LATE-ONSET RHABDOMYOLYSIS IN SARS-COV-2

ABSTRACT

SESSION TITLE Medical Student/Resident Critical Care Posters SESSION TYPE Med Student/Res Case Rep Postr PRESENTED ON October 18-21, 2020 INTRODUCTION: A growing body of evidence has suggested an association between SARS-CoV-2 and non-respiratory sequelae via an inflammatory cascade. Rhabdomyolysis is caused by exertion, prolonged immobilization, medications, seizures, and viral infections such as influenza, leading to acute renal failure. We present a two-patient case series which describes rhabdomyolysis in the setting of SARS-CoV-2. CASE PRESENTATION The first case is a 55-year-old male with a history of hypertension and hyperlipidemia who presented with dyspnea after 6 days of subjective fevers and dry cough. Patient was intubated for hypoxia, and nasopharyngeal swab was positive for SARS-CoV-2 by reverse transcriptase - polymerase chain reaction assay (RT-PCR). On Hospital Day 9, he was extubated but noted to have increased creatine kinase (CK) to a peak of 12391 U/L with a concurrent rise in lactate dehydrogenase (LDH), C-reactive protein (CRP), and total bilirubin. Urinalysis was consistent with myoglobinuria. Creatinine remained below twice his baseline, and he did not require renal replacement therapy. CK and LDH downtrended with intravenous sodium bicarbonate and fluids, and hypoxia improved prior to discharge. The second case is a 59-year-old male with a history of Stage 0 chronic lymphocytic leukemia, hyperlipidemia, gastroesophageal reflux disease, and prior intubation for influenza B. He presented with two weeks of generalized body aches and was intubated for hypoxia secondary to SARS-CoV-2 confirmed by RT-PCR, before progressing to renal failure requiring hemodialysis. He was extubated on Day 16 and dialysis catheter was removed on Day 17. CK rose to a peak of 4617 U/L on Day 20 with a concurrent rise in LDH. Urinalysis showed trace protein, large blood with 4-5 red blood cells per high-powered field. Simvastatin was discontinued after CK elevation, which resolved with fluid resuscitation. DISCUSSION: These cases suggest that SARS-CoV-2 may be associated with late-onset rhabdomyolysis. SARS-CoV-2 may increase the incidence of rhabdomyolysis via a combination of prolonged immobilization and cytokine activation. SARS-CoV-2 may also increase the frequency of statin-induced rhabdomyolysis. Critically ill patients with SARS-CoV-2 warrant screening for rhabdomyolysis, as early intervention likely prevented the first patient from progressing to renal failure. CONCLUSION(S) Clinicians should have an elevated suspicion for delayed rhabdomyolysis in SARS-CoV-2 patients. This suggested association warrants further investigation to determine whether SARS-CoV-2 independently contributes to the incidence of rhabdomyolysis. Reference #1 Huerta-Alardin AL, Varon J, Marik PE. Bench-to-bedside review Rhabdomyolysis - an overview for clinicians. Crit Care. 2005;9(2)158-169. Reference #2 Pesik NT, Otten EJ. Severe rhabdomyolysis following a viral illness a case report and review of the literature. J Emerg Med. 1996;14(4)425-428. Reference #3 Schett G, Sticherling M, Neurath MF. COVID-19 risk for cytokine targeting in chronic inflammatory diseases? Nat Rev Immunol. 2020;20(5)271-272. DISCLOSURES No relevant relationships by Nader Kamangar, source=Web Response No relevant relationships by Dennis Su, source=Web ResponseCopyright © 2020 American College of Chest Physicians