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  • Updated 04.22.2024
  • Released 07.17.2007
  • Expires For CME 04.22.2027

Metabolic encephalopathy and metabolic coma



Metabolic encephalopathy is a syndrome of global cerebral dysfunction that encompasses various clinical presentations ranging from mild executive dysfunction or agitated delirium to deep coma with decerebrate posturing. In this update, the most recent literature on the clinical manifestations, diagnostic evaluation, and management of metabolic encephalopathy are reviewed. This includes new insights into underlying mechanisms and key features of the diagnostic evaluation that can help point toward specific etiologies.

Key points

• The initial phase of impairment of consciousness with metabolic encephalopathies is often delirium, with impairment of attention and fluctuations in alertness, clouding of consciousness, disturbances in the wake-sleep cycle, and, sometimes, agitation and restlessness.

• The anatomic basis for metabolic encephalopathy and metabolic coma relates to diffuse, bilateral cortical dysfunction.

• In conscious patients with metabolic encephalopathies, cognitive function typically fluctuates considerably, in contrast to dementia.

• Specific neurologic symptoms, imaging, and EEG patterns may be seen with certain causes of metabolic encephalopathy.

• Treatment should focus on correcting the underlying etiology, supportive reorientation, and avoidance of sedating medications if possible.

Historical note and terminology

The origin of the term “metabolic encephalopathy” has been attributed to Glaser, who in 1960 described its clinical manifestations in the setting of renal, pulmonary, and hepatic disorders as “acute and chronic disturbances of intellectual performance and motor and sensory activities ranging from mild confusional states to coma” (25; 78). This was followed by Plum and Posner’s classification of encephalopathy into two distinct subgroups: structural and toxic-metabolic, which was published in their monograph, The Diagnosis of Stupor and Coma (57). In clinical practice today, the term metabolic encephalopathy typically refers to global cerebral dysfunction that occurs in the absence of a CNS structural lesion and manifests as delirium or in more severe cases, coma (78).

In this discussion we refer to the “metabolic” conditions as those due to organ dysfunction, nutritional deficiencies, electrolyte imbalances, hypoglycemia, hyperglycemia, endocrine disorders, medications, and systemic sepsis; the following are excluded: metabolic encephalopathies due to inborn errors of metabolism, cardiac arrest and anoxic-ischemic encephalopathy, direct CNS infections, exogenous toxins (including recreational drugs, alcohol, and poisons), hematological conditions, immune-mediated CNS diseases, and direct and indirect effects of cancer on the nervous system.

Of note, metabolic encephalopathy is often due to multiple metabolic derangements rather than just one in isolation, reflecting the interaction among various organ systems. The term “acute encephalopathy” has been recommended by a consensus panel to describe a pathobiological process that develops in less than 4 weeks. Clinically, this may be manifested as (1) subsyndromal delirium (acute cognitive changes compatible with delirium but do not fulfill all DSM-5 delirium criteria), (2) delirium, or (3) coma, and can have additional features like seizures or extrapyramidal signs (68).

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