Pathophysiology and management of critical illness polyneuropathy and myopathy

Abstract

Critical illness associated weakness (CIAW) is an umbrella term used to describe a group of neuromuscular disorders caused by severe illness. It can be subdivided into three major classifications based on the component of the neuromuscular system (i.e. peripheral nerves or skeletal muscle or both) that are affected. This includes critical illness polyneuropathy (CIP), critical illness myopathy (CIM) and an overlap syndrome, critical illness polyneuromyopathy (CIPNM). It is a common complication observed in people with critical illness requiring intensive care unit (ICU) admission. Given CIAW is found in individuals experiencing grave illness, it can be challenging to study from a practical standpoint. However, over the past two decades, many insights into the pathophysiology of this condition have been made. Results from studies in both humans and animal models have found that a profound systemic inflammatory response and factors related to bioenergetic failure as well as microvascular, metabolic, and electrophysiological alterations underlie the development of CIAW. Current management strategies focus on early mobilization, achieving euglycemia, and nutritional optimization. Other interventions lack sufficient evidence, mainly due to a dearth of large trials. The goal of this Physiology in Medicine article is to highlight important aspects of the pathophysiology of these enigmatic conditions. It is hoped that improved understanding of the mechanisms underlying these disorders will lead to further study and new investigations for novel pharmacologic, nutritional, and exercise-based interventions to optimize patient outcomes.

Neurological Sequelae of COVID-19

“…ICUAW is subdivided into two major categories: critical illness polyneuropathy (CIP) or CIM with CIM being more commonly observed [42,43]. CIM is characterized by the selective loss of myosin causing myofiber atrophy and death while CIP is a result of peripheral nerve axonal dysfunction and death, importantly, without a major demyelinating component as seen in GBS.…”

Effect of early mobilization combined with early nutrition on acquired weakness in critically ill patients (EMAS): A dual-center, randomized controlled trial

“…Intensive care unit-acquired weakness (ICU-AW) is a severe neuromuscular complication in critically ill patients, with a global incidence of 25–31% among the critically ill [ 1 ]. ICU-AW can affect the respiratory and limb muscles, leading to prolonged mechanical ventilation (MV), extended intensive care unit (ICU) stay, higher hospital costs, increased mortality, and decreased quality of life [ 2 – 4 ]. It can take weeks to months to achieve functional recovery from ICU-AW, with most severe cases unable to regain their level of function before the onset of critical illness [ 4 , 5 ].…”

“…ICU-AW can affect the respiratory and limb muscles, leading to prolonged mechanical ventilation (MV), extended intensive care unit (ICU) stay, higher hospital costs, increased mortality, and decreased quality of life [ 2 – 4 ]. It can take weeks to months to achieve functional recovery from ICU-AW, with most severe cases unable to regain their level of function before the onset of critical illness [ 4 , 5 ]. Although some risk factors for ICU-AW have been identified, its pathogenesis and etiology remain uncertain, and there are no specific drugs or targeted treatments to offset these changes.…”

Continuously protracted infusion of cisatracurium besilate in patients with ARDS

“…ICU-acquired weakness (ICU-AW), which refers to a group of neuromuscular disorders, is a frequent complication of critical illness with the morbidity about 30%–50% [ 21 ]. It generally affects the limb muscles, the diaphragm muscle, and even the global respiratory muscles [ 22 ].…”

“…4 ). Hyperglycemia is another potential driving force in the onset of ICU-AW [ 21 ]. So we strictly controlled the blood glucose, synthetically by arterial blood (given more weight) and capillary blood, less than 180 mg/dL according to suggestions drawn from previous studies [ 11 , 28 ].…”