CASE REPORT

An unusual cause of exercise-inducedhyponatremiaAdam MortonMater Hospital, Raymond Terrace, South Brisbane, Queensland, Australia

Abstract

A case of exercise-induced hyponatremia due to an unusual cause is presented.

Key words: cystic, fibrosis, exercise, hyponatremia.

Case report

A 48-year-old man became acutely confused and col-lapsed having played lawn bowls in 42 degree Celsiustemperature. His companions denied any intake ofalcohol or illicit drugs. His past history included hyper-tension for 4 years, gastro-oesophageal reflux, oli-gospermia attributed to undescended testis and Gilbertssyndrome. Medications were ramipril and esomepra-zole. On examination he was afebrile, Glasgow ComaScore was 15/15, mental state quotient was 5/10, pulsewas 100 per minute and regular, he was clinically hypo-volemic with blood pressure 120/80 mmHg lying and100/60 mmHg sitting. There was no focal neurologicabnormality. His biochemistry is presented in Table 1.Electrocardiography, chest X-ray radiograph, comput-erized axial tomography of his head and a short syn-acthen test were normal. The provisional diagnosis wasof heat exhaustion, he was treated with intravenoussaline, his mental state rapidly recovered and serumsodium the following day was 137 mmol/L.

He gave a history of recurrent similar episodes overthe preceding 30 years precipitated by exertion. Hedescribed profuse sweating after any exercise such thathis face became crusted with salt, and having to take

salt tablets to avoid cramps, nausea and presyncope.Family history was significant with two brothers, hisfather and five paternal uncles suffering similar symp-toms with exertion, and a sister dying of cystic fibrosisat age 18 years. His identical twin brother had appar-ently fathered three children and his father sevenchildren.

Pilocarpine iontophoresis revealed sweat sodium of103 mmol/L (normal 0–45) and sweat chloride of82 mmol/L (normal 0–45). Cystic fibrosis DNA study

Correspondence: Dr Adam Morton, Mater Hospital, Raymond Terrace, South Brisbane, Qld 4101, Australia. Email: adam.morton@mater.org.au

Adam Morton, FRACP, Senior Staff Specialist Endocrinology.

Table 1. Serum biochemistry on presentation

Normal

Sodium 124 mmol/L 135–145Potassium 3.3 mmol/L 3.2–4.5Chloride 86 mmol/L 100–110Bicarbonate 27 mmol/L 22–33Anion gap 11 mmol/L 5–15Creatinine 0.087 mmol/L 0.070–0.120Urea 6.5 mmol/L 3.0–8.0Urate 0.44 mmol/L 0.15–0.50Osmo (calc) 260 mmol/L 280–300Albumin 43 g/L 33–47Bili total 28 umol/L <20

doi: 10.1111/j.1742-6723.2007.00994.x Emergency Medicine Australasia (2007) 19, 377–378

© 2007 The AuthorJournal compilation © 2007 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine

detected a single Delta F508 mutation. Pancreatic andrespiratory function were normal. Further testing of thefamily revealed that an older sister was heterozygousfor Delta F508 mutation.

Discussion

Exercise-induced hyponatremia has been reported in18% of ultradistance runners in New Zealand, and 29%of Hawaii Ironman triatheletes. Hyponatremia withprolonged endurance activity is associated with inap-propriate antidiuretic hormone (ADH) release, withinappropriately high urine osmolality and sodium levelsand inappropriately non-suppressed levels of ADH.1,2

Risk factors include low body weight, female sex, pro-longed exercise duration, slow running or performancepace, race inexperience, excessive drinking behaviourand weight gain during events. Pain might be the causeof inappropriate ADH release with endurance sportsgiven inappropriate ADH release is also seen with otherpainful conditions including partuition, the postopera-tive state, varicella zoster, porphyria, burns and acuteneuropathy.3–8 One previous case of exercise-associatedhyponatremia has been reported in a 24-year-old infan-tryman who was heterozygous with DeltaF508 andR117H mutations.9 With the two presentations prior todiagnosis he was hypovolemic thus the diagnosis ofinappropriate ADH release could not be entertained.A 5-year-old boy has also been reported as presentingwith dehydration, acute renal failure and hyponatremiaduring a heat wave, and was found to be a compoundheterozygote for DeltaF508 and S1455X mutations.10

It would seem likely that our patient is a compoundheterozygote with a second undetected mutation toexplain his phenotype.

In conclusion, exercise-induced hyponatremia iscommon in prolonged endurance events, and related toexcessive fluid intake accompanied by inappropriaterelease of ADH. These individuals will be clinicallyhypervolaemic. In individuals with exercise-inducedhyponatremia who are hypovolaemic, have a history ofmultiple similar presentations, have a family history ofexercise-induced hyponatremia, or have a familyhistory of cystic fibrosis or male infertility, mutations in

the cystic fibrosis transmembrane conductance regula-tor gene should be considered and sweat chloride levelsmeasured.

Competing interests

None declared.

Accepted 12 March 2007

References

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8. von Bormann B, Weidler B, Dennhardt R, Frings N, Lennartz H,Hempelmann G. [Plasma-antidiuretic hormone level as indicatorof postoperative stress (part II) (author’s transl)]. Anasthesiol.Intensivther Notfallmed. 1981; 16: 319–22.

9. Smith HR, Dhatt GS, Melia WM, Dickinson JG. Cystic fibrosispresenting as hyponatraemic heat exhaustion. BMJ 1995; 310:579–80.

10. Epaud R, Girodon E, Corvol H et al. Mild cystic fibrosis revealedby persistent hyponatremia during the French 2003 heat wave,associated with the S1455X C-terminus CFTR mutation. Clin.Genet. 2005; 68: 552–3.

A Morton

378 © 2007 The AuthorJournal compilation © 2007 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine