scott@vtx-cpd.com

Replying to Areti Tsioka 10/06/2021 - 16:07

That is really disappointing.

You did all the right things with this case. I think you are right, sounds like there were lots of concurrent issues.

Scott 🙂

Sorry for delay!

I will get that uploaded!

Scott 🙂

Hello.

Lovely to hear from you. I hope you are safe and well. I am sorry about the delay in getting back to you. The new website and all!

What dose is the dog on currently? Would you be able to share most recent bloods and the Freestyle results with me?

scott@vtx-cpd.com

Thanks.

Scott 🙂

HAHAH!

Sounds like you are doing all the right things!

USG is really low and you are right… there could be more than one thing going on:

Tumors of the hypophysis as the cause of both Cushing’s syndrome and diabetes insipidus in dogs

Abstract

Invasive tumors of the pituitary gland associated with Cushing’s disease and diabetes insipidus are described in ten dogs. All patients showed typical clinical symptoms including polyuria/polydipsia and acanthosis nigricans. All tumors led to compression and partial destruction of the posterior lobe of the pituitary gland and the infundibular stalk; two of them infiltrated the hypothalamic region. All tumors produced ACTH and caused hyperadrenocorticism. In six cases, additional expression of beta-lipoprotein and MSH were found: in pars intermedia adenomas many cells stained strongly for MSH and/or beta-lipoprotein, whereas in tumors of the pars distalis only occasional cells stained positive. The purpose of the present study was to describe the neuropathological findings and the immunohistochemistry of hormone excretion in pituitary tumors in dogs resulting in Cushing’s disease associated with D.i., to review the literature and to discuss the pathogenesis.

Hey.

Hope you are well.

How did you get on with this case?

Scott 🙂

Lessons are available for 6 months! You have plenty time!

Urinary corticoid excretion, determined from a morning sample, is a reflection of adrenal glucocorticoid secretion over a period of several hours, negating concerns regarding fluctuating blood concentrations. Several studies have demonstrated UCCR as a sensitive screening test (nearly 100%) but with low specificity (20-77%). Due to its sensitivity, UCCR is a good test for ruling out HAC, since a normal result makes the diagnosis extremely unlikely. Since the UCCR is non-specific and increased in dogs with various conditions, further testing is warranted if the UCCR is increased in a dog suspected of HAC. In some studies… dogs with PDH tend to have higher UCCR values than those with FAT and if >100 (reference range, <10), the probability of PDH is 90%.

Scott 🙂

Hello.

I hope you are both well. I totally agree. I still think we know so little about the toxicity. Jenny spoke about the values/minimal amounts reported. Regardless, I think we have to treat every ingestion seriously. I would induce emesis and start IVFT if it was my dog!

My question is… would you be happy making vomit and send home?

Scott 🙂

Hello.

Thank you as always for your questions. Sorry for the delay in getting back to you. I have answered below your questions:

1)With regards to iv fluids, is there a rate of iv fluids (e.g 2xmaintainance, 3x maintainance etc) or a type to calculate how much should replace?

I think it is always important to address dehydration and hypovolaemia separately. Treatment of hypovolemia should be finished within 1-2 hours of presenting to the hospital. This type of resuscitation routinely requires rapid administration of large volumes of fluids intravenously. These are “shock boluses” of replacement crystalloids: 40-50 mL/kg for cats, 20-90 mL/kg for dogs (see below). Typically, I would give a portion (1/3 or 1/4 dose) of the total volume and then reassess endpoints of resuscitation to determine if more volume is truly necessary. After this initial resuscitation, I would calculate a fluid plan based on % dehydration and body weight. I would administer this volume over the next 6-12 hours.

2)With regards to dextrose, do you give like a CRI added on fluids or d you give it straight into the vein and how much?

In these cases, I would only use dextrose as a CRI if the hypoglycaemia is persistent and severe. I would normally give a bolus A dextrose bolus (0.25-0.5 g/kg, diluted 1 : 3) can be given IV.

3)In dogs with atypical HA that require only glucocorticoids p.os , what dose do you use?

Prednisolone can be administered at a relatively high dosage of 0.5 mg/kg PO q 12 h for 2-3 days. Following these first few days, the prednisolone dosage can be quickly decreased to physiologic needs (0.1-0.2 mg/kg PO q 12-24 h).

4) in dogs which require zycortal, do you give p.os prednisolone only until day 3 after diagnosis and then stop and use only in crisis or do they maintained on prednisolone on daily basis but on low dose?

They do need to be maintained on prednisolone but at the lowest possible dose (see above).

5)and last question, you mentioned about a cut off point of 55nmol/l in order to exclude hypoadrenocorticism, but then if post ACTH is between 27-55nmol/l then this not neseccarilly means hypoadrenocorticism, could you please explain this a bit further? I had a dog examined today with basal cortisol of 33.9nmol/l (so less than 55) and i am going to do an ACTH test in 2 days. What result should i expect to diagnose hypoadrenocorticism? If it is still below 55 but above 27 is this not compatible with hypoadrenocorticism?

You are looking for the lack of stimulation ultimately. Many hypoadrenocorticism cases are consistently below the detectable limit. If there are not (as in your case) you are looking for the value not to change (flatline).

Send me the result when you get it!

Scott x