approach to EMS

Presenting signs

·    Overweight

·    Regional adiposity – cresty neck, fat pads, sheath/mammary swelling

·    Laminitis

·    Divergent hoof rings

History

·    Have they had previous events of laminitis?

·    Had EMS before?

Diagnosis

Basal tests:

·    Basal insulin concentration

o  Measure insulin conc. 1-3h after coming off pasture (not after big feed)

o  Hyperinsulinaemia in resting/starved state = EMS

o  Poor sensitivity – if normal, doesn’t rule out EMS

·    Adiponectin concentration

o  Adiponectin = adipose derived, insulin-sensitising horse

o  Low conc – associated with risk of laminitis

Dynamic tests:

·    Oral sugar test

o  Collect baseline insulin, administer oral karo light syrup (45ml/100kg bw)

o  Collect blood sample 60-90m later and measure insulin and glucose – high = EMS

·    Combine glucose insulin test

o  Fast overnight, measure baseline insulin and glucose

o  Administer IV glucose and insulin – measure insulin at 45m and glucose frequently

§ Glucose should be baseline by 45m and insulin <100IU/ml

o  Not involving the gut, only looks at tissue insulin sensitivity

Management 

·    Diet – want to manage obesity

o  Reduce carbohydrate intake – feed 1.75% of bw, soaked hay to leech sugar out

·    Exercise

o  Increases insulin sensitivity, helps management of obesity

o  But only once laminitis is under control

·    Medication

o  SGLT2 inhibitor – ertugliflozin, metformin, levotyroxin

§ Decreases insulin conc. by increasing glucose output in urine

§ But risk of hyperlipaemia so continue to monitor

Causes

·    Risk factors:

o  Genetic predisposition – warm bloods, native breed ponies

o  Obesity, regional adiposity

o  Pregnancy-associated insulin dysregulation

Pathogenesis

·    EMS = collection of resk factors for endocrinopathic laminitis:

o  Insulin dysregulation

§ Prolonged hyperinsulinemia response

§ Basal hyperinsulinemia

§ Tissue insulin resistance – 3 stages

o  Obesity

o  Presence/risk of laminitis  

Consequences

·    Can lead to pancreatic dysfunction

o  Prolonged high insulin conc. ® pancreatic beta cell exhausition

o  Clinical signs: PUPD, hyperglycaemia, weight loss, normal insulin conc.

·    Hyperinsulinemia ® laminitis

o  Lengthening/stretching of secondary epidermal lamellae

o  Different to sepsis-related laminitis (don’t see any destruction of basement membrane)

o  Reduce risk of laminitis:

§ Identify hyperinsulinemia

§ Dynamic tests

§ Measure adiponectin conc. – low conc. = decreased risk of laminitis

§ Assess for concurrent risk factors, e.g. PPID

§ Evidence of previous episodes, e.g. divergent hoof rings

·    Insulin resistance – 3 stages:

1.        Compensated IR – normal glucose conc. maintained by increased insulin output

2.        Uncompensated IR – glucose conc. increasing and increased insulin output

3.        Type 2 DM = endstage – persistent hyperglycaemia due to inadequate insulin output