Journal of neurosurgery · 2015
Aneurysm location and clipping versus coiling for development of secondary normal-pressure hydrocephalus after aneurysmal subarachnoid hemorrhage: Japanese Stroke DataBank.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Yamada Shigeki, Ishikawa Masatsune, Yamamoto Kazuo, Ino Tadashi, Kimura Toru, Kobayashi Shotai, Japan Standard Stroke Registry Study Group
Аннотация
OBJECT: The present study aimed to investigate aneurysm locations and treatments for ruptured cerebral aneurysms associated with secondary normal-pressure hydrocephalus (sNPH) after subarachnoid hemorrhage (SAH) by using comprehensive data from the Japanese Stroke DataBank.
METHODS: Among 101,165 patients with acute stroke registered between 2000 and 2013, 4693 patients (1482 men, 3211 women) were registered as having had an SAH caused by a ruptured saccular aneurysm. Of them, 1448 patients (438 men and 1010 women; mean age 61.9 ± 13.4 years) who were confirmed to have or not have coexisting acute hydrocephalus and sNPH were included for statistical analyses. Locations of the ruptured aneurysms were subcategorized into 1 of the following 4 groups: middle cerebral artery (MCA; n = 354), anterior communicating artery and anterior cerebral artery (ACA; n = 496), internal carotid artery (ICA; n = 402), and posterior circulation (n = 130). Locations of 66 of the ruptured aneurysms were unknown/unrecorded. Treatments included craniotomy and clipping alone in 1073 patients, endovascular coil embolization alone in 285 patients, and a combination of coiling and clipping in 17 patients. The age-adjusted and multivariate odds ratios from logistic regression analyses were calculated after stratification using the Fisher CT scale to investigate the effects of the hematoma volume of SAH.
RESULTS: Acute hydrocephalus was confirmed in 593 patients, and 521 patients developed sNPH. Patients with a ruptured ACA aneurysm had twice the risk for sNPH over those with a ruptured MCA aneurysm. Those with an ACA aneurysm with Fisher Grade 3 SAH had a 9-fold-higher risk for sNPH than those with an MCA aneurysm with Fisher Grade 1 or 2 SAH. Patients with a ruptured posterior circulation aneurysm did not have any significant risk for sNPH. Clipping of the ruptured aneurysm resulted in twice the risk for sNPH over coil embolization alone.
CONCLUSIONS: Patients with low-grade SAH caused by a ruptured MCA aneurysm had a low risk for the development of sNPH. In contrast, patients with high-grade SAH caused by a ruptured ACA aneurysm had a higher risk for sNPH. Endovascular coiling might confer a lower risk of developing sNPH than microsurgical clipping.
METHODS: Among 101,165 patients with acute stroke registered between 2000 and 2013, 4693 patients (1482 men, 3211 women) were registered as having had an SAH caused by a ruptured saccular aneurysm. Of them, 1448 patients (438 men and 1010 women; mean age 61.9 ± 13.4 years) who were confirmed to have or not have coexisting acute hydrocephalus and sNPH were included for statistical analyses. Locations of the ruptured aneurysms were subcategorized into 1 of the following 4 groups: middle cerebral artery (MCA; n = 354), anterior communicating artery and anterior cerebral artery (ACA; n = 496), internal carotid artery (ICA; n = 402), and posterior circulation (n = 130). Locations of 66 of the ruptured aneurysms were unknown/unrecorded. Treatments included craniotomy and clipping alone in 1073 patients, endovascular coil embolization alone in 285 patients, and a combination of coiling and clipping in 17 patients. The age-adjusted and multivariate odds ratios from logistic regression analyses were calculated after stratification using the Fisher CT scale to investigate the effects of the hematoma volume of SAH.
RESULTS: Acute hydrocephalus was confirmed in 593 patients, and 521 patients developed sNPH. Patients with a ruptured ACA aneurysm had twice the risk for sNPH over those with a ruptured MCA aneurysm. Those with an ACA aneurysm with Fisher Grade 3 SAH had a 9-fold-higher risk for sNPH than those with an MCA aneurysm with Fisher Grade 1 or 2 SAH. Patients with a ruptured posterior circulation aneurysm did not have any significant risk for sNPH. Clipping of the ruptured aneurysm resulted in twice the risk for sNPH over coil embolization alone.
CONCLUSIONS: Patients with low-grade SAH caused by a ruptured MCA aneurysm had a low risk for the development of sNPH. In contrast, patients with high-grade SAH caused by a ruptured ACA aneurysm had a higher risk for sNPH. Endovascular coiling might confer a lower risk of developing sNPH than microsurgical clipping.