Factors related to hydrocephalus after aneurysmal subarachnoid hemorrhage

OBJECTIVE: The purpose of this study was to identify factors predictive of shunt-dependent hydrocephalus among patients with aneurysmal subarachnoid hemorrhage. The data can be used to predict which patients in this group have a high probability of requiring permanent cerebrospinal fluid diversion. METHODS: Seven hundred eighteen patients with aneurysmal subarachnoid hemorrhage who were treated between 1990 and 1999 were retrospectively studied, to identify factors contributing to shunt-dependent hydrocephalus. With these data, a stepwise logistic regression procedure was used to determine the effect of each variable on the development of hydrocephalus and to create a scoring system. RESULTS: Overall, 152 of the 718 patients (21.2%) underwent shunting procedures for treatment of hydrocephalus. Four hundred seventy-nine of the patients (66.7%) were female. Of the factors investigated, the following were associated with shunt-dependent hydrocephalus, as determined with a variety of statistical methods: 1) increasing age (P < 0.001), 2) female sex (P = 0.015), 3) poor admission Hunt and Hess grade (P < 0.001), 4) thick subarachnoid hemorrhage on admission computed tomographic scans (P < 0.001), 5) intraventricular hemorrhage (P < 0.001), 6) radiological hydrocephalus at the time of admission (P < 0.001), 7) distal posterior circulation location of the ruptured aneurysm (P = 0.046), 8) clinical vasospasm (P < 0.001), and 9) endovascular treatment (P = 0.013). The presence of intracerebral hematomas, giant aneurysms, or multiple aneurysms did not influence the development of shunt-dependent hydrocephalus. CONCLUSION: The results of this study can help identify patients with a high risk of developing shunt-dependent hydrocephalus. This may help neurosurgeons expedite treatment, may decrease the cost and length of hospital stays, and may result in improved outcomes.     

Factors leading to hydrocephalus after aneurysmal subarachnoid hemorrhage.

Hydrocephalus is not a rare complication following aneurysmal subarachnoid hemorrhage. Hydrocephalus following subarachnoid hemorrhage can progress acutely (0-3 days), subacutely (4-13 days) or chronically (after 13 days). The predisposing factors leading to hydrocephalus after subarachnoid hemorrhage are not known exactly. This study assessed the predictive factors for the development of this condition. All patients presenting with subarachnoid hemorrhage between 1992-2001 were evaluated. All of them had initial computed tomography (CT) and hydrocephalus was diagnosed on CT scans. Age, gender, preexisting diabetes mellitus and hypertension, neurological state according to the Hunt and Hess scale at admission, Fischer grade on CT, the presence of intraventricular hemorrhage and localization of aneurysm were analyzed to see if there was any meaningful relationship between hydrocephalus and these factors. One hundred and fourteen patients with aneurysmal subarachnoid hemorrhage were evaluated. The incidence of hydrocephalus was 28.1 %. The incidence for acute hydrocephalus was 18.4 %, for subacute 5.2 % and for chronic 4.3 %. Sixty-nine percent of patients with hydrocephalus were graded as 3, 4 or 5 according to the Hunt and Hess scale on admission. Fifty-five percent of patients with hydrocephalus were graded as 3 and 4 according to Fisher grade on initial CT scan. Preexisting diabetes, higher Fisher grade and intraventricular hemorrhage were statistically significant predictors for the development of hydrocephalus. But only preexisting diabetes and higher Fisher grade were independent predictors according to multivariate analyses.     

Symptomatic hydrocephalus following aneurysmal subarachnoid hemorrhage

The results of a series of 500 consecutive patients who underwent aneurysmal surgery between 1969 and 1980 are reported. The incidence of significant symptomatic hydrocephalus secondary to spontaneous rupture of an intracranial aneurysm was 16.4%. Hydrocephalus was most frequent after rupture of aneurysms of the anterior communicating artery. Only one-third of the patients had more than one episode of subarachnoid hemorrhage before surgery. In 64% of the patients with preoperative hydrocephalus, there was angiographic evidence of spasm. In certain cases, the hydrocephalus must be treated before the offending aneurysm can be managed.     

Hypomagnesemia after aneurysmal subarachnoid hemorrhage

OBJECTIVE: Hypomagnesemia frequently occurs in hospitalized patients, and it is associated with poor outcome. We assessed the frequency and time distribution of hypomagnesemia after aneurysmal subarachnoid hemorrhage (SAH) and its relationship to the severity of SAH, delayed cerebral ischemia (DCI), and outcome after 3 months. METHODS: Serum magnesium was measured in 107 consecutive patients admitted within 48 hours after SAH. Hypomagnesemia (serum magnesium <0.70 mmol/L) at admission was related to clinical and initial computed tomographic characteristics by means of the Mann-Whitney U test. Hypomagnesemia at admission and during the DCI onset period (Days 2-12) was related to the occurrence of DCI and hypomagnesemia at admission, and hypomagnesemia that occurred any time during the first 3 weeks after SAH was related to outcome. RESULTS: Hypomagnesemia at admission was found in 41 patients (38%) and was associated with more cisternal (P = 0.006) and ventricular (P = 0.005) blood, a longer duration of unconsciousness (P = 0.007), and a worse World Federation of Neurosurgical Societies scale score at admission (P = 0.001). The crude hazard ratio for DCI with hypomagnesemia at admission was 2.4 (95% confidence interval, 1.0-5.6), and after multivariate adjustment it was 1.9 (95% confidence interval, 0.7-4.7). The hazard ratio of hypomagnesemia from Days 2 to 12 for patients with DCI was 3.2 (range, 1.1-8.9) after multivariate adjustment. The crude odds ratio for poor outcome (Glasgow Outcome Scale score, 1-3) with hypomagnesemia at admission was 2.5 (range, 1.1-5.5). Hypomagnesemia at admission did not contribute to the prediction of outcome in the multivariate model. CONCLUSION: Hypomagnesemia is frequently present after SAH and is associated with severity of SAH. Hypomagnesemia occurring between Days 2 and 12 after SAH predicts DCI.     

Cardiac complications after aneurysmal subarachnoid hemorrhage

BACKGROUND: Cardiac complications are frequently encountered by neurointensivists caring for patients with SAH. Our aim was to better characterize the natural history of various cardiac abnormalities in this population. We sought to determine the risk factors for cardiac abnormalities, patient outcome, and impact of treatment type on cardiac abnormalities. METHODS: We performed a single center retrospective review of admissions of patients with aneurysmal SAH to the neurosurgical ICU in a large university hospital. Patient demographics, pertinent history, cardiac tests, hospital LOS, intervention type, and discharge outcome were collected. RESULTS: Data from 266 patients were available for analysis. Of these patients, 50% (n = 133) demonstrated cardiac abnormalities as indicated by abnormal EKG, ECHO, or troponin I. Only age was determined to be an independent statistically significant predictor of cardiac abnormality (P = .01). There was no difference in mortality between the cardiac abnormality and control groups (P = .33). However, there was increased morbidity in the cardiac abnormality group as demonstrated by worse discharge disposition, in addition to increased length of hospital stay (22.6 vs 17.1 days, P < .01). The incidence of cardiac abnormalities was the same among surgical and endovascular treatment groups. CONCLUSIONS: Cardiac abnormalities, including those that meet ACC criteria for MI, are common among patients with SAH. However, in contrast to cardiac events outside the context of SAH, these abnormalities do not increase mortality. They do, however, adversely affect discharge disposition and prolong hospital LOS. The type of aneurysm treatment does not affect the incidence or outcome of cardiac abnormalities.     

Defining survivorship after high-grade aneurysmal subarachnoid hemorrhage

BACKGROUND: Outcome after high-grade aneurysmal SAH is poor. Various treatment paradigms have been advanced to improve treatment outcome and preserve resources, but none have addressed the potential salvageable life lost. METHODS: We retrospectively reviewed all patients with high-grade (H&H score, 4-5) aneurysmal SAH admitted to our institution from January 1998 to June 2002, all aggressively managed, to determine what clinical/radiographic criteria predicted favorable survival. RESULTS: There were 50 patients analyzed. All underwent emergency ventriculostomies or clot evacuations. Twenty-three patients (46%) improved and 7 (14%) worsened; 41 survived to receive definitive therapy. Twenty-one patients (42%) overall achieved a favorable outcome (GOS, 4-5). In the multivariate analysis (stepwise logistic regression), the postresuscitation GCSm alone predicted outcome (P= .004) with 70% cases correctly identified, whereas age, location of aneurysm (anterior circulation or not), presence of intraventricular hemorrhage, time to definitive intervention, clot on computerized tomography, type of therapy used (coil vs clip), pupillary abnormalities, and preresuscitation GCSm did not. Because the sole predictive parameter is obtained postresuscitation, no clinical or radiographic factor on presentation appears valid to determine eligibility for definitive care. CONCLUSION: Overall treatment outcome of our series is comparable with those of other articles. Our experience, as well as review of literature, does not support the existence of a validated "triage" schema to selectively treat patients with high-grade subarachnoid hemorrhage, implying that all such patients should be managed aggressively.     

Magnesium sulfate therapy after aneurysmal subarachnoid hemorrhage

OBJECT: Vasospasm remains a significant source of neurological morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH), despite advances in current medical, surgical, and endovascular therapies. Magnesium sulfate therapy has been demonstrated to be both safe and effective in preventing neurological complications in obstetrical patients with eclampsia. Evidence obtained using experimental models of brain injury, cerebral ischemia, and SAH indicate that Mg may also have a role as a neuroprotective agent. The authors hypothesize that MgSO4 therapy is safe, feasible, and has a beneficial effect on vasospasm and, ultimately, on neurological outcome following aneurysmal SAH. METHODS: A prospective randomized single-blind clinical trial of high-dose MgSO4 therapy following aneurysmal SAH (Hunt and Hess Grades II-IV) was performed in 40 patients, who were enrolled within 72 hours following SAH and given intravenous MgSO4 or control solution for 10 days. Serum Mg++ levels were maintained in the 4 to 5.5 mg/dl range throughout the treatment period. Clinical management principles were the same between groups (including early use of surgery or endovascular treatment, followed by aggressive vasospasm prophylaxis and treatment). Daily transcranial Doppler (TCD) ultrasonographic recordings were obtained, and clinical outcomes were measured using the Glasgow Outcome Scale (GOS). The patients' GOS scores and the TCD recordings were analyzed using the independent t-test. Forty patients were enrolled in the study: 20 (15 female and five male patients) received treatment and 20 (11 female and nine male patients) comprised a control group. The mean ages of the patients in these groups were 46 and 51, respectively, and the mean clinical Hunt and Hess grades were 2.6 +/- 0.68 in the MgSO4 treatment group and 2.3 +/- 0.73 in the control group (mean +/- standard deviation [SD], p = 0.87). Fisher grades were similar in both groups. Mean middle cerebral artery velocities were 93 +/- 27 cm/second in MgSO4-treated patients and 102 +/- 34 cm/second in the control group (mean +/- SD, p = 0.41). Symptomatic vasospasm, confirmed by angiography, occurred in six of 20 patients receiving MgSO4 and in five of 16 patients receiving placebo. Mean GOS scores were 3.8 +/- 1.6 and 3.6 +/- 1.5 (mean +/- SD, p = 0.74) in the treatment and control groups, respectively. Significant adverse effects from treatment with MgSO4 did not occur. CONCLUSIONS: Administration of high-dose MgSO4 following aneurysmal SAH is safe, and steady Mg++ levels in the range of 4 to 5.5 mg/dl are easily maintained. This treatment does not interfere with neurological assessment, administration of anesthesia during surgery, or other aspects of clinical care. We observed a trend in which a higher percentage of patients obtained GOS scores of 4 or 5 in the group treated with MgSO4, but the trend did not reach a statistically significant level. A larger study is needed to evaluate this trend further.     

Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

OBJECT: The pathogenesis of cerebral vasospasm and delayed ischemia after subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET), with its powerful and long-lasting vasoconstricting activity. In this study the author investigated the correlation between serial plasma concentrations of ET and ischemic symptoms, angiographically demonstrated evidence of vasospasm, and computerized tomography (CT) findings after aneurysmal SAH. METHODS: Endothelin-1 immunoreactivity in plasma was studied in 70 patients with aneurysmal SAH and in 25 healthy volunteers by using a double-antibody sandwich-enzyme immunoassay (immunometric) technique. On the whole, mean plasma ET concentrations in patients with SAH (mean +/- standard error of mean, 2.1 +/- 0.1 pg/ml) did not differ from those of healthy volunteers (1.9 +/- 0.2 pg/ml). Endothelin concentrations were significantly higher (p < 0.05) in patients who experienced delayed cerebral ischemia with fixed neurological deficits compared with those in other patients (post-SAH Days 0-5, 3.1 +/- 0.8 pg/ml compared with 2.1 +/- 0.2 pg/ml; post-SAH Days 6-14, 2.5 +/- 0.4 pg/ml compared with 1.9 +/- 0.2 pg/ml). Patients with angiographic evidence of severe vasospasm also had significantly (p < 0.05) elevated ET concentrations (post-SAH Days 0-5, 3.2 +/- 0.8 pg/ml; post-SAH Days 6-14, 2.7 +/- 0.5 pg/ml) as did those with a cerebral infarction larger than a lacuna on the follow-up CT scan (post-SAH Days 0-5, 3.1 +/- 0.8 pg/ml; post-SAH Days 6-14, 2.5 +/- 0.4 pg/ml) compared with other patients. Patients in whom angiography revealed diffuse moderate-to-severe vasospasm had significantly (p < 0.05) higher ET levels than other patients within 24 hours before or after angiography (2.6 +/- 0.3 compared with 1.9 +/- 0.2 pg/ml). In addition, patients with a history of hypertension or cigarette smoking experienced cerebral infarctions significantly more often than other patients, although angiography did not demonstrate severe or diffuse vasospasm more often in these patients than in others. CONCLUSIONS: Endothelin concentrations seem to correlate with delayed cerebral ischemia and vasospasm after SAH. The highest levels of ET are predictive of the symptoms of cerebral ischemia and vasospasm, and ET may also worsen ischemia in patients with a history of hypertension. Thus, ET may be an important causal or contributing factor to vasospasm, but its significance in the pathogenesis of vasospasm remains unknown.     

动脉瘤性蛛网膜下腔出血并发急性脑积水治疗体会

急性脑积水（AHC）是动脉瘤蛛网膜下腔出血3大主要并发症之一。发生率6．8％～30％，是影响病人预后的重要原因。本院收治9例动脉瘤性蛛网膜下腔出血并发急性脑积水，现报道如下。     

Circulatory and vascular changes after aneurysmal subarachnoid hemorrhage

Delayed cerebral ischemia (DCI) is a major complication that afflicts approximately 30% of patients who suffer an aneursymal subarachnoid hemorrhage (SAH). DCI is often associated with neurological infarction, poor outcome and mortality. Though the pathogenesis of DCI is not yet clear, it is traditionally been attributed to angiographic vasospasm. Unfortunately, clinical trials based on this premise have mostly been disappointing, predominantly unable to prevent ischemic damage and improve patient outcome despite reducing angiographic vasospasm. More recently, increasing concern that vasospasm could not fully account for DCI development has incited novel proposals as to the pathogenesis of DCI. A general theme exists among these theories (microcirculatory constriction, cortical spreading depression, blood brain barrier breakdown, microthrombosis) in that a majority seems to revolve around dysfunction and changes to the microvasculature. This purpose of this review was then to juxtapose macrovascular and microvascular changes after SAH, and provide an overview of current and prospective treatments.     

Preoperative ventriculostomy and rebleeding after aneurysmal subarachnoid hemorrhage

OBJECT: Despite the widespread use of ventriculostomy in the treatment of acute hydrocephalus after aneurysmal subarachnoid hemorrhage (SAH), there is no consensus regarding the risk of rebleeding associated with ventriculostomy before aneurysm repair. This present study was conducted to assess the risk of rebleeding after preoperative ventriculostomy in patients with aneurysmal SAH. METHODS: The authors reviewed the records of all patients with acute SAH who were treated at a single institution between 1990 and 1997. Thus, the records of 304 consecutive patients in whom an aneurysmal SAH source was documented on angiographic studies and who had presented to the authors' institution within 7 days of ictus were analyzed. Re-bleeding was confirmed by evidence of recurrent hemorrhage on computerized tomography scans in all cases. Forty-five patients underwent ventriculostomy for acute hydrocephalus after aneurysmal SAH at least 24 hours before aneurysm repair. Ventriculostomy was performed within 24 hours of SAH in 38 patients, within 24 to 48 hours in three patients, and more than 48 hours after SAH in four patients. The mean time interval between SAH and surgery in patients who did not undergo ventriculostomy was no different from the mean interval between ventriculostomy and surgery in patients who underwent preoperative ventriculostomy (3.6 compared with 3.8 days, p = 0.81). Fourteen (5.4%) of the 259 patients who did not undergo ventriculostomy suffered preoperative aneurysm rebleeding, whereas two (4.4%) of the 45 patients who underwent preoperative ventriculostomy had aneurysm rebleeding. CONCLUSIONS: No evidence was found that preoperative ventriculostomy performed after aneurysmal SAH is associated with an increased risk of aneurysm rebleeding when early aneurysm surgery is performed.     

Reversible arterial hypotension after acute aneurysmal subarachnoid hemorrhage

The authors report five patients who developed transient arterial hypotension immediately after the rupture of cerebral aneurysms. They manifested deep coma (three cases), abnormal electrocardiogram (four cases), and remarkable pulmonary edema (two cases). The level of consciousness in all three patients who were in deep coma improved with the normalization of blood pressure. Although two patients died of recurrent hemorrhage, the other three patients were discharged in satisfactory condition. Serious clinical conditions that are not terminal and are caused by arterial hypotension immediately after the rupture of cerebral aneurysms are sometimes reversible with adequate treatment.