Brain dysfunction in critically ill patients--the intensive care unit and beyond

Abstract

Critical care physicians often find themselves prognosticating for their patients, attempting to predict patient survival as well as disability. In the case of neurologic injury, this can be especially difficult. A frequent cause of coma in the intensive care unit is resuscitation following cardiac arrest, for which mortality and severe neurologic disability remain high. Recent studies of the clinical examination, of serum markers such as neuron-specific enolase, and of somatosensory evoked potentials allow accurate and specific prediction of which comatose patients are likely to suffer a poor outcome. Using these tools, practitioners can confidently educate the family for the majority of patients who will die or remain comatose at 1 month. Delirium is a less dramatic form of neurologic injury but, when sought, is strikingly prevalent. In addition, delirium in the intensive care unit is associated with increased mortality and poorer functional recovery, prompting investigation into preventative and therapeutic strategies to counter delirium. Finally, neurologic damage may persist long after the patient's recovery from critical illness, as is the case for cognitive dysfunction detected months and years after critical illness. Psychiatric impairment including depression or post-traumatic stress disorder may also arise. Mechanisms contributing to each of these entities are reviewed.

Figure 1

Potential mechanisms contributing to intensive care unit-associated delirium [18,49,56]. ACh, acetylcholine; GABA, γ-aminobutyric acid; 5HT, serotonin.