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

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Presentation on theme: "by Dr Intekhab Alam Professor of Medicine Department of Medicine Postgraduate Medical Institute, Lady Reading Hospital, Peshawar MANAGEMENT OF ASCITES."— Presentation transcript:



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

4 Objectives 1. Understand the basic mechanisms of portal hypertension (PHT) 2. Study Ascites as a complication of PHT 3. Get an idea on the management of Ascites and its complications

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

6 Causes of Cirrhosis 1. Chronic viral hepatitis 2. Metabolic: hemochromatosis, Wilson dis, alfa-1-antitrypsin, NASH 3. Prolonged cholestasis (primary biliary cirrhosis, primary sclerosing cholangitis) 4. Autoimmune diseases (autoimmune hepatitis) 5. Drugs and toxins 6. Alcohol

7 Anatomy of the portal venous system

8 The Effect of The Liver Nodule

9 Mechanism of Portal HTN Cirrhosis Resistance portal flow Mechanical Nodules Dynamic Nitric oxide

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

11 Ascites Definition: presence of free fluid in the peritoneal cavity

12 Nonperitoneal Causes of Ascites Non-peritoneal causesExamples Intrahepatic portal hypertension Cirrhosis Fulminant hepatic failure Veno-occlusive disease Extrahepatic portal hypertension Hepatic vein obstruction (ie, Budd-Chiari syndrome) Congestive heart failure HypoalbuminemiaNephrotic syndrome Protein-losing enteropathy Malnutrition Miscellaneous disordersMyxedema Ovarian tumors Pancreatic & Biliary ascites ChylousSecondary to malignancy, trauma

13 Peritoneal Causes of Ascites Peritoneal CausesExamples Malignant ascitesPrimary peritoneal mesothelioma Secondary peritoneal carcinomatosis Granulomatous peritonitisTuberculous peritonitis Fungal and parasitic infections Sarcoidosis Foreign bodies (cotton,starch, barium) VasculitisSystemic lupus erythematosus Henoch-Schönlein purpura Miscellaneous disordersEosinophilic gastroenteritis Whipple disease Endometriosis

14 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

15 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.

16 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:

17 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:

18 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:

19 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:

20 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:

21 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:

22 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: Hepatology 2003; 38:

23 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

24 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

25 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.

26 ColorAppearance Translucent or yellowNormal / sterile BrownHyperbilirubinemia GB or biliary perforation Cloudy or turbidInfection Pink or blood tingedMild Trauma Grossly bloodyMalignancy Abdominal trauma Milky ("chylous")Cirrhosis Thoracic duct injury Lymphoma Gross Appearance of Ascitic Fluid

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

28 Diagnostic Studies SAAG > 1.1SAAG < 1.1 Ascites Protein <2.5Ascites Protein > Check serum and fluid albumin Ascites Protein > Check Ascites Protein Hepatic Sinusoid sourcePeritoneum source Capillarized sinusoidNormal sinusoidPeritoneal lymph Cirrhosis Late Budd-Chiari 3. Differential Diagnosis 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

29 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.

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

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

32 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 Hepatology 2003; 38: Dig Dis 2005; 23:30-38

33 Treatment Grade 1 No treatment necessary Modify risk factors Start low sodium diet Hepatology 2003; 38:

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

35 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:

36 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:

37 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:

38 Diuretics Spironolactone start 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:

39 Diuretics Loop diuretics Lasix Initial dose 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 Hepatology 2003; 38: Dig Dis 2005; 23:30-38

40 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 Hepatology 2003; 38: Dig Dis 2005; 23:30-38

41 Paracentesis

42 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

43 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:

44 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 Hepatology 2003; 38: NEJM 350:

45 Paracentesis-Complications Bleeding - can be fatal Ascitic fluid leak Purse string suture Lie with puncture site up Bowel perforation Renal impairment Hypotension/Cardio vascular collapse

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

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

48 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 Hepatology 2003; 38: NEJM 350:

49 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 Am J Gastro 2003;98: NEJM 350:

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

51 TIPS v. Paracentesis Several studies (2 examples) Lebrec 1996 No ascites recurrence benefit in CP class C patients with worsened survival CP class B showed decreased recurrence Small study (25 patients) Salerno Shown to have survival improvement with multivariate analysis (only trend to improved survival without this) Non-blinded 3 center study Had to have 4 taps in the last month Decreased ascites recurrence HR 0.37 ( ) 66 patients Hepatology 2004;40: J Hepatol 1996;25:135-44

52 Cochrane Database No difference in mortality Decreased re-accumulation at 3 and 12 months Increased PSE OR 2.11( ) Surprisingly no difference: GIB, ARF, Infection or DIC Some issues in differences between the studies, not all paracentesis had post- paracentesis albumin, differences in MELD/CP between studies Hepatology 2003; 38:

53 Reasons for TIPS over Paracentesis TIPS better if Loculated ascites Patient unwilling to have repeat taps Frequent recurrences Am J Gastro 2003;98:

54 Peritoneovenous Shunts

55 Creates a communication between the peritoneal cavity and the systemic circulation by a vein Used in only in limited cases currently Used for palliation if TIPS and paracentesis are not available or contraindicated Hepatology 2003; 38:

56 Spontaneous Bacterial Peritonitis H/O Chronic Liver Disease. Fever and abdominal pain (66%) Signs of peritonitis uncommon (<50%) Neutrocytic ascites on diagnostic paracentesis % of pts with CLD develop SBP. Almost always monomicrobial. Anaerobes are not associated with SBP 20% are asymptomatic. Typically due to translocation This is why E. Coli is the most common

57 SBP: Diagnosis. Diagnosed with >250 polys or > 50-70% of the total cell count. Ascitic protein >1gm/dl against SBP % are ascitic fluid culture negative. 3% have secondary Bacterial Peritonitis. Ascitic fluid Glucose, LDH and total proteins may be helpful in DDx. Erect Abd X-ray in suspicious cases. Hepatology 2003; 38: NEJM 350:

58 SBP: Treatment and Prophylaxis Treat with 3rd generation Cephalosporins. Repeat PMN count after 48 hrs. 40% develop HRS during the course of illness. Human Albumin 1.5gm/Kg o day one and 1 gm/Kg on day three has shown improvement in both morbidity and mortality. Prophylaxis: 70% recur within one year. Norfloxacin 400mg qd Ciprofloxacin 750mg q week Tri-Sulpha: Has never been tested in a trial with mortality. Ultimate treatment: Liver transplant.

59 References Moore K, Wong F, Gines P, Bernardi M et al. The Management of Ascites in Cirrhosis: Report on the Consensus Conference of the International Ascites Club. Hepatology 2003;38: Gines P, Cardenas A, Arroyo V, Rodes J. Management of Cirrhosis and Asictes. NEJM. 2004;350: Haskal Z. Improved Patency of TIPS in Humans: Creation and Revision with PTFE Stent-Grafts. Radiology. 1999; 213: Cardenas A, Arroyo V. Refractory Ascites. Dig Dis. 2005; 23:30-38 Russo M, Sood A, Jacobson I, Brown R. TIPS for Refractory Ascites: An Analysis of the Literature on Efficacy, Morbidity and Mortality. Am J Gastroenterol. 2003; 98: Heuman D, Abou-assi S, Habib A et al. Persistent Ascites and Low Serum Sodium Identify Patients with Cirrhosis and Low MELD Scores who are at High Risk for Early Death. Hepatology. 2004; 40: Salerno F, Merli M, Riggio O, Cazzangia M, et al. Randomized Controlled Study of TIPS v. Paracentesis Plus Albumin in Cirrhosis with Severe Ascites. Hepatology 2004;40: Ring-Larsen H, Henriksen J, Wilken C, Clausen J, et al. Diuretic treatment in decompensated cirrhosis and congestive heart failure: effect of posture. Br Med J 1986; 292: Lebrec D, Giuily N, Hadengue A, Vilgrain V, et al. TIPS: comparison with paracentesis in patients with cirrhosis and refractory ascites: a randomized trial. French Group of Clinicians and a Group of Biologists. Saabs, Nieto JM, Ly D, Runyon BA. TIPS versus paracentesis for cirrhotic patients with refractory ascites. The Cochrane database of Systematic Reviews 2004, Issue 3 Art. No.: CD Cattau EL, Stanley BB, Knuff TE, et al. The Accuracy of the Physical Examination in the Diagnosis of Suspected Ascites. JAMA. 1982; 247: Williams JW, Simel DL. Does This Patient Have Ascites?. JAMA. 1992; 267: Mallory A, Schaefer JW. Complications of Diagnositc Paracentesis in Patients with Liver Disease. JAMA. 1978; 239: Runyon BA. Paracentesis of Ascitic Fluid a Safe Procedure. Arch Intern Med. 1986; 146: Simel DL, Halvorsen RA, Feussner JR. Quantitating bedside diagnosis: clinical evaluation of ascites. J Gen Intern Med. 1988; 3: Images:

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