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Simon Patchett

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  • Simon Patchett
    Participant

    Hi :),

    I’m Simon, I am currently the principal veterinary surgeon at an out of hours clinic but in November I am moving into a non-clinical regional leadership position for one of the large corporates. I am hoping to challenge my existing views on leadership and broaden my knowledge.

    Simon

    Simon Patchett
    Participant

    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

    Simon Patchett
    Participant

    There appears to be an alveolar pattern with some air bronchograms and an increase in radiopacity ventrally overlying the heart base. This consolidation and location suggests that the Collie has aspirated when it regurgitated!

    How did the case get on?

    Simon Patchett
    Participant

    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?

    Simon Patchett
    Participant

    Great question and a really tricky one! I’ll not touch on the clinical side.

    But I’ve learnt it’s not what you say but the way that you say it. Having been on the other side of this and actually owing a lot my confidence with decision making now, due to the nurses I worked with when I started practicing just doing little subtle things to suggest that I should maybe double check something, or gauging whether or not I’m sure about something or not. I think a lot of the response I gave (hopefully a positive one) came down to the way the question was asked – They careful signposted to either ask another colleague or suggested an alternative way of doing it because they’ve seen most people do it that way. I was a brand new vet at this point so responded to this, as to be honest, a lot of the time it’s worth that double check and sometimes I wasn’t really sure! and that’s ok. You only get better when you realise what you don’t know.

    In your situation, if that person isn’t wanting to accept that you maybe have more knowledge in that area due to an interest or something, then providing a colleague of a similar level to that person could result in a better response. I’m not in anyway that it’s ok that a doctor/vet wouldn’t take onboard things their team are saying but it does happen – and this maybe is a way around it.

    In time dependent situations this is a little more tricky, perhaps may be worth approaching a few days after the incident and ask them if they’d mind explain their decision making process in those situations as it’s a topic you find interesting. Once that door has been opened you can bring in the why atropine over atipmazole.

    Hope that helps 🙂
    Simon

    Simon Patchett
    Participant

    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 🙂

    Simon Patchett
    Participant

    Apomorphine is an a potent Dopamine 1 and (to a greater degree) Dopamine 2-‘like’ receptor agonist and also has an antagonistic effect on serotonergic receptors 5-HT2 and antagonist effects on alpha adrenergic receptors.
    Metoclopramide is a D2 receptor antagonist (main mechanism of anti-nausea) and also an antagonist of 5-HT3
    Maropitant is an NK-1 antagonist

    So I think it’s the other way round I think! Metoclopramide and Apomorphine act on the same receptors and maropitant is the different one.

    The physiology of vomiting is fairly complicated with loads of receptors (Dopaminergic, serotonergic, adrenergic, histaminergic, neurokinergic) and some other ones I also can’t spell! all in the CRTZ chemoreceptor trigger zone. So when we give apomorphine this is where the action is happening on the D2 receptors. I guess the question pharmacologically is, does metoclopramide have greater affinity for the D2 receptor than apomorphine? Metoclopramide has 28.8 nM affinity at the D2 receptor site and apomorphine 52nM (higher number = lower affinity) so theoretically metoclopramide may diminish the effects of apomorphine but I couldn’t find any studies relating to this. The other question… is antagonism of the NK-1 receptor enough to counter the agonists effect on D2. I’m not sure we have an answer to this one!

    I couldn’t find any literature on the specific question.

    A little counter question why give an anti-emetic at all?

    The duration of action of apomorphine is around 60-90minutes, the induction of vomiting and completion of vomiting will take anywhere between 5-20minutes. The info on the data sheet for maropitant suggests that it takes 45-60minutes to have reliable action (some studies administered at time point zero and then gave apomorphine at 60min, or an opioid at 45min). So when considering the timing – is it really worth it? Are we making a difference or just giving the anti-emetic because it feels like the right thing to do?

    Hope this adds to your discussion!

    #whatareyouthinking

    Simon Patchett
    Participant

    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 🙂

    Simon Patchett
    Participant

    That is really helpful, thanks Scott!

    Good to know we don’t see age related changes in response to anaemia – It must be a real challenge for doctors to interpret the anaemias in the elderly!

    The dog is clinically well at the moment and so further testing hasn’t been pursued.

    Really interesting RE melena and the volume of ingested blood required in humans (it’s not an insignificant amount) – something that seems obvious now you’ve pointed it out but I hadn’t considered there’s a threshold volume. There’s clearly a number of these cases that will fly under the radar or at least have normal histories but may still have a GI bleed!

    Thanks again!
    Simon 🙂

    Simon Patchett
    Participant

    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.

    Simon Patchett
    Participant

    So luckily for us there’s a helpful pneumonic for common causes of metabolic acidosis (With increased anion gap) :).

    DUEL

    Diabetic Keto Acidosis
    Uraemia
    Ethylene Glycol toxicity
    Lactic Acidosis

    Simon Patchett
    Participant

    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

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