Age and outcome after aneurysmal subarachnoid hemorrhage: why do older patients fare worse?

1996 ◽  
Vol 85 (3) ◽  
pp. 410-418 ◽  
Author(s):  
Giuseppe Lanzino ◽  
Neal F. Kassell ◽  
Teresa P. Germanson ◽  
Gail L. Kongable ◽  
Laura L. Truskowski ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Subarachnoid Hemorrhage ◽  
Age Groups ◽  
Age Group ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Age Related ◽  
Increased Risk ◽  
Fine Print

✓ Advanced age is a recognized prognostic indicator of poor outcome after subarachnoid hemorrhage (SAH). The relationship of age to other prognostic factors and outcome was evaluated using data from the multicenter randomized trial of nicardipine in SAH conducted in 21 neurosurgical centers in North America. Among the 906 patients who were studied, five different age groups were considered: 40 years or less, 41 to 50, 51 to 60, 61 to 70, and more than 71 years. Twenty-three percent of the individuals enrolled were older than 60 years of age. Women outnumbered men in all age groups. Level of consciousness (p = 0.0002) and World Federation of Neurological Surgeons grade (p = 0.0001) at admission worsened with advancing age. Age was also related to the presence of a thick subarachnoid clot (p = 0.0001), intraventricular hemorrhage (p = 0.0003), and hydrocephalus (p = 0.0001) on an admission computerized tomography scan. The rebleeding rate increased from 4.5% in the youngest age group to 16.4% in patients more than 70 years of age (p = 0.002). As expected, preexisting medical conditions, such as diabetes (p = 0.028), hypertension (p = 0.0001), and pulmonary (p = 0.0084), myocardial (p = 0.0001), and cerebrovascular diseases (p = 0.0001), were positively associated with age. There were no age-related differences in the day of admission following SAH, timing of the surgery and/or location, and size (small vs. large) of the ruptured aneurysm. During the treatment period, the incidence of severe complications (that is, those complications considered life threatening by the reporting investigator) increased with advancing age, occurring in 28%, 33%, 36%, 40%, and 46% of the patients in each advancing age group, respectively (p = 0.0002). No differences were observed in the reported frequency of surgical complications. No age-related differences were found in the overall incidence of angiographic vasospasm; however, symptomatic vasospasm was more frequently reported in the older age groups (p = 0.01). Overall outcome, assessed using the Glasgow Outcome Scale at 3 months post-SAH, was poorer with advancing age (p < 0.001). Multivariate analysis of overall outcome, adjusting for the different prognostic factors, did not remove the age effect, which suggests that the aging brain has a less optimal response to the initial bleeding. Age as a risk factor is a continuum; however, there seems to be a significant increased risk of poor outcome after the age of 60 years.

scholarly journals Increased levels of lipid peroxides as predictive of symptomatic vasospasm and poor outcome after aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1302-1305 ◽  
Author(s):  
Takao Kamezaki ◽  
Kiyoyuki Yanaka ◽  
Sohji Nagase ◽  
Keishi Fujita ◽  
Noriyuki Kato ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Lipid Peroxides ◽  
Medical Complication ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

Object. Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). Reactive oxygen species and subsequent lipid peroxidation are reported to participate in the causes of cerebral vasospasm. This clinical study was performed to investigate the relationships between levels of lipid peroxides in cerebrospinal fluid (CSF) and both delayed cerebral vasospasm and clinical outcome after SAH. Methods. Levels of phosphatidylcholine hydroperoxide (PCOOH) and cholesteryl ester hydroperoxide (CEOOH) in the CSF were measured in 20 patients with aneurysmal SAH. The patients' CSF was collected within 48 hours of hemorrhage onset and on Day 6 or 7 post-SAH. On Day 7, angiography was performed to verify the degree and extent of the vasospasm. The relationship between the patients' clinical profiles and the levels of lipid peroxides in the CSF were investigated. Both PCOOH and CEOOH were detectable in CSF, and their levels decreased within 7 days after onset of SAH. The levels of CEOOH within 48 hours after onset of hemorrhage were significantly higher in patients in whom symptomatic vasospasm later developed than in patients in whom symptomatic vasospasm did not develop (p = 0.002). Levels of PCOOH measured within 48 hours after onset of hemorrhage were significantly higher in patients with poor outcomes than in patients with good outcomes (p = 0.043). Conclusions. Increased levels of lipid peroxides measured in the CSF during the acute stage of SAH were predictive of both symptomatic vasospasm and poor outcome. Measurements of lipid peroxides in the CSF may be useful prognostically for patient outcomes as well as for predicting symptomatic vasospasm.

Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 98 (6) ◽  
pp. 1222-1226 ◽  
Author(s):  
Matthew J. McGirt ◽  
John C. Mavropoulos ◽  
Laura Y. McGirt ◽  
Michael J. Alexander ◽  
Allan H. Friedman ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Leukocyte Count ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Increased Risk ◽  
Grade 3 ◽  
Fine Print

Object. The identification of patients at an increased risk for cerebral vasospasm after subarachnoid hemorrhage (SAH) may allow for more aggressive treatment and improved patient outcomes. Note, however, that blood clot size on admission remains the only factor consistently demonstrated to increase the risk of cerebral vasospasm after SAH. The goal of this study was to assess whether clinical, radiographic, or serological variables could be used to identify patients at an increased risk for cerebral vasospasm. Methods. A retrospective review was conducted in all patients with aneurysmal or spontaneous nonaneurysmal SAH who were admitted to the authors' institution between 1995 and 2001. Underlying vascular diseases (hypertension or chronic diabetes mellitus), Hunt and Hess and Fisher grades, patient age, aneurysm location, craniotomy compared with endovascular aneurysm stabilization, medications on admission, postoperative steroid agent use, and the occurrence of fever, hydrocephalus, or leukocytosis were assessed as predictors of vasospasm. Two hundred twenty-four patients were treated for SAH during the review period. One hundred one patients (45%) developed symptomatic vasospasm. Peak vasospasm occurred 5.8 ± 3 days after SAH. There were four independent predictors of vasospasm: Fisher Grade 3 SAH (odds ratio [OR] 7.5, 95% confidence interval [CI] 3.5–15.8), peak serum leukocyte count (OR 1.09, 95% CI 1.02–1.16), rupture of a posterior cerebral artery (PCA) aneurysm (OR 0.05, 95% CI 0.01–0.41), and spontaneous nonaneurysmal SAH (OR 0.14, 95% CI 0.04–0.45). A serum leukocyte count greater than 15 × 109/L was independently associated with a 3.3-fold increase in the likelihood of developing vasospasm (OR 3.33, 95% CI 1.74–6.38). Conclusions. During this 7-year period, spontaneous nonaneurysmal SAH and ruptured PCA aneurysms decreased the odds of developing vasospasm sevenfold and 20-fold, respectively. The presence of Fisher Grade 3 SAH on admission or a peak leukocyte count greater than 15 × 109/L increased the odds of vasospasm sevenfold and threefold, respectively. Monitoring of the serum leukocyte count may allow for early diagnosis and treatment of vasospasm.

Blood transfusion and increased risk for vasospasm and poor outcome after subarachnoid hemorrhage

2004 ◽  
Vol 101 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Michelle J. Smith ◽  
Peter D. Le Roux ◽  
J. Paul Elliott ◽  
H. Richard Winn
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Blood Transfusion ◽  
Smoking Status ◽  
Ct Scans ◽  
Content Type ◽  
Poor Outcome ◽  
Increased Risk ◽  
Confounding Variables ◽  
Rbc Transfusion ◽  
Fine Print

Object. Nitric oxide (NO) metabolism may influence vasospasm after subarachnoid hemorrhage (SAH). It has been demonstrated in recent studies that erythrocytes carry NO for release in vessels, whereas transfused erythrocytes may lack stored NO. Several converging lines of evidence also indicate that blood transfusion may exacerbate poor outcomes in some critically ill patients. In this study the authors hypothesized that patients with SAH who received red blood cell (RBC) transfusions were at greater risk for vasospasm and poor outcome. Methods. The authors retrospectively reviewed a prospective observational database, including hospital records, computerized tomography (CT) scans, and pre- and postoperative four-vessel angiograms, in which the management methods used in 441 patients undergoing surgery for ruptured cerebral aneurysms were described. Two hundred seventy patients (61.2%) received an RBC transfusion during their hospital stay. After adjustment for Hunt and Hess grade, SAH grade on CT scans, delay between rupture and surgery, smoking status, and intraoperative aneurysm rupture, a worse outcome was more likely in patients who received intraoperative blood (odds ratio [OR] 2.44, confidence interval [CI] 1.32–4.52; 120 patients). Intraoperative RBC transfusion did not influence subsequent angiographically confirmed vasospasm (OR 0.92, CI 0.6–1.4). Worse outcome was observed in patients who received blood postoperatively (OR 1.81, CI 1.21–2.7), but not after adjustments were made for confounding variables (OR 1.48, CI 0.83–2.63). Angiographic vasospasm was observed in 217 patients and, after adjusting for confounding variables, was more frequent among patients who received postoperative RBC transfusion (OR 1.68, CI 1.02–2.75). Among patients in whom angiographically confirmed vasospasm developed there was a tendency to have received more blood than in those with no vasospasm; however, a clear dose-dependent response was not observed. Conclusions. Development of angiographically confirmed vasospasm after SAH is associated with postoperative RBC transfusion and worse outcome is associated with intraoperative RBC transfusion. Before blood is transfused, patients with SAH should be carefully assessed to determine if they are symptomatic because of anemia.

Hyperglycemia, excess weight, and history of hypertension as risk factors for poor outcome and cerebral infarction after aneurysmal subarachnoid hemorrhage

2005 ◽  
Vol 102 (6) ◽  
pp. 998-1003 ◽  
Author(s):  
Seppo Juvela ◽  
Jari Siironen ◽  
Johanna Kuhmonen
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Patient Outcomes ◽  
Plasma Glucose ◽  
Clinical Condition ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Poor Outcome ◽  
History Of ◽  
Fine Print

Object. Stress-induced hyperglycemia has been shown to be associated with poor outcome after aneurysmal subarachnoid hemorrhage (SAH). The authors prospectively tested whether hyperglycemia, independent of other factors, affects patient outcomes and the occurrence of cerebral infarction after SAH. Methods. Previous diseases, health habits, medications, clinical condition, and neuroimaging variables were recorded for 175 patients with SAH who were admitted to the hospital within 48 hours after bleeding. The plasma level of glucose was measured at admission and the fasting value of glucose was measured in the morning after aneurysm occlusion. Factors found to be independently predictive of patient outcomes at 3 months after SAH onset and the appearance of cerebral infarction were tested by performing multiple logistic regression. Plasma glucose values at admission were found to be associated with patient age, body mass index (BMI), history of hypertension, clinical condition, amount of subarachnoid or intraventricular blood, shunt-dependent hydrocephalus, outcome variables, and the appearance of cerebral infarction. When considered independently of age, clinical condition, or amount of subarachnoid, intraventricular, or intracerebral blood, the plasma glucose values at admission predicted poor outcome (per millimole/liter the odds ratio [OR] was 1.24 with a 95% confidence interval [CI] of 1.02–1.51). After an adjustment was made for the amount of subarachnoid blood, the clinical condition, and the duration of temporary artery occlusion during surgery, the BMI was found to be a significant predictor (per kilogram/square meter the OR was 1.15 with a 95% CI of 1.02–1.29) for the finding of cerebral infarction on the follow-up computerized tomography scan. Hypertension (OR 3.11, 95% CI 1.11–8.73)—but not plasma glucose (OR 1.06, 95% CI 0.87–1.29)—also predicted the occurrence of infarction when tested instead of the BMI. Conclusions. Independent of the severity of bleeding, hyperglycemia at admission seems to impair outcome, and excess weight and hypertension appear to elevate the risk of cerebral infarction after SAH.

Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage

2003 ◽  
Vol 98 (5) ◽  
pp. 978-984 ◽  
Author(s):  
Miriam M. Treggiari ◽  
Bernhard Walder ◽  
Peter M. Suter ◽  
Jacques-André Romand
Keyword(s):  
Systematic Review ◽  
Subarachnoid Hemorrhage ◽  
Relative Risk ◽  
Sensitivity Analyses ◽  
Neurological Deficits ◽  
Content Type ◽  
Risk Of Death ◽  
Symptomatic Vasospasm ◽  
Triple H ◽  
Fine Print

Object. There is uncertainty about the efficacy of hypertension, hypervolemia, and hemodilution (triple-H) therapy in reducing the occurrence of delayed ischemic neurological deficits (DINDs) and death after subarachnoid hemorrhage. The authors therefore conducted a systematic review to evaluate the efficacy of triple-H prevention in decreasing the rate of clinical vasospasm, DINDs, and death. Methods. The authors systematically reviewed studies identified based on a MEDLINE, EMBASE, and COCHRANE Register search of articles published between 1966 and 2001, and reference lists of identified articles. An independent assessment of each study's methodological quality, population, intervention, and outcomes (rates of symptomatic vasospasm, DINDs, and death) was performed. Summary relative risk estimates were calculated for the main outcomes using fixed- or random-effect models, as appropriate. Only four prospective, comparative studies with a total of 488 patients were identified. The median internal validity score was 0.5 (range 0–2); the median external validity score was 3 (range 2–6). Compared with no prevention, triple-H therapy was associated with a reduced risk of symptomatic vasospasm (relative risk [RR] 0.45, 95% confidence interval [CI] 0.32–0.65), but not DIND (RR 0.54, 95% CI 0.2–1.49). The risk of death was higher (RR 0.68, 95% CI 0.53–0.87). Sensitivity analyses including only randomized, controlled trials showed no evidence of statistically significant results for these major end points. Conclusions. The paucity of information and important limitations in the design of the studies analyzed preclude evaluation of the efficacy of triple-H prevention and formulation of any recommendations regarding its use for the prevention of cerebral vasospasm.

Decrease in platelet count as an independent risk factor for symptomatic vasospasm following aneurysmal subarachnoid hemorrhage

2005 ◽  
Vol 102 (5) ◽  
pp. 882-887 ◽  
Author(s):  
Yutaka Hirashima ◽  
Hideo Hamada ◽  
Masanori Kurimoto ◽  
Hideki Origasa ◽  
Shunro Endo
Keyword(s):  
Platelet Count ◽  
Subarachnoid Hemorrhage ◽  
Blood Cells ◽  
White Blood Cells ◽  
Experimental Studies ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Cell Counts ◽  
Fisher Grade ◽  
Fine Print

Object. Increased platelet consumption is expected in patients with cerebral vasospasm, according to data from clinical and experimental studies. The authors investigated sequential changes in platelet counts in patients with subarachnoid hemorrhage (SAH) and the difference in platelet consumption between patients with and those without symptomatic vasospasm (SV). Variables related to platelet count as well as other clinical and radiological variables were analyzed as independent predictors of SV. Methods. One hundred consecutive patients who had undergone surgery within 48 hours after SAH onset were entered in the study. Clinical and radiological variables and blood cell counts, including red blood cells, white blood cells, and platelets, after SAH were retrospectively examined. Twenty of these variables were entered into univariate and multivariate analyses to determine predictors for SV. After SAH, the platelet count decreased to a minimum and then increased rapidly to levels greater than those recorded on admission. This change was specific to SAH, and platelet consumption was more severe in patients with SV than in those without. There were three independent predictors of SV: a ratio of the lowest platelet count and the admission count greater than 0.7 (odds ratio [OR] 0.322, 95% confidence interval [CI] 0.124–0.834, p = 0.0196) and a history of hypertension (OR 0.338, 95% CI 0.126–0.906, p = 0.0311) were negatively significant (that is, decreases the occurrence of SV), and a Fisher Grade 3 (OR 4.42, 95% CI 1.48–13.2, p = 0.0077) was positively significant (that is, increases the occurrence of SV). Conclusions. The association between a decrease in platelet count and the occurrence of SV indicates the important role of platelets in the pathophysiology of vasospasm following SAH.

Subarachnoid hemorrhage of unknown origin: prognosis and prognostic factors

1985 ◽  
Vol 63 (3) ◽  
pp. 349-354 ◽  
Author(s):  
Jan Brismar ◽  
Göran Sundbärg
Keyword(s):  
Prognostic Factors ◽  
Subarachnoid Hemorrhage ◽  
Prognostic Significance ◽  
Delayed Cerebral Ischemia ◽  
Content Type ◽  
Full Activity ◽  
Time Work ◽  
Part Time ◽  
Part Time Work ◽  
Fine Print

✓ The cases of 127 consecutive patients with subarachnoid hemorrhage (SAH), in whom cerebral panangiography revealed no cause for the bleeding nor any sign of an intraparenchymatous hemorrhage, were reviewed in a study of the long-term prognosis and the possible prognostic factors in this condition. Data for all 127 patients in the study were obtained, with an average follow-up period of 5.4 years. After the 1st week post-SAH, only three rebleeds had occurred. In all, 80% of the patients had returned to full activity, 91% to at least part-time work; if the patients with hypertension were excluded, these figures rose to 86% and 95%, respectively. Decreased wakefulness on admission related to a slightly poorer prognosis, whereas age and red blood cell count in the cerebrospinal fluid had no prognostic significance. Of those patients who, at the end of the 2nd week following the SAH, were fully awake and had not developed any symptoms of delayed cerebral ischemia (87% of all patients admitted), 88% returned to full activity, 97% to at least part-time work. The survival rate for this group, as well as causes of death, seem to be within the range for normal individuals. It should thus be possible to inform these patients (at least the normotensive ones) of the benignity of their condition, directly after normal angiography. Even among the patients who were able to return to full activity, symptoms attributable to the SAH were common: 22% experienced problems such as frequent headaches, vertigo, irritability, and increased fatigability.

CSF leukotriene C4 following subarachnoid hemorrhage

1988 ◽  
Vol 69 (4) ◽  
pp. 488-493 ◽  
Author(s):  
Pietro Paoletti ◽  
Paolo Gaetani ◽  
Guido Grignani ◽  
Lucia Pacchiarini ◽  
Vittorio Silvani ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Subarachnoid Hemorrhage ◽  
Arterial Spasm ◽  
Lipoxygenase Pathway ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Csf Levels ◽  
Fine Print

✓ Leukotrienes derive from arachidonic acid metabolism via the lipoxygenase pathway and modulate several cellular events. In the central nervous system, leukotrienes are mainly synthesized in the gray matter and in vascular tissues. Their production is enhanced in ischemic conditions and in experimental subarachnoid hemorrhage (SAH). Previous studies have indicated the ability of the leukotrienes C4 and D4 to constrict arterial vessels in vivo and in vitro and have suggested their involvement in the pathogenesis of cerebral arterial spasm. In the present study, the authors measured lumbar and cisternal cerebrospinal fluid (CSF) levels of leukotriene C4 in 48 patients who had suffered aneurysmal SAH. In 12 of the cases, symptomatic and radiological spasm was evident. The mean lumbar CSF level of immunoreactive-like activity of leukotriene C4 (i-LTC4) was significantly higher (p < 0.005) than in control cases, while the cisternal CSF level was higher than the lumbar mean concentration (p < 0.005). Patients presenting with vasospasm had significantly higher levels of i-LTC4 compared to patients without symptomatic vasospasm. This is the first report concerning monitoring of i-LTC4 levels in the CSF after SAH. The results of this study suggest that: 1) metabolism of arachidonic acid via the lipoxygenase pathway is enhanced after SAH; 2) the higher cisternal CSF levels of i-LTC4 may be part of the biological response in the perianeurysmal subarachnoid cisterns after the hemorrhage; and 3) the higher CSF levels of i-LTC4 in patients presenting with vasospasm suggest that a relationship exists between this compound and arterial spasm and/or reflect the development of cerebral ischemic damage.

Paradoxical aggravation of vasospasm with papaverine infusion following aneurysmal subarachnoid hemorrhage

1996 ◽  
Vol 84 (4) ◽  
pp. 690-695 ◽  
Author(s):  
Brent L. Clyde ◽  
Andrew D. Firlik ◽  
Anthony M. Kaufmann ◽  
MichaelP. Spearman ◽  
Howard Yonas
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Artery ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Left Middle Cerebral Artery ◽  
Xenon Ct ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fine Print

✓ Reports of intraarterial papaverine infusion as treatment for cerebral vasospasm are few and documented complications are uncommon. The authors report the case of a patient with paradoxical aggravation of cerebral arterial narrowing during selective intraarterial papaverine infusion intended to treat vasospasm following aneurysmal subarachnoid hemorrhage (SAH). A 48-year-old man presented to the authors' service with symptomatic vasospasm 10 days after experiencing an SAH. The ruptured anterior communicating artery aneurysm was surgically obliterated the following day, and thereafter maximum hypervolemic and hypertensive therapies were used. However, the patient remained lethargic, and a stable xenon—computerized tomography (CT) cerebral blood flow (CBF) study revealed CBF to be 15 cc/100 g/minute in the left anterior cerebral artery (ACA) and 25 cc/100 g/minute in the right ACA territories. Cerebral arteriography demonstrated diffuse severe left ACA and mild left middle cerebral artery (MCA) vasospasm. In response intraarterial papaverine was infused into the internal carotid artery just proximal to the ophthalmic artery. During the infusion the patient became aphasic and exhibited right hemiplegia. Arteriography performed immediately after the intraarterial papaverine infusion revealed diffuse exacerbation of vasospasm in the distal ACA and MCA territories. A repeat xenon—CT CBF study showed that CBF in the left ACA and the MCA had drastically decreased (2 cc/100 g/minute and 10 cc/100 g/minute, respectively). Despite aggressive management, infarction ultimately developed. This is the first clinical case to illustrate a paradoxical effect of intraarterial papaverine treatment for vasospasm following aneurysmal SAH. The possible mechanisms of this paradoxical response and potential therapeutic reactions are reviewed.

Relationship between intracranial pressure and other clinical variables in patients with aneurysmal subarachnoid hemorrhage

2004 ◽  
Vol 101 (3) ◽  
pp. 408-416 ◽  
Author(s):  
Gregory G. Heuer ◽  
Michelle J. Smith ◽  
J. Paul Elliott ◽  
H. Richard Winn ◽  
Peter D. Leroux
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Clinical Grade ◽  
Icp Monitoring ◽  
Content Type ◽  
Poor Grade ◽  
Symptomatic Vasospasm ◽  
Increased Icp ◽  
Fine Print

Object. Increased intracranial pressure (ICP) is well known to affect adversely patients with head injury. In contrast, the variables associated with ICP following aneurysmal subarachnoid hemorrhage (SAH) and their impact on outcome have been less intensely studied. Methods. In this retrospective study the authors reviewed a prospective observational database cataloging the treatment details in 433 patients with SAH who had undergone surgical occlusion of an aneurysm as well as ICP monitoring. All 433 patients underwent postoperative ICP monitoring, whereas only 146 (33.7%) underwent both pre- and postoperative ICP monitoring. The mean maximal ICP was 24.9 ± 17.3 mm Hg (mean ± standard deviation). During their hospital stay, 234 patients (54%) had elevated ICP (> 20 mm Hg), including 136 of those (48.7%) with a good clinical grade (Hunt and Hess Grades I–III) and 98 (63.6%) of the 154 patients with a poor grade (Hunt and Hess Grades IV and V) on admission. An increased mean maximal ICP was associated with several admission variables: worse Hunt and Hess clinical grade (p < 0.0001), a lower Glasgow Coma Scale (GSC) motor score (p < 0.0001); worse SAH grade based on results of computerized tomography studies (p < 0.0001); intracerebral hemorrhage (p = 0.024); severity of intraventricular hemorrhage (p < 0.0001); and rebleeding (p = 0.0048). Both intraoperative cerebral swelling (p = 0.0017) and postoperative GCS score (p < 0.0001) were significantly associated with a raised ICP. Variables such as patient age, aneurysm size, symptomatic vasospasm, intraoperative aneurysm rupture, and secondary cerebral insults such as hypoxia were not associated with raised ICP. Increased ICP adversely affected outcome: 71.9% of patients with normal ICP demonstrated favorable 6-month outcomes postoperatively, whereas 63.5% of patients with ICP between 20 and 50 mm Hg and 33.3% with ICP greater than 50 mm Hg demonstrated favorable outcomes. Among 21 patients whose raised ICP did not respond to mannitol therapy, all experienced a poor outcome and 95.2% died. Among 145 patients whose elevated ICP responded to mannitol, 66.9% had a favorable outcome and only 20.7% were dead 6 months after surgery (p < 0.0001). According to results of multivariate analysis, however, ICP was not an independent outcome predictor (odds ratio 1.26, 95% confidence interval 0.28–5.68). Conclusions. Increased ICP is common after SAH, even in patients with a good clinical grade. Elevated ICP post-SAH is associated with a worse patient outcome, particularly if ICP does not respond to treatment. This association, however, may depend more on the overall severity of the SAH than on ICP alone.

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