The novel coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has made its presence known on the centerstage of worldwide healthcare in 2020. Although it is widely known about its pulmonary presence and ensuing complications, evidence is emerging that there are other organ systems including the cardiovascular and cerebrovascular systems that may be damaged by this virus. There have been reports of large vessel stroke occurring in coronavirus disease 2019 (COVID-19) positive patients, with very few reported in the age group less than 50 years. In this case, we describe a previously healthy 49-year-old male who presented with signs of stroke, and was found to have the novel coronavirus as he had been suffering from upper respiratory tract symptoms for 3 weeks. He subsequently developed further large vessel stroke while in the hospital despite being started on antiplatelet therapy. He was also found to have new onset cardiomyopathy. He was started on anticoagulation and discharged with follow-up for cardiomyopathy testing outpatient. This case begs the question on which anticoagulation to utilize in COVID-19 positive patients to be effective in preventing thrombotic events. It is postulated that a pro-inflammatory state induced by the virus and the virus' affinity for angiotensin converting enzyme-2 receptors in the cerebral vasculature are predispositions to cause a stroke. The virus also directly damages cardiac myocytes causing a number of cardiac complications including cardiomyopathy. It is crucial that guidelines on anticoagulation choice and indications for when to start anticoagulation be developed in order to prevent the more devastating consequences of thrombosis and embolism and their subsequent clinical sequelae.
Splenic infarction is a recognized complication occurring at high altitudes in patients with sickle cell trait (SCT). There have been a few cases of splenic infarction occurring in the setting of nonhypoxic events at sea level, and some cases of spontaneous splenic infarction without an inciting event in patients with SCT.We present the case of a 25-year-old male with a recent untreated dental infection who was drinking alcohol excessively and moving furniture over the last few weeks. He came to the hospital due to left-sided abdominal pain and was found to have a splenic infarction. He was found to have hemolysis on his blood work, with elevated lactate dehydrogenase, low haptoglobin, and elevated bilirubin levels. He underwent hemoglobin electrophoresis which revealed SCT. His blood cultures grew Streptococcus mitis and Streptococcus oralis, a normal oral commensal, which was thought to be due to the untreated dental infection. His workup for endocarditis as a source of splenic infarction was negative, and he had no other source of emboli. He was treated with antibiotics for the sepsis and fluids for the sickling and hemolysis. He developed multiple complications of the splenic infarction but ultimately recovered. Ours is the first example of nonhypoxic splenic infarction in an SCT patient that has been documented in a scenario of dehydration and sepsis. This link should be understood to prevent splenic infarction even at sea level by preventing overexertion and dehydration in individuals with known SCT.
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