Long-term hypothermia in patients with severe brain edema after poor-grade subarachnoid hemorrhage: feasibility and intensive care complications

The purpose was to evaluate the feasibility and intensive care complications of long-term hypothermia (>72 hours) in the treatment of severe brain edema after poor-grade subarachnoid hemorrhage (SAH) Hunt and Hess grade 4 to 5. Among 156 patients with SAH, 21 patients were treated with mild hypothermia (33.0 to 34.0 degrees C) combined with barbiturate coma because of severe brain edema and elevated intracranial pressure (>15 mm Hg) after early aneurysm clipping. Hypothermia was sustained for at least 24 hours after maintaining an intracranial pressure of <15 mm Hg. Nine patients were treated for <72 hours (group 1: mean 42.2 hours, range 8-66 hours) and 12 for >72 hours (group 2: mean 153.9 hours, range 78-400 hours). Three patients (14%) died during the hypothermia treatment. Good functional outcome after 3 months (Glasgow Outcome Score 4-5) was achieved in 10 patients (48%). The outcome did not differ between the two groups. All patients developed severe infections. In group 2 the mean value of minimal leukocyte counts during hypothermia was significantly lower (6.9 vs. 11.8 x 109/L; P = 0.001), and thrombocytopenia (<150 x 109/L) occurred significantly more often (48 vs. 33%; P = 0.032). In 48% of patients with poor-grade SAH, good functional outcome was achieved with combined mild hypothermia and barbiturate coma after early aneurysm surgery. This may be a feasible treatment even for longer than 72 hours. All patients developed severe infections as potentially hazardous side effects. To determine whether mild hypothermia alone is effective in the treatment of severe SAH patients, controlled studies to compare the effects of barbiturate coma alone, mild hypothermia alone, and combined barbiturate coma with hypothermia are needed.     

Recent Advances and Future Directions of Hypothermia Therapy for Traumatic Brain Injury

For severe traumatic brain injury (TBI) patients, no effective treatment method replacing hypothermia therapy has emerged, and hypothermia therapy still plays the major role. To increase its efficacy, first, early introduction is important. Since there are diverse pathologies of severe TBI, it is necessary to appropriately control the temperature in the hypothermia maintenance and rewarming phases by monitoring relative to the pathology. Currently, hypothermia is considered appropriate for severe TBI patients requiring craniotomy for removal of hematoma, while induced normothermia is appropriate for severe TBI patients with diffuse brain injury. Induced normothermia is expected to exhibit a cerebroprotective effect equivalent to hypothermia, as well as reduce the complexity of whole-body management and systemic complications. According to the Japan Neurotrauma Data Bank of the Japan Society of Neurotraumatology, the brain temperature was controlled in 43.9% of severe TBI patients (induced normothermia: 32.2%, hypothermia: 11.7%) in Japan. Brain temperature management was performed mainly in young patients, and the outcome on discharge was favorable in patients who received brain temperature management. Particularly, patients who need craniotomy for removal of hematoma were a good indication of therapeutic hypothermia. Improvement of therapeutic outcomes with widespread temperature management in TBI patients is expected.     

Hypothermia on admission in patients with severe brain injury

Data from the "National Acute Brain Injury Study: Hypothermia" were examined to identify the impact of hypothermia on admission. In all patients, temperature was measured at randomization using bladder catheters with thermistors. Patients assigned to hypothermia were cooled using fluid-circulating pads. Outcome was assessed at 6 months using the dichotomized Glasgow Outcome Scale (good outcome = good recovery/moderate disability; poor outcome = severe disability/vegetative/dead). One-hundred and two patients (hypothermia, 62; normothermia, 40) were hypothermic on admission (< or =35.0 degrees C). Hypothermia-on-admission patients assigned to normothermia (n = 40) had a 78% poor outcome, and normothermia-on-admission patients assigned to normothermia had a 52% poor outcome (p < 0.004). Hypothermia-on-admission patients assigned to hypothermia had a lower percentage of poor outcomes than those assigned to normothermia (hypothermia, 61%; normothermia, 78%; p = 0.09). Patients over 45 years of age had an adverse effect of hypothermia regardless of admission temperature due to medical complications. Patients who were hypothermic on admission, age < or = 45 years (n = 81), and assigned to hypothermia had a significantly lower percentage of poor outcomes than those assigned to normothermia (hypothermia, 52%; normothermia, 76%; p = 0.02). Factors associated with hypothermia on admission were increased age, prehospital hypotension, smaller size, positive blood alcohol, larger volume of pre-hospital fluids, slightly higher injury severity, and winter enrollment The treatment effect was found in all of the four centers, which randomized the majority (80%) of the patients. It is unclear whether the improved outcome when hypothermia is maintained is a beneficial effect of very early hypothermia induction or an adverse effect of permitting the patients to rewarm passively.     

Effect of moderate hypothermia on experimental severe subarachnoid hemorrhage, as evaluated by apparent diffusion coefficient changes

OBJECTIVE: The aims of this study were to investigate the early changes in the mean apparent diffusion coefficient (ADC) after severe subarachnoid hemorrhage (SAH), as a marker of ischemic damage, and to examine the effects of moderate hypothermia, induced at various time points, on ADC changes. METHODS: ADC maps were calculated from diffusion-weighted, blipped-epi, spin echo, magnetic resonance imaging sequences (2.35-T BIOSPEC 24/40 scanner; Bruker Medizin Technik GmbH, Karlsruhe, Germany) for 21 anesthetized (0.45-1% halothane, temperature-adjusted/30% oxygen/69% nitrogen) and ventilated Wistar rats. After baseline scanning, bolus injection of 0.5 ml of autologous arterial blood or artificial cerebrospinal fluid (control group), into the cisterna magna, was performed. Serial scanning was performed for 3 hours after injection, using normothermic or hypothermic (32 degrees C) rats. In an additional series of experiments, hypothermia was initiated either immediately or 60 minutes after normothermic SAH. The water contents of the removed brains were calculated using the wet/dry weight method. RESULTS: The ADC values did not change in the control group but decreased to 88.6+/-5.2% (P < 0.05 versus baseline) after SAH and remained significantly decreased throughout the experiment in normothermia. An injection of blood during hypothermia caused an initial decrease in ADC to 96.1+/-5.6% (P < 0.05 versus baseline); values continuously increased and reached normal levels within 60 minutes. Delayed hypothermia also normalized ADC values within the observation period. The brain water content in the control group was 80.3+/-0.1%, that after SAH in normothermia was 81.1+/-0.7%, and that after SAH in hypothermia was 79.3+/-0.5%. CONCLUSION: This model of severe SAH in rats causes significant ADC changes, which are reversible by application of moderate hypothermia even when it is induced after a 60-minute delay. These findings support the concept of moderate hypothermia exerting a neuroprotective effect in severe SAH.     

Acute operation and preventive nimodipine improve outcome in patients with ruptured cerebral aneurysms

Sixty-five patients with ruptured aneurysms were operated upon within 48 to 72 hours after subarachnoid hemorrhage (SAH) and were treated with a regimen of intra- and postoperative nimodipine for the prevention of symptomatic vasospasm. The clinical grading (Hunt and Hess) was I to III in 49 patients and IV or V in 16. The SAH was mild in 15 patients, moderate in 27, and severe in 23; 12 patients harbored an intracerebral hematoma, and 6 had intraventricular bleeding. Acute hydrocephalus was observed on preoperative computed tomography (CT) in 19 patients. On CT 3 days postoperatively (i.e., Day 3-4 after SAH), 30 of 65 patients still had subarachnoid blood; however, severe symptomatic vasospasm as the deciding threatening event during the delayed postoperative period was not encountered in this series. Transient symptoms of ischemia were noted in 2 patients (3%) and were accompanied by angiographic spasm in 1. Irreversible neurological deficit occurred in 2 patients (3%); in 1 of these, it was a complication of postoperative control angiography. Of the patients preoperatively graded I or II, 96% had an excellent to fair outcome 6 months postoperatively, and 1 patient (4%) had died because of a surgical complication. Among patients preoperatively graded III or IV, 86% had an excellent to fair outcome, and the remaining 14% had a poor outcome. Shunt-dependent hydrocephalus developed in 7% of the patients. Acute surgical repair of ruptured cerebral aneurysms and preventive topical and intravenous administration of nimodipine reduce management complications and improve outcome; above all, ischemic lesions from symptomatic vasospasm are reduced to a minimum.     

The effect of clipping and coiling in acute severe subarachnoid hemorrhage after international subarachnoid aneurysmal trial (ISAT) results.

Cerebral aneurysms are treated by two methods: direct microsurgical clipping and endovascular coiling. Both are selected based on definite guidelines for clinicoradiological criteria as follows: Endovascular therapy comprising of GDC embolization, CSF wash-out with UK or TP A were performed in cases with Hunt and Kosnik grade 4 (GCS 7, 8), and grade 5 (without hydrocephalus or intracranial hemorrhage), age>70 years, subacute stage (4--14 days of vasospasm), basilar aneurysm and peripheral MCA/PCA aneurysms. Microsurgical clipping with a drainage procedure was performed in cases with Hunt and Kosnik grades 0--3, grade 4 (GCS 9--12), age less than 70 years, grade 5 with hydrocephalus or intracerebral hematoma and acute stage (0--3 days after bleed). The patient's outcome was measured using GOS (Glasgow outcome score) at the time of discharge. In our series of severe (poor grade) SAH cases, 120 cases underwent clipping and 59 cases underwent coiling. Although they accounted for 37.8 % and 48 % of total SAH cases, respectively, the outcome was satisfactory. Good recovery and moderate disability, together termed "favorable outcome" was found in 69.16 % of clipping cases and 44.06 % of coiling cases. Clipping had a better outcome than coiling in cases of acute severe SAH in our series. The golden hour resuscitation, pre-hospital care and the adjunctive treatment strategies like hypothermia are discussed. A critical appraisal of the ISAT of microsurgical clipping versus coiling is used for comparison of our results.     

Therapeutic trial of cerebral vasospasm with the serine protease inhibitor, FUT-175, administered in the acute stage after subarachnoid hemorrhage.

The therapeutic effect of the synthetic serine protease inhibitor, FUT-175, on cerebral vasospasm after subarachnoid hemorrhage (SAH) was investigated. Twenty-three patients with severe SAH who were admitted between February and July 1990 and who underwent surgery within 48 hours of the initial aneurysmal rupture were treated with an intravenous administration of FUT-175 soon after the operation. The patients were divided randomly into three groups, each receiving a different dose of FUT-175 (Group A, 20 mg every 12 hours for 4 days; Group B, 20 mg every 6 hours for 4 days, Group C, 40 mg every 6 hours for 4 days). The results were compared with another group of twenty-two patients with severe SAH who were admitted before February 1990 and received equivalent treatment, except they were not treated with FUT-175. In 64% of all the patients treated with FUT-175 (Groups A, B, C), and in 85% of those treated with higher doses of FUT-175 (Groups B and C), there was no spasm or only mild vasospasm on the angiogram. The incidence of a delayed ischemic neurological deficit significantly decreased from 55% in the control group to 13% in all patients treated with FUT-175 and to 7% in the patients treated with higher doses (P less than 0.05). The incidence of cerebral infarction resulting from vasospasm significantly decreased from 43% in the control group to 9% in patients treated with FUT-175. In the patients treated with higher doses of FUT-175 (Groups B and C), none developed cerebral infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

After spontaneous hypothermia during hemorrhagic shock,continuing mild hypothermia (34 degrees C) improves early but not late survival in rats

BACKGROUND: Spontaneous hypothermia is common in victims of severe trauma. Laboratory studies have shown benefit of induced (therapeutic) mild hypothermia (34 degrees C) during hemorrhagic shock (HS). Clinical data, however, suggest that hypothermia, which often occurs spontaneously in trauma patients, is detrimental. Because critically ill trauma patients are usually cool, the clinical question, which has not been explored in the laboratory with long-term outcome, is whether maintaining hypothermia or actively rewarming the patient improves outcome. We hypothesized that after spontaneous cooling during HS, continuing mild therapeutic hypothermia during resuscitation is beneficial compared with active rewarming. METHODS: In study A, under light isoflurane anesthesia, 24 Sprague-Dawley rats were bled over 10 minutes to, and maintained at, mean arterial pressure (MAP) of 40 mm Hg until reuptake of 30% of maximal shed blood volume was needed. Rectal temperature (Tr) decreased spontaneously to, and was then maintained at, 35 degrees C during HS. Fluid resuscitation included the remaining shed blood and up to 400 mL/kg of lactated Ringer's solution with 5% dextrose over 4 hours. During resuscitation, three groups (n = 8 each) were studied: normothermia (rapid rewarming to Tr 37.5 degrees C at the beginning of resuscitation); hypothermia-2 h (cooling to Tr 34 degrees C to resuscitation time 2 hours); and hypothermia-12 h (cooling to Tr 34 degrees C to 12 hours). Rats were observed to 72 hours. In study B, more severe HS than in study A was studied. HS was induced with 3 mL/100 g blood withdrawal over 15 minutes followed by maintenance of MAP of 40 mm Hg until 50% of maximal shed blood volume was needed. Two groups (n = 8 each) were studied: normothermia and hypothermia-12 h. Data are presented as mean +/- SD or median (range). RESULTS: In study A, both hypothermia groups had higher MAP and lower heart rates during resuscitation than the normothermia group (p < 0.01). Survival to 72 hours was achieved in three of eight rats in the normothermia group and two of eight in each hypothermia group. Thirteen of 17 deaths occurred after 24 hours. In study B, for resuscitation, the hypothermia group needed less fluid (53 +/- 6 mL vs. 79 +/- 32 mL, p < 0.05), but had higher MAP (p < 0.01), lower heart rate (p < 0.01), and lower lactate level (p = 0.06). All rats died before 72 hours. The hypothermia group had longer survival time (24.5 [13-48.5] hours) than the normothermia group (7.5 [1.5-19] hours) (p = 0.003 by life table analysis). CONCLUSION: After spontaneous cooling during moderately severe HS, mild, controlled hypothermia during resuscitation does not seem to affect long-term survival. After more severe HS, hypothermia increases survival time. Hypothermia supports arterial pressure during resuscitation from severe HS.     

Effect of raloxifene on cerebral vasospasm following experimental subarachnoid hemorrhage in rats

The effect of raloxifene on cerebral vasospasm following experimental subarachnoid hemorrhage (SAH) was investigated in a rat model. Seven groups of seven rats underwent no SAH, no treatment; SAH only; SAH plus vehicle; SAH plus 3 days intraperitoneal raloxifene treatment; SAH plus 4 days intraperitoneal raloxifene treatment; SAH plus 3 days intrathecal raloxifene treatment; and SAH plus 4 days intrathecal raloxifene treatment. The basilar artery cross-sectional areas were measured at 72 or 96 hours following SAH. The results showed raloxifene decreased SAH-induced cerebral vasospasm in all treatment groups, and suggested no difference between intraperitoneal and intrathecal application, or between 3 days and 4 days of raloxifene treatment. The present study demonstrates that raloxifene is a potential therapeutic agent against cerebral vasospasm after SAH.     

亚低温治疗重型脑损伤的脑氧代谢和神经电生理临床研究

目的 研究亚低温治疗重型颅脑损伤过程中脑氧代谢和神经电生理变化规律,评估亚低温对重型脑伤的近期疗效。方法 选择受伤后10h内入院GCS（格拉斯哥昏迷评分,Glasgow Coma Scale）3～8分之间的急性重型脑伤患者148例,按病情轻重分为GCS7～8分组、GCS5～6分组和GCS3～4分组,并随机分入亚低温亚组和常温亚组。亚低温亚组（32～34℃）在降温前后的不同时段记录脑氧代谢监测指标、神经电生理指标;常温组在同样的时段记录上述指标。结果GCS7～8分组：SLSEP的N20波幅、BAEP的I／V波幅比值和rSa02在降温后亚低温组较常温组有显著性改善,PbrO2在亚低温组的部分时段低于常温组;GCS5～6分组：亚低温治疗组N20、I／V和rSaO2在部分时段较常温组有改善,PkO2在亚低温组的部分时段高于常温组;GCS3～4分组：亚低温组与常温组上述指标均无显著性差异。结论 亚低温对于GCS7～8分的重型脑伤有明显的治疗作用,对GCS3～4分者无明显疗效,对GCS5～6分者疗效不确定;脑氧代谢和神经电生理指标对颅脑损伤的疗效评价具有重要意义。     

Brain hypothermia relieves severe brain swelling following acute major cerebral artery occlusion

Seven patients were treated with brain hypothermia following acute major cerebral artery occlusion to utilize the suppressive effect against brain swelling. Five patients had internal carotid and two had proximal middle cerebral artery occlusion. Except for the first two cases, hypothermia was introduced early and the temperature reached 35.0 degrees C within 6 hours after the onset. The core temperature finally stabilized between 32 degrees C to 34 degrees C. Hypothermia had a suppressive effect against brain swelling and the temperature showed a significant correlation to intracranial pressure. Recurrence of brain swelling was observed during the rewarming process, but two patients became independent and three patients were moderately disabled in wheelchairs. Only two patients died. Brain hypothermia is an effective treatment for acute major cerebral artery occlusion through the relief of brain swelling. The overall outcome may be improved by combining brain hypothermia with other conventional therapies such as osmotherapy and external decompression implemented with an extended period of rewarming.     

Spinal cord stimulation for cerebral vasospasm as prophylaxis

Cervical spinal cord stimulation (SCS) was used to increase cerebral blood flow (CBF) in 10 patients with secured cerebral aneurysms in Hunt and Hess grade 3 or 4 and with Fisher group 3 subarachnoid hemorrhage (SAH). The patients underwent preemptive electrical stimulation through a percutaneous lead following aneurysm surgery. All patients also received hypervolemic therapy and nicardipine. Efficacy of the treatment was evaluated using xenon computed tomography and cerebral angiography. The CBF in the distribution of the middle cerebral artery significantly increased following SCS (p < 0.05). Four of 10 patients showed angiographic vasospasm, but none developed severe sequelae of cerebral vasospasm. The overall outcome was good or excellent in seven of the 10 patients. No serious adverse effects due to SCS were observed. Fluid management and calcium antagonist have a beneficial effect on cerebral vasospasm following SAH, but is not tolerated or is ineffective in some patients. SCS as an adjunctive therapy for cerebral vasospasm following SAH may have a favorable effect on outcome.     

A study of the effectiveness of the iron-chelating agent deferoxamine as vasospasm prophylaxis in a rabbit model of subarachnoid hemorrhage

The pathogenesis of cerebral vasospasm occurring after subarachnoid hemorrhage (SAH) is unknown. Several lines of experimentation have suggested a free radical mechanism in the etiology of vasospasm. Iron is an important catalyst in the generation of free radicals and lipid peroxides in response to tissue injury. We hypothesize that the elaboration of iron from the subarachnoid clot might result in enhanced generation of free radicals and lipid peroxidation. If so, then treatment with deferoxamine, an iron-chelating compound, might reduce the formation of free radicals and thereby ameliorate vasospasm. This hypothesis was examined in a rabbit model of experimental cerebral vasospasm. New Zealand White rabbits were divided into the following experimental groups: control (normal) animals (n = 7), control animals treated with deferoxamine (n = 3), animals subjected to SAH and killed on Day 2 (n = 7), animals subjected to SAH on Day 2 and treated with deferoxamine (n = 9), animals subjected to SAH killed on Day 3 (n = 7), and animals subjected to SAH on Day 3 and treated with deferoxamine (n = 7). Deferoxamine treatment (50 mg/kg/8 hours) was begun 16 hours before the induction of SAH and continued until the animals were killed by perfusion fixation. The basilar artery caliber was assessed using morphometric techniques. The diameter of the basilar arteries in the control animals was 0.64 +/- 0.02 mm. Deferoxamine treatment alone did not alter the artery diameter.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes of evoked potentials and evaluation of mild hypothermia for treatment of severe brain injury

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Severe cerebral vasospasm caused by non-aneurysmal subarachnoid hemorrhage treatment with transluminal balloon angioplasty.

Non-aneurysmal subarachnoid hemorrhage (NSAH) is a benign form of subarachnoid hemorrhage (SAH). The angiographic changes of cerebral vasospasm (CVS) are uncommon in patients with this type of SAH. NSAH is uniformly associated with an excellent outcome without associated rebleeding or symptomatic CVS. We report a patient with NSAH who developed severe and diffuse CVS. He was treated with transluminal balloon angioplasty because he has been refractory to conventional treatment measures for CVS.     

Effect of long-term mild hypothermia therapy in patients with severe traumatic brain injury: 1-year follow-up review of 87 cases

OBJECT: The goal of this study was to investigate the protective effects of long-term (3-14 days) mild hypothermia therapy (33-35 degrees C) on outcome in 87 patients with severe traumatic brain injury (TBI) (Glasgow Coma Scale score < or = 8). METHODS: In 43 patients assigned to a mild hypothermia group, body temperatures were cooled to 33 to 35 degrees C a mean of 15 hours after injury and kept at 33 to 35 degrees C for 3 to 14 days. Rewarming commenced when the individual patient's intracranial pressure (ICP) returned to the normal level. Body temperatures in 44 patients assigned to a normothermia group were maintained at 37 to 38 degrees C. Each patient's outcome was evaluated 1 year later by using the Glasgow Outcome Scale. One year after TBI, the mortality rate was 25.58% (11 of 43 patients) and the rate of favorable outcome (good recovery or moderate disability) was 46.51% (20 of 43 patients) in the mild hypothermia group. In the normothermia group, the mortality rate was 45.45% (20 of 44 patients) and the rate of favorable outcome was 27.27% (12 of 44 patients) (p < 0.05). Induced mild hypothermia also markedly reduced ICP (p < 0.01) and inhibited hyperglycemia (p < 0.05). The rates of complication were not significantly different between the two groups. CONCLUSIONS: The data produced by this study demonstrate that long-term mild hypothermia therapy significantly improves outcomes in patients with severe TBI.     

Non-aneurysmal subarachnoid haemorrhage

A subarachnoid haemorrhage (SAH) is frequent after a severe head injury. Traumatic-SAH is associated with a bad outcome and may induce cerebral vasospasm. There is no agreement on the treatment based on the amount of traumatic-SAH. Non-aneurysmal SAH accounts for 15% of all causes of non-traumatic SAH. There is a risk of cerebral vasospasm, although less frequent than after aneurysmal rupture. The improvement in imaging techniques has decreased the frequency of idiopathic SAH.     

Aneurysmal subarachnoid haemorrhage and the anaesthetist

The anaesthetist may be involved at various stages in the managementof subarachnoid haemorrhage (SAH). Thus, familiarity with epidemiological,pathophysiological, diagnostic, and therapeutic issues is asimportant as detailed knowledge of the optimal intraoperativeanaesthetic management. As the prognosis of SAH remains poor,prompt diagnosis and appropriate treatment are essential, becauseearly treatment may improve outcome. It is, therefore, importantto rule out SAH as soon as possible in all patients complainingof sudden onset of severe headache lasting for longer than anhour with no alternative explanation. The three main predictorsof mortality and dependence are impaired level of consciousnesson admission, advanced age, and a large volume of blood on initialcranial computed tomography. The major complications of SAHinclude re-bleeding, cerebral vasospasm leading to immediateand delayed cerebral ischaemia, hydrocephalus, cardiopulmonarydysfunction, and electrolyte disturbances. Prophylaxis and therapyof cerebral vasospasm include maintenance of cerebral perfusionpressure (CPP) and normovolaemia, administration of nimodipine,triple-H therapy, balloon angioplasty, and intra-arterial papaverine.Occlusion of the aneurysm after SAH is usually attempted surgically(‘clipping’) or endovascularly by detachable coils(‘coiling’). The need for an adequate CPP (for theprevention of cerebral ischaemia and cerebral vasospasm) mustbe balanced against the need for a low transmural pressure gradientof the aneurysm (for the prevention of rupture of the aneurysm).Effective measures to prevent or attenuate increases in intracranialpressure, brain swelling, and cerebral vasospasm throughoutall phases of anaesthesia are prerequisite for optimal outcome.     

Surgical problems and pathophysiology in severe cases with ruptured aneurysm in the acute stage

Summary We have managed 674 cases of ruptured aneurysms of the anterior part of the circles of Willis during the period 1969 to 1980. For this study, analyses were made to clarify the operative indication, timing and suitable procedures based on the pathophysiology of severe cases in the acute stage.Clinical results of conservative treatment in the era of delayed operation clearly show the inevitable necessity of early operation. The CBF measurement in the acute stage revealed a slight decrease of hemispheric CBF without regulatory dysfunction of cerebral circulation within 3 days of SAH.Results of early operation within 3 days of SAH in the 3rd era showed that 83.1% of cases survived with a good outcome and 3.4% died when they were in Grades 1 and 2. 40 cases with severe grading, operated on within 3 days of SAH, were studied on each site of the aneurysm. Mortality was 12.5% and there was a favourable outcome in 55%. Death was due to brain swelling caused by vasospasm and direct brain damage caused by SAH and an intracerebral haematoma.Extensive evacuation of subarachnoid clotting could be performed only when brain volume could be reduced enough to minimize brain compression, by using ventricular drainage, evacuation of the intracerebral haematoma and Mannitol administration.Surgical procedures for each aneurysm are also described.     

Effects of mild hypothermia and alkalizing agents on brain injuries in rats with acute subdural hematomas

Brain ischemia is the leading pathopysiological mechanism in the development of secondary brain damage after acute subdural hematoma (SDH). Hypothermia has been employed as an effective cerebroprotective treatment on brain injuries, but the control of the general condition is very difficult under hypothermia, and various severe complications have been reported. Cerebral acidosis in the ischemic area is one of the important factors augmenting the brain edema formation. Tris-(hydroxymethyl)-aminomethane (THAM) has been used as an alkalizing agent for acidosis on brain injury and is reported to be effective. In the present study, we used a rat acute SDH model to assess the effect of mild (35 degrees C) hypothermia and THAM combined treatment on brain water content, brain ischemia, and blood-brain barrier (BBB) permeability at 4 h after hematoma induction. Mild hypothermia did not significantly reduce the brain water content beneath the hematoma (79.5 +/- 0.2%) compared to normothermia (80.2 +/- 0.2%), but mild hypothermia combined to THAM resulted in a significant reduction (78.7 +/- 0.0%; p < 0.01). Combined with mild hypothermia, THAM treatment significantly reduced the Evan's blue extravasation (35 +/- 7 ng/g wet tissue; p < 0.05) compared to normothermia (63 +/- 7 ng/g wet tissue). Furthermore, the volume of infarction at 24 h after the hematoma induction (54 +/- 3 mm(3); p < 0.01) was significantly smaller by the combined treatment compared with normothermia (70 +/- 2 mm(3)). The present findings indicate that mild hypothermia of 35 degrees C combined with THAM presents a potent cerebroprotective strategy. The protection of the BBB is one of the possible cerebroprotective mechanisms in this rat acute SDH model.