ABSTRACT
Cardiac valve injury after blunt chest trauma is rare. We present a case of blunt chest trauma resulting in an isolated aortic valve rupture treated with aortic valve replacement.
Subject(s)
Aortic Valve/injuries , Heart Valve Diseases/etiology , Thoracic Injuries/complications , Wounds, Nonpenetrating/complications , Acute Disease , Aged , Aortic Valve/surgery , Echocardiography, Transesophageal , Heart Valve Diseases/diagnostic imaging , Heart Valve Diseases/surgery , Heart Valve Prosthesis Implantation , Humans , Male , Rupture/diagnostic imaging , Rupture/etiology , Rupture/surgery , Thoracic Injuries/diagnostic imaging , Thoracic Injuries/surgery , Wounds, Nonpenetrating/diagnostic imaging , Wounds, Nonpenetrating/surgeryABSTRACT
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.