even when no specific skin complaint is present.
b) Treat apparently minor skin lesions aggressively.

7. In a patient being treated for a new or persistent skin condition (e.g., acne, psoriasis),
determine the impact on the patient’s personal and social life.

322
Somatization - Key Features

1. In patients with recurrent physical symptoms, diagnose somatization only after an adequate
work-up to rule out any medical or psychiatric condition (e.g., depression).

2. Do not assume that somatization is the cause of new or ongoing symptoms in patients
previously diagnosed as somatizers. Periodically reassess the need to extend/repeat the work-up
in these patients.

3. Acknowledge the illness experience of patients who somatize, and strive to find common
ground with them concerning their diagnosis and management, including investigations. This
is usually a long-term project, and should be planned as such.

4. In patients who somatize, inquire about the use of and suggest therapies that may provide
symptomatic relief, and/or help them cope with their symptoms (e.g., with biofeedback,
acupuncture, or naturopathy).

Definition: Patients with somatization disorder experience their emotional distress or difficult life
situation through physical symptoms, where no physiologic explanation can be found

The DSM-IV-TR diagnostic criteria are:

• A history of somatic complaints over several years, starting prior to the age of 30.
• At least four different sites of pain on the body, AND at least two gastrointestinal
problems, AND one sexual dysfunction, AND one pseudoneurological symptom.
• Such symptoms cannot be fully explained by a general medical condition or substance
use OR, when there is an associated medical condition, the impairments due to the
somatic symptoms are more severe than generally expected.
• Complaints are not feigned as in malingering or factitious disorder

Diagnostic Features Suggesting Somatization

Multiple symptoms, often occurring in different organ systems (KEY FEATURE)
Symptoms that are vague or that exceed objective findings
Chronic course (KEY FEATURE)
Presence of a psychiatric disorder
History of extensive diagnostic testing
Rejection of previous physicians

Diagnosis
• Perform a comprehensive physical examination to rule out physical causes for the patient's
somatic complaints. A detailed focus on specific systems, ie, neurological, may be necessary; this
is based on the specific complaint.
• Order appropriate blood work and or imaging to rule out organic disease
• Include a full mental status examination. A patient with somatoform disorder displays the
following on an examination.

323
 o Appearance - Normal
o Attitude and behavior - Attitude is appropriate and behavior demonstrates a
preoccupation with physical symptoms and complaints.
o Mood - Mildly anxious and depressed
o Affect - Full range and appropriate
o Thought disorder - None, although thoughts are limited to issues around physical
symptoms.
o Hallucinations - None
o Delusions - None
o Obsessions - None
o Compulsions - None
o Attention - Within normal range
o Memory - Within normal range
o Concentration - Within normal range
o Orientation - Patient is oriented to time, place, and person.
o Insight and judgment - Insight appears limited in that nonmedical causes of symptoms
are not considered. Judgment appears unimpaired.
o Suicidal and homicidal ideation - No evidence of such

Etiology
-No definitive causes for most of the somatoform disorders have been established.
-Genetic and environmental influences appear to contribute to somatization.
-Children raised in homes with a high degree of parental somatization may model somatization.
-Sexual abuse may be associated with an increased risk of somatization later in life.
-Poor ability to express emotions (alexithymia) may result in somatization

Psychiatric comorbidity
-Alcohol and drug abuse are common in patients with somatoform disorders. Patients may
attempt to treat their somatic pain with alcohol or other drugs.
-Additionally, alcohol or drug intoxication or withdrawal may induce somatic symptoms of
unclear etiology, unless the physician considers the potential role of substances.
-Anxiety disorders and mood disorders commonly include physical symptoms as part of the
presentation. Ruling out a primary anxiety disorder or mood disorder is key before reviewing the
role of somatoform disorders.

-->coexisting depression (up to 60 percent), anxiety disorders such as panic or obsessive-

compulsive disorder (up to 50 percent), personality disorders (up to 60 percent) or a
substance abuse disorder

Patient Management
- Key patient educational issues include the following:

• The physician acknowledges the patient's symptoms and suffering.

• The physician takes on the role of evaluation and monitoring of symptoms.
• Not all symptoms indicate evidence of a pathological disease.
• The patient should attempt to maintain interpersonal function despite symptoms.

324
 • Physical symptoms not due to a defined disease often remit spontaneously.
• Identifying key life stressors and sources of anxiety can be important.
• Stress reduction may produce improvement in physical symptoms.
• Aggressive surgical approaches should be used cautiously and only with the approval of
a primary care physician who knows the patient well.

Family Education
- Family education is often crucial for the successful management of somatoform disorders. For
the patient's family members, this education should include the following:

• Discuss the somatoform diagnosis.

• Expect the patient to improve and return to normal function.
• Direct the patient to discuss any somatic symptoms with the primary care provider.
Patients should not seek assistance from family members in assessing the seriousness of
their symptoms or the diagnosis relating to their symptoms
• The primary care provider should direct any need for subspecialty evaluation.
• Family members should spend time with and pay attention to the patient when
symptoms are absent. For the patient, this reinforces the idea that their symptoms do not
bring special attention from others.
• Family members may help by providing distraction activities if somatic symptoms are
present, eg, going for a walk or going out to a movie

Practice Management Strategies for Somatoform Disorders

-Accept that patients can have distressing, real physical symptoms and medical conditions with
coexisting psychiatric disturbance without malingering or feigning symptoms
-Consider and discuss the possibility of somatoform disorders with the patient early in the work-
up, if suspected, and make a psychiatric diagnosis only when all criteria are met
-Once the diagnosis is confirmed, provide patient education on the individual disorder using
empathy and avoiding confrontation
-Avoid unnecessary medical tests and specialty referrals, and be cautious when pursuing new
symptoms with new tests and referrals
-Focus treatment on function, not symptom, and on management of the disorder, not cure
-Address lifestyle modifications and stress reduction, and include the patient's family if
appropriate and possible
-Treat comorbid psychiatric disorders with appropriate interventions
-Use medications sparingly and always for an identified cause
-Schedule regular, brief follow-up office visits with the patient (five minutes each month may be
sufficient) to provide attention and reassurance while limiting frequent telephone calls and
“urgent” visits
-Collaborate with mental health professionals as necessary to assist with the initial diagnosis or to
provide treatment, including CBT, which has been found to be an effective treatment for
somatization disorder

Stress - Key Features

1. In a patient presenting with a symptom that could be attributed to stress (e.g., headache,
fatigue, pain) consider and ask about stress as a cause or contributing factor.

325
20-25% of Canadians >15yrs rate daily life as “quite a bit” or “extremely” stressful.

Acute Stress

Physical Response Emotional Response

- Denial (defense mechanism)

- ↑ ACTH, epi + norepi, glucocorticoids and endorphins - Disbelief

- Shock
- Anger
- ↓ Insulin+ reproductive hormones (est, prog, test)
- Anxiety
- ↑ Cognition + memory
- Restlessness
- ↓ Pain sensation
- Confusion
- ↑ Energy stores mobilized, heartrate, metabolic rate, bp, resp rate
- Self-doubt
- Forgetfulness
- Fear, anger and excitement

Chronic Stress

Physical Response Emotional Response Behavioural Response

Gl upset
Mental blocks
Sleep disturbances Mistakes or judgment errors
Headaches Hopelessness,
Lethargy frustration
Impulsiveness
Muscle + Back pain Boredom
Inappropriate or aggressive
↓ libido Reduced feelings of
communication
↓ Immune response empathy
Apathy
↑ risk developing mood disorder Chronic fatigue
Increased drug or alcohol use
(GAD, MDD) Anger, cynicism,
Withdrawal, isolation
↑ serum cholesterol pessimism
↑ difficulty maintaining healthy life
↑ blood pressure Depression
style (diet, exercise, sleep)
↑ platelet aggregation Nervousness
Disordered eating
↑ risk of cardiovascular events Self-hate
↑ risk of DM related complications Guilt
and metabolic syndrome

2. In a patient in whom stress is identified, assess the impact of the stress on their function (i.e.,
coping vs. not coping, stress vs. distress).

Stress: any demand on the body, mind and spirit to perform. Function is maintained and coping is
adaptive.
Distress: Coping and adaptation processes fail to return an organism to physiological and/or
psychological homeostasis.
Coping: Behavioral response to reduce stress in non-detrimental way. Function maintained.

326
Not coping: Appreciable decline in social, work, economic, family functioning and/or
maladaptive coping (ETOH, substances, smoking, social withdrawl, etc)

A) Assess function (all domains): school, family, relationships, work, health behaviors (exercise,
diet, sleep), substance use, sexual function, psychological health

B) Identify maladaptive/deleterious coping strategies/behaviors

3 main ways people cope with stress (can be adaptive or maladaptive)

Task-oriented: analyze situation and take action to deal directly with situation.
Emotion-oriented: address feelings and find social supports.
Distraction-oriented: use activities or work as distraction.

3. In patients not coping with stress, look for and diagnose, if present, mental illness (e.g.,
depression, anxiety disorder).

Stress has high comorbidity with anxiety, depression and psychoses

Screen for following:

MDD
Eating disorders
GAD
Panic Disorder
Phobias
Acute Stress disorder (symptoms of PTSD with onset before 4 weeks and duration < 4
weeks)
PTSD

Diagnostic Criteria for Post-traumatic Stress Disorder

A. The person has been exposed to a traumatic event in which both of the following were present:
1. The person experienced, witnessed, or was confronted with an event or events that
involved actual or threatened death or serious injury, or a threat to the physical integrity of
self or others.
2. The person's response involved intense fear, helplessness, or horror.
B. The traumatic event is persistently re-experienced in one (or more) of the following ways:
1. Intrusive distressing recollections(young children, repetitive play)
2. Nightmares
3. Flashbacks/hallucinations
4. Intense psychologic/physiologic distress at exposure to cues resembling the event.
C. Avoidance of stimuli associated with the trauma + numbing of general responsiveness
D. Persistent symptoms of increased arousal (irritable, hypervigilant, ↑ startle, ↓ [ ]
E. Duration is more than one month.
F. Causes clinically significant distress or impairment in function.

327
Prognosis: Spontaneous improvement, lasts 36 months (treatment), 64 months (no
treatment), > 1/3 never fully recover
(+) prognosis if: Rapid engagement of treatment, early/ongoing social support, avoidance
of retraumatization,good premorbid function, and absence of psychiatric disorders or
substance abuse.

Comorbidity Men (%) Women (%)

Alcohol abuse or dependence 51.9 27.9
Drug abuse or dependence 34.5 26.9

Treatment:

NO! Exposure therapy and psychotherapy to relive experiences = (BAD)

Behavioural and cognitive therapy (enroll families in therapy as well)
SSRI (sertraline, Fluvoxamine, paroxetine) ↓ numbing, avoidance, hyperarousal
Clonidine/Risperidone may ↓ intrusive recollections, nightmares, hypervigilance and
outbursts of anger
Benzos: ↓ anxiety but no impact on core symptoms (↑ substance abuse = avoid benzos)

4. In patients not coping with the stress in their lives,

a) Clarify and acknowledge the factors contributing to the stress,
b) Explore their resources and possible solutions for improving the situation.

Stress Reduction Therapies:

Exercise!!!
Control manageable issues
Counseling/ CBT
Encourage peer social support
Massage
Breathing exercises + Progressive muscle relaxation
Mediation (mindfulness, transcendental, guided imagery)
Acupuncture

5. In patients experiencing stress, look for inappropriate coping mechanisms (e.g., drugs,
alcohol, eating, violence).

Screen for:

Substance use
ETOH
Overworking

328
 Eating disorders
Anger/aggressive behaviour
Smoking

Stroke - Key Features

1. In patients presenting with symptoms and/or signs suggestive of stroke, include other
diagnoses in the differential diagnosis (e.g., transient ischemic attack [TIA], brain tumour,
hypoglycemia, subdural hematoma, subarachnoid bleed).

2. In a patient presenting with a stroke, differentiate, if possible, hemorrhagic from

embolic/thrombotic stroke (e.g., through the history, physical examination, and ancillary
testing, such as scanning and electrocardiography), as treatment differs.

3. Assess patients presenting with neurologic deficits in a timely fashion, to determine their
eligibility for thrombolysis.

4. In a patient diagnosed with stroke, involve other professionals as needed (e.g., a physical
therapist, an occupational therapist, social service personnel, a physiatrist, a neurologist) to
ensure the best outcome for the patient.

5. When caring for a stroke patient with severe/serious deficits, involve the patient and her or
his family in decisions about intervention (e.g., resuscitation, use of a feeding tube, treatment
of pneumonia).

6. In patients who have suffered stroke, diagnose “silent” cognitive deficits (not associated with
sensory or motor symptoms or signs, such as inattention and impulsivity) when they are
present. 7. Provide realistic prognostic advice about their disabilities to stroke patients and
their families.

8. In stroke patients with disabilities, evaluate the resources and supports needed to improve
function (e.g., a cane, a walker, home care).

9. In the continuing care of stroke patients with deficits (e.g., dysphagia, being bedridden),
include the prevention of certain complications (e.g., aspiration pneumonia, decubitus ulcer) in
the treatment plan, as they are more common.

10. In patients at risk of stroke, treat modifiable risk factors (e.g., atrial fibrillation, diabetes,
hyperlipidemia, and hypertension).

11. In all patients with a history of TIA or completed stroke, and in asymptomatic patients at
high risk for stroke, offer antithrombotic treatment (e.g., acetylsalicylic acid, clopidogrel) to
appropriate patients to lower stroke risk.

STROKE
Definition

• An acute neurological injury that occurs due to either brain ischemia or brain
hemmorrhage

329
Types

1. Ischemic (87%)
a. Thrombotic
b. Embolic
c. Hypoperfusion related
2. Hemorrhagic
a. Intracerebral(10%) b. SAH(3%)

History

• Typically sudden onset of sx

• Weakness, esp unilateral
• Confusion
• Aphasia
• Visual deficit/diplopia
• Dizziness, gait disturbance, ataxia
• Sudden severe HA with no known cause

• Atypical sx
• SOB
• LOC or syncope
• Sudden pain in chest, arms, legs
• Seizure
• Sudden hiccups, fatigue, palpitations
• Altered mental status

• Risk Factors
• HTN
• DM
• CAD
• A-fib
• Valve replacement
• Recent MI
• Bleeding diathesis (i.e anticoagulation)

Physical Exam

• Assess ABCs
• GCS

330
 • Screening neurological exam assessing visual, motor, sensory, coordination, and
language functions

Work Up

• Capillary blood glucose

• CBC, lytes, BUN, Cr
• INR, PTT
• ECG
• Consider: LP, tox screen, CXR (for aspiration) depending on presentation
• Imaging
• Emergent non-contrast CT head
• Most acute ischemic strokes are not visualized by non-contrast CT in early hours of a
stroke
• Role of CT is primarily to exclude intracranial bleeding, tumour, and other stroke
mimics
• Remember to do LP if suspicion of SAH and normal CT

Management

• Hypertension in ischemic stroke

• If no thrombolytic therapy, should treat if SBP >220 or DBP >120, or if serious other
comorbidities (i.e. ACS, AKI, HF etc)
• Cautiously lower BP by 15% within first 24h
• Can restart previous antihypertensives at ~24h if neurologically stable
• Stricter control if thrombolysis being considered or has been done
• Hyperglycemia
• Less favourable outcomes in the setting of hyperglycemia, so it should be treated if >10
• Thrombolysis
• Need to determine time of symptom onset!defined as last moment patient was at
baseline
• Thrombolysis not recommended if time of onset unclear
• Inclusion criteria
• Acute ischemic stroke
• 18-80 y/o
• Onset of symptoms 3-4.5h before rtPA administration (time varies between
institutions/guidelines)
• Stroke sx present for at least 30 minutes without significant improvement
• Exclusion Criteria
• Lengthy list, but includes ICH, coagulopathy, seizure at onset, significant HTN, or
unclear dx
• Antiplatelet therapy (for ischemic stroke)
• ASA 325mg w/I 24-48h after stroke onset (does not interfere with thrombolysis)
• Other considerations
• Aspiration risk
• NPO until swallowing assessment

331
 • May need NG or PEG feeds!discuss wishes w/ pt/family
• Elevated head of bed to 30 degrees if concerned about increased ICP, aspiration,
oxygen desaturation
• Maintain normothermia
• Pneumonia most common cause of fever w/I 1st 24h
• DVT prophylaxis with UFH or LMWH in patients w/ ischemic stroke and limited
mobility (wait 24h if thrombolyzed)
• Urinary incontinence common
• Most commonly d/t detrusor hyperrflexia from loss of inhibitory input from CNS
• Beware of bedsores
• Frequent repositioning q2h ideally if bed bound
• Pressure reducing products
• High rates of post-stroke depression (18-61%)
• Multi-disciplinary approach
• Involve OT, PT, SLP, stroke rehab if available
• D/C planning-consider need for home support, assisted living, placement

Secondary Prevention

• Antiplatelet therapy for non-cardioembolic stroke/TIA

• ASA 81mg od OR
• Clopidogrel 75mg od OR
• ASA + Aggrenox (ER Dipyridamole)
• Clopidogrel vs ASA
• Clopidogrel slightly more effective (5.3% vs 5.8% rate of stroke, MI, vascular death
annually), but marginal benefit may be offset by cost (CAPRIE Trial)
• Slighly lower rates of GI bleeding w/ clopidogrel vs ASA
• Don’t use ASA and clopidogrel together-no benefit and increased rates of adverse
events-unless there is some other indication (i.e ACS, PCI etc)
• Dyslipidemia/Statin Therapy
• Conflicting evidence, some suggestion that dyslipidemia is not a strong risk factor for
stroke but...
• Atorvostatin 80mg po od for anyone with TIA or ischemic stroke of atherosclerotic
origin
• ARR of fatal/nonfatal stroke at 5 years = 2.2%
• ARR of any coronary event 6.5% (SPARCL trial)
• Consider combining statin with niacin or gemfibrozil if HDL <1
• Treat DM2 and HTN
• Lifestyle modification

Primary Prevention

• Lack of data for ASA in mod –high risk patients (Framingham risk >10%), so use
clinical judgement

332
TRANSIENT ISCHEMIC ATTACK
Definition

• A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or

retinal ischemia, without acute infarction
• Duration (i.e. <24h) no longer included in definition

Prognosis

• Increased risk of stroke (up to 17% 90 day risk)

• Predictor of imminent stroke (4-10% risk w/i 48h)

Clinical Manifestation

• Low flow (i.e. secondary to carotid stenosis, vertebrobasilar lesion etc)

• Usually brief (i.e. minutes), recurrent
• Carotid stenosis/MCA lesion
• Usually stereotyped
• Hand, face, arm, leg numbness/weakness
• Aphasia if dominant hemisphere
• Vertebro-basilar circulation
• Not stereotyped
• Brainstem and cerebellar sx
• Dizziness w/ or w/o vertigo
• Dysarthria
• Diplopia, ptosis
• Arm/leg numbness or weakness-can be bilateral
• Facial numbness
• Embolic
• Typically last hours
• Sx as above, but if in PCA distribution may include
• Ataxia
• Hemianopsia
• Hearing loss
• Crossed face and body numbness

Work-Up

• ABCD2 score
• Prognostic scoring tool designed to identify patients at high risk of ischemic stroke in
the first two days after a TIA
• Can be used to determine inpatient vs outpatient therapy
• Imaging
• CT or MRI brain recommended ASAP, w/i first 24h
• Neurovascular evaluation
• Most patients will get a duplex u/s of carotids initially, or possibly CTA/MRA

333
 • Cardiac evaluations
• ECG
• ECHO if no cause for TIA found on w/u

Management

• Risk factor reduction-see recommendations for secondary prevention of stroke

• Carotid Endarterectomy (CEA)
• Symptomatic and > 50% stenosis, with life expectancy >5 years --> refer to vascular
surgeon
• CEA usually recommended in patients w/ recently symptomatic carotid stenosis of 70-
99% with a life expectancy of >5 years
• Symptomatic stenosis 50-69%-CEA usually recommended in men but not women
• <50% stenosis-medical management
• Near occlusion-CEA not beneficial
• Ideally CES should be done w/I 2 weeks of last event

334
*Note-Above table does not include metabolic causes (i.e. hypoglycemia, other metabolic
disturbances), encephalopathy

335
Substance Abuse - Key Features

1. In all patients, and especially in high-risk groups (e.g., mental illness, chronic disability),
opportunistically screen for substance use and abuse (tobacco, alcohol, illicit drugs).

2. In intravenous drug users:

a) Screen for blood-borne illnesses (e.g., human immunodeficiency virus infection, hepatitis).
b) Offer relevant vaccinations.

3. In patients with signs and symptoms of withdrawal or acute intoxication, diagnose and

336
manage it appropriately.

4. Discuss substance use or abuse with adolescents and their caregivers when warning signs
are present (e.g., school failure, behaviour change).

5. Consider and look for substance use or abuse as a possible factor in problems not
responding to appropriate intervention (e.g., alcohol abuse in patients with
hypertriglyceridemia, inhalational drug abuse in asthmatic patients).

6. Offer support to patients and family members affected by substance abuse. (The abuser may
not be your patient.)

7. In patients abusing substances, determine whether or not they are willing to agree with the
diagnosis.

8. In substance users or abusers, routinely determine willingness to stop or decrease use.

9. In patients who abuse substances, take advantage of opportunities to screen for co-
morbidities (e.g., poverty, crime, sexually transmitted infections, mental illness) and long-term
complications (e.g., cirrhosis).

Presentation and clinical features:

- Substance use disorders are Axis I diagnoses and include two mutually exclusive sub-
categories - substance abuse and substance dependence

Substance Abuse
When any 1 of A and both B and C are "yes," a definite diagnosis of abuse is made:
A. Has the client experienced the following?

1. Recurrent failure to meet important responsibilities due to use?

2. Recurrent use in situations when this is likely to be physically dangerous?
3. Recurrent legal problems arising from use
4. Continued to use despite recurrent problems aggravated by the substance use

B. These symptoms have occurred within a 12 month period

C. Client had never met the criteria for dependence

Substance Dependence
When any 3 of A, and B are "yes," a definite diagnosis of dependence is made:
A. Has the client experienced the following?

1. Tolerance (needing more to become intoxicated or discovering less effect with same
amount)
2. Withdrawal* (characteristic withdrawal associated with type of drug)
3. Using more or for longer periods than intended?
4. Desire to or unsuccessful efforts to cut down?

337
 5. Considerable time spent in obtaining, using, or recovering from the effects of the
substance?
6. Important social, work, or recreational activities given up because of use?
7. Continued use despite knowledge of problems caused by or aggravated by use.

B. Have these symptoms been present during the same 12 month period?
* A clearcut withdrawal syndrome is not present with some classes of drugs: caffeine,
phencyclidine, or hallucinogens.

- Acknowledge warning signs (e.g., school failure, behaviour change) and discuss substance use
and abuse with adolescents and their caregivers

Differential diagnoses:
- Screen for substance use and abuse (tobacco, alcohol, illicit drugs) in all patients, and especially
in high-risk groups (e.g., mental illness, chronic disability)
- Consider substance use or abuse when problems don’t respond to appropriate interventions
(e.g., alcohol abuse in patients with hypertriglyceridemia, inhalational drug abuse in asthmatic
patients, chronic disease)
- Grief

History-taking:
- Conduct multiple assessments over time (e.g. after 2 to 3 weeks of decrease in consumption)
and use multiple assessment methods
- Be sensitive to consumers' concerns;
- Conduct the assessment when he/she is sober, drug-free and reasonably stable emotionally;
- Provide assurance of confidentiality;
- Establish a good rapport before asking for a lot of details;
- Use simple direct questions with clearly defined time frames;
- Do not aim for levels of specificity that exceed assessment goals;
- Frame questions to normalize different substance use patterns (e.g., many people have
experimented with drugs? Have you ever had any experiences with.....?); and
- Verify the information as much as possible with other sources to converge on a consistent set of
conclusions.
- Screen for co-morbidities (e.g., poverty, crime, sexually transmitted infections, mental illness,
depression, anxiety, eating disorders) and long-term complications (e.g., cirrhosis)
- Assess family history of disorders
- Assess childhood variables (e.g., trauma, neglect, abuse)
- Assess natural history (i.e., onset, course, fluctuations, remissions)
- Assess patterns and severity of alcohol consumption (e.g., episodic vs. daily)
- Assess the effect of improvements

A detailed substance use history includes:

- the frequency and pattern of use;
- the level of dependence;
- the consequences that result.
- Get the full substance abuse history: (how old were they when they started ____? How did use
of ______ change with time? How much ______ are they using now? Have they tried quitting
______ in the past? What were the results? Have they experienced withdrawal? How did that go?
- The best predictor of a substance use problem by the consumer was their perception that others
were concerned about their substance use (70% sensitivity: 88% specificity; 76% positive

338
predictive value; and 84% negative predictive value). It is cautiously recommended that the three
following questions be used as potential Level I screening questions for substance use disorders.
A positive response to any one question should indicate the need for further investigation:

1. Have you ever had any problems related to your use of alcohol or other drugs?
2. Has a relative, friend, doctor or other health worker been concerned about your
drinking or other drug use or suggested cutting down?
3. Have you ever said to another person "No, I don't have [an alcohol or drug] problem,
when around the same time, you questioned yourself and FELT, "Maybe I do have a
problem?"

- Determine whether or not they are willing to agree with the diagnosis (assess stage of change)
and routinely determine willingness to stop or decrease use

The "Stages of Change" identifies five stages in the change/recovery process:

• pre-contemplation is the stage at which there is no intention to change behavior in the
foreseeable future;
• contemplation is the stage in which people are aware that a problem exists and are seriously
thinking about overcoming it but have not yet made the commitment to take action;
• preparation combines the intention to take action within the next month with lack of success in
taking action during the past year;
• action is the stage in which individuals modify their behavior, experiences, or environment in
order to overcome their problems;
• in maintenance, people work to prevent relapse and consolidate the gains attained during the
action phase.

Motivational strategies for Behavioral Change:

Stage AIM PLAN

• Encourage patient to consider
• Raise issue in sensitive manner
Pre- change
Contemplation
• Offer neutral exchange of Info
• Increase Pt’s awareness
• Offer opportunity to discuss pros and
Contemplation • Understand Pt’s Ambivalence
cons
• Explore options and choose course
most appropriate for pt
• Offer realistic options for change
Preparation
• ID strategies for relapse
• Discuss inevitable difficulties
• Strengthen confidence and
commitment
• Help pt design way to reward
themselves
• Offer positive reinforcement and explore
Action
• Develop strategies to prevent ways to cope with obstacles
relapse
• Support and reinforce convictions
Maintenance • Help Maintain motivation • Discuss progress and cues for impending
relapse

339
 • ID high risk situations
• Offer non-judgemental discussion about
• View it as a learning experience circumstances
Relapse
• Provide support • How to avoid relapses in the future
• Reassess readiness for change

Physical Exam:
Diagnose signs and symptoms of acute intoxication vs withdrawal:

ABC checklist for a mental health status exam includes:

Appearance: General appearance, hygiene, and dress.

340
Alertness: What is the level of consciousness?
Affect: Elation or depression: gestures, facial expression, and speech.
Anxiety: Is the individual nervous, phobic, or panicky?
Behavior:
Movements: Rate (hyperactive, hypoactive, abrupt, or constant?).
Organization: Coherent and goal-oriented?
Purpose: Bizarre, stereotypical, dangerous, or impulsive?
Speech: Rate, organization, coherence, and content.
Cognition:
Orientation: Person, place, time, and condition.
Calculation: Memory and simple tasks.
Reasoning: Insight, judgment, problem solving.
Coherence: Incoherent ideas, delusions, and hallucinations?

Investigations and diagnostic work:

- Screen for blood-borne illnesses (e.g., HIV infection, hepatitis) in IV drug users

Management
- Treat the context of substance misuse
- Engage client in identifying and managing cues to misuse, practical problem-solving with
emphasis on action and reliance on social supports, and resolving ambivalence about change
- Ensure client choice and tailor to the person's stage and motivation for change
- Offer relevant vaccinations in IV drug users
- Offer support to patients and family members affected by substance abuse
- Consider a harm reduction approach (e.g. flexible goals)
- Consider non-pharmacologic: Alcoholics Anonymous or equivalent, detox, treatment centre,
rehab, psychotherapy
- Manage symptoms of withdrawal or acute intoxication (pharmacological symptom management
which is highly disorder-specific – see below for proposed algorithms)

Proposed algorithm for the diagnosis of drug intoxication and withdrawal:

Drug-Transmitter Actions That Cause Symptom Complexes:

Neurotransmitters:
Drug class: GABA 5-HTP Norepinephrine AcCH β-Endorphin Dopamine
Opiates X X
Dissociatives X X X X X
Psychedelics X
Stimulants X X
Alcohol, sedatives,
X X X X
tranquilizers

Drugs of Abuse: Six Groups That Are Likely to Require Primary Care Medical:

Action on affected
Drug class and members Neuroreceptors
neurotransmitter
Anticholinergics: Acetylcholine Nicotinic and

341
Asthmador, Benztropine (Cogentin),
antagonists muscarinic
Dimenhydrinate (Dramamine), Diphenhydramine
(Benadryl), Hydroxyzine (Atarax), Locoweed
Dissociatives:
Affect actions of all
All receptors
Ketamine (Ketalar), Phencyclidine (PCP), neurotransmitters
Phenylcyclohexylpyrolidine (PHP)
Opiates:
Κ
Butorphanol (Stadol), Pentazocine (Talwin), β-Endorphin agonists
Heroin, Hydromorphone (Dilaudid-Hp), μ
Mesipramine, Methadone, Morphine
Psychedelics:

Borneol, Lysergic acid diethylamide (LSD), Serotonin agonists 5-HT-2

Mescaline, Methylenedioxymeth-amphetamine
(MDA), Psilocybin, Sufrole
GABA-A
Sedative-hypnotics:
GABA agonists
Benzodiazepines:
Barbiturates, Ethchlorvinyl (Placidyl),
Ethyl alcohol: GABA GABA-A-α
Glutethimide (Doriden), Methaqualone, Zolpidem
and opioid agonist Ethyl alcohol:
(Ambien), Benzodiazepines Ethyl alcohol
GABA-A and μ
Stimulants:
Dopamine,
DA-2, 5-HT-2, α
norepinephrine and
Amphetamine, Cocaine Methamphetamine and β
serotonin agonists
(Desoxyn), Methylphenidate (Ritalin)

Specific Treatment Based on Affected Neurotransmitter:

Neurotransmitter: Treatment:
Intoxication and overdose:
Acetylcholine (anticholinergic) Physostigmine (Antilirium)
β-Endorphin Naloxone (Narcan)
Benzodiazepine
Dopamine
Butyrophenone
GABA Mechanical support
Beta blocker
Norepinephrine
Benzodiazepine
Serotonin Benzodiazepine
Withdrawal:
β-Endorphin Methadone

342
 Clonidine (Catapres)
Dopamine Bromocriptine (Parlodel)
GABA Barbiturate or benzodiazepine replacement
Norepinephrine Desipramine (Norpramin)
Serotonin Fluoxetine (Prozac)

Suicide - Key Features

1. In any patient with mental illness (i.e., not only in depressed patients), actively inquire about
suicidal ideation (e.g., ideas, thoughts, a specific plan).

Assessment of Suicidal Ideation

• Onset and frequency of thoughts – “When did this start? How often do you have these
thoughts?”
• Control over suicidal ideation – “Can you stop the thoughts or call someone for help?”
• Lethality – “Do you want to end your life or get a ‘release’ from your emotional pain?”
• Access to means – “How will you get a gun?” “Which bridge do you think you would go to?”
• Time and place – “Have you picked a date and place? Is it in an isolated location?”
• Provocative factors – “What makes you feel worse (e.g. being alone)?”
• Protective factors – “What keeps you alive (e.g. friends, family, pets, faith, therapist)?”
• Final arrangements – “Have you written a suicide note? Made a will? Given away your
belongings?”
• Practiced suicide or aborted attempts – “Have you put the gun to your head? Held the
medication in your hand? Stood at the bridge?”
• Ambivalence – “There must be a part of you that wants to live – you came here for help.”

- >90% of patients who attempt suicide have a major psychiatric disorder

- 95% of patients who commit suicide have a psychiatric diagnosis

Canadian Task force on Preventative Health Care (1994)

- poor evidence (expert opinion alone) to include or exclude routine evaluation of suicide risk in
the periodic health examination
- physicians should remain alert to the possibility of suicide in high-risk patients
- routinely evaluate the risk of suicide, particularly if there is evidence of:

- psychiatric disorder (especially psychosis)

- depression
- substance abuse
- if the patient lives alone
- recently attempted suicide
- family member has committed suicide

- special attention paid to young Native and Aboriginal males

2. Given a suicidal patient, assess the degree of risk (e.g., thoughts, specific plans, access to
means) in order to determine an appropriate intervention and follow-up plan (e.g., immediate
hospitalization, including involuntary admission; outpatient follow-up; referral for
counselling).

343
- Prior history of attempted suicide = strongest single factor predictive of suicide

SAD PERSONS
- Sex (male)
- Age (>60 y.o.)
- Depression
- Previous attempts
- Ethanol abuse
- Rational thinking loss (delusions, hallucinations, hopelessness)
- Suicide in family
- Organized plan
- No spouse (no support systems)
- Serious illness / intractable pain

- Scoring Guide (based on total number of risk factors present)

- 0-2 : consider sending home with family

- 3-4 : close follow-up, consider hospitalization
- 5-6 : strongly consider hospitalization
- 7-10 : hospitalize

- Suicide contracts = unreliable

Clinical Presentation
- symptoms associated with suicide

- hopelessness
- anhedonia
- insomnia
- severe anxiety
- impaired concentration
- psychomotor agitation
- panic attacks

In Elderly Patients
- personality disorders, rigid personality styles
- non-adaptive coping strategies
- functional decline

3. Manage low-risk patients as outpatients, but provide specific instructions for follow-up if
suicidal ideation progresses/worsens (e.g., return to the emergency department [ED], call a
crisis hotline, re-book an appointment).

Management of the Suicidal Individual

- reducing immediate risk

- involve a family member or person close to patient, if allowed

344
 - ask about availability of lethal means (e.g., firearms, medications) and make
inaccessible
- increase the frequency of contact with the patient; communicate a commitment to help
- begin aggressive treatment of psychiatric disorders or substance abuse

- managing underlying factors

- referral to counseling
- engagement of community, religious, and family supports
- CBT
- treatment of depression (e.g., SSRI) / bipolar disorder (e.g., lithium)

- monitoring and follow-up

- risk fluctuates, should be reassessed frequently

- determine if there have been changes, especially a reemergence of precipitating events,
adverse life circumstances, or mental disorders
- assure that previously suicidal patients are actively engaged in ongoing care for any
mental disorders
- continue to receive treatment for prevention of relapse or recurrence of depression,
bipolar disorder, anxiety disorders, psychosis, or other conditions
- for those with a history of alcohol or substance abuse, monitoring and assisting the
patient in remaining in programs that promote adequate control
- days and initial weeks following discharge from psychiatric hospitalization are a time of
increased risk
- particularly if patients perceive that they have lost a therapeutic support system
- high risk for non-adherence to medication regimens

4. In suicidal patients presenting at the emergency department with a suspected drug overdose,
always screen for acetylsalicylic acid and acetaminophen overdoses, as these are common,
dangerous, and frequently overlooked.

- Other common Rx’s

- TCAs
- benzodiazepines
- CCBs
- Β-blockers

- Urine toxicology screen and blood alcohol level are the two most commonly required tests for
patients transferred/admitted to psychiatric facilities from the ED

- Serum levels for other Rx may include:

- Mood stabilizers
- Lithium
- Valproic acid

345
 - Antiepileptic
- Phenytoin
- Carbamazepine
- Phenobarbital
- Digoxin
- Cyclosporine (for transplant patients)
- INR (in patients taking Coumadin)

5. In trauma patients, consider attempted suicide as the precipitating cause.

Trauma - Key Features

1. Assess and stabilize trauma patients with an organized approach, anticipating complications
in a timely fashion, using the primary and secondary surveys.

Primary Survey:
“2 large bore IVs, O2, monitors”
A Airway assessment and protection, while maintaining cervical spine stabilization.
B Breathing and ventilation assessment (maintain adequate oxygenation).
C Circulation assessment (control hemorrhage and maintain adequate end-organ perfusion).
Major areas of hemorrhage are pelvis, abdomen, thorax, and external (from limbs, scalp). FAST
exam using ultrasound can be included as part of circulation assessment.
D Disability assessment (basic neurologic evaluation). Basic exam includes GCS, pupils, neuro
exam of all 4 limbs. If possible, rapid neuro exam prior to paralysis for intubation.
E Exposure, with environmental control (undress patient and search everywhere for possible
injury, while preventing hypothermia).

Secondary Survey:
a) Hx: AMPLE (Allergies, Medications, PMHx, Last meal, Events leading to incident)
b) Head to toe examination, including C-spine, log roll (for spine exam and rectal exam if
necessary)
c) Trauma imaging: Chest XR, C-spine XR, Pelvis XR
d) EKG, trauma labs, +/- additional imaging

2. Suspect, identify, and immediately begin treating life- threatening complications (e.g.,
tension pneumothorax, tamponade).

a) Tension pneumothorax

- if suspected, treat with needle decompression prior to obtaining Chest XR (14G

angiocath in 2nd ICS, midclavicular)
- needle decompression must be followed by chest tube (4th-5th ICS, anterior axillary
line)

b) Cardiac tamponade

- ER needle aspiration, or to OR if available

346
3. When faced with several trauma patients, triage according to resources and treatment
priorities.

The sickest viable patients are managed first.

4. In trauma patients, secure the airway appropriately (e.g., assume cervical spine injury, use
conscious sedation, recognize a difficult airway, plan for back-up methods/cricothyrotomy).

Assessment for difficult airway:

L Look (trauma, teeth, hair, large tongue)
E Evaluate 3-3-2 (what you want is mouth opening to fit 3 finger-breadths, submandibular length
3 finger-breadths, hyoid to cricoid 2 finger-breadths)
M Mallampati score (you want 3 or 4)
O Obstruction, any signs of? Sleep apnea?
N Neck mobility (neck arthritis, C-spine collar)

Assessment for difficult BVM ventilation:

B Beard
O Old
O Obese
T Toothless
S Snores

5. In a patient with signs and symptoms of shock:

a) Recognize the shock.

Pre-shock:

- <10% loss of effective blood volume

- compensated shock
- tachycardia, +/- modest BP change

Shock:

- 20-25% loss of effective blood volume

- s/s organ dysfunction appear
- tachycardia, BP drop, dyspnea, diaphoresis, restlessness, oliguria, cool / mottled skin

End-organ dysfunction:

- untreated shock progresses to end-organ dysfunction and death (renal failure, acidosis,
obtundation)

b) Define the severity and type (neurogenic, hypovolemic, septic).

Hypovolemic shock:

347
 - Decreased preload due to intravascular volume loss.
- DDx: hemorrhage, fluid loss

Cardiogenic shock:

- Cardiac pump failure.

- Cardiomyopathies, MI, arrhythmias

Distributive shock:

- severely decreased systemic vascular resistance.

- DDx: sepsis, SIRS, anaphylaxis, neurogenic (neurogenic shock is disruption of
autonomic pathways causing decreased systemic vascular resistance)

Combined shock:

- combination of the above

c) Treat the shock.

- Bolus 20cc/kg crystalloid

- with hemorrhage give blood soon
- massive transfusion protocols (eg 1:1:1 pRBCs:platelets:FFP)

6. In trauma patients, rule out hypothermia on arrival and subsequently (as it may develop
during treatment).

7. Suspect certain medical problems (e.g., seizure, drug intoxication, hypoglycemia, attempted
suicide) as the precipitant of the trauma.

8. Do not move potentially unstable patients from treatment areas for investigations (e.g.,
computed tomography, X-ray examination).

If you need imaging urgently, a capable physician should accompany the patient.

9. Determine when patient transfer is necessary (e.g., central nervous system bleeds, when no
specialty support is available).

This is very dependent on the center you’re practicing in.

10. Transfer patients in an appropriate manner (i.e., stabilize them before transfer and choose
the method, such as ambulance or flight).

This is very dependent on the center you’re practicing in. Consider intubation for transfer.
Indications for intubation include:

- oxygenation
- ventilation

348
 - expected clinical course (eg with GCS<8 intubate to prevent aspiration, or with transfer
intubate if at all suspecting decompensation during transfer)

11. Find opportunities to offer advice to prevent or minimize trauma (e.g., do not drive drunk,
use seatbelts and helmets).

12. In children with traumatic injury, rule out abuse. (Carefully assess the reported mechanism
of injury to ensure it corresponds with the actual injury.)

Hx factors suspicious for abuse:

- Hx inconsistent with injuries

- Vague or inconsistent Hx
- Injury attributed to actions of other siblings

Px findings suspicious for abuse:

- injuries not consistent with Hx

- multiple fractures or injuries
- likely inflicted injuries (cigarette burns or patterned bruises)
- bruising in a child that is not yet “cruising” (normally 9-12mo)
- bruising to pinna, neck, abdomen
- genitalia injury

Travel Medicine - Key Features

1. Make sure travelers get up to date, timely, itinerary-specific advice from a reliable source
(e.g., travel clinic, travel website).

-seek medical advice at least 4-6weeks before departure to leave time for immunizations
-local travel clinic
-websites: Health Canada, Centre for Disease Control, World Health Organization, Committee to
Advise on Tropical Medicine and Travel (CATMAT) by the Public Health Agency of Canada
-recommendation to register with the Gov't of Canada prior to travelling at www.travel.gc.ca

• in Japan, after the earthquake, people who were registered were evacuated first

2. When seeing patients planning travel, discuss the common, non-infectious perils of travel
(e.g., accidents, safer sex, alcohol, safe travel for women).

- motor vehicle accidents (higher rate of tourist death than all infectious disease combined), safe
sex (countries with higher rates of HIV, Hep B and C, pcn resistant gonorrhoea), alcohol, safe
travel for women, sun exposure, dehydration, travel induced conditions (barotrauma, jet lag,
motion sickness, DVT)
-risk assessment: who (pt), where (destinations), when (departure date and trip duration), why
(purpose), what (activities), how (nature and style of travel)

349
3. In patients presenting with symptoms of infection without an obvious cause, especially those
with a fever, enquire about recent travel history to identify potential sources (especially, but not
exclusively, malaria).

-malaria: blood films

-dengue: IgG testing
-consider stool testing for parasites
-HIV seroconversion

4. Provide prevention and treatment advice and prescribe medications for common conditions
associated with travel (e.g., traveler’s diarrhea, altitude sickness).

-contaminated food and water

• e coli, Hep A (3-5 cases/1000 travellers/month), salmonella, parasites(ex giardi),

typhoid fever, campylobacter
• "boil it, cook it, peel it, or forget it", drink bottled water
• traveller's diarrhea:
◦ Pep to-Bismol 2 tabs qid for prophylaxis (unless ASA allergy)
◦ ciprofloxacin 500 mg po bid M:5days for treatment in adults, azythromycin in children
◦ azithromycin is also recommended (currently) for Thailand, Vietnam, India,Mexico in
the summer, and Nepal (due to Cipro resistance)
◦ loperamide if no fever or bloody stools
◦ electrolyte replacement

- altitude sickness

• acetazolamide 250mg po bid

• allow 2-3 days to acclimatize before strenuous activity

-insect bites

• depends on season, altitude, location

• dusk to dawn biting mosquito risk of malaria
• day biting mosquito risk of dengue
• DEET (no DEET if children <6 mos, 10% DEET if 6mos-2 years), protective clothing,
stay indoors, mosquito nets

-malaria prophylaxis

• chloroquine if chloroquine sens area: start 1 week before, take weekly, take 4 weeks
after
• mefloquine if chl-resistant: start 1 week before, take weekly, 4 weeks after, can cause
nausea, dizziness, difficulty sleeping, moodiness, vivid dreams, do not give if psych or sz
hx
• doxycycline if chl-resistant and can't tolerate mefloquine: start 2 days before, take daily,
4 weeks after, causes photo sens
• malarone if chl-resistant: start 2 days before, take daily, 7 days after, less reactions but
expensive

350
-rabies

• dogs, bats, cats, monkeys, racoons, foxes, skunks are carriers, transmitted by licking,
scratching, biting
• vaccine expensive (600$), post exposure prophylaxis (Ig serum) availability dependent
on country

5. Ensure patients understand how to manage their chronic disease while traveling (e.g.,
diabetes, asthma, international normalized ratios [INRs]).

- diabetes, asthma, pregnancy, cardiovascular and pulmonary disease, INRs

-medical alert bracelets, appropriate medications, travel insurance, rescue meds (ie puffers)

6. Use patient visits for travel advice as an opportunity to update routine vaccinations.

- Td q 10yrs, MMR booster if only received once dose in childhood, Hep B if not received,
Pertussis booster, polio if not received
-single Hep A vaccine gives roughly 95% immunity in 4 weeks, booster given in 6-12 mos
confers immunity for at least 20 yrs
-single Hep B vaccine gives 60% immunity, usual dosage regime is 0, 1, 6 mos but can be given
0, 7, and 21 days
-depending on travel, pts may require yellow fever and meningococcus vaccinations for border
crossings
-food and water risks: typhoid, Hep A
-destination specific: Japanese encephalitis, yellow fever, malaria, meningitis
-long term stay: rabies, Mantoux, Hep B
-high risk travellers: diabetes, pregnancy, immunosuppressed (beware of live attenuated vaccines)

7. Advise patients to check insurance coverage issues especially in regard to recent changes in
chronic disease and any recent treatment changes.

-detailed signed contract with emergency repatriation

8. Advise patients traveling with medications to have an adequate supply, documentation of

need for use, and to transport them securely (e.g., carry-on bag).

-pharmacy labelled, carry-on bag, personal identification (medical alert bracelet)

Upper Respiratory Tract Infection - Key Features

1. Given an appropriate history and/or physical examination:

a) Differentiate life-threatening conditions (epiglottitis, retropharyngeal abscess) from benign
conditions.
b) Manage the condition appropriately.

Clinical Presentation Diagnosis Treatment

Croup -Common, 6 mos to 4 yrs -Clinical -Humidified O2; dexamethasone;
epinephrine

351
 -Fall, early winter -Atypical
-Hoarse voice, barking presentation: -Intubation if unresponsive to
cough, stridor, worse at CXR → ‘steeple treatment
night sign’
-Rare, all age groups
-Clinical -Start croup therapy
-Similar to croup, but
Bacterial
more rapid deterioration
Tracheitis -Definitive Dx -Often requires intubation
and fever
via endoscopy -Antibiotics
-Toxic appearance
-Not respond to croup trt
-Rare -Clinical
-Intubation
diagnosis
-Toxic appearance, rapid
-Antibiotics
Epiglottitis progression, severe airway -Avoid throat
obstruction, drooling, exam to avoid
 Prevented with Hib
stridor, tripod position, further
vaccine
anxiety exacerbation
-Sore throat, fever,
torticollis, dysphagia, neck - IV hydration
pain, muffled voice
Retropharyngeal -Contrast CT
-IV Antibiotics (clinda 600-900mg,
Abscess neck
-Respiratory distress, cefoxitin 2gm, or pip/tazo)
stridor, neck edema, -+/- Surgical intervention
cervical lymphadenopathy
-Often clinical
-Needle aspiration, I&D, or, rarely,
-Fever, sore throat,
tonsillectomy
odynphagia, dysphagia, -Needle
otalgia aspiration
-Although polymicrobial, most
purulent
common grp A Strept → 10 d
Peritonsillar -Trismus, muffled/’hot material if dx in
course Abx against GAS and oral
Abscess potato’ voice, inf & med question
anaerobes (amox/clav,
displacement tonsil, -CT with
PenV+metronidazole, clinda)
contralateral deflection contrast to
-Single dose IV
uvula, drooling, confirm and/or
methylprednisolone
lymphadenopathy if concern of
-F/up 24 hrs post aspiration
spread
-Definitive airway management
-Dysphagia, odynphagia,
(fiberoptic
trismus, edema upper neck -Clinical
intubation/tracheostomy)
& floor of mouth
Ludwigs Angina -Ct with contrast
-Systemic antibiotics (clinda or
-Tongue may displace → may augment
amp + nafcillin, PCN +
airway compromise clinical findings
metronidazole until Cx available)
-Stridor, cyanosis
-+/- I&D

352
2. Make the diagnosis of bacterial sinusitis by taking an adequate history and performing an
appropriate physical examination, and prescribe appropriate antibiotics for the appropriate
duration of therapy.

FYI: Most common sinus involved: MAXILLARY > Ethmoid > frontal > sphenoid

ACUTE RHINOSINUSITIS (< 4 WEEKS)

-VIRAL > bacterial

-Viruses: rhinovirus, parainfluenza, influenza

-Bacterial: S. pneumo, nontypable H. Flu, Moraxella Caterhalis (children), small % staph
aureus
-Fungal: most common in immunocompromised, repetitive & invasive infections

SIGNS & SYMPTOMS:

-Nasal drainage, congestion, facial pain/pressure, headache, cough, sneeze, fever

-Tooth pain & halitosis associated with bacterial sinusitis
-Symptoms may localize with further invasion of sinus: increased symptoms when
bending/supine

-COMPLICATIONS: meningitis, epidural abscess, cerebral abscess

-DIAGNOSIS: clinical

-Recommended reserve bacterial diagnosis to: PERSISTENT SYMPTOMS (>10d in

adult, >10-14d in children), PRURULENT DISCHARGE, NASAL OBSTRUCTION,
AND, FACIAL PAIN
-CT Sinuses: to evaluate persistent, chronic, or recurrent symptoms

-TREATMENT:

-Decongestants, nasal saline lavage, nasal glucocorticoids

-Suspect bacterial/persistent: Antibiotics:
-Amoxicillin 500 mg tid x 10 d
-If PCN allergy: Doxycycline 100 mg bid Day 1, then 100 mg daily for 10-14 d course
-Suspect fungal: REFER (may need biopsy)
-Severe/intracranial complications: IV antibiotics +/- surgical intervention

CHRONIC RHINOSINUSITIS (> 12 WEEKS)

-more commonly bacterial/fungal; high morbidity
-constant congestion, sinus pressure, intermittent increase in severity for YEARS
-CT may identify extent of disease, detect underlying defects/obstruction, assess response to
therapy
-TREATMENT: difficult

-Refer to Otolaryngologist for endoscopic exam +/- biopsy

-Repeated culture guided antibiotics 3-4 wks duration, intranasal glucocorticoids, sinus
irrigation, +/- surgery

353
3. In a patient presenting with upper respiratory symptoms:
a) Differentiate viral from bacterial infection (through history and physical examination).
b) Diagnose a viral upper respiratory tract infection (URTI) (through the history and a
physical examination).
c) Manage the condition appropriately (e.g., do not give antibiotics without a clear indication
for their use).

-Etiology of Nonspecific URTI:

-Rhinovirus (30-40%), influenza, parainfluenza, coronavirus, adenovirus, RSV (pediatric,

elderly, immunocompromised)

-Viral URTIs lack anatomic localization of signs and symptoms

-Course is acute, mild and self limited; median duration approx. one week (2-10d)
-Signs & Symptoms may include: rhinnorhea, nasal congestion, cough, sore throat, fever,
malaise, sneezing, lymphadenopathy, hoarseness
-Secondary Bacterial infections complicate approx. 0.5-2% of viral URTI (e.g. sinusitis, OM,
pneumonia)

-Infants, elderly, chronically ill are at higher risk

-Present with prolonged course, increased severity, anatomic localization of signs and
symptoms, often as a rebound after clinical improvement

-TREATMENT:

-Symptom based: decongestants, NSAIDS, dextromethorphan, lozenges with topical

anaesthetic
-Zinc, vitamin C, Echinacea have not shown consistent benefit in clinical trials
-Antibiotics are NOT indicated for nonspecific/viral URTI without other specific
indication

4. Given a history compatible with otitis media, differentiate it from otitis externa and
mastoiditis, according to the characteristic physical findings.

OTITIS MEDIA (Streptococcus pneumonia, Haemophilus influenza, Streptococcus pyogenes)

-HISTORY: Often preceded by URTI; Otalgia, aural pressure, pyrexia, decreased hearing,
otorrhea
-PHYSICAL EXAM:

AOM: thickened, hyperemic, immobile TM;

OME: dull gray- or yellow tinged, immobile TM, if TM clear may see bubble/air-fluid
levels

-TREATMENT: Analgesia & Antipyretics

354
 -Antibiotics: for all children < 6 mos, children 6 mos – 2 years with certain diagnosis,
and all children with severe infection (moderate to severe otalgia or temperature > 39 deg
C); Otherwise Abx may be deferred provided reliable observation and ready access to
medical care/f-up
-Amoxicillin 80-90 mg/kg/d div bid; Macrolides/Clinda/Cephalosporin in PCN
allergy/resistant infection

OTITIS EXTERNA (gm neg: pseudomonas, proteus; fungi: aspergillus)

-HISTORY: often history of recent water exposure (e.g. swimming) or mechanical trauma (e.g.
scratching/cotton swabs); otalgia, pruritis
-PHYSICAL EXAM: Erythema & edema of external canal, purulent exudate, pain with
manipulation of auricle
-TREATMENT: Acidification with drying agent (50/50 mix isopropyl alcohol/white vinegar)

-infection: acidic otic antibiotic drops containing aminoglycoside/fluoroquinolone +/-

corticosteroid (e.g. neomycin sulf ate, polymyxin B sulfate; used abundantly – 5 or more
drops tid-qid to penetrate the canal)

MASTOIDITIS (S pneumoniae & S pyogenes, with S aureus and H influenzae occasionally)

-HISTORY: usually follows weeks of inadequately treated OM; post-auricular pain & erythema,
spiking fever
-PHYSICAL EXAM: Postauricular pain, edema & erythema; fever; down & outward displaced
pinna; OM on otoscopy
-TREATMENT: IV Antibiotics: ceftriaxone + nafcillin or clindamycin until Cx results; then Cx
guided for 2-3 weeks

-Myringotomy for Cx +/- drainage

-Failure of medical therapy → mastoidectomy

5. In high-risk patients (e.g., those who have human immunodeficiency virus infection, chronic
obstructive pulmonary disease, or cancer) with upper respiratory infections: Lood for
complications more aggressively, and follow up more closely.

6. In a presentation of pharyngitis, look for mononucleosis.

-SIGNS & SYMPTOMS:

-fever, pharyngitis, fatigue, anorexia, myalgia

-tonsillar exudates, splenomegaly (in up to 50% cases), lymphadenopathy (especially
posterior cervical chain), maculopapular (occasionally petechial) rash in <15% of patients
(>90% cases if ampicillin has been given)
-symptoms generally resolve over 2-3 weeks, fatigue may persist for months

-DIAGNOSIS:

-CBC: lymphocytosis (>50% lymphocytes), atypical lymphocytes on smear

355
 -Monospot: identifies heterophile antibodies thought to be diagnostic of EBV infection
-may be negative early in course (i.e. specific, but not sensitive early on, usually positive
by 4 wks)
-sensitivity also decreased in infants and elderly

-COMPLICATIONS: Secondary bacterial pharyngitis (often streptococcal), splenic rupture,

acalculous cholecystitis, hepatitis, pericarditis, myocarditis, transverse myelitis, encephalitis,
Guillain-Barre syndrome
-TREATMENT: rest and analgesia (acetaminophen/NSAIDS)

-AVOID all contact sports for minimum 4 weeks after illness onset to avoid splenic
injury
*Note: Use of corticosteroids is associated with increased complications and is
recommended only for patients with severe disease, such as upper airway obstruction,
neurologic disease, or hemolytic anemia
*Note: Acyclovir decreases viral shedding but with no clinical benefit

7. In high-risk groups:
a) Take preventive measures (e.g., use flu and pneumococcal vaccines).
b) Treat early to decrease individual and population impact (e.g., with oseltamivir phosphate
[Tamiflu], amantadine).

INFLUENZA VACCINE CANDIDATES IN BC 2011 SEASON:

www.healthlinkbc.ca/healthfiles/hfile12d.stm

PNEUMOCOCCAL VACCINE
PNEUMOCOCCAL CONJUGATE (PCV13) VACCINE
www.healthlinkbc.ca/healthfiles/hfile62a.stm
PNEUMOCOCCAL POLYSACCHARIDE VACCINE
http://www.healthlinkbc.ca/healthfiles/hfile62b.stm

USE OF ANTIVIRAL DRUGS FOR INFLUENZA

www.bccdc.ca/resourcematerials/guidelinesandforms/guidelinesandmanuals/
antiviraldrugsinfluenza.htm

Urinary Tract Infection - Key Features

1. Take an appropriate history and do the required testing to exclude serious complications of
urinary tract infection (UTI) (e.g., sepsis, pyelonephritis, impacted infected stones).

History
- Cystitis: Dysuria, frequency, urgency, hematuria and possibly the presence of suprapubic pain.
History of prior UTI and/or renal stones.
- Pyelonephritis: Symptoms of cystitis may be present and and is generally believed to be
associated with fever, flank pain and systemic symptoms such as nausea and vomiting and CVA
tenderness. Hx of prior UTI and/or renal stones.
- Impacted infected stones: Renal colic, hematuria with fever and systemic signs.

356
Testing
1. Urinalysis: Midstream sample. Positive dipstick nitrite or positive leukocyte is sensitive (75%)
and specific (82%).
2. Urine C&S: Positive will be colony count of more than 105 organisms per milliliter. This
provides high specificity but poor sensitivity. However, colony counts of more than 102 obtained
on a clean voided specimen from acutely dysuric women are also diagnostic of true infection.
These women may also have pyuria on urinalysis (more than 2-5 WBCs per high-power field).
3. CBC, Lytes, Cr, BUN, Blood cultures → if there is fever and other systemic signs.
4. If suspecting a renal stone then imagining studies will be necessary.

a. Ultrasound: sensitive for the diagnosis of urinary tract obstruction and can detect
radiolucent stones missed on KUB; however, it may miss small stones and ureteral stones
b. Non-contrast CT scan: it can detect both stones and urinary tract obstruction, and has
become the gold standard for the radiologic diagnosis of stone disease since stones not
visualized on KUB or IVP will usually be detected by CT scan
c. IVP: it has a higher sensitivity and specificity than an abdominal plain film for the
detection of stones and provides data about the degree of obstruction. It was previously
the diagnostic procedure of choice, but is no longer because of potential contrast
reactions, lower sensitivity, and higher radiation exposure. It has been replaced by non-
contrasted helical CT as the test of choice.

2. Appropriately investigate all boys with urinary tract infections, and young girls with
recurrences(e.g., ultrasound).

Rational for imaging studies

- Identify urinary tract abnormalities and possible need for surgical intervention
- Identify patients at risk for subsequent renal damage

Ultrasound: Given the potentially large benefit of detecting correctible malformations for a small
number of children and the low risk of harm, we (uptodate.com) suggest Renal and Bladder U/S
in for the following children:

- Girls < 3 yrs with first UTI

- Boys of any age with first UTI
- Children younger than two years of age with a first febrile UTI
- Children of any age with recurrent febrile UTIs
- Children of any age with a UTI who have a family history of renal or urologic disease
or poor growth
- Children who do not respond as expected to appropriate antimicrobial therapy

Voiding cystourethrogram: for detection of Vesicoureteral reflux (VUR) is indicated in the

following:

- Children of any age with two or more febrile UTIs

357
 - Children of any age with a first febrile UTI who have a family history of renal or
urologic disease; poor growth; hypertension; or non-E. coli organism. Urinary tract
anomalies are more frequent among children with UTI caused by pathogens other than E.
coli

3. In diagnosing urinary tract infections, search for and/or recognize high-risk factors on
history (e.g., pregnancy; immune compromise, neonate, a young male, or an elderly male with
prostatic hypertrophy).

UTI in pregnancy whether it is symptomatic or asymptomatic has been associated with an

increased risk of preterm birth, low birth weight, and perinatal mortality. This is why it must be
treated at all times.

Elderly male with BPH: The increase in UTI that occur in men of age 50-65 years of age parallels
the increase in prostate size that occurs with hyperplasia. This enlargement leads to bladder
outflow tract obstruction and a postvoid residual begins to develop in the bladder. This along with
what is thought to be reduced antibacterial activity of prostatic secretions among men in this age
group puts them at risk for UTIs.

4. In a patient with a diagnosed urinary tract infection, modify the choice and duration of
treatment according to risk factors (e.g., pregnancy, immunocompromise, male extremes of
age); and treat before confirmation of culture results in some cases (e.g.,pregnancy, sepsis,
pyelonephritis).

Treatment of uncomplicated UTI

- Urine C&S is usually not necessary in the management of uncomplicated UTI. It should
however be considered in patients suspected of having a complicated UTI, if the patient did not
respond to the standard therapy or if the patient has recurrent UTIs.
- First line

o TMP/SMX 2 tabs BID or 1 DS tab BID x 3 days

o Trimethoprim 100mg BID or 200mg qdaily x 3days
o Nitrofurantoin 50-100mg QID or Macrobid 100mg BID x 5 days (x 7days for nursing
home population). Not to be used in infants <1 month of age or in renal failure CrCl
<60mL/min.

- Second Line

o Amoxicillin 500mg TID x 7 days (40% of bacteria are resistant)

o Ciprofloxacin 250mg BID or 500mg of extended release qdaily x 3 days

- Third Line

o Cephalexin 250-500mg QID x 7 days

o Levofloxacin 250mg qdaily x 3 days

Treatment of UTIs in Nursing home/LTC patients

358
- Generally 7 days of treatment. For those presenting with fever or more severe symptoms 10-14
days is recommended
- Routine screening and treatment of asymptomatic bacteriuria in nursing home residents is not
recommended.
- Treatment is the same as for Uncomplicated UTI with adjustment to the duration of therapy.

Treatment of complicated UTI

- Includes patients with structural or functional abnormalities such as: obstruction, chronic
catheter, spinal cord injury etc. or any UTI in men.
- Culture required before Ab therapy.
- Duration: if cystitis with mild to moderate symptoms treat for 7-10 days. If upper tract (kidneys)
symptoms or systemic signs such as fever, sepsis, vomiting treat for 10-14 days.
- First Line for mild to moderate

o TMP/SMX 2 tabs BID or 1 DS tab BID

o Trimethoprim 100mg BID or 200mg qdaily
o Nitrofurantoin 50-100mg QID or Macrobid 100mg BID (Not to be used in upper
kidney involvement or if there is obstruction or tissue infection)
o Ciprofloxacin 500mg BID or 1g extended release qdaily
o Levofloxacin 500mg qdaily

- Second line for mild to moderate

o Amox/Clav 500mg TID

- First line for severe

o Ampicillin 1g IV q6h + Gentamicin or Tobramycin 4-7mg/kg IV q24h

- Second line for severe

o Cefotaxime 1-2g IV q12h

o Ceftriaxone 1-2g IV q24h
o Ciprofloxacin 200-400mg IV q12h
o Levofloxacin 250mg IV q24h
o Pip/Tazo 3g/0.375g IV q6h

- Third line for severe

o Imipenem 500mg IV q6h

o Meropenem 500-1000mg q8h

Treatment in Pregnancy
- Aways do f/u urine C&S after treatment
- Acute Cystitis

o Cephalexin 250-500mg QID x 7 days

o Amoxicillin 500mg TID x 7 days (there high E. coli resistance to this and so use after
C&S confirmation)

359
 o Nitrofurantoin 50-100mg QID or Macrobid 100mg BID x 5 days
• ** This is contraindicated in pregnant patients at term (36-42), during labour and in
neonates due to the possibility of hemolytic anemia.
o Second line Options
• TMP/SMX 2 tabs BID or 1 DS tab BID x 3 days
• Trimethoprim 100mg BID or 200mg qdaily x 3days
• ** Avoid use of these antibiotics during the 1st trimester because of concerns that
trimethoprim may limit the availability of folic acid and lead to fetal abnormalities.
• **Avoid TMP/SMX during the last 6 weeks of pregnancy as sulfonamides may displace
bilirubin from albumin bidning sites causing kernicterus in infants.

- Pyelonephritis in pregnancy

o Ceftriaxone 1-2g q24h x 10-14 days

Treatment for Pyelonephritis, Urosepsis

- Start empiric therapy after Blood and urine cultures have been taken.
- These patients need admission to hospital and parenteral antibiotics.
- IV fluids, and broad spectrum antibiotics to cover for pseudomonas species and other resistant
gram negative rods.
- Enterobacteriaceae (Family of Gram negative bacteria that includes pathogens such as
Salmonella, Escherichia coli, Yersinia pestis, Klebsiella and Shigella) account for 90% of cases
- Treatment choices

o Ciprofloxacin 500mg PO BID or 400mg IV q12h x 10-14 days

o Levofloxacin 500mg PO qdaily x 10 days OR 750mg PO qdaily x 5 days (for
uncomplicated cases) OR Levofloxacin 250-500mg IV q24 x 10 days for severe cases.
o Gentamicin 4-7mg/kg IV q24h +/- Ampicillin 1-2g IV q4-6h x 10-14 days for severe
cases
o Cefotaxime 1-2g IV q12h x 10-14 days for severe cases

5. Given a non-specific history (e.g., abdominal pain, fever, delirium) in elderly or very young
patients, suspect the diagnosis and do an appropriate work-up.

6. In a patient with dysuria, exclude other causes (e.g., sexually transmitted diseases, vaginitis,
stones, interstitial cystitis, prostatitis) through an appropriate history, physical examination,
and investigation before diagnosing a urinary tract infection.

- Vaginal discharge, external discomfort, absence of frequency or urgency and negative urine
culture distinguishes vaginitis from UTI. Trichomonas vaginalis and Candida albicans are the
most commonly responsible organisms.
- Women with dysuria and absence of bacteria on urine culture may have urethritis caused by C.
trachomatis, Neisseria gonorrhoeae or HSV.
- Prostatitis: diminished urine flow and signs of bladder outflow obstruction (ex frequency, loss
of stream, dribbling, hesitancy, urgency etc), dysuria, perineal pain. On rectal exam: the gland is
gound to be enlarged, tender and boggy.

360
Vaginal Bleeding - Key Features

1. In any woman with vaginal bleeding, rule out pregnancy.

2. In pregnant patients with vaginal bleeding

a) Consider worrisome causes (e.g., ectopic pregnancy, abruption, abortion), and confirm or
exclude the diagnosis through appropriate interpretation of test results.
b) Do not forget blood typing and screening, and offer rH immunoglobulin treatment, if
appropriate.
c) Diagnose (and treat) hemodynamic instability.

First Trimester (20-40% of pregnancies) Second and Third Trimester

1) Implantation bleeding 1) Bloody show

2) Abnormal pregnancy (ectopic or molar) 2) Placenta previa

3) Miscarriage (threatened, inevitable, incomplete, complete) 3) Placental Abruption
4) Uterine Rupture
4) Uterine, Cervical, Vaginal pathology 5) Vasa previa

1st Trimester bleeding

HX:
Preg Hx
GTPAL, Dates/LMP, Ultrasound
Concerns with current or past pregnancies
Blood type/ Partners blood type
Bleeding Hx
Onset and Duration
Quantity – # of pads
Passing tissue or clots
RF: trauma, Intercourse, bleeding disorder, fibroid, pelvic surgery, PID, STD, IUD
PX:
ABC’s, Orthostatic Vital
Abdominal Exam- ? FHR
Pelvic Exam- look for source, is cervix open or closed, products of conception
Investigation
CBCD, lytes, BUN, Cr
Group and Screen
B-HCG
Transvaginal Ultrasound

Miscarriage Definition and Management

Definition Clinical Management

Threatened Bleeding through a closed os Cervix closed 1) Watch and wait

361
 Bleeding
+FHR
Cervix dilated
1) Watch and wait
Increase cramping
Inevitable SA is imminent
and bleeding
2) Misoprostal
Tissue visualized in
os
Uterus small but not
1) Watch and wait
Membrane ruptured and fetus passed well contracted
Incomplete
2) Misoprostal
Retention of placental tissue Cervix open
3) D&C
++ bleeding
Uterus small and
contracted
No management
Complete Complete passage of sac/gestational tissue
Cervix closed needed
Scant vaginal
bleeding
1) watch and wait
Intrauterine death prior to 20 weeks with
Missed
retention of pregnancy for prolonged period
abortion 2) Misoprostal
of time
3) D&C
*** rh immunoglobulin if RH -

Management of Ectopic Pregnancy

1) Suspect if abdominal pain, vaginal pain and + b-hCG
2) Surgery if vitals unstable
3) Transvaginal ultrasound if stable (should see gestational sac 5.5-6 wks after LMP)
4) Methotrexate if : <3.5cm, unruptured, absent FHR, b-hCG <5000, no liver/renal/heme dz,
willing and able to follow up. HCG is followed until undetectable

2nd and 3rd Trimester Bleed

Differential Diagnosis
Cervix/Vagina- polyps, CA, postcoital, laceration
Bloody show
Uterine Rupture
Placental

1) Abruption - placental separation

Presentation- bleeding plus abdominal/back pain, increased uterine tone, uterine
irritability/contractions, +/- fetal distress/demise
RF include HTN, previous abruption, large uterus (macrosomia, polyhydramnios,
multiple gestation), smoking, EtOH, cocaine, uterine anomaly, trauma

362
 2) Placental Previa • Placenta over OS- Types: Complete or Partial previa. Marginal or
Low lying
Presentation -Painless vaginal bleeding, uterus soft non-tender,+/- fetal distress
RF include history of placenta previa, multiple gestation, multiparity, increased maternal
age, uterine anomalies including surgical scars
3) Vasa previa - rupture of fetal vessels- Painless vaginal bleeding and fetal distress

Physical Exam
Vitals- maternal and fetal
Abdominal exam including measurement of uterine size, Leopolds, increased uterine tone
Doppler for fetal heart NST
Sterile speculum-Amount of bleeding, tissue/clots, cervical dilatation, uterine and
adnexal tenderness
** NO bimanual until previa ruled out with ultrasound
Investigations
CBC, blood type/type and screen, crossmatch- Rh status
Kleihaurer/Apt test- assess fetal blood
Fetal Ultrasound assess for abruption
Management
Maternal stabilization - ABC's, monitors, IV fluids, PRBCs if required
Continuous Fetal monitoring
Rhogam Rh negative -300mcg IM
Consider corticosteroids for fetal lung immaturity (24-34 weeks GA)- Betamethasone
12mg IM q24 hr x2
Abruption
<37 weeks - serial hemoglobin, deliver when hemorrhage dictates o
>37 weeks - stabilize and deliver
Placenta previa-Keep pregnancy intrauterine until the risk of delivery < risk of not
delivering
Vasa previa- Emergency cesarean section

3. In a non-pregnant patient with vaginal bleeding:

a) Do an appropriate work-up and testing to diagnose worrisome causes (e.g., cancer), using
an age-appropriate approach.
b) Diagnose (and treat) hemodynamic instability.
c) Manage hemodynamically stable but significant vaginal bleeding (e.g., with medical versus
surgical treatment).

Abnormal Uterine Bleeding: any persistent change in menstrual period frequency, duration or
amount +/- breakthrough bleeding
Dysfunctional Uterine Bleeding: excessively heavy, prolonged or frequent bleeding of uterine
origin which is not due to pregnancy or to recognizable pelvic or systemic disease

Hx: RULE OUT PREGNANCY

Amt-Def:>80 ml, changing soaked pad >1 hr, changing pad overnight, postural hypotension

363
Ovulatory vs.Anovulatory

Ovulatory Anovulatory
Cyclical bleeding
Irregular bleeding
Premenstrual symptoms
Minimal pain
Midcycle pain Higher risk of endometrial hyperplasia or cancer
Dysmenorrhea

Psychosocial issues-stress
Medication causing bleeding- Anticoagulants, ASA, Phenzothiazines, SSRI, TCA, Tamoxifen,
Corticosteroids, Thyroxine, Contraception-OCP, DEPO, IUD Systemic causes- ie. Thyroid

PX:
Pap + swabs
Pelvic/bimanual exam

*detect genital tract pathology (fibroids. Polyps

* if abnormal consider transvaginal ultrasound

Investigations: CBC, ferritin, TSH

Coagulation work up- of FH/bleeding dyscrasia
Pelvic ultrasound
Endometrial biopsy

Endometrial Cancer Risk Factors

BMI >40
Age >40
DM
Anovulatory cycles/PCOS
Tamoxifen
FH of endometrial CA or colon CA

Management of Acute Bleeding

If stable: Hormonal contraceptive 2-4 pills per day for 7 days and then 1 pill/d for 2
weeks
If unstable: Send to emerg,
Conjugated equine estrogen (premarin) 25mg IV q 6 hr x 4 doses
Once bleeding has subsided oral hormonal therapy is continued for 2-3 weeks with
conjugated estrogen 2.5 mg-10 mg daily along with progesterone (provera )10 mg for the
last 10 days
Should be followed by cyclic hormonal contraceptive or cyclic progestin for 4-6 months
Gyne consult for surgical options- hysteroscopy, endometrial ablation, hysterectomy

364
4. In a post-menopausal woman with vaginal bleeding, investigate any new or changed vaginal
bleeding in a timely manner (e.g., with endometrial biopsy testing, ultrasonography, computed
tomography, a Pap test, and with a pelvic examination).

Post- Menopausal Vaginal Bleeding

* Most common cause in post-menopausal women is endometrial/vaginal atrophy

Ddx/Frequency:
Atrophic Vaginitis 59%
Endometrial polyp 12%
Endometrial hyperplasia 10%
Endometrial CA 10%
Hormonal Effect 7%
Cervical CA 2%
OTHER <1%

Hx Important Question
Amount/Frequency of blood loss
Medication: HRT, anticoagulants, ASA, Tamoxifen

PX
Vitals- Are they hemodynamically stable?
Pelvic Exam- atrophic/infectious vaginitis, cervical polyps, uterine size and contour
Pap and Swabs

Investigation
CBC, ferritin, TSH
Tranvaginal Ultrasound
* Sensitivity 96% for detecting endometrial CA
* If endometrial echo (EE) < 5 mm and symptoms resolve- WATCH
* If endometrial echo (EE) > 5 mm or symptoms persist- NEED ENDOMETRIAL
biopsy
* Either endometrial biopsy, transvaginal US or both can be done to initially assess the
endometrium- can base choice of first investigation upon patient preference, physician
comfort with procedure, US availability

TX
Results of Biopsy
Normal- Symptoms resolve- watch
Hyperplasia without Atypia- Treat with Provera and repeat biopsy in 3-6 months
Hyperplasia with Atypia/Cancer- Gyne consult for surgery

TX for Vaginal Atrophy- Topical estrogen (creams, tablets, vaginal ring)

Vaginitis - Key Features

1. In patients with recurrent symptoms of vaginal discharge and/or perineal itching, have a
broad differential diagnosis (e.g., lichen sclerosus et atrophicus, vulvar cancer, contact
dermatitis, colovaginal fistula), take a detailed history, and perform a careful physical
examination to ensure appropriate investigation or treatment. (Do not assume that the

365
symptoms indicate just a yeast infection.)

2. In patients with recurrent vaginal discharge, no worrisome features on history or physical

examination, and negative tests, make a positive diagnosis of physiologic discharge and
communicate it to the patient to avoid recurrent consultation, inappropriate trreatment, and
investigation in the future.

3. When bacterial vaginosis and candidal infections are identified through routine vaginal
swab or Pap testing, ask about symptoms and provide treatment only when it is appropriate.

4. In a child with a vaginal discharge, rule out sexually transmitted infections and foreign
bodies. (Do not assume that the child has a yeast infection.)

5. In a child with a candidal infection, look for underlying illness (e.g., immunocompromise,
diabetes).

• Presentation:
-itching, burning, irritation, erythema, dyspareunia, spotting, dysuria, change in vaginal discharge
(normal is 1-4 ml/24 hours, white/transparent, mostly doorless)

• Differential:
-BV, candida and trichomoniasis account for 90% of cases
-less commonly: cervicitis, atrophic vaginitis, foreign body, irritants, allergens, lichen sclerosis

• History:
-Don’t forget to ask about abdo pain (suggests UTI or PID) and medications (antibiotics, OCPs,
antifungals, HRT), sexual history (partners, protection), and hygienic practices (panty lines,
spermicides, soaps/perfumes, topical drugs)

• Physical exam:
-should focus on the degree of vulvovaginal inflammation and characteristics of the
vaginal discharge, the presence of cervical inflammation and abdominal or cervical
motion tenderness
-If possible, pH, microscopy (saline wet mount, KOH mount), amine/’whiff’ test
-Swabs (vaginal + cervical culture) if diagnosis not obvious based on above tests

Vulvovaginal Candidiasis Bacterial Vaginosis Trichomoniasis

Sexual intercourse,
DM, antibiotics, increased women who have sex Sexually transmitted, high
Risk estrogen levels (OCP, pregnancy, with women, rate of co-infection with
Factors HRT), immunosuppression, new/multiple sexual other STIs (males are
contraceptive devices partners, douching, carriers)
smoking
Symptoms -Pruritis, soreness, 50-75% asymptomatic Purulent, malodorous, thin
and signs dysuria,dyspareunia discharge’ burning,
-fishy-smelling pruritus, dysuria,
-vulvar erythema +/- edema; discharge (more frequency, dyspareunia
white, clumpy discharge noticeable after coitus),
-sxs often worse prior to homogeneous thin, -sxs +/- worse during
menstruation greyish white menstruation

366
 -Vulvar/vaginal erythema,
-rarely, dysuria,
green-yellow frothey d/c in
dyspareunia (pruritis
10-30%;punctate
and inflammation
hemorrhages on vagina and
typical absent)
cx (strawberry cx)
-pH >4.5
-pH >4.5
-pH 4-4.5
-postive whiff-amine
Special
test -Motile trichomonads on
tests -Pseudohyphae on saline/KOH
-clue cells on saline wet wet mount
mount
mount -TEST for other STIs
-no role for culture!
-Treat if symptomatic
-Fluconazole 150 mg PO x 1 (resolves spontaneously
-Avoid intercourse until
in 1/3 non-preg and ½
after abx and asymptomatic
-Intravaginal preparations pregnant women)
(~7d)
(clotirimazole cream/intravaginal
tablets, miconazole -May reduce risk of
-Flagyl 2 gm PO x 1
cream/vaginal suppository) x 3-7 acquiring STIs
Treatment -Flagyl 500 mg PO BID x
d depending on dose/method including HIV
7d
-in pregnancy, use topical -Flagyl 500 mg BID x
-Treat all cases
-if immune suppressed, use 2-3 7 days
(asymptomatic and
doses diflucan 72 hours apart -Flagyl gel .75% 5gm
symptomatic) and their
-can add topical steroid if PV OD x 5 days
partners
severely inflamed -Clinda 2% cream 5gm
PV HS x 7 days
***Note Re: trichomonas in pregnancy: treat if symptomatic (same Rx). Don’t treat if
asymptomatic as study did not show a decrease in preterm labour, rather an increase with
tx (unsure why). May tx after 37 weeks though to prevent transmission to neonate (can
cause fever, resp probs, uti etc).

Less frequent causes of vaginitis:

• Atrophic vaginitis

o Occurs in peri/postmenopausal women, or hypoestrogenic states

o Dyspareunia, dryness, burning, PV bleeding (post-coital), UTI sxs
o O/E – atrophic vaginal mucosa, thin, pale, loss of rugae
o Rule out vulvar intraepithelial neoplasia (visible/palpable lesion)
o Tx -topical estrogen

• Dermatitis (irritative/allergic)

o Hx of scented items, non-breathable undergarments, douches, creams, latex, spermicide

(rarely semen plasma allergy)
o Treatment – remove offending agent

367
• Vestibulodynia

o Chronic introital pain as primary symptom, at least x 3-6 mos

o Rule out vaginitis
o Tx – TCAs, gabapentin

Violent/Aggressive Patient - Key Features

1. In certain patient populations (e.g., intoxicated patients, psychiatric patients, patients with a
history of violent behaviour):
a) Anticipate possible violent or aggressive behaviour.
b) Recognize warning signs of violent/aggressive behaviour.
c) Have a plan of action before assessing the patient (e.g., stay near the door, be accompanied
by security or other personnel, prepare physical and/or chemical restraints if necessary).

2. In all violent or aggressive patients, including those who are intoxicated, rule out underlying
medical or psychiatric conditions (e.g., hypoxemia, neurologic disorder, schizophrenia) in a
timely fashion (i.e., don`t wait for them to sober up, and realize that their calming down with or
without sedation does not necessariy mean they are better).

3. In a violent or aggressive patient, ensure the safety (including appropriate restraints) of the
patient and staff before assessing the patient.

4. In managing your practice environment (e.g., office, emergency department), draw up a plan
to deal with patients who are verbally or physically aggressive, and ensure your staff is aware
of this plan and able to apply it.

Common Causes of violent behaviour:

• Toxicologic: Alcohol or other drug intoxication/withdrawal (stimulants, sedatives,

steroids)
• Metabolic: Hypoglycemia, hypoxia
• Neurologic: Stroke, intracranial lesion (eg, hemorrhage, tumor), CNS infection, seizure,
dementia
• Other medical conditions: Hyperthyroidism, shock, AIDS, hypo/hyperthermia
• Psychiatric: Psychosis, schizophrenia, paranoid delusions, personality disorder
• Antisocial behaviour

Warning Signs of Impending Violent Behavior

Male gender, a history of violence, and drug or alcohol abuse are associated with
violence.
• Provocative behavior
• Angry demeanor and/or loud, aggressive speech
• Tense posturing (eg, gripping arm rails tightly, clenching fists)
• Frequently changing body position, pacing
• Aggressive acts (eg, pounding walls, throwing objects, hitting oneself)

368
Management Points

• Immediate blood glucose (one-touch finger poke), vital signs and pulse oximetry
• Assume that all violent patients are armed until proven otherwise
• patients must be disarmed before any interview
• interview in private but not isolated area, clear exit path for clinician
• have security present for interview and leave door open
• interview room must not contain any objects that could be used as weapons
• have a panic button, code word/phrase to alert others to danger
• remove glasses, earrings, neckties and necklaces and other potentially dangerous
personal accessories prior to interview
• Actively violent patients and uncooperative, agitated patients, particularly those who
exhibit signs of impending violence, require immediate restraint.

Interview Strategies

• Adopt an honest and straightforward manner

• Perform friendly gestures (eg, offer food)
• Avoid direct eye contact; do not approach the patient from behind or move suddenly;
stand at least one arm's length away
• Address violence directly: The patient should be asked relevant questions, such as, "Do
you feel like hurting yourself or someone else?"
• Avoid arguing, machismo, condescension, or commanding the patient to calm down
• Never lie to the patient, and take all threats seriously

When Verbal Techniques Fail:

• Physical restraints (must monitor patient carefully and frequently; remove as soon as
possible)
• Rapid tranquilization may be required in the agitated or violent patient.
• If severely violent patients requiring immediate sedation, try haloperidol, loxapine or
lorazepam (or combination of haloperidol and lorazepam)
• If drug intoxication or withdrawal, we suggest treatment with a benzodiazepine.
• If violence originates from psychiatric disorder, use first or second generation
antipsychotic

Well-baby Care - Key Features

1. Measure and chart growth parameters, including head circumference, at each assessment;
examine appropriate systems at appropriate ages, with the use of an evidence-based pediatric
flow sheet such as the Rourke Baby Record.

2. Modify the routine immunization schedule in those patients who require it (e.g., those who
are immunocompromised, those who have allergies).

3. Anticipate and advise on breast-feeding issues (e.g., weaning, returning to work, sleep
patterns) beyond the newborn period to promote breast-feeding for as long as it is desired.

369
4. At each assessment, provide parents with anticipatory advice on pertinent issues (e.g.,
feeding patterns, development, immunization, parenting tips, antipyretic dosing, safety issues).

5. Ask about family adjustment to the child (e.g., sibling interaction, changing roles of both
parents, involvement of extended family).

6. With parents reluctant to vaccinate their children, address the following issues so that they
can make an informed decision:
- their understanding of vaccinations.
- the consequences of not vaccinating (e.g., congenital rubella, death).
- the safety of unvaccinated children (e.g., no Third World travel).

7. When recent innovations (e.g., new vaccines) and recommendations (e.g., infant feeding,
circumcision) have conflicting, or lack defined, guidelines, discuss this information with
parents in an unbiased way to help them arrive at an informed decision.

8. Even when children are growing and developing appropriately, evaluate their nutritional
intake (e.g., type, quality, and quantity of foods) to prevent future problems (e.g., anemia, tooth
decay), especially in at-risk populations (e.g., the socioeconomicaly disadvantaged, those with
voluntarily restricted diets, those with cultural variations)

Nutrition
• Exclusive breastfeeding recommended in first 6 months, and breastfeeding (with
complementary foods) is promoted as long as desired
• Vitamin D 400 IU/day for breastfed infants (800 IU/day in Northern communities)
• Solids: introduction at 6 months

o Iron containing foods (cereals, meat, egg yolk, tofu)

o Fruits and veggies to follow
o Introduce cow’s milk products at 9 months
o No egg white, nut products, or honey until 12 months

• Milk

o Switch from formula to homo milk (500-750 mLs/day) at 12 months

o Transition to 1% or 2% milk (~500 mLs/day) at 2-3 years
o Discontinue bottles by 18 months

• Avoid sweetened juices/liquids

• Inquire about vegetarian diets
• Transition to lower fat diet after age 2 as per Canada’s Food Guide

Breastfeeding
• Benefits

o Infant: reduced risk of infections (GI, respiratory, UTIs, AOM, meningitis), SIDS,
obesity, T1DM, childhood CA (leukemia, lymphoma), IBD, Celiac disease, heart and
liver diseases in adulthood

370
 o Mother: decreased risk of breast and ovarian CA, decreased risk of DM improved bone
health, weight loss, lactational amenorrhea

• Weaning

o Eliminate one BF session every 2-5 days (start with midday feed), supplement with age
appropriate alternative (see nutrition)
o Another caregiver could introduce the bottle, as some babies initially refuse the bottle
when the mother’s breast is available

• Return to work: pumping every few hours will help prevent mastitis
• Tips to facilitate sleep: keep baby awake with frequent feeds in evening, bedtime rituals (ie.
bath), keep lights low and do not talk to or stimulate baby during nighttime feeds

Education/Advice
• Sleep safety

o Place on back to sleep (place head in different positions on alternate days), supervised
tummy time while awake
o Soft mattresses, pillows, comforters, stuffed toys and bumper pads should not be used
in cribs
o Rooming-sharing lowers the risk of SIDS
o Avoid bed-sharing, overheating, and maternal or second-hand smoke to decrease the
risk of SIDS
o Pacifier use may decrease risk of SIDS and should not be discouraged in the first year

• Medications

o Antipyretics: acetaminophen 15 mg/kg/dose

o Ibuprofen 10 mg/kg/dose
o Do not use OTC cough/cold medication

Development

Age Gross Motor Fine Motor Speech Social

Prone-lifts head and pushes
2m Coos Smiles, follows
up on arms
Reaches for and
Holds head steady, rolls F
4m holds objects, Begins to babble Laughs
to B
hands to mouth
Palmar grasp,
Begins to sit without Babbles, responds
6m hand to hand Stranger anxiety
support, rolls B to F to name
transfer
Gets into sitting position,
Finger-thumb
9m sits independently, pulls to Mama, dada, baba Peek-a-boo, bye-bye
grasp
stand, stands holding on
12m Independent standing, Pincer grasp, Single words (2) Drinks from cup

371
 cruising, first steps throws
Single words (10), Points to show interest,
Walks independently, stairs Scribbles, tower
18m follows simple points to body parts, uses
with help of 3 blocks
commands spoon
Draws straight 2 word phrases,
Runs, up stairs 2 feet/step,
2y lines, tower of 6 follow 2-step Undresses, knows age/sex
kicks ball
blocks commands
Up stairs 1 foot/step, down Draws circle, 3 word phrases,
Dresses/undresses self,
3y 2 feet/step, stands on 1 turns book pages says name, age, and
toilet trained
foot, jumps one at a time sex, counts to 10

Pediatric Exam Includes

• Growth: correct percentiles until 24-36 months if gestation <37 weeks, regain BW by 1-3 weeks

• Eyes: red reflex, corneal light reflex, cover-uncover test and inquiry for strabismus (6+ months)
• Hearing inquiry/screening
• Fontanelles: posterior closed by 2 months, anterior closed by 18 months
• Muscle tone
• Hips (until at least 1 year, or until child can walk)
• Snoring/tonsils

Immunization
• Understanding vaccines

o Infants can respond to 10,000 different antigens at any one time, giving 6 vaccines does
not add, significantly, to the daily load

• Not vaccinating

o Protection from herd immunity declines, as vaccination rates decline

o Diseases only one flight away – massive outbreaks (eg. diptheria in Russia in the 90’s
and polio in middle east last year with >500 paralyzed) due to lapses in immunization
o Advise against 3rd world travel

• Some contraindications

o Immunocompromised: live vaccines, consult specialist

o IgE-mediated chicken or egg allergy is a contraindication to influenza, yellow-fever
and rabies vaccines (GI intolerance in NOT)
o Anaphylaxis to neomycin or gelatin is a contraindication to MMR

372