Felipe M.
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Hey all!
Right, let’s get this one solved.
Dex/Medetomidine:
Uses (among others!): more reliable sedation that can be titrated to effect; cases when antagonisable drug is preferred (short procedures, liver disfunction); patients that can benefit from shorter onset (brachycephalics); additional analgesia and muscle relaxation; patients over 3 months old; some heart conditions (at lower doses) such as HCM, Sub/aortic stenosis; Boxers (in case of unknown hypersensitivity to acepromazine); Border collies (in case of unknown ABCB1 mutation); laparoscopic procedures (to avoid the spleen vasodilation making access difficult)
Side effects (some at least!): decreased cardiac output, bradycardia, AV blocks, increased diuresis, vasoconstriction (at least initially), potential for hyperthermia in animals predisposed due to vasoconstriction (more so in infusions where vasoconstriction is constant), decreased tissue perfusion (again, more so in infusions or in very high doses where the vasoconstriction is longer lasting).Acepromazine:
Uses (among others!): less reliable sedation but longer lasting effects; alpha-2 sparing effects in animals where we may want to reduce how much we give (geriatrics, very excitable patients that will need a lot of alpha-2 otherwise); some heart conditions (reduced myocardial contractility, MDVD, conduction problems, bradyarrhythmias, mild DCM -at low doses-); renal disease (although being vigilant of dosing as hypotension is also detrimental); hypertensive animals (as alpha-2 agonists will increase pressure further, but beware of decreasing blood pressure too much as organ autoregulation will have shifted up in pressures)
Side effects (some at least!): vasodilation and hypotension that adds to that caused by inhalant anaesthetics and neuraxial anaesthesia, spleen vasodilation and increase in volume; longer lasting sedation that cannot be antagonised; further heat loss due to vasodilation.Hope this helps!
Excellent!
Felipe
Hey Christina!
Great question indeed.
After using alpha-2 agonists, when we see hypotension, usually this means the first phase (peripheral vasoconstriction and bradycardia) has finished and we are now seeing phase two (normal peripheral vascular tone or even vasodilation, but still with bradycardia). The transition from the first to the second phase historically has been timed at around 45 min from IV administration, but the reality is that the time is completely dose and route dependent. So we can actually see it much earlier.
Provided we are certain that the blood pressure is indeed low and not due to spurious inaccurate readings, I would be very happy to skip the atipamezole and treat straight away with muscarinic anticholinergics. This is because if the blood pressure is already low, giving atipamezole will not work as there is no vasoconstriction to reverse. It will indeed increase the heart rate a bit, but not enough to compensate the now established hypotension. Any potential added vasodilation from the atipamezole will actually only worsen the hypotension.
On the other hand, if, for example, after induction, the blood pressure was fairly high and we had marked bradycardia with or without conduction blocks (usually second degree AV block), then this would be a case for administering atipamezole. In this case, we want to undo the still present peripheral effects of alpha-2 agonists (vasoconstriction) as well as the central ones (bradycardia, taking into account that part of it is due to the peripheral vasoconstriction actually).
So you can see this is a bit of myth busting: Never give muscarinic anticholinergics to animals who had alpha-2 agonists!!!! – Actually, in the right setting, yes, you can –
I have to say that there is a reason for this historical guideline. Before practitioners routinely monitored blood pressure, and back when much higher doses were recommended, the heart rate would get worryingly low and they would treat this with muscarinic anticholinergics. However in this case these animals had a very high blood pressure, that would go even higher -worryingly so- after the muscarinic anticholinergics.Hope this makes sense!
Excellent!
Felipe
Hey all!
So let’s get this one answered
In terms of managing fear-aggressive dogs and cats, there are some strategies we can follow:
– Admission:
Very important the environment and keeping the animal as calm as possible. Separated cat waiting areas are great, and or quick admissions with no wait for dogs that are dog-aggressive.
For cats: pre-admission gabapentin the morning of, and sometimes the night before and morning of admission, can help in achieving a calmer admission to the clinic.
For dogs: pre-admission trazodone for a couple of days before the appointment, and in severe cases adding a gabapentin dose the morning of admission.– Administration of drugs:
In this regard the management and handling of the animal are key to keep stress level as low as possible.
Administering the drugs IM can help, and (in healthy animals) combinations of an alpha2 agonist, opioid, and ketamine (dogs) or alpha2 agonist, opioid, midazolam +/- ketamine (cats) can help in achieving a deeper sedations. Don’t forget to administer oxygen while placing IV.
In cats, using a blanket to wrap them can facilitate injecting and is safer than crush cages. In dogs, an injection can be done in the lumbar while the animal is being walked to be kept distracted. If needing extra safety, a hypodermic needle can be attached to an IV extension, and this to a syringe. Then the line is primed with the drugs all the way to the needle, and the syringe will have spare air in to push it in. The needle is then injected in the dog, but now we can walk alongside while injecting remotely and safely. I would recommend syringes of 2mL tops as the pressure will otherwise not be high enough to push the drug in effectively.– Recovery:
If animals are on trazodone, I would avoid acepromazine. I tend to use medetomidine for recovery in dogs and cats (1-2mcg/kg IV at a time) after extubation, to make recovery a bit smoother. In dogs with no trazodone on board, acepromazine can be given before recovery too, however if discharge is planned shortly after, probably best to steer away from it. Giving drugs before extubation may delay this, however in very fear-aggressive animals this can be done for safety reasons.Hope this helps, but let me know if you would like further info!
Excellent!
Felipe
Replying to Samantha S. 19/06/2023 - 20:59
Hi Samantha
Please don’t apologise!! This is what I am here for and it’s a pleasure.
Great, ketamine can help as an analgesic and improving depth of anaesthesia. I would recommend diluting it (I rarely use any more than 1mg/kg but 2mg/kg is not wrong at all!) and giving it slow over 3-5min. This helps reduce the apnoea we sometimes see.
Since ketamine has a moderately long duration, this can be good enough in shorter procedures for us to be able to decrease the isoflurane on the vapouriser. In longer procedures, an infusion will maintain the plasma concentration better and will maintain this benefit of reducing isoflurane needs.
Just keep in mind that ketamine (especially when given as a bolus) can cause the eye to go central and therefore will make a bit trickier to judge confidently depth of anaesthesia! Jaw tone can help you confirm this.
Hope this helps!
Felipe
Hi there Samantha!
Thanks for your question and it’s absolutely fantastic to see that you aim for 70mmHg MAP. I firmly believe that giving a bit extra margin, especially in older animals, makes a difference in maintaining organ perfusion.
I would always intervene as soon as I see hypotension, especially given that from recognition of hypotension to successful treatment sometimes we can see a fair bit of time in between.
I would say that, unless there are other conditions that contraindicate fluid boluses, starting with one is sensible. However, if there is no response, I would not insist as the animal will not respond. If on the other hand the effect lasted 10-15 min but wore off, I’d be happy to give up to 3 or so.
Should the animal not respond to fluids, or need constant bolusing, I would then go on to a pressor. Dopamine tends to be (unless a specific problem makes me choose a different one) my go to. However ephedrine can be an option too, especially for shorter procedures.
I hear you with dentals being the biggest source of headaches in blood pressure matters, first because descaling and so on is usually not painful, and neither are extractions if the blocks work! So the effects of the anaesthetics become then more obvious. However this definitely warrants being more vigilant so great stuff you are looking to improve things. In any case, being proactive definitely pays off.
Something else you could potentially do is using infusions to decrease the amount of isoflurane used. Drugs like dex/medetomidine or ketamine can help as an infusion having an obvious MAC-sparing effect (around 20% for ketamine and 30% for medetomidine!). Using less isoflurane also helps absorb some of the costs of the additional infusion.
Hope this helps but let me know if you need me to go a bit further with anythingExcellent!
Replying to Okba Takieddine C. 09/06/2023 - 02:01
Hi there Okba
First of all, please don’t apologise for your English, it’s great!!! 🙂
Of course, let’s go one by one:
1/ Alfaxalon:
Is the same dose can be used for sedation and induction ? And how can we avoid the apnea with IM inj?– For induction, we tend to draw up 2mg/kg of alfaxalone and give it intravenously to effect, 0.5-1mg/kg at a time, waiting 20-30 seconds between doses. For sedation IM, we generally mix 1-2mg/kg of alfaxalone IM with something like butorphanol, or 0.5-1mg/kg if we mix it with an opioid plus a sedative like medetomidine.
Apnoea is a side effect of any induction agent, which is actually dose-dependent. To decrease the chances of apnoea the way forward would be to decrease the dose of alfaxalone given.2/ In my country we have a combination of Telitamine+ Zolazepam : it should be given with the “sandwich technique”?
– That combination also existed in my country, Spain, actually! Never have used it myself to be honest, however I have used before ketamine/diazepam combination for induction of anaesthesia which follows a similar principle (a dissociative anaesthetic and a benzodiacepine).
In other situations we do use this “sandwich technique” of giving, for example, a bit of propofol, a bit of midazolam, and more propofol if needed. In this case I would actually not follow this principle. I would recommend actually giving both drugs at the same time in incremental doses, following the data sheet. If I’m not wrong the preparation actually contains both drugs already in the lyophilisate for reconstitution. Giving it this way makes sense, given that the onset of the bezodiacepine and the dissociative anaesthetic are similar, which facilitates the benzodiacepine counteracting the side effects of the dissociative (muscle spasms, rigidity, etc.).3/ To avoid hypotension while using a2 : when should we give atropine? As pre-med or only if we had a drop on BP intra-operatively?
– Great question! I would never recommend giving atropine before or at the same time as alpha-2 agonists as the initial change in BP is usually hypertension, which would be severely aggravated by the atropine. I would not hesitate, on the other hand, to treat hypotension with concurrent bradycardia with atropine, once it happens. So I would say, when and if it happens intra-operatively!
4/what’s the best and safest sedative/analgesic that i can use daily(at least the first 4 days) for the same patient for quick and painful procedure (dressing wounds)??
– If the animal is otherwise healthy and not paediatric or geriatric, I would go for methadone 0.2mg/kg plus medetomidine (dose depending on level of sedation needed and demeanour, but somewhere between 5-10mcg/kg in dogs, or 10-15mcg/kg in cats) IM. I would then place an IV cannula and top up the sedation with medetomidine, 1mcg/kg diluted IV at a time, when and if needed to deepen the sedation. I find this way works great and it’s very practical. Titrating the medetomidine to effect also avoids overdosing and side effects.
Something that also works great in cats is to add to the above initial IM sedation 0.2mg/kg midazolam to make it a bit deeper and give some extra relaxation with minimal additional side effects.Hope this helps!
Excellent!
Felipe
Replying to Okba Takieddine C. 08/06/2023 - 14:09
I there Okba!
I am well thank you so much, hope you are well too.
Thanks a lot for sharing your experience and practice. I love to hear you give oxygen even in cases where no inhaled anaesthetic is used. Definitely the way forward, and the safest too.
In terms of dosing, butorphanol, medetomidine and ketamine are very commonly used and with a wide therapeutic window. If you’d want to tweak your dosing, I would personally always recommend dosing drugs per patient weight. The risk of giving a fixed volume of them per cat means that the dosing can be very variable depending on the patient’s body weight, with the increased risk of side effects as well. By calculating each volume for each patient with a fixed dose in mg/kg or mcg/kg, we give the exact same dose to each patient irrespective of body weight (so what is variable is actually the volume we give), making it more predictable and therefore safer as well.
In addition, something else to point out would be to change the butorphanol for methadone for painful procedures or for animals that arrive in pain already.
Definitely right to wait around 45 minutes or so after IM injection of ketamine before antagonising the medetomidine to prevent dysphoria in recovery. I am sure you already do this but just a reminder to still administer oxygen while waiting that time before antagonising the medetomidine.
Lastly, don’t forget that in cats we generally give half the volume of atipamezole of that given of medetomidine, due to them metabolising medetomidine faster than dogs, where we administer the same volume.
Hope this helps.
Excellent!!!
Felipe
Hi there Samantha
I am glad you are finding the information useful, thank you so much!
Great question, and a valid concern.
Indeed, (sidestream, the most common) capnography monitors can get damaged if water is suctioned in the line by the pump and it goes into the infrared spectrometer. However, in order to stop this, there is most often a water trap (where the line connects to the monitor, a plastic receptacle with a clear cup), that prevents this. Condensation suctioned in the line is collected there. It is good practice to always make sure at the end of an anaesthetic or a workday that the water trap is emptied (in most monitors the water trap can be taken off and clear cup comes apart for this reason). This water trap is usually changed every so often (as per manufacturer’s recommendations).
During a dental there is indeed a lot of lavage fluid in the mouth, however this should never be going inside the airway. Use of appropriate size cuffed et tubes, with cuff inflated appropriately and having a leak free airway, together with effective throat packing and head positioning should mean no lavage enters the airway. Should all connections be appropriately tight, the only way of this water to go in the capnograph would be if said water has entered the airway, which would certainly cause major problems in our patients.
Some additional precautions can be taken anyway, which are good practice. Keeping the insert of the capnograph to the breathing system uppermost (by rotating the attachment, never the ET tube inside the trachea!) avoids condensation pick up and prevents the line insert being in a pool of lavage. Covering said insert with swabs can also help. Lastly, something we use for every and any patient is a HME. These filters prevent bacteria and condensation from going into the breathing system, and since the capnograph insert is beyond the filter, no condensation ever makes it to the capnograph. Ensuring the capnograph line is not split (especially where it joins the luer connector) is necessary to avoid isoflurane leaking, artifactual capnography readings and fluids potentially entering the line too.
In any case, lavage should never make it inside the airway, which is the most likely place where it would be picked up by the capnograph.
We use and have always used capnographs for any and every procedure, including those with copious lavage or bleeding around the area and I cannot remember a time fluid has gone in the capnograph.
So in summary, look after your capnographs but look after your airways even more! By all means use your capnograph for all your dentals, just be mindful of connections being tight, airway being secure, and equipment being in good working order and you should always be fine. And in any case, the water trap should be there in case.
Hope this helps!
Felipe
Replying to Christina G. 22/05/2023 - 20:43
Dear all
I hope you are having a great week and managing to catch a bit of sun at the end of the day.
Let’s get this one answered.
The reasons the use of (dex)medetomidine, is controversial in animals with renal disease are:
– They cause a substantial reduction in cardiac output and therefore oxygen delivery to the tissues. Kidneys get 25% of the cardiac output, and reductions in an already dysfunctional organ could cause deterioration. Don’t forget that pressure is not flow.
– The current literature on the effect of alpha 2 agonists on renal arteries (mainly 4 papers last time I checked) is somewhat controversial. Several find the resistive indexes (a way of measuring vasoconstriction) doesn’t really change. However looking at other variables like GFR, renal blood flow or blood velocity, some papers do find a decrease. On the whole it seems changes are not massive, and not consistent across the research, but I guess then it all comes down to risk assessment and risk-benefit balance. I am personally still not convinced about the results.
– Alpha 2 agonists do cause an initial increase in pressure and in a second phase a return to normal or even decrease in pressure (especially under GA). Kidneys do keep a constant flow between around 50-150mmHg of MAP (unless chronically hypertensive – think CKD), and we can support blood pressure should it drop. So this part does not worry me much as I know I can manage side effects.
– In terms of metabolites, (dex)medetomidine is mainly metabolised by the liver (a tiny bit in the kidney) into pretty much inactive metabolites, later excreted by the kidney as they are hydrosoluble. Given the metabolites have very little activity, an impaired kidney will indeed take longer to excrete them, but the clinical effect (especially of a single dose) will be inexistent.What do I do?
I generally avoid these drugs in animals with kidney disease (definitely so in AKI). I tend to rely much more heavily in other drugs like opioids and acepromazine or sometimes different combinations of benzodiacepines with drugs like ketamine or alfaxalone (my choice depends on the species, the level of impairment, the procedure, the route and the behaviour profile).
In animals where I think an alpha 2 agonist would really be beneficial, I tend to go with other drugs first, like an opioid and acepromazine, and only use the smallest amount of alpha 2 I can get away with, usually diluted and given to effect. This way I am giving alpha-2 sparing drugs first, and then titrating to the minimum dose I need.I hope this helps!
Excellent!
Felipe
Replying to Emma S. 17/05/2023 - 17:13
Hi Emma!
That is fantastic to hear, thank you very much! 🙂
Felipe
Replying to Okba Takieddine C. 16/05/2023 - 23:27
Hi there Okba,
Thanks a lot for your questions! Let’s get to them:
1- The pre-anaesthetic evaluation should be done the day of surgery or before?
Very fair point. I would recommend to do it as close to the procedure as possible, so that the information we get is accurate for the timeframe of the procedure. However in other cases we may want to do this assessment some days before the procedure, should we need to plan things with enough time or allow this time for additional tests. As examples, I would do the pre-anaesthetic screening the day before a TPLO for a healthy animal, however if we were considering doing a bone marrow biopsy in an animal with chronic anaemia it would be worth assessing the animal some days before the procedure in case the PCV has dropped too much and we need to organise a transfusion before the procedure.
2- sometimes we find by chance mild elevated liver enzymes on 2 yo cat (looks healthy on physical exam) that came in for a routine spay,if we didn’t do the blood work, the anesthesia can affect the safety of our patients?
Thank youAnother great question. There are a couple of studies (3 last time I checked) looking at the value of pre-operative blood tests. My overall conclusion looking at the three of them together is that, in the absence of clinical signs or previous health problems, pre-operative blood tests tend to be of the highest significance (so detecting pre or subclinical problems that effectively led the anaesthetist to change or cancel the anaesthetic) in animals considered geriatric (around 7 years old for a dog, and around 9 for a cat -the papers only included dogs however-). In young animals these papers did not seem to find a huge amount of value of doing blood tests with no previous history of disease and a normal clinical exam.
However this should be put into context of cost-benefit and personal approach. Some practitioners will not anaesthetise an animal without basic blood tests, and that is very very fair. The more information we have is always best as there will be a potential very small proportion of animals with pre-clinical or subclinical problems, albeit young and apparently healthy, that we could diagnose with these blood tests.Hope this helps!
Excellent!
Replying to Okba Takieddine C. 16/05/2023 - 10:46
Hello everyone!
Be very welcome to this course.
I am so happy you have chosen us to learn a bit more about anaesthesia! I really hope you enjoy this course as much as I have enjoyed creating every lesson.
Anaesthesia, like any other discipline, is a very wide field that can be very challenging to condense to a course format. For this reason I took what I have found over the years that is the basic foundations that have the biggest impact on patient safety and care, put it together with those things I am asked most frequently by colleagues, and made this course in the most practical manner possible.
However, you may find that there are things you wanted to know about that haven’t been touched in the depth you wanted during the course. No problem at all! This forum is here for everyone to ask those questions they would like more information on or clarifying further. Do not be afraid to ask away, even if you think it is a very basic question. There are certainly no silly questions, especially when even the most basic principles in anaesthesia are fundamental to maximising patient safety.
You will hear me repeat “patient safety” endless times during the course. And it is for a reason. In my opinion, anaesthesia has several aims, but one is the most important. Obviously we want to provide analgesia, amnesia, muscle relaxation and overall anaesthesia to the animal undergoing a procedure, but for me the most important is patient safety. When an animal is under the anaesthetist care, the paramount duty of the anaesthetist is to ensure the animal is safe while the needed procedures are performed, so the patient can go back to their normal lives without any impediments. I am convinced little changes and tweaks to our everyday practice can have a massive impact in patient safety, and this then became the priority in the course! I hope you find it very useful.
I will post a question every now and then for everyone to have a think and fire your most wild guesses. Please do not be afraid to answer!
So all in all, thank you once more for being here, and be very very welcome!
Excellent!
Felipe
Replying to Gosia Scherchen 28/03/2023 - 21:59
Hi there Gosia
No problem at all! Always happy to help.
I am very glad you enjoyed the course, thank you so much for the kind words!!
Felipe
Dear Emma
Lovely to read you again!
Great question indeed.
To begin with, I’d say, in additive order my protocols would be:
– OA: Frunevetmab injections (solensia) +\- NSAIDs +\- gabapentin +\- amantadine
– Dental pain: NSAIDs +\- gabapentin +\- amantadine
In terms of NSAIDs in IRIS stage 2 and 3 CKD, there are a couple of studies looking at this:
Meloxicam: it has been tested up to 6 months, with a lower daily dose (0.02mg/kg), in cats with IRIS stage 2 and 3 CKD. No deleterious effects were found. (Reference: 10.1177/1098612X20935750.)
Robenacoxib: it has been tested for up to a month, with a daily dose ranging between 1 to 2.4mg/kg, in a population that included a good number of IRIS stage 3 CKD. No deleterious effects were found (Reference: 10.1177/1098612X15590870)
So in terms of NSAIDs and CKD I would say the current consensus is that its use in this population should still be judicious and on a risk-benefit basis, always aiming to use the lowest dose that gives a clinical effect. On the other hand it is accepted these two drugs seem to be well tolerated chronically, provided the animals are well hydrated (I.e. encouraging extra water intake, etc.). I would still recommend monitoring the renal parameters once or twice a year (at the end of the day no studies have monitored beyond 6 months).
I hope this helps!
Thank you
Felipe
Replying to Gosia Scherchen 11/03/2023 - 18:02
Dear Gosia
Thanks for your reply!
I have been doing a bit of a search and all the reference I could find for this protocol was the table from Cats Protection. In all versions I could not see (I do apologise beforehand if I have missed it) any reference to any research, clinical trial, or book reference. All that is given is the table and the link to the app. There is a publication on In Practice making reference to it (https://doi.org/10.1136/inp.l5007). The references of the publication do not include (that I can see) any research on safety of the anaesthesia protocol.
Just to give additional context, the doses stated in the “quad combination” there are all higher that any of the doses for medetomidine, or equipotentially, for dexmedetomidine, included in the American Association of Feline Practitioners Feline Anaesthesia Guidelines, published in ISFM in 2018 (https://doi.org/10.1177/1098612X18781391).
I could not find myself any research (again, I do apologise if it’s there and I didn’t see it, I did not do an exhaustive search and I will be very happy to be corrected) on the safety for this drug combination, and neither have I found references to its outcomes.
Another bit of context is the fact that both myself in the past, as well as other colleagues working in charities who have reached out to me for advice, found ourselves able to reduce the medetomidine doses very substantially from what some tables give for “triple combination” (in this case for adult cats). As a disclaimer, obviously different tables will give different doses.
Having in hand the above and my own personal training and experience, I cannot personally support the use of those doses in standard practice. This is especially true for animals younger than 3 months, patients in which the use of alpha-2 agonists should be, if any, very judicious and at low doses.
As another disclaimer, although the age is not specified there, it seems the recommendation of pre-pubertal neutering from Cats Protection is from 4 months of age. So by being older than 3 months of age in my opinion the use of alpha-2 agonists would be adequate, but I still think that the dose, especially of medetomidine, is excessive.
Once more, I cannot recommend enough (in standard practice) always aiming to provide an IM pre-anaesthetic medication, securing IV access, pre-oxygenating, inducing anaesthesia with an injectable agent titrated to effect and maintain on isoflurane in oxygen like we do in canine patients. All these steps are basic to anaesthesia and patient safety. I think it is always important to put these protocols in the context of a charity (doses aside), where funds are very limited and throughput is very important.
I hope this helps you, it is not a straight forward answer I am afraid!
Felipe
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