Posttraumatic Intracerebral Haemorrhage of a Patient with Inhibitor Positive Hemophilia A: A Case Report Pusem Patir * , Osman Butun, Mustafa Duran, Fatos Dilan Koseoglu, Nur Akad Soyer, Fahri Sahin and Guray Saydam Ege University, Bornova, Izmir, Turkey * Corresponding author: Pusem Patir, Medical Doctor, Ege University, Bornova, Izmir, Turkey, Tel: 90 232 311 10 10; E-mail: pusemp@yahoo.com Received date: Dec 21, 2015, Accepted date: Jan 27, 2016, Publication date: Jan 31, 2016 Copyright: © 2016 Patir P, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Treatment of hemaophilia patients with inhibitor has been difficult situation especially in emergency rooms. Here, we report the successful treatment of a patient with inhibitor positive severe hemophilia A hospitalized due to intracerebral haemorrhage after traffic accident. Keywords: Hemophilia; Inhibitor; Cerebral haemorrhage Introduction Te development of inhibitor is more common in patients with hemophilia A than in those with hemophilia B. Factor VIII inhibitors have been reported in approximately 25 to 30 percent of patients with severe hemophilia A [1-3]. Both host and product factors infuence the likelihood of inhibitor formation. Research continues to defne the best predictors of inhibitor formation, as well as methods to decrease or prevent formation. Bypassing products have included activated prothrombin complex concentrates (aPCC) and recombinant human factor VIIa (rFVIIa). Here we report the successful treatment of a patient with inhibitor positive severe hemophilia A sufer from intracerebral haemorrhage afer trafc accident. Case Report A 36-year-old Caucasion male with inhibitor positive severe hemophilia A presented with an unconsciousness to emergency room afer heavy trafc accident. Te patient is monitored regularly under prophylactic aPCC treatment twice per week at a dose of 25 IU/kg in our adult hemophilia outpatient unit since 2009. In history, the patient had a trafc accident in a car eight hours ago and although there were no signs of bleeding, aPCC was administered at a dose of 25 IU/kg once to stop any potential bleeding by himself. But, later, deteriorations have occurred in his conscious status. His physical examination revealed no evidence of haematoma formation on the body. His conscious status was observed as stupor and no orientation and cooperation. Other system fndings were normal. Tere were no external fndings of bleeding and no focal neurological defcits. Cranial and whole-body computed tomographies (CT) were urgently performed in terms of intracranial and intraabdominal haemorrhage. Cranial CT revealed subcutaneous haematoma of the lef parietal scalp, haemorrhage in lef lateral ventricle and 3 rd ventricle, subarachnoid haemorrhage, lef insular lobe haematoma about 9 mm diameter and 5 mm shif towards the right of midline structures (Figure 1a and 1b). aPCC was administered immediately at a dose of 100 IU/kg every 12 hours. Te neurosurgery consultation was conducted because of that shif and neurological signs and it was not planned to operate because of positivity of his inhibitor status. And also, there was high bleeding risk for removal of the haematoma. Progression in haemorrhage (Figure 2) was observed in control cranial CT and no objective clinical response to current medical therapy, so his treatment was switched promptly to rFVIIa at a dose of 90 µg/kg every 2 hours. He had a prolonged activated partial thromboplastin time (aPTT) as 44.6 seconds, and his inhibitor level was measured as 5.9 BU/ml. Te medical condition of patient improved day by day and returned completely to normal by the fourth day of rFVIIa treatment. Te dosage of rFVIIa was adjusted to 90 µg/kg every 3 hour, then every 4 hour and 6 hour, each lasting 4 days, for a total treatment period took 2 weeks. Regression of haematoma was detected in serial follow-up cranial CT (Figure 3). He continued to have prophylaxis with aPCC at a dose of 25 IU/kg three times per week as indicated. Afer 1 month, control cranial CT confrmed complete disappearance of the haemorrhage (Figure 4). Figure 1: Te CT of the head, showing an intracerebral (a) and intraventricle (b) haemorrhage at frst arrival. Blood Disorders & Transfusion Patir et al., J Blood Disord Transfus 2016, 7:1 http://dx.doi.org/10.4172/2155-9864.1000338 Case Report Open Access J Blood Disord Transfus ISSN:2155-9864 JBDT, an open access journal Volume 7 • Issue 1 • 1000338