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Acute toxic-metabolic encephalopathy in adults

INTRODUCTION

Confusion is clinically defined as the inability to maintain a coherent stream of thought or action. Delirium is a confusional state with superimposed hyperactivity of the sympathetic limb of the autonomic nervous system with consequent signs including tremor, tachycardia, diaphoresis, and mydriasis. Acute toxic-metabolic encephalopathy (TME), which encompasses delirium and the acute confusional state, is an acute condition of global cerebral dysfunction in the absence of primary structural brain disease [1]. An overview of TME in hospitalized patients will be discussed here; a diagnostic approach to delirium is presented separately. (See "Diagnosis of delirium and confusional states".)

TME is common among critically ill patients. Furthermore, TME is probably under recognized and undertreated, especially when it occurs in patients who require mechanical ventilation [2-4]. TME is usually a consequence of systemic illness, and the causes of TME are diverse. Most TME is reversible, making prompt recognition and treatment important. Certain metabolic encephalopathies, including those caused by sustained hypoglycemia and thiamine deficiency (Wernicke's encephalopathy), may result in permanent structural brain damage if untreated. Alcohol withdrawal syndromes must be excluded in patients with suspected TME. (See "Management of moderate and severe alcohol withdrawal syndromes".)

PATHOPHYSIOLOGY

Normal neuronal activity requires a balanced environment of electrolytes, water, amino acids, excitatory and inhibitory neurotransmitters, and metabolic substrates [5]. In addition, normal blood flow, normal temperature, normal osmolality, and physiologic pH are required for optimal central nervous system function [6]. Complex systems, including those mediating arousal and awareness and those involved in higher cognitive functions, are more likely to malfunction when the local milieu is deranged [5-7].

All forms of acute toxic-metabolic encephalopathy (TME) interfere with the function of the ascending reticular activating system and/or its projections to the cerebral cortex, leading to impairment of arousal and/or awareness [6]. Ultimately, the neurophysiologic mechanisms of TME include interruption of polysynaptic pathways and altered excitatory-inhibitory amino acid balance [8,9]. The pathophysiology of TME varies according to the underlying etiology:

Cerebral edema contributes to acute fulminant hepatic encephalopathy and to hypo-osmolar encephalopathies [7].

                          

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Literature review current through: Aug 2014. | This topic last updated: Aug 9, 2013.
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