JOURNAL ARTICLE

Management and outcome of patients with acute traumatic subdural hematomas and pre-injury oral anticoagulation therapy

Christian Senft, Thomas Schuster, Marie-Thérèse Forster, Volker Seifert, Rüdiger Gerlach
Neurological Research 2009, 31 (10): 1012-8
19570326

BACKGROUND: Acute subdural hematomas (aSDHs) are found in up to one-third of patients with severe traumatic brain injury and are associated with an unfavorable outcome in the majority of cases. Mortality ranges between 40 and 60%, but was reported to be even higher in patients undergoing oral anticoagulation therapy (OAT) at the time of injury. The objective of this study is to specifically report on the peri-operative management and outcome of patients with aSDH and pre-injury OAT.

MATERIAL AND METHODS: From June 2002 to June 2006, all patients with OAT who underwent surgical treatment of aSDH were retrospectively analysed. Results of pre-operative blood tests, the peri-operative and surgical management and the clinical courses were assessed. Patient outcome is reported according to the Glasgow Outcome Scale (GOS) at 6 months.

RESULTS: Eleven (10.3%) out of 107 patients with aSDH were on OAT. Patients with OAT were significantly older than patients without OAT (72.4 +/- 9.3 versus 59.9 +/- 17.5 years; p<0.05, Mann-Whitney U-test). Intensity of head trauma was moderate in four and severe in seven patients with a median pre-operative Glasgow Coma Scale (GCS) of 8. Median pre-treatment prothrombin time and international normalized ratio were 23% (range: 10-65%) and 3.3 (range: 1.5-10.6), respectively. Replacement therapy consisted of administration of prothrombin complex concentrates, vitamin K and FFP (fresh frozen plasma). In four patients, antithrombin was additionally given to prevent disseminated intravascular coagulation. Surgical treatment consisted of craniotomy (n=10) or craniectomy (n=1) and hematoma evacuation with intracranial pressure probe placement. Low molecular weight heparin was administered as pharmacological prophylaxis of thrombembolic events in an increasing dose post-operatively. At 6 months, six out of 11 patients survived with a median GOS of 4. All-cause mortality was 45.5%. A pre-operative GCS of < or = 8 was not associated with an increased risk of mortality (p>0.5, Fisher's exact test). No relevant rebleedings or thrombembolic complications were observed. The mortality rate of patients who did not undergo OAT was 50%.

CONCLUSION: A large number of patients with aSDH are on pre-injury OAT. Specific replacement therapy facilitates successful clot evacuation without bleeding complications. The overall outcome of these patients does not seem to differ from historical cohorts with aSDH without OAT, but a large prospective multicenter study is warranted to answer that question.

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