Abstract

Metabolic Encephalopathy (ME) is a group of diseases with central nervous system dysfunction caused by a variety of etiologies. According to the etiology, it can be divided into Wernicker's encephalopathy (WE) caused by thiamine deficiency, hepatic encephalopathy (HE) caused by liver dysfunction and eventual ammonia poisoning in patients with cirrhosis, hyponatremic encephalopathy caused by plasma hypotonic due to low serum sodium, uremic encephalopathy (UE) caused by toxin accumulation after renal dysfunction, and dysglycemic encephalopathy caused by excessive blood glucose fluctuation. The pathophysiological mechanism of ME is not the same, but for the clinical symptoms, it all show different degrees of neuro-mental symptoms. The mild manifestations are indifference, irritability, time-space sensory disorders, thinking retardation, mental decline etc., and the serious manifestations are delirium, lethargy, coma. In patients with existing metabolic encephalopathy, treating the disease is not an easy task for every clinician, but prevention of metabolic encephalopathy may be much simpler and the return greater than treatment.

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