Introduction Basilar artery thrombosis accounts for a small part of ischemic strokes but contributes to one‐fifth of the posterior circulation strokes. Recurrent basilar artery thrombosis secondary to dolichoectasia is caused by abnormal flow in the dilated artery and can result in cerebral ischemia. We present a similar case of recurrent thrombosis with a missed dose of anticoagulation and dehydration on two separate occasions. Methods An 81‐year‐old man with a past medical history of ulcerative colitis with colostomy, provoked deep venous thrombosis presented as a transfer from an outside hospital with acute onset of dysarthria, nausea/vomiting, unsteadiness, and left hemiparesis. CT angiogram of head and neck revealed right vertebral thrombosis extending into the basilar artery with dolichoectasia involving distal right vertebral artery and basilar artery. He was started on heparin infusion with improvement in symptoms and a return to baseline. He was later transitioned to apixaban and discharged home. On a follow‐up office visit two months later, his repeat CT angiogram revealed resolution of the thrombus. He was advised to continue the medication due to the risk of recurrent occlusion secondary to vessel anomaly. After four months, the patient returned to the emergency department with acute onset dizziness, imbalance, nausea, and vomiting. CT angiogram of the head and neck was performed which revealed non‐occlusive thrombosis in the basilar artery. On evaluation by neurology, he admits to three missed doses of apixaban. Clinical and laboratory data were concerning for volume depletion. On further questioning about his symptoms, he mentions decreased oral intake on the day of colostomy change. He was advised to continue apixaban and stay hydrated. Results After fifteen months of the first presentation, the patient is symptom‐free but was continued on anticoagulation with apixaban to prevent recurrent events. Conclusions The role of short‐term and long‐term anticoagulation in basilar artery occlusion is less studied. No prospective trials were done so far to suggest that antithrombotic therapy lowers the risk of recurrent ischemic events and/or anticoagulation is superior to antiplatelets. Dolichoectasia by itself can increase the risk of recurrent thrombosis and dehydration likely facilitated the thrombosis in our patient during the event of missed anticoagulation.

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Introduction Approximately 10%–15% of acute strokes are spontaneous, nontraumatic intraparenchymal cerebral hemorrhage (IPH). Hypertension (HTN), amyloid angiopathy, or impaired coagulation cause most spontaneous IPHs, in which case the CTA is unlikely to identify an underlying vascular lesion. Prior investigators have identified clinical and non‐contrast CT (NCCT) features that increase the likelihood of identifying a vascular etiology for an IPH, including younger age (< 40–50), absence of hypertension, and presence of subarachnoid (SAH) or intraventricular hemorrhage (IVH). Findings from earlier studies of patients with IPH suggested that older age, HTN, together with certain locations (basal ganglia, thalamus, cerebellum, and pons) could reliably exclude IPH patients with underlying lesions. We aimed to assess the yield of CTA, a costly study with risks of radiation, contrast induced renal injury and death, in identifying vascular lesions in this group. Methods This retrospective study involved reviewing medical records of all patients admitted to Carilion RMH hospital for brain hemorrhage during the period 2008–2020, inclusive. Patients were considered if they were over 50 year of age, had HTN (and/or left ventricular hypertrophy on electrocardiograms or echocardiograpy) and IPH in the thalamus, basal ganglia, cerebellum or pons. Patients with SAH, lobar IPH, traumatic IPH, pure IVH, and patients with known vascular lesions were excluded. Imaging of all patients was reviewed with attention to finding CTAs showing vascular lesions that might have caused of the recent symptomatic IPH (arteriovenous malformations, aneurysms, venous anomalies and dural venous sinus thrombosis). Small saccular aneurysms at remote sites were not considered relevant, nor were intra‐ or extracranial stenoses. Results A total of (446) charts were reviewed, of which 143 met the inclusion criteria (94 males and 49 females). Family history was positive for cerebral aneurysm in one patient and Alzheimer’s with brain hemorrhage in another. Twenty‐six patients were on anticoagulation: 10 on NOAC, 14 on Warfarin (INR was < 2 in 8, 2–3 in 5, and >3 in only one patient). One was on subcutaneous heparin (PTT was 53). No other patient had major coagulation abnormalities; only 5 patients had platelets count < 100K, the lowest was 62K. CTA was negative for underlying vascular lesion at the site of bleeding in all 143 patients, confidence interval 2.6% using Confidence intervals for proportions, using Wilson’s method for proportions. Conclusions In patients over 50 year of age with evidence of hypertension, and ICH in the basal ganglia, thalamus, brain stem and cerebellum; the diagnostic yield of CTA is negligible. Performing this study routinely in the evaluation of these patient increases health care costs, and exposes patients to the risks of unnecessary radiation, contrast induced kidney injury and death. We recommend against the routine use of CTA in patients meeting the above criteria.