Metabolic encephalopathy differential diagnosi

Suggested Alternatives for Differential Diagnosis Bartonellosis, brucellosis, other causes of encephalitis, coxsackieviruses, cryptococcosis, cysticercosis, cytomegalovirus, histoplasmosis, legionellosis, leptospirosis, listeria, lyme disease, malaria, rabies, tuberculosis, mumps, stroke, metabolic encephalopathy, Reye syndrome, Bartonella infection, Naegleria infection, Ebstein-Barr virus, prion disease, toxic ingestions, and AIDS. 

Delirium, toxic confusional state, metabolic encephalopathy or acute confusional state are terms that are used interchangeably and often loosely to describe a syndrome of acutely disordered cognition, sometimes associated with reduced level of consciousness and abnormal attention (see Table 32.1). The syndrome is very common, especially in the elderly and in patients with dementia, and presentations vary widely both in the speed of onset and severity (Siddiqi et al. 2006). The differential diagnosis is broad and includes almost any medical condition, but the commonest causes are sepsis, adverse drug reaction and metabolic derangement (Francis et al. 1990). 

Encephalopathy can occur in a number of extrahepatic diseases, such as toxic, metabolic or circulatory disorders, intracranial space-occupying lesions, hypothyroidism (35) and neurological/psychiatric diseases, (s. tab. 15.2) Identification of neuropsychiatric symptoms always calls for careful differential diagnosis. 

The fasting venous plasma ammonia concentration is useful in the differential diagnosis of encephalopathy when it is unclear if encephalopathy is of an hepatic origin. It is especially helpful in diagnosing Reye s syndrome and the inherited disorders of urea metabolism. However, it is not a useful test to use in patients with laiown liver disease. 

IV. Diagnosis is based on the history of exposure and typical findings of CNS depression and metabolic disturbances. The differential diagnosis is broad and in-oludes most CNS depressants. Encephalopathy and hyperammonemia may mimio Reye s syndrome. 

In its more severe forms thiamine deficiency can present as (1) wet beri-beri with generalized oedema 2md tendency to heart failure, (2) dry beri-beri, a chronic polyneuropathy with degenerative changes in the peripheral nerves, (3) infantile beri-beri, a chronic marasmic state also frequently associated with sudden heart failure, and (4) Wernicke s encephalopathy, which may be seen in chronic alcoholics and may be regarded as a cerebral beri-beri . Less severe states of thiamine deficiency usually manifest themselves as a chronic polyneuropathy. Problems of differential diagnosis from other forms of peripheral neuritis therefore arise, and it is in this connection that studies of pyruvate metabolism may be of help. 

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