CLINICAL STUDY

Early Pressure Dressing for the Prevention of Subdural Effusion Secondary to Decompressive Craniectomy in Patients With Severe Traumatic Brain Injury Gang-Zhu Xu, PhD,*Þ Wen Li, MD,Þ Kai-Ge Liu, PhD,Þ Wei Wu, PhD,Þ Wen-Chao Lu, MD,Þ Jun-Feng Zhang, MD,Þ and Mao-De Wang, PhD*

Abstract: This study was performed to investigate the effect of early pressure dressing on the prevention of postoperative subdural effusion secondary to decompressive craniectomy (DC) in patients with severe traumatic brain injury (STBI). Patients with STBI who had undergone DC for refractory increased intracranial pressure between January 2008 and December 2011 (n = 169) were randomly divided into early pressure dressing (n = 82) and control (n = 87) groups. Early pressure dressing with an elastic bandage or general wrapping (control treatment) was applied 7 to 10 days after DC. Patients’ age, sex, preoperative Glasgow Coma Scale score, incidence rate of subdural effusion, hospitalization time, and postoperative Glasgow Outcome Scale score were compared between groups. Intracranial pressure was measured immediately before and on the day after pressure dressing. No significant difference in age, sex, preoperative Glasgow Coma Scale score, or postoperative Glasgow Outcome Scale score was observed between groups (P 9 0.05). Subdural effusion incidence rates were significantly lower in the early pressure dressing group than those in the control group (W2 = 5.449, P = 0.021), and a larger proportion of patients in the early pressure dressing group was hospitalized for 30 days or less (W2 = 5.245, P = 0.027). Early pressure dressing 7 to 10 days after DC, which is a noninvasive, simple procedure, reduced the incidence rate of subdural effusion and shortened hospitalization time after DC for STBI. Key Words: Traumatic brain injury, decompressive craniectomy, subdural effusion, pressure dressing (J Craniofac Surg 2014;25: 1836Y1839)

M

ortality rates are high in patients with severe traumatic brain injury (STBI) due to increased intracranial pressure (ICP) and brain swelling. The adequate management of increased ICP is thus

From the *Department of Neurosurgery, First Affiliated Hospital, Medical College of Xi’an Jiaotong University; and †Department of Neurosurgery, Affiliated Hospital of Xi’an Medical College, Xi’an, China. Received March 26, 2013. Accepted for publication June 22, 2013. Address correspondence and reprint requests to Mao-De Wang, PhD, or Gang-Zhu Xu, PhD, Department of Neurosurgery, First Affiliated Hospital, Medical College of Xi’an Jiaotong University, No. 277, Yanta West Rd, Xi’an 710061, Shaanxi, China; E-mail: maodewang@ 163.com; [email protected] The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0b013e3182a21056

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critical in these patients, and many studies have shown that surgical decompression effectively achieves this goal.1Y3 Decompressive craniectomy (DC), in which a portion of the skull on the affected side is removed and dural opening is performed simultaneously to provide space for the swelling brain, is a widely used method of managing refractory intracranial hypertension that is unresponsive to maximal medical therapy.4,5 Although technically straightforward, DC has been associated with high complication rates. Yang et al6 documented a surgical complication rate of 50% in patients who had undergone DC. Complications such as subdural effusion may require aggressive treatment because they tend to cause midline shift and neurologic deterioration, which adversely affect clinical outcomes.7 Patients with STBI who undergo DC are at increased risk of developing postoperative complications that can severely affect clinical outcomes.8Y10 Subdural effusion, the most frequent complication, may impede recovery, cause the deterioration of a patient’s clinical condition, or result in the appearance of new symptoms/ signs, such as consciousness disturbance. Such complications can lead to poor quality of life, prolong hospitalization, and increase the patient’s economic burden. The treatment of subdural effusion is challenging, especially in refractory cases, and the prevention of this complication is important. Several methods, such as duraplasty,11 avoidance of excessive dehydration,12 and early cranioplasty,13 have been suggested to prevent subdural effusion after surgical decompression. These methods can help to reduce the incidence of this complication, but cannot prevent it completely. Yang et al6 recommended bandaging of the cranium after the peak time of cerebral edema to prevent subdural effusion as well as brain movement and cephalocele. However, that study did not discuss the bandaging technique further or identify a difference between patients who were bandaged and control subjects, which was not the main purpose of the research; thus, the clinical effectiveness of bandaging remains unexamined. The purpose of this study was to determine whether the early (7Y10 days after DC) application of pressure dressing (bandaging) could prevent subdural effusion secondary to DC in patients with STBI. We based the timing of application on the results of a study of brain edema development and regression after brain contusion and laceration, in which Xiong et al14 found that edema peaked in most patients at 7 to 10 days after trauma and subsided gradually thereafter.

PATIENTS AND METHODS Patients Patients included in this prospective randomized study were drawn from a total of 237 patients with STBI who underwent DC for refractory increased ICP between January 2008 and December 2011 at 2 hospitals: the First Affiliated Hospital of the Medical College of

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Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.

The Journal of Craniofacial Surgery

& Volume 25, Number 5, September 2014

Xi’an Jiaotong University and the First Affiliated Hospital of Xi’an Medical College. The ethics committees of these hospitals approved the study protocol. The following inclusion criteria were applied: preoperative Glasgow Coma Scale (GCS) score of 8 or less; computed tomography findings confirming brain contusion and laceration, midline structure shift, and displaced brain ventricles; and provision of written informed consent to participation in the study. Exclusion criteria were age 80 years or older, subdural effusion within 7 days after DC, elevated (9250 mm H2O) ICP and skin flap tension, incomplete clinical followup data, simple epidural hematoma, and participation in another clinical trial. Table 1 shows the characteristics of patients with STBI who underwent DC and were included in this study.

Surgical Treatment and Postoperative Management Trained and experienced attending physicians performed all operations. All patients underwent DC with wide dural opening, and all dural defects were covered with gelfoam. Using a computer-generated random sequence, study participants were divided postoperatively into 2 groups: an early pressure dressing group and a control group. Patients in the early pressure dressing group received moderate pressure dressing in the bone defect region at 7 to 10 days after DC. A self-stick elastic bandage prepared in the hospital was secured with nylon thread in each patient to enable the regulation of pressure and tension (Fig. 1). Patients in the control group received only light bandaging after DC; the bandage did not extend circumferentially around the head but was applied locally with adhesive tape. All other postoperative management was the same in all patients.

Data Collection and Study Parameters Each patient’s age, sex, and GCS score on admission were recorded preoperatively. The incidence rate of subdural effusion secondary to DC, hospitalization time, Glasgow Outcome Scale (GOS) score, and ICP immediately before and the day after the application of pressure dressing were determined postoperatively. Subdural effusion was defined as newly appearing subdural fluid accumulation (thickness 92 mm) on serial cranial computed tomography scans. Neurologic examination was performed using the GCS.15 Functional outcome was evaluated 6 months after injury using the GOS, as follows: 1, death; 2, vegetative state; 3, severe disability; 4,moderate disability; and 5, good recovery.16 Intracranial pressure was measured by lumbar punctures.

Statistical Analysis

We compared clinical data from the 2 groups using Pearson W2 test for categorical variables and the paired-sample t test for TABLE 1. Features of Patients With Severe Traumatic Brain Injury Who Underwent DC

Total Mydriasis Bilateral Unilateral None Brain contusion and laceration Brain contusion and laceration complicated by subdural hematoma Brain contusion and laceration complicated by multiple intracranial hematomas

Early Pressure Dressing Group

Control Group

82

87

23 49 10 9 51

27 51 9 16 53

22

18

Dressing for Prevention of Subdural Effusion

FIGURE 1. Conceptual diagram of bandage positions used in the pressure dressing method. Before (A) and after (B) pressure dressing with an elastic bandage secured with nylon threads (shaded regions).

continuous data, with P G 0.05 considered to indicate statistical significance. Statistical analysis was performed using SPSS software (version 17.0 for Windows; SPSS Inc, Chicago, IL).

RESULTS After the application of inclusion and exclusion criteria, 169 patients (early pressure dressing group, n = 82; control group, n = 87) were included in the study sample. Baseline clinical data were comparable between groups (P 9 0.05). No significant difference in age, sex, GCS score, or GOS score was observed between groups (P 9 0.05), but significant differences were found in the subdural effusion incidence rate (W2 = 5.449, P = 0.021) and hospitalization time (W2 = 5.245, P = 0.027; Table 2, Fig. 2). Hospital stays of 30 days or less were significantly more frequent in the early pressure dressing group, and the incidence rate of subdural effusion was significantly lower in comparison with the control group. Intracranial pressure was higher immediately before early pressure dressing than on the day after

TABLE 2. Clinical Features of Patients Undergoing Decompressive Craniectomy for Severe Traumatic Brain Injury

Observation Index N Age, y e50 950 Sex Male Female GCS e5 95 Subdural effusion Yes No Duration of hospitalization, d e30 930 GOS e3 93

Early Pressure Dressing Group

Control Group

82

87

70 12

W2

P

72 15

0.214

0.679

56 26

63 25

0.220

0.738

45 37

52 35

0.413

0.537

10 72

23 64

5.449

0.021*

30 52

18 69

5.245

0.027*

53 29

61 26

0.578

0.512

*P G 0.05.

* 2014 Mutaz B. Habal, MD

Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.

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Xu et al

FIGURE 2. Computed tomographic images showing subdural effusion contralateral (A) and ipsilateral and contralateral (B) to the craniectomy site in the control group and demonstrating the absence of subdural effusion after decompressive hemicraniectomy (C) and bilateral DC (D) in the early pressure dressing group.

dressing (178.78 T 25.32 vs 175.06 T 24.45 mm H2O), but this difference was not significant (t = 1.490, P = 0.140).

DISCUSSION To our knowledge, this study is the first to examine the effectiveness of early pressure dressing for the prevention of subdural effusion secondary to DC in patients with STBI. Many studies have reported that DC can reduce mortality and improve clinical outcomes, and this procedure is used widely for the prevention and management of complications in patients with STBI.17Y19 Neurosurgeons have only recently devoted attention to postoperative complications of DC, as much attention has been focused on its initial advantages. In patients who have not undergone DC, 5% to 20% incidence rates of posttraumatic subdural effusion have been reported.20 As craniotomy is a well-known cause of subdural effusion, the development of this complication may easily be anticipated when traumatic brain injury and craniotomy are combined. Incidence rates of 21% to 62% have been reported in patients with STBI who have undergone DC.6,10,21 Subdural effusion is currently managed by bandaging of the head, oral administration of acetazolamide, observation, subdural tapping and drainage, and subduropleural or subduroperitoneal shunting.6,20,22Y26 However, investigations of such treatments have focused primarily on the period following subdural effusion occurrence and have yielded controversial results, especially for refractory subdural effusion. The prevention of this complication is important, and the incidence rate of subdural effusion might be reduced by using simple preventive measures and modifying the surgical technique.

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The pressure gradient after DC is a major reason for the development of subdural effusion, and its early correction could aid rehabilitation and prevent several complications. In patients with STBI, subdural effusion can be prevented and managed by bandaging of the cranium about 7 to 10 days after DC, when edema has abated; this timing was used in the present study and achieved good clinical outcomes. The results of our prospective randomized study provide support for the argument of Yang et al6 that cranial bandaging after the peak time of cerebral edema is useful in preventing subdural effusion secondary to DC in patients with STBI. Jeon et al27 retrospectively reviewed clinical and radiological features and analyzed risk factors for subdural effusion, finding that the mean GOS score was significantly lower in patients with than in those without subdural effusion (P G 0.0001). The authors thus suggested that subdural effusion affected prognosis; however, our results were not in agreement with this conclusion, as we observed no obvious effect of pressure dressing on patients’ prognoses and no significant difference in GOS score between the early pressure dressing and control groups. This discrepancy may be explained by the multitude of factors affecting patients’ prognoses; simple pressure dressing improved the incidence rate of subdural effusion to a certain extent but had no larger ultimate effect. Subdural effusion secondary to DC is known to be caused by traumatic rupture of the dura-arachnoid interface and the resultant change in cerebrospinal fluid (CSF) circulation dynamics.28,29 Tearing or disruption of the arachnoid layer may result in the formation of a 1-way flap valve that promotes CSF leakage and accumulation in the subdural space.29 Thus, the effects of DC on CSF dynamics lead to posttraumatic edema.3,30 In addition, following the reduction of brain volume due to the intraoperative removal of necrotic brain tissue and CSF drainage, normal brain shape cannot be restored. The disruption of normal CSF circulation and absorption increases the risk of CSF leakage through the torn arachnoid layer.31 Because of intracranial hypertension induced by brain edema, pressure remains relatively balanced in the early stage, and the tear in the arachnoid is closed temporarily; thus, subdural effusion rarely develops in this stage. With the gradual resolution of brain edema, ICP is reduced, and the brain tissue shifts to the bone window, where cranial support is lacking. Areas of low pressure develop ipsilateral and contralateral to the craniectomy site and adjacent to the cerebral falx. Cerebrospinal fluid accumulates in these locations through the 1-way flap valve because of the force resulting from the pressure difference, resulting in subdural effusion. To our knowledge, this process has not been described previously; it can be explained as follows. With the progression of therapy, ICP gradually returns to approximately normal, and pressure on the bone window is minimal, but the cephalocele cannot be moved intracranially. Moderate pressure dressing on the bone window at this time helps tore store the closed intracranial environment and CSF circulation. It can prevent cephalocele and pendular movement after DC for STBI. Pressure dressing may induce intracranial hypertension, but total ICP tends to decline with the reduction of brain edema. In this way, early pressure dressing may reduce the incidence of subdural effusion. This finding has significant implications for the management and treatment of patients with STBI who have undergone DC. Carefully structured therapy using simple bandaging material appears to have a beneficial effect. One must consider the limitations of this study when interpreting its findings. The study design did not allow the identification of the mechanism responsible for the observed effect. * 2014 Mutaz B. Habal, MD

Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.

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Furthermore, although the influence of early pressure dressing on ICP was not significant, intracranial hypertension may develop immediately after pressure dressing; this study did not focus on this potential effect. Moreover, the study did not examine whether early pressure dressing had a harmful effect on intracranial blood circulation via blood vessel obstruction. These issues may be resolved by subsequent research examining hemodynamics. Given the potential benefits of early pressure dressing in patients with STBI who have undergone DC, further research on this potentially effective method of preventing subdural effusion in these patients is warranted.

CONCLUSIONS The results of this study suggest that early pressure dressing 7 to 10 days after DC, which is a noninvasive, simple procedure, reduces the incidence rate of subdural effusion and shortens hospitalization time in patients with STBI. Early pressure dressing after DC for STBI appears to be a safe and effective method for the prevention of subdural effusion in appropriately selected patients.

ACKNOWLEDGMENTS The authors thank the patients who kindly agreed to participate in this research project. They also thank Medjaden Bioscience Limited for assisting in the preparation of this manuscript.

REFERENCES 1. Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev 2006;25:CD003983 2. Kontopoulos V, Foroglou N, Patsalas J, et al. Decompressive craniectomy for the management of patients with refractory hypertension: should it be reconsidered? Acta Neurochir (Wien) 2002;144:791Y796 3. Aarabi B, Hesdorffer DC, Ahn ES, et al. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg 2006;104:469Y479 4. Timofeev I, Hutchinson PJ. Outcome after surgical decompression of severe traumatic brain injury. Injury 2006;37:1125Y1132 5. Piek J. Decompressive surgery in the treatment of traumatic brain injury. Curr Opin Crit Care 2002;8:134Y138 6. Yang XF, Wen L, Shen F, et al. Surgical complications secondary to decompressive craniectomy in patients with a head injury: a series of 108 consecutive cases. Acta Neurochir (Wien) 2008;150:1241Y1247 7. Aarabi B, Chesler D, Maulucci C, et al. Dynamics of subdural hygroma following decompressive craniectomy: a comparative study. Neurosurg Focus 2009;26:E8 8. Stiver SI. Complications of decompressive craniectomy for traumatic brain injury. Neurosurg Focus 2009;26:E7 9. Ban SP, Son YJ, Yang HJ, et al. Analysis of complications following decompressive craniectomy for traumatic brain injury. J Korean Neurosurg Soc 2010;48:244Y250 10. Su TM, Lee TH, Huang YH, et al. Contralateral subdural effusion after decompressive craniectomy in patients with severe traumatic brain injury: clinical features and outcome. J Trauma 2011;71:833Y837

Dressing for Prevention of Subdural Effusion

11. Yang XJ, Hong GL, Su SB, et al. Complications induced by decompressive craniectomies after traumatic brain injury. Chin J Traumatol 2003;6:99Y103 12. Yang XF, Wen L, Gong JB, et al. Subdural effusion secondary to decompressive craniectomy in patients with severe traumatic brain injury. Acta Neurochir (Wien) 2010;152:555Y556 13. Liang W, Xiaofeng Y, Weiguo L, et al. Cranioplasty of large cranial defect at an early stage after decompressive craniectomy performed for severe head trauma. J Craniofac Surg 2007;18:526Y532 14. Xiong NX, Zang FC, Zhao HY, et al. Exploring time course of brain edema after cerebral contusion and laceration. Chin J Clin Neurosurg 2004;9:427Y429 15. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974;2:81Y84 16. Jennett B, Bond M. Assessment of outcome after severe brain damage: a practical scale. Lancet 1975;1:480Y484 17. Danish SF, Barone D, Lega BC, et al. Quality of life after hemicraniectomy for traumatic brain injury in adults. A review of the literature. Neurosurg Focus 2009;26:E2 18. Kim KH. Predictors for functional recovery and mortality of surgically treated traumatic acute subdural hematoma in 256 patients. J Korean Neurosurg Soc 2009;45:143Y150 19. Qiu W, Guo C, Shen H, et al. Effects of unilateral decompressive craniectomy on patients with unilateral acute post-traumatic brain swelling after severe traumatic brain injury. Crit Care 2009;13:R185 20. Stone JL, Lang RG, Sugar O, et al. Traumatic subdural hygroma. Neurosurgery 1981;8:542Y550 21. Honeybul S. Complications of decompressive craniectomy for head injury. J Clin Neurosci 2010;17:430Y435 22. Kumar R. External hydrocephalus in small children. Childs Nerv Syst 2006;22:1237Y1241 23. Sakai N, Nokura H, Deguchi K, et al. Surgical indications for infantile subdural effusion. Childs Nerv Syst 1990;6:447Y450 24. Mizoi K, Takaku A, Suzuki J. Subdural effusion following radical surgery for chiasmal region tumors in children. Report of 4 cases. Childs Brain 1981;8:307Y315 25. Arsalo A, Louhimo I, Santavuori P, et al. Subdural effusion: results after treatment with subdural-pleural shunts. Childs Brain 1977;3:79Y86 26. French BN, Cobb CA 3rd, Corkill G, et al. Delayed evolution of posttraumatic subdural hygroma. Surg Neurol 1978;9:145Y148 27. Jeon SW, Choi JH, Jang TW, et al. Risk factors associated with subdural hygroma after decompressive craniectomy in patients with traumatic brain injury: a comparative study. J Korean Neurosurg Soc 2011;49:355Y358 28. Carvi Y Nievas MN, Ho¨llerhage HG. Early combined cranioplasty and programmable shunt in patients with skull bone defects and CSF-circulation disorders. Neurol Res 2006;28:139Y144 29. Yang XF, Wen L, Li G, et al. Contralateral subdural effusion secondary to decompressive craniectomy performed in patients with severe traumatic brain injury: incidence, clinical presentations, treatment and outcome. Med Princ Pract 2009;18:16Y20 30. Mazzini L, Campini R, Angelino E, et al. Posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. Arch Phys Med Rehabil 2003;84:1637Y1641 31. Su FW, Ho JT, Wang HC. Acute contralateral subdural hygroma following craniectomy. J Clin Neurosci 2008;15:305Y307

* 2014 Mutaz B. Habal, MD

Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.

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Early pressure dressing for the prevention of subdural effusion secondary to decompressive craniectomy in patients with severe traumatic brain injury.

This study was performed to investigate the effect of early pressure dressing on the prevention of postoperative subdural effusion secondary to decomp...
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