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Basics ⬇

Outline

BASICS

Overview!!navigator!!

  • Hepatic insufficiency causes altered behavior and conscious proprioception.
  • >80% of liver function must be impaired; can be acute, subacute, or chronic.
  • Possible mechanisms:
    • Toxic metabolites act as false neurotransmitters (i.e. ammonia, mercaptans, phenols, fatty acids).
    • Imbalance between excitatory and inhibitory neurotransmitters.
    • Increase in aromatic amino acids increases false neurotransmitters, some of which cause sedation with decrease in branched chain amino acids, which decreases neurotransmitters.
    • Increased expression benzodiazepine receptors, increased neurosteroid synthesis.
    • Potential increased permeability of blood–brain barrier.
    • Role for inflammation in disease

Signalment!!navigator!!

No breed or sex predilection.

Signs!!navigator!!

  • Behavior changes (depression, somnolence, aggressive or violent behavior mixed with stupor).
  • Head pressing.
  • Circling.
  • Ataxia.
  • Wandering/aimless movement.
  • Anorexia.
  • Recumbency.
  • Icterus.
  • Photosensitization.
  • Pyrexia.
  • Weight loss.
  • Colic—chronic.
  • Coagulopathy.
  • Blindness.
  • Yawning.
  • Inspiratory stridor (laryngeal paralysis)

Causes and Risk Factors!!navigator!!

  • Toxic hepatopathy, including pyrrolizidine alkaloids, mycotoxins, iron.
  • Acute necrotizing hepatitis—Theiler disease.
  • Cholelithiasis.
  • Chronic active hepatitis.
  • Tyzzer disease.
  • Hyperlipemia—ponies; miniature horses more at risk.
  • Neoplasia.
  • Hyperammonemia (adult horses, portosystemic shunts, Morgans)

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Viral encephalitis (e.g. Eastern equine encephalopathy, Western equine encephalopathy, West Nile virus, rabies).
  • Trauma.
  • Verminous encephalitis.
  • Electrolyte abnormalities—hyponatremia, hypernatremia, hypocalcemia, hypomagnesemia.
  • Brain abscess.
  • Meningitis.
  • Neonatal Maladjustment Syndrome, history.
  • Metabolic (foals—hypoglycemia, acidosis)

Progression of these diseases can lead to HE:

  • Theiler disease—history of antitoxin 4–10 weeks prior.
  • Cholangiohepatitis—adults, most >9 years old

CBC/Biochemistry/Urinalysis!!navigator!!

  • Azotemia.
  • Blood urea nitrogen and glucose—may be decreased in liver failure.
  • Liver-specific changes—elevated bilirubin, increased γ-glutamyltransferase, sorbitol dehydrogenase, glutamate dehydrogenase, hypoalbuminemia, hypoproteinemia, elevated resting ammonia levels, and elevated bile acids.
  • Hyperlipemia—may have increased cholesterol and triglycerides.
  • Secondary hypocalcemia, hypokalemia, and metabolic acidosis.
  • Delayed bromsulphthalein (bromosulfophthalein) clearance

Other Laboratory Tests!!navigator!!

Coagulation profiles may be prolonged.

Imaging!!navigator!!

  • Ultrasonography of the liver. Biopsy results help predict prognosis.
  • Radiographs—rule out fractures.
  • CT/MRI—assess for trauma, abscesses, tumors, hydrocephalus

Other Diagnostic Procedures!!navigator!!

  • Cerebrospinal fluid tap—to rule out other infectious causes.
  • Feed analysis to assess for toxins

Treatment ⬆ ⬇

TREATMENT

  • Prognosis is poor, but potentially reversible depending on cause.
  • Decrease inflammation (i.e. flunixin meglumine, DMSO, colchicine, cyclosporine (ciclosporin)).
  • Sedation may be necessary. Xylazine and detomidine can occasionally exacerbate signs. Valium and/or phenobarbital for seizures but can potentiate GABA effect and exacerbate HE signs.
  • Correct fluid, electrolyte, and acid–base deficits.
  • For anorectic or hypoglycemic animals, give 5% dextrose (2 mL/kg/h) to start, then 2.5% in half-strength saline.
  • High-carbohydrate, low-protein (i.e. 10%) diet with branched chain amino acids; need some fiber (i.e. oat, grass hay, beet pulp) to decrease gastrointestinal dysfunction.
  • Feed small amounts frequently (every 2–4 h).
  • Vitamin B1, K, folic acid, and C supplementation.
  • Protect from sunlight to prevent photosensitization

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Lactulose (0.3 mL/kg every 6 h).
  • Hyperlipemic horses can be given insulin, glucose/galactose, and heparin.
  • Mannitol for cerebral edema.
  • Mineral oil or magnesium sulfate if suspect toxins ingested.
  • Septic cholangiohepatitis—antibiotics are warranted.
  • S-adenosylmethionine if expect oxidative injury

Contraindications/Possible Interactions!!navigator!!

Avoid drugs that require hepatic metabolism.

Follow-up ⬆ ⬇

FOLLOW-UP

  • Prognosis depends on the primary cause.
  • Severe fibrosis associated with poor prognosis.
  • Animals with hyperlipidemia/hyperlipemia may respond well to aggressive treatment.
  • Animals with HE from toxins probably experienced the initial insult several weeks/months prior; determine if signs are still progressing. These animals may be stabilized, but if signs continue to progress or recur, a poor prognosis is indicated.
  • Poor prognosis for recumbent animals

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Pregnancy/Fertility/Breeding!!navigator!!

Small percentage of pregnant animals will be hyperlipemic.

Abbreviations!!navigator!!

  • CT = computed tomography
  • DMSO = dimethylsulfoxide
  • GABA = γ-aminobutyric acid
  • HE = hepatic encephalopathy
  • MRI = magnetic resonance imaging

Suggested Reading ⬆ ⬇

Reed SM, Bayly WM, Sellon DC, eds. Equine Internal Medicine, 3e. St. Louis, MO: WB Saunders, 2010.

Author(s) ⬆

Author: Sharon G. Witonsky

Consulting Editor: Caroline N. Hahn