Volume 7 Supplement 2
Early signs of critical illness polyneuropathy in porcine sepsis
© BioMed Central Ltd 2003
Published: 3 March 2003
Critical illness polyneuropathy is a well known complication of critical illness causing prolonged artificial ventilation, increased ICU and inhospital length of stay and higher mortality in critically ill patients. Although two studies reported early signs of polyneuropathy on day 2–5 after ICU admission, the exact time of onset of this complication is still unknown.
To investigate the electrophysiologic manifestations of critical illness polyneuropathy in a porcine model of sepsis during the first 24 hours after the septic insult.
Materials and methods
Seven anaesthetised, artificially ventilated and multicatheterized domestic pigs (body weight 29.7 ± 3.9 kg) were randomly subjected to either live E. coli IV infusion to induce sepsis (n = 4) or to a sham procedure (n = 3). Animals were fluid resuscitated with 20 ml/kg per hour of Ringer's lactated solution. Conduction studies (compound muscle action potential after supramaximal stimulation, latency and duration of the potential) of a motoric peripheral nerve (n. peronaeus) and needle electromyography (insertion activity, presence of positive sharp waves or fibrillations) of one of the corresponding muscles (m. tibialis longus) on the left pelvic extremity were recorded before, and 6, 18 and 24 hours after E. coli infusion. For statistical analysis, ANOVA for repeated measures and Fisher's LSD test were used.
No differences were present in latency and duration of the compound action muscle potential between septic and control animals. No changes in insertion activity and no signs of spontaneous muscle activity (presence of positive sharp waves or fibrillations) were found in either groups. Compound muscle action potentials (CMAP) were significantly reduced compared with baseline in septic animals starting from 6 hours (P < 0.01) after microbial infusion and further decreasing at 18 (P < 0.0001) and 24 hours (P < 0.00001). In control animals, there was significant decrease in CMAP at 24 hours (P < 0.05). The time course of CMAPs was significantly different between the groups (P < 0.04). Positive fluid balance was significantly higher in the septic group (P < 0.00001).
We detected a very early and significant decrease of compound muscle action potential in septic animals. This result may be caused by the changes in peripheral nerve or in the correspondent skeletal muscle analogic to either critical illness polyneuropathy or myopathy, although changes due to tissue edema can not be excluded. To our best knowledge, this is the first animal model of critical illness neuromuscular abnormalities.