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

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

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 abnormalityMalignancies 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 CAShould suspect malignant ascites in pts with malignancy however need to rule out cirrhosisBreast, lung, colon and pancreatic are often complicated by ascitesMalignant 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 adhesionsSupine 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 studiesSAAG= 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 HTNDoes not give pathogenesis or dx cirrhosisNot 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 1975Goal to distinguish SBP from surgical peritonitisDiagnosis 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: 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

Signs + symptoms % of pts

Fever 68

Abdominal pain 49

Tender abdomen 39

Mental status 54

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: PrognosisOld studies 48-95% of pts died despite txNow <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 hemorrhageOral 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 paracentesisDiet education with salt restriction key to management (2gm Na/day)Check urinary Na excretion to ensure complianceFluid restriction not needed unless Na < 120 or pt symptomatic

TreatmentDiuretics: 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

Treatment

Combination diuretics most effective 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 ReplacementAlbumin 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

TIPSRossle 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