ABSTRACT
Introduction Cases of rhabdomyolysis causing myoglobinuria in post-COVID-19 patients have been seen occasionally, and exact mechanisms behind this seem multi-factorial. Some patients have severe myoglobinuria with highly elevated creatinine phosphokinase levels requiring urgent hemodialysis to keep creatinine and blood urea nitrogen levels under control and protect the kidneys from long-term damage. Case presentation We present a case of a 24-year-old man with autism who was admitted to the hospital for COVID-19 viral pneumonia and discharged without major complications. After 3 weeks, he came to the ER with a decreased mental status and asterixis, and labs indicated creatinine had increased from baseline 0.7 mg/dl to 2.9 mg/dl and eventually increased to 6.4 mg/dl despite IV hydration. Creatinine phosphokinase was ordered, and it was 289,500 mcg/L. The patient likely suffered acute tubular necrosis secondary to rhabdomyolysis. Urgent hemodialysis was initiated, and the patient showed clinical improvement after one week and was taken off dialysis in 2 weeks. During an outpatient Nephrology clinic visit, the creatinine level was close to baseline level at 0.9 mg/dl, and the patient was asymptomatic. Discussion Different viruses have been described to cause myositis and rhabdomyolysis. The list is long but not limited to influenza A and B, coxsackie, Epstein-Barr, herpes simplex, parainfluenza, adenovirus, cytomegalovirus, measles, varicellazoster, human immunodeficiency, and dengue. In addition, reports about myoglobinuria post-COVID-19 infection have been emerging. The mechanism is unclear, but one theory suggests muscular necrosis from the direct viral invasion of myocytes, and another one suggests a toxic effect on myocytes by the host response, i.e., cytokine release and other immunological factors. Hence, early clinical recognition of this entity can be lifesaving in some cases.
ABSTRACT
Introduction Coronavirus 19 (COVID-19) is a viral illness that is caused by SARS-CoV-2. It has a surface spike protein that binds to human angiotensin-converting enzyme 2 receptors expressed in the kidneys, lung, and vascular endothelium. Here we present a case of a 73-year-old critically ill male with COVID pneumonia and acute respiratory distress syndrome (ARDS), who developed compartment syndrome and rhabdomyolysis as a consequence of extensive right lower extremity arterial thrombosis related to a COVID induced hypercoagulable state. Case A 73-year-old COVID positive male with past medical history of coronary artery disease status-post triple coronary artery bypass 10 years ago and type 2 diabetes mellitus presented to the emergency department with progressively worsening dyspnea for one week. His initial oxygen saturation on room air measured 85%, so he was placed on 3 liters per minute supplementation via nasal cannula. CXR showed bilateral diffuse alveolar infiltrates and he was admitted for observation. He developed worsening respiratory failure five days into hospitalization, placed on maximum supplementation via high flow nasal cannula (HFNC), and transferred to the medical ICU. Ultimately, he was intubated and mechanically ventilated for the remainder of his hospitalization due to severe ARDS. After three days in the ICU, his right lower extremity was cold, without palpable nor detectable pulses via bedside Doppler from the femoral to pedal landmarks. Formal ultrasound Doppler that morning confirmed arterial clot extending from the right external iliac to posterior tibial arteries. The patient received embolectomy, stenting, and therapeutic heparin. Within 24 hours, though his creatinine kinase was normal, he developed significantly elevated myoglobin, lactate and worsening acidosis. The patient had a fasciotomy to the right lower extremity at bedside. The next day, he was anuric, with severe acidosis, hyperkalemia, and hypotension, requiring continuous renal replacement therapy (CRRT) and vasopressor support. Discussion Compartment syndrome is characterized by increased pressure within fascial compartments, leading to circulatory compromise, cellular necrosis, and rhabdomyolysis. In this case, the COVID-19 viral effect on coagulation led to extensive arterial thrombosis, complicated by compartment syndrome and renal failure necessitating CRRT. While the exact pathophysiology of the hypercoagulable state in COVID-19 illness is debated, we have observed its manifestations ranging from deep venous thrombosis (DVT), pulmonary embolism (PE), to stroke. Conclusion COVID-19 is known to be a virulent, multifactorial, intelligent virus with myriad end-organ and vascular consequences. When attending to the most critically ill patients with COVID-19, it is wise to consider all forms of vascular thromboembolism.