1.6 Acute Equine Laminitis Flashcards

1
Q

How common is acute equine laminitis?

A

1.5-3.4%

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2
Q

What basic anatomy is necessary to know in the case of laminitis?

A
  1. within the hoof is the pedal bone, P3
  2. attached to the outside of P3 is the dermal lamellae (sensitive)
  3. the dermal lamellae interdigitate with the epidermal lamellae on the inside of the hoof
  4. the basement mambrane is anchored together by hemidesmosomes which are maintained and assembled by glocose-consuming phosphorylation reactions
  5. this increases the surface area of attachment and counteracts the weight of the horse pushing down, as well as the DDFT rotatating the P3 tip down into the sole

if the integrity of the system is damaged, P3 can sink and rotate

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3
Q

What are some risk factors for laminitis?

A
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4
Q

What is laminitis in its most basic form?

A

a syndrome not a disease: laminitis is a collection of clinical signs, with three distinct and unrelated forms, and the end result for each is similar:
- morphological derangement leads to loss of strength of lamellar attachment
- P3 is no longer suspended within the hoof capsule leading to pain

[A] healthy primary and secondary epidermal lamellae (PEL, SEL) [B] loss of attachment leading to CS associated with laminitis
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5
Q

What are the three forms of laminitis?

A

(1) sepsis-associated:

  • primary endotoxemia (GI perforation, severe pneumonia, septic metritis), leading to systemic inflammatory response syndrome leading to inflammatory and/or hypoxic injury of the laminar basal epithelial cells

(2) endocrinopathic:

  • primary endocrinopathy (PPID, equine metabolic syndrome, exogenous steroid tx) leads to prolonged hyperinsulinemia; poorly understood mechanism, but NOT inflammation

(3) excessive weight-bearing:

  • severe, prolonged lameness in one leg can cause laminitis in the other leg
  • likely chronic weight-bearing leads to inadequate perfusion c.f. mechanical overload
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6
Q

Regardless of cause, what are the three stages of laminitis progression?

A
  1. developmental stage (contact with trigger: up to 72hrs with no CS)
  2. acute laminitis (CS seen here)
  3. resolution or chronic laminitis (depending on response to tx: P3 remodelling or rotation)
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7
Q

How do you diagnose laminitis?

A

(1) clinical signs:

  • 2 or more limbs affected, stance, pain, temperature

(2) radiography:

  • lateromedial of all four feet: founder distance and rotation

(3) +/- endocrine tests

  • PPID: pituitary pars intermedia dysfunction (equine cushing’s)
  • EMS: equine metabolic syndrome
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8
Q

How do you manage acute laminitis medically?

A

(1) Analgesia

  • NSAIDs
  • +Opioids if NSAIDs not enough

(2) Blood flow

  • vasodilation (ACP may help relax horse and get it to lay down which would be good for the feet)
  • vasoconstriction: will limit endotoxins from reaching limbs; can ice for similar effect with no adverse effects

(3) Endocrine

  • peroglide for PPID
  • weight loss for EMS

(4) Other

note for analgesia (18): NSAIDs are the mainstay of treatment, as they are easy for the owner to give long-term.

Opioids are controlled drugs, short-acting, and usually given by injection -> not nearly as convenient for these reasons, but a possible option for some cases.

(17) treatment will take weeks to months

(19) Icing (digital cryotherapy) is proven effective. Can literally just tape plastic bags of ice around feet.

All horses a risk of complications are iced for 24-48 hours at the QMH. Little to no complications.

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9
Q

What do you look for on hoof radiograph for equine laminitis?

A

Founder distance

Rotation of P3

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10
Q

What are prognistic indicators for laminitis?

A

radiology:

  • rotation >11.5 degrees = significantly reduced prognosis
  • if founder distance has sunk >15mm: 40% chance of returnng to soundness after treatment

physical exam / history:

  • coronary band depression extends completely around hoof = 20% survuval
  • evidence of previous attacks = prognosis reduction by 20%
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11
Q

How do you prevent laminitis?

A

(1) endocrinopathic laminitis:

  • REDUCE the overconsumption of non-structural carbohydrates (NSCs) - sugar, starch, and fructan
  • horses with metabolic diseases such as PPID require less NSCs to maintain physiological functions
  • must analyze feed to be sure

(2) sepsis-associated lamintis:

  • treat underlying cause quickly
  • anti-endotoxic therapy
  • prophylactic digital cryotherapy

(3) supporting limb laminitis:

  • physiotherapy
  • treat underlying lameness
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