Liz Bode

Hi Kerida,

Thanks for uploading the history and the radiographs to the discussion forum, what an interesting case!

I think there is evidence of some cardiomegaly, particularly at the base on the laterals. You can’t really see the right atrium on these as it is buried in the middle of the cardiac silhouette (unless v severe tricuspid dysplasia, which cats do not often get and this is the wrong age). It is hard to confirm specific chamber enlargement on the DV as the silhouette is effaced by the lung pattern. I see what you mean on the left lateral, there looks like there is some sort of mass cranio-dorsal to the heart. I can’t see this on the Dv, but the slight rotation makes it hard to look at the right-cranial thorax. The heart is rounder on the left lateral, but I think we tend to see this so can’t read too much into that.
The lung pattern is diffuse broncho-interstitial with a greater interstitial component in the caudo-dorsal lung fields.
You don’t mention any murmur/ arrhythmia/ gallop so I assume that these are not present?

My DDx would be:

Oedema – cardiogenic vs non-cardiogenic superimposed on feline asthma type pathology
Infection – bronchopneumonia
Possible mass in cranial thorax

Is there any way this cat could have a FAST scan of the thorax to rule in/out cardiomegaly and a mass? I think that would be the single most useful test here?

What did you decide to do with the cat in the end? Interesting that the brother died of resp issues too…

I would be very interested to see what others thought 🙂

Liz

No problem 🙂 That sounds like a cool case. I always think comparing what you find to the human literature is super interesting, so you would want to do that. If there are any case reports/ case series of similar things in the veterinary literature you would want to compare your case to those too (if there aren’t you might consider writing this up!). If there was anything unusual about this case or things you didn’t do due to financial limitations then talk about this in the discussion too.

Hope that helps.

Liz

Well done Scott, definitely something to be proud of. Danielle is a legend and I learnt so much from her as a resident.

Liz

I think both theories are in their infancy, but there appears to be growing evidence for a role of both these theories. The cardioprotective theory involves the intralipid being able to improve myocardial metabolic function, even reversing some of the effects of ischaemia, which will provide more energy for the heart. It also enhances some calcium handling within the heart which improves inotropy and repairs any lost function present that may have been caused by cardiotoxic drugs. Most evidence appears to be in the use of anaesthetics in people.

Hi Ashley,

Poor little guy. This is quite an unusual condition, especially the severe cases when it can cause exercise intolerance and respiratory difficulty. I’ve only ever really seen milder forms in brachycephalic dogs, who seem to have this condition slightly more commonly. I have seen a Pug with this condition when it was more severe, but he exercised fine, the only thing that was unusual with him was that his apex beat was shifted to the right and the mean electrical axis of his ECG also showed R deviation – I think we investigated an asymptomatic murmur that was not related. There is a surgical option – external splinting, and there are a few published reports where this has been successful for certain forms of the condition. It also seems to be more successful the younger the animal as their sternum is still soft/ cartilaginous. However, I have no experience of patients having this procedure – not sure if Scott or anyone else do.

Sorry I can’t be more helpful.

Liz

I might give it some butorphanol if anxious.
I would perform a thoracic POCUS examination – looking for pleural effusion, evidence of B-lines and to check cardiac structure and function. You might also be able to see any evidence of herniation.
Check BP
Check an ECG
Bloods inc electrolytes
More imaging if stable enough and nothing obvious on POCUS examination

(the cardiologist’s perspective)

Hi both,

Feline VHS could be useful if it is increased, which it will be in cases of HF.
However, pre-clinical HCM may have a normal VHS which can complicate the picture.

In terms of further assessment post stabilisation, I think this is indicated. Different types of heart disease have vastly different prognosis and so from that point of view further investigations would be indicated.

Liz 🙂

Hi Scott,

The dose is a good question – generally we consider patients (dogs only, cats it is thought to be lower at 5-8mg/kg/day) have diuretic resistance at doses around 12mg/kg/day when given orally. However, it is an interesting finding that despite having tolerance to oral doses at this level that patients will still respond to IV furosemide. So, for example, the dog that has been on 10-12 mg/kg/day and is ‘rescued’ by a change in diuretic to, for example, torasemide will still respond to IV furosemide if they are re-admitted for decompensation. Oral furosemide will have a lower dose at which tolerance occurs for many reasons, but one of the main points will be the fact that bioavailability is notoriously difficult to predict with figures between 10 and 100%. IV furosemide on the other hand obviously does not have this issue.

I have tried to find some literature on the max dose of furosemide in dogs when it is given via CRI but I haven’t been able to. Most references use between 0.5-1mg/kg/day but you can go higher than this too. You can tailor it to the severity of CHF.

In terms of why switch to intermittent boluses before oral meds – there was a study in horses that showed a CRI gave better diuresis for the first 8 hours of administration, thereafter intermittent boluses gave better results. That is one rationale, but was obviously performed in healthy horses and so may not be the same in dogs. You could switch straight to oral meds if you think that the patient is dry, the only other good thing about intermittent boluses is that you then have a better idea of how much furosemide to send them home with i.e. if you have used 6mg/kg over a 24 hour period IV then you might opt to discharge them on a similar amount orally. The routes of admin aren’t like for like and so you do need to be a bit careful with this, but it can be helpful.

I’ve not encountered precipitation either. However, there must be some fluids with which you combine furosemide and crystals form so the IV route can’t be used. The study that I mentioned in my previous reply showed that, at least visually, those fluids did not cause crystals to form and were safe to administer IV with furosemide (for a maximum of 8 hours at least).

I would say in general my use of CRI depends where I am working and on the patient. I would use it for fulminant heart failure where they are being monitored relatively closely (in theory monitoring may be less intense with a CRI vs boluses as you give boluses depending on RR and so more decisions are needed). A protocol that I might use would be:

Patient in O2 with B-lines/ severe oedema on rads
Give 2mg/kg IV furosemide (or IM if placing an IV line is too stressful – you can use butorphanol IM if they are very anxious, just remember to wait long enough for this to take effect before attempting an IV)
Start a CRI of 0.5-1mg/kg/hr
Monitor RR hourly and when RR is 40 or less stop the CRI
At this point decide if the patient can go on to oral meds or if you prefer intermittent boluses
If using boluses I would go for q4-6 hours IV initially, still monitoring RR and giving additional 1mg/kg boluses IV if RR >40 at these checks (as long as this is believable, which can be an issue)
Once happy that the RR is consistently <40 and the effort is normal swap on to oral meds - If severe HF I would usually discharge on around 2mg/kg TID and then taper that down to the lowest effective dose at home with owner monitoring RR.
Monitor renal parameters and electrolytes at least q24 hours and one week after discharge

If you don't use a CRI I would use an initial bolus at 2mg/kg then 1mg/kg q1-2 hours until RR is <40 then increase the time between administration, give additional 1mg/kg boluses if RR>40 at any check. Once happy that they are stable change to oral meds.

This was a great topic and made me think I will do the next journal club on the use of CRIs in dogs going through the evidence that we have to date (which is a bit mixed for its use).

Thanks for making me think 🙂

Liz