Prep For Clinical Practice Flashcards
-Absorbed dose
total amount of radiation absorbed by an object (International System of unit or SI unit: Gray (Gy)).
Equivalent dose
absorbed dose x radiation weighing factor, to account for how harmful a type of radiation is to biological tissues (SI unit: Sievert (Sv)).
Effective dose:
equivalent dose x tissue weighing factor, to account for the radiosensitivity of different organs and the increased risk of the patient developing stochastic (see below) effects (SI unit: Sievert (Sv)).
Direct damage:
results in break of molecular bonds within cells (eg DNA).
Indirect damage
esults in interaction with water leading to creation of free radicals, which in turn can break molecular bonds within cells.
Deterministic effects
they occur at a specific dose threshold and represent tissue reactions; the severity of these effects is dose-dependent. Rapidly dividing cells are most sensitive and radiation sickness reflects body systems affected (eg dermatitis, burns, cataract, gastrointestinal disturbance or changes in blood). The latter are known as somatic effects.
Stochastic effects
represent effects that have no threshold and occur randomly. The severity of the effects is not dose-dependent, but the probability for the effects to occur is dose-dependent.
Carcinogenic effect: tumors may be induced decades after the radiation exposure Genetic effects: mutations may occur in the chromosomes of germ cells in the ovaries or testes, with potential effects in the offspring.
ALARP
he main goal is to keep the radiation dose As Low As Reasonably Practicable (Achievable) at all times
Doses are kept lower than the threshold for deterministic effects. As there is no threshold for stochastic effects, doses should always be kept as low as possible.
Too high kVp will lead to
increased scatter production by the patient, increased scatter in the radiography room and reduced image contrast
oo low kVp may lead to
increased exposure time, with a likelihood of motion artifacts and a need for repeat examination.
Use a grid for subjects greater than
10 cm thick.
Methods of protection against scatter radiation
time, distance, shielding
Dosimetry
Measurement of radiation exposure
Compton absorption
photon of electromagnetic energy interacts with a loosely bound electron in the outer shell of an atom.
The photon displaces the loosely bound electron which can ionize other atoms.
The photon is diverted and continues in a different direction with a lower energy ’Scattered radiation.
Increases with increasing energy.
As energy increases more of scattered radiation is directed in a forward direction, ie more likely to reach x-ray film.
Independent of atomic number of tissue.
Production of scatter
catter is produced when x-rays interact with matter.
Lower energy than primary beam.
Travel in any direction.
Very important inlarge animal radiography.
At high kV less of the primary beam is converted to scatter but more scattered radiation is moving forward towards the film.
Increases with increasing volume of tissue irradiated.
ncreases radiation exposure to personnel.
Increases radiation dose to patient.
Reduces film contrast (increases overall film density in a non-specific way).
how is scatter reduced?
collumation
Compress patient
Reduces volume of tissue irradiated. Can be achieved using Bucky band - a webbing strap which can be tightened around the body (particularly abdomen).
Reduce kVReduce scatter affecting filmGrids
Placed between film and patient to absorb scatter. Most scatter is travelling in an oblique direction and therefore is unable to pass through grid. Results in increased exposure factors required. Grid lines can appear on film.
Alternative filtration devices
Air gap between patient and film:
Radiation travelling obliquely misses film.
Important in large animal radiography where film is often some distance from object.
Air gap increases magnification and reduces image sharpness.
Filter between patient and film:
Lead backing to film cassettes
Reduce effects of scatter on film
Intensifying screens (particularly rare earth) intensify primary photons more than scatter. Screens also increase gamma so that film contrast is enhanced and effect of scatter is reduced.
When compiling an exposure chart as many variables as possible should be kept constant: what variables are these
Film focal distance.
Object film distance.
Processing
Film type
Intensifying screen type Radiography
Use of grid use.
Line mains compensation.
Variable kV
This is used if:
Machine allows variation in kVp of 1-2. Due to the variation in dog size and shape selecting an exposure based on dogs weight may be inaccurate. Breed variability in conformation can be overcome by basing exposure on tissue thickness. Keep mAs constant and as high as possible and alter kV based on tissue thickness. A grid should be used if tissue depth is >10 cm and may be useful in smaller obese animals.
Grids
If using a grid the exposure will need to be increased.
Multiply grid factor by mAs to obtain new mAs.
X-rays
electromagnetic radiation.
Their usefulness stems from a number of properties:
Travel in straight lines. Can pass through a vacuum. Travel at constant speed. Variably absorbed by body tissue. Affect photographic film to produce a latent image ause certain substances to fluoresce (emit visible light)
X-rays are produced when electrons are rapidly deccelerated
Kilovoltage (kV) control
Alters the potential difference applied across the tube head during exposure.
Alters the speed and energy with which electrons hit the target and hence the pentrating power of the subsequent x-ray beam.
In some machines it is linked to mA so that if high mA is selected, kV must be reduced.
Milliamperage (mA) control
Controls the heating of the filament and hence the number of electrons released by the cathode.
This directly affects the quantity of x-rays produced.
Timer (x rays)
The time for which the exposure is applied affects the number of x-rays produced.
The quantity is usually measured as a combination of amperage and time, ie mAs.
The longer the exposure the more chance there is of a patient moving so it is preferable to use the highest mA permissible with a given kV and reduce the exposure time accordingly.
Older machines had clockwork timers but new machines have electronic timers which are quieter and more accurate.
Portable x ray machines
Stationary anode (heat lost by convection and conduction).
Self or half wave rectified.
Often fixed mA
Occasionally fixed kV.
Run from domestic supply (13 amp).
Cheaper than mobile/3-phase machines to buy and maintain.
Can be dismantled and used for domicillary examinations.
mobile x ray machines
Rotating anode (heat lost by radiation)
Usually full wave rectified - 2-pulse.
May be capacitor discharged.
High and variable mA facilitating shorter exposure times.
Higher output allows grid and grid use to be used more readily.
More expensive to buy and maintain than portable machines.
Limited to use within the practice unless van or trailer used!
3-phase x ray machines
Rotating anode.
Full wave rectified - 6 pulse.
High and variable mA and kV.
Very high exposures and short exposure times possible.
Expensive to buy and service.
Fixed installation ’ dedicated room needed.
Medium frequency (high frequency) x-ray machines
An invertor increases the frequency of the electrical supply so that with vastly increased number of pulses the ripple factor is negligible and the generator is equivalent to a constant potential unit.
Used in some mobile machines which may use a battery supply and some fixed machines which run off a 13 amp supply.
Pharmacokinetics
what the body does to the drugp
Pharmacodynamics (PD)
What the drug does to the body
ADME
Absorption (administration), distribution, metabolism and elimination; ADME
Given the heterogonous structure of bodies, on top of its target a drug will inevitably interact with more than one element (side effects possible).
Understanding the ADME (absorption/distribution/metabolism/excretion) of a compound is central to any therapy.
A - Routes of Administration
Enteral routes:
Directly into the gastrointestinal tract
Sublingual
Swallowing
Rectal
Parenteral routes:
Topical admin.
Intradermal admin.
Subcutaneous admin.
Intramuscular admin.
Intravascular admin.
Inhalation
Intravascular administration
Mostly used when there is a need to control accurately the body concentration of drugs. Typically used when compounds have narrow margins of safety between therapeutic and toxic index (e.g. induction agents/anticancer drugs).
Drawback:
Drug injected cannot be recalled . A slow infusion administration is needed to avoid side effects.
Inhalation administration
Gas and aerosols:
Rapid systemic effect but dependent on:
1- the tidal volume
2- the size of the aerosol particle (not true for gas). The smaller the more likely to reach alveolar ducts and sacs. Otherwise get stacked in bronchi.
D - Distribution
Distribution around the body occurs after drug reaches circulation
It must then penetrate tissues to act
consider Movement of drugs across membranes- passive, active, ionic
Active transport / Carrier mediated transport
In general, compounds that rapidly cross membranes have:
a. Low degree of ionization b. High lipid/water partition in the non ionized form c. Relatively low MW < 1000 d. A biological affinity with transporters/facilitated diffusion (e.g. cephalporins are absorbed by a transporter for dipeptides)
Effect of ionization on drugs crossing membranes
Must be neutral to cross the membrane (if too charged they would associate with many other molecules which would impair their ability to diffuse).
Many drugs are weak acids or weak bases
Recall that weak acids (HA) donate (H+) to form anions: HA↔H++A-
Recall that weak bases (B) accept a proton (H+) to form cations: BH+ ↔B+ H+
Recall Henderson-Hasselbalch equation:
pH=pKa+log[nonprotonated/protonated]
pH=pKa: protonated form equal to nonprotonated concentration
pHpKa: vice versa
(dont need to know this just understad concept)
An example!
Effects of ionization on the macrolide antibiotic erythromycin
Erythromycin pka = 8.8
Plasma pH = 7.4. Milk pH = 6.5
Given pH = pka + log non-ionized/ionized
In milk, 199.5 ionized to every non-ionized, in plasma 25 parts ionized to every nonionized = ION TRAPPING
Chemical Properties of Drugs- isomers
constitutional isomers
setrioisomers- diastereomers (cis/trans)- conformers, rotamers
enantomers
M - Drug metabolism
Lipophilic drugs must follow a very special treatment to become hydrophilic (polar), often inactive, and then be excreted.
The drug transformation may be a two phase reaction (but the phase I may be sufficient to inactive and excrete the drug)
In the liver the major drug metabolising enzymes act in the Smooth
Endoplasmic Reticulum of Liver Cells (hepatocytes)
aneamia can effect
drug metabolism
Metabolism and CYPs
The majority of CYPs are found in the liver, but certain CYPs are also present in the cell wall of the intestine.
The mammalian CYPs are bound to the endoplasmic reticulum, and are therefore membrane bound
CYP 3A4, CYP 2D6, and CYP 2C9 are especially involved in the metabolism of xenobiotics and drugs in humans (and probably veterinary species)
Metabolism & Glucuronidation
The major phase II drug metabolising family of enzymes are the Uridine Diphosphate Glucuronyl Transferases (UGTs)
Cats are deficient in UGTs
– Limited ability to perform glucuronidation
– Paracetamol toxicity
Metabolites known as glucuronide conjugates
– Excreted in bile and urine
– Limited stability and can hydrolyse in the gut
– Undergo enterohepatic recirculation
major routs of Drug excretion
renal
billary- faeces
pulminoary
minor routs of excretion
mammary
salivary
Biliary excretion
Parent drug or metabolites may either be excreted in bile and eliminated via the GI tract or recycle several times before entering the systemic circulation (the drug follows bile salts)
Specific liver transporters are involved in the biliary excretion of metabolized drugs
Drugs can be very long lasting (e.g. Antibiotics)
renal excretion
passive filtration, secretion and reabsorbtion
Pharmacokinetic Drug-DrugInteractions
Tissue/plasma levels of one drug altered by another one
– Absorption
• Change in gastric pH
• Alteration in bacterial flora
• Decreased gastric emptying – metaclopramide
– Excretion
• Sodium bicarbonate makes urine more alkaline – increases excretion of weak acids (why?)
• Probenecid reduces renal excretion of penicillins
– Some drugs reduce circulation and may therefore reduce
• Clearance
• Elimination
– Eg alpha-2 agonists
– Metabolism
• Enzyme inhibition/induction
Quantitative Pharmacokinetics (PK)
Changes in plasma/tissue drug concentration with time
Quantitative Pharmacodynamics (PD)
– Changes in biological response with time
Absorption kinetics
IV infusion = zero order kinetics (straight line on grph)
IM/SC/oral = tend to follow first order kinetics. (increasing line on graph) Absorption rate from oral administration tends to be proportional to amount of drug (first order)
Amount of drug at administration site decreases with time therefore, rate of absorption decreases
Drug Elimination Rate
The amount of parent drug eliminated from the body per unit time – occurs after distribution
Volume of water in glass tank is analogous to the volume of blood plus interstitial fluid (body water) also described as the initial volume of distribution (Vi)
Concentration of contaminant in water = 100 mg / 10 L = 10 mg / L
This is analogous to drug concentration in blood immediately after
IV bolus dosing
Contaminant stuck on glass is in equilibrium with contaminant in solution
Concentration of contaminant in solution = 30 mg / 10 L = 3 mg / L
This is analogous to the concentration of a drug in blood after distribution
to tissue
Volume of distribution
Vd usually given in litres/kg
TBW approx. 0.6LKg
ECF approx. 0.1-0.3L/Kg
Vd of 0.1-0.3L/Kg drug most likely water soluble and mainly in ECF. E.g., midazolam or NSAIDs Vd high (2L/Kg +) drug accumulates in another site – e.g., fentanyl in fat
Properties of X-rays and Gamma Rays:
No charge and no mass
Invisible and cannot be felt
Travel at speed of light
Travel in straight line
Penetrate all matter to some degree
Cause some substances to fluoresce
Expose photographic emulsion
Ionise atoms
X-rays are produced by the interaction of electrons with an atom
2 types:
Characteristic
Bremsstrahlung (braking)
Cathode
coiled tungsten wire
The cathode in an X-ray tube generates a stream of electrons via thermionic emission
Potential difference applied across the X-ray tube accelerates the electrons towards the positively charged anode
These hit and interact with the atoms within the target area of the anode resulting in the release of X-rays
Radiodensity (or radiopacity)
is opacity to the radio wave and X-ray portion of the electromagnetic spectrum: that is, the relative inability of those kinds of electromagnetic radiation to pass through a particular material.
Scatter
The effect of the X-ray beam striking another atom
Lower energy radiation produced in the patient’s body tissues - Compton Effect
Amount depends on:
Density/atomic no. of the patient/tissue
Increases in kV- higher penetration higher dose- may stay in tissues- domino effect of ionisation
Larger area (collimation)
As the size of the field increases, the amount of scatter will increase
Properties
May travel in any direction
Image degradation
Ionisation in tissues
Radiation dose – patient, YOU!
Harmful effects of X-rays
Genetic effects
Increased risk of DNA mutation and inherited abnormalities with ionising radiation
Somatic effects
Skin erythema, BM hypoplasia, abortion..
Carcinogenic effects- Rapidly dividing cells most susceptible
Persons under 18
Pregnant women (foetus)
Bone marrow
Gonadal tissue/repro organs
Germinal layers of skin (and gut)
legilation on radiation saftey
Ionising Radiations Regulations 2017 (IRR17)
BVA Guidance Notes for the Safe use of Ionising Radiations in Veterinary Practice
Must appoint a Radiation Protection Advisor and a Radiation Protection Supervisor
Must define and identify a controlled area
Must draw up and follow Local Rules
Radiation Protection Advisor
External to practice
Advanced knowledge of radiation (e.g. Radiation Physicist or Veterinary Diploma holder)
Must hold a RPA Certificate of Competence
Initially helps design and setup radiography facilities (or when any significant changes)
Establishes Local Rules
Annual visits to advise on:
Room design
Layout and shielding
Siting and use of equipment
Local Rules
Dosimetry
Radiation Protection Supervisor
Member of staff within practice
Responsible for day-to-day supervision and enforcement of rules
Makes sure local rules are followed
Keeps local rules and other paperwork up to date
Understand legal requirements
Ensures radiation doses are kept to a minimum
Manage radiation emergencies
Consults with RPA where necessary
Local Rules
(for x-ray
Code of conduct for performing radiography
Should be in an easily visible place
Should be read and understood by every member of staff involved in radiography
Detail equipment, procedures and access restrictions
List RPA, RPS and any staff involved in radiography
Define controlled areas (in practice and for mobile work)
Includes written arrangements for making radiographs, including restraint, record keeping and protective clothing
Controlled Area
(for x-ray)
Area where there is risk of significant radiographic exposure
Determined by Radiation Protection Advisor
Should be clearly defined with warning signs
Primary beam stopped by 4½ inches of brick (double thickness) or 1mm of lead
Scattered radiation stopped by single brick thickness
Radiation not stopped by wood or glass (lead glass and lead lining may be used in protective doors)
Creating controlled area (for x-rays) in the field
Don’t take radiographs in the stable
Too confined
Cant visualise behind stable wall
Stay in open area/yard with good line of sight in the direction of the primary beam
Work on 20 metre control zone
Based on Inverse Square Law, at that distance, the dose from a single diagnostic radiograph will be negligible
Double the distance reduces the exposure risk 4-fold
Dose Monitoring
Film badges or TLDs (thermoluminescent dosimeters) most commonly used
Must be worn by all staff involved in radiography on a regular basis
Must be regularly checked (usually every 1-3 months, depending on practice)
The badge must be OVER the lead, not underneath it
Worn on the chest/neck area
Film-focal Distance
The closer the x-ray tube to the film or plate, the more “concentrated” the x-ray beam and vice versa
The exposure varies according to the inverse square law
Particularly in-field radiography
Maintain source-image distance (SID) for the radiograph itself
Controlling Scatter
- To reduce scatter produced:
Adequate collimation
Use lowest kV compatible with a diagnostic image - To reduce amount of scatter reaching the plate:
Use of a grid
Functions:
Absorb secondary scattered radiation
Allows primary beam to pass through to form the useful image on the film
Used when x-raying patient/part >10cm thick
Grid factor – when a grid is used, the amount of exposure required increases.
The exposure factors increased is the mAs
- Reduce effect of scatter on personnel
Milliampere-seconds (mAs)
The number of electrons generated at the cathode is determined by the mA (milliamperes) and exposure time
mA relates to the tube current
Milliampere-seconds (mAs) is the product of mA and time in seconds
The mA governs the current applied to the filament and this is applied for a specific time (= sec.)
Increased mA = Increased tube current -> Increased number of electrons ->
Greater number of x-rays are produced
HOWEVER
The energy of the x-rays is unchanged
mA x sec = mAs
mAs is a measure of the number of X-rays produced
the kV (kilovolts)
Potential difference applied across the X-ray tube
Aka The energy of the electrons striking the anode is determined by the kV (kilovolts) applied (sometimes called kVp = kilovolt peak)
Increase kV..
Increased energy of electrons
Increasing kV = Increased electron acceleration Increased energy of electrons =
Greater number of x-rays are produced
AND
X-rays have increased energy = increased penetrating power
Quality (x ray)
penetrating power of the beam
Intensity (xray)
amount of radiation in the beam
mA affects intensity only
3 basic things for Xray production:
Source of electrons (through thermionic emission)
A means of accelerating those electrons (kV)
A means of decelerating the electrons (slamming into the anode)
Attenuation
Reduction in intensity of the X-ray beam as it passes through the matter
Due to absorption or scatter or both!
Absorption
The energy from X-ray photon transferred to atoms of absorber.
As more energy is absorbed, the number of X-rays reaching the film reduces – and therefore affects the appearance of the radiograph!
So tissues are seen on a radiograph in various shades of grey according to how much they absorb.
Interaction of X-rays with tissues
The five basic densities:
Metal – White (all x-rays absorbed)
Bone – nearly white
Soft tissue/Fluid – mid grey
Fat – dark grey
Gas – very dark/black (few x-rays absorbed)
The optimal radiograph
Well positioned
Good collimation, centring
Good definition, no film faults
A wide range of well differentiated shades of grey
This means a balance of kV and mAs to ensure there is enough penetration of the patient with sufficient X-rays passing through
Exposure charts help obtain consistent results!
Pink Camels Collect Extra Large Apples
positioning
centering
collumation
expousure
labling
artifacts
Positioning
Position the area of interest as close as possible to the cassette
Anatomical distortion
Rotation
Standard radiographic positions
Use a reference text for standard views
Described in detail in later lectures and in CS booklets
Centring
Centre the primary beam over the area of interest
Can lead to distortion on the image
Centre in middle of area of interest AND middle of the cassette
Collimation
Scatter contributes to image opacity
And increases radiation hazard
Collimate beam to minimum size necessary
But include enough!
The primary beam should ALWAYS be contained within the area of the cassette
Is it collimated sufficiently?
Safety
Describe the number of unexposed borders seen within the boundary of the film/cassette.
0% 25% 50% 100% for 1,2,3,4 sides seen
Exposure
underexposed- too white
overexposed- too dark
Contrast
Difference between radiographic densities
Seen as shades of grey
Ideal is with extremes of black and white
To improve contrast, must adjust the penetration of the X-ray beam.. How?
… This will change the amount of the x-ray beam absorbed by the tissues and therefore the shades of grey
Labelling
abelling:
Patient details and date
Exposed onto film, digital (embedded)
Side markers – should always be exposed onto the image
Side of body/recumbency (L/R)
Artefacts:
Things that shouldn’t be there!
Sandbags, troughs, driplines, collars!
radiographic quality
Blurring
Magnification
Distortion
Scatter
Good definition?
Any film faults?
Pink Camels..
Blurring
(xray)
Movement
Involuntary e.g. breathing
Voluntary e.g. conscious
How do we overcome this?
Chemical restraint, positioning aids
Magnification/Distortion
(xray)
Primary beam diverges with distance from the tube
Can also lead to geometric distortion if object is positioned obliquely to the beam
Beam intensity
Amount of radiation (number of X-ray photons) in beam
affected by mAs and KV
Beam quality
Beam quality
Penetrating power of beam
affected by KV
Density of the image
Amount of blackening of the image
Affected by mAs and KV (film)
Contrast of the image
The range of shades of grey in the image
Affected by KV (film)
The Ultrasound Machine
(Ultra) Sound Waves
Medium required (liquid, solid, gas) for propagation
Piezoelectric crystals oscillate = sound waves
Reflected differently by different tissue types
Picked up by transducer = image
Piezoelectric crystals – an electric voltage is applied to the crystals which causes them to oscillate which is then transmitted as an ultrasound wave into the body. The wave hits something, bouncing back as an echo. The crystals converts the receiving echo into electricity which is then converted into a real-time image on the screen
The transmitted sound waves pass through the thin layer of skin, but bounce off fluids, tissues and internal organs. These reflected waves are received by the probe, which converts them into electric signals which is the converted into an image
Gain- ultrasound
overall brightness
TGC (Time Gain Compensation)
selectively adjusting the gain at different depths
Near field vs far field
accounts for diffrent layers
Focus zones and position
The pulse of ultrasound can be manipulated to be at its narrowest at a particular depth, the focal position.
Maximise image quality
The focal zone is typically positioned at or just below the object you are evaluating.
like a zoom on a tissue
Depth
“zooms in” in 1cm graduations. Higher the depth, lower the image quality.
Depth = the time it takes for the echo to return from the organ
Frequency
- image resolution at the level of the object being evaluated.
highest frequency for a superficial object (in the near field).
lowest frequency for a deeper object
Higher frequency (ultrasound)
decreased penetration but with increased resolution
lower frequency (ultrasound)
Lower frequency = better penetration with decreased resolution
Echogenicity
Echogenicity is a measure of acoustic reflectance, i.e. the ability of a tissue to reflect an ultrasound wave.
Or “how many echoes are bounced back”
The source of echogenicity is impedance mismatching between tissues
Hyperechoic
= tissues that produce strong echoes
Fat, bone, stones, air
Bright/white as ultrasound is reflected
Hypoechoic
tissues that produce few echoes
Soft tissue, muscle
Grey as some ultrasound passes through the tissue, some is reflected
Anechoic
structures that produce no echoes
Fluid
Dark as no ultrasound waves are reflected
Reverberation echo:
Produced by a pulse bouncing back and forth between two interfaces
Transducer:Tissue or tissue:tissue
More likely to occur from highly reflective surfaces like gas and bone
Homogenous
uniform
Heterogenous
non-uniform
Shadowing
Complete reflection of the sound beam
Zone deep to structure will be anechoic
Bone, gas, calculi
Mirror Image
A strongly reflective, obliquely orientated surface may reflect the sound beam distally instead of returning it to the transducer
Takes longer for the sound waves to return, the image will appear deeper to the structure it is reflecting
drug volume=
(weight x dosage)/ drug concentration
drug dosage=
(mg/kg) /weight
Flow rate =
Volume (ml) / Time (hours) Drop Rate
Total Body (Blood) Clearance
the volume of blood plasma cleared of parent drug per time unit
or
a constant relating to the rate of elimination to the blood/plasma concentration
Bioavailability
how much of the drug taken orally that actually gets to the blood plasma
one compartment model
body is seen as one single compartment
two compartment model
bosy is seen as teo compartments
vessel rich group and then to other tissues in the brain heart and kidneys
vessel rich group
Lung, brain, heart, and major organs (liver, kidney) have a relatively high blood flow (vessel-rich group [VRG]) compared with muscle and fat and are more susceptible to anesthetic drug-related effects
theraputic window
the plasma concentration at which the drug is effective
Tmax
the point on the curve where the drug is most active in the body
Constant rate infusions
a loading dose is given and then a low, constant rate of the drug i given to keep within theraputic window
multiple dosing
giving multiple dosing to keep drug level in theraputic range
can lead to overdose
loading dose
A loading dose is an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower maintenance dose
A loading dose is most useful for drugs that are eliminated from the body relatively slowly, i.e. have a long systemic half-life
Without an initial higher dose, it would take a long time for the concentration of these drugs to reach therapeutic levels
Examples include ketamine and fentanyl
what type of biological molecules can drugs interact with
most often proteins
e.g
Enzymes (e.g. ACE inhibitors, aspirin, neostigmine)
Carrier Molecules (e.g. flavonoid – Pgp antagonist, digoxin)
Ion channels (e.g. verapamil - L-type calcium channel antagonist)
Receptors (e.g. benzodiazepine – GABA receptor agonist, adrenoceptor agonists and antagonists )
Structural proteins (e.g. Taxol – Tubulin “agonist”)
DNA (e.g. anti cancer agents like Doxorubicin) (dont need to memorise)
Lipophilicity (Hydrophobicity)
drugs that are hydrophobic may stay in cell membrane and dissrupt cell membrane
this is how inhaled anathetic drugs have a CNS effect
vey lipid soluble molecules take only low doses to produce an anethetic effect
receptors
Protein molecules whose function is to recognise and respond to endogenous chemical signals.
– Chemicals which mimic the endogenous signals (i.e. drugs) will also elicit an effect. Drugs need to bind to receptors with high affinity and high specificity However…drugs generally lack complete specificity
Dose response curves
how do we know a drug is doing what we want
shaped graphs x axis= concentration y axix= effect of drug
shows at a low does there is little effect
rapid increase in the theraputic window
platues at high does- this could be where you see side effects
Potency
amount of drug required to produce 50% of its maximal effects.
Used to compare drugs within a chemical class (usually expressed in milligrams/kg). Example: if 5 mg/kg of drug A relieves pain as effectively as 10 mg/kg of drug B, drug A is twice as potent as drug B.
Efficacy
the maximum therapeutic response that a drug can produce (example: morphine vs buprenorphine)
the tendency of a drug to activate the receptor once bound
Agonism
an agonist produces a responce in a receptor
a full agonist
If the activation is 100%, namely each time a drug interacts with its
target there is a response then the agonist is said to be a “full agonist”
If the activation is <100%, the agonist is said “partial agonist”. Partial
agonists have lower efficacy than full agonists – even with maximal occupancy of receptors.
An agonist has affinity and efficacy – therefore elicits a biological response
Affinity
the tendency of a drug to bind to the receptor
Antagonism
Antagonist: molecule/drug that binds a receptor without activation
Antagonist have affinity but zero efficacy (as they block the target activity)
Main types of antagonism:
• Competitive
• Non-competitive
• Irreversible
competative antagonists
Competitive agonists compete with agonists for the receptor binding site.
The chemical structure of the agonist and competitive antagonist are often similar (lock and key hypothesis).
Antagonist binds to receptor in such a way as to prevent agonist binding
Competitive antagonism is surmountable – additional agonist can overcome the receptor blockade.
Addition of a competitive antagonist shifts the dose response curve of the agonist to the right (e.g. methadone/naloxone)- more drug will have to be given to overcome the block
decrece potency but not efficacy
Non-competitive Antagonism
Non-competitive antagonists either bind to a different receptor site, blocking the desired receptor
OR
Block the chain of events “post” binding - acting “downstream” of the receptor.
ketamine is an example of this
decrese potency and efficacy
Irreversible Antagonism
Antagonist dissociates from the receptor only very slowly or not at all.
The antagonist forms covalent bonds with the receptor.
Irreversible antagonism is insurmountable – additional agonist cannot overcome the receptor blockade.
Often used in drug discovery, rarely in practice – risky
asprin and omeprozol, anticancer drugs
Inverse agonism
drug that reduces the activation of a receptor with constitutive activity (example: GABAA receptor)- these receptors fire without stimulation
Can be regarded as drugs with negative efficacy.
Therapeutic index =
toxic dose (or LD50) ÷ effective dose (or ED50)
EC50: Effective concentration. The dose required for an individual to experience 50% of the maximal effect.
ED50: Effective dose. The dose for 50% of the population to obtain the therapeutic effect
EC50:
Effective concentration. The dose required for an individual to experience 50% of the maximal effect.
ED50:
Effective dose. The dose for 50% of the population to obtain the therapeutic effect.
Would an ideal drug have a small or large therapeutic index?
large!
ideally you want a large toxic dose and small effective dose
Drug receptor types
Ion channel cell surface transmembrane receptor- things tha topen up to let ions in and out of cells to change polarity and make them less or more likley to fire- drugs can open and close these channels
Ligand regulated enzyme- brings molecules toghther to form active catalitic domain
G-protein coupled receptors
Protein synthesis regulating receptor- can upregulate or decrease. acth stimulation test
Tachyphylaxis (“rapid protection”).
Reduction in drug tolerance which develops after a short period of repeated dosing. Not common. Often due to a lack of a co-factor. the bosy runs out of the effect the drug asks it to produce
happens in mainly IV drugs- addrenaline
not self antagonism
Self-Antagonism
When a drug becomes antagonistic to its own effects
Loss of target sensitivity
Change in receptors- become resistant to drug stimulation/conformational changes
Loss of receptors - endocytosis
Exhaustion of mediators- degradation/low re-expression level
Increased metabolic degradation- higher concentration of drugs are needed
Physiological adaptation- crosstalk between body systems, one takes over
Drug transporters- drug removed from receptor sites
Drug-drug interactions
Potential outcomes of drug-drug interactions:
• Action of one or more drugs is ENHANCED
• Development of totally NEW EFFECTS
• INHIBITORY effects on one drug on the other
• NO CHANGE
ligand regulated enzyme
the binding of an extracellular ligand causes enzymatic activity on the intracellular side
G-protein coupled receptors
integral membrane proteins that are used by cells to convert extracellular signals into intracellular responses
activated by agonists
When a ligand binds to the GPCR it causes a conformational change in the GPCR, which allows it to act as a guanine nucleotide exchange factor (GEF). The GPCR can then activate an associated G protein by exchanging the GDP bound to the G protein for a GTP. The G protein’s α subunit, together with the bound GTP, can then dissociate from the β and γ subunits to further affect intracellular signaling proteins or target functional proteins directly depending on the α subunit type
GPCRs are an important drug target
CRI
constant rate infusion
the use of low levels of agents to maintain theraputic dose
CD
controlled drug
TIVA
total intravenous anaesthesia
PO/SC/IM/IV are all …
dosing routes
describe the diffrent sites analgesia may act on
They may act at the site of injury and decrease the pain associated with an inflammatory reaction (e.g. NSAIDs)
They may alter nerve conduction (e.g. local anaesthetics)
They may modify transmission in the dorsal horn (e.g. opioids & some antidepressants)
They may affect the central component and the emotional aspects of pain (e.g. opioids & antidepressants)
Opioids
Natural (opiate) and synthetic (opioid) drugs
Endogenous opiates
Opioid receptors identified; mu(most important), delta, kappa (important in birds), nociceptin
Effect depends on dose, route, species, stimulus etc
CVS effects, pruritis, urinary retention, ileus, pancreatic duct, temperature, miosis, mydraisis, vomiting & nausea, mania & respiratory depression?- MOSTLY IN PEOPLE, side effects limited in vet species
decrease the likly hood that pain signals will be firesd at primary and secondary neurons- work a t a numebr of sites
Morphine
The most efficacious opioid at relieving pain
It is a full agonist at mu, delta and kappa receptors
Not licensed. (CD II)
Nevertheless still used widely
CRIs and epidurals plus horses
Methadone
opiate
A synthetic mu agonist (full) & affinity for NMDA receptor
Has effects as a norepinephrine and serotonin reuptake inhibitor
Following IV - duration of action is approximately 4 hours (can be longer with sc)
Vomiting – not usually
Use as premed, for sedation, intra op (v slow IV), on recovery, and as CRI
Poor oral availability
Licensed for dogs and cats. CD II
Pethidine (Meperidine)
Synthetic agonist at the mu receptor
Also shown to block sodium channels
Agonist at alpha 2 B subtypes
Negative inotropic effects but tends to increase heart rate
NOT IV- Can induce histamine release, im only
Pethidine should not be administered to dogs receiving selegiline
Monoamine oxidase inhibitor + pethidine ≡ serotonin syndrome
CD II (licensed for dogs, cats, horses)
Spasmodic colic
DOA (duration of action) ≈ 90 minutes- short acting
Fentanyl
Fentanyl is a highly lipid soluble short acting mu opioid agonist. CD II
Uses:
Intraoperatively as bolus, with peak analgesic effects occurring in 3-5 minutes
At induction with a benzodiazepine
For compromised patients, fentanyl + benzodiazepine may be sufficient for intubation
CRIs are very effective
Transdermal fentanyl patches
Respiration slows or may cease following a bolus
Bradycardia can be significant
Fentanyl ‘spot on’ licensed for dogs (Recuvyra)
Codeine
has been used in dogs (often with paracetamol) for mild to moderate pain (post op) but…..
Oxycodone
has also been advocated for use in dogs (post op), but little information is currently available
Naloxone
for antagonism of pure mu opioids
Tramadol
Tramadol is popular! But there is a lack of data in dogs, better in cats
It is commonly prescribed to humans – now licensed in dogs
It is a synthetic analogue of codeine; it is a low potency mu selective partial agonist PRODRUG with LIMITED metabolism in dogs
It has an alpha 2 adrenergic effect and inhibits 5HT reuptake
CDIII
Very limited value in dogs but useful in cats
Buprenorphine
a partial agonist with a strong affinity for mu receptors (mild kappa antagonist)
Highly potent but not as efficacious as pure opioids
Peak effect IV admin 45-60mins- long wait time
Mild to moderate pain, good sedation, long duration of action, preservative in multi dose vials
Licensed for dogs and cats and horses
OTM route works v well (cats>dogs)
- Better than butorphanol for analgesia but as it is a partial agonist you cannot increase the effect by giving more- occupies and blocks the receptors for about 6 hours
Allows patients a night sleep and is good for mild to moderate pain
OTM route
oral trans mucosal
Butorphanol
Only mixed one!
is a kappa opioid agonist and mu antagonist (short-medium duration)
Its actions differ to that of the other opioids
Available as oral form (Torbutrol)
Useful in combination with acepromazine for sedation e.g. cardiac patients
Licensed for dogs, cats & horses
Antitussive- suppresses cough
LIMITED ANALGESIA- Blocks mu receptors for up to 6 hours! But only 10 mins of analgesia and prevents use of other opiod analgesis
Alfentanil, sufentanil and remifentanil
can be used during anaesthesia to blunt sympathetic stimulation
All have context sensitive half lives shorter than fentanyl
Remifentanil is metabolized by plasma esterases
Remifentanil always given by CRI
Given as low dose (for analgesia) or higher doses as part of TIVA
MAC reduction of these opioids has been shown in dogs and cats
None licensed for dogs and cats
Local Anaesthetic (LA) Agents
block the sodium channels in nerve fibers, blocking transmission
the unionised local anethetic enters cell, becomes ionised and is then able to block the sodium channel
it can also affect eh membrane directly
LAs are weak bases and largely ionised at physiological pH. - Problem in inflamed tissue
Their speed of onset is inversely related to their degree of ionization. -Longer to start working in inflamed tissue
Their duration of effect is directly related to their degree of protein-binding.
Their potency is related to their lipid solubility.
Lidocaine
Prilocaine (+lidocaine)
Bupivicaine
Mepivicaine
Ropivicaine
Etidocaine
Amethocaine
Proparacaine
Cocaine
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
Inhibit prostaglandin production by interfering with cyclo-oxygenase (COX)- COX 1, 2
Now thought also to have a spinal action
Synergistic with other drugs
iv, im, sc, po
non sterodials vlock the production of cyclooxygenase and therfore the production of PGG2- steriods also act earlier of this pathway so they should not be used toghter- gastric ulcration
Some licensed for pre-operative use
Carprofen and meloxicam have revolutionized perioperative pain management in UK in last 3 decades
Traditional NSAIDs are contraindicated in patients with:
Renal or hepatic insufficiency
Hypovolaemia
Congestive heart failure & pulmonary disease
Coagulopathies, active haemorrhage
Spinal injuries
Gastric ulceration
Concurrent use of steroids
Shock, trauma (esp head trauma)
Pregnancy
COX 1
NSAI block the production of this enzyme
Prostaglandin (PG) synthesis attributable to COX 1 along length of GIT
PGs play a role in regulating renal blood flow, reducing vascular resistance & enhance organ perfusion
COX 1 is found in neurones and in the foetus, amniotic & uterine tissue
Blood platelets contain COX 1
Cox 1 = ‘housekeeping’?
BUT
Earlier NSAIDS also inhibit COX1
COX 2
NSAIDs with a more favourable GIT profile were being sought before COX 2 was discovered
When COX 2 was discovered in 1991 it was shown that 3 drugs (carprofen, etodolac & meloxicam) with an enhanced GIT protective profile inhibited COX 2
Then assumed that COX 2 selective NSAIDs were the answer…
This has not been shown to hold true
Deracoxib & firocoxib – problems in humans, not all coxibs have problems!
COX 2 induction in heliobacter pylori gastritis, IBD & bacterial infections
Therefore COX 2 inhibition may exacerbate the situation…
Supported by transgenic studies
COX 2 may have a role in GI defence
In summary do not equate COX 2/COX 1 inhibition ratios to overall in vivo safety!
Licensed NSAIDs for horses
Phenylbutazone
Suxibuzone
Firocoxib
Meloxicam
Flunixin meglumine
Vedaprofen
Carprofen
Grapiprant (Galliprant)
New class of piprant NSAIDs- Non-cyclooxygenase inhibiting non-steroidal anti-inflammatory drug- blocks EP4 further down in pathway instead
Licenced for treatment of mild to moderate osteoarthritis pain and inflammation in dogs
Has been called ‘next step’ when ‘traditional’ NSAIDs are not tolerated
Approved for use in dogs from 9 months of age and favourable safety profile
Once daily administration (chewable tablet) – 2mg/kg
Adverse events include vomiting, diarrhoea, decreased appetite and tiredness.
Often dogs will adjust but washout between NSAIDs essential
Not for use in cats
What is paracetamol?
Paracetamol: 10-15 mg/kg PO two to three times daily. Is it a NSAID?
Analgesic & antipyretic
Mechanism of action unknown!
Thought to inhibit COX-3(??) but recent data suggest there may be another site
Alpha-2 Adrenoceptor Agonists
good sedatives
between opiates and nonsteriodals
Bind to alpha 2 receptors
Receptors widespread
Drugs have other actions (sedation, ↓HR etc)
Systemic, epidural, peripherally
Synergism with LA’s
Dogs/cats
Medetomidine (45 minutes)
Dexmedetomidine (45 minutes)
Horses
Xylazine (30 minutes)
Detomidine (45 minutes)
Romifidine (60-70 minutes)
Cattle
Xylazine
Detomidine
Very useful drugs
Sedative action
Analgesic (& reduce MAC)
Compatible with other drugs & potential to antagonise (atipamezole),
IV, IM, epidurally, buccally (detomidine)
Small volume
Alpha 2 receptors:
3 subtypes (4) A,B,C
Diverse sites: CNS & PNS
Side effects-
Hyper (B) then normo/hypotension (A)
Decreased CO & HR, increased SVR
Respiratory depression
Increased urine production
Decreased GI motility
Decreased surgical stress response
Hyperglycaemia, GH enhanced
Thermoregulation affected
Sweating
NMDA Antagonists
Ketamine
As induction agents
As analgesics peri op
Ketamine for fractious cats (sprayed in mouth)
Very versatile
Will improve the patient’s post op comfort
Ketamine
It has been shown that at low doses ketamine can prevent the ’wind up’ and sensitisation of dorsal horn cells
0.5mg/kg after induction
Can be used in the pre-med
CRI e.g. Add 60mg ketamine to 1L LRS and administer at 10ml/kg/hr to dogs intra op (10mcg/kg/min)
NMDA Antagonists
As induction agents
As analgesics peri op
Ketamine for fractious cats (sprayed in mouth)
Very versatile
Will improve the patient’s post op comfort
Premed combinations
Acepromazine + opioid
Alpha 2 agonist + opioid or BZD or ketamine
BZD + Ket
Opioid + BZD
Alpha 2 + BZD + opioid
Post operative period in regards to anelgesic drugs
How long should we provide analgesia for?
24-72 hours for routine ops
Involve the owner
Rescue analgesia (what is yours?)
What options do we have available?
NSAIDs (daily, oed, monthly)
Opioids (patch, long acting formulations, oral forms (tramadol, morphine, OTM buprenorphine)
LA blocks
Adjuncts for chronic pain (amantadine, gabapentin etc)
side effects of antibiotics
Direct toxicity – aminoglycosides
Drug interactions – sulphonamides and alpha-2 agonists
May reduce normal protection – gut flora
May cause tissue site necrosis (tetracyclines)
Chloramphenicol has been shown to cause a reduced immune response
Some can cause reduced metabolism
Potential residues in food producing animals
RESISTANCE
Hypersensitivity
Anaphylactoid reactions
What Influences Success of antibiotics
Bacterial susceptibility
Pharmacokinetics and tissue penetration
Most tissues – concentration is perfusion limited
Free drug concentration in plasma is related to, or equal to that in tissue
In some tissues – concentration is permeability limited where non inflamed
CNS
Eye
Lung
Prostate
Mammary gland
Local factors
Abscess - pus - necrosis – inactivates aminoglycosides and sulphonamides
Foreign material – bacterial glycocalix
Slowed bacterial growth – less susceptible to cephalosporins and penicillins
Low pH/low oxygen – erythromycin, fluoroquinolones
Haemoglobin - penicillins
Wound cleansing and drainage
Compliance
Factors Affecting Choice of antibiotic
Presence of infection (Gram stain culture and sensitivity)
Spectrum
Habitual reliance on broad spectrum indicates low standard of diagnosis
Bacteriocidal versus bacteriostatic
Cost
Toxicity
Concurrent disease
Pregnancy
Habit…..!
Dosage and frequency
Route
Duration and re-evaluation
Acute versus chronic infection
Immunocompromise
Septic arthritis
Osteomyelitis
Combination therapy
Not bacteriostat + bacteriocide
Peptidoglycan is unique to bacteria, making it ….
good antibiotic target
Amoxicillin-clavulanate
Penicillin based – -lactamase inhibitor
Staphs, streps
Gram negatives
Escherichia and Klebsiella spp variable
Pseudomonas enterobacter resistant
Lincosamides
Penicillin based – -lactamase inhibitor
Usually bacteriostatic
GI irritation –do not use in horse except foals, never in rabbits
Basic drugs – ion trapping in milk
Fluoroquinolones
Penicillin based – -lactamase inhibitor
Reserve for serious gram-negative systemic infections
Do not use routinely and non-selectively
If used, use the correct dose!
Potentiated sulphonamides
Penicillin based – -lactamase inhibitor
Old but useful – resistance growing
Aminoglycosides
Penicillin based – -lactamase inhibitor
Gentamicin – gram-negative aerobes
Adjuncts
Probiotics?
Anti-tetanus toxin
Foaming agents –foot rot
prophylactic use of antibiotics
Not indicated for routine, clean surgery where no inflammation is present, GI system not invaded and aseptic technique has not been broken
But do use for:
Dental procedures
Leukopenia
Contaminated surgery
Where infection would be disastrous – orthopaedic
Administer before procedure and within 3-5 hours of contamination
Slow IV
Appropriate to contaminating pathogen
licensed antifungals
Ketoconazole Fungiconazol 200 mg tablets for dogs – dermatphytosis. Used off licence for systemic infections.
Itraconazole oral solution for cats and birds, e.g. Itrafungol 10 mg/ml Oral Solution (treats M. Canis). Used off licence for systemic infections.
Miconazole. In various shampoos and ear drop preparations.
Nystatin ear drops - Canaural
Terbinafine – in various ear drops for dogs
Clotrimazole- in various ear drops for dogs
Enilconazole. Imaverole Concentrate for Cutaneous Emulsion – cattle, horses and dogs vs dermatophytosis
Bovilis® Ringvac MSD Animal Health UK Limited vaccination for cattle
unlicnened antifunglas
Amphotericin b
Climbazole
Fluconazole
Silver sulfadiazine
Tiabendazole
treatment of ringworm
Clipping of the hair coat, especially small animals, removes infected hairs, stimulates new hair growth and hastens recovery
Systemic ketoconazole (dogs), itraconazole (cats) plus a topical treatment (e.g. miconazole)
Treatment with ketoconazole suppresses testosterone concentrations and increases progesterone concentrations and may affect breeding effectiveness in male dogs during and for some weeks after treatment
Treatment of dermatophytosis should not be limited to treatment of the infected animal(s)
Measures to prevent introduction of M.canis into groups of cats may include isolation of new cats, isolation of cats returning from shows or breeding, exclusion of visitors and periodic monitoring by Wood’s lamp or by culturing for M.canis
Bovilis® Ringvac reduces clinical signs of ringworm caused by Trichophyton verrucosum (prophylactic dose) and shortens the recovery time of infected cattle showing clinical signs of ringworm (therapeutic dose)
Initially the whole herd should be vaccinated (two vaccinations 10-14 days apart).
Subsequently, (closed herds) only young calves require revaccination at around 2 weeks of age, followed by a second injection 10-14 days later. New animals should receive a full vaccination course. No subsequent doses are required.
Can be used during pregnancy (?lactation).
Administration is by intramuscular injection.
Aspergillosis treatment
First line treatment = topical clotrimazole formulated in a polyethylene glycol base
Indwelling tubes trephined into the frontal sinuses or via the nares as a single infusion.
The infused solution is left in place for 1 hr, during which the dog’s position is changed periodically
~80% success rate
Also reports of enilconazole (bid for 7–14 days), via tubes implanted surgically into the frontal sinuses
Systemic treatments of ketoconazole, itraconazole, fluconazole, voriconazole, and Posaconazole reported
In horses, surgical exposure and curettage have been used for guttural pouch mycosis.
Topical natamycin and oral potassium iodide have been reported effective
Itraconazole (3 mg/kg, bid for 84–120 days) has been reported effective in Aspergillus rhinitis in horses
aspergiliosis diagnosis
Imaging (radiographs/CT) of the nasal cavity can show turbinate tissue destruction
Visualization of fungal plaques by rhinoscopy together with serologic and either mycologic or radiographic evidence of disease is gold standard .
Culture result alone is not appropriate (ubiquitous and can be isolated from the nasal cavities of healthy patients)
Systemic disease is usually diagnosed by culture of the organism, often from urine
Two pharmacological approaches to viral control
effective vaccines or antiviral therapy
licensed Antiviral agents
One licensed agent
Virbagen Omega
Contains recombinant omega interferon of feline origin
For cats (sc) and dogs (iv)
Licenced for treatment of canine parvovirus, feline leukaemia virus (FeLV), and feline immunodeficiency virus (FIV)
Interferons increase the cell’s resistance to a virus
unlicenced antiviral agents
Aciclovir
Famciclovir
Ganciclovir
Lamivudine
Zidovudine
Oseltamivir for treatment of viral diseases in dogs (parvovirus and parainfluenza) has also been reported
Biochemistry/haematology/serology of FIP
Hypergammaglobulinaemia; raised bilirubin without liver enzymes being raised, lymphopenia; non-regenerative anaemia, high antibody titre to FCoV
FIP treatment
Feline interferon omega (Virbagen Omega) or human interferon alfa-2b have been used – limited success
Stimulate body’s response
Immunosuppressive and anti-inflammatory drugs reduce inflammation. Commonest immunosuppressive drug used in FIP is prednisolone (corticosteroid) but no placebo-controlled trials showing prednisolone to be better than other anti-inflammatories
GS-441524 is a nucleoside analogue
Two published studies from UC Davis in 2018 and 2019. Results were 100% (10/10) recovery rate reported in experimentally infected cats and 84% (25/31) recovery rate in naturally infected cats. Of the recovered cats, owners reported that they returned to “near normal” within two weeks of treatment
The 2019 study proposed the optimized treatment protocol for GS-441624 use as 4.0 mg/kg given as a subcutaneous injection once daily for at least 12 weeks
can only buy it for research currently
Equine vaccines
Routinely equine flu, tetanus, equine herpes virus, equine rotavirus and now strangles
Following 2019 equine flu outbreak in the UK some governing bodies moved from annual to six-monthly requirements
All vaccination records should be kept up to date in the horse’s passport document
Up-to-date vaccination record is a requirement of many sporting governing bodies for horses competing under their rules
Cattle vaccines – what’s available?
Bovine viral diarrhoea
Very common disease in the UK. About 60% of cattle in the EU test positive for exposure to the BVD virus. Timings for all BVD vaccines are to aim for full protection to occur at least two to three weeks prior to service.
Infectious bovine rhinotracheitis
Live and inactivated vaccines are available. Live vaccines have rapid onset of immunity and are of use in the face of an outbreak to reduce clinical signs and improve the immunity quickly but inactivated vaccines appear to be better at producing longer-term immunity
Leptospirosis
Two vaccines are available in the UK for leptospirosis control. In both cases a primary course of two doses four to six weeks apart, followed up with annual boosters, is preferably given in the spring before the period of highest risk.
Calf enteric disease – rotavirus, coronavirus and Escherichia coli
A number of vaccines are available for immunising pregnant cows and heifers to raise antibodies to rotavirus, coronavirus and Escherichia coli. After birth, the calves gain protection in their gut from drinking the colostrum and milk that is fortified with these antibodies.
Some minor differences exist in the timing of the various vaccines.
Pneumonia vaccines
Calf pneumonia vaccines are available for infectious bovine rhinotracheitis, parainfluenza type three, bovine respiratory syncitial virus, Pasteurella, Mannheimia haemolytica and Histophillus somni, and many combinations are available depending on what protection is needed.
It is important to identify the common diseases present and the age calves become infected
Lungworm
The only lungworm vaccine available uses irradiated live lungworm larvae that create an immune response from the animal, but the larvae do not continue to reproduce, so do not cause clinical disease. The vaccine is a two-dose programme given approximately four weeks apart to youngstock at the beginning of their first grazing season. The second dose should be given at least two weeks before turnout, and vaccinated and unvaccinated stock should not be mixed for at least two weeks after the second dose has been given.
It is preferable for calves to be exposed to low levels of lungworm larvae throughout the grazing season to stimulate and maintain this immunity. If the worming protocol on the farm is too effective, there may be small exposure of the calves to lungworm, allowing very little natural immunity to build up, and this leads to insufficient long-term immunity in adult cattle, which can develop the disease in subsequent grazing years.
Clostridial diseases
Vaccinations against clostridial diseases are routinely given to sheep, but the uptake is much less in the cattle sector. A number of products exist on the market.
Ringworm
Mastitis
STARTVac, covers the main mastitis causing pathogens, E coli, Coliforms, Staph aureus and Coagulase-Negative Staphylococci (CNS), but does not protect against Strep uberis. It involves a complicated programme and is quite expensive
Salmonella
In the face of a Salmonella outbreak on farm, a fluid vaccine can be used to improve immunity to S. enterica serovar Dublin and S enterica serovar Typhimurium
Bluetongue
Not routinely used in UK but two vaccinations are available
Pig vaccines – what’s available?
Porcine parvovirus
Porcine reproductive and respiratory syndrome
E.coli
Clostridia
Erysipelas
Mycoplasma hyopneumoniae
Lawsonia intracellularis
Atrophic rhinitis
Glasser’s Disease
Aujeszky’s Disease
Salmonella typhimurium
Also relatively new intramuscular vaccine to control ileitis in pigs
The bacterial disease is present on most pig farms in the UK and causes widespread digestive health problems
There are often no visible signs of ill health, but an infection with the bacterium Lawsonia intracellularis can lead to poor feed conversion ratios (FCR) and reduced growth rates
More serious infection levels also cause diarrhoea and result in increased herd mortality rates.
Sheep vaccines – what’s available?
Vaccines available in the UK for sheep
Clostridial diseases, e.g. lamb dysentery, pulpy kidney, tetanus, braxy, blackleg
Pasteurellosis
Ovine abortion, e.g. toxoplasmosis and enzootic abortion
Louping ill
Contagious pustular dermatitis (Orf)
Footrot
Dog Core vaccines in the UK
Canine Distemper Virus (D)
Canine Adenovirus/Infectious Canine Hepatitis (H)
Canine Parvovirus (P)
Leptospirosis (L). Please be advised that vaccines are multivalent; preparations are available containing different Leptospira strains.
Core vaccines
protect animals from severe, life-threatening diseases that have global distribution and which ALL dogs and cats, regardless of circumstances or geographical location, should receive. Non-core vaccinations protect from disease where the animal’s geographical location, lifestyle or environment puts them at risk, e.g. rabies vaccination before overseas travel. (
Dog non-core vaccines in the UK
Bordetella bronchiseptica +/- Canine parainfluenza virus (“Kennel Cough” vaccine): vaccination should be considered for dogs before kennelling or other situations in which they mix with other dogs (e.g. dog shows, training classes)
Rabies: legal requirement for dogs travelling abroad / returning to the UK
Canine Herpes Virus: for breeding bitches
Leishmaniasis: before travelling to endemic areas
Borrelia burgdorferi (Lyme disease): for dogs at high risk of exposure
Cat core vaccines in the UK
Feline enteritis (feline parvovirus) (P)
Cat flu (feline calicivirus (C) and herpes virus (H)
Cat non–core vaccines in the UK
Feline leukaemia vaccine (FeLV) (this may be considered a core vaccine for all cats that go outdoors or are in contact with cats which go outdoors).
Chlamydophila felis (Chlamydia)
Rabies: legal requirement for cats travelling abroad / returning to the UK
Bordetella bronchiseptica
Rabbit vaccines
Myxomatosis
Two forms of Rabbit Viral Haemorrhagic Disease (RHD) caused by RHDV-1 and RHDV-2 strains where local risks and individual veterinary advice indicate the need
ferret vaccines
Rabies: legal requirement for ferrets travelling abroad / returning to the UK
Distemper: No vaccine currently licensed for use in ferrets in the UK, some owners ask for canine distemper vaccines in discussion with their vet
what is the mode of action and target of penicillin
inhibits cells wall synthesis
gram postitive bacteria
what is the mode of action and target of ampicillin
inhyibits cell wall syntheisis
broad spectrum
what is the mode of action and target of Bacitracin
inhibits cell wall syntheisis
gram positive bacteria (applied as skin ointment)
what is the mode of action and target of cephalosporin
inhibits cell wall syntheisis
gram positive bacteria
what is the mode of action and target of tetracycline
inhibits protien synthesis
broad spectrum
has wide spread, plasmid mediated imunity
what is the mode of action and target of streptomycin
inhibits protien synthesis
gram neg
tuberculosis
what is the mode of action and target of sulfa drug
inhibits cell motabolism
bacterial meningitis
urinary tract infections
what is the mode of action and target of rifampicin
inhibits RNA synthesis
gram positive bacteria
gram negative bacteria
what is the mode of action and target of quinolones
inhibits DNA synthesis
urinary tract infections
what is the mode of action of polyenes
(amphotericin, B Nystatin)
interacts with sterols in cell membrane to cause cellular leak
what is the mode of action of antibiotics (against antifungals)
griseofulvin
inhibits mitosis (via the microtubules)
what is the mode of action of azoles
fluconazole
itraconazole
ketoconazole ect
inhibits ergosterol synthesis (inhibits cell membrane)
what is the mode of action of allylamines
terbinafine
inhibits ergosterol (cell membrane)
what is the mode of action of thicocarbamate
tolnaftate
inhibits ergostero (cell membrane)
what is the mode of action and target of antimetabolite
flucytosine
inhibits dna and rna synthesis
what is the mode of action and target of profens
flurbiprofen
ibuprophen
directly damages the fungal cytoplasmic membrane
what are the components of a surgical theatre
Surgical environment should have several distinct areas:
Changing area
Surgical prep/induction
Scrub area
Operating theatre
Recovery
Utility
Skin disinfectants
Chlorhexidine 2% with or without 70% isopropyl alcohol
Not suitable for broken skin, wounds, mucous membranes
Povidone iodine 7.5%
Suitable for contact with mucous membranes
Non-povidone iodine (alcohol free)
For use with ocular surgery
Equally effective at reducing bacterial counts
Chlorhexidine has greatest residual action
what class of antibiotis inhibit cell wall synthesis
penicillin
ampicillin
bacitracin
cephalosporin
what class of antibiotis inhibit protein synthesis
tetracyclin
streptomycin
what class of antibiotis inhibit cell metabolism
sulfa drug
what class of antibiotis inhibit RNA synthesis
rifampicin
what class of antibiotis inhibit DNA synthesis
Quinolones
comon bacterial agents of Bite wounds, trauma and contaminated wounds
Staphylococcus spp, Streptococcus spp, Pasteurella spp, anaerobes
comon bacterial agents of Osteomyelitis
Staphylococcus spp, Streptococcus spp, Proteus, Pseudomonas (cat/dog), anaerobes
Septic arthritis
Staphylococcus spp, Streptococcus spp, coliforms
What is General Anaesthesia?
Controlled, reversible depression of the CNS so as to produce lack of awareness of painful inputs (nociception)
Minimal depression of hind brain functions – cardiovascular centres
What is Local Anaesthesia/analgesia?
Local anaesthesia (local analgesia) – not aiming for CNS depression
what are the components of the anethetic triad
unconciousness
muscle relaxation
analgesia
one drug does not do all of these therefore we need a cocktail
The less anaesthetic you give…
…the better for the patient’s physiology
Less cell and organ damage
Quicker recoveries
Quicker return to normal appetite
Better functioning immune systems
Balanced Anaesthesia
Using multiple drugs to minimise the dose and the side-effects of any one of them
Results in lower doses of potent anaestheticsless CNS depression
Better achievement of the goal of anaesthesia
Hypnosis
artificially induced sleep
analgesia
Anti-nociception
Muscle relaxation
From the same agent producing hypnosis or
From a centrally acting muscle relaxant - diazepam or
From a specific neuromuscular junction blocking agent - curare
modern stages of anesthesia
Conscious
Anaesthetised
Dead
Unconsciousness is an all or nothing thing
Level of CNS depression
Specific signs related to muscle relaxation
Signs related to brain stem depression
Respiratory rate
Heart rate
Blood pressure
Minimising anesthesia risk
Support
Oxygen
Fluids
Warmth
Monitoring
During anaesthesia
Recovery
Anaesthesia record sheet
Legal record
The trained anaesthetist
Tranquilisation
relief of anxiety
Sedation –
central depression, drowsiness
Narcosis
drug induced sleep produced by narcotics - opium like drugs
Dissociative anaesthesia
induced by drugs such as ketamine that dissociate the thalamo-cortical and limbic systems
The Anaesthetic Process
IDENTICAL for all species
History and examination
The anaesthetic plan
Place iv cannula
Premedicate, allow to settle
Induce anaesthesia – injectable agent
Once intubated do ABC
AIRWAY, BREATHING, CIRCULATION
Connect to anaesthetic machine and supply volatile anaesthetic in oxygen (or us total injectable with top ups)
Alter inspired concentration in response to physical signs
Supply analgesia separately
Recover following anaesthesia
Continue to monitor until patient comfortable/discharged
Why are combinations of agents used for anesthesia?
One agent could be used to induce and produce all 3 desired effects of the triad (unable to perceive painful stimuli, relaxed muscles, unconsciousness) but with massive physiological depression
Eg isoflurane, sevoflurane
But usually injectable agents are used in combination
“Balanced anaesthesia”
E.g. ketamine: if used alone, poor muscle relaxation
Add medetomidine: improved analgesia and muscle relaxation
Why is Airway Management Important?
Allows delivery of oxygen and inhaled anaesthetic gas
Most anaesthetics cause respiratory depression
Loss of airway reflexes = prone to airway obstruction
Brachycephalics obstruct
All the above cause hypoxia- high mortality
Allows scavenging and environmental protection
Allows intermittent positive pressure ventilation (IPPV)
Allows ventilator support in ICU setting
‘Protects the airway’
Under normal anaesthesia
Reflux 40-60% in anaesthetised dogs
Most of this is silent – may not be witnessed
When carrying out oral/pharyngeal procedures
E.g. Dental work and associated debris
Allows airway management during bronchoscopy
Allows one lung ventilation
Pre-Anaesthetic Fasting?
Recommended in adult dogs/cats 3-6 hours, water until premed
<3 = food present. >6 = stomach pH drops so reflux is damaging
Neonates = from 0.5 to 3 hours – monitor glucose
Horses withdraw concentrate overnight (to reduce gas distension) – controversial
Ruminants withdraw 6 hours and reduce concentrates ( to reduce gas distention) 12-24 hours
Small exotics/furries – shorter times depending on species
intubation methods
Endotracheal tubes
Supraglottic airway devices
V-gels (rabbits)/I-gels (cats)
Laryngeal mask airways
Face masks
Others
(Tracheostomy tubes)
(Arndt endobronchial blockers)
Endotracheal Tubes (ETT)
Various types available
Most are cuffed with a visible pilot balloon
Inflate to ~25mmHg – use manometer if possible
Murphy, Magill or Cole
Use of laryngoscope advisable
Flow = ∆𝑃𝜋𝑟4/8∩𝐿
Go as large as possible
What size shall I place?
Selection based on nasal septal width = 21% accurate
Selection based on tracheal palpation = 46% accurate
Best technique = visualise larynx using laryngoscope
Spray lidocaine (only cats as the have larygneal spazm) and WAIT
Try largest but have a range available
Cut to length – minimise dead space
Not possible with armoured tubes
Red Rubber ETT
Red rubber in common use
Crack over time + non-repairable
Prone to kinking
Irritant
Not possible to visualise blockages
Low volume high pressure cuff
Can lead to tracheal trauma but good seal
Difficult to recommend
PVC and Silicone ETT
More popular than rubber
Disposable but reused, silicone tubes repairable
Less prone to kinking compared to rubber
Non-irritant
Allows visualisation of blockages
Usually high volume low pressure cuff
Less risk of tracheal trauma but relatively good seal
Recommended
Armoured Endotracheal Tubes
Wire coil embedded in wall
Resist kinking but more difficult to place without stylet
If bitten may permanently obstruct
Useful in ophthalmic cases
Impossible to reduce dead space
Contraindicated in MRI
Cole Pattern Tubes
Designed for emergency use in paediatric anaesthesia
The shoulder of the tube should impact in the larynx to provide a gas-tight seal
However movement or IPPV tends to dislodge the tube
Still quite useful for exotic animal anaesthesia- snake ect
Supraglottic Airway Devices (SADs)
Developed originally for human anaesthesia
Major cardiovascular and laryngospasm problems in humans
ETT remain ‘gold standard’
veterinary specific LMAs achieving popularity for short uncomplicated procedures
Increasing evidence of their effectiveness in veterinary patients
Veterinary Specific SADs
V-gels are veterinary specific (rabbits and cats)
2 species where ETT placement can be challenging
Designed to anatomical standards
Can be used to protect the airway the same as an ETT
IPPV is possible
Channels to divert regurgitation can be incorporated
Very useful for short procedures and for bronchoscopy
Always use capnography
Face Masks for anesthesia
Should cover nose and mouth
Not whole head
Avoid eyes
Beware of dead space – choose the shape
Transparent masks preferable
Ensure a good seal using rubber diaphragms
Have been used for anaesthetic induction – NOT recommended
Stage 2 excitement and no airway protection
Very useful for provision of supplemental oxygen
Complications of Airway Management
High pressure/low volume (red rubber and some silicone ETT) exert pressure on a small part of the tracheal mucosa.
May see tracheitis or pressure necrosis
This can lead to tracheal strictures
Extreme cases may see tracheal rupture
Post-op subcutaneous emphysema in cats – but still recommended to use a cuff
ALWAYS disconnect from breathing system when changing position whenever a change in recumbency is needed
Especially with dental cases where head and neck movement is common
Always inflate carefully preferably with manometer
Or listen for leaks
ETT over insertion – carefully measure
Should be at level of thoracic inlet
Too long potential one lung ventilation
Cleaning and storage of ETT and LMAs
Usually stored on wall brackets ideally keep covered to avoid contamination
Common cause of tracheitis is insufficient rinsing of ETT tubes
LMAs need to be thoroughly dried after cleaning or tend to degrade
What Type Of Intravenous Cannula?
‘Over the needle’
24-10 gauge, 1.9-13.3 cm long
Relatively stiff material
‘Through the needle’
Large bore insertion needle
Cannula passed through the needle
Central veins
Not used commonly
Peel away – place through an over the needle cannula
Seldinger/over the wire cannula
placment of cannula
Cephalic
Most used site as animals easiest to restrain
Start distally (can then use the higher site)
Saphenous Veins
Requires more assistance
Medial or lateral saphenous
Use vein on caudal aspect of leg as it ascends
Medial easier in cat – straighter
Good choice in brachycephalics
Jugular- horse
Useful for long term therapy & regular sampling
Well tolerated
Multilumen cannulae available
right (straighter in the dog)
The Auricular Veins
Useful in animals with large or floppy ears, rabbits, ruminants too
EMLA cream can help to reduce discomfort
What size of cannula should u use?
22g (blue) for v small patients
20g (pink) or greater for most patients including cats
>20kg dogs use 18g
Very large dogs use 16g or 14g
maintinance of a placed intravenous cannula
Check cannula regularly and flush q 6 hours with heparinised saline (1IU/ml); does this help ????
Normal cannulae can be maintained for up to 3 days after which they should be replaced (exceptions do occur)
Swab ports prior to injection
Replace giving sets, bungs and T ports after 3 days
complications a cannula
Extravasation
Thrombosis (where do the thrombi occur)
Thrombophlebitis
Infection
Emboli (air, catheter)
Exsanguination
What would you do in these situations?
what are the functions of an anesthetic machine?
Delivery of oxygen / nitrous oxide at known rate.
Delivery of known concentration of IAA.
Removal of exhaled gases from patient.
Recirculation or removal of exhaled gases.
Facilitate IPPV/ CPR.Delivery of oxygen / nitrous oxide at known rate.
Delivery of known concentration of IAA.
Removal of exhaled gases from patient.
Recirculation or removal of exhaled gases.
Facilitate IPPV/ CPR.
Gas Source of an enesthetic machine function?
Molybdenum steel cylinders
Specific yokes and Bodok seal
Colour coded (e.g. oxygen = black/white top). Also piped gas from large cylinders. Usual sizes = E,G,F
Oxygen ; pressure = contents
Nitrous oxide ; liquid with vapour above. Therefore volume of gas in cylinder = (Wt. Cylinder – Empty Wt. Cylinder) x 534
Needle valve and flowmeter.
Regulate flow into low pressure side of machine. Flowmeter = graduated glass tube with floating bobbin/ball. Can stick. Read at TOP of bobbin/middle of ball. Rotate.
Back bar
Horizontal part of the anaesthetic machine circuit between the rotameter block and the common gas outlet
Vaporisers are mounted on the back bar, enabling volatile agents to be added to the fresh gases. The pressure in the back bar is approximately 1 kPa at the outlet end, and may be 7–10 kPa at the rotameter end
Contains a ‘blow off’ or pressure relief valve at the outlet end plus safety features to only allow one vaporiser in use
Intermittent positive pressure ventilation (IPPV)
Intermittent manual – ‘sighing’. A good habit! Close valve + short inspiration up to 20cm water. Chest supra-maximal. OPEN VALVE AGAIN.
Continuous manual. Repeated sighing. Can be tiring. Will allow breathing control but turn down vaporiser.
Mechanical. Ventilator. TV – 10-20ml/kg. Use large TV with slow rates. Various types. Frees anaesthetist and regular rhythm.
Soda Lime
USA – baralime.
90% = calcium hydroxide;
Ca(OH)2 +CO2 -> CaCO3 + H2O + Heat. Therefore gas warmed and humidified.
Colour change – usually to purple but NOT permanent so change if needed at end of anaesthetic.
Dust. Tracking of gas. Dead space. Resistance. Hyperthermia.
Exhaustion – colour change, no heat, increased heart/resp rate and bp, wound ooze, red mms.
Gas storage safety aspects
Oxygen/nitrous support combustion – naked flames/heat/electrical sparks.
Puncture cylinders – rocket effect; chain/ secure well. Move with carts. Store upright in dedicated area.
Keep tops dust free – plastic and blow dust off briefly before attachment.
Clearly label full/in use/empty.
Inhaled anaesthetic agent storage safety
Ether – highly flammable.
Halothane/Isoflurane/Sevoflurane.
Store upright in cool cupboard and avoid breakages.
Fill vaporisers at end of each day.
Recap bottles when empty.
If spill – open windows, wear gloves/mask and use absorbent into airtight container.
Scavenging
Prolonged exposure to anaesthetic gases potentially detrimental
Some anaesthetic are ozone gases
Legal requirement to control pollution
Control of substances hazardous to health
(COSHH)
Need to vent waste anaesthetic gases
Recommended max concentrations (UK)
* 100 ppm Nitrous oxide * 50 ppm isoflurane * 10 ppm halothane
Excess gas vented via pressure relief
(pop-off valve/APL valve)
Disc held by weak
spring
Connected to wide –bore
scavenge tubing
Types of scavenging
Charcoal cannister e.g. Cardiff aldasorber
Passive
- window
- hole in wall
- vent to outside
Active
- pumped outside
Charcoal canister
Cardiff aldasorber
Charcoal absorbs halogenated anaesthetics
Does not absorb nitrous oxide
Increasing weight indicates exhaustion
Heating causes release of gases
Active scavenging
Collecting & transfer system
Receiving system
- valveless open-ended reservoir
- bacterial filter
Pump to generate vacuum
Scavenging systems and safety
IMPORTANT – long term exposure to IAAs/nitrous possibly associated with;
Abortion/congenital problems.
Halothane hepatotoxicity.
Neurological problems – memory.
Bone marrow suppression/anaemia (nitrous).
?renal toxicity with methoxyflurane.
Therefore;
Cuffed tubes
Closed breathing systems
Wear gloves and fill vaporisers at end of day in fume hood
Key filling system
Turn on gas flows only if animal connected
Avoid mask induction and ventilate room – 20 air changes an hour
Monitor and inspect equipment
Oxygen failure alarm
Nitrous cut-off or oxygen failure protection device: if oxygen pressure is lost then the other gases can not flow past their regulator
Hypoxic-mixture alarms (hypoxy guards or ratio controllers) to prevent gas mixtures which contain less than 21-25% oxygen being delivered to the patient
Often chain linked (link 25 system). Located on the rotameter assembly, unless electronically controlled.
Ventilator alarms, which warn of low or high airway pressures.
Interlocks between the vaporizers preventing inadvertent administration of more than one volatile agent concurrently
Pin Index Safety System on gas cylinders
Pipeline gas hoses have non-interchangeable Schrader valve connectors, which prevents hoses being accidentally plugged into the wrong wall socket
Ambulatory infusion:
An animal is freely moving without need for a tether to connect with the catheter. This is normally only possible with larger animals that can be fitted with jackets to carry an infusion pump and compound reservoir. Totally implanted pumps can sometimes be used in rodents but have size limitations.
Atraumatic:
Minimal tissue injury is caused during the procedure
Biocompatibility:
Good toleration of implants by animal tissues after implantation.
Biofilm
A coating which develops on implanted materials derived from the animal’s own tissue fluids and cells
Catheter/cannula:
Flexible tube inserted into body cavities or organs for medical or experimental procedures
Dehiscence:
Bursting open or splitting along natural or sutured lines.
Haematogenous spread
Spread of microbial infection through the blood stream
Thrombogenic:
Property of causing or promoting blood clotting (thrombosis).
Breathing system requirements
Supply fresh gas & anaesthetic to patient
Allow removal of carbon dioxide
Allow scavenging
Enable positive pressure ventilation
Easy to use & clean
Inexpensive to buy and use
Re-breathing systems
Expired gas is ‘scrubbed’ of CO2
Chemical CO2 absorber
Low fresh gas flow
Economical
Expensive to buy
Large and cumbersome
Conserves heat and moisture
Increases resistance to breathing
Only suitable for larger animals
e.g. > 10 kg
Large animal systems available
formula Working out gas flow requirements for rebreathing systems
Minimum requirement is metabolic oxygen demand
i.e. 10 ml/ kg/ minute
However, must supply minimum vaporizer flow
e.g.Penlon sigma (sevoflurane) 0.25 Lmin-1
Denitrogenation
With any rebreathing system where carrier gas is oxygen
Use higher flows for ~10 minutes- 2l or 3 l per minute
Risk of alveolar hypoxia
N.B also after short disconnections – movement between theatres etc
can also increase to deliver more anethesia
Non-rebreathing systems
High gas flow requirements
Loss of heat and moisture
Cheap to purchase, expensive to run
Low resistance to respiration
Suitable for very small patients
formula for Working out gas flow requirements for non rebreathing systems
Based on multiples of minute volume, where minute volume is;
Respiratory rate x Tidal volume
OR
200 ml per kg
Magill non rebreathing system
Reservoir bag at fresh gas inlet
Awkward to use
1 x Vm (Vm = Vt x RR) or (Vm =200ml/kg)
no ippv
Lack non rebreathing syste
Co-axial Magill
1 x minute volume
Damage to inner limb results in rebreathing
no ippv
Mini Lack non rebreathing system
Alternative to T-piece for patients under 10 kg
Bodyweight range 1-10kg
1 x minute volume
No bag twist hazard
Very low resistance
Easy to clean smooth bore tubing
no ippv
T-piece
Suitable for very small patients, < 8 kg
2-3 x Vm- half as efficent at lck or magill
Suitable for IPPV
Bain non rebreathign system
Co-axial T-piece
Suitable for 7 – 10 kg
2- 3 X Vm
Beware – damage to inner tub
Humphrey ADE
3 different modes
- lever upright (lack)
- lever down (T-piece)
- circle
Versatile, suitable for 4 kg - >20 kg
Pros
Compact
Well designed
Scavenge at machine end
Straightforward conversion to IPPV (Nb increase flow)
Applies PEEP
Increases FRC
Prevents microatalectasis
Lowers work of breathing in human infants
Cons
Cost
Very heavy – strain on common gas outlet
Flows of 50ml/kg/min in lever up (lack) not substantiated in animals
Relies on 3 human references
Unquantified resistance from inspiratory/expiratory valves
Hoses pinch at valve end and start to crack
Colour codes misleading (S. African)
Excessive (unquantified) mechanical dead space
Surprising lack of veterinary controlled trials
Soda lime canister capacity 690ml
Filled with soda lime capacity 345ml
This intergranular volume falls as anaesthesia progresses as soda lime is used up
Expired volume must not exceed this or expired breath will not be completely scrubbed of carbon dioxide
This leads to maximum limit of 29kg dog with tidal volume of 12ml/kg
Morphology of necrosis
Continued swelling and hypereosinophilia
Nuclear changes:
Pyknosis = shrinkage
Karyorrhexis = fragmentation
Karyolysis = dissolution
Inflammation
Pyknosis
shrinkage or condensation of a cell with increased nuclear compactness or density
Karyorrhexis
the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm.
Karyolysis
he complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases.
Causes of necrosis - anoxia
Reduction or cessation of ATP production due to hypoxia or anoxia respectively will result in loss of function on energy-dependent cell pumps: -Na+/K+ pumps
Results in cell swelling due to osmotic pressure
ONCOTIC NECROSIS- Cell swelling is the typical feature and distinguishes it from apoptosis
-Calcium efflux pumps
are also affected
resulting in accumulation of intracellular calcium
describe membrane damage as a Cause of necrosis –
Membranes can be directly damaged by:
Pore-forming infectious agents/toxins- One of the best examples of membrane damage by pore-forming toxins are those produced by Clostridium perfringens
Reactive oxygen species (ROS)
Phospholipase activation
Protease activation- cytoseletal damage
Viruses can damage cell membranes as they leave the host cell.
Enveloped viruses require incorporation of host cell membrane to form part of their envelope
Viruses that bud off from the outer cell membrane (retroviruses) do so quietly, leaving an intact host cell
Those that bud from the golgi or RER (flavi, corona, arteri, bunya), and those that bud from nuclear membrane (herpes) lyse the cell as they go
Non-enveloped viruses can also only leave the host cell upon lysis
Additionally, viruses may causes cell lysis due to disruption of the cytocavitary network and other homeostatic mechanisms when they “hijack” intracellular processes for replication
Viruses will also induce apoptosis
how do viruses cause cell membrae damage
Viruses can damage cell membranes as they leave the host cell.
Enveloped viruses require incorporation of host cell membrane to form part of their envelope
Viruses that bud off from the outer cell membrane (retroviruses) do so quietly, leaving an intact host cell
Those that bud from the golgi or RER (flavi, corona, arteri, bunya), and those that bud from nuclear membrane (herpes) lyse the cell as they go
Non-enveloped viruses can also only leave the host cell upon lysis
Additionally, viruses may causes cell lysis due to disruption of the cytocavitary network and other homeostatic mechanisms when they “hijack” intracellular processes for replication
Viruses will also induce apoptosis
describe free radicals as a Cause of necrosis –
Free radicals are any molecule with a free electron
Reactive oxygen species (ROS) and reactive nitrogen species (NO)
Produced by oxidative metabolism, therefore most frequently made by mitochondria, but will also damage the mitochondria if cannot be removed.
Vitamin E and selenium are important co-factors in the neutralisation of free radicals
Programmed cell death - apoptosis
Apoptosis is normal- Embryological, Physiological
May be due to a pathological process:
Organ not receiving stimulus- portosystemic shunt
Cell contains infectious agent
Cell is irreparably damaged
DNA is irreparably damaged
Cell is cancerous
Two main mechanisms of apoptosis
Intrinsic- due to something within the cells. meachanism within the cell tell cellt to die
Extrinsic- more complex. binding of death ligand with cell receptor
morphology of apoptosis compared to necrosis
Morphology differs to necrosis:
Cell is shrunken
No/minimal inflammation- only a few inflamatory cells coming to clean up dead cell
Chromatin condensation around nuclear periphery (most characteristic)-
Formation of cytoplasmic blebs = apoptotic bodies as oposed to bursting out as in Karyorrhexis,
Karyolysis
There are different types of programmed cell death
Fresh Gas Flow Calculations
• To calculate fresh gas flow calculations we first need to calculate the animals minute volume (MV).
• All our non-rebreathing systems require 1-1.5 or 2-3 times the minute volume to run effectively and efficiently. This is know as the circuit or system factor.
• To calculate the minute volume (MV) we need to know the volume of air inspired or expired in one breath (tidal volume) and over a minute (minute volume)
• Minute Volume (MV) = Tidal Volume (TV) x Respiration Rate (RR)
• Tidal Volume (TV) = 10-15ml/kg
• We then multiply this amount with the system/circuit factor.
• Alternatively, the MV can be estimated using 200ml/kg/min.
fgf= MV x CF
A 4 year old Male Entire Staffordshire Bull Terrier presents at your practice for a dental descale and polish (routine). His Pre-op bloods and physical exam are normal. He weighs 19.8kg.
- Which of the following would be a suitable choice of breathing system for this patient? If not, why not?
a. Bain
b. Parallel Lack
c. Circle
d. T-piece
b
Aims of premedication
Sedation and anxiolysis (The reduction of anxiety by means of sedation or hypnosis) facilitating handling of the animal
Reduction of the stress for the animal- reduce adrenaline, prevent cardiac problems
Reduction the amount of other anaesthetic agents
Provision of a balanced anaesthesia technique
Provision of analgesia
Counter the effects of other anaesthetic agents to be administered during the anaesthesia procedure e.g. atropine to prevent an opioid mediated bradycardia
Contribute to a smooth, quiet recovery after anaesthesia
ideal Properties of drugs of pre med drugs
Reliable sedation and anxiolysis
Have minimal effects on the cardiovascular system
Cause minimal respiratory depression –animals will not be intubated following premedication until induction of anaesthesia, therefore they should breathe spontaneously after premedication
Provide analgesia, e.g. Opioid component
Be antagonisable: The ability to antagonise the effects of premedication may be desirable to hasten recovery from anaesthesia
Alpha2 Adrenoceptor Agonists (Alpha-2s) as premeds
Potent sedative and analgesic drugs- keeps patient really sedated. very good for very sick patients post op as anelgesia
Xylazine was the first a2 agonist to be used in veterinary practice
Superseded by medetomidine & dexmedetomidine (cats & dogs), both lasting about 45 minutesas xylazine is assosiated with death
Xylazine (30minutes), detomidine (45 minutes)and romifidine (60 minutes, less ataxia) used in horses- only real difference is leanth of action
Xylazine and detomidine used in cattle- licenced for food animals
The superior selectivity of dexmedetomidine makes it the theoretical a2 agonist of choice for use in small animals
work on alpha 2 receptiors on presynaptic neurons- widly distributed on cns- alpha 2s activate alpha 2 receptors and provides negative feedback and reduces release of neurotransmitor
Sedation is profound & dose related
Alpha 2 agonists provide good analgesia through an agonist effect at spinal cord A2 receptors
The duration of analgesia provided by a 10 µg/kg dose of dexmedetomidine is approximately 1 hour
Intra-op analgesia improved
The dose of induction and maintenance agents required after alpha 2 agonists are dramatically reduced in small animals- be careful of this
Intravenous induction agents must be given slowly and to effect (vein to brain circulation time is slowed)
Alpha 2 agonists produces a biphasic effect on blood pressure (initial increase followed by a return to normal or slightly below normal values)
Heart rate is decreased throughout the period of a2 agonist administration HR 45-60bpm dogs and 100-120 bpm cats
Alpha2agonists cause a reduction in cardiac output & in healthy animals.
Urine production is increased due to a reduction in vasopressin and renin secretion
avoid these drugs in patients with heart issues
Endogenous insulin secretion is reduced leading to a transient hyperglycaemia- do not test for diabetes after administration of these drugs
Both liver blood flow and the rate of metabolism of other drugs by the liver are reduced
Peripheral vasoconstriction tends to reduce peripheral heat loss
As a consequence it can be easier to maintain normothermia during the peri-operative period compared to animals given acepromazine
Small ruminants are quite sensitive to alpha 2 agonists
Alpha 2 sedation and analgesia is rapidly antagonised by the administration of atipamezole, a specific alpha2 adrenergic receptor antagonist- wont always antagonise cardiovascular effects
Reversal is advantageous because the recovery period is noted to be a high risk time for anaesthetic complications
IM atipamezole produces smooth and good quality recoveries
IV atipamezole produces a very rapid, excitable recovery from anaesthesia and this route of administration is not recommended
It is important to ensure that analgesia is supplemented with different classes of drugs
Atipamazole rarely used in horses and cattle
Phenothiazines
Acepromazine commonest/only licensed one
Sedation and anxiolysis that is initially dose dependent- less flat out sedation
can last 46 hours- lasts through recovery
With larger doses the duration of action is more prolonged
The quality and reliability of sedation can be improved by combination with an opioid (neuroleptanalgesia)
Addition of an opioid also provides analgesia, advantageous since acepromazine itself is not analgesic
To maximise sedation the animal should be left undisturbed for 30-40 minutes after administration
Less reliable sedation cf dexmedetomidine
Acepromazine (ACP) is an antagonist of a1 adrenoreceptors and can cause peripheral vasodilation and a fall in arterial blood pressure- will bleed more
Avoid in animals with marked cvs disease or animals in shock
Acepromazine is long lasting & non-reversible(!) so avoid in hypotensive animals
Acepromazine has anti-arrhythmic properties which may be advantageous during anaesthesia- decreses central arythmia, very potent at this
Reduction in body temperature occurs due to a resetting of thermoregulatory mechanisms combined with increased heat loss due to peripheral vasodilation
No evidence to suggest that acepromazine alters seizure threshold despite what some say
Giant breeds of dog may be “more sensitive” to the effects of acepromazine
Some boxer dogs are sensitive to even small doses of acepromazine, which has been attributed to acepromazine induced orthostatic hypotension or vasovagal syncope in this breed
Although acepromazine is not contraindicated in boxers, it is not the premedicant of choice in this breed - a very low dose (≤0.01 mg/kg) is recommended and animals should be monitored carefully after administration
Acepromazine is a dopamine antagonist- Anti-emetic
Contraindicated in breeding stallions- causes repro problems
comes in gell for horses and tablet ofr dogs and cats as well as injectable
neuroleptanalgesia
combination of opiod and Phenothiazines (ACP)
Benzodiazepines
Midazolam or diazepam (MA coming for midazolam, diazepam has MA in France)
Benzodiazepines alone produce minimal or no sedation in healthy cats and dogs
May even cause excitation due to loss of learned “inhibitory” behaviour
Benzodiazepines are therefore given in combination with other sedatives
In dogs benzodiazepines often combined with opioids because both classes of drugs are cardiovascularly stable and the combination can provide reliable sedation
In cats benzodiazepine and opioid is not very sedative, so benzodiazepine is most commonly combined with ketamine
These drugs have minor effects on cardiorespiratory systems
Therefore these drugs tend to be used as premedicants in animals with cardiovascular compromise.
Benzodiazepines are commonly used to manage convulsions, particularly as a first line intervention for animals presenting in status epilepticus
Premedication drug combinations (dogs and cats)
Acepromazine + opioid
Alpha 2 agonist + opioid
Alpha 2 agonist + BZD
Alpha 2 agonist + Ketamine
BZD + Ketamine
Opioid + BZD
Alpha 2 agonist + BZD + opioid
how to choose premeds for anethesia
Reason for anaesthesia or sedation
Duration of sedation required
Procedure to be carried out
Degree of pain expected from the procedure
Species and breed of the patient
Age of the patient
ASA classification of the patient
Injectable Induction,Why choose it?
Can be injected:
direct from needle/syringe (IM, SC, IV)
via IV cannula/syringe (IV only)
Renders patient unconscious by drug reaching brain directly via blood - rapid and smooth
Injectable Induction Agents in Common Use – Small Animals
Propofol
Alphaxalone
Dissociative agent & benzodiazepine
Inhalant Induction
Simple
Choice of agent critical
Speed
Pungency
Not generally recommended – VERY POOR for the patient and associated with higher mortality
distressing for animal
propofol
pros- Quick recovery with no hangover
cons-Apnoea if given too quickly
Propofol (‘milk of amnesia’)
Most commonly used anaesthetic in UK (dogs and cats)
Alkyl phenol, white emulsion 10mg/ml
Soyabean oil, glycerol, egg lecithin, no preservative, NaOH (changes pH)
Supports bacteria and endotoxin
Use within 24 hours
A multi-dose vial with preservative was available (‘Propoflo Plus’ – Zoetis) 28d shelf life
Rapid onset of action -rapid uptake by CNS
Short period of unconsciousness (5-10 mins)
Large volume of distribution (lipophilic)
Rapid smooth emergence due to redistribution & efficient metabolism (hepatic and extra hepatic) metabolites inactive
good for patietn swith hepatic problems as it is alos metabolised in the lungs
Respiratory depression (apnoea) - IPPV - Speed of injection should be slow, less needed if given over longer period
Cardiovascular depression
Rapid and smooth recovery
Suitable for top ups or TIVA
Muscle relaxation usually ok- can cause extention and rigisity of legs, wait it out or give muscle relaxant
Anticonvulsant
Not irritant, pain reported
not Analgesic
↓ ICP (patients with raised and normal ICP)
problems-
Rigidity, twitching
Apnoea
Profound bradycardia
Care in hypoproteinaemia
Heinz body anaemia in cats
??? Use for patients with pancreatitis / hyperlipoproteinaemia or diabetic hyperlipidaemia
Pain on injection ?
Local reaction (clear formulation, discontinued)
Alfaxalone
Is suitable for cats and dogs (& other spp)
Alfaxalone is a clear colourless neuroactive steroid
Causes anaesthesia by activating the GABA (inhibitory) receptor
has a short plasma elimination half life and is cleared from the body relatively quickly
Alfaxalone can be give as repeated boluses or as TIVA to maintain anaesthesia
Premedication is preferable
Anaesthesia induction is smooth, and the injection is given slowly over 60 seconds.
Occasional apnoea is seen and IPPV may be necessary (more than propofol)
The drug has good cardiovascular stability, causes no histamine release and produces good muscle relaxation
Animals should not be disturbed during recovery as excitement can occur
Dissociative Agents
Ketamine (also Tiletamine in Europe/USA)
Weak organic base pH 3.5
Racemic 10% solution (100mg/ml)
IV, IM, SC, IP, PO, epidural
Dissociative state
Used in many species for induction and analgesia
What is ‘dissociative anaesthesia’?
Dissociative anaesthesia = detached from surroundings- Patient may have their eyes open and make reflex movements during surgery
In recovery the patient may be agitated- Hallucinations are associated with human ketamine anaesthesia, Can be reduced by premedication with benzodiazepines
Ketamine increases the intracranial pressure- causes rigitity, give other meds along side this
Ketamine
Can be combined with BZD, alpha 2 agonists, acepromazine, opioids
Versatile induction agent and wide safety margin
Invariably needs to be combined with something
Rapid induction
Respiratory effects are mixed – bronchodilation and RR usually preserved but my stop!
GOOD ANALGESIA
CVS effects depend on dose
Muscle tone ↑ and jerky movements
Salivation and lacrimation ↑
Ketamine can be diluted with sterile water or physiological saline
Stormy recovery if disturbed or not adequately premedicated
Depth assessment is different (eyes open)
Corneal drying - use ‘Lacrilube’ or similar tears
Vomiting common with alpha 2 combinations avoid in patients with GI obstruction
Avoid in patients with ↑ Intra ocular pressure, ocular surgery, fever, hyperthyroidism
schedual 2 control drugs- records important
MAC
Minimal Alveolar Concentration (MAC)
The alveolar concentration (at 1 atm) producing immobility in 50% of patients in response to a noxious stimulus
i.e. Potency
MAC is for healthy, un-premedicated patients
MAC affected by
Age, N2O, hypotension, hypoxia, anaemia, opioids, sedatives , LAs, pregnancy
premeds reduce mac- not nsaids though
MAC not affected by
Stimulation, duration, species, sex, CO2, NSAIDs
Concentration of agent rises in plasma at a rate that depends upon
Ventilation
Concentration of agent in carrier gas
Cardiac output (inversely)
Solubility of agent in the body (inversely)- the more soluble the slower the effect
Blood:gas partition coefficient =
Solubility
This is the ratio of the amount of anaesthetic in blood and gas when the two phases are of equal pressure and volume
The LESS soluble agents (low coefficient) are washed away less quickly therefore the alveolar concentration rises FASTER
Blood: gas partition coefficient
The LESS soluble agents (low coefficient) are washed away less quickly therefore the alveolar concentration rises FASTER
a fat animal will recover from anethesia slower than a thin one. why?
Recovery is the reverse of induction, so dependant on blood solubility, redistribution will have occurred into the fat, which then acts as a depot of anaesthetic so (depending on fat solubility) a fat animal will recover slower than a thin one….
ideal anasthetic agent
Stable
No preservatives
Non-inflammable
Cheap
Ozone friendly
Non metabolised
Non-toxic
No CVS effects
Analgesic
What are negative effects of inhaled agents?
To the animal-
Cardiorespiratory depression
Formation of carbon monoxide with soda lime
(Formation of other toxic gases)
To the anaesthetist-
Little or no evidence apart from nitrous oxide
Bone marrow suppression
Teratogenesis
Nitrous oxide – becoming obsolete (why?)
H and S issues
Expensive
Analgesic
Min CVS & resp effects
V high MAC > 100%
Isoflurane
Lower solubility
Different CV depression
‘SAFER’ in dog
CEPSAF
summerise the considerations made with anethetic agents
Most anaesthetics induced by injection and maintained by an inhalational agent.
Recovery faster with a less soluble agent such as sevoflurane but MAC is higher
MAC is altered in states such as pregnancy and with other drugs
Scavenging is important although little evidence for problems
All inhalants are CV depressants
Evidence supports use of isoflurane over halothane
No data supporting further reduction of risk with sevoflurane
methods other than vapors to maintain anaesthesia
TIVA = total intravenous anaesthesia
PIVA = partial intravenous anaesthesia
Often used in horses but increasingly in small animals
Offer environmental advantages
TIVA
total intravenous anaesthesia
Can be used for short procedures in small animals/aggressive patients
E.g. ‘quad’ anaesthesia for cat neuters
The Cat Group
Routinely used for field procedures in horses
E.g. ‘GGE, ketamine, alpha-2 agonist – so called triple drip
Various ‘recipes’
GGE (Guaifenesin, a centrally acting skeletal muscle relaxant with little or no analgesic properties)
Supplied as 5% guaifenesin in 5% dextrose and infused to effect until signs of ataxia are seen, at which time IV bolus of ketamine is given
Maintained with infusion given to effect
However, always remember
Protect the airway – regurgitation risk (which species?)
Supply oxygen
Have a means to ventilate
PIVA
partial intravenous anaesthesia
Goals of PIVA
Reduce MAC
Reduce cardiopulmonary depression
Provide additional analgesia
Improve environmental impact
(Improve plane of anaesthesia)
Reduced cardiopulmonary depression, and less inhalant can be used
Analgesia provision
Less pollution & organ toxicity
Improved intra operative conditions
Improved outcome?
We don’t know yet
Evidence based medicine
Cardiopulmonary depression will still occur
Most IV drugs accumulate over time
Additional equipment required
the ideal drug-
MAC reduction
Analgesic
Minimal toxicity
Minimal effects on the body
Short context sensitive half life
Compatible with other drugs
NO single drug meets these requirements
Hence the need for combinations
combinations for PIVA
Inhalant+
Lidocaine- Analgesic
MAC reduction (25%)- not for cats !!!
Ketamine-
Often given as boluses during anaesthesia
Ketamine CRI (30% MAC reduction)
Alpha 2 agonists (not licensed as CRIs)- Xylazine, detomidine, medetomidine and dexmedetomidine can be given as small (tiny) boluses
Bradycardia !
Can also be given as CRIs
Opioids – various commonly used
Combinations may be the key
Remember most drugs accumulate over time
Lidocaine + ketamine have been shown to improve cardiovascular stability during isoflurane anaesthesia
Many combinations are possible and again we must used evidence based medicine to recommend the recipes
what can be measured on a monitor during anesthesia
Capnograph- The term capnography refers to the noninvasive measurement of the partial pressure of carbon dioxide (CO2) in exhaled breath expressed as the CO2 concentration over time.
Blood pressure
ECG
Pulse oximeter
Cardiac output
What Should We Monitor in a patient under anesthesia?
CNS depression- Eye position, jaw tone, EEG, BIS, etAA
Physiology and homeostasis-
Respiratory: Oesophageal stethoscope, capnograph, pulse oximeter
Cardiovascular : Blood pressure (MAP), pulse, ECG
Delivery of oxygen = how much oxygen is being carried to the tissues by how much blood pressure
Temperature under anesthesia
Anaesthetised, sedated and critical patients unable to regulate temperature
Measure temperature using rectal thermometer (may under read) or oesophageal thermoprobe (gold standard)
Core-periphery differences
Use bubble wrap, socks, hot water beds, lamps, low flow anaesthesia, warm theatre, heated pads, blankets, themovents/HMEs
Temperature affects many aspects of anaesthesia
Increased pain
Increased wound infections
Delayed recovery
Core temperature support?-
Consider warm saline irrigation
Circle systems (rebreathing system)
Consider warm water enemas
Hypothermia during anaesthesia
Temperature falls due to
Reduced shivering
Vasodilation
Reset thermoneutral point- opiods
Open body cavity
Cold gases
Dry gases
Wetting and prep
monitoring pule during anethesia
Use peripheral pulses
Get used to palpating pulses at different sites
Femoral artery
Dorsal metatarsal artery
Lingual artery
Auricular artery
Compare dorsal metatarsal artery and femoral artery
With hypotension dorsal metatarsal artery disappears
use fingertips to locate artery
Pulse Oximetry
Displays percentage oxygen saturation of haemoglobin
Accuracy is affected by
poor circulation (common in critical patients)
ambient light
movement of the probe
chow-chows
Limitations- High/low heart rates
Probe design
Useful post-op
saturating on room air?
Early warning?
Cyanosis – crude estimation
But ‘On a cliff edge
How is the haemoglobin saturation SPO2% (reading from pulse oximeter) related to PaO2 (partial pressure of oxygen in the blood)?
Oxygen content is dependent on both SaO2 and PaO2
Oxygen content
= (1.39 x Hb x SPO2%) + (0.003 x PaO2)
SPO2%
the haemoglobin saturation
PaO2
amount of oxygen disolved in the plasma
drives SPO2%
Cyanosis
not enough oxygen in the blood
Hb of 15g/dL (PCV 45%)
Cyanosis may start to manifest at SpO285% - no other signs
Haemoglobin of 9 g/dL (PCV 27%)
The threshold SaO2 level for cyanosis is lowered to about 73% (PaO2 38 mm Hg), the patient would certainly have other signs
Oxygen Content
Blood gas analysis-
pH
HCO3
PCO2
PO2
Arterial blood gases- the most accurate
Capnography – a good alternative for (PACO2)
Electrocardiogram (ECG)
ECG analysis does not give information about the mechanical activity of the heart
Important for arrhythmia diagnosis and monitoring response to treatment
Various arrhythmias may be seen
Tachycardia (sinus) may be the result of
Nociception- pulling on ovaries
Hypercapnia
Hypovolaemia
Hypokalaemia
And many more…
ECG may show characteristic changes depending on the underlying cause
Bradycardia (less common)
Drugs (e.g. alpha-2 agonists, opioids)
Hypothermia
Electrolyte disturbances e.g. severe hyperkalaemia
Knowledge of the patient is vital to determine treatment;
Alpha-2 agonist-induced bradycardia with second degree AV blocks
treatment is antagonism of the original dose
Opioid-induced bradycardia
treatment is the administration of an anticholinergic (contraindicated following alpha-2 agonist administration)
Capnography
Capnography (carbon dioxide measurement) conveys information relating to both respiratory and cardiac function
The end tidal carbon dioxide concentration is measured from the alveolar plateau and should remain constant with unchanged ventilation and cardiac output
Main-stream (measured directly in the box) and side-stream machines (measured via a water trap are available
need to be scavenged from!
Normal ET CO2 = 35–45 mm Hg
Hyperventilation – Decreased ETCO2
Hypoventilation - Increased ETCO2
obstructive pattern- sharks fin pattern:
asthma
kinked endotrachial tube
not reaching baseline- rebreathing:
sodalime has run out
non rebreathing apperatus has inadiquate flow
Other indicators
Oesophageal intubation
Leak at cuff/Patient disconnection
Adequacy of resuscitation
Normal variation – cardiac oscillations
Arterial Blood Pressure Monitoring methods
Non-invasive blood pressure (NIBP) monitoring, sphygmomanometry, oscillometric ( & HDO)
Doppler
Invasive blood pressure monitoring
Finger on pulse?
NO (Systolic 90-150 feels the same)
Monitoring Blood Pressure- Doppler
Set up takes a few minutes
Piezoelectric crystal placed over artery (clip fur, use gel)
Locate artery with distinct noise of arterial pulse
Cuff placed proximal to probe
Cuff size must be accurate
Audible signal v useful
Systolic pressure only (cats?)
Non-invasive blood pressure (NIBP) monitoring- oscillometric
Cuff size must be accurate- must go 1/3 of the way around
small cuff size makes reading high- large cuf size makes reading low
Unreliable in cats & small dogs
Quite expensive
More accurate methods available
High definition oscillometric devices– the future?, fast can cope with high HR & poor perfusion but clinically poor
Invasive blood pressure monitoring- Artery cannulation
Direct arterial pressure via an arterial cannula “gold standard”
Usually placed in the dorsal pedal artery
Auricular and facial arteries also used
Cannula is attached via saline-filled non-distensible tubing to an electrical transducer which gives continuous ‘beat to beat’ diastolic, mean and systolic arterial pressures
Must label cannula, line & flush regularly (hep saline)
Never inject any other drugs
Tubing must be narrow bore and non-compliant to amplify signal
Causes of decreased blood pressure include
Intravascular fluid loss (haemorrhage, third space losses)
Failing myocardial function
Sepsis
Relative hypovolaemia (vasodilation – drugs/sepsis)
determining renal perfusion
Although blood pressure monitoring is important it does not tell us directly about organ perfusion
Assessing urine output may be of equal value in determining renal perfusion
Aim for 1-2ml/kg/hr intraoperatively
treatment of Hypothermic patient with bradycardia and low blood pressure
Anticholinergic treatment and warming to raise heart rate and subsequently blood pressure
treatment of Septic patient with tachycardia but poor blood pressure
Intravenous fluid therapy to improve status
Patients with advanced sepsis require pressor support
Noradrenaline
Dopamine
Phenylephrine
Central Venous Pressure (CVP)
Used as an approximation of right atrial filling pressure (late guide) but of limited clinical value in anaesthesia
?Acts as a guide to correct fluid therapy (late guide)
May aid in detection of tricuspid valve problems
Central Nervous System Monitoring
Aims -Adequate ‘depth’ for procedure undertaken
Electroencephalogram (EEG)
Experimentally – Bispectral index (BIS)
Electroencephalogram (EEG)
Raw signal data
Spectral edge frequency
Auditory evoked potentials
Very limited clinical value
Anaesthesia Recovery
The process of allowing a patient to regain consciousness after anaesthesia
Recovery is the most common time for an anaesthetic-related death
Recovery Involves-
inhalant- Turn off inhalant.
Remain on oxygen.
Allow inhalant to be breathed off.
injectable-Turn off infusion/stop top-ups.
Drugs are metabolised/re-distributed.
Goal of recovery is to ensure patients return to the physiological norm as quickly as possible
Key points:
Heat loss leading to hypothermia
Extubation
Only perform when patient can swallow and has control of airway
Care with brachycephalic breeds
IV access
Leave cannular in for 1 hour after patient appears stable for patients not on longer term IV fluids
causes and solutions to prolonged recovery
Hypothermia
Excessive pre-med use
Patient too deep during maintenance
Hypoglycaemia
Choice of inhalant
Choice of induction agent
solutions-
Heat supplementation
Reconsider premed use
Closer monitoring to give as little anaesthetic as possible
IV fluids
Use faster acting inhalant
Use shorter acting induction agent
causes and solutions of airway instructions
Debris or gauze left
after dental procedures
Body fluids eg vomit,
blood
solutions-
Clear oral cavity then extubate after patient gains control of swallow reflex
causes and solutions of agitated recovery
Inadequate use of premeds or analgesics
solutions-
Reconsider premed and analgesic protocol and dose rates
Recovery in BOAS Patients
Sedation (acepromazine followed by alpha-2 agonist or vice versa)
Don’t forget analgesia (NSAIDS* +/- opioids)
*caution if steroids
Oxygen supplementation
Monitoring plan
Leave IV cannula in situ
Check for regurgitation prior to extubation
EXTUBATE LATE - after the head is raised
Very well tolerated!
Be prepared to re-intubate
Have a full dose of induction agent ready
Tracheostomy
When to re-intubate?
SPO2 consistently low on room air
If reading 80 something then consider oxygen / re-intubation
Pulling tongue out assists readings
Obvious effort/distress
Cyanosis
Paradoxical breathing
Post operative analgesia
Untreated pain leads to;
Chronic pain states
Wound infection
Wound breakdown and interference
Occasional reports of diabetes mellitus
Catabolic states (insulin resistance)
Welfare concerns
Unhappy owners
Will anything given pre or intraoperatively last into recovery period?
What is the predicted degree of pain post operatively?
Is it a requirement that the animal is fully conscious rapidly post operatively ?
Is a slower recovery required?
What is the preferred route of administration?
Enteral – oral , rectal, transmucosal
Parentral – intravenous, intramuscular, subcutaneous, transdermal
How long is the predicted length of analgesic requirement?
Intermittent bolus
Continuous rate infusion
How Can We Apply Local Anaesthetic Techniques in addition to general anethesia?
Somatic infiltration generally reliable & safe
Multiple intradermal (or s/c) injections
Usually administered in sedated/anaesthetised animals
Lidocaine spray – ‘Intubeaze’ (2%)
Lidocaine jelly (2%) for catheterising the urethra
Lidocaine & prilocaine cream (EMLA) useful for IV cannula placement
Proparacaine 0.5% and butacaine 2% topical on cornea (10-20 minutes)
can improve recovery
How Do We Use Local Anaesthetic?
Intravenous route- Only use lidocaine IV
More benefit in soft tissue pain??
Can be used in both dogs and horses
Decreases MAC and reduces opioid requirements
Can also be useful post-op
AVOID in cats- very sensitive
Somatic infiltration generally reliable & safe
Multiple intradermal (or s/c) injections
Usually administered in sedated/anaesthetised animals
Lidocaine spray – ‘Intubeaze’ (2%)
Lidocaine jelly (2%) for catheterising the urethra
Lidocaine & prilocaine cream (EMLA) useful for IV cannula placement
Proparacaine 0.5% and butacaine 2% topical on cornea (10-20 minutes)
Small animals
Splash blocks
Epidurals
Dental blocks
Limb nerve blocks
Intraoperative articular blocks
Farm animals
Cornual block
Caudal epidural
Inverted L-block
IVRA
Paravertebral
Horses
Diagnostic nerve blocks
Epidural
Eye and dental blocks
Intraoperative + intraarticular
small animal anesthetic techniques
Splash blocks
Epidurals
Dental blocks
Limb nerve blocks
Intraoperative articular blocks
Farm animals anesthetic techeniques
Cornual block
Caudal epidural
Inverted L-block
IVRA
Paravertebral
Horse anesthetic techniques
Diagnostic nerve blocks
Epidural- caudal
Eye and dental blocks
Intraoperative + intraarticular
Local Blocks
Revise anatomy!
Place local anaesthetic in region of the nerve
Nerve Location Techniques- Nerve stimulator, Ultrasound of femoral triangle
Head/Dental Blocks
infraorbital n.- upper lip, nose, roof of nose, skin rosral to canal
maxillary n. - maxilla, upper teeth, nose upper lip
rigeminal n.- akinesia of globe, desensitises eye and orbit
mental n,- lower lip, incisors
mandibular n.- mandible, teeth, akin, mucosa
Infraorbital Block
upper lip, nose, roof of nose, skin rosral to canal
Transbuccal
Transdermal
Place needle into canal
Maxillary Block
Tmaxilla, upper teeth, nose upper lip
ransorbital approach
Transdermal approach
Ventral to notch in zygomatic arch
Transmucosal – cannula into infra-orbital canal
Mental Block
lower lip, incisors
Mandibular nn
Mental foramen
Mandibular Block
Medial mandible
Just rostral to angular process
Or transmucosal – medial aspect mandible
mandible, teeth, akin, mucosa
Ophthalmic Blocks
Auriculopalpebral
Supraorbital
3 point
Petersen block
Retrobulbar
Forelimb Blocks
Brachial plexus
Median
Radial and ulnar
(RUMM block)
Digital
Hindlimb Nerve Blocks
Sciatic
Femoral
Tibial
Fibular
Digital
Motor- ok in small animals but bad in large animals- flighty horse will be stressed by loss of use of limbs
Sensory
Forelimb Blocks
Brachial plexus
Median
Radial and ulnar
(RUMM block)
Digital
Intercostal Blocks
Useful for:
Rib fractures & flail chests
Chest drains
Thoracic surgery
‘Soaker’ Cathetersv
Useful for analgesia for total ear canal ablations (TECA), limb amputations & extensive reconstructive surgery
Relatively large bore (6-12 French) catheters with very tiny holes
Allow distribution of local anesthetic into the surgical site
Placed just before closing incision and secured to the skin at the end of the surgery
Intravenous Regional Anaesthesia (IVRA)
Esmarch bandage applied and tourniquet proximal
After removal of the bandage 0.25-0.5% lidocaine (2.5mg-5mg/kg) injected using a vein distal to tourniquet
Tourniquet can be left in place for up to 90 minutes
Used in conjunction with GA or heavy sedation
Common in cattle -digit amputation
Paravertebral Anaesthesia
Predominantly used in farm animals – traditionally!
Inject L.A around spinal nerves emerging from vertebral canal
Advantages
Desensitizes large area
Good muscle relaxation - motor
Reduced I/abdominal pr
?simple/quick
Less L.A required than infiltration
Epidural Analgesia
Indications
Abdominal and hind quarter surgery in small animals under light GA
Post operative analgesia
Standing surgery in farm animals and horses
Post operative analgesia for above surgeries or injuries
Caudal Epidural Analgesia
Commonest technique in large animals
Inject slowly over 5-10sec
Iml/100kg 2% lidocaine
Max effect in 10 min - lasts c. 60 min
Useful in small animals – tail amputations, perineal surgery
Epidural Analgesia Complications
Accidental vascular injection
Haematoma formation
Subarachnoid injection
Infection
Hypotension
Respiratory depression due to cephalad spread
Nerve damage
Pruritis
Urinary retention
Motor dysfunction
Hypothermia
Supporting Anaesthetised Patients
Influence on outcome – evidence base
Ethical considerations
Common sense….
Supporting oxygenation: Indications
During all anaesthetics
Pre-induction
Recovery
Increased FIO2-
Methods
Flow by
Intranasal
Intratracheal
Tracheostomy
Incubator
Mask
Hypothermia during anaesthesia:
Hypothermia causes
Increased pain
Wound infection
Delayed recovery
Temperature falls due to
Reduced shivering
Vasodilation
Reset thermoneutral point
Behavioural modification
Open body cavity
Cold gases
Dry gases
Wetting and prep
Core temperature support
Active warming
Minimise heat loss
Circle systems (rebreathing system)
Pre-clip
Warm environment
Minimise wetting
Aim for short anaesthesia time
Drug choices?
Support of renal function during anesthesia
Fluids during anaesthesia
5 x maintenance.. Why?
10ml/kg/hr dogs (less for cats)
Estimated output 1-2ml/kg/hr
Measurement
Volume - use of collection systems
specific gravity
Minimal Support for anesthesia
Baseline monitoring
Oesophageal stethoscope
Finger on pulse
Ventilation rate
Monitoring record (BP, capnography, temperature)
Fluids and intravenous access
Oxygen
Analgesia
what breathing system would you use on a 5 kilo patient
a tpiece if you neet to ippv
a lack if not
what breathing system would you use on a 10 kilo or above patient
a rebreathing system
effiecine with lower flows
cant be used for patients lees than ten kilos due to valve and sodalime- resistance
minute volume (MV)
the volume breathed per miniute
on average this is 200ml per kg
risks of equine GA
duration of anesthesia corellates with increased risk
difficult to manage after and hour and a half
factors that effect duration:
-caseload
-skill of surgeon and staff
- current condition of surgeon and staff- time of day or week, have they had a break
why increased risk-
big
flighty
cardiopulmanory depression- nit designed to lie down
- experience with anesthesia- horse thats experienced it before is more acoustomed to it
specific risks- cardiac arrest, fracture (esspecially of a long bone- mares who have recetly had foals most at risk)
feild equine anesthesia
minor procedures
castration, sacrcoid removals ect
Total Intreveneous Anesthesia- TIVA
extra boluses of ketamine to maintain anesthesia
check the feild- stones, watercourses, batteries, holes, slopes, type of fence (barbed wire)- anything that could injusre horse as it goes down
draw up all drugs and palce iv cannula- get all equipment ready
fit horse with padded head collar
have help and a plan
administer drugs and induce anesthesia
position horse- if horse in lateratl, bottom forelimb forward, hind limbs parallel
hospital equine anesthesia
more majour surgery
horse is intubated-same as small animals but cannot visulise the larynx- use gag
endoscope up the nares could be used
dorsal recumbancy is maintianed when using oxygen in isofurane
monitor as usual
pre-oxygen rarly tolerated but used in very sick cases
theater equipmetn must be checked- hoist, inflatable beds
equine premed
aim is to produce a horse sedate enough for ketamine
could use propofol but requires large amount
healthy horses ofter recive acp intramuscularly- only drug assosiated with improved outcome- not good for colic due to vasodilation
iv jugular canula- want to place on uppermost side depending on surgery
alpha 2 agonists also used-
xylazine- quick acting, can top up, good for colics
romifodine- takes 5 to 10 mins, longest acting, less ataxia, could take too long. lasts 45 mins,
detomidine- interediate, lasts 45 mins, small volumes
can tell sedation by knocking on sinuses or indeifference to lip being touched
GGe- used in horses not healthy enough for an Alpha 2 (specifically for cardiovascular problems)- muscle relaxant
infuse IV until horse is “knuckling then give etamine and microdose of APHA 2
equine induction agents
ketamine-
dissociative
good anesthesia
must not be used alone- causes sezures
eyes remain open and central
can be used as top ups (dont exceed induction dose)- every 10-20 mins
takes 2 mins to go down
use head to guide which side horse goes down in
Used in combination with acepromazine, alpha 2 agonists, BZDs or guaifenesin (GGE)
give an example of the “recipe” for a GA eqine feild induction
ACP- wait 30-45 mins
detomidien IV- wait 5 mins, check heart rate (> 20 BPM), chek for adiquate sedation
diazepam/ katamine iv for induction
ketamine iv top ups every 8-15 mins or triple drip (GGE, Ketamine, Alpha 20
add 1/4 doese detomidine after 4/5 doses i using katamine alone
with ketamine continue to give top ups of alpha 2
problems suring equine anesthesia
arterial blood pressure
low PO2
high CO2- vetilate patient
bradycardia- common
tachycardia- rare
aponea
pain
movment
poor recovary
methods of equine hospital recovery
free recovery
rope recovery
anaesthesia of ruminents
licenced drugs for food animals must be considered
many orocedures done standing
usually achived via iv (calves cna be masked)
diffucult cows may drink chloral hydrate
iv cannula placment??
intubation of ruminents
small ruminents -direct visulisation
larger ruminents- intubated by palpation, developed skill
cuffed tubes- regurgitation risk! rumenants have a rumen!!!
induction of anesthesia in pigs
deep im (just behind ear- dont go into back or hindlimb), iv or mask with inhalant
ketamine, alfaxalone, propofol
ketamine combinations
malignant hyperthermia- rare condition of pigs. after exposure to inhalant, rapidly fatal- can be treated with drug
intubation is challenging- larynx is complex
anasthetic risk for rabbits
difficult to intubate- lidocane needed, big fleshy tounge
difficult to handle
lack of familiarity
sublinical disease
small lungs
prone to hypothermia
rabbit premed
if in doubt go low with dose
buprenorphine- 30 40 mins to peak if given Im
maintanence and monitoring or rabbits
difficult to monitor depth
gi support of rabbuts for anestheisa
gut stasis big killer
Why do we Encounter Dysrhythmias?
Older/sick patients
Multiple underlying conditions
Cardiovascular depression
Vasoactive drugs (which?), inhaled anaesthetic agents (effects?)
Hypothermia
Fluid loss
Overstimulation
Nociception
ECG triangle
lead 2 (left leg)- standard lead, most diryhtmias recorded in
lead 1(right arm)
lead 3(left leg)
ecg wave
p wave- atrial depolarisation
qrs complex- ventricular depolarisation
t wave- repolarisation of ventricals
qrs complex is bigger as it is a cordinated movmemt involving punjinke fibres. t wave is doen by individual myocytes
st segment should be at same level as baselinw but is often below- indicates myocardial hypoxia
a big q wave could mean a thickened intraventricular septum
ecg does not tell you anything about the pulse- Pulseless electrical activity can occur- electrical activity without actual beat of the heart
st segment depression indicates…
myocardial hypoxia
Dysrhythmia Interpretation
What is the rate
What is the overall rhythm
Is there a P for every QRS
Is there a QRS for every P
Are there aberrant (usually ventricular) complexes
What do the monitors tell you about the patient?
Sinus arrhythmia
Perfectly normal rhythm
Often seen in fit anaesthetised patients
Sign of high vagal tone?
Be careful of procedures that stimulate vagus such as ocular surgery
(1st degree) and 2nd Degree A-V Block
Occasional p waves with no QRS
Common to see
Can be caused by vagal stimulation or very ‘deep’ anaesthesia
Can be idiopathic
Commonly as a result of alpha-2 agonists
Very rarely HIGH dose opioids
Will be heard as missed heartbeats
Treatment?- do you need to?-
Is treatment necessary?
How would you decide?
If necessary, antagonise the alpha-2 agonist (or administer naloxone?)
Problem with this?
Decrease anaesthetic depth
If still no response and reduced cardiac output?
Consider atropine/glycopyrrolate
3rd degree AV block
P waves and qrs doing own thing
Artial pacemaker cells and avn are not working in sync
Impulse not originating in avn
REAL PROBLEM
Treatment while under anesthesia– Stop further deterioration, ensure all other parameters are normal- depth of anesthesia ect
pacemaker can be places
Atrail Fibrilation and ventricular ectopic
Gap of complexes different
Height of complexes different
No pause after ventricles contract
worring!!!
ventricular ectopic-electric signals in the heart starting in a different place and travelling a different way through the heart.
Treatment?
Stop further deterioration, ensure all other parameters are normal
Recover asap, ?amiodarone
Then cardiology
Rate control if there is underlying heart disease – medical mx
Electrical DC cardioversion may be an option
Ventricular premature complexes (VPCs) plus compensatory pause
Fairly regular but with a few ventricular ectopic beats- strange and occasional variation in size of qrs complex
Is the pause good or bad?
Treatment?
Check physiology – often due to hypoxia or hypercapnia. Sometimes low blood pressure
Add analgesia – may be due to nociception
Possible lidocaine if becoming frequent
Ventricular tachycardia (V tach)
Some normal beats
Others wide, abnormal ventricular beats
Ventricular tachycardia (V tach)
Often a deterioration of SVT – treat underlying cause
Often as a result of sepsis or a major underlying condition
May deteriorate into ventricular fibrillation (often fatal)
Treatment = underlying cause, lidocaine, amiodarone, magnesium
Ensure all other parameters normal
Ventricular escape
Triphasic qrs
Actually quite normal
Ventriclas are firing to restart normal rhythm
Would you treat this?
Possible due to alpha-2 agonists or high dose opioids?
What would you do?
Treat cause otherwise ensure all other physiology is normal- probebly no nead to treat
Whatever the Cause of abnomal ECGs, you should always
Apply First Principles..
Check physiological parameters and correct if possible
Oxygen, carbon dioxide, temperature, heart rate
External factors and correct if possible
Blood loss, surgery, nociception, drug reaction (contrast for example)
Antagonise drugs (or add more – nociception)
Finish surgery as soon as possible – into ICU
Imaging Modalities for imaging the thorax:
Radiography
Widely available
Non-invasive
Time and cost-efficient
Ultrasonography (echocardiography- imaging the heart)
Complementary
First choice for cardiac disease
no good if lungs are full of air
Computed Tomography (CT)
Where radiography and US fail
Higher sensitivity
Assess technical quality
Positioning
Centring/Collimation
Exposure factors
(Inspiratory)
Labelling
No Artefacts
Restraint
methods for imaging the thorax
Chemical
General Anaesthesia-
Avoids voluntary patient movement
Allows control of respiratory movement
Facilitates good oxygenation
Increased atelectasis of the dependent lung
Sedation-
Safer if suspect CVS or pleural disease e.g. butorphanol
Can lead to respiratory depression (so monitor and flow by O2)
No control of respiration
Physical restraint alone – does not mean manual restraint
Difficult to get good quality images
Rabbit burrito/cats in resp distress in a box can work well.
how do you decide which views to take on a radiograph
A minimum of 2 orthogonal views
Beyond that – case dependent!
Routine (inc cardiac) cases – RL and DV
Screening for metastases RL + LL + VD/DV
Specific lung pathology – RL + LL + VD
Appearance unclear on one lateral and DV/VD – take the other lateral
taking a right lateral view
Right lateral preferred
Cardiac silhouette position more consistent
Diaphragm obstructs less lung field
More lung between cardiac silhouette and thoracic wall
Position:
Right lateral recumbency
legs secured cranially, neck extended
foam wedge to prevent rotation
Centering/Collimation
Centre beam slightly caudal to caudal border of scapula
Collimate to thoracic inlet, thoracic spine, sternum and diaphragm (cranial abdomen)
taking a ventral dorsa/ dorsal ventral view
DV/VD centring/collimation
Ensure symmetrical positioning with spine and sternum superimposed (to avoid axial rotation)
Centre beam in midline, at level of caudal border of scapula
Collimate to thoracic inlet, diaphragm and body wall (skin edges) – unless investigation requires otherwise.
vd
Heart rotates to one side and distorts shadow
May produce better pulmonary detail
Can see more of the lung fields
dv
Safer in dyspnoeic patient
Heart lies in anatomically correct position – easier to interpret cardiac silhouette
Timing of exposure when imaging the thorax
Aim for peak inspiration:
Diaphragmatic line straight dorsally – T12/13
Expiration:
Diaphragmatic line domed, increased contact with CS
– T10/11
Avoiding movement blur when imaging the thorax
Good restraint
Good radiographic technique
Exposure time - High kV / low mAs technique
Relevant to film radiography
Low mAs minimises exposure time
High kV reduces the high contrast appearance of the thorax
Less relevant with digital radiography
Use a grid if thickness > 10cm
Controls scattered radiation
Timing of the exposure
At peak inspiration
May need to use the expiratory pause in a conscious panting animal
Radiopacities
The five basic densities:
Metal – White (all x-rays absorbed – most opaque)radiopaque
Bone – nearly white
Soft tissue/Fluid – mid grey
Fat – dark grey
Gas – very dark/black (few x-rays absorbed – most lucent)- radiolucent
Border obliteration
How visible is the border of the structure being evaluated?
Structures of the same opacity which are in contact will appear as one shadow
Border obliteration
(silhouette sign or border effacement)
Mass effect
Displacement of structures due to adjacent space-occupying lesions
e.g. fluid or mass
Interpretation of thoratic Radiology
1.Assess technical quality (Pink Camels..)
- Assess the respiratory system
- Assess the cardiac silhouette
- Assess everything except the heart and lungs
General Principles:
Be consistent!
Ensure you evaluate:
Thoracic boundaries
Pleural space
Lower airways and lung fields
Mediastinum
Heart and blood vessels
Always ask:
Is the radiographic diagnosis consistent with clinical findings?
Is the quality of the radiograph adequate to permit a confident radiographic diagnosis?
Roentgen Signs
Number
Location
Size
Shape
Margination
Radiopacity
Pulmonary Vasculature on imaging
Normal vasculature
Normal pulmonary vessels are clearly visible in central and middle zones
Vessels taper towards the periphery
In lateral view
Artery is dorsal to bronchus and vein
Veins are ventral to bronchus and artery
In DV view
Veins are medial to arteries
so.. veins are ventral and central
Lung Patterns on imaging
Lung disease
different characteristic radiological appearances depending on which component of the lung is affected.
Known as lung patterns:
Bronchial
Alveolar
Vascular
Interstitial
Diffuse
Nodular
lung varitation Dogs vs Cats
In dogs, caudodorsal lungs very close to spine, right up to the tip
In cats, diverge slightly from the spine around caudal T11/cr T12 due to the larger sublumbar muscles
Cardiac Silhouette
Assess the cardiac silhouette
Generalised enlargement
Individual chamber enlargement:
left atrium
right atrium
Left ventricle
Right ventricle
Change in great vessels
VD
Diaphragm often appears as 3 ‘humps’
Distance between diaphragm & heart is greater than for DV
Better visualisation of accessory lobe
Gas should be in the pylorus
Right and ventral
DV
Diaphragm appears as a single dome
Gas should be in the fundus
Left and dorsal
Normal Heart Size - Cat
Cat - Normal width (DV)
< 2/3 width of thorax
Normal short axis (lateral)
= cranial 5th rib to caudal 7th rib
Normal long axis (lateral)
2/3 height of thorax
Vertebral Heart Scores
Leanghth + Width = VHS
Normal values:
Dog = 8.5 – 10.5
Cats = 7.5
Pericardial Effusion on imaging
Cardiac silhouette grossly enlarged
Globoid appearance
Ultrasound = sensitive indicator!
Pneumothorax on imaging
Lung retraction from thoracic wall
Space between heart and sternum
Example recipe for GA Hospital
Acepromazine im, wait approx 30-45 minutes
Detomidine iv, wait 5 minutes, HR>20 bpm, adequate sedation must be apparent
Diazepam/ketamine iv for induction (can use ketamine alone)
Intubate, maintain on isoflurane in oxygen
Monitor depth, keep ABP > 70mmHg, and PCO2 <60mmHg IPPV if necessary. Sedate for recovery
Achieving a secure airway in a rabbit
Obligate nasal breather
need to disengage the soft palate from the epiglottis to visualise larynx
Big fleshy tongue
Narrow gape
cheeks
VERY sensitive larynx
I always use lidocaine spray prior to an ETT
Depth Test - jaw tone??, tongue withdrawal (care), cough when local applied to larynx. Breath holding vs apnoea.
Raise the head and extend the neck to disengage the soft palate
Ideally visualise the larynx to intubate the patient
apply local to larynx
otoscope/laryngoscope
slightly curved ET tube, no cuff
~1 mm diameter for every kg bw
Right parasternal long-axis view
obtained with the transducer in the parasternal window with the transducer index mark pointed toward the patient’s right shoulder (10 o’clock) in the third or fourth intercostal space.
Depth of an ultrasound
this adjusts the field of view (the real-time image should fill the field)
Gain of an ultrasound
power (high gain = white image)
Sector Width of an ultrasound
(the smaller the sector angle, the faster the frame rate and the higher the resolution of the real-time image)
Sector width affects frame rate.
The narrower the width, the higher the frame rate.
Focus of an ultrasound
make sure you place the focal point at the depth level of interest on the image
Right-sided ultrasound views – why do we want them?
Subjective assessment of chamber size and systolic function
Evaluate the mitral and tricuspid valves
Measure chamber size (particularly the left ventricle and left atrium)*
Evaluate some measurements of systolic function
How to perform a basic echo exam
PREPARATION
clip fur
dont sedate when posible
ECG trace – don’t worry about where your ECG clips are. You just want the timing intervals.
Remember your cardiac cycles.
Beginning of the QRS is end-diastole.
End of the T wave is end-systole.
Choose the correct transducer according to patient size.
Palpate the apex beat prior to scanning.
POSTURE – avoid twisting to look at the screen. Use an arm rest. Try to relax and DON’T PRESS TOO HARD! Use more gel….takes a few minutes to soak in.
Try to ultrasound as many patients as possible to get a good technique and develop consistency. PRACTISE!
Understand cardiac pathophysiology well.
make sure image fills screen
obtain Right Parasternal Long-axis Four Chamber View- asses systolic function: Interventricular septum, Interatrial septum, Mitral valve
Watch the left ventricle contract
turn thumb and tip probe till left ventrical is curcular- Right Parasternal Short-axis View (papillary muscle level)
tip transducer upwards ot visulise mitral valve- fish mouth view
tilt it further to visulise the aortic valve
Measurements – How to Make Them on an echocardiogram
As a general rule, measurements should be taken from 3 cardiac cycles then averaged.
Most importantly, ensure that the view is correct and well aligned before taking any measurements. It is best not to make measurements if your image is substandard.
Fractional Shortening
FS (%) = (LVDd – LVDs)/ LVDd
LVDd=Left ventricular internal diameter during diastole
LVDs=Left ventricular internal diameter during systole
FS% is affected by many external factors therefore has its limitations
standard reference ranges can be obained
measure of contractillity and function
can be effected by preload, afterload and contractility
Cornell measurement
When assessing LV diameter, use published breed specific reference ranges when possible, however, these are not always available OR the dog may be a cross breed. What then?
LVDd=Left ventricular internal diameter during diastole
For those dogs which are cross breeds are pure bred dogs with no published reference ranges available, then the “Cornell method” scales the LVDd (cm) to bodyweight (kg).
Cornell formula; LVDd cm/BWˆ0.294
For the “EPIC Study”*, dogs were classified as having enlarged left ventricles when the LVDdALLO was >1.7
E-Point to Septal Separation (EPSS)
an easy measurement to obtain that is accurate in estimating the LVEF. EPSS is measured in the parasternal long axis view (PLAX) of the heart, which gives a view of the left ventricle and is often used to assess its function.
sensitive and specific for ventricular function
Indications for Echocardiography
Investigation of a heart murmur*.
Investigation of breathlessness, cough and/or collapse.
Investigation of an arrhythmia.
Investigation of a gallop rhythm.
Investigation of the presence, significance and cause of pericardial disease.
Investigation of ascites or pleural effusions whereby noncardiac disease has been excluded.
Investigation of unexplained pyrexia.
Breed screening (in particular for preclinical dilated cardiomyopathy).
Assessment pre-chemo.
Eupnoea
Normal respiration
Tachypnoea
Increased respiratory rate (not necessarily depth)
Apnoea
Absence of respiration
Hypoventilation Hyperventilation are both examples of
Alterations in ventilation at the alveolar level
Hypercarbia
Increased CO2 in blood•Hypoventilation•Incprodnof CO2Primary drive for respiration
Hypoxaemia
Decreased O2 in blood•Poor O2 intake•Hypoventilation•Increased O2 consumption•Decreased O2 carrying capacity
Differentials for tachypnoea
Primary cardiac disease
Neurological disease- Damage to respiratory control centre
Metabolic disease- Acidosis/alkalosis, Increased PaCO2
Hyperthermia- Cooling mechanism
Stress
Pain
Abdominal discomfort- Restricted movement of diaphragm
Primary respiratory disease
OBSTRUCTIVE RESPIRATORY PATTERNs
LRT Obstruction- Thickening, inflammation and mucus
Causes increased expiratory effort
Small airways held open during inspiration
Early collapse during expiration
e.g asthma
positive pressure of inspiration created allows easire passage of air. experation needs more effort
dont get stertor or sridor with this pattern
URT Obstruction- Causes marked inspiratory effort
Dynamic collapse of soft tissues due negative pressure associated with inspiration
Inspiratory STRIDOR or STERTOR
as animal breathes in, negative pressure is created meaning there will be more effort needed to inspire than expire with this pattern
Restrictive Respiratory Pattern
Expansion of the thorax restricted> Decreased tidal volumeTachypnoea / short-shallow breaths> Hypoventilation
restriction can be in lungs, in pleural space or withing ribs or diaphram.
Paradoxical Respiratory Pattern
results form significant trauma to the ribcage
road traffic accidents
Paradoxical movement of the chest wall: -Trauma –“Flail” chest
-Terminal respiratory failure –fatigue of muscles
SEROUS
Nasal Discharge
Inc. nasal secretionsAllergic rhinitisAcute InflammationViral infection
MUCOID nasal discharge
Nasal Discharge
PURULENT Nasal Discharge
Bacterial infection1o or opportunisticpathogen
HAEMORRHAGIC Nasal Discharge
TraumaClotting disorderVascular diseas
Nasal Discharge
Can be difficult to identify
•Intermittent nature
•Cleaning / Licking of nasal planum
Character of the discharge + Unilateral or Bilateral Presentation + Knowledge of common diseases
URT Origins (usually unilateral)-
•Nasal cavity
•Paranasal sinuses
•Guttural Pouch (horses)- could be bilateral
•Nasopharyngeal - could be bilateral
•Trachea- could be bilateral
LRT Origins ( will be consistantly and evenly bilateral)-
•Bronchoalveolarspace
•Oedema, Pneumonia
•Pulmonary vasculature
•Haemorrhage
Coughing
Upper respiratory tract-
•Harsh, dry, hacking cough
•Tracheitis or tracheobronchitis
•Often productive
Lower Respiratory Tract-
•Soft, chesty cough
•Pneumonia
•Lower airway inflammation
•Cardiogenic
Respiratory Sounds
Normal:
Tracheal / Bronchovesicular-
•Normal air movement through airways
•Increase airflow > Harsh intensity
Abnormal:
Wheezes-
Air passing through narrow airways
Bronchoconstriction
Crackles/Rales- Air passing through fluid
Oedema, harmorrhage, pneumonia
Dull/Absent- No air movement though lung
Pleural rubs Friction between pleural surfaces
Systematic auscultation- larynx, trachea, multiple points thorax: craniodorsa, caudodorsa, Hilus, cranioventra
Accentuating Respiratory Sounds
Adventitious noises can difficult to detect during normal: respiration-
•Subclinical inflammatory airway disease / asthma •Interstitial disease
Re-breathing exam (plastic bag over horses nose) -Increase tidal> volumeIncrease air flow> Accentuate adventitious noise
PERCUSSION- assessing resonance of air-filled structures
Thoracic percussion–Lung Parenchyma•Pulmonary consolidation•Pleural fluid accumulationGenerally used as adjunct to auscultation
Sinus percussion-
•Altered resonance in paranasalsinuses •Fluid / pus
•Cysts / Masses Very useful assessment in horses
what is visualised in an endoscopy
Nasal meati
Nasopharynx
Ethmoid turbinates
Nasomaxillary opening
Guttural Pouches
Trachea
can be done without sedation in horses, and possibly while ridden (dynamic endoscopy)- can diagnose Laryngeal Hemiplagia (recurrent laryngeal neuropathy)
Laryngeal Hemiplagia
(recurrent laryngeal neuropathy)
Common cause of poor performance in race horses
•Also occurs in dogs, in association with hypothyroidism
paralysis of larangel cartilages, usually of the recurrent laryngeal nerve
RHINOSCOPY
used to investigating URT disorders
Restricted access in small animals-
•Rigid rhinoscope
•Narrow-bore flexible endoscope
•Otoscope
Indications-
•Nasal foreign body
•Nasal mass –biopsy
RADIOGRAPHY to Investigate URT disorders
Commonly used to assess paranasal sinuses-
Lateral, dorsoventral and oblique projections
Cheap•Quick•Readily available•Doesn’t usually require GA•Excellent for assessing lung parenchyma
Identification of;
•Fluid accumulation in sinus (sinusitis) (fluid line)
•Soft tissue masses
•Distortion/destruction of normal bony architecture
Nasal / Nasopharyngeal Swab
Not appropriate as a screening tool-
•Wide array of commensal bacterial flora
•Contamination of sample is impossible to avoid
Only use for identification/isolation of specific pathogen(s)-
•Virus identification
•Bacterial isolation
-Streptococcus equi equi, Influenza, herpes, IBR
nvestigating LRT disorders using radiography
Cheap
•Quick
•Readily available
•Doesn’t usually require GA•Excellent for assessing lung parenchyma
1.Ensure good (and safe) positioning
2.Obtain 3 standard views if possible- RL, LL. DV
3.Expose on inspiration
Radiographic Patterns- Interstitial
•Interstitiumis the space between the alveoli and capillaries
•Interstitiumbecomes more prominent
•Air still present in alveoli and normal vessels seen
Diffuse(unstructured) -e.g. oedema/ diffuse lymphoma. the tissue around the broncheoles is more radiodense
Nodular –e.g. soft tissue mass ie. neoplasia/abscess- tissue around bronchi is more radiodense but in a more “smattered” pattern
Underexposure, expiration or obesity can look similar –often misdiagnosed
Bronchial Radiographic Patterns
Thickened bronchi
•Infiltration/mineralisation of bronchial walls or due to peribronchialchanges
•Classical ‘donuts’ or ‘tramlines’
•Bronchi may be more obvious in the periphery of the lungs where normally wouldn’t be seen
Alveolar Radiographic Pattern
Consolidation or collapse of alveoli
Air in alveoli is replaced by fluid (oedema/haemorrhage) or cells
Air bronchogram is commonly seenCan be focal or diffuse
Examples; bronchopneumonia, aspiration pneumonia, oedema, haemorrhage, neoplasia, lung lobe collapse or torsion
Vascular Radiographic Pattern
Any changes to the size, course or opacity of the pulmonary vessels
•Vessels may be larger or smaller than normal or may be tortuous
•Commonly seen associated with cardiac disease
•Tortuous vessels seen with heartworm
•Differentials depend on vessels affected
Pleural Disease
Pleural effusion:
•Fluid in the pleural space
•Transudate, exudate, haemorrhage, chyle
Pneumothorax:
Air in the pleural space
Both cause lung edges to move away from the thoracic wall
investigating LRT disorders- ULTRASONGRAPHY
Cheap
•Very Quick
•Readily available
•Ideal where sedation/GA is contraindicated
Excellent for assessing; •Pleural space
•Pleural effusion
•Diseased lung tissue
RESPIRATORY SECRETION SAMPLING
investigating LRT disorders
TRACHEAL WASH-
Sampling of tracheal mucus
Trans-endoscopic
Trans-tracheal
Representative of tracheal secretions and ascending lower airway secretions- wont tell if left lung/ right lung
Cytology + Culture
BRONCHALVEOLAR LAVAGE-
Sampling of bronchoalveolarspace
Trans-endoscopic
Blind
Cytology only
Syncope
another word for fainting or passing out
Cardiogenic syncope
Intermittent, profound hypotension resulting in marked reduction in blood flow to brain
Estimated blood pressure fall ≤50%
Arrhythmia:
Asystole – sinus arrest or ventricular standstill
Marked reduction in cardiac output – rapid V Tach
Duration 10-30 seconds:
Activity level and presence/ absence structural heart disease
Pulmonary hypertension
Most common cause bradyarrhythmias
Might be intermittent
Pre-syncope/ episodic weakness
Intermittent, profound hypotension resulting in reduction in blood flow to brain
BUT lesser degree of hypotension cf. syncope
Arrhythmia:
Less rapid v tach
SVT
Less profound bradyarrhythmias
Structural heart disease and pulmonary hypertension may exacerbate- Excitement/ exertion
Bradycardias
Disorder of impulse formation and conduction systems of the heart
Dogs <60bpm and cats <100bpm
Bradycardias to consider:
Advanced AV block (High grade 2nd degree and 3rd degree)
Sinus arrest
Atrial standstill due to hyperkalaemia
Persistent atrial standstill
Can be drug induced:
ACP
Opioids
Alpha2-agonists
B-blockers, calcium channel antagonists and potassium channel blockers are all c/i in sinus bradycardia, SSS and AVB greater than 1st degree
Sinus bradycardia usually high vagal tone and does not result in syncope
Tachycardias
Supraventricular and ventricular tachycardias
Dogs >160bpm and cats >200bpm
Supraventricular tachycardia
Most common is atrial fibrillation (AF)- New onset – weakness, collapse or syncope. no consistent p waves
loss of atrial contraction and also variable diastolic filling time reduce CO
SVT is an umbrella term-AF, accessory pathways, atrial flutter…
Regular SVT less common cause of syncope- less syncope because regular rhythm and activation of the heart is normal sequence.
Ventricular tachycardia-
Boxers and Dobermanns
Can drop CO dramatically
Sudden death – more so when abnormal function of LV
drop of CO due to short diastolic filling time, lack of atrial connection, aberrant sequence of ventricular activation
Neurocardiogenic syncope
Also called vasovagal syncope
Profound hypotension due to combination of bradyarrhythmia AND vasodilation
Sudden autonomic nervous system failure
Withdrawal of sympathetic tone
Abrupt increase in vagal tone
Triggering events are variable
Coughing (tussive)
Excitement e.g. excited boxer
Situational e.g. micturition, defecation, vomiting, sneezing…
Exacerbated by structural heart disease (SAS) or concurrent GIT disease
Neurally mediated syncope represents an exaggeration of the CV reflexes that normally control the circulation. Syncope occurs when these reflees intermittently become inappropriate in response to a trigger. It is likely that dogs that suffer this type of syncope have some sort of disorder of autonomic control.
Remember that bradycardia can occur on its own as can vasodilation or they can occur together. The degree to which one predominates over the other will vary and persist to differing degrees.
The medulla is the control centre of the reflex.
Neurocardiogenic syncope is an adrenergically stimulated vagal reflex bradycardia/ Vagal mechanoreceptors (C-fibres) initiate the reflex when stretched- they are found in the in the ventricle, LA and LA-PV junction and Pas
Triggered by fight or flight scenarios
Apparently healthy individuals or predisposed individuals:
Genetics
DCM
High preload
Diagnosis often presumptive
Common situation is exertion/ excitement in small breed dog with advanced MMVD-
Hyperdynamic ventricle – increased by sympathetic surge
Vagal afferents when suddenly stretched trigger reflex
In this cohort it is often a sign of v high preload and impending/ overt CHF
Can also occur on diuretics if preload reduced too much
Diuertics is usually treatment of MMVd and syncope associated with high preload. Although if over diurese can cause syncope due to empty ventricle
Boxers-
Bimodal age at 6-24 months 0r 7-10 years
Triggered by exertion with excitement
Older Boxers also ARVC!
Both can occur in same dog
Situational syncope-
Easily identified trigger e.g. cough
Common in small, middle-aged or elderly dogs
Often associated with tracheal/ bronchial compression or big LA
Tussive syncope – transient bradycardia +/- reduced cardiac output
Cats with HCM- On exertion
Pulmonary hypertension, outflow tract obstruction (pulmonic/ sub-aortic): Severe - exertional syncope due to inability to increase RV output
Impaired right-sided inflow:
Compression, pericardial effusion with tamponade
Hypoxia and hypoglycaemia (insulinoma)
Severe anaemia with exertion
Exercise induced – Labradors, Border collies
Non-syncopal collapse
Wide range of diseases
Difficult to differentiate from cardiogenic/ neurocardiogenic
Neurological conditions
Profound hypoxaemia-
Can also have tussive syncope
Metabolic disorders-
Hypoadrenocorticism
Hypoglycaemia
Diagnostics for syncopy
Blood tests-
Complete blood count
Biochemistry & electrolytes
Cardiac troponin I
NT-proBNP?
Basal cortisol?
Fasted glucose level?
Ammonia/ BAST?
Thyroid panel?
Blood pressure -Especially if present collapsed
ECG- Bradyarrhythmia
Tachyarrhythmia
Thoracic and abdominal imaging-
POCUS
Radiography
Abdominal ultrasound
Echocardiography-
Structure and function
Viral causes of livestock respiritory diseae
In cattle the most common viral causes of pneumonia are Parainfluenza 3 (PI3) and Respiratory Synctial Virus (RSV).
IBR can affect any age of stock but is rarely found in young calves. In the endemic setting it is insidious, causing low grade respirator disease in stock. The real problems are seen when it enters a naive population as it causes severe disease and transmits rapidly. Following infection it becomes latent in the cows cells, recrudescing at times of stress.
Bovine viral diarrhoea virus (BVD) as the name suggests doesn’t cause respiratory disease directly but it significantly affects the immune system opening the door for other pathogens. It is therefore commonly considered as part of the respiratory disease complex.
bacterial causes of livestock respiritory diseae
Mannheimia haemolytica
Pasturella multocida
Histophilus somnus
Mycoplasma spp.
Others
A variety of bacterial pathogens can act as opportunistic pathogens but we commonly recognise four bacterial species as causing respiratory disease in cattle. M.haemolytica is probably the most significant and most severe. It can act as a primary disease agent, particularly at times of stress (shipping fever), but frequently is the sequel of viral infections. This is also true of P.multocida and H.somnus. Mycoplasma is increasingly recognised as a cause of respiratory disease in all ages of stock, both primary and secondary.
As already discussed, these pathogens rarely act in isolation and diagnostic samples (eg post mortem) yielding these pathogens does not necessarily make them the instigating agent. Possibly the greatest significance of the bacterial species involvement is to explain why we use antimicrobials in the treatment of respiratory disease and why we see different response rates to different antimicrobials on different farms.
fog fever
respiritory disease
Trypthophan toxicity
Fog fever is seen rarely in cattle grazing lush pasture. It is due to an excess of tryptophan in the diet which the animal can’t process quickly enough resulting in toxic damage to the lungs
Farmers lung
respiritory disease
Allergic reaction to moulds
Two Main Causes of Coughing
CARDIAC DISEASE
Cardiomegaly causing left mainstem bronchus compression
Congestive heart failure (fulminant pulmonary oedema)
RESPIRATORY DISEASE
Upper airway dz(laryngeal paralysis, BUAS, tracheal collapse)
Lower airway dz(infectious/ inflammatory/ neoplastic)
CLINICAL EXAM IS SO IMPORTANT
HEART FAILURE (HF)
HF = a clinical syndrome where cardiac output and tissue perfusion are maintained at the expense of increased cardiac filling pressures.
-Forward and backward failure
-Right-and left-sided heart failure
-Systolic and diastolic failure
-Acute and chronic heart failure
will cause drop in blood pressure and therefor trigger THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS)- causes vasoconstriction and odema
AETIOLOGIES of heart failur
-Chronic Myxomatous Mitral Valve Dz/CMVD -Dilated Cardiomyopathy/DCM-Hypertrophic Cardiomyopathy/HCM-Pericardial Effusion/PE-Restrictive Cardiomyopathy/RCM
AETIOLOGIES•Patent DuctusArteriosus•Mitral Valve Dysplasia•Tricuspid Valve Dysplasia•Pulmonic Stenosis
aCUTE HF: TREATMENT
OXYGEN
IV FUROSEMIDE- im if too stressed
MINIMAL STRESS
PIMOBENDAN- vasodilator, increases contractillity
waht to look for in a radiograph to diagnose heart failure
1.Is there cardiomegaly? vhs greater than 8-10 in dogs
2.Is there left atrial enlargement?
3.Is there tracheal elevation?
4.Is there an abnormal lung pattern?
5.Are the pulmonary vessels normal?
Signs of heart failure
Cough (do not trust this as a sign of HF)
Dyspnoea (not always detected by the owner)
Increased sleeping respiratory rate (SRR)
Exercise intolerance
Non-cardiac causes of NT-proBNP
Systemic hypertension
Hyperthyroidism
Renal failure
Calculating the drip rate
The steps to calculate the drip rate are the following..
Calculate the hourly rate according to the total volume requirement (more on this later)
This is all you need to input if you are using an infusion pump
Calculate the minute rate: divide the hourly rate by 60 minutes
Calculate the drops per minute: multiple the minute rate by the giving set drip factor
Calculate the drops per second (drip rate): divide the drop per min by 60 seconds
Creating a fluid therapy plan
Step 1 – Resuscitation
If shock is present step 1 must be followed first. When the patient no longer shows signs of shock, or if no shock is present, move to step 2.
Step 2 – Rehydration
Is the patient is showing signs of dehydration?
Step 3 – Maintenance
Is the patient is not eating/drinking normally?
Step 4 – Ongoing losses
Does the patient have continuous fluid losses (e.g. vomiting)
To create a fluid therapy plan:
- Deal with Step 1 first if required. Stop when the patient no longer shows signs of shock.
- Work out if Steps 2, 3 and 4 apply to your patient. If they do, calculate the volume of fluids needed in each of the Steps 2, 3 and 4 and then add them together. This total must be administered in 24-48 hours.
Monitor the patient to guide continuity of fluids, identify complications and resolution of clinical signs.
Fluid deficit in dehydration is determined by:
Fluid deficit (litres) = Body weight (kg) x % dehydration (as a decimal)
fluid defecit of a patient with No clinical signs, but patient has history of fluid loss
<5%
fluid defecit of a patient with Tacky mucous membranes, ? Thirst,
5-6%
fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT
6-8%
fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT plus Increased pulse rate, cold peripheries
8-10%
fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT, Increased pulse rate, cold peripheries plus prolonged CRT, Tented skin stands in place, Pulses weak
10-12%
fluid defecit of a patient with Collapse, signs of hypovolaemic shock
12-15%
Which route/s might you use to administer fluids to your patient if Dehydration is severe
Intravenous
Which route/s might you use to administer fluids to your patient if it is a Mild case of dehydration
Oral.
Subcutaneous.
The aim of the maintenance step in the fluid therapy plan is to
provide the daily requirements of water and electrolytes lost by sensible and insensible losses for patients that are not eating or drinking normally.
Normal losses of fluid
Insensible e.g. Sweating, panting
Sensible e.g. Urine, faeces
Abnormal fluid losses
Usually secondary to illness
E.g. vomiting, diarrhoea, blood loss, inappetence
Maintenance volume can be calculated in two ways:
Estimate of sensible + insensible losses= 40-60ml/kg/day (2-2.5ml/kg/hour)
(tend to use the higher end for small dogs and lower end for large dogs – this method can under/over estimate requirements)
Accurate method (used in patients <2kg or >40kg)= Daily fluid requirement in ml = Body weight (kg) x 30 + 70
The volume is administered over a 24-48 hour period
The patient must be constantly re-evaluated to assess for signs of over hydration
Ongoing losses can also be estimated as:
0.5ml-2ml/kg/hour
Ongoing losses
This step is to try and replace any abnormal loss of fluids to continue in the next few hours-days. E.g. diarrhoea doesn’t generally stop as soon as they start treatment, it can take a while!
Ongoing losses can be estimated visually or measured directly (e.g. Urine production via urinary catheter or by patient weight loss after an additional fluid loss)
Ongoing losses can also be estimated as:
Patients must be reassessed in 4-6 hrs to check if volumes need to be adjusted
Aims of fluid therapy
Maintenance of normal physiology – e.g. during anaesthesia. many patients will not drink at vets so will be fluid deficient
Improvement of organ function e.g. kidney, heart, liver
The correction of electrolyte disturbances
The correction of hypovolaemia- blood loss
The correction of acid base disturbances
(Total parenteral nutrition (TPN) - usually partial parenteral nutrition (PPN) used in animals)- not commonly done in adult animals
Is there a requirement for therapy? (ie assess patient, consider losses)
What type of fluid?
Which route?
What volume?
How fast?
When to stop? End points?
replace like with like- heatstoke= water loss so replace water
parameters to asses Perfusion status and hydration status
Pulse quality
CRT
Heart rate
Demeanour- collapse ofter due to hypovolemia
Skin tent
Blood pressure
Mucous membranes
Eye position- eyes will sink and third eye often prolapses with dehydration
What is the daily maintenance rate for an animal?
2.5ml/kg/hour
≈60ml/kg/day
{Or (30 x Kg) + 70 ???}
Factor it into your plan
Types of fluid
Crystalloids (hypotonic, isotonic, hypertonic)- electrolites in water that mimic plasma without protien and cells
Colloids- protien in water. mimics plasma without electrolytes and cells
Blood products- HBOCS (hemoglobin-based oxygen carrying solutions) –££ & problems….
heartmans if first line fluid
Isotonic Crystalloid fluids
Isotonic-Lactated Ringer’s solution (LRS) aka Hartmann’s
Na+ 130 mEq/l , Cl– 109mEq/l
Buffered, contains lactate as a bicarbonate precursor- treats and controls acidosis
Inadequate potassium for long term therapy- pk for hypokolemic patients as potassium lever lower than plasma so dilutes plasma levels
Good for shock, diuresis, during anesthesia & can use for maintenance (can add other things to it)
Only 25% remains in vascular space after 12 minutes- need to give more tan you think
If in doubt, choose Hartmann’s!
Hypotonic crystalloid fluids
0.18% NaCl
0.18% NaCl + 5% glucose
Do you really want to use this ???
Hypertonic saline- crystalloid fluids
!!! can easily be mistaken form heartmans and will cause issues!!!
Draws water from interstitial space
Transient effect (10-15 mins)
Rapid restoration of MAP, increased myocardial contractility, CO & oxygen delivery
2ml/kg over 10 min, can repeat once but must follow with isotonic fluids
More commonly used in large animals (e.g. prior to colic surgery) but can be used in dogs and cats (carefully)
Also used in severe life-threatening raised Intra Cranial Pressure
Used in GDVS and colic surgeries
Treatment of raised intercranial pressure
follow up with normal crystaline to restore fluid
Fluid type - colloids
Support circulating blood volume better than crystaliods
e.g. severe hypovolaemia, haemorrhage, hypoproteinaemia
Exert a colloid osmotic pressure
More rapid initial re-expansion of volume
Only 1/4 of crystalloid administered remains in circulation in 40 mins
Support circulation longer than crystalloids
Types
artificial -gelatins, dextrans, starches, HBOCs
natural colloids e.g. albumin, plasma
However, no evidence of clinical superiority
over crystalloids
colloids good for volume expansion
Oxypolygelatin
Dextran 40
Pentastarch
Hetastarch
Albumin
Whole blood
Plasma
colloids good for half life
Hetastarch
Dextran 70
Pentastarch
Dextran 40
Oxypolygelatin
Colloids – Gelatins (ntk)
Oxypolygelatins
Plasma half life 2-4 hours (manufacturer data)
Weight average 30,000 D -pulls an equivalent volume of water from interstitial space
No need for concurrent crystalloid but often do give both
Produces osmotic diuresis
No direct coagulation effects
15 ml/kg total
Colloids – starches (ntk
Plasma half life 25 hours (hetastarch) - due to molar substitution
Initial elimination by tissue uptake
Excretion by metabolism - serum amylase rises
Volume expanded by volume given
Reversal of microvascular permeability
?anti inflammatory effect ?
Direct coagulation effects
Increased APT in dogs (factor VIII precipitation)
Anaphylaxis in 0.0005-0.085% human patients
Nausea and vomiting in cats - slow administration
Up to 40 ml/kg/day
Fluid type – blood products
‘Natural’ colloids
Chosen according to clinical requirement-
Whole blood
pRBCs
Ffp
Cryoprecipitate
Match the fluid to the loss
Replace like for like-
Blood issue?- blood
Liver issue?- plasma
Breaking down red cells? – give packed red cells
Oxyglobin Solution
purified bovine haemoglobin
given to patients without enough red cells to increase oxygen capacity of the blood
very expensive
supply scarse
cause patients to pee hemoglobin
very potent colloid
Intravenous access for fluid therapy
Commonest route used
Relatively simple to master
Consider the different veins that can be used e.g. cephalic, saphenous, jugular, auricular, lateral thoracic
Select large bore cannula (flow α r 4)
more concentrated the solution the less it likes proliferal vein- dextrose
Complications can & do occur
Extravasation
Thrombosis
Thrombophlebitis
Infection
Emboli
Exsanguination
routes for fluid therapy
Oral- best
Rectal
Subcutaneous- good for small furries but not great option
Intraosseous- puppies and kittens particularly. can be treated by vein. lots of LA
Intraperitoneal- experemental situations- rats ect
intravenous- most common
Volume and rate of replacement of fluid
Calculate total deficit (% fluid deficit + losses – see earlier charts)
Add on maintenance fluids
Acute (replace ½ total deficit over first 1-2 hours) then consider rate thereafter (over 24 or 48 hours) – keep monitoring ins and outs
In cases of shock can give 60-90ml/kg/hr (<1hr though, and MUCH less in cats)
Chronic losses – replace over 3-4 days
OR BASE RESPONSE ON CLINICAL SIGNS!!
Monitor regularly and respond to changes
Anaesthesia - Why Give Fluids?
Intravenous fluid therapy is generally recommended for any anaesthetised patient
The aim is to maintain circulating volume to ensure adequate perfusion and oxygen delivery to organs
Allows an ‘open vein’
Ancillary drugs/PIVA
Emergency situations
helps negate bad effects of anesthesia-
Fluid deficits caused by peri-operative fasting
Vasodilatory effects of anaesthetic drugs leading to a relative hypovolaemia
Acepromazine, isoflurane
Losses from the respiratory tract (worsened by endotracheal intubation)
Use HME’s, low flow anaesthesia if appropriate
IPPV (with PEEP/CPAP)-
Reduces urine output via alterations in renal vein pressure and altered ADH
However, alpha-2 agonists increase urine output
Extra(epi)durals with local anaesthesia- Hypovolaemia due to
vasodilation
Surgical site losses-
Evaporative
Third space
Haemorrhage
Contra-Indications of fluids
Risk of volume overload in, for example, cardiac patients
Risk of anaphylactoid reactions and interference with clotting tests (colloids)
?Cost
Common differential diagnoses for respiratory disease in exotics
Infectious-
Bacterial
Viral
Fungal
Non-infectious-
Environmental
Heat stress
Diaphragmatic hernia
Pregnancy toxaemia
Gastric dilatation
Cardiac disease
Pulmonary neoplasia
clinical signs in exotic respiritory disease
Oculonasal discharge
Facial asymmetry
Oral exam
Auscultation
Over trachea
Whole thorax crackles, wheezing, referred sounds & vocalisation
Heart rate & rhythm
diagnosics for exotic upper respiritory infection
Culture and sensitivity from a deep nasal swab
Nasolacrimal duct flush- Cytology, Culture
Rhinoscopy
Skull radiography
Advanced imaging- CT
diagnosics for exotic lower respiritory infection
Thoracic radiography – R & L lateral and DV views
Caudal lung lobes large and are well aerated
Assessment of cranial lung lobes difficult small in some species = normal
Assess lung patterns
Bacterial pneumonia-
Alveolar pattern
Air bronchograms
Diffuse, localised, lobar
Changes may not be present in early stages
Solitary mass-
Neoplasia
Abscessation
Consolidation
exotic respiritory diseases tested for by pcr
Chlamydia PCR – Chlamydia caviae (guinea pigs)
Conjunctival scrapings intracytoplasmic, coccoid, basophilic organisms (elementary and reticulate bodies)
Myxomatosis PCR
Rabbit haemorrhagic disease PCR
Distemper virus
Bordetella bronchiseptica, Mycoplasma pulmonis, Pasteurella multocida
exotic respiritory diseases tested for by post mortem
good for large groups of animals
Lung congestion
Fibrin adhesions
Fibrosis
Suppurative lesions
Pulmonary abscesses
Granulomas
Lung consolidation
Myocarditis
Tracheitis
Bronchitis
Otitis media/interna
Septicaemia
ferret respiritory diseases
Pneumonia uncommon-
Clinical signs are similar to other species
Viral-
Canine distemper virus
Influenza virus
Bacterial – often secondary to another disease process
Streptococcus zooepidemicus
S. pneumoniae
Streptococci groups C and G
Other bacteria-
Escherichia coli, Klebsiella pneumoniae, Bordetella bronchiseptica, Listeria monocytogenes, Pseudomonas aeruginosa
respiritory disease in rats
Very common health problem
Major pathogens-
Mycoplasma pulmonis
Streptococcus pneumoniae
Corynebacterium kutscheri
Minor pathogens-
Cilia-associated respiratory (CAR) bacillus
Haemophilus spp.
Sendai virus
Pneumonia virus of mice
Rat respiratory virus
Sialodacryoadenitis (SDA)
Interact synergistically-
Chronic respiratory disease
Bacterial pneumonia
respiritory disease guinea pigs
Pneumonia is a significant disease
Subclinical infection - clinical signs when stressed
Opportunistic bacteria-
Bordetella bronchiseptica, Streptococcus pneumoniae, Klebsiella pneumoniae, Streptobacillus moniliformis, Staphylococcus aureus, E. coli, Pasteurella pneumotropica, Pasteurella multocida, Streptococcus zooepidemicus, Streptococcus pyogenes, Citrobacter freundii, Yersinia pseudotuberculosis, Pseudomonas aeruginosa, Chlamydia caviae.
Viral aetiologies
Adenovirus, Parainfluenza virus
respiritory disease in chinchillas
Pneumonia is relatively uncommon
Potential pathogens-
Streptococcus, Klebsiella, Pasteurella, Bordetella, Pseudomonas
Viral causes not reported
respiritory disease in rabbits
Viral aetiologies-
Myxomatosis
Rabbit haemorrhagic disease
Other causes-
Neoplasia
Irritants
Nasal foreign bodies
Cardiac disease
Gastric dilatation
Bacterial aetiologies-
Pasteurella multocida, Bordetella bronchiseptica
Pasteurella multocida-
Chronic and acute infections
A commensal
Bordetella bronchiseptica-
Common flora within rabbit respiratory tract
Predisposes to the development of pasteurellosis
clinical signs of respiritory disease in reptiles
open-mouth breathing, exaggerated respiratory effort, increased gulping motions in the throat, repeated yawning in snakes, tracheal discharges, respiratory noise, ocular and nasal discharges (care not to confuse with secretions from salt gland in some species (e.g., green iguana), facial swellings, altered buoyancy in aquatic species.
reptile diagnostics for respiritory disease
History & clinical exam
Radiography
Advanced imaging (CT)
Endoscopy
Haematology & biochemistry
Nasal flush & tracheal wash
Cytology
Culture and sensitivity
PCR
Snakes – differential diagnosis
Viral-
Arenavirus (inclusion body disease)
Ophidian paramyxovirus
Sunshine virus
Nidovirus
Bacterial disease- Often secondary
Chlamydia pneumoniae- Zoonotic potential
Mycobacterium- Zoonotic potential
Birds – clinical signs in respiritory disease
Dyspnoea
Mouth breathing
Tail bobbing
Discharge from nares
Respiratory noise
Loss or change of voice
Exam (if safe to do so)-
Eyes/nares
Rhinoliths
Choanal slit
Auscultate heart, lungs and air sacs
Birds – respiritory disease diagnostic techniques
Haematology and biochemistry
Diagnostic imaging
Sinus flush and aspirates-
Cytology
Culture and sensitivity
Endoscopy
PCR/serology
Birds – respiritory disease Differentials
Bacterial -E.coli, Haemophilus spp., Pseudomonas spp., Streptococcus, Staphylococcus, Mycobacterium spp., Chlamydia psittaci
Fungal - Aspergillus spp., Candidia spp.
Viral - pox
Parasites - trichomoniasis
Nutrition - hypovitaminosis A
Lower respiratory tract disease-
Bacterial air sacculitis
Fungal air sacculitis
Chlamydia psittaci
Transmitted through aerosols of respiratory secretions, faecal material or feather dust
Grey parrots susceptible
Clinical signs-
Respiratory secretions
Diarrhoea
Weight loss
Poor feathering
Conjunctivitis
Component Therapy Versus Whole Blood
Component Therapy:
Benefits-
Maximising resource utilisation
Flexible dosing and administration
Reduced transfusion volume
Minimising immune sensitisation
Immediately available on site
Extended shelf life
Limitations-
Need knowledge of what activity each product has
Multiple storage areas are required due to different product temperature ranges
Whole Blood:
Benefits-
No processing requirement
Storage easier as single storage temperature
Limitations-
Shorter shelf life
Need a suitable in-house donor to be available
Inexperienced staff collecting the blood
Fresh Versus Stored Whole Blood
Collected whole blood is called Fresh Whole Blood (FWB) and it is classed as FWB for 6 hours. During this time it should be kept at room temperature
After 6 hours it is reclassed as Stored Whole Blood (SWB) and must be refrigerated
In SWB the activity of Factor I (Fibrinogen), Factor VIII and von Willebrand’s Factor will likely have declined to below therapeutically useful levels and platelets have been shown to be less responsive and have a poor lifespan once transfused (24 hours max)
There is however new compelling evidence that chilled platelets in SWB retain their ability to contribute to clot formation
Use of Red Cells
Fresh Whole Blood-
Source of all erythrocytes, haemostatic proteins, plasma proteins, immunoglobulins, antiproteases and platelets
Blood loss/ Haemostatic resuscitation
Haemostatic protein deficiency with blood loss
? Arrest active haemorrhage in patient with thrombocytopenia or thrombopathia
Packed Red Blood Cells-
Source of erythrocytes
Anaemia
Blood loss /haemostatic resuscitation +/- Fresh Frozen Plasma
Use of Plasma
Fresh Frozen Plasma (FFP)-
Source of all haemostatic proteins (labile and non labile), antiproteases, immunoglobulins and plasma proteins-
DIC
Adder Bites
Consumptive coagulopathy
Haemophilia A and B
von Willebrand’s Factor Deficiency
Bleeding due to Angiostrongylus
Acute haemorrhagic shock
1 year as Fresh Frozen Plasma + 4 year Fresh Plasma Shelf Life
Frozen Plasma (FP) and Cryosupernatant (Cryo-S):
Source of plasma proteins, immunoglobulins, antiproteases and non labile factors: II, V, VII, IX, X, XI and XII
HGE
Anticoagulant Rodenticide Toxicity
Hepatic coagulopathy
Haemophilia B
Hypoproteinaemia
Resuscitative IVFT
Immunoglobulin transfer
+ Cryo-S can be used to treat hypoalbuminaemia
FP 5 year Shelf Life
Cryo-S 1 year Shelf Life
Cryoprecipitate (Cryo-P):
Source of labile factors: I, VIII, XIII and vWF and fibronectin
Von Willebrand’s Disease- resuces chances of bleeding during surgery
Haemophilia A
Hypofibrinogenaemia
1 year Shelf Life
Use of Platelets
Platelet Concentrate (PC):
Source of platelets-
Uncontrolled or life-threatening haemorrhage due to thrombocytopenia/thrombopathia
Prophylactic treatment in patients with hereditary thrombopathia prior to surgery
Contains some red blood cells – typing recommended
Shelf Life of 3 days
Erythrocyte Antigens
Antigens are surface molecules capable of stimulating an immune response found on lots of things such as drugs, infectious organisms, pollens, plasma proteins and blood cells
Erythrocyte antigens are the antigens found on red blood cells and the presence of an erythrocyte antigen determines the blood type of the individual
Antigens are genetically determined characteristics and each erythrocyte antigen is inherited independently of other erythrocyte antigens meaning a single antigen can be present or multiple different antigens in any combination
Expression of an erythrocyte antigen = Positive for that blood type
No expression of an erythrocyte antigen = Negative for that blood type
10 canine erythrocyte antigens have been identified
Their antigenicity varies as will the degree of the immune response; some antigens will not provoke a response whilst for others the response will be strong- DAE-1, DEA-8
Antigenicity is influenced in part by the antigen’s:
Size
Complexity
Biological activity
The first exposure to a non-self antigen may include the production of antigen-specific alloantibodies which are retained for life
This individual is now sensitised to that antigen
A subsequent encounter will cause an antigen-antibody mediated immune response
: What makes an antigen more clinically significant when performing a blood transfusion?
More antigenic antigens produce a more profound immune response and the greater the strength of an adverse reaction
The greater the likelihood antigen exposure will occur the more it is a concern
High prevalence of Positive dogs = less likely to encounter a Negative dog
Low prevalence of Positive = less likely to encounter a Positive dog
50:50 prevalence of Positive and Negative = high chance of a Positive and Negative encounter
Blood Typing in Dogs
Most antigenic blood type is DEA 1.
Expression of this antigen on the red cell surface in Positive dogs is variable from strong through to weak.
Distribution of DEA 1 antigen in the canine population is around 50:50
Administering DEA 1 Positive red cells to a DEA 1 Negative recipient will result in DEA 1 sensitisation on first exposure
Subsequent exposure in a sensitised dog can cause an Acute Haemolytic Transfusion Reaction (AHTR) as a result of the extravascular +/- the intravascular destruction of the transfused cells
Preferably type and type match recipient and product/donor with regards to DEA 1 status in all dogs prior to red cell and platelet transfusion
Blood Typing Methodologies
In house typing kits available to determine DEA 1 status in the UK
Immunochromatographic, card and gel technologies are used in in-house typing kits
Immunochromatographic kits (QuickTest from Alvedia) consists of porous paper strip along which the sample migrates. The strip is impregnated with a line of monoclonal DEA 1 antibody that attaches to DEA 1 antigen (if present) and a control line impregnated with anti-glycophorin antibody that attaches to red cells regardless of blood type.
Cross Matching in Dogs
In dogs clinically significant alloantibodies will not be present in transfusion naïve individuals but all previously transfused dogs should be cross matched if they were given red cells 4 or more days ago to detect any clinically significant alloantibodies that have been generated that will react with a donor red cell antigen in the pending transfusion
Major cross match evaluates the recipient’s plasma for the presence of alloantibodies against donor erythrocytes to determine the likelihood of a haemolytic transfusion reaction
Minor cross match evaluates the donor’s plasma for the presence of alloantibodies against recipient erythrocytes to determine the likelihood of a haemolytic transfusion reaction
The Major Cross Match
Two reactions indicate incompatibility and the presence of existing recipient alloantibodies when recipient plasma is mixed with donor red cells:
Haemagglutination - a reversible red cell phenomenon caused by antigen-antibody binding and the cross-linking of antibodies causing red cells to clump together
Haemolysis – activation of complement results in lysis of the red cells and release of haemoglobin causing pink or red tinged plasma
Gel based tests: porous gel matrix block in the tube allows single red cells to pass through but not agglutinated clusters of cells
A crude version of the cross match can also be performed in house without the use of a commercial kit
Positive control – the red cells have
agglutinated and are too large to
pass through the sieve-like gel
Negative control – the red cells
Have passed through the gel
Patient test tube
indicating compatibility
when to do this?
Any recipient that has had a previous transfusion reaction
Any recipient with an unknown transfusion history
Any recipient that has received red cell product 4 or more days ago
PBB provides a crossmatch service via IDEXX cross matching the recipient against 6 stored packed red blood cell units.
Minor cross match may be considered if transfusing very large volumes of plasma to ….
detect any clinically significant alloantibodies in the donor plasma to recipient’s red cells
Feline Blood Types
Blood types: A, B, AB and Mik negative or positive
Naturally occurring antibodies to non-self red cell antigens in type A and B and some Mik negative cats
Strength and titre of antibodies varies:
Type B cats have a high titre of anti-A antibodies
Type A cats have a lower titre of weaker anti-B antibodies
Type AB cats have no antibodies to either the A or B antigen
In house kits are available for determining A/B status.
Cats must be blood typed and the recipient and product/donor must be type matched
Feline Cross Matching
Transfusion naïve cats can have clinically significant alloantibodies to other blood types so cross matching even the first transfusion is recommended
Red Cell Transfusions = Major Cross Match Plasma Transfusions = Minor Cross Match (donor plasma for alloantibodies to recipient red cells) Whole Blood = Major and Minor Cross Match (Alvedia/EmMa Test)
What tests can you use to evaluate the Urinary Tract?
Imaging (Radiography, Ultrasound, CT)
Clinical pathology (Haematology and Biochemistry tests) - path
Urinalysis
Surgical – biopsy, visualisation
Stranguria
difficulty urinating
Generally disorders of:
The lower urinary tract (bladder or urethra)
The genital tract (prostate, vagina)
Both
Two processes have potential to cause stranguria:
Non-obstructive stranguria- Mucosal irritation/inflammation of lower urinary/genital tract in fection
Obstructive stranguria - Obstruction or narrowing of the urethra/bladder neck. spasms, stones
A thorough history - ask the right questions
Signalment
Dogs – bacterial cystitis/urethritis, urinary calculi
Cats – idiopathic cystitis, urolithiasis
Palpate the bladder size
Stranguria + large bladder may be obstructed = emergency!
Physical Exam:
Assessment of urethral patency
Bladder Palpation – be very carefull!!! bladders blocked for long period of time are painful and fragile. can also cause backflow of urin into kidneys and cause kidney faliur
Digital rectal palpation- In all stranguric dogs. Especially males!
External genitalia and perineum
Haematuria
haem/blood in the urine
can be macoscopic or microscopic
Haematuria causes:
Iatrogenic haematuria- trauma caused by method used to obtain sample- e.g irritation by catheter
Pathological haematuria
Genital sources (if voided)- trauma to penis
Determine if systemic (coagulopathies) or localised to the urinary tract
Do they have clinical signs associated with LUTD?
Has bleeding been noticed from other sites?
Trauma?
Rodenticides?
Blood in faeces?
Pattern to urine pigmentation?
Clinical exam:
Look for haemorrhage at other sites- look for coagulopathy
Abdomen, thorax, mucosae (especially mouth, axillae, groin)
Palpate and assess kidneys for size, symmetry, discomfort- more reliable in smaller animals
Examine the external genitalia
can be found by
1.Gross “pigmenturia”
red, brown or black urine
2. Urinalysis: positive haem
possible causes:
Haematuria
Haemoglobinuria
Myoglobinuria
Gross haematuria:
>150 RBCs/hpf
Occult haematuria:
Positive Hb on dipstick
>5 RBCs/hpf but not visibly pink
Care re: interpretation if catheterised/cysto
Both can be accompanied by clinical signs (stranguria, dysuria, pollakiuria)
Is it consistent throughout urination?
Initial haematuria: At beginning of voiding - lower urogenital tract (bladder neck, urethra, vagina/vulva, penis, prepuce)
Terminal haematuria: At end of voiding -Upper urinary tract (bladder, ureters, kidneys or intermittent bleeding)
Total haematuria: throughout voiding - upper UT, diffuse bladder dz, prostatic or proximal urethra, coagulopathies
So how do I know if it’s Haematuria?
Clinical signs, gross inspection
Haematology/biochemistry-
Anaemia?
CK?
Positive dipstick
Centrifuge sample to examine for intact RBCs:
Supernatant clear with pellet of RBCs present = haematuria
Supernatant pigmented with absence of RBCs in pellet = haemoglobinuria or myoglobinuria
- Sediment evaluation for RBCs if haematuria
- always take into account collection method
- not always able to tell
Dysuria
pain or discomfort upon urination
Pollakiuria
abnormal frequent passage of small amounts of urine
Periuria
urination at inappropriate sites
Anuria
failure of urine production by the kidneys
Oliguria
reduction in urine production
Polyuria
Increase urine production
Haemoglobinuria
spill over of exess haeomoglobin form plasma
pink-red urine
Intravascular lysis of RBCs- haemolytic anemia
Lysis of RBCs within the urinary excretory- USG <1.008, pH>7
Myoglobinuria
rare in dogs and cats (seen more in horses)
Extensive skeletal muscle damage/myopathies- might see in racing greyhounds and horse
Creatinine Kinase will show on biochem test
Full Urinalysis
Macroscopic examination (colour, transparency/turbidity)
Microscopic examination
Chemical examination (dipstick tests and urine specific gravity)
Microbiological examination by culture
Part of the database for animals with signs of:
Renal disease
Lower urinary tract disease
Many medical problems (particularly those with multi-systemic signs)
Part of a geriatric or pre-anaesthetic screen
Hand-in-hand with biochemistry for any sick patient.
Tubular function
USG – Loop of Henle, Distal Tubules
Proximal Tubules
Dipstick - PT
Glomerular function-
Biochemistry
Dipstick
Haemorrhage, infection, inflammation…
Urine Collection Methods
Micturition
Cystocentesis
Catheterisation
Note: always record in your notes which collection method was used, as results can be significantly affected.
micturition as a urine collection method
“free catch”- can be got form-
Mid-flow- allows intitial flow to wash out contaminants
Naturally voided or Manual expression
Table-top- make sure to make this cea rin notes
Advantages:
Easy (generally) and may be left to owner (naturally voided - dog)
Non-traumatic, non-invasive
Use of modified litter can be used for initial screening of cats (KatKor)
Disdvantages:
Risk of non-compliance, resentment (dog)
Risk of haematuria and bladder rupture with manual expression
Variable volume
Likely to be contaminated - sample unsuitable for culture
Collection vessel may affect results- glucose from food containers, cleaning fluids can contaminate sample
Cystocentesis
Advantages:
Quick with no need to wait for spontaneous urination
Easier than voided sample from cats
Aseptic collection with no urethral contamination (so ideal for culture)
Easy to perform when bladder moderately distended and patient (dog or cat) adequately restrained
Better tolerated (cf. catheterisation)
Lower risk of iatrogenic haematuria and iatrogenic infection (cf. catheterisation)
Disadvantages:
Requires some experience
Needs adequate volume of urine in bladder
Iatrogenic micro-/(macro-)scopic haemorrhage possible
Contraindicated if:
bladder severely diseased – risk of rupture, clotting problems
Catheterisation as a method for urine collection
Advantages:
No need to wait for spontaneous micturition
Relatively, rather than absolutely, free of risk of bacterial contamination- use quantitative urine culture
Usually an ample sample volume
Advantages:
No need to wait for spontaneous micturition
Relatively, rather than absolutely, free of risk of bacterial contamination
use quantitative urine culture
Usually an ample sample volume
Catheterisation in the Queen
Blind insertion
Get body as straight as possible
Advance catheter along ventral vaginal wall along midline
Should enter urethra!
waht makes a good urin sample
Aim is to obtain a urine sample with in vitro characteristics similar to the original urine (in vivo)
If sample is not processed immediately, consideration should be given to sample storage and preservation
Collect and analyse with 60 mins
Or refrigerate (upto 12 hours)- after this cells lyse and crystals form.
Artefacts= Calcium oxolate, Struvite
should be analysed at room temp- affects usg and crystals
Refrigeration artefacts:
In vitro crystal formation (especially calcium oxolate dihydrate)
Falsely decreased results due to inhibition of enzymatic reactions
SG falsely increased
Room temperature artefacts:
Bacterial overgrowth
Alter pH
Decrease chemicals metabolised by bacteria (e.g. glucose)
Alter urine culture results
Timing of Collection:
Early morning or after fasting-
Advantages:
Most concentrated sample (relative water deprivation overnight) – evaluates concentrating capacity
Gives the highest yield of cells, casts and bacteria
Disadvantages:
Glucosuria may be less obvious than in a post-prandial sample
Cytology – cells may be altered due to prolonged exposures to variations in pH and osmolality
Gross Inspection of urin
Colour-
Light yellow or amber
Odour-
Should not be offensive
Transparency/turbidity-
Concentrated and end flow samples more likely to be turbid
Normal = clear/slightly cloudy
Volume-
5ml
Routine Urine Chemistry
Specific gravity (SG)
refractometer
pH
Dipstick- Remember – do not dip the stick!
Urine Specific Gravity
Assessment of concentrating ability
Measured with a Refractometer NOT dipstick
Best practice: Read urine supernatant
Ranges in hydrated patients:
Dogs - 1.015 to 1.045
Cats - 1.035 to 1.060
Interpret in light of animals hydration status, comorbidities, BUN/Creat/Glucose/Protein conc
First morning sample
Isosthenuria - 1.008-1.012 - Specific gravity (SG) of glomerular filtrate
Hyposthenuria – <1.008 = active dilution
Well concentrated - >1.030 (dog) or >1.035 (cat)
Interpret in light of animals hydration status, comorbidities, BUN/Creat/Glucose/Protein conc
Dipstick
Leucocytes- not valid
Nitrite- not valid
Urobilinogen- not valid
Protein
pH
Blood/Haem
USG- not valid
Ketone
Bilirubin
Glucose
pH measurement on a urine dipstick
Rough estimate of systemic acid-base status
pH values stable for 24 hrs (if fridged!)
Meters more precise and accurate than dipstick analysis
Important in management of urolithiasis and UTIs
Direct effect upon crystal type (struvite)
Direct effect on sediment findings: RBCs, WBCs, casts
Causes/examples:
High pH >7.5
UTI by urease-producing bacteria
Metabolic alkalosis
Herbivores
Low pH <7-
UTI caused by acid-producing bacteria
Normal in carnivores (5.5-7.5)
Metabolic acidosis
Bilirubin on urine dipsticks
Normal metabolism of Hb from erythroctyes results in hepatic formation of conjugated bilirubin- Primary excretion via GIT, and to a lesser extent, in urine via kidneys
Urine testing – screen for:
Intravascular haemolytic dz
Cholestatic hepatobiliary dz
Cannot be used to rule-out dz.
Interpret in light of USG
Normal in concentrated urine of dogs (USG >1.030)-Male>Female, Also ferrets
Always abnormal in cats
Haem on urine dipsticks
Screen for presence of haemoglobin
Free haemoglobin from lysis RBCs
Lysis of RBC’s when contact pad = + result
Intravascular (abnormal)
Dilute or extremely alkaline urine can also lyse RBCs – false +!
Free myoglobin from damaged myocytes (abnormal)
Sediment evaluation
<5 RBCs/hpf is normal finding (won’t cause a + on dipstick!)
Always take into account collection method
Glucose on urine dipsticks
Small molecule, freely passes through glomerulus into filtrate- Normally removed from urine by renal tubules
Presence in urine (abnormal >trace):
Exceed renal threshold e.g. hyperglycaemia-
Diabetes mellitus, Stress-induced hyperglycaemia in cats
Proximal renal tubular dysfunction
Serum biochemistry +/- fructosamine
Remember: effect on USG
Renal thresholds:
Cats - 14-15mmol/L
Dogs – 10-12mmol/L
Ketones on urine dipsticks
Ketones:
Acetone
Acetoacetic acid
Beta-hydroxybutyrate- ost abundant
Produced as alternative energy source to meet demands (negative energy balance)- E.g. aberrant carbohydrate metabolism (as in diabetes mellitus)
Ketonuria precedes ketonaemia
Urine screening for DM!
Diuretic effect
Predisposition to hypoNa and HypoK
Ketones on urine dipsticks
Ketones:
Acetone
Acetoacetic acid
Beta-hydroxybutyrate- ost abundant
Produced as alternative energy source to meet demands (negative energy balance)- E.g. aberrant carbohydrate metabolism (as in diabetes mellitus)
Ketonuria precedes ketonaemia-
Urine screening for DM!
Diuretic effect
Predisposition to hypoNa and HypoK
Protein on urine dipsticks
Screen for diseases that cause:
protein loss by the kidneys (e.g. renal proteinuria)- Tubular disease, Glomerular barrier alterations
Excess production of protein (less likely)- Overload proteinuria
Dipstick most sensitive to albumin-
Other proteins at high levels (e.g. Ig, Hb)
Urine electrophoresis
Always interpret in context of:
USG
pH
> 7.5 may cause false positive
Sediment
Normal Urine:
-/trace >1.025
<2+ > 1.030 (dogs)
<1.015 should be none.
Protein:Creatinine ratio (UP:UC)-
Quantitative
Creatinine not reabsorbed/secreted so conc is static
Standardises protein concentration
Evidence for glomerular or tubular proteinuria
UPC should be <0.5 for Dogs and <0.4 for cats (IRIS guidelines)
Interpretation confounded by other causes of protein in urine
E.g. pre-renal overload or post-renal proteinuria e.g. bacteriuria, pyuria, haematuria
Microscopic Examination of urine
Sediment Examination-
Crystalluria
Renal tubular casts
Epithelial cells
Blood cells
Bacteria
Renal Tubular Casts
Proteinaceous plugs of dense, mesh-like mucoprotein +/- cells accumulate in distal portion of nephron
Low number (<2/HPF) can be normal
Increased number relates to tubular disease
Try to identify associated cells, e.g. epithelial, WBC, RBC
Epithelial Cells in microsopic urinary analysis
Routinely see a small number (<= 2-5/HPF)
Type of cell may be difficult to identify, but may help to identify location of disease if increased number:
Renal tubular cells
Transitional cells- renal pelvis, ureter, bladder, proximal 2/3 urethra
Squamous cells- Distal 1/3 urethra
Blood Cells in microsopic urinary analysis
Erythrocytes
Haematuria – prev discussed
Leucocytes:
Cystocentesis sample - <3/HPF. - <8/HPF catheter/voided
High counts = pyuria
+/- bacteria
Bacteria
in microsopic urinary analysis
May be present for reasons other than UTI, e.g. contamination overgrowth in stored sample
Pyuria + bacteriuria = active UTI- Urine Culture & Sensitivity
Silent Urinary tract infections can also occur!
urine samle for Culture & Sensitivity
Obtain urine by cystocentesis
Usually boric acid container- bacteriostatic
Submit to external laboratory
Is patient receiving parenteral antibiotics?
Crystalluria
Precipitate out when urine saturated with dissolved minerals
Do not indicate presence of, or predisposition to form urinary calculi
May get in vivo without disease
Cold temperature/prolonged storage increases formation in vitro – so use fresh, non-refrigerated sample within 1 hour
Useful for:
provisional identification of existing calculi before analysis
When pathological types are identified
Magnesium ammonium phosphate
urinary crystal
struvite
Most commonly seen in dogs and cats
Neutral-alkaline urine-
UTI’s
Diet
Cystine
urinary crystal
Hexagonal
Acidic Urine
Abnormal finding
Inherited defect in proximal renal tubular transport of AA’s
Concentrated, acidic urine
Radiolucent
Calcium oxalate dihydrate
urinary crystal
radiopeic
calcium crystal
can be an artifact of stirage in fridge
Cross-striations, “envelope”
Acidic urine
Can be seen in clinically normal animals or storage artefact
Or urolithiasis, hypercalcuria, hyperoxaluria..
Calcium oxalate monohydrate
urinary crystal
radiopeic
calcium crystal
Picket fence
Abnormal in cats/dogs
Ethylene glycol (anti freeze) ingestion- Not 100% sensitive
Can be seen in normal horse
Calcium Carbonate
urinary crystal
Alkaline Urine
Yellow-brown or colourless
Common in equine
Not seen in dogs and cats
Bilirubin in urine
can be see
Orange-reddish brown
Low number routinely observed in dogs
Ammonium biurate Crystals
urinary crystal
Acidic urine
Abnormal finding in most breeds
Routine finding in Dalmations
Amorphous Crystals
urinary crystal
Aggregates/no defining shape
Urates - acidic
Phosphates – alkaline
Xanthene
Urolithiasis
A calculus (stone) in the urinary tract-
Single or multiple
Cystolith, ureterolith, nephrolith…
Remember – Crystals do NOT = Urolith
Recognised in all species
Common urolith types vary with species
Calcium carbonate – horses, rabbits
Magnesium ammonium sulphate, calcium oxolate – dogs, cats
One mineral normally predominates
Increased precipitation of excretory metabolites
Multi-factoral!
Genetic/breed factors
e.g. cystine stones in SBT
Metabolic disease
e.g. urate stones with PSS
Inappropriate diet
e.g. ram lambs fed concentrate
UTI e.g. struvite stones in dogs
Clinical Signs-
Nephroliths
Asymptomatic
Incidental finding on x-rays
Associated with pyelonephritis
Pain, pyuria, pyrexia
Ureteroliths
As above
Renomegaly – uni/bilateral +/- pain
Renal failure if bilateral
“big kidney-little kidney” cats
Cystoliths
True LUT signs
Dysuria, pollakiuria, haematuria
Occasionally palpable on physical exam
Depending on size/number
Urethroliths
True LUT signs
Abdominal discomfort
Licking at penis/vulva, trying to urinate but can’t
Urethral obstruction - post-renal azotaemia - AKI - renal azotaemia
Does the clinical history/physical exam suggest stones?
Plain radiographs:
Radiopaque stones:
Struvite
Calcium oxolate
Calcium phosphate
Radiolucent stones:
Ammonium urate
Cystine
Abdominal Ultrasound
Easy to miss
Rectal examination to palpate urethra
treating an acute urinary sytem obstruction
Nephroliths, Ureteroliths, Cystoliths and non obstructive urethroliths.. Later.
Urethral Obstruction
Treat as an emergency unless partial obstruction
Stabilise the patient but do not delay
Manage hyperK, IVFT
Decompress the bladder?
Retrograde urohydropulsion using catheter
Urethrostomy- More appropriate for recurrent problems, not emergency treatment
What are the receptors called that detect plasma osmolality and where are they ?
What are the receptors called that detect plasma osmolality and where are they
Where is ADH released from?
ADH is a substance produced naturally in an area of the brain called the hypothalamus. It is then released by the pituitary gland at the base of the brain
Where does ADH act in the kidney?
The main action of ADH in the kidney is to regulate the volume and osmolarity of the urine. Specifically, it acts in the distal convoluted tubule (DCT) and collecting ducts (CD
Name two stimuli that may cause ADH release
elevated plasma osmolality and decreased effective circulating volume. Increased plasma osmolality causes shrinkage of a specialized group of cells in the hypothalamus called osmoreceptors
How does ADH cause urine to be concentrated in the kidney?
ADH increases the permeability to water of the distal convoluted tubule and collecting duct, which are normally impermeable to water
What clinical condition arises in patients which fail to produce ADH?
Diabetes insipidus
What are the clinical consequences of a lack of ADH?
dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases
What conditions might lead to high ECF Sodium
Dehydration
A disorder of the adrenal glands.
A kidney disease.
Diabetes insipidus
Is Sodium maintained within a relatively narrow range?
yes
Which hormone is released as a consequence of a rise in plasma K+?
When K+ plasma levels increase enough, hyperkalemia induces aldosterone secretion. Aldosterone, in turn, promotes renal K+ secretion
What clinical condition arises in patients which fail to produce aldosterone
Addison’s disease
What is the fate of glucose that enters the glomerulus?
Glucose that enters the nephron along with the filtrate after passing through the glomerulus, passes from the tubule of nephron where it is selectively reabsorbed and sent back into the blood.
Why is there glucose in the urine of animals with Diabetes mellitus?
Once blood glucose reaches a certain level, the excess is removed by the kidneys and enters the urine. This is why dogs and people with diabetes mellitus have sugar in their urine (glucosuria) when their insulin levels are low.
What is the consequence of Diabetes Mellitus on the urine volume?
In diabetes, the level of sugar in the blood is abnormally high. Not all of the sugar can be reabsorbed and some of this excess glucose from the blood ends up in the urine where it draws more water. This results in unusually large volumes of urine
How will the presence of glucose in urine affect USG
the addition of glucose caused the USG to increase
How will the presence of glucose in urine affect Osmolality
glucose can also add significantly to the osmolality when it is abundant in urine
Why is there usually no protein detected in the urine?
most protein molecules are too large for the filters (glomeruli)
In what circumstances might you find haemoglobin in the urine?
If the level of hemoglobin in the blood rises too high
In what circumstances might you find myoglobin in the urine?
extensive damage to your skeletal muscles, resulting in the rapid breakdown of muscle
What are the potential outcomes of losing lots of albumin in urine?
kidney disease
Thirst and urination determined by interplay of:
Plasma osmolality - Determines blood pressure – baroreceptors (pressure) and osmoreceptors (water)
Osmolality integrated into thirst centre in the brain
Hypothalamic – Posterior pituitary gland – ADH axis
Regulates water reabsorption in collecting duct
Renal function- Needed to produce concentrated urine
Urine Concentration
Adequate secretion of ADH and kidneys must be able to respond normally
Enough functioning nephrons
A concentration gradient in renal medulla
when 2/3 of kidney lost this process is impares
Mechanisms of PUPD
polyurea
polydypsia
2 basic reasons:
Primary polyuria (insesant urination) with secondary compensatory polydipsia- Most common, Several mechanisms
Primary polydipsia (insesant need to drink) with consequent PU
Primary Polydipsia
Uncommon in small animals- In dogs behaviour resulting in increased drinking referred to as psychogenic polydipsia
Horses>others
Cerebrocortical dysfunction- Central lesion affecting hypothalamus/thirst centre and ADH
Endocrine disorders
Pathophysiology of Primary PU
- Lack of ADH produced by hypothalamus
Cannot concentrate urine
Compensatory PD
Primary central diabetes insipidus- ongenital/idiopathic, rare. (Acquired neoplastic/trama also v.rare) - Inability of DT/CD cells to respond to ADH
ADH has no action in DCT
Nephrogenic diabetes insipidus
Primary - ↓receptors/inability to bind due to mutation
VERY rare
Secondary-
Reduced sensitivity to ADH-
E.coli toxins in pyelonephritis and pyometra/prostatic abscess or any pyogenic infection in the body
Hyperadrenocorticism - cortisol interacts with ADH at the receptor level
Interference with action of ADH at tubule:
Hypercalcaemia
Hypokalemia
ADH receptor downregulation:
Obstuction of ureters/ bladder - post-renal azotaemia conditions
Hypokalemia
- Osmotic Diuresis
A minimum volume of water must be excreted with waste solutes by the kidney.
Concentration of solutes within the glomerular filtrate > proximal tubular capacity for reabsorption
= increased water excreted
= primary polyuria - Reduced medullary concentration gradient
Unable to concentrate urine in Loop of Henle
Controlled by Na+ and urea in medulla
Chronic Kidney Disease
Nephrons are lost and replaced with inflammatory and fibrous tissue:
-Reduced water reabsorption within distal tubules and collecting ducts
-Inability to maintain counter-current mechanism
Signalment:
Older animals (any age!)
Clinical Signs
Weight loss, ↓BCS
Inappetence
PUPD
Oral ulcers
Diagnostics:
Biochem/haematology signs- Renal azotaemia, Non-regenerative anaemia (kidneys produce erythropoietin) , Hypokalaemia +/- hyperphosphatemia
Inappropriate USG
Proteinuria (UP:UC, dipstick)
Pyelonephritis
Inflammation of the renal pelvis-
Acute or chronic
+/- Bacterial infection
Dogs>cats
Clinical signs:
PUPD:
Endotoxins interfere with ADH
Inflammation interferes with medullary osmotic gradient
Chronic ->loss of nephrons - >CKD
LUTD signs- haematuria, pollakiuria, dysuria, stranguria
Renal/lumbar spinal pain
Unilateral/bilateral renomegaly
Acute – pyrexia, lethargy
Diagnostics:
US
Haematology – left shift inflammatory leucogram
Urine culture & sensitivity (cystocentesis, pyelocentesis)
pyometra
Infection in the progesterone-primed uterus
Usually E.coli
Signalment:
Older, entire bitches
Clinical Signs:
Open mucoid to purulent discharge at vulva
Closed lethargy, pyrexia, inappetance, V+D, PUPD
Diagnostics:
Left shift leucogram
Azotaemia
Imaging -> US +/- radiography
Hyperthyroidism
Signalment:
Cats >7yo
Clinical signs:
Polyphagia with weight loss
Intermittent V+D
Hyperactivity and behavioural changes
PUPD
Clinical exam:
↓ BCS
Tachycardia, heart murmur, gallop rhythm
+/- thyroid goitre
Diagnostics:
Biochem -> ↑ ALT, ↑tT4-
+/- free T4, TSH
CKD
Hyperadrenocorticism
Signalment:
Middle aged-older Dog >6-9yo
Clinical signs:
PUPD
Polyphagia
Pot-bellied
Skin thinning, haircoat changes
Diagnostics:
Biochem -> ↑ALP
USG -> <1.020
ACTH stimulation test
Low dose dexamethasone suppression test (LDDS)
Urine Cortisol:Creatinine ratio
Hypoadrenocorticism
Loss of adrenocortical cells = glucocorticoid and mineralocorticoid deficiency
Signalment:
Younger dogs – 2-5yo
Clinical signs:
Vague
“waxing and waning” GI signs
Collapse, shock
Diagnostics:
Biochem -> Na:K ratio<23
ACTH stimulation test
the great pretender- sometimes ccan cuase PUPD due to electrolyte imabalence bu this is not a common presentation
Diabetes Mellitus
Persistent Hyperglycaemia and glucosuria
Signalment:
Dogs & cats, any age
Clinical signs:
Weight loss
Polyphagia
Lethargy
PUPD
Diagnostics:
Biochem -> hyperglycemia
Urine -> Glucose +
Fructosamine
Hypercalcaemia
Hypercalcemia due to number of conditions:
Signalment:
Dogs>Cats
Clinical signs:
PUPD
Variable, depending on cause
Diagnostics:
Biochem ->↑ total Ca (influenced by albumin)- Ionised Ca
Work up depending on cause
Causes: HOGSINYARD
• Hyperparathyroidism
• Osteolysis
• Granulomatous disease
• Spurious (false or fake) sample
• Idiopathic (cats)
• Neoplasia
• Young animals
• Addisons (Hypoadrenocorticism)
• Renal disease
• D Hypervitaminosis D
Hepatic Disease
Variable causes of hepatic disease
Signalment:
Dogs, any age
Cats
Clinical signs:
PUPD
Non specific, depending on cause
Diagnostics:
Biochem -> ↑ liver enzymes (ALT, ALP, GGT)
Function: ↓ urea, cholesterol, albumin, glucose- Bile Acid Stimulation Test
Imaging
Central Diabetes insipidus:
rare
Lack of ADH by the hypothalamus/posterior pituitary
Causes:
Idiopathic
Neoplastic
Head trauma
Clinical signs:
Extreme PUPD
Diagnostics:
Only performed after exclusion of other causes of PUPD
USG <1.008
Water Deprivation Test – DANGEROUS, can caus ekidney faluire
Desmopressin trial
Congenital Nephrogenic Diabetes insipidus:
rare
Lack of response to ADH by the kidney
Clinical signs:
Extreme PUPD
Diagnostics:
Only performed after exclusion of other causes of PUPD
USG <1.008
Water Deprivation Test – DANGEROUS
Desmopressin trial
Primary Psychogenic Polydipsia
Rare
Behavioural, young dogs
Clinical signs:
Extreme PUPD
Diagnostics:
Only performed after exclusion of other causes of PUPD
Water Deprivation Test – Dangerous
water deprivation test
depriving an animal of water then testing the urine specific gravity
if normal then test respones to synthetic ADH
if positive : Central Diabetes insipidus
if negative: Congenital Nephrogenic Diabetes Insipidus
if USG is high: Primary Psychogenic Polydipsia
In PUPD cases, what is more comon? primary polyurea or primary polydypsia
Primary Polyuria
clinical examlple of PUPD-
History
10yo FE Staffordshire Bull Terrier
Drinking more for last 2 weeks
Off colour and vomiting, normal faeces
Possible weight loss?
Not sure whether spayed
No medications
No diet/environmental change
Clinical examination
Mucus membranes slightly tacky
Thoracic auscultation normal
Abdomen tense, difficult to palpate
No visible vaginal discharge
Temperature 39.2C
can rule out that its not drug related
Primary Problems
Polydipsia
Vomiting
Mild pyrexia
Probable secondary problems
Weight loss- due to vomiting
Inappetance - due to naeusea
5% dehydration- due to polydipsia and vominting
Differential diagnoses - PUPD
• Renal
• Hepatic
• Endocrine – diabetes mellitus, diabetes insipidus, hyperadrenocorticism, hypoadrenocorticism
• Infectious – pyelonephritis, pyometra
• Electrolytes – hypokalemia, hypercalcaemia
• Iatrogenic – diuretics, steroids etc
Differential diagnoses - Vomiting
Primary GI tract problem
Inflammatory, infectious, obstructive, motility disorder, toxic
Intra-abdominal, extra GI problem
Pancreatitis, diabetes mellitus, hepatitis, renal disease, pyometra, splenitis, hypoadrenocorticism, obstruction from large mass
Extra-abdominal
Fear, pain, vestibular disease, toxic
diagnostics-
Urinalysis- USG determine whther animal is truly PUPD, can show no protien, whether there is infection
bloods- CBC, can show dehydration (concentrated pcv), neutrophils can show infection, liver enzymes normal (rules out liver disease), electrolystes ok (rules out hyperthyroidism), calcium is fine (rules out hypoclacemia)
azotaemia
azotemia is a biochemical abnormality, defined as elevation, or buildup of, nitrogenous products (BUN-usually ranging 7 to 21 mg/dL), creatinine in the blood, and other secondary waste products within the body
can be normal varitaion
an be pre renal, renal or post real
will not be detected in blood until about 70% of renal function is lost
pre-renal azotaemia
any process that reduces RBF-
Dehydration/hypovolaemia
hypotension/shock
clinical signs- other indicators of hypovolaemia or shock
blood indictaiors of dehydration: PCV/ total protien/ lactate
renal azotaemia
primary rena disease that results in reduced GFR
glomerular disease
tubular disease
interstitial disease
clinical signs- other indicators of hypovolaemia or shock
blood indictaiors of dehydration: PCV/ total protien/ lactate
post renal azotaemia
defective excretion distal to the nephron
obstruction (increased intratubular pressure
rupture of urinary tract
generally distinctive in presentation- dysuria
reversable but may have renal component if nephron becomes damaged
hyposthenuric
the secretion of urine of low specific gravity due to inability of the kidney to concentrate the urine normally.
can activly dilute urine so some function of idney
hypersthenuric
A condition where the osmolality of the urine is elevated
activly concentrating urine, good nephorn function
isosthenuric
Isosthenuria refers to the excretion of urine whose specific gravity (concentration) is neither greater (more concentrated) nor less (more diluted) than that of protein-free plasma, typically 1.008-1.012. Isosthenuria reflects damage to the kidney’s tubules or the renal medulla.
potential loss of nephron function
RENAL FAILURE
Reduced renal function
Loss of renal reserve
Acute Kidney Injury (AKI)?
Chronic Kidney Disease (CKD)?
Acute-on-chronic?
What is causing the damage?
How much damage has been done?
Is it reversible?
What is the prognosis?
clinical signs-
URAEMIA
Polyuria/Polydypsia
Dehydration
Anorexia/inappetance
Weight loss
Vomiting
Halitosis
Oral ulceration
Gastrointestinal bleeding
Weakness / lethargy
Palor of mucous membranes
Neurological signs
AKI
Acute kidney disease
Sudden onset of signs
Polyuria may progress to oliguria/anuria as renal function lost
Advanced signs of uraemia may not have had time to develop
CKD
chronic kidney disease
Most common sign is weight loss
Advanced CKD is most common cause of uraemia
Usually have a long term history of PU & PD
URAEMIA
Polyuria/Polydypsia
Dehydration
Anorexia/inappetance
Weight loss
Vomiting
Halitosis
Oral ulceration
Gastrointestinal bleeding
Weakness / lethargy
Palor of mucous membranes
Neurological signs
URAEMIA
a buildup of toxins in your blood. It occurs when the kidneys stop filtering toxins out through your urine.
Polyuria/Polydypsia
Dehydration
Anorexia/inappetance
Weight loss
Vomiting
Halitosis
Oral ulceration
Gastrointestinal bleeding
Weakness / lethargy
Palor of mucous membranes
Neurological signs
Excretory failure
Due to diminished GFR
Retention of non-protein nitrogenous waste
BUN, Creatinine
(renal) Metabolism Failure
Failure to catabolise some polypeptide hormones
Insulin, Glucagon, GH
(renal) Failure to Synthesise
Failure to make calcitriol (vit D3)
- 2o hyperparathyroidism
Failure to synthesis erythropoietin
-anaemia
effects of acccumulation of ‘uraemic toxins/substances
UREA- Weakness, anorexia, vomiting, glucose intolerance, haemostatic disorders
Creatinine
(Creatine, Guanidine etc)- Weight loss, platelet dysfunction
Peptides and polypeptide hormones:
Parathyoid hormone- Osteodsyrtophy
Insulin- Hyperinsulinamia
Growth Hormone- Insulin resistance
Aromatic amino acid derivatives:
Tryptophan, Tyrosine etc-Anorexia
Alphatic amines- Uraemic breath, encephalopathy
Ribonuclease- Impaired erythropoiesis
cAMP-Abnormal platelet function
renal dysfunction
Inability to produce urine
Inability to concentrate or dilute urine in response to bodies requirements
renal Electrolyte abnormalities
Hyponatraemia
- Renal sodium wastage
Hypo- or hyper- calcaemia
Hypo- or hyper- kalaemia
- alteration to secretory function
Hyperphosphataemia
- Renal retention of phosphate
renal Acid-base homeostasis
Kidneys is vital for normal acid-base homeostasis, and to do so normally it must:
Reabsorb all the bicarbonate from the renal filtrate-
70-80% done in the proximal tubule
20-30% done in the distal convoluted tubule (DCT)
Excrete the daily metabolic acid load (H+ ions) generated - Active excretion takes place at DCT
Tubular dysfunction will result in;
Loss of bicarbonate in urine
Reduce acid secretion from DCT -> METABOLIC ACIDOSIS- RENAL TUBULAR ACIDOSIS
renal dysfunctions role in systemic hypertension
Alteration in function or control of the renin-angiotensin-aldosterone-system (RAAS) can have a profound effect on systemic blood pressure
Common complication of chronic renal failure in cats
Clinical Features of Renal Failure
URAEMIA
Polyuria/Polydypsia
Dehydration
Anorexia/inappetance
Weight loss
Vomiting
Halitosis
Oral ulceration
Gastrointestinal bleeding
Weakness / lethargy
Palor of mucous membranes
Neurological signs
POSSIBLE DIAGNOSTIC FINDINGS
Azotaemia
Hyperphosphataemia
Metabolic acidosis
Systemic hypertension
Hyperkalaemia or hypokalaemia
Hypercalcaemia or hypocalcaemia
Anaemia (normocytic, normochromic)
Haemostatic disorder
Secondary hyperparathyroidism
Osteodystrophy
Hormone imbalances
clinical sign of renal faliure
Acute:
Animal presents with sudden onset dullness, weak, off-food PU/PD or anuric/oliguric
OR, with signs of urinary obstruction/abdominal trauma
OR, with history of access / ingestion of known toxin, or nephrotoxic drug administration
WITH or WITHOUT signs of uraemia
Chronic:
Animal presents with long term weight loss only
Or, with weight loss and recent history of PU/PD for a few weeks
With possible history of vomiting (more likely in dogs)
Progressive weakness and evidence of pale mucous membranes
diagnostic methods of renal faliur
Blood Biochemistry & Haematology
Identify Azotaemia
Investigate presence of;
Electrolyte abnormalities
Acid-base imbalance
Anaemia
Platelet disorders
OBTAIN A URINE SAMPLE
Establish the USG
Dogs = isosthenuric. Cats may have higher SG in CKD
Full urinalysis - look for signs of intrinsic renal failure
Rabbit unique calcium metabolism
Blood calcium levels reflect dietary intake
Readily absorbed from intestines
Does not depend on activated vitamin D
Ionised and total calcium serum concentrations are higher than those in other species
Rabbit absolutely dependent on the kidney for calcium osmoregulation
Renal fractional excretion of calcium = 45-60% compared with <2% in mammals that regulate calcium uptake from the GI tract and eliminate excess in faeces.
acute renal failure signs in exotics
Non specific (anorexia, lethargy)
Pain (bruxism – pain scoring recommended)
Other signs, e.g., GI ileus/stasis
chronic renal failure signs in exotics
Weight loss
PUPD
Poor body condition
Occasionally haematuria
Reduced appetite
GI stasis
Cystitis/urolithiasis signs in exotics
Urine scald
Vocalisation when passing urine
Haematuria
Urinary incontinence
Urine dribbling
Dysuria = Pain or burning sensation while passing urine.
Stranguria = Slow, painful discharge of small volumes of urine expelled only by straining despite a feeling of urgency
Pollakiuria = frequent, abnormal urination during the day.
Common differential diagnoses for urinary disease in exotics
Infectious-
Bacterial
Viral
Parasitic- e.caniculli
Non-infectious-
Environmental
Urine sludge
Calculi – obstruction
Neoplasia
Toxic
Other diseases not related to urinary system
Prostatic cysts (endocrine)
Normal – porphyrin, food pigments
causes of urinary disease in exotics
Diet
water Bottle vs bowl
Design of enclosure
Exercise – sedentary rabbits more prone to sludge
Conspecifics
Recent changes to husbandry or routine- extreme changes in temp
Vaccination status (rabbits & ferrets)- canine distemper , rhd
Neutering status (e.g., neutered male ferret may develop prostatic cysts or prostate enlargement )
Observation
Evaluate demeanour and stance
diagnostics for uriary porblems in exotics
Blood work
Rabbits – Lateral saphenous vein, cephalic vein or marginal ear vein
Ferrets – Jugular vein or cranial vena cava (under GA)
Assess: Blood urea nitrogen (BUN), creatinine (low normall levels in ferrets comparitivly), inorganic phosphate, total calcium, ionised calcium, potassium, PCV
Limitations-
Circadian rhythms
Diet can affect values
Muscle loss
Symmetrical dimethylarginine (SDMA) recommended
Serology for some disease processes: E. cuniculi serology
Radiography-
Abdominal radiography: Plain and contrast
Ultrasonography-
Bladder wall, neck or urethral abnormalities
Identification of cystoliths or urethroliths
Advanced imaging-
CT
Endoscopy
For species where challenging to distinguish between haematuria and vaginal/uterine bleeding e.g., rabbits – urethra opens into the ventral aspect of the vaginal body
Rabbit urinalysis
Rabbits excrete alkaline urine
Average volume produced = 130ml/kg/day (range 20-350ml/kg/day)
Urine pigments gives rabbit urine a yellow, brown or red colour.
Some pigments are a result of the breakdown of endogenous compounds bile pigments, porphyrins, flavins
Food ingested can lead to urine colouration
Distinguish between haematuria and porphyrin pigments-
Positive reaction for blood on dipstick
Identifying >5 RBCs per high-power field on urine sediment examination.
Porphyrins may fluoresce under a Wood’s lamp
Excreted calcium precipitates in the alkaline urine to form calcium complex crystals gives the urine a creamy and thick appearance.
Urine sediment can be seen normally in samples
exotics urine sampling methods
Sampling techniques
Free catch from litter trained rabbits using non-absorbable products designed for cats as a replacement litter
Sedation and cystocentesis - recommended for obtaining a sample for culture
GA urethral catheterisation -diagnostic and therapeutic
Challenges – urinary catheterisation ferrets
Penis
J-shaped penis, making catheterisation tricky.
Os-penis
Palpated easily, caudal to preputial opening
Groove on the bone, supports urethra
urinalysis in exotics
Urinalysis, sediment and bacterial C+S
C+S Only useful BEFORE antibiotic treatment started
Normal values (rabbit – Reusch et al, 2009; Varga Smith, 2022)
pH 7.6-8.3
Specific gravity 1.003-1.036
Leucocytes and erythrocytes occasionally seen <5RBCs hpf
Protein trace
Glucose trace
Ketones and occult blood absent
Casts, epithelial cells and bacteria absent
Crystals = large amounts of calcium carbonate monohydrate, anhydrous calcium carbonate and calcium oxalate and ammonium magnesium phosphate (struvite) may be seen
Urinary protein and creatinine ratio (UPC) 0.11-0.40
Species specific considerations - small rodents-
Urinary obstruction possible in male mice infection of preputial and bulbourethral glands
Urine volume
0.5ml-2.5ml/day (mouse)
13-23ml/day (rat)
5.1-8.4ml/day (hamster)
2-4 drops/day (gerbil)
Most differences seen related to animal’s native environment and water conservation.
Gerbils- Loop of Henle is comparatively longer ->concentrate urine more effectively.
Urinary calculi common
Cystitis
Often older sows
Ascending infection
E. coli
Streptococcus spp.
blood pressure in exotics
Systemic hypertension is a common feature of renal failure due to the renin-angiotensin-aldosterone system
Rabbits
Mean arterial blood pressure = 80-91mmHg
Systolic BP = 92.7-135mmHg
Diastolic BP = 64-75mmHg
Ferrets
Systolic BP = 80-120mmHg
common causes of renal disease in rabbits
Common causes of renal disease
Encephalitozoon cuniculi
Chronic renal failure in older rabbits
Renoliths
Other urinary conditions -
Hypercalciuria/urine sludge
Bacterial nephritis
Hydronephrosis
Papillary necrosis with renal mineralisation.
what is Most common causes of renal disease in pet rabbits
E.cuniculi
Infection with Encephalitozoon cuniculi – a microsporidian parasite
Diagnostics-
IgG & IgM E cuniculi serology
C-reactive protein
PCR
Osmoregulation in birds
Kidneys
Large intestine
Salt glands (some species)
Renal system-
Kidneys
Ureters
Urodeum (structure in the cloaca)
Birds are uricotelic
Avian kidney
Fixed, ventral depressions, synsacrum
Extend from the lungs to the caudal synsacrum
Renal fossa: symmetrical and retroperitoneal
Three distinct renal divisions
Do not have lobes but have lobules
Cortical (reptilian) nephrons – approx 70%
Mammalian (medullary) nephrons – approx. 30%
this means dosing is different
consider portla system
Relevance of the anatomy
Swelling of kidney -> neuropraxia: birds will present as lame
Renal portal system
present in birds and reptiles
Makes a venous ring
Portal blood receives blood though:
External iliac veins
Internal iliac veins
The ischiatic veins
Caudal mesenteric vein
Renal portal valve shunts blood to kidney OR back to heart depending on adrenergic or cholinergic innervation
RELEVANCE = DRUGS AND INFECTION
clinical signs of renal disease in birds
Observations-
Droppings in cage:
White urates = normal
Green = biliverdinuria (severe hepatic disease)
Golden yellow or brownish yellow = hepatic disease or vitamin administration
Red/brown = toxicity (lead), nephritis, haemolysis, polyomavirus, warfarin-type poisons
Clinical signs
Polyuria, anuria or oliguria
Polydipsia
Non-specific signs
Lameness
diagnostics for renal disease in birds
Blood work-
Persistently high uric acid
Filtration decreased by 70-80% before plasma uric acid is elevated
UA may rise with severe dehydration
Will rise postprandially in carnivorous birds
Urinalysis-
Problems with sampling -need ureteral urine
Urinary GGT (some labs) - over 20 U/L suspicious of some renal insult.
NAG (N-acetyl-β-D-glucosaminidase renal tubular enzyme (not available in many labs) studied in chickens
Diagnostic imaging-
Radiography:
Kidney lies in a fossae on ventral surface of the synsacrum
Contrast may be beneficial
Ultrasound:
May be challenging due to air sacs but useful if kidney surrounded by fluid or tissue
CT:
IV in basilic (wing vein)- remember portal system, can cause nephrotoxicity
Endoscopy-
Renal biopsy to achieve a definitive diagnosis
Histopathology
Culture and sensitivity
PCR
Cytology – e.g., look for uric acid crystals
differentials for renal disease in birds
Bacterial -> acquired from haematogenous route
Fungal -> Aspergillus spp.
Viral -> herpesvirus, adenovirus, paramyxovirus and avipoxvirus can affect the kidney as part of a generalised infectious process.
Parasites -> protozoal infections. Microsporidia have been found in association with nephritis
Nutrition ->Fatty liver/kidney syndrome
Neoplasia
Gout
Toxicities -> heavy metals, poisonous plants, potential nephrotoxic drugs
Obstructions ->cloacoliths, tumours, pressure from egg binding
differentials for renal disease in reptiles
Environmental
Bacterial
Viral
Fungal
Parasitic (Hexamita or Entamoeba)
Calculi in species with a bladder
Gout
Neoplasia
Post hibernation complications
risk factors and clinical designs of renal disease in reptiles
Risk factors-
Provision of purine rich high-protein diets
Low humidity
Lack or unsuitable water source
Nephrotoxic medications
Clinical signs-
Depression
Weakness
Dehydration
Pharyngeal oedema
Palpation of enlarged kidney (iguanas – via digital cloacal palpation)
assesing dehydration in reptiles
PCV
BLOOD PROTEINS
URINE SG
SKIN TENTING
TACKY MMS
ALL UNRELIABLE
hibernating tortouses will recycle bladdder contents- can be cause of renal disease if the animal doesnt drink after waking
roentgen signs
The radiologic (roentgen) signs are abnormal:
Number. Position. Size. Shape. Opacity. Margination. Decreased. Congenital absence (rare)
Left Atrial to Aortic root ratio
In veterinary clinical practice, the left atrial-to-aortic root ratio (LA/Ao) in right parasternal short axis view is the most commonly used method to evaluate left atrial (LA) size in dogs [6, 8, 12, 13, 26]. This ratio provides an index of LA size that is independent of body size.
dogs; <1.6
cats ; < 1.5 is normal. Typically cats with heart failure have significantly increased LA:Ao of >1.8.
what are the steps to check the breathing system is safe and ready for use:
- Connect breathing system to anaesthetic machine and scavenging system
2.Cover patient end of breathing system with your thumb and close APL valve
- Fill breathing system with oxygen using flush button or turning oxygen flow meter on
- Squeeze inflated reservoir bag, check whether it keeps its shape/size and listen for sounds of leaking gas in any part of the system
- Open the APL valve with your thumb still in place
- Squeeze reservoir bag and check exit through scavenging tubing is patent
radiography abdominal VD positioning
Positioning:
Use radiolucent cradle to ensure no axial rotation
Centring:
At level of caudal edge of last rib (slightly more caudal in cats)
In midline
Collimation
To greater trochanter caudally
To lateral body wall
Aim to include whole of abdomen in survey films
radiograph anbdominal lateral positioning
Positioning:
Pad sternum +/- between hindlimbs to prevent axial rotation
Pull hindlimbs caudally (and forelimbs cranially)
Centring:
At level of caudal edge of last rib (slightly more caudally in cats)
Half to third way up from ventral body wall
Collimation
To greater trochanter caudally
To ventral body wall and collimate off some dorsal tissues if possible
Aim to include whole of abdomen in survey films
advantages and disadvantages of using radiography to view the kidneys
Advantages:
Number, location, size, shape, symmetry
Presence of mineralised opacities
Addition of contrast agents useful
Disadvantages:
Beware of superimposition
Limited if fluid or lack of fat
No information on internal architecture
Contrast Agents
Used when plain radiography gives insufficient organ detail
Positive Contrast Agents
High atomic number, e.g. compounds containing barium or iodine
Appear more radiopaque than surrounding body tissues
Negative Contrast Agents
Gases, e.g. room air or carbon dioxide
Appear radiolucent
Intravenous Urography (IVU)
Positive contrast media
Anatomical and functional information-
IVU provides only very crude assessment of renal function (excretion)
Sequential radiographs taken
Information obtained at each stage of the IVU:
Immediate VD (kidneys)
5 mins – VD (whole abdomen)
10 mins – lateral (whole abdomen)
15 mins – lateral (bladder neck)
Others as needed
advantages and disadvantages of using ultrasound to view the kidneys
can see images on different planes- saggital, transverse, dorsal
dorsal plane gives best view of pelvis
better view of internal archatechture
Advantages:
Safe, cheap, avoids ionising radiation
Assessment of internal architecture
Focus and diffuse lesions
Disadvantages:
Requires operator experience
kidney ultrasound anatomy
Renal Cortex-
Evenly granular
Hypoechoic (occasionally isoechoic) to the liver in dogs
Often more echogenic in cats
Medulla-
Hypoechoic to cortex
Look for a good ‘cortico-medullary’ definition
Pelvis-
Recognised in the normal kidney by echogenic peripelvic fat
advantages and disadvantages of using radiograph to view the blader
Plain Radiographs:
Advantages:
Detection of radiopaque cystoliths
Size and location
Addition of contrast agents can provide more information
Disdvantages:
Limited value for evaluating for disease without contrast
Retrograde Contrast Cystography
Fast, simple, inexpensive
Sedated/GA required
Negative, positive or double contrast
Uses:
Bladder wall assessment
Location or integrity
Radiolucent cystouroliths
Which contrast media?
Air (pneumocystogram)
Cheap, readily available
Useful to identify bladder and show position and wall thickness
Poor mucosal detail and may miss small tears.
can very rarley casue air embolysm so some peopple use co2
Positive contrast cystogram
Expensive
Main indication is suspected bladder rupture
Double contrast cystogram-
similarly to a conventional cystogram, but gas is also introduced through the Foley catheter
Excellent mucosal detail and contrast puddle provides useful contrast (e.g. radiolucent calculi)
advantages and disadvantages of using ultrasound to view the blader
Advantages:
Detect radiolucent cystourolith
Cystocentesis
Surrounding structure assessment
Disadvantages-
Degree of distension affects shape, size and wall thickness
Ultrasonographic appearance
3-layers
Inner mucosal interface (hyperechoic)
Muscle layer (hypoechoic)
Outer serosal layer (hyperechoic)
polyps will have no shadowing
cystolyths will have shadowing
advantages and disadvantages of using radiography to view the uethra
Plain radiographs yield minimal diagnostic information
Always include entire pelvis and male urethra
2 lateral views: hindlimbs caudally and cranially
Feline Lower Urinary Tract Disease
A collection of conditions that can affect the bladder and/or urethra in cats:
Urolithiasis
Bacterial infections- RELlTIVLY UNCOMMON IN CATS, SEEN MORE IN OLDER CATS
Urethral plugs
Anatomical defects
Neoplasia
Feline Idiopathic cystitis- common, espessialy in younger cats
Clinical Signs of FLUTD
Lower Urinary Tract signs:
Dysuria (77%)- +/- vocalisation &/or pain
Pollakiuria (78%)
Haematuria (71%)
Stranguria (70%)
Periuria (70%)
Signs of urethral obstruction?
Behavioural changes: - associated with PAIN
Loss of litter training
Aggression
Excessive grooming- Not just around rear but around caudoventral abdomen
“Constipation”
Stilted gait as are uncomfortable
Abdominal pain
iFLUTD
The typical Feline Idiopathic cystitis cat:
young or middle aged (<10years)
neutered
overweight
inactive
mainly indoor
dry diet
multi cat house
New Theories:
Interstitial cystitis in people-
neurogenic inflammation
mucosal defects- Increased bladder wall permeability, Altered GAG layer
Neuroendocrine imbalance
triggered by stress
neurogenic inflamation- Characterised by submucosal histopathological changes in the urothelium
Damaged urothelium
vasodilation
haemorrhage
Lymphocytic infiltrate
Muscularis fibrosis
increased mast cells (20% of patients)
diagnosis-
Signalment
Are there any clues to the possible underlying cause?
Age of cat - infection or idiopathic cystitis?
Clinical history
Is this the first episode or a recurrent episode?
Are they a multi cat household? Stressful events recently?
Pattern of behaviour
Are there features that increase the likelihood of:
UTI
Neoplasia
Urolith
rule these out
managment-
iFLUTD…
pain relief – 5-7 days
how do we treat a disease if we don’t understand the cause?
Control the discomfort
Buprenorphine
Glucocorticoids have no benefit in clinical trials and may cause pupd
NSAIDs
placebo controlled trial with meloxicam showed no benefit (Dorsch 2009 ECVIM)
Flush the bladder with
saline –> urohydrodistension
Lidocaine
Self-limiting!
Increase water intake
Produce a dilute urine and increasing flushing out of bladder
wet diet
free access to water
water fountains
tuna water
reduce stress- consider social factors, resources
physical examination of obstructed cat
Bladder palpation-
distended?
firm
painful
Penis discoloured +/or swollen
Dehydrated
Often systemically ill if obstructed
Bradycardia
Non obstructed cat-
Bladder palpation-
small
thickened?
painful?
Systemic signs are uncommon but could indicate concurrent disease
flud diagnostics
Urinalysis
Haematology and Biochemistry-
Unremarkable unless systemic disease
Essential in obstructed cats
Radiography
+/- contrast
Ultrasound- Not for urethra!
Cystoscopy
Exclusion of other causes - iFLUTD
Urethral Obstruction Causes
Uroliths-
Struvite (magnesium ammonium phosphate)
Calcium oxalate
Urethral plugs-
Protein-colloid matrix
Mucoproteins, albumin, globulin
Cells – RBCs, WBCs, epithelial cells
+/- crystalline material
‘Idiopathic’ obstruction-
Functional not physical obstruction
urethral spasm
mucosal oedema
Complicating issue in male cats… a design fault!
Unblocking the blocked cat
Stabilise the patient-
haematology, biochemistry, electrolytes- Correct the electrolyte disturbances; HyperK+-
Calcium gluconate if bradycardic, Dextrose
Fluid therapy in all cases-
Hartmann’s or 0.9% sodium chloride
Cystocentesis? – Care.-
Advance the needle through the bladder wall at a 45-degree angle directed toward the trigone
General anaesthesia
Aseptic technique and a gentle hand are fundamental to urethral catheter placement.-
Extrude the penis and retract it caudally to straighten the urethra.
Advance a urinary catheter into the urethra to the site of obstruction – never force past obstruction!
Saline flushing as catheter advanced
Rectal palpation by assistant
Once the urethra is patent, advance catheter
flush and drain the bladder multiple times with sterile saline to remove debris and help prevent rapid recurrent UO.
Halsted’s Principles
Strict Asepsis
Gentle Tissue Handling
Haemostasis
Preservation of the blood supply
No tension on tissues
Good approximation of tissues
Obliteration of dead space
maintaining haemostasis during surgery
applying Digital pressure- 60 seconds for minor, 5 mins for majour
Haemostats- crushes tissues
Packing with surgical swabs- good for deeper or more delecate tiussues, can disloge blood clots when removed
Lavage with saline- allows visulisation
Ligatures- good for thigs that likly wont clot
Topical haemostatic agents
Tourniquets- limb amputations
Diathermy- electrocautory
Sutures
Placement of sutures in tissue
Sutures are used to:
Close tissue planes
Re-appose vital structures
close dead space
Retract tissues with minimal handling
Stabilize and exteriorize tissue and organs.
Monofilament
Advantages:
Smooth surface
Low friction
less drag
less tissue trauma
No bacterial harbouring as nowhere to stick
No capillarity
Disadvantages
Poor handling
Poor knotting
‘Memory’
Stretch
Multifilament
Advantages:
Strength
Soft & pliable
Good handling
Disadvantages
Harbour bacteria
Capillary action
‘wicking’ in the suture material gaps
Tissue trauma
Drag/chatter/cutting
Absorbable sutures
Absorbable, or soluble, sutures undergo degradation and a rapid loss of tensile strength within 60 days
Intended primary for short term use
Good in feral cats/vicious animal
Absorption routes:
Proteolysis e.g. catgut
Hydrolysis e.g. vicryl
Advantages
Broken down by body
No foreign material left
Disadvantages
Shorter wound support
Examples:
Multifilament:
Catgut- bad for inflamation
Polyglactin 910 (vicryl)- well tolerated, long absorbtion
Monofilament
Polydioxanone (PDS)
Poliglecaprone 25 (monocryl)
Catgut
multifilament
Removed (rapidly) by proteolysis & phagocytosis
Plain catgut approx. 7-10 days tensile strength
Chromic catgut 10-14 days
Any situation that needs short term support
Derived from ruminant intestine
Doesn’t have a predictable absorption rate so don’t know how long its going to last
known to produce intense tissue reactions.
Polyglactin 910 (Vicryl)
multifilament
Braided synthetic absorbable
Good handling
Good knotting
Coating ensures smooth passage through tissue
Also Vicryl Rapide
Lactomer 9-1 (Polysorb)
Strong braided absorbable multifilament
Similar to vicryl
Finer, more compliant
superior handling, less memory
Tensile strength >21 days
Polydioxanone (e.g. PDS, PDS II)
Synthetic absorbable monofilament
High initial strength
Predictable absorption
Long term wound support
e.g. linea alba or other tissues that take a while to heal
Smooth passage through tissue as is monofilament
Poor handling and poor knotting
Minimal tissue reaction
Poliglecaprone 25 (e.g. Monocryl)
Monofilament synthetic absorbable
Excellent strength
Good handling
7 days 50% tensile strength remains
Non-Absorbable sutures
Retained permanently or retain tensile strength >60 days
These elicit a tissue reaction that results in encapsulation of the material by fibrous tissue
Advantages
Permanent wound support (e.g. hernia)
Disadvantages
Suture sinus
Material becomes encapsulated and eventually becomes an abscess
Foreign body
Suture extrusion
Silk
Twisted/Braided biological suture material
Made from silk worm cocoon
Non-absorbable- doeas technically but takes long time
Excellent handling
Suture standard
Good knot security
Nice and soft e.g. good to use for entropian
Disadvantages
Tissue reactions common
Rapid loss of strength
Ultimately fragments - eventually breaks off
Long term foreign body reactions
Never to be used in presence of infection
Polyamide (Nylon e.g. monosof, ethilon)
non-absorbable
Monofilament or multifilament
Usually used for skin closure
High memory
Hydrolysed slowly
principles of chosing suture material
tensile steanght should match streanghth of tissue
rate of loss of streangth should match wound gain of streangth
will sutre alter healing- reaction ect
mechanical prprties should match wound tissue
Suture characteristics
Suture/tissue interaction
Tissue characteristics
Wound characteristics
Patient factors
Surgeon factors
Why spay?
Elective -prevention of breeding potential
Treatment of disease-Neoplasia, pyometra
Stabilise systemic disease e.g. diabetes
Population control
Increased lifespan
Commonly reported advantages for performing sterilisation are:
reduced risk of mammary neoplasia
reduced sexual behavioural problems
Reduced stress of pseudopregnancy
When to spay?
Age:
Younger
Reduced risk mammary tumours https://bestbetsforvets.org/bet/579
Incidence of other neoplasia?
bitches >3 months post-season
Ligaments of he uterus
Broad ligaments:
Mesometrium- uterus, cervix, vagina
Mesovarium- ovary
Mesosalpinx- surrounds oviduct
bursa formed by the mesovarium and mesosalphinx
Proper ligament of the ovary (O to H)
Suspensory ligament of the ovary (O to wall)- break to expose ovary
Round ligament of the uterus
Open OVH/OVE method
Landmarks:
Caudal to umbilicus
Steps:
Stab incision for linea alba- insision extended via sissors
hook ovary
Stretch/break suspensory ligament
make window in mesometrium
Clamp & ligate pedicle
Transect the pedicle distal to ligatures
Check for haemorrhage
Repeat on other side
for ovh- ligate and cut at tip of uterine horn
Laparoscopic OVE
Advantages:
Quicker return to activity
Less post operative pain
Weak evidence
Disadvantages:
Operator training and experience
Kit
Cost
Complications -> convert to open anyway
Ovarian Remnant Syndrome
Oestral activity (2w-9years later)
More common after routine procedures
Hormonal investigations
? R > L ovary
may be easier to find residual tissue in oestrus.
may see enlarged ovarian vessels on functional side.
Submit tissue for histopath
Always open ovarian bursa after surgery to check whole ovary removed.
Urinary Sphincter Mechanism Incompetence (USMI)
Most common non-neurogenic cause of canine incontinence
Typical case = older, spayed bitch
Several factors may be involved:
Ageing or lack of oestrogen cause changes in urethral support structures (collagen)
Abnormal position of bladder or urethra (“intra-pelvic bladder”)
Reduced amount of smooth muscle in the urethra
Obesity - increases intra-abdominal pressure and makes things worse
Breed predispositions (genetic factors?)
Recent systematic review stated evidence not strong enough to determine link between neutering or age of neutering and urinary incontinence in bitches
OVH in the queen
Left flank:
Landmarks: iliac crest, greater trochanter and the caudal ribs
Advantages:
Reduced infection
Easier to monitor – ferals
Disadvantages:
Difficulty exposing repro tract?
Midline:
Umbilicus -> pubic brim
<12 weeks; go 2/3 of way back from umbilicus to pubic brim
halfway for > 12 weeks
Advantages:
Better exposure/visualisation
Larger wound e.g. pregnancy
Disadvantages:
Difficult to monitor e.g. feral
Increased contamination risk
Why castrate?
Advantages
Prevention of some neoplasia
Prevention of testosterone-stimulated disease
Reduced male behaviour
Disadvantages
Increase risk of some neoplasia
Reduced male behaviour (important for guarding / performance dogs)
Delayed growth plate closure (if pre-pubertal neuter)
Can increase risk of fractures
Low testosterone (concern if castrated late)
when to castrate
Early vs. conventional neutering
Fixed age?
Prepubertal?
Cats <4-6 months
Dogs – more variable
Early:
Delayed physeal closure (not shown to be associated with growth plate fracture)
? Increased risk of osteosarcoma in Rottweilers/ joint disease and neoplasia in Golden Retrievers
relevent anatomy of testes
located in an evagination of the peritoneum (vaginal tunic)
covered by
Tunica albuginea
Visceral layer of vaginal tunic
Eight layers:
Skin (scrotum)
Dartos
External spermatic fascia
Cremaster muscle (only in one part)
Internal spermatic fascia
Parietal vaginal tunic
(Vaginal cavity)
Visceral vaginal tunic
Tunica abuginea
(Testis)
q
surgical method of neutering the dog
Pre-operative evaluation:
Physical examination
Palpation of scrotum and inguinal canal
Check there are two descended testicles!
Pre-operative analgesia
General anaesthetic
Dorsal recumbency
Aseptic skin prep
Note: do not clip the scrotal hair!!
Single mid-line incision
Commonly performed as:
Modified (open then subsequently closed)
Closed
Open
Which approach?
Pre-scrotal:
Between scrotum and prepuce- most popular in dogs
Scrotal
Open Castration
Internal spermatic fascia is incised
Provides direct visualisation of the spermatic cord and BV’s
Closed Castration
Parietal vaginal tunic not incised
What is the definition of a fertile ram?
“…capable of getting 85% of 60 normal healthy naturally cycling ewes in lamb in the first cycle in a commercial situation”
“…a mature ram lamb is expected to achieve pregnancies from 85% of 40 normal, healthy, naturally cycling ewes in the first cycle”
stages of fertilaization involving the sperm
Sperm Capacitation- Freshly ejaculated sperm are unable or poorly able to fertilize. Rather, they must first undergo a series of changes known collectively as capacitation.
Sperm-Zona Pellucida Binding-
Binding of sperm to the zona pellucida is a receptor-ligand interaction with a high degree of species specificity. The carbohydrate groups on the zona pellucida glycoproteins function as sperm receptors.
The Acrosome Reaction- acrosome - a huge modified lysosome that is packed with zona-digesting enzymes and located around the anterior part of the sperm’s head.The acrosome reaction provides the sperm with an enzymatic drill to get throught the zona pellucida
Penetration of the Zona Pellucida- The constant propulsive force from the sperm’s flagellating tail, in combination with acrosomal enzymes, allow the sperm to create a tract through the zona pellucida. These two factors - motility and zona-digesting enzymes- allow the sperm to traverse the zona pellucida.
Sperm-Oocyte Binding- Once a sperm penetrates the zona pellucida, it binds to and fuses with the plasma membrane of the oocyte. Binding occurs at the posterior (post-acrosomal) region of the sperm head.
Testosterone
Produced by the Leydig cells of the testes
Initiates Pubertal development of the testis then optimises spermatogenesis in adulthood
Targets the Sertoli cells
Follicle Stimulating Hormone
Targets the Sertoli cells
Produced by the anterior pituitary gland
Initiates pubertal development and maintains spermatogenesis during adulthood
Luteinizing Hormone
Produced by the anterior pituitary gland
Targets the Leydig cells
Ram Fertility exam
3 stage process
1 – Full clinical exam and reproductive tract examination (RAM MOT)
2 - Pre-breeding exam (PBE)
3 – PBE certification
How long does spermatogenesis take in the ram?
47–48days
By what age do 90% of rams have a mature sized scrotal circumference?
> 14 months
Methods of Semen Collection in ram
Artificial Vagina (AV Collection)-
Defined as ‘Gold Standard’
Attempt first if appropriate
Rams require training
Ewe Teaser – Be aware of Welfare Implications
Not practically Feasible in many commercial situations
Vaginal Aspiration (VA)-
Teaser Ewe required
Welfare
Disease Risk
Contamination – blood, pus, inflammatory exudate white cells
Difficult to Interpret
Ensure rams remain separated from ewes, ideally >14 days prior to examination
Electro Ejaculation (EEJ)-
Commonly Used in field conditions
A small population of Rams fail to ejaculate – caution with failing rams
Often highly successful following teasing
asssesing Gross Motility
of sperm
A function of both motility and concentration
Low Power x 40
Scored on a Scale 1-5:
1 – No Swirl, generalised oscillation of individual cells only
2 – Very Slow distinct swirl
3 – Slow Distinct Swirl
4 – Moderately Fast Distinct Swirl
5 – Fast distinct swirl with continuous dark waves
assesing Progressive Motility
of sperm
Perform at 100x and 400x Magnifications
Critical to perform
Previously 30% minimum acceptable
Now 60 % minimum acceptable
No circling, zig-zagging or floating
“… ability of individual cells to achieve progressive, unidirectional, linear motility at a rate of at least 1x times cell length per second”
Morphological examination of semen sample
Relationship to ‘fertility’
Reflects Physiological and/or pathological status of the testes
Reflects maturation and transport processes occurring within the epididymides.
Useful diagnostic tool when dysfunction has been identified.
A MUST DO for PBE
Nigrosin Eosin Stained Smear
High Power magnification X1000 (X100 Lens)
Oil Immersion
Perform Morphology Count
Assess minimum 100 cells
≥70% to achieve Pass
Handling Issues Identified!
Common Sperm abnormalities
Defects of the sperm head-
Pyriform Heads
Micro/Macrocephalic Sperm
Nuclear Vacuoles
Knobbed Acrosome Defect
Detached Heads
Defects of the sperm tail-
Proximal Cytoplasmic Droplets
Distal Cytoplasmic Droplets
Distal Midpiece Reflex
Severely coiled tails/Dag Defect
Coiled Principal Piece
Bent Tails - Hypotonic Shock
Abaxial Tails
Accessory Tails
List 5 common disease of sheep which may affect ram fertility
Epididymitis (Brucella Ovis)-
Epididymitis is a venereal disease of rams caused by the bacteria Brucella ovis. Epididymitis means inflammation of the epididymitis, the tubular portion of the testicle that collects the sperm produced by the testes and stores it until it is ready to transport. Severely affected rams will often have at least one enlarged epididymis and may show pain when the testicle is manipulated.
can also be caused by Corynebac-
terium ovis (the “cheesy gland” germ
Brucellosis-
also known as ‘bruce-o’ is a bacterial disease that permanently infects the testes and epididymis of rams, rendering them infertile. It also temporarily infects the reproductive tracts of ewes, meaning that ewes can potentially spread the infection to uninfected rams. Rams also pick up infection from each other in the ram paddock.
Sheep brucellosis is practically incurable, so control of the disease relies on sound biosecurity and testing to eliminate infected animals.
large worm burdens
“pizzle-rot” or enzootic posthitis. Pizzle-rot is an infection of the sheath of the penis and is caused by the bacteria Corynebacterium renale. Pizzle-rot can also be caused by high protein diets that include a crude protein value higher than 16%.
stages of labour in cattle
Stage one labour (start of contractions) : 8-12 hours
Stage two labour (from amniotic sac rupture to calf out): >2 hours
Stage three labour (passing of fetal membranes): 4-6 hours
Suggested intervention points during stage 2 (Oklahoma state research):
30 mins no progress cow
60 mins no progress heifer
what is assessed in the initial examilation of a calving cow
Local conditions
(Mal)presentation
FM disproportion
Obstruction
Twins
Malformation
(Metabolic – hypocalcaemia- calcium drives muscle contraction)
Feto-maternal disproportion
calf too big/ dam too small
Dam factors-
Age, weight, parity, BCS, nutrition
Calf factors-
Gestation length, breed, sire, exess nutriom
Bones or soft tissue?- bcs
Herd level significance?- cow selection? bull selection?
often causes crossed legs presentation due to stuck shoulders
Obstruction in calving
Normal’- Undilated cervix
Abnormal- Undilated cervix- abnormal presentation causes abnoral factors and cervix doestn dilate
Uterine torsion- often have milk fever when corrected
Pelvic abnormalities
Obstruction in calving
Normal’- Undilated cervix
Abnormal- Undilated cervix- abnormal presentation causes abnoral factors and cervix doestn dilate
Uterine torsion- often have milk fever when corrected
Pelvic abnormalities
Immediate post-calving management
‘Tears and Spares’ check
Rehydration
Nutrition
Management of stress
Client management
Lessons to be learned
Herd-level implications
Retained fetal membranes
Nerve damage
Tears or bleeding
Uterine prolapse
Hypocalcaemia
Trauma
(Other concurrent disease)
Management of the neonate
Start breathing
Shock, rubbing, positioning
Assisted ventilation
Correct acidosis
Iodine navel
Colostrum
ID
Management of the neonate
Start breathing
Shock, rubbing, positioning
Assisted ventilation
Correct acidosis
Iodine navel
Colostrum
ID
if the dominant bull is infertile…
he will stop fertile bulls servicing cows while not servicing cows himself
Fully fertile mature bull running with 50 cycling healthy cows should deliver:
60% in calf in 3 weeks
<10% empty after 9 weeks- this can be skewed by issues with the cows
TAKE CARE!-
Herd circumstances- weather, grass quality , diet, heat stressect
Changing status
name a few causes of infertility in bulls
Poor libido
Injury
Overwork
Nutrition
Corpus cavernosum rupture
Persistent frenulum
Corkscrew deviation
IPBP
Penile trauma
Fibropapilloma
Testicular hypoplasia
Orchitis
Epidydimitis
Seminal vesiculitis
Testicular degeneration
Systemic illness
BVD
Genetic malformation
Iatrogenic
these can be catagorised as:
Failure to mount
Failure to achieve intromission/ejaculate
Failure to achieve fertilization
Reaching the ovum
Producing a viable zygote
Bull Breeding Soundness Evaluation
Physical exam- bull must Sustain himself
Locate females in oestrus
Mount those females
BCS- too thin= underlyign health issue. to fat= testicles retain too much heat
Heart &lungs
Eyes
Jaw
Locomotion- Lameness
Conformation- strain when working, genetics
Abnormalities
External genitalia
Palpation of testes
External genitalia
Scrotal circumference
External genitalia
Penis
Internal genitalia
Accessory sex glands
Semen analysis- bull bust Inseminate
Fertilize
Libido/service assessment- bull must NOT KILL ANYONE IN THE PROCESS
Infectious disease?- bull from small closed heard would be niave to infectous disease
semen collection in bull
Mated female- Internal AV inseted into cow in heat
Artificial vagina
Ampullae massage
Electroejaculation (EEJ)
Fresh cow check
Health check
Temp, smell (infection), rumen fill, hydration
Appetite
+/- Ketones
+/- Vaginal exam
Metritis
Uterine infection post calving (~3 – 21dim, mainly 4-7d)-
Voluminous purulent discharge
Smelly, red-brown usually
Involves the myometrium and the endometrium
Usually results in systemic illness
Fever
Inappetence
Depression
Treatment:
Systemic antibiotics
NSAID
Fluid therapy
Energy – prop glycol
Herd situation?
prevelance- 3%- 25% of cows
~$500/case (J. Perez-Baez 2021)
Post Natal Check
Often around 30 days in milk
Two assessments:
Resumption of normal cyclicity
Uterus involuted and free of infection- Endometritis, Abscesses
Herd level assessment useful-
Proportion of cows cycling
Proportion of cows ‘dirty’
Endometritis
Uterine infection limited to the endometrium
>21days in milk
Often called ‘whites’ – white, purulent discharge
No systemic effects on cow health
~£160/case (AHDB)
Diagnosis – vaginal exam, metricheck, US
Treatment – if CL; PGF2a, or ‘washout’. cow to be taken out of progeserone heavy staye and put into estrus as its protective against infection
discharge can be graed 0-3- metri checker
Post calving uterine infections
thickened wall
see puss on ultrasound
dystocia risk factor- malpresentation, twins
age
metabolic stasis
poor imune function
stress
concurrent disease
hygean
retained fetal membranes
Not Seen Bulling cow check
After voluntary wait period (~50dim)
Assess whether cow not been or not seen in oestrus
Various hormonal interventions available
Interventions escalate in severity as DIM increases
(Heat delay/service delay)
Beware of pregnancy!
Actions depend on DIM, ovarian status, co-morbidities;
PGF2alpha
GnRH
P4
(Oestrogens – not in UK/EU)
Synchronisation protocols
~100% submission rate
Double prost
Ovsynch 56
CIDR/PRID synch
Cosynch…
Pregnant!
Cystic ovaries-
Follicular cyst – thin walled, fluid filled structure >30mm diameter persisting on the ovary for >10 days in the absence of a CL
Luteal cyst/part luteinised cyst – wall
thickness greater than 3mm
True anoestrus
Uterine disease-
Chronic endometritis, pyometra, mucometra
Difficult to truly diagnose ovarian dysfunction at one visit!
cow Pregnancy Diagnosis
Transrectal ultrasonography: >28 days
Manual palpation: >~35 days
Later gestation – fremitus, cotyledon bouncing
PAG testing ( pregnancy assosiated glycoprotien)– milk recording
Progesterone monitoring – eg De Laval VMS systems
Knocking
Non-return (animal does not appear to come back into heat)
Benefits of transrectal ultrasonography vs manual:
More accurate assessment of uterus (and ovarian structures)
Can detect twins
Can detect fetal heartbeat and assess viability
Less likely to cause iatrogenic abortion
Can sex embryos (55-60d)
Benefits of manual palpation
Cheap, no kit required
Possibly easier in later gestation than US?
Aging Pregnancies
Farm records!
Practice
Ultrasonography
Manual palpation
diagnosisng twins in cows
multiple corpora lutea- most commonly double ovulation rather than split embryo
twin line
two fetus visible
often one fetus may dies
Submission Rate
Proportion of eligible animals served within a given time period (usually 21 days)
AYR target: >60%
All about heat detection
Provided cows are cycling
factors effecting it:
enviromental factors- confidence in floor, light, fpace
managment factors- fertility interventions, what other cows they are housed with
cow factors- health, genetics
Conception Rate
Proportion of served animals Pregnant at PD
Not a true measure of fertilisation rate-
effected by when you PD
(Early Eembrionic Death /Late ED)
AYR target >40%
factors:
enviroment- cow comfort, flooring, temp, food and water
managment factors- bull choice, breed choice, teqnique
cow factors- health, uterine enviroment
Pregnancy Rate
Proportion of eligible animals pregnant in a given time period (usually 21 days)
PR = Submission Rate x Conception Rate
For example: (SR 60%) x (CR 40%) = PR 24%
AYR target: >20%
Block Calving Systems
Spring vs Autumn
Resource planning and requirements
Cow choice
Seasonal management strategy
Seasonal output
spring block- smaller cow, lower grazing. peak yeailds= peak grass growth
autumn block= larger cow
Block calving fertility management
Fertility visit structure:
Clean checks
PSM -21d
PSM -7d
PSM +7d
PSM +21d
PDs
Different strategies
12 block calving- 12 block breeding- fertility managment for year over
Block Calving KPIs
Submission Rate: >90%
Conception Rate: >60%
3 week I/C rate: >50%
6 week I/C rate: >75%
12 week empty rate: <8%
Often AI and bulls
KPIs
key performance indicators for cow fertility
Heifer management
Aim to calve in well-grown heifers by 24 months
Which means they need to be In Calf at 15 months-
Heat detection
Synchronisation
start inseminating at 12 months
Age at first calving KPIs…
Av vs %?
Better measures?
% 2nd lact?
follicular stasis
reproductive condition ofchelonians
Pre-ovulatory egg binding
Often seen in the older, female tortoise kept alone
If follicles are not resorbed inflammation of the follicles coelomitis
CS anorexia, HL paresis, generalised weakness
Due to an inability to produce progesterone failure of regression of follicles.
Recent exposure to a male after a period of prior isolation?
Inappropriate diet?
Inappropriate husbandry?
Stress?
Lack of hibernation, light and temperature change?
Still in need of further research
disgnosis-
Blood work – raised calcium, raised proteins
Ultrasonography
Advanced imaging
treatment-
Fluids
Nutritional support
Correct husbandry
Often surgical hormonal implants ineffective for these cases
COELIOTOMY
entering the coelomic cavity
Ligation – haemoclips or absorbable monofilament suture material
Closure - absorbable monofilament suture material
Skin closure
Everting suture pattern
Suture choice often non-absorbable and strong.
Skin suture removal not to be removed for at least 6-10 weeks
PLASTRONOTOMY
Heart > in the midline intersection of the pectoral and abdominal scutes.
Plastron hinge -: often between the abdominal and femoral scutes.
Abdominal veins - parallel, running in a craniocaudal direction below the plastron
Ovariectomy in chelonians
The prefemoral approach-
Preferred method if possible – less traumatic and faster recovery time
Useful in species with a larger prefemoral fossa
Craniocaudal incision is made in the skin
Blunt dissect underlying abdominal muscles
Dissect coelomic membrane
Closure – simple interrupted or continuous pattern for coelomic membrane, muscle and fat.
Closure – everting pattern for the skin
Dystocia – egg retention
Non-obstructive factors
Lack of suitable nesting site
Stress
Hypocalcaemia
Infection of oviduct
Poor muscle tone
Obstructive factors
Oversized eggs
Malformed eggs
Oviductal stricture
Space occupying lesions
Clinical signs-
No presenting signs are pathognomonic for dystocia
No signs
Abnormal posture
Hind limb paresis
Anorexia
Malodorous cloacal discharge
Faecal or urinary retention
Cloacal organ prolapse
treatment- chelonians
Fluids
Nutritional Support
Provision of nesting site
Calcium gluconate
Oxytocin-
Induces parturition/egg laying when uterine inertia is present (as long as there is no evidence of obstruction)
trteatment- lizards and snakes
More commonly seen in oviparous (egg-laying snakes) >pythons, rat snakes, king snakes milk snake
Less commonly seen in ovoviviparous (live-bearing) snakes > boas, garter snakes
cloacla prolapse
Prolapse – advice to client moist substrate (no woodchip or sand), lubricate tissue
Cover with cling film/glove
Identify tissue
Gastrointestinal impactions
Dystocia
Parasitism
Hypocalcaemia
Space occupying lesion
Faecal/foreign body impaction
Dystocia
Ultrasonography – follicles
Blood work – hypocal
Faecal analysis - parasites
treatment-
Address underlying causes
Analgesia
General anaesthetic to replace prolapse-
Manually
Surgically
Care – must check for intussusception
Amputation >necrotic phallus
dystocia of birds
Dystocia-
Caudal uterus
Vagina
Uterovaginal sphincter
EMERGENCY if compresses blood vessels and/or nerves
Radiography (conscious)
treatment-
Stabilisation
Warmth
Fluid therapy
Calcium
PGE2 gel
GA manual delivery
Chronic egg laying in birds
Small psittacines >cockatiels
Produce repeated clutches or a larger than normal clutch
Depletion of calcium and protein stores
Poor bone density
Weight loss
Pathological fractures
Dystocia
prevetion-
Environmental modification-
Reduce photoperiod
Remove nesting material
Behavioural modification-
Training
Leaving in eggs
Nutritional modification-
Encourage foraging
Hormonal manipulation-
Deslorelin (Suprelorin)-
Desensitises GnRH receptors, thereby decreasing release of LH & FSH
Cabergoline (Galastop)-
Potent selective inhibition of prolactin
May have beneficial effect in birds with chronic egg laying.
In birds it also conjectured that its action could be mediated via its effect as a dopamine agonist.
Leuprolide acetate (Lupron)-
Leuprolide acetate is a synthetic nonapeptide that is a potent gonadotropin-releasing hormone receptor (GnRHR) agonist
What is mastitis and how do cows get it?
Pathogen gets into the udder cistern → inflammation of the mammary gland
All mastitis risk factors fit into at least one of 3 categories:
The udders natural defences are compromised
Bacteria numbers are increased at the teat end
The udders natural defences are by-passed
Mastitis is a game of risk and numbers!
Teat skin should be smooth, thick firmly adhered, no glands.
Defenses:
The Teat (Streak) Canal:
Keratinocytes
Lipid secretions
Sphincter muscle
Phagocytes (somatic cells)
Frequent milking
Antibodies
Lactoferrin
Classifications:
Peracute/ acute / chronic
Clinical / sub-clinical
Environmental / contagious
From a therapeutic perspective may be graded as
Mild - abnormal milk
Moderate - abnormal milk and abnormal gland
Severe - abnormal milk, abnormal gland, and sick cow
clinical signs of mastitis in the individual cow
Abnormal milk and/or udder-
Secretion
Size
Texture
Agalactia-n absence or faulty secretion of milk
Blind or non-functional glands
Hungry neonate- esspecially in beef hers, a hungry calf might be a problem with the cow
Pain – altered gait
Enlargement of the supramammary lymph nodes
Teat and skin lesions
Visual examination (Gland and teats)- hard? hot?
Palpation of the gland
Palpation of the supra mammary lymph nodes- inflamed?
Inspect mammary gland secretions (stripping)- thick clots?
Perform a California Mastitis Test (Rapid Mastitis Test)
Check the skin adjacent to the udder
Inspect and palpate the mammary veins
California milk test (CMT)
The test uses a reagent that is added to a sample of milk. If the test is positive and a quarter is infected, the CMT mixture will appear thickened and gel-like.
good for subclinical disease
Septic mastitis
Most commonly caused by coliforms
Systemic signs of endotoxemia in severe cases-
weakness, depression, inappetence
fever, scleral injection
tachycardia, tachypnea
rumen stasis, diarrhea
Endotoxaemia induces hypocalcaemia
Bacteraemia
Mortality common with endotoxic shock,
MODS
Summer mastitis
“Dry cow” or “Summer” mastitis, caused by Trueperella pyogenes
Most infections occur during the dry period
The incidence of infection is increased by filthy, wet, or muddy environments for dry cows
Purulent infection often leads to abscessation of the gland
The organism may be spread by flies
Pathogen diagnosis-mastitic cow
(+/- clinical signs, SCC, response to treatment)
Individual milk culture or PCR
some may be on far- to detect gram neg strainsdue to that being able tobe treated without antibiotics
signs of mastitis in the herd
Bulk Milk Cell Count is too high (over 200) – I’m not being paid the quality bonus
There are too many clinical cases – I’m spending too much time treating cows after milking
Bulk Milk Cell Count is too high (over 400) – the milk company is going to penalise me
I have too many chronic high SCC cows that won’t cure – I am culling too many cows
I’ve lost another cow to E.coli, that’s the 3 one this month- too many cows are dying and they are expesive to replace
common causes from most common to least:
signs of mastitis in the herd
Bulk Milk Cell Count is too high (over 200) – I’m not being paid the quality bonus
There are too many clinical cases – I’m spending too much time treating cows after milking
Bulk Milk Cell Count is too high (over 400) – the milk company is going to penalise me
I have too many chronic high SCC cows that won’t cure – I am culling too many cows
I’ve lost another cow to E.coli, that’s the 3 one this month- too many cows are dying and they are expesive to replace
common causes from most common to least:
Incorrect teat spray volume or application
Teat end damage
Excessive vacuum
Over milking
Under milking
Unsuitable teat cup liners
Cup slip
poor cluster removal
what shoud be investigated whnn investigating a herd wide problem with mastitis
Staff and Farm profile
Bulk and Individual cow SCC
Clinical case data
Milk cultures & PCR
Milking machine static test
Milking machine dynamic test
Milking routine
Cow:parlour interaction
teat cup slips
Teat condition
Cow behaviour
milking time per cow
Completeness of milking
cluster alignment
Teat disinfection
The environment
Drying off
Calving
clinical signs of mastitits within a herd
Genetics report- to inform rate of mastitis resistance improvement?
Age demographic and replacement rate of the herd
Purchases from other herds? Were any herd checks done beforehand?
Any culls for clinical mastitis?
High BMSCC
High Bactoscan
High number of clinical cases
High number of repeat cases
High number of chronic SCC numbers
High number of deaths from mastitis
Milk quality & herd mastitis surveillance
Herd mastitis surveillance:
Tests performed by the milk factory on Bulk Tank Milk include:
Bulk Milk Cell Count (BMCC)
Protein, Fat, Urea
Total plate count or Bactoscan
Coliform count
Thermoduric count
Freeze Point (extraneous water)
On farm data
Clinical case rates
Culling/death rate for mastitis
Antibiotic IMM tube use
Herd recording (Individual Cow Somatic Cell Counts – ICSCC)/ (Conductivity-robots)
Lab tests:
Individual cow milk cultures (or PCR)
Bulk Milk PCR (for Strep agalactiae or Mycoplasma)
Milking machine test report
(eg Vardia/ Advanced Milking Solutions
WHY PERFORM A REPRODUCTIVE EXAM n a mare
Pre-breeding
•Breeding management (detection of follicular growth/optimum time to breed/post breeding problems)
•Infertility workup
•Pre-purchase examination
•Pregnancy diagnosis
•Import/Export- some regulations require it
Poor conformation of the vulva in the mare can lead to
Pneumo-Urovagina
■Vaginitis, cervicitis, endometritis
■Infertility
can be negated with caslick
Windsucker Test
Part the vulvar lips and listen for an in-rush of air•Tests the integrity of the vaginal vestibular sphincter
tr a n s r e c t a l U l t r a s o u n d in the mare
Uterus:Cycle staging-
•Estrus:endometrial folds•Diestrus: homogenus echotexture
Endometrial cysts•Intrauterine fluid•Pregnancy (twins, sexing, viability)•Abnormalities
vaginal exam of the mare
Visual exam:
■Speculum exam
■Vaginoscopy-
Allows to evaluate:
A. Changes in cervix during estrus cycle-
ESTRUS:
■Secretions ↑ (moist)
■Vascularity ↑ (pink)
■Relaxation ↑ (open)
DIESTRUS:
■Secretions↓ (dry
Vascularity↓ (pale)
■Relaxation↓ (closed)
B. Abnormalities■Anatomical■Accumulation material (urine, pus, blood)■Inflammation (vaginitis, cervicitis)■Varicosities■Tears/Lacerations (cervix, vagina)■Adhesions
- Manual Exam (digital evaluation):
■Cervix integrity:■Patency■Tone■Adhesions■Other abnormalities (Better evaluated in diestrus)
■Vagina integrity
how is daily sperm output of the stallion is linearly related to testis mass:
■Mass can be estimated by measuring testis volume:
■TV=0.52heightwidthlength
■DSO=(0.024TV)-0.76 (billions)
semen collection methods from the stallion
First consider:
■Restraint
■Tr a i n e d p e r s o n n e l
■Proper facilities
■Estrous female, phantom
Methods:
■Artificial vagina
■Electroejaculation
■Manual collection
Semen Evaluation in the stallion
Odour
■Volume
■Color
■Sperm concentration (100-400 million/ml)
■To t a l n u m b e r of sperm
■Sperm motility
■Semen pH (optional)
■Sperm morphology
■Cytology - other cell types
■Bacteriology / virology
■Flow cytometry/fluorescence(advanced)
Hemospermia
still fertile
indicates problems within stallion
hard to preserve
Oligospermia/azoospermia
no/ reduced sprem production
Obstructive disease-
■Alkaline phosphatase
■Testicular degeneration (Idiopatic or after insult)
■Te s t i c u l a r h y p o p l a s i a
■Overuse
bitch oestrus cycle
Pro-oestrous (10 days)- peak in oestrogen
Oestrous (10 days)- behavioural definition, bitch is receptive
Luteal phase- metoestrus/ dioestrus (2 month)- progesterone and lh spike
Pregnant or non-pregnant
Anoestrous (4.5 months)
P4 from CL only
LH and prolactin luteotrophic- help maintain cl and therefore progesterone
bitch gestation
Average gestation in the bitch is 63-64 days (range 56-72 days)
calculated either from
preovulatory surge of luteinizing hormone (LH) (65 ± 1 days)
day of ovulation (63 ± 1 days)
time of fertilization (60 ± 1 days)
General principles of small animal pregnancy diagnosis
Detection of protein / endocrinological changes associated with pregnancy
- Detection of the fetus or fetal membranes either directly or indirectly:
Abdominal palpation
Ultrasound examination
Radiographic examination - Detection of physical changes in the dam which are associated with her accommodating a fetus (increased size of the uterus)
- Detection of maternal changes that are secondary to endocrinological changes
History
When was she mated?
Have you noticed any changes in size of abdomen/teats?
Have you noticed any changes in behaviour?
Have you noticed any vulval discharge?
When was her last season?- if shes in luteal phase it could be pyo
clinical signs of small animal pregnacy
Secondary Changes-
Teat and mammary gland-more obvious in first timer-
Reddening
Enlargement
Secretions- small amount o vaginal secretion at beginning
Increase HR
Physical Changes-
Increased appetite
Weight gain
Abdominal enlargement in later pregnancy
Relaxation of the perineal tissue/vulva
Plasma Progesterone Concentration for pregnancy diagnosis in bithc
No rapid return to oestrus
Not sufficiently different between pregnant and non-pregnant bitches
this is why psuedo pregancy occurs
can use plasma relaxin conc instead
Plasma Relaxin Concentration for pregnacy diagnosis in the bitch
Values elevated in pregnancy from day 25 onwards and are diagnostic whilst a viable placenta is present
better than progesterone
when can abdominal palpation diagnose pregnancy in the bitch
From 21 days
Before this, the pregnant and non-pregnant uterus is not reliably palpated
Day 21 – 32
Aprox 1.5-3.5cm, round, firm and well separated
“Chain of walnuts”
After day 32
Gestational sacs become more confluent and lose their distinction - “sausages”
After day 50 the puppies may be balloted directly
radiography for pregancy diagnossi in the bitch
Limited use in early pregnancy as Fetal calcification after day 41-44 (av – 42d)- uterus may be seen to be enlarged but this may also be pyo
So radiographic diagnosis from day 45
Can determine number, position and relative size of fetuses from d50
Valuable in dystocia cases
gold standard for determining number
ultrasonography for pregnancy diagnosis
Fetal structures from day 17
Fetal heartbeats detected from approx. 24-28 days of pregnancy
Cannot assess number of fetuses
Has limitations, particularly in early gestation
Cannot be accurately used to count foetuses
Fetal heart movements 28-30 days after ovulation IF known
False negatives
False positives
using ultrasonography for gestational age
Appearance of certain organs
E.g. kidneys last 20 days of gestation (see table for reference)
Measurement of foetal dimensions – less useful in later gestation-
Gestational sac (or chorionic cavity) diameter in early pregnancy
Crown-rump length
Head diameter
Trunk diameter
Nb. These measurements are breed-specific
Pseudopregnancy
All entire non-pregnant bitches go through pseudopregnancy
Long luteal phase (~66d)
Clinical signs Prolactin
Covert/physiological
Overt/Clinical
Queen-
Sterile matings
Behaviours less commonly seen
Hyperaemia of nipples as in pregnancy - red teats
What do you do?-
Nothing
Prolactin inhibitors-
Cabergoline (galastop, finilac)
Bromocriptine
Do not spay
Pyometra
Occurs during the luteal phase
Due to bacterial colonisation at oestrus
Can be open or closed
Most common in middle aged and elderly bitches
Pyometra may also be induced by:
therapeutic administration of oestrogens for treatment of unwanted pregnancy
therapeutic administration of progestogens for prevention of oestrus
Pregnancy Diagnosis (Queen)
Polyoestrous
Return to oestrous confirms non-pregnancy
BUT lack of return is not specific for pregnancy
Behavioural changes not useful
Physical changes.. Can be subtle
Reddening of mammary glands d21
Enlargement of mammary glands d50
Manual palpation – d21-25 optimal
Relaxin – d25
Ultrasonography – 3 weeks post mating
Radiography – mineralisation of fetal skeleton at d40.
Accidental Pregnancies
Indications:
Unwanted mating (misalliance)
Size mismatch
Age
High risk of dystocia
Medical indications
Get a good history
+/- vaginal cytology
Options:
Surgical Approach- overyhystorectamy in late pregnacy
ovaryectomy in early pregnacy- ONLY IN EARLY PREGNANCY
- Pharmacological Approach
Drugs that act on the uterus:
Oestrogens e.g. oestradiol benzoate
Alters transit time of zygote
Within first 5 days of mating
not common due to side effects
Anti-progestogens
Synthetic steroids that compete with progesterone
Aglepristone (Alizin)
Day 1 - 45
Drugs that act on the ovaries:
Prostaglandins – luteolytic
Bitch and Queen corpora lutea are ‘autonomous’ for first 15 days of luteal phase
PG’s of little use before day 20
Repeated treatments are necessary
dogs very sensitive to it so not first line
Drugs that act on the pituitary gland:
Dopamine agonists (prolactin inhibitors) e.g. bromocriptine and cabergoline
No activity before 30d, moderate activity 30-40d
Suspected/Early pregnancy – Aglepristone
Mid-pregnancy 22-40 days – Aglepristone
Confirm by USS before and after (10d), repeat if necessary
Signs of parturition
Late pregnancy >40d after mating
PGF2a
Dopamine agonists
Combination
Predicting parturition
Bitch
A number of clinical indicators of impending parturition may be used, including:
Measurement of progesterone and LH during oestrous
Behavioural changes close to parturition- Restless
Seek seclusion/excessively attentive
Inappetant
Nesting behaviour
Shivering
Clinical signs close to parturition-
Relaxation of pelvic, perineal and abdominal musculature
Increased HR
Decline in body temperature
Measurement of progesterone in late pregnancy- rappid drop indicates partuition Around ovulation assists in prediction of whelping dates:
the date on which progesterone first exceeds 1.8 ng/mL (~2 ng/mL) predicted the day of parturition within:
±1 day – 67% precision
±2 days – 90%
±3 days - 100%
Around due date:
<2.8ng/ml = 99% chance of whelping within 48 hours
<1.0ng/ml = 100%
>5ng/ml = <2% chance of spontaneous parturition within 12 hrs
Diagnostic imaging
Queen
Induced ovulator – ovulation follows mating by 24-36 hours
Gestation = 52 to 74 days when recorded from the last mating or first mating to parturition, mean pregnancy length is 65– 66 days.
No significant reduction in temperature
stages of partuition- bitch
Stages:
Stage of preparation
Production of relaxin (placenta)
Causes relaxation of the pubic symphysis, vulval and perineal tissues
First stage parturition
Onset of contractions
Restlessness, nesting, temperature drop
Second stage parturition
Expulsion of the foetus
Third stage parturition
Expulsion of the placenta and foetal membranes
Puerperium
Dystocia
Normal birth = expulsive forces are sufficient to propel a fetus of normal size and disposition through a birth canal of adequate size
Dystocia occurs if any of these are abnormal or insufficient.
Inadequate expulsive forces
Inadequacy of birth canal
Presentation or disproportion (relative to the dam) of the fetus
Defects of expulsive forces:
Intrinsic defects of uterine contractility
Nervous voluntary inhibition of labour
Failure of contraction due to mineral/hormonal imbalances (primary inertia)
Exhaustion of uterine muscle or depletion of pituitary oxytocin stores (secondary inertia)
Defects in adequacy of birth canal:
Functional disturbances of genitalia e.g. incomplete cervical dilation
Obstructions e.g. neoplasia
Pelvic malconformations e.g. brachycephalics or past #’
Management of primary inertia (49% of bitches, 37% queens):
Exercise to stimulate contractions
Digital stimulation (feathering) to stimulate endogenous oxytocin
Calcium borogluconate IV
No response to Ca oxytocin
Perform a vaginal exam
If not successful C-section
Management of secondary inertia (23% of both):
Correction of the cause of dystocia
Nothing
OR
Ca2+, oxytocin C-sec as before.
Is the birth premature or overdue?
Has the dam given birth before – if so where there complications and what where these?
What is known about the sire (and his size)?
What has recently been observed in this bitch?
Has there been recent vulval discharge?
Have uterine / abdominal contractions been noted and if so when?
Have any fetal membranes / fluid been expulsed?
Have any fetuses been delivered?
when to get involved in partuition of the bitch
Second stage parturition
Expulsion of the foetus
Weak, irregular straining for more than 2– 4 hours
Strong, regular straining for more than 20– 30 minutes
Fetal fluid was passed more than 2– 3 hours previously, but nothing more has happened
Greenish discharge is seen but no puppy is born within 2– 4 hours
(red-brown in the queen)
More than 2– 4 hours have passed since the birth of the last puppy and more remain
The bitch has been in the second stage of parturition for more than 12 hours.
Foetal distress
Normal fetal HR = 180-240 bpm
<180bmp = Foetal distress
Foetal HR <150bpm at full term = immediate intervention required
Emergency Cesarean Section indications:
Primary or secondary uterine inertia nonresponsive to medical therapy
Uterine rupture or torsion
Fetal malposition without success of correction by manipulation vaginally.
Fetal death with remaining viable but distressed fetuses.
Fetal distress with decreased heart rate.
150-180 bpm consider CS
<150 bpm – immediate CS
Reproduction management of the exotic female.
Approaches
Traditional ventral abdominal midline (rabbits)
Flank (guinea pigs and rats)
Bilateral
Unilateral
Combination of the two
Laparoscopic approach (zoo animals)
Reproduction management of the exotic female.
Approaches
Traditional ventral abdominal midline (rabbits)
Flank (guinea pigs and rats)
Bilateral
Unilateral
Combination of the two
Laparoscopic approach (zoo animals)
Reproduction management of the exotic femaleexotic male
Terminology
‘Castrate’ – removal of the testicles
Scrotal
Open
Closed
Prescrotal
Open
Closed
Abdominal approach
Vasectomy
Vas deferens ligated and incised
Medical management
Implants
Hormonal injections
Options vary depending on the species
Separation of the two sexes
Isolation of social species welfare implications
Housing animals of same sex may lead to fighting
implant-In response to testosterone ferrets produce sebaceous secretions and a musky odour
Can place deslorelin implant, SC between scapulae every 18-24 months
GnRH implan> Plasma FSH and testosterone concentrations, testis size and spermatogenesis were all suppressed after Deslorelin implant
Owners to monitor >once testes increase in size again > time to place another implant
Ferrets – Teaser/vasectomised males
Natural mating (vasectomised male/’teaser’ male)
Good option for owners/working ferreters with many jills.
Mating appears violent biting and dragging the jill by neck
Pseudopregnancy lasts approximately 42 days
Increased aggression towards owners and cage mates
Abdominal enlargement
Mammary gland development
Risk of disease transmission if vasectomised hobs shared.
Will not change smell or hormonal behaviour
Leaves options for future breeding of the female
Vasectomy- ferrets
Vasectomised males are used to take jills out of oestrus without the risk of pregnancy
Vasectomised ferrets will retain their musky odour, as this is dependent on testosterone levels.
The spermatic cord is palpated cranial to the testis, and a 10 mm skin incision made directly over it, approximately 20 mm cranial to one scrotal sac
The vaginal process is identified.
The parietal tunica of the vaginal process is incised and spermatic cord is exposed
The white vas deferens is identified and a short portion is separated from the spermatic cord.
Double ligate at a distance of approximately 0.5cm and excise between the ligatures.
Submission of excised tissue for histological examination is recommended, to confirm proper excision.
Mild scrotal swelling may be observed postoperatively >usually resolves over 2–3 days
The vasectomised hob should not be used for 7 weeks after surgery
Ferrets – management of oestrus
Proligestone (Delvosteron, MSD Animal Health)
Suppresses/postpones the breeding season – maintains jill in anoestrus
Give 50mg per ferret in the Spring = 0.5ml per jill, administered via SC route
Signs of season often reduced within 10 -11 days
One injection often covers whole breeding season – but not always!
Pyometra risk
May be discontinued in 2023
Hormonal implant (Deslorelin acetate)
GnRH agonist
Licensed in males (9.4mg), off license in females
4.7mg used in both sexes but off license
Reversible control of ovarian activity
Ovarian suppression for approximately 18-24 months
Easy to place as an outpatient
Brief GA
Placed SC between scapulae
Surgical neutering
Ovariectomy or ovariohysterectomy depending on concurrent disease
Castration
Permanent method
Likelihood of developing adrenal disease.
Spaying rabbits
prevents
Unwanted pregnancies
Uterine disease
Cystic endometrial hyperplasia
Pseudopregnancy
Aneurysm
Neoplasia
Rabbits are sexually mature at 4-6 months
Neoplasia – adenocarcinoma 50-80% in certain breeds >4 years old
Free living European hares (feral) in Australia 21% of does had reproductive disease
Post mortem examination in pet rabbits
Mean year for neoplasia = 6 years
Youngest with neoplasia confirmed = 12 months.
Can we just perform ovariectomy?
Does depend on how early uterine disease can occur.
Anecdotally, reported in a 6 month old rabbit!
Unique anatomy
Two uterine horns
Two cervices
No uterine body
Long and flaccid vagina
Often large amount of uterine fat in mature rabbits
Vagina fills with urine during micturition
Techniques
Ventral midline abdominal approach
Ovariovaginectomy often described
2 cervices, empty directly into the large vagina
Ligate ovarian pedicles and ligate at cranial vagina
Ligature placed around vaginal side of cervices
Risk of urine leakage through the vaginal stump
Must use a transfixing ligature
Oversew
Risk of including ureters and blood vessels supplying the bladder if ligature placed too low.
Other points to consider
Prone to fat necrosis
Adhesions ‘internal scar tissue’ form around devitalised or traumatised tissue.
To minimise the risk of adhesions
Minimise tissue handling, always use instruments
Gentle surgical technique
Care with haemostasis
Never use dry swabs
Irrigate tissues with warmed sterile saline
Choose suture material wisely!
Use the finest suture material that is practical
Do not use biological sutures (cat gut)
reproductive managment of rodents
Reproductive management of rodents often requires surgery
Approach for the female
Traditional ventral midline
Flank
flank approch to spaying in rodents
Find your landmarks. Identify
The spine
The last rib
The pelvis
Gentle simultaneous pressure on these three points will produce a bulge of soft tissue in the centre > incision site.
Incise through skin (can be thick)
Blunt dissect through muscles
The external oblique
Internal laminar muscles
Once you have incised the muscle there will be internal fat
Fat will be associated with
The reproductive tract
The kidneys
The spleen
The GI tract
Retract the fat until you can see the distal uterine horn and ovary
Ligate the ovarian pedicle
In the guinea pig can perform whole procedure from the one incision
In the rat often a bilateral flank approach is required.
Ventral midline approach
Large incision needed
Challenging – deep body cavity, ovaries located cranially and dorsally
Longer surgery time
Longer recovery time
If large ovarian cysts can still perform flank approach
Remove fluid from cysts with a sterile needle and syringe.
advantages and disadvantages of radiography
Advantages:
Gives a global overview/screening
Assessment of adjacent thorax and skeleton
Good for detecting gas or mineralisation
Very useful for acute conditions (particularly vomiting)
Cheap and widely available
Disadvantages:
Superimposition of structures
Lack of inherent radiographic contrast (cf. thorax)
Soft tissue and fluid appear the same (water radiopacity)
Magnification
Less useful for chronic conditions (particularly diarrhoea)
Minimising scattered radiation
Low kV, collimation, use of a grid
Minimising scattered radiation
Low kV, collimation, use of a grid
Avoiding movement blur in a radiograph
Appropriate physical +/- chemical restraint
how would you deal with Low inherent contrast (soft tissue/fluid and fat) in a radiograph
Low kV (film)
patient preparation for a radiograph
Fasted, empty bladder and bowels, clean coat
important landmarks in an abdominal radiograph
Liver
Stomach
Spleen
Kidneys
Small intestines
Colon
Urinary bladder
border obliteration
Mesenteric fat highlights the serosal surface of the abdominal organs
Structures of the same opacity in contact with each other = border obliteration (border effacement/silhouette sign)
e.g in acites- fluid has same contrast
Abdominal Contrast Studies
Contrast media:
Either more radiopaque or radiolucent than surrounding tissue
Document function by taking sequential still images (e.g. barium series) or using real time radiography (e.g. fluoroscopy)
describe a normal liver on a lateral radiograph
Roughly triangular in shape with smooth distinct margins- when enlarged edges will be rounded instead.
Soft tissue opacity
Demarcated by the diaphragm cranially and the stomach caudally-
Gastric axis should between parallel to the ribs and perpendicular to the spine (lateral) and perpendicular to the spine (VD)
entral lobe-
Fairly sharp angle
Extends to slightly beyond the level of the costal arch
May see gall bladder ventrally in cat
when it is small (hypoplasic)-
Cranial displacement of stomach
Absence of caudoventral angle
Significance dependent on clinical signs, etc.
seen inDeep-chested dogs
hepatomegaly on a radiograph
Projection of caudoventral margin well beyond the costal arch
Rounding of caudoventral angle
Caudal displacement of stomach axis
describe the normal spleen on a radiograph
Location and size variable- Smaller in the cat (usually not visible on lateral views)
Flattened triangle on lateral view (tail of spleen)
Triangular mass next to left abdominal wall on VD (head of spleen)
Splenomegaly on a radiograph
Generalised splenomegaly is common
Subjective assessment
Wide normal range
Overlap maximum physiological/ minimum pathological size
Spleen enlarges following ACP / barbiturates
Localised splenomegaly-
Look for changes in shape as well as size
describe the stomach on radiograph
Rugal folds are often seen as parallel linear soft tissue opacities
If the stomach is completely collapsed and empty it may not be seen at all
Recap:
Fundus and body lie to left of midline
Pylorus to the right and ventrally
radiographs of the stomach can show- Changes in location, size, shape and margination
describe the small intestine on radiograph
Pylorus and duodenum are identifiable by location
Rest of small intestine fills “the space where there is nothing else!”
Cats tend to have less intestinal gas than dogs
Roughly even diameter throughout
Diameter in(dogs):
<1.4 x L5 unlikely obstructed
>2.4 x L5 likely obstructed
Look at the shape and distribution of the intestinal loops
Symmetrical peristaltic constrictions
Beware of “pseudo-thickening”
SI (or stomach) wall may appear thickened in plain images with partial filling with gas
viral causes of bovine Diarrhoea
-Rotavirus
-Coronavirus
-Bovine Viral Diarrhoea- young stock
bacterial causes of bovine Diarrhoea
•E.coli
•Salmonella species- agressive mortality rate
•Clostridia species
•Mycobacterium paratuberculosis (Johne’s)- slow incubation- vertical infection as calves, presents at 3-5 ears
Parasitic causes of bovine Diarrhoea
Protozoal:
•Cryptosporidium- disease of hygene
•Cocci
Worms:
•Strongyles
•Fluke
Nutritional causes of bovine Diarrhoea
•Milk scours
•Peri-weaning Scours
•SARA
•Grain overload
•Dietary changes
Environmental & Husbandry causes of bovine Diarrhoea
Exposure to pathogens usually as a result of failed husbandry
-Failure passive transfer of antibodies
-Poor hygiene of equipment
-Poor hygiene of housing
-Mixing of age groups
-Stress
Scour Check Kits
•Used to detect common pathogens in young calves
•Rotavirus, Coronavirus, Cryptosporidum& E. coli
•Can be used on farm, results in 10 minutes from small faecal sample
•Easy to interpret -two lines positive, one line negative
Faecal Worm Egg Counts for scours
•Preparation of faeces in a salt solution to look for worm eggs or cocci oosysts
•Quick test to indirectly assess parasite burden
•Test performed off farm either in-house or sent off to external lab
•Used to look for gut worms and cocci oocysts in youngstock & adults
•Can also be used in series to test wormer efficacy
Faecal Culture for scours
•Microbiology for bacterial causes of GI disease.
•Can be used for Salmonella, Johnes, Clostridial toxin detection and Rota/Coronavirus
•Can be done in-house or sent to external lab
•Can be slow to yield results
Serology for scours
•Blood sampling for specific diseases
•Can be used if clinical suspicion of Johnes or BVD at an individual animal level
•Tested in an external lab
bulk Milk Surveillance for scours
•Used to monitor disease in adult cows
•Can be used to monitor Fluke, BVD, IBR, Johnes, Salmonella
•Useful comparing results year on year
•Take into account vaccination status for some diseases when interpreting results
disease of the caecum in the horse
One of the most common diseases of the caecum in horses is impaction:
Type 1 = accumulation of dry ingesta
Poor dentition?
Sand
Type 2 = abnormal caecal motility resulting in a more fluid consistency
Much more likely to rupture than the colon
much more prone to rupture than any other part of horse gastro tract
Caecocolic intussusception- colon intercepts into caecum, possibly assosiated with tape worms
Unclear pathogenesis
Motility issue
Ileocaecal intussusception more common
Inflammation of the caecum is referred to as typhlitis
Cyathostomins- mass emergances, may not cause clinical signs
Anoplocephala perfoliata
Small strongyles also known as cyathostomins, are extremely prevalent amongst the equine population worldwide.
Horses can carry large worm burdens without displaying clinically significant symptoms and with a negative faecal worm egg count
The clinical syndrome of larva. cyathostominosis (cyathostomiasis), occurs as a result of mass emergence of hypobiotic intestinal stages.
High fatality rates due to diffuse severe and acute damage to the caecal mucosa.
Caecal infections in birds
Protozoa predominate as the cause of infectious typhlitis in poultry;
Eimeria tenella-
Variably severe clinical signs
Major disease of production
Exudative to erosive
DIFFERENT STRAINS INFECT DIFFERENT PORTIONS OF THE TRACT
Histomonas meleagridis-
Spread by a worm
Turkeys and peafowl
Caecal cores
Necrotizing typhlitis
Hepatitis
Caecal cores can also be seen in Salmonella enterica Pullorum
Other systemic signs- SEPTICEMIA
Right dorsal colitis
NSAID use in horses, as well as being associated with gastric ulcers and renal papillary necrosis, can result in right dorsal colitis
Due to decreased production of prostaglandin via NSAID inhibition of (COX-2) resulting in vasoconstriction.
Infectious colitis
Oedema disease of pigs
Enterotoxaemic colibacillosis
E. coli F18
Pathogenesis:
Associated with dietary changes at weaning
Bacterial overgrowth in small intestine
Produce verotoxin (Shiga-like)
Necrosis of enterocytes and endothelial cells
Leakage from vessels results in oedema, which in the brain results in swelling and neurological signs
Classical gross post mortem presentation is marked oedema of the spiral colone
E.coli
Swine dysentery-
Necrohaemorrhagic enterocolitis
Brachyspira hyodysenteriae
Salmonellosis
Histiocytic ulcerative colitis
Boxer dogs and their kin
E. coli
Histiocytes - granulomatous
E. Coli
Escherichia coli is one of the first bacteria to colonize the GIT of infants and establishes as a life-long resident of the normal intestinal microbiota in humans (Eggesbø et al., 2011).
Non-pathogenic E. coli strains provide benefit to the host in many ways, including aiding absorption of vitamin K and B12 (Blount, 2015)
Some E. coli strains can cause disease:
Enterotoxigenic (ETEC)- covers villi, produces enterotoxins IT and ST resulting in endocytosis
Enteropathogenic (EPEC)- structural injury to enterocites resulting in loss of microvilli and osmotic dirhoea and secretory dihroa
Enterohaemorrhagic (EHEC)- easirer to see post mortem- lysis, damage to cells, haemoragic
E.coli can be typed according to their various pathogenicity factors and surface markers
Adhesins (fimbriae or pillia)- Fimbriae commonly found in pigs: F4 (K88), F5 (K99), F6 (987P), F18, F41
Toxins
Serotype (O, H, K)
Salmonellosis
All salmonella species are enteroinvasive
Zoonotic and reportable
enterica species serovar Typhimurium - Second most important cause of food poisoning in humans
Pathogenicity factors include ability to neutralise NO in phagocyte-Are phagocytosed but able to survive within phagolysosome
Pathophysiology:
Septicaemia-
Fibrinoid necrosis of vessels and DIC
Hepatitis and pneumonia
S. choleraesuis
Acute enteric -
Necrotising ileotyphlocolitis
S. typhimurium
Chronic enteric-
Button ulcers – ddx classical swine fever
S. typhimurium
Rectal strictures
Trichuris
Trichuris spp.
Whipworm
Carnivores, ruminants, pigs people
Direct life cycle
Clinical signs- Transient, recurring large bowel diarrhoea with or without blood
Rarely, severe infestations result in pseudo-Addison’s
Histiocytic ulcerative colitis
Boxer dogs and their kin
genetic issue with response to E. coli
Histiocytes - granulomatous
Rectal prolapse
Often secondary to inflammation
But can be due to other reasons
Dystocia
Urinary disease
Perineal hernia
Anal furunculosis
breed issue- GSDs
Immune-mediated
Peri-anal fistulation- A fistula is an opening between areas of the body that are not usually connected.
In this case between the anus and skin
Furunculosis is generally a term used to imply a deep infection of the dermis, typically with ruptured hair follicles and free hair shafts which themselves add to the immune reaction
Epithelial tumours of the canine intestine
tend to be upper GIT
In the cat, more commonly lower GIT
Papilloma and
polyp- dachhound
Adenoma
Carcinoma
causes of colic
Smooth muscle spasm
Inflammation-
Colitis / Ulceration
Distension
Impaction-
Gas accumulation
Obstruction
Impaction-
Tension on the mesentery
Displacement
Tissue congestion/infarction/necrosis-
Torsion/volvulus
Strangulation
(both could cause endotoxaemia- gut wall is compromised and horse absobs endotoxins from gut bacteria, causing systematic reaction)
Clinical Signs of Colic
Inappetence
Reduced faecal output
Vocalising/grunting
Agitation
Pawing at the ground
Lip curling
Flank Watching
Lying down- For long periods, Repeatedly
Stretching to urinate
Rolling / Thrashing
Sweating excessively
Straining
Mild signs – Restless, Pawing, Flank watching
Gas build up / inflammation of GIT / Smooth muscle spasms
Moderate signs - Lying down flat out, groaning
Impaction or other simple obstruction
Very fractious, violent rolling
Acute, severe strangulation
Dull, unresponsive
End-stage – Severe illness due to colic
“False” colic
Any non-gastrointestinal source of abdominal pain
Liver disease / hepatomegaly
Urinary disease-
Renal pain
Bladder Dz (urolithiasis)
Peritonitis
Intra-abdominal abscess
Intra-abdominal neoplasia
Reproductive disorders- displacments post foaling
Other
Non-abdominal, pain mistaken for colic
Oesophageal obstruction
Rhabdomyolosis (tying-up)
Laminitis
Pleuroneumonia
clinical exam for colicing horse
Aim of clinical examination is to;
Assess the severity of the horse’s condition
Establish appropriate ‘level’ of treatment
Conservative ‘in-field’ treatment
Referral for more intensive medical therapy
Referral for surgical intervention
Examination should be targeted, quick but thorough – be systematic
doese not need to be full clinical examination- aim is to establish prognosis
Observe from a distance
Current status of colic- Pain or signs of depression
Respiratory rate & depth
Abdominal distension
Presence of faeces
Evidence of duration / severity-
Traumatic injuries
Disrupted bedding
Shavings/soil on back
Rapid assessment of cardiovascular status-
Heart Rate
Pulse quality
Jugular refill
MM Colour
CRT
this can show the difference between normal and endotoxaemia
Moisture content of oral MM is an assessment of hydration status; if bad horse should be reffered for fluid therapy
Assessment of hydration status & hypovolaemia-
dehydration
mm moistrure
heart rate- heart rate of 80= tahcycardia and horse is cardiovascularyly compromised
CRT
PCV
lactate- indicates anarobic respiration- necrosis ect
Assessment of Gastrointestinal Tract
Auscultation - GIT borborygmi of the ascending colon (caecum & LC)
Auscultation of GIT has some degree of specificity but low degree of sensitivity.
Hypermotility- Increased smooth muscle activity - ‘spasm’ colic
Local hypomotility- Localised stasis of GIT
General absence- GIT ileus – common finding in most colics
Very useful for monitoring cases – e.g. progressive loss of motility
- =Absent
+ =Hypomotile
++ =Normomotile
+++ = Hypermotile
Other assessment:
Rectal Temperature-
Most uncomplicated colics will have normal rectal temperature-
Low core temp – usually associated with severe/end stage shock-
Pyrexia – Can indicate alternate diagnosis, e.g. peritonitis
Digital pulses
– not appropriate to assess circulation
– only useful to assess for presence of laminitis
Respiration:
Tachypnoea – usually due to pain, but could be associated with endotoxaemia (metabolic acidosis)
Detailed auscultation of lungs rarely necessary
Pain and colic assessment-
Pain will only cause a mild-moderate increase in HR (40-60bpm)
Marked-severe tachycardia (>60bpm) is a sign of hypovolaemia
Pain will cause tachypnoea
Pain can make it very difficult to examine the horse
Administer quick-acting, potent analgesic
alpha 2-agonist
Xylazine (Rompun, Virbaxyl),
Detomidine (Domosedan),
Romifidine (Sedivet)
+/- opioid- Butorphanol (Torbugesic )
Try to assess CV status before giving alpha 2-agonist
diagnostics for colic
Nasogastric Intubation:
Nasogastric reflux
Fluid/ingesta reflux from the stomach
>2 Litres of fluid is abnormal
Usually indicative of small intestinal obstruction (physical or functional)
Can occur due to LC displacement (pressure on duodenum)
Presence of gastric reflux has significant diagnostic value
Majority of cases with reflux need referring to hospital
Relieving reflux is also very therapeutic
>8L will stretch stomach and be a significant source of pain
Trans-Rectal Examination (TRE):
Abnormalities:
- Impaction
- Distension (Gas accumulation)
- Displacement
- Masses
Abdominocentesis-
Assess for presence of changes in peritoneal fluid- good prognostic indicator
Serosanguineous colour change and or Increased protein concentration- Serosal compromise – leakage of blood components
Increased Lactate concentration- Anaerobic tissue metabolism
Presence of ingesta- Rupture of GIT tract
High WBC count- Peritonitis
Abdominal Ultrasonography:
Adjunctive to all other examinations
Can assess structures not palpable on rectal
Excellent for assessing;
Thickness of intestinal wall
Distension of small intestine
Motility of intestine
Presence of displacements
Peritoneal fluid
Foals – can visualise entire abdomen
treatment for colic
Analgesia
Imperative to provide some form of analgesia to a colic case
NSAID-
The most common form of analgesics used to treat colic
Slow onset and long duration of activity
Flunixin meglumine (Finadyne Solution)-
1.1 mg/kg iv
Potent visceral analgesic
Can masks deterioration in CVS status
Ketaprofen (Ketofen)
1.1 - 2.2mg/kg iv
Phenylbutazone (Equipalazone Injection)
4.4mg/kg iv
Alpha-2 agonists
Potent analgesics with rapid onset and short duration of action
Allow rapid re-assessment of case progression
Xylazine (Rompun, Virbaxyl)
Dose rate: 0.2-1.1mg/ml
Analgesia for 15-20min
Detomidine (Domosedan)
Dose rate: 0.01-0.02mg/kg
Analgesia for 1-2 hours
Romifidine (Sedivet)
Dose rate: 0.04-0.08mg/kg
Analgesia for 1-3 hours
Opiods
Not first line analgesic
Usually reserved for higher degree of pain
Butorphanol (Torbugesic)
0.05-0.075mg/kg iv
Potent analgesic; 1 hour duration
Spasmolytics (Anticholinergics)-
N-Butylscopolamine (Buscopan Injectable )
Smooth muscle relaxant
Rapid onset and short duration of activity
Good for;
Treating hypermotile/spasm type colic
‘Gas’ colic
Relaxing rectum prior to rectal examination
General Rules
For first-line treatment, or where diagnosis is uncertain, use short acting analgesic agents
Assessing progression, rapid recurrence of pain or deteriorating CV status is vital in the decision to refer
Beware the potent anti-inflammatory effects of flunixin, which can significantly ‘mask’ the early signs of endotoxaemia.
Only administer NSAIDs after the diagnosis or CV status have been established
Fluid Therapy:
Enteric fluids
Indicated in the vast majority of colic cases- Most cases will have a degree of dehydration
Contraindicated if NG reflux is present, or suspect small intestinal lesion
Excellent way to rehydrate the colonic content (impactions)
Bolus(es) of isotonic fluids (tap water + NaCl + KCl)
5-8L can be given q2hrs
Purgatives
Liquid Paraffin; Magnesium Sulphate (Epsom Salts)
Decision to refer-
Essentially, any indicators that the case won’t resolve with simple conservative therapy (analgesics & enteric fluids)
Non-response to analgesia
Significant CV compromise
Rapid deterioration despite therapy
Complex abnormalities on rectal exam
Presence of NG reflux
Recurrent/chronic cases with unclear Dx
82.9% survival rate for 1st opinion cases
Approach to Weight loss in the Horse
Reduced Intake?- Not wanting to eat
Disease or chronic pain
Not able to eat
Dental disease or Dysphagia
Not being allowed to eat
Social hierarchy
Not being fed enough
Poor or Inadequate diet
Poor Absorption?-
Inadequate presentation of nutrients
Dental Disease
Gastrointestinal Disease
Parasitism
Diarrhoea
Ulcerative GI disease
Inflammatory disease
- Small Intestine, Colon, both
Neoplasia
- Lymphoma
Decreased Utilisation?- Disorder of nutrient metabolism
Liver Disease
Excessive Loss?- Protein losing enteropathy
Increased Requirement ?- Increased demand/Consumption
Bacterial infections
Chronic Viral infection
Neoplasia
HYPOALBUMINAEMIA
Loss of albumin
Protein losing enteropathy
Protein-losing nephropathy
Chronic blood loss
Reduced production
Hepatopathy
Malnutrition
Chronic inflammation
Negative acute phase protein
Anaemia
Low grade, normocytic normochromic (non-regenerative) anaemia is also common finding in weight loss
“Anaemia of chronic disease”
Decreased RBC production
Reduced RBC lifespan
gasteroscopy for weight loss in the horse
Weight loss generally only present in more advanced cases of gastric ulceration
Altered or reduced appetite
Delayed gastric emptying
Other forms of GIT ulceration could cause weight loss through causing malabsorption
Right dorsal colitis associated with NSAID toxicity
Gastroscopic examination used to obtain trans-endoscopic duodenal mucosal biopsies
Indicated where there is evidence of small intestinal malabsorption
Abdominal Ultrasonography for weight loss in the horse
In context of weight loss, can give information on;
Thickness of Small intestine and Colon
Assess characteristic of thickening
Are mural layers visible?
Peritoneal fluid volume
Presence of intra-abdominal masses
Liver evaluation (or u/s guided biopsy)
Abdominocentesis
for weight loss in the horse
Assess for presence of changes in peritoneal fluid
Low sensitivity, but good specificity for:
Peritoneal inflammation / Bacterial involvement
WBC > 5 x109/l
Protein concentration > 20g/l
Increased Lactate concentration
Serosanguineous colour change
Neoplasia
Rare to diagnose intra-abdominal neoplasia on PF alone
<50% solid tumours exfoliate cells
Usually presents as low grade peritoneal inflammation
Oral Glucose Absorption Test (OGAT)
Simple and inexpensive test to assess absorptive capacity of small intestine
Normal
Approximate doubling of baseline serum glucose 2 hours after dosing (70-100% increase)
Partial Malabsorption
15-65% increase in serum glucose at 2 hours, or slower to peak
Total Malabsorption
Serum glucose not increasing above 15% of baseline
Faecal Blood Test
Evidence of frank blood in faeces indicates colonic/rectal bleeding
(Upper GIT bleeding is digested in the colon so not represented in faeces)
Faecal Occult blood test
Detects albumin and haemoglobin separately
Proposed to differentiate between different sources of pathology
Varying evidence for diagnostic value
Osmotic Diarrhoea
results from the presence of osmotically active, poorly absorbed solutes in the bowel lumen that inhibit normal water and electrolyte absorption. Certain laxatives such as lactulose and citrate of magnesia or maldigestion of certain food substances such as milk are common causes of osmotic diarrhea.
Secretory Diarrhoea
occurs when your body secretes electrolytes into your intestine. This causes water to build up. It can be caused a number of factors, including: bacterial infection such as salmonella and E. coli.
diarrhoea caused by Increased gut mucosal permeability
ncreased intestinal permeability or hyperpermeability. That means their guts let more than water and nutrients through — they “leak”.
diarrhoea cause by Abnormal gut motility
hypermotility can casue this
SI Diarrhoea
normal to large volume
watery
Melaena- Black colored stools that occur as a result of gastrointestinal bleeding. This bleeding usually comes from the upper gastrointestinal (GI) tract, which includes the mouth, esophagus, stomach, and the first part of the small intestine.
borborygmi- the sound that the stomach and intestines make as food, fluids, and gas move through them.
weight loss +/- vomiting
inappetance
*SI can still be urgent
LI Diarrhoea
Urgency/increased frequency
straining/tenesmus
haematochezia- Rectal bleeding (or haematochezia) is the passage of fresh blood per rectum
small volume passed more often
mucus
fresh blood
“incontinence”
Adsorbants
May reduce diarrhoea
Efficacy not proven
Kaolin
Pectin
Chalk
Bismuth subsalicylate
Magnesium aluminium silicate
Activated charcoal
Alter intestinal flora/bind flora
Coat or protect mucosa
Absorb toxins
Bind water and possibly antiscretory
Faecal analysis
Is it infectious? History
Systemically unwell
D+ is acute & haemorrhagic
D+ is very severe
Multiple animals in crowded environment
Owner or pet is immunocompromised
Faecal – parasites – SNAP Giardia/ELISA
Faecal – virology– SNAP Parvo
Faecal for microbiology?
Bacteria – Salmonella, Campylobacter, Clostridia
(Viruses)
Faecal for parasites – OR JUST TREAT?
Nematodes
Cestodes
Giardia – multiple pooled samples?
Trypsin-like immunoreactivity
Exocrine Pancreatic Insufficiency
Clinical signs:
Steatorrhea - fatty loose faeces
Dramatic polyphagia
Weight loss
Stages of vomiting
Prodromal phase:
Nausea-
Hypersalivation
Loss of appetite
Lip licking
Excessive swallowing
Retching
Retrograde duodenal contractions
Rhythmic inspiratory movements against a closed glottis
Dilation of the cardia and low oesophageal sphincter
Expulsion
Reduced oesophageal and pharyngeal tone
Contraction of abdominal muscles to actively expulse gastric/duodenal contents
Programmed, overlapping and coordinated events help minimise risk of adverse events such as aspiration
The vomiting reflex
Two separate centres
CRTZ
Humoral pathway
chemical stimuli
BBB is permeable in the area of the CRTZ
Vomiting centre in brainstem
Several brain stem nuclei
Receives nerve impulses via 2 (neural) pathways:
Central
Peripheral
coordinates and integrates vomiting
Also Vestibular apparatus
input for motion sickness
Substance P
neurotransmitter
binds to NK-1 receptors
NK-1 receptors
location: cell membrane
vomiting centre
CRTZ
Dysphagia
can be mistaken for vomiting
Gagging
Dropping food
Retching
Difficulty eating
Exaggerated swallowing
Ptyalism
Fear of eating
swallowing difficulties
Maropitant
Anti-emetic
selective NK1 receptor antagonist
effective against
peripheral pathways
central pathways
Visceral analgesia in cats
Metoclopramide
Anti-emetic
dopamine, 5-HT3 & H1 receptor antagonist
central>peripheral pathway effects
variable prokinetic effect
cats & dogs
indications to investigate vomiting
History:
several days duration or fast deterioration
persistent vomiting
“not keeping anything down”
haematemesis
blood?
coffee grounds?
SI diarrhoea
weight loss
Concurrent signs (anorexia, fever etc)
Physical examination:
weak, collapsed
mm: dry/tacky, pale or congested
tachycardia, bradycardia, arrhythmia
weak & thready or hyperdynamic pulses
hypothermia or pyrexia
abdominal pain or distension
melaena, haemorrhagic diarrhoea
vomiting resulting from Primary GI problem
Primary disease should be suspected if:
An abnormality is palpable in the gut e.g. foreign body
The vomiting is associated with significant and concurrent diarrhoea
The patient is clinically and historically normal in all other respects
The onset of vomiting significantly preceded any development of signs of malaise – depression and/or anorexia.
The vomiting is consistently related in time to eating (although this can also occur with pancreatitis)
vomiting results from a Metabolic problem secondarily causing GI signs (secondary GI disease)
Often have evidence from the history and/or clinical exam of abnormalities affecting other organ systems e.g. jaundice/PUPD
Vomiting is usually intermittent, unrelated to eating and may often occur subsequent to the onset of other signs of malaise.
Generally not usually bright, alert and happy.
Usually ill (depressed/inappetant) before vomiting was observed.
Exception to the rules: Pancreatitis.
Secondary GI disease diagnostics:
Biochemistry, haematology
Urinalysis
+/- imaging
Patients that are unable to digest carbohydrates effectively may require
an increase in protein provisions in place of carbohydrates.
However, high protein diets may be contraindicated in patients with co morbidities such as hepatic disease, pancreatitis and renal disease
calorie dense diets
Fat is calorie dense so is indicated to critically ill patients where nutritional volume is difficult to consume. Therefore, calorie dense diets allow for a reduced portion of food to be given.
High fat content diets ,however, are contraindicated in cases of pancreatitis.
Resting energy requirement (RER)
the energy (number of calories) required for normal function in fasted patients under thermo-neutral conditions.
RER = 70 x (bodyweight BW in kg)0.75
OR
For animals weighing 3kg-25kg
RER = (30 x BW in kg) +70
The calculated RER should always be viewed as a starting point and feeding volumes can be adjusted as required, depending on the status and progression of the patient.
Water volumes should also be taken into consideration, especially when using a diet which requires blending as fluid overload may occur.
Diluting food with water will dilute the calories and reduce calorific density.
Tube flush volumes should be recorded and included in the total volume per feed guidelines.
Enteral feeding of anorexic patients should commence with one third of the patient’s total RER for the first 12 to 24 hours.
If well tolerated, this amount can be increased every 12 hours until full RER is reached.If the patient vomits, feeding should be discontinued until vomiting has resolved. Thereafter reduce the volume when feeding is resumed and increase the volume more slowly.
Excessive nutrition during times of illness may increase the risk for hyperglycemia and other metabolic complications so should be avoided.
Feeding frequency is determined by hospital hours, staff availability, and patient tolerance of volume fed. Ideally, feeding frequency can be every 4 to 6 hours initially and later decreased to every 6 to 8 hours after it is clear that the patient can tolerate the feedings.
calculating energy requirements
Weigh the patient (regularly)
Calculate the RER. This will give you the number of calories required per day (kcal/day)
Select the appropriate diet for the patient and the type of feeding tube
Divide the energy requirement of the patient (kcal/day) by the energy content of the diet (kcal/ml or gram) to provide the daily amount of food required
Divide the total amount of food per day by the number of feeds per day
Do not exceed 5-10ml/kg per feed when reintroducing food
Write up the feeding plan and keep a detailed record.
Entereal vs Parenteral nutrition
Enteral = giving nutrients into the GI system i.e. assisted feeding
Parenteral = giving nutrients IV, sometimes via central line
IF THE GUT WORKS… USE IT! – Enteral feeding best option if possible
Parenteral is more complicated and expensive than enteral feeding. There is also a risk of villous atrophy and risk of bacterial growth at the line site if not kept clean.
Feeding Tubes
There are 4 main types of feeding tubes which can be placed for assisted feeding in dogs and cats:
1. Naso-oesophogeal (NO) or nasogastric (NG) tube- most commonly used as they are easiest to place and manage
2. Oesophagostomy (O) tube
3. Gastrostomy (PEG) tube
4. Enterostomy or jejunostomy tube- usually placed during abdominal surgery and are reserved for patients with gastric or pancreatic disease. They require a near constant infusion of commercially prepared diet.
Tubes are named for where they enter the GI tract.
Tube selection will depend on multiple factors…
Patient condition
Illness/injury
Food required
Availability of resources including staff
Financial factors
Duration of assisted feeding required
Naso-oesophageal Tube
Small bore tube passed through the nostril of the patient
Indicated in any patient with malnutrition that will not undergo oral, pharyngeal, esophageal, gastric, or biliary tract surgery
Can be placed conscious so no need to GA potentially high-risk patient
In place for 3-5 days (up to 10 days)
Small bore tube so requires commercially prepared liquid diet
Advantages – easy to place – no GA required, cheap,can be used immediately and removed at any time, patient can eat and drink around the tube
Disadvantages – short term use only, sometimes patient removes them as irritate the face, placed at the head end – can be difficult to manage in patients that bite, can only give liquid oral medications, not crushed tablets, can increase risk of reflux
Oesophagostomy tube
Surgically placed into the oesophagus (GA required)
Oesophagostomy tube feeding is indicated in anorexic patients with disorders of the oral cavity or pharynx, or anorexic patients with a functional gastrointestinal tract distal to the oesophagus. E.g jaw fracture
Contraindicated in patients with a primary or secondary oesophageal disorder (e.g., oesophageal stricture, after oesophageal foreign body removal or oesophageal surgery, esophagitis, megaesophagus).
Wider bore tube than NG
Can prepare own diets ( blended in ‘gruel’ form) or use commercially prepared
Can be left in place for weeks/months
Advantages – easy to place and manage, can feed own blended diet, the patient can eat and drink around the tube, can be removed at any time, can give crushed oral medications
Disadvantages – requires short GA to place, at the head end so can be difficult in patients who bite, requires some wound management and risk of local infection at placement site, rarely stricture can form where tube enters oesophagus
Gastrostomy tube
Placed directly into stomach through body wall, bypasses oral cavity and oesophagus
Gastrostomy tube placement is contraindicated in patients with primary gastric disease (e.g., gastritis, gastric ulceration, gastric neoplasia) or disorders causing persistent vomiting.
Must stay in place for 10-14 days (minimum 7 days) after placement to allow ‘seal’ to form between stomach and abdominal wall, preventing leaks into abdominal cavity which may lead topancreatitis
Can be left in place for months-years (tube may need to be replaced but this can be performed through the same stoma)
Advantages – long term use, further from head so can be easier to manage in patients who bite, large bore tube so can feed variety of diets in larger volumes, can give crushed medications
Disadvantages – unable to use immediately after placement (24 hours), requires GA to place, risk of local infection at placement site, risk of pancreatitis/peritonitis if incorrectly placed and ‘leaks’
Jejunostomy Feeding Tube or “J-tube”
Invasive, challenging to place
Mid-long term support
Bypasses upper GIT
Patient if able to eat via the oral route still whilst tube is in place if required
Jejunum does not have storage capacity
Required trickle feeding NOT bolus feeding
Tend to be referral cases
Total Parenteral Nutrition (TPN)
The practice of feeding the patient via the intravenous route (usually by a central venous catheter)
Used on short term basis (3-5 days)
Reserved only for use when:
The patient is unable to be fed enterally e.g. failure of the GIT
The patient is at an increased risk of aspiration
Other methods of assisted feeding have failed to ensure adequate intake of nutrition
TPN aims to meet all of the patients energy and protein requirements
Partial parental nutrition (PPN) aims to meet some of the requirements, alongside other methods of nutritional support e.g. tube feeding
Intensive nursing required
Postural Feeding
Typically used for patients presenting with Megaoesophagus
Daily food intake should be split into 3 – 4 smaller meals a day
Food should be soft wet food – never hard kibble
Ideal the patient should be in a sitting position
During each meal, the wet food should be rolled into small balls and fed from a height
HYPERNATRAEMIA
s a deficit of water relative to sodium and can result from a number of causes, including free water losses, inadequate free water intake, and, more rarely, sodium overload
MALOCCLUSION
the teeth are not aligned properly
•VOLVULUS SYNDROME
occurs when a loop of intestine twists around itself and the mesentery that supports it, causing bowel obstruction
Scald/Ovine Interdigital Dermatitis
Seen in sheep continuously exposed to wet pasture – often lambs but can be seen in housed ewes when straw becomes wet and warm
Fusebacterium Necrophorum – can be zoonotic – human wounds have been swabbed and F. Necrophorum found – wear gloves when examining lame sheep!
Mild and transient lameness, rapidly resolves with treatment
Dermatitis involving some or all of the skin between the claws of the feet – skin between claws appears red and inflamed with white discharge
V common, less important than footrot/CODD, but associated with pathogenesis of foot abscesses and foot rot
Footrot
Footrot – 90% of lameness in the national flock
Dichelobacter Nodusus (Bacteroides) BUT needs F. necorphorum to facilitate epidermal invasion
D.nodosus – obligate parasite, can’t survive in the environment for more than 1 week
Also requires devitalised skin – chronic exposure to wet conditions and faecal contamination
Fly strike can occur in affected feetVery effective vaccine against footrot.
Acts as treatment and prevention.
Timing is important
A second injection can be needed 4-6 weeks
One injection will last 6 months.
Diagnosis is essential
genetic element to susceptibility to scald and footrot.
CODD
Contagious Ovine Digital Dermatitis
Relatively ‘new’ disease – ongoing research
Bacteria – treponeme species. Some association with cattle with Bovine Digital Dermatitis
Link between CODD and footrot
Usually SEVERE lameness with one claw of one foot affected
Initially ulcers develop on the coronary band which then under-run the hoof, can lead to whole hoof avulsion
Graded 1-5
Can lead to permanent hoof growth problems
Often needs systemic treatment with antibiotic and NSAIDs
White line separation
Often individual rather than ‘whole flock’ issue
Unknown aetiology – walking on stony ground, nutritional imbalance?
‘Shelley Hoof’
Separation of the hoof wall from the underlying tissues
Lameness caused by dirt packing into space created
Can lead to abscess formation
Toe Granuloma
Painful red swellings caused by:
Over-trimming
Chronic untreated lesions
Chemical irritation
Joint Ill
Most common – Septic arthritis ‘Joint-ill;
Strep. Dysgalactiae, (e.coli, erisypelas sometimes isolated in older lambs)
Transmission still unknown – cord/tagging/tailing/castrating/oral/vaginal canal? Vaginal canal transmission thought to be most significant
Septic arthritis = swollen joints, ill thrift, death
1-2% of flocks, can be up to 50% of lambs in severe outbreaks
Lamb outdoors if possible! Reduces bacterial load for newborn lambs
Research evidence suggests that wearing long disposable gloves for lambing will be the most effective method to reduce the prevalence within a flock
Hyaline Cartilage
The principal component of hyaline cartilage is type II collagen.
Collagen:
The most abundant protein in mammals (up to 35% of the proteome).
At least 28 different types of collagen.
Made of amino acids, wound to form a triple-helix, which are aligned in elongated fibrils (there are also non-fibrillar collagens).
Hyaline cartilage components…
Collagens
Aggrecan
Hyaluronan
Link protein
COMP
Decorin
Fibromodulin
Fibronectin
Chondroadherin
Equine Osteoarthritis (OA)
Age-related degenerative musculoskeletal disease.
Loss of articular cartilage, abnormal bone proliferation, synovial membrane dysfunction and subchondral sclerosis.
Commonly affects hock, pastern, coffin, fetlock, carpal (knee) and stifle joints.
Estimated that up to 60% of equine lameness is related to OA.
Leading welfare issue in horses - resulting in substantial morbidity and mortality.
Abnormal loading (physiological strain) of normal cartilage
or
Normal loading (physiological strain) of abnormal cartilage
or
Both: Abnormal loading (physiological strain) of abnormal cartilage
Initially, OA was been considered to be a disease of articular cartilage. However, recent research has indicated that the condition involves the entire joint.
Loss of articular cartilage - thought to be the primary change, but a combination of cellular changes and biomechanical stresses causes several secondary changes.
Secondary Changes:
Subchondral bone remodelling
Osteophytes
Bone marrow lesions
Changes in the synovium
Changes in the joint capsule
Changes in the ligaments
Changes in the peri-articular muscles
Meniscal tears and extrusion
Evidence supports the hypothesis that OA is a bone disease instead of, or in addition to, a cartilage disease.
Spontaneous OA animal models show a change in the density and metabolism of subchondral bone prior to any signs of cartilage damage
Cartilage Homeostasis
In normal cartilage there is homeostasis between cartilage synthesis and cartilage degradation
Synthesis
Growth factors
Hyaluronic acid / GAGs
Tissue inhibitors of MMPs (TIMPs)
Degradation
Cytokines (TNFα, Il-1β)
ADAMTSs (aggrecanases)
MMPs (collagenases)
OA Pathogenesis
During the early stages of OA, the cartilage surface is still intact.
The molecular composition and organisation of the Extra cellular matrix (ECM) is altered first.
Articular chondrocytes, which possess little regenerative capacity and have a low metabolic activity in normal joints, exhibit a transient proliferative response and increased matrix synthesis (Col2, aggrecan etc.) attempting to initiate repair causing by pathological stimulation.
This response is characterized by chondrocyte cloning to form clusters and hypertrophic differentiation, including expression of hypertrophic markers such as Runx2, ColX, and Mmp13.
Changes in the composition and structure of the articular cartilage further stimulate chondrocytes to produce more catabolic factors involved in cartilage degradation.
As proteoglycans and then the collagen network breakdown, cartilage integrity is disrupted.
Articular chondrocytes then undergo apoptosis and the articular cartilage will eventually be completely lost.
The reduced joint space, resulting from total loss of cartilage, causes friction between bones, leading to pain and limited joint mobility.
Other signs of OA, including subchondral sclerosis, bone eburnation, osteophyte formation, as well as loosening and weakness of muscles and tendons will also appear.
Osteo Arthritis - Altered Metabolism
Metabolism has a key role in the physiological turnover of synovial joint tissues, including articular cartilage.
In OA, chondrocytes and cells in joint tissues other than cartilage undergo metabolic alterations and shift from a resting regulatory state to a highly metabolically active state.
Inflammatory mediators, metabolic intermediates and immune cells influence cellular responses in the pathophysiology of OA.
Key metabolic pathways and mediators might be targets of future therapies for OA.
grading criteria for equine osteoarthritis
wear lines- graded 0-3
erosions- graded 0-3
palmar athrosis (osteochondral lesions distal palmar aspect of metacarpus)- graded- 0-3
Histopathology
of equine osteoarthritis
Chondrocyte Necrosis
Chondrone Formation
Fissuring
Focal Cell Loss
less Stain Uptake (Safranin O)
Gelsolin
Multifunctional protein involved cell shape determination, secretion and chemotaxis.
Gelsolin knockout mouse model - arthritis exacerbation (Aidinis et al., 2005).
Exogenous gelsolin administration - chondroprotective properties, protecting murine cartilage
decreases in horses with OA
Alanine
Alanine is one of the main amino acid residues which constitutes collagen.
It may be that the reduction in alanine abundance identified with OA cartilage is resultant of degradation of the cartilage collagen framework, which are subsequently released into the SF resulting in the elevated synovial abundance
Creatine
Nonessential amino acid involved in cellular energy metabolism, maintaining cellular adenosine triphosphate (ATP) levels (muscle and brain)
Previous human and equine studies also identified elevated SF creatine in OA SF
Approximately 95% of stored creatine is located within skeletal muscle (Snow and Murphy, 2001). Thus, given the association of muscle atrophy with OA, this elevation in synovial creatine may be reflective of an associated muscle mass loss
Stranguria
painful, frequent urination of small volumes that are expelled slowly only by straining
Generally disorders of:
The lower urinary tract (bladder or urethra)
The genital tract (prostate, vagina)
Both
Two processes have potential to cause stranguria:
Non-obstructive stranguria
Mucosal irritation/inflammation of lower urinary/genital tract
Obstructive stranguria
Obstruction or narrowing of the urethra/bladder neck
Palpate the bladder size
Stranguria + large bladder may be obstructed = emergency!
Haematuria
blood in the urine
Haematuria causes:
Iatrogenic haematuria
Pathological haematuria
Genital sources (if voided)
Do they have clinical signs associated with LUTD?
Has bleeding been noticed from other sites?
Trauma?
Rodenticides?
Blood in faeces?
Pattern to urine pigmentation?
Look for haemorrhage at other sites
Abdomen, thorax, mucosae (especially mouth, axillae, groin)
Palpate and assess kidneys for size, symmetry, discomfort
Examine the external genitalia
Gross “pigmenturia”
red, brown or black urine
- Urinalysis: positive haem
3 possible causes:
Haematuria
Haemoglobinuria
Myoglobinuria
Gross haematuria:
>150 RBCs/hpf
Occult haematuria:
Positive Hb on dipstick
>5 RBCs/hpf but not visibly pink
Care re: interpretation if catheterised/cysto
Both can be accompanied by clinical signs (stranguria, dysuria, pollakiuria)
Dysuria
discomfort or burning with urination
Pollakiuria
increased frequency of urination
Periuria
urination at inappropriate sites
Anuria
failure of urine production by the kidneys
Oliguria
reduction in urine production
Polyuria
Increase urine production
signs of a lame cow
head bobbing
stride leanght
joint rigitity
toe tipping
cadence/timing of strides
lordosis
The 90% rule for cattle lamness
90% of the time it’s in the claw
90% of the time it’s on the back feet
90% of the time it’s the lateral claw on the back feet
Foot trimming – Dutch 5 Step
- Toe length
- Match
- Model- correct weight distribution on wall of horn
- Create height
- Investigate/trim loose horn
Non-infectious cow foot lesions
White Line Disease
Sole Ulcers
Trauma
Iatrogenic
Trimming
Experimental
Nutritional?
Presentation of pain elsewhere?
Infectious cow foot lesions
Digital derematitis
Foul in the foot
Foot and Mouth Disease
MCF
Polyarthritis – mycoplasma, joint ill
White Line Disease
a range of presentations, all at the white line.
can travel up to coronary band- if this happens the entire wall of horm must be removed
risk factors-
Horn integrity- more common in aging cattle with weakened horn
Surfaces- deep tracks
Stockmanship- stressed, fearful, pushed around cows, most important risk factor
Treatment:
Block other claw
Remove all loose horn
NSAID
Prevention
Good cow surfaces
Good stockmanship
Appropriate nutrition
Sole Ulcers
one of the commonest causes of lameness in dairy cattle. It is an area of damaged sole horn which has completely lost the horn tissue except for the corium
Disruption to horn growth due to pressure on the corium underneath P3
Risk Factors:
metabolic- pregnancy, relaxation of the ddft, drops p3 and rotates it
Standing time- biggest, lying time 14 hours is optimum
Surfaces- softer surfaces (pasture) mean cows weigh distribution is more optimal
Foot trimming
Fat mobilisation- fat pad reduction during pregnacy and lac due to neg energy
Inflammation
large long term effects- bone spur formation in P3
treatment:
Remove pressure
Block
Trim loose horn
NSAID
Prevention:
Cow comfort – minimise standing times
Maximise transition health
Ensure cows aren’t lame in dry yards
Prompt ID and treatment
Foot trimming technique and strategy
predominantly a result of poor transition (pregnancy and lactation)
Digital Dermatitis in cows
Multifactorial
Strong bacterial component
Treponeme spp
Genetic susceptibility
Hoof hygiene
chronic condition- prior infection huge risk
M1- new infection, not painful
M2- acute active lesions, inflamed
M3- healing, black plauqes
M4- chronic but dormant
M4.1- chronic and reactivated
M2- treat topically
M4- footbath
prevention- clenliness
vigilnce with heifers
foot bathing for M4
Foul in the foot
Bacterial infection of interdigital tissue
F. Necrophorum et al
Painful, swollen ID space
Characteristic fragrance
foul smell
can result in deep infections
Treatment
Systemic antimicrobials
NSAID
Local treatments
Prevention
Similar to DD
Minimise risk of interdigital trauma
Heel horn erosion
a change in the appearance of the surface of the bulb of the heel in cows
Prevention:
Hygiene and trimming of loose heel horn
Interdigital hyperplasia
fibrous mass that protrudes from the interdigital space of the feet of cattle
related to laws spreading adn streaching interdigital skin
may be caused by poor trimming
Fissures in cattle
Horizontal- thimble foot
horizontal fissues indicate stopped horn growth- metabloic
vertical
needs trimming all the way back
axial- iatrogenic- bad hoof triming
Toe lesions
white line, absesses, Thin soles
Thin soles most common- Abrasion, Over-trimming
not much can be done- thn blocks for those with no pain
Corkscrew Claws
Don’t tend to occur on well managed farms…
Medial corkscrew claws are a different phenomenon
Deep Digital Sepsis
Terminal presentation.
deep nfection
Footbathing cattle
3-4x/week
Not too strong/acidic (below pH3)
No more than 200 cows
Effective design required
Commonest ingredients – formalin, CuSO4
common signs of lamness in horses
Heat
Effusion (swelling)
Discharge
Muscle atrophy
Lameness!
Initial examination for lameness
Complete clinical history:
- signalment
- duration
- previous issues
- speed of onset
- exercise induced
- known trauma
- any treatment started
- any pattern?
Observation stationary
- size/shape
- hoof pastern angle
- hoof capsule
- coronary band conformation
- shoe type, wear pattern, position
Palpation
coronary band/ coffin joint(DIPJ)/lateral cartilages/heel bulbs
Remove dirt/false horn
Symmetry/heels?
Hoof testers
Gait assessment
Hard straight line
Flexion tests
Soft and hard lunge
Ridden sometimes required
hard level non slip surface is important
Flexion tests
Apply stress or pressure on an anatomical region of the limb for set period of time
Horse then trotted off and observed for the effects of the test on gait
Controversial amongst the equine population
Can induce lameness that may be unrelated to the baseline lameness
Responses must be interpreted carefully
how can you tell if a horse has forelimb lamness
head is highest during the phase when horse is taking eight on the lambe limb
how can you tell if a horse has hindlimb lamness
increased verticle displacment of the tuber coxae in the lame limb copared to sound limb
what tools are available to diagnose lameness in horses
3 grading systems:
1-5: american
1-8: sue dison
1-10: one to use
10/10- non weight baring
8-9/ 10 - toe touching
3/10 seen every stride
1/10- not lame
Nerve blocks
Time consuming and hazardous!
Valuable tool for localisation
Mepivicaine administered perineurally lasts 90-120min – can be up to 3hours. less tissue reaction than other options
Intra-articularly lasts approximately 1hr
lidocane cheaper but more reaction
in the foot-
Palmar digital
Abaxial sesamoid
Coffin joint
Navicular bursa
DFTS?
False positive
Will the horse warm out of the lameness?
Proximal diffusion?
Clinician bias
False negative
Misdirection of needle outside of the fascia that surrounds the neurovascular bundle or into synovial structure.
Local anaesthetic inadvertently injected into a blood vessel
Clinician bias
Other limitations
Mechanical lameness that doesn’t respond to anaesthesia- dont do if horse warms out of lameness
Desensitisation of skin but not deeper structures.
Palmar digital nerve block
What does it block?
Sole
Navicular apparatus
Soft tissues of the heel
Coffin joint
Distal portion of the DDFT
Distalsesamoideanligament
inserted distally two points on palmar aspect of foot abouve heel bulbs
How?
25g 2/3in needle (25g if cobby!)
Needle separate from syringe- makes sure you are not in blood vessel, makes it easier to keep needle in if trouble with horse
1.5ml mepivicaine- larger volumes give larger spread and so less diagnostic
Proximal edge of the cartilage of the foot- can palpate neurovascular bundle
Evaluate before 10mins
Abaxial sesamoid nerve block
What does it block?
Foot
Middle phalanx
PIPJ
Distopalmar aspects of the proximal phalanx
Distal portion of the SDFT andDDFT
Distalsesamoideanligaments
Distal annular ligament
Fetlock
How?
25g 2/3in needle (25g if cobby!)
Needle separate from syringe- makes sure you are not in blood vessel, makes it easier to keep needle in if trouble with horse
2.5ml mepivicaine
Base of the proximal sesamoids- can feel neurovascular bundle
Direct needle distally.
Coffin joint block
What does it block?
Coffin joint!
Navicular apparatus
Branches of the palmar digital nerves
Toe region of the sole
(larger volumes – heel region of the sole)
Minimal benefit over PDNB
quick block
horse finds it uncomfortable
How?
20g 1.5in needle
Needle separate from syringe
5-6ml mepivicaine
Lateral approach with the limb off the ground
May be better tolerated
May enter navicular bursa or DFTS
Navicular bursa block
What does it block?
Navicular bursa
Navicular bone and associated ligament’s
Solar toe pain
Distal DDFT
Does not block the coffin joint
How?
Hickman block
20g spinal needle
Desensitise skin
Ideally with radiographic guidance- needle will be inserted, radiograph will be takein, if it sits on the palmar aspect of navicular bone, the la will be injected
Omnipaque?
3-4ml
Digital flexor tendon sheath block
What does it block?
Lesions within the DFTS
The portion of DDFT in the foot distal to the DFTS
How?
Palmar aspect of the pastern (out of choice)- sheeth is superficial
Tourniquet applied- encorages la to move distally
20g 1-1.5inc needle
Needle must remain superficial to the DDFT
Foot balance radiographs
Gross imbalance can induce lameness
Correct early on in a lameness investigation
Leave the shoes on
longterm poor foot balence leads to pathology
Lateromedial-
Foot positioned flat
Weight bearing on 2-5cm block
Horizontal beam centred on coronary band halfway between toe and heel
Dorso-palmar imbalance - Long toe/ low heel common finding
What to assess:
Solar surface angle in frontfeet
Long toe/low heel
Osteophyte/entheseophyteassociated with coffinjoint andnaviucularbone
Margin and cortico-medullary definitionnavicular bone
Dorsopalmar (weightbearing)-
How?
Leave shoes on
Foot positioned flat
Weight bearing on 2-5cm block
Horizontal beam centred on coronary band
Often foot not aligned with pastern/fetlock.
What to assess?
Medial –lateral imbalance – abnormal stress though the joints.
Coffin joint space should be even.
Ossification of the lateral cartilages
Dorso proximal palmaro distal oblique-
(Dorsal 65 degree proximal-palmarodistaloblique weight bearing–pedal/ navicular bone)
Shoes off–pack well with putty
Could useDPr-PaDiO
Standing on cassette tunnel
Some elongation of radiographic anatomy
Much easier to perform when limited people.
What to assess:
Navicular bone-
Cyst like lesions
Distal border fragments and lucent zones
Medullary sclerosis
Pedal bone-
Fractures
Keratomas
Osteitis
Palmaroproximal – palmarodistal oblique of the navicular bone (skyline)-
How?
Cassette tunnel
Caudal to the contralateral limb with heel on ground
45o angle
X-ray beam centred between the bulbs of the heel and collimated to the navicular bone
What to assess:
Palmar cortex of the navicular bone
Corticomedullary definition
Lucencies within the spongiosa
Cyst like lesions?
Limited to bony changes
Limited assessment of soft tissues.
By the time radiographic changes are seen its likely disease is well developed.
Advancement in diagnostic imaging has lead to improvement in treatment success rates.
Able to provide a more reliable prognosis with a definitive diagnosis.
MRI
Utilises radiowaves, strong magnetic fields and computer technology
MRI uses the hydrogen nuclei (protons) found in body water due to their magnetic properties
Once a magnetic field is applied the spinning protons rotate to align with the magnetic field.
A radiofrequency pulse is then applied forcing the protons out of alignment
The radiofrequency pulse is then removed and the electromagnetic energy released is converted into black and white images.
Different sequences are set up to look at different aspects
In the equine veterinary world its being used to improve the accurary and efficacy of diagnostics for lameness investigations.
horses must have GA
Radiographs show only bone
Ultrasound provides soft tissue detail
Ultrasound very limited in the foot.
Image bilateral limbs
Pre-fracture pathology and subtle soft tissue damage
Foot penetrations
Able to image within the hoof capsule!
Indications?
Where radiographs are negative or unclear and US access is difficult in a localised area.
Penetrating injuries
When GA is unadvisable
Acute onset lameness during exercise
Cases that do not respond to treatment as expected.
Monitor progress/ readiness for competition.
Computed Tomography
Series of x-rays emitted from various angles and the detectors measure attenuation
Provide a 3D image via advanced mathematical algorithms reconstructing the image
Benefits over radiographs-
No super imposition or complex overlap of anatomy
Can orientate images to view key structures
3D image capture in 60 second scan time.
Gamma Scintigraphy
Radioactive technetium
Bone tracing agent
Identifying fractures
Poor performance cases
Difficult areas to examine/radiograph
SUB–SOLAR ABSCESS
The most common cause of acute lameness in horses
Ascending bacterial infection into the chorium (solar dermis)
Lesions in the white line
“Nail bind”
Penetration injuries
Risk Factors
Poor foot conformation
Seedy Toe
Wet, muddy conditions
Seen both in shod & unshod horses
Chronic Laminitis / PPID- white line streaches and splays
Diagnosis
Acute & severe unilateral lameness
Grade 3 or 4 (AAEP lameness scale)
Increased digital pulsation to affected hoof – “Bounding pulses”
Heat in the hoof
+/- distal limb swelling
Repeatable and marked pain response on application of hoof testers
Differential Diagnosis-
Solar Bruising, Pedal bone fracture,
Laminitis (rare to be unilateral)
TREATMENT
AIM TO ENCOURAGE DRAINAGE- drainage will be black/grey
Remove Shoe
Pare and clean the sole
‘Explore’ any discoloured tracts or defects in the white line
(Sedation infrequently required)
NB: Nerve block contraindicated in NWB lameness
POULTICE
To soften hoof prior to curetting
To maintain drainage after abscess open
Poultice should be changed 2-3 times daily
Provide pain relief
24-48 hours NSAID therapy
Phenylbutazone 4.4 mg/kg IV or PO BID
Antibiotics are not indicated for un-complicated abscess
Tetanus Prophylaxis
Check tetanus vaccination status
If in doubt
Administer tetanus antitoxin
Chronic Abscess
Will rupture at coronary band or heel bulb
Still aim to encourage drainage distally
May require repeat flushing
Purulent Abscess
Deeper/sensitive structure involved
Will require further diagnostics – Radiography
Likely to need more extensive surgery
Antimicrobial therapy indicated
Solar Penetrations
If nail/wire is still in place
Leave it in situ - support leg with bandage/splint
Obtained radiographs if possible
If nail/wire already removed by owner
Try to identify tract and carefully pare sole to expose chorium (solar dermis)
Clean, lavage and dress the lesion
BEWARE delay in onset of lameness
Further investigations ASAP if any suspicion of complications;
Contrast Radiography/MRI
Potential Sequelae-
Damage to Pedal bone-
Pedal osteitis Sequestrum formation
Damage to Soft tissue structures-
Insertion of Deep digital flexor tendon
Impar Ligament
Synovial Infection- 56% survival from hospital
36% return to normal athletic function
Navicular bursa
Distal interphalangeal joint
Digital tendon sheath
Simple, uncomplicated penetration;
As per solar abscess – pare and poultice
Antibiotics only if clear evidence of infection
Judicious use of analgesia / NSAIDs
Penetrations with synovial penetration;
Broad-spectrum antimicrobial therapy
Procaine Penicillin, 22mg/kg IM BID (or IV QID)
Gentamicin, 6.6mg/kg IV SID
SURGICAL INTERVENTION
Arthroscopic lavage of synovial cavity
TETANUS PROPHYLAXIS
Hoof Trauma
FOOT CAST
Support
Sterility
Protection
Pain Relief
fracture managment
PRIORITIES
Establish diagnosis to INFORM PROGNOSIS
Stabilise the limb
Provide analgesia
Situational awareness (finances, logistics, future athletic aims)
Allow owner to make informed decision on treatment
Prioritise welfare and recognize role of euthanasia
parameters for assesing lamness
head nod- down on sound for front lameness
hip drop, hip hike- hindlimb lamenessy
limb movement- joint angle changes, stride leanght, stance duration, adduction/abduction, limb protration
sound of hoof hitting carrage
tail carrige
track
quality of movment- “stifff” ect
what is the best movment paraemter to detect and quantify lameness
alterations in weightbrearing forces on the ground
describe an exam for lamness in small animals
step 1- history
Step 2. Hands off: Observe
Observe sitting and standing
Uneven weight distribution on a particular limb
Muscle asymmetry
Join angulations/conformation
Loading position of feet and toes
Asymmetries in ways limbs are positioned
Swellings
Observe sitting -> standing
Particularly useful if stifle issues
Positive sit test
Weight shifting
Observe - Moving
Analyse gait and lameness
Contraindicated in severe lameness or major traumatic injury
Observe prior to treatments
Walk and trot
Repeat on different surfaces – concrete, gravel, grass
Lameness score 5 or 10 point scale – subjective
Kinematic/kinetic gait analysis - objective
Head nod- down on sound
Stride length and duration
Limb tracking- limb should be stight
Gait abnormalities are not always painful
Some are conformational
Muscle contractures
Limb shortening
Joint arthrodesis
Some are neurological
Ataxia
knuckling
3.Hands-on examination
General Clinical Exam
- Orthopaedic Examination
Be methodical
Minimal restraint
Palpate painful areas last - Neurological Examination
Proprioceptive testing
Reflex testing
Symmetry
Manipulation:
May be painful – be gentle
Some manipulations better performed under sedation or general anaesthesia
instability: laxity (looseness), sub-luxation or luxation (dislocated)
pain
range of motion:
flex, extend, abduct, adduct, rotate
reduced or increased?
Crepitus
Lameness Grading in small animals
0- no lamness
1- subtle and only observed in trot
2- mild lameness in walk, worse in trot
3- obvious in both gautes
4- observeavle in both gautes with periods on non weight baring
5- non wiegh bearing most/all of the time
signs of Forelimb lameness in small animals
Placement on lame limb – head raises
Placement of sound limb – head dips
signs of hindlimb lameness in small animals
Placement of lame limb – pelvis rises
Placement of sound limb – pelvis dips
Weight shift to forelimbs
Bilateral lameness
Abnormal tracking – affected limbs wider
Forelimbs – short choppy strides and circumduction
Hindlimbs
Hips – waddling/oscillating gait at walk
Stifles – short stilted strides and circumduction
Bunny-hopping
lameness effecting the elbow of small animals
Complex hinge joint
Common site of lameness in large breed dogs:
Elbow dysplasia- hard to see sue to it being bilateral
Effusion -> lateral epicondyle and olecranon
lameness effecting the shoulder of small animals
Biceps Tendon test
Abduction test to assess medial instability under GA/sedation
examine after elbow to distinguish between elbow and shoulder pain
lameness effecting the Pelvic Limb
of small animals
Tarsus
Tibiotarsal joint only appreciable motion
Assess for laxity and luxations
Palpated and stressed
Hyperflexion
SDFT
Calcaneal tendon
Tibia & Fibula
Deep palpation to elicit osseus source of pain
Detect focal area of swelling
Abnormal conformation
Stifle Examination
Synovial effusion -> palpate either side of the patellar ligament.
Chronic cranial cruciate ligament instability results in medial fibrosis and thickening -> medial buttress
Patella position ->patellar luxation
Partial CCL rupture
Craniomedial band rupture
Cranial drawer only in flexion
Intact caudolateral band taut in extension – prevents cranial drawer
Caudolateral band rupture
No cranial drawer
Craniomedial band taut in flexion and extension – prevents cranial drawer.
CCL
Positive Sit Test
Cranial Draw
Tibial Compression Test/Tibial thrust
Patella Luxation
Medial>Lateral patella luxation
More common in smaller dogs
Insidious in onset
Skipping intermittent lameness
Graded in severity from I to IV:
Grade 1: subclinical. Patella can be manipulated out of place but will return to its normal position
Grade 2: the patella luxates when the stifle is placed through a normal range of movement, spontaneously.
Grade 3: permanent luxation but the patella can be manually returned (reduced) to the femoral trochlear sulcus by the examiner, but the patella luxates again.
Grade 4: permanent luxation and the patella cannot be returned to the femoral trochlear sulcus.
lamness resulting from te hips in small animals
Hip examination:
Decreased ROM especially in extension
Crepitus
Pain
Laxity
Note ->Hip extension also results in extension of the lumbosacral joint and passive extension of the stifle – beware false-positives.
Extension and abduction of the hip = hip pain
Ortolani test
More objective assessment of hip laxity
Must be done under sedation/GA
Angle of subluxation the point at which the hip subluxates
Angle of reduction the point at which the femoral head returns to the acetabulum
Abnormalities can be classified according to distribution within the skeleton:
Monostotic – involving a single bone (e.g. an osteosarcoma)
Polyostotic – multiple bones are involved (as seen with multiple myeloma or haematogenous osteomyelitis
Focal – may involve a specific bone region (e.g. the metaphysis)
Generalized – involving all bones (as may be seen with metabolic conditions)
Symmetrical or Asymmetrical
Bone reacts to pathological processes in a limited number of ways:
change in alignment
change in contour
increased or decreased bone mass.
Aggressive vs non-aggressive changes in radiographs of bones
Aggressive lesion rapid bony change where there is minimal time for the bone to respond and remodel
Non-aggressive lesion benign, slow-growing, more chronic process with time for bone to remodel.
Wide spectrum in between!
This can be assessed by looking at the nature of any:
Bone destruction (lysis)
Periosteal reaction
Lytic edge character
Cortical disruption
Transition from normal to abnormal bone
Rate of change (10-14 days)
Periosteal Reactions:
New bone production:
Artifact (superimposition)
New bone production secondary to injury
continiuos (solid, lammelar, lamellated) vs interupted (thin brush like, sunburst, amorphus)
bone loss in radiographs
Aggressive vs non-aggressive changes
Patterns of bone lysis:
Artifact (superimposition)
Real due to generalised or focal bone loss
geofraphic lysis- least agressive
moth eaten lysis
permiative bone lysis- most agressive
Stages of wound healing
- Haemorrhage/Coagulation -
Immediate haemorrhage
Vasoconstriction
Vasodilation
Blood clot forms
‘Scab’ - Inflammation/Debridement -
6 hours after injury
Neutrophils -> Monocytes -> Macrophages
Macrophages – ESSENTIAL TO WOUND HEALING
Wound exudate – serosanguinous to purulent – NORMAL finding
Inflammatory phase can be minimal in apposed wound e.g. surgical incision - Reparative .-
Granulation tissue –
Identified between day 3 and 5 of wound healing
Fibroblasts
Angiogenesis – capillaries advance 0.4-1mm/ day
Collagen
Develops from wound margins
Contraction - 5-9 days after injury
Epithelialisation -
Visible 4-5 days after injury
Pink smooth margin to wound
Monolayer of cells
- Maturation
Re-organisation of collagen
Can take Months – Years
80% Strength of normal tissue
stage one of wound healing
Haemorrhage/Coagulation -
Immediate haemorrhage
Vasoconstriction
Vasodilation
Blood clot forms
‘Scab’
stage two of wound healing
nflammation/Debridement -
6 hours after injury
Neutrophils Monocytes Macrophages
Macrophages – ESSENTIAL TO WOUND HEALING
Wound exudate – serosanguinous to purulent – NORMAL finding
Inflammatory phase can be minimal in apposed wound e.g. surgical incision
stage three of wound healing
Reparative-
Granulation tissue –
Identified between day 3 and 5 of wound healing
Fibroblasts
Angiogenesis – capillaries advance 0.4-1mm/ day
Collagen
Develops from wound margins
Contraction
5-9 days after injury
Epithelialisation
Visible 4-5 days after injury
Pink smooth margin to wound
Monolayer of cells
stage four of wound healing
maturation-
Re-organisation of collagen
Can take Months – Years
80% Strength of normal tissue
First Intention wound healing
Healing of a wound where skin edges are closely re-approximated
Second Intention wound healing
Gap left between wound edges and natural healing allowed to occur
nsuitable for surgical closure, extensive contamination or devitalisation
Allow to heal by granulation, contraction and epithelialisation
Immediate Primary wound healing
Incision/Clean e.g. surgical incision
closes imediatly
Delayed Primary wound closure
Clean contaminated – contaminated
closes Up to 2-3 days after wounding. Inflammatory phase over
Secondary wound closure
Contaminated or Dirty
closes Up to 5-7 days after wounding. Granulation tissue present
Approach to wound management in abrasions
partial skin thickness wound
Rapidly re-epithelialise
Can be more severe – shearing injuries e.g. RTA
heals by Second Intention
Approach to wound management in avulsions
valuation – Avulsion
= skin torn from underlying attachments e.g. de-gloving injury of distal
heals by
Delayed Primary Closure
Secondary Closure
Second Intention
Approach to wound management in Incisions
smooth wound edges with minimal trauma e.g. surgical wound
heals by Immediate Primary Closure
Approach to wound management in laceration
= ragged incision with variable damage to surrounding tissues
Immediate Primary Closure?
Delayed Primary Closure
Secondary Closure
Approach to wound management in burns
Classified by depth -
First degree: superficial
Second degree: partial thickness
Third degree: full thickness
Secondary Closure
Second Intention
Approach to wound management in Punctures
e.g. bite wounds or ballistic missile
Minimal external skin damage
Extensive underlying tissue damage
Foreign material e.g. dirt/debris/hair in wound
Surgical exploration indicated
Consider underlying structures! - penetration of body cavities???
Delayed Primary Closure
Secondary Closure
Poor local blood supply to a wound =
slow granulation tissue formation and increased risk of wound infection
Can be difficult to assess in the early stages
pproach to wound management - debriding
emove devitalised tissue, foreign material, bacteria from wound
Sedation/GA/local
Clip hair from around wound
SHARP excision with scalpel
Conservative with skin
Radical with fat/muscle
Preserve bone/tendons/blood vessels/nerves where possible
Bleeding good indicator of tissue viability
NO point leaving in obviously necrotic tissue
Approach to wound management -Lavage
DILUTION IS THE SOLUTION TO POLLUTION
TYPE OF FLUID
TAP WATER – CHEAP and readily available. Useful for grossly contaminated large wounds
HARTMANNS/STERILE SALINE (0.9%) – fluid of choice. Still relatively cheap, minimally toxic to cells
20 or 50ml syringe with 18G needle
DO NOT USE UNDILUTED ANTISEPTICS E.G. CHLORHEXIDINE FOR WOUND LAVAGE
Barriers to wound healing
Infection
Movement
Foreign Material
Necrotic tissue
Local factors – pH, Shape of wound
Poor blood supply
Health Status
Iatrogenic Factors
Cell transformation
Patient Temperament
Client Temperament
Principles of Open Wound Management
Assess at every stage:
Degree of inflammation
Degree of exudate
Presence and quality of granulation tissue
Skin edges
Degree of epithelialisation
Primary contact layer for Bandaging Inflammatory/Debridement
wounds
Wet to dry
Moisture retentive
Honey
Negative pressure
MagPrimary contact layer for Bandaging Inflammatory/Debridement
wounds gots
q24 hours for 1st 3 days then q48 hours
Primary contact layer for Bandaging Reparative – early stages wounds
Wet to dry?
Moisture retentive
Honey
Negative pressure
Primary contact layer for Bandaging Reparative – later stage/good granulation bed wounds
Moisture retentive
Foam/absorptive
Hydrogel if drying out
Nutrition associated diseases in exotics
Commonly referred to as MBD
Results from inadequate dietary calcium and/or vitamin D3, imbalance in the calcium-to-phosphorus ratio and/or lack of UV light provision.
Persistent hypocalcaemia will lead to hyperparathyroidism.
This causes an increase in production of parathyroid hormone (PTH) promotes calcium resorption from the bones .
Uncommon in snakes
Eat warm-blooded whole prey items
Exceptions ->Green snakes
Insectivorous
Most commonly seen in herbivorous, insectivorous and omnivorous reptiles.
Increased incidence in herbivorous and insectivorous species challenging with diets
Diurnal species may be more susceptible
More in juvenile animals due to an increase in demand for growth.
Parents may play an essential role
Vitamin D3
Calcium
Genetic status
Skeletal development during embryonic development influences bone quality in later life
Less common in adult reptiles (with the exception of reproductively active females) as long bones and/or shell are no longer growing, reducing the calcium demand.
Similar clinical signs may be seen in adults and usually are due to other metabolic diseases such as renal secondary hyperparathyroidism (RSHP).
Differentials for bone and joint changes
RSHP
Traumatic fractures
Osteomyelitis
Gout/pseudogout
Abscesses
Cellulitis
Neoplasia
lizards-
Brachycephalic appearance to the head
Deformity of mandibular and maxillary bones
Soft and pliable
Deformed jaw characteristic smile appearance
Kyphosis and scoliosis of the spine
May see decreased neurological function to the rear limbs
Hypocalcaemic tetany
Partial depolarisation of nerves and muscles tremors, twitching and seizures
Tremors and fasciculations may be seen, especially during handling
Seizure, tetany and/or flaccid paresis of limbs/tail.
chelonians-
Beak may be overgrown and can develop a parrot beak-like appearance.
Prolapse of the cloaca, colon, rectum or phallus due to a lack of calcium on smooth muscle.
Carapace and plastron may be soft, the shape of the shell may be distorted and there may be difficulty in ambulating due to the inability to lift the plastron from the ground.
hypocalcaemia birds
Hypocalcaemia
Inadequate dietary calcium and/or vitamin D3
Lack of UV light provision.
Commonly seen in Grey Parrots
Commonly seen in birds fed seed diet.
Lethargy
Fluffed-up
Shaking/tremoring
Seizures
Pathological fractures
Limb deformities
Dystocia
Clinical examination
Full blood profile
Ionised calcium low
Radiography
Serum 25-hydroxycholecalciferol
Exotic mammals – NSHP
Less commonly diagnosed with NSHP
Reported in
Nonhuman primates
Sugar gliders
Skunks
Exotic cats
Guinea pigs
Rabbits
NSHP not uncommon in sugar gliders
Causes
Suboptimal husbandry
Suboptimal nutrition
Low calcium
Low vitamin D3
High phosphorus
Clinical signs
Acute collapse
CNS abnormalities
Seizures
Hind limb weakness
Osteoporosis
Hypovitaminosis E
Birds
Associated with muscle weakness
Localised wing paralysis
Poor digestion
Embryonic and hatchling mortalities
Rabbits
Cause of muscular dystrophy
Degeneration and necrosis of skeletal muscle fibres
Long-term storage of feed can decrease vitamin E content
Vitamin B deficiency
Chondrodystrophy
Short, widened leg bones
Distortion of the hock
Slipped tendon/gastrocnemius tendon movement from trochlear groove – also called perosis
Associated with nutritional deficiencies
Vitamin B deficiencies
Pyridoxine (vitamin B6)
Biotin (vitamin B7)
Folic acid (vitamin B9)
Niacin (vitamin B3)
Manganese deficiency
Choline deficiency
Zinc deficiency
Myopathies in exotics
Myopathy = muscle disease
Capture myopathy = exertional rhabdomyolysis
Occurs as a result of stress & physical exertion
Important in capture and restraint of wild or zoo animals
Ungulates susceptible
Some bird species long legged wading birds and ratites
Myopathy in poultry
Associated with heavy, large birds
Can be associated with different infectious organisms
Fungi
Bacteria
Viruses
Protozoa
Trematodes
Mycobacterial infections
Zoonotic implications
Weight loss, severe muscle wasting, atrophy of pectoral muscles (birds)
Granulomatous lesions in bones and joints
Identification of acid-fast microorganisms
neoplasia in exotic
Tumours of the musculoskeletal system
Squamous cell carcinomas of the mandible
Leiomyosarcomas
Osteoma/Osteosarcomas
Chondrosarcomas
Rhabdomyomas/rhabdomyosarcomas
Sarcomas
Chordomas
Chordoma -ferrets
Commonly occur at tip of the tail
Osteomyelitis in exotics
Osteomyelitis infection of bone or medullary canal
Bacterial osteomyelitis
Staphylococcus spp.
Streptococcus spp.
Gram-negative aerobic bacteria
Sometimes anaerobic infections
Sometimes fungi
Diagnosis
Radiographs
Culture of samples
Culture of implants implants used for internal fixation can act as a nidus of infection, or a sequestrum may be present
Gout
Gout painful!
Visceral gout - crystals within internal organs
Articular gout – crystals in joints
Periarticular gout – crystals in the tissues around the joint
Clinical exam
Poor body condition
Subcutaneous nodules near joints
Pain on palpation
Diagnosis
History
Clinical exam
Bloods Uric acid high
FNA and cytology birefringent needle-shaped urate crystals
Radiography Osteolysis and proliferative densities around joints
Structure of the skin
Epidermis
Superficial
Derived from ectoderm
Dermis
Deeper
Derived from mesoderm
Subcutis/Hypodermis
structure of Epidermis
Most superficial layer
4 cell types :
Keratinocytes ∼ 85%
Langerhans cells ∼ 3– 8%
Melanocytes ∼ 5%
Merkel cells ∼ 2%
Keratinocytes
form the bulk of the epidermis.
Produced from the stratum basale
Constantly reproduced and then shed as dead horny cells.
Anchored to each other by desmosomes
Structural and immune functions:
produce structural keratins
phagocytic and capable of processing antigens
produce cytokines (IL-1, IL-3, prostaglandins, leukotrienes, interferon)
Pemphigus foliaceus- a rare autoimmune condition that causes painful and itchy blisters and sores to form on your skin.
Langerhans cells
mononuclear dendritic cells
immune surveillance of the skin
found basally or suprabasilar
Functions:
antigen processing and presentation to helper T lymphocytes
induction of cytotoxic T lymphocytes directed to modified alloantigens
production of cytokines including IL-1
phagocytic activity.
Melanocytes
Dendritic cells
found within epidermis, hair follicle and ducts of sebaceous and sweat glands.
In epidermis, each melanocyte communicate with 10– 20 keratinocytes to form the ‘epidermal melanin unit’.
Each melanocyte produces eumelanin or pheomelanin within melanosomes melanosomes migrate to the end of dendrites and transfer melanin to adjacent epidermal cells.
functions:
production of protective colouration and for sexual attraction
barrier against ionising radiation
scavengers for cytotoxic radicals
contribution to inflammatory response via production of cytokines
Merkel Cells
Dendritic epidermal cells in basal cell layer of the epidermis or just below.
Functions:
specialised slow-adapting mechanoreceptors
influencing cutaneous blood flow and sweat production
coordinating keratinocytes proliferation
controlling of hair cycle by maintaining and stimulating hair follicle stem cell population.
layers of the epidermis
Stratum Basale
Stratum Spinosum
Stratum Granulosum
Stratum Lucidum
Stratum Corneum
Stratum Basale
Single layer columnar cells
Mostly keratinocytes
Anchoring:
To Basement Membrane Zone (BMZ)/dermis
hemidesmosomes
KC to KC
desmosome
Initial site of keratin production
Stem cell function
Proliferating- very mitotically active, skin produced here
Stratum Spinosum
Generally 1-2 cells thick
Footpads, nasal planum and MCJ’s upto 20 cell layers
Desmosomes mediate adhesion between keratinocytes
Important in barrier function
Stratum Granulosum
Not always present in haired skin (1-2 cell thick if is)
Cornified envelope and degeneration of cells starts in this level
various lipids and enzymes-secreted extracellularly (watertight seal)
Stratum Lucidum
Compact layer of dead keratinocytes only found in footpads and nasal planum.
Stratum Corneum
Outermost layer of skin
Flattened cornified anucleate cells
Constantly shed
Basement Membrane Zone (BMZ)
Separates epidermis from the dermis
Acts as a physical barrier- maintians arcatechtue AND STRUCTURE
Regulates nutrition
Aids in wound healing
The Dermis
The dermis forms the middle of the three layers and is comprised of dense connective tissue that is vascular. - Thickness of dermis determines the thickness of the skin
It is this layer that contains the nerve fibres, nerve endings and elastic fibres in addition to the hair follicles, and the sweat and sebaceous glands that grow down from the epidermis.
Tensile strength and elasticity of skin
Made up of:
Insoluble fibres ->collagen and elastin ->resist tensile forces
Soluble polymers -> proteoglycans and hyaluronan -> dissipate compressive forces
Hypodermis
The hypodermis or subcutaneous layer lies beneath the dermis and consists of loose connective tissue.
Predominant cell type – lipocyte (90%)
Energy reserve
Thermogenesis and insulation
Protective padding and support
Maintaining surface contour/shape
Small blood supply - susceptible to disease
Functions of the integument
- Protection
Mechanical protection from chemical, physical and microbial damage
Epidermal cells, Hair, Specialised secretions e.g. sebaceous and sweat glands
Antibacterial and antifungal activity
Immune system
Nerve sensors to allow the perception of heat, cold, pressure, pain and itch
Pigment production to protect against solar damage - Maintenance of homeostasis
prevent loss of water, electrolytes and macromolecules Temperature regulation - Excretion
Sebaceous glands, sweat glands
Secretion via epitrichial, atrichial and sebaceous glands - Synthesis of vitamin D
Calcium homeostasis
Conversion of Vitamin D precursor into Vit D3
Synthesis of calcitriol by kidney - Storage
Energy reserve
Storage of vitamins, electrolytes, water, fat, carbohydrates and protein - Other
Elasticity to allow movement
Production of adnexa, e.g. hair and claws
Communication as to the health of the individual and sexual identity
structureof hair
Specialised keratinised tubular structure-
Primary (guard hairs)-
Bulb deep in dermis
Have associated sebaceous glands, sweat glands, arrector pili muscles
Secondary (downy hairs)-
Small, not as deep in dermis
May have associated sebaceous gland but not sweat glands or arrector pili muscles
Cortex, medulla & cuticle containing variable pigment
Important for Insulation, Signalling, Physical protection
Sebaceous Glands
Holocrine secretion – produces sebum containing triglycerides, other lipids (e.g. linoleic acid), transferrin, IgA, IgG
Functions of sebum
Lubricates hair, and skin (glossy sheen)
Required for normal hair shaft separation
Excreted via squamous duct to the hair follicle
hair follicles
Simple hair follicles
single hair protrudes from the follicular orifice
Compound hair follicles
multiple hairs use the same follicular orifice (enter at the level of the sebaceous gland)
Species differences:
Omnivores and herbivores – simple follicles (bar sheep)
Dogs – compound – 2-15 hairs per group
Cats – compound follicles – 10-12 hairs per group
The hair cycle
Three phases:
Anagen (growing phase) – deep dermis
New hair produced under previous hair in deep dermis
Distinctive hair bulb containing follicular dermal papilla
Catagen (intermediate phase) – mid dermis
Rarely seen in normal skin – feature of some skin diseases (e.g. alopecia X)
Telogen (resting phase) – mid to upper dermis
Regulated by photoperiod, temperature, hormones and growth factors
Trichograms
a trichogram is the microscopic examination of hair shafts
Telogen bulb-
spear-shaped
rough
no pigment
Inactive hairs
Normally 80-90%
often 100% in endocrinopathies- results in allopecia
Anagen bulb-
rounded
smooth
pigmented centre +/-
bulb may fold around shaft when plucked
Actively growing hairs
Normally 10-20%
But many variations…
Breed variations:
poodles 80-100% anagen
Most dogs/cats telogenic growth patterns
Seasonal variation:
summer <50% anagen
winter 10% anagen
NB 100% telogen never normal. Indicates eg:
Endocrine disease
Telogen effluvium (sudden hairloss 1-2 months post-stress)
Post-clipping alopecia
Look at the hair tips!
Normal hair tips
Smooth pointed tips
Angular broken ends
Indicates self-inflicted hair loss and probable pruritus
Pruritis
Unpleasant sensation that elicits the desire or reflex to scratch (rub, lick, chew)
Classify as
Pruriceptive pruritus – due to stimulation of peripheral receptors in skin (in presence of healthy nervous system). Usually due to skin disease
Neuropathic pruritus – generated in CNS in response to
circulating pruritogens (eg cholestasis)
pharmacological mediators (eg intraspinal morphine)
anatomical lesion of PNS or CNS, eg syringomyelia in CKCS
Psychogenic pruritus recognised in animals/man, poorly understood)
Uncommon but need to differentiate from dermatological causes of pruritus
Somato-sensory activity of skin involves
Mechanoreceptors
Thermoreceptors
Nociceptors – itch and pain
Mainly via unmyelinated slow-conducting C-fibres
Some dedicated purely to itch (and temperature change)
Also A-delta fibres
But complex interaction between itch and pain
Painful stimuli can inhibit itch (eg scratching)
Pruriceptive pruritus
due to stimulation of peripheral receptors in skin (in presence of healthy nervous system). Usually due to skin disease
Neuropathic pruritus
generated in CNS in response to
circulating pruritogens (eg cholestasis)
pharmacological mediators (eg intraspinal morphine)
anatomical lesion of PNS or CNS, eg syringomyelia in CKCS
Sensitisation in chronic pruritus
In man:
Peripheral sensitisation
Scratching ->increase local inflammation -> production of pruritogens by inflammatory cells -> ncrease C-fibre responsiveness
Central sensitisation
Inflammation of skin -> altered perception of gentle mechanical /other stimuli -> perceived as pruritus (allokinesis)
+ Emotional, biochemical, central factors alter pruritic neural impulses in the brain
Likely occurs in animals too…
Therefore in the chronically pruritic animal, marked pruritus may be incited by only minor stimuli (hyperkinesis)
Threshold of itch: summation effect
– an important clinical concept….
Pruritus from multiple sources may coexist, eg:
Allergen concentrations
Often seasonally variable in atopy
Environmental factors
heat enhances itch – lowers threshold of receptors to pruritus
effects on skin microclimate and microbial growth
Ectoparasites -
Flea burden, even if not flea-allergic
Stress factors-
changes in the family, new pets, new baby, move house
Effects summate and may take pruritus over the pruritic threshold -> clinical pruritus.
Identification and elimination of as many factors as possible is important -> return below the threshold where able
Skin lesions
Primary lesions: Those that are a direct result of skin disease. They are usually most obvious in the early stages of the disease and are those upon which a definitive diagnosis should be based.
Macule
Papule
Nodule
Vesicle
Bulla
Pustule
Wheals
Alopecia
Scale
Crust
Comedone
Follicular Cast
Secondary lesions: are mostly non specific and are caused by pathological changes which result from the primary disease and its lesions or by self-inflicted damage by the patient. (more common) result of cutaneous, immunological or metabolic abnormality.
Erosion
Ulcer
Lichenification
Hyperpigmentation
Epidermal collarette
Epidermal responses
Hyperkeratosis
Scale (seborrhoea)
Follicular hyperkeratosis
Acanthosis
Lichenification
Vesicle/pustule formation
Hyperpigmentation/ hypopigmentation
Crusting
Dermal responses
Erythema
Oedema
Thickening
Hyperkeratosis
Increased depth of the cornified layer
Scaling
= production of abnormal or excessive scale
indicates abnormality of keratinisation
also known as seborrhoea (older term)
can be greasy (“oleosa”) or dry (“sicca”)
Can be primary (usually inherited) or secondary
compared to Crusting
formation of dried exudate
variable cellularity, variably coloured
may contain organisms
always secondary
Primary keratinisation defects
unusual/rare in domestic animals
Ichthyosis (fish scales) of Golden Retrievers
secondary defects are common
Non-specific sign indicative of
increased turnover of epidermis, or
imbalance between turnover and desquamation
Feature of many different skin diseases
Metabolic
Infectious
Parasitic
Immune mediated
Neoplastic
Follicular Hyperkeratosis
Follicular Hyperkeratosis
Keratinaceous plugs in hair follicle infundibula
= comedo / comedones (plural)
particular feature of
Demodicosis-parasite lives down hair follicle
Endocrinopathies
Comedones (black heads) in a hypothyroid dog -skin scrapes and hair plucks for Demodex are essential first tests in dogs which present with comedones.
Keratinaceous collar around emerging hair
= follicular cast
Non-specific finding, often seen in many diseases where increased keratin produced in the hair follicle e.g.
Sebaceous adenitis
Demodicosis
Dermatophytosis
Endocrinopathies
Vitamin-A associated dermatosis
Usually seen on trichogram
follicular cast
type of Follicular Hyperkeratosis
Keratinaceous collar around emerging hair
= follicular cast
Non-specific finding, often seen in many diseases where increased keratin produced in the hair follicle e.g.
Sebaceous adenitis
Demodicosis
Dermatophytosis
Endocrinopathies
Vitamin-A associated dermatosis
Usually seen on trichogram
comedo / comedones (plural)
type of Follicular Hyperkeratosis
Keratinaceous plugs in hair follicle infundibula
= comedo / comedones (plural)
particular feature of
Demodicosis-parasite lives down hair follicle
Endocrinopathies
Acanthosis
Increased depth of epidermis - inc no. of layers of cells
usually due to persistant low grade trauma
different from Hyperkeratosis = Increased depth of cornified layer
Lichenification
Thickening and hardening of the skin characterised by exaggeration of the superficial skin markings
Non-specific finding of many diseases with chronic inflammation or friction
: different from Hyperkeratosis = Increased depth of cornified layer
Vesicles of the skin
A small circumscribed elevation of the epidermis containing clear fluid less than 1 cm (“blister”)
Short-lived as epidermis is very fragile
Subsequently see erosions and ulcers.
Usually occur with:
Viruses e.g.
FMD
Feline orthopoxvirus
Orf (sheep)
Autoimmune diseases
Bulla-
As above but more than 1 cm diameter
Erosions vs Ulcers
Erosions
(superficial: basal layer of epidermis not breached)
ulcers
(deeper: dermis exposed)
Papule
Papule
Small solid elevation of skin <1cm diameter
Often erythematous
May –> crusts of serum, pus or blood
Plaque
A large flatter elevation of the skin, sometimes formed by papules coalescing
Plaque
A large flatter elevation of the skin, sometimes formed by papules coalescing
Pustule
Pustule
Small (<1cm) skin elevation, filled with pus
Often start as papule
But not all papules turn into pustules!
Both are always primary lesions… cf scale, crust
Usually associated with infection..
..but some are sterile (eg auto-immune diseases)
do impression smear of contents:
Helps differentiate bacterial vs sterile pustules (pustules often sterile in immune-mediated diseases eg pemphigus foliaceus)
Also used to detect acantholytic keratinocytes
Insert a fine (25-27G) needle into pustule (needle parallel to skin so not puncturing tissue below pustule)
Impress microscope slide directly onto pustule contents. Air dry and stain.
Nodules
Nodules
A solid elevation of the skin greater than
1 cm in diameter that usually extends into the deeper skin layers.
Nodules may result from:
Neoplasia (originating from skin cells, or metastatic)
Inflammatory cell accumulation (especially chronic granulomatous inflammation associated with infections or sterile processes)
or less commonly, tissue dysplasia or hyperplasia or mineral deposition
Pigmentation Disturbances
Melanocytes in basal layer of epidermis-
Important in skin pigmentation
But also role in local modulation of cutaneous inflammation
Skin damage can result in both hyperpigmentation and hypopigmentation
Hyperpigmentation-
Skin pigmentation increased beyond what is normal for that area
Non-specific -
Commonly post-inflammatory
Some endocrine skin disorders
Hypopigmentation
Skin pigmentation decreased beyond what is normal for that area
Feature of diseases affecting the basal epidermis and dermo-epidermal junction in dog, eg
some immune-mediated disorders
epitheliotropic lymphoma (neoplasia)
Hypopigmentation
Skin pigmentation decreased beyond what is normal for that area
Feature of diseases affecting the basal epidermis and dermo-epidermal junction in dog, eg
some immune-mediated disorders
epitheliotropic lymphoma (neoplasia)
But also post-inflammatory, especially after more marked inflammation in the horse
Cutaneous lupus erythematosus
(immune-mediated)
Leucotrichia
Crusting of the skin
Formed when dried exudate, serum, pus, blood, cells, scales or medications adhere to skin surface
Caused by multiple exudative and ulcerative diseases including:
Physical damage- mechanical, thermal, chemical
Many infectious processes- Viral, bacterial, fungal, parasitic
Sterile inflammatory diseases- auto-immune and immune mediated diseases
Ulcerating neoplasms
erythema
dermal response
Damage -> release of pro-inflammatory mediators (incl. histamine) -> vasodilation of dermal vessels -> erythema
Common in infectious and allergic processes…
Epitheliotropic lymphoma
Macule
A circumscribed flat area of change in colour of the skin <1cm in diameter
>1cm = patch
Bacterial pyoderma
Oedema of the skin
dermal reaction
Mediated by histamine and other cytokines increased vascular permeability leakage of tissue fluid urticarial lesions
‘Pit’ on pressure
Classically Type I hypersensitivity but occasional other causes
Wheals: circumscribed, raised lesion consisting of dermal oedema.
-> Reflect localised mast cell degranulation
Thickening of the skin
dermal reaction
Associated with:
Longer-standing allergic reactions
Late-phase reaction cellular infiltrate
Chronic inflammatory conditions
Increased collagen/other connective tissue components
NB Sometimes nodular – need to differentiate from neoplasms (fine-needle aspirate/biopsy)
Alopecia
= Loss of hair
Partial
Complete
Due to
failure to grow properly
Endocrinopathies
Hair follicle dysplasias
damage to hair follicles/shafts
Trauma
Follicular infections
Follicular parasites
Neoplasia
Immune-mediated/autoimmune disease
Nutritional deficiency
Demidocosis (follicular parasite)
Dermatophytosis
(Fungal follicular infection)
Sertoli cell tumour (testicular tumour) -> produces oestrogens -> alopecia
Normal Skin flora
Skin and hairs are not sterile and have a resident flora.
Normal skin is resistant to microorganisms
The resident flora can aid in exclusion of pathogens but may also contribute to disease.
Disease occurs when virulence of pathogen overwhelms or bypasses the cutaneous defences - or the resident flora is disadvantaged by local conditions and overgrowth occurs.
Definitions.
Resident - can replicate on the skin and can persist.
Nomad organisms that can colonise and reproduce on the skin for short times.
Transient - can not replicate so stay for a short time.
Pathogens organisms that become established and can proliferate on the skin surface and deeper that are deleterious to normal physiology of the skin.
staphelococus intermedius- resident
micrococcus - resident
pseudomonas- transient
What should be found on skin microscopy?
some bacteria and yeast.
Malassezia, Gram +ve (Staphylococci)
Treat
only if intractable send to lab
staphelococus psuedointermedius not found on skin but hair and hair folicles
Gram –ve unexpected
Rods unexpected
send to lab – C&S!
start treatment
-
Bacterial Skin disease
IS OFTEN SECONDARY
Primary disease affects defence
Atopic dermatitis
Endocrinopathy
Nutritional deficiencies
Trauma/overcrowding
Environmental damage
Organisms implicated in the dog most commonly Staphylococcus pseudintermedius
Canine Pyoderma
1. Surface pyoderma:
Secondary bacterial colonisation of lesions on the skin surface.
Examples include: acute moist dermatitis, eczemas and intertrigo.
- Superficial pyoderma.
Infection involves skin and hair follicle epithelium.
Examples include: impetigo, superficial bacterial folliculitis, dermatophilosis, pyotraumatic folliculitis and mucocutaneneous pyoderma. - Deep pyoderma.
Infection involves the dermis and subcutaneous tissue.
Examples include: furnculosis, cellulitis, and furunculosis, acral lick furnculosis
Surface pyoderma:
Secondary bacterial colonisation of lesions on the skin surface.
Examples include: acute moist dermatitis, eczemas and intertrigo.
Diagnostic techniques
* Dermatological signs
* Bacterial culture and susceptibility testing
* Skin biopsies – histology +/- culture
Management
Treat the primary disease
Treat the bacterial infection (usually topically)
Anti-Staphylococcal antibacterial
Treat the inflammation (usually topically)
Usually corticosteroid - short-acting to reduce the inflammation
Superficial pyoderma.
Infection involves skin and hair follicle epithelium.
Examples include: impetigo, superficial bacterial folliculitis, dermatophilosis, pyotraumatic folliculitis and mucocutaneneous pyoderma.
Common, often recurrent (SECONDARY) - treat the primary disease
Allergy/endocrinopathy, parasites
Clinical Signs
Often diffuse – ventral abdomen especially
Pustules
Papules
Epidermal collarettes
Alopecia
Variable pruritus
Epidermal collaret is characterisic- circular leasion of crusting, caused by burst pustule
Diagnostic Techniques
Dermatological signs – main diagnostic
Bacterial culture and susceptibility testing - rarely only if recurrent
Skin biopsies – histology +/- culture
Management
Manage any primary cause
Systemic anti-staphylococcal antimicrobial
Minimum 3 weeks
1 week beyond cure
Topical antibacterial shampoo/rinse e.g. Chlorhexidine
Long-term maintenance
Deep pyoderma.
Infection involves the dermis and subcutaneous tissue.
Examples include: furnculosis, cellulitis, and furunculosis, acral lick furnculosis
Furuncle – (“boil”) – follicle infection spreads into hair follicle which ruptures in the dermis
Cellulitis - infection of follicles and surrounding dermis
Difficult to manage
Often secondary
Some breed predispositions?
GSD – immunodeficiency?
Clinical Signs
Papules
Pustules
Alopecia
Nodules – furuncles, palpable lumps in dermis
Sinuses
Draining tracts
Diagnostic techniques:
Dermatological signs
Cytology - aspirate/impression smear
Bacterial culture and susceptibility testing
Skin biopsies – histology +/- culture
Management
* Treat any primary cause
* Topical antibacterial shampoo/rinse
* Long courses of systemic antibacterials
○ Based on culture and sensitivity
○ Minimum 6 weeks
○ 2 weeks beyond cure
Acute moist dermatitis
Surface pyoderma
IS USUALLY A SECONDARY CONDITION
Look for a primary pruritic condition
Otitis externa
Anal gland impaction
Fleas/other ectoparasites
??Function of hair coat
??Breed predosposition – Golden retriever
Intertrigo
Surface pyoderma
skin fold dermatitis
Associated with certain breeds
Facial fold
Vulval fold
Lip fold
Tail fold
Often less acute/chronic
Fungal Skin disease
Dermatophytes:
Microsporum and Trichopyton species
Microsporum canis most common isolate in cats and dogs
Use keratin to grow.
Grow exclusively in the non living tissue of skin nails & hair.
Cause inflammation and irritation.
Yeast and Yeast-like organisms:
Candida
Malassezia
Trichosporon
Dermatophytosis
Microsporum canis
Cats>dogs
Zoonotic!
Reservoirs
Infected by direct contact with infected animal/contaminated environment/fomite
Ringworm spores can survive for many months
Contaminated environment.
Exposure to infected host.
Fomites
Two groups:
Culture positive (dogs or) cats with subtle active infections.
Culture positive (dogs or cats) no active infection
Incubation period is approx 1 week.
Spores of the fungus invades anagen hairs – hence circular lesions
Germinate – produce hyphae - invasion by digestion of keratin
New arthrospores produced
Hair breaks off due to weakening leading to partial alopecia
Inflammatory reaction leads to folliculitis or furunculosis.
Inflammatory disease so animals often pruritic.
Clinical Signs:
Lesions VERY variable
Circular, patchy alopecia (broken hairs)
Variable erythema (peripheral?) and pruritus
Scale, crusts
Local/patchy/generalised
Nails may be affected, lost and grow back deformed – onychomycosis
Diagnostic techniques
Trichogram
Wood’s lamp examination
Fungal culture
McKenzie toothbrush culture
PCR
Skin biopsies – histology +/- culture
Zoonotic! Warn re avoiding handling animals and risk from fomites; esp if immunocompromised people
Environmental decontamination:
Spores very long-lived in environment – essential to clear from here to prevent continuous reinfection
Clip hair around lesions with scissors and dispose carefully of hair
Physical cleaning (e.g. daily vacuuming, seal and burn bag)
Chemical agents
Spontaneous resolution?
Topical tx Miconazole/chlorhexidine shampoo
Systemic tx
Ketaconazole licensed for dogs only. Do not use in cats.
Itraconazole licensed for cats. Off license in dogs.
Clinical resolution reached before mycological cure – base assessment of progress on basis of cultures, not clinical appearance of animal.
Monitor all animals with coat brushing weekly: treat until 2-3 negative cultures at least 7 days apart.
Malassezia pachydermatis
Broad based budding organisms- yeast
Isolated from skin and mucous membranes of a variety of species
M. pachydermatis is a typical on healthy canine skin and mucosa.
It is an opportunistic pathogen of cats and dogs.
Infection 100-10000 fold increase in numbers on skin.
Breed Predisposition for higher levels in some breeds.
Bassett, dachshunds, cocker spaniels, WHWT
Common to have concurrent Staphylococcus psuedointermedius infection.
Malassezia dermatitis
Also known as seborrhoea dermatitis (Seborrhoea = “flow of sebum“)
Normal commensal organism
Secondary condition
Usually generalised
Scale – “dry” seborrhoea (dandruff)
seborrhoea sicca
Greasy coat
Seborrhoea oleosa
Pathogenesis
Primary condition allows yeast overgrowth
Yeast lipases alter surface lipid (hence smell)
Epidermal turnover rises due to damage (hence scale)
Immediate (Type 1) hypersensitivity to yeast develops
Clinical Signs
Variable, usually generalised
Most commonly affected regions are hot and moist!
Worse in SKIN FOLDS (athlete’s foot)
Erythema
Scale
Greasy coat
OTITIS EXTERNA – may be only sign
Variable pruritus
Variable alopecia
“yeasty” smell
Diagnostic techniques
Dermatological signs
Acetate tape prep
Impression smear
Fungal culture
Management
TREAT ANY PRIMARY CAUSE
Reduce organism numbers
Topical treatment very effective
Usually aimed at M.p. AND S.p.
Itraconazole if topical fails
Often use anti fungal shampoos
steps of a hands off neuro exam
mentation/sensorume
posture
gait
asymetry
steps of a hands onneuro exam
proprioseption
spinal reflexes
cranial nerves
nociception
MENTATION vs Levels of Consciousness
mentation means mental activity
Normal
Dull/Depressed
Obtundation
Stuporous- still responds to pain
Comatose
MENTATION: behaviour
Compulsive
Disorientation
Hyperactive
Aggressive
posture in a neuro exam
Head Turn- forebrain problem, head turns to side of problem
Head Turn + Body Turn = Pleurothotonus
Head Tilt- vestibular
muscle weakness and damage-
KYPHOSIS- n excessive curve of the spine results in an abnormal rounding of the upper back
LORDOSIS- a deep curve in the spine resulting in dipped back
SCOLIOSIS- s shape deviation of the spine
special postures
Decerebrate Rigidity
Decerebellate Rigidity
Shiff-Sherrington
Decerebrate Rigidity
Stuporous or Comatose
Extension of all limbs
Extension of head and neck (opisthotonus)
Acute rostral brainstem injury
Decerebellate Rigidity
Mentation normal- cerebellum not involved
Extension of head and neck (opisthotonus)
Thoracic limbs extended
Hips flexed- back musces contract, almst lordotic
Acute rostral cerebellar injury
Shiff-Sherrington
Extension of thoracic limbs
Normal mentation
Reduced to normal tone in pelvic limbs
Normal postural responses in thoracic limbs
Acute thoracolumbar injury- disc herniation
ATAXIA
uncordinated gait
cerebellar- patient strugles to place feet, incordination, hyermetric (exagerated) gaite, hyometria
Vestibular- head tilt, problems with baence, staggering, all four limbs
cerebello- vestibular- the cerebellum is involved with the vestibular sytem, head tilt, hypermetria
General Proprioceptive/Spinal- involves spinal cord, can effect all four legs but also may just effect pelvic limbs
PARESIS
weakness of guate
Spontaneous knuckling
Scuffing of nails
Inability to support weight
Mono – one limb only
Para – pelvic limbs only
Hemi – one thoracic and one pelvic (same side)
Tetra – All four limbs affected
when is lamness neurological
Shifting of weight to the contralateral limb
Reduced protraction of affected limb
Musculoskeletal
Radicular pain/Nerve root signature
Neuropathy
Asymmetry, Spontaneous and Positional abnormalities in a neuro exam
Pupil size: Sympathetic vs parasympathetic dysfunction
Muscles of mastication: drooping (CNVII) or loss (CN V)- drop jaw
Eye Position: (CN III, IV and/or VI)
Positional nystagmus or strabismus (vestibular)
neuro Tests for Body and Limbs
Responses-
Postural
Hopping
Placing
Nociception
Reflexes-
Withdrawal
Patellar
Perineal
Cutaneous trunci-
(Extensor carpi radialis)
(Cranial tibial)
(Triceps)
(Gastrops)
(Biceps)
PROPRIOCEPTION
Postural responses-
Appropriate response: brisk normal placement of paw
Abnormal: delayed response or absence
Hopping
One leg only- TLs only (wheelbarrow)
One side only- PLs only ( Ext postural thrust)
NOCICEPTION
Response to noxious stimuli
Appropriate reaction (vocalization or moving away from noxious stimuli) NOT just movement of limb.
In cases of paralysis (plegia) or suspected sensory neuropathy
Spinal Reflexes: Patellar Reflex
Assessment of Femoral Nerve
Appropriate reflex: Kicking out of limb
Non-neuro causes for abnormal result:
Stifle disease
Old age
Anatomy: Middle patellar lig. Femoral nerve and L4-L6 spinal cord segment
Spinal Reflexes: Withdrawal Reflex
DO NOT TRAVEL TO BRAIN
Does not require noxious stimuli
Appropriate reflex: Flexion of all flexors.
Anatomy: Afferent nerve, C6-T2 or L4-S1 spinal cord segment, LMN to flexors
Spinal Reflexes: Cutaneous Trunci Reflex
Start at L4/5 and pinch with fingers or artery forecepts
Continue cranially up to T2 if no response
Appropriate reflex = bilateral contraction of cutaneous trunci.
Anatomy: Afferent nerve, Spinal cord (C8-L4/5), Brachial plexus, Lateral thoracic nerves, Cutaneous trunci mm.
Spinal Reflexes: Perineal reflex
stroking the spects of the perineaium watch for the anus clamping down
Anatomy: S1-S3 spinal cord segments
neuro tests for head
Responses-
Menace Response
Nasal septal mucosal response
Reflexes-
Pupillary Light Reflex
Palpebral Reflex
Corneal reflex
Vestibulo-ocular reflex
Gag reflex
Menace Response
move hand towards face to cause blink
Learned response: > 12 weeks in dogs
Not reliable in cats
Anatomy: Retina, optic nerve optic chiasm, optic tract, lateral geniculate n. (thalamus), optic radiation, visual cortex (occipital cortex), motor cortex, midbrain, cerebellar cortex, facial nucleus (medulla oblongata), facial n (orbicularis oculi mm)
Nasal septal mucosal response
poke nose with foreceps and watch for dog flinching away- cover eyes for accurate result
Anatomy: nasal septum, ophthalmic branch of CN V, sensory cortex (forebrain)
Pupillary Light Reflex
shine light on pupil and watch for contraction
Anatomy: Retina, optic nerve, optic chiasm, optic tract, pretectal n. (midbrain), parasympathetic n of oculomotor, oculomotor n, ciliary ganglion, short ciliary n, pupillary muscle.
Palpebral reflex
poke next ot eye, watch for blink
Anatomy
Medial: A = CN V (ophthalmic branch)
E = CN VII (orbicularis oculi mm)
Lateral: A = CN V (maxillary branch)
E = CN VII (obicularis oculi mm)
Corneal reflex
poke eye with coton bud, watch for blink(trigeminal nerve) and eye drawing back (facial nerve)
Anatomy
A = CN V (ophthalmic branch)
E = CN VII (obicularis oculi mm)
= CN VI (retractor bulbi mm)
Gag reflex
poke dog in back f throat, watch for swallow
Anatomy:
A= CN IX and X
E= CN IX and X
Vestibulo-ocular reflex
physiological nastagmus
move whole body in asur for small animas
move the head an watch for corection of eye direction
A = CN VIII
E = CN III, IV and CN VI
ranges of motion in a neuro exam
Neck range of motion
Palpation of back and neck
check for signs of pain
signs of a forebrain leasion
circling to side of leasion
menece response absent on opposite side to leasion
visual input affected- dog wont eat food in bowl on side of leasion
signs of bilateral facil nerve leasion
no palpebral rsponse on both eyes
no menace response
response ofn nnasal mucosal response ruling out trigeminal nerve
signs of a bilateral trigeminal nerve leasion
drop jaw
corneal reflex absent insensory section injury but present in motor injury
sings of a cerebellar problem
head tilt on oposite side to leasion
delayed postural reflex on same side as leasion
signs of peripheral nervus sytem issue
muscle wastage
head seems fine- less lilkly to be brain
signs of senstation but withdrawl reduced
no muscle tone in limbs
AUTONOMIC NERVOUS SYSTEM
Activating emergency mechanism
Preservation of the body’s internal environment: homeostasis
E.g change blood supply from skin to guts in aid of preservation
Mainly LMN (motor and efferent systems) system but higher centers present within brain (hypothalamus and autonomic nuclei)
LMN = Two neuron system- differences between sympathetic and parasympathetic- sympathetic longer and releases acetylcholine and eopineferin whie parasympathetic shorter and just uses acetylecholine
Target organ= smooth muscle
Parasympathetic vs Sympathetic- YING and YANG relationship, symbiotic
Sympathetic Nervous System
Flight or Fight response
Majority in Thoracolumbar Division [T1-L4]- feeds into other ganglia
Parasympathetic Nervous System
Rest and Digest
Craniosacral divisions
Cranio part- give rise to function in head area and slightly branches intothoratic and abdominal
Sacral division- pelvic pexus and ganglia
autonomic division of PUPIL CONTROL
PARASYMPATHETIC= CONSTRICTION
SYMPATHETIC = DILATION
assesment of Pupil Size….PARASYMPATHETIC
Pupillary Light Reflex!
Target organ = Sphincter pupillae
Involves oculomotor nucleaus-> oculomotor nerve -> cillary gangleion
PARASYMPATHETIC: Dysfunction
Mydriatic pupil
-ve on direct PLR of affected eye
-ve on indirect PLR when light shone in unaffected eye
INTERNAL OPTHALMAPLEGIA- an ocular movement disorder that presents as an inability to perform conjugate lateral gaze and ophthalmoplegia due to damage to the interneuron between two nuclei of cranial nerves (CN) VI and CN III (internuclear).
assesment of Pupil Size….SYMPATHETIC
1st order-
Hypothalamus ->lateral tectotegmentospinal tract ->Spinal cord segment T1-T3
2nd order
Brachial Plexus-> Cervical Sympathetic trunk (with the vagus nerve)
3rd order
Cranial cervical ganglion -> passes near middle cavity ->base of skull->exits orbital fissure -> dilator pupillae mm
SYMPATHETIC DYSFUNCTION = Horner Syndrome
Miosis
Third eyelid protrusion
Ptosis ( reduced palpebral commissure)
Scleral congestion
Enophthalmos
(Warm ipsilateral pinnae)
symathetic bladder control
STORAGE = SYMPATHETIC
TL division
Hypogastric nerve +
Relaxes the detrusor muscle
Tightens the internal urethral sphincter
parasymathetic bladder control
MICTURITION/PEEING = PARASYMPATHETIC
Sacral division
Stretch receptors in the bladder wall travel up the pelvic n. to brain.
Centers in the brainstem relay information to activate pelvic nerve +- Contracts the detrusor mm
Pudendal nerve
controls External urethral sphincter
Kept closed during Storage phase (mediated by sympathetic)
Opened for micturition (parasympathetic phase)
UMN BLADDER: Dysfunction
UMN lesion T3-L3- Loss of function from hypogastric muscle, no nerve signals to tell detrusor muscle to relax
Increase muscle tone to the external urethral sphincter muscle (lack of inhibition)
Increased detrusor muscle tone
Increased tone in external urethral sphincter
CLINICAL SIGNS-
Firm turgid bladder
Difficult to express
lmn BLADDER: Dysfunction
LMN lesion S1-S3
relaxed muscle tone to the external urethral sphincter muscle
Decreased detrusor muscle tone and loss of contractility
CLINICAL SIGNS
Flaccid large bladder
Easy to express but not fully
Constant leaking of urine
Vestibular System
Controls balance and posture
Stops a cat/dog from falling over
Consists of receptors and specialised nuclei
Affects movements of eyes, head, neck and limbs
CENTRAL vs PERIPHERAL
Peripheral
(extracranial)
nervous system
Vestibular receptors
Vestibular portion of the vestibulocochlear nerve
Central
(intracranial)
nervous system
Vestibular nuclei
Caudal cerebellar peduncle
Flocculonodular lobe
Fastigial nuclei
Peripheral vestibular receptors
Crista Ampullaris
-acceleration/deceleration
Macula
-static changes in posture
Central vestibular apparatus
Vestibular nuclei
Caudal cerebellar peduncle
Flocculonodular lobe
Fastigial nuclei
Pathology of Head Tilt
Unilateral loss of anti-gravity tone on the muscles of the head and neck ipsilateral to the lesion.
Imbalance of tone leads to head tilt
HEAD TILT TO SIDE OF LESION (n.b exception to the rule [paradoxical])
Gait analysis
Vestibular ataxia
Uncoordinated gait
Circling:
Circles to the side of the lesion
Clinical Evaluation: Mentation and Posture
Peripheral:
Normal
Disorientated
Central:
Normal Comatose
(Decerebellate Rigidity)
Jerk Nystagmus
Involuntary rhythmic oscillations of the eyes
Fast phase and slow phase
NOT spontaneous
Elicited via vestibulo-ocular reflex
Physiological nystagmus is a normal finding
Abnormal finding associated with vestibular disease
Spontaneous and positional
Fast phase and slow phase
Fast phase away from the lesion (with exceptions)
Central and peripheral
HORIZONTAL
VERTICAL
ROTATORY
Pendular Nystagmus
Not pathological
Seen in oriental breeds: Siamese overrepresented
Seen often in periods of stress
Strabismus
Abnormal position of the globe of the eye
If spontaneous, consider direct cranial nerve dysfunction; III, IV and/or VI
In vestibular dysfunction:
Positional ventral or ventro-lateral strabismus
Bilateral Vestibular Dysfunction
Loss of balance to both sides
No postural symmetry noted
Crouching posture
Wide head excursions
E.g. thiamine deficiency, metronidazole toxicity, bilateral otitis media/interna
Paradoxical Vestibular dysfunction
Dysfunction of:
Caudal cerebellar peduncle
Fastigial nuclei
Flocculonodular lobe
Lack of inhibition of the vestibular nuclei on affected side -> Greater activation of affected side
Generalised Tonic-Clonic Seizure
looses consciousness and has stiffening and jerking of the muscles. These seizures usually are generalized, starting on both sides of the brain.
Opisthotonus- amatic abnormal posture due to spastic contraction of the extensor muscles of the neck, trunk, and lower extremities that produces a severe backward arching
Piloerection- the contraction of small muscles at the base of hair follicles resulting in visible erection of hair.
Urination
Defecation
Salivation
Chewing movements
Face twitching
Clonic phase- paddling
Loss of consciousness
Mydriasis- dilation of the pupil of the eye
Lateral recumbency
Tonic phase- outstreached limbs
Apnea
What is a seizure?
ACVIM Consensus 2016
“A non-specific, paroxysmal event of the body that represents an abnormality of forebrain neurotransmission”
International Veterinary Epilepsy Task Force 2015
“a transient occurrence of signs due to abnormal excessive or synchronous neuronal activity”
Originated by an imbalance of excitatory and inhibitory influences on the cerebral neurons
When too many cells in the cerebral cortex become too excited and synchronise, a seizure can result
Seizure threshold
Pre-ictal phenomenon
behavioral changes or autonomic signs that may precede an observable seizure
Ictus
a sudden paroxysmal neurologic occurrence
Post-ictal phenomenon
a transient clinical abnormality of the CNS function that appears or becomes more evident when the clinical signs of the seizure have ended
Disorientation
Ataxia
Central blindness
Behavioral changes
Generalised seizures
involvement of both the cerebral hemispheres.
Tonic-clonic seizures Clonic
Tonic
Atonic
Absence seizures
Focal seizures
activation of only part of a cerebral hemisphere
simple focal seizures (consciousness is not impaired)
complex focal seizures (with impairment of consciousness)
Cluster seizures:
:two or more seizures in a 24-hour period or one seizure per day
Status epilepticus
a seizure that shows no clinical signs of arresting after 5 minutes of activity, or recurrent seizures with no recovery between them
give emergency ASD
If patient newly seizuring naïve of ASDs
Haematology
Biochemistry (including glucose and electrolytes)
Ammonia
Bile acids if appropriate (e.g. patient on phenobarbital with signs of adverse effects or uncertain diagnosis)
If returning patient on ASDs
CBC
Biochemistry (including glucose and electrolytes)
Ammonia
Bile acids if appropriate (e.g. patient on phenobarbital with signs of adverse effects or uncertain diagnosis)
Serum levels of anti-seizure drugs (ASD) when appropriate (phenobarbital and potassium bromide – PLAIN SERUM
Treatment of Status Epilepticus: duration 5-30 minutes
diazepam- 0.5mg-1mg/kg, IV or 1mg/kg rectally, repeated administration >/= 5 minutes apart up to 3 times within 24 hour period
Can double the dose in dogs pre-treated with phenobarbital
midazolam-
0.2-0.5mg/kg, IN, IV or IM. Repeated administration >/= 5min apart up to 3 times within 24 hr period.
CRI 0.2-0.5mg/kg/hr. Continue for 24 hrs and taper.
Treatment of SE: duration 30-60 minutes
Phenobarbital:
In pre-treated patients:
3-5mg/kg, i/v as a bolus
In non-pretreated animals:
3-5mg/kg, i/v as bolus (or orally in the event of a cluster seizure)
Loading? 2-4 mg/kg q6-8hours [max 24mg/kg/hr]
CRI? 2-4mg/kg/hr (<100mg/min)
Levetiracetam
Loading dose
40-60mg/kg i/v or rectal
Followed by:
20mg /kg i/v q 8hrs
Treatment of SE: duration 30-60 minutes
Potassium Bromide
In non-pre-treated patients loading doses:
400-600mg/kg/24hr 100mg/kg PO q4-6hours or 100mg/kg per rectum q24 hours for 5-6 days
130mg/kg/day orally for 6 days
Treatment of SE: 60-120 minutes
Levetiracetam
(can be used in 30-60min interval)
Initial dose 40-60mg/kg, i/v or rectally
Following therapy: 20mg/kg q 8 hours until seizure-free for at least 48 hours
Propofol
1-6mg/kg i/v propofol bolus
CRI: 0.1-0.6 mg/kg/min i/v
Refractory/Drug-resistant SE: > 120min
Ketamine:
5mg/kg, i/v as bolus
CRI: 5mg/kg/hr. If seizure-free for 12-24 hrs, continuous rate infusion under observation can be reduced by ~25% every 2 hours.
Inhalant anaesthesia:
Isoflurane
Sevoflurane
Differential diagnoses for sezure
Syncope
Narcolepsy/Cataplexy
Neuromuscular
Paroxysmal dyskinesia
Vestibular episode
Idiopathic Head tremor
Pain
Idiopathic epilepsy
(genetic)
Recurrent seizures
No identifiable cause
Genetic/familial predisposition
Age dependent
Symptomatic epilepsy
(structural-metabolic): result of identifiable intracranial or extracranial disease
Intracranial (structural) causes such as brain tumors, encephalitides, infarcts…
Extracranial (metabolic) diseases such as toxic or metabolic disorders
Cryptogenic epilepsy (epilepsy of unknown cause)
Investigations for seizure activity:
Signalment: age, breed and gender
History:
Description of event and events before and after that, how long lasted, interictal periods
Vaccinations, toxins, head trauma
Family history, littermates
Physical and neurological examination
Abnormal (post-ictal vs inter-ictal)
Lateralised signs (structural?)
. Haematology, Biochemistry, Urinalysis
- More extensive work up:
Bile acids, Ammonia
Serologic studies (infectious diseases)
EEG
CSF analysis
MRI
When to start Anti-Seizure Medication
> 1 seizure within a 6-month period
One period of cluster seizures
One period of status epilepticus
Prolonged or severe post-ictal signs
Suspect structural brain disease
Anti-seizure drugs (ASDs) LICENSED in dogs
Phenobarbitone / Phenobarbital
(Epiphen or Phenoleptil or Epityl®)
Imepitoin (Pexion®)
Potassium bromide (Epilease, Libromide or Bromilep®)
Anti-seizure drugs (ASDs) ‘off-label’ in dogs and cats
Levetiracetam
Zonisamide
Gabapentin
Pregabalin
Topiramate
Phenobarbitone
MOA: GABAA receptor agonist (potentiating inhibition)
Barbiturate
50% protein bound
Metabolised by liver (approx. 75%)
Approximately a third excreted unchanged in urine
Autoinducer of hepatic microsomal enzymes (p450 system)
10-20 days for steady state
Expected side effects
Polyphagia - High ALKP
Polyuria - High ALT
Polydipsia - Ataxia (transient)
Sedation (transient) - low T4
Dose:
2-3mg/kg PO BID in dogs, 2mg/kg PO BID in cats
Monitoring:
2 weeks: CBC, Biochem, pheno serum levels
6 months: CBC, Biochem, pheno serum levels
Yearly: Biochem, pheno serum levels
Ideal phenobarbital serum levels 25-30 mg/L [10-40]
> 35 mg/L associated with hepatotoxicity
Potassium Bromide
anti sezure med
MOA: Bromide hyperpolarises neurons entering via Cl- channels
Halide salt
Excreted in the kidneys (no biotransformation), Half-life in dogs 15-30 days
2-5 months for steady state
NOT FOR CATS- eosinphilic brochitis
Expected
Polyphagia - Polyuria
Polydipsia - Ataxia
-Sedation
DOSE
20-40mg/kg PO SID or dose split BID as monotherapy
10-20mg/kg PO SID if used with phenobarbital.
MONITORING
2 months after starting treatment
Yearly assessment of serum level and kidney function
MANAGEMENT
Dietary chloride intake: Increase Cl- = increase clearance of Br-
On Biochemistry: False hyperchloraemia (bromide is read as choride)
Imepitoin (Pexion®)
anti sezure drug
MOA: Partial GABA agonist
DOSE: 20-40mg/kg PO BID
Linear pharmacokinetic, we are NOT currently monitoring serum levels
Expected Side effects
- Polyphagia - Ataxia
- Sedation - Vomiting
Other benefits:
Anxiolytic; licensed for noise phobia
Not licensed for structural epilepsy or cluster seizuring patients
Levetiracetam
anti sezure med
MOA: Inhibits neurotransmitter release (binds to the synaptic vesicle protein 2A)
DOSE: 20mg/kg PO TID in dogs and cats
Mostly excreted unchanged by the kidneys (biotransformation enzymatic hydrolysis and hepatic metabolism)
EXPECTED SIDE EFFECTS:
-Hypersalivation (cats) - Sedation
- Anorexia
MANAGEMENT
Linear pharmacokinetic, we are NOT currently monitoring serum levels
Zonisamide
MOA:
inhibition of T-type Ca channels and VG-Na channels = inhibit excitation!
Allosterically bind to GABA R to increase function
Regulate transporters to decrease glutamate and increase GABA
Metabolised by CYP3A4 (with pheno, increase clearance by 50% and shortens half-life)
Free-radical scavenger
Weak carbonic anhydrase inhibitor
Expected side effects
- Sedation - Low TT4
- Ataxia - Low albumin
Idiosyncratic
- Renal tubular acidosis - Polyarthritis
- Keratoconjunctivitis sicca
Benzodiazepines
MOA: GABAA agonist
Diazepam and Midazolam
Quick onset of action, short half-life
Hepatic metabolism
Side effects
Avoid oral diazepam in cats = idiosyncratic hepatic necrosis
Anti-seizure drugs in an emergency?
MIDAZOLAM/DIAZEPAM
LEVETIRACETAM
POTASSIUM BROMIDE
PHENOBARBITAL
Treatment of Status Epilepticus: duration 5-30 minutes
Diazepam:
0.5mg-1mg/kg, IV or 1mg/kg rectally, repeated administration >/= 5 minutes apart up to 3 times within 24 hour period
Can double the dose in dogs pre-treated with phenobarbital
Midazolam:
0.2-0.5mg/kg, IN, IV or IM. Repeated administration >/= 5min apart up to 3 times within 24 hr period.
CRI 0.2-0.5mg/kg/hr. Continue for 24 hrs and taper.
Treatment of SE: duration 30-60 minutes
Phenobarbital:
In pre-treated patients:
3-5mg/kg, i/v as a bolus
In non-pretreated animals:
3-5mg/kg, i/v as bolus (or orally in the event of a cluster seizure)
Loading? 2-4 mg/kg q6-8hours [max 24mg/kg/hr]
CRI? 2-4mg/kg/hr (<100mg/min)
Levetiracetam
Loading dose
40-60mg/kg i/v or rectal
Followed by:
20mg /kg i/v q 8hrs
Potassium Bromide
In non-pre-treated patients loading doses:
400-600mg/kg/24hr 100mg/kg PO q4-6hours or 100mg/kg per rectum q24 hours for 5-6 days
130mg/kg/day orally for 6 days
Treatment of SE: 60-120 minutes
Levetiracetam
(can be used in 30-60min interval)
Initial dose 40-60mg/kg, i/v or rectally
Following therapy: 20mg/kg q 8 hours until seizure-free for at least 48 hours
Propofol
1-6mg/kg i/v propofol bolus
CRI: 0.1-0.6 mg/kg/min i/v
Refractory/Drug-resistant SE: > 120min
Ketamine:
5mg/kg, i/v as bolus
CRI: 5mg/kg/hr. If seizure-free for 12-24 hrs, continuous rate infusion under observation can be reduced by ~25% every 2 hours.
Inhalant anaesthesia:
Isoflurane
Sevoflurane
The Tapetum
An aid to vision in dim light for nocturnal animals
A highly reflective coloured layer in the inner choroid reflecting light back onto the photoreceptors
in horse it terminates before optic nerve in sharp line
variabkle in dogs and cats
Aqueous fluid
Watery
Constant production- ciliary body
Constant drainage- drainage angle
Vitreous fluid
Gel
No turnover
Iris musculature
Constrictor muscle-
Circular
Parasympathetic control
Dilator muscle-
Radial
Sympathetic control
Miotic = Drug which constricts the pupil
Mydriatic = A drug which dilates the pupil
The tarsal plate
stiffens the lid marginal areas
contains the tarsal/Meibomian glands
holds sutures much better then adjacent tissues
Distichiasis
Hairs growing on the edge of the lid
from the tarsal/Meibomian glands within the tarsal plate and emerging at the lid margin
treatment-
Plucking – they regrow
Electrolysis
Cryo
Tarsoconjunctival resection
So nothing simple or easily available
Ectopic (conjunctival) cilia
Emerge from the conjunctival surface and impinge directly on the eye
Much more sporadic and far less common than distichiasis
Far more painful
Alert - young dog (especially bulldogs) with a severely painful eye, possible shallow ulcer and no obvious cause
Ectopic cilia can certainly cause shallow ulcers but distichiasis hairs rarely
Entropion
In-rolling of the lid margin so that skin hairs abrade the eye
Chronic severe hair abrasion can cause large masses of corneal granulation tissue.
Once the abrasion is removed they resolve.
in cats-
Kittens/juveniles-
British Short Hairs
Lid usually needs shortening
Older cats-
?pathogenesis
Both groups-
Major problem for the patient
Often not diagnosed
It is not advisable to do excision surgery in young pups as the correction required
is difficult to judge.
A temporary holding procedure – “Tacking” - will buy some time until the pup is more mature
Ectropion
Out turning of the lid margin with conjunctival exposure
More severe ectropion can be part of the “diamond eye” spectrum
Upper lid trichiasis syndrome
Not true entropion but definitely trichiasis“Middle-aged cocker spaniel upper eyelid syndrome”
Middle-aged cocker spaniels (and other breeds and ages) can suffer from a laxity of the upper lid lashes which angle downwards as a result and abrade the eye causing great discomfort and debility.
These patients need a (modified) Stades procedure
rather than a standard skin-muscle excision
Sebaceous adenoma/epithelioma in the eye
The most common eyelid tumour in the dog
Arises from the tarsal/Meibomian gland
Grows as a:
well-defined mass
requiring full thickness excision
but minimal clearances
Very low metastatic potential
not commonm in cats
Squamous cell carcinoma of the eye
Lid tumours are very uncommon in the cat
SCCa can occur in pale areas
It may be nodular and tumour-like OR erosive and destructive
Functions of the Third Eyelid
Secretory – 30% of aqueous tears
Surface protection
Tear film distribution
Immunological
Cherry Eye
prolapse of the nictitans gland
English bulldogs more than other breeds
Burying but preserving the gland (The Pocket Technique)
Preserves function
Pocket technique ?not that difficult
(Relatively) expensive especially if referred
Failure rate
Excision of the gland
30% of aqueous tear capacity lost
Relatively easy and cheap
Recommended by many breeders and some vets
Comes with a guarantee
The Pre-Corneal Tear Film
Air
Lipid- tarsal glands
Aqueou- lacrimal and nictitans gland- Mucus conjunctival goblet cells
Corneal surface
Chronic Dry Eye
Chronic conjunctivitis
Dull appearance to the ocular surface
Mucopurulent discharge - tenacious and adherent
Discomfort
Corneal ulceration (variable)
Corneal vascularisation and pigmentation
Purulent discharge may be hidden in the fornices
Uncomplicatedconjunctivitis-
antibiotic responsive
clears up in a few days
does not affect the cornea
does not affect the pupil
or vision
Tear production can be quantified –
not a specialist procedure- tear test
corneal ulcer
A corneal ulcer is a full thickness defect in the epithelium
pain
potential for progression
In favourable conditions
the corneal epithelium heals rapidly but…
…the corneal stroma is susceptible to enzymatic destruction
Proteolytic enzymes may be released by:
Bacteria
Pseudomonas
β haemolytic streps
Inflammatory cells
Corneal cells
Unexplained/sterile
Signs of a perforation
Sudden pain
Convex protrusion of brown/black tissue with overlying fibrinous material
Blood from the eye
Indolent ulcers
generally don’t:
get infected
deepen
melt
They just don’t heal!
Minor surgery always needed- dont respond to other treatments
Debride away all loose epithelium firmly
Treat the exposed surface to encourage proper adhesion
Local anaesthetic and sedation preferred
Debridement needs to be thorough
Rub firmly and keep going till it stops
“If it comes off it needs to come off”
Don’t repeat too soon…
…and only if there are loose edges again
If the edges are sharp give it longer to heal
Repeats possible, serious complications rare
Don’t grid stromal ulcers…
pathogenesis different
…nor cats
risk factor for a sequestrum
Corneal Foreign Bodies- essentially two types
Adherent to surface
embedded in/on surface with little penetration
can be wiped off or squirted off with a jet of saline under local anaesthesia
Intracorneal = thorns
easier with a reasonable amount protruding
microsurgical problem in many cases
needle(s) for removal
Pigmentary keratitis
Invasion of the cornea by melanocytes
A common non-specific response of the cornea of the dog to a variety of insults
Common in the medial quadrant of brachycephalics
Brachycephalics more prone generally
Dermoid
a congenital malformation where a patch of skin differentiates on the ocular surface
Currently a French bulldog speciality
Pannus
inflammatory and vascular tissue advances across the cornea always from the ventrolateral direction.
Strong association with GSDs
topical cyclosporine/tacrolimus or topical steroids
Paracentral lipid dystrophy
Not proven to be associated with hyperlipidaemia or any systemic disease
Deposits of crystalline fat in the central cornea
Not proven to be associated with hyperlipidaemia or any systemic disease
Peripheral lipid depositions may well be associated with hyperlipidaemia. Investigate
Glaucoma
Definition - an abnormal rise in intraocular pressure
Always a problem of aqueous flow or drainage and not over-production
Acute glaucoma causes great pain
It rapidly destroys the retina and optic nerve
Glaucoma is ultimately the reason for removing most eyes
Primary Closed Angle Glaucoma-
Primary abnormality of the drainage angle
Inherited in several dog breeds
Sudden decompensation in middle age with an acute pressure rise
Acute pressure rise is devastating – hours matter
Bilateral (but not symmetrical) problem
The onset is usually acute
Easily confused with other conditions
The pain is severe and the damage to the eye rapid
As a result the most important eye emergency of all
The second eye is at risk although it usually appears perfectly normal at the time
Primary lens luxation
An insidious degeneration of the apparatus supporting the lens
Affecting both eyes but not simultaneously
If/when the lens luxates anteriorly through the pupil it causes glaucoma, inflammation and secondary corneal oedema presenting as an acute eye
Anterior dislocation
Surgical lens removal
Return the lens to the posterior chamber by external manipulation (“couching”)
Then maintain a constricted pupil to keep it there
Subluxated lens
Maintain a constricted pupil to prevent anterior dislocation
(Surgical lens removal – historical now)
But the prognosis will always be guarded
Enucleation
is a means of pain relief and a good one.
Removal of a blind painful eye is a simple procedure with a low complication rate which provides pain relief without functional loss.
“Without functional loss” – it is not a question of whether the dog “can manage with one eye”.
Chemosis
oedma of the conjunctiva
occurs readily in the cat conjunctiva
looks dramatic
no prognostic significance
Symblepharon
The permanent adhesion of ocular surfaces – conjunctiva/cornea - following herpes infection as kittens
The flu may have cleared up when the kitten/cat is seen
Very variable
Often pain free and functionally minor and can be left
Special techniques may be required for cases needing surgery
Corneal sequestrum
Delayed healing of a corneal ulcer may lead to necrosis of the exposed stroma
The necrotic stroma then turns brown/black
This then acts as a foreign body and causes pain in its own right
very common eye condition of cat
Systemic Hypertension and the Eye
The eyes of cats appear particularly susceptible to the effects of systemic hypertension
Dogs with overt ocular signs are usually in renal failure
Cats may be surprisingly well with alarmingly high blood pressures
Hyphaema in a teenage cat is almost pathognomonic for hypertension unless there has been trauma.
Look in the fellow eye
Corneal response to injury
Epithelium- very good
Stroma- significant cellular infiltration so good
Endothelium- limited capacity for regeneration
corneal odema
blue opacity
ocuurs ddue to disruption of epthelium
Cellular infiltration of the eye
White/ creamy opacity
Response to infection
Scarring and fibrosis
Pentobarbital Sodium (e.g. Dolethal, Pentoject, Euthasol)
SCHEDULE 3
Barbiturate class of drug
200 or 400mg/ml
Coloured solution
Progressive CNS depression
Stages:
i) sedation,
ii) intoxication, possibly with involuntary
excitement,
iii) anaesthesia,
(iv) respiratory arrest and subsequent cardiac failure.
Rapid IV injection – 200mg/ml 0.4ml/kg debilitated animals 0.6-0.8ml fit/healthy animal
(IP, IC, IM, IT)
Dogs, cats, rodents, rabbits, cattle, sheep, goats, horses and mink
Somulose
(SCHEDULE 2)
Quinalbarbitone sodium
Depresses CNS inc respiratory centre and causes loss of consciousness
Cinchocaine hydrochloride
Cardiotoxic effects
Brain function and cardiac output should stop AT THE SAME TIME
CLEAR Solution
Licensed in dogs, cats, horses, cattle
HIGHLY TOXIC TO HUMANS
IV only - VIA 14G CANNULA
Horses and Cattle = 1ml/10KG OVER 10-15 Seconds
TOO SLOW = ‘Normal’ collapse but prolonged period until death
TOO FAST = Premature cardiac arrest (heart attack)
Captive bolt
Large Animals
Stuns by percussive force.
MUST be ‘bled’ or ‘pithed’ immediately following stunning
Declassified in 1998 – no firearms license required to purchase or use
If used in emergency/casualty situations no slaughter license required either
Bleeding
(for euthanasia)
ASAP after stunning – prevents risk of recovery
Ideally in tonic phase
Sever carotid arteries and jugular veins
Emergency – deep transverse cut across angle of the jaw
2 powerful jets of blood
Sharp knife at least 120mm long
Carcass will not be permitted for human consumption
Pithing
Not to be performed in animals intended for human consumption
Insert a flexible wire or polypropylene rod through the hole in the head made by a captive-bolt.
Disposable pithing canes available – Stay inside the carcass
Firearms (for euthanasia)
Free Bullet
Humane Killer – single shot, barrel in contact with animal
Shotgun
Rifle
Hand-gun
Shotgun or Firearms License required
Storage – locked gun cabinet. Locked metal box in car, ammunition separate from gun
health and saftey-
Firearms Legislation
People
Handling and Restraint
Backdrop
How is death confirmed
Absence of rhythmical breathing
Absence of corneal reflex
Absence of heart beat/pulse
Reflex/Agonal ‘gasps’ common
Disposal of carcases
Burial - Barbituates make boies toxic and owners must be made aware
Cremation - Costs involved
Incineration/Collection/Fallen Stock
Euthanasia of dogs and cats
In practice or home visit
Almost always by intravenous injection
PLAN
Gain informed consent
Administer sedation if required
Secure IV access – cephalic or saphenous vein most common
Inject drug IV
Confirm death
Other methods:
Intra-peritoneal
Intra-renal
Intracardiac
Euthanasia of hrses
Considerations -
Positioning
Disposal
Safety
Insurance - BEVA guidelines
Free bullet most common for companion horses
Lethal Injection:
Gain informed consent
Sedate - detomidine IV
LA at cannula site
Secure IV access with 14g cannula
Inject Somulose IV over 10-15 seconds
Confirm death
Euthanasia of cattle
Lethal Injection :
0.4-0.8ml/kg 200mg/ml pentobarbital sodium via rapid IV injection – Jugular vein
1ml/10KG Somulose IV injection over 10-15 seconds – Jugular vein
Sedation not normally required in most cases
Firearms:
Euthanasia of sheep
Lethal Injection:
0.4-0.8ml/kg pentobarbital sodium rapid IV injection – Jugular Vein.
Sedation not normally required
Firearms
Euthanasia of Pigs
Very difficult
Best option is shotgun
Can be done with ga into soft muscle the somulose into peritoneal cavity- death takes time
What are RECOVER Guidelines?
Series of systematic reviews
Conducted by more than 100 specialists in the field
Evidence based
Divided into 5 major topics (domains)
1.Preparedness and prevention
2.Basic life support (BLS)
3.Advanced life support (ALS)
4.Monitoring
5.Post cardiac arrest (PCA) care
A total of 101 clinical guidelines were published
Evidence classified using Class and Level system
What to do in a case of Cardiopulmonary Arrest
Philosophy?- cpr on healthy patient will not do harm, start anyway if in doubt
Team Size?- could be alone, ideally 3 people with chest compressions, 2 people on respiration, 2 people drawing up drugs, 1 person calling owner, 1 person coordinating team
Should we carry out
CPR?
DNR?
Facilities for PCA care
Success of CPR?
Dogs acute arrest under GA – almost 100%
Hospitalised cases
Dogs 3.8-25%
Cats 2.3-22%
People >20%
domain 1 of RECOVER guidelines
Equipment & Training
Ensure:
All staff are familiar with and utilise a standardised crash cart- Regular training?
Needed drugs and equipment in logical sequence- labels pointing forward
Pre drawn seringes of adrenalin and atropine
Ensure:
Cognitive aids are available
Staff receive comprehensive training (including simulations) plus assessment to ensure comprehension
Education & Leadership-
Refresher training every 6 months recommended (I-A)
Specific leadership training for those leading CPR (I-A)
Both vets and nurses are capable of leading CPR (IIb-B)
Debriefing after CPR to discuss performance (I-A)
domain 2 of RECOVER guidelines
Clinical signs of CPA?
Discoloured blood at surgical site
Bleeding stops
‘Gasping’ ventilation or apnoea
Mucous membranes change colour
CRT > 2 s
No heart sounds
No palpable pulse
Central eye
Mydriasis
Dry cornea
Cranial nerve arreflexia
Generalised muscle relaxation
Response-
Respond conservatively- O2 PPV ECC IT drugs indirect DC defibrillation (not very useful)
Respond aggressively- O2 PPV thoracotomy- direct cardiac compressions and deal with sequale ICC IV / IC drugs direct DC defibrillation
Respond conservatively aggressive if no response
DNR
Response depends on;
Owner
Number of assistants available
(time of day)
Equipment available
Drug availability
Size of patient
Type of arrest: “acute” vs “chronic”
Domain 2: Basic life support (BLS)
A – Airway
B – Breathing
C – Circulation
D – Drugs
E – Electric defibrillation
F – Follow up
Accept the fact-
Call assistance
Position
In right lateral recumbency
On hard surface
In head-down position- Drainage of fliud and good blood flow to brain
A: Airway
Clear airway
Cuffed endotracheal tube
Check patency
Position accurately
Breathing-
PPV- Anaesthetic machine + abs 100 % O2
Self-inflating resuscitation bags- Air or 100 % O2
No synchronicity
Ensure expiratory pause
No PEEP
Rate = maximum 10 bpm
DO NOT OVERVENTILATE
C: Circulation-
Check pulse
External cardiac compression (ECC) - Cardiac pump, Thoracic pump
Internal cardiac compression (ICC)
Acute Arrest
Oxygen runs out In myocytes
Good prognosis
Chronic Arrest
Oxygen runs out and there is lactate build up in myocytes- old dog with comorbidities
Cardiac pump
Cats
Dogs < 15 kg
rabbit
Narrow chests
Compression ventral third 3rd - 6th ribs Between thumb and forefinger
Compression rate 80 - 100 per minute, musxle needs time o relax
Thoracic pump
For dogs > 20 kg
“Barrel chests” (?In dorsal)
Compression widest point
Compression rate 80 - 100 per minute
Compressions during peak lung inflation are fine
HANDS OFF BETWEEN COMPRESSIONS
Internal Cardiac Compressions
Open-chest CPR may be considered in cases of intrathoracic
disease if appropriate resources are available for the intensive
PCA care these patients will require
If thorax is open
When ECC fails (2 minutes but can do alot longer)
When ECC futile
‘Chronic’ arrests in dogs > 20 kg
Technique
Rapid clip in long-coats over left 3rd - 6th ic spaces
Identify 5th ic space
Deflate lungs
Boldly incise
Blunt scissors sternum to dorsum
Open pericardium
‘Milk’ ventricles at 80 - 120 min-1
Internal cardiac compression: advantages
More effective
Arrhythmias diagnosis
Assessment of contractility
Atrial & vena caval filling
Lung inflation assessed
Aortic cross-clamping
Cardiac warming
Accurate IC injection
domain 3 of RECOVER guidelines
Advanced Life Support
Have specific list of drug doses
Adrenaline- 10 mg kg -1 (low dose) (x3 for Intra Tracheal (IT), follow up with saline) x3 then one High dose if needed
Atropine - 40 mg kg -1 (x3 IT) every 2/3 rounds- gets rid of low heart rate
ADH (vasopressin) - 0.8IU/kg
Lidocaine- 2 – 4 mg kg -1 25 – 75 mg kg -1 min –1- FOR ARYTHMIAS
Amiodarone – V/A fib- 5mg/kg- FIBRILATION, last resort
NO fluids unless hypovolaemic
(Magnesium)
(Methoxamine - 500 mg kg -1 (X3 IT))
(Calcium)
If in doubt use twice maintanence
E: Electrical Defibrillation
Energy required
Lowest setting
External 1 - 5 - joules kg -1
Internal 0.1 - 0.5
Crank up
Cardiac massage inter discharge
Domain 4 of RECOVER guidelines
Monitoring – Diagnosing CPA
“Rapid identification of a patient requiring CPR allows more rapid institution of BLS and ALS, which increases the chance of ROSC”
Pulse palpation to diagnose CPA is NOT recommended (current human guidelines limit pulse palpation by health care professionals to less than 10 seconds before BLS measures are initiated).
Electrocardiography (ECG) or Doppler blood pressure measurement to diagnose CPA is NOT recommended
ECG or Doppler blood pressure measurement to detect impending CPA is reasonable to perform in at-risk patients
End-tidal carbon dioxide (EtCO2) monitoring is recommended for intubated patients at risk of CPA
EtCO2 correlates well with cardiac output and rapidly drops to zero at CPA onset
ECG recommended for rhythm evaluation- only during intercycle pauses and NOT delay resumption of chest compressions
EtCO2 monitoring during CPR to evaluate efficacy of chest compressions is reasonable - ROSC will cause a sharp increase in EtCO2
10-15 c02 = good cpr
Blood gas and electrolyte analysis may be helpful in evaluating CPR effectiveness and identifying underlying causes
If underlying electrolyte derangements are suspected or known, electrolyte analysis to guide therapy is recommended
In patients with documented hyperkalaemia, treatment is recommended
Domain 5 of RECOVER guidelines
Post Cardiac Arrest Care
Excellent PCA care- Minimises CPA recurrence and maximises patient discharge. >50% of dogs and cats will have another CPA event while hospitalised
Following ROSC patients have:
Haemodynamic instability (vasopressor therapy during CPR or the underlying cause of CPA)
Cardiac ischaemia
Systemic inflammatory response syndrome (inflammatory system activation and excess circulating cytokines)
Anoxic brain injury
Referral to Specialty Centre?- improved survival of patients treated by professionals with experience in PCA care and in facilities with higher staff-to-patient ratios
Research has indicated that patients were more likely to survive when drugs, such as dopamine and vasopressin, were available and more staff were involved in resuscitation efforts
It is reasonable to refer a PCA patient to a facility with-
24-hour care
Higher staff-to-patient ratios
Advanced critical care capabilities
F: Follow Up
Oxygenation & ventilation
Fluids and urine output
Inotropes & anti-arrhythmics
Analgesics
Warmth OR therapeutic hypothermia
Antibiosis
Position
Neurological sequelae, i.e. Diazepam
Monitor
Fee collection
Cardiopulmonary Arrest
Myocardial disease
Myocardial hypoxia-
Systemic hypoxia
Cardiac overwork
Hypotension
Extremes of temperature
Extremes of pH
Altered electrolytes
Toxaemia
Primary Assessment for triage
Done by receptionist, nurse ect
Respiration
Awareness
Perfusion
RAP
Triaging airway
Any change in breathing pattern might be an emergency
Step back and look- still has airway? just reverse sneezing? abdominal effort? mouth breathing in cat?
?? Emergency Ballpark – Above 50 Br/min considered emergency finding
Mucous membranes
Pulse oximeter
Triaging AWARENESS
It is conscious? Yes?
Is it:
Alert? Normal behavior and is responsive BAR/QAR
Depressed? Awake but subdued. Uninterested in environment QAR?
Delirious? Awake but altered perception. Responds inappropriately to stimulus
Watch for change – a decline in level of consciousness could be indicative of a worsening prognosis
Stuporous: Remains in sleep state. Only roused by strong stimulus
Comatose: Deep unconsciousness. Unable to rouse even with strong stimulus
What kind of situations are these most relevant?
What about an animal in a seizure??
Triaging PERFUSION
MUCUS MEMBRANES
They should be PINK
Any colour change could represent an emergency
They should have a capillary refil time of less than 2 seconds (CRT<2). Cardiovascular collapse might have a CRT of 3 seconds or more.
PULSES
Quality – are they weak and hard to feel? Are they bounding or hyperdynamic?
Rate – too fast? Too slow? Does it co-ordinate with the heart rate i.e. Synchronous or are there Pulse Deficits
Rhythm – regular? Irregular?
- AUSCULATE THE HEART
The Rate – too fast or too slow?
The Sounds – murmurs?
The Rhythm – regular or irregular?
Secondary Assessments - Respiratory
OXYGEN – Flowby, mask, oxygen tent, nasal prongs
Airway?! Inspiratory or expiratory issue??
Primary Respiratory vs Primary Cardio?
b lines- lung rocket- seen on t fast scan with wet lungs
pulmonary odema can be seen on radiograph as enlarged radioopaque heart
pleural effusion can be seen on radiograph as lifting of lungs or large field of radioopuaque material
Secondary Assessments - Awareness
What is this about??
Pupil assessment:
Pupillary Light Response PLR
Miosis (bad)? OR Mydriasis(worse)?- progression of this can indicate herniation (no way back)
A change?
Oculocephalic Reflexes?
Strabismus or Nystagmus?
Cerebral Perfusion Pressure = Mean Arterial Pressure – Intracranial Pressure
CPP = MAP – ICP
OXYGEN
MEASURE BLOOD PRESSURE
IDENTIFY AND TREAT HYPOVOLAEMIA
POSITIONING – Keep head at 30^ to ma
Head trauma+ shock= vasodilation, leading to increased icp
Secondary assessment - Perfusion
Hypovolaemic Shock
**NEED TO RECOGNISE AND ADDRESS THIS **
Tachycardic
Delayed CRT on pale mucous membranes
Progresses to weak pulses
Dull mentation
Low temp/cool extremities
Anaemia-
Pale/white mucous membranes
Normal CRT?
Pulse quality bounding – weak
Tachycardia
Is it bleeding?? Where?!
More chronic? Tachypnoea
Cardiac Dysfunction-
Acute Heart Failure
Tachycardia
Tachpnoea/Dyspnoea
Weak pulses
CARDIAC AUSCULATION – changes in RHYTHM, SOUNDS (murmurs or gallop)
LUNG FIELD AUSCULATION – Might hear adventitious lung sounds like crackles
MUCOUS MEMBRANES – Pale, with long CRT
Sepsis-
Aka Septic Shock
High rectal temp as in over 40 ^C OR low rectal temp as in less than 38^C
Tachycardia (OR bradycardia – typically in cats)
Hyperemic (RED) mucous membranes with short CRT (less so in cats)
Hypotension
Other clinical signs assoc with the disease foci.
Other markers to check with triage
Glucose- Check with glucometer
The bladder- Can they urinate?
PAIN-
The 4th vital marker!!!
Pain can confuse your diagnostic picture!! Administer analgesia and re-examine, re-examine, re-examine.
Opiods vs NSAIDS vs Others – what is appropriate?
Horse obstetrics
HEALTH AND SAFETY – PLEASE TAKE CARE
Stage 2 labour (after the membranes are passed) is only 20 mins in a normal foaling.
Foals not delivered within 30 mins have a much lower survival rate
Retained foetal membranes – 6 hour window
What is an emergency in exotics?
Initial phone call
Based on this call need to determine whether an emergency-
Signalment
Species, breed, sex, neutered/entire, age
Clinical signs
When did this start?
Trauma – when and how?
Did owner notice the animal eat anything poisonous/toxic? How much and what? Birds – respiratory toxins?
Instructions to client
Basic first aid
Handling
Correct Transport to the surgery
Examples of signs noted in small mammals needing immediate attention
Anorexia
Bloating
Haemorrhage
Respiratory distress/compromise
Collapse
Diarrhoea or absence of faeces (particularly herbivores)
Dysuria
Dystocia
Neurological signs
Traumatic injuries
Vomiting (ferrets)
Can be divided into two categories
Acute-
A sudden, recent event
Fight/bite wounds (myiasis), haemorrhage
Trauma – falls, crash landings, fractures
Prolapses
Dystocia
Chronic-
A more chronic illness that has reached a critical point- Dental disease, GI disease
Can be just as life threatening!
First aid and basic information in exotic emergencies for client
Basic first aid – allows animal to be transported safely to optimise survival
Bleeding -> apply pressure
Burns -> Cool area immediately
Choking -> keep animal calm, if breathing immediate travel to surgery. If partially obstructed allow animal to cough. If airway obstructed a modified Heimlich manoeuvre performed
Hypothermia -> bubble wrap & towel to prevent further heat loss. Snugglesafe/hotwater bottle covered -> do not want to burn!
Hyperthermia (heat stroke – rabbits/guinea pigs) -> move to cooler area. Cool slowly. Drizzle water over, concentrating on head, stomach, inner thighs and footpads.
Seizures -> darken room, remove hazards. Time how long seizure lasts. Do not restrain
Prolapse -> dampened substrate – damp kitchen towel (no woodchip or sand), cover with cling film/glove
Procedure for exotics emergencies in practice
Stable vs unstable?
Observe the animal
History collection:
Reason for concerns
Diet and husbandry- Hypocalcaemic tetany -> birds & reptiles.
Vaccination history (distemper – ferrets; Myxo/RHD 1& 2 – rabbits)
Neutering status (ferrets – oestrus induced anaemia. Rabbits – uterine adenocarcinoma/pulmonary metastases)
Assess husbandry
1. What do they feed it?
2. Do they feed vitamin/mineral supplements?
3. Is there UVB provision?
4. What temperature gradient do they keep the vivarium at?
5. What hides/cage furniture is present in the tank?
6. What humidity do they keep the vivarium at?
7. Do they have any other reptiles/pets?
8. If a snake-when did it last shed its skin, and was it a complete shed?
Physical examination – primary assessment
Basic exam initially until stabilised.
Alertness
Posture
Facial asymmetry/facial changes
Locomotion
Body condition score
Coughing
Sneezing
Wheezing
Dyspnoea
Open-mouth breathing
Increased respiratory effort
Ocular and/or nasal discharge
Respiratory noise
Poor hair coat
Abnormal stance
Helps to determine level of urgency
Standard clinical exam
ABCDE protocol
Reptiles - triage
Initial Assessment
1. Safety first! Is it potentially hazardous/dangerous to the handler?
2. Is it mouth-breathing and possibly in respiratory distress?
3. Is it a species that can perform autotomy? (many geckos will shed their tails very easily)
4. Is it suffering from metabolic bone disease making it a risk to handle? (deformed limbs, shell, spine and inability to support its own weight may predispose it to pathological fractures)
5. How large is the animal? (many larger species of tortoise are heavy and strong, with the ability to crush fingers. Snakes longer than 3-4 feet require more than one handler).
Birds - triage
Any bird that is unconscious, seizuring, with evidence of head trauma or respiratory
distress should be attended to immediately.
Birds that are off colour should be hospitalised in a quiet, warm (29-30°C), dimly lit area with supplemental oxygen if there is any evidence of respiratory distress and should be examined as soon as possible.
All birds presenting as an emergency should be assumed to be hypothermic
Primary assement of exotics procedure
ABCDE
Airway -> chest & abdominal movements, respiratory effort, respiratory noise, open mouth breathing.
Open mouth breathing = Severe distress for birds. Severe distress for our small mammal patient such as rabbits & guinea pigs-> obligate nasal breathers.
Breathing -> depth, frequency, rate and rhythm of respiratory movements. - Nostril flaring.
Auscultate for respiratory sounds (wheezing/whistling) or for absence of sounds.
Percussion of thorax – pneumothorax/pleural effusion.
Circulation ->pulse rate/strength, mucous membrane colour, heart rate and rhythm.
Reptiles -> use of a Doppler probe applied over the heart/carotid artery can provide an assessment of blood flow -> can assess intensity of flow and turbulence.
Disability/disease
-> assess the animals consciousness and responsiveness to the surroundings. Assess reflexes
Remember menace response frequently ABSENT in rabbits and rodents
Exposure to the environment-
Bruises, fractures, wounds, contamination
Check body temperature
If stable -> proceed to secondary assessment/full physical examination
Handling and Hospitalisation of exotics
Handling
Keep to a minimum
Place on a non-slippery surface
Visualisation within a clear box transillumination
Towel
Constantly monitor for signs of stress stop!
Consider sedation
Hospitalisation
Appropriate environment
Heated vivariums to POTZ
Appropriate temperature and humidity
Escape proof enclosures
Quiet environment – minimise stress – Pet Remedy plug-in or spray (is safe for birds!)
Predator/prey
Differential for a down dry cow
Dystocia- uterine torsion, seen as ime of partuition
Metabolic- milk fever (secondary possibly to dystocia), ca drop from parturition- not seen without calving complication
Toxaemia- recently dried of cows: toxic mastitis, selective dry off, septic peritonitis (quick drop)
Trauma- always possibility, dry cows pregnant and mixed into new groups so increases risk, lamness prevents them form rising
Physical- near calving puts pressure on many body systems and so may just be the cause
Differentials for down fresh cows
Trauma (obstetric)- biggest reason, calving paralysis syndromes (nerve damage): soon or late onset
Metabolic- Milk Fever
Toxic- Mastitis, Metritis
Differentials for Lactating fresh cows
Traumatic
Toxic
Metabolic
Reasons grazing causes a down cow
Toxin Ingestion
Hypomagnasaemia- to treat magnesium goes under skin NOT IN VEIN
Reasons grazing causes a heifer
Trauma
Toxin Ingestion
Chronic?- may think its acute however could be a long term management problem: pnuemonia
Treatment of a down cow
Traumatic
Depends on prognosis
NSAID
Supportive care
Slaughter certificate?- for animla sthat do not show any sign of systemic disease of emaciation. Needs to be close to abitoure as slaughter man must get there. Kill on farm- captive bolt and examination. Need to know meds that they’ve had
Metabolic
Correct underlying challenge
Supportive care
Toxic
Depends on prognosis
Fluids, NSAID, +/- Abs
Supportive care
Continued care essential- farmer input important to prevent sequential conitions. If farmer cannot support cow euthanasia may be option.
IV access exotic mammals
Rabbits – Lateral saphenous vein, cephalic vein or marginal ear vein
Guinea pigs – cephalic vein, lateral saphenous, jugular vein, cranial vena cava
Ferrets – cephalic, saphenous, jugular vein
Hedgehogs – jugular vein, cranial vena cava
Blood sampling - reptiles
Can take up to 1ml/100g in a healthy animal
Advise to collect 0.5ml/100g- Most patients are compromised
Collect in lithium-heparin tubes (birds & reptiles)
Prepare a fresh blood smear
Edta causes haemolysis
Blood collection - chelonians
Jugular vein
Less chance of lymphodilution
Often at level of auricular scale and base of neck
Apply pressure after
Subcarapacial sinus
Haemodilution
Potential for damage to spine
Dorsal coccygeal vein
Haemodilution
Potential for damage to coccygeal vertebrae
Subcarapacial – situated in the midline below the cranial aspect of the carapace, just above the caudal cervical vertebrae
Brachial plexus
Useful in larger chelonians
Extend front limb
Palpate tendon on caudal aspect of radial-humeral joint
Insert needle just caudal or ventral to the tendon
Blood collection - lizards
Ventral tail vein
Care with species that perform autotomy
Jugular vein
Can be considered for leopard geckos
Blood collection - snakes
Ventral tail vein
Recommended site
Care not to insert needle into hemipenes or cloacal musk glands
Cardiocentesis (ADVISE SEDATION FOR THIS METHOD!)
CARE - risks of laceration to ventricle and risk of pericardial haemorrhage
Blood collection - birds
Venepuncture sites
Right jugular vein
Can obtain large volumes
Gentle pressure to achieve haemostasis
Basilic (ulnar/brachial vein)
Extend wing and visualise vein
Vein runs over the elbow area
Care as haematoma formation is common
Medial metatarsal vein
Vein is very short in psittacines
Assessing hydration In exotics
Assess hydration often dehydrated
Methods are subjective +/- in combination with lab tests
Skin turgor – variable greater elasticity in mammals compared with birds & reptiles. Greater elasticity in younger and fatter animals. Assess over pectoral muscles in birds & scruff of neck most mammals.
<5% = no clear sign of skin tenting/loss of elasticity
5-6% = slight skin tenting & loss of elasticity
7-9% = notable skin tenting % significant loss of elasticity
10-12% = marked skin tenting & complete loss of elasticity
12-15% = marked skin tenting & complete loss of elasticity
Mucous membranes – difficult to assess. Tacky at 7-9% and dry at 10-15%
CRT (mammals) & venous refill time (birds) - >2 seconds at 7-9% and >3 seconds at 10-15%
Eyes – varies with species and bodyweight. Slightly sunken at 7-9%, noticeably sunken at 10-12% and markedly sunken at 12-15%
General condition – variable and difficult to assess normal in a wild animal stress response. 7-9% mild changes in mentation, 10-12% marked changes in mentation, 12-15% moderate shock and moribund
Fluid therapy (birds)
Ability to maintain IV lines more challenging in wildlife/zoo birds vs pet
Direct monitoring often more limited
Birds- SC injection inguinal or precrural folds, wing web (propatagium), axilla, interscapular area- Up to 20ml/kg I tend to go LOWER
Can add hyaluronidase – 1500IU/L added to sterile crystalloid fluids – increases absorption
IV or IO (non pneumatised long bone only – ulna or tibiotarsus)
Maintenance – varies with size of bird – very small birds require more per body mass
Average daily maintenance = 100ml/kg/da
Fluid therapy – IO tibiotarsus
- Anaesthetise the bird and administer analgesia
- Aseptic preparation and administer local anaesthesia
- Hold the tibiotarsus in one hand
- Insert the needle into the cnemial crest, through the insertion of the patellar tendon that is aligned with the diaphysis. Gently advance the needle
- Suture in place
Fluid therapy – IO ulna
GA and administer analgesia
2. Flex the carpus and identify the needle insertion site on the dorsal surface of the ulna just distal to the condyle.
3. Infuse local anaesthesia
4. Aseptic skin preparation
5. Hold the limb and insert the needle in the mid portion of the condyle and in the same plane as the bone
6. Seat the tip of the needle into the periosteum. Rotate the needle and advance. A gentle ‘pop’ may be felt.
7. Flush catheter and secure with tape and sutures
Crop tubing
Fluid therapy (birds)
Crop tubing into crop or at level of thoracic inlet for species without a well developed crop (owls)
General rule = crop volume is calculated as 5% bodyweight LOWER in debilitated patients
Fluid therapy (reptiles)
Epicoelomic (chelonians)
Between the plastron and coelomic membrane
Intravenous
Requires surgical cut-down
Intraosseous
Medial tibial crest (lizards)
Tibial crest and gular plastron (chelonians)
Epicoelomic route recommended 10-20 ml/kg can be given
IO requires sedation. In chelonians also reports of IO on the bony bridge but there is debate whether the bridge communicates with vascular system
Cardiopulmonary Resuscitation in reptiles
Establish an airway (reptiles)
Intubation
Glottis situated rostrally (lizards & snakes)
Tortoise – more challenging due to fleshy tongue
Tortoise – Complete tracheal rings
Lizards & snakes – incomplete tracheal rings
IPPV required
Small animal ventilator
Manually
Emergency diagnostics
Conscious radiography
DV – assess for shelled eggs (birds and reptiles)
Gas within intestinal tract (gastric dilatation – rabbits/g pigs; GDV guinea pigs)
Point-of-Care Ultrasound (POCUS)
Detection of free fluid
Evaluation of trauma cases – pneumothorax/penetrating injury patients
- Describe a basic anesthetic plan for a routine bitch spay
- Acp or alpha 2 agonist- give reasons for choice e.g (medetomidine gives good anasthesia and analgesia but produces profound bradycardia. Has effective time of 40 mins (is this enough for op? alpha-2 hump as it wears off once prep is finished- top up alpha 2 or give something else appropriate to give analgesia)
- Opiod-
- buprenorphine?- last up to 6 hours. When dog gets light you must top up with ketamine/ something other than an opiod.
- Methadone is a better choice as as a full mu agonist opiod you can top up, sicker the patient lower the dose. Start low you can always give more top up with half dose. Also, cheaper
-don’t forget recovery- alpha 2s only last 40 mins!!!!.
What is the common arrhythmia associated with alpha 2s-
2nd degree av block. P wave without qrs
Will be herd as missed heartbeats
Can you use lidocaine in cats as an anti arhythmic iv
Only one bolus!!!! For cats with ventricular dysrhythmias
Recommended sedatives for cvrs/ compromised patients
Very sick patient (cartiovascular- gdv)- sicker the patient the more likely methadone and only a methadone (opiod) is best. Treat bradycardia with atropine
Cavvies with mitral valve disease- acp causes less adrenaline, vasodilation, is an antiemetic and calms the dog
Benzodiazapime may be appropriate in very young/ very old patients
Alpha 2s good because they can be antagonized
Why is butorphanol good for birds and exotics
Lots of birds and some reptiles have lots of KAPPA receptors so targeting those is thought to be better
Atropine vs adrenaline-
Atropine increases vagal tone- should be added in every third round of cpr to combat brady cardia
Adenerline increases heart rate and returns blood to heart- drug of choice
Cardiogenic ossilations
Heart beating againt lungs pushes out small bits of co2 and causes “bumpy lines” on capnograph.
Sail shape on capnograph means….
obstruction
A capnograph that does not reach the dotted baseline indicates
This is caused by
Non- rebreathing systems
- The valve being shut (but only in first few seconds)
- Too low flow- flow pushes co2 out
Circle
- Sodalime running out
- Stuck valves in set
- Gas flows are measured in
- Liters per minute
