Surgery for Brain Edema

Peter Hutchinson, F.R.C.S.(SN); Ivan Timofeev, M.R.C.S.; Peter Kirkpatrick, F.R.C.S.(SN)

Disclosures

Neurosurg Focus. 2007;22(5):E14 

In This Article

Abstract and Introduction

Abstract

Brain edema is a common pathophysiological process seen in many neurosurgical conditions. It can be localized in relation to focal lesions or generalized in diffuse types of brain injury. In addition to local adverse effects occurring at a cellular level, brain edema is associated with raised intracranial pressure (ICP), and both phenomena contribute to poor outcome in patients. One of the goals in treating patients with acute neurosurgical conditions in intensive care is to control brain edema and maintain ICP below target levels. The mainstay of treatment is medical therapy to reduce edema, but in certain patients-for example, those with diffuse severe traumatic brain injury (TBI) and malignant middle cerebral artery infarction—such treatment is not effective. In these patients, opening the skull (decompressive craniectomy) to reduce ICP is a potential option. In this review the authors discuss the role of decompressive craniectomy as a surgical option in patients with brain edema in the context of a variety of pathological entities. They also address the current evidence for the technique (predominantly observational series) and the ongoing randomized studies of decompressive craniectomy in TBI and ischemic stroke.

Introduction

Arguably the most fundamental pathophysiological processes following brain injury are brain edema, increased ICP, reduced cerebral blood flow, inadequate oxygen delivery, energy failure, and further edema. These processes are common to a number of neurosurgical conditions, including TBI, SAH, intracerebral hemorrhage, and cerebral infarction. One of the goals of treatment is to interrupt this vicious cycle by controlling swelling and maintaining an adequate blood and oxygen sup ply to meet the needs of the injured brain. Early intervention with simple treatment measures (administration of oxygen and intravenous fluids) to correct hypoxia and hypotension is essential. Following this initial stage of resuscitation, ongoing specialist treatment is designed to minimize the occurrence of secondary insults, which contribute to brain edema. One of the greatest advances in neurointensive care is the implementation of protocols to standardize treatment in patients with cerebral edema. There is now good evidence that such protocols have resulted in an improvement in neurological outcome. The steps of protocol-driven management differ among centers (type and order of intervention), but the overall concept of increasing the intensity of treatment until targets (for example, ICP and cerebral perfusion pressure) are reached is a common theme. Therapies include medical measures such as maintaining oxygenation, inducing hypothermia or mild hyperventilation, and administering mannitol, hypertonic saline, and barbiturates. Drainage of CSF by ventriculostomy is also an effective means of controlling brain swelling in many patients. Whereas these therapies will allow treatment targets to be reached in most patients, there is a cohort with pathophysiologies including TBI, SAH, and ischemic stroke in whom the vicious cycle of brain edema will continue to propagate, culminating in an increase in cell injury and death. Such patients may be candidates for brain edema surgery; that is, decompressive procedures to assist in the control of brain swelling. In this review we will therefore focus on decompressive craniectomy as a therapy in controlling brain edema in patients with TBI, poor-grade SAH, and ischemic stroke.

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