The word ascites is of Greek origin (askos) and means bag or sac. Ascites describes the condition of pathologic fluid collection within the abdominal cavity (see the image below). Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle.[1] This article focuses only on ascites associated with cirrhosis.
View Image
Ascites. This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.
The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Although many pathogenic processes have been implicated in the development of abdominal ascites, about 75% likely occur as a result of portal hypertension in the setting of liver cirrhosis, with the remainder due to infective, inflammatory, and infiltrative conditions.[2]
Three theories of ascites formation have been proposed: underfilling, overflow, and peripheral arterial vasodilation.
The underfilling theory suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention.
The overflow theory suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia.
The peripheral arterial vasodilation hypothesis includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation theory proposes that underfilling is operative early and overflow is operative late in the natural history of cirrhosis.
Although the sequence of events that occurs between the development of portal hypertension and renal sodium retention is not entirely clear, portal hypertension apparently leads to an increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those without ascites.
Regardless of the initiating event, a number of factors contribute to the accumulation of fluid in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.
The prevalence of chronic liver disease and cirrhosis in the United States is estimated to be 4.5 million.[4] The incidence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) is expected to rise, leading to an increased incidence of cirrhosis.[5]
The prognosis for patients with ascites due to liver disease depends on the underlying disorder, the degree of reversibility of a given disease process, and the response to treatment.
Morbidity/mortality
Worldwide, cirrhosis accounts for an estimated 1 million deaths per year.[6] Ambulatory patients with an episode of cirrhotic ascites have a 3-year mortality rate of 50%. The development of refractory ascites carries a poor prognosis, with a 1-year survival rate of less than 50%.[7]
Complications
The most common complication of ascites is the development of spontaneous bacterial peritonitis (ascitic fluid with PMN count of >250 μ L). Note the following:
Performing repeated physical examinations and paying particular attention to abdominal tenderness may be the best way to become aware of the possible development of this complication. In a study of 133 hospitalized patients with ascites, abdominal pain and abdominal tenderness were more common in patients with spontaneous bacterial peritonitis (P< 0.01), but no other physical sign or laboratory test could separate spontaneous bacterial peritonitis cases from other cases.[8]
Any patient with ascites and fever should have a paracentesis with bedside blood culture inoculation and cell count. Patients with a protein level of less than 1 g/dL in ascitic fluid are at high risk for the development of spontaneous bacterial peritonitis. Prophylactic antibiotic therapy with a quinolone is often recommended.
Complications of paracentesis include infection, electrolyte imbalances, bleeding, and bowel perforation. Bowel perforation should be considered in any patient with recent paracentesis who develops a new onset of fever and/or abdominal pain. All patients with long-standing ascites are at risk of developing umbilical hernias. Large-volume paracentesis often results in large intravascular fluid shifts. This can be avoided by administering albumin replacement if more than 5 L is removed.
Acute kidney injury in the setting of ascites and cirrhosis is a medical emergency, requiring prompt diagnosis and multimodal management.[9]
The most important aspect of patient education is determining when therapy is failing and recognizing the need to see a physician. Unfortunately, in most cases, liver failure has a dismal prognosis. All patients must be taught which complications are potentially fatal and the signs and symptoms that precede them.
Abdominal distention and/or pain despite maximal diuretic therapy are common problems, and patients must realize the importance of seeing a physician immediately.
Patients with ascites often state that they have recently noticed an increase in their abdominal girth.
Because most cases of ascites are due to liver disease, patients with ascites should be asked about risk factors for liver disease. These include the following:
Long-term heavy alcohol use
Chronic viral hepatitis or jaundice
Intravenous drug use
Multiple sexual partners
Homosexual activity with a male partner, or heterosexual activity with a bisexual male
Transfusion with blood not tested for hepatitis virus: In the United States, screening of donated blood for hepatitis B virus (HBV) began in 1972; reliable testing of the blood supply for hepatitis C virus (HCV) began in 1992 in developed countries
Tattoos
Living or birth in an area endemic for hepatitis
Patients with alcoholic liver disease who alternate between heavy alcohol consumption and abstention (or light consumption) may experience ascites in a cyclic fashion.
When a patient with a very long history of stable cirrhosis develops ascites, the possibility of superimposed hepatocellular carcinoma (HCC) should be considered.
Obesity, hypercholesterolemia, and type 2 diabetes mellitus are recognized causes of nonalcoholic steatohepatitis, which can progress to cirrhosis.
Patients with a history of cancer, especially gastrointestinal cancer, are at risk for malignant ascites. Malignancy-related ascites is frequently painful, whereas cirrhotic ascites is usually painless.
Patients who develop ascites in the setting of established diabetes or nephrotic syndrome may have nephrotic ascites.
The physical examination in a patient with ascites should focus on the signs of portal hypertension and chronic liver disease. Note the following:
Physical findings suggestive of liver disease include jaundice, palmar erythema, and spider angiomas.
The liver may be difficult to palpate if a large amount of ascites is present, but if palpable, the liver is often found to be enlarged. The puddle sign may be present when as little as 120 mL of fluid is present. When peritoneal fluid exceeds 500 mL, ascites may be demonstrated by the presence of shifting dullness or bulging flanks. A fluid-wave sign is notoriously inaccurate.
Elevated jugular venous pressure may suggest a cardiac origin of ascites. A firm nodule in the umbilicus, the so-called Sister Mary Joseph nodule, is not common but suggests peritoneal carcinomatosis originating from gastric, pancreatic, or hepatic primary malignancy.
A pathologic left-sided supraclavicular node (Virchow node) suggests the presence of upper abdominal malignancy.
Patients with cardiac disease or nephrotic syndrome may have anasarca.
Abdominal ultrasonography, diagnostic paracentesis, and ascitic fluid cultures are recommended by the British Society of Gastroenterology, the European Association for the Study of the Liver (EASL), and the American Association for the Study of Liver Diseases (AASLD), particularly in the setting of suspected infection.[2]
Laparoscopy may be valuable for the diagnosis of otherwise unexplained cases, especially if malignant ascites is suspected.[10] This may be of particular importance in the diagnosis of malignant mesothelioma.
In patients with new-onset ascites of unknown origin, peritoneal fluid should be sent for cell count, albumin level, culture, total protein, Gram stain, and cytology. Note the following:
Inspection: Most ascitic fluid is transparent and tinged yellow. A minimum of 10,000 red blood cells/µL is required for ascitic fluid to appear pink, and more than 20,000 red blood cells/µL will produce distinctly blood-tinged fluid. This may result from either a traumatic tap or malignancy. Bloody fluid from a traumatic tap is heterogeneously bloody, and the fluid will clot. Nontraumatic bloody fluid is homogeneously red and does not clot because the blood has already clotted and lysed. Cloudy ascitic fluid with a purulent consistency indicates infection.
Cell count: Normal ascitic fluid contains fewer than 500 leukocytes/µL and fewer than 250 polymorphonuclear leukocytes (PMNs)/µL. Any inflammatory condition can cause an elevated white blood cell count. A PMN count of greater than 250 cells/µL is highly suggestive of bacterial peritonitis.[11] In tuberculous peritonitis and peritoneal carcinomatosis, lymphocytes usually predominate.
Serum ascites albumin gradient (SAAG): The SAAG is the best single test for classifying ascites into portal hypertensive (SAAG >1.1 g/dL) and non–portal hypertensive (SAAG < 1.1 g/dL) causes. Calculated by subtracting the ascitic fluid albumin value from the serum albumin value, it correlates directly with portal pressure. The specimens should be obtained relatively simultaneously. The accuracy of the SAAG results is approximately 97% in classifying ascites. The terms high-albumin gradient and low-albumin gradient should replace the terms transudative and exudative in the description of ascites.
Total protein: In the past, ascitic fluid has been classified as an exudate if the protein level is greater than or equal to 2.5 g/dL. However, the accuracy is only approximately 56% for detecting exudative causes. The total protein level may provide additional clues when used with the SAAG. An elevated SAAG and a high protein level are observed in most cases of ascites due to hepatic congestion. The combination of a low SAAG and a high protein level is characteristic of malignant ascites (see Etiology).
Culture/Gram stain: Culture has a 92% sensitivity for the detection of bacteria in ascitic fluid, provided that samples are inoculated into blood culture bottles immediately, at the bedside. In contrast, Gram stain is only 10% sensitive for visualizing bacteria in early-detected spontaneous bacterial peritonitis. Approximately 10,000 bacteria/mL are required for detection by Gram stain; the median concentration of bacteria in spontaneous bacterial peritonitis is 1 organism/mL.
Cytology: Cytology smears are reported to be 58-75% sensitive for detection of malignant ascites.
Ascitic amylase cultures/PCR are recommended for suspected pancreatitis, and mycobacterial cultures/PCR for suspected tuberculosis.[2]
Elevation of the diaphragm, with or without sympathetic pleural effusions (hepatic hydrothorax), is visible in the presence of massive ascites. More than 500 mL of fluid is usually required for ascites to be diagnosed based on findings from abdominal films.
Many nonspecific signs suggest ascites, such as diffuse abdominal haziness, bulging of the flanks, indistinct psoas margins, poor definition of the intra-abdominal organs, erect position density increase, separation of small bowel loops, and centralization of floating gas containing small bowel.
The direct signs are more reliable and specific. In 80% of patients with ascites, the lateral liver edge is medially displaced from the thoracoabdominal wall (Hellmer sign). In the pelvis, fluid accumulates in the rectovesical pouch and then spills into the paravesical fossa. The fluid produces symmetric densities on both sides of the bladder, which is termed a "dog's ear" or "Mickey Mouse" appearance. Medial displacement of the cecum and ascending colon and lateral displacement of the properitoneal fat line are present in more than 90% of patients with significant ascites. Although obliteration of the hepatic angle as been suggested as a sign of increased intra-abdominal fluid, this finding is seen in 80% of healthy patients.
Ultrasonography
Real-time ultrasonography is the easiest and most sensitive technique for the detection of ascitic fluid. Volumes as small as 5-10 mL can routinely be visualized. Uncomplicated ascites appears as a homogeneous, freely mobile, anechoic collection in the peritoneal cavity that demonstrates deep acoustic enhancement. Free ascites does not displace organs but typically situates itself between them, contouring to organ margins and demonstrating acute angles at the point at which the fluid borders the organ.
The smallest amounts of fluid tend to collect in the Morison pouch (posterior subhepatic space) and around the liver as a sonolucent band. With massive ascites, the small bowel loops have a characteristic polycyclic, "lollipop," or arcuate appearance because they are arrayed on either side of the vertically floating mesentery.
Certain ultrasonographic findings suggest that the ascites may be infected, inflammatory, or malignant. These findings include coarse internal echoes (blood), fine internal echoes (chyle), multiple septa (tuberculous peritonitis, pseudomyxoma peritonei), loculation or atypical fluid distribution, matting or clumping of bowel loops, and thickening of interfaces between fluid and adjacent structures. In malignant ascites, the bowel loops do not float freely but may be tethered along the posterior abdominal wall, plastered to the liver or other organs, or surrounded by loculated fluid collections.
Most patients (95%) with carcinomatous peritonitis have a gallbladder wall that is less than 3 mm thick. Mural thickening of the gallbladder is associated with benign ascites in 82% of cases. The thickening of the gallbladder is primarily a reflection of cirrhosis and portal hypertension.
Computed tomography (CT) scanning
Ascites is demonstrated well on CT scan images. Small amounts of ascitic fluid localize in the right perihepatic space, the posterior subhepatic space, and the Douglas pouch (rectouterine pouch). See the image below.
View Image
Ascites. This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.
A number of CT scan features suggest neoplasia. Hepatic, adrenal, splenic, or lymph node lesions associated with masses arising from the gut, ovary, or pancreas are suggestive of malignant ascites. Patients with malignant ascites tend to have proportional fluid collections in the greater and lesser sacs; whereas, in patients with benign ascites, the fluid is observed primarily in the greater sac and not in the lesser omental bursae.
Abdominal paracentesis is the most rapid and perhaps the most cost-effective method of diagnosing the cause of ascites formation. Guidelines from the American Association for the Study of Liver Diseases (AASLD) and from the British Society of Gastroenterology on the management of adult patients with ascites due to cirrhosis advocate paracentesis in all patients with clinically apparent new-onset ascites.[12, 13, 14]
Bleeding from paracentesis is sufficiently uncommon that the AASLD does not recommend the prophylactic use of fresh frozen plasma or platelets beforehand.[12]
For more detailed information regarding paracentesis, including images and video, please see the Medscape article Paracentesis [in the Clinical Procedures section].
Sodium restriction (20-30 mEq/d) and diuretic therapy constitute the standard medical management for ascites and are effective in approximately 95% of patients. Note the following:
Water restriction is used only if persistent hyponatremia is present (see Diet, below).
Patients with ascites and hyponatremia may be treated with aquaretics—vasopressin V2-receptor antagonists that promote excretion of electrolyte-free water.[15] Tolvaptan has been approved by the FDA for treating hypervolemic hyponatremia in ascites. Conivaptan has been approved by the FDA for treating hypervolemic hyponatremia in syndrome of inappropriate antidiuretic hormone; however, studies specific to efficacy in cirrhosis are lacking.[16]
In a multicenter study that assessed the safety and efficacy of an automated pump system for the treatment of refractory ascites in 40 patients at 9 centers, Bellot et al reported the automated pump was an efficacious tool to remove ascites from the peritoneal cavity to the bladder.[17] During the 6-month follow-up period, 90% of the ascites was removed with the pump system; there was also a significant reduction in the monthly median number of large volume paracentesis as well as a reduction in the number of cirrhosis-related adverse events.[17]
Therapeutic paracentesis may be performed in patients who require rapid symptomatic relief for refractory or tense ascites. When small volumes of ascitic fluid are removed, saline alone is an effective plasma expander.[18] The removal of 5 L of fluid or more is considered large-volume paracentesis.[2] Total paracentesis, that is, removal of all ascites (even >20 L), can usually be performed safely.
Supplementing 5 g of albumin per each liter over 5 L of ascitic fluid removed decreases complications of paracentesis, such as electrolyte imbalances and increases in serum creatinine levels secondary to large shifts of intravascular volume. Note: The AASLD indicates that postparacentesis albumin infusion may not be necessary for a single paracentesis of less than 4 to 5 L ((class I, level C recommendation); however, for large-volume paracenteses, an albumin infusion of 6-8 g per liter of fluid removed appears to improve survival and is recommended (class IIa, level C recommendation).[19]
To avoid exposing patients to blood products, the use of terlipressin (eg, 1 mg every 4 hours for 48 hours) rather than albumin has been proposed for prevention of circulatory dysfunction after large-volume paracentesis. Initial studies suggest that terlipressin is as effective as albumin for this purpose.[20, 21]
Repeated therapeutic paracentesis can be used to treat refractory ascites (class I, level C recommendation).[19] For palliative care in patients with advanced cancer, an alternative to serial paracenteses is placement of an indwelling peritoneal catheter; ascitic fluid can then be removed by continuous drainage[22] or intermittent drainage with a proprietary system utilizing vacuum bottles, which can be performed in the patient's home.[23] Preservation of good nutrition status is important.[24]
The transjugular intrahepatic portosystemic shunt (TIPS) is an interventional radiologic technique that reduces portal pressure and may be the most effective treatment for patients with diuretic-resistant ascites. In the procedure, which is performed with the patient under conscious sedation or general anesthesia, an interventional radiologist places a stent percutaneously from the right jugular vein into the hepatic vein, thereby creating a connection between the portal and systemic circulations. TIPS is gradually becoming the standard of care in patients with diuretic-refractory ascites.
In a systematic review and meta-analysis of 10 trials comprising 462 patients with cirrhotic ascites, Guo et al reported that midodrine, a vasopressor, used as a novel therapy for the ascites caused by cirrhosis did not improve survival but potentially improved response rates and reduced plasma renin activity.[25] However, when midodrine was used as an alternative to albumin in large-volume paracentesis, the mortality was higher for those receiving midodrine than for those receiving albumin; midodrine and albumin had a similar association with the development of paracentesis-induced circulatory dysfunction.[25]
Conservative management appears to be the treatment of choice for patients with chylous ascites.[3]
Patients can actually be maintained free of ascites if sodium intake is limited to 10 mmol/d. However, this is not practical outside a metabolic ward.
Twenty-four–hour urinary sodium measurements are useful in patients with ascites related to portal hypertension in order to assess the degree of sodium avidity, monitor the response to diuretics, and assess compliance with diet.
For grade 3 or 4 ascites, therapeutic paracentesis may be necessary intermittently.
Consultation with a gastrointestinal specialist and/or hepatologist should be considered for all patients with ascites, particularly if the ascites is refractory to medical treatment.
The peritoneovenous shunt is an alternative for patients with medically intractable ascites. This is a megalymphatic shunt that returns the ascitic fluid to the central venous system. Beneficial effects of these shunts include increased cardiac output, renal blood flow, glomerular filtration rate, urinary volume, and sodium excretion and decreased plasma renin activity and plasma aldosterone concentration. Although it has largely been supplanted by transjugular intrahepatic portosystemic shunt (TIPS), peritoneovenous shunting has been shown to improve short-term survival (compared with paracentesis) in cancer patients with refractory malignant ascites.[26] The AASLD suggests considering peritoneovenous shunting for patients with refractory ascites who are not candidates for paracentesis, transplant, or TIPS (class I, level A recommendation).[19]
Sodium restriction of 500 mg/d (22 mmol/d) is feasible in a hospital setting; however, it is unrealistic in most outpatient settings. A more appropriate sodium restriction is 2000 mg/d (88 mmol). Indiscriminate fluid restriction is inappropriate. Fluids need not be restricted unless the serum sodium level drops below 120 mmol/L.
The best method of assessing the effectiveness of diuretic therapy is by monitoring body weight and urinary sodium levels.
In general, the goal of diuretic treatment of ascites should be to achieve a weight loss of 300-500 g/d in patients without edema and 800-1000 g/d in patients with edema.
Once ascites has disappeared, diuretic treatment should be adjusted to the minimum effective dose to avoid recurrences.[14]
The goals of pharmacotherapy are to reduce morbidity and to prevent complications in patients with ascites.
Diuretics should be initiated in patients whose ascites does not respond to sodium restriction. A useful regimen is to start with spironolactone at 100 mg/d. The addition of loop diuretics may be necessary in some cases to increase the natriuretic effect. If no response occurs after 4-5 days, the dosage may be increased stepwise up to spironolactone at 400 mg/d plus furosemide at 160 mg/d.
V2 receptor antagonists may be considered in the management of patients with cirrhosis, ascites, and dilutional hyponatremia.[15]
Clinical Context:
For the management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions. The peak effect of Aldactone is approximately 3 d.
Clinical Context:
Increases the excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Dose must be individualized to patient.
Depending on the response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until the desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until a satisfactory effect is achieved.
Clinical Context:
A pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. Potassium-conserving (antikaliuretic) drug which, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.
Clinical Context:
Helps treat edema in congestive heart failure. Increases excretion of sodium, water, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal tubules. May be more effective in those with impaired renal function.
Clinical Context:
Tolvaptan is an oral selective vasopressin V2-receptor antagonist. It is indicated for hypervolemic and euvolemic hyponatremia (ie, serum Na level < 125 mEq/L) or less marked hyponatremia that is symptomatic and has resisted correction with fluid restriction. It is used for hyponatremia associated with CHF, liver cirrhosis, and syndrome of inappropriate antidiuretic hormone secretion (SIADH).
Initiate or reinitiate the drug in a hospital environment only since there may be overly rapid correction of the hyponatremia. However, it increases thirst (potentially limiting its effects) and is expensive.
Clinical Context:
Conivaptan is a parenteral nonselective vasopressin receptor antagonist used for the treatment of euvolemic hyponatremia in hospitalized patients. Conivaptan increases urine output of mostly free water, with little electrolyte loss. It is indicated for hospitalized patients with more severe euvolemic or hypervolemic hyponatremia.
The potential benefits of these drugs include the predictability of their effect, rapid onset of action, and limited urinary electrolyte excretion. Conivaptan and tolvaptan are currently the only vasopressin receptor antagonists that are commercially available in the United States and FDA-approved for the treatment of euvolemic hyponatremia in hospitalized patients. These medications should be initiated in a closely monitored setting to prevent rapid correction of serum Na+, which can result in central pontine myelinolysis (CPM).[27]
What are ascites?What is the pathophysiology of ascites formation?What are the morbidity rates for ascites?How does the presence of intraperitoneal fluid in ascites differ between males and females?What is the prognosis of ascites?What information about ascites should patients receive?What is the clinical presentation of ascites?What should be the focus of the clinical history for ascites?Which clinical history is characteristic of ascites?How is peritonitis diagnosed in patients with ascites?What are complications of paracentesis in ascites?How is acute kidney injury in ascites managed?What should be included in the physical exam for ascites?What causes ascites formation in normal peritoneum?What causes ascites formation in diseased peritoneum?What are the differential diagnoses for Ascites?What is included in the workup of ascites?What is the role of lab studies in the workup of ascites?What is the role of radiography in the workup of ascites?What is the role of ultrasonography in the workup of ascites?What is the role of CT scanning in the workup of ascites?What is the role of paracentesis in the workup of ascites?How is ascites staged?What is included in medical management of ascites?What is the treatment of choice for chylous ascites?What is the role of surgery in the treatment of ascites?Which specialist consultations are needed for the management of ascites?What are dietary restrictions for the treatment of ascites?What is included in long-term monitoring for ascites?What are the goals of drug treatment for ascites?Which medications in the drug class Diuretics are used in the treatment of Ascites?
Rahil Shah, MD, Consulting Staff, Lebanon Endoscopy Center
Disclosure: Received consulting fee from Takeda for speaking and teaching.
Coauthor(s)
Janice M Fields, MD, FACG, FACP, Assistant Professor of Internal Medicine, Oakland University William Beaumont School of Medicine; Consulting Staff, Department of Internal Medicine, Section of Gastroenterology, Providence Hospital, St John Macomb-Oakland Hosptial
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Praveen K Roy, MD, MSc, Clinical Assistant Professor of Medicine, University of New Mexico School of Medicine
CDC/National Center for Health Statistics. Chronic liver disease and cirrhosis. Centers for Disease Control and Prevention. January 17, 2023. Available at https://www.cdc.gov/nchs/fastats/liver-disease.htm. Accessed: May 30, 2023.
[Guideline] Runyon BA, American Association for the Study of Liver Diseases. Management of adult patients with ascites due to cirrhosis: update 2012. National Guideline Clearinghouse. Available at http://guideline.gov/content.aspx?id=45103&search=ascites. Accessed: Nov 6, 2014.
){kind=link}
){kind=link}