Laminitis Flashcards
The weight bearing structure of the horse.
Is not the digital cushion – the horse is suspended from the hoof laminae.
SAPD: suspensory apparatus of the digital phalanx
Laminitis is
inflammation of the laminae which results in weakening of the lamellar junction.
What happens in the hoof when the lamellar junction weakens?
The coffin bone (P3) changes position via rotation and sinking.
- Rotation: The tip of the coffin bone rotates caudally and distally. Can also be mediolateral.
- Sinking is distal displacement of P3. Look for a groove around the pastern.
4 Phases of laminitis.
- Subclinical phase: development of laminitis
* Primary changes in the lamellar basal membrane but no clinical signs. - Acute laminitis 24-72h (so 3 days max)
* Clinical signs; the P3 has not displaced yet though.
* But also, P3 can displace faster and the acute phase can last for only 24 hrs or so too. - Subacute laminitis from 72h onward
* Clinical signs stabilize/ ameliorate, P3 has not displaced. - Chronic laminitis
* P3 is displaced
* Can be chronic, active, acutely painful
Clinical signs of laminitis in horses. (4+)
Front limbs usually more severely affected:
will shift weight to hindquarters and stand
“camped under”.
Digital pulses palpated at the level of sesamoid
bones: strong pulsation.
A groove around the pastern may be palpated:
indicates sinking.
Lameness, reluctance to move.
Clinical signs of acute sinking-laminitis.
- Palpate the coronary band: can you feel a sinking line or groove?
- Most severe case: detached coronary band.
Under the sole:
* Tip of P3 protruding out
* Or Sole bulging out
Clinical signs of chronic laminitis.
Persistently stilted gait and a degree of pain (varies from mild to severe).
Distortion of the hoof capsule.
Horizontal lines indicating phases of uneven growth/ weakening of lamellar attachment.
Broad causes of laminitis. (4)
endotoxemic
ischemic
endocrinopathic
corticosteroid-induced
endotoxemic causes of laminitis
SIRS: target organs are liver, kidneys, lungs and dermal lamellae.
Inflammatory mediator release (IL-1ß, IL-10, CXCL-8, TNF-α, COX-2)
Activation of coagulation cascade, neutrophils migrate into lamellar vasculature, microthrombus
formation→ vasoconstriction, local ischemia.
Protease and free O2 radical activation.
Lamellar attachment breakdown due to inflammation and ischemia.
ischemic causes of laminitis
Mechanical impairment of the blood flow to the hoof .
Compressive injuries of the lower limb, wire cut or
degloving injuries.
Prolonged (weeks) weight bearing on one foot with no rest.
endocrinopathic causes of laminitis
Equine metabolic syndrome (EMS) and pituitary pars intermedia dysfunction (PPID)
Hyperinsulinemia (!)
There is no neutrophilic migration but there are several theories.
Basal membrane changes + inflammatory changes leading to lamellar junction weakness.
corticosteroid-induced causes of laminitis
long courses of dexamethasone or long-acting triamcinolone (synthetic corticosteroid)
Is rare
Causes of SIRS/ endotoxemia in horses.
Any severe infection/ inflammation such as septic peritonitis, septic metritis, severe pleuropneumonia, colitis and these can be due to
e.g. Infection, carbohydrate overload, severe parasitism (cyathostomin infection), ingestion of a toxic substance etc.
Laminitis from the above begin with fever and no other clinical signs yet. It takes up to 24 hrs to develop clinical signs like elevated digital pulses, unwillingness to move.
Look for: temps over 38.6 C, heart rate over 60
bpm, tachypnea, WBC below 4000 or over 14 000 per
μl, or marked left shift with over 10% banded
neutrophils.
When you see obesity or regional fat pads - these suggest what? And what 2 diseases should you suspect?
Obesity or regional fat pads suggest insulin resistance
Equine metabolic syndrome (EMS) and/or pituitary pars intermedia dysfunction (PPID)
- Sudden increase in carbohydrates in the diet of an insulin dysregulated horse - high risk of laminitis.
At risk breeds: “easy keepers” or aboriginal breeds:
Estonian, Icelandic, Finnhorse, all pony breeds
If laminitis is acute, don’t do what?
don’t transport the horse.
Describe laminitis radiography.
All 4 feet, on blocks, from 1 m distance, beam perpendicular to the hoof.
Lateromedial and ideally also horizontal dorsopalmar view.
Several distances and angles can be measured with no exact ranges published for each breed.
- Dorsal hoof wall angle vs parietal surface angle
- Sole thickness
- Extensor process distance from coronary band (0…15 mm)
Tx of laminitis.
Treatment always needs to start immediately. The absolute first thing: the horse goes into a softly bedded box and will not come out of it.
Certain basic tenets apply in all cases:
1. Analgesia
2. Prevent /stop/ slow down P3 displacement, hoof support.
3. Try to identify inciting cause and tx it. This includes diet adjustment.
Access to advanced farriery is recommended in
most cases and essential in some cases.
Pain meds you can use in laminitis cases.
NSAIDs
* Flunixin meglumine 1.1 mg/kg per os or iv 2x day
* Firocoxib loading 0.3 mg/kg once, then 0.1 mg/kg orally 1x day. The most COX2 selective NSAID in horses.
* Phenylbutazone 4.4 mg/kg, then drop to 2.2 mg/kg per os 2x day (The most toxic).
* Meloxicam 0.6 mg/kg per os 1x day
Paracetamol 30 mg/kg per os 2x day
* this is in addition to an NSAID
Gabapentin 20-60 mg/kg per os 2x day for neuropathic pain.
Ketamine, morphine if all the former don’t make the horse comfortable.
Steroids (like dexamethasone or prednisolone) can induce or worsen insulin resistance, which is one of the major drivers of endocrinopathic laminitis.
In some horses, especially those with Equine Metabolic Syndrome (EMS) or PPID (Cushing’s), steroids have even been known to trigger laminitis episodes.
Describe hoof support for laminitic horses.
Hoof support aims to reduce the pressure on the hoof wall and provide sole support.
Nip off too long toes to reduce breakover.
Anyone can make hoof supports from blue Styrofoam pads: 5-6 cm thickness for a horse, 3-4 cm for a pony.
Easily cut with a hand saw. Use grey duct tape to attach to hooves. Usually there’s instant relief and the horse walks more readily.
Longer term: soft ride boots
Postpartum laminitis can be caused by?
Retained fetal membranes leading to metritis: when did they come out? 3 hours max!
* Check if intact!
Most typical presentation for postpartum laminitis/ metritis is 2-3 days after foaling, the mare is dull,
febrile, inappetent and has a stiff gait.
Membranes came out but most likely a small remnant was ripped off and is still attached.
Treat postpartum metritis cases aggressively!
Can you prevent laminitis?
SIRS: treat underlying cause aggressively!
* Platinum BioSponge poweder to bind toxins in
hindgut.
* Use low molecular weight heparin for 3 days
after colic surgery. Will inhibit platelet aggregation in capillaries.
Consider digital cryotherapy:
Submerge the legs and feet into ice water 24/7
so that the hoof wall outer temperature drops
to 5’C. Suppresses local inflammation and won’t
cause ischemia. Do until no more signs of SIRS, or at least 7 days if laminitis signs already present.
How can you prevent Ischemia-induced laminitis?
Supporting-limb-laminitis:
Unclear what the exact underlying mechanism is.
Happens in < 20% of all cases where the limb is perpetually loaded. Can even happen months after initial injury. Probably cumulative microdamage.
Weight-shifting/ unloading even a little bit is protective.
Avoid by:
* adequate pain medication to get the horse to bear weight on the affected limb.
* Epidural analgesia in case of a hindlimb
* Suspend the horse in a sling
* Heel elevation in the supporting foot by 10°
Trauma/ wire cut:
* repair the trauma
* encourage circulation (laser, vasodilators)
* thoughts and prayers
Most common cause of laminitis?
endocrinopathic disease like metabolic syndrome and pituitary pars intermedia dysfunction (PPID)
