In Scary Echo of 2014 Ted Agu Cal Football Death, Another Player With Sickle Cell Trait Was Hospitalized in Berkeley With an Overexertion Muscle-Death Syndrome — Here Are Exclusive Details

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August 5, 2018

by Irvin Muchnick


Four years after Ted Agu died of an exertional attack connected to having sickle cell trait (SCT), an SCT carrier on the current California Golden Bears football roster was hospitalized with a serious exertion-related syndrome after being stricken on the first day of this year’s winter conditioning drills.

Concussion Inc. has learned that there was a 911 call, and the player was diagnosed with a mild-to-moderate case of a condition called rhabdomyolysis.

Details of the incident — revealed to this reporter by a campus source concerned about whether the football conditioning program has adequately reformed safety protocols in the wake of the Agu fatality — are not conclusive with respect to the actions of the medical, coaching, and training staffs. But in the fraught environment surrounding the university’s 2016 settlement of $4.75 million in a wrongful death lawsuit by the Agu family, the January episode does appear to be ambiguous with respect to whether certain further clinical tests related to Exertional Collapse Associated With Sickle Cell Trait (ECAST) were indicated but not ordered. (The student-athlete in question did recover and return to the team.)

In rhabdomyolysis, muscles deteriorate from overexertion and the contents of the dead muscle fibers get released into the bloodstream, leading to the risk of life-threatening complications such as kidney failure. “Rhabdo” was identified in the hospitalizations of at least three athletes last year during football conditioning at the University of Oregon.

Our report here follows months of rumors about the January 16 scare in Berkeley. The player is not being identified beyond the fact that he is, like Agu, an SCT carrier. The total number of players on the squad who carry the trait is not even known, in part because student-athletes are allowed to opt out of SCT screening. According to the Centers for Disease Control, SCT is found in approximately one in 12 African-Americans.

News about this incident at Cal breaks two days after Braeden Bradforth, at Garden City Community College in Kansas, became the year’s third recorded fatality in college football conditioning. Earlier, Jordan McNair had died at the University of Maryland and Darius Minor at the University of.Maine.

According to medical journal research by two leading experts — former University of Oklahoma team physician Dr. E. Randy Eichner and current Oklahoma head athletic trainer Scott Anderson — there have been 36 non-traumatic (practice or conditioning) deaths in collegiate football since 2000: 33 in National Collegiate Athletic Association schools, two in junior colleges, and one at a National Association of Intercollegiate Athletics institution.

In an article scheduled for the September issue of Current Sports Medicine Reports, published by the American College of Sports Medicine, Dr. Eichner writes: “We in sports medicine ought to do more to help end these tragedies.  Football ‘conditioning’ is out of control and killing our kids.”

Cal Athletics issued the following statement:

“We are not able to respond to this request for personal medical information without violating federal laws that protect the privacy and confidentiality of student medical records. The health and safety of our student-athletes is our highest priority, and Cal Athletics and Cal Sports Medicine adhere to best practices on medical matters.”


The information disclosed by our campus source shows that the coaches and trainers were aware of this player’s SCT carrier status, and that he had been pulled out of a practice in October 2017. The October and January episodes may not be related: on the earlier date, California wildfires had made the air quality at practice exceptionally poor.

When the player returned to Berkeley from the winter holiday break, he reported that, while he had stayed active, his private workouts were limited by nagging lower back pain.

On that first day of team conditioning, January 16, the player fully participated in circuit weightlifting. The session was believed to have lasted around 90 minutes and consisted of fast repetitions and transitions between stations, as the players did bench presses, planks, and squats.

Near the end of the workout, the player’s lower back pain worsened, with the right side becoming more acute than the left; it was the first time he had experienced such pain on the right. According to the source, the player wondered at the time whether he might be enduring a “sickling” episode, as sickle cell trait exertional attacks are called. It is not clear whether he finished the workout.

Afterward, in the training room, still feeling lower back pain, the player became dizzy and vomited. Though his vital signs were stable and he was alert and talking, the staff decided to call 911, and emergency medical services took him to the hospital.

Experts told me that the most practical marker of rhabdomyolysis is elevated serum creatine kinase (CK). The initial blood tests showed mildly elevated CK. The working diagnosis of “acute kidney injury” based on these tests proved to be unjustified when, 12 hours later, after the athlete had been rehydrated with intravenous fluid, repeat blood tests showed that normal kidney function had resumed. On this second set of blood tests, however, the CK had risen moderately high.

According to the same experts, in light of the major back pain and a moderately high peak CK level, a key open question is why no MRI scan was done. There have been six reported cases of “acute lumbar paraspinal myonecrosis from exertional sickling”; an MRI might have confirmed a seventh here.

Following two nights of hospitalization, the player was released. The principal diagnosis was “non-traumatic rhabdomyolysis.”

Transition back to full conditioning activities was managed across a period of several weeks, in what our source described as a likely abundance of caution. The player continued to train without further incident and he played in the April 28 spring game.


This incident occurred several months before UC Berkeley released a long-delayed second review of the football strength and conditioning program that was ordered by Chancellor Nicholas Dirks shortly before he resigned. The second review followed both the Agu family wrongful death lawsuit settlement and criticism of a very thin and highly conflicted first review that had been conducted in the immediate aftermath of the death. Announced in the summer of 2016, with co-authors Dr. Elizabeth Joy and Wayne D. Brazil appointed in the fall of that year, the second report was not issued until June of this year.

Critics maintain that even the second report falls short of the mark in failing to account for abuses in the 2013-14 football strength and conditioning program under Damon Harrington, an assistant to head football coach Sonny Dykes. Both coaches now hold the same positions at other schools — Harrington at Grambling State and Dykes at Southern Methodist.

Meanwhile, Concussion Inc. is in the 17th month of California Public Records Act litigation against the University of California Regents for production of internal documents related to the Ted Agu death and a precursor incident, a player-on-player assault that is alleged to have been incited by Harrington. At a hearing Wednesday in Alameda County Superior Court, Judge Jeffrey S. Brand suggested that he might soon rule on our request for release of 141 pages of relevant Berkeley campus police reports — much of which had been withheld from the Alameda County Sheriff’s Office during the Agu autopsy investigation.



2017 op-ed article for the Daily Californian on my Public Records Act lawsuit:

Second op-ed article for the Daily Californian (published May 4):

“Explainer: How ‘Insider’ Access Made San Francisco Chronicle and Berkeley J-School Miss Real Story Behind Death of Cal Football’s Ted Agu,”

Complete headline links to our Ted Agu series:

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Concussion Inc. - Author Irvin Muchnick