Here, I cover two topics. The first, “Conditioning Them to Death,” is somber, and calls for our urgent attention. The second, “Keeping it in the Family,” is lighter, and offers pearls and pitfalls. Let me begin.
Conditioning Them to Death
My colleague Scott Anderson, head athletic trainer at the University of Oklahoma, has tracked college non-traumatic football deaths since 2000. None has occurred from the play of the game. Two, both cardiac, have occurred from collapses during practicing for the game. And 30 have occurred from collapses during conditioning for the game! Anderson reported on this in 2017 (1) and has updated it in recent sports medicine meetings.
The most recent college football conditioning death was in June 2018, about two weeks after the player, a huge lineman, collapsed after a session that included 10 repetitions of 110-yard sprints. A few days later, he got an emergency liver transplant. His cause of death has not yet been announced (it seems that no forensic autopsy was done), and an external review of that football program is underway, but the family’s foundation web site says their son died from exertional heat stroke (EHS).
So these 30 college football conditioning deaths comprise 12 from exertional sickling associated with sickle cell trait (ECAST), 10 from cardiac disease, seven from EHS, and one from asthma. It seems that some of our college football coaches, in their fervor to “prepare athletes to play the game,” are conditioning them to death.
Others have expressed similar concerns. In 2010, Christopher McGrew, MD, team physician at the University of New Mexico, wrote in our journal on “NCAA football and conditioning drills.” At that time, 18 of 21 college non-traumatic football deaths (since mid-2000) were tied to conditioning tests or sessions. McGrew noted that conditioning sessions and preseason drills associated with the death of a player seem to have a common theme: too much, too fast, too soon, and too long. He said the burden of preventing overload falls on the shoulders of the coaches who design and conduct the conditioning program. He called for conditioning sessions to be scientifically based, football-specific, reasonably run, and appropriately monitored. He concluded that coaches who enforce inappropriate and unnecessary drills should be held accountable for adverse outcomes that are clearly preventable, including “needless conditioning-related football deaths” (2).
Alas, since 2010, football-conditioning deaths continue apace, with one exception. The NCAA program for screening and commonsense training precautions for sickle cell trait (SCT), which began in 2010, has sharply and significantly cut the ECAST death rate. For example, in NCAA Division-1 football conditioning, 10 ECAST deaths occurred in the 10 years before the program began, but only one ECAST death has occurred in the 8 years of the program. And in that one death, the university has admitted their negligence in failing to follow SCT guidelines. That university underwent not just one, but two external reviews of their program, yet recently sent another SCT football player to the hospital – this one with non-fatal sickling complications from a day 1 winter conditioning session. This suggests that some football programs are slow to learn, that external reviews may not solve the problem, and that constant vigilance and education are needed to prevent ECAST complications and deaths.
Nor are liver transplants for EHS the antidote for reckless coaches. A pioneering liver transplant for EHS failed to save the life of the most gravely ill cadet in the notorious 1988 outbreak of exertional rhabdomyolysis at a Massachusetts police academy (3). A report from Harvard transplant surgeons in 2012 noted only four prior cases in the literature of liver transplant for heat stroke; they reported a successful liver transplant in a young male runner with EHS (4). Another group reported a successful liver transplant in a young male ultra-marathon runner with EHS (5). The same hospital service that performed the liver transplant for the above-mentioned college football player who died from EHS in June 2018 also has recently performed at least two successful liver transplants for EHS in athletes – a recreational triathlete and a college football player. The football player trained back into shape, but after a long court battle, it was judged unsafe for him to return to college football.
Liver transplant for dire EHS in athletes may be on the increase. Wiser to prevent EHS. More common sense among conditioning coaches and other staff can prevent most or all cases of dire or fatal EHS in football. Ditto for asthma deaths.
As for the 10 cardiac deaths, let me posit that some of these athletes may have lived into middle age or beyond, but for encountering reckless coaches. After all, no cardiac collapse occurred during the play of the game — they were in conditioning drills. I do not argue that some had only athlete’s heart and the real killer was ECAST or EHS, although misclassifying the cause of death like this still occurs now and then. Rather, I argue that the epidemiology and natural history of hypertrophic cardiomyopathy (HCM), for example, suggest that some people with diagnosed or covert HCM live long lives (6). I argue that some of these football players, despite underlying HCM (or even myocarditis), may have lived long lives if not pushed over the edge by a football conditioning coach. I could be wrong.
I do know this: We in sports medicine ought to do more to help end these tragedies. Football “conditioning” is out of control and killing our kids.
Splenic Infarction in the Family
On a lighter note, consider splenic infarction in father and son. The first story goes like this: An 18-year-old white man rode a bus from sea-level Texas to Clines Corner, New Mexico (7,200 ft), where he soon developed sharp left upper quadrant abdominal pain. Ultrasound examination on hospital day 3 showed a necrotic spleen; he was then found to have SCT, splenectomy was done, and the spleen had extensive sickling and multiple infarcts. When his father, a 37-yr-old white man, heard his son was ill, he drove from sea-level Texas to New Mexico, where he also developed sharp left upper quadrant pain and, in the same hospital as his son, also had a splenectomy. His spleen was infarcted, with sickling, and he also had SCT. Like father, like son (7).
The second story repeats the theme: A 55-yr-old man from Ganjam (Odisha, INDIA) visited the Amarnath shrine, a high-mountain cave (12,756 ft), a holy place for Hindus. His wife and his son, 27 yr old, were with him. Near the end of their 16-km hike to the shrine, the father and son developed left upper quadrant pain, but they did not let it stop them. The pain worsened in the cave, and the father and son were evacuated to a hospital, where both had splenic infarcts and SCT. Neither had splenectomy; both were managed conservatively; the father was symptom-free in 10 d; the son in 5 d. Again, like father, like son, but the son heals faster (8). And so it goes….
The pearls: SCT has nothing to do with skin color, per se; its roots are “malarial,” not “racial.” Think of splenic sickling and infarct in anyone new to even moderate altitude who develops acute, sharp pain in the left lower chest or left upper abdomen. Recall that Pittsburgh Steeler safety Ryan Clark, who has SCT, had a splenic infarct in a game against the Broncos in mile-high Denver. Sickling splenic infarcts at altitude also have occurred in skiers, runners, basketball players, weightlifters, and even fishermen with SCT. The pitfalls: This unique sickling syndrome has been confused with pleurisy, pneumothorax, “side stitch,” renal colic, gastroenteritis, or bowel obstruction. The good news: Diagnosed early, this painful splenic complication of SCT responds to conservative therapy, including descent. Enough said.
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