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Equine Laminitis

Equine Laminitis. Gary M. Baxter. Definitions. Inflammation of the laminae Numerous inciting causes Laminitis vs. “founder” Separation of the dermal and epidermal junction Attachment of coffin bone to hoof wall Displacement of the coffin bone Rotation Sinking Combination of the two.

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Equine Laminitis

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  1. Equine Laminitis Gary M. Baxter

  2. Definitions • Inflammation of the laminae • Numerous inciting causes • Laminitis vs. “founder” • Separation of the dermal and epidermal junction • Attachment of coffin bone to hoof wall • Displacement of the coffin bone • Rotation • Sinking • Combination of the two

  3. Coffin Bone Displacement

  4. Clinical Forms • Gastrointestinal/toxic • Grain overload, grass founder • Metritis, retained placenta, colitis, colic • Musculoskeletal/mechanical • Metabolic/local • Cushing's disease • Metabolic syndrome • Corticosteroids • Idiopathic

  5. Predisposing Factors • Systemic illness (toxemia) • Excessive carbohydrate/grass • Metabolic/weight problems • Increased glucose/insulin resistance • Older horses and mares • Non-Thoroughbred breeds • Unilateral lameness • Long toe/low heel • Hard surfaces

  6. Stages of Laminitis • Developmental – before clinical signs • Acute • Clinical signs only • No movement of coffin bone on radiographs • Chronic • Movement of coffin bone within hoof • Subacute? • In between the acute and chronic stages

  7. Clinical Signs • Lameness especially when turned • Worse on hard surfaces • Shifting weight between limbs • Increased digital pulses • Heat over dorsal hoof wall • Both front feet commonly affected • All four feet (very sick horses) • Both rear feet (draft horses?) • Single foot (excessive weight-bearing)

  8. Laminitis

  9. Disease Process • Variable developmental period • Grain overload – 24-72 hours • Much happening in foot before laminar damage and clinical signs • Minimal control over initial laminar damage • Many horses with mild acute/subacute laminitis may not be recognized

  10. Gross Pathology • Edema - compartment syndrome • 2. Hemorrhage • 3. Laminar separation • 4. Structural damage

  11. Physiologic Alterations • Hypertension • Sympathetic stimulation/tachycardia • Systemic/local coagulopathy • Metabolic alterations

  12. Causes of Laminitis? • Several potential theories • Vascular theory • Toxic/enzymatic theory • Traumatic/mechanical theory • Glucose/insulin resistance theory • Common end-result in the foot? • Inflammation • Breakdown of basement membrane of laminae • Separation of sensitive and insensitive laminae

  13. Vascular Theory • Too little blood to foot • Laminar ischemia • Reflex hyperemia – compartment syndrome/reperfusion • Secondary inflammation • Structural failure of laminae

  14. Toxic/Enzymatic Theory • Excessive blood to foot • “Trigger factors” within the blood (from gut or uterus) initiate damage • Several enzymes/mediators damage basement membrane • Secondary inflammation • Structural failure of laminae

  15. Mechanical Theory • Different from “classic” GI form • Traumatic tearing of laminae from excessive weight bearing? • Pain contributes to increased cortisol • Increased insulin? • Vasospasm of digital vessels? • Secondary inflammation • Structural failure of laminae

  16. Glucose/IR Theory • Hyperglycemia/insulin resistance • Impaired blood flow • Direct effect of increased insulin • Impaired glucose uptake • Laminar cells have high glucose requirement • Secondary inflammation • Structural failure of laminae

  17. Diagnosis • Clinical signs • Increased digital pulses • Heat over dorsal hoof wall • Variable lameness but often severe • Heel-toe landing/hoof distortion in chronic cases • Pain over toe with hoof testers • Local anesthesia • Improve with palmar digital, basi-sesamoid or abaxial blocks • Radiography • Rotation, sinking or both

  18. Chronic Laminitis

  19. Radiology – “Rotation”

  20. Radiology – “Sinking”

  21. Radiology - chronic

  22. Treatment/Prevention Developmental – to prevent disease progression Acute – to minimize severity of laminar damage Chronic – to limit further movement of coffin bone

  23. Treatment • Remove or treat inciting cause • Minimize toxemia or “trigger factors” • Mineral oil, flunixin meglumine, DMSO • Cushing’s – pergolide • Metabolic syndrome/IR • Decrease glycemic index (CHOs) • Pergolide and thyroxine? • Mechanical • Sling/ improve weight bearing on other limb • Support of contralateral foot

  24. Treatment • Dependent on stage of disease • Cryotherapy (ice) in acute stage? • Vasodilatory drugs? • Anti-inflammatory drugs • Pain control (decrease sympathetic response) • Minimize toe length (remove shoe) • Bevel dorsal hoof wall of toe • Increase weight bearing surface area • Styrofoam, sand, frog pads, soft putty • Corrective shoeing

  25. Initial Foot Support

  26. Corrective Shoeing

  27. Foot Preparation

  28. 6-year old App. Stallion • Unilateral right forelimb laminitis • No known predisposing cause (toe grabs and long toe?) Removed shoe, shortened toe, and applied a lily pad for frog support

  29. Follow-up Radiographs 10 days 4 weeks Progressive rotation of coffin bone Abscess developed at toe region Performed unilateral deep digital flexor tenotomy Applied extended heel shoe with a treatment plate

  30. Thank you from CSU-VTH

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