title: Role of endotoxin in the pathogenesis of critical illness polyneuropathy.
abstract: Critical illness polyneuropathy (CIP) occurs in association with sepsis and multiple organ failure; however, little is known about the pathomechanisms of CIP and its therapy. In order to determine the parameters which interfere with development of CIP, electrophysiological investigations of peripheral nerves and biochemical measures were correlated to each other. The present study includes 20 consecutive patients in an intensive care unit developing severe sepsis or septic shock. Nerve conduction studies and electromyography were performed with occurring sepsis (day 1, 7, 14) and neurophysiological parameters were correlated with biochemical measures, especially indicators of infection and inflammation. It was found that all patients developed neurophysiological signs of axonal motor polyneuropathy. There was a significant correlation between serum concentrations of endotoxin and interleukin-2 receptors (IL2-R) and reduction of the amplitude of the compound motor action potentials. Other clinical and biochemical parameters showed no significant correlations with neurophysiological data. This finding apparently indicates that endotoxin damages nerve axons directly or indirectly, e.g. by activation of inflammatory cascades (IL2-R). Endotoxin appears to be an essential factor in the pathogenesis of CIP in sepsis, and therapeutic options neutralizing endotoxin may prevent development of CIP.
authors.affiliation: Department of Neurology, Medical School Hannover, Carl-Neuberg-Strasse 1, Hannover, Germany. Mohammadi.Bahram@mh-hannover.de
authors.forename: B
authors.initials: B
authors.lastname: Mohammadi
authors.forename: I
authors.initials: I
authors.lastname: Schedel
authors.forename: K
authors.initials: K
authors.lastname: Graf
authors.forename: A
authors.initials: A
authors.lastname: Teiwes
authors.forename: H
authors.initials: H
authors.lastname: Hecker
authors.forename: B
authors.initials: B
authors.lastname: Haameijer
authors.forename: D
authors.initials: D
authors.lastname: Scheinichen
authors.forename: S
authors.initials: S
authors.lastname: Piepenbrock
authors.forename: R
authors.initials: R
authors.lastname: Dengler
authors.forename: J
authors.initials: J
authors.lastname: Bufler
mesh_terms: D001369:Axons / Q000473:pathology; D016638:Critical Illness; D004558:Electric Stimulation; D004576:Electromyography; D004731:Endotoxins / Q000633:toxicity*; D006090:Gram-Negative Bacteria / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000473:pathology; D009046:Motor Neurons / Q000502:physiology; D009431:Neural Conduction / Q000502:physiology; D009460:Neurologic Examination; D009475:Neurons, Afferent / Q000502:physiology; D010525:Peripheral Nerves / Q000473:pathology; D011115:Polyneuropathies / Q000209:etiology* / Q000473:pathology; D015375:Receptors, Interleukin-2 / Q000187:drug effects / Q000378:metabolism; D018805:Sepsis / Q000150:complications*
chemical_list: D004731:Endotoxins; D015375:Receptors, Interleukin-2