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APPENDIX OSCE Scenario Answers
441
third and lower two-thirds. It runs downwards
and laterally across the triangle on levator scapulae
muscle and passes deep to the anterior border of trapezius at the junction of the upper two-thirds and
lower third.
• Injury to the spinal accessory nerve in the right posterior triangle of the neck will result in inability to
shrug the shoulder on that side due to paralysis of
trapezius.
OSCE SCENARIO ANSWER 5.3
A 40-year-old female is to undergo a subtotal thyroidectomy
for a multinodular goitre.
1. Describe the gross anatomy of the thyroid gland.
e gland is composed of two lateral lobes connected
by an isthmus. e lateral lobes extend from the lateral
aspect of the thyroid cartilage to the level of the 6th tracheal ring. e isthmus overlies the 2nd and 3rd tracheal
rings. An inconstant pyramidal lobe extends up from the
isthmus.
2. When exposing the gland at surgery, which structures
are encountered?
Skin, platysma, deep investing fascia (which is opened
longitudinally between the strap muscles and between the
anterior jugular veins) and pretracheal fascia. e strap
muscles are overlapped by the sternocleidomastoid muscles in the lateral part of the incision.
3. Describe the arterial blood supply of the thyroid gland.
e arterial supply comes mainly from two arteries.
• e superior thyroid artery arises from the external
carotid artery and passes to the upper pole.
• e inferior thyroid artery arises from the thyrocer-
vical trunk of the rst part of the subclavian artery.
• A small inconstant artery, the thyroidea ima, arises
from the aortic arch.
4. Where are the nerves situated in relation to the gland
and when are they in danger of damage?
• e external branch of the superior laryngeal nerve
is close to the superior pole of the gland and is in
danger when ligating the superior thyroid artery,
which must be ligated close to the upper pole of the
gland.
• e recurrent laryngeal nerve lies in the groove
between the trachea and oesophagus close to the
inferior thyroid artery, which must be ligated far
away from the gland.
OSCE SCENARIO ANSWER 5.4
A 35-year-old female is referred to the ENT clinic aer
recurrent episodes of nasal congestion, nasal discharge,
fever, headache, tiredness, and facial pain in the right cheek.
COVID-19 swabs were negative on several occasions and
the GP is seeking advice for management of possible chronic
sinusitis and is concerned that the symptoms are unilateral.
1. What are the paranasal sinuses and where are they
located?
e paranasal air sinuses are four, paired, complex airlled cavities that open into the nasal cavity and are lined
by columnar ciliated epithelium. ese are:
• e frontal sinuses are in the frontal bone and are
separated by a bony septum.
• e maxillary sinuses are located within the maxilla
at the lateral margin of the nasal cavity.
• e ethmoid sinuses are a group of 8–10 air-containing
cavities within the lateral mass of the ethmoid bone, in
between the upper nasal cavity and the orbit.
• e sphenoid sinuses lie within the body of the sphe-
noid bone.
2. Where do they drain into?
• e maxillary sinus: opens into the hiatus semilunaris
in middle meatus. e opening of the sinus lies high on
the medial wall just below the oor of the orbit. As the
ostium is high on the wall, drainage depends on ciliary
action and not gravity.
• e anterior and middle ethmoidal sinuses: drain
into the middle meatus.
• e posterior ethmoidal sinus: drains into the supe-
rior meatus.
• e sphenoidal sinus: drains into the sphenoeth-
moidal recess.
3. How would you go about draining the maxillary sinus
surgically?
e maxillary sinus is the largest paranasal sinus and washout can be performed through a cannula insertion via the
inferior meatus of the nasal cavity, most commonly performed endoscopically, while antral drainage through the
gingivolabial fold (known as the Caldwell Luc procedure)
traditionally involved removing part of the anterior bony
wall of the maxillary sinus.
4. How can carcinoma of the maxillary sinus present?
is depends on which surrounding structures it invades.
• Invading the oor of the sinus causes dental
problems.
• Invading the medial wall may block the nasolacrimal
duct causing epiphora or it may invade the nasal cavity causing nasal blockage or epistaxis
• Invading superiorly can cause proptosis
• Invading the posterior wall may involve the palatine
nerves and produce severe pain referred to the teeth
of the upper jaw.
e GP is right to be concerned that the symptoms are
unilateral.
442
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SECTION IV Appendix
OSCE SCENARIO ANSWER 5.5
A 29-year-old male presented to Accident and Emergency
with mandibular pain and inability to occlude the teeth following a bout of excessive laughter while watching a comic
movie in the cinema. Examination of the temporomandibular joint (TMJ) revealed prominent mandibular head
anteriorly.
1. What is the likely diagnosis and what other events can
cause it?
e likely diagnosis is a dislocation of the jaw or temporomandibular joint. Causes range from yawning, laughing,
prolonged dental procedures, trauma or seizures.
2. What would you nd on examination?
e most common symptom is an inability to close the
mouth. Pain is oen present on the aected side. e patient
may nd it dicult to talk and swallow saliva. Palpation
over the pre-auricular area may reveal an emptiness in the
joint space (it may just feel dierent to the other side).
3. What type of joint is TMJ?
Formed by articulation of the head of the mandible with
mandibular fossa and articular eminence of temporal bone,
the TMJ is atypical synovial joint consisting of a bro-cartilaginous disc and brocartilage on the bony surfaces.
4. How would you treat the patient?
is patient has suered from an anterior dislocation which
is the most common type that aects this joint and can be
reduced by pressing down the mandible on the molar teeth
to stretch the masseter and temporalis which are in spasm
then pulling up the chin to lever the condyle back into the
mandibular fossa (essentially downwards and backwards).
is can be done using an auriculotemporal nerve block or
local anaesthetic inltration into the joint or under general
anaesthesia.
OSCE SCENARIO ANSWER 6.1
An 18-year-old male is assaulted at a party. He is struck on
the le temporal region with a bottle. He briey loses consciousness. He is taken to hospital where on examination
his GCS (Glasgow Coma Scale) is 15. Four hours following
admission, he suddenly deteriorates with a GCS of 8 and his
le pupil dilates.
1. What is the most likely diagnosis?
Extradural haematoma.
2. What is the explanation for the ‘lucid’ interval?
e lucid interval occurs aer the patient comes round from
the concussion caused by the force of the initial trauma and
before lapsing into unconsciousness again due to bleeding
into the cranial cavity, which gives rise to increased intracranial pressure with resulting brain damage.
3. What is the anatomical basis for the le pupillary
dilatation?
e haematoma pushes the most medial part of the temporal lobe, the uncus, across the tentorial hiatus, compressing the ipsilateral 3rd (oculomotor) nerve. is paralyses
the constrictor pupillae, allowing unopposed action of the
sympathetic nerves which supply the dilator papillae.
4. Where would you locate the middle meningeal artery
for the purpose of making a burr hole?
• e anterior branch of the middle meningeal artery
lies in the region of the pterion and is the usual
source of extradural haemorrhage.
• e middle meningeal artery enters the skull at a
point level with the midpoint of the zygomatic arch
and divides 2 cm above it.
• e pterion, a point important for making a burr
hole, is 4 cm above the zygomatic arch and 3.5 cm
behind the lateral angle of the eye.
5. What layers of the scalp would you encounter in your
incision?
e layers are:
• skin
• subcutaneous tissue
• aponeurosis
• loose areolar tissue
• temporalis muscle
• periosteum (pericranium).
OSCE SCENARIO ANSWER 6.2
A 55-year-old male presents with low back pain, bilateral sciatica, numbness over the buttock area and weakness in the
lower limbs. He has also developed diculty in passing urine.
Examination reveals reduced lower limb reexes and loss of
anal tone and sensation.
1. What is the most likely diagnosis?
Cauda equina syndrome.
2. At what level does the spinal cord end in the adult?
At the level of the disc between the 1st and 2nd lumbar
vertebrae.
3. Describe the level and type of disc lesion that is likely to
cause the symptoms.
It is likely to be caused by a central disc lesion at L4–5 or
L5–S1 level.
4. Describe the anatomy of an intervertebral disc.
Each intervertebral disc consists of:
• Peripheral annulus brosus, which is adherent to the
thin, cartilaginous plate on the vertebral body above
and below.
• Nucleus pulposus, which is a gelatinous uid sur-
rounded by the annulus brosus.
APPENDIX OSCE Scenario Answers
443
• e posterior part of the annulus brosus is relatively thin and prone to rupture due to degenerational injury. e nucleus pulposus protrudes into
the vertebral canal through intervertebral foramen.
• In the case of cauda equina syndrome, the disc lesion
is directed posteriorly or central.
5. Explain the anatomical basis of bladder and bowel
dysfunction.
• S2, 3, 4 give o nerve bres (pelvic splanchnic
nerves) which are distributed to the pelvic organs.
• e sacral parasympathetic bres supply motor
bres to the bladder and inhibitory bres to the
internal vesical sphincter. Damage to these nerves
leads to accid paralysis of the bladder and internal
sphincter dysfunction.
• e parasympathetic system also supplies motor
bres to the muscles of the rectum and inhibitory
bres to the internal anal sphincter. Damage results
in bowel dysfunction.
6. What investigation would you carry out to conrm the
diagnosis and what action would you take if the diagnosis was conrmed?
• Urgent MRI.
• If the diagnosis is conrmed, urgent referral is required
for surgical decompression.
OSCE SCENARIO ANSWER 6.3
A 55-year-old insulin-dependent diabetic develops a boil on
the right upper lip. She does not seek treatment. A few days
later she develops a severe headache and redness and swelling
around the right orbit. A diagnosis of cavernous sinus thrombosis is made.
1. Describe the anatomy of the cavernous sinus.
• e cavernous sinuses lie one on either side of the
body of the sphenoid bone against the wall of the
pituitary fossa. ey extend from the superior orbital
ssure to the apex of the petrous temporal bone.
ey communicate with one another via the intercavernous sinuses. e internal carotid artery and
abducent nerve (VI) pass through it.
• On the lateral wall from above down are:
• ocular motor nerve (III)
• trochlear nerve (IV)
• ophthalmic nerve (V1)
• maxillary nerve (V2).
• e ophthalmic veins drain into the anterior part of
the sinus.
• Emissary veins pass through foramina of the middle
cranial fossa connecting the cavernous sinus to the
pterygoid plexus and facial veins.
• e optic tract and the internal carotid artery lie
above the sinus, the latter piercing the roof of the
sinus then doubling back to lie against it.
2. Why does cavernous sinus thrombosis develop following an infection on the upper lip?
Cavernous sinus thrombosis may develop as a result of the
spread of infections from the lips and part of the cheek
via the anterior facial and ophthalmic veins, or from deep
infections via pterygoid venous plexus, all of which drain
into the sinus. Diabetics and immunosuppressed patients
are particularly at risk of cavernous sinus thrombosis following infections on the upper lips and cheek.
3. Describe the characteristic clinical picture of cavernous sinus thrombosis.
e characteristic clinical picture consists of:
• oedema of the conjunctiva (chemosis) and eyelids
• exophthalmos with transmitted pulsations from the
internal carotid artery (pulsating exophthalmos)
• ophthalmoplegia due to pressure on the contained
cranial nerves
• papilloedema, venous engorgement and retinal haem-
orrhages are seen on ophthalmoscopy.
OSCE SCENARIO ANSWER 6.4
A 75-year-old male has been referred to you by the Accident
and Emergency department for a possible stroke. His main
symptom is le arm and leg weakness.
1. Which hemisphere has suered a stroke?
When describing carotid symptoms following a TIA it can
be quite confusing; the symptoms are le sided but this
would mean the right carotid is the symptomatic side, so
we would refer to this as a right hemispheric event.
2. If the patient had suered le sided amaurosis fugax
which hemisphere would have been aected?
Amaurosis fugax is a sensation of a curtain closing over
ones eye. It happens when a clot passes through the retinal
artery. Unlike weakness, which is the contralateral carotid,
the side aected by amaurosis is the same as the symptomatic carotid, i.e. a le amaurosis fugax is caused by a le
carotid artery stenosis.
3. e patient is right-handed and has had dysphasia
only. Which hemisphere is the most likely to have been
aected and why?
Dysphasia is diculty nding words and is not an uncommon symptom; indeed it may well be the only presenting
complaint. In 90% of right-handed people the speech area lies
in the le hemisphere. In le-handed people it is not quite so
simple and can be in the le hemisphere in 50% of people. In
the above example one could be condent the patient had a
symptomatic le carotid lesion, as he is right-handed.
444
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SECTION IV Appendix
OSCE SCENARIO ANSWER 6.5
A 70-year-old non-smoking female presents with a hoarse
voice. A CT angiogram is shown below Fig. 6.5Q.
1. What is the diagnosis?
e patient has a thoracic aortic aneurysm.
2. What are the treatment options?
e options, as with any condition, can be divided into
conservative, medical or surgical. Clearly there are no
medical treatment options but conservative management
may be appropriate for patients who do not wish to have
treatment or are not t enough. Surgical treatment can be
divided into open or endovascular. In the majority of conditions the preferred treatment would be an endovascular repair using a thoracic stent gra (TEVAR – thoracic
endovascular aneurysm repair). Surgery may be preferred
in the very young or those with congenital conditions
aecting the aorta, such as Marfans or Ehlers-Danlos
syndrome.
3. What is the anatomical explanation for the hoarse voice?
e le recurrent laryngeal nerve branches o the vagus
nerve as it crosses the aortic arch. e nerve then passes
underneath the aortic arch behind the ligamentum arteriosum and passes superiorly into the neck. As thoracic
aneurysms grow, the nerve is compressed against the ligamentum arteriosum causing nerve palsy (see Fig. 6.5A).
e le recurrent laryngeal nerve supplies all the intrinsic
muscles of the larynx except the cricothyroid muscles.
OSCE SCENARIO ANSWER 7.1
A 64-year-old male is admitted for a right hemicolectomy
and is found to have a serum sodium of 120 mmol/L.
1. What are the possible causes of hyponatraemia in this
patient?
Hyponatraemia has a number of causes, which may be
dened by asking two questions:
• What is the volume status of the patient: is he hypo-
volaemic, hypervolaemic or normovolaemic?
• Is the sodium in the urine >20 mmol/L or <20 mmol/L?
• Hypovolaemia + urine Na >20 mmol/L = exces-
sive renal loss (diuretics and salt losing renal disease), mineralocorticoid deciency.
• Hypovolaemia + urine Na <20 mmol/L = extra-
renal losses or sequestration.
• Hypervolaemia + urine Na >20 mmol/L = renal
failure.
• Hypervolaemia + urine Na <20 mmol/L = cir-
rhosis, cardiac failure, nephritic syndrome.
• Normovolaemia + urine Na >20 mmol/L = glu-
cocorticoid deciency, hypothyroidism, SIADH
(syndrome of inappropriate ADH secretion).
2. Describe what investigations you would carry out in
order to identify the cause of the hyponatraemia.
e investigations are:
• U&Es
• TFTs
• LFTs
• serum and urine osmolality
• urine sodium
• serum cortisol
• serum ADH
• Synacthen test (identies adrenal failure).
3. How would you correct it?
e treatment depends on the cause. If hypervolaemic,
then volume restriction is appropriate. If the patient is volume depleted, then intravenous normal saline is required.
Hyponatraemia should not be rapidly corrected, as this
may lead to central pontine myelinolysis.
OSCE SCENARIO ANSWER 7.2
An 82-year-old male is transferred to ITU following a
Hartmann’s procedure for perforated diverticular disease. He
has been anuric for 3 h. A number of uid challenges have
been given, achieving a BP of 120/90 mmHg, pulse of 87
beats/min and a CVP of 10 mmHg. ABG analysis shows a
pH of 7.2 and U&Es reveal serum potassium of 7.1 mmol/L.
Fig. 6.5A CT angiogram of the Thoracic Aorta show-
ing a large aneurysm (circled).
1. What are the possible causes of hyperkalaemia in this
patient?
APPENDIX OSCE Scenario Answers
445
e possible causes of hyperkalaemia include:
• acute renal failure
• metabolic acidosis
• excess administration of potassium
• adrenal insuciency (rare).
2. What are the ECG changes associated with
hyperkalaemia?
e ECG changes associated with hyperkalaemia are:
• peaked T-waves
• loss of P-waves
• widened QRS complexes.
3. What would be your possible treatment options for this
patient? Explain how each works to lower the serum
potassium.
e treatment options for hyperkalaemia include:
• 10 mL of 10% calcium gluconate intravenously. It
stabilizes cardiac myocytes, decreasing the risk of
arrhythmia. It has no eect on the serum potassium
level and the eect is short lived.
• Insulin and dextrose infusion (10 units of Actrapid
in 50 mL of 50% glucose). Insulin promotes K+ and
glucose inux into cells via stimulation of the Na/K
ATPase pump. Dextrose prevents the development
of hypoglycaemia.
• Salbutamol (can be given by nebulizer). Stimulates β2
receptors, leading to increased cellular uptake of K+.
• Oral or rectal calcium resonium. is is an ion
exchange resin, calcium being exchanged for potassium, which is then lost in the faeces. It takes 24 h
to work and is therefore inappropriate in the emergency situation.
OSCE SCENARIO ANSWER 7.3
A 56-year-old male is admitted with severe dehydration and
vomiting. His urea and creatinine are raised at 15 mmol/L
and 215 µmol/L, respectively. A blood gas analysis shows
the following abnormalities – pH 7.55, PO2 10.9 kPa, PCO2
6.9 kPa and HCO
1. What type of metabolic abnormality is this patient
displaying?
e patient has a metabolic alkalosis – this is indicated
by the pH showing alkalosis. e fact that it is metabolic
in nature is indicated by the raised CO2 (compensatory
hypoventilation) and the low HCO
by the kidneys). e fact that the HCO
gest the cause of the alkalosis is loss of H+ ions rather than
excess HCO
2. How has it occurred?
Vomiting results in a loss of H+ ions and thus a metabolic
alkalosis.
3
–
.
3
–
is 21 mmol/L.
–
(compensatory loss
3
–
is low would sug-
3
3. e patient has a ‘succussion splash’ on examination.
What is the diagnosis?
A ‘succussion splash’ is a characteristic nding in gastric
outlet obstruction which leads to severe vomiting.
4. How would you manage this condition?
e management of this condition would fall into:
• Resuscitation and correction of electrolyte
abnormalities.
• Investigation as to the cause – OGD and/or CT scan.
• Management of the cause – the commonest causes
are peptic ulcer disease or malignancy. If due to
malignancy, then surgical resection of the tumour
or palliative gastro-jejunostomy would be appropriate. If due to peptic ulcer disease, then initial medical
management with i.v. PPI is appropriate for 48–72 h.
If there is no improvement, then surgical resection
may be deemed appropriate.
OSCE SCENARIO ANSWER 7.4
A 35-year-old female patient with weight of 70 kg underwent
uncomplicated appendicectomy. As she arrives back to the
ward, the nurses ask you to prescribe her intravenous uids
for the next 24 h as she is unable to eat and drink due to
nausea.
1. What are the volumes of the uid compartments of the
body?
For a 70-kg man there would be approximately:
• 25 L of intracellular water
• 19 L of extracellular water, comprising:
• 3 L plasma
• 15 L interstitial uid
• 1 L transcellular uid, e.g. CSF, peritoneal uid,
intraocular uid.
2. In general, what are the average daily uid and electrolyte requirements?
• Approximately 40 mL/kg/day of uid
• Sodium: 1–2 mmol/kg/day
• Potassium: 0.5–1 mmol/kg/day
3. What intravenous uids would you prescribe for the
next 24 h?
• For uncomplicated patient, postoperative intrave-
nous uid prescription should include 2.5–3 L of
uid containing 150 mmol of Na+ and 60 mmol of
K+ per day.
• A suitable uid regimen for 24 h would therefore be
as follows:
• 1000 mL 0.9% sodium chloride + 40 mmol KCL
• 1000 mL 5% dextrose
• 1000 mL 5% dextrose + 20 mmol KCl.
Each bag to of uid is given over 8 h.
446
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SECTION IV Appendix
OSCE SCENARIO ANSWER 7.5
A 65-year-old male patient is bought to the Accident &
Emergency department with acute abdominal pain. He looks
very unwell and is in obvious pain and is very confused. He is
wearing a medical alert bracelet informing you he is diabetic.
He has a temperature of 39°C and his blood pressure is 90/50
with a heart rate of 110. He has a rather strange smell of
acetone or ‘pear drop’ sweets.
1. What is the diagnosis?
e clue is in the medic alert bracelet and the characteristic
‘pear drop’ smell. is patient likely has diabetic ketoacidosis. is is oen triggered by an infection, so he quite likely
has an acute abdominal infection that has led to the ketoacidosis. e characteristic smell is ketones in the breath.
2. What would you expect his blood gases to show and
why?
e blood gas will show severe acidosis, the pH will be less
than 7.3 (in severe cases may fall below 7) and the bicarbonate will also be low (around 10 mmol/L) as excess acid
is neutralized. In addition the anion gap will be >10. is
is due to the metabolism of fat (lipolysis) and resulting production of free fatty acids. e fatty acids are metabolized
and produce acetyl CoA, the citric acid cycle (that breaks
down the acetyl CoA) is overwhelmed and acetyl CoA gets
converted to ketoacids. ese are excreted in the urine
(ketonuria) and the breath (hence the characteristic smell).
e anion gap is a measure of acid–base balance and is a
balance of cations (base) and anions (acids). e anion gap
represents the dierence in these. In acidosis the anion gap
may be high, normal or low. As the acid in ketoacidosis is
from an abnormal source, the anion gap will rise (i.e. more
anions than cation).
3. How would you manage this patient, explaining which
electrolyte needs specic management?
e management of patients with diabetic ketoacidosis
(DKA) can be divided into four parts: (1) uid resuscitation,
(2) administration of insulin, (3) correction of electrolyte
abnormalities and (4) treatment of any precipitating cause.
ere are numerous protocols and regimes for DKA but the
basics will involve giving insulin to lower the glucose levels
and monitoring/giving adequate potassium. Potassium may
be elevated at presentation but as insulin is given, it will cause
potassium to be taken back into cells and lead to dangerous
hypokalaemia and thus added potassium will be needed.
OSCE SCENARIO ANSWER 8.1
A 59-year-old male with severe acute gallstone pancreatitis has
been on the ward for 5 days. He is complaining of acute shortness of breath with a respiratory rate of 32 and an SpO2 of 88%
despite oxygen by facemask. e junior doctor has obtained arterial blood gases (ABGs), the results of which are shown below:
pH 7.25
PaO27.7 kPa
PaCO27 kPa
Base excess −9 mmol/L
−
HCO
18 mmol/L.
1. What are the possible dierential diagnoses for the
3
shortness of breath?
e possible causes of shortness of breath in this patient
include:
• ARDS
• pleural eusion (secondary to acute pancreatitis,
usually le sided)
• aspiration pneumonitis
• hospital-acquired pneumonia.
2. How is respiratory failure classied?
Respiratory failure is said to exist when PaO2 <8 kPa. It is
then divided into type I and type II:
• Type I occurs when the PaCO2 is low or normal and
is termed hypoxaemic respiratory failure.
• Type II occurs when the PaCO2 is elevated and is
termed ventilatory failure.
3. What is adult respiratory distress syndrome (ARDS)?
ARDS is the pulmonary component of the systemic inammatory response syndrome and may be caused by direct
lung injury, e.g. aspiration, or indirect injury such as burns
or pancreatitis.
4. How is ARDS diagnosed?
ere are a number of criteria for the diagnosis of ARDS:
• Known cause.
• Acute onset of symptoms.
• Hypoxia unresponsive to O2 therapy.
• New bilateral ‘uy’ inltrates on CXR.
• No cardiac failure or uid overload (dened
as PAWP) (pulmonary artery wedge pressure
<18 mmHg).
5. How is ARDS managed?
Management involves:
• Treating the precipitating cause.
• Preventing multi-organ failure (MOF) with judicious uids and inotropes as needed.
• Respiratory support to maintain reasonable levels of oxygenation while minimizing further lung
injury.
ere are a number of ventilator strategies used in ARDS:
• Lung protective ventilator strategies with lower tidal
volumes and peak airway pressures and allowing
hypercapnia as long as pH <7.1.
• Prone ventilation.
• High-frequency jet ventilation.
APPENDIX OSCE Scenario Answers
447
• Inverse ratio ventilation (inspiration/expiration ratio
prolonged, allowing a longer time for inspiration).
• ECMO (extra-corporeal membranous ventilation).
OSCE SCENARIO ANSWER 8.2
A 52-year-old male, 7 days post-right total knee replacement,
has become acutely short of breath. He has severe chest pain
on inspiration.
1. What is the dierential diagnosis?
Dierential diagnosis includes:
• pulmonary embolism (PE)
• cardiac-related chest pain
• pneumothorax
• pneumonia.
2. What changes on ECG would support a diagnosis of
pulmonary embolism (PE)?
e following changes on ECG would support a diagnosis
of PE:
• sinus tachycardia
• right bundle branch block (RBBB)
• T-wave inversion in V1–V3
• S1Q3T3 (S-wave in lead I, and Q-wave and inverted
T-wave in lead III).
3. What is the treatment of PE?
• e management of PE depends on whether it is a
non-massive PE or massive PE.
• In patients with non-massive PE, management
involves conrming the diagnosis and denitive
treatment. In patients with a high degree of suspicion
of PE, then treatment should be instituted immediately (see following).
• Many hospitals have ow-chart protocols to assess
the probability of PE from a list of clinical points and
a raised D-dimer blood test. e imaging modality
of choice is CT pulmonary angiography (CTPA).
• Management of non-massive PE involves anticoagu-
lation, initially with heparin (either unfractionated
or low molecular weight), followed by oral anticoagulation with warfarin (maintaining the INR between
2 and 3) for a period of 6 months.
• Patients with a massive PE will be acutely unwell and
require immediate resuscitation according to ABC
guidelines. ey will need ITU support with inotropes for cardiovascular collapse while the diagnosis is
conrmed. Options for massive PE include thrombolysis (treatment of choice) and surgical embolectomy (uncommon).
4. Describe the physiological changes that lead to hypoxia
and hypotension, which occur in PE.
Hypoxia is caused by two mechanisms:
• Firstly, there is an increase in dead space due to blockage of pulmonary arteries by thrombus (this leads to
areas of lung that are ventilated but not perfused).
• Aer 24–48 h, the aected area of lung loses surfactant, leading to atelectasis; this may cause further
hypoxaemia.
Hypotension, seen only in large PEs, is essentially due to
right heart failure (cor pulmonale) due to obstruction of
pulmonary arteries. is leads to a reduction in right ventricular output and thus le ventricular preload and therefore hypotension.
OSCE SCENARIO ANSWER 8.3
A 19-year-old male is involved in a ght. He has been stabbed
in the le side of the chest. He is brought into A&E very pale
and struggling to breathe.
1. What possible chest injury could he have?
e possible chest injuries may include pneumothorax, tension pneumothorax, haemothorax or cardiac tamponade.
2. What would be the examination ndings in each?
ese would depend on the injury:
• Pneumothorax – the patient will be short of breath with
tachypnoea. ere may be some mediastinal shi with
large pneumothorax. e patient will have decreased
breath sounds and hyper-resonant percussion.
• Tension pneumothorax – the patient will be in severe
respiratory distress and shock. He will have mediastinal shi away from the injured side, have decreased
breath sounds and will be hyper-resonant to percussion on the injured side.
• Haemothorax – the clinical signs will depend on
the size of the haemothorax. With a small bleed,
there may be very few clinical signs. With a large
haemothorax, the patient will show signs of shock
and respiratory distress. He will have absent breath
sounds and be dull to percussion on the aected side.
• Cardiac tamponade – the patient will be in shock and
may exhibit signs of respiratory distress. He will not
have mediastinal shi or the lungs signs of a tension
pneumothorax which may have a similar clinical presentation. Beck’s triad includes hypotension, raised JVP
and mued heart sounds. ECG may show reduced
complexes. Other signs, such as pulsus paradoxus and
Kussmaul’s sign, are more related to tamponade caused
by chronic pericardial eusion and demonstrating
them is not appropriate in a trauma scenario.
3. How would you manage this patient?
e treatment of all conditions would initially be in line
with ATLS protocols. Each of these chest injuries would be
diagnosed and managed in the primary survey.
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• Pneumothorax – chest drain
• Tension pneumothorax – initial needle decompression followed by chest drain.
• Haemothorax – i.v. uid/blood resuscitation and
chest drain. Depending on the amount of blood
drained, the patient may require urgent thoracotomy.
• Cardiac tamponade – needle thoracocentesis followed by urgent thoracotomy.
OSCE SCENARIO ANSWER 8.4
A 56-year-old male has recently had major knee surgery
and you are called to the ward as he has diculty breathing. He also has pleuritic chest pain. You suspect a pulmonary
embolus (PE).
1. What other signs may be associated with a PE?
Clinical signs associated with PE – along with shortness
of breath and pleuritic chest pain – may include haemoptysis, pyrexia, hypotension and a raised JVP. With massive
PE the rst presentation may be cardiac arrest. Remember
that DVTs that cause PEs are rarely occlusive (i.e. free
oating and more likely to embolize) and thus only 10%
or so of patients with PE will also have symptoms of a
DVT. ECG may also show a number of changes, which
can include:
• Sinus tachycardia is most common
• Classic sign is S1Q3T3 – this is a prominent S wave
in lead I, Q wave and T wave inversion in lead III –
this indicates right heart strain and is not diagnostic
of a PE.
• Atrial brillation or utter.
• Right bundle branch block.
• Right deviation of the QRS complex.
2. What would you expect to see on ABGS and why would
you see these changes?
e changes on an arterial blood gas (ABG) are again not
diagnostic but one would expect to see low oxygen (hypoxaemia) due to a V/Q mismatch from the blocked pulmonary vessels – i.e. alveoli have air but no perfusion. ere
is hypocapnea as a result of hyperventilation. is would
be termed a respiratory alkalosis. In massive PE, there also
maybe an element of metabolic acidosis due to low blood
pressure and systemic hypoperfusion.
3. How would you investigate and treat this patient?
Investigations would include CXR, VQ scanning and
CT pulmonary angiography (CTPA). A CXR is usually taken at the acute episode that the patient became
symptomatic, mainly to rule out other causes and is
rarely diagnostic. VQ scanning uses radioisotopes to
show the difference between ventilated and perfused
lung but is rarely if ever used today, except in pregnancy.
The mainstay investigation is with CTPA, which is very
sensitive at showing clots within the pulmonary veins.
Direct pulmonary angiography is performed prior to
commencing endovascular treatment but is not used as
a standard investigation.
e rst stage in treatment must always be ABC;
further treatment and investigation will depend on the
stability of the patient – stable or unstable. Remember,
treatment can always be divided into conservative, medical or surgical. Conservative treatment has no role unless
a massive PE occurs in a very poorly patient not expected
to survive. In the stable patient, the treatment is medical – this would include oxygen, uids to support BP and
anticoagulation with i.v. or LMW heparin and ensure
the patient is wearing TED stockings if appropriate.
Investigation with CTPA can then be performed when
appropriate. Anticoagulation should be commenced if a
high degree of suspicion before a CT conrms a PE. In
the unstable patient then treatment involves stabilizing
the blood pressure using inotropes before either systemic
or catheter-directed thrombolysis. Clots can also be
sucked out using special catheters. In some centres facilities maybe available to perform median sternotomy and
pulmonary embolectomy.
OSCE SCENARIO ANSWER 8.5
A 26-year-old male has been shot in the chest with a shotgun
and has a sizeable chest injury. He is very short of breath.
Bubbles are coming from the wound.
1. What type of chest injury is this and how would you
treat it?
is patient has what is called an open pneumothorax or
‘sucking’ chest wound. is is when a defect in the chest
wall allows intra-thoracic pressure and atmospheric pressure to equalize. If the defect is >2/3 the diameter of the
trachea, air will preferentially enter the wound and not take
part in gas exchange and thus cause hypoxia. e visible
bubbles are from damaged lung surface. e rst aid treatment is the placement of a dressing over the wound sealed
on three sides to allow air out but prevent air going into
the chest – this is a utter valve. In hospital a sealed dressing can be placed over the wound and a chest drain distant
from the site of injury.
2. He has hypoxia and hypoxaemia – which type of
hypoxia and hypoxaemia does he have?
Hypoxia is a deciency of oxygen in the tissues – this
patient will be suering from hypoxic hypoxia due to low
arterial oxygen levels. Hypoxaemia is low level of oxygen
in the blood and will result from a ventilation perfusion
mismatch.
3. What other types of chest injury can you describe?
ere are a number of other types of chest injury and
these can be divided into immediately life-threatening and
potentially life-threatening. A useful pneumonic is ‘ATOM
APPENDIX OSCE Scenario Answers
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FC’ for immediate and ‘ATOM PD’ for potentially life
threatening injuries.
Immediately LifeThreatening
Airway obstruction Aortic disruption
Tension pneumothorax Tracheobronchial injury
Open pneumothorax Oesophageal injury
Massive haemothorax Myocardial contusion
Flail chest Pulmonary contusion and
Cardiac tamponade Diaphragmatic rupture
Potentially LifeThreatening
pneumothorax
OSCE SCENARIO ANSWER 9.1
An 80-year-old male is 5 days post-repair of abdominal aortic aneurysm. He has suddenly developed a tachycardia and
become hypotensive. His ECG shows atrial brillation with
a rate of 140.
1. What are the causes of atrial brillation?
e causes of atrial brillation can be divided into cardiac
causes and non-cardiac causes.
• Cardiac causes include:
• ischaemic heart disease
• cardiomyopathy
• le ventricular hypertrophy
• hypertension
• valvular heart disease.
• Non-cardiac causes include:
• hyperthyroidism
• PE
• alcohol excess
• sepsis (especially pneumonia)
• hypoxia
• biochemical derangements (e.g. low calcium,
potassium and magnesium).
2. What are the physiological mechanisms which explain
the hypotension seen in fast atrial brillation?
ere are three physiological mechanisms to explain the
hypotension in atrial brillation:
• Loss of atrial contraction leads to poor ventricu-
lar lling and thus reduced stroke volume and
hypotension.
• Increased heart rate leads to reduced time for ven-
tricular lling and thus reduced stroke volume and
consequent hypotension.
• e increased heart rate leads to reduced time in
diastole (coronary artery lling occurs mainly in
diastole), leading to cardiac ischaemia and reduced
strength of contraction.
3. How would you diagnose atrial brillation?
e two ways to diagnose AF are:
• irregular heart rate (both clinically and on ECG)
• absence of P-waves on ECG.
4. Describe your initial management of the patient.
Initial management involves:
• Airway, Breathing and Circulation
• conrmation of diagnosis:
• ECG
• FBC
• U&E
• cardiac markers
• calcium
• magnesium
• CXR
• ABG.
e further management of AF relates to control of the
heart rate. is varies depending on a number of factors:
• If the patient is haemodynamically unstable, com men-
ce i.v. heparin and arrange urgent DC cardioversion.
• If the patient is not unstable, then treatment diers
depending on whether the AF is of new onset or not:
• new-onset AF: electrical or pharmacological cardioversion (amiodarone)
• previous AF: pharmacological rate control (betablockers, calcium antagonists or amiodarone).
OSCE SCENARIO ANSWER 9.2
An 89-year-old male is 8 days post-laparotomy for repair of
a perforated duodenal ulcer. He has developed a severe postoperative chest infection and is pyrexial and hypotensive.
1. Describe your initial management of this patient.
Assessment of any critically ill patient requires initial assessment and resuscitation (Airway, Breathing and Circulation)
followed by appropriate investigations and treatment.
• ABC:
• Airway: patient may require intubation if in
respiratory failure.
• Breathing: patient should be given high-ow
oxygen.
• Circulation: rapid intravenous access should be
gained and a uid bolus of colloid or crystalloid
given; further management will depend on the
response to the uid. If the patient responds to
a simple uid bolus then investigation into the
cause can be initiated. If the patient has been
given adequate uid resuscitation (which in
septic patients can be several litres) then further invasive monitoring (arterial line and CVP
line) should be used to guide treatment, e.g.
inotropes.
• Diagnosis: screening for sepsis (sputum, wound
swab, blood culture), FBC, CRP, CXR.
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• Treatment: empirical broad-spectrum antibiotics
should be commenced against the most likely source
as soon as possible; respiratory support either as
high-ow oxygen, non-invasive ventilation or intubation; and intensive management of hypotension
with invasive monitoring guiding further uid management and inotropic support.
2. Why does sepsis lead to hypotension?
Sepsis leads to hypotension in three ways:
• Profound vasodilatation, leading to pooling of blood
in the venous system.
• ird space losses due to inammatory exudate.
• Poor cardiac contractility secondary to bacterial toxins and inammatory mediators.
3. Which inotrope is commonly used in sepsis and what is
its mode of action?
• e most commonly used inotrope is noradrenaline.
is is given aer adequate uid resuscitation.
• Noradrenaline (via alpha receptors) leads to
vasoconstriction and thus an increase in blood
pressure.
4. What is Starling’s law of the heart and how do inotropes aect it?
• Starling’s law states that the contraction of cardiac
muscle is dependent on the degree of stretch: the
greater the stretch, the greater the degree of contraction and thus the stroke volume. ere is a nite
limit to which the heart muscle can be stretched,
aer which point the heart will begin to fail.
• Inotropes reset the contraction of the heart to a
higher level, and for a given end diastolic volume will
lead to a greater stroke volume.
OSCE SCENARIO ANSWER 9.3
A 58-year-old male is admitted with severe inter-scapular
back pain. He is hypertensive with a BP of 200/140 mmHg. A
CT angiogram shows a type B aortic dissection.
1. What is the dierence between a type A and B dissection?
Type A dissection refers to an aortic dissection which
begins in the ascending aorta. A type B dissection is where
the tear is located in the descending aorta – usually close to
the origin of the le subclavian artery. Both type A and B
dissections may involve the length of the aorta.
2. How is a type A dissection managed?
Type A is a surgical emergency. Without operation the
mortality is extremely high. Urgent transfer to a cardiothoracic centre is required. Surgery basically involves resection
of the ascending aorta and replacement with a Dacron gra
under cardiopulmonary bypass. e distal anastomosis
oen involves a combination of pledgeted sutures and glue
to obliterate the false lumen.
3. How is an uncomplicated type B dissection managed?
Type B dissections are managed medically unless there are
signs of complications such as:
• end-organ ischaemia (renal, bowel or limb)
• rupture
• high BP resistant to treatment
• unremitting pain
• aneurysmal expansion.
Medical management consists of transfer to HDU/ITU and
invasive BP management with a variety of medications.
e most commonly used drug is labetolol – a rapidly acting beta-blocker that lowers BP and heart rate and thus
applies less ‘pressure’ to the dissection ap and thus limits
its propagation. In complicated dissection the management
is similar but will involve the placement of an endovascular
thoracic gra (TEVAR).
OSCE SCENARIO ANSWER 9.4
A 72-year-old male patient underwent elective open abdominal aortic aneurysm repair. An infra-renal aortic cross clamp
was required.
1. What are the physiological and cardiovascular changes
that result from aortic cross clamping?
e main eect of aortic cross clamping is increasing the
aerload which manifests as hypertension. An increase in
aerload results in increased cardiac work and therefore
oxygen consumption. erefore in susceptible patients (i.e.
those with a history of ischaemic heart disease) it can predispose the patient to myocardial ischaemia, arrhythmias,
and le ventricular failure.
2. What techniques would the anaesthetists use to reduce
these eects?
Several techniques can be utilized to reduce aerload, such
as increasing volatile anaesthetic agent and using betablockers or vasodilators such as glyceryl trinitrate (GTN).
Vasodilatation leads to reduction of peripheral vascular resistance and the aerload, resulting in less stress on the heart.
3. What are the physiological and cardiovascular changes
that result from releasing aortic cross clamp?
is can be more signicant than the initial cross clamping
as it results in sudden reduction in the aerload and reperfusion of the ischaemic tissues. e impact is hypotension,
release of vasodilatory metabolites from the pelvis and legs,
an increase in potassium, lactate and CO2, which can result
in a degree of acidosis, and resultant myocardial ischaemia
or arrhythmias.
4. What techniques would the anaesthetists use to reduce
these eects?
e anaesthetists ensure that patients are adequately prelled prior to the release of cross clamping. Vasodilators are
stopped if they have been commenced. e vascular surgeons can also gradually release cross clamping over several minutes by keeping the ow partially clamped, press
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