Guillain-Barre Syndrome Secondary to SARS-CoV-2

Guillain-Barre Syndrome (GBS) is an acute autoimmune disorder that is provoked by a preceding infection. It is characterized by progressive, ascending, symmetrical muscle weakness accompanied by hyporeflexia or areflexia. We describe two cases of GBS associated with COVID-19. 36-year-old Hispanic female presented ten days after diagnosis of COVID-19 with symptoms of headache, bilateral leg and facial weakness, and facial paresthesias for five days. Within 24 hours of admission, she developed areflexia and progressive bulbar and appendicular weakness. Nerve conduction study and electromyography were consistent with demyelinating form of GBS. Due to difficulty with clearing oral secretions, patient was intubated two times during the hospitalization. 79-year-old Caucasian female presented with progressive weakness, weight loss and fevers. She was diagnosed with COVID-19 on the day of admission. She had paralysis of all four extremities with dysphagia and required intubation. She was extubated and re-intubated two more times due to worsening hypoxia and stridor which led to placement of a tracheostomy tube. Both our patients developed features of dysautonomia, including hypotension and tachycardia. Severe respiratory muscle weakness and dysphagia led to recurrent intubations. Their CT head and MRI brains were negative for facial nerve enhancement. Lumbar punctures in both revealed albuminocytologic dissociation. Plasma exchange was initiated in both females immediately after first intubation for total duration of five days. Upon outpatient follow up, they had significant improvement in motor function. Common precipitants of GBS are Campylobacter jejuni, EBV, CMV, HIV and Zika virus. Clearly, GBS is an infrequent complication of COVID-19. It is possible that SARS-CoV-2 evokes an immune response against peripheral nerve components leading to acute polyneuropathy of heterogenous presentation. Typically, demyelinating and axonal forms of GBS have been described. However, in our cases, both had demyelinating features including symmetric weakness with predominant bulbar symptoms of dysphagia and dysphonia. These cases highlight that GBS is a potential neurological complication of COVID-19 that physicians must be aware of. Thorough daily neurological exam is critical, and early recognition of GBS symptoms may prompt regular evaluation of negative inspiratory force and vital capacity. This may lead to early initiation of intravenous immunoglobulin (IVIG) or plasma exchange leading to improvement in motor symptoms thus avoiding ventilatory support. Plasma exchange should be considered as a first line treatment in COVID-19 patients since high concentrations of IVIG can lead to increased blood viscosity in these patients who are already at increased risk for thrombotic complications.