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Ascites
Introduction
Background
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. 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. This article focuses only on ascites associated with cirrhosis.
This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.
[ CLOSE WINDOW ]
This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.
For excellent patient education resources, visit eMedicine's Liver, Gallbladder, and Pancreas Center and Heart Center. Also, see eMedicine's patient education articles Cirrhosis, Hepatitis B, Hepatitis C, and Congestive Heart Failure.
Pathophysiology
The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. 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 most recent theory, 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.
Mortality/Morbidity
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%.
Sex
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.
Clinical
History
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:
o Long-term heavy alcohol use
o Chronic viral hepatitis or jaundice
o Intravenous drug use
o Multiple sexual partners
o Homosexual activity with a male partner, or heterosexual activity with a bisexual male
o 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
o Tattoos
o 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.
Physical
The physical examination in a patient with ascites should focus on the signs of portal hypertension and chronic liver disease.
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.
Causes
Normal peritoneumo Portal hypertension (serum-ascites albumin gradient [SAAG] >1.1 g/dL)
Hepatic congestion, congestive heart failure, constrictive pericarditis, tricuspid insufficiency, Budd-Chiari syndrome
Liver disease, cirrhosis, alcoholic hepatitis, fulminant hepatic failure, massive hepatic metastases
o Hypoalbuminemia (SAAG <1.1 g/dL)
Nephrotic syndrome
Protein-losing enteropathy
Severe malnutrition with anasarca
o Miscellaneous conditions (SAAG <1.1 g/dL)
Chylous ascites
Pancreatic ascites
Bile ascites
Nephrogenic ascites
Urine ascites
Ovarian disease
Diseased peritoneum (SAAG <1.1 g/dL)
o Infections
Bacterial peritonitis
Tuberculous peritonitis
Fungal peritonitis
Human immunodeficiency virus (HIV)-associated peritonitis
o Malignant conditions
Peritoneal carcinomatosis
Primary mesothelioma
Pseudomyxoma peritonei
Hepatocellular carcinoma
o Other rare conditions
Familial Mediterranean fever
Vasculitis
Granulomatous peritonitis
Eosinophilic peritonitis
Differential Diagnoses
Acute Liver Failure Hepatorenal SyndromeAlcoholic Hepatitis Mediterranean Fever, FamilialBiliary Disease Nephrotic SyndromeBudd-Chiari Syndrome Portal HypertensionCardiomyopathy, Dilated Primary Biliary CirrhosisCardiomyopathy, RestrictiveProtein-Losing EnteropathyCirrhosisHepatitis, ViralHepatocellular Adenoma
Workup
Laboratory Studies
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.
o 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.
o 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.1 In tuberculous peritonitis and peritoneal carcinomatosis, lymphocytes usually predominate.
o 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.
o 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 Causes).
o 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.
o Cytology: Cytology smears are reported to be 58-75% sensitive for detection of malignant ascites.
Imaging Studies
Chest and plain abdominal filmso 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.
o 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.
o 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
o 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.
o 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.
o 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.
o 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).
o
This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.
[ CLOSE WINDOW ]
This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.
o 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.
Other Tests
Laparoscopy may be valuable for the diagnosis of otherwise unexplained cases, especially if malignant ascites is suspected.2 This may be of particular importance in the diagnosis of malignant mesothelioma.
Procedures
Abdominal paracentesis: 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) for management of adult patients with ascites due to cirrhosis advocate paracentesis in all patients with clinically apparent new-onset ascites (grade II-3 recommendation).3
Bleeding from paracentesis is sufficiently uncommon that the AASLD does not recommend the prophylactic use of fresh frozen plasma or platelets beforehand (grade III).3
For more detailed information regarding paracentesis, including images and video, please see the eMedicine article Paracentesis [in the Clinical Procedures section].
Staging
Ascites may be semi-quantified using the following system:
o Stage 1+ is detectable only after careful examination.
o Stage 2+ is easily detectable but of relatively small volume.
o Stage 3+ is obvious, but not tense, ascites.
o Stage 4+ is tense ascites.
Treatment
Medical Care
Sodium restriction (20-30 mEq/d) and diuretic therapy constitute the standard medical management for ascites and are effective in approximately 95% of patients.
Water restriction is used only if persistent hyponatremia is present (see Diet, below). Recent research has focused on the treatment of refractory ascites with aquaretics—
vasopressin V2-receptor antagonists that promote excretion of electrolyte-free water and thus might be beneficial in patients with ascites and hyponatremia.4 Although study results have been promising,5 aquaretics still await approval by the Food and Drug Administration (FDA).
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.6 The removal of 5 L of fluid or more is considered large-volume paracentesis. 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; however, for large-volume paracenteses, the AASLD suggests considering an albumin infusion of 8-10 g per liter of fluid removed (Grade II-2).3
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.7,8
Repeated therapeutic paracentesis can be used to treat refractory ascites.3 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 drainage9 or intermittent drainage with a proprietary system utilizing vacuum bottles, which can be performed in the patient’s home.10
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.
Surgical Care
Peritoneovenous shunt.
[ CLOSE WINDOW ]
Peritoneovenous shunt.
The peritoneovenous shunt is an alternative for patients with medically intractable ascites (see image above). 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 TIPS, peritoneovenous shunting has been shown to improve short-term survival (compared with paracentesis) in cancer patients with refractory malignant ascites.11 The AASLD suggests considering peritoneovenous shunting for patients with refractory ascites who are not candidates for paracentesis or TIPS (Grade I).3
The AASLD recommends that patients with cirrhosis and ascites be considered for liver transplantation.3
Consultations
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.
Diet
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.
Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications in patients with ascites.
Diuretics
Diuretic agents are the mainstay of medical therapy in ascites.
Spironolactone (Aldactone)
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.
Dosing Interactions
Contraindications
Precautions
Adult
25-200 mg/d PO qd or divided bid
Pediatric
1.5-3.5 mg/kg/d PO in divided doses q6-24h
Dosing Interactions
Contraindications
Precautions
May decrease the effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity
Dosing Interactions
Contraindications
Precautions
Documented hypersensitivity; anuria; renal failure; hyperkalemia
Dosing Interactions
Contraindications
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in patients with renal and hepatic impairment; may cause gynecomastia and impotence in men
Furosemide (Lasix)
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.
Dosing Interactions
Contraindications
Precautions
Adult
20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states
Pediatric
1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg
Dosing Interactions
Contraindications
Precautions
Metformin decreases concentrations; interferes with the hypoglycemic effect of antidiabetic agents and antagonizes the muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides, hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently
Dosing Interactions
Contraindications
Precautions
Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
Dosing Interactions
Contraindications
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter.
Amiloride (Midamor)
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.
Dosing
Interactions
Contraindications
Precautions
Adult
5-20 mg PO qd
Pediatric
Not established
Dosing Interactions
Contraindications
Precautions
Concomitant therapy with potassium supplementation may increase serum potassium levels; if concomitant use of these agents is indicated because of demonstrated hypokalemia, use caution and monitor serum potassium level frequently; generally, lithium should not be administered with diuretics because this may reduce renal clearance and add a high risk of lithium toxicity; administration of NSAIDs can reduce the diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing, and thiazide diuretics; when used concomitantly, observe patients closely to determine if the desired effect of the diuretic is obtained.
Indomethacin and potassium-sparing diuretics, including amiloride, may be associated with increased serum potassium levels; consider the potential effects on potassium kinetics and renal function.
Dosing Interactions
Contraindications
Precautions
Documented hypersensitivity; elevated serum potassium levels (>5.5 mEq/L); impaired renal function, acute or chronic renal insufficiency, and evidence of diabetic nephropathy; monitor electrolytes closely if evidence of renal functional impairment is present, BUN is >30 mg/100 mL, or serum creatinine level is >1.5 mg/100 mL
Dosing Interactions
Contraindications
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Potassium retention associated with use of an antikaliuretic agent is accentuated in the presence of renal impairment and may result in rapid development of hyperkalemia; monitor serum potassium level; mild hyperkalemia is usually not associated with abnormal ECG findings.
Metolazone (Mykrox, Zaroxolyn)
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.
Dosing Interactions
Contraindications
Precautions
Adult
5-20 mg/dose PO q24h
Pediatric
Administer as in adults.
Dosing Interactions
Contraindications
Precautions
Thiazides may decrease the effect of anticoagulants, sulfonylureas, and gout treatments; anticholinergics and amphotericin B may increase the toxicity of thiazides; the effects of thiazides may decrease when used concurrently with bile acid sequestrants, NSAIDs, or methenamine; when administered concurrently, thiazides increase the toxicity of anesthetics, diazoxide, digitoxin, lithium, loop diuretics, antineoplastics, allopurinol, calcium salts, vitamin D, and nondepolarizing muscle relaxants.
Dosing Interactions
Contraindications
Precautions
Documented hypersensitivity; hepatic coma or anuria
Dosing Interactions
Contraindications
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in patients with hepatic or renal disease, diabetes mellitus, gout, or lupus erythematosus
Mannitol (Osmitrol)
Inhibits tubular reabsorption of electrolytes by increasing the osmotic pressure of glomerular filtrate. Increases urinary output.
Dosing Interactions
Contraindications
Precautions
Adult
0.5-2 g/kg IV over 30-60 min as a 15-25% solution; repeat q6-8h
Pediatric
Not established
Follow-up
Further Inpatient Care
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.
Further Outpatient Care
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 maintain the patient free of ascites.
Inpatient & Outpatient Medications
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.
Complications
The most common complication of ascites is the development of spontaneous bacterial peritonitis (ascitic fluid with PMN count of >250 μ L).
o 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.12
o 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.
Prognosis
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.
Patient Education
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.
Miscellaneous
Medicolegal Pitfalls
The most important consideration in a patient with a new onset of ascites is to perform a peritoneal tap and to ascertain the cause. A peritoneal tap is also indicated in a patient with known liver disease who presents with sudden clinical deterioration, worsening encephalopathy, or unexplained fever. A missed or delayed diagnosis of spontaneous bacterial peritonitis could potentially lead to sepsis and significant morbidity and mortality.