Traumatic basal subarachnoid hemorrhage due to rupture of the posterior inferior cerebellar artery--case report.
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A 20-year-old male presented with traumatic basal subarachnoid hemorrhage after being involved in a fight. Antemortem clinical examinations could not exclude the possibility of rupture of abnormal blood vessels because of the absence of external injuries. Careful postmortem examination of the head and neck regions and histological examination of the intracranial arteries demonstrated traumatic rupture of the left posterior inferior cerebellar artery due to a fist blow to the jaw. This case indicates the need for careful autopsy examination for the differentiation of traumatic and non-traumatic basal subarachnoid hemorrhages. (+info)
Treatment-related outcomes from blunt cerebrovascular injuries: importance of routine follow-up arteriography.
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OBJECTIVE: To assess the impact of routine follow-up arteriography on the management and outcome of patients with acute blunt cerebrovascular injuries (BCVI). SUMMARY BACKGROUND DATA: During the past 5 years there has been increasing recognition of BCVI, but the management of these lesions remains controversial. The authors previously proposed a grading system for BCVI, with grade-specific management guidelines. The authors have noted that a significant number of injuries evolve within 7 to 10 days, warranting alterations in therapy. METHODS: A prospective database of a regional trauma center's experience with BCVI has been maintained since 1990. A policy of arteriographic screening for BCVI based on injury mechanism (e.g., cervical hyperextension) and injury patterns (e.g., cervical and facial fractures) was instituted in 1996. A grading system was devised to develop management protocols: I = intimal irregularity; II = dissection/flap/thrombus; III = pseudoaneurysm; IV = occlusion; V = transection. RESULTS: From June 1990 to October 2001, 171 patients (115 male, age 36 +/- 1 years) were diagnosed with BCVI. Mean injury severity score was 28 +/- 1; associated injuries included brain (57%), spine (44%), chest (43%), and face (34%). Mechanism was motor vehicle crash in 50%, fall in 11%, pedestrian struck in 11%, and other in 29%. One hundred fourteen patients had 157 carotid artery injuries (43 bilateral), and 79 patients had 97 vertebral artery injuries (18 bilateral). The breakdown of injury grades was 137 grade I, 52 grade II, 32 grade III, 25 grade IV, and 8 grade V. One hundred fourteen (73%) carotid and 65 (67%) vertebral arteries were restudied with arteriography 7 to 10 days after the injury. Eight-two percent of grade IV and 93% of grade III injuries were unchanged. However, grade I and II lesions changed frequently. Fifty-seven percent of grade I and 8% of grade II injuries healed, allowing cessation of therapy, whereas 8% of grade I and 43% of grade II lesions progressed to pseudoaneurysm formation, prompting interventional treatment. There was no significant difference in healing or in progression of injuries whether treated with heparin or antiplatelet therapy or untreated. However, heparin may improve the neurologic outcome in patients with ischemic deficits and may prevent stroke in asymptomatic patients. CONCLUSIONS: Routine follow-up arteriography is warranted in patients with grade I and II BCVIs because most of these patients (61% in this series) will require a change in management. A prospective randomized trial will be necessary to identify the optimal treatment of BCVI. (+info)
Periprocedural morbidity and mortality associated with endovascular treatment of intracranial aneurysms.
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BACKGROUND AND PURPOSE: Despite experience and technological improvements, endovascular treatment of intracranial aneurysms still has inherent risks. We evaluated cerebral complications associated with this treatment. METHODS: From October 1998 to October 2002, 180 consecutive patients underwent 131 procedures for 118 ruptured aneurysms and 79 procedures for 72 unruptured aneurysms. We retrospectively reviewed their records and images to evaluate their morbidity and mortality. RESULTS: Thirty-seven (17.6%) procedure-related complications occurred: 27 and six with initial embolization of ruptured and unruptured aneurysms, respectively, and four with re-treatment. Complications included 22 cerebral thromboembolisms, nine intraprocedural aneurysm perforations, two coil migrations, two parent vessel injuries, one postprocedural aneurysm rupture, and one cranial nerve palsy. Fourteen complications had no neurologic consequence. Three caused transient neurologic morbidity; 10, persistent neurologic morbidity; and 10, death. Procedure-related neurologic morbidity and mortality rates, respectively, were as follows: overall, 4.8% and 4.8%; ruptured aneurysms, 5.9% and 7.6%; unruptured aneurysms, 1.4% and 1.4%; and re-treated aneurysms, 10% and 0%. Combined procedure-related morbidity and mortality rates for ruptured, unruptured, and re-treated aneurysms were 13.5%, 2.8%, and 10%, respectively. Nonprocedural complications attributable to subarachnoid hemorrhage in 118 patients with ruptured aneurysm were early rebleeding before coil placement (0.9%), symptomatic vasospasm (5.9%), and shunt-dependent hydrocephalus (5.9%); mortality from complications of subarachnoid hemorrhage itself was 11.9%. CONCLUSION: Procedural morbidity and mortality rates were highest in ruptured aneurysms and lowest in unruptured aneurysms. Morbidity rates were highest in re-treated aneurysms and lowest in unruptured aneurysms. No procedural mortality occurred with re-treated aneurysms. The main cause of morbidity and mortality was thromboembolism. (+info)
Reperfusion activates metalloproteinases that contribute to neurovascular injury.
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Influence of early antioxidant supplements on clinical evolution and organ function in critically ill cardiac surgery, major trauma, and subarachnoid hemorrhage patients.
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Association of MRI markers of vascular brain injury with incident stroke, mild cognitive impairment, dementia, and mortality: the Framingham Offspring Study.
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Chronic systemic infection exacerbates ischemic brain damage via a CCL5 (regulated on activation, normal T-cell expressed and secreted)-mediated proinflammatory response in mice.
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