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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Hyperlipidemia refers to elevated blood concentrations of lipids including TG or cholesterol
  • Hypertriglyceridemia refers to abnormally high serum or plasma TG concentrations
  • Equine hyperlipemia is a clinical condition characterized by markedly increased serum TG concentrations (>500 mg/dL), depression, anorexia, and organ dysfunction
  • Mild hyperlipidemia is an incidental finding in healthy nursing foals and results from normal chylomicron production after feeding
  • Congenital hyperlipidemia characterized by marked hyperlipidemia can occur in newborn foals born to mares affected by EH prior to parturition
  • DM is a cause of EH. Aged horses should be tested for PPID if DM is detected. Hypertriglyceridemia often improves with pergolide treatment
  • Rarely, hypertriglyceridemia is detected in healthy animals; these may be hereditary hyperlipidemia cases

Pathophysiology!!navigator!!

  • Negative energy balance stimulates lipolysis within adipose tissues, causing mobilization of FFAs (also called nonesterified fatty acids) and glycerol
  • Lipolysis is catalyzed by HSL. Glucagon, glucocorticoids, catecholamines, and growth hormone increase HSL activity, whereas insulin inhibits it
  • Mobilization of FFAs from adipose tissues is a normal physiologic response to negative energy balance
  • EH is driven by excessive mobilization of FFAs from adipose tissue TG stores and is caused by an overabundance of substrate (i.e. TG) in the obese animal and ID
  • Insulin normally inhibits the activity of HSL after feeding
  • Most circulating FFAs are removed from the blood by the liver and serve as substrates for energy production or are esterified to TG. In turn, TG is stored within hepatocytes or packaged into VLDLs and exported to other tissues via the blood. The transported TG is hydrolyzed by LPL into FFAs, which are used as a source of energy
  • If a high rate of lipolysis within adipose tissue persists, blood FFA concentrations rise and uptake of FFAs into the liver accelerates. Rates of TG-rich VLDL synthesis and export substantially increase, accumulation of TG-rich VLDL within the blood (i.e. hyperlipidemia) develops as hepatic production exceeds the clearance by LPL
  • In severe cases, accumulation of TG within the liver results in hepatic lipidosis and TG deposits in other tissues, causing fatty infiltration followed by organ dysfunction. A vicious cycle then develops as elevated serum TG concentrations further suppress appetite

Systems Affected!!navigator!!

Genetics!!navigator!!

There is a genetic component of EMS in Arabians, Morgans, and Welsh ponies and this may also contribute to a predisposition towards hyperlipemia.

Incidence/Prevalence!!navigator!!

Low—dependent upon the breed of horse and feeding practices.

Geographic Distribution!!navigator!!

N/A

Signalment!!navigator!!

  • Breeds—ponies, miniature horses, and donkeys
  • Occurs at all ages
  • Foals may be born with congenital hyperlipidemia
  • Mares are more susceptible during pregnancy and lactation
  • Aged horses with PPID can develop hyperlipidemia more readily if DM is present

Signs!!navigator!!

  • Early signs are nonspecific—lethargy, inappetence, and depression
  • As the disease progresses, patients cease eating and drinking. Fetid, fat-covered feces (steatorrhea) are produced (eventually in the form of diarrhea). Clinical signs associated with organ dysfunction may develop, including neurologic signs consistent with hepatic encephalopathy (depression, head pressing, ataxia, and sham drinking)
  • Mild colic caused by stretching of the liver capsule may be observed
  • Pregnant mares may abort
  • Polyuria/polydipsia is reported when DM and/or PPID are present
  • Newborn foals with congenital hyperlipemia are normal in appearance

Causes!!navigator!!

  • Negative energy balance, particularly in obese animals
  • Recent stress

Risk Factors!!navigator!!

  • Breeds—ponies, donkeys, and miniature horses
  • EMS
  • PPID
  • Pregnancy
  • Stress
  • Concurrent disease
  • Endotoxemia
  • Parasitism
  • Lactation

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Acute infectious diseases with nonspecific signs of depression and inappetence
  • Hepatic, neurologic, or GI disease

CBC/Biochemistry/Urinalysis!!navigator!!

Note that markedly elevated blood lipid concentrations may interfere with analyzer functions, particularly biochemical analysis.

  • When the TG concentration is >500 mg/dL, it is not possible to read newsprint through the tube of a gravity-sedimented or centrifuged plasma sample
  • TG concentrations may be reported in mmol/L and the conversion factor is approximately 89 (500 mg/dL = 5.6 mmol/L)
  • Reference range for adult horses is 11–65 mg/dL. Higher concentrations are detected in healthy donkeys and pregnant ponies
  • Hypoglycemia or hyperglycemia
  • Increased total bilirubin, γ-glutamyltransferase, alkaline phosphatase, aspartate aminotransferase, and sorbitol dehydrogenase
  • Azotemia with normal urinalysis. Blood urea nitrogen may be lower than expected because of hepatic failure
  • Metabolic acidosis may be detected

Other Laboratory Tests!!navigator!!

  • Elevated serum insulin concentration or a low insulin to glucose ratio
  • ID detected using the oral sugar test or other glucose or insulin tolerance tests
  • Elevated blood ammonia concentration if hepatic lipidosis
  • Elevated serum bile acid concentration if hepatic lipidosis
  • Prolonged coagulation profile—advanced liver failure
  • Diagnostic evaluation for PPID

Imaging!!navigator!!

Ultrasonography—liver enlargement and alterations in echogenicity are associated with hepatic lipidosis.

Other Diagnostic Procedures!!navigator!!

Liver biopsy to confirm hepatic lipidosis in advanced cases.

Pathologic Findings!!navigator!!

  • Findings are consistent with fatty infiltration of tissues
  • Pituitary hyperplasia or adenoma(s) may be present in older horses

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

  • In mild cases detected early, appropriate care can be provided on the farm
  • Patient assessment is based on plasma/serum TG concentrations, duration of inappetence, and seriousness of concurrent disease conditions
  • Provide treatment early in the course of disease
  • Hospitalize severely affected patients immediately

Nursing Care!!navigator!!

Increase Feed Intake

  • Mildly affected patients improve as their feed intake increases
  • Provide a large variety of feedstuffs or treats until a preferred diet is identified
  • Provide access to pasture.

Enteral and Parenteral Feeding

  • A commercial enteral diet can be used for smaller patients
  • Liquid preparations of alfalfa meal or soaked, pelleted feedstuffs with added dextrose can be administered via nasogastric tube. Administer small quantities frequently (as often as every 4 h)

IV Fluid/Nutritional Support

  • Administer 5–10% dextrose within polyionic fluids as a continuous infusion. An initial rate of 60 mL/kg body weight per day is recommended
  • Ideally, blood glucose measurements and urine dipstick testing should be used to establish a rate that minimizes renal overflow of glucose. Administer insulin if blood glucose concentrations exceed 200 mg/dL
  • Partial parenteral nutrition can be provided using a solution composed of 50% dextrose and amino acids

Activity!!navigator!!

No specific restrictions but minimize stress.

Diet!!navigator!!

See Nursing Care.

Client Education!!navigator!!

  • Clients should seek veterinary advice if inappetence develops in at-risk equids
  • Obesity as a serious predisposing factor, particularly in pregnant animals

Surgical Considerations!!navigator!!

N/A

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

Insulin

  • Administer if blood glucose concentrations are above 200 mg/dL
  • If dextrose is being administered IV, a constant rate infusion of regular (short-acting) insulin is prepared by adding 10 mL (100 IU/mL) Humulin R® to a 1 L bag of fluids and administering IV to effect (maintain blood glucose <200 mg/dL)
  • Intermediate-acting insulin can be administered SC at a starting dosage of 0.10 IU/kg every 8–12 h

Heparin Sulfate

  • Potentiates LPL activity. However, if LPL activity is already maximized, administration of heparin is ineffective
  • Can be administered at a dose of 10–20 IU/kg body weight IV or SC TID
  • Note that heparin lowers hematocrit levels and can inhibit hemostasis

Other Drugs

Pergolide should be administered to equids with PPID. It may be necessary to increase the dose in patients that are already receiving treatment. Starting dosage for pergolide is 0.002 mg/kg PO every 24 h. Treatment should be initiated if DM and hyperlipidemia are detected, even in anorexic patients.

Contraindications!!navigator!!

  • Insulin administration in hypoglycemic patients
  • Use of heparin sulfate in patients that may require surgery (e.g. cesarean section)
  • Corticosteroids are contraindicated as they can exacerbate ID and lipolysis

Precautions!!navigator!!

Monitor blood glucose concentrations.

Possible Interactions!!navigator!!

N/A

Alternative Drugs!!navigator!!

N/A

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Repeated measurement of serum TG concentration.

Prevention/Avoidance!!navigator!!

  • Maintain appropriate body condition (avoid obesity)
  • Minimize stressful conditions for high-risk breeds, particularly when metabolic demands are high—pregnancy or lactation
  • Early intervention when feed intake is reduced

Possible Complications!!navigator!!

Liver and renal failure.

Expected Course and Prognosis!!navigator!!

  • The course of this disease is rapid
  • Mildly affected patients can recover quickly if the negative energy balance is reversed
  • Prognosis is fair. Severely affected patients with signs of organ failure or neurologic deficits have a poorer prognosis
  • Mortality rates of 57–85% have been reported, but these figures do not reflect recent advances in the treatment of this disorder. Patients may be successfully managed with IV dextrose and insulin treatment

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Hepatic lipidosis and subsequent liver failure
  • Hepatic encephalopathy
  • Renal failure

Age-Related Factors!!navigator!!

N/A

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

In pregnant animals, organ failure, metabolic acidosis, and stress may compromise the fetus, resulting in abortion.

Synonyms!!navigator!!

  • Hyperlipoproteinemia
  • Hypertriglyceridemia

Abbreviations!!navigator!!

  • DM = diabetes mellitus
  • EH = equine hyperlipemia
  • EMS = equine metabolic syndrome
  • FFA = free fatty acid
  • GI = gastrointestinal
  • HSL = hormone-sensitive lipase
  • ID = insulin dysregulation
  • LPL = lipoprotein lipase
  • PPID = pituitary pars intermedia dysfunction
  • TG = triglyceride
  • VLDL = very-low-density lipoprotein

Suggested Reading ⬆ ⬇

Dunkel B, Wilford SA, Parkinson NJ, et al. Severe hypertriglyceridaemia in horses and ponies with endocrine disorders. Equine Vet J 2014;46:118–122.

McKenzie 3rdHC. Equine hyperlipidemias. Vet Clin North Am Equine Pract 2011;27:59–72.

Waitt LH, Cebra CK. Characterization of hypertriglyceridemia and response to treatment with insulin in horses, ponies, and donkeys: 44 cases (1995-2005). J Am Vet Med Assoc 2009;234:915–919.

Author(s) ⬆

Author: Nicholas Frank

Consulting Editors: Michel Levy and Heidi Banse