2. THE BASICS
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
3. SIGNALMENT, HISTORY, RISK FACTORS
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
4. PATHOPHYSIOLOGY
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
5. CLINICAL SIGNS
Often referable to the primary disease
Hyperlipemia is typically a secondary problem
Can see severe depression, anorexia
Non-specific signs measure serum [TG] in depressed,
inappetant animals of at-risk breeds
6. DIAGNOSIS
Serum [TG]
May also diagnose with PCV/TS – will see cloudy/white (lipemic)
serum once hemocrit tube is centrifuged
Hepatic/renal function, chemistry profile
Assessing for an underlying cause; can also help prognostically
Any diagnostics need for evaluation of the primary condition
YOU MUST TREAT THE UNDERLYING DISEASE!
7. COMPLICATIONS
Hepatic failure
Renal failure
Death
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
8. TREATMENT
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 present
Heparin 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
9. PROGNOSIS
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
10. REFERENCES
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 Veterinar y
Manual. Whitehouse Station, NJ: Merck Sharp & Dome Corp.
Watson, T et al. (2013). Hyperlipemia Syndrome. Available:
http://www.vetstream.com/equis/Content/Disease/dis0032
9. Last accessed 24 October 2013.