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Background: Traumatic posterior fossa subdural hematomas (SDHs) are rare lesions. Despite improvements in intensive care and surgical management of traumatic brain injuries over the last decades, the outcome for posterior fossa subdural hematomas remains poor., Methods: We conduct a retrospective study over a 2-year period of patients sustaining traumatic brain injury and posterior fossa SDH. Additionally, a systematic review of case series published to date was performed., Results: The incidence of posterior fossa SDH was 0,01% (4/326). All patients in this current series had poor prognosis. Three out of four exhibited ischemic/edema lesions in postoperative CT scans leading to fourth ventricle effacement and persistent brainstem compression. Our literature review retrieved 57 patients from only seven case series. Unfavorable outcomes were seen in 63% of patients., Conclusions: Our data and data from the literature do not provide sufficient evidence to establish an optimal treatment strategy for posterior fossa SDH. However, based on lessons learned with these four cases, together with results from review of the literature, we propose an algorithm for the management of this rare condition.

Introduction: We report the effective use of dexmedetomidine in the treatment of a patient with a history of chronic alcohol abuse and an acute traumatic brain injury who developed agitation that was unresolved if from traumatic brain injury, or alcohol withdrawal or the combination of both. Treatment with benzodiazepines failed; lorazepam therapy obscured our ability to do reliable neurological testing to follow his brain injury and nearly resulted in intubation of the patient secondary to respiratory suppression. Upon admission to hospital, the patient was first treated with intermittent, prophylactic doses of lorazepam for potential alcohol withdrawal based upon our institution's standard of care. His neurological examinations including a motor score of 6 (obeying commands) on his Glasgow Coma Scale testing, laboratory studies, and repeat CT head imaging remained stable. For lack of published literature in diagnosing symptoms of patients with a history of both alcohol withdrawal and traumatic brain injury, a diagnosis of agitation secondary to presumed alcohol withdrawal was made when the patient developed acute onset of tachycardia, confusion, and extreme anxiety with tremor and attempts to climb out of bed requiring him to be restrained. Additional lorazepam doses were administered following a hospital-approved protocol for titration of benzodiazepine therapy for alcohol withdrawal. The patient's mental status and respiratory function deteriorated with the frequent lorazepam dosing needed to control his agitation. Dexmedetomidine IV infusion at a rate of 0.5 mcg/kg/h was then administered and was titrated ultimately to 1.5 mcg/kg/h. After 8 days of therapy with dexmedetomidine, the patient was transferred from the ICU to a step-down unit with an intact neurological examination and no evidence of alcohol withdrawal. Airway intubation was avoided during the patient's entire hospitalization. This case report highlights the intricate balance between the side effects of benzodiazepine sedation for treatment of agitation and the difficulties of monitoring the neurological status of non-intubated patients with traumatic brain injury., Conclusion: Given the large numbers of alcohol-dependent patients who suffer a traumatic brain injury and subsequently develop agitation and alcohol withdrawal in hospital, dexmedetomidine offers a novel strategy to facilitate sedation without neurological or respiratory depression. As this case report demonstrates, dexmedetomidine is an emerging treatment option for agitation in patients who require reliable, serial neurological testing to monitor the course of their traumatic brain injury.

The goal of our study was to determine the interobserver variability between observers with different backgrounds and experience when interpreting computed tomography (CT) imaging features of traumatic brain injury (TBI). We retrospectively identified a consecutive series of 50 adult patients admitted at our institution with a suspicion of TBI, and displaying a Glasgow Coma Scale score < or =12. Noncontrast CT (NCT) studies were anonymized and sent to five reviewers with different backgrounds and levels of experience, who independently reviewed each NCT scan. Each reviewer assessed multiple CT imaging features of TBI and assigned every NCT scan a Marshall and a Rotterdam grading score. The interobserver agreement and coefficient of variation were calculated for individual CT imaging features of TBI as well as for the two scores. Our results indicated that the imaging review by both neuroradiologists and neurosurgeons were consistent with each other. The kappa coefficient of agreement for all CT characteristics showed no significant difference in interpretation between the neurosurgeons and neuroradiologists. The average Bland and Altman coefficients of variation for the Marshall and Rotterdam classification systems were 12.7% and 21.9%, respectively, which indicates acceptable agreement among all five reviewers. In conclusion, there is good interobserver reproducibility between neuroradiologists and neurosurgeons in the interpretation of CT imaging features of TBI and calculation of Marshall and Rotterdam scores.

Decompressive craniectomy is widely used to treat intracranial hypertension following traumatic brain injury (TBI). Two randomized trials are currently underway to further evaluate the effectiveness of decompressive craniectomy for TBI. Complications of this procedure have major ramifications on the risk-benefit balance in decision-making during evaluation of potential surgical candidates. To further evaluate the complications of decompressive craniectomy, a review of the literature was performed following a detailed search of PubMed between 1980 and 2009. The author restricted her study to literature pertaining to decompressive craniectomy for patients with TBI. An understanding of the pathophysiological events that accompany removal of a large piece of skull bone provides a foundation for understanding many of the complications associated with decompressive craniectomy. The author determined that decompressive craniectomy is not a simple, straightforward operation without adverse effects. Rather, numerous complications may arise, and they do so in a sequential fashion at specific time points following surgical decompression. Expansion of contusions, new subdural and epidural hematomas contralateral to the decompressed hemisphere, and external cerebral herniation typify the early perioperative complications of decompressive craniectomy for TBI. Within the 1st week following decompression, CSF circulation derangements manifest commonly as subdural hygromas. Paradoxical herniation following lumbar puncture in the setting of a large skull defect is a rare, potentially fatal complication that can be prevented and treated if recognized early. During the later phases of recovery, patients may develop a new cognitive, neurological, or psychological deficit termed syndrome of the trephined. In the longer term, a persistent vegetative state is the most devastating of outcomes of decompressive craniectomy. The risk of complications following decompressive craniectomy is weighed against the life-threatening circumstances under which this surgery is performed. Ongoing trials will define whether this balance supports surgical decompression as a first-line treatment for TBI.

The aim of this study was to review the current protocols of prehospital practice and their impact on outcome in the management of traumatic brain injury. A literature review of the National Library of Medicine encompassing the years 1980 to May 2008 was performed. The primary impact of a head injury sets in motion a cascade of secondary events that can worsen neurological injury and outcome. The goals of care during prehospital triage, stabilization, and transport are to recognize life-threatening raised intracranial pressure and to circumvent cerebral herniation. In that process, prevention of secondary injury and secondary insults is a major determinant of both short- and longterm outcome. Management of brain oxygenation, blood pressure, cerebral perfusion pressure, and raised intracranial pressure in the prehospital setting are discussed. Patient outcomes are dependent upon an organized trauma response system. Dispatch and transport timing, field stabilization, modes of transport, and destination levels of care are addressed. In addition, special considerations for mass casualty and disaster planning are outlined and recommendations are made regarding early response efforts and the ethical impact of aggressive prehospital resuscitation. The most sophisticated of emergency, operative, or intensive care units cannot reverse damage that has been set in motion by suboptimal protocols of triage and resuscitation, either at the injury scene or en route to the hospital. The quality of prehospital care is a major determinant of long-term outcome for patients with traumatic brain injury.

Object: The "syndrome of the trephined" is an uncommon and poorly understood disorder of delayed neurological deficit following craniectomy. From the authors' extensive experience with decompressive hemicraniectomy for traumatic brain injury (TBI), they have encountered a number of patients who developed delayed motor deficits, also called "motor trephine syndrome," and reversal of the weakness following cranioplasty repair. The authors set out to study motor function systematically in this patient population to define the incidence, contributing factors, and outcome of patients with motor trephine syndrome., Methods: The authors evaluated patient demographics, injury characteristics, detailed motor examinations, and CT scans in 38 patients with long-term follow-up after decompressive hemicraniectomy for TBI., Results: Ten patients (26%) experienced delayed contralateral upper-extremity weakness, beginning 4.9 +/- 0.4 months (mean +/- standard error) after decompressive hemicraniectomy. Motor deficits improved markedly within 72 hours of cranioplasty repair, and all patients recovered full motor function. The CT perfusion scans, performed in 2 patients, demonstrated improvements in cerebral blood flow commensurate with resolution of cerebrospinal fluid flow disturbances on CT scanning and return of motor strength. Comparisons between 10 patients with and 20 patients (53%) without delayed motor deficits identified 3 factors--ipsilateral contusions, abnormal cerebrospinal fluid circulation, and longer intervals to cranioplasty repair--to be strongly associated with delayed, reversible monoparesis following decompressive hemicraniectomy., Conclusions: Delayed, reversible monoparesis, also called motor trephine syndrome, is common following decompressive hemicraniectomy for TBI. The results of this study suggest that close follow-up of motor strength with early cranioplasty repair may prevent delayed motor complications of decompressive hemicraniectomy.

Background and purposeThe development of a delayed epidural hematoma as a result of decompressive craniectomy represents an urgent and potentially lethal complication in traumatic brain injury. The goal of this study was to determine the incidence of delayed epidural hematoma and whether patterns of skull fractures on the preoperative CT scan could predict risk of a delayed epidural hematoma.Materials and methodsWe retrospectively evaluated medical records and imaging studies for patients with acute traumatic brain injury who underwent a decompressive craniectomy during a 9-year period. We compared patterns of skull fractures contralateral to the side of the craniectomy with the occurrence of a postoperative delayed epidural hematoma.ResultsIn a series of 203 patients undergoing decompressive craniectomy for acute traumatic brain injury, the incidence of a delayed epidural hematoma complication was 6% (12 of 203). All 12 patients who developed a delayed epidural hematoma had a contralateral calvarial fracture on preoperative CT at the site where the delayed epidural hematoma subsequently formed. A contralateral calvarial fracture has perfect sensitivity (100%) for subsequent development of delayed epidural hematoma in our study population. Moreover, a contralateral calvarial fracture involving 2 or more bone plates had an especially high diagnostic odds ratio of 41 for delayed epidural hematoma.ConclusionsRecognition of skull fracture patterns associated with delayed epidural hematoma following decompressive craniectomy may reduce morbidity and mortality by prompting early postoperative intervention in high-risk situations.