CICM Second Part Exam Practice SAQs 10092026

a) Differential diagnoses (2 marks)

WHIP:

• Withdrawal
  • GHB withdrawal (most likely — frequent dosing pattern)
  • alcohol withdrawal or BZD
• Wernicke’s encephalopathy
• Hypertensive crisis
• Hypoxia (e.g. fat embolism)
• Hypoglycaemia
• Intracranial event (e.g. occult TBI, ICH)
• Infection (septic encephalopathy, encephalitis)
• Poisoning/ overdose/ co-ingestion
• Porphyria – acute porphyric crisis

Also consider:

• Unmanaged pain
• Metabolic/electrolyte derangement
• Alcoholic ketoacidosis

b) Clinical features and time course (3 marks)

Time course

• More rapid onset than alcohol/benzodiazepine withdrawal — begins within hours of last dose
• Can last up to 2–3 weeks; severe cases may require up to 14 days inpatient treatment
• This patient’s 1–2 hourly dosing frequency is a specific risk factor for severe/delirious withdrawal (other risk factors: waking overnight to dose, high daily dose)

Clinical features

• Mild: anxiety, diaphoresis, restlessness, tremor, insomnia
• Severe: hallucinations, disorientation, paranoia, seizures, delirium, muscle rigidity
• Rare: hyperthermia, rhabdomyolysis, acute renal failure

c) Pharmacological management (5 marks)

• Risk stratification and initial approach: This patient’s very frequent dosing interval (1–2 hourly) places him at high risk of severe GHB withdrawal. Management should therefore be early and aggressive rather than reactive, with early discussion with a Clinical Toxicologist. The rationale is that under-treatment risks rapid progression to delirium and critical care admission.
• First-line therapy — simultaneous dual GABA-agonist loading: The mainstay of treatment is rapid, titrated loading with two GABA receptor agonists given concurrently in high risk situations such as this:
  • Diazepam: 20 mg orally hourly up to a total of 60 mg, then 10–20 mg orally 1-hourly PRN, titrated to a clinical endpoint of gentle sedation (not deep sedation)
  • Baclofen: 25 mg orally three times daily, started at the same time as the diazepam loading
  • Large and frequent doses are typically required in GHB withdrawal (much higher than typical alcohol withdrawal regimens), because severe GHB withdrawal is often relatively resistant to standard benzodiazepine dosing alone.
• Escalation pathway if refractory: If adequate sedation is not achieved despite this regimen (defined as >150 mg diazepam in 24 hours), escalate to barbiturate therapy in discussion with a Clinical Toxicologist:
  • IV phenobarbitone (if intubation is required): 5 mg/kg every 2 hours, to a maximum daily dose of 2 g
  • Oral phenobarbitone (if the patient does not require airway protection and step down from IV): 30 mg hourly, titrated to gentle sedation, to a maximum of 120 mg
  • Once controlled, wean phenobarbitone by approximately 50% of the total daily dose every 24 hours, tapering to cessation over 4–5 days, while concurrently weaning diazepam to <100 mg/day.
  • Propofol IV may also be used as concurrent sedation in intubated patients.
• Adjuncts and disposition:
  • Thiamine if concerned about hypoglycaemia, deficiency, malnutrition, or alcohol use 
  • Antipsychotics can be used as an adjunct to reduce neuropsychiatric symptoms and to help facilitate adequate dosing of diazepam and baclofen, but they are not a substitute for GABA receptor agonist therapy and should not be relied upon as primary treatment. 
  • Adequate analgesia for the fracture should be ensured, as pain may compound agitation. 
  • Patients at risk of severe withdrawal require inpatient admission; those with severe symptoms require HDU/ICU-level care.
  • Surgery may be delayed until the patient is stabilised..

a) Immediate approach to airway management and resuscitation (5 marks)

This presentation meets criteria for life-threatening haemoptysis (large volume, respiratory distress, hypoxaemia). The key life threat is asphyxiation from airway flooding (the adult airway holds only ~150 mL), not exsanguination — this framing should guide the answer.

• Assess airway adequacy:
  • The critical determinant is whether the patient can effectively cough and clear their own airway
  • Avoid intubation if possible if cough is effective and the patient can oxygenate/ventilate safely
  • Intubate with a large-bore ETT (≥8.0 mm, to allow subsequent therapeutic bronchoscopy) if: ineffective cough, severe respiratory distress, worsening respiratory failure, or to facilitate diagnostics/interventions (CT, bronchoscopy)
  • Anticipate a difficult laryngoscopy — blood will obscure the view; have large-bore suction ready and experienced airway operator present
• Oxygenation/ventilation:
  • High-flow oxygen given SpO₂ <90%
  • Escalate to intubation and mechanical ventilation if hypoxaemia/respiratory failure is severe or refractory
  • V-V ECMO as a rescue strategy if oxygenation/ventilation strategies fail
• Protect against aspiration/flooding of the contralateral lung:
  • Position bleeding side down (lateral decubitus) once the bleeding side is identified
  • If ventilation is compromised by airway flooding, consider lung isolation — selective mainstem intubation or a bronchial blocker (preferred over a double-lumen tube for ease of placement, more selective isolation, and lower risk of malposition/displacement)
• Circulatory resuscitation and correction of coagulopathy:
  • Large-bore IV access, group and crossmatch blood
  • Correct coagulopathy: target INR >1.5 reversed, platelets >50, fibrinogen >1.5, correct hypocalcaemia
  • Consider DDAVP if uraemic platelet dysfunction; reverse any anticoagulants/antiplatelets
  • Withhold chemical VTE thromboprophylaxis while actively bleeding
• Early escalation and diagnostics in parallel:
  • Bedside: ABG (hypoxaemia ± hypercapnia), ECG, glucose
  • Bloods: FBC, coagulation profile, group & crossmatch, U&E/LFTs
  • Early CT chest angiography once stabilised — superior to bronchoscopy for both localisation (70–88%) and identifying aetiology (86%); best performed early before ongoing bleeding obscures the source
  • Early multidisciplinary activation: anaesthetics/airway, respiratory, interventional radiology, thoracic surgery — coordinated team-based approach is emphasised given the rapidity with which this can deteriorate

b) Specific therapies to control ongoing haemorrhage (5 marks)

Note the pathophysiological rationale: in life-threatening haemoptysis the bleeding source is the bronchial circulation in ~90% of cases (systemic pressure, ~100 mmHg) rather than the low-pressure pulmonary arterial circulation, which underpins why bronchial artery embolisation is the definitive therapy.

• Bronchoscopy — first-line temporising therapy (1.5 marks):
  • Allows localisation and direct application of haemostatic measures; ideally performed awake/unintubated if feasible
  • Topical adrenaline (epinephrine): 1:10,000 (100 mcg/mL), instilled in 1–2 mL aliquots directly onto the bleeding segment, maximum total initial dose 6 mL (600 mcg), with continuous ECG and blood pressure monitoring
  • Balloon tamponade / bronchial blockers to isolate and compress the bleeding segment
  • Cold saline lavage (50 mL aliquots) — effectiveness uncertain
  • Endobronchial therapies: argon plasma coagulation, laser (avoid if FiO₂ >0.4), stents, glue, spigots
• Tranexamic acid (1 mark):
  • IV: 1 g every 8 hours
  • Nebulised: 500 mg 8–12 hourly (shown effective in an RCT of non-massive haemoptysis)
  • Endobronchial administration also described (500 mg in 15 mL saline)
• Bronchial artery embolisation (BAE) — first-line definitive therapy (1.5 marks):
  • Both diagnostic and therapeutic; performed via angiography
  • Success rate 70–99%, though less effective for large central masses fed by multiple vascular territories
  • Recurrence is common (9–57%), but repeat BAE can still be successful
  • Risk factors for recurrence include aspergilloma, tuberculosis, bronchiectasis, non-bronchial systemic collaterals, and bronchopulmonary shunting
  • Complications: chest pain (relatively common, 1.4–34%), rare spinal cord ischaemia (<5%)
• Surgery — selected cases (1 mark):
  • Indications: failed BAE, recurrent bleeding, localised disease amenable to resection (e.g. aspergilloma)
  • Carries significant mortality if performed emergently (~35–40%), markedly lower if elective — reflects why BAE remains first-line and surgery is reserved for failure/recurrence

a) Differential diagnosis for respiratory failure (4 marks)

The clinical context (APL, day 4 of ATRA, fever, hypotension, tachycardia, diffuse bilateral infiltrates, leucocytosis with rising WCC) should immediately raise differentiation syndrome as the leading diagnosis, but a broad differential must be considered given the profound pancytopenia/coagulopathy.

• Differentiation syndrome (ATRA/retinoic acid syndrome) — most likely diagnosis given classic timing (typically days 2–21, median ~day 11, but can occur earlier), fever, dyspnoea, diffuse pulmonary infiltrates, hypotension, and rising WCC as blasts differentiate
• Neutropenic sepsis / pneumonia — bacterial or fungal (e.g. invasive pulmonary aspergillosis), given functional neutropenia (blasts, not functional neutrophils), fever, tachycardia, hypotension
• Diffuse alveolar/pulmonary haemorrhage — driven by severe thrombocytopenia (22 ×10⁹/L) and coagulopathy (INR 3.2) in the context of APL-associated DIC/hyperfibrinolysis
• Leukostasis — pulmonary microvascular obstruction from circulating blasts (less classical in APL vs other AML subtypes, but relevant given visible blasts and high WCC)
• Transfusion-related lung injury (TRALI) or fluid overload (TACO) — if the patient has received blood products for his cytopenias
• ARDS secondary to sepsis or another precipitant
• Cardiogenic pulmonary oedema — including idarubicin-related cardiotoxicity

b) Major issues and management (6 marks)

Respiratory failure — likely differentiation syndrome

• Treat as a medical emergency: escalate respiratory support — high-flow oxygen/NIV, with a low threshold for intubation and mechanical ventilation if deteriorating (anticipate a difficult, high-risk intubation given coagulopathy/thrombocytopenia)
• Commence empirical high-dose corticosteroids (e.g. dexamethasone 10 mg IV BD) promptly on clinical suspicion — do not wait for confirmatory diagnosis, as early steroid treatment reduces mortality
• ATRA is generally continued unless life-threatening/severe differentiation syndrome, in discussion with haematology — abrupt cessation may worsen leukaemic proliferation; decision to hold should be individualised with the treating haematologist. Often stop other CTX.
• Judicious fluid management — capillary leak is part of the syndrome, so avoid aggressive fluid resuscitation where possible; use vasopressors if hypotensive rather than large volume boluses

Neutropenic sepsis (must be treated empirically in parallel)

• Blood cultures (peripheral ± central), septic screen, then prompt empirical broad-spectrum antibiotics per neutropenic sepsis protocol (e.g. piperacillin-tazobactam or local equivalent; +/- vancomycin) within the hour.
• Fungal and PJP prophylaxis (e.g. posaconazole, bactrim)
• Escalate/add antifungal cover if not responding or if high clinical suspicion (e.g. invasive aspergillosis)
• Source identification: CT chest; bronchoscopy/BAL only after correcting coagulopathy/thrombocytopenia given bleeding risk; remove infected lines

Coagulopathy / DIC (characteristic of APL) (1.5 marks)

• APL is classically associated with severe DIC and hyperfibrinolysis, compounded by chemotherapy-induced blast lysis
• Correct coagulopathy aggressively: FFP to correct INR, cryoprecipitate/fibrinogen concentrate to keep fibrinogen >1.5–2.0 g/L
• Platelet transfusion — higher threshold than standard ICU patients given active bleeding risk/DIC (e.g. keep platelets >30–50 ×10⁹/L, higher if active bleeding or invasive procedures planned)
• Daily coagulation profile monitoring (INR, fibrinogen, D-dimer) while DIC is active
• Consider tranexamic acid only with great caution/specialist guidance (risk of thrombosis in DIC — generally avoided unless clear hyperfibrinolysis-dominant picture and specialist advice)

Haemodynamic instability

• Likely multifactorial (sepsis, differentiation syndrome capillary leak, possible cardiotoxicity) — cautious fluid resuscitation, early vasopressor support, consider invasive monitoring (arterial line, possibly echocardiography to assess cardiac function given idarubicin exposure)

Other hematology issues: Anaemia and cytopenias, tumour lysis syndrome (0.5 marks)

• Red cell transfusion to maintain adequate oxygen-carrying capacity given Hb 88 and ongoing losses/haemolysis risk
• Irradiated, CMV-safe blood products per local leukaemia transfusion protocols
• Cytotoxic precautions as chemotherapy given
• Check and monitor electrolytes (K⁺, phosphate, calcium), uric acid, LDH, renal function
• Rasburicase/allopurinol and aggressive electrolyte correction as needed given high cell turnover

Multidisciplinary coordination and supportive care

• Early, ongoing discussion with haematology regarding ATRA/chemotherapy continuation, differentiation syndrome management, and overall goals of care given critical illness in the context of active leukaemia treatment
• Supportive care: FASTHUGSIN BED Please
• Family meetings and support