Neuromuscular involvement in COVID-19 critically ill patients

Abstract

Objective: Coronavirus disease 2019 (COVID-19) has a high incidence of intensive care admittance due to the severe acute respiratory syndrome (SARS). Intensive care unit (ICU)-acquired weakness (ICUAW) is a common complication of ICU patients consisting of symmetric and generalised weakness. The aim of this study was to determine the presence of myopathy, neuropathy or both in ICU patients affected by COVID-19 and whether ICUAW associated with COVID-19 differs from other aetiologies.

Methods: Twelve SARS CoV-2 positive patients referred with the suspicion of critical illness myopathy (CIM) or polyneuropathy (CIP) were included between March and May 2020. Nerve conduction and concentric needle electromyography were performed in all patients while admitted to the hospital. Muscle biopsies were obtained in three patients.

Results: Four patients presented signs of a sensory-motor axonal polyneuropathy and seven patients showed signs of myopathy. One muscle biopsy showed scattered necrotic and regenerative fibres without inflammatory signs. The other two biopsies showed non-specific myopathic findings.

Conclusions: We have not found any distinctive features in the studies of the ICU patients affected by SARS-CoV-2 infection.

Significance: Further studies are needed to determine whether COVID-19-related CIM/CIP has different features from other aetiologies. Neurophysiological studies are essential in the diagnosis of these patients.

Keywords: COVID-19; Critical illness neuromyopathy; Neuromuscular disorders; Neurophysiology; Pandemic.

Fig. 1

Patient 7: Right peroneal nerve compound muscle action potencial (CMAP) with normal distal motor latency, normal duration and decreased amplitude. Left sural nerve sensory nerve action potential (SNAP) with decreased amplitude.

Fig. 2

Patient 1: (a) Myopathic pattern: short duration and amplitude (5.3 ms, 208 µV) and polyphasic motor unit potentials of the left posterior deltoid muscle. (b) Spontaneous activity (positive sharp waves and fibrillation potentials) of the left posterior deltoid muscle. (c) Sural nerve sensory nerve action potential (SNAP): normal conduction velocity (49.8 m/s) and amplitude (15.5 µV). (d) Peroneal nerve compound muscle action potential (CMAP): normal distal motor latency (3.97 ms), decreased amplitude (0.72 mV) and increased duration (9.8 ms).

Fig. 3

Skeletal muscle biopsy showing (A) scattered necrotic fibers (arrowhead) in the absence of inflammatory infiltrate (hematoxylin-eosin, 20x). (B) Higher magnification of two necrotic fibers being phagocyted by macrophages (H-E, 40x). (C) There were no thrombi or inflammatory infiltrates in the vessels (H-E, 40x). Also note the absence of angulated fibers. (D) There was no deposit of C5b9 by immunohistochemistry in non-necrotic fibers (C5b9, 20x).