Ascites is an abnormal accumulation of free fluid within the peritoneal cavity. Ascites is due to either increased portal venous pressure, low plasma proteins (hypoproteinaemia), chronic peritoneal irritation, leakage of lymphatic fluid into the peritoneal cavity, or fluid overload (Causes of ascites).
Ascites needs to be differentiated from other causes of abdominal distension including bowel obstruction, bleeding and huge intra-abdominal masses or cysts.
Pathophysiology of ascites
Increased portal venous pressure (The pathophysiology of ascites due to cirrhosis.)
Any cause of increased resistance to hepatic or portal venous blood flow can lead to ascites. Gross ascites occurs when increased pressure within the hepatic veins or at the post-sinusoidal level dramatically increases hydrostatic pressure within the hepatic sinusoids in the liver, and within the portal venous system. Collateral vein formation, shunting of blood to the systemic circulation and splanchnic vasodilatation (due in part to the local production of nitric oxide) develop particularly in the later stages of cirrhosis. Systemic arterial pressure is maintained by vasoconstriction and antinatriuretic factors resulting in sodium and water retention. The increased portal pressure combined with splanchnic vasodilation alters the capillary pressure and permeability, enabling intravascular fluid to move through pores between the vascular endothelial cells of the portal system into the extravascular space of the liver and intestine. Lymphatic flow is increased proximal to the point of vascular obstruction and, when the capacity of the lymphatic system is surpassed, the transudate moves across the surfaces of the liver, mesentery and intestine into the peritoneal cavity. Cirrhosis and schistosomal periportal fibrosis are the commonest causes of portal hypertension.
Any cause of hepatic venous outflow obstruction may cause ascites by increasing portal venous pressure (Budd—Chiari syndrome). The site of obstruction may be at the hepatic venules (haematological or liver disease), large hepatic veins, inferior vena cava or right atrium (right heart diseases).
Low concentrations of plasma proteins, particularly albumin, reduce the osmotic pressure of plasma. In health, the relatively high osmotic pressure of intravascular plasma tends to draw extravascular fluid back into the intravascular space. The osmotic gradient is reduced in hypoproteinaemic states so that less fluid is removed from extravascular sites. When the capacity of the hepatic and intestinal lymphatics to remove fluid from the extravascular interstitial space is exceeded, ascites develops.
Sodium and water retention
Reduced circulating plasma volume, as a result of loss of intravascular fluid into the peritoneal cavity and interstitial spaces (third-space fluid loss) and pooling of blood in the splanchnic vascular space secondary to portal venous outflow obstruction, reduces renal blood flow and glomerular filtration. Decreased renal perfusion stimulates increased renin secretion from the juxtaglomerular apparatus in the ascending limb of the loop of Henle of the kidney. The resultant secondary aldosteronism causes retention of sodium and water. Impairment of renal excretion of water and renal vasoconstriction lead to dilutional hyponatraemia and increase the risk of hepatorenal syndrome.
Chronic peritoneal inflammation
Any chronic inflammatory process within the peritoneal cavity results in considerable increases in flow within peritoneal blood and lymphatic vessels. Peritoneal microvascular permeability increases markedly with consequent exudation of plasma proteins and fluid into extravascular spaces. When the capacity of the lymphatics to reabsorb the fluid is exceeded, it accumulates within the peritoneal cavity. The high protein concentration of this peritoneal fluid further retards fluid reabsorption. As the inflammatory process resolves, and microvascular permeability returns to normal, less peritoneal fluid is formed and fluid is removed by absorption. The commonest cause of chronic peritoneal inflammation worldwide is abdominal tuberculosis but other peritoneal infections and foreign matter may also induce ascites.
Metastatic deposits cause ascites by a combination of inflammation, shedding of cells, exudation and sometimes bleeding. Gross ascites does not usually occur until late. Gastric and ovarian cancers are the most notorious for causing ascites due to their ease of transperitoneal spread, but any peritoneal malignant process may be responsible.
Leakage of fluid
Leakage of fluid directly into the peritoneal cavity occurs when intra-abdominal lymphatics are transected (e.g. abdominal surgery, trauma) or obstructed (e.g. primary or secondary lymphatic malignancy, surgical ligation). Ascites forms when the rate of leakage into the peritoneal cavity exceeds the rate of absorption by peritoneal lymphatics.
Exudation of pancreatic fluid from an inflammed pancreas may occur in acute pancreatitis. If the pancreatic duct ruptures due to inflammation or surgical damage, pancreatic ascites may persist as an internally draining pancreatic fistula.
Bile leaks may be termed bilious ascites although the bile is normally very irritant to the peritoneal cavity and normally induces more of a peritonitis/acute abdomen type reaction.
Urine may leak into the peritoneal cavity either from damage to a ureter, the bladder or an obstructed hydronephrotic kidney.
Ascites should be suspected from a history of abdominal distension. Ascites can be detected clinically on examination of the abdomen when the volume reaches approximately 1 L. Inspection of the abdomen reveals distension, which may vary from slight fullness laterally in the flanks to gross distension predominantly in the centre of the abdomen. Sometimes a hernial sac protrudes as it becomes full of ascitic fluid, particularly at the umbilicus. Other abnormal findings on inspection may include signs of liver disease (jaundice, scratch marks because of pruritus, spider naevi, caput medusae and dilated veins on the anterior abdominal wall, hepatomegaly), para-umbilical and other abdominal hernias, pitting oedema and surgical scars.
On palpation the abdomen may feel thicker owing to the fluid asserting more than the expected degree of resistance. In cases of chronic inflammation, particularly tuberculosis, the abdomen may feel ‘doughy’. Gross ascites causes tense abdominal distension that is unyielding to the examining hand. Ascites is confirmed by the presence of a fluid thrill and shifting dullness on percussion.
Large amounts of intraperitoneal fluid, either free or encysted, may give rise to a fluid thrill. The abdomen is flicked on one side and the transmitted shock wave is palpated by the examiner's other hand, which has been placed flat on the far side of the abdomen ((A&B) Clinical examination: palpating for ascites.). An accessory hand prevents transmission of the shock wave through the subcutaneous fat of the anterior abdominal wall. A fluid thrill may also be elicited by tapping in the loin and palpating at the front ((A&B) Clinical examination: palpating for ascites.). To detect a fluid thrill in an abdomen with smaller volumes of ascitic fluid, the area of stony dullness is first determined by percussion.
Free intraperitoneal fluid gravitates to the most dependent parts of the peritoneal cavity, namely the pelvis and paracolic regions, while the gas-filled intestine tends to ‘float’ uppermost. Fluid-filled structures have a stony dull percussion note, while gas-filled structures are resonant or hyper-resonant on percussion. Thus, when a patient with ascites lies supine, the flanks or lateral parts of the abdomen are stony dull to percussion while the peri-umbilical area is resonant. When the patient lies on one or other side, ascitic fluid gravitates to that side because it is then the most dependent part of the abdomen, and so the percussion note over that area becomes stony dull, while the other side becomes resonant.
Shifting dullness is elicited by percussing the abdomen and determining the point at which the percussion note changes from resonant to dull. The patient is then asked to roll about 45°. to one side, and percussion is repeated after waiting for a few seconds. Shifting dullness is confirmed by a significant change in position of the area of stony dullness. It should be noted that slight changes in the percussion note may be caused by positional changes in the small intestine.
Investigation of ascites
Investigation of a patient with ascites aims to detect the cause of the fluid accumulation. This is usually evident from the history and clinical examination, including habits and previous travel or domicile. Specific investigations depend on the likely cause of the ascites (Causes of ascites). Ascites is a multisystem disease and the probable cause will determine which systems require investigation. The choice includes urinalysis, serum concentrations of electrolytes, urea and creatinine, total proteins and albumin, liver function tests, serology, abdominal ultrasonography ((A) Ultrasound showing fluid (black) around the liver. (B) CT scan showing ascitic fluid, anterior abdominal distension and there is contrast in the loops of the bowel.), computed tomography (CT) scan ((A) Ultrasound showing fluid (black) around the liver. (B) CT scan showing ascitic fluid, anterior abdominal distension and there is contrast in the loops of the bowel.), portal vein Doppler scan and echocardiography. Diagnostic aspiration of a small volume of ascitic fluid for biochemical (protein and amylase estimation), microbiological (microscopy and culture) and cytological assessment may be necessary. Laparoscopy or minilaparotomy may be required to perform a peritoneal biopsy to diagnose abdominal tuberculosis and other inflammatory conditions. Schistosomiasis may be suspected from a history of swimming or living in endemic areas and confirmed by rectal or liver biopsy, ultrasound or serology. Plain abdominal films are not a method of diagnosing ascites but sometimes gross ascites give an appearance of ground glass.
Mild to moderate ascites may cause few symptoms. Large-volume ascites (more than 3–4 L) is very unpleasant for patients because it produces a constant feeling of abdominal fullness and discomfort, nausea and anorexia, limitation of movement and leg swelling. Respiratory difficulty and shortness of breath is due to elevation of the diaphragm, atelectasis and pleural effusions. Ascites may be complicated by previously unrecognised abdominal hernias and rarely by primary bacterial peritonitis. Primary or spontaneous bacterial peritonitis may be difficult to diagnose, does not always cause a lot of guarding or rigidity and patients' immune response to the infection may be impaired owing to their underlying disease, for example liver, renal or malignancy. Sometimes the peritonitis presents with general deterioration (e.g. development of hepatic encephalopathy or renal failure) rather than abdominal signs. Reduced renal blood flow and glomerular filtration, poor urine output, and low urinary sodium excretion cause pre-renal renal impairment with increased urea and creatinine, which may progress to acute renal failure (hepato-renal syndrome). Development of ascites in patients with chronic liver disease indicates severe liver impairment, and 1-year survival of such patients with intractable ascites is approximately 50%. Malignant ascites is most commonly due to intraperitoneal metastatic deposits of cancer originating in the ovary, stomach, breast and colon. Survival of these patients is poor, with a median survival of about 3 months.
Most patients with ascites are treated non-operatively. Ascites can be classified as moderate-volume, highvolume and refractory with regard to the approach to treatment. By definition, refractory ascites does not respond to high doses of diuretics (spironolactone and furosemide). Moderate-volume ascites does not require paracentesis and large-volume ascites is controlled by a combination of medical treatment and paracentesis.
Dietary sodium is restricted to approximately onethird of the normal daily intake (i.e. to about 60–90 mEq/day). Diuretic therapy commences with an aldosterone antagonist, such as spironolactone or amiloride. These two measures are successful in controlling ascites in about 60–70% of patients. In addition, a thiazide diuretic may be required. Diuretic therapy must be monitored closely to ensure that progressive renal failure and electrolyte imbalance (potassium, sodium, calcium and magnesium) do not occur.
Prophylactic antibiotics are not given. Primary or spontaneous peritonitis-complicating ascites is treated with appropriate antibiotics, although sometimes a laparotomy is required either for diagnosis or to wash out the peritoneal cavity. Specific causes of ascites such as tuberculosis are treated with appropriate anti-tuberculous chemotherapy according to national guidelines. Surgical intervention is reserved for diagnosis and to treat complications such as acute bowel obstruction, bleeding or perforation due to intestinal tuberculosis.
Paracentesis, or drainage of ascitic fluid, brings immediate though temporary relief to patients with symptomatic tense ascites. Paracentesis is performed under local anaesthetic and with a strict aseptic technique by inserting a cannula through the anterolateral abdominal wall, avoiding the inferior epigastric artery and the colon. It can often be performed under ultrasound or CT control. Fluid is drained into a sterile collecting system and the cannula is either removed immediately or left in situ for 24–48 hours. Rapid removal of large amounts of ascites may lead to serious hypovolaemia because the underlying reason for formation of ascites has not been eliminated and ascites re-forms rapidly with fluid from the extracellular space (interstitial and intravascular fluid). Volume replacement may be required during paracentesis and is undertaken cautiously with concentrated or normal serum albumin, to avoid hypovolaemia on one hand, and fluid overload and rapid reaccumulation of ascites on the other. The complications of infection, intestinal perforation and bleeding are rare when performed with an appropriate technique and an appropriate cannula.
Relief of acute hepatic venous obstruction
When the cause is due to an acute thrombus, thrombolytic therapy or angioplasty may be performed. Where these are unsuccessful a portosystemic shunt should be considered.
Transjugular intrahepatic portosystemic shunts
A shunt is placed between the portal and systemic circulations in the liver using the transjugular route for venous access. It may stabilise the patient while consideration is being given to liver transplantation. The shunts have a fairly high rate of blockage or stenosis (up to 75% after 6–12 months) and the shunt may induce hepatic encephalopathy.
If ascites is due to portal hypertension, portosystemic shunting may be performed in selected patients to reduce portal venous pressure. This may be using transjugular intrahepatic portosystemic shunts (TIPS) or by making a formal anastomosis between the splenic and renal veins (lienorenal shunt) or portal vein and inferior vena cava (portocaval shunt). These shunts do not adress the problem of the underlying liver disease, nor the accompanying oesophageal varices. Shunt surgery may be complicated by hepatic encephalopathy and hepatorenal syndrome. The presence of ascites in patients undergoing shunt surgery for portal hypertension is a poor prognostic sign.
Symptomatic relief by draining ascitic fluid from the peritoneal cavity into the systemic venous system can be achieved by way of a peritoneovenous shunt (PVS). A PVS (Denver shunt, LeVeen shunt) consists of a silastic tube, with multiple side holes at each end and a oneway valve situated in the middle. The PVS is placed entirely subcutaneously, with one end inserted into the peritoneal cavity and the other into the superior vena cava (SVC) via a jugular or subclavian vein, so that the valve allows flow of ascites from the peritoneal cavity to the venous system. A PVS is indicated when medical therapy has failed to control ascites in patients with (i) intractable ascites in the presence of reasonably good liver function, or (ii) rapidly accumulating ascites secondary to abdominal carcinomatosis. Concern about infusing ascitic fluid laden with malignant cells into the circulation is theoretical because these patients have widely disseminated malignant disease before insertion of the PVS.
The post-operative mortality of PVS is 10–20%, reflecting the serious underlying disorder of patients requiring the procedure. However, most patients obtain useful palliation. A minor coagulopathy is common postoperatively but can be partly prevented by completely aspirating the ascites and replacing it with warmed normal saline or Hartmann's solution when inserting the PVS. Long-term complications include occlusion of the PVS (particularly with bloody or highly proteinacious or mucoid ascites), SVC thrombosis, bacteraemia and shunt infection, which may lead to subacute bacterial endocarditis.