Ascites

Definition

Accumulation of fluid within the peritoneal cavity. Small amounts may be

asymptomatic; increasing amounts cause abdominal distention and discomfort,

anorexia,nausea,early satiety, heartburn, flank pain, and respiratory distress.

Detection

PHYSICAL EXAMINATION Bulging flanks,fluid wave, shifting dullness,“

puddle sign” (dullness over dependent abdomen with pt on hands and

knees). May be associated with penile or scrotal edema,umbilical or inguinal

herniation,pleural effusion. Evaluation should include rectal and pelvic examination, assessment of liver and spleen. Palmar erythema and spider angiomata seen in cirrhosis. Periumbilical nodule (Sister Mary Joseph’s nodule) suggests metastatic disease from a pelvic or GI tumor.

ULTRASONOGRAPHY/CT Very sensitive; able to distinguish fluid

from cystic masses.

Evaluation

Diagnostic paracentesis (50–100 mL) essential. Routine evaluation includes

inspection,protein,albumin,glucose, cell count and differential, Gram’s and

acid-fast stains,culture, cytology; in selected cases check amylase, LDH, triglycerides, culture for TB. Rarely,laparoscopy or even exploratory laparotomy

may be required. Ascites due to CHF (e.g.,pericardial constriction) may require

evaluation by right-sided heart catheterization.

DIFFERENTIAL DIAGNOSIS More than 90% of cases due to cirrhosis,

neoplasm,CHF,tuberculosis.

1. Diseases of peritoneum: Infections (bacterial,tuberculous, fungal, parasitic),

neoplasms,connective tissue disease, miscellaneous (Whipple’s disease,

familial Mediterranean fever,endometriosis, starch peritonitis, etc.).

2. Diseases not involving peritoneum: Cirrhosis,CHF,Budd-Chiari syndrome,

hepatic venocclusive disease, hypoalbuminemia (nephrotic syndrome,

protein-losing enteropathy,malnutrition), miscellaneous (myxedema, ovarian

diseases,pancreatic disease,chylous ascites).

PATHOPHYSIOLOGIC CLASSIFICATION USING SERUMASCITES

ALBUMIN GRADIENT Difference in albumin concentrations between serum and ascites as a reflection of imbalances in hydrostatic pressures:

1. Low gradient (serum-ascites albumin gradient _1.1): 2_ bacterial peritonitis,

neoplasm, pancreatitis, vasculitis, nephrotic syndrome.

2. High gradient (serum-ascites albumin gradient _1.1 suggests ascites is

due to portal hypertension): cirrhosis,CHF, Budd-Chiari syndrome.

REPRESENTATIVE FLUID CHARACTERISTICS See Table 55-1.

CIRRHOTIC ASCITES

PATHOGENESIS Contributing factors: (1) portal hypertension,(2) hypoalbuminemia,(

3) hepatic lymph,(4) renal sodium retention—secondary to

hyperaldosteronism,increased sympathetic nervous activity (renin-angiotensin

production). Initiating event may be peripheral arterial vasodilation triggered

by endotoxin and cytokines and mediated by nitric oxide; results in decreased

“effective” plasma volume and activation of compensatory mechanisms to retain

renal Na and preserve intravascular volume.

TREATMENT

Maximum mobilization _700 mL/d (peripheral edema may be mobilized

faster).

1. Rigid salt restriction (400 mg Na/d).

2. Fluid restriction of 1–1.5 L only if hyponatremia.

3. Diuretics if no response to salt restriction after 1 week or if urine Na

concentration _25 meq/L; spironolactone (mild,potassium-sparing, aldosterone-

antagonist) 100 mg/d PO increased by 100 mg q4–5d to maximum

of 400 mg/d; furosemide 40–80 mg/d PO or IV may be added if

necessary (greater risk of hepatorenal syndrome,encephalopathy), can

increase by 40 mg/d to maximum of 160 mg/d until effect achieved or

complication occurs.

4. Monitor weight,urinary Na and K, serum electrolytes, and creatinine.

5. Repeated large-volume paracentesis (5 L) with IV infusions of albumin

(10 g/L ascites removed) is preferable for initial management of massive

ascites because of fewer side effects than diuretics.

6. In refractory cases,consider transjugular intrahepatic portosystemic shunt

(TIPS),though 20–30% risk of encephalopathy and high rate of shunt

stenosis and occlusion. Peritoneovenous (LeVeen,Denver) shunt (high

complication rate—occlusion,infection, DIC) and side-to-side portacaval

shunt (high mortality rate in end-stage cirrhotic pt) have fallen out of

favor. Consider liver transplantation in appropriate candidates (Chap.

157).

Complications

SPONTANEOUS BACTERIAL PERITONITIS Suspect in cirrhotic pt

with ascites and fever,abdominal pain,worsening ascites, ileus, hypotension,

worsening jaundice,or encephalopathy; low ascitic protein concentration (low

opsonic activity) is predisposing factor. Diagnosis suggested by ascitic fluid

PMN cell count _250/_L and symptoms or PMN count _500/_L; confirmed

by positive culture (usually Enterobacteriaceae,group D streptococci, Streptococcus pneumoniae, S. viridans). Initial treatment: Cefotaxime 2 g IV q8h;

efficacy demonstrated by marked decrease in ascitic PMN count after 48 h; treat

5–10 days or until ascitic PMN count is normal. Risk of recurrence can be

reduced with norfloxacin 400 mg PO qd,trimethoprim-sulfamethoxazole 1 double-

strength PO bid 5 days a week,or possibly ciprofloxacin 750 mg PO once a week. Consider prophylactic therapy (before first episode of peritonitis) in pts

with cirrhotic ascites and an ascitic albumin level _10 g/L (_1 g/dL).

HEPATORENAL SYNDROME Progressive renal failure characterized

by azotemia,oliguria with urinary sodium concentration _10 mmol/L,hypotension,

and lack of response to volume challenge. May be spontaneous or

precipitated by bleeding,sepsis, excessive diuresis or paracentesis. Thought to

result from altered renal hemodynamics. Prognosis poor. Treatment: Trial of

plasma expansion; TIPS of doubtful benefit; liver transplantation in selected

cases.