Management Of Severe Brain Injury Research Articles

Towards modern post-coma care based on neuroscientific evidence.

Understanding the mechanisms underlying human consciousness is pivotal to improve the prognostication and treatment of severely brain-injured patients. Consciousness remains an elusive concept and the identification of its neural correlates is an active subject of research, however recent neuroscientific advances have allowed scientists to better characterize disorders of consciousness. These breakthroughs question the historical nomenclature and our current management of post-comatose patients. This review examines the contribution of consciousness neurosciences to the current clinical management of severe brain injury. It investigates the major impact of consciousness disorders on healthcare systems, the scientific frameworks employed to identify their neural correlates and how evidence-based data from neuroimaging research have reshaped the landscape of post-coma care in recent years. Our increased ability to detect behavioral and neurophysiological signatures of consciousness has led to significant changes in taxonomy and clinical practice. We advocate for a multimodal framework for the management of severely brain-injured patients based on precision medicine and evidence-based decisions, integrating epidemiology, health economics and neuroethics. Major progress in brain imaging and clinical assessment have opened the door to a new era of post-coma care based on standardized neuroscientific evidence. We highlight its implications in clinical applications and call for improved collaborations between researchers and clinicians to better translate findings to the bedside.

Surgical techniques for severe brain injury : With special emphasis on polytrauma

In Austria approximately 2000 people suffer from severe brain injury per year. Brain trauma is the most common cause of death under the age of 45years. In polytrauma patients the treatment and management of severe brain injury is particularly challenging because the life-threatening injuries of other organ systems significantly influence the timing of surgery and the outcome. The sequence of the necessary surgery is an interdisciplinary decision already made in the emergency room. The evacuation of space-occupying intracranial hemorrhage can be of secondary importance. The standard approach for acute subdural hematoma is a craniotomy using alarge question mark-shaped incision (trauma flap) and decompression. In acute epidural hematoma and impression fractures the localization of the lesion determines the surgical approach and evacuation. A variety of access procedures are available. Frontobasal injuries are extremely rarely an indication for an emergency operation for life-threatening injuries. Decompressive craniotomy is performed as for craniotomy for acute subdural hematoma by the standard trauma flap. Emergency room computed tomography provides fast and accurate information about the localization and extent of brain injury. The mortality of acute subdural hematoma ranges between 50-90% despite an adequate evacuation. Outcome of epidural hematoma has a much better prognosis (10% mortality). The results of decompressive craniectomy versus conservative treatment for moderate disability and good recovery are quite similar according to the randomized evaluation of surgery with craniectomy for uncontrolled elevation of intracranial pressure (RESCUE-ICP) study. Interdisciplinary cooperation and communication and well-trained trauma surgeons with experience in brain trauma are key factors in the treatment of severe brain injury in polytrauma patients.

Severe brain injury management

Management of severe brain injury, the main cause of death in young population, has now standardized principles that lead to the improving of the outcome. The treatment of this traumatic illness is directly connected to cerebral physiopathology. After the impact, there are some cerebral mechanisms that are modified and are responsible for the appearance of the secondary injury: damaging of the cerebral metabolism, which has characteristic a very high metabolic rate compared to other tissues, altering the cerebral blood flow responsible for the cerebral oxygenation, altering the blood brain barrier with direct consequences on cerebral edema. Therefore, therapeutic aspects are connected to monitoring and will address to ensuring the hemodynamic stability, accurate oxygenation and correction of the factors that may worsen secondary injury (temperature, glycemia, osmolarity).

Application of decompressive craniectomy in management of severe brain injuries

重型颅脑损伤(severe traumatic brain injury,sTBI)患者的死亡率较高,是青壮年人死亡的主要原因之一~([1]).流行病学调查表明,sTBI患者伤后6个月死亡率高达40%,植物生存和重残分别达4%和16%~([2]),如何降低其死残率仍是目前sTBI研究的重要课题。

Brain Imaging in Intensive Care Medicine

The management of severe brain injury requires a comprehensive approach in which imaging is an indispensable complement to the clinical and physiological information acquired at the bedside. Neuroimaging methods are routinely used in the diagnosis and prognosis of a broad spectrum of patients with acute neurological dysfunction. With incremental theoretical and technological refinements, imaging modalities are helping to unravel fundamental questions regarding the pathophysiology and neuroplasticity associated with critical neurological injury, and it is anticipated that this knowledge will lead to new and effective therapeutic interventions. We review some of the established and emerging structural and physiological imaging methods, and discuss their applications in patients with critical injuries including trauma and encephalopathy due to anoxia, liver failure, and sepsis.

Réanimation des patients traumatisés crâniens graves

Severe brain injuries, most often occurring in young subjects, are a major source of lost work years. These injuries are medical and surgical emergencies. Prehospital management of severe brain injuries requires intubation and mechanical ventilation aimed at normal arterial carbon dioxide pressure. Signs of transtentorial herniation: Uni- or bilateral mydriasis requires immediate perfusion of 20% mannitol or hypertonic sodium chloride. Neurological disorders after head injury justify emergency cerebral computed tomography. The presence of a mass syndrome or signs of transtentorial herniation are in principle indications for surgery. Specialized hospital management is essential. In the case of refractory intracranial hypertension, the cerebral perfusion pressure and osmotherapy should be adapted to the volume of the cerebral contusion. The use of deep hypothermia and barbiturates should be minimized as much as possible. Magnetic resonance imaging makes it possible to identify the cerebral lesions.

Primer on medical management of severe brain injury

To review the current understanding of the medical management of severe brain injury. The MEDLINE database, bibliographies of selected articles, and current English-language texts on the subject. Studies related to management of intracranial hypertension, traumatic brain injury, and brain edema. All studies relevant to the subject under consideration were considered, with a focus on clinical studies in adults. 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. 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 monitoring

Intracranial pressure (ICP) is a product of the volume and compliance of the craniospinal contents. The craniospinal axis has only a limited capacity to accommodate any increase in volume without an increase in ICP. In the normal brain, autoregulation ensures that cerebral blood flow (CBF) remains constant even though cerebral perfusion pressure (CPP) can vary widely. In the diseased brain, autoregulation may be impaired such that CBF becomes pressure dependent. A fall in CPP, as such can result from elevation of ICP, results in a profound reduction in CBF. Early identification and treatment of secondary injuries following acute brain injury is of benefit both in terms of mortality and morbidity. Elevation of ICP is an independent predictor of outcome from traumatic coma. Clinical assessment of ICP is difficult in unconscious patients and there is a poor correlation between the appearances on radiological imaging and direct measurement of ICP. Measurement of ICP and the targeting of therapies to reduce elevated ICP and preserve CPP are components in the management of severe brain injury.

The role of hypothermia in the management of severe brain injury: a meta-analysis.

Hypothermia is utilized in the management of severe traumatic brain injury despite the lack of unequivocal evidence supporting its use. Because of its widespread use, the effects of hypothermia are a concern. To determine the effectiveness of hypothermia in the management of severe brain injury. Two investigators working independently abstracted data in a blinded fashion from studies identified using multiple literature databases, including MEDLINE, Ovid, PubMed, the Cochrane Database of Systematic Reviews, EMBASE, and the abstract center for the American Association of Neurological Surgery and the Congress of Neurological Surgery, as well as the bibliographies of these articles. Additionally, experts in the field of hypothermia and neurotrauma provided additional references. Seven studies met predetermined inclusion criteria: (1) the study was a randomized clinical trial comparing the efficacy of hypothermia vs normothermia in patients with posttraumatic head injury, (2) only subjects aged 10 years or older were included in the study, and (3) relative risks (odds ratios [ORs], cumulative incidence, or incidence density measures) and 95% confidence intervals (CIs) or weighted mean differences and 95% CIs could be calculated from the data presented in the article. These criteria were applied in a blinded fashion by 2 independent investigators. No single outcome variable was evaluated in all studies. The following outcome variables were assessed: intracranial pressure, Glasgow Outcome Scale score, pneumonia, cardiac arrhythmia, prothrombin time, and partial thromboplastin time. Either ORs or weighted mean differences (when the data provided did not permit calculation of an OR) comparing the effects of hypothermia vs normothermia were calculated from the data provided. The weighted mean difference (hypothermia - normothermia) for intracranial pressure was -2.98 mm Hg (95% CI, -7.58 to 1.61; P =.2). The OR (hypothermia vs normothermia) for Glasgow Outcome Scale score was 0.61 (95% CI, 0.26-1.46; P =.3). The OR for pneumonia was 2.05 (95% CI, 0.79-5.32; P =.14). The OR for cardiac arrhythmia was 1.27 (95% CI, 0.38-4.25; P =.7). The weighted mean difference for prothrombin time was 0.02 seconds (95% CI, -0.07 to 0.10; P =.7). The weighted mean difference for partial thromboplastin time was 2.22 seconds (95% CI, 1.73-2.71; P<.001). This meta-analysis of randomized controlled trials suggests that hypothermia is not beneficial in the management of severe head injury. However, because hypothermia continues to be used to treat these injuries, additional studies are justified and urgently needed.

Effect of hypothermia on brain tissue oxygenation in patients with severe head injury

There is renewed interest in the use of induced hypothermia as a method of neuroprotection both intraoperatively and in the intensive care management of severe brain injury. In this study we have investigated the effects of hypothermia on brain tissue oxygenation in patients with severe head injury. Thirty patients with severe head injury (Glasgow coma score <8) were monitored with a multimodal sensor inserted into the brain which measures tissue PO2, PCO2, pH and temperature in addition to routine monitoring. Patients were cooled to a minimum of 33 degrees C when clinically indicated. For all 30 patients brain and systemic temperature correlated well (r=0.96). Brain temperature was consistently higher than systemic temperature by 0.41 +/- 0.26 degrees C (confidence limits). Brain tissue PO2 decreased with hypothermia, with a significant reduction below 35 degrees C (P<0.05). These results emphasize the advantage of measuring brain temperature directly, and suggest that decreasing brain temperature below 35 degrees C may impair brain tissue oxygenation.

829 The Role of Hypothermia in the Management of Severe Brain Injury: A Meta-analysis

829 The Role of Hypothermia in the Management of Severe Brain Injury: A Meta-analysis

829 The Role of Hypothermia in the Management of Severe Brain Injury: A Meta-analysis

829 The Role of Hypothermia in the Management of Severe Brain Injury: A Meta-analysis

Late deaths in multiple trauma patients receiving intensive care

We reviewed the cause and timing of death of all the patients who died within hospital following multiple trauma and admission to a multidisciplinary intensive care unit (ICU) that also acts as a tertiary referral centre for neurosurgery. The ICU database identified 101 such patients in a 3-year period and their records were reviewed retrospectively. There were 40 (39%) deaths within 24 h of admission to the ICU, 38 of which resulted from severe brain injury and two from haemorrhagic shock (HS). A further 61 (60%) deaths occurred more than 24 h after the time of admission to ICU (mean 7 days; range 2–49 days), of which 46 (75%) were due to severe brain injury. While these findings do not question the promulgated tri-modal distribution of death following trauma, they are at variance with the view that the third peak of deaths is due mainly to multiple organ failure. When severe head injury accompanies multiple trauma, it is likely to be the major determinant of late mortality. If outcome from major trauma is to be improved, then a greater emphasis needs to be placed on the prevention and optimal management of severe brain injury.

The use of lobectomy in the management of severe closed-head trauma.

A retrospective review is presented of 20 patients with traumatic brain injury who were treated during the course of their illness by lobectomies either after a herniation or other significant deterioration or to reduce elevated intracranial pressure. All the patients suffered from blunt head trauma. Patient ages ranged from 19 to 59 years (average, 34 yr). The initial Glasgow Coma Scale score ranged from 3 to 15 (average, 8.2). There were 14 frontal lobectomies, 2 temporal, 3 frontal and temporal, and 1 occipital. Surgery was performed between 0 and 8 days after injury (average, 2.8). Outcome was favorable (good or moderately disabled) in 11 patients and unfavorable (severely disabled, persistently vegetative, or dead) in 9. No patients survived in a persistently vegetative state. A higher initial Glasgow Coma Scale score was positively correlated with a more favorable outcome (P < 0.03). Younger patients also showed a significant positive relationship to outcome (P < 0.0005). Better pupillary reactivity showed a significant trend toward a more favorable outcome (P < 0.04). The type of lesions identified on computed tomographic scans had no association with outcome. A lobectomy can be a useful adjuvant in the management of severe brain injury, especially in younger patients with relatively higher initial Glasgow Coma Scale scores who subsequently deteriorate or develop elevated intracranial pressure.