Liz Bode
Forum Replies Created
-
AuthorPosts
-
Hi Nathalie,
I’ve finally read it (thanks for asking this question as it made me read it in detail!). So for those of you not familiar with this score the paper can be found here:
This is a scoring system based on echo that uses the LA:Ao, fractional shortening, E wave peak velocity and LVIDDn.
The authors have chosen parameters that are relatively easy to measure, with experience of Doppler. It is interesting that in dogs with stage B1 disease that 6 dogs would have been classified as severe using this system. This shows how the staging system we use currently is probably not a perfect reflection of the disease process.
It is difficult to say how useful it is without using it in practice. I am not sure it will be very useful to predict whether a dog will die of cardiac death or not as the ROC values were not great and the sensitivity and specificity were only moderate (around 78-87%) .
It would be interesting to use it in cases to see how you get on with it. Perhaps this is paving the way for more studies from this group about progression of disease and the MINE score, which would be more useful clinically than what they have done currently. This is because some dogs will stay mild or moderate for their life whilst others will move through the scoring system. What they have shown in this paper is just one time point on echo and so that is less useful.
Interested to hear other people’s thoughts too.
Liz
Hi Nathalie,
I would agree with you. I would not start furosemide unless I had strong evidence for CHF on rads or thoracic ultrasound. IVRT can be difficult to interpret/ measure accurately and interpretation is challenging with E and A wave summation. An LA:Ao of 1,7 is not massive (although it is usually better to use various measures of LA size when evaluating it so I would also look at the 2D on long axis measurement). CLopidogrel might be indicated. There is no clear cut-off of LA size to start this, the consensus just says stage B2 which is moderate enlargement (but I think we take an LA:Ao of 1.9). I would start it if left auricular velocities were <0.4m/s (as we have previously discussed).
Hope that is helpful.
Liz
Hi Alice,
Sorry for the delay in replying to this. I think it sounds most likely GA related. Would be interesting to see what the troponin was afterwards (although I appreciate that’s more of an academic exercise), but I have seen this in other dogs and could be related to transient myocardial hypoxia with a lower BP given ACP and iso. Your plan sounds excellent. I guess this dog could also have an area of abnormal myocardium that was irritated by the GA in some way.
I think in future the anaesthetic protocol would depend on what the dog was going to have done. Id monitor BP throughout and pre-oxygenate. Perhaps don’t use ACP and give an opioid only or combine with an alpha-2. To be honest though it was probably just one of those things and may not happen again so I wouldn’t be changing things too dramatically.
We could revisit this after lesson 8 which covers anaesthesia too 🙂
Liz
Hi Nathalie,
I still need to read this paper, job for this week and I’ll get back to you 🙂
Liz
Hi Anna,
Ooh!!! SVT in a cat, nice case 🙂 do you think she has an accessory pathway? It’s unusual to get an SVT with a normal looking heart in a cat otherwise. Perhaps you could post an ECG here if you can?
Diltiazem might work definitely worth a try. Can you get HyperCard? It was out of stock before I went on maternity leave. Other options to look into would be Summit and BOVA both (I think and if you’re in UK) do, or have been asked to do, re-formulations of diltiazem. If not then I’ve used 3mg/kg in a cat before so that would be 1/4 of 90mg tablet.
Let me know how you go as I’d be interested to find out.
Liz
Hi Francois,
Great questions, as always.
In terms of RCHF I would just start using furosemide. Sometimes, it’s nice to hospitalise these patients for 24hours to give IV furosemide to ensure that it is being delivered to the kidneys effectively and to improve any associated bowel oedema. However, if the ascites is relatively mild you could just send them home with furosemide too. I’d definitely give them pimobendan, probably and ACE inhibitor as we don’t have evidence for or against this currently, and spironolactone. I’d give the spiro less for the portal hypertension (furosemide will sort this out) and more for its other effects.
Matt’s lecture covers a lot of questions but I would use alfaxalone in this instance. I’d use it IV (unless you can’t get access – just IM requires large volumes). I’d draw up approximately 0.5mg/kg and just give to effect after giving an opioid.
I really like alfaxalone.
Liz
Hi Nathalie,
Yes, that’s my go to dose for both cats and dogs.
In dogs that are very stressed or panting a lot I’ll give them it half an hour before their echo. It can REALLY help!
I’ll also give anxious cats gabapentin prior to coming in and I’m going to try trazadone at some point in them too. I’ll also give trazadone to a dog if it’s coming for a recheck and I’ve had to give butorphanol to echo before.
Liz
Hi Julie (and Camilla),
That’s actually a very useful link for me Camilla, thank you.
I’ve no experience with this machine or heard of it. I see that Camilla gives it an excellent review and, for abdomens, it certainly looks like it would do an excellent job.
I have one main concern about using it for heart scans in cats though. It looks like it has a huge footprint which means you won’t get it to sit nicely between the ribs which will make image quality poor and you will probably get quite frustrated.
Camilla, would this be a fair assessment? Please feel free to contradict me as I’ve not used it.
Liz
Hi,
I would expect some improvement in that time frame. It’s not a hard and fast rule but that time gives the heart enough chance to start repairing.
Liz
It was a homemade one. We know that golden retrievers are prone to taurine deficiency even on normal diets, so definitely something to consider. In the USA they are seeing what they think are cases of DCM associated with grain-free or more unusual meats (kangaroo for example) and there is lots of research into the area currently. We don’t seem to see the same in UK or EU but we need to be aware of this too! Always get a good diet history in any cardiac case 🙂 if people are interested there is a questionnaire you can give owners here;
Lots of useful info there.
Liz
Liz
Hi,
Thanks for you comments. The radiographs show marked cardiomegaly with mixed interstitial-alveolar pattern predominantly in the caudodorsal lung fields but also ventrally in cranial lung fields (almost an aspiration type pattern here). The pulmonary veins and arteries are prominent. These findings are consistent with pulmonary oedema secondary to heart failure. In my experience large breed dogs can cough with pulmonary oedema, especially Dobermanns! So this could be the cause of the cough, but the cranial lung lobes do have a very ventral interstitial-alveolar pattern that could be consistent with some aspiration too. However, we treated him for CHF with furosemide, pimobendan and once stable ACE inhibitor (benazepril) and spironolactone and his cough resolved (although this could be coincidence).
This dog was markedly taurine deficient and we supplemented this. When we saw him back 3 months later his heart looked like this:And we actually managed to wean him off furosemide and eventually pimobendan! If they have a truly taurine deficient DCM then we can see this dramatic remodelling. However, sometimes dogs (and cats) will be taurine deficient with DCM and we supplement with taurine and their hearts do not remodel like this. It is very case dependent and needs good follow-up.
Cool case 🙂
Liz
Hi Thita,
Thank you for the questions.
In terms of taurine we usually start at 500mg PO BID but the dose range is wide at 500-1000mg BID to TID. You can recheck taurine blood levels after 3 or so months but the test is expensive to run. I would expect improvement after 3 months but some might respond sooner than this. On echo you would see a smaller heart with improved systolic function.
In terms of anti-thrombotics at the moment I would always choose clopidogrel as that is the drug we have most evidence for. However, if I were to add a drug on top then I would probably choose rivaroxaban as it is cheaper then low molecular weight heparin and is given orally. If the cat was difficult to medicate then I’d stick with the injectable LMWH though.
Hope that helps.
Liz
Hi Nathalie,
It might depend on which assay is being used -it would be interesting to know if they differed between labs (although I assume that whoever taught you on the ESAVA course uses the high-sensitivity assay too). The Idexx assay is highly-sensitive and so I would follow their instructions if that is who you use. If I am not analysing troponin immediately then I will separate the serum and cool, yes. However, that is because I use Idexx for my samples.
I am not aware of any literature on this though. I will have a look!
Liz
Hi Nathalie,
Generally, it has to be severe PHT to cause syncope. I will cover this a little in lesson 6, but in dogs with significant structural heart disease, especially MMVD then syncope is usually preload related, triggering neurocardiogenic syncope. Of course, it could be a combination of things so mild-moderate PHT with high preload, making syncope more likely. I would worry that this dog was in, or very close to CHF and that the PHT was left-heart related. In a syncopal patient such as this I would also do a Holter to evaluate for the possibility of an arrhythmia or to document any bradycardia associated with a syncopal event. If the syncopal events are initiated with coughing etc than it is likely tussive syncope (although I would still Holter these patients too).
Liz
Thanks all for the discussion and questions. My answers are as follows to the case:
The views show:
1. Right parasternal 4 chamber long axis – demonstrates a dilated LV and LA, with a slightly dilated right side (in the normal animal the right side should be 1/3-1/2 the size of the left, in this dog the right side is almost a 1/3 so if the left side is big the right side must also be a little big to maintain the proportions). The LV is round and subjectively hypokinetic and this can be appreciated on the short axis view too. The mitral valve is slightly thickened and appears tethered (doesn’t open properly).
2. Right parasternal 4 chamber long axis with colour over mitral valve – shows a central jet of mitral regurgitation.
3. M-mode at level of papillary muscles shows a hypokinetic septum with relatively normal free wall (posterior wall) motion.
4. Right parasternal short axis view at the level of the left atrium/ aorta demonstrates a markedly dilated LA.The ECG shows sinus rhythm throughout.
I’m not sure I can evaluate PA size on the last view as I can see the body of the left atrium and the auricle, which is dilated. However, there was tricuspid regurgitation at 3.7m/s indicating mild pulmonary hypertension.
There should be relatively normal cardiac output in this case as systolic blood pressure has been maintained and so this can’t explain why the aorta might be a bit smaller (if it is at all – we would need a better view of the pulmonary artery first to evaluate this).
The aortic annulus does look a little bit strange but I think that this is because there is a coronary artery appearing in this view.
Endocarditis lesions do not always produce those nodular/ thickened looking valves that we are used to seeing they can look relatively normal so cannot always exclude based on echo (I don’t particularly like ‘hunt the endocarditis’ in a pyrexia of unknown origin for this reason, unless more obvious things have been excluded first or the animal has a new murmur etc).
My echo diagnosis would be – DCM-phenotype with probable degenerative mitral valve disease. I think it is more likely a DCM-phenotype because of the central jet of MR and the depressed systolic function of the septum. Although it can be difficult in large breed dogs as MMVD can also reduce systolic function.
Our DDx for a DCM-phenotype would be:
Primary DCM
Tachycardia-induced (a dog paced at 180bpm for 4 weeks will develop heart failure. You can also develop this with intermittent tachyarrhythmias as long as they increase your mean heart rate significantly).
Myocarditis – acute or chronic (if chronic and normal troponin then you wouldn’t know this unless you did a biopsy – however the treatment is the same whatever the pathology in this case)
Diet induced (including taurine deficiency).
A shunt is possible, but less likely and I would only do a bubble study if the right side showed changes consistent with pulmonary hypertension).Further tests:
Taurine
Thoracic radiographs
A Holter could also be consideredResults:
Taurine 7umol/l (ref range 50-180 umol/l) measured in this case due to diet AND because we know Golden Retrievers seem to suffer from taurine deficiency that causes DCM.
Thoracic radiographs:How would you interpret these results and radiographs and what treatment would you advise?
I look forward to reading your answers.
Liz
-
AuthorPosts