Approach to Laminitic Horse Flashcards
what are the acute clinical signs of laminitis (10)
- reluctant to move
- characteristic stance & gait (difficulty getting up)
- pulse >50-70/min
- often pyrexic
- digital pulses bounding
- increased sensitivity to hooftester
- painful to coronary pressure
- may be unable to pick up feet
- gas colic
- hypermotile bowel often present
what are important history points to be concerned about with laminitis (5)
- feeding/grazing history
- number of laminitic episodes
- duration of current episode
- medications: before/after onset
- recent/concurrent disease (infectious, orthopaedic, metabolic/endocrine –> PPID, EMS)
what should your physical exam include in laminitic patients (7)
- stance
- foot/hoof conformation
- lameness grade
- obel laminitis grade
- digital pulses
- palpation of coronary band
- evidence of concurrent disease
what is the obel laminitis grading scheme
grade 1: frequent lifting of feet
grade 2: willing to walk, laminitic gait, can lift forefoot without difficulty
grade 3: vigorously resists lifting of forefoot, moves reluctantly
grade 4: must be forced to move +/- recumbent
what should you note about the digital pulses in laminitis
the pulse rate, quality
often bounding with laminitis
where is the digital pulse found
palmar/plantar arteries
what should you observe about the coronary band when examining a laminitic horse
check if there is depression of the coronary band which would indicate sinking of the P3
negative prognostic indicator
how would you investigate acute laminitis (4)
- hematology/biochem
- radiographs
- search for underlying disease
- pasture/feed assessment
how would you investigate a chronic/recurrent laminitis (5)
- hematology/biochem
- blood insulin
- testing for PPID
- testing for EMS
- radiography
what is the signalment of cushing’s disease
common in elderly animals
what is the main cause of cushing’s
pituitary adenoma
what is the pathogenesis of PPID
hyperadrenocorticism
increased secretion of other pituitary peptides
physical compressive effect of adenoma
how do the pituitary and hypothalamus interact
Hypothalamus releases corticotropin releasing hormone which stimulates the pituitary to release:
ACTH
Major POMC products
MSH
CLIP
B-endorphin
ACTH causes the adrenal gland to produce cortisol
Cortisol has a negative feedback on the pituitary gland and hypothalamus
what are the clinical features of PPID (13)
- hair coat changes: retention of winter coat, altered shedding pattern
- weight loss
- changed demeanour & lethargy
- laminitis
- PUPD
- hyperhidrosis
- hirsutism/hypertrichosis
- altered fat deposition: bulging supraorbital fat pads
- tachypnea
- immunosuppression: chronic resp infections, sinusitis, increased parasitism
- neurological signs (intermittent collapse)
- non healing mouth wounds
- chronic bacterial dermatitis
how is PPID diagnosed (5)
- signalment & history: >12y
- clinical signs
- plasma endogenous ACTH or dynamic ACTH response
- characteristic hematology and biochem changes
- altered dynamic insulin response (secondary insulin resistance)
how is the plasma ACTH concentration determined to diagnose PPID
Resting assessment of plasma ACTH
Plastic EDTA tube — spin down sample — chill assay as soon as possible
May be affected by concurrent severe pain
Seasonal fluctuation, with corrected reference range
There would be a persistent increase
how is ACTH measured post TRH stimulation to diagnose PPID
Useful when basal measurement equivocal
Time zero, basal sample
TRH 1mg intravenously
Resample for ACTH measurement after 10 mins
how is the dexamethasone suppression test used to diagnosed PPID
Cortisol production NOT suppressed following dexamethasone administration in PPID cases
Risk of inducing laminitis
Test performed less regular
why is the ACTH stimulation test not useful to diagnose PPID
Basal cortisol is variable
how is PPID treated
Dopamine agonist is most effective treatment
Pergolide (Prascend) starting at 1-4 ug/kg once daily
Lifelong therapy required; dose increase may be required
Management of multiple other conditions required
Laminitis, hirsutism, sweating and electrolyte loss, body condition
Assess response to treatment via clinical improvement & ACTH concentration
how is PPID prevented in predisposed animals
- Have high index of suspicion: particularly if >10 years old with laminitis, even if phenotype is not typical
- Confirm diagnosis
- Assess for concurrent insulin resistance
- Reassess for ACTH after initially starting pergolide
- Re-evaluate at least every 6 months
- Re-measure ACTH: ideally CBC, glucose, insulin and electrolytes
- Dental
- Weight/condition check and FEC
what are the forces that are in the hoof (4)
- DDFT pulls the pedal bone down (if there is a low heel, or if heel is too short)
- Shearing force from the toe as the hoof breaks over —> if toe is long the shearing forces will be increased
- Friction between the ground and the solar surface of the hoof capsule
- Adhesion force between sensitive and insensitive laminae which oppose the shearing force of the toes
where should weight bearing occur in the hoof
Weight bearing should be on the caudal 2/3 of the foot to minimize pressure over the toe and stop the shearing forces
what is the hoof made up of
modified epidermus
what is the blood supply to the hoof
dermal corium with vascular matrix –> attaches to P3
how do the germinal epidermal basal cells attach to basement membrane cells
via collagen/glycoprotein matrix
how do the primary and secondary lamellae align
at right angles
what is the hoof wall composed of (3)
- stratum internum
- stratum medium
- stratum externum
what is the stratum basale
single layer proliferating columnar keratinocytes
lie on and between long dermal papillae
proliferation forces cells toward or at the distal end or part into stratum medium
what does the stratum internum contain
epidermal lamellae interleave with dermal lamellae (500-600)
secondary lamellae (150-200)
what does the stratum medium contain
horn tubules and intertubular horn
provides strength in every direction
what does the stratum externum contain
thin from perioplic region
what is shown here
normal histological finding of the hoof
secondary epidermal lamellae
primary epidermal lamellae
what is shown here
Secondary lamellae become damaged, inflamed and necrotic
Primary lamellae also become damaged
the two start to separate
how does the induction/activation of matrix metalloproteinases occur
Inflammatory challenge there will be upregulation and activation of enzymes that breakdown the protein matrix between the epidermal and dermal lamellae
Endotoxin absorption (ex colitis, metritis)
Bacterial factors that release vasoactive factors that cause vasoconstriction/ischemia/RI —> produces oxygen free radicals
Cells of the vascular endothelium are sensitive to loss of glucose —> insulin resistance causes decreased uptake of glucose and causes a relative hypoglycemia —> inflammatory challenge
what damages the lamellae
inflammation
Appears central to pathogenesis
Evidence of:
Increased pro-inflammatory cytokines
Decreased anti-inflammatory cytokines
WBC infiltration
Increased COX-2 upregulation
what are the phases of laminitis
how is acute laminitis treated (5)
- reduce further absorption in CHO
- reduce stress on laminae
- pain relief
- analgesia
- cyrotherapy
how would you reduce the stress on laminae in acute laminitis (4)
- remove shoes
- deep supportive bedding
- small box confinement
- even weight bearing/heel support
what analgesic options can you use to treat acute laminitis (6)
- NSAIDs
- paracetamol
- aspirin
- acepromazine
- buprenorphine
- gabapentin
what NSAIDs can you use to treat acute laminitis (3)
- ketoprofen 2.2mg/kg (up to 4x daily)
- flunixin meglumine
- phenylbutazone 2.2-4.4 mg/kg BID
why is aspirin useful analgesic in acute laminitis
reduced platelet aggregation
particularly in hypercoagulable conditions
17-21mg/kg once q48h
what are the benefits of acepromazine in acute laminitis
no effect on digital bloodflow but reduced relapse rate in recent BEVA study
encourages horse to lie down which is beneficial
what are the downsides to using buprenorphine as an analgesic
may cause box walking
must be administered with sedation
when might gabapentin be useful in laminitis
may be helpful in chronic laminitis (neuropathic pain)
what does cryotherapy do in laminitis
reduces digital metabolic rate
decreases glucose requirement
decreases matrix metalloproteinases
decreased pro-inflammation cytokine production
decreases neutrophil influx
what would be hospital setting analgesic treatment of acute laminitis include
- morphine 0.1 mg/kg IM every 4 hours + acepromazine 0.011-0.022 mg/kg IM with morphine
or
- lignocaine (3mg/kg/h) + morphine (0.025 mg/kg/h) as constant rate infusion + acepromazine IM –> decreased leukocyte activation with lignocaine
what are the key ingredients that need to be restricted in a laminitic diet
- starch in grains
- fructans in pastures
describe the changes shown here
remodelling at tip of P3
founder distance: tip of the extensor process to the coronary band
gas shadow: separation of sensitive and non-sensitive lamina
thin sole
large heel, not weight bearing
what is the founder distance
verticle distance between coronary band and P3 extensor process
how should the hoof be trimmed to aid in laminitis treated
hoof capsule relaigned to P3
frog support
reduce breakover point
toe to be shortened and heel to be lowered to minimize the shearing forces on the dorsal laminae and the pulling forces on P3
provide support to equalize the pressure
how should a heart bar shoe be placed
front part of the shoe needs to come just beyond the centre of gravity of the foot, if its too far forward it can cause pressure on P3
how do you treat chronic laminitis
farrier: delay until foot is less painful and pedal bone stable
when has acute phase passed? pain, rads
heel support: reduce effect of DDFT
unload toe –> reduce tearing of laminae (reduce formation of hyperplastic lamellar wedge)
how long should exercise be restricted
box rest on deep bed for 6 weeks after free from clinical signs
in hand walk out for 5 min 2x daily once imrpoved
unexplained relapses frequently seen at 8 weeks
several weeks for normal stability to return
cycle of laminitis flare-ups
