acquired factor viii deficiency is caused by the development of autoantibodies directed against circulating coagulation factor viii , which inhibits its function [ 1 , 2 ] . it may be associated with pregnancy , the postpartum period , autoimmune conditions , drugs , lymphoproliferative disorders , or malignancies . in approximately half of the diagnosed cases , we report a rare case of subdual hemorrhage in a man , who acquired factor viii inhibitors and developed coagulopathy after consuming toxin of the cobra , naja naja . a 49-year - old male was admitted with a 10-day history of subcutaneous hemorrhage of the right shoulder ( fig . 1 ) and left thigh . the patient was being treated with losartan 50 mg / day for hypertension and metformin 500 mg twice a day for diabetes . he had eaten 10 g of dried gall bladder of a cobra , naja naja in thailand one month ago . laboratory test showed a prolonged activated partial thromboplastin time ( aptt ) exceeding 120 seconds ( normal range , 30 - 47 seconds ) , not corrected with plasma mixing test . his prothrombin time was 10 seconds ( normal range , 10 - 13 seconds ) , the level of fdp was 11.71 ug / ml ( normal range , below 5 ug / ml ) , and d - dimer was 3.42 ug / ml ( normal range , below 1.3 ug / ml ) . his hemoglobin was 7.0 g / dl and platelet count was 32310/l . the factor viii level was less than 1% , and his factor viii inhibitor antibody titer was 246 bethesda units / ml ( normal range , 0 - 0.7 bethesda units / ml ) . lupus anticoagulant antibody , anti - nuclear antibody and anti - phospholipid antibody were negative . he was diagnosed with acquired factor viii deficiency . magnetic resonance imaging ( mri ) of the thigh showed hematomas in the left vastus medialis muscle ( fig . the patient was treated with an intravenous infusion of factor viii 3,000 u ( 50 u / kg ) every 8 hours . one month after treatment , the patient 's symptoms improved , but his factor viii inhibitor antibody titer was still high ( 147 bethesda units / ml ) . he had an aptt exceeding 120 seconds due to the presence of high titers of factor viii inhibitor ( 217 bethesda units / ml ) . brain ct scan revealed a mixed subacute subdural hematoma in the left fronto - temporo - occipital areas ( fig . 3 ) and recombinant factor vii was infused at a dose of 360 kiu / day . despite treatment , the patient 's bleeding worsened . two weeks later , multifocal subarachnoid hemorrhages and intracranial hemorrhages in both cerebral hemispheres were revealed . it results from the development of inhibitors , that typically interfere with the coagulant properties of factor viii [ 1 , 2 , 7 ] . the clinical picture is characterized by spontaneous and often sudden onset of severe hemorrhage in a patient with no bleeding history . more than 80% of patients have hemorrhages into the skin , muscles or soft tissues , and mucous membranes . however , the spontaneous disappearance of inhibitors is unpredictable and may occur over many years . for a better prognosis , eradication of the inhibitor and maintenance of normal level of clotting factor viii are important . the therapeutic strategy is to stop the hemorrhage and reduce the autoantibody levels . bypassing products currently available for bleeding control are recombinant activated factor vii ( rfviia ) and plasma - derived activated prothrombin complex concentrate ( apcc ) . in patients with a high inhibitor titer and severe hemorrhages , the extracorporeal removal of the autoantibody by therapeutic plasmapheresis can be used before factor concentrate treatment . there are two case reports in korea which were successfully treated with combination therapy that included therapeutic plasmapheresis . once hemostasis is achieved , autoantibody eradication is the second major goal of acquired hemophilia therapy . the inhibitor may also be eradicated with immunosuppressive agents , including corticosteroids and cytotoxic drugs , such as cyclophosphamide , azathioprine , 6-mercaptopurine , and vincristine . we report the first case of acquired factor viii deficiency in a patient , who suffered from coagulopathy after consuming the dried gallbladder of a cobra . coagulopathy is a significant cause of both morbidity and mortality in snakebite patients [ 13 , 14 ] . a wide variety of venom components can act as procoagulants , activating the coagulation system in vivo , and causing the consumption of coagulation factors , resulting in clinical anticoagulation . fibrinogen clotting and fibrinolytic snake venom toxins exert a direct effect on the actual thrombus - forming protein , fibrinogen , but in varying ways . fibrinogen may be split into fibrin and then degradation products , or it may be only partially split , leaving an ineffective form of fibrinogen circulating , the end result being an increased bleeding tendency . snake venom inhibits platelet activity too , thus reducing their effectiveness in hemostasis [ 13 , 14 ] . another study reported there is transient presence of an inhibitor to factors viii , ix and xi in cases of tiger snake envenomation . in our case , cobra toxin was probably the cause of development of factor viii inhibitor , since the acquired factor viii deficiency developed right after consuming the cobra toxin , and we did not find any other possible cause of acquired factor viii deficiency in this patient . perhaps cobra toxin entered the blood stream through damaged oral mucosa , and acted as factor viii inhibitor . in order to make a clear connection between cobra toxin and acquired factor viii deficiency , further evaluation about the effects of snake venom on individual coagulation factors is needed .