British Journal of Neurosurgery, 2014; Early Online: 1–6 © 2014 The Neurosurgical Foundation ISSN: 0268-8697 print / ISSN 1360-046X online DOI: 10.3109/02688697.2014.918578
ORIGINAL ARTICLE
Risk factors for development of significant chronic subdural hematoma following conservative treatment of acute subdural hemorrhage Yosef Laviv & Zvi Harry Rappaport
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Department of Neurosurgery, Beilinson Hospital, Rabin Medical Center, Petah Tiqva, Israel
Introduction
Absract Objective. One of the complications of untreated acute subdural hemorrhage (aSDH) is the late development of chronic subdural hematomas (cSDH). cSDH may cause major neurologic deficits, requiring their surgical evacuation. The aim of our work was to find risk factors for the development of significant cSDH requiring surgery following conservative treatment of traumarelated aSDH. Methods. In a retrospective manner, we analyzed the data of 95 adult patients admitted with a non-surgical, traumatic aSDH. The patients were divided into two groups. The first group contained 52 patients who did not, on follow-up, develop cSDH requiring surgery. The second group contained 43 patients who ended up with a significant cSDH, based on clinical and radiological criteria, requiring surgical evacuation. Data acquisition and comparison between the two groups was performed by analyzing the patients’ charts for diverse medical conditions and other trauma-related parameters. Results. The operation rate was significantly higher in patients with medical history of ischemic heart disease (IHD) or hypertension (66.7% vs. 38%, p ⴝ 0.019 and 56.9% vs. 20%, p ⬍ 0.01, respectively), with a 4-fold increase in the risk for developing surgical cSDH in patients with IHD and a 6-fold increase in the risk in patients with hypertension (odds ratio 4.2 [95% CI for odds, 1.3–13.1] and 5.9 [95% C.I for odds, 1.6–21.5], respectively). Among 21 patients, 20 (95%) patients, who were either on more than 1 anti-aggregant agents (AAA), used Clopidrogrel, or took anti-coagulant drug were in the operative group (OG). A larger initial thickness of the aSDH was statistically significant in the OG as compared to the non-OG (8.9 mm ⴞ 4.6 vs. 5.5 mm ⴞ 2.1, p ⬍ 0.001). Conclusion. Head-trauma patients with a medical history of IHD or hypertension, patients on more than one AAA or anti-coagulant agents and patients with worse initial CT scan parameters are at risk of developing significant cSDH requiring surgery after conservative treatment of aSDH and consequently should have closer follow-up.
Subdural hematomas represent intracranial extra-axial mass lesions which are usually seen after traumatic brain injury. Acute subdural hematoma (aSDH) usually appears in the first 3 days after the trauma and carries mortality ranges of 50–100%.1–5 Despite these high mortality rates, and although it has been shown that a quick surgical evacuation of an aSDH can reduce mortality rate to as low as 30%,4 not every trauma-related aSDH needs to be treated surgically. Several studies tried to demonstrate the impact of conservative (non-operative) management of aSDH. Wong6 tried to identify parameters that would predict the failure of initial nonoperative management. 6 of 31 patients with GCS scores between 6 and 15 who were initially treated without surgery required a later craniotomy because of neurological deterioration (performed within 3 days). The authors found that a midline shift (MLS) greater than 5 mm in patients with a GCS score of lower than 15 on the initial CT scan was significantly related to the failure of nonoperative treatment. Hematoma volume and thickness of the hematoma were not predictive. Mathew et al.3 reviewed the data on 23 patients with GCS scores between 13 and 15 who were initially treated nonoperatively. All patients had an isolated aSDH. Six patients (25%) required delayed (mean, 14 days) evacuation of their SDH. Servadei et al.7 treated 15 of 65 comatose patients with aSDH in a nonoperative way. Of these, two patients required delayed surgery based on increasing ICP and the development of intracerebral hematomas. Good outcome was achieved in 23% of the patients in the surgery group and 67% of the patients in the nonoperative group. The authors concluded that nonoperative treatment can be safely used for a defined group of comatose patients with aSDH. Finally, Feliciano and De Jesús8 prospectively evaluated 38 patients with traumatic aSDH who were conservatively treated. They found that patients less than 65 years old, patients with GCS score greater than 8, and patients with
Keywords: acute; chronic; hemorrhage; risk factors; subdural
Correspondence: Dr. Yosef Laviv, MD, Department of Neurosurgery, Beilinson Hospital, Rabin Medical Center, Petah Tiqva 49100, Israel. Tel:⫹ 03-9376401. Fax: ⫹ 03-9219774. E-mail: [email protected] Received for publication 15 December 2012; accepted 21 April 2014
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hematoma thicknesses 10 mm or lesser and midline shifts 5 mm or lesser had a favorable or functionally independent outcome in 80–85% of the cases. The studies above show that aSDH can be managed conservatively under the appropriate clinical and radiological conditions (even in comatose patients). However, they also demonstrated that some patients may require delayed evacuation of the SDH at the subacute or chronic phase of the hematoma.3,6,9 Since clinically significant chronic subdural hematomas (cSDH) might cause significant morbidity (especially in the elderly) and because the identification and timely treatment of this condition may have great effect on reducing morbidity, it is important to know which patients are at risk for developing this complication. The purpose of this study was to identify special characteristics and risk factors in patients with traumatic aSDH that develops clinically significant cSDH after conservative treatment of the acute hemorrhage.
Patients and methods This study was conducted according to the principles of the local ethics committee. We analyzed the data of 95 patients who were admitted to our neurosurgical department with a non-surgical, traumatic aSDH during the years 2002–2012. All patients were over the age of 40 years and all suffered a relatively low-velocity head trauma. In a retrospective manner, the patients were divided into two groups. The first group contained 52 patients who were treated conservatively for their aSDH and did not develop significant cSDH requiring surgical evacuation on follow-up. The second group contained 43 patients who were also treated initially in a conservative manner, which resulted in cSDH that needed surgical evacuation based on clinical and radiological criteria. Data acquisition and comparison between the two groups was performed by analyzing the patients’ charts for age, sex, and home medication at the time of admission. The patients’ medical histories were also screened for diverse
medical conditions and other parameters related to the patients’ clinical and neurological status at the time of injury and imaging-related parameters of the SDH. In the operative group (OG), the presence of surgical cSDH, unilateral or bilateral, was confirmed using computed tomographic (CT) scans. In the OG, all patients underwent a standard surgical procedure consisting of a burr hole, irrigation, and closed-system drainage. Surgery was performed under general anesthesia. All patients had at least six months of radiological and clinical follow-up after the initial trauma in our out-patient units. Statistical analysis was performed using SAS (version 8.02; SAS Institute Inc., Cary, NC). The tests used for analysis are indicated with the respective results. For all analyses, a p value of less than 0.05 was considered statistically significant.
Results In the majority of cases the head trauma was caused by falling, usually from a standing position (81.4% in the OG and 84.6% in the NOG). The rest of the cases included blunt object trauma (2 OG and 1 NOG) and pedestrian accidents (4 OG and 7 NOG). Time from initial trauma to operation was 23.3 days on average (range, 10–64). Fifteen patients in the OG (34.9%) were operated on the day of recurrent admission. Only one patient in the OG (2.4%) required more than one operation. The clinical data of 95 consecutive cases are summarized in Table I. There were 53 men (55.8%) and 42 women (44.2%). Mean age of patients in the OG (77.5 ⫾ 10.2) was not significantly different from that in the NOG (74.3 ⫾ 10.4). The operation rate was significantly higher in patients with medical history of ischemic heart disease (IHD) or hypertension (66.7% vs. 38%, p ⫽ 0.019 and 56.9% vs. 20%, p ⬍ 0.01, respectively). These differences were maintained during multi-variant logistic regression, with four times the risk for developing surgical cSDH in patients with IHD and six times the risk in patients with hypertension (odds ratio 4.2 [95%
Table I. Characteristics and clinical findings in the operative group (OG) and the nonoperative group (NOG). OG (n ⫽ 43) Sex Male Female Mean age IHD HTN DM Dementia CVA Anti HTN drugs Ca – blocker β – blocker α – blocker ACE – inh AGT – inh Diuretics Anti-diabetic Home discharge 6-month mortality Abnormal lab
NOG (n ⫽ 52)
Total (n ⫽ 95)
p Value
Test
0.685
Chi-square
t test Chi-square Chi-square Chi-square Chi-square Chi-square Chi-square
25 (58.1%) 18 (41.9%) 77.6 ⫾ 10.2 16 (37.2%) 37 (86.0%) 7 (16.3%) 4 (9.3%) 8 (18.6%)
28 (53.8%) 24 (46.2%) 74.3 ⫾ 10.4 8 (15.4%) 28 (53.8%) 11 (21.1%) 7 (13.5%) 2 (3.8%)
53 (55.8%) 42 (44.2%) 75.9 ⫾ 10.3 24 (25.2%) 65 (68.4%) 18 (18.9%) 11 (11.6%) 10 (10.5%)
0.127 0.019 0.001 0.607 0.749 0.039
15 (34.9%) 16 (37.2%) 5 (11.6%) 20 (46.5%) 2 (4.6%) 9 (20.9%) 3 (6.9%) 19 (44.2%) 9 (20.9%) 9 (20.9%)
8 (15.4%) 12 (23.1%) 0 (0%) 13 (25.0%) 5 (9.6%) 14 (26.9%) 8 (15.4%) 35 (67.3%) 2 (3.8%) 5 (9.6%)
23 (24.2%) 28 (29.5%) 5 (5.3%) 33 (34.7%) 7 (7.3%) 23 (24.2%) 11 (11.6%) 54 (56.8%) 11 (11.6%) 14 (14.7%)
0.033 0.176 0.017 0.033 0.451 0.631 0.335 0.037 0.02 0.151
Chi-square Chi-square Chi-square Chi-square
ACE: angiotensin converting enzyme; AGT: angiotensin; Ca: calcium; CVA: cerebro-vascular accident; HTN: hypertension; IHD: ischemic heart disease.
Single center case study 3 Table II. Surgical indications. N (%)
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Radiological Clinical Consciousness disturbance Paresis Headache Dysphasia Gait disturbance Vomiting Sensory disturbance
15 (34.9) 28 (65.1) 11 (39.3) 7 (25) 5 (17.8) 4 (14.3) 3 (10.7) 3 (10.7) 1 (3.6)
CI for odds, 1.3–13.1] and 5.9 [95% CI for odds, 1.6–21.5], respectively). Patients with past medical history of cerebrovascular accidents (CVA) also showed increased risk for developing surgical cSDH (80% vs. 41.2%, p ⫽ 0.039), but this difference did not reach significance in the multivariate logistic regression, probably due to small sample size. The operation rate was higher in patients who took one (or more) of the following anti-hypertensive drugs: calcium channel blockers (65.2% vs.38.9%, p ⫽ 0.033), α blockers (100% vs. 42.2%, p ⫽ 0.017), or Angiotensin converting enzyme (ACE) inhibitors (60.6% vs. 37.1%, p ⫽ 0.033). These statistically significant differences were not maintained during multivariate logistic regression. The indications for surgery are summarized in Table II. In 15 patients (34.9%) the indication for surgery was a worsening in imaging parameters alone, without clinical deterioration. Specifically, we used increase in size of the hematoma as well as in the MLS as criteria for operation. Retrospectively we have found an average increase of 7.3 mm in the hematoma size and a 4.3 mm increase in MLS between the first CT scan and the immediate pre-op CT. Table III summarizes the risk of developing cSDH requiring surgical evacuation in patients on anti-aggregant agents (AAA) or anti-coagulant drugs and shows that these patients had a higher operation rate (100% vs. 41.6%, p ⫽ 0.007 and 85.7% vs. 42.0%, p ⫽ 0.044, respectively). Eight patients were taking Clopidrogel and all developed surgical cSDH (100% vs. 40.2%, p ⫽ 0.001). Altogether, 20/21 (95%) patients that were either on more than 1 AAA, used Clopidrogel or took anti-coagulant drug were in the OG. Other bleeding tendencies such as leukemia, thrombocytopenia, liver disease, and chronic renal failure were not significantly associated with developing symptomatic cSDH (p ⫽ 0.151). Table IV summarizes all trauma-related parameters, including CT findings. The initial thickness of the aSDH was statistically significantly larger in the OG (8.9 mm ⫾ 4.6) as compared to the NOG (5.5 mm ⫾ 2.1), p ⬍ 0.001. The thickness of the acute subdural hematoma remained statistically significant after
multivariate logistic regression, with a mean size of 8.9 mm having a 1.5 times risk for developing cSDH requiring surgical evacuation (95% CI for odds, 1.2–1.8). In the immediate preoperative CT, the average size of the subdural collection was 17.5 mm (range, 8–45). The initial MLS was also significantly larger in the OG (1.1 mm ⫾ 0.9 vs. 0.2 mm ⫾ 0.1, p ⫽ 0.005). In the immediate pre-operative CT, the average MLS was 6.5 mm (range, 0–15). Totally 44.2% of the patients who eventually needed surgical treatment were initially discharged to their home, compare to 67.3% of patients who were managed only conservatively (p ⫽ 0.037). Regarding outcome results, patients in the nonoperative group (NOG) were significantly more likely to have a good outcome [defined as Glasgow Outcome Scale (GOS) of 4–5], with 90.4% (47/52) of them having a 3-months GOS of 4–5, compared with 65.5% (28/43) in the OG, p ⬍ 0.001. The six-month mortality rate was significantly higher in the OG (20.9%) versus the NOG (3.8%), p ⫽ 0.02. Altogether, there were nine mortality cases in the OG. Two occurred during the immediate post-operative period (due to cardiac arrest). All other cases occurred after discharge (1 case of asystole, 2 cases of sepsis, and 4 cases of death outside the hospital from unknown cause). Ten patients (23%) had post-operative morbidity (1 delirium, 1 wound infection, 1 urinary tract infection, 1 subdural empyema, 1 pneumonia, 2 seizures, 1 acute coronary syndrome, 1 intracerebral hemorrhage, and 1 CVA). Finally, patients in the OG has undergone significantly more CT scans (in the pre-operative period) compared to those of the NOG (2.6 ⫾ 0.8 vs. 1.9 ⫾ 1, respectively. p ⬍ 0.001). Table V summarizes all statistically significant differences between OG and NOG.
Discussion Many cSDH probably start out as an acute hematoma. Blood within the subdural space evokes an inflammatory response. Within days, fibroblasts invade the clot, and form neomembranes on the inner (cortical) and outer (dural) surface of the hematoma. This is followed by an in growth of neo-capillaries, enzymatic fibrinolysis, and liquefaction of blood clot. Fibrin degradation products are re-incorporated into new clots and inhibit hemostasis. The course of cSDH is determined by the balance of plasma effusion and/or re-bleeding from the neomembranes on one hand and re-absorption of fluid on the other.10,11 Surgical evacuation of cSDH is indicated for symptomatic lesions (such as focal deficit and mental status changes) or for collections with maximum thickness greater than 1 cm. Only few publications so far specifically addressed the issue
Table III. Use of anti-aggregants and anti-coagulants in the operative group (OG) and nonoperative group (NOG). OG (n ⫽ 43) Anti-coagulants Anti-aggregants Total Aspirin only Clopidrogel only ⱖ 2 drugs Anti-coagulants ⫹ anti aggregants
6 (13.9%) 22 (51.2%) 13 (30.2%) 8 (18.6%) 6 (13.9%) 1 (2.3%)
NOG (n ⫽ 52) 0 (0%) 21 (40.4%) 20 (38.5%) 0 (0%) 1 (1.9%) 0 (0%)
Total (n ⫽ 95)
p value
Test
6 (6.3%)
0.007
Chi-square Chi-square
43 (45.3%) 33 (34.7%) 8 (8.4%) 7 (7.4%) 1 (1%)
0.309 0.517 0.001 0.044 0.453
Chi-square
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Y. Laviv & Z. H. Rappaport Table IV. Trauma-related parameters and CT characteristics in the operative group (OG) and nonoperative group (NOG). GCS Size of aSDH Amount of CT images Midline shift on admission Isolated head trauma isolated aSDH MVA Side of aSDH Left Right bilateral
OG (n ⫽ 43)
NOG (n ⫽ 52)
Total (n ⫽ 95)
p value
Test
13.9 ⫾ 2.7 8.9 ⫾ 4.6 2.6 ⫾ 0.8 1.1 ⫾ 0.8 39 (90.7%) 28 (65.1%) 6 (14.0%)
14.4 ⫾ 1.5 5.5 ⫾ 2.1 1.9 ⫾ 1 0.2 ⫾ 0.05 45 (86.5%) 25 (48.1%) 11 (21.2%)
14.2 ⫾ 2.1 7.2 ⫾ 3.3 2.3 ⫾ 0.9 0.6 ⫾ 0.4 84 (88.4%) 53 (55.8%) 17 (17.9%)
0.127 ⬍ 0.001 ⬍ 0.001 0.005 0.749 0.103 0.428 0.627
t test t test t test t test Chi-square Chi-square Chi-square Chi-square
26 (60.5%) 14 (32.6%) 3 (7.0%)
27 (51.9%) 19 (36.5%) 6 (11.5%)
53 (55.8%) 33 (34.7%) 9 (9.5%)
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aSDH: acute subdural hemorrhage; CT: computed tomography; GCS: Glasgow coma scale; MVA: motor-vehicle accident.
of the rate of developing cSDH after the conservative treatment of trauma-related aSDH. 3–26% of patients with aSDH who were managed conservatively developed chronic SDHs requiring evacuation.3,8,12, These patients may require surgery as early as 11–20 days after the initial injury3 or as late as 3–7 months after the initial injury.12 The aim of our study was to find the possible risks
factor for this complication rather than the rate for it. Mathew et al.3 noted that all patients with an acute hematoma, thickness greater than 10 mm that were initially managed conservatively, required subsequent burr-hole drainage. In our study, the mean acute hematoma thickness was 8.9 mm in the OG compare to 5.5 mm in the NOG, and this difference remained statistically significant in multivariate analysis.
Fig. 1. 82-year-old male after a fall from a standing position. The patient was on GCS ⫽ 15 on admission without any neurologic deficit. He was not on any anti-platelets aggregant or anticoagulant medicine. The patient was treated conservatively. (a) axial CT scan on the day of trauma demonstrating a left acute subdural hematoma measuring 9 mm with minimal mass effect. Axial CT scan of the patient 2 (b), 4 (c), and 6(d) weeks after the head trauma demonstrating complete resolution of the hematoma without development of cSDH. He had a GOS ⫽ 5 on a 3 months follow-up.
Single center case study 5 Table V. Statistically significant differences between operative group (OG) and nonoperative group (NOG). p value odds
Size of aSDH
IHD
HTN
CVA
MLS
Ca - blockers
α-blockers
ACE-inhibitors
ⱖ 2 Anti-aggregants
Clopidrogel only
⬍ 0.001 1.459
0.019 4.198
0.001 5.954
0.039 NS
0.005 NS
0.033 NS
0.017 NS
0.033 NS
0.044 NS
0.001 NS
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ACE: angiotensin converting enzyme; Ca: calcium; CVA: cerebro-vascular accident; HTN: hypertension; IHD: ischemic heart disease; MLS: midline shift; NS: non-significant.
The increase in the use of anticoagulant and AAA in the general population may have changed the incidence of intracerebral hemorrhage and subdural hematomas.13 The effect of these drugs on development of cSDH has been studied mainly in the context of recurrent cSDHs. Tilmann et al.13 have found that the risk of developing a cSDH while taking warfarin is at least 42.5 times higher than if no anticoagulation is used. In another study investigating the predictors for recurrent cSDH, Torihashi et al.14 found that out of 343 surgical cases of cSDH, 61 patients experienced a recurrence
of cSDH. Univariate and multivariate analyses found that although AAA and anticoagulant therapy had no significant effect on recurrence of cSDH, the time interval between the injury and the first operation for patients with AAA and/ or anticoagulant therapy was shorter than that for patients without it (29.9 vs. 44.2 days). Our study shows that although the use of aspirin only is not overtly represented in the OG, any other combination of AAA or anti-coagulants therapy (including Clopidrogel only, more than one AAAs, AAA plus anti-coagulant, or anti-coagulant only) is highly associated
Fig. 2. 86-year-old female after a fall from a standing position. The patient was on GCS ⫽ 15 on admission without any neurologic deficit. She was on anti-platelets aggregant (Aspirin) on the day of trauma. The patient was treated initially conservatively. (a) axial CT scan on the day of trauma demonstrating a right acute subdural hematoma measuring 12 mm with minimal mass effect. (b) Axial CT scan of the patient one day post trauma. The patient was sent for rehabilitation. (c) axial CT scan done 14 days after trauma demonstrating right cSDH measuring 17 mm, causing significant mass effect. The patient had her cSDH evacuated surgically. (d) Post-op CT scan demonstrating good evacuation of the hematoma with improvement of the mass effect. She had a GOS ⫽ 3 on a 3-month follow-up.
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with late development of cSDH requiring surgical evacuation, with 20/21 patients with one of the above treatments being in the OG. Regarding other bleeding tendencies and the risk for cSDH, Ko et al.15 found that bleeding tendency such as in leukemia, liver disease, and chronic renal failure was significantly associated with recurrence of cSDH (p ⫽ 0.037). However, the impact of such factors on the transition from aSDH to cSDH has not yet been studied. Our data did not find a different frequency in those kinds of bleeding tendencies between the OG and NOG in this study, most probably due to small sample size. In another study investigating risk factors for the recurrence of surgically treated cSDH (A total of 310 patients), Weigel et al.16 found that that ACE-inhibitor treatment for the control of arterial hypertension lowers the risk of recurrence in patients undergoing operation for cSDH (5% vs. 18%, P ⫽ 0.00345). Our study did not demonstrate such protective phenomena against the development of cSDH in patients with aSDH treated with ACE-inhibitors. Moreover, we have found that although HTN can be regarded as a risk factor for developing cSDH after conservative treatment of a SDH, some anti-HTN drugs were actually more common in the OG compared to those of the NOG, including ACE-inhibitors. We have no explanation for these results and it should be mentioned that these differences disappeared during multivariate analysis. Although most of the patients who were at risk for developing significant cSDH were detected relatively early (the patients in the OG underwent statistically significant more CT scans and most of them were not sent home after their hospitalization), our study demonstrates that, nonetheless, 35% of the surgeries occurred on the day of arrival to the hospital and we had 20% six-month mortality rate and a 23% post-operative morbidity rate (although only 2/9 mortality cases occurred during the same hospitalization of the surgery). Figures 1 and 2 are an example of the difficulty in predicting which patient with traumatic aSDH will develop significant cSDH requiring surgical evacuation. These results demonstrate the importance of early recognition of high-risk patients for the development of significant cSDH after the conservative treatment of traumatic aSDH.
Conclusion cSDH carries a significant morbidity in the elderly. Detecting significant, surgical cases, as early as possible may reduce the morbidity and mortality rates in these patients. Since nonsurgical, traumatic aSDH may become a surgical cSDH, it is important to identify those patients at risk for developing this complication. We have found that patients who develop significant chronic subdural collections differ in their medical characteristic compared to patients who did not develop this condition. Specifically, patients with a medical
history of IHD or HTN, patients on more than one AAA or anti-coagulant agents and patients with worse initial CT scan parameters are at risk of developing significant cSDH after conservative treatment of aSDH and should accordingly have closer follow-up. The relation between HTN and IHD and the risk for developing cSDH, as well as the relation between some anti HTN drugs and this illness needs further study.
Declaration of interest: The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.
References 1. Kawamata T, Takeshita M, Kubo O, et al. Management of intracranial hemorrhage associated with anticoagulant therapy. Surg Neurol 1995;44:438–42. 2. Massaro F, Lanotte M, Faccani G, Triolo C. One hundred and twenty- seven cases of acute subdural haematomas operated on. Correlation between CT scan findings and outcome. Acta Neurochir 1996;138:185–91. 3. Mathew P, Oluoch-Olunya DL, Condon BR, Bullock R. Acute subdural haematoma in the conscious patient: outcome with initial non-operative management. Acta Neurochir 1993;121:100–8. 4. Seelig JM, Becker DP, Miller JD, et al. Traumatic acute subdural hematoma. Major mortality reduction in comatose patients treated within four hours. N Engl J Med 1981;304:1511–8. 5. Zumkeller M, Behrmann R, Heissler HE, Dietz H. Computed tomographic criteria and survival rate for patients with acute subdural hematoma. Neurosurgery 1996;39:708–13. 6. Wong CW. Criteria for conservative treatment of supratentorial acute subdural haematomas. Acta Neurochir (Wien) 1995;135:38–43. 7. Servadei F, Nasi M, Cremonini A , et al. Importance of a reliable admission Glasgow Coma Scale score for determining the need for evacuation of posttraumatic subdural hematomas: a prospective study of 65 patients. J Trauma 1998;44:868–73. 8. Feliciano CE, De Jesús O. Conservative management outcomes of traumatic acute subdural hematomas. P R Health Sci J 2008;27:220–3. 9. Croce MA , Dent DL, Menke PG, et al. Acute subdural hematoma. Nonsurgical management of selected patients. J Trauma 1994;36:820–7. 10. Drapkin AJ. Chronic subdural hematoma: pathophysiological basis of treatment. Br J Neurosurg 1991;5:467–73. 11. Labadie EL. Fibrinolysis in the formation and growth of chronic subdurol hematomas. In: Sawaya R, ed. Fibrinolysis and the central nervous system. Hanley and Belfus: Philadelphia, 1990:141–8. 12. Lindvall P, Koskinen LO. Anticoagulants and antiplatelet agents and the risk of development and recurrence of chronic subdural haematomas. J Clin Neurosci 2009;16:1287–90. 13. Tilmann R, Kiemer N, Erasmus A . Chronic subdural haematomas and anticoagulation or anti-thrombotic therapy. J Clin Neurosci 2006;13:823–7. 14. Torihashi K, Sadamasa N, Yoshida K , et al. Independent predictors for recurrence of chronic subdural hematoma: a review of 343 consecutive surgical cases. Neurosurgery 2008;63:1125–9. 15. Ko BS, Lee JK, Seo BR, et al. Clinical analysis of risk factor related to recurrent chronic subdural hematoma. J Korean Neurosurg Soc 2008;43:11–5. 16. Weigel R, Hohenstein A , Schlickum L, Weiss C, Schilling L. Angiotensin converting enzyme inhibition for arterial hypertension reduces the risk of recurrence in patients with chronic subdural hematoma possibly by an antiangiogenic mechanism. Neurosurgery 2007;61:788–92.
ORIGINAL ARTICLE
Risk factors for development of significant chronic subdural hematoma following conservative treatment of acute subdural hemorrhage Yosef Laviv & Zvi Harry Rappaport
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Department of Neurosurgery, Beilinson Hospital, Rabin Medical Center, Petah Tiqva, Israel
Introduction
Absract Objective. One of the complications of untreated acute subdural hemorrhage (aSDH) is the late development of chronic subdural hematomas (cSDH). cSDH may cause major neurologic deficits, requiring their surgical evacuation. The aim of our work was to find risk factors for the development of significant cSDH requiring surgery following conservative treatment of traumarelated aSDH. Methods. In a retrospective manner, we analyzed the data of 95 adult patients admitted with a non-surgical, traumatic aSDH. The patients were divided into two groups. The first group contained 52 patients who did not, on follow-up, develop cSDH requiring surgery. The second group contained 43 patients who ended up with a significant cSDH, based on clinical and radiological criteria, requiring surgical evacuation. Data acquisition and comparison between the two groups was performed by analyzing the patients’ charts for diverse medical conditions and other trauma-related parameters. Results. The operation rate was significantly higher in patients with medical history of ischemic heart disease (IHD) or hypertension (66.7% vs. 38%, p ⴝ 0.019 and 56.9% vs. 20%, p ⬍ 0.01, respectively), with a 4-fold increase in the risk for developing surgical cSDH in patients with IHD and a 6-fold increase in the risk in patients with hypertension (odds ratio 4.2 [95% CI for odds, 1.3–13.1] and 5.9 [95% C.I for odds, 1.6–21.5], respectively). Among 21 patients, 20 (95%) patients, who were either on more than 1 anti-aggregant agents (AAA), used Clopidrogrel, or took anti-coagulant drug were in the operative group (OG). A larger initial thickness of the aSDH was statistically significant in the OG as compared to the non-OG (8.9 mm ⴞ 4.6 vs. 5.5 mm ⴞ 2.1, p ⬍ 0.001). Conclusion. Head-trauma patients with a medical history of IHD or hypertension, patients on more than one AAA or anti-coagulant agents and patients with worse initial CT scan parameters are at risk of developing significant cSDH requiring surgery after conservative treatment of aSDH and consequently should have closer follow-up.
Subdural hematomas represent intracranial extra-axial mass lesions which are usually seen after traumatic brain injury. Acute subdural hematoma (aSDH) usually appears in the first 3 days after the trauma and carries mortality ranges of 50–100%.1–5 Despite these high mortality rates, and although it has been shown that a quick surgical evacuation of an aSDH can reduce mortality rate to as low as 30%,4 not every trauma-related aSDH needs to be treated surgically. Several studies tried to demonstrate the impact of conservative (non-operative) management of aSDH. Wong6 tried to identify parameters that would predict the failure of initial nonoperative management. 6 of 31 patients with GCS scores between 6 and 15 who were initially treated without surgery required a later craniotomy because of neurological deterioration (performed within 3 days). The authors found that a midline shift (MLS) greater than 5 mm in patients with a GCS score of lower than 15 on the initial CT scan was significantly related to the failure of nonoperative treatment. Hematoma volume and thickness of the hematoma were not predictive. Mathew et al.3 reviewed the data on 23 patients with GCS scores between 13 and 15 who were initially treated nonoperatively. All patients had an isolated aSDH. Six patients (25%) required delayed (mean, 14 days) evacuation of their SDH. Servadei et al.7 treated 15 of 65 comatose patients with aSDH in a nonoperative way. Of these, two patients required delayed surgery based on increasing ICP and the development of intracerebral hematomas. Good outcome was achieved in 23% of the patients in the surgery group and 67% of the patients in the nonoperative group. The authors concluded that nonoperative treatment can be safely used for a defined group of comatose patients with aSDH. Finally, Feliciano and De Jesús8 prospectively evaluated 38 patients with traumatic aSDH who were conservatively treated. They found that patients less than 65 years old, patients with GCS score greater than 8, and patients with
Keywords: acute; chronic; hemorrhage; risk factors; subdural
Correspondence: Dr. Yosef Laviv, MD, Department of Neurosurgery, Beilinson Hospital, Rabin Medical Center, Petah Tiqva 49100, Israel. Tel:⫹ 03-9376401. Fax: ⫹ 03-9219774. E-mail: [email protected] Received for publication 15 December 2012; accepted 21 April 2014
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hematoma thicknesses 10 mm or lesser and midline shifts 5 mm or lesser had a favorable or functionally independent outcome in 80–85% of the cases. The studies above show that aSDH can be managed conservatively under the appropriate clinical and radiological conditions (even in comatose patients). However, they also demonstrated that some patients may require delayed evacuation of the SDH at the subacute or chronic phase of the hematoma.3,6,9 Since clinically significant chronic subdural hematomas (cSDH) might cause significant morbidity (especially in the elderly) and because the identification and timely treatment of this condition may have great effect on reducing morbidity, it is important to know which patients are at risk for developing this complication. The purpose of this study was to identify special characteristics and risk factors in patients with traumatic aSDH that develops clinically significant cSDH after conservative treatment of the acute hemorrhage.
Patients and methods This study was conducted according to the principles of the local ethics committee. We analyzed the data of 95 patients who were admitted to our neurosurgical department with a non-surgical, traumatic aSDH during the years 2002–2012. All patients were over the age of 40 years and all suffered a relatively low-velocity head trauma. In a retrospective manner, the patients were divided into two groups. The first group contained 52 patients who were treated conservatively for their aSDH and did not develop significant cSDH requiring surgical evacuation on follow-up. The second group contained 43 patients who were also treated initially in a conservative manner, which resulted in cSDH that needed surgical evacuation based on clinical and radiological criteria. Data acquisition and comparison between the two groups was performed by analyzing the patients’ charts for age, sex, and home medication at the time of admission. The patients’ medical histories were also screened for diverse
medical conditions and other parameters related to the patients’ clinical and neurological status at the time of injury and imaging-related parameters of the SDH. In the operative group (OG), the presence of surgical cSDH, unilateral or bilateral, was confirmed using computed tomographic (CT) scans. In the OG, all patients underwent a standard surgical procedure consisting of a burr hole, irrigation, and closed-system drainage. Surgery was performed under general anesthesia. All patients had at least six months of radiological and clinical follow-up after the initial trauma in our out-patient units. Statistical analysis was performed using SAS (version 8.02; SAS Institute Inc., Cary, NC). The tests used for analysis are indicated with the respective results. For all analyses, a p value of less than 0.05 was considered statistically significant.
Results In the majority of cases the head trauma was caused by falling, usually from a standing position (81.4% in the OG and 84.6% in the NOG). The rest of the cases included blunt object trauma (2 OG and 1 NOG) and pedestrian accidents (4 OG and 7 NOG). Time from initial trauma to operation was 23.3 days on average (range, 10–64). Fifteen patients in the OG (34.9%) were operated on the day of recurrent admission. Only one patient in the OG (2.4%) required more than one operation. The clinical data of 95 consecutive cases are summarized in Table I. There were 53 men (55.8%) and 42 women (44.2%). Mean age of patients in the OG (77.5 ⫾ 10.2) was not significantly different from that in the NOG (74.3 ⫾ 10.4). The operation rate was significantly higher in patients with medical history of ischemic heart disease (IHD) or hypertension (66.7% vs. 38%, p ⫽ 0.019 and 56.9% vs. 20%, p ⬍ 0.01, respectively). These differences were maintained during multi-variant logistic regression, with four times the risk for developing surgical cSDH in patients with IHD and six times the risk in patients with hypertension (odds ratio 4.2 [95%
Table I. Characteristics and clinical findings in the operative group (OG) and the nonoperative group (NOG). OG (n ⫽ 43) Sex Male Female Mean age IHD HTN DM Dementia CVA Anti HTN drugs Ca – blocker β – blocker α – blocker ACE – inh AGT – inh Diuretics Anti-diabetic Home discharge 6-month mortality Abnormal lab
NOG (n ⫽ 52)
Total (n ⫽ 95)
p Value
Test
0.685
Chi-square
t test Chi-square Chi-square Chi-square Chi-square Chi-square Chi-square
25 (58.1%) 18 (41.9%) 77.6 ⫾ 10.2 16 (37.2%) 37 (86.0%) 7 (16.3%) 4 (9.3%) 8 (18.6%)
28 (53.8%) 24 (46.2%) 74.3 ⫾ 10.4 8 (15.4%) 28 (53.8%) 11 (21.1%) 7 (13.5%) 2 (3.8%)
53 (55.8%) 42 (44.2%) 75.9 ⫾ 10.3 24 (25.2%) 65 (68.4%) 18 (18.9%) 11 (11.6%) 10 (10.5%)
0.127 0.019 0.001 0.607 0.749 0.039
15 (34.9%) 16 (37.2%) 5 (11.6%) 20 (46.5%) 2 (4.6%) 9 (20.9%) 3 (6.9%) 19 (44.2%) 9 (20.9%) 9 (20.9%)
8 (15.4%) 12 (23.1%) 0 (0%) 13 (25.0%) 5 (9.6%) 14 (26.9%) 8 (15.4%) 35 (67.3%) 2 (3.8%) 5 (9.6%)
23 (24.2%) 28 (29.5%) 5 (5.3%) 33 (34.7%) 7 (7.3%) 23 (24.2%) 11 (11.6%) 54 (56.8%) 11 (11.6%) 14 (14.7%)
0.033 0.176 0.017 0.033 0.451 0.631 0.335 0.037 0.02 0.151
Chi-square Chi-square Chi-square Chi-square
ACE: angiotensin converting enzyme; AGT: angiotensin; Ca: calcium; CVA: cerebro-vascular accident; HTN: hypertension; IHD: ischemic heart disease.
Single center case study 3 Table II. Surgical indications. N (%)
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Radiological Clinical Consciousness disturbance Paresis Headache Dysphasia Gait disturbance Vomiting Sensory disturbance
15 (34.9) 28 (65.1) 11 (39.3) 7 (25) 5 (17.8) 4 (14.3) 3 (10.7) 3 (10.7) 1 (3.6)
CI for odds, 1.3–13.1] and 5.9 [95% CI for odds, 1.6–21.5], respectively). Patients with past medical history of cerebrovascular accidents (CVA) also showed increased risk for developing surgical cSDH (80% vs. 41.2%, p ⫽ 0.039), but this difference did not reach significance in the multivariate logistic regression, probably due to small sample size. The operation rate was higher in patients who took one (or more) of the following anti-hypertensive drugs: calcium channel blockers (65.2% vs.38.9%, p ⫽ 0.033), α blockers (100% vs. 42.2%, p ⫽ 0.017), or Angiotensin converting enzyme (ACE) inhibitors (60.6% vs. 37.1%, p ⫽ 0.033). These statistically significant differences were not maintained during multivariate logistic regression. The indications for surgery are summarized in Table II. In 15 patients (34.9%) the indication for surgery was a worsening in imaging parameters alone, without clinical deterioration. Specifically, we used increase in size of the hematoma as well as in the MLS as criteria for operation. Retrospectively we have found an average increase of 7.3 mm in the hematoma size and a 4.3 mm increase in MLS between the first CT scan and the immediate pre-op CT. Table III summarizes the risk of developing cSDH requiring surgical evacuation in patients on anti-aggregant agents (AAA) or anti-coagulant drugs and shows that these patients had a higher operation rate (100% vs. 41.6%, p ⫽ 0.007 and 85.7% vs. 42.0%, p ⫽ 0.044, respectively). Eight patients were taking Clopidrogel and all developed surgical cSDH (100% vs. 40.2%, p ⫽ 0.001). Altogether, 20/21 (95%) patients that were either on more than 1 AAA, used Clopidrogel or took anti-coagulant drug were in the OG. Other bleeding tendencies such as leukemia, thrombocytopenia, liver disease, and chronic renal failure were not significantly associated with developing symptomatic cSDH (p ⫽ 0.151). Table IV summarizes all trauma-related parameters, including CT findings. The initial thickness of the aSDH was statistically significantly larger in the OG (8.9 mm ⫾ 4.6) as compared to the NOG (5.5 mm ⫾ 2.1), p ⬍ 0.001. The thickness of the acute subdural hematoma remained statistically significant after
multivariate logistic regression, with a mean size of 8.9 mm having a 1.5 times risk for developing cSDH requiring surgical evacuation (95% CI for odds, 1.2–1.8). In the immediate preoperative CT, the average size of the subdural collection was 17.5 mm (range, 8–45). The initial MLS was also significantly larger in the OG (1.1 mm ⫾ 0.9 vs. 0.2 mm ⫾ 0.1, p ⫽ 0.005). In the immediate pre-operative CT, the average MLS was 6.5 mm (range, 0–15). Totally 44.2% of the patients who eventually needed surgical treatment were initially discharged to their home, compare to 67.3% of patients who were managed only conservatively (p ⫽ 0.037). Regarding outcome results, patients in the nonoperative group (NOG) were significantly more likely to have a good outcome [defined as Glasgow Outcome Scale (GOS) of 4–5], with 90.4% (47/52) of them having a 3-months GOS of 4–5, compared with 65.5% (28/43) in the OG, p ⬍ 0.001. The six-month mortality rate was significantly higher in the OG (20.9%) versus the NOG (3.8%), p ⫽ 0.02. Altogether, there were nine mortality cases in the OG. Two occurred during the immediate post-operative period (due to cardiac arrest). All other cases occurred after discharge (1 case of asystole, 2 cases of sepsis, and 4 cases of death outside the hospital from unknown cause). Ten patients (23%) had post-operative morbidity (1 delirium, 1 wound infection, 1 urinary tract infection, 1 subdural empyema, 1 pneumonia, 2 seizures, 1 acute coronary syndrome, 1 intracerebral hemorrhage, and 1 CVA). Finally, patients in the OG has undergone significantly more CT scans (in the pre-operative period) compared to those of the NOG (2.6 ⫾ 0.8 vs. 1.9 ⫾ 1, respectively. p ⬍ 0.001). Table V summarizes all statistically significant differences between OG and NOG.
Discussion Many cSDH probably start out as an acute hematoma. Blood within the subdural space evokes an inflammatory response. Within days, fibroblasts invade the clot, and form neomembranes on the inner (cortical) and outer (dural) surface of the hematoma. This is followed by an in growth of neo-capillaries, enzymatic fibrinolysis, and liquefaction of blood clot. Fibrin degradation products are re-incorporated into new clots and inhibit hemostasis. The course of cSDH is determined by the balance of plasma effusion and/or re-bleeding from the neomembranes on one hand and re-absorption of fluid on the other.10,11 Surgical evacuation of cSDH is indicated for symptomatic lesions (such as focal deficit and mental status changes) or for collections with maximum thickness greater than 1 cm. Only few publications so far specifically addressed the issue
Table III. Use of anti-aggregants and anti-coagulants in the operative group (OG) and nonoperative group (NOG). OG (n ⫽ 43) Anti-coagulants Anti-aggregants Total Aspirin only Clopidrogel only ⱖ 2 drugs Anti-coagulants ⫹ anti aggregants
6 (13.9%) 22 (51.2%) 13 (30.2%) 8 (18.6%) 6 (13.9%) 1 (2.3%)
NOG (n ⫽ 52) 0 (0%) 21 (40.4%) 20 (38.5%) 0 (0%) 1 (1.9%) 0 (0%)
Total (n ⫽ 95)
p value
Test
6 (6.3%)
0.007
Chi-square Chi-square
43 (45.3%) 33 (34.7%) 8 (8.4%) 7 (7.4%) 1 (1%)
0.309 0.517 0.001 0.044 0.453
Chi-square
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Y. Laviv & Z. H. Rappaport Table IV. Trauma-related parameters and CT characteristics in the operative group (OG) and nonoperative group (NOG). GCS Size of aSDH Amount of CT images Midline shift on admission Isolated head trauma isolated aSDH MVA Side of aSDH Left Right bilateral
OG (n ⫽ 43)
NOG (n ⫽ 52)
Total (n ⫽ 95)
p value
Test
13.9 ⫾ 2.7 8.9 ⫾ 4.6 2.6 ⫾ 0.8 1.1 ⫾ 0.8 39 (90.7%) 28 (65.1%) 6 (14.0%)
14.4 ⫾ 1.5 5.5 ⫾ 2.1 1.9 ⫾ 1 0.2 ⫾ 0.05 45 (86.5%) 25 (48.1%) 11 (21.2%)
14.2 ⫾ 2.1 7.2 ⫾ 3.3 2.3 ⫾ 0.9 0.6 ⫾ 0.4 84 (88.4%) 53 (55.8%) 17 (17.9%)
0.127 ⬍ 0.001 ⬍ 0.001 0.005 0.749 0.103 0.428 0.627
t test t test t test t test Chi-square Chi-square Chi-square Chi-square
26 (60.5%) 14 (32.6%) 3 (7.0%)
27 (51.9%) 19 (36.5%) 6 (11.5%)
53 (55.8%) 33 (34.7%) 9 (9.5%)
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aSDH: acute subdural hemorrhage; CT: computed tomography; GCS: Glasgow coma scale; MVA: motor-vehicle accident.
of the rate of developing cSDH after the conservative treatment of trauma-related aSDH. 3–26% of patients with aSDH who were managed conservatively developed chronic SDHs requiring evacuation.3,8,12, These patients may require surgery as early as 11–20 days after the initial injury3 or as late as 3–7 months after the initial injury.12 The aim of our study was to find the possible risks
factor for this complication rather than the rate for it. Mathew et al.3 noted that all patients with an acute hematoma, thickness greater than 10 mm that were initially managed conservatively, required subsequent burr-hole drainage. In our study, the mean acute hematoma thickness was 8.9 mm in the OG compare to 5.5 mm in the NOG, and this difference remained statistically significant in multivariate analysis.
Fig. 1. 82-year-old male after a fall from a standing position. The patient was on GCS ⫽ 15 on admission without any neurologic deficit. He was not on any anti-platelets aggregant or anticoagulant medicine. The patient was treated conservatively. (a) axial CT scan on the day of trauma demonstrating a left acute subdural hematoma measuring 9 mm with minimal mass effect. Axial CT scan of the patient 2 (b), 4 (c), and 6(d) weeks after the head trauma demonstrating complete resolution of the hematoma without development of cSDH. He had a GOS ⫽ 5 on a 3 months follow-up.
Single center case study 5 Table V. Statistically significant differences between operative group (OG) and nonoperative group (NOG). p value odds
Size of aSDH
IHD
HTN
CVA
MLS
Ca - blockers
α-blockers
ACE-inhibitors
ⱖ 2 Anti-aggregants
Clopidrogel only
⬍ 0.001 1.459
0.019 4.198
0.001 5.954
0.039 NS
0.005 NS
0.033 NS
0.017 NS
0.033 NS
0.044 NS
0.001 NS
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ACE: angiotensin converting enzyme; Ca: calcium; CVA: cerebro-vascular accident; HTN: hypertension; IHD: ischemic heart disease; MLS: midline shift; NS: non-significant.
The increase in the use of anticoagulant and AAA in the general population may have changed the incidence of intracerebral hemorrhage and subdural hematomas.13 The effect of these drugs on development of cSDH has been studied mainly in the context of recurrent cSDHs. Tilmann et al.13 have found that the risk of developing a cSDH while taking warfarin is at least 42.5 times higher than if no anticoagulation is used. In another study investigating the predictors for recurrent cSDH, Torihashi et al.14 found that out of 343 surgical cases of cSDH, 61 patients experienced a recurrence
of cSDH. Univariate and multivariate analyses found that although AAA and anticoagulant therapy had no significant effect on recurrence of cSDH, the time interval between the injury and the first operation for patients with AAA and/ or anticoagulant therapy was shorter than that for patients without it (29.9 vs. 44.2 days). Our study shows that although the use of aspirin only is not overtly represented in the OG, any other combination of AAA or anti-coagulants therapy (including Clopidrogel only, more than one AAAs, AAA plus anti-coagulant, or anti-coagulant only) is highly associated
Fig. 2. 86-year-old female after a fall from a standing position. The patient was on GCS ⫽ 15 on admission without any neurologic deficit. She was on anti-platelets aggregant (Aspirin) on the day of trauma. The patient was treated initially conservatively. (a) axial CT scan on the day of trauma demonstrating a right acute subdural hematoma measuring 12 mm with minimal mass effect. (b) Axial CT scan of the patient one day post trauma. The patient was sent for rehabilitation. (c) axial CT scan done 14 days after trauma demonstrating right cSDH measuring 17 mm, causing significant mass effect. The patient had her cSDH evacuated surgically. (d) Post-op CT scan demonstrating good evacuation of the hematoma with improvement of the mass effect. She had a GOS ⫽ 3 on a 3-month follow-up.
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with late development of cSDH requiring surgical evacuation, with 20/21 patients with one of the above treatments being in the OG. Regarding other bleeding tendencies and the risk for cSDH, Ko et al.15 found that bleeding tendency such as in leukemia, liver disease, and chronic renal failure was significantly associated with recurrence of cSDH (p ⫽ 0.037). However, the impact of such factors on the transition from aSDH to cSDH has not yet been studied. Our data did not find a different frequency in those kinds of bleeding tendencies between the OG and NOG in this study, most probably due to small sample size. In another study investigating risk factors for the recurrence of surgically treated cSDH (A total of 310 patients), Weigel et al.16 found that that ACE-inhibitor treatment for the control of arterial hypertension lowers the risk of recurrence in patients undergoing operation for cSDH (5% vs. 18%, P ⫽ 0.00345). Our study did not demonstrate such protective phenomena against the development of cSDH in patients with aSDH treated with ACE-inhibitors. Moreover, we have found that although HTN can be regarded as a risk factor for developing cSDH after conservative treatment of a SDH, some anti-HTN drugs were actually more common in the OG compared to those of the NOG, including ACE-inhibitors. We have no explanation for these results and it should be mentioned that these differences disappeared during multivariate analysis. Although most of the patients who were at risk for developing significant cSDH were detected relatively early (the patients in the OG underwent statistically significant more CT scans and most of them were not sent home after their hospitalization), our study demonstrates that, nonetheless, 35% of the surgeries occurred on the day of arrival to the hospital and we had 20% six-month mortality rate and a 23% post-operative morbidity rate (although only 2/9 mortality cases occurred during the same hospitalization of the surgery). Figures 1 and 2 are an example of the difficulty in predicting which patient with traumatic aSDH will develop significant cSDH requiring surgical evacuation. These results demonstrate the importance of early recognition of high-risk patients for the development of significant cSDH after the conservative treatment of traumatic aSDH.
Conclusion cSDH carries a significant morbidity in the elderly. Detecting significant, surgical cases, as early as possible may reduce the morbidity and mortality rates in these patients. Since nonsurgical, traumatic aSDH may become a surgical cSDH, it is important to identify those patients at risk for developing this complication. We have found that patients who develop significant chronic subdural collections differ in their medical characteristic compared to patients who did not develop this condition. Specifically, patients with a medical
history of IHD or HTN, patients on more than one AAA or anti-coagulant agents and patients with worse initial CT scan parameters are at risk of developing significant cSDH after conservative treatment of aSDH and should accordingly have closer follow-up. The relation between HTN and IHD and the risk for developing cSDH, as well as the relation between some anti HTN drugs and this illness needs further study.
Declaration of interest: The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.
References 1. Kawamata T, Takeshita M, Kubo O, et al. Management of intracranial hemorrhage associated with anticoagulant therapy. Surg Neurol 1995;44:438–42. 2. Massaro F, Lanotte M, Faccani G, Triolo C. One hundred and twenty- seven cases of acute subdural haematomas operated on. Correlation between CT scan findings and outcome. Acta Neurochir 1996;138:185–91. 3. Mathew P, Oluoch-Olunya DL, Condon BR, Bullock R. Acute subdural haematoma in the conscious patient: outcome with initial non-operative management. Acta Neurochir 1993;121:100–8. 4. Seelig JM, Becker DP, Miller JD, et al. Traumatic acute subdural hematoma. Major mortality reduction in comatose patients treated within four hours. N Engl J Med 1981;304:1511–8. 5. Zumkeller M, Behrmann R, Heissler HE, Dietz H. Computed tomographic criteria and survival rate for patients with acute subdural hematoma. Neurosurgery 1996;39:708–13. 6. Wong CW. Criteria for conservative treatment of supratentorial acute subdural haematomas. Acta Neurochir (Wien) 1995;135:38–43. 7. Servadei F, Nasi M, Cremonini A , et al. Importance of a reliable admission Glasgow Coma Scale score for determining the need for evacuation of posttraumatic subdural hematomas: a prospective study of 65 patients. J Trauma 1998;44:868–73. 8. Feliciano CE, De Jesús O. Conservative management outcomes of traumatic acute subdural hematomas. P R Health Sci J 2008;27:220–3. 9. Croce MA , Dent DL, Menke PG, et al. Acute subdural hematoma. Nonsurgical management of selected patients. J Trauma 1994;36:820–7. 10. Drapkin AJ. Chronic subdural hematoma: pathophysiological basis of treatment. Br J Neurosurg 1991;5:467–73. 11. Labadie EL. Fibrinolysis in the formation and growth of chronic subdurol hematomas. In: Sawaya R, ed. Fibrinolysis and the central nervous system. Hanley and Belfus: Philadelphia, 1990:141–8. 12. Lindvall P, Koskinen LO. Anticoagulants and antiplatelet agents and the risk of development and recurrence of chronic subdural haematomas. J Clin Neurosci 2009;16:1287–90. 13. Tilmann R, Kiemer N, Erasmus A . Chronic subdural haematomas and anticoagulation or anti-thrombotic therapy. J Clin Neurosci 2006;13:823–7. 14. Torihashi K, Sadamasa N, Yoshida K , et al. Independent predictors for recurrence of chronic subdural hematoma: a review of 343 consecutive surgical cases. Neurosurgery 2008;63:1125–9. 15. Ko BS, Lee JK, Seo BR, et al. Clinical analysis of risk factor related to recurrent chronic subdural hematoma. J Korean Neurosurg Soc 2008;43:11–5. 16. Weigel R, Hohenstein A , Schlickum L, Weiss C, Schilling L. Angiotensin converting enzyme inhibition for arterial hypertension reduces the risk of recurrence in patients with chronic subdural hematoma possibly by an antiangiogenic mechanism. Neurosurgery 2007;61:788–92.
