Article Text
PDF
Abstract
The case histories are presented of four athletes taking part in a 95-mile ultra-endurance foot race in Scotland who were hospitalised after developing exercise-associated hyponatraemia and rhabdomyolysis. Exercise-associated hyponatraemia is relatively uncommon in temperate climates. Risk factors disposing to this disorder are discussed. Exercise-associated hyponatraemia is thought to be due to overconsumption of hypotonic fluid with other associated pathophysiology including an inability to suppress fully antidiuretic hormone during exercise or to mobilise adequate sodium from osmotically inactive internal stores. Non-specific symptoms make this disorder difficult to diagnose on site without the assistance of serum sodium measurement, but any delay in treatment of patients with encephalopathy can prove fatal. Mainstays of treatment include fluid restriction, hypertonic saline, loop diuretics and mannitol.
Statistics from Altmetric.com
The hazards of ultra-endurance exercise are many.1 We describe a series of four athletes competing in the West Highland Way Race in Scotland between 2005 and 2007 who suffered from exercise-associated hyponatraemia (EAH) and rhabdomyolysis. The race had passed uneventfully since its inception in 1991. As far as we are aware, there are no previously reported cases of EAH in the temperate climate of Scotland. Emergency and critical care personnel should be aware of the difficulties in diagnosing these disorders and the serious risk of harm to the athlete.
Case reports
The West Highland Way Race is a 95-mile off-road running race which takes place annually in mid-summer.2 It begins near Glasgow and finishes in Fort William, including 14 000 feet of ascent and descent. Around 75% of the highly trained participants complete the race, exercising continuously for 15–35 h. Typically, in 2005 temperatures varied from 15.9°C to 21.5°C with humidity of 60%, partial cloud cover and 0.4 h of sunshine.
Athlete A, a 32-year-old man, was withdrawn from the race at 75 miles (23 h) due to adverse weather. Half an hour following withdrawal he suffered a seizure. He remained confused and agitated on arrival at hospital. He was diagnosed with exercise-associated hyponatraemia with encephalopathy (EAHE) and rhabdomyolysis with mild renal impairment. Treatment included intravenous fluids, diuretics and invasive monitoring and he improved over the next 72 h with no further deterioration in renal function. Table 1 shows the relevant blood tests on admission to hospital in all affected athletes.
Hospital admission blood results for all four athletes
Athlete B, a 47-year-old woman, suffered a seizure 15 min after completing the race in 27 h. Diagnoses were EAH and rhabdomyolysis without renal impairment. She required observation in hospital for 72 h and was then discharged.
Athlete C, a 36-year-old man, completed the race in 23 h and then developed persistent vomiting lasting for 12 h. Serum sodium was marginally subnormal. He had rhabdomyolysis and acute renal failure which did not require renal replacement therapy.
Athlete D, a 41-year-old man, completed the race in 20 h and developed vomiting several hours after completion. He presented with diagnoses of EAH and rhabdomyolysis with acute renal failure. His recovery was complicated by pulmonary and peripheral oedema but he did not require renal replacement therapy.
Discussion
EAH is defined as a serum sodium level below the normal reference range (usually 135 mmol/l) in an individual engaged in prolonged physical activity.3 It may or may not be associated with symptoms and was first described in 1981 in South Africa.4 There have been at least eight reported deaths in athletes as a result of EAH.4
It is generally accepted that the principal cause of EAH is excess intake of hypotonic fluid during exercise, resulting in a dilutional hyponatraemia with an increase in total body water and body weight.3 4 Other influencing factors may include retention of excess fluid due to inadequate suppression of antidiuretic hormone, similar to the syndrome of inappropriate antidiuretic hormone, or failure to mobilise osmotically inactive sodium from internal stores in bone and cartilage.5
Risk factors for EAH are many and include low body weight, prolonged exercise, slow speed of running associated with ease of drinking, access to fluids and female sex. Loss of sodium in sweat which is hypotonic in relation to plasma is not the primary cause of EAH but may be a contributing factor in some cases, especially in very hot weather.4
Athletes experience various non-specific symptoms with EAH including bloating, swollen extremities, nausea, headache and breathlessness which is due to pulmonary oedema. Progression to encephalopathic symptoms of confusion, seizures, coma and death may occur if untreated. Many of these initial symptoms occur normally following prolonged exercise and make diagnosis on site without the help of serum sodium measurement difficult.
Treatment of EAH is similar to that of any other acute onset dilutional hyponatraemia. In mild cases, close monitoring and fluid restriction until a diuresis occurs may be all that is required. In more severe cases the use of hypertonic saline (1–2 ml/kg of 3% saline hourly initially) will increase serum sodium levels.3 The rate of infusion should be closely monitored and can be decreased when a spontaneous diuresis commences. In cases with significant volume overload, loop diuretics and mannitol may be required with monitoring in a critical care setting and hourly measurement of serum sodium levels.
Footnotes
-
Competing interests None.
-
Patient consent Obtained.