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| | | Year : 1996 | Volume : 2 | Issue : 2 | Page : 80-86 | | | Ascites: Tips on diagnosis and management | | | Ibrahim A Al Mofleh, Rashed S Al Rashed
Department of Medicine, College of Medicine & KKUH, King Saud University, Riyadh, Saudi Arabia
Click here for correspondence address and email | |     | |  Abstract | | | Clinical evaluation and diagnostic paracentesis with estimation of the serum-ascitic albumin gradient (SAAG) is the most important step in identifying the etiology of ascites. At a level of 1.1 g/dl, SAAG, accurately (96.7%) differentiate portal hypertension from nonportal hypertension-associated ascites. The majority of patients with ascites (>80%) have portal hypertension associated etiology mainly, liver cirrhosis. Approximately 90% of patients with ascites complicating cirrhosis respond to salt restriction and diuretics. The remainder (10%),have refractory ascites which commonly respond well to large volume paracentesis (LVP). Asymptomatic complications occurring in patients treated with LVP may not necessitate treatment. Other alternative methods for treatment of refractory ascites include: ascitic fluid recirculation (AR), peritoneovenous shunting (PVS),transjugular intrahepatic portosystemic stent-shunting (TIPS) and orthotopic liver transplantation (OLT). How to cite this article:
Al Mofleh IA, Al Rashed RS. Ascites: Tips on diagnosis and management. Saudi J Gastroenterol 1996;2:80-6 |
Ascites is a pathological intraperitoneal fluid accumulation which may complicate a variety of disorders including parenchymal liver disease, neoplasm, peritoneal tuberculosis, congestive cardiac disorders, nephrosis, pancreatitis and myxedema. Parenchymal liver disease represented mainly by cirrhosis accounts for over 75% of the causes of ascites [1],[2] . Development of ascites as a consequence of liver cirrhosis is a bad prognostic sign with probable survival rates of 48 and 18% for one and five years, respectively [3] .
Ascites complicating liver cirrhosis with portal hypertension develops as a consequence of hepatic and renal function alteration with splanchnic and systemic hemodynamic changes. Underfilling, overflow and peripheral arterial vasodilatation theories have been proposed to explain the initiating event of renal sodium and water retention. While in the under-filling theory, renal sodium and water retention complicate hypovolemia due to ascites formation, the overflow is due to ascites formation and hypervolemia induced by primary renal retention of water and sodium. Hypovolemia, due to arterial vasodilatation or sequestration of large amounts of intravascular fluid into the peritoneal cavity, results in triggering compensatory mechanism by releasing renin and aldosterone, enhanced secretion of antidiuretic hormone, activation of sympathetic nervous system with further sodium and water retention [4] . The elevation of some plasma peptides concentration such as kinin [4] and endothilin [5] in cirrhotic patients may contribute to altered renal function and sodium retention.
The mechanism of ascites formation in congestive cardiac disorders may be explained by diminished cardiac output, or a decreased peripheral resistance resulting in hypovolemia. The sympathetic nervous system, renin-aldosterone and vasopressin will be activated resulting in renal vasoconstriction with sodium and water retention [2],[6] . Similarly in nephrosis, hypoalbuminemia results in hypovolemia and subsequent triggering of humoral compensation mechanism with sodium and water retention [2] .
Ascites formation in peritoneal tuberculosis and carcinomatosis is initiated by exudation of protein with subsequent fluid extravasation to maintain an oncotic balance [2] . As the mechanism of ascitic formation differs according to the etiological factor, a proper diagnosis helps in the choice of treatment.
| Diagnosis | |  |
Clinical evaluation of ascites
History and physical examinations are valuable in determining the etiology of ascites. History of jaundice, blood transfusion, hematemesis, melena, drugs and alcohol are suggestive of parenchymal liver disease. The presence of stigmata of chronic liver disease is supportive.
On the other hand, history of hypertension, ischemic heart disease, valvular disease, dyspnea together with a raised jugular venous pressure, peripheral edema,dependent edema and anasarca favors a cardiac origin.
Hypertension, diabetes mellitus, chronic renal failure with puffiness of the face, peripheral edema and anasarca are suggestive of nephrosis. Ascites associated with abdominal pain and fever indicate spontaneous bacterial peritonitis (SBP). Additionally, anorexia and weight loss are indicative of peritoneal tuberculosis or carcinomatosis.
A small amount of ascites is usually asymptomatic. As the amount increases, symptoms may occur in the form of flank fullness, abdominal distension and discomfort. Respiratory distress may complicate massive ascites. Intraperitoneal fluid amounts as small as 0.3-0.4 liter, can be detected physically by placing the patient in the knee-elbow position.
Amounts exceeding 1.5 liters can be detected in a supine position. Fluid wave is the most specific, and flank dullness is the most sensitive sign [7] .
Hematological and biochemical tests
Complete blood count and biochemical tests may give clues to the etiology of ascites. Pancytopenia for instance may indicate hypersplenism complicating liver cirrhosis. Leukocytosis with predominance of polymorphonuclear cells (PMN) in the presence of fever and abdominal pain indicate SBP. Lymphocytosis may suggest tuberculosis.
Abnormal liver enzymes with hypoalbuminemia and altered coagulation parameters are suggestive of hepatic origin of ascites. On the other hand, hypercholesterolemia together with hypoalbuminemia and heavy albuminurea indicate a nephrotic disorder.
Imaging
Although ultrasonography and computed tomography can be useful in detecting and aspirating small amounts of fluids and lobulated ascites as well as helping to diagnose the etiology, they are usually not implemented as the first line investigations of ascites.
Diagnostic paracentesis
Diagnostic ascitic taping is the most rapid and cost-effective test for identifying the cause of ascites and the only method of diagnosing ascitic fluid infection [2] . Therefore, parancentesis should be included in the firstline investigation of patients with new-onset or complicated ascites. Characteristics of ascitic aspirate are shown in [Table - 1],[Table - 2]. Routine tests should include albumin concentration in the first tap, leukocytes with differential count and bacterial culture in blood culture bottles [Figure - 1]. Other tests including ascitic fluid total protein (AFTP), glucose, lactate dehydrogenase (LDH), cytology, acid fast bacilli smear, gram stain, culture and amylase are performed selectively. Simultaneous serum investigation should include albumin, while blood culture, glucose, LDH and amylase are done selectively, when indicated [2] .
Routine Tests
Ascitic fluid albumin: Ascitic fluid albumin with simultaneous serum albumin concentration measurement is necessary for calculation of the serumascitic fluid albumin gradient (SAAG). It is calculated by subtraction of ascitic fluid albumin from the serum albumin concentration. The SAAG correlates directly with portal pressure. At > 1.1. g/dl, SAAG accurately (96.7%) differentiates portal hypertension from other disorders. Similarly, mixed ascites (portal hypertension with another disorder i.e. tuberculosis) is associated with an elevated SAAG [8],[9],[10] . Diuresis and therapeutic paracentesis do not alter SAAG. Therefore, in many places, SAAG has replaced the exudate-transudate concept [8] .
Tuberculosis and neoplasm are associated with a low SAAG. Low SAAG (< 1.1 g/dl) has been found to be the most helpful test in the diagnosis of malignant ascites [1] . On the other hand, a high SAAG (>1.1 g/dl) has been found in patients with peritoneal tuberculosis associated with hepatic cirrhosis [8] and in all patients suffering from malignant ascites with liver involvement.
Cell count and culture: White cell count and PMN count are useful to detect ascitic fluid infections. A PMN count of 250 cells/mm 3 with growth of bacteria in the absence of external or intraabdominal source of infection are diagnostic for SBP [12],[13] . When the culture is negative in patients not treated with antibiotic treatment over one month, it is called culture negative neutrocytic ascites (CNNA), which is an important variant of SBP [14],[15] . Nowadays CNNA is less frequently diagnosed, since the bedside inoculation of blood culture bottle has been adopted with an accuracy rate of 93% compared to 43% for the conventional broth and agar inoculation technique [14] . Another variant of ascitic fluid infection is the monomicrobial nonneutrocytic ascites (MNA), characterized by culture growth of a single microorganism and PMN < 250 cells/mm 3 [16] and also known as bacterascites. A lymphocytes predominance indicates peritoneal tuberculosis, or malignant ascites
Selective tests
In certain conditions, some of the following tests may help supporting the etiological diagnosis of ascites proposed by the routine investigation.
Ascitic fluid total protein: It was the mainstay of classifying ascites into exudate ( 25 g/L) or transudate (< 25g/L). While transudate is found in association with liver cirrhosis, cardiac ascites and nephrotic syndrome, peritoneal carcinomatosis and tuberculosis are associated with an exudative ascites. Due to AFIP low accuracy, SAAG has been proposed to replace it [8] . However, AFTP is valuable in differentiating SBP from secondary perforation- associated peritonitis. A very low AFTP (< 1 g/dl) favors SBP and predispose in noninfected ascites to SAP [7] . On the other hand, a high AFTP with high SAAG advocateste cardiac disorder as the cause of ascites [18] .
Ascitic fluid glucose and ascitic fluid-serum glucose ratio: In patients with neoplasm and SBP, glucose consumption is increased, resulting in a decrement of glucose and glucose ratio compared to cirrhotics [11] .
Ascitic fluid lactate dehydrogenase (LDH): LDH concentration increases significantly in SBP and in malignant ascites compared to cirrhotics [10],[11] .
Ascitic fluid pH and gradient: Patients with SBP and malignant ascites have a low pH and high blood-ascitic fluid pH gradient compared to cirrhotics [11] .
Ascitic fluid amylase: Amylase concentration may help in differentiating ascites due to pancreatitis from other causes [1] .
Ascitic fluid cytology: Cytology should only be performed when neoplasm is suspected. It is essentially positive in all patients with carcinomatosis contrary to those without peritoneal involvement, where cytology remains negative [19] .
Ascitic fluid gram stain: Gram stain may help to differentiate ascitic fluid infection. It is more frequently positive in secondary peritonitis [20] . Ascitic fluid pH, lactate and humoral test for malignancy including fibronectin and cholesterol have rather been considered as a relatively useless test [21] .
| Management | | |
A proper diagnosis is a prerequisite for a successful treatment of ascites. SAAG helps to identify the cause of ascites. It is low (< 1.1 g/dl) in patients with nonportal hypertensive-associated ascites induced by a variety of disease responding to specific treatment including tuberculosis, neoplasm and pancreatic disorders.
A high SAAG ( 1.1 g/dl) is found in portal hypertensive ascites which contributes to approximately 80 % of all causes of ascites and represented mainly by liver cirrhosis. Other forms of portal hypertensive ascites include mixed ascites, cardiac ascites and venous occlusion.A vast majority (90 %) of patients with portal hypertensiveassociated ascites (PHA) respond well to firstline treatment [22],[23],[24] . Management of ascites due to liver cirrhosis is summarized in [Figure - 2].
Firstline treatment:
Bedrest: In patients with liver cirrhosis and ascites, upright position is associated with a reduction of glomerular filtration rate (GFR) and sodium excretion as a result of blood pooling. Consequently, renin-angiotensin and sympathetic nervous system activities are enhanced with further sodium and water retention. In contrary, bedrest is associated with a better renal perfusion, increased GFR, sodium excretion and a better response to diuretics. Therefore, bedrest may benefit in the treatment of mild ascites and ascites with inappropriate response to diuretics [25].
Sodium restriction: It is considered as the conservative treatment of PHA. A daily dietary sodium of 2g (88mEq) has been considered appropriate [26] . Approximately 10 % with mild-moderate ascites respond to sodium restriction and bedrest [27] . Water restriction is not indicated except in the presence of severe hyponatremia (< 125 mEq/L) [26] .
Diuretics: Patients with PHA not responding to dietary sodium restriction require addition of diuretics. Spironolactone and furosemide are the most frequently used diuretics. Spironolactone, a potassium-sparing diuretic acting at the distal tubules, is considered as the standard therapeutic agent. It is more effective than the loop diuretic, furosemide [28] but has a delayed onset of diuresis (approximately two weeks) [23] . Spironolactone may be used alone, but commonly, it is combined with furosemide in a dose of 100 mg and 40 mg, respectively. The treatment response is assessed by monitoring of body weight and urinary sodium excretion. The optimal diuresis is achieved at a negative sodium balance and weight loss of 500 g/day. In patients with ascites and edema, greater negative sodium balance and more weight loss are better tolerated. Since mobilization of ascites is limited, weight loss greater than one kg/day may be complicated with azotemia [29] . Urinary sodium levels below 10 mmol/L with 24-hours urinary volume less than one liter necessitate further dose increment, maximally up to 400 and 160 mg for spironolactone and furosemide, respectively [30] . Approximately 90 % of liver cirrhosis-induced ascites respond to salt restriction combined with spironolactone and furosemide [24] .
Diuresis is associated with a number of adverse effects including hypokalemia, alkalosis and encephalopathy. Hypokalemia and encephalopathy have been reported in 15.7 and 11.6 % of cirrhotic patients treated with furosemide, respectively [31] .
Secondline treatment:
A small proportion (10%) of patients not responding to diuretics require an alternative treatment. Secondline management of ascites is provided by a variety of modalities including large volume paracentesis (LVP), extracorporeal ascitic fluid ultrafiltration and reinfusion, peritoneovenous shunting (PVS), tranjugular intrahepatic portosystemic stent-shunting (TIPS) and orthotopic liver transplantation (OLT).
Large volume paracentesis (LVP): LVP (4-6 liters) is effective, safe and widely practiced. Asymptomatic LVP complications may not necessitate treatment. Repeated, long-term LVP is associated with protein-loss with reduction of complement and opsonines predisposing to ascitic fluid infections. LVP has been considered as the mainstay treatment for tense and drug-resistant ascites [32] . The benefit if i.v plasma expansion is controversial. While in some studies intravenous albumin infusion (6-8 g/L removed ascites) have been found beneficial in reducing complications [33] . Other uncontrolled studies reported no significant alteration in plasma volume, serum electrolytes and renal functions in patient with tense ascites treated by LVP without albumin infusion [34] .
Total paracentesis (TP) with a mean volume removal of 10.7 ± 0.5 L (range 6.3 - 22.5) over a median of 60 minutes in adjunction with i.v albumin infusion has also been found to be safe. Plasma volume, as well as plasma renin, aldosterone, GFR and liver function remained unaffected [35] .
Other plasma expanders such as dextran 70 (6 g/L) and hemaccel (150 ml/L evacuated ascites) have been comparable in effect and safety with albumin infusion in patients with LVP and TP [36],[37] . Dextran 70 and hemaccel are good alternatives for albumin with a considerably lower cost, 15.5 compared to 364.3 dollars per patient for dextran 70 and albumin, respectively [36] .
Ascitic fluid recirculation (AR): AR using extracorporeal ultrafiltration, and i.v. reinfusion of ascitic fluid concentrate has been reported in 1975 (38). Due to associated complications in the form of infection and disseminated intravascular coagulopathy (DIC), the method has not gained popularity. Large controlled trials are required to evaluate the efficacy and safety of the newer hemodialysis membranes [24] .
Peritoneovenous shunting (PVS): Le Veen introduced in 1974 the PVS for management of patients with refractory ascites [39] . A connecting tube between the peritoneal cavity and systemic circulation allows a continuous volume expansion with adequate renal perfusion resulting in a better GFR and diuresis. Due to frequent obstruction of Le Veen shunt, two other types with an external pumping device, the Denever and the Hakim-Cordis PVS have been developed with uncertain advantages [22] .
The use of PVS is associated with a number of serious complications including a high operative mortality in cirrhotics (25%), septicemia, DIC, obstruction, upper gastrointestinal bleeding, hepatic coma and heart failure [40] . PVS may be still considered in patients unable to attend repeated LVP [24] .
Transjugular intrahepatic prostosystemic stent-shunting (TIPS): This technique has initially been used for treatment of refractory esophageal bleeding with a significant reduction of the mean portal pressure [41] . Refractory ascites has also responded well to TIPS [42],[43] . In association with clinical responses, there has been an improvement of nutrition and creatinine clearance [43] . Encephalopathy complicating TIPS will limit its use.
However, TIPS appears to be a beneficial alternative for treatment of refractory ascites. Efficacy and safety need to be evaluated by large scale studies.
Orthopedic liver transplantation (OLT): The only curable treatment for a liver disease with ascites is OLT. The 12 months survival rate for patients with refractory ascites is as low as 25% [44] . However, the overall 3-5 years survival rate of transplanted adult patients with liver cirrhosis and ascites increases up to 70 % [45].
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Correspondence Address:
Ibrahim A Al Mofleh
Department of Gastroenterolgy (59) P.O. Box 2925, Riyadh 11461
Saudi Arabia
PMID: 19864832
[Figure - 1], [Figure - 2]
[Table - 1], [Table - 2] | |
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