Hepatitis (acute vs chronic)

Adnan Menderes UniversityFaculty of Veterinary Small Animals Internal Diseases

Hepatitis(acute vs chronic)

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Presented By: María Zarco Jiménez

What is "hepatitis"?

Hepatitis: inflammation of the liver that causes cell damage, necrosis and infiltration of inflammatory cells; it can be acute or chronic, and have infectious, toxic, metabolic or immunomediated origin.

Importance in small animals: common in dogs and cats; affects vital liver functions (metabolism, detoxification, protein synthesis); it can be subclinical at the beginning and evolve into fibrosis, cirrhosis or liver failure, impacting the prognosis and quality of life.

General classification: acute vs chronic

The liver has a huge capacity for regeneration, but when it is exceeded, chronicity appears

Acute hepatitis:• Sudden and short-term start • Reversible hepatocellular lesion in many cases • Predominance of necrosis and degeneration

Chronic hepatitis: • Prolonged evolution (weeks or months) • Persistent inflammation → fibrosis and possible cirrhosis • Irreversible liver damage

ETIOLOGY

ACUTE HEPATITIS

CHRONIC HEPATITIS

Pathophysiology

Hepatitis is initiated by hepatocellular damage caused by infectious, toxic or metabolic agents, which triggers an inflammatory response and alters essential liver functions such as metabolism, detoxification and protein synthesis. The evolution of the process will depend on the persistence of the harmful stimulus and the capacity for hepatic regeneration. • Acute hepatitis: Sudden and intense damage → hepatocellular degeneration and necrosis → release of enzymes (ALT, AST) → acute inflammatory response (predominance of neutrophils) → hepatic functional alteration → if the cause is eliminated → regeneration and complete recovery • Chronic hepatitis: Persistent damage → chronic inflammation (lymphocytes and plasma cells) → progressive cell death → activation of hepatic star cells → collagen deposit → fibrosis → alteration of hepatic architecture → progression to cirrhosis → portal hypertension and liver failure → onset of complications (ascites, hepatic encephalopathy)

CLINICAL SIGNS

The clinical signs of hepatitis depend on the speed of onset and the duration of liver damage. In the acute form, abrupt and intense signs predominate, while in the chronic form they are usually progressive and, at the beginning, not very specific, which delays the diagnosis.

Acute hepatitis • Sudden start • Marked lethargy • Anorexia • Vomiting ± diarrhoea • Abdominal pain • Fever (occasional) • Variable jaundice • In serious cases: • Coagulopathies • Acute liver failure

Chronic hepatitis • Slow and progressive evolution • Initial non-specific signs: • Mild lethargy • Variable appetite • Progressive weight loss • Frequent jaundice • Ascitis (portal hypertension) • Hepatic encephalopathy (neurological signs) • Chronic weakness

DIAGNOSIS

It is based on the combination of tests that allow to evaluate liver damage, function and structure: • Blood analysis: • ALT, AST → ↑ hepatocellular damage • FA, GGT → ↑ cholestasis • Bilirubin → ↑ jaundice • Albumin → ↓ in chronic disease • Bile acids: • ↑ indicates liver disfunction • Coagulation (PT, aPTT): • Prolonged → failure in factor synthesis • Abdominal ultrasound: • Size, shape and echogenicity of the liver • Liver biopsy (gold standard): • Confirm diagnosis and type of injury

TREATMENT

The treatment of hepatitis depends on whether the disease is acute or chronic, as the underlying pathology, reversibility, and complications differ. In all cases, the main principles are to remove or control the causative factor, support liver function, and manage clinical complications. Acute Hepatitis (Sudden Insult) • Definition: Rapid onset of liver dysfunction due to toxins (e.g., Xylitol, Blue-green algae), infections (Leptospirosis), or trauma. • Management Focus: Emergency stabilization and detoxification. • Fluid Support: IV crystalloids to maintain hepatic blood flow. • Antidotes: N-acetylcysteine (NAC) for toxicities (Acetaminophen). • Antibiotics: Targeted therapy for infectious agents (e.g., Doxycycline for Lepto). • Supportive Care: Strong antiemetics (Maropitant) and GI protectants. Chronic Hepatitis (Persistent Inflammation) • Definition: Long-term inflammation (often immune-mediated or breed-related) leading to fibrosis/cirrhosis. • Management Focus: Controlling inflammation and slowing scarring. • Immunosuppression: Prednisolone or Cyclosporine to reduce auto-immune damage. • Copper Chelation: D-penicillamine if biopsy shows copper accumulation. • Bile Support: Ursodiol (Ursodeoxycholic acid) to thin bile and reduce toxicity. • Antifibrotics: Colchicine to help prevent progressive scarring. Universal Supportive Therapy • Hepatoprotectants: SAMe, Silybin (Milk Thistle), and Vitamin E to boost glutathione and combat oxidative stress. • Dietary Modification: Low-copper, high-antioxidant, and highly digestible protein diets (e.g., Hill's l/d or Royal Canin Hepatic). • Monitoring: Regular ALT/ALP biochemistry and serial ultrasounds.

PROGNOSIS

Acute Hepatitis * Outlook: Guarded initially, but high recovery potential. * Recovery: If the patient survives the first 48–72 hours, the prognosis for full liver regeneration is excellent. * Key Risks: Mortality is usually linked to liver failure or systemic "storm" (DIC, hypoglycemia). Chronic Hepatitis * Outlook: Variable; manageable but progressive. * Early Stage: Good; many pets live 2–3+ years with proper medication and diet. * Late Stage: Poor; once cirrhosis or ascites (fluid buildup) develops, survival is often <6 months. Critical "Red Flag" Indicators * Poor Prognosis: Persistent jaundice (high bilirubin), low albumin, and the presence of ascites. * Better Prognosis: Early detection via routine bloodwork before clinical symptoms appear.

THANK YOU SO MUCH!

• Idiopathic (most frequent cause) • Immunomediated • Copper cluster (predisposed breeds: Bedlington Terrier, Doberman, Labrador) • Sequelae of poorly resolved acute hepatitis • Chronic toxic (prolonged exposure to drugs or toxins) • Metabolic or genetic (inherited alterations that affect the liver)

Chronic hepatitis: • ALT/AST → moderate or persistent • FA, GGT → higher (chronic cholestasis) • Albumine → ↓ • Bile acids → ↑ • Ultrasound → small liver, irregular, hyperechoic, possible ascitis • Biopsy → fibrosis, mononuclear infiltrate, cirrhosis

Acute hepatitis: • ALT/AST → very high (recent and intense damage) • Bilirubin → ↑ variable • Coagulation → altered in severe cases • Ultrasound → hepatomegaly, more hypoechoic liver • Biopsy → necrosis, degeneration, neutrophilic inflammation

VS

• Viral: Canine infectious hepatitis • Bacterial: Leptospirosis

INFECTIOUS

• Drugs (e.g. anticonvulsants, NSAIDs) • Toxic plants • Mycotoxins (aflatoxins) • Chemical substances

TOXIC

• Shock • Prolonged anaesthesia • Severe hypotension

ISCHEMIC / HYPOXIC

• Acute hepatic lipidosis • Severe hypoglycaemia or prolonged fasting • Acute hyperlipidaemia • Congenital metabolic errors

METABOLIC

The cause cannot be identified

IDIOPATHIC