A 68-year-old female, compliant and controlled on her medications for hypertension, diabetes, and with paroxysmal atrial fibrillation (AF) on new oral anticoagulants with a controlled rate diagnosed positive for COVID-19 on clinical basis as well as through polymerase chain reaction (PCR) in September 2021. Patient was admitted to quarantine hospital with an oxygen saturation of 90% and discharged home after 20 days. Few days later the patient began to complain of severe throbbing headache radiating to the back of head and increasing on lying flat that was followed by a single unprovoked generalized tonic clonic seizure followed by disturbed conscious level with a Glasgow coma scale (GCS) of 10/15. Patient was readmitted to an intensive care unit and on retesting PCR it was still positive.
Ten days later the patient was discharged yet with a bilateral convergent squint more on her right eye and left sided weakness with national institute of health stroke scale (NIHSS) of 12. Patient sought medical advice at emergency room (ER) and was admitted to stroke center, where magnetic resonance imaging (MRI) (Philips 1.5 Tesla, Germany) stroke protocol was done as well as magnetic resonance venography (MRV) that revealed bilateral cortical border zone infarcts with restricted diffusion along DWI (Fig. 1) with diffuse atherosclerosis and mural irregularity, attenuated beaded lumen and hypo plastic left anterior cerebral artery A1 segment (normal variant) on magnetic resonance angiography (MRA) (Fig. 2) and altered signal of left lateral dural venous sinuses as well as deep venous system thrombosis with no flow related signal in MRV (Fig. 3).
Basic laboratory samples were ordered and results were going with mild elevation of Prothrombin time / activated Partial thromboplastin time (PT / aPPT) 12.3/23.2 (normal range 9.8–12.1/26.4–37.5), D-dimer 0.95, ferritin 726.2, CRP 9.03, low normal platelet count 160.000, relative lymphopenia 14.9% (normal range 20–40%).
Laboratory blood samples for collagen disorders and thrombophilia were obtained including anti-thrombin III, Protein C and S, factor V Leiden, ANA, anti DNA, anti-cardiolipin antibody and lupus anticoagulant and all were within normal limits, beside absence of clinical history suggestive of collagen disorders or previous history of thrombosis.
Neurosonology with color coded duplex study of both extracranial carotid tree and vertebral system and Doppler spectral wave analysis as well as transcranial duplex (Acuson Juniper, Siemens, Seoul) revealed diffuse atherosclerosis with no evidence of hemodynamic changes or stenosis.
Electrocardiogram (ECG) (CM 300A, Comen, China) revealed normal sinus rhythm and long term monitoring revealed controlled rate paroxysmal AF. Transthoracic echocardiography (Vivid E9 machine, General Electric, Vingmed Ultrasound, Horten, Norway) was within accepted limits with ejection fraction 76% and left atrium diameter of 32 with no evidence of intracardiac thrombus or wall abnormality.
Patient was tested for COVID-19 by PCR that was negative on two successive tests within a 48 h interval as for IgG it was positive donating previous infection and IgM was weak positive donating convalescence phase.
Patient was placed on full dose anticoagulation beside antiepileptic and dehydrating measures with initial improvement regarding sensorium yet recurrent deterioration took place with GCS 6. Follow-up MRI revealed cortical venous infarction donating unresponsive venous system thrombosis to treatment (Fig. 4). Patient was intubated and ventilated and unfortunately died 3 days later.
A final diagnosis was that the patient had dual arterial as well as venous thrombosis, venous thrombosis had no other possible explanation rather than COVID-19 induced hyper coagulopathy (CIC), while arterial thrombosis was either COVID-19 associated or secondary to the patient medical past history.