Metabolic encephalopathy and metabolic coma

Margaret Yu MD (

Dr. Yu of Northwestern University, Chicago, has no relevant financial relationships to disclose.

)
Jinny O Tavee MD (

Dr. Tavee of Northwestern University Feinberg School of Medicine has no relevant financial relationships to disclose.

)
Douglas J Lanska MD FAAN MS MSPH, editor. (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

)
Originally released July 17, 2007; last updated January 7, 2020; expires January 7, 2023

Overview

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 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” (Glaser 1960; Wijdicks 2018). This was followed by Plum and Posner's classification of encephalopathy into 2 distinct subgroups: structural and toxic-metabolic, which was published in their monograph, The Diagnosis of Stupor and Coma (Plum and Posner 1966). 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 (Wijdicks 2018).

In this discussion we shall refer to those disorders 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 is due to multiple metabolic derangements rather than just one in isolation, reflecting the interaction among various organ systems.

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