Acute toxic-metabolic encephalopathy in children

INTRODUCTION

Acute toxic-metabolic encephalopathy (TME) is a condition of acute global cerebral dysfunction manifested by altered consciousness, behavior changes, and/or seizures in the absence of primary structural brain disease or direct central nervous system (CNS) infection. The causes of TME are diverse (table 1). The presentation of this condition in the infant or child may be subtle and not easily recognized. Because TME often is reversible and interruption of neuronal activity in the developing brain can have a long-lasting effect, prompt recognition and treatment are important.

An overview of the causes, clinical features, and an approach to the diagnostic evaluation and management of TME in children will be reviewed here. Neonatal encephalopathy is discussed separately. (See "Clinical features, diagnosis, and treatment of neonatal encephalopathy" and "Etiology and pathogenesis of neonatal encephalopathy".)

DEFINITION

Acute TME is a broad term used to describe a condition of acute global cerebral dysfunction manifested by altered consciousness, behavior changes, and/or seizures occurring as a consequence of systemic disorders or exposures. The term is not used to describe cerebral dysfunction due to primary brain disease, including structural pathology (eg, tumor, hemorrhage, hydrocephalus), central nervous system (CNS) infection (eg, meningitis, encephalitis), or immune-mediated inflammation (eg, autoimmune encephalitis, acute disseminated encephalomyelitis) [1]. All forms of TME interfere with the function of the ascending reticular activating system and/or its projections to the cerebral cortex, thus leading to impairment of arousal and/or awareness, and/or seizures [2].

PATHOPHYSIOLOGY

Normal neuronal activity requires a balanced environment of electrolytes, water, amino acids, excitatory and inhibitory neurotransmitters, and metabolic substrates [3]. In addition, normal blood flow, normal temperature, normal osmolality, and physiologic pH are required for optimal brain function [2]. Complex systems, such as those mediating arousal and awareness and those involved in higher cognitive functions, are more likely to malfunction when the local milieu is deranged [2-4].

Despite a wide array of pathophysiologic mechanisms (table 1), the clinical manifestations of acute TME tend to be very similar because of a common final mechanism: interruption of polysynaptic pathways and altered excitatory-inhibitory amino acid balance and cerebral edema [5-8]. (See 'Specific etiologies of encephalopathy' below.)

Literature review current through: Jul 2021. | This topic last updated: Apr 09, 2021.

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