scott@vtx-cpd.com

Hello lovely Inga,

I hope you are safe and well. I have popped some thoughts below:

1- I generally advise owners to inject as or after a dog is eating. If for some reason they have an off day and don’t eat or we are intentionally starving prior to surgery etc I advise to carry on but inj with half dose of insulin. was curious if you have a similar or different approach.

I would totally agree. We talk to our anaesthesia team a lot about this too. I would agree with the half dose if starving for a procedure or not eating for any other reason. I think it is important that if they are ‘sick’ for another reason and then do not eat, some insulin (1/2 dose) is still important. Obviously, prolonged sickness and anorexia would require investigation.

2- Have a couple of cases with very fussy toy breeds who were previously grazers. I have really struggled to get them to eat a 50% daily food ration in the morning to get their insulin and have one situation currently where the owner hand feeds some of the am ration to be able to inject then the dog has more at lunch and then normal 50% dinner and second injection. It means I cannot accurately check a trough BG level through the day but clinically the dog seems better with this approach. I just wondered for these fussy dogs do ever give a different insulin dose am and pm if meal rations is not equally split and should we relax a bit and just let them graze and inject 50:50 am and pm dose regardless…

This is a really interesting one. I certainly have seen a split/different dose regime used. I thnk it is hard to accurately dose insulin in this way. I think that as long as the dog is well clinically and DM signs have reduced/controlled, then I would allow them to graze! I would treat them more like a cat. This may not get the best control, but we have to be sensible too!

Scott 🙂

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