Omega CantrellVMC 979

HYPERLIPEMIA IN EQUIDS

Clinical manifestation of a severe imbalance between energy intake and demand Similar to ketosis in dairy cattle, but with triglycerides

(TGs) rather than ketones as a consequence of this negative energy balance

Definitions Hyperlipidemia

Serum [TG] increased but <500ng/dL Hyperlipemia

Serum [TG] >500ng/dL

THE BASICS

Breed predilection Ponies, pony crosses, mini horses, donkeys, mini donkeys

Body condition Obese animals (greater fat stores)

Risk factors Obesity, lactation/pregnancy, stress/transportation Concurrent disease/state of increased demand with

decreased intake (especially in high risk breeds) Chronic internal parasitism, colitis, colic, poor nutrition, etc. Anything that would cause an animal to go off-feed, thus

resulting in decreased energy intake compared to increased metabolic demands

SIGNALMENT, HISTORY, RISK FACTORS

Negative energy balance = fatty acids (FAs) mobilized from adipose tissue Most animals = production of ketones from FAs Equids ≠ ketones large amounts of mobilized lipids in

circulation Problem is TG overproduction, not catabolic failure

Hyperlipemic ponies = lipoprotein lipase (LPL) activity is 2x that of healthy animals of the same breed

May be precipitated by insulin resistance Insulin inhibits hormone sensitive lipase (HSL, responsible for

mobilization of fatty acids from adipose tissue) Resistance = increased HSL activity = more FA mobilization,

increased TGs Exacerbated by risk factors (obesity, pregnancy, stress)

High serum [TG] may prolong/complicate recovery

PATHOPHYSIOLOGY

Often referable to the primary disease Hyperlipemia is typically a secondary problem

Can see severe depression, anorexiaNon-specific signs measure serum [TG] in

depressed, inappetant animals of at-risk breeds

CLINICAL SIGNS

Serum [TG] May also diagnose with PCV/TS – will see cloudy/white

(lipemic) serum once hemocrit tube is centrifugedHepatic/renal function, chemistry profi le

Assessing for an underlying cause; can also help prognostically

Any diagnostics need for evaluation of the primary condition YOU MUST TREAT THE UNDERLYING DISEASE!

DIAGNOSIS

Hepatic failureRenal failureDeath

If it can be identified, YOU MUST TREAT THE PRIMARY DISEASE! = often ends up being an expensive treatment, due to

need for diagnostics and aggressive treatment in most cases

COMPLICATIONS

Nutritional support Reverses negative energy balance, increases serum [GLUC],

promotes endogenous insulin release, inhibits lipid mobilization from peripheral stores

“Smorgasbord” approach, enteral, parenteral (rarely)Resolve the primary disease! Insulin therapy

May not be effective if insulin resistance is presentHeparin therapy

Enhances lipogenesis via stimulation of LPL, but no longer recommended (LPL high in affected individuals)

Contraindicated if coagulopathic due to liver dysfunction No longer recommended as a mainstay of therapy

TREATMENT

Poor to grave Mortality 43-80%

Survival in mini horses and donkeys (78%) vs. ponies (20-57%)

Prognosis worsens if renal involvement is present Development or worsening of azotemia Renal failure can cause further anorexia, which will

exacerbate hyperlipemia; also results in build up of toxins in the body

Death is more often from failure to treat the primary disease

These animals are typically presented when signs are advanced, thus rapid, aggressive treatment is often required Can become very expensive very quickly combination of

poor prognosis with a large estimate for care often results in euthanasia

PROGNOSIS

Boyce, M. (1999). Hyperlipemia in Ponies and Miniature Horses. Available: http://wwwchem.csustan.edu/chem4400/sjbr/99boyce.htm. Last accessed 24 October 2013.

Semrad, SD. (2012). Hyperlipemia and Hepatic Lipidosis in Large Animals. In: Aiello, SE et al. The Merck Veterinary Manual. Whitehouse Station, NJ: Merck Sharp & Dome Corp.

Watson, T et al. (2013). Hyperlipemia Syndrome. Available: http://www.vetstream.com/equis/Content/Disease/dis00329. Last accessed 24 October 2013.

REFERENCES