Prolonged paralysis after treatment with neuromuscular junction blocking agents. 1991

J L Gooch, and M R Suchyta, and J M Balbierz, and J H Petajan, and T P Clemmer
Department of Physical Medicine and Rehabilitation, University of Utah Health Sciences Center, Salt Lake City.

OBJECTIVE Previous reports have described prolonged paralysis after treatment with neuromuscular junction blocking agents in critically ill patients. The purpose of this study was to further describe a group of patients who developed prolonged weakness after treatment with these agents. METHODS Clinical information, electrodiagnostic and muscle pathology results are described in this group of patients. Clinical information includes diagnoses, dosage of neuromuscular junction blocker, other medications affecting the neuromuscular system, and neuromuscular examination and clinical course. METHODS All patients were seen in the ICUs of three local hospitals. METHODS Included were critically ill patients with a variety of diagnoses, all of whom developed severe weakness after discontinuation of neuromuscular junction blocking agents. METHODS Electrodiagnostic studies and muscle biopsies were performed on several of the patients. RESULTS All patients had pronounced weakness without sensory loss. Electrodiagnostic and muscle pathology findings were consistent with failed neuromuscular transmission. Although many patients had disorders or were taking medications that can injure the neuromuscular system, no disorder or medication was common to all. Recovery of strength often took several months and most patients were slow to wean from mechanical ventilator support. CONCLUSIONS Although alternative explanations cannot be excluded with certainty, the use of neuromuscular junction blocking agents may lead to neurogenic atrophy and care must be taken when using them.

UI MeSH Term Description Entries
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D009123 Muscle Hypotonia A diminution of the skeletal muscle tone marked by a diminished resistance to passive stretching. Flaccid Muscle Tone,Hypotonia,Decreased Muscle Tone,Floppy Muscles,Hypomyotonia,Hypotony, Muscle,Muscle Flaccidity,Muscle Tone Atonic,Muscle Tone Poor,Muscular Flaccidity,Muscular Hypotonia,Neonatal Hypotonia,Unilateral Hypotonia,Flaccidity, Muscle,Flaccidity, Muscular,Floppy Muscle,Hypotonia, Muscle,Hypotonia, Muscular,Hypotonia, Neonatal,Hypotonia, Unilateral,Hypotonias, Neonatal,Hypotonias, Unilateral,Muscle Hypotony,Muscle Tone Atonics,Muscle Tone, Decreased,Muscle Tone, Flaccid,Muscle, Floppy,Muscles, Floppy,Muscular Flaccidities,Neonatal Hypotonias,Tone Atonic, Muscle,Tone Poor, Muscle
D009132 Muscles Contractile tissue that produces movement in animals. Muscle Tissue,Muscle,Muscle Tissues,Tissue, Muscle,Tissues, Muscle
D009466 Neuromuscular Blocking Agents Drugs that interrupt transmission of nerve impulses at the skeletal neuromuscular junction. They can be of two types, competitive, stabilizing blockers (NEUROMUSCULAR NONDEPOLARIZING AGENTS) or noncompetitive, depolarizing agents (NEUROMUSCULAR DEPOLARIZING AGENTS). Both prevent acetylcholine from triggering the muscle contraction and they are used as anesthesia adjuvants, as relaxants during electroshock, in convulsive states, etc. Neuromuscular Blocker,Neuromuscular Blocking Agent,Neuromuscular Blockers,Agent, Neuromuscular Blocking,Agents, Neuromuscular Blocking,Blocker, Neuromuscular,Blockers, Neuromuscular,Blocking Agent, Neuromuscular,Blocking Agents, Neuromuscular
D010197 Pancuronium A bis-quaternary steroid that is a competitive nicotinic antagonist. As a neuromuscular blocking agent it is more potent than CURARE but has less effect on the circulatory system and on histamine release. Pancuronium Bromide,Pancuronium Curamed,Pancuronium Organon,Pavulon,Bromide, Pancuronium
D010243 Paralysis A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45) Palsy,Plegia,Todd Paralysis,Todd's Paralysis,Palsies,Paralyses,Paralysis, Todd,Paralysis, Todd's,Plegias,Todds Paralysis
D011782 Quadriplegia Severe or complete loss of motor function in all four limbs which may result from BRAIN DISEASES; SPINAL CORD DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; or rarely MUSCULAR DISEASES. The locked-in syndrome is characterized by quadriplegia in combination with cranial muscle paralysis. Consciousness is spared and the only retained voluntary motor activity may be limited eye movements. This condition is usually caused by a lesion in the upper BRAIN STEM which injures the descending cortico-spinal and cortico-bulbar tracts. Quadriparesis,Spastic Quadriplegia,Tetraplegia,Flaccid Quadriplegia,Flaccid Tetraplegia,Paralysis, Spinal, Quadriplegic,Spastic Tetraplegia,Flaccid Quadriplegias,Flaccid Tetraplegias,Quadripareses,Quadriplegia, Flaccid,Quadriplegia, Spastic,Quadriplegias,Quadriplegias, Flaccid,Quadriplegias, Spastic,Spastic Quadriplegias,Spastic Tetraplegias,Tetraplegia, Flaccid,Tetraplegia, Spastic,Tetraplegias,Tetraplegias, Flaccid,Tetraplegias, Spastic
D004568 Electrodiagnosis Diagnosis of disease states by recording the spontaneous electrical activity of tissues or organs or by the response to stimulation of electrically excitable tissue. Electrodiagnoses
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

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