Efficacy of large decompressive craniectomy in severe traumatic brain injury

Objective： To investigate the role of large decompres- sive craniectomy （LDC） in the management of severe and very severe traumatic brain injury （TBI） and compare it with routine decompressive craniectomy （RDC）.
Methods： The clinical data of 263 patients with severe TBI （GCS~8） treated by either LDC or RDC in our department were studied retrospectively in this article. One hundred and thirty-five patients with severe TBI, including 54 patients with very severe TBI （GCS ≤ 5）, underwent LDC （LDC group）. The other 128 patients with severe TBI, including 49 patients with very severe TBI, underwent RDC （RDC group）. The treatment outcome and postoperative complications of the two treatment methods were compared and analyzed in a 6-month follow-up period.
Results： Ninety-six patients （71.7 %） obtained satisfactory treatment outcome in the LDC group, while only 75 cases （58.6 %） obtained satisfactory outcome in the RDC group （P〈 0.05）. Moreover, the efficacy of LDC in treating very severe TBI was higher than that of RDC （63.0 % vs. 36.7 %, P 〈 0.01）. The chance of reoperation due to refractory intracranial pressure （ICP） in the LDC group was significantly lower than that of the RDC group （P 〈 0.05）, while the incidences of delayed intracranial hematoma and subdural effusion were significantly higher than those of the RDC group （ P 〈 0.05）.
Conclusions： LDC is superior to RDC in improving the treatment outcome of severe TBI, especially the very severe ones. LDC can also efficiently reduce the chances of reoperation due to refractory ICP. However, it increases the incidences of delayed intracranial hematoma and contralateral subdural effusion.     

单额开颅治疗双额叶挫裂伤伴血肿

目的总结单额开颅治疗双额叶挫裂伤的经验。方法回顾性分析21例双额叶挫裂伤患者的临床资料,均采用单额开颅治疗。入院时GCS评分:9～11分13例,6～8分6例,3～5分2例。结果术后第1 d所有病例均行头颅CT复查,无一例出现迟发性颅内血肿或残余血肿。对侧挫裂伤及血肿基本清除(>75%)15例,部分清除(50%～75%)6例。术后6个月按GOS分级标准,恢复良好13例,中残4例,重残3例,死亡1例。结论采用单额开颅能有效清除双额叶挫裂伤及血肿,并具有缩短手术时间、减轻手术创伤等优点,具有较好的临床实用价值。     

Incidence and risk factors for post-traumatic hydrocephalus following decompressive craniectomy for intractable intracranial hypertension and evacuation of mass lesions

There continues to be a considerable interest in decompressive craniectomy in the management of severe traumatic brain injury (TBI). Though technically straightforward, the procedure is not without significant complications. In this study we assessed the incidence and risk factors for the development of subdural hygroma and hydrocephalus after decompressive craniectomy. A total of 195 patients who had had a decompressive craniectomy for severe TBI between 2004 and 2010 at the two major trauma centers in Western Australia were considered. Of the 166 patients who survived after the acute hospital stay, 93 (56%; 95% confidence interval [CI] 48,63%) developed subdural hygroma; 45 patients (48%) had unilateral and 48 patients (52%) had bilateral subdural hygromas. Of the 159 patients who survived more than 6 months after surgery, 72 (45%; 95% CI 38,53%) developed radiological evidence of ventriculomegaly, and 26 of these 72 patients (36%; 95% CI 26,48%) developed clinical evidence of hydrocephalus and required a ventriculoperitoneal (VP) shunt. Maximum intracranial pressure prior to decompression (p=0.005), subdural hygroma (p=0.012), and a lower admission Glasgow Coma Scale score (p=0.009), were significant risk factors for hydrocephalus after decompressive craniectomy. Hydrocephalus requiring a VP shunt was associated with a higher risk of unfavorable neurological outcomes at 18 months (odds ratio 7.46; 95%CI 1.17,47.4; p=0.033), after adjusting for other factors. Our results showed a clear association between injury severity, subdural hygroma, and hydrocephalus, suggesting that damage to the cerebrospinal fluid drainage pathways contributes to the primary brain injury rather than the margin of the craniectomy as the factor responsible for these complications.     

Effective ICP reduction by decompressive craniectomy in patients with severe traumatic brain injury treated by an ICP-targeted therapy

Severe traumatic brain injury (TBI) is one of the major causes of death in younger age groups. In Ume?, Sweden, an intracranial pressure (ICP) targeted therapy protocol, the Lund concept, has been used in treatment of severe TBI since 1994. Decompressive craniectomy is used as a protocol-guided treatment step. The primary aim of the investigation was to study the effect of craniectomy on ICP changes over time in patients with severe TBI treated by an ICP-targeted protocol. In this retrospective study, all patients treated for severe TBI during 1998-2001 who fulfilled the following inclusion criteria were studied: GCS 10 mm Hg, arrival within 24 h of trauma, and need of intensive care for >72 h. Craniectomy was performed when the ICP could not be controlled by evacuation of hematomas, sedation, ventriculostomy, or low-dose pentothal infusion. Ninety-three patients met the inclusion criteria. Mean age was 37.6 years. Twenty-one patients underwent craniectomy as a treatment step. We found a significant reduction of the ICP directly after craniectomy, from 36.4 mm Hg (range, 18-80 mm Hg) to 12.6 mm Hg (range, 2-51 mm Hg). During the following 72 h, we observed an increase in ICP during the first 8-12 h after craniectomy, reaching approximately 20 mm Hg, and later levelling out at approximately 25 mm Hg. The reduction of ICP was statistically significant during the 72 h. The outcome as measured by Glasgow Outcome Scale (GOS) did not significantly differ between the craniectomized group (DC) and the non-craniectomized group (NDC). The outcome was favorable (GOS 5-4) in 71% in the craniectomized group, and in 61% in the non-craniectomized group. Craniectomy is a useful tool in achieving a significant reduction of ICP overtime in TBI patients with progressive intracranial hypertension refractory to medical therapy. The procedure seems to have a satisfactory effect on the outcome, as demonstrated by a high rate of favorable outcome and low mortality in the craniectomized group, which did not significantly differ compared with the non-craniectomized group.     

Decompressive craniectomy for the management of patients with refractory hypertension: should it be reconsidered?

Summary. Summary.   Introduction: The management of refractory post-traumatic cerebral oedema remains a frustrating endeavor for the neurosurgeon and the intensivist. Mortality and morbidity rates remain high, despite refinements in medical and pharmacological means of controlling intracranial hypertension.   Method and Material: In this retrospective study we have evaluated the efficacy of decompressive craniectomy as a last resort therapy, from the data of nine patients with severe brain injury and delayed cerebral oedema (diffuse injury type III), treated between January 1997 and September 1999. The following parameters were considered: age, Glascow Coma Scale, injury severity, intracranial pressure, CT findings, pupil reaction/posturing. Follow-up period was over at least 2 years and outcome measured on the GOS.   Results: Patients have been operated on post-trauma median day 3, mean age 26±9, GCS 7±3.7, mean APACHE II 16±6.4, mean ISS 27.8±16.1, mean preoperative ICP 37.7±10.0, mean postoperative ICP 18.1±16.01. Seven patients have been operated by a frontotemporoparietal approach (six of them bilateral, one unilateral) and two patients have been operated on by a bilateral subtemporal approach. Mortality rates 22%, severe disability 11%, good recovery 66%.   Discussion: Patients with STBI, developing delayed intracranial hypertension caused by diffuse cerebral oedema, definitely benefit from craniectomy when current medical treatment has failed. The encouraging results of outcome in this and more recent studies, indicate the need for a multi-institutional randomized prospective study evaluating early indicators of raised ICP, timing, efficacy of treatment, operative technique and complications of decompressive craniectomy. Published online August 12, 2002     

Cerebral oxygenation, vascular reactivity, and neurochemistry following decompressive craniectomy for severe traumatic brain injury

OBJECT: This study addresses the changes in brain oxygenation, cerebrovascular reactivity, and cerebral neurochemistry in patients following decompressive craniectomy for the control of elevated intracranial pressure (ICP) after severe traumatic brain injury (TBI). METHODS: Sixteen consecutive patients with isolated TBI and elevated ICP, who were refractory to maximal medical therapy, underwent decompressive craniectomy over a 1-year period. Thirteen patients were male and 3 were female. The mean age of the patients was 38 years and the median Glasgow Coma Scale score on admission was 5. RESULTS Six months following TBI, 11 patients had a poor outcome (Group 1, Glasgow Outcome Scale [GOS] Score 1-3), whereas the remaining 5 patients had a favorable outcome (Group 2, GOS Score 4 or 5). Decompressive craniectomy resulted in a significant reduction (p < 0.001) in the mean ICP and cerebrovascular pressure reactivity index to autoregulatory values (< 0.3) in both groups of patients. There was a significant improvement in brain tissue oxygenation (PbtO(2)) in Group 2 patients from 3 to 17 mm Hg and an 85% reduction in episodes of cerebral ischemia. In addition, the durations of abnormal PbtO(2) and biochemical indices were significantly reduced in Group 2 patients after decompressive craniectomy, but there was no improvement in the biochemical indices in Group 1 patients despite surgery. CONCLUSIONS: Decompressive craniectomy, when used appropriately in protocol-driven intensive care regimens for the treatment of recalcitrant elevated ICP, is associated with a return of abnormal metabolic parameters to normal values in patients with eventually favorable outcomes.     

颅脑损伤患者Rotterdam评分与术后挫伤性脑出血扩大的相关研究

目的探讨重型颅脑损伤患者Rotterdam头颅CT评分与去骨瓣减压术后挫伤性脑出血扩大的关系,明确挫伤性脑出血增加量与预后的关系。方法 212例行单侧去骨瓣减压术的颅脑损伤患者进入研究,记录年龄,GCS评分,瞳孔,实验室检查和最初的、术前最近的、术后首次的头颅CT数据。预后指标:外伤后6个月GOS评分。结果最初头颅CT的Rotterdam评分与去骨瓣减压术后的挫伤性脑出血是否扩大及血肿增加量相关。Rotterdam评分与死亡率和预后相关。去骨瓣减压术后挫伤性脑出血增加量与死亡率和预后相关。结论重型颅脑损伤患者最初的Rotterdam头颅CT评分可以预测去骨瓣减压术后脑挫伤出血扩大的风险,且与预后相关。     

Long-term complications of decompressive craniectomy for head injury

There is currently much interest in the use of decompressive craniectomy for intracranial hypertension. Though technically straightforward, the procedure is not without significant complications. A retrospective analysis was undertaken of 164 patients who had had a decompressive craniectomy for severe head injury in the years 2004 to 2009 at the two major hospitals in Western Australia. Eighty-six patients had a bifrontal decompression and seventy-eight had a unilateral decompression. Two patients died due to post-operative care issues. Complications attributable to the decompressive surgery were: herniation of the cortex through the bone defect (42 patients, 25.6%), subdural effusion (81 patients, 49.4%), seizures (36 patients, 22%), hydrocephalus (23 patients, 14%), and syndrome of the trephined (2 patients, 1.2%). Complications attributable to the subsequent cranioplasty included: sudden death due to massive cerebral swelling in 3 patients (2.2%), infection requiring removal of the bone flap in 16 patients (11.6%), and bone flap resorption requiring augmentation in 10 patients (7.2%). After excluding simple complications such as subdural effusion and brain herniation through the skull defect and some patients who died as a direct consequence of traumatic brain or extracranial injury, 81 patients (55.5%) had at least one complication after decompressive craniectomy. The occurrence of at least one complication after decompressive craniectomy was significantly associated with an increased risk of prolonged stay in the hospital or rehabilitation facility (odds ratio 2.54, 95%confidence interval 1.22,5.24, p=0.013), after adjusting for predicted risk of unfavorable outcome.     

Outcome following decompressive craniectomy for malignant swelling due to severe head injury

OBJECT: The aim of this study was to assess outcome following decompressive craniectomy for malignant brain swelling due to closed traumatic brain injury (TBI). METHODS: During a 48-month period (March 2000-March 2004), 50 of 967 consecutive patients with closed TBI experienced diffuse brain swelling and underwent decompressive craniectomy, without removal of clots or contusion, to control intracranial pressure (ICP) or to reverse dangerous brain shifts. Diffuse injury was demonstrated in 44 patients, an evacuated mass lesion in four in whom decompressive craniectomy had been performed as a separate procedure, and a nonevacuated mass lesion in two. Decompressive craniectomy was performed urgently in 10 patients before ICP monitoring; in 40 patients the procedure was performed after ICP had become unresponsive to conventional medical management as outlined in the American Association of Neurological Surgeons guidelines. Survivors were followed up for at least 3 months posttreatment to determine their Glasgow Outcome Scale (GOS) score. Decompressive craniectomy lowered ICP to less than 20 mm Hg in 85% of patients. In the 40 patients who had undergone ICP monitoring before decompression, ICP decreased from a mean of 23.9 to 14.4 mm Hg (p < 0.001). Fourteen of 50 patients died, and 16 either remained in a vegetative state (seven patients) or were severely disabled (nine patients). Twenty patients had a good outcome (GOS Score 4-5). Among 30-day survivors, good outcome occurred in 17, 67, and 67% of patients with postresuscitation Glasgow Coma Scale scores of 3 to 5, 6 to 8, and 9 to 15, respectively (p < 0.05). Outcome was unaffected by abnormal pupillary response to light, timing of decompressive craniectomy, brain shift as demonstrated on computerized tomography scanning, and patient age, possibly because of the small number of patients in each of the subsets. Complications included hydrocephalus (five patients), hemorrhagic swelling ipsilateral to the craniectomy site (eight patients), and subdural hygroma (25 patients). CONCLUSIONS. Decompressive craniectomy was associated with a better-than-expected functional outcome in patients with medically uncontrollable ICP and/or brain herniation, compared with outcomes in other control cohorts reported on in the literature.     

Post-operative expansion of hemorrhagic contusions after unilateral decompressive hemicraniectomy in severe traumatic brain injury

Decompressive hemicraniectomy is commonly performed in patients with traumatic brain injury (TBI) with diffuse brain swelling or refractory raised intracranial pressure. Expansion of hemorrhagic contusions in TBI patients is common, but its frequency following decompressive hemicraniectomy has not been well established. The aim of this retrospective study was to determine the rate of hemorrhagic contusion expansion following unilateral hemicraniectomy in severe TBI, to identify factors associated with contusion expansion, and to examine whether contusion expansion is associated with worsened clinical outcomes. Computed tomography (CT) scans of 40 consecutive patients with non-penetrating TBI who underwent decompressive hemicraniectomy were analyzed. Hemorrhagic contusion volumes were measured on initial, last pre-operative, and first post-operative CT scans. Mortality and 6-month Glasgow Outcome Scale (GOS) score were recorded. Hemorrhagic contusions of any size were present on the initial head CT scan in 48% of patients, but hemorrhagic contusions with a total volume of >5 cc were present in only 10%. New or expanded hemorrhagic contusions of >or=5 cc were observed after hemicraniectomy in 58% of patients. The mean volume of increased hemorrhage among these patients was 37.1+/-36.3 cc. The Rotterdam CT score on the initial head CT was strongly associated with the occurrence and the total volume of expanded hemorrhagic contusions following decompressive hemicraniectomy. Expanded hemorrhagic contusion volume greater than 20 cc after hemicraniectomy was strongly associated with mortality and poor 6-month GOS even after controlling for age and initial Glasgow Coma Scale (GCS) score. Expansion of hemorrhagic contusions is common after decompressive hemicraniectomy following severe TBI. The volume of hemorrhagic contusion expansion following hemicraniectomy is strongly associated with mortality and poor outcome. Severity of initial CT findings may predict the risk of contusion expansion following hemicraniectomy, thereby identifying a subgroup of patients who might benefit from therapies aimed at augmenting the coagulation system.     

Acute subdural hematoma: Outcome and outcome prediction

Patients with traumatic acute subdural hematoma were studied to determine the factors influencing outcome.Between January 1986 and August 1995, we collected 113 patients who underwent craniotomy for traumatic acute subdural hematoma. The relationship between initial clinical signs and the outcome 3 months after admission was studied retrospectively.Functional recovery was achieved in 38% of patients and the mortality was 60%. 91% of patients with a high Glasgow Coma Scale (GCS) score (9–15) and 23% of patients with a low GCS score (3–8) achieved functional recovery. All of 14 patients with a GCS score of 3 died. The mortality of patients with GCS scores of 4 and 5 was 95% to 75%, respectively. Patients over 61 years old had a mortality of 73% compared to 64% mortality for those aged 21–40 years. 97% of patients with bilateral unreactive pupil and 81% of patients with unilateral unreactive pupil died. The mortality rates of associated intracranial lesions were 91% in intracerebral hematoma, 87% in subarachnoid hemorrhage, 75% in contusion.Time from injury to surgical evacuation and type of surgical intervention did not affect mortality. Age and associated intracranial lesions were related to outcome. Severity of injury and pupillary response were the most important factors for predicting outcome.     

Bilateral hemicraniectomy in non-penetrating traumatic brain injury

Traumatic brain injury is a heterogeneous entity that encompasses both surgical and non-surgical conditions. Surgery may be indicated with traumatic lesions such as hemorrhage, fractures, or malignant cerebral edema. However, the neurological exam may be clouded by the effects of medications administered in the field, systemic injuries, and inaccuracies in hyperacute prognostication. Typically, neurological injury is considered irreversible if diffuse loss of grey/white matter differentiation or if brainstem hemorrhage (Duret hemorrhage) exists. We aim to characterize a cohort of patients undergoing bilateral hemicraniectomy for severe traumatic brain injury. A retrospective consecutive cohort of adult patients undergoing craniectomy for trauma was established between the dates of January 2008 and November 2011. The primary outcome of the study was in-hospital mortality. Secondary outcomes were ICU length of stay, surgical complications, and Glasgow Outcome Score at most recent follow-up. During the study period, 210 patients undergoing craniectomy for traumatic mass-occupying lesion (epidural hematoma, subdural hematoma, or parenchymal contusion) were analyzed. Of those, 9 met study criteria. In-hospital mortality was 67% (6 of 9 patients). The average ICU length of stay was 12 days. The GOS score was 3 in surviving patients. Bilateral hemicraniectomy is a heroic intervention for patients with severe TBI, but can be a life-saving procedure.     

The management of traumatic brain injury

Traumatic brain injury (TBI) is a huge global problem with an increasing socioeconomic impact. Current understanding of the pathophysiology of TBI has led to a systematic approach towards management in the pre-hospital, operating theatre and critical care settings, with early management directed towards protecting the brain from secondary injury. TBI is a spectrum of diseases, and rapid radiological identification of the underlying pathology is paramount to determine appropriate surgical intervention. Most modern neurocritical care centres augment intracranial pathophysiology with intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targeted therapies at a minimum. Decompressive craniectomy (DC) can be a useful mechanism to control medically refractory intracranial hypertension and reduce mortality; however, it also results in a spectrum of outcome categories and remains a controversial topic. There is emerging evidence that TBI is a chronic illness, with increased incidence of cognitive and behavioural deficits, neurodegenerative disease, and an increased mortality that extends well beyond the initial TBI stage. Ongoing research into novel biomarkers may yield future therapeutic targets to improve clinical outcomes.     

Aspects on decompressive craniectomy in patients with traumatic head injuries

In patients with traumatic brain injury (TBI), intracranial hypertension secondary to cerebral edema is a major problem. A last-tier treatment in these cases is decompressive craniectomy. The aim of the present retrospective investigation was to (1) study the long-time outcome in patients with traumatic head injuries with intracranial hypertension treated with decompressive craniectomy; (2) examine the effects on intracranial pressure (ICP) by the craniectomy; and (3) investigate the possible relationship between the size of the removed bone-flap and the effects on ICP. Among the about 150 patients with severe TBI treated at our neurointensive care unit during 1997-2002, 19 patients were treated with decompressive craniectomy. All patients were young (mean 22 +/- 11 years, range 7-46 years), and 68% were male. The mean ICP was reduced from 29.2 +/- 3.5 before to 11.1 +/- 6.0 mm Hg immediately after the craniectomy; at 24 h after the craniectomy, the mean ICP was 13.9 +/- 9.7 mm Hg. Paired-samples t-test revealed a statistically significant decrease, both when comparing the preoperative values to the values immediately postoperative as well as to the values after 24 h (p < 0.01). A significant correlation between the size of the craniectomy and the decrease in ICP was found using Pearson regression analysis. The outcome of all patients could be assessed. The survival rate was 89%. Two patients died (both day 4 after the trauma); 68% of the patients had a favorable outcome (Glasgow Outcome Scale [GOS] score of 4 or 5); 16% were severely disabled (GOS score of 3); and one patient (5%) was left in a vegetative state.     

The management of traumatic brain injury

Traumatic brain injury (TBI) is a global problem with a huge socioeconomic impact. Current understanding of the pathophysiology of TBI has led to a systematic approach towards management in the pre-hospital, operating theatre and critical care settings. Early management is directed towards protecting the brain from secondary injury. TBI is a spectrum of diseases, and rapid radiological identification of the underlying pathology is paramount to determine appropriate surgical intervention. Perioperative management frequently requires neurocritical care, with most modern centres using intracranial pressure and cerebral perfusion pressure targeted therapies. Decompressive craniectomy can be a useful mechanism to control medically refractory intracranial hypertension and reduce mortality; however, it also results in a spectrum of outcome categories and remains a controversial topic. Finally, there is emerging evidence that TBI is a chronic illness, with increased incidence of cognitive and behavioural deficits, neurodegenerative disease and an increased mortality that extends well beyond the initial TBI stage.     

Subdural hematoma following traumatic brain injury causes a secondary decline in brain free magnesium concentration

A number of studies have demonstrated that neurologic motor and cognitive deficits induced by traumatic brain injury (TBI) can be attenuated with administration of magnesium salts. However, many severe traumatic brain injuries have a significant hematoma that develops subsequent to the primary events, and it is unclear whether magnesium salts are effective in this situation. In the present study, an impact-acceleration rodent model of TBI was used to produce an injury that causes an extensive subdural hematoma in over 50% of injured animals. At 30 min after TBI, rats were randomly administered 250 micromoles/kg intravenous MgSO4 or equal volume saline before being monitored by magnetic resonance spectroscopy for 8 h to determine brain intracellular free magnesium concentration. Animals were then assessed for neurologic motor deficits over 1 week using a rotarod device, followed by postmortem examination for presence of subdural hematoma. Animals with subdural hematoma treated with MgSO4 showed no improvement in motor outcome when compared to nontreated controls. Animals with no visible subdural hematoma demonstrated a significant improvement (p < 0.05 by ANOVA) in rotarod scores with MgSO4 treatment. Brain free magnesium concentration in the magnesium treated/hematoma group demonstrated a biphasic decline made up of an immediate initial decline, recovery of brain magnesium levels with MgSO4 treatment, and then a significant second magnesium decline (p < 0.05). Such a secondary decline did not occur in the Mg treated/no hematoma animals. Our results suggest that development of a subdural hematoma following TBI results in a decline in brain magnesium, even after bolus administration of magnesium salts. Such effects of hematoma development will need to be considered in trials examining efficacy of magnesium salts as an intervention following TBI.     

Acute subdural hematoma and diffuse axonal injury after severe head trauma

The association of acute subdural hematoma (SDH) and diffuse axonal injury has received little attention in the literature. The authors report the clinicopathological findings in six patients who died of severe head injury in whom computerized tomography revealed acute SDH as the predominant lesion. All patients were injured in road traffic accidents and lost consciousness on impact. The mean total contusion index was 17.4 and sever contusions were seen in only two cases. All patients presented histological criteria of intracranial hypertension (pressure necrosis focus in one or both parahippocampal gyri). Hypoxic brain damage was evident in the postmortem examination of three patients. In three cases, macroscopic hematic lesions were observed in the corpus callosum. All patients had widespread axonal retraction balls disseminated in the white brain matter. Three patients who survived for more than 11 days had microglial clusters. In some patients with a head injury, acute SDH may be only an epiphenomenon of a primary impact lesion of variable severity: that is, a diffuse axonal injury. In these cases, the final outcome is fundamentally dependent on the severity of the subjacent diffuse axonal injury.     

Delayed onset of intraventricular hemorrhage following removal of acute subdural hematoma--case report.

A 68-year-old male presented with neurological deterioration after a lucid interval following head trauma. Computed tomographic (CT) scans on admission demonstrated a subdural hematoma in the right frontotemporal region accompanied by subarachnoid hemorrhage in the right Sylvian and interhemispheric fissures. The subdural hematoma was removed via a right frontotemporoparietal craniectomy. However, immediate postoperative CT scans revealed hemorrhage in the third and both lateral ventricles, apparently separate from the primary hemorrhages. Decompressive rupture of damaged subependymal veins is suggested as the cause of the delayed traumatic intraventricular hemorrhage.     

一侧开颅清除双侧额叶挫裂伤伴出血

目的探讨一侧开颅切开额前部大脑镰清除双侧额叶挫裂伤的手术治疗可行性。方法对8例经一侧开颅清除双侧额叶挫裂伤的病例进行回顾性分析。结果术后CT复查示所有病例血肿清除满意,出院GOS评分7例为良好,1例并肺部感染自动出院。结论一侧开颅清除双侧额叶挫裂伤具有创伤小、手术时间短、失血少、患者预后好的优点,对部分病例适用。