ascitis
dr moshtal wtwt FIBMS
it is accumulation of free fluid in the peritoneal cavity
Small amounts of ascites are asymptomatic, but with larger accumulations of fluid (> 1 L
there is abdominal distension, fullness in the flanks, shifting dullness on percussion and, when the ascites is marked, a fluid thrill (*) Other features include eversion of the umbilicus, herniae, abdominal striae, divarication of the recti and scrotal oedema. Dilated superficial abdominal veins may be seen if the ascites is due to portal hypertension
Causes of ascites ()
Common causes
Malignant disease
Hepatic
Peritoneal
Cardiac failure
Hepatic cirrhosis
Other causes
Hypoproteinaemia
Nephrotic syndrome
Protein-losing enteropathy
Malnutrition
Hepatic venous occlusion
Budd-Chiari syndrome
Veno-occlusive disease
Pancreatitis
Lymphatic obstruction
Infection
Tuberculosis
Rare causes
Meigs syndrome*
Hypothyroidism
Investigations
() Ultrasonography is the best means of detecting ascites
() Paracentesis can also be used to confirm the presence of ascites but is most useful for obtaining ascitic fluid for analysis. The appearance of ascitic fluid may point to the underlying cause
Pleural effusions are found in about 10% of patients, usually on the right side (hepatic hydrothorax); most are small and only identified on chest X-ray, but occasionally a massive hydrothorax occurs
Ascitic fluid: appearance and analysis
Cause/appearance
Cirrhosis: clear, straw-coloured or light green
Malignant disease: bloody
Infection: cloudy
Biliary communication: heavy bile staining
Lymphatic obstruction: milky-white (chylous)
Useful investigations
Total albumin (plus serum albumin) and protein*
Amylase
Neutrophil count
Cytology
Microscopy and culture
Measurement of the protein concentration and the serum-ascites albumin gradient are used to distinguish a transudate from an exudate
Cirrhotic patients typically develop a transudate with a total protein concentration below 25 g/L (*) A gradient of more than 11 g/L is 96% predictive that ascites is due to portal hypertension ,Venous outflow obstruction due to cardiac failure or hepatic venous outflow obstruction can cause a transudative ascites
Exudative ascites (ascites protein concentration above 25 g/L or a SAAG of less than 11g/L) raises the possibility of infection (especially tuberculosis), malignancy, hepatic venous obstruction, pancreatic ascites or, rarely, hypothyroidism
Ascites amylase activity above 1000 U/L identifies pancreatic ascites, and low ascites glucose concentrations suggest malignant disease or tuberculosis, Cytological examination may reveal malignant cells (one-third of cirrhotic patients with a bloody tap have a hepatoma). Polymorphonuclear leucocyte counts above 250 × 106/L strongly suggest infection (spontaneous bacterial peritonitis
Laparoscopy can be valuable in detecting peritoneal disease
Causes of high SAAG ("transudate") are Cirrhosis
Heart failure
Hepatic Venous occlusion: Budd-Chiari syndrome or veno-occlusive disease
Constrictive pericarditis
Kwashiorkor
Causes of low SAAG ("exudate") are Cancer (primary peritoneal carcinomatosis and metastasis)
Infection: Tuberculosis or Spontaneous bacterial peritonitis
Pancreatitis
Serositis
Nephrotic syndrome or Protein losing enteropathy
Hereditary angioedema
Other Rare causes
Meigs syndrome
Vasculitis
Hypothyroidism
Renal Dialysis
Peritoneum Mesothelioma
Classification
Ascites exists in three grades
Grade 1: mild, only visible on ultrasound and CT
Grade 2: detectable with flank bulging and shifting dullness
Grade 3: directly visible, confirmed with fluid thrill
Management
Successful treatment of ascites relieves discomfort but does not prolong life, and if over-vigorous, can produce serious disorders of fluid and electrolyte balance and precipitate hepatic encephalopathy (*) Treatment of transudative ascites is based on restricting sodium and water intake, promoting urine output with diuretics and, if necessary, removing ascites directly by paracentesis
Exudative ascites due to malignancy should be treated with paracentesis but fluid replacement is generally not required
During management of ascites, the patient should be weighed regularly. It is important to avoid removing more than 1 L of fluid daily, so body weight should not fall by more than 1 kg daily if fluid depletion in the rest of the body is to be avoided
Sodium and water restriction
Restriction of dietary sodium intake is essential to achieve negative sodium balance in ascites, and a few patients can be managed satisfactorily on this treatment alone.
Restriction of sodium intake to 100 mmol/day ( no added salt diet ) is usually adequate
Drugs containing relatively large amounts of sodium and those promoting sodium retention, such as non-steroidal anti-inflammatory drugs, must be avoided Restriction of water intake to 1.0-1.5 L/day is necessary only if the plasma sodium falls below 125 mmol/L
Most patients require diuretics in addition to sodium restriction. Spironolactone (100-400 mg/day) is the drug of choice for long-term therapy because it is a powerful aldosterone antagonist; unfortunately, it can cause painful gynaecomastia and hyperkalaemia
Some patients also require loop diuretics, such as furosemide, but these can cause fluid and electrolyte imbalance and renal dysfunction
Diuresis is improved if patients are rested in bed, perhaps because renal blood flow increases in the horizontal position
Patients who do not respond to doses of 400 mg spironolactone and 160 mg furosemide are considered to have refractory or diuretic-resistant ascites and should be treated by other therapeutic measures
Paracentesis
The first-line treatment of refractory ascites is large-volume paracentesis with intravenous albumin replacement
Paracentesis to dryness or the removal of 3-5 L daily is safe, provided the circulation is supported with an intravenous colloid such as human albumin (6-8 g per litre of ascites removed, usually as 100 mL of 20% human albumin solution (HAS) for every 3 L of ascites drained
Peritoneo-venous shunt
The peritoneo-venous shunt is a long tube with a non-return valve running subcutaneously from the peritoneum to the internal jugular vein in the neck; it allows ascitic fluid to pass directly into the systemic circulation
It is effective in ascites resistant to conventional treatment but complications, including infection, superior vena caval thrombosis, pulmonary oedema, bleeding from oesophageal varices and disseminated intravascular coagulopathy, limit its use and insertion of these shunts is now rare
Transjugular intrahepatic portosystemic stent shunt (TIPSS
can relieve resistant ascites but does not prolong life; it may be an option where the only alternative is frequent, large-volume paracentesis It can be used when liver function is reasonable or in patients awaiting liver transplantation
Spontaneous bacterial peritonitis
Patients with cirrhosis are highly susceptible to spontaneous bacterial peritonitis (SBP)
This usually presents suddenly with abdominal pain, rebound tenderness, absent bowel sounds and fever in a patient with obvious features of cirrhosis and ascites. Abdominal signs are mild or absent in about one-third of patients, and in these patients hepatic encephalopathy and fever are the main features
Diagnostic paracentesis may show cloudy fluid, and an ascites neutrophil count above 250 × 106/L almost invariably indicates infection. The source of infection cannot usually be determined, but most organisms isolated from ascitic fluid or blood cultures are of enteric origin and Escherichia coli is the organism most frequently found
Treatment should be started immediately with broad-spectrum antibiotics, such as cefotaxime. Recurrence of SBP is common but may be reduced with prophylactic quinolones such as norfloxacin (400 mg daily) or ciprofloxacin (250 mg 12-hourly)