Laminitis: A Comprehensive Guide PDF

Summary

This document provides a comprehensive overview of equine laminitis, a serious hoof condition in horses. It covers various aspects including gross and micro anatomy, histological breakdowns, and different treatment methods. The insights into the pathophysiology and radiographic examination of laminitis are also included.

Full Transcript

Laminitis- As BAD as it gets Gal Kelmer DVM MS DACVS DECVs Gross Anatomy Micro Anatomy  Laminitis Dermal Laminae occurs when the attachment between hoof & coffin bone fails ▪ Basement membrane is weak link Histological Breakdown ...

Laminitis- As BAD as it gets Gal Kelmer DVM MS DACVS DECVs Gross Anatomy Micro Anatomy  Laminitis Dermal Laminae occurs when the attachment between hoof & coffin bone fails ▪ Basement membrane is weak link Histological Breakdown Laminitis  Chronic & acute phases  Chronic is loosely defined as clear failure of the attachment between the hoof wall & P3 ▪ Or could be defined as the stable form of the condition Kind of.…chronic Laminiti s  Lamellae of the inner hoof wall fail  Weight of horse & locomotion drive the bone into the hoof capsule  Damages vasculature & crushes corium of sole Laminitis Pathophysiology  Ischemic necrosis may occur  Dorsal laminar perfusion of the foot is poorest & thus most likely compromised ▪ Leads to necrosis & pedal rotation (because of pull of DDF tendon) Laminitis Pathophysiology  If insult is severe enough, all laminae are compromised ▪ Entire foot sinks ▪ Horse is referred to as a "sinker" Bilateral Severe Laminar detachment Laminitis Pathophysiology  “New” theory (Pollitt’s)  Matrix metalloproteinase enzymes (MMP 2 & MMP 9), maintain & remodel attachments of hoof wall to distal phalanx as hoof wall grows (Controlled enzymatic remodeling).  Metalloproteinase enzymes become activated by trigger factors, causing breakdown of attachments  Other proteases are activated as well Laminitis Pathophysiology Research model: Laminitis induced by over load of oligofructose Trigger factors are Strep Bovis (+other Streps) Exotoxins Hemodynamic changes, fluid shifts, & microthrombosis are a result, not a cause, of failure of the bond between P3 and the hoof wall Laminitis Pathophysiology  Pollitt’s theory challenges the view that laminitis develops because the flow of blood is impeded to cause ischemic necrosis of epidermal lamellae  Evidence shows that foot circulation during developmental (or prodromal) phase of laminitis is vasodilated What is most accurate regarding ?laminitis pathophysiology 1. It is still a mystery- nobody really knows 2. Blood flow is the key- vasoconstriction leads to decreased lamellar activity and detachment 3. Exotoxin induced protease activity that causes breakdown the basal membrane 4. Endotoxemia induced MMP’s activity and that cause vasoconstriction and leads to ischemia 5. MMP 9 & 2 are activated by the vasodilatation and cause crushing of the lamella Laminitis Pathophysiology ▪ Laminitis does not occur if the foot is in a state of vasoconstriction during the developmental phase, suggesting that the trigger factors cause laminitis only if they reach the lamellar tissues at a high enough concentration & over a long enough time. CLLL- Contra Lateral Limb Laminitis  Occurs due to severe prolonged lameness  More common in forelimbs  Can occur in OTHER limbs!  No circulating factors only mechanical load  Again – prevention is the key!  Cast is a significant predisposing factor  Mechanical support is the key for prevention  Modified Ultimate Shoes are a helpful preventative factor Grades of Severity of Laminitis  Obel grades (1948):  Grade 1. At rest, the horse alternately & incessantly lifts its feet. Lameness is not evident at a walk, but a short stilted gait is noted at a trot.  Grade 2. Horse moves willingly at a walk, but gait is stilted. A foot can be lifted of the ground w/o difficulty  Grade 3. Horse moves very reluctantly & vigorously resists attempts to have a foot lifted.  Grade 4. The horse refuses to move & will not do so unless forced.  Good correlation w/ Obel grade & pathologic changes seen histologically Radiographic Examination  Important for establishing a Tx protocol & prognosis  Latero-medial view helps establish if condition is acute or an exacerbation of a more chronic problem Radiographic Examination Abnormal thickness Extreme Sports of dorsal hoof wall, w/ or w/o modeling of toe of distal phalanx, implies chronic laminitis Radiographic examination  Rotation or sinking of distal phalanx  Increased thickness of dorsal hoof wall = HLZ ▪ Should be

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