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Module 17 > Approach to Laminitic Horse > Flashcards

Approach to Laminitic Horse Flashcards

1
Q

what are the acute clinical signs of laminitis (10)

A
  1. reluctant to move
  2. characteristic stance & gait (difficulty getting up)
  3. pulse >50-70/min
  4. often pyrexic
  5. digital pulses bounding
  6. increased sensitivity to hooftester
  7. painful to coronary pressure
  8. may be unable to pick up feet
  9. gas colic
  10. hypermotile bowel often present
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2
Q

what are important history points to be concerned about with laminitis (5)

A
  1. feeding/grazing history
  2. number of laminitic episodes
  3. duration of current episode
  4. medications: before/after onset
  5. recent/concurrent disease (infectious, orthopaedic, metabolic/endocrine –> PPID, EMS)
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3
Q

what should your physical exam include in laminitic patients (7)

A
  1. stance
  2. foot/hoof conformation
  3. lameness grade
  4. obel laminitis grade
  5. digital pulses
  6. palpation of coronary band
  7. evidence of concurrent disease
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4
Q

what is the obel laminitis grading scheme

A

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

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5
Q

what should you note about the digital pulses in laminitis

A

the pulse rate, quality

often bounding with laminitis

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6
Q

where is the digital pulse found

A

palmar/plantar arteries

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7
Q

what should you observe about the coronary band when examining a laminitic horse

A

check if there is depression of the coronary band which would indicate sinking of the P3

negative prognostic indicator

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8
Q

how would you investigate acute laminitis (4)

A
  1. hematology/biochem
  2. radiographs
  3. search for underlying disease
  4. pasture/feed assessment
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9
Q

how would you investigate a chronic/recurrent laminitis (5)

A
  1. hematology/biochem
  2. blood insulin
  3. testing for PPID
  4. testing for EMS
  5. radiography
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10
Q

what is the signalment of cushing’s disease

A

common in elderly animals

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11
Q

what is the main cause of cushing’s

A

pituitary adenoma

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12
Q

what is the pathogenesis of PPID

A

hyperadrenocorticism

increased secretion of other pituitary peptides

physical compressive effect of adenoma

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13
Q

how do the pituitary and hypothalamus interact

A

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

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14
Q

what are the clinical features of PPID (13)

A
  1. hair coat changes: retention of winter coat, altered shedding pattern
  2. weight loss
  3. changed demeanour & lethargy
  4. laminitis
  5. PUPD
  6. hyperhidrosis
  7. hirsutism/hypertrichosis
  8. altered fat deposition: bulging supraorbital fat pads
  9. tachypnea
  10. immunosuppression: chronic resp infections, sinusitis, increased parasitism
  11. neurological signs (intermittent collapse)
  12. non healing mouth wounds
  13. chronic bacterial dermatitis
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15
Q

how is PPID diagnosed (5)

A
  1. signalment & history: >12y
  2. clinical signs
  3. plasma endogenous ACTH or dynamic ACTH response
  4. characteristic hematology and biochem changes
  5. altered dynamic insulin response (secondary insulin resistance)
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16
Q

how is the plasma ACTH concentration determined to diagnose PPID

A

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

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17
Q

how is ACTH measured post TRH stimulation to diagnose PPID

A

Useful when basal measurement equivocal

Time zero, basal sample

TRH 1mg intravenously

Resample for ACTH measurement after 10 mins

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18
Q

how is the dexamethasone suppression test used to diagnosed PPID

A

Cortisol production NOT suppressed following dexamethasone administration in PPID cases

Risk of inducing laminitis

Test performed less regular

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19
Q

why is the ACTH stimulation test not useful to diagnose PPID

A

Basal cortisol is variable

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20
Q

how is PPID treated

A

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

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21
Q

how is PPID prevented in predisposed animals

A
  1. Have high index of suspicion: particularly if >10 years old with laminitis, even if phenotype is not typical
  2. Confirm diagnosis
  3. Assess for concurrent insulin resistance
  4. Reassess for ACTH after initially starting pergolide
  5. Re-evaluate at least every 6 months
  6. Re-measure ACTH: ideally CBC, glucose, insulin and electrolytes
  7. Dental
  8. Weight/condition check and FEC
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22
Q

what are the forces that are in the hoof (4)

A
  1. DDFT pulls the pedal bone down (if there is a low heel, or if heel is too short)
  2. Shearing force from the toe as the hoof breaks over —> if toe is long the shearing forces will be increased
  3. Friction between the ground and the solar surface of the hoof capsule
  4. Adhesion force between sensitive and insensitive laminae which oppose the shearing force of the toes
23
Q

where should weight bearing occur in the hoof

A

Weight bearing should be on the caudal 2/3 of the foot to minimize pressure over the toe and stop the shearing forces

24
Q

what is the hoof made up of

A

modified epidermus

25
Q

what is the blood supply to the hoof

A

dermal corium with vascular matrix –> attaches to P3

26
Q

how do the germinal epidermal basal cells attach to basement membrane cells

A

via collagen/glycoprotein matrix

27
Q

how do the primary and secondary lamellae align

A

at right angles

28
Q

what is the hoof wall composed of (3)

A
  1. stratum internum
  2. stratum medium
  3. stratum externum
29
Q

what is the stratum basale

A

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

30
Q

what does the stratum internum contain

A

epidermal lamellae interleave with dermal lamellae (500-600)

secondary lamellae (150-200)

31
Q

what does the stratum medium contain

A

horn tubules and intertubular horn

provides strength in every direction

32
Q

what does the stratum externum contain

A

thin from perioplic region

33
Q

what is shown here

A

normal histological finding of the hoof

secondary epidermal lamellae

primary epidermal lamellae

34
Q

what is shown here

A

Secondary lamellae become damaged, inflamed and necrotic

Primary lamellae also become damaged

the two start to separate

35
Q

how does the induction/activation of matrix metalloproteinases occur

A

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

36
Q

what damages the lamellae

A

inflammation

Appears central to pathogenesis

Evidence of:

Increased pro-inflammatory cytokines

Decreased anti-inflammatory cytokines

WBC infiltration

Increased COX-2 upregulation

37
Q

what are the phases of laminitis

A
38
Q

how is acute laminitis treated (5)

A
  1. reduce further absorption in CHO
  2. reduce stress on laminae
  3. pain relief
  4. analgesia
  5. cyrotherapy
39
Q

how would you reduce the stress on laminae in acute laminitis (4)

A
  1. remove shoes
  2. deep supportive bedding
  3. small box confinement
  4. even weight bearing/heel support
40
Q

what analgesic options can you use to treat acute laminitis (6)

A
  1. NSAIDs
  2. paracetamol
  3. aspirin
  4. acepromazine
  5. buprenorphine
  6. gabapentin
41
Q

what NSAIDs can you use to treat acute laminitis (3)

A
  1. ketoprofen 2.2mg/kg (up to 4x daily)
  2. flunixin meglumine
  3. phenylbutazone 2.2-4.4 mg/kg BID
42
Q

why is aspirin useful analgesic in acute laminitis

A

reduced platelet aggregation

particularly in hypercoagulable conditions

17-21mg/kg once q48h

43
Q

what are the benefits of acepromazine in acute laminitis

A

no effect on digital bloodflow but reduced relapse rate in recent BEVA study

encourages horse to lie down which is beneficial

44
Q

what are the downsides to using buprenorphine as an analgesic

A

may cause box walking

must be administered with sedation

45
Q

when might gabapentin be useful in laminitis

A

may be helpful in chronic laminitis (neuropathic pain)

46
Q

what does cryotherapy do in laminitis

A

reduces digital metabolic rate

decreases glucose requirement

decreases matrix metalloproteinases

decreased pro-inflammation cytokine production

decreases neutrophil influx

47
Q

what would be hospital setting analgesic treatment of acute laminitis include

A
  1. morphine 0.1 mg/kg IM every 4 hours + acepromazine 0.011-0.022 mg/kg IM with morphine

or

  1. lignocaine (3mg/kg/h) + morphine (0.025 mg/kg/h) as constant rate infusion + acepromazine IM –> decreased leukocyte activation with lignocaine
48
Q

what are the key ingredients that need to be restricted in a laminitic diet

A
  1. starch in grains
  2. fructans in pastures
49
Q

describe the changes shown here

A

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

50
Q

what is the founder distance

A

verticle distance between coronary band and P3 extensor process

51
Q

how should the hoof be trimmed to aid in laminitis treated

A

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

52
Q

how should a heart bar shoe be placed

A

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

53
Q

how do you treat chronic laminitis

A

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)

54
Q

how long should exercise be restricted

A

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

Module 17 (31 decks)

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