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Ascites

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Overview of Ascites

Publicada em: Saúde e medicina
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Ascites

  1. 1. DR. SAI LAKSHMIKANTH BHARATHI De Medicina
  2. 2. Aulus Cornelius Celsus Roman 25 B.C to 50 A.D Coined “ASCITES” ; askites – baglike (Greek)
  3. 3. Definition Pathogenesis & theories of ascites formation Approach Differential Diagnosis Management
  4. 4. Accumulation of fluid in the peritoneal cavity Hydroperitoneum Hydraskos or abdominal dropsy
  5. 5. Similar to edema formation I. Increased hydrostatic pressure II. Reduction in colloid osmotic pressure III. Disturbance of capillary permeability IV. Insufficiency of lymphatic drainage
  6. 6. Portal hypertension IVC obstruction Anatomic disruption of Hepatic veins
  7. 7.  Minimum albumin concentration – 2.5 to 3g/100ml  Decreased albumin production  Increased excretion of albumin Hypoalbuminenia + Portal HTN- a pre-requisite for ascites
  8. 8. Trauma Inflammation Immune mediated
  9. 9. Mesentric lymph adenopathy Parasitic lymphatic obstruction
  10. 10. Underfill theory Overflow theory Lymph imbalance theory Vasodilation theory
  11. 11. Primary • Imbalance of Starling’s forces • Reduced effective plasma volume • Stimulation of Volume receptors,RAAS & sympathetic system • Increased circulating ADH levels • Increased Sodium reabsorbtion and reduced GFR • Ascites formation Lymphatic insufficiency secondary to portal HTN Opening of Portosystemic shunts Decreasing PVR Formation or breakdown of vasodilatory substances
  12. 12. Primary • Liver damage • Portal hypertension sends salt retaining signal • Retention of Sodium • Volume expansion • Overflow from Intravascular volume • Ascites formation
  13. 13. Do not explain in each case Both theories not mutually exclusive Doesn’t effectively explain the initial event
  14. 14. Contradicts “classical” theories Extravasation from intravascular space (Lymph Production) Reflux into vascular system (Lymphatic Drainage)
  15. 15. Obliteration of diaphragmatic lymphatics Dilated lymphatic vessels – reduced flow Limited lymph kinetics at the communion of lymphatics and venous systems
  16. 16. • Portal Hypertension • Peripheral vasodilation • Plasma volume reduction • Volume retention • Salt retention • Plasma volume expansion • Ascites formation
  17. 17. Clinical features Laboratory findings
  18. 18. Is the distension due to Ascites?? Acute or Chronic?? Possible etiological factors?? Grade of Ascites??
  19. 19. Manifest ascites – 1.5 to 2 liters Puddle sign 100-150 ml Shifting dullness 1-1.5 liters Fluid thrill >2 liters
  20. 20. Colour Cell count & Differential Protein Sugar(Glucose < 50g/dL – Bacterial infection) LDH Bacteriology-Culture & Gram Stain, TB ADA
  21. 21. Clear and straw coloured Turbid Hemorrhagic Chylous
  22. 22. Exudate ->1000/cu.mm; Transudate < 250cu.mm PMN > 250/cu.mm – Bacterial Lymphocytes >20% of Total Counts – TB (also Ascitic:Blood Glucose <0.7)
  23. 23. SAAG – Serum albumin: Ascitic Albumin >1.1 – Ascites secondary to Portal Hypertension <1.1 – Malignancy or Inflammation Transudate Exudate Protein <2.5g/L Protein >2.5g/L Specific Gravity <1,015 Specific gravity >1,016
  24. 24. Gram stain Culture – Aerobic and anaerobic AFB staining PCR for Tuberculosis
  25. 25. Ascites:serum <1.4 – portal hypertension Absolute value >400 IU/L
  26. 26. Ferritin Fibronectin Cholesterol α1- antitrypsin
  27. 27. Parameters Portal hypertension Infectious etiology malignancy Clinical features Splenomegaly, spider naevi, jaundice, Dupytren’s contracture Fever, tenderness, guarding.. Sister Mary Joseph nodules, Troisier’s sign Loss of weight SAAG Protein >1.1 <2.5g/dL <1.1 >3g/dL <1.1 >3g/dL Cell count <250cells/cu.mm >1000cells/cu.mm >>1000cells/ cu.mm Ascites: Serum LDH <1.4 >1.4 >>1.4 Color Clear Clear to turbid Clear, turbid, hemorrhagic or chylous
  28. 28. Portal hypertension Infective etiology Malignancy
  29. 29. Salt restriction Diuretics Beta blockers Aldosterone antogonist Paracentesis
  30. 30. Based on culture & sensitivity Empirically, cefotaxime 2g IV q12h for min. 5 days Alternatively, Oral ofloxacin 400mg q12h ESBL antibiotics and aminoglycosides- avoided
  31. 31. Norfloxacin daily; At risk -ascitic fluid protein <1g/dL, UGI bleed, previous SBP

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