CICM Second Part Exam Practice SAQs 27082026

a) Cardiorespiratory physiological effects (2 marks) 

Cardiac

• Acute rise in RV afterload from loss of ~50% pulmonary vascular bed
• Right-to-left shunt through a PFO — driven by raised RV filling pressures
• High incidence of atrial arrhythmias — atrial stretch/handling

Respiratory

• Pulmonary blood flow to remaining lung roughly doubled — raises PA/RV pressure and oedema risk
• Decreased diffusion capacity — reduced alveolar surface area
• Increased work of breathing and O2 consumption — reduced compliance of remaining lung

b) Six early complications (6 marks)

1. Cardiac herniation — through pericardial defect, surgical emergency
2. Post-pneumonectomy pulmonary oedema — non-cardiogenic, 4–15%, worse with fluid overload
3. Atrial arrhythmias — AF/flutter, typically day 2–3
4. Right-to-left shunt via PFO — due to raised right heart pressures
5. Surgical haemorrhage into pneumonectomy space — may be concealed, can be fatal
6. Bronchopleural stump rupture/fistula — more common right-sided, causes massive air leak
7. Chlyothorax
8. Recurrent laryngeal nerve injury

c) Post-operative fluid management strategy and rationale (2 marks)

• Rationale for restrictive approach
  • High risk of post-pneumonectomy pulmonary oedema. Carries high mortality.
    • Remaining lung takes full cardiac output. Reduced vascular reserve.
    • Lymphatics and capillary integrity disrupted by surgery.
  • Exception: active haemorrhage. Then prioritise resuscitation over restriction.
• Strategy
  • Restrictive fluid approach. Aim for euvolaemia, not fluid loading.
  • Limit total IV fluids. e.g. 15–20 mL/kg in first 24 hours.
  • Accept neutral-to-negative balance.
  • Treat hypotension with vasopressors. Avoid fluid boluses.
  • Accept lower urine output. 0.5 mL/kg/hr is acceptable. Don’t chase urine output with fluids.
  • Give blood products only for active bleeding/coagulopathy. Guide by clinical picture and point-of-care tests.

Pneumonectomy

a) Clinical features by phase (5 marks)

Incubation (10–14 days)

• Asymptomatic; viral dissemination via lymphoreticular system

Prodrome (2–4 days before rash)

• Fever, malaise, anorexia
• 3 C’s: cough, coryza, conjunctivitis
• Koplik spots — pathognomonic white/grey buccal mucosal spots, precede rash by 1–2 days
• Period of peak infectivity

Exanthem phase

• Erythematous maculopapular rash — begins face/hairline, spreads cephalocaudally to trunk/limbs over ~3 days
• Fever typically peaks with rash onset, may be high-grade
• Rash may become confluent

Convalescence

• Rash fades in order of appearance over 5–7 days, ± fine desquamation
• Fever resolves within days of rash; cough may persist longest
• Transient post-infectious immune suppression follows, predisposing to complications for weeks

b) Six ICU-level complications (3 marks) — any six:

1. Primary measles pneumonitis → ARDS
2. Secondary bacterial pneumonia
3. Secondary sepsis
4. Acute measles encephalitis (subacute sclerosing panencephalitis is rare and unlikely to need ICU)
5. Croup/laryngotracheobronchitis (and otitis media)
6. Myocarditis
7. Severe dehydration/ electrolyte derangement
8. Haemorrhagic (“black”) measles (extensive echymoses, DIC)
9. Hepatitis

c) Infection control strategy (2 marks)

• Airborne precautions immediately
  • AIIR (negative pressure), door closed
  • N95 (or higher) for all staff entering, regardless of immunity status
  • Mask patient for any transport
• Isolation
  • until 4 days post-rash onset (immunocompetent); duration of illness if immunocompromised
• Staff safety
  • Only immune staff to provide care where possible
  • Screen and manage exposed non-immune contacts (PEP: MMR <72h or IV IgG up to 7d )
  • Only immune staff to provide care where possible
• Notify infection control/public health — notifiable disease

Fever, Rash and a Vuvuzela

a) Mechanisms of antifungal resistance (3 marks)

Unlike C. albicans, C. auris commonly resistant (to azoles at least)

• Azole resistance — ERG11 mutations alter the drug target (14α-demethylase); upregulated efflux pumps reduce intracellular drug levels. Majority of isolates fluconazole-resistant (MIC ≥256 mg/L in ~90%).
• Echinocandin resistance — FKS1 mutations alter glucan synthase target. Less common than azole resistance but increasing.
• Amphotericin B resistance — mutations reducing membrane ergosterol content, impairing pore formation. Less predictable/well characterised.
• Multiple mechanisms can co-exist → pan-resistant isolates reported.

b) Immediate management priorities (5 marks)

Address life threats/ manage underlying condition

• Assess ABCs – risk of respiratory failure (e.g. hypoxaemia from pneumonia), shock (e.g. cardiogenic and/or septic shock)
• Exclude ongoing cardiac surgery complications

Source control

• Remove existing CVC promptly; site new line at a different location (biofilm formation on indwelling devices reduces effective antifungal penetration)

Antifungal therapy

• Empirical echinocandin (e.g. caspofungin or anidulafungin, standard loading then maintenance dose) — first-line given reliable fluconazole resistance; do not use azoles empirically
• Send isolate to confirm identification and for formal susceptibility testing
• Escalate to liposomal amphotericin B if echinocandin resistance demonstrated or clinical failure

Further workup

• Echocardiography (TOE) to exclude endocarditis
• Ophthalmology review — screen for endophthalmitis (haematogenous seeding)
• Assess for other sources/ removable foci (prosthetic material, other lines)

Supportive care and monitoring

• Repeat blood cultures to document clearance
• Treat for a minimum of 14 days from first negative culture
• Continue supportive ICU management of multi-organ dysfunction as per standard sepsis care

c) Infection control measures (2 marks)

Unlike C. albicans, C. auris is a transmissible environmental public health emergency in the ICU setting

• Contact precautions — single-room isolation, dedicated equipment where possible
• Enhanced environmental cleaning — standard disinfectants are inadequate; sporicidal agents required due to biofilm formation and organism resistance to routine cleaning
• Notification — C. auris is a notifiable condition; report to infection control/public health
• Contact screening — skin swabs of ward contacts to detect colonisation and prevent onward transmission