Severe thrombotic and bleeding complications in a baby with heterozygous factor V Leiden and acquired von Willebrand disease on ECMO.

We aim to present the case of a 5-week-old girl with severe respiratory failure placed on veno-venous extracorporeal membrane oxygenation (ECMO) that was then switched to veno-arterial ECMO. She required up to 60 units/kg/hr of heparin to keep her heparin level within the target range at .3-.7 units/mL. During the ECMO course, substantial thrombus formation was observed within the venous site of the ECMO cannula, which led to two circuit changes on ECMO day 9 and day 20. On ECMO day 15, she was noticed to have purpuric lesions on her chest and her right hand with no obvious arterial or venous clot detected by Doppler ultrasound. She was also noted to have remarkable hemolysis as the plasma free hemoglobin levels were substantially elevated up to 700 mg/dL. She was noted to have continuous oozing from the catheter insertion sites despite adequate underlying coagulation status. Her subsequent platelet function analysis, the thromboelastography, and thromboelastography platelet mapping suggested substantial platelet dysfunction. Her von Willebrand panel revealed absence of high molecular weight multimers. Further coagulation workup was prompted which revealed heterozygosity for factor V Leiden. The patient developed severe pulmonary hemorrhages and ECMO was discontinued on day 40.

[1]  R. Bartlett,et al.  Hemolysis and ECMO pumps in the 21st Century , 2011, Perfusion.

[2]  J. Teruya,et al.  Evaluation of heparin assay for coagulation management in newborns undergoing ECMO. , 2010, American journal of clinical pathology.

[3]  N. Uriel,et al.  Acquired von Willebrand syndrome after continuous-flow mechanical device support contributes to a high prevalence of bleeding during long-term support and at the time of transplantation. , 2010, Journal of the American College of Cardiology.

[4]  C. Brizard,et al.  Improved outcomes of paediatric extracorporeal support associated with technology change. , 2010, Interactive cardiovascular and thoracic surgery.

[5]  R. Schelonka,et al.  Plasma Concentrations of Inflammatory Cytokines Rise Rapidly during ECMO-related SIRS due to the Release of Pre-formed Stores in the Intestine , 2009, Laboratory Investigation.

[6]  M. Ruggieri,et al.  Stroke in children: inherited and acquired factors and age‐related variations in the presentation of 48 paediatric patients , 2009, Acta paediatrica.

[7]  R. P. Guillerman,et al.  Acquired von Willebrand syndrome and Wilms tumor: Not always benign , 2009, Pediatric blood & cancer.

[8]  M. Gladwin,et al.  Platelet activation in patients with sickle disease, hemolysis-associated pulmonary hypertension, and nitric oxide scavenging by cell-free hemoglobin. , 2007, Blood.

[9]  M. Gladwin,et al.  The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease. , 2005, JAMA.

[10]  T. Agorastos,et al.  Factor V Leiden and prothrombin G20210A mutations in pregnancies with adverse outcome , 2002, The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians.

[11]  Mattson,et al.  Inherited Thrombophilia due to Factor V Leiden Mutation. , 1998, Molecular diagnosis : a journal devoted to the understanding of human disease through the clinical application of molecular biology.

[12]  U. Nowak‐Göttl,et al.  Prevalence of factor V Leiden in children with thrombo-embolism , 1996, European Journal of Pediatrics.

[13]  T. Quattrociocchi-Longe,et al.  Influence of Platelet Factor 4 on the Neutralization of Heparin by Protamine a , 1989, Annals of the New York Academy of Sciences.