Considerations for Specific Conditions: Life Stage/Pathologies Flashcards

1
Q

What are the different risks for the different trimesters of pregnancy?

A

1st - embryotoxicity
2nd - placental separation - can lead to blood loss for mum and decreased or cessation of oxygen delivery to the foetus. 3rd - major physiological changes

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2
Q

Describe the changes associated with the CVS during pregnancy

A

CO and Blood volume increase to meet placenta needs. Plasma volume increases proportionally more so that red cell mass so results in a dilution anaemia.

Albumin concetrations decrease by dilution. Leads to greater free fractions of drugs in bloodstream, risk of overdose.

Cardiac reserve decreases and decrease in SVR. Vasodilation contributes to hypotension. Large belly can put pressure on vessels e.g. vena cava. Positioning is key.

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3
Q

Describe the changes associated with the respiratory system during pregnancy

A

Increase in minute volume, o2 consumption and metabolic o2 reuirements.

Decrease in functional residual capacity (FRC)- volume of gas left in lungs at end of a normal breath. More likely to destaturate/become hypoxaemic.
Supplement o2 before and after GA due to reduced FRC and increased metabolic oxygen requirement.

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4
Q

Describe the changes associated with the GI system during pregnancy

A

Uterus puts pressure on stomach, alters its position, changing the angle where the oesophagus enters the stomach making sphincter incompetent.

Progesterone decreases the tone of the oesophageal sphincter and slows digestion, food is in the stomach for longer.
Animal is prone to regurge - head up induction, sternal, secure ETT cuffed.

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5
Q

Describe the changes associated with the renal system during pregnancy

A

Increased CO, increasing renal blood flow. Increasing Glomerular filtration rate (GFR) - therefore concentrations of urea and creatnine therefore decrease because of this dilution.

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6
Q

What are our aims/concerns in non-pregnancy related surgeries on pregnant patients?

A
  • Maintain oxygenation (pre-o2 and supplemetn in recovery. Measure spo2)
    -Maintain co2 - want to prevent changes in SVR and acidaemia
  • Maintain BP systolic >90mmHg
  • Avoid teratogenic drugs(that cause developmental malformations.
  • Avoid drugs which will initiate labour (e.g. xylazine is an alpha 2 that is a know ecbolic drug - avoid!)
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7
Q

In short, what are our aims during a caesarean GA?

A
  • Maintain placental oxygen delivery and blood flow until foetus deliveered.
  • Use short-acting drugs or ones that do no cross placental barrier, reducing drugs that pass to foetus.
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8
Q

What properties affect whether a drug will be bale to cross the placental barrier?

A
  • thickness of the tissue
  • ionisation
  • lipid solubility
  • foetal concentration
  • maternal concentration
  • foetal metabolism
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9
Q

What are the pros and cons of using pre-meds in caesareans?

A

Pros:
- pre-emptive analgesia
- reduce induction/volatile agents, therefore reduce CVS and R depression
- smooth GA and avoid responses to Sx
- Smoother recovery

Cons:
- Mum already exhausted . doesnt require sedation
- drugs risk transferring to foetus
- cause respiratory, CV depression and lower Apgar score

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10
Q

What does an Apgar score assess? How?

A

Assesses the viability of foetuses at birth. Scores 1-3 for each parameter.
Measures HR <180, 180-220. >220.
Resp Effort <6bpm not crying, Mild crying 6-15bpm, crying >15bpm.
Reflex irritability - absence, grimace, vigorous
Motility - Flaccid, some flexion, active motions
MM colour Cyanotic, pale, pink

Score 7-10 no distress, 4-6 mod distress, 0-3 severe distress.

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11
Q

What drug is recomended by WSAVA for emergency C-sections

A

Fentanyl 3-5ug/kg

One off dose of NSAID at end of surgery also paracetemol in dogs. Use of local anaesthetics.

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12
Q

How much of a dose of opioids will be transferred into the milk?

A

1-2%

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13
Q

What can pain in a new mum cause?

A

Uterine vasoconstricyion, reduced blood flow and milk production.

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14
Q

Describe the considerations when preparing a caesarian for GA?

A
  • if normotensive, start on maintenance IVFT.
  • Clip and prep as much conscious to reduce GA time, sternal and lateral.
  • Pre-o2 to maintain placental blood oxygencation and dam’s reduced FRC.
  • Head-up induction as regurge prone
  • Short-acting titratable drugs for induction
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15
Q

Describe the considerations when maintaining a caesarian under GA?

A
  • intubated and on a low resistance breathing system.
  • Cuffed ETT incase of regurge, use of IPPV.
  • Low solubility volatile agents to ensure speedy recovery. MAC dcreased in pregnancy so may need less volatile agent percentage.
    -Once in dorsal, uterus puts pressure on diaphragm, reducing FRC and ventilation and impeding venous return. Tilt animal slightly to left.
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16
Q

Describe the monitoring when doing a caesarian GA? and why is it important

A

Capnograph - important due to possibility of hypoventilation due to reduced tidal volume from uterus pressing on diaphragm.
Pulse ox - monitor close as reduced FRC, and to ensure good placental oxygenation.
BP - BP needs to be maintained to keep placental perfusion but can be reduced because of positioning and venous compression.
ECG - no specific risks

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17
Q

What is the difference between a paediatric patient and a neonate?

A

< 4 weeks old is neonate
4-12 weeks old is paediatric
Over 12 weeks, most things are well-developed so dont need to worry too much.

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18
Q

Describe the differences in a paediatric/ Neonatal patient’s Respiratory physiology

A

Limited reserve capacity (less FRC).
2-3 times increase in tissue o2 demand.
Higher RR.
Narrower trachea. Larger tongue proportionally than adults.

Neonatal animals have super compliant lungs so are pulled right in by chest wall movements so not much FRC.

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19
Q

Describe the differences in a paediatric/ Neonatal patient’s CVS

A

A foetus’ blood doesnt need to go through the lungs to pick up o2 as its supplied by maternal side. So instead it shunts blood from R to L heart without passing the lungs. By: The foramen ovale (which moves blood from the R atrium to the L atrium) and the ductus arteriosus (which moves blood from the pulmonary artery to the aorta).
When the neonatal animal takes its 1st breath, the oxygen casues vasdilation in the pulmonary vessels and makes PVR less than SVR causing blood to move from the R atrium into the pulmonary artery and the two now useless gaps in the heart close over in the first few days of life.
So if we have to GA a neonate that is less than a few days old we have to be careful not to increase PVR as it will revert to shunting blood except this time the mother doesnt oxygenate it and the neonate will become hypoxic.

Neonates are dependant on their HR to maintain CO (they cannot alter SV) so avoid bradycardia e.g. use of fentanyl, medetomidine and dexmedetomidine.

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20
Q

Describe the differences in a paediatric/ Neonatal patient’s hepatic physiology

A

Slower to metabolise drugs due to immature microsomal enzyme system until they are 8-12 weeks old.
Glycogen storage is low and not good at making new glucose so often hypoglycaemic. Tend to also have lower albumin levels.

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21
Q

Describe the differences in a paediatric/ Neonatal patient’s renal physiology

A

Neonates and paediatric patients total body water and extracellular fluid volume are higher so water requirements are higher.
Renal funciton is reduced so have poor ability to concentrate urine, poor ability to excrete a water load and poor acid/base regulation up until 6-8 weeks.

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22
Q

Describe the differences in a paediatric/ Neonatal patient’s thermoregulation

A

Born with little sc fat.
Poor thermoregulatory ability
Poor vasomotor tone
Super prone to hypothermia.
Worsened by pre-op starvation as metabolism generates heat.
High surface area to volume ratio so lose more heat.

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23
Q

Describe the differences in a paediatric/ Neonatal patient’s ability to deal with drugs

A

Seem resisitant to non-depolarising NMBAs but also have prolonged action. Start will small dose and titrate.
Renal and hepatic clearance of drugs is prolonged -base re-administration on pain scoring.
Due to higher extracellular water volume, water-soluble drugs such as ketamine may require higher doses.
Low albumin concentrations more pront to over dose.
Less sc fat for redistribution of drugs.

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24
Q

What specific considerations are there for GA’ing neonates/paediatric patients in addition to the underdevelopment of body systems?

A

Avoid prolonged starvation- promotes hypothermia and prone to hypoglycaemia.
<8 weeks or 2kgs starve for 1-2 hours.

Check for hypoglycaemia before induction.
Measure temperature and prevent hypothermia as best can.
Accurate weight and appropriate sized equipment.

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25
Q

How can we assess pain in a paediatric puppy or kitten?

A
  • anthropomorphic approach
  • pain assesmments designed for adults
  • respose to palpation
  • check for diminshed response of noted behaviour after administrtion of analgesic.
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26
Q

What considerations are there for selecting a pre-med for a pediatric patient?

A
  • is pre-med necessary? Will reduce volumes of other drugs needed and pre-emptive analgesia.
  • short acting drugs as clearance will be slower
  • avoid drugs that cause bradycardia
    -pthidine is a good choice as short acting full mu opoid. Can also use benzodiazepines to produce some sedation.
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27
Q

What considerations are there for inducing anaesthesia in a paediatric patient?

A
  • IV access and pre-oxygenate (reduced FRC, increased MOD, intubation can be difficult due to large tongue and narrow trachea).
  • Cut down ETTs so not excessive lengths.
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28
Q

What considerations are there for maintaining anaesthesia in a paediatric patient?

A

Inhalational is preferred to IV as less injectable drug to be metabolised.
A low solubility volatile agent such as sevo/iso will allow fast recovery.

Circuit - low drag, low resistance, low dead space. Chest wall is more compliant so will be less compression on venous return if IPPV needed.

IVFT indicated. Stiff myocardium less responsive to fluid loading. Monitor blood loss closely.

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29
Q

What considerations are there for recovery from anaesthesia in a paediatric patient?

A
  • later extubation due to underdevelopment of gag reflex
  • o2 supplementation esp if shivering
  • food offered asap (check glucose intermittently under GA)
  • Temperature monitored + warming
  • IVFT until good intake
  • Pain assessments.
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30
Q

The liver is a site of protein production, what can happen if this production is decreased? i.e. hypoproteinaemia

A
  • Ascites (fluid in abdomen) which leads to compromised ventilation and reduced FRC.
  • Peripheral Oedema (makes it hard to place IV)
  • Lowered plasma oncotic pressure (this is a form of osmotic pressure induced by proteins, notably albumin, in the blood vessles plasma that draws water in from the interstitial space to the intravascular space).
  • Affects drug - binding
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31
Q

What are the main functions of the liver

A
  • Protein production
  • Glucose homeostasis
  • Erythopoietin production (hormone that stimulates RBC production)
  • Involved in synthesis of blood coagulation factors
  • Filtering out bacteria from the bloodstream.
  • Biotransformation of drugs
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32
Q

If the liver is damaged what consequences may we see in a patient?

A
  • lowered protein production - ascites, oedema, affects drug binding.
  • Hypoglycaemia (then causes systemic neuronal damage and muscle weakness).
  • Anaemia - due to blood loss due to clotting abbormalities, interferes with o2 carrying capacity and our ability to monitor mm colour (also jaundice does this).
  • Hypocalcaemia secondary to reduced albumin (can cause muscle wekness - may need IPPV)
  • Toxin build up and bacteraemia. Ammonia build up as liver isnt able to process it properly (AKA hepatic encephalopathy) - this affects the brain causing dull, depressed and seizures. Need thorough skin prep.
  • Enlarged liver (hepatomegaly) can compress diaphragm and compromise ventilation and oxygenation (prone to hypoxia and hypercapnia).
  • Some patients will concurrently get GI sigsns - v+, d+ etc.
  • delayed recovery due to slower metabolism of drugs. Pain scoring instead of interval dosing.
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33
Q

What considerations are there for anaesthesia of a liver patient?

A
  • liver already has poor oxygen delivery and perfusion - GA will make this worse.
  • We aim for these 2 things: Providing adequate oxygenation and maintaining BP.

Propofol increases hepatic blood flow probably through significant vasodilation.

-Should use sgort-acting drugs with alternative route of metabolism/can be antagonised.
- Avoid benzodiazepines as have been linked to hepatic encephalopathy.
- Blood loss a worry in surgical repair of a shunt.
- If a shunt is ligated you may see drop in CVP as now have same volume going round the long way. This may compromise intestinal perfusion.

In recovery, we may see portal hypertension which can cause loss of blood circulation to abdominal organs. Animals may show signs of ascites, v+, d+, depression or respiratory distress. May even see seizures.

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34
Q

What is a porto-systemic shunt? What can we do? What effects does it have?

A

PSS is an abnormal vein that connects the blood supply returning from the intestines to the vein returning the blood to the heart, by-pasing the liver.
Can be congenital or aquired through liver disease. Often present with hepatic encephalopathy (increased ammonia levels) and require medical stabilisation before GA. Stabilisation includes:
- antibiotics to eliminate toxin-producitng bacteria
- lactulose - promotes the expulsion of faeces and decreases bacterial load in colon
- Low protein diet.

These patients haev reduced liver function so prone to hypothermia, and slower biotransformation of drugs, anaemia, low albumin and less clotting factors.

35
Q

What si the differences between pre-renal, renal and post-renal azotaemia (increased urea and creatnine).

A

-Pre-renal azotaemia is due to circulatory disturbances. which decrease renal blood flow. e.g. dehydration or hypovolaemia. Should still be able to adequately concentrate urine (>1.030 dog and >1.035 cat) and no proteniuria.

-Renal Azotaemia - occurs when more than 75% of nephrons are non-funcitonal. Can be due to primary intrinsic renal disease (glomerulonephritis) or renal injury secondary to pre-renal causes. SG may be the same as plasma USG (1.008-1.012). May see excessive proteinuria, casts and glucoseuria (without hyperglycaemia)

  • Post-renal azotaemia - results from obstruction or rupture of urinary outflow tract. Varying USG results. The back pressure from being unable to void urine can cause renal failure. Patietn should only be anaesthetised if its to correct the cause of the renal failure! e.g. obstruction/ruptured bladder.
36
Q

What can cause dehydration?

A

Fluid shifts
Third space losses e.g. uroabdomen
Decreased intake of water and food
GI losses such as vomitting

37
Q

What is uraemia and what impacts does it have on the body and on anaesthesia?

A

Urea build up in the bloodstream (urea is a nitrogenous waste product that is usually excreted by the kidneys).
It can cause nausea and vomitting, dullness and depression, seizures, hypothermia and decreased metabolic rate.

Lower doses ofsedatives and induction agents are required because of the CNS depression .
Monitor temperature.
IVFT will lower blood levels or urea.
Pain relief - visceral pain from distended bladder or urethra, uroabdomen will also cause painful peritonitis.

38
Q

Describe the acid base and electrolyte changes that occur with acute renal failure

A

In acute renal failure, hydrogen and potassium ions that are usually excreted in the urine accumulate in the bloodstream.

Hydrogen ions are acidic so when they accumulate in the blood, they cause acidaemia. The body will try to correct the acidosis using other body systems e.g. respiratory.

Potassium ions are safe if in the cells, but cause problems when outside the cells i.e. increasing the serum potassium level above 3.5-5.5mmol/L. Only way for potassium to exit is urine so if blocked then accumulates. Hyperkaleamia can cause muscle weakness and neurological signs and dysrhythmias.

Metabolic acidosis will worsen hyperkalaemia because hydrogen ions move into the cells and push out potassium ions.

39
Q

What effects can acidosis have?

A
  • Disrupt enzymatic processes
  • Change where the oxygen dissociation curve lies
  • disrupt ionic and cell membrane charges
  • affect drug binding
  • worsen hyperkalaemia
40
Q

How can we stabilise a patient with electrolyte imbalances?

A

Fluid therapy will improve dehydration, hypovoleamia, uraemia, metabolic acidosis and hyperkaleamia. Can use pre-GA boluses. Need to get blood pH back to above 7.2 and K+ less than 6mmol/L before GA.
Patient should stay on fluids throughout GA and 24 hours after.

Also should be given pain relief and monitor temperature.

41
Q

Why is it okay to use Hartmanns solution for hyperkaleamia even though it contains K+?

A

Low level
Dilutes the potassium due to crystalloid administration
Due to the lactate, Hartmanns is an alkalinising solution (increases the pH) which encourages K+ to go back into the cells.
It also has lower chloride than Saline solution which can damage kidneys.
Some worried about fluids incase rupture bladder but little urine will be produced due to dehydration and lower renal blood flow anf GFR.

42
Q

What can we treat hyperkaleamia with if fluid therapy boluses doesnt work?

A

Glucose (+/- insulin) transports k+ back into the cells as glucose is taken up.

Use of calcium compounds can cause a temporary stabilisation of the cardiac action potential although does not affect serum potassium levels.

IVFT - No11

In severe cases, slow administration of sodium bicarbonate can be infused but can cause hypokaleamia and hypocalceamia.

43
Q

Discuss the changes associated with chronic renal failure and how they can affect GA?

A
  • Anaemia - kidneys are damaged and dont make enough erythropoeitin so patient becomes anaemic. High levels of urea will also suppress bone marrow production of RBCs. Uraemia can also cause blood loss through gastric ulceration. These will affect the patietns oxygen-carrying capacity (making it harder to detect cyanosis) and alter drug dose requirements (MAC).
  • Hypoalbuminaemia - can occur if protein losing nephropathy is present.
  • Can be calcium and phosphorous derrangements which can predispose to arrythmias
  • Hypertension - RAA system is stimulated by reduced renal blood flow so patietns can have chronic hypertension (e.g. CKD patients). This chronic hypertension can lead to cardiomegaly and ventricular hypertrophy.
  • Bleeding - due to platelet defects, decreased platelet aggregation and impaired adhesiveness. Check clotting times.
  • vomitting and nausea from uraemia - also may predispose acid-base abnormalities and dehydration
  • Immunosuppression - high levels of urea suppress bone marrow function. Care with skin prep etc.
  • Decreased renal drug clearance - esp those with active metabolites. E.g. some opioids and some NMBAs
44
Q

How can anaesthesia affect the kidney?? What shoudl we do to alleviate these?

A

Main aim is to maintain renal blood flow and oxygenation of renal tissue.

Renal blood flow will remain constant ( if MAP lies within 60-160mmHg ) - so we try and maintian this MAP.
This range will shift up in a patient with chronic hypertension and we should maintian it higher.

Control depth to avoid drops in BP when too deep. and avoid sympathtic stimulation when too light which will cause vasoconstriction of renal blood vessels.

45
Q

What effects do NSAIDs have on the kidneys?

A

The kidneys rely on prostaglandind PGI2 and PGE2 to maintian renal blood flow in times of low blood pressure. They are blocked by NSAIDs.

46
Q

What drugs have the potential for nephrotoxicity?

A

Volatile agents - due to potential production of fluoride. e.g. sevoflurane.
Sevoflurane also produces a vinyl ether called compund A which is produced when it is used in rebreathing systems - compound A has been implicated in causing renal dysfunction in rats.

47
Q

Describe what is considered geriatric

A

over 80% of anticipated lifespan

48
Q

Describe the physiological changes of a geriatric animal’s CNS

A

Reduced CNS activity, reduced neurotransmittersand receptors.
Lower levels of drugs can be used to acheive expected effects.
Visual and auditory acuity reduced.
Thermoregulation reduced.

49
Q

Describe the physiological changes of a geriatric animal’s CVS

A

Gradual CVS perform decline.
Reduced baroreceptor activity - slower response to changes in BP
Increased vagal tone - slower HR, reduced CO and slower circulation time.
CO becomes pre-load dependant

Older anmals are more prone to hypotension or volume overload. May develop chronic valvular diseases of the heart.
Autonomic responses are slower

50
Q

Describe the physiological changes of a geriatric animal’s respiratory system?

A

Lung loses elasticity
Small airways close at higher lung volume
Reduction in vital lung capacity and FRC (thereofre more likely to desaturate and become hypoxic)
Increase in closing volume (the amount of gas that is trapped in the alveolus when the external pressure becomes greater than the internal pressure and alveoli forced shut)
Greater risk of atelectasis and V/Q mismatch
Greater risk of hypoxia and hypercapnia
Increased incidence of respiratory tract pathologies.
Decreased chest wall compliance (greater squashing of vessels)
Increased diameter of trachea and larynx, increased dead space.
Protective laryngeal reflexes diminished - aspiration more likely.
Increased risk of GO reflux

51
Q

Describe the physiological changes of a geriatric animal’s Renal system

A

Reduced no. nephrons. Kidneys get 25% of CO and this is reduced in geriatric patients therefore renal blood flow is alos reduced.
Reduction in renal mass - decreasing ability to correct acid-base or electrolyte imbalances. Need supportive IVFT.
More prone to fluid overload.

52
Q

Describe the physiological changes of a geriatric animal’s Hepatic system

A

Liver receives 25% CO and this is reduced in geriatric patients so liver blood flow is also reduced.

Reduced hepatic function leads to slower drug metabolism.
Lesser metabolism = less generated heat.
Reduced albumin formation influencing binding of drugs.

53
Q

Describe the altered pharmacokinetics of drugs in geriatric patients.

A
  • less body mass for IM injections
  • More adipose tissues so IM injection end up in fat.
  • Decreased albumin means less drug is bound and more is free. Induction agents given slowly to avoid overdose.
  • Decreased total body water - lower doses of water-soluble drugs e.g. ketamine, can be used.
  • MAC of volatile agents decreased by 30%
  • Hepatic elimination of drugs reduced so effects prolonged
  • Renal reserve decreased - effects of renal eliminated drugs prolonged.
  • Epidural injections will spread more cranially as intervertebarl foramen become narrowed. Therefore reduced volume of epidural drugs advised.
54
Q

What are some common endocrinopathologies in older patients

A

Canine hypothyroidism
Cushings Disease
Diabetes Mellitus
Feline Hyperthyroidism

55
Q

What can do to maximise the stabilisation of a geriatric patietn prior to an elective surgery?

A
  • dieting (not crash!) Protein restriction may be indicated in renal disease/ hepatic dysfunction.
  • administration of antitussives, mucolytics +/- bronchodilators to produce clean, dry, wide airways.
  • Pre GA bloods
  • ## Help with anxiety
56
Q

What considerations are there for geriatric anaesthesia

A
  • Approach carefully as visual/hearing impaired.
  • More prone to emergence delerium
  • Padding under GA as tendency for arthritic joints.
  • Lower doses of sedatives required
  • shorter acting drugs due to slower metabolism
  • IV access
  • IVFT indicated even if urea is normal (becuase need to lose 75% of nephrons to see an increase in urea). Start prior to GA na dinto recovery.
  • Pre-o2 for 3-5mins
  • Induction agents slowly to effect to avoid overdose.
  • Maintainance with a low solubility volatile agent.
  • May need ventilatory support
  • Multi-modal anaesthesia although renal function checked before NSAIDs given.
  • Empty bladder prior to recovery for comfort.
  • Quick return to owners to minimise stress.
57
Q

What is diabetes mellitus?

A

DM is a chronic disorder of carbohydrate metabolism resulting from an absolute or relative deficiency of insulin.

Insulin is responsible for inhibition of gluconeogenesis (production of glucose) and stimulation of glucose uptake into cells.

58
Q

What procedures may be performed in DM patients?

A

Ovariohysterectomy - prgesterone production during oestrus/pregnancy destabilises DM patients so may want to spay.

Animals with DM can get catarachts due to sorbitol deposition in the lens. Removal required GA.

Sedation may be required for USS to investigate unstable DM

59
Q

What are the anaesthetic considerations for a diabetic patient ?

A

-Hypoglycaemia and Hyperglycaemia - hyper will cause glucosuria(if BG goes over renal threshold) causing dehydration, lactic acidosis and hyperosmolarity and can even lead to coma. Hypo produces neurological damage at BG <2.7mmol/L. (Normla BG is 3-7mmol/L)

  • Chronic organ dysfunction - Renal system can have diabetic nephropathy, pre-renal azotaemia, UTIs. Liver can be affected by lipidosis, impaired function or hepatomegaly. Also electrolyte imbalances with depleted stores of potassium and sodium.
  • Immunosuppression due to the negative effects of elevated blood sugar on the immune system.
  • Loss of body and muscle mass can influence drug distribution and cause heat loss.
60
Q

What are the signs of hypoglycaemia in a consious patient?
What signs may we see under GA?

A

Lethargy, uncoordinated, trembling, twitching, weakness, seizures.

May see sympathetic stimulation (increasing HR and BP) but not always.

61
Q

What are the aims when anaesthetising a diabetic patient?

A
  • Maintain glucose in a normal range to prevent keto-acidosis and neurological damage.
  • Maintain pH and electrolytes
  • Rapidly restore post-op eating and drinking
  • Prevent sepsis
62
Q

What can be done to stabilise a diabetic patient prior to GA?

A

Stable on insulin ideally.
Correct any acid-base or electrolyte imbalances.
Minimal disruption to their normal feeding/insulin routine with starvation period for ga.

63
Q

What are the pre-op instructions for a diabetic patient?

A
  • perform procedure first
  • give patietn half a portion of their normal food 2-4 hours prior to GA then starve.
  • Have water until pre-med
  • Give half dose of insulin 2-4 hours before GA
    Another approach would be to starve the animal from midnight and then take a BG on the morning of procedure and administer correct dose of insulin.

BG should be checked before induction and then every 15-30mins during GA

64
Q

What dose of insulin should be given for a BG of:
<6
6-15
>15

What dose of insuling should be given if BG under GA is:
Excessively high
Drops below 3

A

No insulin
Half dose insulin
Full dose of insulin

0.1IU/kg/hr insulin given
0.25-0.5g/kg glucose slow IV

Glucose is hypertonic and will need to be diluted with crystalloids to avoid thrombophlebitis.

65
Q

Describe what drugs we would use for GA of a diabetic patient and why?

A

Pre-meds- dont want to flatten them as want a quik recovery. Use opioid +/- low dose ACP. Alpha 2s can disrupt glucose control even tough its beneficial they can be antagonised.

Low solubility volatile agents for maintainance and short acting drugs for induction.

Multi-modal analgesia. Must manage pain to get to eat. . NSAIDs can be administered if vet is sure no diabetic nephropathy or pre-renal azotaemia.

IVFT at surgical rates and reduced 25% each hour.
Post-op anti-emetics to counteract nausea and encourage eating.
Once the patient eats in recovery, the rest of the insulin can be given. If dont eat, monitor BG and administer insulin as necessary.

66
Q

What are insulinomas. What are the risks with this GA?

A

Malignant functional pancreatic tumours of the Beta cells that retain the ability to produce and secrete insulin.
Most common pancreatic tumour in dogs and cause hypoglycaemia, secondary neurological effects (collapse, seizures) and adrenergic effects from catecholamine release.

Need surgical resection. Patients most at risk of hypoglycaemia under GA. high sympathetic tone and possibility of arrythmias as catecholamines are counter-regulatory to insulin.

67
Q

What should the pre-op steps be for a patient with an insulinoma undergoign GA?

A

Bloods - potassium levels
Starvatoin time reduced due to risk of hypoglycaemia or administer glucose IV during starve.
BG checked before premed +/- IV glucose.

68
Q

What drugs/monioring should be used for GA of an insulinoma patient?

A

Premed
- opioid due to laparotomy painful.
- + low dose of alpha 2/ACP based on temperament and history.
Alpha 2s block insulin so may help combat the need for glucose IV and reduce incidence of hypoglycaemia.

Induction
- Alfaxalone over propofol due to risk of development of pancreatitis post op and high lipid content of propofol.
- Regular blood sampling Q15m whilst pancreas being handled as can release insulin.
- regular BG measurements.

69
Q

What is hypoadrenocorticism?

A

Addisons disease is characterised by a mineralocorticoid (e.g. aldosterone) - produced in the outer layer of the cortex of the adrenal gland) or glucocorticoid (e.g. cortisol) produced in the middle layer of cortex of adrenal gland- deficiency because of failure of the adrenal glands.

The inner zone of the adrenal glands produces sex hormones e.g. androgens and oestrogens.

Patients with Addisons can have a mineralocorticoid deficiency, a glucocorticoid deficiency or both.

70
Q

What is the role of glucocorticoids e.g. cortisol?

A
  • Gluconeogenesis
  • Fat and protein metabolism
  • Immunity
  • BP regulation
  • Counteracting the effects of Stress
71
Q

What are the clinical signs of a dog with a mineralocorticoid deficiency? And glucocorticoid deficiency?

A
  • Hyperkaleamia
  • Hyponatraemia (low blood sodium)
  • Azotaemia
  • Hypovoleamia / dehydration
  • Lethargy/weakness
  • Polyuria/polydipsia
  • v+/d+
  • abdominal pain
  • weight loss
72
Q

What is the treament for a patient presented in addisionian crisis?

Why shouldnt we GA this patient?

A
  • Aggressive IVFT with No9 or No11 to restore fluid volume, improve renal perfusion and decrease potassium concentrations.
  • Replacement of glucocorticoids (e.g. IV dexamethasone) +/- mineralocorticoids

Patients in addisonian crisis should NOT be GA’d - would be at high risk of CV collapse due to decreased venous return , peripheral vasocontriction and decreased CO and contractility.

73
Q

What are our anaesthetic/hospital considerations for an addisonian patient?

A
  • Minimise stressors as stress worsens illnesses and lacks glucocorticoids to counteract stress.
  • Continue to give medications in morning as usualy and allow time to absorb orally.
  • Correct any abnormalities in Na, K, or acid base balance prior to GA using IVFT. Abnormalities should not be corrected any faster than 0.5mmol/hr to avoid demyelinating parts of the brain. No11 preferable due to alkaising effect.
  • Administration of steroid pre-op to supplemetn cortisol to fight the stress associated with surgery.
  • Avoid vasodilating drugs that may worsen hypotension during an adrenal crisis.
    -Avoid etomidate for induction as suppresses cortisol production.
  • Choose circuit suitable for IPPV as pre-disposed to hypoventilation.
  • Multi-modal analgesia including local
  • IVFT
  • Monitoring: capno for hypoventilation, ECG for any rythm changes due to electrolyte changes, BP to see indication of adrenal crisis-related hypotension.

NSAIDs contradicted as already using steroids.

74
Q

What happens to a patient if it goes into addisonian crisis periop? What action should be taken in an adrenal crisis intra-op?

A

Loss of vasomotor tone, impaired alpha adrenergic responses to noradrenaline, leading to hypotension and possibly shock.
Often not responsive to bolus fluids so administer 2-4mg/kg hydrocortisone IV or 5-10mg/kg pred IV.

75
Q

What is hyperadrenocorticism?

A

Cushings. Caused by overprooduction of cortisol. Cause by either a tumour of the adrenal gland or a tumour of the pituitary gland.

The pituitary gland in the brain produced Adrenocorticotropic hormone (ACTH) that stimulates the adrenal gland to produce cortisol.

76
Q

List some clinical signs associated with an excess of cortisol in the bloodstream?

A
  • polyuria
  • polydipsia
  • polyphagia
  • pendulous abdomen
  • hepatomegaly
  • muscle weakness
  • thin skin
  • hypervoleamia and fluid retention. Leads to hyperptension and often heart conditions. Increases myocardial workload and often results in myocardial hypertrophy.
    Cushings is more common in older dogs who might also already have valvular disease.
77
Q

What are the consideration when thinking about anaesthetising a patient with cushings?

A
  • Muscle weakness affects the ventilatory muscles, and hepatomegaly will limit thoracic excursion, PPV may be required.
  • More prone to IV infections from catheters due to suppressed immune system.
78
Q

What are our anaesthesia goals if the vet wants to perform an adrenalectomy on a cushings patient?

A
  • extremely good muscle relaxation as adrenal glands lie deep in abdomen.
  • Adrenal masses tend to invade vena cava so blood loss is a concern. Typing patients prior to GA and ensure blood products available. Directly monitor arterial BP.
  • Supplement steroids during GA to avoid addisonian crisis.
79
Q

What is hypothyroidism? How is t3 and t4 usually released?

A

Reduced function of thyroid gland. Usually in dogs.

Usually, the hypothalamus secretes thyrotropin-releasing hormone (TRH) which acts on the pituitary gland by stimulating it to secrete thyroid-stimulating hormon (TSH). Which in turn acts on the thyroid gland to release t3 and t4.

80
Q

What are the considerations for anaesthetising a patient with hypothyroidism?

A
  • Thyroid hormones predominantly affect metabolic rate.
  • Ideally they are supplemented with thyroid hormones and stabilised prior to GA.
  • geriatric considerations are applicable (lower MR, prone to hypothermia, slower action of drugs)
  • often overweight, lethargic - may require lower doses of sedatives.
  • Thyroid hormones can affect bone marrow function so patient may be anaemic.
  • Hypothyroid patients also tend to have peripheral neuropathies e.g. laryngeal paralysis, megaoesophagus, so GI transit. Pre-o2 and take spteps to avoid aspiration.
  • Prone to bradyarrythmias and slower circulation. Give induction agents slowly, to effect.
  • CO reduced, increasing risk of hypotension.
  • Coagulopathies may be present and skin changes.
81
Q

What is hyperthyroidism?

A

Due to adenoma or carcinoma tumours of the thyroid gland producing excessive levels of thyroid hormone. Usually in cats.

82
Q

What does hyperthyroidism cause?

A

-Increased metabolism and appetite are seen, along with restlesness and aggression.
- often geriatric
- weight loss
- throid hormones affect multiple body systems causing multi-organ dysfunction:

  • Hepatotoxicity caused by excessive thyroid hormones.
  • Renal dysfunction - Glomerular hypertension reducing functional nephron mass, or hyperphosphotaemia that can cause mineralisation of soft tissues and worsening of renal function.
    (hyperthyroidism can mask declining renal function). Excess thyroid hormones artificially increase renal blood flow and GFR which would decrease the serum concentrations of urea and creatnine. Treating the hyperthyroidism will lower GFR and unveil the true urea and creatnine concentrations.
  • HCM - hyperthyroidism causes heart to beat faster with greater force. Eventually heart enlarges with a thicker wall. Limites perfusion of heart muscle itself even though good CO. Sometimes the thickness of the heart muscle can cause subaortic occlussion - affecting the volume of the ventricle, SV and left ventricle outflow.
83
Q

What are the considerations for anaesthetising a cat with hyperthyroidism?

A
  • large tumours can press on trachea, compromise airway - possible difficult intubation - preo2.
  • thyroid tumours can cause laryngeal dysfunction and possible horners syndrome (3rd eyelid protrusion, drooped upper eyelid, small pupil).
  • Blood loss if removing tumours.
  • Sharing neck region with vet so think about circuit and monitoring.
  • possibilty of laryngeal paralysis if nerves are damamged during surgery - airway kit on recovery.
  • Hypocalcaemia can be seen if parathyroid glands are damaged during surgery.
  • Stabilise cat prior to GA ideally
  • Tachycardia drugs should be avoided e.g. ketamine as increased myocardial work and oxygen consumption and may lead to ventricular arrythmias in these cats.
  • Avoid vasodilation e.g. ACP, reducing afterload increases pressure gradient across LVOT. Also hypotension may reduce coronary perfusion.
  • Want to produce mild bradycardia and mild vasoconstriction. E.g. medetomidine.
  • Ensure oxygenation and maintain preload with IVFT.
  • Multimodal analgesia.
  • Thorough monitoring as many organ systems affected:
    - ECG to identify arrthmias
    - BP to monitor CO and ensure maintainance of renal blood flow
    - Temp - poor body consition, higher sa:v ratio so prone to heat loss.
    - Pulse ox - resp system should be okay once intubated.
    - capno - shared head space and indicator of CO.