Baseline characteristics and outcome for aneurysmal versus non-aneurysmal subarachnoid hemorrhage: a prospective cohort study

AbstractThis study aims to investigate the characteristics of patients with mild aneurysmal and non-aneurysmal perimesencephalic and non-perimesencephalic subarachnoid hemorrhage (aSAH, pmSAH, npmSAH) with emphasis on admission biomarkers, clinical course, and outcome. A prospective cohort of 115 patients with aSAH (Hunt and Hess 1–3) and of 35 patients without aneurysms (16 pmSAH and 19 npmSAH) admitted between January 2014 and January 2020 was included. Demographic data, blood samples on admission, complications (hydrocephalus, shunt dependency, delayed cerebral ischemia DCI, DCI-related infarction, and mortality), and outcome after 6 months were analyzed. Demographic data was comparable between all groups except for age (aSAH 55 [48–65] vs. npmSAH 60 [56–68] vs. pmSAH 52 [42–60], p = 0.032) and loss of consciousness (33% vs. 0% vs. 0%, p = 0.0004). Admission biomarkers showed poorer renal function and highest glucose levels for npmSAH patients. Complication rate in npmSAH was high and comparable to that of aSAH patients (hydrocephalus, shunt dependency, DCI, DCI-related infarction, mortality), but nearly absent in patients with pmSAH. Favorable outcome after 6 months was seen in 92.9% of pmSAH, 83.3% of npmSAH, and 62.7% of aSAH (p = 0.0264). In this prospective cohort of SAH patients, npmSAH was associated with a complicated clinical course, comparable to that of patients with aSAH. In contrast, such complications were nearly absent in pmSAH patients, suggesting fundamental differences in the pathophysiology of patients with different types of non-aneurysmal hemorrhage. Our findings underline the importance for a precise terminology according the hemorrhage etiology as a basis for more vigilant management of npmSAH patients. NCT02142166, 05/20/2014, retrospectively registered.

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Plasma glucose levels and outcome after aneurysmal subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/jns.1993.79.6.0885 ◽

1993 ◽

Vol 79 (6) ◽

pp. 885-891 ◽

Cited By ~ 87

Author(s):

Giuseppe Lanzino ◽

Neal F. Kassell ◽

Teresa Germanson ◽

Laura Truskowski ◽

Wayne Alves

Keyword(s):

Subarachnoid Hemorrhage ◽

Plasma Glucose ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Delayed Cerebral Ischemia ◽

Ct Scans ◽

Good Recovery ◽

Glucose Levels ◽

Poor Outcome ◽

Elevated Glucose ◽

Mean Glucose

✓ Plasma glucose levels were studied in 616 patients admitted within 72 hours after subarachnoid hemorrhage (SAH). Glucose levels measured at admission showed a statistically significant association with Glasgow Coma Scale scores, Botterell grade, deposition of blood on computerized tomography (CT) scans, and level of consciousness at admission. Elevated glucose levels at admission predicted poor outcome. A good recovery, as assessed by the Glasgow Outcome Scale at 3 months, occurred in 70.2% of patients with normal glucose levels (≤ 120 mg/dl) and in 53.7% of patients with hyperglycemia (> 120 mg/dl) (p = 0.002). The death rates for these two groups were 6.7% and 19.9%, respectively (p = 0.001). The association was still maintained after adjusting for age (> or ≤ 50 years) and thickness of clot on CT scans (thin or thick) in the subset of patients who were alert/drowsy at admission. Increased mean glucose levels between Days 3 and 7 also predicted a worse outcome; good recovery was observed in 132 (73.7%) of 179 patients who had normal mean glucose levels (≤ 120 mg/dl) and 160 (49.7%) of 322 who had elevated mean glucose levels (> 120 mg/dl) (p < 0.0001). Death occurred in 6.7% and 20.8% of the two groups, respectively (p < 0.0001). It is concluded that admission plasma glucose levels can serve as an objective prognostic indicator after SAH. Elevated glucose levels during the 1st week after SAH also predict a poor outcome. However, a causal link between hyperglycemia and outcome after delayed cerebral ischemia, although suggested by experimental data, cannot be established on the basis of this study.

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Associations of renin-angiotensin system genetic polymorphisms and clinical course after aneurysmal subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/2016.4.jns16409 ◽

2017 ◽

Vol 126 (5) ◽

pp. 1585-1597 ◽

Cited By ~ 7

Author(s):

Christoph J. Griessenauer ◽

R. Shane Tubbs ◽

Paul M. Foreman ◽

Michelle H. Chua ◽

Nilesh A. Vyas ◽

...

Keyword(s):

Single Nucleotide Polymorphism ◽

Subarachnoid Hemorrhage ◽

Clinical Course ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Delayed Cerebral Ischemia ◽

Renin Angiotensin System ◽

Nucleotide Polymorphism ◽

Single Nucleotide ◽

Angiotensin System ◽

Renin Angiotensin

OBJECTIVERenin-angiotensin system (RAS) genetic polymorphisms are thought to play a role in cerebral aneurysm formation and rupture. The Cerebral Aneurysm Renin Angiotensin System (CARAS) study prospectively evaluated associations of common RAS polymorphisms and clinical course after aneurysmal subarachnoid hemorrhage (aSAH).METHODSThe CARAS study prospectively enrolled aSAH patients at 2 academic centers in the United States. A blood sample was obtained from all patients for genetic evaluation and measurement of plasma angiotensin converting enzyme (ACE) concentration. Common RAS polymorphisms were detected using 5′exonuclease genotyping assays and pyrosequencing. Analysis of associations of RAS polymorphisms and clinical course after aSAH were performed.RESULTSA total of 166 patients were screened, and 149 aSAH patients were included for analysis. A recessive effect of allele I (insertion) of the ACE I/D (insertion/deletion) polymorphism was identified for Hunt and Hess grade in all patients (OR 2.76, 95% CI 1.17–6.50; p = 0.0206) with subsequent poor functional outcome. There was a similar effect on delayed cerebral ischemia (DCI) in patients 55 years or younger (OR 3.63, 95% CI 1.04–12.7; p = 0.0439). In patients older than 55 years, there was a recessive effect of allele A of the angiotensin II receptor Type 2 (AT2) A/C single nucleotide polymorphism (SNP) on DCI (OR 4.70, 95% CI 1.43–15.4; p = 0.0111).CONCLUSIONSBoth the ACE I/D polymorphism and the AT2 A/C single nucleotide polymorphism were associated with an age-dependent risk of delayed cerebral ischemia, whereas only the ACE I/D polymorphism was associated with poor clinical grade at presentation. Further studies are required to elucidate the relevant pathophysiology and its potential implication in the treatment of patients with aSAH.

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Comparison of Initial Vasopressors Used for Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage

Cerebrovascular Diseases ◽

10.1159/000458536 ◽

2017 ◽

Vol 43 (5-6) ◽

pp. 266-271 ◽

Cited By ~ 9

Author(s):

Bhaskar Roy ◽

Louise D. McCullough ◽

Rajat Dhar ◽

James Grady ◽

Yu-Bo Wang ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Cerebral Ischemia ◽

Adverse Effects ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Delayed Cerebral Ischemia ◽

Response To Therapy ◽

Discharge Disposition ◽

Induced Hypertension ◽

Baseline Characteristics ◽

The Impact

Background: The main reason for morbidity after aneurysmal subarachnoid hemorrhage (aSAH) is delayed cerebral ischemia (DCI). The mainstay of medical therapy for treating DCI is induced hypertension with vasopressors to restore cerebral perfusion. Both phenylephrine (PE) and norepinephrine (NE) are commonly used for induced hypertension, but the impact of the initial choice of vasopressor on the efficacy, adverse effects, or outcome after hemodynamic therapy for DCI is unknown. Methods: Sixty-three patients with aSAH between January 2012 and October 2014, who developed DCI (defined as new focal deficit or decline in Glasgow Coma Score) and in which PE (n = 45) or NE (n = 18) treatment was initiated were evaluated in this retrospective study. Baseline characteristics, adverse effects, the need to change or add vasopressors, the response to therapy, the need for endovascular therapy, new infarct development, discharge disposition, and 3 months modified Rankin score were all compared between pressor groups. Results: Baseline characteristics (e.g., Hunt Hess and Fisher grades) were similar. There were no differences in the overall rate of complications including arrhythmia, pulmonary edema, or kidney injury. However, those initiated on PE were more likely to be changed to an alternate vasopressor (64 vs. 33%, p = 0.016), mostly for bradycardia or failure to reach therapeutic targets. Patients initially treated with PE were less likely to respond neurologically (71 vs. 94%, p = 0.01) or to be discharged to home or acute rehabilitation facilities (73 vs. 94%, p = 0.02) and were more likely to have a delayed infarct on imaging (62 vs. 33%, p = 0.04). Conclusions: Our study suggests that patients with DCI after aSAH initiated on PE are more likely to require treatment change to another vasopressor and are at greater risk for poor clinical outcomes compared to patients started on NE. Larger comparative studies are warranted.

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