A 78-year old female with a history of atrial fibrillation (AF) presented to our institution with complaints of hematuria, epistaxis, hematochezia, hematemesis and fever. She was on anticoagulation with coumadin therapy for AF and had been recently started on levofloxacin for a urinary tract infection. On examination her pulse rate was 110/minute and blood pressure was 80/40 mm Hg. Investigations revealed hemoglobin of 9.4 g/dl, a hematocrit of 27.8 %, prothrombin time (PT) > 40 and international normalized ratio (INR) >10. She was given intravenous fluids to correct hypotension, fresh frozen plasma (FFP) and vitamin K to correct the coagulopathy. She developed acute renal failure and respiratory failure requiring intubation. Over the period of first week, patient had received a total of 26 units of FFPs, 5 units of cryoprecipitate, 17 units of packed red blood cells and multiple doses of Vitamin K without any improvement of her coagulopathy. She developed disseminated intravascular coagulation (Platelet 42,000/nl, D-Dimer 4032ng/l, fibrinogen degradation products >40 mg/l, fibrinogen 157 mg/dl) and her prognosis appeared poor. She also received 18 units of platelets and 2500 units of Autoplex T (anti-inhibitor coagulant complex), however her INR was persistently >10 and she continued to bleed. Then patient was given recombinant factor VIIa (RF VIIa) at dose of 90 mg/kg and she responded well to single dose of RF VIIa and cessation of her bleeding was noticed within two hours. Repeat coagulation studies showed PT of 13.1 and INR of 1.2. Subsequently patient was extubated, her renal failure reversed and she was discharged home in a stable condition. Originally used for treatment of bleeding in patients with hemophila, rF VIIa, a single chain protease has been used in patients with serious and complicated coagulation defects to arrest or to prevent bleeding. The mechanism of action of rF VIIa remains unclear. It has been suggested that rF VIIa, when administered leads to saturation of tissue factor and this leads to generation of thrombin via the factor Xa. There is evidence that rFVIIa can generate thrombin independently of above pathway. In view of its potent prohemostatic effect, rF VIIa appears to be a promising agent that can be used for application in patients with life-threatening bleeding, in whom all other hemostatic treatments have failed as seen in our patient. However at present time it is not completely clear at what stage recombinant factor VIIa should be administered. Since the efficacy and safety of recombinant factor VIIa have not been established in randomized controlled studies, it may be argued that the safest approach is to administer the agent only if all other treatment has failed. However, if the agent is given too late, ongoing bleeding and transfusion may have resulted in such a derangement of the coagulation system that the drug is less effective. Further studies comparing early versus late administration of rF VIIa are needed. While we await the result of these studies and until more information is available on the safety of rFVIIa, its use in our view should be restricted to life-threatening situations.