Document Type

Conference Proceeding

Publication Date


Publication Title

J Gen Intern Med


CASE: A 64-year-old male with history of atrial fibrillation on apixaban with hospitalization one month prior for acute PE and ACS with PCI to LAD presented with acute heart failure exacerbation secondary to known severe aortic valve regurgitation. Once euvolemic, clopidogrel was transitioned to eptifibatide in anticipation of urgent surgical aortic valve replacement. However, the patient developed significant hemoptysis two days following the initiation of eptifibatide requiring endotracheal intubation for airway management. At that time, eptifibatide was inevitably discontinued and aspirin was continued as antiplatelet monotherapy. Chest x-ray demonstrated diffuse alveolar infiltrates and blood was visualized in all lobes on bronchoscopy. Topical lidocaine was injected with improvement of bleeding and apixaban was subsequently held. Patient received course of high dose steroids with gradual resolution of hemoptysis allowing for extubation. Autoimmune work up was negative and platelets remained stable. Ultimately, patient underwent successful coronary artery bypass grafting with aortic valve replacement and was discharged home.

IMPACT/DISCUSSION: As dual antiplatelet therapy has become protocol medical management following PCI, it does not come without intrinsic risk of major bleeding events. While major bleeding events are recognized, diffuse alveolar hemorrhage is a rare manifestation of bleeding complications associated with antiplatelet therapy. This case describes a case of eptifibatide induced diffuse alveolar hemorrhage in a post PCI surgical patient. DAH secondary to GP IIb/IIIa inhibitors has been previously documented, however, the volume of published cases remains seldom. The first documented case of GP IIb/ IIIa inhibitor induced DAH was described by Stigles and Villa in 1997. Since, there has been an increase in reports of alveolar hemorrhage in relation to this class of antiplatelets. In 2012, Gou et al. composed a comprehensive list of published cases, including 21 isolated cases of GP IIb/IIIa inhibitor induced DAH, three of which were caused by eptifibatide. There have been several more cases describing DAH in patients receiving GP IIb/IIIa inhibitors, and antiplatelet medications in general. Reflecting, the true incidence of DAH due to antiplatelets has yet to be studied extensively. In retrospect, DAH may be a minority in major bleeding complications of antiplatelet therapy, however, it does present as a severe but treatable manifestation if recognized and addressed promptly. This may suggest that DAH should be understood as a potential adverse effect of antiplatelet use and providers must be aware of such presentations.

CONCLUSION: GP IIb/IIIa inhibitors have been associated with several instances of DAH as outlined in literature and providers should be aware of such adverse event. Thorough history and coordination of patient care amongst consultants may prevent undesirable hospital courses, unnecessary exposures, and adverse events during admission.



First Page