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What is laminitis characterised by?

failure of attachment of epidermal cells of the epidermal (insensitive) laminae to the underlying basement membrane of the dermal (sensitive) laminae


Risk factors - laminitis

- sepsis and systemic inflammation (GIT disease, pneumonia, septic metritis)
- endocrine diseases (PPID and EMS)
- Mechanical overload (if one severely lame non weight-bearing limb, weight transferred to another)
- access to pasture
- pony > horses
- spring and summer
- female
- increasing age
- obesity
- recent increase in body weight
- recent new access to grass
- increased time since worming (but not directly related to parturition)
- insulin resistance (IR)


3 stages of laminitis

1. DEVELOPMENTAL: contact with trigger, lasts up to 72 hours, no overt signs
2. ACUTE: see CS, lasts a few days or else --> chronic
3. RESOLUTION or CHRONIC: exact cascade of events and interactions b/w these processes yet to be elucidated


What are the 4 main pathogenesis categories of laminitis?

- inflammation
- ECM degradation
- metabolic disease
- endothelial and vascular dysfunction
* cascade and interactions of factors yet to be elucidated


Outline role of inflammation

- previously questioned
- systemic inflammatory response that accompanies hindgut carbohydrate overload somehow initiates lamellar inflammatory events


Outline role of ECM degradation and laminitis pathogenesis

- MMP activation does occur, not an initiating event
- laminar separation may occur following a failure of epithelial adhesion molecules (hemidesmosomes)
- dysregulation of cell adhesion most likely caused by inflammatory and/or hypoxic cellular injury


Outline metabolic diseases in pathogenesis of laminitis

- greatest risk have metabolic phenotype (obesity and IR)
- similar to human metabolic syndrome (HMS)
- summer pasture appears to produce metabolic responses in laminitis prone ponies leading to expression of this at risk metabolic phenotype
- strong positive relationship b/w pasture NSC content and circulating insulin concentrations
- increased CHO consumption exacerbates IR In horses
- feeding a fructan-type CHO produces an exaggerated insulin response in laminitis prone ponies


Outline vascular and endothelial dysfunction

- digital venoconstriction (early)
- consequent laminar oedema (early)
- venoconstriction d/t platelet activation and platelet-neutrophil activation --> release of vasoactive mediator 5-HT
- amines from hindgut fermentation of CHO are vasoactive
- IR in other spp alters endothelial function (proinflammatory condition, platelet and leukocyte activation, increased ET1 and production of mediators of inflammation and oxdant stress)
- digital vascular haemodynamic alterations (d/t inflammation, platelet activiation, action of vasoactive amines from GIT) --> lamellar injury


Aims in approach to suspect case

- make definitive diagnosis
- determine underlying cause
- determine if likely to recover the expected level of soundness


Dx - laminitis

- CS (lameness affecting 2+ limbs, characteristic stance of leaning back on heels, bounding digital pulses, increased hoof wall temperature, pain on hoof tester pressure at point of frog, palpable depression of coronary band)
+/- radiography (1st presentation - if concerned P3 moved, later - if CS not improving)
+/- enodcrine tests


What might indicate P3 has moved? 2

- depression at coronary band
- softening of sole at point of hoof


What radiographs need to be taken for suspect laminitis?

- lateromedial
- ensure good foot preparation
- put markers on feet (one on dorsal hoof wall starting at coronary band and one at point of bone)
- assess pedal bone rotation and founder distance (sinking)


Which endocrine diseases might you want to r/o with laminitis?



Dx tests - PPID

- CS
- basal ACTH (seasonally adjusted reference range)
- Dex suppression test (not autumn)
- TRH suppression test


Dx - EMS

- Hx
- CS
- Demonstration of IR (fasting insulin and glucose, dynamic test)


T/F: once CS become apparent all of the pathological changes have already occurred in the foot



Aims - laminitis tx - 2

analgesia and foot support


Analgesia - laminitis

- NSAIDs (PBZ, flunixin, carprofen, iv or oral)
- Opiates (morphine, pethadine, fentanyl) in hospital as controlled drugs, short acting and side effects


Outline vasodilator therapy in laminitis

- controversial: d/t conflicting evidence as to whether the blood supply to foot is increased o rdecreased during developmental phase
- onc eCS occur, this will have passed


Vasodilator drug to affect equine digital blood flow

only ACP effective (NOT nitroglycerine ointment/ Percutol)


How can you cause distal limb vasoconstriction in horse?

- ice
- limb distal to carpus/ tarsus should be chilled continueously to


How can foot support be provided in laminitis cases?

- essential
- increase bedding: depth, bring to door
- Frog support: bandages, lilypads, NFS etc
- Frog and sole support: styrofoam, dental impression material etc.


Management changes - laminitis

- bx rest
- change diet: no grass, 1.5-2% bodyweight poor quality hay, no or minimal concentrates (HiFi = a chaff, or unmollassed sugar beet = fibre, only)



= dopamine-R antagonist
- controls ACTH output


Tx - EMS

- weight loss
- increased exercise
+/- pharmacological agents


What does laminitis prognosis depend on?

- CS - if there is a depression which extends all the way round the coronary bank suggests SINKER = 20 % survival
- evidence of previous attacks = success rate decreased by 20%
o rotation > 11.5 degrees = significantly reduced prognosis
o Founder >15mm 40% chance of returning to soundness
* overall one study found 95% survival after 8 weeks
- lower BWt, optimal BCS and mild laminitis (Obel grade 1 and 2) were significantly associated with survival
- trend towards ACP tx with survival
- 72% sound at trot (significantly more likely in small horses)
- 59% being ridden again (significantly more likely if no previous hx of laminitis)


Define NSC

Non-structural carbohydrate


What is the #1 priority for pasture-associated laminitis?

Prevention and laminitis is associated with overconsumption of NSC (fructan+starch+ sugar) which provides energy for growth of plants


Outline how NSC levels fluctuate

- decreases when plant growing
- increases when plant photosynthesising (high light intensity, low temperature, lack of water)
- season (low early spring, greater late spring)
- hay content depends on content of grass at cutting
- NSC of haylage generally low but more palatable
* AIM = minimise NSC intake


How should pasture be managed regarding NSC?

- encourage growth (use fertiliser, regularly topped) as this lowers NSC content
- hay should ideally be made from mature crop post seed dispersal (lower NSC content)
- ideally want NSC