ECMO Anticoagulation and Hemostasis 5 — Questions and Answers
Question 1: What pattern on ROTEM/TEG is most consistent with acquired hypofibrinogenemia in an ECMO patient?
- Short clot formation time with high maximum amplitude
- Normal clotting time with significantly reduced maximum clot firmness on FIBTEM (Correct answer)
- Prolonged lysis onset with normal amplitude
- Very short clotting time with early lysis
Correct answer: Normal clotting time with significantly reduced maximum clot firmness on FIBTEM
FIBTEM (which inhibits platelet contribution) showing reduced maximum clot firmness specifically indicates fibrinogen deficiency as the cause of impaired clot strength.
Question 2: A pediatric ECMO patient on heparin develops catheter-site bleeding with an ACT of 190 seconds and platelet count of 110,000/μL. What additional test helps identify platelet dysfunction as a contributor?
- Prothrombin time/INR
- Platelet function assay (PFA-100) or TEG platelet mapping (Correct answer)
- Fibrinogen level
- Anti-Xa level
Correct answer: Platelet function assay (PFA-100) or TEG platelet mapping
Platelet function assays or TEG platelet mapping can identify acquired platelet dysfunction from ECMO circuit exposure even when platelet count appears adequate.
Question 3: What is the theoretical advantage of using heparin-bonded ECMO circuits regarding anticoagulation management?
- They eliminate the need for systemic anticoagulation in all patients
- They reduce circuit thrombogenicity, potentially allowing lower systemic heparin doses (Correct answer)
- They provide therapeutic anticoagulation equivalent to full-dose heparin
- They prevent all forms of circuit clotting indefinitely
Correct answer: They reduce circuit thrombogenicity, potentially allowing lower systemic heparin doses
Heparin-bonded circuits reduce surface thrombogenicity, allowing some programs to use lower systemic heparin doses or, in select stable patients, brief anticoagulation-free periods.
Question 4: In ECMO patients with both active bleeding and circuit clot, which viscoelastic TEG parameter guides the decision to use antifibrinolytic therapy?
- R time (reaction time)
- LY30 (percent lysis at 30 minutes) (Correct answer)
- Maximum amplitude (MA)
- K time (clot kinetics time)
Correct answer: LY30 (percent lysis at 30 minutes)
LY30 greater than 3% on TEG indicates significant fibrinolysis, guiding use of antifibrinolytics like tranexamic acid to reduce ongoing clot dissolution and bleeding.
Question 5: Which factor most significantly increases thrombin generation on ECMO beyond the circuit surface itself?
- Therapeutic hypothermia
- Systemic inflammatory response activating the extrinsic coagulation pathway (Correct answer)
- Supranormal oxygen delivery
- Hyperglycemia
Correct answer: Systemic inflammatory response activating the extrinsic coagulation pathway
ECMO triggers a systemic inflammatory response that activates tissue factor expression on monocytes and endothelium, driving extrinsic pathway thrombin generation beyond circuit contact activation alone.
Question 6: An ECMO patient's ACT is 350 seconds, well above the target of 180–220 seconds. Which reversal agent can partially reduce heparin effect while continuing the circuit?
- Vitamin K
- Protamine sulfate at a reduced neutralizing dose (Correct answer)
- Fresh frozen plasma
- Tranexamic acid
Correct answer: Protamine sulfate at a reduced neutralizing dose
Low-dose protamine (1–2 mg/kg) can partially reverse heparin over-anticoagulation without full reversal, allowing ACT to be brought into therapeutic range while continuing ECMO.
Question 7: What hemostatic change occurs specifically during the transition from VA-ECMO to VV-ECMO configuration in a recovering cardiac patient?
- Immediate normalization of all coagulation parameters
- Increased turbulence and shear from circuit reconfiguration may transiently worsen platelet consumption (Correct answer)
- Anticoagulation requirements double due to added circuit length
- Von Willebrand factor levels rapidly normalize within 1 hour
Correct answer: Increased turbulence and shear from circuit reconfiguration may transiently worsen platelet consumption
Circuit reconfiguration introduces turbulence and new surface contact areas, which can transiently increase platelet activation and consumption during and immediately after the transition.
What pattern on ROTEM/TEG is most consistent with acquired hypofibrinogenemia in an ECMO patient?