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  1. 1. Ascietes bydr naila masood
  2. 2. Cirrhosis is the late result of any disease thatcauses scarring of the liver.Patients with cirrhosis are susceptible to avariety of complications that include ascites,hepatic encephalopathy, and portalhypertension.Quality of life and survival are often improvedby the prevention and treatment of thesecomplications.
  3. 3. Ascites is defined as the accumulation offree fluid in the peritoneal cavity.It is a common clinical finding with a variety ofboth extraperitoneal and peritoneal etiologies.It is most often caused by liver cirrhosis whichaccounts for over 75% of patients while theremaining 25 % is due to malignancy (10%),heart failure (3%), pancreatitis (1%), TB (2%),or other rare causes.
  4. 4. Nonperitoneal Causes of AscitesNon-peritoneal causes ExamplesIntrahepatic portal Cirrhosishypertension Fulminant hepatic failure Veno-occlusive diseaseExtrahepatic portal Hepatic vein obstructionhypertension (ie, Budd-Chiari syndrome) Congestive heart failureHypoalbuminemia Nephrotic syndrome Protein-losing enteropathy MalnutritionMiscellaneous disorders Myxedema Ovarian tumors Pancreatic & Biliary ascitesChylous Secondary to malignancy, trauma
  5. 5. Peritoneal Causes of AscitesPeritoneal Causes ExamplesMalignant ascites Primary peritoneal mesothelioma Secondary peritoneal carcinomatosisGranulomatous peritonitis Tuberculous peritonitis Fungal and parasitic infections Sarcoidosis Foreign bodies (cotton ,starch, barium)Vasculitis Systemic lupus erythematosus Henoch-Schönlein purpuraMiscellaneous disorders Eosinophilic gastroenteritis Whipple disease Endometriosis
  6. 6. PrognosisThe development of ascites is an indication ofdeterioration in clinical status and poor prognosis.Prognosis is worse for those with refractory ascitesand SBP.Approximately 60% of patients with cirrhosis willdevelop ascites requiring therapy and/or livertransplantation in 10 years duration.Mortality in cirrhotic patients hospitalized with ascitesis 40% at 2 years.
  8. 8. Ascites is derived from the vascular compartmentsubserving the hepatosplanchnic viscera.Factors important in the formation of ascites: Increased total body sodium and water Increased sinusoidal portal pressure.In cirrhosisHepatic dysfunction and sinusoidal portal pressuresend a message to the kidney to retain excesssodium and fluid.PH serves to localize excess fluid to the peritonealcavity rather than the periphery.
  9. 9. The pathogenesis of ascites formationremains controversial.“Underfill" theoryAscites occurs as a primary event.Sequestration of fluid into the peritonealcavity as a result of changes in Starlingsforces leads to reduction of the circulatoryvolume and stimulation of the sympatheticnervous & RAAS that promote renal sodium& water retention.
  10. 10. “Overflow theory"Renal Na retention occurs as a primaryevent.It may be due to increased production of asodium retaining factor or reduced synthesisof a natriuretic factor by the diseased liver.The circulatory volume is expanded & theretained fluid is preferentially localized to theperitoneal cavity as ascites.
  11. 11. The currently accepted theory of ascites formation which include features of both the underfill and overflow theories is the“Peripheral Arterial Vasodilation Hypothesis"According to this theory, Portal pressure >12mm Hg is required for the development ofPH which will lead to formation of ascites.
  12. 12. As PH develops, vasodilators are releasedaffecting the splanchnic arteries resulting indecrease in effective arterial blood flow andarterial pressures .The precise agent (or agents) responsiblefor vasodilation is a subject of wide debate;however, most recent literature has focusedon the role of: Nitric Oxide
  13. 13. Chronic endotoxemia associated withcirrhosis may stimulate the synthesis andrelease of a potent endothelin-derivedrelaxing factor, Nitric oxide.NO is the likely mediator in cirrhosis:(1) Increased activity of NO synthase .(2) High serum nitrite and nitrate levels (anindex of NO synthesis).(3) Inhibition of NO leads to increased arterialpressures and systemic vascular resistance.
  14. 14. Portal hypertension Vasodilatation, Decrease Splanchnic Systemic vascular resistance Reduction in arterial blood volumeActivation of neurohumoral pressor systems Renal sodium & water retention
  15. 15. When Na reabsorption cannot compensate forvasodilation, arterial underfilling leads tofurther activation of vasoconstrictor &antinatriuretic mechanisms which leads toincreased Na retention & ultimately ascites isformed.In the late stages of cirrhosis, free wateraccumulation is more pronounced than the Naretention leading to dilutional hyponatremia.
  16. 16. DIAGNOSIS
  17. 17. I) HistoryApproximately 85% of patients with asciteshave cirrhosis.Patients who don’t have cirrhosis should bequestioned about lifetime body weight asNASH may be the cause.Past history of cancer, heart failure, or TB.
  18. 18. II) Physical ExaminationApproximately 1.5 L must be present beforeflank dullness is detected.If no flank dullness is present, the patient hasless than 10% chance of having ascites.Shifting dullness & fluid thrill mean that morefluid is present.Abdominal ultrasound to determine withcertainty if fluid is present and in obese.
  19. 19. Two grading systems for ascites have beenused in the literature.An old system which grades ascites from 1+to 4+, depending on the detectability of fluidon physical examination.More recently, the International Ascites Clubhas proposed a system of grading from 1 to 3.
  20. 20. The older system1+ is minimal and barely detectable.2+ is moderate.3+ is massive but not tense.4+ is massive and tense.The International Ascites Club grading (2003)Grade 1: mild ascites detectable only by US.Grade 2: moderate ascites manifested bymoderate symmetrical abdominal distension.Grade 3: large or gross ascites with markedabdominal distension.
  21. 21. III) Diagnostic ParacentesisIndications(1)Evaluation for a non-cirrhotic patient developingclinically apparent ascites of recent onset.(2)New development of ascites in a cirrhotic patientdoes not routinely require paracentesis only if :(a) General condition deteriorates.(b) In presence of unexplained fever, abdominalpain, encephalopathy.(c) Admission to hospital for any cause (SBP).(3)Laboratory investigations indicating infection: Leucocytosis Acidosis Worsening of renal functions
  22. 22. SiteMidline was usually chosen.Abdominal wall in the left lower quadrant, 2finger breadths cephalic & 2 finger breadthsmedial to ASIS, has been shown to bethinner with larger pool of fluid than midline.Complications (1% of patients)Abdominal wall hematomas.Hemoperitoneum or bowel entry.ContraindicationsClinically evident fibrinolysis or DIC.
  23. 23. Gross Appearance of Ascitic FluidColor AppearanceTranslucent or yellow Normal/sterileBrown Hyperbilirubinemia GB or biliary perforationCloudy or turbid InfectionPink or blood tinged Mild TraumaGrossly bloody Malignancy Abdominal traumaMilky ("chylous") Cirrhosis Thoracic duct injury Lymphoma
  24. 24. Ascitic Fluid TestingRoutine Sometimes useful Rarely helpfulCell count & Total protein pHdifferentialAlbumin LDH LactateCulture Glucose Gram stain Amylase Triglycerides Bilirubin Cytology TB smear and culture
  25. 25. Ascitic fluid analysis (Routine)I) Cell count with differentialAbnormal results are an indication for further nonroutine tests.If the PMN count is >250 cells/mm3, anotherspecimen is injected into blood culture bottles atbedside.Bacterial growth occurs in about 80% of specimenswith count of >250 cells/mm3.The PMN count is calculated by multiplying the whitecells/mm3 by the percentage of neutrophils in thedifferential.
  26. 26. In a "bloody" sample that contains a highconcentration of RBC, the PMN count must becorrected:one PMN is subtracted from the absolute PMNcount for every 250 red cells/mm3 in thesample.The results must be available within 1 hour, sothat important diagnostic and therapeuticdecisions can be made.A Gram stain is of particular low yield unlessfree gut perforation, is suspected.
  27. 27. II)Total protein ,albumin & serum albumin .Serum-ascites albumin gradient(SAAG) = serum albumin - ascitic fluidalbumin.If > 1.1 g/dL, the patient has PH-relatedascites.If < 1.1 g/dL (about 97% accurate), thepatient does not have PH-related ascites.The SAAG does not need to be repeatedafter the initial measurement.
  28. 28. III)Based on clinical judgment, additionaltesting can be performed :a) Cytology ,smear & culture for mycobacteria.b) Cytology : in peritoneal carcinomatosis(sensitivity increased by centrifuging largevolume).c) Elevated bilirubin level suggest biliary or gutperforation.
  29. 29. d) LDH >225mU/L, glucose <50mg/dL, totalprotein >1g/dL and multiple organisms ongram stain suggest secondary bacterialperitonitis.e) High level of TGs confirms chylousascites.f) Elevated amylase level suggestpancreatitis or gut perforation.
  30. 30. AASLD Recommendations1.Paracentesis should be performed ,ascitic fluidshould be obtained from inpatients & outpatients withclinically apparent new-onset ascites2. Since bleeding is uncommon ,prophylactic use ofFFP or platelets is not recommended.3. Initial evaluation of ascitic fluid should include cellcount ,differential, total protein & SAAG.4. If infection is suspected, ascitic fluid should becultured at the bedside in blood culture bottles.5. Other studies can be ordered based on pretestprobability of disease.
  31. 31. Management of Ascites - Guideline• Treat the Underlying Cause• Childs C – 75% 3-year survival Vs. 0%• Non-Alcoholic less reversible therefore consider referral for transplant earlier
  32. 32. Treatment Options• Bed rest• Diet• Diuretics• Fluid Restriction• Paracentesis• TIPSS• Shunts• Transplant
  33. 33. Management of ascites - Bed Rest• Bed rest : No clinical trials• Upright posture activates sodium retaining mechanisms , impairs renal perfusion and sodium excretion.
  34. 34. Management of ascites- Sodium RestrictionSodium restriction :Water will follow SodiumEducate the PatientAim for 2000mg (88 mmol) per dayStudies show severe restriction (22mmol/day) compared with less restricted is associated with longer duration of evolution of ascites, but higher incidence of diuretic induced renal impairment and hyponatraemia
  35. 35. MANAGEMENT OF ASCITES- Salt restriction (cont)• One controlled study, showed slightly reduced salt diet (120mmol/day) was equally effective when compared to a low salt diet ( 50mmol/day).• No significant survival difference, although low salt diet (50mmol/day ) improved survival in those with previous GI bleed
  36. 36. MANAGEMENT OF ASCITES- WATER RESTRICTION• Central hypovolaemia - > stimulates ADH receptors• - > decreases free water clearance - > dilutional hyponatraemia.•• Therefore, treat by water restriction – no trials to assess effect of water restriction in patients with cirrhosis and dilutional hyponatraemia. Restriction may worsen central hypovolaemia.• Water restriction not first option, sodium restriction appropriate first line, water restrict if Na <125mmol/L
  37. 37. MANAGEMENT OF ASCITES- DIURETICS• Antimineralocorticoids –• Secondary hyperaldosteronism promotes sodium retention in distal tubules and collecting ducts• Controlled and uncontrolled trials - > Spironolactone effective antimineralocorticoid• S.E gynaecomastia, renal impairment, hyperkalaemia• Other K sparing diuretics: amiloride, triamterene• Loop Diuretics : Frusemide – S.E : hyponatraemia, hypokalaemia, hypovolemia, renal impairment of prerenal origin
  38. 38. ASCITES- Assess response to diuretics :• Weight loss of 0.5kg/day in absence of oedema and 1kg/day when oedema present• Use Spironolactone & Frusemide 100mg/40mg ratio• Medical treatment based on sodium restricted diet, diuretics – response in 90 % without renal failure.
  39. 39. ASCITES- Assess response to diuretics :• Weight loss of 0.5kg/day in absence of oedema and 1kg/day when oedema present• Use Spironolactone & Frusemide 100mg/40mg ratio• Medical treatment based on sodium restricted diet, diuretics – response in 90 % without renal failure.
  40. 40. Ascites- Refractory Ascites • Unresponsive to Salt restriction & high dose diuretics (400mg Spironolactone & 160mg Frusemide)• Recurs rapidly after Paracentesis (< 4/52)• Diuretic induced complication – encephalopathy, renal impairment, hyponatraemia (<125mmol/L), hypo (3mmol/L) or hyperkalaemia (6mmol/L)
  41. 41. Ascites- Paracentesis• Repeated daily paracentesis ( 5L/day )• Single total paracentesis- reduced hospital stay
  42. 42. Refractory Ascites - Treatment Options• Serial Paracentesis• Liver Transplantation• TIPSS• Peritoneovenous Shunts
  43. 43. Refractory Ascites - Treatment Options• Liver Transplantation
  44. 44. THANK YOU