Muscle Relaxants in Critically Ill Patients with Renal Disease

Abstract

Critical illness often results in renal dysfunction. Renal disease includes acid base imbalance, electrolyte shift and neuromuscular disturbances in critically ill patients, who are influenced by the pharmacodynamics and pharmacokinetics of muscle relaxants, with kidney dependent metabolism and excretion. In terms of renal dysfunction, not only decreased circulating levels of normal cholinesterase, but also cholinesterase depletion after plasmapheresis and dialysis draw the attention of clinicians, when administering a muscle relaxant to critically ill patients who are compromised with renal function. These patients have a lower clearance of renal excreted drugs, changes of the volume of distribution, water retention, and pH changes that alter the protein bond and degree of ionization of the drugs. Immobilization of the limb and respiratory muscles, leading to muscle atrophy and the up-regulation of nicotinic acetylcholine receptors, associated with critical illness, is observed in many patients hospitalized in the intensive care unit with renal dysfunction. Disease related conditions or iatrogenically induced factors, including sedation, lead to immobilization of skeletal muscles. Aside from systemic inflammation, immobilization is a key contributing factor to the development of critical illness myopathy. Physicians who care for critically ill patients with renal dysfunction should pay attention to the adequate choice of muscle relaxants and their antagonists.