Rehydration-related hyponatraemia occurs in about 13% of athletes [
2] making it a potentially difficult logistic problem (with tens of thousands of runners participating in high-profile marathons worldwide). The development of symptoms in acute hyponatraemia depends on the rate of fall of serum Na rather than the absolute degree of hyponatraemia [
3]. The osmotic gradient produced between the blood and the brain parenchyma may cause potentially lethal cerebral oedema by increasing the intracranial pressure, leading to tentorial herniation, depression of the respiratory centre and death [
3,
4,
8‐
10]. In presence of normal blood glucose levels there is no reason to give 5% dextrose (as happened in the present case) because the risk of brain oedema in the presence of hyponatraemia is increased. The level of hyponatraemia in the present case was relatively mild (130 mM) compared to other reported cases of hyponatraemic encephalopathy (Table
1). However, there are important differences in comparison with our case. Firstly, the patient reported by Garigan et al. [
9] and by O'Brien et al. [
10] was severely fluid-overloaded (9.46 liters of pure water over 90 minutes at one point) and arrived in the Emergency Room with a florid pulmonary oedema [
9]. Our patient received only 3 liters of isotonic solutions over 4 hours. Admittedly, the amount of fluid intake during the 4 hour run was not known, but his normal haematocrit on admission of 0.373 and his normal chest X-ray suggests that he was not in fluid overload. The other patient, reported by Ayus et al. [
4], died primarily because of mismanagement. She was treated with fluid restriction, a strategy for which there is no supporting data (A Arieff, personal communication).
Table 1
Death due to brainstem herniation in rehydration related hyponatremia.
[1] | F | 28 | Equatorian | Marathon | --- | Said she felt dehydrated, rubber-legged and fell to the pavement. She received rehydration. The time to brainstem herniation was not published. She lost consciousness prior to admission and died in hospital the following day. |
[9,10] | M | 18 | Alaska native (Inuit, Yupik) | Military marksmanship training at a temperature of 1190 F (43 C). | 121 | Dizziness, throbbing headache and nausea. With aggressive rehydration (at one stage, 10 U.S. Quarts/9.5 liter in 90 minutes) he started to vomit. Within four hours from the first symptoms, fixed and dilated pupils were recorded. A chest X-ray showed pulmonary oedema. In intensive care he developed sepsis and disseminated intravascular coagulation and died several days later of cardiac arrest. The postmortem showed diffuse cerebral and brainstem oedema, pituitary infarction [9] and hydrocephalus [10]. (Reference 9 and 10 refer to the same patient. Dr Karen O'Brien, personal communication) |
[4] | F | 32 | --- | Marathon1
| 117 | Details on symptoms or time course not published2. She developed nephrogenic diabetes insipidus and ws treated with fluid restriction. She died of cardiac arrest due to brainstem herniation. The autopsy confirmed brainstem herniation and showed pituitary infarction. (Dr Allen Arieff, personal communication) |
Present | M | In his 30's | Caucasian | Marathon | 130 | Light-headedness and headaches. After rehydration he started to vomit and afterwards suffered a respiratory arrest. The CT brain scan showed midbrain herniation into the foramen magnum and severe hydrocephalus (Figure 1A&B). Formal brainstem death testing was performed 16 hours after he collapsed. |
We therefore suspect that our patient may have already suffered from a SAH, producing substantial hydrocephalus prior to the race, thus allowing for only for a small degree of parenchymal brain swelling leading to herniation. It has been suggested that hyponatraemic encephalopathy be named Varon-Ayus syndrome [
11].