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The perioperative complications associated with cerebral aneurysm surgery require a specific anaesthetic management. Four major perioperative accidents are discussed in this review. The anaesthetic and surgical management in case of rebleeding subsequent to the re-rupture of the aneurysm is mainly prophylactic. It includes haemodynamic stability assurance, maintenance of mean arterial pressure (MAP) between 80-90 mmHg during stimulation of the patient such as endotracheal intubation, application of the skull-pin head-holder, incision, and craniotomy. The aneurysmal transmural pressure should be adequately maintained by avoiding an aggressive decrease of intracranial pressure. Once the skull is open, the brain must be kept slack in order to decrease pressure under the retractors and avoid the risks of stretching and tearing of the adjacent vessels. If, despite these precautions, the aneurysm ruptures again. MAP should be decreased to 60 mmHg and the brain rendered more slack, in order to allow direct clipping of the aneurysm, or temporary clipping of the adjacent vessels. The optimal agents in this situation are isoflurane (which decreases CMRO2), intravenous anaesthetic agents (inspite their negative inotropic effect, they may potentially protect the brain) and sodium nitroprusside. Vasospasm occurs usually between the 3rd and the 7th day after subarachnoid haemorrhage. It may be seen peroperatively. The optimal treatment, as well as prophylaxis, is moderate controlled hypertension (MAP > 100 mmHg), associated with hypervolaemia and haemodilution, the so-called triple H therapy, with strict control of the filling pressures. Other beneficial therapies are calcium antagonists (nimodipine and nicardipine), the removal of the blood accumulated around the brain and in the cisternae, and possibly local administration of papaverine. Abrupt MAP increases are controlled in order to maintain adequate aneurysmal transmural pressure. Beta-blockers, local anaesthetics administered locally or intravenously, a carefully titrated level of anaesthesia, a maintained volaemia play a protective role. Cerebral oedema is sometimes already present at the opening of the skull or may arise later, due to a high pressure under the retractors, to the surgical manipulations of the brain or to brain ischaemia subsequent to temporary clipping. Its treatment is aggressive, with intravenous agents, mannitol, deep hypocapnia and/or lumbar drainage. Prophylaxis, according to the "brain homeostasis concept", is the preferred method to avoid these four peroperative accidents. It includes normal blood volume, normoglycaemia, moderate hypocapnia, normotension, soft manipulation of the brain and optimal brain relaxation.
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PMID:[Peroperative risks in cerebral aneurysm surgery]. 875 91

Published medical evidence pertaining to the management of aneurysmal subarachnoid hemorrhage (SAH) was critically reviewed in order to prepare practice guidelines for this condition. SAH should be considered as a possible cause of all sudden and/or unusual headaches, and every attempt should be made to recognize mild SAHs, as they are still frequently misdiagnosed. The first test for SAH is computed tomography (CT), followed by lumbar puncture when the CT is negative for intracranial bleeding (the case in only several per cent of patients within 24 hours of aneurysm bleeding). Urgent cerebral angiography is necessary to detect the underlying cerebral aneurysm. The advantage of rapid diagnosis of SAH followed by early aneurysm repair is minimizing the risk of catastrophic aneurysm rebleeding. Early surgery for aneurysm repair is often possible and is recommended, unless the aneurysm location or size renders it technically difficult to expose in clot-laden subarachnoid cisterns beneath an acutely swollen brain. Aneurysm ablation is optimally accomplished with open microsurgery and clipping of the aneurysm neck, although other options include proximal parent artery occlusion, "trapping" of the aneurysmal segment of the artery, and embolization of thrombogenic materials (e.g., platinum "microcoils") directly into the aneurysm dome using endovascular techniques. Neurological outcome following SAH is also optimized through the prevention of secondary SAH complications, and further management specific for ruptured cerebral aneurysms can include anticonvulsants, neuroprotectants, and various agents and techniques to prevent or reverse delayed-onset cerebral vasospasm. All patients with aneurysmal SAH should be treated with the calcium antagonist nimodipine, and in certain circumstances patients should receive anticonvulsants. Induced arterial hypertension, hypervolemia and in some instances percutaneous balloon angioplasty are recommended to reverse vasospasm causing symptomatic cerebral ischemia prior to cerebral infarction.
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PMID:Current management of aneurysmal subarachnoid hemorrhage guidelines from the Canadian Neurosurgical Society. 916 96

An estimated 1% to 5% of adults have a cerebral aneurysm. Each year, approximately 1 in 10,000 North Americans suffer an aneurysmal subarachnoid hemorrhage, with greater than 50% combined morbidity and mortality. Cerebral aneurysm formation and rupture is associated with a variety of factors, including increasing age, female gender, hypertension, alcohol, smoking, and genetic factors.
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PMID:Epidemiology of aneurysmal subarachnoid hemorrhage. 933 91

Reports of Ask-Upmark kidney, initially described as a congenital defect in renal development, are uncommon. We report a case with the features of bilateral asymmetrical segmental atrophy in a patient with childhood-onset hypertension. As an adult, she developed cerebral, celiac, and renal artery aneurysms. She underwent successful clipping of the cerebral aneurysm and renal artery repair with preservation of renal function. Novel radiologic techniques make possible the noninvasive diagnosis of segmental atrophy and its complications.
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PMID:Ask-Upmark kidney associated with renal and extrarenal arterial aneurysms. 1019 35

From January 1992 to December 1997, 13 parturients with cerebrovascular diseases had childbirth at our institution. Among them, 8 patients received anesthesia for delivery. Five patients had a history of ruptured arteriovenous malformation (AVM), cerebral aneurysm, or intraventricular bleeding due to moyamoya disease, and they had radical operations. Of these 5 patients after radical operations, three had a repeat cesarean section under spinal anesthesia, and two had a vaginal delivery under epidural anesthesia to avoid excessive hypertension and hyperventilation. There were two patients with a history of cerebrovascular diseases but had no radical operations. Of these two, one patient who was diagnosed as having aneurysm underwent elective cesarean section under spinal anesthesia, and another patient with a history of cerebral bleeding underwent cesarean section under general anesthesia for abruptio placentae. These 7 patients did well during pregnancy and puerperium. The eighth patient experienced severe headache followed by loss of consciousness caused by ruptured AVM, and required an emergency operation. Simultaneous cesarean section and craniotomy were performed at another hospital. Intrauterine fetal death (IUFD) occurred, but mother survived.
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PMID:[Anesthetic management of parturients with cerebrovascular diseases]. 1043 20

Intraventricular hemorrhage (IVH) in adults usually occurs in the setting of aneurysmal subarachnoid hemorrhage or hypertension-related intracerebral hemorrhage. Thus, the underlying cause of IVH is apparent from history and radiographic findings. If the underlying cause of IVH is not apparent, additional studies, including cerebral angiography, magnetic resonance imaging, and toxicology screening, should be performed to identify etiologic agents that may alter management of IVH. Management of IVH is thus done amidst (and must be tempered by) the multiple pharmacologic, surgical, and critical care interventions directed toward the diagnosis and treatment of the underlying cause of IVH. The most immediate threat to life posed by IVH is the development of acute obstructive hydrocephalus. If the hydrocephalus is contributing to a neurologic decline, it must be treated emergently with external ventricular drainage (EVD) through an intraventricular catheter (IVC). The patient with IVH should be evaluated and treated for deficient clotting function before an IVC is inserted. For this purpose, clotting function can be adequately assessed by prothrombin and partial thromboplastin times. Insertion of an IVC may significantly lower intracranial pressure, increasing the transmural pressure difference across the wall of a ruptured cerebral aneurysm and precipitating rerupture of the aneurysm. Therefore, with IVH secondary to a ruptured cerebral aneurysm, it is advisable to delay treatment of hydrocephalus that is not contributing to a neurologic decline until the aneurysm is repaired. Hydrocephalus contributing to significant neurologic decline in the setting of a ruptured aneurysm must be treated immediately despite the unprotected status of the aneurysm. Extreme diligence must be used to allow for the slow, controlled release of cerebrospinal fluid after IVC insertion. This will mitigate the effects of increasing the transmural pressure gradient across the wall of the ruptured aneurysm. In the patient with a neurologic deficit who has IVH-related hydrocephalus and an associated intracerebral hemorrhage, it is best to assume that the hydrocephalus is a significant contributor to the deficit and that it should be treated with EVD. An IVH that is not causing hydrocephalus but is apparently occluding one or both foramina of Monro or the third ventricle should be treated with EVD because obstructive hydrocephalus may develop precipitously and, if unrecognized, may cause irreversible brain damage or death. An IVH that is not likely to cause hydrocephalus because of small volume relative to its location can be followed expectantly. Intraventricular injections of thrombolytic agents through an IVC is a treatment option that may be considered in all patients with IVH that is causing or threatening to cause obstructive hydrocephalus. Unrepaired cerebral aneurysms, untreated cerebral arteriovenous malformations, and clotting disorders are contraindications for this intervention. The surgical evacuation of IVH has a role only in very rare cases in which the IVH is causing a significant mass effect independent of hydrocephalus and associated intraparenchymal brain hemorrhage.
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PMID:Intraventricular Hemorrhage in Adults. 1109 7

We report a 73-year-old woman with Ehlers-Danlos syndrome (EDS) and hypertension who had developed various types of cerebrovascular disease. She had suffered from cerebral hemorrhage of the left putamen at the age of 58, of the left parietal lobe at 64 and cerebral infarction of right internal capsule at 71. EDS type II or III was suggested by two times of skin biopsies. A brain CT at the age of 73 revealed a comparatively large cerebral aneurysm in the territory of the anterior cerebral artery. The patient was treated conservatively, but died due to rupture of the aneurysm. The wall of the aneurysm was made up thin collagen fibers without elastic fibers. There were other multiple small aneurysms in the cerebral arteries, but none in other organs. Deposition of acid mucopolysaccharides was noted in the media of the abdominal aorta. Finally, the present case was thought most likely to be of EDS type IV. It was suggested that one of the causes of the cerebral hemorrhage at the ages of 58 and 64 and the infarction at 71 was related to hypertension, since brain MR angiography at 71 showed no clear aneurysms. In cases of EDS, one should consider the possible formation or rupture of cerebral aneurysm even though the course is favorable.
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PMID:[An autopsy case of Ehlers-Danlos syndrome showing various types of cerebrovascular disease]. 1148 58

Delayed vasospasm as a result of subarachnoid blood after rupture of a cerebral aneurysm is a major complication. It is seen in over half of patients and causes symptomatic ischemia in about one third. If left untreated, it leads to death or permanent deficits in over 20% of patients. The essential cause and the relative contribution of true muscle spasm and other changes in the vessel wall remain uncertain. The mainstays of treatment are careful maintenance of fluid balance, induced hypervolemia and hypertension, calcium antagonists, balloon or chemical angioplasty, and, in some centers, cisternal fibrinolytic drugs. Promising future lines of treatment include gene therapy, nitric oxide donors, magnesium, sustained release cisternal drugs, and several other drugs that are under experimental or clinical trial.
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PMID:Therapeutic approaches to vasospasm in subarachnoid hemorrhage. 1238 13

The abdominal compartment syndrome (ACS) is a clinical entity that develops after sustained and uncontrolled intra-abdominal hypertension. ACS has been demonstrated to affect multiple organ systems including the cardiovascular, respiratory, gastrointestinal, genitourinary, and neurologic systems. To date most descriptions of ACS are found in the trauma literature, but the development of ACS in the general surgical population is being increasingly observed. In this study the development of ACS in a nontrauma surgical population is described and examined. The records of 18 surgical intensive care unit patients with documented ACS were reviewed retrospectively. Data acquired included demographics, urine output in mL/hour, cardiac index in L/m2/min: systemic vascular resistance index in mm Hg/L/m2/min: and pulmonary artery occlusion pressure, peak inspiratory pressure, partial pressure of oxygen in arterial blood, pH, partial pressure of carbon dioxide, and intra-abdominal pressure (all in mm Hg). When they were available values were obtained before and after decompression. Data are presented as mean +/- standard deviation and are analyzed by Student's t-test; significance was accepted to correspond to a P value <0.05. Nineteen episodes of ACS were identified in 18 patients. The average age was 69.2 years, and the observed mortality of the group was 61.1 per cent (11 of 18). Diagnoses included abdominal aortic aneurysm (eight), postoperative laparotomy (six), pancreatitis (three), and cerebral aneurysm (one). Of the parameters examined urine output, peak inspiratory pressure, and cardiac index demonstrated a significant change before and after decompression. The average intra-abdominal pressure was 43.4 mm Hg. Five of 18 patients (two with abdominal aortic aneurysm, two with postoperative laparotomy, and one with pancreatitis) were found to have necrotic bowel on decompressive laparotomy. The development of ACS is described in a surgical intensive care unit. ACS is the end result of uncontrolled intra-abdominal hypertension and results in systemic derangements. Surgical decompression of ACS significantly reduces peak inspiratory pressure while increasing urine output and cardiac index. The observed association between ACS and ischemic bowel may result from decreased mucosal perfusion as a direct result of abdominal hypertension. In our patient population ACS resulted in a 61.1 per cent mortality.
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PMID:Abdominal compartment syndrome in the surgical intensive care unit. 1246 11

Despite the catastrophic consequence of ruptured intracranial aneurysms, very little is understood regarding their pathogenesis, and there are no reliable predictive markers for identifying at-risk individuals. Few studies have addressed the molecular pathological basis and mechanisms of intracranial aneurysm formation, growth, and rupture. The pathogenesis and rupture of cerebral aneurysms have been associated with inflammatory processes, and these have been implicated in the digestion and breakdown of vascular wall matrix. Epidemiological data indicate that the risk of cerebral aneurysm pathogenesis and rupture in women rises during and after menopause as compared to premenopausal women, and has been attributed to hormonal factors. Moreover, experimental evidence supports a role for estrogen in the modulation of each phase of the inflammatory response implicated in cerebral aneurysm pathogenesis and rupture. While the risk of aneurysm rupture in men also increases with age, this increased risk has been attributed to other recognized risk factors including cigarette smoking, use of alcohol, and history of hypertension, all of which are more common in men than women. We hypothesize, therefore, that decreases in both circulating estrogen levels and cerebrovascular estrogen receptor density may contribute to an increased risk of cerebral aneurysm pathogenesis and rupture in women during and after menopause. To test our hypothesis, experiments are needed to identify genes regulated by estrogen and to evaluate gene expression and intracellular mechanisms in cells/tissues exposed to varying concentrations and duration of treatment with estrogen, metabolites of estrogen, and selective estrogen receptor modulators (SERMs). Furthermore, it is not likely that the regulation of cerebrovascular homeostasis is due to the actions of estrogen alone, but rather the interplay of estrogen and other hormones and their associated receptor expression. The potential interactions of these hormones in the maintenance of normal cerebrovascular tone need to be elucidated. Additional studies are needed to define the role that estrogen and other sex hormones may play in the cerebrovascular circulation and the pathogenesis and rupture of cerebral aneurysms. Efforts directed at understanding the basic pathophysiological mechanisms of aneurysm pathogenesis and rupture promise to yield dividends that may have important therapeutic and clinical implications. The development of non-invasive tools such as molecular MRI for the detection of specific cells, molecular markers, and tissues may facilitate early diagnosis of initial pathophysiological changes that are undetectable by clinical examination or other diagnostic tools, and can also be used to evaluate the state of activity of cerebral aneurysm pathogenesis before, during, and after treatment.
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PMID:Deficiencies in estrogen-mediated regulation of cerebrovascular homeostasis may contribute to an increased risk of cerebral aneurysm pathogenesis and rupture in menopausal and postmenopausal women. 1635 55


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