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J Neurol Neurosurg Psychiatry doi:10.1136/jnnp-2013-305369
  • Neurological picture

Successful outcome after traumatic rupture and secondary thrombosis of the superior sagittal sinus

  1. Philip C De Witt Hamer
  1. Neurosurgical Center Amsterdam, VU University Medical Center, Amsterdam, The Netherlands
  1. Correspondence to E A Oudeman, Neurosurgical Center Amsterdam, VU University Medical Center, De Boelelaan 1117, Amsterdam 1081 HV, The Netherlands; e.a.oudeman{at}gmail.com
  • Received 12 March 2013
  • Revised 7 April 2013
  • Accepted 9 April 2013
  • Published Online First 4 May 2013

A 15-year-old adolescent was admitted to the emergency department after a car accident because of severe traumatic brain injury. Upon arrival, he was sedated and intubated because of a Glasgow Coma Scale score below 8. He had isocoria with reactive pupils. An occipital puncture wound (diameter 2 cm) was profusely bleeding. His blood pressure was 85/45 mm Hg. Laboratory values identified a haemoglobin level of 4.6 mmol/l. A CT scan of the brain demonstrated a comminuted-depressed fracture of the parietal bone in the midline with a rupture of the superior sagittal sinus (SSS) and secondary thrombosis (figure 1). After prompt resuscitation including packed blood cells, a large biparietal decompressive craniectomy was performed centred at the skull fracture anticipating on intracranial hypertension due to venous oedema or infarction. The sinus haemorrhage was initially packed with haemostatic material and manually compressed with cottonoids and spatula until the roof of the sinus was reconstructed using inverted dural flaps. The craniectomy bone flap was left out, the fractured skull elements were partially removed and antibiotics were provided. A ventricular catheter was inserted for intracranial pressure monitoring while the patient was sedated for a week. The intracranial pressure remained below 20 mm Hg. Three days after surgery, brain MRI showed a persistent sinus thrombosis (figure 2) without venous infarction or haemorrhage. Subsequently, anticoagulation with unfractionated heparin was initiated at 4-day postoperative. After discontinuation of the sedatives, he became fully conscious without focal neurological deficits. The ventricular catheter was removed and after 2 weeks, the craniectomy bone flap was replaced. A brain MRI at 30 days showed recanalisation of the SSS (figure 3). Anticoagulation therapy with warfarin was prescribed for 3 months and the patient remained stable.

Figure 1

Axial and coronal brain CT 2 h after the injury demonstrating a compound comminuted depressed fracture of the parietal bone in the midline involving the superior sagittal sinus. Sagittal CT venogram identifying a superior sagittal sinus interruption and secondary sinus thrombosis up to the torcular herophili.

Figure 2

Sagittal brain MRI time of flight sequence at 3 days after first surgery demonstrating collateral venous drainage with a persistent thrombosis of the superior sagittal sinus. The patient's head is on a silicone donut.

Figure 3

Sagittal brain CT venogram at 30 days after first surgery with recanalisation of the superior sagittal sinus. A deep bone fragment remains located in the occipital lobe.

Comment

Compound depressed skull fractures in general require surgical exploration with dural repair.1 For closed depressed skull fractures overlying a venous sinus without active bleeding, a conservative strategy is generally advocated to avoid excessive blood loss during surgery.2 In our patient haemorrhage control, venous sinus reconstruction and removal of contaminated elements were considered more important than the risk of intraoperative blood loss. Only anecdotal evidence is available for this approach.2 ,3 Reconstruction techniques for the SSS have been described, such as direct suturing, graft patching or bypass using venous graft or silicone tubing.4 We used inverted dura as autograft patch for reconstruction. Another concern is avoidance of infection. In general, debridement with bone fragment removal and antibiotics is recommended.1 We removed the superficial fractured bone fragments, but the fragments penetrating the brain were not further explored due to considerable brain swelling and to avoid secondary damage to the visual cortex. The risk of infection from remaining bone fragments is unknown.

Early anticoagulant therapy is now widely accepted for spontaneous cerebral venous sinus thrombosis, whereas evidence is lacking for traumatic sinus thrombosis or sinus thrombosis in the paediatric population.5 ,6 Anticoagulant therapy carries a risk of haemorrhagic complications, which, in addition to the potential of haemorrhagic transformation of venous infarcts, can be particularly severe following traumatic brain injury, decompressive craniectomy and in the presence of a ventricular catheter. We estimated that the benefits of anticoagulant treatment outweighed the risks. The risk of anticoagulation shortly after surgery was considered too high, given the deranged coagulation profile after severe blood loss and major surgery. Subsequently, the risk of brain damage due to persistent SSS obliteration as confirmed by MRI at 3-day postoperative was considered too high, so that anticoagulation was commenced after 4 days. Usually, a therapeutic dose of low-molecular weight heparin is recommended over unfractionated heparin. This provides a more stable anticoagulant concentration without dose adjustments and, most importantly, is associated with a more favourable clinical outcome.6 Nevertheless, we opted for unfractionated heparin, given the availability of rapid reversal in case of acute haemorrhagic complications or emergency surgery.

Footnotes

  • Contributors EAO wrote the first and consecutive drafts. PdWH revised drafts and designed images.

  • Competing interests None.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

References

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