Horses 5 Flashcards
(100 cards)
1
Q
High cervical (C1-C5) lesions what clinical signs seen, which limbs more affected
A
- Hemiparesis/plegia or tetraparesis/plegia
- Clinically dominated by signs of proprioceptive ataxia
○ Disruption of descending UMN tracts cause paresis
○ Paresis can be (very) difficult to appreciate in mildly affected animals - Pelvic limbs (more severely affected)»_space;» thoracic limbs
○ Longer tracts in the pelvic limbs so metabolically affected
○ Neural tracts pelvic are more superficial in the spinal cord - more susceptible to damage
2
Q
High cervical (C1-C5) lesions what if severe lesions, what results with muscle tone, spinal reflexes and bladder
A
- If severe lesions
○ Recumbent
○ Die suddenly following respiratory paralysis
○ Can raise the head and neck only when lying with the lesion side facing down (with unilateral lesions) - Muscle tone? - HYPERTONIC
- Spinal reflexes? - HYPER-REFLEXIA
- Distended bladder, difficult to express
3
Q
Cervicothoracic (C6-T2) lesions what clinical signs seen, what occurs in terms of muscle tone, spinal reflexes with fore and hindlimbs and bladder
A
- Lesions also result in tetraparesis/plegia
○ BUT nature of deficits differs between front and hind limbs - Forelimbs - damaged the cell bodies (LMN)
○ Muscle tone - hypotonia
○ Spinal reflexes - hypo-reflexia
○ Thoracic limb muscle atrophy - rapid, can occur over 3 weeks - Hindlimbs - damaged the neural tracts (UMN)
○ Muscle tone - hypertonia
○ Spinal reflexes - hyper-reflexia
○ Distended bladder, difficult to express
4
Q
Thoracolumbar (T3-L2) what clinical signs seen with incomplete and complete lesions
A
- Incomplete lesions
○ Normal activity of the forelimbs
○ Proprioceptive ataxia in the hindlimbs - Complete lesions
○ Recumbent
○ May assume a “dog sitting” position - paralysis
○ Hindlimbs may show hypertonia and hyper-reflexia - difficult to assess
5
Q
Lumbosacral (L3 - S2) what does it contain, clinical signs in forelimbs and hindlimbs for incomplete and complete lesions
A
- Contains the LMN Efferents for pelvic limbs
- Normal forelimbs
- Incomplete lesions
○ Appear unable to support weight
○ Stride length is shortened
○ Hypometria
○ Joints might be overly flexes (crouches stance and gait) - Complete
○ Flaccid paraplegia
○ Hyporeflexia or areflexia (no reflexes)
○ Hypotonia
6
Q
Sacrococcygeal (S3 - C5) what clinical signs seen with lesions
A
- Flaccidity of the tail and anus
- Paraphimosis in males
- Desensitization of the tail, penis, vulva, anus and perineum
- Urethral sphincter is dilated
○ Urinary incontinence - Unable to defecate
7
Q
Neuromuscular disease what are the 2 main ones and how common
A
Tetanus and botulism -> not that common
8
Q
How does the tetanus and botulism toxin work (mechanism of action)
A
- Cell binding: toxin circulate in bloodstream
○ Both BoNT and TeNT bind receptors on the pre-synaptic membranes of the NMJ
○ Specific receptors for each toxin -> different intracellular routing - Internalization: neurotoxins internalised within vesicles (pinocytosis) in the neuron
○ Tetanus neurotoxin -> transported to spinal cord
○ Botulinum neurotoxin -> mostly remains at NMJ - Blockade of neurotransmitter release: both toxins have proteolytic activity
○ Disrupt specific components of the neuroexocytosis apparatus -> prevents release of neurotransmitters into the synaptic cleft
9
Q
Tetanus what does it lead to and pathogenesis
A
Tetanospasmin -> spastic paresis
○ Toxin diffuses from production site (wound) into bloodstream
○ Distributed to the pre-synaptic membrane of the motor end-plate (of the alpha motor neuron)
○ Travels centripetally toward spinal cord and enters inhibitory interneurons (Renshaw cells)
○ Blocks release of inhibitory neurotransmitters by the interneuron:
§ Glycine and gamma-aminobutyric acid (GABA)
○ Dis-inhibition of the gamma-motor neuron
10
Q
Tetanus epidemiology when generally occur and sites of growth
A
- Horse -> puncture wounds to the foot or soft tissues
○ ENSURE THAT IT HAS BEEN VACCINATED AGAINST BEFORE SURGERY OR WHEN SEE WOUNDS - Other sites for growth of C. tetani include:
○ Uterine infections
○ Castration wounds (especially when using elastrator bands)
○ Tail docking
○ Dehorning
○ Bull rings
○ Infected umbilical stalks
11
Q
Tetanus clinical signs and what result in
A
- Vague stiffness and lameness initially
○ Reflect local effects of the absorbed toxins - Generalised stiffness
○ Hypertonia most evidence in anti-gravity muscles
○ Sawhorse stance
○ Excessive facial muscle tone -> lock jaw
○ Eyeball retracted into orbit with menace -> 3rd eyelid flashes across the cornea
○ Lips retracted -> sardonic grin
○ Ears pulled slightly downward and caudally
○ Tailhead elevated - Tetanic spasm elicited by auditory, visual or tactile stimulation
○ Severely affected animals become recumbent with opisthotonus (totally rigid)
○ Increased muscle activity -> pyrexia (sweating in horse) - Aspiration pneumonia develops in some cases -> contributes to mortality
- Death due to respiratory muscle paralysis and heart failure
12
Q
Tetanus what are the 6 main things need to do
A
1) provide muscular relaxation
2) ensure good footing
3) elimination of infection
4) neutralise unbound toxin
5) maintain hydration adn nutritional status
6) establish active anti-toxic immunity - if unsure on vaccination history
13
Q
in terms of treating tetanus what is involved in providing muscular relation and ensuring good footing
A
1. Provide muscular relaxation ○ Quiet darkened stall ○ Pack ear with cotton wool ○ Acetylpromazine - long acting mild sedation 2. Ensure good footing ○ Sling support - may not tolerate
14
Q
in terms of treating tetanus what is involved in eliminating infection and neutralising unbound toxin
A
- Elimination of infection
○ Surgical debridement
○ Systemic and local penicillin - Neutralize unbound toxin
○ Infiltration area around wound with TAT (tetanus anti-toxin)
○ Systemic TAT ( 2 to 5000 IU/kg slow IV - broad dose range)
§ Not particularly expensive -> generally pick in the middle
○ Theiler’s disease (acute hepatic necrosis or serum hepatitis) - concern when give TAT
15
Q
in terms of treating tetanus what is involved in establishing active anti-toxin immunity
A
○ TAT and tetanus toxoid can be administered simultaneously but must not be mixed and should be given at different sites
§ Opposite side of the neck
16
Q
How do you diagnose tetanus
A
- Clinical signs and history
- No reliable diagnostic test
- Attempt to culture C. tetani
17
Q
Hypocalcaemia clinical signs
A
- Clinical signs very similar to tetanus
○ Clinically quite different to hypocalcaemic in cattle
○ Synchronous diaphragmatic flutter - thumps
§ Diaphragm contracts in time with the heart (due to phrenic nerve being close to the heart)
□ Hypocalcaemia leads to hyperexcitable nerves
18
Q
Hypocalcaemia in horses what associated with
A
○ Lactating mares
○ GIT disease
○ Renal disease
○ Prolonged transport with food deprivation
○ Endurance events (esp during hot weather) - sweat a lot which contains a lot of calcium
○ Cantharidin (blister beetle) toxicity (oxalate, cadmium)
○ Idiopathic
19
Q
Botulism what lead to, caused by and the 3 ways to become infected and how common
A
- BoTN block the release of acetylcholine at the NMJ -> flaccid paralysis
- Caused by toxins produced by clostridium botulinum
○ Soil organisms
○ Most common risk factor is horse being fed with round bail hay
1. Ingestion of the preformed toxin
○ Most common form in cattle and adult horses
2. Ingestion of spores and toxins production within the GIT:
○ Toxico infectious botulism (shaker foal syndrome)
3. Contamination of wounds with Cl. Botulinum spores:
○ Subsequent production and absorption of toxins
○ Rare in horses (not uncommon in cattle)
20
Q
In terms of types of toxins within botulism what is the most common one and why shouldn’t fee cattle chicken poo
A
○ Type B: 85% of cases of botulism in horses, associated with forage - MOST COMMON - just learn this one
§ Commonly associated with round bale hay
○ Type D: associated with poultry litter -> sporadic disease in cattle - SHOULDN’T FEED CATTLE CHICKEN POO
21
Q
What are common clinical signs in foals with botulism
A
- Lie down more often than normal
○ When forced to rise, stands for a few moments, then develops generalised muscle tremors (shaker foal) and drops to the ground - Typically well- nourished, bright and alert
○ Normal heart rate, respiratory rate and rectal temperature - Clinical pathology findings are often normally
- Progressive symmetric myasthenia -> recumbency
22
Q
what are some additional clinical signs of botulism in foals and 2 main complications
A
- Additional clinical signs include: ○ Drooling milk ○ Tongue easy to pull from the mouth ○ Mild mydriasis and weak eyelid tone ○ Constipation and ileus consistent - As disease progresses… increase HR and RR - Complications include ○ Aspiration pneumonia ○ Decubital ulceration
23
Q
Botulism what are the early clinical signs in adults
A
- Clinical signs are always symmetric and progressive
- Early clinical signs include:
○ Decreased exercise tolerance
○ Dysphagia -> slow to eat, diminished ability to swallow
○ Mild depression
○ Colic -> gastrointestinal ileus and gas accumulation - Decreased tongue, eyelid and tail strength
○ Typically occur before obvious skeletal muscle weakness - Vital signs usually normal initially
24
Q
Botulism what are the moderately affected and late clinical signs in adults
A
- Moderately affected -> shuffling gait, evidence of muscle weakness:
○ Elephant on a ball stance - shuffling gait
○ Muscle tremors begin in triceps -> extend to involve other muscle groups
○ Some horses have difficult lifting their head -> oedema of the muzzle and face - Can progress to difficult rising and recumbency
○ HR and RR increase
○ Increase abdominal component to respiration
○ Decreased borborygmi - Death -> respiratory paralysis
25
How to diagnose botulism
- Often diagnosis of exclusion
○ Clinical signs can be very suggestive and response to treatment
○ Might be supported by history (round bale hay)
- Haematology and serum biochemistry usually normal
- Definitive diagnosis can be difficult - NOT DONE COMMONLY
○ Demonstration performed toxins in the serum or intestinal contents
○ Presence of botulinum spores and toxin in recently consumed feedstuff - suggestive
26
What are the 4 main parts of therapy for botulism
1) anti-toxin administration
2) excercise restriction
3) antimicrobial therapy
4) supportive care
27
in terms of botulism therapy what is involved with anti-toxin administration and excercise restriction
1. Anti-toxin administration
○ Antitoxin has no effect on the toxin after it has bound to the cell receptor
○ Single dose of antitoxin should provide passive protection for more than 60 days -> only single dose needed
2. Exercise restriction
○ Confined to a stall or limit muscular activity
○ Frequent attempts to force animals to rise or move are contraindicated -> depletes acetylcholine stores
○ Can use slings to keep horse up (don't want compartment syndrome)
28
In terms of botulism therapy what is involved with antimicrobial therapy and supportive care and prognosis
```
3. Antimicrobial therapy
○ Aspiration pneumonia
○ Infected pressure sores
○ Avoid drugs that might potentiate neuromuscular weakness (procaine, penicillin, aminoglycosides, and the tetracycline)
4. Supportive care
○ Fluids, analgesia
○ Ventilator
Good prognosis if have the money
```
29
Snake and tick bites clinical signs and the 3 main types of vectors
```
- Common clinical signs to botulism
○ Anti-toxins available and effective
- Types
○ Notechis scutatus (tiger snake)
○ Demansia textilis (common brown snake)
○ Ixodes holocyclus
```
30
Stringhalt what is it, how generally occurs, when worse
- Involuntary flexion of one or both hindlimbs (occasionally forelimbs)
○ Pasture derived neurotoxin (flatweed) -> not sure on the exact toxin
○ Injury to the hock
- Generally gets worse when cold or nervous and excited
31
Stringhalt treatment and what can be confused for
- Treatment
○ Many of the pasture associated cases will resolve eventually with removal
○ Phenyoin - not sure how works
○ Resection of the lateral extensor tendon
Can be confused for shivers (where you pick up the hindlimb and it hoovers and shivers before being placed back down)
- Possible cross-over with the diseases
32
in horses what is a common cause of polyphagia and anorexia
```
Polyphagia
- Equine metabolic syndrome
Don't eat
- Hyperlipemia and hepatic lipidosis
- Re-feeding syndrome
```
33
Equine metabolic syndrome what is it, associated with is it related to PPID and certain breds
- Endocrine and metabolic abnormalities associated with development of laminitis
- Hyperinsulinemia, insulin resistance, insulin dysregulation
- Genetic predisposition + exposure to environmental factors = EMS
- Some similarities, but DIFFERENT from PPID
○ Both have lameness as an issue
○ May have both
○ One can influence the other
- Why certain breeds
○ Evolution within different environments
§ Ponies - harsh mountain areas, donkeys - Arad areas -> metabolism made to get most out of the feed
34
Equine metabolic syndrome pathophysiology and what is the most important clinical consequence
- Incompletely understood
- Thought genetic predisposition in combination with environmental factors (overfeeding, high CHO pastures/diets) leads to EMS phenotype & disease
- High CHO diet → insulin dysregulation
○ Similar to metabolic syndrome/type II diabetes in humans
- Inflammatory role of excess adipose tissue
○ Production of inflammatory cytokines
- Hyperinsulinemia linked to laminitis
- Laminitis most important clinical consequence
35
Equine metabolic syndrome clinical picture
- Generalised obesity –BCS 7/9 or greater
○ Regional adiposity - neck, ribs, rump - or just generally
○ Crestyneck
- Laminitis - multiple founder lines (repeated subclinical)
- Pony breeds, some horse breeds
○ Morgans, paso fino
36
Equine metabolic syndrome what is important to consider
- Client education
○ Lots of owners underestimate the obesity of their animal
○ Or just think that is normal
○ Laminitis is NOT NORMAL
37
In terms of equine metabolic syndrome what are the 6 main tests for diagnostics and what is important
1. BCS, crestyneck score, midneck circumference, girth circumference at withers and umbilicus
2. Basal plasma insulin concentration
3. Oral glucose tolerance test/oral sugar test
4. Oral sugar test
5. Insulin tolerance test
6. Combined glucose-insulin test
- Minimise stress
38
Basal plasma insulin concentration what used for how to perform and when highly likely
Diagnosis of equine metabolic syndrome
○ Fasting no longer recommended - just low sugar hay
§ (can induce ID)
○ Try to limit dietary influences (no grain 4-5 hours prior)
○ Reference range will vary depending on lab and type of assay used
§ Generally ID suspected if 20-50 μIU/ml
§ Highly likely if >50 μIU/ml
39
Oral glucose tolerance test/oral sugar test what used for, what does it measure, how to perform
Diagnosis of equine metabolic syndrome - most common
○ Bodies insulin response to glucose - different to glucose absorption in gut test
○ Overnight fasting
○ Baseline blood sample in morning
○ Horse given small meal (low sugar feed e.g. chaff) with 1 g/kg dextrose powder
○ Blood collected again 2 hours later for insulin concentration
40
Oral sugar test what used for and how to perform
Diagnosis of equine metabolic syndrome
○ Fast at least 3 hours, not >12 hours
a. Baseline blood sample
b. Karo light syrup 0.15 ml/kg PO (dosing syringe) - not as commonly found in AUS
c. Blood sample again at 60 and 90 minutes
○ Insulin > 45 μIU/ml at 60 or 90 minutes suggests ID
41
Insulin tolerance test what used for, what tests and how to perform and what is consistent
Diagnosis of equine metabolic syndrome
ooking at tissue uptake of glucose
○ No prior fasting –feed hay/pasture (not grain)
a. Baseline blood sample
b. 0.1 IU/kg regular insulin
c. Blood sample at 30 minutes for GLUCOSE
§ FEED IMMEDIATELY AFTERWARDS - be careful that don't make hypoglycaemic
○ <50% reduction from baseline consistent with insulin resistance
42
What additional testing may need to be performed on a horse with equine metabolic syndrome
concurrent testing for PPID
- Consider especially in older horses
- Endogenous ACTH
- (TRH stim test –not concurrently with dynamic tests for ID)
43
What is involved in the management of equine metabolic syndrome
- Assess factors present that can be modified
○ High sugar diet
○ Inadequate exercise
○ Obesity
○ Concurrent PPID
1) Weight loss- Dietary modification and excercise (hard if laminitis present)
2) treat concurrent PPID if needed - pergolide
3) medical treatment
44
What dietary modification is needed for the management of a mildy affected equine metabolic syndrome case
```
□ Lower energy intake
□ Many are overfed → remove grain
® Low CHO feed if necessary
□ Limit pasture access
® Restrict to small paddock
® Grazing muzzle - reduce the massive glucose absorption at once
® Short periods (i.e. 1 hour) of turnout
□ Grazing at night/early morning (except after frost)
® Lower sugar content in grass
□ Get hay analysed, can be high sugar
® <10% (DM) NSC ideal
```
45
What dietary modification is needed for the management of a moderate-severely affected equine metabolic syndrome case
□ Remove from pasture entirely
® Adjust once EMS controlled
□ Soak hay (1-2 hours) - not too long for nutrient leakage
□ Reduce hay fed if removal from grain and pasture doesn’t help
® Start at 1.5% bodyweight (to maintain need 2%) - therefore reduce body weight
® ↓ to 1% (minimum recommended) if no weight loss in 4 weeks
46
What medical treatment is used to control equine metabolic syndrome
```
○ MANAGEMENT FACTORS ARE MOST IMPORTANT - just can add the medical treatment
○ Metformin
§ 15-30 mg/kg PO BID
§ Poorly bioavailable
§ Blunts insulin response
○ Levothyroxine?
§ Assist with weight loss
§ Not available in Australia
```
47
Hyperlipidaemia and hyperlipaemia define and which can lead to hepatic lipidosis
```
Hyperlipidaemia
- Increase in triglycerides
○ Usually < 500 mg/dLor 5.5 mmol/L
- No gross lipaemia
- No hepatic lipidosis
Hyperlipaemia
- Increase in triglycerides
○ Usually > 500 mg/dLor 5.5 mmol/L
- Gross lipaemia
- May lead to hepatic lipidosis
```
48
What is the pathophysiology of hyperlipaemia and hepatic lipidosis
- Induced by period of inappetence/anorexia due to a primary disease process (or lack of access to feed
- MAJOR Negative energy balance and mobilisation of fat stores
- Exacerbated if
○ Pregnant/early lactation
○ Overweight/obese –ponies and donkeys
- Hepatic lipidosis→ inappetance→ propagation of disease process
49
Hepatic lipidosis what occurs, what may lead to
- Deposition of triglycerides within hepatocytes
- May lead to → hepatic rupture
- Fatty infiltrate into other organs
○ Kidney
○ Adrenals
○ Heart
○ Skeletal muscle
50
What are the 4 main ways to diagnose hepatic lipidosis
1) Signalment& history
2) Plasma triglyceride concentration
○ Consider treatment when TGs > 1.1 mmol/L (100 mg/dL)
3) Biochemistry
○ GGT, SDH, bile acids, bilirubin, ammonia
§ Not always evidence of hepatic impairment
○ Check for azotaemia
§ Impedes lipid removal from blood (inhibits LPL (lipoprotein lipase))
4) Ultrasound (liver)
51
What are the 4 main aims for treatment of hyperlipaemia/hepatic lipidosis
○ Treat primary disease
○ Reduce fat in liver
○ Increase formation of VLDLs -> so then can be taken up into the tissues and out of the blood
○ Reverse negative energy balance
52
Treatment for hyperlipaemia/hepatic lipidosis what are the 2 main things and thing within
```
1) reduce negative energy balance
○ Nutritional support
○ Termination of pregnancy
§ Foals usually don’t do well if labour induced/early c-section
§ Value of fetus vs. mare/jenny
○ Termination of lactation
§ Alternative milk source for foal
2) Pharmacological treatment
- insulin and heparin
```
53
what is involved in nutritional support for treatment of hyperlipaemia/hepatic lipidosis
○ Enteral feeding
§ Feed slurry administered via NGT
§ Need functional gastrointestinal tract
○ Glucose in IV fluids
§ Will not be able to meet total energy requirements
500 kg horse requires ~ 67,000 kJ/day maintenance
Glucose provides ~ 17 kJ/gram
Start at 2.5-5% at maintenance fluid rate of 1 L/hour= 25-50 g/hour = 600-1200 g/day
x 17 kJ = 10,200-20,400 kJ/day
Increase to 10% if will tolerate = 40,800 kJ/day - may not due to insulin dysregulation
□ Monitor blood glucose
○ TPN (total parenteral nutrition)
§ Usually cost-prohibitive in adult horses
54
What are the 2 main pharmacological treatment for hyperlipaemia and hepatic lipidosis and why do they work
```
1) Insulin
§ Promotes lipoprotein lipase activity
□ Increases TG uptake into adipocytes
§ Inhibits hormone sensitive lipase
□ Decreases release of FFAs/NEFAs from body stores
2) Heparin?
§ Increases lipoprotein lipase activity
```
55
What are the 3 main principles with hepatic lipidosis
- Reduce treatment as appetite improves and triglycerides return to normal
- Appropriate course of weight loss once stable and primary disease resolved
- Severe lipid accumulation in the liver is hard to reverse, often the prognosis is poor at this stage.
56
Re-feeding syndrome when/ why occurs and what is important
- Horses in very poor body condition that suddenly get fed too much
○ Inadequate nutrition (rescue cases)
○ Poor dentition
○ Severe parasitic disease
○ Other causes of weight loss...
- Important to determine the cause of weight loss
○ Parasitic disease, poor dentition, not enough nutrients, competition
57
Starving horses clinical signs and pathogenesis
Clinical signs
- Dull demeanour, low head carriage, minimal/no interaction with other horses
○ Energy conserved as much as possible
- Prominent skeleton, head appears disproportionately large for body
Pathogenesis
- Once deprived of adequate calories, first use fat stores, then protein (from muscle) for energy
- Take 60-90 days to become recumbent after failure to meet energy requirements
- After 36-48 hours of recumbency, unable to lift head, seizure-like activity
58
Starving horses clinpath findings and prognosis
```
Clinpath findings
- Anaemia
- Lymphopenia
- ↓ TP, albumin, phosphate, magnesium, BUN
- ↑ triglycerides (then low as no fat to mobilise), bilirubin, NEFA
Prognosis poor if
- Recumbent (esp. > 72 hours)
- Lost > 50% bodyweight
```
59
re-feeding syndrome what is the general situation and the main issue
- Syndrome of sudden nutrient provision after a period of malnutrition
○ Metabolic and electrolyte derangements
- Classically “rescue horses” being fed by new owners with lack knowledge
- Can be life threatening
60
When are horses mainly at risk for re-feeding syndrome
Horses at risk if:
- BCS of less than 3.5/9 and an unknown dietary history
- Fasted for greater than 5 –10 days regardless of body condition score
- Lost greater than 10% of their body weight over less than a 2 month period
- Hepatic lipidosis
61
re-feeding protocol in order to prevent re-feeding syndrome in starving horses, what monitoring is needed
- Lucerne hay (high protein, P and Mg)
○ Start at 25-30% of maintenance energy requirements for current bodyweight divided into 6 feeds/day
○ Build up to 100% maintenance energy requirements for current bodyweight over 2-3 days (4-6 feeds/day)
○ Gradually increase to maintenance energy requirements for ideal bodyweight over 7-10 days (4-6 feeds/day)
○ Gradually decrease frequency of feeding and increase amount fed at each feed (2-3 feeds/day)
62
What is involved in monitoring re-feeding starving horses to ensure don't get re-feeding syndrome
- Monitoring
Physical exam and monitor blood glucose, P, Mg, Ca, K every 1-2 days for first 7-10 days
- May require IV fluids to correct electrolyte derangements
- If very severe may require feeding via NGT (lucerne slurry)
63
Starving horses what other issues need to consider
- Other important issues for neglected horses
○ Hoof trimming
○ Teeth
○ FEC and de-worming
- Ensure horse doing well after 2-3 weeks of re-feeding before further stressing with these procedures
64
What are typical complaints for poor performance in race and general sport horses
- Racehorses
○ Performed below expectations, "faded" in final stages of race, slow to recover after race, jockey compliant "not quite right"
- Sport horses
○ Lack of willingness to go forward, lack of power, shortened stride, stiffness, changed quality of canter, not handling correct lead limb, refusing jumps, altered behaviour
65
What history questions do you ask specially for poor performance
- Does the horse have proven ability
- Is inadequate fitness possible
- Could overtraining be possible
- May point to specific body systems
○ Complaints with movement - musculoskeletal
○ Abnormal respiratory noise - upper respiratory
66
When does a immediate post-excercise vet check get performed and what is involved
- Requested by officials/stewards for PP horses
- Horse is still recovering from exercise-need to know normal recovery parameters
1. Brief inspection - EIPH? Injuries?, wounds? Level of fatigue, heat stress, increase temp, increase RR, behaviour
2. Auscultation - HR recovery, arrhythmia, murmur
3. Brief palpation limbs and saddle area
4. Trot out in hand
5. Endoscopy (not always available)
- May not have evidence until horse cools down
67
What are the 9 steps in a detailed examination of a poor performing horse
1. Detailed clinical exam
○ Auscultate heart, lungs (and with rebreathing bag)
○ Ensure no oral problems, vision okay and no ataxia
2. CBC and biochemistry panel
3. +/- pre- and post-exercise muscle enzyme
4. Lameness examination
○ Detailed visual and palpation assessment, walk, straight trot in-hand, lunge (trot, canter, transitions between gaits) +/- ridden
5. Endoscopy - resting +/- exercising
6. +/- tracheal wash, BAL
7. +/- ECG-resting, during exercise; echocardiogram-resting, 'stress', cardiac troponin enzyme
8. +/- gastroscopy
9. +/- exercise testing (treadmill or in the field)
68
What area is the most common cause of poor performance, what doesn't preclude as a cause and what else is common
MUSCULOSKELETAL SYSTEM - most common cause of PP (poor performance)
- Trainer's or rider's inability to detect lameness doesn't preclude it as a cause of PP
- Absence of overt lameness doesn't preclude a MS problem or lameness when ridden
- Often several MS problems coexist - small airway disease as well
Combinations of MS problems and medical problems are also common
69
Investigation of mucsculoskeletal system as a cause of poor performance what are important principles
- Challenging and often time consuming
- Often lame in multiple limbs rather than overt lameness seen in hand trot +/- TLS pain
- Crucial role of diagnostic analgesia to determine source of MS pain
- Challenging to determine whether PP is pain related - course of PBZ can be useful but be aware of potential placebo effect
○ Thoracolumbar pain doesn't always respond to analgesics
70
In terms of investigation of the musculoskeletal system as a cause of poor performance what are the 4 main ways
1) diagnostic anaglesia - crucial
2) objective gait assessment - inertial measure units (use sensors, give objective giat assessment on symmetrical movement)
3) follow with diagnostic imaging the area
4) serum muscle enzyme levels before and after excercise
71
How does diagnostic imaging and serum muscle enzyme levels help with the investigation of the musculoskeletal system
3. Follow with diagnostic imaging the area
○ Very sensitive to alterations in bone turnover
○ Some muscle problems also evident
○ IRU (hot spots) not necessarily synonymous with pain and lameness
○ Very useful but not a substitute for thorough clinical assessment and diagnostic anaglesia
4. Serum muscle enzyme levels before and after exercise
○ +/- muscle biopsy and genetic tests
○ As a few horses have chronic RER and some of these have polysaccharide storage myopathy
○ May not have typical clinical signs
○ AST persistently increased and CK increases with exercise
72
Thoracolumbarosacral region lesions leading to poor performance what could be the cause, how to asses/diagnose
- Problems can be primary, but most often secondary or co-existing (horses adapt to lameness by stiffening this region)
- Palpation and assessment of spinal movement
- Imaging-radiograph (limited), US, scintigraphy
- Diagnostic analgesia important to determine significance
73
What is involved in the management and prognosis of musculoskeletal issues leading to poor performance
- Required accurate diagnosis
- Successful rehabilitation required a team approach-rider, trainer, veterinarian, farrier, nutritionist, physiotherapist or chiropractor, saddle fitter
- Prognosis depends on many factors - conformation, chronicity, concurrent problems
- Just as in man, horses show varying willingness and ability to perform with some MS pain
74
Respiratory system leading to poor performance why lead to and main causes
- Important cause of PP
- Reduced oxygen delivery and gas exchange
- URT obstruction during exercise (+/- abnormal noise)
- Lower airway disease - IAD, RAO, EIPH
+/- slow recovery after work, +/- cough
75
Cardiovascular disease how common in causing poor performance, what are the most common causes and diagnosis
```
- Less common than MS and respiratory disease
○ Arrhythmias most common
§ Persistent or paroxysmal
§ Exercise intolerance, poor recovery
○ Abnormal flow within the heart
§ Murmur-valve/structural abnormalities
○ Myocardial disease
- Auscultation resting, post exercise
- Resting ECG and echo
- Exercising ECG and stress echo
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76
Lack of fitness as a cause of poor performance what tests can be used to test the fitness
- Monitor fitness of horse overtime
- May help detect subclinical disease or overtraining
- Exercise test must be specific to discipline, sufficient duration and intensity, incremental steps with blood collection during brief stops
- HR recovery often used by trainers
- HR vs speed (HR monitor or ECG-telemetry and GPS) - also give incline, distance - determine V200
- Blood lactate vs speed (determine VLa4 - velocity of the horse when lactate is at 4)
77
What occurs in terms of training adaption
- Improved capillarisation, oxidative capacity and ability to store and utilise substrates, changes in fibre type composition
- Improved muscle adaptation
- Maintain respiratory capacity
- Increase O2 transport capacity
- Increase CO
- CVS - increase heart size, stroke volume and blood volume - no change in HR (max)
○ HR during exercise 7 x resting
- Adapt musculoskeletal system
- Increase VO2 max (volumes of oxygen in mls/minute that can be used for
○ Depends on: pulmonary diffusion capacity, o2 carrying capacity of blood, muscle diffusion capacity, capillary density in muscle, mitochondrial enzymes
○ 4 major components - respiratory, cardiac, blood and muscle
○ HORSE IS TWICE THE HUMAN ATHLETE
- Improve thermoregulation
78
what is the main muscle adaptation with training
- VO2max can increase by 25%
○ Improvement of oxidative capacity: on type I and IIA fibres
○ Improvement of anaerobic capacity: type II fibres
- Aerobic capacity - can measure VO2max but difficult in the field with very high flow rates in horses, equipment not readily available
79
What is important to remember when measuring HR during excercise and what 8 things that can effect HR
- Linear relationship between HR and VO2
○ Speed at which HRmax is reached is correlated with speed at which VO2max is reached
Beware of factors that can effect HR
1. Lameness or other painful condition
2. Dehydration
3. Exercise conducted in hot or hot and humid conditions
4. Loss of fitness (detraining or inappropriate training or overtraining)
5. Respiratory disease
6. Cardiovascular disease or anaemia
7. Increased body mass, or a greater percentage of bodyweight as fat or water
8. Physiologically inferior horse
Best to compare measurements in the same individual overtime - TRENDS OVERTIME
80
VLa4 what is it an indicator of, how measured and what used for
used for fitness testing
Vla4 - an indicator of aerobic capacity
- Blood samples are taken during incremental exercise test, after each speed step
81
overtraining as a cause of poor performance how to diagnose
- Difficult to diagnose
- No specific testing
- Either doing too much or not having enough recover
○ Can be both
82
Overheating as a cause of poor performance what are the 2 main causes
heat stress and anhydrosis"
83
Heat loss during excercise where and what occurs
- Normally during exercise 70-80% of energy is lost as heat, mostly by sweating
- Normally during exercise increase by 1-2 degrees
- Yet if increase to 41-42 can limit performance, cause tissue damage, effect brain function, cause death
84
Heat stress what is it and clinical signs
- Environmental temperature and humidity important
- Increase risk if recently moved from a cooler climate, local horse not yet adapted to warmer/more humid conditions, dehydrated, larger horses, overweight horses, darker colour, inadequate fitness
Range of signs - can rapidly progress
- Know the signs as may be unsafe to take temp - may lash out with hindlegs and become ataxia
- Increase HR (125-150/min 10-15min after exercise) - should be down to 90-120
- Increase RR (panting 120-140/min), flared nostrils - should be down to 60
- Slower than normal recovery mentation normal -> irritable, uncooperative, kicking out, head shaking, gait changes -> incoordination disorientation -> seizure, coma and death
85
heat stress prevention and management and what not to do
- Acclimatization to conditions, clipping hair coat
- Cold hosing, ice-keep scraping off and repeating - want to evaporate the heat
- Fans or breeze, shade
- If behavioural signs - sedation (Detomidine)
- Fluids
- NOT PLACING WET TOWELS ON THE HORSE
○ Film of water heats up quickly (acts as a thermal layer)
86
Anhydrosis what is it, when occur and what can lead to
( dry coat, puffs)
- Partial or total loss of ability to sweat - sweat glands stop working
- Can occur if moved from temperature to hot humid climate or in horse native to hot country
○ Kept in airconditioned stables in areas like this
- Cause PP and can lead to serious hyperthermia
87
Anhydrosis signs and diagnosis
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Signs
- Gradual or sudden onset
- Increase HR and temperature
- Panting and nostril flare at rest
- Patchy dry coat after exercise
- Flakey/scurfy skin (forehead)
- Hair loss (face, chest) over time
Diagnosis
- Sweat test - terbutaline intradermal injections - little or no response is abnormal
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88
Anhydrosis management
- Move to a cooler climate is the only curative solution
○ Partial remission in winter
○ Full remission possible if remove from climate early
○ Keep valuable athletic horses in air conditioning
- Diet - reduce grain/protein
- No strenuous exercise especially in heat
- Ensure well hydrated
89
What are the 5 main cardiac diagnostic tests and when use
1. Echocardiography - most indicated when have a murmur
2. ECG - more important for arrythmias
○ Single time point
○ Continuous monitoring
§ Exercising ECG - can be better in field (able to replicate what normally occurs) can also do on treadmills (better for comparison over time)
§ 24 hour Holter
Use both 1 and 2 commonly in racehorses
3. Cardiac troponin I (CTnI) - marker of myocardial damage
○ Quick and easy blood test
4. Electrolytes, blood gas
○ Fractional excretion of electrolytes
5. Treadmill exam
Multiple testing at the same time - dynamic respiratory scoping and ECG at the same time
90
Does every equine athlete with abnormal cardiac ausculatation need referral? 3 main times referral is indicated and when do these situations arise (specific)
- Does every equine athlete with abnormal cardiac auscultation need referral? -NO
- Referral indicated when:
○ Pre-purchase exam
○ Complex diagnostics are required
○ Management may be complicated
- These situations arise when:
○ Pathologic arrhythmia diagnosed
○ Murmurs become louder on serial auscultations - suggests progression
○ Mitral or aortic murmur ≥ grade 3/6
○ Tricuspid murmur grade ≥ 4/6 (can be normal under this grade)
○ VSD or other congenital heart lesion suspected
○ Continuous or multiple murmurs auscultated
○ Myocardial injury/damage suspected
91
Murmurs what caused by and what 4 things result of this, is intensity indicator of lesions severity
- Caused by turbulent blood flow
○ Physiologic (flow) murmurs -
○ Valvular insufficiency - most common
§ Effect of mild-moderate murmurs on performance uncertain
§ Can have >1 valve affected
○ Valvular stenosis (very rare)
§ Relative pulmonic stenosis occurs with VSD
○ Congenital cardiac defect e.g. VSD
- Intensity of murmur not reliable indicator of lesion severity
92
What are the 4 ways to describe a murmur
1) grade 1-6
2) systolic/diastolic
○ Systolic between S1-S2
○ Diastolic between S2-S1
3) Holo-or pan-systolic/diastolic
4) location/point of maximal intensity
93
What is the grade 1-6 scale fr cardiac murmurs
1. Just detectable after prolonged auscultation; very localised
2. Quite localised murmur that is heard immediately once the stethoscope is placed over the point of maximum intensity
3. Moderately loud; easily heard
4. Loud murmur heard over a wide area with no palpable thrill
5. Very loud murmur with an associated precordial thrill
6. Very loud murmur with thrill; may be heard with stethoscope just off the skin surface
94
What is the difference with pan-systolic, holo-systolic and holo-diastolic murmurs
○ Pan-systolic - murmur begins with or replaces S1, continues through systole and ends beyond S2
○ Holo-systolic - murmur begins at the end of S1 and continues to the start of S2
○ Holo-diastolic - murmur begins at the end of S2 and continues to the start of S1
95
Valvular heart disease how affects performance, what most commonly affected and how to diagnose
- Usually acquired, causes insufficiency
- Valvular regurgitation reduces CO (via ↓ SV) - HOW AFFECTS PERFORMANCE
- Mitral and aortic valves most commonly affected (degeneration)
- After murmur has been auscultated, echocardiography is most useful for diagnosing valvular disease
○ Colour flow doppler
- Usually no clinical signs, only auscult able murmur
○ Degenerative valvular disease often progresses slowly
96
Valvular heart disease what problems can arise with the valves and how can this lead to arrhythmias
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- Problems with valves...
○ Degeneration
○ Cardiac chamber enlargement
○ Prolapse
○ Ruptured chordaetendinae - relatively rare
○ Flail leaflets - mitral and tricuspid
○ Fenestrations
○ Vegetative lesions
- Chamber enlargement can lead to arrhythmias
○ Especially A fib
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97
Left-sided murmurs what valves involved, what issue if systolic or diastolic murmur and other murmur
- Mitral, aortic or pulmonic (Rare) valves
○ PMI
- Systolic or diastolic? –valvular insufficiency
○ Mitral = systolic
○ Aortic and pulmonic= diastolic (pulmonic rare)
- (Systolic pulmonic murmur accompanying VSD)
○ Relative stenosis
98
Right-sided murmur what are the 2 types and diastolic or systolic
- Tricuspid regurgitation
○ Systolic
- VSD
○ Systolic
99
Mitral vale insufficiency how common, what murmur create, performance, what can see on cardio and function of heart
Most common cause of CHF in horses - rare anyway though
○ Murmur (systolic) PMI L heart apex, may radiate dorsally towards aortic valve
§ S3 may be pronounced if severe - usually S1 systolic murmur
○ Usually mild, normal performance
○ Increased LA and LV chamber size reflect severity of regurgitation
§ L-sided volume overload
§ Enlarged LA increases risk of A fib
○ LV function
§ Normal
§ Increased fractional shortening
100
Mitral valve insufficiency what monitoring horse for and worse case scenario
Monitoring
§ Exercising ECG –assess HR and response to exercise
§ Monitor horse for progression
§ Monitor horse for development of A fib
Worse case - Chordae tendinae rupture →acute onset L-sided CHF (rare) but poor prognosis
