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Neuropathology of septic shock
Author(s) -
Gray F.,
Sharshar T.,
De La Grandmaison G. Lorin,
Annane D.
Publication year - 2002
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.1365-2990.2002.39286_30.x
Subject(s) - septic shock , medicine , encephalopathy , neuropathology , shock (circulatory) , sepsis , leukoencephalopathy , disseminated intravascular coagulation , pathology , cardiology , intensive care medicine , disease
Septic shock is the most frequent cause of death in intensive care units. It is often complicated by an encephalopathy and there is increasing evidence that central autonomic nervous system (CANS) dysfunction plays a crucial role in the onset and persistance of the haemodynamic failure. However, only a few neuropathological studies are available; they are always retrospective and often disagree. Material and methods: Twenty consecutive patient who died from septic shock were examined and compared with eight patients who died from nonseptic shock in the same unit and five ‘normal’ controls collected from the Forensic Medicine Service. Results and conclusion: A variety of lesions, including microabscesses, multifocal necrotizing leukoencephalopathy, haemorrhages and disseminated intravascular coagulation, were found, and were most probably related to the biological disturbances associated with sepsis. These lesions may contribute to the ‘septic encephalopathy’. Ischaemic changes in ‘susceptible’ areas were comparable in septic shock and in nonseptic shock. In contrast, ischaemic changes in the nuclei of the CANS were significantly more severe in septic shock than in nonseptic shock. Neuronal apoptosis in these nuclei was significantly more frequent and more severe in septic shock; apoptosis did not correlate exactly with neuronal ischaemia and was associated with only mild microglial activation suggesting that circulating factors may also play a role in its causation.