University of Iowa
Family Practice Handbook, Fourth Edition, Chapter 5
And Hepatology: Ascites and Spontaneous Bacterial Peritonitis
Jatinder P. S.
Ahluwalia, MD, Mark A. Graber, MD, and William B. Silverman,
Division of Gastroenterlogy and Hepatology and Departments of
Internal Medicine, Family Medicine, and Emergency Medicine
University of Iowa Hospitals and Clinics and College of
Peer Review Status:
Externally Peer Reviewed by Mosby
- Ascites is a pathologic accumulation of serous
fluid within the abdomen. It may be caused by decompensated
liver disease (alcohol- and virus-related cirrhosis),
heart failure, abdominal carcinomatosis, tuberculosis,
fulminant liver failure, pancreatic disease, pelvic
inflammatory disease, connective tissue diseases and
- Cirrhosis is the underlying cause in ~80% of
the patients with ascites.
nonalcohol-related causes of liver disease, ascites
may be reversible in alcoholic liver disease with
abstinence and salt restriction.
abrupt development of ascites after many years in a
patient with stable cirrhosis should suggest the
possibility of hepatocellular carcinoma.
Examination and Radiologic Assessment
of the flanks helps differentiate ascites from other
causes of increased abdominal distention. The dullness
should shift upon rotating the patient in the right or
left lateral positions. Shifting dullness indicates the
presence of at least 1.5 liters of ascites.
abdominal X-ray may show the ground glass appearance
with centrally located bowel loops, but is not necessary
or recommended in the assessment or treatment of ascites.
may be necessary to determine the presence or absence of
ascites. Doppler studies of the portal system are
helpful in cases in which Budd-Chiari syndrome or a vena
caval web are suspected.
chest X-ray and an echocardiogram are helpful in
assessing patients suspected to have ascites of cardiac
and Ascitic Fluid Analysis
- Diagnostic paracentesis
should be performed routinely in all patients with new
onset ascites and in all patients admitted to the
hospital with ascites. A 22-gauge needle can be inserted
in a Z-tract fashion, to minimize leakage of fluid after
the paracentesis, in midline between the umbilicus and
the pubis symphysis in order to avoid collateral
vessels. In the presence of a midline scar, a position
~1.5 inches above and medial to the anterior superior
iliac spine can be used safely.
- Ascitic fluid is mostly straw colored
or yellow tinged. Cloudiness or opacified appearance is
due to the presence of neutrophils. Milky appearing
ascites is due to the presence of triglycerides and is
also known as chylous ascites. Non-traumatic bloody
ascites should raise the suspicion for tuberculosis and
malignancy. A tea-colored fluid is occasionally seen in
- The initial ascitic fluid analysis should include
the following studies: cell count with WBC
differential (mandatory test in all cases), albumin,
total protein and culture (in blood culture bottles to
increase the yield). Glucose, amylase, and Gram stain
are of little or no value except in cases of suspected
- Patients with >250 polymorphonuclear leukocyte
count (PMN) per milliliter are assumed to be infected and
need to be treated. In cases of bloody taps, only 1
PMN per 250 red cells can be attributed to
contamination of the ascitic fluid with blood.
- In ascites due to tuberculous peritonitis
and peritoneal carcinomatosis, lymphocytes
- The serum-ascites albumin gradient (SAAG)
is equal to [albu-min]serum - [albumin]ascites.
A gradient of >1.1 g/dl is indicative of
portal hypertension with greater than 90% reliability.
causes of Ascites
- High SAAG
- Cardiac ascites is due
to congestion of hepatic sinusoids and has high total
- Nephrogenous ascites
occurs in patients on hemodialysis with volume
overload and tends to have high total protein as well.
- Massive liver metastases
can result in portal venous inflow obstruction and
tumor emboli in portal vein radicals cause- portal
hypertension. The ascites total protein is <2.5
mg/dl in two-thirds of the cases. Consider also Budd-Chiari
- In myxedema, ascites
forms due to congestive heart failure and also has
high protein (>2.5 mg/dl).
- Low SAAG
- Tuberculous peritonitis
is most often diagnosed in Asians and immigrants from
- Peritoneal carcinomatosis
accounts for ~50% of all cases of ascites due to a
malignancy. Cytology is positive in 97% to 100% of the
- Pancreatic ascites
accounts for <1% of ascites. Patients often have
underlying liver disease due to alcohol abuse. The
fluid has high amylase and the total protein of the
ascites is usually high.
- Biliary ascites is due
to leakage of bile into the peritoneum, is dark brown,
has bilirubin value $6 mg/dl and an ascitic
fluid/serum bilirubin ratio of >1.
- Ascites with low SAAG may be seen in patients
with connective tissue diseases due to
serositis in the absence of portal hypertension.
- Nephrotic syndrome is a
cause of ascites with low protein.
- Ascites in a febrile,
sexually active young woman should raise a suspicion
for chlamydia peritonitis. This ascites has high
protein and has elevated WBC.
- Discontinue any prostaglandin inhibitors or other
drugs which reduce GFR (e.g., NSAIDS).
- Sodium restriction is the
key to successful treatment of ascites. Patient should
be instructed to follow a 2 g/day sodium diet. Fluid
restriction is not necessary unless hyponatremia is
- Avoidance of salt substitutes
that contain KCl and potassium-enriched foods should be
emphasized especially if the patient is also on a
- If salt restriction alone is not effective,
oral diuretics can be initiated. A combination of
spironolactone and furosemide is usually successful in
causing natriuresis without precipitating hyper- or
hypokalemia. The usual beginning doses are
spironolactone 100 mg QD and furosemide 40 mg QD.
- Random urinary sodium and urinary potassium can be
checked and the diuretics’ doses adjusted to effect Na/K
ratio >1. (Increase in furosemide dose causes
increased urinary sodium and potassium loss and increase
in spironolactone dose causes increased potassium
- The doses of spironolactone and furosemide can be
titrated to a maximum of 400 mg qd and 160 mg QD, respectively,
using the 100 mg:40 mg ratio to maintain normokalemia.
The goal of diuretic therapy should be to effect a 1-2
lb weight loss daily.
weight, serum electrolytes, urea and creatinine are
important pa-rameters to follow.
- Diuretic therapy should be stopped
in the event that encephalopathy, hyponatremia (Na
<120 mmol/L despite fluid restriction), or renal
insufficiency (creatinine >2 mg/dl) develop.
Overaggressive diuresis can also lead to hepatorenal
syndrome, a non-reversible condition resulting in
progressive renal failure due to renal hypoperfusion in
patients with advanced liver disease. Avoid diuresis of
greater than 1 liter per day.
- Large volume paracentesis
can be performed in patients with tense ascites
affecting satiety and respiration. Approximately 4-6 L
can be removed resulting in improvement of symptoms. No
albumin replacement is recommended for removal of up to
5 liters of ascitic fluid. Intravenous albumin (8
g/liter of ascitic fluid removed) can be given for
larger volume paracentesis.
- Refractory or diuretic-resistant ascites,
defined as minimal to no weight loss despite diuretics
or development of complications of diuretic therapy,
occurs in <10% of cirrhotic patients with ascites. It
can be managed by repeated therapeutic paracenteses,
peritoneovenous shunt or TIPS placement. TIPS is
superior to repeated large volume paracentesis in
resolving ascites and there is a trend towards better
survival. However, patients with TIPS must be monitored
for shunt malfunction and hepatic encephalopathy which
may be more frequent than in those undergoing
paracentesis (data is contradictory). While orthotopic
liver transplantation should be considered initially
after the onset of ascites, eligible patients who are
diuretic-resistant need to be prioritized for
transplantation as 50% die in 6 months.
- Spontaneous Bacterial Peritonitis.
Patients with ascitic fluid total protein concentration
<1.0 g/dl and gastrointestinal hemorrhage are at high
risk for spontaneous bacterial peritonitis. There is
good evidence that Bactrim (1 DS tablet daily 5 days a
week) is effective in preventing spontaneous bacterial
peritonitis and decreasing mortality. Norfloxacin 400 mg
qd has been used but there is rapid development of
resistant organisms. Weekly use of ciprofloxacin 750 mg,
as well as levofloxacin 250 mg qd are being used
increasingly. Also see treatment for SBP below.
as the presence of a large pleural effusion that is seen
as a complication of ascites in 5% to 9% of the cirrhotic
patients with ascites, is often right-sided and can
occasionally be found in the absence
of ascites. It is most likely due to defect(s) in
the tendinous portion of the right hemi-diaphragm. The
pleural fluid tends to recur and, like ascites, is usually
transudative in nature.
diagnosis can be confirmed by obtaining a
nuclear study that establishes the presence of a peritoneo-pleural
communication. The study involves the instillation of
99mTc-sulfur colloid into the peri- toneum and documenting
the presence of the radiotracer in the pleural space.
hydrothorax is a relative contraindication to chest tube
due to the potential for life-threatening fluid and
electrolyte depletion. Rather,
it is treated like ascites. In cases not responding
to usual therapy, pleurodesis with tetracycline or
thoracotomy to repair the diaphragmatic defect can be
Bacterial Peritonitis (SBP)
- SBP is a common complication
in patients with cirrhosis and ascites, and occurs
mostly in the setting of low ascitic fluid total protein
level (<1 g/dl).
- Pathogenesis involves
bacterial translocation from the gut to the systemic
circulation and then to ascitic fluid.
- E. coli, Klebseilla
pneumoniae, and pneumococcus
are the three most common isolates.
- Renal failure occurs in approximately one-third of
the patients despite treatment of the
- Abdominal pain and fever are the most
characteristic symptoms, but hepatic
encephalopathy, gastrointestinal bleeding, vomiting,
diarrhea, shock, or hypothermia may be the presenting
symptom(s) in a large number of patients.
can also be totally asymptomatic.
Therefore one must have a low threshold for performing a
paracentesis to obtain ascitic fluid for analysis.
- SBP is diagnosed when there is a positive ascitic
fluid culture or when the ascitic fluid PMN count is >250
cells/mm3 in the absence of an
identifiable intraabdominal source of infection.
- Ascitic fluid culture
must be placed directly into blood culture preferably at
bedside to increase the sensitivity of culture.
- Secondary peritonitis
due to perforated viscus usually results in PMN count in
the thousands, multiple organisms on gram stain and
culture, and at least 2 of the following: total protein
>1 g/dl, LDH > the upper limit of normal for
serum, and glucose <50 mg/dl.
- Empiric antibiotic
treatment should be begun before the culture results
become available to prevent demise of the patient.
- A broad-spectrum therapy is recommended in
suspected ascitic fluid infection until culture
results and susceptibility are available. Cefotamine 2 g
IV Q8h or a comparable third-generation cephalosporin is
the treatment of choice. Five days of treatment is
appropriate. A repeat paracentesis can be performed
after completion of 5 days of therapy with IV
antibiotics to ensure efficacy of the treatment
especially in patients with atypical presentation or
- Intravenous albumin at a
dose of 1.5 g per kilogram body weight on day 1 and 1 g
per kilogram on day 3 has been shown to reduce
significantly the incidence of renal impairment and
death in comparison with treatment with antibiotics
these patients should be placed on SBP prophylaxis
therapy (norfloxacin 400 mg QD or levofloxacin 250 mg QD)
for the remaining part of their hospital stay.