Post COVID 19 multisystem inflammatory syndrome in an older adult

Abstract

The novel coronavirus disease (COVID 19) caused by SARS-CoV-2 has caused widespread illness and death across the world and we continue to identify new sequelae of this disease. We present a case of a post COVID 19 multisystem inflammatory syndrome in an older adult with debilitating neurological and gastrointestinal manifestations and acute kidney injury (AKI) requiring hemodialysis. There have been over 1000 cases of post COVID 19 multisystem inflammatory syndrome in children (MIS-C) described, but none in older adults. The exact mechanism of MIS-C is unknown but is believed to be due to a delayed cytokine storm related to the initial infection. Given the vast number of cases of COVID 19 worldwide, we should be conscious of the possibility of a post COVID 19 multisystem inflammatory syndrome in adults as we work toward effectively treating this virus. We present a 67-year-old male with a past medical history of cirrhosis and hypertension, diagnosed with COVID 19 pneumonia 68 days prior. During the initial admission for COVID 19 pneumonia, he required oxygen via high flow nasal cannula and was treated with doxycycline, ceftriaxone, vitamin C, hydroxychloroquine, zinc, therapeutic enoxaparin, thiamin, dexamethasone, and convalescent plasma. Inflammatory markers were initially high but improved prior to discharge. He returned to our institution 3weeks after discharge with complaints of generalized weakness, anorexia, and weight loss. He also had nausea, dyspnea on exertion, lower extremity swelling and cognitive difficulties, but denied fevers. He was admitted with tachycardia, leukocytosis, AKI and severe hyponatremia. Initial blood pressure 151/98mmHg, heart rate 115 beats per minute, respiratory rate 20 breaths per minute, temperature 98.1 F, and oxygen saturation 96% on room air. On physical examination, he was tachycardic with a regular rhythm, clear lungs with edema in all extremities and generalized muscle weakness. Labs revealed sodium of 109mEq/L, WBC of 35.9 K/cmm, creatinine of 1.1mg/dL (Table 1). Chest x-ray revealed bibasilar infiltrates, CT showed atelectasis. Urinalysis showed protein 100mg/dL, moderate blood, 10 WBC/hpf, 5 RBC/hpf, and muddy brown casts. SARS-CoV-2 PCR was negative, but antibody testing was positive. Echocardiogram showed grade 1 diastolic dysfunction, elevated pulmonary pressures, and normal left ventricular ejection fraction. Hyponatremia corrected appropriately with normal saline. Leukocytosis persisted despite treatment with broadspectrum antibiotics, and all cultures were negative. Due to a high d-dimer and clinical suspicion for pulmonary embolus, therapeutic unfractionated heparin and thrombotic evaluation were initiated. Ventilation/perfusion scan was inconclusive for pulmonary embolism; lower extremity duplex was negative for deep vein thrombosis. Renal function deteriorated and hemodialysis was initiated. Percutaneous renal biopsy showed moderate to marked acute tubular necrosis (ATN), no significant fibrosis, inflammation, immune complexes, or viral inclusions. Given that the patient was never hypotensive and AKI developed prior to the hospitalization, ATN was attributed to cytokine surge. He required 5 treatments of hemodialysis before renal function improved. Due to persistent symptoms and elevated inflammatory markers, dexamethasone 6mg daily was started due to concern for a post COVID 19 multisystem inflammatory syndrome. After 4 days, he improved and was discharged on a prednisone taper. Follow up showed rapid improvement in symptoms and significant reduction in inflammatory markers after 15 days of steroid initiation. His appetite normalized, he gained 10 pounds, and was able to walk 150 feet. BNP and inflammatory markers decreased significantly correlating with improvement in symptoms.