Exertional rhabdomyolysis (ER) seems to be on the rise in the United States military and — as judged by a recent spate of “team rhabdomyolysis” outbreaks — in athletics. What about in the general public? How commonly is ER seen in “civilian” clinics and hospitals? What can we learn by studying ER in soldiers versus civilians? I will begin with an epidemiologic, population-based, retrospective cohort study of ER by Mayo Clinic researchers.
ER in Civilians
Persons who developed ER in Olmsted County, MN from 2003 to 2015 were identified via the Rochester Epidemiology Project, using ICD-9 codes for “rhabdomyolysis” or “myoglobinuria” and an electronic search for key words in clinical notes. The authors reviewed the selected medical charts and diagnosed ER if the setting was right and the serum creatine kinase (CK) was more than five times the upper limit of normal.
Of 430 rhabdomyolysis cases identified, 21 (5%) were ER. Most were men. The age-adjusted incidence rate for men, at two cases per 100,000 person-years, was 10 times greater than for women, but was far below that seen in our military (considered below). The most common cause of the ER was endurance exercise, followed by manual labor and then weight lifting.
Most ER cases seemed mild or moderate, with only brief hospital stays, but the four ER patients who had exertional heat stroke (EHS) tended to be more severe, and one with EHS was dire (16 hospital days, but survived). No one got compartment syndrome or needed hemodialysis, and no one died. All recovered fully, and in a median 3-year follow-up, there was only one recurrence (1).
In their conclusion, the authors say that elevated transaminases, which they found in most of their ER cases, have not been described in ER, and they advise us to include “liver function testing” in our evaluation of ER. This advice is off the mark. As I have said before, not all “liver chemistries” are liver chemistries. I have seen hard-training athletes with staleness, fatigue, and “heavy legs” who were thought to have “hepatitis” based on elevations in transaminases and lactic dehydrogenase. But these enzymes come from muscle as well as from the liver, and these athletes had mild ER, not hepatitis. So the wise advice is to include a CK in the complete metabolic panel in college health centers (2).
Finding few cases of ER (only 21 in 13 years), these authors could not compare incidence rates over time. But 80% of the ER cases occurred in the last half of their study period, so they speculate that ER may be increasing or is being better recognized (1). In a recent study of hospital incidence of ER in Brisbane, Australia, the authors studied 89 cases of ER from early 2005 through 2016. They showed a steady increase in ER cases over those 12 years, which they attributed mainly to the increasing popularity of high-intensity gym workouts by weekend warriors (3).
ER in Our Military
ER also is increasing in our real warriors. Among active service members in 2018, there were 545 incident cases of ER, for an incidence rate of 42 cases per 100,000 person-years, or >20 times greater than the rate for civilian men in the Mayo Clinic study. This partly reflects the greater intensity of military exercise. Risk factors for ER in the military include younger age, male sex, lesser fitness, prior heat illness, and exertion in the warmer months of the year. New recruits, who are not yet accustomed to the physical exertion required of basic training, may be at particular risk. Most cases of ER occur at installations that train recruits in the Army or Marine Corps.
Annual cases of ER increased from 2014 to 2016, dipped slightly in 2017, but rose to a peak in 2018. Annual incidence rates of ER in black service members were higher than in other race/ethnicity groups in 4 of these 5 years, which was attributed, in part, to a greater risk of ER associated with sickle cell trait (SCT). More on this below.
The military calls for greater awareness and preventive actions by commanders. The risk of ER can be reduced, the military advises, by taking into account fitness and fatness, by emphasizing graded, individual preconditioning before starting more strenuous training, and by adhering to recommended work/rest ratios and hydration schedules, especially in hot weather (4). Indeed.
SCT and ER
In a recent study by Army and Stanford epidemiologists, of nearly 48,000 black soldiers tested for SCT and followed up on active duty for 4 years, SCT was not associated with a higher risk of death, but was associated with a roughly 50% higher risk of ER (5).
There are two big problems with this Army study. First, the authors somehow missed some exertional sickling (ES) deaths during their study. Second, they studied “the wrong population.” These soldiers were screened for SCT only after they had completed basic combat training (BCT), the time of greatest risk of ES death. These SCT soldiers are the “survivors;” despite SCT, they survived BCT. So you would expect their risk of ES death to be very low during the rest of their Army career (6). This study is misleading because ES death is still a huge problem in the military. More on this below.
First, a quiz. Twelve black football players at Howard University were hospitalized for heat illness and ER over 23 years; 10 of them in August, at the start of football practice when players were more apt to be detrained (7). One had SCT. All responded to conservative treatment and returned to football. But one had a peak CK of 110,000 IU·L−1, nearly 18 times higher than the mean CK of the other 11 players. Can you guess which one had SCT?
And that's my pearl. Absent EHS or ES, the acute ER from just novel overexertion in otherwise healthy warfighters or athletes — whether individual or “team rhabdomyolysis” — never kills anyone. Or let me know if you can find even a single such fatal case in the medical literature. Yes, EHS can and does kill, but not from rhabdomyolysis. EHS kills with rhabdomyolysis, not from it. EHS kills from heat damage to brain, liver, and other vital organs. There is only one unique syndrome in all of sports and military medicine that kills directly from the rhabdomyolysis, and that is ES collapse, where the ischemic rhabdomyolysis can be so “explosive” that it can create a metabolic storm that can soon stop the normal heart (8).
It is important to do what we can to prevent garden-variety ER (from novel overexertion alone) in civilians, in athletes, and in soldiers, because such ER causes pain and misery. But only one type of ER can kill you: ES. Also, ES is still a huge problem in the military. In 2019 alone, up to eight U.S. military men and women and two potential British Army recruits died from ES, most collapsing in timed “fitness” runs of 1.5 to 2.0 miles. Ten military deaths from ES last year alone. Ten too many.
In contrast, we had 10 ES deaths in National Collegiate Athletic Association (NCAA) Division-1 football conditioning in the decade before we began (in 2010) the NCAA program of screening and sensible training precautions for SCT. But in the now decade of our NCAA program, only one such death, and in that ES death, the university admitted their negligence. This sharp reduction in the ES death rate in football is not only vital, but statistically significant by any test you choose. Maybe the Army can learn something from the NCAA.
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