Metabolic encephalopathy and metabolic coma

Katharina M Busl MD MS (Dr. Young of the University of Florida, Gainesville has no relevant financial relationships to disclose.)
Christopher Robinson DO MS (Dr. Robinson of University of Florida, Gainesville, has no relevant financial relationships to disclose.)
Originally released July 17, 2007; last updated November 27, 2017; expires November 27, 2020


In this article, the authors discuss the commonly encountered clinical scenarios associated with metabolic encephalopathy and metabolic coma. We discuss the anatomical considerations, differential diagnoses, and pertinent objective data relative to encephalopathy in an attempt to better educate the examiner and improve patient care. In this article, an update of the most recent literature and attempt to include localization as a means of diagnostic certainty is provided.

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.


• Motor findings that are strongly suggestive of a metabolic or toxic encephalopathy include postural-action tremor, asterixis, and multifocal myoclonus.


• In comatose patients with metabolic or diffuse or bihemispheric disturbances in cerebral function, the pupillary reactions are typically spared, even if other cranial nerve reflexes are lost and the patient is exhibiting decerebrate or decorticate posturing.


• Respiratory patterns, along with blood gas (acid-base balance) testing can narrow the differential diagnosis considerably.

Historical note and terminology

The term “metabolic encephalopathy” was coined by Kinnier Wilson in 1912 to describe a clinical state due to various causes in which the brain's integrated activity is impaired in the absence of structural abnormalities. Metabolic encephalopathy is, thus, not a diagnosis but a syndrome of global cerebral dysfunction induced by systemic stress, and can vary in clinical presentation from mild executive dysfunction or agitated delirium, to deep coma with decerebrate posturing. There are also some differences in presentation depending on the metabolic disorder at hand.

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

It should be understood that various metabolic disorders causing encephalopathy are combined, rather than occur in isolation, especially in critically ill patients. This reflects the interaction among various organ systems, causing multiple metabolic derangements.

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