1. Equine Laminitis Gary M. Baxter

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

3. Coffin Bone Displacement

4. Clinical Forms Gastrointestinal/toxicGastrointestinal/toxic –Grain overload, grass founder –Metritis, retained placenta, colitis, colic Musculoskeletal/mechanicalMusculoskeletal/mechanical Metabolic/localMetabolic/local –Cushing's disease –Metabolic syndrome –Corticosteroids IdiopathicIdiopathic

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

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

7. Clinical Signs Lameness especially when turnedLameness especially when turned –Worse on hard surfaces –Shifting weight between limbs Increased digital pulsesIncreased digital pulses Heat over dorsal hoof wallHeat over dorsal hoof wall Both front feet commonly affectedBoth 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 periodVariable developmental period –Grain overload – 24-72 hours Much happening in foot before laminar damage and clinical signsMuch happening in foot before laminar damage and clinical signs Minimal control over initial laminar damageMinimal control over initial laminar damage Many horses with mild acute/subacute laminitis may not be recognizedMany horses with mild acute/subacute laminitis may not be recognized

10. Gross Pathology 1.Edema - compartment syndrome 2. Hemorrhage 3. Laminar separation 4. Structural damage

11. Physiologic Alterations HypertensionHypertension Sympathetic stimulation/tachycardiaSympathetic stimulation/tachycardia Systemic/local coagulopathySystemic/local coagulopathy Metabolic alterationsMetabolic alterations

12. Causes of Laminitis? Several potential theoriesSeveral potential theories –Vascular theory –Toxic/enzymatic theory –Traumatic/mechanical theory –Glucose/insulin resistance theory Common end-result in the foot?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 footToo little blood to foot Laminar ischemiaLaminar ischemia Reflex hyperemia – compartment syndrome/reperfusionReflex hyperemia – compartment syndrome/reperfusion Secondary inflammationSecondary inflammation Structural failure of laminaeStructural failure of laminae

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

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

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

17. Diagnosis Clinical signsClinical 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 anesthesiaLocal anesthesia –Improve with palmar digital, basi-sesamoid or abaxial blocks RadiographyRadiography –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 causeRemove or treat inciting cause –Minimize toxemia or “trigger factors” –Mineral oil, flunixin meglumine, DMSO Cushing’s – pergolideCushing’s – pergolide Metabolic syndrome/IRMetabolic syndrome/IR –Decrease glycemic index (CHOs) –Pergolide and thyroxine? MechanicalMechanical –Sling/ improve weight bearing on other limb –Support of contralateral foot

24. Treatment Dependent on stage of diseaseDependent on stage of disease –Cryotherapy (ice) in acute stage? –Vasodilatory drugs? –Anti-inflammatory drugs –Pain control (decrease sympathetic response) Minimize toe length (remove shoe)Minimize toe length (remove shoe) –Bevel dorsal hoof wall of toe Increase weight bearing surface areaIncrease 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 laminitisUnilateral right forelimb laminitis No known predisposing cause (toe grabs and long toe?)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 days4 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