General Critical Care, Systemic Complications, and Neuroprognostication
General Critical Care, Systemic Complications, and Neuroprognostication
Neurocritical care patients die from systemic complications as often as from the brain injury. Manage oxygenation and ventilation, avoiding both hypoxia and hypercapnia; use lung-protective ventilation for ARDS. Treat sepsis promptly, but adjust antibiotic dosing for renal and hepatic function. Sodium disorders are common: correct hyponatremia slowly (typically no more than 8–10 mmol/L in 24 hours) to avoid osmotic demyelination; distinguish SIADH from cerebral salt wasting by volume status and urine sodium. Monitor glucose, potassium, and acid-base status. Provide VTE prophylaxis once bleeding risk allows, stress ulcer prophylaxis for high-risk patients, and early nutrition. Fever worsens brain injury-treat it.
Cardiac complications include neurogenic stunned myocardium and Takotsubo cardiomyopathy after SAH or TBI, with troponin elevation and reversible wall-motion abnormalities. Do not mistake this for acute coronary syndrome requiring aggressive anticoagulation.
Neuroprognostication after cardiac arrest requires multimodal assessment at least 72 hours after rewarming: clinical exam (pupillary and corneal reflexes, motor response), EEG, somatosensory evoked potentials (bilaterally absent N20), neuron-specific enolase, and imaging. Avoid early withdrawal based on a single test; confounders include sedation, hypothermia, metabolic derangement, and hypotension. Brain death determination requires a known cause, absence of brainstem reflexes, apnea testing, and exclusion of confounders.
Trap: declaring poor prognosis on day one or using one modality alone.
Rule of thumb: in a comatose post-arrest patient, combine at least two independent prognostic modalities before discussing withdrawal.