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CU trauma surgery team at conference

CU Surgery Residents Win Big in Western Trauma Association Paper Competition

Ben Stocker, MD, and Morgan Hallas, MD, took home first- and second-place wins, respectively, at the organization’s annual meeting in February. 

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Written by Greg Glasgow on April 9, 2024

Two residents from the University of Colorado Department of Surgery took home top honors in the resident paper competition at the annual meeting of the Western Trauma Association, which took place February 25 through March 1 in Snowmass, Colorado.

Third-year resident Ben Stocker, MD, took first place in the contest for his paper, “Beyond the Von Willebrand Factor: Type O Blood Exhibits Downregulation of the Lectin Complement Pathway in Trauma,” and fourth-year resident Morgan Hallas, MD, placed second for his paper, “Plasma From Severely Injured Trauma Patients Induces Endothelial Cell Mitochondrial Dysfunction.”

“This is one of the more prestigious conferences in the trauma world,” Hallas says. “They typically only accept two abstracts per institution, but this year, they took three from Colorado, because we submitted some good research. We each gave 10-minute presentations in front of 300–400 people, with 10 minutes of questions after, and a panel of judges picked the winners.”

Endothelial insults

Hallas’ research which took place in the trauma lab at the CU Department of Surgery, looked specifically at mitochondrial dysfunction in the endothelium caused by traumatic injury and hemorrhagic shock.

“The mitochondria are responsible for producing energy in the cells, and when someone is severely injured and has low blood pressure and is in shock, the mitochondria don’t function properly,” Hallas says. “The cells aren’t able to produce enough energy to sustain themselves, and that causes all kinds of problems that lead to what we call the endotheliopathy of trauma, which is where the blood vessels get leaky and don’t hold on to fluid like they should.”

For their study, Hallas and his fellow researchers took plasma samples from two sets of trauma patients — severely injured and minimally injured — and examined the effects of each on endothelial cells. A metabolomic analysis showed higher levels of endotheliopathy in the cells treated with plasma from severely injured patients.

“We coined the term ‘energy crisis’ for what happens following this mitochondrial dysfunction,” Hallas says. “The mitochondria typically produce energy in the form of ATP, and this endotheliopathy process results in no ATP being generated. Our theory now is that we might be able to target specific points in this pathway to reverse this process, so that ATP can be generated.”

It’s even possible, Hallas says, that trauma teams could sample a patient’s blood when the patient first arrives, with an eye toward delivering personalized treatment based on their condition.

“We might have a specific medication we could give that would block some of this from happening or reverse it,” he says. “That way, we can give them something rather than just trying to resuscitate. And it might be that not everyone gets the same thing, but people get what they need at that specific time, depending on what their specific problems are.”

Blood type and trauma

Stocker, meanwhile, was part of a research team looking at the effects of trauma on people with type O blood. 

“It’s been shown throughout the research over the past couple of decades that patients with type O blood have a lower level of a coagulation factor that’s necessary for blood clotting,” says Stocker, who is in the first year of the two-year research portion of his residency. “It's been hypothesized that in general, patients with type O blood should bleed more often than others, since they have less of this protein. And in the trauma world, when people have traumatic injuries and bleed after getting shot, stabbed, or being in a car accident, these patients theoretically are more likely to die or have more complications because of the lack of this protein but results have been mixed in the literature.” 

Stocker and his fellow researchers set out to look at other differences between type O blood and other blood types in trauma, looking for other distinctions, beyond the lack of the clotting protein known as the Von Willebrand factor, that may explain differential outcomes.

“A lot of people know about antibodies, which is how our body fights off bacteria and viruses,” Stocker says. “But we also have other systems to fight bacteria and injury, and one of those is the complement system, which is a cascade of proteins that forms special proteins that rev up the immune system and lead to vascular leakage and inflammation.”

In trauma, Stocker says, the complement system is upregulated and active, leading to much of the inflammation and immune system activation see in trauma patients. 

His research found that patients with type O blood had lower levels of mannose-binding lectin (MBL), a protein that is essential for activating the complement system to create the cascade of proteins. 

“When someone is critically injured, inflammation is ramped up, and that interacts with their coagulation system, which actually makes trauma patients less likely to form clots in the first several hours,” he says. “That’s bad, because we want blood clots, we want them to stop bleeding. So the fact that there’s less of this initiator protein, which would theoretically lead to less overall inflammation, could be beneficial for trauma patients.”

There is much more research to be conducted on the issue, Stocker says — his next step is to use animal models to see what happens when the MBL protein is deactivated in other blood types.

“We want to see if we can mitigate some of that inflammation and that regulation of the coagulation system,” he says. “The ideal scenario would be to have a molecule that can inhibit MBL for a short time, just a day or two, and then it wears off so the immune system can get back to its normal state.”

Morale boost

For Stocker, who hopes to one day integrate clinical research into his surgical practice, the win at the Western Trauma Association paper contest was motivation to keep going.

“The fact that they liked my paper and my presentation was fantastic,” he says. “I wasn't expecting to win at all given that I have just entered my research time. It was a great step for my first year of research, and it gave me some positive motivation. Much of basic science work is pretty grueling and slow going, so to get recognized definitely gave me a morale boost.”

Featured image: Trauma research mentor Mitchell Cohen, MD, with residents Ben Stocker, MD, Lauren Gallagher, MD, and Morgan Hallas, MD, at the Western Trauma Association annual meeting.

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