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3. ASCITES part 1.pdf
This document provides a comprehensive overview of ascites, including its definitions, causes, pathophysiology, and management approaches. Common causes of ascites are categorized primarily into cirrhosis and less common conditions such as malignancies and infections, with diagnostic approaches involving history, examination, imaging, and fluid evaluation. It also details the significance of the serum-ascites albumin gradient (SAAG) and discusses spontaneous bacterial peritonitis, emphasizing treatment options for recurring cases.
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3. ASCITES part 1.pdf
- 1. Hepatology lectures for 5thSem;MBBS Pratap Sagar Tiwari MBBS,MD (Medicine),DM (Hepatology)
- 2. Summary ? Predisposing conditions Etiologies Liver Fibrosis/cirrhosis PortalHypertension Varices Splenomegaly Ascites Normal Liver
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- 4. DEFINITION: ASCITES H/o VH VHprevention measures for pts with a known H/o VH Secondary Prophylaxis • Ascites is the pathological accumulation of fluid within the peritoneal cavity. The peritoneal cavity normally contains approximately 50–75 mls of fluid that serves to lubricate the tissues that line the abdominal wall and viscera.1,2 1. Rumack C, Wilson S, Charboneau J, et al. Diagnostic ultrasound, 4th ed St Louis, MO: Mosby, 2011. 2. Hanbidge A, Lynch D, Wilson S. US of the peritoneum. Radiographics 2003; 23: 663–685. Pleural fluid: 10-20 ml Pericardial fluid: 15-50 ml
- 5. CAUSES OF ASCITES Causesof ascites can be categorized on basis of several aspects like • etiology (infection, malignancy), • pathophysiology (portal hypertension-related, non-PHTN related), • organ/system specific (cirrhotic, cardiac, renal ) • others (exudative vs transudative: (protein < 25 g/L) ) However the common causes of ascites are;
- 6. CAUSES OF ASCITES CommonCauses Less Common causes Cirrhosis -84 % • Massive hepatic metastasis Cardiac causes • Infection (tuberculosis, chlamydia infection) Peritoneal carcinomatosis • Pancreatitis • Primary peritoneal malignancies- mesothelioma and sarcoma • Abdominal malignancies- gastric or colonic adenocarcinoma • Metastatic disease from breast or lung carcinoma • Melanoma • Renal disease
- 7. RARE CAUSES OFASCITES Rare Causes • Hypothyroidism • Familial mediterranean fever • Collagen vascular disease • Amyloidosis • Fitz-hugh-Curtis syndrome • Protein-loosing enteropathy, malnutrition • Trauma (Bile ascites, urine ascites), Chylous ascites
- 8. PATHOPHYSIOLOGY Portal hypertension-related Non-portalhypertension related Exudation Lymphatic obstruction Hypoalbuminemia Transudation PATHOPHYSIOLOGY
- 9. PATHOPHYSIOLOGY Normally; • The peritoneumbehaves like a semipermeable membrane that enables the continuous exchange of water and solutes between the peritoneal cavity and the intraperitoneal blood and lymph vessels. PATHOPHYSIOLOGY
- 10. PATHOPHYSIOLOGY Non-portal hypertension related Exudation Lymphatic obstruction Hypoalbuminemia Anycauses leading to hypoalbuminema Protein-loosing enteropathy Malnutrition Nephrotic syndrome • Albumin comprises 75-80% of normal plasma colloid oncotic pressure and 50% of protein content. • When plasma proteins, especially albumin, no longer sustain sufficient colloid osmotic pressure to counterbalance hydrostatic pressure, edema/ascites develops. PATHOPHYSIOLOGY
- 11. PATHOPHYSIOLOGY IN ASCITES:due to Portal HTN
- 12. APPROACH ✓ Small amountsof ascites are asymptomatic, but with larger accumulations of fluid (> 1 L) there is abdominal distension, fullness in the flanks, shifting dullness on percussion and, when the ascites is marked, a fluid thrill/fluid wave. ✓ Other features include eversion of the umbilicus, herniae, abdominal striae, divarication of the recti and scrotal oedema. ✓ Dilated superficial abdominal veins may be seen if the ascites is due to portal hypertension. HISTORY EXAMINATION INVESTIGATION
- 13. Approach to Ascites History Examination Investigation •Bowel obstruction, severe constipation and ileus- inability to pass stool and flatus together with nausea/ vomiting • Weight loss, night sweats and anorexia • ↑ eructation or flatus- aerophagia or ↑ intestinal production of gas • Symptoms of other medical conditions- heart failure and tb • Question about risk factors like excessive alcohol use, iv drug abuse, chronic viral infection and jaundice APPROACH TO ASCITES
- 14. Approach to Ascites History Examination Investigation Cluesfor Cardiac disease • Elevated JVP • Kussmaul’s sign • Pericardial knock • Murmur of TR APPROACH TO ASCITES
- 15. Approach to Ascites History Examination Investigation Cluesfor Chronic liver disease • Pt is sarcopenic with distended abdomen • Peripheral signs of CLD Jaundice ,Parotid swelling, Gynaecomastia in males, Breast atrophy in females, Loss of axillary hairs, Spider naevi, Caput medusae, Testicular atrophy, palmar erythema, Dupytrens contracture, Leuconychia APPROACH TO ASCITES
- 16. Approach to Ascites History Examination Investigation AbdomenExamination • Inspection: generalized distention (localized incase of loculated ascites or mass), bulging flanks, distended superficial veins, everted umbilicus and umbilical nodule may be seen in malignancy • Grey-Turner's or Cullen's sign can be present in case of Acute Pancreatitis APPROACH TO ASCITES
- 17. Approach to Ascites History Examination Investigation AbdomenExamination • Palpation: tenderness, guarding( peritonitis) ,enlarged liver or splenomegaly • Percussion: Shifting dullness, fluid thrill APPROACH TO ASCITES
- 18. INSPECTION • Asymptomatic • Abdominaldistension • fullness in the flanks Shifting dullness on percussion, a fluid thrill/fluid wave. • Eversion of the umbilicus • Hernia • Abdominal striae • Divarication of the recti • Scrotal oedema Other features include *Dilated superficial abdominal veins may be seen if the ascites is due to portal hypertension. PERCUSSION SUMMARY
- 19. Approach to Ascites History Examination Investigation Imaging,eg USG Ascites fluid Evaluation Others; like ECHO
- 20. ➢IMAGING: ULTRASOUND &CT SCAN
- 21. ASCITES FLUID EVALUATION •Appearance • SAAG ? • Exudative ascites ? SBP ? • Others Why SAAG ? The presence of a gradient ≥1.1g/dL indicates that the pt has PHTN-related ascites with 96% accuracy. A SAAG <1.1g/dL indicates that the pt does not have PHTN-related ascites, and another cause of the ascites should be sought.
- 22. SAAG (SERUM ASCITESALBUMIN GRADIENT)
- 23. OTHERS; ASCITES EVALUATION ➢Pancreaticascites: Ascitic amylase > 1000 mg/dl ➢Cytology ➢Tuberculous peritonitis: • lymphocytosis and ADA> 40 U/L • Ascitic fluid AFB smear: sensitivity 0-3 % • Ascitic fluid culture: sensitivity 35-50 % • Elevated ADA: sensitivity >90% (cutoff value 35-40 U/L) Laparatomy or Laparascopy with biopsy- gold standard if cause is uncertain
- 24. OTHERS; LABORATORY EVALUATION ➢Serumamylase and lipase- to rule out pancreatitis ➢24 hr. urinary protein- nephrotic syndrome ➢Malabsorption and increased small intestinal bacterial overgrowth- detection of hydrogen and methane gas in expired breath ➢ECHO ➢Hepatic venous pressure gradient ➢Liver biopsy
- 25. SPONTANOUS BACTERIAL PERITONITIS Definition:an infection of initially sterile ascitic fluid without a detectable intra- abdominal surgically treatable source of infection. The presence of infection is documented by - positive ascitic fluid bacterial culture (essentially monomicrobial) & - an elevated ascitic fluid absolute PMN count (>250 cells/mm3) Note; Absolute PMN count = total white blood cell count X % of PMN
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- 27. TREATMENT Note: The ascitesthat recurs at least on three occasions within a 12-month period despite dietary sodium restriction and adequate diuretic dosage is defined as recidivant ascites. ➢ Ascites is uncomplicated when it is not infected, refractory or a/with HRS.
- 28. TREATMENT ➢ Sodium andwater restriction ➢ Diuretics ➢ Paracentesis ➢ TIPSS ➢ Liver Transplantation ➢ OTHERS;