Overdrinking-induced hyponatraemia in the 2007 London Marathon

Abstract

We report a case of overdrinking-induced hyponatraemia from the 2007 London Marathon. The patient was a 37-year-old experienced female marathon runner. She was brought to the emergency room more than 6 h after completing the marathon suffering from diarrhoea, vomiting and confusion, and was unable to recall any detail of the race. An arterial blood sample confirmed hyponatraemia ([Na⁺] 117 mmol.l⁻¹) associated with hypokalaemia (serum potassium concentration 3.4 mmol.l⁻¹) and respiratory alkalosis (pH 7.62, bicarbonate 16.1 mmol.l⁻¹ and Pco₂ 2.14 kPa). A diagnosis of uncomplicated exercise-associated hyponatraemia due to voluntary overdrinking was made and the patient was catherised and treated with a slow (1 h) intra-venous infusion of 500 ml of 1.8% sodium chloride (NaCl) solution. The following morning her serum [Na⁺] had normalised at 135 mmol.l⁻¹ and she was discharged in the afternoon. She has recovered fully without sequelae.

BACKGROUND

Exercise associated hyponatraemia (EAH) first described in 1985,¹ has become increasingly prevalent in the past decade^2,3 and may cause sometimes fatal cerebral and pulmonary oedema.⁴ The condition is caused by the over-consumption of fluids during and after exercise,⁵ associated with impaired diuresis.⁶ We report a case of EAH occurring at the 2007 London Marathon to highlight the preventable nature and the important diagnostic features of the condition. It remains of concern that this potentially fatal condition continues to occur even though it is entirely preventable.^7,8

CASE PRESENTATION

A 37-year-old otherwise healthy female (height 1.57 m; weight 51 kg; BMI 20.7) was brought to a hospital emergency room some 6 h after she had completed the 2007 London Marathon in a time of 4 h 35 min. She had run three previous marathon with a best time of 3 h 38 min. During the race she had suffered from episodes of diarrhoea and vomiting and had finished in a mild state of confusion. Her level of consciousness had fallen progressively after the race, mandating hospital admission. On presentation in the emergency room, she was confused and agitated, with her legs moving continuously, mimicking the running motion. On questioning, she could not recall any detail of the race, which she believed she was still running. Nor could she describe the volume of fluid she had consumed, although her partner who had been with her before and after the race was convinced that she had followed her normal drinking strategy for the race. Her partner reported that her face looked bloated.

INVESTIGATIONS

On clinical examination, it was noted that although the patient was not clinically oedematous and even though she was not wearing rings her hands appeared swollen. Her heart rate was 95 b.min⁻¹, supine blood pressure 112/73 mm Hg, respiratory rate 28 br.min⁻¹, tympanic temperature 37.2°C and Spo₂ 96%. The lung fields were clear and there were no added heart sounds or murmurs. An initial venous blood sample revealed hyponatraemia (serum sodium concentration [Na⁺] 121 mmol.l⁻¹) with low osmolality (245 mOsm.kg⁻¹). In addition, venous chloride (82 mEq.l⁻¹), magnesium (0.61 mmol.l⁻¹) and calcium (2.06 mmol.l⁻¹) concentrations were low, and there were high concentrations of creatinine (86 μmol.l⁻¹), amylase (U.l⁻¹), alanine aminotransferase (U.l⁻¹) and creatine kinase (5140 U.l⁻¹). An arterial blood sample confirmed the hyponatraemia ([Na⁺] 117 mmol.l⁻¹) associated with hypokalaemia (serum potassium concentration 3.4 mmol.l⁻¹), and respiratory alkalosis (pH 7.62, bicarbonate 16.1 mmol.l⁻¹ and Pco₂ 2.14 kPa). Arterial metabolite values were normal (1.4 and 7.0 mmol.l⁻¹ for glucose and lactate concentrations, respectively). A chest x ray was normal as was the rectal temperature (37.3°C). A suprasternal ultrasound investigation suggested an elevated cardiac output (11 l.min⁻¹).

DIFFERENTIAL DIAGNOSIS

A diagnosis of uncomplicated exercise-associated hyponatraemia due to voluntary overdrinking was made.

TREATMENT

The patient was catherised and treated with a slow (1 h) intra-venous infusion of 500 ml of 1.8% sodium chloride (NaCl) solution since a more concentrated sodium chloride solution was not available.

OUTCOME AND FOLLOW-UP

The patient’s condition improved rapidly. Within the first 2 h of treatment she passed more than 2000 ml of urine and her serum [Na⁺] improved to 125 mmol.l⁻¹. Her mental state also improved, although she was easily distracted. Even though she received no further treatment, she continued to pass large volumes of urine throughout the night. The following morning her serum [Na⁺] had normalised at 135 mmol.l⁻¹ and she was discharged in the afternoon. She has recovered fully without sequelae.

Follow-up investigation revealed that the patient had drunk excessive fluids during the race. In her previous marathons she had followed a strategy (as advised by fellow experienced marathon runners) to begin the race “well hydrated” (drinking greater volumes than her thirst dictated) and take on a small volume of water or sports drinks at each drinking station, and had suffered no ill effects. On this occasion she had consumed larger volumes at each station because she thought this necessary in the high temperatures. She also noted that the increase in the number of competitors running (making it difficult to break from the mass) intensified her perceptions of heat. Her understanding, based on advice from fellow marathon runners and running publications was that heat stress was the primary risk and she had never perceived water intoxication as a real hazard. Warnings were issued over the public address system at the race start relating to ensuring a high intake of fluids was maintained.

DISCUSSION

Exercise-associated hyponatraemic encephalopathy (EAHE) is a potentially fatal condition that is caused by voluntary overdrinking during exercise.⁸ Since the cause has been established since at least 1991,⁹ the condition should not continue to occur especially in big city marathons such as the London Marathon which has access to the very best medical expertise and knowledge about the physiology of marathon running. However, in addition to the case reported here, another runner in the 2007 London Marathon reportedly died from EAHE.¹⁰ That death was the first reported from EAHE since 2003.¹¹ Besides the confirmation that a preventable potentially-fatal condition continues to occur in a major European marathon race,^2,11 the case highlights three additional lessons.

First, the condition is due solely to excessive fluid consumption before, during or after exercise. During the first 12 h of her recovery, the patient passed more than 4 l of fluid while receiving only 500 ml of fluid and 150 mmol of Na⁺ intravenously. A fluid excess of this magnitude is frequently measured in patients whose serum [Na⁺] concentrations are below 122 mmol.l⁻¹.^9,12

Second, the patient’s choice to drink so much during exercise was likely driven by the prevalence of the “importance of drinking” message at the race. Prior to the start of the race and at drinking stations competitors were instructed not to waste fluids (drinks were 330 ml volumes) by pouring them over themselves or throwing them aside after sipping because race organisers were concerned that drinks would run out. In particular, runners are advised to drink “as much as tolerable” and to “stay ahead of thirst”. In addition, because of the unseasonally warm weather, runners in the 2007 London Marathon were advised to ensure a high fluid intake even though there is no evidence that fluid ingestion plays any role in the prevention of heatstroke or collapse during or after exercise.¹³

The 2007 London Marathon was the hottest in its 27-year history with temperatures peaking at 23.5°C. There were also 30 seconding stations and 250 000 litres of fluid available during the race. With in excess of 9 l of fluid available for each competitor (and a clear message from the race organisers that this was likely to run out), it is perhaps understandable why overdrinking is possible (and perhaps likely) under these conditions.

Evidence that the patient was overdrinking during exercise should have been noted from her diarrhoea and vomiting. She suffered episodes of diarrhoea and experienced sloshing sensations in her stomach during the closing miles of the race. She was assisted by race stewards in the final part of the race as she was obviously in some distress and proceeded to vomit clear fluids on regular occasions (approximately every half hour) following the race. Due to crowds around the finish area it took a long time for her and her partner to walk to transport back to the hotel and episodes of vomiting were severe enough that she was seen and rested at a race first aid station. The continued consumption of fluids was because she believed her symptoms were the result of heat stress rather than fluid excess. The warnings regarding the problems of dehydration and heat stress led her to drink regardless of symptoms both during and following the race.

Third, the diagnosis was made immediately on the basis of a high index of suspicion. As a result, her serum [Na⁺] was measured on hospital admission so that the diagnosis could be made early before inappropriate and potentially lethal treatment, in particular the administration of intravenous fluids at high flow rates to treat a fictitious “dehydration”.^11,14 Instead, the patient received appropriate treatment with the slow intravenous infusion of 1.8% NaCl solution. Seigel and colleagues have also reported the effective use of intravenous hypertonic solutions, and advocate 3% NaCl for the treatment of EAHE.^6,15

In summary, the exhortation that athletes should drink beyond thirst and “as much as tolerable” places some at risk of fatal EAHE. This case shows that even in races held in sophisticated European countries, this completely preventable condition still continues to occur. In contrast, in scientifically-less advanced countries like South Africa and New Zealand, the condition has been eradicated⁸ by simple but effective messaging that encourages athletes to drink according to the dictates of thirst and not according to the guidelines promoted by the sports drink industry and its marionettes.⁷

LEARNING POINTS

• The hyponatraemia was caused by overdrinking.

• Participants may be prone to over-consumption of fluids because of the “importance of drinking” message propagated at endurance events.

• Assessment of sodium status is vital in avoiding inappropriate and potentially lethal treatment.

• Educating sportspersons to drink according to the dictates of thirst is vital in eradicating this entirely avoidable condition.