Decompressive Craniectomy in Diffuse Traumatic Brain Injury

Cooper, Jamie; Rosenfeld, Jeffrey V.; Murray, Lynnette; Arabi, Yaseen M.; Davies, Andrew R.; D’Urso, Paul; Kossmann, Thomas; Ponsford, Jennie Louise; Seppelt, Ian; Reilly, Peter; Wolfe, Rory

doi:10.1056/nejmoa1102077

Cited by 1,352 publications

(857 citation statements)

References 33 publications

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“…Some practices, such as the use of hypothermia in TBI patients, decompressive craniectomy, and ICP monitoring, have been reported to lack efficacy at improving outcomes in preliminary clinical trials. [44][45][46] Nevertheless, our findings are in agreement with multiple observational studies suggesting that the development of specialized neurocritical care unitsusually supported by the presence of neurointensivists and utilizing evidence-based protocols-may contribute to improved patient outcomes. 28 International studies involving neurocritical care patients have suggested that there is considerable variability in outcomes between countries and individual centers.…”

Section: Discussionsupporting

confidence: 90%

Declining mortality in neurocritical care patients: a cohort study in Southern Alberta over eleven years

Kramer

Zygun

2013

Can J Anesth/J Can Anesth

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Section: Discussionsupporting

confidence: 90%

Declining mortality in neurocritical care patients: a cohort study in Southern Alberta over eleven years

Kramer

Zygun

2013

Can J Anesth/J Can Anesth

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“…These findings may have been influenced by the "early" timing of craniectomy in their protocols, potentially averting secondary brain damage associated with cerebral edema [47], although the inclusion of patients who may not have truly needed decompression also may have favorably influenced outcome. In contrast, worse outcomes were reported for decompressive craniectomy in traumatic brain injury when compared to maximal medical therapy alone [48]. However, applicability of these findings is tempered based on choice of operative technique (bifrontal procedure), a long study accrual time, differences in study arms (significantly more patients with bilaterally unreactive pupils included in the surgical group), and minimal mean elevations in intracranial pressure leading up to randomization.…”

Section: Osmotherapymentioning

confidence: 97%

Novel Treatment Targets for Cerebral Edema

2012

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Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(−) co-transporter (NKCC1) and the SUR1-regulated NC Ca-ATP (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A-and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.Keywords Cerebral edema . Hyponatraemia . Osmotherapy . NKCC1 . SUR1/TRPM4 . Vaptan . Glyburide Overview of Perturbations in Brain Fluid HomeostasisCerebral edema in the neurointensive care setting can occur with a heterogenous group of neurological diseases, which typically fall under the categories of metabolic [1, 2], infectious [3], neoplastic [4], cerebrovascular [5][6][7], and traumatic [8,9] brain injury. Irrespective of the inciting process, cerebral edema results in the pathological accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs secondary to alterations in the complex interplay between 4 distinct fluid compartments within the cranium; fluid is present within: 1) the blood in the cerebral blood vessels, 2) the cerebrospinal fluid in the ventricular system and subarachnoid space, 3) the interstitial fluid of the brain parenchyma, and 4) the intracellular fluid of the neurons and glia. These fluid compartments are not isolated, and specific movements of solutes and water from one compartment to another occur under normal conditions. When dysregulation of this normally tightly controlled fluid balance...

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“…In addition to improving ICP, DC has also been shown to improve cerebral oxygenation in pediatric patients with TBI [75,99]. The recently published "Decompressive Craniectomy in Diffuse TBI" and the Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intra-Cranial Pressure (RESCUEicp) trials in adults may lay the groundwork for a similar study to be performed with pediatric patients [100]. Large, randomized trials in pediatric patients that address long-term outcomes, including quality of life measures, are needed to address optimal patient selection, timing of intervention, and surgical methods.…”

Section: Decompressive Craniectomymentioning

confidence: 99%

Pediatric Neurocritical Care

Murphy

2012

Neurotherapeutics

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Pediatric neurocritical care is an emerging multidisciplinary field of medicine and a new frontier in pediatric critical care and pediatric neurology. Central to pediatric neurocritical care is the goal of improving outcomes in critically ill pediatric patients with neurological illness or injury and limiting secondary brain injury through optimal critical care delivery and the support of brain function. There is a pressing need for evidence based guidelines in pediatric neurocritical care, notably in pediatric traumatic brain injury and pediatric stroke. These diseases have distinct clinical and pathophysiological features that distinguish them from their adult counterparts and prevent the direct translation of the adult experience to pediatric patients. Increased attention is also being paid to the broader application of neuromonitoring and neuroprotective strategies in the pediatric intensive care unit, in both primary neurological and primary non-neurological disease states. Although much can be learned from the adult experience, there are important differences in the critically ill pediatric population and in the circumstances that surround the emergence of neurocritical care in pediatrics.

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Decompressive Craniectomy in Diffuse Traumatic Brain Injury

Cited by 1,352 publications

References 33 publications

Declining mortality in neurocritical care patients: a cohort study in Southern Alberta over eleven years

Declining mortality in neurocritical care patients: a cohort study in Southern Alberta over eleven years

Novel Treatment Targets for Cerebral Edema

Pediatric Neurocritical Care

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