The patient was a known epileptic that had been having a seizure around every 3 – 6 months over the proceeding 8 years or so. However it had worsened in 2020 to having clusters.
She had been on the keppra for around 3 months prior to this cluster.
I was under the impression that the owner’s believed the seizures were because of the liver disease. The dog had no clinical signs between episodes and was only on keppra and hepatocare. Although it did become extremely polyphagic during the cluster. I wasn’t entirely sure why it was so ravenous and put it down to post ictal behaviour. Would you be considering something else?
I didn’t make this particular patient sick as they were handed over to me having already been admitted and on ivft for several hours.
I have previously made a puppy vomit after gorging on food. It only brought up about 8 pieces of kibble but I did wonder if it resulted in faster digestion of the remaining food. My theory being that the stomach could then contract more efficiently as it wasn’t stretched to it’s max, whilst also allowing for remaining food to swell.
No, not any specific case. I was just thinking about the standard ooh scenario whereby a dyspnoeic cat presents to the clinic, has a scan and has an increased La:Ao ratio and b lines. So it’s in oxygen and started on furosemide.
Just trying to work out the best protocol to get that type of case, out of oxygen and discharged home again.
I was under the impression that furosemide at a dose >12mg/kg/24hrs didn’t provide much additional effect. Is that incorrect?
I’m trying to work out a protocol that I’d switch to.
So far I have:
-Start with 2mg/kg IV
-Then start a cri at 1mg/kg/hr until rr <40bpm
(Is there a max time that you’d keep them on this rate?)
-Switch to intermittent bolus
-Switch to oral meds
If cri is superior, then why switch to intermittent bolus before oral meds?
I’ve not encountered precipitation with furosemide before. Could you possibly explain this?
As faecal testing typically takes time to get results back, would you simply consider a normal faecal motion from a clinically normal dog, as a suitable donation?
“Puppies” is quite a broad classification. To implement this in practice, do you have a g/kg type of dose that you use. I appreciate it’s not an exact science.
Are there studies that could indicate a potential use for faecal transplantation in cases of acute haemorrhagic diarrhoea?
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