CEREBRAL ARTERIAL SPASM AFTER PENETRATING CRANIOCEREBRAL GUNSHOT WOUNDS - TRANSCRANIAL DOPPLER AND CEREBRAL BLOOD-FLOW FINDINGS

Citation
Rk. Kordestani et al., CEREBRAL ARTERIAL SPASM AFTER PENETRATING CRANIOCEREBRAL GUNSHOT WOUNDS - TRANSCRANIAL DOPPLER AND CEREBRAL BLOOD-FLOW FINDINGS, Neurosurgery, 41(2), 1997, pp. 351-359
Citations number
46
Categorie Soggetti
Surgery,"Clinical Neurology
Journal title
ISSN journal
0148396X
Volume
41
Issue
2
Year of publication
1997
Pages
351 - 359
Database
ISI
SICI code
0148-396X(1997)41:2<351:CASAPC>2.0.ZU;2-8
Abstract
OBJECTIVE: The goals of the study were to determine the incidence and time course of cerebral arterial spasm in patients with penetrating cr aniocerebral gunshot wounds, to study the relationship between vasospa sm and subarachnoid hemorrhage (SAH) in these patients, and to evaluat e the effects of vasospasm on outcome. METHODS: Thirty-three patients with craniocerebral gunshot wounds underwent computed tomography at ad mission and then underwent transcranial doppler ultrasonography (TCD). Velocities in the middle cerebral artery and the extracranial interna l carotid artery were measured. Vasospasm was defined as a middle cere bral artery velocity greater than 120 cm per second and a hemispheric index (ratio of middle cerebral artery to internal carotid artery velo city) greater than 3. Intravenous xenon-133 cerebral blood flow (CBF) studies were performed for 10 patients. RESULTS: TCD was initiated, on average, 1.1 days after injury; 205 studies (mean, 6.3 studies/patien t) were performed 0 to 33 days after injury. TCD showed vasospasm in 1 4 patients (42.4%). Xenon-133 studies performed within 24 hours of TCD measurements indicating spasm demonstrated normal or low CBF in three of five patients with spasm, ruling out hyperemia as the cause of ele vated flow velocities in these three patients. Seven patients had unil ateral vasospasm, and seven had bilateral spasm. Vasospasm was most pr ominent from Days 5 through 11. Vasospasm was distributed across all l evels of injury severity, as defined by the Glasgow Coma Scale. Initia l computed tomographic scans demonstrated SAH in all 14 patients with vasospasm but in only 9 of 19 without spasm (100 versus 47%, P < 0.000 1, binomial distribution probability test). Outcomes for patients with vasospasm were slightly worse than for those without spasm (35.7 vers us 47.4% good outcomes, respectively); however, this difference did no t reach statistical significance (P = 0.12). CONCLUSION: These finding s demonstrate that delayed cerebral arterial spasm is a frequent compl ication in patients with craniocerebral gunshot wounds and is strongly associated with SAH. The frequency, time course, and severity of spas m are comparable with those observed with aneurysmal SAH and traumatic SAH caused by closed head injury. This study offers new insights into the hemodynamic pathophysiology after gunshot wounds to the brain and suggests that increased vigilance for vasospasm may be of benefit.