Laminitis - equine Flashcards
(38 cards)
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
- DEVELOPMENTAL: contact with trigger, lasts up to 72 hours, no overt signs
- ACUTE: see CS, lasts a few days or else –> chronic
- 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?
- PPID
- EMS
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
True
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)
Tx - PPID
pergolide
= dopamine-R antagonist
- controls ACTH output