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Principles of Science BVetMed 3 > Equine anaesthesia > Flashcards

Equine anaesthesia Flashcards

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1
Q

Does inhalation or IV anaesthesia carry the greatest risk of death?

A

inhalation because these are most often used for long duration anaesthesia which are the most risking.

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2
Q

What must be considered when anaesthetising a horse?

A

In Europe, horses are considered food animals.

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3
Q

What do you do if you want to do a procedure under sedation and LA but the horse is too excited?

A

Horse will not sedate well –> come back another day or use GA

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4
Q

Name 2 drugs that can be used to sedate a horse.

A
  • PHENOTHIAZINES - Acepromazine

- ALPHA-2 AGONISTS - xylazine, detomidine and romifidine

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5
Q

Outline acepromzaine as a sedative - effects, ROA, combinations, side effects, CIs

A
  • on own produces limited sedation
  • calms horse and makes other procedures possible (clipping)
  • ROA = IV, IM, oral and transmucosal
  • COMBINE - opioids to give better sedation
  • EFFECTS - hypotension
  • CONTRAINDICATIONS - hypovolaemia, stallions (priapism risk), competition (abuse)
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6
Q

What is the effect of acepromzaine on volatile agent

A

considerably reduces dose and easier to maintain stable anaesthesia

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7
Q

What are the mainstay of equine sedation?

A

alpha 2 adrenoceptaor agonists (xylazine, detomidine and romifidine)

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8
Q

Outline alpha 2 agonists as a sedative - effects, side effects and ROA

A
  • deep sedation is dose related to a maximum
  • horse can still kick under deep sedation (adding a low dose opioid reduces this risk)
  • SIDE EFFECTS (major) - bradycardia, decreased CO due to a biphasic BP change, hyperglycaemia, increased urine productine, gut atony, ecbolic (xylazine especially)
  • ROA - IV or IM or sublingual gel (detomidine)
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9
Q

What are the differences between the alpha 2 agonists? 3

A
  1. ) extent of ataxia - romifidine the least
  2. ) duration of action - short xylazine, detomidine and romifidine (longest)
  3. ) cost
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10
Q

Is medetomidine licensed in horses?

A

NO - nevertheless it is used widely as an infusion during anaesthesia. Given on its own –> severe ataxia –> falling

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11
Q

Can all alpha 2 agonists be given with opioids in horses??

A

Yes (beware increased ataxia with romifine and) and/or to horses which have already received low doses of acepromazine (a phenothiazine).

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12
Q

T/F: opioids alone sedate horses

A

False (however a low dose of an opioid increases the depth of sedation of both phenothiazines and alpha 2 agonists), reduces touch response but can increase ataxia. This is not an analgesic dose.

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13
Q

T/F all sedation (except Mg) is banned in equine competition

A

True

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14
Q

What sedative can be used for horse box rest?

A

Out of competition, low dose acepromazine can be very effective without obvious sedation. In USA - a very long acting phenothiazine. Alpha-2 agonists tend to sedate too much. Reserpine used to be used, nasty side effects.

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15
Q

What should you consider when doing local anaesthesia of horse limbs?

A

consider if you want full weight on affected limb

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16
Q

Outline different analgesics in horses - 4

A
  • local vs. epidural
  • NSAIDs
  • Opioids
  • alpha 2 agonists
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17
Q

Outline NSAID use

A

excellent analgesia, especially as swelling often causes pain. High dose (flunixin) can mask surgical colic. BEWARE overdose toxicity is mainly colitis/chronic ulceration –> diarrhoea

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18
Q

Outline opioids use

A
  • controversion - balance analgesia and excitement properties.
  • BEWARE - gut effects can cause impacted colic, sedative reduce or prevent excitement effects
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19
Q

OUtline examples of opioids and ROA

A
  • BUTORPHANOL - L, widely used, limited analgesia
  • PETHIDINE (meperidine) L, antispasmodic for gut so useful in spasmodic colic,
  • ROA = ONLY by IM injection - occasional dramatic anaphylactic reactions if given IV.
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20
Q

Outline alpha 2 agonist use

A

as for other species good analgesia but associated with sedation which may not be wanted, useful for anaesthesia and epidural protocols

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21
Q

Outline epidural analgesia

A
  • easy to perform caudal analgesia - care (especially local and xylazine) –> ataxia, recumbency. For non-surgical a combination of detomidine and morphine is popular (detomidine works quickliy, morphine slow onset - several hours but long action. Morphine epidurally –> pruiritis..
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22
Q

How are longer surgeries maintained under anaesthesia?

A

volatile agents is most usual, although recently a few TIVA methods are becoming practicable.

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23
Q

How long does a horse need to be starved?

A

controversial - classically 8-12 hours - probably 2-4 hours sufficient.

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24
Q

Where should you place an IV catheter as a premed?

A

jugular vein

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25
Q

Outline preoperative preparation - 6-

A
  • starvation
  • place IV catherter - jugular
  • pre-op analgesia as relevant
  • remove shoes
  • AB/anti-tetanus (as relevant)
  • wash out mouth
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26
Q

Name 3 potential IV accidents

A
  • SC injection of irritant drugs
  • intracarotid injection
  • air embolism
  • jugular thrombosis (esp guiaphenesin).
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27
Q

Outline a normal premed protocol

A

Acepromazine (long acting and reduces anaestheic death by half) followed LATER by (as part of induction combination) an alpha 2/ butorphanol PLUS further analgesia as required.

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28
Q

Name 3 ways a horse can be controlled during anaesthetic induction

A
  • free fall
  • padded gate
  • tilting tables
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29
Q

What is the most common IV induction technique?

A

Ketamine based techniques

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30
Q

Outline ketamine IV induction

A

hallucinogenic and convulsant - must be given in combination with agents which reduce this effect (alpha 2 agonists usually). The sedative (xylazine, detomidine or romifidine) is given IV and allowed to take full effect (2-5 minutes). Ketamine then given IV with or without a benzodiazepine (diazepam or midazolam). The horse becomes recumbent in 1-3 minutes.

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31
Q

What should you do when a horse has gone down with ketamine?

A

wait until the recumbent horse relaxes (1-2 minutes later) before attempts are made to position the horse.

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32
Q

When does the influence of ketamine disappear after induction?

A

approximately 15-30 minutes after induction - the duration of action of the alpha 2 agonists used then governs the ease with which subsequnet anaesthesia is kept stable.

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33
Q

What is the tiletamine-zolazepam combination used for?

A

to induce anaesthesia in horses sedated with xylazine.

34
Q

Outline the hypnotic method of anaesthesia induction

A
  • propofol, alfaxalone or thiopental
  • large doses needed rapidly, cost
  • strictly experimental.
  • thiopentane very irritant if given outside the vein (always give via a catheter, dose depends on premeds used, generally used following an alpha 2 premedication). Can be used in combination with chloral hydrate or with guaiphenesin).
35
Q

Describe thiopentane pharmacokinetics

A
  • IV administration ,blood levels are reduced by redistribution, so although small doses are short acting, larger doses are cumulative –> prolonged sedation.
  • higher doses –> longer and worse recoveries
36
Q

What do GG and GGE stand for?

A

Guiaphenesin (a centrally acting mm relxant, it is NOT an anaesthetic

37
Q

Outline the use of guiaphenesi

A
  • always combine with an anaesthetic agent
  • for induction, give by infusion until horse becomes ataxic, then anaesthesia is induced with thiopentone or ketamine. Alternatively for induction, thiopentane or ketamine can be mixed with GG then the horse is infused with this mixture till the horse becomes recumbent.
  • very long lasting (mm weakness after an hour) –> lower dependence on volatile agents
38
Q

Describe ETT intbation in the horse

A

Easy - horse laryngeal reflexes are weak.

  • blind method
  • cuffed tubes (25mm for 450-500kg horse, 20mm for ponies, 30 mm for very large warmbloods and heavy breeds) - very expensive and easily damage
  • horses don’t usually obstruct prior to intubation but colics may regurgitate
39
Q

What volatile agent is licensed for use in the horse?

A

isoflurane is the only licensed agent but not all makes of isoflurane are licensed.

40
Q

Outline isoflurane in the horse

A
  • onset and recovery rapid
  • very fst recovery can be poor (sedation in recovery can improve this)
  • more of a respiratory depressant than halothane –> IPPV often required
  • hypotension worse than tahothane
  • less cardiac depressing than halothane
41
Q

Although halothane is no longer available, what are its properties?

A
  • slow but good quality recovery
  • less respiratory depressing so horses can usually maintain spontaneous respiration
  • PROBLEMS - reduce myocardial contractility, reduced CO, low BP and poor perfusion
42
Q

Name 2 new volatile agents

A

Desflurane and sevoflurane

43
Q

What are desflurane and sevoflurane’s properties?

A

may well prove preferable to isoflurane for equine anaesthesia becase of their low solubility, therfore fast indction, ease of stabilising anaesthesia and rapid recovery.
- Neither are licensed for equine use

44
Q

Outline the use of NO in horses

A
  • controversial
  • NO diffuses into gut spaces causing increased pressure on the lungs and further worsening the RR
  • only use if arterial blood oxygen tension can be monitored.
45
Q

Describe the breathing circuit used in horses

A

must be rebreathing (i.e. circuit) incorporating ‘absorbant’ to absorb the expired CO2, most economical too.

46
Q

What is the minimal acceptable monitoring with halothane anaesthesia? 6

A
  • DEPTH - reflexes have variable reliability, response to surgery, CV measurements (esp BP) and inspired and the end tidal level of the volatile agent
  • HR AND RHYTHM
  • ARTERIAL BP - direct pressure can be measured via a cannula in the facial artery and an inexpensive aneroid manometer
  • ETCO2 and VOLATILE ANAESTHETIC AGENT - most useful monitor of all
  • pulse oximetry (peripheral BF and Hb saturation)
  • arterial blood gas and acid base concentrations
47
Q

What are the 2 main positions for sx

A
  • lateral and dorsal recumbency
  • in both you must have the head raised, don’t overstretch the head/neck as you can stretch the recurrent laryngeal nn –> laryngeal paralysis
48
Q

Describe lateral recumbency for - 4

A
  • under front leg pulled forward
  • upper limbs supported parallel to table
  • preferably HLs pulled back
  • don’t pull limbs over abdomen (prevents venous return and leads to upper limb myopathy)
49
Q

What shouldn’t you do to a horse in dorsal recumbency for sx

A

DO NOT LOCK stifles on HL

50
Q

Define PIVA

A

Partial intravenous anaesthesia

51
Q

What is the use of infusions to improve analgesia known as?

A

Supplementary analgesia or as Partial Intravenous Anaesthesia (PIVA)

52
Q

What options are available for intra-operative analgesia? 6

A
  • Local analgesic blocks - best
  • NSAIDs - work post-op but don’t work intra-operatively
  • OPIOIDS - controversial, don’t decrease MAC in the horse, high doses cause stimulation in the anaesthetised horse.
  • ALPHA 2 AGONISTS - intermittent injection or infusion
  • LIDOCAINE - reduces MAC - reduces isoflurane but combined CV effects not improved versus isoflurane so? must stop infusion 20 minutes before end of anaesthesia or poor recovery
  • KETAMINE - probably most effective
53
Q

List the 6 main anaesthetic complications when using volatile agents

A
  • hypotension
  • hypercapnia
  • hypoxaemia
  • cardiac arrhythmias
  • cardiac arrest
  • muscle and nerve damage
54
Q

Outline hypotension as a complication of volatile agents - 5

A
  • minimum BP at 30 minutes after induction
  • BP improves after, especially once surgery starts
  • improvement due to increase in systemic vascular resistance (peripheral perfusion becomes poor)
  • Severe (MAP inadequate coronary perfusion –> cardiac arrest
  • Non-directly lethal (MAP hypoxic mm damage
55
Q

How can hypotension due to anaesthesia be treated? What shouldn’t you use?

A
  • reduce volatile agents, replace with injectables
  • large volumes of fluids (Hartman’s)
  • Inotropic agents* to improve CO, notably DOBUTAMINE by infusion but slow this if HR falls when BP rises. Care if an anti-cholinergic was included in the pre-meds as a marked tachycardia follows.
  • Don’t use vasoconstrictors such as phenylephidrine (it will increase BP at the expense of peripheral perfusion –> CO falls)
56
Q

How do you treat hypercapnia

A

IPPV but this reduces CO by increasing intrathoracic pressure BUT the significance of hypercapnia is not known.

57
Q

Define hypercarbia

A

the same as hypercapnia, an increase in the level of CO2 in the blood (normal is 40mmHg in the horse)

58
Q

Describe 2 stages of hypercapnia/hypercarbia

A
  • moderate (50mmHg or 7kPa) –> increases CO and BF

- very high (75 mmHg or 10kPa) –> muscle tremor (horse appears to be awakening)

59
Q

T/F; despite breathing high O2 concentrations, arterial oxygen levels may fall, particularly in horses in lateral recumbency.

A

FALSE - despite breathing high O2 concentrations, arterial oxygen levels may fall, particularly in horses in DORSAL recumbency.

60
Q

How can hypoxaemia be treated?

A

DIFFICULT - ask surgeon to be quicker!

  • IPPV doesn’t significantly improve oxygenation
  • occasionally the use of a salbutamol inhaler improves oxygenation
  • improve CO (to provide more O2 to the tissues)
61
Q

Why do horses become hypoaxaemic under GA?

A

Main factor is V/Q mismatch in lngs –> blood shunts (worsened by low CO, further lowered by IPPV). Mismatching is worse the larger the horse.

62
Q

Does hypoxia in horses under GA matter?

A

A lot of evidence suggests horses tolerate hypoxia very well with minimal problems. A reason for this:
1.) the Hb dissociation curve in the horse is shifted to the left versus the dog so the Hb is fully saturated at arterial oxygen tensions lower than other species.

63
Q

Outline how cardiac arrhythmias occur as a consequence of anaesthesia

A

horses are particularly sensitive to vagal stimulation whilst under inhalation anaesthesia and any such stimulation may precipitate a cardiac arrest with no prior bradycardia. Severe bradycardia sometimes occurs for no apparent reason.

64
Q

How can cardiac arrhythmias be prevented? 1 What is the problem with this?

A

anticholinergics BUT tachycardia and tachyarrhythmias are seen following the use of anti-cholinergics when animals are toxic, short of fluid, have adrenaline and sometimes following the use of non-anaesthetic IV agents (e.g. TMPS).

65
Q

How can tachyarrhythmias be treated? 3

A
  1. remove the cause
  2. reduce arterial CO2
  3. if above fail –> anti-arrhythmic agents
66
Q

Why might cardia arrest occur due to anaesthesia?

A
  • hypotension (severe where MAP <40 mmHg as this causes inadequate coronary perfusion)
  • can also occur in well monitored horses with good arterial pressures and blood gases in which there is no reason for vagal reflexes.
67
Q

How can cardiac arrest be detected?

A
  • capnograph very useful
  • a primary cardiac arest is often followed by apparent signs of lightening of anaesthesia, hyperventilation, nystagmus and jerking movements which continue until brain death occurs and resuscitation is impossible at this stage.
68
Q

How do you resuscitate a horse following cardiac arrest? 4

A
  • switch off volatile agent
  • external cardiac massage (jump on chest and land on knees, not practical to be fast enough really)
  • provide IPPV (even if horse appears to be breathing)
  • after instituting cardiac massage use drugs to restart the heart (epinephrine, atropine)
69
Q

What are the causes of paralysis of different nerves (facial, radial/obturator, spinal)

A
  • facial - fall at induction or pressure during sx
  • radial or obturator paralysis - if all limbs are adducted
  • spinal damage - sporadically, usually young horses in dorsal recumbency
  • prolonged anaesthesia not needed for this damage, aetiology unknonw*
70
Q

Outline equine post-anaesthetic myopathy

A
  • major cause of post-op morbidity and can be a cause of mortality
  • due to reduction in perfusion through hypotension adn weight of the animal
71
Q

How can you reduce the risk of equine post-anaesthetic myopathy?

A
  • padding and positioning
  • mm damage likely to occur in any anaesthetic which exceeds 2 hours.
  • improve CO (keep MAP <70mmHg or higher if surgery is likely to be long)
  • reduce surgical time if possible
72
Q

What are the advantages of total intravenous anaesthesia (TIVA)?

A

BP better maintained (not necessarily CO). Johnson’s survey showed no cardiac arrests either BUT all short anaesthetics.

73
Q

What are the different methods for TIVA?

A
  • SHORT duration anaesthesia-induction agents + top ups
  • MEDIUM anaesthesia - infusion of induction agents (i.e. alpha 2 agonist/ ketamine)
  • LONG anaesthesia - currently only experimental work because very expensive. Combinations include:
    1. propofol + analgesic (alpha 2 agonist and/or ketamine)
    2. midazolam/ketamine/alpha 2 agonist (reverse midazolam at end of anaesthesia with flumazenil but reversal of the alpha 2 agonist is not usually necessary)
74
Q

How should you position the horse for recovery?

A
  • surgery in dorsal recumbency - place in left lateral recumbency (i.e. right lung up)
  • surgery in lateral recumbency - position depends on whether hypoxia or mm damage is the most serious risk. Leaving it on the same side reduces hypoxia. Turning it over reduces mm damage.
75
Q

When should the ETT be removed?

A

controversial. perhaps as soon as horse is in the recovery box to prevent damage to the tube (v expensive) OR until horse is on its feets

76
Q

Can hypoxia occur in recovery?

A

Yes - once the horse is no longer breathing 100% O2, hypoxia can be severe. Oxygen can be administered by nasal tube.

77
Q

What determines the quality and speed of recovery?

A

which induction agents were used and on the depth of anaesthesia at the end of surgery. slow recoveries are advisable. very rapid recovers (e.g. ketamine followed by isoflurane) are usually violent. more sedative agent (xylazine) can be given to slow recovery.

78
Q

When is post-op analgesia most effective?

A

if given before pain commences - adequate analgesia will improve the quality and often speed of recovery.

79
Q

What should be done post-op before the horse is removed from the table for comfort?

A

catheterise the bladder

80
Q

Differentiate myopathy from spinal cord malacia

A
  • both complications seen post-op
  • MYOPATY - a reperfusion injury, very painful
  • SPINAL CORD MALACIA - totally painless, descending SC damage, usually results in euthanasia

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