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

In a patient undergoing craniotomy for clipping of an anterior communicating artery aneurysm, sodium nitroprusside was used to lower systemic arterial blood pressure to 80/35 mm Hg (mean arterial blood pressure (MABP) = 50 mm Hg), at which time the electroencephalogram (EEG) changed abruptly from normal to a burst suppression pattern. At the onset of burst suppression, PaCO2 was 18 mm Hg. After PaCO2 had been increased to 28 mm Hg, the patient tolerated a blood pressure of 45/25 mm Hg (MABP = 32 mm Hg) during aneurysm clipping without EEG change. The observations reported here support the conclusion that, with moderate hypotension, hypocarbia may cause brain ischemia and that the level of PaCO2 may influence the degree of hypotension that may be safely used during aneurysm surgery. The importance of repeated arterial blood gas measurements when induced hypotension is employed for berry aneurysm surgery is stressed. Intraoperative EEG monitoring may be employed to help judge safe levels of intraoperative hypotension during intracranial aneurysm surgery.
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PMID:The critical importance of PaCO2 during intracranial aneurysm surgery. Case report. 735 2

Eighty patients are reported with ischaemic complications developing during subarachnoideal haemorrhage due to aneurysm rupture. Ischaemic complications developed in 12.82% of cases in the whole group of subarachnoideal haemorrhages caused by aneurysm rupture. The causes of ischaemia were: closure or stenosis of the afferent artery during the operation, arterial spasm, thrombosis at the site of the aneurysm and brain oedema. Ischaemia during intracranial aneurysm rupture caused in most cases pale infarcts. Ischaemic complications of aneurysm rupture had a serious prognosis, nearly half the patients with this complication died.
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PMID:[Ischemic complications of ruptured intracranial aneurysms]. 745 26

Temporary arterial occlusion has been routinely used as an adjunct in intracranial aneurysm surgery. This has commonly been performed using a protocol of multiple short periods of occlusion alternating with periods of restoration of normal circulation. Recently, the logical basis of this method has come under scrutiny. There is extensive experimental evidence to suggest that repetitive, brief periods of global ischemia may cause more severe cerebral injury than an equivalent single period of global ischemia. Only recently has this issue begun to be addressed with regard to focal ischemia. Hence, despite the common use of temporary clipping, little experimental data are available regarding the ischemic consequences of temporary arterial occlusion with periods of reperfusion versus uninterrupted temporary occlusion. To investigate this issue, a protocol of occlusion/reperfusion that simulates the temporal profile that occurs during surgery was performed in a rat model of focal ischemia. Sixteen anesthetized Sprague-Dawley rats were divided into two groups. The animals in Group I underwent 60 minutes of uninterrupted middle cerebral artery occlusion and the animals in Group II were subjected to six separate 10-minute occlusion periods with 5 minutes of reperfusion between occlusions. Histopathological analysis was performed 72 hours postischemia. Group I had significantly increased mean infarction volumes (50.0 +/- 12.1 mm3) compared to Group II (8.7 +/- 3.1 mm3) (p = 0.008). Injuries in Group I occurred in both the cortex and striatum, whereas Group II showed only striatal injuries. Furthermore, the extent of the injuries in Group II was less severe, characterized by ischemic neuronal injury rather than frank infarction. The results indicate that intermittent reperfusion is neuroprotective during temporary focal ischemia and support the hypothesis that intermittent reperfusion is beneficial if temporary clipping is required during aneurysm repair.
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PMID:Cerebral protection by intermittent reperfusion during temporary focal ischemia in the rat. 889 33

Despite years of research, delayed cerebral vasospasm remains a serious complication of subarachnoid hemorrhage (SAH). Recently, it has been proposed that endothelin-1 (ET-1) mediates vasospasm. The authors examined this hypothesis in a series of experiments. In a primate model of SAH, serial ET-1 levels were measured in samples from the perivascular space by using a microdialysis technique and in cerebrospinal fluid (CSF) and plasma during the development and resolution of delayed vasospasm. To determine whether elevated ET-1 production was a direct cause of vasospasm or acted secondary to ischemia, the authors also measured ET-1 levels in plasma and CSF after transient cerebral ischemia. To elucidate the source of ET-1, they measured its production in cultures of endothelial cells and astrocytes exposed to oxyhemoglobin (10 microM), methemoglobin (10 microM), or hypoxia (11% oxygen). There was no correlation between the perivascular levels of ET-1 and the development of vasospasm or its resolution. Cerebrospinal fluid and plasma levels of ET-1 were not affected by vasospasm (CSF ET-1 levels were 9.3 +/- 2.2 pg/ml and ET-1 plasma levels were 1.2 +/- 0.6 pg/ml) before SAH and remained unchanged when vasospasm developed (7.1 +/- 1.7 pg/ml in CSF and 2.7 +/- 1.5 pg/ml in plasma). Transient cerebral ischemia evoked an increase of ET-1 levels in CSF (1 +/- 0.4 pg/ml at the occlusion vs. 3.1 +/- 0.6 pg/ml 4 hours after reperfusion; p < 0.05), which returned to normal (0.7 +/- 0.3 pg/ml) after 24 hours. Endothelial cells and astrocytes in culture showed inhibition of ET-1 production 6 hours after exposure to hemoglobins. Hypoxia inhibited ET-1 release by endothelial cells at 24 hours (6.4 +/- 0.8 pg/ml vs. 0.1 +/- 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05) and at 48 hours (6.4 +/- 0.6 pg/ml vs. 0 +/- 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05), but in astrocytes hypoxia induced an increase of ET-1 at 6 hours (1.5 +/- 0.6 vs. 6.4 +/- 1.1 pg/ml, control vs. hypoxic astrocytes; p < 0.05). Endothelin-1 is released from astrocytes, but not endothelial cells, during hypoxia and is released from the brain after transient ischemia. There is no relationship between ET-1 and vasospasm in vivo or between ET-1 and oxyhemoglobin, a putative agent of vasospasm, in vitro. The increase in ET-1 levels in CSF after SAH from a ruptured intracranial aneurysm appears to be the result of cerebral ischemia rather than reflecting the cause of cerebral vasospasm.
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PMID:Source and cause of endothelin-1 release into cerebrospinal fluid after subarachnoid hemorrhage. 925 95

Forty-five patients underwent surgery for anterior circulation aneurysms using intraoperative neurophysiologic monitoring at the Johns Hopkins Hospital during 1996. There were seven intraoperative strokes. Two were cortical strokes associated with irreversible somatosensory evoked potential (SEP) changes during temporary arterial occlusion. The remaining five were subcortical strokes, one of which was associated with transient SEP changes during temporary arterial occlusion, but the other four occurred despite normal SEPs throughout surgery. Somatosensory evoked potential monitoring is not sensitive for the detection of subcortical ischemia and infarction in the distribution of the deep perforating arterial branches during intracranial aneurysm surgery. Although attenuation of loss of cortical SEP responses may indicate cerebral ischemia from inadequate collateral circulation during temporary arterial occlusion, normal SEPs can not exclude subcortical ischemia sufficient to cause significant postoperative deficits, and may therefore provide a false sense of security during these surgeries.
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PMID:Subcortical strokes from intracranial aneurysm surgery: implications for intraoperative neuromonitoring. 982 Oct 71

Temporary arterial occlusion (TAO) is commonly used in the surgery of intracranial giant aneurysms. Its usefulness and safety in the surgical management of all cases of aneurysms remains to be proved. We report a series of 54 patients operated on for an intracranial aneurysm with the use of TAO. Among the 27 patients, admitted before the 4th day following post subarachnoid hemorrhage with I or II on WFNS score clinically, 24 had early aneurysm surgery. The size of the aneurysm was small in 16 cases, medium in 22, large in 13 and giant in 3 cases. The protocol proposed by Batjer in 1988 for large and giant aneurysms (etomidate, normotention and hypervolemia) was used without any electrophysiological monitoring. All patients underwent a post-operative cerebral CT scan to evaluate the incidence of a cerebral ischemia. Serial transcranial doppler was used to evaluate the severity of vasospasm. Clinical results were assessed using the GOS. TAO was elective in 51 patients and done after peroperative aneurysm rupture in 3 patients. The duration of TAO was less than 5 mn in 25 patients, between 5 and 10 min in 12, between 10 and 15 in 11, between 15 and 20 in 5 and more than 20 min in one patient. The last one developed a reversible neurological deficit secondary to ischemia attribuated to TAO. Intracranial aneurysm peroperative rupture was noted in 3 patients, clinical vasospam in 13 patients. These results allow us to recommend the routine use of TAO in the surgery of intracranial aneurysm. When application time is limited and cerebral protection used, TAO is safe. It decreases the risk of intraoperative rupture from a 18% rate in literature to 4.2% in our present experience and the risk of symptomatic vasospasm is not increased.
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PMID:[Temporary occlusion in surgical management of intracranial aneurysm. Report of 54 cases]. 1037 31

Retrospectively, subarachnoidal hemorrhage can be misdiagnosed when the acute event did not bring the patient to medical attention, when clinical history is unclear and the CT scan is normal. Moreover, days after subarachnoid hemorrhage, cerebral vasospasm can result in neurological deficits that are indistinguishable from that produced by other causes of stroke. We report our experience with two patients who presented with symptoms of ischemia due to an arterial vasospasm that followed unrecognized rupture of an intracranial aneurysm. In both cases, CT scan failed to detect subarachnoid hemorrhage while MR detected the presence of signal changes in the subarachnoidal spaces associated with an ischemic stroke in one case. Neurological symptoms resolved completely after aneurysm treatment. MR can be a critical for the diagnosis of stroke secondary to vasospasm in order to prescribe an adapted treatment, avoid anticoagulant or thrombolytic therapy, and rapidly exclude the recently ruptured aneurysm to protect the patient from the risk of rebleeding.
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PMID:[The value of MRI for the diagnosis of meningeal hemorrhage during vasospasm]. 1078 53

Orbital infarction syndrome is defined as ischemia of all intraorbital and intraocular structures. It is a rare disease caused by rich anastomotic vascularization of the orbit. It can occur secondary to different conditions, such as, acute perfusion failure, systemic vasculitis, orbital cellulitis and vasculitis. It results in orbital and ocular pain, total ophthalmoplegia, anterior and posterior segment ischemia, and acute blindness. We report here upon two cases of orbital infarction with similar presentations but with different causes, namely, mucormycosis and as a postoperative complication of intracranial aneurysm, discuss the possible mechanisms of orbital infarction, and present a review of the literature on the topic. The prompt recognition of clinical pictures and rapid diagnosis is essential for the early treatment of orbital infarction, since its progression is very rapid and it can be even fatal.
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PMID:Two cases of orbital infarction syndrome. 1121 34

Extracorporeal circulation (ECC) is not only used for open heart surgery. There are also other surgical and medical applications. ECC can be used for encephalic arteries surgery to induce hypothermia and maximally protect the brain. Femoro-femoral ECC may be needful for urgent traumatologic surgery of the supra-aortic trunci. Intracranial aneurysm repair can occasionally necessitate deep hypothermia and circulatory arrest with ECC. Renal cell carcinomas may metastasize to the right atrium and surgery with ECC is mandatory for complete excision. Some reports in the literature mention use of ECC for hepatic surgery of intra-hepatic aneurysms. With acute peripheral ischemia, metabolites in the affected limb can be washed out with good results. Medical indications for ECC are numerous with pulmonary assistance as one of the foremost when mechanical ventilation failed. Homogeneous and rapid rewarming of hypothermic patients can be achieved with ECC. Finally, some groups have reported the use of ECC to administer chemotherapy in limb melanoma.
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PMID:[Extracorporeal circulation: an extraordinary tool that is not just for cardiac surgeons]. 1241 Jan 43

The aim is to give a review of the anesthesiological approach to neuroradiological endovascular treatment of intracranial aneurysm in Croatia since 2004, when the first procedure was done. It took place at University Department of Radiology, Zagreb University Hospital Center. The optimal conduct of anesthesia in the neuroradiology suite requires careful planning of each individual procedure. Essential components are detailed patient evaluation and due understanding of the underlying neuropathology. An open channel of communication between the radiologist and the anesthesiologist is important for routine care but is crucial in case of disasters that may occur during the procedure. In the patient management the basic principles of neuroanesthesia cannot be avoided. This includes optimization of CBF, perfusion pressure, control of intracranial pressure (ICP) and close monitoring of blood pressure (BP), fluid status and body temperature. The choice of anesthetic agents and techniques remains in the hands of the anesthesiologist. The needs of the neuroradiologist and the procedure have to be considered. Most institutions have their protocols and some favor conscious sedation whereas others prefer general anesthesia. There is little evidence in favor of either technique. The better image quality obtained from the motionless patient during digital subtraction angiography favors the use of general anesthesia over any other technique. Since the procedure is becoming very complex, the need for precise BP control and preparation for potential catastrophic complication are considerations for general anesthesia. Aneurysm rupture during endovascular procedures is not common but remains a potential risk. The incidence ranges from 2.3% to 3% and even higher in patients with already ruptured aneurysms. The mortality rate is up to 20% in case of rupture, especially if massive subarachnoid hemorrhage occurs. Anesthesiologic treatment depends on the severity of bleeding and includes maintaining CPP, lowering ICP, reversal of anticoagulation and patient transfer to the neurosurgical operating room if immediate ventriculostomy is needed. During a six month period, 55 patients underwent endovascular treatment of cerebral aneurysm at our hospital. They all were managed under general anesthesia. Since one of the critical roles of the anesthesiologist in the interventional radiology suite is to provide anticoagulation, the protocol of giving clopidogrel was followed, loading dose of 225 mg p. o. to each patient on the day of the procedure and immediately upon introducing microcatheter, heparin iv 70 IU/kg (average of 5000 IU), followed by boluses of 15 IU/kg (approx. 1000 IU) every 60 minutes. Activated clotting time was monitored for the effect of heparin. All patients except four were brought out of anesthesia at the table, immediately after the procedure for their neurological status to be assessed. None of the patients died during the procedure or within the first 24 hours. The mortality was up to 3.6% (two patients died on days 3 and 5 of the procedure). We had only one case of aneurysm rerupture during embolization with Guglielmi detachable coil, followed by cardiac arrest, but the patient (a 32-year-old woman) was resuscitated successfully and underwent standard neurosurgical procedure with full recovery in ICU after 14 days. There were 4 (7.2%) cases of vasospasm followed by ischemia, nimodipine treated, 2 with transient neurological dysfunction and another 2 with permanent hemianopsia. Interventional neuroradiology is rapidly and continually evolving, providing opportunities for the anesthesiologist to be part of this branch of medicine. It is essential to keep up-to-date in the knowledge of neuroanesthesia, neuropathology and interventional neuroradiology. In spite of the relatively non-invasive nature of the procedures, serious, even fatal complications may occur. Therefore, the role of anesthesiologist and his/her cooperation with neuroradiologist is crucial for successful results.
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PMID:[Role of anesthesiologist in endovascular management of intracranial aneurysms]. 1836 4


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