| Ascites |
|
The abdomen of a person with cirrhosis showing massive ascites and prominent superficial veins
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| Classification and external resources |
| ICD-10 |
R18 |
| ICD-9 |
789.5 |
| DiseasesDB |
943 |
| MedlinePlus |
000286 |
| eMedicine |
ped/2927 med/173 |
| Patient UK |
Ascites |
| MeSH |
D001201 |
Ascites ( ə-SY-teez, from Greek askites, "baglike")[1] is a gastroenterological term for an accumulation of fluid in the peritoneal cavity. The medical condition is also known as peritoneal cavity fluid, peritoneal fluid excess, hydroperitoneum or more archaically as abdominal dropsy. Although most commonly due to cirrhosis, severe liver disease or metastatic cancer, its presence can portend other significant medical problems, such as Budd–Chiari syndrome. Diagnosis of the cause is usually with blood tests, an 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 (diuretics), paracentesis, or other treatments directed at the cause.
Contents
- 1 Signs and symptoms
- 2 Classification
- 3 Diagnosis
- 4 Causes
- 5 Pathophysiology
- 6 Treatment
- 6.1 High SAAG
- 6.1.1 Salt restriction
- 6.1.2 Diuretics
- 6.1.3 Water restriction
- 6.1.4 Paracentesis
- 6.1.5 Liver transplantation
- 6.1.6 Shunting
- 6.2 Low SAAG
- 7 Complications
- 7.1 Spontaneous bacterial peritonitis
- 7.2 Hepatorenal syndrome
- 7.3 Thrombosis
- 8 Society and culture
- 9 References
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.
Ascites is detected on physical examination of the abdomen by visible 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" (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:[2]
- Grade 1: mild, only visible on ultrasound and CT
- Grade 2: detectable with flank bulging and shifting dullness
- Grade 3: directly visible, confirmed with the fluid wave/thrill test
Diagnosis
Ascites in a person with abdominal cancer as seen on ultrasound
Routine complete blood count (FBC), 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, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as microbiological culture, Gram stain and cytopathology.[3]
The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.[4] 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.
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 (thrombosis of the hepatic vein) 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. An abdominal CT scan is a more accurate alternate to reveal abdominal organ structure and morphology.[citation needed]
Causes
Causes of high SAAG ("transudate") are:[3]
- Cirrhosis - 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
- Heart failure - 3%
- Hepatic venous occlusion: Budd-Chiari syndrome or veno-occlusive disease
- Constrictive pericarditis
- Kwashiorkor (childhood protein-energy malnutrition)
Causes of low SAAG ("exudate") are:
- Cancer (metastasis and primary peritoneal carcinomatosis) - 10%
- Infection: Tuberculosis - 2% or Spontaneous bacterial peritonitis
- Pancreatitis - 1%
- Serositis
- Nephrotic syndrome[5]
- Hereditary angioedema[6]
Other Rare causes:
- Meigs syndrome
- Vasculitis
- Hypothyroidism
- Renal dialysis
- Peritoneum mesothelioma
Pathophysiology
Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 35 liters are possible.
Roughly, transudates are a result of increased pressure in the hepatic portal vein (>8 mmHg, usually around 20 mmHg[7]), 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.[3]
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 hepatorenal syndrome. Other complications of ascites include spontaneous bacterial peritonitis (SBP), due to decreased antibacterial factors in the ascitic fluid such as complement.
Treatment
Diagram showing ascites being drained
Ascites is generally treated while an underlying etiology is sought, in order to prevent complications, relieve symptoms, and 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.[8] In those with severe ascites causing a tense abdomen, hospitalization is generally necessary for paracentesis.[9][10]
High SAAG
Treatments in high SAAG ("transudate") are:
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.[11]
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.[12] Diuretics for ascites should be dosed once per day.[13] Generally, the starting dose is oral spironolactone 100 mg/day (max 400 mg/day). 40% of patients will respond to spironolactone.[11] 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.[13] Serum potassium level and renal function should be monitored closely while on these medications.[14]
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.[8] 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.[13] A random urine sodium-to-potassium ratio of > 1 is 90% sensitivity in predicting negative balance (> 78-mmol/day sodium excretion).[15]
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.[16]
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.[17][18]
Water restriction
Water restriction is needed if hyponatremia < 130 mmol per liter develops.[14]
Paracentesis
Main article: Paracentesis
In those with severe (tense) ascites, therapeutic paracentesis may be needed in addition to medical treatments listed above.[9][10] 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 article: liver transplantation
Ascites that is refractory to medical therapy is considered an indication for liver transplantation. In the United States, the MELD score (online calculator)[19] 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"[20]
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 article: Spontaneous bacterial peritonitis
Hepatorenal syndrome
Main article: Hepatorenal syndrome
Thrombosis
Complications involve portal vein thrombosis and splenic vein thrombosis: clotting of blood affects the hepatic portal vein or varices associated with splenic vein. This can lead to portal hypertension and reduction in blood flow. When a liver cirrhosis patient is suffering from thrombosis, it is not possible to perform a liver transplant, unless the thrombosis is very minor. In case of minor thrombosis, there are some chances of survival using cadaveric liver transplant.
Society and culture
It has been suggested that ascites was seen as a punishment especially for oath-breakers among the Proto-Indo-Europeans.[21] 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".[citation needed] Comparable is also Numbers 5:11ff, where a confirmed adulteress is punished with swelling of the abdomen.
References
- ^ "Ascites". Dictionary.com: An Ask.com Service. Oakland, CA: IAC. 2010. Retrieved March 29, 2010.
- ^ Moore, K. P.; 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 (2003). "The Management of Ascites in Cirrhosis: Report on the Consensus Conference of the International Ascites Club". Hepatology 2003 (38): 258–66. doi:10.1053/jhep.2003.50315. PMID 12830009.
- ^ a b c Warrell DA, Cox TN, Firth JD, Benz ED. Oxford textbook of medicine. Oxford: Oxford University Press, 2003. ISBN 0-19-262922-0.
- ^ Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG (August 1992). "The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites". Ann. Intern. Med. 117 (3): 215–20. doi:10.7326/0003-4819-117-3-215. PMID 1616215.
- ^ Kumar & Clark's Clinical Medicine e.8 Chapter 7: Liver, biliary tract and pancreatic disease Pg. 335
- ^ Branco-Ferreira M, Pedro E, Barbosa MA, Carlos AG (1998). "Ascites in hereditary angioedema". Allergy 53 (5): 543–5. doi:10.1111/j.1398-9995.1998.tb04098.x. PMID 9636820.
- ^ [Ascites in Cirrhosis Relative Importance of Portal Hypertension and Hypoalbuminemia] DONALI) O. CASTELL, LCDR (MC), USN
- ^ a b Shear L, Ching S, Gabuzda GJ (1970). "Compartmentalization of ascites and edema in patients with hepatic cirrhosis". N. Engl. J. Med. 282 (25): 1391–6. doi:10.1056/NEJM197006182822502. PMID 4910836.
- ^ a b Ginés P, Arroyo V, Quintero E et al. (1987). "Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study". Gastroenterology 93 (2): 234–41. PMID 3297907.
- ^ a b Salerno F, Badalamenti S, Incerti P et al. (1987). "Repeated paracentesis and i.v. albumin infusion to treat 'tense' ascites in cirrhotic patients. A safe alternative therapy". J. Hepatol. 5 (1): 102–8. doi:10.1016/S0168-8278(87)80067-3. PMID 3655306.
- ^ a b Gatta A, Angeli P, Caregaro L, Menon F, Sacerdoti D, Merkel C (1991). "A pathophysiological interpretation of unresponsiveness to spironolactone in a stepped-care approach to the diuretic treatment of ascites in nonazotemic cirrhotic patients". Hepatology 14 (2): 231–6. doi:10.1002/hep.1840140205. PMID 1860680.
- ^ Fogel MR, Sawhney VK, Neal EA, Miller RG, Knauer CM, Gregory PB (1981). "Diuresis in the ascitic patient: a randomized controlled trial of three regimens". J. Clin. Gastroenterol. 3 Suppl 1: 73–80. doi:10.1097/00004836-198100031-00016. PMID 7035545.
- ^ a b c Runyon BA (1994). "Care of patients with ascites". N. Engl. J. Med. 330 (5): 337–42. doi:10.1056/NEJM199402033300508. PMID 8277955.
- ^ a b Ginès P, Cárdenas A, Arroyo V, Rodés J (2004). "Management of cirrhosis and ascites". N. Engl. J. Med. 350 (16): 1646–54. doi:10.1056/NEJMra035021. PMID 15084697.
- ^ Runyon BA, Heck M (1996). "Utility of 24-hour urine sodium collection and urine Na/K ratios in the management of patients with cirrhosis and ascites". Hepatology 24: 571A.
- ^ Spahr L, Villeneuve JP, Tran HK, Pomier-Layrargues G (2001). "Furosemide-induced natriuresis as a test to identify cirrhotic patients with refractory ascites". Hepatology 33 (1): 28–31. doi:10.1053/jhep.2001.20646. PMID 11124817.
- ^ Hunt SA, Abraham WT, Chin MH et al. (2005). "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". Circulation 112 (12): 154–235. doi:10.1161/CIRCULATIONAHA.105.167586. PMID 16160202.
- ^ 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. (2006). "Heart Failure Society of America (HFSA) 2006 Comprehensive Heart Failure Practice Guideline.". J Cardiac Failure 12 (1): e1–e122. doi:10.1016/j.cardfail.2005.11.005. PMID 16500560.
- ^ Cosby RL, Yee B, Schrier RW (1989). "New classification with prognostic value in cirrhotic patients". Mineral and electrolyte metabolism 15 (5): 261–6. PMID 2682175.
- ^ Saab S, Nieto JM, Lewis SK, Runyon BA (2006). "TIPS versus paracentesis for cirrhotic patients with refractory ascites". Cochrane database of systematic reviews (Online) (4): CD004889. doi:10.1002/14651858.CD004889.pub2. PMID 17054221.
- ^ Oettinger, Norbert. Die Militärischen Eide der Hethiter. Wiesbaden, 1976. ISBN 3-447-01711-2.
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Symptoms and signs: digestive system and abdomen (R10–R19, 787,789)
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Gastrointestinal (GI)
tract |
| Upper GI tract |
- Nausea/Vomiting
- Heartburn
- Dysphagia (Oropharyngeal, Esophageal)
- Halitosis
- Xerostomia
- Hypersalivation
|
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| Lower GI tract |
- Flatus: Flatulence
- Abdominal distension
- Bloating
- Burping
- Tympanites
- Stool: Fecal incontinence
- Blood: Fecal occult blood
- Rectal tenesmus
- Constipation
- Obstructed defecation
- Diarrhea
- Rectal discharge
- Football sign
- Psoas sign
- Obturator sign
- Rovsing's sign
- Heel tap sign
- Aure-Rozanova's sign
- Dunphy sign
- Alder's sign
- Lockwood's sign
- Rosenstein's sign
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| Accessory |
- Hepatosplenomegaly/Hepatomegaly
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| Abdominopelvic |
|
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| Abdominal – general |
- Abdominal pain
- Acute abdomen
- Colic
- Baby colic
- Abdominal guarding
- Abdominal mass
- Rebound tenderness
- Shifting dullness
- Bulging flanks
- Puddle sign
- Fluid wave test
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Index of digestion
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| Description |
- Anatomy
- Physiology
- Development
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| Disease |
- Congenital
- Neoplasms and cancer
- Inflammatory bowel disease
- Gluten sensitivity
- Other
- Symptoms and signs
- Blood tests
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| Treatment |
- Procedures
- Drugs
- anabolic steroids
- antacids
- diarrhoea and infection
- bile and liver
- functional gastrointestinal disorders
- laxatives
- peptic ulcer and reflux
- nausea and vomiting
- other
- Surgery
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Pathology: hemodynamics
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| Decreases |
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Thrombus/thrombosis
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Renal vein thrombosis
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Ischemia
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- Brain ischemia
- Ischaemic heart disease
- large intestine: Ischemic colitis
- small intestine: Mesenteric ischemia
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Infarction
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general:
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- Anemic infarct
- Hemorrhagic infarct
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regional:
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- Myocardial infarction
- Cerebral infarction
- Splenic infarction
- Limb infarction
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| Increases |
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Hemorrhage
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general
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- Bruise/Hematoma
- Petechia
- Purpura
- Ecchymosis
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regional
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- head
- Epistaxis
- Hemoptysis
- Intracranial hemorrhage
- Hyphema
- Subconjunctival hemorrhage
- torso
- Hemothorax
- Hemopericardium
- Pulmonary hematoma
- abdomen
- Gastrointestinal bleeding
- Haemobilia
- Hemoperitoneum
- Hematocele
- Hematosalpinx
- joint
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Edema
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general
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- Anasarca
- Angioedema/Lymphedema
- Exudate/Transudate
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regional
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- Cerebral edema
- Pulmonary edema
- Hydrothorax
- Ascites/hydroperitoneum
- Hydrosalpinx
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Other
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