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 Ascites and its complications

ROBERT M. STRAUSS AND JULES L. DIENSTAG

Definition: The term ascites denotes the presence of excessive fluid in the peritoneal cavity.

CLASSIFICATION OF ASCITES AND DIFFERENTIAL DIAGNOSIS

Ascites may be caused by hepatic, renal, or cardiac decompensation; by hepatic venous outflow obstruction; and by malignant, inflammatory, or infectious processes in the peritoneum. (table1_classification_ascites) 378.

Differential diagnosis: Ascites is not the only cause of marked abdominal swelling.

 may be confused with ascites.

PATHOGENESIS

Normally, there is just enough free fluid in the peritoneal cavity to lubricate the peritoneal surfaces. Ascites occurs when there is an imbalance of factors that favour the flow of fluid from the vascular space or when there is exudation of fluid through infection or malignant implantation on the peritoneum, and represents a state of excess total body sodium. Normally, the higher pressure at the arteriolar end of the capillary allows passage of fluid without protein into the pericapillary space, while reabsorption takes place at the venous end of the capillary where hydrostatic pressure is lower than oncotic pressure. In cirrhosis, portal venous hypertension increases the filtration pressure at the capillary level with transudation of fluid, while low albumin levels decrease vascular oncotic pressure.

Two potential mechanisms have been proposed to explain the pathogenesis of Ascites:

    I.The underfilling hypothesis suggests that the primary abnormality is a sequestration of fluid within the splanchnic vascular bed secondary to portal hypertension and reduced oncotic pressure. These events cause a decrease in effective circulating blood volume, which leads to compensatory renal retention of sodium by increasing aldosterone production.

II.The  overflow hypothesis  suggests that renal dysfunction (perhaps mediated by a hepatorenal reflex) is the primary event leading to sodium and water accumulation in the absence of intravascular volume depletion. This hypothesis is supported by the fact that acute constriction of the portal vein in dogs is associated with renal vasoconstriction, renal sodium and water retention, and renin stimulation. Not all data, however, substantiate the  overflow  hypothesis. For example, patients with decompensated cirrhosis show an activation of the sympathetic nervous and renin-angiotensin-aldosterone systems and non-osmotic release of vasopressin, which should be suppressed, not stimulated, by renal sodium and water retention with volume expansion.

III.A new hypothesis that integrates the underfill and overfill hypothesis into one is that of peripheral arterial vasodilation. The underlying assumption of this hypothesis is that patients have peripheral vasodilation as a consequence of arteriovenous shunts in the splanchnic, dermal, and pulmonary circulations. The peripheral vasodilation that accompanies arteriovenous shunts causes renal sodium retention. Because sodium retention may not be sufficient to fill the enlarged vascular compartment, renin, angiotensin, aldosterone, and vasopressin are not suppressed.

CLINICAL FEATURES

Patients may initially not be aware of the presence of fluid within the abdomen. As the amount increases, the patient may become aware of

. Tense ascites may be associated

Physical examination of patients with massive ascites reveals

By inspection:

On palpation:

Smaller amounts of fluid (in excess of 120 ml) may be detected by eliciting

. When massive ascites is present, it is not uncommon to find

Investigations:

1.    Ultrasonography and computed tomography can detect as little as 30 ml of ascitic fluid.

Even routine plain radiographs of the abdomen may be helpful, demonstrating

2.    Examination of the ascitic fluid (Diagnostic paracentesis)

1)    Traditionally, the concentration of protein in the ascitic fluid and the ascites: serum lactate dehydrogenase ratio are used to determine whether the ascites is exudative (protein ›2.5 g/100 ml, ascites serum lactate dehydrogenase ratio ›0.6) or transudative (protein <2.5 g/100 ml, ascites serum lactate dehydrogenase ratio <0.6). Unfortunately, the distinction between exudative and transudative ascites is not absolute.

2)    Ascitic fluid white blood and differential counts should be determined. An absolute count lower than 250 polymorphonuclear cells/mm³; usually denotes uninfected ascites, while counts of above this suggest infection.

3)    Cytology and bacteriological analysis should also be performed.

4)    Chylous ascites refers to a milky or creamy appearance of peritoneal fluid resulting from the presence of thoracic or intestinal lymph.

MANAGEMENT

Some patients may respond to simple measures, while others may require a series of therapeutic approaches that will be only palliative. Generally speaking, the more advanced the liver disease, the worse the prognosis, and, therefore, the less effective therapy will be.

Medical management

General measures

Attempts to improve liver function are worthwhile: patients should abstain from alcohol and receive optimal nutrition. Bedrest is usually recommended but is of little practical value. The theoretical benefit of bedrest derives from the fact that an upright posture activates the renin-angiotensin-aldosterone and α-adrenergic systems. Sodium intake should be restricted to 1.5 to 2 g day. In cirrhotic patients with ascites, prostaglandins are helpful in preserving renal function by maintaining glomerular filtration rate and free water clearance. Administration of drugs that inhibit prostaglandin synthetase, such as non-steroidal anti-inflammatory drugs, should be avoided in such patients.

Diuretics

Most patients require diuretic therapy. However, excessive diuresis may result in azotaemia, hyponatraemia, encephalopathy, and hepatorenal syndrome.

Aldosterone antagonists

·  Spironolactone is an aldosterone antagonist that promotes natriuresis and potassium retention. The initial dose ranges from 50 to 200 mg/day given in two or four doses. Theoretically, there is no absolute dose limit; however, hyperkalaemia and azotaemia usually prevent unlimited dose escalation. If spironolactone causes hyperkalaemia, a potassium-wasting diuretic can be added.

Amiloride is another potassium sparing diuretic which, although not an aldosterone antagonist, has been used successfully to treat ascites. It increases renal excretion of sodium and chloride without significantly affecting the glomerular filtration rate.

Loop diuretics

These agents act by increasing the delivery of sodium to the distal tubule, where ability to reabsorb sodium is exceeded.

·  Frusemide and an initial dose of 20 mg/day may be sequentially increased, especially in patients with peripheral oedema. Loop diuretics should be used as supplements to spironolactone, not as the primary diuretic. Hypokalaemia may develop, despite administration of potassium-sparing diuretics, and hyponatraemia may also develop or worsen. Metabolic alkalosis and hepatic encephalopathy are other potential complications.

Thiazide diuretics: These are usually ineffective when given alone, and they may increase renal production of ammonia; they can, however, be used in conjunction with spironolactone either to reduce potassium retention or to provide a synergistic effect.

Large volume paracentesis

 Large volume paracentesis is associated with intravenous albumin infusion is a fast, effective, and safe treatment for cirrhotic ascites. In general, patients undergoing paracentesis have a shorter hospital stay than those treated with diuretics.

Complications of paracentesis include

However, these complications are rare in experienced hands.

Surgical management

Peritoneovenous shunt

It is a pressure activated one-way valve. One limb of the shunt lies free in the peritoneal cavity, and the venous opening of the efferent limb inserts into the superior vena cava near its entrance into the right atrium. Flow in the shunt is maintained if there is a 3 to 5 cm H&sub2;O pressure gradient between the valve and its venous end. If the gradient falls below this level, the valve closes, preventing blood from flowing back into the shunt tubing.

Early complications of peritoneovenous shunts

Late complications are

At least half of the patients will experience one or more complications.

This procedure is contraindicated in patients with sepsis, heart failure, and active peritonitis. The best results are obtained in a limited subset of patients with diuretic-resistant ascites but relatively well preserved hepatic function.

Portasystemic shunts

Use of portasystemic shunts for treatment of cirrhotic ascites is warranted only in those patients in whom all other forms of therapy have failed. The shunt operation that is most effective at relieving ascites has not been established; in fact, ascites is reduced after any type of portasystemic shunt as a consequence of decreased portal flow and decreased intrahepatic congestion. They include splenorenal and portacaval. The side-to-side portacaval shunt, which decompresses both the splanchnic and hepatic sinusoidal beds, is very effective in relieving ascites; it is the decompressive shunt of choice for the treatment of ascites in the Budd-Chiari syndrome (when hepatic function is well-preserved).

Transjugular intrahepatic portasystemic shunt (TIPS)

Angiographically guided insertion of a metal stent between an intrahepatic hepatic vein and portal vein has been used to reduce portal hypertension in patients with bleeding oesophageal varices. Such transjugular intrahepatic portasystemic shunts (TIPS) have been shown to relieve intractable ascites as well.

Liver transplantation

Liver transplantation is the treatment of choice for patients with liver failure and otherwise intractable ascites, unless contraindications exist.

SPONTANEOUS BACTERIAL PERITONITIS

Definition: infection of ascites fluid in the absence of any obvious intraabdominal source. It is an important complication of ascites.

Pathogenesis

Spontaneous bacterial peritonitis can occur in patients with ascites of any cause; the mechanisms underlying it remain unknown. Plausible contributing factors include

Bacteriology

A single organism is the cause of over 90 per cent of cases. The most common organisms are Escherichia coli and Streptococcus species; other organisms may also be implicated.

Diagnosis

This requires not only an awareness of the presenting symptoms and signs but also a high index of suspicion in any patient with ascites and clinical deterioration. Spontaneous bacterial peritonitis can vary in its presentation from being clinically dramatic to totally asymptomatic.

Clinical features:

Once the diagnosis is entertained, paracentesis is indicated, for both curative & diagnostic purposes. To increase the likelihood of a positive ascites fluid culture, the operator should inoculate 10 ml of ascitic fluid directly into blood culture bottles at the bedside.Bedside  inoculation increases the sensitivity of ascites culture and decreases the time between inoculation of the culture and appearance of bacterial growth.

The diagnosis of spontaneous bacterial peritonitis is based on a

Hallmarks of  surgical  peritonitis include

Treatment: Once a presumptive diagnosis of spontaneous bacterial peritonitis has been made, prompt and appropriate intravenous antibiotic therapy should be instituted, long before culture results are known, and even if cultures are negative

1.    . Empirically, a third-generation cephalosporin should be used. Treatment should continue for 10 to 14 days, although, shorter duration therapy with third-generation cephalosporins is effective.

N.B.: Aminoglycosides should be avoided; they are associated with a high risk of nephrotoxicity and have unpredictable distribution in cirrhotics.

2.    Repeated paracentesis in 48 h may be helpful.

3.    Prophylaxis with daily quinolone therapy has been shown to reduce the frequency of recurrent spontaneous bacterial peritonitis.

HEPATORENAL SYNDROME

Progressive  functional  renal failure occurs in patients with advanced liver disease, all of whom have decompensated cirrhosis, and most of whom have tense ascites. The kidneys are anatomically and histologically normal; if hepatic deterioration is reversed, for example by liver transplantation, the renal failure is also reversible.

Pathology:

i)     Altered renal blood flow appears to be the primary abnormality. There is vasoconstriction of arterioles of the outer renal cortex with shunting of blood to the renal medulla, which results in decreased glomerular filtration rate and urine flow.

ii)  These abnormalities are probably a result of decreased  effective  blood volume and sympathetic overdrive.

iii)     Accumulation of false neurotransmitters at nerve endings has also been proposed.

iv) Derangements in the renin-angiotensin and in the kallikrein-kinin system as well as altered synthesis of renal prostaglandins, vasoactive intestinal peptide, and endotoxins are also thought to be involved in the pathogenesis of the hepatorenal syndrome.

Diagnosis the typical features are

Note: Oliguria may occur spontaneously but usually follows

 To establish this diagnosis, decreased intravascular volume must be excluded by fluid loading.

Treatment

There is no effective therapy for hepatorenal syndrome; however, precipitating factors should be eliminated. Diuretics should be withheld, blood volume replaced, serum electrolyte abnormalities corrected, infections treated promptly, and drugs known to inhibit prostaglandin synthesis as well as other nephrotoxic drugs discontinued.

A fluid challenge to increase effective plasma volume should be attempted; a combination of saline and salt-poor albumin should be administered while close monitoring.. Numerous vasodilatory drugs (e.g. phentolamine, papaverine, metaraminol, phenoxybenzamine) have also been administered. If the liver disease is reversible (for example, fulminant hepatitis), dialysis may be helpful, but dialysis is of no value in patients with end-stage chronic liver disease. Recovery from hepatorenal syndrome has been reported anecdotally following portasystemic shunts and liver transplantation. Occasionally peritoneovenous shunting reverses the hepatorenal syndrome.

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Thompson JE, Forlenza S, Verna R. Amoebic liver abscess: a therapeutic approach. Rev Infect Dis