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Approach to the Patient with Ascites

Henryk Dancygier and Jason N. Rogart

Greek physicians. See also Chapter 80 for the discussion 
of formation and treatment of cirrhotic ascites.


Ascites denotes the accumulation of fluid in the peritoneal 


Several main forms of ascites may be distinguished 

  • Portal
  • Cardiac
  • Malignant
  • Inflammatory/infectious, and
  • Chylous
The features of portal and cardiac ascites are overlapping. 
Many different causes underlie these main forms 
of ascites.

The most common cause of ascites is liver cirrhosis 
in approximately 80% of cases, followed by malignant 
(12%) and cardiovascular diseases (5%). 
ascites is predominantly due to peritoneal carcinomatosis 
(e.g. in gastric or ovarian cancer) or to massive 
liver metastases. 
Congestive right heart failure and 
constrictive pericarditis are the leading cardiac causes 
of ascites. Disturbances of venous hepatic outfl ow such
as Budd-Chiari syndrome or veno-occlusive disease  
are rare etiologies, as are infectious, renal and other 
causes. An isolated portal vein thrombosis, without
concomitant parenchymal disease of the liver usually 
does not cause ascites. The numerous causes and various 
forms of ascites are reported in Tables 54.1–54.4.


The pathophysiology of ascites in peritonitis is self evident. Malignant and infl ammatory/infectious ascites is caused by the formation of an exudate due to peritoneal irritation.

The peritoneum, having a surface area of approximately 2 m2 in the adult, behaves like a semipermeable membrane that enables the continuous exchange of water and solutes between the peritoneal cavity and the intraperitoneal blood and lymph vessels. Under physiologic conditions water and low molecular weight substances are absorbed by the hematogenous route, while high molecular weight substances are drained by the lymphatics, especially via the subdiaphragmatic lymph vessels. This process is facilitated by fenestrations
in the peritoneal mesothelium and in the endothelium. The maximal transport capacity for fluids from the peritoneal cavity to plasma is approximately 720–
840 mL/24 h. This flow cannot be further increased even by forced diuresis. In a healthy person the secretory
activity of the peritoneal mesothelium is in equilibrium with its drainage systems, so that normally only a few
millilitres of a transudate are present in the peritoneal cavity to keep the peritoneal lining moist. Inflammatory peritoneal irritation regardless of its cause or conditions associated with impairment of lymphatic drainage compromise this balance and lead to an accumulation of fluid into the peritoneal cavity.

In contrast to peritonitis, the pathophysiologic mechanisms in the development of cirrhotic ascites
are still not completely understood. However, decade long research has considerably improved our understanding
of its pathogenesis. Patients with advanced cirrhosis regularly exhibit changes in the systemic circulation
(such as an increased cardiac output, decreased peripheral vascular resistance, arterial hypotension,
splanchnic vasodilation) and have an impaired renal excretion of Na+ and water. These alterations, to some
extent are already present in the preascitic stage of cirrhosis. Whether they represent secondary adaptation
processes to primary renal Na+ and water retention with consequent enlargement of extracellular and
plasma volume, or whether they are the initiating factors in the wake of which renal dysfunction develops,
is controversial. The present data favor the latter possibility. Formation of ascites in liver cirrhosis is
essentially regarded as a consequence of a primary peripheral and splanchnic vasodilation with reduction
of the effective arterial blood volume, combined with an impairment of renal Na+ and water excretion. The total body content of Na+ correlates directly with and is the most important determinant of extracellular fluid volume. In a healthy person a balance exists between the uptake of Na+ and its renal excretion, an increased uptake being followed by an increased excretion. Whatever might be the initiating mechanism, in patients with liver cirrhosis this balance is disrupted; i.e., despite an elevated extracellular fluid volume, Na+ is inadequately retained [33]. In addition, local factors must be operative which explain the preferred accumulation of fluid within the peritoneal cavity.

Regulation of Extracellular Fluid Volume

The volume of extracellular fluid in a healthy person is tightly controlled and regulated. This homeostatic process involves 
  • Afferent neural signals, and
  • Efferent neuro-hormonal mechanisms.

Afferent Signals

The filling state of the arterial system is the primary afferent signal, which determines whether or not the kidneys will retain Na+ and water. The most important determinants of arterial
filling are cardiac output and peripheral vascular resistance. A decrease in cardiac output and arterial vasodilation signal a state of “arterial underfilling” and elicit mechanisms that lead to
renal Na+ and water retention [36, 37]. Sensors within the cardio-pulmonary circulation, the kidneys, and not yet precisely defined receptors in the peripheral circulation and central nervous system register the vascular filling state. High pressure baroreceptors are located in the left cardiac ventricle, carotid sinus, aortic arch, and in the renal juxtaglomerular apparatus. A decrease in pressure with diminished distension of these receptors leads to
  • Activation of the sympathetic nervous system
  • Activation of renin-angiotensin-aldosterone (RAA) system, and
  • Non-osmotic release of arginine-vasopressin
All three mechanisms reduce renal water and Na+- excretion. In addition, the release of norepinephrine from sympathetic nerve fibers directly activates the RAA system. Both stimulate the hypothalamic supraoptic and paraventricular nuclei to secrete arginine-vasopressin.

Sensitive low pressure receptors, which are stimulated by distension, are located in the cardiac atria, right heart chamber, and pulmonary arterial vessels. Distension of these receptors causes increased secretion of cardiac natriuretic peptides, and inhibition of vasopressin secretion, followed by enhanced diuresis. Compared to the volume sensitive sensors within the
low-pressure system, arterial baroreceptors seem to play the major role in the pathogenesis of cirrhotic ascites, with renal Na+ and water retention prevailing.

Efferent Mechanisms

The efferent neuro-hormonal factors that affect renal Na+ and water handling are, among other things, vasoconstricting and antinatriuretic substances, such as 
  • Norepinephrine
  • Angiotensin II
  • Aldosterone
  • Arginine-vasopressin, and
  • Endothelins
as well as vasodilating and natriuretic compounds, especially
  • Nitric oxide (NO)
  • Vasodilating peptides
  • Natriuretic peptides, and
  • Prostaglandins
Patients with liver cirrhosis already exhibit arterial
vasodilation in the precirrhotic stage. This “arterial underfilling” leads to a number of compensatory neuroendocrine responses that lead to vasoconstriction and to an increased renal Na+ and water retention (see above). Initially these compensatory mechanisms are beneficial. By increasing intravascular volume they help to correct, at least partially, arterial underfilling,
and thereby prevent the development of ascites. Once the increase in plasma volume is no longer able to normalize the homeostatic mechanisms, liver cirrhosis decompensates, and ascites develops.

Stimulation of the sympathetic nervous system causes peripheral and renal vasoconstriction. As a result of the preferential constriction of the efferent arterioles, vascular resistance initially increases, and renal blood flow diminishes. The filtration fraction is increased in the presence of normal or only slightly reduced glomerular filtration. The constriction of the efferent arterioles also alters the hemodynamic parameters in the peritubular capillaries with a decrease in hydrostatic and a rise in oncotic pressure, which leads to enhanced tubular Na+ and water retention. Thus, increased sympathetic activity in patients with liver cirrhosis is pivotal  for the maintenance of cardiovascular homeostasis. The sympathetic nervous system, by its action on renal vessels and tubules, may contribute to the expansion of extracellular fluid volume and to the development of ascites. By increasing the hepatic vascular resistance,
the sympathetic system also contributes to the generation of portal hypertension (see Chapter 53) [5, 12].

Arterial underfilling and hyponatremia activate the renin-angiotensin-aldosterone system. Angiotensin II stimulates the secretion of aldosterone, which furthers renal tubular Na+ resorption. In addition, angiotensin II itself may enhance Na+ resorption in the proximal tubule and constricts the efferent arterioles with the above mentioned consequences. Recently it has been suggested that the apparent mineralocorticoid effect is only partially explained by increased aldosterone concentrations, and that in addition to aldosterone, cortisol confers mineralocorticoid action. The underlying molecular pathology for this mineralocorticoid receptor activation by cortisol is a reduced activity of the
11b-hydroxysteroid dehydrogenase type 2, an enzyme protecting the mineralocorticoid receptor from promiscuous activation by cortisol in healthy individuals [13].

Arginine-vasopressin stimulates renal V2-receptors thereby enhancing water resorption in the collecting tubules. Inadequately elevated vasopressin levels in plasma are documented in patients with liver cirrhosis, ascites, peripheral edema and hyponatremia [32]. They correlate with the clinical and hemodynamic severity of the disease. In patients with cirrhosis, in contrast to normal persons, a water load does not reduce these increased hormone levels. This suggests that in cirrhotic patients elevated plasmatic vasopressin concentration is mediated by non-osmotic mechanisms [6].

Endothelins are potent vasoconstrictors and important regulators of liver blood flow (see Chapter 4). The intrahepatic endothelin-1 (ET-1) concentration is increased in patients with liver cirrhosis and it correlates with the severity of liver disease and the degree of ascites [1]. ET-1 may have a role in modulating intrahepatic resistance in cirrhotic portal hypertension. The endothelial cells in the splenic sinuses and potentially also B lymphocytes residing in the spleen, appear to be an important source of ET-1 in cirrhotic patients [27].

The counterpart of vasoconstrictory and antinatriuretic substances are atrial and brain natriuretic peptides (ANP and BNP), vasodilating peptides, NO, and the vasodilating prostaglandins. The precise significance of these substances in patients with liver cirrhosis is currently under intensive investigation.

The serum concentrations of cardiac and brain natriuretic peptides (ANP and BNP) in some patients with cirrhosis is increased [28]. These peptides are natriuretic by increasing the glomerular filtration rate, increasing the amount of sodium filtered, and by inhibiting sodium resorption in the collecting tubules. Furthermore, they inhibit the RAA-system and possibly
also vasopressin and sympathetic activity, and they release vascular tension.

Their effects are attenuated in states of arterial underfilling. The causes of “ANP resistance” in liver cirrhosis are unclear. Downregulation of renal ANP and BNP receptors, secretion of biologically less active natriuretic peptides, increased enzymatic degradation in the kidneys, and hyperaldosteronism are among the factors discussed [15, 31].

Nitric oxide is a short-lived intercellular messenger that is primarily synthesized by endothelial cells. Its actions are mediated by intracellular cyclic GMP. NO is a potent vasodilator and plays an important role in regulating vascular tone. In patients with liver cirrhosis an increased synthesis of NO and an increased plasmatic NO concentration already can be demonstrated
in the preascitic, compensated stage [34]. NO concentration in portal venous blood is higher than in the peripheral venous circulation, which suggests increased NO synthesis in the splanchnic circulation [4]. Patients with liver cirrhosis and ascites show an increased endotoxin-induced release of NO as well as an increased activity of NO-synthase in polymorphonuclear granulocytes and monocytes [23]. From the data available it emerges that NO plays an important role in the pathogenesis of cirrhotic ascites, but a final assessment
of its pathogenetic signifi cance is not yet possible. NO could play a role in primary vasodilation (especially in the splanchnic area), in decreased vascular reactivity to vasoconstrictors such as angiotensin II, arginine-vasopressin and norepinephrine, and also be co-responsible for arterial hypotension in patients with advanced cirrhosis [26].

The plasma concentrations of vasodilating peptides such as glucagon, calcitonin gene-related peptide (CGRP), substance P and adrenomedullin are increased in patients with liver cirrhosis and ascites. These peptides could contribute to the hyperdynamic circulation of cirrhotic patients, either directly through their vessel relaxing effects or by inducing constitutive endothelial e-NO synthase [16]. Adrenomedullin, a potent endogenous vasodilating peptide of 52 amino acids, has been isolated from a human pheochromocytoma. Its circulating levels correlate with the hemodynamic and renal changes and with the activation of vasoconstrictor systems in patients with liver cirrhosis and ascites [10, 11, 18].

Prostaglandins normally do not regulate renal sodium handling. In patients with liver cirrhosis, however, vasodilating prostaglandins seem to assume an important role in sustaining renal blood flow and glomerular filtration. In decompensated liver cirrhosis prostaglandin synthesis is diminished with a consequent decrease in renal blood fl ow, glomerular filtration rate,
sodium and free water excretion. Cyclooxygenase inhibitors my cause an renal failure in patients with liver cirrhosis and ascites. 

Theories of Ascites Formation 

"Volume Deficiency" Hypothesis

According to this classic hypothesis, ascites is a result of increased hydrostatic pressure within the hepatic and splanchnic circulation, induced by portal hypertension. Impairment of the Starling-balance leads to movement of fluids from intravascular compartment to the interstitial space [22]. The accumulation of fluid is compensated initially by an increased lymphatic outflow via thoracic duct into the systemic circulation. If, howefer, with increasing portal hypertension the lymphatic system is overburdened, fluid crosses into peritoneal cavity, and the intravascular volume decreases [40, 41].  The decrease in intravascular volume results in hypovolemia (secondary underfilling) wich activates neurohormonal regulatory mechanisms resulting in compensatory renal sodium retention. Since the retained fluid continuously flows into the peritoneal cavity a vicious circle develops with ongoing stimulation of Na+   retaining mechanisms. However, this classic hypothesis is not able to explain the systemic hemodynamic changes observed in patients with liver cirrhosis, and nowadays is mainly of historical importance. 

"Overflow" Hypothesis 

This hypothesis assumes that the expansion of intravascular volume is the crucial event in the pathogenesis of ascites formation. Failure to escape from mineralocorticoid action in compensated cirrhosis is considered a major argument supporting the overflow theory of ascites. Portal hypertension combined with hypervolemia are then assumed to lead to an "overflow" of fluid into into peritoneal cavity. 

However, experimental and clinical data do not support this hypothesis. Failure to escape from mineralocorticoids is uncommon in patients with compensated cirrhosis, is related to an inadequate expansion of effective plasma volume due to the accumulation of ascites, and occurs in patients with marked peripheral arteriolar vasodilation [25]. Thus, the arterial system is not "overfilled", and increased renal sodium retention in the preascitic stage due to vasodilation and does not lead to intravascular hypervolemia. 

"Underfilling or Peripheral Arterial Vasodilation" Hypothesis 

Primary arterial vasodilation with decreased effective arterial volume currently is considered to be the initiating and perpetuating event that results in increased renal sodium and water retention [38, 39]. The cause of peripheral and splanchnic vasodilation is not completely understood. Potential factor are an impaired clearance, porto-systemic shunts, or an increased synthesis of vasodilators such as NO, substance P, CGRP, glucagon, adrenomedullin and prostacyclin (see above). As a reaction to primary arterial vasodilation with decreased effective arterial volume, cardiovascular and renal receptors are activated that, via neurohormonal mechanism, result in increased renal  retention of sodium and water. The compensatory increase (normalization) in plasma volume prevents the development of ascites. If these compensatory mechanisms succeed in normalizing effectively circulatory homeostasis, the activity of sodium retaining systems and renal sodium excretion normalize again - cirrhosis remains compensated. If, however, the compensatory systems are not sufficient to restore effective plasma volume, activation of sodium retaining systems persists and ongoing Na retention results in ascites formation. 

The severity of liver disease is direclty related directly to renal dysfunction, possibly induced by a biochemically or neurally mediated hepatorenal reflex [20, 24]. The hepatorenal syndrome with systemic vasodilation and renal vasoconstriction is probably the most extreme manifestation of a disease with reduced effective plasma volume [14]. 

The theory of primary arterial vasodilation best unifies the numerous hemodynamic alterations observed in patients with liver cirrhosis and ascites. The preferential accumulation of fluid within the abdominal cavity is explained by splanchnic vasodilation seen in portal hypertension. Figure 54.1 summarizes our current pathophysiologic ideas of ascites formation according
to the theory of peripheral arterial vasodilation.


History will provide the first clues to the presence and possible etiology of liver disease. Physical examination is unreliable in diagnosing small amounts of ascites. Special attention should be paid to signs of chronic liver disease. Bulging flanks in the supine position, flank dullness to percussion, tympany at the top of the abdominal wall, shifting dullness when the
patient turns to one side, and a fluid wave are sensitive (80%) but less specific (60%) signs of ascites. The most informative examination finding is dullness to percussion. However, dullness requires at least 1,000 mL of ascites (see Chapter 33).

Abdominal sonography is the imaging method of choice in demonstrating as little as 100 mL of ascites.

In addition, pleural and pericardial effusions may be demonstrated during the same examination. The sonographic evaluation of the liver, spleen and intraabdominal vessels will often provide an assessment of the cause of ascites as well as potential complications and the severity of portal hypertension. Ultrasound guided paracentesis allows for obtaining ascitic fluid for further
laboratory examination [29]. Small amounts of ascites, especially in the retrogastric and periduodenal areas may also be visualized by endosonography, which, however, is rarely required in clinical practice. Since the presence of malignant ascites significantly alters patient management, especially in pancreaticobiliary malignancy, an active search for ascites and the use of EUS-guided fine-needle aspiration of ascites has been advocated to be included in the management of patients with known or suspected pancreaticobiliary malignancies [21].

Provided ultrasound images are technically satisfactory, cost-intensive techniques such as CT and MRI are usually not mandatory.

Paracentesis is the gold standard for the further evaluation of ascites by biochemical, cytologic and bacteriologic techniques. Ascites should be inspected macroscopically, be sent for a complete blood count with differential, albumin, total protein, and cholesterol levels, and cultures (10–20 mL of ascitic fluid should be inoculated into two [aerobic and anaerobic] blood
culture bottles at the bedside). The macroscopic appearance of ascitic fluid often allows for a rough etiologic diagnosis (Table 54.3). A clear serous ascites usually has a portal hypertensive or cardiac etiology. In hemorrhagic ascites one should suspect malignancy. A cloudy fluid points towards infection.

Simple parameters such as the serum-ascites-albumin gradient (SAAG; serum albumin minus ascitic albumin concentration), the ascitic fluid to serum bilirubin concentration ratio, the protein and cholesterol levels and the number of leukocytes and differential are useful in determining the cause of ascites. They allow for classifying ascites into a transudate or an exudate and give hints to a possible malignant etiology or to a bacterial peritonitis (Tables 54.5–54.8) [9, 29, 30, 35].

Chylous ascites has a milky or creamy appearance due to lymph in the abdominal cavity. Its triglyceride concentration exceeds that of plasma. The underlying mechanisms for the formation of chylous ascites are related to disruption of the lymphatic system. Traumatic injury or obstruction by tumors, especially malignant lymphomas are the most frequent causes (Table 54.4) [8]. Chylous ascites is seen in 0.5–1% of patients with liver cirrhosis.

Three basic mechanisms for then formation of chylous ascites have been proposed [7]. (1) Leakage from the dilated subserosal lymphatics into the peritoneal cavity, (2) exudation of lymph through the walls of massively dilated retroperitoneal lymphatics, which leak fluid through a fi tula into the peritoneal cavity (i.e. congenital lymphangiectasia), and (3) thoracic duct
obstruction from trauma or tumor with resulting dilated retroperitoneal lymphatic vessels with consequent direct leakage of chyle through a lymphoperitoneal fi stula.

In liver cirrhosis chylous ascites may develop as a result of increased hydrostatic pressure within the splanchnic lymphatics, with their consequent disruption.

Differential Diagnosis

Four initial questions are especially important in the differential diagnosis of ascites, since the answers will impact treatment and prognosis.
  • What is the underlying cause?
  • What is the SAAG (i.e., is it a transudate or an exudate) and the total ascitic protein content?
  • Is ascites malignant?
  • Is ascites infected?
The history and physical findings already yield important etiologic clues. Spider nevi, splenomegaly, dilated and prominent abdominal wall veins point toward liver cirrhosis. Congested neck veins, systolic pulsations of jugular veins or of the liver may be observed in congestive right heart failure. Pulsus paradoxus and a positive Kussmaul sign suggest a constrictive pericarditis.
Visible veins on the patient’s back suggest obstruction of the inferior vena cava, while palpable abdominal masses, an immobile mass at the umbilicus (Sister Mary Joseph nodule) or a coarse and nodular liver surface are highly suggestive of peritoneal carcinomatosis and metastatic liver disease.

In Western countries liver cirrhosis is the most frequent cause of ascites. (see Table 54.1). The differential diagnosis must consider the various etiologies of liver cirrhosis (see Chapter 79). Complications of longstanding cirrhosis such as hepatocellular carcinoma or portal vein thrombosis should be searched for specifically by ultrasound, CT or MRI.

The differentiation between a transudate and an exudate is important, since portal hypertensive ascites usually is a transudate, while malignant ascites is usually an exudate. Measuring total protein content in ascites is the most widely used initial biochemical method in differentiating between a transudate and an exudate (Table 54.6), as well as for further differentiating
ascites with a SAAG greater than 1.1 g/dL. The ascitic fluid to serum bilirubin concentration may also help in this differentiation (see above) [9].

The cytologic examination of ascitic fluid is of prime importance in differentiating between a benign and malignant ascites. The sensitivity of cytology varies between 40% and 70%. The specifi city and the positive predictive value reach nearly 100% by experienced examiners, if at least three specimens are examined (Table 54.7). In addition, elevated levels of lactic
dehydrogenase, tumor markers such as carcinoembryonic antigen, fibronectin and cholesterol in ascites also suggest a malignant cause. Notably the latter two are of great differential diagnostic value, with cholesterol concentrations > 45–48 mg/dL strongly favoring a malignant cause of ascites [35]. Increased peritoneal permeability with increased diffusion of cholesterol
from plasma to ascites in peritoneal carcinomatosis is thought to underlie this finding.

Ascites infection may occur either as spontaneous bacterial peritonitis (SBP) which may be acquired in or outside the hospital, or be due to secondary bacterial peritonitis, for example following paracentesis or intestinal perforation. SBP is ten times more frequent than secondary peritonitis and is seen in 10–20% ofpatients with liver cirrhosis (see Chapter 80). While
SBP usually is monomicrobial, secondary bacterial peritonitis is nearly always polymicrobial, with Gram negative bacteria predominating in two thirds of cases. Because of the high mortality rate (up to 50% in SBP and 80% in the secondary forms), early diagnosis and treatment are of crucial importance. A high index of suspicion is necessary, since in approximately one third of patients with SBP fever, abdominal pain, guarding, or diminished bowel sounds are absent. The diagnosis is made by bacteriologic examination of ascites and by determining the number of granulocytes in ascites (Table 54.8). In order to ensure a high diagnostic accuracy (80–90%) freshly obtained ascitic fluid must be inoculated immediately at the bedside in
appropriate aerobic and anaerobic culture bottles. An infected ascites nearly always contains > 250/mmpolymorphonuclear leukocytes (PMN), and usually more than 500/mm3 white blood cells. In the case of a “bloody tap,” 1 PMN should be subtracted for every 250 red blood cells.

Rare causes of an infected ascites are tuberculous peritonitis and peritoneal chlamydial infection. Tbcperitonitis is found particularly in HIV infected patients with advanced immunodefi ciency and in alcoholics with liver cirrhosis. Ascites cultures in peritoneal tuberculosis yield variable results and are positive in 20–80% of cases. In addition to ascitic mycobacterial culture, PCR should also be performed. Laparoscopy with biopsy is the best test to diagnose peritoneal tuberculosis. Chlamydial infection must be included in
the differential diagnosis in sexually active, young women who present with fever and an infected ascites. Currently Fitz-Hugh-Curtis syndrome is caused more often by chlamydiae than by gonococci.


Complications of ascites are predominantly SBP, the hepatorenal syndrome, and hepatic hydrothorax (see Chapter 80). In longstanding cirrhosis the risk of hepatocellular
carcinoma should be kept in mind. Disease exacerbation by a superimposed acute alcoholic hepatitis should be taken into account in patients with alcoholic cirrhosis. The development of tense ascites that does not respond to sole diuretic therapy also indicates a complicated course.


The management of ascites is discussed in detail in Chapter 80.


The diagnostic evaluation of a patient with liver cirrhosis and ascites includes the assessment of liver function, description of liver morphology, analysis of ascitic fluid, and the appraisal of hemodynamic parameters, endogenous vasoactive systems, and renal function. The prognosis of a patient with ascites depends on the results of these examinations, on the cause of ascites, and on the presence or absence of complications.

The development of ascites in a patient with liver cirrhosis is the expression of an advanced disease stage. Thus, ascites itself is an adverse prognostic sign. The one and five year survival probability after the first ascites episode is approximately 50% and 20%, respectively. A rise of serum creatinine concentration to >1.5 mg% in a patient with liver cirrhosis and ascites is
associated with mortality rates of up to 80% within 6–12 months. Therefore, whenever the level of serum creatinine rises in a cirrhotic patient with ascites the need for a liver transplant should be discussed prior to the development of hepatorenal syndrome [2, 3].

The efficiency of diuretic therapy may be estimated in advance by determining urinary sodium excretion, glomerular filtration rate, serum creatinine, urea nitrogen and the degree of activation of the reninangiotensin-aldosterone system. In order to avoid false results the patient should be placed on a Na+ -poor diet (50–60 mEq/day) and should not take any drugs that
may affect renal function (e.g. diuretics, nonsteroidal antiinfl ammatory drugs, b-adrenergic blocking agents, arterial vasodilators) before determining these parameters. Depending on the probability of whether the ascites will respond to sole diuretic therapy, it may be classified as simple or problematic (tense). The features of simple and problematic ascites are summarized in Table 54.9.


The term refractory ascites encompasses two conditions
  • Ascites resistant to diuretics, and
  • Ascites intractable with diuretics
An ascites is termed diuretic resistant if it cannot be mobilized despite dietetic sodium restriction (50 mEq/
day) and intensive diuretic therapy (e.g. spironolactone 400 mg/day and furosemide 160 mg/day) for at least
1 week or if, despite intensive therapy, it recidivates early.

An ascites intractable with diuretics is present when complications associated with diuretic treatment such
as diuretic-induced hepatic encephalopathy, renal insufficiency, hyponatremia, and hypo- or hyperkalemia preclude the administration of effective doses of diuretics.

A valid prognostication of the survival time in patients with cirrhotic ascites is extremely difficult. The usual laboratory parameters such as aminotransferases, coagulation parameters, serum albumin levels or quantitative tests of liver function are weak predictors of prognosis. Parameters that include kidney function such as the MELD score (see Chapter 30), and alterations in systemic hemodynamics are better suited for estimating prognosis.

Parameters of a poor prognosis in patients with still normal urea nitrogen and serum creatinine levels are
  • Impaired ability of free water excretion (water diuresis after a water load)1
  • Dilutional hyponatremia
  • Marked Na+ retention (diminished Na+ excretion)
  • Decrease in glomerular fi ltration rate
  • Increased plasma renin activity
  • Increased plasma concentration of norepinephrine, and
  • Arterial hypotension

15% glucose i.v. 20 mL/kg body weight within 45 min. Fifteen minutes after the end of infusion urine volume is determined over 90 min. Urine volume: > 8 mL/min = normal water diuresis, 3–8 mL/min = moderate restriction of water diuresis, <3 mL/min = marked restriction of water diuresis


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