creation date: 2025-12-27 23:48
tags: Workups
Ascites
Background
Ascites is the result of the accumulation of fluid within the peritoneal cavity.
Pathophysiology
The exact pathophysiology varies based on the etiology. The broad mechanisms and the associated changes to Starling forces are described here.
Elevated portal or venous pressure
Portal hypertension or conditions that increase venous pressures (such as right-sided heart failure) increases the hydrostatic pressure of the splanchnic capillary bed, promoting the movement of fluid into the peritoneal compartment.
As the vessels are unaffected, fluid moves through transudation and the normal vessels effectively filter fluid and lymph, resulting in transudative fluid.
In addition to hydrostatic pressures, chronic underfilling of the effective arterial circulation activates RAAS, sympathetic nervous system, and non-osmotic vasopressin, which increases sodium and water retention. As peritoneal permeability favours third spacing, fluid accumulates as ascites.
Low plasma oncotic pressure and protein distribution abnormalities
Reduced plasma proteins/osmoles reduce the oncotic pressure drawing fluid back into vessels.
The lack of protein can occur from decreased synthesis, increased losses, or malnutrition. In exudative states, increased vascular leakage draws protein-rich fluid into the peritoneal cavity which favours further fluid movement out of the vessels.
Peritoneal disease
In normal circumstances, peritoneal fluids is continuously cleared via diaphragmatic and mesenteric lymphatics. However, in conditions with chronic high draining demand, the clearing capacity will be overwhelmed.
Conditions that cause infiltration or obstruction of lymphatic channels or inflammation of the peritoneum can compromise the resorption mechanisms.
Differential Diagnosis
The most common cause is cirrhosis (80%). The following are causes organized by primary underlying pathophysiology.
Portal hypertension
- Cirrhosis
- Alcoholic hepatitis
- Acute liver failure
- Hepatic veno-occlusive disease (eg. Budd-Chiari syndrome)
- Heart failure
- Constrictive pericarditis
- Hemodialysis-associated ascites (nephrogenic ascites)
Hypoalbuminemia
- Nephrotic syndrome
- Protein-losing enteropathy
- Severe malnutrition
Peritoneal disease
- Malignant ascites (eg. ovarian cancer, mesothlioma)
- Infectious peritonitis (eg. tuberculosis, fungal infection)
- Eosinophilic gastroenteritis
- Starch granulomatous peritonitis
- Peritoneal dialysis
- Multicystic mesothelioma
Others
- Chylous ascites
- Pancreatic ascites
- Myxedema
- Hemoperitoneum
- Urologic injury
Initial Evaluation
History
History may suggest certain etiologies (eg. alcohol use, liver disease). Ascites is typically described as:
- Progressive abdominal distension
- May be painless or associated with abdominal discomfort
- Develops over days (eg. trauma) to weeks (eg. alcohol-associated)
Associated symptoms include:
- Weight gain
- Shortness of breath
- Early satiety
- Dyspnea
Be cognizant of symptoms relating to:
- Spontaneous bacterial peritonitis
- Decompensated cirrhosis
Physical Exam
On examination, findings include:
- Flank dullness
- Shifting dullness
An abdominal exam should be completed. Look for:
- Signs of hepatic insufficiency
- Cirrhosis stigmata
- Umbilical nodule that is not bowel or omentum (cancer)
Cardiovascular exam may find signs of heart failure.
Investigations
Laboratory tests
Testing should be completed to investigate suspected etiology. This typically consist of:
- Cirrhosis workup
- Heart failure workup
- Kidney function tests
Imaging
Ultrasound is a cost-effective modality for diagnosing ascites. A complete abdominal ultrasound should provide information on:
- Liver and gallbladder
- Abdomen
- Spleen
Paracentesis
Paracentesis and ascitic fluid analysis provides information on diagnosing underlying etiology.
Initial appearance
Clear fluid:
- Cirrhosis typically translucent yellow
- Clear if bilirubin is normal and protein concentration is very low
Turbid or cloudy: - Spontaneously infected fluid
- 98% sensitive, 23% specific for detecting SBP
Opalescent: - Due to slightly elevated triglyceride concentration
- No apparent clinical significance
- May be misinterpreted as “pus”
Milky: - High triglyceride concentration (> 2.2 mmol/L)
- Referred to as chylous ascites
- Associated with malignancy
Pink or bloody: - RBC >10,000 cells/mm3
- Blood may be due to traumatic tap; confirm with repeat paracentesis on other side of abdomen to confirm if needed
- Associated with cirrhosis, leakage from punctured collateral, malignancy
Brown: - Associated with severe jaundice (ascitic fluid 40% of serum)
- Molasses brown + bilirubin > serum value suggests ruptured gallbaldder or perforated duodenal ulcer
Serum-to-ascites albumin gradient (SAAG)
Identifies presence of portal hypertension and to a lesser extent, whether the ascites is transudate or exudate.
SAAG = serum albumin - ascitic fluid albumin
A SAAG ≥11 g/L suggests the patient has portal hypertension (97% accurate) and a gradient <11 g/L suggests otherwise.
Cell count and differential
Very useful for evaluating infection and should be ordered on all specimens. Note that WBC and neutrophil counts need to be corrected if sample is bloody (subtract 1 WBC for every 750 RBC; subtract 1 neutrophil per 250 RBC).
Total protein concentration
For classification of transudative vs exudative ascitic fluid, total protein concentration can be use although with lesser clinical significance owing to the preferred SAAG system of portal hypertension.
A cut off of 2.5 g/L is used (exudate if greater). This may be useful for:
- Distinguishing SBP from bowel perforation in conjunction with glucose and LDH
- Distinguishing between cirrhotic ascites and cardiac ascites (cirrhosis is transudative while cardiac is exudative)
Additional tests of ascitic fluids include:
- Culture (infection, bowel perforation)
- Glucose concentration (malignancy, infection, bowel perforation)
- Lactate dehydrogenase concentration (malignancy, infection, bowel perforation)
- Amylase concentration (pancreatic ascites or bowel perforation)
- Tuberculosis workup (tuberculous peritonitis)
- Cytology (malignancy)
- Triglyceride concentration (chylous ascites)
- Bilirubin concentration (bowel or biliary perforation)