Neurological complications in critically ill patients; septic encephalopathy, critical illness polyneuropathy
Septic encephalopathy and critical illness polyneuropathy are two syndromes, appearing at different stages in critically ill patients. Their aetiology is unclear, but many arguments seem to associate them with respiratory insufficiency in a context of systemic inflammatory response syndrome (S.I.R.S...
Saved in:
Published in | Acta clinica belgica (English ed. Online) Vol. 53; no. 2; p. 92 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
01.04.1998
|
Subjects | |
Online Access | Get more information |
Cover
Loading…
Summary: | Septic encephalopathy and critical illness polyneuropathy are two syndromes, appearing at different stages in critically ill patients. Their aetiology is unclear, but many arguments seem to associate them with respiratory insufficiency in a context of systemic inflammatory response syndrome (S.I.R.S.) and multiple organ dysfunction syndrome (M.O.D.S.). Septic encephalopathy appears early in the course of sepsis, diagnosis is based on clinical picture and electro-encephalogram. The exact pathogenesis is unclear. Prognosis is related to the underlying pathology, and treatment is supportive. Critical illness polyneuropathy is a predominantly motor axonal dysfunction, occurring in a setting of respiratory insufficiency, S.I.R.S., and M.O.D.S. A weaning problem often indicates the presence of critical illness polyneuropathy. Diagnosis is made on history, clinical picture and electromyographic studies. Indeed, motor and sensory conduction studies show a reduction of the amplitude of action potentials. In a later stage fibrillations and positive sharp waves emerge, with a further reduction of action potentials. Follow-up examinations reveal signs of axonal regeneration. The exact aetiology is unknown, but may be related to sepsis and M.O.D.S. Sepsis and M.O.D.S. are associated with the release of "mediator" substances, and somewhere in this cascade, there might be a toxin, influencing the nerve. A differential diagnosis with myopathy and neuromuscular transmission defects has to be made. Specific treatment is absent, and prognosis is related to the underlying pathology. |
---|---|
ISSN: | 1784-3286 |
DOI: | 10.1080/17843286.1998.11754149 |