6/19 - Fiona to ER, but OK

[Sharyn & Fiona]

My vet wanted Fiona back this AM for more fluids but neglected to mention that to me. When we connected in afternoon, he said she would need fluids every 6 hours. Seemed to me that IV would be better. He said yes, 24 hours at least. Took her to ER leaving a $1200 deposit - ugh. Less than two hours later, ER Vet called to let me know that her potassium was so low it didn't even register and that Fiona rallied within minutes of receiving potassium - including eating. He's assumption was that I was giving too much insulin, he'd never shoot a 181 or a 215 (whatever!) and too much insulin depletes potassium - hmmm... I should be able to pick her up in the morning. YAY! I'm sure ketones are still an issue but they should be a lot lower when I pick her up.

Both ER vets said cats needed carbs to clear ketones. huh? I knew food but carbs? Did we know that? But I don't think "white" carbs - good carbs? ER Vet also said beware of injectable Baytril. Knew of cat that sloughed off skin reportedly cause by injectable Baytril. Anyone else hear of that?

Thanks for the snowflakes. They helped!

 

[Marje and Gracie]

Sending her more healing vines! I've not heard of issues with injectable baytril but dont know.

Too much Insulin depletes potassium? Cats need food to help with ketones....

All I can say is I hope she is better soon.

 

[Vyktors Mum]

Just had a bit of a google turns out insulin can deplete potassium

http://www.medicaltextbooksrevealed.com/files/11161-53.pdf

Patients with diabetes mellitus
Patients who present to hospital with acute diabetic ketoacidosis often
have normal or slightly raised potassium levels as the systemic acidosis
promotes the exit of potassium from cells into the extracellular
fluid. Treatment with insulin drives potassium back into the intracellular
compartment and the serum potassium level may rapidly fall
such that hypokalaemia is a real risk. These dehydrated patients typically
receive large volumes of intravenous fluid and are markedly
polyuric. They therefore require very close monitoring of serum potassium
level (2–4-hourly) combined with judicious potassium supplementation.
Patients with long-standing diabetes mellitus may also
develop a type IV renal tubular acidosis, which may lead to troublesome
hyperkalaemia. This often results in an intolerance to ACE inhibitors
and to renal replacement therapy being commenced slightly
earlier in diabetic patients than in patients with other causes of renal
failure.

However, as for the carbs, your vet seems to be confusing diabetic ketoacidosis with dietary ketosis. Ketones appear in humans who have very low carb diets (e.g. atkins diet) but it is not ketoacidosis and I can't see how that would apply to cats anyway - they are carnivores we are not.

 

[PeterDevonMocha]

Hi guys .. I don't have any answers for you but I am glad to hear fiona is feeling better and eating more! Continued get well thoughts sent her way!

 

[Michelle and Mannie (GA)]

No answers here, but I a also lad that Fiona is better.

 

[Dyana]

Sending healing vines and feel much better today vines, to Fiona.

 

[Sienne and Gabby (GA)]

That kind of potassium level is terrifying! I'm glad Fiona is doing better.

Here's another explanation of the relationship between potassium and insulin:

Insulin is the first-line defense against hyperkalemia (high potassium). A rise in plasma K+ stimulates insulin release by the pancreatic beta cell. Insulin, in turn, enhances cellular potassium uptake, returning plasma K+ towards normal. The enhanced cellular uptake of K+ that results from increased insulin levels is thought to be largely due to the ability of insulin to stimulate activity of the sodium potassium ATPase located in cell plasma membranes. The insulin induced cellular uptake of potassium is not dependent on the uptake of glucose caused by insulin. Insulin deficiency allows a mild rise in plasma K+ chronically and makes the subject liable to severe hyperkalemia if a potassium load is given. Conversely, potassium deficiency may cause decreased insulin release. Thus plasma potassium and insulin participate in a feedback control mechanism. (From: http://www.uhmc.sunysb.edu/internalmed/nephro/webpages/Part_D.htm)

With DKA, potassium and phosphorus levels can shift with an eventual precipitous drop. This change in electrolyte levels is a large part of what makes DKA potentially so dangerous. My hunch is that by giving higher carbs, whatever insulin is there is being offset by the food and allowing potassium levels to get better regulated. In many cases, when a cat is being treated for DKA, they are getting insulin AND a glucose drip along with very gradual administration of the specific electrolytes that are needed. The glucose may be functioning to prevent too big a drop in BG levels but it also seems to be helping potassium to get back into the cells and thereby increase the potassium level.