Liz Bode
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Hi Annette,
Case report writing can be really tricky. You have to do a few for your Cert. Here are some of my tips;
– make sure it has some structure – signalment, history, clinical exam (thoroughly reported and if something was normal state that), problems, differentials, diagnostics, treatment, discussion etc
– structure your differential list as you point out and highlight the most likely differentials for the problem. Put them in order of likelihood.
– during the case report state why certain differentials are excluded by your findings
– you can group differentials together or state that things like anorexia are due to the underlying condition.
– don’t reference apart from in the discussion (only very rarely do you need to reference elsewhere)
– state facts and only discuss aspects of the case in the discussion
– stick to the word count
– follow the guidelines that they provide you (you’ll be amazed how often people don’t do this)
– it doesn’t have to be a perfect case but where there are gaps due to e.g. financial limitations make sure you point these outHope that is helpful 🙂 good luck and remember you can post any interesting cases you have one here.
Best wishes
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
Hi Sophie,
Excellent questions. The individual variability in dogs with DCM wasn’t tested but I’d imagine it would be the same as the healthy dog. You could serial sample in dogs where you were suspicious of heart disease (generally speaking this is where a dog has a murmur – it is rare to see heart disease without a murmur in a dog, unlike a cat). NT-proBNP has been used to track changes in dogs with mitral valve disease for example and I believe the RVC is looking at this currently. So if a client can’t afford repeated echo then you could consider doing this, but I’d always advise echo for monitoring if you can just to avoid false positives and false negatives with NT-proBNP.
In the ACVIM discussion one of the authors of the Lab paper said the following; “I think more breed-specific information on NT-proBNP would be very useful – although a low index of individuality for NT-proBNP has been reported (as we also found in Labradors – see above), meaning that the individual variability is low compared to the group and individual changes over time may be masked by the background “noise” of the wider population.
That suggests that we should probably track individual changes rather than compare one dog to a population reference. However, I think that’s rather impractical in most cases where people use NT-proBNP for disease screening (certainly common in UK practitioners), so a reference interval should be a guide that is considered less useful than tracking a trend in one dog if they are considered high risk (family history, equivocal echo, etc).”
Hope that’s helpful.
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 all,
Interesting case Scott and generated some good discussion.
Distal limb swelling is unusual in small animals with cardiac disease. I think I’ve seen it most commonly with blocked lymph drainage not associated with cardiac disease. Dogs and cats with right sided heart failure can get brisket oedema, but this is unusual and only seen (at least in my experience) with severe disease. This can extend down their limbs if bad enough.
Hope you are all safe and well.
Liz
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
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)
No problem 🙂
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 Gail,
In my opinion radiographs in the acute setting of an animal presenting with dyspnoea should not be the first diagnostic test performed. I’d always do a TFAST over a radiograph in this setting. I wouldn’t say that assessing the VHS is necessary in most cases but perhaps they are thinking that in a case where you aren’t sure from ultrasound and you then radiograph it that knowing how to perform a VHS is a skill that is good to have. If the VHS is normal, heart failure is very unlikely, if the VHS is increased then heart failure is possible but by no means definite!Not sure if the ECC guys have anything to add on this.
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 dischargeIf 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
Hi Scott,
Thanks for this good question.
I use furosemide CRI for acute, fulminant HF (when you have a pretty much white out on rads or coalescing B-lines on POCUS exam). I generally use it until the resting RR falls to around 40 breaths per minute and then stop it swapping for boluses thereafter before starting oral meds. I think the majority of papers have shown that it has a superior diuretic effect when compared to intermittent boluses, at least until 8-12 hours of starting the CRI. Ohad et al. (2019) also showed a trend to suggest shorter hospitalisation times with a CRI vs bolus.
I always use a 2mg/kg IV dose first as this will ensure (as much as you can) that furosemide is delivered to the nephron and into the proximal convoluted tubule. The CRI concentration will take longer to reach peak effect. I use a CRI rate of around 1mg/kg/hour, hence why a loading dose in combination with CRI is probably faster at achieving sufficient plasma levels.
Personally, I use the CRI in a syringe driver that is pretty accurate so I don’t tend to dilute with fluids. Adin et al (2003) showed that you can dilute without precipitation to 10mg/ml with lactated Ringer’s, normal saline, sterile water or D5W and to 5mg/ml with sterile water or D5W for a max of 8 hours without precipitation.
You do tend to see hypokalaemia when using either boluses or a CRI. I don’t supplement with potassium routinely as it is probably best to keep an eye on electrolyte balance. If the animal is eating then potassium will be relatively maintained in dogs, but can be more of a problem in cats. I would usually check renal params and electrolytes prior to starting diuresis and if all is normal then check them again 24 hours later and daily until they go home. If not normal or they fall over that time period I will supplement with oral potassium and only use fluid supplementation if I feel that they are symptomatic for hypokalaemia (which tends to only be an issue in our feline friends).
Hope that helps.
Liz
I’ve come across this too, we used it quite commonly when I was at Liverpool as we all know how difficult it is getting feline blood donors (usually in unfriendly hours!).
My understanding is that the RBCs don’t last that long (perhaps Scott can help with specifics) and you can only do it once, but it is life saving in many cases.I am not used to looking at images of the bladder either, the heart is further forwards!! Getting my excuses in early 🙂
It appears that there is normal contrast within the urethra to the level of the prostate. At the prostate you have an odd pattern of accumulation of contrast and there is a small stream of contrast that enters the bladder, but this is less well opacified than the prostate/ urethra. There also appears to be contrast uptake within a tubular structure that moves cranially from the prostate. I am not sure what this is, I initially thought it was the descending aorta, but that doesn’t makes sense. Is there some sort of fistula to bowel/ venous system?
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