ASCITES

by
Glen E. Hastings MD
September 26, 2005

I History & Physical Examination 1,2 : Ascites is a swelling of the abdomen, caused by the
accumulation of extracellular fluid in the abdominal cavity. Ascites generally accumulates slowly &
often at first attributed to weight gain from dietary indiscretion. Not all patients with abdominal
swelling have ascites. One may usually discern both the diagnosis & its Table 1: Symptom Descriptors
cause on the basis of the medical history & physical findings. Associated Signs or Symptoms
Table 1 is a list of questions that may be helpful in delineating the Precipitating Factors
etiology of the problem. For example: Should the ascites have Ameliorating Factors
Abrupt or Gradual Onset
accumulated over a brief period of time, accompanied by pedal edema Duration
and right upper quadrant discomfort, the diagnosis of congestive heart Has It Happened Before?
failure should be considered. Pain is an unusual accompanying Pattern of Prior Occurrences
symptom. When it occurs it indicates the presence of an inflammatory or infectious process,
neoplastic studding of the visceral cavity, or stretching of an intra-abdominal viscus. Painless ascites
evolving slowly & insidiously suggests end stage cirrhosis of the liver, especially in those with a
history of alcoholism or hepatitis &/or “spider nevi” on the skin, erythematous “liver palms”, testicular
atrophy or other stigmata of hyperestrogenemia. Ascites that recurs & abates suggests cirrhosis as
the underlying condition. Painless ascites with pedal edema, “puffiness” of the faces & proteinurea
>3 to 3.5g/24 hours are characteristic of nephrotic syndrome. A history of a pelvic mass suggests
malignant ascites. An abrupt onset with epigastric pain radiating to the back followed by progressive
ascites suggests a pancreatic etiology.
At the same time that pain is unusual in ascites secondary to cirrhosis or nephrotic syndrome,
patients often complain of a sensation of increased intra-abdominal pressure & tension in the flanks.
Tense ascites may be painful and it may cause dyspnea by interfering with diaphragmatic excursions
(a form of restrictive lung disease) as well as gastroesophageal reflux disease (GERD).
Obviously not everyone with a protuberant abdomen has ascites. Examination of the abdomen in the
supine position will reveal dullness to percussion in the flanks when ascites is present & resonance in
its absence in 90% of cases. When dullness is found, the presence of ascites is confirmed when the
area of dullness shifts when the patient is repositioned in the lateral decubitus position.
Tenderness to percussion of the liver suggests hepatitis, relatively acute liver congestion or biliary
tract obstruction. Palpation of a firm liver edge is characteristic of cirrhosis; nodularity suggests
malignancy; pulsations suggest tricuspid regurgitation & an enlarged palpable gall bladder suggests
prostatic carcinoma with biliary tract obstruction.
II Diagnostic Paracentesis & Peritoneal Fluid Analysis1,2 is performed in all patients with new onset
ascites & routinely in all patients with ascites who are sick enough for hospital admission. The
purposes of examining the fluid are: (1) to exclude subacute bacterial peritoneal peritonitis (SBP),
which is found in 20 to 27% of routine cases. (2) To distinguish whether or not portal hypertension is
the cause of the ascites.
Paracentesis may be performed using a standard 1.5 inch 22 gauge needle or a 3.5 inch spinal
needle, either in the midline, midway between the umbilicus & the symphisis pubis or laterally, about
1.5 inches above and medial to the anterior superior iliac spine. 25 to 30 cc of peritoneal fluid should
be sent to the lab for cell count, differential & albumin determinations & 2 culture bottles should be
inoculated with 10cc of blood at the bedside.
Nonhomogeneous blood in the ascitic fluid that clots upon standing indicates a traumatic tap rather
than preexistent hemoperitonium. True hemoperitoneum usually means malignancy. Chylous ascitic
fluid is milk like in color & opalescent in texture & indicates malignancy in ≈80%. 20% of cases are
among cirrhotics with hypertriglyceridemia. Pancreatitis ascites ranges from “tea-colored” to black.
Essential tests of ascitic fluid include cell count, albumen & bedside bacterial cultures. A serum
albumin drawn at the same time as the pericentesis is also essential. Optional tests include ascitic
fluid protein, LDH, glucose, amylase, Gram’s stain & serum LDH, TBC smears & culture, triglycerides,
cytology & bilirubin are other tests that must be obtained when the circumstances warrant them.
 Ascites: Page 2 of 4

The average WBC count in uncomplicated cirrhosis with ascites is 280cells/mm3. The upper limit is
500cells/mm3. 27 to 30% of the WBCs are usually PMNs; the cut off point is 250PMNs/mm3.
Elevated WBC & PMNs are taken as presumptive evidence of SBP (SBP is asymptomatic in up to 2/3
of cases). In tuberculous & carcinomatosis ascitic fluid, lymphocytes usually predominate.
The presence or absence of portal hypertension is determined by calculating the serum albumin to
ascitic fluid albumin ratio (SAAG). An elevated SAAG means the patient has portal hypertension.
That’s why you need to draw the blood at the same time as you do the peritoneal tap. Table 2 shows
which conditions exhibit high a vs low SAAG: Table 2:Classification of Ascites by SAAG
2

If the difference between the serum & ascitic High (≥1.1g/dL) Low (<1.1g/dL)
fluid albumin ≥1.1g/dL, the patient is >90% Cirrhosis Nephrotic syndrome
certain to have portal hypertension; if the Congestive heart failure Peritoneal carcinomatosis
difference <1.1g/dL he does not. Parenthetically Fulminant hepatic failure TBC without cirrhosis
Fatty liver of Pregnancy Pancreatitis without cirrhosis
it should be noted that the “SAAG gradient” has Liver metastases Biliary disease without cirrhosis
replaced the older classification of ascitic fluid as Portal vein thrombosis Connective tissue disease
either “exudative” or “transudative” based on the Alcoholic hepatitis (Serositis)
serum protein gradient & LDH. The older Budd-Chiari syndrome Pelvic inflammatory disease (PID)
Veno-occlusive disease (Chlamidial or gonococcal)
classification classified ascites correctly only Myxedema
55.6% of the time, while the SAAG gradient Dialysis related ascites
worked in 96.7% of cases.
III Conditions Causing High SAAG Ascites1,2,3 : Table 2 is a list of causes of ascites indicating the
approximate percentage of patients with ascites who Table 2: Causes of Ascites
1,2,3

have each type of diagnosis. Cause %

Cirrhosis & other related causes of hepatic portal Liver Disease: 80-85%
hypertension are the cause of ascites in 80% of Cirrhosis
cases in the US. All patients should be screened for Fulminant Hepatic Failure
Fatty liver of pregnancy
alcoholism, IV drug use PMH of jaundice sexual
Neoplasms: 10%
preference, tattoos & other risk factors for liver Hepatoma
disease. FH should be reviewed for diabetes & Liver, peritoneal or lymphatic metastases
arthritis suggestive of hemochromatosis, & for Lymphoma with Lymph Obstruction
Wilson’s disease. A PMH of recurrent ascites Pseudomyxoma peritonei
Meig’s Syndrome (Ovarian Fibroid)
suggests alcoholic cirrhosis which will sometimes Heart Failure: 3%
improve during periods of alcohol abstinence & salt Cor pulmonalé heart disease & COPD
restriction. The abrupt onset of ascites in a cirrhotic ASHD or VHD with biventricular CHF
Constrictive Pericarditis 1%
patient who has been stable for years may herald
Infections:
the emergence of a hepatoma, especially if the Tuberculosis
patient is alcoholic & is also positive for hepatitis C Spontaneous Bacterial Peritonitis
or B. Pelvic Inflammatory Disease (Chlamydia)
HIV <1%
The physiological basis of the SAAG gradient is that Venous occlusion:
the SAAG gradient is simply a reflection of the Supradiaphragmatic IVC Occlusion
body’s need to maintain balance between the Budd-Chiari Syndrome
o
Veno-occlusive disease 2 to toxins
oncotic & hydrostatic pressures in the vascular & (ie. seneciosis) <1%
extravascular extracellular spaces. As the intra- Renal:
o
abdominal hydrostatic pressure increases 2 to Dialysis Related
portal hypertension, the vascular to ascites fluid Nephrotic Syndrome <1%
Inflammatory:
albumin concentration would be expected to widen Pancreatitis
because albumin is the major vehicle for maintaining Bile Peritonitis
intravascular oncotic osmolality. Chronic lymphatic inflammation/fibrosis
Connective Tissue Disease <1%
Cardiac Ascites is related to arteriosclerotic heart Trauma:
disease (ASHD) in 31% of cases, in 21% Ruptured Viscus
cardiomyopathy, valvular disease in 23%, Trauma to the abdominal cysterna chyli
obstructive or restrictive lung disease in 15% & 8% Nutritional: <1%
Marasmus
to constrictive pericarditis. Optimal management is Kwashiokor <1%
control of the CHF. The pathophysiological Endocrine:
mechanism of CHF causing cirrhosis is that after a Myxedema
time, passive congestion of the hepatic sinusoids Endometriosis
engenders periventricular fibrosis, progressively elevating portal pressure & consequently SAAG.
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Budd-Chiari Syndrome & veno-occlusive disease associated with bone marrow transplantation &
chemotherapy or seneciosis produce severe liver congestion obstructing venous portal egress.
Fulminant Hepatic Failure produces rapidly accumulating ascites, hepatic coma & severe
coagulopathies with a high fatality rate. Ascites is 2o to portal hypertension related to hepatic
sinusoidal congestion.
Myxedema does not cause ascites directly. The ascites occurs because of myxedema related
congestive heart failure. Thyroid hormone treatment usually leads to rapid reversal.
Massive Liver Metastasis is the cause of ascites in 26% of malignancy associated cases. SAAG is
elevated in all cases Serum protein is <2.5g/dL in 67% of cases & the serum alkaline phosphatase is
typically elevated.
Dialysis Related Ascites occurs in fluid overloaded dialysis patients, most of whom also have
cirrhosis. The SAAG is high in 75% of cases as is the total protein.
Protein Loosing Enteropathy is not a disease but is a condition related to one of over 65 specific
causes of excessive loss of protein into the GI tract through ulcerated mucosa (as in Crohn’s Disease
& ulcerative colitis), intact mucosa with increased permeability (as in celiac sprue) or lymphatic
dysfunction or obstruction (as in intestinal lymphoma). Total protein is low, SAAG is high.
IV Conditions Causing Low SAAG Ascites:
Peritoneal Carcinomatosis is the etiological basis for ≈50% of malignancy caused ascites. Alkaline
phosphatase is usually elevated & cytology is usually negative. The fluid is exuded by the peritoneal
cells affected by metastatic implants, most frequently from breast or colon. The diagnosis is made by
endoscopic or open peritoneal biopsy. SAAG is high as is total protein in 67% of cases.
Tuberculous Peritonitis without cirrhosis produces low SAAG ascites, but in the US TBC usually
occurs among alcoholics or drug users, many of whom have concomitant cirrhosis, in this country
TBC peritonitis about 50% of the time produces high SAAG ascites. A similar picture may occur with
coccidiodomycosis or histoplasmosis.
Pancreatic Ascites is rare. It may occur early as a result of chemical burns as proteolytic enzymes
leak onto the mucosal & peritoneal surfaces. Later, ascites may form when digestive enzymes leak
more slowly from pancreatic ductile tears or pseudocysts. The fluid is usually clear & yellow in color,
but may be “tea-colored”. Ascitic fluid amylase is usually higher than the upper limits of the normal
range for serum amylase.
Biliary Ascites rarely occurs as a complication of rupture or surgery of the gallbladder bile ducts or
gut, because of the irritant effect of bile salts. The fluid is usually brown in color with a bilirubin level
above 6mg/dL &a fluid/serum bilirubin ratio >1.0.
Nephrotic Syndrome rarely causes produces ascites. When it does, all serum proteins are low as is
the SAAG.
Connective Tissue Disease. Rarely someone with systemic lupus erythematosis, familial
Mediterranean fever or sarcoidosis will develop a serositis with pleural effusion. The SAAG is low.
The WBCs may be high
Chlamydia or Gonococcal Peritonitis should always be considered in febrile young women with
ascites. The perihepatitis (Fitz-Hugh Curtis syndrome is most frequently due to Chlamydia). Serum
protein is very high. SAAG is low. WBCs are elevated.
HIV related Ascites occurs from a myriad of causes ranging from Kaposi’s sarcoma to lymphomas to
nephrosis or pericarditis to cirrhosis contracted through hepatitis B or C infections or alcoholism.
Ascites in an HIV infected patient requires consideration of almost every known cause of ascites.
V Other Laboratory Tests may be indicated in special circumstances. Abdominal ultrasound is the
modality of choice for confirming the presence of ascites in equivocal cases or for locating the optimal
pericentesis site. Abdominal CT may also confirm the diagnosis & may also reveal
lymphadenopathy, organ enlargement a tumor mass or metastasis or a fibrotic liver. Barium contrast
studies may be indicated to identify intrinsic GI tract abnormalities, varices or displacement by
extrinsic lesions. Retrograde venous angiography may occasionally be useful in identifying
thrombotic diseases, cardiac & pericardial causes of ascites.
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VI Treatment hinges upon discerning the cause of the ascites. In the case of cirrhosis which represents
80% of ascites cases, direct treatment of the ascites itself frequently becomes necessary in the
interest of patient comfort & to relieve restrictive lung disease caused by limitation of diaphragmatic
excursions by the ascites.
The keystone of treatment is salt restriction. Fluid restriction may also be necessary to prevent
hypokalemia. In advanced cirrhosis the renin-angiotensin-aldosterone system is almost always
stimulated, so the optimal first diuretic to use in cirrhotic patients is spironolactone (100mg/d), the
competitive aldosterone receptor blocker. Since spironolactone is a competitive blocker it requires a
few days to reach its peak effect. This effect can be observed by daily determinations of urine Na+ &
K+. When the urinary K+ exceeds the daily Na+ excretion, a loop diuretic may be added to augment
the diuresis 4 .
Alternatively, ascites may be treated by “large-volume paracentesis”, using strict aseptic techniques
while monitoring the patient’s hemodynamic status. As much as 7 liters of fluid may be withdrawn if
albumin (1 gm/kG) is infused during the procedure in order to avoid precipitation of a hypotensive
event. Large volume paracentesis may be used sequentially alone or to “jump-start” diuretic therapy.
Eventually cirrhotic patients become refractory to treatment & require TIPS or portocaval shunting for
control of the ascites (at the same time increasing risk of hepatic encephalopathy).
VII Prognosis like treatment hinges on the etiology of the ascites, comorbidities, complications & age of
the patient. The cumulative actuarial mortality of a cohort of 100 Norwegian patients with alcoholic
cirrhosis followed for 15 years was 18% at 1 month, 28% at 3 months, 36% at 6 months & 49% at one
year, 71% at 5 years, 84% at 10 years & 90% at 15 years 5 .
In that study 58% died of bleeding or hepatic encephalopathy or a combination of the two. & 11%
died of hepatocellular carcinoma. In that study the Child-Pugh class didn’t predict mortality although
it does predict mortality in most series. The Child-Pugh class is determined as shown in Table 4 & it
should be determined when cirrhosis is present. The 12 month survival of Child-Pugh Class A
patients with compensated cirrhosis is >90%, for Class B about 80% & for Class C, 35-45% 6 .
Table 4: The Child-Pugh Classification of Cirrhosis
Assessment Category Assessment Score
1 Point 2 Points 3 Points
Stage of Encephalopathy None Stage 1-2 Stage 3-4
Ascites None Mild Moderate
Total Bilirubin (mg/dL) ≤2.0 mg/dL 2.1-2.9 mg/dL≥3.0 mg/dL
Exception: Primary Biliary Cirrhosis ≤4.0 mg/dL 4.1-9.9mg/dL≥10.0mg/dL
Serum Albumin (mg/dL) <3.5mg/dL 2.8-3.5mg/dL < 2.8mg/dL
Prothrombin Time Ratio (International Normalized Ratio) < 1.4 1.4-2.0 > 2.0
Scoring:
Class A (Well Compensated) 5-6 Points. Class B (Mildly Decompensated): 7-9 Points. Class C (Decompensated) 10-15 Points.

VIII References:
1
Glickman RM, Abdominal Swelling & Ascites. Chapter 39 in Harrison’s Principles of Internal Medicine 16thEdition.
Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005 Pages 243-6.
2
McHutchison JG, Differential diagnosis of ascites. Seminars in Liver Disease. 1997;17(3):191-202.
3 th
Frank BW, Ascites Page 193 in Problem Oriented Medical Diagnosis. 7 Edition. Editor Friedman HH. Lippincott,
Williams & Wilkins, Philadelphia, PA 2001 Page 193.
4
Chung RT, Podolsky DK., Cirrhosis & its Complications. Chapter 39 in Harrison’s Principles of Internal Medicine
16thEdition. Editors: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL. McGraw-Hill NY,NY 2005
Pages 1858-69.
5
Bell H, Jahnsen J, Kittang E et al. Long term prognosis of patients with alcoholic liver cirrhosis: a 15-year follow-up study
of 100 Norwegian patients admitted to one unit. Scand J Gastroenterol. 2004;39(9):858-63.
6
Albers I, Hartmann H, Burcher J, Creutzfeldt W. Superiority of the Child-Pugh classification to quantitative liver function
tests for assessing prognosis of liver cirrhosis. Scand J Gastroenterol. 1989;24(3):269-76.