Feline cholangitis / cholangiohepatitis complex

©Scherk, M (2007) Focus on feline medicine, PGFVSc Conference proceedings, University of Sydney, NSW, Australia

Inflammation of the biliary tree and/or liver parenchyma may be suppurative  or non-suppurative. The non-suppurative form is more common and is often lymphocytic/plasmacytic in character. The clinical presentation includes a vague history of inappetence / anorexia or polyphagia, lethargy, as well as possibly nausea, vomiting, diarrhoea and weight loss. The clinical signs may have a chronic intermittent occurrence.

On physical examination, signs of dehydration, weight loss, muscle wasting, icterus, salivation, palpable liver margins, cranial abdominal tenderness or firmness may be present. Suppurative and non-suppurative CCHC cannot be differentiated on the basis of history and physical examination alone; both forms may or may not present with elevated temperature. Biopsy is required for differentiation. Wedge biopsy provides necessary architectural information that a Tru-cut or fine needle aspirate doesn't.

Cats with CCHC often have hyperbilirubinemia and bilirubinuria but these don't differentiate the conditions from other hepatic, prehepatic and post-hepatic causes of icterus. In patients with bilirubinuria, lack of urobilinogen should increase suspicion of extrahepatic bile duct obstruction. Increases in activity of serum alkaline phosphatase (AP), alanine transferase (ALT) and gamma glutamyl transferase (GGT) may be present to varying degrees but do not distinguish between suppurative and non-suppurative CCHC. Cats with hepatic lipidosis usually have markedly increased ALP activity compared with ALT activity and have normal GGT activity. In contrast, cats with CCHC usually have ALP and ALT increases of equal magnitude or the increase in ALT is greater than ALP; GGT activity is usually increased as well. Bilirubinuria is always significant  in the cat.

It is important to realise that some patients may have chronic CCHC resulting in decreased functional liver mass and therefore no increases in LAT, ALP or bilirubin may occur. There may be variable changes in albumin, glucose, BUN, cholesterol. If you believe that liver disease is possible, a liver function test is indicated. Use the combination of pre- and post-prandial serum bile acid measurement to assess liver function. With cirrhosis, penicillamine or methotrexate may be beneficial in reducing the progression of fibrosis.

Hepatic biopsy is preferred over FNA or Tru-cut biopsy. With FNA, not only are you restricted in what you harvest, but the condition of that sample is mutilated by the aspiration action and slide preparation. Some types of cells do not exfoliate readily (mesenchymal neoplasias such as fibrosarcoma for example) and so with FNA you only get a cytological diagnosis of whatever cells are sampled easily and may not get a real picture of the underlying disease process. Additionally, orientation of the cellular reaction within tissue is critical in differentiating what role neutrophils or lymphocytes play. For example, peribiliary inflammation and periportal inflammation define different disease processes and may indicate different therapy and different prognosis.

Vitamin K1 is required since approximately 50% of cats with hepatic lipidosis have prolonged clotting times. It takes cats less than 7 days to become Vitamin K deficient. Cats who have been on antibiotics may have fewer organisms in their bowels to make Vitamin K. Vitamin K is absorbed in the proximal small bowel (duodenum and jejunum) and recycled by the liver (Vitamin K epoxidase cycle). Thus, in small bowel diseases (such as IBD induced fat malabsorption), as well as in liver diseases (especially in hepatic lipidosis), low Vitamin K levels may predispose to occult coagulopathies. Factors II, VII, IX and X, as well as protein C and protein S (antithrombotic proteins) are Vitamin K dependant. Supplementation is most effective using Vitamin K1. If the patient is jaundiced or nauseous, then Vitamin K1 must be given SQ rather than orally because intestinal absorption is poor (0.5-1.0 mg/kg q24 hrs for 3-4 days or until coagulopathy normalises). If too much Vitamin K1 is given, an oxidative toxicity may develop and supplementation of Vitamin E as an antioxidant may be required.

Cholecystitis

Cholecystitis generally presents as a vague malaise with inappetence and dehydration (pretty much like everything else in the cat). Vomiting may be present. While this too may involve a lymphocytic plasmacytic inflammatory infiltrate of the gall bladder wall, it more often is suppurative. If surgical evaluation occurs, and the gall bladder looks inflamed or if it does not compress and empty normally, or if ultrasound is suggestive of cholecystitis, bile aspiration and culture (aerobic and anaerobic) should be performed.

Extrahepatic bile duct obstruction

This is a cause for acute onset of vomiting and malaise in a patient. Plain radiographs may show radiodense object in the region of the gall bladder; ultrasound confirms the location is the bile duct as well will detect inspissations that aren't radiodense. A urinalysis will detect this problem early as there will be the presence of bilirubin but a lack of urobilinogen in the sample. Blood work will show a marked increase increase in bilirubin and eventually cholestasis (increased SAP) and some hepatocellular injury (increased ALT). This constitutes an emergency constitution and requires surgical correction.