Felipe M.
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Replying to scott@vtx-cpd.com 04/04/2024 - 05:29
Hi all!
Hope you are well
Let’s get this one sorted:
Starting with Scott’s points:
1- Please allow me to direct you (if you haven’t seen it!) to the forum thread on recovering brachycephalic animals with owners. Such an interesting topic.
2- I always give omeprazole and maropitant. As much as I do care about the gut microbiome and recognise giving omeprazole is not benign, I think increasing gastric pH does protect the oesophagus from reflux (especially the silent type), staying there during GA and causing oesophagitis and/or strictures. If the content is accidentally aspirated, it will have a higher bacterial load but will be less abrasive (reducing the initial pneumonitis hopefully). I also think being diligent with airway protection greatly reduces the chances of aspiration anyway.
3- I would recommend giving maropitant at least 30 minutes before pre-anaesthetic medication, to ensure the drugs we administer do not cause nausea or vomiting (which I guess can worsen regurgitation). This way we get the maximum benefit.Now in terms of bullet-point approach:
– Airway airway airway: be ready to intubate from the moment the animal walks through the door.
– Manage stress: be prepared to sedate these animals as soon as walking through the door if they start panting or showing signs of respiratory distress.
– Prevent anxiety: consider pre-treating these patients with trazodone if adequate, before the appointment to reduce anxiety in travel and admission.
– Laryngoscopy: be proficient at it by practicing it everyday, so that the time you need it in an emergency it is second nature.
– Be prepared: have plenty of tubes of adequate length and gauge, including a very small and long one we can place temporarily in an emergency to give oxygen and stabilise before placing a more suitable one.
– Be vigilant: before, during GA and also in recovery. Monitoring these animals closely is key to make sure they are safe.
– If you cannot hear them, assume they have obstructed: during sedation or induction of GA, it is very unlikely that the animal breathes happily much more silently than normal. Most likely in this case they are moving the chest with no air passage. Open the mouth, give oxygen and proceed to induction in a very swift manner.
– Maintain sedation times short: as soon as animal is sedated proceed to induction and intubation in a controlled but fast manner.
– Assume they can regurgitate any time: sedate and induce with head elevated until ET tube is cuffed, and also position the head adequately in recovery. If in doubt suction the oesophagus and definitely do so if you see any reflux.
– Late extubation: extubate when not tolerating the ET tube any more.
– Careful recovery: administer oxygen and ensure animals can breathe and are not obstructing.
– Fast discharge: discharge as fast as clinically sound to do so. Prolonged unnecessary hospitalisation many times causes stress.Thanks a lot!
Felipe
Hi all
Great, so let’s go one by one in a summarised manner:
Noradrenaline: as mainly an alpha-1 agonist, with a bit of beta-1 (and 2) agonism too, it increases SVR and a bit of contractility and rate. So mainly a vasoconstrictor with some inotropic effects too. This is the absolute go-to for animals in sepsis as it has been shown to have better outcomes. I also use it in animals needing higher blood pressure but with a high heart rate (due to vasodilation, for example). Heart rate tends to decrease and MAP to increase when giving noradrenaline. Very predictable in its effects, however bear in mind that increasing BP by mostly vasoconstriction gives a lovely MAP with poor peripheral perfusion, and that’s why I do not use it as first instance.
Ephedrine: it works mainly through the release of endogenous noradrenaline, so it does mainly what noradrenaline does. However it is usually given as a bolus (although an infusion can be also administered). It tends to be handy for animals just needing 10-20 minutes worth of effect, having low MAP with a normal to high heart rate. Heart rate tends to decrease, MAP to increase, and sometimes depth of anaesthesia can lighten (as in itself ephedrine is a sympathomimetic). After a couple of doses, ephedrine may not work any more (it shows what we call tachyphylaxis) as its effect depends on endogenous reserves of NA. Some animals actually show tachycardia when given ephedrine, if the sympathomimetic effect overcomes the baroreceptor activation).
Dobutamine: mainly a beta-1 agonist with some b-2 agonism too. So it causes an increase in contractility and rate, with some vasodilation. It is the one of choice in animals with low contractility, or in which increasing contractility will improve cardiac performance (like mitral valve disease or geriatric animals). It tends to increase heart rate and blood pressure, however it can also cause tachycardia. In animals with several vasodilators on board (pimobendan, acepromazine, isoflurane…), it can cause a moderate to severe tachycardia with almost no improvement in MAP, due to the compounding vasodilatory effect. It can cause arrhythmia.
Dopamine: a bit of an odd one. Low to moderate doses clinically cause mostly beta agonism (up to 10mcg/kg/min), making it behave like dobutamine, and when doses go beyond 10mcg/kg/min alpha effects become more evident, causing vasoconstriction on top. It makes it handy for the average healthy animal as increasing doses if necessary will give an additional different effect to increase BP, when accurate targeting is not necessary. However it can cause tachycardia, bradycardia and arrhythmia. And as I said above, it does a bit of everything in a not-so-clear-cut manner, so not adequate when we want to target how we increase MAP (or cardiac output).
Hope this helps!
Excellent!
Felipe
Hi everyone!
I also wanted to thank you for having chosen us, and having joined me in this journey through everything anaesthesia.
I hope you have enjoyed this course as much as I have enjoyed preparing the sessions and interacting in the forum.
I have tried to condense in this course what I believe are the foundations of anaesthesia practice, however I know there will be things that I didn’t include and you may have wanted to see. By all means give us any feedback you have, as it is this way we continue improving! I sincerely hope this course makes you enjoy practicing anaesthesia a bit more (or much more!), and become (even!) more confident in taking all those decisions that we need to take daily for our patients when needing to sedate or anaesthetise them. It is in these decisions that we can make a massive impact on patient safety and comfort.
I would like to also thank Scott, Andy and Liz at Vtx for being such a lovely bunch of colleagues to work with, it is such an honour for me to be part of this.
Wishing you all the very best
Felipe
Replying to Rachel L. 28/03/2024 - 18:12
Hi Rachel
Cardiac cases are probably one of my favourite! Thank you for your thoughts Liz, so interesting and helpful. As Liz very well said, the best way of decreasing anaesthetic risk would be so solve the problem at hand by ballooning the stenosis if this is the case. I say this for completion, however I totally understand this may not be a possibility.
Please bear in mind all the below suggestions are based on the assumption the animal has moderate to severe pulmonic stenosis and that I am obviously not examining the dog myself.
I would probably put the anaesthetic risk at moderate. Obviously we have a cardiac problem that decreases the fitness of the animal for an anaesthetic, but I have to say generally a balanced anaesthetic is well tolerated.
If animal is very stressed, I would consider giving 10mcg/kg acepromazine IM or 5mcg/kg IV 20 minutes before starting to decrease the dose of other drugs.
I would rely heavily on opioids for pre-anaesthetic medication, methadone at a dose of 0.3-0.4mg/kg IM/IV to achieve some sedation.
A low dose of alpha-2 agonists diluted and given very slow to effect is usually well tolerated too, if needed. I would suggest 1-2mcg/kg medetomidine diluted in 3-6mL, given over 5minutes IV to effect. I would try to go with the absolute lowest that allows a calm induction of anaesthesia. If HR drops too much I would also stop administering medetomidine, although if given slow this is less likely to be a problem.
Preoxygenation is very important in this case.
Induction of anaesthesia can be done with alfaxalone or propofol, depending on heart rate. If on the low side, I would use alfaxalone, if normal to high, propofol. Slow titration to effect is key to decrease the effect on SVR.
Maintenance can be done with isoflurane.
Local blocks as necessary.
Fluid therapy at maintenance rate only, with the allowance of one single 5ml/kg bolus if needing to support MAP.
Maintaining the anaesthetic as short as possible would be advisable, with special emphasis on maintaining BP (MAP of 70 as lowest) and ECG and SpO2 monitoring during GA and in recovery. Oxygen therapy in recovery also highly recommended.Hope this helps!
Felipe
Replying to Jo C. 25/03/2024 - 22:06
Hi Jo!
Such a great question, and unsure there is a right answer for every patient! As a rule of thumb, I would say I do extubate brachycephalic cats as early as the rest, whenever there is ear flick reflex.
Most of the brachycephalic cats are still better off airway-wise than your average Pug and therefore do not obstruct that easily. However some do, and if I was dealing with one of these more extreme cases in which extubating early would mean airway obstruction, I would re-spray lidocaine in the larynx before turning off my inhalant (to reduce the chance of laryngospasm) and extubate a bit later. I would probably still extubate as soon as swallowing and be ready to re-intubate if necessary. With brachycephalic dogs we can leave the tube in literally until sitting up and they do not resent it or have laryngospasm, but cats are a bit less forgiving in this regard!Again, I do gauge this on a risk-benefit ration and case-by-case!
Hope this helps
Felipe
Replying to Natalie Niven 28/03/2024 - 22:09
Hi there Natalie
Thanks a lot for your thoughts! Very interesting points there.
– In terms of the timing, there is no consensus to my knowledge. Obviously giving it beforehand follows the principles of preventive analgesia and maximises its effects by being in the tissues before surgical manipulation happens. However by decreasing the production of PGE2, we are taking away one of the autoregulation mechanisms of the kidney. Given that general anaesthesia can cause hypotension, I am of the opinion of having all the protection mechanisms we can. For this reason I prefer to give the NSAID in recovery, when I know the blood pressure is fine and will not drop. Alternatively, if the animal has been cardiovascularly very stable I may choose to give it towards the end of the procedure. I think the key point is to ensure renal perfusion whichever way we want to go with the NSAIDs (and in any situation, really!).
– In terms of which one to use peri-operatively, robenacoxib, meloxicam and carprofen are licensed for intraoperative use (so we can be confident they will not tamper with the coagulation to a point that will be clinically relevant). I tend to reach for meloxicam due to having more experience with it. However if the animals are on a different one I will continue with the same. Studies in general show similar enough outcomes to not have a strong preference for one or the other, so experience plays a big part.
– When it gets to chronic use, the main factor is how well the animals tolerate the drug and side effects. Both meloxicam and robenacoxib have been tested in cats with renal disease, with good results (10.1177/1098612X20935750) (10.1177/1098612X15590870). So I tend to favour one or the other for OA, depending which one gives less side effects, and always at the lowest dose that gives a benefit. Anecdotally, I seem to find some cats which will get GI side effects with meloxicam but tolerate robenacoxib very well.
– In terms of orthopaedic vs soft tissue cases, I do not treat them differently given I cannot find enough evidence to favour one or the other.
– When treating osteoarthritis, I do also find many animals respond nicely to anti-NGF antibodies. However it is important to not forget that those antibodies block pain, but do not do much for inflammation. For this reason I would still assess case by case, and always keep NSAIDs as an option even if as a pulse therapy (a week’s worth of treatment when weather is worse or the animal has done a bit too much exercise) as they will still yield the best results for OA pain, and help towards slowing the progression. Physiotherapy, either in clinic or at home, still plays an essential part of ensuring the muscle stays in shape and provides the support the joint is unable to do by itself.
Hope this helps!
Great stuff!
Felipe
Hi all!
Hope you are well.
So, in terms of drugs for oral/home analgesia we do have some options. NSAIDs are always a great option, and I would say the foundation. However as Scott very well said, they are sometimes not suitable for some animals.
– In dogs, I love paracetamol. We have a veterinary product (Pardale V) which is licensed for 5 days only. Longer courses can be given, but this is off label and I would reduce the dose to around 20mg/kg (even more in very long periods). It is my first line treatment when NSAIDs are not suitable, or as an add-on to NSAIDs. Cats cannot have paracetamol due to their not fully competent glucuroconjugation. However we do have other options:
– Gabapentin: great for neuropathic pain, but I do also thing it plays a role in acute pain. I introduce this one many times. It has been shown to be useful in cats with acute pain, and it’s my go-to as a first line in feline patients who cannot have NSAIDs, or as an add on.
– Amantadine/memantine: I introduce this when pain is musculoskeletal or due to osteoarthritis. Also in cases where the pain has been going on for a while and I suspect sensitisation.
– Buprenorphine: oral transmucosal buprenorphine can be a good transition opioid for home use, in both dogs and cats. I do introduce this when the animal needs additional pain relief to the above.
– Tramadol: it is an option, and a very popular one. Unfortunately its effectiveness depends a lot on the individual. It is a suitable drug provided we monitor the animal’s reaction to it, as it could be totally ineffective. Cats seem to fare better than dogs on it in the studies, however the palatability tends to not be great. I am not personally very keen on it as I like reliability, however it is an option!
Excellent!
Felipe
Hi all
Hope you are well and had a lovely Easter!
So, my personal take is that they are very much comparable at equipotent doses. And this is a very important point. We know that dexmedetomidine is the isolated isomer that is active. Racemic mixtures have 50% of each isomer, and for this reason dexmedetomidine is twice as potent as medetomidine (which is 50% dexmedetomidine and 50% levomedetomidine -inactive-). This is why medetomidine is 1mg/mL whilst dexmedetomidine is 500mcg/mL, as the volumes given by the charts will yield equipotent dosing. Levomedetomidine has cardiovascular effects similar to dexmedetomidine, and actually reduces its sedative effects, however only at very high doses (10.2460/ajvr.2001.62.616).
In my opinion, this is pretty much where it ends for dexmedetomidine. This paper actually shows they are very similar (10.3390/ani10071240).
The only instance where I may favour dexmedetomidine is in animals where liver metabolism is not fully competent. By giving half the number of molecules per kilogram, I assume I am giving less metabolic load for the liver to deal with. However, I have serious doubts this makes any difference given the low doses commonly used, and the non-activity of levomedetomidine at normal clinical doses. Potentially in long-term infusions dexmedetomidine could be favoured as we would be giving less molecules for the liver metabolise as a constant infusion. But again, I cannot say I see a clinical difference.
Hope this helps!
Excellent!
Replying to Rachel C. 20/03/2024 - 13:33
Hi Rachel
Please do not apologise! This is what I am here for, and very glad to answer as many questions as you have.
– Sterilising ET tubes should only be done according to the guidelines provided by the manufacturer. PVC tubes have none as they are single use. Silicone tubes are veterinary specific and reusable, however all the ones I have used are not autoclavable. But I totally understand, some disinfectant products may still cause deterioration or staining of silicone, causing it to harden and at times split. I have to say PVC tubes are much cheaper and much more forgiving with care. And when they deteriorate (or are used with some infectious patients), discarding them only means a few pounds cost.
– For both tubes (silicone and PVC), we rinse and brush them first, and then disinfect them with F10SC, following the dilution and instructions that come with product. This has been proven to be effective and airway safe. We have not seen any deterioration of any tubes, silicone or PVC. We also use F10 wipes to clean all monitoring (including SpO2 probes that go on mucous membranes, due to the safety for the probe and the patient). Just a disclaimer, I am in no way sponsored by F10! The choice was a result of one of my colleagues’ research and now a year’s experience.
– The safe cuff pressure limits are the same for any type of ET tube, as it determines the pressure on the tracheal mucosa (and therefore what affects its perfusion). However the issue is that in a low volume high pressure, the same pressure is less effective at sealing the airway, as the overall size of the cuff is smaller. The name “low volume high pressure” actually means that they are low in volume, and need to be at high pressures to make the airway leak-free. However we now know this is detrimental and not recommended. High volume-low pressure is definitely the way forward!
Hope this helps, but please keep firing away any questions!
Excellent!
Felipe
Very interesting indeed Scott
A lot to be said about this, and definitely early discharge is a trend among soft tissue surgeons, which I agree with in many cases. These patients have a very low stress tolerance and I think getting them back to their families as soon as it’s safe does prevent issues.
I think I would find difficult to manage actual recovery from anaesthesia with owners present. Given the interventions we sometimes need to implement urgently, I think this can be quite difficult for some owners to witness. So maybe having the right owner would be a must, to also protect them from a very stressful experience.
Doing this in a busy environment could also prove difficult as careful planning of the case to avoid excessive waiting time for the owner would be required.
I wonder if a hybrid method of standard ICU recovery plus early visit as soon as airway is safe would be a happy middle ground?
However there is definitely the owner experience of the whole process and the planning to take into account too I would say.
Very interesting indeed.
Felipe
Replying to scott@vtx-cpd.com 04/03/2024 - 19:13
Hi all
Scott, you are not being unfair actually! And there is a reason for it.
In healthy animals, normocapnoeic and on 100% oxygen, the chances of hypoxaemia are low. So many times a low SpO2 is artifactual due to pressure on tissues or bad signal acquisition by the probe. And therefore we play a bit with it. This is because we have quickly ruled out a real possibility of the low SpO2 being low, and we are assuming an artifact is the cause.
A word of caution, however! I would always advise ruling out causes for hypoxaemia (definitely so in cases where this is a possibility -ie thoracic surgery-) before blaming the probe. This is because if hypoxaemia was real, 5 minutes of it can cause irreversible brain damage. So before spending minutes re-applying the probe, definitely rule out things like O2 failure, FGF off, breathing system disconnection…etc.
However SpO2 is great!
Can we get a normal or high SpO2 and be lied to by it? Yes, but unlikely: reallistically only carbon monoxide poisoning (and sometimes methaemoglobinaemia -which in my experience usually rather gives you a non-changing low reading- and sulfhaemoglobinaemia)
Can we get a low reading and be lied to by it? Yes, many times!: Severe anaemia, low perfusion (alpha 2 agonists), venous pulsation, movement, pigmentation, fur, compression of the tissues by the probe, fluorescent light.
However, even in a healthy animal where hypoxaemia is very unlikely, we should always run a fast check before start playing with the probe, to ensure we are not dismissing a true reading indicating an adverse event!
SpO2 is a great tool that increases hugely patient safety for a modest investment, during and after anaesthesia.
Excellent!
Felipe
Hi Rachel
Great question. And it seems that in general the approach is quite diverse! I will give you my take on it:
I recommend giving omeprazole the night before anaesthesia (if possible) and the morning of. Evidence says omeprazole will increase gastric pH. This will decrease the chance of oesophagtis and stricture in case of regurgitation. In the case of aspiration, the pneumonitis due to acid will hopefully be less severe. On the other hand, another point of view is that the higher pH will make the stomach content less anti-bacterial and therefore in the case of regurgitation the chances of bacterial pneumonia will be higher. Due to the fact that good airway management and profilaxis makes aspiration pneumonia unlikely, I tend to favour the use of omeprazole as many animals will have silent or overt regurgitation during general anaesthesia.
This paper here gives evidence about a dose 3-4h before anaesthesia making a difference for the pH of the stomach and the incidence of reflux.
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1748-5827.2009.00818.x
In this paper, the use of a dose the night before plus another one 3h before anaesthesia made a difference on the gastric pH and the incidence of reflux. However only one dose the day before did not have an effect.
https://onlinelibrary.wiley.com/doi/10.1111/jsap.13328
So very often I will give omeprazole IV as soon as possible, when IV access is in place. I also administer maropitant to these patients at the same time. Granted, maropitant does not have any effect on gastro-oesophaegeal reflux, but in my head trying to reduce as much as possible any nausea (from drugs and so on) is very advisable in animals with already less-than-competent lower oesophageal sphincter and tendency to regurgitate anyway.
In animals suffering from frequent regurgitation needing a routine planned procedure (like airway surgery), omeprazole is usually prescribed for several days (as part of the treatment for the regurgitation), together with cisapride, to try to reduce incidence before anaesthetising.
Hope this helps!
Excellent!
Felipe
Replying to Jo C. 08/03/2024 - 10:59
Hi Jo
Hope you are well!
Great question, and it’s something I didn’t go into in the course but definitely interesting.
Pulseoximetry waveform has been used to assess cardiovascular status and even fluid responsiveness, many times as a surrogate for arterial line waveform. Just something to bear in mind, when doing a simple visual assessment (dicrotic notch, area under the curve…) it is important to ensure our plethysmogram has no auto-gain on. Many monitors do this as a default to always make it look as good as possible regardless of the changes, but turning this feature off (in some monitors it is not possible!) allows us to appreciate these changes.
This is a human study where they looked at it in big numbers:
https://doi.org/10.1186%2Fcc1219Another one from human anaesthesia with its use in hypovolaemia:
https://doi.org/10.1097/ALN.0b013e3181da839fA very nice review of its uses for haemodynamic monitoring:
https://doi.org/10.1016/S1036-7314(00)70611-4A veterinary one this time, on the use of PVI (derived from plethysmography) and its similarities to PPV in monitoring outcomes:
https://doi.org/10.1016/j.vaa.2017.07.007Another veterinary one, on the use of PI (also derived from plethysmography) in haemodynamic monitoring:
https://doi.org/10.1111/vec.12985Hope this helps, happy reading!
Felipe
Hi there all!
Right, as promised, here you have some examples.
– Free: patient handover sheets; pre-anaesthesia, time-out and pre-recovery patient checklists; anaesthesia machine checklists; emergency drug sheets for every patient; meetings to discuss difficult cases beforehand; debriefs after incidents or mistakes; having an open, no blame culture; ensuring everyone has proper rest; promoting a culture where people can say if they feel out of depth or not at their best; handover sheets; M&M rounds; monthly (or more frequently even!) training;
– Under 300 pounds: PVC tubes, laryngoscope, overpressure valves for circle breathing systems, airway manometers, cuff inflating devices, oxygen tubing and masks, portable oxygen cylinder, T-pieces with paediatric APL valve, ambu bag, airway box (with tubes, ambu bag, induction agent, disposable laryngoscope), bougies for difficult airways, tuohy needles for epidurals.
– Under 1000 pounds: portable pulseoximeter, portable suction unit, crash trolley/backpack, syringe driver for infusions
I am sure there are many more, but these are the ones I can think of at the moment!
Felipe
Replying to Christina L. 04/03/2024 - 08:41
Hi Christina!
Great question actually, and I have to disclose I am not a rabbit specialist at all!
Rabbits seem to have a similar blood pressure to dogs and cats, with systolic around 90-130 and diastolic of 70-90 (while conscious). So I always apply same rule as for dogs/cats, young and healthy minimum MAP 65mmHg, and in. geriatrics or there is any disease that makes me worry about organ perfusion, then minimum MAP is 70mmHg. This is only a general guide, as sometimes I will even increase this minimum MAP to even 75mmHg, and this is anyway always tailored to every animal. As an example, a patient with hypertension may require even higher (for example 80mmHg), if their normal MAP while conscious is 130-140mmHg.
Hope this makes sense!
Excellent!
Felipe
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