Temporary Artery Occlusion Research Articles

Transient Cardiac Standstill Induced by Adenosine in the Management of Intraoperative Aneurysmal Rupture: Technical Case Report

OBJECTIVE AND IMPORTANCE Intraoperative aneurysmal rupture represents a potentially catastrophic event. We describe the use of an intravenous adenosine bolus to induce transient cardiac asystole to control a severe intraoperative aneurysmal rupture. This treatment resulted in a brief period of severe hypotension, which enabled successful clipping of the aneurysm. CLINICAL PRESENTATION A 55-year-old man was referred to our institution 7 days after experiencing a mild subarachnoid hemorrhage from a fusiform, multilobulated aneurysm of the anterior communicating artery. The patient was found to have multiple additional fusiform aneurysms as well as a large parietal arteriovenous malformation. INTERVENTION A craniotomy was performed to clip the aneurysm, but surgical dissection was complicated by premature rebleeding that could not be controlled satisfactorily with tamponade or temporary arterial occlusion. Infusion of adenosine resulted in the rapid onset of profound hypotension, allowing for safe completion of the dissection and clipping of the aneurysm with a good outcome. There were no complications identified in relation to the use of adenosine. CONCLUSION In the setting of severe intraoperative aneurysmal rupture, intravenous adenosine represents a potential means of achieving a near-immediate profound decrease in the blood pressure that may allow for safe completion of the dissection and aneurysm clipping.

Temporary Balloon Occlusion of the Internal Iliac Arteries for Control of Hemorrhage during Cesarean Hysterectomy in a Patient with Placenta Previa and Placenta Increta

Temporary Balloon Occlusion of the Internal Iliac Arteries for Control of Hemorrhage during Cesarean Hysterectomy in a Patient with Placenta Previa and Placenta Increta

Temporary and Permanent Occlusion of Cerebral Arteries: Indications and Techniques

Permanent occlusion of the carotid and vertebral arteries has long been used as a treatment for certain aneurysms, tumors, arteriovenous fistulae, and traumatic injuries. Temporary occlusion of these vessels often is used to predict patient tolerance before permanent vessel occlusion. When inadvertent arterial occlusion or injury is considered to be a significant risk of an open or endovascular surgical procedure, temporary arterial occlusion may be used to assess tolerance for permanent occlusion. The results of temporary arterial occlusion testing are often used to determine the need and type of bypass graft to augment cerebral blood flow. Temporary arterial occlusion also may be used to arrest proximal blood flow during open or endovascular surgery.

Brachial Neuropathy After Hemodialysis Shunt Placement Under Axillary Blockade

Brachial Neuropathy After Hemodialysis Shunt Placement Under Axillary Blockade

Evaluation of lipid peroxidation, cathepsin L and acid phosphatase activities in experimental brain ischemia–reperfusion

This investigation was conducted in rat brain tissues to elucidate the free radical induced cellular and subcellular membrane injuries in two different depth of global ischemia. Global moderate (penumbral) ischemia was performed on rat brains by bilateral vertebral arteries cauterization and temporary occlusion of the bilateral carotid arteries. Global severe ischemia was produced by a neck tourniquet in addition to four vessel occlusion. Somatosensory evoked potentials (SSEPs) were used as a feed back parameter to monitor electrophysiologically the ischemia. At the end of ischemic insult (0 min reperfusion) or various reperfusion periods (20, 60 and 240 min), all rats were decapitated and brains were frozen in liquid nitrogen. The brain tissues were prepared for the determination of cathepsin L (CL) and acid phosphatase (AP) activities in the supernatant (cytosolic) fraction (SF) and the fraction enriched with lysosomes (FEL). Further the level of thiobarbituric acid reactive substances (TBARS) of lipid peroxidation was assessed by the spectrophotometric methods. Severe ischemia–reperfusion was accompanied by a significant increase in TBARS levels and the SF/FEL ratio for CL and AP activities compared to the sham operated group and the concurrent reperfusion groups of moderate ischemia ( p<0.05). There were no significant differences between the sham operated and moderate ischemia–reperfusion groups for the same parameters. Our data clearly demonstrate that; in rat brain although severe ischemia–reperfusion causes lipid peroxidation in cellular membranes and redistribution of lysosomal enzymes from lysosomes to cytoplasm due to lysosomal membrane injury, there are no changes in lysosomal membrane stability in moderate ischemia–reperfusion.

Combination drug therapy and mild hypothermia: a promising treatment strategy for reversible, focal cerebral ischemia.

Hypothermia has been suggested to be the most potent therapeutic approach to reduce experimental ischemic brain injury identified to date, and mild hypothermia is increasingly used for neuroprotection during neurovascular surgery. We have recently demonstrated that combined administration of tirilazad mesylate and magnesium provides for an overall enhanced neuroprotective effect. The present study was designed to determine whether the efficacy of mild hypothermia (33 degrees C) can be increased by combination pharmacotherapy with tirilazad and magnesium (MgCl(2)). Forty Sprague-Dawley rats were subjected to transient, middle cerebral artery occlusion and were randomly assigned to 1 of 4 treatment arms (n=10 each): (1) normothermia+vehicle, (2) normothermia+tirilazad+MgCl(2), (3) hypothermia+vehicle, or (4) hypothermia+tirilazad+MgCl(2). Cortical blood flow was monitored by a bilateral laser-Doppler flowmeter, and the electroencephalogram was continuously recorded. Functional deficits were quantified by daily neurological examinations. Infarct volume was assessed after 7 days. Tirilazad+MgCl(2), hypothermia, and hypothermia+tirilazad+MgCl(2) reduced total infarct volume by 56%, 63%, and 77%, respectively, relative to controls. In animals treated with both hypothermia and combination pharmacotherapy, cortical infarction was almost completely abolished (-99%), and infarct volume in the basal ganglia was significantly reduced by 55%. In addition, this treatment provided for the best electrophysiological recovery and functional outcome. The neuroprotective efficacy of hypothermia can be increased by pharmacological antagonism of excitatory amino acids and free radicals by using clinically available drugs. This treatment strategy could be of great benefit when applied during temporary artery occlusion in cerebrovascular surgery.

Abstracts of literature

Abstracts of literature

Current results of the surgical management of aneurysms of the basilar apex.

To provide current information regarding the expected clinical outcomes and sources of morbidity and mortality in the modern surgical management of basilar apex aneurysms. A retrospective review was conducted of 303 cases of such aneurysms that were treated surgically during 18 years at one institution. Postoperative angiography was performed in 81% of the cases. Clinical grading using the Glasgow Outcome Scale was conducted at the time of hospital discharge and for 91% of the surviving patients at 6 months after surgery. The preoperative parameters that were linked statistically to poor clinical outcome were identified through the use of single and multivariate analyses. More than 80% of the patients were operated on using some modification of the trans-sylvian exposure, and temporary arterial occlusion was used routinely. Good outcomes (Glasgow Outcome Scale scores of 4 or 5) were achieved in 76% of the patients at the time of discharge and in 81% of the patients at 6 months after surgery. There was no incidence of postoperative subarachnoid hemorrhage. Residual aneurysm was revealed by postoperative angiography in 6% of the cases. Factors found to be statistically linked to poor outcome included poor admission grade (Hunt and Hess Grades IV and V), patient age older than 65 years, computed tomographic demonstration of thick basal cistern clot, aneurysm size greater than 20 mm, and symptoms attributable to brain stem compression. Direct microsurgical repair of basilar apex aneurysms should result in good clinical outcomes in 80 to 85% of cases, with reliable prevention of subarachnoid bleeding and routine elimination/reduction of symptoms secondary to mass effect. Those patients who are at high risk for poor outcomes can be identified by the presence of certain clinical, radiographic, and demographic features before undergoing surgery and can be considered for alternative or adjunctive modes of therapy if long-term efficacy of such treatment is demonstrated.

Neuroprotective effects of combination therapy with tirilazad and magnesium in rats subjected to reversible focal cerebral ischemia.

Cell death after cerebral ischemia is mediated by release of excitatory amino acids, calcium influx into cells, and generation of free radicals. We examined the hypothesis that concurrent administration of tirilazad, a well-known antioxidant, and magnesium, an antagonist of calcium and excitatory amino acids, would result in a synergistic neuroprotective effect. Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion and assigned to one of four treatment arms (n = 10 in each): 1) vehicle, 2) tirilazad, 3) MgCl2, or 4) tirilazad and MgCl2. Cortical blood flow was recorded using laser Doppler flowmetry. Functional deficits were quantified by performing daily neurological examinations. Infarct volume was assessed after 7 days. There was no difference in cortical blood flow among groups. Animals that received tirilazad or MgCl2 monotherapy had significantly better neurological function compared with control animals only on postoperative Days 3 and 4, whereas animals treated with both drugs had significantly better neurological function than did control animals from postoperative Days 2 through 7. Magnesium reduced total infarct volume by 25% (nonsignificant), tirilazad by 48% (P<0.05), and combination therapy by 59% (P<0.05) compared with control data. Combined therapy with antagonists of excitatory amino acids and free radicals provides better neuroprotection from the effects of transient focal ischemia than does therapy with either antagonist alone. In contrast to many experimental agents, tirilazad and magnesium offer the advantage of being licensed for clinical use. This drug combination could be of great benefit when administered before temporary artery occlusion in patients undergoing cerebrovascular surgery.

Temporary Vascular Occlusion During Cerebral Aneurysm Surgery

Temporary artery occlusion is an effective way to reduce the detrimental effects of intraoperative aneurysm rupture and to facilitate aneurysm dissection. The major risk incurred is of cerebral infarction. Dilemmas in the use of this technique include the amount of time that arterial flow may be interrupted safely and whether or not there is benefit to intermittent reperfusion. Protocol for the use of temporary occlusion is described.

The laparoscopic cooling sheath: novel device for hypothermic preservation of kidney during temporary renal artery occlusion.

Hypothermia is commonly used to prevent ischemic renal damage during complex nephron-sparing surgical procedures requiring temporary renal artery occlusion. We developed a novel Cooling Sheath device, which is compatible with laparoscopy, to protect the kidney hypothermically during 60 minutes of temporary arterial occlusion in a laparoscopic swine model. Comparison of temperature curves and histology to control groups undergoing open slush surface cooling and laparoscopic warm ischemia for similar time periods was performed. Optimal hypothermic temperatures were reached rapidly and maintained with the use of the Cooling Sheath. Ischemic damage, present in all kidneys subjected to warm ischemia, was not found on histopathologic examination of the cooled kidneys. This new device provides hypothermic protection of the kidney during ischemia. The use of the Cooling Sheath combined with temporary arterial occlusion will allow more complex nephron-sparing renal surgery to be performed using laparoscopy.

Neuroprotector effects of Magnesium Sulfate (MgSO4) used in Piglets after Hypoxic-Ischemic Insult † 1903

Magnesium sulfate has been proposed as a potential strategy for hypoxic-ischemic insult because its ability to block calcium entry through NMDA receptor. Objetive: the aim of this work was to examine the neuroprotector effect of MgSO4 in an experimental piglet model of hypoxic-ischemic insult when is administrated as a rescue strategy, 15 minutes after the insult. Methods: Piglets (5 days old) were assigned to (S) Sham (n=8), (SM) Sham+MgSO4 (n=8), (HI) hypoxic-ischemic (n=8), (HIM) hypoxic-ischemic+MgSO4 (n=8) group. In the groups HI and HIM temporary occlusion of carotid arteries during 30 minutes (FiO2 8%), and hemorragic hypotension (15 min) after 15 min of hypoxic insult was made. A loading dosis of 300 mg/kg of MgSO4 followed by 150 mg/kg/h iv were administrated during 12 h to SM and HIM groups. CSF neuron specific enolase(NSE) levels were measured by EIA. Cerebral neuropathologic examination was performed and graded following a score; neuronal necrosis was assesed in diferents regions of the brain. Results: Significant increase in CSF NSE levels in the inmediately before sacrifice were found in the HI and HIM groups (p<0.05). Severe brain damage was found in groups HI and HIM in all of the sections examined, mainly in cortex, basal ganglia and hippocampus.Conclusion: We did not find neuroprotector effect when MgSO4 was administrated 15 minutes after the hypoxic-ischemic insult in this experimental model.

Temporary Arterial Occlusion During Anterior Communicating or Anterior Cerebral Artery Aneurysm Operation Under Tibial Nerve Somatosensory Evoked Potential Monitoring

Background Median nerve somatosensory evoked potentials (SEP) have been used as an indicator of cerebral ischemia in the territory of the middle cerebral artery. This study was designed to examine whether tibial nerve SEPs are a useful technique for detecting ischemia in the territory of the anterior cerebral artery (ACA) during aneurysm surgery. Methods Tibial nerve SEP monitoring was employed in 15 patients who underwent temporary arterial occlusion during surgery for aneurysms of the anterior communicating artery (ACoA) or ACA. To evaluate tibial nerve SEPs, the data after anesthesia induction but before the start of surgery were used as the control and a more than 50% decrease in the amplitude of P40-N50 was regarded as a significant change. Results Changes in SEP were recognized in 11 of these 15 patients. Unilateral A1 occlusion resulted in SEP changes in 4/7, while bilateral A1 interruption caused changes in 6/8 of the patient group. The allowable duration of interruption of the ACA cannot be determined by A1 dominance or the extent of development of the ACoA that can be recognized by angiography. The significance of the collateral circulation via the leptomeninges was indicated. Following the release of the occlusion, SEPs were restored to the control level in all patients and no new motor deficits were found. Conclusions It was concluded that tibial nerve SEP monitoring is a useful system to determine the extent of cerebral ischemia of the ACA territory during temporary arterial occlusion associated with surgery for aneurysms involving the ACA system.

Organ Pathology following Mild Hypothermia Used as Neural Rescue Therapy in Newborn Piglets

The aim of this study was to assess the possible adverse effects of hypothermia, used as neural rescue therapy in a newborn piglet model. Sixteen newborn piglets were subjected to transient cerebral hypoxia-ischaemia by temporary occlusion of the carotid arteries and reduction of the fractional inspired oxygen to 0.12. On resuscitation 11 piglets were maintained normothermic (38.5–39.0°C) and, in order to assess the cerebroprotective effect of hypothermia, 5 piglets were cooled to 35°C for 12 h before normothermia was resumed. At 48 or 64 h following resuscitation the animals were sacrificed and the heart, left kidney, specimens of distal small bowel, lung and liver were removed and histologically sectioned. No microscopic abnormalities of the heart, bowel or lung were observed in hypothermic or normothermic animals. All kidney specimens were normal except one from the normothermic group. Abnormal liver pathology suggestive of hypoperfusion injury was found in 5 normothermic and 3 hypothermic piglets. There was no significant difference in the proportion of piglets with liver abnormality between the two groups. Mild hypothermia following cerebral hypoxia-ischaemia in the newborn piglet was not associated with an increased incidence of non-cerebral organ damage. The hepatic injury observed may be related to umbilical venous catheterisation and has potential relevance to neonatal intensive care.

Temporary occlusion of the middle cerebral artery in intracranial aneurysm surgery: time limitation and advantage of brain protection

The risk of focal infarction secondary to the induced reversible arrest of local arterial flow during microsurgical dissection of middle cerebral artery (MCA) aneurysms was evaluated further to define the optimal approach to temporary arterial occlusion. To compare the effectiveness of potential brain-protection anesthetics, a group of patients treated with the intravenous agents propofol, etomidate, and pentobarbital, administered individually or in combination, was compared to a group treated with the inhalational agent isoflurane. Forty-nine consecutive MCA aneurysm surgeries involving the temporary clipping of the parent vessel were retrospectively reviewed. Thirty-eight patients received intravenous brain-protection (IVBP) anesthesia. Groups of patients with and without infarctions, and receiving and not receiving IVBP anesthesia, were compared based on the duration and nature of temporary arterial occlusion. Postoperative radiographic evidence of new infarction was used as the threshold for failure of occlusion tolerance. The overall infarction rate was 22.4% (11 of 49 patients), including 15.8% (six of 38 patients) in the IVBP group versus 45.5% (five of 11 patients) in the group that did not receive brain protection (NBP). In the NBP group, the mean duration of temporary occlusion was 3.9 +/- 2.2 minutes for patients without infarction versus 12.2 +/- 4.3 minutes for patients with focal infarction (p < 0.01). In contrast, the mean duration was 13.6 +/- 10.6 minutes for patients without infarction and 18.5 +/- 9.9 minutes for patients with infarction in the IVBP group. All patients (four of four) in the NBP group who underwent occlusion lasting 10 minutes or longer suffered an infarction versus five of 23 patients in the IVBP group (p < 0.0001). Patients with multiple aneurysms were found to be at increased risk of developing focal infarction, whereas those treated with intermittent temporary clip application were at decreased risk. It is concluded that patients in whom focal iatrogenic ischemia is induced during MCA aneurysm clip ligation have a significant advantage compared with those receiving isoflurane when they are given pentobarbital as the primary neuroprotective agent or when they receive propofol or etomidate titrated to achieve electroencephalographic burst suppression, particularly if more than 10 minutes of occlusion time is required. It is also concluded that 10 minutes is a general guideline for safe, temporary occlusion of the MCA. The use of intermittent temporary arterial occlusion and its use in patients with multiple aneurysms need further evaluation before specific recommendations can be made.

P-1-49 - Temporary arterial occlusion during the surgical treatment of intracranial aneurysms

P-1-49 - Temporary arterial occlusion during the surgical treatment of intracranial aneurysms

O-24-355 - New advances in monitoring during temporary arterial occlusion

O-24-355 - New advances in monitoring during temporary arterial occlusion

Temporary occlusion of the middle cerebral artery in intracranial aneurysm surgery: time limitation and advantage of brain protection

The risk of focal infarction secondary to the induced reversible arrest of local arterial flow during microsurgical dissection of middle cerebral artery (MCA) aneurysms was evaluated further to define the optimal approach to temporary arterial occlusion. To compare the effectiveness of brain-protection anesthetics, a group of patients treated with the intravenous agents, propofol, etomidate, and pentobarbital, administered individually or in combination, was compared to a group treated with the inhalational agent isoflurane. Forty-nine consecutive MCA aneurysm surgeries involving the temporary clipping of the parent vessel were retrospectively reviewed. Thirty-eight patients received intravenous brain-protection (IVBP) anesthesia. Groups of patients with and without infarctions, and receiving and not receiving IVBP, were compared based on the duration and nature of temporary arterial occlusion. Postoperative radiographic evidence of new infarction was used as the threshold for failure of occlusion tolerance. The overall infarction rate was 22.4% (11 of 49 patients), including 15.8% (six of 38 patients) in the IVBP group versus 45.5% (five of 11 patients) in the isoflurane (ISO) group. In the ISO group, the mean duration of temporary occlusion was 3.9 ± 2.2 minutes for patients without infarction versus 12.2 ± 4.3 minutes for patients with focal infarction (p &lt; 0.01). In contrast, the mean duration was 13.6 ± 10.6 minutes for patients without infarction and 18.5 ± 9.9 minutes for patients with infarction in the IVBP group. All patients in the ISO group who underwent occlusion lasting 10 minutes or longer suffered an infarction versus five of 23 patients in the IVBP group. Patients with multiple aneurysms were found to be at increased risk of developing focal infarction, whereas those treated with intermittent temporary clip application were at a decreased risk. It is concluded that patients in whom focal iatrogenic ischemia is induced during MCA aneurysm clip ligation have a significant advantage compared with those receiving ISO when they are given pentobarbital as the primary neuroprotective agent or when they receive propofol or etomidate titrated to achieve electroencephalographic burst suppression, particularly if more than 10 minutes of occlusion time is required. It is also concluded that 10 minutes is a general guideline for safe, temporary occlusion of the MCA. The use of intermittent temporary arterial occlusion and patients with multiple aneurysms need further evaluation before specific recommendations can be made.

Proton magnetic resonance spectroscopy of the brain during acute hypoxia-ischemia and delayed cerebral energy failure in the newborn piglet.

Studies of the brains of severely birth-asphyxiated infants using proton (1H) magnetic resonance spectroscopy (MRS) have shown changes indicating a rise in cerebral lactate (Lac) and a fall in N-acetylaspartate (Naa). The aim of this study was to test two hypotheses: 1) that these changes can be reproduced in the newborn piglet after transient reversed cerebral hypoxiaischemia, and their time course determined; and 2) that changes in Lac peak-area ratios are related to changes in phosphorylation potential as determined by phosphorus (31P) MRS. Eighteen piglets aged < 24 h were anesthetized and ventilated. Twelve underwent temporary occlusion of the carotid arteries and hypoxemia, and six served as sham-operated controls. 1H and 31P spectra were acquired alternately, both during the insult and for the next 48 h, using a 7-tesla spectrometer. During hypoxiaischemia, the median Lac/total creatine (Cr) peak-area ratio rose from a baseline of 0.14 (interquartile range 0.07-0.27), to a maximum of 4.34 (3.33-7.45). After resuscitation, Lac/Cr fell to 0.75 (0.45-1.64) by 2 h, and then increased again to 2.43 (1.13-3.08) by 48 h. At all stages after resuscitation Lac/Cr remained significantly above baseline and control values. Naa/Cr was significantly reduced below baseline and control values by 48 h after resuscitation. The increases in the Lac peak-area ratios were concomitant with the falls in the [phosphocreatine (PCr)*]/ [inorganic phosphate (Pi)] ratio, during both acute hypoxiaischemia and delayed energy failure. The maximum Lac/Naa during delayed energy failure correlated strongly with the minimum [nucleotide triphosphate (NTP)]/[exchangeable phosphate pool (EPP)] (r = -0.94, p < 0.0001). We conclude that both hypotheses have been confirmed.

Mild hypothermia after severe transient hypoxia-ischemia reduces the delayed rise in cerebral lactate in the newborn piglet.

This study tested the hypothesis that mild hypothermia after severe transient hypoxia-ischemia reduces the subsequent delayed rise in cerebral lactate peak-area ratios as determined by proton (1H) magnetic resonance spectroscopy (MRS) in the newborn piglet. Nine piglets aged < 24 h underwent temporary occlusion of the common carotid arteries and hypoxemia. Resuscitation was started when cerebral [phosphocreatine]/[inorganic phosphate] had fallen close to zero and [nucleotide triphosphate (NTP)]/[exchangeable phosphate pool (EPP)] was below about a third of baseline. On resuscitation rectal and tympanic temperatures were lowered to 35 degrees C for 12 h after which normothermia (38.5 degrees C) was resumed. 1H MRS data collected over 48 or 64 h after resuscitation were compared with concurrently established data from 12 piglets similarly subjected to transient cerebral hypoxia-ischemia, but maintained normothermic, and six sham-operated controls. The severity of the primary insult (judged from the time integral of depletion of [NTP]/[EPP]) was similar in the hypothermic and normothermic groups. The maximum lactate/N-acetylaspartate ratio observed between 24 and 48 h after resuscitation in the hypothermic group was 0.10 (0.05-0.97), median (interquartile range), which was significantly lower than that observed in the normothermic group, 1.28 (0.97-2.14), and not significantly different from that observed in the control group, 0.08 (0.06-0.11). Similar results were obtained for lactate/choline and lactate/total creatine. We conclude that mild hypothermia after a severe acute cerebral hypoxic-ischemic insult reduces the delayed elevation in lactate peak-area ratios, thus reflecting reduced lactate accumulation.