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by Dr Intekhab Alam Professor of Medicine Department of Medicine Postgraduate Medical Institute,

MANAGEMENT OF ASCITES. by Dr Intekhab Alam Professor of Medicine Department of Medicine Postgraduate Medical Institute, Lady Reading Hospital, Peshawar. Objectives. Understand the basic mechanisms of portal hypertension (PHT) Study Ascites as a complication of PHT

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by Dr Intekhab Alam Professor of Medicine Department of Medicine Postgraduate Medical Institute,

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  1. MANAGEMENT OF ASCITES by Dr Intekhab Alam Professor of Medicine Department of Medicine Postgraduate Medical Institute, Lady Reading Hospital, Peshawar

  2. Objectives • Understand the basic mechanisms of portal hypertension (PHT) • Study Ascites as a complication of PHT • Get an idea on the management of Ascites and its complications

  3. What is Liver Cirrhosis? • Diffuse fibrosis of the liver with nodule formation • Abnormal response of the liver to any chronic injury

  4. Causes of Cirrhosis • Chronic viral hepatitis • Metabolic: hemochromatosis, Wilson dis, alfa-1-antitrypsin, NASH • Prolonged cholestasis (primary biliary cirrhosis, primary sclerosing cholangitis) • Autoimmune diseases (autoimmune hepatitis) • Drugs and toxins • Alcohol

  5. Anatomy of the portal venous system

  6. The Effect of The Liver Nodule

  7. Mechanism of Portal HTN

  8. Complications of Portal Hypertension in cirrhosis liver. Development of Ascites. Varices formation. Hepatic encephalopathy. Hepatorenal syndrome.

  9. Ascites Definition: presence of free fluid in the peritoneal cavity

  10. Nonperitoneal Causes of Ascites

  11. Peritoneal Causes of Ascites

  12. Etiology • Cirrhosis (75%) • Most common cause of ascites • Most common complication of cirrhosis • Other causes occur more frequently in cirrhotics • Malignancy (10%) • Cardiac (3%) • TB (2%) • Pancreatic Ascites(1%) • Various others Hepatology 38:258-66

  13. Pathophysiology of ascites in CLD: • Splanchnic HTN due to outflow obstruction • Increased vasodilatation (NO) • This sequesters volume in the abdomen • Decreases systemic filling • Decreases systemic BP • Activates antinatriuretic factors • Combination of increased splanchnic BP with vasodilatation leads to capillary leak • Lymph return can only keep up for sometime then ascites develops.

  14. Physical Examination • Bulging Flanks • Flank Dullness • Shifting Dullness • Fluid Wave • Puddle sign • Approximately 1.5 L must be present before flank dullness is detected. If no flank dullness is present, the patient has less than 10% chance of having ascites. JAMA 1992; 267:2645-48

  15. Bulging Flanks • Occur when weight of ascites is sufficient to push the flanks outwards • Difficult to distinguish from obesity • Sensitivity-72-93% • Pooled data 81% • Specificity-44-70% • Pooled data 59% JAMA 1992; 267:2645-48

  16. Flank Dullness • Similar to bulging flanks, although uses percussion • Typically bowel will float to the top and ascitic fluid sinks to the bottom • Sensitivity-80-94% • Most sensitive test • Pooled data 84% • Specificity-29-69% • 69% outlying value • Pooled data 59% JAMA 1992; 267:2645-48

  17. Shifting Dullness • Find the point where flank dullness occurs • Mark it • Roll the patient away from the examiner • Repeat percussion and ensure that the point moves to the dependent side • Sensitivity-60-83% • Pooled data 77% • Specificity-56-90% • Pooled data 72% JAMA 1992; 267:2645-48

  18. Fluid Wave (fluid thrill) • Medial edges of both hands down midline • Tap flank firmly and feel for an impulse on the other side • Sensitivity-50-80% • Pooled data 62% • Specificity-82-92% • Most specific test • Pooled data 90% JAMA 1992; 267:2645-48

  19. Puddle Sign • Have patient prone 3-5 minutes then rise to crawling • Place the diaphragm of the stethoscope over the most dependent area of the abdomen • Flick a finger until sound detected • No longer recommended • Formerly used for high sensitivity • Sensitivity-43-55% • Pooled data 45% • Specificity-51-83% • Pooled data 73% JAMA 1992; 267:2645-48

  20. International Ascites Club Grading • Grade 1 • Mild, only detectable by U/S • Grade 2 • Moderate, symmetrical distension • Grade 3 • Gross or large with marked distension • Large typically means painful/uncomfortable • Refractory Ascites (5-10%) • Can not be mobilized or early recurrence refractory to medical management NEJM 350:1646-54 Hepatology 2003; 38: 258-266

  21. Diagnosing Ascites • Ultrasound is the most sensitive test for ascites (100mL detection) • Have to use caution as small or even moderate ascites may be difficult to tap (even when marked) • Ensure mark is appropriate • Go with patient to U/S (ideal) • If not possible, in order specify location where you want to place your needle Image from www.gastro.org

  22. Paracentesis: General Tips • Do NOT do paracentesis to see if ascites present, should know before • If unclear need U/S • Ensure patient has voided • FFP/Platelet transfusion if indicated • Ensure landmarks • Get Quick-Tap kit, plastic catheter does not work as well as the metal one. Picture from www.kchealthcare.com

  23. Paracentesis: • Site:5cm cephalic & 5 cm medial to ASIS in the left lower quadrant of the abdomen has been shown to be the ideal site with larger pool of fluid. • Complications: (1% of patients) Abdominal wall hematomas. Hemoperitoneum or bowel entry. • Contraindications:Clinically evident fibrinolysis or DIC.

  24. Gross Appearance of Ascitic Fluid

  25. Recommended Studies Albumin Protein Cell count Looking for PMNs Cultures If clinically appropriate Glucose LDH Amylase RBC count TB smear/culture Cytology Triglycerides Diagnostic Studies www.gastro.org

  26. Diagnostic Studies 1. Check serum and fluid albumin SAAG > 1.1 SAAG < 1.1 Hepatic Sinusoid source Peritoneum source 2. Check Ascites Protein Ascites Protein <2.5 Ascites Protein >2.5 Ascites Protein >2.5 Capillarized sinusoid Peritoneal lymph Normal sinusoid 3. Differential Diagnosis Cirrhosis Late Budd-Chiari Cardiac ascites Early Budd-Chiari Veno-occlusive disease Malignancy Tuberculosis The SAAG does not need to be repeated after the initial measurement. Note: Exceptions exist: may have mixed features Adapted from www.gastro.org

  27. Ascitic fluid analysis: If the PMN count is >250 cells/mm3, another specimen is injected into blood culture bottles at bedside. Bacterial growth occurs in about 80% of specimens with count of >250 cells/mm3. In a "bloody" sample that contains a high concentration of RBC, the PMN count must be corrected: One PMN is subtracted from the absolute PMN count for every 250 red cells/mm3 in the sample.The results must be available within 1 hour, so that important diagnostic and therapeutic decisions can be made.A Gram stain is of particular low yield unless free gut perforation, is suspected.

  28. Based on clinical judgment, additional testing can be performed • Cytology ,smear & culture for mycobacteria. • Cytology : in peritoneal carcinomatosis (sensitivity increased by centrifuging large volume). • Elevated bilirubin level suggest biliary or gut perforation. • LDH >225mU/L, glucose <50mg/dL, total protein >1g/dL and multiple organisms on gram stain suggest secondary bacterial peritonitis. • High level of TG's confirms chylous ascites. • Elevated amylase level suggest pancreatitis or gut perforation.

  29. Prognosis • Poor outcomes • Refractory ascites • SBP • HRS • MELD (Model for end-stage liver disease) is not specifically validated for patients with ascites NEJM 350:1646-54

  30. Prognosis • Any person with ascites due to cirrhosis needs transplant evaluation • If MELD is <15 can stop there • Average US wait time 500d • Average wait less in some other countries • 120 days in UK • 180 days in Spain • If admitted for ascites 40% chance of dying within 2 years • Improves to 70-80% 5 year survival after transplant Dig Dis 2005; 23:30-38 Hepatology 2003; 38: 258-266

  31. Treatment • Grade 1 • No treatment necessary • Modify risk factors • Start low sodium diet Hepatology 2003; 38: 258-266

  32. Treatment • Grade 2 • Bed rest • Diuretics work better supine • studied bemetanide • GFR lower standing as well • Sodium and water restriction • Diuretics Br Med J. 1986;292:1351-3 Hepatology 2003; 38: 258-266

  33. Treatment • Grade 3 • Paracentesis is the treatment of choice • Shown to have fewer complications than diuresis • Faster response • After this would do Grade 2 treatment options Hepatology 2003; 38: 258-266

  34. Treatment • Refractory ascites • Paracentesis with colloid infusion • TIPS • Choice between these is controversial • If repeated paracentesis is contraindicated,TIPS not an option then consider porto-venous shunt • PVS shown inferior to repeat paracentesis in NEJM study Hepatology 2003; 38: 258-266

  35. Sodium Restriction • No survival benefit related to ascites shown, does have benefit in GIB mortality • 50mm restriction is equivalent to 120mm (approx. 2g/day) • Tighter restriction had faster resolution • Higher incidence of renal dysfunction and hyponatremia Hepatology 2003; 38: 258-266

  36. Diuretics • Spironolactone • start 100-200 per day • Titrate to max of 400 per day in severe hyper-aldo • Can use potassium sparing diuretics • Amiloride inferior to canrenoate (anti-mineralocorticoid) • No other comparison trials, but spironolactone accepted as first line • Use second line if spironolactone not possible 2/2 complications (ie gynecomastia) Hepatology 2003; 38: 258-266

  37. Diuretics • Loop diuretics • Lasix • Initial dose 20-40 per day • Can adjust up to 160mg per day • Should be used only as an adjunct to spironolactone • Risks of K depletion, hyperchloremic alkalosis, hyponatremia and hypovolemia with subsequent renal dysfunction Dig Dis 2005; 23:30-38 Hepatology 2003; 38: 258-266

  38. Assessing Diuretic Response • Weight loss • Lose 0.5kg a day when no edema • Lose 1kg a day when edema is present • Avoid renal failure • Response rate in up to 90% patients who do NOT have renal dysfunction Dig Dis 2005; 23:30-38 Hepatology 2003; 38: 258-266

  39. Paracentesis

  40. Paracentesis • First used by the Ancient Greeks • Decreased in the 1950s when diuretics were discovered • Resurgence in 1980s after 1987 article found paracentesis with lower complications than diuretics • More effective than diuresis • Shorter hospital stay Dig Dis 2005; 23:30-38

  41. Paracentesis • Total volume paracentesis is as effective and as safe as sequential 3L paracentesis • Hemodynamics • RA pressure drops immediately • PCWP takes 6h to decrease Hepatology 2003; 38: 258-266

  42. Paracentesis • Post paracentesis volume expansion • Side effects and albumin • without 30% • with 16% • Albumin prevents increased renin/aldo better than synthetic agents • HRS decreases • Less Hyponatremia NEJM 350:1646-54 Hepatology 2003; 38: 258-266

  43. Paracentesis-Complications • Bleeding - can be fatal • Ascitic fluid leak • Purse string suture • Lie with puncture site up • Bowel perforation • Renal impairment • Hypotension/Cardiovascular collapse

  44. TIPS • Transjugular Intrahepatic Portosystemic Shunt • Creates a conduit from the high pressure portal system to the lower pressure systemic circulation

  45. TIPS • Ascites can only form when portal pressure is >12 • Response rates 51-79% in RCT Dig Dis 2005; 23:30-38

  46. TIPS - Benefits • May improve nitrogen balance • Will decrease portal pressure reducing GIB risk • Improves hemodynamics • Increased CO, RA pressure, PCWP and decreased SVR with increased Na excretion • Improves response to diuresis NEJM 350:1646-54 Hepatology 2003; 38: 258-266

  47. TIPS - Risks • Encephalopathy • 30% those treated • Typically can improve with shunt revision or medical management • Increased risk if • Age >60 • History of Encephalopathy • 100% mortality if refractory to TIPS occlusion • CHF - this is due to increased preload NEJM 350:1646-54 Am J Gastro 2003;98:2521-27

  48. TIPS - Complications • Capsule perforation • Stenosis • 75% in 6-12 months • Decreased risk with stents coated in polytetrafluoroethylene (PTFE) • Increased cost relative to paracentesis NEJM 350:1646-54 Radiology 1999;231:759-766

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