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Y4 Equine - Lameness & Orthopaedics > Laminitis > Flashcards

Laminitis Flashcards

1
Q

Definition

A
  • inflammation of the laminae of the foot
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2
Q

Founder

A
  • laminitis so severe that all the laminae in the hoof cease functioning and the pedal bone has dropped down
    BUT
  • term used interchangeably with laminitis
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3
Q

What is the weight bearing structure of the hoof?

A
  • the hoof wall
  • (the frog takes some of it)
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4
Q

What are the 2 types of laminae in the hoof

A
  • sensitive laminae (attached to the coffin bone)
  • insensitive laminae (attached to the hoof wall)
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5
Q

Pathophysiology

A
  • dermal lamellae (P3) and epidermal lamellae (hoof) are strongly bonded
  • to allow hoof growth this bond is released slightly via the action of matrix metalloproteinase (MMP)
  • MMP are catabolic enzymes
  • laminitis is the degeneration then failure of interdigitation between P3 and inside of hoof wall -> breakdown & separation
  • excess MMP activity is involved
  • mechanisms not fully understood but several dz processes are implication
  • sliding scale of severity (not a binary dz)
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6
Q

Where does hoof wall grow from?

A
  • the coronary band
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7
Q

How long does it take the hoof wall to grow from the coronary band to the sole?

A
  • 6m
  • less (~4m) for the palmar/plantar aspect
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8
Q

Endocrine causes

A
  • EMS
  • PPID
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9
Q

Non-endocrine causes

A
  • toxic
  • support limb laminitis
  • corticosteroid induced
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10
Q

Obesity/EMS causing laminitis

A
  • increased bodily fat reduces the cellular response to insulin -> insulin resistance/dysregulation
  • cells remove less glucose from bloodstream ->hyperglycaemia
  • body produces more insulin to try to combat the hyperglycaemia (negative feedback loop) -> hyperinsulinaemia
  • excess insulin in bloodstream stimulates excess MMP production increasing the risk of laminitis

Probably the most common cause of laminitis

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11
Q

Toxic causes of laminitis

A

concurrent to:
1. compromised bowel e.g. colitis, enteritis, strangulation
2. severe infection e.g. RFM/sepsis

  • bacterial endotoxin enters the bloodstream -> endotoxaemia
  • MMP production is increased
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12
Q

PPID causing laminitis

A
  • excess ACTH also causes hyperinsulinaemia
  • endocrinopathic causes of laminitis are closely interlinked
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13
Q

Support limb laminitis

A
  • severe lameness in 1 limb causes excessive weight bearing in contra-lateral limb, e.g. fracture with inadequate stabilisation
  • prolonged pressure within the hoof of the ‘non-lame’ limb reduces blood flow to the laminae causing hypoxia
  • hypoxia causes inflammation and MMP production
  • therefore, support limb laminitis is often unilateral
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14
Q

Corticosteroid induced laminitis

A
  • exogenous glucocorticoid
    – rare (0.15% in a study)
    – different glucocorticoids have different risks, e.g. preds very low, others (e.g. triamcinolone) much higher
  • stress
    – endogenous glucocorticoids increase
  • induce hyperinsulinaemia and subsequent increased MMP production
  • risk greater in animals that are already susceptible e.g. EMS
  • discuss this risk with O before corticosteroid injection
  • recommend taking blood insulin test before administering corticosteroids (even for asthma) in fat horses
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15
Q

Signalment

A

Age
- no consistent predisposition but foal & weanlings rarely affected (likely bc they’re growing so all their glucose is going into growing, also they’re not old enough for the endocrine disorders)

Breeds
- occurs in all breeds of horse, but natives/ponies predisposed
- donkeys can be severely affected
- the heavier the horse the more difficult it will be to treat, e.g. draughts/shires

Sex
- no predisposition

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16
Q

Incidence in UK

A
  • 1/10 equines may have at least 1 laminitis epidote each year
  • as common as colic
  • approx. 15% equine deaths linked to laminitis
  • year round problem with incidence peaks in spring and autumn
  • most cases are endocrine
    – toxic and support limb less common
17
Q

History q’s

A
  • when did signs begin?
  • progression - getting better or worse?
  • any recent management changes?
  • previous episodes of laminitis?
  • any concurrent dz/injury?
  • received any medications recently?
  • current diet?
  • when last trimmed/shod?
  • horse’s use?
  • exercise history?
18
Q

General CE

A
  • recumbent?
  • stance?
    – leaning backwards
    – weight shifting
  • rr/panting?
  • hr?
  • temp?
  • sweating?
  • pained expression?
19
Q

CE - evidence of endocrinopathy

A

PPID
- hirsutism
- decreased muscle mass
- ‘pot belly’ appearance
- supraorbital fat pads

EMS
- excess body condition
- abnormal fat distribution

20
Q

CE - limb specific

A
  • often affects both front limbs
  • may be all 4 limbs, just 1 or just the hind limbs
  • increased digital pulse
  • hooves warm to touch
  • visible growth rings indicate previous episodes
  • able to life legs?
  • often show pain to hoof testers at point of frog
  • shod/unshod and type of shoe?
  • depression at coronary band and loss of concavity of sole suggest severe dz (sinking)
21
Q

CE - dynamic

A
  • degree of lameness varies
  • may be mild (walks almost normally) to severe (unable to walk)
  • usually worse when turning and on hard ground
  • foot lands heel first to spare the toe region from weight bearing
  • sometimes show a high stepping gait with hind limb laminitis
22
Q

Modified Obel grade 0

A
  • sound
23
Q

Modified Obel grade 1

A
  • weight shifting at rest
  • sound walking in straight line
  • stilted gait when turning or trotting
24
Q

Modified Obel grade 2

A
  • stilted gait when walking in straight line
  • clearly lame when turning
  • legs can be lifted without difficulty
25
Q

Modified Obel grade 3

A
  • reluctant to walk
  • legs can only be lifted with great difficulty
26
Q

Modified Obel grade 4

A
  • will only move if forced to
  • spends long periods recumbent
27
Q

Radiography

A

Latero-medial view
- rotation
– <5° mild
– 5-10° moderate
– >10° severe
- sinking
- remodelling/degeneration at tip of P3?
- hoof overgrowth?

Dorso-palmar view
- rare collapse on just the lateral or medial side

28
Q

Metabolic testing - EMS

A

1) Baseline insulin (serum)
- Feed only hay / grass for 12 hours prior
- Positive result (increased baseline insulin) is diagnostic for EMS
- Negative result (normal baseline insulin) does not rule the disease out – lots of false negatives

2) Oral sugar challenge tests
- Feed only hay / grass for 12 hours prior
- Feed Karo light corn syrup or dextrose powder
- Blood sample for insulin 60-90 mins later

29
Q

Metabolic testing - PPID

A

1) Baseline ACTH (EDTA)
- Usually diagnostic
- Reference range changes through the year
- Usually most accurate in the autumn

2) Thyrotropin Releasing Hormone stimulation test
- Rarely required
- Collect baseline ACTH
- Inject TRH
- Collect another ACTH 10 minutes later

30
Q

Metabolic testing

A

▪ Results are inaccurate if animal is in pain – maybe wait a few days until more comfortable.
▪ Repeat samples are required to assess the response to treatment and adjust management & drug dosages

31
Q

Initial Management

A

▪Pain Relief
- NSAIDs (phenylbutazone), paracetamol, opiates (butorphanol good for short term analgesia)

▪ Vasodilator
- Improve blood supply to distal limbs
- Acepromazine (has additional benefit of reducing anxiety)

▪Support feet
- Confine to stable on deep shavings bed - Remove shoes?
- Use frog supports
- In the per-acute phase (not after 24h) ice packs can help

▪ Diet - Weight loss
- 1.5-2% body weight dry weight hay, soaked for 1 hour to reduce sugar content
- Tiny amount of low sugar food (alfalfa) to put medication in
- Vitamin / mineral balancer

▪ Warn owner that this is not a quick fix
- 3w bost rest minimum to start with

▪ Euthanasia?

32
Q

Subsequent management

A

▪ Regular re-examinations (initially 1x weekly)
▪ Adjust medication & management
accordingly
▪ Endocrine testing once pain reduced
▪ EMS – metformin, levothyroxine, ertugliflozin
▪ PPID – pergolide, cabergoline
▪ Farriery – trim heels & toes, heart bar shoes (good as utilises the frog to reduce weight bearing on the sole)
▪ Carefully and gradually introduce exercise
▪ Repeat radiographs if not improving / as required by farrier
▪ Euthanasia?

33
Q

Salvage procedure

A

▪ Deep digital flexor tenotomy
▪Mid cannon
▪ Removes the palmar traction on P3
▪ Salvage only (some believe)
▪ Only for rotational laminitis
▪ Instantly reduces lameness by 1 Obel grade

34
Q

Prognosis

A

▪ Lameness severity ▪Degree of rotation
▪ Sinking
▪Patient weight
▪ Ability to control endocrine disease
▪ Improvement takes many months
- As the new hoof grows down – 1 year
▪ Repeat episodes are common

Y4 Equine - Lameness & Orthopaedics (34 decks)

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