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