Case Presentation: A 64-year-old woman with a past medical history of hypertension presented with a sudden onset of slurred speech, right gaze preference, and left-sided body weakness while at a hair salon. In the Emergency Department, she was afebrile, blood pressure 110/70 mmHg, and heart rate 105 beats per minute. CT head without contrast revealed no acute intracranial pathology. CT angiogram head and neck revealed thrombus within the right MCA, M1/M2 junction, and an incidental finding of large acute right-sided pulmonary embolism. She received intravenous tissue plasminogen activator (tPA) and she was orally intubated for airway protection, subsequently she underwent emergent cerebral angiogram with distal right MCA thrombectomy. The patient was admitted to the neurological ICU for post-procedural monitoring. A follow-up CT angiogram of the head and neck revealed a new occlusion of the left MCA at M1/2 junction and ischemia involving the left MCA territory. Neurosurgery recommended no intervention due to established infarction. The initial COVID-19 nasopharyngeal swab was negative. However, due to multiple thrombotic events, hypercoagulable workup was thought, including a repeat COVID-19 swab, which was reported positive. Laboratory findings were remarkable for CRP of 25.10 mg/dL, LDH 980 U/L, and D-Dimer of more than 10,000 ng/mL. The patient’s mental status remained poor; she remained on IV heparin and requiring mechanical ventilatory support. Treatment options discussed with the family for tracheostomy placement versus palliative extubation.
Discussion: COVID-19 frequently causes severe acute respiratory syndrome and has a wide range of other non-respiratory presentations. There is growing evidence showing diverse neurological complications related to COVID-19, including venous and arterial origin’s thromboembolic stroke.The reported incidence of cerebrovascular accidents (CVA) in patients testing positive for COVID-19 ranges from 1-6%, potentially affecting many individuals.These CVAs’ proposed mechanism includes a hypercoagulable state from systemic inflammation and cytokine storm, direct viral-induced endothilitis, and endarteropathy, potentially leading to angiopathic thrombosis.Another proposed theory is the COVID-19 glycoprotein spike binding to angiotensin-converting enzyme 2 (ACE2) present on brain endothelium leading to extensive tissue damage. ACE2 plays a vital role in the renin-angiotensin system (RAS). It acts as a counterbalance to angiotensin II which is a pro-inflammatory hormone that causes vasoconstriction and promotes organ damage. Thus, the depletion of ACE2 by COVID-19 may alter the balance between ACE2/Angiotensin II, promoting tissue injury in the brain and leading to CVAs.
Conclusions: COVID-19 is primarily a respiratory disease affecting lungs in various degrees of severity, ranging from asymptomatic carriers to fatal acute respiratory distress syndrome (ARDS). Recent reports have suggested an increased prevalence of thrombotic events suggesting a coagulopathic pathology in COVID-19 infection. Despite emerging reports confirming COVID-19 associated coagulopathy, there are no prophylaxis and treatment guidelines as of yet.