Foot: laminitis in Horses (Equis) | Vetlexicon
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Foot: laminitis

ISSN 2398-2977

Synonym(s): Founder


  • 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: acepromazine, digital 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.

Presenting signs

  • Characteristic stance with the weight being taken on the heels of the affected feet, and as the forelimbs are usually more severely affected, increased weight carriage on hindlimbs.
  • Bounding digital pulses palpable.
  • Pain in sole anterior to apex of frog.
  • Depression on palpation of the dorsal coronary band if pedal bone has sunk.

Acute presentation

  • Very severe bouts may see hoof sloughing or sinking of the pedal bone through the sole within 48 h.

Geographic incidence

  • Worldwide.

Age predisposition

  • Depends on underlying cause; risk of certain endocrinopathies such as PPID increases with age.

Breed/Species predisposition

  • Higher incidence of EMS in certain breeds.
  • Higher incidence of PPID in ponies compared to horses.
  • Generally perceived higher incidence of endocrinopathic laminitis in ponies, but this is not substantiated by all surveys.

Cost considerations

  • Cost associated with medical treatment and farriery as recovery can be prolonged.

Special risks

  • The underlying cause must always be identified and treated/removed if possible.



  • 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 with two possible mechanisms with some supporting evidence, either:
    • Toxic endothelium → endothelial dysfunction → continued production of vasoconstrictor mediators, but decreased production of vasodilator mediators → altered lamellar perfusion.
    • Or binding to and inappropriate stimulation of insulin-like growth factor 1 (IGF-1) receptors in lamellae → cellular proliferation → lamellar stretching.
  • 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 → lamellar ischemia.

Clinical syndromes associated with laminitis

  • Endocrinopathies: EMS Equine metabolic syndrome which is a cluster of clinical abnormalities associated with an increased risk of laminitis. The central feature is insulin dysregulation which may manifest as hyperinsulinemia, an excessive insulin response to oral carbohydrate and/or tissue insulin resistance. Additional features include dyslipidemia and altered circulating adipokine concentrations with or without obesity Weight gain: pony - laminitis PPID Pituitary pars intermedia dysfunction (PPID); iatrogenic corticosteroid administration.
  • Sepsis: retained placenta Placenta: retained, endotoxemia, 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 insulin dysregulation including 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 dysregulation 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 dysregulation 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. There is also evidence to suggest inappropriate stimulation of lamellar insulin-like growth factor 1 (IGF-1) receptors by insulin leading to cellular proliferation.
    • A significant proportion of laminitis cases occur at pasture. It is thought that consumption of non-structural carbohydrate triggers an excessive insulin response directly in response to the absorbed glucose and indirectly via incretin hormones secreted by gastrointestinal tract.
  • 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 focused 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 tissue insulin resistance → endothelial dysfunction →  vasoconstriction and platelet and leukocyte adhesion, all of which are implicated in the pathogenesis of laminitis. And/or → binding to and inappropriate stimulation of insulin-like growth factor 1 (IGF-1) receptors in lamellae → cellular proliferation → lamellar stretching.
  • PPID: increased released of hormones normally produced by the pituitary pars intermedia some of which → 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 (Enterobacteriaceae) → 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.