HUS Treatment
The following information on the treatment of hemolytic uremic syndrome is not medical advice. We are a law firm that represents E. coli victims throughout the United States and are publishing this information as a public service. Contact us about compensation for pain and suffering, emotional distress and other damages.
There is very little that can be done to treat hemolytic uremic syndrome (HUS). Most commonly used treatments for infection have been shown to be ineffective or actually worsen the illness. Typically therapy is mainly supportive, essentially making sure that food and nutrient intake are sufficient and that fluid and electrolytes are at proper levels. If acute renal failure does develop, dialysis will be necessary to remove waste and maintain relative homeostasis.
Platelet transfusion is not recommended because it can increase likelihood of blood clot formation (1). Other therapies such as plasmapheresis (plasma is removed from the body, filtered and returned), anti-thrombotic agents (prevent blood clots), steroids and Shiga toxin-binding agents (the cause of kidney damage in HUS) have been found not to be effective (2).
Antibiotics, especially intravenous cephalosporin, have been found to greatly increase the likelihood of the development of HUS (3). Antimotility drugs such as Imodium® and Lomotil®, anticholinergic agents such as Detrol® and Ditropan®, and opioid narcotics like morphine and oxycodone have all been found to increase the risk for HUS. Although different, all these drugs have effects that include relaxing the muscles of the colon or small intestine which increases water uptake, and results in firmer stools. They can also help relieve abdominal pains common in diarrheal illnesses. But this muscle relaxation allows E. coli and associated shiga toxin to remain in the bowels for a longer period of time which increases absorption of the toxin. A study by Bell et al. found that children treated with antimotility agents had approximately a 2 times greater risk for developing HUS (4).
Sources:
1. Tarr PI, Gordon CA, Chandler WL. 2005. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet. 365: 1073-86.
2. Razzaq S. 2006. Hemolytic uremic syndrome: an emerging health risk. Am Fam Phys. 74:6: 991-996.
3. Higami S, Nishimoto K, Kawamura T, Tsuruhara T, Isshiki G, Ookita A. 1998. Retrospective analysis of the relationship between HUS incidence and antibiotics among patients with Escherichia coli O157 enterocolitis in the Sakai outbreak. Kansenshogaku Zasshi. 72:3: 266-72.
4. Bell B, Griffin P, Lozano P, et al. 1997. Predictors of hemolytic uremic syndrome in children during a large outbreak of Escherichia coli O157:H7 infections. Pediatrics, 100: E12.
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