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The Mystery of Swimming Deaths in Athletes

Eichner, E. Randy MD, FACSM

doi: 10.1249/JSR.0b013e318205e0f6
Pearls and Pitfalls

Address for correspondence: E. Randy Eichner, MD, FACSM, 321 Baudin Way, Sonoma, CA 95476 (E-mail:

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Swimming deaths of athletes in races can be shocking and puzzling. Two recent reports are vivid examples. First, in October 2010, Fran Crippen, 26, a medal-winning, open-water swimmer on the U.S. national team, died while competing in the International Swimming Federation (FINA) Open Water 10-k World Cup, in the Gulf of Oman, at Fujairah, east of Dubai (17). Second, in July 2008, three men, ages 32, 52, and 60 respectively, died in the swim portion of triathlons in the United States (4). From 2004 to mid-2008, among deaths recorded by USA Triathlon and including the three men above, 20 (80%) of 25 deaths were during the swim (4). So although triathlon deaths are rare, 1.5 per 100,000 participants (10), they occur disproportionally during the swim. We need to learn more about swimming deaths in athletes so we can better prevent them. This column considers the causes of these deaths.

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Exertional Heat Stroke

At this writing, the hypothesis for the death of Fran Crippen is drowning from exertional heat stroke (EHS). According to press accounts, the race was held in blazing heat - the water temperature was 84°F or higher, and the air temperature was nearly 100°F. Crippen told a coach on the last of five laps that he felt ill, but he was driven to finish. Other swimmers struggled in the race, the winner said it was too hot for racing, and three female swimmers were treated for dehydration and heat exhaustion. Two hours after the race ended, Crippen's body, goggles still in place, was found by divers, approximately 400 m from the finish line (6,9,15). His family said, on a death certificate they received, the cause of death was heat exhaustion and drowning (15).

Dehydration surely can occur in endurance swimming. During a 10-k swim we held in a pool on a warm day in Oklahoma, as research on exertional hemolysis, the swimmers drank ad hoc but finished dehydrated (14). Competitive adolescent swimmers are more dehydrated day-to-day than less active peers, and competitive male swimmers in an interval training session in moderate conditions can finish dehydrated and mildly hyperthermic (11,16). The conditions Crippen faced were extreme: he raced in hot salt water under a blazing sun. This may be the first time an elite swimmer has drowned because of EHS in a race.

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One would think some triathlon swimming deaths would be from heart attack. This seems to be true, as in the 63-yr-old man, a former college swimmer newly returned to the sport, who struggled in the 1.5-mile swim of the 2008 Alcatraz Triathlon, rolling over to rest several times, including 100 yd from the finish, where he stopped breathing and could not be resuscitated. Also, one of the three male triathletes who died in July 2008 died from hypertensive cardiovascular disease. But the other two died of accidental drowning (4).

Most swimming deaths in triathlons, however, seem not from heart attack. In a recent study of 13 such deaths from 2006 to 2008, drowning was declared the cause of death in each case. Nine had autopsies performed, and although one had a congenital coronary artery abnormality, one had a clinical history of Wolff-Parkinson-White syndrome, and six had mild left ventricular hypertrophy and increase in wall thickness (likely athlete's heart), the authors concluded that logistical factors (to be considered later in this column) and adverse environmental conditions may have caused the drownings (10).

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Swimming deaths have been tied to the long QT syndrome (LQTS). In a study of 35 LQTS cases, six had a personal or family history of drowning or near drowning (1). LQT1, from a loss-of-function mutation in a cardiac potassium-channel gene, is the most common LQTS. One third of the events in LQT1 occur during swimming (12). Syncope from LQTS is from torsades de pointes, and the deaths are from ventricular fibrillation. Swimming may trigger cardiac events in nearly 15% of children and young adults with LQTS, especially LQT1; the pathophysiology may involve sympathetic and parasympathetic stimulation from exertion, voluntary apnea, and cold-water face immersion (7).

In a study of 43 patients with a personal or family history of drowning or near drowning, 33 had likely LQTS, mainly LQT1, but some had another genetic channelopathy that triggers catecholaminergic polymorphic ventricular tachycardia (7). Therefore, at least two genetic channelopathies predispose to fatal arrhythmia while swimming. Although LQTS can be confirmed postmortem by genetic analysis of heart tissue, as in a young woman who drowned while swimming in a lap pool (2), so far no swim death in a triathlon has been tied to LQTS.

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Pulmonary Edema

Swimming-induced pulmonary edema (SIPE) theoretically could contribute to triathlon deaths. SIPE presents during or after a strenuous distance swim, usually in cold water, with dyspnea, cough, tachypnea, hemoptysis, confusion from hypoxemia, and physical signs of pulmonary edema. It seems most common in combat swimmers, where it may relate to swim posture. The Israeli navy described 70 cases of SIPE (in nearly 2% of all trainees) in a 3-yr period and speculated that the bilateral pulmonary edema was potentiated by swimming in a semi-supine (half-sitting) posture, using fins, with head and shoulders out of water (3). In contrast, three cases of SIPE in U.S. Navy combat swimmers who swam right-side down were unilateral, only in the right lung (13). The pathophysiology is multifactorial, with increase in cardiac preload and afterload, central blood pooling, and high capillary pressures in parts of the lung, breaking some capillaries and allowing egress of fluid and red cells into alveoli, as in galloping racehorses (3,19).

SIPE usually is not severe and reverses quickly with supportive therapy. Mild cases likely are underreported, and unlike combat swimmers, recreational swimmers may stop when symptoms are mild and self-limited. SIPE can recur, but swimmers also can change their style or early intensity to avoid it. SIPE can occur in triathletes (18), and one study of eight male triathletes found a decrease in diffusing capacity and increase in lung density (but not pulmonary edema) after a triathlon (5). But SIPE rarely is fatal - I found only two deaths reported, both in scuba divers (8) - and no triathlon swim death yet has been tied to SIPE.

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Triathletes may drown if they are knocked unconscious or suffer a panic attack. This was implied from the study of the 13 triathlon swim deaths (10), that "logistical and adverse environmental conditions may have been responsible for these events." The authors note that these deaths are more common in large triathlons that "begin with chaotic, highly dense mass starts." As one triathlete said, "Nothing can prepare a newbie for the start. It can be like jumping into a washing machine. You get swum over, kicked, hit, and banged into" (4).

Identifying distressed athletes and initiating timely resuscitation also can be a problem on open water (10). We may best prevent triathlon swimming deaths if we key on the consequences of chaos, trauma, and panic. Enhanced safety measures and a "no-start" rule when it is too hot to race also may prevent tragedies like the death of Fran Crippen.

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