Here is a puzzling case sent by Crystal Azevedo: Hi George! I have a question for you from one of my pathologists. 24 hours after an uneventful coronary bypass procedure a 51 kg patient developed acute hemorrhage. A post-protamine thromboelastogram (TEG) on the day of surgery was completely normal. At the time bleeding occurred, the patient was found to have a fibrinogen of 104 mg/dL and a platelet count of 43,000. A TEG was performed that showed a markedly prolonged R-time in the kaolin cup (21 minutes) but substantial correction in the heparinase cup (to 8.8 minutes). Alpha, K and MA were low, as expected. Heparin was felt to be present based on the TEG results, but the physician and nurse caring for the patient insisted that no heparin had been administered.
An anti-Xa assay performed on the same sample as that used for the TEG analysis showed no anti-Xa activity. A paired partial thromboplastin time (PTT) with and without heparinase showed a markedly prolonged PTT but with a difference of 50 seconds with the heparinase cup. Can these results be explained? I would also like to add, George, that the patient had a markedly decreased antithrombin of 20%. Thanks so much for this wonderful resource!
Hi, Crystal, and thank you for your question. I usually like to acknowledge your location workplace, but want to maintain the privacy of your patient. I checked separately with three respected colleagues, and all agreed that, despite the claims of the patient’s nurse and physician, the patient had received some heparin. It is likely that someone flushed a line or collected blood in a heparin-coated syringe and did not document. My colleagues say they see this happen frequently, though they can seldom document the incident. The heparinase results are partly an accident of timing. The PTT and the fibrinogen could also be the result of the heparin, presuming you are performing fibrinogen using the clot-based method. A heparin flush may not provide enough heparin to raise the anti-Xa levels, though the anti-Xa may be low as a function of the reduced antithrombin level.
The presence of heparin does not explain the bleeding or the low platelet count, however, nor does it explain the prolonged (though shortened compared to untreated) PTT in the heparinase-treated specimen. I hope the patient was further worked up using fresh (non-heparin) specimens to check for DIC, which seems to be the most likely explanation. Please let me know what happens in follow-up. Geo.