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Approach to ascites


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Approach to ascites

  2. 2. Definition -Ascites is of greek derivation(askos) which refers to bag or sack -The word describes pathological fluid accumulation in peritoneal cavity
  3. 3. Background • • • • Peritoneum Portal HTN Impaired drainage in lymphatic system Hypoalbuminemia
  4. 4. Pathophysiology • Under filling theory primarily there is inappropriate sequestration of fluid within the splanchnic vascular bed as a consequence of portal hypertension (PHT) that produces decrease in effective circulating blood volume. This activates the plasma rennin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention
  5. 5. Overflow theory primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. Basis of this theory is that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia
  6. 6. Peripheral arterial vasodilatation • The major factor of ascites formation is splanchnic vasodilation. • Cirrhosis causes increased hepatic resistance to portal flow that results in PHT and shunting of blood to the syst emiccirculation. • Local production of vasodilators, mainly nitric oxide due to PHT results in splnchnic and peripheral arterial vasodilatation. This leads to decrease in effective arterial blood volume (EABV)
  7. 7. Pathogenic mechanism • Increased hydrostatic pressure • Decreased colloid osmotic pressure • Increased permeability of peritoneal capillaries • Leakage of fluid into peritoneal cavity • Misc.
  8. 8. Etiology • Neonatal ascites/congenital ascites 1.Associated with hydrops > -cardiovascular rhythm dist. cardiac malformn. -hematological isoimmune hemolytic dis. homo alpha thal.
  9. 9. 2. Isolated ascites - chylous congenital anomaly of lymphatic channels -biliary spontaneous perforn of biliary tree - pancreatic duct anomaly
  10. 10. -chromosomal turner synd trisomy 13,18,21 -infections TORCH syphillis -renal nephrosis PUV
  11. 11. -pulmonary diaphragmatic hernia -gastrointestinal atresia -maternal condn toxemia diabetes -placenta/cord cord compression chorangioma
  12. 12. -misc wilms tumour neuroblastoma -storage dis. mucopolysachharadosis 8 -skeletal abn. osteogenesis imperfecta achondrogenesis
  13. 13. -cirrhosis alpha antitrypsin def. -liver failure neonatal hemochromatosis -unknown
  14. 14. 2.Isolated asictes - chlylous congenital anomaly of lymphatics - biliary spontaneous perforation of biliary tree - pancraetic duct anomaly 3. Peritonitis - chemical bile,meconium - bacterial
  15. 15. Etiology In Children 1.Associated with portal hypertension -extrahepatic venous obstruction misc -intrahepatic biliary tract dis. hepatocellular dis. toxins misc -others
  16. 16. Etiology of acute ascites -Venous obstruction -Peritonitis -Fulminant hepatic failure
  17. 17. Etiology in ref to normal /diseased peritoneum Normalportal HTN liver dis. hypoalbuminemia misc Diseasedinfections malignancy others
  18. 18. Presentation • • • • Abdominal distension Increasing wt Respiratory embarras. Pedal oedema
  19. 19. Risk factors • • • • • • Chronic viral hepatitis Intravenous drug use Sexual promiscuity Transfusions Tattos Habitation or origination from endemic hepatitis
  20. 20. Examination • • • • • • Flank dullness 90% sensitive Increased abdominal girth and wt loss Puddle sign Shifting dullness Fluid thrill Peritoneal tap
  21. 21. Monitoring • Abdominal girth and weight -jugular venous distension -heart murmur/signs of CHF -signs of pulmonary oedema -skin changes -asterixis/anasarca -virchows node
  22. 22. • Grading 1.Mild Puddle sign/usg • Staging 2.Moderate Shifting dullness/no thrill 2+ easily detectable 3.Tense Fluid thrill/resp. difficulty 4+ tense ascites 1+ careful examin 3+ obvious but no tense
  23. 23. Confirm >cause >complications • Blood tests > Complete blood counts Complete urine examination LFT Clotting screen
  24. 24. Imaging studies • Chest and abdominal films -elevation of diaphragm -nonspecific signs -hellmer sign -obliteration of hepatic angle -dogs ear/mickey mouse sign -med displacement of cecum & ascending colon & lat displacement of properitoneal line
  25. 25. • USG -site for paracentesis -100ml fluid -uncomplicated ascites homogenous ,freely mobile, anechioc collection in peritoneal cavity,deep acoustic enhancement -massive ascites small bowel loops-polycyclic,lollypop like arcuate app.
  26. 26. -coarse internal echoes(blood) -fine internal echoes(chyle) -multiple septa(TB,pseudomyxoma peritonei) -loculated /atypical fluid distribution -matting or clumping bowel loops -thickening of interface betn fluid & adjacent structure
  27. 27. • Upper GI endoscopy -oesophageal/fundal varices CT/MRI -rt perihepatic space,morrisons pouch,douglas pouch -malignant ascites prop fluid in lesser & greater sac -benign ascites fluid in greater sac
  28. 28. Abdominal paracentesis • • • • Position Site Technique Ascitic fluid analysis routine/optional tests total protein/gram stain albumin/AFB smear and culture cell count cytology amylase/LDH/glucose Complications
  29. 29. • white cell count<500 leukocytes/ml & <250 PMN L-N Red cell count>50000/ml hemorrhagic Grosstransluscent/yellow-N brown-hyperbili/GB perforatn cloudy/turbid-infection pink/blood tinged-mild trauma gross blood-malignanacy/trauma milky-cirrhosis/thor.duct injury/lymphoma
  30. 30. • • • • • • • • • Toatl protein Gram stain Cytology SAAG-sr albumin-ascitic fluid albumin portal/nonportal Culture LDH Triglycerides Amylase Bilirubin
  31. 31. Classification of ascitic fluid infection Type PMN count Cells/mm3 Bacterial culture Spont bact peritonitis > 250 + Culture negative >250 _ monomicrobial <250 + Polymicrobial <250 + Sec.bact.perito nitis >250 +
  32. 32. Types of ascitis acc to sr ascitis albumin gradient High gradient >1.1g/dl Cirrhosis Hepatitis Fulminant hepatic failure Cardiac ascitis Portal vein thromb. Veno-occlusive dis. Myxedema Massive liver metastasis Low gradient <1.1g/dl Tb peritonitis Nephrotic syndrome Pancreatic ascitis Bowel obst/infarction Biliary ascitis Postop lymph leak Serositis in CTD
  33. 33. Indication for admssion • • • • • • • • • • For investigation Not responsive Diet limited to 88mmol of Na per day Monitoring Grade 3 ascitis Susp bact peritonitis Electrolyte imbalance Hepatorenal syndrome Hepatic encephalopathy Refractory ascitis
  34. 34. Management 1.non drug – bed rest medical care diet fluid restriction 2.drugs diuretics b blockers
  35. 35. 3.Diuretic resitance therapeutic paracentesis le veen or denver peritoneovenous shunt liver transplantation extracorporeal ultrafiltration with reinfusion TIPSS
  36. 36. Surgical • TIPSS-hepatic vein and portal vein -reduces pressure gradient betn portal and systemic
  37. 37. Peritoneovenous shunt • A peritoneovenous shunt (also called Denver shunt) is a shunt which drains peritoneal fluid from the peritoneum into veins, usually the internal jugular vein or the superior vena cava
  38. 38. Portocaval shunt • A portacaval shunt (or portal caval shunt) is a treatment for high blood pressure in the liver. A connection is made between the portal vein, which supplies 75% of the liver's blood, and the inferior vena cava, the vein that drains blood from the lower two-thirds of the body.
  39. 39. • • • • • • • • Liver transplantation Follow up Spontaneous bacterial peritonitis Prevention Patient education Monitoring Prognosis Lows albumin gradient ascites
  40. 40. Refractory ascitis • Fluid load that is non responsive to restriction of dietary sodium to 88mmol/day and maximal dose diuretic therapy in absence of ingestion of prostaglandin inhibitors(NSAID) • Management serial large volume paracentesis 100ml/kg at a time iv albumin 6-8g/lit
  41. 41. Others • • • • • ANP V2 receptor antagonist OPC-3126 Niravoline FK352
  42. 42. • Chylous ascitis • Pseudochylous ascitis • Management low fat,high protein,paracentesis
  43. 43. THANK YOU