Coagulopathic-induced membrane dysfunction during extracorporeal membrane oxygenation: a case report

Abstract

This paper describes an unusual complication of membrane dysfunction during extracorporeal membrane oxygenation (ECMO) for treatment of neonatal respiratory distress. A 2.8-kg term infant presented to our facility in severe respiratory distress and was diagnosed with primary pulmonary hypertension. After routine priming of the extracorporeal circuit, the patient was placed on veno-arterial ECMO with 8 F arterial and 12 F venous cannulae. Transfusion criteria were established which included trigger values of the following: platelet count 100,000/microliters, fibrinogen 150 mg/dl, haematocrit 40%. The ECMO course was uneventful until approximately the 132nd hour on support when the patient developed a consumptive coagulopathy, as evidenced by 55-60% reductions in both platelet count and fibrinogen concentrations, despite transfusion therapy. Total autogeneic blood product transfusion during the first 120 h of ECMO averaged 4.4 +/- 2.2 ml/h, while the transfusion rate for the final 35 h was 7.8 +/- 3.5 ml/h. Coinciding with this rise in transfusion requirements was an increase in transmembrane pressure from 0.29 to 1.52 mmHg/ml blood flow. The patient was separated from ECMO after 175 h due to a continuing coagulopathy and haemothorax. The patient was then treated with nitric oxide therapy before succumbing on the twelfth postoperative day due to refractory respiratory failure. The circuit was dissected and significant clots found in both the venous bladder and oxygenator. In addition, approximately one-third of the membrane compartment had a 'fused' circumferential pattern of dessicated clot which interrupted blood path continuity. In conclusion, this report describes an unusual complication of the ECMO oxygenator that occurred during long-term extracorporeal life support which most likely resulted from a coagulopathy.

Unfractionated Heparin Activity Measured by Anti-Factor Xa Levels Is Associated With the Need for Extracorporeal Membrane Oxygenation Circuit/Membrane Oxygenator Change

“…A decision that the circuit or membrane oxygenator requires change is at the discretion of the attending physician. Such a change typically is performed for the following reasons: (1) visible thrombus on the arterial limb of the circuit; (2) steadily worsening thrombus formation in components of the venous limb of the circuit; (3) worsening thrombus formation within the membrane oxygenator as assessed by worsening gas exchange across the oxygenator or increasing circuit pressures; or (4) development of the “sick circuit syndrome” [18-20] consisting of platelet and fibrinogen consumption, signs of worsening patient capillary leak, and increasing circuit visible thrombus or fibrin stranding.…”

Coagulation and Anticoagulation in Extracorporeal Membrane Oxygenation

“…This uniform approach does not seem to be very satisfactory if one considers that bleeding and thrombosis remain frequent and often severe complications during ECMO. Many studies report bleeding or thromboembolic complications with a frequency of up to 60% of ECMO patients, and in many patients, bleeding or thromboembolic complications may lead to termination of ECMO (2–6).…”

Effect of Heparin, Platelets, Activated Platelets, Platelet Fragments, and Hematocrit on Activated Clotting Time

“…Insufficient anticoagulation might cause malfunction of the extracorporeal circuit and endanger the patient by inducing hypercoagulability following contact of the clotting system with artificial surfaces. On the other hand, this therapy has a considerable risk of bleeding (1–4). To achieve adequate administration of heparin and to reduce the risk of circuit malfunction or bleeding, anticoagulation must be monitored closely during therapy and after heparin reversal.…”