CRITICAL CARE

Ghulam Mujtaba
Pharm.D, M.phil, BCPS
Assistant Manager –Clinical pharmacy
ASHP Accredited Preceptor- Critical Care
CASE SCENARIO
A 62-year-old woman is admitted to your ICU for respiratory dysfunction necessitating mechanical ventilation.
Her medical history is nonsignificant, and she is taking no medications at home. Her chest radiograph shows
bilateral lower lobe infiltrates, her white blood cell count (WBC) is 21 × 103 cells/mm3, lactate is 1.7 mmol/L,
temperature is 103.3°F(39.6°C), blood pressure is 82/45 mm Hg (normal for her is 115/70 mm Hg), heart rate is
110 beats/minute, and respiratory rate is 22 breaths/minute.
After she receives a diagnosis of community-acquired pneumonia, she is empirically initiated on ceftriaxone 2
g/day and levofloxacin 750 mg/ day intravenously. After fluid resuscitation with 6 L of lactated Ringer solution,
her blood pressure is unchanged. Dopamine is initiated and titrated to 9 mcg/kg/minute, with a resulting
blood pressure of 96/58 mm Hg, and her heart rate is 138 beats/ minute. She has made less than 100 mL of
urine during the past 6 hours, and her creatinine (Cr) has increased from 0.9 mg/dL to 1.3 mg/dL. Her serum
albumin concentration is 2.1 g/dL. Which therapyis best for this patient at this time?

A. Administer 5% albumin 500 mL intravenously over 1 hour and reassess mean arterial pressure (MAP).
B. Initiate hydrocortisone 50 mg intravenously every 6 hours.
C. Change dopamine to norepinephrine 0.01 mcg/kg/minute to maintain an MAP greater than 65 mm Hg.
D. Reduce the dopamine infusion to 1 mcg/kg/minute to maintain urine output of at least 1
mL/kg/hour.

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 HEMODYNAMIC PARAMETERS

• INTERPRETATION OF HEMODYNAMIC PARAMETERS:

Arterial blood pressure = cardiac output x resistance to flow (systemic
vascular resistance [SVR].
a. Cardiac output (milliliters of blood pumped per minute) consists of stroke
volume (milliliters of blood ejected from the left ventricle per beat) and heart
rate.
b. Stroke volume is determined by
Preload (amount of blood available to eject)
Afterload (resistance to ejection
Contractility (amount of force generated by the heart).
• MAP = [SBP + (2 × DBP)]/3.
a. Normal MAP is 70–100 mm Hg.
Preload is defined as ventricular end-diastolic volume, and it increases
proportionally with stroke volume
Commonly used measures of preload include CVP, PCWP, or pulmonary artery
occlusion pressure (PAOP), and newer measures such as stroke volume
variation (SVV) and pulse pressure variation (PPV).
Lactic acid
a. Lactic acid is formed during anaerobic metabolism.
b. During states of hypo-perfusion, the tissues receive less blood and therefore
less oxygen.
c. If there is less oxygen for the tissues, they will use anaerobic metabolism,
with the subsequent production of lactic acid.
d. Lactate clearance can be used as a therapeutic end point in shock

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HEMODYNAMIC PARAMETERS AND NORMAL VALUES

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TYPES OF SHOCK

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Treatment of hypovolemic shock

1. Fluid resuscitation
2. Patients may need vasopressors if hypotension is not rapidly reversed with
fluid resuscitation.
a. The efficacy of vasopressors is reduced in patients who have not received
adequate intravascular volume resuscitation.
b. Adverse events associated with vasopressors (e.g., arrhythmias, ischemia)
are greater in patients who have not received adequate fluid resuscitation.

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Treatment of obstructive shock

1. Fluids and vasopressors can be used temporarily to improve end organ

perfusion, but may not improve outcomes.
2. Treatment of the actual obstruction is the only way to reverse the shock
state.
a. Massive pulmonary embolism: Thrombectomy or administration of systemic
or catheter-directed thrombolytics may be indicated if the patient has a high
risk of death.
b. Cardiac tamponade: Drainage or removal of fluid in the pericardial sac is the
only definitive treatment.

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SEPSIS

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• The hallmark treatment of septic shock is rapid antibiotic administration,
ideally within the first hour of hypotension.

The Surviving Sepsis Campaign (SSC) is an initiative to reduce mortality from

sepsis and septic shock.
The SSC recommends the following bundle for patients presenting with sepsis
or septic shock.

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To be completed within 1 hour

(a) Measure lactate concentration.

(b) Obtain blood cultures before administering antibiotics.
(c) Administer broad-spectrum antibiotics.
(d) Begin administering 30 mL/kg crystalloid for hypotension or lactate 4
mmol/L or greater.
(1) Albumin can be considered when patients need a substantial amount of
crystalloids. There is no evidence that colloids are superior to crystalloids in
improving outcomes, and they are more expensive.

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The use of “balanced crystalloids” (solutions with electrolyte concentrations
similar to those of extracellular fluid, such as lactated Ringer solution and
Plasmalyte) for volume replacement can lead to less acute kidney injury than
the use of other fluids (0.9% NaCl or 5% albumin).

(e) Initiate vasopressors if the patient is hypotensive during or after fluid

resuscitation to maintain MAP 65 mm Hg or greater

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• Norepinephrine is the initial vasopressor of choice.
• Epinephrine can be added to or substituted for norepinephrine if needed.
• Vasopressin (0.03 unit/minute) can be added to norepinephrine if needed.
The efficacy of vasopressin when added to norepinephrine is similar to that
of norepinephrine alone.
• Dopamine is an alternative to norepinephrine, but it is associated with a
higher incidence of arrhythmias compared with norepinephrine. Dopamine
use should be limited to patients with a low risk of tachy-arrhythmias and
absolute or relative bradycardia.
• Low-dose dopamine should not be used for renal protection.

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VASOPRESSORS EXAMPLES

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Appropriate use of antimicrobials in patients with sepsis

1. Empiric antimicrobials should cover likely pathogens according to suspected location of

infection and risk of multidrug-resistant pathogens.
2. Common sources of infection are lung, abdomen, blood, and urinary tract. Please refer
to the infectious diseases chapter for discussion of specific agents.
3. Consider empiric fungal therapy with either tri-azoles such as fluconazole, an echino-
candin, or a lipid formulation of amphotericin B if patients have several risk factors,
including recent abdominal surgery, long-term PN, indwelling central venous catheters,
or recent treatment with broad-spectrum antibiotics or if patients are
immunocompromised .An echino-candin is preferred in patients with septic shock,
recently treated with antifungal agents, or if Candida glabrata or Candida krusei
infection is suspected.
4. Other considerations when choosing appropriate antimicrobials include the patient’s
history of drug allergy or intolerance, recent antibiotic use, comorbidities, and
antimicrobial susceptibility patterns in the community and hospital.
5. Consider empiric antiviral therapy with oseltamivir for patients presenting with flulike
symptoms during flu season.

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A 62-year-old woman is admitted to your ICU for respiratory dysfunction necessitating mechanical ventilation.
Her medical history is nonsignificant, and she is taking no medications at home. Her chest radiograph shows
bilateral lower lobe infiltrates, her white blood cell count (WBC) is 21 × 103 cells/mm3, lactate is 1.7 mmol/L,
temperature is 103.3°F(39.6°C), blood pressure is 82/45 mm Hg (normal for her is 115/70 mm Hg), heart rate is
110 beats/minute, and respiratory rate is 22 breaths/minute. After she receives a diagnosis of community-
acquired pneumonia, she is empirically initiated on ceftriaxone 2 g/day and levofloxacin 750 mg/ day
intravenously. After fluid resuscitation with 6 L of lactated Ringer solution, her blood pressure is unchanged.
Dopamine is initiated and titrated to 9 mcg/kg/minute, with a resulting blood pressure of 96/58 mm Hg, and
her heart rate is 138 beats/ minute. She has made less than 100 mL of urine during the past 6 hours, and her
creatinine (Cr) has increased from 0.9 mg/dL to 1.3 mg/dL. Her serum albumin concentration is 2.1 g/dL.
Which therapy is best for this patient at this time?

A. Administer 5% albumin 500 mL intravenously over 1 hour and reassess mean arterial pressure (MAP).
B. Initiate hydrocortisone 50 mg intravenously every 6 hours.
C. Change dopamine to norepinephrine 0.01 mcg/kg/minute to maintain an MAP greater than 65 mm Hg.
D. Reduce the dopamine infusion to 1 mcg/kg/minute to maintain urine output of at least 1
mL/kg/hour.

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➢This patient meets the definition for septic shock. Treatment with 5%
albumin (Answer A) is unlikely to offer additional benefit because the
patient’s MAP is at goal (more than 65 mm Hg). Furthermore, colloids are no
more effective than crystalloids for fluid resuscitation, and a serum albumin
concentration does not predict the efficacy of albumin administration.
Hydrocortisone (Answer B) is incorrect because the patient is not persistently
hypotensive after receiving fluids and vasopressors. Although this patient’s
blood pressure is responding to the infusion of dopamine, the heart rate has
increased. Norepinephrine (Answer C) is correct because it has similar
efficacy, but with fewer tachy-arrhythmias than dopamine. Dopamine should
not be reduced (Answer D) because lower doses are not renal protective.

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INTERPRETATION OF ACID-BASE
DISTURBANCES
CLINICAL CASES
• A 62-year-old woman has been hospitalized in the ICU for several weeks. Her
hospital stay has been complicated by aspiration pneumonia and sepsis,
necessitating prolonged courses of antibiotics. For the past few days, she has been
having high temperatures again, and her stool output has increased dramatically.
Her most recent stool samples have tested positive for Clostridium difficile toxin,
and her laboratory tests show serum sodium 138 mEq/L, potassium (K) 3.5 mEq/L,
Cl 115 mEq/L, HCO3 15 mEq/L, albumin 4.4 g/dL, pH 7.32, and Paco2 30 mm Hg.
Which is most consistent with this patient’s primary acid-base disturbance?
A. AG metabolic acidosis.
B. Non-AG metabolic acidosis.
C. Chloride-responsive metabolic alkalosis.
D. Acute respiratory acidosis.

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NORMAL ARTERIAL GAS VALUES

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Acidosis: Any pH less than 7.35 indicates a primary acidosis.
Alkalosis: Any pH greater than 7.45 indicates a primary alkalosis.
1 Metabolic disorders
. Acidosis: Decreased HCO3
. Alkalosis: Increased HCO3
2. Respiratory disorders
. Acidosis: Increased Pco2
. Alkalosis: Decreased Pco2

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STEPS TO EVALUATE ACID-BASE DISORDERS
1. Assess pH, Pco2 and HCO3
a. Acidosis if pH less than 7.35
i . If Pco2 is elevated, the primary disorder is respiratory acidosis.
ii. If HCO3 is decreased, the primary disorder is metabolic acidosis.

b. Alkalosis if pH is greater than 7.45

i. If Pco2 is decreased, the primary disorder is respiratory alkalosis.
ii. If HCO3 is elevated, the primary disorder is metabolic alkalosis.

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• 2. Calculate the anion gap (AG) = [Na+] − [Cl+ HCO3]
• a. Normal range is 6–12 mEq/L.
• b. If AG is more than 12, there is a primary metabolic acidosis regardless of
pH or HCO3. Some patients have a mixed acid-base disorder in which they
have more than one primary disorder.
• c. Hypoalbuminemia decreases the AG by 2.5–3 mEq/L for every 1-g/dL
decrease in serum albumin less than 4 g/dL.
3. Calculate the excess AG = Total AG − Normal AG. Add excess AG to serum
bicarbonate.

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• A 62-year-old woman has been hospitalized in the ICU for several weeks. Her
hospital stay has been complicated by aspiration pneumonia and sepsis,
necessitating prolonged courses of antibiotics. For the past few days, she has been
having high temperatures again, and her stool output has increased dramatically.
Her most recent stool samples have tested positive for Clostridium difficile toxin,
and her laboratory tests show serum sodium 138 mEq/L, potassium (K) 3.5 mEq/L,
Cl 115 mEq/L, HCO3 15 mEq/L, albumin 4.4 g/dL, pH 7.32, and Paco2 30 mm Hg.
Which is most consistent with this patient’s primary acid-base disturbance?
A. AG metabolic acidosis.
B. Non-AG metabolic acidosis.
C. Chloride-responsive metabolic alkalosis.
D. Acute respiratory acidosis.

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• This patient’s ABG is consistent with metabolic acidosis. The pH is less than
7.40, indicating primary aci-dosis (Answer C is incorrect). The HCO3and
PaCO2 are lower than normal, indicating this is metabolic inorigin (Answer D
is incorrect).
• In metabolic acidosis,the decrease in HCO3 is the primary disorder. When
metabolic acidosis is present, the AG should be calcu-lated to provide
additional insight about the potential cause of the disorder. The AG is
calculated by subtracting the sum of measured anions (Cl−and HCO3)
fromcations (Na+). This patient’s AG (8 mEq/L) is within the reference range
of 6–12 mEq/L; therefore, it is called a normal AG metabolic acidosis or non-
AG metabolic acidosis (Answer B is correct, answer A is incorrect).c difficile–
induced diarrhea is the most likely cause of this patient’s acid-base disorder.

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CARDIAC ARREST
• A. Training: Any pharmacist who participates in codes should complete basic
life support (BLS) and advanced cardiac life support (ACLS) training.
• Medication administration
a. Central venous administration is preferred.
b. If medications are administered through a peripheral vein, it is important to
follow the medication with 20 mL of intravenous fluid to facilitate drug flow
from the extremity to the central circulation.

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Post–cardiac arrest care

1. After ROSC, systematic post–cardiac arrest care can improve survival and
quality of life.
2. Initial therapy should optimize ventilation, oxygenation, and blood pressure.
a. Sao2should be maintained at 94% or higher.
i. Insertion of an advanced airway may be necessary.
ii. Hyperventilation and excess oxygen delivery are harmful and should be
avoided, especially after ROSC.
b. Hypotension (SBP of 90 mm Hg or less) should be treated with fluid boluses
and vasopressors if necessary.

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Target temperature management (therapeutic hypothermia)
a. Induction of hypothermia (32°C–36°C) for at least 24 hours beginning as
soon as possible after ROSC can improve neurologic recovery and mortality.
b. Rewarming should be done slowly (0.3°C–0.5°C every hour), and patients
should remain afebrile.

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Complications
i. Shivering
ii. Altered drug metabolism
iii. Coagulopathy
iv. Increased renal excretion of water and subsequent volume depletion
v. Arrhythmia and hypotension
vi. Hyperglycemia and hypoglycemia
vii. Electrolyte disturbances

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PAIN, AGITATION, DELIRIUM, AND
NEUROMUSCULAR BLOCKADE
General considerations

1. Nonpharmacologic strategies to improve patient comfort include lighting,

music, massage, verbal reassurance, avoidance of sleep deprivation, and
patient positioning based on patient preferences.
2. Determine patient goals using validated scales and routinely assess pain and
sedation.
a. Routine assessment of pain and sedation should be performed in every
patient in the ICU.

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BEHAVIORAL PAIN SCALE

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RASS SCORE

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• Goal sedation scores should be individualized for each patient, but generally
an SAS score of 3 to 4 or a RASS score of 0 to –1 is recommended.

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Pain and discomfort are primary causes of agitation; therefore, treat pain first and add a sedative if needed.
This is often referred to as analgosedation.

i. Use bolus dose analgesics and/or non-pharmacologic interventions before potentially painful procedures.

ii. Opioid analgesics are considered first line for the treatment of non-neuropathic pain (gabapentin or
carbamazepine can be considered for neuropathic pain).

iii. Nonopioid analgesics (e.g., acetaminophen, ketamine) can be used in conjunction with opioids as a
“multimodal analgesia” approach to optimize pain control and to avoid dose-related adverse effects.

iv. Nonsteroidal anti-inflammatory drugs are usually avoided because of the risk of bleeding and kidney injury
in critically ill patients.

v. Nonbenzodiazepine sedatives may be preferred to benzodiazepines to improve clinical outcomes in

mechanically ventilated patients.

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Dosing strategies for analgesics and sedatives

i. Analgesics and sedatives should be dosed to achieve pain and sedation goals. Adjust
sedative medications to achieve a light level of sedation (RASS 0 to –1). Light sedation is
needed for evaluating pain and delirium and for early patient mobility.

ii. Goals can be achieved using intermittent dosing administered routinely or as needed.
iii. If unable to achieve goals with intermittent dosing, use a combination of bolus dosing
with a
continuous infusion.

(a) In patients receiving a continuous infusion, use a bolus dose before or instead of
increasing the infusion rate (a bolus dose has a faster onset and can eliminate the need for
an increase in the infusion rate). An exception is with drugs such as propofol or dexmedeto-
midine, which can cause hypotension or bradycardia when bolused.
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SEDATIVES
1. Benzodiazepines should be avoided when possible to prevent adverse outcomes,
including prolonged duration of mechanical ventilation, increased ICU length of stay,
and development of delirium
Lorazepam
a. Intermittent dosing 1–4 mg every 2–6 hours
b. Continuous infusion: Start at 1 mg/hour and titrate to goal (e.g., RASS, SAS). Total
daily doses as
low as 1 mg/kg can cause propylene glycol toxicity. Monitor for an osmolal gap
greater than 10–12
mOsm/L, indicating propylene glycol toxicity.
c. Lorazepam is the preferred benzodiazepine in severe hepatic dysfunction because
of its metabolism.

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3. Midazolam
a. Intermittent dosing 1–4 mg every 15 minutes to 1 hour
b. Continuous infusion: Start at 1 mg/hour and titrate to goal (e.g., RASS, SAS).
c. Often used for procedural sedation or daily dressing changes because of its
rapid onset and short duration

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3. Propofol
a. Rapid onset (1–2 minutes) and short duration (3–5 minutes or longer if
prolonged infusion)
b. Initiate at 5 mcg/kg/minute and titrate to achieve sedation goals by 5
mcg/kg/minute every 5 minutes. Avoid prolonged infusions greater than 50
mcg/kg/minute.
c. Avoid loading doses because of the risk of hypotension.

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4. Dexmedetomidine
a. Sedative properties through central and peripheral α2-receptor agonist
activity
b. Extent of analgesic activity in patients in the ICU is not well described.
c. Does not cause respiratory depression

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Assessment and management of delirium
1. Delirium is an acute change in cognitive function characterized by
disorganized thought, altered level of consciousness, and inattentiveness.

2. Delirium is associated with increased mortality, prolonged length of stay in

the ICU, and cognitive impairment after ICU discharge..

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 MANAGEMENT
• Nonpharmacologic interventions are preferred to pharmacologic treatment.
These interventions include maintaining communication with the patient,
reorienting the patient (to person, place, and time), maximizing
uninterrupted sleep.
• Pharmacologic treatment of delirium

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An older woman is admitted to the ICU for acute decompensated heart failure and acute kidney injury with
an ejection fraction of less than 30%. She is administered a continuous infusion of bumetanide; however, the
benefit is limited because of her acute-on-chronic kidney disease. She is intubated on ICU day 2 because of
worsening pulmonary edema and hypoxia. After intubation, she scores a zero on the RASS, but her CAM-
ICU is positive for delirium. Her BPS score is 4. Her blood pressure is 120/70 mm Hg, and heart rate is 88
beats/minute. What is the best recommendation for achieving her analgesia, sedation, and delirium goals?

A. Initiate propofol at 5 mcg/kg/minute and titrate as needed.

B. Administer haloperidol 5 mg intravenously and double the dose every 20 minutes as needed.
C. Initiate morphine 4 mg intravenously every 4 hours as needed.
D. Offer the patient verbal reassurance.

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PREVENTING STRESS ULCERS
A. Mucosal bleeding in critically ill adults
1. The incidence of stress-related mucosal bleeding in critically ill adults is
estimated to be about 6%.
2. Signs and symptoms of stress ulcers include hematemesis, gross blood in
gastric tube aspirates, coffee ground emesis or aspiration from gastric tube,
and melena. Clinically significant stress ulcers are defined as those that cause
hemodynamic compromise or necessitate blood transfusion.

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Prophylactic therapy for stress ulcers
1. Prophylactic medications are recommended for any one of the following
major risk factors:
a. Respiratory failure necessitating mechanical ventilation (for more than 48
hours)
b. Coagulopathy, defined as platelet count less than 50,000 cells/mm3
, INR greater than 1.5, or activated partial thromboplastin time greater than
twofold the control value. (Note: Prophylactic or treatment doses of
anticoagulants do not constitute coagulopathy.)

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• Strategies for stress ulcer prophylaxis (see Table 17 for specific medications)
• 1. Efficacy of intravenous histamine-2 (H2)-blockers in preventing stress-
related upper GI bleeding has been shown in several clinical trials. These
blockers are commonly administered enterally when possible because of
excellent bioavailability; however, evidence of efficacy is primarily with the
intravenous administration of H2-blockers.

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PHARMACOLOGIC THERAPY FOR
PREVENTING VENOUS
THROMBOEMBOLISM
RISK FACTORS
1. Critically ill patients are usually at high risk of VTE.
2. Additional risk factors include surgery, major trauma, lower extremity injury, immobility,
malignancy,
sepsis, heart failure, respiratory failure, venous compression, previous VTE, increasing age,
pregnancy,
erythropoiesis-stimulating agents, obesity, and central venous catheterization.
C. Nonpharmacologic prevention of VTE
1. Early mobility is the ideal non pharmacologic therapy.
2. Mechanical prophylaxis with intermittent pneumatic compression or graduated compression
stockings
is recommended for medical patients at risk of VTE who have a contraindication to pharmacologic
anticoagulation (e.g., thrombocytopenia, severe coagulopathy, active bleeding, recent intracerebral
hemorrhage).
3. Mechanical prophylaxis can be used in combination with pharmacologic treatment.

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D. Recommendations for critically ill patients
1. American College of Chest Physicians, ninth edition
a. Recommends low-molecular-weight heparin (LMWH) or low-dose
unfractionated heparin over no prophylaxis

b. For patients who are bleeding or at high risk for major bleeding, the
guidelines recommend mechanical thromboprophylaxis and institution of
pharmacologic prophylaxis when the bleeding risk decreases.

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PREVENTING VENTILATOR-
ASSOCIATED PNEUMONIA
A. The Institute for Healthcare Improvement has developed a ventilator bundle with the following elements
that directly target ventilator-associated pneumonia and complications arising from it.
1. Head of the bed elevation: Maintain the head of the bed elevated (about 30–45 degrees).
2. Daily sedation interruptions and assessment of readiness to extubate
3. Stress ulcer prophylaxis
4. VTE prophylaxis
5. Daily oral care with chlorhexidine (0.12% oral rinse)
B. Additional methods
1. Selective decontamination of the digestive tract
a. It is a short course of antimicrobial therapy aimed at eradicating potential pathogens to minimize ICU-acquired
infections.

b. Selective decontamination is still not routinely performed.

2. Endotracheal tubes coated in an antimicrobial (silver) reduce infection but are cost prohibitive in manycenters.

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INTRACRANIAL
HEMORRHAGE
General overview
1. Intracranial hemorrhage (ICH) is a broad term that encompasses many
clinical scenarios. Goals of careare to minimize hemorrhage expansion and to
treat associated organ dysfunction, thereby decreasing
mortality and improving quality of life.
2. ICH is classified by the anatomic location of the bleeding.
a. Intraparenchymal hemorrhage (IPH): Nontraumatic bleeding into the brain
parenchyma

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• Severity of ICH and resulting neurologic injury guide diagnostic tests,
treatment, and prognosis.

• Commonly used scales include the Glasgow Coma Scale (GCS; Table 19) to
assess the level of consciousness and the National Institutes of Health Stroke
Scale.

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Management
1. Blood pressure control
a. Acute hypertension should be controlled after the diagnosis of SAH. The goal blood
pressure has not been definitively established. AHA Guidelines for the Management
of Aneurysmal Subarachnoid
Hemorrhage recommend balancing the risk of stroke, rebleeding because of
hypertension, and
maintenance of cerebral perfusion pressure in determining a patient’s goal blood
pressure. They
further state that a goal systolic blood pressure less than 160 mm Hg is reasonable.

b. Blood pressure should be controlled with an intravenous, titratable agent such as

nicardipine or clevidipine.

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2. Antifibrinolytic therapy
a. For patients who will have a delay in surgical intervention, short-term (less than 72 hours or until
angiography) treatment with tranexamic acid or aminocaproic acid (preferred) is reasonable.

b. Many different dosing protocols exist for aminocaproic acid and tranexamic acid. Typically, ami-
nocaproic acid is administered as a 4- to 5-g load followed by 1 g/hour.

c. Patients who receive antifibrinolytic therapy should be monitored for the development of a VTE.

3. Coagulation factors: In a study of ICH not caused by anticoagulant therapy, recombinant activated
factor VII decreased the size of ICH but did not improve outcomes.

4. Seizure prophylaxis in aneurysmal SAH

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For Questions and Queries please email at

ghulam.mujtaba37@gmail.com
ghulammujtaba@skm.org.pk

19-06-2021 BCPS Preparatory Class 66