Venous thromboembolism (VTE) continues to be a problem — and may even be on the increase — in athletes. Ice hockey notably has had a rash of VTE. Meantime, we have made progress on preventing fatal exertional sickling in college football conditioning, but we have continuing challenges for athletes — and for military men and women — with sickle cell trait (SCT). Here is the story.
VTE in Ice Hockey
A young female professional ice hockey player developed influenza and missed a game while sedentary for a week. Then she awoke with left leg pain, swelling, rubor, and numbness. In the prior month, she had been on three plane flights for games. She was taking an oral contraceptive and was found to be heterozygous for Factor V Leiden.
Duplex venous ultrasound showed occlusive thrombus in the femoral-popliteal system, along with May-Thurner syndrome. No pulmonary embolism was seen. She underwent catheter removal and pharmacologic thrombolysis of the clot, then stenting of the left common iliac vein. She was begun on apixaban (Eliquis) and aspirin (81 mg daily). The question was: Can she safely play ice hockey while on anticoagulants? She was getting mixed advice.
Among athletes with VTE, females tend to be younger than males, and most of the females are on oral contraceptives (1). Among the general public, when female risk factors for VTE (pregnancy, oral contraception, postmenopausal hormone therapy) are adjusted for, the risk of a first VTE is twice as high in men as in women (2). By and large, VTE recurrence rate also is higher in men than in women. Among athletes with VTE, it is not unusual for the correct diagnosis to be delayed for days or even weeks (3). Delayed diagnosis of VTE also is common in the general public. This female hockey player was quickly diagnosed correctly.
VTE is a problem in ice hockey. In just the past decade or so, at least 12 male professional hockey players have had VTE. Five had effort thrombosis or thrombosis of the subclavian and/or axillary vein; at least three had rib resection for it. The other seven players had VTE that began in the lower extremity; several VTE cases followed hockey injuries to the foot or leg. Immobility and plane trips may have played roles. Some men had inborn thrombophilia, such as Factor V Leiden or protein C deficiency. VTE — including recurrences — ended the careers of some players. Some with bouts of VTE continued to play ice hockey — one played for years — trying to time anticoagulation (e.g., injections of low-molecular weight heparin) to wear off for games (4). All considered, VTE can be a major challenge for some ice hockey players.
The tough call for the female ice hockey player featured here was whether she could return to play on anticoagulants. Conventional practice is that collision sports — for example, football and ice hockey — are avoided on anticoagulants. However, some experts claim that medical advances could obviate this practice. They argue that the “fast on/fast off” profiles of the direct oral anticoagulants (DOAC) can change how sports medicine physicians approach anticoagulation. They say that after taking a DOAC pill, therapeutic anticoagulation occurs quickly (peak activity within 1 to 4 h) and the DOAC drugs are cleared rapidly (half-lives, 7 to 14 h). They propose a pharmacokinetic study, wherein the athlete ingests a DOAC and has interval measurements of plasma drug levels over 24 h. Then, they say they can figure out how long before the hockey game to stop the DOAC, and it can be restarted maybe 1 to 2 h after the game. They note that professional athletes may have the most to gain by continuing to compete and are more likely to be able to afford this “labor-intensive and costly” treatment plan (5).
I doubt this intermittent anticoagulation scheme will sweep the high school and college ranks of athletes. The professional hockey player here discussed all this with her sports medicine physician and clotting experts and decided not to play competitive ice hockey while on anticoagulants. Wise decision, I would think.
We have progress and challenges in exertional sickling. The vital progress is in college football, where the NCAA program for SCT has sharply and significantly cut the death rate from exertional collapse associated with sickle trait (ECAST). In the decade before this program began, there were 10 ECAST deaths in NCAA Division 1 football conditioning. In the near-decade now of the program — screening and sensible training precautions for SCT — only one such death, and the university at fault admitted their negligence.
Challenges remain, however, in high school and youth sports and especially in the US military, where ECAST deaths continue apace. In the past decade, similar to prior decades, I know of at least 13 deaths from ECAST in the military (seven Army, four Air Force, one Navy, one Coast Guard). Also, we do not identify all Army ECAST deaths, because the Army does not screen recruits for SCT. Early Army field research, misinterpreted, suggested that the trigger for ECAST death in recruits is heat and/or dehydration. The Army decided that all recruits — SCT or not — would be safe if they held back some and drank more water when training in the heat. This seemed to work for a while — few ECAST deaths — maybe only from the Hawthorne effect (6). In any case, after a decade of fewer deaths, the military ECAST death rate rose back to its former high baseline and has stayed there — up to 15 deaths per decade — ever since.
The latest military ECAST death was at Naval Station Great Lakes, in February 2019. A recent Air Force ECAST death also was in February. It is not hot on the Great Lakes in February. Nor was the Navy recruit likely dehydrated when she began the 1.5-mile fitness run. She collapsed near or at the end of that run and soon died in a nearby hospital. As we have reported, most military ECAST collapses occur during or after a timed fitness run (7). We can hope the military will come to understand that athletes or recruits with SCT can take the field fully hydrated, physically fit, and on a cool day, yet still collapse from exertional sickling if pushed beyond their limit. The trigger for ECAST is not heat or dehydration, but all-out exertion sustained for at least a few minutes.
The Air Force screens recruits for SCT. This enabled military researchers to compare results in their standard physical fitness test for recruits with and without SCT. Examined retrospectively was performance in >200,000 recruits from January 2009 to December 2014. Time to run 1.5 miles was used as a rough marker of aerobic fitness, and the maximal number (in 1 min) of push-ups and sit-ups was used as a rough marker of mainly anaerobic fitness.
After adjusting for key variables, recruits with and without SCT were similar in performance of push-ups and sit-ups, but SCT recruits averaged nearly 10 s slower in the initial 1.5-mile fitness run. The researchers concluded that SCT recruits had “slightly inferior aerobic fitness.” I do not buy this. More likely, I think, is that SCT recruits as a group were slowed by exertional sickling late in the run. It seems clear, studying the field as a whole, that exertional sickling occurs along a continuum, from mild to lethal. To their credit, the military researchers do pose this point (8).
A final point is that last year a quarterback in a military academy collapsed from exertional sickling in a 1.5-mile annual timed fitness run for which he had not specifically trained. He was being paced to hit a fast mark, and he collapsed near the end of the run. The pearl here is that even a top athlete can suffer ECAST if circumstances push him beyond his limit.
Thanks to fast action by a stellar athletic trainer and to good medical care in the hospital, this quarterback survived ECAST and even returned to football. Go Navy! Go Army!
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