Abstract
BackgroundAlthough coagulopathy have been proved to be a contributor to a poor outcome of aneurysmal subarachnoid hemorrhage (aSAH), the risk factors for triggering coagulation abnormalities have not been studied after aneurysm clipping.MethodsWe investigated risk factors of coagulopathy and analyzed the relationship between acute coagulopathy and outcome after aneurysm clipping. The clinical data of 137 patients with ruptured CA admitted to our institution was collected and retrospectively reviewed. Patient demographic data (age, sex), smoking, alcohol use, hypertension, diabetes, Hunt-Hess grade, Fisher grade, operation time, intraoperative total infusion volume, intraoperative blood loss, intraoperative transfusion, intraoperative hemostatic drug treatment, calcium reduction (preoperative free calcium concentration–postoperative free calcium concentration) were recorded. Coagulation was assessed within 24 h. Postoperative hemorrhage and infarction, deep venous thrombosis (DVT), and mortality were analyzed.ResultsCoagulopathy was detected in a total of 51 cases (group I), while not in 86 cases (group II). Univariable analysis demonstrated that age, smoking, alcohol use, intraoperative total infusion volume, intraoperative blood loss, intraoperative transfusion, and calcium reduction (≥ 1.2 mg/dl) were related to coagulopathy. Non-conditional logistic regression analysis showed that age [OR, 1.037 (95% CI, 1.001–1.074); p = 0.045] and calcium reduction (≥ 1.2 mg/dl) [OR, 5.509 (95% CI, 1.900–15.971); p = 0.002] were considered as the risk factors for coagulopathy. Hunt-Hess grade [OR, 2.641 (95% CI, 1.079–6.331); p = 0.033] and operation time [OR, 0.107 (95% CI, 1.012–0.928); p = 0.043] were considered as the risk factors for hypocoagulopathy. There were 6 cases (11.7%) with cerebral infarction in group I, while 6 cases (6.98%) in group II (χ2 = 0.918, p = 0.338). There were 4 cases (7.84%) with rebleeding in group I, while 5 cases (5.81%) in group II (χ2 = 0.215, p = 0.643). The mortality was 9.80% (5/51) in group I, while 1.16% (1/86) in group II (χ2 = 5.708, p = 0.017). DVT was not detected in all cases.ConclusionsIn conclusion, age (≥ 65 years) and calcium reduction (≥ 1.2 mg/dl) were considered as the risk factors for coagulopathy and have been proved to be associated with higher mortality after aneurysm clipping.
Highlights
Coagulopathy have been proved to be a contributor to a poor outcome of aneurysmal subarachnoid hemorrhage, the risk factors for triggering coagulation abnormalities have not been studied after aneurysm clipping
Neurosurgical clipping following aneurysmal subarachnoid hemorrhage (aSAH) prevents rerupture of aneurysms, reduces the mortality and cognition, and improves the Glasgow Coma Scale (GCS), neurological deficits were detected after intracranial aneurysm clipping [3,4,5,6,7]
There were a total of 252 aneurysms: 13 located at anterior cerebral artery (ACA), 32 at the posterior communicating artery (PCoA), at the middle cerebral artery (MCA), at the anterior communicating artery (ACoA), 52 at the internal carotid artery (ICA), 3 at the posterior cerebral artery (PCA), 4 at the ophthalmic artery, 7 at the anterior choroidal artery, 1 at the basilar artery, and 2 at vertebral artery
Summary
Coagulopathy have been proved to be a contributor to a poor outcome of aneurysmal subarachnoid hemorrhage (aSAH), the risk factors for triggering coagulation abnormalities have not been studied after aneurysm clipping. Aneurysmal subarachnoid hemorrhage (aSAH) accounts for 3–5% of strokes, which is serious harmful to human health for its high mortality and morbidity [1, 2]. Neurosurgical clipping following aSAH prevents rerupture of aneurysms, reduces the mortality and cognition, and improves the Glasgow Coma Scale (GCS), neurological deficits were detected after intracranial aneurysm clipping [3,4,5,6,7]. Elevated serum fibrinogen degradation product (FDP) was associated with intracranial hemorrhage and mass effect following TBI [10]. Coagulative/fibrinolytic abnormalities are the frequently cause for intracranial re-hemorrhage [11]. Giroud et al demonstrated that significant activation of the coagulation was observed in the patients with cortical infarction [13]
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