Metabolic Encephalopathy - Part I

Abstract

Encephalopathy can range from the acute confusional state to frank coma, and is broadly defined as a constellation of symptoms and signs reflecting diffuse cerebral dysfunction. The potential causes of encephalopathy are vast requiring a thorough initial assessment and systematic diagnostic approach. Obtaining a comprehensive history may be challenging and ancillary sources of information are often helpful in narrowing the differential diagnosis. The general examination may provide hints as to the cause of encephalopathy and the neurologic examination can guide both acute management and focus the diagnostic investigations on specific etiologies which fit the clinical presentation. The systemic manifestations of infection and toxic exposures are common causes of encephalopathy. In sepsis, not only is brain perfusion compromised, multi system dysfunction is common and additional factors related to the specific infection such as hypoxia in pneumonia or secondary CNS involvement can complicate management. An understanding of the common physical examination findings of toxic exposures can aid in the diagnosis and rapid treatment of reversible toxic encephalopathies such as narcotics, benzodiazepines or environmental toxins. Cardiopulmonary dysfunction can lead to hypoxic-ischemic encephalopathy and advances in critical care, and particularly targeted temperature management following cardiac arrest, have improved the neurologic outcome in these patients. This review contains 2 figures, 3 tables, and 25 references. Key words: encephalopathy, delirium, ascending reticular activating system, acute confusional state, subclinical seizures, Glasgow Coma Scale, Full Outline of Unresponsiveness (FOUR) Score , hypoxic-ischemic encephalopathy, neuroleptic malignant syndrome, serum neuron-specific enolase