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: 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.

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 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 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 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.

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 Rec 176 (3), 70-71 PubMed.
  • Menzies-Gow N J et al (2014) The effect of exercise on plasma concentrations of inflammatory markers in normal and previously laminitic ponies. Equine Vet J 46 (3), 317-321 PubMed.
  • Borer-Weir K E et 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 J 45 (6), 688-693 PubMed.
  • 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 J 45 (6), 681-687 PubMed.
  • Sherlock C & Parks A (2013) Radiographic and radiologic assessment of laminitis. Equine Vet Educ 25 (10), 524-535 Wiley Online Library.
  • Tadros E M & Frank N (2013) Endocrine disorders and laminitis. Equine Vet Educ 25 (3), 152-162 VetMedResource.
  • Cornelisse C J & Robinson N E (2013) Glucocorticoid therapy and the risk of equine laminitis. Equine Vet Educ 25 (1), 39-46 VetMedResource.
  • Leise B E et al (2012) Hindlimb laminar inflammatory response is similar to that present in forelimbs after carbohydrate overload in horses. Equine Vet J 44 (6), 633-639 PubMed.
  • Schvartz G, Kelmer K & Berlin D (2012) Chronic laminitis in a 10-month-old Arabian filly. Equine Ved Educ 24 (8), 408-414 VetMedResource.
  • Milner P & Hughes I (2012) Remedial farriery Part 4: Chronic laminitis. UK Vet 17, 8-12 VetMedResource.
  • 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 J 43 (6), 737-743 PubMed.
  • 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 J 43 (6), 744-749 PubMed.
  • Chameroy K A et 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 J 43 (4), 494-499 PubMed.
  • Visser M B & Pollitt C C (2011) The timeline of lamellar basement membrane changes during equine laminitis development. Equine Vet J 43 (4), 471-477 PubMed
  • Wilford S, Fowke G D, McKane S & Cromer R (2011) Post-foaling laminitis: A case report. UK Vet 16, 4-9 VetMedResource.
  • 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 J 43 (1), 45-53 PubMed.
  • 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 J 43 (1), 54-61 PubMed.
  • 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 J 43 (1), 62-68 PubMed.
  • Asplin K E et al (2010) Histopathology of insulin-induced laminitis in ponies. Equine Vet J 42 (8), 700-706 PubMed.
  • Menzies-Gow N J et al (2010) Epidemiological study of pasture-associated laminitis and concurrent risk factors in the South of England. Vet Rec 167 (18), 690-694 PubMed.
  • Menzies-Gow N J et al (2010) Severity and outcome of equine pasture-associated laminitis managed in first opinion practice in the UK. Vet Rec 167 (10), 364-369 PubMed.
  • Menzies-Gow N J et al (2010) Repeatability and reproducibility of the Obel grading system for equine laminitis. Vet Rec 167 (2), 52-55 PubMed.
  • Williams J M et al (2010) Effect of intravenous lidocaine administration on laminar inflammation in the black walnut extract model of laminitis. Equine Vet J 42 (3), 261-269 PubMed
  • 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), 129-135 PubMed.
  • 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 J 41 (9), 852-858 PubMed.
  • van Eps A W & Pollitt C C (2009) Equine laminitis model: Lamellar histopathology seven days after induction with oligofructose. Equine Vet J 41 (8), 735-740 PubMed.
  • 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 J 41 (8), 741-746 PubMed.
  • Nourian A R et al (2009) Equine laminitis: Ultrastructural lesions detected in ponies following hyperinsulinaemia. Equine Vet J 41 (7), 671-677 PubMed.
  • Van Weyenberg S, Hesta M, Kalmar I D, Vandermeiren J & Janssens G P J (2009) Nutritional management of laminitis in a horse. Vet Rec 164 (22), 694-695 PubMed.
  • 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 J 41 (2), 171-178 PubMed.
  • 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 Educ 21 (2), 91-99 VetMedResource.
  • Parks A H & Mair T S (2009) Laminitis: A call for unified terminology. Equine Vet Educ 21 (2), 102-106 Wiley Online Library.
  • O'Grady S E & Steward M L (2009) The wooden shoe as an option for treating chronic laminitis. Equine Vet Educ 21 (2), 107-112 VetMedResource.
  • Thomason J J, Faramarzi B, Revill A et al (2008) Quantitative morphology of the equine laminar junction in relation to capsule shape in the forehoof of Standardbreds and Thoroughbreds. Equine Vet J 40 (5), 473-480 PubMed.
  • Keen J A, Hillier C, McGorum B C & Nally J E (2008) Endothelin mediated contraction of equine laminar veins. Equine Vet J 40 (5), 488-492 PubMed.
  • 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 J 40 (5), 482-487 PubMed.
  • 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 J 39 (4), 360-364 PubMed.
  • Belknap J K et 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 J 39 (1), 42-47 PubMed.
  • Loftus J P et al (2007) Laminar xanthine oxidase, superoxide dismutase and catalase activities in the prodromal stage of black-walnut induced equine laminitis. Equine Vet J 39 (1), 48-53 PubMed.
  • O'Grady S E (2006) Realignment of P3 - the basis for treating chronic laminitis. Equine Vet Educ 18 (4), 214-218 VetMedResource.
  • Menzies Gow N (2006) Equine acute pasture-associated laminitis - Part 1. UK Vet 11 (4), 10-12 VetMedResource.
  • Van Eps A W & Pollitt C C (2006) Equine laminitis induced with oligofructose. Equine Vet J 38 (3), 203-208 PubMed.
  • Peroni J F et al (2005) Black walnut extract-induced laminitis in horses is associated with heterogeneous dysfunction of the laminar microvasculature. Equine Vet J 37 (6), 546-551 PubMed.
  • 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 Rec 154 (21), 647-652 PubMed.
  • Kyaw-Tanner M & Pollitt C C (2004) Equine laminitis: increased transcription of matrix metallopoteinase-2 (MMP-2) occurs during the developmental phase. Equine Vet J 36 (3), 221-225 PubMed
  • 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 J 36 (3), 230-235 PubMed.
  • French K R & Pollitt C C (2004) Equine laminitis: cleavage of laminin 5 associated with basement membrane dysadhesion. Equine Vet J 36 (3), 242-247 PubMed.
  • Mobasheri A et al (2004) Chronic equine laminitis is characterised by loss of GLUT1, GLUT4 and ENaC positive laminar kertinocytes. Equine Vet J 36 (3), 248-254 PubMed.
  • Van Eps A W & Pollitt C C (2004) Equine laminitis: cryotherapy reduces the severity of the acute lesion. Equine Vet J 36 (3), 255-260 PubMed.
  • French K R & Pollitt C C (2004) Equine laminitis: glucose deprivation and MMP activation induce dermo-epidermal separation in vitroEquine Vet J 36 (3), 261-266 PubMed.
  • Berhane Y et al (2004) In vitro and in vivo studies of homocysteine in equine tissues: implications for the pathophysiology of laminitis. Equine Vet J 36 (3), 279-284 PubMed.
  • Weguespack R W et al (2004) Increased expression of MAIL, a cytocine-associated nuclear protein, in the prodromal stage of black walnut-induced laminitis. Equine Vet J 36 (3), 285-291 PubMed.
  • Johnson P J et al (2004) Tissue-specific dysregulation of cortisol metabolism in equine lamintis. Equine Vet J 36(1), 41-45 PubMed.
  • Cornelisse C J & Robinson N E (2004) Glucocorticoid therapy in equine laminitis: fact or fiction? Equine Vet Educ 16 (2), 90-93 VetMedResource.
  • Parks A H , Balch O K & Collier M A (2003) Treatment of acute laminitis. Equine Vet Educ 15 (5), 273-280 VetMedResource.
  • Parks A & O'Grady S E (2003) Chronic laminitis: current treatment strategies. Vet Clin North Am Equine Pract 19 (2), 393-416 PubMed.
  • Cripps P J & Eustace R A (2000) Factors involved in the prognosis of equine laminitis in the UK. Equine Vet J 31(5), 433-442 PubMed.
  • Eustace R A & Cripps P J (2000) Radiological measurements from the feet of normal horses with relevance to laminitis. Equine Vet J 31 (5), 427-442 PubMed.
  • Katwa L C et al (1999) Expression of endothelin in equine laminitis. Equine Vet Educ 31 (3), 243-247 PubMed.
  • Bailey S R et al (1998) Evidence for different 5-HT1B/1D receptors mediating vasoconstriction of equine digital arteries and veins. Eur J Pharmacol 355 (2-3), 175-187 PubMed.
  • Bailey S R et al (1998) Plasma 5-hydroxytryptamine constricts equine digital blood vessels in vitro - implications for pathogenesis of acute laminitis. Equine Vet J 30 (2), 124-130 PubMed.
  • Pollitt C C (1998) The anatomy and physiology of the hoof wall. Equine Vet Educ 10 (6), 318-325 VetMedResource.
  • Robinson N E (1998) Step by painful step, increasing knowledge about laminitis. Equine Vet J 30 (2), 89-90 PubMed.
  • Polzer J et al (1997) Age, breed, sex and seasonality as risk factors for equine laminitis. Prev Vet Med 29 (3), 179-184 PubMed.
  • Owens H G et al (1996) Evaluation of detomidine-induced analgesia in horses with chronic hoof pain. J Pharmacol Exp Ther 278 (1), 179-184 PubMed.
  • Riber C et al (1995) Hematologic changes observed in Andalusian horses with laminitis. J Vet Med Sci 57 (5), 981-984 PubMed.
  • Slater M R et al (1995) Descriptive epidemiologic study of equine laminitis. Equine Vet J 27 (5), 364-367 VetMedResource.
  • Owens J G et al (1995) Effects of ketaprofen and phenylbutazone on chronic hoof pain and lameness in the horse. Equine Vet J 27 (4), 296-300 PubMed.
  • Rowe J B et al (1994) Prevention of acidosis and laminitis associated with grain feeding horses. J Nutr 124 (12), 2742S-2744S PubMed.
  • Baxter G M et al (1994) Acute laminitis. Vet Clin North Am Equine Pract 10 (3), 627-642 PubMed.
  • Hunt R J et al (1993) A retrospective evaluation of laminitis in horses. Equine Vet J 25 (1), 61-64 PubMed.
  • Fagliari J J et al (1988) Changes in plasma protein concentrations in ponies with experimentally induced alimentary laminitis. Am J Vet Res 59 (10), 1234-1237 PubMed.

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 et al (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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