SARS-Cov-2 infection: pneumonia and ischemic stroke

ABSTRACT

Introduction: Thromboembolism is a known phenomenon of coronavirus disease. Patients hospitalized with severe covid-19 demonstrate clinical and laboratory markers compatible with hypercoagulability. Case Report A 85-old-man with a previous history of hypertension and diabetes. He presented to emergency room afebrile, oriented, cooperative (CGS 15), with cough, dyspnea and hypoxemia (oxygen saturation 88% on room air) requiring non-invasive-ventilation (C-PAP Fi O2 50% PEEP 5). Vital signs were BP 100/70 mmHg, HR 88 bpm, RR 26/min;ECG no arrhythmia;PCR for Sars- CoV2 was positive;the ChestX-Ray revealed bilateral consolidations. Laboratory findings at admission WBC 10.4 K/microL, Neutrophils 9.7 K/microL, Lymphocytes 0,5 K/microL, Platelet Count 306 mm3, D-Dimer 703 ng/ml, CRP 158 mg/L. The patient started therapy with Piperacillin/Tazobactam, LMWH, steroids in addition to standard supportive care and admitted in covid department. On the second day he didn't respond to painful stimulations, neurological examination revealed bilateral babinski, left sides hemiplegia followed by absent corneal and vestibule-ocular reflexes (CGS 4);brain CT-Scan revealed acute large ischemic infarct. Laboratory findings after onset of stroke WBC 17.6 K/microL, Neutrophils 16.4 K/microL, Lymphocytes 0,3 K/microL, Platelet Count 457 mm3, D-Dimers 7464 ng/ml, CRP 166 mg/L. Conclusions: Systemic inflammation and the potential direct action of the coronavirus may cause endothelial disfunction, resulting in a hypercoagulable state that could be considered a potential cause of ischemic stroke.