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.
A technique is described for exposure of the descending aorta, allowing separate arterial cannulation for perfusion of the upper and lower body during reconstruction of the aortic arch, maintaining continuous full-flow cardiopulmonary bypass to the entire body. This single technique is applicable to all aortic arch pathologies and allows an unhurried aortic reconstruction in an unobstructed field.
Uncontrolled systemic-to-pulmonary shunt results in decreased systemic flow during extracorporeal life support (ECLS). Ligation of systemic-to-pulmonary shunts during ECLS is associated with poor outcome and is not always readily achieved. In ex vivo preparations, alveolar hypoxia results in pulmonary vasoconstriction despite normoxic pulmonary perfusate. We hypothesized that anoxic ventilation would result in reduced pulmonary shunting and increased systemic flow during ECLS in piglets with systemic-to-pulmonary shunt. Four piglets were placed on ECLS with right and left atrial drainage. A shunt was created between the bicarotid trunk and pulmonary artery, using 5-mm ePTFE tubing. Inspired oxygen was reduced to <1% for 10 minutes, then returned to room air; pH, hematocrit, temperature, ventilatory pressures, and total pump flow were maintained constant. Systemic arterial pressure and right atrial return volume and hemoglobin saturation were measured: All decreased significantly upon shunt unclamping. Anoxic ventilation caused increased systemic pressure (34 vs. 28 mm Hg, p < 0.05), flow (335 vs. 278 mL/min, p < 0.05), and systemic venous saturation (53% vs. 48%, p = 0.13) compared with room air ventilation. In conclusion, anoxic ventilation during normoxic ECLS in subjects with systemic-to-pulmonary shunts results in a significant and potentially clinically useful reduction in pulmonary shunting.
Background: The timeframe for safely using previously setup dry, crystalloid, and blood-primed extracorporeal circuits has long been debated. This study was undertaken to determine a safe deviation from standardized recommendations. Methods: Open (cardiopulmonary bypass) circuits and closed extracorporeal membrane oxygenation circuits were setup dry for up to 60 days and wet primed for up to 6 weeks with one control inoculated with Escherichia coli. Open circuits were cultured daily, closed circuits weekly. Circuits were primed with blood, albumin, heparin, NaHCO3, and CaCl2. Baseline pCO2, pO2, hemoglobin, lactate dehydrogenase, and plasma free hemoglobin were measured. Circuits were recirculated at a blood flow of 6 Liters/minute with a sweep gas of 1 Liter/minute at 100% FiO2 for 1 minute. Post oxygenator blood gases were collected at 8-, 16-, and 24-hour intervals. Results: There was no observed compromise to the sterility of the circuits and no clinically significant gas exchange abnormalities observed over the duration of the study period. Statistical significance (p < 0.01) was seen in free hemoglobin and lactate dehydrogenase levels, most significant in between the 16- and 24-hour time point in the closed systems intentionally inoculated with E. coli. Conclusion: Open and closed circuits can be safely setup dry for up to 60 days. Open, wet-primed circuits can be used safely up to 5 days. Closed, wet-primed circuits can be used safely up to 6 weeks. Blood-primed circuits can be safely run up to 16 hours prior to patient use but should be validated in a randomized clinical study.
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