is a common condition, especially in ponies, causing considerable welfare problems and often leading to euthanasia. Management in practice is constrained by facilities and owner compliance. Although many treatments have been described, few are proven and some contradict each other e.g. raise / lower heels and vasoconstriction vs. vasodilation. Due to these difficulties, too often veterinary treatment is limited to providing more ‘Bute. 

• Carbohydrate overload (grass; cereals)

•   Septicaemia / endotoxaemia (endometritis; colitis)

•   Mechanical - excess weightbearing (severe prolonged lameness contralateral limb,

  galloping on cobbled streets...)

•   Corticosteroid administration (controversy re. level of risk / dose required)

•   Cushing’s disease; hypothyroidism (see Medicine lectures)

  Fat ponies and horses especially at risk; peak incidence at times of lush pasture growth. See notes on Equine Metabolic Syndrome 

0. Acute laminitis is the result of systemic disease (exception = mechanical).
   Laminitis can be experimentally induced therefore mechanisms have been much studied After noxious stimulus (e.g. stomach-tube with excess carbohydrate) the development period lasts 2-3 days before clinical signs appear
   During the development (or prodromal) phase various inflammatory mediators act on the laminae. 

0. (1) Intestinal acidosis:

 excess carbohydrate in caecum (Figure 1)
o increase in lactic acid-producing bacteria

o drop in caecal pH damages gram-negative bacteria o endotoxin release into circulation

 peripheral vasoconstriction and activation of A-V shunts, decreases laminar perfusion, exacerbated by microthrombi

o laminar ischaemia causes necrosis and loss of pedal bone support.

•   The dorsal laminae are vascularised last within the foot, so they are most affected. Once the laminae are damaged the pull of the DDFT is no longer resisted and the bone rotates (Figure 2 A)

•   If all laminae are affected at the same time, as can occur in acute and severe laminitis, then complete laminar separation may result and the pedal bone will sink ventrally without rotation (:”sinker” or “founder”) or the whole hoof capsule can even be shed, as illustrated in Figure 2 (B).

  
  

  2. Inflammatory activation of proteolytic enzymes:

   A more recent theory postulates that systemic disease activates proteolytic

  enzymes (mainly matrix metalloproteinases) which unravel type IV collagen that connects the hoof wall laminae to those of the pedal bone 

Typical cases adopt a “saw horse” stance, with the fore feet placed forwards and the hind limbs under the body. This is because both front feet are painful, especially the toes.

• This is a condition affecting primarily the front feet; severe cases have all 4 feet affected, although the fore feet are usually worse than hinds

• Depressed, inappetant, increased HR & RR
• Markedly increased digital pulsation
• Heat in feet
• Painful across sole to pressure from hoof testers (if rotation has occurred then pain will

be worst just dorsal to frog and sole pay become convex at this point) • Coronary band depression 

• intermittent bouts of lameness
• flat or convex sole; “seedy toe” and abscesses common
• prominent hoof wall rings, narrowing at dorsal hoof wall (ddx from nutritional rings) 

 Remove potential causes (placenta; pasture; give liquid paraffin if appropriate) • Support the feet by using:

Styrofoam support pads or Soft-Ride boots

Very deep bedding (sand or peat better than shavings).
Once lameness improves, use glue-on plastic (“Imprint”) shoes

• Analgesia (NSAIDs)
• ACP QID iv or im for vasodilation effect
• Feed hay only +/- Farriers Formula +/- methionine to promote hoot growth

Many other treatments used but of dubious efficacy: glyceryl nitrate (“Percutol”); isoxsuprine; ice or cold water; hot water; aspirin or heparin for anticoagulation

Radiography to establish severity of condition and provides baseline for monitoring progress. Lateromedial views with markers to indicate position of coronary band and point of frog. Measure angle of rotation (if present) and founder distance (= “d distance”). Prognosis worse with increasing values, as well with severity of lameness, solar prolapse and increasing number of feet affected. “Ski tip” new bone formation at tip of pedal bone indicates previous bouts of laminitis 

•   Trim feet – often overgrown

•   Shoe – egg bar; reverse; heart bar or wide webbed normal shoes have all

  been used

•   Consider surgery:

o dorsal hoof wall resection
o ALLDDFT (check ligament) or DDFT transection