Definition |
Ascites is a detectable collection of
free fluid in the peritoneal cavity. Ascetic
fluid is derived from the vascular
compartment subserving the hepatosplanchnic
viscera.
|
|
Two factors are important in the formation
of ascites: |
1-Increase of total body sodium and
water
2- Increase of the sinusoidal portal
pressure.
|
|
Blood volume and pressure controls
|
|
|
Initial Assessment and Diagnosis |
1. History
2. Physical examination
3. Abdominal ultrasound
4. Abdominal paracentesis
5. Ascitic fluid analysis including a cell
count and differential, ascitic fluid total
protein, and serum-ascites albumin gradient
6. Culture of ascitic fluid at bedside in
blood culture bottles
|
|
Pathogenesis of ascites: |
Hepatic dysfunction and sinusoidal
portal pressure probably both send a message
to the kidney to retain excess sodium and
fluid, while the portal hypertension serves
to localize excess fluid to the peritoneal
cavity rather than the periphery. Portal
hypertension alone without hepatic
dysfunction rarely results in ascites.
The pathogenesis of ascites formation
remains controversial.
►►The "under
fill theory" proposes that ascites
occurs as a primary event. Sequestration of
fluid into the peritoneal cavity as a result
of changes in Starling's forces within the
splanchnic circulation results in a
reduction of the circulatory volume. This in
turn leads to stimulation of the sympathetic
nervous and renin-angiotensin-aldosterone
systems, which promote renal sodium and
water retention.
►►The
"overflow theory" on the other hand,
proposes that renal sodium retention occurs
as a primary event. This may be due to the
increased production of a sodium-retaining
factor or the reduced synthesis of a
natriuretic factor by the diseased liver.
The circulatory volume is expanded. In the
presence of abnormal Starling's forces in
the splanchnic circulation, the retained
fluid is preferentially localized to the
peritoneal cavity as ascites.
►►More recently,
"the peripheral arterial vasodilation
hypothesis" which encompasses features
of both the underfill and overflow theories,
was put forward. It proposes that in
cirrhosis, arterial vasodilation leads to a
decrease in splanchnic and systemic vascular
resistance with pooling of blood in the
splanchnic circulation, leading to a
reduction in the effective arterial blood
volume. This in turn activates neurohumoral
pressor systems, promoting renal sodium and
water retention in an attempt to restore the
effective arterial blood volume and maintain
blood pressure. When increased renal sodium
reabsorption cannot compensate for the
arterial vasodilation, arterial underfilling
occurs. Then the cascade of further
activation of various neurohumoral pressor
systems leading to increased sodium
retention begins, and ultimately ascites is
formed.
Arterial vasodilation is also responsible
for the hyperdynamic circulation that is
often evident in cirrhosis. This clinically
manifests as:
►Increased
cardiac output
►Bounding pulse
►Wide pulse
pressure
►Systemic
hypotension
Locally produced vasodilators may be
responsible.
►►More
recently, it has been proposed that chronic
endotoxemia associated with cirrhosis may
stimulate the synthesis and release of a
potent endothelin-derived relaxing factor,
nitric oxide, resulting in splanchnic and
systemic vasodilation.
|
|
Signs and Symptoms: |
Clinically, the first evidence of ascites is
an increase in abdominal girth accompanied
by weight gain. Peritoneal fluid of less
than 2 L is difficult to detect clinically,
and ultrasound is useful in defining small
amounts of ascites. The patient is sallow
and intravascularly depleted. Muscle wasting
is profound. The abdomen is distended, often
with fullness in the flanks and an everted
umbilicus. Scrotal edema is frequent.
Distended abdominal wall veins that radiate
from the umbilicus represent the presence of
portal-systemic collaterals. The earliest
sign of ascites is dullness to percussion in
the flanks. Shifting dullness and a fluid
thrill mean that more fluid is present.
A pleural effusion is found in a small
percentage of patients with ascites, usually
on the right side. This is due to the
presence of a diaphragmatic defect that
allows ascitic fluid to pass into the
pleural cavity.
|
|
Examintation
& Laboratory Tests |
Examination of ascitic fluid by diagnostic
paracentesis should be performed at first
presentation, or when there is alteration of
the patient's clinical state, such as a
sudden increase in the amount of ascitic
fluid, worsening of encephalopathy or
presence of fever.
The purpose of the examination is to rule
out other complications such as:
►Spontaneous
bacterial peritonitis
►Tuberculosis
►Hepatocellular
carcinoma.
Ascitic fluid analysis should include:
►Total
polymorph count
►Protein and
albumin concentrations
►Direct
inoculation of at least 10 mL of ascitic
fluid each into blood culture bottles at the
bedside, as this increases the positive
culture yield.
Results:
►A
serum-ascitic fluid albumin gradient >
11 g/L represents cirrhotic rather than
malignant ascites.
►A high protein content may be associated with the Budd-Chiari Syndrome or seen in pancreatic ascites.
►A total
polymorph count
> 250/µL is diagnostic of spontaneous
bacterial peritonitis. |
|
|
|
Although bed rest will result in a
redistribution of body fluid, fluid and salt
restriction is required to mobilize the
ascites.
►The patient is usually prescribed a
no-added-salt diet containing 2 g (100 mmol)
sodium/day, and monitored carefully with
daily weights.
►Measurement of abdominal
girth is unreliable, as gaseous distention
is common.
Too rapid mobilization of fluid
will result in worsening of renal function;
one should aim at a weight loss of 0.5
kg/day. Patients with peripheral edema can
have their fluid mobilized more rapidly, as
the edema fluid can easily be absorbed to
replenish the intravascular volume.
Diuretic therapy is usually required in
addition to salt and fluid restriction. The
potassium-sparing diuretic
spironolactone
can be given in a single daily dose,
starting at a dose of 100 mg/day, and may be
increased by 100 mg per week up to 400
mg/day if the response is inadequate.
Spironolactone has a slow onset of action,
and therefore frequent dose adjustments are
unnecessary. Its half-life in cirrhotic
patients can be as long as 10 days;
therefore, it also has a slow offset of
action and patients should still be
monitored after
spironolactone is
discontinued. One of its unacceptable side
effects is painful gynecomastia. Other
potassium-sparing diuretics, such as
amiloride and triamterene, are less potent
but acceptable alternatives.
If there is no
diuretic response and the patient is
compliant with the sodium intake, a loop
diuretic such as
furosemide is added.
Electrolyte abnormalities are common with
diuretic therapy and should be monitored
regularly. Hypokalemia and hypochloremic
alkalosis can precipitate
encephalopathy.
Too rapid diuresis can lead to azotemia and hepatorenal syndrome.
|
|
NEXT |
