Lamanitis

Question 1

laminitis

Answer 1

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

Question 2

hoof anatomy

Answer 2

• 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

Question 3

coffin bone

Answer 3

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

Question 4

hoof wall

Answer 4

• grows from epithelium

- horn tubules cover dermis covering coffin bone

Question 5

hoof, top to bottom, front to back external anatomy

Answer 5

-coronary, sensitive laminae, sole, bulbs

Question 6

general points of laminitis

Answer 6

• 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

Question 7

acute vs chronic lamanitis

Answer 7

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

Question 8

clinical signs of acute laminitis

Answer 8

-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

Question 9

conditions associated with laminitis

Answer 9

acute GIT diseases like colitis, strangulation

• carb overload with fructans
• endocrine and metabolic diseases: increased steroids in blood/glucotoxicity
• endotoxemia or sepsis
• fractures
• obesity

Question 10

theories on pathogenesis

Answer 10

• 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

Question 11

3 forms of laminitis

Answer 11

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

Question 12

insulin resistance

Answer 12

• 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

Question 13

mechanical trauma

Answer 13

• 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

Question 14

endotoxemia or SEPSIS

Answer 14

• 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

Question 15

diagnosis

Answer 15

• history

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

Question 16

level of treatment

Answer 16

acute is EMERGENCY

-horses should NOT be moved or transported,

Question 17

treatment 1: eliminate predisposing factor and primary disease

Answer 17

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

Question 18

treatment 2

Answer 18

reduce pain and inflammation

-NSAIDs and opiods

Question 19

treatment 3: minimize edema/swelling in hoooves

Answer 19

• do not give too much fluid therapy

- provide colloids into blood to increase oncotic pressure, drawing fluids into blood

Question 20

treatment 4: improve blood flow

Answer 20

-heparin, asprin, dilate vessels

Question 21

treatment 5

Answer 21

prevent movement of P3 within hoof capsule

• no exercise
• deep bedding, sand
• frog support to reduce weight bearing via padding , shoes

Question 22

complications

Answer 22

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

Question 23

prognosis

Answer 23

variable, long recovery period

• pain useful predictor, high pain=worse prognosis
• rotation, sinking, prolapse=bad prognosis
• prolaspe=some success

Question 24

chronic laminitis

Answer 24

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

Question 25

chronic characteristics

Answer 25

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

Question 26

chronic complications

Answer 26

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

Question 27

chronic treatment

Answer 27

- reduce pain - shoes - 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