Severe Acute Respiratory Syndrome Coronavirus 2-induced Acute Aortic Occlusion

A Case Report

Artem Minalyan; Franklin L. Thelmo; Vincent Chan; Stephanie Tzarnas; Faizan Ahmed

Disclosures

J Med Case Reports. 2021;15(112) 

In This Article

Case Presentation

A 59-year-old Caucasian male presented to the emergency department (ED) from a nursing home for evaluation of shortness of breath, fevers, and dry cough. His past medical history included schizophrenia, epilepsy, and peripheral vascular disease. As per the patient, his symptoms started 5–7 days prior to the ED visit. He was treated in the outpatient setting with azithromycin for concern of community-acquired pneumonia. He presented to the ED due to progressive dyspnea from his facility where staff found the patient to be hypoxemic with an O2 saturation in the 80s on room air. Of note, the patient was exposed to facility residents with confirmed SARS-CoV-2 infection. However, he tested negative for SARS-CoV-2 infection prior to arrival.

In the ED, he was found to be febrile with oral temperature of 38.2 °C, tachypnea at 22 breaths per minute, and persistent hypoxemia requiring supplemental oxygen delivery via a non-rebreather mask. Physical exam revealed no aberrations in his heart or lungs. Chest X-ray showed bilateral airway opacities concerning for multifocal pneumonia. A complete metabolic panel (CMP) and complete blood count (CBC) with differential revealed lymphopenia with an absolute lymphocyte count 0.5 K/μL (reference range 1.5–3.2). The patient was started on intravenous antibiotics (vancomycin, cefepime, levofloxacin) for presumed bacterial pneumonia. Hydroxychloroquine was initiated to cover possible COVID-19 pneumonia. The patient was admitted to hospital. On day 2, the patient remained hypoxemic and developed increased work of breathing for which he was placed on bilevel positive airway pressure (BiPAP). D-dimer, ferritin, lactate dehydrogenase, and C-reactive protein were all elevated (Figure 1). SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) was positive. On day 3, the patient was upgraded to the intensive care unit (ICU) where he was later intubated. Soon after he was intubated, he developed a mottled appearance of skin that extended from his bilateral feet up to the level of the subumbilical plane. Pulses were unable to be detected both via palpation and Doppler. Bedside ultrasound was performed, and absence of anterograde flow was noted from the mid-aorta down to both common iliac arteries (Figure 2); a deep venous thrombosis (DVT) in the left femoral vein was also revealed. The patient became hypotensive in the ICU with mean arterial pressure (MAP) of 50 mmHg. He was started on a norepinephrine drip for pressure support. Given hemodynamic instability and the high likelihood of venous thromboembolic event, the decision was made to start thrombolytic therapy with tissue plasminogen activator (tPA) of 50 mg intravenously once as well as systemic anticoagulation with a heparin drip. The patient was evaluated emergently by the vascular surgery team. The patient was deemed too unstable to be taken for computed tomography (CT) angiography. No AAA was identified in the patient. After a discussion with the family, it was decided to proceed with comfort-directed care, and the patient died later that day.

Figure 1.

Trends of inflammatory markers during hospitalization

Figure 2.

Ultrasound Doppler imaging of patient's aorta and iliac arteries (a) proximal aorta, (b) mid aorta, (c) left common iliac artery, and (d) right common iliac artery

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