Incidence Of Symptomatic Cerebral Vasospasm Research Articles

The Nimodipine-Sparing Effect of Perioperative Dexmedetomidine Infusion During Aneurysmal Subarachnoid Hemorrhage: A Prospective, Randomized, Controlled Trial.

Background: Nimodipine can block the influx of calcium into the vascular smooth muscle cell and prevent secondary ischemia in patients with aneurysmal subarachnoid hemorrhage. However, the reduction of blood pressure after long-term intravenous administration of nimodipine has been associated with neurological deterioration. Yet, no effective solutions have been suggested to address this phenomenon. The use of neuroprotective drug combinations may reduce the risk of sudden blood pressure loss. This prospective, randomized, controlled trial was performed to evaluate the nimodipine-sparing effect of perioperative dexmedetomidine infusion during aneurysmal subarachnoid hemorrhage. Methods: One hundred nine patients who underwent aneurysm embolization were divided into three groups: group C (n = 35, infused with 0.9% sodium chloride at the same rate as other two groups), group D1 (n = 38, dexmedetomidine infusion at 0.5 µg·kg–1 for 10 min, then adjusted to 0.2 µg·kg–1·h–1), and group D2 (n = 36, dexmedetomidine infusion at 0.5 µg·kg–1 for 10 min, then adjusted to 0.4 µg·kg–1·h–1). Patient-controlled analgesia was given for 48 h after surgery. The primary outcome measure was the total consumption of nimodipine during the first 48 h after surgery. The secondary outcome measures were recovery time at post-anesthesia care unit (PACU), postoperative pain intensity scores, dexmedetomidine and sufentanil consumption, hemodynamic, satisfaction of patients and neurosurgeon, neurologic examination (Glasgow Coma Scale, GCS), Bruggemann comfort scale, and adverse effects. Intraoperative hemodynamics were recorded at the following time-points: arrival at the operating room (T1); before intubation (T2); intubation (T3); 5 min (T4), 10 min (T5), and 15 min (T6) after intubation; suturing of femoral artery (T7); end of surgery (T8); extubation (T9); and 5 min (T10), 10 min (T11), and 15 min (T12) after arrival at the PACU. The level of sedation was recorded at 15 min, 30 min, 1 h, and 2 h after extubation. We also recorded the incidence of symptomatic cerebral vasospasm during 7 days after surgery, Glasgow Outcome Score (GOS) at 3 months, and incidence of cerebral infarction 30 days after surgery. Results: The consumption of nimodipine during the first 48 h after surgery was significantly lower in group D2 (P < 0.05). Compared with group C, HR and MAP were significantly decreased from T2 to T12 in group D1 and D2 (P < 0.05). Patients in group D2 showed a significantly decreased MAP from T5 to T9 compared with group D1 (P < 0.05). The consumption of sevoflurane, remifentanil, dexmedetomidine, and nimodipine were all significantly reduced in groups D1 and D2 during surgery (P < 0.05). Compared with group C, MAP was significantly decreased in groups D1 and D2 during the first 48 h after surgery (P < 0.05). Compared with group C, consumption of sufentanil and dexmedetomidine at 1 h, pain intensity at 1 h, and 8 h after surgery were significantly decreased in groups D1 and D2 (P < 0.05). FAS was significantly higher in group D2 at 8 h, 16 h, and 24 h after surgery. LOS was significantly lower only in group D2 at 0.5 h after surgery (P < 0.05). Compared with group C, BCS was significantly higher group D2 at 4 h and 8 h after surgery (P < 0.05). There were no significant differences among the three groups in consumption of propofol, cisatracurium, fentanyl, and vasoactive drugs during operation, recovery time at PACU, satisfaction of patients and neurosurgeon, and number of applied urapidil and GCS during the first 48 h after surgery. The incidence of symptomatic cerebral vasospasm during 7 days after surgery, GOS of 3 months, and cerebral infarction after 30 days were also comparable among the three groups. Conclusions: Dexmedetomidine (infusion at 0.5 µg·kg–1 for 10 min, then adjusted to 0.4 µg·kg–1·h–1 during the surgery) significantly reduced the total consumption of nimodipine during the first 48 h after surgery and promoted early rehabilitation of patients although the incidences of symptomatic cerebral vasospasm, GOS, and cerebral infarction were not reduced.

Pituitary hormone level changes and hypxonatremia in aneurysmal subarachnoid hemorrhage

The aim of this study was to investigate the changes in serum pituitary hormone levels and the mechanism of hyponatremia in aneurysmal subarachnoid hemorrhage (SAH). Nuclear medical tests and serum electrolyte monitoring were performed in 49 aneurysmal SAH cases and 10 healthy volunteers. The levels of serum pituitary hormones were significantly higher in the SAH patients compared with the control group on days 1–3 and 7–9 after SAH onset (P<0.05). The peak value occurred on days 7–9. The rate of hyponatremia was 49.0% in the 49 SAH patients. The incidence of severe hyponatremia was significantly higher in Fisher grades III–IV and Hunt-Hess grades III–IV compared with Fisher grades I–II and Hunt-Hess grades I–II, respectively (P<0.05). There was no correlation between the site of aneurysm and the rate of hyponatremia. The incidence of symptomatic cerebral vasospasm was significantly higher in the hyponatremia group and Fisher grades III–IV compared with the normal serum sodium group and Fisher grades I–II, respectively. Serum pituitary hormone levels were positively correlated with blood loss and disease severity in patients with aneurysmal SAH. Hyponatremia may be considered an important indicator of SAH. SAH patients are likely to benefit from intense monitoring and regulation of serum sodium.

Intravenous Magnesium Infusion for the Prevention of Symptomatic Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

ObjectiveThe study examined the difference in the incidence of symptomatic cerebral vasospasm with magnesium supplementation in aneurysmal subarachnoid hemorrhage (SAH) in a Korean population.MethodsThis retrospective analysis was performed in 157 patients diagnosed with aneurysmal SAH from January 2007 to December 2011 at a single center. Seventy patients (44.6%) received a combination treatment of nimodipine with magnesium and 87 patients (55.4%) received only nimodipine. A matched case-control study using propensity scores was conducted and 41 subjects were selected from each group. A dosage of 64 mmol/day of magnesium was administrated.ResultsThe infusion of magnesium did not reduce the incidence of symptomatic cerebral vasospasm (n=7, 17.1%, p=0.29) compared with simple nimodipine injection (n=11, 26.8%). The ratios of good clinical outcome (modified Rankin scale 0-2) at 6 months were similar, being 78% in the combination treatment group and 80.5% in the nimodipine only group (p=0.79). The proportions of delayed cerebral infarction was not significantly lower in patients with combination treatment (n=2, 4.9% vs. n=3, 7.3%; p=0.64). There was no difference in the serum magnesium concentrations between the patients with symptomatic vasospasm and without vasospasm who had magnesium supplementation. No major complications associated with intravenous magnesium infusion were observed.ConclusionMagnesium supplementation (64 mmol/day) may not be beneficial for the reduction of the incidence of symptomatic cerebral vasospasm in patients with aneurysmal SAH.

Diabetes Mellitus Increases Risk of Vasospasm Following Aneurysmal Subarachnoid Hemorrhage Independent of Glycemic Control

Symptomatic cerebral vasospasm (SCV) is a morbid sequela of subarachnoid hemorrhage (SAH). Its etiology is multifactorial and predicting onset can be challenging. Diabetes mellitus (DM) is known to affect vasoactive properties of vessels, but it has not been definitively correlated with SCV. We report that pre-existing DM is independently and strongly correlated with SCV, despite intensive glycemic control. This is a retrospective chart review of all patients with aneurysmal subarachnoid hemorrhage (aSAH) admitted to a single academic medical center between January 2002 and January 2008 (n = 145). Patients presenting greater than 14 days after ictus, as well as those not surviving the first 3 days post-ictus were excluded from analysis. Remaining patients (n = 113) were assessed for study parameters including pre-existing DM, mean daily blood glucose, and additional known correlates to SCV. Multivariate analysis was performed to assess risk factors for SCV development. The primary outcome measure was SCV, defined as neurological change in conjunction with evidence of vessel spasm by either angiography or transcranial ultrasound. Of 113 patients included in the study, 42 (37%) had SCV. Patients with DM (80% incidence of SCV) had an increased risk of subsequently developing SCV (OR 9.90, P = 0.031). Elevated blood glucose was not associated with increased risk of vasospasm and no difference in glycemic control was noted between patients with or without DM. SCV resulted in worsened mortality and Glasgow Outcome Score for survivors (P < 0.005). In this group of patients with SAH, diabetes mellitus is identified as a risk factor for development of SCV. Blood glucose management during hospitalization was similar in diabetics and non-diabetics, suggesting that the longstanding effects of microvascular disease may be more relevant in the development of SCV then acute glycemic control in these patients.

Simvastatin for the prevention of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage: a single-institution prospective cohort study

Vasospasm is the major cause of disability and death after aneurysmal subarachnoid hemorrhage (aSAH). Although the results of 2 randomized clinical trials demonstrated that statin decreases the incidence of symptomatic cerebral vasospasm after aSAH, retrospective studies have failed to confirm this. The authors conducted a prospective observational study to determine whether a standardized regimen of simvastatin would reduce the incidence of cerebral vasospasm and improve neurological outcomes in patients with aSAH. Since 1991, all patients with aSAH admitted to the authors' institution have been prospectively followed up with standardized outcomes recording. Starting in September 2005, all patients admitted with aSAH were given enteral simvastatin (80 mg/day for 14 days) in addition to the standard care. The incidence of symptomatic cerebral vasospasm, length of hospitalization, in-hospital mortality rate, and discharge Glasgow Outcome Scale scores in these 170 patients were compared to data obtained in 170 consecutive patients who underwent treatment in our unit prior to the introduction of statin therapy. The 5-year study period included 340 consecutively treated patients (170 who received statins and 170 who did not). Patients who received simvastatin therapy were more frequently male (29 vs 20%) and had a smaller median aneurysm diameter (6 vs 7 mm). Baseline characteristics were otherwise similar between the cohorts. There were no differences in the incidence of symptomatic vasospasm (25.3 vs 30.5%; p = 0.277), in-hospital mortality rate (18 vs 15%; p = 0.468), length of hospitalization (21 +/- 15 vs 19 +/- 12 days; p = 0.281), or poor outcome at discharge (Glasgow Outcome Scale Scores 1-2: 21.7 vs 18.2%; p = 0.416) between the simvastatin and nonstatin cohorts. There were no statin-related complications. The uniform introduction of simvastatin did not reduce the incidence of symptomatic cerebral vasospasm, death, or poor outcome in patients with aSAH. Simvastatin was well tolerated, but its benefit may be less than has been previously reported.

Does Prophylactic Postoperative Hypervolemic Therapy Prevent Cerebral Vasospasm and Improve Clinical Outcome After Aneurysmal Subarachnoid Hemorrhage?

Delayed cerebral vasospasm is a common cause of morbidity and mortality after acute aneurysmal subarachnoid hemorrhage. Hypovolemia and fluid restriction are risk factors for delayed vasospasm; hypervolemic therapeutic approaches are commonly used in patients with subarachnoid hemorrhage to prevent and to treat cerebral vasospasm. To determine if postoperative prophylactic hypervolemic therapy prevents cerebral vasospasm and improves clinical outcome in patients with aneurysmal subarachnoid hemorrhage. The objective was addressed through the development of a structured critically appraised topic. This included a clinical scenario, structured question, search strategy, critical appraisal, results, evidence summary, commentary, and bottom line conclusions. Participants included consultant and resident neurologists, a medical librarian, clinical epidemiologists, and content experts in the field of vascular neurology. One randomized controlled trial addressed the questions. There was no difference in the incidence of symptomatic cerebral vasospasm (20% each) or clinical outcome at 14 days and 3 months between the hypervolemic and normovolemic groups. Hypervolemic therapy also had no effect on measures of cerebral blood flow. A second quasi-randomized trial reached the same conclusions. Available evidence is insufficient to support use of prophylactic hypervolemic therapy after surgery in patients with aneurysmal subarachnoid hemorrhage. Although completed studies may be insufficiently sensitive (underpowered) to detect a treatment effect, the magnitude of any as yet undetected benefit of prophylactic hypervolemic therapy is likely modest and its risks have not been systematically evaluated.

塞栓術を行った破裂脳動脈瘤例における脳血管攣縮の検討

We analyzed the incidence of vasospasm (VS) of the cerebral arteries in the patients treated with coil embolization using Guglielmi detachable coils (GDCs) for ruptured cerebral aneurysms, and herein we report the details. Between March 1997 and March 2005, 52 patients underwent coil embolization within 7 days following rupture of cerebral aneurysms. We excluded 8 patients in whom VS could not be judged due to prolonged disturbance of consciousness resulting from early brain damage consequent to subarachnoid hemorrhage (SAH); early mortality; or other causes, as well as 2 patients in whom VS was already detected at the time of coil embolization. The remaining 42 patients (mean age: 64.4 years) were the subjects of our study. When thick hematomas were revealed on CT scans, spinal drainage was placed until SAH disappeared, while 3H therapy was actively conducted if the patients showed any manifestations of VS. In addition, when no improvement could be achieved, intra-arterial injection of papaverine hydrochloride was administered or (simultaneous) vascular reconstruction was performed. Preoperatively, H & H grade was I in 1 case, II in 16 cases, III in 6 cases, IV in 17 cases, and V in 2 cases. In the Fisher CT group, the grade was 1 in 1 case, 2 in 13 cases, 3 in 25 cases, and 4 in 3 cases. In 11 of the 42 patients (26.2%), cerebral VS was noticed, and the manifestations such as hemiplegia persisted in 3 (7.1%). The incidence of symptomatic cerebral VS following craniotomy is reportedly about 15% to 30%, but in our present study we found that the incidence was relatively slightly lower following coil embolization. Our results suggest that comparative studies on post-craniotomy cerebral VS should be conducted.