Laminitis – Causes and Consequences Flashcards

1
Q

Why is laminitis such an important disease?

A
  • Very common problem in First-opinion practice.
    -Causes huge amount of equine suffering and welfare issues.
  • A considerable drain owner emotions/finance/time
  • A common cause of euthanasia
  • Often (badly) dealt with by owners without (enough) veterinary involvement
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2
Q

Define laminitis

A

Inflammation of the lamellae
“An acute onset lameness of variable severity involving one or more feet”
“the failure of the attachment between the distal phalanx (coffin bone) and the inner hoof wall”

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3
Q

Describe the anatomy of the hoof

A
  • Underneath the horn is the dermis
  • Horn produced by the coronary band
  • Junction between the sensitive and insensitive tissue (area that goes wrong in laminitis)
  • Lamellae = “Thin sheet”
  • About 600 Primary lamellae per hoof
  • About 150 Secondary lamellae per primary lamellae
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4
Q

Describe the anatomy of the sole and describe weight bearing in the hoof

A
  • No lamellae on sole of foot
  • Weight bearing mostly done through lamellae, frog and walls of hoof.
  • So the sole isn’t designed for weight bearing
  • Excessive pressure on solar corium (dermis) tissue = painful
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5
Q

Describe the blood supply in the hoof

A

Foot – very well vascularised.
Aterio-venous shunts present in laminae

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6
Q

Why does the foot need to be well vascularised?

A

Constant supply of glucose needed to keep basement membrane structures intact.
- A single horses’ hoof uses more glucose per day than its brain.
- Glucose uptake in the foot not insulin mediated.

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7
Q

Name some of the modern theories for laminitis

A
  1. Vascular Theory
  2. Endotoxaemic\sepsis\inflammatory theory
  3. Carbohydrate overload theory
  4. Supporting limb laminitis
  5. Mechanical laminitis
  6. Glucose deprivation theory
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8
Q

Name a real and common cause of laminitis

A

Endocrinopathic laminitis

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9
Q

Name 5 real and uncommon causes of laminitis

A

Endotoxic/septic/inflammatory laminitis
Mechanical laminitis
Supporting limb laminitis
Glucocorticosteroid induced laminitis
Carbohydrate overload

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10
Q

What is the vascular theory of laminitis

A

Laminitis caused by alterations in blood flow to digit – leading to tissue hypoxia, ischemia, tissue necrosis, inflammation and ultimately laminar failure

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11
Q

Compare the evidence for and against the vascular laminitis theory

A

For: Vascular changes well proven - both vasoconstriction and vasodilation
Against:
- No consistent pattern of change found
- Histopathological signs of inflammation not always present in pasture associated laminitis.
- What initiates the vascular changes?

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12
Q

What is the endotoxic/sepsis/inflammatory theory of laminitis

A

Laminitis caused by the effects of endotoxins and other inflammatory substances on the foot.

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13
Q

Compare the evidence for and against the endotoxic/sepsis/inflammatory theory of laminitis

A

For: Laminitis well recognised as a potential complication of SIRS/Endotoxemia in horses e.g. retained foetal membranes, colitis, post colic surgery, pleuropneumonia
Against:
- Not every endotoxic horse gets laminitis.
- Most laminitics not endotoxic.
- Injection of endotoxins to horses does not reliably induce laminitis

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14
Q

Describe the supporting limb laminitis theory

A

Horses which are non-weight bearing on one leg often develop laminitis in the contralateral limb

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15
Q

Compare the evidence for and against the supporting limb laminitis theory

A

For: Definitely does occur – in very severe lameness (fractures etc.)
Against:
- Limited to severe lameness: not every lame horse gets laminitis
- Not representative of pasture associated laminitis

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16
Q

Describe the mechanical laminitis theory

A

Any force which physically tears hoof from the laminae is technically laminitis.
Either occurs as a (very) traumatic one-off incident or as a result of chronic forces on an already weakened digit.

17
Q

Compare the evidence for and against the mechanical theory

A

For: Logically can occur. Probably quite common in severe chronic laminitis
Against: Little researched evidence, mostly anecdotal, difficult to prove condition exists

18
Q

Describe the glucocorticoid induced laminitis theory

A

Glucocorticoid administration to horses can cause laminitis.
Long held belief that glucocorticoids practically contra-indicated in horses

19
Q

Compare the evidence for and against the glucocorticoid induced theory

A

For: Well documented evidence that this can occur - even after one-off intra-articular doses.
Against:
- Modern epidemiological studies shown risk is genuine, but actually quite low.
- Deliberately trying to induce laminitis by giving steroids (for research purposes) rarely works
- Using high doses of steroids or using them in animals already predisposed to laminitis likely to increase the risk.
- Oral prednisolone shown to be quite safe.

20
Q

Describe the fructans and carbohydrate overload theory for laminitis

A
  • Mammalian digestive tracts lack the enzymes to digest fructans therefore they spill into the large bowel intact.
  • Bacteria can digest fructans.
  • Fructan overload therefore implicated as the source of pasture-associated laminitis.
21
Q

Fructan level in plants depends on which factors?

A
  • Type of plant, part of plant, growing season, ambient temperature, sunlight levels, “stress” levels
  • Highly variable, can change from hour-to-hour – can’t predict pasture levels.
22
Q

Compare the evidence for and against the the fructans and carbohydrate overload theory for laminitis

A

For:
- Large quantities of oral fructans will reliably induce laminitis in experimental studies.
- Could easily explain pasture-associated laminitis
Against:
- Can horses physically consume enough fructans in a day to cause laminitis ?
Controversial – most experts consider it unlikely, although some disagree.

23
Q

Describe the practical relevance of the fructans and carbohydrate overload theory for laminitis

A
  • Carbohydrate overload is just a form of endotoxic/septic/inflammatory laminitis (since a form of colitis is induced) and does not reflect pasture-associated laminitis.
  • Concept still widespread with horse owners.
  • Lead to use of in-feed antibiotics to prevent hindgut fermentation
24
Q

Name 3 underlying endocrinopathies that can lead to laminitis

A
  • Equine metabolic syndrome
  • Equine pars pituitary intermedia dysfunction
  • EMS and PPID together
25
Q

The chance of an individual suffering from laminitis if it does not have EMS or PPID is …

A

Low

26
Q

Describe equine metabolic syndrome

A

Syndrome obesity, insulin dysregulation and laminitis

27
Q

What is the trigger cause of equine metabolic syndrome related laminitis?

A

Hyperinsulinaemia due to insulin dysregulation

28
Q

How does hyperinsulinaemia lead to laminitis?

A

Sustained hyperinsulinaemia will reliably induce laminitis in normal (non-EMS) horses.
Hyperinsulinaemia damages cytoskeleton of laminar cells and also has vasoactive properties (remember foot glucose metabolism insulin independent).

29
Q

Describe the features of Pituitary Pars Intermedia Dysfunction

A
  • Equine Cushing’s Syndrome.
  • Equines 15 years or older.
  • Extremely common in UK aged horse populations.
  • Testing for PPID and monitoring treatment large part of modern leisure horse practice - good for preventing laminitis
  • Exact mechanism by which PPID initiates laminitis unknown
30
Q

What are the consequences of laminar failure in the hoof?

A

The pedal bone is free to move within the foot.
- Where it goes and how far depend on the forces acting on the bone and the extent and severity of laminar failure

31
Q

Describe how a normal hoof should appear on radiography

A
  • Depth from coronary band to tip of extensor process is variable but approx. 10 mm in normal horses
  • Distance form dorsal surface PIII to hoof should be constant.
  • Dorsal surface of PIII and PII in line
32
Q

Describe cases of laminitis when there is no movement of the pedal bone

A

Mild cases might not have any pedal bone movement (or it is so slight not to be visible on radiographs).
Important to explain to owner that this does not imply the animal has not got laminitis

33
Q

Describe capsular rotation of the pedal bone

A

The hoof capsule diverges form the dorsal surface of PIII, but PIII itself remains aligned with PII. Common.

34
Q

Describe bony rotation of the pedal bone

A

The hoof capsule diverges form the dorsal surface of PIII, and PIII itself is rotated palamarly around the DIP. Implies significant pull of DDF and usually a sign of severe damage. Less common.

35
Q

Describe the appearance of a ‘sinker’ laminitis on radiography

A
  • Vertical displacement of PIII downwards
  • Sole depth thin
  • Distance from tip of extensor process to coronary band increased
  • Usually implies very serious pathology, horses usually very painful
36
Q

Describe the consequences of pedal bone movement

A
  • In the acute stage: resultant gap becomes a haematoma/seroma /necrotic mess
  • If this gets infected a foot abscess will result.
  • Foot abscesses are a common complication of laminitis: usually 2-3 weeks post the acute stage – warn the client.
  • Forces on the foot stretch the white line junction, providing an easy ingress route for abscess causing bacteria
  • Eventually the haematoma is replaced by poor quality, dysplastic horn – a lamellar “wedge”
37
Q

How does pedal bone movement affect the blood supply?

A

Downward the pedal bone drags the coronary band with it leading to a compromised (crushed) blood supply to the coronary band.

38
Q

How can the visual conformation of the hoof change due to pedal bone movement?

A
  • Abnormal horn growth results: the toe goes slower than the heels leading to diverging hoof rings (parallel growth rings just indicate a change in growth rate)
  • The hoof attempts to remodel itself around the new position of the pedal bone leading to abnormal hoof shapes (which may lead to chronic lameness).