COVID-19 AND NEUROLOGICAL AUTOIMMUNITY: A CASE OF SARS-COV-2-INDUCED GUILLAIN-BARRE SYNDROME

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: With the ongoing COVID-19 pandemic, a number of rare complications have been reported. We present a case of a rare neurological complication in a patient with a newly diagnosed COVID-19 infection. CASE PRESENTATION: A 64-year-old man with recently treated intraabdominal infection (antibiotics and drainage) presented to the Emergency Department (ED) with a 3-day history of fevers, intermittent right-sided flank pain, and urinary symptoms. He was found to have a complicated urinary tract infection (UTI) due to Klebsiella pneumoniae. He was started on intravenous antibiotics. He was tested positive for the SARS-CoV2 virus. On day 5, he developed progressive hypoxemia with bilateral infiltrates on the chest x-ray. Remdesivir and dexamethasone were initiated. Despite that, the patient developed further progression of respiratory failure requiring intubation. He then failed extubation. On exam, the patient was noted to have profound bilateral lower extremity weakness (motor strength: upper extremities - 4/5 bilaterally; lower extremities - 2/5), absent deep tendon reflexes. Magnetic resonance imaging (MRI) of the brain and spine did not show any abnormal lesions. Lumbar puncture showed an elevated protein (147 (15-40 mg/dL)) with absent cells in the cerebrospinal fluid (CSF) (albuminocytologic dissociation). He was diagnosed with Guillain-Barré syndrome (GBS). Therapeutic plasma exchange (TPE) was initiated (IVIG was not recommended given the potential risk of hypercoagulability). The patient completed 5 days of TPE. The patient noted some improvement in the strength of upper extremities. Unfortunately, the patient later developed a multiorgan failure with recurrent aspiration events and renal failure. The patient and his family decided to proceed with hospice. DISCUSSION: GBS is a heterogenous acute immune-mediated polyneuropathy commonly triggered by various viral infections. There have been several reports of SARS-CoV-2 infection triggering both primary and recurrent GBS. It is thought to be induced by the cross-reactivity of viral antigens with myelin. The diagnosis of GBS should be suspected in patients with progressive symmetric muscle weakness and absent deep tendon reflexes. Electrodiagnostic (not done in our patient) and CSF studies are usually done to confirm the diagnosis. Albuminocytologic dissociation (elevated protein with normal WBC count in the CSF) can be detected in most patients, especially if CSF is obtained after 7 days since the onset of symptoms. Supportive treatment with close monitoring of respiratory function is extremely important in affected patients. Disease-modifying therapies include the use of IVIG or TPE. CONCLUSIONS: With the myriad of publications related to SARS-CoV-2 infection, we continue to learn more about the culprit virus. We believe that healthcare workers should be aware of autoimmune complications of COVID-19 infection given the ongoing pandemic. REFERENCE #1: Caress JB, Castoro RJ, Simmons Z, et al. COVID-19-associated Guillain-Barré syndrome: The early pandemic experience. Muscle Nerve. 2020 Oct;62(4):485-491. doi: 10.1002/mus.27024. Epub 2020 Aug 11. PMID: 32678460; PMCID: PMC7405390 REFERENCE #2: Rahimi K. Guillain-Barre syndrome during COVID-19 pandemic: an overview of the reports [published correction appears in Neurol Sci. 2020 Sep 23]. Neurol Sci. 2020;41(11):3149-3156. doi:10.1007/s10072-020-04693-y DISCLOSURES: No relevant relationships by Vincent Chan, source=Web Response No relevant relationships by Artem Minalyan, source=Web Response No relevant relationships by Franklin Thelmo, source=Web Response No relevant relationships by Qian Zhang, source=Web Response