mcq 2 pcp Flashcards
vsmall animal oestrus cycle
Pro-oestrous (10 days)
Oestrous (10 days)
Luteal phase (2 month)
Pregnant or non-pregnant
Anoestrous (4.5 months)
P4 from CL only
LH and prolactin luteotrophic
Average gestation in the bitch
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)
principles of 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
Plasma Progesterone Concentration
No rapid return to oestrus
Not sufficiently different between pregnant and non-pregnant bitches
Plasma Relaxin Concentration in small animals
Values elevated in pregnancy from day 25 onwards and are diagnostic whilst a viable placenta is present
describe what can be felt on abdominal palpation 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 small animal pregnancy diagnosis
Limited use in early pregnancy
Fetal calcification after day 41-44 (av – 42d)
So radiographic diagnosis from day 45
Can determine number, position and relative size of fetuses from day -50
Valuable in dystocia cases
Fetal skeleton – >day 42
Skull day 45-59
Pelvic bones day 53-57
Teeth day 58-63
ultrasonography for small animal 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
what can be used to measure gestational age in small animals
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
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.
treatment of Accidental Pregnancies
Surgical Approach
- Pharmacological Approach
Drugs that act on the uterus:
Oestrogens e.g. oestradiol benzoate
Alters transit time of zygote
Within first 5 days of mating
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
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
pregnancy diagnosis in the bitch
NOT a lack of return to oestrus
NOT elevated plasma progesterone
Trans-abdominal ultrasound: from day 25
Plasma relaxin: from day 25
Plasma acute phase proteins: from day 35
Abdominal palpation for discrete swellings: from day 28
Radiographic examination: from day 45
Predicting parturition in the 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
Diagnostic imaging
Progesterone and whelping
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
stages of Normal Parturition
- 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
3.Second stage parturition
Expulsion of the foetus
4.Third stage parturition
Expulsion of the placenta and foetal membranes
- Puerperium
Maternal dystocia
Inadequate expulsive forces
Inadequacy of birth canal
Foetal dystocia
Presentation or disproportion (relative to the dam) of the fetus
dystocia- 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)
dystocia- 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 #’s
Management of primary inertia
Primary uterine inertia is the failure to initiate labor at term
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
Secondary uterine inertia is the failure to progress once labor is initiated (uterine fatigue).
Correction of the cause of dystocia
Nothing
OR
Ca2+, oxytocin C-sec as before.
Faulty foetal disposition
Presentation: longitudinal axis of the foetus and the maternal birth canal
Longitudinal (anterior/posterior), transverse (V/D)
Position: the surface of the maternal birth canal to which the fetal vertebral column is applied (D/V/LL/RL)
Posture: position of the appendages (flexion/extension of neck or limbs)
Disproportion:
Foetomaternal disproportion – when the foetus is larger than the capacity of the pelvis
Normal fetal disposition is described as cranial longitudinal presentation, dorsal position, extended posture.
When to get involved with dystocia
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
managment for dystocia
Establish a tentative treatment plan:
Conservative treatment
Manipulative treatment
Drug therapy-
Ecbolic (oxytocin)
Calcium
Tocolytic (clenbuterol-reduces contractions)
Surgical treatment-
Epidural anaesthesia
Episiotomy-enlarge birth canal
Caesarean operation
Euthanasia
Manipulative Treatment:
Repulsion-
Pushing the fetus out of the pelvis back into the abdomen to give more room (may be impossible if dam straining)
Correction-
Correction of the abnormal orientation
Rotation or version-
Alteration of alignment of long axis or transverse axis of fetus
LOTS of lubrication and a normal sized foetus required!
Traction:
Vectis forceps
Cup like structure over back of head of the fetus
USE WITH CAUTION
Medical management:
Ecbolic drugs e.g. Oxytocin
Contraindicated in cases of obstructive dystocia
Calcium gluconate
ONLY when:
Bitch is healthy
Cervix is dilated
Foetal size and positioning are appropriate
Foetal HR is normal
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
managment of Postpartum bitches/queens
Normal
Slightly elevated temperature (upto 39.2)
Serosanguinous vaginal discharge 3-6 weeks
Uterine involution 12-15 weeks
Abnormal
Temperature >39.5
Thick dark vaginal discharge
Haemorrhagic discharge more than a drop
Serosanguinous discharge >6 weeks
When to get involved-
Third stage parturition
Expulsion of the placenta
All the placentas have not been passed within 4– 6 hours (although placental numbers may be difficult to determine if the bitch eats them)
The rectal temperature is higher than 39.5°C (101.3°F)
There is continuing severe genital haemorrhage
The lochia are putrid or foul smelling
The general condition of the bitch is abnormal
The general condition of any of the puppies is abnormal.
comon female rabbit reproductive conditions
Normal pregnancy – need to know normal
Extrauterine pregnancy
Not uncommon
Escape of fertilised ovum or rupture of a pregnant uterus
Fetus becomes mummified
Dystocia
Rare
Pseudopregnancy
Reflex ovulators
Ovulation occurs approx. 10 hours after mating
Or by being mounted by another female PSEUDOPREGNANCY
Lasts for 16-18 days
Territorial, nest building
Condition self-limiting
Pregnancy toxaemia-
Susceptible during late gestation
Predisposing factors = obesity, stress, reduced appetite
Depression, weakness, collapse, abortion, seizures and death
Diagnostics: history, clinical signs, acidic urine, ketonuria, proteinuria
Uterine disorders
Pyometra
Purulent vaginal discharge
Lethargy
Inappetent
Enlarged uterus palpable, ultrasonography, cytology, haematology, serum biochemistry
Mucometra
Build up of mucus within uterine lumen
Hydrometra
Build up of transudate fluid in the uterus
Weight gain, but decline in body condition, anorexia, respiratory compromise, abdominal enlargement
Clinical signs, ultrasonography
Neoplasia-
Uterine adenocarcinoma-
Most common tumour in female entire rabbits
Serosanguinous vaginal discharge or haematuria
Nonspecific signs -> anorexia, depression
Dyspnoea if pulmonary metastasis
Diagnosis -> palpation, radiography (chest as well), ultrasonography, histopathology
Often multicentric and involve both horns of the uterus
Metastasis via local spread into the peritoneum and other abdominal organs -> liver
Metastasis via haematogenous route lungs, brain, skin or bones
Cystic mammary glands may be seen in association with this
pregnancy landmarks of rabbits
Gestation = 30-32 days
Often can gently palpate olive-sized masses from day 10
Fetuses can be seen on ultrasound from day 12
Fetuses difficult to feel abdominally from day 14
Parturition often day 30-32 – usually in the morning and quick
Fetuses will not survive after day 35
mamary gland disease in rabbits
Mammary masses
Progression from cystic mastitis
Development of irregular sized, fluctuant, subcutaneous nodules
Discharge – milk or amber fluid
Clinical signs, FNA and cytology
Mastitis
Lactating or pseudopregnant does
Common isolates
Staphylococcus aureus
Pasteurella spp.
Streptococcus spp.
Hot, swollen, firm, painful glands
Pyrexia
Depression
Clinical signs, culture and sensitivity.
male rabbit repro issues
Testicular tumour-
Seminomas, interstitial cell tumours, Sertoli cell tumours, lymphoma
Non-painful, firm, nodular testicular enlargement
Cryptorchidism-
Normally descend by 12 weeks
Scrotal sac does not develop on the side of the cryptorchid testicle
Orchitis and epididymitis
Bacteria Pasteurella multocida
Viral Myxomatosis
Trauma- Bite wounds, testicular evisceration and secondary infection
Swollen testes/scrotum, depression, anorexia
Venereal spirochetosis-
Treponema paraluis cuniculi
Redness, oedema, vesicles, ulcers, scabs around perineum and genitalia (+ face)
Clinical signs, microscopic visualisation, silver stains on biopsy, serological testing
repro disease in ferrets
Hyperoestrogenism (prolonged oestrus in entire female ferret)
Pseudopregnancy
Uterine disease
Pyometra, mucometra and hydrometra
Neoplasia
Mastitis
Prostatic disease
Adrenal disease (surgically neutered ferrets)
Oestrus cycle - ferrets
Seasonally polyoestrus.
Jills remain in oestrus until they are mated, or chemically brought out of oestrus, or the day length shortens.
Pro-oestrus indicated by increase in vulva swelling. Oestrus follows – will see large, swollen vulva & behavioural changes.
Prolonged oestrus = increases risk of persistent hyperoestrogenism development of pancytopenia due to bone marrow suppression.
Induced/reflex ovulators
Mating a rough process
Gestation 42 days
Litter size 6-8
Persistent oestrus ->pancytopenia
Subcutaneous and mucosal petechiae
Ecchymoses
Swollen vulva
Pale mucous membranes
Abdominal distension
Blood from cephalic vein
Poor prognosis
pseudo pregnancy in jills
Susceptible to pseudopregnancy ->implantation failure due to effects of photoperiod or lack of conception.
Associated with HCG injection or mated with a vasectomised hob
CS – weight gain, mammary enlargement & nesting behaviour.
Pseudopregnant jills may develop a fuller hair coat.
After the ‘whelping’ date jill will cycle back to normal
adrenal disese in ferrrets
Correlation with surgical neutering
Increase in concentrations of gonadotrophins loss of negative feedback stimulation of adrenal cortex adrenocortical hyperplasia and tumour formation
CS symmetrical alopecia, ‘rat tail’, pruritis
Vulva swelling
Recurrence of sexual behaviour
Urinary incontinence prostatic enlargement
repro considerations in gerbils
High incidence of ovarian disease
Ovarian cysts
Neoplasia
Clinical signs: abdominal distension, bilateral alopecia, weight loss, decrease appetite, respiratory effort.
Diagnosis: clinical signs, imaging
repro considerations in hamsers
Pyometra (hamsters & gerbils)
Care not to misinterpret in hamsters
Diagnosis: clinical signs, ultrasonography, cytology.
repro considerations in rats and mice
Neoplasia (mammary tumours)
Rats - subcutaneous fibroadenoma
Oestrogen and prolactin are thought to playa role in tumour development.
? Early neutering as a preventative measure
repro consideration in guinea pigs
Reproductive disease common
Cystic ovaries
Dystocia
Pregnancy toxaemia
Neoplasia
Cystic ovaries
Abdominal distension, lethargy, depression, bilateral alopecia in the area of the flank.
Cysts often contain clear fluid
May see subsequent uterine pathology
Diagnosis Ultrasound
Dystocia
Fusion of the pubic symphysis in older sows that have not given birth predisposes to dystocia
Normal parturition is quick (within 30 minutes)
Gestation 59-72 days (average = 65 days)
Clinical signs: unproductive contractions, straining, bloody-green/brown vulvar discharge
Pregnancy toxaemia
Last 2 weeks of gestation or the week following birth.
Acute onset lethargy, anorexia, dyspnoea, decreased urine production, acetone breath.
Hypoglycaemia, ketonemic, proteinuric and aciduric
How common is infertility in bulls?
Complete infertility
~ 5-10%
Sub fertility
20%+
Fully fertile mature bull running with 50 cycling healthy cows should..
60% in calf in 3 weeks
<10% empty after 9 weeks
Bull Breeding Soundness Evaluation
Physical exam- BCS, Heart &lungs, Eyes, Jaw, Lameness, Conformation, Abnormalities, External genitalia, Scrotal circumference
Semen analysis
Libido/service assessment
Infectious disease?
how is sperm assesed
Gross motility-
Grade 1-5
Beware dilution effect
Progressive motility-
% actively swimming forward
Beware temperature
New technology-
Dynescan
Slide preparation-
Eosin nigrosin stain
Smear
Microscope x 100
Wet prep-
Formal saline
Bioxcell
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
Obstruction in cow partuition
‘Normal’-
Undilated cervix
Abnormal-
Undilated cervix
Uterine torsion
Pelvic abnormalities
Fresh cow check
Health check- Temp, smell, 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?
Post Natal Check for cattle
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
>21dim
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’.
outcomes of a cow not seen bulling
90% - did
10%- 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!
Pregnancy Diagnosis in cattle - Techniques
Transrectal ultrasonography: >28 days
Manual palpation: >~35 days
Later gestation – fremitus, cotyledon bouncing
PAG testing – 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
Conception Rate
Proportion of served animals Pregnant at PD
Not a true measure of fertilisation rate
(EED/LED)
AYR target >40%
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%
Fertility visit structure on a block calving farm
Clean checks
PSM -21d
PSM -7d
PSM +7d
PSM +21d
PDs
Different strategies
PSM= planned start of mating
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
aims of calving with heifers
Aim to calve in well-grown heifers by 24 months
Which means they need to be I/C at 15 months
Heat detection
Synchronisation
Age at first calving KPIs…
Av vs %?
Better measures?
% 2nd lact?
Why would nutrients not be getting to the tissues?
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
Protein losing nephropathy
Increased Requirement-
Increased demand/Consumption
Bacterial infections
Chronic Viral infection
Neoplasia
Abdominal Ultrasonography 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)
Gastroscopy In context of weight loss, can give information on;
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
Abdominocentesis
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) in horses
Simple and inexpensive test to assess absorptive capacity of small intestine
horse is fasted for 12 hours
baseline oxalate-fluoride blood sample are taken
1g/kg 20% warm glucose solution is given by stomach tube. bloods are taken every 4-5 hours or until return to base line
samples are analysed for glucose and the percentage abouve the baseline is calculated
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
exotic Reproductive conditions – follicular stasis
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
Blood work – raised calcium, raised proteins
Ultrasonography
Advanced imaging
CT – follicles and shelled eggs- Follicle, helled egg
Ultrasonography - follicles
Treatment - medical-
Fluids
Nutritional support
Correct husbandry
Often surgical hormonal implants ineffective for these cases
COELIOTOMY
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
plastronotomy site between heart and plastron hinge
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 in reptiles
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
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-
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)
chelonians- Hydrate the tortoise soak in warm shallow bath
Prepare suitable nest site
Calcium gluconate if appropriate
Oxytocin
SURGERY
Cloacal ovocentesis
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
dystocia in 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
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
breeding Soundness Exam for stallions
■ History
■ General physical evaluation-
Vision, cardiopulmonary, locomotor
Potential genetic/hereditary (e.g: parrot
mouth, cataract, chriptorchidism)
Blindness
lameness
Ataxia
Penis, prepuce
Penile paralisis
Scrotum and testes
Internal genitalia (manual palpation and
ultrasound)
■ Semen collection and evaluation ( 2
collections 1 h apart)
■ Libido and mating behavior
■ Examination of internal and external genitalia
■ culture of urethra/penile/fossa glandis
■ Ancillary procedures
■ Serology, virology, endocrinology, endoscopy,
genetics/karyotype
Estimation of Daily Sperm Output (DSO)
■ DSO is linearly related to
testis mass:
■ Mass can be estimated
by measuring testis
volume:
■ TV=0.52heightwidth
length
■ DSO=(0.024TV)-0.76
(billions)
Semen Evaluation methods
■ Odour
■ Volume
■ Color
■ Sperm concentration (100-400 million/ml)
■ Total number of sperm
■ Sperm motility
■ Semen pH (optional)
■ Sperm morphology
■ Cytology - other cell types
■ Bacteriology / virology
■ Flow cytometry/fluorescence(advanced)
Sperm Motility
■ Subjective estimate:
■ Temperature
■ Dilution
■ Total motility
■ Progressive motility
■ Computerized motility analysis
Sperm Morphology
■ Classification systems:
■ Primary vs secondary
■ Major vs minor
■ compensable vs
noncompensable
■ Methods:
■ Stains (eosin-nigrosin)
■ FORMOL-saline wet
mount preparations
■ 1000x magnification
Oligospermia/azoospermia
■ Obstructive disease
■ Alkaline phosphatase
■ Testicular degeneration (Idiopatic or after
insult)
■ Testicular hypoplasia
■ Overuse
Diseases Of Scrotum, Testis And Epididymis in stallions
■ Hydrocoele/
haematocele
■ Inguinal hernia
■ Orchitis/epididymitis:
■ Trauma
■ Infectious
Thermal Injury To The Testis
Thermoregulation:
■ pampiniform plexus
■ cremaster muscle
■ scrotum
■ Spermatocytes appear most vulnerable to
thermal injury
■ Acute thermal injury may require 60 days
(duration of spermatogenesis) for recovery
Diseases Of The Accessory Glands
■ Vesicular adenitis (seminal vesiculitis):
■ Bulls
■ stallions
■ Prostatitis:
■ Dogs
■ Prostatic hyperplasia / neoplasia
■ Congenital defects (rare)
Lesions Of Penis And Prepuce
Trauma
■ common problem
■ paraphimosis
■ phimosis
■ rupture of corpus cavernosum
■ denervation
■ Congenital
■ Infectious
viral GI disease in cattle
- Rotavirus
- Coronavirus
- Bovine Viral Diarrhoea
bacterial GI disease in cattle
E.coli
* Salmonella species
* Clostridia species
* Mycobacterium paratuberculosis (Johne’s)
Parasitic GI disease in cattle
- Protozoal-
- Cryptosporidium
- Cocci
- Worms-
- Strongyles
- Fluke
nutritional GI disease in cattle
- Milk scours
- Peri-weaning Scours
- SARA
- Grain overload
- Dietary changes
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
Faecal Worm Egg Counts
* 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 cattle
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 result
bulk Milk Surveillance
- 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
Windsucker Test
Part the vulvar lips and
listen for an in-rush of air
* Tests the integrity of the
vaginal vestibular sphincter in mares
Caslick’s ind
a x l
where a= the angle of declination of the mares external genitles compared to the anus
l= the effective leanth of the vulva
tests the nesesity of a caslick procedure
Caslick’s procedure
Vulvoplasty in mares
what can be felt on rectal palpation of the mare
Uterus:
– Size & symmetry (pregnancy,
pyometra)
– Tone (estrus, diestrus,
pregnancy)
– Contents (fluid, fetus)
– Other abnormalities (masses,
adhesions)
Ovaries
– Size & position
– Shape (ovulation fossa)
– Consistency
– Follicular activity
– CL not palpable
* Cervix:
– Length
– Tone (Estrus, Diestrus,
Pregnancy)
– Abnormalities (difficult to feel
rectally)
visual exam of the mare repro tract
peculum exam
■ Vaginoscopy
Allows to evaluate:
A. Changes in cervix during estrus
cycle
ESTRUS
■ Secretions ↑ (moist)
■ Vascularity ↑ (pink)
■ Relaxation ↑ (open)
B. Abnormalities
■ Anatomical
■ Accumulation material (urine, pus,
blood)
■ Inflammation (vaginitis, cervicitis)
■ Varicosities
■ Tears/Lacerations (cervix, vagina)
■ Adhesions
surgical Reproduction management of female mammles
‘Spay’ – removal of the ovaries and uterus.
Ovariectomy
Hysterectomy (total vs supracervical/subtotal)
Ovariohysterectomy
Ovariohystero-partial vaginectomy - rabbits
surgical Reproduction management of
male mammels
‘Castrate’ – removal of the testicles:
Scrotal-
Open
Closed
Prescrotal-
Open
Closed
Abdominal approach
Vasectomy
Vas deferens ligated and incised
medicla Reproduction management of mammels– male & female.
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
reproductive managemnt of ferrets
Reproductive management of ferrets
Unique ->females must be taken out of season
If surgically neutered -> may predispose to adrenal disease
Pineal gland
A small conical endocrine gland
Attached by stalk to the dorsal wall of the third ventricle of the cerebrum
Major source of melatonin biosynthesis
Melatonin
Hormone synthesised and released during hours of darkness
Responsible for function of body related to photoperiod
Melatonin produced during dark phase of the day -> as longer days this suppression is lost-> get pulsatile release of GnRH Stimulates production of LH and FSH-> Stimulates the gonads to produce either oestradiol or testosterone.
Negative feedback on hypothalmus to prevent excessive secretion
What happens when we neuter them?
Loss of negative feedback-> Increase in the release of LH and FSH-> Persistently stimulate respective receptors in the adrenal cortex
Hobs usually reach puberty at approximately 9 months old
Jills reach sexual maturity in the first Spring after birth, at approximately 9 months old
Occasionally jills will show signs of oestrus in the first AUTUMN if
females were born early in the season
weather conditions are suitable
photoperiod is suitable.
Persistent oestrus pancytopenia
Subcutaneous and mucosal petechiae
Ecchymoses
Swollen vulva
Pale mucous membranes
Abdominal distension
Natural mating (vasectomised 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
Delvosteron injection (jill jab)- 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)- (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.
reproductive managment of female rabbits
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
Techniques
Ventral midline abdominal approach
Ligate ovarian pedicles and ligate around the uterine side of the cervices
Disadvantage
Leaves a small amount of residual uterine tissue
Advantages
Prevents the risk of urine leakage
Minimises the risk of infection from the vagina entering the abdomen cervices are a natural barrier
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 male rabbits
Medical reproductive management in rabbits is not used
Testicles descend into scrotal sacs at 10-12 weeks
Remember open inguinal ring
Options for castration
Scrotal
Open
Closed
Pre-scrotal
Open
Closed
Abdominal Indicated for true cryptorchids
reproductive managment of female rodents
Reproductive management of rodents often requires surgery
Approach for the female
Traditional ventral midline
Flank
Flank approach – advantages
Less invasive
Quicker recovery time
Less risk of infection
Less risk of suture disruption and complications
Less risk of evisceration secondary to dehiscence of wound
Achieved via a bilateral or unilateral flank incision
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.
spaying in guinepigs
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.
reproductive managment of male rodents
Options for castration
Scrotal - true aseptic surgical preparation difficult
Open
Closed
Prescrotal - improved aseptic surgical preparation: requires 2 separate incisions
Open
Closed
Abdominal approach
Considered fertile for up to 8 weeks following castration
defences agianst mastitis
Defenses:
The Teat (Streak) Canal
Keratinocytes
Lipid secretions
Sphincter muscle
Phagocytes (somatic cells)
Frequent milking
Antibodies
Lactoferrin
clinical signs of mastitis in the individual cow
Abnormal milk and/or udder
Secretion
Size
Texture
Agalactia
Blind or non-functional glands
Hungry neonate
Pain – altered gait
Enlargement of the supramammary lymph nodes
Teat and skin lesions
California Milk Test
detects SUB-CLINICAL disease
thickening in the fluid indicates mastitis- degree of thickening is concurent with cell count
grades of mastitis
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
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
gi disorders in cows
Upper GI tract issues/Choke
“Hardware” disease
Acidosis
Ketosis
GI tract displacements/torsions-
Left displaced abomasum
Right displaced abomasum +/- volvulus
Caecal torsion
Small intestinal torsion
Enteritis
Energy requirements dairy cow
Maintenance
Pregnancy
Milk production
Activity
Condition gain
Fog fever
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
an allergic reaction to the inhalation of fungal spores usually from mouldy silage
club foot
in horses
conformation issue with hoof
Broken forward hoof pastern axis
change in digital cushion composure
risk factors-
Common digital extensor tendon injury
Navicular syndrome
Pedaloestitis
Medio lateral imbalance of a horse
risk factors-
Collateral ligament injury
Articular cartilage damage
Degenerative joint disease
Sidebone
Corns
Sheared heels
Interference injury
Heel bruising/possible navicular syndrome
Margination
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)
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)
appearance of the liver on radiograph
Roughly triangular in shape with smooth distinct margins
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)
Ventral lobe-
Fairly sharp angle- softer angle can idicate Hepatomegal
Extends to slightly beyond the level of the costal arch
May see gall bladder ventrally in cat
Hepatomegaly on a radiograph
Projection of caudoventral margin well beyond the costal arch
Rounding of caudoventral angle
Caudal displacement of stomach axis
meaning of a small liver on a radiograph
Cranial displacement of stomach
Absence of caudoventral angle
Significance dependent on clinical signs, etc.
Deep-chested dogs
spleen apearence on 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
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
Fundus and body lie to left of midline
Pylorus to the right and ventrally
Distribution of gas and fluid depends on the position
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
colon and rectum on radiograph
Often easy to identify because they are filled with faeces
However poor preparation limits interpretation
Colic
Clinical syndrome associated with abdominal pain
Predominantly associated with GIT
May involve a number of body systems
Spontaneous recovery 28.7 %
Medical recovery 63.1 %
Surgical Recovery 2.0 %
Smooth muscle spasm
Inflammation-
Colitis / Ulceration
Distension-
Impaction
Gas accumulation
Obstruction-
Impaction
Tension on the mesentery-
Displacement
Tissue congestion/infarction/necrosis-
Torsion/volvulus
Strangulation
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
> 50% cases return non-specific diagnoses
Making a diagnosis is not as important as making an accurate assessment of the severity of the condition
Assess severity and duration
When was the horse last seen ‘normal’
Acute or chronic onset?
What signs are being displayed?
– persistent, intermittent, progressive?
Food and water intake since colic started
Faecal output
Has any treatment been administered?
Previous history of colic
Identify risk factors
Current management and any Recent Changes
Feeding
Stabling
Pasture access
Changes in exercise
Dental history
Parasite control programme
Vices
‘Differential Diagnoses’ for 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
Other
Non-abdominal, pain mistaken for colic
Oesophageal obstruction
Rhabdomyolosis (tying-up)
Laminitis
Pleuroneumonia
factors that can be assesed or the prognosis of colic
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
assessment of cardiovascular status-
a strong pulse, heart rate of 32-46, rapid jugular refil, pink mm and <2 sec capillary refil time is normal
higher heart rate, weaker pulse, slower jugular refil, darker mm and longer crt is indicative of edotoxemia from colic
Moisture content of oral MM is an assessment of hydration status;
Moist – Normal
Tacky or Dry - Dehydration
Compromised CV status is an important indicator for referral;
Deteriorating CV status is associated with poorer prognosis
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
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
2-agonist
Xylazine (Rompun, Virbaxyl),
Detomidine (Domosedan),
Romifidine (Sedivet)
opioid
Butorphanol (Torbugesic )
Try to assess CV status before giving 2-agonist
Nasogastric Intubation
diagnostic for colic
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
what is palpable on a trans resctal examination of a horse
ventral band of cecum
great vessels
caudal pole of left kidney
caudodorsal aspect of spleen
nephrosplenic space +/- ligamnet
fecal balls in small colom
uterus and ovaries
ingunal rings
bladder when full
Abnormalities: - Impaction
- Distension (Gas accumulation)
- Displacement
- Masses
structures palpable when abnomal-
deuodenum
jejunum
illeum
mesenteric root
Abdominocentesis
diagnostic in colic
Assess for presence of changes in peritoneal fluid
Not indicated in every case
Serosal compromise – leakage of blood components- Serosanguineous colour change
Increased protein concentration
Anaerobic tissue metabolism -Increased Lactate concentration
Rupture of GIT tract- Presence of ingesta
Peritonitis
analgesia for colic
Imperative to provide some form of analgesia to a colic case
NSAIDs
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
when should colic cases be refered
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
Periodontal disease
Periodontal disease is the most common disease in small animal medicine
> 87% of dogs and 70% of cats >3yrs.
May be obvious on clin exam Radiographs to see true extent
See number of teeth involved and extent of involvement
Can then determine treatment options or use to monitor progression
Dental disease
Clinical Signs of periodontal disease
gingivitis, plaque and calculus build up, gingival recession, bone loss, mobile teeth and eventually tooth loss.
Plaque: When bacteria collects within a matrix of salivary glycoproteins and extracellular polysaccharides and adheres to tooth surface
Calculus = tartar - when the plaque mineralises.
The bacteria and their by-products plus immune system = inflammation, infection and destruction of tissues
Plaque forms
Leads to gingivitis
Proliferation of plaque and deepening of the sulcus
biofilm accumulates reduction in oxygen transition from aerobic to anaerobic toxins produced immune response tissue destruction and breaches junctional epithelium deepening the gingival sulcus
Further attachment loss
plaque mineralises, calculus forms prevents healing and allows plaque to further colonise the tooth surface.
Tooth loss
the junctional epithelium separates, the tissues move away from the tooth surface, alveolar bones resorbs which causes the tooth to become mobile and eventually is lost.
Mesial
toward the front midline of the maxilla or mandible
Coronal
toward the tip of the crown of the tooth
Periodontal probe
Blunt-ended, graduated instrument used to:
Measure attachment loss
Assess gingival inflammation through probing
Evaluate furcation lesions
Measure tooth mobility
Check for subgingival calculus/pathology
Dental explorer
Sharp-ended instrument designed to give tactile sensitivity on hard tissue and is used to:
Detect softened enamel
Explore other defects, such as fracture sites and tooth resorption
Check the margins of restorations and crowns
Check for pulp exposure in GA patients
Gingivitis index
Stage 0 – no gingivitis
Stage 1 – Mild – slight change in colour, no bleeding on probing
Stage 2 – Moderate – Redness and oedema, bleeding on probing
Stage 3 – Severe inflammation – ulceration, prone to spontaneous bleeding.
Periodontal Grading Index
Stage 0 – Healthy periodontum, pink in colour, firmly attached.
Stage 1 – Gingivitis only due to calculus deposition, reversible by brushing/S+P, no attachment loss.
Stage 2 – upto 25% detachment loss, sulcus deepened
Stage 3 – 25-50% attachment loss,
Stage 4 – Over 50% attachment loss, disease has progressed, may see horizontal bone loss, severe inflammation
> 0.5mm in cats, >3mm in dogs = significant
Furcation Index
“furcation” anatomical area where roots divide on multi-rooted teeth
Exposure = Indicator of severity of periodontitis
0 = no bone loss
1 = less than 1/3 bone of the width of the tooth lost
2 = more then 1/3 but not total
3 = open furcation
Mobility Index
Loss of normal support around a tooth
0 – no mobility (<0.2mm)
1 = <1mm horizontal movement of the tooth
2 = >1mm horizontal movement of the tooth
3 = any vertical mobility
Bisecting angle technique radiograph
Creating a shadow and capturing it
Identification of axes
Film “flat” or as perpendicular as it can be to tooth root
Measure angle between them
Cut the angle in half
Beam bisects this angle
Too steep = short/compressed image = miss pathology
Too shallow = elongated = exaggerate “normal”
dental radiograph techniques
- Parallel technique
- Bisecting angle technique
- Extra-oral
Parallel dental radiograph technique
Film parallel to target with a perpendicular beam
Simplest
Same as conventional radiography
Use for caudal mandibular teeth
- Extra-oral dental radiograph techniquw
Cats
Caudally maxillary teeth
Superimposition of the zygomatic arch
Gives a skyline view of maxillary arcade
Chevron sign
e widened periodontal ligament spaces in the apical areas of endodontically sound teeth, often in the shape of a chevron, resembling radiographic signs of apical periodontitis (Figure 14). This occurs most frequently at the maxillary incisors, canines, and mandibular first molar teeth.
Vertical bone loss
Vertical bone loss was defined as the resorption of inter-dental marginal bone of at least 2 mm with typical angulation toward either the mesial or distal aspect of the root on intraoral radiographs.
Horizontal bone loss
manifests as a somewhat even degree of bone resorption so that the height of the bone in relation to the teeth has been uniformly decreased, as indicated in the radiograph to the rig defects occur adjacent to a tooth and usually in the form of a triangular area of missing bone,
Type 1 resorption
commonly begin resorption on the coronal third of the root, but can begin further apically. As resorption progresses, the coronal dentin often becomes involved. Eventually, dentinal loss undermines the enamel, causing it to fracture and resulting in a defect in the tooth.
Type 2 resorption
radiographically the root appears to be disintegrating and not easily discernible from bone. This is referred to as replacement resorption.
trauma in the tooth
Uncomplicated crown fractures = dentin exposure but not pulp
Complicated crown fractures = pulp exposure
indications for toothe extraction
Periodontitis
Pulp Necrosis
Dental Fractures
Tooth Resorption
Cavities
Chronic Gingivostomatitis
Persistent Deciduous Teeth
Malocclusion
Supernumerary Teeth
Unerupted Teeth
Teeth Associated with pathologic lesions
Failed Endodontic Treatment
Open extractions:
Require elevation of a mucoperiosteal flap and bone removal. Often with multi-rooted teeth, sectioning of the tooth into single-rooted sections.
Closed Extractions:
Require neither but do require incision into gingival attachment and breakdown of periodontal ligament. Most commonly used in single root teeth.
Diarrhoea:
altered pattern in normal pattern of defaecation
Increased:
faecal volume
water content
frequency of defaecation
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
when electrolyte absorbtion is impared and the intestine does not complete absorption of electrolytes and water from luminal contents
Increased gut mucosal permeability
leading to diarrhoea
guts let more than water and nutrients through — they “leak”
abnormal gut motility leading to diarrhoea
abnormal muscle and nerve contractions that cause spasms or lack of motion anywhere along your gastrointestinal (GI) tract. Your esophagus, stomach, small and large intestine, as well as your colon and rectum may be unable to perform their functions in the digestive process leading to abnormal stools
Acute Diarrhoea:
3 weeks
Change in diet
Diet history – raw feeding?
Scavenger? Table food?
Vaccination history (think age!)
Deworming history
In contact animals
humans with signs
How long its been going on for?
Character of D+ - etiology – SI, LI, mixed
Concurrent signs e.g. Weight loss, vomiting
Physical exam:
Dehydration?
Cardiovascular status?
Rectal temperature normal?
Oral exam
Abdominal palpation
Rectal exam
Minimum database:
PCV/TP -> dehydrated
SI Diarrhoea
normal to large volume
watery
Melaena- black stools that occur as a result of gastrointestinal bleeding. This bleeding typically originates from the upper gastrointestinal (GI) tract
borborygmi- a rumbling or gurgling noise made by the movement of fluid and gas in the intestines.
weight loss +/- vomiting
inappetance
*SI can still be urgent
LI Diarrhoea
Urgency/increased frequency
straining/tenesmus
haematochezia
small volume passed more often
mucus
fresh blood
“incontinence”
parasitic causes of dihorea
Essential to rule out
Shedding not continuous
Protozoa e.g. Giardia spp. – 3-5 day stool sample
ELISA
Helminth GI
Toxocara
Trichuris
Uncinaria
Faecal flotation
OR..
Fenbendazole 5-day course
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
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 samples?
Chronic Diarrhoea
in a well patient-
Dietary sensitivity/Adverse food reaction
Immunological reaction
Diet trials
Elimination trial
novel protein – a good diet history!!
Hypoallergenic
hydrolysed protein
Dietary challenge to elicit recurrence
LI fibre
Any change in diet should be progressive
Owner compliance is essential
in an unwell patient-
Blood work-
Biochemistry- Panhypoproteinaemia (low albumin and globulin) PLE
Haematology- Mild non-regenerative anaemia
Urinalysis check for protein
Basal cortisol
Vit B12
TLI
PLI
Trypsin-like immunoreactivity -
Exocrine Pancreatic Insufficiency
Clinical signs:
Steatorrhea
Dramatic polyphagia
Weight loss
Indicated if:
All of above fails
Hypoproteinaemic
Significant weight loss
Neoplasia suspected
Endoscopy
Upper GI only
Ex-lap
Further work up..
Immunosuppressive trials
Antibiotic trials
Faecal transplants..
in cats-
A bit trickier!
Chronic>acute
Tritrichomonas – PCR
Hyperthyroid – run a T4
Primary complaint might just be weight loss
Vomiting
Active expulsion of gastric/duodenal contents
Protective function
A common clinical presentation
Do not assume vomiting = GI disease!
A disease of many body systems
Can range from inconsequential to life-threatening
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
What causes vomiting via the peripheral nervoud system?
Abdominal visceral receptors, Dz/irritation of: GIT, biliary system, peritoneum, urogenital system
->Vomiting Centre (medulla oblongata)
What causes vomiting via the central nervous system?
Cerebral cortex, cerebral dz, pain, anxiety, fear,
->
Vomiting Centre (medulla oblongata)
What causes vomiting via the Vestibular system?
Motion
Ear Disease
Vestibular Disease
->
Vestibular system
->
CRTZ
4th ventricle
->
Vomiting Centre (medulla oblongata)
What causes vomiting via the primeraly CRTZ
4th ventricle?
Drugs, toxins, uraemia, keto-acids, infection
->
CRTZ
4th ventricle
->
Vomiting Centre (medulla oblongata)
dietary causes of vomiting
change of diet
spoiled food
food intolerance
food allergy
immune mediated
types I, III and IV
proteins (glycoproteins)
causes of vomiting in the stomach
inflammatory-
“gastritis” (acute or chronic)
ulceration
physical-
foreign body
outflow obstruction
functional-
motility disorder
neoplastic
intestinal causes of vomiting
inflammatory-
inflammatory bowel disease
physical-
foreign body
intussusception
Volvulus
Functional-
Ileus
neoplastic
abdominal causes of vomiting
pancreas (examples only!)- acute or chronic pancreatitis
peritonitis-
liver disease (examples only!)-
cholangiohepatitis
biliary obstruction +/- rupture
Renal disease-
AKI/CKD
Urinary tract obstruction
Uterine e.g. pyometra
Prostatic disease
metabolic causes of vomiting
Hyperthyroidism (cats only)
Uraemia
Hypoadrenocorticism
Diabetic ketoacidosis
central/cns causes of vomiting
Motion sickness
Vestibular disease
Encephalitis
tumours
bacterial causes of vomiting
Salmonella
Clostridium perfringens
E.coli
Campylobacter jejuni
viral causes of vomiting
Parvovirus
Feline panleukopenia
FELV/FIV/FIP
Distemper, Canine adenovirus
parasitic causes of vomiting
Worms-
Toxocara
Taenia
Trichuris
protoxoal causes of vomiting
Isospora
Cryptosporidium
Giardia
Tritrichomonas (cats)
toxic and drug causes of vomiting
Antibiotics
NSAIDs
cyclosporine
Ethylene glycol
Raisins or grapes (dogs)
Theobromine
Ivy, daffodils, lilies
Conkers, acorns
Adder bites, toads
Dysphagia
the medical term for swallowing difficulties
Clinical signs:
Gagging
Dropping food
Retching
Difficulty eating
Exaggerated swallowing
Ptyalism
Fear of eating
Anti-emetics
Maropitant-
selective NK1 receptor antagonist
effective against
peripheral pathways
central pathways
Visceral analgesia in cats
Metoclopramide-
dopamine, 5-HT3 & H1 receptor antagonist
central>peripheral pathway effects
variable prokinetic effect
cats & dogs
vomiting from a primary Gi problem should be uspected 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)
Primary GI disease diagnostics:
Survey and contrast radiographs
Abdominal ultrasonography
Endoscopy
Exploratory laparotomy
vomiting from a secondary Gi problem should be uspected if…
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
Megaoesophagus
recognize variations of normal (transient)
persistent abnormal dilation of the esophagus with gas or fluid
First line - plain lateral radiographs
+/- contrast radiography
+/- use fluoroscopy in cases of less severe or dynamic disease
Can be induced by anaesthesia/sedation/drugs
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
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-
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
The 90% rule of 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
hence easions most common on the hind lateral claws
Foot trimming – Dutch 5 Step
- Toe length
- Match
- Model
- Create height
- Investigate/trim loose horn
non infectious foot lesions
White Line Disease
Sole Ulcers
infectious foot lesions
Digital derematitis
Foul in the foot
White Line Disease
Degeneration of the horn at the white line leads to separation of the hoof wall from the underlying structures and weakening of the hoof wall
Risk factors:
Horn integrity
Surfaces
Stockmanship
Treatment:
Block other claw
Remove all loose horn
NSAID
Prevention-
Good cow surfaces
Good stockmanship
Appropriate nutrition
Sole Ulcers
Disruption to horn growth due to pressure on the corium underneath P3
Risk Factors:
Standing time
Surfaces
Foot trimming
Fat mobilisation
Inflammation
log term isseus cause bone spurs
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
Digital Dermatitis
Multifactorial
Strong bacterial component
Treponeme spp
Genetic susceptibility
Hoof hygiene!
treat active leasions (m2) topically and chronic inactive leasions with footbathing (m4)
Foul in the foot
an acute and highly infectious disease of cattle characterised by swelling of the foot and resulting in lameness.
Treatment-
Systemic antimicrobials
NSAID
Local treatments
Prevention-
Similar to DD
Minimise risk of interdigital trauma
claw horn disorders
white line leasion
soul ulcer
digital dermatitis
foul in the foot
Heel horn erosion- Prevention:
Hygiene and trimming of loose heel horn
Inderdigital hyperplasia
Toe lesions-
Thin soles!
Abrasion
Over-trimming
Fissures (hor,ver, axial)
Corkscrew claws-
Don’t tend to occur on well managed farms…
Medial corkscrew claws are a different phenomenon
Deep digital sepsis-Terminal presentation.
Hoof health assessments
Not all feet need trimming!
Examine all cows 2x/year (more if required)-
Pre-dry off
Early lactation
Ensure foot trimming to a high standard
Footbathing
3-4x/week
Not too strong/acidic (below pH3)
No more than 200 cows
Effective design required
Commonest ingredients – formalin, CuSO4
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 feet
early stage footrot – dermatitis and under-run horn visible
later stage, large amount under-run horn present
Very 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
identify risk periods and vaccinate before these (usually housing/lambing) or times of regular gathering.
Before high risk periods such as housing/lambing
This is where the vet comes in – doesn’t protetct against ay other form of lameness – if you are advising your clients to use it – be sure of the diagnosis!
H+S – make sure clients are aware of self injection risks – oil adjuvant in vaccine can cause unpleasant injection site reactions
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 in sheep
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
causes of lamness in sheep
foot rot
CODD
white line seperation
scauld/ ovine digital dermatitis
ORF
strawberry foot rot
bluetongue
Laminitis – all 4 feet, often after grain gorging or over-fat rams
Injuries – fractures etc
Neuro disease – spinal abscess
foot and mouth
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
Gait assessment of horses
Hard straight line
Flexion tests
Soft and hard lunge
Ridden sometimes required
Flexion tests?!
Thoughts?
Controversial amongst the equine population
Can induce lameness that may be unrelated to the baseline lameness
Responses must be interpreted carefully
How?
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
What nerve blocks do we have available in the foot?
Palmar digital
Abaxial sesamoid
Coffin joint
Navicular bursa
DFTS?
Palmar digital nerve block
What does it block?
Sole
Navicular apparatus
Soft tissues of the heel
Coffin joint
Distal portion of the DDFT
Distalsesamoideanligament
How?
25g 2/3in needle (25g if cobby!)
Needle separate from syringe
1.5ml mepivicaine
Proximal edge of the cartilage of the foot
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
2.5ml mepivicaine
Base of the proximal sesamoids
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
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
Omnipaque?
Digital flexor tendon sheath
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)
Tourniquet applied
20g 1-1.5inc needle
Needle must remain superficial to the DDFT
Nerve blocks limitations
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
Desensitisation of skin but not deeper structures.
Foot balance radiographs
Gross imbalance can induce lameness
Correct early on in a lameness investigation
Leave the shoes on
Lateromedial radiograph
How?
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) radiograph
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 radiograph
(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) radiograph
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?
MRI in equine medicine
Imaging method of choice in human medicine.
Every major hopsital is equipped with one
Used to diagnose everything from cancer to spinal and joint diseases.
In the equine veterinary world its being used to improve the accurary and efficacy of diagnostics for lameness investigations.
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!
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
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
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
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-
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
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
Orthopaedic examination
Aims:
Localise bone/joint pain
Assess muscle atrophy
Localise crepitus
Assess joint ROM
Examine for joint effusion/thickening
Assess joint stability
Signs of pain:
Turning to look
Attempting to move away
Withdrawal of affected limb
Attempting to bite
Cessation of panting
Lip-licking
Fidgeting
Dilated pupils
Vocalisation
Palpation: Muscles, bones, joints
Symmetry (both legs at same time)
muscle atrophy
thickening
joint effusion
heat
pain
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
lamness stemming from the distal limb
Both thoracic and pelvic limbs:
Paw pad!!
Corns in greyhounds
90% thoracic digital pads, digit III & IV
Be thorough
Examine individual digits, pads, interdigital webbing
Thickening of IP and MCP joints common in older dogs – may be incidental
Significance should be assessed by applying pressure and checking for pain response
lamness stemming from the elbow
Complex hinge joint
Common site of lameness in large breed dogs:
Elbow dysplasia
Effusion lateral epicondyle and olecranon
lamness stemming from the shoulder
Biceps Tendon test
Abduction test to assess medial instability under GA/sedation
lamness stemming from the pelvic limb
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
Stifle - CCL
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.
Stifle – 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 in small animals origination from the hips
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
Bone reacts to pathological processes in a limited number of ways
change in alignment
change in contour
increased or decreased bone mass.
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
Aggressive vs non-aggressive changes in bone
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:
Aggressive vs non-aggressive changes
continiuos (solid, lamellar, lammalated)- least agressive
interupted (thick brush like, thin brush like, sunburst, amorphous bone production) - most agressive
New bone production:
Artifact (superimposition)
New bone production secondary to injury
Bone loss or destruction- Aggressive vs non-aggressive changes
Patterns of bone lysis:
Artifact (superimposition)
Real due to generalised or focal bone loss
geographic lysis- least agressive
moth eaten lysis
permiative 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
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
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
Evaluation – 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 Incision
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
Approach to wound management - debriding
Remove 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
Primary contact layer for Bandaging Maturation
wounds
Non-adherent
PU Foam
Change every 4-7 days
