Is plasma calcium concentration implicated in the development of critical illness polyneuropathy and myopathy?

One hundred and ninety consecutive adult critically ill patients with prolonged ICU stay (longer than 7 days) were prospectively evaluated. Patients with acute weakness and/or weaning difficulties were subjected to extensive electrophysiological measurements in order to establish the diagnosis of CIPNM. All recognized and/or possible risk factors for development of CIPNM were recorded.The diagnosis of CIPNM was confirmed in 40 patients (21.05%). By applying a logistic regression model, hypocalcemia (P = 0.02), hypercalcemia (P = 0.01) and septic shock (P = 0.04) were independently associated with the development of CIPNM in critically ill patients.We found that septic shock and abnormal fluctuations of plasma Ca2+ concentration represent significant risk factors for the development of CIPNM in critically ill patients.Acutely acquired neuromuscular dysfunction is a common phenomenon among critically ill patients in the ICU, with a prevalence ranging between 25 and 60% depending upon the criteria used for the diagnosis, the population studied and the timing of examination [1]. Critical illness polyneuropathy and critical illness myopathy have been established as separate entities of muscular weakness leading to considerable weaning difficulties and prolonged ICU stay. These two entities often coexist [2] and have been related to systemic inflammatory response syndrome and sepsis [3]. Several risk factors, such as the administration of neuromuscular blocking agents, aminoglycosides and high-dose corticosteroids, have so far frequently but controversially been considered [4-7].In recent years there has been considerable interest in the role of intracellular calcium homeostasis disturbances as an early event leading to cell injury or death. Calcium is an important intracellular messenger and regulator of cell function. Calcium is essential for the excitation-contraction coupling in muscle, neurotransmission, digestive enzyme activation, inhibition of ATP synthesis and fr