Ascites

What is ascites?

Ascites is the abnormal accumulation of fluid in the peritoneal cavity, the space between the abdominal organs and the abdominal wall. A small amount of fluid in this space is normal. Ascites occurs when fluid production exceeds reabsorption, typically because of elevated pressure in the portal venous system, low albumin levels, or peritoneal involvement from infection or malignancy.

The most common causes determine the fluid type and its clinical characteristics. Ascites is broadly classified by its serum to ascites albumin gradient (SAAG):

• High SAAG ascites (above 1.1 g/dL) indicates portal hypertension as the driver, most commonly from liver cirrhosis, heart failure, or portal vein thrombosis.

• Low SAAG ascites (below 1.1 g/dL) indicates a non-portal hypertensive cause such as peritoneal malignancy, tuberculosis, or nephrotic syndrome.

This distinction is made through ascitic fluid analysis performed by a specialist, guided by the clinical picture that imaging and blood testing first establishes.

Symptoms of ascites

Small amounts of ascites cause no symptoms. As fluid accumulates, symptoms reflect increasing abdominal pressure and displacement of surrounding organs:

• Progressive abdominal distension and a sensation of fullness or tightness

• Abdominal discomfort or pain from pressure on surrounding structures

• Shortness of breath when fluid pushes against the diaphragm

• Difficulty eating full meals from gastric compression

• Ankle and leg swelling, frequently coexisting with ascites from the same underlying cause

• Nausea and reduced appetite

• Reduced ability to move comfortably or bend forward

• In infected ascites (spontaneous bacterial peritonitis): fever, worsening abdominal pain, and confusion requiring immediate medical attention

What causes ascites?

Ascites develops when the normal mechanisms for fluid balance in the abdominal cavity are overwhelmed. Common contributing causes include:

• Liver cirrhosis is the most common cause, responsible for approximately 75% of cases. Cirrhosis raises portal venous pressure and reduces albumin production, both driving fluid into the peritoneal space.

• Heart failure causes elevated venous back-pressure that impairs fluid reabsorption from the peritoneal cavity alongside peripheral oedema.

• Malignancy including ovarian cancer, colorectal cancer, gastric cancer, and peritoneal metastases from other primary tumours causes peritoneal irritation and direct fluid production.

• Chronic kidney disease and nephrotic syndrome cause severe hypoalbuminaemia, reducing the oncotic pressure that normally holds fluid in the bloodstream.

• Tuberculosis can cause peritoneal infection with characteristic low SAAG ascitic fluid.

• Pancreatitis causes pancreatic ascites through leakage of pancreatic fluid into the peritoneal space in severe cases.

• Portal vein thrombosis obstructs portal blood flow, causing ascites without necessarily involving cirrhosis.

How is ascites detected?

Ascites is detected primarily through abdominal imaging, with blood tests identifying the underlying cause and assessing systemic impact.

Abdominal MRI: Elfcare's full body MRI images the abdomen directly and can identify even small amounts of peritoneal fluid before they become clinically apparent. It simultaneously assesses the liver for cirrhosis and structural changes, the kidneys, the pancreas, and any abdominal masses suggesting malignancy. For ascites, MRI provides both detection of the fluid itself and the most likely structural cause in a single examination.

Blood tests: Blood tests assess the underlying conditions most commonly driving ascites formation. Relevant markers in Elfcare's panel include:

• Albumin: low levels of this protein are the most common cause of fluid leaking into the abdomen.

• Liver enzymes (ALT, AST, GGT, bilirubin): comprehensive markers used to check for cirrhosis or liver failure.

• Platelet count: low levels often signal advanced liver disease and increased pressure in the abdominal veins.

• Creatinine and eGFR: evaluates kidney health, as advanced liver issues can often trigger kidney failure.

• NT-proBNP: a marker used to determine if heart failure is the reason for the fluid buildup.

• CRP: high levels suggest the fluid may be caused by an infection or serious inflammatory condition.

• PSA (for men): screens for prostate cancer, which can metastasise to the peritoneum and present with malignant ascites in advanced disease.

• HbA1c and glucose: assesses metabolic health, as diabetes can accelerate the progression of liver disease.

Why early detection matters

Ascites is a marker of advanced disease in most cases, and its development significantly changes prognosis. In cirrhosis, the development of ascites marks the transition from compensated to decompensated liver disease, with a two-year mortality of approximately 50% without treatment. In malignancy, peritoneal involvement with ascites indicates advanced spread requiring systemic treatment. Identifying the underlying condition, whether liver disease, heart failure, or an abdominal malignancy, before ascites develops offers the greatest opportunity for meaningful intervention. Finding liver cirrhosis, cardiac dysfunction, or an abdominal mass before fluid accumulates is where early detection has the greatest impact.

How Elfcare can help

Elfcare's abdominal MRI directly images the peritoneal cavity, liver, kidneys, pancreas, and any abdominal masses, identifying ascites and the most likely structural cause in a single examination. For a condition that frequently reflects serious underlying disease, this structural assessment is the most clinically important finding Elfcare can provide.

Our blood panel covers albumin, liver function, platelet count, kidney function, NT-proBNP, and metabolic markers, together providing the systemic picture of the conditions most commonly driving ascites formation.

If our MRI or blood tests identify ascites or a finding consistent with its underlying cause, we take care of further diagnostics or refer you to the appropriate specialist.