Traumatic brain injury (TBI) affects up to 2% of the population per year, and constitutes the major cause of death and severe disability among young people. By far, the most important complication of TBI is the development of an intracranial hematoma, which complicates 25 to 45% of severe TBI cases, 3 to 12% of moderate TBI cases, and approximately 1 in 500 patients with mild TBI20. Without effective surgical management, an intracranial hematoma may transform an otherwise benign clinical course with the expectation of recovery to a situation in which death or permanent vegetative survival will occur. Moreover, prolonged delay in the diagnosis or evacuation of an intracranial hematoma may produce a similar result.

As many as 100,000 patients per year may require surgical management for a posttraumatic intracranial hematoma in the United States alone. For these reasons, the impact that neurosurgeons can have on the care of such patients is enormous, and perhaps, more than in any other area of emergency medicine, the aggressiveness and rapidity with which care is provided for an intracranial hematoma will determine the outcome8. Picard et al.13 have shown that craniotomy for evacuation of an acute epidural hematoma is one of the most cost-effective of all surgical procedures. For this particular subgroup, which may represent up to 5% of patients with severe and moderate TBI, the quality of outcome has been shown to vary dramatically among different hospitals with different levels of commitment to acute neurotrauma care2, 6, 11. It is for this reason, more than any other, that neurosurgical consultation in the Emergency Room should be promptly available and is a mandated requirement for Level I certification of Trauma centers1.

Although there is evidence that posttraumatic intracranial mass lesions have been removed surgically up to 4000 years ago by the Egyptians and Meso-Americans, it was not until a series of publications emerged in the late 1960s that it became generally accepted that excellent results could be achieved with craniotomy for removal of extradural hematomas9. For acute subdural hematomas and intraparenchymal lesions, such as contusions and traumatic intracerebral hematomas, the outcome has historically been much worse, because up to 60% of patients with acute subdural hematomas will die or remain severely disabled10.

During the early 1970s, a series of publications from the Medical College of Virginia demonstrated that wide decompressive craniotomy with duraplasty was one of the most effective forms of therapy for raised intracranial pressure in patients with mass lesions4. Subsequently, most neurosurgical centers with an interest in TBI have also applied the same craniotomy technique to patients with intraparenchymal contusions, with improvements in outcome. However, there is also widespread dissent and controversy regarding the surgical management of intraparenchymal lesions, with some neurosurgeons maintaining that aggressive surgical intervention, although able to preserve life, will result in a very poor quality of life for survivors7, 15.

With our increasing understanding of the pathomechanisms in severe and moderate TBI have come changes in our approach to management of patients with posttraumatic intracranial mass lesions. For example, it is now well accepted that most intraparenchymal mass lesions (contusions and intracerebral hematomas) will enlarge with time, necessitating serial computed tomographic scanning, and usually intracranial pressure monitoring during the first few days12, 17. Similarly, the propensity of patients with posttraumatic coagulation disorders to develop intraparenchymal bleeding that is more severe is now well accepted, and has led to management of coagulation disorders in the head injured population that is much more aggressive18.

In turn, these practices led to an increase in the performance of craniotomy, both for evacuation of intraparenchymal mass lesions and as a decompressive measure. Recently, several publications have shown that, within the context of modern aggressive neuro-intensive care therapy, decompressive craniotomy is an effective means of controlling raised intracranial pressure after severe TBI, especially in those patients with intraparenchymal lesions14,19. Many neurosurgeons, however, are reluctant to implement such aggressive surgical techniques in patients with raised intracranial pressure after severe TBI, claiming that improved quality of life has never been conclusively demonstrated.

It is, therefore, the overall aim of these Guidelines is to present rigorous literature-based recommendations for the surgical management of patients with posttraumatic intracranial mass lesions. We have chosen to focus on those acute mass lesions that develop within 10 days of injury and, thus, we have chosen not to cover chronic subdural hematoma, subdural hygroma, and posttraumatic hydrocephalus, which usually are delayed. Similarly, we have chosen to focus on closed TBI in general because a comprehensive set of management guidelines for patients with penetrating TBI has already been formulated3.

Compared with the Guidelines for The Management of Severe Traumatic Brain Injury5, the literature regarding surgical management after TBI suffers from extensive limitations, in both quality and scope. Most notably, although our group reviewed more than 700 manuscripts for the preparations of these Guidelines, there are no controlled clinical trials in the literature to support different forms of surgical management, or to support surgical versus conservative therapy. Consistent with these limitations, we have been unable to formulate recommendations at the standard level requiring Class I evidence.

As in all other areas of "evidence-based medicine," these Guidelines have been formulated strictly in accordance with externally imposed constraints. Only clinical human-based literature has been reviewed. Only literature from 1975 through 2001 has been reviewed. Mainly literature in English, with far fewer articles in other languages, was reviewed. For these reasons, the reader must clearly understand that the scope and level of magnitude of the recommendations made here are distilled from the available literature and interpreted according to the rules of "evidence-based medicine"16.

An important aspect of this document is, therefore, to also formulate critical questions that need to be resolved by future clinical trials or prospective cohort studies, to determine the most effective forms of therapy for the future. As with the other guidelines in severe TBI, therefore, this is a document in evolution, and frequent revisions will be made to keep up with the evolving state of knowledge in this area.

These Guidelines have been organized on the basis of the traditional literature-based classification of posttraumatic mass lesions: namely, epidural hematoma, acute subdural hematoma, intraparenchymal lesions (contusion and intracerebral hematoma), acute posterior fossa mass lesions, and depressed fractures of the cranium. We recognize, however, that, for most patients with severe TBI, and for some patients with moderate TBI, more than one of these acute posttraumatic mass lesions may coexist at the same time. For example, the majority of patients with acute subdural hematomas will also demonstrate concomitant intraparenchymal contusions on their computed tomographic scan. In some patients, there may be multiple sites in which intraparenchymal mass lesions occur - e.g., bifrontal contusions, bitemporal contusions, or temporal and frontal lesions. For high-volume lesions (>50 cm3), management decisions are easier, and generally are in favor of surgery. Low-volume lesions (<25 cm3) are usually not operated on, however, for lesions between high and low volumes, the decisions may be very difficult and associated factors, e.g., shift, cisterns, and Glasgow Coma Scale, become especially important.

Within the literature, the terms surgical decompression, decompressive craniectomy, evacuation, and internal decompression are often used interchangeably. This aspect is clarified as much as possible in the individual sections.

We describe methods for posttraumatic mass volume measurement in Appendix 1 and simple methods and definitions of midline shift, subarachnoid hemorrhage, and status of basal cisterns in Appendix 2.