March 7, 2002
Controlling the body’s response to severe injury
| Pamela Wyngate |
| HS News & Community Relations |
One of the results of training highly skilled paramedics and first responders is a significant increase in the number of severely injured patients making it to the emergency room. This influx of critically injured patients has changed more than just the hospital patient counts—it has greatly increased the challenges in treating acute injuries.
“More and more patients, who would have died had they sustained the same injuries five or 10 years ago, are surviving due to improvements in acute surgical care,” says Dr. Ronald Maier, professor and vice-chair of surgery and surgeon in chief at Harborview Medical Center. “I’ve found that the critically injured are the most challenging patients. They frequently develop a process called multiple organ failure, causing much more damage than the injuries alone and producing a high rate of mortality.”
When a person suffers an acute injury, the body produces an intense but localized, controlled response. This inflammatory response fights bacteria and resolves wounds. However, if the injury is severe enough, control of the localized responses is lost and a massive, indiscriminate inflammatory response develops. This systemic response results in organ injury and failure.
“Evolution did not plan on people with such massive injuries surviving. While the localized responses to injury are appropriate,” explains Maier, “the systemic inflammatory response is more like a massive, uncontrolled explosion. After a patient survives the acute injury, we’re left with treating the patient’s own aberrant response to the injury.”
Maier, director of the Surgical Intensive Care Unit at Harborview since 1983, investigates the macrophage in relationship to immunopathology and a patient’s inflammatory response to severe injury. Macrophages are cells that produce protein mediators responsible for orchestrating a patient’s inflammatory response.
“We’re trying to control these protein mediators and understand the mechanisms and targets for therapeutic intervention,” Maier says. “By focusing on the macrophage, we’ve identified potential methods to treat critically injured patients, including injecting hypertonic solutions, vitamins C and E, as well as other antioxidants to shut down the excessive inflammatory response.”
Hypertonic solutions, he explains, alter the shape of the macrophage and decrease the efficiency of enzymes and other cell signaling apparatuses necessary in the inflammatory process. Antioxidants decrease oxidation, a critical process in the inflammatory response.
“We can use what we learn about the molecular biology of the inflammatory response and the macrophage to help us improve the treatment and care of critically injured patients,” says Maier.
Maier will present “Evolution Did Not Plan on Survival in the ICU” at the Science in Medicine lecture, noon, Thursday, March 14, in D-209 Turner Auditorium, Health Sciences Center. Everyone is welcome.
Maier obtained a B.S. from the University of Notre Dame and a M.D. from Duke University Medical School. Following his general surgery residency training at the UW, he completed a postdoctoral fellowship in immunopathology at the Scripps Clinic and Research Foundation in La Jolla, Calif. He has been a member of the UW faculty in the Department of Surgery since 1981.
Maier has served as chair and a member of the NIH Surgery, Anesthesiology and Trauma Study Section. He is past-president of the Society of University Surgeons and the Shock Society, current president of the American Association for the Surgery of Trauma and president-elect of the Surgical Infection Society and the International Association for the Surgery of Trauma and Surgical Intensive Care. He is also a director and chair-elect of the American Board of Surgery. Maier has been a fellow of the American Association for the Advancement of Science since 1994.
