POST-INFECTIOUS DEMYELINATING POLYNEUROPATHY SECONDARY TO COVID-19 INFECTION

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Coronavirus disease 2019 (Covid-19) began late 2019 in Wuhan, China, declared health care emergency in January 2020 and by March 2020 was declared a pandemic by the WHO. Although respiratory symptoms are most commonly reported, it is important to notice that neurologic complications have been increasingly recognized. Symptoms include headache, dizziness, anosmia, ageusia, and encephalopathy. Demyelinating polyneuropathy presenting as post infectious sequela has not yet been well described. CASE PRESENTATION: Three weeks after being diagnosed with Covid-19, when fully recovered, a 66-year-old man presented with sudden onset walking difficulties owning to symmetric weakness in the lower extremities that rapidly progressed to the upper extremities. Once in respiratory distress with a negative inspiratory force of negative 12, he was intubated due to neuromuscular failure. The diagnosis of Guillain-Barre syndrome (GBS) was made through clinical evaluation in junction with Cerebrospinal Fluid (CSF) analysis (revealing albumin-cytological dissociation), electromyography, and magnetic resonance imaging. He had no significant improvement with intravenous immunoglobulin (400mg/kg/day for five days) and, thus, was started on plasmapheresis treatment (five sessions every other day). Although he only had a mild response, the patient was able to answer simple questions and was enrolled in a long-term physical and occupational therapy. DISCUSSION: Guillain-Barre is an immune-mediated disease that affects the peripheral neurons and nerve roots usually after a preceding respiratory or gastrointestinal illness. There are several proposed mechanisms through which Covid-19 can affect the nervous system. It is thought that the virus can enter the cells via an angiotensin-converting enzyme 2 receptor, invading the peripheral nerve terminals and spreading to the dorsal root ganglion. Then, it potentially shares epitopes similar to neurons, allowing the activation of a cell-mediated immunity leading to neuronal dysfunction. GBS as a sequela of Covid-19 has not been well reported in literature. The case hereby presented had a temporal relationship between the resolution of Covid-19 and the neurologic symptoms. Its rapid progression affecting the peripheral nerves and the albumin-cytological evidence dissociation on CSF analysis led us to consider Guillain-Barre as a strong differential. The poor clinical response despite aggressive treatments is usually associated with a worse prognosis and significant likelihood of reliance on mechanical ventilation. CONCLUSIONS: By reporting this case, we aim to reiterate the importance of fully understanding the spectrum of Covid-19 related complications, in order to prevent further mortality. REFERENCE #1: Huang C, Wang Y, Li X et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497-506. REFERENCE #2: Zubair AS, McAlpine LS, Gardin T, et al. Neuropathogenesis and Neurologic Manifestations of the Coronaviruses in the Age of Coronavirus Disease 2019: A Review. JAMA Neurol. 2020;77(8):1018–1027. REFERENCE #3: Hughes RA, Cornblath DR. Guillain-Barré syndrome. Lancet. 2005 Nov 5;366(9497):1653-66. DISCLOSURES: No relevant relationships by Christiana Atuaka, source=Web Response No relevant relationships by Nishil Dalsania, source=Web Response No relevant relationships by Claudia De Araujo Duarte, source=Web Response No relevant relationships by Bruno De Brito Gomes, source=Web Response No relevant relationships by Varun tej Gonuguntla, source=Web Response No relevant relationships by Ravikaran Patti, source=Web Response No relevant relationships by Chanaka Seneviratne, source=Web Response No relevant relationships by Navjot Somal, source=Web Response