Toxic metabolic encephalopathies (TMEs) present as an acute derangement in consciousness, cognition and behavior, and can be brought about by various triggers, including endocrine and metabolic disturbances, exogenous toxins, pain and infection. Also referred to as "delirium" or "acute confusional states," TMEs are characterized by (1) an altered level of consciousness and activity, (2) global changes in cognition with inattention, (3) a fluctuating course with disturbances in the sleep-wake cycle, and (4) asterixis and myoclonus. The pathophysiology of this syndrome is poorly understood. Imbalanced neurotransmitter signaling and pathologically heightened brain inflammatory cytokine signaling have been proposed as candidate mechanisms. Focal brain lesions can also occasionally mimic TMEs. A neurological examination is required to identify the presence of focal findings, which when present, identify a new focal lesion or the recrudescence of prior ischemic, inflammatory or neoplastic insults. Diagnostic testing must include a search for metabolic and infectious derangements. Offending medications should be withdrawn. Magnetic resonance imaging, cerebrospinal fluid analysis and electroencephalography should be considered in select clinical situations. In addition to being an unpleasant experience for the patient and family, this condition is associated with extended hospital stays, increased mortality and high costs. In individuals with diminished cognitive reserve, episodes of TME lead to an accelerated decline in cognitive functioning. Starting with an illustrative case, this paper provides a neurologist's approach to the diagnosis, differential diagnosis and management of toxic metabolic encephalopathies.
Keywords: Confusion; Confusional state; Delirium; Encephalopathy; Metabolic encephalopathy.
Copyright © 2013 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.