Organ failure syndrome
18 December 2013
The battle to save accident victims in Intensive Care often extends beyond treating the original injury, with multiple organ failure (MOF) presenting a constant threat. While the precise cause of the body's sequential 'shut down' is unknown, results from a recent Hunter Medical Research Institute (HMRI) study may help to solve the puzzle.
"Our key research area is looking at the body's inflammatory response to injury – what is the molecular connection between tissue damage and organ failure," Professor Zsolt Balogh, Director of Trauma Surgery at John Hunter Hospital and head of the University of Newcastle's Traumatology Research Group, said.
"We have found four independent predictors of multiple organ failure. One is the severity of injury, the second is the severity of blood loss, third is the patient's genetics, and fourth is the so-called second hit."
'Second hit' refers to the management of a patient's injuries and condition after arriving at hospital, particularly how surgical operations can trigger their immunological response.
"Patients are stirred up by the trauma and we hit them again with surgery and interventions," Professor Balogh explained. "We can't do anything about how severely they're injured or their blood loss, we can't change how genetically prone they are to inflammation, but the way we manage their treatment can directly impact on the degree of organ failure they will suffer."
Trauma is the major killer for people aged below 45 and a leading cause of burden on society.
Organ failure is the leading cause of death among accident patients who survive the first few days in hospital. The mortality rate is 25 per cent once a patient develops MOF, regardless of what initial injury they sustained, compared with a rate of only 3 per cent for those who aren't afflicted.
In collaboration with an HMRI immunology group led by Professor Phil Hansbro and University of Newcastle genomics expert Dr Doug Smith, Professor Balogh's team has identified a key marker for post-injury inflammation – it is the naturally occurring mitochondrial DNA within cells.
Professor Balogh likens them to a Trojan horse: "Every cell has hundreds of mitochondria living happily inside but when the cells die due to trauma the mitochondrial DNA leaks out," he said.
"It actually looks like bacterial DNA and, because it's recognised as bacterial product, it activates the white blood cell receptors which then kill more tissue … a vicious cycle.
"These activated white cells can also release their mitochondrial DNA, and we are the first to show that this mechanism happens without any bacteria or infection."
Results of the study were published this month in the international Journal of Critical Care and previously in The Lancet.
There is no "magic silver bullet" for medical staff other than preventing the syndrome. Depending on patient response, surgeons can decide when to operate and whether to initially perform major or minimally invasive surgery.
HMRI is a partnership between the University of Newcastle, Hunter New England Health and the community.
Contact: Mark Rothfield, HMRI.
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