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Thrombosis of the internal carotid artery is an unusual complication of neck compression, and even more infrequently observed in manual strangulation. It is important in such cases to exclude spontaneous thrombosis which may result from atherosclerotic narrowing of the vessel.
Fourteen patients with bilateral internal carotid artery thrombosis were analysed with respect to long-term prognosis and the prevalence of risk factors of cerebrovascular disease. The patients comprised seven per cent of all patients with internal carotid thrombosis treated in 1966-73 at the Department of Neurology, University of Helsinki. During the follow-up period of 3 to 86 months (median 50 months) five patients died, three during the first, and two during the second year of follow-up. Of the surviving patients: two needed institutionalization; three were able to take care of themselves; and four who were virtually symptom-free, were able to work. The risk factors of cerebrovascular disease were analysed: 91 per cent were cigarette smokers; 70 per cent had serum triglycerides of 140 mg/100ml or higher; and 62 per cent had cholesterol values of 280 mg/100 ml or higher. Fasting glucose values higher than 95 mg/100 ml, and ECG abnormalities were encountered in every third, and obesity and hypertension in every fourth patient. Cigarette smoking and high triglycerides were more prevalent than in the general population. No association between the number of risk factors in the individual patients and the prognosis could be found.
BACKGROUND AND PURPOSE: Thromboembolic events are a major cause of ischemic stroke. To obtain evidence for platelet embolization after cerebrovascular injury, the accumulation of indium-labeled platelets was documented after photothrombosis of the rat common carotid artery. METHODS: Heterologous blood was collected from donor rats, and the isolated platelets were labeled with 111In-tropolone. Labeled platelets were then infused into Wistar rats 30 minutes before right carotid artery thrombosis. Nonocclusive common carotid artery thrombosis was induced by a laser-driven rose bengal-mediated photochemical insult to the vascular endothelium, and the rats were killed 15 minutes or 3 hours later. Carotid arteries and brains were immediately removed and dissected for regional radioactivity assessment or sectioned for the autoradiographic visualization of platelet emboli. RESULTS: At 15 minutes after thrombosis, the ratio of right-to-left common carotid artery radioactivity was significantly elevated compared with control (33 +/- 12 [mean +/- SEM] versus 0.97 +/- 0.2). Within individual brain regions, including the frontal and frontoparietal cortices and hippocampus, significant elevations in right-to-left radioactivity ratios were also documented. Autoradiographic images revealed multiple foci of 111In-labeled platelets throughout the thrombosed hemisphere. At the level of the frontal cortex, bilateral platelet accumulation was seen. Regional counts demonstrated significantly increased platelet density within selective cortical and subcortical regions. In contrast to the 15-minute findings, right-to-left ratios of carotid arteries or brain regional radioactivities were not significantly elevated at 3 hours after injury. In addition, the areal densities of autoradiographically visualized platelets in the 3-hour group were not different from control except in the right frontal cortex. CONCLUSIONS: These data demonstrate (1) the acute accumulation of labeled platelets in downstream vessels after nonocclusive common carotid artery thrombosis, (2) that platelet accumulation is widespread and also involves contralateral areas, and (3) that platelet accumulation within the thrombosed carotid artery and brain is largely transient.
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A case is presented of cerebral infarction secondary to carotid artery thrombosis in a patient with hemolysis, elevated liver function, and low platelets (HELLP) syndrome. The patient's rebound thrombocytosis may have contributed to a hypercoagulable state. Severe preeclamptic patients with HELLP syndrome who experience a reactive thrombocytosis may represent a subset of women who have postpartum thrombosis.
Two cases of internal carotid artery thrombosis associated with a maxillary Le Fort III and mandibular angle fractures after maxillofacial blunt injuries are described. Both patients had delayed neurologic deficit and hemiparesis. The diagnosis was made by carotid angiography after clinical evidence of thromboembolism. Clinical aspects and etiology, with special attention to mechanism of injury, are discussed.
PURPOSE: To develop a porcine carotid artery thrombosis model for the evaluation of thrombolytic therapy and adjunctive angioplasty procedures. METHODS: Bilateral carotid thrombosis was induced in 16 pigs using endothelial crush injury followed by external polytetrafluoroethylene (PTFE, 5 x 2 cm2) wrap placement to create segmental carotid stenosis. Light microscopy was used to examine thrombus composition. Selective carotid catheterization was performed via a femoral approach. Two hours following carotid artery occlusion, a urokinase (250,000 IU) and heparin (1000 U) solution was pulse-sprayed in 1 carotid artery while the contralateral vessel received the control saline vehicle. The efficacy of thrombolytic therapy was assessed using carotid arteriography and intravascular ultrasound. The feasibility and technical efficacy of balloon angioplasty within the carotid stenosis model were also evaluated. RESULTS: Carotid artery occlusion occurred in 30 +/- 6 minutes following endothelial injury plus PTFE wrap placement. Histological examination of carotid arteries showed endothelial irregularity with fibrin-rich and platelet-rich thrombus. Urokinase was effective in recanalizing all occluded arteries (100%), while the control saline vehicle showed no effective thrombolysis (p < 0.001). Angioplasty was successful in restoring normal diameter in all arteries (100%). CONCLUSIONS: This carotid artery thrombosis model, which incorporates intimal injury with segmental stenosis, is simple to create and reproducible. It provides not only a model for the evaluation of thrombolytic therapy but also a practical training tool for adjunctive endovascular interventions.
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This is believed to be the first reported case of carotid artery thrombosis after elective maxillary or mandibular osteotomy. The most likely cause was a sudden, sharp blow to the right carotid artery region either when the mandibular split was completed or when the maxillary tuberosity was separated. The blow was associated with neck hyperextension and some lateral flexion. In a patient with tight, underdeveloped soft tissue, the resultant intimal tear caused thrombosis of the artery. Although this event is associated with a 40% mortality and further 52% serious morbidity, our patient has regained nearly full neurological function--probably thanks to a competent circle of Willis that allowed adequate collateral flow to the brain.
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The antithrombotic activity of a 2-kDa heparin fragment was studied in a rat model of common carotid artery thrombosis that causes a completely occlusive thrombus with cessation of the blood flow within 10-15 min. The compound reduced thrombus formation in a dose-dependent manner, starting from an intravenous dose of 5 mg kg-1. A dose of 20 mg kg-1 completely prevented thrombus formation and apparently induced the almost complete lysis of the already formed occlusive thrombus. At none of the doses used did the compound cause increased bleeding or the formation of haematomas. The present results indicate that low molecular weight heparins, which have an established, highly beneficial effect in venous thromboembolism, are also highly effective in an animal model of arterial thrombosis.
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INTRODUCTION: In the rat model of topical ferric chloride-induced carotid artery thrombosis, a transient blood flow velocity (VEL) increase is observed immediately following ferric chloride application. The immediacy of the response suggested vasoconstriction, as thrombotic narrowing of the vessel lumen was hypothesized to be too slow to account for the rapidity of the response. METHODS: To explore this phenomenon, the effects of two mechanistically distinct vasodilators, sodium nitroprusside (SNP) and hydralazine (HYD), on velocity increase, ex vivo platelet aggregation and thrombosis, were assessed in the rat ferric chloride-induced thrombosis model. RESULTS: Sodium nitroprusside (10, 30 and 50 microg/kg/min i.v.) and hydralazine (0.1, 0.3 and 1.0 mg/kg/min i.v.) reduced the mean arterial pressure with the higher dose regimens eliciting equivalent hypotensive effects. Both sodium nitroprusside and hydralazine blunted the initial velocity increase, but only sodium nitroprusside significantly reduced the incidence of thrombotic occlusion. No differences in ex vivo platelet aggregation responses to adenosine diphosphate (ADP), collagen (COLL) and arachidonic acid (AA) were observed between the sodium nitroprusside and hydralazine treatment groups. However, platelet aggregation response to thrombin was significantly reduced in the 50 microg/kg/min i.v. sodium nitroprusside compared to the 1.0 mg/kg/min i.v. hydralazine and vehicle groups. CONCLUSIONS: Inhibition of the initial velocity increase by two mechanistically distinct vasodilators, and the dissociation between this velocity change and antithrombotic efficacy, support the hypothesis that the early velocity increase results from a change in vascular tone rather than due to enhanced platelet activation and thrombus formation. Inhibition of thrombin-induced platelet activation may contribute to the antithrombotic actions of sodium nitroprusside in this preparation.