Acute Laminitis Flashcards

0
Q

What are the risk factors for laminitis?

A

Sepsis and systemic inflammation (GI disease, pneumonis, septic metritis)
Endocrine disorders (PPID and EMS)
Mechanical overload
Access to pasture

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1
Q

What is the pathology that causes laminitis?

A

Failure of the attachment of the epidermal cells of the epidermal laminae to the underlying basement membrane of the dermal laminae

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2
Q

What signalment can predispose to laminitis?

A

Pony, spring/summer, female, increasing age, obesity, recent increase in body weight, recent new access to grass, increasing time since worming, insulin resistance

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3
Q

What are the three stages of laminitis? What occurs at each stage?

A

Developmental/prodromal - contact with trigger, lasts up to 72 hours, no clinical signs, when all changes occur
Acute laminitis - onset of clinical signs
Resolution or chronic laminitis

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4
Q

How is inflammation linked to the pathogenesis of laminitis?

A

Minimal neutrophil infiltration caused doubt but recent research shows abundant evidence of inflammatory changes
Mechanisms linking pasture consumption and lamellar inflammation not fully determined but systemic inflammation accompanying hindgut carbohydrate overload is thought to initiate lamellar inflammatory events

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5
Q

How is ECM degradation linked to the pathogenesis of laminitis?

A

Previously thought that dysregulation of MMPs was fundamental but now known not to be an initiating event
Laminar separation may occur following a failure of epithelial adhesion molecules
Dysregulation of cell adhesion is most likely caused by inflammatory and/or hypoxic cellular injury

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6
Q

What pathologic mechanisms associated with EMS could increase chance of laminitis?

A

Changes in insulin signalling
Inflammatory cytokines
Endothelial dysfunction caused by adipose tissue-derived mediators

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7
Q

Why do laminitis prone individuals become more at risk during spring and summer?

A

Strong positive relationship between pasture NSC content and circulating insulin concentrations, increased CHO consumption increases IR
Exacerbation of IR by increased CHO consumption during summer months => laminitis

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8
Q

What are the vascular events that occur in the early stages of laminitis?

A

Digital venoconstriction and consequent laminar oedema

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9
Q

What are the hypothesised causes of vascular events in laminitis?

A

Platelet activation and platelet-neutrophil activation causing release of 5-HT causing venoconstriction
Amines from hindgut fermentation of CHO are vasoactive
IR in other species alters endothelial function creating a pro-inflammatory condition leading to platelet and leucocyte activation, increased ET-1 and production of inflammatory mediators and oxidant stress

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10
Q

What are alterations in digital vascular haemodynamics associated with?

A

Inflammation, platelet activation, action of vasoactive amines absorbed from the intestinal tract

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11
Q

What are your aims in a suspected case of laminitis?

A

Make a definitive diagnosis
Determine the underlying cause
Determine if horse is likely to recover to expected level of soundness

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12
Q

What is diagnosis of laminitis made on?

A

Clinical signs
+/- radiography showing sunken/rotated pedal bone
+/- endocrine tests for PPID and EMS

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13
Q

What are the clinical signs of laminitis?

A
Lameness affecting two or more limbs
Leaning back on heels
Bounding digital pulses
Increased hoof wall temperature
Pain on hoof tester at the point of the frog
Palpable depression at the coronary band
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14
Q

What radiographs are taken to diagnose laminitis?

A

Lateromedial radiographs of feet following good foot preparation
Mark feet with one mark on dorsal hoof wall and one at the point of the frog

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15
Q

What tests are performed to evaluate likelihood of PPID and EMS?

A
PPID = basal ACTH, dexamethosone suppression test, TRH stimulation test
EMS = demonstration of insulin resistance by fasting insulin and glucose levels
16
Q

What medical treatment should be given to a horse diagnosed with laminitis?

A

Analgesia - NSAIDs such as bute, flunixin, carprofen or opiates such as morphine, pethadine, fentanyl
Vasodilator (ACP)/vasoconstrictor (ice) therapy is controversial as once clinical signs appeared damage caused by change in blood supply will have occurred

17
Q

How can foot support be provided?

A

Increase bedding in depth and bring to door
Frog support with bandages, lilypads, NFS etc
Frog and sole support using styrofoam or dental impression material

18
Q

What management changes should be made?

A

Box rest

Change diet to 1.5-2% body weight poor quality hay, no or minimal concentrates

19
Q

What are the treatments if an endocrine disorder is diagnosed?

A
PPID = pergolide
EMS = weight loss, increased exercise, +/- pharmacological agents
20
Q

What is prognosis for laminitis linked to?

A

Extent of clinical signs

21
Q

What are the different prognoses depending on extent of disease?

A

Depression around coronary band = 20% survival
Previous attacks = decrease success rate by 20%
Rotation of >11.5 degrees = reduced prognosis
Reduced founder distance of >15mm = 40% chance of returning to soundness
After 8 weeks 95% alive, 72% sound at trot, 59% ridden again

22
Q

What preventative measures can be taken against laminitis?

A

Minimise intake of NSC (<10%) (lowest when plant is growing)
Diet based on forage/fibre not sugar starch
Regular exercise to prevent obesity

23
Q

What grazing changes should be advised to prevent laminitis?

A

Consider zero grazing, turn out late night to early morning, restrict grazing in spring and summer, avoid if frost with bright sunshine/drought, rotate paddocks to keep grass at appropriate height, restrict intake by strip grazing/muzzle