The liver is the largest single organ in the horse, weighing between 10 and 20 pounds (4.5–9.0 kg). Physiologically, the liver is involved in a variety of metabolic and detoxification functions. It possesses large functional reserve and regeneration capacities. When the liver fails, a variety of organ systems fail. Liver disease may be present long before liver failure develops. Equine liver diseases are relatively infrequent when compared with other animal species despite the many diseases primarily affecting the equine gastrointestinal tract. Predictable clinical signs of liver failure in the horse are icterus, hypoalbuminemia, coagulopathy, hypoglycemia, hyperlipoproteinemia, and hepatic encephalopathy. This chapter summarizes liver diseases unique to the equine animal species. Pathologic entities include metabolic disorders, toxic and immunologic insults, infectious agents, endoparasites, neoplastic disorders, and incidental findings.
I. Liver
Figure 7.1. Horse. Liver. Diaphragmatic Surface. Normal. Color as expected. Numbers denote the anatomic identification of the hepatic lobes.
Figure 7.2. Horse. Liver. Visceral Surface and Hilus. Normal. Numbers identify anatomic configurations. The equine liver lacks a gallbladder.
1. Hemodynamic changes
a. Lobar atrophy
In clinically normal horses, the right liver lobe constitutes half of the total liver weight. The condition of lobar atrophy is believed to be the result of ischemia in this part of the liver from long-standing atony of the adjacent right dorsal colon and base of the cecum.
Figure 7.3. Horse. Liver. Hepatic Atrophy. The right liver lobe is markedly reduced in size. Differential diagnosis is generalized liver atrophy due to starvation.
b. Portosystemic shunt
Foals and juvenile horses are mainly affected. Clinical signs are vague and may include depression, lethargy, and ataxia due to hepatic encephalopathy. Livers may be grossly reduced on size.
c. Chronic congestive heart failure
Back flow and insufficient return of venous blood from the liver results in hepatomegaly and excessive flow of blood from the cross section.
Figure 7.4. Horse. Liver In-situ. Passive Hepatic Congestion. Right-sided Heart Failure. The liver is dark blue and markedly enlarged indicating congestion. Pulmonary edema and hydropericardium are also visible. Ascites can be expected.
Figure 7.5. Horse. Liver. Venous Congestion (“Spider Veins”). Right-sided Heart Failure. Enlarged liver with spiderweb-like congestion of stretched Glisson capsule vessels.
Figure 7.6. Horse. Liver Cross Section. Passive Venous Congestion. Right-Sided Heart Failure. Stagnating blood has caused a mottled pattern sometimes compared with a nutmeg.
d. Focal ischemia
Figure 7.7. Horse. Liver. Focal Ischemic Lipidosis. This is an incidental finding on the diaphragmatic surface of the liver and the result of focal inflammatory adhesion between the liver surface and diaphragm surface. The condition is also coined as tension lipidosis. (Courtesy Dr. J. King, Cornell University.)
2. Metabolic, necrotic, and toxic diseases
a. Lipidosis
This metabolic disorder occurs mainly in ponies, donkeys, and Miniature horses. Anorexia and lethargy are clinical signs. Hepatic encephalopathy may ensue. The condition is associated with hyperlipidemia and hyperlipemia indicative of an underlying disturbance of the lipid metabolism. Hepatic lipidosis results when the rate of hepatic triglyceride synthesis exceeds the formation and release of very low density lipoprotein substance into the circulation. The two major hormones regulating lipid metabolism are glucocorticoids and insulin. Insulin resistance may play a role in the pathogenesis of hyperlipidemia.
Figure 7.8. Horse. Liver In-situ. Hepatic Lipidosis. The liver exhibits large areas of yellow discoloration.
Figure 7.9. Horse. Liver. Hepatic Lipidosis. The entire liver is enlarged and yellow. Edges are rounded. On touch the parenchyma may easily rupture. Differential diagnosis: amyloidosis.
Figure 7.10. Horse. Liver. Surface Rupture in Hepatic Lipidosis. Hemoperitoneum may be a fatal complication.
b. Amyloidosis
Figure 7.11. Horse. Liver. Amyloidosis. The interstitial accumulation of amyloid (yellow) progressively compresses and atrophies the hepatic parenchyma (brown). Hepatic amyloidosis typically is encountered in serum-producing horses and is of AA-type. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
c. Idiopathic acute hepatic disease
A recent publication suggested a divergent virus belonging to the Flaviviridae family as possible etiologic cause. Synonyms for this condition are Theiler’s disease or serum hepatitis. It is mainly a sporadic disease and typically occurs 40–60 days after injection of an equine-based product (e.g., tetanus antitoxin). Affected horses may show signs of hepatic failure. A type III hypersensitivity reaction originally had been suggested as the cause. Acute mortality may be as high as 50–60%. Affected horses present anorexia, hepatic encephalopathy, and icterus. Hepatic liver enzyme levels are increased. Serum total bile acid concentration will be elevated. Differential diagnoses include hepatotoxins and acute infectious diseases.
At necropsy, the liver is usually small and flattened. It may be bile-stained. Microscopic changes are characterized by severe panlobular necrosis and a mild to moderate mixed inflammatory infiltrate.
Figure 7.12. Horse. Liver. Acute Hepatic Necrosis. Theiler’s disease. The affected liver is on the right and has a shrunken, flat profile with indentations on the capsular surface. A healthy liver is depicted on the left. (Courtesy Dr. J. King, Cornell University.)
Figure 7.13. Horse. Liver. Acute Hepatic Necrosis. Theiler’s disease. There is distortion of the hepatic lobular pattern due to a loss of intrinsic hepatocytes. A few remaining hepatocytes show vacuolar swelling. Intermixed are mainly mononuclear inflammatory cells. (H&E)
d. Degeneration and necrosis
The liver is highly susceptible to unspecific and specific toxins. Despite a high threshold toward toxins, long exposure to these induces degenerative and necrotic changes. Histologically, there are specific lobular patterns of response to bloodborne toxic injuries to the liver. Recognition of these patterns may be indicators of and may lead to narrowing the nature of the toxins involved. Depending on the duration, sequence, and dosage of the toxins, the liver will respond to toxic injury with fibrosis, cirrhosis, or regeneration.
Figure 7.14. Horse. Liver. Focal Necrosis. The green brown areas of discoloration indicate the anatomic site of the necrosis.
Figure 7.15. Horse. Liver. Lobar and Multifocal Necrosis. One lobe is markedly swollen and discolored. The other lobes reveal focal involvement of necrosis. Depending on blood flow and susceptibility of the detoxifying enzyme, the pattern of injury is not uniform in this case.
Toxins affecting the equine liver generally are derived from plants, fungi, chemicals, drugs, and heavy metals. Most commonly plants producing pyrrolizidine alkaloids (PAs) are responsible for liver failure in horses. These alkaloids are found in Crotalaria, Amsinkia, Senecio spp., and others.
i. Crotalaria toxicosis.
Crotalaria, found predominantly in the South and Southeast of the United States has been the cause of many pastured horse losses. Known as wild pea or rattlebox, Crotalaria is planted as an agricultural cover crop. Two species, Crotalaria sagittalis and Crotalaria spectabilis, are particularly toxic to the equine liver. Horses, unlike small ruminants, are 30–40 times more susceptible to PA poisoning due to a poor capability to detoxify alkaloids in the liver.
Alkaloids are metabolized to toxic pyrrol esters in the liver by the hepatic PFO system (cytochrome P450). The pyrrol esters act as alkylating agents and ligate to hepatocellular nuclear proteins and nucleic acid (DNA) to become anti-mitotic. Cellular division occurs, but no DNA replication leading to nuclear DNA accumulation and increased nuclear size resulting in the formation of megalocytes. The megalocytes eventually die and are replaced by fibrous connective tissue. Reactive PA metabolites may also damage the lung alveolar and renal tubular epithelium, albeit to a lesser degree. Photosensitivity dermatitis develops as clinical complication.
Figure 7.16. Horse. Equine Body. Head Pressing. Hepatic Encephalopathy from PA Toxicosis. The posture is a typical clinical sign seen in this condition.
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