Toxic epidermal necrolysis and hemolytic uremic syndrome after allogeneic stem-cell transplantation

  1. Johan Arvidson1,
  2. Morten Kildal2,
  3. Torbjörn Linde3,
  4. Rolf Gedeborg4

Article first published online: 16 JUN 2007

DOI: 10.1111/j.1399-3046.2007.00743.x

Issue

Pediatric Transplantation

Pediatric Transplantation

Volume 11, Issue 6, pages 689–693, September 2007

Additional Information

How to Cite

Arvidson, J., Kildal, M., Linde, T. and Gedeborg, R. (2007), Toxic epidermal necrolysis and hemolytic uremic syndrome after allogeneic stem-cell transplantation. Pediatric Transplantation, 11: 689–693. doi: 10.1111/j.1399-3046.2007.00743.x

Author Information

  1. 1

    Department of Women’s and Children’s Health and Pediatrics, Uppsala University Hospital

  2. 2

    Department of Surgical Sciences Plastic Surgery, Uppsala University Hospital

  3. 3

    Department of Medical Sciences and Internal Medicine, Uppsala University Hospital

  4. 4

    Department of Surgical Sciences, Anaesthesiology and Intensive Care, Uppsala University Hospital, Uppsala, Sweden

*Rolf Gedeborg, Department of Surgical Sciences, Anesthesiology and Intensive Care, Uppsala University Hospital, SE-751 85 Uppsala, Sweden Tel.: +46 18 6114893 Fax: +46 18 559357 E-mail: rolf.gedeborg@surgsci.uu.se

Publication History

  1. Issue published online: 16 JUN 2007
  2. Article first published online: 16 JUN 2007
  3. Accepted for publication 12 April 2007

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Keywords:

  • children;
  • allogeneic stem cell transplantation;
  • hemolytic uremic syndrome;
  • toxic epidermal necrolysis;
  • cyclosporine A;
  • plasmapheresis

Abstract:  TEN and HUS are challenging complications with excessive mortality after HSCT. We report the development of these two conditions in combination in a nine-yr-old boy after HSCT from an unrelated donor. TEN with skin detachment of more than 90% of body surface area developed after initial treatment for GvHD. Within a few days of admission to the burns unit, the patient developed severe hemolysis, hypertension, thrombocytopenia, and acute renal failure consistent with HUS, apparently caused by CSA. The management included intensive care in a burns unit, accelerated drug removal using plasmapheresis, and a dedicated multi-disciplinary team approach to balance immunosuppression and infections management in a situation with extensive skin detachment. The patient survived and recovered renal function but requires continued treatment for severe GvHD. Suspecting and identifying causative drugs together with meticulous supportive care in the burns unit is essential in the management of these patients and long-term survival is possible.

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