ABSTRACT
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been found to cause multiple complications across several organ systems in patterns not typically observed in previous iterations of the virus. Hemostatic mechanisms have been noted to be significantly altered in particular, resulting in a disseminated intravascular coagulation (DIC)-like picture with elements of coagulopathy as well as hypercoagulability. A 65-year-old man with hypertension, hyperlipidemia, prior tobacco use, chronic kidney disease, and diabetes presented from a correctional facility with hypoxia. The diagnosis of COVID-19 was confirmed. With his elevated D-dimer of >7,955 ng/mL (reference: 90-500 ng/mL) in the setting of COVID-19 and hypoxia, he was empirically started on therapeutic anticoagulation with enoxaparin. His oxygen requirements increased, mental status deteriorated, and platelets began falling, raising concern for heparin-induced thrombocytopenia versus DIC. Heparin products were discontinued in favor of a direct oral anticoagulant. He later became obtunded and unable to tolerate oral medications. Fondaparinux was initiated. Two days later, he was found to have acute limb ischemia of the right lower extremity. He underwent surgical thrombectomy but required an above-the-knee amputation the following day. Shortly after he died secondary to hypoxic respiratory failure. This case highlights the derangement of hemostatic mechanisms seen prominently in COVID-19 infection and raises questions as to appropriate anticoagulant choices to adequately prevent thrombosis. Thorough physical exams should be performed on all patients with COVID-19, taking into account this documented hypercoagulability. Further investigation is warranted into the use of heparin products as the anticoagulant of choice in these patients given observed deficiencies of antithrombin III (ATIII).
ABSTRACT
A 74-year-old female with a history of diabetes presented with chest pain and shortness of breath for two days. She was hypoxic to an oxygen saturation of 60% in the emergency department, requiring bilevel positive airway pressure (BiPAP) to maintain saturations. Chest X-ray demonstrated bilateral hazy opacities suspicious for viral pneumonia. Coronavirus disease 2019 (COVID-19) was confirmed. Right bundle branch block (RBBB) with left anterior fascicular block was noted on admission electrocardiogram (ECG). Cardiac enzymes and brain natriuretic peptide levels were within normal limits. After noting frequent pauses on telemetry, a repeat ECG was performed that demonstrated RBBB with left posterior fascicular block as well as second-degree atrioventricular block (Mobitz type II). Transcutaneous pacing pads were placed, and atropine was placed at the bedside. Cardiac enzymes remained negative. Interleukin-6 levels were elevated at 159 pg/mL. Hydroxychloroquine was deferred due to the patient's arrhythmia and prolonged QTc. Tocilizumab was deferred due to the patient's age. The patient's oxygen requirements and mental status continued to worsen. She continued to desaturate despite maximal BiPAP therapy and eventually died. Cardiac involvement in COVID-19, whether caused primarily by the virus, secondary to its clinical sequelae, or even due to its treatment, cannot be ignored. Further high-quality research is needed to clarify the cardiac pathophysiology. Thorough cardiac exams with electrocardiographic correlation should be performed on all patients with COVID-19. Clinicians should not hesitate to consult cardiovascular services in the event of abnormality.
