Outcome after severe brain trauma due to acute subdural ......March 2009, and 16 centers enrolled 448 patients until April 2010. Both projects were conducted after approval ... GCS

J Neurosurg 117:324–333, 2012

324 J Neurosurg / Volume 117 / August 2012

TraumaTic brain injuries represent a serious public health problem. This injury is the leading cause of death in people younger than 45 years old in the

US, Europe,27 and most other countries.11 It has been es-timated that each year 1 million admissions to European hospitals are caused by TBI.11 Incidence, mortality, and

morbidity of TBI are even higher in developing coun-tries.11

Acute SDH has been recognized as a devastating in-jury. In patients with severe TBI due to acute SDH, mor-tality rates of 60% and more, depending on GCS scores, have been published.13 Some authors have developed algorithms to estimate the probability of functional re-covery29 or poor outcome.22 However, most of the studies on acute SDH came from single centers, were performed more than 10 years ago, and enrolled comparatively few patients. In addition, most previous studies enrolled pa-tients with mild, moderate, and severe TBI. The goal of this study was to identify factors influencing outcomes after severe TBI due to acute SDH using fairly recent

Outcome after severe brain trauma due to acute subdural hematoma

Clinical articleJohannes Leitgeb, M.D.,1 WaLter Mauritz, M.D., Ph.D.,2,3 aLexanDra brazinova, M.D., Ph.D., M.P.h.,4,5 ivan Janciak, Ph.D.,6 Marek MaJDan, Ph.D.,5,7 ingriD WiLbacher, M.sc., Ph.D.,8 anD Martin rusnak, c.sc., M.D., Ph.D.5,9

1Department of Traumatology, Medical University of Vienna; 2Department of Anesthesiology and Intensive Care Medicine, Trauma Hospital “Lorenz Boehler”; 3Vice President, 4Executive Director, 6Information and Data Manager, 7Statistician, 8Senior Research Fellow, and 9President, International Neurotrauma Research Organization, Vienna, Austria; and 5Department of Public Health, Faculty of Health and Social Services, Trnava University, Trnava, Slovakia

Object. In this paper, the authors’ goal was to identify factors contributing to outcomes after severe traumatic brain injury (TBI) due to acute subdural hematoma (SDH).

Methods. Between February 2002 and April 2010, 17 Austrian centers prospectively enrolled 863 patients with moderate and severe TBI into observational studies. Data regarding accident, treatment, and outcomes were col-lected. Data sets from patients who had severe TBI (Glasgow Coma Scale score < 9) and acute SDH were selected. Six-month outcomes were classified as “favorable” if the Glasgow Outcome Scale (GOS) scores were 5 or 4, and they were classified as “unfavorable” if GOS scores were 3 or less. The Rotterdam score was used to classify CT findings, and the scores published by Hukkelhoven et al. were used to estimate the predicted rates of death and of unfavorable outcomes. Univariate (Fisher exact test, t-test, chi-square test) and multivariate (logistic regression) statistics were used to identify factors associated with hospital mortality and favorable outcome.

Results. Of the 738 patients with severe TBI, 360 (49%) had acute SDH. Of these, 168 (46.7%) died in the hos-pital, 67 (18.6%) survived with unfavorable outcome, and 116 (32.2%) survived with favorable outcome. Long-term outcome was unknown in 9 survivors (2.5%). Mortality rates predicted by the Rotterdam CT score showed good cor-relation with observed mortality rates. According to the Hukkelhoven scores, observed/predicted ratios for mortality and unfavorable outcome were 1.09 and 1.02, respectively.

Conclusions. Age, severity of TBI, and neurological status were the main factors influencing outcomes after severe TBI due to acute SDH. Nonoperative management was associated with significantly higher mortality.(http://thejns.org/doi/abs/10.3171/2012.4.JNS111448)

key WorDs • traumatic brain injury • acute subdural hematoma • outcome • prognostic score

Abbreviations used in this paper: AIS = Abbreviated Injury Score; GCS = Glasgow Coma Scale; GOS = Glasgow Outcome Scale; ICP = intracranial pressure; INRO = International Neu-rotrauma Research Organization; ISS = Injury Severity Score; IVH = intraventricular hemorrhage; PD = probability of hospital death; PU = probability of unfavorable long-term outcome; SDH = subdural hematoma; TBI = traumatic brain injury.

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Outcome after severe TBI due to acute SDH

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data from a large sample of patients enrolled in Austrian trauma centers.

MethodsBetween 2001 and 2010 the INRO (a nongovernmen-

tal research organization, founded in 1999 and based in Vienna, Austria) coordinated 2 projects that focused on Austrian patients with TBI. The first project analyzed epi-demiology and hospital treatment of patients with severe TBI as well as the effects of guideline-based treatment.23 This project was begun in March 2002, and 5 centers en-rolled 415 patients until June 2005. The second project focused on prehospital and early hospital management of patients with moderate and severe TBI. It started in March 2009, and 16 centers enrolled 448 patients until April 2010. Both projects were conducted after approval was obtained from the local ethics committees.

Databases developed by INRO were used to collect data for these projects. Data from the 2 projects were compared by examination for significant differences in epidemiology, treatment, and outcomes. No relevant dif-ferences were found, and the 2 databases were merged. The merged database now holds data from 863 patients. Since both projects were purely observational, pediatric and geriatric patients, patients with TBI with multiple trauma, and patients with low GCS scores were enrolled; these patients are usually excluded from industry-spon-sored studies.

The data for this study were collected in 17 Austrian centers. All centers were of tertiary care level and were able to provide patient management according to the Brain Trauma Foundation guidelines for the management of pa-tients with severe TBI.1 The number of patients enrolled by these centers (median 28 [IQR 21–65], range 3–150 patients) varied considerably, as 4 centers participated in both projects, and some centers joined the second project with just a few weeks remaining for patient inclusion.

Treatment in the field was provided by emergency physicians. All patients underwent rapid examination, which included documentation of vital signs (GCS score, pupil status, blood pressure, heart rate, and oxygen satura-tion). Rapid-sequence intubation facilitated by hypnotics and relaxants, ventilation, treatment of hemorrhage, and fluid resuscitation were done as appropriate. After admis-sion, each patient was examined by a trauma team (an-esthesiologists, trauma surgeons, and/or neurosurgeons, radiologists, and nurses), and a CT scan was obtained. The patients then underwent surgery as appropriate and/or were admitted to the ICU. Neurosurgery was provided by neurosurgeons (6 centers) or by trauma surgeons (11 centers) who had the option of consulting neurosurgeons for more difficult cases. Intensive care was provided by anesthesiologists in cooperation with neurosurgeons or trauma surgeons.

Basic patient demographic data, cause and location of trauma, prehospital status and treatment, mechanism and severity of trauma (AIS and ISS), CT scanning findings, laboratory test results, and data on surgical procedures and outcomes were recorded prospectively. Prehospital data were documented by the local paramedics, and these

data were then transferred into the databases. Computed tomography scans were interpreted by neurosurgeons, trauma surgeons, and radiologists, and the summarized findings were entered into a separate page in the databas-es. This page collected detailed data on the appearance of the basal cisterns (open, compressed, or absent), midline shift, and main findings (such as edema, hematoma, and contusions). No central review of CT scans was done in the first project, as no actual images were uploaded into the databases. Central review of the CT scans was done in the second project; CT scans were collected on compact discs, and a radiologist and a trauma surgeon checked the accuracy of the data entered into the database. Data regarding duration of various treatments, complications, and outcome were collected at discharge from the ICU and at hospital discharge. Information on status and lo-cation was recorded at 6 months after injury. This was done by phone calls to the patients and/or their relatives; in some cases the GOS score was recorded at the patients’ follow-up visits to the centers. In all centers, data were collected by local research fellows; the data quality was monitored by the INRO project manager (A.B.). Missing or implausible data were reported to local investigators who then submitted missing or corrected values. Personal data protection was observed, and the identifiers were kept separately from the data.

All patients for whom an acute SDH was noted on their first CT scan were selected for this analysis. Only patients with severe TBI (defined as a GCS score of 8 or less in the field and/or following resuscitation) and who survived at least until admission to the ICU were in-cluded. Data on trauma mechanism, trauma severity, CT findings, treatment, and outcomes were retrieved for each patient. The 6-point Rotterdam CT score15 was used to classify CT findings, and the PD according to this score was calculated using the formula given in the paper. In addition, the Marshall classification19 was also used to classify CT findings. The prognostic scores developed by Hukkelhoven et al.9 were used to estimate the PD and the PU. To describe long-term outcomes, the GOS12 was used. “Favorable outcome” was defined as a GOS score of 5 or 4, and “unfavorable outcome” was defined as a GOS score of 3 or less at 6 months after trauma. According to their hospital outcomes, patients were assigned to the groups “alive” and “dead.” The differences between these 2 groups of patients were analyzed.

The free software provided by P. Wessa (Free Sta-tistics Software version 1.1.23-r6, http://www.wessa.net) was used for calculations. The 2-tailed t-test (for compar-isons of mean values), Fisher exact test (for analysis of 2 × 2 tables), and chi-square test (for analysis of N × 2 contin-gency tables) were done as appropriate to identify differ-ences between the groups. To check for associations with outcomes, 2 logistic regression models were constructed: 1 each for hospital survival and favorable long-term out-come. The parameters age, injury mechanism, sex, ISS, head AIS, direct transfer, prehospital hypotension, pre-hospital hypoxia, pupil reactivity, GCS score, presence of IVH, Rotterdam CT score, and treatment strategy (opera-tive vs nonoperative treatment) were used as confound-ing variables, with backward exclusion of nonsignificant

J. Leitgeb et al.


parameters. A p value < 0.05 was considered statistically significant.

ResultsThere were 863 data sets in the database. Of these,

outcome was not recorded in 18 patients, 9 patients died prior to ICU admission, and 98 patients had only moder-ate TBI (GCS scores of 9–12 after admission); this left 738 patients for analysis. Of these, 360 (48.8%) had an acute SDH on their CT scan and were selected for this analysis.

Demographic data for the 2 groups of patients are given in Table 1. About 70% of the patients were male, and there was no significant difference between the

groups. Sex had no effect on outcome, although female patients were significantly older than males. There was a significant effect of age; patients who survived were significantly younger. Fifty-six percent of the patients who died (94 of 168 patients) were older than 60 years of age. There was a significant increase in mortality rates (from 25% to 63%) with increasing age. With regard to trauma mechanism, there were no significant differences, although the rate of low-level falls was higher in nonsur-vivors. Type of trauma (blunt vs penetrating trauma) had no effect on mortality.

Trauma severity was significantly lower in patients who survived (Table 2); mean ISS, head AIS, GCS score, the number of patients with unreactive pupils, and the number with hypotension and hypoxia in the field were

TABLE 1: Age, sex, and trauma mechanism in 360 patients who suffered a TBI

Value*Parameter Alive Dead Total % Mortality p Value†

patients female 59 (30.7) 55 (32.7) 114 (31.7) 48.2 male 133 (69.3) 113 (67.3) 246 (68.3) 45.9 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.73mean age (yrs) female 63.7 ± 18.6 68.5 ± 19.8 66.0 ± 19.3 male 49.0 ± 19.9 56.7 ± 21.4 52.6 ± 20.9 <0.001 total 53.5 ± 20.6 60.6 ± 21.6 56.8 ± 21.3 <0.001age group (yrs) 1–15 3 (1.6) 1 (0.6) 4 (1.1) 25.0 16–30 34 (17.7) 20 (11.9) 54 (15.0) 37.0 31–45 33 (17.2) 21 (12.5) 54 (15.0) 38.9 46–60 36 (18.8) 32 (19.0) 68 (18.9) 47.1 61–75 53 (27.6) 39 (23.2) 92 (25.6) 42.4 >76 33 (17.2) 55 (32.7) 88 (24.4) 62.5 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.018trauma mechanism blunt assault 4 (2.1) 1 (0.6) 5 (1.4) 20.0 gunshot 0 (0.0) 4 (2.4) 4 (1.1) 100.0 fall <3 m 69 (35.9) 79 (47.0) 148 (41.1) 53.4 fall >3 m 23 (12.0) 16 (9.5) 39 (10.8) 41.0 traffic related 46 (24.0) 34 (20.2) 80 (22.2) 42.5 bicycle 12 (6.2) 11 (6.6) 23 (6.6) sports related 12 (6.2) 4 (2.4) 16 (4.4) 25.0 work related 8 (4.2) 5 (3.0) 13 (3.6) 38.5 unknown 6 (3.1) 2 (1.2) 8 (2.2) 25.0 other 12 (6.2) 12 (7.1) 24 (6.7) 50.0 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.065type of trauma blunt 177 (92.2) 156 (92.9) 333 (92.5) 46.8 penetrating 15 (7.8) 12 (7.1) 27 (7.5) 44.4 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.84

* Mean values are presented as the mean ± SD. All other values are the number of patients (%).† The p values refer to differences between surviving versus nonsurviving patients.



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significantly lower. Fifty-five percent of the patients had GCS scores of 3 or 4; more than 70% of the patients who died, but only 42% of those who survived, had GCS scores of 3 or 4. Nearly two-thirds of the patients from both groups had isolated TBI. Associated injuries with an AIS greater than 2 were seen more frequently in survi-vors, but this difference was not significant. The number of additionally injured regions had no effect on mortality.

With regard to CT findings (Table 3), increasing values of the Rotterdam CT score were significantly as-sociated with increasing mortality rates. No patient had the best score of 1. There was a significant correlation between the PD predicted by the score and the observed mortality rates (y = 1. 2281x + 6.11; R2 = 0.933; p = 0.007

for scores 2–6). According to the Marshall classification, 198 patients (55%) had an evacuated mass lesion, and 162 (45%) had a nonevacuated mass lesion. Mortality was lower in the patients with evacuated mass lesions (42.9% vs 51.2%), but this difference was not significant (p = 0.14). With the exception of IVH, additional CT findings were not associated with significantly increased mortal-ity.

With regard to treatment, indirect transfer was asso-ciated with significantly lower mortality (Table 4). The mode of transport, rates of prehospital intubation, and timing of CT scanning and surgery were not significantly different. Conservative management without ICP moni-toring was associated with the highest mortality (64.2%);

TABLE 2: Parameters relevant to severity of brain injury and overall severity of injury, and incidence of field hypotension and hypoxia

Value*Parameter Alive Dead Total % Mortality p Value†

additional regions w/ AIS >2 0 119 (62.0) 113 (67.3) 232 (64.4) 48.7 1 41 (21.4) 32 (19.0) 73 (20.3) 43.8 2 24 (12.5) 16 (9.5) 40 (11.1) 40.0 >2 8 (4.2) 7 (4.2) 15 (4.2) 46.7 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.72GCS score 3 70 (36.5) 96 (57.1) 166 (46.1) 57.8 4 11 (5.7) 23 (13.7) 34 (9.4) 67.6 5 23 (12.0) 19 (11.3) 42 (11.7) 45.2 6 34 (17.7) 19 (11.3) 53 (14.7) 35.8 7 25 (13.0) 6 (3.6) 31 (8.6) 19.4 8 29 (15.1) 5 (3.0) 34 (9.4) 14.7 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 <0.001mean ISS 24.1 ± 10.5 38.7 ± 23.3 31.0 ± 19.1 <0.001mean head AIS 4.1 ± 0.5 4.8 ± 0.9 4.4 ± 0.8 <0.001mean enrollment GCS score 5.1 ± 1.9 4.0 ± 1.4 4.6 ± 1.8 <0.001pupils 0 reactive 11 (5.7) 49 (29.2) 60 (16.7) 81.7 1 reactive 1 (0.5) 2 (1.2) 3 (0.8) 66.7 2 reactive 143 (74.5) 86 (51.2) 229 (63.6) 37.6 unknown 37 (19.3) 31 (18.5) 68 (18.9) 45.6 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 <0.001prehospital hypotension no 183 (95.3) 147 (87.5) 330 (91.7) 44.5 yes 9 (4.7) 21 (12.5) 30 (8.3) 70.0 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.012prehospital hypoxia no 174 (90.6) 140 (83.3) 314 (87.2) 44.6 yes 18 (9.4) 28 (16.7) 46 (12.8) 60.9 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0 .041

* Mean values are presented as the mean ± SD. All other values are the number of patients (%).† The p values refer to differences between surviving versus nonsurviving patients.

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mortality rates were significantly lower (p = 0.01) with conservative management with ICP monitoring (38.3%) or with operative management (42.9%). Primary craniec-tomy was associated with lower mortality than cranioto-my (39% vs 46%), but the difference was not significant (p = 0.32). The use of ICP monitoring was associated with significantly lower mortality (42% vs 54%, p = 0.037).

The observed hospital mortality rate was 46.7% (168 of 360 patients), and the PD predicted by the Huk-kelhoven score was 42.7% ± 22.3%. The observed versus predicted ratio for mortality was 1.09; this ratio equals 32 unexpected deaths but is within the predicted range. The PD predicted by the Rotterdam CT score was 52.6 ± 18; the observed versus predicted ratio for mortality for this score was 0.89; this equals 39 unexpected survivors and is also within the predicted range. Most of the non-survivors died in the ICU (146 [87%]), and 22 died on intermediate or regular wards. Most patients died of brain death (113 [67.3%] of 168), cardiovascular problems (24 [14.3%] of 168), hemorrhage (7 [4.2%] of 168), or multiple organ failure (6 [3.6%] of 168). Four patients (2.4%) died of other causes, and the cause of death was unknown in the remaining 14 patients (8.4%). Logistic regression re-

vealed that age, GCS score, pupil reactivity, head AIS, prehospital hypoxia, and nonoperative treatment were significantly associated with hospital mortality (Table 5). Sex, injury mechanism, ISS, indirect transfer, prehospital hypotension, Rotterdam CT score, and presence of IVH had no significant influence on hospital mortality.

Of the 192 hospital survivors 116 (60.4%) had favor-able outcomes, 67 (34.9%) had unfavorable outcomes, and long-term outcome was unknown in 9 patients (4.7%). Of all patients in this study, 116 (32.2%) had favorable outcomes, 235 (65.3%) had unfavorable outcomes (168 patients who died in the hospital plus 67 patients who survived with unfavorable outcomes), and long-term out-come was unknown in 9 patients (2.5% of all patients). The PU predicted by the Hukkelhoven score was 63.8% ± 21.9%; the observed/predicted ratio for unfavorable out-come was 1.02. This ratio equaled 7 patients with unex-pected unfavorable outcome and was within the range of the predicted PU. If all patients with unknown long-term outcome were classified as “unfavorable” the observed/predicted ratio for unfavorable outcome would be 1.06 and would still be within the predicted range. Logistic re-gression analysis revealed that age, GCS score, head AIS,

TABLE 3: Rotterdam CT scores and various additional CT findings*

No. of Patients (%)Parameter Alive Dead Total % Mortality p Value†

Rotterdam CT score 2 42 (21.9) 22 (13.1) 64 (17.8) 34.4 3 91 (47.4) 55 (32.7) 146 (40.6) 37.7 4 42 (21.9) 44 (26.2) 86 (23.9) 51.2 5 14 (7.3) 35 (20.8) 49 (13.6) 71.4 6 2 (1.0) 8 (4.8) 10 (2.8) 80.0 ND 1 (0.5) 4 (2.4) 5 (1.4) 80.0 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 <0.001additional EDH no 169 (88.0) 142 (84.5) 311 (86.4) 45.7 yes 23 (12.0) 26 (15.5) 49 (13.6) 53.1 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.36additional SAH no 93 (48.4) 70 (41.7) 163 (45.3) 42.9 yes 99 (51.6) 98 (58.3) 197 (54.7) 49.7 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.21additional IVH no 180 (93.8) 143 (85.1) 323 (89.7) 44.3 yes 12 (6.3) 25 (14.9) 37 (10.3) 67.6 total 192 (100.0) 168 (10 0.0) 360 (100.0) 46.7 0.009additional contusion no 104 (54.2) 93 (55.4) 197 (54.7) 47.2 yes 88 (45.8) 75 (44.6) 163 (45.3) 46.0 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.83

* EDH = epidural hematoma; ND = no data; SAH = subarachnoid hemorrhage.† The p values refer to differences between surviving versus nonsurviving patients.



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TABLE 4: Selected parameters of prehospital and hospital treatment*

No. of Patients (%) Parameter Alive Dead Total % Mortality p Value†

indirect transfer no 147 (76.6) 148 (88.1) 295 (81.9) 50.2 yes 45 (23.4) 20 (11.9) 65 (18.1) 30.8 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.006mode of transport air 70 (36.5) 54 (32.1) 124 (34.4) 43.5 ground 122 (63.5) 114 (67.9) 236 (65.6) 48.3 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.44prehospital intubation no 67 (34.9) 50 (29.8) 117 (32.5) 42.7 yes 125 (65.1) 118 (70.2) 243 (67.5) 48.6 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.31time btwn admission & CT scan (mins) 0–30 116 (60.4) 97 (57.7) 213 (59.2) 45.5 31–60 48 (25.0) 44 (26.2) 92 (25.6) 47.8 61–90 13 (6.8) 7 (4.2) 20 (5.6) 35.0 >90 14 (7.3) 14 (8.3) 28 (7.8) 50.0 unknown 1 (0.5) 6 (3.6) 7 (1.9) 85.7 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.73time btwn CT scan & start of op (mins) 0–20 31 (19.6) 25 (22.1) 56 (20.7) 44.6 21–40 45 (28.5) 32 (28.3) 77 (28.4) 41.6 41–60 16 (10.1) 18 (15.9) 34 (12.5) 52.9 61–120 28 (17.7) 23 (20.4) 51 (18.8) 45.1 >120 38 (24.1) 15 (13.3) 53 (19.6) 28.3 total 158 (100.0) 113 (100.0) 271 (100.0) 41.7 0.19neurosurgery no surgery 29 (15.1) 52 (31.0) 81 (22.5) 64.2 ICP monitoring 50 (26.0) 31 (18.5) 81 (22.5) 38.3 ASDH evacuation 93 (48.4) 72 (42.9) 165 (45.8) 43.6 ASDH + EDH evacuation 16 (8.3) 9 (5.4) 25 (6.9) 36.0 ASDH + ICH evacuation 4 (2.1) 2 (1.2) 6 (1.7) 33.3 ASDH + EDH + ICH evacuation 0 (0.0) 1 (0.6) 1 (0.3) 100.0 decompressive 0 (0.0) 1 (0.6) 1 (0.3) 100.0 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.01surgical technique craniectomy 55 (48.7) 35 (41.2 90 (45.5) 38.9 craniotomy 58 (51.3) 49 (57.6) 107 (54.0) 45.8 decompressive 0 (0.0) 1 (1.2) 1 (0.5) 100.0 total 113 (100.0) 85 (100.0) 198 (100.0) 42.9 0.32ICP monitoring no 61 (31.8) 72 (42.9) 133 (36.9) 54.1 yes 131 (68.2) 96 (57.1) 227 (63.1) 42.3 total 192 (100.0) 168 (100.0) 360 (100.0) 46.7 0.037

* ASDH = acute SDH; ICH = intracerebral hematoma.† The p values refer to differences between surviving versus nonsurviving patients.

J. Leitgeb et al.


and the Rotterdam CT score were significantly associated with long-term outcomes (Table 5). All other variables had no significant influence on long-term outcome.

DiscussionThis study presents a large sample of patients from 17

Austrian centers who had severe TBI due to acute SDH. Our findings show that acute SDH is the mass lesion with the highest incidence (49%) in patients with severe TBI. They also show that acute SDH is associated with high mortality (47%) and a low rate of favorable long-term outcomes (32%) in this group of patients. These poor re-sults, however, were well within the ranges predicted by the scores developed by Hukkelhoven et al.9 and by Maas et al.15 Our study also shows that age, neurological status,

and severity of trauma are the main factors determining outcomes after severe TBI due to acute SDH.

The results presented here, however, are actually bet-ter than those published by some other authors. Koç et al.13 reported 60% mortality and 38% favorable outcome for patients with acute SDH who needed surgery; that study included patients with moderate TBI, whereas our study included only patients with severe TBI. Hospital mortality for patients who had acute SDH evacuation was 43% in our study. It seems that nearly all survivors in the study by Koç et al.13 had favorable outcomes, and more than one-third of the survivors had unfavorable outcomes in our study. Hatashita et al.5 found an overall mortal-ity of 55% and favorable outcome of 30% in surgically treated patients with acute SDH; their study also included patients with moderate TBI. These results are somewhat closer to our own results than those of Koç et al.13 In

TABLE 5: Coefficients of logistic regressions for hospital outcome and 6-month outcome*

Variable Parameter Standard Error t Statistic 2-Sided p Value Significant

hospital outcome† intercept 1.4391 2.2788 0.6315 0.5281 age −0.0304 0.0077 −3.9777 0.0008 yes GCS score 0.3019 0.0815 3.7072 0.0002 yes pupils 1.2261 0.4089 2.9985 0.0029 yes head AIS score −1.0352 0.2730 −3.792 0.0002 yes field hypoxia 1.1149 0.3621 2.5499 0.0032 yes op treatment 1.3882 0.4023 3.4508 0.0006 yes sex −0.3046 0.2997 −1.0161 0.3102 no mechanism −0.2381 0.1771 −1.3443 0.1797 no ISS −0.0221 0.0129 −1.7096 0.0882 no field hypotension −0.2802 0.5455 −0.5138 0.6077 no transfer 0.3403 0.2081 1.6348 0.1029 no IVH 0.1991 0.2816 0.7072 0.4799 no Rotterdam score 0.2034 0.2957 0.6881 0.4918 no6-mo outcome‡ intercept 2.7676 2.3698 1.1678 0.2437 age −0.0333 0.0075 −4.3893 0.0002 yes GCS score 0.2049 0.0762 2.6893 0.0075 yes head AIS score −1.1776 0.2803 −4.2019 0.0003 yes Rotterdam score 0.9242 0.4689 1.9709 0.0596 yes pupils 0.8248 0.4088 2.9714 0.1665 no field hypoxia 0.1825 0.4446 0.4106 0.6817 no op treatment 0.0203 0.3020 0.0673 0.9463 no sex −0.2438 0.3009 −0.8102 0.4183 no mechanism −0.2298 0.1716 −1.3389 0.1815 no ISS −0.0069 0.01415 −0.4939 0.6217 no field hypotension −0.3723 0.5868 −0.6344 0.5262 no transfer 0.4029 0.3583 1.1245 0.2616 no IVH 0.2480 0.2817 0.8805 0.3792 no

* All parameters that were included in the model are presented, including those that had no significant influence.† Survival = 1.‡ Favorable = 1.



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another study, Servadei et al.25 reported a 35.4% favor-able outcome in 65 patients with severe TBI due to acute SDH, and they managed 20% of the patients conserva-tively. These results are in accordance with our own ex-periences. According to Dent et al.2 only 24% of patients with severe TBI due to acute SDH who required urgent surgery had a favorable outcome, which is the worst result published so far. However, it has to be noted that none of the other authors provided data on the expected mortal-ity of their patients, because no score had been available at the times of their studies. Trauma severity and, thus, expected mortality might have been different from that seen in our study.

With regard to factors influencing outcomes, the impact of GCS scores has been studied most frequently. The most detailed analysis of the effects of GCS scores on outcomes after severe TBI was done in the IMPACT (International Mission for Prognosis and Analsysis of Clinical Trials in TBI) study.16 It was shown that the GCS score at hospital admission was strongly related to the GOS score at 6 months after trauma (OR 1.7–7.5). Hatashita et al.5 also found a strong correlation between GCS scores and mortality: nearly all patients with acute SDH and GCS scores of 3 died (93% mortality), patients with GCS scores of 4–6 had a mortality of 45%–67%, and all patients with GCS scores of 7 or higher survived. These results are confirmed by the study by Koç et al.13 Gennarelli et al.3 published mortality rates of 74% for pa-tients with acute SDH and GCS scores of 3–5, and 36% for those with GCS scores of 6–8. This significant as-sociation between GCS scores and outcomes was also found in our study.

Age is one of the most important factors influencing survival as well as recovery after severe TBI, as demon-strated in the large study done by Hukkelhoven et al.10 They estimated that the odds for poor outcome increased by 40%–50% per 10 years of age. With regard to patients with acute SDH, Howard et al.7 reported that overall mor-tality was more than 4 times higher in patients older than 65 years than in those 18–40 years. In the study by Koç et al.,13 age did not significantly influence outcome, although their findings demonstrated that an older age was associ-ated with increased mortality. The significant influence of age on outcomes was also found in our study.

Koç et al.13 reported that patients with acute SDH who presented with bilateral or unilateral unreactive pu-pils had mortality rates of 97% and 81%, respectively. In the study by Marmarou et al.,16 one or both unreactive pupils were significantly associated with poor outcome (OR 2.71–7.31). With regard to hospital outcome, this as-sociation was also observed in our study; however, pupil reactivity had no significant effect on long-term outcome.

Lefering et al.14 analyzed data from patients with head injury from the German Trauma Registry and re-ported that patients with concomitant injuries with an AIS greater than 3 had a 5% higher mortality rate than patients without concomitant injuries. Heinzelmann et al.6 came to different conclusions. They found that extra-cranial injuries had no significant effect on outcomes of patients with epidural hematoma. In our study, additional injuries also had no effect on outcomes.

With regard to CT findings, our study showed that the PD predicted by the Rotterdam CT score correlated significantly with the observed mortality rates. Unfortu-nately, this correlation could only be calculated for scores 2–6, as our study had no patient with a score of 1. The Rotterdam CT score was much better suited for our group of patients than the Marshall score, since our patients fell into 2 of the 6 possible groups. The Rotterdam CT score had significant effect on long-term outcome but not on hospital mortality.

With regard to surgical management, Seelig et al.24 reported a mortality of 30% for comatose patients treated less than 4 hours after injury versus 90% mortality for those treated after 4 hours. Other authors, however, came to different conclusions. Wilberger et al.28 found that mor-tality in patients with admission GCS scores less than 8 who underwent surgery within 4 hours of injury was 59% versus 69% for those who underwent surgery after 4 hours. They were not able to confirm a significant influ-ence of timing of surgery on outcome. These findings are supported by the studies done by Stone et al.,26 Hatashita et al.,5 and Koç et al.13 Timing of surgery also had no effect on outcome in our study. Craniotomy and crani-ectomy were associated with comparable mortality rates in our study. This confirms earlier results from Paci et al.21 However, these authors found higher mortality rates with craniectomy, which is in contrast to our findings. The multivariate analysis showed that conservative man-agement of patients with acute SDH had significant ef-fect on hospital mortality but not on long-term outcome. However, this might reflect a conscious decision by the medical team and the patients’ families not to treat the most severely injured patients. The conservatively man-aged patients had the highest PD (0.47) of all patients with acute SDH, while the PD of all surgically treated patients was 0.41.

Another treatment aspect that may influence out-comes is direct transfer to a specialized neurosurgical center. Stone et al.26 found that in patients with acute SDH, mortality was significantly lower for those who had been transported directly to their center (50% vs 76%). More recently Härtl et al.4 reported that indirect trans-fer was associated with a 50% increase in mortality for patients who had suffered severe TBI. We were unable to demonstrate an effect of direct transfer on outcomes in our study; mortality was actually lower in the patients with indirect transfer. This, however, was not significant in the logistic regression analysis. There are 2 possible reasons for this surprising result. First, only patients who were admitted to the ICU were enrolled into the first study; patients who did not survive until ICU admission might have been lost. Second, there could be a “selection bias;” it might be that only patients who were considered to have a chance of survival were transferred to the study centers, and the patients in the worst condition might have died at the primary hospital.

Limitations of the StudyThe scores used to estimate PD and PU have not been

validated for our study population. These scores were created from the international and North American data

J. Leitgeb et al.


from the tirilazad trial8,18 and were validated against the core data set of the EBIC (European Brain Injury Consor-tium) survey20 and data from the Traumatic Coma Data Bank.17 It is quite likely that our patients are comparable to those from the EBIC centers and the international arm of the tirilazad trial. There could, however, be subtle dif-ferences, and the observed/expected ratios for mortality and unfavorable outcome estimated for our groups of pa-tients may be incorrect. The use of these scores seemed justified, however, because interpretation of our results would be difficult without comparison with the predic-tions.

ConclusionsAcute SDH was found in almost half of the patients

with severe TBI. Forty-seven percent of the patients died in the hospital, 19% survived with unfavorable out-comes, and 32% had favorable outcomes. These results were within the predicted ranges. Age, severity of TBI, and neurological status were the main factors influenc-ing morbidity and mortality. Nonoperative management was associated with significantly higher mortality. The mortality predictions made by the Rotterdam CT score correlated well with the observed mortality rates.

Disclosure

The data used for this study were collected for a project funded by the Austrian Workers’ Compensation Board (AUVA; FK 33/2003) and by the “Jubilee Fund” of the Austrian National Bank (Project 8987), and for a project funded by the Ministry of Health (Contract October 15, 2008) and the AUVA (FK 11/2008 and FK 11/2010). INRO is supported by an annual grant from Mrs. Ala Auersperg-Isham and Mr. Ralph Isham, and by small donations from various sources.

Author contributions to the study and manuscript preparation include the following. Conception and design: Leitgeb, Mauritz. Acquisition of data: Leitgeb, Brazinova. Analysis and interpreta-tion of data: Leitgeb, Janciak. Drafting the article: Leitgeb, Majdan. Critically revising the article: Leitgeb, Mauritz, Brazinova, Majdan, Wilbacher, Rusnak. Reviewed submitted version of manuscript: Leitgeb, Mauritz, Brazinova, Majdan, Wilbacher, Rusnak. Approved the final version of the manuscript on behalf of all authors: Leitgeb. Administrative/technical/material support: Wilbacher. Study super-vision: Rusnak.

Acknowledgments

The authors are very grateful to the investigators from the participating centers: H. Artmann, M.D. (Schwarzach), N. Bauer, M.D. (Linz UKH), F. Botha, M.D. (Linz WJ), F. Chmeliczek, M.D. (Salz burg LKA), G. Clarici, M.D. (Graz Uni), D. Csomor, M.D. (Wr. Neustadt), R. Folie, M.D. (Feldkirch), R. Germann, M.D., Ph.D. (Feldkirch), F. Gruber, M.D. (Linz AKH), H.-D. Gulle, M.D. (Klag en furt), T. Haidacher, M.D. (Graz UKH), G. Herzer, M.D. (Wr. Neustadt), P. Hohenauer, M.D. (Salzburg LKA), A. Hüblauer, M.D. (Horn), J. Lanner, M.D. (Salzburg UKH), V. Lorenz, M.D. (Wien UKH XII), C. Mirth, M.D. (St. Pölten), W. Mitterndorfer, M.D. (Linz AKH), W. Moser, M.D. (Klagenfurt), H. Schmied, M.D. (Amstetten), K.-H. Stadlbauer, M.D., Ph.D. (Innsbruck), H. Stelt zer, M.D., Ph.D. (Wien UKH XII), Ernst Trampitsch, M.D. (Klag enfurt), A. Waltensdorfer, M.D. (Graz Uni), and A. Zechner, M.D. (Klagenfurt).

References

1. Bullock R, Chesnut RM, Clifton G, Ghajar J, Marion DW, Na-rayan RK, et al: Guidelines for the management of severe head injury. Eur J Emerg Med 3:109–127, 1996

2. Dent DL, Croce MA, Menke PG, Young BH, Hinson MS, Kudsk KA, et al: Prognostic factors after acute subdural he-matoma. J Trauma 39:36–43, 1995

3. Gennarelli TA, Spielman GM, Langfitt TW, Gildenberg PL, Harrington T, Jane JA, et al: Influence of the type of intracra-nial lesion on outcome from severe head injury. J Neurosurg 56:26–32, 1982

4. Härtl R, Gerber LM, Iacono L, Ni Q, Lyons K, Ghajar J: Di-rect transport within an organized state trauma system reduc-es mortality in patients with severe traumatic brain injury. J Trauma 60:1250–1256, 2006

5. Hatashita S, Koga N, Hosaka Y, Takagi S: Acute subdural he-matoma: severity of injury, surgical intervention, and mortal-ity. Neurol Med Chir (Tokyo) 33:13–18, 1993

6. Heinzelmann M, Platz A, Imhof HG: Outcome after acute ex-tradural haematoma, influence of additional injuries and neu-rological complications in the ICU. Injury 27:345–349, 1996

7. Howard MA III, Gross AS, Dacey RG Jr, Winn HR: Acute subdural hematomas: an age-dependent clinical entity. J Neurosurg 71:858–863, 1989

8. Hukkelhoven CW, Steyerberg EW, Farace E, Habbema JD, Marshall LF, Maas AI: Regional differences in patient charac-teristics, case management, and outcomes in traumatic brain injury: experience from the tirilazad trials. J Neurosurg 97: 549–557, 2002

9. Hukkelhoven CW, Steyerberg EW, Habbema JD, Farace E, Marmarou A, Murray GD, et al: Predicting outcome after traumatic brain injury: development and validation of a prog-nostic score based on admission characteristics. J Neurotrauma 22:1025–1039, 2005

10. Hukkelhoven CW, Steyerberg EW, Rampen AJ, Farace E, Habbema JD, Marshall LF, et al: Patient age and outcome fol-lowing severe traumatic brain injury: an analysis of 5600 pa-tients. J Neurosurg 99:666–673, 2003

11. Hyder AA, Wunderlich CA, Puvanachandra P, Gururaj G, Ko-busingye OC: The impact of traumatic brain injuries: a global perspective. NeuroRehabilitation 22:341–353, 2007

12. Jennett B, Bond M: Assessment of outcome after severe brain damage. Lancet 1:480–484, 1975

13. Koç RK, Akdemir H, Oktem IS, Meral M, Menkü A: Acute subdural hematoma: outcome and outcome prediction. Neurosurg Rev 20:239–244, 1997

14. Lefering R, Paffrath T, Linker R, Bouillon B, Neugebauer EA: Head injury and outcome—what influence do concomitant in-juries have? J Trauma 65:1036–1044, 2008

15. Maas AI, Hukkelhoven CW, Marshall LF, Steyerberg EW: Prediction of outcome in traumatic brain injury with com-puted tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. Neurosurgery 57:1173–1182, 2005

16. Marmarou A, Lu J, Butcher I, McHugh GS, Murray GD, Stey-erberg EW, et al: Prognostic value of the Glasgow Coma Scale and pupil reactivity in traumatic brain injury assessed pre-hospital and on enrollment: an IMPACT analysis. J Neurotrauma 24:270–280, 2007

17. Marshall LF, Becker DP, Bowers SA, Cayard C, Eisenberg H, Gross CR, et al: The National Traumatic Coma Data Bank. Part 1: Design, purpose, goals, and results. J Neurosurg 59: 276–284, 1983

18. Marshall LF, Maas AI, Marshall SB, Bricolo A, Fearnside M, Iannotti F, et al: A multicenter trial on the efficacy of using tirilazad mesylate in cases of head injury. J Neurosurg 89: 519–525, 1998



333

19. Marshall LF, Marshall SB, Klauber MR, van Berkum Clark M, Eisenberg HM, Jane JA, et al: A new classification of head injury based on computerized tomography. J Neurosurg 75: S14–S20, 1991

20. Murray GD, Teasdale GM, Braakman R, Cohadon F, Dearden M, Iannotti F, et al: The European Brain Injury Consortium survey of head injuries. Acta Neurochir (Wien) 141:223–236, 1999

21. Paci GM, Sise MJ, Sise CB, Sack DI, Shackford SR, Kureshi SA, et al: Preemptive craniectomy with craniotomy: what role in the management of severe traumatic brain injury? J Trauma 67:531–536, 2009

22. Phuenpathom N, Choomuang M, Ratanalert S: Outcome and outcome prediction in acute subdural hematoma. Surg Neurol 40:22–25, 1993

23. Rusnak M, Janciak I, Majdan M, Wilbacher I, Mauritz W: Se-vere traumatic brain injury in Austria VI: effects of guide-line-based management. Wien Klin Wochenschr 119:64–71, 2007

24. Seelig JM, Becker DP, Miller JD, Greenberg RP, Ward JD, Choi SC: Traumatic acute subdural hematoma: major mortal-ity reduction in comatose patients treated within four hours. N Engl J Med 304:1511–1518, 1981

25. Servadei F, Nasi MT, Cremonini AM, Giuliani G, Cenni P, Nanni A: Importance of a reliable admission Glasgow Coma Scale score for determining the need for evacuation of post-

traumatic subdural hematomas: a prospective study of 65 pa-tients. J Trauma 44:868–873, 1998

26. Stone JL, Lowe RJ, Jonasson O, Baker RJ, Barrett J, Older-shaw JB, et al: Acute subdural hematoma: direct admission to a trauma center yields improved results. J Trauma 26:445–450, 1986

27. Tagliaferri F, Compagnone C, Korsic M, Servadei F, Kraus J: A systematic review of brain injury epidemiology in Europe. Acta Neurochir (Wien) 148:255–268, 2006

28. Wilberger JE Jr, Harris M, Diamond DL: Acute subdural he-matoma: morbidity, mortality, and operative timing. J Neurosurg 74:212–218, 1991

29. Yanaka K, Kamezaki T, Yamada T, Takano S, Meguro K, Nose T: Acute subdural hematoma—prediction of outcome with a linear discriminant function. Neurol Med Chir (Tokyo) 33:552–558, 1993

Manuscript submitted August 26, 2011. Accepted April 23, 2012.Please include this information when citing this paper: pub-

lished online May 25, 2012; DOI: 10.3171/2012.4.JNS111448.Address correspondence to: Johannes Leitgeb, M.D., Depart-

ment of Traumatology, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria. email: [email protected].

Outcome after severe brain trauma due to acute subdural ......March 2009, and 16 centers enrolled 448 patients until April 2010. Both projects were conducted after approval ... GCS

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