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Ascites

Ascites. Associate Professor Dr Meltem Ergun Yeditepe University Department of Gastroenterology. Points of this lecture. What is ascites? Etiologies of ascites Clinical presentations Pyhsical examination findings Laboratory tests Prognosis Spontaneous bacterial peritonitis.

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Ascites

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  1. Ascites AssociateProfessorDr Meltem Ergun Yeditepe University Department of Gastroenterology

  2. Points of thislecture • What is ascites? • Etiologies of ascites • Clinical presentations • Pyhsical examination findings • Laboratory tests • Prognosis • Spontaneous bacterial peritonitis

  3. Definition Pathological accumulation of fluid in abdominal cavity >50 ml

  4. Pathophysiology of Ascites From: Robbins Basic Pathology

  5. Causes of Ascites

  6. Rare Causes of Ascites

  7. Imaging • Ultrasound with Dopplers • Easily confirms ascites • May see nodularity of cirrhosis • Evaluate patency of vasculature • No radiation, contrast • CT / MRI • Evaluation for malignancy

  8. Serum to Ascites Albumin Gradient • Is portal hypertension present? • 97% accurate SAAG > 1.1 g/dL  Portal HTN SAAG < 1.1 g/dL  Other causes The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Runyon BA; Montano AA; Akriviadis EA; Antillon MR; Irving MA; McHutchison Ann Intern Med 1992 Aug 1;117(3):215-20.

  9. Serum to Ascites Albumin Gradient

  10. Tests on Ascitic Fluid

  11. Cell Count, differential and culture • Is ascites infected? • Greater than 250 PMN = SBP • If ascites is bloody ( > 50,000 RBC/mm3), correct by subtracting 1 PMN / 250 RBC • Is ascites bloody? • 5% of pts w/ cirrhosis - spontaneous or s/p traumatic tap. • Non-traumatic  associated with malignancy • 20% of malignant ascites • 10% of peritoneal carcinomatosis

  12. Total Protein • Exudate ( > 2.5 g/dL) or Transudate? • Supplanted by SAAG • Is there gut perforation? (vs SBP) • Total protein >1 g/dL • Glucose <50 mg/dL (2.8 mmol/L) • LDH greater than serum ULN

  13. Glucose and LDH • Consistent with infection or malignancy? • Infection and cancer consume glucoselow • LDH is a larger molecule than glucose, enters ascitic fluid with difficulty. • Ascitis/Serum LDH ratio • ~ 0.4 in cirrhotic ascites • Approaches 1.0 in SBP • >1.0, usually infection or tumor

  14. Other tests • Amylase • Uncomplicated cirrhotic ascites • About 40 IU/L. The AF/S ratio is about 0.4 • Pancreatic ascites • About 2000 IU/L. The AF/S ratio is about 6 • Triglycerides — run on milky fluid. • Chylous ascites - TG > 200 mg/dL, usually 1000 mg/dL • Bilirubin — run on brown ascites. • Biliary perforation – AF Bili > serum Bili

  15. Tests for TB • Smear – extremely insensitive • Culture – 62-83% when large volumes cultured • Cell count – mononuclear cell predominance • Adenosine deaminase – • Enzyme involved in lymphoid maturation • Falsely low in pts with both cirrhosis and TB

  16. Cytology • “almost 100%” with peritoneal carcinomatosis have positive cytology • Malignant ascites from massive hepatic mets, HCC, lymphoma are usually negative • Overall sensitivity for detection of malignancy-related ascites is 58 to 75 %

  17. Not helpful • “Some tests of ascitic fluid appear to be useless. These include pH, lactate, and ‘humoral tests of malignancy’ such as fibronectin, cholesterol, and many others”

  18. Biopsy Fatty Liver Cirrhosis http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html#2

  19. Causes of Cirrhosis

  20. Malignant Ascites • Definition: abnormal accumulation of fluid in the peritoneal cavity as a consequence of cancer. • Commonly caused by cancers of: • Breast, bronchus, ovary, stomach, pancreas, colon • 20% of cases have tumors of unknown primary • Survival poor – usually less than 3 months Becker, G. Malignant ascites: Systematic review and guideline for treatment. European Journal of Cancer 42 (2006) 589 - 597

  21. Malignant Ascites: Pathophysiology • Obstruction of lymphatics by tumor • Prevents absorption of fluid and protein • Alteration in vascular permeability • Hormonal mechanisms (VEGF, IL2, TNF alpha) • Decreased circulating blood volume • Activates RAAS leading to Na retention

  22. Pathophysiology of Malignant Ascites

  23. Management of Malignant Ascites • Therapeutic paracentesis • Removing up to 5L appears safe • No good data on role of volume expanders • Diuretics • Equivocal evidence of efficacy • May be helpful for portal HTN • Less/minimally useful when no portal HTN • Drainage Catheters • Peritoneovenous shunts

  24. Peritoneovenous Shunt Contraindications • Protein > 4.5 g/l (occlusion) • Loculated ascites • Coagulopathy • Advanced renal/cardiac disease • GI malignancy Complications • Infection • Hematogenous spread of mets • DIC • Pulmonary edema • Pulmonary emboli Denver Shunt (Similar to LaVeen Shunt)

  25. Transjugular intrahepatic portosystemic shunt (TIPS)

  26. 66 yrs old, man presented with abdominal distension and jaundice , started 3 months ago. He had been diagnosed HBS Ag carrier 20 years ago but had no follow up.

  27. Ascites and peripheral edema

  28. Examination of Abdomen • Percussion • liver • Spleen • Palpation • Liver • Spleen • Examination of ascites

  29. Radiological findings • Abdominal ultasonography • Irregular and nodular surface of the liver • Splenomegaly • Ascites • Abdominal MRI and CT • Sometimes better than USG

  30. How about liver biopsy • Itshighlyinvasive • %1-2 severe bleedingand sometimesmortality • Hematologicproblems • Sowhenbiopsy? • ifclinically, radiologicallyandlaboratuaryfindings do not clearlyindicatecirrhosis • Ifwe do not clarifytheetiologicfactorandsuspect of treatablecondition

  31. Staging of Cirrhosis Interpretation:Class A: 5-6Class B: 7-9Class C: 10-15

  32. Prognosis of Cirrhosis Mortality is usually related with the occurence of complications

  33. Model of End Stage Liver Disease Score (MELD)

  34. Treatment At Early Stage • Early treatment may affect prognosis • Stop alcohol drinking • Eradication of viruses • Treatment of the cause • Autoimmune • Wilson • Hemachromatosis • Sclerozing Cholangitis • Very good followup • Prevention of complications • Low Na Diet

  35. Treatment for Ascites • Diuretics (Spironolactone, furosemide) • Low sodium diet • Therapeutic parasentesis • Transplantation

  36. Ascites; usuallythefirstcomplication !! • Sometimes no symptom • Abdominal distension • Feeling abdominal tenderness • Treatment • Na restriction • Dıuretics • Terapeutic parasentesis

  37. Serum alb – ascites alb >1.1 • LDH, protein, glucose • Cell count • Cytology • Culture

  38. Spontaneous bacterial peritonitis • Spontaneousinfection of ascites • Anycirrhoticpatientwith • Fever • Abdominalpain • Abdominaltenderness • Detoriation of clinicalsituation • Parasentesis • Neutrophilcount>250/ml • Ascitesculture: mostly E.coli • Treatment • i.v antibiotics: 3th generationcephalosporins (cefotaxim) firstchoise, • quinalonsorpenicilins

  39. Spontaneus Bacterial Peritonitis: Mechanism Abdominal Cavity Ascitic Fluid Systemic Circulation Intesine • Loss of opsanization • Decreased complemant amount Decreased RES Function Intestinal Permeability Bacterial Overgrowth LIVER Collaterally pass Kupfher Cell Loss Portal Vein

  40. Liver Transplantation • Each patient who has the complications must be listed for transplantation • Child Score > 9 • MELD Score > 10 • Urgent Tx • Acute fulminant liver failure • Acute on chronic liver failure

  41. Cadaveric Tx • Living donor Tx • 600-700 Tx each year in Turkey • Mostly living donor • Survival % 80 in 2 years, % 70 in 5 yrs • Immunsupressive treatment after Tx

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