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 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)

Causes of Ascites History should make diagnosis 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

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

Pathogenesis

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

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

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

                                                                                                                      

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

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

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

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

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

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

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)

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

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

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

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

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

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

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

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

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

Begin here to finish presentation

SBP: Pathogenesis MNB: CNNA: 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

SBP: presentation

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.

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

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

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%)

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

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

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

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

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

Treatment Diuretics: Spironolactone Furosemide Amiloride 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

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

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

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

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

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

Refractory Ascites Therapeutic abdominal paracentesis- one of the oldest medical procedures first line therapy in pts with TENSE ascites and second line therapy for refractory ascites large taps tolerated

Colloid Replacement Albumin Expensive: $2-$25/g or $100-$1250 per tap markedly increase albumin degradation 58% of infused albumin was accounted for by increased degradation 15% increase in serum albumin led to 39% increase in degradation Barcelona study used pts with tense ascites, not refractory ascites (31% not on diuretics)

Colloid Replacement Albumin Tense ascites paracentesis > 10L with or without albumin No albumin developed statistically sig. Changes in electrolytes, plasma renin and creatinine All changes were asymptomatic No increased morbidity or mortality in pts who did not receive albumin pilot study by Runyon showed no difference in morbidity, hepatorenal or mortality p1330

TIPS Side-side portocaval shunt placed by IR Local anaesthesia Originally used for variceal bleeding

TIPS Rossle used a RCT to compare TIPS vs LVP (NEJM 2000) 60 pts with good hepatic and renal function, refractory or recurrent ascites survival 1 and 2 year was 69 and 58% vs 52 and 32% respectively 40% required stent opening cost $25,000 to $50,000 trial of LVP and if unsuccessful in “select” pts refer for TIPS

Liver Transplant 12-month survival for refractory pts ranges from 25-50% Early referral after decompensation: refractory ascites encephalopathy gi hemorrhage Transplant has a 12-month survival close to 75%

Summary