Identifying and treating secondary complications
Secondary complications of feline inflammatory hepatobiliary disease include coagulopathy, bacterial infection, extrahepatic
bile duct obstruction, ascites, and hepatic encephalopathy (Table 3).
Table 3: Treatment of Feline Inflammatory Hepatobiliary Disease-Associated Complications
Feline inflammatory hepatobiliary disease may result in coagulopathy secondary to decreased synthesis of clotting factors
and impaired vitamin K absorption. Initiate empirical vitamin K1 therapy in all cases before any invasive procedures. Vitamin K1 therapy, given subcutaneously, may be continued in hyperbilirubinemic cats every 14 to 21 days. Overdosing vitamin K1 may cause hemolytic anemia associated with Heinz body formation.1 In cases in which decreased synthesis of clotting factors is suspected (elevation in prothrombin time, partial thromboplastin
time, or both) consider administering fresh frozen plasma, or, if the cat is also anemic, performing a fresh whole blood transfusion.
People with hepatobiliary disease are predisposed to bacterial infection because of impaired Kupffer cell function, decreased
neutrophil function secondary to complement deficiency, and bacterial translocation due to portal hypertension. It is thought
that some of these same predisposing factors may make cats with inflammatory hepatobiliary disease more prone to bacterial
infection. In most cases, prophylactic broad-spectrum antibiotic therapy is indicated once a diagnosis is made. Patients with
acute suppurative cholangitis are at a higher risk of developing sepsis and should be monitored closely for 1) an acute change
in body temperature (increase or decrease); 2) the onset of abdominal pain; 3) the development of a neutrophilia, neutropenia,
or a monocytosis; 4) a sudden increase in serum bilirubin concentration; or 5) an acute onset of hypoglycemia.
Extrahepatic bile duct obstruction
Cats with inflammatory hepatobiliary disease may develop extrahepatic bile duct obstruction due to strictures secondary to
chronic biliary inflammation and fibrosis, a predisposition to biliary adenocarcinoma, or extraluminal constriction from pancreatic
fibrosis. Consider periodically reassessing the hepatobiliary tree ultrasonographically in cases that are refractory to treatment.
Ascites is a rare complication of feline inflammatory hepatobiliary disease and is generally indicative of end-stage liver
disease with concurrent portal hypertension. Treatment consists of spironolactone and a low-sodium diet.
Hepatic encephalopathy is caused by the inhibition of excitatory neurotransmission secondary to inadequate hepatic detoxification
of gut-derived neurotoxins. Hepatic encephalopathy may be present initially or may develop during the course of therapy. Signs
include ptyalism, lethargy, depression, stupor, blindness, and ataxia. Treatment consists of lactulose and metronidazole.
Adjust the lactulose dose to achieve three or four soft stools a day. Metronidazole decreases gastrointestinal ammonia production
by reducing the population of urease-producing bacteria. Protein restriction is not instituted unless medical management is
inadequate; it is adjusted to the maximally tolerated amount.
In cases of suppurative cholangitis, treatment is considered successful if biochemical abnormalities normalize within four
weeks and the cat is clinically doing well. Ongoing inflammation should be presumed in cases of persistent increases in serum
liver enzyme activities or serum bilirubin concentrations, especially in the presence of a neutrophilic leukocytosis.1 In these cases, abdominal ultrasonography, liver biopsy, and bile collection with cultures should be repeated. It is suspected,
but not proven, that suppurative cholangitis may evolve into a nonsuppurative cholangitis.1,2 If nonsuppurative inflammation is verified, culture results are negative, and no underlying source of chronic infection
is found, treatment with anti-inflammatory drugs is appropriate.1