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• W3205990467 abstract "TOPIC: Pulmonary Manifestations of Systemic Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Advancements in oncologic therapies have generated novel agents that promise good clinical effect in cancer management. While pneumonitis is a commonly observed complication for newer biologic and small molecule therapies, there are other respiratory complications that are important to recognize. CASE PRESENTATION: A 63 year-old female with a history of resected malignant melanoma, morbid obesity and possible OSA presented with progressive exertional dyspnea that began two weeks after her first treatment with adjuvant nivolumab for melanoma. In the ED, she was found to be tachypneic and hypoxic with accessory muscle use. Exam demonstrated bibasilar crackles, JVP elevation to 12cm and 2+ pitting edema of her lower extremities. VBG showed a pH of 7.31 and PCO2 of 76mmHg. EKG and echocardiogram were unremarkable, but troponin was 0.2. Chest x-ray demonstrated bilateral patchy infiltrates, suggestive of pulmonary edema. She was placed on high flow nasal cannula (HFNC) and transferred to the ICU. It was determined that the patient was in acute decompensated heart failure secondary to nivolumab-induced myocarditis. She was started on methylprednisolone and diuresed with mild symptomatic improvement over several days. Right heart catheterization ultimately showed normal hemodynamics and filling pressure. However, during this time, she had difficulty tolerating non-invasive ventilation, but could not maintain eucapnia on HFNC. She subsequently developed bulbar weakness with increasing fatigue and hypercarbic respiratory failure, requiring intubation. After she was intubated, her negative inspiratory force was found to be -10cm H2O. MRI brain and lumbar puncture were unremarkable. However, a myasthenia gravis panel returned with elevated acetylcholine receptor-binding and anti-striated muscle antibodies. She was diagnosed with immune checkpoint inhibitor-related myasthenic crisis and started on pyridostigmine. Her condition gradually improved and she was successfully extubated. DISCUSSION: This case highlights an unusual and interesting cause of neuromuscular weakness, which is an important yet often overlooked etiology of dyspnea. Myasthenic crisis should be suspected in any patient with dyspnea and bulbar or proximal muscle weakness. With regard to PDL-1 inhibitors such as nivolumab, these are most commonly associated with mucosal toxicity, colitis, hepatotoxicity, pneumonitis and endocrinopathies.[1] However, a broad range of neurological manifestations have also been documented and typically present within 3 months after starting therapy.[2] CONCLUSIONS: Increasing use of checkpoint inhibitor immunotherapy in the treatment of a variety of malignancies necessitates an understanding of their common adverse events, including, as highlighted in this case, recognition of neurologic causes of respiratory failure. REFERENCE #1: Naidoo J, Page DB, Li BT, et al. Toxicities of the anti-PD-1 and anti-PD-L1 immune checkpoint antibodies. Ann Oncol 2015; 26:2375. REFERENCE #2: Reynolds KL, Guidon AC. Diagnosis and Management of Immune Checkpoint Inhibitor-Associated Neurologic Toxicity: Illustrative Case and Review of the Literature. Oncologist 2019; 24:435. DISCLOSURES: No relevant relationships by Howard Freeman, source=Web Response No relevant relationships by Aaron Trimble, source=Web Response" @default.
• W3205990467 created "2021-10-25" @default.
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• W3205990467 date "2021-10-01" @default.
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• W3205990467 title "IMMUNE CHECKPOINT INHIBITOR-INDUCED MYASTHENIC CRISIS" @default.
• W3205990467 doi "https://doi.org/10.1016/j.chest.2021.07.1873" @default.
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