Summary of Clinical approach to patient with ascites

Summary of "Clinical approach to patient with ascites"

This lecture presents a comprehensive clinical approach to evaluating a patient with ascites, illustrated through a detailed case study of a 50-year-old male with chronic liver disease secondary to Hepatitis C virus (HCV) infection. The discussion emphasizes the importance of systematic history taking, clinical examination, laboratory investigations, imaging, and Ascitic fluid analysis to reach a differential and clinical diagnosis.

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Main Ideas and Concepts

• Clinical Approach Framework:
  • Focus on key points in:
    • History taking
    • Clinical examination
    • Laboratory investigations
    • Imaging studies
    • Ascitic fluid analysis
  • These steps guide toward differential diagnosis and management.
• Case Presentation:
  • 50-year-old male with vague abdominal pain, low-grade fever, chronic liver disease due to HCV.
  • Signs: jaundice, spider nevi, splenomegaly, moderate ascites.
  • Labs: elevated AST > ALT, hyperbilirubinemia (mainly direct), low albumin, prolonged INR.
  • Ultrasound: nodular liver, coarse echotexture, focal hepatic lesion, splenomegaly, ascites.
  • Ascitic fluid albumin: 1.6 g/dL; Serum Ascitic Albumin Gradient (SAAG) = 0.8.
• History Taking and Clinical Examination:
  • Important to clarify:
    • Characteristics and causes of abdominal pain in chronic liver disease.
    • Symptoms/signs of infection (fever, chills, urinary symptoms, respiratory symptoms).
    • History of liver disease etiology (HCV treatment status, other viral hepatitis, alcohol, autoimmune).
    • Symptoms of complications: jaundice, bleeding, encephalopathy, edema.
  • Physical exam to detect:
    • Chronic liver disease stigmata (fetor hepaticus, palmar erythema, gynecomastia, tremors, edema).
    • Abdominal signs: liver size, consistency, tenderness; spleen size and features; abdominal collaterals.
• Interpretation of Laboratory Data:
  • AST/ALT ratio >1 suggests cirrhosis.
  • Elevated direct bilirubin and alkaline phosphatase indicate intrahepatic cholestasis.
  • Low albumin and high INR reflect impaired synthetic liver function.
  • SAAG <1.1 suggests non-portal hypertensive causes of ascites.
  • Additional labs needed:
    • Viral load (HCV RNA), hepatitis B markers.
    • Autoimmune markers if indicated.
    • Complete blood count to evaluate anemia, leukocytosis, thrombocytopenia.
    • Renal function tests (urea, creatinine) to assess hepatorenal syndrome.
    • Alpha-fetoprotein for Hepatocellular carcinoma (HCC) screening.
• Ascitic fluid analysis:
  • Essential for all moderate/severe ascites.
  • Tests include:
    • Albumin level (to calculate SAAG).
    • Polymorphonuclear leukocyte count (>250 cells/mm³ diagnostic for spontaneous bacterial peritonitis [SBP]).
    • Culture and sensitivity.
    • Acid-fast bacilli staining (to exclude tuberculosis).
    • Cytology for malignant cells.
• Serum Ascitic Albumin Gradient (SAAG):
  • SAAG ≥ 1.1 g/dL indicates ascites due to portal hypertension (e.g., cirrhosis).
  • SAAG < 1.1 g/dL suggests other causes (infection, malignancy, pancreatic ascites).
  • High sensitivity and specificity but not 100% accurate.
• Differential Diagnosis of Ascites:
  • Portal hypertensive ascites:
    • Liver cirrhosis (most common)
    • Budd-Chiari syndrome (hepatic vein obstruction)
    • Portal vein thrombosis
    • Cardiac causes (right heart failure, constrictive pericarditis)
  • Non-portal hypertensive ascites:
    • Infections (SBP, tuberculosis, fungal)
    • Malignancy (primary peritoneal tumors, metastases, HCC)
    • Pancreatic disease (pancreatic ascites)
    • Endocrine, nephrotic syndrome, malnutrition, others
• Focal Hepatic Lesions in Cirrhosis:
  • Most common cause: Hepatocellular carcinoma (HCC).
  • Other benign lesions: hemangioma, adenoma, focal nodular hyperplasia.
  • Other malignancies: cholangiocarcinoma, metastases, lymphoma.
  • Diagnosis primarily by Triphasic spiral CT or MRI:
    • HCC is a hypervascular tumor with characteristic arterial phase enhancement and rapid washout in portal venous/delayed phases.
    • Biopsy reserved for inconclusive imaging.

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