Liver diseases in horses – 31 May 2016

Liver disease occurs commonly in horses. Classical clinical signs of liver disease in horses are vague but generally include jaundice (yellowing of the whites of the eye), weight loss, mild diarrhoea and in severe cases, neurological signs and uncontrolled bleeding tendencies.

Liver disease occurs commonly in horses. Classical clinical signs of liver disease in horses are vague but generally include jaundice (yellowing of the whites of the eye), weight loss, mild diarrhoea and in severe cases, neurological signs and uncontrolled bleeding tendencies. Neurological signs could include depressed mentation, wobbly gait and head pressing.

Common causes of equine liver disease in Australia include plant toxicosis and cholangiohepatits. Other causes of equine liver disease include hepatic lipidosis, hepatic abscess and neoplasia, liver fluke and parasitic migration.

The most common type of plant causing liver disease in horses are a group of plants species containing pyrrolizidine alkaloids (PAs). PAs are naturally occuring alkaloids, produced by plants as a defence mechanism against insects. Ingestion of these toxic alkaloids lead to formation of toxic by products in the liver. These toxic by products, called pyrroles inhibits DNA function in liver cells. Liver cells fail to undergo normal mitosis and forms megalocytes (cells with large ares of cytoplasm). These liver cells eventually die and are replaced by connective tissue over time (fibrosis, or cirrhosis).

Plants containing PAs include fireweed, Patterson’s curse, Heliotrope and Darling Peas. Horses are quite sensitive to the effects of PA plants while other ruminant species such as cattle and sheep appear to show more resistance towards their toxic effects. Toxic effects are cumulative and ingestion of PA plants over the course of weeks to months may be required to produce clinical signs. Animals that are naïve to the plants may be more sensitive to their effects. PA plants are thought to be non palatable to horses but some individuals appear to have developed a taste for these plants.

Horses with PA toxicosis usually present with weight loss and various degree of inappetence depending on the severity of toxicosis. The condition whereby neurological signs develop as a complication of liver disease is called hepatic encephalopathy, and carries a poorer prognosis. Signs of hepatic encephalopathy can range from mild depression and ataxia to severe depression, head pressing, aggression and recumbency. One consistent clinical sign of liver disease is the presence of jaundice. PA toxicosis suspected when there is a history of possible ingestion of PA plants and clinical signs of liver disease.

A full blood analysis should be performed in horses suspected of PA toxicosis. An increase in liver derived enzymes such as GGT and GLDH points towards liver injury and the magnitude of their increase provides a clue to the severity of liver disease. A liver function test (total bile acid) should also be conducted, as liver injury can occur in the absence of liver failure. An increase in total bile acid suggests liver failure and carries a poorer prognosis compared to an animal without liver failure. These biochemical tests should also be repeated serially (weekly or fortnightly) to assess response to therapy instituted. A serial and gradual decrease in liver derived enzymes and total bile acid will suggest a more favourable prognosis, while a liver profile that deteriorates despite therapy carries a less favourable prognosis for recovery.

In addition to laboratory tests, ultrasound can also be performed to visualise the liver. Horses suffering from PA toxicosis may have a change in liver size. The liver could also appear “brighter” on ultrasound, termed increase in echogenicity. The ultrasound examination is also useful to rule out other possible liver diseases such as abscesses or neoplasia.

The definitive diagnosis for PA toxicosis is histopathology from a biopsied sample from the liver. Prior to performing a liver biopsy, a coagulation panel should be performed to investigate the animal’s clotting ability. Horses with severe liver failure are unable to clot their blood as clotting factors are normally produced in the liver. A liver biopsy is generally contraindicated in these patients as the risk of uncontrolled hemorrage from the procedure is high. The liver biopsy can be performed with the aid of the ultrasound machine, called ultrasound guided liver biopsy. The liver is visualised and the area of interest identified using the ultrasound. The area is then cleaned in a sterile manner and the veterinarian will obtain small liver samples using an automated biopsy needle. The samples are then sent for histopathological processing and the slides viewed under high power microscopes for definitive diagnosis.

Treatment of horses with suspected or diagnosed PA toxicosis revolves around removal of the toxic plant and supporting the liver for regeneration:
1.Remove horse from “offending” pasture, or remove offending plants from pasture
2.Ensure adequate nutrition. Horses that are showing signs of inappetence generally has a poorer prognosis compared to a horse that still has good appetite:
3.a. Addition of molasses into feed may entice/increase appetite of the patient.
4.b.Nutrition in horses with inappetence can be provided via enteral route. This can be performed by making a “slurry” of pellets mixed with molasses and administering a portion of this slurry using stomach tube every few hours. Some horses do not tolerate repeated stomach tubing and other horses may develop colic or diarrhoea from “force-feeding”.
5.c. In horses that are intolerant of enteral nutrition, a total parenteral nutrition (TPN) can be provided “through the vein”. This involves formulating a complete “diet” with a specific combination of amino acids (protein), glucose (carbohydrate) and lipids (fat). This complete liquid diet is then administered in a controlled rate through an intravenous catheter for as long as the patient requires it. This is only performed in hospital as frequent monitoring of blood glucose level and tight control of TPN is required to prevent hyperglycaemia.
6.Avoid adminstration of any drugs that require metabolism by the liver, to provide the liver adequate “rest” and reduce workload.
7.Patients that exhibit neurological signs will likely require greater intensive care.

Prognosis Factors/Clinical signs

Good prognosis · Horse is appetent, eating.
· No neurological signs.
· Acute and short exposure to suspected toxic plants.
· Exhibits significant improvement in serial liver biochemistry panel.
· No liver failure.
· No fibrosis noted on histopathology of liver biopsy

Poorer prognosis · Inappetent, require enteral or parenteral nutrition.
· Neurological signs, especially in cases where horses are recumbent
· Chronic and large exposure to suspected toxic plants.
· Exhibits no improvement or deterioration in serial liver biochemistry panel.
· Liver failure noted on biochemistry panel. Total bile acids of >50mmol/L carries a poorer prognosis.
· Bridging fibrosis noted on histopathology of liver biopsy.

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