MONDAY, June 18, 2007 (HealthDay News) -- A powerful clot-busting drug used in stroke and heart attack patients might also reduce amputations in people with severe frostbite, researchers say.
The standard treatment for frostbite hasn't changed for decades and involves re-warming the affected area and sometimes amputation, according to the report in the June issue of the Archives of Surgery.
"This is an excellent article, which opens a new venue of a more dynamic frostbite treatment," said Dr. Patrizio Petrone, from the division of trauma and critical care and the department of surgery at the University of Southern California's Keck School of Medicine.
"However, there is a need of a large multi-institutional prospective study in order to validate these extremely important findings," added Petrone, who was not involved in the study.
In their research, a group of University of Utah researchers, led by Dr. Kevin J. Bruen, looked at the possibility of using tissue plasminogen activator, (tPA), for treating frostbite.
Between 2001 and 2006, the team identified six patients with frostbite who had abnormal blood flow within the affected area. These patients were given tPA within 24 hours of contracting severe frostbite.
To see if the treatment was effective, Bruen's team compared the patients' outcomes to those of 25 frostbitten patients treated from 1995 to 2006 without tPA, plus one patient who received tPA more than 24 hours after injury.
The Utah team found that for the six patients who received tPA within 24 hours of injury, six of 59 affected fingers or toes (10 percent) required amputation, compared with 97 of 234 affected fingers or toes (41 percent) among people who did not receive the drug.
Moreover, none of the patients who received tPA within 24 hours after frostbite needed to have any part of their arm or leg amputated. However, among those who didn't receive tPA, there were 14 amputations, including five below the knee, Bruen's group reported.
"The preservation of limbs, which maximizes patient functional outcome, is perhaps the greatest benefit conferred by use of tPA in frostbite injury," the researchers said.
Bruen suspects that tPA works by reducing injury caused when frozen skin is re-warmed. Inflammation that occurs when the affected area thaws stimulates clotting that blocks small blood vessels, leading to cell death. Since tPA stops this clotting, blood flow is restored before permanent damage is done.
"Based on the dramatic improvements in perfusion and reduction in rates of amputations when tPA was administered within 24 hours of frostbite injury, we anticipate the continued use of tPA in patients who are admitted to our institution with acute frostbite," the authors wrote.
But Petrone said the number of patients involved in this study is too small to draw any definitive conclusions.
"In addition, because of the nature of this kind of patients, the follow-up is sometimes very difficult; therefore, the incidence of complications can not be accurately recorded," Petrone said. "Also, the absence of the adequate and matched controls -- especially in terms of severity scores -- makes me think that the study subjects could have improved anyway without tissue plasminogen activator treatment," he said.
More information
For more information on frostbite, visit the U.S. National Library of Medicine.
