Predictors of unfavourable outcome in aneurysmal subarachnoid haemorrhage

Abstract

Background. Mortality rates following aneurysmal subarachnoid haemorrhage (aSAH) have decreased due to improvements in diagnoses and the management of complications, as well as early obliteration of the aneurysms. Neurogenic pulmonary oedema (NPO) is a clinical syndrome associated with an acute increase in intracranial pressure and a release of catecholamines into the circulation. This study investigated independent predictors of unfavourable outcomes (Glasgow Outcome Scores 1, 2 or 3) in patients with aSAH. Materials and methods.A total of 262 patients with aSAH (162 females) were included in this prospective study. Clinical characteristics were assessed, and electrocardiographic, serum cardiac and inflammatory biomarker measurements were recorded on admission. Outcomes were assessed three months after admission. Univariate and multivariate analyses of these data were used to predict unfavourable outcomes. Results.A total of 156 patients (59.54%) had unfavourable outcomes. Compared to those who had favourable outcomes, patients with unfavourable outcomes were significantly older (54.37 ± 10.56 vs. 49.13 ± 10.77 years; p < 0.001) and had more severe aSAHs (Hunt and Hess grades ≥ 3: 82.7% vs. 39.6%; p < 0.001). Patients with unfavourable outcomes were more likely to have NPO (10.3% vs. 2.8%; p = 0.023), hydrocephalus (34.0% vs. 20.8%; p = 0.02), and aneurysm reruptures (28.2% vs. 3.8%; p < 0.001). Independent predictors of an unfavourable outcome included Hunt and Hess grades ≥ 3 (odds ratio [OR], 4.291; 95% confidence interval [CI], 2.168-8.491; p < 0.001), increased systolic blood pressure on admission (OR, 1.020; 95% CI, 1.002-1.038; p = 0.03), increased heart rate (HR) on admission (OR, 1.024; 95% CI, 1.001-1.048; p = 0.04), and aneurysm rerupture (OR, 4.961; 95% CI,; p = 0.01).Conclusions. These findings suggest that aneurysm reruptures, as well as increased blood pressure and HR, are associated with unfavourable outcomes in patients with aSAH.

Prognostic factors affecting the ruptured intracranial aneurysms: A 9-year multicenter study in Fujian, China

“…Hypertension may cause extensive intimal hyperplasia, causing poor surgical vascular conditions to increase the difficulty of the operation and raising cerebral edema risk and secondary bleeding greatly. [ 26 ] Nastasovic et al [ 27 ] demonstrated that 46% of patients developing CVS after aSAH suffered from hypertension, which indicated that the hypertensive population was susceptible to the complications of IAs rupture, and adverse prognostic events. Furthermore, Kurtz revealed that blood glucose was positively correlated with stroke mortality.…”

“…[ 28 ] A large-scale follow-up study found that elevated blood glucose was significantly associated with mortality within 14 days after aSAH, and further confirmed the significant impact of glucose on stroke prognosis. [ 27 ] There is extensive systemic inflammatory basis for diabetics, and SAH induces intracranial hypertension and cerebral edema, affecting neuroendocrine function and insulin resistance. [ 29 ] Moreover, hyperglycemia induced the expression of p-selectin and von Willebrand factor (vWF), enhancing platelet activation and the release of intracellular oxidative stress to further aggravate the systemic inflammatory injury.…”

Endovascular treatment of vertebrobasilar system aneurysms — long term results

“…As far as the clinical results at admission were concerned, the majority of our patients were hypertensive and tachycardic (average blood pressure 143/87 mmHg, average heart rate 83). In their recent paper, Nastasovic et al concluded that increased blood pressure and HR are associated with unfavourable outcomes in patients treated due to ruptured intracranial aneurysms [17].…”

Recanalisation of cerebral artery aneurysms treated endovascularly — a midterm follow-up

“…flow velocity and wall shear stress) indicates a significantly lower amplitude reduction of the velocity on the neck plane in patients undergoing recanalisation [22,23]. The role of inflammation in the recanalisation process is not yet established, which is probably important bearing in mind other factors in the process of formation, progression and rupture of aneurysms [24,25].…”