Page 598 - Small Animal Internal Medicine, 6th Edition
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570    PART IV   Hepatobiliary and Exocrine Pancreatic Disorders


            The cat should be monitored carefully for any leakage of bile   of clinical and histologic presentations suggests more than
            after the procedure; any suspicion of leakage and bile peri-  one cause. Some researchers have suggested an immune-
  VetBooks.ir  tonitis warrants surgery. Cytology of bile usually shows bac-  mediated etiology, but the disease does not resolve with
                                                                 immunosuppressive medication. Other studies have sug-
            teria and neutrophils, and culture and sensitivity tests should
                                                                 gested possible infectious etiologies, such as Helicobacter or
            be performed.
                                                                 Bartonella spp. (Boomkens et al., 2004; Greiter-Wilke et al.,
            Treatment and Prognosis                              2006;  Kordick et al., 1999), although recent work has not
            Cats should be treated for 4 to 6 weeks with an appropriate   supported infectious causes (Warren et al., 2011). However,
            antibiotic on the basis of the results of culture and sensitiv-  the use of immunosuppressive medication in all these cases
            ity tests. Amoxicillin is a good initial choice at a dose of 15   is subject to question.
            to 20 mg/kg PO q8h. Ursodeoxycholic acid may be given
            as an additional choleretic and antiinflammatory agent at   Clinical Features
            a dose of 15 mg/kg PO q24h, although there are no studies   Cats with lymphocytic cholangitis were previously reported
            demonstrating its benefit in cats with neutrophilic cholan-  to be typically young to middle-aged, and Persians appeared
            gitis. Septic or extremely sick cats may require hospitaliza-  to be overrepresented, but recent studies report it in older
            tion for IV fluid and IV antibiotic administration during the   cats with no obvious breed predisposition (Callahan Clark
            initial stages of therapy. Careful attention should be paid to   et al., 2011; Warren et al., 2011). Affected cats tend to have
            feeding anorexic cats to prevent the concurrent develop-  a long history (months to years) of waxing and waning low-
            ment of hepatic lipidosis, which was found in one third of   grade illness. Many become jaundiced, and they often lose
            the cats with cholangitis in a recent study (Callahan Clark   weight and have intermittent anorexia and lethargy, but they
            et al., 2011); a high-protein diet designed for critical care   are less likely to be pyrexic than cats with neutrophilic chol-
            use, as outlined in the lipidosis section, is more appropriate   angitis. About one third of cats may also present with a high-
            for these animals than a protein-restricted liver diet. The   protein  ascites,  reportedly  most  commonly  in  the  United
            prognosis is generally good, and these cats usually recover   Kingdom. This makes differentiation from feline infectious
            completely  provided  they  are  treated  early  and  appropri-  peritonitis (FIP) important. Ultimately, the differentiation in
            ately. It is thought that some cases of the more chronic form   these cats can be made only on histopathology.
            of neutrophilic cholangitis may represent long-term persis-
            tence of a low-grade infection in untreated or only partially   Diagnosis
            treated cats.                                        Diagnosis in these cases relies ultimately on hepatic histopa-
                                                                 thology, although ultrasonographic and clinicopathologic
            Lymphocytic Cholangitis                              findings can support a presumptive clinical diagnosis.
            Lymphocytic cholangitis is also termed lymphocytic cholan-  Increases in liver enzyme levels are mild to moderate and
            giohepatitis, lymphocytic portal hepatitis, and nonsuppurative   tend to be less marked than in cats with neutrophilic chol-
            cholangitis. Some cases of chronic neutrophilic cholangitis as   angitis. Peripheral blood neutrophilia is less common than
            defined by the WSAVA may also overlap with lymphocytic   in cats with the acute disease but may be present. A particu-
            cholangitis.                                         lar feature of most cats with lymphocytic cholangitis is an
                                                                 increase in γ-globulin concentration, which again may cause
            Pathogenesis and Etiology                            confusion with FIP. However, some cats have normal white
            Lymphocytic cholangitis is a slowly progressive chronic   blood cell counts and liver enzyme levels, so these findings
            disease characterized by infiltration of the portal areas of the   are neither sensitive nor specific (Callahan Clark et al.,
            liver with small lymphocytes. Occasionally, plasma cells and   2011). Radiographic signs are also nonspecific; there may be
            eosinophils can be seen. The presence of neutrophils might   hepatomegaly (which is often caused by enlargement of the
            change the name of the disease to chronic neutrophilic chol-  larger bile ducts) and in some cases abdominal effusion but
            angitis, but some authors include a predominantly lympho-  radiographs are often normal (Fig. 35.6). Ultrasonography is
            cytic disease with a small number of neutrophils in the   more helpful and reveals dilation of the biliary tract in some
            lymphocytic chronic cholangitis category. Histologic changes   patients (see  Fig. 34.11). The common bile duct typically
            vary among cases, probably reflecting a variety of as yet   appears dilated, and there may be dilation of the gallbladder
            unknown etiologies. In the largest study on the histology of   and sludge in it. The main differential diagnosis for these cats
            the disease (Warren et al., 2011), many cats had biliary   is EBDO; the ultrasonographer should attempt to rule this
            hyperplasia and peribiliary fibrosis, but a small number of   out by carefully imaging the surrounding pancreas, small
            cases showed ductopenia (loss of bile ducts). The lymphocyte   intestine, and mesentery, although it can be difficult to rule
            infiltrate was predominantly of T cells, but portal B-cell   out EBDO completely particularly if it is caused by an echo-
            aggregates seemed to be a particular feature of the disease.   lucent lesion or sphincter of Oddi spasm.
            Bile duct targeting by inflammatory cells was common. In   It is very important to evaluate a hemostasis profile before
            severe cases the main differential diagnosis on histology is   performing a liver biopsy in view of how commonly coagula-
            lymphoma, and in some cases, differentiating the two dis-  tion times are prolonged in cats with liver disease. Vitamin
            eases can be difficult. The cause is unknown, and the variety   K should be given before the biopsy (0.5 mg/kg of vitamin
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