scott@vtx-cpd.com

Hello.

Thank you again for your feedback and questions. These are really tricky cases, don’t beat yourself up!

1. Regarding the urine glucose. It may well be that even in the most stable cases that never completely disappears. Are there ketones in the urine too?

2. I would not be making any changes to the amount of insulin. I would then repeat the BGC in 2-4 weeks’ time. Make sure that feeding and insulin are as accurate as possible.

3. If it were not for the 2.9mmol/l BG, this would all indicate that you should be increasing the dose.

I think there is a good argument for then investing in a sensor. With the code of a sensor and then the owner using her phone app., this should keep costs down.

I will try and find a good placement resource and post it here.

Hope that helps.

Scott 🙂

Thanks so much for this other information. Really useful:

1) If a dog develops hyperglycaemia/DM due to acute pancreatitis can this be transient? Would the pancreatitis have to be so severe that clinical signs would be very obvious?

In a study of 80 dogs with severe acute pancreatitis, 29 dogs had concurrent diabetes mellitus (Papa et al. 2011), making the prevalence of DM much higher in this population than in dogs without acute pancreatitis. The relationship between these two conditions is complex and not totally understood. Overall, at this level and the persistent glucosuria, it is unlikely to be transient. I would definitely treat the DM (as you have done) in this case.

2) If you have a patient that you suspect may have HAC as well as DM what is the best test for HAC to use? Is it LDDST?

There is not a best test in this situation. Both the LDDST and ACTH stim can be affected by the concurrent disease. I would prioritize optimizing the insulin dose as much as possible and stabilizing the DM as a priority and HAC testing later. The HAC is a much more long-term concern. Once a bit more stable DM-wise and still wanting to test, I would do the LDDST.

What was included on the pancreatic panel? I will leave the diet question up to RC… I have no idea! Sorry. Let me know what they say though!

Scott 🙂

Hello Emma.

Hope you are safe and well. I think your comments above are really valid regarding pre-treatment. That is definitely a really important step. Otherwise, I would treat as any anaphylaxtic reaction. Thankfully I have not been in this situation many times either!

Initial treatment of a dog or cat with anaphylaxis consists of the basics of emergency medicine and the administration of adrenaline. A patent airway and effective breathing/ventilating should be confirmed immediately. Respiratory distress can result from upper airway obstruction, necessitating intubation with an endotracheal tube or tracheostomy if intubation is not possible. If respiratory distress without airway obstruction is present, oxygen should be administered by mask or flow-by during initial assessment and stabilization, and then by nasal catheter or oxygen cage. Hypovolemic shock is a significant contributor to morbidity and mortality in anaphylaxis. Hypovolemia occurs secondary to increased vascular permeability and venous pooling. Ongoing crystalloid therapy usually will be necessary at rates higher than maintenance to keep up with ongoing losses and will need to be tailored to the individual patient.

Regarding adrenaline (taken from Ettinger); traditionally, a dosage of 0.01 mg/kg given slowly IV is recommended, although 0.02 mg/kg can be given into the trachea if the patient is intubated and IV access cannot be obtained. A maximum dose of 0.5 mg IV for patients weighing >40 kg is recommended. Adrenaline also can be administered IM at a dosage of 0.01 mg/kg. Doses can be repeated every 5-15 minutes as needed. Adrenaline is useful because of its inotropic and chronotropic effects on the heart as well as vasoconstriction. Adrenaline also causes bronchodilation and increased intracellular concentrations of cyclic adenosine monophosphate, which decreases synthesis and release of inflammatory mediators of anaphylaxis. A single dose of adrenaline given IV, IM, or SC after maximal hypotension had developed did not produce a sustained improvement in hemodynamic parameters in a study on dogs with induced anaphylactic shock; only the IV dose produced a transient improvement (<15 minutes) in mean arterial pressure, stroke volume, and pulmonary wedge pressure. A later study of anaphylaxis induced in dogs showed that administration of adrenaline by constant rate intravenous infusion (CRI) was the only route that caused sustained improvement in hemodynamic parameters compared to the nontreatment group and the groups that received a bolus given IV, SC, or IM. The dosage used for the IV CRI was 0.05 mcg/kg/min. These studies suggest that adrenaline acts primarily as a vasopressor rather than specifically improving immunologic recovery. Consideration should be given to administering adrenaline as a CRI rather than an IV bolus.

Other medications that can be useful in the treatment of systemic anaphylaxis include vasopressors, glucocorticoids, antihistamines, aminophylline, and atropine. Dopamine at a dosage of 5-10 mcg/kg/min IV CRI or norepinephrine at a dosage of 0.01-1 mcg/kg/min IV CRI can be used if refractory hypotension is present. Vasopressin (0.5-1.25 mU/kg/min IV CRI) can be used if the patient is refractory to fluid and catecholamine therapy. Aminophylline or a selective beta2 agonist such as albuterol may be used if bronchoconstriction is refractory to adrenaline.

I hope that helps!

Scott x

Thanks so much for these great questions!

With the patient with pancreatitis… how high has the blood glucose been? How did the patient present?

What is the reason for testing for HAC in the case with DM and suspected HAC.

Sorry for answering with more questions, just want to make sure I give the right answer.

Scott 🙂

Interesting!

I understand what they, are saying, but it is still quite a significant result. Normally the portal vein hypoplasia cases do not have such significant increases in bile acids.

Was the bilirubin increased?

P.s. I am not disagreeing with them! It is just an interesting discussion!

Scott x

Areti!

So lovely to hear from you. Thank you so much for your questions as always.

I have popped some ideas under your questions below:

1)how long would you withdraw from meds causing lower T4 before consider testing for hypothyroidism?

It depends a little bit on the medication and the half-life of the medication. I would normally give a good couple of weeks free of medication before testing thyroid hormone levels. If there are any equivocal results I would wait a further 2 weeks and test again!

2)if you find elevated TgAA with normal fT4 what should you do? do you start tx or retest later on?

Positive TgAA results are associated with lymphocytic thyroiditis but may be present in the circulation long before a dog becomes clinically hypothyroid. As such, TgAAs provide no information on thyroid function. TgAA positivity, uncommon in dogs with non-thyroidal illness, is suggestive of underlying pathology. A positive TgAA does, indirectly, support a diagnosis of hypothyroidism. However, if the free T4 is normal I probably not treat at that point and re-test at a later time point as you suggest.

3) I am a bit confused with lymphocytic thyroiditis. Is it not the cause of hypothyroidism? or is it a concurrent condition? as on the chart of how to interpret results says if low fT4 and positive TgAA then lymphocytic thyroiditis with hypothyroidism. Are they not the same? (hope not silly question)

Acquired primary thyroid disease accounts for the overwhelming majority of dogs with hypothyroidism. The two main causes on a cellular level are lymphocytic thyroiditis and thyroid atrophy (equally common). Lymphocytic thyroiditis is a destructive autoimmune process characterized by multifocal or diffuse infiltration of the thyroid gland by lymphocytes, macrophages and plasma cells and progressive replacement by fibrous connective tissue. By contrast, idiopathic atrophy is described as a degenerative process with minimal inflammatory change and gradual replacement of thyroid tissue by adipose and connective tissue.

Ultimately both will result in hypothyroidism.

Lymphocytic thyroiditis is slowly progressive, causing signs of hypothyroidism after about 75% of the gland has been destroyed. Its progression can be divided into four stages. The rate of progression through these stages is variable, and not all dogs develop functional hypothyroidism. Approximately 20% of TgAA-positive euthyroid dogs develop hormonal evidence of thyroid dysfunction within a year of testing, but only 5% become clinically hypothyroid. Most dogs remain TgAA positive and asymptomatic, while a small number later test negative without evidence of thyroid dysfunction. Some TgAA-positive hypothyroid dogs later become TgAA negative, supporting the concept that thyroid atrophy represents an end stage of lymphocytic thyroiditis. Theoretically, the complete destruction of all thyroid tissue leads to a reduction in immune stimulation, absence of histologic thyroiditis, and conversion to autoantibody negativity.

Yes, low free T4 and positive TgAA are part of the same process and supportive of hypothyroidism. However, patients can be hypothyroid with a low free T4 without being positive for TgAA (see about). Please let me know if this is not clear.

4)would you start oral suppl. of T3 only if on higher end of dosage and no response or would you check for concurrent diseases first?

I would definitely check for a concurrent disease first. It would be very unusual to have to use T3 supplementation.

5)How do you support the diagnosis in breeds with lower circulating t4 especially in Greyhounds?

The key thing has to be compatible clinical signs and clinicopathological tests (is the cholesterol increased). TSH, free T4 and TgAA would then all be used to support a diagnosis. The fundamental thing would only to look for this condition in dogs with compatible clinical signs.

6)is there anything we can do in patients with congenital hypothyroidism? what is the prognosis/life expectancy?

With appropriate supplementation, they can do well and actually can have a relatively normal life. It all depends on how quickly the problem is detected as if not detected early, the growth abnormalities may be left as permanent changes.

7)and last question, when we say about concurrent illness, do we mean only serious diseases or could be anything like a simple infection on a nail base for example?

It really could be anything, definitely does not have to be a severe concurrent disease.

Thanks again for your questions. If any of this is not clear, let me know.

Scott 🙂