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A variety of neuromuscular entities contribute to the weakness associated with critical illnesses. These include critical illness polyneuropathy, [1,2] prolonged neuromuscular junction blockade by nondepolarizing blocking agents, [3] and the acute myopathies consisting of thick filament myosin myopathy [4,5] and acute necrotizing myopathies. [6,7] We describe two patients with unique pathologic changes characterized by acute type II fiber atrophy with features of regeneration.
Case reports.
Patient 1.
A 67-year-old man was admitted with status asthmaticus and no preexisting neuromuscular disease. Three weeks before admission, he had an upper respiratory infection. He received prednisone 40 mg/d for 5 days but had no improvement. He was admitted to the hospital and placed on IV methylprednisolone 300 to 500 mg/d. He became septic and required intubation 5 days later, having neuromuscular blockade for 4 days (vecuronium 2 to 6 mg/h). Two weeks after admission, a progressive marked generalized weakness and muscle wasting was first noted, more pronounced on the left and proximally more than distally. Deep tendon reflexes were absent in all but the right upper extremity. Otherwise, his examination was normal. Methylprednisolone was reduced to 100 to 200 mg/d and then discontinued 3 weeks after initiation, and oral prednisone 40 to 100 mg/d was begun. He was on IV aminophylline throughout his hospitalization, up to 40 mg/h. Serum CK peaked at 785 (mostly skeletal muscle type) 3.5 weeks after admission. Nerve conduction studies and needle EMG were performed at this time. Muscle biopsy was performed 4 weeks after admission. The patient died of Aspergillus pneumonia 3 days later.
Patient 2.
A 60-year-old man with a history of chronic obstructive pulmonary disease, diabetes mellitus, alcoholic cirrhosis, and hypothyroidism was admitted for a partial colon resection for adenocarcinoma. He had no known neurologic deficits on admission. Six days after surgery, he became hypoxic, required intubation, and was found to have …
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