BOXERS and ACEPROMAZINE

Date: Mon, 8 Apr 96

Nor can I, also anecdotal..
Long time ago, when in Bristol, England studying for my DVA, I premedicated
a Boxer with ACP, usual dose i.m. When brought to the prep room, the dog was
in a condition as if it had been deeply anaesthetized with bradycardia.
Surgery was cancelled and after atropine and oxygen administration recovery=
was uneventfull.
Also, some ten years ago, a colleague (not an anaesthetists) asked me what=
is the dose of Acepromazine in dogs. Later on, I was informed that an eye=
operation had to be cancelled as the dog (a Boxer) had collapsed
following the i.m.administration of Ace. I have no more info for this case.

Professor D. Raptopoulos
Faculty of Veterinary Medicine
Aristotle University of Thessaloniki, Greece

Date: 96-04-09
From: Jacky.XXXX@udcf.gla.ac.uk

For what it is worth, we premed otherwise healthy boxers with low dose ACP
(0.02-0.03mg/kg max) + pethidine, and an anticholinergic (atropine or
glycopyrrolate) to counteract side effects of the acepromazine - no horror
stories to tell so far, touch wood!!

Date: 96-04-10

Jacky wrote:
>For what it is worth, we premed otherwise healthy boxers with low dose ACP
>(0.02-0.03mg/kg max) + pethidine, and an anticholinergic (atropine or
>glycopyrrolate) to counteract side effects of the acepromazine - no horror
>stories to tell so far, touch wood!

I had a request for clarification of what Jacky meant by the use of an
anticholinergic to counteract the side effects of acepromazine. I presume
that you're referring to the reports of bradycardia being associated w/
aceprom in these dogs, but thought I'd check.

thanks,

Date: 96-04-10
From: XXX@ovcnet.uoguelph.ca

We teach that Boxers are sensitive to ace. Occasionally for interest and
learning experience, we use it at a low dose (0.02 mg/kg) with glyco and show the students the odd occurrences. Since we have all the monitoring at hand, I haven't been too afraid to do so when the dog is young, apparently healthy and no preexisting arrhythmias diagnosed. We have seen PVC's and severe sedation (ussually related to hypotension rather than to bradycardia) which has been
interesting to diagnose and treat. i believe in this 'sensitivity' but feel that it may be unmasking a preexisting undiagnosed condition. I have found it interesting and challenging in our intensive monitoring environment, but not worth using in the real world, due to these concerns.

Date: ??

I think that Jacky's statement on antichol to counteract side effects
of aceprom meant the bradycardia that's supposed to be assoc w/ aceprom in
boxers specifically. I agree that normally you don't see profound
bradycardia assoc w/ aceprom & if anything might see incr HR due to
baroreceptor reflex, as you said. In normal dogs HR might decr some if the
animal was excited b/f aceprom. I saw one horse which developed normal 2nd
degr HB following aceprom premed (not present in pre-premed ECG).

Date: 96-04-11 11:32:43 EDT
From: Jacky.XX@udcf.gla.ac.uk

Yes, that's right. According to Hall & Clarke in Veterinary Anaesthesia, the
'fainting' seen in Boxers given ACP has been attributed to vasovagal syncope.
Jacky

Date: 96-04-12

XXX wrote:
>We teach that Boxers are sensitive to ace. Occasionally for interest and
>learning experience, we use it at a low dose (0.02 mg/kg) with glyco and show
>the students the odd occurrences. Since we have all the monitoring at hand, I
>haven't been too afraid to do so when the dog is young, apparently healthy and
>no preexisting arrhythmias diagnosed. We have seen PVC's and severe sedation
>(ussually related to hypotension rather than to bradycardia) which has been
>interesting to diagnose and treat. I believe in this 'sensitivity' but feel
>that it may be unmasking a preexisting undiagnosed condition. I have found it
>interesting and challenging in our intensive monitoring environment, but not
>worth using in the real world, due to these concerns.

When I went to vet school (KSU 1979), Dr. Upson, professor extraordinaire
of veterinary pharmacology, did great labs with us. One that I was very
impressed with dealt with the ANS and included the difference in a dog's
response to epinephrine unpremedicated and after premedication with ace.
This dramatically demonstrated an "epinephrine reversal" effect of ace. If
I remember correctly, this was attributed to an alpha antagonist effect of
ace. If this is part of the "boxer ace syndrome" I would think that a few
micrograms bolus of neosynephrine would reliably increase the blood
pressure in a safe and predicable fashion. Neosynephrine tends to also
cause a relative bradycardia, vagally mediated, which should not usually
require intervention, but does respond to atropine. Have you used
neosynephrine in this scenario? ( Or can anyone else comment on this?)

Although boxers may be more sensitive to the adverse effects of ace, my
impression when I was working as a clinical veterinarian (not a specialist
at that time) was that non-boxers also occasionally developed apparrent
hypotension and severe sedation to modest im doses of ace. I had at least
one veterinarian friend relate an experience of a very mean german shepard
who was in fact only lightly sedated (still required physical restraint)
that "dropped dead" totally unexpectedly immediately after going making an
extreme effort to attack the vet. ( He swears this was not the result of
unsafe physical restraint.)

In relation to the PVCs mentioned, one possible explanation might be that
brachycephalic breeds when heavily sedated with ace may develop pvcs
secondarily to hypercarbia. If this is the case, controlled ventilation
may take care of it. PVCs in fact may not really be that big a deal, in
regards to the hypotension.

I haven't practiced veterinary medicine much for about 10 years, although I
maintain my license and will always be a DVM at heart. I am currently an
ASA board certified anesthesiologist but do not have the wealth of recent
experience and training in veterinary anesthesiology that most of the
readers of this discussion group have, so I hope my thoughts are not to far
of base. (Comments welcome.)

I do want to express my thanks to all the participants of this group for
your interesting comments which in a small way help me to keep in touch
with veterinary medicine and "real doctors".

Vancouver, Washington

Date: 96-04-12
From: XXX@ovcnet.uoguelph.ca

I treat the hypotension with fluids usually. I also find that hypotension
occurs in others premedicated with ace. When we notice excessive sedation, we

always check BP before inducing and treat with fluids before if hypotension
detected. It has not stopped me from using ace in other breeds though. The
advantages seem to far outweigh the risks. (20-40mL/kg)
If arrhythmias are noted, I like to see if they are responsive to lidocaine
before anesthesia is considered. I also get the primary clinician to consult
our cardiologist and inform the owner that a concern exists.
Maybe the use of ace makes us aware of potential risks before getting into
the
middle of anesthesia and allows us to make owners aware. Somehow I doubt that

vets will use this as a diagnostic tool! I find it interesting and a good
learning experience for students when the caseload is a bit mundane.
I may also keep the dopamine and/or lidocaine handier during the anesthesia.

Date: 96-04-05
I was recently asked to avoid giving acepromazine as part of an
anesthetic protocol for a Boxer. The client brought in a magazine cutting
which strongly stated acepromazine was contraindicated in Boxers. I am sure
all of
us could quote numerous unsubstantiated and anecdotal recommendations
concerning canine breed - specific anesthetic complications ( Innovar vet
and Australian Terrier, Anesthetics and Collies, Belgian Sheepdogs, Shetland
Sheepdogs, Anatolian Sheepdogs, Soft - coated Wheaten Terrier, etc.
etc.). My interest in these problems lead me years ago to work on one,
which to my knowledge is the only scientifically proven breed -
specific problem viz. thiobarbiturate metabolism and Racing Greyhounds. So my
usual response to these concerns of breeders and owners is that with proper
preanesthetic work - up and identification of pre - existing disease,
proper selection of an anesthetic protocol and carefully management and
monitoring, their dog will 'be fine'. However it does put a little mar on
my day because now I consider this individual might be 'fragile' in some
unknown way. Years ago I started to collect a file on breed - specific
anesthetic complications quoted in articles to try to ascertain if there
is any validity to the claims. One suspicion I have is that we are
breeding more purebred dogs ( as a dog - breeder I am particularly
concerned with this responsibilty) with genetic susceptibilty to various
diseases all of which might pose anesthetic risk (brachycephalic
syndrome, vWD, hypothyroidism, cardiomyopathy, juvenile renal
disease, chronic active hepatitis, etc. etc. and who know what other
genetic flaws).

I would be interested in adding to my collection of scientically -
documented and anecdotal breed - specific anesthetic problems if any one
has any interesting references.

Back to the Boxer: I did turn up an old reference of interest:

Garland and White: Unusual Reactions to Acetyl Promazine, Vet Rec 83,
641, 1968 ( a letter from my own hometown of Slough !!)


Date: 96-04-05
I am afraid that I can't add to the science. I did try to get some local
breeders of Boxers to bring their dogs in so we could do a study but only
had two people reply. I am convinced that there is a problem and we have
had three cases at UCD since I have been here and it is mentioned in Hall's
text as well as being quoted now in Plum's book. One of the cases here was
a dog which received ace for x-rays and was returned to the waiting room.
It collapsed and quit breathing and was taken to ICU where it was
successfully resuscitated. A second case was a dog being examined by the
cardiology service. One of the students on the rotation was a Boxer owner
and was aware of the problem and questioned the faculty member who had
ordered the ace for this dog. The faculty said something to the effect
that - "We've done lots of them and never had a problem"!! Following the
ace the dog had an episode of profound bradycardia (read asystole) which
was succesfully managed with atropine!! A local practitioner asked me
about three Boxers she had seen where there had been similar problems as
well. In the UK and in Australia it seems to be one of those
idiosyncracies that everyone knows about but it is clearly not widely
recognized in the US. Anyone know of a source of Boxers we could test to
find out the reason for this "collapse" (vagal bradycardia or massive
hypotension or?????). There is a reference in JAVMA from the 60's or early
70's on ace in brachycephalic dogs but I can't lay my hands on it!!

Date: 96-04-06
From: XXX@sydney.healey.com.au
> I am afraid that I can't add to the science.

Nor can I!

> I am convinced that there is a problem and we have
> had three cases at UCD since I have been here and it is mentioned in Hall's
> text as well as being quoted now in Plum's book. One of the cases here was
> a dog which received ace for x-rays and was returned to the waiting room.
> It collapsed and quit breathing and was taken to ICU where it was
> successfully resuscitated. A second case was a dog being examined by the
> cardiology service. One of the students on the rotation was a Boxer owner
> and was aware of the problem and questioned the faculty member who had
> ordered the ace for this dog.

> In the UK and in Australia it seems to be one of those
> idiosyncracies that everyone knows about but it is clearly not widely
> recognized in the US.

True. Just for annecdote's sake:
We have known about this very real problem for some time, and while our
usual S.C. dose of Ace is 0.05mg/kg, when I was still at Uni of Sydney,
one of our anaesthetists gave a boxer a premed of 0.01 mg/kg plus
pethidine (I think it was 2 mg/kg) S.C.

Syrgery for OHE was not attempted, until it had chilled out in the ICU
for two days with an ECG, NIBP and I think it was a Noradrenaline (Norepi-
nephrine to those in US) infusion!

We remain convinced of the reality of this syndrome!

Date: 96-04-06
From: XXX@duke.usask.ca

Also anecdotal. Following one death, many, many years ago (and multiple
other confounders), I stopped using acepromazine in Boxers. I have seen
others with severe hypotension. I believe it is real. However, there may be
a genetic linkage and not all Boxers would react similarly.

I believe this 'sensitivity' is also mentioned in Charlie Short's book
(don't have a copy handy).

Subj: Re:Acepromazine in Boxers
Date: 98-01-11 11:24:01 EST
From: EmilyMeg
Posted on: America Online

Paul asked me "What is your impression?"

I use it. However, those of you who know me from the anesthesia board also know that I seldom say "all dogs get this dose"...so I adjust the dose to the dog. A bounce young boxer may well get 0.1 mg/kg IM if I think it needs it while an older dog may only 0.01 mg/kg. Also, I NEVER use it IV in dogs. I do usually back my dose off a bit in brachycephalic dogs due to the relaxation of the muscle/tissues in the pharynx and hence increase in upper airway obstructions, but this is true for me for any brachycephalic dog. Again, I don't necessarily NOT use it, I just change how I use it.
Did that muddy it up well enough? :-)
Meghan

Subj: Re:Acepromazine in Boxers
Date: 98-01-11 11:34:26 EST
From: EmilyMeg
Posted on: America Online

"Anyone know what this is ?

Rare, idiosyncratic reaction to acepromazine in dogs."

Yeah, there are reports, mostly British in origin, of profound hypotension and bradycardia with resultant collapse in boxers. There are several "odd" factors in these anecdotal reports: often the reports are of British origin (so are they only ones reporting it, is it a gene pool thing, is related to the dose or route or some other technique, is there a difference in the "inert" ingredients between US ace and British/european ace??), the doses vary; the age of dog varies; the underlying problem varies; the work up varies. IE not very standardized, and I would bet if you seriously looked at ALL other breeds, eps brachycephalics, there is a similar incidence.

Corry says they watch like a hawk for the first 2-5 minutes after IM injection. In that time, the ace hasn't even started to work, at least based on what there is for onset time, etc. If it were given IV, I would maybe buy it a bit more. Another thing to remember is that ace is a potent alpha blocker, causing profound vasodilitation and hypotension, even an miniscule doses. Add to that a puppy that has been NPO for 12 hrs or so, and you have a relative hypovolemia to begin with. (The trend now a days to not withhold "clear liquids" in pups until a couple hours pre-induction). I can see how these things could happen, to any dog, esp a high strung brachycephalic dog like a boxer. Think about it: how many other brachycephalic dogs do we do LOTS of ear crops in?? Bostons are the only one I can think of, and few of them any more.

Stir the pot...make ya' think...:-)
Meghan

Subj: Re:Acepromazine in Boxers
Date: 98-01-11 11:38:34 EST
From: EmilyMeg
Posted on: America Online

Corry's dose "My present dose of acepromazine for a 8-10 week old Boxer pup is "the hub of a needle" of 10mg/ml ace. That translates into not even 1 mg per 15lb pup"

Corry, if my math is right: 15# is 6.8 kg. at 1mg/6.8 kg this si 0.15 mg/kg. That is ALOT of ace to a young pup that may be dehydrated and stressed. Try this: dilute some ace to make it 1 mg/ml--use a sterile vial and as asepticly as possible. Then dose at 0.5 mg/kg, or less, and DON'T put anything else in the syringe so as to not aspirate the dead space of the hub. I will bet you this solves 99% of your problems. Try it and let us know.

Meghan

Subj: Re:Acepromazine in Boxers
Date: 98-01-12 01:35:24 EST
From: ScoVetHosp
Posted on: America Online

Excuse my math. It's the position of the decimal point gets me every time. I use a tuberculin syringe which translates to a 1cc syringe, so "the hub of the needle" is less than 0.01cc of a 10mg/ml solution, ie the 15-20 lb pup gets less than 0.1mg or 0.01mg/kg. I hope my calculations are correct this time.

I never use it i.v. and agree that a reaction so quickly after i.m administration barely gives it time to hit the blood stream, so it's certainly is idiosyncratic! One client's older Boxer couldn't even take a quarter of a 10mg tablet orally without plummeting its heart rate to less than 40bpm

Corry


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