Horses 2 Flashcards
(101 cards)
1
Q
Ovarian haematoma size, what look like, treatment and cause
A
- Very large ovary (>15cm) ○ Differential for granulosa theca cell tumor - Wont luteinise - Might have to be removed surgically - Cause unknown
2
Q
Silent oestrus how to detect, possible causes, how to treat
A
- Teasing technique
○ Not observing well
○ Foals at foot -> not showing oestrus
○ Dominant or submissive - may never or always look like in heat - Synchronize cycle (PGF2alpha) and tease every second day
- AI (if possible)
3
Q
Persistence of the CL define, 3 causes and treatment
A
- Characterized by lifespan > 13-16days
- Can be caused in 3 ways:
1. Dioestral (mid-cycle) ovulation - day 10-11 from first follicular wave - not common
2. Chronic endometrial disease (loss of functional endometrium)
§ Pyometra, endometrium eroded so prostaglandin not being made
3. Early embryonic death: CL will persist until D70 - Treatment: PGF2alpha injection
4
Q
Retention of endometrial cups when should remove and how long persist, how to identify, diagnosis and treat
A
- Should only be around to day 100-120 until immune system removes
- Persist throughout pregnancy and beyond
- Therefore foal and then shows no signs of heat - no foal heat
- Diagnose: generally not via ultrasound alone, use an endoscope
○ Generally at the base of the horn - Treatment: have to cut them out -> Referral case
5
Q
Endometritis how common, when occur, and common bacterial causes
A
- Probably most common cause for infertility in the mare
- Most common: opportunistic bacteria take advantage of compromised immune defences but can be non-infectious
○ Post-partum breeding endometritis - Primary uterine pathogens possible
- Remember: bacteria are commonly introduced into mare’s uterus without causing disease
Commonly isolated pathogens - Streptococcus equi sp. zooepidemicus
- E. coli
3 below - primary causes - Pseudomonas aeruginosa
- Klebsiella pneumoniae
- Tayorella equigenitalis
Opportunistic -> treated for bacterial - Yeast
- Fungi
6
Q
Endometritis what are important anatomical defences and how does doiestrus change this
A
Defence mechanisms
- Phagocytosis by macrophages and neutrophils
- Cilial activity of endometrial cups
- Antibody binding
- Muscle contractions
- Barriers - cervix, vestibulo-vaginal sphincter, vulva
Dioestrus dangers
- Defences are physiologically compromised in dioestrus
○ Decreased immune functions
○ Closed cervix prevents drainage
○ No flushing effect (that are present in oestrus)
○ Muscle contractions ↓
7
Q
Endometritis diagnosis
A
- Possible signs:
○ Breeding history with infertility
○ Anatomical defects - negative pressure should be present so suck air in after put in endoscope
○ Vaginal discharge (also check tail) - Cytology: rarely false results
- Culture: may yield false positive or false negative
- Swab should be taken in dioestrus
8
Q
Endometritis treatment
A
- Treat during oestrus when endogenous defences are high - can start end of dioestrus
- Aim at breeding during same oestrus
- Uterine flushes with or without antibiotics
○ Make sure intrauterine drugs do not cause irritation and/or fibrosis
§ Yeast -> give 0.5% iodine flush leads to irritation -> prostaglandin -> short cycle - Breed mares by minimal contamination technique (MCT)
9
Q
Cervical defects what is general history and how to detect
A
- Often “classic history”: barren since last foaling for unexplained reason (esp. if hx. Of dystocia)
Manual Exam to be done during dioestrus -> may have cervical tear
10
Q
What are the 3 main techniques for assessing stallions
A
- Physical examination of the reproductive organs
○ Tease stallion with a mare to get penis out - Observation of sexual behaviour and Mating ability
- Collection and examination of semen (field &Lab)
○ Tests for infectious disease
○ Tests for inherited disease
11
Q
Where to collect samples for serology, what testing for
A
- Culture sites = pre-and post-ejaculatory urethral swabs, semen, penis, prepuce, accessory gland fluid.
- Pseudomonas aeruginosa, Klebsiella pneumoniae, Tayorella equigenitalis(CEM), EHV-3(coital exanthema) lesions?
- Serology: EHV-3 (equine herpes virus) - cause ulcerations on penis
12
Q
Testicles how suspended and measured
A
- Testes are suspended in a horizontal plane
- Measured using scrotal calipers across their width (average 80-100mm) and length (80-140mm)
13
Q
Total scrotal width what used for and how
A
- Assuming testicular consistency is satisfactory, TSW can be used to estimate sperm production and output
○ Length is related to the amount of sperm produced
○ Sperm output = concentration of sperm x by the volume on the 5-7 days following serial ejaculations
§ Daily sperm output = different to the amount of sperm within 1 ejaculate within a day
WIDTH not always normal -> may be pathological why so large
14
Q
What is involved with examination of accessory sex glands
A
- Palpation/endoscopic ○ Pelvic urethra ○ Body of prostate -> prostate not as well involved in large animals ○ Seminal vesicles § Size, consistency ○ Lobulation and symmetry § Bulbo-urethral glands § Ampullae - diameter, consistency
15
Q
Sperm production how much produced per day and how long does it take so what is important about this and 2 ways to collect semen
A
- 5-6 billion spermatozoa per day
- Takes about 2 months to produce -> IF HAVE ISSUE WHAT 2 MONTHS TO REEXAMINE
1) artifical vagina - most common
2) dummy mare or surrogate mare
16
Q
How to prepare an artifical vagina for a stallion
A
- Temperature 42 to 48 degrees
- Pressure, lubrication
- Protection of sample from cold shock and sunlight
- Strict hygiene
17
Q
What evaluating with sperm characteristics and stain used
A
- Vol of the ejaculate (40-200 ml) x concentration = total sperm count. ( 500mill per dose)
- Sperm cell morphology
- pH of semen - 7.2-7.9
- Bacterial cultures, e.g. for Taylorella equigenitalis(contagious equine metritis; CEM), Pseudomonas, Klebsiella spp.
- Motility analysis (motility = % moving acitvely forward), chromosomal analysis, sperm chromatin assays, acrosome reactions etc.
Stain nigrosineosin stained smear - black sperm DEAD
18
Q
Semen extension for artifical insemination what are the 6 main functions
A
- Increases volume of the ejaculate
- Permits effective antibiotic treatment of semen containing pathogenic or potentially pathogenic organisms
- Prolongs survival of spermatozoa
- Protects spermatozoa from unfavourable environmental conditions
- Aids in proper evaluation of sperm motility
- Increases pregnancy rates due to more viable spermatozoa
19
Q
Squamous cell carcinoma characteristic, where commonly occur, treatment and prevention
A
Characteristics - Locally aggressive but rarely metastasise
Where else do these commonly occur
- Eye lids, Nose, Third eyelid, Genitalia - penis, prepuce
Areas without hair protecting the unpigmented skin
Treatment
1. Surgical resection - wide margins and checked with histopathology
2. Local chemotherapy, cryotherapy
If small lesion on the eye
- Removal of eyelid
Prevention
- Keep out of the sun
- Keep inside during day and outside at night to graze - ideal
- Sunscreen
- Light rug in summer
- Face mask
20
Q
Sarcoid what is it, characteristics and causes
A
Common tumour of horses
- Non-regressing and locally invasive
- Involve both the epidermis and dermis but will invade
Causes - association with bovine papilloma virus 1 and 2 (BPV-1,2)
- Always found in Sarcoids but also normal skin
21
Q
Sarcoid treatment and what if located around the eye
A
Goals - destroy all tumours cells and minimise damage to healthy tissue
- Immunstimulant creams - imiquimod, flurouracil
OWNERS SHOULD WEAR GLOVES
- Resection of the sarcoid
○ If don’t remove all cells will then come back so need histopathology to ensure adequate margins
- Leave it until active (starts to change)
EYE
- Hard to resect with good margins
- Don’t use caustic creams near the eye
22
Q
What are the 4 types of sarcoids and appearance
A
- Occult sarcoids, which are smooth, flat and usually hairless.
- Verrucous sarcoids, which have wart-like appearance.
- Fibroblastic or nodular sarcoids – these are sometimes referred to as two different types, with fibroblastic sarcoids usually being ulcerated and nodular sarcoids being lumps under otherwise normal-appearing skin. However, fibroblastic sarcoids are more likely a progression of the nodular form.
- Mixed sarcoids contain components of two or more of the above types. They most likely represent a transition between different types.
23
Q
Melanoma common locations and therefore main presenting problems
A
Common locations
- Ventral tail, anus, perineum, external genitalia, parotid region
What are the main problems
- Generally benign
- Physically obstructing ability to defecate
NOT GOING TO KILL THE HORSE
24
Q
Melanoma treatment 3 options
A
- Surgery resection? -> anal sphincter issues
- Palliative care - intralesional chemotherapy
- Cimetidine - unsure on how works but can help
25
Eosinophilic granulomas characteristics, cause and how to confrim diagnosis
```
Characteristics
- Non-tumour nodular skin disease
- Lumps - smooth nodules that are well-circumscribed, haired, firm and non-pruritic
Cause - unknown
Confirm with biopsy!
- Presence of eosinophils
```
26
Eosinophilic granulomas treatment
- Anti-inflammatories -> prednisolone
- Insect control
- If small amount could excise them
- Corticosteroids can inject into the lesions -> avoid systemic (hard if multiple lesions
27
viral papillomas cause, transmission, treatment and prevention
Cause
- Viral papilloma's that are species specific
Transmission
- Via direct contact
Treatment
- Nothing - spontaneously resolve
- If large - cryosurgery
No vaccines
Prevention
- Disinfection of track, brushes to minimise fomite transmission
Housing young horses individually rather than in large groups but may not be practical
28
Rain scald (dermatophilosis) clinical signs, cause and how transmitted
- Significant hair loss over face, dorsum, extending ventrally
- Crusting bald/ulcerative
- Housed outdoors, recent rainfall
- No scratching/itching but painful
Cause - Dermatophilus congolensis
Required for development
1. Moisture
2. Skin abrasions
3. A carrier animal
Transmission
- Flies, biting insects, fomites
29
Rain scald treatment and prevention
```
Treatment
1. Wash with benzamidine, chlorhexidine
2. Topical disinfectants
3. Get horse out of the rain
Prevention
- Collect ulcerations as act as carrier of the spores
Keep dry with adequate shelter
```
30
Dermatophytosis (ringworm) cause, transmission
cause - trichophyton and Microsporon - Warmth and humidity
Transmission
- Contact with other infected animals or infected hair shafts
- Younger animals more susceptible - immunity after exposure
31
Dermatophytosis (ringworm) treatment
- Probably go away by itself but if want resolved quickly
1. Malaseb - medicated wash
2. Imaverol - systemic antifungal? - only if immunosuppressive - NOT IN PREGNANT ANIMALS
Still takes time for hair to grow back
32
Pastern dermatitis predispoing factor and treatment
Predisposing factors
- Draft or feathered breeds
- Excess hair aids in keeping the area wet and prepetuation of bacterial growth
Also predisposed to chorioptic mange that can lead to dermatitis
Treatment
1. GET OUT OF THE MUD
2. Dry and clip the hooves
3. Topical disinfectants - dilute chlorhexidine scrub and topical ointments such as silversulfadiazine
4. Systemic antibiotics in severe cases -> procaine penicillin G
○ Should do culture and sensitivity if infection remains
33
Cutaneous habronemiosis what known as, cause and locations
Also known as "summer sores" due to increased occurrence during warm months
Cause
- Deposition of larvae Habronema microstoma/muscae or Draschia by flies (intermediate host) into wounds or moist skin sites rather than mouth (normally)
- Results in hypersensitivity reactions to dead and dying larvae
Locations
- Media canthus of the eye
- Third eyelids
- Distal limb
- Penis or prepuce
34
Cutaneous habronemiosis diagnosis, treatment and prevention
Diagnosis
Biopsy with histopathology usually revealing granulomatous inflammation
Treatment
- Ivermectin (moxidectin)
- Corticosteroids may be needed to control hypersensitivity reaction
Prevention
- Good fly control - with prompt removal and disposal of manure containing larvae and insect repellent application to affected and at-risk horses
35
Culicoides hypersensitivity "queensland itch" what results from, where located and age of onset in what climates
- Hypersensitivity reaction to midge saliva proteins
○ May be a hereditary predisposition for developing hypersensitivity (most likely type 3 - antibody/antigen mediated)
○ Nature of the hypersensitivity response to unknown
- Present mainly over the base of the mane, neck, dorsum and ventral midline
- Age of onset usually 2-4 years and more common in warm, tropical climates - where midges are
36
Culicoides hypersensitivity "queensland itch" problem list diagnosis
Problem list
- Pruritis - presenting complaint
- Crusty/ulcerated skin lesions
○ Dorsal distribution - head, neck, back, tail
- Tropical/subtropical geographical location
Diagnosis
- Clinical based on history, pruritis, typical distribution of lesions and geographical location
37
Culicoides hypersensitivity "queensland itch" what are the important treatment/prevention
Insect control
- Midges active at dawn and dusk
1. Spraying horses with insect repellents
2. Use of rugs and hoods to prevent contact with midges and the skin
3. Keeping horses indoors, especially during peak midge activity
4. Fans placed in barns -> prevent midges from entering?
38
Lice main problems and diagnosis
Main problems
- Pruritis - self-trauma is very common
- Patchy alopecia as damages the hair follicles
- Anaemia for chronic severe sucking lice infestations
Diagnosis
- Physical examination
- Presence of lice on the horse -> generally can find
- Type of lice via skin or hair scraping under microscope
39
Lice treatment what medications and how many applications
- Most only kill lice and NOT EGGS -> 2-3 treatment administered 2 weeks apart
○ In order to kill emerging nymphs and adults from pre-existing eggs
1. Ivermectin - administered systemically for SUCKING LICE ONLY
2. Topical insecticides may be used FOR NOTH TYPES - fipronil and pyrethroids spray
- Single application include imidacloprid (advantage)
○ Kill the larvae and adults
ALL in-contact horses should also be treated
40
Atopic skin disease what type, how develop, desposition and common allergens
- Allergic, pruritic skin disease -> type 1 hypersensitivity - IgE mediated
- Develop sensitising antibodies to certain allergens
- Breed disposition -> thoroughbred and Arabian horses
Owners - can try doing elimination trials however some cannot be eliminated -> environment
1. Parasites
2. Insects
3. Drugs - common NSAIDS, phenothiazines, sulfa drugs, ANY DRUG
4. Vaccines
5. Plants - environmental
Feed - not as common as small animals
41
Atopic skin disease problem list
- Severe pruritus -> due to antibodies cross-link mast cells, causing degranulation and release of inflammatory mediators
○ May not be present
- Mild patchy alopecia
- Seasonal
- Secondary pyoderma may develop
- Urticaria - "wheals" - transient focal swelling that result of dermal oedema arising from vasodilation
○ Found on the neck and cranial third of the body but may be diffuse over the body
○ Size variable from 1-10cm in diameter
○ Resolve if left untreated
42
Atopic skin disease diagnosis
- Often clinical
- But atopy isn't a diagnosis in itself
○ HISTORY IS VERY IMPORTANT - to determine trigger
○ Intradermal skin testing and serologic IgE assays -> can be positive without being the real issue
§ No anti-hisatmine or corticosteroids for a month before this test - hard to keep pruritis under-control in these situations
43
Atopic skin disease treatment describe the 5 options
1. Corticosteroids if severe (short term solution)
○ Possible association with laminitis
○ Cannot have in their system if eventing -> withholding period important
2. Elimination of allergen…
○ If drug or vaccine can prevent administration of those
3. Antihistamines?
○ Variably helpful to horses -> try it and see how respond
○ Hydroxizine
4. Environmental management
○ Turnout, insect control, rugging, etc.
○ Especially if seasonal -> keep inside and rugged in those times
5. Hyposensitisation
○ Success rate of 65-70%
○ A prolonged infection course is required (12months) and owners need to remain committed
○ May be required throughout life
44
Mites what are the 3 mites and where present and transmission
- Several species of mites affecting horses - chorioptes bovis (leg mange), psoroptes equi (body mange), sarcoptes scabiei (scabies or head mange)
transmission - Via direct contact or contact with fomites
45
Chorioptic mange (leg mange) lifecycle, location, when most common, problem list and diagnosis
○ Entire lifecycle on the host however can survive many weeks off the host
§ Can infest cattle and goats
○ Draft or feathered breeds are predisposed to developing
○ More common in winter
○ Problem list
§ Distal limb lesions
§ Crusting alopecia
§ Pruritis
○ Diagnosis
§ Skin scraping - generally don't burrow into skin
46
Psoroptic mange (body mange/ear mites) signifiance, problem list and diagnosis
○ Have been eradicated in some countries where it is a reportable disease
○ Problem list
§ Base of the mane, tail, ears and spread down the trunk
§ Pruritis - intensity varies
§ Ear infestations - headshake or rub their heads on posts
○ Diagnosis
§ Skin scraping - don't burrow deep into skin
§ Serological assay - not widely available
47
Sarcoptic mange (head mange) how common, problem list, diagnosis
○ Rare in horses
○ Problem list
§ Begin on the head and ears but spread to the rest of the body
§ Pruritis is intense
§ Rubbing of head and ear on solid objects
○ Diagnosis
§ Burrow deep into the skin -> difficult to diagnose on skin scraping
§ Biopsy - may be required
48
Mites treatment what are the 3 main steps and what NOT TO USE
1. Shave their legs -> clip the feathers
2. Ivermectin or moxidectin administered every 2 weeks for 2-3 treatments
○ Eggs will not be killed so need to do again (Same as lice)
○ Systemic Ivermectin and moxidectin may not eliminate all live mites - resistance possible
3. Topical treatment - fibronil (frontline spray -administered once weekly for 1 month), lime sulphur, malathion
- ALL in contact horses should be treated as well as DECONTAMINATION of fomites in the environment
- NOTE -> Amitraz - DO NT USE IN HORSES
○ May cause ileus in horses that may be IRREVERSIBLE
If in early stages -> alpha2 antagonists
49
Cutaneous onchocerciasis what cause and how cause, transmission
- Common filarial dermatitis caused by microfilariae of Onchocerca cervicalis - hypersensitivity reaction to dying microfilariae
- Adult worms live in the nuchal ligament and microfilariae migrate to the superficial dermis
Transmission - via Culicoides vector
50
Cutaneousonchocerciasis problem list
- Lesions normally on face, base of mane, proximal forelimb, ventral midline and pectoral region
- Pruritis - occasionally with Culicoides hypersensitivity
- Ocular and cutaneous lesions
○ Ocular - uveitis, conjunctivitis, keratitis, depigmentation
○ Skin - patchy alopecia, erythema and scaling
- Non-seasonal and affects older horses more commonly
51
Cutaneous onchocerciasis diagnosis and treatment
Diagnosis
- Biopsy - detect microfilariae - can be distributed unevenly so hard to find
○ Mincing skin biopsy in saline - allow to sit for 30mins and use microscope
- Based on clinical findings, history, response to treatment
Treatment
- Ivermectin (or moxidectin)
○ Minor adverse reactions (swelling of face, midline) may occur due to death of microfilariae
○ No effective adulticide so may recur after 2 months
○ Many horses remain without clinical signs for 6-12 months following treatment
52
List 8 essentials supplies for a equine eye examination
1. Schirmer tear test strips - use schering-plough strips with the dye indicator
2. Stains - fluorescein
3. Mydriatic - mydriacyl NOT atropine
4. Saline for flushing
5. Topical anaesthetic (alcaine)
6. Microscope slides
7. Sterile spatula - bottom end of a scalpel blade
8. Stains - diff-quick, gram, methylene blue
53
Eyelid laceration treatment
- DO NOT trim lid margin
○ Eyelid margins have a very important role - specialised tissue
- May need to delay surgery
- Cover eye/wound with pad covered in antibiotic cream
- Careful debridement if necessary, then suture
○ Use appropriate suture material 4/0-6/0 nylon
54
Penetrating foreign body within the eye treatment
- May need ocular U/S
- Surgery common - GA, exploration of any sinus tracts
- Antibiotics
- Anti-inflammatories
55
Corneal infection general signs, causes and treatment
General signs
1. Usually unilateral
2. Yellow-white in appearance
3. Severe uveitis/hypopyon
4. Miosis
5. very painful - NEED TO EXAMINE WITH SEDATION
NOT ALL CORNEAL ULCERS ARE INFECTED
Bacteria - pseudomonas, staphs, streps
Fungi - more common in horses (rare in dogs)
- Aspergillus , hyphae
Treatment
- Topical antibiotics/antifungals (if fungal still give antibiotics to prevent secondary infection)
○ Ofloxacin - gram negatives
○ Fortified cefazolin - gram positive
○ Voriconazole - BEST ANTIFUNGAL
- Consider compounded oral antifungals
- Serum topically
- Surgery - keratectomy/conjunctival graft
○ If antibiotics/antifungals doesn't work
Transpalpebral lavage tube - IMPORTANT
Pain control important - give Bute TWICE daily
56
Bullous keratopathy what is it, caused by and treatment
- When bullae formed on cornea due to endothelial dysfunction
Caused by
- Trauma
- Corneal infection
Treatment
- Cover cornea - temporary or third eyelid flap
- Keratectomy - debride devitalised cornea and conjunctival flap/graft
Appropriate topical antibiotic, anti-inflammatories and topical atropine
57
Acute uveitis primary and secondary causes and treatment
- Primary - equine recurrent uveitis
- Secondary - to other ocular diseases
Treatment
- Treat primary cause
- Timely anti-inflammatory therapy, corticosteroids, NSAIDS
- Atropine
Poor treatment = loss of vision
58
What are 8 chronic signs of uveitis
1. Phthisis bulbi (shrunken non-function eye)
2. Secondary cataracts from chronic uveitis
3. Posterior synechia
4. Retinal detachment
5. Hyperpigmented iris
6. Vitreous opacity
7. Lens luxation
8. Glaucoma
59
What are the 3 main causes of lameness and causes within
```
1) Load
○ Single
§ External mass - hit by a car
○ Multiple loads
§ Athlete
§ Conformation
2) Inflammation
○ Autoimmune
○ Sepsis
○ Infectious
3) Inadequate structural integrity
○ Developmental
○ Nutritional
○ Local pathology
```
60
What are the important components of a equine lameness examination
Horses important components
- Clinical examination
- Gait examination
- Nerve blocks
- Imaging
61
Most common cause of lameness in non-athletic, athletic and neonates and yearlings
```
○ Non – athletic
§ Feet
○ Athletic
§ Feet, fetlocks and carpi
○ Young growing
§ Neonates – septic joints
§ Yearlings – osteochondrosis, bone cysts
```
62
What are the following bones called P1,P2,P3, Metacarpal 3 and metacarpal 2 and 4
```
P1 = long pastern
P2 = short pastern
P3 = coffin bone
Metacarpal 3 = cannon bone
Metacarpal 2 and 4 = splint bones -> have what they call "buttons" on the end of the splint bones
```
63
What are the important joints in the horse limb
Tarsal joint = hock
P1-P2 = pastern joint (proximal interphalangeal joint)
P2-P3 = coffin joint (distal interphalangeal joint)
Metacarpal phalangeal joint = fetlock joint
Carpal joint = knee
64
How to determine between the hind and forelimbs
Forelimb - base of the hoof tends to be more circular -> 60% weight bearing -> circular is better equip to -> also carpal bones
Hindlimb - base of the hoof tends to be elongated -> 40% weight bearing -> also tarsal bones
65
What are the vessels and nerves in the forelimb
- Major arterial supply is via the medial palmar artery which is the continuation of the median artery - 4 branches below:
1) Medial and lateral palmar veins, arteries and nerves
○ Course distally between the interosseous and the flexor tendons
2) Medial and lateral palmar metacarpal veins, arteries and nerves
○ Course distally on the palmar surface of the third metacarpal bone deep to the interosseous ligament
Minor variations and anastomoses are common in this region
66
Annular ligaments of the limb what are the 3 ones
- Palmar annular ligament of the fetlock
- Proximal digital annular ligament
- Distal digital annular ligament
67
What are the 3 main tendon structures on the palmar surface of the limb
1) Deep digital flexor tendon
- Has an accessory ligament (distal check ligament) midway along the carpus
○ Only obvious in the forelimb
2) Superficial digital flexor tendon
- Has an accessory ligament (proximal check ligament) that originates from the distal radius
○ Only present in the forelimb
3) Interosseous ligament - made up of origin, body and branches
68
Interosseous ligament location and how spans the limb
- Lies against the palmar surface of the metacarpal bone III
- Originates from the palmar aspect of the carpus and proximal metacarpus (with the accessory ligament (check ligament) of the deep digital flexor)
- Bifurcates in the distal metacarpus before it inserts into the proximal sesamoids and branches extend over each other the lateral and medial aspects of the fetlock joint to merge with the extensor tendon on the dorsum of the digit
- Common name is the suspensory ligament -> it suspends the fetlock
69
What are the 3 main types of sesamoidean ligaments
1) proximal sesamoidean ligaments
2) middle sesamoidean ligament
3) distal sesamoidean ligaments
70
Proximal and middle sesamoidean ligaments what are they and where do they coarse
1) Proximal sesamoidean ligaments
- Metacarpal segment of the interosseous ligament
- 2 metacarposesamoidean ligaments which are slender, elastic, strands arising from the palmar aspect of the distal metacarpal bone
2) Middle sesamoidean ligaments
- Palmar ligament (intersesamoidean) - Fibrocartilage which unites with the two axial surface of the sesamoid bones -> proximal scutum is continuous with this
- Collateral sesamoidean ligaments - medial and lateral aspects of the fetlock
○ Attach the abaxial surfaces of the sesamoid bones to the distal extremity of the metacarpal bone and the tuberosity of P1
71
Distal sesamoidean ligaments what are the 4 ligaments and where do they coarse
1) Straight sesamoidean ligaments - from the base of each sesamoid to P1 and P2
2) Oblique sesamoidean ligaments - on either side of the straight ligament and partially covered by it, run to the palmar surface of P1
3) Cruciate sesamoidean ligaments - deep the oblique and straight ligaments, from the base of one sesamoid to the proximal P1 adjacent to the base of the other sesamoid - they cross over each other
4) Short sesamoidean ligaments - from the base of each sesamoid to the underlying region of P1
72
Synovial structures clinical signs, what to do with and emergency treatment
- Open synovial structures may not be very lame
- Synovial fluid: WCC/TP/diff present diagnostic
- Distend from distant site
- If in doubt offer referral
Emergency Treatment
- Broad spec abx
- NSAID
- Collect SF if aspirate joint
○ Blood culture bottle
○ EDTA: cytology
73
What are the 2 main normal treatments for synovial structure involvement
```
1. Surgery - $7K
○ Effective lavage and debridement essential
○ Arthroscopy
2. Cheaper option
○ Needle lavage/large catheter 18G - can be done in the field
○ Sedate horse, nerve block
○ May not be as effective
Most suited to recent penetrations
```
74
Prognosis for synovial structure involvement and what involved
- Variable
- Chronicity - longer been going on than lower prognosis
- Bone/tendon involvement
- Lots of money
- Bacteria involved
- 70% survival
75
List the general treatment for tendons and specifics for extensor and flexor tendons
- Debride tendon ends
- Debride and flush tendon sheaths
- Provide support
○ Extensor tendons
§ Bandage, Simple splint
§ Tow extension shoe
○ Flexor tendons
§ Rescue splint*, Support bandage, Cast*
§ Heel extension shoe
§ Raised heel shoe
- Suture
○ Clean simple transection only
○ Special suture patterns
§ Locking loop
§ Tendon pulley suture
76
Prognosis for tendon injuries with specific tendons
```
- Extensor tendons
○ Depends on extent of wound
○ Open (ext) tendon sheaths heal well
○ Can impair high performance athletes
○ Stringhalt (hock hyperflexion) occasional complication in hind limbs
- Flexor tendons: depends on extent/site/quality of healing.
○ SDFT
§ Most athletically sound except for racing
○ SDF and DDFT
§ Guarded-poor prognosis
○ SDF, DDF and SL
§ Significant support lost- salvage only
○ involving tendon sheath?
§ Poor prognosis unless minimal injury
§ Heal poorly, Adhesions
```
77
Luxations what can result in, diagnosis, treatment and prognosis
- Severe trauma to articulation. Injury to collateral ligaments
- Diagnosis
○ Exploration of wound/periarticular swelling
○ Stressed radiographs
○ (Ultrasound of ligaments)
- Treatment
○ Distal limb
§ Cast application
§ Arthrodesis
○ Proximal limb
§ Stall rest
- Prognosis
○ Guarded
○ Often develop osteoarthritis
○ Depends on site and ability to stabilise
78
Fracture diagnosis in the distal and proximal limb
```
○ Distal limb
§ Clinical examination and radiographs
§ Severe lameness
§ Joint/limb swelling - generally have joint effusion
○ Proximal limb
§ Diagnosis more difficult
§ Radiographs
§ Ultrasound
§ Scintigraphy
```
79
Fracture stabilisation reasons to and principle
```
○ Reasons to
§ Minimise additional damage
□ Neurovascular structures
□ Penetration of skin
□ Bone ends
§ Prevent anxiety
○ Principle
§ “Joint above and joint below”
§ Rigid support
```
80
Fracture stabilisation distal metacarpus and below
§ Commercial splint
§ (Kimsey/monkey splint)
§ Align dorsal cortices
OR
§ Padded heavy bandage - 3 times width of the leg
§ Splint dorsally forelimb, plantarly in hind limb and under foot
§ Cover with cast material
81
Fracture stabilisation from mid-metacarpus to distal radius and mid to proximal radius
○ Fractures from mid-metacarpus to distal radius
§ Robert-Jones bandage
□ Multiple layers
□ Approximately 3 times diameter of limb
§ 2 splints from elbow to ground laterally and caudally
○ Fractures of mid to proximal radius
§ Robert-Jones bandage
§ Extend lateral splint proximally up lateral aspect of chest
§ Lateral muscular pull distracts fracture
82
Fracture stabilisation from mid to proximal tibia and proximal fractures
○ Fractures of mid to proximal tibia
§ Robert-Jones bandage
§ Wide board on lateral aspect of limb extending to proximal thigh
○ More proximal fractures cannot be stabilised
§ Muscles provide splinting
83
Fracture stabilisation for transportation
a. Confine well
b. Face forward for HL
c. Face back for FL
d. Other treatment
§ NSAIDs**
§ Antibiotics if open
84
Vascular how too know how much is too much blood, CV stabilisation
```
- How much is too much?
○ 8L /500kg horse
○ HR>80, (PCV/TP)
○ Lactate >2
○ Pale mmbs
○ ‘Colic’ ** -> can look like colic if lose enough blood -> possibly leads to ileus
- CV stabilisation
○ Pressure bandage
○ Ligate vessel?
○ Crystalloids
○ Transenamic acid? (10mg/kg slow IV)
○ Avoid field GA if unstable CV
```
85
Avascular necrosis how to diagnosis and warning signs
- Cold foot unreliable
- Bleeding unreliable
- Difficult to be sure
- Best way to know whether blood flow -> Scintigraphy flow phase
- Warning signs
○ Excessive lameness initial days
○ Then very comfortable
○ Coronary band serum ooze
86
When first see soft tissue injuries what is preliminarily treatment and medications used
- Sedate/ local nerve block
- Clip, clean, debride- DECOMTAMINATE
○ dilute CHX/saline
- Soil significantly decreases infective dose of bugs
- High volume lavage
- Wear gloves!
Medications?
○ Check tetanus status: TAT/TT
○ Broad spec abx?
○ NSAID
○ Protect from contamination
87
Wound healing what is first and second intention healing
```
- First intention
○ Primary closure
○ Skin apposed
- Second intention
○ Skin not apposed
○ Granulation tissue
○ Contraction
○ Epithelialisation
```
88
What is involved with deciding when to suture or not to suture
- Acute wounds - not contaminated
- Ability to debride effectively
- Help prevent skin loss and protect underlying structures
○ Tension relieving sutures
○ Infection-minimise sutures - try to reduce amount of suture material
§ Gap better than xs tension
○ Minimise movement
- Need to consider Skin tension
- (Client wants cosmetic result?)
89
What are the 3 stages of wound healing and which are poor in distal limbs and therefore 3 reasons wounds break down in this area
Stages of wound healing;
1. Cellular debridement**
2. Proliferation/angiogenesis (granulation tissue)
3. Contraction**/Epithelialisation
- ** poor in horse distal limbs
THEREFORE
1. Poor cellular debridement** /infection
- Horses > ponies
- Distal limb
2. Movement: Tension at suture lines
3. Orientation of skin vs blood supply - Upside down flap get tension in suture and will break down
90
Proud flesh what is it, what it promotes and differenetial diagnosis
- Poor cellular debridement
○ Chronic infection
○ Chronic inflammation
○ Promotes growth of unhealthy granulation tissue -> exudate released
○ extra GT prevents contraction and epithelialisation
Differential diagnosis that look like proud flesh
- Sarcoid /squamous cell carcinoma transformation
- EGT uncommon on proximal limb
- Histology required
- Exacerbated by trimming
91
Proud flesh treatment what are the 3 main ones
```
1) Trim with blade - no nerve supply
○ Level with skin and distal
○ WILL BLEED
○ Removes superficial contamination/inflammation mediators
○ Keep doing it time and time again until healthy and will close up
2) Topical treatments
○ Corticosteroids
○ Yellow lotion - Zinc sulphate
3) Movement prevention
○ Bandages provide stability and promotes healthy granulation tissue
○ Cast is optimal
○ Bandage cast easier in the field
```
92
Non-healing wound what are the 3 main things it is caused by and treatment
```
- Caused by:
○ Discharging tract
○ Sequestrum: due to infected avascular bone
§ X-ray to highlight surface under tract
○ Tendon infection / motion
- Treatment
○ Remove sequestrum, standing without general anaesthetic
○ Curette underlying bone
```
93
Non healing wound what results if leave and don't treat
```
○ Chronicity decreases contraction
○ Epithelialisation
§ slow
§ poor quality tissue
§ suboptimal cosmetics
§ prone to injury
```
94
what is best treatment for non-healing wounds
- Graft healthy granulation tissue to speed closure and improve quality of the scar
1) Pinch/punch grafting -> take grafts from the neck
2) Complex grafting
95
Pinch/punch grafting how complicated, comestics and mechanism
```
§ Cheap, Easy, Field procedure
§ Poor cosmetics - scarring
□ Islands of sparse hair
§ Mechanism
□ Prepare granulation tissue bed by trimming 2 stages prior
® Biopsy punch from neck
® 2mm smaller diameter punch in wound bed
□ Primary dressing + heavy bandage 3-4 days
□ 10 days until grafts take
□ Careful bandage changes in between
□ Immobilise
□ Topical antibiotic cream
□ Wound closes 2-3months
```
96
Complex grafting what is involved, comestics and what is needed
```
§ Full thickness /split thickness sheets
§ Modified Meek grafts ($6K+)
§ Cosmetic outcome better
§ Referral cases
§ Wound bed must be optimal
§ Immobilisation critical
```
97
heel lacerations what structures involved
```
§ Coronary band
§ Collateral cartilage
§ DIP joint
§ Navicular bursa
§ Digital sheath
§ Collateral ligaments
§ Digital vessels
§ Digital nerves
```
98
Treatment for heel lacerations and complications
Debridement
○ GA or nerve block
○ Tourniquet* -> bleed profusely
○ Debride collateral cartilage
○ Sharp sectioning of nerve/ ligate vessels
○ Apposition of coronary band
○ Check synovial structures
○ Stabilise with hoof cast
- Complications
○ *Abnormal hoof growth (coronary band/instability)
○ *Synovial infection
○ Excessive granulation tissue (instability)
○ Quittor - inflammation of cartilage of lower limb
99
Sole penetration what structres may be involved and prognosis and treatment with these
1) Sensitive laminae
2) Pedal bone
□ Bandage initially
□ Hospital plate
□ Good prognosis
3) DDFT* - deep digital flexor tendon
4) Navicular bursa*
□ Prognosis guarded- poor
□ Early dx critical
® Take sample of the navicular bursa
□ Treatment
® Referral
◊ Arthroscopy – 50% survivors sound
◊ Street nail – 30% sound
® Broad spectrum antibiotics
§ Distal interphalangeal joint*
§ Digital sheath*
100
Hoof wall avulsion what is involved, complication and treatment
```
○ Rip the hoof wall off the laminae -> not weight bearing as very painful
○ P3 fracture common therefore xray
○ Treatment
§ Remove unstable wall
§ Debride contaminated tissue
§ Cast until stable growth from coronet
§ Bar show until grown out
```
101
Chest wounds complications and treatment
```
Complications
- Subcutaneous emphysema* - SO COMMON WILL HAPPEN
- Elbow joint sepsis
- Penetrate pleural space
○ Respiratory compromise
Treatment
- Strict confinement
- Close/cover to reduce emphysema
- Daily lavage
- TAT, Abx
- Pneumothorax req emergency tx
```
