Acute Weakness Syndromes in Critically Ill Patients—A Reappraisal

Abstract

Over the last twenty years, increasing numbers of critically ill, mechanically ventilated patients who develop acute profound muscle weakness have been described. These acute weakness syndromes have not been well understood and they have been given many names including: acute steroid myopathy, acute quadriplegic myopathy, the floppy person syndrome, critical illness polyneuropathy, critical illness polyneuromyopathy, and prolonged neurogenic weakness. Many of these “syndromes” either overlap or represent the same disease process in different patients. Many have been incompletely diagnosed. During this review it became evident that the acute weakness syndromes currently recognized in critically ill patients could be categorized into four major groups: myopathy, neuromuscular junction abnormalites, neuropathy and polyneuromyopathy. Each had different possible aetiologies. “Myopathy” includes acute necrotizing myopathy and disuse atrophy. Neuromuscular junction abnormalities are subdivided into myasthenia-like syndromes and prolonged neuromuscular blockade. Neuropathies are divided into critical illness polyneuropathy and acute motor neuropathy. The anterior horn cell injury in Hopkins syndrome should also be considered in this group. Polyneuromyopathies include various combinations of neuropathy and myopathy in the same patients.

Critical illness polyneuropathy: risk factors and clinical consequences. A cohort study in septic patients

“…Previous studies have failed to reveal specific vitamin or nutritional deficiencies as well as toxic factors [7]. Malnutrition, hyperalimentation, hyperosmolar states and certain drugs, especially aminoglycosides and neuromuscular blocking agents (NMBAs), have been postulated as causes that might contribute to CIP development in small series and case reports [8]. Several studies excluded patients with previous potential risk factors of peripheral nerve disease such as cancer, alcoholism or diabetes mellitus, which may influence risk factor analysis.…”

Experimental animal models of muscle wasting in intensive care unit patients

“…The poor understanding of basic mechanisms underlying AQM in the clinical setting is in part due to the fact that basic distinctions between myopathy and neuropathy have often not been clearly made and because the complex clinical, electrophysiologic, and histologic abnormalities are often incompletely reported (16). Diagnosis and classification has frequently been based on clinical observations and electrophysiologic measurements, but both are weak diagnostic indicators (17,18).…”

Altered diaphragm contractile properties with controlled mechanical ventilation

“…Unfortunately, in both studies, the control group did not receive the same duration of anesthesia, sedation, or paralyzing drugs. The confounding effects of paralyzing agents (26) with or without anesthetic drugs (33) may have played a role in the reduced diaphragm muscle function. In addition, neither study assessed the time course of the decrease in diaphragm muscle force.…”