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Liver ascites

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.

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