Simon Patchett

Hey Scott,

I had actually looked into do this for two kittens I was treating recently. On reading around I found the following from the shelter medicine section at the University of Maddison-Wisconsin

“As there is no data to support its use in treating congestion at this time, I cannot speak to how effective it may be or any potential side effects”

It’s quite a PC statement and I thought it odd they’d choose to say that whilst also decribing how it might be used… providing a dilution and dose etc.

I opted to not use at that time point… I hadn’t found anything on a literature research recently Is there anything I have missed? Any conference abstracts or presentations?
With limited options for decongestants and with cats being obligate nasal breathers would you recommend using it? Are there other things you would reach for first?

Cheers
Simon

Looks to me like Acute Lymphoblastic Leukaemia from the blood smear. There is a large peripheral expansion of lymphoid origin cells, they are large (larger than neutrophils if there were any for comparison) lymphoid cells with a higher nuclear:cytoplasmic ratio with visible nucleoli and condensed chromatin and intensely basophilic cytoplasm.

As noted the lack of neutrophils is not surprising as many of these dogs have concurrent neutropenia, thrombocytopenia and anaemias.

VBG
Looking at the blood gas we have a mixed respiratory alkalosis and metabolic acidosis – we can see this acidosis is not lactic in origin. There is moderate to severe anaemia, mild hypoglycaemia and mild azotaemia.

On the biochemistry there is moderate to severe Hypoalbuminaemia.

On the haematology there is significant thrombocytopenia, spontaneous bleeding is possible at this count with trauma or surgery but would need confirmation on a smear.

Overall this is one very sick pup. The mild hypoglycaemia is concerning as we know these dogs are at risk of sepsis, DIC and haemorrhage. If wanting to treat this dog (Prognosis considered very poor – variation depending on phenotype) I’d consider whole blood transfusion. But before that making sure we had samples to send for flowcytometry to confirm the diagnosis and 4DX to r/o Erhlichia. Amox/clav 20mg/kg Q6 IV, Glucose CRI as required, and placement of feeding tube for nutritional support. Then aggressive chemotherapy (Vinc + Pred I think is in literature).

Did the owners opt to attempt treatment in this case?

Hey Andy – sorry hadn’t seen this!

For sure absolutely a consideration. I tend to use Intralipid when clinical signs start, I guess that way I’d know if it was being effective or not! But absolutely would have considered it in this case (I’d actually calculated a dose whilst the dog was vomiting) but didn’t end up using it as the dog remained clinically normal.

Yes Scott, evidence to support worse outcomes, or at least no benefit demonstrated and more complications when compared to activated charcoal alone. But yes absolutely they acknowledge your very point about case selection – the ones we would look to be more aggressive with are those that have ingested a more potent toxin.

Simon 🙂

Hi Gail,

You got me thinking about what evidence there is for ranitidine use in rabbits, it’s something I was taught to give at university and have used it in practice without ever really looking for an evidence base.

So evidence wise, I found this (amongst others)… as you said largely a prokinetic, and a convincing one at that!

https://www.sciencedirect.com/science/article/abs/pii/S1043661800907850?via%3Dihub

In this paper they removed the intestines of rabbits duodenum to rectum and then assessed its contractility in an organ bath following administration of ranitidine. Ranitidine demonstrates a concentration dependent contractile effect on the duodenum, ileum and ascending colon. They also looked at whether cisapride potentiated the effect (main aim of the paper) and concluded that up to a certain threshold it did but thereafter it actually antagonised the effects of ranitidine. There aren’t any doses in the paper but I think it nicely demonstrates the effects of the medication.

Hope that it is of interest..!
Simon 🙂

I think you’ve got it! Don’t know the level of detail required?

Sensitivity and specificity are test-based calculations and are independent of the population.

I always think it’s useful to remember there are 2 groups within your population. Those with disease and those without and the ability of the test to perform in each of these groups is different which is where the 4 categories below come from.

True positive = Animals who have the condition and test positive for the condition.
False positive = Animals who do not have the condition but test positive for the condition
True negative = Animals who do not have the condition and test negative for the condition
False negative = Animals who have the condition and test negative for the condition

Sensitivity is the tests ability to detect those who DO have the condition.
It is in relation to positives. So for this test say we use 100 dogs (easy maths) we know have the disease as the population. 96% of them test positive, 4% are false negatives (we know they have the disease but the test fails to recognise it).

Sensitivity (True positive rate) = True positives / (true positives + false negatives)

So the proportion of the population that does have the condition as a percentage of animals that test positive. So your sensitive test is very good detecting your positives. So 96% of the time a negative is reliable.

Specificity is the tests ability to detect those who DO NOT have the condition.
It is in relation to negatives. So for this test say we use 100 dogs we know do not have the disease and run the test 94% of them test negative, 6% are false positives (we know they do not have the disease but the test thinks they do).

Specificity (True negative rate) = True negatives / (True negatives + False positives)

So the proportion of the population that does not have the condition as a percentage of animals that test negative. So 94% of the time a positive is reliable.

This test overall is pretty good as in either camp it’ll return you a reliable result.

Hopefully this helps in what is often a really confusing topic.

Hi Gail,

So in traditional acid-base analysis the changes we see are related to the equation below.

CO2 + H2O ←→ H2CO3 ←→ H+ + HCO3−

You’re absolutely right that changes in HCO3- are therefore dependent on PCO2 (respiratory component). Usually PCO2 and HCO3- would go the same way (decrease to one results in decrease of the other) as we see in the question, the body loves to compensate and achieve equilibrium where possible and so tries to achieve this via the above equation.This creates difficulty when you’re trying to evaluate the two values separately.

Base excess is a ‘better’ way of measuring metabolic disturbance because it is independent of the respiratory system (PCO2). It is defined as the amount of acid or base that must be added to a sample of oxygenated whole blood to restore the pH to 7.4 at 37°C and at a PCO2 of 40mmHg.

Essentially if there are minimal changes to the PCO2 then either Base excess or bicarb to evaluate the metabolic component should be fine.

In your question they have only given you bicarb to evaluate the metabolic component and so that’s all you’ve got to go on here, and I would agree with Annette’s interpretation.

In terms of the lactate this would effect your base excess in an equimolar fashion. In terms of getting more complicated with acid-base analysis you can actually get a numerical contribution of things like lactate, albumin, chloride to base excess.

Hope that helps
Simon