Anaesthetic Considerations for Specific Conditions II

What is the main risk of the first trimester and anaesthesia?

Embryotoxicity

What is the main risk of the second trimester and anaesthesia?

Placental separation

What is the main risk of the third trimester and anaesthesia?

Major physiological changes and in this trimester anaesthesia is most often required

What are the physiological changes in the third trimester?

• Dam's cardiac output and blood volume increase to meet needs of growing placenta (diluted anaemia)

• Albumin levels are decreased

• Cardiac reserve decreases

• Systemic vascular resistance (SVR) decreases; vasodilation contributes to potential hypotension. > also uterus puts pressure on great vessels running along the dorsum vena cava and oarta. Dorsal recumbency > uterus compresses vessels reducing venous return and therefor cardiac output

• Minute volume is increased > oxygen consumption increasing and metabolic oxygen requirement also increases

• Decrease in Functional Residual Capacity (FRC, volume of gas left in lungs at end of normal breath) because uterus pushing forward and compressing diaphragm which limits lung capacity and volume

• More prone to regurgitation > stomach alters position because of uterus> angle where oesophagus enters stomach changes making oesophagus sphincter incompetent. Progesteron decreases sphincter tone and slows digestive progress

• Urea and creatinine concentrations decrease because of dilution > because of increased cardiac output more blood flows through kidneys > glomular filtration rate increases

What is dilutional anaemia?

For the blood volume both plasma volume and red cell mass increase, but plasma volume increases proportionally more resulting in diluted anaemia

Aims for anaesthesia for non pregnancy reasons

• Maintain placenta and foetal oxygenation (pre oxy, oxy suppl in recovery, SpO2 measurement)

• Carbon dioxide should be maintained within normal limits; has effects on vasodilation and vasoconstriction and ensuring it remains normal levels is advisable to avoid foetal acidaemia

• Blood pressure should be maintained with systolic value >90mmHg

• Teratogenic drugs should be avoided (cause developmental malformations)

• Drugs that induce labour (ecbolic drugs) should be avoided (an alpha2-adrenergic agonist) Xylazine is known to be ecbolic

General aims for anaesthesia for caesarean sections

• Maintain placental blood flow and delivery of oxygen until foetuses are delivered

• Use short acting drugs or drugs which do not cross the placental barrier (also small amount of drug transferred via milk)

Drugs crossing the placenta depend on;

• Thickness of tissue

• Ionisation

• Lipid solubility

• Foetal concentration

• Maternal concentration

• Foetal metabolism

What are the benefits of premedication for a caesarean section:

• Pre emptive analgesia > reduction of the amount of induction and volatile agent required thus reducing cardiovascular and respiratory depression

• Smoothing the anaesthetic and avoiding responses to surgical stimulation (possible regurgitation when patient becomes light)

• Smoother recovery from anaesthesia

What is an APGAR score?

Scoring system which indicates neonatal viability (appearance, pulse, grimace, activity and respiration)

What opiod for caesarean section and what drug can you add if only opioid is not enough?

For emergency c-section is fentanyl IV 3-5 microgram/kg.

Acepromazine can be added at the lower end of the dose range

Which opioid specifically NOT for caesarean?

Buprenorphine.

Morphine unlicensed in dog/cat.

What opioid CAN you use for caesarean

Fentanyl

Methadone low dose (0,1-0,2mg/kg) and can be antagonised in the neonates with naloxone

What other analgesia can you give the dam?

One off dose of NSAID at the end of anaesthesia because hypotension may occur during anaesthesia.

Paracetamol can be given sagely to dogs aftr caesarean

What local anaesthetics for caesarean sections?

• Line block preincision or at closure into abdominal wall/skin

• Epidural (with morphine +/- Lidocain avoid prolonged postoperative motor blockade)

Why is appropriate analgesia importent with caesareans?

So that the dam is comfortable enough to feed the neonates.

Untreated pain causes uterine vasoconstriction and redcued blood flow and reduced milk production

Can you use both alfaxalon and propofol for induction with caesarean?

Yes, although alfaxalon was associated with better neonatal viability during the first 60min after delivery

Is MAC increased or decreased in pregnant animal?

Decreased and therefor it may be possible to reduce vaporiser settings.

Low solubility volatile agent such as iso or sevoflurane should be used.

How should the dam's abdomen be clipped?

In both lateral recumbencies; avoid dorsal until the last possible moment

What is important when the dam is put in dorsal recumbency?

Tilting the animal slightly to the left.

The uterus puts pressures on the diaphragm (causing hypoventilation and reduced FRC) and vena cava/oarta (causing decreased venous return). Vena cava is most easily compressed; is a vein and thinner walled and lies to the right.

What is the difference between neonate, paediatric and juvenile?

Neonate = <4wks

Paediatric = 4-12wks

Juvenile = >12wks

Why is there more concern with anaesthetics for animals <12wks?

There organ systems are under developed; circulatory, ventilatory, thermoregulation,hepatic and renal function

What is different with the respiratory system of a paediatric patient?

• They have 2-3x the tissue oxygen demand of an adult and higher respiratory rate.

• FRC is also lower in paediatric patients. Because the chest wall in a neonate is very compliant and is easily pulled in by the inward forces created by the elastic recoil of the lung.

• Tongue is relatively large but diameter of airway narrow

Difference between the heart of the neonate in utero and when born?

• In utero the blood does not need to go through the lungs to be pick up oxygen; oxygen is provided by placenta.

• 2 shunts allow blood to go from right side of the heart to left without going through lungs

» foramen ovale which moves blood from the right atrium to left atrium

» ductus arteriosus which moves blood from the pulmonary artery to the oarta

Of you need to anaesthetise a patient in the first few days of life what should be avoided?

• Increases in Pulmonary Vascular Resistance (PVR).

This may increase the resistance to blood flow through the lungs and encourage blood to flow through shunts again > can become hypoxic

Ventilating with high peak inspiratory pressures is a potential cause of increased PVR

• Bradycardia > myocardium is stiff in neonates and therefor cannot increase stroke volume if increased cardiac output js required. Maintenance of cardiac output is heart rate dependant. Avoid drugs that cause bradycardia

What is different with a neonates hepatic physiology?

• They have an immature microsoft enzyme system untill 8-12wks old > slow to metabolise drugs

• Poor gluconeogenic ability > prone to hypoglycaemia. Glycogen storage is minimal

• Lower album levels

What is different with a neonates renal physiology?

• Renal function is reduced until 6-8wks of age

• Poor ability to concentrati urine

• Poor ability to excrete a water load

• Poor acid-base regulation

• Their daily water requirement is higher > total body water nd extra cellulair fluid volume is higher than an adult

Why do neonates have trouble with thermoregulation/prone to hypothermia?

• Born with little subcutaneous fat

• Poor thermoregulatory capabilities

• Immature controle of vasomotor tone (limited control of vasodilation and vasoconstrictio)

• Prolonged preanaesthetic starvation = metabolism produces (less) body heat

• Small size = high surface area to volume ratio = prone to heat loss

What to think of with drugs and neonates?

• May appear to be resistant to non-depolarising neuromuscular blocking drugs, but these have a prolonged action so low dose should be used to start with and titrated to an adequate level of muscle relaxation for surgery

• Use lower doses of drugs because renal and hepatic clearance can be prolonged

• Some drugs (like opioid analgesics) repeat doses should be administered based on pain scoring since duration of action may be longer than anticipated

• Water soluble drugs (like ketamine) may require higher doses

• Lower albumin levels mean patient is more prone to overdose with highly protein bound drugs

• Less subcutaneous fat for redistribution of drugs

Preanaesthetic preparation?

• Limited starvation > under 8wks of age or 2kg body weight, starved for only 1-2hrs. Prolonged starvation also promotes hypothermia

• Blood sample to check for hypoglycaemia

• Weighed accurately and appropriate sized equipment ready

• Small animal is also easy to overheat so temperature regulation is important

How to pain asses in neonates;

• No validated pain scoring system designed for use in puppies or kittens

• Anthropomorphic approach: if procedure/condition is expected to be painfull analgesia is warranted

• Pain assesment tools (especially composite one with different categories) validated for adult cat/dog, give more thorough evaluation of patient

• Response to papation of painfull area

• Observaties of preanaesthetic pain free behaviour is vital for comparison postsurgery

• If behaviour is painrelated it should diminish after appropriate analgesia administration

Why not use alpha2-adrenergic on neonate?

To avoid bradycardia

Why should you use lower concentrations of local anaesthetics on paedeatrics?

• The myelination is not complete in neonates

• Spinal cord ends more caudally so more chance of dural puncture

• Larger volumes of more dilute anaesthetics are commonly used (not high concentrations such as 0,5%)

What to think of during anaesthesia of paediatrics

• Inhalational maintenance preferable > less injectable drug to metabolise > low solubiity = fast recovery

• Breathing system with low drag, resistance and dead space > Ayre's T-piece with Jackson Rees modicification or Mapleson D T-piece

• Chest wall is more compliant is less effect on blood pressure if lPPV is performed

• Fluid therapy administered with accuracy > myocardium is stiff > not responsive to fluis loading

• Intermittent blood glucose monitoring

Recovey of paedatrics?

• Tube left in place longer (without swallowing) gag reflexes are less developed)

• Supllementary oxygen, especially if patient is shivering

• Food offered as soon as patient can sjt up and maintain their own airway

• Temperature monitoring

• Fluid therapy contonued untill good oral intake

• Pain assesed for pain to be managed effectively

What is a geriatric patient?

For different breeds >80% of anticipated lifespan lived.

Age related changes (geriatric) - Central Nervous System (CNS)

• progressive reduction in CNS activity with reduced amounts of neurotransmittors and receptors > lower doses of sedative, induction, maintenance achieve same lvl of sedation as expected in youger animal

• Visual and auditory acuity may be reduced

• Thermoregulatory ability also reduced

Age related changes (geriatric) - cardiovascular

Cardiac performance decreases gradually with age

• Reduced barometer activity which means a slower response to changes in blood pressure

• Increased vagal tone which leads to slower heart rate which in turn leads to a reduced cardiac output and slower circulation time

• Cardia output becomes preload dependant

• Prone to hypotension or volume overload

• May have chronic valvular disease (mitral valve or tricuspid valve endocarsiosis = progressive myxomatous degeneration of atrioventricular valves)

• Autonomic responses are slower

• Exercise tolerance tests are influenced by other sieraden processes like arthritis

Age related change (geriatric) - respiratory

• Reduction in vital capicity and functional residual capacity (FRC) > lung loses elasticity and small airways close at a higher lung volume

• Increased risk of atelectasis and ventilation perfusion mismatch (where part of the lung receives oxygen without blood flow or blood flow without oxygen)

• Chest wall compliance is decreased therefor positive pressure ventilation has a greater effect on venous return

• Trachea and larynx are increased in diameter leading to increased anatomical dead space

• Protectie laryngeal reflexes may be dimished making aspiration of any regurgitated material more likely

Age related changes (geriatric) - renal

• Reduced number of nephrons (functional unit of kidney)

• Kidneys receive 25% of cardiac output > renal blood flow decreases with reduced cardiac coutput

• Reduction of renal mass

• Reduced ability to correct for fluid, electrolyte and acid-base derangements

• Benefit from fluid therapy but prone to fluid overload so must be monitored carefully

Ventilation perfusion mismatch is where part of the lung receives oxygen without blood flow or blood flow witout oxygen. The V/Q ratio refers to the ratio of ventilation to perfusion: V = the flow of air that reaches the alveoli through the alveolar duct; Q = the flow of blood that reaches the alveoli through the capillary beds

High V/Q is oxygen without blood flow (V= ventilation Q= blood flow)

Age related changes (geriatric) - heptatic

• Liver also receives 25% of cardiac output = reduced liver blood flow and reduced hepatic function leading to slower drug metabolism

• Liver generates a lot of body heat as an exothermic (chemical change that us accompanied by liberation of heat) by product of metabolism

• When liver is not functioning, animal more prone to hypothermia

• Reduced albumin formation, which influences binding of protein bound drugs

Altered drug disposition, why?

• Less muscle mass: less mass available for IM injections

• Increased adipose tissue: some IM injections may end up intrafat if the needle is not long enough

• Decreased albumin: less drug is bound and more drug is free (=active). Induction agents must be given slowly to effect to avoid overdose

• Decreased total body water: lower doses of water soluble drugs (ketamine) should be used to achieve the same effect as in younger dog with lower dose

• Minimum alveolar concentration (MAC) values of volatile agents decrease by 30%

• Decreased hepatic elimination; effects of drugs may be prolonged

• Decreased renal reserve so drugs relying on renal clearance have a prolonged duration of action

• Extradural (epidural) injections spread more cranially > volume moves less sideways into the epidural cuffs via the foramen between the vertebrae but moves more cranially. Reduction in volume is beneficial

Name 4 diseases that are more common in older animals

• Canine hypothyroidism

• Cushing's disease

• Diabetes mellitus

• Feline hyperthyroidism

What can you do to stabilise prior to anaesthesia (up to 2wks)

• Dieting (not crash dieting)

• Antitussives

• Mucolytics

• Bronchodilators (3 last for wide clean airways)

• Dietary protein restriction (renal)

• Low protein multiviamins (hepatic)

What is emergence delirium?

Temporary state of confusion and uncontrolled agitation that happens when an animal wakes up from general anesthesia

Aims for anaesthesia for geriatric patients

• Lower doses of premedication with shorter acting drugs due to patient slower metabolism

• Benzodiazepines may be sedative in geriatrics

• IV acces

• Fluid therapy (75% of nephrons need to be lost before urea start to increase in bloodwork)

• Preoxygenation via mask for 3-5min (unless this stresses the animal)

• Short acting induction agents should be used injected slowly and to effect

• Low solubility volatile agent such as sevo and isoflurane are preferred

• May need ventilation support

• Multi modal analgesia but renal function checked before administering any NSAID

• THOROUGH monitoring

Effects of liver dysfunction on anaesthesia

• Hypoproteinaemia > ascites, peripheral oedema, reduced plasma oncotic pressure, drug binding

• Anaemia > erythropoietin, clotting abnormalties, oxygen carrying capacity, detection of cyanosis,

• Hypocalcemia

• Hypoglycaemia

• Hypothermia (liver is one of main exothermic organs)

• Clotting disorders (hepatocytes are involved in the synthesis of most blood coagulation factors)

• Hepatic encephalopathy

• Bacteraemia (liver is responsible for filtering bacteria out of bloodstream)

• Jaundice (icterus)

• Hepatomegaly

• Gastrointestinal disturbances (vomiting, diarrhoea. Check for dehydration, hypovolaemia,electrolyte and pH abnormalities)

• Drug biotransformation

Hypoproteinaemia: the liver is a site of production of several plasma proteins, incl albumin so if protein production is decreased the following may occur:

• Ascites > fluid accumulation in the abdomen which can compromise ventilation and reduce the functional residual capacity

• Peripheral oedema which can make it difficult to get peripheral IV acces

• Reduced plasma oncotic pressure > or colloid osmotic pressure is a form of pressure induced by proteins, notably albumin, in the plasma in blood vessels that draw water into the intravascular space from the interstitial space

• Drug binding > many anaesthetic drugs bind to albumin, the less albumin available the less drug is bound and more is free and active

Reasons why a liver patient may be anaemic

• Erythropoietin: liver is one of the sites of production of erythropoietin a hormone that stimulates red blood cell production

• Clotting abnormalities: blood loss anaemia due to clotting abnormalities which occur due to lover dysfunction

• Oxygen carrying capacity: moderate to severe anaemia influences the patients blood oxygen carrying capacity and anaesthetic requirements (lower MAC valur of volatile agents)

• Detection of cyanosis: can be seen by the human eye when deoxygenated haemoglobin level is above 5g/dl. If patient is anaemic their haemoglobin concentration in total may not even reach 5g/dl but patient is still extremely hypoxic but blue discoloration may not be seen

What does hypocalcemia predisposes to with anaesthesia

Predisposes to muscle weakness and arrhythmias.

Reduction in total serum calcium can result from a decrease in albumin secondary to liver disease.

How does hypoglycaemia relate to liver disease and anaesthesia?

Liver is key to glucose homeostasis. Any disruption of its metabolism, structural integrity or intracellular dynamics may alter the livers ability to maintain normal glucose homeastasis.

Hypoglycaemia causes systemic effects > neuronal damage, immunosupression and muscle weakness

What is hepatic encephalopathy?

Condition that occurs when liver is too diseased/damaged to properly process ammonia. Ammonia building up in the blood and affects the brain leading to dullness, depression and seizures. Must be corrected before a anaesthesia takes place

What is hepatomegaly?

An enlarged liver, can be causes by hepatitis or hepatic tumours.

As the liver sits just behind the diaphragm when enlarged it may limit thoracic excursion and reduce ability to ventilate and oxygenate properly predisposing to hypoxia and hypercapnia

What does drug biotransformation mean in relation to liver dysfunction?

Liver is the site op biotransformation of may anaesthetic drugs and so their metabolism may be slower and recovery delayed.

Top ups of analgesia should be done on pain assesment not on strict dosing regime.

If prodrugs are given formation of the active drug is delayed

Effects of anaesthesia on the liver

• Ensure adequate oxygenation

• Measuring and maintaining blood pressure

• All volatile agents decrease arterial blood pressure and therefor portal flow

• IV anaesthetics have a modest impact in hepatic blood flow

» etomidate decreases hepatic blood flow secondary to increased hepatic arterial vascular resistance and reduced blood pressure

» propofol increases hepatic blood flow probably through a significant vasdilator effect

» ketamine has little impact on hepatic blood flow

Normal hepatic blood flow (photo)

What is a portosystemic shunt? (PSS)

An abnormal vein which bypasses the liver (shunting) and connects the blood supply returning from the intestines to the vein returning blood to the heart.

• Can either be congenital (present at birth) of acquired (through liver disease)

• Most are congenital and identified when patients are young

• Often present with neurological signs due to hepatic encephalopathy from raised blood ammonia > stabilisation often for some weekse required before attempting sedation/anaesthesia

• Stabilisation includes antibiotics, lactulose and dietary management with the aim of decreasing bacterial population in the intestines and minimizing the production of toxins. Lactose promotes the expulsion of faecal matter as well as decreasing bacterial load in the colon whilst antibiotics helps to eliminate bacteria that promote the formation of toxins

• Decreased liver function usually indicated by increased bile acids.

• Less exothermic activity, slower biotransformation of drugs, low plasma proteins (incl albumin), microcytic normochromic anaemia and decreased clotting factors

What to think about with anaesthesia for a live patient

• Short acting drugs should be used

• Those with an alternate route of metabolism or those that can be antagonised

• Benzodiazepines have been avoided because of endogenous (produced in the body) benzodiazepines are implicated in the pathogenesis of hepatoencephalopathy

• Usually attenuated via laparotomy approach. Intra/extrahepatic shunts > risk of blood loos with intrahepatic is greater as liver dissection is required

• A significant decrease in central venous pressure may be seen after shunt ligation because the same blood volume is now flowing through an additional new capillary netwerk (the liver). Intestinal perfusion may become compromised at this time

• Complications after surgery include portal hypertension (high blood pressure in portal vein which carries blood from intestines to the liver) which can lead to loss of proper blood circulation to abdominal organs and death. Animals may show signs of > ascites, vomiting, diarrhoea, depression, respiratory distress

• Rare complication is seizures which are refractory to treatment; cause is unknown. Seizures may be managed with antiseizure medication like levetiracetam.

Functions of the kidney

• Urine production

• Blood pressure and osmolarity regulation

• Hormonen secretion

• Maintain acid-base balance

How to differ between prerenal, renal or postrenal azotaemia (an increase in urea+/-creatinine)

Pre anaesthetic blood test and urine specific gravity (USG)

Prerenal azotaemia

• Is due to circulatory disturbances which decrease renal blood flow such as dehydration or hypovolaemia

• Usually distinguished from renal azotaemia by clinical signs and urinalysis (urine is adequately concentrated but there is usually no evidence of renal tubule dysfunction (such as excessive proteinuria) » USG >1030 dog >1035 cat

Renal azotaemia

• When more than 75% of nephrons (functional unit of kidney) are non functional

• May be due to primary intrinsic renal disease (glomerulonephritis, ethylen glycol toxicity) or renal injury which soccurs secondary to renal ischaemia (do not get enough blood flow/oxygen) or urinary tract obstruction (postrenal azotaemia)

• Isothenuria (USG is no different to that of plasma 1008-1012) is common in renal azotaemia

• Other evidence of renal tubular dysfunction in urinalysis includes excessive proteinuria, casts, glucosuria without hyperglycaemia

Postrenal azotaemia

• Rsulda from obstruction or rupture of urinary outflow tracts

• USG resjlts are quite variable so best to diagnose based on clinical signs

• The types of renal failure are not mutually exclusive. One can leas to another

Acute renal failure - what signs may animals exhibit

• Dehydration and potential hypovolaemia if dehydration is severe; from fluid shifts, third space losses (uroabdomen), decreased oral intake of water and food, gastrointestinal losses such as vomiting. Hydration status should be assessed and corrected before anaesthesia

• Electrolyte imbalances and acid-base imbalances

• Uraemia indicates that urea (a nitrogenous waste product usually excreted by the kidneys) is building up in the bloodstream. This can cause nausea and vomiting, dulness, depression, seizures, hypothermia and decreased metabolic rate. Generally low doses of sedative/induction agents are required because of CNS depression. Warm if needed, fluid therapy will decrease bood levels of urea

• Pain, especially postrenal failure cases, where the blader or urethra are distended, as this produces visceral pain. Uroabdomen causes peritonitis which is also painfull

Metabolic acidosis

In acute renal failure, potassium ions and hydrogen ions which are usually excreted in urine, are retained. Hydrogen ions are acidic and acidaemia develops if they cannot be excreted in urine and accumulate in blood stream. As this is of metabolic origin, it is metabolic acidosis

(More hydrogen ions mean lower pH and higher acidity)

If there is a primary acid-base derangment (such as metabolic acidosis) the body tries to compensate using the otber body system (in this case respiratory) Carbon dioxide is an acidic gas and therefor the patient breaths faster to increase elimination

Hyperkalaemia and its problems

• Serum potassium levels above normal range (3,5-5,5mmol/l)

• Potassium is mainly intracellular ion, but outside the cell can be problematic

• It occurs if urine cannot be voided; only route of exrection for potassium is via urine, so it accumulates

• Causes muscle weakness, neurological abnormalities and possibility of dysrhythmias

• Typical dysrhythmias; bradycardia, spike T waves, flattened or lost P waves and QRSbcomplexes which look like they have been picked up and pulled apart

• Metabolic acidosis worsens hyperkalaemia because as hydrogen ions move into cells, potassium ions are pushed out

Describe what happens to the ECG PQRST complex with hyperkalaemia

What are the minimum levels of pH and potassium at which you can anaesthetise an animal again who had hyperkalaemia

PH at least >7,2 and potassium <6 mmol/l

Dehydration, hypovolaemia, uraemia, metabolic acidosis and hyperkalaemia are all improved with what?

Fluid therapy.

• 0,9%NaCl or Hartmann's solution (lactated ringers)

• Level of potassium in Hartmanns is low and administering a crystalloid fluid dilutes potassium

• It is an alkalising solition (because of the lactate), pH is brought back up which encourages potassium to go back into cell (=safe place) and it actually reduces potassium serum concentrations

Isn't it dangerous to give fluid therapy to an animal with obstructive renal disease? (In case of bladder rupture)

Not really, these animals are probably dehydrated and hypovolaemic so renal blood flow and therefor golmerular filtration rate is lower. In addition , back pressure from the obstruction reduces the stimulus to produce urine, so until blockage is relieved little urine is produced

If fluid boluses are insufficient to bring potassium down to safe levels for anaesthesia, what more can you do?

• Glucose (+/-Insulin) can be used to shift potassium back into the cell via contransporter system as glucose is take up

• If this is unsuccesfull, the use of calcium compounds can cause a temporary stabilisation of the cardiac action potential, although this effect is only transient and does not affect serum potassium levels

If IV fluid therapy with Hartmann's (ringers lactate) is not enough what else could you add?

In severe situations, sodium bicarbonate can be infused slowly (ensuring it is not mixed with a calcium containing solution otherwise precipitation occurs which may potentially block the catheter).

However it can produce multiple side effects incl hypernatraemia, hyocalcemia, hypokalaemia and carbon dioxide production so it is usually reserved unless the base excess is more negative than -10mmol/l

Chronic renal failure - clinical changes, many that are evident on haematological/ biochemicus blood panels (name 8 changes)

• Anaemia: kidneys do not make enough erythropoietin (hormone that stimulates bone marrow to make red blood cells). High levels of urea supress bone marrow production of red blood cells and increase fragility of red blood cells limiting their life span. Uraemia can also cause blood loss anaemia through gastrointestinal ulceration. This alters the animals oxygen carrying capacity

• Hypoalbuminaemia (where a protein losing nephropathy is present) this means more drug is free and active and therefor animals are at a higher risk of overdose

• Calcium phosphorus derangements may predispose to arrhythmias

• Hypertension: renal disease, espically chronic kidney disease (CKD) is most common cause of hypertension in dogs and cats. The renin angiotensin aldosterone system (RAAS) (hormone system that is essential for regulation of blood pressure and fluid balance) is regulated by the rate of renal blood flow and therefor stimulated in CKD, producing hypertension. Chronic hypertension may lead to cardiomegaly and ventricular hyperthrophy.

• Bleeding tendencies may occur due to intrinsic platelet defects, decreased platelet aggregation and impaired platelet adhesiveness: therefor, if from the history there is suspicion of coagulopathies, clotting times should be checked before large bore vessels are cannulated or surgery performed

• Acid-base abnormalties: uraemia may cause nausea and vomiting which predisposes to acid-base abnormalties and dehydration

• Immunosupression: high levels of urea supress bone marrow function and therefor immunosupression; care should therefor be taken with skin preparation for catheters and surgeries

• Decreased drug clearance: there is decreased renal clearance of some drugs, especially those with active metabolites. In anaesthesia , examples of these drugs incl some opioids and some neuromuscular blockers

Main aims for anaesthesia with a kidney patient, chronic or acute

• Maintain renal blood flow and oxygenation of renal tissue

• Get depth of anaesthesia correct

How is renal blood flow regulated?

It is autoregulated across a bandwidth of mean arterial pressure of 60-160 mmHg.

It does not matter where within that range it is, renal blood flow stays the same.

If an animal suffers from chronic hypertension, in this circumstance the aim must be to maintain blood pressure within the higher end of the bandwith range

Why is depth of anaesthesia so important with a kidney patient?

If patient is too deeply anaesthetised, blood pressure may fall below the autoregulation bandwidth which reduces renal blood flow.

If patient is too light and they respond to nociception, the stimulation of the sympathetic nervous system causes vasoconstriction of the renal blood vessels, again affecting blood flow

Why should NSAID's not be used during anaesthesia of a kidney patient?

Kidneys rely on certain prostaglandines (PGI2 and PGE2 and other) to maintain renal blood flow at times of low blood pressure. These prostaglandines are blocked by NSAIDs and therefor during anaesthesia normotension cannot be guaranteed.

What other class of drugs has the potential for nephrotoxicity?

Volatile agents; 2 older agents > methoxyflurane and enflurane. (They yield a fluoride ion).

Metabolism of sevoflurane also yields fluoride but studies have not shown evidence of fluoride-induced nephrotoxicity.

Sevoflurane does produce a vinyl ether; Compound A, which is produced when its used in rebreathing systems during low flow anaesthesia. Compound A has been implicated in causing renal dysfunction in rats. In all other veterinary species this should cause few problems. But dont use in circle systems at low flows for long periode of time.

What does the endocrine system consist of?

Consists of different glands which secrete hormones into the blood stream, which affect the activity of cells at another site in the body.

The system is integral to homeostasis.

• Hypothalamus (control center linking nervous system to endocrine system)

• Pituitary gland (‘master gland’)

• Pineal body (melatonin)

• Thyroid (metabolism/energy use)

• Parathyroid (calcium)

• Thymus (specific white blood celss)

• Adrenal glands (cortisol/adrenaline)

• Pancreas (insulin/glucagon)

• Gonads (ovary and testes)

What is diabetes mellitus ?

A chronic disorder of carbohydrate metabolism resulting from absolute or relative deficiency of insulin.

Insulin is responsible for inhibiton of fluconeogenesis (prosuction of glucose) and stimulation of glucose uptake into cells.

Animals are usually polyphagic, polyuric, polydipsic and losing weight.

Name 3 situations when anaesthesia is required to treat or investigate conditions associated with diabetes

• Ovariohysterectomy - entire female dogs with diabetes mellitus tend to destabilise during oestrus or pregnancy due to the production of progesterone, therefor ovariohysterectomy if often performed in diabetic bitches to aid stabilisation

• Phaecoemulsion - animals with diabetes can develop diabetic cataracts due to sorbitol deposition in the lens. Phaecoemulsification for the treatment if cataract (where the lens is emulsified and then aspirated from the eye) requires general anaesthesia

• Abdominal ultrasound - may be required to investigate why a patients diabetes is poorly controlled and sedation may be required to facilitate this

What is a normal blood glucose and what are the risks with hyper- and hypoglycaemia?

Approximately 3-7 mmol/l

Hyperglycaemia causes glucosuria (if the blood glucose goes over the renal threshold (=dog 10-12mmol/l, cat 13-17 mmol/l)) causing osmotic diuresis and dehydration.

Severe hyperglycaemia can lead to coma, theough dehydration, lactate acidosis and hyperosmolality.

Hypoglycaemia produces neurological damage (<2,7mmol/l)

What type of chronic organ dysfunction can a diabetic patient have?

• Renal system - diabetic nephropathy, prerenal azotaemia, urinary tract infections

• Liver - lipidosis, impaired function, hepatomegaly

• Electrolyte imbalances where total body stores of potassiumnand sodium become depleted

• Immunosupressed - negative effects elevated blood sugars have on immune system. Loss of body and muscle mass can influence drug distribution and increased potential for heat loss

Generic starvation and insulin protocol for a diabetic patient

• Procedure performed first on the days's list

• Patient given half a portion if their normal food 2-4hrs before anaesthesia and then starved

• Water offered until preanaesthetic medication

• Half-dose of insulin should be given 2-4hrs before anaesthesia

Individualised approach based on glucose levels, what are the levels and portions of insulin?

• Starve from midnight, feed no breakfast, morning of anaesthesia check blood glucose levels and administer appropriate dose of insulin:

— <6mmol/l : no insulin given

— 6- 15 mmol/l : half-dose of insulin given

— >15mmol/l : foll-dose of insulin given

What is the nadir?

Lowest point of the blood glucose curve after insulin administration

At what point do you give glucose and how much during anaesthesia?

Below 3 mmol/l.

0,25-0,5 g/kg glucose slow IV.

Glucose stock solution Is hypertonic and must be diluted with a crystalloid to avoid thrombophlebitis.

If blood glucose become excessively high, soluble insulin (0,1IU/kg/hr) IM should be administered

What kind of anaesthetics should or should not be used for a diabetic patient?

• Antiemetic (maropitant)

• Dont over sedate; patient needs to recover quickly

• Opioid +/-Low dose acepromazine

• Short acting drugs

• Low solubility volatile agents for quick recovery

• Fluid therapy 5ml/kg/hr (dog), 3ml/kg/hr (cat) reduced by 25% each hour (until maintenance rate is reached)

• Be carefull with: alpha2- adrenergic agonist; it blocks insulin and can disrupt glucose control

• Check for diabetic nephropathy or prerenal azotaemia before administering NSAID

Can you give insulin after the procedure when the animal starts eating again?

• When patient can sit up and swallow give small test feed.

• When patient does not vomit, give usual breakfast

• When breakfast is eaten, remainder of insulin (which had not been given that morning) should administered

• If animal does not want to eat breakfast > monitor blood glucose for rest of the day and further insulin given if blood glucose concentrations start to increase significantly

What are insulinomas?

Malignant functional pancreatic tumours of the beta cells, which retain the ability to produce and secrete insulin.

Most common pancreatic neuroendocrine tumour in dogs, which induce a variety of clinical signs that result from hypoglycaemia and secondary neurological effects (incl collapse and seizures) to adrenergic effects from catecholamine release incl anxiety.

Rarely reported in cats.

What are the risks of anaeathesia with insulinoma resection?

• Primarily risk of debeloping hypoglycaemia when CNS signs are less noticable

• In addition to high sympathetic tone and possibly of arrhythmias (as catecholamines are counter regulatory to insulin= they raise blood sugar levels)

Important things before and during anaesthesia for insulinoma resection

• Blood chemistry and electrolyte evaluation, particularly potassium

• Remove food at midnight with small calorie dense meal at 4 am = option

• Or administering a glucose containing solution IV during starvation time

• Check blood glucose before preanaesthetic medication

• Check blood every 15min during anaesthesia

• More regularly when pancreas is handled > this may cause aditional release of insulin into blood stream

• Keep blood glucose between 3-7mmol/l

• ECG and blood pressure during procedure

• Epidural analgesia and lidocaine CRI are options

What medication could be of use (in low dose) to aid with the anaesthesia? What did one drug had as side effect?

Low dose of alpha2- adrenergic agonist.

This blocks the action of insulin, so it can raise plasma glucose concentration and decrease plasma insulin concentrations.

(Dose was 5microgram/kg IM)

Alfaxalon or propofol with insulinomas?

Both are an option.

Occasional reports of pancreatitis in humans with propofol due to the high lipid content of the drug, could be reason to choose alfaxalon.

Risk of pancreatitis following surgery is fairly high due to handling of the pancreas and should be monitored (in addition of signs of diabetes mellitus) postoperatively

What is hypoadrenocorticism?

Addison’s disease.

• Characterised by glucocorticoid and/or mineralcorticoid deficiency due to a failure of the adrenal glands

What are the names of the layers of the adrenal glands?

And what do they produce?

Outer cortex and inner medulla

Cortex is composed of 3 layers:

• Outer zona glomerulosa: production of mineralcorticoids (aldosteron)

• Middle zona fasciculata: production of glucocorticoids (cortisol)

• Inner zona reticularis: production of sex hormones (androgens and oestrogens)

What are glucocorticoids (cortisol) vital for?

• Gluconeogenesis (metabolic process that synthesizes new glucose from non-carbohydrate precursors, primarily occurring in the liver and kidneys to maintain blood sugar during fasting or intense exercise)

• Fat and protein metabolism

• Immunity

• Blood pressure regulation

• Counteracting the effects of stress

Clinical signs of dogs deficient in mineralocorticoids

• Hyperkalaemia

• Hyponatraemia

• Azotaemia

• Hypovolaemia/dehydration

• Bradycardia due to hyperkalaemia (despote being hypovolaemic)

Clinical signs of dogs deficient in glucocorticoids

Overall vague clinical signs:

• Lethargy/weakness

• Polyuria/polydipsia

• Vomiting/diarrhoea

• Abdominal pain

• Weight loss

• Depending on the severity of the gastrointestinal signs; anaemia, hypoalbuminaemia or metabolic acidosis may be present