Ascites 197574 225686711 2008-07-14T22:12:22Z Queenmomcat 6687298 /* Diuretics */ corrected a type? {{Infobox_Disease | Name = Ascites | Image = | Caption = | DiseasesDB = 943 | ICD10 = {{ICD10|R|18||r|10}} | ICD9 = {{ICD9|789.5}} | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = ped | eMedicineTopic = 2927 | eMedicine_mult = {{eMedicine2|med|173}} | MeshID = }} In [[medicine]] ([[gastroenterology]]), '''ascites''' (also known as '''peritoneal cavity fluid''', '''peritoneal fluid excess''', '''hydroperitoneum''' or more archaically as '''abdominal dropsy''') 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. Diagnosis of the cause is usually with [[blood test]]s, an [[medical ultrasonography|ultrasound scan]] of the abdomen and direct removal of the fluid by needle or [[paracentesis]] (which may also be therapeutic). Treatment may be with medication ([[diuretic]]s), paracentesis or other treatments directed at the cause. ==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 (anatomy)|diaphragm]]. Ascites is detected on [[physical examination]] of the abdomen by visible [[Bulging flanks|bulging of the flanks]] in the reclining patient ("flank bulging"), "[[shifting dullness]]" (difference in percussion note in the flanks that shifts when the patient is turned on the side) or in massive ascites with a "fluid thrill" or "[[Fluid wave test|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 etiology. For instance, in [[portal hypertension]] (perhaps due to cirrhosis or fibrosis of the liver) patients may also complain of leg swelling, bruising, [[gynecomastia]], [[hematemesis]], or mental changes due to [[encephalopathy]]. Those with ascites due to [[cancer]] (peritoneal carcinomatosis) 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. ==Classification== Ascites exists in three grades:<ref>Moore KP, Wong F, Gines P, Bernardi M, Ochs A, Salerno F, Angeli P, Porayko M, Moreau R, Garcia-Tsao G, Jimenez W, Planas R, Arroyo V. The management of ascites in cirrhosis: report on the consensus conference of the International Ascites Club. ''Hepatology'' 2003;38:258-66. PMID 12830009.</ref> * Grade 1: mild, only visible on ultrasound * Grade 2: detectable with flank bulging and shifting dullness * Grade 3: directly visible, confirmed with fluid thrill ==Diagnosis== Routine [[complete blood count]] (CBC), basic metabolic profile, [[liver enzymes]], and [[coagulation]] should be performed. Most experts recommend a diagnostic [[paracentesis]] be performed if the ascites is new or if the patient with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, [[serum albumin|albumin]], and cell counts (red and white). Additional tests will be performed if indicated such as [[Gram stain]] and [[cytology]].<ref name=OTM>Warrell DA, Cox TN, Firth JD, Benz ED. ''Oxford textbook of medicine''. Oxford: Oxford University Press, 2003. ISBN 0-19-262922-0.</ref> The ''[[Serum-ascites albumin gradient]]'' (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.<ref>Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. ''Ann Intern Med'' 1992;117:215-20. PMID 1616215.</ref> 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 etiology. [[Medical ultrasonography|Ultrasound]] investigation is often performed prior to 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 detecting [[Budd-Chiari syndrome]] and [[portal vein thrombosis]]. Additionally, the sonographer can make an estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. Abdominal [[CT scan]] is a more accurate alternate to reveal abdominal organ structure and morphology. ==Causes== Causes of high [[Serum-ascities albumin gradient|SAAG]] ("transudate") are:<ref name=OTM/> * [[Cirrhosis]] - 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%) * [[Heart failure]] - 3% * [[Budd-Chiari syndrome]] or [[veno-occlusive disease]] * [[Constrictive pericarditis]] * [[Kwashiorkor]] Causes of low [[Serum-ascities albumin gradient|SAAG]] ("exudate") are: * [[Cancer]] (primary peritoneal carcinomatosis and metastasis) - 10% * [[Tuberculosis]] - 2% * [[Pancreatitis]] - 1% * [[Serositis]] * [[Nephrotic syndrome]] * Hereditary [[angioedema]]<ref name="pmid9636820">{{cite journal |author=Branco-Ferreira M, Pedro E, Barbosa MA, Carlos AG |title=Ascites in hereditary angioedema |journal=Allergy |volume=53 |issue=5 |pages=543–5 |year=1998 |pmid=9636820 |doi=10.1111/j.1398-9995.1998.tb04098.x}}</ref> ==Pathophysiology== Ascitic fluid can accumulate as a [[transudate]] or an [[exudate]]. Amounts of up to 25 liters are fully possible. Roughly, transudates are a result of increased pressure in the [[hepatic portal vein|portal vein]] (>8 mmHg, usually around 20 mmHg<ref>[Ascites in Cirrhosis Relative Importance of Portal Hypertension and Hypoalbuminemia] DONALI) O. CASTELL, LCDR (MC), USN</ref>), ''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 cell]]s. 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.<ref name=OTM/> 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 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 system|complement]]. ==Treatment== Ascites is generally treated simultaneously while an underlying etiology is sought in order to prevent complications, to relieve symptoms and to prevent further progression. In patients with mild ascites, therapy is usually as an outpatient. The goal is weight loss of no more than 1.0 kg/day for patients with both ascites and [[peripheral edema]] and no more than 0.5 kg/day for patients with ascites alone.<ref name="pmid4910836">{{cite journal |author=Shear L, Ching S, Gabuzda GJ |title=Compartmentalization of ascites and edema in patients with hepatic cirrhosis |journal=N. Engl. J. Med. |volume=282 |issue=25 |pages=1391–6 |year=1970 |pmid=4910836 |doi=}}</ref> In those with severe ascites causing a tense abdomen, hospitalization is generally necessary for paracentesis.<ref name="pmid3297907">{{cite journal |author=Ginés P, Arroyo V, Quintero E, ''et al'' |title=Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study |journal=Gastroenterology |volume=93 |issue=2 |pages=234–41 |year=1987 |pmid=3297907 |doi=}}</ref><ref name="pmid3655306">{{cite journal |author=Salerno F, Badalamenti S, Incerti P, ''et al'' |title=Repeated paracentesis and i.v. albumin infusion to treat 'tense' ascites in cirrhotic patients. A safe alternative therapy |journal=J. Hepatol. |volume=5 |issue=1 |pages=102–8 |year=1987 |pmid=3655306|doi=10.1016/S0168-8278(87)80067-3}}</ref> ===High SAAG=== ====Salt restriction==== Salt restriction is the initial treatment, which allows [[diuresis]] (production of urine) since the patient now has more fluid than salt concentration. Salt restriction is effective in about 15% of patients.<ref name="pmid1860680">{{cite journal |author=Gatta A, Angeli P, Caregaro L, Menon F, Sacerdoti D, Merkel C |title=A pathophysiological interpretation of unresponsiveness to spironolactone in a stepped-care approach to the diuretic treatment of ascites in nonazotemic cirrhotic patients |journal=Hepatology |volume=14 |issue=2 |pages=231–6 |year=1991 |pmid=1860680 |doi=}}</ref> ====Diuretics==== 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. This choice has been confirmed in a [[randomized controlled trial]].<ref name="pmid7035545">{{cite journal |author=Fogel MR, Sawhney VK, Neal EA, Miller RG, Knauer CM, Gregory PB |title=Diuresis in the ascitic patient: a randomized controlled trial of three regimens |journal=J. Clin. Gastroenterol. |volume=3 Suppl 1 |issue= |pages=73–80 |year=1981 |pmid=7035545 |doi=10.1097/00004836-198100031-00016}}</ref> Diuretics for ascites should be dosed once per day.<ref name="pmid8277955">{{cite journal |author=Runyon BA |title=Care of patients with ascites |journal=N. Engl. J. Med. |volume=330 |issue=5 |pages=337–42 |year=1994 |pmid=8277955|doi=10.1056/NEJM199402033300508}}</ref> Generally, the starting dose is oral spironolactone 100 mg/day (max 400 mg/day). 40% of patients will respond to spironolactone.<ref name="pmid1860680"/> For nonresponders, a [[loop diuretic]] may also be added and generally, [[furosemide]] is added at a dose of 40 mg/day (max 160 mg/day), or alternatively ([[bumetanide]] or [[torasemide]]). The ratio of 100:40 reduces risks of potassium imbalance.<ref name="pmid8277955"/> Serum [[potassium]] level and renal function should be monitored closely while on these medications.<ref name="pmid15084697">{{cite journal |author=Ginès P, Cárdenas A, Arroyo V, Rodés J |title=Management of cirrhosis and ascites |journal=N. Engl. J. Med. |volume=350 |issue=16 |pages=1646–54 |year=2004 |pmid=15084697 |doi=10.1056/NEJMra035021}}</ref> '''Monitoring diuresis''': Diuresis can be monitored by weighing the patient daily. The goal is weight loss of no more than 1.0 kg/day for patients with both ascites and [[peripheral edema]] and no more than 0.5 kg/day for patients with ascites alone.<ref name="pmid4910836">{{cite journal |author=Shear L, Ching S, Gabuzda GJ |title=Compartmentalization of ascites and edema in patients with hepatic cirrhosis |journal=N. Engl. J. Med. |volume=282 |issue=25 |pages=1391–6 |year=1970 |pmid=4910836 |doi=}}</ref> 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.<ref name="pmid8277955"/> A random urine sodium-to-potassium ratio of > 1 is 90% [[sensitivity (tests)|sensitivity]] in predicting negative balance (> 78-mmol/day sodium excretion).<ref name="Runyon1996">Runyon BA, Heck M. Utility of 24-hour urine sodium collection and urine Na/K ratios in the management of patients with cirrhosis and ascites [abstract]. Hepatology. 1996;24:571A.</ref> '''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.<ref name="pmid11124817">{{cite journal |author=Spahr L, Villeneuve JP, Tran HK, Pomier-Layrargues G |title=Furosemide-induced natriuresis as a test to identify cirrhotic patients with refractory ascites |journal=Hepatology |volume=33 |issue=1 |pages=28–31 |year=2001 |pmid=11124817 |doi=10.1053/jhep.2001.20646}}</ref> If a patient exhibits a resistance to or poor response to diuretic therapy, [[ultrafiltration]] or [[aquapheresis]] 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 patients with diuretic resistance and may restore responsiveness to conventional doses of diuretics.<ref name="pmid16160202">{{cite journal |author=Hunt SA, Abraham WT, Chin MH, et al |title=ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines |journal=Circulation |volume=112 |issue=12 |pages=154–235 |year=2005 |pmid=16160202 |doi=10.1161/CIRCULATIONAHA.105.167586}}</ref><ref name="pmid16500560">{{cite journal |author=Adams KF, Lindenfeld J, Arnold JMO, Baker DW, Barnard DH, Baughman KL, Boehmer JP, Deedwania P, Dunbar SB, Elkayam U, Gheorghiade M, Howlett JG, Konstam MA, Kronenberg MW, Massie BM, Mehra MR, Miller AB, Moser DK, Patterson JH, Rodeheffer RJ, Sackner-Bernstein J, Silver MA, Starling RC, Stevenson LW, Wagoner LE. |title=Heart Failure Society of America (HFSA) 2006 Comprehensive Heart Failure Practice Guideline. |journal=J Cardiac Failure |volume=12 |pages=e1–e122 |year=2006 |pmid=16500560}}</ref> ====Water restriction==== Water restriction is needed if hyponatremia < 130 mmol per liter develops.<ref name="pmid15084697"/> ====Paracentesis==== {{main|Paracentesis}} In those with severe (tense) ascites, therapeutic [[paracentesis]] may be needed in addition to medical treatments listed above.<ref name="pmid3297907"/><ref name="pmid3655306"/> As this may deplete [[serum albumin]] levels in the blood, albumin is generally administered intravenously in proportion to the amount of ascites removed. ====Liver transplantation==== {{main|liver transplantation}} Ascites that is refractory to medical therapy is considered an indication for [[liver transplantation]]. In the United States, the [[Model for End-Stage Liver Disease|MELD score]] ([http://www.unos.org/resources/meldPeldCalculator.asp online calculator])<ref name="pmid2682175">{{cite journal |author=Cosby RL, Yee B, Schrier RW |title=New classification with prognostic value in cirrhotic patients |journal=Mineral and electrolyte metabolism |volume=15 |issue=5 |pages=261–6 |year=1989 |pmid=2682175 |doi=}}</ref> is used to prioritize patients for transplantation. ====Shunting==== In a minority of patients 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]]. A [[meta-analysis]] of [[randomized controlled trials]] by the international [[Cochrane Collaboration]] concluded that "TIPS was more effective at removing ascites as compared with paracentesis...however, TIPS patients develop hepatic encephalopathy significantly more often"<ref name="pmid17054221">{{cite journal |author=Saab S, Nieto JM, Lewis SK, Runyon BA |title=TIPS versus paracentesis for cirrhotic patients with refractory ascites |journal=Cochrane database of systematic reviews (Online) |volume= |issue=4 |pages=CD004889 |year=2006 |pmid=17054221 |doi=10.1002/14651858.CD004889.pub2}}</ref> ===Low SAAG=== Exudative ascites generally does not respond to manipulation of the salt balance or diuretic therapy. Repeated paracentesis and treatment of the underlying cause is the mainstay of treatment. ==Complications== ===Spontaneous bacterial peritonitis=== {{main|Spontaneous bacterial peritonitis}} ==Cultural significance== It has been suggested that ascites was seen as a punishment especially for [[oath]]-breakers among the [[Proto-Indo-Europeans]].<ref>Oettinger, Norbert. Die Militärischen Eide der Hethiter. Wiesbaden, 1976. ISBN 3-447-01711-2.</ref> This proposal builds on the [[Hittite military oath]] as well as various [[Veda|Vedic]] hymns ([[Rigveda|RV]] 7.89, [[Atharvaveda|AVS]] 4.16.7). A similar curse dates to the [[Kassites|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".{{Fact|date=February 2007}} Comparable is also [[Numeri]] 5:11ff, where a confirmed adulteress is punished with swelling of the abdomen. ==References== {{reflist|2}} {{Digestive system and abdomen symptoms and signs}} [[Category:Gastroenterology]] [[Category:Symptoms]] [[ar:استسقاء (مرض)]] [[cs:Ascites]] [[de:Aszites]] [[es:Ascitis]] [[fr:Ascite]] [[fy:Bûkfocht]] [[it:Ascite]] [[nl:Ascites (medisch)]] [[ja:腹水]] [[pl:Wodobrzusze]] [[pt:Ascite]] [[ru:Асцит]] [[fi:Askites]] [[sv:Ascites]] [[te:జలోదరం]] [[uk:Асцит]]