CHAPTER 1
INTRODUCTIONM. Ross Bullock, M.D., Ph.D.Department of Neurological Surgery,Virginia Commonwealth UniversityMedical Center,Richmond, Virginia
Randall Chesnut, M.D.Department of Neurological Surgery,University of WashingtonSchool of Medicine,Harborview Medical Center,Seattle, Washington
Jamshid Ghajar, M.D., Ph.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David Gordon, M.D.Department of Neurological Surgery,Montefiore Medical Center,Bronx, New York
Roger Hartl, M.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David W. Newell, M.D.Department of Neurological Surgery,Swedish Medical Center,Seattle, Washington
Franco Servadei, M.D.Department of Neurological Surgery,M. Bufalini Hospital,Cesena, Italy
Beverly C. Walters, M.D., M.Sc.Department of Neurological Surgery,New York UniversitySchool of Medicine,New York, New York
Jack E. Wilberger, M.D.Department of Neurological Surgery,Allegheny General Hospital,Pittsburgh, Pennsylvania
Reprints requests:Jamshid Ghajar, M.D., Ph.D.,Brain Trauma Foundation,523 East 72nd Street,New York, NY 10021.Email: [email protected]
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Traumatic brain injury (TBI) affects up to2% of the population per year, and con-stitutes the major cause of death and
severe disability among young people. By far,the most important complication of TBI is thedevelopment of an intracranial hematoma,which complicates 25 to 45% of severe TBIcases, 3 to 12% of moderate TBI cases, andapproximately 1 in 500 patients with mild TBI(20). Without effective surgical management,an intracranial hematoma may transform anotherwise benign clinical course with the ex-pectation of recovery to a situation in whichdeath or permanent vegetative survival willoccur. Moreover, prolonged delay in the diag-nosis or evacuation of an intracranial hema-toma may produce a similar result.
As many as 100,000 patients per year mayrequire surgical management for a posttrau-matic intracranial hematoma in the UnitedStates alone. For these reasons, the impact thatneurosurgeons can have on the care of suchpatients is enormous, and perhaps, more than inany other area of emergency medicine, the ag-gressiveness and rapidity with which care isprovided for an intracranial hematoma will de-termine the outcome (8). Picard et al. (13) haveshown that craniotomy for evacuation of anacute epidural hematoma is one of the mostcost-effective of all surgical procedures. For thisparticular subgroup, which may represent up to5% of patients with severe and moderate TBI,the quality of outcome has been shown to varydramatically among different hospitals with dif-ferent levels of commitment to acute neuro-trauma care (2, 6, 11). It is for this reason, morethan any other, that neurosurgical consultationin the Emergency Room should be promptlyavailable and is a mandated requirement forLevel I certification of Trauma centers (1).
Although there is evidence that posttraumaticintracranial mass lesions have been removedsurgically up to 4000 years ago by the Egyptiansand Meso-Americans, it was not until a series ofpublications emerged in the late 1960s that itbecame generally accepted that excellent resultscould be achieved with craniotomy for removal
of extradural hematomas (9). For acute subduralhematomas and intraparenchymal lesions, suchas contusions and traumatic intracerebral hema-tomas, the outcome has historically been muchworse, because up to 60% of patients with acutesubdural hematomas will die or remain severelydisabled (10).
During the early 1970s, a series of publica-tions from the Medical College of Virginia dem-onstrated that wide decompressive craniotomywith duraplasty was one of the most effectiveforms of therapy for raised intracranial pressurein patients with mass lesions (4). Subsequently,most neurosurgical centers with an interest inTBI have also applied the same craniotomy tech-nique to patients with intraparenchymal contu-sions, with improvements in outcome. How-ever, there is also widespread dissent andcontroversy regarding the surgical managementof intraparenchymal lesions, with some neuro-surgeons maintaining that aggressive surgicalintervention, although able to preserve life, willresult in a very poor quality of life for survivors(7, 15).
With our increasing understanding of thepathomechanisms in severe and moderate TBIhave come changes in our approach to man-agement of patients with posttraumatic intra-cranial mass lesions. For example, it is nowwell accepted that most intraparenchymalmass lesions (contusions and intracerebral he-matomas) will enlarge with time, necessitatingserial computed tomographic scanning, andusually intracranial pressure monitoring dur-ing the first few days (12, 17). Similarly, thepropensity of patients with posttraumatic co-agulation disorders to develop intraparenchy-mal bleeding that is more severe is now wellaccepted, and has led to management of coag-ulation disorders in the head injured popula-tion that is much more aggressive (18).
In turn, these practices led to an increase inthe performance of craniotomy, both for evac-uation of intraparenchymal mass lesions andas a decompressive measure. Recently, severalpublications have shown that, within the con-text of modern aggressive neuro-intensive
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care therapy, decompressive craniotomy is an effective meansof controlling raised intracranial pressure after severe TBI,especially in those patients with intraparenchymal lesions (14,19). Many neurosurgeons, however, are reluctant to imple-ment such aggressive surgical techniques in patients withraised intracranial pressure after severe TBI, claiming thatimproved quality of life has never been conclusively demon-strated.
It is, therefore, the overall aim of these Guidelines is topresent rigorous literature-based recommendations for thesurgical management of patients with posttraumatic intracra-nial mass lesions. We have chosen to focus on those acutemass lesions that develop within 10 days of injury and, thus,we have chosen not to cover chronic subdural hematoma,subdural hygroma, and posttraumatic hydrocephalus, whichusually are delayed. Similarly, we have chosen to focus onclosed TBI in general because a comprehensive set of manage-ment guidelines for patients with penetrating TBI has alreadybeen formulated (3).
Compared with the Guidelines for The Management of SevereTraumatic Brain Injury (5), the literature regarding surgical man-agement after TBI suffers from extensive limitations, in bothquality and scope. Most notably, although our group reviewedmore than 700 manuscripts for the preparations of these Guide-lines, there are no controlled clinical trials in the literature tosupport different forms of surgical management, or to supportsurgical versus conservative therapy. Consistent with these lim-itations, we have been unable to formulate recommendations atthe standard level requiring Class I evidence.
As in all other areas of �evidence-based medicine,� theseGuidelines have been formulated strictly in accordance withexternally imposed constraints. Only clinical human-basedliterature has been reviewed. Only literature from 1975through 2001 has been reviewed. Mainly literature in English,with far fewer articles in other languages, was reviewed. Forthese reasons, the reader must clearly understand that thescope and level of magnitude of the recommendations madehere are distilled from the available literature and interpretedaccording to the rules of �evidence-based medicine� (16).
An important aspect of this document is, therefore, to alsoformulate critical questions that need to be resolved by futureclinical trials or prospective cohort studies, to determine themost effective forms of therapy for the future. As with theother guidelines in severe TBI, therefore, this is a document inevolution, and frequent revisions will be made to keep upwith the evolving state of knowledge in this area.
These Guidelines have been organized on the basis of the tra-ditional literature-based classification of posttraumatic mass le-sions: namely, epidural hematoma, acute subdural hematoma,intraparenchymal lesions (contusion and intracerebral hema-toma), acute posterior fossa mass lesions, and depressed frac-tures of the cranium. We recognize, however, that, for mostpatients with severe TBI, and for some patients with moderateTBI, more than one of these acute posttraumatic mass lesionsmay coexist at the same time. For example, the majority ofpatients with acute subdural hematomas will also demonstrate
concomitant intraparenchymal contusions on their computed to-mographic scan. In some patients, there may be multiple sites inwhich intraparenchymal mass lesions occur—e.g., bifrontal con-tusions, bitemporal contusions, or temporal and frontal lesions.For high-volume lesions (�50 cm3), management decisions areeasier, and generally are in favor of surgery. Low-volume lesions(�25 cm3) are usually not operated on, however, for lesionsbetween high and low volumes, the decisions may be very dif-ficult and associated factors, e.g., shift, cisterns, and GlasgowComa Scale, become especially important.
Within the literature, the terms surgical decompression,decompressive craniectomy, evacuation, and internal decom-pression are often used interchangeably. This aspect is clari-fied as much as possible in the individual sections.
We describe methods for posttraumatic mass volume mea-surement in Appendix 1 and simple methods and definitions ofmidline shift, subarachnoid hemorrhage, and status of basalcisterns in Appendix 2.
REFERENCES
1. ACS-COT: American College of Surgeons-Committee on Trauma: Resourcesfor Optimal Care of the Injured Patient. Chicago, American College of Sur-geons, 1999.
2. Alberico A, Ward J, Choi S, Marmarou A, Young H: Outcome after severehead injury. Relationship to mass lesions, diffuse injury, and ICP course inpediatric and adult patients. J Neurosurg 67:648–656, 1987.
3. Anonymous: Management and prognosis of penetrating brain injury.J Trauma 51[Suppl]: S1–S49, 2001.
4. Becker D, Miller J, Ward J, Greenberg R, Young H, Sakalas R: The outcomefrom severe head injury with early diagnosis and intensive management.J Neurosurg 47:491–502, 1977.
5. Brain Trauma Foundation, American Association of Neurological Surgeons,Joint Section on Neurotrauma and Critical Care: Guidelines for the manage-ment of severe traumatic brain injury. J Neurotrauma 17:457–554, 2000.
6. Bricolo A, Pasut L: Extradural hematoma: Toward zero mortality. A pro-spective study. Neurosurgery 14:8–12, 1984.
7. Clark K, Nash TM, Hutchison GC: The failure of circumferential craniotomyin acute traumatic cerebral swelling. J Neurosurg 29:367–371, 1968.
8. Consensus conference: Rehabilitation of persons with traumatic brain in-jury. NIH Consensus Development Panel on Rehabilitation of Persons withTraumatic Brain Injury. JAMA 282:974–983, 1999.
9. Jamieson KG, Yelland JD: Extradural hematoma: Report of 167 cases.J Neurosurg 29:13–23, 1968.
10. Jamieson KG, Yelland JD: Surgically treated subdural hematomas.J Neurosurg 37:137–149, 1972.
11. Klauber MR, Marshall LF, Luerssen TG, Frankowski R, Tabaddor K,Eisenberg HM: Determinants of head injury mortality: Importance of thelow risk patient. Neurosurgery 24:31–36, 1989.
12. Lobato RD, Gomez PA, Alday R, Rivas JJ, Dominguez J, Cabrera A,Turanzas FS, Benitez A, Rivero B: Sequential computerized tomographychanges and related final outcome in severe head injury patients. ActaNeurochir (Wien) 139:385–391, 1997.
13. Picard J, Bailey S, Sanderson H, Reese M, Garfeld JS: Steps towards costbenefit analysis of regional neurosurgical care. BMJ 301:629–635, 1990.
14. Polin R, Shaffrey M, Bogaev C, Tisdale N, Germanson T, Bocchicchio B, JaneJ: Decompressive bifrontal craniectomy in the treatment of severe refractoryposttraumatic cerebral edema. Neurosurgery 41:84–92, 1997.
15. Ransohoff J, Benjamin MV, Gage EL Jr, Epstein F: Hemicraniectomy in themanagement of acute subdural hematoma. J Neurosurg 34:70–76, 1971.
16. Sackett DL, Rosenberg WM, Gray JA, Haynes RB, Richardson WS: Evidencebased medicine. What it is and what it isn’t. BMJ 312:71–72, 1996.
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17. Soloniuk D, Pitts LH, Lovely M, Bartkowski H: Traumatic intracerebralhematomas: Timing of appearance and indications for operative removal.J Trauma 26:787–794, 1986.
18. Stein SC, Young GS, Talucci RC, Greenbaum BH, Ross SE: Delayed braininjury after head trauma: Significance of coagulopathy. Neurosurgery 30:160–165, 1992.
19. Taylor A, Butt W, Rosenfeld J, Shann F, Ditchfield M, Lewis E, Klug G,Wallace D, Henning R, Tibballs J: A randomized trial of very early decom-pressive craniectomy in children with traumatic brain injury and sustainedintracranial hypertension. Childs Nerv Syst 17:154–162, 2001.
20. Thurman D, Guerrero J: Trends in hospitalization associated with traumaticbrain injury. JAMA 282:954–957, 1999.
INTRODUCTION
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CHAPTER 2
METHODOLOGYM. Ross Bullock, M.D., Ph.D.Department of Neurological Surgery,Virginia Commonwealth UniversityMedical Center,Richmond, Virginia
Randall Chesnut, M.D.Department of Neurological Surgery,University of WashingtonSchool of Medicine,Harborview Medical Center,Seattle, Washington
Jamshid Ghajar, M.D., Ph.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David Gordon, M.D.Department of Neurological Surgery,Montefiore Medical Center,Bronx, New York
Roger Hartl, M.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David W. Newell, M.D.Department of Neurological Surgery,Swedish Medical Center,Seattle, Washington
Franco Servadei, M.D.Department of Neurological Surgery,M. Bufalini Hospital,Cesena, Italy
Beverly C. Walters, M.D., M.Sc.Department of Neurological Surgery,New York UniversitySchool of Medicine,New York, New York
Jack E. Wilberger, M.D.Department of Neurological Surgery,Allegheny General Hospital,Pittsburgh, Pennsylvania
Reprints requests:Jamshid Ghajar, M.D., Ph.D.,Brain Trauma Foundation,523 East 72nd Street,New York, NY 10021.Email: [email protected]
Neurosurgery 58:S2-4-S2-6, 2006 DOI: 10.1227/01.NEU.0000210362.83548.0B www.neurosurgery-online.com
The concept of formulating a set of rec-ommendations for patient managementhas its basis in the advent of scientific
investigation in clinical medicine. Along withthis came the realization that deriving recom-mendations from our own experience as clini-cians, although tempting, has limitations re-lated to the fact that humans remember thebest or the worst of their experiences, andcannot easily objectify their results. What clin-ical experience does do for us is to help withthe formulation of hypotheses that can betested through human clinical trials experi-mentation. Rather than seeing clinical experi-ence and clinical trials as dichotomous, polarsources of information regarding outcomes ofpatient care, it is probably more useful tothink of the gamut of clinical testing along acontinuum. On one end, we have the more-subjective impressions of care delivery thatare attractive because they are grounded inpersonal experience in the real world of caringfor patients. This is expressed well by one ofthe fathers of clinical epidemiology, AlvanFeinstein. Dr. Feinstein, in his seminal work,Clinical Judgment (2), writes: “. . .any decentdoctor reflects on alternatives, is aware of un-certainties, modifies judgments on the basis ofaccumulated evidence, balances risks of vari-ous kinds, considers the potential conse-quences of his or her diagnoses or treatments,and synthesizes all of this in making a rea-soned decision that he or she decrees right forthe patient.” He further goes on to underscorethe value of clinical experience when hewrites, “In caring for patients, clinicians con-stantly perform experiments. During a singleweek of active practice, a busy clinician con-ducts more experiments than most of his lab-oratory colleagues do in a year.”
This philosophy underscores and supportsthe notion that we can make recommenda-tions from the wealth of clinical experienceprovided by direct, day-to-day clinical care.However, a close look at the process of trueexperimentation yields a long list of potentialerrors that can be made in the gathering and
interpretation of data, even in highly con-trolled circumstances. Sources of error havebeen classified into two broad categories: sys-tematic error (bias) and random error. In gen-eral, the former source of error is controlled bycareful study design, and the latter is dealtwith by randomization. Without these protec-tors against error, the chances of making mis-takes in deriving recommendations from prac-tice are great. For this reason, the notion ofcategorizing recommendations into groups as-sociated with various strengths of clinicalstudies on the basis of scientific rigor wasintroduced in the last decade-and-a-half of the20th century.
In 1990, the Institute of Medicine published alandmark work entitled Clinical Practice Guide-lines: Directions for a New Program (1). The insti-gating factors for this publication were the ob-servation of wide variability of practicethroughout American healthcare and the devel-opment of mechanisms for establishing qualityassurance and review within Medicare, alongwith the increasing use of technology and con-comitant costs of care delivery. In this docu-ment, the authors made recommendations re-garding attributes defining the validity ofrecommendations. These include the following:1. The available scientific literature should besearched using appropriate and comprehensivesearch terminology. 2. A thorough review of thescientific literature should precede guideline de-velopment. 3. The evidence should be evaluatedand weighted, reflecting the scientific validity ofthe methodology used to generate the evidence.4. There should be a link between the availableevidence and the recommendations, with thestrength of the evidence being reflected in thestrength of the recommendations, reflecting sci-entific certainty (or lack thereof). 5. Empiricalevidence should take precedence over expertjudgment in the development of guidelines. 6.Expert judgment should be used to evaluate thequality of the literature and to formulate guide-lines when the evidence is weak or nonexistent.7. Guideline development should be a multidis-
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ciplinary process, involving key groups affected by the recom-mendations.
SEARCH OF THE LITERATURE
The literature is generally searched using the National Li-brary of Medicine computerized database, either through in-dividual search engines in academic medical centers orthrough the internet. This, by definition, will limit the scope ofthe search to 1966 and forward. In addition, if modern neuro-imaging techniques are pertinent, as in this document, thesearch should be limited to the years since the modality wasavailable. Therefore, our searches were limited to the period of1975 to the present. Because guidelines are applicable to pa-tient care, the literature is limited to human studies in the areaof traumatic brain injury and surgical management, alongwith the imaging characteristics in patients with surgicallyamenable lesions. In addition, further limitations in the searchwere imposed by the fact that most of the literature is inEnglish, and limited ability existed for reading the usefularticles that appear in different languages. Therefore, mostsearches were limited to the English language. Appropriatesearch terms were chosen, as demonstrated in each of theindividual Guideline sections.
EVALUATION AND WEIGHTING OF THELITERATURE
The journal articles found have been carefully read andevaluated, including an assessment of the methodology usedin the studies. This not only includes the establishment of theclinical question addressed (e.g., therapeutic effectiveness, di-agnostic tests, prognostic studies, etc.) and type of study (ran-domized controlled trial, case-control study, case series, etc.),but also the quality of the study with respect to potentialerrors in design, execution, or conclusions reached. Therefore,studies that might, on the surface, represent evidence support-ing one level of recommendation, may instead be flawedenough to be devalued to support a recommendation of lesserstrength. The quality of the literature was evaluated in thisway according to well-established criteria (3). All articles werecross-reviewed and disagreements were resolved by consen-sus.
LINK BETWEEN EVIDENCE ANDGUIDELINES
The general concept of relating strength of recommenda-tions to strength of evidence reflecting varying degrees ofclinical certainty was formalized into a scheme that has beenfollowed by medical societies, including organized neurosur-gery, from the inception of the Guideline development process.Despite problems with the strict application of this paradigm(some of which are displayed and discussed in this supple-ment), the scheme has the benefit of using scientific evidencerather than expert opinion for the substrate of the recommen-dations, although expert opinion is used to formulate therecommendations themselves, as well as to make judgmentsregarding the quality of the evidence. The evidence-basedscheme used in these and all Guidelines regarding therapeuticeffectiveness endorsed by the American Association of Neu-rological Surgeons and the Congress of Neurological Surgeonsbegins with classification of the literature into three categoriesof evidence, as outlined next and in Table 1.
The classification of evidence into these three categoriesleads to the formulation of recommendations called Standards,Guidelines, and Options. Class I evidence is used to supporttreatment recommendations of the strongest type, practiceStandards, reflecting a high degree of clinical certainty. Class IIevidence is used to support Guidelines, reflecting a moderatedegree of clinical certainty. Class III evidence supports practiceOptions reflecting unclear clinical certainty. This terminologywas developed to indicate, in normal vocabulary, the strengthof the recommendations on the basis of strong to weak med-ical evidence. In neurosurgery, this scheme has been used toformulate Guidelines, rather than a scheme that uses letters ornumbers that have no grounding in language and are, there-fore, more easily misinterpreted. The link between scientificevidence and recommendations has been highlighted in theseGuidelines by presenting those studies in the scientific founda-tion that support the stated recommendation in boldface type.
Recommendations are not necessarily weak in cases inwhich the evidence is weak. Examples of this appear in manyof the Guidelines developed in neurosurgery to date, and au-thors and readers alike feel frustrated at the impotency of therecommendations when the evidence is weak, especially whenthe logic of the recommendation and all of the evidence sup-porting it, however weak, support the recommendation. Oneexample of this, among many that can be found in this sup-
TABLE 1. Classification of Evidence on Therapeutic Effectiveness
Class I Evidence from one or more well-designed, randomized, controlled clinical trials, including overviews of such trialsClass II Evidence from one or more well-designed comparative clinical studies, such as nonrandomized cohort studies, case-control
studies, and other comparable studiesClass III Evidence from case series, comparative studies with historical controls, case reports, and expert opinion
METHODOLOGY
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plement, is in the recommendation regarding timing of evac-uation of epidural hematomas. According to the paradigmembraced and used in this set of Guidelines, case series indi-cating that patients who have a Glasgow Coma Scale score of8 or below with evidence of a “blown pupil” and who areoperated on early achieve better outcomes can only support apractice “Option.” However, no competent neurosurgeonwould allow a patient in this clinical scenario to be neglectedwhen the need for surgical relief of brain compression is soclear. It is fairly certain to say that there will never be arandomized controlled trial for this circumstance, and, thus,never a practice “Standard.” However, a patient databasecould be used to generate a case-control study, thus, yieldinga higher recommendation. However, there is no evidence thatwaiting to operate on such a patient is beneficial, and, there-fore, an “Option” to delay surgical evacuation will also prob-ably never be promulgated. If, indeed, such a recommenda-tion were put forward, it would never be accepted by theprofession, and rightfully so.
EXPERT JUDGMENT AND EMPIRICALEVIDENCE
There are two ways in which expert judgment comes intoGuideline development. The most common use of expert opin-ion is in developing recommendations for practice. This hasbeen a usual method in the past (as well as the present, in theform of textbook chapters), but has more recently given way tomore formalized approaches embraced by evidence-basedmedicine methodology, such as that used in this supplement.However, even in evidence-based methodology, expert opin-ion is used to evaluate the literature as well as to frame theconcepts and wording of the recommendations. In addition, ifthe evidence is weak and conflicting, expert opinion is used toderive recommendations. This use is unavoidable, but theexpert opinion is guided by the evidence published in theliterature, rather than from personal experience alone.
OPTION LEVEL RECOMMENDATION
All of the recommendations in the Surgical Management ofTraumatic Brain Injury are at the option level, supported only
by Class III scientific evidence. Unfortunately, option canmean choice and, as discussed above, it would be unethicalnot to operate on surgical mass lesions in salvageable patients.Currently, all neurological guidelines approved by the Amer-ican Association of Neurological Surgeons and the Congressof Neurological Surgeons use option recommendations forClass III evidence. In the future, this may change because thesesurgical guidelines put maximized strain on using such ter-minology.
Given that the recommendations in these surgical guide-lines are at the option level (Class III evidence) we state therecommendation at the beginning of the chapter on each topic,and refer the reader to this methodology section for an expla-nation of the level of evidence.
MULTIDISCIPLINARY PROCESS
In all Guidelines published under the auspices of the BrainTrauma Foundation and the American Association of Neuro-logical Surgeons, other professional organizations were in-volved in either developing the Guidelines or reviewed andapproved them. In these Surgical Management of TraumaticBrain Injury Guidelines, however, only neurosurgeons wereinvolved. These neurosurgeons represent a wide range oforganizations. There were representatives from the AmericanAssociation of Neurological Surgeons, the Congress of Neu-rological Surgeons, the European Brain Injury Consortium, theAmerican College of Surgeons (Committee of Trauma) and theWorld Federation of Neurological Surgeons (Neurotraumasection) involved in the development of these Surgical Man-agement of Traumatic Brain Injury Guidelines.
REFERENCES
1. Committee to Advise the Public Health Service on Clinical Practice Guide-lines (Institute of Medicine): Clinical Practice Guidelines: Directions for a NewProgram. Washington, D.C., National Academy Press, 1990.
2. Feinstein A: Clinical Judgement. Baltimore, Williams & Wilkins, 1967.3. Walters B: Clinical Practice Parameter Development, in Bean J (ed): Neuro-
surgery in Transition. Baltimore, Williams & Wilkins, 1998, pp 99–111.
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
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CHAPTER 3
SURGICAL MANAGEMENT OF ACUTE
EPIDURAL HEMATOMASM. Ross Bullock, M.D., Ph.D.Department of Neurological Surgery,Virginia Commonwealth UniversityMedical Center,Richmond, Virginia
Randall Chesnut, M.D.Department of Neurological Surgery,University of WashingtonSchool of Medicine,Harborview Medical Center,Seattle, Washington
Jamshid Ghajar, M.D., Ph.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David Gordon, M.D.Department of Neurological Surgery,Montefiore Medical Center,Bronx, New York
Roger Hartl, M.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David W. Newell, M.D.Department of Neurological Surgery,Swedish Medical Center,Seattle, Washington
Franco Servadei, M.D.Department of Neurological Surgery,M. Bufalini Hospital,Cesena, Italy
Beverly C. Walters, M.D., M.Sc.Department of Neurological Surgery,New York UniversitySchool of Medicine,New York, New York
Jack E. Wilberger, M.D.Department of Neurological Surgery,Allegheny General Hospital,Pittsburgh, Pennsylvania
Reprints requests:Jamshid Ghajar, M.D., Ph.D.,Brain Trauma Foundation,523 East 72nd Street,New York, NY 10021.Email: [email protected]
RECOMMENDATIONS(see Methodology)
Indications for Surgery● An epidural hematoma (EDH) greater than 30 cm3 should be surgically evacuated
regardless of the patient’s Glasgow Coma Scale (GCS) score.● An EDH less than 30 cm3 and with less than a 15-mm thickness and with less than
a 5-mm midline shift (MLS) in patients with a GCS score greater than 8 without focaldeficit can be managed nonoperatively with serial computed tomographic (CT)scanning and close neurological observation in a neurosurgical center.
Timing● It is strongly recommended that patients with an acute EDH in coma (GCS score �
9) with anisocoria undergo surgical evacuation as soon as possible.Methods● There are insufficient data to support one surgical treatment method. However,
craniotomy provides a more complete evacuation of the hematoma.
KEY WORDS: Coma, Computed tomographic parameters, Craniotomy, Epidural, Head injury, Hematoma,Surgical technique, Timing of surgery, Traumatic brain injury
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OVERVIEW
Incidence
Since the introduction of CT scanning as theimaging study of choice to detect intracraniallesions after trauma, the incidence of surgicaland nonsurgical EDH among traumatic braininjury (TBI) patients has been reported to be inthe range of 2.7 to 4% (8, 11, 25, 41). Amongpatients in coma, up to 9% harbored an EDHrequiring craniotomy (10, 35). The peak inci-dence of EDH is in the second decade, and themean age of patients with EDH is between 20and 30 years of age ( 3, 8, 9, 13, 16–18, 20, 22,26, 29, 32, 37, 39). EDH are a rare entity inpatients older than 50 to 60 years of age. Inpediatric patients, the mean age of patientsharboring EDH is between 6 and 10 years (21,34), and EDH is less frequent in very youngchildren and neonates (27, 30).
Pathogenesis
Traffic-related accidents, falls, and assaultsaccount for 53% (range, 30–73%), 30% (range,
7–52%), and 8% (range, 1–19%), respectively,of all EDH (3, 8, 20, 22, 26, 27, 36, 40). Inpediatric patients, falls are the leading causeof EDH in 49% of cases (range, 25–59%) andtraffic-related accidents are responsible for34% (range, 25–41%) of all EDH (21, 25–27, 30,34). EDH can result from injury to the middlemeningeal artery, the middle meningeal vein,the diploic veins, or the venous sinuses. His-torically, bleeding from the middle meningealartery has been considered the main sourcefor EDH. In a recent report on EDH in 102pediatric patients and 387 adults, arterialbleeding was identified as the source of theEDH in 36% of the adults and only in 18% ofthe children (27). In 31% of the pediatric pa-tients, a bleeding source could not be identi-fied and venous bleeding accounted for ap-proximately 32% of EDH in both age groups.
Location
In surgical series, EDH are more frequentlylocated in the temporoparietal and temporal re-gions as compared with other locations (3, 6, 25,
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27, 29, 32). In 2 to 5% of patients, bilateral EDH are found (11, 18,40), and there seems to be a slight predominance of right-sidedEDH over left-sided lesions (6, 40).
Clinical Presentation
In patients with EDH, 22 to 56% are comatose on admissionor immediately before surgery (3, 17, 20, 22, 25, 32). Theclassically described “lucid interval,” i.e., a patient who isinitially unconscious, then wakes up and secondarily deterio-rates, was observed in a total of 456 of 963 patients (47%)undergoing surgery for EDH in seven studies (3, 8, 18, 22, 28,31, 39). Between 12 and 42% of patients remained consciousthroughout the time between trauma and surgery (3, 8, 17, 22).Pupillary abnormalities are observed in between 18 and 44%of patients, and up to 27% (3–27%) of patients are neurologi-cally intact. Other presenting symptoms include focal deficits,such as hemiparesis, decerebration, and seizures. Early sei-zures are noted in 8% of pediatric patients presenting withEDH (21).
Mortality
The mortality in patients in all age groups and GCS scoresundergoing surgery for evacuation of EDH is approximately10% (range, 7–12.5%) (7, 8, 14, 17, 18, 20, 22, 28, 31, 32).Mortality in comparable pediatric case series is approximately5% (25, 30).
Determinants of Outcome in Patients UndergoingSurgical Evacuation of an EDH
GCS, age, pupillary abnormalities, associated intracraniallesions, time between neurological deterioration and surgery,and intracranial pressure (ICP) have been identified as impor-tant factors determining outcome from EDH.
Age and GCS
The influence of age on outcome in the subgroup of patientswith EDH is not as pronounced as it is in TBI patients overall.Three studies using multiple regression analysis found thatGCS was a better predictor of outcome than age in patientsundergoing surgery for EDH (20, 22, 38). In a retrospectiveanalysis of 98 patients of all age groups with EDH undergoingcraniotomy, van den Brink et al. (39) investigated determi-nants of outcome at 6 months. They identified GCS, age, andthe CT diagnosis of subarachnoid hemorrhage as significantfactors correlated with outcome, using multivariate analysis.Admission GCS or GCS before surgery is the single mostimportant predictor of outcome in patients with EDH under-going surgery (3, 10, 20, 22, 24, 38, 39). In three studies usingmultivariate analysis in a total of 284 patients, the admissionGCS score was identified as the most significant factor deter-mining outcome at 6 months (20, 38, 39). In one study with 200patients undergoing craniotomy, admission and preoperativeGCS both correlated with functional outcome at 1 year (22).Gennarelli et al. (10) analyzed the relationship between type oflesion, GCS score on admission, and 3-months outcome in
1107 comatose patients with TBI. The highest mortality wasfound in patients with a subdural hemorrhage and a GCSbetween 3 and 5 (74%). Patients with an EDH and a GCS of 3to 5 had a mortality of 36%, and patients with an EDH and aGCS of 6 to 8 had a mortality of only 9%.
Pupils
Pupillary abnormalities, such as pupillary asymmetry orfixed and dilated pupils occur in approximately 20 to 30% ofpatients with EDH undergoing surgery (3, 16, 20, 40) and in62% of patients who are comatose on admission (32). Onestudy showed that ipsilateral mydriasis was not associatedwith adverse outcome and was reversible when operated onwithin 70 minutes after pupillary dilation (6). Bilateral mydri-asis, however, is associated with a high mortality (3, 6, 8, 24,32, 39). Mydriasis contralateral to the hematoma is also asso-ciated with high mortality (24, 32). Van den Brink et al. (39), ina multivariate model evaluating the relative prognostic valueof predictive parameters, found that, in patients in all agegroups and GCS scores, pupillary abnormalities were signifi-cantly related to unfavorable outcome. Adverse outcome wasobserved in 30% of normal pupillary responses, in 35% ofunilateral fixed pupils, and in 50% of bilateral fixed pupils.Bricolo and Pasut (3) achieved a good outcome in 100% ofpatients who presented with anisocoria and in 90% of patientswho presented with anisocoria and hemiparesis. The onlypatient with bilateral mydriasis in their case series died.
Associated Lesions
Associated intracranial lesions are found in between 30 and50% of adult patients with surgically evacuated EDH (3, 8, 13,16, 20, 22, 23, 27, 29, 31, 32, 35). These are predominantlycontusions and intracerebral hemorrhage followed by sub-dural hematoma (SDH) and diffuse brain swelling (8, 16, 29,32, 35). The incidence of associated lesions is less in the pedi-atric age group (25, 27, 30). SDH and/or parenchymal lesionsin association with EDH lower the chance of a good outcome.In two studies with a total of 315 patients operated on forevacuation of an EDH, the frequency of associated intracraniallesions was 33% (20, 22). In both studies, a significant relation-ship was found between the presence of other lesions inaddition to the EDH and an adverse outcome. Lee et al. (22)identified associated brain lesions as one of four independentpredictors of unfavorable outcome after surgery for EDH andthis has been confirmed by several others (8, 13, 16, 23, 32).Cranial fractures are present in between 70 and 95% of cases(15, 17, 20, 25, 30, 37). The impact of fractures on outcome iscontroversial. Kuday et al. (20) observed a significant relation-ship between cranial factures and adverse outcome in 115patients undergoing surgery for EDH. Lee et al. (22) did notsee this relationship in a series of 200 patients managed sim-ilarly, and Rivas et al. (32) actually reported a significantlylower mortality rate in patients with cranial fractures. Signif-icant extracranial injury is present in 7 to 23% of patientsoperated on for an EDH (8, 13, 17, 24, 27). Lobato et al. (24)
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found extracranial injury in 20% of their patients, and themortality rate in this subgroup was lower than the overallmortality (7.6% versus 28%). No data were found on theassociation of hypotension and outcome in patients with anacute EDH.
ICP
There is only one study available in which postoperativeICP and its relationship to outcome 6 months after trauma wasstudied. Lobato et al. (24) monitored ICP in 54 (83%) of 64comatose patients after removal of an EDH. Elevated ICP (�15mm Hg) was found in 67% of cases, and ICP greater than 35mm Hg was significantly associated with a higher mortality.
PROCESS
A MEDLINE computer search using the following key-words for the years 1975 to 2001 was performed: “traumaticbrain injury” or “head injury” and “epidural” or “extradural”and “hematoma” or “hematoma” or “hemorrhage.” Thesearch was narrowed by including the keywords “surgicaltreatment” or “surgery” or “operation” or “craniotomy” or“craniectomy” or “craniostomy” or “burr holes” and exclud-ing “spinal.” These searches combined yielded 168 articles.The reference lists of these publications were reviewed and anadditional 22 articles were selected for analysis. Case reports,publications in books, and publications regarding penetratingbrain injuries on spinal EDH and on exploratory burr holeswithout a preoperative CT scan were not included. Articleswere excluded if the diagnosis of EDH was not based on CTscanning, or if subgroups of patients who did not undergo CTscanning were not clearly identified. Publications with fewerthan 10 patients or publications that did not include informa-tion on outcome were excluded. Of these 190 articles, 18 wereselected for analysis.
SCIENTIFIC FOUNDATION
Indication for Surgery
The decision to operate on an acute EDH is based on thepatient’s GCS score, pupillary exam, comorbidities, CT find-ings, age, and, in delayed decisions, the patient’s ICP. Neuro-logical deterioration over time is also an important factorinfluencing the decision to operate. Trauma patients present-ing to the emergency room with altered mental status, pupil-lary asymmetry, and abnormal flexion or extension are at highrisk for either an SDH and/or EDH compressing the brain andbrainstem.
CT Characteristics and Outcome
CT is the imaging study of choice for the diagnosis of anEDH. CT scanning is recommended in patients at risk forharboring an acute EDH. It allows not only diagnosis of theprimary lesion but also identification of additional featuresthat affect outcome, such as MLS, traumatic subarachnoid
hemorrhage, obliteration of the basal cisterns, thickness of theblood clot, and hematoma volume.
In a series of 200 patients who were treated surgically forEDH, Lee et al. (22) found that a hematoma volume greaterthan 50 cm3 was significantly related to higher mortality andunfavorable functional outcome. Unfavorable functional re-covery was observed in 6.2% of patients with a hematomavolume less than 50 cm3, and in 24% of patients with ahematoma volume greater than 50 cm3. Mixed density of theblood clot, indicating acute bleeding, was observed in 32% oftheir patients and correlated with unfavorable outcome butnot with mortality. Patients with an MLS greater than 10 mmshowed a higher mortality and more unfavorable outcomewhen compared with those with less displacement. Partial ortotal obliteration of the basal cisterns was observed in 59% oftheir patients and correlated with both mortality and func-tional outcome. Multivariate analysis identified only hema-toma volume as an independent predictor of unfavorableoutcome.
In contrast, in 98 patients with EDH who underwent sur-gery, van den Brink et al. (39) found that the status of the basalcisterns, MLS, and hematoma volume were not related tooutcome. The authors only identified the presence of trau-matic subarachnoid hemorrhage to be significantly associatedwith unfavorable outcome. Patients with favorable outcomehad a hematoma volume of 56 � 30 cm3 and, with unfavorableoutcome, the hematoma volume was 77 � 63 cm3, but thisdifference was not significant.
Rivas et al. (32) found that hematoma volume and severityof MLS were related to preoperative coma in patients withEDH. In comatose patients, a hematoma volume greater than150 cm3 and an MLS greater than 12 mm were associated withincreased mortality. Mixed-density blood clots were observedin 62% of their patients and were related to poor outcome.Location of the lesion did not influence outcome. Seelig et al.(35) did not find a relationship between location of blood clot,MLS, and outcome in 51 comatose patients undergoing sur-gery for EDH.
In summary, most authors could not detect a relationshipbetween blood clot location and outcome. However, it is likelythat hematoma volume, MLS, mixed density of the blood clot,and traumatic subarachnoid hemorrhage are related to out-come, but more studies are needed to clarify this issue.
Surgery and Nonoperative Treatment
Prospective, randomized trials comparing surgical treat-ment with nonoperative management are not available. Somestudies compared patients who were treated either surgicallyor nonoperatively, and used logistic regression analysis andmultivariate analysis models to determine factors that wereassociated with either treatment (36, 37). Some investigatorslooked at patient series that were initially all treated nonop-eratively and analyzed the factors associated with subsequent,delayed surgery (2, 7, 19, 37). There are no studies on nonop-erative treatment of comatose patients with EDH.
ACUTE EPIDURAL HEMATOMAS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-9
What are the factors leading to surgery? The followingstudies compared characteristics between patients who weretreated with either surgery or were managed nonoperatively.The value of such analyses is doubtful because it merelydocuments the criteria used to select patients for surgery.
Servadei et al. (36) conducted a prospective study including158 consecutive patients with GCS 14 and 15 with EDH whowere admitted to three neurosurgical units. A treatment pro-tocol was not defined for these hospitals. One hundred-sixteenpatients underwent surgery and 42 patients were managednonoperatively. Ninety-three percent of patients with an MLSgreater than 5 mm, and 91% of patients with a hematomathickness greater than 15 mm underwent surgery. A logisticregression analysis identified hematoma thickness and MLS asthe factors associated with surgery. Location and the presenceof associated lesions did not reach significance. Outcome wasgood in all patients. Similar results were obtained in 33 pedi-atric patients, 20 of whom were treated surgically (1). Bothgroups did not differ in terms of age, GCS, and outcome.Multivariate logistic regression analysis revealed that MLS,hematoma thickness, and volume, as well as temporal locationof the blood clot were related to surgery. Hematoma volumeand MLS were 41 cm3 and 8 cm3, and 4 mm and 0.5 mm, forthe surgical and nonsurgical groups, respectively.
A review of 30 patients who were treated with craniotomyand 18 patients treated nonoperatively revealed that patientsmanaged with surgery had lower GCS scores, were morelikely to present with pupillary abnormalities and hemipare-sis, and had larger blood clots and more MLS (12). Temporallocation of the hematoma and the presence and location of afracture were not related to surgery.
Factors Determining Delayed Surgery
Bezircioglu et al. (2) conducted a prospective study on thenonoperative management of 80 patients with EDH and GCSscores between 9 and 15. Patients with a GCS score greaterthan 8, an EDH volume less than 30 ml, a hematoma thicknessless than 2 cm, and without neurological deficit were treatednonoperatively. Five patients deteriorated and underwent cra-niotomy. One of these patients died, the others had goodoutcomes. The only factor significantly associated with de-layed surgery was a temporal location of the hematoma,which was observed in all five surgical patients but only in24% of the 75 patients treated without operation.
In a study of 74 patients with initially asymptomatic EDHmanaged nonoperatively, 14 required delayed surgery be-cause of neurological deterioration or increase in the size ofthe hematoma (5). The authors found that a hematoma volumegreater than 30 cm3, a hematoma thickness greater than 15mm, and an MLS greater than 5 mm were significantly morefrequent in patients requiring surgery. A hematoma volumegreater than 30 cm3, an EDH thickness greater than 15 mm,and an MLS greater than 5 mm were observed in 5%, 27%, and28% of patients managed without surgery, and in 57%, 71%,and 79% of patients who had surgery, respectively. The au-
thors used the “ellipsoid” or “ABC/2” method to estimate thevolume of EDHs (see Appendix I). Hematoma location, bonefractures, and time-to-initial CT scan were not related to out-come. In a small study on 22 patients, 7 of whom required latersurgery, a time interval of less than 6 hours after injury to thefirst CT scan and a cranial fracture that crossed a major vesselwere significantly related to surgery (19).
Studies Describing Successful Nonsurgical Management
Bullock et al. (4) treated 12 of 123 patients presenting withEDH nonsurgically. All patients were conscious (GCS 12–15)with a hematoma volume between 12 and 38 cm3 (mean, 26.8cm3) and an MLS less than 10 mm on the initial CT scan. Noneof the hematomas were in the temporal region. All patientsmade a good outcome. Cucciniello reported on 57 patientswith EDH who were treated nonoperatively (9). Initial GCSwas between 10 and 15. Five hematomas were in the temporalregion. The maximum hematoma thickness ranged between 6and 12 mm. Only one patient had an MLS. All patients madea good recovery.
Timing of Surgery
Time between Injury and Surgery
The effect of surgical timing on outcome from EDH isrelevant for a subgroup of patients in whom the EDH causescompression of brain structures that, with time, could causepoor outcome. This subgroup is usually categorized as havingpupillary abnormalities and/or a GCS score less than 9(coma). Generally, studies of EDH reveal that only 21 to 34%of patients present to the hospital with a GCS score less than8 or 9 (3, 20, 22, 25). Studies do not find a relationship betweensurgical timing and outcome if patients of all GCS scores areincluded. In 200 patients with EDH that were surgically evac-uated, Lee et al. (22) failed to demonstrate a significant rela-tionship between surgery within 4 hours of trauma or surgerywithin 2 hours of admission and outcome, using multivariateanalysis. However, a significant correlation was observed be-tween the duration of brain herniation, as evidenced by aniso-coria, and the outcome. The time lapse between the onset ofpupillary abnormalities and surgery is related to outcome.Cohen et al. (6) studied 21 patients with EDH and GCS scoreless than 9 who underwent surgery. Ten of these patientsdeveloped anisocoria after admission. All 5 patients withanisocoria for longer than 70 minutes before surgical evacua-tion of the EDH died. Patients with anisocoria for shorter than70 minutes achieved a good outcome. Haselsberger et al. (13)studied 60 patients with EDH, and 34 patients developedcoma before surgery. They found that patients treated within2 hours after loss of consciousness exhibited a mortality rate of17% and good recovery in 67%, compared with a mortalityrate of 56% and good results in 13% in patients operated onlater. Sakas et al. (33) found that all patients with either SDHor EDH with fixed and dilated pupils for longer than 6 hourdied.
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Patient Transfer and Timing of Surgery
The question of whether a patient with acute EDH shouldbe treated at the nearest hospital or transferred to a specializedtrauma center has been debated but poorly documented instudies. This is an important timing issue and is significant inthe group of patients who are deteriorating. Another issue isthe surgical evacuation of EDH by nonneurosurgeons withsubsequent transfer to a neurosurgical center. Obviously,these studies are uncontrolled with regard to the efficacy ofsurgery and the type of patients included in both arms. In theabove timing of surgery, the group of patients in a coma andwith pupillary abnormalities can be expected to do worse thelonger the interval to evacuation of the EDH. Thus, because ofthe delay, transferred patients would have longer intervaltimes to surgery.
Wester (40) studied 83 patients with acute EDH that under-went craniotomy. Twenty-eight patients were transferredfrom other hospitals and 11 of these underwent emergencysurgery at those outside institutions. Patients who underwentsurgery outside the parent institution by nonneurosurgeonshad a significantly worse outcome at 3 months as comparedwith patients who were directly admitted to the study hospi-tal. This was mainly attributed to the technical inadequacy ofthe primary operation at the outside institution. The authorsinterpreted this as support for the strategy of directly trans-ferring patients to an adequate trauma center, but they did notcontrol for other confounding variables, such as admissionGCS and pupillary exam.
Another study analyzed 107 patients operated on for EDH(3). The majority (67%) of these patients were transferred fromoutlying hospitals. The authors noted that only 6% of thedirect admissions experienced a poor outcome, as comparedwith 18% of patients who were transferred after undergoingCT scanning at an outside institution. This difference failed toreach statistical significance. Poon and Li (31) studied 71 pa-tients with EDH managed surgically primarily at a neurosur-gical hospital and 33 patients transferred from an outsideinstitution. Time delay from neurological deterioration to sur-gery was 0.7 � 1 hour and 3.2 � 0.5 hours for the direct versusindirect transferred group, respectively. Six-months outcomewas significantly better in patients who were directly admittedwith a minimal delay from deterioration in neurological examto surgery.
SUMMARY
In patients with an acute EDH, clot thickness, hematomavolume, and MLS on the preoperative CT scan are related tooutcome. In studies analyzing CT parameters that may bepredictive for delayed surgery in patients undergoing initialnonoperative management, a hematoma volume greater than30 cm3, an MLS greater than 5 mm, and a clot thickness greaterthan 15 mm on the initial CT scan emerged as significant.Therefore, patients who were not comatose, without focalneurological deficits, and with an acute EDH with a thickness
of less than 15 mm, an MLS less than 5 mm, and a hematomavolume less than 30 cm3 may be managed nonoperativelywith serial CT scanning and close neurological evaluation in aneurosurgical center (see Appendix II for measurement tech-niques). The first follow-up CT scan in nonoperative patientsshould be obtained within 6 to 8 hours after TBI. Temporallocation of an EDH is associated with failure of nonoperativemanagement and should lower the threshold for surgery. Nostudies are available comparing operative and nonoperativemanagement in comatose patients. The literature supports thetheory that patients with a GCS less than 9 and an EDHgreater than 30 cm3 should undergo surgical evacuation of thelesion. Combined with the above recommendation, it followsthat all patients, regardless of GCS, should undergo surgery ifthe volume of their EDH exceeds 30 cm3. Patients with anEDH less than 30 should be considered for surgery but may bemanaged successfully without surgery in selected cases.
Time from neurological deterioration, as defined by onset ofcoma, pupillary abnormalities, or neurological deterioration tosurgery, is more important than time between trauma andsurgery. In these patients, surgical evacuation should be per-formed as soon as possible because every hour delay in sur-gery is associated with progressively worse outcome.
KEY ISSUES FOR FUTURE INVESTIGATION
•Effect of transfer versus direct admission to a traumacenter on timing of surgery and outcome from EDH.
•Identification of subgroups that do not benefit from sur-gery: old patients with low GCS scores, pupillary abnormali-ties, and associated intracerebral lesions.
•Surgical technique.
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EVID
ENTI
AR
YTA
BLE
TAB
LE1.
Surg
ical
man
agem
ent
ofac
ute
epid
ural
hem
atom
asa
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Bej
jani
etal
.(1
)33
IIIA
llG
CS
Surg
ery
and
nons
urgi
cal
Dis
char
geR
etro
spec
tive
anal
ysis
offa
ctor
saf
fect
ing
the
deci
sion
toop
erat
ein
33pe
diat
ric
patie
nts
with
EDH
.13
patie
nts
unde
rwen
top
erat
ive
trea
tmen
t.
Mas
sef
fect
,te
mpo
ral
loca
tion
ofbl
ood
clot
,M
LS,
thic
knes
sof
clot
,an
dvo
lum
ew
ere
inde
pend
ently
rela
ted
tosu
rger
y.O
ther
clin
ical
fact
ors,
such
asag
e,G
CS,
and
asso
ciat
edfr
actu
res
wer
eno
t.O
utco
me
was
good
in�
90%
ofpa
tient
s.
EDH
Ope
rati
vetr
eatm
ent
Non
oper
ativ
etr
eatm
ent
Thic
knes
s(m
m)
209
Vol
ume
(cm
3 )41
8
MLS
(mm
)4
0.5
Bez
irci
oglu
etal
.(2
)80
IIIG
CS
�8
Surg
ery
and
nons
urgi
cal
GO
Sat
2m
oPr
ospe
ctiv
est
udy
onno
nope
rativ
em
anag
emen
tof
patie
nts
with
EDH
.Pa
tient
sw
itha
EDH
volu
me
�30
ml,
thic
knes
s�
2cm
,G
CS
�8,
none
urol
ogic
alde
ficit,
and
adm
itted
with
in24
hof
TBI
wer
etr
eate
dno
nope
rativ
ely.
Of
80pa
tient
sw
how
ere
trea
ted
nono
pera
tivel
y,5
dete
rior
ated
and
need
edsu
rger
y.O
nedi
ed,
and
4ha
da
good
outc
ome.
Tem
pora
llo
beED
Hw
asre
late
dto
dela
yed
surg
ery.
Bri
colo
and
Pasu
t(3
)10
7III
All
GC
SA
llsu
rger
yG
OS
at6
mo
Neu
rolo
gica
lsi
gns
onad
mis
sion
No.
ofpa
tien
tsG
ood
outc
ome
(%)
Non
e17
100
One
dila
ted
pupi
l8
100
Hem
ipar
esis
only
2391
Hem
ipar
esis
and
one
dila
ted
pupi
l10
90
Dec
ortic
atio
n9
44
Dec
ereb
ratio
n4
25
Bot
hpu
pils
fixed
10
GC
Son
adm
issi
onN
o.of
pati
ents
GR
/MD
(%)
SD/V
S(%
)D
ead
(%)
3–4
425
2550
5–7
3278
139
8–1
571
973
0
Bul
lock
etal
.(4
)12
IIIG
CS
12–1
5N
onsu
rgic
alD
isch
arge
Ret
rosp
ectiv
ean
alys
isof
the
nono
pera
tive
trea
tmen
tof
12pa
tient
sw
ithED
H.
All
patie
nts
mad
ea
good
reco
very
.N
ote
mpo
ral
EDH
patie
nts
wer
ein
clud
ed,
and
basa
lci
ster
nsw
ere
open
oron
lypa
rtia
llyef
face
din
all
patie
nts.
MLS
was
�10
mm
inal
lpa
tient
s.M
ean
volu
me
ofth
eED
Hw
as26
.8cm
3 .
Che
net
al.
(5)
74III
GC
S�
12Su
rger
yan
dno
nsur
gica
lG
OS
at1
mo
Ret
rosp
ectiv
ean
alys
isof
111
of46
5pa
tient
sw
ithED
Hw
houn
derw
ent
initi
alno
nope
rativ
etr
eatm
ent.
All
nono
pera
tive
case
sha
da
GC
S�
12,
and
14pa
tient
sun
derw
ent
dela
yed
surg
ery
beca
use
ofne
urod
eter
iora
tion
orin
crea
sein
the
size
ofth
eED
H.
37pa
tient
sw
ere
excl
uded
beca
use
ofin
com
plet
eC
Tda
ta.
All
patie
nts
achi
eved
ago
odG
OS.
Patie
nts
requ
irin
gde
laye
dsu
rger
ypr
esen
ted
mor
efr
eque
ntly
with
anED
Hvo
lum
e�
30cm
3 ,cl
otth
ickn
ess
�15
mm
,or
MLS
�5
mm
onth
ein
itial
CT
scan
.
Ope
rati
vetr
eatm
ent
Non
oper
ativ
etr
eatm
ent
Pva
lue
No.
ofpa
tient
s14
97
Tem
pora
l/fr
onto
tem
pora
llo
catio
nof
EDH
42.8
%36
.6%
n.s.
EDH
�30
cm3
83
P�
0.00
1
MLS
�5
mm
1117
P�
0.00
1
EDH
�15
mm
thic
knes
s10
16P
�0.
01
(Tab
leco
ntin
ues)
ACUTE EPIDURAL HEMATOMAS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-13
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Coh
enet
al.
(6)
21III
GC
S�
8A
llsu
rger
yN
otdo
cum
ente
dPr
ospe
ctiv
eda
taco
llect
ion
on21
adul
tpa
tient
sad
mitt
eddu
ring
3yr
with
acut
eED
Han
dG
CS
�8,
who
unde
rwen
tsu
rger
y.10
patie
nts
deve
lope
dne
wan
isoc
oria
afte
rad
mis
sion
.O
nly
14pa
tient
sha
dC
Tsc
ans.
3pa
tient
sha
dem
erge
ncy
cran
ioto
my
with
out
radi
ogra
phic
stud
ies.
Ani
socr
iafo
rm
ore
than
70m
inw
asas
soci
ated
with
100%
mor
talit
y,an
dfo
rle
ssth
an70
min
with
GO
S4
and
5.
Tim
efr
oman
isoc
oria
tocr
anio
tom
yN
o.of
pati
ents
GR
/MD
(%)
Dea
d(%
)
�71
min
510
00
�89
min
50
100
Cuc
cini
ello
etal
.(9
)57
IIIG
CS
10–1
5N
onsu
rgic
alN
otdo
cum
ente
dR
etro
spec
tive
anal
ysis
ofa
case
seri
esof
57pa
tient
sou
tof
144
with
EDH
who
wer
em
anag
edno
nope
rativ
ely.
All
patie
nts
had
good
outc
ome.
Onl
yon
epa
tient
dem
onst
rate
dM
LSan
dm
axim
umhe
mat
oma
thic
knes
sw
asbe
twee
n6
and
12m
m.
Ham
ilton
and
Wal
lace
(12)
48III
All
GC
SSu
rger
yan
dno
nsur
gica
lD
isch
arge
Ret
rosp
ectiv
ean
alys
isof
patie
nts
who
unde
rwen
tsu
rgic
alan
dno
nope
rativ
etr
eatm
ent
for
EDH
.
Patie
nts
who
unde
rwen
tsu
rgic
altr
eatm
ent
had
low
erG
CS
scor
es,
mor
epu
pilla
ryab
norm
aliti
es,
larg
erED
H,
grea
ter
MLS
,an
dw
ere
mor
elik
ely
tosh
owun
cal
hern
iatio
non
CT.
Has
elsb
erge
ret
al.
(13)
60III
All
GC
SA
llsu
rger
yN
otdo
cum
ente
dA
revi
ewof
171
patie
nts
who
pres
ente
dw
ithei
ther
subd
ural
(111
patie
nts)
orep
idur
al(6
0pa
tient
s)he
mat
oma.
The
influ
ence
ofsu
rgic
altim
ing
onm
orta
lity
and
func
tiona
lre
cove
ryw
asan
alyz
ed.
Patie
nts
with
anac
ute
subd
ural
orep
idur
alhe
mat
oma
had
alo
wer
mor
talit
yan
dim
prov
edfu
nctio
nal
reco
very
whe
nop
erat
edon
�2
haf
ter
onse
tof
com
a.
Tim
efr
omco
ma
onse
tto
surg
ery
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS
(%)
D(%
)
�2
h18
6716
17
�2
h16
1331
56
Knu
ckey
etal
.(1
9)22
IIIA
llG
CS
Surg
ery
and
nons
urgi
cal
Not
docu
men
ted
Ret
rosp
ectiv
ean
alys
isof
22pa
tient
sof
all
age
grou
psw
how
ere
initi
ally
trea
ted
nono
pera
tivel
y.7
patie
nts
need
edsu
bseq
uent
cran
ioto
my.
Earl
yC
Tsc
an�
6h
afte
rtr
aum
aan
dcr
ania
lfr
actu
res
cros
sing
big
vess
els
orth
em
iddl
em
enin
geal
arte
ryw
ere
asso
ciat
edw
ithde
teri
orat
ion.
Initi
alG
CS,
age,
and
size
ofth
eED
Hw
ere
not.
Kud
ayet
al.
(20)
115
IIIA
llG
CS
All
surg
ery
GO
Sat
6m
oR
etro
spec
tive
anal
ysis
ofpr
ospe
ctiv
ely
colle
cted
data
on11
5pa
tient
sof
all
age
grou
psun
derg
oing
surg
ery
for
�sig
nsof
hern
iatio
n.�
GC
Sis
the
para
met
erco
rrel
atin
gm
ost
clos
ely
with
outc
ome.
The
pres
ence
ofa
cran
ial
frac
ture
and
“lon
g”in
terv
albe
twee
non
set
ofsy
mpt
oms
and
inte
rven
tion
also
affe
ctou
tcom
e.
Lee
etal
.(2
2)20
0III
All
GC
SA
llsu
rger
yG
OS
at1
yrA
retr
ospe
ctiv
est
udy
of20
0pa
tient
sw
ithep
idur
alhe
mat
omas
requ
irin
gop
erat
ion.
Ana
lysi
sof
fact
ors
lead
ing
toa
poor
outc
ome.
Func
tiona
lou
tcom
eco
rrel
ated
with
decr
ease
dle
ngth
ofhe
rnia
tion
time,
nopo
stur
ing,
norm
alpu
pils
,an
da
high
GC
Ssc
ore.
Unf
avor
able
radi
olog
ical
sign
sw
ere
asso
ciat
edbr
ain
inju
ry,
MLS
�1
cm,
oblit
erat
edba
sal
cist
erns
,an
dsi
zean
dde
nsity
ofth
ebl
ood
clot
.
Inte
rval
betw
een
anis
ocor
iaan
dde
com
pres
sion
(h)
No.
ofpa
tien
tsSD
/VS/
D(%
)
No
126
7.9
�1.
518
22.2
1.5–
2.5
2725
.9
2.5–
3.5
1330
.8
3.5–
4.5
1353
.8
�4.
53
66.7
Hem
atom
avo
lum
e(m
l)N
o.of
pati
ents
SD/V
S/D
(%)
�50
816.
2
51–1
0081
14.8
101–
150
3138
.7
�15
07
71.4
MLS
(mm
)N
o.of
pati
ents
SD/V
S/D
(%)
�5
859.
4
6–1
069
8.7
11–1
535
37.1
�15
1163
.6
(Tab
leco
ntin
ues)
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-14 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Poon
and
Li(3
1)10
4III
All
GC
SA
llsu
rger
yG
OS
at6
mo
Apr
ospe
ctiv
est
udy
of10
4pa
tient
sof
all
age
grou
psw
ithis
olat
edED
H.
One
-thi
rdof
the
patie
nts
wer
etr
ansf
erre
dfr
oman
outs
ide
hosp
ital.
Asi
gnifi
cant
incr
ease
inm
orta
lity
and
mor
bidi
tyw
asre
late
dto
incr
ease
dtim
efr
omne
urol
ogic
alde
teri
orat
ion
tosu
rger
y.
No.
ofpa
tien
ts
Tim
ebe
twee
nde
teri
orat
ion
ofco
nsci
ous
leve
lan
dsu
rger
y(h
)
D(%
)V
S/SD
/MD
(%)
GR
(%)
710.
7�
14
1086
333.
2�
0.5
2427
49
Saka
set
al.
(33)
11III
“Com
atos
e”A
llsu
rger
yG
OS
at1
yrA
naly
sis
of40
seve
reTB
Ipa
tient
sw
houn
derw
ent
cran
ioto
my
afte
rde
velo
ping
bila
tera
lfix
edan
ddi
late
dpu
pils
.
Patie
nts
with
SDH
had
asi
gnifi
cant
incr
ease
inm
orta
lity
(64%
)co
mpa
red
with
thos
ew
ithED
H(1
8%).
Patie
nts
who
unde
rwen
tde
laye
d(�
3h)
surg
ery
had
aw
orse
outc
ome.
Tim
efr
ompu
pilla
ryno
nrea
ctiv
ity
tosu
rger
y
No.
ofpa
tien
tsG
R/M
D(%
)SD
(%)
VS/
D(%
)
�3
h20
3030
40
�3
h16
2512
63
Seel
iget
al.
(35)
51III
“Com
atos
e”A
llsu
rger
yG
OS
at3
mo–
2yr
Pros
pect
ive
mul
ticen
ter
data
base
anal
yzed
retr
ospe
ctiv
ely,
look
ing
atth
efa
ctor
sin
fluen
cing
outc
ome
afte
rsu
rger
yfo
rED
H.Th
em
ost
pow
erfu
lin
dica
tor
ofou
tcom
ew
asm
otor
scor
ebe
fore
surg
ery.
Mot
orsc
ore
No.
ofpa
tien
tsG
R/M
D/S
D(%
)V
S/D
(%)
1–3
1932
68
4–
632
6931
Serv
adei
etal
.(3
6)15
8III
GC
S14
/15
Surg
ery
and
nons
urgi
cal
GO
Sat
6m
oPr
ospe
ctiv
est
udy
of15
8co
nsec
utiv
epa
tient
sw
ithm
inor
TBI
(GC
S14
/15)
adm
itted
to3
neur
osur
gica
lun
its.
No
trea
tmen
tpr
otoc
olw
assp
ecifi
edan
da
logi
stic
regr
essi
onan
alys
isw
asco
nduc
ted
toid
entif
yth
efa
ctor
sle
adin
gto
surg
ery.
116
patie
nts
unde
rwen
tsu
rger
yan
d42
patie
nts
wer
em
anag
edno
nope
rativ
ely.
Of
all
fact
ors
anal
yzed
,on
lyth
ickn
ess
ofhe
mat
oma
and
MLS
wer
ere
late
dto
the
deci
sion
toop
erat
e.O
utco
me
was
the
sam
ein
both
grou
ps.
MLS
(mm
)N
o.of
pati
ents
Cra
niot
omy
(%)
Non
oper
ativ
em
anag
emen
t(%
)
0–5
130
7030
6–1
019
89.5
10.5
�10
810
00
van
den
Bri
nket
al.
(39)
98III
All
GC
SA
llsu
rger
yG
OS
at6
mo
Ret
rosp
ectiv
ean
alys
isof
CT
para
met
ers
and
outc
ome
in98
patie
nts
ofal
lag
egr
oups
with
acut
eED
H.
Vol
ume
ofth
eED
Hdi
dno
tco
rrel
ate
with
outc
ome.
Suba
rach
noid
bloo
dan
dpu
pilla
rydy
sfun
ctio
n,ag
e�
20yr
,an
dG
CS
onad
mis
sion
wer
epa
ram
eter
sco
rrel
atin
gw
ithou
tcom
e.
Age
(yr)
SD/V
S/D
(%)
�20
6
21–
4017
41–
6031
�60
50
Mot
orsc
ore
SD/V
S/D
(%)
1–3
50
4–
67
Pupi
lsSD
/VS/
D(%
)
Nor
mal
3
Uni
late
ral
fixed
and
dila
ted
35
Bila
tera
lfix
edan
ddi
late
d50
Wes
ter
(40)
83III
All
GC
SA
llsu
rger
yG
OS
at3
mo
Ret
rosp
ectiv
est
udy
ofth
em
anag
emen
tof
pure
EDH
inpa
tient
sof
all
age
grou
psin
Nor
way
.In
form
atio
non
thei
rin
itial
neur
olog
ical
exam
islim
ited.
The
outc
ome
of11
patie
nts
trea
ted
atth
epr
imar
yho
spita
lw
asw
orse
than
the
outc
ome
ofpa
tient
sth
atw
ere
adm
itted
dire
ctly
.Th
eau
thor
sco
nclu
deth
atpa
tient
ssh
ould
betr
ansf
erre
ddi
rect
lyfo
rne
uros
urgi
cal
man
agem
ent.
aG
CS,
Gla
sgow
Com
aSc
ale;
EDH
,ep
idur
alhe
mat
oma;
MLS
,m
idlin
esh
ift;
GO
S,G
lasg
owou
tcom
esc
ore;
TBI,
trau
mat
icbr
ain
inju
ry;
GR
,go
odre
cove
ry;
MD
,m
oder
ate
disa
bilit
y;SD
,se
vere
disa
bilit
y;V
S,ve
geta
tive
stat
e;D
,de
ath;
CT,
com
pute
dto
mog
raph
icsc
an;
n.s.
,no
tsi
gnifi
cant
.
ACUTE EPIDURAL HEMATOMAS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-15
CHAPTER 4
SURGICAL MANAGEMENT OF ACUTE
SUBDURAL HEMATOMASM. Ross Bullock, M.D., Ph.D.Department of Neurological Surgery,Virginia Commonwealth UniversityMedical Center,Richmond, Virginia
Randall Chesnut, M.D.Department of Neurological Surgery,University of WashingtonSchool of Medicine,Harborview Medical Center,Seattle, Washington
Jamshid Ghajar, M.D., Ph.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David Gordon, M.D.Department of Neurological Surgery,Montefiore Medical Center,Bronx, New York
Roger Hartl, M.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David W. Newell, M.D.Department of Neurological Surgery,Swedish Medical Center,Seattle, Washington
Franco Servadei, M.D.Department of Neurological Surgery,M. Bufalini Hospital,Cesena, Italy
Beverly C. Walters, M.D., M.Sc.Department of Neurological Surgery,New York UniversitySchool of Medicine,New York, New York
Jack E. Wilberger, M.D.Department of Neurological Surgery,Allegheny General Hospital,Pittsburgh, Pennsylvania
Reprints requests:Jamshid Ghajar, M.D., Ph.D.,Brain Trauma Foundation,523 East 72nd Street,New York, NY 10021.Email: [email protected]
RECOMMENDATIONS(see Methodology)
Indications for Surgery• An acute subdural hematoma (SDH) with a thickness greater than 10 mm or a midline
shift greater than 5 mm on computed tomographic (CT) scan should be surgicallyevacuated, regardless of the patient’s Glasgow Coma Scale (GCS) score.
• All patients with acute SDH in coma (GCS score less than 9) should undergo intracranialpressure (ICP) monitoring.
• A comatose patient (GCS score less than 9) with an SDH less than 10-mm thick and amidline shift less than 5 mm should undergo surgical evacuation of the lesion if the GCSscore decreased between the time of injury and hospital admission by 2 or more pointson the GCS and/or the patient presents with asymmetric or fixed and dilated pupilsand/or the ICP exceeds 20 mm Hg.
Timing• In patients with acute SDH and indications for surgery, surgical evacuation should be
performed as soon as possible.Methods• If surgical evacuation of an acute SDH in a comatose patient (GCS � 9) is indicated, it
should be performed using a craniotomy with or without bone flap removal andduraplasty.
KEY WORDS: Coma, Computed tomographic parameters, Craniotomy, Decompressive craniectomy, Headinjury, Hematoma, Intracranial pressure monitoring, Salvageability, Subdural, Surgical technique, Timing ofsurgery, Traumatic brain injury
Neurosurgery 58:S2-16-S2-24, 2006 DOI: 10.1227/01.NEU.0000210364.29290.C9 www.neurosurgery-online.com
OVERVIEW
SDH represents one type of intracranialmass lesion, and surgical management at-tempts to define the subset of patients whowould benefit from surgical evacuation of anacute SDH. SDH are diagnosed on a CT scanas extracranial, hyperdense, crescentic collec-tions between the dura and the brain paren-chyma. They can be divided into acute andchronic lesions. Herein, “acute SDH” is de-fined as an SDH diagnosed within 14 days oftraumatic brain injury (TBI).
Incidence
Studies conducted after the introduction ofCT scanning report an incidence of acute SDHbetween 12 and 29% in patients admitted with
severe TBI. Combining several publications,acute SDH was diagnosed in 21% of 2870 pa-tients (8, 26, 27, 36). When including mild, mod-erate, and severe head injuries, 11% (360 of 3397patients) present with SDH (21, 28). The meanage for this combined group is between 31 and47 years, with the vast majority of patients beingmen (6, 11, 17, 21).
Mechanism
The mechanism of injury responsible for thedevelopment of an SDH differs between agegroups. Most SDH are caused by motorvehicle-related accidents (MVA), falls, and as-saults. In one study, 56% of SDH in theyounger group (18–40 yr) were caused byMVA and only 12% were caused by falls,whereas, in the older groups (�65 yr), these
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mechanisms were responsible for 22% and 56% of SDH, re-spectively (15). Falls have been identified as the main cause oftraumatic SDH in two studies looking specifically at patientsolder than 75 and 80 years (3, 16). Studies with comatosepatients describe MVA as the mechanism of injury in 53 to75% of SDH. This indicates that MVA causes more severeinjury, possibly because of high-velocity accidents and diffuseaxonal injury (18, 26, 36).
Clinical Presentation
Between 37 and 80% of patients with acute SDH presentwith initial GCS scores of 8 or less (4, 6, 21, 28, 33). A lucidinterval has been described in 12 to 38% of patients beforeadmission but there is no conclusive evidence that this corre-lates with outcome (1, 9, 31, 34, 36). The definition of lucidinterval is vague. Authors interpret the lucid interval differ-ently and analysis of its frequency requires documentationduring the prehospital phase. Pupillary abnormalities are ob-served in 30 to 50% of patients on admission or before surgery(6, 10, 28, 33).
Mortality
Studies looking at patients from all age groups with GCSscores between 3 and 15 with SDH requiring surgery quotemortality rates between 40 and 60% (10, 11, 13, 14, 17, 27, 39).Mortality among patients presenting to the hospital in comawith subsequent surgical evacuation is between 57 and 68% (7,12, 18, 20, 26, 36).
Associated Injuries
Only 30 to 40% of SDH requiring surgery are isolatedlesions (21, 28). In the majority of cases, the SDH is associatedwith other intracranial and extracranial injuries. Contusions andintracerebral hematomas are the most frequently associated in-tracranial abnormalities. Associated intracranial and extracraniallesions have been reported in larger series to occur in 47 to 57%of patients presenting with GCS scores between 3 and 15 (4, 11,15, 28) and in 65 to 82% of patients with GCS scores less than 10(18, 26). In patients with SDH, contusions and fractures arefrequent associated injuries (16, 19, 25, 31, 36, 37). An associatedsubarachnoid hemorrhage has been observed in 14 to 25% ofpatients with SDH (4, 28) and epidural hematomas are observedin 6 to 14% of patients (4, 28). Significant extracranial injuries areobserved in 18 to 51% of patients and the majority of these casesinclude facial fractures, extremity fractures, and thoracic andabdominal trauma (5, 6, 11, 28, 31). Because of the frequentassociation of SDH with parenchymal injury, surgical manage-ment decisions should take into consideration the recommenda-tions for both lesion types.
PROCESS
A MEDLINE computer search using the following key-words for the years 1975 to 2001 was performed: “traumaticbrain injury” or “head injury” and “subdural” or “intradural”
and “hematoma” or “hemorrhage.” The search was narrowedby including the keywords “surgical treatment” or “surgery”or “operation” or “craniotomy” or “craniectomy” or “cranios-tomy” or “burr holes” and excluding “chronic” and “spinal.”These searches combined yielded 161 articles. The referencelists of these publications were reviewed and an additional 18articles were selected for analysis. Case reports, publicationsin books, and publications regarding penetrating brain inju-ries, or spinal or chronic SDH were not included. Chronic SDHwas defined as an SDH occurring or diagnosed more than 14days after trauma. Articles were excluded if the diagnosis ofSDH was not based on CT scanning, or if subgroups of pa-tients who did not undergo CT scanning were not clearlyidentified. Publications with fewer than 10 patients or publi-cations that did not include information on outcome wereexcluded. Of these 179 articles, 21 were selected for analysis.
SCIENTIFIC FOUNDATION
Indications for Surgery
The decision to operate on an SDH is based on the patient’sGCS score, pupillary exam, comorbidities, CT findings, age, and,in delayed decisions, ICP. Neurological deterioration over time isalso an important factor influencing the decision to operate.Trauma patients presenting to the emergency room with alteredmental status, pupillary asymmetry, and abnormal flexion orextension are at high risk for either an SDH and/or an epiduralhematoma compressing the brain and brainstem.
CT Parameters
Many investigators have tried to define a relationship be-tween CT parameters, such as hematoma volume, clot thick-ness, midline shift (MLS), and patency of the basal cisterns,and outcome. Two studies using multivariate analysis to iden-tify factors affecting outcome from SDH found contradictoryresults. Howard et al. (15) reported on 67 patients, with GCSscores between 3 and 15, who were undergoing surgery, andfound a significant correlation between poor outcome and thevolume of the SDH and the MLS. The volume of the SDH, theMLS, and mortality were significantly greater in older pa-tients. van den Brink et al. (33) found no difference in hema-toma volumes, MLS or status of the basal cisterns when com-paring surgical patients, who had a GCS of 3 to 15, andfavorable versus unfavorable outcome. Zumkeller et al. (39)investigated CT scan parameters in 174 patients with SDH anda GCS between 3 and 15 undergoing surgery. The findingsrevealed a 10% mortality rate in patients with a clot thicknessof less than 10 mm, and a 90% mortality for patients with clotsthicker than 30 mm. For an MLS greater than 20 mm, therewas a steep increase in mortality. Both parameters correlatedwell with the Glasgow outcome score (GOS). In a mixed groupof patients treated with or without surgery, Servadei et al. (28)also found a correlation between outcome and clot thickness,MLS, and status of the basilar cisterns. Kotwica and Brzezinski(18) found a significant relationship between MLS and out-
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come in 200 patients with GCS scores lower than 10, who wereundergoing surgery for SDH. In summary, there seems to bea relationship between CT parameters and outcome, but it isdifficult to determine specific threshold values.
Surgical Versus Nonoperative Treatment of SDH
The decision for nonoperative versus surgical managementof SDH is influenced by the GCS score; CT parameters, such asMLS, SDH clot thickness and volume, and patency of the basalcisterns; and the salvageability of the patient (i.e., whether theprimary injury is so extensive that evacuation of the SDH willnot make a difference in outcome). On the basis of the re-viewed literature, a clot thickness greater than 10 mm or aMLS greater than 5 mm are suggested as critical parametersfor surgical evacuation of an acute SDH, regardless of theGCS.
Wong (37) tried to identify parameters that would predictthe failure of initial nonoperative management. No treatmentprotocol was defined. Six of 31 patients with GCS scoresbetween 6 and 15 who were initially treated without surgeryrequired a later craniotomy because of neurological deteriora-tion (performed within 3 d). The authors found that an MLSgreater than 5 mm in patients with a GCS score of lower than15 on the initial CT scan was significantly related to the failureof nonoperative treatment. Hematoma volume and thicknessof the hematoma were not predictive. Good outcome wasachieved in all patients.
Matthew et al. (22) reviewed the data on 23 patients withGCS scores between 13 and 15 who were initially treatednonoperatively. No criteria were defined for nonoperativemanagement. All patients had an isolated SDH and all wereobserved in the neurosurgical intensive care unit. Six patientsrequired delayed (mean, 14 d) evacuation of their SDH. Sig-nificant differences in clot thickness and hematoma volumewere found between the operative and the nonoperativegroups. In addition, all patients with an initial hematomathickness greater than 10 mm required surgery. Finally, Ser-vadei et al. (27) developed a protocol to select comatose pa-tients with SDH for nonoperative management. The criteriaused to select comatose patients for nonoperative treatmentwere clinical stability or improvement during the time frominjury to evaluation at the hospital, hematoma thickness lessthan 10 mm and MLS less than 5 mm on the initial CT scan,and ICP monitoring in the neurosurgical intensive care unit.Surgery was performed if the ICP exceeded 20 mm Hg. Fifteenof 65 comatose patients with SDH were treated nonopera-tively. Of these, two patients were identified that requireddelayed surgery based on increasing ICP and the developmentof intracerebral hematomas. Good outcome was achieved in23% of the patients in the surgery group and 67% of thepatients in the nonoperative group. The authors concludedthat nonoperative treatment can be safely used for a definedgroup of comatose patients with SDH.
Age and Salvageability
Increasing age is a strong independent factor in prognosisfrom severe TBI, with a significant increase in poor outcome inpatients older than 60 years of age (2). Among patients withacute SDH, there is also a tendency for older patients to havea poorer outcome, especially those patients presenting withlow GCS scores (3, 16, 18, 19, 36). In comatose patients withGCS scores less than 9 who underwent craniotomy for SDH,Wilberger et al. (36) found that age older than 65 years wasstatistically correlated with poorer outcome. In patients withGCS scores less than 10 undergoing surgery for SDH, Kotwicaand Brzezinski (18) found that there was a statistically signif-icant difference in 3-months outcome between younger pa-tients (18–30 yr of age, 25% mortality) and older patients (�50yr, 75% mortality). Three smaller studies looked specifically atpatients between 70 and 100 years of age with an admissionGCS (one study) or preoperative GCS (two studies) equal to orless than 9. The 49 patients from these three studies all under-went surgery. Forty-eight patients died and one had a pooroutcome (severely disabled or vegetative) (3, 16, 19). No pa-tient older than the age of 75 years who preoperatively wasextensor posturing, flaccid to pain, or had unilateral or bilat-eral fixed and dilated pupils made a good recovery (GOS, 3–5)(16). In 23 comatose patients aged 66 years and older whopresented with an acute SDH, Howard et al. (15) found that 17died and the others survived in a vegetative state or withsevere disabilities.
Functional outcomes in older patients with low GCS scoreshave also been reported. However, these articles did not doc-ument whether patients showed signs of cerebral herniation.Hatashita et al. (14) reported 9 deaths in 12 patients older than65 years who presented with GCS scores between 4 and 6 andunderwent surgery for SDH, as compared with 34% for thoseaged 19 to 40 years. Two older patients survived with a GOSof 4 or 5. In another publication, 1 of 28 comatose patientsolder than 65 years made a functional recovery after craniot-omy for SDH (36). Although some studies that included pa-tients with all GCS scores undergoing surgery for SDH founda relationship between age and outcome (15, 21, 28), otherauthors failed to describe such a relationship (13, 17, 26, 33,39). Three studies using multivariate analysis in patients op-erated on for SDH did not identify age as an independentpredictor of outcome (15, 26, 33). In summary, there is arelationship between poor outcome and age, low GCS, andsigns of herniation, but it is not possible to predict death onthe basis of old age and poor GCS with certainty.
Timing of Surgery
The time from injury to entering the operating room is oneof the few factors that can be affected by intervention. Unfor-tunately, the relationship between time from injury to opera-tion and outcome is difficult to study because patients who areoperated on soon after TBI tend to have more severe injuriesthan those who undergo delayed surgery. Therefore, outcomein patients operated on a short time after injury is frequently
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worse when compared with patients undergoing delayed sur-gery. Furthermore, time from TBI to surgery may not be asimportant as time from clinical deterioration or onset of cere-bral herniation to surgery. The literature supports the state-ment that the length of time from clinical deterioration tooperative treatment of an SDH is significantly related to out-come. Haselsberger et al. (13) studied the time interval fromonset of coma to surgery in 111 patients with SDH. Thirty-fourpatients were operated on within 2 hours after onset of coma.Of those patients, 47% died and 32% recovered with goodoutcome or moderate disability. However, 54 patients whounderwent surgery longer than 2 hours after the onset of comahad a mortality of 80% and only 4% had a favorable outcome.These differences were statistically significant.
Seelig et al. (26) studied the delay to surgery in 82 patientswith SDH who were all comatose on admission. They found a30% mortality rate in patients operated on within 4 hours afterinjury and a 90% mortality in patients who had surgery morethan 4 hours after injury. The mean time for evacuation was390 � 39 minutes in patients who died and 170 � 18 minutesin patients who made a functional recovery. Multivariate anal-ysis identified time to surgery as one of the factors determin-ing outcome from SDH. The weaknesses of this study are thata proportion of patients did not undergo CT scanning and thatSDH was diagnosed using air ventriculography. In comatosepatients undergoing surgery for SDH, Wilberger et al. (36)found that the time interval from TBI to surgery was 374 � 31minutes for patients who died and 280 � 26 minutes forpatients who made a functional recovery. Mortality in patientsundergoing surgery within 4 hours of injury was 59% versus69% in patients operated on after 4 hours. A statistically sig-nificant difference could only be found in patients who un-derwent surgery after 12 hours, in which case, mortality roseto 82%.
Sakas et al. (24) looked at outcome from surgery for intra-cerebral hematoma, epidural hematoma, and SDH in 40 pa-tients who developed bilateral pupillary abnormalities duringtheir hospital course. The authors found a significant relation-ship between the time from onset of bilateral pupillary abnor-malities and 6-months outcome. Patients who had surgerymore than 3 hours after herniation had a higher morbidity andmortality than those undergoing surgery earlier (mortality,63% versus 30%).
Most studies focusing on the time between injury and sur-gery did not find a correlation with outcome (15, 17, 18, 21, 28,32). Some investigators even reported that early surgery wasassociated with worse results than delayed surgery (6, 14, 29).As mentioned, this may be related to the fact that most inves-tigators do not control for other variables affecting outcome,such as prehospital hypotension, hypoxia, GCS score, andassociated intracranial lesions. In 82 patients undergoing sur-gery for SDH, Dent et al. (6) found that time to surgery of lessthan 4 hours was associated with a significantly lower rate offunctional outcome when compared with surgery delayed forlonger than 4 hours (24% versus 51%). Mortality was approx-imately 30% in both groups. The authors also found that
patients who underwent surgery within 4 hours were morelikely to have obliterated basal cisterns and showed a ten-dency for lower GCS scores and more associated intracranialinjuries, suggesting a more severe TBI.
The only large study with patients with low GCS scores(GCS � 10) that did not find a relationship between earlysurgery and better outcome was the study by Kotwica andBrzezinski (18). In that study, mortality was approximately60% in all patients, regardless of whether they had surgerywithin 4 hours or between 4 and 16 hours after TBI. A detailedanalysis reveals that although GCS scores were the same,almost 90% of patients undergoing early surgery had associ-ated intracranial lesions. Associated lesions were found in 78%and 64% of patients surviving the first 5 and 12 hours, respec-tively. This indicates that patients with early surgery hadmore severe injuries. In summary, there is evidence that pa-tients who undergo surgery within 2 to 4 hours after clinicaldeterioration have a better outcome than those who undergodelayed surgery.
Surgical Technique
Different surgical techniques have been advocated for theevacuation of an SDH. The most commonly used techniquesare:
• Twist drill trephination/craniostomy procedures.• Burr hole trephination.• Craniotomy with or without dural grafting.• Subtemporal decompressive craniectomy.• Large decompressive hemicraniectomy, with or without du-
ral grafting.
Most investigators do not specify the type of surgical treat-ment used for evacuation of the SDH and, if they do, theyusually do not address the effectiveness of the procedure.Except for two studies (14, 30) no papers were found lookingat the impact of procedure type on outcome. The choice ofoperative technique is influenced by the surgeon’s expertise,training, and evaluation of the particular situation. Some cen-ters treat all SDH with decompressive craniectomies (18, 23),whereas other centers used solely osteoplastic craniotomies(36). Most studies report a mixture of procedures dependingon the clinical and radiographic evaluation (13–15, 17, 38), orcombined approaches in the same patient, i.e., subtemporaldecompression plus subsequent craniotomy (26) or cranioto-mies with contralateral decompressive craniectomies in somechildren (31). One study evaluated decompressive hemicrani-ectomies for the treatment of selected patients with SDH (30).
Only two investigators addressed the effect of the operativetechnique on outcome from SDH. Hatashita et al. (14) lookedat 3-months GOS in 60 patients with GCS scores between 3and 15 admitted for SDH evacuation. All patients underwentsurgery. The authors performed 24 burr holes, 25 cranioto-mies, 8 craniotomies with dural grafting, and 3 decompressivecraniectomies. In patients with GCS scores between 4 and 6,the authors found a statistically significant increased mortality
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and reduced functional recovery rate in patients undergoingburr hole trephination versus craniotomy. Koc et al. (17) com-pared craniotomy, craniotomy with dural grafting, and de-compressive craniectomy in 113 patients with GCS scoresbetween 3 and 15 undergoing SDH evacuation. Seventeenpatients underwent decompressive craniectomy and all died.No other significant differences were found between treat-ment groups. The results of all of these studies have to beviewed with caution because groups undergoing differenttypes of surgical treatment were not comparable.
SUMMARY
In patients with an acute SDH, clot thickness or volume andthe MLS on the preoperative CT correlate with outcome. Instudies analyzing CT parameters that may be predictive fordelayed surgery in patients undergoing initial nonoperativemanagement, an MLS greater than 5 mm or a clot thicknessgreater than 10 mm on the initial CT scan emerged as signif-icant prognostic factors (see Appendices for measurement tech-niques). Therefore, patients with SDH presenting with a clotthickness greater than 10 mm or an MLS greater than 5 mmshould undergo surgical evacuation, regardless of their GCS.Patients who present in a coma (GCS � 9) but with an SDHwith a thickness less than 10 mm and an MLS less than 5 mmcan be treated nonoperatively, providing that they undergoICP monitoring, they are neurologically stable since the injury,they have no pupillary abnormalities, and they have no intra-cranial hypertension (ICP � 20 mm Hg). Because of the fre-quent association of SDH with parenchymal injury, surgicalmanagement decisions should take into consideration the rec-ommendations for both lesion types.
KEY ISSUES FOR FUTURE INVESTIGATION• Craniotomy versus decompressive craniectomy and dural
grafting for the initial evacuation of SDH. Effect of differentprehospital ambulance systems on timing of surgery andoutcome from SDH.
• Incidence and impact of prehospital hypotension and hyp-oxia on outcome from SDH.
• Identification of subgroups that do not benefit from surgery:older patients with low GCS scores, pupillary abnormalities,and associated intracerebral lesions.
• Prospective evaluation of the treatment option for comatosepatients (GCS � 9) presented above: does operating on allcomatose patients, regardless of their hematoma thicknessand MLS lead to a better outcome than following the treat-ment option presented above.
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16. Jamjoom A: Justification for evacuating acute subdural haematomas inpatients above the age of 75 years. Injury 23:518–520, 1992.
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TAB
LE1.
Surg
ical
man
agem
ent
ofac
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subd
ural
hem
atom
asa
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(ref
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tmen
tpr
otoc
olw
asno
tsp
ecifi
ed.
Adm
issi
onG
CS,
inju
ryse
veri
tysc
ore,
and
pupi
llary
reac
tivity
wer
ein
depe
nden
tpr
edic
tors
ofou
tcom
ein
the
entir
epa
tient
popu
latio
n.
<4
hfr
omTB
Ito
surg
ery
(%)
>4
h(%
)P
valu
e
GR
/MD
2451
0.02
SD/V
S48
19
D28
30n.
s.
Ope
nci
ster
ns5
190.
0004
Effa
ced
cist
erns
7653
0.00
2
GC
S7.
0po
ints
8.4
poin
tsn.
s.
Has
elsb
erge
ret
al.
(13)
111
IIIA
llG
CS
All
surg
ery
GO
Sat
9m
oA
retr
ospe
ctiv
ere
view
of17
1pa
tient
sw
hopr
esen
ted
with
eith
era
subd
ural
(111
patie
nts)
oran
epid
ural
(60
patie
nts)
hem
atom
a.Th
ein
fluen
ceof
surg
ical
timin
gw
asan
alyz
edin
rela
tion
tom
orta
lity
and
func
tiona
lre
cove
ry.
Patie
nts
with
anac
ute
subd
ural
orep
idur
alhe
mat
oma
had
alo
wer
mor
talit
yan
dim
prov
edfu
nctio
nal
reco
very
whe
nop
erat
edon
�2
haf
ter
onse
tof
com
a.
Tim
efr
omco
ma
onse
tto
surg
ery
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS
(%)
D(%
)
�2
h34
3221
47
�2
h55
416
80
Hat
ashi
taet
al.
(14)
60III
All
GC
SA
llsu
rger
yG
OS
at3
mo
Ret
rosp
ectiv
ean
alys
isof
60pa
tient
san
dth
ein
fluen
ceof
surg
ical
timin
gon
the
outc
ome
from
SDH
.
Patie
nts
oper
ated
onw
ithin
4h
ofin
jury
had
ahi
gher
mor
talit
yco
mpa
red
with
thos
eop
erat
edon
afte
r4
h.Pa
tient
sw
itha
GC
Sbe
twee
n4
and
6w
houn
derw
ent
acr
anio
tom
yha
da
sign
ifica
ntly
bette
rou
tcom
eco
mpa
red
with
thos
ew
how
ere
trea
ted
with
burr
hole
s.
GO
S<
4h
from
TBI
tosu
rger
y,n
�43
(%)
4–1
0h,
n�
17(%
)
GR
/MD
2641
D63
35
How
ard
etal
.(1
5)67
IIIA
llG
CS
All
surg
ery
GO
Sat
2m
oR
etro
spec
tive
anal
ysis
of2
age
grou
ps(1
8–
40yr
and
�65
yr)
ofpa
tient
sw
ithac
ute
SDH
.A
ge�
65yr
,si
zeof
the
hem
atom
a,an
dM
LSw
ere
rela
ted
toou
tcom
e,bu
tno
tin
depe
nden
tly.
Size
ofth
ehe
mat
oma
and
MLS
wer
egr
eate
rin
the
olde
rpa
tient
grou
p.M
orta
lity
inth
eol
der
patie
ntgr
oup
was
74%
,in
the
youn
ger
grou
p,it
was
18%
(P�
0.00
1).
Jam
joom
(16)
27III
All
GC
SA
llsu
rger
yG
OS
at6
mo
Are
view
of27
patie
nts
aged
75yr
orol
der
who
requ
ired
oper
atio
nfo
ran
acut
eSD
H.
No
patie
ntol
der
than
75yr
who
preo
pera
tivel
yw
asex
tens
orpo
stur
ing,
flacc
idto
pain
,or
had
unila
tera
lor
bila
tera
lfix
edan
ddi
late
dpu
pils
mad
ea
good
reco
very
(GO
S3–
5).
Evac
uatio
nof
acut
esu
bdur
alhe
mat
oma
isno
tre
com
men
ded
inth
issu
bgro
upof
patie
nts.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/V(%
)D
(%)
Preo
pera
tive
dete
rior
atio
nto
GC
S�
8
138
92
Pupi
lsre
activ
e15
2727
46
Uni
/bila
tera
lun
reac
tive
pupi
ls12
100
Adm
issi
onG
CS
�4
1921
1663
Adm
issi
onG
CS
�5
813
87
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-22 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Koc
etal
.(1
7)11
3III
All
GC
SA
llsu
rger
yG
OS
at3
mo
Rev
iew
of11
3co
nsec
utiv
epa
tient
sof
all
age
grou
psop
erat
edon
for
acut
eSD
H.
Preo
pera
tive
GC
San
dpu
pilla
ryex
amco
rrel
ated
with
func
tiona
lou
tcom
e.A
ssoc
iate
din
trac
ereb
ral
hem
atom
a,ce
rebr
alco
ntus
ion,
and
SAH
wer
eal
sore
late
dto
poor
erou
tcom
e.Ti
me
from
inju
ryto
surg
ery
did
not
affe
ctm
orta
lity.
No.
ofpa
tien
tsG
R(n
o.)
MD
(no.
)SD
(no.
)D
(no.
)
GC
S3–
437
235
b
GC
S5–
628
42
22b
GC
S7–
825
21
1125
GC
S9
–12
1110
1
GC
S13
–15
1211
1
Bila
tera
lpr
esen
tlig
htre
flex
6337
32
21
Uni
late
ral
abse
ntlig
htre
flex
111
19c
Bila
tera
lab
sent
light
refle
x39
138
c
b P�
0.05
,c P
�0.
01
Kot
wic
aan
dB
rzez
insk
i(1
8)20
0III
GC
S�
10A
llsu
rger
yG
OS
at3
mo
Ret
rosp
ectiv
ean
alys
isof
200
adul
tpa
tient
sw
houn
derw
ent
surg
ical
evac
uatio
nof
anac
ute
SDH
.
AG
CS
betw
een
3an
d6,
age
�50
yr,
and
MLS
�1.
5cm
wer
eas
soci
ated
with
poor
outc
ome.
Ther
ew
asno
diffe
renc
ein
outc
ome
betw
een
earl
y(le
ssth
an4
h)an
dla
tesu
rgic
alev
acua
tion.
No.
ofpa
tien
tsG
R(n
o.)
MD
(no.
)SD
(no.
)V
S(n
o.)
D(n
o.)
GC
S3–
616
629
625
799
GC
S7–
934
56
26
15
MLS
�1.
5cm
4115
26
216
MLS
1.5–
3cm
9618
612
1050
MLS
�3
cm63
14
91
4
Age
18–
40yr
7016
512
829
Age
50–
65yr
703
47
353
Kot
wic
aan
dJa
kubo
wsk
i(1
9)27
IIIA
llG
CS
All
surg
ery
Not
docu
men
ted
Ret
rosp
ectiv
ean
alys
isof
27pa
tient
s�
70yr
with
SDH
unde
rgoi
ngsu
rger
y.O
ldag
eis
asso
ciat
edw
itha
high
mor
talit
yfr
omSD
H.
All
17pa
tient
sw
itha
GC
S�
9di
ed.
Mas
saro
etal
.(2
1)12
7III
All
GC
SA
llsu
rger
yG
OS
at18
mo
Ret
rosp
ectiv
ean
alys
isof
127
patie
nts
unde
rgoi
ngsu
rger
yfo
rSD
H.
GC
Sis
the
mos
tim
port
ant
pred
icto
rof
outc
ome.
No.
ofpa
tien
tsG
R/M
D(%
)SD
(%)
D(%
)
GC
S�
128
100
GC
S9
–12
3534
2046
GC
S�
984
1121
68
Mat
hew
etal
.(2
2)23
IIIG
CS
13–1
5Su
rger
yan
dno
nsur
gica
lG
OS
at3–
8m
oR
etro
spec
tive
anal
ysis
of23
patie
nts
with
SDH
who
wer
ein
itial
lym
anag
edno
nope
rativ
ely.
6pa
tient
sun
derw
ent
dela
yed
surg
ery.
All
patie
nts
had
ago
odou
tcom
eat
3–8
mo.
All
patie
nts
with
acl
ot�
10m
mth
ick
onin
itial
CT
scan
requ
ired
surg
ery.
Saka
set
al.
(24)
22III
Com
atos
eA
llsu
rger
yG
OS
at1
yrA
naly
sis
of40
seve
reTB
Ipa
tient
sw
houn
derw
ent
cran
ioto
my
afte
rde
velo
ping
bila
tera
lfix
edan
ddi
late
dpu
pils
.
Patie
nts
with
SDH
had
asi
gnifi
cant
incr
ease
inm
orta
lity
(64%
)co
mpa
red
with
thos
ew
ithED
H(1
8%).
Patie
nts
who
unde
rwen
tde
laye
d(�
3h)
surg
ery
had
aw
orse
outc
ome.
Tim
efr
ompu
pilla
ryno
nrea
ctiv
ity
tosu
rger
y
No.
ofpa
tien
tsG
R/M
D(%
)SD
(%)
VS/
D(%
)
�3
h20
3030
40
�3
h16
2512
63
Serv
adei
etal
.(2
7)65
IIIG
CS
�9
Surg
ery
and
nons
urgi
cal
GO
Sat
6m
oR
etro
spec
tive
anal
ysis
ofco
mat
ose
patie
nts
with
SDH
who
wer
etr
eate
dno
nope
rativ
ely
acco
rdin
gto
pred
efin
edcr
iteri
a.
15of
65co
mat
ose
patie
nts
with
SDH
wer
etr
eate
dno
nope
rativ
ely
and
2pa
tient
sre
quir
edde
laye
dsu
rger
ybe
caus
eof
incr
easi
ngIC
Pan
din
trac
ereb
ral
hem
atom
as.
The
auth
ors
conc
lude
dth
atno
nope
rativ
etr
eatm
ent
can
besa
fely
used
for
sele
cted
com
atos
epa
tient
sw
ithSD
H.
Serv
adei
etal
.(2
8)20
6III
All
GC
SSu
rger
yan
dno
nsur
gica
lG
OS
at6
mo
Pros
pect
ive
anal
ysis
of20
6pa
tient
sof
all
age
grou
pspr
esen
ting
with
anac
ute
SDH
ofat
leas
t5
mm
thic
knes
s.14
8pa
tient
sun
derw
ent
oper
ativ
etr
eatm
ent.
The
initi
alC
Tsc
anid
entif
ies
patie
nts
atri
skfo
run
favo
rabl
eou
tcom
e.H
emat
oma
thic
knes
s,M
LS,
stat
usof
basa
lci
ster
ns,
and
pres
ence
ofSA
Hin
all
patie
nts
(sur
gica
lan
dno
nsur
gica
l)ar
ere
late
dto
outc
ome.
Shig
emor
iet
al.
(30)
15III
GC
S�
9A
llsu
rger
yG
OS
at6
mo
Ret
rosp
ectiv
ean
alys
isof
15pa
tient
sw
ithSD
Hun
derg
oing
deco
mpr
essi
vehe
mic
rani
ecto
my
beca
use
ofra
pid
neur
olog
ical
dete
rior
atio
n.
10pa
tient
sdi
edan
d2
patie
nts
mad
ea
good
reco
very
.G
ood
reco
very
was
only
seen
inpa
tient
sw
ithlo
wpo
stop
erat
ive
ICP.
The
patie
nts
who
mad
ea
good
reco
very
wer
ebo
th9
yrol
d.
ACUTE SUBDURAL HEMATOMAS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-23
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Uza
net
al.
(32)
18III
Com
atos
eA
llsu
rger
yG
OS
at6
mo
Pros
pect
ive
stud
yof
71pa
tient
sw
ithED
H,
SDH
,an
din
trac
ereb
ral
hem
orrh
age,
ofal
lag
egr
oups
oper
ated
onfo
rsi
gns
ofun
cal
hern
iatio
n.
Tim
ing
ofsu
rger
ydi
dno
taf
fect
outc
ome.
GC
Sco
rrel
ated
with
GO
S.
van
den
Bri
nket
al.
(33)
91III
All
GC
SA
llsu
rger
yG
OS
at6
mo
Ret
rosp
ectiv
ean
alys
isof
the
CT
scan
para
met
ers
in91
patie
nts
with
acut
eSD
H.
Vol
ume
ofth
esu
bdur
albl
ood
did
not
corr
elat
ew
ithou
tcom
e.Su
bara
chno
idbl
ood
and
pupi
llary
dysf
unct
ion
wer
eth
eon
lysi
gnifi
cant
para
met
ers
corr
elat
ing
with
apo
orou
tcom
e.
SD/V
S/D
(%)
Bila
tera
lab
norm
alpu
pils
89
GC
Sm
otor
scor
e�
480
GC
Sm
otor
scor
e�
352
Wilb
erge
ret
al.
(35)
101
IIIG
CS
�9
All
surg
ery
GO
Saf
ter
18m
oR
etro
spec
tive
anal
ysis
of10
1co
mat
ose
patie
nts
ofal
lag
egr
oups
with
acut
eSD
H.
Asi
gnifi
cant
incr
ease
inm
orta
lity
was
asso
ciat
edw
ithG
CS
3or
4,ag
egr
eate
rth
an65
yr,
ICP
grea
ter
than
45m
mH
gan
dev
acua
tion
ofhe
mat
oma
�12
haf
ter
inju
ry.
No.
ofpa
tien
tsG
R/M
DD
Pva
lue
Tim
efr
omin
jury
toop
erat
ion
101
280
�26
min
374
�31
min
n.s.
Age
(yr)
No.
ofpa
tien
tsG
R/M
D(%
)D
(%)
Pva
lue
�35
3531
.454
.3n.
s.
35–5
021
23.8
61.9
n.s.
51–
6517
11.8
70.6
n.s.
6528
3.6
82.1
P�
0.01
GC
SN
o.of
pati
ents
%G
R/M
D%
DP
valu
e
319
590
P�
0.05
432
1076
P�
0.05
527
1862
n.s.
6–7
2344
51n.
s.
Won
g(3
7)31
IIIA
llG
CS
Surg
ery
and
nons
urgi
cal
GC
Sat
2w
kto
5yr
Ret
rosp
ectiv
ean
alys
isof
31ad
ult
patie
nts
(1ch
ild)
of30
0pa
tient
sw
ithSD
Hw
how
ere
initi
ally
trea
ted
nono
pera
tivel
y.6
patie
nts
requ
ired
dela
yed
surg
ery
for
neur
olog
ical
dete
rior
atio
n.N
odi
ffere
nce
was
foun
din
outc
ome.
MLS
�5
mm
(onl
yin
patie
nts
with
GC
S�
15)
and
thic
knes
sof
the
hem
atom
a�
10m
mon
the
initi
alC
Tsc
anar
esi
gnifi
cant
lyre
late
dto
the
failu
reof
nono
pera
tive
trea
tmen
t.H
emat
oma
volu
me
was
not
pred
ictiv
e.
Yan
aka
etal
.(3
8)17
0III
All
GC
SSu
rger
yan
dno
nsur
gica
lG
OS
at3
mo
Are
tros
pect
ive
stud
yon
170
patie
nts
ofal
lag
egr
oups
with
SDH
adm
itted
duri
ng7
yr,
trea
ted
eith
ersu
rgic
ally
orno
nsur
gica
lly.
Ast
rict
prot
ocol
was
follo
wed
and
patie
nts
with
MLS
�5
mm
unde
rwen
tsu
rger
y.
77pa
tient
sun
derw
ent
surg
ery.
Prog
nost
icin
dica
tors
ofou
tcom
efo
rth
ew
hole
grou
pof
patie
nts
wer
e:G
CS,
pupi
ls,
age,
hem
atom
asi
ze,
MLS
,cl
otth
ickn
ess,
asso
ciat
edco
ntus
ions
,SA
H,
stat
usof
basa
lci
ster
ns,
and
ICP.
Zum
kelle
ret
al.
(39)
174
IIIA
llG
CS
All
surg
ery
Post
oper
ativ
em
orta
lity
Ret
rosp
ectiv
ean
alys
isof
174
patie
nts
oper
ated
onfo
rac
ute
SDH
.SD
Hth
ickn
ess
ofle
ssth
an1
cmor
mid
line
shift
less
than
12m
mar
ew
ell
tole
rate
d,w
ithhi
ghsu
rviv
alra
tes.
Mor
talit
ycl
imbs
stee
ply
whe
nM
LSsu
rpas
ses
clot
thic
knes
s.
aG
CS,
Gla
sgow
Com
aSc
ale;
EDH
,epi
dura
lhem
atom
a;SD
H,s
ubdu
ralh
emat
oma;
GO
S,G
lasg
owou
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SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-24 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
CHAPTER 5
SURGICAL MANAGEMENT OF TRAUMATIC
PARENCHYMAL LESIONSM. Ross Bullock, M.D., Ph.D.Department of Neurological Surgery,Virginia Commonwealth UniversityMedical Center,Richmond, Virginia
Randall Chesnut, M.D.Department of Neurological Surgery,University of WashingtonSchool of Medicine,Harborview Medical Center,Seattle, Washington
Jamshid Ghajar, M.D., Ph.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David Gordon, M.D.Department of Neurological Surgery,Montefiore Medical Center,Bronx, New York
Roger Hartl, M.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David W. Newell, M.D.Department of Neurological Surgery,Swedish Medical Center,Seattle, Washington
Franco Servadei, M.D.Department of Neurological Surgery,M. Bufalini Hospital,Cesena, Italy
Beverly C. Walters, M.D., M.Sc.Department of Neurological Surgery,New York UniversitySchool of Medicine,New York, New York
Jack Wilberger, M.D.Department of Neurological Surgery,Allegheny General Hospital,Pittsburgh, Pennsylvania
Reprints requests:Jamshid Ghajar, M.D., Ph.D.,Brain Trauma Foundation,523 East 72nd Street,New York, NY 10021.Email: [email protected]
RECOMMENDATIONS(see Methodology)
Indications• Patients with parenchymal mass lesions and signs of progressive neurological
deterioration referable to the lesion, medically refractory intracranial hypertension,or signs of mass effect on computed tomographic (CT) scan should be treatedoperatively.
• Patients with Glasgow Coma Scale (GCS) scores of 6 to 8 with frontal or temporalcontusions greater than 20 cm3 in volume with midline shift of at least 5 mm and/orcisternal compression on CT scan, and patients with any lesion greater than 50 cm3
in volume should be treated operatively.• Patients with parenchymal mass lesions who do not show evidence for neurological
compromise, have controlled intracranial pressure (ICP), and no significant signs ofmass effect on CT scan may be managed nonoperatively with intensive monitoringand serial imaging.
Timing and Methods• Craniotomy with evacuation of mass lesion is recommended for those patients with
focal lesions and the surgical indications listed above, under Indications.• Bifrontal decompressive craniectomy within 48 hours of injury is a treatment option
for patients with diffuse, medically refractory posttraumatic cerebral edema andresultant intracranial hypertension.
• Decompressive procedures, including subtemporal decompression, temporal lo-bectomy, and hemispheric decompressive craniectomy, are treatment options forpatients with refractory intracranial hypertension and diffuse parenchymal injurywith clinical and radiographic evidence for impending transtentorial herniation.
KEY WORDS: Coma, Computed tomographic parameters, Craniotomy, Decompressive craniectomy, Headinjury, Herniation, Intracranial pressure monitoring, Parenchymal mass lesion, Surgical technique, Timingof surgery, Traumatic brain injury
Neurosurgery 58:S2-25-S2-46, 2006 DOI: 10.1227/01.NEU.0000210365.36914.E3 www.neurosurgery-online.com
OVERVIEW
Traumatic parenchymal mass lesions arecommon sequelae of traumatic brain injury(TBI), occurring in up to 8.2% of all TBI (37)and 13 to 35% of severe TBI, (6, 35, 44, 47, 57,58) and comprising as much as 20% of opera-tive intracranial lesions in representative se-ries (44, 68). Most small parenchymal lesionsdo not require surgical evacuation (18, 19, 57).However, the development of mass effect fromlarger lesions may result in secondary brain in-jury, placing the patient at risk of further neu-
rological deterioration, herniation, and death(6). Because parenchymal lesions tend to evolve,(36, 54, 55, 58) and because timing of surgerywith respect to the occurrence of neurologicaldeterioration clearly affects outcome (41), mucheffort has been directed at defining patients atrisk of progressive neurological compromise asa result of their traumatic injuries (6, 50). Beckeret al. (3) advocated early evacuation of traumaticintracranial hematomas and contusions for thepurpose of avoiding secondary complications.A selective approach was envisioned by Gall-braith and Teasdale (18), who stated, “if those
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who are going to deteriorate could be identified soon after thehematoma has been detected they could be operated on imme-diately without incurring the risks of delay, and the remainderwould be spared unnecessary operation.” The literature address-ing these issues in the CT era is reviewed here in an attempt todefine appropriate surgical indications, methods, and timing forthe patient with traumatic parenchymal injuries.
Although the majority of relevant data retrospectively ad-dresses prognostic variables, differential classification, andclinical course of parenchymal lesions, several studies attemptto assess the efficacy of surgical intervention in a retrospective,historically controlled fashion. Only one randomized, con-trolled trial has been published (61). In addition, the topics ofdelayed traumatic intracerebral hematoma (DTICH) and de-compressive operations for diffuse parenchymal injury andpersistent intracranial hypertension deserve specific consider-ation, and are also addressed here.
PROCESS
A MEDLINE computer search using the following keywords: “intracerebral” or “intraparenchymal” or “ICH” or“IPH and “hematoma” or “hematoma” or “hemorrhage” and“surgery” or “craniotomy” or “craniectomy” or “burr hole” or“craniostomy” and “trauma” or “traumatic” or “TBI” or“CHI” between 1975 and 2001 and limited to humans wasperformed. A total of 330 documents were found. An addi-tional search using the following key words: “brain” or “cor-tex” and “laceration” between 1975 and 2001 was performed,yielding 101 additional articles. This search was narrowed toinclude the following key words: “surgery” or “operative” or“craniotomy” or “craniectomy” or “decompressive craniec-tomy” or “repair” and “outcome,” yielding 49 articles. A thirdsearch using the following key words: “contusion” or “hem-orrhagic contusion” and “brain” and “surgery” or “craniot-omy” or “craniectomy” or “burr hole” or “craniostomy” wasperformed, yielding 174 articles. A fourth search, using thekey words “DTICH” or “DTIPH,” yielded 11 articles. A fifthsearch, using the key word “TICH,” yielded eight articles. Allfive searches were combined. Duplicates between searcheswere discarded. A total of 495 references resulted. In addition,the reference lists of selected articles were reviewed, and atotal of 51 articles were selected for critical analysis. Theresults of this analysis were incorporated into the reviewpresented here. Papers primarily addressing the followingtopics were not included: nontraumatic lesions (e.g., sponta-neous intraparenchymal hemorrhage or infarction), patientswith other associated nontraumatic lesions (e.g., tumors orarteriovenous malformations), posttraumatic aneurysms,chronic lesions, penetrating trauma, carotid-cavernous fistu-lae, patients undergoing anticoagulation therapy, patientswith associated illnesses (e.g., acquired immunodeficiencysyndrome; concomitant infection; hemophilia; thromboticthrombocytopenic purpura; or hemolysis, elevated liver en-zymes, and low platelet count), pregnant patients, birthtrauma, traumatic intraventricular hemorrhage, traumatic hy-
drocephalus, external ventricular drainage, sagittal sinus in-jury, pre-CT era reports, and book chapters. Papers with thefollowing characteristics were also excluded: case series withfewer than 10 patients evaluated by CT scan and with incom-plete outcome data (mortality or Glasgow outcome score[GOS]), case reports, operative series with operations occur-ring greater than 14 days from injury. Posterior fossa paren-chymal injuries are addressed in Surgical Management of Pos-terior Fossa Mass Lesions. Selected articles were evaluated fordesign, prognostic significance, therapeutic efficacy, and over-all outcome. In addition, several articles were reviewed for thepurposes of historical perspective.
SCIENTIFIC FOUNDATION
Traumatic Parenchymal Lesions
Traumatic parenchymal lesions are a heterogeneous group,and are traditionally divided into focal and nonfocal lesions.Focal lesions include intracerebral hematomas (ICH), DTICH,contusions, and infarctions. Nonfocal lesions include cerebraledema, hemispheric swelling, and diffuse injury. Althoughthese lesions often do not occur in isolation, their presence hasbeen shown to adversely affect prognosis (16, 44). Indeed,Fearnside et al. (16) prospectively collected data on 315 se-verely head-injured patients and found that “the model whichprovided the most accurate prediction of poor outcome in-cluded age, hypotension and three different CT characteristics:subarachnoid blood, ICH or intracerebral contusion (accuracy72.5%).” Parenchymal lesions have been further subclassifiedby multiple authors, and outcome has clearly been shown todiffer among lesion types (19, 35, 39–41, 44, 65). Marshall (39)demonstrated that CT-defined injury type was a highly sig-nificant independent predictor of mortality, even when ageand GCS motor score were included in the predictive model.Given the heterogeneity of the pathophysiology and prognos-tic significance of “parenchymal” lesions, the task of definingclear surgical indications and methods becomes difficult.
Prognostic Factors
Despite proven differences among lesion types, outcomewithin the broad category of “parenchymal” lesions correlateswith known prognostic variables of TBI in general (5). Theseinclude age (26, 44, 45, 56, 58, 66, 70), admission or postresus-citation GCS (6, 19, 23, 40, 44, 45, 49, 51, 58), presence of cranialfracture (56), presence of pupillary response/brainstem re-flexes (7, 44), respiratory insufficiency (8), ICP (6, 7, 23, 39, 44,50, 51), and the status of the basal cisterns (6, 41, 62) or thirdventricle (6, 41, 62) on CT scan. Moreover, other variables signif-icantly correlate with outcome. These include location of thelesion (2, 32, 50, 58), ICH volume (8, 63), GCS at time of follow-upCT (63), lowest recorded GCS (7), severity of surrounding edema(6), timing of surgery (41, 51, 53), occurrence of preoperativeneurological deterioration (41), and presence of acute hemi-spheric swelling or concomitant subdural hematoma (7, 35). Al-though their study included nontraumatic lesions, Andrews et al.
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(2) showed that patients with a temporal or temporoparietal ICHof 30 cm3 or greater, as defined by product of anteroposterior,mediolateral, and superoinferior diameters on CT scan, weresignificantly more likely to develop signs of brainstem compres-sion or tentorial herniation, implying that these patients shouldundergo early evacuation of the offending mass lesion. However,these prognostic variables alone do not define the patient whoshould undergo operative intervention.
Operative Indications
As stated above, in Overview, several studies have focusedon defining the patient at risk for subsequent neurologicaldeterioration, making the assumption that operative interven-tion for this patient will improve the likelihood of a morefavorable outcome. Predictors of failure of nonoperative man-agement (defined by subsequent neurological deteriorationand need for craniotomy) include lesion location (50), intra-cranial hypertension (6, 18, 50), presence of subarachnoidhemorrhage (41), cisternal effacement (41), lesion volume (41),and hypoxic events (41).
Bullock et al. (6) prospectively studied 85 patients with ICHwhose initial need for craniotomy was uncertain. These pa-tients underwent ICP monitoring in an attempt to better de-fine the need for surgical intervention. The authors then ret-rospectively reviewed the CT scans of those patients for whomICP monitoring failed to predict late deterioration and, thus,the need for ICH evacuation. With multiple linear regressionanalysis, they found the peak ICP to be the strongest predictorof outcome. However, ICP monitoring failed to predict latedeterioration or death secondary to high ICP in 5 of 30 patientswho did not undergo initial surgery. After critical analysis ofCT factors, they concluded that the decision to operate“should be based on a spectrum of clinical, CT scanning andICP findings”. CT and clinical predictors included cisternalstatus, edema severity, and admission GCS. Interestingly, theauthors found that the weight of each predictor depended onthe location of the ICH. For temporoparietal lesions, hema-toma size, degree of edema, GCS, basal cistern status, and ICPdata correlated with outcome. However, for frontal lesions,peak ICP alone was predictive of outcome. These findingsexpand on those reported by Gallbraith and Teasdale (18),who found that all patients with “intradural” lesions (includ-ing subdural hematoma, ICH, and “burst lobes”) and sus-tained ICP greater than 30 mm Hg, versus only one patientwith an ICP less than 20 mm Hg, required operative interven-tion, as defined by clinical deterioration or failure to improvein the setting of increased ICP.
Mathiesen et al. (41) reviewed data collected prospectively forthe Head Injury Trial-2 nimodipine trial on 218 TBI patients notobeying commands within 24 hours of injury. These authorsfound that the initial CT characteristics of presence of subarach-noid hemorrhage, presence of focal lesion with volume greaterthan 40 cm3, and compressed or absent cisterns were associatedwith neurological deterioration, defined as a fall in GCS by 2points or from 4 to 3, or as the development of pupillary dilation.
They also found that the incidence of secondary (greater than 5 dafter injury) deterioration was associated with the occurrence ofhypoxic events. The occurrence of neurological deterioration, inturn, was found to adversely affect outcome from craniotomy,suggesting that patients with factors strongly associated withneurological deterioration should be considered for early surgery(i.e., before the onset of neurological deterioration). The authorsdirectly demonstrated that a subgroup of patients with admis-sion GCS of at least 6 and focal lesion volume of at least 20 cm3
who underwent surgery without previous neurological deterio-ration had significantly better outcomes compared with thosewho either did not undergo surgery or who underwent surgeryafter deterioration. Furthermore, if a radiological sign of masseffect (i.e., compression or obliteration of the cisterns and/or amidline shift � 5 mm) was present, craniotomy significantlyimproved the outcome in this group. Craniotomy was also di-rectly shown to improve outcome in a small subgroup of patientswith admission GCS of at least 10, temporal contusions, and aradiological sign of mass effect (i.e., a midline shift and/or com-pression or obliteration of the basal cisterns. Additionally, pa-tients admitted with a GCS of at least 6 and a lesion volume of atleast 50 cm3 had better outcome with surgery before or immedi-ately after deterioration than without surgery or with delayedoperation.
Although the goal of identifying those patients who arelikely to deteriorate neurologically is paramount, the questionof whether surgery itself is beneficial remains unanswered.Few studies compare surgical outcome with matched, nonsur-gically managed controls. In a retrospective study of 21 pa-tients with frontal lobe contusions and medically intractableintracranial hypertension (�40 mm Hg), mortality was signif-icantly decreased in the surgical group compared with a non-surgical historical group (22% versus 88%, respectively) (28).These patients were matched for age, sex, GCS, and ICP levels,although statistics for these variables are not provided by theauthors. Choksey et al. (8) retrospectively reviewed 202 pa-tients with traumatic ICH and showed, with logistic regres-sion analysis, that craniotomy significantly improved theprobability of good outcome. Factors taken into considerationfor this analysis included low GCS and hematoma volumegreater than 16 cm3, each of which independently predictedpoor outcome in these patients. Several other studies examineoutcome relative to specific decompressive procedures, andare discussed in the surgical treatment section.
For the purposes of CT classification, Marshall (39) defineda �mass lesion� as a lesion of volume greater than 25 cm3. Theyshowed differential outcome between patients with evacuatedand nonevacuated mass lesions (23% versus 11% favorableoutcome, respectively) in a series of 746 severe TBI patients(i.e., after resuscitation, GCS � 8). In contrast, a recent paperfrom the European Brain Injury Consortium (54) evaluating aseries of 724 TBI patients with a GCS of 3 to 12 showed a 45%rate of favorable results in evacuated mass lesions versus 42%in nonevacuated mass lesions using the same classificationsystem. Sample size between these two studies was noticeablydifferent: the former series included 276 patients with evacu-
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ated mass lesions and 36 with nonevacuated mass lesions,whereas the latter included 195 and 148 patients, respectively.These studies reviewed illustrate that a classification systembased solely on lesion volume is unable to consistently showthe relationship between surgery and outcome. Surgical indi-cations are, in fact, related to many factors, including CTparameters (i.e., volume, midline shift, and basal cistern com-pression), clinical status, and the occurrence of clinical deteri-oration, among others.
One fundamental problem in using initial CT parameters asindependent indications for surgery is that CT pathology hasclearly been shown to be a dynamic process. Using the TraumaticComa Data Bank classification system (39), Lobato et al. (36)showed that 51.2% of 587 severely injured patients (GCS � 8)developed significant changes between initial and “control” CTscans, the latter of which more accurately predicted outcome.Similarly, Servadei et al. (54) showed that 16% of moderately-to-severely injured patients (GCS of 3–12) with diffuse injuryshowed radiological progression across Traumatic Coma DataBank classes. Yamaki et al. (69) showed that only 56% of ICHgreater than 3 cm in diameter developed within 6 hours of injury,and that only 84% of ICH reached maximal size within 12 hours.These studies highlight the dynamic nature of parenchymal in-juries and the dangers inherent in placing too much emphasis ona single, static CT scan for management decisions.
The data reviewed shows that there are subpopulations ofpatients with traumatic intraparenchymal lesions that willbenefit from surgical intervention. However, the precise char-acteristics of these subpopulations are not, as yet, clearly de-fined. The literature supports taking into account an amalgamof clinical and radiographic criteria, including GCS, location,volume, CT appearance, ICP, and the presence of neurologicaldeterioration, to make an informed decision to subject a pa-tient with a parenchymal lesion to a craniotomy. It seems thatall factors must be taken into consideration to best define thepatient population that will benefit from surgery.
DTICH
ICH have been shown to evolve over time (55, 58, 69). Theentity of DTICH was initially described by Bollinger in 1891(4), and is now defined by most authors as occurring in areasof radiographically normal brain in patients with otherwiseabnormal initial CT scans (20, 22, 59, 63). It is defined byGentleman et al. (20) as a �lesion of increased attenuationdeveloping after admission to hospital, in a part of the brainwhich the admission CT scan had suggested was normal”.Other authors, however, have noted DTICH to occur in areasof contusion on initial, high-resolution CT scan (72). The inci-dence of DTICH ranges from 3.3 to 7.4% in patients withmoderate-to-severe TBI (15, 20, 22, 29, 59, 63). EvacuatedDTICH represent approximately 1.6% of all evacuated trau-matic ICH (20), and mortality ranges from 16 to 72% (15, 20,22, 59, 63) Therefore, the importance of careful monitoring andof serial CT scanning cannot be overemphasized (55, 63, 72).
In a retrospective review of 32 patients with DTICH, Tseng(63) found that greater lesion volume, cisternal compression,earlier timing of appearance, occurrence of clinical deteriora-tion, and lower GCS at time of a second, follow-up CT ad-versely affected outcome. Mortality occurred only with clini-cal presentation of DTICH within 48 hours of injury. In thissmall series, no patient with DTICH requiring craniotomypresented after 72 hours of injury. Sprick et al. (59) similarlyfound that approximately 70% of clinically significant DTICHpresented within 48 hours of injury. Additionally, DTICH hasbeen shown to be significantly associated with an increasedincidence of secondary, systemic insults (22), an increasedincidence after decompressive surgery for other mass lesions(22), and an increased incidence of abnormal clotting param-eters (29), suggesting a complex etiology for this lesion beyondthe mechanical disruption of the parenchyma (22, 27).
Although DTICH is most likely a distinct pathophysiologi-cal entity, it is still a parenchymal lesion from which manypatients either fail to recover or clinically deteriorate. Thefindings of Mathiesen et al. (41) indicate that patients withintracerebral lesions undergoing surgery before neurologicaldeterioration have improved outcomes. It follows logicallythat a subset of DTICH patients would benefit from rapidsurgical intervention after discovery of the lesion. However noCT-era studies have critically examined surgical outcome. Be-cause the majority of studies show that all patients who de-velop clinically relevant DTICH have abnormal initial CTscans (20, 63, 72), it is essential that patients with initiallyabnormal scans undergo intensive monitoring and serial im-aging to ensure rapid intervention, if necessary.
Surgical Methods
The standard surgical treatment of focal lesions, such asintracerebral hemorrhages or contusions, is craniotomy withevacuation of the lesion. Location of the lesion and proximityto critical structures are considerations when contemplatingthe choice of surgical options. Evacuation of traumatic masslesions is often effective in amelioration of brain shift andreduction of ICP, and can decrease the requirement for inten-sive medical treatment. Other methods, such as stereotacticevacuation of focal mass lesions, have also been used, al-though much less commonly (12). These procedures, however,become less effective when the patient’s intracranial pathol-ogy is diffuse and involves intracranial hypertension as aresult of posttraumatic edema or hemispheric swelling—fac-tors known to be associated with poor outcome (6, 19, 35, 38,44, 51). Even with focal ICH, a significant proportion of pa-tients have medically intractable intracranial hypertension af-ter standard craniotomy, and these patients fare the worst (44).
Surgical Treatment of Intracranial Hypertension
Rationale
A variety of operations have been developed for, or applied to,decompression of the brain at risk for the sequelae of traumati-
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cally elevated ICP. These include Cushing’s subtemporal decom-pression (13), temporal lobectomy (34, 48), manual reduction ofthe temporal lobe (64), circumferential craniotomy (9), and themore widely used hemispheric decompressive craniectomy (52)and bifrontal decompressive craniectomy (30). The rationale forsuch an approach is supported from a physiological perspectiveby both human and animal studies. Particular attention has beendirected at the study of changes in ICP and CT scan features,such as cisternal effacement and midline shift, after decompres-sion, with the goal of correlating significant postoperative reduc-tion of these parameters with improved outcome.
Hatashita and Hoff (25) showed that decompressive fronto-parietal craniectomy in cats led to significant reduction in ICP,reduction in cortical gray and white matter tissue pressure, in-creased pressure-volume index, and increased tissue compliance.The authors found that craniectomy significantly increased thevolumetric compensatory capacity of the intracranial cavity, afinding consistent with those of Hase et al. (24), in which ven-tricular catheter ICP measurements in 47 severe TBI patients, 33of whom underwent external decompression, documented a dra-matic increase in intracranial compliance after decompression.Yoo et al. (71) studied intraoperative ventricular pressures in acohort of 20 patients with refractory intracranial hypertensionafter both traumatic and nontraumatic insults who underwentbilateral frontotemporoparietal decompressive craniectomy withdural expansion and grafting. These authors found a 50.2 �16.6% reduction of initial ICP after craniectomy, and a furtherreduction to 15.7 � 10.7% of initial ICP after dural opening.
Polin et al. (51) showed a significant decrease in ICP afterbifrontal decompressive craniectomy, as well as a significantdifference in postoperative ICP when compared with ICPmeasured 48 to 72 hours after injury in a cohort of historicallymatched controls. Gower et al. (21) found that 7 of 10 patientswho underwent subtemporal decompression for medically re-fractory intracranial hypertension had an average decrease inICP of 34%. Kunze et al. (33) found a reduction in mean ICP from41.7 to 20.6 mm Hg in 28 patients after unilateral or bilateraldecompressive craniectomy for posttraumatic edema refractoryto maximal medical therapy. And Whitfield et al. (67) demon-strated a significant reduction of ICP from 37.5 to 18.1 mm Hg (P� 0.003) in 26 patients who underwent bifrontal decompressivecraniectomy for refractory intracranial hypertension managedusing a standardized ICP/cerebral perfusion pressure (CPP)treatment algorithm. The amplitude of the ICP waveform and ofslow waves were significantly reduced, and compensatory re-serve was significantly increased postoperatively in a subgroupof eight patients in this study. Munch et al. (45), however, failedto show a significant postoperative reduction in ICP or increasein CPP after unilateral hemispheric decompression. From a ra-diological perspective, however, this group found a significantimprovement in the visibility of mesencephalic cisterns and asignificant decrease in midline shift after decompressive craniec-tomy—both known to correlate with improved outcome. Fur-thermore, the change in cistern visibility correlated with thedistance between the lower craniectomy border and cranial base.Additionally, Alexander et al. (1) found an average increase in
intracranial volume of 26 cm3 in an analysis of CT scans inpatients with traumatic and nontraumatic lesions undergoingsubtemporal decompression. In contrast, experimental evidencefrom Cooper et al. (10) supports the notion that decompressiveprocedures may aggravate cerebral edema formation, thus, re-sulting in increased secondary injury. Such studies may helpexplain why, despite laboratory success, actual improvement inpatient outcome has not been consistently demonstrated.
Procedures and Outcome
There are several studies that suggest an important role fordecompressive procedures in the management of parenchy-mal injury. In a retrospective review of 28 patients undergoingunilateral or bilateral decompressive craniectomy for posttrau-matic edema and intracranial hypertension refractory to headelevation, moderate hyperventilation, osmodiuretics, barbitu-rates, tromethamine, and cerebrospinal fluid drainage, 57% ofpatients had good outcome or moderate disability at 1 year.However, the authors excluded patients with “vast” primarylesions, hypoxia, ischemic infarction, brainstem injury, “central”herniation, and primary anisocoria, thus, biasing results towardfavorable recovery (33). Nussbaum et al. (48) showed that com-plete temporal lobectomy performed within 2 hours of the de-velopment of clinical signs of transtentorial herniation in 10patients with unilateral hemispheric swelling and a GCS of lessthan 7 resulted in 40% functional independence. All patientsdemonstrated displacement of the brainstem, compression of thecontralateral peduncle, and progressive obliteration of the para-sellar and interpeduncular cisterns on CT scan, along with fixedpupillary dilation, and therefore, represent a particularly com-promised patient population.
Guerra et al. (23) prospectively performed decompressivecraniectomy following a standardized treatment protocol withstandardized surgical technique for posttraumatic diffusebrain swelling in 57 severe TBI patients (GCS, 4–6). Thirty-nine of these patients underwent primary decompression, and18 others underwent secondary decompression because ofpersistent intracranial hypertension after evacuation of a sur-gical mass lesion. Intracranial hypertension in these patientswas refractory to a standardized medical protocol that in-cluded hemodynamic stabilization, head elevation, sedationwith or without muscle relaxation, controlled hyperventilationto an arterial carbon dioxide pressure of 28 to 32 mm Hg,mannitol, tromethamine for acute rises in ICP, and electroen-cephalogram burst suppression with barbiturates. Fifty-eightpercent of the first group and 65% of the second group expe-rienced good outcome or moderate disability at 1 year. Theseresults compare favorably with published outcomes of alter-native second-tier therapy. However, a direct comparisonwith matched nonsurgical controls was not performed. Whit-field et al. (67) demonstrated a favorable outcome (GOS, 4–5)in 61% of a severe TBI population that underwent bifrontaldecompressive craniectomy for ICP greater than 30 mm Hgwith CPP less than 70 mm Hg, or for ICP greater than 35 mmHg, irrespective of CPP, despite a medical management pro-
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tocol that involved head elevation, propofol sedation, manni-tol and/or hypertonic saline, normocarbia, mild hypothermiato 33°C to 35°C, and electroencephalogram burst suppression.Only 55% of eligible patients, however, underwent craniec-tomy, and the reasons for nonsurgical management despiteeligibility were not documented or discussed.
Munch et al. (45) were able to show a significant differencein outcome between patients undergoing rapid decompressivecraniectomy and those undergoing delayed decompressivecraniectomy. However, the nature of the lesions differed be-tween the two groups, and, thus, the outcomes cannot bemeaningfully compared. Tseng (64) noted that the addition ofgentle elevation of the temporal lobe until the tentorium wasvisualized and CSF egress was noted decreased mortality andimproved the incidence of good outcome when comparedwith a standard craniotomy with hematoma evacuation andcontusion resection in a series of 32 severe TBI patients withanisocoria, hemiparesis, and CT evidence for uncal herniation.However, no statistical analysis was performed, and the au-thor notes that preoperative selection was biased and thatoperative timing and intraoperative judgements may haveinfluenced the choice of surgical procedure. Gower et al. (21)retrospectively studied 115 patients with admission GCS of 8or less who had adequate ICP monitoring data and no oper-ative mass lesion on admission. These patients were managedunder a standard treatment protocol. Outcome was comparedbetween 10 patients who underwent subtemporal decompres-sion and 17 patients managed by induction of pentobarbitalcoma. They found that subtemporal decompression affordedsignificantly lower mortality than pentobarbital coma, despitethe fact that the surgical group had a lower (but not statisti-cally significant) average admission GCS. However, 10 of thepatients treated medically had been determined not to beoperative candidates and subsequently died, greatly biasingresults in favor of the operative group. In a retrospectivereview of 29 patients undergoing operation for a combinationof acute subdural hematoma and severe contusion and swell-ing of the temporal lobe with uncal herniation, Lee et al. (34)documented a significant improvement in outcome with theaddition of temporal lobectomy to subtemporal decompres-sion and debridement of contused brain. Mortality decreasedfrom 56% to 8%, with a concomitant increase in average GOSfrom 2.2. to 4.0. These two surgical groups did not differ withrespect to preoperative GCS, age, or sex. However, patientswith intraoperative “overswelling,” defined as herniation ofbrain more than 2 cm above the craniectomy window, wereexcluded and underwent decompressive craniectomy withdural expansion, thus, potentially biasing these results.
Coplin et al. (11) retrospectively reviewed 29 consecutivepatients with GCS of at most 9 and CT scans with a midlineshift greater than the volume of a surgically amenable lesion toevaluate the safety and feasibility of decompressive craniec-tomy with duraplasty versus traditional craniotomy as theinitial surgical procedure. No significant differences in age,gender, admission GCS, time to surgery, or serum ethanolconcentration existed between the two groups. Despite a sig-
nificantly lower GCS at time of surgery and significantlygreater percentage of Diffuse Injury III and IV injuries (39),there was no significant difference in mortality, GOS, acutehospital length of stay, functional independence measurescore on admission to a rehabilitation unit, change in func-tional independence measure score, or length of rehabilitationstay between craniectomy and craniotomy groups. Althoughthis study is subject to the biases inherent in a retrospective,uncontrolled design, it strongly supports the safety of decom-pressive craniectomy as a first-line surgical intervention asopposed to its traditional role as a salvage procedure.
The studies briefly outlined here support the potential use-fulness of decompressive procedures, but are clearly ham-pered by inherent biases.
The study by Polin et al. (51) deserves particular mention,because it offers more concrete evidence that a decompressiveprocedure may result in improved patient outcome. Theseauthors report a retrospective evaluation of outcome in 35patients undergoing bifrontal decompressive craniectomy forrefractory posttraumatic cerebral edema matched for age, ad-mission GCS, sex, and maximal ICP with historical controlsselected from the Traumatic Coma Data Bank. Only patientswith Diffuse Injury III (39) were eligible as controls. Highestpostoperative ICP less than 24 hours after surgery in cases wasmatched with highest ICP 48 to 72 hours after injury in con-trols. Preoperative ICP in cases was matched with highest ICPless than 48 hours after injury in controls. Several findings areparticularly relevant. In the operative group, surgery per-formed less than 48 hours after injury was significantly asso-ciated with favorable outcome when compared with surgeryperformed longer than 48 hours after injury (46% versus 0%,respectively). Medical management alone carried a 3.8 timesrelative risk of unfavorable outcome compared with decom-pressive craniectomy. Maximum benefit was achieved in pa-tients undergoing decompression within 48 hours of injuryand whose ICP elevations had not yet been sustained above 40mm Hg (60% favorable outcome versus 18% in matched con-trols). This study argues strongly in favor of bifrontal decom-pressive craniectomy for patients with medically refractoryposttraumatic cerebral edema and resultant intracranial hy-pertension not yet sustained above 40 mm Hg within 48 hoursof injury, but does not have contemporaneous controls (51).
Overall, the literature suggests, but does not prove, that de-compressive procedures may be the intervention of choice giventhe appropriate clinical context. A recent study by Taylor et al.(61) examined the use of early (median 19.2 h after injury) bitem-poral craniectomy in addition to intensive medical managementversus intensive medical management alone in 27 children withsustained intracranial hypertension in a prospective, random-ized, controlled fashion. Their results showed a trend towardsgreater improvement in ICP, less time required in the intensivecare unit, and improved outcome with surgical decompression.These trends, although promising, did not reach statistical sig-nificance. Additional prospective, controlled studies are, thus,needed to strengthen the argument for the use of surgical de-
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
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compression in the management of intracranial hypertensionand refractory cerebral edema.
SUMMARY
The majority of studies regarding surgical treatment ofparenchymal lesions are case series. Only one prospectiveclinical trial of treatment using surgical versus nonsurgicalmanagement has been published (61). The majority of evi-dence indicates that the development of parenchymal masslesions, which are associated with progressive neurologicaldysfunction, medically refractory intracranial hypertension, orradiological signs of mass effect, are associated with a pooroutcome if treated nonsurgically. Specific surgical criteria,however, have not been firmly established.
Evidence also suggests that decompressive craniectomymay be the procedure of choice in patients with posttraumaticedema, hemispheric swelling, or diffuse injury, given the ap-propriate clinical context. This context has yet to be defined.
KEY ISSUES FOR FUTURE INVESTIGATION
The majority of studies on traumatic parenchymal lesions isobservational, and the studies offer no means to meaningfullycompare outcome between surgical and nonsurgical groups.Those studies that attempt this comparison fail to adequatelycontrol for known prognostic variables between surgicallyand nonsurgically managed groups in a prospective fashion.Prospective, controlled trials, such as that of Taylor et al. (61)need to be pursued and supported to define appropriate clin-ical criteria and surgical methods.
Additionally, the data of Coplin et al. (11) and Taylor et al.(61) strongly support the feasibility of performing trials ofdecompressive operations in the first instance, as opposed to asecond- or third-tier therapy for posttraumatic intracranialhypertension.
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TRAUMATIC PARENCHYMAL LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-33
TAB
LE1.
Surg
ical
Man
agem
ent
ofTr
aum
atic
Pare
nchy
mal
Lesi
onsa
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Bul
lock
etal
.(6
)85
IIIM
ean
GC
S9
Non
surg
ical
GO
S3
mo
Pros
pect
ive
stud
yof
85pa
tient
sw
ithIC
Hw
ithun
cert
aint
yre
gard
ing
need
for
imm
edia
tecr
anio
tom
y.Th
ese
patie
nts
wer
ese
lect
edfo
rIC
Pm
onito
ring
inan
atte
mpt
tobe
tter
defin
ene
edfo
rcr
anio
tom
y.A
retr
ospe
ctiv
ean
alys
isof
CT
scan
char
acte
rist
ics
was
then
perf
orm
edfo
rth
ose
patie
nts
for
who
mIC
Pm
onito
ring
did
not
pred
ict
late
dete
rior
atio
nto
crea
tea
bette
rpr
edic
tive
mod
elof
thos
ein
need
ofIC
Hev
acua
tion.
●M
anag
emen
t�s
houl
dbe
base
don
asp
ectr
umof
clin
ical
,C
Tsc
anni
ng,
and
ICP
findi
ngs.
�●
Peak
ICP
was
the
stro
nges
tpr
edic
tor
ofou
tcom
e,bu
tfa
iled
topr
edic
tla
tede
teri
orat
ion
orde
ath
in16
.7%
.●
For
tem
pora
l/par
ieta
lle
sion
s,he
mat
oma
size
,de
gree
ofed
ema,
GC
S,ba
sal
cist
ern
stat
us,
and
peak
ICP
corr
elat
edw
ithou
tcom
e;fo
rfr
onta
lle
sion
s,pe
akIC
Pal
one
pred
icte
dou
tcom
e.●
Prem
esen
ceph
alic
cist
ern
stat
usfa
lsel
ypr
edic
ted
low
ICP
inon
ly2.
3%of
patie
nts
with
elev
ated
ICP
(fals
ene
gativ
e).
●A
utho
rsco
nclu
de:
1)B
asal
cist
ern
effa
cem
ent
onin
itial
CT
scan
isin
dica
tion
for
surg
ery,
rega
rdle
ssof
GC
S. 2)Ex
tens
ive
surr
ound
ing
edem
ash
ould
prom
ptIC
Pm
onito
ring
orse
rial
CT
scan
ning
.If
cist
erns
are
effa
ced,
evac
uatio
nsh
ould
beco
nsid
ered
.
3)IC
Pm
onito
ring
shou
ldbe
carr
ied
out
inpa
tient
sin
com
a.
No.
ofpa
tien
tsG
R/m
inim
aldi
sabi
lity
(%)
MD
(%)
VS/
D(%
)
Surg
ery
5547
2033
No
initi
alsu
rger
y30
4723
30
Car
oli
etal
.(7
)36
IIIA
vera
geG
CS
9.3
Surg
ery
and
nons
urgi
cal
GO
S6
mo
Ret
rosp
ectiv
ere
view
of95
patie
nts
with
mul
tiple
trau
mat
icin
trac
rani
alle
sion
sto
iden
tify
clin
ical
fact
ors
and
radi
olog
icpr
edic
tors
ofpr
ogno
sis
toes
tabl
ish
man
agem
ent
crite
ria.
Patie
nts
wer
edi
vide
din
to3
grou
psba
sed
onpr
edom
inan
tle
sion
type
;36
patie
nts
with
pure
ICH
asth
epr
edom
inan
tle
sion
wer
ein
clud
edin
this
anal
ysis
.Pa
tient
sw
ithpa
renc
hym
alle
sion
s�
2cm
wer
eex
clud
edby
the
auth
ors.
●C
iste
rns
(P�
0.01
),sh
ift(P
�0.
05),
prol
onge
din
crea
sed
ICP
(P�
0.00
01)
diffe
red
sign
ifica
ntly
betw
een
surg
ical
and
nons
urgi
cal
grou
ps.
●80
.6%
neur
olog
ical
lyw
orse
ned
with
in12
–24
hof
initi
alas
sess
men
t.●
44.4
%in
cide
nce
ofD
TIC
H.
●Ty
peof
lesi
on(S
DH
�IC
H),
low
est
reco
rded
GC
S,pr
esen
ceof
prol
onge
din
crea
sed
ICP,
abse
nce
ofpu
pilla
ryre
flexe
sw
ere
sign
ifica
ntpr
edic
tors
ofba
dou
tcom
e(V
S/D
)ba
sed
onm
ultip
lere
gres
sion
anal
ysis
.●
Dec
ompr
essi
vecr
anie
ctom
yw
asa
“use
ful
mea
nsof
cont
rolli
ngin
trac
rani
alpr
essu
rein
19/2
2pa
tient
sun
derg
oing
proc
edur
e.”
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
ICH
3633
.338
.916
.70
11.1
Ope
rate
d13
.3
Non
oper
ated
219.
5
Cho
ksey
etal
.(8
)20
2III
All
GC
SSu
rger
yan
dno
nsur
gica
lG
OS
6m
oR
etro
spec
tive
stud
yof
202
patie
nts
with
trau
mat
icIC
Hto
asce
rtai
nfa
ctor
sin
fluen
cing
outc
ome.
●H
emat
oma
volu
me
�16
cm3
incr
ease
dpr
obab
ility
ofcl
inic
alde
teri
orat
ion.
●R
espi
rato
ryin
suffi
cien
cy,
low
GC
San
dhe
mat
oma
volu
me
�16
cm3
wer
esi
gnifi
cant
lyas
soci
ated
with
apo
orou
tcom
e.
●W
ithth
ese
fact
ors
take
nin
toco
nsid
erat
ion,
cran
ioto
my
sign
ifica
ntly
impr
oved
prob
abili
tyof
good
outc
ome.
●Lo
catio
nof
peri
pher
alhe
mat
omas
did
not
pred
ict
outc
ome.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
1H
emat
oma
169
5842
2H
emat
omas
1921
79
�3
Hem
atom
as14
010
0
Hyp
oxia
,re
spir
ator
yin
suffi
cien
cy35
2080
No
resp
irat
ory
insu
ffici
ency
167
5743
Evac
uatio
n84
6238
Non
evac
uatio
n11
842
58
Age
0–2
0yr
5629
71
Age
21–
40yr
5467
33
Age
41–
64yr
4468
32
Age
�65
yr48
4258
GC
S3–
711
231
69
GC
S8
–11
4562
38
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-34 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
GC
S12
–15
4587
13
Vol
ume
1–5
cm3
2681
19
Vol
ume
6–1
5cm
358
5743
Vol
ume
16–3
5cm
367
4654
Vol
ume
�36
cm3
5133
67
Neu
rolo
gica
lde
teri
orat
ion
135
4753
No
neur
olog
ical
dete
rior
atio
n49
8020
Initi
alG
CS
�4
200
100
Fron
tal
9348
52
Pari
etal
1250
50
Tem
pora
l63
6337
Occ
ipita
l9
6733
Cen
tral
2520
80
Cop
linet
al.
(11)
29III
GC
S3–
9D
ecom
pres
sive
cran
iect
omy
GO
Sat
disc
harg
e;FI
Mat
adm
issi
onan
ddi
scha
rge
from
reha
bilia
tion
Ret
rosp
ectiv
ere
view
of29
cons
ecut
ive
patie
nts
with
GC
S�
9an
dC
Tsc
ans
with
mid
line
shift
grea
ter
than
the
volu
me
ofa
surg
ical
lyam
enab
lele
sion
toev
alua
teth
esa
fety
and
feas
ibili
tyof
deco
mpr
essi
vecr
anie
ctom
yw
ithdu
rapl
asty
vers
ustr
aditi
onal
cran
ioto
my
asth
ein
itial
surg
ical
proc
edur
e.Ex
clus
ion
crite
ria
incl
uded
age
�16
yr,
inju
ry�
24h
befo
read
mis
sion
,D
iffus
eIn
jury
II(T
CD
Bcl
assi
ficat
ion)
,is
olat
edED
H,
pree
xist
ing
illne
sslim
iting
life
expe
ctan
cyto
�1
yrfr
omic
tus,
age
�40
yrw
ithex
tens
orpo
stur
ing,
and
bila
tera
lun
reac
tive
pupi
ls�
4m
min
diam
eter
.
●N
onsi
gnifi
cant
diffe
renc
ebe
twee
ncr
anio
tom
yan
dcr
anie
ctom
ygr
oups
with
rega
rds
toag
e(P
�0.
8),
gend
er(P
�1.
0),
adm
issi
onG
CS
scor
e(P
�0.
07),
time
tosu
rger
y(P
�1.
0),
seru
met
hano
lco
ncen
trat
ion
(P�
0.6)
.●
Cra
niec
tom
ygr
oup
had
sign
ifica
ntly
low
erG
CS
scor
eat
surg
ery
(P�
0.04
).●
Cra
niec
tom
ygr
oup
had
sign
ifica
ntly
mor
epa
tient
sw
ithD
iffus
eIn
jury
IIIan
dIV
(56%
vers
us9%
).●
No
sign
ifica
ntdi
ffere
nce
betw
een
grou
psw
ithre
spec
tto
mor
talit
y,G
OS,
acut
eho
spita
lle
ngth
ofst
ay,
initi
alFI
Msc
ore,
chan
gein
FIM
scor
e,or
leng
thof
reha
bilit
atio
nst
ay.
●D
espi
tesi
gnifi
cant
lylo
wer
GC
Sat
time
ofsu
rger
yan
dw
orse
inju
rycl
assi
ficat
ion
byC
Tsc
an,
deco
mpr
essi
vecr
anie
ctom
yw
ithdu
rapl
asty
affo
rded
equi
vale
ntou
tcom
eto
trad
ition
alcr
anio
tom
y,es
tabl
ishi
ngits
safe
tyan
dfe
asib
ility
asa
first
-lin
esu
rgic
alin
terv
entio
nas
oppo
sed
toits
trad
ition
alro
leas
a“s
alva
ge”
proc
edur
e.●
Aut
hors
emph
asiz
eim
port
ance
ofcr
anie
ctom
yex
tend
ing
dow
nto
the
floor
ofth
em
iddl
ecr
ania
lfo
ssa
atth
ero
otof
the
zygo
ma.
All
Cra
niot
omy
Cra
niec
tom
yP
valu
e
No.
ofpa
tient
s29
1712
Dis
char
geG
OS
44
40.
8
Mor
talit
y(%
)34
.541
.225
0.4
Hos
pita
lle
ngth
ofst
ay(d
)17
1818
0.4
Adm
issi
onFI
M63
6438
0.7
Dis
char
geFI
M90
9271
0.6
Cha
nge
inFI
M27
2723
1.0
Cor
addu
etal
.(1
2)37
IIIG
CS
3–5
to�
7St
ereo
tact
icev
acua
tion
Mor
talit
yat
disc
harg
eR
etro
spec
tive
seri
esof
37pa
tient
sw
ithtr
aum
atic
ICH
trea
ted
byst
ereo
tact
icev
acua
tion
thro
ugh
anen
larg
edbu
rrho
leto
eval
uate
outc
ome
usin
gth
iste
chni
que.
Surg
ical
indi
catio
nsin
clud
edco
ma,
dete
rior
atin
gco
nsci
ousn
ess,
orfo
cal
neur
olog
ical
defic
it.
●N
om
orta
lity
with
adm
issi
onG
CS
�7.
●A
dmis
sion
GC
Sre
late
din
vers
ely
tom
orta
lity
(no
stat
istic
s).
●Te
mpo
ral
loca
tion
had
high
erm
orta
lity
(no
stat
istic
s).
No.
ofpa
tien
tsD
(%)
ICH
,to
tal
3730
GC
S3–
510
80
GC
S6
–712
25
GC
S�
715
0
Fron
tal
185.
5
Tem
pora
l18
55
TRAUMATIC PARENCHYMAL LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-35
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
De
Luca
etal
.(1
4)22
IIIG
CS
3–12
Dec
ompr
essi
vecr
anie
ctom
yG
OS
atdi
scha
rge
Ret
rosp
ectiv
ere
view
of22
patie
nts
who
unde
rwen
tde
com
pres
sive
cran
iect
omy
for
cere
bral
edem
aw
ithre
frac
tory
intr
acra
nial
hype
rten
sion
orfo
r�i
mm
inen
the
rnia
tion�
duri
ngth
eev
acua
tion
ofa
spac
e-oc
cupy
ing
trau
mat
icle
sion
.Su
rgic
alm
etho
dsar
ede
scri
bed.
No.
ofpa
tien
tsG
R/M
D(%
)SD
(%)
VS
(%)
D(%
)
Dec
ompr
essi
vecr
anie
ctom
y22
4118
2318
Dia
zet
al.
(15)
9III
Unk
now
nSu
rger
yM
orta
lity
atdi
scha
rge
Ret
rosp
ectiv
ese
ries
of9
patie
nts
with
DTI
CH
toev
alua
tecl
inic
alch
arac
teri
stic
san
dou
tcom
e.
●55
.6%
mor
talit
y.●
Incl
uded
with
n�
9fo
rw
ell-
pres
ente
dda
taon
DTI
CH
.●
Def
initi
onof
DTI
CH
:1)
hist
ory
ofhe
adin
jury
with
head
inm
otio
npr
oduc
ing
tran
sien
tor
perm
anen
tLO
C,
foca
lne
urol
ogic
alfin
ding
s,or
cran
ial
frac
ture
;2)
inte
rval
betw
een
inju
ryan
dde
velo
pmen
tof
DTI
CH
of�
2w
k.
No.
ofpa
tien
tsD
(%)
DTI
CH
955
.6
Gaa
bet
al.
(17)
37III
Unk
now
nD
ecom
pres
sive
cran
iect
omy
GO
S1
yrPr
ospe
ctiv
ese
ries
of37
patie
nts
who
unde
rwen
tde
com
pres
sive
cran
iect
omy
beca
use
oftr
aum
atic
brai
nsw
ellin
gto
asse
ssef
ficac
yof
trea
tmen
tpr
otoc
olat
1yr
afte
rtr
aum
a.Su
rgic
alin
dica
tions
and
excl
usio
ncr
iteri
ade
taile
d.
●14
.7%
mor
talit
yus
ing
stan
dard
ized
prot
ocol
.●
Initi
alG
CS
�6,
day
1G
CS
�8
asso
ciat
edw
ithbe
tter
outc
ome
(no
stat
istic
s).
●A
llpa
tient
sw
ithG
OS
1–2
had
GC
S3
with
pupi
llary
abno
rmal
ity.
●R
epre
sent
sea
rly
repo
rtof
Gue
rra
etal
.st
udy.
No.
ofpa
tien
tsFu
ll(%
)D
isab
led
(%)
VS
(%)
D(%
)
Dec
ompr
essi
vecr
anie
ctom
y34
41.2
35.3
8.8
14.7
Gen
nare
lliet
al.
(19)
1107
IIIG
CS
3–8
Surg
ery
and
nons
urgi
cal
GO
S3
mo
Mul
ticen
ter
pros
pect
ive
seri
esof
1107
patie
nts
with
seve
rebl
unt
trau
mat
icbr
ain
inju
ry(G
CS
�8)
toex
amin
edi
ffere
nces
inty
peof
inju
ry,
seve
rity
ofin
jury
,an
dG
OS
at3
mo.
Subg
roup
sof
patie
nts
with
�oth
erfo
cal
inju
ry�
(n�
205)
and
�diff
use
inju
ry�
(n�
487)
wer
eex
amin
edfo
rth
isch
apte
r.O
fno
te,
�oth
erfo
cal
inju
ry�
incl
uded
ICH
,co
ntus
ions
,bu
tal
sode
pres
sed
cran
ial
frac
ture
,SD
H,
and
EDH
that
wer
eno
tth
epr
imar
yle
sion
s,an
dco
mbi
ned
EDH
/SD
Hin
whi
chth
em
ost
impo
rtan
tle
sion
was
unkn
own.
●Lo
wer
GC
Sw
asst
rong
lyco
rrel
ated
with
wor
seou
tcom
efo
rea
chle
sion
type
.●
Giv
enth
esa
me
pres
entin
gG
CS,
lesi
onty
pes
diffe
red
mar
kedl
yw
ithre
spec
tto
outc
ome.
●A
utho
rsm
ain
poin
tis
that
outc
ome
diffe
rsm
arke
dly
amon
gle
sion
type
sw
ithin
the
real
mof
seve
rehe
adin
jury
,an
dth
atou
tcom
ede
pend
sin
part
onty
peof
lesi
onas
wel
las
onin
jury
seve
rity
asm
easu
red
byG
CS.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Oth
erfo
cal
lesi
on,
tota
l20
521
1819
339
GC
S3–
511
27
1418
456
GC
S6
–8
9338
2319
218
Ope
rate
d71
2115
204
39
Ope
rate
d,G
CS
3–5
359
920
657
Ope
rate
d,G
CS
6–
836
3322
193
22
Non
oper
ated
134
2119
183
39
Non
oper
ated
,G
CS
3–5
776
1717
456
Diff
use
inju
ry,
tota
l48
734
1711
532
GC
S3–
523
716
1014
851
GC
S6
–8
250
5224
92
13
Com
a6
–24
h92
6315
21
15
Com
a6
–24
h,G
CS
3–5
2752
77
430
Com
a6
–24
h,G
CS
6–
865
6818
50
9
Com
a�
24h
395
2817
136
36
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-36 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Com
a�
24h,
GC
S3–
521
011
1015
954
Com
a�
24h,
GC
S6
–8
185
4625
103
15
Com
a�
24h,
not
dece
rebr
ate
219
3821
125
24
Com
a�
24h,
not
dece
rebr
ate,
GC
S3–
577
218
1312
47
Com
a�
24h,
not
dece
rebr
ate,
GC
S6
–8
142
4729
111
11
Com
a�
24h,
dece
rebr
ate
176
1513
147
51
Com
a�
24h,
dece
rebr
ate,
GC
S3–
513
66
1216
957
Com
a�
24h,
dece
rebr
ate,
GC
S6
–8
4048
158
328
Gen
tlem
anet
al.
(20)
23III
Com
ave
rsus
not
com
a
Surg
ery
and
nons
urgi
cal
GO
S6
mo
Ret
rosp
ectiv
ere
view
of27
01he
ad-i
njur
edpa
tient
sdi
still
edto
aco
hort
of23
patie
nts
with
DTI
CH
.V
olum
eof
hem
atom
aan
dtim
ing
ofre
peat
CT
scan
are
rela
ted
tom
anag
emen
t.O
pera
tive
vers
usno
nope
rativ
em
anag
emen
tis
rela
ted
toG
OS
at6
mo.
●O
pera
tive
vers
usno
nope
rativ
ele
sion
sdi
ffere
din
aver
age
volu
me
(24
vers
us7
cm3 )
and
time
tore
peat
CT
base
don
clin
ical
crite
ria
(41
vers
us99
h).
Out
com
ebe
twee
ngr
oups
was
not
stat
istic
ally
sign
ifica
nt.
●39
%of
DTI
CH
requ
ied
evac
uatio
n;cr
iteri
ano
tde
scri
bed.
●A
llpa
tient
sw
ithD
TIC
Hha
dab
norm
alC
Ton
adm
issi
on.
●D
efin
ition
ofD
TIC
H:
�les
ion
ofin
crea
sed
atte
nuat
ion
deve
lopi
ngaf
ter
adm
issi
onto
hosp
ital,
ina
part
ofth
ebr
ain
whi
chth
ead
mis
sion
CT
scan
had
sugg
este
dw
asno
rmal
.�
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
Ope
rate
dD
TIC
H9
5644
b
Non
oper
ated
DTI
CH
1457
43
DTI
CH
,to
tal
2357
43b
P�
n.s.
Gow
eret
al.
(21)
10III
GC
S�
8Su
btem
pora
lde
com
pres
sion
vers
uspe
ntob
arbi
tal
com
a
Mor
talit
y1
yrR
etro
spec
tive
seri
esof
115
patie
nts
with
GC
S�
8w
ithno
oper
ativ
em
ass
lesi
onat
time
ofad
mis
sion
man
aged
ona
stan
dard
trea
tmen
tpr
otoc
ol.
10pa
tient
sun
derw
ent
subt
empo
ral
deco
mpr
essi
onbe
caus
eof
med
ical
lyre
frac
tory
intr
acra
nial
hype
rten
sion
,an
dou
tcom
ew
asco
mpa
red
with
thos
epa
tient
sm
anag
edby
pent
obar
bita
lco
ma
with
out
surg
ery.
Tech
niqu
ede
scri
bed.
●Pa
tient
sun
derg
oing
subt
empo
ral
deco
mpr
essi
onha
dsi
gnifi
cant
lylo
wer
mor
talit
yth
anth
ose
trea
ted
with
pent
obar
bita
lco
ma
desp
iteha
ving
low
er(b
utno
tst
atis
tical
lysi
gnifi
cant
)av
erag
ead
mis
sion
GC
S(4
.9ve
rsus
6.1)
.H
owev
er,
10pa
tient
sun
derg
oing
pent
obar
bita
lco
ma
wer
ede
term
ined
not
tobe
oper
ativ
eca
ndid
ates
and
subs
eque
ntly
died
;bi
ases
resu
ltsin
favo
rof
oper
ated
grou
p.●
70%
ofop
erat
edpa
tient
sha
dav
erag
ede
crea
sein
ICP
of34
%.
No.
ofpa
tien
tsD
(%)
Pent
obar
bita
lco
ma
1782
.4
Subt
empo
ral
deco
mpr
essi
on10
40c
cP
�0.
039.
Gud
eman
etal
.(2
2)III
12G
CS
4–1
0Su
rger
yan
dno
nsur
gica
lG
OS
3m
o,1
yrPr
ospe
ctiv
est
udy
of16
2pa
tient
sw
ithse
vere
head
inju
ry,
12of
who
mde
velo
ped
DTI
CH
byC
Tsc
an.
Thes
epa
tient
sw
ere
anal
yzed
for
clin
ical
asso
ciat
ions
and
outc
omes
tobe
tter
unde
rsta
ndth
isle
sion
.
●92
%D
TIC
Hde
tect
ed�
48h
from
inju
ry.
●50
%de
velo
ped
afte
rde
com
pres
sive
surg
ery.
●D
TIC
Hha
d50
%m
orta
lity;
high
erbu
tno
tst
atis
tical
lysi
gnifi
cant
com
pare
dw
ithal
lse
vere
head
inju
ries
duri
ngth
esa
me
peri
od.
●Si
gnifi
cant
lyhi
gher
inci
denc
eof
seco
ndar
ysy
stem
icin
sults
attim
eof
adm
issi
onin
DTI
CH
patie
nts
vers
usal
lse
vere
CH
Ipa
tient
s(9
2%ve
rsus
44%
).●
No
sign
ifica
ntte
mpo
ral
rela
tions
hip
betw
een
deve
lopm
ent
ofD
TIC
H,
ICP
leve
ls,
neur
olog
ical
chan
ge.
●A
utho
rsbe
lieve
that
deve
lopm
ent
ofD
TIC
His
anep
iphe
nom
enon
ofse
cond
ary
insu
ltto
ada
mag
edbr
ain
asop
pose
dto
aca
usat
ive
fact
orfo
rne
urol
ogic
alde
teri
orat
ion—
thus
,tr
eatm
ent
shou
ldbe
aim
edat
prev
entio
nof
seco
ndar
yhy
poxi
cin
sults
.
●D
efin
ition
ofD
TIC
H:
new
pare
nchy
mal
high
dens
ityle
sion
whe
nno
lesi
onor
ane
glig
ible
abno
rmal
ityw
aspr
esen
ton
initi
alC
T.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
DTI
CH
1225
250
050
TRAUMATIC PARENCHYMAL LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-37
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Gue
rra
etal
.(2
3)57
IIIG
CS4
–6
Dec
ompr
essi
vecr
anie
ctom
yG
OS
1yr
Pros
pect
ive
seri
esof
57pa
tient
sw
houn
derw
ent
deco
mpr
essi
vecr
anie
ctom
yun
der
ast
anda
rdiz
edtr
eatm
ent
prot
ocol
and
stan
dard
ized
surg
ical
tech
niqu
efo
rpo
sttr
aum
atic
diffu
sebr
ain
swel
ling.
The
patie
nts
wer
edi
vide
din
toa
grou
pun
derg
oing
prim
ary
deco
mpr
essi
on(n
�39
)an
da
grou
pun
derg
oing
seco
ndar
yde
com
pres
sion
beca
use
ofth
erap
y-re
sist
ant
intr
acra
nial
hype
rten
sion
afte
rev
acua
tion
ofa
surg
ical
mas
sle
sion
(n�
18).
Surg
ical
indi
catio
nsan
dm
etho
dsar
ede
taile
d.Pa
tient
sw
ithG
CS
3an
d/or
bila
tera
lfix
ed/
dila
ted
pupi
lsw
ere
excl
uded
.A
ge�
30yr
,�
40yr
,an
d�
50yr
vari
ably
used
asex
clus
ion
crite
ria
thro
ugho
utst
udy.
●37
%G
OS
5,19
%m
orta
lity
over
all.
●G
CS
onpo
sttr
aum
ada
y1
pred
ictiv
eof
outc
ome.
●Si
gnifi
cant
lybe
tter
outc
ome
with
nolo
ssof
Bw
aves
and
pres
ence
ofpl
atea
uw
aves
onIC
Pm
onito
ring
.●
Incl
usio
nof
SEP,
ICP/
CPP
,an
dA
EPm
onito
ring
tech
niqu
eshe
lped
tode
fine
indi
catio
nsfo
rth
eau
thor
s.●
Aut
hors
conc
lude
that
deco
mpr
essi
vecr
anie
ctom
ysh
ould
be1s
tam
ong
seco
nd-t
ier
ther
apie
sfo
rre
sist
ant
intr
acra
nial
hype
rten
sion
.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
Prim
ary
deco
mpr
essi
on38
5842
Seco
ndar
yde
com
pres
sion
1765
35P
�n.
s.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
All
patie
nts
5537
2111
919
Kat
ayam
aet
al.
(28)
21III
Unk
now
nSu
rger
yan
dno
nsur
gica
lM
orta
lity
Ret
rosp
ectiv
eca
seco
ntro
lst
udy
of21
patie
nts
with
fron
tal
lobe
cont
usio
nsan
dm
edic
ally
intr
acta
ble
intr
acra
nial
hype
rten
sion
�40
mm
Hg,
com
pari
ngm
orta
lity
betw
een
the
grou
ptr
eate
dm
edic
ally
(n�
8)an
dth
egr
oup
trea
ted
with
surg
ical
evac
uatio
nof
cont
used
brai
n(n
�13
).A
utho
rsst
ate
that
age,
sex,
GC
S,an
dIC
Ple
vels
wer
eco
mpa
rabl
ebe
twee
ngr
oups
,bu
tdo
not
prov
ide
stat
istic
s.
●M
orta
lity
was
sign
ifica
ntly
decr
ease
din
the
surg
ical
grou
p(2
2%ve
rsus
88%
).●
Aut
hors
note
that
prog
ress
ive
ICP
incr
ease
and
neur
olog
ical
dete
rior
atio
nof
ten
cont
inue
dpa
stth
etim
ing
ofm
axim
alen
larg
emen
tof
intr
acer
ebra
lle
sion
son
CT.
●A
utho
rsad
voca
tesu
rgic
alex
cisi
onof
cont
used
brai
nin
the
setti
ngof
med
ical
lyun
cont
rolla
ble
ICP
elev
atio
n.
No.
ofpa
tien
tsD
(%)
Non
oper
ativ
e8
88
Surg
ery
1322
d
dP
�0.
01
Kau
fman
etal
.(2
9)8
IIIA
llGC
SSu
rger
yan
dno
nsur
gica
lM
orta
lity
atdi
scha
rge
Ret
rosp
ectiv
ese
ries
of12
patie
nts
with
DTI
CH
orre
curr
ent
hem
atom
aaf
ter
head
inju
ryto
exam
ine
the
asso
ciat
ion
ofdi
ssem
inat
edin
trav
ascu
lar
clot
ting
and
fibri
noly
sis
with
occu
rren
ceof
thes
ele
sion
s.A
subs
etof
8pa
tient
sw
ithD
TIC
Hw
asev
alua
ted
for
this
chap
ter.
●7
of8
DTI
CH
patie
nts
had
abno
rmal
clot
ting
para
met
ers.
●In
clud
edw
ithn
�8
beca
use
ofpr
esen
tatio
nof
data
and
eval
uatio
nof
clot
ting
para
met
ers.
No.
ofpa
tien
tsD
(%)
Clo
ttin
gab
norm
alit
ies
(%)
DTI
CH
,to
tal
837
.587
.5
Kot
wic
aan
dJa
kubo
wsk
i(3
1)48
IIIA
llGC
SSu
rger
yan
dno
nsur
gica
lG
OS,
not
spec
ified
Ret
rosp
ectiv
ese
ries
of13
6pa
tient
sag
ed70
–91
yrw
ithTB
Ito
eval
uate
outc
ome
from
TBI
inan
aged
popu
latio
n.48
patie
nts
with
ICH
/con
tusi
onre
view
ed.
●O
vera
llm
orta
lity
from
ICH
/con
tusi
ons
was
50%
;8
of13
inop
erat
edca
ses,
and
16of
35in
nono
pera
ted
case
s.●
Mor
talit
yco
rrel
ated
with
adm
issi
onG
CS
(no
stat
istic
s).
●A
utho
rsfe
elth
atbe
caus
eth
em
orta
lity
rate
for
patie
nts
�70
yrw
ithG
CS
�9
isso
high
(�80
%),
limite
dat
tem
pts
shou
ldbe
mad
eat
resu
scita
tion,
inte
nsiv
eca
re,
and
surg
ery.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
ICH
�co
ntus
ion,
surg
ery
137.
77.
715
.47.
761
.5
ICH
�co
ntus
ion,
nosu
rger
y35
11.4
11.4
22.9
8.6
45.7
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-38 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Kum
chev
etal
.(3
2)79
IIIG
CS
3–6
to12
–15
Surg
ery
and
nons
urgi
cal
Mor
talit
yR
etro
spec
tive
revi
ewof
79pa
tient
sw
ithin
trac
ereb
ral
hem
atom
as,
com
pari
nglo
catio
nof
hem
atom
aw
ithm
orta
lity,
and
outc
ome
ofsu
rger
yve
rsus
nons
urgi
cal
ther
apy.
Trea
tmen
tpr
otoc
olw
asno
tst
anda
rdiz
ed;
surg
ical
indi
catio
nsw
ere
not
repo
rted
.
●Th
ose
patie
nts
with
tem
pora
lIC
Hw
ere
mor
elik
ely
todi
e.●
Surg
ery
did
not
alte
rm
orta
lity.
Surg
ical
lym
anag
edpa
tient
sw
ere
mor
elik
ely
tosh
owcl
inic
alim
prov
emen
t.
Loca
tion
No.
ofpa
tien
tsD
(%)
Pva
lues
Fron
tal
166
�0.
001
Tem
pora
l36
57.6
�0.
01
Pari
eto-
occi
pita
l14
18.2
�0.
01
Mul
tiple
site
s13
18.2
�0.
01
Kun
zeet
al.
(33)
28III
All
GC
SD
ecom
pres
sive
cran
iect
omy
GO
S1
yrR
etro
spec
tive
stud
yof
28pa
tient
sun
derg
oing
uni/b
ilate
ral
deco
mpr
essi
vecr
anie
ctom
yfo
rpo
sttr
aum
atic
edem
aaf
ter
�max
imal
�m
edic
alth
erap
y.
●57
%ov
eral
lfa
vora
ble
outc
ome
(GO
S4
–5)
at1
yr.
●M
ean
ICP
decr
ease
dfr
om41
.7to
20.6
mm
Hg
afte
rde
com
pres
sion
.●
Patie
nts
with
“vas
t”pr
imar
yle
sion
s,hy
poxi
a,is
chem
icin
farc
tion,
brai
nste
min
jury
,“c
entr
al”
hern
iatio
n,an
dpr
imar
yan
isoc
oria
excl
uded
.
No.
ofpa
tien
tsG
R/M
D(%
)SD
(%)
VS
(%)
D(%
)
Dec
ompr
essi
vecr
anie
ctom
y28
5718
1411
Lee
etal
.(3
4)29
IIIG
CS
�8
Subt
empo
ral
deco
mpr
essi
on�
tem
pora
llo
bect
omy
GO
S1
yrR
etro
spec
tive
seri
esof
29pa
tient
sop
erat
edon
for
acut
eSD
Han
dse
vere
cont
usio
n/sw
ellin
gof
tem
pora
llo
bew
ithun
cal
hern
iatio
n.16
patie
nts
unde
rwen
tsu
btem
pora
lde
com
pres
sion
and
debr
idem
ent
ofco
ntus
edbr
ain
whe
reas
13su
bseq
uent
patie
nts
unde
rwen
tte
mpo
ral
lobe
ctom
yin
addi
tion.
Thes
etw
ogr
oups
wer
eco
mpa
red
with
resp
ect
toou
tcom
eat
1yr
orlo
nger
.
●A
dditi
onof
tem
pora
llo
bect
omy
tosu
btem
pora
lde
com
pres
sion
and
debr
idem
ent
ofco
ntus
edbr
ain
sign
ifica
ntly
decr
ease
dm
orta
lity
from
56%
to8%
and
sign
ifica
ntly
impr
oved
aver
age
GO
Sfr
om2.
2to
4.0.
Preo
pera
tive
GC
S,ag
e,an
dse
xw
ere
not
sign
ifica
ntly
diffe
rent
betw
een
grou
ps.
●In
cide
nce
ofm
otor
reco
very
,co
gniti
vede
ficits
,an
dse
izur
esw
ere
not
sign
ifica
ntly
diffe
rent
betw
een
grou
ps.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)D
(%)
STD
,deb
ridem
ent
1625
7556
STD
,de
brid
emen
t,TL
1377
238e
STD
,de
brid
emen
t,co
mpl
ete
TL10
100
00
STD
,de
brid
emen
t,an
teri
orTL
30
100
33
eP
�0.
01.
Loba
toet
al.
(35)
277
IIIG
CS
3–7
Surg
ery
and
nons
urgi
cal
GO
S6
mo
Pros
pect
ive
seri
esof
277
seve
rely
head
-in
jure
dpa
tient
scl
assi
fied
byC
Tsc
anin
to8
inju
ryty
pes
toex
amin
eG
OS
at6
mo
rela
ted
tole
sion
type
.IC
Pw
asm
onito
red
inal
lpa
tient
s.Pa
tient
sbr
ain
dead
onar
riva
lw
ere
excl
uded
.A
stan
dard
ized
man
agem
ent
prot
ocol
was
used
and
isde
scri
bed.
GC
S,IC
P,an
din
terv
alto
oper
atio
nva
ried
betw
een
CT
grou
ps.
●Pa
tient
sw
ithpu
reex
trac
ereb
ral
hem
atom
a,si
ngle
brai
nco
ntus
ion,
gene
ral
brai
nsw
ellin
g,an
dno
rmal
CT
scan
sha
da
sign
ifica
ntly
bette
rou
tcom
eth
anpa
tient
sw
ithex
trac
ereb
ral
hem
atom
aan
dac
ute
hem
isph
eric
swel
ling,
mul
tiple
brai
nco
ntus
ions
,an
dpa
tient
sw
ithdi
ffuse
axon
alin
jury
.●
Acu
tehe
mis
pher
icsw
ellin
gsi
gnifi
cant
lyin
crea
sed
mor
talit
y.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Sing
leco
ntus
ion
(SC
)25
728
44
12
SC�
EDH
714
860
00
SC�
SDH
1315
4615
023
MU
C20
015
100
75
MU
C�
SDH
120
178
075
Mul
tiple
bila
tera
lco
ntus
ion
4219
265
050
GB
S25
768
40
12
GB
S�
EDH
1688
60
06
DA
I43
59
2112
53
Nor
mal
CT
2839
2918
114
TRAUMATIC PARENCHYMAL LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-39
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Loba
toet
al.
(36)
587
IIIG
CS
3–8
Surg
ery
and
nons
urgi
cal
GO
S6
mo
Ret
rosp
ectiv
ese
ries
of58
7pa
tient
sw
ithG
CS�
8an
dat
leas
ton
eco
ntro
lC
Tsc
an(a
vera
ge36
.7h
afte
rin
itial
CT)
toev
alua
tein
cide
nce
ofch
ange
sin
CT
clas
sific
atio
nov
ertim
ean
dto
asse
ssth
ere
lativ
epr
ogno
stic
sign
ifica
nce
ofa
seco
ndC
Tsc
anve
rsus
the
first
.
●51
.2%
deve
lope
dsi
gnifi
cant
CT
chan
ges
requ
irin
gch
ange
indi
agno
stic
cate
gory
.●
Fina
lou
tcom
ew
asm
ore
accu
rate
lypr
edic
ted
byco
ntro
lC
Tdi
agno
sis
than
byin
itial
CT
diag
nosi
s.●
19%
ofdi
ffuse
inju
ries
evol
ved
tom
ass
lesi
ons.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS
(%)
D(%
)
Diff
use
inju
ryI
2475
8.3
16.6
Diff
use
inju
ryII
247
54.6
19.4
25.9
Diff
use
inju
ryIII
123
20.3
10.5
69.1
Diff
use
inju
ryIV
2516
480
Man
dera
etal
.(3
7)31
IIIG
CS
3–8
to13
–15
Surg
ery
and
nons
urgi
cal
GO
S,no
tsp
ecifi
edR
etro
spec
tive
stud
yof
31ch
ildre
nw
ithtr
aum
atic
ICH
toex
amin
efa
ctor
sre
late
dto
surg
ical
deci
sion
mak
ing
and
asse
ssou
tcom
e.
●O
utco
me
did
not
diffe
rbe
twee
nsu
rgic
alan
dco
nser
vativ
egr
oups
desp
iteth
efa
ctth
atm
ore
patie
nts
with
seve
rein
jury
wer
etr
eate
dsu
rgic
ally
.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Surg
ery
2035
2030
015
Non
surg
ical
1145
1818
018
Mar
shal
l(3
9)41
4III
GC
S3–
8N
onsu
rgic
alG
OS
11d–
2yr
Pros
pect
ive
seri
esof
746
patie
nts
from
TCD
Bto
iden
tify
patie
nts
atri
skfo
rde
velo
ping
intr
acra
nial
hype
rten
sion
inth
eab
senc
eof
sign
ifica
ntm
ass
lesi
ons
onin
itial
CT.
The
auth
ors
prop
ose
ane
wcl
assi
ficat
ion
ofhe
adin
jury
base
don
CT
and
rela
teth
ene
wcl
assi
ficat
ion
cate
gori
esto
outc
ome.
Non
surg
ical
diffu
sein
jury
cate
gori
esar
ein
clud
ed.
●C
Tdi
agno
sis
was
ahi
ghly
sign
ifica
ntin
depe
nden
tpr
edic
tor
ofm
orta
lity
whe
nag
ean
dm
otor
scor
ew
ere
incl
uded
inth
em
odel
.●
InD
iffus
eIn
jury
III,
high
est
ICP
and
post
resu
scita
tion
pupi
llary
reac
tivity
wer
esi
gnifi
cant
pred
icto
rsof
outc
ome.
Mar
shal
let
al.
(40)
502
IIIG
CS
3–8
Surg
ery
(ICH
)an
dno
nsur
gica
l(D
iffus
eIn
jury
I–IV
)
GO
S11
d–2
yrPr
ospe
ctiv
ese
ries
of74
6pa
tient
sse
lect
edfr
omTC
DB
toas
sess
impo
rtan
ceof
prog
nost
icva
riab
les
inde
term
inin
gou
tcom
efr
omse
vere
head
inju
ry.
Subg
roup
sof
nono
pera
ted
patie
nts
with
Diff
use
Inju
rypa
ttern
sI–
IVan
dpa
tient
sw
ithev
acua
ted
ICH
are
incl
uded
.
●90
%of
deat
hsoc
curr
edw
ithin
2w
k.●
Intr
acra
nial
diag
nosi
sst
rong
lyco
rrel
ated
with
outc
ome;
e.g.
,hi
gher
%of
Diff
use
Inju
ryIII
/IVpa
tient
sw
ere
vege
tativ
e.●
InD
iffus
eIn
jury
IIgr
oup,
age
�40
yrst
rong
lyco
rrel
ated
with
poor
outc
ome.
●G
OS
for
evac
uate
dIC
Hpa
tient
sco
rrel
ated
nega
tivel
ywith
age
�40
yr.
●Fo
ral
lpa
tient
s,po
stre
susc
itatio
nG
CS,
pupi
llary
reac
tivity
,an
dag
eco
rrel
ated
with
outc
ome.
CT
diag
nosi
sf
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Diff
use
Inju
ryI
5227
34.6
19.2
9.6
9.6
Diff
use
Inju
ryII
177
8.5
2640
.711
.313
.5
Diff
use
Inju
ryIII
153
3.3
13.1
26.8
22.9
34
Diff
use
Inju
ryIV
323.
13.
118
.818
.856
.2
Diff
use
Inju
ryII,
age
�40
yr15
310
28.7
41.1
11.1
9.1
Diff
use
Inju
ryII,
age
�40
yr24
08.
337
.512
.541
.7
fP
�0.
001
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-40 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Mat
hies
enet
al.
(41)
218
IIIM
ean
GC
S6.
9Su
rger
yan
dno
nsur
gica
lG
OS
6m
oR
etro
spec
tive
revi
ewof
data
accu
mul
ated
inpr
ospe
ctiv
e,ra
ndom
ized
,do
uble
-blin
dH
IT-2
stud
yon
nim
odip
ine
inhe
adin
jury
.21
8pa
tient
sno
tfo
llow
ing
com
man
dsw
ithin
24h
oftr
aum
aw
ithin
trac
ereb
ral
lesi
ons
only
onC
Tw
ere
chos
enfo
ran
alys
is.
Patie
nts
with
extr
acer
ebra
lle
sion
s,no
rmal
CT,
guns
hot
wou
nds,
preg
nanc
y,bi
late
rally
fixed
/dila
ted
pupi
ls,
GC
S3
for
�2
h,an
dpr
evio
usdr
ugad
min
istr
atio
nin
terf
erin
gw
ithne
urol
ogic
alas
sess
men
tw
ere
excl
uded
.C
linic
alm
anag
emen
tw
asno
tst
anda
rdiz
ed.
Patie
nts
wer
edi
vide
din
to4
subg
roup
sba
sed
onC
Tap
pear
ance
with
in24
hof
trau
ma:
1)co
ntus
ions
;2)
frac
ture
cont
usio
ns(d
irec
tlyun
derl
ying
depr
esse
dfx
);3)
DA
I;an
d4)
ICH
(�10
cm3 ),
and
anal
yzed
with
resp
ect
toG
OS
at6
mo.
Asu
bgro
upof
patie
nts
with
GC
S�
6an
dle
sion
�20
cm3
wer
ean
alyz
edfo
rth
eef
fect
ofsu
rger
yan
dtim
ing
ofsu
rger
yon
outc
ome.
Asu
bgro
upof
patie
nts
who
�tal
ked
and
died
�w
ere
anal
yzed
tode
term
ine
the
valu
eof
earl
ysu
rger
y.
●In
itial
CT
char
acte
rist
ics
asso
ciat
edw
ithne
urol
ogic
alde
teri
orat
ion,
defin
edas
fall
inG
CS
by2,
GC
Sfr
om4
to3,
orpu
pilla
rydi
lata
tion,
wer
eSA
H,
foca
lle
sion
with
volu
me
�40
cm3 ,
and
com
pres
sed/
abse
ntci
ster
ns.
●Se
cond
ary
(�5
d)de
teri
orat
ion
corr
elat
edw
ithSA
Hon
initi
alC
T,hy
poxi
cev
ents
.●
For
the
4gr
oups
:1)
Con
tusi
ons:
outc
ome
adve
rsel
yaf
fect
edby
pres
ence
ofIV
H.
2)Fr
actu
re/c
ontu
sion
s:ou
tcom
esi
gnifi
cant
lyw
orse
than
othe
rgr
oups
;ou
tcom
ead
vers
ely
affe
cted
bypr
esen
ceof
SAH
.3)
DA
I:m
ean
adm
issi
onG
CS
sign
ifica
ntly
wor
seth
anot
her
grou
ps.N
opa
tient
sop
erat
ed.
4)IC
H:m
ean
adm
issi
onG
CS
sign
ifica
ntly
bette
rth
anot
her
grou
ps;o
utco
me
adve
rsel
yaf
fect
edby
pres
ence
ofIV
H.
●Pa
tient
sw
ithle
sion
s�
20cm
3an
dad
mis
sion
GC
S�
6:1)
Patie
nts
oper
ated
with
outp
revi
ous
dete
riora
tion
(n�
9)ha
dbe
tter
outc
ome
than
thos
eno
top
erat
edon
orop
erat
edon
afte
rde
terio
ratio
n(n
�66
).2)
Patie
nts
with
radi
olog
ical
sign
sof
mas
sef
fect
(com
pres
sion
/obl
itera
tion
ofci
ster
nan
d/or
mid
line
shift
�5
mm
)had
bette
rou
tcom
ew
ithsu
rger
yve
rsus
nosu
rger
y,an
dth
ose
oper
ated
befo
rede
terio
ratio
nha
dbe
tter
outc
ome
than
thos
eop
erat
edaf
ter
dete
riora
tion.
3)Su
rger
ydi
dno
tinf
luen
ceou
tcom
ein
patie
nts
adm
itted
with
GC
S�
5.●11
patie
nts
with
tem
pora
lcon
tusi
on,r
adio
logi
cals
igns
ofm
ass
effe
ct,a
dmis
sion
GC
S�
10:
outc
ome
sign
ifica
ntly
bette
rin
thos
eop
erat
edbe
fore
orim
med
iate
lyaf
ter
dete
riora
tion
com
pare
dw
ithde
laye
dor
nosu
rger
y.●A
utho
rspo
ints
:1)
Patie
nts
with
front
alor
tem
pora
lcon
tusi
ons
with
mid
line
shift
orci
ster
nalc
ompr
essi
onha
dst
atis
tical
lybe
tter
outc
ome
with
surg
ery.
2)Su
rgic
alou
tcom
ew
asbe
tter
the
earl
ier
itw
aspe
rfor
med
rela
ted
tode
teri
orat
ion.
3)Pa
tient
sw
ithte
mpo
ral
cont
usio
nsan
dra
diol
ogic
alsi
gns
ofm
ass
effe
ctsh
ould
beop
erat
edon
befo
rede
teri
orat
ion.
4)A
utho
rsof
fer
indi
catio
nsfo
rsu
rger
y:al
lpa
tient
sw
ithco
ntus
ions
�20
cm3
with
radi
olog
ical
sign
sof
mas
sef
fect
orw
ithan
yle
sion
�50
cm3 .
No.
ofpa
tien
tsG
R/M
D(%
)D
(%)
Mea
nG
OS
All
patie
nts
218
5627
.53.
2
Lesi
onty
peN
o.of
pati
ents
GR
(%)
MD
(%)
SD(%
)V
S(%
)D
(%)
Con
tusi
ons
122
2430
115
30
Con
tusi
ons/
depr
esse
dcr
ania
lfr
actu
reg
2412
1725
442
DA
I39
2325
305
17
ICH
3231
2816
322
No.
ofpa
tien
tsG
R/M
D/S
D(%
)V
S/D
(%)
GC
S�
6,vo
lum
e�
20cm
3
No
surg
ery
4250
50
Surg
ery
befo
rede
teri
orat
iong
610
00
Surg
ery
onda
yof
dete
rior
atio
n9
6733
Surg
ery
�1
daf
ter
dete
rior
atio
n9
5544
GC
S�
6,vo
lum
e�
20cm
3 ,C
Tm
ass
effe
ct
No
surg
ery
1926
74
Surg
ery
befo
rede
teri
orat
iong
610
00
Surg
ery
onda
yof
dete
rior
atio
n8
62.5
37.5
Surg
ery
�1
daf
ter
dete
rior
atio
n1
010
0
GC
S�
6,vo
lum
e�
50cm
3
No
surg
ery
1436
64
Surg
ery
befo
rede
teri
orat
iong
310
00
Surg
ery
onda
yof
dete
rior
atio
ng10
7030
Surg
ery
�1
daf
ter
dete
rior
atio
n1
010
0
GC
S�
10cm
3 ,te
mpo
ral
cont
usio
n,C
Tm
ass
effe
ct
Del
ayed
orno
surg
ery
80
100
Surg
ery
befo
reor
attim
eof
dete
rior
atio
ng3
100
0g
P�
0.05
.
TRAUMATIC PARENCHYMAL LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-41
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Mei
eret
al.
(42)
38III
All
GC
SSu
rger
yG
OS
atdi
scha
rge
Ret
rosp
ectiv
ese
ries
of93
6pa
tient
sw
houn
derw
ent
surg
ery
for
TBI,
38of
who
mw
ere
child
ren
with
ICH
/con
tusi
onas
prim
ary
path
olog
y.G
OS
isre
late
dto
adm
issi
onG
CS.
●C
hild
ren
with
adm
issi
onG
CS
6–
8ha
dbe
tter
over
all
outc
ome
than
adul
tsw
ithad
mis
sion
GC
S6
–8.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS
(%)
D(%
)
Chi
ldre
nw
ithco
ntus
ions
3853
1037
Mei
eret
al.
(43)
19III
GC
S3–
12D
ecom
pres
sive
cran
iect
omy
GO
Sat
disc
harg
eR
etro
spec
tive
seri
esof
19pa
tient
sw
ithin
trac
tabl
ein
trac
rani
alhy
pert
ensi
onun
derg
oing
deco
mpr
essi
vecr
anie
ctom
yto
eval
uate
fact
ors
rela
ted
topr
ogno
sis.
Surg
ical
indi
catio
nsin
clud
edfa
ilure
ofco
nser
vativ
ein
terv
entio
nfo
rin
trac
rani
alhy
pert
ensi
on,
age
�50
yrw
ithou
tm
ultip
letr
aum
a,ag
e�
30yr
inpr
esen
ceof
maj
orex
trac
rani
alin
juri
es,
seve
rebr
ain
swel
ling
onC
T(o
rin
trao
pera
tivel
y).
11pa
tient
sun
derw
ent
deco
mpr
essi
vecr
anie
ctom
ybe
caus
ege
nera
lized
brai
ned
ema
was
evid
ent
duri
ngev
acua
tion
ofa
spac
e-oc
cupy
ing
lesi
on;
8pa
tient
sun
derw
ent
deco
mpr
essi
vecr
anie
ctom
yse
cond
ary
tofa
ilure
ofco
nser
vativ
etr
eatm
ent.
●2
patie
nts
�60
yrha
dG
OS
2(V
S).
●A
gean
dG
CS
rela
ted
toG
OS
(no
stat
istic
s).
●M
orta
lity
incr
ease
dw
ithth
epr
esen
ceof
extr
acra
nial
inju
ries
(no
stat
istic
s).
No.
ofpa
tien
tsG
R/M
D(%
)SD
(%)
VS
(%)
D(%
)
All
1926
526
43
Ope
rate
d63
Non
oper
ated
27
Mill
eret
al.
(44)
20III
GC
S3–
8Su
rgic
alan
dno
nsur
gica
lG
OS
3m
oPr
ospe
ctiv
ese
ries
of22
5pa
tient
sw
ithse
vere
head
inju
rym
anag
edby
stan
dard
ized
prot
ocol
toid
entif
ypr
ogno
stic
vari
able
san
dto
valid
ate
resu
ltsof
apr
evio
usst
udy.
Subg
roup
sw
ithsu
rgic
alan
dno
nsur
gica
lle
sion
sar
eid
entif
ied
and
outc
ome
issp
ecifi
edfo
rea
chle
sion
.Th
ede
finiti
onof
ICH
incl
uded
�5
mm
mid
line
shift
,an
d,th
us,
all
wer
eta
ken
tosu
rger
y.
●C
orre
latio
nbe
twee
nag
e,ab
norm
alm
otor
resp
onse
,bi
late
ral
loss
oflig
htre
flex,
impa
ired
/abs
ent
ocul
ocep
halic
refle
x,an
dou
tcom
ein
nono
pera
tivel
ym
anag
edpa
tient
s.●
Pare
nchy
mal
lesi
ons
ofin
crea
sed
dens
ityon
CT
wer
eas
soci
ated
with
seve
redi
sabi
lity/
vege
tativ
est
ate
com
pare
dw
ithot
her
lesi
ons.
●31
%in
cide
nce
ofun
cont
rolla
ble
post
oper
ativ
eel
evat
edIC
Pin
ICH
patie
nts.
Surg
ical
and
nons
urgi
cal
grou
psw
ere
not
com
para
ble.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS
(%)
D(%
)
ICH
2026
1658
Con
tusi
on,
nosu
rger
y31
6413
23
Diff
use,
nosu
rger
y10
173
1017
Mun
chet
al.
(45)
49III
GC
S�
8to
�8
Dec
ompr
essi
vecr
anie
ctom
yG
OS
6m
oR
etro
spec
tive
seri
esof
49pa
tient
sun
derg
oing
unila
tera
lde
com
pres
sive
cran
iect
omy
for
TBI
unde
rst
anda
rdiz
edtr
eatm
ent
prot
ocol
toev
alua
tepr
eope
rativ
ean
dpo
stop
erat
ive
CT
char
acte
rist
ics,
ICP/
CPP
chan
ge,
and
toas
sess
outc
ome.
Asu
bdiv
isio
nin
tora
pid
and
dela
yed
grou
psw
asal
soan
alyz
edac
cord
ing
toou
tcom
e.Su
rgic
alin
dica
tions
deta
iled.
Patie
nts
with
bila
tera
lin
trac
rani
alle
sion
s;bi
late
rally
fixed
and
dila
ted
pupi
ls;
and
life-
thre
aten
ing
conc
omita
ntm
edic
aldi
seas
ew
ere
excl
uded
.A
llpa
tient
sun
derg
oing
rapi
dde
com
pres
sion
had
acut
eSD
H.
All
patie
nts
unde
rgoi
ngde
laye
dde
com
pres
sion
had
diffu
sebr
ain
swel
ling.
●41
%go
odou
tcom
eat
6m
o.●
Vis
ibili
tyof
mes
ence
phal
icci
ster
nsan
dm
idlin
esh
iftim
prov
edsi
gnifi
cant
lyaf
ter
cran
iect
omy;
gyra
lpa
ttern
and
visi
bilit
yof
vent
ricl
esdi
dno
t.●
No
chan
gein
mea
nth
erap
eutic
inte
nsity
leve
lbe
fore
vers
usaf
ter
deco
mpr
essi
on.
●A
ge�
50yr
,G
CS
�8
corr
elat
edsi
gnifi
cant
lyw
ithbe
tter
outc
ome.
●G
OS
at6
mo
sign
ifica
ntly
bette
rin
rapi
dve
rsus
dela
yed
deco
mpr
essi
ongr
oups
,bu
tG
OS
atdi
scha
rge
from
ICU
not
sign
ifica
ntly
diffe
rent
.●
No
sign
ifica
ntdi
ffere
nce
betw
een
befo
rean
daf
ter
deco
mpr
essi
onIC
Pan
dC
PP.
●C
hang
ein
mes
ence
phal
icci
ster
nvi
sibi
lity
corr
elat
edw
ithdi
stan
cebe
twee
nlo
wer
cran
iect
omy
bord
eran
dcr
ania
lba
se(m
ore
than
area
ofde
com
pres
sion
).
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
At
disc
harg
efr
omIC
U49
2872
At
6m
o49
4159
GC
S8
GC
S<
8R
apid
Del
ayed
Age
<50
yrA
ge50
yr
Mea
nG
OS
3.9
1.4h
3.1
1.9i
3.0
1.9i
hP
�0.
023,
iP
�0.
046.
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-42 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Nag
abha
ndan
dSa
ngch
am(4
6)10
IIIU
nkno
wn
Surg
ery
Mor
talit
yR
etro
spec
tive
revi
ewof
71pa
tient
sun
derg
oing
surg
ery
for
intr
acra
nial
hem
atom
a.M
orta
lity
com
pare
dbe
twee
ndi
ffere
ntin
trac
rani
alle
sion
s,an
dbe
twee
ngr
oups
trea
ted
befo
rean
daf
ter
intr
oduc
tion
ofC
Tto
the
hosp
ital.
Asu
bset
of10
patie
nts
with
ICH
rece
ivin
gpr
eope
rativ
eC
Tis
incl
uded
No.
ofpa
tien
tsD
(%)
ICH
/con
tusi
on10
50
Nor
dstr
omet
al.
(47)
587
IIIG
CS
3–8
Surg
ery
and
nons
urgi
cal
GO
S6
mo
Ret
rosp
ectiv
ese
ries
of58
7pa
tient
sw
ithse
vere
TBI,
prim
arily
toan
alyz
eef
fect
ofin
stitu
tion
ofm
anag
emen
tpr
otoc
olin
are
gion
inSw
eden
onou
tcom
e.Pr
otoc
olin
stitu
ted
in19
83.
For
our
purp
oses
,ep
idem
iolo
gyan
dou
tcom
eof
ICH
and
seve
reTB
Iw
ithno
mas
sle
sion
are
eval
uate
d.
●Pa
tient
sw
ithIC
H(in
clud
ing
asso
ciat
edSD
H/E
DH
)ha
d64
%m
orta
lity
and
15%
good
reco
very
at6
mo.
●%
ofex
plor
ator
ycr
anio
tom
ies
and
%m
orta
lity
inlo
cal
hosp
itals
decr
ease
dfo
llow
ing
inst
itutio
nof
man
agem
ent
prot
ocol
.C
Tw
asno
tun
iver
sally
avai
labl
eat
loca
lho
spita
ls.
No.
ofpa
tien
tsG
R(%
)D
(%)
ICH
205
1564
No
mas
sle
sion
,ex
plor
ator
ycr
anio
tom
y30
73j
No
mas
sle
sion
,no
expl
orat
ion
150
61jP
�n.
s.
Nus
sbau
met
al.
(48)
10III
GC
S3–
6Te
mpo
ral
lobe
ctom
yB
arth
elin
dex,
min
imum
8m
oR
etro
spec
tive
seri
esof
10pa
tient
sw
ithG
CS
3–6
and
clin
ical
sign
sof
tran
sten
tori
alhe
rnia
tion
who
unde
rwen
tst
anda
rdiz
edte
mpo
ral
lobe
ctom
yfo
run
ilate
ral
hem
isph
eric
swel
ling.
All
patie
nts
dem
onst
rate
dfix
edpu
pilla
rydi
latio
n;un
ilate
ral
in7,
bila
tera
lin
3.A
llfa
iled
med
ical
ther
apy
and
unde
rwen
tsu
rger
yw
ithin
2h
ofsi
gns
ofhe
rnia
tion.
●O
vera
ll40
%fu
nctio
nally
inde
pend
ent
surv
ival
with
30%
mor
talit
y.
No.
ofpa
tien
tsFu
ncti
onal
inde
pend
ence
(%)
Min
imal
assi
stan
ce(%
)D
(%)
Tota
l10
4030
30
Papo
etal
.(4
9)29
IIIG
CS
4–5
to�
10Su
rger
yan
dno
nsur
gica
lM
orta
lity
atdi
scha
rge
Ret
rosp
ectiv
ese
ries
of29
patie
nts
with
trau
mat
icIC
H/b
rain
lace
ratio
nto
anal
yze
the
corr
elat
ion
betw
een
GC
S,C
T,an
dIC
Pda
taan
dou
tcom
ew
ithor
with
out
oper
ativ
etr
eatm
ent.
ICP
data
reco
rded
via
intr
aven
tric
ular
cath
eter
.
●Pa
tient
sw
ithG
CS
4–5
onad
mis
sion
trea
ted
byop
erat
ion
with
in48
hof
inju
rydi
ed(n
ost
atis
tics)
.
No.
ofpa
tien
tsD
(%)
GC
S4
–55
100
GC
S6
–10
1346
.2
GC
S�
1011
0
Pate
let
al.
(50)
38III
GC
S�
8to
�13
Non
surg
ical
Mor
talit
yR
etro
spec
tive
seri
esof
57pa
tient
sin
itial
lym
anag
edno
nope
rativ
ely
who
subs
eque
ntly
requ
ired
cran
ioto
my
toat
tem
ptto
iden
tify
fact
ors
that
led
tofa
ilure
ofno
nope
rativ
em
anag
emen
t.A
subg
roup
of38
patie
nts
with
ICH
revi
ewed
.
●54
.5%
ofpa
tient
sw
ithIC
P�
20m
mH
gfa
iled
nono
pera
tive
man
agem
ent
in�
24h.
●Fr
onta
lIC
Hw
ere
sign
ifica
ntly
mor
epr
one
toea
rly
vers
usla
tefa
ilure
.●
Mor
talit
yin
faile
dIC
Hpa
tient
sw
as10
.5%
.
No.
ofpa
tien
tsD
(%)
Faile
dIC
H38
10.5
TRAUMATIC PARENCHYMAL LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-43
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Polin
etal
.(5
1)35
IIIM
ean
GC
S5.
62B
ifron
tal
deco
mpr
essi
vecr
anie
ctom
y
GO
Sat
disc
harg
eR
etro
spec
tive
case
-con
trol
seri
esof
35pa
tient
sun
derg
oing
bifr
onta
lde
com
pres
sive
cran
iect
omy
for
refr
acto
rypo
sttr
aum
atic
cere
bral
edem
aco
mpa
ring
preo
pera
tive
and
post
oper
ativ
eIC
P,ag
eve
rsus
outc
ome,
and
com
pari
ngth
egr
oup
asa
who
lew
ithth
egr
oup
from
TCD
Bm
atch
edfo
rag
e,ad
mis
sion
GC
S,se
x,an
dm
axim
alIC
Pin
term
sof
outc
ome.
Onl
yTC
DB
patie
nts
with
diffu
sein
jury
,no
sign
ifica
ntm
ass
lesi
on,
nom
idlin
esh
ift(II
I)(M
arsh
all
etal
.[3
9])
wer
eel
igib
lefo
rco
nsid
erat
ion
asco
ntro
ls.
●A
dmis
sion
GC
Sre
late
dto
outc
ome.
●O
pera
tion
�48
has
soci
ated
with
favo
rabl
eou
tcom
e(4
6%)
com
pare
dw
ith�
48h
(0%
).●
Sign
ifica
ntch
ange
inIC
Pbe
fore
vers
usaf
ter
deco
mpr
essi
on.
●Si
gnifi
cant
diffe
renc
ein
post
oper
ativ
eIC
Pve
rsus
cont
rol
ICP
48–7
2h
afte
rin
jury
.●
Coa
gulo
path
ydi
dno
taf
fect
outc
ome
insu
rgic
algr
oup.
●IC
P�
40m
mH
gsu
stai
ned
and
oper
atio
n�
48h
afte
rin
jury
had
sign
ifica
ntly
less
favo
rabl
eou
tcom
es.
●A
ge�
18yr
had
high
erra
teof
favo
rabl
eou
tcom
ein
surg
ical
grou
p.●
Surg
ery
age
�18
yrha
dhi
gher
rate
offa
vora
ble
outc
ome
than
mat
ched
cont
rols
ifop
erat
ed�
48h
and
ICP
�40
mm
Hg.
●M
edic
alm
anag
emen
tal
one
carr
ied
3.86
times
rela
tive
risk
ofun
favo
rabl
eou
tcom
eco
mpa
red
with
deco
mpr
essi
vecr
anie
ctom
y.●
Max
imum
bene
fitis
achi
eved
inpa
tient
sop
erat
edon
�48
haf
ter
inju
ryan
dw
ithIC
Pel
evat
ions
sust
aine
d�
40m
mH
g(6
0%fa
vora
ble
vers
us18
%in
mat
ched
cont
rols
).
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Surg
ery
k35
11.4
25.7
31.4
8.6
22.9
Cas
eco
ntro
l92
7.6
8.8
35.2
18.7
30.8
No.
ofpa
tien
tsG
R/M
D(%
)D
(%)
Coa
gulo
path
y18
33l
28
No
coag
ulop
athy
1741
18
ICP
�40
mm
Hg,
OR
�48
h15
6.7m
ICP
�40
,O
R�
48h
2060
Age
�18
yr18
44
Age
�18
yr17
29
OR
�48
h,IC
P�
4020
60n
ICP
�40
,co
ntro
l58
18
Age
�18
,IC
P�
40,
OR
�48
h10
80o
Age
�18
,IC
P�
40,
cont
rol
2524
kfa
vora
ble
outc
ome,
P�
0.01
4;lP
�n.
s.,
mP
�0.
0004
,n
P�
0.00
01,
oP
�0.
02.
Serv
adei
etal
.(5
4)72
4III
GC
S3–
12Su
rger
yan
dno
nsur
gica
lG
OS
6m
oPr
ospe
ctiv
est
udy
of72
4pa
tient
sw
ithm
oder
ate-
to-s
ever
eTB
Ito
dete
rmin
eth
efr
eque
ncy
ofch
ange
sin
CT
findi
ngs
and
thei
rpr
ogno
stic
impl
icat
ions
.
●16
%of
diffu
sein
juri
eson
initi
alC
Tde
mon
stra
ted
dete
rior
atio
non
subs
eque
ntC
T.●
12%
ofdi
ffuse
inju
ries
evol
ved
tom
ass
lesi
ons.
●Ev
olut
ion
from
diffu
sein
jury
with
out
swel
ling
orsh
ift(T
ype
II)to
am
ass
lesi
onw
asas
soci
ated
with
sign
ifica
ntin
crea
sein
risk
ofun
favo
rabl
eou
tcom
e.
●Tr
end
tow
ards
mor
efa
vora
ble
outc
ome
inpa
tient
sw
ithno
neva
cuat
edve
rsus
evac
uate
dm
ass
lesi
ons.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
Diff
use
inju
ryI,
noch
ange
7587
13
Diff
use
inju
ryI,
evol
utio
n5
8020
Diff
use
Inju
ryII,
noch
ange
185
6238
Diff
use
Inju
ryII,
evol
utio
np34
3862
Diff
use
Inju
ryIII
,no
chan
ge57
3367
Diff
use
Inju
ryIII
,ev
olut
ion
757
43
Diff
use
Inju
ryIV
,no
chan
ge14
2179
Diff
use
Inju
ryIV
,ev
olut
ion
475
25
Mas
sle
sion
343
4357
pP
�0.
01.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD (%
)V
S(%
)D (%
)
Diff
use
inju
ryI
8074
129
05
Diff
use
inju
ryII
219
3622
202
21
Diff
use
inju
ryIII
6420
169
253
Diff
use
inju
ryIV
1811
2211
056
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-44 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Sing
ouna
s(5
7)16
IIIG
CS
8–1
0U
nkno
wn
Mor
talit
yR
etro
spec
tive
revi
ewof
48ch
ildre
n�
14yr
with
seve
rehe
adin
jury
(ext
radu
ral
and
subd
ural
hem
atom
asex
clud
ed)
toco
mm
ent
onre
lativ
ely
good
prog
nosi
s.M
orta
lity
for
16pa
tient
sw
ithbr
ain
edem
aon
lyw
asre
port
ed.
No.
ofpa
tien
tsD
(%)
Diff
use
edem
a,no
foca
lle
sion
1612
.5
Solo
niuk
etal
.(5
8)35
IIIG
CS
�8
or�
8Su
rger
yG
OS
6m
oR
etro
spec
tive
revi
ewof
35pa
tient
sun
derg
oing
cran
ioto
my
for
evac
uatio
nof
ICH
toev
alua
tech
arac
teri
stic
sof
timin
gof
appe
aran
ceof
ICH
and
fact
ors
rela
ted
toou
tcom
e.IC
Hde
fined
asho
mog
eneo
usco
ales
cent
area
ofhi
ghat
tenu
atio
nm
easu
ring
2cm
orgr
eate
r.
●O
nly
26%
ofIC
Hre
quir
ing
evac
uatio
nar
epr
esen
ton
CT
with
in6
hof
inju
ry.
●49
%ov
eral
l1-
yrm
orta
lity;
71%
with
GC
S�
8.●
Mor
talit
yva
ries
with
loca
tion,
with
panh
emis
pher
ic,
tem
pora
l,an
dfr
onta
lra
tes
of80
%,
57%
,an
d37
%,
resp
ectiv
ely.
No.
ofpa
tien
tsD
(%)
ICH
,op
erat
ed35
49
Spri
cket
al.
(59)
34III
GC
S3
to�
7Su
rger
yan
dno
nsur
gica
lG
OS,
not
spec
ified
Ret
rosp
ectiv
ese
ries
of34
patie
nts
with
DTI
CH
ofat
leas
t2.
5-cm
diam
eter
inpr
evio
usly
norm
alar
eaon
initi
alC
Tto
eval
uate
outc
ome
and
clin
ical
char
acte
rist
ics.
●53
%D
TIC
Hde
velo
ped
with
in24
haf
ter
adm
issi
onan
d79
%w
ithin
48h
No.
ofpa
tien
tsG
R(%
)D
isab
led
(%)
D(%
)
All
3417
.655
.926
.5O
pera
ted
714
.342
.942
.9
Stat
ham
etal
.(6
0)18
IIIG
CS
5–14
Surg
ery
(n�
1)an
dno
nsur
gica
lG
OS
6m
oR
etro
spec
tive
revi
ewof
18pa
tient
sw
ithpr
imar
yC
Tdi
agno
sis
offr
onta
lco
ntus
ion,
defin
edas
regi
ons
ofm
ixed
high
and
low
orlo
wat
tenu
atio
nin
the
fron
tal
lobe
s,to
atte
mpt
tode
term
ine
fact
ors
that
may
lead
tone
urol
ogic
alde
teri
orat
ion
and
wor
seou
tcom
e.
●G
ood
outc
ome
was
achi
eved
in72
%of
patie
nts
with
fron
tal
cont
usio
n.●
Bot
hca
ses
ofde
teri
orat
ion
wer
eas
soci
ated
with
exte
nsiv
ebi
late
ral
inju
ry(n
ost
atis
tics)
.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Uni
late
ral
cont
usio
n10
900
00
10Li
mite
dbi
late
ral
cont
usio
ns5
4040
200
0
Exte
nsiv
ebi
late
ral
cont
usio
ns3
670
00
33
Fron
tal
cont
usio
ns,
tota
l18
72.2
11.1
5.6
011
.1
Tayl
oret
al.
(61)
27II
GC
S4
–11
Dec
ompr
essi
vebi
tem
pora
lcr
anie
ctom
yan
dno
nsur
gica
l
GO
S6
mo;
Hea
lthSt
ate
Util
ityIn
dex
6m
o
Pros
pect
ive,
rand
omiz
ed,
cont
rolle
dtr
ial
of27
child
ren
with
TBI
and
sust
aine
din
trac
rani
alhy
pert
ensi
onto
eval
uate
effe
ctof
earl
yde
com
pres
sive
bite
mpo
ral
cran
iect
omy
onou
tcom
ean
don
cont
rol
ofIC
P.
●Tr
end
tow
ards
grea
ter
decr
ease
inIC
Pin
deco
mpr
essi
ongr
oup
(P�
0.05
7).
●Tr
end
tow
ards
shor
ter
ICU
stay
inde
com
pres
sion
grou
p(P
�0.
12).
●Tr
end
tow
ards
impr
oved
outc
ome
inde
com
pres
sion
grou
p(P
�0.
046
[P�
0.02
21re
quir
edfo
rsi
gnifi
canc
e]).
No.
ofpa
tien
tsFa
vora
ble
(%)
Unf
avor
able
(%)
Dec
ompr
essi
on13
53.8
q46
.1
Con
trol
1414
.385
.7q
P�
0.04
6(P
�0.
0221
requ
ired
for
sign
ifica
nce)
.Fa
vora
ble:
norm
alor
func
tiona
llyno
rmal
but
requ
irin
gm
edic
atio
nor
med
ical
supe
rvis
ion.
Unf
avor
able
:m
oder
ate
disa
bilit
y,de
pend
ent,
seve
rely
disa
bled
/veg
etat
ive,
orde
ad.
Teas
dale
etal
.(6
2)37
IIIG
CS
3–8
Non
surg
ical
GO
S6
mo
Ret
rosp
ectiv
ese
ries
of37
patie
nts
diag
nose
dw
ithse
vere
diffu
sehe
adin
jury
(with
out
mid
line
shift
of�
5m
m)
tode
term
ine
the
rela
tions
hip
betw
een
com
pres
sion
ofba
sal
cist
erns
/3rd
vent
ricl
ean
del
evat
edIC
P.
●H
ighl
ysi
gnifi
cant
rela
tions
hip
betw
een
stat
usof
basa
lci
ster
ns/II
Ive
ntri
cle
and
leve
lof
ICP.
●Pr
esen
ceve
rsus
abse
nce
ofci
ster
ns/II
Ive
ntri
cle
seem
edto
corr
elat
ew
ithou
tcom
ew
ithin
GC
Sgr
oups
(no
stat
istic
s).
No.
ofpa
tien
tsG
R/M
D(%
)SD
(%)
VS/
D(%
)
GC
S3–
5,ab
sent
cist
erns
/3rd
vent
ricl
e11
9.1
090
.9
GC
S3–
5,pr
esen
tci
ster
ns/3
rdve
ntri
cle
520
2060
GC
S6
–8,
abse
ntci
ster
ns/3
rdve
ntri
cle
837
.525
37.5
GC
S6
–8,
pres
ent
cist
erns
/3rd
vent
ricl
e13
61.5
15.4
23.1
TRAUMATIC PARENCHYMAL LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-45
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Tsen
g(6
3)32
IIIA
llG
CS
Surg
ery
and
nons
urgi
cal
GO
S1
yrR
etro
spec
tive
seri
esof
32pa
tient
sw
ithD
TIC
Hto
eval
uate
clin
ical
and
radi
olog
icfa
ctor
saf
fect
ing
outc
ome.
●H
emat
oma
volu
me,
cist
erna
lef
face
men
t,tim
ing
ofde
tect
ion,
occu
rren
ceof
clin
ical
dete
rior
atio
n,an
dG
CS
attim
eof
follo
w-u
pC
Tw
ere
rela
ted
sign
ifica
ntly
toou
tcom
e.●
16%
over
all
mor
talit
y.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
GC
S3–
7at
follo
w-u
pC
Tr12
3367
GC
S8
–12
atfo
llow
-up
CT
1610
00
GC
S13
–15
atfo
llow
-up
CT
410
00
Cis
tern
effa
cem
ents
50
100
No
cist
ern
effa
cem
ent
2788
.911
.1r
P�
0.00
5,s
P�
0.00
1.
Tsen
g(6
4)32
IIIG
CS
5–7
Cra
niot
omy
�m
anua
lte
mpo
ral
lobe
redu
ctio
n
GO
S3
mo
Ret
rosp
ectiv
est
udy
of32
patie
nts
with
GC
S5–
7,C
Tev
iden
cefo
run
cal
hern
iatio
n,an
isoc
oria
,an
dhe
mip
ares
istr
eate
dei
ther
with
stan
dard
surg
ical
proc
edur
e(i.
e.,
cran
ioto
my
with
hem
atom
aev
acua
tion
and
cont
usio
nre
sect
ion)
orw
ithst
anda
rdpr
oced
ure
plus
man
ual
redu
ctio
nof
hern
iate
dte
mpo
ral
lobe
.G
OS
mea
sure
dat
�3
mo
post
opto
com
pare
outc
ome
betw
een
grou
ps.R
educ
tion
proc
edur
ede
scri
bed
asge
ntle
elev
atio
nof
tem
pora
llo
beun
tilte
ntor
ium
isvi
sual
ized
and
CSF
egre
ssis
note
d.
●A
dditi
onof
tem
pora
llo
bere
duct
ion
toth
est
anda
rdsu
rgic
alpr
oced
ure
seem
edto
resu
ltin
bette
rou
tcom
e(n
ost
atis
tics;
sele
ctio
nbi
as).
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD (%
)V
S(%
)D (%
)
Cra
niec
tom
y�
cont
usio
n�
redu
ctio
n10
2070
00
10
Cra
niec
tom
y�
cont
usio
n,no
redu
ctio
n
220
279
955
Uzz
ell
etal
.(6
5)11
7III
GC
S4
–6
Non
surg
ical
GO
S6
mo;
neur
o-ps
ycho
logi
cal
mea
n4.
8m
o(n
�30
)
Ret
rosp
ectiv
ese
ries
of11
7pa
tient
sw
ithD
AI,
diffu
sesw
ellin
g,or
foca
lin
jury
byC
Tto
char
acte
rize
diffe
rent
ial
outc
ome.
Neu
rops
ycho
logi
cal
test
ing
was
perf
orm
edin
asu
bset
of30
patie
nts
toch
arac
teri
zedi
ffere
ntia
lne
urop
sych
olog
ical
sequ
elae
base
don
lesi
onty
pe.
Patie
nts
with
SDH
,ED
H,
SAH
,or
deve
lopm
ent
ofa
seco
ndm
ajor
lesi
onw
ere
excl
uded
.D
AI
defin
edas
�mid
line
hem
orrh
ages
orm
ultip
lesm
all
hem
orrh
ages
atgr
ay-w
hite
mat
ter
inte
rfac
es�;
diffu
sesw
ellin
gde
fined
as�n
arro
win
gor
oblit
erat
ion
ofve
ntri
cles
orba
sila
rci
ster
ns�;
foca
lin
juri
esde
fined
as�u
nila
tera
lin
trac
ereb
ral
hem
orrh
ages
orco
ntus
ions
.�
●Pa
tient
sw
ithD
AI
had
sign
ifica
ntly
high
erm
orta
lity
and
sign
ifica
ntly
less
“goo
dre
cove
ry”
than
othe
rgr
oups
.●
Mem
ory
and
lear
ning
scor
ebu
tno
tin
telli
genc
eor
visu
omot
orsp
eed
scor
esi
gnifi
cant
lydi
ffere
dam
ong
CT
grou
ps.
●Le
vels
ofm
emor
y,le
arni
ng,
and
visu
omot
orsp
eed
wer
ehi
gher
afte
rdi
ffuse
swel
ling
inju
ries
,bu
tim
prov
emen
tw
asle
ssov
ertim
e.●
Patie
nts
with
DA
Iha
dgr
eate
rim
prov
emen
tov
ertim
eof
mem
ory,
lear
ning
,an
dvi
suom
otor
spee
d.●
Patie
nts
with
foca
lin
juri
esha
dim
prov
emen
tov
ertim
ein
visu
omot
orsp
eed,
but
not
reca
llor
lear
ning
.●
Dia
gnos
ticgr
oups
did
not
diffe
rsi
gnifi
cant
lyin
age,
year
sof
educ
atio
n,G
CS,
timin
gof
neur
opsy
chol
ogic
alte
stin
g,se
x,ha
nded
ness
,or
GO
Sat
6m
o.
CT
grou
ptN
o.of
pati
ents
GR
(%)
MD
(%)
SD (%)
VS
(%)
D (%)
DA
I33
1815
1512
40D
iffus
esw
ellin
g34
6217
60
15
Foca
lin
jury
5048
1514
022
tP
�0.
01.
Vol
lmer
etal
.(6
6)32
1III
All
GC
SSu
rger
yan
dno
nsur
gica
lG
OS
6m
oPr
ospe
ctiv
est
udy
from
1984
–198
7of
patie
nts
with
GC
S3–
15to
eval
uate
effe
ctof
age
onou
tcom
ein
diffe
rent
popu
latio
ns,
incl
udin
gpa
tient
sw
ithla
rge
(�15
cm3 )
ICH
requ
irin
gev
acua
tion
(n�
54)
and
patie
nts
with
�15
cm3
ICH
(n�
267)
.
●Pr
esen
ceof
ICH
and
ofla
rge
ICH
(�15
cm3 )
incr
ease
dsi
gnifi
cant
lyw
ithag
e.●
Incr
easi
ngag
ew
asin
depe
nden
tlypr
edic
tive
ofpo
orou
tcom
ein
larg
ean
dsm
all
ICH
subg
roup
s.
No.
ofpa
tien
tsV
S/D
(%)
ICH
�15
cm3u
267
Age
16–2
5yr
31.8
Age
26–3
5yr
27.7
Age
36–
45yr
42.4
Age
46–5
5yr
62.2
Age
�56
yr82
.2u
P�
0.00
1
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-46 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Whi
tfiel
det
al.
(67)
26III
GC
S3–
13B
ifron
tal
deco
mpr
essi
vecr
anie
ctom
y
GO
S6
mo
Ret
rosp
ectiv
ere
view
ofou
tcom
efo
r26
patie
nts
unde
rgoi
ngbi
fron
tal
deco
mpr
essi
vecr
anie
ctom
yfo
rre
frac
tory
intr
acra
nial
hype
rten
sion
(ICP
�30
mm
Hg
with
CPP
�70
mm
Hg;
orIC
P�
35m
mH
gir
resp
ectiv
eof
CPP
)m
anag
edus
ing
ast
anda
rdiz
edIC
P/C
PPtr
eatm
ent
algo
rith
m.
Con
tinuo
usIC
P,A
BP,
and
CPP
data
wer
ean
alyz
edfo
r8
patie
nts
toex
amin
eef
fect
ofbi
fron
tal
deco
mpr
essi
vecr
anie
ctom
yon
thes
eva
riab
les.
Surg
ical
tech
niqu
ede
scri
bed.
●61
%of
seve
reTB
Isu
bgro
upha
dfa
vora
ble
outc
ome
(GO
S4
–5).
●IC
Pw
assi
gnifi
cant
lyre
duce
dfr
om37
.5to
18.1
mm
Hg
(P�
0.00
3).
●C
PPdi
ffere
nces
wer
eno
tsi
gnifi
cant
.●
Am
plitu
deof
ICP
wav
efor
m,
ampl
itude
ofsl
oww
aves
,an
dR
AP
coef
ficie
nt(r
efle
ctin
gin
crea
sed
com
pens
ator
yre
serv
e)w
ere
sign
ifica
ntly
redu
ced
bysu
rger
yin
asu
bgro
upof
eigh
tpa
tient
s.●
Tim
ing
ofsu
rger
yw
asno
tpr
edic
tive
ofou
tcom
e.N
o.of
pati
ents
GR
/MD
(%)
SD(%
)V
S(%
)D
(%)
All
2669
80
23A
ge�
166
83.3
00
16.7
GC
S3–
818
61.1
11.1
027
.8G
CS
9–1
25
100
00
0G
CS
133
66.7
00
33.3
Tim
ing
ofsu
rger
yN
o.of
pati
ents
Favo
rabl
e(%
)U
nfav
orab
le(%
)O
R�
48h
afte
rin
jury
2060
40O
R�
48h
afte
rin
jury
610
00
Wu
etal
.(6
8)35
IIIA
llG
CS
Surg
ery
GO
S6
mo
Ret
rosp
ectiv
ese
ries
of48
9pa
tient
str
eate
dsu
rgic
ally
for
intr
acra
nial
hem
atom
asto
asse
sspr
ogno
stic
fact
ors
rela
ted
toG
OS
at6
mo.
Asu
bgro
upof
35pa
tient
sw
ithIC
His
incl
uded
.
●Po
stre
susc
itatio
nG
CS,
preo
pera
tive
chan
gein
pupi
llary
size
,N
o.of
oper
atio
ns,
No.
ofhe
mat
omas
,an
dty
peof
lesi
onw
ere
sign
ifica
ntly
rela
ted
tosu
rgic
alou
tcom
e.●
Goo
dou
tcom
e:si
ngle
,ev
acua
ted
EDH
�IC
H�
SDH
.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Acu
teIC
H,
evac
uate
d35
6022
.98.
62.
85.
7
Yam
aki
etal
.(6
9)48
IIIU
nkno
wn
Surg
ery
and
nons
urgi
cal
GO
S;tim
eof
max
imal
hem
atom
adi
amet
er
Ret
rosp
ectiv
ere
view
of48
patie
nts
with
trau
mat
icIC
H�
3-cm
diam
eter
who
sefir
stC
Toc
curr
edw
ithin
6h
ofin
jury
toev
alua
teth
etim
ing
ofhe
mat
oma
evol
utio
nan
dto
asse
ssou
tcom
e.C
Tsc
ans
of32
nono
pera
ted
patie
nts
wer
eus
edto
asse
ssna
tura
lhi
stor
yof
hem
atom
aev
olut
ion.
●A
llIC
H�
3-cm
diam
eter
deve
lope
dw
ithin
24h
ofin
jury
.●
Onl
y56
%of
ICH
�3-
cmdi
amet
erde
velo
ped
with
in6
hof
inju
ry.
●IC
Hre
ache
dm
axim
alsi
zein
84%
ofpa
tient
sw
ithin
12h.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
ICH
,to
tal
5853
142
328
ICH
,op
erat
ed26
358
47
46N
o.of
pati
ents
GR
(%)
Non
oper
ated
3213
Ope
rate
d26
46A
dmitt
edim
med
iate
lyaf
ter
TBI
1631
Adm
itted
�6
haf
ter
TBI
1070
You
nget
al.
(72)
15III
Gra
dyC
oma
Scal
e1–
5
Surg
ery
Mod
ified
GO
S,no
tsp
ecifi
edR
etro
spec
tive
seri
esaf
ter
intr
oduc
tion
ofC
Tof
15pa
tient
str
eate
dsu
rgic
ally
for
DTI
CH
toex
amin
ecl
inic
alan
dra
diol
ogic
corr
elat
es,
and
tore
late
clin
ical
stat
usto
outc
ome.
●M
orbi
dity
/mor
talit
yas
soci
ated
with
com
asc
ore
onad
mis
sion
(no
stat
istic
s).
●80
%oc
cipi
tal/p
arie
tooc
cipi
tal
impa
ct;
cont
reco
upfr
onto
tem
pora
lle
sion
s.●
Def
initi
onof
DTI
CH
:de
velo
psin
area
ofpr
evio
usco
ntus
ion.
No.
ofpa
tien
tsIn
tact
(%)
Mild
disa
bilit
y(%
)
Sign
ifica
ntdi
sabi
lity
(%)
D(%
)
Gra
dy1–
26
83.3
16.7
00
Gra
dy3–
49
00
22.2
77.8
DTI
CH
,to
tal
1533
.36.
713
.346
.7
Zum
kelle
ret
al.
(73)
53III
GC
S�
5to
11–1
5Su
rger
yan
dno
nsur
gica
lPo
orve
rsus
good
,no
tsp
ecifi
ed
Ret
rosp
ectiv
ese
ries
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tient
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ithIC
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who
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esen
ted
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mat
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ive
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rativ
etr
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ent
with
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ome.
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ost
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tical
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renc
ein
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ome
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dbe
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edan
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rate
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.
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ood
(%)
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Ope
rate
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ated
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.959
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ngle
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ed17
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race
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geta
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edi
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lity;
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,del
ayed
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mat
icin
trac
ereb
ralh
emat
oma;
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,sub
dura
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atom
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otsi
gnifi
cant
;FIM
,fun
ctio
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ende
nce
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sure
;ED
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ural
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atom
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oss
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ess;
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raum
atic
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ata
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k;SE
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mat
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oked
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on;
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mat
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ain
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bara
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e;IV
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aven
tric
ular
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orrh
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P,ar
teri
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ood
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sure
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lar
tery
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sure
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U,
inte
nsiv
eca
reun
it;O
R,
oper
atio
n.
CHAPTER 6
SURGICAL MANAGEMENT OF POSTERIOR FOSSA
MASS LESIONSM. Ross Bullock, M.D., Ph.D.Department of Neurological Surgery,Virginia Commonwealth UniversityMedical Center,Richmond, Virginia
Randall Chesnut, M.D.Department of Neurological Surgery,University of WashingtonSchool of Medicine,Harborview Medical Center,Seattle, Washington
Jamshid Ghajar, M.D., Ph.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David Gordon, M.D.Department of Neurological Surgery,Montefiore Medical Center,Bronx, New York
Roger Hartl, M.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David W. Newell, M.D.Department of Neurological Surgery,Swedish Medical Center,Seattle, Washington
Franco Servadei, M.D.Department of Neurological Surgery,M. Bufalini Hospital,Cesena, Italy
Beverly C. Walters, M.D., M.Sc.Department of Neurological Surgery,New York UniversitySchool of Medicine,New York, New York
Jack Wilberger, M.D.Department of Neurological Surgery,Allegheny General Hospital,Pittsburgh, Pennsylvania
Reprints requests:Jamshid Ghajar, M.D., Ph.D.,Brain Trauma Foundation,523 East 72nd Street,New York, NY 10021.Email: [email protected]
RECOMMENDATIONS(see Methodology)
Indications• Patients with mass effect on computed tomographic (CT) scan or with neurological
dysfunction or deterioration referable to the lesion should undergo operative inter-vention. Mass effect on CT scan is defined as distortion, dislocation, or obliterationof the fourth ventricle; compression or loss of visualization of the basal cisterns, orthe presence of obstructive hydrocephalus.
• Patients with lesions and no significant mass effect on CT scan and without signs ofneurological dysfunction may be managed by close observation and serial imaging.
Timing• In patients with indications for surgical intervention, evacuation should be performed as
soon as possible because these patients can deteriorate rapidly, thus, worsening theirprognosis.
Methods• Suboccipital craniectomy is the predominant method reported for evacuation of
posterior fossa mass lesions, and is therefore recommended.
KEY WORDS: Cerebellum, Coma, Computed tomographic parameters, Contusion, Head injury, Occipital,Posterior fossa, Surgical technique, Timing of surgery, Traumatic brain injury
Neurosurgery 58:S2-47-S2-55, 2006 DOI: 10.1227/01.NEU.0000210366.36914.38 www.neurosurgery-online.com
OVERVIEW
Posterior fossa injury is rare, occurring in lessthan 3% of head injuries in most published series(8, 12, 22). The vast majority of these series dealexclusively with posterior fossa epidural hemato-mas (EDH), representing 1.2 to 12.9% of all EDH(7, 20, 21, 30). A small number of observationalstudies address subdural and intraparenchymalhematomas of the posterior fossa (5, 8, 17, 22, 24),representing 0.5 to 2.5% and 1.7% of all subduralhematomas and intraparenchymal hematomas,respectively (22, 24). Additionally, there is a sepa-rate literature that focuses on parturitional hemor-rhages, up to 48% of which primarily involve theposterior fossa (27). Because of the physiology andanatomy of the neonate, and the unique mecha-nism of these injuries, this subgroup of patientswarrants independent analysis, and will not beaddressed in these Guidelines.
Despite the rarity of these lesions, the impor-tance of timely recognition and surgical evacu-
ation, when indicated, cannot be overstated.Many patients can undergo rapid clinical dete-rioration because of the limited size of the pos-terior fossa and the propensity for these lesionsto produce brainstem compression.
PROCESS
A MEDLINE computer search using the fol-lowing key words: “posterior fossa” or “cerebel-lum” or “cerebellar” or “occipital” and “sub-dural” or “epidural” or “extradural” or“intradural” or “parenchymal” or “intraparen-chymal” or “intracerebellar” or “fracture” be-tween 1975 and 2001 was performed. A total of1828 documents were found. The search wasnarrowed to include the key words: “surgery”or “operative” or “craniotomy” or “craniec-tomy” or “decompressive craniectomy” or “re-pair” and “trauma” or “traumatic” or “TBI” or“CHI.” A total of 430 articles were found. Atertiary search adding the key words “contu-
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-47
sion,” “hemorrhagic contusion,” “surgical decompression,” “cra-niostomy,” “TICH,” and “DTICH” was performed, yielding 421articles. The secondary and tertiary searches were combined,yielding a total of 433 articles. In addition, the reference lists ofselected articles were reviewed, and 24 articles were selected forcritical analysis. The results of this analysis were incorporatedinto the review presented here. Papers primarily addressing thefollowing topics were not included: nontraumatic lesions, pa-tients with associated posterior fossa anomalies (e.g., Chiari mal-formation), posttraumatic aneurysms, chronic subdural hemato-mas, vertebral artery dissection, patients undergoinganticoagulation therapy, patients with associated illnesses (e.g.,acquired immunodeficiency syndrome, idiopathic thrombocyto-penia purpura, hemophilia, arteriovenous malformation, aftercraniotomy, or von Willebrand’s disease), pre-CT era reports,and book chapters. In general, papers with the following char-acteristics were also excluded: case series with less than 10 pa-tients evaluated by CT scan and with incomplete outcome data(mortality or Glasgow outcome score [GOS]), case reports, andoperative series with operations occurring longer than 14 daysfrom injury. Several articles with case series of less than 10patients were examined and reviewed because of the limitednumber of patient series evaluating primary traumatic posteriorfossa mass lesions that exist in the literature. Selected articleswere evaluated for design, prognostic significance, therapeuticefficacy, and overall outcome. In addition, several articles werereviewed for the purposes of historical perspective.
SCIENTIFIC FOUNDATION
Because of the rapid and life-threatening nature of neuro-logical deterioration secondary to expanding mass lesions inthe limited compartment of the posterior fossa, surgery isgenerally viewed as required therapy in symptomatic patientswith progressive dysfunction. Because of the potential adverseconsequences of withholding or delaying surgery for such pa-tients, studies depend on retrospective analyses. As a result,there is no Class I or Class II evidence to support recommenda-tions for the surgical management of these injuries. However, thepredominantly observational studies that were reviewed yieldan important and relatively clear picture of the prognosis for thepatient with a posterior fossa mass lesion as patients are cur-rently managed. Admission Glasgow Coma Scale (GCS) score (5,7, 8, 12, 24, 26) and GCS score at surgery (6, 14, 19, 20, 22)correlate with outcome (GOS and mortality). D’Avella et al. (5)retrospectively reviewed the clinical and radiographic character-istics of 81 patients with traumatic intracerebellar hemorrhages.Subjecting their data to multivariate analysis, they found thatonly GCS and the presence of concomitant supratentorial lesionsindependently predicted outcome at 6 months. Outcome wasfavorable (GOS, 4 or 5) in 95% of patients with admission GCSscore of at least 8, whereas outcome was poor (GOS, 1–3) in 81%of patients with a GCS score less than 8. Class III data suggeststhat a neurologically deteriorating patient should undergo emer-gent evacuation of the mass lesion.
Neurologically intact patients with a posterior fossa lesionand no CT evidence for mass effect (compression of cisterns,distortion of 4th ventricle, hydrocephalus) have been success-fully managed nonoperatively with close observation and se-rial imaging (1, 5, 15, 25, 28).
Wong (28) conducted a retrospective study of 25 patientswith posterior fossa EDH and compared clinical and radiolog-ical characteristics and outcomes between 17 patients under-going early surgery and 8 patients managed nonoperatively.Patients with a posterior fossa EDH of at most 10 cm3 involume, at most 15 mm in thickness, and responsible for atmost a 5-mm midline shift had excellent survival rates witheither surgical or nonsurgical treatment. Patients managednonsurgically with a posterior fossa EDH greater than 10 cm3
in volume, greater than 15 mm in thickness, and responsiblefor greater than 5 mm of midline shift had a significantlygreater mortality than those with similar CT characteristicsundergoing early surgery. The disparity in mortality, how-ever, is confounded by the strong correlation between thepresence of an associated frontal lesion (which was foundmore commonly in the latter group) and death. This reportraises the concept of conservative management for patientswith posterior fossa lesions on the basis of objective CT char-acteristics. This concept is also supported by a two-centerstudy performed by Bozbuga et al. (1). The authors dividedpatients into management groups on the basis of CT charac-teristics. All patients (n � 14) without evidence of mass effecton CT scan, defined by obliteration of the perimesencephaliccisterns, compression and/or displacement of the fourth ven-tricle, or the presence of hydrocephalus, were managed non-operatively and had a good outcome (GOS, 5). According tothe authors, these objective criteria were “earlier, more pre-dictive, and more reliable” than the clinical findings, althoughno statistics regarding this statement were performed. Severalother case series add additional support (9, 16, 25).
There are several prognostic factors that adversely affectoutcome regardless of management. These include the pres-ence of associated intracranial lesions ( 4, 5, 12, 14, 18–22, 24,28), extension of an infratentorial lesion into the supratentorialcompartment (19), the location of the lesion (e.g., intraparen-chymal versus extra-axial, and midline versus hemispheric)(17, 22), the presence or absence of associated hydrocephalus(7, 8, 14), and the acuity of presentation, with subacute pre-sentation portending a better outcome than acute presentation(4, 14, 19, 23–25). There are no controlled studies measuringthe impact of these variables on surgical versus nonsurgicalmanagement of posterior fossa mass lesions.
SUMMARY
There are no controlled, prospective clinical trials of treat-ment using surgical versus nonsurgical management of pos-terior fossa mass lesions. The available data support rapidevacuation of posterior fossa mass lesions that 1) show CTevidence of mass effect, or 2) result in progressive neurologicaldysfunction. Moreover, data support expectant management
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-48 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
with serial imaging for select cases in which there is neuro-logical stability and no radiological evidence for mass effect.
KEY ISSUES FOR FUTURE INVESTIGATION
There are several patient groups in which the distinction be-tween surgical and conservative management is blurred. Onesuch group includes patients who present with neurologicaldeficit and a traumatic posterior fossa mass lesion without clin-ical evidence for neurological deterioration or radiological evi-dence for mass effect. Conversely, another group includes theneurologically intact patient with radiological evidence for masseffect from an offending hematoma. These groups have not beenadequately addressed in the current literature, and, when re-ported, are managed at the discretion of the individual neuro-surgeon, thus, precluding an accurate assessment of efficacy oftreatment. The literature contains methodological problems out-lined in this supplement that preclude the establishment of man-agement standards, and even of treatment guidelines, for poste-rior fossa injury. Most series present prognostic data regardingoutcome after either conservative or surgical treatment of poste-rior fossa mass lesions. In those few studies that attempt tocompare outcomes, important prognostic factors known to berelevant to TBI outcome, such as cardiorespiratory instability,other systemic injuries, comorbidities, etc. (2), are not controlledbetween the surgical and nonsurgical cohorts. As a result, wehave important prognostic information regarding operativelyand nonoperatively managed posterior fossa injury, but nomeans for valid, direct comparison between the two. This com-parison is essential if we are attempting to establish a standard ofcare. Thus, attention needs to be directed to controlled studies ofpatients with similar CT and clinical characteristics who aremanaged with operative versus nonoperative intervention.
REFERENCES
1. Bozbuga M, Izgi N, Polat G, Gurel I: Posterior fossa epidural hematomas:Observations on a series of 73 cases. Neurosurg Rev 22:34–40, 1999.
2. Brain Trauma Foundation, American Association of Neurological Surgeons,Joint Section on Neurotrauma and Critical Care: Guidelines for the manage-ment of severe traumatic brain injury. J Neurotrauma 17:457–462, 2000.
3. Brambilla G, Rainoldi F, Gipponi D, Paoletti P: Extradural haematoma of theposterior fossa: A report of eight cases and a review of the literature. ActaNeurochir (Wien) 80:24–29, 1986.
4. Ciurea AV, Nuteanu L, Simionescu N, Georgescu S: Posterior fossa extra-dural hematomas in children: Report of nine cases. Childs Nerv Syst 9:224–228, 1993.
5. d’Avella D, Servadei F, Scerrati M, Tomei G, Brambilla G, Angileri FF,Massaro F, Cristofori L, Tartara F, Pozzati E, Bruni P, Delfini R, TomaselloF: Traumatic intracerebellar hemorrhages: A clinicoradiological analysis of81 cases. Neurosurgery 50:16–25, 2002.
6. Ersahin Y, Mutluer S: Posterior fossa extradural hematomas in children.Pediatr Neurosurg 19:31–33, 1993.
7. Holzschuh M, Schuknecht B: Traumatic epidural haematomas of the poste-rior fossa: 20 new cases and a review of the literature since 1961. BrJ Neurosurg 3:171–180, 1989.
8. Karasawa H, Furuya H, Naito H, Sugiyama K, Ueno J, Kin H: Acutehydrocephalus in posterior fossa injury. J Neurosurg 86:629–632, 1997.
9. Kawakami Y, Tamiya T, Tanimoto T, Shimamura Y, Hattori S, Ueda T,Ishida T: Nonsurgical treatment of posterior fossa epidural hematoma.Pediatr Neurol 6:112–118, 1990.
10. Koc RK, Pasaoglu A, Menku A, Oktem S, Meral M: Extradural hematoma ofthe posterior cranial fossa. Neurosurg Rev 21:52–57, 1998.
11. Lui T, Lee S, Chang C, Cheng W: Epidural hematomas in the posteriorcranial fossa. J Trauma 34:211–215, 1993.
12. Mahajan R, Sharma B, Khosla V, Tewari M, Mathuriya S, Pathak A, Kak V:Posterior fossa extradural haematoma—Experience of nineteen cases. AnnAcad Med Singapore 22:410–413, 1993.
13. Mohanty A, Kolluri V, Subbakrishna D, Satish S, Mouli B, Das B: Prognosisof extradural haematomas in children. Pediatr Neurosurg 23:57–63, 1995.
14. Neubauer UJ: Extradural haematoma of the posterior fossa. Twelve yearsexperiences with CT-scan. Acta Neurochir (Wien) 87:105–111, 1987.
15. Otsuka S, Nakatsu S, Matsumoto S, Sato S, Motozaki T, Ban S, Yamamoto T:Study on cases with posterior fossa epidural hematoma—Clinical featuresand indications for operation. Neurol Med Chir (Tokyo) 30:24–28, 1990.
16. Pang D, Horton J, Herron J, Wilberger JJ, Vries J: Nonsurgical managementof extradural hematomas in children. J Neurosurg 59:958–971, 1983.
17. Pozzati E, Grossi C, Padovani R: Traumatic intracerebellar hematomas. JNeurosurg 56:691–694, 1982.
18. Pozzati E, Tognetti F, Cavallo M, Acciarri N: Extradural hematomas of theposterior cranial fossa. Observations on a series of 32 consecutive casestreated after the introduction of computed tomography scanning. SurgNeurol 32:300–303, 1989.
19. Prusty GK, Mohanty A: Posterior fossa extradural haematoma. J IndianMed Assoc 93:255–258, 1995.
20. Rivano C, Altomonte M, Capuzzo T, Borzone M: Traumatic posterior fossaextradural hematomas. A report of 22 new cases surgically treated and areview of the literature. Zentralbl Neurochir 52:77–82, 1991.
21. Roda J, Gimenez D, Perez-Higueras A, Blazquez M, Perez-Alvarez M:Posterior fossa epidural hematomas: A review and synthesis. Surg Neurol19:419–424, 1983.
22. Sripairojkul B, Saeheng S, Ratanalert S, Pheunpathom N, Sriplung H: Trau-matic hematomas of the posterior cranial fossa. J Med Assoc Thai 81:153–159, 1998.
23. St John JN, French BN: Traumatic hematomas of the posterior fossa. Aclinicopathological spectrum. Surg Neurol 25:457–466, 1986.
24. Tsai FY, Teal JS, Itabashi HH, Huprich JE, Hieshima GB, Segall HD: Com-puted tomography of posterior fossa trauma. J Comput Assist Tomogr4:291–305, 1980.
25. Vrankovic DJ, Splavski B, Hecimovic I, Kristek B: Acute traumatic hemato-mas of the posterior fossa: Experience with eleven cases. Neurol Croat43:21–30, 1994.
26. Wang EC, Lim AY, Yeo TT: Traumatic posterior fossa extraduralhaematomas (PFEDH). Singapore Med J 39:107–111, 1998.
27. Welch K, Strand R: Traumatic parturitional intracranial hemorrhage. DevMed Child Neurol 28:156–164, 1986.
28. Wong CW: The CT criteria for conservative treatment—but under closeclinical observation—of posterior fossa epidural haematomas. ActaNeurochir (Wien) 126:124–127, 1994.
29. Zuccarello M, Andrioli G, Fiore D, Longatti P, Pardatscher K, Zampieri P:Traumatic posterior fossa haemorrhage in children. Acta Neurochir (Wien)62:79–85, 1982.
30. Zuccarello M, Pardatscher K, Andrioli GC, Fiore DL, Iavicoli R, Cervellini P:Epidural hematomas of the posterior cranial fossa. Neurosurgery 8:434–437,1981.
POSTERIOR FOSSA MASS LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-49
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
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TAB
LE1.
Surg
ical
man
agem
ent
ofpo
ster
ior
foss
am
ass
lesi
onsa
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Boz
buga
etal
.(1
)73
IIIU
nkno
wn
Surg
ery
and
nons
urgi
cal
GO
S,no
tsp
ecifi
edPr
ospe
ctiv
est
udy
of73
patie
nts
with
PFED
Hm
anag
edby
CT
crite
ria
eith
ersu
rgic
ally
orno
nsur
gica
llyba
sed
onpr
esen
ceof
sign
sof
mas
sef
fect
onC
T.
●Pa
tient
sw
ithPF
EDH
and
noas
soci
ated
CT
evid
ence
for
mas
sef
fect
may
bem
anag
edef
fect
ivel
yw
ithou
tsu
rger
y.●
No
patie
ntw
ithm
ass
effe
cton
CT
was
man
aged
nons
urgi
cally
,th
us,
prec
ludi
ngdi
rect
com
pari
son
betw
een
grou
ps.
●N
om
orbi
dity
orm
orta
lity
insu
bacu
teca
ses
(pre
sent
atio
n24
h–7
d).
No.
ofpa
tien
tsG
R(%
)M
D(%
)D
(%)
Non
surg
ical
1410
00
0
Surg
ical
5986
77
Acu
te(�
24h)
5485
77
Suba
cute
(24
h–7
d)19
100
00
Bra
mbi
llaet
al.
(3)
8III
GC
S4
–15
Surg
ery
Dea
thve
rsus
com
plet
ere
cove
ry,
not
spec
ified
Ret
rosp
ectiv
ese
ries
of8
patie
nts
surg
ical
lytr
eate
dfo
rPF
EDH
toev
alua
tecl
inic
alch
arac
teri
stic
san
dou
tcom
e.
●A
utho
rsem
phas
ize
high
mor
talit
yra
teth
ough
tse
cond
ary
toco
ncom
itant
brai
nste
man
dba
sal
gang
liain
jury
seen
atau
tops
y.*N
ote:
pape
rin
clud
edw
ithn
�8
beca
use
oflim
ited
num
ber
ofca
sese
ries
with
�10
patie
nts.
No.
ofpa
tien
tsG
R(%
)D
(%)
PFED
H8
62.5
37.5
Ciu
rea
etal
.(4
)9
IIIG
CS
13–1
4Su
rger
yG
OS,
not
spec
ified
Ret
rosp
ectiv
ese
ries
of9
patie
nts
aged
2–12
ysu
rgic
ally
trea
ted
for
PFED
Hto
eval
uate
clin
ical
char
acte
rist
ics
and
outc
ome.
●Su
bacu
tepr
esen
tatio
npr
edom
inat
ed(8
8.8%
)an
d,th
us,
may
have
bias
edou
tcom
eda
ta.
●A
ssoc
iate
din
trac
rani
alin
juri
esse
emed
asso
ciat
edw
ithw
orse
outc
ome
(no
stat
istic
s).
Not
e:pa
per
incl
uded
with
n�
9be
caus
eof
limite
dnu
mbe
rof
case
seri
esw
ith�
10pa
tient
s.
No.
ofpa
tien
tsG
R(%
)M
D(%
)
PFED
H9
8911
PFED
H�
asso
ciat
edle
sion
475
25
d’A
vella
etal
.(5
)81
IIIG
CS
3–5
to14
–15
Surg
ery
and
nons
urgi
cal
GO
S6
mo
Ret
rosp
ectiv
ese
ries
of81
patie
nts
with
trau
mat
icin
trac
ereb
ella
rhe
mor
rhag
e/co
ntus
ion
toev
alua
tepr
ogno
stic
fact
ors
and
exam
ine
clin
icor
adio
logi
cal
pres
enta
tion.
●44
.4%
poor
resu
lt(G
OS
1–3)
;55
.6%
favo
rabl
ere
sult
(GO
S4
–5).
●G
CS,
pres
ence
ofsu
prat
ento
rial
lesi
on,
stat
usof
basa
lci
ster
nsan
dfo
urth
vent
ricl
e,m
echa
nism
ofin
jury
,an
dcl
otsi
zeco
rrel
ated
with
outc
ome.
●G
CS
and
pres
ence
ofco
ncom
itant
supr
aten
tori
alle
sion
wer
ein
depe
nden
tpr
ogno
stic
fact
ors.
●9.
4tim
esre
lativ
eri
skof
poor
outc
ome
with
GC
S�
8.
●2.
3tim
esre
lativ
eri
skof
poor
outc
ome
with
asso
ciat
edsu
prat
ento
rial
lesi
on.
●Tr
aum
atic
intr
acer
ebel
lar
clot
sob
serv
edto
incr
ease
insi
zeup
to4
daf
ter
inju
ry—
auth
ors
advo
cate
repe
atC
Tsc
ans
until
lesi
onst
abili
zes.
●A
utho
rsre
com
men
dsu
rger
yfo
rpa
tient
sw
ithla
rger
clot
sca
usin
gpo
ster
ior
foss
am
ass
effe
ct.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
Intr
acer
ebel
lar
hem
orrh
age/
cont
usio
n,to
tal
8155
.644
.4
GC
S�
839
946
GC
S�
8b42
1981
OR
c27
4852
bP
�0.
000,
cP
�n.
s.
Hol
zsch
uhan
dSc
hukn
echt
(7)
20III
GC
S3–
15Su
rger
yG
OS
6m
oR
etro
spec
tive
seri
esof
20pa
tient
ssu
rgic
ally
trea
ted
for
PFED
Hto
eval
uate
clin
ical
and
radi
olog
icch
arac
teri
stic
san
dou
tcom
e.
●G
CS
corr
elat
edw
ithG
OS
(no
stat
istic
s)●
Mor
talit
yof
acut
e(�
24h)
and
suba
cute
(24
h–7
d)ca
ses
was
50%
and
20%
,re
spec
tivel
y.●
Aut
hors
emph
asiz
eim
port
ance
ofC
Tfo
rpa
tient
sw
ithsi
gns
ofoc
cipi
tal
trau
ma
todi
agno
sePF
EDH
befo
recl
inic
alde
teri
orat
ion.
Not
e:C
Tin
18/2
0ca
ses.
No.
ofpa
tien
tsG
R(%
)M
D(%
)D
(%)
PFED
H,
tota
l20
4520
35
GC
S15
–14
210
00
0
GC
S13
–8
862
.512
.525
GC
S7–
310
2030
50
Acu
te(�
24h)
1428
.621
.450
Suba
cute
(24
h–7
d)5
6020
20
Chr
onic
(�7
d)1
100
00
POSTERIOR FOSSA MASS LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-51
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Kar
asaw
aet
al.
(8)
53III
GC
S3–
8to
13–1
5Su
rger
yan
dno
nsur
gica
lG
OS
atdi
scha
rge
Ret
rosp
ectiv
ese
ries
of53
patie
nts
with
post
erio
rfo
ssa
inju
ryco
mpa
ring
thos
ew
ithan
dw
ithou
tas
soci
ated
HC
Pto
eval
uate
CT
fact
ors
asso
ciat
edw
ithth
ede
velo
pmen
tof
HC
Pan
dth
edi
ffere
nces
inou
tcom
ebe
twee
nsu
bgro
ups
with
and
with
out
HC
P.
●Su
prat
ento
rial
exte
nsio
n,he
mat
oma
thic
knes
s�
15m
m,
and
abno
rmal
mes
ence
phal
icci
ster
nsw
ere
sign
ifica
ntly
asso
ciat
edw
ithH
CP
(P�
0.05
).●
Bila
tera
lle
sion
san
din
abili
tyto
visu
aliz
eth
efo
urth
vent
ricl
ew
ere
sign
ifica
ntly
asso
ciat
edw
ithH
CP
inin
trac
ereb
ella
rhe
mat
oma/
cont
usio
n.●
No
sign
ifica
ntdi
ffere
nce
inm
orta
lity
betw
een
patie
nts
with
PFED
Hw
ithor
with
out
HC
P.●
HC
Pin
crea
sed
mor
talit
yin
patie
nts
with
ICH
/con
tusi
on(1
00%
vers
us15
.4%
;P
�0.
05).
●Su
rger
ydi
dno
tal
ter
mor
talit
yin
patie
nts
with
asso
ciat
edH
CP,
thou
ghnu
mbe
rof
patie
nts
was
too
smal
lfo
rco
mpa
riso
n.
●A
dmis
sion
GC
Sw
asin
vers
ely
rela
ted
tom
orta
lity
(P�
n.s.
).
●A
utho
rsad
voca
teex
tern
alve
ntri
cula
rdr
aina
gein
patie
nts
with
ICH
/con
tusi
onan
dH
CP,
not
with
PFED
H.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Post
erio
rfo
ssa
inju
ry,
tota
l53
747
22
15
EDH
2588
80
04
ICH
/con
tusi
on13
46.2
07.
77.
738
.5
SAH
710
00
00
0
SDH
580
00
020
Bra
inst
emhe
mor
rhag
e3
066
.70
033
.3
EDH
�su
rger
y�
HC
P7
8614
00
0
EDH
�su
rger
y,no
HC
P7
7114
00
14
ICH
�su
rger
y�
HC
P2
00
00
100
ICH
�su
rger
y,no
HC
P1
100
00
00
HC
P�
surg
ery
966
.711
.10
022
.2
HC
P,no
surg
ery
366
.70
00
33.3
Koc
etal
.(1
0)11
IIIG
CS
7–15
Surg
ery
GC
Sat
disc
harg
eR
etro
spec
tive
seri
esof
14pa
tient
s(1
1w
ithC
Tsc
ans)
trea
ted
surg
ical
lyfo
rPF
EDH
toex
amin
ecl
inic
alan
dra
diol
ogic
feat
ures
and
toas
sess
outc
ome.
●A
utho
rsre
port
that
lesi
onsi
ze,
pres
ence
ofco
exis
ting
intr
acra
nial
lesi
ons,
and
incr
easi
ngag
ear
eno
tas
soci
ated
with
prog
nosi
s,ho
wev
er,
all
mor
bidi
tyan
dm
orta
lity
occu
rred
inpa
tient
sw
ithou
tC
Tsc
ans.
No.
ofpa
tien
tsG
R(%
)D
(%)
PFED
Hw
ithC
T11
100
0
Lui
etal
.(1
1)89
IIIA
llG
CS
Surg
ery
GO
S,1
yr;
mor
talit
y,1
wk
Ret
rosp
ectiv
ere
view
of89
patie
nts
trea
ted
surg
ical
lyfo
rPF
EDH
toev
alua
teou
tcom
ere
late
dto
CT
char
acte
rist
ics,
age,
GC
S.
●M
orta
lity
17.9
%.
●M
orta
lity
inve
rsel
yre
late
dto
GC
Sbe
fore
surg
ery.
●A
ge�
16yr
asso
ciat
edw
ithde
crea
sed
mor
talit
y.
●Pr
esen
ceof
mix
edle
sion
(i.e.
,ex
tens
ion
into
occi
pita
lre
gion
)an
dco
ncom
itant
,no
ncon
tiguo
ussu
prat
ento
rial
lesi
onas
soci
ated
with
incr
ease
dm
orta
lity.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
PFED
H,
tota
l89
74.2
5.6
1.1
1.1
17.9
GC
S(s
urge
ry)
3–5
1764
.7
GC
S6
–8
195.
2
GC
S9
–12
2913
.8
GC
S13
–15
240
Age
�16
yr29
10.3
Age
�16
yr60
21.7
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-52 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Mah
ajan
etal
.(1
2)19
IIIG
CS
�7
to13
–15
Surg
ery
GO
S,no
tsp
ecifi
edR
etro
spec
tive
seri
esof
19pa
tient
str
eate
dsu
rgic
ally
for
PFED
Hto
exam
ine
clin
ical
char
acte
rist
ics
and
outc
ome.
●M
orta
lity
15.8
%.
●A
dmis
sion
GC
Sco
rrel
ated
with
outc
ome
(no
stat
istic
s).
●B
oth
patie
nts
with
conc
omita
ntsu
prat
ento
rial
intr
acra
nial
lesi
ons
died
.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
PFED
H,
tota
l19
57.9
26.3
00
15.8
GC
S(a
dmis
sion
)15
–13
710
00
00
0
GC
S12
–8
757
.128
.60
014
.3
GC
S7–
35
060
00
40
Moh
anty
etal
.(1
3)24
IIIG
CS
3–5
to13
–15
Surg
ery
GO
Sat
disc
harg
eR
etro
spec
tive
seri
esof
489
patie
nts
with
surg
ical
lyev
acua
ted
EDH
com
pari
ngpr
ogno
sis
betw
een
child
ren
and
adul
tsan
dev
alua
ting
diffe
renc
ein
asso
ciat
edcl
inic
alpa
ram
eter
sbe
twee
nch
ildre
nan
dad
ults
.A
subg
roup
of24
patie
nts
with
surg
ical
lytr
eate
dPF
EDH
isin
clud
ed.
●In
cide
nce
ofPF
EDH
/ED
Hhi
gher
inch
ildre
nve
rsus
adul
ts(1
1%ve
rsus
3%).
●PF
EDH
had
bette
rou
tcom
eve
rsus
supr
aten
tori
alED
Hin
both
age
grou
ps(n
ost
atis
tics)
.
No.
ofpa
tien
tsG
R/M
D(%
)SD
/VS/
D(%
)
PFED
H,
tota
l24
87.5
12.5
age
�15
yr11
919
age
�16
yr13
8515
Neu
baue
r(1
4)18
IIIG
CS
3–14
Surg
ery
GO
Sno
tsp
ecifi
edR
etro
spec
tive
seri
esof
18pa
tient
ssu
rgic
ally
trea
ted
for
PFED
Hto
eval
uate
outc
ome
rela
tive
toac
uity
ofpr
esen
tatio
n,pr
esen
ceof
hydr
ocep
halu
s,an
dpr
esen
ceof
asso
ciat
edle
sion
s.
●M
orta
lity
22%
—al
lpr
esen
ted
with
acut
eco
urse
.●
GC
Sim
med
iate
lybe
fore
surg
ery,
acut
epr
esen
tatio
n,an
dpr
esen
ceof
hydr
ocep
halu
sse
emed
toco
rrel
ate
with
mor
talit
y(n
ost
atis
tics)
.●
Con
com
itant
lesi
ons
did
not
alte
rm
orta
lity
but
corr
elat
edw
ithin
crea
sed
disa
bilit
y(n
ost
atis
tics)
.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
PFED
H,
tota
l18
5511
5.5
5.5
22
With
asso
ciat
edle
sion
825
2512
.512
.525
No
asso
ciat
edle
sion
1080
00
020
Acu
te(�
24h)
1040
Suba
cute
(2–7
d)8
0
With
HC
P6
33
No
HC
P12
16
Ots
uka
etal
.(1
5)11
IIIA
llG
CS
Surg
ery
and
nons
urgi
cal
GO
Sat
disc
harg
eR
etro
spec
tive
seri
esof
11pa
tient
sw
ithPF
EDH
toev
alua
tecl
inic
alan
dra
diol
ogic
feat
ures
,an
dto
com
pare
outc
ome
betw
een
oper
ated
and
nono
pera
ted
grou
ps.
●M
orta
lity
18.2
%.
●O
utco
me
was
sim
ilar
betw
een
grou
psw
hen
surg
ical
indi
catio
nsw
ere
dete
rior
atio
n/no
nim
prov
emen
tof
neur
olog
ical
sign
san
dsy
mpt
oms
ofhe
adac
he,
naus
ea,
and
vom
iting
inpr
esen
ceof
CT
para
met
ers
ofm
axim
alhe
mat
oma
thic
knes
s�
15m
m,
poor
visu
aliz
atio
nof
post
erio
rfo
ssa
cist
erns
,m
arke
dde
form
ity/d
ispl
acem
ent
ofIV
vent
ricl
e,an
dex
tens
ion
ofPF
EDH
into
supr
aten
tori
alre
gion
(no
stat
istic
s).
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Surg
ery
666
.716
.70
016
.7
Non
surg
ical
580
00
020
Pozz
ati
etal
.(1
7)32
IIIG
CS
�7
to14
(14
poin
tsc
ale)
Surg
ery
(n�
30)
and
nons
urgi
cal
(n�
2)
Mod
ified
GO
S,no
tsp
ecifi
ed
Ret
rosp
ectiv
ese
ries
of32
patie
nts
with
PFED
H,
30of
who
mun
derw
ent
surg
ery,
toev
alua
tecl
inic
alch
arac
teri
stic
san
dou
tcom
e.
●M
orta
lity,
15.6
%.
●Pr
esen
ceof
asso
ciat
edin
trac
rani
alle
sion
corr
elat
esw
ithpo
orou
tcom
e(i.
e.,
disa
bilit
y,m
orta
lity)
com
pare
dw
ith“p
ure”
PFED
H(n
ost
atis
tics)
.
●A
llpa
tient
sw
ithG
OS
�5
had
asso
ciat
edle
sion
s.
●N
onsu
rgic
alm
anag
emen
tw
assu
cces
sful
in2
patie
nts
with
smal
lcl
ots.
No.
ofpa
tien
tsG
R(%
)D
isab
led
(%)
D(%
)
Pure
PFED
H,
oper
ated
1410
00
0
Ass
ocia
ted
lesi
on,
oper
ated
1650
18.8
31.3
Smal
l,no
nsur
gica
l2
100
00
POSTERIOR FOSSA MASS LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-53
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Pozz
ati
etal
.(1
8)7
IIIG
CS
5–11
Surg
ery
and
nons
urgi
cal
GO
Sat
disc
harg
eR
etro
spec
tive
seri
esof
7pa
tient
sto
exam
ine
the
role
ofC
Tin
cons
erva
tive
vers
ussu
rgic
altr
eatm
ent
ofis
olat
edin
trac
ereb
ella
rhe
mat
oma.
●Po
orer
outc
ome
was
asso
ciat
edw
ithm
idlin
eve
rsus
hem
isph
eric
clot
s(n
ost
atis
tics)
.
●C
Tal
low
edsu
cces
sful
cons
erva
tive
man
agem
ent
ofse
lect
edpa
tient
s.
●N
ogo
odou
tcom
ew
asac
hiev
edw
ithcl
ot�
3cm
.N
ote:
pape
rin
clud
edw
ithn
�7
beca
use
oflim
ited
num
ber
ofca
sese
ries
with
�10
patie
nts.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Mid
line
clot
30
00
010
0
Hem
isph
eric
clot
450
500
00
Surg
ery
30
330
067
Non
surg
ical
450
250
025
�3
cm3
067
00
33
�3
cm4
500
00
50
GC
S�
74
5025
00
25
GC
S�
73
033
00
67
Prus
tyan
dM
ohan
ty(1
9)17
IIIG
CS
4–1
5Su
rger
y(n
�16
)an
dno
nsur
gica
l(n
�1)
GO
Sat
disc
harg
ean
d6
mo
Ret
rosp
ectiv
ese
ries
of17
patie
nts
with
PFED
H,
16of
who
mun
derw
ent
surg
ery,
toex
amin
ecl
inic
alch
arac
teri
stic
san
dou
tcom
e.
●M
orta
lity
17.6
%—
all
patie
nts
who
died
pres
ente
dac
utel
y(�
24h
from
inju
ry)
and
had
conc
omita
ntin
trac
rani
alle
sion
s.
●G
OS
5at
6m
ofo
ral
lpa
tient
spr
esen
ting
with
suba
cute
orch
roni
cco
urse
.N
ote:
CT
perf
orm
edin
14/1
7pa
tient
s.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
PFED
H,
tota
l17
5923
00
18
Riv
ano
etal
.(2
0)22
IIIG
CS
4–1
5Su
rger
yG
OS
atdi
scha
rge
Ret
rosp
ectiv
ese
ries
of22
patie
nts
unde
rgoi
ngsu
rger
yfo
rPF
EDH
toev
alua
tecl
inic
alan
dra
diol
ogic
feat
ures
with
resp
ect
toou
tcom
e.
●M
orta
lity
13.6
%—
all
patie
nts
who
died
pres
ente
dw
ithac
ute
clin
ical
cour
se.
●G
CS
atsu
rger
yre
late
dto
outc
ome
(no
stat
istic
s).
●Pr
esen
ceof
asso
ciat
edin
trac
rani
alle
sion
sde
crea
sed
good
outc
ome,
incr
ease
dm
orbi
dity
,an
din
crea
sed
mor
talit
yco
mpa
red
with
patie
nts
with
isol
ated
PFED
H(n
ost
atis
tics)
.N
ote:
2/22
patie
nts
eval
uate
dby
angi
ogra
phy.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Acu
te(O
R�
24h)
1464
77
022
Suba
cute
(OR
24h–
10d)
683
170
00
GC
S(s
urge
ry)
15–1
45
100
00
00
GC
S13
–8
1385
150
00
GC
S7–
34
00
250
75
Ass
ocia
ted
lesi
on7
4314
140
29
No
asso
ciat
edle
sion
1384
.67.
70
07.
7
Srip
airo
jkul
etal
.(2
2)22
IIIG
CS
3T–1
5Su
rger
yG
OS
6m
oR
etro
spec
tive
seri
esof
22pa
tient
sw
ithsu
rgic
ally
trea
ted
post
erio
rfo
ssa
hem
atom
asev
alua
ting
outc
ome
byag
e,ty
peof
hem
atom
a,an
din
terv
albe
twee
nin
jury
and
surg
ery.
●M
orta
lity
38%
.●
GC
S�
9at
time
ofsu
rger
yco
rrel
ated
with
poor
outc
ome.
●In
terv
albe
twee
nin
jury
and
surg
ery
�1
dco
rrel
ated
with
bette
rou
tcom
eth
ansu
rger
y�
6h—
this
may
beca
used
bya
sele
ctio
nof
patie
nts
with
suba
cute
pres
enta
tion.
●C
onco
mita
ntsu
prat
ento
rial
and
infr
aten
tori
alle
sion
sin
crea
sed
mor
bidi
tyan
dm
orta
lity
(mor
talit
y20
%ve
rsus
0%).
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-54 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
Age
�40
yr16
756.
26.
20
12.5
Age
�40
yr6
16.7
16.7
16.7
050
GC
S(s
urge
ry)
3–8
d9
33.3
11.1
11.1
044
.4
GC
S9
–12
666
.70
16.7
016
.7
GC
S13
–15
785
.714
.30
00
EDH
710
00
00
0
EDH
�as
soci
ated
lesi
on
955
.622
.20
022
.2
SDH
110
00
00
0
SDH
�IC
H1
00
100
00
ICH
20
050
050
ICH
�su
prat
ento
rial
lesi
on
20
00
010
0
Inju
ryto
OR
�6
h9
55.6
011
.10
33.3
Inju
ryto
OR
6h–
1d
742
.914
.314
.30
28.6
Inju
ryto
OR
�1
d6
83.3
16.7
00
0
dO
dds
ratio
,0.
057
(sta
tistic
ally
sign
ifica
nt).
St.
John
and
Fren
ch(2
3)8
IIIG
CS
6–1
4Su
rger
yG
OS,
not
spec
ified
Ret
rosp
ectiv
ese
ries
of8
patie
nts
surg
ical
lytr
eate
dfo
rtr
aum
atic
post
erio
rfo
ssa
hem
atom
ato
eval
uate
clin
ical
char
acte
rist
ics
and
outc
ome.
●M
orta
lity
25%
.●
Suba
cute
pres
enta
tion
seem
edto
corr
elat
ew
ithbe
tter
outc
ome,
but
num
ber
ofpa
tient
sto
osm
all
toev
alua
te.
Not
e:pa
per
incl
uded
with
n�
8be
caus
eof
limite
dnu
mbe
rof
case
seri
esw
ith�
10pa
tient
s.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
All
patie
nts
850
12.5
12.5
025
Acu
te(�
24h)
633
.316
.716
.70
33.3
Suba
cute
(24
h–7
d)2
100
00
00
Tsai
etal
.(2
4)57
IIIA
llG
CS
Surg
ery
and
nons
urgi
cal
GO
Sva
riab
leR
etro
spec
tive
seri
esof
57pa
tient
sw
ithpr
imar
ypo
ster
ior
foss
ain
jury
toev
alua
teC
Tch
arac
teri
stic
san
dco
rrel
ate
type
ofin
jury
with
prog
nosi
s.
●PF
EDH
patie
nts
who
wer
eco
mat
ose
onad
mis
sion
died
with
orw
ithou
tsu
rger
y.
●2/
2PF
SDH
patie
nts
with
asso
ciat
edin
jury
wer
eco
mat
ose
onad
mis
sion
,di
dno
tun
derg
osu
rger
y,an
ddi
ed.
●Ev
iden
cefo
rbr
ains
tem
inju
ry,
post
erio
rfo
ssa
swel
ling/
cist
ern
oblit
erat
ion
corr
elat
edw
ithin
crea
sed
mor
talit
y(n
ost
atis
tics)
.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
PFED
H14
500
00
50
PFSD
H8
62.5
12.5
00
25
Cer
ebel
lar
inju
ry14
00
28.6
14.3
57.1
Bra
inst
emin
jury
210
00
23.8
76.2
Vra
nkov
icet
al.
(25)
11III
Unk
now
nSu
rger
yan
dno
nsur
gica
lG
OS
atdi
scha
rge
Ret
rosp
ectiv
ese
ries
of11
patie
nts
with
ATP
FHtr
eate
dei
ther
surg
ical
ly(n
�8)
orno
nope
rativ
ely
(n�
3)to
eval
uate
clin
ical
and
radi
olog
icch
arac
teri
stic
san
dou
tcom
e.
●9
of11
patie
nts
had
occi
pita
lfr
actu
res
and
8.1%
ofpa
tient
sw
ithoc
cipi
tal
frac
ture
sha
dA
TPFH
,em
phas
izin
gim
port
ance
ofC
Tfo
rpa
tient
sw
ithsi
gns
ofoc
cipi
tal
trau
ma.
●3
patie
nts
with
intr
acer
ebel
lar
hem
atom
asan
dno
sign
sof
mas
sef
fect
onC
Tw
ere
succ
essf
ully
man
aged
with
out
surg
ery.
●A
utho
rsad
voca
teim
med
iate
surg
ery
for
all
case
sof
PFED
Hbe
caus
eof
unpr
edic
tabi
lity
ofde
teri
orat
ion.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
All
patie
nts
1154
.536
.40
09.
1
POSTERIOR FOSSA MASS LESIONS
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-55
TAB
LE1.
Con
tinu
ed
Aut
hors
(ref
.no
.)N
o.of
pati
ents
Cla
ssIn
clus
ion
GC
STr
eatm
ent
Out
com
eD
escr
ipti
onC
oncl
usio
n
Wan
get
al.
(26)
13III
All
GC
SSu
rger
yG
OS
3–6
mo
Ret
rosp
ectiv
ese
ries
of13
patie
nts
who
unde
rwen
tsu
rger
yfo
rPF
EDH
toid
entif
ycl
inic
alfe
atur
esth
atm
ayle
adto
earl
ydi
agno
sis
and
toev
alua
teou
tcom
ew
ithre
spec
tto
initi
alG
CS.
●Ea
rly
CT
shou
ldbe
prom
pted
byth
epr
esen
ceof
occi
pita
lso
fttis
sue
inju
ry,
drow
sine
ss,
occi
pita
lfr
actu
re,
and
dias
tasi
sof
lam
bdoi
dsu
ture
.
●G
CS
inve
rsel
yre
late
dto
outc
ome
(no
stat
istic
s).
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
GC
S15
–14
710
00
00
0
GC
S13
–8
250
500
00
GC
S7–
34
500
250
25
Won
g(2
8)25
IIIA
llG
CS
Surg
ery
and
nons
urgi
cal
Mor
talit
yat
disc
harg
eR
etro
spec
tive
seri
esof
25pa
tient
sw
ithPF
EDH
com
pari
ngou
tcom
eof
surg
ical
vers
usno
nsur
gica
lm
anag
emen
tw
ithre
spec
tto
initi
alC
Tch
arac
teri
stic
s,in
clud
ing
volu
me,
thic
knes
s,de
gree
ofsh
ift,
and
pres
ence
ofas
soci
ated
fron
tal
cont
usio
n.
●Pa
tient
sm
anag
edex
pect
antly
with
PFED
Hvo
lum
e�
10cm
3 ,th
ickn
ess
�15
mm
,an
dsh
ift�
5m
mha
dsi
gnifi
cant
lyhi
gher
mor
talit
yth
anpa
tient
sm
anag
edsu
rgic
ally
with
equi
vale
ntC
Tch
arac
teri
stic
s.
●10
0%su
rviv
alin
all
patie
nts
with
PFED
Hvo
lum
e�
10cm
3 ,th
ickn
ess
�15
mm
,an
dsh
ift�
5m
m,
rega
rdle
ssof
trea
tmen
t.
●A
ssoc
iate
dfr
onta
lIC
Hsi
gnifi
cant
lyin
crea
sed
mor
talit
yin
both
grou
ps.
No.
ofpa
tien
tsD
(%)
Vol
�10
cm3 /e
arly
OR
e9
11.1
Vol
�10
cm3 /e
xpec
tant
475
Vol
�10
cm3 /e
arly
OR
f8
0
Vol
�10
cm3 /e
xpec
tant
40
Thic
knes
s�
15m
m/e
arly
OR
g13
7.7
Thic
knes
s�
15m
m/e
xpec
tant
475
Thic
knes
s�
15m
m/e
arly
OR
f4
0
Thic
knes
s�
15m
m/e
xpec
tant
40
Shift
�5
mm
/ear
lyO
Re
50
Shift
�5
mm
/exp
ecta
nt1
100
Shift
�5
mm
/ear
lyO
Rf
128.
3
Shift
�5
mm
/exp
ecta
nt7
28.6
Ass
ocia
ted
fron
tal
cont
usio
nh6
66.7
No
fron
tal
cont
usio
n19
0e
P�
0.05
,fP
�n.
s,g
P�
0.01
,h
P�
0.00
1.
Zuc
care
lloet
al.
(29)
10III
Unk
now
nSu
rger
yan
dno
nsur
gica
lM
orta
lity
Ret
rosp
ectiv
ese
ries
of10
patie
nts
with
trau
mat
icpo
ster
ior
foss
am
ass
lesi
ons
tode
scri
befa
ctor
sre
late
dto
man
agem
ent
and
prog
nosi
s.
●M
orta
lity
40%
(incl
udes
all
lesi
onty
pes)
.●
No
com
pari
son
betw
een
grou
psab
leto
bem
ade.
No.
ofpa
tien
tsD
(%)
EDH
20
Cer
ebel
lar
hem
orrh
age
�su
rger
y2
50
Cer
ebel
lar
hem
orrh
age,
nons
urgi
cal
30
Bra
inst
emin
jury
310
0
Zuc
care
lloet
al.
(30)
8III
GC
Sm
otor
4–5
Surg
ery
GO
Sat
disc
harg
eR
etro
spec
tive
clin
ical
seri
esof
8pa
tient
sw
ithsu
rgic
ally
trea
ted
PFED
Hto
eval
uate
outc
ome.
●Im
port
ance
ofC
Tis
emph
asiz
ed.
Not
e:pa
per
incl
uded
with
n�
8be
caus
eof
limite
dnu
mbe
rof
case
seri
esw
ith�
10pa
tient
s.
No.
ofpa
tien
tsG
R(%
)M
D(%
)SD
(%)
VS
(%)
D(%
)
PFED
H,
tota
l8
5037
.50
012
.5
aG
CS,
Gla
sgow
Com
aSc
ale;
GO
S,G
lasg
owou
tcom
esc
ore;
PFED
H,p
oste
rior
foss
aep
idur
alhe
mat
oma;
CT,
com
pute
dto
mog
raph
icsc
an;G
R,g
ood
reco
very
;MD
,mod
erat
edi
sabi
lity;
D,d
eath
;SD
,sev
ere
disa
bilit
y;V
S,ve
geta
tive
stat
e;n.
s.,n
otsi
gnifi
cant
;HC
P,hy
droc
epha
lus;
ATP
FH,a
cute
trau
mat
icpo
ster
ior
foss
ahe
mat
oma;
ICH
,int
race
rebr
alhe
mor
rhag
e;ED
H,e
pidu
ralh
emat
oma;
SAH
,su
bara
chno
idhe
mor
rhag
e;SD
H,
subd
ural
hem
atom
a;O
R,
oper
atio
n.
CHAPTER 7
SURGICAL MANAGEMENT OF DEPRESSED
CRANIAL FRACTURESM. Ross Bullock, M.D., Ph.D.Department of Neurological Surgery,Virginia Commonwealth UniversityMedical Center,Richmond, Virginia
Randall Chesnut, M.D.Department of Neurological Surgery,University of WashingtonSchool of Medicine,Harborview Medical Center,Seattle, Washington
Jamshid Ghajar, M.D., Ph.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David Gordon, M.D.Department of Neurological Surgery,Montefiore Medical Center,Bronx, New York
Roger Hartl, M.D.Department of Neurological Surgery,Weil Cornell Medical College ofCornell University,New York, New York
David W. Newell, M.D.Department of Neurological Surgery,Swedish Medical Center,Seattle, Washington
Franco Servadei, M.D.Department of Neurological Surgery,M. Bufalini Hospital,Cesena, Italy
Beverly C. Walters, M.D., M.Sc.Department of Neurological Surgery,New York UniversitySchool of Medicine,New York, New York
Jack Wilberger, M.D.Department of Neurological Surgery,Allegheny General Hospital,Pittsburgh, Pennsylvania
Reprints requests:Jamshid Ghajar, M.D., Ph.D.,Brain Trauma Foundation,523 East 72nd Street,New York, NY 10021.Email: [email protected]
RECOMMENDATIONS(see Methodology)
Indications• Patients with open (compound) cranial fractures depressed greater than the thick-
ness of the cranium should undergo operative intervention to prevent infection.• Patients with open (compound) depressed cranial fractures may be treated nonop-
eratively if there is no clinical or radiographic evidence of dural penetration,significant intracranial hematoma, depression greater than 1 cm, frontal sinusinvolvement, gross cosmetic deformity, wound infection, pneumocephalus, or grosswound contamination.
• Nonoperative management of closed (simple) depressed cranial fractures is a treat-ment option.
Timing• Early operation is recommended to reduce the incidence of infection.Methods• Elevation and debridement is recommended as the surgical method of choice.• Primary bone fragment replacement is a surgical option in the absence of wound
infection at the time of surgery.• All management strategies for open (compound) depressed fractures should include
antibiotics.
KEY WORDS: Antibiotic prophylaxis, Burr hole, Cranial fracture, Craniotomy, Depressed cranial fracture,Depressed skull fracture, Head injury, Skull fracture, Surgical technique, Traumatic brain injury
Neurosurgery 58:S2-56-S2-60, 2006 DOI: 10.1227/01.NEU.0000210367.14043.0E www.neurosurgery-online.com
OVERVIEW
The presence of a cranial fracture has con-sistently been shown to be associated with ahigher incidence of intracranial lesions, neu-rological deficit, and poorer outcome (4, 8, 12,14). Indeed, Chan et al. (4) found cranial frac-ture to be the only independent significantrisk factor in predicting intracranial hemato-mas in a cohort of 1178 adolescents. Macpher-son et al. (12) found that 71% of 850 patientswith a cranial fracture had an intracranial le-sion (i.e., contusion or hematoma), comparedwith only 46% of 533 patients without a cra-nial fracture. Hung et al. (8) determined thatpatients with both loss of consciousness andcranial fracture were at significantly greaterrisk of developing a “surgically significant in-tracranial hematoma” than those with one or
neither condition. Servadei et al. (14) showedthe importance of cranial fracture in predict-ing the presence of intracranial lesions, evenin minor head injuries (Glasgow Coma Scalescore 14 or 15). These studies underscore theimportance of cranial fractures as indicators ofclinically significant injuries, as well as theimportance of computed tomographic (CT)scans in evaluation of all patients with knownor clinically suspected cranial fractures.
Depressed cranial fractures may complicateup to 6% of head injuries in some series (7),and account for significant morbidity andmortality. Compound fractures account for upto 90% of these injuries (3, 6, 17), and areassociated with an infection rate of 1.9 to10.6% (9, 13, 16, 17), an average neurologicalmorbidity of approximately 11% (6), an inci-dence of late epilepsy of up to 15% (10), and a
S2-56 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
mortality rate of 1.4 to 19% (3, 5–7, 17). By convention, com-pound depressed cranial fractures are treated surgically, withdebridement and elevation, primarily to attempt to decreasethe incidence of infection. Closed (“simple”) depressed cranialfractures undergo operative repair if the extent of depressionis greater than the full thickness of the adjacent calvarium,with the theoretical benefits of better cosmesis, a diminution inlate-onset posttraumatic epilepsy, and a reduction in the inci-dence of persistent neurological deficit. There is, however,very little literature to support these management strategies,despite their widespread, and theoretically sound, practice.There is Class III literature that addresses the efficacy ofsurgical management of these injuries, and it argues againstautomatic surgical treatment of all compound fractures (7).
Most of the literature reviewed focuses predominantly oninfectious complications, seizures, surgical technique (e.g., bonefragment replacement versus removal), or the predictive powerof cranial fracture for the presence of other intracranial pathol-ogy. Several large studies of patients with cranial fracture shedlight on the breadth of issues associated with such lesions and arediscussed below, under Scientific Foundation. However, some ofthese studies were conducted before the CT-scan era, and thus,although important for our understanding of the injury itself, arenot included for critical analysis.
PROCESS
A MEDLINE computer search using the following key words:“skull” and “fracture” and “depressed” between 1975 and 2001was performed. A total of 224 documents were found. The searchwas narrowed to include the key words: “surgery” or “opera-tion” or “elevation”. A total of 122 articles were found, 5 of whichmet the criteria for critical analysis. In addition, the reference listsof all articles were reviewed, and additional articles were se-lected for background information. The results of this analysiswere incorporated into the review presented here. Papers pri-marily addressing the following topics were not included: pa-tients with associated medical illnesses, sinus fractures, cranialbase fractures, isolated orbital or facial fractures, and pre-CT erareports. In general, papers with the following characteristicswere also excluded: case series with less than 10 patients evalu-ated by CT scan and with incomplete outcome data (mortality orGlasgow outcome score), case reports, operative series with op-erations occurring longer than 14 days from injury. Several arti-cles with case series of less than 10 patients were examined andreviewed because of the limited number of patient series evalu-ating the acute surgical management of depressed cranial frac-tures in the CT era. Selected articles were evaluated for design,prognostic significance, therapeutic efficacy, and overall out-come. In addition, several articles were reviewed for the pur-poses of historical perspective.
SCIENTIFIC FOUNDATION
Closed, linear cranial fractures are considered nonoperativelesions unless associated with surgical intracranial masses.
Controversy surrounds appropriate management of de-pressed cranial fractures. Compound depressed cranial frac-tures are depressed fractures with an overlying scalp lacera-tion in continuity with the fracture site and with galealdisruption, and have conventionally been treated with de-bridement and surgical elevation (3, 6, 9, 14). Simple de-pressed cranial fractures have no galeal disruption and aretraditionally managed with surgical elevation only if the ex-tent of depression equals or exceeds the thickness of adjacent,intact bone, or if there is an associated intracranial hematomawith mass effect that requires evacuation.
The rationale for aggressive treatment of depressed cranialfractures stems from their association with infection and lateepilepsy. Cosmetic deformity also plays a role in surgicaldecision making. Such complications, and their potential se-quelae, are well documented. In a series of 359 patients withcompound cranial fractures, Jennett and Miller (9) docu-mented a 10.6% incidence of infection, which was associatedwith a significantly higher incidence of persistent neurologicaldeficit, late epilepsy (defined as seizures longer than 1 wkfrom injury), and death. Operative debridement reduced theincidence of infection to 4.6% in their series. Operative delaygreater than 48 hours from injury dramatically increased theincidence to 36.5%. There was no difference in infection ratebetween surgical cohorts who had bone fragments replacedversus removed—results supported by a series of 225 patientswith depressed cranial fracture reported by Braakman (3), anda treatment strategy reported as early as Macewan in 1888 (9).In a separate report of 1000 patients with nonmissile de-pressed cranial fractures, Jennett et al. (10) documented a 15%incidence of late epilepsy, which was significantly associatedwith posttraumatic amnesia longer than 24 hours, torn dura,the presence of focal neurological signs, and the presence ofearly epilepsy (i.e., within 1 wk of injury). In the closed-fracture patients in this series, there was no difference inincidence of epilepsy between the elevated and nonelevatedcases. Additionally, there was a higher incidence of late epi-lepsy in patients with elevated compound fractures. The au-thors explain this finding by documenting a higher incidenceof those factors independently associated with late epilepsy,such as dural tearing and long posttraumatic amnesia, in theelevated-fracture patient cohort. These series were reportedbefore the CT era, however, they offer us a clear picture ofboth the range of complications associated with nonmissiledepressed cranial fractures and the controversies surroundingmanagement strategies.
The primary question facing the neurosurgeon regardingdepressed cranial fracture is whether to operate. Heary et al.(7) reported a group of patients with compound depressedcranial fractures in which nonsurgical therapy was used for asubgroup of 26 patients without clinical or radiographic evi-dence of dural violation or significant underlying brain injury.They concluded that patients with open (compound) de-pressed cranial fractures may be treated nonoperatively ifthere is no clinical or radiographic evidence of dural penetra-tion, significant intracranial hematoma, depression greater
DEPRESSED CRANIAL FRACTURES
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-57
than 1 cm, frontal sinus involvement, gross deformity, woundinfection, pneumocephalus, or gross wound contamination.No infectious complications occurred. Similarly, van denHeever and van der Merwe (16) reported an equally lowincidence of infection in a group of nonoperatively treatedpatients that included 139 compound depressed fractures.Surgical indications in their series included clinical character-istics of the wound. CT scans were not routinely used unlessa neurological deficit was present on admission.
Although these studies are retrospective and nonrandom-ized, and, thus, subject to inherent biases, they clearly dem-onstrate that at least a select group of patients with compounddepressed cranial fractures will do well without surgery.
Another challenge to traditional thinking that has surfaced inthe literature involves the proper surgical management of com-pound depressed cranial fractures with respect to the bone frag-ments. Conventional treatment involves operative debridement,elevation of the fracture, removal of bone fragments, and delayedcranioplasty. However, this subjects the patient to a second op-eration (i.e., cranioplasty), with its attendant risks and complica-tions. Kriss et al. (11), Jennett and Miller (9), and Braakman (3)showed that infectious complications are not increased by pri-mary bone fragment replacement. Wylen et al. (17) retrospec-tively reviewed a series of 32 patients who underwent elevationand repair of a compound depressed cranial fracture with pri-mary replacement of bone fragments within 72 hours of injury.Patients treated longer than 72 hours after injury and patientswho presented with existing infection were excluded from thestudy. There were no infectious complications. Blankenship et al.(2) also demonstrated a 0% infection rate in 31 children withcompound depressed cranial fractures treated with primarybone fragment replacement, regardless of the degree of contam-ination of the wound at the time of surgery. Thirty patients in thisseries were treated within 16 hours of injury. Likewise, Adeloyeand Shokunbi (1) report the success of immediate bone replace-ment, without infectious sequelae, in 12 patients with compounddepressed fractures, 11 of whom were treated within 10 hours ofinjury. Four patients in their series were treated with free-fragment removal secondary to the greater severity of parenchy-mal injury, suggesting benefit from the decompression that boneremoval would provide. Despite the retrospective, uncontrolled,nonrandomized design of these observational studies, theyclearly demonstrate the feasibility of immediate bone fragmentreplacement without a corresponding increase in infectious se-quelae, thus, obviating the need for a second surgical procedure.
SUMMARY
The majority of studies are case series. No controlled, prospec-tive clinical trials of treatment using surgical versus nonsurgicalmanagement have been published. The majority of data supportdebridement and elevation of grossly contaminated compounddepressed cranial fractures as soon as possible after injury. How-ever, several retrospective studies demonstrate successful non-operative management of some patients with less-severe com-pound depressed cranial fractures on the basis of CT and clinical
criteria. In the absence of gross wound infection at the time ofpresentation, immediate replacement of bone fragments seemsnot to increase the incidence of infection if surgery is performedexpeditiously, and this replacement eliminates the need for sub-sequent cranioplasty and its attendant risks and complications.No controlled data exist to support the timing of surgery or theuse of one technique over another.
KEY ISSUES FOR FUTURE INVESTIGATION
To improve the strength of recommendations above theoption level, well-controlled trials of surgical technique arewarranted, and should examine issues of bone fragment re-placement versus removal, dural laceration repair, etc., andtheir respective relationship to outcome variables, such asincidence of infection, incidence of epilepsy, need for reopera-tion, surgical complications, and, most importantly, neurolog-ical and neuropsychological outcomes.
REFERENCES
1. Adeloye A, Shokunbi MT: Immediate bone replacement in compound de-pressed skull fractures. Cent Afr J Med 39:70–73, 1993.
2. Blankenship JB, Chadduck WM, Boop FA: Repair of compound-depressedskull fractures in children with replacement of bone fragments. PediatrNeurosurg 16:297–300, 1990.
3. Braakman R: Depressed skull fracture: Data, treatment, and follow-up in 225consecutive cases. J Neurol Neurosurg Psychiatry 35:395–402, 1972.
4. Chan KH, Mann KS, Yue CP, Fan YW, Cheung M: The significance of skullfracture in acute traumatic intracranial hematomas in adolescents: A pro-spective study. J Neurosurg 72:189–194, 1990.
5. Colak A, Berker M, Ozcan OE: Occipital depression fractures in childhood.A report of 14 cases. Childs Nerv Syst 7:103–105, 1991.
6. Cooper PR: Skull fracture and traumatic cerebrospinal fluid fistulas, in Cooper PR(ed): Head Injury. Baltimore, Williams and Wilkins, 1993, pp 115–136 ed 3.
7. Heary RF, Hunt CD, Krieger AJ, Schulder M, Vaid C: Nonsurgical treatmentof compound depressed skull fractures. J Trauma 35:441–447, 1993.
8. Hung CC, Chiu WT, Lee LS, Lin LS, Shih CJ: Risk factors predictingsurgically significant intracranial hematomas in patients with head injuries.J Formos Med Assoc 95:294–297, 1996.
9. Jennett B, Miller J: Infection after depressed fracture of skull. Implicationsfor management of nonmissile injuries. J Neurosurg 36:333–339, 1972.
10. Jennett B, Miller J, Braakman R: Epilepsy after monmissile depressed skullfracture. J Neurosurg 41:208–216, 1974.
11. Kriss F, Taren J, Kahn E: Primary repair of compound skull fractures byreplacement of bone fragments. J Neurosurg 30:698–702, 1969.
12. Macpherson BC, MacPherson P, Jennett B: CT evidence of intracranialcontusion and haematoma in relation to the presence, site and type of skullfracture. Clin Radiol 42:321–326, 1990.
13. Mendelow AD, Campbell D, Tsementzis SA, Cowie RA, Harris P, Durie TB,Gillingham FJ: Prophylactic antimicrobial management of compound de-pressed skull fracture. J R Coll Surg Edinb 28:80–83, 1983.
14. Servadei F, Ciucci G, Pagano F, Rebucci GG, Ariano M, Piazza G, Gaist G:Skull fracture as a risk factor of intracranial complications in minor headinjuries: A prospective CT study in a series of 98 adult patients. J NeurolNeurosurg Psychiatry 51:526–528, 1988.
15. Steinbok P, Flodmark O, Martens D, Germann ET: Management of simpledepressed skull fractures in children. J Neurosurg 66:506–510, 1987.
16. van den Heever CM, van der Merwe DJ: Management of depressed skullfractures. Selective conservative management of nonmissile injuries.J Neurosurg 71:186–190, 1989.
17. Wylen EL, Willis BK, Nanda A: Infection rate with replacement of bone fragmentin compound depressed skull fractures. Surg Neurol 51:452–457, 1999.
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-58 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
DEPRESSED CRANIAL FRACTURES
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-59
TAB
LE1.
Surg
ical
man
agem
ent
ofde
pres
sed
cran
ial
frac
ture
sa
Aut
hors
No.
ofpa
tien
tsC
lass
Incl
usio
nG
CS
Trea
tmen
tO
utco
me
Des
crip
tion
Con
clus
ion
Ade
loye
and
Shok
unbi
(1)
16III
GC
S15
Bon
efr
agm
ent
repl
acem
ent
vers
usre
mov
al
Infe
ctio
nra
te;
GO
S;tim
ing
not
spec
ified
Ret
rosp
ectiv
ese
ries
of16
patie
nts
trea
ted
eith
erw
ithim
med
iate
bone
frag
men
tre
plac
emen
t(n
�12
)or
free
frag
men
tre
mov
al(n
�4)
toco
mpa
rein
fect
ion
rate
and
outc
ome
betw
een
grou
ps.
●N
oin
cide
nce
ofin
fect
ious
com
plic
atio
nin
eith
ergr
oup,
supp
ortin
gth
esa
fety
ofbo
nefr
agm
ent
repl
acem
ent.
●Se
lect
ion
bias
and
smal
lnu
mbe
rof
patie
nts
prec
lude
com
pari
son
ofou
tcom
e.
No.
ofpa
tien
tsG
R(%
)In
fect
ion
(%)
Rep
lace
men
t12
100
0
No
repl
acem
ent
410
00
Bla
nken
ship
etal
.(2
)31
IIIU
nkno
wn
Bon
efr
agm
ent
repl
acem
ent
Infe
ctio
nor no
nuni
on,
aver
age
26.5
mo
Ret
rosp
ectiv
ere
view
of31
child
ren
aged
20m
oto
17yr
surg
ical
lytr
eate
dw
ithpr
imar
ybo
nefr
agm
ent
repl
acem
ent
for
com
poun
dde
pres
sed
cran
ial
frac
ture
toex
amin
eth
ein
cide
nce
ofin
fect
ious
com
plic
atio
ns.
Thir
tyof
31pa
tient
sw
ere
trea
ted
with
in16
hof
inju
ry.
●N
oin
stan
ces
ofin
fect
ious
com
plic
atio
nsan
dno
need
for
subs
eque
ntcr
anio
plas
ty,
rega
rdle
ssof
degr
eeof
wou
ndco
ntam
inat
ion.
No.
ofpa
tien
tsIn
fect
ion
(%)
Rep
lace
men
t31
0
Bra
akm
an(3
)22
5N
/AN
/AB
one
frag
men
tre
plac
emen
tve
rsus
rem
oval
Infe
ctio
nra
te;
inci
denc
eof
epile
psy
Ret
rosp
ectiv
ere
view
of22
5pa
tient
sw
ithde
pres
sed
cran
ial
frac
ture
toex
amin
eep
idem
iolo
gy,
asse
ssou
tcom
ew
ithre
spec
tto
inci
denc
eof
epile
psy
and
pers
iste
ntne
urol
ogic
alde
ficit,
and
toas
sess
the
effe
ctof
prim
ary
bone
frag
men
tre
plac
emen
ton
infe
ctio
nra
te.
●4.
4%in
cide
nce
ofea
rly
epile
psy.
●7.
1%in
cide
nce
ofla
teep
ileps
y.●Pr
imar
yre
plac
emen
tof
bone
frag
men
tsdi
dno
tal
ter
infe
ctio
nra
te.
No.
ofpa
tien
tsIn
fect
ion
(%)
Rep
lace
men
t82
2.4
Part
ial
repl
acem
ent
2711
.1
Rem
oval
5610
.7
Hea
ryet
al.
(7)
54III
Exce
llent
,go
od,
fair
,po
or
Surg
ery
and
nons
urgi
cal
Mea
nG
OS,
9.5
mo
Ret
rosp
ectiv
ere
view
of54
pros
pect
ivel
ytr
eate
dpa
tient
sw
ithco
mpo
und
depr
esse
dcr
ania
lfr
actu
res
com
pari
ngpa
tient
str
eate
dsu
rgic
ally
vers
usno
nsur
gica
llyba
sed
ona
stan
dard
ized
trea
tmen
tpr
otoc
olin
volv
ing
clin
ical
and
CT
crite
ria.
●N
odi
ffere
nce
inou
tcom
ebe
twee
npa
tient
str
eate
dsu
rgic
ally
vers
usno
nsur
gica
llyw
ithco
mpo
und
depr
esse
dcr
ania
lfr
actu
res
that
have
nocl
inic
alor
radi
ogra
phic
evid
ence
ofdu
ral
pene
trat
ion,
sign
ifica
ntin
trac
rani
alhe
mat
oma,
depr
essi
on�
1cm
,fr
onta
lsi
nus
invo
lvem
ent,
gros
sde
form
ity,
wou
ndin
fect
ion,
orgr
oss
wou
ndco
ntam
inat
ion.
●N
oin
fect
ious
com
plic
atio
nsoc
curr
edin
eith
ergr
oup
with
stan
dard
ized
trea
tmen
tpr
otoc
olin
clud
ing
prop
hyla
ctic
antib
iosi
s.●Pa
tient
sw
ithsu
rgic
alle
sion
sha
dsi
gnifi
cant
lyin
crea
sed
inci
denc
eof
SAH
and
cere
bral
cont
usio
n(P
�0.
01an
dP
�0.
05,
resp
ectiv
ely)
.●M
orta
lity
5.6%
ofth
ose
anal
yzed
,19
%to
tal.
No.
ofpa
tien
tsEx
celle
nt(%
)G
ood
(%)
Fair
(%)
Poor
(%)
D(%
)
Surg
ery
2864
.321
.410
.70
3.6
Non
surg
ical
2680
.83.
87.
70
7.7
Jenn
ett
and
Mill
er(9
)35
9N
/AN
/AEa
rly
vers
usde
laye
d;bo
nefr
agm
ent
repl
acem
ent
vers
usre
mov
al;
dura
clos
edve
rsus
open
Infe
ctio
nra
te,
CN
Ssi
gns,
late
epile
psy,
mor
talit
y
Ret
rosp
ectiv
ere
view
of35
9pa
tient
sw
ithco
mpo
und,
depr
esse
dcr
ania
lfr
actu
res
toex
amin
eth
eca
uses
and
cons
eque
nces
ofin
fect
ion
and
toas
sess
the
effe
ctof
surg
ical
timin
gan
dm
etho
dson
infe
ctio
nra
te.
●10
.6%
over
all
infe
ctio
nra
te.
●In
fect
ion
was
sign
ifica
ntly
asso
ciat
edw
ithin
crea
sed
mor
talit
y,pr
olon
ged
CN
Ssi
gns,
late
epile
psy.
●In
cide
nce
ofin
fect
ion
was
sign
ifica
ntly
grea
ter
inpa
tient
sw
ith�
48h
dela
ybe
twee
nin
jury
and
oper
atio
n.●N
odi
ffere
nce
inin
fect
ion
rate
betw
een
the
grou
pw
hose
dura
was
clos
edan
dth
egr
oup
who
sedu
raw
asle
ftop
en.
●Pr
imar
ybo
nefr
agm
ent
repl
acem
ent
did
not
sign
ifica
ntly
affe
ctpo
stop
erat
ive
infe
ctio
nra
teor
inci
denc
eof
late
epile
psy.
Jenn
ett
etal
.(1
0)10
00N
/AN
/ASu
rger
yve
rsus
nosu
rger
yIn
cide
nce
ofea
rly
and
late
epile
psy
Ret
rosp
ectiv
ere
view
of10
00pa
tient
sw
ithno
nmis
sile
depr
esse
dcr
ania
lfr
actu
res
tost
udy
risk
fact
ors
asso
ciat
edw
ithpo
sttr
aum
atic
epile
psy.
●10
%in
cide
nce
ofea
rly
epile
psy
(1w
k).
●15
%in
cide
nce
ofla
teep
ileps
y(�
1w
k).
●In
crea
sed
risk
ofla
teep
ileps
yw
ithpo
sttr
aum
atic
amne
sia
�24
h,to
rndu
ra,
foca
lne
urol
ogic
alsi
gns,
occu
rren
ceof
earl
yep
ileps
y.●Lo
wer
risk
ofea
rly/
late
epile
psy
with
occi
pita
lfr
actu
res.
SURGICAL MANAGEMENT OF TBI AUTHOR GROUP
S2-60 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
TAB
LE1.
Con
tinu
ed
Aut
hors
No.
ofpa
tien
tsC
lass
Incl
usio
nG
CS
Trea
tmen
tO
utco
me
Des
crip
tion
Con
clus
ion
No.
ofpa
tien
tsIn
fect
ion
(%)
Initi
ally
clea
n,in
jury
toO
R�
36h
283
3.91
Initi
ally
clea
n,in
jury
toO
R�
48h
214.
8
Inju
ryto
OR
�48
hor
neve
r76
36.5
2
Bon
efr
agm
ent
repl
acem
ent
166
3.6
Bon
efr
agm
ent
rem
oval
135
4.4
1P
�n.
s,2
P�
0.00
1
Men
delo
wet
al.
(13)
176
N/A
N/A
Prop
hyla
ctic
antib
iotic
sve
rsus
noan
tibio
tics
Infe
ctio
nra
teR
etro
spec
tive
seri
esof
176
patie
nts
with
com
poun
d,de
pres
sed
cran
ial
frac
ture
sto
dete
rmin
efa
ctor
sth
atpr
edis
pose
toin
fect
ion
and
the
effe
ctof
prop
hyla
ctic
antib
iotic
son
infe
ctio
nra
te.
●6.
3%ov
eral
lin
fect
ion
rate
.●Pr
ophy
lact
icus
eof
ampi
cilli
nan
da
sulp
hona
mid
ew
asas
soci
ated
with
asi
gnifi
cant
lylo
wer
infe
ctio
nra
te(1
.9%
)th
anw
ithan
yot
her
com
bina
tion
(15.
6%)
orno
antib
iotic
sat
all
(10.
5%).
●D
ural
pene
trat
ion,
prim
ary
vers
usse
cond
ary
clos
ure,
sinu
sin
volv
emen
t,su
rger
yve
rsus
nosu
rger
y,bo
nere
plac
emen
tve
rsus
rem
oval
did
not
sign
ifica
ntly
affe
ctin
fect
ion
rate
.
No.
ofpa
tien
tsIn
fect
ion
(%)
Am
pici
llin
�su
lpho
nam
ide
107
1.9
No
antib
iotic
s19
10.5
1
All
othe
ran
tibio
tics
4515
.62
1P
�0.
05,
2P
�0.
01,
com
pare
dw
itham
pici
llin
�su
lpho
nam
ide
Stei
nbok
etal
.(1
5)11
1III
Dur
atio
nof
com
aSu
rger
yan
dno
nsur
gica
lIn
cide
nce
ofse
izur
es,
neur
olog
ical
dysf
unct
ion,
cosm
esis
;tim
ing
not
spec
ified
Ret
rosp
ectiv
ese
ries
of11
1ch
ildre
n�
16yr
with
sim
ple
depr
esse
dcr
ania
lfr
actu
res
toex
amin
eou
tcom
ew
ithre
spec
tto
the
occu
rren
ceof
seiz
ures
,ne
urol
ogic
aldy
sfun
ctio
n,an
dco
smes
isbe
twee
nsu
rgic
ally
and
nons
urgi
cally
man
aged
patie
nts.
●N
odi
ffere
nce
inse
izur
es,
neur
olog
ical
dysf
unct
ion,
cosm
etic
defo
rmity
betw
een
surg
ical
and
nons
urgi
cal
trea
tmen
t.G
roup
sdi
ffere
dw
ithre
spec
tto
max
imum
depr
essi
onof
frac
ture
(P�
0.00
0),
but
not
todu
ratio
nof
com
a,ag
e.●D
ural
lace
ratio
nw
assi
gnifi
cant
lyas
soci
ated
with
neur
olog
ical
defic
it.
No.
ofpa
tien
tsSe
izur
es(%
)C
osm
etic
defo
rmit
y(%
)R
esid
ual
defic
it(%
)
Surg
ery
1910
.521
0
Non
surg
ical
234.
317
.40
van
den
Hee
ver
and
van
der
Mer
we
(16)
284
IIIU
nkno
wn
Surg
ery
vers
usno
nsur
gica
l
Sept
icco
mpl
icat
ion;
outc
ome
offo
cal
neur
olog
ical
abno
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fect
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rgic
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)
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agm
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ctio
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ry.
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ical
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tsIn
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ion
(%)
Rep
lace
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t32
0
aG
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sgow
Com
aSc
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ore;
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ry;
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mpu
ted
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ogra
phic
scan
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gnifi
cant
.
APPENDICES
APPENDIX I: POST-TRAUMATIC MASS VOLUME MEASUREMENT IN
TRAUMATIC BRAIN INJURY PATIENTS
1. Direct volumetric measurement with imaging softwareusing a modern computer tomographic CT scanner is thegold standard. This has been applied only on rare occa-sions.
2. The “ellipsoid method” was developed to calculate thevolume of arteriovenous malformations (3). It is based onthe concept that the volume of an ellipsoid is approxi-mately one-half of the volume of the parallelepiped (asix-faced polyhedron, all of whose faces are parallelo-grams lying in pairs of parallel planes) into which it isplaced. By measuring three diameters of a given lesion inthe arterial phase of an angiogram, a parallelepiped isconstructed, and its volume, divided in half, is close tothe actual volume of the malformation. By extending thisconcept from angiography to CT scanning, calculation ofspace-occupying lesions becomes possible (4). The“ABC” method has been described by Kothari et al. (2)for the measurement of intracerebral hemorrhages, andis also based on the concept of measuring the volume ofan ellipsoid. The formula for an ellipsoid is:
Ve � 4/3 � (A/2) (B/2) (C/2)where A, B, and C are the three diameters.For � � 3, the formula becomes Ve � ABC/2
The volume of an intracerebral hemorrhage can be approx-imated by following the steps listed below:
• Identify the CT slice with the largest area of hemorrhage(Slice 1)
• A: measure the largest diameter, A.• B: measure the largest diameter 90° to A on the same slice,
B.
• C: count the number of 10-mm slices.• Compare each slice with slice 1.• If the hemorrhage is greater than 75% compared with slice 1,
count the slice as 1.• If the hemorrhage is 25 to 75%, count the slice as 0.5.• If the hemorrhage less than 25%, do not count the slice.• Add up the total C.
3. More recently, the “Cavalieri direct estimator” methodhas been introduced (1). It breaks down the lesion on theCT scan into a corresponding number of points. Thevolume of a lesion is the product of the sum of the pointsthat fall into the lesion, the area associated with eachpoint, and the distance between the scan slices. A gridthat is used to determine the number of points can beobtained by photocopying a template provided in theoriginal article or by preparing a uniformly spaced pointgrid by computer (4).
REFERENCES
1. Clatterbuck R, Sipos E: The efficient calculation of neurosurgically relevantvolumes from computed tomographic scans using Cavalieri’s Direct Estima-tor. Neurosurgery 40:339–342, 1997.
2. Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M,Khoury J: The ABCs of measuring intracerebral hemorrhage volumes. Stroke27:1304–1305, 1996.
3. Pasqualin A, Barone G, Cioffi F, Rosta L, Scienza R, Da Pian R: The relevanceof anatomic and hemodynamic factors to a classification of cerebral arterio-venous malformations. Neurosurgery 28:370–379, 1991.
4. Stocchetti N, Croci M, Spagnoli D, Gilardoni F, Resta F, Colombo A: Massvolume measurement in severe head injury: Accuracy and feasibility of twopragmatic methods. J Neurol Neurosurg Psychiatry 68:14–17, 2000.
NEUROSURGERY VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT | S2-61
APPENDICES
APPENDIX II: EVALUATION OF RELEVANT COMPUTED
TOMOGRAPHIC SCAN FINDINGS
Computed tomographic (CT) scanning is the imagingmodality of choice for traumatic brain injury because ofits widespread availability, the rapid imaging time, the
low associated costs, and its safety. CT scanning measures thedensity of tissues using x-rays. To standardize the imagingprocedure, 5-mm slices should be obtained from the foramenmagnum to the sella and 10-mm slices should be obtainedabove the sella, parallel to the orbitomeatal line. The followingearly CT scan findings correlate with outcome (1):
• Status of the basal cisterns.• Midline shift.• Subarachnoid hemorrhage in the basal cisterns.
Basal Cisterns at the Midbrain Level
Compressed or absent basal cisterns indicate a threefoldrisk of raised intracranial pressure and the status of the basalcisterns is related to outcome. The degree of mass effect isevaluated at the level of the midbrain. Cerebrospinal fluidcisterns around the midbrain are divided into three limbs, oneposterior and two laterally (Fig. 1). Each limb can be assessed
separately as to whether ornot it is open or com-pressed. Basal cisterns canbe:
• Open (all limbs open).• Partially closed (one or
two limbs obliterated).• Completely closed (all
limbs obliterated).
Midline Shift at theForamen of Monro
The presence of midlineshift is inversely related toprognosis. However, inter-action exists with the pres-ence of intracranial lesions and other CT parameters (1). Mid-line shift at the level of the foramen of Monro should bedetermined by first measuring the width of the intracranialspace to determine the midline (“A”). Next, the distance fromthe bone to the septum pellucidum is measured (“B”) (Fig. 2).The midline shift can be determined by calculating:
Midline shift � (A/2) � B
Traumatic Subarachnoid Hemorrhage
Traumatic subarachnoid hemorrhage occurs in between 26and 53% of all patients with severe traumatic brain injury.Mortality is increased twofold in the presence of traumaticsubarachnoid hemorrhage. The presence of subarachnoidhemorrhage in the basal cisterns carries a positive predictivevalue of unfavorable outcome of approximately 70%.
REFERENCE
1. Chesnut R, Ghajar J, Maas A, Marion D, Servadei F, Teasdale G, Unterberg A,von Holst, Walters B: Early indicators of prognosis in severe traumatic braininjury. J Neurotrauma 17:535–627, 2000.FIGURE 1. Evaluation of the basal cisterns on computed tomographic scan.
FIGURE 2. Assessment of midlineshift on computed tomographic scan.
S2-62 | VOLUME 58 | NUMBER 3 | MARCH 2006 SUPPLEMENT www.neurosurgery-online.com
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