Laminitis (Menzies-Gow) Flashcards
What is laminits?
- failure of attachement of epidermal cells of insensitive laminae (epidermal) to underlying basement membrane of sensitive laminae (dermal)
What 2 direction can the pedal bone move in?
Rotate or sink down
Risk factors for laminits
> sepsis and sysetmic inflammation
- GI disease, sick neumonia, septic metritis
endocrine disorders
- PPID and EMS
mechanical overload
- non-weight bearing lame for significant period of time (contralateral laminitis)
access to pasture
PDF for laminitis
- pony
- spring/summer (related to grass)
- female (maybe)
- ^ age
- obesity
- recent ^ BCS
- recent access to new grass
- ^ time since worming(? reason for link)
- insulin resistance
3 stage of laminitis?
- developmental
- lasts ~72hrs
- contact w/ trigger and breakdown of attachemnts
- NO CLINICAL SIGS - acute
- clinical signs seen - Resolution or progression to chronic laminitis
Main 4 aspects of pathogenesis?
- inflammation
- ECM degradation
- metabolic disease
- endothelial and vascular dysfunction > exact mechanism not elulcidated
How is inflammation involved in laminitis?
- minimal neutrohil infiltration histopathologially - role questioned
- lamellar inflammation definiely involved now
- ## hindgut fermentation of carbs in gut -> systemic inflam with only overt signs in the pony’s feet ? Inflam seen elsewhere in the body too
How is ECM degradation involved in laminitis?
- (ECM = structural proteins, proteoglycans, regulatory proteins, proteases, protease inhibitiros. Responsible for maintainance of structural support, remodelling, healing)
- previously thought MMPs fundamental - now shown not an initiating event (but is involved)
- now shown laminar separation = failre of adhesion molecules called hemidesmisomes (attach epidermal cells to basement membrane)
- somehow these are moe liekly to fail in the feet (inflam? hypoxia and reperfusion injury?)
How is metabolic disease linked to laminitis?
- greatest risk of laminitis assocaited with ‘metabolic phenotype’ (eg. obesity, insulin resistance)
- endothelial cell dysfunction caused by mediators from adipose tissues
- hypertension?
- may be exaccerabation of IR by increased carbs (grass intake) -> laminitis in summer/spring
> NB not all laminitis prone ponies are obese and not all obese ponies are laminitis
How are ascualr and endothelial cells indicate in lamintis?
- digital vasoconstriction and consequent laminar oedema
- venoconstriction d/t platelet activation and platelet neutrophil acitvation -> vasoactive mediator 5HT
- amines from hidgut fermentation of CHO are vasoactive
- IR in other species alters endothelial function -> pro-inflam condition -> platelet and leucocyte activation, ^ production ET1 and production of mediators of inflame and oxidant stress
What aret he aims of the workup?
- definitive dx
- determine cause
- prognosis of recovery and soundness?
How many legs are commonly affected in laminitis?
More than one (can be one, but very unlikely)
Clinical signs of laminitis
- 2+ limbs
- leaning on heels
- bounding digital pulses
- hoof wall may feel warm
- pain in hoof testers at the point of the frog
- palpable depression at the coronary band (extensor process of pedal bone should -> solid uncompressable area, otherwise indicates pedal bone has sunk. POOR PROG)
What further diagnostics can be carried out for lamintis?
- Imaging
- Endocrine tests
When would radiographs be indicated?
> concern P3 has moved - palpable softening at point of frog - depression at coronary band > if not improing * can be difficult, may need +- nerve blocks*
What rads are needed?
Lat med rads of affected foot
- marker dorsal hoof wall (top level with coronary band)
- marker point of frog
> look for founder and rotation
What endocrine tests may be performed?
> PPID
- basal ACTH (seasonally adjusted ref range)
- dex suppression (not autumn)
- TRH stim
EMS
- Hx and lcincial signs
- demonstration of IR (fasting insulin and glucose)
Medical tx of laminitis
- medical emergency (see on the day, changes already occoured in developemental stage) *
> analgesia longterm - NSAIDs [at home] (PBZ, flunixin, carprofen IV/oral)
+- opioids [require hospitalisation] (morphine, pethidine, fentanyl etc. NB controlled drugs and short acting, side effects)
> foot support to prevent pedal bone movement - deep bed
- frog support (bandage, lilypad, NFS)
- frog and sole support (styrofoam, dental impression material)
> vasodilators - ACP, [nitroglycerine percutol in the past but SHOWN NOT EFFECTIVE] to prevent ischaemia
- questionable efficacy because vasoactive stage is subclinical and has passed
- still useful as sedative to make horse lie down
> vasoconstriction - ice, chill to distal carpus/tarsus, 10*, no complications but only useful for prevention in high risk/first aid tx not long term
> box rest
> diet - no grass, 1.4%-2% body weight poor quality hay
- no/min concentrate
- HiFi or unmolassed sugar beet
> PPID tx: Pergolide (Prosend)
> EMS tx: weight loss, excercise, medical
Give some indicators of prognosis.
- clinical signs
> depression all the way around the coronary band suggest sinker (20% survival)
> evidence of previous attacks (succes rate v 20%) - radiographs
> rotation >11.5* significantly v prog
> founder distance >15mm 40% = chance returning to soundness
egs stats
- 95% alive @ 8 weeks
- 72% sound at trot
- 60% ridden again
What is the moecule in grass causing problems?
> overconsumption NSC (fructan + starch + sugar)
- NSC = energery for growth of plants (non-structural carbs)
- decreases when grass is growing
- ^ when plant photosythesising (^ light intensity, v temp and lack of water)
- NSC hay related to grass content
- NSC haylage generally low but more palatable so will eat more
Preventative measures
> minimise NSC consumption
- manage pasture to encourage growth (to v NSC)
- fertilise but top regularly
- ideally hay made from mature hay post seed dispersal
base diet on forage/fibre not sugar/starch
- extra energy sugar beet pulp/oil
- if cereals ensure cooked
- vitamin supplements
some ponies need zero grazing
- sand paddocks
- grass muzzle
- turn out over night (carbs lowest as not photosynth)
- restrict spring and sutumn
- avoid grazing with frost and bright sunlight (photosyth but not growing)
excercise and prevent obestiy
Neutroceuticals/supplements for prevention?
> cinnamon - ? insulin sesntiising - no equine studies - = results in man and rats > magnesium - ?mpdulates action of insulin - no equine studies - mixed in humans - ensure adequate intake > chromium - potentiates the action of insulin *probably do no harm but no good evidence either*
Prevalence of laminits in the UK
~3%
