Epidemiology

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Etiology

• Cardiac cirrhosis
  • A complication of right-sided heart failure characterized by cirrhosis due to chronic hepatic vein congestion.
  • Associated with “nutmeg liver” (diffuse mottling on imaging due to ischemia and fatty degeneration).

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Pathophysiology

• Cytokine‑mediated activation of hepatic stellate cells has been identified as a central element for developing fibrosis.
  • A cell found in the perisinusoidal space of the liver
    • Quiescent phase: vitamin A storage
    • Activated phase: transform into myofibroblast to secrete collagen (primary cell involved in hepatic fibrosis)

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Clinical features

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Diagnostics

CT abdomen

• Relative hypertrophy of the left lobe and caudate lobe
• Regenerative nodules
• Irregular liver surface
• Indirect findings: ascites, splenomegaly, portosystemic collaterals

Pathology

• Fibrosis (fibrous septa)
• Replacement of normal liver tissue with collagenous regenerative nodules

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Treatment

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Complications

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Portal hypertension

• Portal vein collateral circulation
  • Portal vein → Left gastric vein → Esophageal venous plexus → Azygos vein → Superior vena cava
  • Portal vein → Inferior mesenteric vein → Rectal venous plexus → Internal iliac vein → Inferior vena cava
  • Portal vein → Paraumbilical vein → Periumbilical venous network → Abdominal wall vein → Superior and inferior vena cava

Pulmonary complications of cirrhosis

Hepatic hydrothorax

• Definition: pleural effusions (typically one-sided; 70% right, 18% left) with transudate characteristics in the absence of any other cardiac, pulmonary, or pleural disease
• Pathophysiology: increased permeability of the diaphragm (small defects, increased abdominal pressure)
• Clinical presentation
  • May be asymptomatic
  • Signs and symptoms of pleural effusion: cough, dyspnea, hypoxia
• Diagnosis: Thoracocentesis shows transudate.