Acute Coronary Syndromes

Chapter 65 Acute Coronary Syndromes

Case 1: Bleeding After Fibrinolytic Therapy

A 63-year-old man with a history of hypertension presents to a rural hospital with sudden onset of severe retrosternal chest pain. An ECG performed in the emergency department demonstrates 4-mm anterior ST segment elevation. The nearest hospital with a cardiac catheterization laboratory is more than 6 hours away. He is treated with aspirin (300 mg loading dose), clopidogrel (300 mg loading dose), and an IV infusion of front-loaded alteplase, with rapid resolution of pain and normalization of ST-segment elevation. Toward the end of the alteplase infusion, he complains of abdominal pain, becomes hypotensive, and develops melena. Hemoglobin is 10.2 g/dL, the aPTT is 89 seconds, the international normalized ratio (INR) is 1.7, and the fibrinogen level is below 100 mg/dL.

Aspirin and clopidogrel are held; the patient receives 10 units of cryoprecipitate and is started on an IV infusion of a proton pump inhibitor. He undergoes urgent upper gastrointestinal tract endoscopy with injection of a bleeding ulcer. He does not receive platelets because of concerns about the risk of recurrent MI. No further bleeding occurs, and after 48 hours, he resumes aspirin. Clopidogrel is restarted 1 week later after repeat endoscopy demonstrates a healing ulcer.


Fibrinolytic trials report a 1% to 6% incidence of major bleeding and a 10% incidence of moderate bleeding during the first 30 days. The most common sources of major bleeding are the gastrointestinal tract and procedure-related bleeding. The principles of management of major bleeding in STEMI patients treated with fibrinolytic therapy are summarized in Table 65-2. Steps include (1) stop antithrombotic therapies; (2) use local measures when possible to control bleeding; (3) draw blood to measure fibrinogen, prothrombin time (PT), aPTT, and possibly anti-Xa levels (to measure the anticoagulant effect of low-molecular-weight heparin) and to crossmatch blood; and (4) administer therapies to mitigate or reverse the effects of fibrinolytic, antiplatelet, and anticoagulant drugs.

The extent and duration of the lytic effects of fibrinolytic drugs is determined by their fibrin specificity. Whereas streptokinase produces profound and sustained depletion of fibrinogen (<100 mg/dL) that lasts for up to 24 to 48 hours, alteplase and other more fibrin-specific agents exert a less pronounced and more short-lived effect on fibrinogen levels. The aPTT and PT can be markedly prolonged in patients with hypofibrinogenemia. Normal coagulation can be restored by elevating fibrinogen level to at least 100 mg/dL. This can be readily achieved by infusing cryoprecipitate (recommended dose, 10 units). Fresh-frozen plasma also contains fibrinogen but requires administration of much larger volumes.

Platelet dysfunction caused by aspirin, clopidogrel, and fibrinolytic therapy cannot be specifically reversed, but infusion of donor platelets can help to restore platelet function. Platelet transfusion is generally reserved for patients with life-threatening bleeding because of concerns about the risk of recurrent MI. A single unit of single donor platelets can be expected to increase the platelet count by 50 to 60 × 109/L. Even a small number (e.g., 10%-20%) of functional (nonaspirinated) platelets are sufficient to generate sufficient thromboxane to sustain normal platelet aggregation, but a much larger number of transfused platelets are need to overcome the antiplatelet effects of clopidogrel. In this case, bleeding was controlled with cryoprecipitate, and local measures and platelet infusions were not required.

Jun 12, 2016 | Posted by in HEMATOLOGY | Comments Off on Acute Coronary Syndromes
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