So this is some interesting stuff – well, I think so anyway! I want to thank my good friend Kate Russell for raising this with me as well. The basic question at hand here is can a puppy drink so much water in a single episode as to cause water intoxication and a hyponatraemic seizure?
Before I get into that, a quick reminder about the theory around hyponatraemia. Essentially the clinical consequences are meant to be more related to the speed of onset than the absolute decrease. Sodium is the main osmotically active substance in the body:
- If hyponatraemia of sufficient severity develops quickly enough ((per)acutely) water will move out of the extracellular space into the cells of the central nervous system*; cerebral oedema occurs with subsequent neurological signs. These signs can vary but seizures are possible.
- If hyponatraemia develops more slowly (chronically) then the brain has time to ‘defend’ itself which it does by losing potassium and other osmotically active particles (organic osmolytes) from the cells; this means that there is less of an osmotic gradient and less tendency for water to move into the cells.
[*Remember ‘osmosis’? Essentially the tendency for water to move from an area of low concentration of osmotically active particles (more dilute) through a semipermeable membrane (like a cell membrane) to an area where there is a higher concentration of osmotically active particles.]
Back to the point
Phew. Okay with that theory out the way, what am I going on about in this blog? Well Kate recently saw a crossbreed puppy, a few weeks old, that by all accounts had been fine until the day of presentation; let me say from now, no other historical signs suggestive of a portosystemic shunt. On that day the puppy drank ‘a lot of water’ and then vomited a couple of times. In the hours that followed she worsened becoming more lethargic until shortly after presenting to the clinic 5 hours after drinking the water, she started to have generalised seizures. The most – and more or less only – noteworthy finding on emergency database blood tests was a marked hyponatraemia of 124 mmol/l (reference interval 139-150 mmol/l); mild hyperglycaemia – definitely no hypoglycaemia. To the best of my knowledge, plasma sodium concentration in a puppy of this age is the same as for adult dogs. Anticonvulsive therapy was implemented, the hyponatraemia was corrected, the puppy slept off the drugs (!) with no further seizure activity and as far as I know is doing fine now with no recurrence.
Kate and I are also aware of another case, that time a German Shepherd puppy, with basically exactly the same history/clinical story, diagnosed marked hyponatraemia presumed to be acute in onset, same therapy and the same progression.
So back to my question, did both these puppies drink so much water in a single episode as to cause water intoxication and a hyponatraemic seizure?
A few things to say from briefly exploring online but I guess overall I am saying that yes, in theory, this could be the case..it may not seem very probable but it certainly seems possible..to me anyway...you?
Acute water intoxication is meant to be more likely if for some reason the animal is unable to adequately excrete the excess water consumed. This was induced for example experimentally in dogs given vasopressin at the time of the water load. As far as I know puppies if anything have reduced urine concentrating ability relative to adult animals, i.e. they excrete more dilute urine, rather than retain excess water. So they should not be more prone to retaining excess water consumed.
There is one* clinical case in the literature of an adult Labrador retriever who developed acute hyponatraemia (125 mmol/l) and acute neurological signs (coma) after swimming for many hours in a lake. Marked diuresis occurred spontaneously and the patient recovered with supportive care. This suggests that the dog was able to suppress vasopressin (anti-diuretic hormone) release in response to the water load…so I guess maybe this response was delayed in onset, ‘took a while to get going’? Was this what occurred with our puppies? I am not aware of diuresis being noted in either case. But maybe the vomiting that followed the water consumption relatively caused them to lose more sodium than water??
[* Toll J, Barr SC, Hickford FH. Acute water intoxication in a dog. J Vet Emerg Crit Care 1999. 9:19.]
I did find some reports in calves that were given ad lib access to water for the first time where acute water intoxication led to clinically significant hyponatraemia; but actually red cell lysis due to changes in plasma osmolality with haemoglobinaemia/haemoglobinuria seemed to be the more notable development.
I did find plentiful mention of hyponatraemic seizures in human infants that were inadvertently given low solute drinks/feed at home, especially with concurrent vomiting/diarrhoea and hence sodium loss – but diving into the reports this was at least over a few days not a one-off episode.
Psychogenic polydipsia is one of the differentials for normovolaemic hyponatraemia – but there we are talking about recurrent episodes of excessive water consumption and a chronic hyponatraemia that can be acutely decompensated by a suitable trigger. These puppies mentioned above did not have that in their life stories.
I don’t think our puppies had syndrome of inappropriate antidiuresis.
There are also lots of reports of humans drinking too much water during endurance events resulting in clinically significant acute hyponatraemia – but again I believe this is over hours-days, multiple episodes of water intake.
Anyway, that’s me done. If I am over-complicating this, if anyone knows any references I have not uncovered, if anyone can shed any more light or discussion…as always, please do!
See further discussion about this HERE.