http://informahealthcare.com/bij ISSN: 0269-9052 (print), 1362-301X (electronic) Brain Inj, Early Online: 1–5 ! 2015 Informa UK Ltd. DOI: 10.3109/02699052.2015.1004560
ORIGINAL ARTICLE
Surgical management of the patients with chronic subdural haematoma and contralateral subdural effusion: Operation or no-operation? Haifeng Wang1, Jingwei Zhao2, Ye Li3, Yan Feng3, & Li Bie1,4 Department of Neurosurgery of the First Clinical Hospital, Jilin University, Changchun, PR China, 2Department of Neurosurgery, China–Japan Union Hospital, Jilin University, Changchun, PR China, 3Department of Radiology, and 4Department of Pathology and Laboratory Medicine, University of California, Irvine, CA, USA
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1
Abstract
Keywords
Objective: Patients with chronic subdural haematoma and contralateral subdural effusion are rare after head injury. Surgery might reduce clinical progression of subdural effusion, but is not used routinely. This study aimed to investigate the effect of surgery on subdural effusion and clinical outcome. Methods: A retrospective study was performed, comparing operation and non-operation in the patients with chronic subdural haematoma and contralateral subdural effusion, in a series of 47 patients divided into two groups. The operation group of 21 patients underwent bilateral surgery. The non-operation group of 26 patients underwent surgery on the side with chronic subdural haematoma. Neurological status was assessed by the Glasgow Coma score and Modified Rankin Scale score on admission and at follow-up. All cases underwent pre- and postoperative computed tomography scans. Results: Pre-operative clinical and radiological data were similar in the two groups. The rate of subdural effusion progression was significantly lower in the operation group than in the nonoperation group (p50.05). Thirteen cases (50%) in the non-operation group and three cases (14.3%) in the operation group had progression of subdural effusion to chronic subdural haematoma (p50.05). Chronic subdural haematoma recurrence rate, mortality and neurological recovery were similar, with no significant difference between groups. Conclusions: The patients benefitted from surgery for subdural effusion when they had chronic subdural haematoma and contralateral subdural effusion.
Chronic subdural haematoma, outcome, subdural effusion, surgery
Introduction Chronic subdural haematoma (CSDH) is a post-traumatic disease frequently in neurosurgery [1]. Burr-hole drainage (BHD) followed by irrigation of the subdural space is a widespread treatment for CSDH [2] and, in most cases, surgical treatment is straightforward and clinical outcomes are good. Subdural effusion (SDE) occurs rarely in patients with head injury, but SDE progresses to CSDH in some cases [3]. There is no consensus on how to treat patients with CSDH with contralateral SDE. This study reports the retrospective results of a comparison of the efficacy of operation with non-operation on the SDE side.
Methods Patients This was a retrospective review of 52 adult patients who were treated for CSDH and contralateral SDE at a clinical hospital Correspondence: Li Bie, Department of Neurosurgery of the First Clinical Hospital, Jilin University, 71 Xinmin St., Changchun, Jilin 130021, PR China. E-mail: [email protected]
History Received 8 August 2014 Revised 17 November 2014 Accepted 3 January 2015 Published online 19 March 2015
between January 2004 and December 2013. Three patients were excluded with serious medical illness, not suitable for surgery. Two patients had incomplete follow-up or were lost to follow-up. There were 32 males and 15 females ranging in age from 18–85 years (mean age ¼ 65.2 ± 10.8 years). All patients had the symptoms of CSDH confirmed to require surgery based on computed tomography (CT). According to Zanini et al. [4], subdural effusion creates a significant mass effect in the patients. All patients underwent a single burrhole irrigation on the CSDH. Twenty-one patients had drainage in the SDE side. Twenty-six patients were not receiving treatment in the SDE side. The clinical courses and outcomes were evaluated and data included patient information, Glasgow Coma score (GCS), Modified Rankin Scale (MRS) score, recurrence rate, mortality and complaints. All patients underwent 3 months’ follow-up. All cases underwent pre- and post-operative CT scan to evaluate haematoma density and midline shift. Measurements were calculated by two independent neurosurgeons from data derived CT scans images. Written informed consent for participation in the study was obtained from all participants or their guardians. The study was approved by the Institutional Review Board
2
H. Wang et al.
(IRB) of The (IRB00008484).
Brain Inj, Early Online: 1–5
First
Hospital
of
Jilin
University
Operation Surgical procedure for CSDH [5]
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A single burr-hole was made under general or local anaesthesia for all patients. After diathermy and incising the dural mater, the outer membrane of the haematoma was incised and a soft silicone drain was inserted into the subdural space through the burr hole. Irrigation was performed using saline solution and repeated until the drainage fluid was clear. The subdural cavity was then filled with saline solution and the scalp was closed in two layers. The silicone drain was connected to a closed drainage system that was kept in a dependent position for 48 hours and then removed. The location of the silicone drain was verified on a CT scan before removal (Figure 1). Surgical procedure for SDE The surgical procedure was identical, but the silicone drainage system was placed. Statistical analysis Categorical frequencies were compared with a 2 or Fisher’s exact test. The corresponding coefficients on the odds scale (with 95% CIs) were included. For all statistical tests, the level of significance was set at 0.05. Statistical analysis was performed with SPSS software version 17.0.0 (SPS, IBM Inc., Chicago, IL).
seizure (4.3%) and coma (14.9%). GCS scores upon admission were 13–15 for 29 patients, 9–12 for 11 patients and 3–8 for seven patients. Twenty-six patients had an MRS of 0–3 and 21 patients had an MRS 4–5. Twelve patients received anticoagulant/antiplatelet therapy (26.1%). Mean mid-line shift was 9.8 mm and 8.7 mm, in the operation and nonoperation groups, respectively. The CT-based characteristics of the primary subdural haematomas were hypodense in 11, isodense in six and of mixed density in 30 patients. The clinical characteristics of patients are no significant differences between groups (p40.05). The primary surgical interventions were a burr-hole irrigation and drainage on the CSDH side and irrigation alone on the SDE side in 21 patients (operation group). The non-operation group patients underwent single burr-hole irrigation and drainage on the CSDH side only. The rate of SDE progression into CSDH was significantly lower in the operation group than in the non-operation group (p50.05, Table II). The volume of subdural effusion increased in one case in the operation group and in three cases in the non-operation group. Thirteen cases (50%) in the non-operation group and three cases (14.3%) in the operation group showed progression of SDE to CSDH (p50.05). The recurrence rate of CSDH showed no significant difference between the two groups (p40.05) and mortality did not differ between the groups at 1- and 3-months’ follow-up. A discharge GCS score of 15 was recorded at a higher rate with an operation than in those without (81.0% vs. 69.2%, p40.05). A similar rate of complications was seen after both operation and non-operation.
Results
Discussion
Table I shows the demographic and clinical data from a retrospective chart review used to identify 47 patients with CSDH and contralateral SDE treated at the hospital between 2004–2013. There was a predominance of males, with a sex ratio of 2.1/1. The mean age of the participants was 65.2 ± 10.8 years (range ¼ 18–85 years). Headache was the most common symptom (68.1%). Table I shows the frequencies of the presenting symptoms, including headache, vomiting (40.4%), drowsiness (31.9%), visual disturbance (25.5%), speech impairment (34.0%), hemiparesis (31.9%),
Neurosurgical practice frequently encounters the problem of treating patients with CSDH and contralateral SDE. To the authors’ knowledge, there has been no previous research comparing the outcome of surgical intervention vs. conservative treatment on the SDE side. This study reports the preliminary results of a retrospective study comparing the results in an operation group and a nonoperation group to guide future treatment in these patients. The results are based on a population of 47 patients divided into the two groups not selected to match for epidemiological,
Figure 1. Serial axial CT scans showing the process of treatment. (a) Pre-operative axial CT scan shows the patients with CSDH and contralateral SDE; (b) Post-operative axial CT scan shows the right side CSDH was cleared, the left side SDE volume significantly reduced, (c) Post-operative axial CT scan shows no CSDH or SDE recurrence 3-months after operation.
Surgical management of CSDH and contralateral SDE
DOI: 10.3109/02699052.2015.1004560
group and 38.5% in the non-operation group (p ¼ 0.044), showing a trend that it is hypothesized could become significant with larger case numbers. Traumatic subdural effusion (TSE) refers to accumulation of cerebrospinal fluid (CSF), xanthochromic or slightly
clinical and radiological parameters. Comparison of postoperative results showed a significant difference in the SDE progression rate (p50.05), in favour of the operation group (Table II). The number of cases at 3-months’ follow-up who progressed from SDE to CSDH was 9.5% in the operation
Table I. Demographic and clinicopathologic data of patients (p50.05).
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Female Age (years) Drug history Anticoagulant Antiplatelet Admission Glasgow coma scale 15–13 12–9 8–3 MRS score 0 1 2 3 4 5 CT (CSDH) Location Right Left Density Hypodense Isodense Mixed Mean mid-line shift (mm) Symptom Headache Vomiting Drowsiness Visual disturbance Speech impairment Hemiparesis Seizure Coma
Operation (n ¼ 21)
Non-operation (n ¼ 26)
p
6/21 (28.6%) 66.1 ± 9.0 (47–83)
8/26 (30.8%) 64.5 ± 12.2 (18–85)
1.00 40.05 40.05
4/21 (19.0%) 5/21 (23.8%)
5/26 (19.2%) 7/26 (26.9%)
14 (66.7%) 4 (19.0%) 3 (14.3%)
15 (57.7%) 7 (26.9%) 4 (15.4%)
40.05
40.05 2 4 3 3 4 5
(9.5%) (19.0%) (14.3%) (14.3%) (19.0%) (23.7%)
4 4 5 1 5 7
(15.4%) (15.4%) (19.2%) (3.9%) (19.2%) (26.9%) 40.05
9/21 (42.9%) 12/21 (57.1%)
12/26 (46.2%) 14/26 (53.8%)
5/21 (23.8%) 3/21 (14.3%) 13/21 (61.9%) 9.8 ± 5.5
6/26 (23.1%) 3/26 (11.5%) 17/26 (65.4%) 8.7 ± 5.1
40.05
32/47 19/46 15/47 12/47 16/47 15/47 2/47 7/47
40.05
(68.1%) (40.4%) (31.9%) (25.5%) (34.0%) (31.9%) (4.3%) (14.9%)
Table II. The outcome of patients measures in operation and non-operation groups (p50.05). Operation Recurrence CSDH SDE SDE!CSDH* SDE clinical progress* Mortality 1 month 3 months GCS (15) Discharge MRS (0–3) Discharge Complications Infection Seizure Pneumocephalus Speech impairment *p50.05.
3/21 1/21 2/21 3/21
(14.3%) (4.8%) (9.5%) (14.3%)
Non-operation
Odds ratio (95% CI)
4/26 3/26 10/26 13/26
1.006 1.077 1.437 1.714
(15.4%) (11.5%) (38.5%) (50.0%)
p Value
(0.795–1.273) (0.910–1.274) (1.043–1.981) (1.124–2.651)
0.959 0.617 0.044 0.014
1/21 (4.8%) 1/21 (4.8%)
1/26 (3.8%) 2/26 (7.7%)
0.990 (0.876–1.120) 1.032 (0.891–1.195)
0.877 0.683
17/21 (81.0%)
18/26 (69.2%)
1.889 (0.479–7.442)
0.505
19/21 (90.5%)
23/26 (88.5%)
0.807 (0.122–5.340)
0.824
0.380 0.952 0.915 0.929
0.579 0.447 0.684 0.644
2/21 1/21 4/21 3/21
(9.5%) (4.8%) (19.0%) (14.3%)
3
1/26 0/26 3/26 2/26
(3.8%) (0.0%) (11.5%) (7.7%)
(0.032–4.508) (0.866–1.048) (0.713–1.175) (0.755–1.142)
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H. Wang et al.
blood-tinged fluid between the dura and the arachnoid membrane [6]. Head injury can cause a separation of the dura–arachnoid interface, which is a basic requirement for the development of subdural effusion [7]. When the subarachnoid barrier is broken, CSF accumulates in the subdural space. Another proposed mechanism for SDE is that it results from deceleration injury or is an epiphenomenon with increased vascular permeability in the Sylvian veins or cortical capillaries [6]. Most SDEs are asymptomatic and resolve when brain expansion or absorption exceeds effusion [7]. An arachnoid tear forming a one-way valve gradually increases the amount of fluid in some cases [8] and 4.0–58.0% of all SDEs progressed to CSDH in the literature [8]. The following research to explain the development of SDE is widely accepted [9]: The cycle of persistent SDE, rebleeding, coagulation and fibrinolysis contributes to the development and maintenance of CSDH [10]. Hypercoagulative and hyperfibrinolytic activities are enhanced after head injury and this may cause CSDH [11]. Additionally, the levels of TNF-a, IL-1b, IL-6, IL-8, IL-10 and procollagen propeptides are significantly increased during CSDH formation [12–14]. The pathological process of SDE and CSDH indicates that local inflammation plays a leading role in the pathogenesis of the evolution and propagation of CSDH [15]. Mid-line structures will return to their pre-injury position following operation on the CSDH side in patients with CSDH and contralateral SDE. Brain movement may increase pathological blood vessels ruptured in the SDE side and especially with high pre-operative intracranial pressure (ICP) patients may show a significant mid-line shift. Therefore, SDE is more likely to progress into CSDH after operation in these patients. Operation opens the effusion membranes and addresses neovascularization. Saline irrigation clears inflammatory cytokines, proteins and plasma, possibly preventing SDE progressing to CSDH. In this research, the operation group showed significantly reduced progression (2/21, 14.3%) and the non-operation group had more cases that progressed to CSDH (10/26, 38.5%). The SDE side was irrigated without drainage in the operation group. If subdural effusion and subarachnoid is inter-linked, a ‘reservoir effect’could make it difficult to remove the drain. The operation group had a higher rate of a GCS score of 15 than did the non-operation group at discharge (81.0% vs. 69.2%), suggesting that subdural effusion and subdural haematoma affect the clinical prognosis of patients simultaneously. However, there was no significant difference between the two groups (p40.05). Studies with larger sample sizes are needed. Single burr-hole drainage is currently widely accepted worldwide [2, 5, 16]. The drainage hole was placed at the highest point intra-operatively and a continuous irrigation system was used. These techniques reduce the complications, including pneumocephalus, infection and seizure. The postoperative complication rate was not significantly different compared with other studies [17, 18].
Conclusions The results showed similar outcomes in the two groups on the CSDH side, although the operation group showed less SDE
Brain Inj, Early Online: 1–5
severity and high GCS 15 at discharge. In the authors’ opinion, patients with CSDH and contralateral SDE benefitted from the operation for subdural effusion.
Acknowledgments The research has been performed in accordance with the Declaration of Helsinki and has been approved by the First Hospital of Jilin University ethics committee (IRB00008484)
Declaration of interest The authors report no conflict of interest. This work was supported by the National Natural Science Foundation of China (No. 81201980) and Natural Science Foundation of Jilin Province, China (No. 20130522028JH).
References 1. Cenic A, Bhandari M, Reddy K. Management of chronic subdural hematoma: A national survey and literature review. Canadian Journal of Neurological Sciences 2005;32:501–506. 2. Belkhair S, Pickett G. One versus double burr holes for treating chronic subdural hematoma meta-analysis. Canadian Journal of Neurological Sciences 2012;40:56–60. 3. Park SH, Lee SH, Park J, Hwang JH, Hwang SK, Hamm IS. Chronic subdural hematoma preceded by traumatic subdural hygroma. Journal of Clinical Neuroscience 2008;15: 868–872. 4. Zanini MA, de Lima Resende LA, de Souza Faleiros AT, Gabarra RC. Traumatic subdural hygromas: Proposed pathogenesis based classification. Journal of Trauma 2008;64:705–713. 5. Santarius T, Kirkpatrick PJ, Ganesan D, Chia HL, Jalloh I, Smielewski P, Richards HK, Marcus H, Parker RA, Price SJ, et al. Use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: A randomised controlled trial. Lancet 2009; 374:1067–1073. 6. Kumar R, Singhal N, Mahapatra AK. Traumatic subdural effusions in children following minor head injury. Childs Nervous System 2008;24:1391–1396. 7. Lee KS. The pathogenesis and clinical significance of traumatic subdural hygroma. Brain Injury 198;12:595–603. 8. Lee KS, Bae WK, Bae HG, Yun IG. The fate of traumatic subdural hygroma in serial computed tomographic scans. Journal of Korean Medical Science 2000;15:560–568. 9. Markwalder TM. Chronic subdural hematomas: A review. Journal of Neurosurgery 1981;54:637–645. 10. Ito H, Saito K, Yamamoto S, Hasegawa T. Tissue-type plasminogen activator in the chronic subdural hematoma. Surgical Neurology 1988;30:175–179. 11. Reisser D, Lejeune P, Lagadec P, Onier N, Dasilva C, Lindley I, Jeannin JF. Interleukin-8 antitumour effect is associated with a local infiltration but not with a systemic activation of T lymphocytes. Anticancer Research 1994;14:977–979. 12. Wada T, Kuroda K, Yoshida Y, Ogasawara K, Ogawa A, Endo S. Local elevation of the anti-inflammatory interleukin-10 in the pathogenesis of chronic subdural hematoma. Neurosurgical Review 2006;29:242–245. 13. Frati A, Salvati M, Mainiero F, Ippoliti F, Rocchi G, Raco A, Caroli E, Cantore G, Delfini R. Inflammation markers and risk factors for recurrence in 35 patients with a posttraumatic chronic subdural hematoma: A prospective study. Journal of Neurosurgery 2004;100: 24–32. 14. Heula AL, Sajanti J, Majamaa K. Procollagen propeptides in chronic subdural hematoma reveal sustained dural collagen synthesis after head injury. Journal of Neurology 2009;256: 66–71. 15. Feng JF, Jiang JY, Bao YH, Liang YM, Pan YH. Traumatic subdural effusion evolves into chronic subdural hematoma: Two stages of the same inflammatory reaction? Medical Hypotheses 2008;70:1147–1149.
DOI: 10.3109/02699052.2015.1004560
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16. Smith MD, Kishikova L, Norris JM. Surgical management of chronic subdural haematoma: One hole or two? International Journal of Surgery 2012;10:450–452. 17. Almenawer SA, Farrokhyar F, Hong C, Alhazzani W, Manoranjan B, Yarascavitch B, Arjmand P, Baronia B, Reddy K, Murty N, et al. Chronic subdural hematoma management: A systematic review and
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meta-analysis of 34,829 patients. Annals of Surgery 2013;259: 449–457. 18. Rohde V, Graf G, Hassler W. Complications of burr-hole craniostomy and closed-system drainage for chronic subdural hematomas: A retrospective analysis of 376 patients. Neurosurgical Review 2002;25:89–94.
ORIGINAL ARTICLE
Surgical management of the patients with chronic subdural haematoma and contralateral subdural effusion: Operation or no-operation? Haifeng Wang1, Jingwei Zhao2, Ye Li3, Yan Feng3, & Li Bie1,4 Department of Neurosurgery of the First Clinical Hospital, Jilin University, Changchun, PR China, 2Department of Neurosurgery, China–Japan Union Hospital, Jilin University, Changchun, PR China, 3Department of Radiology, and 4Department of Pathology and Laboratory Medicine, University of California, Irvine, CA, USA
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1
Abstract
Keywords
Objective: Patients with chronic subdural haematoma and contralateral subdural effusion are rare after head injury. Surgery might reduce clinical progression of subdural effusion, but is not used routinely. This study aimed to investigate the effect of surgery on subdural effusion and clinical outcome. Methods: A retrospective study was performed, comparing operation and non-operation in the patients with chronic subdural haematoma and contralateral subdural effusion, in a series of 47 patients divided into two groups. The operation group of 21 patients underwent bilateral surgery. The non-operation group of 26 patients underwent surgery on the side with chronic subdural haematoma. Neurological status was assessed by the Glasgow Coma score and Modified Rankin Scale score on admission and at follow-up. All cases underwent pre- and postoperative computed tomography scans. Results: Pre-operative clinical and radiological data were similar in the two groups. The rate of subdural effusion progression was significantly lower in the operation group than in the nonoperation group (p50.05). Thirteen cases (50%) in the non-operation group and three cases (14.3%) in the operation group had progression of subdural effusion to chronic subdural haematoma (p50.05). Chronic subdural haematoma recurrence rate, mortality and neurological recovery were similar, with no significant difference between groups. Conclusions: The patients benefitted from surgery for subdural effusion when they had chronic subdural haematoma and contralateral subdural effusion.
Chronic subdural haematoma, outcome, subdural effusion, surgery
Introduction Chronic subdural haematoma (CSDH) is a post-traumatic disease frequently in neurosurgery [1]. Burr-hole drainage (BHD) followed by irrigation of the subdural space is a widespread treatment for CSDH [2] and, in most cases, surgical treatment is straightforward and clinical outcomes are good. Subdural effusion (SDE) occurs rarely in patients with head injury, but SDE progresses to CSDH in some cases [3]. There is no consensus on how to treat patients with CSDH with contralateral SDE. This study reports the retrospective results of a comparison of the efficacy of operation with non-operation on the SDE side.
Methods Patients This was a retrospective review of 52 adult patients who were treated for CSDH and contralateral SDE at a clinical hospital Correspondence: Li Bie, Department of Neurosurgery of the First Clinical Hospital, Jilin University, 71 Xinmin St., Changchun, Jilin 130021, PR China. E-mail: [email protected]
History Received 8 August 2014 Revised 17 November 2014 Accepted 3 January 2015 Published online 19 March 2015
between January 2004 and December 2013. Three patients were excluded with serious medical illness, not suitable for surgery. Two patients had incomplete follow-up or were lost to follow-up. There were 32 males and 15 females ranging in age from 18–85 years (mean age ¼ 65.2 ± 10.8 years). All patients had the symptoms of CSDH confirmed to require surgery based on computed tomography (CT). According to Zanini et al. [4], subdural effusion creates a significant mass effect in the patients. All patients underwent a single burrhole irrigation on the CSDH. Twenty-one patients had drainage in the SDE side. Twenty-six patients were not receiving treatment in the SDE side. The clinical courses and outcomes were evaluated and data included patient information, Glasgow Coma score (GCS), Modified Rankin Scale (MRS) score, recurrence rate, mortality and complaints. All patients underwent 3 months’ follow-up. All cases underwent pre- and post-operative CT scan to evaluate haematoma density and midline shift. Measurements were calculated by two independent neurosurgeons from data derived CT scans images. Written informed consent for participation in the study was obtained from all participants or their guardians. The study was approved by the Institutional Review Board
2
H. Wang et al.
(IRB) of The (IRB00008484).
Brain Inj, Early Online: 1–5
First
Hospital
of
Jilin
University
Operation Surgical procedure for CSDH [5]
Brain Inj Downloaded from informahealthcare.com by Universitat de Girona on 03/24/15 For personal use only.
A single burr-hole was made under general or local anaesthesia for all patients. After diathermy and incising the dural mater, the outer membrane of the haematoma was incised and a soft silicone drain was inserted into the subdural space through the burr hole. Irrigation was performed using saline solution and repeated until the drainage fluid was clear. The subdural cavity was then filled with saline solution and the scalp was closed in two layers. The silicone drain was connected to a closed drainage system that was kept in a dependent position for 48 hours and then removed. The location of the silicone drain was verified on a CT scan before removal (Figure 1). Surgical procedure for SDE The surgical procedure was identical, but the silicone drainage system was placed. Statistical analysis Categorical frequencies were compared with a 2 or Fisher’s exact test. The corresponding coefficients on the odds scale (with 95% CIs) were included. For all statistical tests, the level of significance was set at 0.05. Statistical analysis was performed with SPSS software version 17.0.0 (SPS, IBM Inc., Chicago, IL).
seizure (4.3%) and coma (14.9%). GCS scores upon admission were 13–15 for 29 patients, 9–12 for 11 patients and 3–8 for seven patients. Twenty-six patients had an MRS of 0–3 and 21 patients had an MRS 4–5. Twelve patients received anticoagulant/antiplatelet therapy (26.1%). Mean mid-line shift was 9.8 mm and 8.7 mm, in the operation and nonoperation groups, respectively. The CT-based characteristics of the primary subdural haematomas were hypodense in 11, isodense in six and of mixed density in 30 patients. The clinical characteristics of patients are no significant differences between groups (p40.05). The primary surgical interventions were a burr-hole irrigation and drainage on the CSDH side and irrigation alone on the SDE side in 21 patients (operation group). The non-operation group patients underwent single burr-hole irrigation and drainage on the CSDH side only. The rate of SDE progression into CSDH was significantly lower in the operation group than in the non-operation group (p50.05, Table II). The volume of subdural effusion increased in one case in the operation group and in three cases in the non-operation group. Thirteen cases (50%) in the non-operation group and three cases (14.3%) in the operation group showed progression of SDE to CSDH (p50.05). The recurrence rate of CSDH showed no significant difference between the two groups (p40.05) and mortality did not differ between the groups at 1- and 3-months’ follow-up. A discharge GCS score of 15 was recorded at a higher rate with an operation than in those without (81.0% vs. 69.2%, p40.05). A similar rate of complications was seen after both operation and non-operation.
Results
Discussion
Table I shows the demographic and clinical data from a retrospective chart review used to identify 47 patients with CSDH and contralateral SDE treated at the hospital between 2004–2013. There was a predominance of males, with a sex ratio of 2.1/1. The mean age of the participants was 65.2 ± 10.8 years (range ¼ 18–85 years). Headache was the most common symptom (68.1%). Table I shows the frequencies of the presenting symptoms, including headache, vomiting (40.4%), drowsiness (31.9%), visual disturbance (25.5%), speech impairment (34.0%), hemiparesis (31.9%),
Neurosurgical practice frequently encounters the problem of treating patients with CSDH and contralateral SDE. To the authors’ knowledge, there has been no previous research comparing the outcome of surgical intervention vs. conservative treatment on the SDE side. This study reports the preliminary results of a retrospective study comparing the results in an operation group and a nonoperation group to guide future treatment in these patients. The results are based on a population of 47 patients divided into the two groups not selected to match for epidemiological,
Figure 1. Serial axial CT scans showing the process of treatment. (a) Pre-operative axial CT scan shows the patients with CSDH and contralateral SDE; (b) Post-operative axial CT scan shows the right side CSDH was cleared, the left side SDE volume significantly reduced, (c) Post-operative axial CT scan shows no CSDH or SDE recurrence 3-months after operation.
Surgical management of CSDH and contralateral SDE
DOI: 10.3109/02699052.2015.1004560
group and 38.5% in the non-operation group (p ¼ 0.044), showing a trend that it is hypothesized could become significant with larger case numbers. Traumatic subdural effusion (TSE) refers to accumulation of cerebrospinal fluid (CSF), xanthochromic or slightly
clinical and radiological parameters. Comparison of postoperative results showed a significant difference in the SDE progression rate (p50.05), in favour of the operation group (Table II). The number of cases at 3-months’ follow-up who progressed from SDE to CSDH was 9.5% in the operation
Table I. Demographic and clinicopathologic data of patients (p50.05).
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Female Age (years) Drug history Anticoagulant Antiplatelet Admission Glasgow coma scale 15–13 12–9 8–3 MRS score 0 1 2 3 4 5 CT (CSDH) Location Right Left Density Hypodense Isodense Mixed Mean mid-line shift (mm) Symptom Headache Vomiting Drowsiness Visual disturbance Speech impairment Hemiparesis Seizure Coma
Operation (n ¼ 21)
Non-operation (n ¼ 26)
p
6/21 (28.6%) 66.1 ± 9.0 (47–83)
8/26 (30.8%) 64.5 ± 12.2 (18–85)
1.00 40.05 40.05
4/21 (19.0%) 5/21 (23.8%)
5/26 (19.2%) 7/26 (26.9%)
14 (66.7%) 4 (19.0%) 3 (14.3%)
15 (57.7%) 7 (26.9%) 4 (15.4%)
40.05
40.05 2 4 3 3 4 5
(9.5%) (19.0%) (14.3%) (14.3%) (19.0%) (23.7%)
4 4 5 1 5 7
(15.4%) (15.4%) (19.2%) (3.9%) (19.2%) (26.9%) 40.05
9/21 (42.9%) 12/21 (57.1%)
12/26 (46.2%) 14/26 (53.8%)
5/21 (23.8%) 3/21 (14.3%) 13/21 (61.9%) 9.8 ± 5.5
6/26 (23.1%) 3/26 (11.5%) 17/26 (65.4%) 8.7 ± 5.1
40.05
32/47 19/46 15/47 12/47 16/47 15/47 2/47 7/47
40.05
(68.1%) (40.4%) (31.9%) (25.5%) (34.0%) (31.9%) (4.3%) (14.9%)
Table II. The outcome of patients measures in operation and non-operation groups (p50.05). Operation Recurrence CSDH SDE SDE!CSDH* SDE clinical progress* Mortality 1 month 3 months GCS (15) Discharge MRS (0–3) Discharge Complications Infection Seizure Pneumocephalus Speech impairment *p50.05.
3/21 1/21 2/21 3/21
(14.3%) (4.8%) (9.5%) (14.3%)
Non-operation
Odds ratio (95% CI)
4/26 3/26 10/26 13/26
1.006 1.077 1.437 1.714
(15.4%) (11.5%) (38.5%) (50.0%)
p Value
(0.795–1.273) (0.910–1.274) (1.043–1.981) (1.124–2.651)
0.959 0.617 0.044 0.014
1/21 (4.8%) 1/21 (4.8%)
1/26 (3.8%) 2/26 (7.7%)
0.990 (0.876–1.120) 1.032 (0.891–1.195)
0.877 0.683
17/21 (81.0%)
18/26 (69.2%)
1.889 (0.479–7.442)
0.505
19/21 (90.5%)
23/26 (88.5%)
0.807 (0.122–5.340)
0.824
0.380 0.952 0.915 0.929
0.579 0.447 0.684 0.644
2/21 1/21 4/21 3/21
(9.5%) (4.8%) (19.0%) (14.3%)
3
1/26 0/26 3/26 2/26
(3.8%) (0.0%) (11.5%) (7.7%)
(0.032–4.508) (0.866–1.048) (0.713–1.175) (0.755–1.142)
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H. Wang et al.
blood-tinged fluid between the dura and the arachnoid membrane [6]. Head injury can cause a separation of the dura–arachnoid interface, which is a basic requirement for the development of subdural effusion [7]. When the subarachnoid barrier is broken, CSF accumulates in the subdural space. Another proposed mechanism for SDE is that it results from deceleration injury or is an epiphenomenon with increased vascular permeability in the Sylvian veins or cortical capillaries [6]. Most SDEs are asymptomatic and resolve when brain expansion or absorption exceeds effusion [7]. An arachnoid tear forming a one-way valve gradually increases the amount of fluid in some cases [8] and 4.0–58.0% of all SDEs progressed to CSDH in the literature [8]. The following research to explain the development of SDE is widely accepted [9]: The cycle of persistent SDE, rebleeding, coagulation and fibrinolysis contributes to the development and maintenance of CSDH [10]. Hypercoagulative and hyperfibrinolytic activities are enhanced after head injury and this may cause CSDH [11]. Additionally, the levels of TNF-a, IL-1b, IL-6, IL-8, IL-10 and procollagen propeptides are significantly increased during CSDH formation [12–14]. The pathological process of SDE and CSDH indicates that local inflammation plays a leading role in the pathogenesis of the evolution and propagation of CSDH [15]. Mid-line structures will return to their pre-injury position following operation on the CSDH side in patients with CSDH and contralateral SDE. Brain movement may increase pathological blood vessels ruptured in the SDE side and especially with high pre-operative intracranial pressure (ICP) patients may show a significant mid-line shift. Therefore, SDE is more likely to progress into CSDH after operation in these patients. Operation opens the effusion membranes and addresses neovascularization. Saline irrigation clears inflammatory cytokines, proteins and plasma, possibly preventing SDE progressing to CSDH. In this research, the operation group showed significantly reduced progression (2/21, 14.3%) and the non-operation group had more cases that progressed to CSDH (10/26, 38.5%). The SDE side was irrigated without drainage in the operation group. If subdural effusion and subarachnoid is inter-linked, a ‘reservoir effect’could make it difficult to remove the drain. The operation group had a higher rate of a GCS score of 15 than did the non-operation group at discharge (81.0% vs. 69.2%), suggesting that subdural effusion and subdural haematoma affect the clinical prognosis of patients simultaneously. However, there was no significant difference between the two groups (p40.05). Studies with larger sample sizes are needed. Single burr-hole drainage is currently widely accepted worldwide [2, 5, 16]. The drainage hole was placed at the highest point intra-operatively and a continuous irrigation system was used. These techniques reduce the complications, including pneumocephalus, infection and seizure. The postoperative complication rate was not significantly different compared with other studies [17, 18].
Conclusions The results showed similar outcomes in the two groups on the CSDH side, although the operation group showed less SDE
Brain Inj, Early Online: 1–5
severity and high GCS 15 at discharge. In the authors’ opinion, patients with CSDH and contralateral SDE benefitted from the operation for subdural effusion.
Acknowledgments The research has been performed in accordance with the Declaration of Helsinki and has been approved by the First Hospital of Jilin University ethics committee (IRB00008484)
Declaration of interest The authors report no conflict of interest. This work was supported by the National Natural Science Foundation of China (No. 81201980) and Natural Science Foundation of Jilin Province, China (No. 20130522028JH).
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