Cell count: Leukocyte>500/cc or absolute neutrophil
>250/cc suggests infection.
Protein < 1g/dL in spontaneous peritonitis; >1 g/dL in
Glucose <50 mg/dL or increased LDH in secondary peritonitis.
Albumin serum-ascites gradient = serum albumin - ascitic albumin
- Gradient of > 1.1 g/dL suggests portal hypertension; seen in
cirrhosis, alcoholic hepatitis, CHF, massive liver metastasis, fulminant
liver failure, portal-veiin thrombosis, Budd-Chiari synd, veno-occlusive
disease, fatty liver of pregnancy, myxedema.
- Gradient of < 1.1 g/dL seen in peritoneal carcinomatosis, TB,
pancreatic ascites, biliary ascites, nephrotic synd, bowel obstruction or
Gram stain & C/S
Amylase in pancreatic or perforation.
Cytology or TB smear & culture prn.
A. Transudative ascites (Serum Albumin - Ascites Albumin
Congestive heart failure
Hepativ vein obstruction (Budd Chiari syndrome) a. Assoc. with tumors (hepatoma,
hypernephroma, pancreatic Ca) b. Assoc. with hematologic disorders
(myeloproliferative disease, polycythemia vera, myeloid metaplasia c. Due
Meig's ovarian tumor syndrome
Inferior vena cava obstruction
Viral hepatitis with submassive or massive hepatic necrosis
B. Exudative ascites (Serum Albumin - Ascites Albumin <1.1
Neoplastic diseases involving the peritoneum: Peritoneal carcinomatosis,
Post surgery talc or starch powder peritonitis
Transected lymphatics following portal caval shunt surgery
Lymphatic obstruction: a. Intestinal lymphangiectasia, b. Lymphoma
Prior abdominal trauma with ruptured lymphatics
Hemodialysis CRF related ascites
C. Disorders simulating ascites
RX of ascites depending on underlying cause.
Paracentesis to remove large amount of ascitic fluid 4-6 L/day.
Several large randomized, controlled trials have shown that repeated large-volume
paracentesis (4 L-6 L) is safer and more effective for the treatment of tense
ascites compared with larger-than-usual doses of diuretics.
Low salt diet <2 g NaCL/d and fluid restriction <1500 mL/day.
It is defined as an ascitic fluid infection associated with
a positive bacterial culture and
an ascitic fluid polymorphonuclear cell count of > 250/mm3,
in the absence of a surgically treatable abdominal source of infection.
In hospitalized patients with cirrhosis, 10% to 25% will have an episode
of SBP with a mortality rate of 17% to 50%, with outcome dependent on the
association with a recent gastrointestinal bleed, the severity of infection,
and degree of renal and liver failure.
Bacteremia is most often from intestinal bacterial overgrowth, but may also
result from bacteriuria or intravascular catheters.
Types of SBP
Culture-positive neutrocytic ascites (SBP) (the most common
form of SBP) with a positive bacterial culture and a polymorphonuclear (PMN)
cell count of >/= 250/mm3. About two thirds of ascitic fluid infections
belong to this subgroup and are almost invariably monomicrobial. Other
variants of SBP include
Culture-negative neutrocytic ascites (CNNA) characterized by PMN cell
count of >/= 250/mm3 with negative ascitic fluid cultures
The differential diagnosis of CNNA includes peritoneal carcinomatosis,
pancreatitis, and tuberculous peritonitis. CNNA has the same prognosis as
SBP and should therefore be treated similarly.
Monomicrobial nonneutrocytic bacterascites (MNB), characterized by
isolation of bacteria in cultures but with a PMN cell count of </= 250
Asymptomatic MNB usually signifies colonization and does not require antibiotic
therapy unless there are clinical signs and symptoms suggestive of infection.
Polymicrobial bacterascites occurs when ascitic fluid contains multiple
organisms and the PMN cell count is < 250/mm3. The latter usually results
from inadvertent puncture of the intestines during attempted paracentesis
and occurs in about 1/1000 paracenteses. Risk factors include ileus,
presence of multiple surgical scars, and operator inexperience. If the ascitic
fluid contains > 1 g/dL of protein and the opsonic activity of fluid is
adequate, colonization usually resolves spontaneously. Secondary bacterial
peritonitis is also polymicrobial but has a PMN cell count of > 250/mm3.
The latter can be distinguished from SBP by a total protein > 1 g/dL,
glucose concentration < 50 mg/dL, and a lactate dehydrogenase level >
225 U/mL. Prompt diagnosis through imaging is necessary because without surgical
correction, death is the usual outcome.
A rigid abdomen is not necessary for diagnosis, especially in patients with
large-volume ascites, which prevents the contact of visceral and parietal
peritoneal surfaces to elicit the spinal reflex that causes rigidity.
Treatment of SBP
Treatment should be started empirically if SBP is suspected
clinically, regardless of the availability of laboratory results.
In community-acquired SBP and in patients not on SBP prophylaxis, Escherichia
coli and Klebsiella pneumoniae are seen in up to 60% of isolates. About 25%
are Gram-positive cocci, mostly streptococcal species. Anaerobes are rarely
Intravenous cefotaxime 2 gm q12h for a minimum of
5 days is the empiric antibiotic of choice and has been shown
to cure SBP episodes in 85% of patients compared with in 56% of those receiving
ampicillin and tobramycin.
Intravenous amoxicillin-clavulanic acid followed by oral therapy has
been shown to be as effective as cefotaxime, but may not be widely available.
Intravenous ciprofloxacin followed by oral treatment has also been
shown to be effective.
Trials of oral ofloxacin vs intravenous cefotaxime in patients without
septic shock, encephalopathy, azotemia, gastrointestinal bleed, or ileus
showed an SBP resolution rate of 84% in the ofloxacin group vs 85% in the