Horses Flashcards
1
Q
parasitic skin diseases
i) ectoparasites
ii) endoparasites
b) Insects
A
a) i)
Pediculosis (suck - haematopinus, chew - damalinia)
chorioptosis (chorioptes bovis, psoroptes equi = ear canker)
Thrombiculosis - “harvet mites (thrombiculata autumnalis)
sarcoptic manage (sarcoptes scabei) - eradicated in the UK (rare elsewhere)
Demodicosis - demodex cabali
ii)
onchocerciasis (onchocera cervicalis, reticulata) - VMD is NB
oxyuris equi
strongyloides westerii
Habronema megastoma ("summer sores")
b) Tabanids + haematopota - horse flies stomoxys haematobia irritans - horn fly (VMD) similidae - black flies (deposit habronema) culicoides - hypersensitivity + oncocherosiss hypoderma bovis, diana - warble Parafilariosis --> exudative nodules dracunculosis --> exudative nodules
2
Q
Treatment of
i) ectoparasites
ii) endoparasites
A
Permethrin, moxidectin, ivermectin
Pro: toltrazuril, metronidazole, permethrin and trimethaprim
Trem: praziquantel
Cest: praziquantel
Hel: benzimidazoles
3
Q
Hypersensitivities of the skin
inc. photosensitivity
A
Long term issues that are managed not cured, characterised by (eosinophilic) pruritis from self trauma
insect hypersensitivity - “sweet itch”
Atopic dermatitis (IgE production to environmental allergens)
Contact dermatitis (no immune mediation, contact with irritants such as chemicals, metals or fabrics)
food allergies
Photosensitivity
- primary (ingestion of photodynamic agent or tetracycline)
- secondary (impaired liver clearance)
- ulceration
4
Q
DDX of skin hypersensitivities
A
Skin patch test
IgE production serum tests
elimination tests
5
Q
Treatment of skin hypersensitivities
A
Removal
Symptomatic - CCS, NSAID’s, anti-histamines or OFA’s
Immunotherapy - ID’ed Ag is targeted and neutralised (60% efficacy)
6
Q
Bacterial skin diseases of horses
Their treatment
A
Dermatophilosis - (Dermatophilus congolensis)
- known as rain scald
- Cs: nobbly crusts with toothbrush appearance
- Dx - smear, biopsy, impression - railroad cytology
Superficial pyoderma - (staphyloccocal usually)
- 2nd to many skin disorders
- Dx: neutrophils on smear with cocci inside
Deep pyoderma (folliculitis + furunculosis) - penetrating wound or spread from superficial pyoderma
Ulcerative lymphangitis (occationally affects subcutaneous lymph nodes causing erupting through the skin and ulceration)
- Cornybacterium pseudoTb
- Rhodococcus equi
Anthrax - most common is cutaneous form (95%), less acute in equids and looks like insect bite with inflammation of local LN’s
Farcy - (Pseudomonas mallei)
- cutaneous glanders
- zoonosis
- T - Euthanasia in non endemic areas
T
- chlorhexidine shampoo
- systemic Atb (penecillin)
7
Q
fungal diseases the skin
Dx
T
A
Dermatophytosis - “ringworm”
- trichophytoon equinum
- microsporum canis
- stabled horses in winter
- usually 2nd to skin damage
- Dx - woods lamp (m.canis), saborhads, MS
- T - Lime sulfur wash
Deep cutaneous myocosis
- sporotrichosis, cryptococcus, histoplasmosis
Pythiosis - “swamp cancer”
- prolonged water exposure
- phythium sp.
- ulcerative sinuses (Leeches)
8
Q
Immune mediated skin diseases
A
pemphigas foliaceus
- immune mediated acantholysis –> sloughing
- waxes and wanes
- head and coronary band –> generalised
- Dx: cytology (lysed acanthocytes and neutrophils)
- T - immunosuppression (prenisolone), in foals (gold flakes)
Alopecia areata
- immune mediated destruction of hair bulb
- Non-inflammatory alopetic lesions
- leukotrichia
- Dx: trichogram (broken ! shape), lymphocytic infiltration of hair follicles
- T - Minoxidil (vasodilator)
Pemphigus erythymatosus (discoid or systemic)
9
Q
Other skin diseases of the horse
- seborrhea
- misc.
A
Seborrhea sicca/olesa
- primary (problem with overproduction of keratin)
- secondary (problem with desquamation or epithelialisation)
MEED (multisystemic eosinophilic epitheliotropic disease)
Epitheliotropic lymphoma
exudative dermatitis
urticaria - multiple oedematous lesions
Exuberant granulation tissues (“proud flesh”)
- Dx with cytology
Amyloidosis - deposits of amyloid A
Pastern dermatitis (“greasy heel”)
- superficial pyo
- dermatophilosis
- chorioptes
- vasculitis
- contact irritation
10
Q
Viral skin diseases in horse
A
EHV - 3 (ECE) EVA (manifests as urticara) Papilomavirus (EPV) - aural plaques (DDx w/ psoroptes) Vesicular stomatitis
11
Q
Neoplastic skin lesions
A
Melanoma - perioccular, perianal and distal limbs - almost exclusively in white/grey horses SSC epitheliotropic lymphoma sarcoid - types of sarcoid -- Verrucous (wart like) -- occult (flat) -- fibroblastic (pendulous) -- nodular -- malevolent (metastasise into lymphatics) -- mixed
12
Q
Diseases of depigmentation of skin
A
Vitaligo
- immune mediated destruction of melanocytes
- eyes, muzzle, lips common
- arabs
albuminism
- congenital aplasia of melanin production
- partial blindness and deafness
- Lethal white foal (albuminism + colonic atresia –> meconium retention –> death)
- lavender foal syndrome (very cool)
leukotrichia/derma
- derma - occurs commonly after trauma
- trichia - spotted or reticulated (cross hatch)
13
Q
Equine recurrent uveitis - “moon blindness”
- Aetiology
- 3 types
- cs, dx, t
NB FOR EYE Q
A
A: genetic, infectious (EHV-1, Lepto, Onchocera)
types: Anterior, posterior, panuveitis
cs - photophobia, blepherospasm, hypopyon, cattaracts (chronic), vitrious haze/ nuclear sclerosis (chronic)
Dx - tonometery (decreased IOP), vitrious humour sample Ag test (ELISA)
T -
- Medical: anti inflammatory (NSAID, CCS), mydriatic agent (uveitis = miosis)
- Surgical (vitriectomy Ag-Ab’s are here) + cyclosporin implant or replace vitrium with saline
14
Q
Diseases of the globe and orbit
- congenital
- acquired
A
Congenital
- microphalmus
- anophalmus
- bupthalmus - enlarged globe (increased IOP)
- strabism - cross eyed
Acquired
- exopthalamus
- due to trauma, neoplasia, cysts, ethmoid haematomas
- lubricate and drain + antiinflamms
- enopthalamus
- loss of fat or dehydration
- rehydrate (can lead to entropion)
Glaucoma (increased IOP)
- rare in equids
- due to damage to uveoscleral drainage of VH (as well as iridocorneal angle)
- lower production of VH is treatment - B-blockers (timolol)
15
Q
Diseases of the eyelids in a horse
- Congenital
- Acquired
A
Congenital
- entropion (eyelid folded inwards)
- ankyloblepheron ( failure to open at birth)
Acquired
- ectropion (blepheroplasty to treat)
- third eyelid prolapse (NB: often a golden sign of tetanus)
- Trauma - very common due to
16
Q
Corneal diseases in a horse
- congenital (RARE)
- acquired (COMMON)
NB FOR EYE Q
A
congenital
Pannus
- this is excessive granulation tissue formed over the cornea
- Keratomalacia
- immune mediated destruction of cornea
Acquired
Keratoconjunctivitis sicca (KCS) - “Dry eye”
– lower tear quality/quantity
–Dx:STT, fluroscein test
–T: Cholinergics (increase tear production)
Mineralisation - Ca2+ deposits in the eye due to trauma
- T – keratectomy or EDTA (binds calcium)
Traumatic keratitis
- mild –> penetrating
- often due to entropion, ectopic cilia, FB, trauma
- mild –> penetrating
- T - mild –> topical ATB, severe –> systemic ATB, penetrating –> reform VH and suture
Ulcerative keratitis - infection with pyogenic agent (staph, strep, aspergillus)
- bacteria cannot enter the eye through the cornea unless damaged –> then adhere to the stroma
- Pyogenic exudate + LIQUIFICATON (keratomalacia) - due to bacterial enzymes
- DDx - fluorescein (check for damage to cornea as aspergillus can enter without damage to cornea)
- T -topicals
Stromal ulcer
- 2nd to ulcerative keratitis where the cornea grows over the top of the infected tissue sealing it inside
- Dx: fluorescein to check for no corneal breakage with opacity seen behind the cornea
- T - debride and ATB
Viral keratitis - EHV -2
- Dx: rose bengal (binds EHV infected cells)
- T - acyclovir (anti viral)
Parasitic keratitis
- onchocerosis
- Theilazia lacrimalia
- T - remove and ivermectin
17
Q
diseases of the lens in horses
A
Equine lens turns yellow with age Cataracts - 3 types --incipient (small foci) --immature (will spread with no treatment) --mature (will go blind with no T)
In young it is genetic but is usual in older horses of around 20 years old
Cs: partial blindness
Dx: small stellate scars in the eye using a slit lamp
T: US waves can disintegrate the cataracts and they can be removed
Sub/luxation of lens
18
Q
Diseases of the conjunctica in horses
- conjunctiva = Limbus, episclera and sclera
–limbus = retina, optic disc, choroid
A
conjunctivitis
- primary: infective agent (AHS, onchocerosis), trauma, irritants, AI
- secondary: respiratory infection (Flu, EHV-1) , FB, other occular disease
- T - antiinflammatores
Neoplasia - SCC
Amyloidosis
19
Q
Nasolacrimal system diseases
A
Dysgenesis
- usually nasal septum side
- Epiphora
- no passage of Fluor through NLS
- can pass folley catheter through and leave for 2-4 weeks to reopen
Stenosis
- FB
- neoplasia
- ethmoid haematoma
KCS
- disruption of aqueous part of tears
- dry eye
- Cs: blepherospasm, chemosis, keratitis
- Dx: STT/ fluorescein
- T - cholinergics
20
Q
Functional disorders of the heart
Valves and septums
A
Patent ductus arteriosis
- should close to form ligament arteriosum
- if not blood mixes in the aorta
- LV hypertrophy due to hypoxia –> pulmonary oedema
- Cs: strong pulse, exercise intolerence, cyanosis
- Dx: echocardiogram
- T: furosemide (diuretic), ACE inhibitors (prevent hypertension, vasodilator), surgical ligation of PDA
Atrial septal defect
- blood shunts from LA to RA causing
- RA dilation
- LA hypertrophy
ventricular septal defects
- Blood shunts from left ventrical to right ventricle
- RV dilation
- LV hypertrophy –> pulmonary oedema
pulmonic stenosis
- narrowing of PA –> RV hypertrophy
- T: furesomide, b-blockers (lower HR), ACE inhibitors/NO compounds
Valvular and sub valvular aortic stenosis
- narrowing of aorta –> LV hypertrophy
- also affects coronary arteries increasing chance of myocardial infarct
- Dx: can be heard as murmur over 4th ICS
- T: furesomide, B-Blockers, ACE inhibitors
Tetralogy of fallot
- pulmonic stenosis
- RV hypertrophy
- ventricular septal defect
- dextroposition of aortic blood
- less blood to lungs –> dyspnea + cyanosis + exercise intolerance
- oxygen has decreased O2 carrying capacity –> kidneys –> EPO –> more RBC –> thickening of blood –> increased clot or embolism incidence as well as decreased perfusion
21
Q
Acquired CV disorders in the horse
A
Mitral valve insufficiency (regurg)
- valvular disorder caused by
- endocarditis (bacterial)
- fibrosis
- cordae tendinae rupture
- increased LA pressure –> A Fib and dilation
- Dx: echo, USG
- T - ACE inhibitors, furesomide, b-blockers, acepromazine (to increase forward stroke)
tricuspid valve insufficiency
- in racehorses due to high pulmonary pressure
Aortic valve regurg
-blood regurgitates into LV
Pericarditis
- Viral, bacterial, traumatic, autoimmune
- fluid surrounds the heart –> tamponade
- decrease cardiac output
- Cs: exercise intolerance, cyanosis
- Dx: echo, USG, pericardiocentesis (see fibrotic fluid), auscultation (hear “splashing sounds”)
- T - furesomide CI’ed due to further lowering of cardiac output and potential for hypovolemic shock to set it
Myocardial infarct - vit e and selenium
22
Q
Infectious processes of CV system in horses
- Viral
- parasitic
A
Viral
- EIA (lentivirus)
- transmitted by culicoides sp.
- Cs: anaemia and weight loss with fever
- Dx: coggins test (AGID)
- -T: euthanasia (if not, life long isolation), can try acyclovir (anti viral)
- EVA (aterivirus)
- -transmitted by aerosol and VENEREAL
- Cs: oedema in perianal area, limbs and ventrum, conjunctivitis
- -Usually self limiting
- AHS (orbivirus)
- culicoides
- affinity for endothelium (resp or BV’s + heart)
Parasitic
- Piroplasmosis
- babesia caballi +theilera equi
- -destruction of RBC’s –> anaemia
- -T - imidocarb
- Setaria equi
- -mosquitos
- microfilaria in blood
- parasitic thrombophlebitis
- strogylus vulgaris hangs out in A. mesenterica cranialis, aorta thoracic and abdominalis –> infarcts
- infarcts –> colic
- T: moxidectin + pyrantel
- -NB: RESISTANT to ivermectin and albendazole
23
Q
Equine CV BPM?
A
28-48 bpm
24
Q
what is the most common arrthymia in horses? (racehorses especially)
How does this look on ECG?
Causes?
A
Atrial fibrillation
- ECG: no discrete P wave
- -Causes: electrolyte imbalance, hypovolemia, mitral regurgitation, HCM
- -T:
- –Young: digoxin (slows heart), rebalance electrolytes
- –Old: box rest, less exercise
25
What is thrombophlebitis?
Cs?
Dx?
T?
Inflammation to a vein (usually after blood draw/catheterisation) that causes a blood clot.
Cs: pain, swelling, oedema in the area and heat
Dx: USG doppler effect can detect abnormal blood flow
T: LMWH, EDTA, NSAID's, cold compress, ATB's if suspected infection
26
Punctum optimums?
```
Mitral - 5th IC
Tri - 3-4th OC (right side)
Pulmonic - 3rd IC
Aortic - 3-5th IC
Heart - 3-5th IC
```
27
Lab tests for heart function
PCV - anaemia
K
- increased = fatal arrythmia
- decreased = bradycardia
Creatinine + Tropanin - myocardial injury
28
Functional disorders of URT (Nares, nasal passage and sinuses)
Nares
Alar fold hypertrophy
-- alar fold vibrates during inspiraton usually
-- We suspect hypertrophy when vibration occurs during exspiration or exercise
--results in less O2 --> lowers performance
--surgical resection or ligation to hold the nostril open is Dx and T
atheroma of nose
- soft mass forming on the nose purely cosmetic
Nasal passage
ethmoid haematomas
- continuous epistaxis (non-fresh blood) seems idiopathic
Dx: endoscopy
T: chemical ablation (formalin) - WILL SOMEONE CHECK THIS?!?!?!?!, surgical removal or cryotherapy
Sinuses
sinusitis --> empyema of sinuses
-primary - sinus infection
-secondary - tooth abscess
-Cs: purulent or bloody discharge from the nose, Facial swelling - (primary: maxilla sinus, secondary: facial crest)
Dx: dull sinus percussion, endoscopy, X-Ray, scintigraphy, CT
T: ATB lavage (if primary), trephination, sinusotomy
29
Functional disorders of the URT (laryngopharynx, GP and trachea)
GP
Guttural pouch tympany
-Result of malformation, air sucking or inflammation (from URT infection) causing accumulation of air inside the GP
--this then compresses the oesophagus and trachea --> CS:dysphagia and dyspnea
Dx: endoscopy
T: folly catheter to release gas. fenestration of GP, NSAID's
Laryngopharynx
Hemilaryngeal paralysis
-L > R (due to looping laryngeal nerve)
- Results in partial obstruction of airway --> less O2
- CS:("whistling sounds"), lowered performance and cyanosis
Dx:
Slap test (palpate larynx while slapping side of horse to feel for arytenoid contraction)
Stick-to-grunt test --> startle horse, if LHP we hear stridor sounds
Endoscopy
T: laryngoplasty (suture arytenoid cartilages)
Arytenoidectomy (only as last ditch effort) can cause aspiration
Trachesotomy can be used to allow performance horses to train while undergoing other treatment
Epigloital entrapment
- epiglottis becomes trapped under tongue
- usually secondary to DDSP
- CS: whistling and exercise intolerance
- Dx: endoscopy
- T: surgical or laser resection
4th brachial arch defects (TC,CTAM,CoPS)
- 1)thyroid cartilage
- cricothyroid 2)articulation and 3)muscles
- 4)cricopharangeal sphincter
wind-sucking (stereotypie)
DDSP (dorsal displacement of soft palate)
-caudal soft palate moves over the epiglotis
-this is due to either laryngeal nerve (branch of vagal) damage, hypoplasia of the epiglotis or muscle damage to SP
-we hear "gurgling" noises and "choking" on soft palate
-Dx: endoscopy
T: Palatoplasty "tiring forward", can also scarify the soft palate or resect
Trachea
-Obstruction
- caused by collapse (grade 1-4), FB, compression from neighbouring structures, trauma
T: resect or external fixation
30
Infectious diseases of URT
Equine rhinotracheitis
- EHV 1, 4 - Respiratory form
- Cs: nasal discharge, cough, sneeze, head shake
- Dx: nasal lavage - ELISA
- T: Rest, NSAID's, acyclovir, mucolytics (ambroxol), bronchodilators (clenbuterol)
- P: Yearly vaccine
Equine Flu - orhtomyxoviridae H7N7
- 100% infection in unvaccinated horses
- Cs(dependant on strain): nasal discharge, sneeze, cough, head shake
- Dx: nasal lavage - HIT, PCR
- T : Rest, NSAID's, bronchodilators, mucolytics
- P: Yearly vaccine (2x a year in competitive horses)
Strangles (streptoccocus equi)
- seen as lymphadentitis on LN's and ulceration of head
- can metastasise to other LN's (mesenteric = colic)
- Cs: nasal discharge (serous --> purulent),
- Dx: nasal lavage - serology
- T: ATB
Glanders (Pseudomonas/burkholdaria mallei)
- Ulcerative disease of URT
- 3 forms (Nasal, pulmonary, cutaneous)
- Cs: stellate (ulcers --> scars) in nasal passage producing purulent discharge and epistaxis, enlargement of submaxillary LN's
- Dx: characteristic scars, EYE HYPERSENSITIVITY TEST
- T: Only in endemic areas (M.East) otherwise cull all in stable
Gutural pouch mycosis
- aspergillus infection of guterall pouch
- forms plaques that can damage BV's or nerves (n. hypoglossus = dysphagia)
- CS: horner's syndrome, epistaxis
- Dx: endoscopy
- T: ligation of a. carotis interna, anti fungals (amphoptericin b), lavage
Rhinoestrosis (Oestrus purpureus)
- like sheep bot fly but in Eq
- nasal discharge (usually bloody)
- T: ivermectin
31
Locomotion and respiration
- relationship between breaths and strides at canter and gallop
- when does the horse inspire/expire
At canter and gallop there exists a 1:1 ratio of breaths to strides, any higher is suggestive of pathology
- inspiration on stride
- expiration on weight baring phase
32
Physiological respiratory rate for a horse
Position of lung field
Localisation of pathology
8-16 RPM
Tuber coxae - 18ICS
mid thorax - 13ICS
shoulder - 11ICS
Elbow
Inspiratory sounds - intra-thoracic
expiratory sounds - extra-thoracic
33
Dx techniques in respiratory tract
```
Endotracheal/bronchoalveolar lavage (cytology)
endoscopy
X-Ray
USG
Percussion
```
34
Infectious diseases of LRT
- Bacterial
- Viral
- Fungal
- Parasitic
Bacterial
- Bacteria pneumonia (s.zooepidemicus, c.tetani)
- Cs: typical resp signs (cough, sneeze, etc)
- Dx: BAL, Serology, PCR
- T: ATb, bronchodilators (clenbuterol), mucolytics (ambroxol), rest, NSAID's
- Glanders (P/B mallei)
- respiratory form
- Cs: purulent discharge
- Dx: stellate shaped ulcers/scars on LRT, BAL serology
- T: Only in endemic areas otherwise cull
Rhodoccocus equi - foal pneumonia
Pleuoppneumonia
- bacterial infection secondary to viral infection
- 3 stages
- -exudative (inflammation)
- -fibropurulent (bacteria in pleual space)
- -organisational (fibrin --> fibrous peel)
Viral
- EHV 1,4 - can be passed in utero
- -vaccinating mother with EHV passes to foal
- Flu
- EVA (endothelium affinity in lungs)
- AHS (resp signs)
Fungal (primary or secondary)
- primary: cryptococcus, histoplasmosis
- second: aspergillus, candida sp.
- - usually due to iatrogenic use of ATB's or immunosupression
- Dx: USG, saborhads agar
- T: Lime-sulphur, fluconazole, amphptericin B
Parasitic
- parascaris equorum
- -heptogastropumonic migration
- -Dx: BAL (esosinophilic) lack of fever is DDX for bacteria
- -T: ivermectin
- Dictyocaulus arnfieldi
- - FH is donkeys but Eq are dead end host
- - L3 migrate to lungs and damage
- - Cs: paroxysmal coughing
- -Dx: larvascopy + endoscopy
- -T: iverectin --P: dont pasture horses w/ donkeys
-Echinococcus equinum
35
Non-infectious processes of LRT
| COPD/EA/RAO
COPD
-associated with stabled horses with dry hay
- environmental allergens build up in bronchioles producing a hypersensitivity reaction
- 3 forms
--subclinical
--mild - infrquent cough and normal RR
--severe - consistent cough with elevated RR
Dx - Tracheal pinch, Ausculatation (crackles, wheezes), endoscopy, BAL, intradermal skin allergen test, elimination test (remove dry bedding etc)
-T: environmental management, bronchodilators (clenbuerol), mucolytics (ambroxol), atropine
Summer pasture associated obstrcutive pulmonary disease (SPAOPD)
- very similar aetiology and Cs to COPD but occurs in the summer in relation to grass/tree pollen allergens
```
IAD
bacterial - bacterial, mycoplasma
non-bacterial - immune mediated, viral
-complex of 3
--airway inflammation
--mucus cell hyperplasia
--hypersensitivity
```
Cs: mucopurulent discharge, ex intolerance
Dx: BAL (cytology), endoscopy
T: CCS, NSAID's, mucolytics, bronchodilators
EIPH
assosciated with racehorses
increased pulmonary pressure during exercise --> mechanical damage of capiliaries and neovascularisation --> thickening of lumen --> increased pressure --> bleeding
Cs: subclinical --> mild --> massive fatal haemorrhage (graded based on blood amount)
Dx: Endoscopy, BAL (haemosiderosis of sample - stain with prussian blue)
T: furesomide (diuretic)
36
what type of dentition does a horse have?
What is the dental formula for a horse?
Hypsodont (root continuously grows)
I:3/3 C:1/1 P:3/3 M:3/3
37
What nerve innervates the
a) maxillary teeth
b) mandibular teeth
a) CN V (trigeminal) - infraorbital branch
| b) CN V (trigeminal) - alveolar inferior branch
38
what age do deciduous inscisors erupt?
what age do adult inscisors errupt?
I1: 8 days, I2: 8 weeks, I3: 8 months
I1: 1.5 years, I2: 2.5 years, I3 3.5 years
39
What is galvanyes line?
A line that moves dorsally to ventrally along the tooth as the horse ages between 10 --> 30 years old
40
What are dental
a) stars?
b) cups?
and what age do they appear disappear?
Stars - coincide with dentin (appear at 8 years and only become very small by 25 years)
Cups - top of infundibulum (appear at 3 years disappear at 8 years)
41
infectious diseases of equine mouth
stomatitis/gingivitis
- Primary
- -bacterial (pseudomonas)
- - viral (horse pox, viral stomatitis)
- -fungal (candida - thrush)
- secondary
- -uraemia
- -ulceration
```
Oral ulcers
Primary
-vesicular stomatitis
secondary
- trauma, FB's
- dental issues - hooks, caries
```
Wooden tongue - Actinobaccilus liegresii
- phlegmon of the tongue develops when the tongue is injured as actinobacillus is a comensal of the mouth
- T: flush with iodine and give ATB
Lumpy jaw - actinomyces bovis
- infrequently reported in horses
- has been known to cause fistulus withers
Gastrophilus innermis
-can moult in molar gaps (RARE)
42
Signs of dental disease
```
Dysphagia --> weight loss
dropping food
pain on palp of head
hypersalivation
unilateral chewing
bleeding gums
halithosis
nasal discharge
```
43
Non-infectious dental disease
Inscisors
- overbite
- underbite
- Hooks
- wave mouth
- fractures
Molars
- "bumps"
- anisognathia - maxilla wider than mandible
- - upper damages buccal side
- - lower damages lingual side
- fractures
- Hooks (improper diet or improper alignment)
Dental caries
- high carbs --> stuck in teeth --> fermented --> acids --> wears away cementum and enamel
- graded 0 -4
- Cs appear when they fracture --> dysphagia
- T: Debride --> lavage with acid gel --> Fill
- -if it has infiltrated the pulp --> extract
Diastema - between P2 and canine
- food becomes lodged (food stasis)
- can cause infection --> periodontal disease
- extract
EORD
- >20 years old
- extremely painful - carrot test
- extract
44
Methods of tooth extraction in the horse
Levator / fulcrom
Surgical
- MITE (minimal invasion transbuccal extraction)
- cortical screw extraction
- Rupulsion --> using existing tooth tracts
45
Diseases of the adnexa of the mouth
Salivary glands (submand, parotoid, sublingual)
- mucocele (ranula)
- sialolith
- sialoadentitis - inflammation of sl.gl.
Periodontal dieease
- inflammation of tooth support structures (ligaments)
- most often seen at diastema due to food stasis
endodontal disease
- pulp disease
- bacterial infiltration + necrosis
- secondary to fractures, caries, periodontal disease
- purulent discharge
- T: extraction
Neoplasia
- odontoma
- osteoma/sarcoma
- ameloblastomas
46
Diseases of the oesophagus
megaoesophagus
- primary - congenital
- secondary - EHV-1 (nerve damage), chronic obstruction,
Obstruction
- intralumenal - dry food that absorps water and gets stucks
- extralumenal - neoplasia, cyst, FB
Stricture
- previous injury
- congenital
Cs: regurgitation (nose), extended head, dysphagia, coughing
Dx: passing of NGT, contrast x-ray,
T: sedation (ketamine + butorphanol) and spasmolytics (diazepam)
Diverticulum
- True (traction) - entire oesophagus is outpouched
- False (pulsion) - through the muscular layer
Rupture
- abuse of NGT
- compression necrosis from chronic obstruction
- reflux necrosis
- T: suture/anastomosis
Parasites
- gongylonema pulcharum
- sarcocystis equicanis
- gastrophilus innermis
47
Diseases of the equine stomach
EGUS
- EGSD (80%)
- EGGD (20%)
- Factors
- -stress
- -diet (low roughage high conc)
- -Infrequent eating
- -NSAID's
3 factors protect stomach
- mucus lining
- stomach vascularisation (PG regulated)
- saliva (raises pH)
```
Cs: inappetance (weight loss), bruxism, abdominal pain (colic), hypersalivation
Dx: endoscope (graded 0-4)
T: H2 agonist (omeprazole)
histamine antagonist (cimetidine)
mucus protectant (sucralfate)
antacid (bicarb)
```
Tympany
-impaction of the stomach due to:
--dry feed (absorbs water and becomes stuck)
--stenosis / obstruction (trichobezors)
--gastric hypomotility
--hepatic disease
--poor dentition (inadequate mastication)
Cs: colic, distended abdomen
Dx: exploratory coeiliotomy, USG
T: NSG, abdominocentesis, prokinetics (CI'ed in obstruction)
48
Parasites of the stomach
Gastrophilus innermis, pecorum
- licked from lips and forelimbs
- releases haemolytic agents causing ulceration and intense colic
Habronema muscae, drachia megastoma
- passed in blood meal from culcoides
- microfilaria in stomach --> ulcers
trichostrongylus axeii --> muscosal folds
49
Diseases of the SI
Simple obstruction
strangulating obstruction
internal incarceration
```
Simple obstruction
-causes
--LI displacement
--food impaction (intramural)
--ascarid (parasitic) impaction
--cysts, neoplasia (extramural)
--muscular hyperplasia (mural)
PG: obstruction leads to;
-decrease in water absorption (distally to block) = hypovolemia
-increased pressure from fluid and gas build up (proximally to block) --> pain and abdominal distention + leakage of protein rich fluid into peritoneum = hypovolemia + loss of acid-base balance
```
hypovolemia = decreased cardiac output --> shock--> death
Proximal block = alkalosis + sudden death
distal block = acidosis
Cs: increased HR, sweating, kicking abdomen (all signs of pain), tachypnoe (acidosis), bradypnoe (alkalosis)
Strangulating obstruction
- Causes
- -pendulous lipoma
- -volvulus
- -adhesions
internal incarceration
- causes
- -Intussusception
- -herniation (epiploitic foramen)
PG: Acute abdominal crisis
-vascular compromise (venous -hyperaemia, arterial - hypoxia) --> necrosis --> ulceration --> perforation of bowel --> leakage of blood and SI content into abdomen
Cs: increased HR, sweating, kicking abdomen (all signs of pain), cyanosis, weak pulse and sudden death
50
Infectious and AI diseases of the SI
- bacterial
- viral
- parasitic
```
Chronic inflammatory bowl disease (IBS)
aetiology is suspected to be AI
factors
-mycobacterium paratuberculosis
-rhodococcus equi
-histoplasma capsulatum
Cs: malabsorption syndrome
--D+
--inappretance
--protein losing enteropathy (albumin)
--peripheral oedema
```
Enteritis
- bacterial
- -salmonelosis --> PLE + endotoxemia --> sepsis (septic shock)
- -clostridium dificile, perferinges --> toxin A (enterotoxic) + B (cytotoxic)
- -Pontomac horse fever (neoricketsia sp.) - american painted horses
- Viral
- -Rotavirus - foals mainly (high mortality) (vaccine available)
- -coronavirus
- -Cause malabsorption syndrome by damaging villi endothelium (atrophy)
Parasitic
- eimeria leukarti --> toltrazuril
- cryptosporidium --> nitosoxomide
- giardia --> metronidazole
- anoplocephala magna --> albendazole/praziquantel
- -80% obstructive colic
- -20% spasmodic colic
- parascaris equorum
- strogyloides westerii
- -> ivermectin (moxidectin if not done for a while and worm burden is high)
51
Large intestine conformation
```
Cecum - 60L (NG fluids)
Large colon
-right ventral
-strenal flexure
-left ventral
-pelvic flexure
-left dorsal
-diaphragmatic flexure
-right dorsal
Transverse colon
Small colon
Rectum
```
52
Cecal pathology
Tympany
- accumulation of gas due to obstruction, torsion, displacement
- Cs: pain, addominal enlargement
- Dx: metallic ping on paralumbal fossa,
- RE: can feel hard band of cecum
- T: gas release by catheter
Ceaco-colic intussusception
- apex of cecum through the body of cecum
- related to anoplocephala in yearlings
- high risk of rupture --> peritonitis
- Cs: scant feces, pain
- Dx: exploratory coliotomy, X-Ray, USG
- T: partial typhlectomy
cecal impaction
- food in base of cecum becomes dry and impacted
- caused by poor dentition, dehydration or general anaesthesia
- Cs: pain,
- Dx: RE: heavy weight of cecal band
- T: rehydration, jejuno-colic anastomosis, laxatives, analgesia
Hind-gut acidosis
- normal pH 6.5-7
- addition of concentrates or sugars --> fermentation and lowering of pH
- acid --> kills bacteria --> endotoxaemia
- Cs: ulcer, laminitis, colic, shock
- Dx: cecal sample pH test
- T: 1.5% BW in forage (fibre)
53
Ascending (large) colon pathology
Pelvic flexure impaction
-common due to diameter change here
-dry or inadequately chewed food fails to transport
Cs: obstruction, pain, dehydration
Dx: USG, X-Ray, lack of intestinal sounds
T: laxatives, fluids, do not feed
```
Sand impaction
-feeding on sandy terrain
-Cs: obstructive signs, pain
Dx: glove test, X-Ray, USG, sounds like waves
T: laxatives, fluids, lubrication (oils)
```
enteroliths
-struvite crystals formed around a nidus
-feeding alfalfa is risk factor (Mg)
-can cause partial or complete obstruction --> necrosis and rupture
- Dx: X-Ray, USG
T: surgical removal
Volvulus
- mesentery between dorsal and ventral colon
- causes strangulating obstruction
- Dx: x-ray, no response to analgesia
- T:surgical colopexy
LDD
- large colon becomes entrapped in the nephrosplenic space (L kidney, spleen, nephrospelenic ligament)
- Cs: intermitten pain
- Dx: RE can feel colon by caudal L kidney
- T: Rolling (RIGHT recumbancy, roll LEFT), fenephrine (shrinks spleen)
RDD
- large colon becomes entrapped between abdominal wall and cecum
- Cs: impaction, tympany
- Dx: RE: feel tenia on colon
- T: Rolling (LEFT recumbancy, roll RIGHT)
54
Descending colon pathology
Impaction - sinks into caudal abdomen
enteroliths
- struvite crystals
- alfalfa is risk factor (Mg)
- Cs: partial or complete obstruction
- Dx: X-Ray, USG
- T: surgical removal
diverticulitis/diverticulosis
- out-pouching of mucosa through muscularis (diverticulitis)
- as these become filled with faeces they become infected (diverticulosis)
55
Infectious diseases of the LI
- Bacterial
- Parasitic
Bacterial
- Salmonellosis
- -young and immunosupped
- -Cs: (colitis)D+ --> endotoxaemia --> sepsis, laminitis, colic
- -Dx: faecal culture, elisa
- Clostridial D+ - C.difficile, perfringes
- -Toxin A + B
- -Cs: (colitis) D+
- -Dx: faecal culture, serology
- Potomac horse fever (neorickettsia
- -american paint horses
- -Cs: colitis, D+ , 2nd lamintis
- -T: oxytetracycline
Parasitic
-Strongyles
--Large: vulgaris (AMC), equis (liver and pancreas), edentatus (liver)
--Small: cyathostomum
Cs: granulomatous colitis --> ulceration --> haemorrhage and rupture
Dx: CoproAg test, larvascopy
T: benzimidazoles
Anoplocephala magna, perfoliata
- associated with ileocecal lesions in yearlings
- can cause intussusception
- Dx: proglittids in faeces
- T: praziquantel
```
PINWORM - oxyuris equi
-lays eggs in perianal region
-Cs: rat tail (NB)
Dx: Cs, floatation
T: flu/fen/albendazole
```
56
The equine acute abdomen (colic)
Types of pain
Types of colic (causes)
Pain
- mild: lip curling, pawing, kicking abdomen
- moderate: straddling as if to urinate, rolling
- severe: violent rolling, tachypnoe/cardia, kicking out
Types of colic
-spasmodic - loss of/disorganisation of peristaltic waves - vagal tone - grass sickness, idiopathic
- obstructive - physical obstruction - volvulus, pendulous lipoma, herniation, intussusception, incarceration, enteroliths, parasites (parascaris)
- impaction - impaction of food (dehydration, poor dentition) or sand
- Tympanic - change in diet causing increased fermentation and gas accumulation disrupting peristalsis, hind gut acidosis
- infarcts - S. vulgaris thromboembolism
- enteritis - EGUS
- idiopathic
57
Dx-ing colic
History
- Previous colic?
- changes in environment (grazing esp)
- dental history?
- Deworming protocol (not deworming for ages and then using ivermectin can cause high load of dead worms and cause impaction)
Signalment (age related changes)
- Foals - meconium retention, GI ulcers, uroperitoneum
- yearlings - ascarid impaction
- young - Ileocecal intussusception, FB, S. vulgaris infarct
- Adult - volvulus, enteroliths, cecal rupture
- Old - pendulous lipoma, colic rupture
Observations (physical exam)
- Signs of pain (posture)
- -abrations to face or body
- -mild, moderate, severe
- abdominal size
- -paralumbal fossa = cecal
- -generalised = SI
- Apathy (endotoxaemia)
Auscultation
- top left: SI
- top right: Cecum
- bottom L/R: LI
- increased sounds: spasmodic
- no sounds: obstructive
- gas sounds: impaction/obstructive
NGT
- NGT passage and reflux
- -pH >5 = reflux from LI = blockage
RE
-size, pain, position, lesions
Peritonial fluid
- normal: clear/yellow <5000WBC, <2.5g P
- pathology: turbid/red >5000WBC, >2.5g P
USG
- Large colon on ventral abdomen
- olympic ring structure
58
Treatment of colic
- medical
- surgical
Medical
- In mild cases walking will work
- passage of NGT can also be attempted (nares to 6-8 ICS stomach)
Aims:
reduce pain
restore perfusion
mitigate endotoxaemia
Medicaments
Analgesia
-NSAID'S - Flunixin
Sedative
- -Xylazine (short lived and mild)
- -detomidine - highly effective (if still showing signs of pain after this then surgery is needed)
Fluids
- Hartmans - increases tissue perfusion
- NGT > IV give more if obstruction is proximal to cecum as cecum absorbs 90% of water
Laxatives
-parafin oil
Narcotic
- morphine is CI due to lowered GIT motility
- butorphanol is a good one
Spasmolytics
- buscopan
- atropine (very long lasting can cause tympany)
Endotoxaemia
-polymyxin B
Surgical
- indications
- - >4L reflux
- - no gut sounds (volvulus)
- - uncontrollable pain (after analgesia)
- - enteroliths, FB, displaced colon
- - suspected peritonitis
Aims
- anastomose any necrotic intestine
- decompress any gas
- remove any obstruction
- correct any torsion/volvulus
- biopsy
59
Equine euthanasia
- Indications
- methods (inc. emergency)
Indications:
- rabies
- eq encephalitis
- glanders (non-endemic region)
- brucella
- inoperable trauma/lameness/colic
Methods:
-Pentobarbital - IV Jugular
-sedation (xylazine + butorphanol) --> anaesthesia (ketamine + diazepam) --> inject to stop heart (K + Mg OR NaCl)
Emergency methods:
- Captive bolt
- shotgun to face
- severing abdominal aorta transrectal
60
Urinary tract of the horse
- position
- function
- Dx of urinary tract disease
- -Lab exam (signs of failure)
position
- L: L3
- R: Last 2 ribs/L1
Function
- excretion - nitric compounds
- reabsorption - water and ions
- BP regulation - RAAS
- hormones - EPO, calcitrol (Vit d), renin
```
Glom - filters small ions
PCT - maintains pH and electrolytes
DLoH - reabsorbs water
ALoH - reabsorbs ions
DCT - maintains pH and electrolytes
CT - reabsorbs water and ions
```
Dx (Lab exam)
-BUN + creatinine increased shows GFR disrupted
- Loss of electrolytes (Na, K, Cl)
- increased Ca (unique to Eq)
SG - 1.03-1.06 (decreased shows CRF)
pH - 7.8 - 8.5
Cellular inclusions
-crystals, bacterial, leucocytes --> infection
RE - palpation
- Left kidney caudal boarder
- feel atrophy, enlargement, calculi, neoplasia
61
Renal disease/failure
Failure - >75% of nephrons damaged
pre-renal azotemia
- haemorhage, dehydration, D+
- hypovolemia
- decreased perfusion + GFR
- increased N compounds in blood
Renal azotemia
- primary
- -metal ions, drugs, toxins
- -NSAID's (suppress PG's so less blood to kidneys)
- -obstruction (urolithiasis, cysts, neoplasia)
- -hydro/pyonephritis (ascending UTI)
- secondary
- -colic endotoxaemia
- -shock --> ischemia --> infarct
Chronic glomerular nephritis - thickening of basement membrane (decreasing GFR)
Cs:
- PU/PD
- Oedema (protein loss)
- anorexia
- anaemia (less EPO)
- loss of ions (Na,Cl)
- hypercalcaemia
- azotemia
62
Bladder pathology
| Urethra pathology
Bladder
Cystitis
-primary - ascending UTI
-secondary - renal stasis + bacterial proliferation (calculi or nerve damage)
Cs: polakuria, dysuria, stranguria
Dx:>10,000 CFU on urinary exam, neutrophil casts, USG
Cystic urolithiasis
- CaCO3 most commonly (high Ca diet, low acidity in the kidneys)
- Cs: As above + haematuria
- Dx: RE palpate calculi, USG
- T: US waves to break down and pass
Rupture --> uroperitoneum
Foals: patent urachus --> uroperitoneum
neoplasia
- TCC (Highly metastatic)
- SCC
Ureter
-Ectopic ureters
Urethra
- Urethritis - usually due to kick from mare
- urethrolithiasis
- urethral diverticulum - smegma accumulation
63
Equine liver
- position
- blood flow
13th IC inside the rib cage - no gall bladder
Aorta --> hepatic artery (+SI) --> hepatic sinusoid
-->SI --> hepatic portal vein --> hepatic sinusoid
Hepatic sinusoid --> central vein --> Hepatic vein --> VCCau
64
Infectious liver diseases
- Bacterial
- viral
- parasitic
Bacterial
- Cholangiohepatitis
- -starts in liver --> billiary tracts
- Tyzzer's disease (C.difficile)
- -Hepatic in foals (necrosis)
- -GIT in adults
- -T: broad spec (oxytetracycline, cephlosporins)
Viral
- EHV-1
- -necrotic lesions with IB's
Parasitic
- Fasciola hepatica/magna
- -metacircaria on grass
- -T: praziquantel
- Parascaris equorum
- -migratory damage (milk spots)
- -T: benzimidazoles
- Ecchinococcus equinus - cystic lesion on liver
Cs:
- Enlarged liver --> billiary obstruction --> colic
- Jaundice
- Clotting issues
- heptoencephalopathy (billirubinaemia)
Dx: USG, Biopsy,
- Serology
- -Glutamate dehydrogenase - liver
- -AST - liver
- -ALT - billiary
- -GGT - billiary
- -billirubin increase
- -cholesterole increase
- -NH4+ increase
- -hypoglycaemia
- -fewer clotting factors
- -hypoalbuminaemia
```
T:
Fluids (K + dextrose)
LACTULOSE (takes NH4+ out of blood into GIT)
anti-inflammatory (NSAID)
anti-oedema (mannitol)
anti-oxidant (Vit E)
Low protein diet
Xylazine can help hepatic encephalopathy
```
65
Non-infectious liver disease
Chronic "active" hepatitis
- active in terms of PMN cells present in inflammatory state
- Auto immune indicated
Iron overload
- Foals given iron supplements can get iron toxicity of the liver
- Dx: kuppfer cells with heamosiderin (haemosiderosis)
Theilers disease - tetanus antitoxin can cause liver damage
portosystemic shunts
```
Cs:
jaundice
colic (hepatic enlargement and billiary stasis)
clotting issues
hepatic encephalopathy
```
```
Dx:
USG, serology
Glu dehy
AST
ALP
GGP
raised (NH4+, cholesterol, billirubin)
decreased (glucose, albumin, clotting factors)
```
```
T:
Fluids (K + dextrose)
LACTULOSE (takes NH4+ out of blood into GIT)
anti-inflammatory (NSAID)
anti-oedema (mannitol)
anti-oxidant (Vit E)
Low protein diet
Xylazine can help hepatic encephalopathy
```
66
Common equine intoxifications
Ragwort --> alkaloid --> liver damage
Locoweed + water hemlock --> CNS damage
Castor bean --> ricin --> sudden death
Cherries + hydrangeas --> cyanogenic glycosides --> cyanide --> death
Maple --> MtHbaemia --> hypoxia
Oak --> renal failure
Foxglove --> cardiogenic gycosides --> heart failure
Photosensitising plants
- st.johnswort
- clover
Aflatoxins
stringhalt - false dandilion
sycamore - myopathy
Rotten Cows creepily licking organic flags...must push ahead swiftly swiftly
67
Skeletal muscle disorders
Exertional rhabdomyolysis
- 2 forms
- -sporadic: high carbs with little exercise, glycogen stored in muscles --> exercise --> hypoxic environment --> anaerobic resp --> LA --> Pain --> more contraction in response --> more LA
--recurrent: congenital issue with Ca2+ release (too much during exercise causing extreme contractions)
Cs: stiffness, pain, myoglobinuria
T: (sporadic) rest, NSAID's, Vit E + Selenium fluids (myoglobinuria)
(recurrent) dantrolene that binds Ca2+ 1hr before exercise
Nutritional rhabdomyolysis
- Vit E + Selenium (anti-oxidants)
- lack of causes zenkers necrosis
- Cs: high k+ (bad for heart), stiffness, pain
- Dx: PM white lines in muscle
- T: supplements
post-anaesthesia myopathy
- long term recumbency causes ischemia and necrosis
- triceps, masseter, quads, glutes most commonly
- local / generalised
- Cs: stiffness unable to stand after long GA
- P: padding, light plane of anaesthesia, maintain BP >70mmHg
sycamore myopathy - sycamore has hypoglycin A which causes myopathy
Sarcocystis equicanis
```
Dx:
enzymes -
-Creatinine phosphatase - muscle specific (skeletal and cardiac)
-AST - liver, muscles
-lactate dehydrogenase - muscle, liver
```
68
CNS parameters
- Reflexes
- levels of conciousness
- levels of ataxia
```
reflex
-pupillary - II + III
-menace - II + VII
-Corneal - V + VI
-palpebral- V + VII
-swallowing - XI + X + XI
(Prime ministers crown prosecution service)
```
Levels of conc
- BAR
- obtunded
- stuporous
- comatose
```
Ataxia
0- none
1- very hard to ID intermittent
2- hard to ID consistent
3- easily ID'ed
4-anyone can see
5- recumbant
```
69
4 nerve blocks of the head
Infraorbital
maxillary
mentalis
mandibular
70
Infectious diseases of the CNS
- viral
- bacterial
- parasitic
Viral
WNV (flavivirus)
-carried by birds
T: supportive only
```
Eq encephalitis
-rodents and birds
-EEE, WEE, VEE
EEE - higher mortality
WEE - higher morbidity
VEE - mild disease
T: euthanasia
```
Rabies (lyssavirus)
- furious form (3 stages, prodromal, excitatory, paralytic)
- dumb form
- vaccine exists
EHV - 1 myeloencephalitic form
equine protozoal myoencephalitis
- sarcocystis neurona
- opossum is FH
- eq in dead end host (cysts in brain)
- Dx: W blot of CSF
- T: sulfadiazine + trimethoprim
Bacterial
-metastatic abscesses from strangles or glanders
Botulism - c.botulinum
- flaccid paralysis (inhibits ACh release)
- can pass in utero
- "shaker foal syndrome" --> ingestion of bacteria NOT toxin (honey)
- T: fluids, laxatives and anti toxin
- P: vaccine given 2x before birth
Tetanus - c. tetani
- cleves snare protein (cant release ACh from receptors)
- T: sedation and anti toxin
Parasitic
- verminous encphalitis
- -S.vulgaris migrating through BV's causing a encephalic embolism
- -hypoderma bovis can overwinter and form nodules in CNS
71
Non-infectious processes of CNS
Brain
Hydrocephalus - congenital acc. of water
abiotrophy of arabs - congenital degen of neurones
temporohyoid osteoarthropathy - ossification around this joint causes compression of VII CN - lip and nose droop
trauma - mannitol for swelling, xylazine for sedation
SC
Wobblers syndrome - cervicalspondylopathy
-compression of SC between atlas and axis causing wobbly gait
-Dx: myelography x-ray
Peripheral nerves
- Horners syndrome (ptosis, enopthalmus, miosis)
- stringhalt - hyperflex of hock
- vestibular syndrome - head tilt
Nerve damage
Suprascapular n - seen as supra and subscapular atrophy due to entrapment of nerve under scapula
-T: physiotherapy
Radial n - due to humeral break
facial n - long recumbancy in GA or temporohyoid osteoarthropathy
-T: warm pads, laser treatment
72
Hoof diseases
sclerosis - replacing hoof with connective tissue
cracks - due to trauma or sclerosis
pin + wire --> cover (unless infected)
hoof hypoplasia
- congenital or nutritional (Vit B,A,E,Cu,S,Fe)
- soft hood makes showing difficult
- T: warm to increase blood supply
White line disease (line is golden)
- line that connects outer hoof to inner hoof
- opportunistic bacteria/fungi or chronic pododermatitis
- Dx: can see line will go black and if chronic can become hollow (knock to see)
- T: iodine flush
Hoof imbalance
congenital - skeletal deformities
acquired - heel, toe, off to side
Cs: poor gait, visible imbalances in hoof
Dx: lunging, inspecting hooves
T: Trim, fit appropriate shoe
pastern dermatitis (greasy heel)
Bruising
- pressure causing bleeding into the hoof
- imbalances, improper shoeing, FB
- bruises on the bar = corns
Abscesses
- corns often develop into abscesses
- seen as discharge from the hoof as well as pain on contact and lameness
- T: natural drain (drill and apply epsom salt)
thrush - fuscobacterium necrophorum in central sulcus
-superficial / deep
canker - FN spreads from central sulcus to frog and eventually outer hoof
-Cs: cottage cheese discharge
T:ATB (superficial = topical, deep = systemic)
Laminitis - inflamation of articulation between coffin bone and hoof wall
-multifactorial disease
--diet (overweight, cushings), colic, hoof imbalances, predispositions (stallions more likely due to higher testosterone), exercise on hard surfaces
-more common in FL
-Cs: acute - sudden lameness + frenimus digital artery
chronic: lameness that lasts >48 hours, likely deviation of coffin bone
Dx: X-Ray rotation of coffin bone
--can be rotated or sunken (through hoof)
T: supportive, soft pads and bedding, NSAID's cryotherapy
if rotation is >10 degrees = poor prognosis
Podotrochleosis (navicular syndrome)
-chronic degradation of navicular bone and DDFT
-sclerosis, cartilage degeneration
Cs: progressive disease unilateral inconsistent --> constnt
Dx: MRI (gold standard)
X-Ray - osteophytes on NB and DDFT calcification
Lameness exam (flexion test, lunging, nerve blocks)
T: supportive shoeing (rise heel), desmotomy of suspensory ligament
73
Classification of synovial fluid
Non-inflammatory - yellow w/ low protein
inflammatory - yellow opaque w/ high protein
infectious - green, opaque w/high protein
haemorrhagic - red, opaque variable protein
74
Diseases of joints
Osteochondrosis
-developmental abnormality of cartilage on long bones leading to thickening and inability of chondrocytes to be perfused and as such necrotise
caused by trauma, overfeeding (overweight) and genetic predisposition
-originates from
--Joint cartilage
--Bone cyst
--growth plate - physitis
Cs: joint effusion with no pain - lameness
Dx: arthroscopy, X-Ray
T:box rest, PRP, MSC, laser
OC --> OCD
OCD
-the bone underlying the cartilage of OC becomes detached and a such the cartilage loses all perfusion --> OA
T: remove fragment
Osteoarthritis
- osteoarthritis develops after cartilage is worn away and changes being to occur on the bone
- osteophytes, subchondral sclerosis, lysis
Septic
-common in foals due to umphelophlebitis or mAb failure
-less common in adults but can be haematogenous or penetrating trauma of joint
Cs: swelling, fever, lameness
Dx: foal (serum fibrinogen), adult (serum amyloid A)
T: joint lavage, ATB, arthroscopic removal of necrotic process if lavage fails
Aseptic (<4g TP in synovial fluid)
- repeated trauma + loading
- secondary to OC, septic OA
- inflammation causes effusion-->effusion eliminates joint space and limits perfusion of cartilage inhibiting healing --> constant lameness
```
Dx: X-Ray, arthrocentesis, flexion test
T: PRP, CCS (less inflamation less destruction), IRAP (Interleukin receptor agonist protein), Glycosaminoglycan (lower inf, builds cartilage matrix)
hyaluronic acid (cartilage matrix)
```
Bursitis
- inflamation of fluid filled sac around joints
- true - bicipital + navicular
- acquired - olecranon + patella
cs: swelling without lamness
dx: arthroscopy, arthrocentesis
t: nsaids, cold compress, rest, ccs
Tenosynovitis
- inflammation of tendon sheath
- usually due to trauma
- nsaid, ccs, lavage, hot press
75
Bone fractures
- salter harris
- types
Salter harris (all in relation to growth plate)
- Straight through
- Above
- Lower than
- Through Everything (Di, GP, Meta)
- cRush
```
Types
Simple - one break and bones in line
complex - one break but displaced bones
communicated - broken in many places
compound (open) - through skin
Greenstick (incomplete) - fracture
```
76
Bones diseases
Osteochondrosis
- thickening of cartilage leading to less perfusion of chondrocytes --> necrosis of cartilage --> physitis, OCD, Bone cysts
```
anular deformities
-vargus + valus
-acquired - diet, trauma
-congenital - in utero infection, twins, premature birth
T: Splint and bandage
periosteal stripping
cortical screw fixation
```
Osteitis - inflammation of cortical bone
- septic - haematogenous inf. or penetrating trauma --> sequestration of bone
- aseptic - consistent overloading (doral metacarpal osteopathy) often confused with laminitis
osteomyelitis - inflammation of cortical and medullary bone
- seen in foals due to haematogenous infection
- often causes fissure fractures
- if it penetrates haversian system then euthanasia is only option
T: debride, flush, ATB's, stabilise fracture (if present)
Fractures
-classify the fracture firstly
-simple/complex/complicated/compound
-SALTER HARRIS
Minimise damage to soft tissue, fix bone
distal simple fractures - bandage + splint
proximal/complex fracture - DCP/LCP
LCP (prefered for long bones), DCP
Navicular bone or coffin bone fractures can be healed with shoeing
Ringbone (navicular exostosis)
-high (pastern) or low (coffin)
77
Tendon pathologies
Tendon laxities
-tend to be congenital can be acquired (more common in HL)
-laxities of DDFT + SDFT cause falling of the fetlock
Cs: weird gait and fallen fetlock
Dx: X-ray (cuboidal bone ossification)
T: raise the heel with shoe
Flexural deformities
- Congenital flexural deformities
- Due to malposition in utero, intoxification, hypothyroidism
- Localisation of lesion
- -Coffin joint - DDFT
- --walk on toe (ballerina walking)
- -Fetlock - SDFT
- --over-knuckling
- -metatarsal/carpal - Suspensory ligament
- --buckling forward/cant stand
T: oxytetracycline (binds Ca2+ to lower contractility)
-Acquired flexural deformities
-Overfeeding grains, overload, trauma
--DDFT - ballerina walking
--SDFT - over-knuckling
T: elevate the heel, desmotomy of inf. check ligament
Tendinosis (degeneration of tendon)
-seen commonly in racehorses due to repetitive overload --> scars --> less flexible --> reoccurance --> lameness
--SDFT (racehorses esp) - metacarpal
--DDFT (showjumpers/dessage esp) - annular ligament thickening
Dx: USG (Hyperechoic), MRI
T: CCS, cryotherapy, rest, NSAIDs, PRP, MSC, arthroscopic debridement
Degenerative suspensory ligament desmitis (DSLD)
-common in racehorse HL
-repetative overload or proteoglycan storage disease
T: MSC, neurectomy, shockwave therapy
Trauma/wounds
- 18 weeks to heal --> scar --> reoccurance
- T: scaffold, PRP, MSC, HA, IRAP, glycosaminoglycan
Rupture
-congenital rupture of extensor tendon
--enlargement of tendon sheath
T:bandage
-acquired rupture
--DDFT: elevated toe
--SDFT, Sus Lig, seasamoid lig: dropping of fetlock
--m.peroneus tertious - HL straight and back (dragging)
--Collaterals - luxation of hoof
Dx: USG (hypoechoic where lig should be)
T: debride damage, cast, arthrodesis
78
Equine lameness Dx
- what is lameness?
- exam
- -physical
- -lameness specific
- -gait evaluation
Dx anaesthesia of lameness
Types of lameness and its classification (grading)
Lameness is a disorder of stand or swing phase of gait
History
-age, use (work, show, race, pleasure), previous injury or disease, DIET
Physical
- observe symmetry, swelling, lameness
- palpate joints for crepitus or lesions
Lameness exam
- assess at walk and trot
- -(will only see at walk if severe pain or neurological)
- assess on hard and soft ground
- -soft overloads tendons
- lunge L and R
- -overloads collateral ligaments
Gait evaluation
- FL: head bob while placing weight on lame limb
- HL: rump will raise up on the side of lameness when lame foot contacts ground
Evaluate:
- stride length
- foot dragging
- displacement of landing
Dx anaesthesia
- Used to localise lameness
- CI'ed in severe lameness or trauma due to likelihood of exacerbating the issue
Start proximal --> distal
i) abaxial sesamoid (P1 downwards)
ii) palmer/planter (heel only)
iii) navicular (distal tibia to planter/palmer surface)
iv) coffin bone (cranial aspect only)
Types of application
- perineural
- intrasynovial
- direct (into lesion)
- ring (around suspected area)
Drugs
- lidocaine (short + irritating)
- mepivacaine (long + no irritation)
Provocation tests
- exacerbate lameness to make ID easier
- -flexion test
- --to ID extensor tendon
- -extension test (wedge test 30 degrees)
- --to ID suspensory ligament
- -navicular apparatus (toe raised)
- --to ID DDFT
Types of lameness
- Swing phase
- -lack of cranial swing = patellar
- -lack of caudal swing = sesamoid fracture
- Stand phase - lack thereof
- diagonal/ipsilateral
- hind/front
- shame lameness
```
Grading of lameness (AAEP)
0-none
1- Difficult to ID, intermittent
2-Difficult to ID, consistent
3-Obvious lameness on trot
4-very clearly abnormal gait
5-no weight bearing at all or recumbent
```
79
Diseases of the reproductive tract of the stallion (andrological, infectious diseases of the reproductive tract of the stallion; etiology, diagnosis, differential diagnosis and therapy)
LH --> leydig --> testosterone
FSH --> sertolli --> ABP, inhibin, oestrogen
Stallion pre-purchase exam
-history: previous impregnantions, did they carry to term? did they have any genetic issues?
-physical: palpate testes, prolapse penis (xylazine, medetomidine)
-Lesions: Dourine, EHV 1,3,4, EVA, EIA
Semen quality
-60% motile
-70ml
-7.2-7.6pH
```
Andrological diseases
-Phimosis (inability to extrude penis)
--due to persistent frenulum, trauma and inflammation, behavioural or genetically short prepuce
--Dx: use xylazine to determine physiological or behavioural
--T:
frenulum: cut and ligate
Too short - dont breed
inflammation - NSAID's + hot packs
Behavioural - train
```
Paraphimosis (inability to retract penis)
- due to spinal cord lesions (m. retractor penis), dourine or inflammation or short prepuce
- Must act quickly --> drying, keratitis and ischemia
- T: lubricate and replace ASAP
Testicular degeneration
-age related mineralisation or due to trauma, radiation or a spermatocele
-Nutritional (zinc and Vit A) deficiency
Cs: subfertility
T:Castrate
```
Testicular torsion
-trauma, idiopathic
>180 degrees we see vascular compromise
Cs: pain, swelling and subfertility
T: Hemi-castrate
```
Neoplasia
- Testes
- -germ cell (seminoma)
- -leydig cell tumour --> hypertestosterone (prostate)
- -sertoli cell tumour --> hyperoestrogenism (feminisation)
- prepuce
- -SSC
- -melanoma
Hernias
- inguinal hernia
- -extravaginal - in scrotum but not t.vaginalis
- -intravaginal - necrosis and blockage --> castrate if not corrected in hours
Infectious diseases
-balantitis (penis), posthitis (prepuce), balantoposthitis (penis and prepuce)
causes:
EHV 3 - ECE
-red nodules that ulcerate and rupture
EVA
-preputial inflammation due to endothelial affinity
Dourine (OIE --> cull)
-silver dollar plaques on penis and inability to retract penis
Dx: preputial flush and culture (EHV - IB's)
```
Cystitis, urethritis,
-usually bacterial UTI (ascending or descending)
-S.zooepidemicus
-brucella --> no breed, no T, cull
-salmonella abortus
Cs: discharge, dysuria, unwillingness to mate, excessive licking
Dx: preputial flush, cystocentesis
T: ATB
```
80
Castration and cryptorchidectomy of the stallions (etiology, diagnosis, differential diagnosis, complications, therapy)
Castrate
- performed approx 18 months
- -too young - too small
- -too old - high chance of haemorrhage
Reasons
- lower testicular tumour occurance
- behavioural
- testicular torsion
- heritable diseases
Done in spring/fall - fewer insects and winter the horse moves less so more chance of oedema build up
Pre-op
- fasting (12 hours)
- tetanus vaccine check
- both testes descended?
- prep area (wash iodine, tie tail, etc)
Procedure
- Standing - only in tall and well mannered horses
- -sedation only (xylazine + butorphanol)
- -high risk of evisceration but cheaper and quicker
- recumbent (left lateral or dorsal) - using full GA (sedation + ketamine and diazepam/guaifenasine)
- -remove lower teste first
Types:
Closed (neoplasia or infection)
-incision of skin and tunica daros (along raphae)
-Do not open tunica vaginalis, strip the parietal side from the daros
-emasculate above testis + epididymis
Advantages
-lower risk of infection, haemorrhage, evisceration and hydrocele (fluid between parietal and visceral T.vaginalis)
Disadvantages
-can cause incomplete removal of epididymis
Semi-open
-As above, with small incision into t.vaginalis to inspect structures.
Open
- As above, with 10cm incision into t.vaginalis, sripped away and then emasculator is used to after ligature of the cauda epididymis and spermatic cord (DD).
- This wound if often left open to allow for drainage
Post-op care
- 6-8 weeks to heal
- 24 hour box watch for herniation or bleeding
- hand walking to allow for drainage and decrease swelling
Complications
- haemorrhage
- evisceration
- septic funiculitis
- persistent behavioural issues (incomplete removal)
Cryptorchidism
-heritable disease (drafts, ponies)
--testes too big, inguinal ring too small or failure of gubernaculum
Types
-abdominal
-incomplete abdominal
-inguinal
Dx:RE absent (abdominal), vessels (inc ab or inguinal)
Can give hCG, if testosterone rises --> tissue in the body
T: castrate inguinally or laparoscopically
81
Reproductive management (breeding season, transition period, influencing the onset of breeding season, postpartum breeding, control of reproduction in mares);
Artificial insemination management (semen collection; preparation, storage and transport of the insemination dose);
Management of early embryo transfer; risk analysis from infectious and reproductive point of view
Reproductive management
-puberty ~18 months
Seasonal polyoestrus (16 hour daylight)
-March/april --> July/August
light --> pineal (decrease in melatonin) --> hypothalamus (GnRH) --> pituitary (LH, FSH) --> ovaries (E2) -->signs of oestrus
Signs of oestrus
- vaginal winking with micturation position
- tail lifting
- frequent urination
- flehmens response from male
Transition period is time between oestrus and anestrus where behavioural signs may not line up with physiological oestrus
- determined by melatonin + GnRH
- demarcated by 3 follicles in a row developing but not ovulating
```
Influencing cycle
encouraging
-artificial light 16 hours
-warmer temp - earlier cycle
hCG
-20cm follicle - induces cyclicity,
->35cm follicle - will ovulate in 24 hours
PGF2-a
- ovulation
```
Suppressing cycle
-P4 (for eventing)
postpartum breeding
- foal-heat: often in primiparous mares they will be more interested in looking after foal than breeding
- giving PGF2-a 1-5 days PP can stimulate cycle again
- oxytocin PP can help clear uterus PP
Artificial insemination
- semen collection by artificial vagina
- one/day
- 60% motility, 70ml, 7.2-7.5pH
- Filtered and extender added (eq semen low in fructose)
fresh insemination - 20ml + ATB's immediate
frozen insemination - 2ml in 4 cotton balls (0.5ml each)
Early embryo transfer
-Done to allow a valuable mare to breed many foals or in mares with previous dystocia or abortion issues
collection
- folley catheter into uterus
- flush 60L of water with buffer (Phosphate Buffered Saline) (3-6x)
- store in PBS
Recipient
- placed transvaginally or laparoscopically
- 2 days post oestrus
- P4 is given 1 week before insemination up to day 140 (CL dependant)
Risks
EVA + stallion can pass through infected semen
Rectovaginal fistulation can occur also
82
Diseases of the reproductive tract of the mare
– diseases of ovaries and tubular organs (reproductive disorders of reproductive tract of the mare; irregularities of the oestrus cycle and ovulation in mares; anestrus; equine post-breeding endometritis; endometriosis; endometrial cysts; poor vulvar conformation; (etiology, diagnosis, differential diagnosis and therapy), risk analysis from infectious point of view
Ovarian diseases
-oophoritis - inflammation of ovaries --> peritonitis + adhesions
-neoplasia - granulosa cell tumour --> increased inhibin --> regression of other follicle
T:ovariectomy
-haematoma --> corpus haemorrhagicum --> can become cystic --> abbscess if infected (usually calcifies and regresses)
Tubular organs
- salpingitis - ascending cervical/uterine infection
- Cervicitis + vaginitis - often 2nd to breeding or due to "wind-sucking" during oestrus also seen in mares with poor vulvar conformation - T: Caslick procedure
Infective agents
- salmonella abortus equi
- brucella --> carrier --> cull
- chlamydia
- EVH 1 --> Embryonic mortality
- EHV 3 --> ECE ulcers --> 2nd inf
- EVA --> inflammation
- Dourine --> cull OIE
```
Contagious equine metritis
-Taylorella equigenitalis
--Stallion is asymptomatic
--mare: metritis, short cycle, mucopurulent discharge
Dx - lavage/swab and anaerobic culture
T: ATB's
```
```
endometritis
-inflammation of endometrium
-windsucking, mating, parturition, gyno exams
-3 barriers to infection
--vulva, vest. vulvovag (hymen), cervix
--if these break down --> persistent endometritis
Cs: few (subfertility)
Dx: neutrophils in lavage
```
Persistent endometritis
-occurs as an inflammatory response up to 5 days after initial endometritis occurance
-causes early CL regression --> embryo mortality
Dx: USG (purulent oedema)
T: Oxytocin (clear uterus), ATB lavage, repair 3 barriers
Endometriosis
- chronic changes due to persistent endometritis
- fibrosis of glands
- gland dilation
- endometrial cyst formation
Endometrial cysts
- embryonic loss due to inability of cups to attach
- Dx:USG - anechoic cysts
- T: progestins (altrenogest), surgical removal
```
poor vulvar conformation
-wind-sucking --> pneumovagina (increased infection risk)
-urovagina --> urine in vagina
Dx: part vagina and listen for air
T: Caslick vulvoplasty
```
Oestrus cycle irregularities
Intra-cycle time
- short - Taylorella equigenitalis, silent,
- long - Neoplasia, older mares, global warming, transition period
inter-cycle time
- short - Uterine disease --> PGF2-a
- long - Abortion, NSAID's (block PGF2-a), nutritional (poor nutrition can delay April cycle)
83
Diseases of the reproductive tract of the mare
- pathology of pregnancy (twins reduction, embryonic mortality, dystocia; fetotomy; cesarean section),
- postparturient abnormalities (mastitis, traumatic injuries of the birth canal, retained placenta); etiology, diagnosis, differential diagnosis and therapy; risk analysis from infectious point of view
Pregnancy detection
MIP (mare immunological pregnancy test) - tests for eCG in serum/urine
USG - 15-25 days (heartbeat + detection of twins)
Twin reduction - Aim to ID and eliminate twins before day 40 (endometrial cup formation)
-Bicornal or unicornal
-often occurs naturally due to placental insufficiency
-Dx: USG (15-25 days)
-T:
--Day 16-25 can crush follicle easily, recheck unicorn at (33 days)
--Day 36: needle puncture and NSAID's
After day 60 it becomes difficult and can damage allantochorion
Day 60 - 100 - procaine and KCl penicillin injection
Day 110+ - break head from neck (wolfsdorf technique)
Embryonic mortality (before day 40)
- intrinsic causes
- -uterine disease (cysts, inflammation, neoplasia)
- -P4 faiure (early CL regression - Persistent endometritis)
- -chromosomal abnormalities
- -twins
- Extrinsic causes
- -endotoxaemia --> PGF2-a
- -Poor handling (RE crush follicle)
- -nutritional
- -Stress/pain
Dystocia - failure of explosive forces of uterus
- Foal should start to arrive 30 ins after CA rupture
- caused by age, primiparous, nutritional status, diaphragmatic rupture, nerve damage
- Primary inertia
- -myometrial defects (overstretch/degenerated)
- -deficiencies (Ca2+, glucose, PGF2-a)
- -premature birth (CA in tact)
- Secondary inertia (rupture/obstruction)
- -obstruction
- --Bone - pelvis too narrow
- --soft tissue - adhesions, stenosis, torsion, displacement, rupture
- Foetal causes
- -Lack of PGF2-a
- -malposition (spine to spine)
- --foal turns vent --> dorsal in late gestation
- -Malpresentation (front or breach)
- -Malposture (limbs in relation to head)
C-Section
- indicated for dystocia or abortion
- foal only viable for 30 mins after stage II
- Procedure
- -inscise 40cm from umbilicus
- -inscise greater curvature
- -remove foetus holding close to mare to allow placental blood transfer
- -close (lambert, cushing, utretch)
- -4 layers (Peritoneum, muscle, subQ, skin)
- Post-op
- -Analgesia, colostral transfer, mild laxative to foal for meconium
- Complications
- -Placental retention (give oxytocin >6hrs)
- -peritonitis
- -seroma
- -haemorrhage
Fetotomy
- retained foetus (aborted only)
- -hold nose of foetus, feel for carotid/rectal artery, USG (doppler)
- <6 cuts, <1hr
- Partial/complete
- Head, thorax, pelvis, HL in breach
- embryotome
- epidural (lidocaine + xyl)
```
Post-partum pathology
-Mastitis
-Cs: hot, pain, swelling, milk changes
-Dx: milk culture (CMT)
T: ATB
```
Uterine trauma
- tears from parturition
- peritonitis + toxaemia
- fuscobacterium necrophorum --> necrotising vagintis
```
Retained placenta
>3hrs placenta should be expelled
-uterine contractions
--inflammatory
--endocrinological
--adhesion
3 factors to expulsion
-placental maturation
-exsanguination of placenta
-uterine contraction
Dx: visible protrusion
T: tie up, oxytocin, remove
```
84
Equine anesthesia (standing sedation of the horse, total intravenous anesthesia (TIVA), inhalation anesthesia, clinical examination of horse before anesthesia, perioperative and postoperative monitoring of the patient)
Pre-anaesthesia
- assess CV and BP
- arrythmia with fibrillation is CI for anaesthesia
- vagotonia --> bradycardia is physiological
- Fast for 6-12 hour prior
Standing sedation
- lower risk than GA
- minor procedures - rasping, arthroscopy, obstetric work, rectals, hoof work, castrate
A2 (xylazine) + opioid (butorphanol, romifidine)
Acepromazine is CI'ed due to penile prolapse
TIVA - GA
Sedation + ketamine + diazepam (midazolam) - 10-20 mins
-prolong: xylazine + ketamine
Foal: NO A2 (ketamine and diazapam)
never >45 unless on O2
give xylazine first as ketamine without sedation can cause seizures
>90 mins - more diazepam
Inhalation
-used for prolongation of TIVA
Isofluroane (sevoflurance provides too light and is expensive)
However 1.2% too light - 1.5% resp block
-give medetomidine first and will give great anaesthesia at 1% as well as analgesia
flow rate
- adult induction (15 mins) - 20ml/kg/hr
- adult maintain - 10ml/kg/hr
- foal - 40-60ml/kg/hr
reflexes
- corneal - light
- pupillary - if absent = dead
- palpebral - absent
Complications
- Hypoxia - 6-18 rpm
- prolonged recumbency - myopathy (triceps, quads, glutes, masseters), neuropathy (facial, radial)
- bradycardia - 24-48 bpm --> atropine (suppresses vagal tone)
- hypotension - >70mmHg can cause ischemic myopathy --> dopamine
- hypercapnia - PoCO2
85
A comprehensive veterinary - medical approach to the traumatized patient (trauma during exercise, work, sport event)
Aim: ID issue and stabilise for transport
- fractures
- luxations
- lacerations
- head + eye trauma
Jumpers - FL fractures (coffin and cannon bones)
Racers - Tendon and ligament issues (DDFT, SDFT, Sus Lig, Collateral ligs, seasamoid ligs)
```
Fractures and luxations
-NB: check pulse, if low give fluids
-sedate
Level 1 - distal to cannon bone
-FL: splint cranial aspect
-HL: splint caudal aspect
-SDFT, DDFT : elevate heel (take pressure off tendons)
-Common extensor tendon - elevate toe and cranial splint
```
Level 2 - cannon bone, hock, olecranon, radial nerve
- FL: 2 splints caudal and lateral (hoof to elbow)
- HL: 2 splint caudal and lateral (hoof to stifle)
Level 3 - tibia or radius
- FL: lateral splint, hoof --> withers (tie to chest)
- HL: lateral splint, hoof --> hip
Level 4 - pelvic, scapula, femur, humerus
- FL: caudal splint
- HL: No splint (RE to determine localisation of damage)
- box rest for 6 months
- poor prognosis for ever eventing again
Wounds and laceration
- primary healing - suture (<6 hours)
- secondary healing - debride --> granulation tissue
Aims: minimise haemorrhage (compression bandage), tetanus prophylaxis, ATB
Head injuries --> NSAID's + mannitol
Thoracic injuries - due to incomplete mediastinum any penetrating injury to the thorax causes bilateral pneumothorax
Dx: loss of resp sounds over lung field
T: drain air with catheter (12ICS)
Synovial injuries - determine if joint space has been compromised --> flush to see if leaks
Tendons
- SDFT: fetlock falls --> support heel
- DDFT: toe lifts up --> support toe
- Sus. lig: drop the fetlock --> cranial splint
Hoof puncture - FB
--white line disease, canker, abscess
Exhaustion
-Rehydrate + electrolytes (6L BGT)
Hyperthermia - horse down
exertional rhabdomyolysis
- Vit E + selenium
- fluids
86
Diseases of foals (etiology, diagnosis, differential diagnosis and therapy)
T: 37-39
P: 80-100
R: 40-60
Needs 2L of colostrum in first 6 hrs (madigan windows)
-Snap test for foal exists to test serum IgG
```
APGAR - neonatal score
Appearance Pulse Grimace Activity Respiration
score based on
HR 0-2
Resp 0-2
Reflexes 0-2
Muscle tone 0-2
```
Total score
- 0-3 - life threatening
- 4-6 - intervene
- 7-8 - normal
Prematurity
- 320-360 days gestation
- Cs: floppy ears, joint ROM, domed head, small
Pulmonary immaturity - atelectasis
T: clear airways perform mouth to nose (10-20 bpm)
GIT immaturity - no IgG absorption
T: IV plama and fluids
Musculoskeletal - carpal bone ossification
-Grade 1-4
--1 - metacarpal growth plate still visible
--2 - oval bones
--4 - all bone rectangular
T: warmth
Righting reflex (suckle within 1 hour)
Cardiac insufficiency - no pulse/bradycardia
-right recumbency and compressions (90-120/min) for 2-3 mins if no response --> adrenaline (atropine doesn't work in foals)
```
Congenital diseases
-flexural deformities = T: oxytetra (binds Ca2+)
-laxities
-varus & valgus
-portosystemic shunts
--intrahepatic - patent ductus venosus
--extrahepatic - other vessel issues
Dx: BUN, NH3-, jaundice
T: Lactulose + vinger (NGT)
```
lethal-white syndrome - am. paint horse
-white, blind, colonic atresia --> meconium retention --> death
Lavender foal syndrome - arabs
Acquired
Infectious
-sepsis
--impaired mAb's transfer + poor hygiene (from umbilicus, resp, git)
-Cs: swollen joints, recumbency, fever, >CRT
-Dx: fibrinogen in serum
T: lavage joints, fluids and ATB's
- Foal heat D+ --> 14 days of self limiting D+
- D+ - e.coli, parascaris, eimeria, giardia
Foal pneumonia - rhodococcus equi
-pyogranulomatous lesions in lungs
Shaker foal - c.botulinum
-ingestion of bacteria --> toxin
progressive flaccid paralysis
T:Anti-toxin
```
EHV1 - in utero --> resp + git
EVA - in utero --> high mortality
parasites
-parascaris
-eimeria
-giardia
-s.westeri --> deworm mare (in utero)
```
Non-infectious
- Osteoarthritis
- -2nd to septicaemia
- -Types (PEST)
- Physial
- epiphyseal
- synovial
- tarsal cuboidal
-Osteomyelitis - failure to heal fracture
dummy foal - neonatal hypoxia
-dystocia --> early rupture from CA --> hypoxia --> acidosis
T: ventilation, mouth to nose , bicarb
```
Neonatal erythrolysis
-mAb's lyse RBC's
Cs: jaundice, anaemia
Dx: coombs test
T: IV colloids and serum from stallion
```
meconium retention
- should pass in 3hrs, >12 is retained
- obstruction --> colic --> death
- T: laxative, oils, fluids
```
Patent urachus
-no regression to ligament of bladder
-articulates with CA
-see urine leaking from urachus
T: surgical
```
Uroperitoneum
-rupture bladder or patent urachus
T: surgical
87
Veterinary care at stud farms, at competitions, preventive and control measures (immunoprophylaxis and immunotherapy of infectious diseases of horses; parasite control; herd examination)
Farm classification
- stallion farm - health care and semen collection/quality assessment
- -tested for EVA, Dourine, EHV, EIA
- mare farm - health care and birthing
- -Tested for EVA, EIA, Taylorrela
-foal + yearlings
```
Vet care at competitions
drug testing
-steroids - performance
-clenbuterol - bronchodilator
-acepromazine - anti-anxiety
-furosemide - EPIH
```
Veterinary care
- ID + stabilisation of injuries
- Transport of injured horses
- emergency care/euthanasia
Passport checks, vaccination checks, chip checks
Preventative and control measure
Vaccines
1st - 4-6 months: Flu, EHV, tetanus, WNV, slamonella, rabies
2nd - 4-6 weeks later: ALL
3 months from first:Flu, EHV (10-12 weeks old)
6 months from second:WNV (13-14 weeks old)
Boosters
- 6 months: EHV
- per year: Flu (racehorse gets 2x / year), Rabies, WNV,
- per 2 years: tetanus (once per year if competing)
Inter-gestational vaccines
-5, 7, 9 months - EHV
6 weeks prior to foaling - tetanus
Optional - rotavirus
Stallions
28 days prior to breeding season - EVA + Taylorella
Strangles (endemic areas) - 4 months --> 4 weeks later --> 4 weeks later again
Leptospirosis
Parasitic control
- Start deworming at 4 weeks, then every 4 until 6 months
- 200 egg/g faeces is good for building immunity in the foal
- DO NOT pasture with donkeys
- Can pasture with cows
density 2Eq/acre
Husbandry
- regular cleaning and changing of bedding
- disinfection, insect and rodent control
- do not house young with old
Prophylaxis
protozoa - Toltrazuril, metronidazole
sarcocystic neurona - sulfadiazine and trimethoprim
Trematodes - praziquantel
Cestodes - praziquantel + moxidectin
Nematodes - benzimidazoles
Ectoparasites - iver/moxidectin + permethrin
Herd exam
- Vaccination status - yearly
- Teeth - 6-12 months
- hooves - 4-6 weeks
