| Ascites | |
|---|---|
| Other names | Peritoneal cavity fluid, peritoneal fluid excess, hydroperitoneum, abdominal dropsy[1] |
 | |
| Theabdomen of a person withcirrhosis that has resulted in massive ascites and prominent superficial veins | |
| Pronunciation | |
| Specialty | Gastroenterology,general surgery |
| Symptoms | Increased abdominal size, increased weight, abdominal discomfort,shortness of breath[3] |
| Complications | Spontaneous bacterial peritonitis,hepatorenal syndrome,low blood sodium[3][4] |
| Causes | Liver cirrhosis,cancer,heart failure,tuberculosis,pancreatitis,blockage of the hepatic vein[4] |
| Diagnostic method | Physical exam,ultrasound,CT scan[3] |
| Treatment | Low-salt diet, medications,draining the fluid[3] |
| Medication | Spironolactone,furosemide[3] |
| Frequency | >50% of people with cirrhosis[4] |
Ascites (/əˈsaɪtiz/;[5]Greek:ἀσκός,romanized: askos, meaning "bag" or "sac"[6]) is the abnormal build-up of fluid in theabdomen.[1] Technically, it is more than 25 millilitres (0.88 imp fl oz; 0.85 US fl oz) of fluid in theperitoneal cavity, although volumes greater than one litre (0.22 imp gal; 0.26 US gal) may occur.[4] Symptoms may include increased abdominal size, increased weight, abdominal discomfort, andshortness of breath. Complications can includespontaneous bacterial peritonitis.[3]
In thedeveloped world, the most common cause isliver cirrhosis, whose underlying mechanism involveshigh blood pressure in the portal system and dysfunction ofblood vessels. Other causes includecancer,heart failure,tuberculosis,pancreatitis, andblockage of the hepatic vein.[4] Diagnosis is typically based on an examination together withultrasound or aCT scan. Testing the fluid can help in determining the underlying cause.[3]
Treatment often involves alow-salt diet, medication such asdiuretics, anddraining the fluid. Atransjugular intrahepatic portosystemic shunt (TIPS) may be placed but is associated with complications.[3] Attempts to treat the underlying cause, such as by aliver transplant, may be considered. Of those with cirrhosis, more than half develop ascites in the ten years following diagnosis. Of those in this group who develop ascites, half will die within three years.[4]
TheLatin ascites, originally fromGreek (askites [ασκίτης]), meant "bag-like dropsy," from askós (ἀσκός), a leather bag or sheepskin ("wineskin") used for carrying wine, water or oil.[7]
Mild ascites is hard to notice, but severe ascites leads toabdominal distension. People with ascites generally will complain of progressive abdominal heaviness and pressure as well asshortness of breath due to mechanical impingement on thediaphragm.[8]
Ascites is detected withphysical examination of the abdomen by visible bulging of the flanks in the reclining person ("flank bulging"), "shifting dullness" (difference in percussion note in the flanks that shifts when the person is turned on the side), or in massive ascites, with a "fluid thrill" or "fluid wave" (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite side of the abdomen).
Other signs of ascites may be present due to its underlying cause. For instance, inportal hypertension (perhaps due to cirrhosis or fibrosis of the liver) people may also complain of leg swelling, bruising,gynecomastia,hematemesis, or mental changes due toencephalopathy. Those with ascites due tocancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due toheart failure may also complain of shortness of breath as well as wheezing and exercise intolerance.
Causes of highserum-ascites albumin gradient (SAAG or transudate) are:[9]
Causes of low SAAG ("exudate") are
Routinecomplete blood count (CBC), basic metabolic profile,liver enzymes, andcoagulation should be performed. Most experts recommend diagnosticparacentesis if the ascites is new or if the person with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level,albumin, and cell counts (red and white). Additional tests will be performed if indicated such asmicrobiological culture,Gram stain, andcytopathology.[9]
Theserum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.[12] A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive as a cause.[13]
Ultrasound investigation is often done before attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detectingBudd–Chiari syndrome (thrombosis of the hepatic vein) andportal vein thrombosis. The sonographer also can estimate the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. An abdominalCT scan is more accurate than a sonogram to reveal abdominal organ structure and morphology.[13]
Uncomplicated ascites is characterized by receding or nonrecurring ascites post-paracentesis, and is treatable with diet control and diuretic treatment. Refractory ascites is characterized as ascites that recurs or does not recede post-paracentesis, despite diet control and diuretic treatment.[14]
Uncomplicated ascites is more common, responsive to treatment, and exists in three grades:[15]
Refractory ascites is less common, difficult to treat, and exists in two subtypes: i) diuretic intractable ascites makes up the majority of refractory ascites cases, where diuretic treatment is difficult due to diuretic-induced complications such as elevated creatinine andhypokalemia; ii) diuretic resistant ascites does not respond to diuretic treatment.[16][17]
Ascitic fluid can accumulate as atransudate or anexudate. Amounts of up to 35 liters are possible.
Roughly, transudates are a result of increased pressure in thehepatic portal vein (>8 mmHg, usually around 20 mmHg[18] (e.g., due to cirrhosis), while exudates are actively secreted fluid due toinflammation or malignancy. As a result, exudates are high in protein andlactate dehydrogenase and have a lowpH (<7.30), a lowglucose level, and morewhite blood cells. Transudates have low protein (<30 g/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 andserum albumin concentrations. A difference of less than 1 g/dl (10 g/L) implies an exudate.[9]
Portal hypertension plays 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 additionalfluid retention by the kidneys due to stimulatory effect on blood pressure hormones, notablyaldosterone. Thesympathetic nervous system is also activated, andrenin production is increased due to decreased perfusion of the kidney. Extreme disruption of the renal blood flow can lead tohepatorenal syndrome. Other complications of ascites includespontaneous bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic fluid such ascomplement.
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Ascites is generally treated while an underlying cause is sought, in order to relieve symptoms and to prevent complications and progression. In people with mild ascites, therapy is usually as an outpatient. The goal is weight loss of no more than 1.0 kg/day for people with both ascites andperipheral edema and no more than 0.5 kg/day for people with ascites alone.[19] In those with severe ascites causing a tense abdomen, hospitalization is generally necessary forparacentesis.[20][21]
Salt restriction is the initial treatment, which allowsdiuresis (production of urine) since the person now has more fluid than salt concentration. Salt restriction is effective in about 15% of these people.[22] Water restriction is needed ifserum sodium levels drop below 130 mmol L−1.[23]
Because salt restriction is the basic concept in treatment, andaldosterone is one of the hormones that increase salt retention, a medication that counteracts aldosterone should be sought.Spironolactone (or other distal-tubule diuretics, such astriamterene andamiloride) is the drug of choice, because it blocks the aldosterone receptor in the collecting tubule. This choice has been confirmed in arandomized controlled trial.[24] Diuretics for ascites should be taken once a day.[25] Generally, the starting dose is oral spironolactone 100 mg/day (max 400 mg/day).40% of people will respond to spironolactone.[22] For nonresponders, aloop diuretic may also be added and generally,furosemide is added at a dose of 40 mg/day (max 160 mg/day), or alternatively (bumetanide ortorasemide). The ratio of 100:40 reduces risks of potassium imbalance.[25] Serumpotassium level and renal function should be monitored closely while the patient is on these medications.[23]
Monitoring diuresis: Diuresis can be monitored by weighing the person daily. The goal is weight loss of no more than 1.0 kg/day for people with both ascites andperipheral edema and no more than 0.5 kg/day for people with ascites alone.[19]If daily weights cannot be obtained, diuretics can also be guided by the urinary sodium concentration. Dosage is increased until a negative sodium balance occurs.[25] A random urine sodium-to-potassium ratio of > 1 is 90%sensitivity in predicting negative balance (> 78-mmol/day sodium excretion).[26]
Diuretic resistance: Diuretic resistance can be predicted by giving 80 mg intravenous furosemide after 3 days without diuretics and on an 80 mEq sodium/day diet. The urinary sodium excretion over 8 hours < 50 mEq/8 hours predicts resistance.[27]
If the person exhibits a resistance or poor response to diuretic therapy,ultrafiltration oraquapheresis may be needed to achieve adequate control of fluid retention and congestion. The use of such mechanical methods of fluid removal can produce meaningful clinical benefits in people with diuretic resistance and may restore responsiveness to conventional doses of diuretics.[28][29]
In those with severe (tense) ascites, therapeuticparacentesis may be needed in addition to medical treatments listed above.[20][21] As this may depleteserum albumin levels in the blood, albumin is generally administered intravenously in proportion to the amount of ascites removed.
Ascites that is refractory to medical therapy is considered an indication forliver transplantation. In the United States, theMELD score[30] is used to prioritize people for transplantation.
In a minority of people with advanced cirrhosis that have recurrent ascites, shunts may be used. Typical shunts used are theportacaval shunt, theperitoneovenous shunt, and thetransjugular intrahepatic portosystemic shunt (TIPS). However, none of these has been shown to extend life expectancy, and they are considered to be bridges toliver transplantation. A 2006meta-analysis concluded that "TIPS was more effective at removing ascites [than] paracentesis[,] without a significant difference in mortality, gastrointestinal bleeding, infection, and acute renal failure. However, TIPS patients develop hepatic encephalopathy significantly more often."[31]
Another option for people with refractory or malignant ascites is the automated low-flow ascites pump (Alfapump), an implanted machine, which uses a pump to move ascites from the peritoneal cavity to the bladder for urination.[32][33]
Exudative ascites generally does not respond to manipulation of the salt balance or diuretic therapy.[34] Repeated paracentesis and treatment of the underlying cause is the mainstay of treatment.
It has been suggested that ascites was seen as a punishment especially foroath-breakers among theProto-Indo-Europeans.[35] This proposal builds on theHittite military oath as well as variousVedic hymns (RV 7.89,AVS 4.16.7). A similar curse dates to theKassite dynasty (12th century BC).
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