LAUSR

Introduction: Myasthenia Gravis is an autoimmune condition that affects the neuromuscular junction. Acute respiratory failure due to myasthenic weakness is a known complication of Myasthenia Gravis. Rituximab infusion for refractory myasthenia gravis has been well reported to improve symptoms. Description: We report a case of a 25 year old African American female who is known to have anti-acetylcholine receptor positive myasthenia gravis, managed on mycophenolate mofetil and monthly Intravenous immunoglobulin (IVIG) until recently, when IVIG was switched for rituximab due to worsening renal function. She presented to the emergency department (ED) with generalized weakness, dysarthria and shortness of breath 2 days after her first Rituximab therapy. She required emergent intubation and mechanical ventilation for acute hypercapnic respiratory failure in the ED. Her initial vital signs were BP 128/85, pulse 86, respiratory rate 30, temperature of 97.8, SpO2 7587% on room air. Arterial blood gas showed pH 7.21, pCO2 69, pO2 307. Chest X-ray showed bibasilar infiltrates versus atelectasis with no leukocytosis and normal procalcitonin and lactic acid. Multidisciplinary approach to her care was taken with involvement of the hematologist, neurologist and intensivist. Patient underwent a total of 5 sessions of plasmapheresis with improvement of her negative inspiratory force (NIF) from -14 to -30 and forced vital capacity (FVC) from 799 to 1497. She was extubated 5 days later, and with the guidance of neurology, she was discharged on mycophenolate mofetil and pyridostigmine to follow up with outpatient care. Discussion: Rituximab is an anti-CD20 monoclonal immunoglobulin therapy that has increasing utility in the treatment of myasthenia gravis that does not respond to first line immunosuppressive therapy. Myasthenic crisis has many triggers; however treatment relapse and acute respiratory distress should be considered following rituximab infusion therapy. The underlying mechanism is not fully elucidated; however, it is believed to be mediated by release of proinflammatory cytokines in other clinical settings. Our patient reports strict adherence to her oral medications and there were no other known precipitants at the time of her presentation.