gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit den Benelux-Ländern und Bulgarien

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

24. - 27.05.2009, Münster

Treatment of traumatic cerebral venous and sinus thrombosis

Meeting Abstract

  • H. Stegmaier - Neurozentrum, Berufsgenossenschaftliche Unfallklinik Murnau
  • K. Mainka - Neurozentrum, Berufsgenossenschaftliche Unfallklinik Murnau
  • M. Schaan - Neurozentrum, Berufsgenossenschaftliche Unfallklinik Murnau
  • M. Strowitzki - Neurozentrum, Berufsgenossenschaftliche Unfallklinik Murnau
  • H. Jaksche - Neurozentrum, Berufsgenossenschaftliche Unfallklinik Murnau

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocP01-09

DOI: 10.3205/09dgnc257, URN: urn:nbn:de:0183-09dgnc2570

Veröffentlicht: 20. Mai 2009

© 2009 Stegmaier et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Posttraumatic cerebral venous and sinus thrombosis (tCVST) is an infrequent complication after head injury. There are no consistent treatment recommendations. We reviewed patients with tCVST after head injury from the last 4 years and looked for predisposing trauma locations. Then we compared our treatment with the EFNS guidelines on treatment of non‑traumatic CVST to decide whether they are applicable to tCVST.

Basilar bone fracture has already been suspected of being a risk factor for transverse and sigmoid sinus thrombosis (ST/SS). Since all our patients with these thrombosis locations had sustained petrosal bone fracture (PBF), CT-scans were reviewed.

Methods: A retrospective review of 10 patients who developed a CVST after head injury between 2004 and 2008 was performed using radiological imaging (CCT and CTA) and patient charts. 441 patients with head injury suffered PBF during these four years. Their CT scans were reviewed.

Results: 7 male and 3 female patients with head injury developed a tCVST. Mean age was 47 years. 7 patients developed ST/SS thrombosis. In 3 the jugular vein was also occluded. One patient showed occlusion of the SS only. All 8 patients had suffered an ipsilateral PBF. The 2 patients with thrombosis of the superior sagittal sinus also showed adjacent skull fractures. Symptoms of CVST were ICP elevations in 3 patients. 4 patients showed otherwise inexplicable increases of brain edema in CT-scans. Mean onset was 6.3 days after trauma. Anticoagulation (AC) started immediately after diagnosis and was carried on for 23 days. One patient received oral AC for 6 months. Recanalization was seen in all patients after an average interval of 32 days with no signs of recurrent thrombosis during follow-up. Two patients died of secondary infarctions and intracerebral hemorrhage (I/ICH). Final outcome with respect to tCVST is difficult to assess due to the different influence of concomitant injuries.

Conclusions: Initial treatment followed EFNS recommendations. AC was carried out for 23 days. Except for one patient, no further oral AC was given. 2 patients died shortly after their accident due to secondary I/ICH only potentially related to tCVST. There were no treatment related complications. We therefore conclude that AC can be safely used to treat tCVST in patients with traumatic brain injury. Finally, tCVST seems to yield a better prognosis than spontaneous CVST with a high rate of recanalization and no signs of recurrent thrombosis even after cessation of anticoagulative therapy.