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APPENDIX OSCE Scenario Answers
451
on the femoral artery to perfuse the pelvis rst prior to perfusing the leg and release one leg at a time.
OSCE SCENARIO ANSWER 9.5
A 75-year-old female patient underwent dicult open
anterior resection. She has past medical history of hypertension, ischaemic heart disease and transient ischaemic
attack (TIA). e procedure was complicated with signicant
blood loss that necessitated intraoperative blood transfusion.
Postoperatively, she was admitted to the high-dependency
unit as she required vasopressors support.
1. What methods can be utilised to monitor the cardiovascular system?
• ECG
• blood pressure measurement (via cu or arterial line)
• central venous pressure
• pulmonary wedge pressure (pulmonary artery occlu-
sion pressure) via a Swann-Ganz catheter
• pulse oximetry
• cardiac output
• urine output
• echocardiogram
• echo Doppler.
2. What is the best indicator to assess adequate uid
balance?
Urine output remains the best indicator to assess adequate uid balance. Normal urine output is 0.5–1 mL/
kg/h. Assessment of the central venous pressure can be
also a useful guide to uid replacement in hypovolaemic
patients.
3. How does the pulse oximetry work?
It relies on the measurement of the dierent absorption
of oxyhaemoglobin and deoxyhaemoglobin at dierent
wavelengths. e pulse oximeter uses two dierent light
emitting diodes at two wavelengths: 660 nm (red light) and
960 nm (infrared light)
4. What are the problems and pitfalls that can occur
when reading pulse oximetry?
• delay: calculations are made from several pulses and
there is a 20s delay between actual and displayed values
• irregular pulse: atrial brillation
• venous pulsation (tricuspid incompetence)
• hypotension
• vasoconstriction
• abnormal Hb (carboxy-), and methaemoglobin
• bilirubin
• methylene blue dye
• other factors: electrical interference (diathermy),
ickering lights, patient movement, shivering, nail
varnish (coloured or not).
5. What is a vasopressor? Give some examples used in
common clinical practice.
Vasopressors are drugs that constrict blood vessels through
α-eect. Metaraminol and noradrenaline are commonly
used vasopressors. Adrenaline has both vasopressor
(α-eect) and inotropic (β-eect) mechanisms of action,
depending on the dose given.
OSCE SCENARIO ANSWER 10.1
A 40-year-old male presents with recurrent attacks of right
upper quadrant pain exacerbated by fatty food. His only
signicant past medical history is a right hemicolectomy 5
years previously for acute regional ileitis (Crohn’s disease).
Investigations reveal normal liver function tests but FBC
reveals anaemia with a raised MCV. Abdominal ultrasound
scan demonstrates gallstones.
1. Explain the pathophysiology underlying the develop-
ment of gallstones in this patient.
• e terminal ileum is the site of bile salt absorption.
Because the terminal ileum has been removed during
the right hemicolectomy for terminal ileal Crohn’s
disease, the absorption of bile salts is reduced and
they are lost in the faeces.
• Due to the loss of enterohepatic circulation, there is
a decrease in the bile salt pool. ere is therefore not
enough bile salt to keep cholesterol dissolved and
thus cholesterol gallstones form.
2. What is the cause of the patient’s anaemia?
e terminal ileum is the site of absorption of vitamin B12.
Intrinsic factor (secreted in the stomach) binds to its specic receptor. e intrinsic factor–vitamin B12 complex is
then taken up into the cell. Absence of the terminal ileum
results in lack of B12 absorption and consequently B12 deciency, leading to a megaloblastic anaemia (i.e. the cells are
large), thus explaining the raised MCV.
3. What would be the eects of failing to treat the anaemia?
• Body stores of vitamin B12 far exceed requirements
and deciency may take years to develop.
• Apart from the general symptoms of anaemia, paraesthesia and peripheral neuropathy may be present.
• Less commonly spasticity, unsteadiness and altered
gait may occur due to subacute combined degeneration of the spinal cord (damage to the posterior and
lateral columns).
• Visual disturbances (due to optic atrophy), dementia
and weight loss (due to eects of the vitamin deciency on intestinal mucosal cells) can also occur.
• Cardiomyopathy may occur.
4. How would you treat the anaemia?
Megaloblastic anaemia due to vitamin B12 deciency is
treated by replacement with intramuscular injections of
1 mg of hydroxocobalamin. Initially this is performed 3
times per week for 2 weeks. e maintenance dose is 1 mg
every 3 months continued for life.
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SECTION IV Appendix
OSCE SCENARIO ANSWER 10.2
A 32-year-old female is admitted with jaundice and right
upper quadrant pain. Liver function tests reveal a bilirubin
of 112 µmol/L, a markedly raised alkaline phosphatase and
gamma GT. Liver enzymes are normal.
1. What is jaundice?
Jaundice is a yellow discoloration of the tissues noticed
especially in skin and sclera due to the accumulation of
bilirubin.
2. At what level of bilirubin is jaundice clinically
apparent?
For jaundice to be clinically apparent, the circulating bilirubin levels should be in excess of 35 µmol/L.
3. Classify the types of jaundice.
Jaundice may be:
• pre-hepatic (due to haemolysis)
• hepatic (due to intrinsic liver disease)
• post-hepatic/cholestatic (due to either intrahepatic
cholestasis or post-hepatic biliary tract obstruction).
4. What is the most likely cause in this case?
Given the markedly elevated levels of alkaline phosphatase
and gamma GT and the fact that the liver enzymes are normal, this would suggest a cholestatic cause.
5. Describe the dierent types of gallstone.
ere are three types of gallstone:
• Mixed (80%): these are predominantly cholesterol
with small amounts of calcium and bile pigment.
• Cholesterol stones (10%): these are usually solitary and
can be up to 5 cm in diameter. ey are usually formed
in bile which is supersaturated with cholesterol.
• Pigment stones (10%): these are usually multiple,
small and black in colour. ey result most commonly due to haemolytic anaemia.
6. List the complications of gallstones.
e complications of gallstones are:
• cholecystitis (acute, chronic, acute-on-chronic)
• obstructive jaundice
• mucocoele of the gall bladder
• empyema of the gall bladder
• perforated gall bladder
• ascending cholangitis
• acute pancreatitis
• gallstone ileus
• carcinoma of the gall bladder.
OSCE SCENARIO ANSWER 10.3
A 63-year-old male is admitted with central abdominal pain
radiating through to his back. He is hypotensive with a BP of
90/60 mmHg and tachycardic. e results of blood investigations are shown below:
WBC 19 × 109/L
Glucose 8 mmol/L
AST 390 U/L
LDH 500 U/L
Amylase 2235 U/L.
1. e raised amylase suggests acute pancreatitis. What
are the common causes of acute pancreatitis?
e commonest causes of acute pancreatitis are gallstones
(40%) and alcohol excess (35%). Other causes include hyperlipidaemia, hypercalcaemia, viral infections (mumps and
Coxsackie virus), hypothermia, trauma, drugs, hereditary/autoimmune disorders, scorpion bites, post Endoscopic Retrograde
Cholangiopancreatography (ERCP) and pancreatic cancer.
2. What is the patient’s initial Ranson score?
On admission, Ranson’s criteria are
• WBC > 16 × 109/L
• Age >55 years
• Glucose >10 mmol/L
• AST >250 U/L
• LDH >350 U/L.
is patient thus scores 4. Amylase has no prognostic value.
3. What are the criteria measured at 48 h for the Ranson
score?
At 48 h post-admission the following criteria are examined:
• Haematocrit drop >10% from admission
• Urea increase >5 mg/dL from admission
• Calcium <2 mmol/L
• Arterial PaO2 < 8 kPa
• Base decit <4
• 6 L uids within 48 h.
e more factors present, the higher the predicted mortality.
4. What pancreas-related complications can occur with
acute pancreatitis?
Complications of acute pancreatitis include:
• pancreatic necrosis
• pancreatic abscess
• pancreatic pseudocyst formation
• chronic pancreatitis
• diabetes.
OSCE SCENARIO ANSWER 10.4
A 50-year-old male patient presented to Accident and Emergency
with epigastric pain aer starting a course of NSAIDs 2 weeks
ago for a are-up of arthritis. His pain was getting worse over
the last 24 h. Abdominal examination revealed peritonism with
guarding. His HR was 130/min, temperature 38.5°C and BP
130/70. You suspect perforated peptic ulcer.
1. What is the volume of daily gastric secretion? And
what is its content?
e stomach secrets 2-3 L/day; it contains
• Hydrochloric acid: helps to break down tissue, con-
verts pepsinogen to active pepsin, and provides
immunity against microorganisms.
APPENDIX OSCE Scenario Answers
453
• Pepsinogen: when activated to pepsin, it hydrolyses
peptide bonds in proteins.
• Mucus: helps neutralize gastric acid to protect the
stomach from digestion.
• Intrinsic factor: binds to vitamin B12 which is then
absorbed as a complex in the ileum.
• Salt and water.
2. What are the classes of medications that are used to
treat peptic ulcers and what are their mechanisms of
action?
Medical treatment of peptic ulcers frequently involves
antibiotic therapy to eradicate H. pylori and drugs that
reduce the gastric acid secretion or produce mucosal
protection.
• Drugs that reduce gastric secretion can be divided
into three groups:
• histamine (H2-receptor) antagonists, e.g. cimetidine and ranitidine: these drugs act by blocking
H2-receptors on parietal cells which prevents
the intracellular increase in cAMP, and thus acid
production
• muscarinic antagonists are historic and not in
clinical use.
• proton pump inhibitors (PPI), e.g. omeprazole:
activated at stomach low pH; these block the proton pump (H+/K+ ATPase).
• Drugs that produce mucosal protection can be
divided into three types:
• sucralfate: forms a sticky layer that adheres to the
base of the ulcer
• bismuth chelate: acts the same; in addition, it
helps eradicate H. pylori
• misoprostol: stimulates secretion of mucus and
bicarbonate and increases the mucosal blood ow.
3. e patient undergoes emergency laparotomy, and a
large friable perforated duodenal ulcer is found that
could not be closed with a patch. e surgeon decides
to perform distal gastrectomy with Roux-en-Y gastrojejunostomy. What are the potential complications of
gastrectomy?
• malnutrition
• iron deciency anaemia
• vitamin B12 deciency
• dumping syndrome
• diarrhoea
• bilious vomiting
• infection
• carcinoma
• risk of vagotomy.
4. Why does dumping syndrome develop?
• Early dumping (30–45 min aer eating): due to the
rapid gastric emptying of a hyperosmolar meal into
the small bowel, resulting in uid moving into the
small bowel by osmosis (third space loss), and results
in dizziness, weakness, and palpitations.
• Late dumping (1–3 hours aer eating): due to the
rapid swings in insulin secretion in response to the
glucose load in the small bowel, this leads to rebound
hypoglycaemia.
OSCE SCENARIO ANSWER 10.5
A 65-year-old female patient with background of smoking
and hypertension presents with chronic postprandial pain
(sitophobia), weight loss and loose stools. She is found to be
cachexic due to food fear and admission is for urgent investigations and addressing nutritional problems with total parenteral nutrition (TPN).
1. A CT abdomen is arranged (see Fig. 10.5Q). What is the
main nding on this CT scan? What is the diagnosis?
e CT scan clearly shows that there is occlusion of the
superior mesenteric artery (SMA) from its origin (see
ar row, Fig. 10.5A). e SMA is the main artery that supplies
the small intestine and right colon; however, rich anastomoses take place between the SMA and the celiac artery
and inferior mesenteric artery (IMA) via their terminal
branches; hence, signicant ischaemia usually occurs when
more than one mesenteric artery is aected. is is called
chronic mesenteric ischaemia. e CT scan also shows that
the patient is cachexic.
Fig. 10.5A CT angiogram showing occlusion of the
Coeliac artery (top arrow) and tight stenosis of the
superior mesenteric artery (SMA).
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SECTION IV Appendix
2. What are the pros and cons of enteral and parenteral
feeding?
Enteral feeding should be always preferred to maintain mucosal integrity of bowels. It is also associated with lower cost and
infective complications than TPN. However, it can be dicult
to adopt in cases of poor abruption/ileus, it can cause diarrhoea and increases risk of ventilator-associated pneumonia
and sinusitis in ITU patients. TPN, on the other hand, does
not depend on bowel integrity and function and provides
easy route for full energy requirements. However, it is associated with risk of infection, liver dysfunction and metabolic
complications such as mineral or trace element deciency.
3. How would you treat this condition?
As the patient is symptomatic and continues to lose weight,
revascularization of the SMA would be indicated; however,
before that, the patient’s nutritional status should be optimized by referring the patient to the dietician; occasionally TPN is indicated. In addition, the patient should be on
the best medical therapy for atherosclerotic disease in the
form of antiplatelet therapy and statin. In addition, lifestyle
modication, including smoking cessation and control of
other risk factors such as diabetes, hypertension and hyperlipidaemia, should be addressed. Revascularization of the
SMA can be via the endovascular route such as stent insertion or through open surgery such as endarterectomy of
aorto- (or ilio)-mesenteric bypass.
4. Five days aer her admission, the patient is found to
have low levels of K, Mg and PO4. What is this condition called? And why does it develop?
is is called refeeding syndrome. is metabolic disturbance is important to consider prior to feeding malnourished patients. e body adapts to a state of starvation and
refeeding can cause insulin levels to rise in response to glycaemia, resulting in cellular uptake of K, PO4 and Mg and
causing their catastrophic depletion. Hypophosphataemia
can reduce ATP and 2,3-DPG, causing cellular dysfunction that can cause respiratory and cardiac failure. It is
also important to replenish thiamine, particularly in
alcoholics.
OSCE SCENARIO ANSWER 11.1
A 70-year-old male is 2 days post-repair of a ruptured abdominal aortic aneurysm. Urine output has been poor, the last 4 h
having been 20 mL, 10 mL, 5 mL and 5 mL per hour, respectively. e patient has been haemodynamically unstable.
1. How would you dene oliguria?
Oliguria is a urine output of <0.5 mL/kg/h.
A specimen of urine is sent for examination and reveals
the following results:
Specic gravity >1020
Urine osmolality >500 mOsm/kg
Urine sodium <20 mmol/L
Fractional sodium excretion <1.
2. What is the likely cause of the oliguria?
is is physiological (pre-renal) oliguria. Likely causes
are either dehydration, hypovolaemia or impaired cardiac
function.
3. What action would you take based on these results?
• Fluid challenge with a bolus of 250–500 mL of uid.
CVP monitoring is oen required in these patients.
Fluid should be given until there is a sustained rise in
the CVP, indicating that the patient is well lled.
• If uid challenges do not produce a diuresis, the next
step is to ensure adequate renal perfusion pressure
using inotropes such as noradrenaline. Furosemide
rarely has a place in the acute management of poor
urine output as it results in depletion of intravascular
volume, although it may increase urine output; and
dopamine has never been shown to improve outcome from acute renal failure, even though it may
increase urine output.
Appropriate measures fail to produce a diuresis. Serum
creatinine is now 350 mmol/L and urine analysis reveals
the following:
Specic gravity <1010
Urine osmolality 290 mOsm/kg
Urine sodium >40 mmol/L
Fractional sodium excretion >2
4. What is now the cause of the patient’s renal dysfunction?
e patient is developing acute tubular necrosis.
5. What techniques are available for renal replacement
therapy in this patient?
• e available techniques are:
• haemodialysis
• haemoltration
• haemodialtration.
• Peritoneal dialysis is inappropriate in this patient as
he has recently undergone major abdominal surgery
and a prosthesis has been inserted (risk of infection).
6. What are the absolute indications for renal replace-
ment therapy?
e absolute indications for renal replacement therapy are:
• hyperkalaemia (>6.5 mmol/L)
• severe metabolic acidosis (HCO
• uid overload with pulmonary oedema
−
<10 mmol/L)
3
• symptoms of severe uraemia, e.g. ts, pericarditis.
7. Which mode of renal replacement therapy will be the
most appropriate in this patient?
• Haemoltration is the most appropriate.
• Haemodialysis involves movement of large volumes
between body compartments, and risk of gross
hypotension and cardiac arrhythmias in the haemodynamically unstable patient. With haemoltration,
APPENDIX OSCE Scenario Answers
455
uid removal can be achieved gradually over a
period of time.
• It is highly ecient, giving good ECF volume control, and can be used in the hypotensive patient.
• With continuous veno-venous haemoltration,
almost any quantity of uid can be removed in a 24 h
period, allowing administration of other uids, e.g.
parenteral nutrition.
OSCE SCENARIO ANSWER 11.2
A 19-year-old male is admitted to A&E having been
stabbed in the abdomen. On examination he is pale, sweating, with a tachycardia of 120 and a systolic blood pressure
of 80 mmHg.
1. What are the grades of haemorrhagic shock?
Haemorrhagic shock can be classied from 1 to 4 and
allows a rough clinical assessment of the amount of blood
lost.
• Class 1: 15% blood loss or <750 mL, pulse is <100,
BP is normal, pulse pressure is normal and there
may be a mild increase in respiratory rate. Urine
output is normal. Clinically this occurs when donating blood.
• Class 2: 15–30% blood loss or >750 mL and
<1500 mL, the pulse is elevated, the BP is normal but
the pulse pressure has narrowed due to an increase
in diastolic pressure owing to the release of natural
vasoconstrictors. e patient has a mild tachypnoea
(20–30 breaths/min) and urine output may fall
(20–30 mL/h).
• Class 3: 30–40% blood loss or >1500 to <2000 mL,
the patient looks in shock from the end of the bed,
and is anxious or confused, pale and tachypnoeic.
e pulse rate is above 120, the systolic blood pressure is <100 mmHg and urine output is markedly
reduced (<10 mL/h).
• Class 4: >40% or >2000 mL blood loss, the patient
is in extremis and is white, barely rousable and will
die very soon if haemorrhage is not arrested. Pulse
rate is >140, blood pressure may be unrecordable
(or sometimes only systolic) and the urine output is
negligible.
2. What is renal blood ow autoregulation and how is it
aected by shock?
• Autoregulation is the physiological ability of the kidney to maintain perfusion at a constant level across a
range of perfusion pressures. Autoregulation occurs
between 80 mmHg and 180 mmHg. e main site of
autoregulation in the kidney is the aerent glomerular arteriole. Two main factors aect vascular tone in
the aerent arteriole:
• myogenic: with an increase in transmural pressure the arterioles are distended, thus stretching
the muscle in the wall, resulting in vasoconstriction, an increase in vascular resistance and
decrease in renal blood ow
• tubulo-glomerular feedback via the juxtaglomerular apparatus: complex signals pass from the
macula densa to the aerent arteriole, regulating
its tone.
• ese mechanisms fail below around 80 mmHg, i.e.
in a state of severe shock, and other mechanisms,
namely hormonal, will attempt to compensate, e.g.
antidiuretic hormone (ADH), aldosterone and the
renin–angiotensin system (RAS).
3. Describe the hormonal response to shock with specic
reference to ADH, aldosterone and the renin–angiotensin system.
e eect of ADH, aldosterone and the RAS all aim both to
increase blood pressure (and thus perfusion pressure) and
to maintain intravascular volume. ey have the following
eects:
• ADH: leads to an increase in the permeability of the
distal tubule and collecting ducts to water and thus
increases absorption and increases intravascular volume. It is also a potent vasoconstrictor.
• Aldosterone: leads to an increased absorption of
sodium in the distal convoluted tubules and thus acts
to increase plasma volume and blood pressure.
• RAS: renin leads to the conversion of angiotensinogen to angiotensin II. is is a powerful vasoconstrictor (thus increasing blood pressure) and also
stimulates the release of both ADH and aldosterone.
OSCE SCENARIO ANSWER 11.3
A 75-year-old male with a known lung malignancy is admitted in an acute confusional state. He is found to have a
sodium level of 117 mmol/L. He is not dehydrated and has
no signs of sepsis.
1. What possible explanation is there for the electrolyte
abnormality?
e lung malignancy and hyponatraemia in the presence of
normovolaemia would suggest SIADH (syndrome of inappropriate antidiuretic hormone secretion).
2. What other tests would help conrm it?
Measuring the urine sodium content and urine/plasma osmolality. In the face of hyponatraemia the urine will have sodium
level >40 mmol/L and urine osmolality will be >100 mOsm/
kg and the plasma osmolality is <280 mOsm/kg.
3. Which type of lung cancer most commonly causes it?
Small cell lung cancer is the commonest cause of SIADH.
4. How would you treat it?
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SECTION IV Appendix
An endocrinologist should be consulted. Treatment in the
acute setting consists of:
• 3% hypertonic saline
• water restriction 0.5–1.5 L per day
• loop diuretics to excrete free water
• vasopressin receptor antagonists (e.g. tolvaptan);
these block the AVP V2 receptors.
OSCE SCENARIO ANSWER 11.4
A 40-year-old male who was a restrained driver in a motor
vehicle crash was found to be paraplegic at the level of T10.
Aer primary and secondary survey, he was admitted to the
high-dependency unit and abdominal examination revealed
palpable bladder.
1. What is the normal innervation to the urinary bladder?
• L1–2: sympathetic outow via the hypogastric plexus
that acts to inhibit micturition by suppressing detrusor contraction and stimulating internal sphincter
contraction.
• S2–4: parasympathetic outow via the pelvic
splanchnic and pudendal nerves which stimulate
micturition by stimulating the detrusor muscle and
suppressing the internal sphincter contraction.
• Eerent sensory bres enter the spinal cord at L1–2
and S2–4.
2. What are the three bladder abnormalities that can
occur following spinal injury?
• Atonic bladder: or accid bladder, refers to a bladder whose muscles do not fully contract. Hence, the
patient might sense that they need to urinate, but
they are unable to because their bladder muscles will
not contract. As a result, the bladder can overow
with urine, causing leakage and discomfort.
• Automatic reex bladder: with a reex bladder, the
nerve impulses (known as the reex arc) between
the bladder and spinal cord remain intact but messages no longer reach the brain. A reex bladder
allows automatic, involuntary control of the bladder
so when the bladder lls above a certain level it contracts and urine ows out automatically. However,
the reex bladder may not empty completely due to
the sphincter not relaxing fully. is can leave a pool
of urine in the bladder which increases the risk of
infection and back pressure on the kidneys.
• Autonomous bladder: with autonomous bladder,
there is interruption in both the aerent and eerent
limbs of the reex arcs. Bladder sensation is absent;
dribbling is constant; residual urine amount is large.
3. Describe the bladder function following the initial
phase of spinal injury.
Atonic bladder occurs during the initial phase of spinal
shock and may last for several weeks; the following abnormalities are seen:
• Bladder wall muscle is relaxed.
• Sphincter vesicae is contracted.
• Sphincter urethra is relaxed.
• Bladder becomes distended and eventually empties
by overow. If the level of injury is above L1–2 then
the patient becomes unaware of the bladder distension; if the injury is below L1–2 then the patient is
aware of the distended bladder.
OSCE SCENARIO ANSWER 11.5
A 70-year-old male is admitted to the emergency surgical
unit with suprapubic pain and inability to pass urine for
12 h. He reported recent history of hesitancy, weak stream
and nocturia. Abdominal examination revealed a palpable
distended bladder. His creatinine is found to be 220 μmol/L
and GFR of 32 mL/min/1.73 m2, while his baseline test
2 months ago showed GFR of 60 mL/min/1.73 m2 and Cr
of 87 μmol/L.
1. What volume in the bladder normally triggers the urge
to urinate?
e intravesical pressure is normally around 3 cmH2O and
the pressure does not change much until the intravesical
volume reaches 200–300 mL, at which point the desire to
pass urine is felt. As the volume increases further, the intravesical pressure rises steeply.
2. What is the dierential diagnosis?
e clinical scenario suggests acute on chronic bladder urinary retention with a background of symptoms of benign
prostatic disease. e commonest cause is benign prostate
hypertrophy. Other causes include prostate cancer, severe
constipation, urethral stricture, urinary tract infection,
drugs, general anaesthesia and a mass or cancer in the
pelvis.
3. What is the likely cause of his renal function
deterioration?
Causes of acute kidney injury can be classied into prerenal, renal, or post-renal. In this case, the cause is postrenal due to obstructive uropathy and inability to void,
which results in tubulointerstitial injury. is tends to be
reversible if urinary retention is treated promptly.
4. e patient was found to have been recently com-
menced on tamsulosin by his GP. How does tamsulosin
work?
Tamsulosin is a drug that inhibits α1 sympathetic receptors
located in the prostate smooth muscles which in turn relax
the bladder neck and relieve some of the symptoms associated with benign prostatic disease.
APPENDIX OSCE Scenario Answers
457
OSCE SCENARIO ANSWER 12.1
A 32-year-old female is admitted with suspected acute appendicitis. She is sweating, agitated, confused and complaining of
palpitations. Her symptoms do not t with a straightforward
diagnosis of acute appendicitis. Examination reveals a temperature of 40°C and a tachycardia of 140 with an irregularly
irregular pulse. You check her thyroid function, which reveals
an elevated T3 and T4 with suppressed TSH.
1. What is the most likely diagnosis?
e symptoms and signs suggest a thyroid storm (crisis).
2. What may precipitate the condition?
yroid storm is an uncommon condition but has a mortality rate >50%. It is a hypermetabolic state that occurs
in undiagnosed patients with hyperthyroidism and also in
inadequately treated patients with hyperthyroidism. It is
commonly precipitated by infection, trauma or surgery.
3. How is the condition managed?
Immediate recognition of the condition is the key to managing patients with a thyroid storm (crisis). yroid storm
(crisis) is manifest by hyperpyrexia, tachycardia, hypertension, severe tremor, agitation, confusion and high output
cardiac failure. Conrmation of the diagnosis is with urgent
thyroid function tests. Medical management consists of:
• ABC: high-ow oxygen i.v. access and uids
• if infection is suspected, treat empirically with
antibiotics
• high-dose propylthiouracil: prevents the production
of more T4 and T3 and blocks the peripheral conversion of T4 to T
• 1 h aer administration of propylthiouracil, admin-
3
ister Lugol’s iodine. is blocks the release of stored
T4 and T3. If it is given before the propylthiouracil
works, it will increase the release of thyroid hormone
• hydrocortisone: blocks the peripheral conversion of
T4 to T
• beta-blocker: used to treat tachycardia, tremor and
3
agitation.
OSCE SCENARIO ANSWER 12.2
A 40-year-old male presents to his GP with intermittent headaches, palpitations, sweating, anxiety and intermittent chest
pains. Examination reveals a blood pressure of 180/110 mmHg.
1. What endocrine condition do you need to consider?
Explain the condition.
• A diagnosis of phaeochromocytoma must be consid-
ered in this case.
• Phaeochromocytomas are tumours of the chromaf-
n cells. Around 90% arise in the adrenal glands.
Phaeochromocytomas are known as the ‘10%’ tumour
as 10% are bilateral, extra-adrenal, multiple or familial
(especially MEN IIa and IIb) and malignant.
2. How could you conrm the diagnosis?
e diagnosis is conrmed by:
• Biochemical diagnosis: 24 h acidied urine sample
for VMA (vanillylmandelic acid), which is a breakdown product of catecholamines.
• Imaging diagnosis: CT and MRI are accurate in the
majority of cases. MRI is preferred as it is more accurate in identifying extra-adrenal tumours. Radioisotope MIBG scans (
131
I-metaiodobenzylguanidine)
may be used for extra-adrenal tumours and metastases in cases of malignancy.
3. What measures would you take to prepare the patient
for surgery?
Two main forms of medication are required:
• Alpha-adrenergic blockade with phenoxybenzamine. Treatment should be given prior to surgery
until nasal stuness and postural hypotension occur.
High dosage may need to be gradually introduced to
block the adrenergic eects of the tumour.
• Beta-blockade with propanolol should be used only
when alpha-blockade is complete. If used before, it
may precipitate a hypertensive crisis.
OSCE SCENARIO ANSWER 12.3
A 64-year-old female is admitted for major gastrointestinal
surgery. She is taking 5 mg prednisolone and has been doing
so for 6 months.
1. What are the risks of failing to replace steroids
pre-operatively?
Steroids will cause adrenal suppression. At the time
of major surgery the body needs increased steroids as
a part of the acute phase response. If this is not met
due to the adrenal suppression, then an Addisonian
crisis may occur. This presents as low BP, hypoglycaemia, confusion, hyponatraemia, hyperkalaemia and
hypercalcaemia.
2. How would you manage her steroid administration
prior to major surgery?
For major surgery the patient takes the usual pre-operative
steroid dose. She should have 25 mg of hydrocortisone i.v.
on induction and then 100 mg i.v. daily for 48–72 h unless
there are post-operative complications.
3. How long aer stopping steroids would a patient not
require pre-operative replacement?
If the patient has stopped taking steroids, a period of stress
may still cause an Addisonian crisis. is is a potential risk
up to 3 months from the time of stopping steroids. Aer 3
months, steroid replacement is not required.
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SECTION IV Appendix
OSCE SCENARIO ANSWER 12.4
A 46-year-old female has undergone a total thyroidectomy –
you are called to the ward as the patient is suering from
severe cramps and numb peripheries.
1. What are Chovstek’s and Trousseau’s signs?
Chovstek’s sign is a contraction of the facial muscles when
you tap the facial nerve just in front of the external auditory meatus. Trousseau’s sign is a spasm of the hand when
a blood pressure cu is inated.
2. What is causing the above symptoms and why? What
would you expect to see on an ECG and how would you
treat it?
e above symptoms are due to hypocalcaemia. e likely
cause for this in this patient is either ischaemia or inadvertent removal of all parathyroid glands. An ECG would
typically show a prolonged QT interval. Treatment is with a
combination of i.v. calcium gluconate acutely and a combination of oral calcium and vitamin D.
3. Why has the hypocalcaemia happened and what will
be the long-term treatment?
e parathyroid glands are intimately related to the thyroid
gland and may be removed or damaged during surgery. In
addition, ligation of the inferior thyroid artery may render them ischaemic. Preservation during surgery is the
mainstay of preventing this complication. If the gland is
removed accidentally it can be diced and then placed in an
intra-muscular pocket in the sternomastoid where it will
eventually be revascularized. Even if this is not done, parathyroid function will eventually return to normal as ectopic islands will grow or retained parathyroid tissue will
revascularize. In the short term, the hypocalcaemia may
need to be managed with i.v. calcium gluconate acutely or
vitamin D and oral calcium in the long term if symptoms
persist.
OSCE SCENARIO ANSWER 12.5
A 45-year-old male attends a GP surgery with some strange
symptoms – he describes episodes of sweating, palpitations,
being confused and forgetting things, and also abdominal
pain and diarrhoea. A friend thought it might be diabetes
and measures his blood sugar during an episode and found
it to be 3 mmol/L.
1. What is the diagnosis and what is the classic triad asso-
ciated with this condition?
ere are a number of possibilities but the symptoms
would be highly suggestive of an insulinoma. Symptoms
are either due to a lack of glucose, i.e. weakness, sweating, lack of cerebral glucose (confusion, forgetfulness or
odd behaviour) or from GI tract problems, such as hunger
or diarrhoea. e classic triad is Whipple’s triad, which
is symptoms due to hypoglycaemia, a diagnosis of low
glucose at the time of the symptoms and having glucose
relieves the symptoms.
2. What cells does the disorder arise from?
Insulin is produced in β-cells so insulinomas arise from
pancreatic β-cells.
3. What percentages are benign or malignant?
Malignancy is not common and only around 10% are
malignant.
4. What syndrome are they associated with?
Insulinomas can be related to a group of conditions known
as multiple endocrine neoplasia; this is an autosomal dominant condition and there are three types. Most typically
insulinomas are associated with MEN I. MEN I is associated with hyperparathyroidism, pancreatic/duodenal
tumours and pituitary tumours. MEN IIA is associated
with medullary thyroid carcinoma, phaeochromocytoma
and hyperparathyroidism. MEN IIB is associated with
same as IIa but patients have multiple ganglioneuromas
and a marfanoid appearance.
OSCE SCENARIO ANSWER 13.1
An 18-year-old male is admitted to A&E following an assault.
He has severe head injuries. His GCS is 6.
1. How is brain injury classied?
Brain injury is classied as primary or secondary.
• Primary: this is the damage caused as an immediate
result of trauma. It results in contusions, lacerations
and diuse brain damage. ere are two mains types:
focal damage or diuse axonal injury. Treatment
cannot reverse primary brain injury.
• Secondary: this develops as a result of complications.
Complications include intracranial haemorrhage,
cerebral hypoxia, cerebral oedema, intracranial herniation and cerebral infection, e.g. meningitis. e
prevention, recognition and treatment of these secondary complications are the mainstay of treatment
of the patient with head injuries.
2. Describe the mechanism of compensation for an acute
rise in intracranial pressure.
• e skull, which is a rigid container, contains the
brain, CSF and blood. e volume of the brain is
static and cannot alter. Compensation occurs following head injury as the swelling/haematoma pushes
CSF and blood out of the skull vault. is will compensate for a mass of approximately 100–150 mL.
Aer this point the ICP sharply increases as compensation can no longer occur.
• is is referred to as the Monro–Kellie hypothesis,
which states that the ICP will increase if the volume
of one component is increased. e increase in ICP
APPENDIX OSCE Scenario Answers
459
can only be compensated for by a decrease in one or
both of the other components.
e patient is transferred to ITU and you are called because
the intracranial pressure (ICP) has risen acutely.
3. Describe the possible management options.
As with any critically ill patient, the initial management
should be according to ABC principles. In an isolated
head injury, ICP should be kept below 20 mmHg. In a
patient with an ICP above this, options for management
include:
• Position the patient head up 30° to improve venous
drainage (removing a spinal collar can only help if
safe to do so).
• Sedate the patient: this decreases cerebral metabolism and can be achieved with propofol or thiopental.
• Hyperventilation: normally a patient should be normocarbic but in instances of sudden increase in ICP,
a period of hyperventilation may buy time.
• Treat with i.v. mannitol, an osmotic diuretic that
reduces brain water and thus volume.
• Inducing hypothermia may be protective.
• Contact the neurosurgical team. ey may advise
re-scanning of the patient to identify a reason for
deterioration. Surgical options include CSF drainage, evacuation of haematoma, craniectomy and
lobectomy.
OSCE SCENARIO ANSWER 13.2
A 55-year-old male presents to a pain clinic with a long history
of lumbar back pain that has become more severe recently.
ere is no history of sciatica and there is no neurological
decit on examination. Paracetamol has been of no benet.
1. Why is paracetamol unlikely to have been of benet?
• Paracetamol is an eective analgesic and anti-pyretic.
It is believed to inhibit COX-3 (cyclo-oxygenase-3)
in the spinal cord and brain, and this results in
analgesia. It has little eect on COX-1 and 2, thus
explaining its poor anti-inammatory action.
• is patient is likely to have a signicant inammatory component to his pain and this explains the lack
of benet from paracetamol.
He is commenced on ibuprofen.
2. Why is this more likely to be of benet than
paracetamol?
Ibuprofen is an inhibitor of COX-1 and COX-2 enzymes,
leading to inhibition of a number of prostaglandins involved
in pain transmission (thus explaining the analgesic eect).
It also inhibits prostaglandins involved in inammation.
Treatment with ibuprofen brings about little improve-
ment and he is treated with a TENS machine.
3. What is the mechanism of action of TENS?
• TENS is thought to work by closing the gate on
pain, i.e. preventing onward transmission of pain
signals from the dorsal horn of the spinal cord
to the ascending sensory nerves (spinothalamic
tract) which connect to the pain centres in the
brain.
• TENS signals arrive at the dorsal horn by large sensory A-bres at the same time as pain signals arriving
via small sensory C-bres. If the large A-bre input
is signicantly strong, the C-bre input is inhibited,
producing pain relief.
TENS provides initial improvement but the benet is
slowly lost. He is treated by facet joint injections with local
anaesthetic and steroid.
4. What is the purpose of the local anaesthetic injec-
tion and what is the mechanism of action of local
anaesthetics?
• e combination of steroid and local anaesthetic
injections produces a combination of the short-lived
pain relief given by local anaesthetic followed by the
longer-term relief provided by the anti-inammatory action of the steroids.
• Local anaesthetics reversibly block nerve conduction
by inactivating sodium channels. is preferentially
aects smaller nerve endings that transmit sharp
pain.
Facet joint injections with steroid fail to give lasting relief
and he is commenced on Oramorph (morphine).
5. What is the mechanism of action of Oramorph and
what side eects might be expected?
• Oramorph is a liquid form of morphine, a member
of a group of drugs known as opiates. Opioid painkillers work by mimicking the action of naturally
occurring pain-reducing chemicals called endorphins. Endorphins are found in the brain and spinal cord and reduce pain by combining with opioid
receptors.
• Oramorph interacts predominantly with the opioid
mu receptor in the brain (posterior amygdala, thalamus, caudate nucleus and putamen) and spinal cord
(substantia gelatinosa).
• Side-eects of opiates include dependence, respiratory depression, sedation, itching, nausea and
constipation.
OSCE SCENARIO ANSWER 13.3
A 24-year-old male is in a critical condition on ITU following
a road trac accident. He has severe head injuries. e ITU
consultant has discussed his poor prognosis with the family
and they ask about organ donation. Answer the following
questions regarding testing for brainstem death.
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SECTION IV Appendix
1. What are the preconditions required before diagnosing
brainstem death?
ere are four preconditions for diagnosing brainstem death:
• patient must be in a coma
• known cause for coma
• cause is irreversible
• patient dependent on ventilator.
2. What are the exclusion criteria?
ere are three exclusion criteria prior to carrying out
brainstem death tests:
• no residual eects from drugs: e.g. narcotics, hypnotics, tranquilizers, muscle relaxants, alcohol or
illicit drugs
• core body temperature >35°C
• no reversible causes that may contribute coma (circulatory, endocrine or metabolic).
3. Which cranial nerves are involved in the following
tests:
Corneal reex
Gag reex
Cough reex
Vestibulocochlear reex
e cranial nerves involved in each test are as follows:
• Corneal reex – V and VI
• Gag reex – IX and X
• Cough reex – IX and X
• Vestibulocochlear reex – III, VI and VIII.
OSCE SCENARIO ANSWER 13.4
A 75-year-old male patient is found confused during a night
shi, 5 days following le hemicolectomy. He has past medical history of TIA, IHD and BPH. On examination, his GCS
is 13/15, he appears combative and hallucinating, his temperature is 38.9°C, RR is 25/min, PR is 120/min and irregular
and blood pressure is 115/65. His chest examination shows
possible reduced air entry on the le side, he is diusely tender in the abdomen, and he has a urinary catheter with urine
output averaging 20/h over the last 3 h. Bedside ECG shows
new fast AF. You are the night surgical SPR and asked to
review the patient.
1. How would you manage this patient?
is patient is suering from acute onset postoperative
confusion and management should be along the guidance of the care of critically ill surgical patients’ course
(CCrISP) with assessment of ABCDE, etc. In summary,
oxygen therapy and commencement of intravenous uid
resuscitation should be followed by history and examination, including a review of his medical notes, drug chart,
vital signs, uid balance charts and recent lab results. In
addition to bedside ECG, up-to-date blood tests including FBC, U&E, LFT, glucose and ABGs should be sought.
As the patient has signs of sepsis, it is important to look
for a source and initial assessment with blood cultures,
chest X-ray, sputum culture (if applicable), midstream
urine and wound swabs should be sent. Assessment
should include examination for infected lines and early
commencement of broad-spectrum intravenous antibiotics. While the patient is very confused and has fast AF,
these are secondary signs to sepsis and addressing the
acute presentation with sedation, e.g. haloperidol, and
medical control of fast AF, e.g. digoxin, might be required
at certain points in his management but should not be
the sole management plan.
2. What is the dierential diagnosis?
e presence of fever in this scenario suggests infection
as the underlying cause; however, other causes should be
ruled out with a detailed assessment. Other causes can be:
• dehydration
• electrolyte abnormalities
• hypoxia
• drugs
• uraemia
• hypoglycaemia
• pre-existing psychiatric disorder or dementia
• alcohol and drug withdrawal
• urinary retention
• pain and anxiety
• cerebrovascular accident (CVA)
• head injury (especially trauma patients)
• sleep deprivation
• ITU syndrome: pain, fear and sleep deprivation can
lead to visual and auditory hallucinations and inability to dierentiate reality from fantasy.
3. What is the most likely cause?
e clinical scenario suggests infection as the underlying
cause of confusion and the patient has mainly abdominal
signs. In the context of recent colonic surgery, the possibility of anastomotic leak or intra-abdominal infected collection should be considered, and CT abdomen and pelvis
would be indicated.
4. Who would you inform at this stage?
In addition to the surgical consultant on call, it would be
relevant to inform the on-call radiologist regarding the
urgency of the CT scan; the critical team outreach as the
patient might need perioperative admission to critical care;
the on-call anaesthetic and theatre team as he might need
emergency laparotomy and patient’s next of kin to inform
them of his progress.
OSCE SCENARIO ANSWER 13.5
A 65-year-old male patient has been stepped down from the
high-dependency unit to the ward on day 2 following open
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