Approach to ascites: Clinical sciences

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Approach to ascites: Clinical sciences

Block 9 Gastrointestinal partial

Block 9 Gastrointestinal partial

Colon histology
Esophagus histology
Gallbladder histology
Liver histology
Pancreas histology
Small intestine histology
Stomach histology
Gastroesophageal reflux disease (GERD)
Barrett esophagus
Eosinophilic esophagitis (NORD)
Esophageal cancer
Mallory-Weiss syndrome
Esophageal atresia and tracheoesophageal fistula: Year of the Zebra
Achalasia
Achalasia: Year of the Zebra
Esophageal disorders: Clinical
Esophageal disorders: Pathology review
Esophagitis: Clinical
Gastroesophageal reflux disease (GERD): Clinical
Gastroesophageal reflux disease: Clinical sciences
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Plummer-Vinson syndrome
Gastrointestinal bleeding: Clinical
Gastrointestinal bleeding: Pathology review
Diffuse esophageal spasm
Scleroderma: Pathology review
Scleroderma
Boerhaave syndrome
Pediatric gastrointestinal bleeding: Clinical
Jaundice
Jaundice: Pathology review
Jaundice: Clinical
Neonatal jaundice: Clinical
Approach to jaundice (unconjugated hyperbilirubinemia): Clinical sciences
Approach to jaundice (conjugated hyperbilirubinemia): Clinical sciences
Cholestatic liver disease
Cirrhosis: Clinical
Hepatitis B and Hepatitis D virus
Viral hepatitis: Pathology review
Viral hepatitis: Clinical
Viral hepatitis
Cirrhosis
Cirrhosis: Clinical sciences
Cirrhosis: Pathology review
Portal hypertension
Pulmonary arterial hypertension (NORD)
Approach to ascites: Clinical sciences
Pancreatitis: Clinical
Hepatocellular carcinoma
Hepatocellular adenoma
Peptic ulcer
Peptic ulcer disease: Clinical sciences
Peptic ulcers and stomach cancer: Clinical
Zollinger-Ellison syndrome
Approach to melena and hematemesis: Clinical sciences
Acid reducing medications
Antidiarrheals
Acute pancreatitis
Pancreatitis: Pathology review
Chronic pancreatitis
Chronic pancreatitis: Clinical sciences
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Pancreatic cancer: Clinical sciences
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Multiple endocrine neoplasia: Pathology review
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Diabetes mellitus: Pathology review
Diabetes mellitus (Type 2): Clinical sciences
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Large bowel obstruction: Clinical sciences
Small bowel obstruction: Clinical sciences
Irritable bowel syndrome
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Short bowel syndrome (NORD)
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Diverticular disease: Clinical
Abdominal hernias
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Congenital gastrointestinal disorders: Pathology review
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Colorectal polyps and cancer: Pathology review
Diverticular disease: Pathology review
Gallbladder disorders: Pathology review
Biliary atresia
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Gilbert's syndrome
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Anal fissure
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Anal fissure: Clinical sciences

Decision-Making Tree

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Ascites refers to an abnormal collection of fluid in the peritoneal cavity, which can be a sign of various underlying conditions. In some cases, ascites can arise in the absence of portal hypertension, which is typically seen in conditions such as peritoneal carcinomatosis; pancreatic ascites, protein-losing enteropathy, and nephrotic syndrome.

More commonly, ascites is associated with portal hypertension, which can occur due to prehepatic, hepatic, and posthepatic causes. The most common prehepatic cause is portal vein thrombosis; while common hepatic causes include cirrhosis, infiltrative liver disease, and acute liver failure. Finally, important posthepatic causes include right-sided heart failure, constrictive pericarditis, and pulmonary hypertension.

Now, when approaching a patient with new ascites, you should first obtain focused history and physical examination, as well as labs, including CBC, CMP, and coagulation profile. History typically includes progressive abdominal distension; while physical exam reveals bulging flanks, a palpable fluid wave, and shifting dullness to percussion.

Additionally, order an abdominal ultrasound, which can help you detect free fluid in the peritoneal cavity, which is commonly seen as an anechoic space.

Next, obtain a diagnostic paracentesis to remove a small amount of ascitic fluid for analysis. Initial tests on the ascitic fluid include albumin, total protein, and cell count with differential. With these values, calculate the serum ascites albumin gradient, or SAAG for short, by subtracting the ascites albumin from the serum albumin. The SAAG results will help you determine if portal hypertension is present or absent. Moreover, SAAG less than 1.1 means there’s no portal hypertension, so your next step is to assess the ascitic fluid WBC count and differential.

Elevated WBCs in ascitic fluid with predominant lymphocytes should make you think of peritoneal disease, so test ascitic fluid for TB cultures and order cytology. Positive cultures confirm the diagnosis of peritoneal tuberculosis; while positive cytology for malignant cells confirms the diagnosis of peritoneal carcinomatosis. Keep in mind that peritoneal carcinomatosis can be caused by a primary cancer of the peritoneum, but more often it happens when cancer metastasizes to the peritoneum.

Ok, let’s say the ascitic fluid has elevated WBCs, but the differential reveals a neutrophilic predominance. In this case, you should consider pancreatic ascites or secondary bacterial peritonitis. Individuals with pancreatic ascites may have a history of chronic pancreatitis, or they may have suffered recent abdominal trauma.

To differentiate the two, measure ascitic amylase level and order ascitic fluid cultures. High amylase confirms the diagnosis of pancreatic ascites. On the other hand, positive ascitic fluid cultures for more than one pathogen, or in other words, positive polymicrobial cultures, confirm the diagnosis of secondary bacterial peritonitis. Secondary bacterial peritonitis occurs when bacteria from an underlying intraabdominal infection spread to the peritoneal cavity.

Finally, let’s take a look at patients that present with normal WBC count with lymphocyte predominance. If your patient presents with ascites and a history of diarrhea, steatorrhea, or abdominal bloating, in combination with pitting edema, consider protein-losing enteropathy.

In this case, order a 24-hour stool alpha-1 antitrypsin test to evaluate for excessive protein loss in the stool. Elevated alpha-1 antitrypsin confirms the diagnosis of protein-losing enteropathy.

But, what if your patient presents with a history of frothy urine and facial edema? In this case, consider nephrotic syndrome. To confirm the diagnosis, you should order a urinalysis and 24-hour urine protein. Urinalysis in a patient with nephrotic syndrome will show greater than 3.5 g of protein per 24 hours, as well as lipiduria.

Now, let’s go back to the SAAG and take a look at individuals with SAAG equal to or greater than 1.1, which is suggestive of portal hypertension. In these individuals, your next step is to assess the ascitic fluid total protein and determine whether or not the cause of portal hypertension is a liver problem.

If the ascitic fluid total protein is equal to or greater than 2.5 g/dL, there’s a low likelihood of liver conditions, so consider posthepatic causes.

These individuals typically report dyspnea on exertion, while their physical exam usually reveals jugular venous distention, bilateral lower extremity edema, and hepatomegaly. If your patient presents with these findings, order a transthoracic echocardiogram, or TTE for short. TTE can help you detect elevated pressure in the right side of the heart, which is associated with increased central venous pressure and conditions such as right-sided heart failure, constrictive pericarditis, and pulmonary hypertension.

Sources

  1. "Diagnosis, Evaluation, and Management of Ascites, Spontaneous Bacterial Peritonitis and Hepatorenal Syndrome: 2021 Practice Guidance by the American Association for the Study of Liver Diseases" Hepatology (2021)
  2. "Guidelines on the management of ascites in cirrhosis" Gut (2021)
  3. "EASL Clinical Practice Guidelines: Vascular diseases of the liver" J Hepatol (2016)
  4. "Unexplained ascites" Clin Liver Dis (Hoboken) (2016)
  5. "Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients With and Without Cirrhosis" Gastroenterology (2019)