4.6 Review

Pathophysiology of septic encephalopathy: A review

Journal

CRITICAL CARE MEDICINE
Volume 28, Issue 8, Pages 3019-3024

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00003246-200008000-00057

Keywords

astrocytes; blood-brain barrier; brain edema; cerebrovascular circulation; inflammation; intensive care; leukocytes; neurons; sepsis; vascular endothelium

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Objectives: Encephalopathy is a common complication of sepsis. This review describes the different pathologic mechanisms that may be involved in its etiology. Data Sources: The studies described here were derived from the database PubMed (http:\\www.nlm.nih.gov) and from references identified in the bibliographies of pertinent articles and books. The citations are largely confined to English language articles between 1966 and 1998. Older publications were used if they were of historical significance. Study Selection: All investigations in which any aspect of septic encephalopathy was reported were included. This selection encompasses clinical, animal, and in vitro cell culture work. Data Extraction: The literature cited was published in peer-reviewed clinical or basic science journals or in books. Data Synthesis: Contradictions between the results of published studies are discussed. Conclusions: The most immediate and serious complication of septic encephalopathy is impaired consciousness, for which the patient may require ventilation. The etiology of septic encephalopathy involves reduced cerebral blood flow and oxygen extraction by the brain, cerebral edema, and disruption of the blood-brain barrier that may arise from the action of inflammatory mediators on the cerebrovascular endothelium, abnormal neurotransmitter composition of the reticular activating system, impaired astrocyte function, and neuronal degeneration. Currently, there is no treatment.

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