Aneurysmal Subarachnoid Hemorrhage: Neurosurgical Frontiers and Nursing Challenges

1991 ◽  
Vol 2 (4) ◽  
pp. 665-674
Author(s):  
Helen A. Cook

Despite increases in survival beyond the initial hemorrhage, the devastating consequences of subarachnoid hemorrhage persist. Ruptured intracranial aneurysms are the most likely cause of subarachnoid hemorrhage, with morbidity and mortality rates approaching 75%. Complications arising from aneurysmal subarachnoid hemorrhage include rebleeding, delayed cerebral ischemia, hydrocephalus, hypothalamic dysfunction, and seizure activity. In order to positively influence outcome after subarachnoid hemorrhage, preservation of an adequate cerebral blood flow and prevention of secondary aneurysmal rupture is essential. This article reviews aneurysmal subarachnoid hemorrhage, relating the management of complications to currently accepted treatment strategies

2015 ◽  
Vol 123 (4) ◽  
pp. 862-871 ◽  
Author(s):  
Matthew R. Reynolds ◽  
Robert T. Buckley ◽  
Santoshi S. Indrakanti ◽  
Ali H. Turkmani ◽  
Gerald Oh ◽  
...  

OBJECT Vasopressor-induced hypertension (VIH) is an established treatment for patients with aneurysmal subarachnoid hemorrhage (SAH) who develop vasospasm and delayed cerebral ischemia (DCI). However, the safety of VIH in patients with coincident, unruptured, unprotected intracranial aneurysms is uncertain. METHODS This retrospective multiinstitutional study identified 1) patients with aneurysmal SAH and 1 or more unruptured, unprotected aneurysms who required VIH therapy (VIH group), and 2) patients with aneurysmal SAH and 1 or more unruptured, unprotected aneurysms who did not require VIH therapy (non-VIH group). All patients had previously undergone surgical or endovascular treatment for the presumed ruptured aneurysm. Comparisons between the VIH and non-VIH patients were made in terms of the patient characteristics, clinical and radiographic severity of SAH, total number of aneurysms, number of ruptured/unruptured aneurysms, aneurysm location/size, number of unruptured and unprotected aneurysms during VIH, severity of vasospasm, degree of hypervolemia, and degree and duration of VIH therapy. RESULTS For the VIH group (n = 176), 484 aneurysms were diagnosed, 231 aneurysms were treated, and 253 unruptured aneurysms were left unprotected during 1293 total days of VIH therapy (5.12 total years of VIH therapy for unruptured, unprotected aneurysms). For the non-VIH group (n = 73), 207 aneurysms were diagnosed, 93 aneurysms were treated, and 114 unruptured aneurysms were left unprotected. For the VIH and non-VIH groups, the mean sizes of the ruptured (7.2 ± 0.3 vs 7.8 ± 0.6 mm, respectively; p = 0.27) and unruptured (3.4 ± 0.2 vs 3.2 ± 0.2 mm, respectively; p = 0.40) aneurysms did not differ. The authors observed 1 new SAH from a previously unruptured, unprotected aneurysm in each group (1 of 176 vs 1 of 73 patients; p = 0.50). Baseline patient characteristics and comorbidities were similar between groups. While the degree of hypervolemia was similar between the VIH and non-VIH patients (fluid balance over the first 10 days of therapy: 3146.2 ± 296.4 vs 2910.5 ± 450.7 ml, respectively; p = 0.67), VIH resulted in a significant increase in mean arterial pressure (mean increase over the first 10 days of therapy relative to baseline: 125.1% ± 1.0% vs 98.2% ± 1.2%, respectively; p < 0.01) and systolic blood pressure (125.6% ± 1.1% vs. 104.1% ± 5.2%, respectively; p < 0.01). CONCLUSIONS For small, unruptured, unprotected intracranial aneurysms in SAH patients, the frequency of aneurysm rupture during VIH therapy is rare. The authors do not recommend withholding VIH therapy from these patients.


2015 ◽  
Vol 35 (7) ◽  
pp. 1163-1168 ◽  
Author(s):  
Kenji Shimada ◽  
Hajime Furukawa ◽  
Kosuke Wada ◽  
Yuan Wei ◽  
Yoshiteru Tada ◽  
...  

Angiotensin-(1-7) (Ang-(1-7)) can regulate vascular inflammation and remodeling, which are processes that have important roles in the pathophysiology of intracranial aneurysms. In this study, we assessed the effects of Ang-(1-7) in the development of intracranial aneurysm rupture using a mouse model of intracranial aneurysms in which aneurysmal rupture (i.e., aneurysmal subarachnoid hemorrhage) occurs spontaneously and causes neurologic symptoms. Treatment with Ang-(1-7) (0.5 mg/kg/day), Mas receptor antagonist (A779 0.5 mg/kg/day or 2.5 mg/kg/day), or angiotensin II type 2 receptor (AT2R) antagonist (PD 123319, 10 mg/kg/day) was started 6 days after aneurysm induction and continued for 2 weeks. Angiotensin-(1-7) significantly reduced the rupture rate of intracranial aneurysms without affecting the overall incidence of aneurysms. The protective effect of Ang-(1-7) was blocked by the AT2R antagonist, but not by the Mas receptor antagonist. In AT2R knockout mice, the protective effect of Ang-(1-7) was absent. While AT2R mRNA was abundantly expressed in the cerebral arteries and aneurysms, Mas receptor mRNA expression was very scarce in these tissues. Angiotensin-(1-7) reduced the expression of tumor necrosis factor-α and interleukin-1β in cerebral arteries. These findings indicate that Ang-(1-7) can protect against the development of aneurysmal rupture in an AT2R-dependent manner.


2009 ◽  
Vol 26 (5) ◽  
pp. E2 ◽  
Author(s):  
Rohan R. Lall ◽  
Christopher S. Eddleman ◽  
Bernard R. Bendok ◽  
H. Hunt Batjer

Aneurysmal subarachnoid hemorrhage continues to have high rates of morbidity and mortality for patients despite optimal medical and surgical management. Due to the fact that aneurysmal rupture can be such a catastrophic event, preventive treatment is desirable for high-risk lesions. Given the variability of the literature evaluating unruptured aneurysms regarding basic patient population, clinical practice, and aneurysm characteristics studied, such as size, location, aspect ratio, relationship to the surrounding vasculature, and the aneurysm hemodynamics, a metaanalysis is nearly impossible to perform. This review will instead focus on the various anatomical and morphological characteristics of aneurysms reported in the literature with an attempt to draw broad inferences and serve to highlight pressing questions for the future in our continued effort to improve clinical management of unruptured intracranial aneurysms.


2020 ◽  
Vol 54 (2) ◽  
Author(s):  
Ronnie E. Baticulon ◽  
Kevin Ivan P. Chan ◽  
Peter Paul P. Rivera ◽  
Gerardo D. Legaspi ◽  
Willy G. Lopez

Objectives. To identify factors that predict the occurrence of seizures in patients with aneurysmal subarachnoid hemorrhage (SAH) and to evaluate the efficacy of antiepileptic drugs (AEDs) in preventing in-hospital seizures among patients who undergo clip occlusion of ruptured intracranial aneurysms. Methods. In this retrospective study, the medical charts of 205 patients admitted for aneurysmal SAH in Philippine General Hospital (PGH) and who underwent craniotomy and clipping of aneurysm from January 2011 to June 2014 were reviewed. Demographic, radiologic, and clinical factors were converted into categorical variables and their association with the occurrence of seizures analyzed. The incidence of seizures among patients who received an AED (AED cohort) and those who did not receive an AED (No AED cohort) were compared. Secondarily, the effects of seizures and AED use on early postoperative outcomes were determined using the Glasgow Outcome Scale (GOS) on the day of discharge. Results. Among 205 patients with aneurysmal SAH, 31 (15.1%) developed seizures. 21 (10.2%) had seizures at onset of SAH and only seven (3.4%) had in-hospital seizures. Aneurysm re-rupture (OR 5.26, p-value 0.045) and the presence of a parenchymal clot (OR 2.90, p-value 0.043) were independent predictors for seizure occurrence. There was no significant difference in the incidence of seizures in the AED cohort and in the No AED cohort (4/100, 4% vs. 3/99, 3%, p-value 0.714). AED use was associated with a higher proportion of patients with a discharge GOS score of 3 or less (28.0% vs 12.1%, p-value 0.005). Conclusion. The results of the study do not support the routine use of AEDs in patients with aneurysmal SAH.


Author(s):  
Hanna Schenck ◽  
Eliisa Netti ◽  
Onno Teernstra ◽  
Inger De Ridder ◽  
Jim Dings ◽  
...  

The glycocalyx is an important constituent of blood vessels located between the bloodstream and the endothelium. It plays a pivotal role in intercellular interactions in neuroinflammation, reduction of vascular oxidative stress, and provides a barrier regulating vascular permeability. In the brain, the glycocalyx is closely related to functions of the blood-brain barrier and neurovascular unit, both responsible for adequate neurovascular responses to potential threats to cerebral homeostasis. An aneurysmal subarachnoid hemorrhage (aSAH) occurs following rupture of an intracranial aneurysm and leads to immediate brain damage (early brain injury). In some cases, this can result in secondary brain damage, also known as delayed cerebral ischemia (DCI). DCI is a life-threatening condition that affects up to 30% of all aSAH patients. As such, it is associated with substantial societal and healthcare-related costs. Causes of DCI are multifactorial and thought to involve neuroinflammation, oxidative stress, neuroinflammation, thrombosis, and neurovascular uncoupling. To date, prediction of DCI is limited, and preventive and effective treatment strategies of DCI are scarce. There is increasing evidence that the glycocalyx is disrupted following an aSAH, and that glycocalyx disruption could precipitate or aggravate DCI. This review explores the potential role of the glycocalyx in the pathophysiological mechanisms contributing to DCI following aSAH. Understanding the role of the glycocalyx in DCI could advance the development of improved methods to predict DCI or identify patients at risk for DCI. This knowledge may also alter the methods and timing of preventive and treatment strategies of DCI. To this end, we review the potential and limitations of methods currently used to evaluate the glycocalyx, and strategies to restore or prevent glycocalyx shedding.


Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Carolina Rouanet ◽  
Natalia Vasconcellos ◽  
Feres Eduardo Chaddad Neto ◽  
Gisele Sampaio Silva

Introduction: Delayed cerebral ischemia (DCI) is one of the main determinants of prognosis in aneurysmal subarachnoid hemorrhage (aSAH). Hypertension induction (HI) and inotropics are frequently used strategies to treat DCI. However, little is known about clinical improvement immediately after those therapies. Methods: All patients with aSAH admitted to our hospital from 2016 to 2018 were evaluated. DCI was defined as a new focal neurological deficit or decrease in level of consciousness or the appearance of new infarctions on brain imaging. Patients who developed DCI and received vasopressors or inotropics and were included in the study. They were evaluated before (t0), 45 (t1) and 90 (t2) minutes after therapy initiation using NIHSS scores and Glasgow Coma Scale (GCS). Results: A total of 98 aSAH were evaluated, and 21 of them developed DCI (21.4%). Six patients received both treatment strategies, leading to a total of 27 DCI treatments (norepinephrine =12, milrinone =15). Mean NIHSS score had a significant decrease in t1 and t2 when compared to t0 (17 [95%CI 13-24], 16 [95%CI 11-23], 15 [95%CI 9-22], p<0.001 and p<0.002). The same happened among those treated with IH (t0=18 [95%CI 13-25]; t1=16 [95%CI 11-23], p=0.002; t2=14 [95%CI 9-22], p=0.027) and with milrinone (t0=17 [95%CI 12-24]; t1=15 [95%CI 10-23], p=0.007; t2=14 [95%CI 9-23], p=0.001). Mean GCS had a significant improvement in t1, that was not sustained in t2 (9 [95%CI 8-11], 10 [95%CI 9-12], 10 [95%CI 9-12], p=0.008 and p=0.098). In those treated with HI GCS scores did not change significantly (t0=9 [95%CI 7-11]; t1=10 [95%CI 8-12], p=0.054; t2=10 [95%CI 8-12], p=0.177). Those treated with inotropics significantly improved across time (t0=10 [95%CI 8-12]; t1=11 [95%CI 9-13], p=0.004; t2=11 [95%CI 9-13], p=0.001). Conclusions: DCI treatment with HI or inotropic therapy seems effective in immediately improving neurological deficits in patients with aSAH and DCI.


1999 ◽  
Vol 6 (2) ◽  
pp. E2
Author(s):  
James V. Byrne ◽  
Min-Joo Sohn ◽  
Andrew J. Molyneux ◽  
B. Chir

Object During a 5-year period 317 patients presenting with aneurysmal subarachnoid hemorrhage were successfully treated by coil embolization within 30 days of hemorrhage. The authors followed these cases to assess the stability of aneurysm occlusion and its longer-term efficacy in protecting patients against rebleeding. Methods These cases were followed for 6 to 65 months (median 22.3 months) by clinical review, angiography performed at 6 months posttreatment, and annual postal questionnaires. Conclusions Stable angiographic occlusion was evident in 86.4% of small and 85.2% of large aneurysms with recurrent filling in 38 (14.7%) of 259 aneurysms. Rebleeding was caused by aneurysm recurrence in four patients (between 11 and 35 months posttreatment) and by rupture of a coincidental untreated aneurysm in one patient. Annual rebleeding rates were 0.8% in the 1st year, 0.6% in the 2nd year, and 2.4% in the 3rd year after aneurysm embolization, with no rebleeding in subsequent years. Rebleeding occurred in three (7.9%) of 38 recurrent aneurysms and in one (0.4%) of 221 aneurysms that appeared stable on angiography. Periodic follow-up angiography after coil embolization is recommended to identify aneurysm recurrence and those patients at a high risk of late rebleeding.


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