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

Introduction

  • 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.

Pathogenesis

Etiology

  • 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

General

Pathophysiology

  • 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  .

Timecourse

  • 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.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Wells-Smith L (2015)Laminitis in the 21st century.Vet Rec176(3), 70-71PubMed.
  • Menzies-Gow N Jet al(2014)The effect of exercise on plasma concentrations of inflammatory markers in normal and previously laminitic ponies.Equine Vet J46(3), 317-321PubMed.
  • Borer-Weir K Eet al(2013)Seasonal and annual influence on insulin and cortisol results from overnight dexamethasone suppression tests in normal ponies and ponies predisposed to laminitis.Equine Vet J45(6), 688-693PubMed.
  • Wylie C E, Collins S N, Verheyen K L P & Newton J R (2013)A cohort study of equine laminitis in Great Britain 2009-2011: Estimation of disease frequency and description of clinical signs in 577 cases.Equine Vet J45(6), 681-687PubMed.
  • Sherlock C & Parks A (2013)Radiographic and radiologic assessment of laminitis.Equine Vet Educ25(10), 524-535 Wiley Online Library.
  • Tadros E M & Frank N (2013)Endocrine disorders and laminitis.Equine Vet Educ25(3), 152-162VetMedResource.
  • Cornelisse C J & Robinson N E (2013)Glucocorticoid therapy and the risk of equine laminitis.Equine Vet Educ25(1), 39-46VetMedResource.
  • Leise B Eet al(2012)Hindlimb laminar inflammatory response is similar to that present in forelimbs after carbohydrate overload in horses.Equine Vet J44(6), 633-639PubMed.
  • Schvartz G, Kelmer K & Berlin D (2012)Chronic laminitis in a 10-month-old Arabian filly.Equine Ved Educ24(8), 408-414 VetMedResource.
  • Milner P & Hughes I (2012)Remedial farriery Part 4: Chronic laminitis.UK Vet17, 8-12VetMedResource.
  • Keller M D, Pollitt C C & Marx U C (2011)Nuclear magnetic resonance-based metabonomic study of early time point laminitis in an oligofructose-overload model.Equine Vet J43(6), 737-743PubMed.
  • Venugopal C S, Eades S, Holmes E P & Beadle R E (2011)Insulin resistance in equine digital vessel rings: An in vitro model to study vascular dysfunction in equine laminitis.Equine Vet J43(6), 744-749PubMed.
  • Chameroy K Aet al(2011)Effects of a supplement containing chromium and magnesium on morphometric measurements, resting glucose, insulin concentrations and insulin sensitivity in laminitic obese horses.Equine Vet J43(4), 494-499PubMed.
  • Visser M B & Pollitt C C (2011)The timeline of lamellar basement membrane changes during equine laminitis development.Equine Vet J43(4), 471-477PubMed
  • Wilford S, Fowke G D, McKane S & Cromer R (2011)Post-foaling laminitis: A case report.UK Vet16, 4-9VetMedResource.
  • Faleiros R R, Nuovo G J, Flechtner A D & Belknap J K (2011)Presence of mononuclear cells in normal and affected laminae from the black walnut extract model of laminitis.Equine Vet J43(1), 45-53PubMed.
  • Leise B S, Faleiros R R, Watts M, Johnson P J, Black S J & Belknap J K (2011)Laminar inflammatory gene expression in the carbohydrate overload model of equine laminitis.Equine Vet J43(1), 54-61PubMed.
  • Vinuela-Fernandez I, Jones E, McKendrick I J & Molony V (2011)Quantitative assessment of increased sensitivity of chronic laminitic horses to hoof tester evoked pain.Equine Vet J43(1), 62-68PubMed.
  • Asplin K Eet al(2010)Histopathology of insulin-induced laminitis in ponies.Equine Vet J42(8), 700-706PubMed.
  • Menzies-Gow N Jet al(2010)Epidemiological study of pasture-associated laminitis and concurrent risk factors in the South of England.Vet Rec167(18), 690-694 PubMed.
  • Menzies-Gow N Jet al(2010)Severity and outcome of equine pasture-associated laminitis managed in first opinion practice in the UK. Vet Rec167(10), 364-369PubMed.
  • Menzies-Gow N Jet al(2010)Repeatability and reproducibility of the Obel grading system for equine laminitis.Vet Rec167(2), 52-55PubMed.
  • Williams J Met al(2010)Effect of intravenous lidocaine administration on laminar inflammation in the black walnut extract model of laminitis.Equine Vet J42(3), 261-269PubMed
  • de Laat M A, McGowan C M, Sillence N M & Pollitt C C (2010)Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses.Equine Vet J  42(2), 129-135PubMed.
  • Toth F, Frank N, Chameroy K A & Boston R C (2009)Effects of endotoxaemia and carbohydrate overload on glucose and insulin dynamics and the development of laminitis in horses.Equine Vet J41(9), 852-858PubMed.
  • van Eps A W & Pollitt C C (2009)Equine laminitis model: Lamellar histopathology seven days after induction with oligofructose.Equine Vet J41(8), 735-740PubMed.
  • van Eps A W & Pollitt C C (2009)Equine laminitis model: Cryotherapy reduces the severity of lesions evaluated seven days after induction with oligofructose.Equine Vet J41(8), 741-746PubMed.
  • Nourian A Ret al(2009)Equine laminitis: Ultrastructural lesions detected in ponies following hyperinsulinaemia.Equine Vet J41(7), 671-677PubMed.
  • Van Weyenberg S, Hesta M, Kalmar I D, Vandermeiren J & Janssens G P J (2009)Nutritional management of laminitis in a horse.Vet Rec164(22), 694-695PubMed.
  • Carter R A, Treiber K H, Geor R J, Douglass L & Harris P A (2009)Prediction of incipient pasture-associated laminitis from hyperinsulinaemia, hyperleptinaemia and generalised localised obesity in a cohort of ponies.Equine Vet J41(2), 171-178PubMed.
  • Eustace R A & Emery S L (2009)Partial coronary epidermectomy (coronary peel), dorsodistal wall fenestration and deep digital flexor tenotomy to treat severe acute founder in a Connemara pony.Equine Vet Educ21(2), 91-99VetMedResource.
  • Parks A H & Mair T S (2009)Laminitis: A call for unified terminology.Equine Vet Educ21(2), 102-106Wiley Online Library.
  • O'Grady S E & Steward M L (2009)The wooden shoe as an option for treating chronic laminitis.Equine Vet Educ21(2), 107-112VetMedResource.
  • Thomason J J, Faramarzi B, Revill A, Sears W, Thomason J J, Faramarzi B, Revill A & Sears W (2008)Quantitative morphology of the equine laminar junction in relation to capsule shape in the forehoof of Standardbreds and Thoroughbreds.Equine Vet J40(5), 473-480PubMed.
  • Keen J A, Hillier C, McGorum B C & Nally J E (2008)Endothelin mediated contraction of equine laminar veins.Equine Vet J40(5), 488-492PubMed.
  • Kyaw-Tanner M T, Wattle O, van Eps A W & Pollitt C C (2008)Equine laminitis: Membrane type matrix metalloproteinase-1 (MMP-14) is involved in acute phase onset.Equine Vet J40(5), 482-487PubMed.
  • Nourian A R, Baldwin G I, Brawner W, Taintor J & Pinto N (2007)Equine laminitis: ultrastructural lesions detected 24-30 hours after induction with oligofructose.Equine Vet J39(4), 360-364PubMed.
  • Belknap J Ket al(2007)Lamellar pro-inflammatory cytokine expression patterns in laminitis at the developmental stage and at the onset of lameness: innate vs. adaptive immune response.Equine Vet J39(1), 42-47PubMed.
  • Loftus J Pet al(2007)Laminar xanthine oxidase, superoxide dismutase and catalase activities in the prodromal stage of black-walnut induced equine laminitis.Equine Vet J39(1), 48-53PubMed.
  • O'Grady S E (2006)Realignment of P3 - the basis for treating chronic laminitis.Equine Vet Educ18(4), 214-218VetMedResource.
  • Menzies Gow N (2006)Equine acute pasture-associated laminitis - Part 1.UK Vet11(4), 10-12VetMedResource.
  • Van Eps A W & Pollitt C C (2006)Equine laminitis induced with oligofructose.Equine Vet J38(3), 203-208PubMed.
  • Peroni J Fet al(2005)Black walnut extract-induced laminitis in horses is associated with heterogeneous dysfunction of the laminar microvasculature.Equine Vet J37(6), 546-551PubMed.
  • Kempson S A & Robb R (2004)Use of topical disinfectant as part of a hoof care programme for horses with diseases of the hoof capsule.Vet Rec154(21), 647-652PubMed.
  • Kyaw-Tanner M & Pollitt C C (2004)Equine laminitis: increased transcription of matrix metallopoteinase-2 (MMP-2) occurs during the developmental phase.Equine Vet J36(3), 221-225PubMed
  • French K R & Pollitt C C (2004)Equine laminitis: loss of hemidesmosomes in hoof secondary epidermal almellae correlates to dose in an oligofructose induction model: an ultrastructural study.Equine Vet J36(3), 230-235PubMed.
  • French K R & Pollitt C C (2004)Equine laminitis: cleavage of laminin 5 associated with basement membrane dysadhesion.Equine Vet J36(3), 242-247PubMed.
  • Mobasheri Aetal (2004)Chronic equine laminitis is characterised by loss of GLUT1, GLUT4 and ENaC positive laminar kertinocytes.Equine Vet J36(3), 248-254PubMed.
  • Van Eps A W & Pollitt C C (2004)Equine laminitis: cryotherapy reduces the severity of the acute lesion.Equine Vet J36(3), 255-260PubMed.
  • French K R & Pollitt C C (2004)Equine laminitis: glucose deprivation and MMP activation induce dermo-epidermal separationin vitro.Equine Vet J36(3), 261-266PubMed.
  • Berhane Yet al(2004)In vitroandin vivostudies of homocysteine in equine tissues: implications for the pathophysiology of laminitis.Equine Vet J36(3), 279-284PubMed.
  • Weguespack R Wet al(2004)Increased expression of MAIL, a cytocine-associated nuclear protein, in the prodromal stage of black walnut-induced laminitis.Equine Vet J36(3), 285-291PubMed.
  • Johnson P Jet al(2004)Tissue-specific dysregulation of cortisol metabolism in equine lamintis.Equine Vet J36(1), 41-45PubMed.
  • Cornelisse C J & Robinson N E (2004)Glucocorticoid therapy in equine laminitis: fact or fiction?Equine Vet Educ16(2), 90-93VetMedResource.
  • Parks A H , Balch O K & Collier M A (2003)Treatment of acute laminitis.Equine Vet Educ15(5), 273-280VetMedResource.
  • Parks A & O'Grady S E (2003) Chronic laminitis: current treatment strategies.Vet Clin North Am Equine Pract19 (2), 393-416PubMed.
  • Cripps P J & Eustace R A (2000)Factors involved in the prognosis of equine laminitis in the UK.Equine Vet J31(5), 433-442PubMed.
  • Eustace R A & Cripps P J (2000)Radiological measurements from the feet of normal horses with relevance to laminitis.Equine Vet J31(5), 427-442PubMed.
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  • Bailey S Ret al(1998)Evidence for different 5-HT1B/1D receptors mediating vasoconstriction of equine digital arteries and veins.Eur J Pharmacol355(2-3), 175-187PubMed.
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  • Robinson N E (1998)Step by painful step, increasing knowledge about laminitis.Equine Vet J30(2), 89-90PubMed.
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  • Riber Cet al(1995)Hematologic changes observed in Andalusian horses with laminitis.J Vet Med Sci57(5), 981-984PubMed.
  • Slater M Ret al(1995)Descriptive epidemiologic study of equine laminitis.Equine Vet J27(5), 364-367VetMedResource.
  • Owens J Get al(1995)Effects of ketaprofen and phenylbutazone on chronic hoof pain and lameness in the horse.Equine Vet J27(4), 296-300PubMed.
  • Rowe J Bet al(1994)Prevention of acidosis and laminitis associated with grain feeding horses.J Nutr124(12), 2742S-2744SPubMed.
  • Baxter G Met al(1994)Acute laminitis.Vet Clin North Am Equine Pract10(3), 627-642PubMed.
  • Hunt R Jet al(1993)A retrospective evaluation of laminitis in horses.Equine Vet J25(1), 61-64PubMed.
  • Fagliari J Jet al(1988)Changes in plasma protein concentrations in ponies with experimentally induced alimentary laminitis.Am J Vet Res59(10), 1234-1237PubMed.

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.
  • O'Grady S E (2003)How to Restore Alignment of P3 in Horses with Chronic Laminitis.In:Proc 49th AAEP Convention.pp 328-336.
  • Redden R F (2003)Preventing Laminitis in the Contralateral Limb of Horses with Non-Weight-Bearing Lameness.In:Proc 49th AAEP Convention.pp 320-327.
  • Pollitt C C, Kyaw-Tanner M, French K R, van Eps A W, Hendrikz J K & Daradka M (2003)Equine Laminitis.In:Proc 49th AAEP Convention.pp 103-115.
  • Eustace R A (2000)Explaining laminitis and its prevention.Equilife Ltd 0870 444 0676.
  • Pollitt C C (1999)Equine laminitis - a revised pathophysiology.In:Shoeing for Soundness - an AEVA seminar for veterinarians and farriers.

Organizations

  • The Laminitis Trust.


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