Ischemic Stroke due to Intracranial Embolization of a Pelvic Phlebolith in a Pregnant Patient Successfully Treated by Surgical Embolectomy following Attempted Endovascular Thrombectomy.

An unusual case of ischemic stroke due to calcified cerebral embolus occurring in a pregnant patient during the peripartum period is reported. The source of the embolus was suspected to be a pelvic phlebolith in origin which paradoxically embolized via a patent foramen ovale to the supraclinoid right internal carotid artery. To our knowledge, this is the first reported case of calcified cerebral embolus attributed to paradoxical embolism of a pelvic phlebolith, and we theorize that introduction of the phlebolith into the venous system may have occurred as a consequence of vascular remodeling due to pregnancy-related hemodynamic changes. Clinicians should be aware of this potential source of calcified cerebral emboli in patients with a patent foramen ovale during pregnancy. Our patient ultimately achieved an excellent outcome with surgical endarterectomy and embolectomy following an unsuccessful attempt at mechanical thrombectomy.

Cerebral venous congestion as indication for thrombolytic treatment.

PURPOSE: To carry out a retrospective analysis of patients with acute dural sinus thrombosis, and the role of cerebral venous congestion in patient management. METHODS: Twenty-five patients were identified with the clinical and imaging diagnosis of acute dural sinus thrombosis. The imaging diagnosis was by magnetic resonance (MR) and/or computed tomography (CT) venography. There was a female predominance with a female to male ratio of 1.5 to 1 (16 women, 9 men). The age range was from 19 to 64 years old with an average age of 37 years. The first 10 patients, who ranged in age from 21 to 64 years old (average 37 years), received only anticoagulation therapy with heparin and warfarin for periods ranging from 5 days to 2 months. The remaining 15 patients ranged in age from 19 to 57 years old (average 38 years). They either underwent subsequent thrombectomy after a trial of anticoagulation therapy, or went straight to thrombectomy. These latter 15 patients had initial evidence of cerebral venous congestion, either clinically by severe or worsening symptoms despite anticoagulation therapy, or on initial or subsequent CT or MR imaging. In our experience, the cerebral venous congestion imaging findings included intracranial hemorrhage, a hematoma, or edema. The thrombolytic treatment technique consisted of the advancement of a 6 Fr guiding catheter to the jugular bulb or sigmoid sinus from a transfemoral approach. A microcatheter was then advanced to the proximal portion of the thrombus and then either tissue plasminogen activator (tPA) or urokinase was injected to prevent clot propagation. A balloon catheter was used to perform thrombectomy since the thrombolytic agents can be injected via the inner lumen with an inflated balloon. The inflated balloon helped to keep the venous flow from washing out the thrombolytic agent, thus facilitating the agent's effect. RESULTS: The first 10 patients received only anticoagulation therapy with heparin and warfarin for periods ranging from 5 days to 2 months. Eight of these were diagnosed with dural sinus thrombosis only, and had a stable hospital course without worsening of symptoms. These patients also did not have imaging evidence of cerebral venous congestion. The remaining 2 patients had cerebral edema on the CT scan. One had only a small amount of edema in the right cerebellum, but the other had severe edema in the bilateral basal ganglia and thalamic areas. Nine of these patients had a stable hospitalization course and experienced a symptom-free recovery, but 1 died with severe cerebral edema and hemorrhage. Seven of the remaining 15 patients were initially treated with anticoagulation therapy for periods ranging from 2 days to 2 months (average 11 days). These 7 patients were considered to have failed anticoagulation therapy since they had worsening symptoms, and 5 of these had developed hemorrhage on subsequent CT or MR imaging scans. Five of the 7 then underwent thrombectomy with the administration of tPA. Of the remaining 2, 1 underwent thrombectomy alone without the administration of tPA, and the other was given 1 million units of urokinase instead of tPA. Three of these patients had a symptom-free recovery, but 2 had residual left-sided weakness, 1 patient had a minimal gait disturbance, and another patient developed a transverse sinus arteriovenous fistula 7 months after thrombolytic therapy. The remaining 8 patients did not receive anticoagulation therapy, and went straight to treatment with thrombectomy and administration of tPA. All of these presented with worsening clinical symptoms. Six had hemorrhage on their imaging studies, 1 had new edema on a subsequent CT scan, and 1 had edema along with the dural sinus thrombosis, but experienced worsening clinical symptoms consisting of headache and atypical dystonia. Five of these 8 patients experienced a symptom-free recovery, and 3 patients had mild residual weakness. CONCLUSION: In patients with acute dural sinus thrombosis, an indication for thrombectomy or thrombolytic therapy may be the development of cerebral venous congestion which appears to include (1) worsening or severe clinical symptoms, and/or (2) CT or MR imaging findings including intracranial hemorrhage, a hematoma, or edema. It appears that anticoagulation therapy alone is not adequate in patients with acute dural sinus thrombosis when they develop cerebral venous congestion. This may be due to a lack of sufficient collateral flow. Those patients who went straight to thrombectomy because of worsening symptoms, or the imaging findings of cerebral vascular congestion, survived with either a symptom-free recovery or only mild residual neurologic deficit. The patient with evidence of cerebral venous congestion died while on anticoagulation therapy. Thus, the presence of cerebral venous congestion in patients with dural sinus thrombosis, even while on anticoagulation therapy, appears to be an indication for thrombectomy and infusion of thrombolytic agent through a balloon catheter to the site of thrombosis. Our experience suggests that this approach appears to improve the chance of survival, with either a symptom-free recovery or a recovery with only mild residual neurologic deficit.

Endovascular recanalization of basilar artery occlusion 80 days after symptom onset.

BACKGROUND AND PURPOSE: Acute basilar artery occlusion portends high risk of stroke and death. Thrombolysis or endovascular therapy has been limited to patients who present within hours of symptom onset. Without recanalization, acute basilar artery occlusion almost always results in death or severe disability. SUMMARY OF CASE: We report a case of basilar artery occlusion and successful endovascular recanalization 80 days after symptom onset. CONCLUSIONS: Endovascular therapy can be feasible and safe for symptomatic basilar artery occlusion at chronic stage.