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Flashcards in Laminitis (Menzies-Gow) Deck (24):

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?

1. developmental
- lasts ~72hrs
- contact w/ trigger and breakdown of attachemnts
2. acute
- clinical signs seen
3. Resolution or progression to chronic laminitis


Main 4 aspects of pathogenesis?

1. inflammation
2. ECM degradation
3. metabolic disease
4. 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?

- basal ACTH (seasonally adjusted ref range)
- dex suppression (not autumn)
- TRH stim
- 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