To date, several studies have suggested a severe acute respiratory syndrome coronavirus 2 (SARS-CoV2)mediated hypercoagulability in the forms of pulmonary embolism, stroke, gangrene, "COVID toes," as well as other acute thrombotic complications, warranting the use of systemic anticoagulation. Currently, there are no definitive recommendations as to the timing and dosing of prophylactic or therapeutic anticoagulation in coronavirus disease 2019 (COVID-19) patients. In this manuscript, we report a case of SARS-CoV2-mediated hypercoagulability and review the literature pertaining to the incidence and pathophysiology of coronavirus-mediated coagulopathies. A 64-year-old female, with a medical history of hypothyroidism and remote tobacco abuse, presented to the ED with fever and nonproductive cough. She had multiple negative SARS-CoV2 nasopharyngeal PCR tests during her hospital stay, but chest imaging and elevated inflammatory markers were suggestive of SARS-CoV2 infection. Computed tomography showed a left upper lobe pulmonary embolism with associated right heart strain, and an enlargement of the main pulmonary artery, for which she was initiated on therapeutic anticoagulation with low molecular weight heparin. Despite the medical management of her pulmonary embolism and conservative management of her SARS-CoV2, her clinical condition worsened requiring intubation and mechanical ventilation. After seven days, she was successfully extubated and was transferred to the medical service where her clinical course remained stable and subsequently discharged home on apixaban. In patients with SARS-CoV1-, SARS-CoV2-, and the Middle East respiratory syndrome coronavirus (MERS-CoV)-mediated hypercoagulability, the risk of thrombosis appears to be multifactorial -direct viral cytopathological effects, a pro-inflammatory state, cytokine storm, hypoxia-inducible thrombosis, and endothelial inflammation culminating in the formation of intra-alveolar or systemic fibrin clots. While initial guidelines have been developed to assist clinicians in selecting appropriate chemoprophylaxis as well as therapeutic anticoagulation, a consensus statement remains lacking. Further studies are needed to evaluate the pathogenesis and treatment of coronavirus-induced thrombosis.

Hepatic portal venous gas, while a rare finding with a classically poor prognosis, is not always fatal. Mortality varies depending on the underlying etiology; bowel ischemia carries the highest mortality rate. Other etiologies include gastrointestinal obstruction, gastric ulcer, infectious processes (intraperitoneal abscess and gastroenteritis), inflammatory processes (ulcerative colitis, Crohn disease, chemotherapy-induced), and complications from endoscopic procedures. We report a case of a 68-year-old woman who presented with a week-long history of diminished intake, nausea, and vomiting, with unremarkable abdominal examination, who was found to have significant portal venous gas that completely resolved within 16 hours without surgical intervention.

While cardiac myxomas are the most common primary cardiac tumours, their overall incidence remains rare. Most cases (90%) are sporadic and occur in the third–sixth decades of life with a female predominance and have a specific predilection for the left atrium (75%). While often asymptomatic, clinical presentations depend on the tumour size, architecture and location. Echocardiography remains the mainstay for diagnostic evaluation. Tumour resection is the only definitive treatment. Histopathology using H&E and immunohistochemical stains, such as calretinin and CD34, confirms the diagnosis. We present a case of a patient with reported history of asthma who presented with recurrent acute on chronic shortness of breath refractory to inhaler therapy, multiple outpatient visits and hospitalisations for ‘asthma exacerbations’. After further evaluation, she was diagnosed with a left atrial myxoma attached to the inferior aspect of the intra-atrial septum complicated by severe functional mitral stenosis.

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