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177

Section 7: Digestive system

Chapter 177

Ascites

DEFINITION

DIFFERENTIAL DIAGNOSIS

Ascites is the accumulation of excess uid in the peritoneal cavity, most commonly caused by liver cirrhosis.

CLINICAL PRESENTATION

Important information to elicit within history:


Viral hepatitis
Alcoholism
Increasing abdominal girth, umbilical hernia (Fig. 1771)
Increasing lower extremity edema
Intravenous drug use
Sexual history (i.e., men who have sex with men)
History of transfusions
Important physical examination ndings:
Bulging anks
Flank dullness to percussion
Fluid wave on abdominal examination (Fig. 1772)
Lower extremity edema
Shifting dullness succusion splash (see Fig. 1772) on
abdominal examination
Physical signs associated with liver cirrhosis: spider angiomas (see Fig. 1764), jaundice (see Fig. 1762), loss of
body hair, Dupuytrens contracture (see Fig. 30411),
muscle wasting, bruising, palmar erythema, gynecomastia
(see Fig. 2842), testicular atrophy, hemorrhoids (see Fig.
1691), caput meduse (see Fig. 1766)

CAUSE

Pathophysiology of ascites: increased hepatic resistance to portal ow leads to portal hypertension. The splanchnic vessels
respond by increased secretion of nitric oxide causing splanchnic artery vasodilation. Early in the disease increased plasma
volume and increased cardiac output compensate for this vasodilation. However, as disease progresses the effective arterial
blood volume decreases causing sodium and uid retention
through activation of the renin-angiotensin system. The change
in capillary pressure causes increased permeability and retention of uid in the abdomen.

LABORATORY TESTS

Initial evaluation should always include:


Diagnostic paracentesis. Laboratory tests on this uid
should include a CBC with differential, albumin, total protein, culture and a Gram stain. Optional tests on paracentesis uid (depending on patients history) include amylase,
LDH, acid-fast bacilli and glucose levels
AST, ALT, total and direct bilirubin, albumin, alkaline
phosphatase, GGTP
CBC, coagulation studies
Electrolytes, BUN, creatinine
A serum to ascites albumin gradient (SAAG) should be calculated in all patients. If the SAAG is greater than 1.1, the cause
of ascites can be attributed to portal hypertension. If SAAG is
less than 1.1, a nonportal hypertension etiology of ascites must
be sought.
IMAGING STUDIES

Endoscopy of the upper GI tract to evaluate for esophageal


varices if ascites is secondary to portal hypertension.
Abdominal ultrasound is the most sensitive measure for
detecting ascitic uid; a CT scan is a viable alternative (Fig.
1773).

Fig 1771

Fig 1772

Ascites with umbilical hernia.

Succusion splash technique for assessing distention of abdominal


viscera.

(From Swartz MH: Textbook of Physical Diagnosis, 5th ed. Philadelphia,


WB Saunders, 2006.)

620

Chronic parenchymal liver disease, leading to portal hypertension


Peritoneal carcinomatosis
Congestive heart failure
Peritoneal tuberculosis
Nephrotic syndrome
Pancreatitis

(From Swartz MH: Textbook of Physical Diagnosis, 5th ed. Philadelphia,


WB Saunders, 2006.)

Chapter 177: Ascites

177

Fig 1773
Ascites. On a plain lm of the abdomen (A), only gross amount of ascites (a) can be identied. This is usually seen, because the ascites have
caused a rather gray appearance of the abdomen and pushed the gas-containing loops of small bowel (SB) toward the most nondependent and
central portion of the abdomen. A transverse computed tomography scan (B) shows a cross-sectional view of the same appearance with the airand contrast-lled small bowel (SB) oating in the ascitic uid (A).
(From Mettler FA, Guibertau MJ, Voss CM, Urbina CE: Primary Care Radiology. Philadelphia, Elsevier, 2000.)

Liver biopsy in select patients (i.e., those with portal hypertension of uncertain etiology).

TREATMENT

Sodium-restricted diet (maximum 60-90 milliequivalents


per day).
Fluid restriction to 1 liter per day in patients with hyponatremia.
Patients with moderate-volume ascites causing only moderate discomfort may be treated on an outpatient basis with
the following diuretic regimen: spironolactone 50-200 mg
daily or amiloride 5-10 mg daily. Add furosemide 20-40 mg
per day in the rst several days of treatment, monitoring
renal functions carefully for signs of prerenal azotemia (in
patients without edema goal weight loss is 300-500 grams/
day, in patients with edema 800-1000 grams/day).
Patients with large-volume ascites causing marked discomfort or decrease in activities of daily living may also be
treated as outpatients if there are no complications. There
are two options for treatment in these patients: (1) largevolume paracentesis or (2) diuretic therapy until loss of
uid is noted (maximum spironolactone 400 mg daily and
Lasix 160 mg daily). There is generally no difference in longterm mortality; however paracentesis is faster, more effective, and associated with fewer adverse effects.
Five percent to 10% of patients with large-volume ascites will
be refractory to high-dose diuretic treatment. Treatment strategies include repeated large-volume paracentesis with infusion of albumin every 2-4 weeks or placement of a transjugular intrahepatic portosystemic shunt (TIPS) (Fig. 1774).

Fig 1774
Transjugular intrahepatic portosystemic stent-shunt (TIPS). An intrahepatic tract has been created between the right hepatic vein and the
right portal vein. The tract is dilated and stented, creating a shunt as
demonstrated on shuntogram. (Courtesy of Dr. W. K. Tso.)

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