scott@vtx-cpd.com

Replying to Kathryn B. 23/10/2022 - 20:13

Hello again!

I’m this case you would definitely treat the potassium regardless. Depending on the underlying condition, IVFT is often enough to treat some cases. We were worried about the cardiac consequences in this case.

Calcium infusions are considered “cardioprotective” in severe hyperkalaemia, even though they do not change the circulating potassium concentration. Hyperkalaemia raises the resting membrane potential, and providing additional calcium raises the threshold for depolarization, re-establishing a more normal ionic gradient across the cell membrane. IV calcium gluconate (50 mg/kg slow IV over 10-30 minute period, given to effect) is a logical first-line treatment for severe hyperkalaemia in these patients.

If severe hyperkalemia persists following 6-8 hours of fluid therapy or if bradycardia is profound, IV dextrose can be administered. Glucose stimulates insulin secretion, which moves K from the extracellular fluid into cells, quickly decreasing circulating K concentrations. If dextrose administration alone fails to decrease the K, IV insulin can be safely administered. When insulin is administered, glucose must be monitored closely to ensure that hypoglycaemia can be quickly identified and treated, if needed. Severe hypoglycaemia at admission or after insulin administration should be addressed with adequate glucose added to the IV saline to create a 5% dextrose solution. Alternatively, a dextrose bolus (0.25-0.5 g/kg, diluted 1 : 3) can be given IV. It is important to remember that glucose administration may cause transient hyperglycaemia. Hyperglycaemia, in turn, causes serum Na concentrations to measure low because the increasing glucose concentration results in fluid shifting to the extracellular space, diluting Na. In the very unlikely event that acidosis is severe (pH < 7.1) and does not correct with fluid therapy, bicarbonate can be administered at increments of 1/4 (0.3 × base deficit × body weight in kg) every 20 minutes while monitoring venous pH. We did do an ACTH stim in this case... https://ibb.co/MZv0WrB

Addison's indeed! But for me the big learning point was the crazy potassium!

Scott 🙂

Replying to Andrea Scott 01/11/2022 - 20:26

Hello.

Hope you are well.

The session will be edited and uploaded ASAP. Andy will pop out a post/message when it is avaiable.

It was a great session, so definitely worth watching back.

Scott 🙂

Replying to Clare McConville 01/11/2022 - 11:30

It made my day to see you pop up here!

Yes, please to continue to ask questions when you get round to watching the sessions.

Happy to help in any way we can.

Scott 🙂

Replying to Kathryn B. 26/10/2022 - 20:00

Great questions!

Let me speak to the nutrition lot and get back to you ASAP!

Scott 🙂

Replying to Helen S. 25/10/2022 - 10:27

Hello Helen.

Thank you so much for this, really interesting.

We can maybe chat through the DISC profiling at the next Q&A?

Thanks again.

Scott 🙂

Replying to Kathryn B. 23/10/2022 - 20:13

My exact reaction!

My first thought was indeed, is this compatible with life!!!! I discussed the following wit the clinet first:

Pseudohyperkalaemia – translocation of potassium from cells post-collection
Asian dog breeds (Akita, Shiba Inu, Jindo, Chow Chow, Shar pei)
Haemolysis
Delayed serum separation
Markedly increased platelets or white blood cell count

Artifact:
Collection from IV line where potassium was administered
EDTA contamination

The sample was run again on the same machine with the same result. The sample was then run at another practice and at the reference lab and was indeed real!

The DDX for high potassium are as follows:

Decreased potassium excretion
Hypoadrenocorticism (Addison’s disease)
Acute anuric or oliguric kidney failure
Urinary obstruction or ruptured bladder
Hypoaldosteronism
Drugs (e.g. ACE inhibitors, trimethoprim, spironolactone)
Selected gastrointestinal diseases (e.g. whipworms, salmonellosis, perforated duodenal ulcer)
Potassium translocation from intracellular fluid to extracellular fluid
Metabolic acidosis due to increased organic acids (e.g. ketones, lactate)
Diabetes mellitus with hyperosmolar syndrome
Tissue necrosis, severe
Acute tumour lysis syndrome
Reperfusion syndrome
Aortic thromboembolism
Rhabdomyolysis/muscle necrosis (e.g. post-seizure, strenuous exercise)
Hyperkalaemic periodic paralysis
Post-exercise in hypothyroid dogs (mild increase)
Increased intake
Administration of potassium rich fluids
Dietary excess
Pleural effusion and ascites

As you mentioned, many of these DDX are ruled out from examination etc. My other big concern was the low sodium. I thought an ACTH would be sensible!

Will update soon!

Scott 🙂

• This reply was modified 2 years, 10 months ago by scott@vtx-cpd.com.

Replying to Inga-Lill F. 21/10/2022 - 14:06

Hello Inga!

Welcome. It sounds like you have had a very interesting career. Thank you for joining the course.

Allocated CPD time sounds amazing! We need more of that in the world. I think we are all so keen to learn more… fining the time is the problem!

Scott 🙂