2026 Volume 13 Pages 425-432
Traumatic dural venous sinus injury is uncommon but potentially fatal because of massive hemorrhage at presentation or during surgery, and intracranial hypertension caused by impaired venous outflow. We report a case of a young woman with an open depressed skull fracture over the vertex caused by repeated blunt assault. Computed tomography revealed a large midline depressed fracture with bony fragments penetrating the superior sagittal sinus. On arrival, the patient was in hemorrhagic shock, with a semicoma status and right hemiparesis. Emergency surgery was performed for hemostasis and wound debridement. Because the wound was contaminated, irregular, and associated with a crushed sinus wall, direct sinus suturing was considered unsuitable for this patient. After temporary hemostasis with head elevation and Gelfoam compression, the injured superior sagittal sinus was reconstructed using an autologous fascia lata patch reinforced with fibrin glue. A postoperative epidural hematoma at the fracture site required immediate evacuation. On day 2, severe intracranial hypertension developed despite the initial surgery, and multimodal neurocritical care was instituted, including intracranial pressure monitoring, external ventricular drainage, deep sedation and analgesia, neuromuscular blockade, hypertonic saline, targeted temperature management, and pentobarbital infusion. The intracranial pressure gradually stabilized, and the patient was extubated on postoperative day 14. She was transferred for rehabilitation and ultimately achieved an excellent functional outcome, with a modified Rankin Scale score of 1. This case highlights the importance of preserving superior sagittal sinus patency using autologous patch repair in contaminated open injuries and promptly escalating intracranial pressure-directed intensive care when delayed venous outflow impairment is suspected.
Traumatic dural venous sinus injury is rare, accounting for approximately 1.5% to 5% of head injuries, and 70% to 80% of these injuries involve the superior sagittal sinus (SSS).1,2) A classic older series reported mortality as high as 41%, underscoring the severity of this condition.2) Open depressed fractures overlying the sinus are particularly hazardous because they may cause uncontrollable venous hemorrhage and air embolism during surgical exploration.1,3,4)
In addition to acute bleeding, postoperative deterioration may occur due to venous outflow obstruction, sinus stenosis, or traumatic cerebral venous sinus thrombosis (tCVST). A systematic review found that the pooled frequency of venous sinus thrombosis was 26.2% among patients with traumatic brain injury and skull fractures adjacent to a dural venous sinus, indicating that this is mainly a problem in selected high-risk patients rather than in all patients with blunt head trauma.5) Recent literature also emphasizes that occlusive thrombosis and persistent intracranial pressure (ICP) elevation may complicate early post-traumatic care.6)
We describe a young woman with an open depressed skull fracture and direct SSS injury caused by repeated blunt trauma. This case illustrates 2 practical challenges: immediate surgical hemostasis while preserving sinus patency and aggressive postoperative management of refractory intracranial hypertension, likely related to impaired venous drainage.
A woman in her 20s sustained repeated blunt trauma to her head from behind. On arrival at our emergency department, her Glasgow Coma Scale score was E3V4M5, and she had an evident right hemiparesis. Multiple lacerations and an open cranial wound with bone loss were observed at the vertex. Marked peripheral coldness suggested hypovolemic shock due to massive blood loss from the scalp and cranial wounds (Figure 1).
At the time of arrival after injury, a photograph of the scalp at the vertex. Due to numerous wounds, flap formation is severely compromised, and the subdural space is visible through the depressed skull fracture.
Initial laboratory studies showed hemoglobin 8.6 g/dL, platelet count 264,100/μL, prothrombin time-international normalized ratio 1.08, and activated partial thromboplastin time 20.7 seconds, indicating acute blood loss anemia without major coagulopathy. After airway protection, head computed tomography revealed a large midline depressed skull fracture at the vertex (Figure 2-1). A free bone fragment protruded deeply into the SSS, strongly suggesting direct sinus wall injury with persistent intracranial venous bleeding (Figure 2-2).
Initial CT demonstrating a free bony fragment deeply penetrating the superior sagittal sinus at the midline. The upper four images are standard head CT scans, and the bottom row shows a head CT scan with bone window settings. The superior sagittal sinus is affected by fractures and damage.
Reconstructed image from initial CT. A bone fragment is lodged in the superior sagittal sinus.
CT: computed tomography
Emergency surgery was performed on the day of admission. Because wide sinus reconstruction might be required, the fascia lata was harvested from the left thigh before cranial exposure. The standard scalp incision design was difficult because of multiple irregular lacerations; therefore, the existing wounds were connected and reflected as a posteriorly based scalp flap.
After exposure of the depressed fracture, extensive dural laceration was not evident; however, one sharp bone fragment was found to penetrate the wall of the SSS. The sinus was exposed as far as possible rostral and caudal to the injury in preparation for proximal and distal control, and the fragments were carefully removed. As expected, brisk venous bleeding from the SSS occurred immediately. The head was elevated in the reverse Trendelenburg position, and temporary hemostasis was attempted using Gelfoam compression (Figure 3). However, compression alone was insufficient to achieve hemostasis. Direct sinus suturing was considered unsuitable because the wound edges were irregular and contused, and primary closure was considered likely to cause luminal narrowing or rebleeding from the fragile sinus wall. Therefore, after temporary control of bleeding, the defect was reconstructed using an autologous fascia lata patch reinforced with fibrin glue. This achieved satisfactory hemostasis while attempting to preserve the sinus patency. Postoperative computed tomography demonstrated a new epidural hematoma away from the fracture site, and urgent reoperation for hematoma evacuation was performed.
Schematic diagram of intraoperative hemostatic procedures. After identifying the bleeding site at the site of injury, Gelfoam was applied, followed by compression hemostasis with cotton.
Technical tips. The fascia lata patch was harvested approximately 4 × 3 cm, which was deliberately larger than the estimated sinus defect, to provide sufficient overlap with the surrounding dura. Before placing the patch, the sinus was exposed approximately 2 cm rostral and caudal to the injury so that proximal and distal control could be obtained promptly in case of rebleeding. The Gelfoam used for initial tamponade was intentionally left in place against the bleeding sinus surface and incorporated beneath the patch, rather than being removed, to avoid re-initiating venous bleeding. The patch was laid flat, in the same plane as the surrounding dura, without tension or invagination, and was tacked at its peripheral edges to the surrounding dura with single interrupted sutures. Fibrin glue was then applied along the entire margin to obtain a watertight seal and secure the patch in position (Figure 4).
Schematic diagram of the repair of an injured dural sinus. The Gelfoam used for compression hemostasis at the injury site was left in place, cotton was removed, and the harvested fascia lata was spread to cover the Gelfoam and placed in the same layer as the dura mater. Subsequently, fibrin glue was applied around the area to achieve watertight sealing and fixation.
Because hemodynamics were stabilized by resuscitation in the emergency department, circulation remained stable despite total intraoperative blood loss of approximately 600 mL. However, due to suspected progression of anemia and deficiency of coagulation factors, a total of 12 units of RBC and 18 units of FFP were transfused intraoperatively and postoperatively.
The patient was admitted to the intensive care unit following surgery. On postoperative day 1, an ICP sensor was placed. On day 2, the ICP remained above 30 mmHg, and external ventricular drainage was performed for cerebrospinal fluid diversion. Deep sedation with propofol and fentanyl, and continuous neuromuscular blockade with rocuronium were administered. On day 3, because intracranial hypertension persisted, hypertonic saline was initiated, and endovascular targeted temperature management was started with a target temperature of 35.8°C. On day 4, continuous pentobarbital infusion was initiated for refractory ICP elevation (Figure 5).
Postoperative intracranial pressure trend and major neurocritical care interventions. ICP gradually stabilized after ventricular drainage, deep sedation with neuromuscular blockade, hypertonic saline, endovascular temperature control, and pentobarbital infusion.
ICP: intracranial pressure
After these stepwise interventions, the ICP gradually stabilized. Pentobarbital and hypertonic saline were discontinued on day 6, the ventricular drain was removed on day 7, and the ICP sensor was removed on postoperative day 12. No rebound ICP elevation occurred during the weaning from sedation. On day 13, she obeyed commands with a motor score of 6 and was extubated on day 14. She was subsequently transferred for rehabilitation and ultimately achieved excellent functional outcomes, with a modified Rankin Scale score of 1.
On the CT images taken 15 days after surgery, no findings suggestive of increased intracranial pressure were observed. In addition, there were no findings indicating sinus occlusion, such as the delta sign, and the venous sinus was considered to be patent (Figure 6).
CT images were obtained on postoperative day 15. The upper and middle rows show axial images, and the lower row shows reconstructed coronal images. No delta sign or other abnormalities were observed in the venous sinus, and patency was presumed to be preserved.
CT: computed tomography
This case highlights 2 clinically important aspects of traumatic SSS injuries. First, hemostasis must be achieved without unnecessarily sacrificing sinus patency. Second, even after apparently successful surgical control of bleeding, delayed intracranial hypertension may develop because of venous outflow impairment and requires early, structured neurocritical care.
Current literature supports a stepwise approach to the repair of venous sinus injury. Techniques described include compression, topical hemostatic agents, bipolar coagulation in selected situations, tack-up sutures, dural flaps, direct suturing, patch reconstruction, venous bypass, and ligation.7) In the 15-case series by Behera et al.,2) many smaller tears were controlled with Gelfoam and head elevation alone, whereas larger injuries sometimes required direct repair.2) More recent reviews likewise emphasize tailoring the repair strategy to the location and morphology of the injury.7)
In our patient, direct suturing was avoided because the sinus wall was crushed, and the wound edges were irregular. Under such circumstances, forced primary closure may worsen luminal narrowing and provoke additional tearing. Therefore, patch reconstruction was a reasonable option. Autologous fascia lata was chosen because the injury was open and contaminated. Although semisynthetic materials may reduce operative preparation time, autologous grafts remain widely used in contaminated or high-risk fields because they avoid implantation of foreign material and have longstanding neurosurgical use as dural substitutes.8-10)
The second major lesson was the importance of recognizing the venous pathophysiology after surgery. Despite satisfactory initial hemostasis, our patient developed severe ICP elevation beginning on postoperative day 2. This clinical course is consistent with impaired venous return due to postoperative sinus narrowing, local thrombosis, external compression, or a combination thereof. Reviews of tCVST in traumatic brain injury note that venous sinus thrombosis is particularly relevant when skull fractures cross or abut a venous sinus, and that venous hypertension may impair cerebrospinal fluid absorption and promote vasogenic edema and venous infarction.5,6)
A particularly important practical point is that worsening neurological or ICP status may precede the appearance of obvious new mass lesions on routine computed tomography. When there is a mismatch between persistent intracranial hypertension and relatively nondiagnostic routine imaging, additional venous imaging, such as computed tomographic venography, should be considered early, especially in patients with fractures or surgery involving the sinus.5,6)
Our neurocritical care strategy is noteworthy. The management of refractory intracranial hypertension was broadly aligned with the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC) concept of a stepwise escalation. SIBICC recommends ICP-guided tiered management, beginning with basic measures and escalating through cerebrospinal fluid drainage, sedation, osmotherapy, and selected advanced rescue therapies when needed.11,12)
In this case, the escalation sequence was logical: ICP monitoring, ventricular drainage, deep sedation and analgesia, neuromuscular blockade, hypertonic saline, targeted temperature management, and finally, pentobarbital infusion. With regard to temperature control, SIBICC does not support routine profound hypothermia for all patients with severe traumatic brain injury, but mild temperature reduction around 35°C to 36°C may be used in selected refractory cases.11) Our target of 35.8°C was consistent with that framework. Likewise, barbiturate therapy is considered a rescue measure for refractory ICP elevation and should be used cautiously because of the risks of hypotension and reduced cerebral perfusion pressure.11,12)
The excellent final outcome in this patient suggests that even severe SSS injury can be survivable with good recovery when 2 objectives are pursued simultaneously: preservation of venous sinus patency during surgery and aggressive postoperative control of secondary brain injury. Although early cranioplasty with titanium mesh and central tack-up sutures has been proposed by others as a possible way to reduce postoperative dead space and support venous sinus contour in selected skull defects, this was not performed in our patient and should be regarded only as a potential consideration for future cases rather than a conclusion from this case.
LimitationDuring this patient's clinical course, dedicated evaluation of the dural venous sinuses by magnetic resonance venography or contrast-enhanced computed tomographic venography was not performed. At the time of management, the possibility that elevated intracranial pressure was related to impaired venous outflow through the SSS was not adequately recognized. Accordingly, the absence of dedicated venous sinus imaging means that we cannot definitively confirm whether the refractory intracranial hypertension was attributable to compromised sinus patency, and this limitation should be taken into account when interpreting the present case.
ConclusionOpen depressed skull fractures involving the SSS pose a dual threat of catastrophic intraoperative hemorrhage and delayed intracranial hypertension due to impaired venous drainage. In the present case, autologous fascia lata patch repair provided effective hemostasis while preserving the sinus lumen in a contaminated open injury, and structured escalation of ICP-directed neurocritical care resulted in excellent functional recovery. In patients with postoperative ICP elevation after sinus injury, venous outflow impairment and traumatic cerebral venous sinus thrombosis should be considered early on.
T.M. drafted the manuscript. Y.N. and K.S. were involved in the clinical management of the patient. T.M. critically revised the manuscript for important intellectual content. All authors read and approved the final manuscript.
All authors have no conflict of interest.
With the patient's consent, this case was properly anonymized, and the content was submitted.
During the preparation of this work, the author (s) used Paperpal in order to check grammar and Nano Banana in order to generate the schematic figures. After using these tools, the author (s) reviewed and edited the content as needed and take full responsibility for the content of the published work.
