A Computational Model of Blood D-Dimer, Cystatin C, and CRP Levels Predicts the Risk of Intracranial Aneurysms and their Rupture.

Objective: The aim of this study is to construct a computational model of blood D-dimer, cystatin C, and CRP levels and to predict the risk of intracranial aneurysms and their rupture. Methods: A total of 69 intracranial aneurysms patients were selected as the case group, including 28 cases in the ruptured group and 41 cases in the unruptured group. Another 64 non-intracranial aneurysm patients were selected as the control group. The detection results of serum D-dimer, cystatin C, and CRP were collected. The logistic regression computational model was used to analyze the occurrence and risk factors of intracranial aneurysms. The receiver operating curves (ROC) of serum D-dimer, cystatin C, and C reactive protein (CRP) levels for predicting intracranial aneurysms and their rupture were drawn, and the area under the curve (AUC), sensitivity, and specificity were calculated. Results: The serum levels of D-dimer, cystatin C, and CRP in patients with intracranial aneurysms were significantly higher than those in the control group and the differences were statistically significant (P < 0.05). The serum levels of D-dimer, cystatin C, and CRP in patients with ruptured intracranial aneurysms were higher than those in patients with unruptured intracranial aneurysms, and the differences were also statistically significant (P < 0.05). The combined detection of serum D-dimer, cystatin C, and CRP levels has a higher AUC (0.9014) for predicting intracranial aneurysms and higher AUC (0.9412) for predicting ruptured intracranial aneurysms than D-dimer (0.7118 and 0.8750, respectively), cystatin C (0.6489 and 0.6180, respectively), and CRP (0.7764 and 0.6551, respectively) independent detection; the combined detection had a sensitivity of 93.75% and 87.80 for predicting the occurrence and rupture of intracranial aneurysms, and the specificity was 68.12% and 92.86%, respectively. Conclusion: The combined detection of serum D-dimer, cystatin C, and CRP levels is a very valuable indicator for predicting the occurrence and rupture of intracranial aneurysms, and combined detection can provide scientific evidence-based guidance for clinical prediction of the occurrence and rupture of intracranial aneurysms.

Elevation of inflammatory S100A8/S100A9 complexes in intracranial aneurysms.

BACKGROUND: Inflammation-related factors might give further insight into the pathophysiology of vessel wall inflammation and intracranial aneurysm (IA) rupture. One of these factors is the protein complex S100A8/A9, which is released by neutrophils, monocytes, and activated macrophages and is known for its role in cardiovascular disease. OBJECTIVE: To determine if venous S100A8/A9 levels in patients with a ruptured IA (rIA) or unruptured IA (uIA) are elevated compared with a control group. Second, to assess differences between venous and intra-aneurysmal S100A8/A9 levels of rIA and uIA patients. METHODS: A prospective case study was performed between June 2016 and May 2017 in patients harboring a ruptured or unruptured saccular IA. Primary outcome measures were individual S100A8/A9 serum concentrations as measured in venous and intra-aneurysmal blood samples during endovascular treatment. Venous serum S100A8/A9 concentrations from a healthy control group served as a reference. RESULTS: We included 16 patients with either a rIA or uIA and 47 healthy controls. Venous S100A8/A9 concentrations were higher in aneurysm patients (rIA and uIA) than those of healthy controls (P≤0.001). S100A8/A9 concentrations were higher in intra-aneurysmal samples than in venous samples of rIA patients (P=0.011). This difference was not found in uIA patients (P=0.054). Intra-aneurysmal S100A8/A9 levels were higher in rIAs than in uIAs (P=0.04). CONCLUSIONS: Venous S100A8/A9 levels are elevated in patients with both rIAs and uIAs compared with healthy controls and likely represents aneurysm wall inflammation. S100A8/A9 causes macrophage-induced inflammation and degeneration of the vessel wall which might explain higher intra-aneurysmal S100A8/A9 levels found in rIAs than in uIAs.

Serum myelin basic protein as a marker of brain injury in aneurysmal subarachnoid haemorrhage.

BACKGROUND: Myelin basic protein (MBP) is the second most abundant protein in central nervous system myelin. Since the 1980s, it has been regarded as a marker of brain tissue injury in both trauma and disease. There have been no recent reports regarding MBP in aneurysmal subarachnoid haemorrhage (SAH). METHODS: One hundred four SAH patients with ruptured aneurysms underwent endovascular treatment within 24 h of rupture, and 156 blood samples were collected: 104 on days 0-3, 32 on days 4-6 and 20 on days 9-12 post-SAH. MBP levels were assayed using ELISA and compared with the clinical status on admission, laboratory results, imaging findings and treatment outcome at 3 months. RESULTS: MBP levels on days 0-3 post-SAH were significantly higher among poor outcome patients (p < 0.001), non-survivors (p = 0.005), patients who underwent intracranial intervention (p < 0.001) and patients with intracerebral haemorrhage (ICH; p < 0.001). On days 4-6 post-SAH, significantly higher levels were found following intracranial intervention (p = 0.009) and ICH (p = 0.039). There was clinically relevant correlation between MBP levels on days 0-3 post-SAH and 3-month Glasgow Outcome Scale (cc = - 0.42) and also ICH volume (cc = 0.48). All patients who made a full recovery had MBP levels below detection limit on days 0-3 post-SAH. Following endovascular aneurysm occlusion, there was no increase in MBP in 86 of the 104 patients investigated (83%). CONCLUSIONS: The concentration of MBP in peripheral blood after intracranial aneurysm rupture reflects the severity of the brain tissue injury (due to surgery or ICH) and correlates with the treatment outcome. Endovascular aneurysm occlusion was not followed by a rise in MBP in most cases, suggesting the safety of this technique.

Decreased Total Iron Binding Capacity May Correlate with Ruptured Intracranial Aneurysms.

Iron and its derivatives play a significant role in various physiological and biochemical pathways, and are influenced by a wide variety of inflammatory, infectious, and immunological disorders. We hypothesized that iron and its related factors play a role in intracranial aneurysm pathophysiology and investigated if serum iron values are associated with ruptured intracranial aneurysms. 4,701 patients with 6,411 intracranial aneurysms, including 1201 prospective patients, who were diagnosed at the Massachusetts General Hospital and Brigham and Women's Hospital between 1990 and 2016 were evaluated. A total of 366 patients with available serum iron, ferritin and total iron binding capacity (TIBC) values were ultimately included in the analysis. 89% of included patients had anemia. Patients were categorized into ruptured and non-ruptured groups. Univariable and multivariable logistic regression analyses were performed to determine the association between ruptured aneurysms and iron, ferritin, and TIBC. TIBC values (10-3 g/L) within 1 year of diagnosis (OR 0.41, 95% CI 0.28-0.59) and between 1 and 3 years from diagnosis (OR 0.52, 95% CI 0.29-0.93) were significantly and inversely associated with intracranial aneurysm rupture. In contrast, serum iron and ferritin were not significant. In this case-control study, low TIBC was significantly associated with ruptured aneurysms, both in the short- and long term. However, this association may not apply to the general population as there may be a selection bias as iron studies were done in a subset of patients only.

Levels of MMP-9 in patients with intracranial aneurysm: Relation with risk factors, size and clinical presentation.

BACKGROUND: Intracranial aneurysms are arterial anomalies affecting 2% to 3% of the general population in the world and these ruptures are associated with a high mortality. Some risk factors, such as age, gender, smoking, alcohol, hypertension and familial history are associated with the number of aneurysms and their size. In addition, inflammatory processes within the blood vessels of the brain can activate matrix metalloproteinase-9 (MMP-9), which degrades various components of the extracellular matrix, such as elastin. Thereby, this work has aimed at evaluating the relationship between plasma MMP-9 levels and the risk factors that are associated with intracranial aneurysm, as well as investigating the aneurysm statuses (ruptured and unruptured) and comparing them with the control volunteers. METHODS: Between August 2014 to June 2016, blood samples were collected from 282 patients (204 ruptured and 78 unruptured saccular intracranial aneurysms) and 286 control volunteers. The MMP-9 plasma levels were measured by ELISA. Statistical analyzes were performed with SPSS software when using parametric or nonparametric tests, after the normality tests. RESULTS: Higher levels of MMP-9 were found in the aneurysm groups as a whole and when they were stratified by rupture status, then compared with the control group (p < 0.0001). When stratifying them by diameter, those smaller than 7 mm presented high levels of MMP-9 (p < 0.0001), especially in the ruptured ones. As for risk factors, hypertension and smoking were the most important. However, hypertension was mostly associated with the ruptured aneurysms (p < 0.0001). CONCLUSIONS: High levels of MMP-9 were found in smaller ruptured and unruptured intracranial aneurysms (<7 mm) with strongest statistical associations than other sizes, especially when associated with smoking and hypertension.

[Prognostic significance of leukocyte count in the venous blood in the acute stage of cerebral aneurism rupture]. / Prognosticheskaia znachimost' kontsentratsii leikotsitov v venoznoi krovi v ostrom periode razryva tserebral'nykh anevrizm.

AIM: To determine a prognostic role of leukocyte count in the venous blood in the acute stage of cerebral aneurysm (CA) rupture. MATERIAL AND METHODS: Fifty-one patients with CA rupture, aged from 20 to 65 years, hospitalized in the first 72 h over the period from 01.10.12 to 01.02.16 were examined. The severity of disease and anatomical form of hemorrhage was corresponded to III-IV degree on the W. Hunt - R. Hess scale and Fisher scale. All patients underwent surgery. Outcomes after open and endovascular surgeries were similar. RESULTS: Normal leukocyte number in the venous blood at admission was identified in 12 (24%) of patients (on average 7.3±1.4·109/L), leukocytosis in 39 (76%) (14.3±3.1·109/L) (p<0.0001). Leukocyte number in the acute stage of CA rupture was correlated with the frequency and severity of the vessel spasm. In 28 (55%) of patients with ischemic lesions of the brain matter, mean leukocyte number in the first 72 h after hemorrhage was higher by 2-24% (3±4.8·109/L) compared to patients without ischemia (11.9±2.5·109/L) (p=0.06). The level of leukocytes in survivors was lower by 3 - 28% (122±3.4·109/L) compared to patients with fatal outcome and patients with severe neurological deficit after the surgery (14.5±3.9·109/L) (p>0.05). CONCLUSION: The increase in leukocyte number in the venous blood in the first 72 h after CA rupture ≥10,1·109/L is a reliable risk factor of marked vessel spasm. The level of leukocytes in patients with cerebral ischemia and poor prognosis in the first 72h after aneurysmal hemorrhage was higher by 2-28% compared to survivors without neurological impairment or mild neurological deficit.

Myeloperoxidase is increased in human cerebral aneurysms and increases formation and rupture of cerebral aneurysms in mice.

BACKGROUND AND PURPOSE: Cerebral aneurysm (CA) affects 3% of the population and is associated with hemodynamic stress and inflammation. Myeloperoxidase, a major oxidative enzyme associated with inflammation, is increased in patients with CA, but whether myeloperoxidase contributes to CA is not known. We tested the hypotheses that myeloperoxidase is increased within human CA and is critical for formation and rupture of CA in mice. METHODS: Blood was drawn from the lumen of CAs and femoral arteries of 25 patients who underwent endovascular coiling of CA, and plasma myeloperoxidase concentrations were measured with ELISA. Effects of endogenous myeloperoxidase on CA formation and rupture were studied in myeloperoxidase knockout mice and wild-type (WT) mice using an angiotensin II-elastase induction model of CA. In addition, effects of myeloperoxidase on inflammatory gene expression in endothelial cells were analyzed. RESULTS: Plasma concentrations of myeloperoxidase were 2.7-fold higher within CA than in femoral arterial blood in patients with CA. myeloperoxidase-positive cells were increased in aneurysm tissue compared with superficial temporal artery of patients with CA. Incidence of aneurysms and subarachnoid hemorrhage was significantly lower in myeloperoxidase knockout than in WT mice. In cerebral arteries, proinflammatory molecules, including tumor necrosis factor-α, cyclooxygenase-2 (COX2), chemokine (C-X-C motif) ligand 1 (CXCL1), chemokine (C motif) ligand (XCL1), matrix metalloproteinase (MMP) 8, cluster of differentiation 68 (CD68), and matrix metalloproteinase 13, and leukocytes were increased, and α-smooth muscle actin was decreased, in WT but not in myeloperoxidase knockout mice after induction of CA. Myeloperoxidase per se increased expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 in endothelial cells. CONCLUSIONS: These findings suggest that myeloperoxidase may contribute importantly to formation and rupture of CA.

Surgical treatment of giant aneurysm of hepatic artery: report of three cases.

BACKGROUND/AIMS: To explore the surgical way of treating giant hepatic artery aneurysm(HAA). METHODOLOGY: Three hepatic artery aneurysm patients who were performed aneurysm resection without revascularization of the hepatic artery were reviewed. After surgery, the values of liver function and enhanced CT scan of the patients were followed. RESULTS: All the three patients were recovered well postoperatively and only several values of biochemistry marks of liver function as ALT, AST, TBIL and DB in one case with liver cirrhosis were elevated and decreased to normal ranges in a few days postoperatively. The values of biochemistry marks of liver function in other two cases were within normal limits. The enhanced CT scan also showed arteries in the liver after hepatic artery aneurysm resection. CONCLUSIONS: Giant HAA may be safely removed without revascularization of the hepatic artery.

Circulating microRNAs serve as novel biological markers for intracranial aneurysms.

BACKGROUND: Biological markers that can be used to predict the risk of intracranial aneurysms (IAs) are not available. METHODS AND RESULTS: To clarify whether circulating microRNAs could be used as biomarkers for IA, we carried out microarray assays in a screening cohort of 40 IA patients (20 unruptured and 20 ruptured) and 20 healthy volunteers. We identified 20 microRNAs that were unanimously changed in both ruptured and unruptured patients. We confirmed 60% of these changed microRNAs by a separate microarray test with an independent validation cohort (n=143 including 93 IA patients). To identify potential biomarkers, we combined the 2 cohorts and performed quantitative real-time polymerase chain reactions for selected target microRNAs. Logistic regression analysis demonstrated that miR-16 and miR-25 were independent factors for IA occurrence (P<0.001). After controlling for age, sex, smoking, and history of hypertension, the contributions of miR-16 and miR-25 were still highly significant (P<0.001). The adjusted odds ratio values for miR-16 and miR-25 were 1.52 (95% CI 1.31 to 1.77) and 1.53 (1.30 to 1.79). Combining both miR-16 and miR-25 in a single model did not improve the performance of risk association. CONCLUSIONS: Our data suggest that circulating miRNAs may be novel biological markers that are useful in assessing the likelihood of IA occurrence.

Gene expression profiling of blood in ruptured intracranial aneurysms: in search of biomarkers.

The molecular mechanisms underlying the systemic response to subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms (RAs) are not fully understood. We investigated whether the analysis of gene expression in peripheral blood could provide clinically relevant information regarding the biologic consequences of SAH. Transcriptomics were performed using Illumina HumanHT-12v4 microarrays for 43 RA patients and 18 controls (C). Differentially expressed transcripts were analyzed for overrepresented functional groups and blood cell type-specific gene expression. The set of differentially expressed transcripts was validated using quantitative polymerase chain reaction in an independent group of subjects (15 RA patients and 14 C). There were 135 differentially expressed genes (false discovery rate 1%, absolute fold change 1.7): the abundant levels of 78 mRNAs increased and 57 mRNAs decreased. Among RA patients, transcripts specific to T lymphocyte subpopulations were downregulated, whereas those related to monocytes and neutrophils were upregulated. Expression profiles of a set of 16 genes and lymphocyte-to-monocyte-and-neutrophil gene expression ratios distinguished RA patients from C. These results indicate that SAH from RAs strongly influences the transcription profiles of blood cells. A specific pattern of these changes suggests suppression in lymphocyte response and enhancements in monocyte and neutrophil activities. This is probably related to the immunodepression observed in SAH.

Mobilization of circulating endothelial progenitor cells after endovascular therapy for ruptured cerebral aneurysms.

Emerging evidence shows that circulating endothelial progenitor cells (EPCs) promote regeneration of the endothelium at sites of vessel injury. This study was designed to test the hypothesis that EPCs are mobilized in patients who had ruptured cerebral aneurysm (CA) and underwent endovascular therapy. Fourteen patients with ruptured CAs were recruited and blood samples were analyzed after coil embolization surgery. Blood samples were also obtained from 18 healthy control subjects who had no evidence of CAs and did not undergo endovascular surgery. We measured the numbers of circulating EPCs, levels of plasma vascular endothelial growth factor (VEGF) and platelet counts. EPCs significantly increased in patients with ruptured CAs and underwent surgical coil embolization, reaching a peak level on day 14 post operation. The levels of plasma VEGF and platelet counts also significantly increased in parallel with the increase in EPCs, leading to significant positive correlations of circulating EPCs with VEGF in plasma (r=0.636, P<0.01) and platelet counts (r=0.721, P<0.001), respectively. The finding suggests that EPCs are mobilized upon surgery and may play a critical role in repairing injured vascular endothelium. Levels of EPCs in peripheral blood could also serve as a prognostic marker for the outcomes of ruptured cerebral aneurysms after surgical repair.

TNF-alpha and sICAM-1 in intracranial aneurismal rupture.

INTRODUCTION: Subarachnoidal hemorrhage (SAH) occurring after aneurysmal rupture produces an inflammatory response in the cerebral circulation. Tumor necrosis factor (TNF)-alpha is a major cytokine in this process. Adhesion molecules provide information on inflammatory reactions taking place in the walls of blood vessels. Clinical evidence suggests a role of soluble intercellular adhesion molecule (sICAM)-1 in early hemorrhagic events. This study aimed to evaluate the implementation of early TNF-alpha and sICAM-1 serum measurement for the prognosis of patient outcome after intracranial aneurysmal rupture. MATERIALS AND METHODS: The study consisted of 27 patients with a diagnosis of intracranial aneurysm. SAH was evaluated on admission according to the Fisher scale, patients' consciousness with the Glasgow Coma Scale, clinical grading with the Hunt and Hess scale, and clinical outcome with the Glasgow Outcome Scale (GOS). Blood samples were drawn within 72 h after arrival at the emergency room. Serum concentrations of TNF-alpha and sICAM-1 were assayed with the ELISA method. RESULTS: The initial serum TNF-alpha concentration in the aneurysmal patients was low and did not correlate with radiological and clinical scores. The serum sICAM-1 level positively correlated with the severity of bleeding assessed by the Fisher scale and negatively with the patient's scoring in the GOS. CONCLUSIONS: This study demonstrated the absence of a systemic TNF-alpha-mediated inflammatory response at the onset of subarachnoid hemorrhage. Early measurement of serum sICAM-1 levels offers a potential prognostic value in the assessment of patients' outcome after brain aneurysmal rupture.

Changes in laboratory values and their relationship with time after rupture of an abdominal aortic aneurysm.

PURPOSE: Many laboratory values are abnormal after surgery for a ruptured abdominal aortic aneurysm (RAAA). However, these changes have not been comprehensively evaluated. We analyzed the changes in routine laboratory values and how these changes related to outcome in a consecutive series of RAAA patients. METHODS: All patients who underwent surgery for an RAAA between January 1990 and June 2003 at our hospital were included in this study. We analyzed laboratory data acquired during the first week for all patients and at discharge for survivors. We categorized 29 different measurements into six categories based on the related pathological process, including hematology and coagulation, metabolism, systemic inflammation, renal function, liver function, and electrolytes. RESULTS: A total of 290 patients underwent RAAA surgery, with a hospital mortality of 34%. Hemorrhage was the most common cause of early death, whereas multiple-organ failure (MOF) was the most common cause of death several days after surgery. Most laboratory values deviated from normal at multiple time points and they differed significantly between survivors and nonsurvivors. CONCLUSIONS: Both survivors and nonsurvivors of RAAA surgery displayed characteristic time-dependent laboratory abnormalities. Awareness of these responses may help us predict patients prone to complications.

Acute lung injury after ruptured abdominal aortic aneurysm repair: the effect of excluding donations from females from the production of fresh frozen plasma.

OBJECTIVES: Transfusion-related acute lung injury may contribute to the development of acute lung injury in the critically ill, due to plasma from female donors containing antileukocyte antibodies. In July 2003, the U.K. National Blood Service stopped using female donor plasma for the production of fresh frozen plasma. Patients undergoing repair of a ruptured abdominal aortic aneurysm receive large amounts of fresh frozen plasma and often develop acute lung injury. We investigated whether the change to male fresh frozen plasma was associated with a change in the frequency of acute lung injury in these patients. DESIGN: A retrospective, before and after, observational, single-center study. SETTING: Tertiary care center and a regional blood center. PATIENTS: The study included 211 patients undergoing open repair of a ruptured abdominal aortic aneurysm between 1998 and 2006. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Primary outcome was the development of acute lung injury in the first 6 hrs after surgery. Secondary outcomes were significant hypoxia (PaO2/FiO2 ratio <300), time to extubation, and survival at 30 days. Groups were well matched and received similar volumes of intravenous fluids and blood components. There was significantly less acute lung injury following the change to male fresh frozen plasma (36% before vs. 21% after, p = .04). At 6 hrs after surgery, fewer patients were hypoxic (87% before vs. 62% after, p < .01). In multivariate analysis, the change in donor policy was associated with a decreased risk of developing acute lung injury (odds ratio 0.39; 95% confidence interval, 0.16-0.90). Time to extubation and survival at 30 days were not statistically different between groups. CONCLUSIONS: The policy to exclude female donors from the production of fresh frozen plasma was associated with a decrease in the frequency of acute lung injury in patients undergoing repair of a ruptured abdominal aortic aneurysm.

Late massive uterine hemorrhage caused by ruptured uterine artery pseudoaneurysm after laparoscopic-assisted myomectomy.

Diagnosis and management of ruptured uterine artery pseudoaneurysm after laparoscopic-assisted myomectomy is described.

Elevated plasma MMP1 and MMP9 are associated with abdominal aortic aneurysm rupture.

BACKGROUND: The role of matrix metalloproteinases (MMPs) in abdominal aortic aneurysm (AAA) formation is well established. However the changes in plasma MMP levels with AAA rupture have not been reported. The aim of this study was to determine circulating levels of MMPs in non-ruptured and ruptured AAA immediately prior to open repair. METHODS: Concentrations of MMPs and their endogenous tissue inhibitors (TIMPs) were quantified using ELISA in pre-operative plasma samples from non-ruptured and ruptured AAA. RESULTS: MMP1 and MMP9 were elevated in the plasma of ruptured AAA versus non-ruptured AAA. A four-fold elevation in pre-operative plasma MMP9 was associated with non-survival at 30 days from rupture surgery compared with those surviving for greater than 30 days. CONCLUSION: In conclusion, these findings support the role of MMPs in AAA pathogenesis. Elevation of MMP9 was associated with ruptured aneurysm related 30-day mortality and may represent a survival indicator in this group.

Assessment of the haemostatic system in patients surgically treated for ruptured cerebral aneurysm.

BACKGROUND AND PURPOSE: The aim of the study was to evaluate selected markers of thrombin generation and subsequent fibrinolysis in patients with aneurysmal subarachnoid haemorrhage (SAH) and to assess the relationship between thrombin generation/fibrinolysis and clinical course and outcome. MATERIAL AND METHODS: This prospective study included 72 patients after aneurysmal SAH who underwent surgery within 72 hours after onset of symptoms. The results were compared with 84 control patients without SAH. Selected markers of thrombin generation (thrombin-antithrombin complexes, TAT), fibrinolysis (D-dimer) and fibrinogen level were examined in blood just after admission and on day 7 after surgery. The relationship between levels of those markers and selected clinical and radiological data, and outcome at 3-6 months after surgery, were assessed. RESULTS: On admission, patients with SAH had higher levels of TAT (p<0.001), D-dimer (p=0.048), and fibrinogen than the control group (p<0.001). Also, patients with severe bleeding demonstrated higher TAT (p<0.001) and D-dimer (p=0.04) levels. The admission level of TAT (higher than 24 g/l; odds ratio = 10.8) and the elevated blood fibrinogen level (odds ratio = 1.2) showed a strong correlation with mortality. Furthermore, a level of TAT higher than 24 g/l (odds ratio = 9.98) and the level of fibrinogen (odds ratio = 1.3) strongly correlated with poor outcome. There was no significant correlation between markers of coagulation on the 7th day after surgery for SAH and the outcome. CONCLUSIONS: Activation of blood coagulation as well as the fibrinolytic system occurred early in the course of SAH. Such activation was associated with poor clinical status of patients on admission, greater amount of subarachnoid blood, and poor clinical outcome. Thus, blood levels of TAT and fibrinogen are independent factors associated with mortality and morbidity after aneurysmal SAH.

How does spontaneous hemostasis occur in ruptured cerebral aneurysms? Preliminary investigation on 247 clipping surgeries.

BACKGROUND: Rupture of cerebral aneurysms results in subarachnoid hemorrhage. In many cases, bleeding from aneurysms spontaneously arrests. Although bleeding from cerebral aneurysms has been reported to arrest from outside, bleeding from some aneurysms can arrest in different ways. METHODS: Between April 2002 and March 2004, we prospectively investigated mechanisms of spontaneous hemostasis in ruptured aneurysms by macroscopic examination when performing craniotomy and clipping surgeries. RESULTS: Hemostatic mechanisms were investigated in 247 patients with ruptured aneurysm (77 men, 170 women; age range, 25-95 years). Hemostatic mechanisms were divided into 3 different patterns. In the most common pattern (79.4%), the surface of the aneurysm rupture point was sealed from the outside by a platelet plug or fibrin net (outside-arrest pattern). In some aneurysms (10.1%), a thrombus or platelet plug was attached to the rupture point from inside the aneurysm (inside-arrest pattern). In a very small number of aneurysms (1.6%), a naked thrombus covered the hole made on the arterial wall or small remnant of the aneurysmal dome (bursting pattern) The mechanism remained unclear in the remaining 8.9% of aneurysms. Multivariate analysis revealed that alert consciousness on admission (WFNS grade I) significantly associated with usual hemostasis (outside arrest pattern: OR, 3.8; 95% CI, 1.4-10.0; P = .008). Borderline association with usual hemostasis was found in aneurysms with a size of 5 or smaller than 5 mm (OR, 2.6; 95% CI, 0.99-7.1; P = .052). CONCLUSIONS: The present preliminary study revealed that arrest of bleeding from a ruptured cerebral aneurysm does not always occur from outside the aneurysm. Unusual mechanisms of hemostasis are seen in approximately 12% of ruptured aneurysm. The outside-arrest-pattern aneurysm was more common for smaller aneurysms, and these patients tended to be of better grade. Further studies are necessary to explore the mechanism of hemostasis for ruptured cerebral aneurysms.