Revista de Gastroenterología del Perú - Volumen 18, Nº2 1998

Ascites in Hepatic Círrhosis : Recognition, investigation and treatment

Ha Shoh*, N D C Finlayson*



La cirrosis hepática es la causa más común de ascitis. Es causada por insuficiencia hepática que lleva a cambios complejos renales y circulatorios interrelacionados, que resultan en retención de sodio y agua e hipertensión portal, localizandoel sodio y el agua en el peritoneo. La ascitis es una complicación importante de la cirrosis, que implica generalmente un pobre pronóstico a largo plazo. La investigación de la ascitis es importante, porque no siempre se debe a cirrosis, puede ser la consecuencia de complicaciones de esta, tales como carcinoma hepatocelular y puede estar asociado con infección, la cual es fatal, si no es tratada. La mayoría de pacientes responden a tratamiento con restricción de sodio y diuréticos. Este tratamiento toma tiempo y cada vez más médicos recurren a la paracentisis terapéutica con restricción de sodio y uso de diuréticos para prevenir la recurrencia de la ascitis. La paracentesis sin embargo no está libre de complicaciones, por lo que es particularmente importante dar coloides como reemplazo, para prevenirla hipovolemia que puede llevara insuficiencia renal. Los pacientes que no responden a este tratamiento pueden ser ayudados con un procedimiento de TIPS ó un shunt peritoneo venoso. Sin embargo esos pacientes tienen una función hepática muy pobre y se considerará la posibilidad del transplante hepático. La infección es una complicación muy seria de la ascitis (peritonitis bacteriana espontánea) y generalmente tiene un pobre pronóstico. La profilaxis antibiótica es importante para prevenir la recurrencia y se considerará el transplante hepático.

Palabras clave: Ascitis, cirrosis, detección, diagnóstico, pronóstico, complicaciones, tratamiento.


Hepatic cirrhosis is the most common cause of ascites. It is caused by liver failure leading to complex interrelated circulatory and renal changes resulting in retention of sodium and water and portal hypertension localising that sodium and water in the peritoneum. Ascites is an important development in cirrhosis as it implies a generally poor long term prognosis. Investigation is important as ascites is not always dueto cirrhosis, may bethe consequence of complications of cirrhosis such as hepatocellular carcinoma, and may be associated with infection which is fatal if untreated. Most patients respond to treatment with sodium restriction and diuretic drugs. This treatment takes time, and increasingly doctors use therapeutic paracentesis with sodium restriction and diuretics to prevent recurrence of ascites. Paracentesis, however, is not without complications, and it is particularly important to give colloid replacement to prevent hypovolaemia which can lead to renal failure. Patients who do not respond to this treatment may be helped by a TIPSS procedure or a peritoneovenous shunt. However, these patients usually have very poor liverfunction and the possibility of fiver transplantation should be considered. Infection is a very serious complication of ascites (spontaneous bacterial peritonitis) and carries a generally poor prognosis.Antibiotic prophylaxis is important to prevent recurrence and liver transpiantation shoulcl be considered.

Key words: Ascites, cirrhosis, detection, diagnosis, prognosis, complications, treatment.

Rev. Perú Gastroenterol. 1998; 18 (2): 135-44


Ascites, free fluid in the peritoneal cavity, indicates the presence of serious disease. Chronic liver disease is the most common cause of ascites and it is always a sign of acívanced liver damage. This paper considers the ascites of chronic liver disease, including its detection, diagnosis, prognosis, complications and treatment.


Ascites in hepatic cirrhosis develops because of a considerable increase of total body sodium and water, and portal hypertension which localises much of that sodium and water to the peritoneal cavity (Arroyo et al 1988).

Sodium and water retention

Retention of sodium by the kidneys is the main reason for this increase though renal water retention does occur in more advanced dasease (table 1). Renal excretion is the means whereby the body rids itself of excess sodium, and normal urinary excretion varies widely in relation to sodium intake, Marked renal sodium retention, however, is characteristic in hepatic cirrhosis and ascites; the total daily excretion of sodium in such patients is usually less than 10 mmol/24 hours and in severe cases no sodium can be detected in the urine. Water retention occurs primarily as a consequence of sodium retention. Three general theories have been proposed to explain renal retention of sodium in hepatic cirrhosis (Ring-Larsen and Henriksen, 1986). One suggests that portal hypertension causes a loss of fluid into the peritoneun and leads to depletion of the intravascular volume (underfilling theory) with secondary and compensatory renal retention of sodium and water; another suggests that the fiver disease itself causes primary renal sodium and water retention leading to expansion of the vascular volume and hence the ascites (overflow theory); a third theory proposes a primary circulatory derangement resulting in a reduced effective arterial plasma volume with consequent renal retention of sodium and water (Henriksen et al 1989). The mechanisms underlying these theories are complex, poorly understood, and beyond the scope of this paper as they do not yet have important implications for the management of hepatic ascites. All, however, are associated with poor liver function and include activation of the renin-angiotensin-aldosterone system with high plasma and urine aldosterone, increased sympathetic activity possibly via a hepatorenal reflex arc, and the actions of such agents as arterial natriuric peptide, kallikrein-kinin prostaglandins, nitrous oxide, endothelin, and endotoxin. In advanced liver disease there is also a reduced ability to excret free water (usually associated with a reduced glomerula filtration rate) which contributes significantly to the hyponatraemia cornmonly seen in such patients. As would expected, impaired free water clearance is associated with hyponatraemia and a poor prognosis (Table 2)


Renal sodium retention
Renal water retention 
Portal hypertension    
Poor liver function      


Free Water
(<130 nmol/L)
Died in Hospital p
< 1 17 13 11(65%) < 0.05
> 1 38 3 4(11%)


Portal Hypertension and Ascites

Portal hypertension is caused primarily by an increased resistance to blood flow which, in hepatic cirrhosis, occurs in the hepatic parenchyma. In addition, there is an increased portal blood flow which acts to maintain and aggravate portal hypertension (Bosch et al 1992 ). These factors cause an increased filtration pressure in the hepatic sinusoids and in the mesenteric capillaries leading to increased passage of fluid into the peritoneal cavity (Witte et al 1971). Initially, this increased fluid is removed by the lymphatics; the thoracic duct flow of lymph is normally 60120 ml/hr and it is increased 5-10 times in portal hypertension due to hepatic cirrhosis. Once the transport capacity of the lymphatics is exceeded fluid accumulates in the peritoneal cavity and eventually ascites becomes evident. It is notable that the rate of passage of fluid into the peritoneum is low and is normally less than 5% of that passing to the thoracic duct ( Henriksen and Ring-Larsen 1984 ). Most of the peritoneal fluid originates from the hepatic sinusoids which are high1y permeable and produce protein-rich interstitial fluid explaining the high ascites protein content in acute obstruction of the hepatic venous outflow ( e.g.acute Budd Chiari syndrome ) and in many cases of ascites due to heart failure. The hepatic sinusoids become 'capillarised', (by connective tissue) progressively in hepatic cirrhosis and are less permeable which accounts for the generally low protein content of ascites in this condition.

'Capillarisation', however, is variable and the ascites protein is not always low in hepatic cirrhosis.

The mesenteric capillaries also contribute to ascites and produce interstitial fluid with a low protein content as in other arts of the body (Witte et al 1971). Local diseases in the peritoneal cavity such as TB, malignant disease,and pancreatitis, damage capillaries and produce protein-rich ascites (exudates).


Clinically evident ascites causes abdominal distention and bulging of the flanks. Three bedside signs have been advocated for determining that these appearances are due to ascites. The most widely used is "shifting clullness". The "puddle sing" is said to be able to detect as little as 120 ml of ascites (Lawson and Weissbein 1959), and a "fluid thrill" is considered very specific. It is, however, important to be realistic and recognise the limitations and practicality of these clinical signs. Cattau et al (1982) have shown that clinical examination detects peritoneal fluid in only a half of patients with less than a litre of ascites (Table 3).


Sign Sensitivity(%) Specificity(%)
Bulging flanks 78 44
Frank dullness 94 29
Shifting dullness 83 56
Fluid wave 50 82
Puddle sign 55 51
Sensitivity=true positive/total with ascitesx100
Sensitivity=true negative/total with ascitesx100


They found that bulging and dullness in the flanks and shifting dullness were most sensitive but of limited specifity, that a fluid thrill was specific but of limited sensitivity, and that the puddle sign in their hands was of very limited value. In practice, shifting dullness is the sign most used though it generally requires the presence of more than a litre of fluid and probably more in obese patients. The puddle sign is little used, and the fluid thrill is an interesting observation in patients with ascites visible even to the casual observer.

Lack of flank dullness is useful as it makes ascites very unilikely.

Ascites can give rise to a number of secondary abdominal features including umbilical eversion, herniae, pale abdominal striae, scrotal oedema, and meralgia paresthetica from entrapment of the lateral cutaneous nerve of the thigh . Mechanical effects on the chest impair cardiopulmonary function and can cause dyspnoea which is relieved by removal of the ascites (Table 4). Pleural effusion and hydrothorax can also occur (below).



Ascites can often be detected confidently from clinical examination, but in some cases the findings are equivocal usually because the amount of ascites is small or the patient is obese. In these circumstances, ultrasonography is a good noninvasive means of confirming ascites. Ultrasonography is particularly useful in identifying small amounts of ascites as it can detect as little as 100 mI of free peritoneal fluid (Goldberg et al 1970), and in such cases it allows the aspiration of fluid for analysis.

Observation Paracentesis
Before After*
Cardiac Ouput (L/min) 4.7 +/- 0.5 5.9 +/- 0.2
Right atrial pressure(mm Hg) 10 +/- 4.5 5 +/- 2.2
Total lung capacity(L) 5.1 +/- 1.2 5.7 +/- 1.3
Functional residual capacity(L) 2.5 +/- 0.9 3.0 +/- 1.0
Intra-abdominal pressure(mm Hg) 18 +/- 3.8 10 +/- 4.2
*p<0.03 after removal of 3-5 L ascities



Ascites in cirrhosis is usually clear and straw or light green in colour, but it can also be cloudy, bloo -stained chylous or bile -stained.


Cloudy or slightly or opaque ascites suggests the presence of infection (below) and indicates the need for an immediate ascites polymorphonuclear leucocyte cell count. Ascitic fluid and blood culture shoulcl also be done (below).


Blood-stainedascites (haemoperitoneum) in hepatic cirrhosis is uncommon and occurs in only about 5% of patients ( Akriviadis 1997). It usually develops insidiously without causing haemodynamic instability, and is most often due to a hepatocellular carcinoma. Bloody ascites can also be caused by rupture of intra-abdominal varices or possibly leakage from dilated liver lymphatics as liver lymph in cirrhosis contains significant numbers of red blood cells ( Dumont and Mulholland 1960). Hepatocellular carcinoma and ruptured intra-abdominal varices can also cause acute bleeding leading to hypovolaernic shock. Bloody ascites can be due to trauma caused by liver biopsy, fine-needle piration, TIPPS insertion or, rarely, paracentesis.


Chylous ascites has a milky white appearance and is characterised by microscopic fat, an ascitic triglyceride concentration greater than the serum triglyceride concentration, a protein concentration usually > 30 g/l and no growth on culture. It is usually caused by malignant disease in adults but rarely it has been found in cirrhosis possibly due to leakage from lymphatics (Malagelada et al 1974 ). It is a poor prognostic sign.



Bile-stained ascites points to a biliary communication usually caused by gallstones, neoplasia or trauma.



Analysis of the ascitic fluid is helpful in identifying the cause of the ascites and in recognising complications such as infection and neoplasia (Table 5). Chronic parenchymal liver disease is the most cornmon cause of ascites, and Table 6 shows the main conditions from which it needs to be differentiated. Ascites is usually classified as an exudate when its protein content is above 25 g/I and a transudate when its protein content is below 25 g/l. Hepatic cirrhosis is generally regarded as giving rise to ascites which is a transudate. Unfortunately, a review of large series has shown that the ascites protein in cirrhosis exceeds 25 g/lin up to 20% of cases (Sampliner and Iber 1974). Accordingly, an ascites protein < 25 g/I can be regarded as compatible with cirrhosis but a higher concentration does not exclude the diagnosis. Furthermore, the ascites protein may rise during diuretic therapy (Hoefs 1981).

Total Protein
Serum - ascites albumin

The serum/ascites albumin gradient (serum albuminascites albumin) is more reliable in identifying ascites due to cirrhosis as a gradient <II 9/1 (Runyon et al 1992) indicates underlying portal hypertension with a sensitivity of 80-93% and a specificity of 97-98%. An ascites polymorphonuclear leucocyte count is valuable in identifying infections as the resultis available quickly and counts >250/mm3 reliably indicate bacterial infection (Pinzello et al 1983). Blood and ascites culture should also be done, and the chance of isolating an organism from the ascites is best if the fluid is drawn into blood culture bottles (Runyon et al 1988). Culture for M. tuberculosis should also be done. Cytology of ascites is important as malignant cells can be identified reliably in ascites sediment by this technique. Unfortunately, the sensitivity of ascites cytology for malignancy is low.

Hepatic cirrhosis 78
Malignant disease 12
Cardiac failure 5
Pancreatitis 1
Nephrotic syndrome 0.5
Others 3.5
Hepatitic cirrhosis includes coexistant hepatocellular carcinoma and malignant disease ecludes hepatocellular carcinoma. TB shows large variation in geographics distribution

The ascites amylase is high in pancreatic ascites and should be measured particularly when the protein content of ascites is high.

Other Investigations

Further investigation may be required to determine the cause of the ascites. In the case of hepatic cirrhosis, this includes imaging to detect cirrhosis, portal hypertension and complications of cirrhosis such as hepatocellular carcinoma, the causes of cirrhosis, and endoscopy for detection of oesophago-gastric varices which imply portal hypertension. Rarely, measurement of the portal venous pressure may reveal otherwise occult hepatic cirrhosis by revealing portal hypertension. This is done most safely by measuring the wedged hepatic venous pressure. Ascites not attributed to cirrhosis is usually due to intra-abdominal malignant disease and other causes are uncommon (Table 6).


Ascites in hepatic cirrhosis is associated with advanced liver disease and with poor hepatic function and portal hypertension, and consequently it is also associated with a poor prognosis. About a half of all patients die within six months of first presentation, a third to a half of those remaining die over the next 2 years, and the overall five year survival is about 10-20% (Fig.1). Many early deaths are attributable to serious complications such as hepatocellular carcinoma and spontaneous bacterial peritonitis, but patients with severe ascites who do not have such complications also often have a poor prognosis. About a half of patients with tense ascites who do not have gastrointestinal bleeding, infection, encephalopathy, severe renal failure or hepatocellular carcinoma at presentation die within a year, and poor prognostic factors in these patients are shown in Table 7. Prognosis is related largely to liver function, and patients with lesser degrees of ascites and better liver function respond better to treatment and survive longer. In view of its prognostic implications, the development of ascites should always lead to consideration of liver transplantation.


Mild to moderate ascites can be treated as an outpatient, but more severe ascites is treated best in hospital as these patients usually have more severe liver damage and they more often have adverse reactions to therapy. Important factors intreating ascites include removing precipitating factors, controlling sodium intake (and sometimes water intake), promoting sodium excretion with diuretic drugs, removing ascites by paracentesis, and diverting ascitic fluid into the systemic circulation via a transjugular intrahepatic portal systemic stent (TIPSS) shunt or a Le Veen shunt lt is very doubtful whether any of this treatment prolongs life, and as the prognosis for patients with hepatic cirrhosis and ascites is generally poor, liver transplantation shoulcl be considered.

- Malnutricion
- Small(impalpable) liver
- Mean arterial pressure < 82 mmHg
- Serum albumin <28 g/l
- Urine sodium < 1.5 mmol/24 hrs.
- Glomerular filtration rate(< 50 ml/min)
SURVIVAL(with any factor)
- 20 - 40 % at one year
Mean arterial presure=Diastolic presure +1/3 (Systolic presure - Diastolic pressure)

Precipitatinq Factors

Precipitating factors should be sought though in many cases none can be found . Such factors include recent heavy alcohol abuse, ingestion of unusually salty foods, and medicines.


Drugs sometimes contain significant amounts of sodium including some antacids and alginates, aspirin, fybogel, phenytoin and all effervescent preparations. Other drugs can promoje renal retention of sodium and these include nonsteroidal anti-inflammatory drugs, corticosteroids, oestrogens and metociopramide. ACE-inhibitors reduce glomerular filtration rate and sodium excretion even in doses which do not reduce the blood pressure. Ascites arising or worsening in hospital shoulcl always lead to a review of therapy, especially the use of parenteral antibiotics and of intravenously administered fluids which often contain much sodium.


Renal sodium retention is marked in ascites caused by hepatic cirrhosis (above), particularly when the ascites is severe and hepatic dysfunction marked, and accordingly restriction of sodium intake is important, particulary in initial treatment. Occasionally, sodium restriction alone will allow resolution of ascites, particularly where a precipitating cause has been found and removed, but the great majority of patients require also diuretic drugs. Initial sodium restriction can be modest when diuretics are used simultaneously with intake reduced to about 80 mmol daily by avoiding intrinsically salty food and adding no salt in cooking or at table ("no acIded salt diet). Patients with cirrhosis and ascites are often malnourished, and this modest reduction in salt intake allows the diet to remain reasonably palatable which is important in maintaining nutrition. Diuresis can then be produced by gradually increasing the dose of diuretics given. Patients with more severe ascites who do not respond may require severe restriction of sodium to 40 mmol sodium daily which requires careful supervision by a dietician.

    Sodium depletion Rarely, patients become truly sodium and water depleted following large fluid losses by paracentesis, diuresis or enteric losses. These patients have lost their ascites and oedema and show clinical features of dehydration, tachycardia, hypotension and uraemia. These patients need to be given sodium and water parenterally to replace their losses.

    Urine sodium estimation. Measurement of the daily urine sodium output is useful in patients who do not respond to dietary salt restriction and diuretics as the finding of a good sodium excretion implies the intake of excess salt. This source needs to be identified and excluded.


Mild hyponatraemia is common in cirrhosis with ascites (above) and does not require treatment. Treatment is only needed in patients with more marked hyponatraermia and should not be used without good reason as it can only add to the patient's discomfort. Moderate hypo-natraernia (115-124 mmol/I), especially if there is no uraemia and no other electrolyte abnormality, shoulcl be treated by restricting water intake to 1 litre dialy till the serum sodium exceeds 124 mmol/l. More severe hyponatraemia (110-114 mmol/I) in asymptomatic patients and in those with mild symptoms such as anorexia, nausea, and headache should be treated by restricting water intake to 500 ml/day. Severe symptoms such as fits, vomiting , confusion and ataxia or very severe hyponatraemia requires treatment in an intensive care unit owing to the risks of respiratory arrest. The serum sodium is raised gradually to 130 mmol/I over 24-48 hours with hypertonic sodium chIoride infusion via a constant infusion pump.

The serum sodium shoulcl not rise at a rate greater than 1 mmol/I/hr so as to avoid central nervous system damage (Nairus 1986, Grieff 1993).


Potassium depletion is widely regarded as cornmon in hepatic cirrhosis, but this may only be the case when diuretic drugs have been given (Mas et al 1981). There is no good simple measure of potassium stores as 90% of body potassium is intracellular, but in practice potassium replacement shoulcl be given when the plasma potassium is <3. 0 mmol/I particularly where diuretic drugs have been given.

Potassium 50 mmol/day can be given orally as potassium chloride or potassium bicarbonate if the blood urea or creatinine is normal. Potassium and spironolactone (below) should not be given together when the plasma potassium is >3 mmol/l.


Most patients require diuretic drugs, and those available currently are sufficiently powerful to allow sodium restriction to be relaxed and nutrition improved as treatment progresses. Only about 10% of patients are resistant to these drugs (below). The horizontal position approximately doubles the urinary excretion of sodium and water in response to diuretics and accordingly, at least in the early stages of treatment, Up to 6 hours of bed rest alter diuretic drugs are given is worthwhile (Ring-Larsen et al 1986). Even with diuretic drugs, not more than about 900 ml/day of ascites can be mobilised from the peritoneal cavity and amounts excreted beyond this come from the extraperitoneal fluid. Excessive diuresis can cause hypovolaemia and renal failure, and accordingly daily fluid losses shoulcl be limited to 500 ml. (0.5kg. weight) in those with no peripheral oedema and 1 litre (1kg weight) in those with peripheral oedema. Spironolactone is generally regarded as the drug of choice for longterin treatment, other diuretics are added when spironolactone produces an inadequate diuresis, and bendrofluazide is needed only very occasionally.

Potassium-sparing diuretics
Spironolactone, an aldosterone antagonist, is widely regarded as the drug of first choice for ascites in hepatic cirrhosis, perhaps because hyperalclosteronism is relatively so important in sodium retention in this condition. lt is a specific competitive antagonist of aldosterone action on the distal renal tubules and consequently reduces sodium resorption and increases urinary sodium excretion. Patients with obvious ascites require a starting dose of 100 mg, diuretic action begins after 3-4 days, and the dose in increased dy 100 rng/clay at weekly intervals until sodium) excretion as reflected by weight loss is satisfactory or a dose of 500 mg/day is reached. This maximum dose will give a satisfactory response in about a half of patients (Gatta et al 1991). The addition of a loop diuretic in those whose response is inadequate increases the response rate to about 90%. Spironolactone is a safe drug but it can cause hyperkalaemia and potassium supplements (including salt substitutes) must not be given concomitantly. Gynaecomastia, often painful, is the most troublesome side-effect and when it occurs sodium canrenoate (which has a similar diuretic action) can be used. Gastrointestinal symptoms, headache, drowsiness, skin rashes, impotence and agranulocytosis are uncornmon or rare side- effects.

Amiloride (10-20mg/day) and triamterine (10-25Omg/day) act directly on the distal renal tubules to increase sodium excretion and reduce potassium excretion but they are not aldosterone antagonists. They produce a diuresis starting 6 hours and ending 24 hours after administration, and are usually used to potentiate loop diuretics and reduce urinary potassium loss. They can produce hyperkalaemia and should not be given with spironolactone or potassium supplements or when renal failure is present. They are not wiclely used.

Loop diuretics.
The loop diuretics are the most powerful diuretics available acting on the ascending loop of Henle and to a lesser extent on the proximal tubules to inhibit sodium and chloride absorption. Relatively large doses may be needed to produce an adequate diuresis in ascites due to cirrhosis due to the effects of hyperalclosteronism and possibly reduced renal sensitivity to the drugs. Potassium excretion is increased in response to increased sodium reabsorption in the distal tubules; calcium and magnesium excretion is also increased and metabolic alkalosis may occur. Diuresis starts within an hour (within minutes of an intravenous dose) and lasts for about six hours after an oral dose. Frusemide 40mg/day increasing by 4Omg/day to 240mg/day is used most often, or bumetanide (1-5 mq/day) may be used as an alternative. Side-affects are usually due to fluid and electrolyte imbalances, but gastrointestinal symptoms, skin rashes, parasthesiae, blood dyscrasias and hepatic and renal dysfunction occasionally occur. Hiperuricaemia and hyperglcaemia occur but are rarely significant.

The thiazides are diuretics of intermediate potency which are little used in ascites due to hepatic cirrhosis. They act by inhibiting sodium and chloride absorption in the distal tubule and cause increased secretion of potassium by the distal tubules. Side-effects are uncommon, but thiazide can produce hepatic encephalopathy perhaps due to hypokalaernia alkalosis and an increased blood ammonia. The main indication for giving a thiazide is in patients not responding to spironolactone and a loop diuretic as the thiazides act at sites different from these drugs (Olesen and Sigund 1971).


Paracentesis of large volumes of ascites (>5 litres) can be carried out without undue hazard provided that care is taken to prevent circulatory dysfunction, and even the complete removal of all ascites at a single paracentesis can be used safely as a treatment for ascites (Gines et al 1987, Tito et al 1990, Ruiz-del-Arbol et al 19979). Paracentesis also improves respiratory function rapidly and relieves the respiratory distress of marked ascites, though diuretic treatment achieves the same end more slowly (Chang et al 1997). Indeed, although most patients will respond well to sodium restriction and diuretic drugs, paracentesis is used increasingly as a treatment of first choice probably because it is quicker and can reduce the length of hospital stay (Gines et al 1987). A survey of participants at a meeting of the European Association of the Study of the Liver found that 95% of respondents used paracentesis to manage cirrhosis ascites (Arroyo et al 1994). Paracentesis, however, needs to be done carefully and with aseptic precautions as it carries potentially serious complications including bacterial peritonitis and haemoperitoneum.

Feature Circulatory present dysfunction Absent
Cardiac index -> ->
Systemic vascular resistance <- <-
Right arterial pressure <- <-
Pulmonary capillary pressure <- <-
Hepatic venous pressure gradient -> <-
Renin -> -
Aldosterone -> -
Norepinephrine -> -
Creatinine -> -
Note: ->=increase, decrease= <-, - = no change

Paracentesis leads to circulatory changes and these can persist for up to a week (Table 8). The removal of 51 of fluid withoud replacement may not be followed by any and circulatory change (Peltekian et al 1997), but larger amounts cause an immediate increase in cardiac output which soon returns to normal, and a fall in mean arterial pressure, systemic vascular resistance, right atrial pressure and pulmonary capillary pressure which can still be present a week later (Ruiz del-Arbot et al 1997). Paracentesis reduces the free and wedged hepatic venous pressure without changing the hepatic venous pressure gradient and this persists for at least a week . The hepatic venous have been used, including dextran (Ruiz-del Arbol et al 1997), polygeline (Salerno et al 1991), and albumin (Tito pressure gradient may, however, rise when circulatory dysfunction occurs indicating that the intrahepatic vascular resistance increases in these patients (Ruiz-del-Arbol et al 1997). Circulating dysfunction, indicated by increased plasma renin, aldosterone and noradrenaline may be associated with renal impairment, and though this impairment is often reversible, this is not always the case. Accordingly, preventative measures to support the circulation with a colloidal solution at the time of paracentesis are important as this prevents circulatory dysfunction. Several such solutions et al 1990), and all are effective. Albumin solution is perhaps the most effective, but it is also the most expensive (Table 9). Half of the infusion can be given over 2 hours and the remainder over the following six hours after the procedure. The pulse, blood pressure and urine output should be measured regularly during and for 24 hours after the procedure, and the plasma urea and/or creatinine should be measured before and one and six days after the procedure.

Plasma Expander

Plasma Expander 1/2 life

Circulatory dysfunction (%)
None - 70
Dextran - 40 Hours 40 - 50
Polygeline Hours 40 - 50
Dextran - 70 Days 30
Albumin Weeks 15

Paracentesis is an effective way of getting rid of ascites but it does not prevent the continuing accumulation of more ascites. Accordingly, diuretic drugs and sodium restriction will be needed (above) after paracentesis, and a recent trial suggest that spironolactone 200 m/g started inmediately after paracentesis in satisfactory (Fernández-Espaurach et al 1997).

Parecentesis and oesphageal varices. Total paracentesis of all ascites reduces the wedged hepatic venous pressure and recently it has been reported also to decrease intravariceal pressure (Kravetz et al 1997). There may, therefore, be a case for paracentesis in patients with bleeding oesophageal varices and marked ascites, especially where other treatments are unsuccessful.

Resistant Ascites

Refractory or resistantascites is broadly definedas ascites resistant to medical therapy (Arroyo et al 1996). This is generally taken to mean a combination of sodium restriction and diuretic drugs, but paracentesis is used increasingly as an initial treatment for ascites owing to the speed with which it can be applied and a consequent reduction in hospital stay (above). Accordingly, refractory ascites has been defined as failure to respond to sodium restriction of 50 mmol/d, a combination of spironolactone 400 mmol/d and frusemide 160 mg/d or bumetanide 4 mg/d, evidenced by weight loss of less than 200 g/d and urine sodium below 50 mmol/d over 4 days of intense diuretic therapy, or recurrance of ascites within 4 weeks of medical therapy of paracentesis which cannot be prevented by medical therapy.

Such refractory ascites has been described as diureticresistant (i.e.cannot be benefitted by sodium restriction and diuretic drugs) or diuretic-intractable (i.e.sodium restriction and diuretic drugs produce hepatíc encephalopathy), renal failure(creatinine increased 100%to>2mg/I), hyponatraemia (serum sodium reduced 10 mmol/I to <125 mmol/I) or hypo-or hyperkalaemia. Before diagnosing refractory ascites it is important to exclude unrecognised inappropriate sodium intake, failure to take diuretic drugs concomitant drug therapy causing sodium retention (above) and ascites due to causes other than cirrhosis (Table 6) even in a patient with cirrhosis.

Portal Systernic Shunts. Portal hypertension is an important factor in the development of ascites (above), and relief of portal hypertension should therefore improve ascites.


Surgical Shunts.

Surgical portasystemic shunts proved effective in the secondary prevention of variceal bleeding but have fallen into disuse because thay were associated with an increased occurrance of hepatic encephalopathy and did not prolong fife. They were, however, also effective in preventing ascites and consequentially spontaneus bacterial peritonitis. Castells et al (1994) followed up patients treated for variceal bleeding and found that 15% of those treated by a distal splenorenal shunt developed ascites and 2% spontaneus bacterial peritonitis compared to 73% and 21% respectively of those treated by sclerotherapy. Previous reports had shown had shown that surgical shunts can elieve intractable ascites and reverse hepatorenal failure (Ariyan et al 1975, Franco et al 1998). However surgical portal systemic shunts are not used for treating ascites as patients with intractable ascites generally have poor liver function and are poor candidates for such major surgical procedures.

Transjugular intrahepatic portasystemic stent shunts (TIPSS). The introduction of TIPSS has allowed the placement of portasystemic shunts by interventional radiological means applicable even in patients with poor liver function. These shunts are used primarily for treating variceal haemorrhage, but intractable ascites has emerged as the second most frequent indication (Stanley et al 1997).

Uncontrolled trials have shown that full or partial resolution of ascites follows a TIPPS in three quarters more of patients but hepatic encephalopathy appears for the first time in about a fifth, the need for diuretic treatment continues, and a half to two thirds of patients die within two years (Ochs et al 1995, Martinet et al 1997). A small randomised trial showed improvement in refractory ascites following TIPSS in Child B patients but not Child C patients by comparison with no improvement in either group with paracentesis but the mortality at two years was greater after TIPSS (71%) than after paracentesis (44%) (Lebrec et al 1996). In short, TIPSS can improve refractory ascites but the mortality is not improved and may even be increased, especially in Child C patients where liver function is very poor. This emphasises the need to consider liver transpiantation in refractory ascites but where this is inappropriate TIPPS should be used particularly in Child B patients where liver funtion is better.

Spontaneous Bacterial Peritonitis (SBP).

To the occurrence of bacterial peritonitis in patients with cirrhosis and ascites without any local source such as an organ perforation or abscess. It is a serious complication of ascites as it carries a high mortality, a high frequency of recurrence after resolution, and a poor longterm prognosis. Patients who develop SBP tend to have advanced cirrhosis with obvious ascites, but this is not always the case. Ascites can sometimes be difficult to detect clinically and accordingly ultrasonic examination and diagnostic paracentesis should be done where a patient becomes ill for no obvious reason. Patients may present with a combination of a systemic illness with fever and leucocytosis, often associated with hepatic encephalopathy, and abdominal features of pain, peritonism and absent bowel sounds or with either independently. Thus, when a patient with ascites becomes unwell or develops hepatic encephalopathy for no obvious reason, SBP should be sought.


SBI develops in patients with advanced cirrhosis who are susceptible to infection generally and specifically in their ascitic fluid collections. They are often jaundiced, have hypoprothrombinaemia and hypoalbuminaemia, and classify as Group C in the Child-Pugh system. Features indicating general susceptibility to infection include poor reticuloendothelial activity, reduced complement activy and impaired leucocyte function. Increased susceptibility to infection of the ascitic fluid is reflected in low ascites protein concentrations which includes low ascites concentrations of opsonic factors such as immunoglobulins,complement, and fibronectin. Bacteria probably reach the ascitic fluid as a result of bacteraemia, and as a high proportion of ascitic infections are with gut-related organisms, many must reach the blood by passing through the bowel wall. Occasionally, infection reaches the ascitic fluid from recognised sources elsewhere in the body and unusual sources include dental infections and the fallopian tubes. Many patients acquire SBP while in hospital, and though these are likely the more ill and susceptible patients, intravascular cannulae and invasive investigations producing bacteraemia are additional important factors.


The most important investigation is immediate analysis of the ascites for polymorphonuclear leucocyte content and culture. A polymorphonuclear leucocyte count >250/mm3 can be regarded as establishing infection and antibiotic treatment should be started (Rimola et al 1995, Pinzello et al 1983). A total leucocyte count is not helpful as it is the short-lived polymorph cells which reflect infection. Bacterial culture should be carried out by innoculating ascitic fluid into blood culture bottles as this gives the highest yield of bacteria (Runyon et al 1988). The concentration of organism in the ascites is low, making Gram staining of limited value and accounting for failure to culture organisms in a third to a half of cases (Runyon et al 1984). Blood culture should also be done as organisms are isolated in some cases and they reflect those found in the ascitic fluid (Conn et al, 1971). SBI is almost always caused by a single organism, and alternative diagnoses such as organ perforation should be considered when multiple organisms are found.


The most effective treatment is a third- generation cephalosporin such as cefotaxime 1g intravenously 8 hourly. Treatment should be continued for five days and can then be stopped if the ascitic polymorph count has fallen by over 50% (Runyon et al 1991). Alternative antibiotics include other cephalosporins such as ceftriaxone, aztreonane and augmentin (amoxicillin-clavulanic acid ). Aminoglycosides were used previously but are now avoided owing to their renal toxicity. Patients who are clinically well can be treated with broadspectrum quinolones such as ciprofloxacin.

Prognosis and prevention

SBP carries a high mortaly and a high recurrence rate. Resolution of the SBP can be achieved with cefotaxime in about three quarters of cases but the in-hospital mortality in these patients is about 40% (Toledo et al;, 1993). Community-acquired SBP carries a more favourable prognosis than hospital-acquired SBP, perhaps because patients in hospital tend to be sicker. The development of uraemia is a serious prognostic sign. Recurrence of SBP after recovery is common and occurs in about two thirds of patients within a year and in three quarters within two years (Tao et al; 1988). Recurrance is particularly frequent in patients with jaundice (bilirubin>70mmol/I), a prolonged prothrombin time or an ascites protein < 10 g/l. Survival after recovery from SBP is bout 40% at one year and 16% at three years. Death is due largely to l¡ver failure but also to recurrent SBP.


Norfloxacin is a poorly absorbed quinolone which reduces the aerobic Gram negative gut flora without suppressing the anaerobic flora and it has proved successful in reducing recurrance of SBP. lt should be given orally (400 mg/d) to all patients recovering from SBE (Gines et al; 1990). Infection, including SBP, is also cornmon following acute gastrointestinal bleeding and these infections can be prevented by Norfloxacin 400 mg twice daily (Rimola et al; 1985).


This is defined by the finding of bacteria in ascitic fluid with the ascites neutrophil count < 250 mm3 . lt has been regarded previously as occurring in asymptomatic patients but this is not aIways the case (Runyon Hep. 12 1990).

These patients should be regarded as having SBP and although asymptornatic patients may clear the ascitic infection spontaneously, it is probably safer to treat them with antibiotics.

Hepatic hydrothorax. Pleural effusion occurs in about 6% of patients with cirrhosis and ascites (Krowka and Coutese 1989).

Most are small and right-sided, but occasionally ascitic fluid accumulates in the pleural space in large amounts to cause a hepatic hydrothorax. Most patients have obvious ascites which is thought to reach the pleural space through diaphragmatic defects, but occasionally ascitic fluid passes preferentially to the pleural space and hepatic hydrothorax occurs in the absence of clinically detectable ascites (Rubenstein et al 1985). Analysis of the pleural and peritoneal fluids shows that both share the features of a transudate, and in difficult cases 99m Tc sulphur colloid injected into the peritoneum can be shown subsequently to accumulate in the pleura (Rubenstein et al 1985). The treatment of hepatic hydrothorax is difficult and often unsuccessful. Initial treatment should be with diuretic drugs and sodium restriction (above), but his is often unsuccessful and many patients become uraemic as the dose of drugs is increased of or better effect. Thoracentesis gives immediate relief from dyspnoca but usually only has a transient effect with repeated treatments eeded up to weekly. Pleurodesis and surgical repair of diaphragmatic defects is often unsuccessful and fraught with serious complications. Peritonovenous shunts have been used successfully but are of limited value owing to frequent side-effects (Stanley 1979). A TIPSS shunt is probably the best treatment currently available as about half of patients have complete relief and aquarter partial relief (Gordon et al 1979, Strauss et al 1994). Patients requiring this treatment have advanced disease and encephalopathy and deterioration of fiver function can occur fter TIPSS. Liver transplantation needs to be considered in such a situation.

Spontaneous Bacterial Empyema. This is characterised by infection in a pleural effusion which cannot be attributed to any local cause (Xiol et al 1990). lt usually occurs in patients with ascites, and bacteria probably reach the pleural space directly from the ascites or via the blood.

The clinical features are those of cough, dyspnoea, chest pain or fever in a patient with a pleural effusion, of an associated spontaneous bacterial peritonitis, or of unexplained deterioration in a patients condition. A chest radiograph is needed to exclude underlying conditions, such as pneumonia, and pleural fluid, ascites and blood shoulcl be cultured. A pleural fluid polymorphonuclear leucocyte count >500/mm3 should be taken as establishing infection. The most cornmon organisms are E col¡, K. pneumonia and CI. perfringens. Initial treatment with cefotaxime 1g 6-hourly intravenously is recommended. Mortality is around 20% as patients usually have advanced hepatic cirrhosis, and antibiotic prophylaxis is suggested after recovery though its value has not been proved.


1 . ARROYO V, BERNARDI M, EPSTEIN M et al. Pathophysiology of ascites and functional renal failure in cirrhosis. Journal of Hepatology 6,239-257, 1988.

2. ARROYO V, NAVASA M, RIMOLA A.. Spontaneous Bacteria¡ Peritonitis in Liver Cirrhosis : Treatment and Prophylaxis. Infection 22 Suppl. 3. 167-175, 1994.

3. BOSCH J, PIZCUETAP, FEUF et al. Pathophysiology of portal hypertension. Gastroenterol. Clin North Am. 21; 1-14., 1992.

4. CATTAU EL JR, BENJAMIN SB, KNUFFTE et al. The accuracy of the physical examination in the diagnosis of suspected ascites. Journal of the American Medical Association 247, 1164-1166, 1982.

5. CONN H 0, FESSEL J M. Spontaneous bacterial peritonitis in cirrhosis: variations on a theme. Medicine 50, 161-197, 1971.

6. FERNANDEZ-ESPARRACH G, GUEVARA M, SORT P et al. Diuretic requirements after therapeutic paracentesis in non-azotemic patients with cirrhosis. A randomized double-blind trial of spironolactone versus placebo. Journal of Hepatology, 26, 614-620, 1997.

7.- FRANCO D, LABIANCA M, SMADJA C et al. Titanium catheter tip for peritoneovenous shunts. Artificial Organs 12, 81-82, 1987.

8. GINES P, RIMOLA A, PLANAS R et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of adouble-blind, placebo-controlled trial. Hepatology 12, 716-724, 1990.

9. GORDON F D, ANASTOPOULOS H T, CRENSHAW W et al. The successful treatment of symptomatic, refractory hepatic hydrothorax with transjugular intrahepatic portosystemic shunt. Hepatology 25: 6, 1366-1369, 1997.

10. HENRIKSEN J H, BENDTSEN F, SRENSER TIA et al. Reduced central blood volume in cirrhosis. Gastroenterology 97, 1506-1513, 1989.

11. HOEFS JC.The mechanismofascicfiuid protein concentration during diuresis in patients with chronic liver disease. American Journal of Gastroenterology 76, 423-431, 1981 b.

12. KRAVETZ D, ROMERO G, ARGONZ J et al. Total volume paracentesis decreases variceal pressure, size, and variceal wall tension in cirrhotic patients. Hepatology 59-62, 1997.

13. LAWSON J D, WEISSBEN A. S. The Puddle Sing-and aid in the diagnosis of minimal ascites. New England Journal of Medicine, 652-654, 1959.

14. LEBREC D, GlUILY N, HADENGUE A et al. Transjugular intrahepatic portosystemic shunts: comparison with paracentesis in patients with cirrhosis and refractory ascites : a randomized trial. Journal of Hepatology 25, 135-144, 1996.

15. MALAGELADA J R, IBER F L, LINSCHEER W G. Origin of fat in chylous ascites of patients with l¡ver cirrhosis. Gastroenterology 67, 878-886, 1974.

16. OLESENKH, SIGURD B. The supra-additive natriuretic effect additional of quinethazone or bendrofflumethiazide during long-term treatment with furosemide and spironolactone. Acta Médica Scandinavica 190: 223-240, 1971.

17. PARE P, TALBOT J, HOEFS J C. Serum-ascites albumin concentration gradient: a physiologic approach to the differential diagnosis of ascites. Gastroenterology 85, 240-244, 1983.

18. PELTEKIAN K M, WONG F, LIU P et al. Cardiovascular, Renal and Neurohumoral Responses to Single Large-Volume Paracentesis in Patients with Cirrhosis and Diuretic-Resistant Ascites. The American Journal of Gastroenterology Vol 92, No. 394-399, 1997.

19. PINZELLO G, SIMONETTI RG, CRAXI A et al Spontaneous bacterial peritonitis: a prospective investigation in predominantly nonalcoholic cirrhotic patients . Hepatology 3, 545-549, 1983.

20. PRIETO M, GÓMEZ-LECHÓN M J, HOYES M et al. Diagnosis of malignant ascites . Comparison of ascitic fibrinectin, cholesterol and serum-ascites albumin difference. Digestive Diseases and Sciences 33: 833-838, 1988.

21. RIMOLAA, BORY F, TERES Jetal. Oral, Nonabsorbable antibiotics prevent infection in cirrhotics with gastrointestinal haemorrhage. Hepatology 5, 463-467, 1985.

22. RIMOLA A, SALMERÓN J, CLEMENTE G et al. Two different dosages of cefotaxime in the, treatment of spontaneous bacterial peritonitis in cirrhosis. Results of a prospective, randomized, multicenter study Hepatology 21, 674, 1995.

23. RING-LARSEN H, HENRIKSEN JH. Pathogenesis of ascites formation and hepatorenal syndrome: humoral and hemoclynamic factors. Seminars in Liver Disease 6, 341-352,1986.

24. RUIZ-DEL ARBOLL, MON ESCILLO A, JIMÉNEZ W et al. Paracentesis-induced Circulatory Dysfunction: Mechanism and Effect on Hepatic Hemodynamics in Cirrhosis. Gastroenterology, 113, 579-586, 1997.

25. RUNYONBA, HOEFS JC.Culture-negative neutrocytic ascites: a variant of spontaneous bacteria¡ peritonitis. Hepatology 4, 1209-1211, 1984b.

26. RUNYON B A. Spontaneous bacterial peritonitis: an explosion of information. Hepatology 8, 171-175, 1988.

27. RUNYON B A. Monomicrobial nonneutrocytic bacterascites: A variant of spontaneous bacterial peritonitis. Hepatology 12, 710-715, 1990.

28. RUNYON B A, MCHUTCHISON J G, ANTILLON M R et al. Short-course versus long-course antibiotic treatment of spontaneous bacterial peritonitis: a randomized controlled study of 100 patients. Gastroenterology 100: 1737-1742, 1991.

29. RUNYON B MONTANO A, ARKIVIADIS E et al. The serum ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann. Intem. Med. 117: 215, 1992.

30. SALERNO F, BADALAMENTIS, LORENZANO E et al. Randomized comparative study of hemacel vs. albumin infusion after total paracentesis in cirrhotic patients with refractory ascites. Hepatolgy 13: 707-713, 1991.

31. SAMPLINER R E, IBER F L. High protein ascites in patients with uncomplicated hepatic cirrhosis. American Journal of the Medical Sciences 267, 275-279, 1974.

32. STANLEY M M. Treatment of intractable ascites in patients with alcoholic cirrhosis by peritoneo-venous shunting (LeVeen). Med. Clin. North Am. 62: 523-536, 1979.

33. STRAUSS R M, MARTIN LG, KAUFMAN S L et al. Transjugular intrahepatic portal systemic shunt for the management of symptomatic cirrhotic hydrothorax . Am J Gastroenterol. 89, 15520-1522, 1994.

34. TITO L, GINES P, ARROYO V et al. Total paracentesis associated with intravenous albumin management of patients with cirrhosis and ascites. Gastroenterology 98. 146-151, 1990.

35. TOLEDO C, SALMERÓN J, RIMOLA A et al. Spontaneous Bacterial Peritonitis in cirrhosis: Predictive Factors of Infection Resolution and Survival in Patients treated with Cefotaxime. Hepatology Vol 17, No. 1, 251-257, 1993.

36. WITTE M H, WITTE C L DUMONT A E. Progress in l¡ver disease: physiological factors involved in the causation of cirrhotic ascites. Gastroenterology 61: 742-750, 1971.

37. XIOL X, CASTELLOTE J, BALIELLAS C et al. Spontaneous bacterial empyema in cirrhotic patients: analysis of eleven cases. Hepatology 11: 365-370, 1990.