Traumatic brain injury (TBI) is a multifaceted and varied condition resulting from an external mechanical force that inflicts damage on the brain. TBI can arise from several causes, such as motor vehicle collisions, falls, sports-related injuries, and acts of violence. The World Health Organization (WHO) reports that TBI is a major contributor to mortality and disability globally, impacting millions of individuals annually. Traumatic brain injury (TBI) represents a significant health issue worldwide, leading to severe neurological consequences for those affected.(1)

The incidence of TBI varies widely depending on the

population, location, and criteria used to define TBI. A systematic review of 22 studies on TBI epidemiology reported that the global incidence of TBI ranges from 150 to 600 per 100,000 people per year. The same review found that the mortality rate for TBI ranges from 10 to 30 per 100,000 people per year (2).

TBI can cause both primary and secondary brain damage. Primary brain damage occurs immediately after the injury and is caused by the mechanical forces of the injury. Secondary brain damage occurs in the hours and days following the injury and is caused by a variety of mechanisms, including inflammation, oxidative stress, and excitotoxicity. TBI can be classified into three categories based on the severity of the injury; Mild TBI: This category includes injuries that result in minimal or no loss of consciousness, and no-significant neurological deficits. Moderate TBI: This category includes injuries that result in a loss of consciousness lasting from a few minutes to a few hours, and some neurological deficits. Severe TBI: This category includes injuries that result in a prolonged loss of consciousness, significant neurological deficits, and often require intensive care and rehabilitation. The clinical presentation of TBI can vary widely depending on the severity and location of the injury. Common symptoms of TBI include: Headache, Dizziness, Nausea and vomiting, Confusion and disorientation, Memory loss, Mood changes, Sleep disturbances and Seizures.

Imaging studies, such as computed tomography (CT) and magnetic resonance imaging (MRI), are commonly used to diagnose and evaluate the severity of TBI.(3)

The Glasgow Coma Scale (GCS) is also widely used to assess the severity of TBI. The treatment and management of TBI depend on the severity and location of the injury. Mild TBI is often managed conservatively with rest, pain management and monitoring for signs of worsening. Moderate and severe TBI often require more aggressive management which includes surgical intervention to relieve pressure or repair damaged tissue, Intensive care and monitoring, Rehabilitation and physical therapy, Cognitive and behavioral therapy. TBI can result in a range of complications, including post-concussive syndrome, post-traumatic epilepsy, hydrocephalus, cerebrospinal fluid leaks, meningitis and brain abscess. The outcomes of TBI can vary widely depending on the severity and location of the injury. Generally, mild TBI has a good prognosis, while moderate and severe TBI can result in significant disability and mortality.(4)

Despite advances in the management of TBI, there is still much to be learned about the pathophysiology and treatment of this complex condition. Future research directions include: developing more effective treatments for TBI including pharmacological and cell-based therapies, improving diagnostic and prognostic tools for TBI, enhancing rehabilitation and recovery outcomes for individuals with TBI, Investigating the long-term effects of TBI on cognition, behavior, and quality of life. Approximately one-third of patients with severe TBI exhibit the existence of acute subdural hematomas. TBI with Acute Traumatic SDH leads to an increase in mortality rate of 40-60%, with a functional recovery rate of 19-45%. (5) Trauma is the most common cause of Acute SDH, with most cases of road accidents, falls, and assaults.(6) Initial presentation in 50% of cases at the time of injury is coma.(7) In the developing countries burden related to TBI is very high, because of the use of motor vehicles while in developed countries falls are highly reported as a cause of head injury.(8)

After the approval by ethical review committee for the research, all patients with head injuries who met the inclusion criteria were enrolled in this study. Written informed consent was obtained from either the patient or their guardian. The patients were randomly divided into two distinct groups using a lottery method. Group A underwent craniectomy with a wide dural flap duraplasty, while Group B was treated with dural slits. Both groups were monitored for cerebrospinal fluid (CSF) leaks for four weeks post-surgery. All data were meticulously recorded on a designed proforma. Follow-up was facilitated by collecting addresses and contact numbers. Data was analyzed using SPSS version 25.0. Quantitative variables like, duration of trauma, age and baseline GCS were measured as mean ± SD. Frequencies and percentages were calculated for gender and frequency of CSF leak in both groups. Frequency of CSF leak in both groups was compared by employing Chi-square test. P-value was considered significant at ≤ 0.05. Effect modifiers like age, gender, duration of trauma and baseline GCS were controlled by stratification and chi-square test was applied. P value < 0.05 was considered significant.

A total of two hundred and ninety-two adult patients of either gender between age 15 – 55 years presented with unilateral isolated traumatic ASDH with midline shift of 5mm (diagnosed on CT scan) were enrolled and equally divided into two groups. There is significant difference in overall frequency of CSF leak in both groups as shown in Table 1.

Post stratification frequency of CSF leak is found significant in male (P = 0.003), 15-35 years age (P = 0.060) and in Duration of trauma < 6 hours (P = 0.10) but these groups did not show any significant difference when stratified with respect to female, 36-55 years age, duration of trauma 6-12 hours and baseline GCS (table 2). P value (chi-square) was > 0.05 in these cases. Mean age, duration of trauma and baseline GCS was 31 ± 9, 4 ± 2 and 9 ± 2 respectively.

Table 1: CSF Leak in Both Groups of Patients

Table 2: CSF Leak with Respect to Gender, Age, Duration of Trauma, Baseline GCS

Acute subdural hematoma resulting from a traumatic brain injury is a neurosurgical emergency that frequently necessitates surgical intervention. A decompressive craniectomy is conducted to evacuate the hematoma, during which the bone is not reconstructed. Following the evacuation of the hematoma, a wide dural flap duraplasty is performed to create space for the edematous brain; however, this procedure can often lead to severe brain herniation. To mitigate this risk, an alternative surgical technique is employed, which involves creating multiple dural slits parallel to the dural blood vessels. These slits facilitate the gradual removal of the hematoma, thereby preventing brain herniation. Nevertheless, this method is frequently linked to postoperative cerebrospinal fluid (CSF) leaks. This study aimed to compare the incidence of CSF leaks in decompressive craniectomy with a wide dural flap versus decompressive craniectomy with dural slits. The results of this study demonstrate a significantly lower frequency of CSF leak in group A (DC with wide dural flap) compared to group B (DC with dural slits). CSF leak was observed in 11.1% (n =16/145) in group A (DC with wide dural flap) and in 21.3% (n = 31/145) in group B (DC with dural slits) (P=0.02). However, upon stratification of the data, this significant difference does not persist across all population subgroups (P = > 0.05). Notably, in certain subgroups, the sample size was limited, which may have contributed to the observed discrepancy. Our results are in contrast to previous studies that have reported similar rates of CSF leak between the two techniques.(9) The reduced frequency of post-operative CSF leak observed in this study can be attributed to several factors. Firstly, the use of wide dural flap duraplasty may provide a more watertight closure of the dura, reducing the risk of CSF leak (10). Secondly, this technique may also allow for better apposition of the dural edges, reducing the risk of CSF leak (11). In contrast, dural slits may not provide as secure closure of the dura, increasing the risk of CSF leak. (12) The findings of this study have significant implications for the management of ATSDH. Decompressive craniectomy with wide dural flap duraplasty may be a preferable technique to dural slits in reducing the risk of post-operative CSF leak. However, further studies are needed to confirm these findings and to determine the optimal surgical technique for the management of ATSDH.

This study demonstrates a significant reduction in the frequency of post-operative CSF leak in patients undergoing decompressive craniectomy with wide dural flap duraplasty compared to those with dural slits for the management of acute traumatic subdural hematoma. However, stratified analysis reveals that this significant difference may not be consistent across all population subgroups, potentially due to limited sample sizes in certain subgroups. These findings suggest that wide dural flap duraplasty may be a preferable technique to dural slits in reducing the risk of post-operative CSF leak, but further investigation with larger sample sizes is necessary to confirm these results and fully elucidate the relationships between surgical technique, patient characteristics, and CSF leak risk.

1. Khellaf A, Khan DZ, Helmy A. Recent advances in traumatic brain injury. Journal of neurology. 2019;266(11):2878-89.
2. Theadom A, Mahon S, Hume P, Starkey N, Barker-Collo S, Jones K, et al. Incidence of sports-related traumatic brain injury of all severities: a systematic review. Neuro-epidemiology. 2020;54(2):192-9.
3. Meyfroidt G, Bouzat P, Casaer MP, Chesnut R, Hamada SR, Helbok R, et al. Management of moderate to severe traumatic brain injury: an update for the intensivist. Intensive care medicine. 2022;48(6):649-66.
4. Abdallah A, Demaerschalk BM, Kimweri D, Aden AA, Zhang N, Butterfield R, et al. A comparison of the Full Outline of Unresponsiveness (FOUR) and Glasgow Coma Scale (GCS) scores in predicting mortality among patients with reduced level of consciousness in Uganda. Neurocritical care. 2020;32:734-41.
5. Atalay T, Ak H, Gülsen I, Karacabey S. Risk factors associated with mortality and survival of acute subdural hematoma: A retrospective study. Journal of research in medical sciences. 2019;24(1):27.
6. Farzaneh N, Williamson CA, Jiang C, Srinivasan A, Bapuraj JR, Gryak J, et al. Automated segmentation and severity analysis of subdural hematoma for patients with traumatic brain injuries. Diagnostics. 2020;10(10):773.
7. Bodnar CN, Roberts KN, Higgins EK, Bachstetter AD. A systematic review of closed head injury models of mild traumatic brain injury in mice and rats. Journal of neurotrauma. 2019;36(11):1683-706.
8. Khan M, Yaqoob U, Hassan Z, Uddin MM. Immediate Outcomes of Traumatic Brain Injury at a Tertiary Care Hospital Of Pakistan-A Retrospective Study. 2020.
9. Khan B, Khan Afridi EA, Khan B, Khan SA, Aurangzeb A, Khan AA, et al. Decompressive Craniectomy for acute subdural haematoma with expansile duraplasty versus dural slits. JAMC Abbott:. 2016;28(2):285-8.
10. Miyake S, Fujita A, Aihara H, Kohmura E. New technique for decompressive duraplasty using expanded polytetrafluoroethylene dura substitute--technical note. Neurologia medico-chirurgica. 2006;46(2):104-6; discussion 6.
11. Phan K, Moore JM, Griessenauer C, Dmytriw AA, Scherman DB, Sheik-Ali S, et al. Craniotomy Versus Decompressive Craniectomy for Acute Subdural Hematoma: Systematic Review and Meta-Analysis. World neurosurgery. 2017;101:677-85.e2