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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analyzed the management of 310 patients with acute subarachnoid hemorrhage from a ruptured intracranial aneurysm, 280 of whom survived to operation, according to preoperative neurologic function, location and size of the aneurysm and timing of operation. Severe initial bleeding, rebleeding (usually within two weeks) and delayed ischemia were major preoperative problems; 10 per cent died, and 13 per cent deteriorated before operation. Operative mortality was 5 per cent, ranging from 1.6 per cent of patients with normal preoperative neurologic function to 35 per cent of severely disabled patients. Intraoperative complications (5 per cent of cases) related chiefly to the size and location of the aneurysm, but postoperative delayed ischemia (minor and reversible in 10 per cent and severe in 5 per cent) related to timing of operation and occurred primarily in patients afflicted within the previous 10 days. The results of surgical treatment, including preoperative deaths, were better than the natural history of the illness, the difference being apparent after one month's observation.
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PMID:Subarachnoid hemorrhage from intracranial aneurysms. Surgical management and natural history of disease. 66 71

The authors have analyzed a total of 96 consecutive cases in which vasospasm followed subarachnoid hemorrhage (SAH). The SAH was caused by ruptured intracranial aneurysm or developed after aneurysm surgery. Usually at least 4 days elapsed between SAH and the onset of vasospasm. Vasospasm subsided an average of 2 weeks after onset. Of 68 patients with preoperative vasospasm, eight died due to cerebral edema resulting from ischemia, and 49% of survivors had neurological deficits. Preoperative vasospasm was not aggravated by surgical intervention when operations were carried out more than 7 days after the onset of vasospasm. Postoperative vasospasm was found in 25 of 52 patients who underwent operation within 1 week after SAH (excluding cases in Grade V). Five of these patients died, all of whom underwent surgery between the fourth and seventh day after SAH (the day of SAH was counted as the first day). There were no deaths among 20 patients operated on within the first 3 days after SAH. Postoperative vasospasm was always mild in these cases, when it occurred, probably because blood clot or blood-stained cerebrospinal fluid was removed by operative procedures. In all cases, 4 to 11 days elapsed between the last SAH and the onset of postoperative vasospasm regardless of the timing of surgery.
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PMID:Significance of vasospasm in the treatment of ruptured intracranial aneurysms. 89 45

The clinical course, operative technique, and angiographic outcome are reported for a patient with a giant intracranial aneurysm of the proximal middle cerebral artery (MCA) who presented with symptoms of ischemia. Treatment of the aneurysm required bypassing the involved MCA bifurcation, but the patient lacked a suitable donor superficial temporal artery. The involved arterial segment was therefore bypassed with a side-to-side anastomosis of the anterior temporal artery to one of the secondary trunks of the MCA. This bypass eliminated the need to harvest a vein graft and re-established flow using in situ intracranial vessels of similar diameter, minimal arterial dissection, and only one suture line.
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PMID:Anastomosis of the anterior temporal artery to a secondary trunk of the middle cerebral artery for treatment of a giant M1 segment aneurysm. Case report. 156 47

A review of a series of 56 patients with a giant intracranial aneurysm showed that 28 presented with signs related to the mass effect and 19 with subarachnoid hemorrhage (SAH). Additional clinical signs observed were seizures, ischemia, and endocrinological disturbances. Fourty-five aneurysms involved the carotid artery territory and eleven the vertebrobasilar system. On computed tomography (CT) images partially thrombosed aneurysms (23 cases) showed 1) a marginal or central "target" appearance on contrast enhanced scans corresponding to the non-thrombosed lumen as demonstrated by angiography, 2) capsular enhancement in 16 cases and 3) calcifications in 9. SAH occurred in 13 and 6 cases of non-thrombosed and partially thrombosed aneurysms, respectively. Magnetic resonance imaging (MRI) in 6 cases showed several layers of thrombosis in 4 cases and a small signal void close to the parent artery. In one case of a non-thrombosed aneurysm, thrombosis was mimicked by flow artifacts of MRI.
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PMID:Clinico-radiological spectrum of giant intracranial aneurysms. 179 40

Cerebral vasospasm (specifically, intracranial arterial spasm) is variously defined as: (1) an arteriographically evident narrowing of the lumen of one or more of the major intracranial arteries at the base of the brain due to contraction of the smooth muscle within the arterial wall, or due to the morphological changes in the arterial wall and along its endothelial surface that occur in response to vessel injury; (2) the delayed onset of a neurological deficit following subarachnoid hemorrhage, thought to be due to ischemia or infarction of a portion of the brain; or (3) the combination of these two features (symptomatic vasospasm). The arterial contraction of intracranial arterial spasm typically develops a few days after the rupture of an intracranial aneurysm and lasts 2 to 3 weeks. Such arterial spasm can also occur in other conditions such as head trauma. If it is severe enough it can lead to cerebral infarction. The pathogenesis of this condition is still unclear. Many ingenious attempts have been made to prevent or treat cerebral vasospasm, but most have failed. The best current approach is to ensure adequate blood volume, and to elevate the patient's blood pressure (especially if the aneurysm has been secured by an early operation). The continuing investigation of drugs such as calcium channel blocking agents to improve the cerebral circulation has begun to provide additional help.
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PMID:Cerebral vasospasm. 222 95

Recent studies have demonstrated that the computerized EEG (CEEG) is a reliable indicator for the early detection of brain ischemia during carotid surgery. During intracranial aneurysm surgery, different cerebral monitoring techniques are proposed, and the benefits and limitations of conventional EEG, evoked potentials and transcranial doppler are discussed. The authors also give the results of their experience with the CEEG monitoring during intracranial aneurysm surgery. In conclusion, they insist on the necessity for some type of cerebral monitoring during this type of surgery.
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PMID:[Cerebral monitoring during surgery of intracranial aneurysm: review of various techniques and contribution of computerized EEG]. 228 6

Cerebral vasospasm is one of the most dreaded consequences of a ruptured intracranial aneurysm. Although exceptions may be found, the relationship between angiographic narrowing of cerebral arteries and deterioration of clinical status is supported by many authors. The cause of cerebral vasospasm still remains obscure. Several substances such as serotonin, prostaglandins, catecholamines appear to have a vasoconstrictive effect on the cerebral vessels. Recent evidence indicates that erythrocyte lysis within the subarachnoid spaces may play a major role in the genesis of delayed clinically relevant cerebral vasoconstriction following aneurysmal subarachnoid hemorrhage (SAH). The pathophysiology of brain ischemia following aneurysmal rupture, and the correlation between angiographic vasospasm, neurological condition, intracranial pressure (ICP) value, cerebral blood flow and CT findings are briefly discussed. It is concluded that, at present, blood volume expansion and/or induced hypertension, and pharmacological control of increased ICP provide the best basis for clinical management of the cerebral ischemic complications of SAH. Preoperative antifibrinolytic therapy and delayed surgical obliteration of the bleeding aneurysm, i.e. the policy at present most frequently adopted, are currently undergoing critical review in the light of the fact that antifibrinolytic therapy seems to be accompanied by a higher rate of ischemic SAH complications and vasospasm, whilst there are very recent suggestions that the results of early intracranial aneurysm surgery may be better than those of delayed surgery, if account is taken of the patients lost because of recurrent SAH or ischemia during the waiting period.
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PMID:Cerebral vasospasm as a complication of aneurysmal subarachnoid hemorrhage: a brief review. 388 14

The presence of intracranial aneurysm in association with arteriovenous malformation has been well documented. Aneurysms have been described in typical proximal sites along the feeding system to the arteriovenous malformation, in abnormal distal locations along feeding vessels, and in sites remote and apparently hemodynamically unrelated to the arteriovenous malformation. Little attention has been focused on the most appropriate medical and surgical care of patients harboring these lesions. Since 1977, 22 patients with this combination of lesions have been evaluated at our institution. Nine patients (41%) presented after intracranial hemorrhage. The remaining 13 patients were investigated because of seizures in 5 patients (23%), headaches in 4 patients (18%), and progressive ischemia in 4 patients (18%). Among the patients suffering intracranial hemorrhage, 78% had bled from an aneurysm, with 22% having hemorrhaged from their arteriovenous malformation. All 7 of the patients who suffered aneurysmal hemorrhage bled from atypical distal aneurysms on major feeding vessels. Our experience and that of others has led us to believe that the safest approach to patients with this combination of lesions is to treat the aneurysm before microsurgical resection of the associated arteriovenous malformation. Hemodynamic changes associated with the abrupt elimination of an arteriovenous malformation may place associated aneurysms at immediate risk.
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PMID:Intracranial arteriovenous malformations associated with aneurysms. 394 76

Transient focal cerebral ischemia may occasionally be due to distal embolization of a clot from an unruptured intracranial aneurysm. Follow-up data in 12 such patients revealed no ischemic strokes, subarachnoid or parenchymal hemorrhages in a mean follow-up period of 6.5 years. The aneurysms ranged in size from 2 to 12 mm in diameter, and only two were larger than 10 mm. Two patients had clip ligation of the aneurysm, five patients were given platelet antiaggregation therapy, one was given oral anticoagulants after aortic valve surgery, and four had no specific therapy. The prognosis for unruptured aneurysms presenting with transient focal ischemia was good, regardless of therapy.
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PMID:Unruptured intracranial aneurysm and transient focal cerebral ischemia: a follow-up study. 396 Mar 39

The progression of changes in cerebral blood flow (CBF) and neurological status were measured in 12 patients in whom profound hypotension (mean arterial blood pressure (MABP): 30 to 40 mm Hg) was used during intracranial aneurysm surgery. Nine patients (Group I) showed autoregulation of CBF to an MABP of 40 to 50 mm Hg during surgery. None of these patients had arterial spasm preoperatively. Postoperatively, mild flow disturbances were noted at the site of retraction. Three Group I patients developed arterial spasm postoperatively, but there was no associated neurological deterioration. The remaining three patients (Group II) had impaired autoregulation during surgery, and CBF decreased by 35% to 65% at an MABP of 50 mm Hg. Two of these patients had angiography immediately before surgery, and both showed moderate to severe arterial spasm. Relatively severe flow disturbances were noted postoperatively at the site of retraction, and two patients developed ischemic deficits of late onset. Brain retractor pressure and the degree and duration of hypotension were equivalent in the two patient groups. There was no correlation between intraoperative reductions in CBF (to as low as 20 ml/100 gm/min in the unretracted hemisphere) and immediate postoperative neurological deficits. The use of halothane and mannitol and the relatively short duration of the flow reductions were suggested as factors contributing to the protection from ischemia that was observed. Arterial spasm was found to produce hemodynamic instability and reduced CBF, although neurological status was unaffected in the majority of patients. Patients with impaired autoregulation during surgery were at increased risk of delayed ischemic complications postoperatively, and showed characteristic flow disturbances at all three stages of their clinical course.
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PMID:Effects of profound hypotension on cerebral blood flow during surgery for intracranial aneurysms. 729 61


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