Non-penetrating trauma to the carotid artery with secondary thrombosis and embolism: Treatment by Thrombolysin

101

SUMMARYThe capacity of intracarotid Infusion of urokinase to salvage neurologic function in a baboon model of acute thrombotk stroke has been studied. The model consists of reversible eccentric balloon compression (3 hours) of the right middle cerebral artery (MCA) proximal to the take-off of the lentlculostriate arteries (LSA), resulting in in situ thrombosis of perforating branches supplying the right corpus striatum. Neurologic endpoints included quantitative assessment of neurologic function (NE), estimation of cerebral infarction volume by computerized tomographic (CT) scan, and carotid angiography. In untreated acute stroke control animals (n = 6), a persistent decrease in functional score (from 100 to 36 ± 11) at 14 days and a defined region of cerebral infarction (volume = 3.2 ± 1.5) were detected at 10 days. Intracarotid urokinase administered to five animals (1.2 x 10* II) over 60 min) following the 3 hour period of MCA occlusion improved neurologic function (NE = 50, 55, 85,100,100) and reduced infarction size (0.3, 0.5, 0.8,0.7,1.1 cm 3 , respectively) without evidence of intracranial hemorrhage. Systemk fibrinogenolysis was produced in all five treated animals. We conclude that thrombolytic therapy given within 3 hours of experimental thrombotic ocdusion may salvage neurologic function and reduce cerebral Infarction volume without CT scan detectable intracranial bleeding.

Section: Discussionmentioning

confidence: 88%

The beneficial effect of intracarotid urokinase on acute stroke in a baboon model.

Zoppo¹,

Copeland²,

Waltz³

et al. 1986

101

“…and selected peripheral arteries, 15 ' 23~34 traumatic internal carotid artery occlusion, 35 as well as of pulmonary embolism 36 " 39 and peripheral deep venous thrombosis.…”

mentioning

confidence: 99%

Thrombolytic therapy in stroke: possibilities and hazards.

Zoppo¹,

Zeumer²,

Harker³

1986

202

patients with various thrombolytic agents, and to weigh the relative risk of intracerebral hemorrhage in patients treated with fibrinolytic agents for stroke and for other thrombotic disorders. Mechanism of ThrombolysisArterial thrombosis and thrombus extension involve to varying degrees the processes of endothelial injury, platelet aggregation and release, and thrombin generation. Thrombin-mediated fibrinogen cleavage results in fibrin formation which is required for thrombus stabilization.80 Thrombin-mediated fibrin formation occurs in direct relation to platelet activation by several mechanisms. Platelets promote activation of the early stages of intrinsic coagulation by a process that involves a factor XI receptor and high molecular weight kininogen.81 Also, factors V and VHI interact with platelet membrane phospholipids to facilitate the activation of factor X to Xa and the conversion of prothrombin to thrombin.82 Platelet-bound thrombinmodified factor V (factor Va) serves as a high affinity platelet receptor for factor Xa. 83 Consequently, the rate of thrombin generation is accelerated 10 3 fold, providing a potent positive feedback mechanism for initiation of thrombin formation on the platelet surface, fibrin network formation in the thrombus, and indirectly, fibrinolysis.Thrombus dissolution is, in large part, mediated by fibrinolysis localized within the thrombus.84 " 86 Fibrin (and fibrinogen) degradation is catalyzed by plasmin, the product of plasminogen activation. 87 In the consolidating thrombus plasminogen binds to fibrin and to platelets, allowing local release of plasmin within the thrombus. The circulating plasminogen activators, tissue plasminogen activator (tPA) and single chain urokinase plasminogen activator (scuPA), catalyze plasby guest on

“…An early review noted a high morbidity (50%) and mortality (40%), 10 but if those patients diagnosed only at autopsy are excluded, the mortality drops to 30%. 6 More recently, rates of 20-30% have been reported 8 ' " and one small series noted no mortality. 8 The diagnosis of traumatic ICA dissection is made angiographically, although, as noted above, it is usually the fortuitous finding of angiography in a head-injured patient who is deteriorating.…”

Section: Discussionmentioning

confidence: 99%

Traumatic dissection of the internal carotid artery treated by ECIC anastomosis.

Bergquist¹,

Boone²,

Whaley³

1981

INTERNAL CAROTID ARTERY (ICA) dissection following blunt trauma to the head and neck is a well described, but uncommon entity. The patient, usually a young male involved in a motor vehicle accident, presents with hemispheric symptoms after a lucid interval of hours to days. Ultimate outcome and treatment are highly variable. We describe a patient with traumatic ICA dissection, who was treated by extracranial-intracranial (ECIC) anastomosis and a middle cerebral artery embolectomy. S.B., a 20-year-old, right-handed male was admitted to the Neurosurgery Service at the University of North Carolina because of suspected left internal carotid artery occlusion. He was in good health until August 19, 1978, when he was involved in a motor vehicle accident. He was riding in the passenger's seat during a low speed, front end collision. On the collision he struck his head and neck on the steering wheel and dashboard. Following an unconscious interval of 15-20 minutes, he recovered in a local hospital. No focal neurologic deficits were recorded, but he did complain of persistent headache and left neck pain. A dynamic radionuclide brain scan demonstrated decreased flow on the left side, and he was transferred to the University of North Carolina for further evaluation. His medical history was complicated by a Wolfe-Parkinson-White syndrome which had occasionally caused supraventricular tachycardia.Examination revealed an alert, healthy, young male with minimal tenderness of the left neck anteriorly, but no apparent trauma. There were no bruits and the neurological examination was normal. Admission laboratory studies and plain skull and cervical spine radiographs were normal. Non-invasive vascular studies were then carried out. Carotid phonoangiography (CPA) did not demonstrate a bruit on either side, while Kartchner-McRae occuloplethysmography (OPG) showed a differential pulse skewed to the left. These indicated a left carotid stenosis of 85-100%.1 The Gee OPG 2 showed a significant decrease in the left ophthalmic artery pressure relative to the right and a significantly decreased ophthalmic From the Division of Neurosurgery, Department of Surgery, and Department of Radiology, University of North Carolina, Chapel Hill, NC 27514.Reprints-Division Neurosurgery, Department Surgery, University of North Carolina, Chapel Hill, NC 27514. artery/brachial artery pressure ratio. These findings prompted a transfemoral bilateral carotid arteriogram, which revealed an 80% left ICA stenosis secondary to dissection, beginning 3 centimeters distal to the bifurcation of the common carotid artery and extending to the base of the skull ( fig. 1). As the patient remained asymptomatic, he was discharged the following morning. That evening (10 days post trauma), he experienced a syncopal spell lasting a few minutes following which he could not speak to, but apparently understood his father.He was readmitted to the Neurosurgery Service approximately one hour later, at which time he was again without neurological deficit. Repeat carotid arteriography...