Surgery Long Cases Scripts N Q&A

PREPARING FOR THE MBBS | CHAPTER THREE
Surgery Long Cases

presentation scripts & Q&A
NIGEL FONG & MARIANNE TSANG | V1.0

SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A CONTENTS
Contents
Overall Strategy 115
General Surgery:
Abdominal Pain: Acute Cholecystitis 118
Abdominal Pain: Acute Pancreatitis 123
Abdominal Pain: Aortic Aneurysm 128
Abdominal Pain: Diverticulitis 131
Abdominal Pain: Urolithiasis 134
Bleeding GIT, Lower: Diverticular Bleed 138
Bleeding GIT, Upper: Peptic Ulcer Disease 142
Bleeding GIT, Upper: Variceal Bleed 146
Breast Cancer 149
Dysphagia: Esophageal Cancer 154
Gastric Outlet Obstruction: Gastric Cancer 158
Hematuria: Bladder Cancer 164
Hematuria: Renal Cell Carcinoma 167
Hepatocellular Carcinoma 170
Intestinal Obstruction: Colon Cancer 175
Intestinal Obstruction: Crohn’s Disease 182
Jaundice, Painful: Cholangitis 186
Jaundice, Painless: Pancreas Cancer 191
Leg Pain: Claudication, Critical Limb Ischemia 195
Leg Pain: Venous Insufficiency 199
Lower Urinary Tract Symptoms: BPH & Prostate CA 202
Thyroid Cancer 208
Orthopaedic Surgery:
Hip: Osteoarthritis & AVN 211
Knee: Osteoarthritis 215
Spine: Cervical Myelopathy 220
Spine: PID & Cervical Radiculopathy 224
Spine: Lumbar Spinal Stenosis 228
NIGEL FONG & MARIANNE TSANG | V1.0 PREPARING FOR THE MBBS | 114
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A STRATEGY
Strategy
What are surgical long cases like? You begin with 20 min for history taking, targeted
physical examination, and consolidation. Examiner 1 observes you. Examiner 2 arrives at the
21st minute and begins a 20min discussion, which is more in-depth than the medical longs.
[For orthopedics: 10min + 10min, only 1 examiner] *
Examiners want you to:

• Take a good history: have a reasonable approach to the presenting complaint, be able
to diagnose and consider differentials, etiology and complications. Explore how the
patient has been managed, including his/her progress up to your exam day.
• Interact with the patient, not simply use a memorized template (a memorized template
will inevitably lead to an examiner’s comment along the lines of “appear to have little
experience or interactions with patients in real life”)
• Do targeted physical exam (tailor to your history), with good technique and accuracy.
Please do not neglect the physical exam as this has a rather high weightage; do not
take ‘shortcuts’ e.g. examine through clothes!
• Show professionalism (e.g. after doing per-rectal exam, please wipe the patient).
• Present your case in full (more detailed than in medicine longs), not merely repeating
what the patient told you, but ‘adding value’ with your interpretation and synthesis.
• Discuss just about anything: e.g. your clerking, what is atypical in the history, read lab
results and X-ray / CT scans, suggest management, and answer basic science
questions. You are expected to tailor your answer to this patient. Many examiners like
to probe if you have been in the wards, and will be a safe HO.
Your strategy: Surgical long cases are quite high-stakes (because of the points system),
although patients are generally less complicated than the medical ones. The longer
presentation and in-depth questioning can also be a challenge. Our advice is:
• Be comfortable with clerking patients. History-taking is not easy. You need to be logical
and comprehensive (covering diagnosis, differentials, severity, etiology, complications,
and management), and yet have a conversation with the patient (not do a checklist).
Patients are very different from textbooks; it takes experience to make sense of what
they say, to probe for information, and piece things together on the go. There is no
shortcut to practice with real patients - we only became comfortable after clerking ~50
cases. As you practice, do so intentionally – blind yourself to the case, take full histories
as you would in an exam and also practice presenting. Get a friend or senior to observe
and give feedback. Think about whether you covered what you need to achieve, what
you did well and what you can do better (we too have made ‘rookie’ mistakes like
clerking ‘dark urine’ as approach to hematuria when it was obstructive jaundice).
Develop your own style and template, and at MBBS stick to what you have practiced.
• Think through cases you have seen. The long discussion tests your overall ability to
clinically assess and apply knowledge to this patient (from history till management).
Do not simply float through your SIP posting, but ask your team the ‘why’ questions –
why this diagnosis, why not the other diagnosis, why this treatment? For every patient
think – if this is your patient, how will you manage? Only then, flip the file and ask why
did the team’s approach differ from yours. Read up on what you do not know.
Refer to Approaches to Symptoms of Disease for how to get from presenting complaints to
diagnosis. This chapter begins at diagnosis, samples possible presentations and discussion.
Common things being common, they will cover about 80% of all possible surgical long cases
– but there are oddballs. These cases were mostly written based on real patients we clerked,
to help us learn from what we saw. Please do not take them as a gold standard to memorize
- they are just an example. You would do far better to attempting the exercise yourself - think
through or write out the cases you clerk in this manner, in your own style.
* Orthopaedic long cases are also covered here. These are shorter and a lot more standard
(fewer permutations), but otherwise the approach and strategy is not too different.
Troubleshooting:
• Don’t ask the patient for his/her diagnosis at the start. This causes you to fixate on
certain ideas and clouds your thinking – at best you are highly likely to be less
comprehensive in approaching the presenting complaint, neglecting to consider
differentials, at worst you may be led down an entirely wrong track. You should trust in
your ability to arrive at a diagnosis more than you trust the patient’s ability to give you
one! It is, however, generally acceptable to ask a patient towards the end of your
history, ‘what do you understand about your condition’ – you can use this to gauge
patient’s understanding of disease, verify your suspicions, and probe any
discrepancies.
• Patient can’t give a good history. Despite due diligence to list good patients, some do
not turn up and are replaced by random patients grabbed from the wards. Those who
have clerked many real patients generally handle suboptimal patients better. For the
long-winded patient, guide him/her along with targeted questions, and try to stay
focused on what is important. For the reserved patient, keep probing and tease out
information patiently. For an unsure patient, ask direct questions that will allow you to
form one clinical impression or the other. Do not depend on patients to be primed, or
to give you answers (if you need to know about a specific past medical history, ask
specifically, and do not assume a ‘no’ if the patient does not respond to an open-ended
question on ‘what medical history do you have’). The bottom line: clerk real patients,
not just your medically-trained friends!
• Patient can’t speak English. You are expected to to clerk in English or your mother
tongue (translator may not be provided if patient speaks your mother tongue). In any
case, having a translator is bad news – it cuts your time in half. Therefore, please
practice clerking your mother tongues (and better, in other languages and dialects).
• I have difficulty presenting: Remind yourself not just to report, but to interpret and to
put things together – ready to present. For each case you clerk, practice presenting to
someone (preferably a tutor, or a senior, if not then a batchmate). Try to present
immediately after clerking, do not sit down to ‘prepare’ a presentation – you do not
have this luxury in the exam.
• I cannot read CT scans: Start practicing early in SIP. Look at the scans of your patients,
first attempting them yourself, before reading the report.
• I am scared of difficult questions: Taking a good history and putting things together
puts you in good stead for any questions on history or diagnosis (always go back to
what the patient tells you). As for investigation and management questions, focus on
being a safe HO – if you do not know, admit it humbly and offer to escalate to seniors.
• I don’t have enough time: Manage your time well, be disciplined and know when to
move on. Practice, practice, and you will take a history more effortlessly. You need to
do this without talking too quickly (neither patient nor examiner understands you) or
appearing rushed/flustered.
• I don’t know what to expect. Look at the senior’s accounts from the hospital you are
going to. Each hospital has a slightly different character. Your aim is to get the idea
and flavor, not freak out at every single question that is asked.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A ABDO PAIN: ACUTE CHOLECYSTITIS
SURGICAL LONG CASES
Abdo Pain: Acute Cholecystitis
PRESENTATION
Sir, my patient Mdm Liew is a 50 year old Chinese lady with past medical history of DM, HTN,
HLD, presents now with 3 days of right hypochondrium pain and low-grade fever.
Her presentation first started as right hypochondrial pain, sharp, constant, gradually becoming
worse. It does not radiate to the back or shoulder and is not better on sitting forward. This was
associated with low-grade fever of Tmax 37.8 degrees, and 2 episodes of nonbilious
nonbloody vomiting. She is not jaundiced and does not have dark coloured urine or pale stools.
[Risk fx / etio] This is on a background of recurrent episodes of biliary colic. In the last 2 years,
she has had at least 5 episodes of right hypochondrial pain which begin after a fatty meal,
reach a crescendo over 3-4 hours, and then subsided. These episodes have been much milder
than her presentation currently, and she was never febrile during these episodes. [Etio] She
does not have history of mechanical heart valve replacement, or family history of jaundice and
anemia (hemolytic anemias)
[Ddx]
• [Hepatitis] I note that she has had raw oysters last week and has not been vaccinated
against viral hepatitis. She is in a stable monogamous relationship, has no hx of IV
drug abuse, and has never received blood products from outside singapore.
• [PUD] Otherwise she does not have hematemesis, coffee grounds vomitus, PR
bleeding, or malena. She is not on long-term NSAID or steroid therapy and has no
known peptic ulcer disease.
• [Referred] On systematic review there is no chest pain / shortness of breath /
palpitations to suggest a coronary event, and no cough / shortness of breath to suggest
right basal pneumonia. She has no cough, shortness of breath, positive travel history
or sick contact
Other than DM HTN and HLD, all of which are well controlled on medications, she does not
have any other past medical or surgical history. She has no known drug allergies.
She stays with her husband and children in a HDB flat, works as a business executive and is
financially well to do.
On examination, Mdm Liew is alert, comfortable. She is currently receiving IV fluids as well as
IV rocephin and flagyl. She has no scleral icterus and no conjunctival pallor. Her urine bag is
draining clear yellow urine. Abdomen was not distended. There is tenderness and guarding
over the right hypochondrium and epigastrium. Otherwise the rest of the abdomen is soft and
non-tender, no signs of peritonism. Murphy’s was positive. There was no organomegaly.
Bowel sounds were present. Cough impulse over bilateral groins were negative. Breath
sounds were clear and equal bilaterally. Heart sounds were dual, no murmurs, pulse was
regular at 95. I would like to complete my examination by doing a digital rectal examination
looking for PR bleed or melena.
In summary my patient is a 50/Chinese/lady with recurrent episodes of biliary colic, now

presenting with right hypochondrial pain and low-grade fever of 2 days duration, with a positive
murphy’s sign. My primary diagnosis is cholecystitis and my differentials include biliary colic,
hepatitis, pancreatitis, peptic ulcer disease, and dengue.
QUESTIONS
How would you investigate?

Sir, I need to investigate to confirm my diagnosis, rule out differentials and find the etiology.
Initial bloods include

• FBC for raised TW
• LFT which should be normal or at most mildly raised. If severe cholestatic LFTs, I will
suspect cholangitis. If hepatocellular picture I will suspect hepatitis.
• UECr for prerenal AKI since patient has been vomiting / to guide fluid therapy
• Blood cultures if the patient looks septic.
• CRP, procalcitonin
For differentials, I will do

• Amylase, lipase to look for pancreatitis (if present, to do full glasgow bloods).
• Hepatitis viral serologies for viral hepatitis
• Cardiac enzymes, ECG - to rule out AMI.
• CXR - looking for basal lobe consolidation, rule out air under diaphragm
Imaging modalities include

• US HBs for evidence of cholecystitis
• CT abdomen for the same especially overnight where US cannot be easily obtained.
Can you please read this ultrasound?

Sir I note there is a thickened gallbladder wall with intraluminal gallstones casting a posterior
acoustic shadow. There is pericholecystic fluid and I will like to ask if there is positive
sonographic murphy sign. I will also like to look at the common bile duct which I expect to be
not dilated.
You are the HO on call. How would you manage?

Sir, my main goals would be to (1) Resuscitate the patient according to ABC (2) Confirm the
diagnosis and rule out differentials (3) Initiate treatment and plan for definitive treatment.
1. Resuscitate the patient according to

A Assess airway
B Ensure breathing, saturation
C Take vitals
Set IV plugs
IV fluid rehydration
Keep NBM
Transfer GW or HD
Chart: strict I/O, Q2h paras
Serial monitoring for complications
2. Confirm diagnosis and rule out differentials

As discussed above.
3. Initiate treatment
Empiric IV antibiotics with gram negative and anaerobic coverage - 3rd gen
cephalosporin like ceftriaxone, and metronidazole.
4. Definitive treatment
> Laparoscopic KIV open cholecystectomy
When would you perform cholecystectomy?

Sir I would prefer early cholecystectomy within first 72h as opposed to interval
cholecystectomy because there is no increased risk of bile duct injury, and we do not risk the
patient having a recurrence while waiting for interval cholecystectomy
If patient too sick for op then how?

Alternative is percutaneous cholecystostomy
• Involves percutaneous catheter placement in the gallbladder lumen under imaging
guidance (alternative to surgical cholecystectomy)
• Indications: moribund patients who are not fit for surgery or when early surgery is
difficult due to extensive inflammation
• Drains the gallbladder and alleviates the inflammation (resolves acute episode)
• Followed by elective cholecystectomy 4-6 weeks later
Please counsel Mdm Liew on cholecystectomy.
Mdm Liew, I am Dr ____. I’m going to explain to you (1) your current condition (indication) (2)
What is a cholecystectomy and why we recommend it (3) risks and complications of
cholecystectomy (4) risk of not going for cholecystectomy and alternative. Do you have any
other questions or concerns you would like me to address along the way? If not, still feel free
to stop me any time along the way to clarify anything you don’t understand.
*Recommend drawing it out!
(1) Your current condition

You have inflammation of your gallbladder. This is likely due to irritation and infection
of the stones that your gallbladder had formed. Thankfully none of the stones have
dropped out into the bile ducts and caused any blockage.
(2) Cholecystectomy
So the best solution is to just remove the whole gallbladder with the stones inside. This
will both remove the infection and also prevent the possibility of any more such
infections in the future! The operation is called cholecystectomy. It will be done under
general anesthesia so you do not feel any pain. We normally try to do this by a camera
through keyhole surgery, but that sometimes does not work so we need to make it
open through a small cut (draw).
(3) Risks and complications of cholecystectomy

(a) Risk from general anesthesia
Can get heart attack and stroke, but there is a lower risk of this as you have no
previous heart or blood vessel problems
(b) Risk from procedure itself
*If lap, risk of conversion to open
Injury to common bile duct, injury to cystic artery, injury to bowel
Spillage of bile → peritonitis, sepsis
Infection, hemorrhage
(4) Risk of not going for cholecystectomy and alternatives

The alternative to cholecystectomy is percutaneous cholecystostomy, poking a hole
through the skin into the GB to drain it. However this is just a temporary measure and
once the tube is removed without removing the gallbladder, there is a risk that this can
happen again. Furthermore, the stones can drop out and cause cholangitis or
pancreatitis.
The last option is to not do anything, but other problems may arise: the GB can become
gangrenous and burst, the stones can burrow a hole through to the intestine and cause
blockage of the intestine, mucous or pus can accumulate there, the infection can
spread to the whole body and cause sepsis & death, and in rare cases GB cancer can
develop after a long time.
So let’s say the OT very full, and we have not been able to do the cholecystectomy on
the same day. The next day you see the patient. It is now day 4 of illness, the patient is
more tender in the RHC and the temperature is going up. What is happening?
Sir I am worried about local complications of cholecystitis such as mucocele → empyema →

gangrenous → perforation. I think the patient needs early cholecystectomy.
Start suspecting these when there are signs of failure of conservative mx (peritonism, non-
resolving fever/pain)
OK what are the other complications of cholecystitis?

• Gallstone complications: cholecystoenteric fistula → gallstone ileus
• Long term: GB cancer.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A ABDO PAIN: ACUTE PANCREATITIS
SURGICAL LONG CASES
Abdo Pain: Acute Pancreatitis
PRESENTATION
HLD, presents now with acute epigastric pain of 2 days.
Her epigastric pain was sudden in onset, constant, sharp and excruciating with radiation to
the back, slightly better when sitting up and leaning forward. This was associated with a low
grade fever of 37.8 no chills no rigors, as well as nausea and 2 episodes non-billous non-
bloody vomiting over the same duration.
[Ddx]
• [Acute cholangitis] She did not have jaundice, tea coloured urine, pale stools.
• [PUD] There is no hematemesis, coffee ground vomitus, PR bleed, melena, nor does
she have risk factors of peptic ulcer disease such as long term NSAID or steroid use,
known peptic ulcers or H. pylori.
• [Aortic dissection] No migratory pain from chest to abdomen, no suggestion of distal
embolization.
• [DKA] She has no polyuria, polydipsia, no intercurrent illness or non-compliance to
medications that could precipitate DKA.
• [AMI] She did not have crushing chest pain with shortness of breath, palpitations,
diaphoresis.
As for underlying etiology,

• [Gallstone disease] She has longstanding post-meal dyspepsia symptoms.
• [Instrumentation] She has never had an OGD or ERCP.
• [Alcohol] She drinks only occasionally and in small quantities
• [Metabolic] She does not have past medical hx of hypercalcemia or parathyroid
problems. She is however hyperlipidemic and may have high triglycerides.
• [Drugs] There is no long term use of TCM, corticosteroids, NSAIDs, loop diuretics
• [Viral] No recent history of bilateral jaw pain/swelling (mumps)
Her past medical history is that of well-controlled DM, HTN, HLD. Her latest HbA1c is 6.0 and
compliance is good. She has no past surgical hx and has no drug allergies.
Socially, she stays with her husband and children in a HDB flat, works as a business executive
and is financially well to do. She does not smoke.
On examination, Mdm Liew is alert and sitting forward, not in respiratory distress. She is
currently receiving IV fluids. She is not jaundiced, has no scleral icterus or conjunctival pallor,
and her urine bag is draining clear yellow urine. I do not note any abdominal scars. Abdomen
was not distended, soft and non-tender on palpation with no guarding or rebound. Murphy’s
was negative. There was no organomegaly. No pulsatile expansile mass. Bowel sounds were
present. Cough impulse over bilateral groins were negative. Breath sounds were clear and
equal bilaterally. Heart sounds were dual, no murmurs, pulse was regular at 95. I would like
to complete my examination by doing a digital rectal examination looking for PR bleed or
melena.
In summary my patient is a 50/F/Chinese who presents with epigastric pain radiating to the
back on a background hx of longstanding post-meal dyspepsia symptoms. My top differential
is acute gallstone pancreatitis. My ddx include cholecystitis, and I want to make sure it is not
cholangitis.
QUESTIONS
You are the HO on call. How would you manage this lady?
Sir, on call my initial goal will be (1) resuscitate the patient, (2) confirm my diagnosis and rule
out differentials, (3) stratify severity to determine disposition and prognosticate and to look out
for complications, and (4) identify the etiology so that this can be treated.
(1) Resus
A Assess airway
Supplemental oxygen
Be wary of systemic inflammatory response syndrome
C Take vitals
2 large bore IV plugs
Aggressive fluid rehydration - 2 pint normal saline fast
Keep NBM
Insert IDC
Transfer GW (if mild) or HD/ICU (if severe)
Chart: strict I/O, Q1h paras + SpO2 + hypocount
Also ensure patient has adequate analgesia (tramadol, pethidine)
I would then do investigations to:

(2) Confirm diagnosis and rule out differentials
(3) Stratify severity using Glasgow’s scoring system
(4) Determine etiology
(5) Prepare for ERCP
Blood work:
• FBC - raised TW (Glasgow)
• RP - raised urea (Glasgow) and Cr in pre-renal AKI (SIRS), raised glucose (Glasgow),
rule out DKA (low bicarb, high glucose)
• Ca/Mg/Phos - hypocalcemia (Glasgow)
• LFT - looking for cholestatic picture (?choledocholithiasis, cholangitis), albumin and
AST/ALT and LDH (Glasgow)
• Amylase Lipase -- normal range <100, <140
• ABG - PaO2 (Glasgow)
• CRP - to trend
• Cardiac enzymes ECG - to rule out AMI
• GXM PT/PTT (ERCP)
• Dengue serology - since we are in the midst of an outbreak.
Imaging:
• Ultrasound for evidence of cholelithiasis, rule out dilated CBD, look for cholecystitis
• Also do CXR - looking for whiteout (ARDS) or air under diaphragm
• Supine AXR - for sentinel loop (ileus secondary to para-pancreatic inflammation)
• Acutely there is no role for CTAP, this is not required for diagnosis of pancreatitis in
the presence of a typical hx and raised amylase/lipase, and I don’t expect
complications like necrosis so early. In practice however I often see CT abdo being
ordered for radiological confirmation and to rule out other ddx.
What are the complications of acute pancreatitis?

The complications of pancreatitis can be divided into local and systemic complications.
Local complications include

• Pseudocyst formation which can cause mass effect (GOO, obstructive jaundice), pain,
persistently increased amylase.
• Pancreatic necrosis which is initially sterile but can become secondarily infected (pain,
sepsis). CT scan look for gas > necrosis. If suspect infection, aspirate and culture and
cover with Abx. If not infected discontinue Abx. Infected necrosis may also require
surgical necrosectomy.
• Pancreatic pseudoaneurysm
• Functional complications like exocrine or endocrine deficiency.
Systemic complications
• Organ failure e.g. ARDS, AKI, DIVC
• Hypocalcemia
• Pancreatic ascites
You may be asked this content in various permutations… e.g.

• When rounding the patient the next morning, you notice that he has desaturated. CXR
shows bilateral infiltrates… [ARDS]
• 1 week later the patient complains of abdominal pain, and develops a high fever.
Amylase is still elevated… [infected necrosis]
What is the definitive treatment for Mdm Liew?

• ERCP within 48-72h, especially if severe, evidence of ductal stones, cholangitis, or not
responding.
• Cholecystectomy (same admission)
No ductal stones were seen on the CTAP, just some in the GB. No dilated ducts seen.
Pancreatitis improves with supportive treatment. Please counsel Mdm Liew on
cholecystectomy.
Mdm Liew, I am Dr Tsang. I’m going to explain to you (1) your current condition (indication)
(2) What is a cholecystectomy and why we recommend it (3) risks and complications of
cholecystectomy (4) risk of not going for cholecystectomy and alternative. Do you have any
other questions or concerns you would like me to address along the way? If not, still feel free
to stop me any time along the way to clarify anything you don’t understand.
*I recommend drawing the HBS system in this case!

You have inflammation of your pancreas, which is a gland you have in your body that
helps produce juices for digestion and also helps control blood sugar. This
inflammation happened because a stone inside your gallbladder dropped out and
blocked the pancreas. The pancreas juices cannot flow out, get stuck inside the
pancreas and cause irritation and inflammation, sometimes the tissue will die and form
fluid collections. Currently your pancreas inflammation has improved. The stone
causing blockage has passed out by itself OR has been removed by the scope
(ERCP).
(2) Cholecystectomy
Now, the next step is to remove the source of the stones - the gallbladder. The name
of the operation for this is ‘cholecystectomy’. This can be done laparoscopically (if
ERCP already done) or open (if ERCP was not done and need to do CBDE). We will
leave a drain from the surgery area coming out of your skin, but only for a few days
then we will take it out. Therefore after the operation you should have a scar like this
and a drain coming out (draw!).
If CBDE: We will also need to open the bile ducts to make sure there are no more
stones left behind. After that we will close back the bile duct and leave a another drain
from the bile duct.

(a) Risk from general anesthesia
*If lap, risk of conversion to open
Injury to common bile duct, injury to cystic artery, injury to bowel
Spillage of bile → peritonitis, sepsis
Infection, hemorrhage
Steatorrhea on eating fatty food

The alternative to cholecystectomy is conservative management.
However the risk if you don’t remove the gallbladder is that it can happen again. The
source of gallstones will still be there… stones can still drop out and cause pancreatitis.
There is a 40% of recurrence within 6 weeks.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A ABDO PAIN: AORTIC ANEURYSM
SURGICAL LONG CASES
Abdo Pain: Aortic Aneurysm
PRESENTATION
Mr Muthu is a 69 year old gentleman who is retired. He is a vasculopath with HTN HLD IHD,
and previous cardiac bypass. Other medical problems include BPH.
He now presents with a 4 day history of epigastric pain radiating to the back. He describes
this as multiple episodes of dull aching pain, pain score 5/10, each episode lasting 30 minutes
and then resolving. He has not had any prior episodes
[Ddx]
• [Spine]: Pain is not related to spine flexion or extension, and
• [Biliary: cholelithiasis, cholangitis, pancreatitis]: is not relieved on leaning forward. He
has no jaundice, tea coloured urine, or fever. He has no known gallstone disease, past
episodes of fatty dyspepsia, or recent alcohol binge.
• [Peptic ulcer / Dyspepsia]: There are no gastrointestinal symptoms of vomiting or
diarrhoea, and no melena, hematemesis, or per-rectal bleeding.
• [Urolithiasis]: There is no hematuria and no past episodes of loin to groin colic.
• [AMI]: There is also no diaphoresis, palpitations, dyspnoea,
• [DKA]: new-onset polyuria/polydipsia,
• [Dengue]: and does not stay in a dengue cluster.
He was first seen in primary care and treated as for gastritis with proton pump inhibitors, but
did not improve. He then came to the accident and emergency, where he was diagnosed with
abdominal aortic aneurysm. He has received endovascular aneurysm repair and is post-op
day 5, recovering well in general ward.
In terms of complications, he was not hemodynamically unstable when admitted, and has no
chest pain / shortness of breath (backward dissection / AR), no giddiness / blackouts /
weakness / facial droop (dissection involving carotids). He has no sudden severe abdominal
pain (rupture), no oliguria (renal artery involvement), no sudden leg gangrene (distal
embolization).
In terms of past medical history, he is a vasculopath with ischaemic heart disease requiring
coronary artery bypass 10 years ago, and has not had anginal symptoms since. He does not
know his latest ejection fraction. He has hypertension and hyperlipidemia, for which he is on
multiple medicines. He misses his medications about twice a week and latest clinic blood
pressure was systolic 160. He is an ex smoker of 30 pack years and has quit smoking since
his bypass.
His is functionally good, able to walk 10 bus stops.
Socially, he is a retiree. He stays with his wife in a condo and they do not have any financial
concerns.
On examination, he is alert, comfortable, not on any external intervention at present. I note an

old midline sternotomy with old saphenous vein graft scar, likely from old coronary bypass. I
also note fresh surgical scars over bilateral femoral arteries, both of which are healing well
with no hematoma. His abdomen is soft non-tender, there is an mass palpable deep in the
epigastrium - this is a firm 3cm x 2cm mass, not expansile or pulsatile, regular margins and
not nodular; it is likely the repaired AAA. On examination of the lower limbs, there were no
gangrene, ulcers, arterial skin changes. Pulses were well felt and capillary refill time was < 2
seconds. A brief cardiac examination was unremarkable.
In summary, Mr Muthu is a 69 year old vasculopath presenting with symptomatic aortic

aneurysm status post endovascular repair.
QUESTIONS
At his initial presentation, what would be your differentials for his epigastric pain?
See above; remember to cast your net wide.
How do AAA present?

• Asymptomatic, detected incidentally on (hopefully) abdominal palpation or (sadly) CT
scan for some other reason
• Symptomatic but unruptured: pain due to local compression, rapid expansion; distal
embolism causing trash feet
• Rupture: a catastrophic event with hypotension, hemoperitoneum and rapid demise
OK so you are the HO on call, what will you do?

Sir, my initial goals are to (1) resuscitate the patient, (2) establish the diagnosis and consider
differentials (as AAA may be incidental and pain may be due to another pathology, and (3)
prepare the patient for urgent intervention.
Resus A Assess airway

C Take vitals
Set 2 large bore IV plugs
Start fluids
Bloods FBC - Hb drop, Plt

PT/PTT
GXM
UECr - for contrast scan
LFT - ddx hepatobiliary pathology
Amylase, lipase - ddx pancreatic pathology
Glucose, dengue duo
Troponins
ECG
Imaging CT aortogram (if unstable - bedside ultrasound).

Looking for to confirm AAA, exclude ddx, identify size and branches involved
Look for dissection or contained leak/rupture and plan for stenting
Initial Mx To HD/ICU with hourly monitoring and strict i/o

Insert IDC
Keep NBM
Analgesia
(Stop antiplatelet)
CT aortogram shows a 5cm aneurysm. What is the management?

Sir, this patient has a symptomatic aneurysm and needs to be repaired urgently (regardless
of size). I would opt for endovascular aneurysm repair over open repair in view of lower
perioperative risk, assuming endovascular repair is anatomically feasible (These days even
suprarenal AAA can be repaired endovascularly).
What complications will you counsel the patient on?

Aortic surgery is not low risk.
• Anaesthetic/general risks include myocardial infarction, stroke, and death.
• Surgical risks can be divided into aortic and systemic organ risks.
o Aortic risks include endoleak, stent migration, stent occlusion, stent infection.
o Organ risks include paralysis (spinal artery involvement), kidney injury (renal
artery involvement or contrast nephropathy), bowel ischaemia, trash feet from
distal embolization.
• Transfusion risks: hemolytic transfusion reaction, hepatits/HIV, and ARDS.
• If endovascular repair, post-op complications also include stent migration, stent
infection, endovascular leak
Let’s say he has the same 5cm aneurysm but this was asymptomatic and detected on
CTAP performed for some other reason. What will you do?
Sir, for an asymptomatic AAA, my threshold to repair is 5.5cm (UK small aneurysm trial). At
5cm therefore I will follow up with ultrasound in 3-6 months with a view to repair when the
aneurysm reaches 5.5cm.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A ABDO PAIN: DIVERTICULITIS
SURGICAL LONG CASES
Abdo Pain: Diverticulitis
PRESENTATION
Mdm Verasamy is 35 year old Indian lady with a 2 day history of right iliac fossa pain with
fever and vomiting.
With regards to her abdominal pain, this started as a mild ache 2 days ago and got worse over
the course of the day, reaching a pain score of 5/10 at presentation to A&E. She describes it
as a constant dull pain localized in the right iliac fossa. There is no prior migration from
umbilicus to right iliac fossa [appendicitis], and no radiation from loin to groin [urolithiasis], to
the back [pancreatitis or AAA], or anywhere else.
This was associated with fever, also of 2 days’ duration; she did not measure her temperature
at home. She also had 3 episodes of non-bloody non-bilious vomiting over these 2 days. There
is no constipation, diarrhoea, or jaundice [cholecystitis]. There was also no pyuria
[pyelonephritis], hematuria [urolithiasis], no per-vaginal bleed [ectopic pregnancy] or
discharge [PID], or back pain [spine dx]. She has been well until these 2 days, with neither
prior episodes of abdominal pain, nor any loss of weight or appetite. Her last menstrual period
was last week (remember to ask!).
Since admission she has received IV antibiotics with symptomatic improvement. She has also
undergone a computed tomography scan, but has not had any interventional procedures or
surgeries.
In terms of past medical history, I note that she has childhood asthma for which she no longer
requires follow up. She has also had one termination of pregnancy 10 years ago. Otherwise
there is no past medical history, no past surgeries and no drug allergy. She does not have any
family history of malignancy or inflammatory bowel disease.
Socially, she is single, unmarried, and is sexually active with multiple partners without use of
condoms. She works as an advertising executive and is financially comfortable. She stays in
a 4 room flat with her parents and does not smoke or drink.
On examination, she is alert and comfortable, receiving IV ceftriaxone and metronidazole via
an IV plug which is clean. Peripherally there is no cachexia, jaundice, or pallor. On inspection
of the abdomen, there is no scar, no distension. She has mild tenderness in the right iliac
fossa with no guarding or rebound, and the abdomen is otherwise soft. There is no RIF mass.
There is no flank tenderness and no positive Murphy. Renal punch is negative.
I will like to complete my examination by doing digital rectal examination to rule out a bleed,
and doing per-vaginal examination looking for cervical excitation and cervical discharge.
In summary my patient is a 35 year old Indian lady with 2 days of right iliac fossa pain and
fever. She is not peritonitic and has clinically improved after 2 days of IV antibiotics.
QUESTIONS
What are the differentials you will like to consider for her initial presentation?
Sir, I will like to consider gastrointestinal, urological, gynaecological, and miscellaneous
causes (cast net broad as presentation nonspecific).
• The gastrointestinal causes include diverticulitis and appendicitis, although there is no
classic migratory pain.
• I must also consider gynaecological causes especially due to her sexual activity with
multiple partners, and I feel that her reported menses does not exclude ectopic
pregnancy.
• In terms of urological causes, I am considering pyelonephritis or urolithiasis
complicated by pyonephrosis, although my patient has no hematuria or loin to groin
pain to suggest urolithiasis.
How will you investigate the patient?

Sir, my investigations are directed to (1) confirm dx, (2) look for cx, and (3) guide further mx.
• At the bedside I want a urine pregnancy test, capillary blood glucose, and urine
dipstick.
• I will then send initial blood work such as FBC looking for raised TW in infection, UECr
for hypochloraemic metabolic alkalosis due to vomiting, LFT to rule out hepatobiliary
causes, amylase to rule out pancreatitis, CRP and cultures since she is febrile, dengue
duo just to be sure, and GXM and PT/PTT in case the patient needs interventional
procedure.
• I will send urine for formed element microscopy looking for evidence of hematuria.
• If vaginal examination shows discharge I will also like to send for culture.
• I will order erect chest X ray and KUB, looking for urolithiasis, and seeking to exclude
air under diaphragm or Rigler’s sign in perforation.
• I will discuss with my senior and the patient will likely eventually need a CTAP.
OK here is the CTAP please read -

Sir this is a slice of my patient’s CTAP taken yesterday morning. I note that there is fat
stranding surrounding the cecum, with thickening of the colonic wall and multiple diverticulae.
I also note a small hyperdense collection adjacent to one of the diverticulae and I wonder if
this is an abscess. Otherwise I do not note any free air in this cut. Overall this scan confirms
my impression of diverticulitis, with a paracolic abscess.
Can you explain how colonic diverticuli form?

Diverticuli are outpouchings of the colonic wall at a point of weakness where the vessels
penetrate the circular muscle layer of the colon. It arises due to increased intraluminal
pressure especially in patients with chronic constipation and low fibre diet.
What is diverticular disease?

Outpouchings in the colonic mucosa and submucosa through weaknesses in the muscles
layers where colonic arteries penetrate the colonic wall.
How can diverticular disease present?

Diverticular disease can be asymptomatic, present as lower gastrointestinal bleeding, or
present as diverticulitis. Diverticulitis may be simple with just abdominal pain which is
classically LIF in textbooks but more commonly RIF in asians. Alternatively diverticulitis can
be complicated and present with perforation, palpable mass due to abscess formation, or
fistulation causing pneumaturia, fecaluria, per-vaginal feculent discharge. Chronic diverticulitis
can form benign strictures, causing intestinal obstruction
OK so how would you manage the patient?

Sir, my patient has Hinchey 1 diverticulitis (pericolic perforation) so I would initially attempt
conservative management most importantly with IV antibiotics. Supportive measures include
hydration, keeping patient NBM, and analgesia. If she fails to improve she may require
percutaneous drainage by interventional radiology. I could consider offering an interval
colonoscopy to rule out underlying colorectal malignancy.
You give your patient IV antibiotics. On call you are called to see her because of severe
abdominal pain. When you palpate the abdomen it is rigid. How now brown cow?
Sir, I am worried about perforated diverticulitis. I will attend to the patient immediately and
resuscitate the patient. I will inform my senior and obtain a stat erect chest X ray unless the
patient is crashing. The patient needs to go for laparotomy with surgical resection for example
right hemicolectomy with defunctioning ileostomy.
(If you know the diverticulum is right sided, please don’t say Hartmann’s!)
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A ABDO PAIN: UROLITHIASIS
SURGICAL LONG CASES
Abdo Pain: Urolithiasis
PRESENTATION
Sir, my patient is Ms Jolene, a 33 year old Chinese lady with hypercalcemia from an underlying
parathyroid tumor, presenting with recurrent urolithiasis and pyelonephritis, and currently
admitted for pyonephrosis.
May I begin with Ms Jolene’s significant past medical history. In the past 4 years, she has
recurrent pyelonephritis with fever and loin pain, each time treated by GPs with oral Abx. She
has also had multiple episodes of loin to groin pain suggestive of ureteric colic, but has never
had loss of weight or appetite in all these years.
Five days ago, she presented yet again with loin pain, fever, chills and nausea of one day’s
duration. No other storage symptoms such as dysuria, frequency, urgency, or urge
incontinence; no voiding symptoms; and no hematuria. She was started on IV antibiotics with
little improvement. In fact on the 3rd day of admission her loin pain worsened. CTAP was
done, which showed pyonephrosis with ureteric stones. Right percutaneous nephrostomy was
done, after which her symptoms improved.
In terms of the etiology of her urolithiasis, I note that she was found to be hypercalcemic with
elevated parathyroid hormone levels. Sestamibi scan found a parathyroid adenoma although
there was no palpable goitre. She is otherwise not on any medications that could cause
hypercalciuria. In terms of other etiologies, she has no known hx of gout or joint pains, and
drinks at least 2 litres of water each day. She is not known to have congenital structural
abnormalities of the urinary tract. She does not have any family history of parathyroid tumours,
urolithiasis (RTA), urological cancers, or other endocrine tumors (MEN).
I understand that she has recently underwent parathyroidectomy for her parathyroid adenoma.
In terms of social, functional and financial history,

• She does not smoke or drink
• She has been able to work as per normal in her job as a magazine editor, as it is a
mostly desk bound job
• She stays with her husband in a HDB flat in tampines, does not have any children
• Financially okay as she is covered by insurance
• The only concern/struggle she has is with the restrictions that come with the new low
purine diet as per dietician recommendation, to reduce risk of kidney stones
On examination, Ms Jolene was alert and comfortable. She is still receiving antibiotics. She
does not have an indwelling catheter. I note a horizontal scar in the midline of the neck over
the level of the thyroid cartilage. The right percutaneous nephrostomy is draining
hemopurulent fluid, the collecting bag currently contains about 200ml of fluid. Otherwise I do
not note any other scars, her abdomen is soft and non-tender. The left kidney was renal punch
negative and not ballotable. I did not touch the right side in view of the right PCN.
In summary Ms Jolene is a 33 year old Chinese lady with hypercalcemia from an underlying
parathyroid tumor, presenting with recurrent urolithiasis and pyelonephritis. She is currently
admitted for pyonephrosis and is now status post parathyroidectomy.
What are the risk factors for urolithiasis?

Sir, risk factors include:
• Dehydration
• Diet: high protein and salt intake, high purine diet.
• Drugs: probenecid, loop diuretics, antacids, salicylate acid, indinavir, chemotherapy
• Systemic diseases: Crohn’s disease, gout, renal tubular acidosis, patients on chemo
for haem malignancies, hyperparathyroidism, inborn errors of purine metabolism
• Infection with urea splitting organism (struvite stone)
• Biodata: Male to female 3:1, age 40-60
Assuming that you are the HO when she first presented, how would you manage her?
Sir, pyonephrosis is a urological emergency and requires drainage as soon as possible. I
would see her immediately, get a set of vitals and assess her airway breathing and circulation,
set an IV plug and start IV fluid resuscitation. I would then send off the following basic
investigations:
• FBC for raised total whites
• RP for raised Cr (both pre and post renal AKI), electrolyte abnormalities
• Ca/Mg/Phos, for hypercalcemia
• CRP for trending
• Blood cultures, to guide antibiotic treatment
• ABG and lactate if she is sick
• PT/PTT and GXM as she is going for an invasive procedure
• UFEME, Urine gram stain and cultures
• XR KUB looking for radio-opaque stones
• Subsequent CT KUB or CT urogram looking for pyonephrosis.
I would then start her on empiric broad spectrum IV antibiotics, insert an IDC and put her on
Q1H paras plus strict IO monitoring, transfer her to a HD ward, escalate to my senior and
make an urgent urology referral once the CT KUB or urogram confirms pyonephrosis. The
patient will need percutaneous drainage.
Note: the diagnosis of pyonephrosis is seldom as apparent from the start! Many patients come
in with what appear to be pyelonephritis - think of pyonephritis if they do not get better with
Abx (worsening pain, more septic, not responding), have a ballotable kidney. Have a low
threshold to scan if the patient is very sick. Be suspicious of pyonephrosis if the patient is
known to have urolithiasis.
Outline the definitive treatment of urolithiasis.

My patient has pyonephrosis and will require emergent drainage via percutaneous
nephrostomy tube. Thereafter her urolithiasis will need to be managed for example with
percutaneous nephrolithotomy or ESWL.
General principle:
Treatment depends on the size and location of stones.
• Conservative for stones <5mm (70% spontaneously expelled):
o Analgesia, high fluid intake, medical expulsive therapy with alpha blocker
o If uric acid stone → alkalinize urine.
• Intervention if conservative is unlikely to succeed (larger than 5mm), fails, recurrent,
or complicated (e.g. pyonephrosis, hydronephrosis).
o Extracorporeal shockwave lithotripsy -- for renal and upper ureter stone
o Ureteroscopy plus laser lithotripsy -- for ureteric stones
o Percutaneous nephrolithotomy -- for renal stones especially when PCN
inserted already.
o If worried that stone fragments may cause obstruction, add a means to ensure
drainage e.g. double J stent.
• Address underlying cause of stone formation: e.g. drink more water, decrease intake
of oxalate rich food (e.g. spinach) and purine rich food (alcohol, red meat), normal
calcium diet
How do you know when you can remove the PCN?

After successful decompression and drainage, the next step is evaluate the patency of the
collecting system. This is usually done with an antegrade urogram, where contrast is injected
through the PCN. It is imperative to ensure there is no obstruction before removing the drain,
otherwise the patient will leak from the nephrostomy site or the pyonephrosis will recur.
• Therefore if there is free flow of contrast, → can pull out PCN
• If still obstructed/narrowing seen (dDx stone vs benign stricture vs malignant stricture)
→ insert DJ stent via ureteroscopy and ensure free flow before pulling out PCN
o With DJ stent in place, you can also perform ESWL on any kidney/ureteric
stones without worrying about obstructing the system again.
o DJ stents should be left in only about 6-8 weeks, no more than 3 months,
otherwise stent crystallization may occur. Crystallized stents are extremely
hard to remove.
How would you evaluate her kidney function?

• Renal panel - Cr, eGFR >> evaluate both kidney overall function, if there is only one
working kidney Cr can still be normal. So need to evaluate differential function.
• A MAG3 renogram would be the investigation of choice. This is a dynamic radioisotope
study that allows me to evaluate the differential function of right vs left kidney, by
looking at how well each kidney excretes the radioisotope tracer. In normal individuals,
differential kidney function should be ~50% on each side, out of 100% for both kidneys
combined. If one kidney has <15% total renal function, it is not worth saving that
kidney.
• What about DMSA? This is a static scan that can allow visualization of scarring. But
does not give information about function.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A BGIT, LOWER: DIVERTICULAR BLEED
SURGICAL LONG CASES
BGIT, Lower: Diverticular Bleed
PRESENTATION
Mr Ng is a 57 year old Chinese gentleman who presents with a 1-day hx of painless per-rectal
bleeding.
This is his first episode of gastrointestinal bleeding. He first noticed dark red blood mixed with
stool yesterday morning, followed a few hours later by one episode of large amount of dark
red blood with no stool. Since admission yesterday evening he has had 5 more episodes,
each time passing ~1 cup amount of fresh red blood with no stool. All of these episodes were
painless.
[Ddx]
• [UBGIT] His stools are not malenic and he has no hematemesis or melena to suggest
bleeding from the upper part of the GIT. No epigastric pain, long term use of NSAIDs
or steroids, no personal history of chronic liver disease or peptic ulcer disease.
• [CA colon] There is no recent change in bowel habits (baseline 1x a day), no change
in stool caliber, tenesmus, recent loss of appetite or weight.
• [Haemorrhoids] He does not have any history of haemorrhoids and does not notice
any lumps or sensation of rectal prolapse while defecating.
• Not associated with any pain on defecation, does not have history of constipation
In terms of complications, he was hemodynamically stable on admission and not in

haemorrhagic shock. I do not note any symptoms of anemia such as chest pain, SOB,
palpitations, giddiness/syncope.
In terms of past medical history, he has ischaemic heart disease of NYHA class 1 on aspirin;
he has never required percutaneous angioplasty or stent (if angioplasty or stent, must know
when, so can decide whether to hold aspirin). He has well controlled hypertension and
hyperlipidaemia on medications. He has never had a colonoscope but a fecal occult blood test
done last year was negative. There are no known drug allergies.
In terms of family history there is no suggestion of a family history of colorectal or colorectal

associated malignancies.
Social history wise, he is a high-functioning engineer. He stays with wife and 2 doctor children
in a HDB mansionette. He does not smoke or drink.
On examination, Mr Ng was alert and comfortable. He does not have any surgical scars. There
was no conjunctival pallor. Abdomen was soft and non-tender, no organomegaly no masses.
I would offer to do a digital rectal examination with proctoscopy, looking for piles or colonic
masses as well as the nature of the blood.
In summary, my patient is a 57 year old gentleman with 1 day of painless per rectal bleed. He
is hemodynamically stable and his bleed has stopped spontaneously
QUESTIONS
What are the differentials for lower BGIT?

• Sir, my patient is most likely to have a diverticular bleed given his history of dark blood
mixed with stool followed by fresh blood passed without stool.
• I need to rule out massive upper gastrointestinal bleed although I do not note any risk
factors suggestive of variceal or peptic ulcer bleed.
• I will also need to rule out colorectal cancer although these tend to present as chronic
bleed, mixed with stools, and iron deficiency anaemia rather than as an acute episode
of per rectal bleeding.
• Another differential would be hemorrhoids, however this is classically bright red blood
after defecation, spraying or dripping blood staining whole toilet bowl and on wiping
with toilet paper.
• Other differentials include colitis which may be inflammatory (Crohn’s) or infective
(parasites), however these tend to be bloody diarrhoea with abdominal pain, which is
not what my patient has
• Angiodysplasia is another relatively rare cause that is difficult to elicit on history and is
usually picked up incidentally on scopes (can be torrential)
• Coagulopathy (I would not attribute a bleed to coagulopathy alone unless everything
else is ruled out!)
If you were the house officer on call, how would you investigate and manage this patient
in the acute setting?
I would
• Resuscitate according to airway breathing and circulation
• Get a set of vitals
• Set 2 large bore IV cannulae and commence IV fluid resuscitation
• Keep the patient nil by mouth and start IV omeprazole/pantoprazole
• Suspend his aspirin for now
• Catheterize.
• Send to high dependency with hourly parameters, strict I/O monitoring and stool
charting
Then I would send off some basic investigations:

• Full blood count: looking at Hb for anemia and Plt count
• Renal panel: looking at the urea to creatinine ratio that would suggest bleeding from
the upper GIT
• PT/PTT: for any bleeding diasthesis
• GXM: in anticipation for any blood products the patient may require
• Lactate, ABG
• Cardiac enzymes and ECG: looking out for type 2 MI, especially in view of the patient’s
history of ischemic heart disease
• Chest XR looking for free air under diaphragm
If patient develops symptoms of anemia or has a Hb below the requirement for scopes (9),
then I would call for packed red cells
I would then counsel the patient and take consent for OGD to rule out upper GIT bleed and
an interval colonoscopy to confirm the presence of diverticular disease and screen for
colorectal cancer.
Your patient has stopped bleeding by the time you clerk him and your registrar says
that he will do the scope outpatient. However, that night you are called to see him for a
large spontaneous per rectal bleed. He is now tachycardic - he asks you if he can get a
scope right away. Can you counsel him?
Mr Ng, you must be worried about suddenly bleeding again. We take this seriously and need
to investigate you. I understand that you are asking for a colonoscope - you do need a
colonoscope eventually but right now our priority is to find the source of bleeding and stop the
bleed. Colonoscopy is not so good in patients who are currently bleeding, it often cannot find
the source because you may have more than one abnormal area / outpouching which can
bleed and we don’t know which one is bleeding. May I suggest we send you for a scan which,
if there is currently fast bleeding, will show us exactly where is bleeding?
Principles of subsequent management (after resuscitation)

• Stable patient (either stable from beginning or responded after resus) with no further
bleed (consider that 80% of bleeds stop by themselves): stop antiplatelets/warfarin,
give outpatient / interval scope to rule out cancer.
• Initially unstable, transient response to resuscitation (rebleeds or unstable): CT
mesenteric angiogram looking for arterial blush (minimum 0.3ml/min flow to see) -
o CTMA finds bleed: proceed to conventional angiogram + embolise
o Negative CTMA: either stopped bleeding or bleed too slow to detect. Continue
to monitor, should not be massive bleed.
o Offer scope if unfit for CTMA, or when bleeding has stopped.
• Does not respond to resuscitation: surgery stat.
When do you need surgery for bleeding diverticula?

• Please please always rule out UGBIT or hemorrhoidal bleeding (done via on table
OGD and proctoscopy) before chopping
• Emergency
o If bleeding cannot be controlled with angiographic or endoscopic therapy, and
source of bleed has already been identified on CTMA → targeted segmental
resection.
o If pt unstable despite aggressive resuscitation, and source of bleed is still
unknown → total colectomy. Blind segmental resection contraindicated (high
rebleed rate).
• Elective – if more than 2 episodes of significant bleeding (symptomatic anemia or
requiring transfusion)
So Mr Ng is very happy with you and refers his friend to see you. His friend has been
complaining of blood staining his toilet paper, with a ‘lump’ that prolapses out of the
anal canal with defecation but reduces spontaneously. Proctoscopy reveals
haemorrhoids. How would you counsel Mr Ng’s friend?
Mr Ng’s friend sounds like he has grade 2 internal haemorrhoids. I will first attempt
conservative treatment with stool softeners and bulking agents, Daflon, and topical
nitroglycerine / nifedipine. If this fails I can counsel the patient for rubber band ligation or
sclerotherapy. If all else fails the patient can be referred for surgical haemorrhoidectomy.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A BGIT, UPPER: PEPTIC ULCER DISEASE
SURGICAL LONG CASES
BGIT, Upper: Peptic Ulcer Disease
PRESENTATION
Sir, Mr Hong is a 40 year old Chinese gentleman with significant past medical history of
migraine requiring frequent analgesia. He presented 3 days ago with three episodes of coffee
ground vomitus, malena, and epigastric pain of one day duration.
His pain was sharply felt in the epigastrium and did not radiate to the back or shoulder, pain
score was 7/10. 4 hours after onset of the epigastric pain, he had 4 episodes of coffee ground
vomitus each about 50ml and 3 episodes of malenic stools. (If possible, note time of last
episodes). There was no hematemesis or fresh PR bleed.
[Etiology]
• [Variceal bleed] He is not an alcoholic and has no known hx of chronic liver disease or
alcoholism. He is not jaundiced and does not have dark coloured urine. He does not
have known hepatitis but has never been vaccinated or tested.
• [PUD] He has had previous episodes of epigastric pain worse at night. These were
milder and self-limiting, and without hematemesis or malena. He has been taking
NSAIDs chronically for his migraine. He is also quite stressed at work, often skips
meals, and is a smoker of 20 pack years.
• [Gastric CA] He has not had any early satiety, loss of weight or loss of appetite recently.
• [Mallory weiss] There was no retching before the hematemesis started.
• [Reflux esophagitis] He has no history of heartburn or gastroesophageal reflux
symptoms]
• Prior to this incident he has not had any past scopes or H. pylori testing or treatment.
[Complications]
• On admission he was hemodynamically stable with no chest pain, palpitations,
giddiness, shortness of breath (haemorrhagic shock / anaemia).
• There was no severe abdominal pain to suggest peritonitis.
I note that he was resuscitated, received blood transfusion, and IV medication. An

oesophagoduodenoscopy was performed on the same day. He is currently stable and
received no further transfusions or repeat OGD. He tested positive for H. pylori and has
commenced triple therapy.
In terms of past medical history, he has bad migraine on follow up with neurology. He has
been prescribed beta blockers, NSAIDs, and ergot drugs. He has required his analgesics
almost daily when he is stressed. Otherwise, he has no other medical or surgical history, no
past scopes. He has no known drug allergies.
Socially, Mr Hong is a top lawyer and is married with 2 children. He is financially well to do
and stays in landed property. He smokes (as discussed above) and drinks one can of beer a
day.
On examination, Mr Hong was alert and comfortable, receiving IV fluids and proton pump
inhibitors. He does not have conjunctival pallor. On inspection, the abdomen has no scars,
herniae, and was not distended. On palpation, it was soft non-tender without rebound or
guarding. No palpable masses or organomegaly. Percussion note over the abdomen is
normal, not tympanic. Bowel sounds are present. I would like to complete my examination with
a digital rectal examination looking for melena or fresh PR bleed.
In summary, Mr Hong is a middle aged Chinese lawyer with first episode of upper GI bleeding
likely secondary to peptic ulcer disease, status post endoscopic hemostasis
Sir, goals for this patient are to (1) resuscitate him, (2) rule out ddx and cx (3) initiate medical
therapy, (4) prepare for endoscopy.
(1) Ensure patient is stable

Assess airway, breathing, circulation
Set 2 large bore IV plugs
Start fluid resuscitation with normal saline.
Insert IDC.
Q1H parameters with strict IO charting and stool charting
Keep NBM.
(2) FBC - Hb for anemia, Plt

RP - raised U to Cr ratio, prerenal AKI, dehydration
PT/PTT, GXM - to call for blood
Cardiac enzymes, ECG - for cx of AMI
Chest XR looking for free air under diaphragm
(3) Start IV PPI e.g. omeprazole 80mg bolus then 8mg/h infusion
(4) Prepare for endoscopy
What if the initial Hb is 13?

Sir, I am aware that in acute blood loss the Hb can be normal. I will not be fooled by a Hb of
13 and will still need to resuscitate as above.
If he comes in with free air under diaphragm, what will you do?
Sir, perforation is a surgical emergency. Patient needs laparotomy and
• Duodenal ulcer: omental patch repair +/- vagotomy
• Gastric ulcer: partial gastrectomy including the ulcer, or patch closure with biopsy.
If there is no free air under the diaphragm, what is your definitive mx?
Sir, patient needs Oesophagogastroduodenoscopy. This is diagnostic, therapeutic, and
prognostic.
• Diagnostic:
o Directly visualize source of bleed (diagnostic)
o Biopsy to do clo testing for H. pylori
o Biopsy for histology in gastric ulcer.
• Therapeutic: endoscopic hemostasis using two modalities - e.g. clipping, submucosal
adrenaline injection, argon plasma coagulation, etc.
• Prognostic: predict risk of rebleed using Forrest classification
What are the indications for emergency (stat) endoscopy?

• Hemodynamic instability
• Evidence of continued bleeding e.g. hematemesis (malena can be existing blood in
the GI tract)
• Suspected variceal bleed
if not - scope within 24h.
Tell me about Forrest Classfication.

It is a scoring system to predict risk of re-bleeding.
Forrest 1: Active bleed 1a - spurting
1b - oozing
Forrest 2: Recent bleed 2a - visible vessel
2b - blood clot
2c - hematin stain
Forrest 3: Lesion without bleeding: healed ulcer, clean base
Other scores available - Rockall, Blatchford
Please counsel Mr Hong on OGD.

Mr Hong, I am Dr Tsang. I’m going to explain to you (1) your current condition (indication) (2)
what is an OGD (3) risks and complications of OGD (4) risk of not going for OGD and
alternative. Do you have any other questions or concerns you would like me to address along
the way? If not, still feel free to stop me any time along the way to clarify anything you don’t
understand.

You are currently bleeding from your stomach or intestine. We have given you a
transfusion but we must also find and stop this bleeding . We usually do this with an
OGD
(2) OGD
This involves putting a small camera through your mouth, down your food pipe into the
stomach and first part of the small intestine. With the camera, we can see where the
bleeding is, and once we find the problem we can put a clip and injection to stop the
bleeding. You will be sedated so that you won’t feel any pain.
(3) Risks and complications of OGD
(a) Risk from sedation
Can get heart attack and stroke, but there is a low risk of this as you have no
previous heart or blood vessel problems and the dosage given is lower than for
bigger operations
Perforation (accidently poke through the wall of the intestine), failure to stop
bleeding, re-bleeding, infection
(4) Risk of not going for OGD and alternatives
If you don’t go for the OGD then there is a chance you will keep bleeding and keep
needing transfusion of blood. The only other way to stop the bleeding is with an
operation, but that is even more invasive and comes with even higher risks.
OK so you have done OGD, Mr Hong tests positive for H. Pylori. How would you treat?
• Triple therapy with PPI (Omeprazole) 20mg BD + Clarithromycin 500mg BD +
Amoxicillin 1g BD or Metronidazole 400mg BD x 2/52 then Omeprazole 20mg BD
x6/52.
• Follow with test for cure with urea breath test. If H. Pylori –ve, then continue PO PPI.
You treat for H. Pylori. Next day Mr Hong rebleeds. How?

• First rebleed: rescope.
• Second rebleed: surgery (oversewing or underrunning of ulcer, duodenotomy/partial
gastrectomy)
OGD showed gastric ulcer. How would you follow up?

In addition to following up on H. pylori eradication, need to re-scope 6 weeks later to document
clearance. Need to rule out malignant ulcer.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A BGIT, UPPER: VARICEAL BLEED
SURGICAL LONG CASES
BGIT, Upper: Variceal Bleed
PRESENTATION
Sir, Mr Lee is a 34 year old gentleman with past medical history of chronic alcoholic liver
disease, presents now with 2 episodes of painless hematemesis over 1 day’s duration. The 2
episodes of painless hematemesis were unprovoked, each time of about 200ml of fresh blood,
associated with 2 episodes of fresh PR bleed followed by 2 episodes of melena. This was
preceded by worsening abdominal distension and bilateral lower limb swelling of 1 weeks
duration.
[Complications] He does not have symptoms of anemia such as chest pain, giddiness,
syncope, palpitations. He does have some shortness of breath but only on lying supine,
possibly due to diaphragmatic splinting from his ascites.
In terms of etiology, I note a longstanding history of alcoholic cirrhosis with a recent admission
6 months ago for variceal bleed. He required several blood transfusions and intubation then,
and bleeding was stopped successfully via OGD. Since then he has defaulted follow up, and
did not undergo interval endoscopic variceal ligations to obliterate any remaining varices.
He admits that he still drinks about 6 cans of guinness stout a day (his baseline since before
previous admission), and is unable to cut down. CAGE screen for ethanol use disorder was
positive. There is no known hepatitis infection or risk factors such as IVDU or sexual exposure;
he is however not vaccinated against hep B.
Other differentials that I considered -

• [PUD] he did not have any abdominal pain, no preceding history of gastritis, no risk
factors such as long term corticosteroid use, NSAID use, smoking. He has never been
tested for H pylori.
• [Gastric CA]. He does not have early satiety or loss of weight or appetite.
• [Mallory Weiss tear] he did not have severe nausea, vomiting or wretching before.
• [Hemoptysis] no preceding coughing or history of TB
Otherwise in terms of his social, functional and financial situation,

• He used to work as a cook in a kopitiam but is currently in between jobs
• He is not on talking terms with his wife, children due to his drinking habits, and currently
stays with his elderly mother
• He is not coping well financially and has been receiving some financial support from
his mother
On examination, Mr Lee is alert and oriented to time place and person. He does not have
asterixis. He has conjunctival and palmar pallor. I note peripheral stigmata of chronic liver
disease, namely: jaundice, clubbing, scleral icterus, spider naevi, gynaecomastia, loss of
axillary hair. His abdomen is grossly distended. It is tense but non-tender, with a positive fluid
thrill. I am unable to palpate for any hepatomegaly. Bowel sounds are active. I measured his
blood pressure supine and standing and there is significant postural drop. I would like to
complete my examination with a digital rectal examination looking for fresh blood or melena.
In summary, Mr Lee is a 34 year old Chinese gentleman with 2nd episode of hemetemesis
secondary to alcoholic liver cirrhosis. My main issues are (1) hematemesis, (2) alcohol use
disorder, (3) liver cirrhosis.
QUESTIONS

Sir, this is a medical emergency. I will attend to the patient immediately and escalate rapidly
to my senior. My management will be (1) to resusitate the patient according to ABC, (2) to
initiate therapy for variceal bleed, (3) to send the patient for urgent endoscopic hemostasis,
and (4) to treat underlying condition
(1) Resusitation
A Assess airway (blood > airway compromise)
If compromised, intubate.
C 2 large bore IV plugs
Take vitals
Fluid - 2 pint normal saline fast
Call blood bank for transfusion
Keep NBM
Insert IDC
Transfer HD/ICU
Chart: strict I/O, stools, CIWA, Q1h paras
(2) Initiate emergent therapy while awaiting OGD

Bloods: FBC (Hb), UECr (raised urea to Cr, AKI), LFT, PT/PTT, GXM, Trop
ECG, CXR
IV pantoprazole (clot stabilization)
80mg bolus, then 8mg/h infusion for 3 days
IV somatostatin (splanchnic vasoconstrictor → decrease portal flow & thus pressure)
250ug bolus followed by 250ug/h infusion for 3-5days
IV ciprofloxacin or ceftriaxone (prevent 2ndary bacterial infection, clot stabilization)
Ciprofloxacin 500mg bd or ceftriaxone 1g od for 7 days
Glucose and thiamine (prophylaxis for wernicke encephalopathy)
(3) Emergent OGD

Always emergent in suspected variceal bleeds
o Endoscopic variceal ligation (preferred for esophageal varices)
o Sclerotherapy (preferred for gastric varices)
(4) Treat underlying condition

See below (treat underlying portal HTN)
QUESTIONS
What is the definitive management for the varices?

Oesophagealgastroduodenoscopy for visual confirmation of varices with red stigmata of
recent hemorrhage, with endoscopic variceal band ligation or sclerotherapy. This is followed
by 3-weekly endoscopic variceal ligation until all remaining varices are obliterated.
If 2nd bleed → attempt scope again

If 3rd bleed → consider temporizing measures such as sengstaken blakemore tube
How do you treat the underlying portal hypertension?

• Prevention of progression of CLD, prevent further insults to liver
o Refer NAMS (national addiction management service), pharmacological
abstinence therapy
o Treat any underlying Hep B/C, if no underlying Hep infection then vaccinate
• Medical: non-selective beta blockers i.e. propanolol
• Radiological: transjugular intrahepatic portosystemic shunt (beware hepatic
encephalopathy)
• Surgical: surgical shunts (not done anymore)
How do you use a Sengstaken Blakemore tube?

• Secure airway first - intubation
• Measure SB tube as per nasogastric tube (usually ~40cm)
• Advance SB tube via nose
• Fill gastric balloon with 150ml of water or gastrograffin (for position check)
• Tug gently to ensure gastric balloon is sufficiently inflated, then anchor with pulley and
traction
• Inflate esophageal balloon to 20-25mmHg
• Can aspirate blood in stomach
• Confirm position of tube with CXR
• Release intermittently to prevent pressure necrosis
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A BREAST CANCER
SURGICAL LONG CASES
Breast Cancer
PRESENTATION
Sir, my patient is Mdm Chin a 73-year-old Chinese retiree who presented with an
asymptomatic right breast lump.
The lump was picked up on mammogram during a free neighbourhood breast cancer
screening program. The lump is painless. She is unaware of how long she has had it, and
does not know if it has been increasing in size. She has not noticed any nipple discharge or
skin changes over the lump. She also has not experienced any constitutional symptoms such
as LOW or LOA, nor any shortness of breath, constant progressive headache, increase or
change in nature of her back pain that might suggest distant spread.
In terms of risk factors, she has a significant family history of breast cancer -- 5 out of her 7
sisters, have breast cancer as well. Age of diagnosis ranges from 55 to 67. She is the youngest
in her family. There is no personal or family history of colon, ovarian, pancreas, thyroid or skin
cancers. Otherwise she does not have prolonged estrogen exposure -- she had her menarche
at 14 years of age, has had 3 children all breastfed, has never taken oral contraceptive pills,
went into menopause at 50, and has not been on hormone replacement therapy for her
osteoporosis. She also has never received radiotherapy, and being a seamstress does not
have occupational exposure to radiation.
She has never had any procedures or surgeries to the breast. She had done a mammogram
done 10 years ago when the 1st of her sisters got diagnosed with breast cancer. It was normal
at the time. She did not feel the need to do any more mammograms since, and decided to go
for the mammogram screening this time because it was free.
Otherwise she has a past medical history of osteoporosis, previous compression fractures in
2013 and left neck of femur fracture in 2014 s/p fixation, HTN HLD and DM well controlled on
medications, and bilateral cataracts s/p insertion of intraocular lense in 2015. No drug
allergies.
In terms of social history, she does not smoke or drink. She stays with her daughter and son
in a HDB flat with a lift landing. She is ADL independent and community ambulant with a
walking stick. The family is able to cope financially with the cost of treatment.
On examination, Mdm Chin is alert and comfortable. She does not look cachectic, her
temporalis muscles are not wasted. On inspection, the breasts are symmetrical with no
obvious masses, scars, skin changes or nipple changes. There is no tethering of the skin
accentuated by the patient tensing her pectoralis majors. On palpation, I note a irregular ill-
defined mass in the right breast at the 10 o’clock position 5 cm from the nipple, measuring
about 4cm by 4cm. It is non-tender and not warm, not fixed to the overlying skin or underlying
structures. There were no other masses felt in the right breast, no masses felt behind both
nipples, and the contralateral breast was normal. She is not able to express any discharge.
On examination of the axilla, I found a small non-tender mobile node about 1.5cm by 1.5cm.
There was no cervical lymphadenopathy. There was no tenderness on percussion of the
spine, auscultation of the lungs was clear and no hepatomegaly on abdominal exam.
In summary, Mdm Chin is a 73 year old lady with a significant family history of breast cancer,
who now presents with a right breast lump for investigation.
QUESTIONS
How would you investigate this lady?

Sir, I would like to complete the triple assessment, which in addition to clinical evaluation would
involve radiological assessment with mammogram and ultrasound and histopathological
assessment with core biopsy. Tissue should be sent for histology, plus estrogen/progesterone
receptor and HER2 receptor staining. After which, if the diagnosis of breast cancer is
confirmed, I would proceed to stage the patient with a CT Thorax and liver +/- bone scan.
Please interpret Mdm Chin’s mammogram.

Sir, these are the cephalocaudal and medial lateral oblique views of Mdm Chin’s
mammogram. I see a ill-defined spiculated hyperdensity located in the upper outer quadrant
(MLO: lateral, CC: superior). There are pleomorphic microcalcifications around the lesion.
There is some architectural distortion causing tethering of the skin.
Yes it was reported as BIRADS 5. What does this mean?

The breast imaging reporting and data system (BIRADS) is a standardized way of
communicating mammogram findings. BIRADS 5 means a highly suggestive of malignancy
and biopsy should be done.
BIRADS 0 = incomplete assessment

1 = normal
2 = benign finding, go back to routine screening
3 = likely benign, needs close interval follow up in 6 months.
4 = suspicious for malignancy, must biopsy
5 = highly likely malignancy
6 = biopsy proven malignancy.
Please interpret the ultrasound image

Sir, this is an ultrasound image of Mdm Chin’s right breast lump. It is solid-cystic, taller than
wide. Its margins are irregular and I note internal microcalcification casting posterior acoustic
shadow.
CTTAP confirmed no metastasis elsewhere, no other axillary or internal mammary

lymphadenopathy other than the axillary node you found on examination. Bone scan is
normal. What stage is Mdm Chin?
T1 <2cm
à T2 2-5cm
T3 >5cm
T4 direct ext to chest wall or skin
à N1 ipsilateral axillary level 1-2 nodes that are mobile

N2 ipsilateral axillary level 1-2 nodes that are matted OR internal mammary nodes
N3 ipsilateral axillary level 1-2 nodes that are matted
AND internal mammary nodes, infracalvicular nodes OR supraclavicular nodes
Stage 1: Max T1 N0
à Stage 2: Max T2 N1, T3 N0
Stage 3: A = T0-3 N2, T3 N1-2, B = T4 any N, C = any T N3
Stage 4: Any T, any N, M1
According to the TNM classification, Mdm Chin is Stage 2b = early stage breast cancer.
Please outline the principles of management of breast cancer.

Sir my goal of treatment for this patient is curative. She should receive multidisciplinary,
multimodality care and needs to be discussed at tumour board.
The options are that of breast conserving surgery with postoperative radiotherapy vs
mastectomy. As she has a palpable lymph node, axillary clearance should be done (no role
for sentinel lymph node biopsy if LN already palpable). I will need to discuss this with the
patient and look for contraindications to breast conserving surgery such as
• Small breast to tumor ratio: small breast, large tumor
• Multifocal tumor
• Contraindication to RT: connective tissue disease, unable to comply, (pregnancy - not
in this lady)
• Recurrence of breast cancer (not in this lady)
Following surgery she may be offered adjuvant chemotherapy depending on surgical staging,
hormonal therapy if she is hormone receptor positive (aromatase inhibitor since
postmenopausal, tamoxifen in younger ladies), or herceptin if HER2 positive. Need to monitor
contralateral breast with screening mammogram!
General principles
DCIS Early stage Locally advanced Unresectable

(max T2N1) (T ≥3 or N ≥2) / Metastatic
Goal Curative Palliative #
Local Rx BCT +/- RT or BCT + RT or Neoadjuvant chemo/RT Toilet

Simple mastec Simple mastectomy Mastectomy (no BCT) mastectomy
+ RT (since high stage)
+/- reconstruction +/- reconstruction +/- reconstruction
Regional BCT: no need SLNB Clinical nodes: Axillary clearance

Rx Mastec: do SLNB* Axillary clearance
No clinical nodes:
SLNB; if +ve,
axillaryclearance
Systemic No chemo, Chemotherapy - multiple potential agents.

Rx Herceptin If ER/PR +ve: hormonal therapy
Can give tamoxifen. Tamoxifen (premenopausal) vs AI (menopausal)
If HER2 +ve: targeted therapy - Herceptin
* Need for SLNB in DCIS is disputed. If the patient is going for total mastectomy, it may no
longer be possible to do SLNB at a later date because there is no more breast tissue in which
to inject blue dye -- so if invasive cancer is unexpectedly found in resection tissue, a full axillary
clearance would be required. Hence DCIS going for total mastectomy, SLNB is favoured.
However for DCIS going for BCT, there may not be a need to do SLNB.
^ Axillary clearance prognosticates (to decide on systemic Rx) but not cures
# Modalities for symptom control include

o Brain mets: RT
o Bone pain: RT
o #: prophylactic fixation
o Cord compression: RT, steroid
o Pleural effusion: tap
Can you explain what is sentinel lymph node biopsy?

SLNB Is the standard of care to assess regional lymph nodes in early breast cancer (patients
with locally advanced breast CA do not qualify). As most early stage breast cancers have a
lower clinical suspicion for lymph node involvement, the sentinel lymph node biopsy saves
many of these patients from the morbidity of axillary clearance, which includes lymphedema
and recurrent cellulitis of that arm.
To do a SLNB, dye is injected into the breast tissue and the first lymph node the dye drains to
(i.e. the sentinel node) is removed to be assessed under frozen section.
The sentinel lymph node is taken to be representative of the nodal status of the rest of the
axillary nodes.
• If the sentinel node is negative, then axillary node clearance is not done.
• If the sentinel node is positive for metastasis, then full axillary clearance is done. This
is to determine nodal status, to prognosticate and guide (systemic) treatment (NOT to
remove disease).
What are some other variants of breast cancer and when do you think of them?
• Phyllodes tumor - a fibroepithelial tumor which ranges from what resembles a benign
fibroadenoma, to a clearly malignant lesion which grows much faster and larger than
the other breast cancers
• Inflammatory breast cancer - an aggressive form of locally advanced breast cancer
where tumor emboli within dermal lymphatics cause lymphedema. The breast is
painful, swollen, with erythematous skin and a peau d orange appearance. This has a
poor prognosis.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A DYSPHAGIA: ESOPHAGEAL CANCER
SURGICAL LONG CASES
Dysphagia: Esophageal Cancer
PRESENTATION
Mr Teo is a 60 year old Chinese gentleman who presents with a one month history of painless
progressive dysphagia.
He describes his dysphagia as a feeling of food getting stuck in his chest, rather than difficulty
with swallowing itself. Dysphagia was initially worse with solid food than with liquids, and he
noted a gradual change in food preference from rice and meat, to porridge and soup. There
is associated regurgitation of undigested food 5 minutes after swallowing. Over the past month
his dysphagia has gotten progressively worse and in the past few days he struggled to tolerate
even liquids. What prompted him to seek treatment at A&E was that he vomited liquids
yesterday.
He has clinically significant loss of weight of 10 kg over the past month, with very poor oral
intake and postural giddiness suggesting dehydration.
There are no symptoms to suggest local invasion such as hoarseness of voice (recurrent
laryngeal nerve involvement) or hemoptysis (tracheal-esophageal fistula). He also does not
note any hematemesis or malena, no symptomatic anaemia, and has no symptoms of
aspiration pneumonia (or esophago-pulmonary fistula) such as fever or shortness or breath.
He is not jaundiced (distal mets).
In terms of risk factors,

• [For SCC] I note that he is a heavy smoker of 200 pack years and is also a heavy
drinker with frequent binges. He drinks very hot tea. Otherwise, he has no ingestion of
caustic chemicals,
• [For adenoCA], no history of gastroesophageal reflux symptoms.
He does not have any past medical or surgical history, nor any past scopes. He is not on any
long term medications and has no drug allergies.
Socially and functionally, he works as a delivery man which requires him to able to carry heavy
loads, but he has been struggling to keep up with this work. He cannot afford to stop working,
however, as he is the main breadwinner of his family with two kids. He stays with wife and
children in a 3-room HDB flat and they are financially tight.
On examination, Mr Teo is cachectic with wasted temporalis and intrinsic muscle of the hand.
He is on an IV drip and his mucous membranes appear dry. I find conjunctival pallor but no
scleral icterus. I do not note any scars over his neck, chest, or abdomen. His abdomen was
soft and non-tender with no hepatomegaly. His lungs were clear. There was no goitre and no
cervical lymph nodes palpable.
In summary, my patient is a 60 year old Chinese gentleman, with a 1 month history of

progressive esophageal dysphagia and significant LOW 10 kg.
QUESTIONS
What are the differentials you would consider for this gentleman?
Sir my primary differential for this gentleman is that of a malignancy of his esophagus or
gastroesophageal junction (may also consider gastric CA). I am also considering other causes
such as -
• Benign strictures, although he does not have any history of caustic chemical ingestion.
• Achalasia, although I would expect achalasia to present with difficulty swallowing
solids and liquids from the start
• Extraluminal compression by the 4 Ts - thyroid, thymoma, teratoma, or terrible
lymphoma.
How would you investigate this gentleman?

Sir my goals are to (1) confirm the diagnosis, (2) stage the disease, and (3) prepare for
surgery.
I would like to start with some blood tests

• FBC: looking for anemia, raised total whites in asp pneumonia
• RP: looking for raised urea and creatinine in view of dehydration, as well as
hyponatremia (can cause difficulty swallowing, lethargy → misconstrued as decreased
effort tolerance)
• LFT: albumin, liver metastasis → ALP, liver enzyme derangements
• CXR to rule out aspiration pneumonia
Definitive confirmation of diagnosis can be undertaken via

• Gastrograffin swallow looking for irregular shouldering, and ruling out the rat-tail
appearance of achalasia.
• Esophagealgastroduodenoscopy which will allow me to directly visualize the lesion,
measure its distance from the incisors as well as take tissue biopsies.
Staging can be divided into locoregional and distant staging

• Locoregional staging for T and N stage is best undertaken with endoscopic ultrasound.
(difficulty: less accurate if the scope cannot pass the tumor)
• Distant staging wise, patient will need CT thorax abdo pelvis +/- PET looking for lung,
liver, and adrenal mets.
Pre-operatively patient will also require lung function test, PT/PTT, GXM.
OK can you read this OGD photo please?

• Sir I see a tight stricture with slight erythematous change and contact bleeding of the
mucosa. The scope is unable to pass the stricture,
• OR sir I see an ulcerative fungating mass with contact bleeding
OK so a biopsy is taken. What is the likely histological type in this gentleman?

Sir I think a squamous cell carcinoma is more likely than adenocarcinoma in this gentleman
given his risk factors are smoking and alcohol and there is no GERD.
How would you treat this gentleman if -
(a) Tumor invades mucosa only (T1a), N0, M0

Sir the patient is suitable for endoscopic mucosal resection with spares patient the morbidity
of esophagectomy. However patient will need frequent repeat endoscopes.
(b) Tumor invades submucosa or muscularis propria (T1, T2), N0, M0

Sir this patient should be discussed at a multidisciplinary tumor board. He can receive
esophagectomy with complete (R0) resection, adequate proximal and distal margins, and
appropriate nodal dissection. Options are
• Transthoracic: either
o Two-stage (Ivor Lewis): with intra-thoracic esophageal anastamosis,
abdominal and right thoracotomy scars
o Three stage (McKeown):
o with cervical esophagogastric anastamosis, abdominal, thoracic, and cervical
scars
• Transhiatal: done in 4 stages, with cervical esophagogastric anastamosis, abdominal
and cervical scars
(c) Tumor invades adventitia (T3) +/- adjacent resectable structures (T4)
As for (b) but with neoadjuvant chemoradiotherapy.
(d) Unresectable or metastatic disease

Sir this patient should receive palliative chemoradiotherapy. For palliative mitigation of
dysphagia, he can receive palliative stenting and/or palliative radiotherapy (must be done
before stenting or stent will drop). Patient can also have insertion of NG tube or PEG to
facilitate feeding.
(e) Gastroesophageal junction tumors

Sir, I am aware that GEJ tumors are mostly staged as esophageal tumors (unless epicentre
in stomach >5cm from EGJ or not extending into esophagus). Management depends on
location from GEJ
• Siewert 1: Esophagectomy plus partial gastrectomy, plus appropriate lymph node
dissection
• Siewert 2 & 3: Total gastrectomy with distal esophagectomy (only abdominal incision),
plus appropriate lymph node dissection
How do you optimise the patient for surgery?

• Nutritional: NG vs TPN
• Lung: LFT, chest physiotherapy.
What are the post-op complications?

• Anastamosis-related
o Anastomosis leak → mediastinitis
o Anastomotic stricture → GOO symptoms
• Injury to surrounding structure:Recurrent laryngeal nerve, chylothorax
• Cardiovascular: AMI, VTE
• Pulmonary: Atelectasis, pneumonia
• Related to altered anatomy (stomach now functioning as esophagus): GERD, dumping
syndrome
Another patient with dysphagia is diagnosed with achalasia. What is achalasia?

Aperistalsis of distal esophagus due to degeneration of ganglion cells in myenteric plexus.
This results in failure of lower esophageal sphincter to relax. Diagnosis is via barium swallow
showing smooth distal rat-tailing (vs shouldering in esophageal CA), esophageal manometry
showing failure of peristalsis, increased lower esophageal sphincter resting tone and failure
of lower esophageal sphincter to relax on swallowing.
How do you treat achalasia?

Aim is to decrease lower esophageal sphincter tone. Can be done with medical, endoscopic
or surgical means.
! Medical: Calcium channel blockers, nitrates
! Endoscopic: Injection of botulinium toxin, pneumatic balloon dilatation
! Surgical: Laparoscopic Heller’s esophagomyotomy with partial fundoplication
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A GOO: GASTRIC CANCER
SURGICAL LONG CASES
GOO: Gastric Cancer
PRESENTATION
Sir, my patient Mdm Goo is a 70 year old Chinese lady with past medical history of peptic
ulcer disease, now presenting with symptoms of gastric outlet obstruction of 2 weeks duration,
with significant loss of weight.
I note that she has a significant history of peptic ulcer disease. She was admitted in 2007 for
what sounds like a perforated peptic ulcer s/p emergency repair (sounds like patch repair).
She was again admitted in 2010 with malena requiring endoscopic hemostasis. Both times
she has received triple therapy but defaulted the follow up urea breath tests and scope. She
has been asymptomatic until this year.
Over the last 2 months, however, she has been complaining of early satiety and vague
epigastric discomfort which has been getting worse. She has gravitated towards small
frequent meals of semi-solid foods like porridge or just liquids like soup. In the last 2 weeks,
she also has post-meal vomiting (forceful, vs regurg which is not), 5 minutes after meals.
Vomitus is non-bilious, non-bloody, and consists of the undigested food she had just ingested.
This is associated with clinically significant weight loss of 10kg over 2 months.
Her presentation sounds like gastric outlet obstruction and I am considering malignant
obstruction, benign strictures, as well as extraluminal compression
• First, I am most worried about gastric cancer.
• It may also be benign fibrotic stricture due to previous peptic ulcer disease
• There is no progressive painless jaundice, or dark urine / pale stools, to suggest a
periampullary tumor that could compress on the gastric outlet.
In terms of other complications of gastric cancer, there is no hematemesis, coffee grounds

vomitus, or malena from a bleeding malignant ulcer; and the patient does not have symptoms
of anaemia such as chest pain / SOB / giddiness / palpitations. There is no sudden severe
generalized abdominal pain suggestive of perforation. There is no ascites from transcoeliomic
spread. Systemic review was unremarkable for distant spread.
In terms of past medical history, she has well controlled DM HTN and HLD, and no other past
medical or surgical history. No previous gastrectomy, no history of GERD. She has had no
more scopes since the 2010 admission and no known drug allergies.
She is retired, stays with her husband a HDB flat, and spends most of her time helping to look
after her grandchildren. Financially, she is well-supported by her children. She does not smoke
or drink.
On examination, Mdm Goo is alert and comfortable, slightly cachectic. She is currently on IV
drip. She does not have scleral icterus or conjunctival pallor. Her abdomen has no scars, is
not distended, and is soft and non-tender on palpation, no rebound tenderness or guarding.
There is no masses in epigastrium or anywhere else, no hepatomegaly, no palpable
gallbladder. There was no shifting dullness. Succussion splash was positive. Bowel sounds
were present and active. No inguinal hernia. She did not have any cervical lymphadenopathy
specifically no Virchow’s node.
I would like to complete my examination by doing a digital rectal examination looking for PR
bleed or melena, and masses in the rectouterine pouch or fixed adnexal masses in the
blumer’s shelf suggestive of metastatic disease.
In summary, Mdm Goo is a 70 year old Chinese lady presenting with symptoms of gastric
outlet obstruction, preceded by 2 months vague epigastric discomfort and loss of weight, and
positive succussion splash on examination. There is no palpable abdominal mass or jaundice.
I am most worried about gastric cancer, not complicated by bleeding or perforation. My other
ddx are benign strictures or extraluminal compression.
QUESTIONS
What are the risk factors for gastric cancer?

Sir, the development of gastric cancer is multifactorial due to the interplay of past gastric
conditions, environmental factors including infection, and host factors including genetics.
1. Premalignant and other gastric conditions
! Peptic ulcer disease
! Atrophic gastritis
! Previous gastric resection with bile reflux
! Gastric polyps
2. Environmental factors
! Infection: H. pylori infection
! Diet: nitrosoamines in preserved food, smoked food
! Smoking
! Low socioeconomic status
3. Genetic and other host factors.
! Obesity
! Family history
What are the various ways gastric cancer can present, and what are their differentials?
Presentation DDx
Asymptomatic, picked up incidentally
Nonspecific - Early satiety, dyspepsia Peptic ulcer disease

Biliary colic.
Constitutional - LOW, LOA
Anemia Colon cancer

Peptic ulcer disease
Post-gastrectomy anemia (B12, Fe def)
Menorrhagia, endometrial cancer
Epigastric mass Pancreatic tumor (or pseudoaneurysm etc)

HCC of left lobe
Transverse colon CA
Gastrointestinal stromal tumour
Cx of ulcer - Bleeding, Perforation Peptic ulcer, variceal bleed
GOO Peptic ulcer disease cx stricture

Head of pancreas cancer
Dysphagia Esophageal cancer

Gastroesophageal junction tumor
Obstructive jaundice Periampullary cancers
Transcoelomic metastasis: Ascites Cirrhotic/tuberculous ascites

Sir, I would start off with some basic investigations:
• FBC looking at Hb for anemia
• RP looking for hypokalemia hypochloremic metabolic alkalosis with paradoxical
aciduria, rise in Cr from pre-renal AKI (dehydration)
• LFT looking for cholestatic pattern (possible in HOP or LN at porta hepatis) vs
hepatocellular pattern (liver metastasis)
• CXR looking for free air under the diaphragm
• ECG PT/PTT GXM - pre-op w/u
Then I would like to prepare the patient for an OGD, which is both diagnostic and therapeutic.
It will allow us to confirm GOO (presence of food debris, absence of duodenal visualization),
directly visualize the lesion and location, and take a biopsy for histological confirmation, and
placement of a stent for temporary relief of GOO symptoms.
Can you please read this scope picture?

• Sir this is an endoscopic view of the gastric outlet showing a large fungating tumor with
contact bleeding. The gastric outlet is almost entirely occluded and I think the scope
cannot intubate past the pylorus.
• Sir this is an endoscopic view of the stomach. I note a large ulcer with heaped up
edges. There is contact bleeding from the ulcer.
Histology confirms adenocarcinoma. Please outline your management for Mdm Goo.
I would first stage the lesion with:
(1) Endoscopic ultrasound for T and N staging
(2) CTTAP for N and M staging
(3) PET scan also for M staging
Thereafter the patient should be discussed at tumor board and managed by a multi-
disciplinary team.
Further discussion depends on the scans they show you -
(a) Early gastric cancer i.e. superficial to muscularis propria.

• Can be treated with endoscopic mucosal resection
(b) Non-early gastric cancer -- for curative Rx

• Pre-operatively there is a role for laparoscopy to rule out peritoneal metastases which
may be occult on CT scan.
• If there are no peritoneal metastases I will offer curative resection involving
o Wide resection with oncological margins (≥6cm confirmed with frozen section):
partial / subtotal / total gastrectomy
o En-bloc resection of lymphovascular supply and any structures involved by
local invasion
• Re-establish GI continuity with Roux-en-Y (alternatives: Bilroth I, Bilroth II)
• Couple with 6 cycles of chemotherapy (3 neoadjuvant and 3 adjuvant)
o Chemotherapy regimen: 5FU, epirubicin, cisplatin
(c) Palliative Mx:

• Painful bony mets - external beam radiotherapy
• Bleeding - transcatheter embolization, palliative gastrectomy
• Obstruction - palliative gastrectomy, self-expanding metal stent, feeding jejunostomy
• Perforation - palliative gastrectomy
What are the post-op complications to look out for, and what to do about them?
Early: bleeding, infection, injury to surrounding organs, anastomotic leak, stump blowout
Late:
• Pre-meal: Early satiety due to loss of gastric reservoir → take small frequent meal
• Post-meal: early dumping syndrome (hypovolaemic symptoms from fluid shift) vs late
(hypoglycaemic symptoms) → take small frequent meal
• Between meals: Nutritional deficiencies - B12 (loss of intrinsic factor), Fe → give B12
injections, Fe supplements
• Afferent loop syndromes
• Retained antrum syndrome
• Bile reflux gastritis
OK apart from adenocarcinomas what other gastric cancers do you know of?
While the majority of gastric cancers are adenocarcinomas (diffuse type or intestinal type -
Lauren classification), other histological types include GIST, carcinoid tumors, and
lymphomas.
Yay! I love GIST! Tell me about GIST?

GIST stands for Gastrointestinal Stromal Tumour. It is the most common stromal/
mesenchymal neoplasm arising from the GI tract. It is characterised by cKIT mutation which
causes tyrosine kinase hyperactivity, picked up as CD117 antigen expression (part of the KIT
membrane receptor’s tyrosine kinase). PDGFRA (Platelet derived growth factor receptor alpha
polypeptide) gene mutation is also seen in GIST.
While GISTs occur throughout the GI tract from the esophagus to the anus, they are most
common in the stomach (40 to 60 percent) and jejunum/ileum(25 to 30 percent), and less
commonly in the duodenum (5 percent), colon/rectum (5 to 15 percent), and esophagus (≤1
percent). They can also occur in the retroperitoneum, mesentery and omentum. They
frequently metastasize to liver, omentum, peritoneal cavity and rarely to regional lymph nodes.
They uncommonly metastasize to the lungs, the most common site of metastasis for most soft
tissue sarcomas (dDx for GIST).
The clinical behavior of GISTs is highly variable; the main prognostic determinants for are
tumor size, mitotic rate, and tumor location. Tumours with high risk of recurrence are those
>2cm, high mitotic rate and extra-gastric location.
How do GIST present?

GIST tumours can be asymptomatic and discovered incidentally. More often, they are
associated with nonspecific symptoms (ie, early satiety, bloating) unless they ulcerate and
bleed, or grow large enough to become a palpable mass or cause intestinal obstruction.
What is the diagnostic work-up?

The preoperative diagnosis of a GIST requires a high degree of suspicion and familiarity with
its radiologic appearance.
1. CT/MRI scan: Appears as a solid smoothly contoured mass that enhances brightly with
IV contrast. Very large tumors (>15 cm) may appear more complex/heterogenous due
to necrosis, hemorrhage, or degenerating components. It may be difficult to identify
the origin of a large mass because of exophytic growth.
2. OGD: Appears as a submucosal mass with smooth margins, a normal overlying
mucosa, and bulging into the gastric lumen, occasionally with central ulceration
o Leiomyomas have the exact same appearance
3. Endoscopic Ultrasound: Can help to characterize lesion and determine if benign or
malignant. Tumors that disrupt the normal tissue planes, contain cystic spaces, and
are associated with enlarged lymph nodes are more likely to be malignant.
4. Pre-op Biopsy, EUS guided preferred: Preoperative biopsy is not generally
recommended for a resectable lesion in which there is a high suspicion for GIST, and
the patient is otherwise operable. However, a biopsy is preferred to confirm the
diagnosis if metastatic disease is suspected or if preoperative imatinib is considered
prior to attempted resection in a patient who has a large locally advanced lesion
thought to represent a GIST.
How do you treat a GIST?

• Local control: Surgical resection
• Systemic control: neoadjuvant or adjuvant targeted therapy with tyrosine kinase
inhibitors (imatinib) --- TKIs have transformed the treatment of GIST.
• Hypothyroidism is a common side effect of antiangiogenic tyrosine kinase inhibitors
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A HEMATURIA: BLADDER CANCER
SURGICAL LONG CASES
Hematuria: Bladder Cancer
PRESENTATION
Sir, my patient Mr Pradeep is a 55 year old indian man with past medical history of urolithiasis
in 2014 status post extracorporeal shock wave lithotripsy. He now presents with a 2 week
history of painless gross hematuria.
This gross hematuria is painless, persistent and mixed with urine/throughout micturation, no
blood clots. It does not occur in between micturition and he does not notice any blood staining
his underwear. This is associated with some storage symptoms such as frequency and
urgency, but no voiding symptoms such as hesitancy, slow and intermittent flow, terminal
dribbling, incomplete voiding, and double voiding.
[Ddx]
• [RCC/Urolithiasis] It is not associated with any dull flank ache or sharp loin to groin
pain
• [Cystitis] There is no fever, dysuria or pyuria
• He has had no recent instrumentation to the urethral tract.
• [Anticoagulant] He is not on any anticoagulants.
• [Renal] I also considered renal causes but he does not have lower limb swelling,
decreased urine volumes, or recently diagnosed hypertension. He does not have any
joint pain, rashes, or history of autoimmune disease.
Otherwise he has no pneumaturia or recurrent urinary tract infections to suggest local

invasion, no constitutional symptoms such as LOW LOA, and no SOB, bone, pain or
neurological symptoms to suggest distant spread.
In terms of risk factors, he does not smoke, does not have occupational exposure to industrial
chemicals as a cabin crew member, and does not have family history of any urological cancers
or colorectal cancers.
In terms of past medical history, he had hematuria and sharp flank pain secondary to kidney
stones in 2014 s/p ESWL, as well as previous testicular torsion s/p orchidopexy when he was
18. He has no other past medical, surgical or drug history and no known drug allergies.
Social, functionally and financially, he stays with his wife and 2 children, is able to work as per
normal as a cabin crew member and is financially stable.
On examination, Mr Pradeep was alert and comfortable at rest. He is not cachexic. Abdominal
examination found no scars and a soft non-tender abdomen. There was no organomegaly,
most notably no ballotable masses and no palpable bladder. In the groin there was no left-
sided varicocele. Digital rectal exam revealed a normal prostate of 1.5 breadths that was
smooth, firm, no nodules, median sulcus felt, overlying rectal mucosa mobile over it. Anal tone
was intact. No spinal tenderness, lungs clear.
In summary Mr Pradeep is a 55 year old indian man with 2 weeks of painless gross hematuria
for investigation. I am most suspicious for bladder cancer, with a differential of renal cell
carcinoma, prostate cancer, and although less likely in the absence of pain or infective
symptoms, urolithiasis and urinary tract infection.
QUESTIONS
How would you investigate this patient?

Sir, I would (1) confirm diagnosis (2) look for complications (3) stage disease and (4) plan for
treatment
I would start with the following basic investigations -

• FBC looking at Hb for anemia, and total whites
• Renal panel looking at Cr for kidney function and for contrast studies
• PT/PTT, GXM in preparation for procedures
• UFEME looking at RBC WBC bacteria casts and crystals
• Urine gram stain and cultures
• Urine cytology for malignant cells
In terms of imaging I would do

• CT urogram looking for any renal tumours or any synchronous tumours in the upper
tracts (field change effect); also to stage N and M.
• CXR to rule out lung metastases
To confirm the diagnosis he will require cystoscopy which can visualize the lesion and its
location as well as take a biopsy.
Subsequently if cystoscopy confirms a tumor, he will require transurethral resection of bladder

tumor. This is both diagnostic to determine depth of invasion (superficial vs muscle invasive),
as well as therapeutic.
If there is muscle invasive disease, then we will also need to look for metastases with CT
thorax and with the CT urogram already done.
OK a 4cm exophytic papillary lesion seen. TURBT was performed. Mr Pradeep’s

histology comes back as superficial bladder cancer. What now?
For superficial bladder cancer, the TURBT would already have been the primary treatment.
He would benefit from intravesical therapy with Bacillus Calmette Guerin (BCG) or mitomycin
C as a >3cm tumor is high risk*. Following treatment careful surveillance for recurrence and
second tumors is required, e.g. cystoscopy and urine cytology in 3 months.
* High-risk features are:

• high grade
• multi-focality
• multiple recurrences
• tumour size >3cm
• primary or coexisting carcinoma in-situ
• prostatic urethral involvement
Mr Pradeep decided he does not want intravesical therapy. He returned to his job as a
cabin crew and was lost to follow up. 4 years later he comes back with the same
symptoms, and was found to have recurrence of bladder tumour -- this time muscle
invasive. Repeat CT urogram and bone scan show no synchronous lesions and no
mets. What would you offer him?
• I would offer him curative management with neoadjuvant platinum-based
chemotherapy and then radical cystectomy and pelvic lymphadenectomy with urinary
diversion, usually an ileal conduit or with a neobladder.
• If he refuses surgery - I suppose multimodal therapy with TURBT, chemotherapy, and
radiotherapy is possible but if this fails then cystectomy becomes difficult.
• Note: if metastatic, chemotherapy is the mainstay of treatment.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A HEMATURIA: RENAL CELL CARCINOMA
SURGICAL LONG CASES
Hematuria: Renal Cell Carcinoma
PRESENTATION
Sir, my patient Mr Cui is a 75 year old Chinese gentleman on warfarin for old mitral and aortic
valve replacement, who presents now with 1 month of painless gross hematuria, left flank
discomfort and loss of weight.
With respect to his painless gross hematuria, this has been persistent for 1 month, mixed with
urine throughout micturition, and associated with vermiform blood clots. There is no urethral
bleed or staining of underwear between micturation. He also complains of dull left flank
discomfort, which has been become more prominent recently. Occasionally he also feels a
sharp flank pain radiating to the groin, which will be followed by passage of a blood clot. I also
note weight loss of 5kg over the past month.
[Ddx]
• Otherwise, there is no fever or pyuria to suggest pyelonephritis
• No LUTS symptoms such as dysuria, urgency, and frequency (cystitis), hesitancy
intermittancy double-voiding (BPH), no pneumaturia or recurrent UTIs (e.g. bladder
tumor with local invasion)
• He does not have any history of urolithiasis, parathyroid tumor, gout, or endocrine
tumors (MEN). He is not on any medications that could cause hypercalciuria, has no
known hx of gout or joint pains, and drinks at least 2 litres of water each day.
• I also considered renal causes but he does not have lower limb swelling, decreased
urine volumes, or new hypertension. He does not have any joint pain, rashes, or history
of autoimmune disease.
• His last INR 3 months ago was said to be within range. He has no other symptoms
such as per rectal bleeding or easy bruising. He does not drink at all, has not been
prescribed any new medications recently, sticks religiously to a stable diet and has
never in the past 20 years been admitted for complications from warfarin.
He has not had any jaundice, shortness of breath, bone pain or constant progressively
worsening headache suggestive of metastasis. In terms of paraneoplastic syndromes, I note
there is no symptoms of hypercalcemia, and no painful leg swelling to suggest deep vein
thrombosis, no weakness and rash to suggest dermatomyositis.
In terms of risk factors, he is a smoker of 50 pack years but does not have any family history
of kidney tumours. No risk factors such as industrial chemical exposure or pelvic irradiation
As for his past medical history, I note he had aortic and mitral valve replacements 20 years
ago for rheumatic heart disease. He is stable on warfarin. Otherwise there is no other medical
or surgical history, and no other long term medications other than warfarin. He does not drink
because of his warfarin. No known drug allergies.
Socially functionally and financially, he stays with his wife in a 2 room studio flat. Both are
retired and well-supported financially by their 3 children.
On examination, Mr Cui is alert and comfortable. His blood pressure is 120/70. I note that he
is slightly cachectic. He has a midline sternotomy scar and audible metallic clicks by bedside.
I note that he has an IDC, urine bag containing gross hematuria.There is no scleral icterus,
conjunctival pallor OR suffusion, no easy bruising. His abdomen is not distended, soft and
non-tender. There is a left ballotable mass but no other organomegaly. No palpable bladder.
Bowel sounds are present. Hernia orifices are intact. There is a left varicocele. Digital rectal
examination revealed a normal prostate and no PR bleeding.
In summary, this is a 75 year old gentleman who has had 1 month of painless gross hematuria
with vermiform clots, left flank discomfort and significant loss of weight, associated with a
ballotable left flank mass and left varicocele on physical examination. I am most suspicious of
left renal cell carcinoma.
QUESTIONS
What are your differentials?

Other differentials include
• Urolithiasis but the sharp loin to groin pain is always in relation to passing of a blood
clot and he has persistent hematuria in between the loin to groin pain episodes.
• Bladder cancer
What are some of the paraneoplastic syndromes associated with RCC?

• Hypertension - due to overproduction of renin
• Hypercalcemia - due to production of PTH-like protein
• Polycythemia - due to overproduction of erythropoietin
• Venous thromboembolism
• Non-metastatic hepatic dysfunction.

Sir, I would investigate with the aim of (1) confirming diagnosis and ruling out differentials (2)
looking for complications (3) staging.
But I would like to start with the following basic investigations:

• FBC looking at Hb for anemia or polycythemia, TW for infection
• UECr looking at Cr in view of contrast studies
• PT/INR make sure it is in range
• GXM as patient may be going for surgery
• UFEME for RBC, WBC, bacteria, casts, crystals
• Urine cytology for malignant cells
• Most importantly a triphasic CT Kidney looking for a renal parenchymal mass with
irregular borders and enhancement after contrast injection, any lymph node
involvement, perinephric extension beyond gerota’s fascia, renal vein or IVC extension
Then staging should be completed with

• CT thorax and abdomen looking for distant metastasis to the lung, liver
• Bone scan for bone mets
• KIV MRI w gadolinium abdomen and heart (IVC and right atrium)
Mr Cui’s corrected calcium is 4.0mmol/L. How would you manage?

Sir this is severe hypercalcaemia (>3.5mmol/L). For severe hypercalcaemia or even if not
severe but patient is symptomatic, I will
• Immediately begin aggressive hydration (1st line therapy, onset in hours) with 3L of
saline a day
• Give calcitonin (onset in 4-6hrs, has tachyphylaxis after a few days)
• Consider bisphosphonate i.e. IV zoledronic acid or pampidronate (onset in 24-72
hours): used if due to excessive bone resorption e.g. malignancy related
hypercalcemia, hypervitaminosis D etc.
• Glucocorticoid (onset in 2-5days): not applicable in this case, better for lymphoma,
sarcoidosis, other granulomatous disease
• If all else fails - dialysis (onset in hours)
Mr Cui’s CT Kidney shows a 12cm left renal parenchyma mass that enhances with
contrast, extension into the renal vein stopping just before the IVC, but contained within
the Gerota’s fascia. No enlarged lymph nodes seen. No distant metastasis. How would
you treat this patient?
This is a T3N0M0 tumour, it is resectable. I would counsel Mr Cui for a radical nephrectomy.
This will involve en-bloc resection of the entire kidney with the Gerota’s fascia together with
it’s lymphovascular supply, as well as resection of the renal vein. Surgery is the mainstay of
treatment. There is no role for adjuvant chemotherapy or radiotherapy.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A HEPATOCELLULAR CARCINOMA
SURGICAL LONG CASES
Hepatocellular Carcinoma
PRESENTATION
Sir, my patient Mr Buang is a 43 year old Malay gentleman with hepatocellular carcinoma on
a background of hepatitis B cirrhosis, currently admitted for transarterial chemoembolisation.
4 years ago, he was admitted for symptomatic ascites and diagnosed with cirrhosis secondary
to hepatitis B. Since then he has had multiple admissions for decompensated liver cirrhosis,
about 2-3 times a year. Triggers are usually fluid and salt indiscretion, or intercurrent illnesses
such as upper respiratory tract infection or gastroenteritis. He has never had variceal bleeding.
He is compliant to propranolol, frusemide and spironolactone, but misses his clinic
appointments sometimes. He is not on antiviral medication at present and does not know his
current Child’s score, viral load or HBe status.
He was diagnosed with HCC last month when a follow-up ultrasound showed a small lesion
which CT confirmed as HCC. He is otherwise asymptomatic with no abdominal pain,
worsening jaundice, symptomatic ascites, encephalopathy, or variceal bleeding. There is no
loss of appetite or loss of weight.
He does not have any family history of hepatocellular carcinoma. He has no other liver
problems such as autoimmune liver or biliary disease. As for his underlying hepatitis B, his
mother and siblings do not have hepatitis or cirrhosis. He does not have IV drug use and has
not received blood products overseas. He declines to comment on sexual history.
He is currently admitted for transarterial chemoembolisation and is post-procedure day 2. He

does not have any bleeding manifestations or fever, and is planned for home tomorrow.
He is functionally good and is able to work normally as a lab technician. Socially, he does not
smoke or drink. He stays with wife and children in a hepatitis B flat. His wife is vaccinated
against hepatitis B. They are coping well financially.
On examination, Mr Buang was alert and comfortable. He has peripheral stigmata of chronic
liver disease such as marked jaundice, scleral icterus, spider naevi, loss of axillary hair, but
no palmar erythema, clubbing, or gynaecomastia. There is no conjunctival pallor, no needle
marks, no parotidomegaly or dupuytren’s contractures. The abdomen was not distended, had
no scars, and was soft non tender even over the RHC. There was splenomegaly of 2cm below
costal margin but no hepatomegaly. I did not find any shifting dullness or pitting lower limb
edema. I note multiple tattoos over his arms and legs. There was no cough impulse over both
groins, and I would like to complete my examination by doing a digital rectal examination.
In summary Mr Buang is a 43 year old Malay gentleman with recently diagnosed HCC on a
background of hepatitis B liver cirrhosis, status post transarterial chemoembolization.
QUESTIONS
What are the ways in which HCC can present?

Sir, HCCs can
• Be completely asymptomatic and picked up only on screening (AFP/US).
• Have local symptoms such as right hypochondrial pain, either when the tumour grows
fast enough to stretch the liver capsule or when it invades into the liver capsule.
• Precipitate decompensation of chronic liver disease
• Present with constitutional symptoms such as LOW LOA or symptoms of distant
metastasis such as SOB or back/bone pain.
• Present with tumour rupture, with sudden severe abdominal pain, hypotension, and
signs of peritonism.
How is HCC diagnosed?

HCC is usually diagnosed via surveillance ultrasound and/or AFP* monitoring of patients with
chronic hepatitis or cirrhosis; that is the only way to diagnose in a timely fashion.
If the ultrasound finds a nodule >1cm, workup with further imaging modality is carried out -
triphasic CT or dynamic contrast MRI. Classic imaging features (see below) is diagnostic of
HCC. If the initial imaging features are not diagnostic, a second imaging modality (MRI with
liver-specific contrast e.g. primovist, contrast enhanced ultrasound) or biopsy is carried out
(otherwise, Biopsy is not routine due to risk of seeding)
A smaller subcentimeter lesion would be followed up on serial ultrasound and investigated if

it is growing.
* AFP is routinely measured but not needed for diagnosis and insufficiently sensitive or specific
(not all HCCs secrete AFP, and AFP can be elevated in the absence of HCC). AFP is now used
more for trending on follow-up.
Please read Mr Buang’s CTAP.

Sir, this is Mr Buang’s CT scan. The arterial phase (contrast lights up in aorta) shows a 4 cm
x 4 cm arterially enhancing lesion in the right liver. The venous phase shows the same lesion
which is now hypodense, consistent with venous washout as is expected in HCC. I do not note
any other lesions in the liver. The background liver is cirrhotic with nodularity, caudate lobe
hypertrophy, and corkscrewing of hepatic arterioles. I do not note any ascites and I do not see
any distant metastases in these cuts.
Mr Buang’s albumin is 25, bilirubin is 40, and PT/PTT is normal. Please calculate his
Child-Pugh Score.
A = 3 pts, B = 2 pts, C = 1 pt, D = 1 pt, E = 1 pt. Total 8 points, i.e. Child’s B.
Scoring table:
1 point 2 points 3 points
Albumin g/L >35 28-35 <28
Bilirubin µmol/L <34 34-51 >51
Coag: PT prolongation (INR) <4 (<1.7) 4-6 (1.7-2.3) >6 (>2.3)
Distension (ascites); None Controlled on diuretics Refractory to diuretics
Encephalopathy None West Haven 1-2 West Haven 3-4

1: Change in behaviour 3: Marked confusion,
alone mostly sleeping but
2: Disorientation, arousable
drowsy, asterixes 4: Comatose
Interpretation: Child’s A: 5-6 points, Child’s B: 7-9 points, Child’s C: 10-15
What is TACE?
TACE is the selective intra-arterial administration of chemotherapeutic agents followed by
embolization of major tumour artery (principle: HCC draws vascular supply mainly from artery
not hepatic vein). A guidewire is inserted from from groin (femoral artery) going up to the aorta
and then into the hepatic artery. Contrast is used to localize the exact artery supplying the
tumour. Chemotherapy and oily contrast (lipiodol) is then injected through a catheter, and the
artery supplying the tumour embolized.
Suppose Mr Buang has just come back from TACE. You are now the HO reviewing him
in the ward. How would you assess him, and what would you do for him?
The main concern is post-TACE syndrome which is usually self-limiting but there is a small
risk of hepatic decompensation after TACE, especially if premorbid liver function is poor.
• I will get a set of vitals looking for fever.
• Ask for symptoms of right hypochondrial pain, nausea, vomiting. Ensure there is no
malena or hematemesis (UBGIT is another cx of TACE)
• Examine general condition: drowsiness, asterixes; palpate abdo for RHC tenderness
• Order FBC UECr LFT PT/PTT; there may be transient elevation of AST ALT and bil.
• Order analgesia, antiemetics, and ensure that he is on antibiotics e.g. 5 days of
ampicillin/sulbactam
Why do you think Mr Buang received TACE instead of another treatment option?
Sir, Mr Buang has a 4cm x 4cm nodule and is Child’s B at present. Technically a single 4 cm
nodule should be resectable. Perhaps there is another contraindication to resection such as
poor liver function or inadequate future liver remnant volume should he be resected.
Radiofrequency ablation would not be curative in his case as his nodule is too big.
General principles of management:
• Is this a good liver or bad liver? Assess liver function -

o Child Pugh scoring: most liver surgeons will only be comfortable operating on
a Child’s A or a good Child’s B; surgical morbidity is 40% for Child’s C
o Indocyanine green: Patient must have a r15 of >14% for major liver resection,
and a r15 of >20% for segmental liver resection
• Is this a good tumor or a bad tumor?

o Principle: A good tumor is a tumor that can be resected and yet leave sufficient
functional liver for the patient to survive. Leaving insufficient functional liver
behind can cause hepatic encephalopathy and liver failure.
o A tumor with vascular invasion, metastasis is clearly a bad tumor. A multifocal
tumor may be good or bad - if they are all on the same side of the liver which
can be resected, then it is a good tumor; if all over the place, then bad.
o Estimate future liver remnant volume: measured by CT volumetry = remnant
liver / (current liver - tumor size). The larger the the tumour volume, the smaller
the volume of functional liver removed. The minimum % of future remnant liver
varies depending on function - about 25% for healthy liver, to 40% for cirrhotics1
• Various algorithms of varying complexity are available.

o Can I cure this patient? > Curative options are resection or RFA (if qualify3), or
transplant (see note2).
o If cannot cure > how best to palliate?
o Motherhood statements: multidisciplinary care, discuss at tumor board… etc.
Good Liver (Child A, early B) Bad Liver (Child late B or C)

and patient fit or patient unfit (comorbids)
3
Good tumor Curative resection RFA
3 2
(resectable) RFA Transplant: if within Milan
criteria
2 2
Bad tumor: Transplant: if within UCSF Transplant: if within UCSF
locally advanced expanded criteria expanded criteria
Local-regional therapies e.g. Best supportive care
4
TACE, SIRT
Extrahepatic Sorafenib Best supportive care

metastasis Best supportive care
Footnotes:
1. Sometimes, to improve residual functional liver volume, can try portal vein embolization of the
diseased lobe. Hope is that shunting blood supply to the contralateral lobe results in atrophy of
the diseased lobe and hypertrophy of the normal lobe, improving future liver remnant volume.
2. Transplantation is a curative option for virtually all patients who fulfill the transplant criteria
(below) and are fit for a big operation + can tolerate post-operative immunosuppression. It is
considered especially in those who cannot be cured by resection or RFA. Unfortunately it is the
hardest to come by simply due to lack of supply - donor organs are allocated on a waitlist
prioritised according to MELD (model for end-stage liver disease) score. Transplant criteria are:
○ Traditional milan criteria: 1 lesion no more than 5cm OR 3 lesions less than 3cm AND
no lymphovascular involvement AND no distant metastasis.
○ Can also be considered within expanded UCSF criteria (less strict).
3. Radiofrequency ablation (RFA): curative for lesions that are 3cm or smaller, and cannot be
performed on lesions near any major vessels due to heat sink effect.
4. Locoregional therapy options include the following (all are palliative except RFA for a small
tumor; and usually should not be offered to a child’s C).
○ Transarterial chemoembolisation (TACE)
○ Selective Internal Radiation Therapy (commonly with Yttrium-90 microspheres)
○ Ablative therapies, which include radiofrequency ablation, percutaneous ethanol
injection, microwave ablation, cryotherapy
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A IO: COLON CANCER
SURGICAL LONG CASES
IO: Colon Cancer
PRESENTATION
Sir, my patient Mr Mok is a 66 year old Chinese cook. He has no significant past medical or
surgical history, and has good premorbid function.
He presents with a 1-month history of change in bowel habit, and loss of weight. In terms of
his change in bowel habit, he notes a decrease in stool calibre and progressively watery stools
in the last month which is non-bloody and non-fatty. This is associated with clinically significant
loss of weight of 10 kg over 3 months. In the last week, he also complains of abdominal
distension and mild colic over the central abdomen (pain score 1-3/10), without
nausea/vomiting or constipation. There is no tenesmus and no severe unremitting pain that
could suggest perforation. He has no per-rectal bleeding and no symptoms to suggest
anaemia such as chest pain, dyspnoea, giddiness, palpitations, or lethargy. He also does not
have any pneumaturia, fecaluria, or urinary tract infection. Systemically he is well with no
jaundice or dyspnoea.
In terms of risk factors, he does not have any personal history of polyps, and no known family
history of colorectal cancer or CRC-associated cancers. He had a colonoscope 10 years ago
which was clean, and no further fecal occult blood test or scopes since then.
He was diagnosed with colon cancer and is currently post-op day 4. He is systemically well
and tolerating escalation to soft diet. He did not receive neoadjuvant chemotherapy and does
not know if he is planned for adjuvant chemotherapy.
Examination revealed a pleasant middle-aged chinese gentleman who is alert and comfortable
at rest. He is not receiving any active interventions at the moment. There is mild temporal
wasting, no pallor or jaundice. On inspection of the abdomen, there is a midline laparotomy
scar, a surgical drain in the left iliac fossa connected to a closed active drain system and
draining small quantities of hemoserous fluid, and a loop ileostomy in the right iliac fossa. I
say that it is an ileostomy because it is draining liquid material, and the lumen size is <1cm; it
is however less spouted than I would expect and I will like to remove the base plate to check
for skin excoriations. Otherwise the stoma is pink. The abdomen is soft and generally non-
tender, except for mild tenderness at the surgical scar, with no hepatomegaly or other organ
masses felt. Hernia orifices are intact and there are no parastomal or incisional hernias.
Ideally I would like to complete my examination by performing a digital rectal exam however I
feel that this may not be wise considering that it is POD4. I do not expect any findings as a
loop ileostomy usually serves to defunction a left hemicolectomy or anterior resection; if he
had a abdominal-perineal resection he would have had an end-ileostomy instead.
In summary, my patient Mr Mok is a 66 year old Chinese gentleman who presented with
change in bowel habit, loss of weight, and symptoms suggestive of partial intestinal
obstruction. He was diagnosed with colon cancer which is most likely left-sided, and
underwent either a left hemicolectomy or anterior resection with defunctioning loop ileostomy.
QUESTIONS
You mention colorectal cancer associated malignancies, what are those?

These are seen in hereditary non-polyposis colorectal cancer, also known as Lynch
Syndrome. This is an autosomal dominant syndrome due to defective mismatch repair (MMR)
proteins. HNPCC is divided into
• Lynch syndrome I : familial colon cancer. Defined by Amsterdam Criteria, remembered
as the 3-2-1 rule
o At least 3 relatives with histologically confirmed colorectal cancer, 1 of whom
is a first degree relative of the other 2.
o At least 2 successive generations involved;
o At least 1 of the cancers diagnosed before age 50.
o Exclusion of FAP
• Lynch syndrome II : HNPCC associated with other cancers of the GI or reproductive
system - namely endometrial cancer and, to a lesser extent, cancers of the ovary,
stomach, small intestine, hepatobiliary tract, pancreas, upper urinary tract, prostrate,
brain, and skin.
OK what are your differential diagnoses in this patient?

Sir, my differential diagnoses for his presentation with intestinal obstruction include other
infective and inflammatory pathologies of the colon. These include -
• Diverticular disease complicated by stricture, which can explain the decrease in stool
calibre and spurious diarrhoea. However the loss of weight is somewhat unexpected,
as is an extensive resection for the condition.
• Infective strictures such as that due to TB.
• Inflammatory bowel disease, especially ulcerative colitis, which can present with toxic
megacolon
• Infective colitis
Note: please tailor your differentials to the patient’s predominant presenting symptom e.g.
intestinal obstruction, lower BGIT / iron deficiency anaemia, or change in bowel habit
Why do you think this patient’s tumor is left sided?

This patient presents as intestinal obstruction which is consistent with that of a left sided
tumours (in the right side the feces is more liquid, hence tends not to obstruct).
Localizing presentations:
• Left sided - change in bowel habits, decreasing stool calibre, eventually intestinal
obstruction +/- bleeding.
• Rectal - tenesmus
• Right sided - tend to present more insidiously with just weight loss and anemia, and
typically present with more advanced disease.
If you were the first doctor seeing him at A&E, how would you investigate this patient?
In the acute setting, my goals are to (1) rule out any emergent complications such as
perforation or impending perforation, (2) diagnose the underlying cause IO, and (3) prepare
for further management.
• First I will need to resuscitate the patient and ensure that he is hemodynamically stable.
• I would begin with simple blood investigations
o FBC to look for microcytic hypochromic anaemia
o UECr for electrolyte imbalance for diarrhoea and to ensure renal function for
contrast scan
o LFT to rule out liver dysfunction from extensive hepatic metastases
o PT/PTT and GXM as pre-procedural investigations.
• My first line imaging modality will be erect CXR to rule out air under diaphragm, and
supine KUB on which I expect dilated right-sided large bowel loops. Cecal dilation
>9cm or the absence of dilated small bowel loops will be worrysome (impending
perforation or close loop obstruction). I must also make sure that I don’t see any
Rigler’s sign.
• The patient will subsequently require a CTAP
The patient will also require

• CXR or CT thorax for metastatic disease
• Colonoscopy to visualize the lesion and biopsy for tissue diagnosis.
When would you worry of impending perforation?

• RIF tenderness
• Diameter >3cm in small bowel, >6cm in large bowel, >9cm in cecum
• Pneumatosis intestinalis.
In this setting would you do CTAP first or colonoscope first?

Sir, in the emergent setting I do CT first.
1. CT provides more information. It allows me to confirm a tumor, rule out other causes of
obstruction, and look for impending perforation i.e. pneumatosis intestinalis, diameter (or
existing sealed perforation). Even if I am considering colonoscopic stenting, the CT helps see
if the tumor is stentable (ascending colon, flexures are technically difficult to stent).
2. CT is safer. If there is impending perforation, the patient must be sent to OT immediately

and not for colonoscope. In such a situation a biopsy is unnecessary - surgical resection will
provide the histology. Colonoscopy involves air insufflation which risks causing an iatrogenic
perforation! I need to make sure there is no 9cm cecum or pneumatosis intestinalis before
sending an obstructed patient to scope room.
3. CT is faster. Preparing the distal colon for a scope takes time and even then there is no
guarantee that the tumor can be visualized. In the acute situation a CT scan is much faster.
In contrast in the elective setting (patient presents with PR bleed for investigation) - you would
do colonoscopy first.
Suppose he indeed presented with an obstructed tumor, how would you manage him?
• First i will need to resuscitate him and rule out complications e.g. perforation (add in if
not previously discussed).
• Will rule out other causes of obstruction such as hernia.
• I would prepare the patient for procedural intervention -
o Non-surgical: colonscopy with stenting; this converts an emergency procedure
into an elective one.
o Surgical: resection with primary anastamosis, proximal washout and
defunctioning ileostomy. If patient is sick, Hartmann procedure is an option.
What is the benefit of colonoscopic stenting instead of immediate resection?

Sir, colonoscopic stenting may allow decompression of the obstruction and is of value in
certain circumstances, assuming expertise and equipment is on standby
1. Interval stenting as a bridge to elective resection (2 weeks later). Benefits are:

• Avoid emergency surgery which has more complications
• To perform a one stage procedure without diverting ileostomy -- in the obstructed
setting, a diverting ileostomy is important. This because the proximal bowel is
distended and the distal bowel is collapsed, so there is an issue with matching lumen
size while making anastomosis. The proximal bowel will also be edematous which
results in higher rates of anastomotic leak later. (note: if rectal CA, will need
defunctioning anyway)
• Allow completion of staging before op.
2. Advanced metastatic cancer: emergency laparotomy will defer chemotherapy at least 1

month. Emergency surgery will not change prognosis but palliative chemo can prolong survival
-- so it helps to get palliative chemo fast.
However even if I prepare to stent the patient, I will prepare for laparotomy (standby EOT, call
for blood, resuscitate pt) in case stenting is unsuccessful (15%) or there is a complication.
Would you give him bowel prep for colonoscopy?

Sir, my patient is obstructed, I cannot give him bowel prep which will make the obstruction
worse. I do not expect to be able to scope past the obstruction and hence I can make do with
giving the patient fleet enema to clear the distal bowel.
How do you stage him?

• I will stage him according to the T, N, M system.
• CTAP + CT chest or CXR is the first line modality to determine clinical stage. I am
looking at the primary tumor in terms of size and depth of invasion to determine T stage
(T1 = mucosal, T2 = muscularis, T3 = serosa, T4 = locally invasive) and for nodes to
determine N stage (may not be obvious on scan, only confirmed post resection). The
presence of hepatic or lung metastases signifies M1 i.e. stage 4 disease
• I am aware that stage 4 colorectal cancer is potentially still curative, e.g. if there is a
single small live metastasis which can be resected.
• After operation pathological examination of the resection specimen allows
determination of pathological stage, at which point decision on chemotherapy can be
undertaken by a multidisciplinary tumor board.
Would you do CEA levels?

• Sir, I am aware of the utility of CEA levels as a tumor marker, particularly to monitor
for relapse.
• But I would not do CEA for diagnosis.
How would you manage this patient if CT shows -
(a) Descending colon tumor, no obvious nodes, no mets?

• Sir I would want to achieve oncologic resection of the tumour with 5cm margins
proximally and distally
• Likely op is left hemicolectomy
• with lymph node dissection (at least 20 lymph nodes to complete histopathological N
staging)
• and primary anastomosis
• KIV defunctioning ileostomy
• If nodes are positive, patient will require adjuvant chemotherapy
(b) Rectal tumor 8cm from anal verge, no nodes, no mets?

• Neoadjuvant chemoRT (survival benefit - do for all tumors below peritoneal reflection
i.e. <12cm)
• Oncologic resection of the tumour with 5cm proximally and 2cm distally. If the distal
2cm margin does not hit the anal canal (i.e. where the anal spincters are) → sphincter
saving surgery. If the distal 2cm hits the anal canal, then have to sacrifice sphincters
and do APR. Length of anal canal can range 2-5cm from anal verge.
• Sphincter sparing surgery: anterior resection (anastomosis above peritoneal reflection
>12cm) or low anterior resection (anastomosis below peritoneal reflection, 7-12cm),
ultra-low (<7cm)
• With Total Mesorectal Excision (survival benefit)
• Followed by primary anastomosis
• And creation of a defunctioning ileostomy (if low AR)
• Adjuvant chemotherapy if nodes +ve
(c) Rectal tumor 3cm from anal verge, no nodes, no mets?

• Sir, as the tumour is too low to save the sphincter (minimum 2cm distal and 5cm
proximal margins)
• Neoadjuvant chemoradiotherapy
• Abdominal perineal resection with creation of an end-stoma.
• Total mesorectal resection
• If nodes are positive, patient will require adjuvant chemotherapy
(d) Descending colon tumor with solitary liver mets?

• Intent of treatment can still be curative if solitary liver met is resectable.
• E.g. left hemicolectomy with lymph node dissection and primary anastomosis (as in
the case without liver mets)
• Plus resection of liver met.
(e) Multiple liver mets

• Palliative chemotherapy
• If obstructed, endoscopic stenting
• Palliative symptom management
What is the purpose of loop ileostomy?

This is a defunctioning stoma to protect a distal anastomosis, especially for low anterior
resection where blood supply is poorer and anastomotic leak rates are higher. It does not
decrease the incidence of anastomotic leak however it reduces the morbidity of a leak.
Can you please counsel the patient about stoma?

• Indication: Mr Mok, you will be going for an operation to cut out a part of your intestine
and join the other two ends. This joint can sometimes leak and to reduce the severity
of complications, we intend to do a stoma for you
• Procedure: A stoma is when we take out a part of the intestine and connect it to the
skin.
• What it means for patient: You will go home with a bag into which fecal material will
drain. The bag is airtight so there is no smell. You will need to change the bag once it
becomes half full, about 3-4 times a day. This is temporary, about 1-2 months later we
will do a contrast X-ray to make sure the joint has no leak, and then we will put the
intestine we took out back inside your tummy after.
• Site marking: We will choose convenient place to put the stoma, away from your belt
line, belly button, or bone (ASIS); not too near the operation site.
• Risks:
o In the first few days the output may be quite high and you may need top-up
with intravenous fluids, but this usually gets better within the week.
o Sometimes the skin can get a bit irritated but we try to minimise this by
designing the stoma accordingly.
o With time the opening can become a bit weak and the stoma can either sink
inside or drop out more; if it doesn’t interfere with the appliance we do not need
to do anything, if it does then you will need a small operation to adjust the stoma
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A IO: CROHN’S DISEASE
SURGICAL LONG CASES
IO: Crohn’s Disease
PRESENTATION
Sir, my patient Mr Ai Oh is a 60 year old Chinese man with Crohn’s disease with recurrent
admissions for intestinal obstruction and 2 previous small bowel resections in 2002 and 2010,
presenting now with 2 days abdominal pain, abdominal distension and vomiting.
His abdominal pain began in the night after CNY reunion dinner where he had an enormous
helping of mushrooms. It is generalized, colicky, non-radiating. He had 6 episodes of bilious
non-bloody vomiting, and also has abdominal distension. He was still passing small amounts
of stool and flatus at the time.
[Ddx for abdo pain] Otherwise, he has no fever, diarrhoea, jaundice, dysuria/pyuria,
polyuria/polydipsia.
[Ddx for cause of IO] He has no change in bowel habits, decrease in stool calibre, PR bleed,
tenesmus, LOW or LOA in the preceding months.
[Complications of IO] He has not had any sudden worsening of pain and extreme pain on
movement to suggest perforation and peritonitis.
More on his past medical history of Crohn’s:

• He first presented in his 30s with mucous-y diarrhea 20x day, with bloatedness relieved
on passing motion. He was initially labeled as irritable bowel syndrome, however
persistent symptoms prompted an OGD and colonoscopy, and Crohn’s was diagnosed
after biopsy found caseating granulomas.
• Since diagnosis till now he has only had 2 flares, each usually with fever, melena,
intestinal symptoms like his first presentation and raised CRP.
• In between those flares he has grappled with recurrent small bowel IO due to strictures,
averaging about 1-2 admissions a year mostly managed conservatively.
• Thankfully he does not have the other complications of the disease, such as:
o Fistula formation - there have been no enterocutaneous or anal fistulas, nor
any recurrent UTIs, pneumaturia, or fecaluria to suggest rectovesical fistula
o PR bleeding
o And colorectal cancer - last scope 3 months ago did not have any suspicious
lesions or polyps
• I do not note any extra-intestinal manifestations - no joint pain (spondyloarthritis),

tendon pain (enthesitis), eye problems (uveitis), skin rash or ulcers pyoderma
gangrenosum, erythema nodosum), and no oral ulcers.
• In terms of medical management, he is steroid dependant (the two previous flares
happening when attempts were made to wean him off), with steroid induced
hyperglycemia. He also takes daily sulfasalazine and monthly infliximab injections
which he is tolerating well.
• In terms of surgical management, he has had 2 small bowel resections in 2002 and
2010 for IO, complicated by steatorrhea and malnutrition (short gut syndrome). He is
on vitamin supplementation.
He has no family history of inflammatory bowel disease.
And in terms of current functional, social and financial situation, he is single and stays alone,
works as an administrator and has been able to support himself financially. He has a good
understanding of his disease and generally feels he is coping well. He sometimes gets
frustrated about the recurrent IOs but is still grateful that he is ADL-I and community ambulant.
On examination, Mr Ai Oh is alert and comfortable. He has being kept NBM, and has an NG
tube on active suction, and on IV drip. He is thin but not cachectic, no temporalis muscle
wasting. He has no conjunctival pallor or jaundice. He is not clubbed. I note a midline
laparotomy scar and a paramedian scar in keeping with his previous surgeries. His abdomen
is distended, soft and non-tender on palpation, no RIF mass or organomegaly, tympanic on
on percussion, bowel sounds are sluggish but not tinkling. No incisional hernias or inguinal
hernias. No enterocutaneous or perianal fistulas.
In the peripheries, I do not note any joint swelling, red eye, skin ulcers. I do not note any signs
of cushing syndrome
I would like to complete my examination with a digital rectal examination looking for masses
or PR bleed or fistulae.
In summary, Mr Ai Oh is a 60 year old Chinese gentleman with refractory, steroid-dependant

Crohn’s disease who has had recurrent admissions for IO and 2 small bowel resections in
2002 and 2010, presenting once again and symptoms and signs of intestinal obstruction.
QUESTIONS
Why was he initially still passing stool if this is IO?

Sir, in a proximal IO, vomiting occurs early and constipation occurs late; so this presentation
is not inconsistent with distal IO.
What are the possible causes of IO in this patient?

Sir, causes of IO in this patient can be disease related and non-disease related.
• Related to Crohn’s, he could have inflammatory strictures or development of a
colorectal tumour as well as post-op complications such as anastomotic strictures,
adhesions and incisional hernias.
• Unrelated to Crohn’s, he could have bezoars from high fibre food such as Chinese
mushrooms. I looked for but did not find any inguinal hernia.
You are HO on call. What are you going to do?

• FBC UECr PT/PTT GXM
• Erect CXR looking for free air under diaphragm
• Supine AXR looking for intestinal obstruction, and what type
• Barium meal and follow through looking for site of obstruction
• Drip and suck, keep NBM, NGT, IDC in interim.
Please interpret this patient’s AXR.

• Sir, I see dilated bowel with plicae circularis and ‘stack of coins’ appearance located
centrally. This is small bowel obstruction.
• OR Sir, I see dilated large bowel loops located peripherally. There are no dilated small
bowel loops, therefore ileocecal valve is competent. There is no rectal gas. I am
worried about a closed loop obstruction of the large bowel.
What are the indications for surgical management of IO in such a patient?

It is important to aim to avoid surgery until absolutely necessary, as repeated small bowel
resections can lead to short gut syndrome (like what Mr Ai Oh has) which in turn causes
problems like steatorrhea and malnutrition. The indications Mr Ai Oh might have had for bowel
resection include failure of response to medical therapy, closed loop obstruction or impending
perforation, perforation of bowel, long segments of strictures >12cm (be it due to Crohn’s itself
or from the surgical anastomosis). Mr Ai Oh has not had other indications such as fistula or
abscess formation and malignancy.
Let’s say this patient came in with a flare. How would you investigate?
Sir, I would investigate with the aim of (1) confirming diagnosis and ruling out differentials (2)
looking for complications (3) guide management
I will start with basic investigations such as:

• FBC looking at raised total whites and Hb for anemia
• RP looking at hypokalemia and dehydration from prolonged diarrhea
• ESR, CRP for disease activity
• LFT for hypoalbuminemia due to poor nutritional intake and also as baseline before
initiation of therapy
• Stool cultures and ova cysts parasites
• Fecal elastase, fecal calprotectin
Then I will bowel prep patient and prepare for colonoscopy and OGD
Lastly, can do TB spot and hepatitis screen (TRO TB, hepatitis before initiation of steroids or
immunotherapy)
How else would you manage the patient?

Refer to gastroenterologist for optimization of his medical therapy. Our patient Mr Ai Oh has
refractory disease, as he is unable to be weaned off corticosteroids. This is the reason why
he is on monthly infliximab injections, in addition to sulfasalazine and corticosteroids at the
moment. (Refer to medical case > IBD)
OK how about surgically, how would you follow up Mr Ai Oh when he sees you in clinic?
Mr Ai Oh is at elevated risk of colorectal malignancy and therefore needs surveillance
colonoscopy. Recommendations differ but MOH recommends for pancolitis, to begin scopes
8 years after onset of symptoms and thereafter every 1-2 years.
How does Ulcerative Colitis differ from Crohn’s disease?

In ulcerative colitis, there is superficial inflammation and ulceration limited to mucosa of the
large bowel, It always involves the rectum but may extend in a proximal and continuous
fashion to involve other portions of the colon and occasionally even the terminal ileum
(backwash ileitis). In Crohn’s, there is transmural inflammation with deep ulceration, fistula
and abscess formation. It occurs throughout the GIT from mouth to anus but in skip lesions
with normal mucosa in between, and typically spares the rectum.
On endoscopy, Crohn’s has a cobblestone appearance with deep ulcers and fissures whereas
ulcerative colitis has shallow ulcers, pseudo-polyps and mucosal bridges.
Medical therapy for UC, like Crohns, consist of 5-ASA, glucocorticoids, immunomodulators
like azathioprine and biologic/immunotherapy like infliximab.
Surgical Management of UC:

• Emergent Indications
o Acute fulminant colitis with acute abdomen Toxic megacolon (colon > 5.5cm)
o Impending Perforation (i.e. dilatation with thumb-printing or pneumatosis) or
o Free/walled off perforation
o Acute fulminant colitis without acute abdomen unremitting bloody diarrhoea
→ Total colectomy + end ileostomy
• Elective Indications
o Disease refractory to medical therapy with severe & extensive colitis (most
common)
o Serious complications of medical therapy
o Malignancy – precancerous lesions or prophylactic risk reduction
o Debilitating extra-intestinal manifestation – i.e. thromboembolic complications
→ Proctocolectomy + ileal pouch anal anastomosis
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A JAUNDICE, PAINFUL: CHOLANGITIS
SURGICAL LONG CASES
Jaundice, Painful: Cholangitis
PRESENTATION
HLD. She now presents with 2 day hx of fever, jaundice and right hypochondrium pain.
This started 2 days ago with sudden onset right hypochondrium pain, sharp and constant, not
radiating to back or shoulder and not better sitting forward. She also had jaundice, tea coloured
urine, and lightening of stool colour. Her fever started the next day with Tmax of 38.0, chills
and rigors. She has also had 4 episodes of non-bilious non bloody vomiting.
In terms of etiology,
• [Gallstone disease] I note that she has longstanding post-meal dyspepsia but has
never been investigated with ultrasound or OGD.
• [Malignant] There is no loss of weight...
• [Stricture] … and no past ERCP (past - stricture, recent - iatrogenic).
• [Metabolic cause of gallstone] She does not have any chronic hemolytic anaemia (e.g.
thalassaemia) or mechanical heart valve replacement.
In terms of differentials, I note that she has had raw oysters last week and has not been
vaccinated against viral hepatitis. She is in a stable monogamous relationship, has no hx of
IV drug abuse, and has never received blood products from outside singapore.
Other than DM HTN and HLD, all of which are well controlled on medications, she does not
have any other past medical or surgical history. She has no known drug allergies.
Socially, she stays with her husband and children in a HDB flat, works as a business executive
and is financially well to do.
On examination, Mdm Liew is alert, comfortable. She is currently receiving IV fluids as well as
IV ceftriaxone and metronidazole. She has scleral icterus but no conjunctival pallor. Her urine
bag is draining tea coloured urine. Abdomen was not distended. There is tenderness and
guarding over the right hypochondrium. Otherwise the rest of the abdomen is soft and non-
tender, no signs of rebound or guarding. Murphy’s was negative. There was no organomegaly.
Bowel sounds were present. Cough impulse over bilateral groins were negative. Breath
sounds were clear and equal bilaterally. Heart sounds were dual, no murmurs, pulse was
regular at 95. I would like to complete my examination by doing a digital rectal examination
looking for PR bleed or melena.
In summary, this is a 50 year old Chinese lady presenting with 2 days of fever, jaundice and
right hypochondrial pain on a background of dyspepsia. My top differential is acute cholangitis,
but I would like to consider hepatic abscess, acute cholecystitis, acute hepatitis, and acute
pancreatitis.
QUESTIONS

Sir, I need to investigate to confirm my diagnosis, rule out differentials and find the etiology.
Initial bloods include

• FBC for raised TW
• LFT for cholestatic picture of raised LFT in cholangitis; hepatocellular picture if
hepatitis.
• UECr for prerenal AKI since patient has been vomiting / to guide fluid therapy
• Blood cultures
• CRP, procalcitonin
For differentials, I will do

• Amylase, lipase to look for concomitant pancreatitis (if present, to do full glasgow
bloods).
• Hepatitis viral serologies for viral hepatitis
Imaging modalities include

• US HBs for dilated CBD, evidence of gallstone disease
• CT abdomen for the same especially overnight where US cannot be easily obtained.

Sir, cholangitis is a surgical emergency. I would see the patient immediately and escalate to
my senior. My goals are to (1) Resuscitate the patient, (2) Initial investigations to confirm dx,
rule out ddx, look for etiology, (3) Initiate medical therapy, (4) Send patient for emergent
decompression, (5) Treat underlying condition.
(1) Resus
A Assess airway
C Take vitals
2 large bore IV plugs
Aggressive fluids as I expect the patient to turn septic - 2 pint normal saline fast
Keep NBM
Insert IDC
Transfer HD/ICU
Chart: strict I/O, Q1h paras + SpO2
(2) Confirm diagnosis and rule out differentials

As discussed above.
(3) Initiate treatment

Empiric IV antibiotics with gram negative and anaerobic coverage - 3rd gen
cephalosporin like ceftriaxone, and metronidazole (alternative: augmentin plus
gentamicin/amikacin, plus metronidazole).
(4) Send patient for emergent decompression of the biliary system

Either by ERCP and stenting (or stone retrieval with sphincterotomy) or PTC
(5) Treat underlying cause (definitive treatment)

If ERCP → Early cholecystectomy
If PTC → ERCP → Cholecystectomy OR
If PTC → cholecystectomy with intra-op cholangiogram, CBD exploration and T tube
What is a normal ERCP?

• Normal intrahepatic ducts
• Smooth CBD
• No narrowing of the CBD
• No filling defects
• Free flow of contrast into duodenum
What are the contraindications to ERCP and what is the alternative?

• Patient is too sick for ERCP (cannot be put in prone position, not fit for anesthesia)
• Abnormal anatomy (previous gastrectomy, bilroth, roux-en-y, etc)
• Coagulopathic → can opt for stenting, forgo sphincterotomy
• Previously failed ERCP (relative)
The alternative is percutaneous transhepatic biliary drainage.
In the context of definitive stone removal after PTC, what are the indications for
operative removal of stone (instead of ERCP)?
• Stone >25mm
• Intrahepatic stone
• Large number of stones
• Impacted stone
• Dual pathology
• Tortuous duct
• Previous Billroth II (unsuitable anatomy for ERCP)
Please counsel Mdm Liew on ERCP.

Mdm Liew, I am Dr Tsang. I’m going to explain to you (1) your current condition (indication)
(2) What is a ERCP and why we recommend it (3) risks and complications of ERCP (4) risk of
not going for ERCP and alternative. Do you have any other questions or concerns you would
like me to address along the way? If not, still feel free to stop me any time along the way to
clarify anything you don’t understand.
*I recommend drawing the HBS system in this case!

You have stones in your gallbladder, and one has dropped out into the bile duct. This
stone is blocking flow of bile from the liver to the intestine. The blockage has caused
infection → this is called cholangitis. Cholangitis is not something we can take lightly,
because the bacteria can spread everywhere in your body and you can become very
sick very quickly. Therefore it is very important that we take out the stone and relieve
the obstruction, as well as treat the infection with antibiotics.
(2) ERCP
Removal of the stone is commonly done through ERCP, which stands for a very long
name - “Endoscopic retrograde cholangiopancreatigogram”. First we give you sedation
so that you don’t feel any pain. Then we put a camera through your mouth into your
intestine. From there, we either remove the stone, or put a stent so that bile can flow.

(a) Risk from sedation
You have to be very closely monitored during the procedure.
Perforation of bowel
Bleeding, esp from sphincterotomy
Infection
Pancreatitis
Failure of ERCP

The alternative method to relieve the obstruction is percutaneous transhepatic
cholangiography. This is where we insert a tube through the skin and through the liver
into the bile duct to allow the infected bile to drain out. However this is just a temporary
measure as it cannot remove the stone. This still has to be followed up by an ERCP or
an operation to remove clear the stone from the bile duct + remove the gallbladder at
the same time.
The last option is to not do anything, but the risk of that is the infection will spread to
your whole body and can lead to death.
Please counsel Mdm Liew on cholecystectomy.

Refer to Acute Pancreatitis
Mdm Liew is very worried about whether this could be pancreatic cancer. She heard
that you can do a blood test tumor marker to tell her if it is so. What do you say?
CA19-9 is a tumor marker for pancreatic cancer but it is also elevated in other diseases of the
biliary tree such as cholangitis, gallstones. It is not specific and can be elevated in other
cancers (gallbladder, cholangioCA); so it is generally unwise to do CA 19-9 in the setting of
acute cholangitis.
Suppose Mdm Liew goes for the cholecystectomy but comes back again 3 months later
with cholangitis once. US HBS shows stones in the CBD. What are you suspecting?
Recurrent pyogenic cholangitis
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A JAUNDICE, PAINLESS: PANCREAS CA
SURGICAL LONG CASES
Jaundice, Painless: Pancreas CA
PRESENTATION
Sir, my patient Mr Huang is a 68 year old Chinese gentleman who presents with 1 month of
painless progressive jaundice and significant loss of weight.
In terms of of his jaundice, his relatives first noticed that he was yellow 1 month ago, during
Chinese New Year visitations. This was not associated with any abdominal pain. He has
noticed tea-coloured urine and lightening of stool colour, and also complains of pruritus. There
is clinically significant weight loss of 10kg over 3 months. [Cx] There is no steatorrhoea or new
onset polyuria/polydipsia (DM)
[Ddx / etio]
• He does not have fever or right hypochondrial pain to suggest cholangitis.
• He has never had post-meal dyspepsia or known gallstone disease.
• He has no previous instrumentation to the biliary tree, and no stay overseas in a rural
country to suggest strictures.
• I also considered hepatic causes of jaundice, however he does not have any known
chronic liver disease, chronic hepatitis, no IV drug use, alcoholism, or high risk sexual
exposure.
In terms of family history, he has no family history of periampullary, biliary tree, or gastric
cancer.
His other past medical history includes well-controlled DM, HLD, and IHD on aspirin. He also
has L4/5 disk disease and BPH. He has no past surgeries and no known drug allergies.
Socially, he is a retiree who stays with wife and children. He is comfortable financially. He
does not smoke or drink and is ADL-independent and community ambulant.
On examination, Mr Huang was alert and comfortable. He appears slightly cachectic with
wasting of temporalis muscle and intrinsic hand muscles. I note that he is jaundiced and has
scleral icterus. There are no stigmata of chronic liver disease such as clubbing, palmar
erythema, asterixes, loss of axillary hair, or telangiectasia. On examination of the abdomen,
there were no surgical scars, distension, or herniae. It was soft non tender. There was a
palpable gallbladder. I say that it is a gallbladder because it is a globular shaped right
hypochondrial mass, dull to percussion, moves inferiorly with respiration, and I cannot get
above it. There was no other organomegaly and no shifting dullness. I looked for but did not
find cervical or supraclavicular lymphadenopathy. I would like to complete my examination by

performing digital rectal examination to look for stool colour.
In summary, Mr Huang is a 68 year old Chinese gentleman who presents with painless
progressive jaundice, palpable gallbladder, and significant loss of weight.
QUESTIONS
What are your differential diagnoses?

• My first diagnosis is a periampullary cancer e.g. head of pancreas, ampulla of vater,
or distal CBD.
• Differential diagnosis is gallstone disease but this is less likely given lack of pain or
fatty dyspepsia.
• I also considered hepatic causes of jaundice such as decompensated cirrhosis or
hepatitis however these were less likely.
• Other causes of obstructive jaundice include strictures and extrinsic compression by
porta hepatis lymph node
What is Courvoisier’s law? What are the exceptions?

Courvoisier’s law states that jaundice in the presence of a palpable gallbladder is unlikely to
be due to stones. This is because the gallbladder with stones is likely to be chronically fibrosed
and shrunken. Exceptions include Mirizzi’s syndrome (stones impacted in hartmann’s pouch
of cystic duct compress on the common hepatic duct), primary ductal stone formation
(recurrent pyogenic cholangitis), mucocele formation.
How would you investigate this patient?

For this patient, my goals are to (1) establish the diagnosis, (2) consider ddx.
I will start with blood investigations including

• LFT - for cholestatic pattern of derangement, albumin for nutrition state
• FBC - Hb (anaemia), Plt (thrombocytopenia), TW (cholangitis)
• UECr - as contrast studies will be done
• PT/PTT - measure hepatic function
• Glucose - measure hepatic function
• Tumor markers i.e. CA 19-9
I understand is that US HBS is the usual first line investigation for obstructive jaundice, but as
my suspicion for CA is high, I would like to go straight for a contrasted CT abdomen looking
for dilated biliary ducts, double duct sign, causes of obstruction, local invasion of the superior
mesenteric vein or artery, regional spread to para-aortic lymph nodes or distant spread. This
is usually followed up by a more detailed imaging scan such as CT or MRI pancreas to further
delineate anatomy. Patient would also need a CT thorax for staging.
Whether to biopsy the lesion for histological confirmation depends on the index of suspicion
for malignancy, surgeon and patient preference (generally no need unless uncertain of dx,
patient unwilling to accept risk of negative whipples - if do, use endoscopic ultrasound guided).
Would you relieve the obstructive jaundice in this patient?

Sir, I would not relieve the obstruction in this patient. He is not cholangitic and does not have
severe symptoms of coagulopathy, encephalopathy, or pruritus. I am aware that tumor
obstruction is usually sterile and stenting may cause contamination and make subsequent
tissue dissection more difficult. However if he develops cholangitis then definitely he requires
a drain.
Can you read this CTAP

Sir there is a large mass in the head of pancreas not involving SMA or SMV. I see a double
duct sign with enlarged gallbladder. I do not note any lesions in the liver and there is no ascites.
I do not note obvious para aortic nodes. The liver does not appear cirrhotic. There are no other
metastasis to the liver, lung or peritoneum.
OK so given his CTAP how will you manage?

Sir, my patient is fit and his tumor is resectable. I want to offer curative therapy yet knowing
that 5-year survival after Whipple’s is around 10%. I will discuss him at a multidisciplinary
tumor board with a view towards Whipple’s procedure and adjuvant chemotherapy. Prior to
surgery I will optimise his nutritional state.
General principles
• Resectable = no SMA invasion, no paraaortic lymph nodes involvement, no mets.
(SMV is resectable but difficult). 80% of patients are not suitable for curative resection.
• If resectable, Whipple’s then adjuvant chemotherapy
• Unresectable or distant mets or unfit:
o Relieve GOO: stenting
o Relieve obstructive jaundice: stenting vs feeding jejunostomy
o Nutrition support, enzyme replacement for steatorrhoea
o Surgical triple bypass (gastrojejunostomy, hepatojejunostomy,
jejunojejunostomy) is an option to relieve both GOO and obstructive jaundince,
but is now not commonly done due to the advancement of endoscopic stenting
technique.
OK a Whipple’s performed and the tissue is sent for histology. What are the possible
types of periampullary cancer?
Sir, the periampullary cancers include carcinoma of head of pancreas, ampulla of vater, and
distal cholangiocarcinoma. All can present as obstructive jaundice.
How about a body or tail of pancreas tumor? How will this present?
Sir, a body or tail of pancreas tumor does not cause obstructive jaundice. It often presents late
as back pain, mass, loss of weight, incidental finding on CT scan, new-onset diabetes, or
paraneoplastic manifestations (e.g. migratory thrombophlebitis).
Tell me about cholangiocarcinoma.

Cholangiocarcinoma arise from the bile duct and may be intrahepatic, Klatskin, or distal CBD.
Distal tumors may cause obstructive jaundice but intrahepatic tumors do not, presenting
instead with vague symptoms of RHC discomfort, hepatomegaly, and weight loss. ALP +/-
bilirubin may be raised. Patients with primary sclerosing cholangitis are at particular risk.
Diagnosis is via MRCP for proximal lesions and EUS for distal lesions, and the task in
intrahepatic lesions is to distinguish from HCC.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A LEG PAIN: CLAUDICATION, CRITICAL LIMB
SURGICAL LONG CASES
Leg Pain: Claudication, Critical Limb
PRESENTATION
Mdm Tan is a 66 year old known vasculopath with claudication status post arterial bypass.
She now presents with rest pain and tissue loss of her left lower limb for 2 weeks duration.
With regards to her known peripheral vascular disease, she was first seen by a vascular
surgeon 2 years ago. At that time she had a 2-year history of claudication symptoms, worse
on exertion, worse walking uphill than downhill, with no back pain or change with spine flexion
or extension. Her function then was good and claudication was not disabling. She was
managed conservatively for a year with risk factor control and exercise.
Over that year, however, her claudication distance decreased from 2 bus stops to barely 100
meters which severely affected function. Pain was worse on the right than on the left. She
underwent balloon angioplasty followed by arterial bypass to the right lower limb, with
significant symptomatic improvement and good function.
In the past 2 weeks, however, her claudication distance has fallen from 1.5 bus stops to 0.5
bus stops and she has experienced symptoms of critical limb ischaemia. She complains of
rest pain over the dorsum of bilateral feet and lateral aspect of calf, severe enough to wake
her up, however pain was not better when leg put in a dependent position. She also noted a
new ulcer over the back of her left heel, which was dry, no discharge, no fever. She also has
paresthesia over L LL over the past 3-4 months, with no weakness.
Since admission she has undergone balloon angioplasty to her left lower limb, with significant
improvement to pain.
In terms of vascular risk factors, I note that she has a longstanding history of diabetes mellitus,
hypertension, and hyperlipidaemia. She is maintained on increasing doses of oral medications
which she appears to be unfamiliar with and poorly compliant to. She does not know her
HbA1c or home glucose and blood pressure readings. In terms of vascular complications, she
has had a myocardial infarction 3 years ago, status post percutaneous coronary intervention.
She does not know her 2DE findings. I do not note any renal disease or cerebrovascular
disease. Her medications include aspirin, oral hypoglycaemics, antihypertensives, and statins
which she is unable to provide me the names of. She does not smoke.
In terms of function, she stopped working due to her vascular claudication symptoms a few
years ago. She is however still ADL independent and community ambulant with a walking
stick, until these two weeks.
Social wise, she is a widower who stays with the oldest of four children. Social and financial
support is good from 4 children.
On examination, Mdm Tan was comfortable and alert. On inspection I noted a 4cm x 4cm
round ulcer with gangrenous edges and visible extensor tendon over the back of her left heel.
This was clean with no discharge and no surrounding erythema. Bilaterally there were multiple
healed scars and arterial skin changes such as shiny hairless skin in both lower limbs. On
palpation, the R LL was colder than L LL below the knee. Capillary refill time in R LL was 3s,
and <2s in the L LL. DP, PT, popliteal, femoral pulses all felt bilaterally. Buerger’s test was
negative. There were no varicose veins and no loss of pinprick sensation bilaterally.
Dressing over the right femoral access site was dry, no hematoma. I looked for but did not find
any AAA. Cardiovascular examination found first and second heart sounds with ejection
systolic murmur over aortic region radiating to the carotids. I would like to complete my
examination by measuring her blood pressure and ankle brachial pressure index.
In summary, Madam Tan is a 66 year old vasculopath currently admitted for L LL critical limb
ischemia status post balloon angioplasty.
QUESTIONS
What are your initial investigations?

Sir, I need to investigate to (1) confirm arterial disease, (2) look for complications, and (3) plan
for surgical intervention
I would start off with the following basic blood investigations:

• Full blood count, looking at whether her total white count is raised which may suggest
infection of her heel wound, and also at her platelet count as she is going for an
invasive intervention
• Renal panel, with an eye on the Cr especially knowing she is likely going to need
contrast
• Pre-operative investigations: PT/PTT, CXR, ECG, 2DE
• Risk factors: HbA1c, fasting glucose, fasting lipids, if none were done recently
To confirm arterial disease, I will like to do

• Ankle brachial pressure index as very basic assessment to confirm critical limb
ischaemia and also a reference point to compare post-op and quantify improvement.
• Ultrasound duplex of her lower limb arterial system to trace the arterial anatomy, look
for stenosis, look at flow velocity and pattern i.e. monophasic/biphasic/triphasic, as
well as to plan for angiography.
Her ulcer is clinically not infected at present and therefore I will withhold workup for infection
i.e. wound swab and culture, foot X ray (to exclude OM), CRP and blood cultures.
How do you interpret the ABPI?

• Normal ABI is > 0.9 (can be > 1.0 as ankle pressures tend to be higher than brachial)
• ABI between 0.5 - 0.9 – occlusion, often associated with claudication
• ABI <0.5: Critical limb ischaemia
• If >1.40, suggests non-compressible calcified vessel esp. seen in DM patients
→ Do Toe pressures index (TPI) instead (an abnormal TBI is <0.70)
How would you manage Mdm Tan?

Sir Mdm Tan has critical limb ischaemia. My goals are to (1) revascularize, (2) modify risk
factors, and (3) rehabilitate.
I would counsel for surgical management to her left lower limb (her previous bypass was to
the right limb). Look at the scans (inflow i.e. aortoiliac, outflow i.e. femoral, and runoff i.e.
below knee) and decide, for example reasonable answers are-
• She has a short focal segment of stenosis which is amenable to endovascular
intervention such as angioplasty +/- stenting. However I think her life expectancy likely
exceeds 2 years and hence I will suggest bypass surgery as the initial treatment
because of better long-term outcomes in spite of higher immediate morbidity (BASIL
study).
• She has extensive disease with long segment stenosis but has good runoff vessels, I
would opt for femoral-popliteal bypass grafting.
• She has inflow (aortoiliac) disease and hence my first task will be to do aortobifemoral
bypass.
In terms of risk factor control I believe that this patient needs multidisciplinary care with medical
colleagues such as a cardiologist and endocrinologist, as well as allied health professionals
like a dietitian. It is important to optimise blood pressure, lipids, and glucose control, as well
as to treat her comorbids.
After surgery I will send her for rehabilitation with supervised exercise to maximise function. I
will also maintain her on an antiplatelet e.g. aspirin 100mg or clopidogrel 75mg (? role for
medications such as cilastazol, a type III PDE inhibitor which inhibits platelet aggregation and
causes vasodilatation). I will emphasize compliance to therapy otherwise she is sure to
restenose and get critical limb ischaemia again!
While awaiting surgery what will you do?

• Give analgesia
• Optimise diabetes and blood pressure control in the ward
• Give high dose statin if not already on.
• Start aspirin - recommend to continue during perioperative period.
If she refuses surgery what is her prognosis?

At one year, there is a 50% chance she is alive with two legs, 25% chance of one leg
amputated, and 25% chance of death due to cardiovascular disease.
When will you amputate?

Sir I will amputate if the limb is
• Dead (ischemic): peripheral vascular disease (80-90% of all cases)
• Damaged (trauma): unsalvageable limb, burns
• Dangerous: Gangrene, ascending sepsis, malignancy (soft tissue / bone)
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A LEG PAIN: VENOUS INSUFFICIENCY
SURGICAL LONG CASES
Leg Pain: Venous Insufficiency
PRESENTATION
Mdm Latifah is a 49 year old Malay lady with bilateral leg swelling and discomfort at the end
of each day, and a nonhealing right leg ulcer which has become infected in the past week. If I
may discuss each of her complaints in turn -
She gives a chronic history of bilateral leg swelling and discomfort of two years duration. This
is not present when she wakes up each morning, occurring only at the end of each day,
especially on work days where she stands for long hours as a McDonalds counter staff.
Discomfort is mild and aching in nature; there is no pain radiating from the back to her legs,
and no exacerbation of discomfort on walking. Swelling and discomfort is relieved when she
gets home and props her legs up to watch TV. She has also tried wearing stockings with mild
relief.
Moving on to her ulcer, in the last 3 months she developed an ulcer just above the medial
malleolus on her right leg, which has not healed since then. This is the first ulcer she has ever
had. It was associated with bilateral varicosities which Mdm Latifah has noticed for a year.
The ulcer was initially painless and did not bother my patient. She has attempted to apply
some powder provided by a traditional medicine physician without success. However in the
past week she has developed a low-grade fever, and has noted a foul smelling discharge from
the ulcer which stains her stockings.
I looked for the presence of concomitant arterial disease and note that Mdm Latifah has no
symptoms of vascular claudication or tissue loss. She is however a vasculopath with poorly
controlled diabetes of HbA1c 8.8%, hypertension, and hyperlipidemia. She is also morbidly
obese. I note that she is on glipizide, metformin, nifedipine, as well as a statin; she is however
poorly compliant to her medications.
In terms of other contributory factors to bilateral lower limb edema, I note that she is on
nifedipine which can contribute to pedal edema. Otherwise there was no history of cardiac or
renal or liver disease, and systemic review found no shortness of breath on exertion, angina
symptoms, frothy urine, and no heat or cold intolerance to suggest thyroid disease.
She also does not have any prior episodes of deep vein thrombosis. Apart from what I have
mentioned there is no other past medical history or drugs or drug allergy. There is no family
history of varicose veins.
Socially, she is married with five children, and stays in a HDB flat on a lift landing floor with
her husband and children. She is still able to work in McDonalds but the discomfort at the end
of the shift troubles her. She has attempted to lose weight unsuccessfully, and enjoys staff
meal and unlimited coke provided by McDonalds at least 2 meals a day. She does not smoke
or drink. She is coping alright financially.
Examination found a pleasant Malay lady, alert and comfortable at rest, quite obese. On
inspection of the lower limb, there was a 4cm x 3cm ulcer on the gaiter region of the right leg
which appeared shallow, with well defined edges, a base with slough, and a weeping yellow
discharge. There are no heaped edges or fleshy appearance to suggest Marjolin’s ulcer.
I note bilateral venous skin changes of hyperpigmentation and lipodermatosclerosis, as well

as bilateral varicosities in the great saphenous vein distribution. Tourniquet test found that
there is incompetence distal to the saphenofemoral junction. Lower limb pulses were well felt
and capillary refill time was less than 2 seconds. On palpation of the abdomen there was no
pelvic mass.
In summary, my patient is a 49 year old Malay lady with bilateral chronic venous insufficiency
complicated by infected venous ulcer. I do not note any evidence of concomittant arterial
disease.
QUESTIONS
What CEAP grade is she?

Sir, she has an active ulcer so she is CEAP 6.
What are this patient’s risk factors for venous ulcer?

• Long periods of standing
• Obesity
• Multiparity
How do you distinguish venous vs an arterial ulcer?

See Approaches to Symptoms of Disease
What investigations will you order?

Sir, my goal will be to (1) guide treatment of infection, (2) diagnose venous disease, (3)
exclude arterial disease.
(1) FBC, CRP, blood and wound c/s. (If can see bone, Xray)
(2-3) ABPI, arterial duplex and venous duplex ultrasound.
OK you confirm pure venous disease. how will you manage her?
Sir, in the acute setting my priority is to treat infection and to relieve venous hypertension. In
terms of treating infection, I would start antibiotics, initially broad spectrum then culture guided.
I will also give wound care and analgesia.
To relieve her venous hypertension and aid wound healing, I will give four layer compression
bandage after excluding arterial disease (very important - if resting arterial pressure is systolic
75mmHg and the compression bandaging exerts 25-30mmHg, you are going to make the
patient 45mmHg i.e. tip the patient over into critical limb ischemia).
I may also offer her surgery for underlying venous insufficiency, I know that this does not
accelerate ulcer healing but reduces recurrence (ESCHAR study). Surgical options include
endovenous radiofrequency ablation or traditional open surgery (high tie, stripping, and
avulsion). Thereafter she will need stockings for life.
Say this patient was lost to follow up and came back to you 3 years later. The ulcer is
now bigger and more fleshy. What would you do?
Sir, in a long standing non-healing ulcer I would be wary of Marjolin’s ulcer i.e. malignant
transformation into sqamous celll carcinoma. I would need to take a biopsy of the edge of the
ulcer.
A more detailed discussion is found under venous short case as veins appear more commonly
as short cases.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A LUTS: BPH & PROSTATE CANCER
SURGICAL LONG CASES
LUTS: BPH & Prostate Cancer
PRESENTATION
Sir, my patient Mr Pang is a 63 year old Chinese gentleman who presents with 2 days of fever,
dysuria, frequency, and later acute urinary retention, on a background of a few months of
voiding type lower urinary tract symptoms.
In terms of his acute presentation, in the last 2 days he has been passing small amounts of
urine q15minutes, with urgency and dysuria, even throughout the night. In the 6 hours before
he came to the A&E, he was not able to pass urine and developed suprapubic tenderness. At
A&E he was noted to be febrile at 38.5 degrees. There was no pyuria or hematuria, back or
loin pain. There is no painful ejaculation to suggest prostatitis.
He has a background of voiding type of lower urinary tract symptoms for 5 months. This is
mainly poor and intermittent flow but otherwise no hesitancy or sensation of incomplete
voiding or double voiding, and no storage symptoms such as frequency, urgency and nocturia.
GP started alpha blockers, to some effect. He has not had any side effects such as postural
giddiness.
Other than BPH, he does not have other risk factors for urinary tract infection such as kidney
or bladder stones, or known congenital abnormalities of the urinary system. He is in a stable
monogamous relationship and I do not note any high risk sexual exposure.
I do not note any other possible precipitants of acute urinary retention such as constipation,
new medications, neurological disease, painful ejaculation (prostatitis) or recent
instrumentation to the urinary tract.
A second issue is that the GP found that he had high prostate specific antigen, but Mr Pang
has not decided whether to biopsy. There are no red flags such as painless gross hematuria,
loss of weight or appetite, shortness of breath, bone pain or back pain, or neurological
symptoms. He does not have a family history of prostate cancer.
He has no other medical or surgical history, the only long term medications he is on are for
his BPH, and he has no drug allergies.
In terms of social, functional and financial history,

• He stays with wife and children
• Is still actively working in company as engineer, no functional impairment
• Financially good
• Not smoker not drinker.
On examination, Mr Pang was alert and comfortable. Currently receiving IV antibiotics and on
indwelling catheter draining small amounts of clear yellow urine. On examination of the
abdomen, there are no scars, no hernias, no organomegaly, no palpable/percussible bladder.
Renal punch was negative.
Digital rectal examination revealed an enlarged prostate of 3 finger breadths. This was
smooth, symmetrical, firm and not nodular. I could feel the median sulcus and the rectal
mucosa was smooth mobile over the prostate. Prostate was non-tender, no boggy areas felt.
Stool in the rectum was soft and not impacted. Anal tone was intact.
There was no tenderness on percussion of the spine or any decreased breath sounds. There
was no conjunctival pallor or pitting pedal edema to suggest chronic kidney impairment and
there there was no cough impulse over both groins (hernia).
In summary, Mr Pang is a 63 year old Chinese gentleman. His issues are

1. Cystitis precipitating acute urinary retention, now stable post catheterization and
receiving IV antibiotics
2. Background benign prostatic hyperplasia on alpha blockers
3. Elevated PSA for investigation.
QUESTIONS
What is the difference between voiding and storage symptoms, which does he have?
• His chronic history sounds like mainly voiding symptoms (hesitancy, slow stream,
intermittency, straining to void, double micturition, terminal dribble) → this is
characteristic of BPH.
• In the last two days he has developed new storage symptoms (urgency, frequency)
with dysuria → due to UTI
• Most recently his ARU is the ultimate voiding symptom.
Tell me about his UTI. Is this upper or lower; what ddx do you have?
• More likely lower UTI due to the storage symptoms.
• No features of upper UTI such as loin pain, renal punch negative, or septic shock (note:
fever does not equal upper UTI, severe cystitis can have fever too).
• Ddx is prostatitis - also dysuria + fever +/- ARU. Key points are pain on ejaculation,
and on DRE, tender prostate +/- bogginess (abscess)
What are some other predisposing factors to UTI?

Sexually transmitted diseases, recent instrumentation of urethra, urolithiasis/cystolithiasis,
structural abnormalities of the collecting system
What are the possible precipitants of acute urinary retention?

Causes can be divided into structural and functional.
Structural causes include:
• Intraluminal causes such as stones, blood clots and foreign bodies
• Luminal causes include tumour of bladder neck, urethritis (UTI), urethral strictures
• Extra luminal causes include BPH, prostate CA (less common as usually peripheral),
constipation, pelvic masses, pregnancy, UV or rectal prolapse
Functional causes include
• Infection e.g. prostatitis
• Neurological causes, which can be further divided into
o Central nervous systems pathologies like stroke, parkinson’s, hydrocephalus,
spinal cord injuries or lesions
o Peripheral nervous system pathologies like DM autonomic neuropathy
• Medications such as anticholinergics, antihistamines, some analgesics esp opioids,
anti-parkinsonian drugs, anti-depressants/anti-psychotics
• Post-op, post-anesthesia, pain and trauma
You are the HO on call, what will you do for this patient?
Sir, Mr Pang must be in a lot of discomfort from ARU; I will see to him as soon as possible.
• First I will assess his ABC and resuscitate accordingly.
• I will quickly insert a urinary catheter under aseptic technique which I expect to relieve
his discomfort from acute urinary retention; I will also collect a urine sample and send
for UFEME, gram stain, and urine culture - looking for pyuria and for microbiological
diagnosis so that I can treat him better
• I will also set an IV plug and send off a septic workup which includes FBC for total
white, CRP, blood cultures. I also want UECr looking for obstructive nephropathy
• I will do X ray KUB looking for stones.
• I will start empiric antibiotics for community acquired UTI, for example augmentin plus
a dose of gentamicin, aiming for 7 days, to adjust based on culture and sensitivity.
His BPH will also need to be worked up later.

I would not do PSA in acute setting especially with ARU and catheterization (see later)
You have trouble catheterizing the patient. What do you do?

• Upsize the catheter
• Call urologist - bedside cystoscopy and insertion of catheter under direct vision
• Suprapubic catheterization (not really done anymore with the advent of bedside
cystoscopy)
It is now the next morning; Mr Pang is now asking what to do about his BPH. What are
some ddx you must consider before concluding it is BPH?
• Stricture → past hx of STD, urethral discharge, instrumentation
• Neurogenic bladder → any neurologic disease, lax anal tone, lower limb weakness or
numbness
• CA prostate or bladder neck → ensure no painless hematuria, loss of weight, prostate
normal on DRE; can do PSA to screen.
• Drugs
How would you manage his BPH?

I will like to confirm my diagnosis by doing uroflowmetry, expecting peak flow rate <15ml/s;
and doing ultrasound bladder for increased post-void residual volume and intravesical
prostatic protrusion. I will also do screening PSA (also do UFEME and Cr - already done in
this case). I can also do IPSS (international prostate symptoms scale) scoring to find out how
badly it is affecting him.
In view that he has had an episode of ARU despite being on alpha blockers, and knowing that
such patients are high risk for recurrence of ARU, I am keen to offer surgery i.e. transurethral
resection of prostate. An alternative is combination medical therapy with alpha blockers and
5-alpha reductase inhibitors, but the latter takes 3-6 months to work. I must also make sure
that all drugs that predispose to ARU are taken off
Overview of treatment for BPH -

• Non-medical: avoid diuretics, caffeine, alcohol; reduce fluids after dinner
• Medical
o For most patients, start with alpha blockers (tamsulosin, alfuzosin); counsel on
hypotension, try to take at night.
o Switch to 5-alpha reductase inhibitors (finasteride, dutasteride) if not tolerating
(e.g. hypotension)
o If not effective enough: combination alpha blocker + 5-alpha reductase inhibitor
• Surgical: transurethral resection of prostate
o For patients who fail medical therapy, develop complications (repeated ARU,
UTI, hydronephrosis, obstructive uropathy, bladder stones)
o Risks: TURP syndrome (less with bipolar TURP, no need to use glycine for
irrigation), retrograde ejaculation, incontinence, recurrence, structure.
Mr Pang prefers to continue with medical management for now. He asks about his high
PSA - would you repeat his PSA now? What are the causes of high PSA?
• PSA can be falsely elevated as it is organ specific but not disease specific.
• Other than prostate cancer, it can also be elevated in BPH, prostatitis, UTI, ARU, and
recent instrumentation of the urethra (including catheterization), recent TRUS biopsy,
or even DRE!
• Therefore I would not repeat PSA this admission as it is likely to be falsely elevated.
How do you distinguish BPH vs Prostate CA?

• DRE: nodular, hard, asymmetrical prostate, obliteration of median sulcus, rectal
mucosa fixed down to prostate
• PSA level (Prostate CA elevates PSA much more than BPH). Ranges: <4 normal, 4-
10 abnormal (TRUS), >10 suspicious for CA (TRUS)
• If unsure > TRUS biopsy.
Mr Pang is discharged home well and came back for follow up in clinic, with repeat PSA
on arrival. Repeat PSA comes back as 12. You proceed to do a TRUS biopsy. What are
the complications of TRUS biopsy?
• Pain (cover with analgesia)
• Bleeding (counsel patient to expect PR bleed for a few days),
• Infection (cover with gentamicin)
• Lower urinary tract symptoms
Histology confirms prostate CA. Outline your management plan.

Sir, my patient’s life expectancy is >10 years so I will like to treat actively.
• First I need to stage the patient; e.g. for high risk (Gleason 8-10, PSA >20) need MRI
pelvis, CTAP for pelvic and paraaortic lymph nodes, and bone scan for bone mets.
[Don’t stage if don’t intend to treat i.e. life expectancy <10y]
• Based on the risk stratification I will treat. For example if the patient is gleason 7, PSA
15, long expected life expectancy, I will offer radical prostatectomy vs radiotherapy.
• Thereafter need serial monitoring of PSA to look for recurrence.
General principles:
Risk class If life expectancy >10y If life expectancy <10y
Localized disease, low risk Active surveillance: regular PSA, TRUS Watchful waiting; no repeat
(Gleason ≤6, PSA <10) Individualize timing of resection: if short TRUS or PSA (pt likely
PSA doubling time, higher grade on to die of comorbids, not
biopsy→ treat prostate CA)
Localized disease, med risk Radical prostatectomy + pelvic LN diss Active surveillance or
(Gleason 7, PSA 10-20) (SE: incontinence, impotence) watchful waiting.
Or Radiotherapy (SE: impotence,
cystitis, proctitis; less incontinence)
Or Brachytherapy
Localized disease, high risk As for mod risk,

(Gleason ≥8, PSA >20) May need post-op androgen deprivation
Locally advanced disease RT with androgen deprivation therapy
Metastatic disease Androgen deprivation therapy

- Castration (surgical vs medical - LHRH agonist)
- Antiandrogen
If hormone refractory → chemotherapy
If bone mets, painful → palliative RT
Patient is lost to follow up and now has unresectable /metastatic prostate CA with
painful bone mets. How do you manage?
• Palliative RT
• Androgen deprivation
o Castration: surgical vs medical (LHRH agonist)
o Antiandrogen
• Analgesia.
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A THYROID CANCER
SURGICAL LONG CASES
Thyroid Cancer
PRESENTATION
Sir, my patient Mdm Tai is a 38 year old Chinese lady with no past medical history, who
presents with a painless neck lump.
She first realized this lump two months ago when her relatives pointed it out during Chinese
New Year visitations. Since Chinese New Year it has slowly increased in size. It is entirely
asymptomatic with no pain, and she does not notice any other neck lumps.
[Ddx]
• [Thyroid cancer]: In terms of local symptoms, there is no change in voice, dysphagia,
or dyspnoea (local invasion). She does not have constitutional symptoms of loss of
weight or loss of appetite; also she does not have shortness of breath, bone pain, or
jaundice.
• [Autoimmune thyroid disease]: In terms of thyroid status, she does not note heat
intolerance, palpitations, diarrhoea, and oligomenorrhoea to suggest hyperthyroidism,
neither does she notice cold intolerance, lethargy, and constipation to suggest
hypothyroidism.
• [Parathyroid adenoma/carcinoma] No symptoms of hypercalcemia such as bone pain,
loin to groin pain (kidney stones), colicky abdominal pain, confusion/lethargy
• [Lymph nodes]: She does not have any other symptoms of infection or malignancy in
the head and neck region such as sinusitis or bloody nasal discharge.
[Risk fx] She has no known past medical or surgical history, is not on any long term
medications, and has no known drug allergies. In particular, I do not note any history of MNG,
radiation exposure, or autoimmune disease. She was born in Singapore and has stayed here
all her life (MNG). Systemic review was unremarkable with no joint pain, rash
She has no family history of thyroid or parathyroid malignancy, no suggestion of colonic polyps
(FAP) or other endocrine neoplasms (MEN2)
Socially, she does not smoke or drink. She is a full time housewife staying with her husband
and 2 young children in a 5-room flat, and they are financially stable.
On examination, Mdm Tai is alert and comfortable at rest, not in respiratory distress, and not
cachectic looking. On inspection I noted a central neck mass, just to the right of the midline,
which ascends on swallowing but not tongue protrusion. There are no overlying scars or skin
changes. Palpation confirms a firm nodule, 4cm x 5cm, which has an irregular surface but is
not fixed to overlying skin or underlying structures. It is not warm or tender. I can feel the lower
border of mass. There were no other palpable nodules, and no cervical lymphadenopathy or
retrosternal dullness. The trachea is central. Her voice is not hoarse. On examination of her
thyroid status I find her euthyroid. There are no signs of thyroid eye disease.
In summary, Mdm Tai is a 38 year old Chinese lady with no past medical history presenting
with a painless slow growing right thyroid nodule for investigation. There are no symptoms or
signs of local invasion or distant spread, and she is euthyroid.
QUESTIONS
What are your differentials for a neck lump?

See short case thyroid and Approaches to Symptoms of Disease
How would you investigate this mass?

• TFT
• US thyroid
• Fine needle aspiration of the right lobe mass.
Can you please read this ultrasound?

Sir this is the ultrasound thyroid of my patient taken on ___. I note that there is a hypoechoic
nodule (vs anechoic - cyst) measuring 3cm x 3cm, it appears to be taller than wide. Margins
are irregular and I see microcalcifications. Doppler imaging confirms intranodular vascularity.
Sir I am worried that this ultrasound shows features of malignancy.
FNAC was sent. Tell me about the Bethesda scoring system?

Sir the Bethesda system is a system for histopathological reporting of thyroid FNAC
1 : non-diagnostic, unsatisfactory → repeat FNA with US guidance
2 : benign → clinic follow-up
3 : atypia/follicular lesion of undetermined significance → repeat FNA
4 : follicular neoplasm → surgery
5 : suspicious for malignancy → surgery
6 : malignant → surgery
His FNAC came back as follicular neoplasm. What are your thoughts on this?
Sir a follicular lesion may be an adenoma or a carcinoma, and the only difference is capsular
invasion which a FNAC cannot tell. I need to counsel the patient for hemithyroidectomy KIV
completion thyroidectomy (removal of other lobe) if histology shows follicular carcinoma
(capsular invasion).
Further questions
• How about frozen section? Previously the teaching was to do frozen section intra-op,
but nowadays it has been found that frozen sections are inadequate for differentiating
adenoma vs carcinoma… frozen sections only take a few cuts, high chance of missing
the capsular invasion… therefore sending the whole hemithyroid for histology is
currently the preferred option.
• Why is the completion thyroidectomy needed? Can do TSH suppression, can follow
up with thyroglobulin levels, can do RAI ablation of any residual tissue
So patient goes for hemithyroidectomy, you review her in the ward post-op. What do
you look for?
• Neck hematoma causing airway compression: airway, stridor, saturations, dyspnoea,
visible hematoma, see drain amount and make sure not clogged > if present, need to
undo stitches and return to OT
• Hoarseness of voice > injury to recurrent laryngeal nerve
• Check calcium levels (hypocalcemia), ensure no tingling and numbness of peri-oral
region and hands, Chvostek and Trosseau sign are late.
Histology says follicular carcinoma. So how?

• Complete staging with CT neck thorax liver.
• Completion thyroidectomy with central compartment lymph node clearance
• KIV adjuvant radioactive iodine ablation depending on risk stratification, to be
discussed at tumor board.
How do you prognosticate a thyroid cancer?

Sir differentiated thyroid cancers are generally of good prognosis especially since she is young
(Age <40), has no metastases (M), extrathyroid invasion (E), and the size of her nodule was
small (Size <4cm) - [AMES score].
After surgery how would you manage her in the long term?
• Give thyroxine at high doses for TSH suppression
• Monitor thyroglobulin levels (if RAI ablation done)
• RAI can be used to look for recurrence (lower doses than ablation)
Apart from thyroid cancer what are the other indications for thyroidectomy?
• Graves disease failed medical therapy and radioactive iodine (e.g. not compliant, not
tolerated)
o Beware thyroid storm: must ensure controlled before surgery, give Lugol’s
iodine pre emptively.
• Multinodular goitre causing compression symptoms, bad cosmesis
> Can do subtotal thyroidectomy in these cases
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A HIP: OSTEOARTHRITIS & AVN
SURGICAL LONG CASES
Hip: Osteoarthritis & AVN
HISTORY & EXAMINATION
Background: Age, PMHx, Drug Allergy (esp NSAIDs), Baseline function (ADL, Occupation -
make sure not deep sea diving)
About the pain:

• Is this hip pain? → Please point to pain, any radiation? Differentiate hip vs back pain -
o Hip: classically groin pain +/- radiation to anterior thigh (obturator nerve) but
does not go past knee
o Back: classically back pain radiating down side or back of leg past the knee
o Other ddx: abdominal (retrocecal appendicitis, gynaecological disease,
urolithiasis)
• Duration and course: How long has it been? Progressively worsening?
o OA: elderly patient with longstanding progressive hip pain
o AVN: beware in younger patient esp if risk factors present.
• Inflammatory vs mechanical: Worse on moving, better with rest? Worse in the morning
+ stiffness?
Etiology:
• History of fall / trauma?
• Rule out infection: fever?
• Rule out cancer: LOA/LOW?
• Could this be AVN?
o Ortho hx: previous fracture, septic arthritis, congenital (Perthes, slipped capital
femoral epiphysis)
o Medical hx: steroid use, autoimmune disease
o Lifestyle: e.g. deep sea diving, TCM (steroid)
o Note that NOF# and septic arthritis are ddx of hip pain AND causes of avascular
necrosis and secondary OA,
Function: ADLs? Ambulation requiring walking aid/orthosis? Are you still able to weight bear,
walk? Clip toe nails? Able to continue work?
Examination: Sir, my patient Mr Tan is an 50 year old Chinese man who is alert and
comfortable at rest. [Ensure adequate exposure and start with patient standing up]
On inspection, I do not note any scars, sinuses, swelling or deformities of of the hip. I do not
note any wasting of the quadriceps or hamstrings. Sir can you walk there and back for me
please? I note that he has a right antalgic gait. There is no trendelenberg gait. I will now
perform the Trendelenberg test. Sir can you place your hands on top of mine and maintain
your balance while standing on your right leg? I note that the patient’s left hip sags when she
stands solely on her right lower limb, therefore this is a positive tredenlenberg on the right.
Trendelenberg test is negative on the left side.
Sir can you lie back down please? I am now palpating for bony landmarks, namely the ASIS,
hip joint, greater trochanter. The right hip joint is tender on palpation, but not warm or swollen.
I will now move on to limb length measurement. Apparent limb length, measured from the
xiphisternum to the medial malleolus, is __ on the right and __ on the left. True limb length,
measured with the pelvis sqaured from the ASIS to the medial malleolus, is __ on the right
and __ on the left. As there is true limb length discrepancy, I will now perform the Galleazi
test. Sir can you flex your knees to 90 degrees? Looking from the side, there is shortening of
the femur but no shortening of the tibia. The patient’s footwear does not have a heel raise.
I am now going to assess the ROM of the hip joints. All movements are limited (state the
degree as you do each movement) and painful in the right hip, but normal in the left hip.
N.B. normal ROMs of the hip joint:

• Hip flexion: 110 to 120 degrees
• Hip abduction: 30 to 50 degrees
• Hip adduction: 20-30 degrees
• Hip extension: 10 to 15 degrees
• Hip external rotation: 40 to 60 degrees
• Hip internal rotation: 30 to 40 degrees
I am now doing the Thomas’ test looking for fixed flexion deformities of the hip. Ma’am I’m
going to place one hand below your lower back. Bring your left knee up to your chest for me.
There is fixed flexion deformity of about 20 degrees in the right hip. Ok put your left leg down.
Bring your right knee up to your chest (or as high as you can) for me. Patient is limited by pain,
unable to assess if there is fixed flexion deformity in the left hip. There is crepitus felt over the
right hip.
I would like to complete my examination by examining the lumbar spine and the neurovascular
status of the lower limbs.
Summary: My patient is a 50 year old Chinese gentleman who fell on his hip 2 year ago and
never saw a doctor. Since then he has had progressively worsening mechanical right hip pain.
Examination shows positive right trendelenburg, shortened right femur on galeazzi, reduced
ROM of the right hip joint in all directions and right FFD. I am worried about avascular necrosis
from occult neck of femur fracture causing secondary osteoarthritis.
QUESTIONS
What are the causes of AVN?

1. Apparent: trauma, dislocation, fracture, septic arthritis
2. Insidious:
o Drugs (steroids, alcohol, smoking)
o Metabolic (Sickle cell, Gaucher)
o Autoimmune (SLE, RA)
o Pro-thrombotic states (e.g. Factor V Leiden, Protein C or S deficiency,
hyperhomocysteinemia, antithrombin III deficiency)
o Occupational (diving)
3. Paediatric age group: SCFE, Perthes
What are the causes of OA?

• Primary (degenerative)
• Secondary
o Infective: septic arthritis
o Inflammatory: RA, gout
o Traumatic: untreated neck of femur fracture
o Avascular necrosis

• Pelvis XR AP. Weightbearing XR of the hip AP and lateral views, looking for crescent
sign or collapsed head of femur (Ficat stage 3), OA changes secondary to AVN (Ficat
stage 4), also to rule out any fractures
• MRI of the right hip. T1 weighted scan – fat is white. Look for decreased signal in the
femoral head, represents edema. T2 scan -- may find a double line sign (low density
and high density line, corresponds to dead bone and surrounding inflammation for
repair)
What treatment would you offer this patient?

Sir this patient has advanced OA of the hip... I will first attempt trial of conservative
management which includes nonpharmacological and pharmacological therapy
• Nonpharmacological
o Weight loss
o Exercise in water
o Walking aids
o Physiotherapy for muscle strengthening exercises.
• Pharmacological:
o Analgesia: paracetamol, NSAIDs with PPI cover
o Intraarticular injection of steroids (triamcinolone)
o Intraarticular viscosupplementation with Synvisc injections (hyaluronic acid
which helps to lubricate the joint)
I think he will eventually need total hip replacement.
What if he came to you with earlier AVN?

Precollapse Ficat 0-2
• Bisphosphonates
• Core decompression (relieve intraosseous hypertension)
• Rotational osteotomy for small lesions - rotate lesion away from a weight bearing
surface
• Curettage and bone grafting.
Collapsed
• Remove necrotic area and replace with fibular strut
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A KNEE: OSTEOARTHRITIS
SURGICAL LONG CASES
Knee: Osteoarthritis
HISTORY contributions from Teo Ling Li
Mdm Teo is a 50 yo female who has been complaining of progressively worsening right knee
pain over the past two years. This is worse on exercise, especially on going downstairs, and
relieved with rest. There is stiffness of 10min in the morning and swelling especially after
exercise. Paracetamol used to relieve the pain but does not completely do so now. There are
no red flags (fever, weight loss, calf pain, trauma, etc) or suggestion of referred pain (hip/back
pain)
Notably Mdm Teo has had a previous sports injury s/p ACL reconstruction and meniscal repair
20 years ago. Currently she still experiences some locking/instability/catching especially when
turning sharp corners (suspicious of ACL graft failing). She has no other past medical history
and does not smoke or drink.
Functionally, she is a housewife who stays with husband and son. She is coping okay without
walking aids but it bothers her that she cannot do housework. At home they stay on a lift
landing floor and have a sitting toilet.
Examination: My patient is a middle aged Chinese

lady in her 50s who is alert and comfortable.
Inspecting from the front, side, and back with the
patient standing; there is a short midline scar* over
the anterior knee with arthroscopic scars over the
medial aspect, suggestive of previous cruciate
ligament repair using the patella tendon. There is
swelling of right knee (loss of parapetellar fossa),
but no Baker’s cyst (associated with OA) or other
swellings. There are no genu varus or valgus
deformities of her knees, but I note a fixed flexion
deformity of the right knee from the side
Maam can you walk for me please? Her gait is antalgic on the right, and she requires a walking
stick. Can you squat? I note that she is not able to squat
Maam can you lie down please. Measuring thigh circumference 10cm superior to the lateral
femoral condyle, the right thigh is 35cm whereas the left thigh is 39cm. Both knees are not
warm. On palpation there appears to be positive patellar grind, medial and lateral joint
tenderness. There is also a positive fluid shift test.
I will now like to demonstrate movements. Ma’am can you straighten your knee? Ok let me try
to help you. There is a fixed flexion deformity of 30 degrees in the right knee. Ma’am can you
bend your right leg to touch your thigh? Ok ma’am I’m going to help you bend a bit more. Actie
and passive flexion are both 160 degrees. Range of movement is 0 degrees to 160 degrees
in the left knee. Internal rotation of both hips are full and not painful. There is crepitus in the
right knee, but not in the left.
I will now perform the drawer tests. [Position patient]. There is no posterior sag. Anterior
drawer test on the right knee is postitive with a spongy endpoint, but negative on the left knee
with a good end point. I will now perform the Lachmann test. Again it is positive on the right
knee with a good end point, but negative on the left with a good end point.
I will examine the other ligaments. I am now performing the valgus stress test in full extension,
and again in 20 degree of flexion. The test is negative. I am now performing the varus stress
test in full extension and again in 20 degrees of flexion. This is also negative.
I will now like to perform the McMurray test for the medial meniscus. I am flexing and externally
rotating the knee, applying a valgus stress and now gradually extending the knee. There is no
clunk and the test is negative.
I will like to complete my examination by examining the hip, lumbar spine, and doing a
neurovascular examination of the lower limb.
Summary: Sir, my patient is a 50 year old Chinese lady who was an avid soccer player in her
youth, presenting now with secondary osteoarthritis of the right knee on a background of
ruptured right ACL repair. This is affecting her ability to do housework. There are no red flag
symptoms such as fever, rest pain, LOW, LOA. Physical examination was consistent with
osteoarthritis of the right knee, and a right ACL tear.
* Note: scars for ACL repair include arthroscopic port scars, plus a graft scar -
! Semitendinosus graft: Hockey shaped scar along the medial aspect of the tibia
! Patellar tendon graft: short anterior midline scar [patellar tendon should not be used in
individuals who have high use for it: Malays (kneeling to pray) or high jumpers as much of the
explosive power of the extensor mechanism hinges on an intact patella tendon)]
! Distinguish from TKR scar which is a long midline scar.
QUESTIONS
Can you tell me how you do fluid shift test?

• Milk the supra-patellar pouch.
• Milk the median sulcus from bottom to up, up and around the top border of the patella
and down into the lateral sulcus.
• THEN milk the lateral sulcus from bottom to up and watch for re-filling of the median
sulcus --> positive fluid shift test.
Is this primary or secondary OA? Why?

This is secondary OA
• Unilateral
• History of previous ligamentous injury.
What are the causes of secondary OA?

• Previous trauma and injuries (e.g. patella fracture, tibial plateau fracture, meniscal
tears and resections, ligamentous tears)
• Inflammatory arthritis: gout, RA
• Septic arthritis
What are your differentials?

• Knee pain: Rheumatoid arthritis, gouty arthritis, psoriatic arthropathy
• Locking symptoms: medial meniscus injury
• Also offer spine and hip.

I would start with weightbearing AP, lateral and skyline X-rays of the knee. I am looking for
osteoarthritic changes namely reduced joint space, subchondral sclerosis, subchondral cysts
and osteophyte formation.
Can also do long leg film looking at the mechanical axis of the leg (line from femoral head to
ankle joint) which in this patient with varus deformity may go through the medial joint
compartment instead of centre of the knee. (Alternative: look at tibial-femoral angle
I would also consider doing some basic blood investigations such as FBC RP ESR RF ANA,
to rule out rheumatoid arthritis.
How would you manage?
I would like to attempt conservative management first
Nonpharmacological measures:
• Weight loss
• Physiotherapy: knee strengthening (esp vastus medialis for varus knee), aerobic
exercises (improve function and reduce pain)
• Modalities
o Aquatherapy (exercise in water)
o Transcutaneous electrical nerve stimulation (TENS): short term pain relief,
improve ROM
o Thermal modalities
• Orthotics to ameliorate varus deformity:
o Valgus knee brace
o Lateral wedge insoles
• Acupuncture (adjunct)
• Occupational therapy: walking aids, activity modification
Pharmacological measures:
• Topical NSAIDs e.g. ketoprofen patch.
• Analgesia - know exactly what and what dose (ensure no contraindication)
o Paracetamol 1mg QDS
o Diclofenac 75mg BD
o Arcoxia 60mg or 90mg OM
o Tramadol 25mg or 50mg TDS
• Glucosamine: helps with inflammation, not with repair. Evidence shows >6 month
regular use no benefit compared to placebo.
Intraarticular injections
• H&L: steroids (triamcinolone)
• Viscosupplementation with Synvisc injections (intraarticular hyaluronic acid which
helps to lubricate the joint)
However as her osteoarthritis is quite severe and pain is significantly limiting her function, I
think she may require total knee replacement in order to preserve her mobility (if she is fit for
operation).
What are the risks of total knee replacement?

• Early: Injury to surrounding structures esp peroneal nerve → foot drop, numbness over
dorsum of foot, complications from general anesthesia, deep vein thrombosis and
pulmonary embolism, surgical site infection
• Late: stiffness, periprosthetic fracture, implant failure
How do you do a TKR?

1. Make incision, usually 8-10 inches longitudinally on anterior aspect of knee
2. Rotate the patella to the side, to gain access to the knee joint
3. Resurface femur
4. Attach metal femoral component (titanium) to the end of the femur and secure with
bone cement (PMMA)
5. Resurface tibia
6. Attach bottom portion of the implant, called the tibial tray (titanium), to the tibia and
secure with bone cement (PMMA)
7. Put a polyethylene (medical-grade plastic) insert to sit between the tibial tray and the
femoral component. This will serve as a kind of buffer, reducing wear and tear of the
articulating surfaces of the implant.
8. Patella will be flattened and fitted with an additional plastic component to ensure proper
fit with the rest of the implant
9. Bend and flex the knee to ensure that the implant is working correctly, and that
alignment, sizing, and positioning is suitable
10. Close the incision with stitches or staples
How long would a TKR last and why doesn’t it last longer?
A typical TKR lasts about 15 years. It may not last as long if patient is very active and the
implant wears out faster.
So how about a young patient, what can you offer them?

If the patient has unicompartmental OA, can offer -
• Medial compartment: tibial osteotomy to correct varus knee (good for 5 - 10 years),
medial unicompartmental arthroplasty
• Lateral compartment: distal femoral osteotomy to correct valgus knee, lateral
unicompartmental arthroplasty
• Isolated patellofemoral: Patellectomy, tibial tubercle elevation, lateral retinacular
release (+/- partial facetectomy)
Others
• Arthroscopic debridement: especially for mechanical symptoms e.g. loose
bodies/flaps of meniscus or cartilage that are causing mechanical symptoms esp
locking, catching, giving way
• Cartilage regeneration techniques e.g. harvest from non weightbearing part of knee
joint, culture in vitro, then autologous chondrocyte implantation
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A SPINE: CERVICAL MYELOPATHY
SURGICAL LONG CASES
Spine: Cervical Myelopathy
History
• Background: Age, PMHx, Drug Allergy, Baseline function (ADL, Occupation)
• Elicit presenting symptoms & time course (progressive or stepwise)
o Neck pain → Ensure that pain is mechanical. May have ‘electric shock’
sensation down spine on forward flexion (Lhermitte sign)
o Gait disturbance:spastic, ataxic
o LMN in UL: loss of fine motor control / clumsy, numbness
o UMN in LL: weakness, spasticity
o Bladder/bowel symptoms (develops late)
• Rule out red flags
o Trauma
o Inflammatory pain: at rest, at night, disturbs sleep
o Loss of appetite/weight
o Fever
• Consider ddx: aside from cervical radiculopathy the rest are non-orthopaedic and neck
pain does not feature prominently
o Cervical radiculopathy: main complaint will be pain shooting from neck to arm
in a dermatomal distribution; no gait, bladder/bowel, or LL disturbance
o Discogenic disk pain: neck pain only with no other symptoms
o Transverse myelitis: e.g. multiple sclerosis, neuromyelitis optica
o Syringomyelia
• Evaluate complications
o Falls
o Anterior cord syndrome / spinal cord injury after minor trauma.
• Evaluate function: able to work?
• Explore PMHx
• What has been done for the patient so far?
Examination: Sir, my patient is a middle-aged Chinese gentleman who is alert and

comfortable at rest. He uses a walking stick.
On inspection there are no scars, sinuses,swellings or deformities of the neck. Sir, can you
walk there and back please. I note that he has an unsteady, broad-based gait (if normal, stress
patient with tandem gait).
On palpation, there is no step deformity of the spine, no warmth or tenderness. There is some
paraspinal muscle spasm
Sir can you now follow my movements - bend your neck forward, do you feel anything? On
forward flexion of the neck, the patient complains of pain shooting down his spine which is a
positive Lhermitte’s sign. Neck extension, lateral flexion and rotation are otherwise full and
without pain.
I will now do a targeted neurological examination.

• Tone: Sir I am going to move your hands and legs, I want to see how relaxed you can
be. Tone is normal in upper limbs and slightly hypertonic in lower limbs with no clonus.
• Reflexes: Sir, this is a tendon hammer, I’m going to tap your arms and legs gently. I
note that bilateral upper limbs have an absent biceps jerk, inverted supinator jerk and
an exaggerated triceps jerk. Ankle and knee jerk are slightly hyperreflexic and Babinski
is equivocal
• Power: Sir I’m going to test how strong you are now. Don’t let me push you up/down.
Power is 5 in all limbs.
• Sensory: Sir I want to see how well you can feel. This is a satay stick - I am now
touching your forehead, this is 100%. Can you close your eyes and tell me how many
% each time. I note that sensation is intact over all limbs
Special tests:
• Hoffman’s sign (flick down) is present in both upper limbs.
• Sir, open and close your hands as quickly as you can in 10 seconds. My patient has
slow grip and release of less than 20 times in 10 seconds.
• Sir, stretch out your hands as straight as you can. There is ulnar drift in both hands.
Sir, can you write something for me / button your clothes / pick up this coin? In terms of
function, his writing is impaired
I would like to complete my examination with a digital rectal examination
Summary: Sir, my patient is a 70/M/Chinese with no significant PMHx who presents with 6
months of progressively worsening mechanical neck pain, associated with loss of finger
dexterity and gait disturbance. I do not note any red flags such as rest pain, night pain, loss of
weight, of fever. Functionally he is disturbed by difficulty writing and using chopsticks. Physical
examination is consistent with cervical myelopathy at the C6 level
QUESTIONS

• XR cervical spine, AP lateral views
• MRI cervical spine looking for spinal canal AP diameter <10mm, level of disease, and
ruling out differentials such as mitotic lesion
• If prompted - pre-op: FBC, RP, PT/PTT, GXM, ECG, CXR, 2DE
Can you please read this X-ray?

Have a systematic approach to reading!
• Introduce: Sir this is the lateral cervical spine X ray of my patient.
• Adequacy: This is an adequate radiograph showing up till C7/T1 junction. There is
good penetrance.
• Alignment: The alignment of the vertebrae (anterior vertebral, posterior vertebral,
spinolamellar line, posterior spinous line) is intact although I note loss of cervical
lordosis. There is no spondylolisthesis (always look).
• Bone: Bone is intact, no fractures.
• Discs: There is decreased height of the C4/5, C5/6, C6/7 discs
• Conclusion: This is consistent with spondylotic changes although I will like an MRI to
look at the spinal canal itself
Can you please read this MRI?

• Introduce: Sir this is the T2-weighted MRI of the patient’s cervical spine in axial / lateral
view
• Lateral view: Cervical spine has lost its physiological lordosis. There is disc protrusions
at the C4/C5, C5/C6, C6/C7 level resulting in effacement of the CSF (no more CSF
space) and indenting the spinal cord. There is high T2 signal noted in the cord
(=marrow edema, sign of chronicity). The discs also appear dessicated (no white
inside)
• Axial view: There is central disc protrusion indenting the spinal canal and reduced
spinal diameter of <10mm (kidney bean shape).
o In contrast - for radiculopathy, look for lateral disc prolapse, foraminal
narrowing.
How would you manage this gentleman?

Sir as my patient’s has progressive symptoms affecting function, and because the natural
history of cervical myelopathy is not to spontaneously resolve, I will like to offer the patient
surgical decompression. In view of multi-level disease I would opt for posterior approach
(1) When to offer surgery

• Natural hx of cervical myelopathy: will progress but may be slow
• Functional disturbance, progressive symptoms → surgical
• Mild symptoms, good premorbids, severe disease on MRI → surgical to minimise risk
of deterioriation
• Mild symptoms, poor premorbids → conservative (analgesia, neck strengthening
exercise, collar, fall caution)
• Asymptomatic → do nothing.
(2) What surgery to offer

• 1-2 levels affected → Anterior cervical discectomy and fusion (less infection, blood loss
than posterior approach)
• ≥3 levels affected → Laminectomy with posterior fusion (higher cx of dysphagia,
difficulty breathing for anterior approach in multi-level disc)
PID, cervical radiculopathy Lumbar spinal stenosis Cervical myelopathy

(no cauda equina)
Ntl hx 80-90% recover in 6 weeks 1/3 improve Progressively worsen

1/3 same Acute decompensation
1/3 require surgery after trauma
When to offer Symptoms > 8 weeks Failed conservative Mx Prevent progression

surgery Severe weakness or cauda and function poor Offer to most, unless
equina syndrome Progressive neurology mild symptoms mild &
normal function, or
poor premorbids
Surgical PID 1 level: decompression No spondylolisthesis: 1-2 levels: ACDF

option e.g. microdiscectomy or decompressive ≥3 levels: posterior
open discectomy +/- laminectomy laminectomy and
laminectomy Spondylolisthesis or back fusion
PID multiple levels: need pain > leg pain: add
fusion e.g. TLIF fusion e.g. TLIF
C-spine: ACDF
How do you counsel for surgery?

• Goal of surgery is to reduce risk of progression, may not have fully normal neurologic
function after, and 5-30% may not feel better.
• Early complications:
o Nerve root injury: C5, C6, recurrent laryngeal nerve → dyspnoea, hoarseness
o Anaesthetic risk
o Epidural hematoma
o Wound infection
• Late complications: nonunion, pseudoarthrosis
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A SPINE: PID & CERVICAL RADICULOPATHY
SURGICAL LONG CASES
Spine: PID & Cervical Radiculopathy
History:
• Back pain
o Is this neck/back pain? → Consider ddx: hip (unable to squat), knee, shoulder.
o Onset + surrounding circumstances (suddenly after heavy lifting?), duration,
progressive or stable
o Mechanical vs inflammatory - worse on movement, better on rest
o Better on flexion (disc pathology) or extension (facet joint disease, pars
interarticularis)?
• Neurologic symptoms
o Sciatica i.e. shooting/radiation of pain from back to arm/leg. Usually a single
dermatome in PID. Identify which
L2: to the groin
L3: anterior thigh
L4: medial thigh and calf
L5: lateral thigh and calf, dorsum of foot
S1: back of thigh and calf, sole/heel
C6: Neck, deltoid, radial forearm, thumb ± index finger.
C7: similar going to middle finger.
o Weakness, numbness
• Red Flags
o Loss of urinary or bladder bowel incontinence, saddle anesthesia
o Fever
o Rest pain, night pain that disturbs sleep
o LOW, LOA → Cancer
o Abdominal pain → AAA
• Previous treatment
• Function
Examination: Sir, my patient is alert and comfortable at rest. *inspect from front, side, back*
There are no scars, skin changes or deformities such as kyphoscoliosis or scoliosis. He is
listing to the right.
Sir I’m going to feel along your spine now. On palpation, there are no step deformities of the
spine. There is tenderness on palpation of the vertebrae, associated with paraspinal muscle
spasm on the left.
Sir I’m going to see how well you can move. I am now performing Schober’s test by marking
the level of the posterior iliac spines, and marking a point 10cm above and 5cm below. Sir can
you bend forward please? Flexion of spine is restricted to 40 degrees by pain, lumbar
excursion is only 2cm. Sir can you follow my movements please? Extension, bending
sideways and rotation are also with some pain but able to demonstrate full range of movement.
Sir can you sit down please? (fix the pelvis) Rotation is normal.
Ok please lie down now sir. I’m going to do raise your leg slowly, please tell me what do you
feel? > Can you tell me where is the pain. Straight leg raise of right leg positive at 40 degrees
flexion, with positive Lasegue’s test. Left leg normal.
I will now do a targeted neurological examination.

• Tone: Sir I am going to move your hands and legs, I want to see how relaxed you can
be. Tone is normal.
• Reflexes: Sir, this is a tendon hammer, I’m going to tap your arms and legs gently.
Knee reflexes are present but ankle is absent on the right.
Big toe and ankle dorsiflexion was MCR 3 on the right. Hip flexion, knee flexion, knee
extension, and ankle plantarflexion were full power, and all movements on the left leg
were normal.
% each time. There is decreased sensation over the lateral aspects of the right leg,
top of feet including 1st dorsal webspace
I would like to complete my examination by doing

• Digital rectal examination to assess anal tone and saddle anesthesia.
• Abdominal examination to check for pulsatile mass and palpable bladder.
Summary: In summary, this is a middle aged Indian loading officer with mechanical back pain
and sciatica radiating to L5 dermatome on right foot. This started acutely 3 months ago when
he was lifting heavy objects, and has persisted since then with worsening foot drop rendering
him unable to work. There is no signs and symptoms of cauda equina syndrome, rest pain,
night pain, LOW, or fever. Physical examination is consistent with prolapsed intervertebral
disk at L4/L5 position causing L5 nerve root symptoms.
Note: Differential in an older patient can be spondylolisthesis
QUESTIONS

Sir, I would first do XRays of the lumbar/cervical spine, both AP and lateral views
• This is the lateral lumbar/cervical spine XR of this patient taken on ____. There is good
penetrance. There is preservation of cervical/lumbar lordosis. Most notably there is
loss of disk space between the ____vertebrae (count from odontoid process of C2, or
count from sacrum). I do not see any spondylolisthesis. There are no spondylotic
changes such as end plate sclerosis, syndesmophytes formation or facet joint
osteoarthritic changes.
o In a lateral lumbar spine XR, can also always comment on hip joint
• This is the AP lumbar/cervical spine XR of this patient taken on ____. There is good
penetrance. The psoas shadows preserved (therefore no paraspinal abscess). There
is no winking owl sign (disappearance of pedicle). I do not note any vertebral fractures,
scoliosis. SI joints look normal (sacroileitis: blurring of joint lines, sclerosis, widening
of joint space).
• An MRI spine would then be needed, looking for lateral recess prolapse causing
impingement of transversing nerve root
How would you manage this patient?

Sir as 80-90% of patients recover within 6 weeks I will first offer conservative management
• Nonpharmacological
o Bed rest
o Lifestyle modification: avoid heavy lifting, educate patient to lift properly (squat
down instead of bending back), stop smoking and alcohol
o Physiotherapy: strengthening of back muscles, heat therapy, ultrasound
therapy
o Orthosis: lumbar spine support
• Pharmacological
o NSAIDs with PPI
o Nerve root agents: gabapentin, pregabalin, amitryptyline.
If he is still symptomatic at 8 weeks I would offer him surgical decompression with

• As his disease affects a single level gold standard is microdiscectomy (old one:
discectomy +/- laminectomy or laminotomy), or
• As his disease affects multiple levels I would offer decompression and fusion e.g.
transforaminal lumbar Interbody fusion
• Post-op: rehab is very important, light work only after 1 month and heavy work only
after 3 months
[Please refer to table comparing treatment of various spine disease; see Cervical Myelopathy]
If this patient also has urinary symptoms what would you do?
Sir I am worried about cauda equina syndrome. I would arrange urgent MRI scan. The patient
needs decompression within 48 hours.
What are the complications of surgery?

! Early: paralysis, loss of urinary continence, infection (including meningitis), epidural
hematoma, anaesthesia risk.
! Late: recurrence of slip disk (10%), adjacent disk develops slipped disk, implant failure
(no fusion)
SURGERY LONG CASES: PRESENTATION SCRIPTS & Q&A SPINE: LUMBAR SPINAL STENOSIS
SURGICAL LONG CASES
Spine: Lumbar Spinal Stenosis
History:
• Elicit presenting symptoms & time course (progressive or stepwise)
o [Axial] Back pain → Ensure that pain is mechanical. Is it worse on flexion
(discogenic) or extension (facet joint)?
o [Appendicular] Neurogenic claudication: unilateral or bilateral
cramping/tingling/discomfort in calf/thigh/butt on walking, variable claudication
distance, relieved on flexion, worse walking downhill, can have
numbness/weakness if more severe
o Differentiate from sciatica, which would be sharp shooting pain radiating down
from back down the leg, present both at rest and on movement (spinal stenosis
can sometimes have radicular symptoms, albeit less commonly than in PID)
o Is leg pain worse or back pain worse? (Affects management)
• Consider ddx:
o Vascular claudication -- this has a fixed claudication distance (vs variable),
worse walking uphill (vs downhill), relieved on rest (vs spine flexion), no
numbness or weakness
o Prolapsed intervertebral disc -- younger patient, radicular (shooting) rather than
cramping pain, has neurology; spinal stenosis patients do not often have
neurology, but osteophytes may sometimes press on exiting nerve roots and
cause radicular symptoms
o Hip pain: if able to squat, less likely hip.
• Rule out red flags
o Trauma
o Cauda equina syndrome: Bladder/bowel dysfunction
o Inflammatory pain: at rest, at night, disturbs sleep
o Loss of appetite/weight → Cancer
o Fever → Infection
o Abdominal pain → AAA.
• Evaluate function
• Explore PMHx
• What has been done for the patient so far?
Examination: Sir, Mr Ahmad is alert and comfortable at rest; I do not any walking aids next
to him. On inspection there are no scars, skin changes or deformities. I note that he is standing
in slight flexion. Can you please walk there and back? The patient’s gait appears normal, not
broad based or antalgic.
Sir I’m going to feel along your spine now. On palpation, I do not note any step deformity,
midline tenderness, or paraspinal muscle spasm.
Sir I’m going to see how well you can move. I am now performing Schober’s test by marking
the level of the posterior iliac spines, and marking a point 10cm above and 5cm below. Sir can
you bend forward please? There is only an increase of 4cm indicating reduced forward flexion.
Sir can you follow my movements please? Lumbar extension and lateral flexion is normal. Sir
can you sit down please? (fix the pelvis) Rotation is normal.
Sir I will skip straight leg raise in this patient as he does not appear to have symptoms of
sciatica (do if there are radicular symptoms)
I will now do neurological examination

• Tone: Sir I am going to move your legs, I want to see how relaxed you can be. Tone
appears to be normal and there is no clonus.
• Reflexes: Sir, this is a tendon hammer, I’m going to tap your arms and legs gently. Sir
I note depressed reflexes over bilateral ankles. Knee jerk is normal. Plantars are
downgoing.
Power is 5 in all myotomes.
% each time. I note that sensation is intact over all limbs
I would like to complete my examination by

• Palpating dorsalis pedis pulses to rule out vascular claudication
• Doing digital rectal examination assessing anal tone and perianal sensation
• Abdominal examination to check for palpable bladder
Summary: Mr Ahmed is an 70 year old Malay gentleman presenting with 3 years lower back
pain and worsening neurogenic claudication. I do not note any red flags such as rest pain,
weight loss, fever, or suggestion of cauda equina. Function wise, there is mild limitation of
mobility but as a retiree with low functional demand he is not extremely bothered. His
premorbids are good with only well controlled diabetes, hypertension, hyperlipidemia.
Examination findings are that of reduced lumbar spine flexion with slightly depressed LL
reflexes but full power. There was no step deformity. In summary Mr Ahmed is a 70 year old
Malay gentleman with symptoms of lumbar spinal stenosis.
QUESTIONS

• XR lumbar spine AP lateral, looking for degenerative changes
• MRI lumbar spine looking for reduced spinal canal anteroposterior diameter
• FBC - rule out myeloma (think of myeloma if anaemia), lymphoma, infection
• UECr - so that I can give NSAID
• Pre-op also: FBC, RP, PT/PTT, GXM, ECG, CXR, 2DE; add HbA1c and fasting
glucose for this patient.
Can you read this X-ray please

• Introduce: Sir this is a lateral X-ray of my patient’s lumbar spine
• Adequacy: There is good penetrance.
• Alignment: I note that there is grade 2 spondylolisthesis of the L4 upon L5 (grade based
on ratio of overhanging part of superior vertebral body vs AP length of inferior vertebral
body, grade 1 = 0-25%, grade 2 = 26-50%, grade 3 = 51-75%, grade 4 = 76-100%). I
will also like a oblique view looking for spondylosis (pars interarticularis break)
• Disk: There are changes of spondylosis with reduced disk height of L3/L4, L4/L5,
L5/S1, endplate sclerosis, osteophyte formation, +/- facet joint OA change.
• Bone: Bone is intact (all square shaped)
• Hip shows no OA changes.
• In summary this X-ray shows spondylotic changes with spondylolisthesis
What is the prognosis of lumbar spinal stenosis?

1/3 improve, 1/3 same, 1/3 require surgery
How would you manage this patient?

As Mr Ahmed’s function is not too badly affected I will first offer a trial of conservative
management with weight loss, analgesia, and physiotherapy to strengthen muscles and
correct posture. If he does not improve and symptoms worsen to limit function I would offer
surgery - in his case he has spondylolisthesis; decompression alone would worsen instability,
so he also needs a fusion procedure e.g. transforaminal lumbar intervertebral body fusion
(TLIF)
[Please refer to table comparing treatment of various spine disease; see Cervical Myelopathy]
If for op what will you counsel the patient on?

• Risk that symptoms may not improve or may recur due to adjacent level disease (20%)
• Operative risk: e.g. infection, epidural hematoma, nerve injury, anaesthetic
complications (depending on premorbids)

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PREPARING FOR THE MBBS | CHAPTER THREE

Surgery Long Cases

NIGEL FONG & MARIANNE TSANG | V1.0

Examiners want you to:

SURGICAL LONG CASES

Abdo Pain: Acute Cholecystitis

In summary my patient is a 50/Chinese/lady with recurrent episodes of biliary colic, now

How would you investigate?

Initial bloods include

For differentials, I will do

Imaging modalities include

Can you please read this ultrasound?

You are the HO on call. How would you manage?

1. Resuscitate the patient according to

2. Confirm diagnosis and rule out differentials

When would you perform cholecystectomy?

If patient too sick for op then how?

Please counsel Mdm Liew on cholecystectomy.

*Recommend drawing it out!

(1) Your current condition

(3) Risks and complications of cholecystectomy

(4) Risk of not going for cholecystectomy and alternatives

Sir I am worried about local complications of cholecystitis such as mucocele → empyema →

OK what are the other complications of cholecystitis?

SURGICAL LONG CASES

Abdo Pain: Acute Pancreatitis

As for underlying etiology,

I would then do investigations to:

What are the complications of acute pancreatitis?

Local complications include

You may be asked this content in various permutations… e.g.

What is the definitive treatment for Mdm Liew?

*I recommend drawing the HBS system in this case!

(1) Your current condition

(3) Risks and complications of cholecystectomy

(4) Risk of not going for cholecystectomy and alternatives

SURGICAL LONG CASES

Abdo Pain: Aortic Aneurysm

His is functionally good, able to walk 10 bus stops.

On examination, he is alert, comfortable, not on any external intervention at present. I note an

In summary, Mr Muthu is a 69 year old vasculopath presenting with symptomatic aortic

How do AAA present?

OK so you are the HO on call, what will you do?

Resus A Assess airway

Bloods FBC - Hb drop, Plt

Imaging CT aortogram (if unstable - bedside ultrasound).

Initial Mx To HD/ICU with hourly monitoring and strict i/o

CT aortogram shows a 5cm aneurysm. What is the management?

What complications will you counsel the patient on?

SURGICAL LONG CASES

Abdo Pain: Diverticulitis

How will you investigate the patient?

OK here is the CTAP please read -

Can you explain how colonic diverticuli form?

What is diverticular disease?

How can diverticular disease present?

OK so how would you manage the patient?

SURGICAL LONG CASES

Abdo Pain: Urolithiasis