Internal Medicine/Abdominal Swelling and Ascites

Abdominal Swelling

Abdominal swelling can indicate various medical conditions. Patients may describe feelings of bloating or fullness in the abdomen and might notice an increase in their abdominal size, leading to tighter clothing or belt adjustments. While abdominal discomfort is common, abdominal pain is less frequent. However, when abdominal pain does accompany swelling, it is often due to intraabdominal infections, peritonitis, or pancreatitis. In cases of abdominal distention caused by ascites (fluid accumulation in the abdomen), patients may also report the sudden appearance of an inguinal or umbilical hernia. Pressure on the diaphragm from abdominal swelling can result in breathing difficulties.

Causes

The causes of abdominal swelling can be remembered using the six Fs: flatus, fat, fluid, fetus, feces, or a "fatal growth" (usually a neoplasm).

• Flatus: Abdominal swelling can occur due to increased gas in the intestines. The small intestine naturally contains about 200 mL of gas, including nitrogen, oxygen, carbon dioxide, hydrogen, and methane. Factors like swallowing air (aerophagia), anxiety, or bacterial fermentation of certain substances can lead to increased intestinal gas. In some cases, it's the sensation of abdominal pressure, rather than actual gas volume, that causes abdominal distention.
• Fat: An increase in abdominal fat due to weight gain can cause a noticeable increase in abdominal girth, resembling abdominal swelling. This can result from a poor diet, sedentary lifestyle, or conditions like Cushing's syndrome.
• Fluid: Accumulation of fluid in the abdominal cavity, known as ascites, often leads to abdominal distention. Ascites severity is categorized into grades, with grade 3 resulting in significant abdominal swelling.
• Fetus: Pregnancy naturally leads to increased abdominal girth. This enlargement becomes apparent around 12–14 weeks of gestation as the uterus moves from the pelvis into the abdomen.
• Feces: Severe constipation or intestinal obstruction can cause increased abdominal girth due to stool buildup in the colon. These conditions often come with abdominal discomfort, pain, nausea, and vomiting.
• Fatal Growth: Abdominal masses like neoplasms, abscesses, or cysts can cause abdominal swelling. Enlargement of intraabdominal organs such as the liver or spleen, or the presence of an abdominal aortic aneurysm, can also result in abdominal distention. Bladder distention may cause abdominal swelling as well.

Approach to the Patient History

Determining the cause of abdominal swelling starts with a thorough history. Patients should be asked about symptoms like weight loss, night sweats, and anorexia, which may suggest malignancy. Symptoms such as the inability to pass stool or gas, along with nausea or vomiting, can point to bowel issues like obstruction, constipation, or ileus. Increased belching and flatulence may indicate aerophagia or excessive gas production. Risk factors for liver disease, including alcohol consumption and jaundice, should also be explored, along with symptoms of other conditions like heart failure and tuberculosis that can lead to ascites.

Physical Exmination

A comprehensive physical exam should be performed, including an assessment for signs of systemic disease. Specific findings like lymphadenopathy, elevated jugular venous pressure, cardiac abnormalities, liver disease-related signs, and abdominal abnormalities should be carefully evaluated. Percussion and palpation techniques can help differentiate between abdominal gas, fluid, or a solid mass.

Imaging and Laboratory Evaluation

Depending on the suspected cause, abdominal x-rays, ultrasonography, or CT scans may be ordered to visualize the abdomen and identify potential issues like intestinal obstruction, ascites, or tumors. Laboratory tests such as liver function assessments, complete blood counts, and specific enzyme tests may also be conducted to evaluate liver function and rule out other systemic issues. Additionally, breath tests may be used to diagnose certain malabsorption or bacterial overgrowth conditions. In some cases, hepatic venous pressure gradient measurement or liver biopsy may be necessary for diagnosis.

Ascites

Pathogenesis in the Presence of Cirrhosis

Ascites in individuals with cirrhosis develops due to both portal hypertension and the retention of salt and water by the kidneys. Similar mechanisms contribute to ascites formation in heart failure. Portal hypertension is characterized by elevated pressure in the portal vein. According to Ohm's law, pressure is the result of resistance and flow. Increased hepatic resistance occurs through several mechanisms. Firstly, the development of hepatic fibrosis, which is a defining feature of cirrhosis, disrupts the normal structure of hepatic sinusoids and hinders regular blood flow through the liver. Secondly, activation of hepatic stellate cells, which promote fibrogenesis, leads to the contraction of smooth muscle and fibrosis. Lastly, cirrhosis is linked to reduced production of endothelial nitric oxide synthetase (eNOS), resulting in lower nitric oxide production and increased vasoconstriction within the liver.

Cirrhosis development is also associated with increased systemic levels of nitric oxide, as well as elevated levels of vascular endothelial growth factor and tumor necrosis factor, leading to vasodilation in the splanchnic arteries. This vasodilation causes blood pooling and a decrease in the effective circulating volume, which is perceived by the kidneys as hypovolemia. This triggers compensatory vasoconstriction through the release of antidiuretic hormone, resulting in the retention of free water and activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, leading to the retention of renal sodium and water.

Pathogenesis in the Absence of Cirrhosis

Ascites without cirrhosis typically results from peritoneal carcinomatosis, peritoneal infection, or pancreatic disease. Peritoneal carcinomatosis can occur due to primary peritoneal malignancies (like mesothelioma or sarcoma), abdominal malignancies (such as gastric or colonic adenocarcinoma), or metastatic disease from breast, lung carcinoma, or melanoma. Tumor cells lining the peritoneum produce a protein-rich fluid that contributes to ascites development. Fluid from the extracellular space is drawn into the peritoneum, further contributing to ascites development. Tuberculous peritonitis can also cause ascites by a similar mechanism, with tubercles on the peritoneum releasing proteinaceous fluid. Pancreatic ascites results from leakage of pancreatic enzymes into the peritoneum.

Causes

Cirrhosis accounts for 84% of ascites cases. Cardiac ascites, peritoneal carcinomatosis, and "mixed" ascites resulting from cirrhosis and another disease make up 10-15% of cases. Less common causes include massive hepatic metastasis, infections (like tuberculosis or Chlamydia), pancreatitis, and renal disease (nephrotic syndrome). Rare causes include hypothyroidism and familial Mediterranean fever.

Evaluation

Once ascites is confirmed, its cause is best determined by paracentesis, a procedure where ascitic fluid is extracted from the peritoneum using a needle or small catheter. Paracentesis is generally performed in the lower quadrants, with the left lower quadrant preferred due to deeper ascites and a thinner abdominal wall. It is considered safe, even in patients with coagulopathy, with infrequent complications.

After ascitic fluid extraction, its appearance is examined. Turbid fluid can indicate infection or tumor cells, white milky fluid can signify chylous ascites, dark brown fluid can reflect a high bilirubin concentration, and black fluid may suggest pancreatic necrosis or metastatic melanoma.

Ascitic fluid is sent for albumin and total protein level measurement, cell and differential counts, and, if infection is suspected, Gram's stain and culture. A serum albumin level is also measured simultaneously to calculate the serum-ascites albumin gradient (SAAG). SAAG is valuable for distinguishing ascites caused by portal hypertension from nonportal hypertensive ascites.

A high SAAG (≥1.1 g/dL) reflects portal hypertension and indicates that ascites results from increased hepatic sinusoidal pressure. A low SAAG (<1.1 g/dL) suggests ascites unrelated to portal hypertension.

In high-SAAG ascites, the ascitic protein level can provide further diagnostic information. An ascitic protein level of ≥2.5 g/dL indicates normal hepatic sinusoids that allow protein passage, while <2.5 g/dL indicates damaged, scarred hepatic sinusoids. The presence of high serum pro-brain-type natriuretic peptide (BNP) levels can suggest heart failure as the cause of high-SAAG ascites.

Additional tests are performed in specific clinical circumstances, such as glucose and lactate dehydrogenase measurement for suspected secondary peritonitis and amylase measurement for suspected pancreatic ascites. Cytology is used to diagnose peritoneal carcinomatosis, and adenosine deaminase levels can help identify tuberculous ascites.

When the cause of ascites remains uncertain, laparotomy or laparoscopy with peritoneal biopsies may be necessary for histological and cultural examination.

Treatment

Cirrhotic Ascites: The initial treatment involves limiting sodium intake to 2 g/d. When sodium restriction alone is insufficient, oral diuretics, typically a combination of spironolactone and furosemide, are used to increase urinary sodium excretion. Refractory cirrhotic ascites, which doesn't respond to sodium restriction and maximal diuretic use, may require pharmacological therapy with agents like midodrine or clonidine in addition to diuretics. Repeated large-volume paracentesis (LVP) or transjugular intrahepatic peritoneal shunt (TIPS) may be considered in cases where medical therapy alone is ineffective. Patients undergoing LVP should receive intravenous (IV) albumin to decrease the risk of postparacentesis circulatory dysfunction.

Malignant Ascites: Malignant ascites does not respond to sodium restriction or diuretics. Management involves serial LVPs, transcutaneous drainage catheter placement, or in rare cases, a peritoneovenous shunt or placement of the Alfapump system.

Ascites Caused by Tuberculous Peritonitis: This is treated with standard antituberculosis therapy.

Noncirrhotic Ascites: Ascites resulting from other conditions is treated by addressing the underlying cause.

Complications

• Spontaneous Bacterial Peritonitis (SBP): This is a common and potentially life-threatening complication of cirrhotic ascites. SBP may present with increased abdominal girth, fever, nausea, vomiting, or hepatic encephalopathy. Prompt paracentesis is essential for diagnosis, and treatment with antibiotics like IV cefotaxime is generally effective. Prophylactic antibiotics may be considered in certain high-risk cirrhotic patients.
• Hepatic Hydrothorax: This occurs when ascites, often from cirrhosis, enters the pleural space, causing respiratory and infectious issues. Treatment options include sodium restriction, diuretics, and thoracentesis or TIPS placement when needed.