Introduction

• Cause: most cases idiopathic; copper associated chronic hepatitis common; some cases believed to be autoimmune; chronic infections (eg chronic leptospira) or toxicities possible causes. Lobular dissecting hepatitis in young dogs. 
• Signs: lethargy, depression, anorexia, jaundice, ascites, polydipsia-polyuria, vomiting, diarrhea, melena, coagulopathy, hepatic encephalopathy.
• Diagnosis: hepatic biopsy.
• Treatment: supportive and symptomatic; use of copper chelators, low copper diet or immunosuppressives may be indicated.
• Prognosis: reasonable in early stages particularly if cause can be treated. Poor in more advanced disease.

Pathogenesis

Pathophysiology

• Chronic hepatitis is a heterogenous group of inflammatory-necrotizing diseases of the liver in which lymphocytes and plasma cells are the predominant inflammatory infiltrate.
• Pathophysiologic mechanisms of chronic hepatitis in dogs are poorly understood; although immune mechanisms and copper accumulation play roles, chronic toxicity and chronic leptospirosis also implicated.
• Chronic hepatitis can progress to hepatic cirrhosis (end-stage liver disease).
• Copper accumulation in liver → significant hepatic injury → acute/chronic hepatitis → cirrhosis.
• Immune mechanisms directed against cell nuclei, liver membranes, smooth muscle and mitochondria may → chronic active hepatitis.

• Periportal and sinusoidal fibrosis → portal hypertension → ascites and gut wall edema → diarrhea +/- melena 
• Decreased production of clotting factors → bleeding tendencies.
• Hepatcyte swelling → intrahepatic cholestasis → icterus.
• Inflammation of biliary system → partial obstruction to biliary flow → icterus.
• Decreased production of albumin → hypoalbuminemia → ascites.
• Failure to detoxify ammonia from intestine → hepatic encephalopathy.

Timecourse

• Weeks to months to years.

Diagnosis

Treatment

Outcomes