New Device Could Detect Septic Shock Early On

2013_03_280008d (Photo credit: Gwydion M. Williams)

Septic shock affects around 750,000 people and kills over 200,000 patients per year within the United States.

Septic shock, which is also known as severe sepsis, occurs when the body’s immune system gets triggered by a bacterial infection or some kind of serious physical injury and starts an inflammatory response that could lead to a dangerously low blood pressure, multiple organ failure and death. Septic shock affects around 750,000 people and kills over 200,000 patients per year within the United States.

Due to the dangers behind this reaction and the difficulty in detecting its onset, researchers from CALS at the University of Wisconsin Madison have come up with a potentially powerful tool that would detect septic shock roughly 12 to 48 hours faster than traditional methods. The team had developed a breath biomarker technology that was patented in 2008. It is currently going through clinical trials and if the results are successful, it could change how doctors treat and handle septic shock.

“If you can detect septic shock earlier, then you can begin to explore ways of treating it earlier,” commented one of the researchers, Mark Cook, who is an animal sciences professor at CALS.

For the research, Cook, who worked with scientist Jordan Sand, focused on the gastrointestinal tract, which has been tied to being the primary site of the massive inflammatory response carried out by the immune system. The team looked at a protein called sPLA2, which has been linked to the chain of events that triggers septic shock, and attempted to interfere with its activity. The protein is known for having two functions as either an enzyme or a signaling molecule.

First, the team blocked sPLA2 from carrying out its signaling function. Even after the protein was inhibited, the researchers found that it made the situation worse for the mice models. The team then created antibodies that would block the protein’s ability to perform as an enzyme. They were shocked to find that by prohibiting sPLA2 to act as an enzyme, the mice models were able to survive.

“We had 100 percent survival across the board,” Sand commented according to Medical Xpress.

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