Felipe M.
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Hi there Gosia
Thanks a lot for this question, I am very happy to hear you are finding the course helpful!
Excellent question indeed, and a very common topic.
As I elaborated on in the course, the dose of medetomidine used and even recommended by some charts can be astonishingly high. In addition, and in my opinion, the induction of general anaesthesia via a single intramuscular injection is only justified in exceptional circumstances. In the vast majority of cases and standard clinical environments, I cannot find a justification for not using an IM pre-anaesthetic medication, IV access, pre-oxygenation, and IV induction with the agent titrated to effect. This is indeed how I manage all my feline patients, and how I have done it for years now with the main reason being sheer patient safety.
In first place, very well done for pursuing change!
Secondly, I completely agree on the concern of using high doses (if any) medetomidine in animals younger than 3 months. The direct evidence might not be overly available but we can make a very reasonable inference and recommendations are made in some books. We know paediatric patients (up to 3 months old, approximately) have a limited myocardial contractility and therefore the cardiac output is largely heart rate dependent (this is detailed in Lumb & Jones Veterinary Anaesthesia, in chapter 53, Neonatal and Paediatric patients). We know as well alpha-2 agonists produce a marked decrease in cardiac output, and especially heart rate (plenty of evidence, but one of the main research papers would be Pypendop et al 2011, in Vet Anaesth Analg, DOI: 10.1111/j.1467-2995.2011.00663.x). With this two things in hand, alpha-2 agonists should be used, if at all, “judiciously at low doses, in selected young patients with no cardiovascular disease” (this is again from Lumb & Jones, same chapter). They go on afterwards to elaborate on the potentially detrimental effects they may have anyway on very young animals, which should be taken into account.
With all this in hand, my personal recommendation and my clinical praxis, is to avoid alpha-2 agonists in animals younger than 3 months, and use low doses in animals older than 3-months but not far from this age. Other combinations like opioid+midazolam+ketamine or opioid+midazolam+alfaxalone, administered IM to achieve sedation (not at anaesthetic doses) can be used instead to a satisfactory result. This is then followed by IV placement and pre-oxygenation and induction with IV alfaxalone given to effect, plus maintenance with isoflurane.
As a general thought, paediatric animals are not “stronger” and therefore can cope/need higher doses, but quite the opposite in some respects.
I hope this helps, but by all means let me know if you’d like me to elaborate on any of the above or if you need additional help!
Once again thank you so much, and great to hear you are working towards tweaking you anaesthetic protocols!
Felipe
Hi there all!
Apologies for only saying hi now! My name is Felipe Márquez Grados and I am a specialist in Veterinary Anaesthesia and Analgesia. I am based in Wear Referrals, in North East England. Although I love all aspects of anaesthesia, I do have a special interest in patient safety and the prevention of peri-anaesthetic morbidity and mortality. It’s lovely to meet you all!
I will be taking you through a condensed session on the basic aspects of anaesthesia, with an emphasis on patient safety.
Whether it’s your main area of interest or maybe not so much (which is totally fine too!), general anaesthesia or sedation are many times the first steps in the diagnostic procedures or surgical treatment of our patients, so my aim with this session is to boost your confidence in their practice, help you maximise your patients’ safety, as well as make the whole process (even!) more enjoyable too!
I really hope you enjoy this session as much as I did preparing it!
A very warm welcome to all!
Felipe
Replying to Idris Vandekinderen 11/09/2022 - 18:44
Dear Idris
Thanks a lot for your questions! Let’s have a look.
1 – Yes, you are absolutely right! This was my mistake when narrating the webinar which I didn’t even notice when I proof watched it. Apologies for this! For clarification: the yellow lead goes on LF, red on RF, and green on LH. In ECGs where there is an additional black lead, this one goes on the RH.
2 – Capnography can be expressed in several units actually! Millimetres of mercury (mmHg) is the most often used, however the SI unit is actually the kilopascal (kPa). Some monitors will come in kPa as it is very often used in human anaesthesia this way. Some also come in %. This means % of gas pressure, which we can assume is atmospheric, and at sea level (which we can take as the pressure in our clinics) it is 760mmHg. So 1% of 760 = 7.6mmHg, while 7% would be 53.2mmHg. As a rule of thumb: CO2 (%) x 7.6 = CO2 (mmHg). Coincidentally, 7.5mmHg=1kPa. So the pretty much the same factor can be applied to convert kPa to mmHg. However, many capnographs do have the option to change the unit of the capnograph, although in some cases it is in the installation/service menu, needing of the appropriate code to access it. So for the normal limits of normocapnoea, 35-45mmHg would be 4.6 – 5.9%.
I hope this helps!
Kind regards
Felipe
Replying to Idris Vandekinderen 05/09/2022 - 23:34
Hi there Idris!
My apologies! Acronyms should always be explained before their use. My bad!
FGF means “Fresh Gas Flow” which is the flow of oxygen (or oxygen and air mixture if you were using that) that goes into your breathing system, and is displayed in your flowmeter.
IPPV means “Intermittent Positive Pressure Ventilation”. This is the inflation of the lungs artificially by positive pressure, and it can be mechanically (using a ventilator) or manually (giving “breaths” by squeezing the reservoir bag.
I hope this helps!
Kind regards
Felipe
Hi there Rumyana!
First of all, thank you ever so much for the kind words! Means a lot to hear you liked the course. Also, you don’t bother me at all! Let’s have a look at this question, I will break down the calculation:
– Your patient weighs 6.7kg, and you want to do a ketamine infusion.
– The only thing you have not mentioned is the dose of ketamine you want to administer. I will do a calculation for 2microg/kg/min, 5mcg/kg/min and 10mcg/kg/min.
– You have prepared a 0.4mg/mL solution.So!
– Ketamine is 100mg/mL in the bottle. If we put 0.4mL (40mg) into 100mL saline, we will have a 0.4mg/mL (same as 400microg/mL) solution.
– If we administer 2microg/kg/min: 2microg/kg/min * 6.7kg = 13.4mcicrog/min; 13.4microg/min*60min = 804microg/h OR 0.804mg/h; 0.804mg/h / 0.4mg/mL= 2.01mL/h you should program your pump/syringe driver to.
– If we administer 5microg/kg/min: 5microg/kg/min * 6.7kg = 33.5mcicrog/min; 33.5microg/min*60min = 2010microg/h OR 2.01mg/h; 2.01mg/h / 0.4mg/mL= 5.025mL/h you should program your pump/syringe driver to.
– If we administer 10microg/kg/min: 10microg/kg/min * 6.7kg = 67mcicrog/min; 67microg/min*60min = 4020microg/h OR 4.02mg/h; 4.02mg/h / 0.4mg/mL= 10.05mL/h you should program your pump/syringe driver to.
We all approach calculations in our own way and this is my way so I don’t get lost in numbers! In any way I think it is always helpful to operate in mg or microg/kg/h (or min), when calculating doses. By knowing how much drug we need, then it’s just a matter of dividing by the concentration in the bag to obtain the mL/h. Also be mindful if the dose is in per minute or per hour to maintain the same time units.
I hope this helps!
Excellent!
Felipe
Thank you very much Victoria and Grigori for your kind words!!!
And thank you very much as well for having joined me in this course and having supported it. It means a lot!
I hope you enjoy anaesthesia as much as I do, and wish you all the very best
Kindest regards
Felipe
Replying to Emma Holt 15/07/2022 - 12:52
Hi Emma
Great! Please let me know how it goes!
Excellent!
Felipe
Replying to Mark Laloo 13/07/2022 - 10:59
Hi there Mark
Urine retention related to trazodone is a side effect that is reported in humans, but I think there is not much in veterinary patients, maybe because it does not happen as often or because it has not been reported as much. After all, trazodone has only been administered in our patients since relatively recently.
Looking at the human literature, it seems this side effect is related to the central increase of serotonin concentrations (due to the inhibition of its reuptake) together with some anticholinergic effects.
So as you well say, absolutely. This could be a factor to be taken into account, especially in animals that can potentially already show some urinary retention. However as you say, if an IDUC is in place, it is not such a big problem. On the other hand, I would say that with the evidence we have to this date, I would still use trazodone regardless (unless urinary retention MUST be avoided -cystotomies, etc..-) and only stop it if we need to rule out causes for urinary retention, should it happen.
Excellent!
Felipe
Replying to Mark Laloo 12/07/2022 - 10:45
Hi Mark
We actually use it a lot as well. Generally with quite good results but it is true that some animals do respond better than others. I guess this is something we can see with any drug, as effects are always to some extent individual dependent, but another factor that can affect the clinical effects are how much of the behaviour we are observing is due to anxiety and how much due to general excitation. Since trazodone is an antidepressant, it is fair to expect best results when treating animals where anxiety is a big part of the observed behaviour (although it is many times not obvious at all!).
We actually did a Facebook post on trazodone, that I will paste below. A couple of bits in your question we did not touch on:
Dosing: Usually I use 3-5 mg/kg SID or BID, up to 10mg/kg. I usually start at 3-5mg/kg SID or BID as I judge best for the animal’s needs and increase over days (to prevent side effects) up to 10mg/kg if the animal does not respond as I like. I do not exceed 19mg/kg/day.
Contraindications: Glaucoma, seizures, high sensitivity to antidepressants or urine retention. Used with caution in liver, heart and kidney disease.
In terms of drug interactions and other particulars related to anaesthesia, please find that below in the excerpt from the Facebook post I did for Vtx.
“Trazodone is a very useful drug for anxiety and stress in our canine patients, however there are some considerations when anaesthetising an animal receiving it:
Trazodone, a triazolpyrimidine, is primarily both a serotonin (5HT) antagonist and a reuptake inhibitor.
However, it also has some alpha-1 adrenorreceptor antagonism activity, which can cause vasodilation and hypotension (similarly to acepromazine).
It has quite a wide therapeutic window, making it fairly safe on its own.So taking into account that trazodone inhibits the reuptake of serotonin, therefore increasing its levels in the interneuronal synapse, it interacts with drugs that can also cause an increase in serotonin. A list of some important examples is included below:
Antidepressants: inhibitors of the monoaminooxidase (MAOIs), such as selegiline; selective and non-selective serotonin reuptake inhibitors (SSRIs, SNRIs), such as fluoxetine and duloxetine; and tricyclic antidepressants (TCAs), such as amitryptiline.
Serotonin releasing agents (SRA), such us carbamazepine.
Most commonly used opioids: such as methadone, pethidine, tramadol, fentanyl.
Amantadine
Mirtazapine
Metochlopramide
Domperidone
Ondasentron
Some herbal products and spices: nutmeg, ginseng, St. John’s Wort…Concomitant use of trazodone with any of the drugs above can lead to what is known as “serotonin syndrome”. This is due to an excessive amount of serotonin being present in the central nervous system, and can cause among other signs: cardiovascular instability (usually tachycardia but also potentially bradycardia and usually hypertension but sometimes also hypotension), hyperaesthesia, myoclonus, shivering, seizures, apnoea, nystagmus, urinary incontinence, diarrhoea.
For this reason, it is very important to be vigilant of early signs when more than one drug that increases serotonin levels are administered concomitantly. In clinical practice, it is very rare to observe serotonin syndrome if only two of these described drugs are administered (at normal doses) at the same time, however as a rule of thumb we recommend never administering more than two concomitantly.In relation to anaesthesia, it is important to remember that trazodone also shows a drug interaction with acepromazine, however in this case, in a different way. The well-known vasodilation potentially leading to hypotension action of acepromazine is mediated by blockade of alpha-1 adrenorreceptors. As described above, trazodone exhibits a secondary similar pharmacological action, which can exacerbate the aforementioned vasodilation and hypotension. Additionally, trazodone plasma levels increase in the presence of acepromazine due to delayed breakdown, potentiating its effects. For this reason, acepromazine should be best avoided in these patients, or if no other alternative is available, administered with caution and a at a lower dose.”
I hope this helps.
Excellent!
Felipe
Dear Emma
That is a very sensible plan actually! You can even increase your butorphanol to 0.4mg/kg and decrease a bit your alfaxalone to 1.5mg/kg IM. Sometimes with 2mg/kg animals can go totally anaesthetised. However not having seen the dog myself, I cannot recommend one or the other better since it depends on how you perceive the dog and whether you think you have a second chance to IM inject him/her! In any case, the combination makes perfect sense and I would use it too. Oxygen therapy, although basic in any sedation, will in this case help relieve some pressure on the right heart by vasodilating the lung. The clinical relevance of this is unknown since in normal conditions the pulmonary circulation is a low resistance/low pressure system anyway, but I guess that anything that helps is worth trying!
Giving some gabapentin and trazodone orally before the appointment is a great idea. The combination is also compatible with the sedation you describe. Just make sure you gauge the effect it’s had in the animal since any sedative will have at least additive effect and potentially even synergistic effect with both drugs. If the animal comes much calmer than normal, a lower dose of alfaxalone may work nicely already. Again, your judgement will be key here.
Very interesting case indeed!
Kind regards
Felipe
Hi all
I hope you are well and keeping safe.
Let’s get this question solved! Emma, excellent job, you got it right!
ECG becomes key in the first assessment of some animals, and cats with urethral blockage are an example.
As Emma well said, as serum potassium levels increase, the ventricular depolarisation will start being affected, which will give the increased voltage T waves. As it keeps increasing, the p waves may start disappearing as SA node depolarisation is affected, and the QRS complex will begin widening in time, being proof of interference with ventricular depolarisation. The ECG becomes a sinus-like wave, and full arrest can ensue as kalaemia keeps increasing. Over this whole process, the heart rate will also decrease, with the animal showing bradycardia that tends to not respond to sympathetic stimulation or anticholinergics.
Although in humans there are much more defined serum potassium level limits that correspond with different ECG abnormalities, my experience says that in cats and dogs these levels do not necessarily correlate with the ECG abnormalities. I also think that the rate increase of the potassium as well as the chronicity of the problem plays a role in how the ECG changes in relation to the serum potassium levels.
However, any ECG abnormality will help us more or less have an idea of either how high the kalaemia is, or at least how much of an effect it is having on the electrical activity of the heart. Sometimes the ECG looks perfectly normal, but the rate might be inadequately low -or normal- considering the animal is painful and stressed. I also use this to assess those effects of the potassium on the heart’s electrical automaticity.
With all this in hand, I can begin making decisions on a couple different things:
– Do I need to stabilise the animal further? I.e. decrease kalaemia with glucose and insulin or begin a calcium infusion to counteract the effects of potassium on the heart.
– Is the animal a good candidate for anaesthesia as he/she is? We might actually see the animal is showing an adequate heart rate for their state, therefore giving us a window to sedate/anaesthetise and unblock the urethra, which will resolve the problem.
Obviously, having a serum potassium measurement is key in the management of these cases, but an ECG is a fast, effective way of having a head start in the approach to the case.
Excellent!
Felipe
Hi there Emma
I hope you are well. I had a very lovely weekend thank you! Hope you did too. Thanks for the questions, they are very interesting questions indeed!
Let’s get them answered:
1.Even though a mini-lack anaesthetic circuit is an economical choice over a T-piece in regards to fresh gas flow, it does not have the ability to perform IPPV. So if we are thinking of patient safety, the ability to perform IPPV seems crucial. So when would you choose a mini-lack over a t-piece, and vice versa?
– It is a fantastic approach indeed how you are analysing your clinical choices from a patient safety perspective. This is how I try to focus all aspects of anaesthesia at the hospital, since patient safety is the most important part of anaesthesia. As you well say, a Lack breathing system (which is a Mapleson A breathing system) is much more economical than a T piece (Mapleson D) in terms of fresh gas flow used. And this is great from a economical but also environmental point of view. However as you say, a Lack (or a mini-Lack), does not allow IPPV. This is because the reservoir is at the inspiratory flow, and as soon as we give one or two ventilations, the reservoir is filled with alveolar gas. However, it does allow to give one or two breaths, should the animal need it. So I would say in absolute terms of safety, a Lack is AS safe as a T-piece in terms of what a breathing system is. But if the animal is for example apnoeic or requires mechanical ventilation, a Lack will be impractical and a different breathing system will be necessary (i.e. a circle, or a Mapleson D -T piece, Bain).
In terms of safety on the other hand, it is best to minimise breathing system swaps during an anaesthetic to avoid introducing factors that can lead to human error (wrong connections, valves closed), so planning ahead if the animal is likely going to need IPPV definitely makes sense. However if an animal happens to need IPPV during an anaesthetic, the breathing system can be carefully changed if necessary. As a side note, consider that a Lack breathing system can behave in a more or less similar way to a Mapleson D when high fresh gas flows are used (3-4 times minute volume). This can buy us time while using a Lack to ventilate, if the animal has transient apnoea or while we are setting up a different breathing system. I would generally recommend using this feature only temporarily. Another feature to bear in mind is that (depending on the make) many Lacks have an APL valve that when closed is totally closed, whereas a modified T-piece generally has a paediatric APL valve that will open even if closed, at a certain pressure (which we call an overpressure safety feature of the valve). So, with this assumption, maybe this does put things in favour of the T-piece but not due to the breathing system itself, because of the type of APL valve equipped (which I guess depending on the make of the Lack it could be also installed in it, so it’s really just a circumstantial advantage). So to sum up, both breathing systems are equally safe, but the Lack has the impracticality of not allowing IPPV. Safety depends on other things involved, including how we plan our choices and even what the suppliers equip different breathing systems with. But having said this, provided it makes clinical sense, a Lack is a very adequate and economical breathing system ( as an example, we use it instead of circles when a circle would not be used too often in the room, to avoid having dry soda lime).2.When using a circle circuit, is it preferable to take the circuit you’ve been using through to theatre or have a new circuit already in there? Is there a safer/better option?
– Again, excellent approach to this. I have also given this a lot of thought in the past when building routines for everyday practice. And in this case I have a clearer answer! In my opinion, it is better to have a different breathing system waiting in theatre. The reason is that this way, you will have performed your machine check and checklist for your prep area before induction, and you will have done both things as well for the theatre machine. This means that both machines are checked, safe and that this is the routine you follow -making it repeatable-. On the other hand if the normal routine is for the breathing system to be taken through from prep, that will mean that the anaesthetic machine check in theatre will never be complete, since it will be left without a breathing system waiting for the other one to come through, This also introduces a source of complications/human error, which is the connection of a breathing system to the machine while an animal is connected to it. As an example, the breathing system could be potentially connected in an incorrect manner, especially if something is happening with the patient while moving through. For this reason, I always prefer to keep key transitions where complications or errors could occur as simple as I possibly can.
3.I also wondered if I could ask you about the use (or not use) of ALfaxan in cats with HCM. All of the cardiologists that I have discussed cases with are very happy to give Alfaxan to cats if needed to perform echos (if the cat is anxious normally they would give Butorphanol 0.2mg/kg IM and then ALfaxan (2mg/kg) IM) to allow echo. In lesson three you say that you would not be happy using Alfaxan with HCM due to the possible tachycardia as a side effect, therefore should I be avoiding Alfaxan when performing echos and if so why are the cardiologists happy using it? I hope that makes sense.
– Of course! It makes sense actually. Let me elaborate a bit to explain why I may have sounded inconsistent. Animals with HCM have a diastolic failure, which results in the incomplete relaxation of the ventricles in diastole and suboptimal ventricular filling (or end diastolic volume). As heart rate increases, diastolic time decreases, exacerbating this phenomenon. For this reason, we prefer to avoid too high heart rates in these animals. As I probably said in the video, a typical occurrence in theatre is that in a severe HCM, as soon as they show nociception and the HR increases, the BP decreases, which is counter intuitive (when compared to the healthy animal). For completeness, just a reminder that we also want to avoid too low heart rates as that can also cause a drop in cardiac output when the stroke volume is limited due by a diastolic failure.
Alfaxalone does not inhibit the baroreceptor reflex and allows the heart rate to increase as a compensation to the vasodilation during induction. However some animals show a very marked tachycardia, which in the animals at hand is undesirable. However there are a couple of things to clarify. This tachycardia does not happen in every animal (actually a marked tachycardia is much less common than an unaltered or just moderate increase of the HR), and in my experience, it is much rarer when the drug is administered IM as opposed to IV. These two factors, combined with the fact that alpha-2 agonists will greatly affect the measurements of an echo and that propofol is not suitable for IM injection, make the combination you mention a very sensible option (except in cases where any of the drugs could be contraindicated for any reason) for echo cardiography.
To be fair and to complete the background, in mild HCM I would quite likely be still happy to induce with alfaxalone. In moderate and cases I would definitely favour propofol, if adequate, to try to avoid tachycardia. Should propofol not be an option for any reason, I would potentially look at a co-induction with an agent that would decrease the amount of alfaxalone required to minimise the likelihood of tachycardia.
But just to emphasise again, one vital difference as well is the effects we usually see when given IV versus those when given IM.
I hope this makes all sense!Very interesting stuff.
Excellent!
Felipe
Hello everyone!
Very well done with your answers. Very interesting stuff over here. And as I said, there is no right or wrong, as we all prepare for our emergencies a bit different. At the end of the day it is what works for you.
A couple of general ideas that come to mind:
– Keep it simple: in an emergency you don’t want to have to look for things, also because you will not be as efficient at it. Other times, you may be verbally guiding someone to get you things. So having drawers looking almost “bare” with the essentials and clearly labeled will increase that effectiveness.
– Do I need this?: when we think about an emergency we automatically want to have EVERYTHING with us. But this contradicts the above point. Don’t forget that you are still within your practice and probably 30 seconds away from pretty much anything you always have around. So before including things in your trolley, always think: can’t I really spend 30s getting to this? And for some things the answer will be no, but for many others it will be a yes. An example that comes to mind: as an anaesthetist pain relief is ALWAYS at the back of my head. However in an actual emergency, it is barely a priority. And it is something I can definitely spend 30s going to the dispensary to prepare if the animal is stable enough. So it doesn’t go in the trolley.
– Make sure it’s checked: Once a week, or earlier if used, the contents should be checked to ensure nothing is missing. Once a month things should be checked for expiry of drugs or sterile instruments. A tape can be placed across all drawers, with initials and date of check. If drawers are opened, the tape will be removed, showing that it needs checking. The tape should never be replaced if the trolley has not been re-stocked!
– Make it ultra-clear: a stressful situation is barely the moment to do complicated calculations. Have tables with pre-calculated doses for emergency drugs (adrenaline, atropine) but don’t have too many that you struggle to find the right one. Make them very clear. Also, label everything so that looking for things is very easy.
– Keep it small: an emergency trolley will fail in its task if it cannot be quickly wheeled around, so keep it a size that works for you and your practice.
– Keep it an emergency trolley: maintain a culture of using it for what it’s meant to be. They tend to easily become an extra surface to keep things that should not be there. If everybody gets into the habit of treating it as what it is from the beginning, it will be easier to keep it usable.And as an example, some things we keep in ours (please bear in mind this is in a referral hospital environment so your needs may be different):
Top surface: Suction machine with tubing attached, two different tips (long tracheal and hard Yankauer) sterile next to it. Power cable ready to be plugged; Defibrillator
Side pocket: Dose charts for emergency drugs, recover algorithm, defibrillator energy chart
First drawer – IV access: Cannulae, clippers, tourniquet, tape, extensions, pre-drawn flush.
Second drawer – Drugs: adrenaline, atropine, lidocaine, diazepam, glucose, EO sterilised pre-attached and labeled syringes for everything. Pre-drawn flush in 20ml syringes. A couple of Hartmann’s bags and a bag squeezer.
Third drawer – Airway management: (Everything in foam cut-outs so that it is in display) Laryngoscope with all Miller blade sizes. Full length tubes of all sizes. Tube tie. Bougies of different sizes (to use as an over-the-stylet intubation device or to do an airway exchange. This is the actual tool that we sometimes substitute by a long rigid urinary catheter, especially in small animals like cats). Big cannulae (like a grey) for temporary “tracheostomy” – this buys a bit of time while we prepare for an actual one-. Temporary “tracheostomy” device (short and wide bore needle attached to an 2.5mL syringe without a plunger, connected to an ETT connector (I think from memory it’s a 6.5 or 7 ETT connector that attaches to it). This can then be attached to a T piece as a temporary means to give O2 while preparing for a tracheostomy. Couple of HME’s. Ambu bag.
Fourth drawer – Thoracocentesis: Needles, cannulae, butterfly needles, three way taps, extension sets and 20 – 50mL syringes to be able to drain a pleural effusion or pneumothorax. No drain kits here as that is best done sterile and can be prepared without rushing once the chest has been drain via thoracocentesis -following the principle of “do I really need this here”-. Means to quickly prepare the area (like “chloraprep”).
Fifth drawer – Thracheostomy: Small sterile surgical kit with essentials to perform and secure a tracheostomy in situ. Means to quickly prepare the area. Tracheostomy tubes of different sizes. (you could think “do you really need this here?” but in our experience if we cannot intubate the trachea and we only secured a needle tracheocentesis to provide oxygen we really only have minutes to resolve the situation -which is securing a tracheostomy-, and getting the sterile kit together in a hospital could mean doing a bit of walking and searching, so this means it is here with us ready to go, so while we place the needle the surgeon can be opening the kit and getting gloves on, saving a lot of time).
Back of the trolley – Oxygen: Our trolley is a purpose made emergency trolley and it has two straps to secure a C or E oxygen cylinder for oxygen administration. We currently do not use this as we have oxygen everywhere in the hospital so it is not practical, but in a practice with oxygen access maybe only in theatre this would be very useful. CF oxygen cylinders incorporate a flow meter and the outlet fits into “green” oxygen tubing, so it is very handy. Do not forget that this can only be attached to the ambu bag or given as flow by. This is not a breathing system and doesn’t have a valve, therefore we should NEVER connect directly to an ET tube or tracheostomy tube.
Again, this is only an example of what we find most useful ourselves and the kind of emergencies we encounter. The choices of things to keep in and out depend on how far they are for us otherwise and how quickly we need them.
I hope this helps.
Excellent!
Felipe
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This reply was modified 3 years, 1 month ago by
Felipe M..
Hi there Mark
Great question actually.
Rapid sequence induction is actually a human term that describes the administration of a pre-calculated dose of anaesthetic plus a neuromuscular blocking agent. In human anaesthesia usually the induction agent is only used to cause loss of consciousness (when we stop communicating or counting backwards) and then a NMBA is administered to relax the larynx and intubate the trachea. In veterinary anaesthesia we are fortunately able to get away without NMBAs for intubation, but it means that we rely more on the anaesthetic agent to facilitate muscle relaxation too.
When RSI is used in veterinary context, it usually means the administration of the anaesthetic agent at a set dose in a fast fashion, so as to gain airway access fast. This is the choice sometimes in cases like: high risk of regurgitation, oesophageal or gastric obstructions, constant vomiting, hypersalivation, obesity, upper airway obstruction, among others.
The technique is used to gain rapid airway access and avoid problems like aspiration or obstruction, but is a trade-off with titration of the agent, as you say. However, when a RSI is needed, usually it is the best option for the animal in the big scheme of things. Side effects of the induction agent like apnoea and cardiovascular depression may be more apparent, but usually their importance in these animals is lower than the ongoing airway risk and therefore the latter is addressed first.
Pros: fast airway access and protection, ability to control ventilation faster.
Cons: no titration of agent, potentially more side effects from higher dose, less pleasant induction if pre-anaesthetic medication is not a possibility, complete dependency on anaesthetist as all airway reflexes are abolished fast, need for rapid airway control, need for all equipment and staff to be ready (these last two are more a requirement than a con)So all in all, if we are a bit literal, what we do in veterinary anaesthesia is more a modified RSI (mRSI) at best as we do not give a NMBA. However the purpose and the effect is similar indeed.
In terms of drugs, propofol or alfaxalone are very adequate. Ketamine I would say is not a preferred agent if an alternative is available as the onset is slightly longer.
Co-inductions (which will also be covered in the course!) many times are overall slower in nature due to more than one agent being administered. Also we need to consider what we need the co-inductor to do for the patient and if it is then justified to introduce it as a factor. If the co-inductor is fentanyl for example, the animal could lose ability to effectively control the airway after it, hindering us taking control as the inductor has not yet been administered. If the co-inductor is midazolam, it is best given after an initial dose of inductor agent to prevent agitation and disinhibition, therefore not serving the purpose either as it will increase the induction time. Ketamine does not seem to fit the profile since its onset is longer than propofol and we will be dealing with delayed effects or having to wait, which defeats the purpose. The only one I could possibly be happy with is lidocaine, which can be given with the animal totally awake and will not cause sedation (therefore “the clock has not started ticking” for us to have to rush to gain airway control) but once the induction agent is given will blunt the cough reflex to some extent -if this is what we need-. However in the case of lidocaine, the animal needs to be stable before induction so that the time to administer the lidocaine is justified. In general terms, when considering doing a mRSI in a patient, we usually do not want to be dealing with many drugs and benefit from having a simple plan of action as we will be dealing with the airway in a very fast sequenced manner.
So in summary, yes, we will likely see more side effects from the induction as a titration is always preferable, however when we choose to implement an mRSI, it is because the benefits offset the aforementioned side effects.
I hope this helps!
Excellent!
Felipe
Hi there Mark
That is an excellent case example! The anaesthetic considerations in end pregnancy for caesarean are covered but this is actually different since it is mid-pregnancy and not for delivery. Very interesting indeed, since it is not often given as much thought as the former.
As an overall thought, generally if needing to anaesthetise a pregnant animal mid-pregnancy for an non-urgent procedure (that can be scheduled but maybe not postponed until after delivery), the middle third is considered the safest for the foetuses. Anaesthesia in the first third can cause abortion, while the same in the last third can cause premature birth.
It is always key to keep in mind that the homeostasis of the foetuses is directly dependent on the mother’s, so keeping a close control on it will be the best way of controlling the foetuses’.
If anaesthetising a pregnant animal in this situation, we need to ensure:
– Placental blood flow: avoid aortocaval compression (position in lateral or sternal if possible, or if in dorsal, 15 degrees tilted to the left), not to administer any vasoconstrictors (alpha 2 agonists, vasopressors like phenylephrine) and ensure maternal normotension (I would aim for a lowest tolerated MAP of 75mmHg).
– Placental oxygenation: Ensure mother never experiences hypoxaemia (meticulous preoxygenation, monitor SpO2 closely, oxygen in recovery, IPPV if necessary).
– Placental acid-base stability: ensure mother’s acid base status is preserved so that the foetuses is also stable. In an otherwise healthy mother, the most likely cause of acidosis is respiratory, so ensure EtCO2 is kept around 30-35mmHg (PaCO2 in mothers is around 32mmHg, which is lower than the 35-45mmHg in non-pregnant animals; hypercapnoea can cause foetal acidosis but hypocapnoea can cause uterine vasoconstriction too). IPPV as necessary to control this. If another acid base disturbance is present, treat accordingly.Since the foetuses are to stay still in mum for plenty of time, most of the anaesthetic drugs are quite safe at this time. Some exceptions:
– NSAIDs: better not administered since prostaglandin E2 is responsible for keeping the Ductus Arteriosus open during foetal life, which is necessary for foetal viability. NSAIDs or steroids can inhibit PGE2, causing premature closure.
– Nitrous oxide: related to teratogenicity and therefore best avoided.
– Benzodiacepines: in humans there was some association with earlier delivery, cleft palate and heart defects. The current evidence seems to actually counter that, so I would say only use if really needed.
– Alpha 2 agonists: due to a decrease in cardiac output and peripheral vasoconstriction, they will decrease uterine blood flow, so best avoided.
– Ketamine can cause uterine contraction in early pregnancy, so would avoid it until late pregnancy. Also, NMDA antagonism can have an effect on neuronal apoptosis during periods of synaptogenesis. The clinical relevance is not conclusive but maybe using it lower down in the list might make sense.
– Vasoconstrictors like phenylephrine, high doses of dopamine, or noradrenaline (obviously there will be some situations where the use of noradrenaline will be the only way forward -like septic shock-)In terms of infusions, I would try to always go in general with the lowest amount of drug possible that keeps the mother comfortable. Paracetamol would be my first line due to the excellent safety profile. Then I would escalate to low dose methadone. Then to a higher methadone dose, and if still insufficient, I would go to infusions (lidocaine or ketamine -following the above-). Infusions can cause drug accumulation in the foetuses, especially if acidosis happens, so would use them with care. The trade-off is that if the mother is in pain, uterine blood flow will also be affected, so we then find ourselves in the “between a rock and a hard place” situation.
If the animal you describe was to undergo general anaesthesia, I would have probably placed an IV cannula, administered methadone IV as a pre-anaesthetic medication, and then induced with propofol or alfaxalone and maintained on isoflurane on oxygen. If loco-regional anaesthesia can be used, it is definitely recommended.
I hope this helps.
Excellent!
Felipe
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