Encyclopedia of Ayurvedic Medicinal Plants

ASCITES

 

Introduction

             Ascites is an abnormal accumulation of fluid in the abdomen.In medicine (gastroenterology), ascites is an accumulation of fluid in the peritoneal cavity. Although most commonly due to cirrhosis and severe liver disease, its presence can portend other significant medical problems. Typically described in terms of transudate (low protein concentration) and exudate (high protein), the serum-ascites albumin gradient (SAAG) is probably a better discriminate.

              In Ayurveda, there have a similar condition to ascites named Udara.

 Synonyms and related keywords

                Fluid collection, fluid accumulation, fluid retention, distended abdomen, portal hypertension, hypoalbuminemia, hepatic congestion, congestive heart failure, constrictive pericarditis, tricuspid insufficiency, Budd-Chiari syndrome, liver disease, cirrhosis, alcoholic hepatitis, fulminant hepatic failure, massive hepatic metastases, nephrotic syndrome, protein-losing enteropathy, severe malnutrition, anasarca, chylous ascites, pancreatic ascites, bile ascites, nephrogenic ascites, urine ascites, ovarian disease, bacterial peritonitis, tuberculous peritonitis, fungal peritonitis, HIV-associated peritonitis, malignancy, peritoneal carcinomatosis, primary mesothelioma, pseudomyxoma peritonei, hepatocellular carcinoma, HCC, familial Mediterranean fever, vasculitis, granulomatous peritonitis, eosinophilic peritonitis, alcohol use, chronic viral hepatitis, jaundice, intravenous drug use, blood transfusions, alcoholic liver disease, obesity, hypercholesterolemia, type 2 diabetes mellitus, nonalcoholic steatohepatitis, gastrointestinal cancer, malignant ascites, cirrhotic ascites, nephrotic ascites, palmar erythema, spider angiomas, puddle sign, Sister Mary Joseph nodule, gastric malignancy, pancreatic malignancy, hepatic primary malignancy, left-sided supraclavicular node, Virchow node, anasarca

 

 

Background

          The word ascites is of Greek origin (askos) and means bag or sac. Ascites describes the condition of pathologic fluid accumulation 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 the menstrual cycle. This article focuses only on ascites associated with cirrhosis.

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.

              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. According to the vasodilation theory, the underfilling theory is proposed to be operative early and the overflow theory is proposed to be 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. Patients with ascites have greater hepatic artery nitric oxide synthase activity compared to patients 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.

                    Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 25 litres are fully possible.

                   Roughly, transudates are a result of increased pressure in the portal vein (>8 mmHg), e.g. due to cirrhosis, while exudates are actively secreted fluid due to inflammation or malignancy. As a result, exudates are high in protein, high in lactate dehydrogenase, have a low pH (<7.30), a low glucose level, and more white blood cells. Transudates have low protein (<30g/L), low LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm³. Clinically, the most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1 g/dl (10 g/L) implies an exudate.

                     Portal hypertension lays an important role in the production of ascites by raising capillary hydrostatic pressure within the splanchnic bed.

                  Regardless of the cause, sequestration of fluid within the abdomen leads to additional fluid retention by the kidneys due to stimulatory effect on blood pressure hormones, notably aldosterone. The sympathetic nervous system is also activated, and renin production is increased due to decreased perfusion of the kidney. Extreme disruption of the renal blood flow can lead to the feared hepatorenal syndrome.

                      Other complications of ascites include spontaneous bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic fluid such as complement.

 

                     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 the menstrual cycle.

Description

                Rapidly developing (acute) ascites can occur as a complication of trauma, perforated ulcer, appendicitis, or inflammation of the colon or other tube-shaped organ (diverticulitis). This condition can also develop when intestinal fluids, bile, pancreatic juices, or bacteria invade or inflame the smooth, transparent membrane that lines the inside of the abdomen (peritoneum). However, ascites is more often associated with liver disease and other long-lasting (chronic) conditions.

Types of ascites

                  Cirrhosis, which is responsible for 80% of all instances of ascites in the United States, triggers a series of disease-producing changes that weaken the kidney's ability to excrete sodium in the urine.

                  Pancreatic ascites develops when a cyst that has thick, fibrous walls (pseudocyst) bursts and permits pancreatic juices to enter the abdominal cavity.

                  Chylous ascites has a milky appearance caused by lymph that has leaked into the abdominal cavity. Although chylous ascites is sometimes caused by trauma, abdominal surgery, tuberculosis, or another peritoneal infection, it is usually a symptom of lymphoma or some other cancer.

                   Cancer causes 10% of all instances of ascites in the United States. It is most commonly a consequence of disease that originates in the peritoneum (peritoneal carcinomatosis) or of cancer that spreads (metastasizes) from another part of the body.

                    Endocrine and renal ascites are rare disorders. Endocrine ascites, sometimes a symptom of an endocrine system disorder, also affects women who are taking fertility drugs. Renal ascites develops when blood levels of albumin dip below normal. Albumin is the major protein in blood plasma. It functions to keep fluid inside the blood vessels.

Causes

Low levels of albumin in the blood that cause a change in the pressure necessary to prevent fluid exchange (osmotic pressure). This change in pressure allows fluid to seep out of the blood vessels.

An increase in the pressure within the branches of the portal vein that run through liver (portal hypertension). Portal hypertension is caused by the scarring that occurs in cirrhosis. Blood that cannot flow through the liver because of the increased pressure leaks into the abdomen and causes ascites.

Other conditions that contribute to ascites development include:

• hepatitis
• heart or kidney failure
• inflammation and fibrous hardening of the sac that contains the heart (constrictive pericarditis)

Persons who have systemic lupus erythematosus but do not have liver disease or portal hypertension occasionally develop ascites. Depressed thyroid activity sometimes causes pronounced ascites, but inflammation of the pancreas (pancreatitis) rarely causes significant accumulations of fluid.

 

Causes of high SAAG are:

Cirrhosis - 81%

alcoholic - 65%

viral - 10%

cryptogenic - 6%

Heart failure - 3%

Budd-Chiari syndrome or veno-occlusive disease

Constrictive pericarditis

Causes of low SAAG are:

Cancer (primary peritoneal carcinomatosis and metastasis) - 10%

Tuberculosis - 2%

Pancreatitis - 1%

Serositis

Nephrotic syndrome

Signs and symptoms

           Mild ascites is hard to notice, but severe ascites leads to abdominal distension. Patients with ascites generally will complain of progressive abdominal heaviness and pressure as well as shortness of breath due to mechanical impingement on the diaphragm.

            Other signs of ascites may be present due to its underlying etiology. In those with portal hypertension, such as due to cirrhosis, patients may also complain of lower extremity swelling, progressive problems with clotting after major trauma/surgery, hematemesis, or mental status changes. In some cases, patients will also complain of gynecomastia (due to hyperestrogenism), spider angiomata, palmar erythema, or caput medusa. Jaundice and skin itching may or may not be present depending on the level of liver congestion and bilirubin build-up.

            Those with ascites due to cancer (peritoneal carcinomatosis or peritoneal cavity seeding from metastases from elsewhere) may complain of chronic fatigue or weight loss.

         Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance. Ascites can also be due to tuberculosis, in which case patients may complain of night sweats, dry cough, and chronic fatigue. Rarely, ascites may be a component of Meigs' syndrome --- a combination of ascites, hydrothrorax (unilateral pleural effusion), and benign tumors of the ovary.

Small amounts of fluid in the abdomen do not usually produce symptoms. Massive accumulations may cause:

• rapid weight gain
• abdominal discomfort and distention
• shortness of breath
• swollen ankles

 

Diagnosis

           In addition to the routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation factors, diagnostic paracentesis should be performed to sample about 50 to 100 mL of fluid. The fluid is then reviewed for its gross appearance, protein level, serum-ascites albumin gradient (SAG, SAAG), and cell counts (red and white). Additional tests will be performed if indicated such as gram stain and cytology.

           The serum-ascites albumin gradient is important because it is paramount to determine if the ascites is due to portal hypertension or otherwise, since the diagnostic pathways are different for each cause. A high gradient (> 1.1 g/dL) indicates the ascites is due to uncomplicated cirrhotic ascites and is likely due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertension etiology.

             Skin stretches tightly across an abdomen that contains large amounts of fluid. The navel bulges or lies flat, and the fluid makes a dull sound when the doctor taps the abdomen. Ascitic fluid may cause the flanks to bulge.

              Physical examination generally enables doctors to distinguish ascites from pregnancy, intestinal gas, obesity, or ovarian tumors. Ultrasound or computed tomography scans (CT) can detect even small amounts of fluid. Laboratory analysis of fluid extracted by inserting a needle through the abdominal wall (diagnostic paracentesis) can help identify the cause of the accumulation.

 

              If the cause is not apparent, serology for viruses known to cause hepatitis may contribute to the analysis. Iron studies (serum iron, ferritin, TIBC) may reveal rare causes such as hemochromatosis. Serum copper and ceruloplasmin may reveal Wilson's disease. a1-antitrypsin may reveal a1-antitrypsin deficiency disease. All of these causes may contribute to formation of cirrhosis.

          Ultrasound investigation with doppler studies can be an important help, and may identify vessel architecture and reveal such problems as Budd-Chiari syndrome, portal vein thrombosis and cirrhosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid.

 

Abdominal CT scan is an alternate to reveal abdominal organ structure and morphology.

Classification

Ascites exists in three grades:

Grade 1: mild, only visible on ultrasound

Grade 2: detectable with flank bulging and shifting dullness on physical examination

Grade 3: directly visible, confirmed with fluid thrill (or fluid wave)

 

History: Most cases of ascites are due to liver disease. Patients often state that their increasing abdominal girth has been noted for a short period.

• Patients with ascites should be asked about risk factors for liver diseases. These include the following:

• Alcohol use and duration of use

• Chronic viral hepatitis or jaundice

• Intravenous drug use

• Sexual promiscuity

• Sexual orientation

• Transfusions: Hepatitis C has been linked to transfusions occurring before 1980.

• Tattoos

• Habitation or origination from an area endemic for hepatitis

• Patients with alcoholic liver disease who intermittently cease or reduce alcohol consumption may experience ascites in a cyclic fashion. When the patient has a very long history of stable cirrhosis and then develops ascites, the possibility of superimposed hepatocellular carcinoma should be considered.

• Obesity, hypercholesterolemia, and type 2 diabetes mellitus are now 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 known diabetes or nephrotic syndrome may have nephrotic ascites.

Physical: The physical examination 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 often, the liver is enlarged. The puddle sign indicates that 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 peritoneum

• 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

• Hypoalbuminemia (SAAG <1.1 g/dL)
  • Nephrotic syndrome
  • Protein-losing enteropathy
  • Severe malnutrition with anasarca

• 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)

• Infections
  • Bacterial peritonitis
  • Tuberculous peritonitis
  • Fungal peritonitis
  • HIV-associated peritonitis

• Malignant conditions
  • Peritoneal carcinomatosis
  • Primary mesothelioma
  • Pseudomyxoma peritonei
  • Hepatocellular carcinoma

• Other rare conditions
  • Familial Mediterranean fever
  • Vasculitis
  • Granulomatous peritonitis
  • Eosinophilic peritonitis

 

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.

• Therapeutic paracentesis should be reserved for patients who need rapid symptomatic relief of tense ascites.

• TIPS is an interventional radiologic technique that reduces portal pressure and may be the most efficacious for treatment of patients with diuretic-resistant ascites. This procedure consists of inserting a long metal needle from the right jugular vein into the hepatic vein. This is slowly becoming the standard of care in patients with diuretic-refractory ascites.

Surgical Care

            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. No evidence indicates that these shunts improve patient survival. With the advent of the TIPS procedure, this form of therapy is almost obsolete.

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.

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Diuretics -- Mainstay of medical therapy in ascites.

 

Drug Name	Spironolactone (Aldactone) -- For 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.
Adult Dose	25-200 mg/d PO qd or divided bid
Pediatric Dose	1.5-3.5 mg/kg/d PO in divided doses q6-24h
Contraindications	Documented hypersensitivity; anuria; renal failure; hyperkalemia
Interactions	May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity
Pregnancy	D - Unsafe in pregnancy
Precautions	Caution in renal and hepatic impairment; may cause gynecomastia and impotence in men

 

Drug Name	Furosemide (Lasix) -- Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until a satisfactory effect is achieved.
Adult Dose	20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states
Pediatric Dose	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
Contraindications	Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
Interactions	Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes 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
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

 

Drug Name	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.
Adult Dose	5-20 mg PO qd
Pediatric Dose	Not established
Contraindications	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
Interactions	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 may reduce renal clearance and add a high risk of lithium toxicity; administration of NSAIDs can reduce diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing, and thiazide diuretics; when used concomitantly, observe patient closely to determine if desired effect of diuretic obtained Indomethacin and potassium-sparing diuretics, including amiloride, may be associated with increased serum potassium levels; consider potential effects on potassium kinetics and renal function
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Potassium retention associated with use of an antikaliuretic agent accentuated in presence of renal impairment and may result in rapid development of hyperkalemia; monitor serum potassium level; mild hyperkalemia usually not associated with abnormal ECG findings

 

Drug Name	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.
Adult Dose	5-20 mg/dose PO q24h
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; hepatic coma or anuria
Interactions	Thiazides may decrease effect of anticoagulants, sulfonylureas, and gout treatments; anticholinergics and amphotericin B may increase toxicity of thiazides; effects of thiazides may decrease when used concurrently with bile acid sequestrants, NSAIDs, or methenamine; when administered concurrently, thiazides increase toxicity of anesthetics, diazoxide, digitoxin, lithium, loop diuretics, antineoplastics, allopurinol, calcium salts, vitamin D, and nondepolarizing muscle relaxants
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution in hepatic or renal disease, diabetes mellitus, gout, or lupus erythematosus

 

Drug Name	Mannitol (Osmitrol) -- Inhibits tubular reabsorption of electrolytes by increasing osmotic pressure of glomerular filtrate. Increases urinary output.
Adult Dose	0.5-2 g/kg IV over 30-60 min as a 15-25% solution; repeat q6-8h
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure
Interactions	May decrease serum lithium levels
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Carefully evaluate cardiovascular status before rapid administration because a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination; when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood

 

                  Ascites is generally treated simultaneously while an underlying etiology is sought (see above, diagnosis) in order to prevent complications (i.e., spontaneous bacterial peritonitis) and to prevent further progression. In patients with mild ascites, therapy can be done in the outpatient but should be gradual. If both ascites and peripheral edema is present, the goal of loss is no more than 1.0 kg/day and no more than 0.5 kg/day for those with ascites alone. In those with severe ascites, hospitalization is generally necessary.

              Salt restriction is generally the baseline step in therapy, which allows diuresis since the patient now has more fluid than salt concentration. Since salt restriction is the basic concept in treatment, and aldosterone is one of the hormones that acts to increase salt retention, a medication that counteracts aldosterone should be sought. Spironolactone (or other distal-tubule diuretics such as triamterene or amiloride) is the drug of choice since they block the aldosterone receptor in the collecting tubule. Generally, the starting dose is spironolactone PO 100 mg/day (max 400 mg/day). A loop diuretic (furosemide, bumetanide, torasemide) may also be added to the regimen to further enhance diuresis and generally, furosemide (Lasix) is added at a dose of 40 mg/day (max 160 mg/day). Serum potassium level and renal function should be monitored closely while on these medications.

            In those with severe ascites, therapeutic paracentesis may be needed in addition to medical treatments listed above. Ascites that is refractory to medical therapy is considered to be a classic indication for liver transplantation.

             In a minority of the patient with advanced cirrhosis that have recurrent ascites, shunts may be used. Typical shunts used are portacaval shunt, peritoneovenous shunt, and the transjugular intrahepatic portosystemic shunt (TIPS). However, none of these shunts has been shown to extend life expectancy, and are considered to be bridges to liver transplantation.

 

Reclining minimizes the amount of salt the kidneys absorb, so treatment generally starts with bed rest and a low-salt diet. Urine-producing drugs (diuretics) may be prescribed if initial treatment is ineffective. The weight and urinary output of patients using diuretics must be carefully monitored for signs of

• hypovolemia (massive loss of blood or fluid)
• azotemia (abnormally high blood levels of nitrogen-bearing materials)
• potassium imbalance
• high sodium concentration. If the patient consumes more salt than the kidneys excrete, increased doses of diuretics should be prescribed

Moderate-to-severe accumulations of fluid are treated by draining large amounts of fluid (large-volume paracentesis) from the patient's abdomen. This procedure is safer than diuretic therapy. It causes fewer complications and requires a shorter hospital stay.

Large-volume paracentesis is also the preferred treatment for massive ascites. Diuretics are sometimes used to prevent new fluid accumulations, and the procedure may be repeated periodically.

 

 

Cultural significance

                It has been suggested that ascites was seen as a punishment especially for oath-breakers among the Proto-Indo-Europeans (Oettinger, StBoT 22:71). This proposal builds on the Hittite military oath as well as various Vedic hymns (RV 7.89, AVS 4.16.7). A similar curse dates to the Kassite dynasty (12th century BC), threatening oath-breakers: "May Marduk, king of heaven and earth, fill his body with dropsy, which has a grip that can never be loosened". Comparable is also Numeri 5:11ff.

 

Alternative treatment

Dietary alterations, focused on reducing salt intake, should be a part of the treatment. In less severe cases, herbal diuretics like dandelion (Taraxacum officinale) can help eliminate excess fluid and provide potassium. Potassium-rich foods like low-fat yogurt, mackerel, cantaloupe, and baked potatoes help balance excess sodium intake.

Prognosis

               The prognosis depends upon the condition that is causing the ascites. Carcinomatous ascites has a very bad prognosis. However, salt restriction and diuretics can control ascites caused by liver disease in many cases.

Therapy should also be directed towards the underlying disease that produces the ascites. Cirrhosis should be treated by abstinence from alcohol and appropriate diet. The new interferon agents maybe helpful in treating chronic hepatitis.

Prevention

Modifying or restricting use of salt can prevent most cases of recurrent ascites.

Computed tomography scan (CT)

An imaging technique in which cross-sectional x rays of the body are compiled to create a three-dimensional image of the body's internal structures.

Interferon

A protein formed when cells are exposed to a virus. Interferon causes other noninfected cells to develop translation inhibitory protein (TIP). TIP blocks viruses from infecting new cells.

Paracentesis

A procedure in which fluid is drained from a body cavity by means of a catheter placed through an incision in the skin.

Systemic lupus erythematosus

An inflammatory disease that affects many body systems, including the skin, blood vessels, kidneys, and nervous system. It is characterized, in part, by arthritis, skin rash, weakness, and fatigue.

Ultrasonography

A test using sound waves to measure blood flow. Gel is applied to a hand-held transducer that is pressed against the patient's body. Images are displayed on a monitor

Lab Studies:

• Peritoneal fluid should be sent for cell count, albumin level, culture, total protein, Gram stain, and cytology for new-onset ascites of unknown origin.

• Inspection: Most ascitic fluid is transparent and tinged yellow. A minimum of 10,000 red blood cells/L is required for ascitic fluid to appear pink, and more than 20,000 red blood cells/L is considered distinctly blood tinged. This may be attributed to 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 it has already clotted and lysed. Neutrophil counts of more than 50,000 cells/L have a purulent cloudy consistency and indicate infection.

• Cell count: Normal ascitic fluid contains fewer than 500 leukocytes/L and fewer than 250 polymorphonuclear leukocytes/L. Any inflammatory condition can cause an elevated white blood cell count. A neutrophil count of more than 250 cells/L is highly suggestive of bacterial peritonitis. In tuberculous peritonitis and peritoneal carcinomatosis, a predominance of lymphocytes usually occurs.

• 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. Those patients with malignant ascites have a low SAAG and a high protein level (see Causes).

• Culture/Gram stain: The sensitivity with bedside inoculation of blood culture bottles with ascites results in 92% detection of bacterial growth in neutrocytic ascites. Gram stain is only 10% sensitive for helping visualize 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 smear results are reported to be 58-75% sensitive for helping detect malignant ascites.

Imaging Studies:

• Chest and plain abdominal films

• 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 indicate 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). Obliteration of the hepatic angle is visible in 80% of healthy patients. 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.

• Ultrasound

• Real-time sonography 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 homogenous, 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 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 sonographic findings suggest that the ascites may be infected, inflammatory, or malignant. 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 they may be 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.

• CT scan: Ascites is demonstrated well on CT scan images. Small amounts of ascitic fluid localize in the right perihepatic space, the posterior subhepatic space (Morison pouch), and the Douglas pouch. A number of CT 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 if malignant ascites is suggested. 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. Therapeutic paracentesis may be performed for refractory or tense ascites. The removal of 5 L of fluid is considered large-volume paracentesis. Total paracentesis, ie, removal of all ascites (even >20 L), can usually be performed safely. Recent studies demonstrate that supplementing 5 g of albumin per each liter over 5 L decreases complications of paracentesis, such as electrolyte imbalances, and increases in serum creatinine secondary to large shifts of intravascular volume.

• Transjugular intrahepatic portacaval shunt (TIPS): This is a side-to-side portacaval shunt placed by an interventional radiologist under local anesthesia. This is often used for diuretic refractory ascites.

Staging:

• Ascites may be semiquantified using the following system:

• Stage 1+ is detectable only after careful examination.

• Stage 2+ is easily detectable but of relatively small volume.

• Stage 3+ is obvious ascites but not tense ascites.

• Stage 4+ is tense ascites.