Intensive Care Medicine Flashcards

A 58-year-old patient with septic shock is on noradrenaline 0.4 mcg/kg/min and vasopressin 0.03 units/min. Despite adequate fluid resuscitation, MAP remains 58 mmHg. Echocardiography shows a hyperdynamic left ventricle with LVEF 65% and a dilated, poorly contracting right ventricle. Which intervention is most appropriate?

Answer: Add inhaled nitric oxide and consider milrinone

The echocardiogram reveals acute cor pulmonale with RV dilation and dysfunction — a common but underrecognised pattern in septic shock, especially with ARDS-associated pulmonary hypertension. The LV is hyperdynamic, so inotropes targeting the LV (dobutamine) risk worsening RV afterload or causing hypotension. Increasing noradrenaline may further increase pulmonary vascular resistance. Fluid bolus is inappropriate with RV dilation. Inhaled nitric oxide selectively reduces pulmonary vascular resistance without systemic hypotension, and milrinone adds RV inotropy while also causing pulmonary vasodilation — the correct combined approach for RV failure in this context.

A 72-year-old patient develops refractory status epilepticus (RSE) in the ICU. After failure of two benzodiazepines and levetiracetam, they are intubated and started on propofol infusion 4 mg/kg/h. After 48 hours, the nurse reports new-onset metabolic acidosis (pH 7.18, lactate 6.2 mmol/L), elevated triglycerides 9.8 mmol/L, and dark urine. Which diagnosis must be immediately considered?

Answer: Propofol infusion syndrome

Propofol infusion syndrome (PRIS) is characterised by metabolic acidosis, rhabdomyolysis (dark urine = myoglobinuria), hypertriglyceridaemia, cardiac dysfunction, and renal failure. It is triggered by high-dose propofol (>4 mg/kg/h) for >48 hours, especially in the context of high catecholamines, corticosteroids, and carbohydrate deficiency — all present in RSE management. The mechanism involves impaired mitochondrial respiratory chain function. Immediate cessation of propofol and transition to an alternative sedative/anaesthetic agent is mandatory. PRIS can be fatal if not recognised early.

A 45-year-old with severe ARDS (P/F ratio 68) is on lung-protective ventilation (Vt 6 mL/kg IBW, PEEP 16 cmH₂O, FiO₂ 0.85) and prone positioning for 18 hours/day. Despite this, driving pressure remains 22 cmH₂O. Oesophageal manometry reveals end-expiratory oesophageal pressure of +12 cmH₂O. What is the most appropriate next step?

Answer: Increase PEEP guided by transpulmonary pressure targeting positive end-expiratory transpulmonary pressure

Oesophageal pressure is a surrogate for pleural pressure. An end-expiratory oesophageal pressure of +12 cmH₂O indicates high chest wall elastance (obesity, abdominal hypertension, etc.), meaning current PEEP may be insufficient to keep alveoli open despite appearing high by airway pressure. Transpulmonary pressure (Ptp = airway pressure − pleural pressure) at end-expiration = 16 − 12 = +4 cmH₂O, which is acceptable, but optimising Ptp by titrating PEEP to achieve a slightly positive end-expiratory Ptp (0–5 cmH₂O) is the physiologically correct approach. ECMO is premature when physiology-guided ventilation strategies haven't been exhausted. Reducing PEEP would worsen alveolar collapse. Recruitment manoeuvres with fixed inflation carry haemodynamic risk and the 40/40 method is no longer preferred in modern ARDS guidelines.

A patient with known cirrhosis is admitted with acute-on-chronic liver failure (ACLF) grade 3, hepatic encephalopathy grade III, and AKI stage 2. Urine sodium is <10 mmol/L, urine osmolality 520 mOsm/kg, no response to 2 days of albumin 1 g/kg and cessation of diuretics. Creatinine rises from 180 to 290 µmol/L. Which treatment has the strongest evidence to bridge to liver transplantation?

Answer: Terlipressin plus albumin

This presentation is consistent with hepatorenal syndrome type 1 (HRS-AKI). Terlipressin, a vasopressin analogue causing splanchnic vasoconstriction, combined with albumin (to expand effective circulatory volume) has the highest level of evidence (multiple RCTs and meta-analyses, FDA approval in 2022) for reversal of HRS-AKI. Noradrenaline is an alternative in ICU settings where terlipressin is unavailable (especially in the USA prior to approval), but has less robust RCT data. Midodrine plus octreotide is a less effective outpatient regimen. TIPS improves portal hypertension but is contraindicated in advanced HE and ACLF grade 3 due to high risk of further decompensation and mortality.

During management of a patient with severe TBI (GCS 6, CT showing diffuse axonal injury), ICP is consistently 28 mmHg despite head positioning, sedation, osmotherapy with mannitol, and normoventilation (PaCO₂ 35–38 mmHg). CPP is 62 mmHg. You are considering decompressive craniectomy versus barbiturate coma. Which statement best reflects current evidence regarding these two options?

Answer: Decompressive craniectomy reduces ICP effectively but the DECRA and RESCUEicp trials showed conflicting results regarding functional outcomes, with RESCUEicp showing survival benefit but more survivors with severe disability

The DECRA trial (2011) showed that early bifrontal decompressive craniectomy reduced ICP and ICU stay but was associated with worse functional outcomes at 6 months. The RESCUEicp trial (2016) evaluated craniectomy as a last-tier therapy and found a significant reduction in mortality (26.9% vs 48.9% at 6 months), but more survivors were left with severe disability or vegetative state. This nuance — reduced mortality but at a cost of increased disability — is the defining tension in TBI decompression decisions. Barbiturate coma has evidence for ICP reduction (Pentobarbital) but no proven neurological outcome benefit and carries significant risks (immunosuppression, cardiovascular depression). Decompressive craniectomy is not contraindicated in diffuse injury.

A 34-year-old woman is admitted to ICU 5 days postpartum with severe headache, blurred vision, BP 168/112 mmHg, and new-onset confusion. MRI shows bilateral posterior white matter T2 hyperintensities. Platelet count is 88,000/µL, LDH 940 U/L, total bilirubin 42 µmol/L, and haptoglobin is undetectable. Creatinine is 1.9 mg/dL. Which condition is the MOST LIKELY primary diagnosis, and which additional test most critically differentiates it from thrombotic thrombocytopaenic purpura (TTP)?

Answer: HELLP syndrome with superimposed PRES; ADAMTS13 activity level to exclude TTP

This patient has postpartum HELLP syndrome (haemolysis, elevated liver enzymes, low platelets) with concurrent posterior reversible encephalopathy syndrome (PRES) — a recognised neurological complication of severe hypertension in HELLP/eclampsia. The clinical overlap with TTP is dangerous: both cause microangiopathic haemolytic anaemia (MAHA), thrombocytopenia, and neurological symptoms. The critical differentiator is ADAMTS13 activity: TTP typically shows severely reduced ADAMTS13 activity (<10%), while HELLP has normal or mildly reduced levels. This distinction is clinically vital because TTP requires urgent plasma exchange, whereas HELLP is managed with magnesium, antihypertensives, and delivery (already delivered here, so supportive care continues). A peripheral smear showing schistocytes alone cannot differentiate the two. Gadolinium MRI confirms PRES but doesn't differentiate from TTP.