Autopsy results probed

As Aaron O’Neal’s high school remembered him over the weekend, questions remained about the circumstances of his death. Boone County Medical Examiner Valerie Rao says viral meningitis, not sickle cell trait, was a key factor in his death; other experts say the sickle cell trait that O’Neal carried was likely the cause.
Sunday, September 11, 2005 | 12:00 a.m. CDT; updated 3:10 p.m. CDT, Tuesday, July 22, 2008

Months after Aaron O’Neal’s death, numerous authorities disagree about the role sickle cell trait, which O’Neal had, played in his death and how to stop deaths for others with the trait.

In February 2001, Florida State University freshman Devaughn Darling, a 6-foot-2, 220-pound linebacker, collapsed after a vigorous off-season indoor conditioning practice and later died. He was 18.

In July 2005, MU redshirt freshman Aaron O’Neal, a 6-foot-3, 220-pound linebacker, collapsed after a voluntary off-season practice and later died. He was 19.

Both athletes were carriers of sickle cell trait, an inherited disorder of red blood cells.

Two parallel cases, one key difference — the official cause of death.

Leon County, Fla., Medical Examiner David E. Craig found no definitive cause of death but noted in his autopsy report that Darling had red cell sickling in most blood vessels, which could lead to a fatal cardiac arrest.

“Although rare, sudden unexpected death has been associated with healthy, athletic males with sickle cell trait,” Craig wrote in the autopsy report. “No definite morphologic cause of death.”

Boone County Medical Examiner Valerie Rao found lymphocytic meningitis to be O’Neal’s probable cause of death and has repeatedly and emphatically refuted a connection with sickle cell trait despite a neuropathologist’s assertion in the autopsy report that sickle cell trait played a part in O’Neal’s death. Douglas Anthony, the neuropathologist at University Hospital who examined O’Neal’s brain, wrote to Rao in his evaluation, “In my opinion, both lymphocytic meningitis and sickle cell trait are potential contributing factors in this sudden death.”

Sports medicine and sickle cell experts who analyzed the autopsy findings for this story say that sickle cell trait with heat stroke or rhabdomyolysis — exercise-related muscle damage — most likely killed Aaron O’Neal.

Some in the medical community willing to discuss the trait and sudden death say the most minimal adjustments can prevent these rare deaths: a slow buildup to strenuous exercise when the weather is hot and humid and attention to how much water an athlete is drinking. But other medical professionals say that athletic trainers should treat all players the same — making sure they’re not being overworked or becoming dehydrated. That approach is safe and doesn’t create the danger of discrimination against the athlete with the trait.

Bob Blitz and Scott Rosenblum, attorneys for Aaron O’Neal’s father, have cited negligence in suing 14 MU athletic department employees. The wrongful death suit accuses trainers and coaches of waiting too long and doing too little to respond to a football player’s obvious distress.

Darling’s parents filed a wrongful death suit against FSU and were awarded $2 million by a Tallahassee judge last year. Most of the award remains to be decided by the Florida legislature.

Rao’s autopsy report indicates that O’Neal’s liver, spleen, kidneys and brain contained sickled red blood cells. Craig’s autopsy report indicated Darling’s lungs, liver, stomach, kidneys and heart contained sickled red blood cells.

Anthony went on to write, “While 8 percent of African Americans have sickle cell trait, it is worth noting that sickle cell trait is associated with a 40-fold increased risk of sudden death.”

Rao disagreed with Anthony’s opinion.

“The neuropathologist and the sickle cell trait experts are not medical examiners. The neuropathologist is only looking at the brain slides, but you have to look at the whole picture,” Rao said. “Everyone has an opinion but in the court of law, none of that matters. It’s what the medical examiner says.”

Rao concluded that O’Neal’s meningitis was lymphocytic because of the virus-fighting white blood cells — lymphocytes — found in the brain. The Centers for Disease Control and Prevention has to confirm the meningitis was viral. That determination could take several months.

Rao was hired as an associate professor of clinical pathology and anatomical sciences in 2004 by MU and is contracted out as a medical examiner for Boone and Callaway counties.

John Kark is convinced sickle cell trait played a role in O’Neal’s death.

“This wasn’t a death from viral meningitis — if he really had viral meningitis, which I doubt,” said Kark, a retired Army physician and expert in heat-related deaths who authored a pioneering study on sickle cell trait. “I’m not too convinced that’s the correct interpretation there.”

Steven Van Camp, past president of the American College of Sports Medicine, agreed: “This case sounds very consistent with exertional rhabdomyolysis and sickle cell trait.”

A dangerous combination

Sickle cell trait has caused the death of up to 10 college football players since 1974, usually occurring during heavy exertion such as wind sprints, timed miles, ramp running, mat drills and weight training, according to the article “Youth Football: Heat Stress and Injury Risk” in the August 2005 edition of the Medicine & Science in Sports & Exercise Journal, the official journal of the American College of Sports Medicine. Players with severe sickling collapse due to muscle pain and malfunction and then lose the ability to talk before vital signs begin to deteriorate, leading to “acidosis (overproduction of lactic acid) impairing the pumping power of the heart.”

Greg Flaker, the cardiologist who attended to O’Neal in the emergency room of University Hospital in the final minutes before the player died, identified O’Neal as having “pulseless electrical activity.”

“He had an electrical signal that was telling the heart to pump, but the heart wasn’t pumping,” he said.

The NCAA describes sickle cell trait as a “benign condition that does not affect the longevity of the individual” and says it is not a barrier to “outstanding athletics performance.” Eight to 10 percent of the black population in the United States has the trait, according to the NCAA. The NCAA Committee on Competitive Safeguards and Medical Aspects of Sports does not recommend requiring screening for the trait.

Chad Moller, MU athletics media relations director, said the university does not test athletes for sickle cell trait. But on the pre-participation medical history form that all MU athletes must fill out, obtained through a Freedom of Information Act request under the Missouri Sunshine Law, an athlete is asked to disclose if a blood relative has had “sickle cell trait/disease” and if the athlete has “sickle cell anemia.” On another form, the pre-participation medical evaluation form also obtained by a FOIA request, the athlete is asked if he or she has had “sickle cell.” None of the forms directly asks if the athlete has sickle cell trait.

When asked if O’Neal disclosed that he had sickle cell trait, Moller said, “I’m not aware either way.”

Blitz, O’Neal’s attorney, said he also had no idea if his client’s son knew he had the trait.

It is a thing that Aaron O’Neal would most likely have known about himself. The state of New York, where he was born in 1985, began testing all newborns for sickle cell trait in 1975. Ninety-eight percent of newborns are tested for conditions such as sickle cell disease and sickle cell trait, according to the Centers for Disease Control and Prevention. Missouri began statewide testing for the trait in 1989.

People with the trait are normally thought of as healthy, and athletic performance is unaffected unless cells sickle.

“Especially vulnerable appear to be those athletes with sickle cell trait who perform maximal, or ‘heroic’ exercise in pre-season conditioning sessions,” Van Camp wrote in the book “Catastrophic Injuries in High School and College.” The question is whether those conditions existed on that day in July when O’Neal collapsed on the turf.

Michael Bergeron, an applied physiologist at the Medical College of Georgia and American College of Sports Medicine fellow, described a potentially deadly scenario for a person with the trait. “Our research would support that, given the right conditions of strenuous exercise, dehydration and heat strain, sickling can occur and that can lead from mild symptoms of discomfort to severe pain to significant organ damage and ultimately to death,” Bergeron said.

At 2:39 p.m. on July 12, the time Aaron O’Neal collapsed, according to photographs taken by Columbia Daily Tribune photographer Jenna Isaacson, the temperature was between 86 and 88 degrees — the peak for the day. Noting the temperature in her report, Rao points out the practice was the same for all 12 players on the field. She concluded “the environmental factor” played no role in O’Neal’s death.

Bergeron and Kark disagree.

“It’s unique to him because he’s the one with the trait,” Bergeron said. “Moreover, the mid-80s — or somewhat higher on-field temperatures — is plenty hot enough to cause significant heat strain.”

Kark called Rao’s statement “absolute, total nonsense.”

“That’s how it almost always is,” Kark said. A former associate professor at Howard University in Washington D.C., Kark is a pioneer in heat-related sickle cell research. He and other researchers performed a study on military recruits in the late ’70s and early ’80s suggesting black recruits with sickle cell trait had a nearly 28-fold increased chance of dying of sudden death than black recruits without the trait.

“When people have severe heat illness, two or three people get mildly sick and the rest don’t,” he said. “It has to do with a lot of other factors, not just environmental exposure.”

Bergeron said O’Neal’s symptoms listed on the autopsy narrative such as “sluggish” behavior, significant performance changes, “wobbling,” “blurred vision” and having to lie down would be enough to suggest excessive heat stress and clinical risk. He said at that point it is critical to cool the body down immediately and activate the emergency response system. Icing is a quick solution, Kark said.

Rao’s notes from interviews with players indicate that water was poured on O’Neal after he collapsed and that he had easy access to drinking water. He drank water during the stretch after the last drill. Since O’Neal’s death, “players get enough water breaks” and “(trainers) ask if everything is OK,” according to notes Rao took from her interview with MU player Trenile Washington.

Enhanced heat sensitivity

Jerry Weber, the chair of the NCAA Sports Science Safety Subcommittee, said NCAA guidelines are just that — guidelines. It is up to individual schools to develop their own policies.

Among the Big 12 schools that test for sickle cell trait during athletes’ annual physicals are Oklahoma University, Oklahoma State University, Baylor University, Colorado University and the University of Nebraska, where Weber is head athletic trainer.

“There’s no doubt because of the situations that can arise, you do want to know all that you can about your athletes,” Weber said.

The American College of Sports Medicine is one of the most outspoken organizations in the country on the potential dangers of sickle cell trait and heat stress. But not everyone agrees. Cage Johnson, director of the University of Southern California Comprehensive Sickle Cell Center and professor of medicine at USC, said O’Neal’s death could not have been caused by sickle cell trait because it is a condition that has no known accompanying illness. He said the death could be heat-related.

“I believe that (people with the trait) are more sensitive to heat stroke than the general population because they do have a renal (kidney) defect in about half of the cases,” Johnson said. “They can’t concentrate their urine so they have difficulty saving water.”

Johnson said oxygen levels, acid-base balances and red blood cell hydration — all issues in a heat illness — affect the sickling of red blood cells. He said sickling occurs in venous blood — blood that is going back to the lungs to be re-oxygenated before traveling to the heart to be pumped back to the body. When sickled cells receive oxygen from the lungs, a body should correct any sickling on its own, he said.

Jon R. Thogmartin, the medical examiner for Pinellas-Pasco County, Fla., took an interest in Darling’s 2001 death. Thogmartin had published an article in a 1998 issue of the Journal of Forensic Sciences, “Sudden Death in Police Pursuit,” describing the death of a 13-year-old black boy after a chase. The boy had sickle cell trait and no other medical problems.

Thogmartin said he thinks Darling died as a direct result of sickle cell trait combined with extreme exertion, and he thinks the trait could have been a contributing factor in O’Neal’s death “if the liver, spleen and blood vessels were extensively examined.”

Thogmartin was trained by Rao, who worked as medical examiner in Lake, Citrus, Hernando, Marion and Sumter counties in Florida before arriving in Columbia last year.

An NFL player’s story

There is a postscript to the story of Devaughn Darling’s death.

Devard Darling is Devaughn’s identical twin brother.

He also played at FSU, and both learned when they were tested as freshmen that they had sickle cell trait. After Devaughn died, Devard was not medically cleared to continue playing at the university despite passing several tests “with flying colors,” he said. Devard said FSU knew his family was going to take legal action against the university.

He said he tried to transfer to Purdue University, USC and the University of Tennessee, but wasn’t cleared to play. Devard firmly believes he was “black-balled” although he is less certain of the reason. He finally transferred to Washington State University and was later drafted by the Baltimore Ravens in the third round of the 2004 NFL draft. The Ravens’ coaches did research and concluded he was healthy, Devard said.

The NFL does not exclude athletes with sickle cell trait. In a survey of 579 NFL players, 6.7 percent had sickle cell trait, according to the August 2005 article in the Medicine & Science in Sports & Exercise.

Knowing that Devard has the trait, trainers still treat him the same as his teammates, he said.

“The trainers will act more promptly and make sure I’m hydrated,” he said. “They won’t take any procedures that are different than anyone else.”

That’s exactly as it should be, said Van Camp, the past president of the American College of Sports Medicine.

While Van Camp said the trait may not be “benign,” he said he doesn’t think it calls for drastic changes. He said trainers and coaches should treat all athletes the same — with care during high-intensity workouts and with people who aren’t acclimatized. Generalized muscle cramps that last longer than 15 minutes should be treated as medical emergencies. “It’s not necessary to screen (for the trait),” he said. “Just do the right thing.”

MU defensive back Trenile Washington had similar advice for the medical examiner when asked how things should change on the MU practice field. “Pay more attention to all the players,” he said in an interview with Rao. “Ask if everything is OK — they do it only for players they think are going to play.”


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