Ascites R18

Excessive accumulation of serous fluid in the free abdominal cavity. Ascites is always an indication of an advanced disease and therefore requires diagnostic clarification. In addition to the medical history and physical examination, laboratory tests of liver values, kidney function and serum and urine electrolytes are part of the primary diagnosis. This is followed by specific etiologically oriented diagnostics according to the probability of a specific organ disease.

• Portal ascites (80% of cases: cirrhosis of the liver)
• Cardiac ascites (right heart failure; Budd-Chiari syndrome, pericarditis constrictiva)
• Malignant ascites (lymphatic drainage obstructions, peritoneal carcinosis, retroperitoneal tumours and fibrosis, up to 10% of cases)
• Inflammatory ascites (bacterial peritonitis, collagenosis, genitoanal infections e.g. chlamydia)
• Pancreatogenic ascites (acute or chronic pancreatitis)
• Hypalbuminemic ascites (nephrotic syndrome, exudative enteropathy; Ménétrier's disease)
• Rare forms of ascites: mesenteric vein thrombosis, uremia, hypothyroidism, hematoperitoneum (trauma), Meigs syndrome (ovarian tumor)

The pathophysiology of ascites formation is not yet fully understood (John S et al. 2015). Common to all causes is the transfer of fluid from the blood vessels into the peritoneal cavity. The most frequent cause, at around 80 %, is liver cirrhosis, which leads to fluid leaking from the blood vessels due to an increase in pressure in the portal vein circulation. Ascites can also occur in (right) heart failure or pericarditis constrictiva, as well as in liver tumours or metastases into the peritoneal cavity. In the case of perforations of hollow organs, secondary peritonitis leads to ascites formation. Likewise, acute or chronic pancreatitis, fistulae of the biliary or pancreatic system or a lack of albumin can lead to ascites formation. Increased sodium reabsorption through activation of the RAAS (Renin-Alosterone-angiotensin system) with release of ADH and catecholamines is a response to reduced blood volume.

Visible swelling (protruding flanks in a lying patient, in contrast to the upturned abdomen in obese patients). The navel is elapsed or convex. The lower clinical detection limit of ascites is about 1000-1500ml.

Percussion: Flank damping which can be changed when changing position.

Ballottement (undulation phenomenon): When the abdomen is pushed sideways, a wave is formed which can be palpated on the other side (from about two litres of ascites fluid).

Sonography: Lower detection limit about 50ml. Small amounts of fluid are most likely to be detected at the lower edge of the liver or just above the bladder. The space between liver and kidney (Morison's pit or recessus hepatorenalis) is the lowest point of the upper abdomen when lying down.

The ascites fluid is examined for cell count and germs. Based on the protein content, a distinction is made between transudates (protein content <30g/l) and exudates (protein content > 30g/l). Exudates indicate malignant tumours, infections, collagenoses or pancreatogenic ascites.

SAAG: Albumin content of ascites in relation to the albumin content of the blood (serum ascites-albumin gradient = SAAG). The SAAG can give an indication of the cause. SAAG > 1.1 g/dl: portal hypertension likely.

SAAG > 2.5 g/dl: ascites formation in heart failure or early Budd-Chiari syndrome.

SAAG < 1.1 g/dl portal hypertension less likely; indicates pancreatitis, peritoneal carcinomatosis, a bile leak, tuberculosis or nephrotic syndrome.

Clinic and clinical examination

• Computer tomography
• Sonography
• Analysis of ascites after puncture of the peritoneal cavity.
• Lactic ascites indicates an injury or disruption of lymphatic drainage (for example due to trauma), but can also occur in other diseases.
• Dark brown ascites usually contains a high proportion of bilirubin.
• Black ascites is formed by necroses of the pancreas; more rarely by diffuse metastasis in malignant melanoma.
• Amber ascites indicates right heart failure or nephrotic syndrome.
• Purulent ascites is found in purulent peritonitis.
• Cloudy or hemorrhagic ascites is found in purulent or tuberculous peritonitis.
• Mucinous or mucous ascites (gall bladder) is mainly found in pseudomyxoma peritonei from the appendix (mucocele) or ovarian cysts.

Essential for the differential diagnosis of ascites is the diagnostic paracentesis. In particular, it must clarify the questions of whether the ascites is malignant or infected.

Any deterioration of the general condition in cirrhosis of the liver with ascites or deterioration of liver function parameters (such as bilirubin, INR, albumin) as well as other laboratory chemical parameters such as creatinine, urea should be followed by a diagnostic ascites puncture to exclude spontaneous bacterial peritonitis (SBP).

Diet: Patients with cirrhosis of the liver and ascites should receive an adequate protein diet (recommended protein intake: 1.2-1.5g× kg-1×day-1) with sufficient energy content (non-protein energy 25kcal×kg-1×day-1). All patients should be informed that an additional salt intake can lead to a worsening of the clinical picture.

Control of the therapy by daily weight control. Optimal weight loss 0.5-0.6kg/day. The weight loss cannot be realized faster.

Diuretics: are generally only used when strict sodium restriction does not respond. Spironolactone (100-300mg/day) in 2 or 3 doses is usually effective. If not sufficiently effective, additional application of a loop diuretic (hydrochlorothiazide 50-100mg/day p.o.), xipamide (10-40mg/day p.o.) or furosemide (40-160mg/day p.o.). Fluid restrictions are usually not necessary.

An alternative therapeutic approach is therapeutic puncture. The removal of 4-6l of ascites is possible without risk, provided that a low-salt albumin solution (about 40g i.v./puncture appointment) is infused at the same time (Wong F 2012). It appears, however, that after puncture the ascites will rebuild faster than with conservative therapy.

TIPS: TIPS(Transjugular intrahepatic portosystemic shunt), i.e. a connection between the portal vein and the inferior vena cava is an alternative in cases of portal hypertension and therapy-resistant ascites.

Transplantation is a further therapeutic option for liver cirrhosis.

Paracentesis: malignant ascites is often treated with repeated paracentesis. In addition, shunts and chemotherapies are used, some of which are administered directly into the peritoneal cavity (intraperitoneally), as well as the antibody catumaxomab, which is specially approved for the treatment of malignant ascites.

PleurX drain: an alternative to therapeutic puncture is the "PleurX drain", a catheter tunneled into the subcutaneous fatty tissue. The patient, his relatives or the nursing service can use it to drain the ascites on an outpatient basis and independently (Tapping CR et al. 2012).

In healthy people, the peritoneal cavity contains about 50 to 70 ml of fluid. Smaller amounts of ascites are usually asymptomatic. Only larger volumes become noticeable as predominantly painless swelling of the abdomen.

1. Gerbes Al et al (2011) S3 guideline "Ascites, spontaneous bacterial peritonitis, hepatorenal syndrome". Z Gastroenterol 49:749-779
2. Geraint B et al (2013) Ascitic Microbiota Composition Is Correlated with Clinical Severity in Cirrhosis with Portal Hypertension. PLoS ONE 8: e74884
3. John S et al (2015) Hyponatremia in cirrhosis: pathophysiology and management. World J Gastroenterol 21:3197-3205.https://www.ncbi.nlm.nih.gov/pubmed/25805925
4. Kimer N et al (2015) Beta-blockers in cirrhosis and refractory ascites: a retrospective cohort study and review of the literature. Scand J Gastroenterol 50:129-137.
5. Matthew P et al (2013) Tunneled Peritoneal Drainage Catheter Placement for Refractory Ascites: Single-center Experience in 188 Patients. Journal of Vascular and Interventional Radiology 24: 1303-1308
6. John S et al (2015) Hyponatremia in cirrhosis: pathophysiology and management. World J Gastroenterol 21:3197-3205.
7. Tapping CR et al (2012) PleurX drain use in the management of malignant ascites: safety, complications, long-term patency and factors predictive of success. The British Journal of Radiology 85: 623-628
8. Wong F (2012) Management of ascites in cirrhosis. J Gastroenterol Hepatol 27:11-20.