Abstract
Critical illness polyneuropathy (CIP) and myopathy (CIM) are major complications of severe critical illness and its management. CIP/CIM prolongs weaning from mechanical ventilation and physical rehabilitation since both limb and respiratory muscles can be affected. Among many risk factors implicated, sepsis, systemic inflammatory response syndrome, and multiple organ failure appear to play a crucial role in CIP/CIM. This review focuses on epidemiology, diagnostic challenges, the current understanding of pathophysiology, risk factors, important clinical consequences, and potential interventions to reduce the incidence of CIP/CIM. CIP/CIM is associated with increased hospital and intensive care unit (ICU) stays and increased mortality rates. Recently, it was shown in a single centre that intensive insulin therapy significantly reduced the electrophysiological incidence of CIP/CIM and the need for prolonged mechanical ventilation in patients in a medical or surgical ICU for at least 1 week. The electrophysiological diagnosis was limited by the fact that muscle membrane inexcitability was not detected. These results have yet to be confirmed in a larger patient population. One of the main risks of this therapy is hypoglycemia. Also, conflicting evidence concerning the neuromuscular effects of corticosteroids exists. A systematic review of the available literature on the optimal approach for preventing CIP/CIM seems warranted.
Highlights
Critical illness polyneuropathy (CIP), first described by Bolton and colleagues in 1986 [1], is a frequent complication of critical illness, acutely and primarily affecting the motor and sensory axons
Improvement of diagnostics later on revealed that muscle may be primarily involved, which is called myopathy in critical illness or critical illness myopathy (CIM) [2,3,4,5]
The effect of intensive insulin therapy on CIP/CIM and the need for prolonged mechanical ventilation have been studied in surgical (SICU) and medical (MICU) intensive care unit (ICU) populations
Summary
Critical illness polyneuropathy (CIP), first described by Bolton and colleagues in 1986 [1], is a frequent complication of critical illness, acutely and primarily affecting the motor and sensory axons. Evidence for these mechanisms and a possible ‘myotoxic’ factor responsible for this comes from animal data in which sera of patients with CIM had differential effects on resting and action potentials, sodium channels, and the excitation-contraction coupling process at the level of the SRCa2+ release [76].
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