Prevention of secondary ischemic insults after severe head injury.

OBJECTIVE: The purpose of this study was to compare the effects of two acute-care management strategies on the frequency of jugular venous desaturation and refractory intracranial hypertension and on long-term neurologic outcome in patients with severe head injury. DESIGN: Randomized clinical trial. SETTING: Level I trauma hospital. PATIENTS: One hundred eighty-nine adults admitted in coma because of severe head injury. INTERVENTIONS: Patients were assigned to either cerebral blood flow (CBF)-targeted or intracranial pressure (ICP)-targeted management protocols during randomly assigned time blocks. In the CBF-targeted protocol, cerebral perfusion pressure was kept at >70 mm Hg and PaCO2 was kept at approximately 35 torr (4.67 kPa). In the ICP-targeted protocol, cerebral perfusion pressure was kept at >50 mm Hg and hyperventilation to a PaCO2 of 25-30 torr (3.33-4.00 kPa) was used to treat intracranial hypertension. MEASUREMENTS AND MAIN RESULTS: The CBF-targeted protocol reduced the frequency of jugular desaturation from 50.6% to 30% (p = .006). Even when the frequency of jugular desaturation was adjusted for all confounding factors that were significant, the risk of cerebral ischemia was 2.4-fold greater with the ICP-targeted protocol. Despite the reduction in secondary ischemic insults, there was no difference in neurologic outcome. Failure to alter long-term neurologic outcome was probably attributable to two major factors. A low jugular venous oxygen saturation was treated in both groups, minimizing the injury that occurred in the ICP-targeted group. The beneficial effects of the CBF-targeted protocol may have been offset by a five-fold increase in the frequency of adult respiratory distress syndrome. CONCLUSIONS: Secondary ischemic insults caused by systemic factors after severe head injury can be prevented with a targeted management protocol. However, potential adverse effects of this management strategy may offset these beneficial effects.     

Intracranial pressure and cerebral perfusion pressure in near-drowning

Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were strictly controlled in 11 pediatric victims of near-drowning. Three outcome groups were defined: complete recovery, persistent vegetative state, and death. In the early postimmersion phase (first 72 h), CPP was consistently above 50 mm Hg in all patients. There were occasional, nonrepetitive, and easily controllable ICP spikes above 15 mm Hg in three patients from each group. Repeated ICP spikes above 15 mm Hg were observed in some patients with adverse outcome only after 72 h. Successful control of ICP and CPP did not ensure intact survival, and sustained late intracranial hypertension is more likely a sign of profound neurologic insult rather than its cause.     

Pyrexia in head-injured patients admitted to intensive care

OBJECTIVES: (a) To quantify the occurrence of pyrexia during the first week after head injury; (b) to elucidate the relationships between pyrexia and neurological severity, length of stay in the ICU, intracranial hypertension, and cerebral perfusion pressure (CPP); and (c) to describe the effects of antipyretic therapy on temperature, intracranial pressure (ICP) and CPP. DESIGN AND SETTING: Multicenter retrospective observational study in three ICUs in the Milan area. PATIENTS: 110 patients with traumatic brain injury. MEASUREMENTS AND RESULTS: Eighty patients suffered pyrexia, defined as an external temperature higher than 38 degrees C or internal temperature higher than 38.4 degrees C. Occurrence and duration of pyrexia were associated with the degree of neurological impairment and with prolonged ICU stay. In patients with normal perimesencephalic cisterns the episodes of increased ICP were more frequent in febrile cases. Various antipyretic therapies were used in 66 patients. Pharmacological treatment was slightly effective (mean temperature reduction 0.58+/-0.7 degrees C) but caused a significant drop in CPP (6.5+/-12.5 mmHg). CONCLUSIONS: Pyrexia is extremely frequent in the acute phase after head injury. Its incidence is higher in more severe cases and is correlated with a longer ICU stay. It may affect ICP, but its contribution is difficult to assess when other major causes of increased intracranial volume are present. Antipyretic therapy is poorly effective for controlling body temperature and may be deleterious for CPP.     

颅内动脉瘤介入治疗后早期持续腰大池引流对脑血管痉挛的影响

目的:探讨颅内动脉瘤破裂出血介入治疗后早期持续腰大池引流对脑血管痉挛(CVS)的影响.方法:对60例Hunt-Hess分级为Ⅲ级的颅内动脉瘤破裂出血患者行介入治疗,并将其随机分为观察组36例和对照组24例,观察组给予早期持续腰大池引流,对照组给予间断腰穿释放脑脊液,比较两组并发症发生情况及脑脊液红细胞和压力参数等相关指标.结果:观察组脑脊液中红细胞计数和脑脊液压力从术后第3天开始明显低于对照组(P＜0.05),观察组CVS发生率明显低于对照组(P＜0.05).结论:动脉瘤介入治疗术后早期持续腰大池引流可有效防治CVS,值得临床推广应用.     

不同方法测量的颅内压值之差异

目的　比较在急性颅脑损伤患者使用不同方法测量的颅内压值 (intracranialpressure ,ICP)之差异。方法　 1 6例急性颅脑损伤在术后同时采用硬脑膜外压 (extraduralpressure ,EDP)监护、脑室内脑脊液压力 (ventnricle cerebrosinalfluidpressure,V CSFP)和腰蛛网膜下腔脑脊液压力 (lumber subarachnoidspaceCSFP ,L CSFP)方法测量ICP值 ,每天一次 ,共 6d。结果　V CSFP与L CSFP所测量的ICP值相似 ,而在多数时间段 ,EDP测量的ICP值低于上述两种方法的ICP值 ,有统计学差异 (P <0 0 5 )。结论　EDP测量的ICP值可能与V CSFP与L CSFP测量的ICP值有差异     

Fluid thresholds and outcome from severe brain injury

OBJECTIVE: To determine, by retrospective analysis, critical thresholds for intracranial pressure, mean arterial pressure, cerebral perfusion pressure, and fluid balance associated with poor outcome in patients with severe brain injury. DESIGN: Retrospective review of patient data from the prospective, randomized, multicenter National Acute Brain Injury Study: Hypothermia, comparing outcome results at 6 months after injury with intracranial pressure, mean arterial pressure, cerebral perfusion pressure, and fluid balance measurements recorded during the 96-hr period after randomization. SETTING: Emergency departments and intensive care units in 11 metropolitan tertiary care university hospitals. PATIENTS: A total of 392 patients, aged 16-65 yrs, with severe, nonpenetrating brain injuries and a Glasgow Coma Scale score of 3-8 after resuscitation, who were enrolled in a study designed to determine the treatment effect of moderate hypothermia in patients with severe brain injury. INTERVENTION: Standard brain injury treatment for 193 randomly assigned patients and standard treatment plus hypothermia for 48 hrs for 199 patients. MEASUREMENTS AND MAIN RESULTS: Intracranial pressure levels of 20, 25, and 30 mm Hg, mean arterial pressure levels of 70 and 80 mm Hg, cerebral perfusion pressure levels of 50, 60, and 70 mm Hg, and fluid balance levels in quartiles were examined for their effect on outcome as measured by the Glasgow Outcome Scale at 6 months after injury. When considered separately, any of the following-intracranial pressure >25 mm Hg, mean arterial pressure <70 mm Hg, or cerebral perfusion pressure <60 mm Hg and fluid balance lower than -594 mL-was associated with an increased percentage of patients with poor outcome. When the variables were combined into a stepwise logistic regression model, Glasgow Coma Scale score at admission, age, mean arterial pressure <70 mm Hg, fluid balance lower than -594 mL, and intracranial pressure > 25 mm Hg, in that order, were the most powerful variables in determining outcome. CONCLUSIONS: Exceeding thresholds of intracranial pressure, mean arterial pressure, cerebral perfusion pressure, and fluid volume may be detrimental to severe brain injury outcome. Fluid balance lower than -594 mL was associated with an adverse effect on outcome, independent of its relationship to intracranial pressure, mean arterial pressure, or cerebral perfusion pressure.     

腰穿脑脊液持续引流治疗蛛网膜下腔出血的系统评价

目的评价腰穿脑脊液持续引流治疗蛛网膜下腔出血（SAH）的疗效及安全性。方法通过电子检索和手工检索,运用Cochrane协作网系统评价的方法对纳入所有应用腰穿脑脊液持续引流治疗SAH的随机对照试验（RCT）进行系统评价。结果共检出21个RCT,其中7个（390例）符合纳入标准,但试验方法学质量普遍低下。所有试验均未提及随访期末（至少3个月）SAH患者病死、植物状态或残疾等不良结局。其余指标Meta分析结果显示：在治疗和随访期末引流组的总病死率低于对照组,其差异有统计学意义[RR=0．32,95％CI（0．15,0．70）];并发症发生率（除再出血地是如此,其中脑血管痉挛RR=0．15[95％CI（0．06,0．33）]、脑积水RR=0．22[95％CI（0．10,0．52）]、脑梗死RR=0．25[95％CI（0．08,0．82）];仅1篇文献报道了该疗法的不良反应包括颅内感染和低颅压反应的发生,其余试验未提及不良反应。结论本系统评价纳入RCT质量均低,虽腰穿脑脊液持续引流有降低SAH患者病死率和并发症的趋势,但缺乏评价其远期功能性结局以及不良反应的指标,尚不能对其疗效是否有效、安全得出确切的结论,其疗效和安全性还需要更多设计严格的多中心、大样本的RCT予以进一步证实。     

术后早期脑脊液引流对颅内动脉瘤破裂出血患者早期并发症的疗效分析

目的探讨颅内动脉瘤破裂出血患者术后早期脑脊液引流对术后早期并发症的疗效。方法将70例颅内动脉瘤破裂出血并接受手术患者随机分为2组,A组行术后早期脑脊液引流,B组术后1周行脑脊液引流,比较2组术后早期并发症发生率。结果 A组交通性脑积水、脑血管痉挛、切口脑脊液漏等术后并发症发生率明显低于B组(P<0.05)。A、B组的颅内感染率差异无统计学意义(P>0.05)。结论颅内动脉瘤破裂出血开颅患者于术后早期引流脑脊液可降低脑积水、脑血管痉挛、切口脑脊液漏等并发症发生率,疗效安全可靠。     

Ventriculosubgaleal shunting for acute head trauma

In 12 cases of closed head injury without fracture or hematoma, but with clinical signs of increased intracranial pressure (ICP) and brain stem compression and with computed tomographic (CT) scan evidence of cerebral edema and contusion, subgaleal shunts were inserted for immediate decompression of the ventricular system and continuous drainage of hemorrhagic cerebrospinal fluid (CSF). Three patients with fixed dilated pupils and no reflexes or spontaneous respiration on admission did not improve and expired within 72 h. Nine patients who manifested Cushing's triad (bradycardia, bradypnea, and hypertension) shortly after admission made significant recovery and underwent catheter removal 1 wk later; 8 were able to be discharged home after extended periods of physiotherapy. No complications, postoperative hemorrhage or infection, were recorded.     

Critical care and anesthetic management of Reye's syndrome.

The encephalopathy of Reye's syndrome is frequently complicated by increased intracranial pressure (ICP) which may lead to death or severe neurologic sequelae. An understanding of the pathophysiology of increased ICP is necessary to prevent further increases in pressure and to reduce pressure while maintaining adequate cerebral perfusion. Four of seven children with Reye's syndrome and increased ICP survived after reduction of increased ICP by controlled hyperventilation and osmotherapy while being monitored with the Richmond intracranial bolt. Careful anesthetic and critical-care management, appropriate, reliable monitoring, and pentobarbital therapy may constitute the most successful therapy to date for patients with Reye's syndrome and increased ICP.     

Management of intracranial hypertension

Effective treatment of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased intracranial pressure. When intracranial pressure becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. medical management of increased intracranial pressure should include sedation and paralysis, drainage of cerebrospinal fluid, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from traumatic brain injury.     

Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension

OBJECTIVES: To review the literature on the use of hypertonic saline (HS) in treating cerebral edema and intracranial hypertension. DATA SOURCES: Review of scientific and clinical literature retrieved from a computerized MEDLINE search from January 1965 through November 1999. STUDY SELECTION: Pertinent literature is referenced, including clinical and laboratory investigations, to demonstrate principles and efficacy of treatment with HS in patients with intracranial space-occupying pathology. DATA EXTRACTION: The literature was reviewed to summarize the mechanisms of action, efficacy, adverse effects, systemic effects, and comparisons with standard treatments in both clinical and laboratory settings. DATA SYNTHESIS: HS has an osmotic effect on the brain because of its high tonicity and ability to effectively remain outside the bloodbrain barrier. Numerous animal studies have suggested that fluid resuscitation with HS bolus after hemorrhagic shock prevents the intracranial pressure (ICP) increase that follows resuscitation with standard fluids. There may be a minimal benefit in restoring cerebral blood flow, which is thought to be mitigated through local effects of HS on cerebral microvasculature. In animal models with cerebral injury, the maximum benefit is observed in animals with focal injury associated with vasogenic edema (cryogenic injury). The ICP reduction is seen for < or =2 hrs and may be maintained for longer periods by using a continuous infusion of HS. The ICP reduction is thought to be caused by a reduction in water content in areas of the brain with intact blood-brain barrier such as the nonlesioned hemisphere and cerebellum. Most comparisons with mannitol suggest almost equal efficacy in reducing ICP, but there is a suggestion that mannitol may have a longer duration of action. Human studies published to date reporting on the use of HS in treating cerebral edema and elevated ICP include case reports, case series, and small controlled trials. Results from studies directly comparing HS with standard treatment in regard to safety and efficacy are inconclusive. However, the low frequency of side effects and a definite reduction of ICP observed with use of HS in these studies are very promising. Systemic effects include transient volume expansion, natriuresis, hemodilution, immunomodulation, and improved pulmonary gas exchange. Adverse effects include electrolyte abnormalities, cardiac failure, bleeding diathesis, and phlebitis. Although unproven, a potential for central pontine myelinolysis and rebound intracranial hypertension exists with uncontrolled administration. CONCLUSIONS: HS demonstrates a favorable effect on both systemic hemodynamics and intracranial pressure in both laboratory and clinical settings. Preliminary evidence supports the need for controlled clinical trials evaluating its use as resuscitative fluid in brain-injured patients with hemorrhagic shock, as therapy for intracranial hypertension resistant to standard therapy, as firstline therapy for intracranial hypertension in certain intracranial pathologies, as small volume fluid resuscitation during spinal shock, and as maintenance intravenous fluid in neurocritical care units.     

颅内压增高患者短时轻度过度通气的观察与护理

目的探讨重型颅脑损伤后的患者使用短时轻度过度通气（HV）的观察与护理。方法2004年5月-2005年12月复旦大学附属华山医院神经外科急救中心收治的重型颅脑外伤的患者31例，使用短期轻度的过度通气治疗，严密观察治疗前后的呼吸指标（PaCO2、PaO2）、颅内压（intracranial pressure，ICP）、平均动脉压（MAP）、脑灌注压（CPP）、意识和瞳孔等动态变化。结果30例患者在使用过度通气1h后，ICP降至20mmHg以下；1例患者出现颅内压反跳性增高，行去骨瓣减压术控制颅内压。31例患者脑灌注压均〉60mmHg。结论 使用短时轻度过度通气可使患者的颅内压下降，通过对呼吸指标、颅内压、脑灌注压的全面仔细观察及护理，有助于保证过度通气的治疗效果，减少因使用过度通气而发生脑缺血加重的并发症。     

Survey of the use of intracranial pressure monitoring in children in the United Kingdom

OBJECTIVE: To establish current practice for the monitoring and management of acute intracranial hypertension in children in United Kingdom intensive care units (ICUs). DESIGN: Postal questionnaire, targetted by prior telephone survey, to all ICUs admitting five or more children per annum with acute neurological illness. RESULTS: Of the units contacted 70 % responded, approximately one-half of which reported the use of intracranial pressure (ICP) monitoring. Only data from these units are presented. Nearly all of these units consider monitoring following serious head injury, but its use in non-traumatic brain injury is less widespread. The decision to institute ICP monitoring is based mainly upon neuroimaging appearances and Glasgow Coma Scale score. ICP and cerebral perfusion pressure targets differ markedly between centres, with only 46 % and 65 % of units, respectively, setting age-dependent parameters. Mannitol and varying degrees of hyperventilation are employed by all units to lower ICP. The majority also use barbiturates, diuretics, and fluid restriction. Controlled hypothermia is used in 52 % of units. Paediatric units are more likely to employ age-dependent cerebral perfusion pressure targets. Specific therapies employed to lower ICP are similar to those used in adult centres. CONCLUSION: Faced with a lack of both evidence and consensus, the management of acute intracranial hypertension in childhood varies widely. National or international guidelines for the management of children with raised intracranial pressure are needed. These should incorporate the physiological differences between children of different ages.     

Primer on medical management of severe brain injury

OBJECTIVE: To review the current understanding of the medical management of severe brain injury. DATA SOURCE: The MEDLINE database, bibliographies of selected articles, and current English-language texts on the subject. STUDY SELECTION: Studies related to management of intracranial hypertension, traumatic brain injury, and brain edema. DATA EXTRACTION: All studies relevant to the subject under consideration were considered, with a focus on clinical studies in adults. DATA SYNTHESIS: Basic rules of resuscitation must apply, including adequate ventilation, appropriate fluid administration, and cardiovascular support. The control of intracranial pressure can be considered in three steps. The first step should be initial slight hyperventilation with a target PaCO2 of 35 mm Hg and cerebrospinal fluid drainage for intracranial pressure of >15-20 mm Hg. The second step should be mannitol or hypertonic saline and hyperventilation to target PaCO2 of 28-35 mm Hg. The third step should be barbiturate coma or decompressive craniectomy. Additional management issues, including seizure prophylaxis, sedation, nutritional support, use of hypothermia, and corticosteroids, are also discussed. CONCLUSIONS: Brain injury is frequently associated with the development of brain edema and the development of intracranial hypertension. However, with a coordinated, stepwise, and aggressive approach to management, focusing on control of intracranial pressure without adversely affecting cerebral perfusion pressure, outcomes can be good.     

Intracranial pressure waveform analysis: clinical and research implications.

Assessment of intracranial adaptive capacity is vital in critically ill individuals with acute brain injury because there is the potential that nursing care activities and environmental stimuli to result in clinically significant increases in intracranial pressure (ICP) in a subset of individuals with decreased intracranial adaptive capacity. ICP waveform analysis provides information about intracranial dynamics that can help identify individuals who have decreased adaptive capacity and are at risk for increases in ICP and decreases in cerebral perfusion pressure, which may contribute to secondary brain injury and have a negative impact on neurologic outcome. The ability to identify high-risk individuals allows nurses to initiate interventions targeted at decreasing adaptive demand or increasing adaptive capacity in these individuals. Changes in the ICP waveform occur under various physiologic and pathophysiologic conditions and may provide valuable information about intracranial adaptive capacity. Simple visual assessment of the ICP waveform for increased amplitude and P2 elevation is clinically relevant and has been found to provide a rough indicator of decreased adaptive capacity. Advanced ICP waveform analysis techniques warrant further study as a means of dynamically assessing intracranial adaptive capacity.     

Effect of therapeutic hypothermia on the incidence and treatment of intracranial hypertension.

Therapeutic hypothermia initiated immediately after a severe head trauma holds promise for improving outcomes. However, the effect of hypothermia on intracranial pressure (ICP) is not yet known. This study was a secondary analysis, conducted within a National Institutes of Health clinical trial on the efficacy of therapeutic hypothermia, to determine the effects of therapeutic hypothermia on ICP and of interventions (i.e., cerebrospinal fluid drainage and mannitol administration) on intracranial hypertension. There were no significant differences in the overall incidence or treatment of intracranial hypertension between patients who were treated with therapeutic hypothermia and normal controls. Therapeutic hypothermia maintained the ICP at lower levels during the cooling phase, but once patients were rewarmed, the ICP elevated to the levels of normothermic patients.     

Intensive care management of head-injured patients in Europe: a survey from the European Brain Injury Consortium

OBJECTIVES: (a) to describe current practice in the monitoring and treatment of moderate and severe head injuries in Europe; (b) to report on intracranial pressure and cerebral perfusion pressure monitoring, occurrence of measured and reported intracranial hypertension, and complications related to this monitoring; (c) to investigate the relationship between the severity of injury, the frequency of monitoring and management, and outcome. METHODS: A three-page questionnaire comprising 60 items of information has been compiled by 67 centres in 12 European countries. Information was collected prospectively regarding all severe and moderate head injuries in adults (> 16 years) admitted to neurosurgery within 24 h of injury. A total of 1005 adult head injury cases were enrolled in the study from 1 February 1995 to 30 April 1995. The Glasgow Outcome Scale was administered at 6 months. RESULTS: Early surgery was performed in 346 cases (35%); arterial pressure was monitored invasively in 631 (68%), ICP in 346 (37%), and jugular bulb saturation in 173 (18%). Artificial ventilation was provided to 736 patients (78%). Intracranial hypertension was noted in 55% of patients in whom ICP was recorded, while it was suspected in only 12% of cases without ICP measurement. There were great differences in the use of ventilation and CPP monitoring among the centres. Mortality at 6 months was 31%. There was an association between an increased frequency of monitoring and intervention and an increased severity of injury; correspondingly, patients who more frequently underwent monitoring and ventilation had a less favourable outcome. CONCLUSIONS: In Europe there are great differences between centres in the frequency of CPP monitoring and ventilatory support applied to head-injured patients. ICP measurement disclosed a high rate of intracranial hypertension, which was not suspected in patients evaluated on a clinical basis alone. ICP monitoring was associated with a low rate of complications. Cases with severe neurological impairment, and with the worse outcome, were treated and monitored more intensively.     

Monitoring of cerebral perfusion pressure during intracranial hypertension: a sufficient parameter of adequate cerebral perfusion and oxygenation?

OBJECTIVE: A cerebral perfusion pressure (CPP) oriented treatment is a widely accepted standard for patients with intracranial hypertension. In an animal model of controlled intracranial hypertension we investigated whether CPP is a reliable parameter of sufficient cerebral perfusion and oxygenation. Using near-infrared reflexion spectroscopy the effect of decreasing CPP due to increasing intracranial pressure (ICP) on cerebral tissue oxygenation was studied. METHODS: Ten rabbits were subjected to artificially elevated ICP using the cisterna-magna infusion technique. Regional cerebral O(2) saturation of hemoglobin (tiSO(2)), regional tissue concentration of hemoglobin (tiHb), and CPP were recorded continuously. CPP was investigated with respect to tiSO(2). Electrocortical activity was simultaneously recorded by two-channel EEG to determine the onset of ischemia. RESULTS: Reduced CPP due to increased ICP led to a continuous decrease in tiSO(2.) There was progressive suppression of EEG frequency and amplitude with decreasing CPP in all animals. Onset of EEG-silence due to elevated ICP was observed in a wide range of CPP-values between 9 and 42 mmHg. At the same time tiSO(2) varied merely between 0 and 5%. CONCLUSIONS: Regarding the EEG effects due to increased ICP (EEG silence), CPP values showed a wide interindividual variability, in contrast to tiSO(2). In our animal model the sole calculation of CPP did not reflect adequate cerebral perfusion.