Intensive Care Medicine Flashcards

A 58-year-old patient with ARDS on lung-protective ventilation (VT 6 mL/kg IBW, PEEP 14 cmH2O, FiO2 0.7) has a PaO2/FiO2 ratio of 68 mmHg despite prone positioning for 20 hours. The driving pressure is 18 cmH2O and plateau pressure is 32 cmH2O. Which intervention has the strongest evidence for improving 90-day mortality in this clinical scenario?

Answer: Initiate venovenous ECMO

The EOLIA trial demonstrated that VV-ECMO can be used as rescue therapy in severe ARDS (P/F < 80 mmHg despite optimized conventional ventilation including prone positioning). While EOLIA did not reach statistical significance for its primary endpoint, subsequent Bayesian analysis and the crossover-adjusted analysis strongly support mortality benefit. Inhaled nitric oxide improves oxygenation but has not demonstrated mortality benefit. Recruitment maneuvers (sustained inflation technique) were associated with harm in the ART trial. Increasing plateau pressure beyond 30 cmH2O violates lung-protective ventilation principles and worsens VILI.

A patient on day 7 of ICU admission for septic shock develops new thrombocytopenia (platelets 48,000/μL, down from 220,000/μL on admission). She is receiving unfractionated heparin infusion for DVT prophylaxis and has a suspected DVT in her left leg. The 4T score is calculated as 6 points. Which of the following is the MOST appropriate next step in anticoagulation management?

Answer: Switch to argatroban with dose adjusted to achieve aPTT 1.5–3× normal

A 4T score of 6 represents high probability of heparin-induced thrombocytopenia (HIT). All heparin products, including LMWH, must be immediately discontinued as LMWH has >90% cross-reactivity with HIT antibodies. Fondaparinux is not approved for treatment of HIT-associated thrombosis and has insufficient evidence in this setting. Argatroban is a direct thrombin inhibitor approved for HIT treatment that does not cross-react with HIT antibodies; it is particularly favored in patients with renal impairment. Bivalirudin is an alternative. Dose reduction of heparin is never appropriate when HIT is suspected — cessation is mandatory.

During management of refractory status epilepticus in a 34-year-old, continuous EEG monitoring shows a burst-suppression pattern after pentobarbital coma induction. On day 3 of barbiturate coma, the patient develops hypotension requiring norepinephrine 0.4 μg/kg/min and a new fever of 39.2°C. Serum lactate is 4.8 mmol/L. Which diagnosis must be immediately excluded as the MOST life-threatening complication of current therapy?

Answer: Pentobarbital-induced adrenal insufficiency

Prolonged high-dose barbiturate (pentobarbital) therapy for refractory status epilepticus causes suppression of the hypothalamic-pituitary-adrenal axis, leading to relative or absolute adrenal insufficiency. This presents with refractory hypotension, fever, and elevated lactate — a potentially fatal combination. A random cortisol level and empirical hydrocortisone supplementation should be initiated immediately. Propofol infusion syndrome is not applicable here as the patient is on pentobarbital. VAP is possible but would not cause such acute hemodynamic collapse on this timeline without other signs. Phenobarbital is a different compound and metabolic conversion to it from pentobarbital in clinically significant amounts does not occur.

A 67-year-old patient with Child-Pugh C cirrhosis is admitted to the ICU for hepatic encephalopathy grade III and an acute kidney injury (creatinine 3.2 mg/dL, baseline 0.9 mg/dL). Urinalysis shows no casts, urine sodium is 6 mEq/L, and FENa is 0.3%. He has received 1.5 L of albumin over 48 hours with no improvement in creatinine. Which pharmacological treatment, if initiated within this timeframe, has the strongest evidence for improving 90-day transplant-free survival in this condition?

Answer: Terlipressin combined with continued albumin infusion

This presentation is consistent with hepatorenal syndrome type 1 (HRS-AKI). The CONFIRM trial (2021) demonstrated that terlipressin (a vasopressin analogue) combined with albumin significantly improved verified HRS reversal and 90-day transplant-free survival compared to placebo plus albumin. Terlipressin is now the preferred first-line vasopressor for HRS-AKI based on highest-quality RCT evidence. Norepinephrine + octreotide + midodrine (the 'triple therapy') has supporting evidence but weaker trial data compared to terlipressin. N-acetylcysteine has no established role in HRS. Rifaximin addresses encephalopathy, not renal vasoconstriction.

A 72-year-old post-cardiac arrest patient (ROSC achieved after 22 minutes of CPR) undergoes targeted temperature management at 36°C. On day 3, with sedation discontinued, the patient has absent pupillary light reflexes bilaterally, absent corneal reflexes bilaterally, and a GCS motor score of 1. EEG shows a burst-suppression pattern with identical bursts (20% suppression ratio). Which prognostication finding would provide the HIGHEST specificity (closest to 100%) for poor neurological outcome in this patient?

Answer: Bilaterally absent N20 cortical responses on median nerve SSEP

Bilaterally absent N20 SSEP responses at ≥24 hours post-arrest have a false positive rate (FPR) approaching 0% (specificity ~100%) for poor neurological outcome and are recommended as a major prognosticator by ERC/ESICM 2021 guidelines. This finding indicates complete disruption of thalamocortical pathways. NSE >60 μg/L at 72 hours is a strong predictor but has a higher false positive rate (~5%) due to hemolysis and other confounders. MRI ADC mapping is increasingly useful but depends on protocol and timing; it has not achieved the near-zero FPR of SSEP. EEG reactivity absence has specificity of ~85–90% but not approaching 100%. SSEP N20 absence is the gold standard for high-specificity prognostication.

A 55-year-old patient with known Type 2 diabetes is admitted to the ICU with septic shock secondary to necrotizing fasciitis. Despite adequate fluid resuscitation, MAP remains 58 mmHg on norepinephrine 0.35 μg/kg/min. Vasopressin 0.03 units/min is added. Cortisol stimulation testing reveals a delta cortisol of 4 μg/dL after 250 μg ACTH. The intensivist initiates hydrocortisone 200 mg/day by continuous infusion. Four hours later, the nurse notes capillary glucose of 18.2 mmol/L (328 mg/dL). What is the MOST physiologically accurate explanation for this glucose elevation in this specific context?

Answer: Hydrocortisone induces hepatic gluconeogenesis and peripheral insulin resistance, compounded by counter-regulatory catecholamine effects and impaired insulin secretion due to vasopressin-mediated V1b receptor inhibition on pancreatic beta cells

Hydrocortisone causes hyperglycemia through multiple mechanisms: it stimulates hepatic gluconeogenesis and glycogenolysis, promotes peripheral insulin resistance by reducing GLUT-4 expression and post-receptor signaling, and enhances the hyperglycemic effects of catecholamines. Additionally, vasopressin acts on V1b (V3) receptors on pancreatic beta cells to inhibit glucose-stimulated insulin secretion, contributing to reduced endogenous insulin response. This multi-mechanism explanation is the most complete. Vasopressin acts via V1b not V2 in the pancreas; V2 receptors are renal and mediate water retention, not glycogenolysis. Alpha-1 receptor activation by norepinephrine does cause some glucose elevation but GLUT-4 inhibition is not the primary mechanism cited. Hydrocortisone does not cause acute beta-cell apoptosis within hours.