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Approach to ascites
This document provides an overview of ascites, including: - Ascites is an accumulation of fluid in the peritoneal cavity. It is usually caused by cirrhosis and portal hypertension which increases hydrostatic pressure in blood vessels in the abdomen. - Diagnosis involves physical exam findings like abdominal distension. Imaging like ultrasound can identify fluid levels. Paracentesis analyzes fluid for causes like spontaneous bacterial peritonitis. - Treatment depends on the underlying cause but may include dietary sodium restriction, diuretics, large volume paracentesis, TIPSS procedure to lower pressure, or liver transplantation for cirrhosis. Refractory ascites requires more aggressive management.
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Approach to ascites
- 1. APPROACH TO ASCITES DRRUSHIKESH KUTE NIRMAL HOSPITAL PVT LTD SURAT
- 2. Definition -Ascites is ofgreek derivation(askos) which refers to bag or sack -The word describes pathological fluid accumulation in peritoneal cavity
- 3. Background • • • • Peritoneum Portal HTN Impaired drainagein lymphatic system Hypoalbuminemia
- 5. Pathophysiology • Under fillingtheory 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
- 6. Overflow theory primary abnormalityis 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
- 7. 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)
- 8. Pathogenic mechanism • Increasedhydrostatic pressure • Decreased colloid osmotic pressure • Increased permeability of peritoneal capillaries • Leakage of fluid into peritoneal cavity • Misc.
- 9. Etiology • Neonatal ascites/congenitalascites 1.Associated with hydrops > -cardiovascular rhythm dist. cardiac malformn. -hematological isoimmune hemolytic dis. homo alpha thal.
- 10. 2. Isolated ascites -chylous congenital anomaly of lymphatic channels -biliary spontaneous perforn of biliary tree - pancreatic duct anomaly
- 11.
- 12.
- 13. -misc wilms tumour neuroblastoma -storage dis. mucopolysachharadosis8 -skeletal abn. osteogenesis imperfecta achondrogenesis
- 14. -cirrhosis alpha antitrypsin def. -liverfailure neonatal hemochromatosis -unknown
- 15. 2.Isolated asictes - chlylous congenitalanomaly of lymphatics - biliary spontaneous perforation of biliary tree - pancraetic duct anomaly 3. Peritonitis - chemical bile,meconium - bacterial
- 16. Etiology In Children 1.Associatedwith portal hypertension -extrahepatic venous obstruction misc -intrahepatic biliary tract dis. hepatocellular dis. toxins misc -others
- 17. Etiology of acuteascites -Venous obstruction -Peritonitis -Fulminant hepatic failure
- 18. Etiology in refto normal /diseased peritoneum Normalportal HTN liver dis. hypoalbuminemia misc Diseasedinfections malignancy others
- 19. Presentation • • • • Abdominal distension Increasing wt Respiratoryembarras. Pedal oedema
- 20. Risk factors • • • • • • Chronic viralhepatitis Intravenous drug use Sexual promiscuity Transfusions Tattos Habitation or origination from endemic hepatitis
- 21. Examination • • • • • • Flank dullness 90%sensitive Increased abdominal girth and wt loss Puddle sign Shifting dullness Fluid thrill Peritoneal tap
- 22. Monitoring • Abdominal girthand weight -jugular venous distension -heart murmur/signs of CHF -signs of pulmonary oedema -skin changes -asterixis/anasarca -virchows node
- 23. • 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
- 24. Confirm >cause >complications •Blood tests > Complete blood counts Complete urine examination LFT Clotting screen
- 25. Imaging studies • Chestand 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
- 26. • USG -site forparacentesis -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.
- 27. -coarse internal echoes(blood) -fineinternal echoes(chyle) -multiple septa(TB,pseudomyxoma peritonei) -loculated /atypical fluid distribution -matting or clumping bowel loops -thickening of interface betn fluid & adjacent structure
- 29. • Upper GIendoscopy -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
- 31. Abdominal paracentesis • • • • Position Site Technique Ascitic fluidanalysis routine/optional tests total protein/gram stain albumin/AFB smear and culture cell count cytology amylase/LDH/glucose Complications
- 33. • white cellcount<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
- 34. • • • • • • • • • Toatl protein Gram stain Cytology SAAG-sralbumin-ascitic fluid albumin portal/nonportal Culture LDH Triglycerides Amylase Bilirubin
- 35. Classification of asciticfluid infection Type PMN count Cells/mm3 Bacterial culture Spont bact peritonitis > 250 + Culture negative >250 _ monomicrobial <250 + Polymicrobial <250 + Sec.bact.perito nitis >250 +
- 36. Types of ascitisacc 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
- 37. Indication for admssion • • • • • • • • • • Forinvestigation 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
- 38. Management 1.non drug – bedrest medical care diet fluid restriction 2.drugs diuretics b blockers
- 39. 3.Diuretic resitance therapeutic paracentesis leveen or denver peritoneovenous shunt liver transplantation extracorporeal ultrafiltration with reinfusion TIPSS
- 40. Surgical • TIPSS-hepatic veinand portal vein -reduces pressure gradient betn portal and systemic
- 41. Peritoneovenous shunt • Aperitoneovenous 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
- 42. Portocaval shunt • Aportacaval 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.
- 43. • • • • • • • • Liver transplantation Follow up Spontaneousbacterial peritonitis Prevention Patient education Monitoring Prognosis Lows albumin gradient ascites
- 44. Refractory ascitis • Fluidload 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
- 45.
- 46. • Chylous ascitis •Pseudochylous ascitis • Management low fat,high protein,paracentesis
- 47.