Recommended
More Related Content
Similar to ascitesbymohammed-160614173622.pdf
Similar to ascitesbymohammed-160614173622.pdf (20)
More from Kemi Adaramola
More from Kemi Adaramola (20)
Recently uploaded
Recently uploaded (20)
ascitesbymohammed-160614173622.pdf
- 1. Ascites Dr Mohammed Hussien Assistant Lecturer of Hepatology & Gastroentrology Kafrelsheik University
- 2. What is Ascites ? • Ascites is the presence of excess fluid in the peritoneal cavity. • It is a common clinical finding with a wide range of causes, but develops most frequently as a part of the decompensation of previously asymptomatic chronic liver disease.
- 4. • Ascites occurs in 50% of patients within 10 years of diagnosis of compensated cirrhosis. • It is a poor prognostic indicator, with a 50% 2-year survival. • Worsening significantly to 20 - 50% at 1 year when the ascites becomes refractory to medical therapy.
- 6. A)Incresased hydrostatic pressure • Cirrhosis • Hepatic vein occlusion (Budd- Chiari syndrome) • Inferior vena cava obstruction • Constrictive pericarditis • Congestive heart failure
- 7. B) Decreased colloid osmotic pressure • End-stage liver disease with poor protein synthesis • Nephrotic syndrome with protein loss • Malnutrition • Protein-losing enteropathy 2004 7
- 8. C) Increased permeability of peritoneal capillaries • Tuberculous peritonitis • Bacterial peritonitis • Malignant disease of the peritoneum
- 9. D) Leakage of fluid into the peritoneal cavity • Bile ascites • Pancreatic ascites • Chylous ascites • Urine ascites
- 10. E) Miscellaneous causes • Myxedema • Ovarian disease (Meigs' syndrome) • Chronic hemodialysis
- 11. Pathogenesis of ascites in cirrhosis
- 12. 2004 cirrhosis cirrhosis Hemodynamic changes Hemodynamic changes. . VC substances VD substances Favoring VD Systemic & splanchnic VD Decrease effective circulating blood volume Imbalance
- 13. Perceived hypovolemia activates various VC systems ↑ RAAS , SNS , ADH Renal VC renal Na & water reabsorption Decrease in GFR Ascites Decrease in effective circulating blood volume ↓ oncotic pressure
- 14. 2004 SNS SNS RAS RAS ADH ADH SNS SNS RAS RAS ADH ADH Kidney Kidney R perfusion R perfusion & GFR & GFR R perfusion R perfusion & GFR & GFR Ability to Ability to Exc. Sod Exc. Sod Ability to Ability to Exc. Sod Exc. Sod Ability to Ability to Exc. water Exc. water Ability to Ability to Exc. water Exc. water HRS HRS HRS HRS Ascites Ascites Ascites Ascites Dilutional Dilutional Hyponat Hyponat “ “Sod<130 Sod<130” ” Dilutional Dilutional Hyponat Hyponat “ “Sod<130 Sod<130” ” Renal Dysfunction in Cirrhosis Renal Dysfunction in Cirrhosis
- 15. Commonest causes (90% of cases ( •Cirrhosis (Cirrhotic Ascites) •Cancer (Malignant Ascites) •Congestive Heart Failure •Mycobacterium tuberculosis
- 17. Symptoms • Small amount of ascites • Asymptomatic • Large amount of ascites • Abdominal distention and discomfort • Anorexia • Nausea • Early satiety • Heartburn (Gastroesophageal Reflux) • Flank pain • Respiratory distress
- 18. Signs • Umbilicus may evert • Bulging flanks with patient lying supine • Weight of ascitic fluid pushes against side walls • Tympany at the top of the abdominal curve • Patient lies supine • Gas filled bowel floats upward over ascites • Fluid Wave Test • Shifting Dullness Test • Puddle Sign
- 19. Grades of ascites • Grade 1 :– Mild ascites detectable only by ultrasound examination • Grade 2: Moderate ascites manifested by moderate symmetrical distension of the abdomen • Grade 3 : Large or gross ascites with marked abdominal distension
- 20. Ultrasonography • Ultrasound is probably the most cost- effective modality. • It involves no radiation or intravenous access, & no risk of contrast allergy or nephropathy. • If a computed tomographic (CT) scan is performed, ascites is easily seen 20
- 21. • Ultrasound findings in patients with portal hypertension may include : - may reveal evidence of a nodular liver. - dilation of the portal vein to ≥13 mm, - dilation of the splenic and superior mesenteric veins to ≥ 11 mm, - reduction in portal venous blood flow velocity, splenomegaly (diameter >12 cm), and recanalization of the umbilical vein. - may reveal evidence of hepatocellular carcinoma
- 23. Investigations Peritoneal fluid analysis Peritoneal fluid Cell and differential PMN count Gram stain Direct inoculation in routine blood culture bottles Other studies of ascitic fluid Other studies of ascitic fluid to be considered to be considered Cytology Cytology Lactate Lactate pH pH
- 24. Calculated by subtracting the albumim concentration of the ascitic fluid from the albumin concentration of a serum specimen obtained on the same day.
- 25. Serum Ascites Albumin Gradient (SAAG (
- 26. SAAG • It is the best single test for classifying ascites into portal hypertensive (SAAG >1.1 g /dL) and non–portal hypertensive (SAAG <1.1 g /dL) causes. • Calculated by subtracting the ascitic fluid albumin value from the serum albumin value, • It correlates directly with portal pressure. • The accuracy is approximately 97% .
- 27. • This phenomenon is the result of Starling's forces between the fluid of the circulatory system and ascetic fluid. • Under normal circumstances the SAAG is < 1.1 because serum oncotic pressure (pulling fluid back into circulation) is exactly counterbalanced by the serum hydrostatic pressure (which pushes fluid out of the circulatory system).
- 28. • This balance is disturbed in certain diseases (such as the Budd-Chiari syndrome , heart failure, or liver cirrhosis) that increase the hydrostatic pressure in the circulatory system. • The increase in hydrostatic pressure causes more fluid to leave the circulation into the peritoneal space (ascites).
- 29. • The SAAG subsequently increases because there is more free fluid leaving the circulation, diluting the albumin in the ascitic fluid. • The albumin does not move across membrane spaces easily because it is a large molecule. DR.Mohammed Hussien 29
- 30. 2004 30 SAAG Helpful diagnostically, as well as Helpful diagnostically, as well as therapeutically in decision making therapeutically in decision making Low SAAG > 1.1 High SAAG < 1.1 Non –portal hypertensive cases Portal hypertensive cases Does not respond to salt restriction nor Diuretics Respond to salt restriction & Diuretics
- 31. 2004 31
- 32. 2004 32 high-albumin high-albumin gradient gradient > 1.1g/dl > 1.1g/dl low-albumin low-albumin gradient gradient < < 1.1 1.1 g/dl g/dl Transudative Transudative Exudative Exudative Terms should be replaced
- 33. Types of ascites according to SAAG High Gradient ) < or = 1.1 g/dl)PHT Portal vein thrombosis Cirrhosis Cardiac Failure Budd Chiari syndrome Alcoholic hepatitis Fulminant hepatic failure Massive hepatic metastasis Fatty liver of pregnancy Myxedema Mixed ascites Low Gradient ) > 1.1 g/dl ( Non PHT Peritoneal Carcinomatosis Pancreatic ascites Biliary ascites Peritoneal Tuberculosis Nephrotic Syndrome Serositis Bowel obstruction or infarction 2016 33
- 34. High gradient ( SAAG > 1.1 ( • A high gradient (> 1.1 g/dL) indicates that ascites is due to portal hypertension with 97% accuracy. • This is due to increased hydrostatic pressure within the blood vessels of the hepatic portal system, which in turn forces water into the peritoneal cavity but leaves proteins such as albumin within the vasculature. 34
- 35. Important causes of high SAAG ascites (> 1.1 g/dL) include: - High protein in ascitic fluid (> 2.5 (: Heart failure & Budd Chiari syndrome - Low protein in ascitic fluid (< 2.5 (: - Liver cirrhosis
- 36. Low gradient ( SAAG <1.1) • Indicates causes of ascites not associated with increased portal pressure. • Examples include : - Tuberculosis - Pancreatitis . - Nephrotic syndrome • Various types of peritoneal cancer.
- 37. 2. The amylase concentration which is elevated in pancreatic ascites. 3. The triglyceride concentration which is elevated is chylous ascites.
- 38. 4. White cell count : - When greater than 250/microliter is suggestive of infection. - If most cells are PMNLs , bacterial infection should be suspected. - When mononuclear cells predominated tuberculosis or fungal infection is likely.
- 39. 5.Red cell count : • When greater than 50.000/microliter denotes hemorrhagic ascites, which usually is due to : - malignancy - tuberculosis - Pancreatitis - or trauma.
- 40. 6.Gram stain and culture : which can confirm the diagnosis of bacterial infection. 7.pH : when less than 7 suggests bacterial infection 8.Cytology : can be positive in malignancy.
- 41. Ascites Fluid: Cell Count with Differential RBCs elevated • Malignant ascites • Tuberculous peritonitis • Pancreatitis WBC elevated >1000 • Neoplasm (>50% Lymphocytes) • TB peritonitis (>70% Lymphocytes) • Bacterial peritonitis (WBC > 10,000) • Spontaneous Bacterial Peritonitis (PMN > 250)
- 43. 2016 43 Treatment of Treatment of ascites ascites Bed rest Bed rest Water restriction Diuretics Refractory ascites Reversible Causes Reversible Causes Na+ restriction
- 44. Role of bed rest no controlled trials to support this practice. Upright posture may aggravate plasma renin Bed rest may lead to muscle atrophy, stasis, and extended hospital stay. Bed rest is NOT recommended for treatment of ascites. Low Sodium diet Sodium restriction has been associated with lower diuretic requirement, faster resolution of ascites, and shorter hospitalization. But, it is less palatable and may further worsen the malnutrition. when given a choice, most patients would prefer to take some diuretics and have a more liberal sodium intake than take no pills and have a more severe sodium restriction.
- 45. Spironolactone • aldosterone antagonist, acting mainly on the distal tubules as Potassium-sparing diuretic (inhibit Na+ re-absorption and K+ excretion). • It is the drug of choice in the initial treatment. • There is a lag of 3–5 days between the beginning of treatment and the onset of the natriuretic effect • Side effects are those related to its anti-androgenic activity, such as decreased libido, impotence, and gynaecomastia in men and menstrual irregularity in women
- 46. Frusemide • Frusemide is a loop diuretic that generally used as an adjunct to spironolactone • it inhibit re-absorption of Na+/K+/2Cl- in the ascending limb of the loop of Henle. • High doses of frusemide are associated with severe electrolyte disturbance and metabolic alkalosis, and should be used cautiously.
- 47. Other diuretics • Amiloride and triamterene act on the distal tubule. It blocks Na reabsorption and induces diuresis in 80% of patients at doses of 15–30 mg/day. It is less effective compared with spironolactone. • Bumetanide is similar to frusemide in its action and efficacy
- 48. Single or combination therapy • The initial combination treatment shortens the time to mobilization of moderate to tense ascites and better for inpatient treatment. • So it is preferred approach in achieving rapid natriuresis and maintaining normokalemia. • An alternative approach would be to start with Spironolactone, in particular in the outpatient setting, then monitoring the patient for adding loop diuretics after 400mg Spironolactone failure.
- 49. Dosage • The doses of both oral diuretics can be increased simultaneously every 3-5 days (maintaining the 100 mg:40 mg ratio) if weight loss and natriuresis are inadequate. • This ratio maintains normo-kalemia. • Usual maximum doses are 400 mg/day of spironolactone and 160 mg/day of furosemide • Over diuresis is associated with intravascular volume depletion leading to renal impairment, hepatic encephalopathy, and hyponatraemia.
- 50. Therapeutic Paracentesis • Although initially the recommendation was to perform daily 5-L paracentesis until the disappearance of ascites, it was subsequently determined that total paracentesis (i.e., removal of all ascites in a single procedure accompanied by the concomitant infusion of 6– 8 g albumin per liter of ascites removed) was as safe as repeated partial paracenteses
- 51. LVP • LVP associated with i.v. plasma expander is effective and associated with a significantly faster resolution and a lower rate of complications than repeated paracentesis with intensive diuretics. • However, it is a local therapy (does not act on the mechanisms of ascites formation) and ascites recurrence is the rule. • Additionally, it is more costly and requires more resources than the administration of diuretics.
- 52. Use of plasma expanders • Paracentesis of <5 L of uncomplicated ascites does not require volume expansion • Plasma volume expander should always be used whenever >5 L of ascites are removed.
- 53. Stepwise treatment of ascites • Sodium restriction (88 mmol /d = 2 g) • Titrate spironolactone (to Na+u / K+u > 1) • If no success add loop diuretic • Fluid restriction only if Na+ < 120 mmol/l • Bed rest is not recommended. • Aim for weight loss < 1/2 kg/d in non-edematous pts , but should not exceed 1 kg/day when edema is present. • Please don’t forget
- 54. • Serum potassium, blood urea nitrogen (BUN), and creatinin levels should be serially followed. • In the event of marked hyponatremia, hyperkalemia or hypokalemia, renal insufficiency, dehydration, or encephalopathy , diuretics should be reduced or discontinued. • The spot urine Na+ to-K+ ratio might ultimately replace the cumbersome 24-hour collection: • A random urine Na+ concentration higher than the K+ concentration has been shown to correlate with a 24-hour sodium excretion higher than 78 mmol/day with approximately 90% accuracy. 54
- 55. 2004 55
- 56. Avoid NSAIDs & Stop alcohol Restrict Na = 2g/day Oral Diuretics Spironolactone100 mg + Furosemide 40 mg /day Progressive increase of dose by one /one till maximum 4 tablets of each drug Frequent large volume paracentesis with albumin (infusion ( 6-8 gm for each liter ascitic fluid TIPS Liver transplantation Stepwise Management of ascites Failed Refractory ascites Failed Failed
- 57. 2004 57 Effective management of ascites Effective management of ascites improves patient well-being & eliminates improves patient well-being & eliminates the patient's risk for these life threatening the patient's risk for these life threatening complications complications HRS SBP Refractory ascites
- 59. 2004 59
- 60. 2004 60 Refractory ascites Refractory ascites ) ) 10-15% 10-15% of cirrhotic ascites of cirrhotic ascites ( ( Diuretic-resistant Diuretic-resistant ascites ascites Diuretic- intractable Diuretic- intractable ascites ascites Ascites fail to respond to full dose of diuretics for 2 weeks Patients who cannot tolerate Patients who cannot tolerate diuretics because of side diuretics because of side effects effects
- 61. Non-compliance with sodium restriction is a major & often overlooked cause of refractory ascites . 61
- 62. 2004 62 Management of Refractory Management of Refractory Ascites Ascites Liver Liver transplantation transplantation Large Large volume volume paracentesis paracentesis Peritoneovenous Peritoneovenous shunt shunt TIPS TIPS
- 63. Liver transplantation •It is the most effective & definitive treatment but
- 65. 2004 65
- 66. 2004 66 OV Before TIPS After TIPS
- 67. TIPS Advantages of TIPS ■ High success rate. ■ Low complication rate. ■ Short hospitalization. Disadvantages of TIPS ■ Stenosis of the shunt. ■ Encephalopathy due to wide shunt. ■ Difficult LTX due to stent projection into I.V.C.
- 68. Large volume paracentesis • Repeated LVP is a safe and effective mean of controlling refractory ascites. • Single LVP can be safely performed without the infusion of plasma expanders such as albumin. • However, patients who require frequent repeated LVP or a single total paracentesis should receive albumin infusion.
- 69. 2004 69
- 70. Peritoneovenous shunt Le Veen Shunt • It is a device that returns ascitic fluid from the peritoneal cavity to the systemic circulation. • Its use is restricted to patients with well preserved hepatic function since survival following it falls off dramatically in patients with severe liver dysfunction. • The associated complications, including technical problems, makes this an option for only selected patients.
- 71. 2004 LeVeen Shunt Effect of Increased effective circulating Increased effective circulating volume volume ↓ ↓ Plasma rennin Plasma rennin activity activity ↓ ↓ Aldosterone Aldosterone ↓ ↓ Norepinephrine Norepinephrine Diuresis and Diuresis and mobilization of ascites mobilization of ascites
- 74. Definition • It is an acute bacterial infection of ascitic fluid without an evident intra- abdominal, surgically treatable cause . • SBP is defined as an ascites fluid polymorph nuclear leukocyte (PMN) count > 250/mm3 (regardless of culture results, which may be negative (. 2004 74
- 75. Symptoms& signs 69% 59% 54% 49% 32% 30% 21% 17% 0% 10% 20% 30% 40% 50% 60% 70% F e v e r P a i n E n c e p h a l o p a t h y T e n d e r n e s s D i a r r h e a I l e u s H y p o t e n s i o n H y p o t h e r m i a 2004 75 McHutchison JG et al., 1994 McHutchison JG et al., 1994
- 76. Other Clinical Manifestations • Asymptomatic : 30% . • Ascites that does not improve following administration of diuretics . • Worsening or new-onset renal failure . 2004 76
- 77. Secondary vs. SBP Secondary bacterial Secondary bacterial peritonitis peritonitis SBP SBP Organisms Organisms Multiple Multiple Single Single Ascitic protein Ascitic protein >1 g/dL >1 g/dL < 1 g/dL < 1 g/dL Ascitic glucose conc. Ascitic glucose conc. < 50 mg/dL < 50 mg/dL ~ serum value ~ serum value Response to Tx Response to Tx PMN cell count PMN cell count Continues to rise Continues to rise despite treatment despite treatment Falls Falls exponentially exponentially Ascitic culture Ascitic culture Remains positive Remains positive Rapidly Rapidly becomes sterile becomes sterile 2004 77
- 78. Management Cefotaxime Cefotaxime •Less nephrotoxic Less nephrotoxic •Broad spectrum Broad spectrum •1 -2 g, 8 hourly 1 -2 g, 8 hourly Cefoxitin Cefoxitin •Enterococcal coverage Enterococcal coverage •1 g, 6 to 8 hourly 1 g, 6 to 8 hourly Aztreonam Aztreonam •0.5 0.5 – – 1 gm, 8 hourly 1 gm, 8 hourly Amoxicillin- Amoxicillin- clavulanic acid clavulanic acid •1 g amoxicillin & 200 mg 1 g amoxicillin & 200 mg clavulanic acid, 8 hourly clavulanic acid, 8 hourly 2004 78
- 80. Definition of HRS Major Criteria (5 ( 1 - Chronic or acute liver disease with liver failure and portal hypertension . 2 - Low GFR : • Cr>1.5 mg/dL or Cr. clearance <40 mL/min . 3 - Absence of Shock, bacterial infection, nephrotoxic drugs or excessive fluid loss . • No sustained improvement in renal function following expansion with 1.5 L of isotonic saline . • Proteinuria < 0.5 g/d with no ultrasonographic evidence of renal disease . 1 - Chronic or acute liver disease with liver failure and portal hypertension . 2 - Low GFR : • Cr>1.5 mg/dL or Cr. clearance <40 mL/min . 3 - Absence of Shock, bacterial infection, nephrotoxic drugs or excessive fluid loss . • No sustained improvement in renal function following expansion with 1.5 L of isotonic saline . • Proteinuria < 0.5 g/d with no ultrasonographic evidence of renal disease . 2004 80
- 81. Minor Criteria (5 ( 1 - Urine Volume <500 mL/d . 2 - Urine Sodium <10 mmol/d . 3 - Urine osmolality > plasma osmolality . 4 - Urine red cell count < 50 per HPF . 5 - Serum sodium < 130 mmol/L . 1 - Urine Volume <500 mL/d . 2 - Urine Sodium <10 mmol/d . 3 - Urine osmolality > plasma osmolality . 4 - Urine red cell count < 50 per HPF . 5 - Serum sodium < 130 mmol/L . 2004 81
- 82. Type I HRS Type I HRS • Rapidly progressive renal failure • With a doubling of serum creatinine to a level > 2.5 mg/dL or creatinine clearance < 20 mL/min . • In less than 2 weeks . 2004 82
- 83. Type II HRS Type II HRS • Is a more chronic form • With a slowly progressive increase in serum creatinine level >1.5 mg/dL or creatinine clearance <40 mL/min . 2004 83
- 85. Treatment • Liver Transplantation . • MARS “Molecular Adsorbent Recirculating System ” • TIPS . • Pharmacological Therapy 2004 85
- 86. 2004 86