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MRCEM Part C · OSCE Preparation

OSCE Station Bank 12

The final bank — completing the full MRCEM Part C syllabus across 125 stations. Vertigo and HINTS exam, meningococcal rash, fundoscopy and papilloedema, diabetic foot, BLS teaching, safeguarding adults, anaphylaxis, ABG interpretation and end-of-life communication.

0/ 10 completed
10Stations
5Domain types
8Min / station
0/10 completed
📋 History Taking
📋
Dizziness and Vertigo History — Peripheral vs Central Cause (HINTS Exam)
History · 8 minStation 1 of 10
✓
▼
8:00
Station type
History Taking
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

You are the ED doctor. Mrs Anita Sharma, 52 years old, has presented with a 3-day history of dizziness. She describes the room spinning. She has nausea and has vomited twice. She is visibly unsteady.

Obs: HR 82, BP 136/84, RR 16, SpO₂ 98% on air, BM 5.6 mmol/L, GCS 15.

Please take a focused history, determine the type of dizziness, differentiate peripheral from central causes, and outline which bedside tests you would perform. You have 8 minutes.

💡 Vertigo — SOCRATES, Peripheral vs Central, HINTS Exam, ABCD² ▼
  • Step 1 — Clarify the type of dizziness (critical first question):
    • True vertigo — illusion of rotatory movement, world spinning or patient spinning. Caused by disorder of the peripheral vestibular system (inner ear, CN VIII) or central vestibular pathways (brainstem/cerebellum). Mrs Sharma describes room spinning = true vertigo.
    • Presyncope / near-faint — lightheadedness, "going to pass out," grey-out, tunnel vision. Caused by cerebral hypoperfusion: vasovagal, cardiac arrhythmia, orthostatic hypotension, dehydration.
    • Disequilibrium — unsteadiness without spinning, particularly on walking. More common in elderly. Causes: cerebellar ataxia, proprioceptive loss, Parkinsonism, drug effects.
    • Non-specific dizziness — ill-defined, floating, swimming sensation. Often psychiatric (anxiety, hyperventilation, depression), medication-related, or poorly-described vertigo.
    • Ask: "When you feel dizzy — does the room spin around you, as if you've been on a roundabout? Or do you feel like you're going to faint? Or do you feel unsteady on your feet?"
  • SOCRATES for vertigo:
    • Onset: Sudden vs gradual. Sudden onset with no preceding illness = BPPV or posterior circulation stroke/TIA. Sudden onset following URTI = vestibular neuritis (viral). Gradual progressive = acoustic neuroma, central cause.
    • Duration of individual episodes:
      • Seconds (5–30 seconds) = BPPV — triggered by specific head movements, brief, recurrent. Classic: rolling over in bed, looking up.
      • Hours (20 min to several hours) = Ménière's disease — triad: episodic vertigo + fluctuating sensorineural hearing loss + tinnitus + aural fullness.
      • Days (continuous) = Vestibular neuritis (no hearing loss) or labyrinthitis (with hearing loss). Often follows viral infection. Mrs Sharma: 3 days continuous = vestibular neuritis/labyrinthitis pattern.
      • Seconds to minutes, recurrent = BPPV, TIA (posterior circulation), perilymph fistula.
    • Character: Rotatory (true vertigo) vs non-rotatory.
    • Radiation/Associated symptoms — CRITICAL:
      • Hearing loss and/or tinnitus = labyrinthitis, Ménière's, acoustic neuroma. Mrs Sharma: no hearing loss, no tinnitus — points away from Ménière's and labyrinthitis.
      • Neurological symptoms = central cause until excluded. Ask specifically: double vision (diplopia — CN VI/III), facial numbness/weakness, dysarthria, dysphagia, limb weakness, limb numbness, loss of balance (falling to one side), headache (especially occipital). These are posterior circulation stroke/TIA features (PICA or AICA territory).
      • Nausea and vomiting — common in both peripheral and central vertigo (not discriminating).
      • Ear pain, discharge, fullness — suggests middle ear pathology, cholesteatoma, otitis media complication.
    • Timing and triggers: Positional (BPPV — triggered by specific head movements, reproducible). Constant (vestibular neuritis). Episodic (Ménière's, TIA).
    • Exacerbating/Relieving: Better lying still (peripheral vestibular — any movement worsens it). Persistent regardless of position (may suggest central).
    • Severity: Able to walk? (gait ataxia = central feature). Vomiting frequency.
  • Past medical history and medications:
    • Vascular risk factors — hypertension, diabetes, hypercholesterolaemia, AF, smoking, previous stroke/TIA. Important for posterior circulation stroke risk.
    • Ototoxic medications — aminoglycosides (gentamicin — bilateral vestibular toxicity, oscillopsia), loop diuretics (furosemide), quinine, cisplatin, vancomycin. Cause bilateral sensorineural hearing loss and vestibular dysfunction.
    • Other medications — antiepileptics (phenytoin, carbamazepine — cerebellar ataxia/dizziness), antihypertensives (orthostatic hypotension), benzodiazepines, antihistamines (dizziness as side effect).
    • Previous ear surgery, head trauma, recurrent ear infections (cholesteatoma risk).
    • Recent viral illness (upper respiratory tract infection — vestibular neuritis).
    • Anxiety and panic disorder (hyperventilation-induced dizziness).
  • HINTS exam (bedside examination — distinguishes peripheral from central vertigo in patients with acute continuous vertigo):
    • H — Head Impulse Test (HIT): Patient fixes gaze on examiner's nose. Examiner rapidly rotates head 10–15° to one side. In peripheral vestibular disease (e.g. vestibular neuritis) — VOR (vestibulo-ocular reflex) is impaired on the affected side → eyes lag behind, then make a corrective saccade back to target (positive HIT = peripheral disease). In central disease (stroke) — VOR is intact → eyes remain fixed on target, no corrective saccade (negative HIT = central disease — MORE DANGEROUS). A normal head impulse test in a patient with acute continuous vertigo suggests a central cause — do not be falsely reassured.
    • I — nystagmus direction: In peripheral vestibular disease: nystagmus is unidirectional (fast phase always in the same direction regardless of gaze direction), horizontal, typically reduced by visual fixation. In central disease: nystagmus may be direction-changing (fast phase changes direction with gaze direction — gaze-evoked nystagmus), purely vertical, or torsional. Direction-changing nystagmus = central.
    • T — Test of Skew (alternating cover test): Examiner alternately covers each eye. In peripheral disease: no vertical misalignment of eyes. In central disease (brainstem): vertical skew deviation — one eye higher than the other — is revealed on alternating cover test. Vertical skew = central.
    • HINTS interpretation: All 3 reassuring (positive HIT + unidirectional nystagmus + no skew) = peripheral cause likely (sensitivity 100%, specificity 96% for posterior circulation stroke — superior to MRI in first 24–48 hours). Any 1 worrying sign (negative HIT + direction-changing nystagmus + vertical skew) = central cause until proven otherwise → CT/MRI head urgently.
    • Important caveat: HINTS should only be performed in patients with acute spontaneous continuous vertigo — it is NOT valid for episodic vertigo (e.g. BPPV).
  • ABCD² score (for TIA/posterior circulation event risk): Age ≥60 (1), BP ≥140/90 (1), Clinical features — unilateral weakness (2), speech disturbance (1), Duration ≥60 min (2), 10–59 min (1), Diabetes (1). Score 0–3 = low risk; 4–5 = moderate; 6–7 = high. Mrs Sharma: age 52, BP 136/84, no neurological symptoms — low-moderate risk. But if HINTS worrying → urgent imaging regardless of ABCD².
  • Management of vestibular neuritis (likely diagnosis here — 3 days continuous, no neurological symptoms, no hearing loss, follows pattern):
    • Symptomatic treatment: prochlorperazine 3–6 mg buccal BD or 12.5 mg IM (antiemetic and vestibular sedative). Avoid prolonged use (>3 days) — delays central compensation.
    • Reassurance: usually resolves in days to weeks. Head movement exercises (Cawthorne-Cooksey exercises) accelerate vestibular compensation.
    • Exclude central cause first with HINTS — if all reassuring, MRI not mandatory in straightforward vestibular neuritis. MRI if HINTS uncertain or any neurological features.
    • Admit if unable to mobilise, unable to tolerate oral fluids, or central cause suspected.

⚠️ Examiner / Role-player Instructions — Not for Candidate

Play Mrs Sharma — articulate, slightly anxious. The room spins, worse when she moves her head. Started 3 days ago after a cold. No hearing loss, no tinnitus. No diplopia, no facial weakness, no limb weakness, no dysarthria. She has hypertension (on ramipril) and is a non-smoker, non-diabetic. No ototoxic medications. She had a similar milder episode 6 months ago that resolved. She can walk but feels unsteady. If candidate asks about HINTS exam: tell them they can perform it — HIT is positive (left-beating corrective saccade on right head impulse), nystagmus is unidirectional horizontal left-beating, no vertical skew. This is a peripheral pattern. Key checkpoints: Did candidate clarify the type of dizziness first? Did they ask duration of episodes (days = not BPPV)? Did they specifically ask for neurological symptoms? Did they describe the HINTS exam correctly? Did they know a positive HIT = peripheral?

🎭 Patient Script ▼
  • Type of dizziness: "The room is spinning — like I've been on a fairground ride and I can't make it stop."
  • Duration/onset: "It started 3 days ago. I had a cold the week before. It's been there the whole time — not coming and going, just constant. Worse when I move my head."
  • Hearing/tinnitus: "No, my hearing is fine. No ringing."
  • Neurological symptoms: "No double vision. No weakness in my face or arms. I can speak fine. Just the spinning and feeling sick."
  • Medications/risk factors: "Ramipril for blood pressure. Nothing else. I don't smoke. No diabetes."
  • Previous episode: "Yes — about 6 months ago, not as bad. My GP said it was a 'labyrinthitis' — it went away in about 2 weeks."
🔔 Examiner Cues ▼
  • If candidate doesn't clarify type of dizziness at outset: "Mrs Sharma uses the word 'dizziness' — is this enough to proceed, or do you need to characterise it further?"
  • If candidate diagnoses BPPV based on positional worsening alone: "In BPPV, how long does each episode typically last — and how does that compare to Mrs Sharma's 3-day continuous symptoms?"
  • If candidate doesn't perform/describe HINTS: "You're about to discharge her with vestibular neuritis — how are you excluding a posterior circulation stroke at the bedside?"
  • At 7 minutes: "If the head impulse test were normal (no corrective saccade) and the nystagmus changed direction on lateral gaze — how would your management change?"
CriterionMarks
Type and Character of Dizziness
Type of dizziness clarified as first step — true vertigo (rotatory) vs presyncope vs disequilibrium vs non-specific; Mrs Sharma correctly identified as true vertigo2
Duration of episodes characterised — continuous 3 days distinguishes vestibular neuritis from BPPV (seconds) and Ménière's (hours); onset after URTI noted2
Key Symptoms and Red Flags
Neurological symptoms specifically asked — diplopia, facial weakness/numbness, dysarthria, limb weakness, dysphagia; absence of these reduces central probability2
Hearing loss and tinnitus asked — absent here (points away from Ménière's and labyrinthitis); ototoxic medications and vascular risk factors screened2
HINTS Exam
HINTS exam described correctly — Head Impulse (positive = peripheral; negative = central), Nystagmus direction (unidirectional = peripheral; direction-changing = central), Skew (vertical = central)4
Correct interpretation — positive HIT + unidirectional nystagmus + no skew = peripheral pattern; knows negative HIT is the dangerous finding suggesting central cause2
Management
Vestibular neuritis likely diagnosis stated; prochlorperazine for symptom relief; avoid prolonged vestibular sedatives; MRI if HINTS uncertain or neurological features; ABCD² considered4
Total20
📋
Rash History — Meningococcal Septicaemia (Non-Blanching Rash, Immediate Treatment)
History · 8 minStation 2 of 10
✓
▼
8:00
Station type
History Taking
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

You are the ED doctor. Kieran Murphy, 19 years old, a university student, has been brought in by his flatmate with a 12-hour history of fever, headache, neck stiffness, and a rash on his legs.

On arrival: HR 126, BP 94/60, RR 22, Temp 39.4°C, SpO₂ 96% on air, GCS 14 (E3 V5 M6), capillary refill 3 seconds. He is lying still, photoophobic.

Please take a focused history, perform the glass test on the rash, and outline your immediate management. The examiner will provide positive and negative findings as you examine. You have 8 minutes.

💡 Meningococcal Septicaemia — Non-Blanching Rash, Immediate IV Antibiotics, LP, Notifiable Disease ▼
  • CRITICAL TEACHING POINT — Non-blanching rash + fever = meningococcal septicaemia until proven otherwise. Do NOT delay treatment to complete the history. In this scenario: haemodynamic compromise (HR 126, BP 94/60, CRT 3s) + non-blanching rash + fever + meningism = immediate antibiotics within minutes of assessment, not after history, not after LP, not after CT.
  • The glass test: Press a clear glass tumbler (or a transparent plastic cup) firmly against the rash. If the rash disappears under pressure (blanches) = blanching rash (most commonly viral exanthem, drug reaction, vasodilation — less immediately dangerous). If the rash remains visible through the glass (does not blanch) = non-blanching = petechiae or purpura = blood has leaked out of capillaries into the dermis = cannot be pressed back = highly concerning for meningococcal septicaemia or other causes of thrombocytopenia/DIC/vasculitis. A non-blanching rash on a febrile patient is a medical emergency regardless of how well the patient looks.
  • Rash history — key questions:
    • When did the rash first appear? Where did it start and how has it spread? (Meningococcal: often starts on legs/trunk, spreads rapidly — can be purpuric within hours.)
    • Did you do the glass test at home? (Many patients/parents know this now.)
    • What does the rash look like? (Small pin-prick spots = petechiae. Larger irregular bruise-like areas = purpura — indicates DIC, worse prognosis.)
    • Is it spreading? (Spreading rash = active septicaemia, worsening DIC.)
  • Associated symptoms — meningitis and septicaemia:
    • Fever onset and height: When? How high? Preceding rigors?
    • Headache: Is it severe? Sudden thunderclap (SAH DDx) vs gradual? Worse on bright light (photophobia), noise (phonophobia)?
    • Neck stiffness: Classic meningism. Kernig's sign (inability to extend knee when hip flexed 90° due to meningeal irritation). Jolt accentuation (worsening headache with rapid horizontal head rotation). In meningococcal — neck stiffness may be absent in early or fulminant septicaemia.
    • Nausea and vomiting — almost universal.
    • Consciousness level — GCS 14 here = altered (normal = 15). Deteriorating GCS = worsening disease.
    • Preceding URTI — meningococcus can colonise the nasopharynx and invade during URTI. Sore throat in preceding days?
    • Joint pains, limb pain — meningococcal arthritis, myalgia (severe sepsis).
  • Exposure and epidemiology:
    • Close contacts at risk — university students in halls of residence are a high-risk population for meningococcal disease (close living, shared spaces). Who has he been in close contact with in the last 7 days? Flatmates, romantic/kissing contacts, people who shared drinks/utensils. Close contacts will require prophylactic antibiotics (ciprofloxacin or rifampicin) via Public Health England/UKHSA.
    • Immunisation history — MenACWY vaccine (now given to all UK adolescents at Year 9 and university freshers). MenB vaccine (Bexsero — given to infants in UK schedule since 2015, not routinely to all teenagers). Any vaccines missed? Asplenic patients are at extreme risk (give antibiotics immediately regardless of vaccination status).
    • Recent travel — sub-Saharan Africa (meningitis belt), Hajj/Umrah (MenW disease cluster), Saudi Arabia. Travel raises MenW and MenA risk.
    • Immunocompromise — asplenia (functional or surgical), complement deficiency, HIV, immunosuppressants — extreme risk for encapsulated organisms including Neisseria meningitidis.
  • Immediate management — do NOT delay for further history or investigations:
    • Airway, Breathing, Circulation — simultaneous: High-flow oxygen via NRM (SpO₂ 96% — supplemental O₂ while assessing), 2× large-bore IV cannulas, bloods (FBC, U&E, LFT, coag, CRP, lactate, blood cultures × 2 sets — before antibiotics if can be done within 5 minutes of decision but DO NOT delay antibiotics for blood cultures), IV fluid resuscitation (crystalloid 500 mL bolus — haemodynamic compromise).
    • IV antibiotics immediately:
      • IV Cefotaxime 2 g (or ceftriaxone 2 g) IV immediately — first-line for suspected bacterial meningitis/meningococcal septicaemia in adults.
      • If penicillin allergy (non-anaphylactic): Ceftriaxone/cefotaxime still likely safe (10% cross-reactivity with penicillin — very low with 3rd gen cephalosporins). If anaphylactic penicillin allergy: chloramphenicol 25 mg/kg IV or meropenem.
      • Benzylpenicillin 1.2 g IV — the pre-hospital standard (GPs give this before transfer). In ED with access to cefotaxime — use cefotaxime first. If only penicillin available — use it.
      • IV Dexamethasone 0.15 mg/kg QDS for 4 days — given with or just before first antibiotic dose. Reduces neurological complications (hearing loss, brain damage) in bacterial meningitis — especially pneumococcal. NICE guidance: give if bacterial meningitis suspected, regardless of organism.
    • Lumbar puncture (LP) — when safe and appropriate:
      • LP is NOT the immediate priority. Antibiotics must NOT be delayed for LP.
      • LP contraindicated if: signs of raised ICP (papilloedema, focal neurology, GCS <12, pupil changes), haemodynamic instability (perform LP only once stabilised), coagulopathy (INR >1.4 or platelets <50), thrombocytopenia, local infection at LP site.
      • CT head before LP if: GCS <12, focal neurology, papilloedema, seizure, immunocompromised (risk of coning).
      • LP CSF findings in bacterial meningitis: turbid/purulent appearance, high white cells (predominantly neutrophils — >1000 × 10⁶/L), high protein (>1 g/L), low glucose (<2.2 mmol/L or <60% of simultaneous blood glucose), Gram stain and culture (positive in ~60–80% if no prior antibiotics). PCR — Neisseria meningitidis, Streptococcus pneumoniae (stays positive even after antibiotics started).
    • Notifiable disease: Meningococcal disease (meningococcal meningitis and meningococcal septicaemia) is a statutory notifiable disease in England. Must notify the local health protection team (PHE/UKHSA) immediately — they will arrange contact tracing and prophylaxis. The on-call consultant at the Health Protection Unit handles this out of hours.
    • Contact prophylaxis: Ciprofloxacin 500 mg oral single dose (preferred) or rifampicin 600 mg BD for 2 days (second-line — more side effects, drug interactions, stains contact lenses). Given to all household and intimate contacts within 24 hours of index case identification.

⚠️ Examiner / Role-player Instructions — Not for Candidate

Play Kieran — unwell, lying still, photophobic, answers questions briefly. If candidate performs glass test: "The rash does not disappear under the glass — it remains clearly visible." Rash is petechial on both lower legs, extending to the trunk. It is spreading. Headache onset 12 hours ago, sudden onset, 10/10. Neck is stiff. GCS 14. No focal neurology. MenACWY given at age 16 (Year 9). MenB not given. University halls — 7 flatmates. Last ate and drank 12 hours ago. No known allergies. No recent travel. Key checkpoints: Did candidate perform glass test and correctly identify non-blanching rash? Did they give antibiotics IMMEDIATELY (before further workup)? Did they prescribe dexamethasone? Did they state notifiable disease? Did they know ciprofloxacin for contacts?

🔔 Examiner Cues ▼
  • If candidate takes a full detailed history before prescribing antibiotics: "While you're taking the history, the nurse interrupts — Kieran's BP has dropped to 82/50. At what point should antibiotics have been given?"
  • If candidate orders LP before antibiotics: "NICE guidance on meningococcal disease — should LP or antibiotics come first in a haemodynamically compromised patient?"
  • If candidate doesn't add dexamethasone: "There is an adjunctive treatment recommended by NICE to reduce neurological sequelae — what is it and when should it be given relative to antibiotics?"
  • At 7 minutes: "Kieran is stabilising on IV antibiotics. His flatmate calls the ED — he feels fine but is worried. What advice do you give him?"
CriterionMarks
Recognition and Immediate Action
Glass test performed and interpreted correctly — non-blanching rash identified; meningococcal septicaemia stated as diagnosis until proven otherwise2
IV antibiotics given IMMEDIATELY — not delayed for LP, CT, or further history; cefotaxime/ceftriaxone 2g IV or benzylpenicillin stated; correct dose3
IV dexamethasone 0.15 mg/kg given with/before first antibiotic dose — NICE guidance; reduces neurological complications2
History
Rash progression asked (spreading = active DIC/septicaemia); onset, duration, distribution characterised; fever height, headache, photophobia, neck stiffness, GCS2
Close contacts asked — university flatmates, kissing contacts; immunisation history (MenACWY, MenB); recent travel; immunocompromise2
LP and Public Health
LP safety criteria explained — anticoagulation, GCS <12, focal neurology, papilloedema = CT first; LP done after stabilisation, not before antibiotics2
Notifiable disease — immediate notification to UKHSA/PHE; contact prophylaxis — ciprofloxacin 500 mg single oral dose for close contacts within 24 hours3
Resuscitation — IV fluids for haemodynamic compromise; blood cultures before antibiotics if achievable without delay; ITU/HDU referral if deteriorating2
Total20
🩺 Clinical Examination
🩺
Fundoscopy — Papilloedema and Raised Intracranial Pressure
Examination · 8 minStation 3 of 10
✓
▼
8:00
Station type
Clinical Examination
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

You are the ED registrar. Mr Stuart Black, 44 years old, has a 3-week history of progressive headache, worst in the mornings, worse on coughing and straining. He also has nausea. He now reports brief visual disturbances — "the lights flicker for a few seconds" on standing. No fever. No trauma. No history of malignancy.

Obs: HR 62, BP 162/98, RR 14, SpO₂ 99% on air, GCS 15.

Please perform fundoscopy on this patient. Talk through your technique, describe the findings the examiner provides, and state your diagnosis and immediate management plan. You have 8 minutes.

💡 Fundoscopy Technique — Normal vs Papilloedema — Raised ICP Management ▼
  • Clinical context — raised ICP headache features (critical to recognise):
    • Morning headache: ICP rises during REM sleep due to hypercapnia-induced cerebral vasodilation and supine position reducing CSF drainage. Headache worst on waking = classic raised ICP pattern.
    • Worse on Valsalva (coughing, straining, bending over): These manoeuvres raise intrathoracic pressure → reduce venous return → raise ICP transiently. Any headache worsened by Valsalva = raised ICP until excluded.
    • Visual obscurations: Transient visual loss (seconds, in one or both eyes) triggered by posture change = papilloedema-related. Due to transient ischaemia of the optic nerve as ICP compresses optic nerve head blood supply. A key symptom of raised ICP.
    • Bradycardia + hypertension (Cushing's reflex): HR 62, BP 162/98 — this is Cushing's triad (bradycardia + hypertension + irregular respirations). Late, serious sign of raised ICP — brainstem herniation imminent. This patient needs urgent intervention.
    • Nausea with headache without fever — raised ICP pattern. Vomiting without nausea is a classic "pressure vomiting" feature.
  • Fundoscopy technique:
    • Preparation: Dim the room (darkness dilates the pupil — improves view). Seat or lay the patient comfortably. Ask patient to fix their gaze on a distant point straight ahead and not to move their eyes during the examination. Remove glasses (keep contact lenses if worn). Ophthalmoscope set: wheel to 0 diopters initially (adjust for refractive error during examination).
    • Approach: Use your right eye to examine the patient's right eye; left eye for left eye. This keeps your face out of the patient's visual field and allows you to get close without bumping noses. Stand slightly to the temporal side (lateral) of the patient — approach from about 15° lateral to visual axis to find the disc more easily.
    • Red reflex: From arm's length — shine the light at the pupil. Normal: bright orange-red reflex from the retina. Absent or white reflex = cataract, corneal opacity, retinoblastoma (in child — urgent ophthalmology).
    • Finding the disc: Move in close (ophthalmoscope almost touching eyelashes). Follow a blood vessel toward the disc — vessels on the nasal retina branch toward the disc. Or approach from temporal side and look nasally for the disc. Adjust the diopter wheel to focus.
    • Systematic examination of the disc:
      • Disc margins — sharp/distinct or blurred?
      • Disc colour — pink (normal), pale (optic atrophy), hyperaemic/red (papilloedema, papillitis)
      • Cup:disc ratio — the pale central cup relative to total disc diameter. Normal <0.5. Increased (>0.6) = glaucoma.
      • Disc elevation — is the disc raised above the surrounding retina?
      • Venous pulsations — spontaneous pulsation of the central retinal vein at the disc = normal (present in ~80% of healthy individuals) and indicates ICP is not significantly elevated. Absence of venous pulsations = earliest sign of raised ICP.
    • Macula: Ask patient to look directly at the light briefly. The macula should appear darker than the surrounding retina. Macular degeneration, cherry red spot (central retinal artery occlusion), oedema.
    • Vessels: A:V ratio (normal arteries slightly narrower than veins — 2:3). AV nicking (hypertension). Flame haemorrhages (hapertension, CRVO, papilloedema). Silver/copper wiring (hypertension). Neovascularisation (diabetic retinopathy).
  • Papilloedema — fundoscopic findings (examiner will describe):
    • Earliest finding: Loss of venous pulsations — absence of spontaneous venous pulsation at the disc (normal pulsation present → raised ICP makes pulsation disappear).
    • Blurring of disc margins — begins superiorly and inferiorly, then nasally, lastly temporally. Margins appear hazy, indistinct.
    • Disc hyperaemia — disc becomes pink-red due to venous congestion.
    • Disc elevation — the disc appears raised, 3-dimensional, protruding toward the examiner. You need to adjust the diopter wheel toward + (green numbers) to keep it in focus relative to surrounding retina.
    • Flame haemorrhages at disc margin — splinter haemorrhages.
    • Cotton wool spots — white fluffy patches of ischaemic nerve fibre layer infarcts.
    • Peripapillary retinal folds (Paton's lines) — concentric folds around the disc in severe papilloedema.
    • In severe/chronic papilloedema: macular oedema, enlarged blind spot on visual fields.
  • Differential diagnosis of disc swelling:
    • Papilloedema = disc swelling due to raised ICP (bilateral, no visual loss acutely until late, no RAPD initially).
    • Papillitis (optic neuritis) = disc swelling due to optic nerve inflammation (usually unilateral, painful eye movements, RAPD, visual loss). MS association.
    • Central retinal vein occlusion (CRVO) = disc swelling + widespread flame haemorrhages in all 4 quadrants ("blood and thunder" fundus), tortuous veins, unilateral.
    • Hypertensive retinopathy = disc swelling in malignant/accelerated hypertension (BP >180/110 with end-organ damage) + AV nicking, flame haemorrhages, cotton wool spots, arteriolar narrowing.
    • Infiltrative — lymphoma, sarcoidosis, leukaemia, malignant infiltration of optic nerve.
  • Causes of raised ICP (in this clinical context): Space-occupying lesion (primary or secondary brain tumour — most likely given 3-week history, no fever), cerebral abscess, subdural haematoma, venous sinus thrombosis, idiopathic intracranial hypertension (IIH — obese young woman typically, but can occur in males), hydrocephalus, meningitis/encephalitis (if fever present).
  • Immediate management:
    • Medical emergency — do not perform LP before CT head. LP in raised ICP can cause transtentorial herniation (coning) → brainstem compression → death.
    • Urgent CT head immediately — looking for mass lesion, midline shift, hydrocephalus, cerebral oedema, haemorrhage.
    • Neurosurgical referral — urgent.
    • Head of bed at 30° — optimises cerebral venous drainage, reduces ICP.
    • Avoid hypotonic fluids (0.45% NaCl, 5% dextrose) — worsen cerebral oedema. Use isotonic fluids (0.9% NaCl, Hartmann's).
    • Osmotherapy if herniation signs — IV mannitol 0.25–1 g/kg 20% over 15–30 minutes, or hypertonic saline (3% NaCl). Reduces ICP acutely.
    • Dexamethasone 8–16 mg IV/oral — reduces oedema around tumour (vasogenic oedema). Not effective for ischaemia or haemorrhage.
    • Treat pain and nausea (opioids increase ICP — use with caution; anti-emetics safe).
    • Restrict IV fluids to maintenance — avoid overhydration.

⚠️ Examiner Instructions — Not for Candidate

Either use a fundoscopy simulator or describe findings verbally as candidate performs the technique. Findings to describe when asked: "Bilateral disc margin blurring — more prominent superiorly and inferiorly. Disc margins indistinct and hazy. Both discs appear pink and slightly elevated. Venous pulsations absent bilaterally. Flame haemorrhages at the margin of the right disc. No AV nicking. No cotton wool spots." Allow candidate to diagnose papilloedema and manage. If candidate asks about red reflex: "Both eyes — normal orange-red reflex bilaterally." Key checkpoints: Did candidate dim the room? Did they use right eye for right fundus? Did they follow the vessel to the disc? Did they diagnose bilateral papilloedema? Did they state CT before LP? Did they mention head of bed 30°?

🔔 Examiner Cues ▼
  • If candidate doesn't dim the room: "Is there an environmental adjustment that would significantly improve the quality of fundoscopy?"
  • If candidate uses right eye for left fundus: "Which eye does the examiner use when examining the patient's right eye — and why?"
  • If candidate requests LP after diagnosing papilloedema: "Given your fundoscopy findings, is LP safe to perform now? What must come first?"
  • At 7 minutes: "CT shows a 4 cm ring-enhancing lesion in the right frontal lobe with surrounding oedema and 8 mm midline shift. What is your immediate management?"
CriterionMarks
Clinical Recognition
Raised ICP headache features recognised — morning headache, worse on Valsalva, visual obscurations, Cushing's triad (bradycardia + hypertension)2
Fundoscopy Technique
Room dimmed; patient fixes on distant target; red reflex assessed first; right eye for right fundus, approach from temporal side2
Systematic disc examination described — margins, colour, cup:disc ratio, elevation, venous pulsations (absent = earliest sign)3
Papilloedema Findings
Bilateral papilloedema correctly identified from examiner's description — blurred margins (superior/inferior first), disc hyperaemia, elevation, absent venous pulsations, flame haemorrhages3
Differential diagnosis of disc swelling — papilloedema vs papillitis vs CRVO vs hypertensive retinopathy; causes of raised ICP listed2
Management
LP contraindicated without CT first — risk of coning stated; urgent CT head immediately; neurosurgical referral3
Head of bed 30°; avoid hypotonic fluids; osmotherapy (mannitol/hypertonic saline) if herniation; dexamethasone for vasogenic oedema around tumour3
Total20
🩺
Peripheral Vascular Examination — Diabetic Foot Ulcer (Wagner, ABPI, Buerger's)
Examination · 8 minStation 4 of 10
✓
▼
8:00
Station type
Clinical Examination
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

You are the ED registrar. Mr Noel Fitzpatrick, 68 years old, has type 2 diabetes mellitus (T2DM) for 20 years. He is referred by his GP with a right foot ulcer that has not healed for 6 weeks. He is on insulin, metformin, and atorvastatin. He smokes 10 cigarettes/day.

Obs: HR 78, BP 148/88, RR 16, SpO₂ 97% on air, Temp 37.8°C, BM 12.4 mmol/L.

Please perform a focused peripheral vascular and neurological examination of the lower limbs. The examiner will provide positive and negative findings. Describe your examination and classify the ulcer. You have 8 minutes.

💡 Diabetic Foot — Examination, ABPI, Buerger's, Wagner Classification, MDT ▼
  • Ulcer characterisation — inspection first:
    • Site:
      • Neuropathic ulcer — over pressure areas and bony prominences: metatarsal heads (plantar aspect), heel, tips of toes (especially claw toes). Areas of callus formation.
      • Ischaemic ulcer — tips of toes, between toes, lateral border of foot, heels. Areas with least collateral supply.
      • Neuroischaemic ulcer — combination, commonly lateral border of foot and toes.
    • Appearance:
      • Neuropathic: Punched-out edges (sharp, well-defined border), surrounded by callus, painless (neuropathy), pink/granulating base, warm foot. May be deep (penetrating to bone — osteomyelitis).
      • Ischaemic: Irregular sloughy edges, painful (unless also neuropathic), pale or necrotic base, black necrotic eschar, cold foot, atrophic shiny skin, hairless, pale.
    • Skin changes indicating ischaemia: Shiny, thin, atrophic skin. Hairless (hair follicles ischaemic). Pale or dusky. Dependent rubor (red when dependent). Dry, fissured. Toe nails: thickened, dystrophic (ischaemia or fungal).
    • Charcot joint (neuropathic arthropathy): Warm, swollen, erythematous foot/ankle with destruction of bony architecture. No pain despite severe deformity (neuropathy). Rocker-bottom deformity. Requires urgent offloading and non-weight bearing.
    • Signs of infection: Cellulitis (erythema, swelling, warmth, induration), discharge (purulent), tracking erythema (spreading cellulitis, lymphangitis), crepitus (gas-forming organism — gas gangrene, Clostridium, Gram-negative anaerobes). Systemic signs: fever 37.8°C, BM 12.4 (hyperglycaemia in infection).
  • Temperature assessment:
    • Dorsum of examiner's hand along the limb — compare both limbs.
    • Cold foot = peripheral arterial disease (ischaemia).
    • Warm foot with cellulitis = infection, Charcot (hot, red, swollen).
    • Asymmetric temperature = vascular occlusion on cold side.
  • Peripheral pulses — must examine all:
    • Femoral pulse (inguinal ligament midpoint — ASIS to pubic symphysis).
    • Popliteal pulse (knee slightly flexed, both thumbs on tibial tuberosity, fingers curl around posterior knee — press firmly into popliteal fossa). Difficult to palpate — absent in significant PAD.
    • Dorsalis pedis (DP) pulse — lateral to extensor hallucis longus tendon on the dorsum of the foot. Absent in ~5% of normal population.
    • Posterior tibial (PT) pulse — posterior to medial malleolus.
    • Absent DP + absent PT = significant peripheral arterial disease.
  • Capillary refill time — press nail bed for 5 seconds, release, count to colour return. Normal ≤2 seconds. >2 seconds = poor perfusion.
  • Neuropathy assessment — stocking distribution:
    • 10 g Semmes-Weinstein monofilament: Gold standard for peripheral neuropathy screening. Apply to plantar aspect of 10 sites (1st, 3rd, 5th metatarsal heads, tips of toes, plantar heel). Press until monofilament buckles (applies 10 g force). Patient's eyes closed — ask "yes or no" whether they feel it. Inability to feel monofilament = loss of protective sensation → at risk of pressure ulceration.
    • Vibration sense: 128 Hz tuning fork on big toe (interphalangeal joint), medial malleolus. Patient reports when vibration ceases. Reduced perception = peripheral neuropathy. Normal: patient feels vibration for at least as long as the examiner.
    • Pinprick sensation — stocking distribution loss (both feet, bilateral symmetric).
    • Proprioception — big toe position sense.
    • Ankle reflexes — reduced/absent = peripheral neuropathy (also B12 deficiency, hypothyroidism).
  • Ankle-Brachial Pressure Index (ABPI):
    • Doppler probe over DP or PT artery. Inflate BP cuff on ankle until signal disappears. Note ankle SBP. Repeat for brachial SBP (arm). ABPI = ankle SBP ÷ brachial SBP.
    • Normal: 0.9–1.3.
    • 0.7–0.9 = mild PAD.
    • 0.5–0.7 = moderate PAD — claudication.
    • <0.5 = severe PAD — rest pain, critical ischaemia.
    • >1.3 = vessel calcification (common in diabetes and renal disease — medial calcinosis makes vessels non-compressible → falsely elevated ABPI). In this scenario, Mr Fitzpatrick's vessels may be calcified → ABPI may be unreliable. Use toe-brachial index (TBI) instead (toe vessels less affected by calcification — normal TBI >0.7).
  • Buerger's test:
    • Step 1 (elevation test): Elevate legs to 45° for 1–2 minutes. Observe foot colour. In ischaemia: foot becomes pale (cadaveric pallor) within 30 seconds because arterial perfusion pressure cannot overcome gravity. Normal: foot stays pink.
    • Step 2 (dependency test / reactive hyperaemia): After pallor is noted, sit patient up and hang legs over side of bed. In ischaemia: foot turns bright red-purple (reactive hyperaemia — maximal vasodilation after ischaemia). This is called Buerger's sign (sunset rubor/dependent rubor). A positive Buerger's test = significant peripheral arterial disease.
    • Buerger's angle: The angle of elevation at which pallor develops. Less than 20° = critical ischaemia.
  • Wagner classification of diabetic foot ulcers:
    • Grade 0: No open lesion; bony deformity, callus, pre-ulcerative lesion.
    • Grade 1: Superficial ulcer — skin only, not through full thickness.
    • Grade 2: Deep ulcer — through full thickness to tendon, capsule, or fascia, but not bone.
    • Grade 3: Deep ulcer with osteomyelitis, abscess, or joint sepsis.
    • Grade 4: Localised gangrene (toe or forefoot).
    • Grade 5: Extensive gangrene involving whole foot.
    • Grades 3–5 = surgical/vascular emergency.
  • Referral:
    • Diabetic foot MDT within 24 hours for any infected or ischaemic ulcer (NICE NG19 — Diabetic Foot in Hospital).
    • Vascular surgery if ABPI <0.5 or critical ischaemia (rest pain, gangrene).
    • Orthopaedic surgery if osteomyelitis suspected (plain X-ray — periosteal reaction, cortical destruction; MRI gold standard).
    • IV antibiotics if deep infection, cellulitis >2 cm, systemic signs. MRSA screen. Wound swab.
    • Offloading — total contact cast or removable cast walker for neuropathic ulcers.
    • Glucose optimisation — hyperglycaemia impairs wound healing and immune response.

⚠️ Examiner Instructions — Not for Candidate

Provide findings as candidate examines: "Inspection — right plantar forefoot ulcer, 2 cm diameter, punched-out edges, surrounded by callus, base appears pink but with yellow slough. Surrounding skin is erythematous extending 3 cm proximally. No crepitus. Left foot appears shiny and hairless with no ulcers." "Temperature — right foot slightly warmer than left in area of cellulitis; left foot cool." "Pulses — femoral palpable bilaterally; popliteal present right, absent left; dorsalis pedis and posterior tibial absent on left, present on right." "Monofilament — unable to feel 10 g monofilament at any site on the right foot." "ABPI — right 0.82, left 1.4 (calcified vessels)." "Buerger's — right foot: pallor at 45° elevation, dependent rubor on hanging. Left foot: same pattern." Key checkpoints: Did they classify the ulcer (neuropathic vs ischaemic)? Did they note ABPI >1.3 suggests calcified vessels? Did they perform Buerger's test? Did they state MDT within 24 hours?

🔔 Examiner Cues ▼
  • If candidate doesn't examine all four pulses: "You've palpated the DP — are there other pulses in the lower limb vascular examination you need to assess?"
  • If candidate doesn't flag ABPI >1.3 as unreliable: "The ABPI on the left is 1.4 — does this mean perfusion is better than normal on that side?"
  • If candidate omits neuropathy testing: "The ulcer is on a pressure area with callus — what aspect of diabetic foot pathology does that suggest, and how would you test for it?"
  • At 7 minutes: "Wagner classification — where does this ulcer fit, and what does that mean for management?"
CriterionMarks
Inspection and Ulcer Classification
Ulcer site, size, edges, base, surrounding tissue described; neuropathic vs ischaemic vs neuroischaemic pattern distinguished; skin changes (shiny, hairless, atrophic = ischaemia)3
Signs of infection assessed — cellulitis, erythema extent, crepitus (gas), discharge, systemic signs (fever, hyperglycaemia)2
Vascular Assessment
All four pulses assessed bilaterally — femoral, popliteal, DP, PT; absence at multiple levels indicates multi-segment disease2
ABPI performed; normal 0.9–1.3 stated; <0.5 = critical ischaemia; >1.3 = calcified vessels unreliable in diabetes — TBI alternative2
Buerger's test — elevation pallor (ischaemia), dependent rubor (reactive hyperaemia); Buerger's angle <20° = critical ischaemia2
Neuropathy and Classification
10 g monofilament, 128 Hz vibration, pinprick, proprioception, ankle reflexes — stocking distribution; loss of protective sensation identified3
Wagner classification applied — Grade 2 (deep to tendon/fascia, no bone involvement) or Grade 3 if osteomyelitis; MDT referral within 24 hours (NICE NG19)4
IV antibiotics if systemic infection; X-ray/MRI for osteomyelitis; glucose optimisation; vascular surgery if critical ischaemia; offloading device2
Total20
🔧 Practical Procedures
🔧
BLS Teaching — Teaching CPR to a Layperson (Tell-Show-Do)
Procedure / Teaching · 8 minStation 5 of 10
✓
▼
8:00
Station type
Procedure / Teaching
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

You are an ED doctor. Tyler, 16 years old, has just experienced the traumatic death of his parent from a cardiac arrest at home. The resuscitation attempt was unsuccessful. Tyler approaches you in a corridor and says:

"I didn't know what to do. I just stood there. I want to learn CPR so if it ever happens again I can actually help."

A manikin and AED trainer are available. The examiner will play Tyler. Please teach Tyler basic life support. You have 8 minutes.

💡 BLS Teaching — Tell-Show-Do, Technique, AED, Emotional Intelligence ▼
  • Setting and emotional acknowledgement — before any teaching:
    • Tyler has just lost a parent. He is 16. He is asking this immediately after a traumatic bereavement. Do NOT immediately dive into CPR teaching — this risks feeling cold and clinical.
    • Brief acknowledgement first: "Tyler, first — I'm so incredibly sorry about what happened today. You were incredibly brave being there. The fact that you want to learn this shows real courage." Pause. "Are you sure you feel up to this right now? We could do this today or I could arrange for someone to come back and teach you — whatever feels right."
    • If he says yes, he wants to learn now — respect that. Learning can be therapeutic and empowering after helplessness. It addresses his stated need.
    • Move to a private, quiet area (not the corridor — too public, too clinical, he may feel exposed). A side room with a manikin is ideal.
    • Check in on his emotional state throughout — not just at the start. "Are you okay to continue?" at 3–4 minutes.
  • Teaching framework — Tell-Show-Do (structured approach to teaching practical skills):
    • Tell: Explain what you're about to do and why. Establish prior knowledge: "Have you ever seen CPR before — on TV, or in real life?" Use plain language throughout — no medical jargon. Explain the rationale briefly: "When someone's heart stops, blood stops flowing to the brain. CPR pumps the heart manually from the outside, keeping blood moving until the heart can be restarted. Every second counts — starting CPR quickly can double someone's chance of survival."
    • Show: Demonstrate on the manikin before asking Tyler to try. Narrate each step as you do it. "Watch me first, then you'll have a go."
    • Do: Guided practice — "Now you try. I'll guide you." Hands-on learning with immediate feedback. Correct gently, not critically: "That's great — just try to push a little deeper, like this." Supervised repetition until confident.
  • BLS sequence — what to teach (UK Resuscitation Council 2021 guidelines):
    1. Safety: "Before anything — make sure it's safe for you to approach. Look for hazards (traffic, electricity, chemicals). Don't put yourself at risk."
    2. Call for help / Check response: "Tap their shoulders firmly and shout 'Are you alright?' If no response — shout for help. Ask someone to call 999 immediately — or call it yourself on speakerphone. Don't do CPR and call at the same time — delegate."
    3. Open the airway: "Tilt the head back, lift the chin gently up — this opens the airway so they can breathe."
    4. Check breathing: "Look, listen, and feel for normal breathing for no more than 10 seconds. If they're not breathing normally — start CPR."
    5. Call 999 / Get AED: "If alone — call 999 first. If others present — send someone to call 999 AND get the nearest AED (defibrillator). Tell them where you are and what's happening."
    6. Chest compressions:
      • "Kneel beside them. Put the heel of one hand on the centre of their chest — lower half of the breastbone."
      • "Put your other hand on top. Interlock your fingers. Keep your fingers off the chest — just the heel of your hand."
      • "Keep your arms straight, shoulders directly over your hands."
      • "Push down hard and fast — 5 to 6 centimetres deep (about 2 inches). That's deeper than you think."
      • "Let the chest fully come back up between each compression — full recoil. Don't lean on the chest."
      • "Aim for 100 to 120 compressions per minute — the beat of 'Stayin' Alive' by the Bee Gees is exactly the right speed."
    7. Rescue breaths (30:2 ratio): "After 30 compressions, give 2 rescue breaths if you're trained and willing. Tilt head back, pinch nose, make a seal with your mouth, blow in until you see the chest rise. 1 second each. If you're not comfortable with mouth-to-mouth, compression-only CPR is still very effective — especially in the first few minutes."
    8. Continue 30:2: "Keep going — 30 compressions then 2 breaths — until the ambulance arrives, the AED tells you to stop for analysis, or the person starts breathing normally."
    9. When to stop: "If you're exhausted, swap with someone else if available. If paramedics arrive — they'll take over. You only stop CPR if you're told to stop or if it becomes unsafe to continue."
    10. AED use: "Turn it on — it will talk you through every step. Peel and stick the pads as shown in the picture. One above the right nipple, one on the left side below the armpit. The AED analyses the heart rhythm. If it says 'stand clear, delivering shock' — make sure no one is touching the person and press the button. Then go straight back to CPR. The AED will tell you when to stop for the next analysis."
  • Common layperson errors to correct during Do phase:
    • Insufficient depth — "Push harder than you think. It's okay if it feels uncomfortable — it needs to be deep."
    • Leaning on chest — "Fully release between each push."
    • Too slow — check against timer: "Count out loud to keep the rhythm."
    • Hands in wrong position — "Heel of hand only, centre of chest."
  • Assess learning: After demonstration — ask Tyler to do it back. "Now show me what you've learned — I'll be here to guide you." Observe and give positive corrective feedback. Ask a check question: "If someone hands you the AED — what's the first thing you do?"
  • Resources and signposting:
    • British Heart Foundation (BHF) CPR guide — free printout and online video. "Heartstart" community CPR courses.
    • Hands-Only CPR app (BHF) — guides through real-time CPR.
    • Bereavement support: "Tyler, I also want to make sure you have support for what happened today — this is an incredibly hard thing to go through. Our bereavement team can offer counselling. Can I arrange for someone to speak with you today?" Signpost school counsellor, CRUSE Bereavement Care, or NHS mental health support if needed.

⚠️ Examiner / Role-player Instructions — Not for Candidate

Play Tyler — a 16-year-old who is composed but visibly sad. He is motivated and engaged. He has no medical knowledge — use this to test candidate's plain language. React naturally to the teaching — if the candidate uses medical jargon, Tyler looks confused: "What do you mean, 'compress the sternum'?" During the Do phase, deliberately make mistakes: (1) put hands too high (on upper sternum), (2) push too shallowly, (3) not let the chest recoil fully. Expect candidate to correct each gently. At 5 minutes, ask: "What if I get it wrong and hurt them more?" — expect candidate to reassure (you cannot make it worse if they're already in cardiac arrest — CPR is always better than nothing). Key checkpoints: Did candidate acknowledge his grief before teaching? Did they find a private space? Did they use Tell-Show-Do structure? Correct technique (5–6 cm, 100–120/min, full recoil, 30:2)? Did they address emotion throughout? Did they signpost bereavement support?

🎭 Tyler's Script ▼
  • Opening: "I just stood there. I didn't know what to do. I could have helped and I didn't." [Looks down, emotional but controlled].
  • During teaching — deliberate errors: Hands too high. Pushes with fingers rather than heel. Doesn't let chest recoil. [Expect gentle correction].
  • Question at 5 minutes: "What if I hurt them? What if I break their ribs?" [Expect candidate to say: ribs can break during CPR — that's okay, they were already in cardiac arrest, CPR is always better than nothing, paramedics accept this as a known complication].
  • Question about AED: "What if I can't find one? What if it's too far away?" [Expect candidate to say: start CPR immediately, send someone else to find AED — do not leave the patient to go get it yourself unless completely alone].
  • End: "Thank you. I feel like I could actually do something now." [Brief emotional moment — expect candidate to acknowledge this and signpost bereavement support].
🔔 Examiner Cues ▼
  • If candidate uses jargon ("compress the sternum at a rate of 100 bpm"): Tyler looks confused — "What does that mean?"
  • If candidate doesn't acknowledge the bereavement at all before starting: "Tyler says 'aren't you going to ask if I'm okay?' — how should you have started this encounter differently?"
  • If candidate only tells and shows but doesn't let Tyler try: "Is watching enough to learn a practical skill? What's missing from this teaching approach?"
  • At 7 minutes: "Tyler asks: should I give mouth-to-mouth or is that dangerous with strangers?"
CriterionMarks
Setting and Emotional Intelligence
Bereavement acknowledged sincerely before teaching; private space arranged; Tyler's emotional state checked throughout; not rushed into teaching3
Teaching Structure
Tell-Show-Do framework used — explains rationale first (tell), demonstrates on manikin (show), supervised hands-on practice (do); plain language throughout, no jargon3
Prior knowledge established before teaching; learning assessed at end — Tyler asked to demonstrate back; check questions used2
BLS Technique
Safety first; 999 call delegated; head tilt-chin lift; assess breathing ≤10 seconds; compressions: centre of chest, heel of hand, arms straight2
Correct depth 5–6 cm; rate 100–120/min (Stayin' Alive); full recoil between compressions; 30:2 ratio; compression-only CPR acceptable alternative3
AED use — turn on, follow voice prompts, pad placement, stand clear for shock, immediately resume CPR; reassurance re broken ribs (CPR always better than nothing)2
Follow-up
BHF resources provided; bereavement support signposted (counselling, CRUSE, school counsellor)3
Total20
📊 Data Interpretation
📊
Urinalysis and Dipstick Interpretation — Pregnancy UTI and DKA
Data Interpretation · 8 minStation 6 of 10
✓
▼
8:00
Station type
Data Interpretation
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

Part 1: Mrs Priya Okonkwo, 28 years old, 24 weeks pregnant, attends the antenatal clinic with mild dysuria. Urine dipstick: protein 2+, blood 1+, nitrites positive, leukocytes 2+, glucose negative, ketones negative.

Obs: HR 84, BP 142/90, RR 16, Temp 37.6°C, SpO₂ 99%.

Part 2: Mr David Clarke, 45 years old, known T1DM, vomiting and drowsy. Urine dipstick: glucose 4+, ketones 3+, protein 1+. Venous BM: 28.4 mmol/L.

For each part: interpret each dipstick finding systematically, state your diagnoses, and outline immediate management. You have 8 minutes.

💡 Dipstick Interpretation — Systematic Approach, Pregnancy Considerations, DKA ▼
  • Systematic urine dipstick interpretation — ten components:
    • Glucose: Normal = negative. Positive = hyperglycaemia (>10 mmol/L renal threshold) or, less commonly, renal glycosuria (low renal threshold, normal blood glucose — common in pregnancy). Always check blood glucose. In pregnancy, mild glycosuria can be normal due to lowered renal threshold — do NOT diagnose gestational diabetes on dipstick alone (requires OGTT).
    • Ketones: Normal = negative. Positive = ketonaemia: DKA (trace to 3+ with hyperglycaemia), starvation (negative/trace glucose), alcoholic ketoacidosis (low/normal glucose), prolonged vomiting, high-fat diet. Grade: trace, 1+, 2+, 3+. Ketones 3+ with glucose 4+ = strongly suggests DKA — check blood ketones and ABG.
    • Protein: Normal = negative/trace. Significant = 1+ or more. Causes: UTI (inflammation allows protein leakage), glomerulonephritis, nephrotic syndrome, pre-eclampsia (in pregnancy), orthostatic proteinuria (benign — only when standing). In pregnancy: protein 2+ = investigate for pre-eclampsia. Quantify with urine protein:creatinine ratio (PCR) — significant if >30 mg/mmol, severe if >100 mg/mmol.
    • Blood (haematuria): Normal = negative. Positive = haematuria (macroscopic or microscopic) or haemoglobinuria (haemolysis), myoglobinuria (rhabdomyolysis — brown urine, no RBCs on microscopy). Causes of haematuria: UTI, renal calculus, glomerulonephritis, malignancy (bladder/renal), trauma, catheter trauma, menstrual contamination, anticoagulation. Microscopy confirms RBCs. Any haematuria in age >40 without obvious cause = urgent urology referral (2-week wait rule).
    • Nitrites: Normal = negative. Positive = gram-negative bacteria present (nitrate → nitrite via bacterial reductase). Gram-negative bacteria: E. coli (most common UTI organism — 80%), Klebsiella, Proteus. Gram-positive organisms (Staphylococcus saprophyticus, Enterococcus, Streptococcus) do NOT produce nitrites → false negative. Requires urine to dwell in bladder ≥4 hours — early morning sample best. Sensitivity ~50%, specificity ~95%.
    • Leukocytes (leukocyte esterase): Normal = negative. Positive = pyuria (white cells in urine). Causes: UTI, urethritis, pyelonephritis, contamination (vaginal secretions — common in women), sterile pyuria (TB, interstitial nephritis, renal calculus, appendicitis adjacent to bladder). Sensitivity ~75%, specificity ~82% for UTI.
    • Bilirubin: Conjugated bilirubin in urine = obstructive jaundice (gallstones, cholangiocarcinoma, pancreatic head tumour) or hepatocellular jaundice. Unconjugated bilirubin (haemolysis) is water-insoluble and NOT excreted in urine → dipstick negative in haemolytic jaundice.
    • Urobilinogen: Increased in haemolysis (increased bilirubin production) and hepatocellular disease. Absent in complete biliary obstruction (no bilirubin reaching gut, no urobilinogen produced).
    • pH: Normal 4.5–8. Alkaline urine (>7): UTI (urease-producing organisms — Proteus, Pseudomonas), metabolic alkalosis, renal tubular acidosis (type I — inability to acidify urine). Acid urine (<5.5): low-carbohydrate diet, starvation, metabolic acidosis.
    • Specific gravity (SG): Normal 1.003–1.030. High (>1.020) = concentrated urine (dehydration, SIADH). Low (<1.005) = dilute urine (overhydration, diabetes insipidus, renal failure — inability to concentrate).
  • Part 1 — Interpretation and diagnosis:
    • Nitrites positive + leukocytes 2+ + blood 1+ + protein 2+ in a febrile pregnant woman = urinary tract infection / ascending pyelonephritis in pregnancy.
    • UTI in pregnancy — always treat regardless of symptoms: Asymptomatic bacteriuria in pregnancy carries 25% risk of progression to pyelonephritis (vs 2–4% in non-pregnant). Pyelonephritis in pregnancy is associated with preterm labour, low birth weight, maternal sepsis. Any positive urine culture in pregnancy = treat.
    • Urine MC&S first — before starting antibiotics in non-critically unwell patient. Mid-stream urine (MSU) correctly collected.
    • Safe antibiotics in pregnancy:
      • Nitrofurantoin 100 mg MR BD × 5 days — safe in first two trimesters; avoid at term (≥36 weeks) and near delivery — risk of neonatal haemolytic anaemia (immature red cell enzyme systems).
      • Trimethoprim — avoid in first trimester — folate antagonist, risk of neural tube defects. Can use in 2nd and 3rd trimester. Mrs Okonkwo: 24 weeks → trimethoprim acceptable if nitrofurantoin not suitable.
      • Amoxicillin 500 mg TDS × 7 days — safe in pregnancy if sensitivity confirmed. Many E. coli strains are resistant — do not empirically use without sensitivities.
      • Cephalexin 500 mg QDS × 7 days — safe in all trimesters, reasonable empirical choice.
      • Avoid: fluoroquinolones (ciprofloxacin — cartilage toxicity in animal models, avoid in pregnancy), tetracyclines (teeth staining, hepatotoxicity).
    • Protein 2+ in pregnancy at 24 weeks + BP 142/90 = investigate for pre-eclampsia:
      • Pre-eclampsia: hypertension (>140/90) + proteinuria (>300 mg/24h or PCR >30 mg/mmol) after 20 weeks gestation.
      • Investigations: urine PCR, FBC (thrombocytopenia), LFTs (elevated transaminases, epigastric pain), U&E (creatinine rising), uric acid (elevated in pre-eclampsia), coagulation. LDH, fibrinogen if HELLP syndrome suspected.
      • Admit and refer to obstetric team urgently. Even if investigations normal — repeat in 24–48 hours, close surveillance, anti-hypertensives if BP >150/100 (labetalol first-line in pregnancy).
  • Part 2 — Interpretation and DKA diagnosis:
    • Glucose 4+ + ketones 3+ + clinical context (T1DM, vomiting, drowsy, BM 28.4) = Diabetic Ketoacidosis (DKA).
    • DKA diagnostic criteria (JBDS/ADA): Blood glucose >11 mmol/L (or known DM), blood ketones ≥3.0 mmol/L (or urine ketones ≥2+), pH <7.3 or bicarbonate <15 mmol/L.
    • Protein 1+ in DKA — non-specific, can occur due to dehydration, UTI precipitating DKA, or underlying diabetic nephropathy.
    • DKA management (JBDS 2023): IV 0.9% NaCl resuscitation (500 mL over 15 min if haemodynamically compromised). Fixed rate insulin infusion (FRII) 0.1 units/kg/hour — do NOT give stat IV insulin bolus (worsens hypokalaemia). Add glucose 10% when BM <14 mmol/L (maintain insulin running). Potassium replacement (hypokalaemia from insulin driving K⁺ intracellularly — if K⁺ <3.5 mmol/L do not start insulin until replaced). Monitor hourly BM, 2-hourly VBG until ketones <0.6 and pH >7.3. Find and treat precipitant (infection — urine/chest, omitted insulin, new diagnosis).

⚠️ Examiner Instructions — Not for Candidate

Part 1: Read dipstick values aloud for Mrs Okonkwo. If candidate interprets correctly: "Good — can you explain the significance of protein 2+ in this context, given her blood pressure?" Expect candidate to raise pre-eclampsia. Part 2: Read David's dipstick. Then: "Blood ketones measured at 4.8 mmol/L, pH 7.19, bicarbonate 11 — what is your diagnosis and immediate management?" Key checkpoints: Did they interpret all ten components systematically? Did they note nitrofurantoin is unsafe at term (Mrs Okonkwo is 24 weeks — safe now but candidate should demonstrate this knowledge)? Did they link protein 2+ + elevated BP to pre-eclampsia? Did they correctly diagnose DKA and cite JBDS criteria? Did they know NOT to give IV insulin bolus?

🔔 Examiner Cues ▼
  • If candidate prescribes trimethoprim for Part 1 without considering gestation: "Is trimethoprim safe at all gestations of pregnancy — are there any trimesters where it should be avoided?"
  • If candidate misses the pre-eclampsia concern: "Her blood pressure is 142/90 and protein is 2+ — at 24 weeks gestation, what condition must you exclude?"
  • If candidate gives IV insulin stat bolus for DKA: "JBDS 2023 guidelines advise against stat insulin boluses in DKA — why, and what is the recommended approach?"
  • At 7 minutes: "Mrs Okonkwo's PCR returns at 85 mg/mmol. What does this mean and who do you refer to?"
CriterionMarks
Systematic Dipstick Interpretation
All ten components addressed — glucose, ketones, protein, blood, nitrites, leukocytes, bilirubin, urobilinogen, pH, SG; each finding interpreted with clinical significance3
Part 1 — Pregnancy UTI and Pre-eclampsia
UTI/pyelonephritis in pregnancy diagnosed — nitrites + leukocytes + fever; urine MC&S before antibiotics; treat regardless of symptoms in pregnancy2
Safe antibiotic choice — nitrofurantoin (safe at 24 weeks; unsafe at term), trimethoprim (avoid 1st trimester), amoxicillin if sensitive, cephalexin; unsafe antibiotics named (fluoroquinolones, tetracyclines)3
Protein 2+ + BP 142/90 at 24 weeks → pre-eclampsia investigated; PCR, FBC, LFT, U&E, uric acid ordered; obstetric team referral3
Part 2 — DKA
DKA diagnosed — glucose 4+, ketones 3+, blood glucose 28.4, ketones 4.8, pH 7.19; JBDS criteria applied (BG >11, ketones ≥3.0, pH <7.3)3
DKA management — IV 0.9% NaCl resuscitation, FRII 0.1 units/kg/hour (NO stat bolus — hypokalaemia risk), potassium replacement, add glucose 10% when BM <14; find precipitant4
Haematuria significance noted — blood 1+ in pregnancy; MSU microscopy; age >40 haematuria without obvious cause = urology referral2
Total20
📊
VBG Interpretation — Mixed Acid-Base, Post-ROSC, Metabolic Alkalosis, Paediatric Respiratory Failure
Data Interpretation · 8 minStation 7 of 10
✓
▼
8:00
Station type
Data Interpretation
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

Three VBG results. For each: interpret systematically, state the diagnosis, and outline management.

Part 1: Mr Howell, 68, ROSC after 25-minute cardiac arrest. VBG: pH 7.18, pCO₂ 6.8, HCO₃ 14, BE −14, lactate 8.2, glucose 14, K⁺ 5.8, Na⁺ 138.

Part 2: Mrs Patel, 72, on furosemide for heart failure, 5 days vomiting, confused. VBG: pH 7.52, pCO₂ 5.1, HCO₃ 32, BE +8, lactate 1.2, K⁺ 2.8, Cl⁻ 88, Na⁺ 142.

Part 3: Finn, 5 years old, 3-day viral illness, worsening respiratory distress, now lethargic. VBG: pH 7.28, pCO₂ 8.2, HCO₃ 22, BE −2, lactate 1.8. SpO₂ 91% on 10L O₂.

💡 VBG Systematic Approach — Post-ROSC, Metabolic Alkalosis, Paediatric Type 2 RF ▼
  • VBG systematic interpretation framework (apply to each):
    1. pH — acidaemia (<7.35), alkalaemia (>7.45), or normal.
    2. Primary disturbance — CO₂ (respiratory) or HCO₃ (metabolic). The one moving in the same direction as pH change is the compensation; the one moving in the opposite direction is the primary disorder.
    3. Compensation — is it appropriate? (Winter's formula for metabolic acidosis: expected pCO₂ = 1.5 × HCO₃ + 8 ± 2. For metabolic alkalosis: expected pCO₂ = 0.7 × HCO₃ + 21 ± 2.)
    4. Mixed disorder — if compensation is inappropriate (too little or too much), a second primary process is present.
    5. Lactate — elevated (>2 mmol/L) = Type A lactic acidosis (hypoperfusion) or Type B (metabolic, drug-related).
    6. Electrolytes, glucose — act on what you find.
  • Part 1 — Post-ROSC VBG:
    • pH 7.18 = acidaemia (severe).
    • pCO₂ 6.8 = elevated → respiratory acidosis component (normal = 4.5–6.0 kPa).
    • HCO₃ 14 = low → metabolic acidosis component (normal = 22–26 mmol/L).
    • Both CO₂ elevated and HCO₃ low in the context of acidaemia = mixed respiratory and metabolic acidosis.
    • Lactate 8.2 = severely elevated → Type A lactic acidosis (tissue hypoperfusion during cardiac arrest and post-arrest low-output state).
    • K⁺ 5.8 = hyperkalaemia — acidosis drives K⁺ out of cells (H⁺/K⁺ exchange). Dangerous: can cause arrhythmias post-ROSC. Treat if symptomatic or worsening.
    • Glucose 14 = stress hyperglycaemia (catecholamine surge during arrest).
    • Post-ROSC management targets (ILCOR/ERC 2021):
      • SpO₂ target: 94–98% — avoid hyperoxia (free radical injury) and hypoxia. Titrate FiO₂.
      • pCO₂ target: normocapnia (4.5–5.0 kPa) — avoid hypo- and hypercapnia (both worsen neurological outcome).
      • Avoid hyperthermia — temperature target 36°C (TTM2 trial — targeted temperature management 36°C vs 33°C equivalent outcomes).
      • BP target: MAP ≥65 mmHg (vasopressors if needed — noradrenaline first-line).
      • 12-lead ECG for STEMI → primary PCI regardless of consciousness level.
      • CT brain if no obvious non-cardiac cause.
      • Treat hyperkalaemia if K⁺ >6.5 or ECG changes: calcium gluconate 10 mL 10% IV, insulin-dextrose, sodium bicarbonate if severe metabolic acidosis.
      • Lactate will improve with reperfusion — serial lactate every 1–2 hours to assess adequacy of resuscitation.
  • Part 2 — Metabolic alkalosis (furosemide + vomiting):
    • pH 7.52 = alkalaemia.
    • pCO₂ 5.1 = slightly elevated = respiratory compensation for metabolic alkalosis (hypoventilation — appropriate).
    • HCO₃ 32 = elevated → primary metabolic alkalosis.
    • K⁺ 2.8 = hypokalaemia. Cl⁻ 88 = hypochloraemia.
    • Diagnosis: Hypochloraemic hypokalaemic metabolic alkalosis — classic pattern of loop diuretic use + vomiting.
    • Mechanism: Furosemide → Cl⁻ and K⁺ loss in urine → hypokalaemia + hypochloraemia → HCO₃ rises to maintain electrochemical neutrality (contraction alkalosis). Vomiting → additional H⁺ and Cl⁻ loss → worsens alkalosis. Contraction alkalosis: volume contraction → renin-angiotensin-aldosterone activation → Na⁺ and H₂O retention, H⁺ and K⁺ loss → sustains alkalosis.
    • Management:
      • IV potassium chloride (KCl) — replace both potassium and chloride. Max rate 10–20 mmol/hour via peripheral IV (faster via central line with monitoring). Target K⁺ >3.5 mmol/L.
      • IV 0.9% NaCl — provides chloride for renal bicarbonate excretion and corrects volume depletion.
      • Stop or reduce furosemide temporarily.
      • Treat underlying cause of vomiting.
      • Monitor ECG — hypokalaemia: U waves, flattened T waves, prolonged QU interval, arrhythmias (AF, VT).
  • Part 3 — Paediatric acute respiratory acidosis (bronchiolitis/viral lower respiratory tract infection):
    • pH 7.28 = acidaemia.
    • pCO₂ 8.2 = markedly elevated → primary respiratory acidosis (CO₂ retention).
    • HCO₃ 22 = near normal → no metabolic compensation yet = acute respiratory acidosis (compensation takes 24–48 hours for kidneys to generate bicarbonate).
    • Lactate 1.8 = mildly elevated — borderline (normal <2), not alarming but bears watching.
    • SpO₂ 91% despite 10L O₂ = Type 2 respiratory failure (hypoxia + hypercapnia) — inability to clear CO₂ = ventilatory failure.
    • Diagnosis: Acute respiratory acidosis — Type 2 respiratory failure in viral bronchiolitis, approaching ventilatory failure.
    • PICU threshold criteria: Rising pCO₂ (>8 kPa), pH <7.25 or <7.30 with fatigue, SpO₂ <92% on high-flow O₂, exhausted child (lethargic, apnoeic episodes), poor feeding, worsening clinically.
    • Escalation ladder for respiratory support in bronchiolitis:
      • Supplemental O₂ — first-line (nasal cannula/face mask): correct hypoxia.
      • High-Flow Nasal Cannula (HFNC) (e.g. Optiflow) — warms and humidifies high-flow O₂/air mix. Provides mild positive pressure, reduces WOB, reduces CO₂. Starting point: 2 L/kg/min, titrate to effect. First-line escalation for moderate bronchiolitis in most paediatric units. Does NOT reliably reduce intubation rates vs standard O₂ in RCTs but improves comfort and oxygenation.
      • CPAP (continuous positive airway pressure) — maintains alveolar patency, reduces atelectasis, improves oxygenation. Useful when oxygenation the primary problem but patient can initiate breaths. Not effective for pure CO₂ retention (does not augment tidal volume).
      • BiPAP / NIV — provides inspiratory pressure support (reduces CO₂ by augmenting tidal volume) + PEEP. Better than CPAP for hypercapnoea. Requires cooperative patient and intact airway reflexes. Consider early in Finn given rising pCO₂.
      • Intubation and mechanical ventilation — if NIV fails or contraindicated, GCS dropping, apnoeas, exhaustion, pH <7.20. RSI with ketamine/rocuronium. Ventilator settings: rate 25–30/min, tidal volume 6 mL/kg IBW, PEEP 5–8 cmH₂O for bronchiolitis, long expiratory time (I:E 1:3) to prevent air trapping. Risk of post-extubation stridor.
    • PICU referral: This child needs urgent PICU review now — pH 7.28, SpO₂ 91% on 10L, pCO₂ 8.2, lethargic = on the threshold of ventilatory failure. Do not wait.

⚠️ Examiner Instructions — Not for Candidate

Read each VBG in turn and pause after each for interpretation. Part 1 prompts: "What does the lactate of 8.2 indicate and what are your post-ROSC SpO₂ and CO₂ targets?" Part 2 prompts: "What is causing the metabolic alkalosis — name both mechanisms. What is your treatment?" Part 3 prompts: "This 5-year-old is on 10L O₂ with SpO₂ 91% — what respiratory support would you escalate to, and in what order?" Key checkpoints: Mixed acidosis diagnosis in Part 1 (not just metabolic)? Post-ROSC targets correct (SpO₂ 94–98%, normocapnia, temp 36°C)? Hypochloraemic hypokalaemic alkalosis named in Part 2? KCl and 0.9% NaCl for Part 2? Escalation ladder for Part 3 — HFNC → BiPAP → intubation? PICU referral urgency stated?

🔔 Examiner Cues ▼
  • If candidate diagnoses only metabolic acidosis in Part 1: "The CO₂ is also elevated — does this fit with compensation, or is there a second primary disorder?"
  • If candidate targets SpO₂ 100% post-ROSC: "What are the risks of hyperoxia post-cardiac arrest and what is the current target range?"
  • If candidate treats Part 2 alkalosis with 5% dextrose: "Which electrolyte and IV fluid combination specifically addresses both the low chloride and the potassium deficit?"
  • At 7 minutes: "For Part 3 — Finn deteriorates on HFNC, pH now 7.20, pCO₂ 9.8. What is your next step and who do you call?"
CriterionMarks
Part 1 — Post-ROSC
Mixed respiratory and metabolic acidosis identified — both elevated CO₂ and low HCO₃ in acidaemia context; not described as single disturbance2
Lactate 8.2 = Type A lactic acidosis (tissue hypoperfusion); hyperkalaemia (5.8) from acidosis-driven K⁺ efflux — treatment plan stated; post-ROSC targets: SpO₂ 94–98%, normocapnia pCO₂ 4.5–5.0, temp 36°C, MAP ≥65, ECG for STEMI4
Part 2 — Metabolic Alkalosis
Hypochloraemic hypokalaemic metabolic alkalosis correctly named; dual mechanism — furosemide (Cl⁻/K⁺ loss) AND vomiting (H⁺/Cl⁻ loss) both identified3
Management: IV KCl (restores K⁺ and Cl⁻), IV 0.9% NaCl (Cl⁻ for renal HCO₃ excretion), stop furosemide, ECG monitoring for hypokalaemia-related arrhythmias3
Part 3 — Paediatric Respiratory Failure
Acute respiratory acidosis identified — elevated CO₂, normal HCO₃ (no compensation yet = acute); Type 2 respiratory failure diagnosed (hypoxia + hypercapnia)2
Escalation ladder — O₂ → HFNC → BiPAP/NIV (for CO₂ retention) → intubation; correct threshold for intubation stated; PICU referral urgently now given pH 7.28, pCO₂ 8.2, fatigue4
CPAP limitation in CO₂ retention explained (no inspiratory pressure augmentation); BiPAP preferred for hypercapnoea2
Total20
📊
POCUS — Cardiac Tamponade Recognition and Pericardial Effusion Interpretation
Data Interpretation · 8 minStation 8 of 10
✓
▼
8:00
Station type
Data Interpretation
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

You are the ED registrar. Mr Brendan Kearney, 52 years old, has known lung cancer (recently diagnosed, not yet treated). He presents with 3 days of progressive dyspnoea and reduced exercise tolerance. He looks unwell.

Obs: HR 118, BP 90/60, RR 24, SpO₂ 94% on 4L O₂. JVP raised 5 cm. Heart sounds muffled. Pulsus paradoxus 18 mmHg on measurement.

You have performed a POCUS (point-of-care ultrasound). The examiner will describe the echo findings. Please interpret the findings, state your diagnosis, and outline immediate management. You have 8 minutes.

💡 POCUS — Tamponade Echo Signs, Constrictive Pericarditis, Pericardiocentesis, Fluid Analysis ▼
  • POCUS echo findings for cardiac tamponade (examiner will describe):
    • Large circumferential anechoic (echo-free) space around the heart — pericardial fluid appears as a dark black band around the ventricles on 2D echo. "Anechoic" = no echoes = fluid. Location: anterior and posterior to the heart in the pericardial space.
    • Right ventricular diastolic collapse (RV diastolic collapse) — the most sensitive echo sign of tamponade physiology. The RV free wall collapses inward during diastole (when RV pressure is at its lowest) because pericardial pressure exceeds RV diastolic pressure. Seen on parasternal long axis (PLAX) or subcostal view.
    • Right atrial systolic collapse — RA free wall invaginates during systole. Less specific than RV diastolic collapse but adds specificity when present.
    • IVC plethora with <50% respiratory variation — the IVC is dilated (>2.1 cm) and shows less than 50% collapse on inspiration (normal = >50% collapse = low RA pressure). In tamponade: elevated RA pressure prevents venous return from collapsing the IVC on inspiration. Sign of elevated right atrial pressure — high sensitivity for tamponade when combined with effusion.
    • Swinging heart — the heart swings back and forth within the pericardial effusion on echo (electrical alternans on ECG — alternating QRS amplitude corresponding to cardiac swinging). Seen in large effusions.
    • Respiratory variation in mitral and tricuspid inflow — on Doppler: >25% variation in mitral E-wave on inspiration = tamponade physiology. Corresponds to pulsus paradoxus.
  • Clinical context — malignant pericardial effusion:
    • Known lung cancer + pericardial effusion = malignant pericardial effusion until proven otherwise. Lung cancer, breast cancer, lymphoma, leukaemia, melanoma are the most common causes of malignant pericardial effusion.
    • Other causes of pericardial effusion: viral pericarditis (usually smaller, rarely causes tamponade), hypothyroidism, uraemia, TB, connective tissue disease (SLE, rheumatoid), aortic dissection (haemopericardium — Type A — surgical emergency), post-cardiac injury syndrome (Dressler's), post-procedural (pacemaker insertion, cardiac surgery).
  • Cardiac tamponade vs constrictive pericarditis — key POCUS distinction:
    • Tamponade: Large effusion, RV diastolic collapse, IVC plethora, swinging heart. Haemodynamics improve with fluid and/or pericardiocentesis.
    • Constrictive pericarditis: No (or minimal) pericardial effusion. Pericardium is thickened, calcified, rigid — encases the heart. Echo: septal bounce (rapid early ventricular filling causes interventricular septum to bounce laterally), pericardial thickening/calcification, hepatic venous flow reversal on expiration, IVC plethora. CT/MRI: pericardial calcification and thickening (>4 mm). Treatment: surgical pericardiectomy — not drainage. Fluid and diuretics are harmful in constriction. Beck's triad present in both — differentiate on echo.
  • Immediate management:
    • IV fluid bolus (250–500 mL 0.9% NaCl) — temporising measure only. Increases preload → increases RV filling despite elevated pericardial pressure → maintains cardiac output temporarily. Does NOT treat tamponade.
    • Avoid vasodilators (GTN, morphine, ACE inhibitors) — reduce preload and worsen tamponade.
    • Avoid diuretics — reduce preload, worsen tamponade.
    • Pericardiocentesis — definitive ED treatment (as covered in Bank 11, Station 5). Subxiphoid approach, 45° angle toward left shoulder, echo guidance reduces complications. Even 50 mL aspiration can dramatically improve haemodynamics.
    • Cardiothoracic surgery referral — malignant effusions frequently reaccumulate after pericardiocentesis. Pericardial window (surgical) provides longer-term drainage. Indwelling pericardial drain as bridge.
    • Pericardial fluid analysis:
      • Cytology — malignant cells (diagnostic for malignant effusion).
      • MC&S — bacterial pericarditis (rare).
      • LDH, protein, glucose — exudate vs transudate (Light's criteria).
      • ADA (adenosine deaminase) — elevated in TB pericarditis (sensitivity ~87%).
      • AFB smear and culture — TB.
      • Haematocrit — bloody fluid: haematocrit >50% of blood = haemopericardium (aortic dissection, cardiac rupture, trauma).
    • Oncology referral — systemic treatment of underlying lung cancer may reduce effusion recurrence.

⚠️ Examiner Instructions — Not for Candidate

Describe POCUS findings aloud: "On subcostal view — large circumferential anechoic space surrounding the heart, approximately 2.5 cm anteriorly and posteriorly. The RV free wall collapses inward during diastole — RV diastolic collapse present. RA free wall invaginates during systole. IVC is 2.6 cm and shows less than 30% collapse on inspiration. The heart appears to swing within the effusion." Allow candidate to diagnose and manage. Then: "How does this distinguish from constrictive pericarditis on echo?" Then: "You aspirate 80 mL of straw-coloured fluid — what do you send it for?" Key checkpoints: RV diastolic collapse named as most sensitive sign? Fluid bolus as temporising (not definitive) treatment? Vasodilators and diuretics avoided? Pericardiocentesis as ED treatment? Fluid sent for cytology?

🔔 Examiner Cues ▼
  • If candidate gives diuretics: "He has raised JVP — is diuresis appropriate in cardiac tamponade, and why not?"
  • If candidate doesn't name RV diastolic collapse as the key sign: "Which specific echo finding is considered the most sensitive sign of cardiac tamponade physiology?"
  • If candidate confuses tamponade with constrictive pericarditis: "This patient has a large effusion — constrictive pericarditis typically shows what features on echo that are different from what you've described?"
  • At 7 minutes: "After pericardiocentesis HR 92, BP 110/70. Three weeks later he re-presents with the same picture. What definitive treatment should be considered?"
CriterionMarks
POCUS Interpretation
All five echo findings interpreted correctly — large circumferential effusion, RV diastolic collapse (named as most sensitive sign), RA systolic collapse, IVC plethora <50% variation, swinging heart4
Cardiac tamponade diagnosed confidently; Beck's triad on clinical exam corroborated by echo; pulsus paradoxus 18 mmHg significance explained (>10 = significant)2
Differential — Constrictive Pericarditis
Constrictive pericarditis distinguished — no/minimal effusion, pericardial thickening/calcification, septal bounce, no RV diastolic collapse; treatment difference (pericardiectomy, not drainage)3
Management
IV fluid bolus as temporising only — increases preload; vasodilators and diuretics explicitly avoided (reduce preload, worsen tamponade)3
Pericardiocentesis — ED definitive treatment; technique referenced; pericardial window for recurrence; oncology referral3
Fluid analysis — cytology (malignant cells), MC&S, LDH/protein/glucose, ADA (TB), AFB, haematocrit (haemopericardium)3
Malignant aetiology in lung cancer context recognised — pericardial effusion as oncological emergency2
Total20
💬 Communication & Teaching
💬
Teaching Cannulation to a Medical Student — SET-DIALOGUE-CLOSURE
Communication / Teaching · 8 minStation 9 of 10
✓
▼
8:00
Station type
Communication / Teaching
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

You are an ED registrar. Sophie, a 3rd-year medical student on her first ED placement, approaches you during a quiet moment and says:

"I've watched cannulation a few times but I've never done one myself. Could you teach me? I want to be able to do it by the end of this placement."

A cannulation training arm and equipment tray are available. The examiner will play Sophie. Please teach IV cannulation using a structured approach. You have 8 minutes.

💡 Teaching Cannulation — SET-DIALOGUE-CLOSURE, Pendleton's Feedback, Cannula Technique ▼
  • Structured teaching framework — SET-DIALOGUE-CLOSURE (SDC):
    • SET:
      • Learning objectives: Be explicit — "By the end of this session, you should be able to: (1) select appropriate cannula size and vein, (2) perform the technique safely on a training arm, (3) name the complications and how to avoid them." Written objectives if time allows.
      • Prior knowledge assessment: "What have you seen so far? Have you had a go before? Do you know the equipment?" Establish baseline — do NOT assume zero knowledge or advanced knowledge. Tailor teaching accordingly.
      • Time and environment check: "We have about 8 minutes — this should be enough for a demonstration and a supervised attempt. Let's go to a quiet area with the training arm."
    • DIALOGUE (teaching content — Tell-Show-Do integrated):
      • Equipment overview:
        • Cannula colour coding and sizes — this is a high-yield OSCE topic: Grey (16G) — fastest flow, major trauma/theatre. Green (18G) — standard adult. Pink (20G) — standard, most common in ED for medications. Blue (22G) — paediatric, elderly, fragile veins. Yellow (24G) — neonatal. Size (gauge) inversely related to flow — smaller number = bigger cannula = faster flow.
        • Tourniquet — apply 5–10 cm above intended site. Not too tight (occludes artery) — just enough to distend veins.
        • Skin prep — 2% chlorhexidine in 70% alcohol wipe. Allow to dry for 30 seconds (wet chlorhexidine skin prep is ineffective and stings).
        • Equipment: cannula (appropriate size), 10 mL flush syringe pre-filled with 0.9% NaCl, adhesive dressing (Tegaderm/IV3000), tape, blood bottles if samples needed.
      • Vein selection: Antecubital fossa (ACF) — large, easy, good for rapid infusion but limits elbow movement and phlebitis risk. Forearm veins — cephalic and basilic — preferred for dwell time. Dorsum of hand — last resort, small and uncomfortable. Avoid: areas of infection, lymphoedema arm (post-mastectomy), AV fistula arm (dialysis patient), paralysed arm, joint flexures (high phlebitis risk).
      • Technique (step-by-step):
        1. Hand hygiene — 6-step WHO technique. Non-sterile gloves.
        2. Apply tourniquet. Select vein — look and palpate. Straight, soft, bouncy = good. Hard = calcified. Rolly = will roll. Tap vein to dilate if needed.
        3. Skin prep — swab and allow 30 seconds to dry.
        4. Warn patient: "Sharp scratch" — not "small scratch" or "tiny prick" (minimises complaint if painful).
        5. Anchor skin distally with non-dominant thumb (prevents vein rolling).
        6. Insert cannula with bevel (bevelled tip) facing UP. Angle 15–30° to skin (shallower for superficial veins, steeper for deeper veins).
        7. Watch for flashback — blood enters the cannula hub. Advance 2–3 mm further (ensures cannula tip is in the lumen, not just the bevel).
        8. Lower angle to near skin level. Advance the plastic cannula off the metal stylet — hold stylet still, advance cannula only. Do NOT advance stylet further (risk of through-and-through puncture).
        9. Release tourniquet before removing stylet — prevents blood spill.
        10. Apply finger pressure proximal to cannula tip to occlude vein. Remove stylet.
        11. Sharps disposal immediately — stylet directly into sharps bin. Never resheath.
        12. Connect extension set or cap. Flush with 5–10 mL 0.9% NaCl — check flows freely without swelling (infiltration/tissuing = cannula not in vein).
        13. Secure with transparent dressing (allows visual inspection). Document: date, time, size, site, inserter's name.
    • Complications:
      • Haematoma — through-and-through puncture or excessive probing. Management: remove, direct pressure 3–5 minutes.
      • Phlebitis — inflammation of vein wall. Causes: long dwell time, ACF site, irritant drugs (potassium, amiodarone, concentrated glucose). Signs: erythema, pain, warmth, induration along vein track (VIP score). Remove if VIP ≥2.
      • Extravasation / infiltration — vesicant drug leaks into tissues. Prevention: check flashback and flush before starting. Cytotoxic agents → tissue necrosis. Management: stop infusion, aspirate, elevate, specialist review (plastic surgery for some cytotoxics).
      • Arterial puncture — bright red, pulsatile blood, rapid fill. Do NOT use as IV line. Remove, apply firm pressure 5–10 minutes. Risk: inadvertent intra-arterial drug injection (severe — ischaemia).
      • Infection / bacteraemia — skin flora introduced at insertion. Prevention: strict aseptic non-touch technique (ANTT), skin prep, remove all cannulas not clinically needed (48–72 hour review policy).
      • Nerve injury — avoid antecubital fossa (median nerve, lateral cutaneous nerve), wrist (radial nerve at anatomical snuffbox).
    • CLOSURE (feedback — Pendleton's model):
      • Ask Sophie to have a supervised attempt on the training arm. Observe without interrupting unless safety issue.
      • Pendleton's feedback rules (4 steps):
        1. Ask the learner what they thought went well first. "What did you feel went well with that?"
        2. You (the teacher) add what went well. "I also noticed that your vein anchoring technique was excellent — you prevented it rolling."
        3. Ask the learner what they would do differently. "Is there anything you'd change?"
        4. You add what could be improved. "Just one thing I noticed — when you had flashback, try to lower the angle a little more before advancing the cannula — this helps thread it in without kinking."
      • Set next steps: "The next step is to do this on a real patient — supervised. Would you like me to call you when I'm going to put a cannula in and you can do it with me watching?"
      • Signpost resources: Geeky Medics, RCN cannulation standards, local hospital clinical skills lab.

⚠️ Examiner / Role-player Instructions — Not for Candidate

Play Sophie — enthusiastic, slightly nervous, asks good questions. Prior knowledge: "I've watched about 5 so far. I know you need a needle and a tube thing. I'm not sure what all the colours mean." During the supervised attempt: (1) inserts at too steep an angle (>45°), (2) attempts to advance stylet after flashback (not just the cannula). Expect candidate to gently correct both errors during or after the attempt. Ask: "What's the difference between pink and green?" — expect colour-coding knowledge. Ask: "What if I accidentally stick myself?" — expect: remove gloves, wash wound under running water for minimum 2 minutes, do NOT suck the wound, report to occupational health immediately, donor blood sample requested. Key checkpoints: Learning objectives stated at SET? Prior knowledge assessed? Colour coding taught? Bevel up angle 15–30° stated? Sharps disposal immediately? Pendleton's feedback used?

🔔 Examiner Cues ▼
  • If candidate teaches without setting learning objectives: "Sophie asks — 'What am I supposed to be able to do by the end of this?' — how should you have started?"
  • If candidate doesn't demonstrate before asking Sophie to try: "Is watching a demonstration part of an effective practical teaching framework? What model does this follow?"
  • If candidate gives feedback without asking Sophie's self-assessment first: "Pendleton's rules ask you to do something specific before giving your own feedback — what is that?"
  • At 6 minutes: "Sophie asks — 'I accidentally stuck myself — what do I do?'"
CriterionMarks
SET Phase
Learning objectives stated clearly at outset; prior knowledge assessed before teaching; environment and time checked3
DIALOGUE — Content
Equipment explained — cannula colour coding and sizes correct (grey 16G, green 18G, pink 20G, blue 22G, yellow 24G); tourniquet application; skin prep (chlorhexidine, allow to dry)3
Technique correct and in logical sequence — bevel up, 15–30° angle, flashback, lower angle, advance cannula only (not stylet), release tourniquet before removing stylet, flush and check patency3
Sharps disposal immediately (never resheath); infection control — hand hygiene, gloves, ANTT; needlestick management stated if asked (wash 2 min running water, report OH)2
Complications taught — haematoma, phlebitis, extravasation, arterial puncture, infection; prevention strategies for each2
CLOSURE — Feedback
Supervised practice on training arm; errors corrected gently during/after attempt (angle too steep, advancing stylet after flashback)3
Pendleton's model used — Sophie's self-assessment first, then teacher's additions; positives before improvements; next steps set (supervised real patient attempt)4
Total20
💬
Leadership — Major Trauma Team Briefing (ATLS, Closed-Loop, Role Allocation)
Communication / Leadership · 8 minStation 10 of 10
✓
▼
8:00
Station type
Communication / Leadership
Time allowed
8 minutes
Pass mark
12 / 20
📄 Candidate Briefing
👁 Examiner Instructions
✅ Mark Scheme

📄 Candidate Instructions

You are the ED registrar leading the trauma team. A pre-alert has just been received:

"45-year-old male unrestrained driver, high-speed RTC at approximately 70 mph, passenger side impact. GCS 10 on scene (E2 V3 M5). BP 90 systolic on scene. Suspected multiple rib fractures, abdominal tenderness, right femoral deformity. ETA 4 minutes. One large-bore IV en route, 500 mL NaCl running."

The following team is assembled in the trauma bay: anaesthetic registrar, two ED nurses (Nurse A and Nurse B), radiographer, ED consultant (observing, not leading).

Please conduct the pre-arrival team briefing. The examiner will play the team. You have 8 minutes (4 minutes for briefing before patient arrives, then 4 minutes to manage the arrival).

💡 Trauma Team Briefing — Role Allocation, ATMIST, Anticipatory Preparation, Leadership ▼
  • Why team briefings matter — situational awareness and shared mental model: A trauma team briefing before the patient arrives ensures every team member knows: (1) what is coming, (2) their specific role, (3) what equipment is needed, (4) what the immediate priorities will be. Shared mental model reduces errors, duplication, and omissions. Time spent briefing saves time during resuscitation.
  • Team briefing structure — mnemonic ATMIST (pre-alert information structure):
    • A — Age: 45-year-old male.
    • T — Time of incident: Stated in pre-alert.
    • M — Mechanism: High-speed RTC, 70 mph, unrestrained driver, side impact.
    • I — Injuries (known/suspected): Multiple rib fractures (likely pneumothorax/haemothorax), abdominal tenderness (solid organ injury — spleen, liver), right femoral fracture (haemorrhage — femur holds 1–2 litres blood).
    • S — Signs: GCS 10, BP 90 systolic (haemodynamic compromise — Class III-IV haemorrhagic shock), presumed HR unknown from pre-alert.
    • T — Treatment given: Large-bore IV access, 500 mL NaCl running en route.
  • Team introductions and role allocation (explicit, by name):
    • "Good afternoon everyone — I'm [name], the ED registrar, and I'll be leading this trauma. We have 4 minutes before arrival. Let me quickly go through roles."
    • Team leader (candidate): Stands at foot of bed — maintains overview, directs <C>ABCDE, calls for investigations and specialist input, makes key decisions. Does NOT perform procedures — delegates. Situational awareness.
    • Airway doctor (anaesthetic registrar): "You're on airway — please position at the head of the bed. GCS 10 — high likelihood this patient will need RSI. Please draw up RSI drugs now: ketamine or thiopentone induction, rocuronium. Cricoid pressure preparation. Prepare for failed airway — bougie and surgical airway kit within reach."
    • Circulation/IV access nurse (Nurse A): "Please take the right side — you're on IV access and haemodynamic monitoring. We'll need 2 large-bore IV cannulas confirmed. Prepare blood tubes for trauma bloods (FBC, coag, crossmatch — 6 units pRBC, 6 FFP — activate massive transfusion protocol)."
    • Procedure/exposure nurse (Nurse B): "Please take the left side — you'll handle exposure (cutting clothing — trauma shears), catheter when appropriate, and monitoring leads. Start on chest assessment once exposed — rib fractures on exam."
    • Radiographer: "Please position for immediate trauma chest X-ray and pelvis X-ray after the primary survey. Have the portable ready."
    • Scribe: "Is there a scribe? If not, Nurse B — please document all interventions with timestamps once your initial tasks are done."
    • ED consultant (observing): Acknowledge their presence — "Dr [name] is here as clinical supervisor." Do not defer leadership to them unless asking for specific guidance.
  • Anticipatory preparation — equipment (call out each item and confirm):
    • Massive transfusion protocol (MTP) activation: GCS 10 + BP 90 systolic at scene + suspected haemorrhage from femur + abdominal injury = early MTP. "Has the blood bank been called? 6 units O-negative pRBC and 6 units FFP — please confirm." Ratio: 1:1:1 (pRBC:FFP:platelets).
    • RSI drugs drawn up: Anaesthetic registrar confirms. Ketamine 1–2 mg/kg IV, rocuronium 1.2 mg/kg IV. Suxamethonium alternative if not pre-treated. Video laryngoscope at head of bed.
    • Pelvic binder: "Pelvis binder on standby — unrestrained driver with BP 90, pelvic fracture must be excluded. Place as soon as exposed, before CT."
    • Thoracostomy kit: "Bilateral thoracostomy kit available — multiple rib fractures, haemopneumothorax likely." (Bilateral thoracostomies in traumatic cardiac arrest — see previous stations.)
    • Warming: Warm IV fluids, warming blanket, heated trauma bay. Hypothermia worsens coagulopathy in trauma (lethal triad: hypothermia + acidosis + coagulopathy).
    • Level 1 rapid infuser: Confirmed ready for blood product administration.
    • Trauma CT plan: "If he survives the primary survey and is haemodynamically stable after initial resuscitation — immediate CT trauma (pan-scan: head, C-spine, chest, abdomen, pelvis). If haemodynamically unstable — FAST scan first, and to theatre if positive."
  • Closed-loop communication:
    • Every instruction given by the team leader should be read back by the recipient to confirm receipt and understanding.
    • Example: "Nurse A — can you activate the MTP please?" → Nurse A: "MTP activated — understood." → Team leader: "Thank you, MTP activated."
    • This prevents missed or misunderstood instructions in a noisy, high-stress environment.
    • Use names, not roles: "James" not just "anaesthetist" — increases accountability.
  • Invitation for questions: Before closing the briefing: "Any questions or concerns before they arrive? Is there anything I've missed?" Psychological safety — any team member can speak up.
  • Leadership style — calm and authoritative:
    • Speak clearly, loudly enough for all to hear, but not panicked.
    • Maintain eye contact when allocating roles.
    • Stand at the foot of the bed or a position with line of sight to the whole team — do NOT perform procedures yourself (lose situational awareness).
    • Acknowledge good team performance during: "Good work, airway secured." Positive reinforcement maintains team morale and focus.

⚠️ Examiner Instructions — Not for Candidate

Play the assembled team — respond when roles are allocated. If candidate does NOT introduce themselves: "Could you tell us who you are and who is leading this?" If candidate allocates roles vaguely ("anaesthetist, you do the airway"): "What specifically would you like me to do now, before the patient arrives?" At 4 minutes: "The patient arrives. BP 80/50, HR 136, GCS 8. Paramedics are handing over — how do you receive the patient?" Expect candidate to maintain leadership, not abandon it to the paramedics. If candidate tries to personally cannulate: "You've left the foot of the bed to cannulate — who is maintaining situational awareness?" Key checkpoints: ATMIST briefing given? Roles allocated explicitly by name? MTP activated? RSI drugs and pelvic binder anticipated? Closed-loop communication demonstrated? Questions invited before arrival?

🔔 Examiner Cues ▼
  • If candidate doesn't activate MTP pre-emptively: "GCS 10, BP 90, unrestrained high-speed RTC with suspected femoral and abdominal injury — at what point would you activate the MTP?"
  • If candidate doesn't use closed-loop: "You've asked Nurse A to call the blood bank — how do you confirm she's received and understood that instruction?"
  • If candidate abandons foot-of-bed position to perform a procedure: "As team leader, what is the risk of you performing procedures during a trauma resuscitation?"
  • At 7 minutes: "FAST shows free fluid in Morrison's pouch. BP now 70/40 despite 2 units pRBC. What is your decision — CT or theatre?"
CriterionMarks
Briefing Structure
Self-introduced as team leader; ATMIST pre-alert information shared clearly with full team; mechanism, injuries, haemodynamic compromise, treatment en route all communicated3
All team members introduced and roles allocated explicitly by name — anaesthetic registrar (RSI/airway), Nurse A (IV/haemodynamic), Nurse B (exposure/monitoring), radiographer, scribe3
Anticipatory Preparation
MTP activated pre-emptively (GCS 10, BP 90, suspected haemorrhage from femur + abdomen); pelvic binder on standby; RSI drugs drawn up; thoracostomy kit available; warming protocol4
Trauma CT vs theatre decision framework explained — haemodynamically stable → CT; unstable → FAST then theatre; Level 1 infuser and blood products confirmed available2
Leadership and Communication
Closed-loop communication demonstrated — instructions given, read back confirmed; uses names not just roles; calm authoritative tone maintained3
Foot-of-bed position maintained throughout (situational awareness); does NOT personally perform procedures; questions invited before patient arrives; psychological safety maintained3
Manages patient arrival — receives ATMIST from paramedics, begins <C>ABCDE, directs team by name, does not lose control of briefing structure2
Total20
🎓 All 125 Stations Complete
You have completed the full ReviseMRCEM OSCE bank — covering every domain of the MRCEM Part C syllabus.
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