ASCITES - Udara
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
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.
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.
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.
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.
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:
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
Causes of low SAAG are:
Cancer (primary peritoneal carcinomatosis and metastasis) - 10%
Tuberculosis - 2%
Pancreatitis - 1%
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:
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.
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.
Physical: The physical examination should focus on the signs of portal hypertension and chronic liver disease.
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.
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.
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.
of 500 mg/d
is 2000 mg/d
Drug Category: Diuretics -- Mainstay of medical therapy in ascites.
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
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.
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.
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.
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.
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.
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.
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.
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
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