Lamanitis Flashcards Preview

Equine biology > Lamanitis > Flashcards

Flashcards in Lamanitis Deck (27):


inflammation of soft tissues (laminae) of equine foot, ultimately leading to separation of epidermis from dermis and hoof wall from phalanx


hoof anatomy

-primary and secondary dermal epidermal lamellae interdigitate to coffin bone, hoof capsule, and sole
-tendons and ligaments can be pulled and rotated
-vascular supply of corium; arteries and veins crushed when bone rotates
-60-65% of weight bearing is on front feet


coffin bone

-conforms to shape of hoof wall
-attached to hoof wall via dermis
-porous to allow blood vessels through overlying dermis


hoof wall

-grows from epithelium
-horn tubules cover dermis covering coffin bone


hoof, top to bottom, front to back external anatomy

-coronary, sensitive laminae, sole, bulbs


general points of laminitis

-complex, occurs mostly in adults and ponies (ponies any age, breed, or use)
-15% of all horses develop laminitis, 75% of which will develop chronic debilitating disease requiring euthanasia
-treatment must be aggressive and early
-all 4 feet affected, but usually front feet since they are weight bearing


acute vs chronic lamanitis

-occurs in stages
-chronic/founder associated with physical evidence of rotational or vertical displacement of third phalanx
-chronic follows acute


clinical signs of acute laminitis

-very painful, caused by bruising, inflammation, abscess formation
-unwilling to move, lameness
-rock backwards, shifting weight on rear legs
-exaggerated lifting of legs
-anxiety, sweating, increased heart and resp rate
-sweeling of coronet band
-unwillingness to lift leg for cleaning
-sensitive to hoof testers
rotation indicated by depression of coronet band, bulging sole


conditions associated with laminitis

acute GIT diseases like colitis, strangulation
-carb overload with fructans
-endocrine and metabolic diseases: increased steroids in blood/glucotoxicity
-endotoxemia or sepsis


theories on pathogenesis

-vascular, lack of oxygen to digit
-toxic metabolism, damage to epithelial cells of laminae result in vascular lesions
-both lead to death of laminae cells, causing hoof wall to separate from dermis and phalanx


3 forms of laminitis

-insulin resistance: CHO overload from derangement of glucose regulation
-mechanical trauma
-secondary result of systemic inflamm response syndrome (SEPSIS) or endotoxemia


insulin resistance

-found in horses with pituitary pars intermedia dysfunction (cushings)
-experimentally induced by HYPERINSULINEMIA
-common in horses on PASTURE due to high level of fructans in grass, which may lead to increase in insulin resistance and high blood glucose


mechanical trauma

-reduces blood flow to laminae
-caused by support limb laminitis or long trailers rides
-inflamm results in swelling, damage to vessels and loss of laminae
-cows deal with it better because they can lie down


endotoxemia or SEPSIS

-models using grain overload as model of laminitis show damage to lining of gut allows microbial products to enter blood stream
-gram -ve bac cell walls contain toxins
-reults in vasodilation and unresponsive vessels, blood shunts away from crucial tissues, damaging walls and clots



-radiographic evidence may see P3 (coffin bone) starting to sink


level of treatment

acute is EMERGENCY
-horses should NOT be moved or transported,


treatment 1: eliminate predisposing factor and primary disease

-treat endotoxemia or sepsis
-grain overload-gastric lavage or mineral oil
-corrective trimming and shoeing
-deep bedding
-cryotherapy=cold water


treatment 2

reduce pain and inflammation
-NSAIDs and opiods


treatment 3: minimize edema/swelling in hoooves

-do not give too much fluid therapy
-provide colloids into blood to increase oncotic pressure, drawing fluids into blood


treatment 4: improve blood flow

-heparin, asprin, dilate vessels


treatment 5

prevent movement of P3 within hoof capsule
-no exercise
-deep bedding, sand
-frog support to reduce weight bearing via padding , shoes



-pressure sores from prolonged recumbency
-weight loss
-chronic laminitis



variable, long recovery period
-pain useful predictor, high pain=worse prognosis
-rotation, sinking, prolapse=bad prognosis
-prolaspe=some success


chronic laminitis

-collapse of lamellae and displacement/rotation of P3
-causd by acute or recurrent chronic
-prognosis variable


chronic characteristics

space between wall and p3 filled with proliferation of cells of laminae, connective and dead tissue
-hoof continues to grow distortion occurs and see
'founder rings'
-white line widens


chronic complications

recurrent abscesses
-infection of p3, fractures
-perforation in sole
-hoof contraction pauses pain
-flexor tendon causes pain


chronic treatment

-reduce pain
-avoid excess body weight
-chronic NSAID therapy, tho does cause ulcers
-antibiotics when concerend with infection in bone
surgery: cut deep digital tendon to prevent pull, and drain abscesses