Hi everyone!
I want to share this (simple) case with you. Ricky is a 13yo male chihuahua that underwent a sedation with low dose dexmedetomidine + butorphanol IM to investigate a otitis caused by f.b. He had a 2-3 year old assintomatic grade II left systolic murmur that was never investigated before.
Accordingly to my colleague during the sedation he was ok and was discharged 2 hours later (reversed 1h previously with same volume atipamezol IM), already walking and active.
Hi everyone!
I want to share this (simple) case with you. Ricky is a 13yo male chihuahua that underwent a sedation with low dose dexmedetomidine + butorphanol IM to investigate a otitis caused by f.b. He had a 2-3 year old assintomatic grade II left systolic murmur that was never investigated before.
Accordingly to my colleague during the sedation he was ok and was discharged 2 hours later (reversed 1h previously with same volume atipamezol IM), already walking and active.
Two hours later he had a syncope-like episode at home, with supposedly loss of consciousness with involuntary micturion and irresponsiveness. He arrived already awaken, agressive as always.
At the time it was referred to me. I did an ECG and echocardiography. He had a severe decrease of the shortening fraction, low HR, minimal mitral regurgitation, moderate aortic regurgitation, decreased aortic and pulmonic velocities, mild LA dilation, and obvious mitral degenerative valve disease. Also, the myocardium didn’t seem very healthy. No arrithmias detected.
I started pimo twice a day and discharged him home after few hours.
The next day he was re-evaluated. The decreased FS% was gone, no more Ao regurgitation and normal P/Ao velocities.
(the first 3 videos are from the 1st day and the fourth is from the next day)
My questions are – Do you believe that he had a ‘real’ syncope? Have you ever seen a syncope induced by dexmedetomidine (low output, arrithmias…)? Would you do pimo ad eternum in this case (small breed, B2)?
Comments
The use of Dexmedetomidine
The use of Dexmedetomidine probably was a risky choice in this age chihuahua with known heart disease.
Adverse Effects
The adverse effects reported with medetomidine or dexmedetomidine are essentially extensions of their pharmacologic effects including bradycardia, vasoconstriction, muscle tremors, transient hypertension, reduced tear production, occasional AV blocks, decreased respiration, hypothermia, urination, vomiting, hyperglycemia, and pain on injection (IM). Rare effects that have been reported include: prolonged sedation, paradoxical excitation, hypersensitivity, pulmonary edema, apnea, and death from circulatory failure. Adverse effects that require treatment can generally be alleviated with atipamezole, however analgesic effects will also be reversed.
My guess is that he likely
My guess is that he likely got hypotensive as all the meds were likely not out of his system and being the charged up type his pressure couldnt keep up wiht his attitude:) the echo there is some trivial MR and AI but no volume overload and some myocardial fibrosis. In this breed and wiht MR the FS% typical runs on the compensatory higher end so eyeballing a FS% of 22-25% here… he gets up fast and th efs% drops under 20 and he falls over…. the meds completely wear off and his fs% comes back to normal and he has no more episodes…?? Is he having any mor eepisodes? If not IM guess temporary and he should scan now normally wiht FS% in th e40s+. just a theory but plausible. Otherwise paraoxysmal arrythmia potentially owing to the myocardial remodeling here..??
Without the volume overload and DCM criteria is not present and wrong breed not sure pimo is needed here long term and could be damaging if not at least in stage B2 VD.
How was the BP? maybe a holter monitor or an event monitor? We have holters if need be info@sonopath.com
Yes, I absolutely agree that
Yes, I absolutely agree that the dexmedetomidine was not a good choice here. Nevertheless the episode happened about 4 or 5 hours later, he was reversed and I was told that the sedation went well and he was fine at the discharge. I was a little bit confused since I’me very new on echo, so I just wanted to ask you experts what were your thoughts.
EL – The BP was normal and you are right, the FS% went from 19% to 39%. Thanks for the tip on the holter, but I’m writing you from overseas, we’re a little far away :).
I think I’ll check him a week from now to run a 5 minute ECG and FS%, if everything is OK I’ll stop the pimo.
Even with reversal I dont
Even with reversal I dont think anesthetics or their effects are completely out of system for some time but I dont know the pharmaco i only got a B+ in that course:) With the hypocontractility on your echo that fits systemic disease/sluggishness which is exactly what sedatives, shock, hypothyroidism, addisons hearts look like. Ever want to check shock do a rapid echo and see what the heart is doing… compensatory = tachycardia and solid fs%… decompensating shock starts to look like yours.
Cool thread:)
Hi!
Basically, this dog
Hi!
Basically, this dog does have some underlying valvular disease (mitral valve thickening and prolapse). But the changes seen on the first 3 videos are typical of alpha-2 agonists. This is exactly, what they do and why I hate them. Typically, systolic function drops and valvular regurgitations increase or develop. They mimic a shock – not only on echo but as well clinically. Watch their mucous membranes and palpate the pulse…
And I would never never ever use a alpha-2 agonist in an old dog. Young dogs do tolerate them better if you need a little shot for taking orthopedic radiographs or sth.
Maybe the antagonist was erroneously administered s c and did not really act. I have used alpha-2 agonists and sometimes the owners report that their pets were very tired at home the whole day long even though they had been antagonized.
When you release patients from the hospiatal after alpha-2-agonist sedation, pls pay particular attention to the heart rate! If it’s still slow, don’t let the patient go home. Maybe he needs a bit more antagonisation.
Even though many anesthesiologists recommend alpha-2- agonists in some cardiac patients, particularly aortic stenosis or HCM, I would not use them.
Once I instructed a course on cardiac ultrasound in cats and all patients had been sedated with domitor – the attendees were shocked!! They would not have expected these severe changes.
After having gotten this off my chest – some recommendations re this particular patient>
I totally agree with Eric – maybe the patient has some underlying arrhythmia that could have caused the syncope – it’s hypothetical but has to be ruled out – a Holter is recommended. And the valvular disease needs some re-check, maybe in 6-9 months. Pimobendan in asymtomatic DMVD is only recommended if it’s B2 or more – see one of the previous threads.
Best regards!
Peter