Equis ISSN 2398-2977

Foot: laminitis

Synonym(s): Founder

Contributor(s): Gordon Baker, Olin Balch, Simon Curtis, Robert A Eustace, Graham Munroe, Vetstream Ltd, Nicola Menzies-Gow


  • Failure of the attachment between the distal phalanx and the inner hoof wall (lamellae).
  • Cause: laminitis can arise in association with sepsis, eg gastrointestinal disease, pleuropneumonia, metritis; endocrinopathies, eg pars pituitary intermedia dysfunction (PPID), equine metabolic syndrome (EMS), corticosteroid administration; weight overload, ie supporting limb laminitis (SLL).
  • Signs:
    • Bounding digital pulse   Foot / shoe: examination  .
    • Uni-, bilateral or quadripedal foot pain, stilted gait   Musculoskeletal: gait evaluation  .
    • Reluctant to move, characteristic, toe-relieving, stance   Musculoskeletal: physical examination - adult  , forelimbs extended in front   Forelimb: stance 01 - extension  , or all feet brought towards center of gravity   Forelimb: stance 02 - upright - laminitis  .
    • Rapid progression of laminar necrosis may   →   sinking or rotation of distal phalanx within hoof capsule    →   penetration of the apex of pedal bone through sole   Sole: collapsed 03 - laminitis  .
    • Chronic cases may have a variety of hoof changes   Hoof: rings - laminitis  , including divergent growth rings.
    • There may be signs of systemic illness if the disease is associated with sepsis.
  • Diagnosis: clinical signs, radiography   Forelimb: radiography  to quantify P3 displacement in hoof capsule.
  • Treatment: vasodilators, cryotherapy, anti-inflammatories/analgesics; farriery; as for primary problem.
  • Prognosis: depends on cause and pedal bone movement.
Print off the Owner factsheets on Caring for your horse's feetEmergencies - when to call the vet and Laminitis - the facts to give to your clients.



  • In the normal foot tightly regulated enzymatic remodeling at the junction between the corium and the basal cell layer of the epidermal lamellae allows continued proliferation of hoof wall and movement past the pedal bone.
  • Failure of this regulation at the junction is the key factor in the pathogenesis of laminitis. Failure of adhesion of the cells to the underlying basement membrane occurs   →   detachment and mechanical deformation of the dermal/epidermal junction.

Trigger factors

  • Depends on the form of laminitis.
  • Endocrinopathy-associated laminitis; hyperinsulinemia   →    toxic endothelium   →   endothelial dysfunction   →   continued production of vasoconstrictor mediators, but decreased production of vasodilator mediators   →   altered lamellar perfusion.
  • Sepsis-associated laminitis: absorption of trigger factors from the source of the sepsis, eg gastrointestinal tract into the circulation results in activation of inflammatory cascade   →   dysregulation of cell adhesion.
  • Supporting limb laminitis: failure of normal limb cycling   →   altered lamellar perfusion.

Clinical syndromes associated with laminitis

  • Endocrinopathies: EMS   Equine metabolic syndrome   which is a cluster of clinical abnormalities, including hyperinsulinemia and/or insulin resistance, dyslipidemia and altered circulating adipokine concentrations with or without obesity   Weight gain: pony - laminitis  ; PPID   Pituitary: adenoma  ; iatrogenic corticosteroid administration.
  • Sepsis: retained placenta   Placenta: retained  , endotoxemia   Endotoxemia: overview  , colitis   Colitis X  .
  • Supporting limb laminitis: failure to bear weight on contralateral limb; see complications of internal fixation.

Predisposing factors



  • Still unclear.
  • Four distinct phases.
    • Developmental phase:
      • Prior to development of clinical signs; may go unrecognized.
      • Lamellar separation is triggered.
      • May occur in 8 h to longer.
    • Acute phase:
      • From onset of clinical pain/lameness to evidence of displacement of the distal phalanx.
      • Complete recovery may occur or the disease progresses to the chronic phase.
    • Chronic:
      • Indefinite duration.
      • Persistent mild lameness   →   severe pain and hoof slough.
    • Chronic laminitic feet:
      • Intermittent variable lameness resulting from chronically distorted feet.
  • Endocrinopathic laminitis:
    • Encompasses laminitis associated with obesity, insulin dysfunction, pasture-associated laminitis, EMS, PPID or glucocorticoid administration.
    • Recent research has shown that prolonged hyperinsulinemia can induce laminitis in healthy ponies and horses. In contrast to sepsis-associated laminitis, inflammation does not appear to be a major feature and evidence of systemic or gastrointestinal inflammation is not apparent. In addition, the histological changes seen in the lamellae are more consistent with stretching rather than separation of the basement membrane, accompanied by increased mitotic activity and cellular proliferation.
    • A number of different theories have been postulated to explain the potential relationship between hyperinsulinemia or insulin dysfunction and the development of laminitis. Most of the considered mechanisms involve an indirect relationship, as glucose uptake in the tissue appears to be insulin independent. Instead it would appear that insulin dysfunction is associated with endothelial dysfunction which in turns results in vasoconstriction and platelet and leukocyte adhesion, all of which are implicated in the pathogenesis of laminitis.
    • A significant proportion of laminitis cases occur at pasture and these animals generally have a metabolic predisposition. Pasture can contain large amounts of fructan, consumption of which may increase plasma insulin concentrations and may cause changes in the hind gut microflora. Thus, it may be the combination of hyperinsulinemia and hindgut fermentation of fructans that contribute to the development of acute laminitis in these animals.
  • Sepsis-associated laminitis:
    • Absorption of laminitis trigger factors from source of sepsis.
    • Systemic activation of the inflammatory cascade.
    • There is evidence of endothelial activation, leukocyte adhesion and emigration, pro-inflammatory cytokine expression and oxidative injury occurring in the laminae and it would appear that this is a local manifestation of a systemic disease.
    • Whilst matrix metalloproteinases (MMPs) were initially thought to play a decisive role in the dysadhesion process, this has since been disproven. Instead dysadhesion appears to be associated with elevated expression of another extracellular matrix protease known as ADAMTS-4 and consequent depletion of the proteoglycan versican which contribute to lamellar failure by affecting critical laminar basal epithelial cell functions such as expression of adhesion proteins.
  • Supporting limb laminitis:
    • There has been little or no primary research focussed on the mechanisms that result in SLL, but rather than being due to direct mechanical overload, it seems more likely that SLL is a consequence of inadequate perfusion of the lamellar tissue due to reduced digital blood flow associated with excessive and continuous weight-bearing. Metabolic, vascular and/or lymphatic compromise occur secondary to prolonged and enforced changes in load distribution, decreased cyclic loading of the digit and/or inflammatory responses to these events within the compensatory limb(s).

Possible inciting conditions

  • EMS: hyperinsulinemia and/or insulin resistance   →    endothelial dysfunction   →    vasoconstriction and platelet and leukocyte adhesion, all of which are implicated in the pathogenesis of laminitis.
  • PPID: increased circulating glucocorticoids   →   protein catabolism and antagonism of insulin   →   hyperinsulinemia   →   laminitis.
  • Grain overload: excessive grain intake   →   rapid fermentation and production of lactic acid within hindgut   →   acidic conditions in the hindgut   →   increased intestinal permeability and death and lysis of bacteria (Enterobacteriasceae)   →   endotoxins from the release of the lipopolysaccharide components of the cell wall   →   systemic circulation   →    activation of inflammatory cascade   →    sepsis-associated laminitis.
  • Sepsis: Gram-negative bacterial infection   →    endotoxin production (part of Gram-negative bacterial cell wall)   →    increased circulatory absorption   →    activation of inflammatory cascade   →    laminitis.

Chronic laminitis

  • Acute bouts of laminitis   →    temporary alteration in hoof growth   →    rings in hoof wall   →    'slipper toe' conformation.
  • Persistent pressure from the tip of the rotated pedal bone   →    convex sole   →    necrosis and ulceration of the dermis   Foot: subsolar abscess / infection  .
  • Dead space between rotated pedal bone and hoof wall is filled in with epidermal scar tissue   →    white line on solar surface   →    'seedy toe'   Hoof: seedy toe  .


  • Severe acute cases may deteriorate in a matter of hours though this is rare.
  • Chronic cases result from several bouts of laminitis over a long period of time, eg months to years.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
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Other sources of information

  • Pollitt C C (2008)Equine Laminitis - Current Concepts.Australian Government Rural Industries Research and Development Corporation Publication No 08/062.
  • Steward M L (2003)How to Construct and Apply Atraumatic Therapeutic Shoes to Treat Acute or Chronic Laminitis in the Horse.In:Proc 49th AAEP Convention.pp 337-346.
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  • Pollitt C C (1999)Equine laminitis - a revised pathophysiology.In:Shoeing for Soundness - an AEVA seminar for veterinarians and farriers.


  • The Laminitis Trust.