TOPIC: Critical Care
TYPE: Medical Student/Resident Case Reports
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 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 COVID-induced hypercoagulable state.
CASE PRESENTATION: A 73-year-old male with 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. He was diagnosed with COVID-19 pneumonia by nasopharyngeal swab. His initial oxygen saturation on room air was 85%; he was placed on supplemental oxygen. CXR showed bilateral diffuse alveolar infiltrates and he was admitted to the hospital. 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 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. He received embolectomy, stenting, and therapeutic heparin. Within 24 hours, though his creatinine kinase was normal, he developed significantly elevated myoglobin, lactate and worsening acidosis. He had a fasciotomy to the right lower extremity. The next day, he was anuric, with severe acidosis, hyperkalemia, and hypotension, requiring continuous renal replacement therapy (CRRT) and vasopressor support. After three days on dialysis, without signs of improvement, the family decided to pursue comfort measures. He was compassionately extubated and died.
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 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.
CONCLUSIONS: 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.
REFERENCE #1: Jamal M, Bangash HI, Habiba M, et al. Immune dysregulation and system pathology in COVID-19. Virulence. 2021;12(1):918-936. doi:10.1080/21505594.2021.1898790
REFERENCE #2: Hu Y, Meng X, Zhang F, Xiang Y, Wang J. The in vitro antiviral activity of lactoferrin against common human coronaviruses and SARS-CoV-2 is mediated by targeting the heparan sulfate co-receptor. Emerg Microbes Infect. 2021;10(1):317-330. doi:10.1080/22221751.2021.1888660
REFERENCE #3: Bibbo C. Reconstruction of COVID-19-Related Compartment Syndrome With Massive Soft Tissue Necrosis. Wounds. 2021;33(4):99-105.
DISCLOSURES: No relevant relationships by Kendall Creed, source=Web Response
No relevant relationships by Navkiran Randhawa, source=Web Response
No relevant relationships by Sima Shahbandar, source=Web Response
No relevant relationships by Sabrina Siddiqui, source=Web Response
No relevant relationships by Victor Test, source=Web Response