Protamine sulfate for the reversal of enoxaparin associated hemorrhage beyond 12 h.

Clinical practice guidelines recommend protamine sulfate for reversal of enoxaparin associated bleeds dependent on the time from last administration and dose of enoxaparin. We present a case of a hemodynamically unstable patient with an enoxaparin induced abdominal wall hematoma/hemorrhage and the previous enoxaparin administration 21.5 h prior to presentation with a therapeutic anti-Xa assay (0.8 IU/mL) upon assessment in the emergency department. Along with resuscitative efforts, an interdisciplinary team collaborated to administer protamine sulfate 50 mg intravenous once (0.5 mg per 1 mg of enoxaparin) to reverse the therapeutic anticoagulation. Our case demonstrates the importance of monitoring renal function and the potential for accumulation of enoxaparin in patients with renal dysfunction leading to prolonged therapeutic anti-Xa assays. With the availability of anti-Xa assays, future reversal recommendations of enoxaparin associated bleeds using protamine sulfate should include the initial anti-Xa assay as a guide for the dosing regimen.

Eptifibatide-associated acute, profound thrombocytopenia.

OBJECTIVE: To describe 3 cases of eptifibatide-associated acute, profound thrombocytopenia. CASE SUMMARIES: A 40-year-old black female received eptifibatide 180-microg/kg double bolus followed by a continuous infusion of 2 microg/kg/min for percutaneous coronary intervention (PCI). The platelet count decreased from 308 x 10(3)/mm3 to 2 x10(3)/mm3 4 hours after initiation of eptifibatide. Eptifibatide was discontinued and platelets were transfused. The patient developed a hematoma and petechiae. A 67-year-old white female received the same dosage regimen of eptifibatide for PCI with no serious adverse effects, with the treatment repeated one month later. At that time, she developed chest and back pain, dyspnea, wheezing, and hypotension after the first bolus. Her platelet count decreased from 334 x10(3)/mm3 to 6 x10(3)/mm3 24 hours after initiation. Eptifibatide was discontinued and platelets were transfused. The patient died due to shock. A 72-year-old white male received eptifibatide 180-microg/kg double bolus followed by a continuous infusion of 2 microg/kg/min for acute coronary syndrome. His platelet count decreased from 189 x10(3)/mm3 to 17 x10(3)/mm3, and eptifibatide was discontinued. Eptifibatide was readministered with bivalirudin for PCI once the platelet count increased to 94 x10(3)/mm3. Sixteen hours later, the platelet count decreased to 1 x 10(3)/mm3. Eptifibatide was discontinued and platelets were transfused. The patient developed a hematoma. DISCUSSION: Acute, profound thrombocytopenia is a rare complication of glycoprotein IIb/IIIa inhibitor therapy characterized by a precipitous decline in platelet count to <20 x10(3)/mm3 within 24 hours of therapy. An objective causality assessment revealed that the adverse drug event was probable in 2 cases and possible in the other. CONCLUSIONS: Increasing use of the glycoprotein IIb/IIIa inhibitors and enhanced recognition of the potential for acute, profound thrombocytopenia reinforce the need for more vigilant monitoring and alternative management strategies.