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ISVPS Ncert Anaesthesia & Analgesia > Considerations For Specific Conditions: Specific Surgeries/Traumas > Flashcards

Considerations For Specific Conditions: Specific Surgeries/Traumas Flashcards

1
Q

fWhat is the motor nerve terminal

A

Large nerve from the spinal cord carries impulses to the skeletal muscle. There are multiple nerve branches stimulating a vast number of nerve fibres which must be activated simultaneously for muscle contraction.

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2
Q

Where would you find the motor end plate?

A

At the neuromuscular junction, the post synaptic membrane is highly folded

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3
Q

Where would you find the most nicotinic ACh receptors ?

A

These are most concentrated on the shoulders of the folded post-junctional membrane

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4
Q

What happens when an ACh neurotransmitter is triggered?

A

Once triggered (when the impulse reaches travel down the nerve and depolarises the nerve terminal), it’s release from vesicles in the pre-synaptic membrane and crosses the junction to stimulate receptors on the post-synaptic membrane where it sets off an sectional potential and the muscle fibre contracts.

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5
Q

What is the synaptic cleft?

A

The gap between the nerve terminal and the motor end plate.

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6
Q

What happens to the ACh once it’s activated the post-synaptic receptors?

A

The ACh is rapidly hydrolysed by a cholinesterase enzyme. Its constituent parts (acetyl and choline) are recycled and taken back to the pre-synaptic membrane to form more ACh.

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7
Q

What is the difference between the 2 types of acetylcholine receptors: muscarinic and nicotinic?

A

Muscarinic AChR are involved in physiological functions (HR, force, contraction of smooth muscles and release of neurotransmitters).

NAChR are involved in either neuronal or muscle-type physiological processes. Muscle-types are localised at NMJ. Each NAChR consists of 5 glycoproteins: 2 alpha, 1 beta, 1 delta and 1 gamma. They are arranged in a cylinder with a pore in the centre. One ACh molecule must bind to the two alpha subunits simultaneously for channel activation to occur and pore to open.

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8
Q

When would we want to perform a neuromuscular blockade?

A

To facilitate intubation
To aid muscle relaxation for surgery
To facilitate PPV
To create a central eye for ophthalmic surgery
As part of a balanced anaesthesia

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9
Q

Simply, how to neuromuscular blocking drugs work?

A

The block or antagonise, the binding of ACh to NAchR

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10
Q

What are the two main types of neuromuscular blocking drugs?

A

Depolarising (one drug group: suxanethonium or succuinylcholine) and Non-depolarising (two groups: aminosteroids and benzylisoquinoliniums)

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11
Q

Describe the succinylcholine drug molecule and its action

A

Two ACh molecules back to back. When they bind to ACh receptors, they cause widespread muscle fasciculations, they then stay bound to the receptor and the channel remains open until it’s ready to disengage so remains flaccidly paralysed. It causes no fade and is non-competitive- it’s an agonist of the ACh receptor. It stays there until it’s broken down- it cannot be antagonised.

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12
Q

What problems are associated with succinylcholine?

A
  • widespread muscle faciculations due to depolarising nature
  • reported muscle pain afterwards in humans
  • increases serum potassium (relaeased when muscle contracts)
  • possible malignant hyperthermia trigger
  • occasionally can cause histamine release
  • muscles faciculations can cause increase in IOP, ICP and IAP
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13
Q

Describe non-depolarising drug molecules and how they work?

A

Large polar molecules with a positive end (N+ atom) and a negative end.
The positive atom binds with the alpha subunit and prevents ACh molecules binding (so they are an antagonist of this receptor). It’s a competitive block - only 75% of receptors need to be blocked to create muscle relaxation. Fade is present.

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14
Q

What is the difference between the two classes of non-depolarising neuromuscular blocking drugs.

A

Aminosteroids are accurate- short sticky molecules. Metabolised in the liver and likely to produce active metabolites. Dont cause histamine release.

Benzylisoquinoliniums are leptocurare molecules and are long and spindly. Probe to degradation and broken down by hydrolysis and enterases. Prone to causing histamine release.

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15
Q

Describe the characteristics of Pancuronium

A
  • can cause tachycardia and hypertension
  • no histamine release IV
  • long half life
  • 80% renal excretion- rest liver.
  • active metabolites produced
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16
Q

Describe the characteristics of vecuronium

A
  • dry powder reconsistitued with water
  • no histamine release IV
  • 40% renal excretion- rest liver
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17
Q

Describe the characteristics of rocuronium

A
  • fast onset of action
  • more CVS effects Than other aminosteroids
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18
Q

Describe the characteristics of atracurium

A
  • contains 10 isomers
  • can cause histamine release IV
  • must be kept in the fridge
  • 10% excreted in urine. 40% Hoffmann elimination. 50% plasma hydrolysis (broken down in the blood stream by non-specific enzymes)
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19
Q

Describe the characteristics of Cis-atracurium

A
  • one of the active isomers of atracurium
  • more potent than parent drug
  • much less histamine release that atracurium
  • mostly cleared by Hoffmanns elimination
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20
Q

Describe the characteristics of mivacurium

A

3 isomers (2active)
Wrong shape for hoffmans eliminations so broken down by hydrolysis and cholinesterase.
Histamine release IV
NO OTHER CARDIAC EFFECTS

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21
Q

What is hoffmans elimination

A

Spontaneous degradation in plasma and tissue at normal body oh and temperature

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22
Q

List the order of which skeletal muscles are blocked by NMblocking drugs in small animals

A

Facial expression muscles
Jaw muscles
Tail muscles
Neck and distal limbs
Proximal limbs
Swallowing
Abdominal muscles
Intercostal muscles
Diaphragm

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23
Q

How does the order of blocked skeletal muscles differ in horses and cows

A

Facial expression muscles are more resistant so further down the list

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24
Q

How does administration of a NMBlockade affect our anaesthetic?

A

Won’t be able to monitor Resp parameters (need manual ventilation)
Can’t monitor eye position or palpaebral reflex.
Can’t monitor jaw tone
Can’t see movement if patient light.

We need to use HR, BP, lacrimation and salivation.

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25
Q

How can we monitor a NMB itself?

A

Monitor for reflexes returning or ideally use a peripheral nerve stimulator

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26
Q

Where are the electrodes of a peripheral nerve stimulator placed?

A

There is a positive and negative electrode. The positive (often red) is placed proximal to the nerve.

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27
Q

What small animal peripheral nerves can we stimulate with a stimulator?

And in equine?

A

Facial, ulnar, peroneal

Facial and peroneal

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28
Q

What is fade

A

Fade is an unsustained tension in a muscle under non-dep NMB after a supramaximal stimulus. Usually seen as decreasing twitch heights.

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29
Q

What twitch patterns are available on a nerve stimulator

A

Single twitch (TW)
Tetanus stimulus (TET)
Double Burst Stimulus (DBS)
Train of four stimulus (TOF)

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30
Q

Why is a single twitch of limited use?

A

Wouldn’t see fade

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31
Q

How many twitches per second (Hz) in a tetanic stimulus?

A

50Hz

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32
Q

How many twitches in a double burst stimulus?

A

50 twitches per second, 750ms apart

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33
Q

How many twitches in a train of four?

A

2 twitches per second, over 2 seconds - most commonly used.

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34
Q

How can we check if a MNB is wearing off and what can we do to prolong it?

A

Should check twitches after 30mins has lapsed, every few minutes. If twitches return, the duration of the blockage can be prolonged same time again by administering half the original dose

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35
Q

How can we end NMB?

A
  1. Let it wear off naturally. Using the TOF ratio (the height of the fourth twitch compared to the full height of the first twitch). This ratio must be >0.9.
    Or
  2. Give drugs. For depolarising NMB, give exogenous plasma cholinesterase. For non-dep NMB give anti-cholinesterase.
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36
Q

How does giving an anti-cholinesterase help reverse a NMB?

A

Stops the acetylcholinesterase working so ACh isn’t broken down and you increase the concentration in the synaptic cleft so it competes with the non-dep drugs for receptors and helps recover. Must wait for twitches to return before giving as need some receptors free.

Care: increasing ACh will act on the muscarinic receptors as well as the desired NAChR! So you’ll see physiological effects such as bradycardia and bronchoconstriction. Often administer an anticholinergic alongside e.g atropine, glyco.

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37
Q

Describe the characteristics of the 2 common used anti cholinersterases

A

Neostigme- ++ muscarinic effects, + pre/ synaptic effects, + acetylcholinesterase inhibitor, ++ plasma cholinesterase inhibitor. Best suited with glyco and slower onset of action.
Edrophonium: +/- muscarinic effects, ++ pre-synaptic effects, ++ acetylcholinesterase inhibitor, - plasma cholinesterase inhibitor. Best suited with atropine and faster onset of action.

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38
Q

What is suggamadex? When is it used?

A

A sugar ring molecule reversal agent for rocuronium and vecuronium. It encapsulates the molecule and doesn’t have any muscarinic effects. And you don’t have to wait until twitches return to give it.

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39
Q

What is peep?

A

Positive end expiratory pressure. It keeps 3-20cmh2o in the alveoli so it doesn’t allow the lungs to empty to atmospheric pressure at the end of ventilation. Helps recruiting closed alveoli also- improves oxygenation and prevents atelectasis.

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40
Q

What powers ventilators

A

Electrical power or gas supply

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41
Q

Describe a mechanical thumb ventilator

A

Mechanical principle of the thumb closing the valve to deliver a breath.

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42
Q

Describe a bag in a bottle ventilator

A

Bellows may be squeezed pneumatically by placing it in a canister and feeding a gas into the space between. Or squeezed mechanically by a motor

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43
Q

What is a minute volume divider?

A

Ventilators that have pressurised gas fed into a reservoir bag that is continually pressurised by a spring or its own eleastic recoil. The patients minute volume is calculated and the dialled up as fgf. The ventilator then divides up the MV into tidal volumes

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44
Q

What ventilator settings should we start with?

A

RR 10-20 bpm
Inspiratory TV 10-15mls/kg
Maximum peak inpiratory pressure (20 in dog, 12in cat)
I:E ratio of minumum 1:2

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45
Q

What effects does mechanical ventilation have on BP?

A

Causes hypotension due to positive pressure in thorax reduces venous return by compressing vena cava.
Reduces pre-load and therefore will reduce CO and BP. More likely to happen if patient is hypovoleamic.

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46
Q

What effects can mechanical ventilation have on the renal system?

A

Inappropriate ADH release.
Kidneys recognise theres a drop in CO abd lowered renal blood flow, so the kidneys release ADH in response so the body retains water and reduces UO.

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47
Q

What effects does mechanical ventilation have on carbon dioxide levels?

A

Overzealous ventilation can cause hypocapnia which may result in respiratory alkalosis or cerebral vasoconstriction.
Hypoventilation may result in hypercapnia and respiratory acidosis and cerebral vasodilation.

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48
Q

How can mechanical ventilation cause oxygen toxicity?

A

If on 100% (>60%) o2 for more than 12 hours, exhaust the free radical scavengers which usually mop up the free oxygen radicals. This damages the alveolar basement membrane.

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49
Q

What can oxygen toxicity cause in a ventilated patient and what can we do to avoid it?

A

Tracheobronchitis and absoprtive atelectasis to alveolar damage.
If patient ventilated long-term, get o2 % to less than 60 whilst maintaining an spo2 of 95%

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50
Q

What is the formula for oxygen delivery

A

O2 delivery = CO x content of o2 in blood

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51
Q

Define CO

A

Volume of blood ejected from the heart in a minute
= HR X SV

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52
Q

How is O2 carried in the body?

A

97% carried bound to haemoglobin (SaO2)
3% carried dissolved in blood (PaO2)

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53
Q

What is the formula for calculating oxygen content of the blood (CaO2)?

A

CaO2= (1.34 x Hb x SaO2) + (PaO2 x 0.003)

1.34 is Hufners constant - indicated the theoretical maximum oxygen-carrying capacity e.g. 1.34ml of oxygen per 1g of Hb.

Hb concentration in blood can be measured by running haematology or blood gas.

0.003 is solubility co-efficient of oxygen in blood

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54
Q

What is the formula for MABP?

A

CO X SVR

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55
Q

What is SVR affected by?

A

Changes in vessel diameter
Changes in blood viiscocity

56
Q

If a patient is in heart failure, what happens to their blood flow?

A

Usually diverteed to central compartment decreasing peripheral perfusion.

57
Q

What influence can drugs to treat heart diseases have on an anaesthetic?

A

Some drugs e.g. acce inhibitors, cause vasodilation which may cause hypotension under GA.
Frusemide may cause patients to have low potassium levels.

58
Q

What special consideratios are there for anaesthetising patients with cardiac disease generally?

A

Oxygenate pre and post to maximise the oxygen content of blood

Ensure adequate analgesia to lower doses of induction agent and volatile agent which both may cause myocardial depression.

Avoid fluid overload and use lower sodium fluids as easier to cope with e.g. Hartmanns.

59
Q

What should be included in a pre-GA clinical exam for a patient with suspected heart disease?

A

MM colour, moistness, CRT
Ausc of all 4 chambers, noting point of intensity of any murmurs.
Auscultate lung fields
Palpation of pulses when listenting to heart to identify any lung deficits.
Observation of respiratory rate and pattern
Peripheral pulse quality and rate.

Also history incl exercise tolerance, any coughing or distended abdomen.

60
Q

Where can we auscultate the mitral, aortic, pulmonic and tricuspid valves?

A

Mitral - btw LA&LV. Heard at 5th Intercostal space on L side
Aortic - LV & body. Hears @ 4th ICS on L side
Pulmonic - btw RV & lungs. Heard 3rd ICS at sternal border
Tricuspid - Btw 3&4th ICP R side.

61
Q

What are our anaesthetic aims in a patient with mitral valve disease?

A
  • Mild vasodilation (decrease resistance so blood takes easiesst path out of the heart)
  • Avoid bradycardia. Lets the heart have more time to fill with blood before contraction making regurgitation worse.
62
Q

Descibe the changes and concerns with a hypertrophic cardiomyopathy?

A

Thickening of left ventricle, decreased volume of heart chamber and abnormal relaxation of heart muscle.

Causes:
- tachycardia
- decreased myocardial oxygenation
- development of arrythmias due to worsening function of heart.

63
Q

What are our anaesthetic aims in a patient with HCM?

A
  • Decrease HR
  • Suppress ventricular arrythmias
  • Maintain fillling pressures
  • Maintain or slightly increase SVR by vasoconstriction
  • reduce outflow obstruction in cats (alpha 2s)

Use of medetomidine or dex will cause an increase in SVR and a decrease in HR so may be good for these patients.

64
Q

What are the issues with the heart in a patient with pulmonic stenosis?

A

Narrowing of the pulmonary valve, limiting R ventricular outflow. This in turn will increase the R ventricular systolic pressure and render the tricuspid valve inefficient

65
Q

What are our anaesthetic aims in a patient with pulmonic stenosis?

A
  • maintain contractility (use MAC sparing drugs to limit volatile agent and the effects on myocardial contractility)
  • maintain or slightly reduce HR. Avoid tachycardia
  • Maintain preload with fluid therapy
  • Avoid excessive IPPV pressures as can make it harder for blood to flow out of the R side of the heart into the lungs.
66
Q

What is aortic stenosis?

A

There is a stenotic valve - narrwing of the aortic valve - which limits left ventricular outflow

67
Q

What are our anaesthetic aims in a patient with aortic stenosis?

A
  • Avoid hypotension by maintaining SVR (try not to vasodilate or constrict)
  • Maintain HR within 20% of baseline
  • Avoid factors that reduce myocardial oxygenation
68
Q

What is dilated cardiomyopathy (DCM)?

A

Happens as a result of heart muscle degeneration causing the heart muscle to become thinner. The thin stretched walls make the heart much larger.
Due to its large size, atrial fibrillation can occur. (Irregularly irregular HB where no p waves).

69
Q

What are our anaesthetic aims in a patient with DCM?

A

-Maintain myocardial contractility and oxygenation
- Avoid bradycardia and maintian the normla HR( patient will already likely be tachycardia to compensate for the poor stroke volume)
- Maintain preload with fluid therapy and avoid increases in afterload (e.g. vasocontriction).

70
Q

What is the pleural space?

A

The space between the parietal layer (lying over the inside of the ribcage) and the visceral layer (lying over the outside of the lungs)

71
Q

What should we monitor during thoracotomy and why?

A

Capnograph - tell us if things get disconnected, obstructions in ETT, reduced ETCO2 if lungs ‘ packed out way’ by vet.

Pulse ox - alerts poor o2 content in blood. Spo2 may drop if obstruction of large airways with debris or lungs packed away.

ECG - phrenic nerve, vagus nerve etc run through thorax - may see arrthmyias if tweaked or patient goes hypoxic or hypercapnic.

BP- drops from compression of vena cava.

72
Q

Why is pain relief so important in thoracoctomy surgery?

A

Extremely painful surgery and patient may be reluctant to breath properly if sore.

73
Q

What drugs can we give for thoracic surgery and why?

A

Opioids - may depress respiratory drive facilitating mechanical ventilation.
Ketamine - can be used on opening and closure as very good for somatic pain. Care in Cardio and onco patients.
NSAIDs - usual contraindications - wait until recovery. +/- paracetemol (dogs)
Alpha 2 adrenergic agonists - contribute to multi-modal analgesia
Others - including gabapaentin, maropitant, tramadol.
Local Anaesthetics - intercostal, interpleural blocks. Wound diffusion catheters and epidurals with morphine. Can use CRI of lidocaine in dogs also.

74
Q

Why is nitrous oxide contraindicated in thoracic surgery?

A

Those with lung pathology require higher concentrations of oxygen inspired.
NO will expand a pneumothorax rapidly.

75
Q

What would stabilisation of a patient about to have thoracic surgery entail?

A
  • Draining pericardial and pleural effusions
  • Oxygen therapy
  • Antibiotic therapy in some cases e.g. pyothorax
  • Cardiac medications
76
Q

What steps should be taken if a patient presents for emergency thoracoctomy due to e.g. flail chest, punctured thorax or intrathoracic bleeding.

A
  • Pain relief! Opioids.
  • Oxygen therpay if doesnt cause stress
  • Blood loss calculations once in chest +/- fluid therapy
  • Gain control of ventilation once animal under GA (dont wait for chest to be opened)Contraindicated in tension pneumothorax - have equipment for thoracocentesis
77
Q

What are the knock-on effects of lung contusions and cardiac contusions?

A

Pulmonary - bruising of lungs, blood and other fluid can gather in lungs. Excessive fluid interferes with gas exchange , potentially leading to hypoxia

Cardiac - Bruises of heart muscle can cause life-threatening arrythmias.

78
Q

How shoudl we stabilise a diaphragmatic hernia patient?

A

Fluids, analgesia (non-emetic) and oxygen

79
Q

What can we check in terms of other organs with a diaphragmatic hernia?

A

Any obstructed organs may have impaired function. Take bloods to check liver function etc.

80
Q

What drug is contraindicated in diaphragmatic hernias if the spleen is in the thoracic cavity?

A

ACP - can cause splenic enlargement.

81
Q

What ventilatory pattern should be used during diaphragmatic hernia repair and why?

A

Low volume high frequency.
Because of the presence of abdominal contents in the chest, the tidal volume is reduced, so minute volume is maintained by increasing the respiratory rate.
Also do this to prevent over-inflating atelectic lungs once repaired and cause pulmonary oedema.

82
Q

What is atelectasis?

A

Collapse of lung or lobe pf lung due to deflation/compression or filling with fluid of the alveoli

83
Q

Why should dorsal recumbency be minimised in diaphragmatic hernia repair surgery?

A

It may precipitate haemoglobin oxygen desaturation

84
Q

What is a thymoma and what effects do they have on the patient?

A

Common tumour of the thoracic cavity
- Size compromises tidal volume, may compress trachea and caudal vena cava, can wrap about large blood vessels causeing blood loss on dissection.
Often cause myasthenia gravis (an autoimmune reaction to ACh receptors) - often treateed with anticholinesterase, however these drugs may alter the duration of action of opioids and response to NMB (so start at low doses).
Myaesthenia gravis can cause megaoesophagus so prone to regurge. So head up, pre-o2 and suction, secure airway.

85
Q

What is a persistant right aortic arch (PRAA)?

A

A PRAA is a restrictive lesion around the oesophagus. Its caused by failure of the foetal vessel to regress and causes stricture of the oesophagus.

86
Q

What are our anaesthetic aims in a patient with PRAA?

A

Uusally neonatal so consider this
Prone to regurge so head up induction and suction.
May also have aspiration pneumonia already so o2 therpay , monitoring spo2 and o2 in recovery.

87
Q

What are our anaesthetic aims in a patient with pulmonary lesions (abscesses, tumours, foreign bodies etc.)

A

Oxygenation will be comprised so need o2 therapy. Surgeon may pack e including healthy lung out way so will see changes in bp, co2 and spo2.
Atmospheric contamination will happen so consider TIVA.
Can use bronchial blockers to prevent leakage of pus into airways.

88
Q

When is a pericardectomy used?

A

Used to relieve pericardial effusion (fluid trapped between the pericardial sac and the heart muscle)

89
Q

What is cardiac tamponade?

A

When there is so much fluid inside the pericardial sac that it interferes with the performance of the heart.

90
Q

What are our anaesthetic aims in a patient with pericardectomy?

A
  • Fluid therapy to maintain venous return
  • Avoid myocardial depression (use MAC sparing drugs)
  • Avoid drugs which produce bradycardia (alpha 2s) as it will blunt the patient’s compensatory tachycardia.
  • arrythmias will happen when touch epicardium +/- lidocaine
  • may not use interpleural LAs as no pericardium to protect heart from cardiotoxic effects potentially.
    Monitor blood loss
91
Q

What is a patent ductus arteriosus?

A

A PDA is a connection between the aorta and pulmonic artery and represents a shunt between pulmonary and systemic circulation. It should close after birth.

92
Q

What are our anaesthetic aims in a patient with PDA?

A

Paediatric considerations
May be ventricular enlargement
Diastolic pressure is often low (because of the connection to low pressure respiratory system) Aim to maintian BP - Avoid use of vasodilators.
Avoid vasoconstriction and dont use too high inflation pressures as can reverse the shunt.
When tying off the shunt may see a reflex bradycardia (Branham’s reflex) as a as a respomse to the increase in systemic BP.
+/- anticholinergic to correct.

93
Q

What is Monroe-Kellie Doctrine?

A

The rule that the brain is made up of 3 parts: the brain parenchyma 84%, blood perfusing the brain 4% and the CSF 12%. If the volume of one component increases it has to be compensated by a decrease in another.

94
Q

What are the clinical signs of increased intra-cranial prssure

A
  • altered mentation and changes in behaviour
  • cranial nerve deficits (deafness, dysphagia, dysphonia, visual disturbance.
  • blindness, changes in pupil size
  • seizures
  • circulatory and respiratory changes (including the cushings triad)
95
Q

What is the cushings triad?

A

Its a CNS hypoxic response in which there is a massive sympathetic discharge which is a neurological emergency.
Includes: systolic hypertension, bradycardia, bradypnoea.

96
Q

What may cause an increase in volume of brain parenchyma?

A

Oedema
Haemorrhage
Inflammation
Space-occupying lesions

97
Q

What may cause an increase in volume of CSF?

A

increased production (e.g. due to a tumour)
Decreased drainage (e.g. due to space occupying lesions).

98
Q

What may cause an increase in volume of blood in the brain?

A

Increased CVP
Increased Jugular pressure
Degree of vasodilation/vasoconstriction in the brain

99
Q

What considerations should we have when anaesthetising a patient with ICP?

A

-Position of patient’s head should be kept raised at 30o to help drain blood out of the skull and into jugular vein.
- avoid occlusion of jugular vein.
- avoid valsalva manoeuvres (forced expiration against a closed glottis e.g. coughing, sneezing, gagging, v+)
- keep PIPs low during IPPV (as may increase CVP)
- Avoid changes in vasomotor tone
- avoid hypoxia (lowers PaO2)
- avoid hypercapnia (increases PaCO2)

100
Q

How we try and normalise a raised ICP prior to GA?

A

Diuretics may reduce volume of brain parenchyma. Mannitol can cause an immediate effect because it draws water from the interstitial space to blood vessels, increasing blood viscocity and brain oxygenation.
Could also remove CSF from the ventrices and craniotomy and durotomy (small hole to relieve pressure) could be done.

101
Q

What pre-medication considerations should we have for neurological patients?

A

Benzodiazepines could be used as lower seizure threshold.
High doses of opiods should be avoided as can depress respiratory drive and stop the brain responsding to high levels of CO2.
Drugs that can cause vomitting should be avoided. (valsalva manouevre)

102
Q

What drugs have a decreasing effect on ICP?

A

Propofol
Etomidate
Alfaxalone

103
Q

What parameters will affect cerebral blood flow?

A

Oxygen and Carbon dioxide tensions
Arterial BP
Central venous pressure

104
Q

Where does a sample of CSF get sampled from ? And where does myleograohy contrast get injected?

A

The cisterna magna of the subaracnoid space of the lumbo-sacral spine. Done with a flexed head and neck and can cause the ETT to kink.

105
Q

What minimises the incidence of seizes when performing myelography?

A
  • using a lumbar puncture
  • minimise the total volume of contrast and the speed of injection
  • ensure GA’d for 45 mins posst-injection
  • maintian patient’s head-up position
  • Ensure adequate depth of GA
  • warm the contrast
106
Q

What is the difference between hansen type 1 and 2 disc disease?

A

Hansen type 1 tends to be young-middle aged chondrodystrophic breeds, due to the degeneration of the nucleus of the disc and extrusion of the nuclear material causing compression of the spinal cord.
Hansen type 2 is caused by fibroid degeneration of the disc nucleus resulting in protrusion of the annulus of the disc. Gradually causes compression of the spinal cord. Less severe signs. Tends to happen in older pets.

107
Q

What condition do dogs that usually present with non-painful paresis after jumping off furniture?

A

Fibrocartilaginous embolic myopathy (FCE)

108
Q

What is explosive disc?

A

Traumatic extrusion of the normal disc nucleus , not compressive injuries.

109
Q

What is wobblers disease?

A

Animal presents with malformation of the cervical vertebrae causing compression of teh spinal cord.

110
Q

How would we triage a spinal/neurological patient?

A

Airway, Breathing, Circulation as normal
then…
- are they paretic (weak)?
- are they ataxic (wobbly)?
- does the patient have paralysis or paraplegia (loss of limb funciton)?
- Proprioception
- Is there spinal pain? (not advisable in trauma)
- do they have superficial and deep pain? (pinch reflex)

111
Q

What drugs may we use for pre-medication of a spinal/neuro patient and why?

A
  • opiod (avoid emetics)
  • ACP may make hypothermia worse which is a concern in spinal patients, but it does not influence the incidence of seizures post-myelogram.
  • Benzodiazepine to try reduce seizures however sometimes not a long enough effect to last post-GA. Also useful to relieve muscle spasm pain - however care with loss of protective muscle tone in spinal fractures.
  • ## Alpha 2s may exacerbate bradycardia and can be emetic esp in cats
112
Q

What considerations are there for the induction of anaesthesia in spinal/neuro patients?

A

IV access
Induction agent given slowly, to effect
Lateral or ‘head-flat’ intubation to prevent strain on the neck during ETT placement.
Pre-oxygenation as this intubation technique is more difficult.

113
Q

What considerations are there for the maintainance of anaesthesia of the spinal patient?

A

ETT placed
Inhalational anaesthetic
Analgesia CRI
Fluid therapy
Regular temp checks due to prone to hypothermia (remember that MAC value of volatile agent will reduce in hypothermia so can down turn). Can pre-warm these patients for 20mins before pre-med.

114
Q

What considerations are there for the anaesthetist during myelography?

A

Flexing of head to get CSF sample through cisterna magna, care with kinking of ETT
- use silicone or PVC tubes
If getting sample from lumbar spine, hind legs need to be pulled forward which can compromise ventilation due to increased pressure on abdomen.

After injection of contrast, can see changes in RR,HR and BP. Constant monitoring required. Can cause a patient to ‘lighten’.
Can also cause hypothermia and difficult to warm patients up.
Contrast agent can cause seizures in recovery.

115
Q

Why are seizures occuring in recovery after myelography? What can we do to minimise this?

A

Caused if the contrast enters the brain so using lumbar puncture will reduce this risk. Risk of seizure will also be reduced if the volume of contrast use is reduced and the rate at which it’s injected is slower.

Keeping the patient under GA for 45 mins after injection will allow time for the contrast to metabolise and prevent seizures in recovery.
More common in patients >25kg.

  • keep patients head up at 30 degress angle in recovery to prevent contrast going into cranial vault
  • ensure adequate depth of GA before injection with contrast
  • warm the contrast agent in your hands before injection
116
Q

What considerations are there for Gadolinium contrast injected IV during an MRI

A

It is nephrotoxic so dose is reduced in kidney patients
Can lighten depth of anaesthesia
Ensure adequate depth prior to injection as can cause a burning sensation in humans.
Constant monitoring for any reactions.

117
Q

What fluid therapy is recommended for spinal patients and why?

A

IVFTindicated as lengthy GAs, support blood volume during gA and aid in elimination of contrast agents.

Dogs: 5mls/kg/hr if CVS stable, then reduced by 25% each hour until maintainance.
Cats: 3mls/kg/hr if CVS stable and then reduced 25% each hr until maintainance.

118
Q

In what condition of patient would we be concerned about sternal positioning?

A

Foramen Magnum decompression patients.

119
Q

What are the position considerations for ventral slot surgery?

A

Usually dorsal recumbency and arms taped to keep still. Has an impact on ability to ventilate so need IPPV.
Care with air emboli forming and haemorrhage as above level of heart in vascular area.
Monitoring a capnograph will alert you to air emboli.

120
Q

What peri-anaesthetic deaths can occur suring spinal surgery?

A

Air emboli
Haemorrhage - monitor BP
Arrythmias and Dysrythmias
Respiratory Arrest

121
Q

Why would an indwelling arterial catheter be useful during ventral slot surgery?

A

Helps detect air emboli.
If there is a sudden drop in ETCO2, can take an arterial blood sample can be drawn from it and run POC sample to check PCO2 and assess V/Q Mismatch

122
Q

Why is it important to monitor the ECG during spinal surgery?

A

Any touching of nerves may cause sympathetic or parasympathetic stimulation. May have bradycardia due to lesions affecting spinal outflow tract, vagal stimulation etc.

123
Q

Why is mechanical ventilation indicated during spinal surgeries?

A

Allow the surgeon predicatble and consistent movements of the chest and also good incase surgeon enters thorax.
Also during cervical spinal cases, the spinal outflow tracts are the phrenic nerve which supplies the diaphragm and therefore affects ventilation

124
Q

What general recovery considerations are there for post-spinal surgery?

A
  • elevated head 30 degrees
  • empty bladder to increase comfort of patient
  • continued fluid therapy
  • Analgesia to facilitate physio in recovery
  • Maintain spinal blood flow by preventing pain-induced vasocontriciton.
  • Can use CRI of alpha 2 for pain relief and keep patietn still if required.

Longer term pain relief incliding cryotherapy to surgical site every 6-8hrs, TENS, acupuncture.

125
Q

What actions do we need to take when ‘sharing’ an airway with the surgeon during head and neck surgery?

A
  • Ensure ETT is well secured
  • May use an oro-tracheal ETT or alternative intubations via pharyngostomy.
  • Circuit with little drag, and valves away from the head.
126
Q

Describe how you would place a pharyngostomy ETT?

A

Place as normal via oro-tracheal intubation.
Incise over the lateral aspect of the pharynx.
Push ETT past side of incision and pull back through incision (connector is detatched and may need forceps).
May require TIVA or top-ups during procedure.
Secure using finger-trap suture. Remove as normal.

127
Q

Describe Trans mylohyaloid intubation

A

Place ETT as normal
Make incision at level of 1st molar tooth over mandible. Bluntly dissect through the mylohyoid muscle. Make an incision through the oralmucosa over postiioned haemostats. Push ETT further down trachea and pull through the incision, holding the pilot balloon then ETT.

128
Q

Describe the procedure for placing a tracheostomy tube

A

Clip and prep ventral surface of neck over 2nd-4th tracheal rings.
Midline incision made through the sternohyoideus muscle.
2 sutures are placed around the tracheal rings rostral and causal to the incision site. A transverse incision is made between the two rings (less than 50% of the circumference of the annular ligament). The sutures are lifted up and out to open the trachea nad place the cuffed tracheostomy tube. Secure by tying round neck usually.

129
Q

What are the immediate and leter signs of tracheal rupture under GA

A

Immediate:
- pneumomediastinum
- subcutaneous emphysema
- pneumothorax
-pneumopericardium
- decompensation

Later:
- dyspnoea
- coughing/gagging
- anorexia
- stridor
-lethargy

130
Q

What is the problem with using mouth gags in cats?

A

Cerebral blood supply in the cat comes solely from maxillary artery. Gags cause constant bulging of soft tissues between mandible and tympanic bulla decreasing maxillary blood flow.
The decreaesd cerebral blood flow manefests as post-procedure blindness.

Keep angle of open mouth to miniumum and have breaks.

131
Q

What anasethetic considerations are there for a pharyngeal stick injury?

A
  • dehydrated due to previous inability to eat/drink
  • debris in the pharynx during intubation
  • pre-o2 for tricky intubation
  • avoid emetic opioids
  • avoid NO incase pneumothorax
  • arrythmias/blood loss once stick is removed.
  • haemorrhage risk as exploring near large vessels in neck
  • emergency airway kit in recovery incase of excessive swelling of pharynx
  • steroids to reduce swelling or NSAIDs once patient is fully re-hydrated.
132
Q

What considerations are there for a jaw fracture patient?
What special considerations are there if its caused by neoplasia?

A
  • any head trauma or raised ICP?
  • any other injuries e.g. pneumothorax, ruptured diaphragm.
  • pre o2 and prepare for difficult intubation
  • Monitor blood loss
  • analgesia
  • on revocery, keep a scissors or wire cutters near incase need to allowpatietn to open mouth, e.g. if vomits.

If due to neoplasia,
Secure airway incase pus, blood into trachea.
Also can have hypercalciaemia of malignancy, anaemia, clotting issues, cancer cachexia (muscle wastage).
Ketamine and high opioid doses tend to worsen spread of tumour whereas LAs help.

133
Q

What is the physiological change of a dog with BOAS?

A

Elongated soft palatte and stenotic nares. +/- hypoplastic trachea (abnormal growth of cartilage and narrowing of trachea).

134
Q

What are the considerations for anaesthetising a BOAS patient?

A
  • Head-up intubation due to prone to regurge, secure cuffed airway.
  • Pre-treatment with omeprazole.
  • Pre-O2 and wise range of ETT sizes.
    -Protect eyes - prone to drying of corneal surface
  • Airway kit in recovery
135
Q

What causes laryngeal paralysis?

A

Loss of innervation of intrinsic muscles of the larynx which move the voal fold opening the airway. Results in obstruction to breathing.

136
Q

What are the anaesthetic considerations for a dog with laryngeal parlaysis.

A

Usually geriatric - these considerations.
Stablising hypoxia, hypercapnia and hyperthermia prior to GA to prevent arrythmias. May need a quick sedation/GA to stop stress and worsening of condition. May require laryngeal tie-back, but must stabilise first!:…

Cool, calm and oxygenate!
- IV and blood sample(if geriatric)
- IVFT to help cool and support older organs
- cooling methods, fans, cool mats. Stop cooling when one degree above desired temp.
- Pre-meds, non-emetic (often ACP included as anti-emetic and vasodilation will reduce the body temperature).
-Provide o2.

Sedation may be enough to break the cycle, but may need future surgery.

For surgery once stable:
- non-emetic opioid
- small amount of induction agent to keep movement of larynx and allow vet to visualise.
- Secure airway
- High risk of aspiration pneumonia
- Monitor post-op swelling +/- NSAIDs/steroids.

137
Q
A

ISVPS Ncert Anaesthesia & Analgesia (8 decks)

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