Intractable subdural effusion after decompressive craniectomy for traumatic brain injury: A case report

Abstract

BACKGROUND

Traumatic subdural effusion is a common complication of traumatic brain injury, especially after decompressive craniectomy (DC). For neurosurgeons, early diagnosis and timely treatment are particularly important, which can help improve patient prognosis and enhance quality of life.

CASE SUMMARY

A 47 year old male underwent DC for traumatic brain herniation. After surgery, he developed stubborn subdural effusion (SDE) on the contralateral side and underwent multiple subdural drilling and drainage surgeries, but only temporarily improved the patient’s symptoms. After the final cranioplasty, the contralateral SDE completely disappeared. The patient did not experience any new contralateral neurological dysfunction, and the Glasgow prognostic score was 11 points (E4V1M6).

CONCLUSION

For neurosurgeons, accurate assessment of the condition is necessary when treating patients with stubborn SDE after DC surgery, and timely cranioplasty can be performed to avoid multiple surgeries. This is a safe and effective surgical method for treating traumatic subdural effusion.

Key Words: Traumatic brain injury; Traumatic subdural effusion; Decompressive craniectomy; Cranioplasty; Case report

Core Tip: Traumatic subdural effusion is a common complication of traumatic brain injury, especially after decompressive craniectomy (DC). For neurosurgeons, early diagnosis and timely treatment are particularly important, which can help improve patient prognosis and enhance quality of life. This article reports a case of refractory subdural fluid accumulation after DC, providing reference for clinical work. Contralateral subdural effusion is one of the complications after DC surgery, especially in cases of stubborn subdural effusion, and cranioplasty is an effective treatment method. Our research can provide reference value for the clinical treatment of refractory subdural fluid accumulation after DC.

INTRODUCTION

Traumatic subdural effusion (TSE) is a common complication in patients with traumatic brain injury, particularly in those who have undergone decompressive craniectomy (DC). While most asymptomatic cases can be managed conservatively, some may progress to significant intracranial hypertension and associated neurological deficits, necessitating surgical intervention. Surgical options for TSE include external drainage, lumbar cistern drainage, hydrocephalus abdominal diversion, craniotomy for the resection of the hydrocephalic capsule, and subarachnoid communication surgery[1]. In cases complicated by skull defects, early cranioplasty is crucial to prevent the development of TSE[2]. Here, we present the case of a patient who, following DC and subsequent traumatic brain herniation, developed refractory TSE. The patient showed significant improvement after multiple surgical interventions and was discharged in stable condition.

CASE PRESENTATION

Chief complaints

4 hours of unconsciousness caused by car accident trauma.

History of present illness

Four hours ago, the patient was hit by a car and lost consciousness. The traffic police sent him to our emergency department for treatment. After completing the cranial computed tomography scan, it was found that there was bleeding in the left frontal and temporal regions and swelling of the brain.

History of past illness

Past physical health.

Personal and family history

The patient is a non-smoker and has no history of alcohol abuse. The patient’s mother and father are healthy. No history of hypertension, diabetes, stroke, or myocardial infarction is present in the family.

Physical examination

On presentation, he was unconscious and intubated, with a Glasgow Coma Scale score of 5 (E1VTM4). The pupils were anisocoric, with the left pupil measuring approximately 4.0 mm and non-reactive to light, while the right pupil measured 3.0 mm with a sluggish light reflex. Neurological examination revealed absent coordination and overextension to painful stimuli, with normal muscle tone in the limbs. Bilateral Babinski signs were positive.

Laboratory examinations

No obvious abnormalities were found in the laboratory examination.

Imaging examinations

Brain computed tomography shows left frontal and temporal hemorrhage with significant brain swelling.

FINAL DIAGNOSIS

Moderate traumatic brain injury.

TREATMENT

Emergency left intracerebral hematoma evacuation and left DC after admission (Figure 1). After surgery, he developed stubborn subdural effusion (SDE) on the contralateral side and underwent multiple subdural drilling and drainage surgeries (Figures 2-5), but only temporarily improved the patient’s symptoms. After the final cranioplasty, the contralateral SDE completely disappeared (Figure 6).

Figure 1  Brain computed tomography scan before and after decompressive craniectomy. A-C: Brain computed tomography scan on admission; D-F: Brain computed tomography scan on the first day after decompressive craniectomy.

Figure 2  Brain computed tomography scan 7 days after decompressive craniectomy. A-C: Brain computed tomography scan 7 days after decompressive craniectomy. White solid arrow: Postoperative left subdural fluid accumulation.

Figure 3 Computed tomography scan tenth day after decompressive craniectomy. A-C: On the tenth day after decompressive craniectomy, a computed tomography scan was performed again, and an increase in bilateral subdural fluid accumulation was observed compared to before (white solid arrows); On the right side, there is a clear deviation of the midline to the left, and the right lateral ventricle is compressed (white dashed arrows); D-F: After the first subdural puncture drainage surgery, re-examination showed that the bilateral subdural fluid accumulation had basically disappeared (white solid arrows), and the midline was centered with improved compression of the right lateral ventricle (white dashed arrows).

Figure 4 Computed tomography scan twentieth day after decompressive craniectomy. A-C: On the twentieth day after decompressive craniectomy, a computed tomography scan was performed again, showing a recurrence of subdural fluid accumulation on the right side (solid white arrow), with the midline shifting to the left again and significant compression on the right ventricle (dashed white arrow); D-F: After the second subdural puncture drainage surgery, a 7-day follow-up examination showed that the right-sided subdural effusion had basically disappeared (white solid arrows), the midline was basically centered, and the compression of the right lateral ventricle had improved (white dashed arrows).

Figure 5 Computed tomography scan on day 32 after cranial decompression osteotomy. A-C: On the 32^nd day after decompressive craniectomy, a computed tomography scan was performed again, and it was observed that there was a significant increase in subdural fluid accumulation on the right side compared to before (solid white arrow). The midline shifted again to the left and the right ventricle was significantly compressed (dashed white arrow); D-F: After the third subdural puncture drainage surgery, a 7-day follow-up examination showed that the right-sided subdural effusion had basically disappeared (white solid arrows), the midline was basically centered, and the compression of the right lateral ventricle improved (white dashed arrows represent 3D skull defect protective caps).

Figure 6 Computed tomography scan on day 53 after cranial decompression osteotomy. A-C: On the 53^rd day after decompressive craniectomy, a computed tomography scan was performed again, and a recurrence of subdural fluid on the right side was observed (white solid arrow), with the midline shifted to the left (white dashed arrow represents the 3D skull defect protective cap); D-F: After skull repair surgery and puncture of the right subdural fluid, the right subdural fluid has basically disappeared (white solid arrows), the midline is centered, and there is no obvious compression on the brain tissue.

OUTCOME AND FOLLOW-UP

The patient did not experience any new contralateral neurological dysfunction, and the Glasgow prognostic score was 11 points (E4V1M6).

DISCUSSION

TSE is often caused by arachnoid tear and cerebrospinal fluid (CSF) circulation disorder caused by trauma. Its incidence rate is about 5%-21%, and the incidence rate in patients receiving DC is significantly higher than that in patients without DC[3-5]. At present, there is no consensus on the pathogenesis of TSE, and there are significant differences in its treatment methods. We will discuss and review the literature on its pathogenesis and treatment methods. At present, the main theories explaining the mechanism of SDE after DC surgery include one-way valve theory, blood-brain barrier disruption theory, and CSF absorption disorder theory[2,6]. The unidirectional valve theory suggests that external violence causes relative displacement between the brain tissue and the cranial cavity, resulting in tearing of the arachnoid membrane on the surface of the brain and forming a structural change similar to a unidirectional valve. And the pulsation of brain tissue caused by traumatic brain injury and the change in intracranial pressure gradient caused by increased intracranial pressure cause CSF to flow into the subdural space along the unidirectional valve, and CSF cannot flow back, thus accumulating in the subdural space. The theory of blood-brain barrier disruption suggests that traumatic brain injury disrupts the integrity of the blood-brain barrier, leading to increased vascular permeability, a large amount of high-density components such as plasma and proteins exuding, and a change in intracranial pressure gradient, further promoting fluid infiltration into the subdural space[7-9]. The theory of CSF absorption disorders suggests that subarachnoid hemorrhage caused by traumatic brain injury can cause aseptic intracranial inflammation, which leads to adhesion of the arachnoid membrane and blockage of the chorionic villi, resulting in obstruction of CSF reflux. At the same time, in severe traumatic brain injury, extensive cerebral vascular spasm can also hinder CSF reflux, causing absorption disorders of CSF[9-11].

We propose that a single theory may not sufficiently explain the development of SDE following DC. Traumatic brain injury disrupts the intrinsic structure and stability of the brain, involving intracranial tissue damage, blood-brain barrier disruption, and skull defects resulting from DC. These factors, coupled with changes in intracranial pressure (ICP) and exacerbation of CSF circulation disturbances due to ICP gradients, contribute to the pathophysiology of SDE. Additionally, the arachnoid membrane, which functions as a pressure-dependent one-way valve, may play a role in the formation of SDE following DC surgery[8,12]. Post-DC, the contralateral subdural space may expand due to pressure gradients between the bilateral cerebral hemispheres, brain tissue atrophy, and decreased brain compliance, all of which increase the likelihood of SDE formation[13]. In the case we reported, the patient underwent multiple puncture and drainage procedures for SDE recurrence. We hypothesize that the instability of intracranial pressure contributed to the persistence of SDE. However, due to the patient’s severe pneumonia, timely cranioplasty was not feasible. To address this, a 3D skull defect protective cap was applied to temporarily restore the balance and stability of ICP. This intervention limits the protrusion of brain tissue through the skull defect, reduces the relative negative pressure space beneath the contralateral dura mater, and achieves results comparable to cranioplasty. After DC, the intracranial arachnoid membrane is usually incomplete, and ICP is influenced by both body position and surrounding atmospheric pressure, making it easy for fluid to accumulate from the subarachnoid space gap in the subdural space. Wearing a 3D skull defect protective cap in the early stage, although it cannot achieve a tight fit with the missing skull, can form a relatively complete structure with the missing skull, which helps maintain stable pressure in the cranial cavity. The fluctuation of CSF under the entire bone window and in areas without bone windows will not produce pressure differences, thereby reducing the probability of subdural fluid accumulation. Our experience suggests that the use of a skull defect protective cap significantly prolonged the interval before recurrence of SDE. Ultimately, following cranioplasty, the patient’s SDE resolved completely.

Stubborn SDE can lead to brain swelling and worsening neurological function. While most cases of TSE following DC do not require specific treatment, a subset of patients with large effusions and symptoms of intracranial hypertension necessitate intervention. Treatment options include drilling and drainage, craniotomy for resection of the subdural fluid cyst wall and/or partial arachnoid resection, and peritoneal shunting. However, drilling and drainage are considered temporary measures. A review of the literature indicates that cranioplasty is the standard and most effective treatment for SDE after DC surgery[13-15]. In cases of refractory SDE, alterations in intracranial pressure gradients and the one-way valve function of the arachnoid membrane are thought to be key mechanisms contributing to the effusion. Early cranioplasty, or a combined approach with drilling and drainage, has proven to be more effective in these cases[16]. Looking back at the entire treatment process of this patient, we repeatedly performed puncture and drainage treatment on subdural fluid, but there is a certain lack of understanding. We believe that there are two basic strategies for treating the mechanism of subdural fluid accumulation. The first step is to ensure that CSF is drained from other areas, such as early drainage of the lumbar cistern or frontal angle drainage; The second is to maintain the integrity of the skull and perform skull repair surgery as early as possible. Therefore, in the treatment of this patient, while wearing a skull defect protective cap, lumbar drainage or frontal angle drainage can be used to reduce the trauma caused by repeated punctures, which may be a better treatment plan. Moreover, neurosurgeons must remain vigilant for the potential development of hydrocephalus in patients with SDE. Contralateral DC can disrupt CSF circulation, increasing the risk of hydrocephalus[17]. In such cases, timely ventriculoperitoneal shunting remains a safe and effective treatment[18]. In summary, contralateral SDE is a known complication following DC, particularly in cases of refractory SDE. Cranioplasty has proven to be an effective treatment for such cases. However, as the existing literature reports only a single case of stubborn SDE following DC surgery, further clinical case-control studies are needed to assess the efficacy of cranioplasty in managing refractory SDE after DC surgery.

CONCLUSION

For neurosurgeons, accurate assessment of the condition is necessary when treating patients with stubborn SDE after DC surgery, and timely cranioplasty can be performed to avoid multiple surgeries. This is a safe and effective surgical method for treating TSE.