Reviewing the chemistry panel: Liver cases (Proceedings)

Article

Neurological disease represents 0.3% (affecting between 0.2 and 0.5% of horses depending on age) of all health problems identified by owners in the latest 2005 Equine National Animal Health and Monitoring Study (NAHMS).14 Likely this is much higher given losses in young horses due to non-infectious neurological causes, in all ages of horses from underreporting of encephalitis, and misdiagnoses of these diseases as lameness and trauma.

The Serum Chemistry Profile

5 Components:

      1. Electrolytes / Acid-Base

      2. Kidney

      3. Glucose

      4. Proteins

      5. Muscle enzymes

      6. Liver parameters

Liver Components

      1. Enzymes

          • SDH

          • AST

          • GGT

          • SAP

      2. Functional components

          • BUN

          • Glucose

          • Albumin

          • Iv. Bilirubin

Enzymes

      Hepatocellular enzymes:

1. SDH

     • Short half-life

     • Cytosolic (means necrosis present)

     • Liver specific

2. AST

     • Intermediate half-life

     • Cytosolic (means necrosis present)

     • Not specific: also from muscle

Biliary:

1. GGT

          • Very long half-life (several days) and upregulated

          • Secreted (It means the ducts have been irritated/inflamed, Increase does not mean necrosis of cells)

          • Biliary-specific (nearly...also found in pancreatic ducts)

2. SAP (serum alkaline phosphatase)

          • Intermediate half-life

          • Secreted (Increase means cells are irritated, not necessarily necrotic)

          • Found in several other tissues:

          • SAP also from bone, placenta, inflammatory cells...

Clinical Relevance

          • SDH tells what is on-going (current status)

          • GGT stays increased for weeks after insult

          • SDH and GGT confer specificity

               o indicate liver/biliary disease

          • SDH and AST indicate hepatocellular necrosis

          • GGT and SAP indicate biliary disease

Functional Indicators in the Chem Panel

These analytes are made by the liver:

Liver dysfunction / failure:

          • BUN ↓ - except neonate

          • Glucose ↓ – late finding

          • Albumin ↓ – late finding; < 20 % of cases

          • Cholesterol ↓

Bilirubin

          • Indirect (unconjugated)

          • Direct (conjugated)

One or both increase with liver disease

Direct fraction = 25 % of the total BR strong evidence of biliary disease

General Guidelines in Interpretation

1. Relatively greater increases of biliary enzymes (GGT, SAP) over hepatocellular enzymes (SDH, AST) indicate primary biliary disease:

Examples include:

          • Cholangitis/cholangiohepatitis

          • Cholelithiasis or other biliary obstruction, including GI displacements

          • Pyrrolizidine Alkaloid Toxicity

          • Biliary tumors

2. Relatively greater increases of hepatocellular enzymes over biliary enzymes indicate primary hepatocyte disease:

Hepatitis/ cholangiohepatitis

Liver Toxicities

          • Theiler's disease (serum hepatitis) in adults

          • Tyzzer's disease in foals

          • Carcinomas

General Guidelines

3. Relatively equal increases in biliary and hepatocellular enzymes:

          • Variations of all of the above differential diagnoses

          • Gut disease – secondary to colic or colitis

          • Hyperlipemia

          • Other toxicities

Treatment Guidelines

Liver Disease

1. IV fluid therapy

Optimal crystalloids: Normosol R or Plasma-Lyte 148

          • Contain acetate and gluconate, no lactate which is primarily liver metabolized

          • Alkalinizing compared to 0.9% saline

          • Supplement fluids with potassium!

               o Aids in preventing hyperammonemia

               o 20 mEq/L KCl even if potassium normal

      PCV may remain elevated due to primary polycythemia

2. Nutritional Support

          • Dextrose in fluids: 0.5-2 mg/kg/min

               o Example: 1.5-5 % in 1 liter/h

          • B complex vitamins:

               o May be deficient

               › Aid in glucose metabolism

               › Neuroprotective

               › 1 cc per 100 lb in fluids/ day

          • Parenteral nutrition- be careful of excessive amino acids if hyperammonemic

          • If eating:

               o Beet pulp, grass hay and grain

               › BCAA

               › Be careful tubing horses with liver failure! – bloody nose

3. Avoid sedation, especially diazepam

4. Low dose flunixin meglumine (Banamine)

          • For endotoxemia

          • For inflammation

5. Plasma transfusion if coagulopathy present

6. Antioxidants - vitamin E, selenium

7. Treatment of hepatoencephalopathy:

     • Lactulose 0.2-0.25 ml/kg PO q 8 h

               o Decreases ammonia concentrations in gut and therefore plasma through ion trapping

          • If neurologic signs present:

               o Mannitol or DMSO

Conclusion

1. Increases in liver enzymes alone signify liver disease, not necessarily failure

          • GGT and SAP indicate primary biliary diseases

               o Cholangiohepatitis

               o Cholelithiasis

               o PA toxicity

          • SDH and AST indicate primary hepatocellular disease

               o Theiler's

               o Tyzzer's

               o Hepatitis

          • Increases in both

               o Any of above diseases

               o Secondary to GI disease

               o Hyperlipemia

Conclusion

2. Liver failure is suggested by

          • Low BUN, glucose, albumin; high BR

3. Remember colic and diarrhea cases can have secondary increases in liver enzymes

Colon displacements

          • Colon torsions

          • Enteritis

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