Laminitis Flashcards
Definition
- inflammation of the laminae of the foot
Founder
- laminitis so severe that all the laminae in the hoof cease functioning and the pedal bone has dropped down
BUT - term used interchangeably with laminitis
What is the weight bearing structure of the hoof?
- the hoof wall
- (the frog takes some of it)
What are the 2 types of laminae in the hoof
- sensitive laminae (attached to the coffin bone)
- insensitive laminae (attached to the hoof wall)
Pathophysiology
- dermal lamellae (P3) and epidermal lamellae (hoof) are strongly bonded
- to allow hoof growth this bond is released slightly via the action of matrix metalloproteinase (MMP)
- MMP are catabolic enzymes
- laminitis is the degeneration then failure of interdigitation between P3 and inside of hoof wall -> breakdown & separation
- excess MMP activity is involved
- mechanisms not fully understood but several dz processes are implication
- sliding scale of severity (not a binary dz)
Where does hoof wall grow from?
- the coronary band
How long does it take the hoof wall to grow from the coronary band to the sole?
- 6m
- less (~4m) for the palmar/plantar aspect
Endocrine causes
- EMS
- PPID
Non-endocrine causes
- toxic
- support limb laminitis
- corticosteroid induced
Obesity/EMS causing laminitis
- increased bodily fat reduces the cellular response to insulin -> insulin resistance/dysregulation
- cells remove less glucose from bloodstream ->hyperglycaemia
- body produces more insulin to try to combat the hyperglycaemia (negative feedback loop) -> hyperinsulinaemia
- excess insulin in bloodstream stimulates excess MMP production increasing the risk of laminitis
Probably the most common cause of laminitis
Toxic causes of laminitis
concurrent to:
1. compromised bowel e.g. colitis, enteritis, strangulation
2. severe infection e.g. RFM/sepsis
- bacterial endotoxin enters the bloodstream -> endotoxaemia
- MMP production is increased
PPID causing laminitis
- excess ACTH also causes hyperinsulinaemia
- endocrinopathic causes of laminitis are closely interlinked
Support limb laminitis
- severe lameness in 1 limb causes excessive weight bearing in contra-lateral limb, e.g. fracture with inadequate stabilisation
- prolonged pressure within the hoof of the ‘non-lame’ limb reduces blood flow to the laminae causing hypoxia
- hypoxia causes inflammation and MMP production
- therefore, support limb laminitis is often unilateral
Corticosteroid induced laminitis
- exogenous glucocorticoid
– rare (0.15% in a study)
– different glucocorticoids have different risks, e.g. preds very low, others (e.g. triamcinolone) much higher - stress
– endogenous glucocorticoids increase - induce hyperinsulinaemia and subsequent increased MMP production
- risk greater in animals that are already susceptible e.g. EMS
- discuss this risk with O before corticosteroid injection
- recommend taking blood insulin test before administering corticosteroids (even for asthma) in fat horses
Signalment
Age
- no consistent predisposition but foal & weanlings rarely affected (likely bc they’re growing so all their glucose is going into growing, also they’re not old enough for the endocrine disorders)
Breeds
- occurs in all breeds of horse, but natives/ponies predisposed
- donkeys can be severely affected
- the heavier the horse the more difficult it will be to treat, e.g. draughts/shires
Sex
- no predisposition
Incidence in UK
- 1/10 equines may have at least 1 laminitis epidote each year
- as common as colic
- approx. 15% equine deaths linked to laminitis
- year round problem with incidence peaks in spring and autumn
- most cases are endocrine
– toxic and support limb less common
History q’s
- when did signs begin?
- progression - getting better or worse?
- any recent management changes?
- previous episodes of laminitis?
- any concurrent dz/injury?
- received any medications recently?
- current diet?
- when last trimmed/shod?
- horse’s use?
- exercise history?
General CE
- recumbent?
- stance?
– leaning backwards
– weight shifting - rr/panting?
- hr?
- temp?
- sweating?
- pained expression?
CE - evidence of endocrinopathy
PPID
- hirsutism
- decreased muscle mass
- ‘pot belly’ appearance
- supraorbital fat pads
EMS
- excess body condition
- abnormal fat distribution
CE - limb specific
- often affects both front limbs
- may be all 4 limbs, just 1 or just the hind limbs
- increased digital pulse
- hooves warm to touch
- visible growth rings indicate previous episodes
- able to life legs?
- often show pain to hoof testers at point of frog
- shod/unshod and type of shoe?
- depression at coronary band and loss of concavity of sole suggest severe dz (sinking)
CE - dynamic
- degree of lameness varies
- may be mild (walks almost normally) to severe (unable to walk)
- usually worse when turning and on hard ground
- foot lands heel first to spare the toe region from weight bearing
- sometimes show a high stepping gait with hind limb laminitis
Modified Obel grade 0
- sound
Modified Obel grade 1
- weight shifting at rest
- sound walking in straight line
- stilted gait when turning or trotting
Modified Obel grade 2
- stilted gait when walking in straight line
- clearly lame when turning
- legs can be lifted without difficulty
Modified Obel grade 3
- reluctant to walk
- legs can only be lifted with great difficulty
Modified Obel grade 4
- will only move if forced to
- spends long periods recumbent
Radiography
Latero-medial view
- rotation
– <5° mild
– 5-10° moderate
– >10° severe
- sinking
- remodelling/degeneration at tip of P3?
- hoof overgrowth?
Dorso-palmar view
- rare collapse on just the lateral or medial side
Metabolic testing - EMS
1) Baseline insulin (serum)
- Feed only hay / grass for 12 hours prior
- Positive result (increased baseline insulin) is diagnostic for EMS
- Negative result (normal baseline insulin) does not rule the disease out – lots of false negatives
2) Oral sugar challenge tests
- Feed only hay / grass for 12 hours prior
- Feed Karo light corn syrup or dextrose powder
- Blood sample for insulin 60-90 mins later
Metabolic testing - PPID
1) Baseline ACTH (EDTA)
- Usually diagnostic
- Reference range changes through the year
- Usually most accurate in the autumn
2) Thyrotropin Releasing Hormone stimulation test
- Rarely required
- Collect baseline ACTH
- Inject TRH
- Collect another ACTH 10 minutes later
Metabolic testing
▪ Results are inaccurate if animal is in pain – maybe wait a few days until more comfortable.
▪ Repeat samples are required to assess the response to treatment and adjust management & drug dosages
Initial Management
▪Pain Relief
- NSAIDs (phenylbutazone), paracetamol, opiates (butorphanol good for short term analgesia)
▪ Vasodilator
- Improve blood supply to distal limbs
- Acepromazine (has additional benefit of reducing anxiety)
▪Support feet
- Confine to stable on deep shavings bed - Remove shoes?
- Use frog supports
- In the per-acute phase (not after 24h) ice packs can help
▪ Diet - Weight loss
- 1.5-2% body weight dry weight hay, soaked for 1 hour to reduce sugar content
- Tiny amount of low sugar food (alfalfa) to put medication in
- Vitamin / mineral balancer
▪ Warn owner that this is not a quick fix
- 3w bost rest minimum to start with
▪ Euthanasia?
Subsequent management
▪ Regular re-examinations (initially 1x weekly)
▪ Adjust medication & management
accordingly
▪ Endocrine testing once pain reduced
▪ EMS – metformin, levothyroxine, ertugliflozin
▪ PPID – pergolide, cabergoline
▪ Farriery – trim heels & toes, heart bar shoes (good as utilises the frog to reduce weight bearing on the sole)
▪ Carefully and gradually introduce exercise
▪ Repeat radiographs if not improving / as required by farrier
▪ Euthanasia?
Salvage procedure
▪ Deep digital flexor tenotomy
▪Mid cannon
▪ Removes the palmar traction on P3
▪ Salvage only (some believe)
▪ Only for rotational laminitis
▪ Instantly reduces lameness by 1 Obel grade
Prognosis
▪ Lameness severity ▪Degree of rotation
▪ Sinking
▪Patient weight
▪ Ability to control endocrine disease
▪ Improvement takes many months
- As the new hoof grows down – 1 year
▪ Repeat episodes are common
