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ASCITES & PERITONITIS

ASCITES & PERITONITIS. Diagnosis of Ascites. Physical exam: Shifting dullness Fluid wave Organ ballotment For cirrhosis related ascites: stigmata of cirrhosis Jaundice Spider angioma Muscle wasting Abdominal wall collaterals. Physical Exam for Ascites.

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ASCITES & PERITONITIS

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  1. ASCITES& PERITONITIS

  2. Diagnosis of Ascites • Physical exam: • Shifting dullness • Fluid wave • Organ ballotment • For cirrhosis related ascites: stigmata of cirrhosis • Jaundice • Spider angioma • Muscle wasting • Abdominal wall collaterals

  3. Physical Exam for Ascites • Sensitivity and specificity related to volume and body habitus • 50-90% sensitive • 30-80% specific • Absence of any flank dullness is best indicator of no/minimal ascites (under 1500 cc)

  4. Causes of Ascites • Cirrhosis/Acute hepatic injury (~80%) ( 5% have multifactorial cause) • Malignancy ( ~ 10%) • Right sided heart failure (3%) • Renal disease (1%) • Pancreatic (1%) • TB (2%) • Other ( SLE, myxedema, surgical complication: chylous: 2%) • HIV ( 75% cirrhosis and 25 % HIV related: TB, fungal, lymphoma) History should make diagnosis

  5. Causes • Cirrhosis causes 80-85% of ascites • Underfill vs Overlow theories • Recent Peripheral Arterial Vasodilation theory: incorporates both • Fundamental abnormality is Portal HTN • PHT--> nitric oxide--> vasodilation--> renal Na retention--> overfill of intravasc vol--> ascites formation--> neurohumoral activation • figure 78.1

  6. Pathogenesis

  7. Physical Exam Related to Pathophysiology of Hepatic Ascites • Portal hypertension • Ascites • Varices/ collaterals • Palmer erythema and gonadal atrophy • estrogen metabolic impairment • Arterial vascular “under filling” • Flat neck veins • System relative hypotension • Tachycardia

  8. Evaluation • Radiology: US supplanted by CT • Signs of cirrhosis • Malignancy • Portal vein thrombosis • Hepatic vein thrombosis Caveat is risk of IV contrast with the common underlying renal insufficiency/volume depletion of associated conditions

  9. Paracentesis • Ascites fluid analysis in all patients with • New onset ascites • Abdominal pain and known ascites • Fever and ascites Clinical deterioration of any kind

  10. Pathogenesis: Non-Liver disease • Depends on site of abnormality • Malignancies • peritoneal carcinomatosis- exudation of proteinaceous fluid from tumor cells lining peri • Massive liver mets- portal HTN • Hepatocellular CA- underlying cirrhosis, PVT • Lymphoma- chylous ascites, obstruction of LN • Cardiac- hear failure, PHT

  11. Clinical Features • Pts with stable cirrhosis and “sudden”ascites, suspect hepatocellular CA • Should suspect malignant ascites in pts with malignancy however need to rule out cirrhosis • Breast, lung, colon and pancreatic are often complicated by ascites • Malignant ascites is usually painful

  12. Diagnosis: Paracentesis • Complications of Paracentesis: • Rare and related to inexperience • Perforation • Past surgery and adhesions to peritoneum • Absence of ascites • Bleeding • Coagulapathy (clotting factors and thrombocytopenia) • Abdominal wall collaterals • Studies have excluded those with INR over 1.6 /PT over 21 seconds and Plt under 50,000 or clinically evident DIC • Leak • Large bore catheter • Tense ascites

  13. Paracentesis: technique • Avoid surgical scar- risk of adhesions • Supine or lateral decubitus • Tap out area of shifting dullness • Head of bed slightly elevated • Avoid collaterals and inferior hypogastric artery • Left or Right lateral versus midline • Main issue is to examine for contraindications to use of site and optimal area of shifting dullness • Scant ascites, scars and or obesity w/o shifting dullness • Prone near midline: “puddle” • US guided if not emergently needed in this setting

  14. Paracentesis: technique • Needle • Bruce Runyon: Up to Date and Slesinger and Fortran • 1.5” 22 gauge diagnostic and 16 gauge for large volume • 3.5” spinal for obese abdominal wall • Steel needle or blunt tipped cannula with sharp stylet that can be removed • Goldkind: Boston University/Boston City Hospital • Angiocath : do not reinsert metal stylet after insertion in to abdominal wall to prevent sheering off of plastic • Angiocath may be less likely to perforate bowel or nick vessel after metal stylet removed • Kinking is an issue

  15. Culture • SBP most common bacterial infection • usually monomicrobial • low bacteria count • Conventional plating not sensitive (50%) • Bedside inoculation of blood culture bottles 80% sensitive

  16. Appropriate Tests • Cell count single most helpful test • EDTA purple top tube • WBC in cirrhotics usually < 500cells/m3 • PMN > 250cells/m3 ABNORMAL • SBP most common cause of increased WBC • Traumatic tap accounts for most bloody ascites (subtract 1 PMN for each 250 RBCs)

  17. Diagnosing TB • AFB from ascites almost always negative • centrifuged pellet only 50% sensitive • Best method- peritoneal biopsy and culture combined for close to 100% sensitivity

  18. Cytology • Should be expected in malignancies with cells lining the peritoneum • Essentially 100% of pts with peritoneal carcinomatosis have positive cytology • Other malignancies (mets, hepatocellular CA) may cause ascites but may have negative cytology

  19. Serum-Ascites Albumin Gradient • Before the 1980s we used transudate vs. exudate, never fully validated • SAAG has been shown superior to exudate-transudate categories and total protein values in several studies • SAAG= serum albumin - ascites albumin (same day specimens) • Correlates with portal pressure Discard Transudate and Exudate terminology

  20. Serum-Ascites Albumin Gradient • SAAG > 1.1 g/dL (11 g/L), • pt has portal HTN (97% accuracy) • SAAG < 1.1 g/dL, no portal HTN • Does not give pathogenesis or dx cirrhosis • Not affected by: • infection, diuresis, etiology of liver disease • Not a test for peritonitis • cell count and culture used for this question

  21. Cirrhosis Alcoholic Hepatitis Cardiac ascites “Mixed” ascites Hepatic failure Budd-Chiari syndrome Portal vein thrombosis Veno-occlusive dis. Myxedema Fatty liver of pregnancy SAAG: high gradient >1.1g/dL

  22. Peritoneal Carcinomatosis Tuberculous peritonitis Pancreatic ascites Bowel obstruction or infarction Biliary ascites Nephrotic Syndrome Post-op lymphatic leak Serositis in CTD SAAG: low gradient < 1.1g/dL

  23. Complications of Ascites • Infection • SBP • Tense Ascites • Respiratory compromise ( restriction) • Pain • Pleural Effusions (hepatic hydrothorax) • Abdominal Wall Hernias

  24. Spontaneous bacterial peritonitis • Correia and Conn coined term in 1975 • Goal to distinguish SBP from surgical peritonitis • Diagnosis • positive ascitic fluid culture • elevated ascitic PMN count > 250cells/mm3 and • no intra-abdominal surgically treatable source

  25. Spontaneous bacterial peritonitis • Spontaneous bacterial peritonitis (variants) • Monomicrobial non-neutracytic: • (culture + without 250 polys) • Culture negative Neutrocytic • high poly count but culture negative: simply presumed false neg culture • SBP and variants • only occur in severe liver disease • In the presence of pre-existing ascites • Almost always in patients with elevated bili and INR

  26. Begin here to finish presentation

  27. SBP: Pathogenesis • MNB: • more common than SBP • probably early stage of SBP • good opsonic activity results in sterile ascites • poor opsonic activity results in SBP • CNNA: • probably poor culture technique • resolving SBP after killing of bacteria but before normalization of PMN count

  28. SBP: presentation

  29. SBP: Prevalence • Overall 10% of pts. with ascites are infected on admission • 27% of cirrhotic ascites are infected • Secondary bacterial peritonitis occurs in <2% of pts.

  30. SBP: organisms • E. coli most common 37% • Klebsiella 17% • Pneumococcus 12% • Strep. viridans 9% • Miscellaneous • gram positive 14% • gram negative 10%

  31. SBP: Diagnosis • High index of suspicion: • Ascitic fluid PMN>250 • Signs and symptoms of infection • Rule out secondary peritonitis- imaging, surgical consult • Repeat tap after 48 hours of treatment • antibiotics can’t control secondary peritonitis but rapidly cure SBP

  32. SBP: Treatment • Empiric antibiotics for all suspected SBP • 5 days of IV antibiotics • cefotaxime 2 gm q8 better than amp and tobra • cefotaxime covered 98% of the flora • no renal toxicity • sterile culture after 1 dose in 86% of pts • change spectrum according to sensitivities • repeat tap in 48 hours to assess for change in PMN count (decline often >80%)

  33. SBP: Prognosis • Old studies 48-95% of pts died despite tx • Now <5% die of infection if timely and appropriate antibiotics are used • earlier detection, treatment • avoidance of nephrotoxic agents • Maximize survival: • tap all pts admitted to hospital • repeat if deterioration, change in sx • tap all outpatients with NEW ascites

  34. SBP: Prevention • Risk factors • previous SBP • low ascitic protein • variceal hemorrhage • Norfloxin 400 mg QD prevents SBP in low protein and previous SBP and 400mg BID for pts with variceal hemorrhage • Oral antibiotics do not prolong survival

  35. Treatment: depends on etiology • Low SAAG: • Peritoneal Carcinomatosis- most common • outpt therapeutic paracentesis • Tuberculous ascites • cured by anti-TB therapy • Pancreatic ascites • may resolve spontaneously

  36. Treatment: depends on etiology • High SAAG: • hospitalization (large volume) • diet education (low sodium) • urine sodium excretion • fluid restriction (hyponatremia) • DIURETICS • no bed rest, sodium bicarb, foleys

  37. Treatment • Hospitalization for diagnosis, large volume paracentesis • Diet education with salt restriction key to management (2gm Na/day) • Check urinary Na excretion to ensure compliance • Fluid restriction not needed unless Na < 120 or pt symptomatic

  38. Treatment • Diuretics: • Spironolactone • is mainstay of tx, better than furosemide • long half life=slow onset (2 weeks to full effect), gynecomastia, hyperkalemia • Furosemide • faster onset, hypokalemia • Amiloride • more rapid onset, more expensive • less gynecomastia

  39. Treatment • Combination diuretics most effective • Spironolactone 100mg • Furosemide 40mg • Single day dosing • Double dose when ineffective • Start simultaneously • IV not needed

  40. Treatment • No limit to weight loss in pts with massive edema • Then 0.5 Kg/day • Stop diuretics for • encephalopathy • creatinine > 2 mg/dL • sodium < 120 mmol/L

  41. Treatment: outpt management • Re-evaluate in 1-2 weeks • Goal of diuretics is weight loss (negative sodium balance) • Check urine sodium • if excretion of Na> than 88mmol/day and pt is on 88mmol Na diet, they should lose weight

  42. Refractory Ascites • Defined as fluid overload unresposive to salt restriction and high-dose diuretics • < 10% of pts with cirrhotic ascites are refractory • Viable options include peritoneovenous shunt, LVP and transplant

  43. Refractory Ascites • Peritoneovenous shunts: • complications include shunt failure, fatal complications of insertion • no survival advantage in RCT • relegation to 3rd line therapy of cirrhotic ascites

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