SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
A 73-year-old man had been diagnosed with an abdominal aortic aneurysm. Surgery was impossible due to poor cardiopulmonary condition. The patient collapsed due to rupture of the aneurysm.
Ruptured cerebral aneurysm is the most common cause of non-traumatic subarachnoid hemorrhage. Subsequent to this catastrophe, patients have usually evidence of severe headache with sudden onset, signs of meningeal irritation, and depression of consciousness. Difficulties in diagnosis arise when the clinical picture is not classical. Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is the leading cause of death and disability after aneurysm rupture. In the presence of a typical history and a normal CT scan, lumbar puncture should be performed with spectrophotometry analysis of the supernatant. After subarachnoid hemorrhage has been confirmed, four-vessel angiography should be performed as soon as possible. The surgical treatment of subarachnoid hemorrhage caused by ruptured aneurysm is the method of choice.
Rupture of cerebral aneurysms is a complex and devastating pathophysiologic event. The successful management of aneurysm rupture requires a dedicated multidisciplinary team. This article reviews pathophysiology; clinical grading that can be used to predict outcome and guide therapy; factors that may affect outcome such as rebleeding, poor clinical grade, intracerebral hemorrhage, intraventricular hemorrhage, and acute hydrocephalus; preoperative care and assessment; pharmacological therapy; anesthetic, surgical, and endovascular considerations; and postoperative care following aneurysm rupture.
Aneurysm rupture occurs when local wall stresses exceed the tensile strength of vascular tissues. Knowledge of vascular wall stresses, and insight into the factors that change wall stresses, will lead to a better understanding of how aneurysms grow and rupture. In this study, stress distributions in the walls of small aneurysms were calculated using finite element analysis (FEA), a numerical technique able to predict stress distributions with greater accuracy than the Law of Laplace. Stresses were calculated for an initial small aneurysm and compared to stresses produced by increasing the aneurysm diameter, decreasing the wall thickness, and changing the material properties of the aneurysm wall. FEA calculations indicate that wall stresses are generally greatest on the inner surface of an aneurysm, and decrease nonlinearly as the outer wall is approached. Maximum wall stresses occur along the region of greatest diameter, and circumferential stresses tend to be significantly greater than longitudinal stresses. Doubling the diameter of an aneurysm produced a twofold increase in the maximum wall stress. Decreasing the wall thickness by half also produced a doubling of the maximum wall stress. Changing material properties produced no appreciable change in wall stresses. However, weaker materials fail at lower stresses, thus halving material strength would be equivalent to doubling wall stresses. We conclude that the Law of Laplace is inaccurate in predicting the complicated stress distributions that exist in aneurysm walls, and that more sophisticated tools, such as FEA, will be needed to understand this complex phenomenon. We also conclude that proportional changes in the diameter, wall thickness, or aneurysm tissue strength have roughly equivalent effects on aneurysm growth and rupture.
Sixty four multiple intracranial aneurysm cases have been analysed for the purpose of identifying the relation between aneurysm rupture and aneurysmal features, mass signs, vasospasms and locations of the aneurysms. 1) 85% of the larger and largest aneurysm in each case were the ruptured aneurysm. 2) Aneurysms with a greater ratio of length to width showed a high frequency of rupturing. 3) Irregularities of the aneurysmal wall and the existence of a daughter aneurysm attached to the main aneurysm have a tendency to rupture. 4) Evidence of mass signs, associated with intracerebral, subarachnoid and subdural hematoma or a cerebral edema is also useful for the identification of the ruptured aneurysm. 5) Anterior communicating artery aneurysms have a relatively high frequency of being the ruptured aneurysm in cases of multiple aneurysm. 6) By utilizing all the investigated factors of the angiogram, the ruptured aneurysm might be identified in about 90% of the cases of multiple aneurysms.
An altered equilibrium of protease/protease-inhibitor factors may be involved in the pathogenesis of aneurysm rupture: alpha 1-antitrypsin (alpha 1-AT) represents the most relevant inhibitor of elastase, a proteolytic enzyme enhancing catabolic processes of collagen metabolism. Cigarette smoking has been shown to significantly reduce the inhibitory effect of alpha 1-AT on proteases. In the present study we test the hypothesis whether the activity of alpha 1-AT is altered in patients with subarachnoid haemorrhage (SAH) and if is there any relationship between alpha 1-AT activity and the high risk of aneurysm rupture in smokers. The patients were subdivided in the following groups: (a) patients with unruptured aneurysm (n = 10); (b) patients presenting with SAH admitted within 48 h after the episode (n = 20); (c) patients presenting with SAH admitted > 48 h after the episode (n = 14); (d) controls (n = 10): patients with neither cerebrovascular nor acute disease. Blood samples were obtained immediately at admission. Measurement of alpha 1-AT level was determined by immunoturbidimetric method. In order to obtain qualitative data about the anti-protease activity of alpha 1-AT (expressed as collagenase inhibitory percentage capacity (CIC) at different doses) we consider the 20 cases admitted for SAH within 48 h. The mean serum level of patients with unruptured aneurysms is significantly lower than that of patients with SAH (p < 0.01), while the mean serum level of alpha 1-AT in controls does not significantly differ from other groups. The mean serum level of alpha 1-AT in patients admitted > 48 h after SAH is significantly higher than that of patients admitted within 48 h after the haemorrhage (p < 0.02). Considering the smoking habit of patients, there is no significant difference in alpha 1-AT levels in each subgroup of patients. A multivariate analysis considering alpha 1-AT CIC, showed that alpha 1-AT CIC in patients with ruptured aneurysms is significantly reduced if compared to controls and unruptured aneurysms (F = 50.759; p < 0.001). Moreover, considering alpha 1-AT CIC and smoking habit in each group the covariance analysis showed that while in controls and unruptured aneurysms there is no difference in alpha 1-AT CIC between smokers and non smokers, in cases of SAH, cigarette smoking significantly influences the alpha 1-AT CIC. The present results suggest that the basic mechanism behind the increased risk of SAH in smokers involves a qualitative deficiency of alpha 1-AT.
Explore the source record for details and available documents.
Headache is a common complaint in emergency departments, but only a small percentage of patients have a serious disease. Nevertheless, some forms of headache, such as "warning headaches", need special attention. By far the most common symptom associated with aneurysmal minor bleed (warning leak) is a sudden headache that is considered to be a warning symptom of impending aneurysmal rupture. In the presence of sudden severe headache with or without meningeal signs or nausea, subarachnoid hemorrhage should always be considered. Recognition of these warning headaches probably offers the best opportunity of reducing the otherwise serious mortality and morbidity of aneurysmal subarachnoid hemorrhage. This report describes 7 non-consecutive patients presenting warning headaches before major aneurysm rupture. Based on our experience and a review of the literature, we recommend a management algorithm for patients presenting with sudden severe headache.
Aneurysms of the sinus of Valsalva are uncommon disorders and are usually congenital in origin. When these aneurysms rupture into an intracardiac chamber, they may be silent initially but later give rise to progressive heart failure due to left or right shunting and aortic regurgitation. The mortality and morbidity in untreated cases is high. We report 13 patients with ruptured aneurysms of the sinus of Valsalva who underwent surgical repair. There were seven males and six females with a mean age of 24.5 years. Three patients were asymptomatic and five were in congestive cardiac failure. The majority of patients (61.5%) had insidious onset of symptoms, only 2 cases presenting acutely. The connection was between the right aortic sinus and the right ventricle in 11 cases and the non coronary sinus and the right ventricle in 2 cases. Associated cardiac anomalies included a ventricular septal defect (8 patients) and aortic regurgitation (6 patients). There was 1 post operative death and 1 patient required re-operation three months later for a recurrence of the fistula. All 6 patients with aortic regurgitation required aortic valve replacement. All patients remained well and asymptomatic during follow up ranging from 2 to 19 years.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The purpose of the present study was to describe the clinical course of patients with Grade-5 ruptured aneurysms (WFNS grading). Among 250 consecutive cases of ruptured aneurysms, 60 Grade-5 patients were reviewed retrospectively, consisting of 24 males and 36 females with an average age of 58 years. Thirty-two patients were directly transferred to our clinic, while the remaining 28 were referred from other clinics. Duration from rupture to arrival at our clinic was within 1 hour in 25 cases and within 2 hours in 43 cases. Systolic blood pressure on admission was 186 mmHg on average. Obvious misdiagnoses by primary physicians were made in 7 cases. Ventricular drainage and clipping/trapping of the aneurysms were performed in 7 and 25 cases, respectively. Forty-nine patients died and the remaining 11 survived. One made a good recovery, 1 was moderately disabled, 8 severely disabled, and 1 in a vegetative state. The prognosis for Grade-5 patients is well known as being extremely poor, which also was the case in our series. Early referral and early surgical intervention have not changed this poor prognosis. Possible improvement of the outcome of this group might be expected by 1) public health and primary physician education on aneurysmal subarachnoid haemorrhage, and 2) control of blood pressure during referral.
Subdural hematomas (SDH) from ruptured aneurysm (RA) are much less common than intracerebral (ICH) hematomas or subarachnoid (SAH) or intraventricular hemorrhage (IVH). With computerized tomography, preoperative diagnosis is now made more often. The authors have collected 18 such cases from a review of 897 cases of RA admitted to eleven medical centers in 1980 and 1981. Nine (50%) of these patients died prior to discharge from hospital. Four (22%) had surgery and died postoperatively and 9 (50%) were operated upon and survived. Thirteen (72%) of the patients showed anisocoria, decreased consciousness and unilateral weakness prior to surgery. Eight (89%) of the fatalities had shown preoperative herniation as opposed to only 5 (56%) of the survivors. The overall incidence of delayed ischemia due to vasospasm was 11% (2 cases). Those who died had greater midline shift and larger SDH on the admission CT scan. Sixteen (89%) of these patients were female. Thirteen (72%) had ruptured aneurysms on the internal carotid artery. All of these hematomas were unilateral and uniformly hyperdense, and the convexity hematomas were crescentic in shape. Seventeen (94%) had evidence of blood in locations other than the subdural space. If the patient is potentially salvageable and has a midline shift, the SDH should probably be evacuated immediately and the aneurysm clipped at the same operation since the development of a tentorial herniation has such an adverse effect on outcome.
The efficacy of intravenous Nimodipine (used at the rate of 2 mg.h-1) was investigated in the treatment of delayed ischemic deterioration or angiographic vasospasm after subarachnoid haemorrhage caused by a ruptured aneurysm in a randomized, double-blind, placebo-controlled multicenter study. A total of 127 case reports was validated: 73 patients received Nimodipine, 54 received placebo. The two groups were comparable in demographic and clinical status data. Analysis of number of deaths and of patients with severe deficit related to vasospasm alone showed a significant statistical difference (Nimodipine = 19%; Placebo = 49%; p = 0.01). The risk of mortality connected with vasospasm was reduced by 82% in the treated group. Side effects were equally frequent in the two groups. The only difference noted was the increase in heart rate in group Nimodipine. The results of this study demonstrate the efficacy of intravenous Nimodipine in the treatment of consequences of cerebral vasospasm after a subarachnoid haemorrhage caused by a ruptured aneurysm.
BACKGROUND AND PURPOSE: We describe four cases of aneurysmal rupture during embolization with Guglielmi electrodetachable coils (GDCs) in an attempt to identify those aneurysms whose rupture during embolization represents a life-threatening risk; our emphasis is on emergency management, in particular, ventriculostomy. METHODS: Medical records were reviewed retrospectively for 91 aneurysms treated with GDCs 0 to 21 days after subarachnoid hemorrhage. Rupture was ascertained by the presence of extravascular effusion of contrast medium. RESULTS: Of the perforated aneurysms, two involved the anterior communicating artery, one the posterior inferior communicating artery, and one the basilar artery. Only two patients, whose aneurysms were located in the posterior fossa, had major complications (arterial hyperpressure, mydriasis, angiographically documented circulatory arrest or slowing). One of these patients died and the other improved after emergency ventriculostomy. CONCLUSION: Aneurysmal perforation during embolization may be accompanied by severe intracranial hypertension, which causes either a decrease or arrest of cerebral perfusion, the duration of which determines clinical outcome. Emergency ventriculostomy (which should be performed in the angiographic suite) is an effective means to reduce intracranial pressure. Recognition of aneurysms associated with a high risk of mortality by rupture in the course of embolization (recently ruptured small aneurysms, posterior fossa aneurysms, associated ventricular dilatation, massive cisternal hemorrhage) and use of proper logistics should ensure the effective management of this devastating complication.
The definition of an elderly person is debateable; however, age is a recognised negative prognostic factor for outcome after subarachnoid haemmorrhage, and the age cut-off of 60 years is accepted to define a high risk population. The goal of this article is to access the outcome in this precise population of patients that underwent endovascular treatment (EVT) after aneurysm rupture. Forty-two patients (mean age = 70.24) had 40 aneurysms located at the anterior circulation and nine at the posterior circulation. Thirty-seven (87.9%) patients had Fisher III or IV. Forty-six (93.8%) aneurysms were smaller than 15 mm. Twenty-eight (66.7%) patients were in good neurological state on admission (Hunt and Hess I-III) and 14 (33.3%) in poor state. Satisfactory occlusion rate (total occlusion or neck flow) was achieved in 75% of patients. Follow-up was available in 19 (43.18%) out of the 44 aneurysms treated. Aneurysm recanalization was disclosed in three cases. Satisfactory outcome was achieved on: 60.7% of good grades, 21.4% of poor grades, 43.7% of patients with and 57.6% of patents without comorbidites. Fisher grade (P = 0.0346), comorbidities (P = 0.525) and risk factors (P = 0.515) were not associated with clinical outcome. No age cut-off (65,70 and 75) for favourable outcome could be established, P-values were 0.723, 0.741 and 0.738, respectively. Advancing of age was not associated with an increase number of unfavourable outcome (P = 0.125). Poor neurological status on admission was the only variable associated with unfavourable outcome (P = 0.02). Mortality and morbidity rate related to the procedure were 4.8% and 9.5% respectively. Age should not be taken alone for precluding treatment in ruptured aneurysms, EVT can be considered as a first therapeutic option for elderly persons, since an overall favourable outcome could be achieved in most cases, mainly in non-comatose patients.
Rupture of a splenic artery aneurysm is a rare and usually catastrophic event, most commonly associated with pregnancy. In spite of increasingly common reliance on abdominal angiography, magnetic resonance imaging, and computerized tomography during the past quarter century, clinicians uncommonly recognize any of the various splanchnic arterial aneurysms absent premonitory signs or symptoms. Accordingly, rupture of a visceral aneurysm, including splenic artery aneurysm, typically presents as sudden, unexpected obtundation or death. As a consequence, the initial recognition and diagnosis of splenic artery aneurysm rupture take place only at autopsy. This report presents two such cases of sudden death resulting from splenic artery aneurysm in a pregnant woman and a postpartum woman, respectively.
BACKGROUND: It is well-known that arachnoid cysts of the middle fossa are associated often with chronic subdural hematomas and/or intracystic hemorrhages. However, reports of an arachnoid cyst associated with an aneurysm are rare. CASE DESCRIPTION: A 45-year-old man was admitted with headache due to intracystic hemorrhage in the sylvian fissure, associated with a saccular aneurysm at the bifurcation of the internal carotid artery. The aneurysm ruptured into the arachnoid cyst, without causing a subarachnoid hemorrhage. Subsequently, the neck of the aneurysm was clipped successfully. The patient's postoperative course was uneventful, and there was no vasospasm. CONCLUSIONS: This is the first reported case of an intracystic hematoma due to a ruptured aneurysm. We discuss the possible etiology of the association between the aneurysm and the arachnoid cyst, and the formation mechanism for the intracystic hematoma that did not result in a subarachnoid hemorrhage.