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CHOLANGIOHEPATITIS IN A TENNESSEE WALKING HORSE GELDING

CHOLANGIOHEPATITIS IN A TENNESSEE WALKING HORSE GELDING. Becky Urion PO Box 1188 Crystal Beach, FL 34681 (727) 430-0060 Mentors: Johanna Elfenbein , DVM, DACVIM; Sarah Reuss , VMD, DACVIM University of Florida Veterinary Medical Center Gainesville, Florida. SIGNALMENT & HISTORY.

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CHOLANGIOHEPATITIS IN A TENNESSEE WALKING HORSE GELDING

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  1. CHOLANGIOHEPATITIS IN A TENNESSEE WALKING HORSE GELDING Becky Urion PO Box 1188 Crystal Beach, FL 34681 (727) 430-0060 Mentors: Johanna Elfenbein, DVM, DACVIM; Sarah Reuss, VMD, DACVIM University of Florida Veterinary Medical Center Gainesville, Florida

  2. SIGNALMENT & HISTORY • 15 year old Tennessee Walking Horse gelding • Trail horse living in central Florida • History of fever and anorexia in July 2010 • Evaluated by referring veterinarian • Serum chemistry & Lyme titer performed at the time • Treated with month-long course of doxycycline • Lyme’s disease suspected based on high titer • Clinical signs resolved with therapy

  3. RECENT HISTORY • Presented to referring veterinarian again for fever and anorexia of one week’s duration in March 2011 • Fever non-responsive to several oral doses of flunixinmeglumine • On day of presentation: • Owner noted passage of chocolate-colored urine • Bloodwork performed by referring veterinarian • Referred to UF CVM for further diagnostics

  4. RECENT HISTORY • Biochemistry - performed by referring veterinarian on day of presentation

  5. RECENT HISTORY • Hematology - performed by referring veterinarian on day of presentation

  6. CLINICAL FINDINGS • Bright, alert, responsive • Body condition score: 5/9 • Oral mucous membranes pink with yellow tinge • Pale yellow sclera • Temperature: 103.8 °F • Pulse: 48 beats per minute • Respiratory rate: 36 breaths per minute • Inappetance with no overt colic behavior and normal gastrointestinal borborygmi • 500 mg of flunixinmeglumine given intravenously

  7. DIAGNOSTIC PLAN • Urinalysis • Additional bloodwork • SDH • Bile acids • Ammonia • PT, PTT • Rebreathing examination • Thoracic & abdominal ultrasound • Liver biopsy Fever likely hepatic in origin but additional diagnostics pursued in order to rule out extra-hepatic causes, e.g. peritonitis, pneumonia, neoplasia, abscesses

  8. LABORATORY FINDINGS Urine Dipstick (free catch sample) *Proteinuria considered spurious due to alkalinity of urine

  9. DIAGNOSTIC PLAN Additional Laboratory Testing Cytosolic enzyme with short half-life, making it ideal for evaluating ongoing disease; increased value indicates hepatocellular damage Increased levels indicate decreased hepatic function and resulting inability of liver to clear ammonia from blood and convert to blood urea nitrogen Measure of hepatic function; increased value indicates bile acids ineffectively cleared from blood by liver; may be due to failure of uptake, conjugation, or excretion, or regurgitation due to biliary obstruction

  10. DIAGNOSTIC PLAN Additional Laboratory Testing • Tests of extrinsic and intrinsic pathways of clotting cascade, respectively • Performed prior to biopsy to ensure adequate clotting ability • Mildly prolonged PT was considered clinically insignificant as it represented <20% increase above normal reference range • Rebreathing Exam & Thoracic Ultrasound • Performed to rule out non-hepatic causes of fever, e.g. pneumonia, neoplasia, abscesses • Both exams unremarkable

  11. DIAGNOSTIC PLAN Trans-Abdominal Ultrasound • Evaluation of liver shape, size, position, texture • Identification of abscesses, cysts, neoplastic masses, dilated bile ducts, choleliths, fibrosis, peritonitis • Liver seen on right side, caudoventral to lung in 8th-14th intercostal spaces; can also be seen on left cranioventral abdomen • Allows for biopsy instrument guidance • Liver edges rounded • Likely indicates some degree of liver disease and fibrosis • Parenchymal pattern difficult to assess due to large abdominal fat stores • No evidence of biliary tree distension, choleliths • Does not entirely rule out presence • No other abnormalities noted

  12. PROBLEM LIST • Fever* • Increased serum GGT, AST, SDH* • Increased serum bile acids* • Icterus, hyperbilirubinemia, bilirubinuria* • Rounded liver edges* • Hyperfibrinogenemia & neutrophilia* • Inappetance • Tachycardia *Denotes most significant problems

  13. DIFFERENTIAL DIAGNOSES • Icterus, Bilirubinemia • & Bilirubinuria • Pre-Hepatic • Anorexia • Hemolysis • Hepatic • Cholangiohepatitis • Pyrrolidizinealkaloid toxicity • Hepatic abscessation • Streptococcus spp., Corynebacteriumpseudotuberculosis • Serum-associated hepatitis • Acute or chronic hepatitis • Neoplasia • Post-Hepatic • Cholelithiasis • Anterior enteritis Fever • Infection • Inflammation • Neoplasia Increased liver enzymes & bile acids • Chronic active hepatitis • Hepatic abscessation • Pyrrolizidine alkaloid toxicity • Aflatoxicosis • Cholangiohepatitis • Cholelithiasis • Serum-associated hepatitis • Neoplasia • Hemochromatosis

  14. DIAGNOSTIC PLAN Percutaneous Liver Biopsy – infectious or inflammatory process involving liver considered most likely • Performed to determine diagnosis & prognosis • (Durham 2003; Equine Vet J.;35:534-40) • Diffuse or zonal lesions (e.g. most toxic, infectious, metabolic liver diseases) can usually be diagnosed by biopsy • Focal lesions (e.g. abscesses, granulomas, neoplasias) easily missed • Bleeding is major complication; occurs in 13% of cases but is mostly subclinical • (Johns 2008; J Vet Intern Med.;22:185-189)

  15. DIAGNOSTIC PLAN • Performed in right 9-14th ICS at intersection of line drawn from tuber coxae to mid-humerus • Site aseptically prepared, anesthetized with lidocaine • Stab incision made with #15 blade before placement of 14-gauge Tru-cut biopsy instrument • Ultrasound guidance used • At least 4 samples taken • One for aerobic & anaerobic cultures • Remainder fixed in formalin for histopathology • Percutaneous Liver Biopsy

  16. DIAGNOSTIC PLAN Percutaneous Liver Biopsy Gross samples greenish in color • Consistent with biliary stasis Aerobic and anaerobic culture • No growth on either plate at 48 hours • Approximately 50% of bacterial cholangiohepatitis cultures yield no results Normal hepatocytes Inflammation Fibrosis H&E 20x; Photo courtesy of Dr. William Craft HISTOPATHOLOGIC ANALYSIS Suppurativecholangiohepatitis, multifocal, marked, with marked portal abscessation, chronic Portal fibrosis, biliary proliferation, periportal hepatocyte loss, multifocal, severe, chronic Nodular hepatocellular regeneration, multifocal, marked, chronic

  17. DIAGNOSIS Common Causes • Primary • Secondary • Cholelithiasis or biliary stasis • Chronic active hepatitis • Duodenal inflammation • Intestinal obstruction • Neoplasia • Parasitism • Certain toxins • Often ascending bacterial infection PRESUMPTIVE BACTERIAL CHOLANGIOHEPATITIS • Common Clinical Findings • Anorexia • Pyrexia • Icterus • Intermittent signs of colic • Hyperammonemic hepatic encephalopathy possible • Diagnosis Supported By • Elevated cholestatic&hepatocellular enzymes • Hyperbilirubinemia • Inflammatory leukogram • Hyperfibrinogenemia

  18. THERAPEUTIC PLAN Enteric organisms common • Salmonella species • Escherichia coli • Citrobacter • Klebsiella • Aeromonas • Acinetobacter • Commonly used antibiotics • Trimethoprim-sulfonamide • Ceftiofur • Enrofloxacin • Penicillin and gentamicin • Ampicillin • Chloramphenicol * Usually 4-6 weeks of antimicrobial therapy required based on culture & sensitivity results • Started one month course of chloramphenicol (50 mg/kg TID) • Empirical choice based on lack of positive culture • Excreted in bile ducts • Broad spectrum of activity • Good penetration of abscesses • Can be given orally for long-term treatment • **Owners warned to wear gloves while handling chloramphenicol because of potential for aplastic anemia in humans**

  19. ADDITIONAL THERAPEUTIC OPTIONS Dietary Modification • Grain with high carbohydrates, low protein Ex: 2 parts beet pulp (or sorghum, bran, or milo), one part cracked corn in molasses • Divide ration into multiple small meals • Oat hay is best roughage, followed by other grass hays • Encourage to graze in grass pastures • Alfalfa & legumes should be avoided if possible because of high protein (Can be included if more calories needed) • Anti-inflammatories • Flunixinmeglumine • Dimethyl sulfoxide • May help dissolve interbiliary sludge or small calcium bilirubinate stones • Pentoxifylline • Provides anti-endotoxic effects

  20. PROGNOSIS • Can be successfully treated but depends on long-term antimicrobial therapy and appropriate supportive care • Clinical signs usually not manifested until ~75% of liver function lost • Severe periportal and bridging fibrosis generally poor prognostic indicators, with or without hyperammonemic encephalopathy • Leukocytosis associated with poorer prognoses (Durham 2003; Equine Vet J.;35:542-547) • Often result of neutrophilia due to systemic inflammatory response following loss of Kupffer cells or glucocorticoid-mediated stress response

  21. OUTCOME • Serum biochemistry repeated by referring veterinarian after one month of treatment with chloramphenicol *Clinical recovery often precedes normalization of biochemical values All other parameters within normal limits • Treatment recommended to continue until normalization of GGT levels • Decision made to pursue additional month of therapy with chloramphenicol with recheck of GGT & bile acid levels following completion • Two months after presentation, continues to do well at home with good appetite & no fevers

  22. REFERENCES & FURTHER READING • Durham, AE, Newton, JR, Smith, KC, et al. Retrospective analysis of historical, clinical, ultrasonographic, serum biochemical and haematological data in prognostic evaluation of equine liver disease. Equine Vet J. 2003;35:542-547. • Durham, AE, Smith, KC, Newton, JR. An evaluation of diagnostic data in comparison to the results of liver biopsies in mature horses. Equine Vet J. 2003;35:554-559. • Durham, AE, Smith, KC, Newton, JR, et al. Development and application of a scoring system for prognostic evaluation of equine liver biopsies. Equine Vet J. 2003;35:534-540. • Johns, IC, Sweeney, RW. Coagulation abnormalities and complications after percutaneous liver biopsy in horses. J Vet Intern Med. 2008;22:185-189. • Reed, SM, Bayly, WM, Sellon, DC. Disorders of the liver. In: Equine Internal Medicine, 2nd ed. Ed: FathmanL, Elsevier, St Louis, MO. 2004. Pp. 951-994. • Peek SF and Tivers TJ. Medical treatment of cholangiohepatitis and cholelithiasis in mature horses: 9 cases (1991-1998). Equine Vet J. 2000;32:301-306.

  23. ACKNOWLEDGMENTS Photographs courtesy of Dr. Johanna Elfenbein and Dr. Sarah Reuss Thanks to both for their time, assistance, and patience Thanks to Drs. Barbara Sheppard and William Craft for histopathology evaluation

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