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British Journal of Anaesthesia, 2000, Vol. 84, No. 5 688-689
© 2000 The Board of Management and Trustees of the British Journal of Anaesthesia


Abstract

Early detection of the covert onset and evolution of critical illness polyneuromyopathy

D. D. Kennedy1, S. N. Fletcher1, I. R. Ghosh1, C. J. Hinds1 and J. H. Coakley1

1 Intensive Care Units, St Bartholomews Hospital, West Smithfield, London EC1A 7BE, and Homerton Hospital, London E9 6SR, UK

Abstract

Introduction: Critical illness polyneuropathy was first identified by Bolton and colleagues1 and weakness due to neuropathic and/or myopathic abnormalities is now recognized as a common complication of prolonged critical illness.2 The presence of abnormally low compound motor action potentials (CMAPs) is considered an important diagnostic criterion. The onset and evolution of this condition following intensive care unit admission has not previously been systematically investigated.

Methods: A prospective, sequential study of all patients thought likely to require intensive care for 7 days or more was performed over a 12-month period. Admission APACHE II score, daily organ failure score, presence of sepsis, ventilation mode and routine haematology and biochemistry results were recorded. A daily neurological examination and weekly neurophysiological studies were performed for the duration of the patients’ ICU stay. The neurophysiological studies included CMAPs, nerve conduction velocities, sensory action potential amplitudes and electromyography. The Spearman correlation coefficient was used to analyse associations between the recorded physiological data and serial CMAPs. In our institution the lower limits of normal for ulnar and common peroneal nerve CMAPs are 2.5 and 2.8 mV respectively.

Results: Thirty-two patients were recruited to the study, of whom 23 survived for 7 days or longer. One patient was withdrawn at a relative’s request and two patients continued to receive muscle relaxants until death. The median age was 61 yr (range 33–80) and median admission APACHE II score was 20 (9–33). A significant positive correlation was found between serum albumin and CMAPs (P<0.05). CMAPs of one patient are shown in Fig 3. Thirteen patients had three or more sets of neurophysiological studies. CMAPs were found to be low or fell during episodes of sepsis, at a time when it was not possible to detect weakness clinically, and CMAPs recovered as sepsis subsided. Of the eight patients who survived, six had severe clinical weakness of MRC grade 3 or less.

Conclusions: The onset of critical illness motor syndrome may precede by days or weeks clinically detectable weakness, seems to be associated with episodes of sepsis and can occur within days of the onset of sepsis. Recovery in CMAPs may be equally rapid as sepsis subsides.


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