Septic Encephalopathy
Of in-patients with positive blood cultures, we found that over 70% had some evidence of brain dysfunction [1]. Forty-six percent of these were in the intensive care unit (ICU), with the rest on the wards. The encephalopathy associated with systemic infec
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I Introduction Of in-patients with positive blood cultures, we found that over 70% had some evidence of brain dysfunction [1]. Forty-six percent of these were in the intensive care unit (ICU), with the rest on the wards. The encephalopathy associated with systemic infections is a diffuse disturbance in cerebral function. Septic encephalopathy is a diagnosis of exclusion: there should be no clinical or laboratory evidence of direct central nervous system (CNS) infection (e.g., meningitis, macroscopic intracranial abscess or empyema), head trauma, fat embolism, adverse reactions to medications, sedative or paralyzing drug effects.
I Pathology and Pathophysiology In fatal cases, watershed brain infarctions from sustained hypotension are rarely encountered, however, the brain may show microscopic abnormalities [2]. Eight of 12 of our patients with post-mortem examinations had disseminated microabscesses. The cerebral cortex is the most commonly involved site, but deep structures and even the spinal cord may be affected. Other less common lesions include multiple microscopic infarctions, brain purpura, and central pontine myelinolysis [2]. Some cases may show no abnormality on gross or light microscopic examination. The mechanism of sepsis-associated encephalopathy is uncertain. In advanced cases it is likely multifactorial, given the variety of pathological findings. The early, fully reversible cases are not likely associated with structural change and are probably 'metabolic' in nature. Other mechanisms, in addition to the metabolic disturbances, operate in more advanced cases. The following mechanisms have been proposed:
Microvascular Disorder. The blood-brain barrier, which normally rigidly maintains a homeostatic environment for brain cells, becomes leaky in a dynamic, patchy manner within the first few hours of endotoxemia in experimental animals [3]. In addition the differential flux of chemicals across the blood-brain barrier is altered, e.g., in sepsis aromatic amino acids are more readily transported than branched chain amino acids from blood to brain. Reduced cerebral blood flow (CBF) and increased cerebrovascular resistance are found in human cases of septic encephalopathy; microthromboses may also occur. Most, if not all of these phenomena likely relate to the production of cytokines (tumor necrosis factor [TNF] and interleukins [IL]-l and -2) and their effects on endothelial nitric oxide (NO) synthase (eNOS) produc-
J.-L. Vincent (ed.), Yearbook of Intensive Care and Emergency Medicine 2002 © Springer-Verlag Berlin Heidelberg 2002
Septic Encephalopathy
tion. Inhibition of eNOS leads to impairment of the microcirculation of the brain and other organs by causing vasoconstriction [4]. Free radical production may also alter capillary permeability.
Free Radical-excitotoxic Injury. Endotoxin lipopolysaccharides (LPS) trigger increases in interferon (IFN)-y, inducible/inflammatory nitric oxide synthase (iNOS) in nonneuronal (glial and microglial) cells and reactive oxygen and nitrogen species [5]. In the f
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