A recent coroner’s finding about the death of a Tasmanian bushwalker has reinforced the need for awareness of Exercise Associated Hyponatraemia, particularly in those participating in prolonged exercise and ultra-endurance events.
What is EAH?
Exercise associated hyponatraemia is a condition of low blood sodium (salt) levels which can occur with exercise. It can cause people to be severely unwell suffering confusion and seizures and can even cause death. It usually occurs with prolonged exercise but there have been cases of people requiring treatment in Intensive Care from EAH in events as short as 10km (running).
What causes EAH?
In general it is due to one or both of overdrinking and excess ADH (a hormone) production.
- Overdrinking – If people over drink, the relative concentration of sodium in the blood drops. People often think that drinking electrolyte solutions protects against this however as these drinks all contain sodium concentrations less than our blood then we will still dilute blood sodium levels by overdrinking them. There is some evidence that drinking fluids containing salt may actually increase our desire to over drink.
- ADH is a hormone that regulates body water. Excess ADH is produced when we are exercising, stressed, at altitude and in extremes of cold and (especially) heat; and causes us to retain water (become ‘waterlogged’). This is important as people with low urine volumes are often assumed to be dehydrated but this is not necessarily the case. Although somewhat difficult to measure there is now good evidence of the role increased ADH production plays in EAH.
- Salt loss. In longer (eg. 100mile ultramarathon) events sodium loss from sweat becomes more important though how best to replace these losses is poorly defined. It is possible in these very long events to have EAH with dehydration. Data from the Western States 100 mile event suggests that (when defined as >3% weight loss) over 30% of athletes with EAH were dehydrated.
- Other proposed mechanisms include lack of salt/sodium stores in bone and cartilage. Atrial Naturetic Factor/Peptide (ANF) may also be important.
What are the risk factors for EAH?
There are several risk factors including over drinking, female, slower finish time, lower body weight, inexperience, extremes of heat and cold and consumption of NSAIDs (non-steroidal anti-inflammatories). Availability of hydration is a risk factor ie. More drink stations leads to increased risk. Examples of drink station placement guidelines for events are in the 2007 EAH consensus statement (eg. 5km for a standard road marathon). There is a role for obtaining pre, during and post race weights in longer events.
What are the symptoms/signs of EAH?
People often quote nausea, vomiting, headache, fatigue, puffiness and bloating as early symptoms however none of these are specific to either EAH or overhydration. Obviously anyone who has confusion or a seizure is very unwell and could have EAH. In situations where scales are present a persons’ weight can help assessment of hydration levels. When people exercise they metabolize carbohydrates and actually produce water so it is quite normal to lose a small amount of weight (1-2% of body weight during a marathon) whilst still being ‘normally’ hydrated. A person who is thirsty, has infrequent very yellow urine and has lost 3kg is most likely dehydrated. A person who isn’t thirsty and has gained 2kg is likely overhydrated and much more at risk of EAH.
In longer events (eg. 100 mile ultramarathons) the correlation between hydration and sodium levels becomes a lot more complicated due to the prolonged loss of sodium through (especially) sweat.
How do I prevent EAH? – The main message.
The easiest method is simply to ‘drink to thirst’.
It’s why we have the thirst mechanism! Avoid any ‘hydration rules’ (eg. mls per hour). Gaining experience in your own hydration assessment is important. How much fluid do you need during training sessions? How much weight did you lose? What is your urine output and how did you feel? Avoid using NSAIDs. The most important thing is to be aware of and educated about EAH. For race directions and trek leaders consideration must be given to participant education about EAH and hydration issues as well as availability of hydration stations and access to medical care including sodium level testing.
Treatment of EAH.
The most important step in treatment is recognition. The 2007 EAH consensus statement states medical directors of events should have access to onsite Sodium (Na+) analysis and hypertonic saline. Obviously this is difficult and many events simply do not have this. Under these circumstances education of medical of participants and medical personnel is even more important and logistics (including education/notification) for emergency transport systems to places of testing and treatment vital. With mild cases the usual treatment is rest, oral salty foods/solutions and restricting fluid intake until urination starts. With rest ADH should ‘switch off’ and the athlete should simply void/urinate the excess water. Note that people can initially deteriorate post race due to a number of factors including delayed water absorption from the stomach/gastrointestinal tract.
In severe cases onsite Sodium testing and treatment with hypertonic saline (3% HTS) is the gold standard.
3% HTS is given as 100ml boluses (repeated up to twice, 10mins apart) with each bolus rising serum sodium by 1-2mmol. Note that no cases of central pontine myelinosis (a neurological complication) have occurred with this method – this can be a concern with rapid correction of sodium in non-excersie associated and chronic hyponatraemia. It is important to note that treatment with Normal (0.9%) Saline carries significant risks and is not advised. Although this fluid carries a higher Sodium concentration that plasma a patient with ADH still “switched on” will simply lose the salt through urine and retain the water. This increases risk of seizures/coma/death so advice is to use 3% HTS and not Normal saline. There are several cases of athletes with both EAH and rhabdomyolysis (muscle breakdown leading to renal failure); and in these circumstances the treatment is a little more complicated!