Ascites

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Ascites

Ascites is the pathological accumulation of fluid within the peritoneal cavity. It is one of the most common complications of cirrhosis and carries significant prognostic implications.

Epidemiology & Prognosis

Cirrhosis accounts for 84% of all ascites cases
Cardiac ascites, peritoneal carcinomatosis, and "mixed" ascites account for 10-15%
~80% of ascites is non-malignant; only ~10% is due to malignancy
Of malignant ascites, 80% arises from epithelial cancers (colon, gastric, pancreatic, ovarian, breast, endometrial)
Median survival: 2 years (non-malignant) vs. 4 months (malignant)
Harrison's Principles of Internal Medicine, 22E
Sleisenger and Fordtran's Gastrointestinal and Liver Disease

Pathophysiology

In Cirrhosis (Portal Hypertension Mechanism)

The mechanism involves three interrelated processes:

1. Increased Intrahepatic Resistance

Hepatic fibrosis disrupts sinusoidal architecture
Activated hepatic stellate cells cause smooth-muscle contraction
Decreased eNOS leads to reduced nitric oxide and increased intrahepatic vasoconstriction

2. Splanchnic Vasodilation

Paradoxically, cirrhosis increases systemic nitric oxide, VEGF, and TNF, causing splanchnic arterial vasodilation
Blood pools in the splanchnic circulation, decreasing effective circulating volume
Kidneys perceive this as hypovolemia

3. Renal Sodium and Water Retention

Compensatory ADH release causes free water retention
Activation of the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) leads to renal Na+ and H2O retention
This is the "peripheral arterial vasodilation hypothesis"

Systemic Inflammation: Decompensated cirrhosis also features bacterial translocation from the gut (PAMPs and DAMPs), which activates innate immune cells, releasing proinflammatory cytokines (IL-6, IL-8, TNF-α), further worsening circulatory dysfunction.

Harrison's Principles of Internal Medicine, 22E
Sleisenger and Fordtran's Gastrointestinal and Liver Disease

In Non-Cirrhotic States

Mechanism	Example
Protein-rich exudation + lymphatic blockage	Peritoneal carcinomatosis, tuberculous peritonitis
Increased capillary pressure (systemic)	Heart failure, constrictive pericarditis, IVC obstruction
Increased capillary pressure (portal)	Budd-Chiari syndrome, portal vein thrombosis
Hypoalbuminemia	Nephrotic syndrome, protein-losing enteropathy, malnutrition
Pancreatic enzyme leakage	Pancreatic ascites
Lymphatic impairment	Chylous ascites

Bailey and Love's Short Practice of Surgery, 28th Ed.

Grading (International Club of Ascites)

Grade	Definition
Grade 1	Mild - detectable only by ultrasound
Grade 2	Moderate - detectable by clinical examination
Grade 3	Large - marked abdominal distention

Refractory ascites = recurs ≥3 times within one year despite appropriate treatment.

Clinical Features

Abdominal distension, discomfort, early satiety
Shifting dullness and fluid thrill on examination
Respiratory compromise when tense
Signs of underlying cause: jaundice, spider angiomata, caput medusae (portosystemic shunt via umbilical vein), palmar erythema (cirrhosis); raised JVP, S3 gallop (cardiac)

CT scan of peritoneal carcinomatosis (white arrow) with ascites (yellow arrow):

CT showing peritoneal carcinomatosis and ascites

Diagnosis

Diagnostic Paracentesis - Always Send:

Cell count (PMN >250/mm³ = SBP)
Albumin (for SAAG calculation - simultaneous serum albumin needed)
Total protein

Additional Studies (Situational):

Test	Indication
Gram stain + culture	Infection
Glucose, LDH	Bacterial peritonitis
Amylase	Pancreatic ascites
Triglycerides	Chylous ascites
Cytology	Malignancy
Bilirubin	Bilious ascites
TB culture/PCR	TB peritonitis

Yamada's Textbook of Gastroenterology, 7th Ed.

Serum-Ascites Albumin Gradient (SAAG)

SAAG = Serum albumin - Ascites albumin (both measured same day)

SAAG reflects hepatic sinusoidal pressure and is ~97% accurate in diagnosing portal hypertension as the cause.

SAAG	Interpretation	Causes
≥1.1 g/dL (high)	Portal hypertension	Cirrhosis, alcoholic hepatitis, congestive heart failure, Budd-Chiari, portal vein thrombosis, fulminant liver failure, myxedema, fatty liver of pregnancy
<1.1 g/dL (low)	Non-portal hypertensive	Nephrotic syndrome, peritoneal carcinomatosis, mesothelioma, TB peritonitis, chylous ascites, pancreatic ascites, bile ascites

Ascites total protein provides additional information:

In cardiac ascites: light yellow fluid, low specific gravity, protein <25 g/L
In malignant/TB ascites: dark yellow, often blood-stained, protein >25 g/L
Yamada's Textbook of Gastroenterology, 7th Ed.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease

Management

1. Salt Restriction + Diuretics (First-line for Cirrhotic Ascites)

Dietary sodium restricted to ≤2 g/day (more restrictive diets compromise nutrition)
Spironolactone (aldosterone antagonist): start 100 mg/day, titrate every 3-4 days to max 400 mg/day - more effective than loop diuretics
Furosemide: start 40 mg/day, escalate to 160 mg/day; add concurrently if tense ascites, or if hyperkalemia or inadequate weight loss on spironolactone alone
Target weight loss: 1 kg/week (first week), then 2 kg/week thereafter
Do not exceed: 0.5 kg/day without edema; 1 kg/day with edema
Avoid: ACEIs, ARBs, NSAIDs (worsen renal function)

Diuretic side effects: hypovolemic hyponatremia, hyperkalemia, renal dysfunction, encephalopathy, gynecomastia (spironolactone)

2. Albumin Infusion

Long-term albumin (40 g twice weekly x 2 weeks, then 40 g weekly) added to diuretics significantly reduces recurrent ascites and improves 18-month survival
After large-volume paracentesis (>5L): albumin 6-8 g IV per liter removed to prevent paracentesis-induced circulatory dysfunction (PICD)

3. Large-Volume Paracentesis (LVP)

Used in 10-20% of patients refractory to diuretics
Goal: removal of all or most fluid
Mandatory albumin supplementation when >5 L removed (8 g/L removed)
Improves comfort, respiratory effort, oral intake, and reduces SBP risk

4. TIPS (Transjugular Intrahepatic Portosystemic Shunt)

More effective than LVP + albumin in preventing recurrent ascites
BUT associated with higher rate of hepatic encephalopathy
Polytetrafluoroethylene-covered TIPS in patients needing >2 LVP/month: may improve survival

5. Peritoneovenous Shunt

Silicone tube placed subcutaneously transferring ascitic fluid from peritoneal cavity to systemic circulation
For patients not candidates for TIPS or liver transplantation

6. Automated Flow Pumps

Move ascitic fluid to the bladder; reduce need for LVP and improve QoL
Require surgical placement; risk of infection

7. Liver Transplantation

Definitive treatment for cirrhotic ascites
Goldman-Cecil Medicine
Rosen's Emergency Medicine
Sleisenger and Fordtran's Gastrointestinal and Liver Disease

Complications

Spontaneous Bacterial Peritonitis (SBP)

Defined as infection of previously sterile ascitic fluid without an intraabdominal source (no GI perforation)
Most common cause of primary peritonitis
Pathogens: mainly gram-negative aerobes (E. coli, Klebsiella) and anaerobes
Diagnosis: ascitic fluid PMN >250 cells/mL
Treatment: broad-spectrum antibiotics covering gram-negatives + anaerobes, tailored to cultures
Suspect SBP in: abdominal pain/tenderness, fever, leukocytosis, sepsis, renal insufficiency, hepatic encephalopathy
Gram stain often negative (low bacterial counts in the fluid)

Hepatorenal Syndrome (HRS)

Functional kidney injury from hemodynamic abnormalities in end-stage liver disease + severe portal hypertension
High mortality despite specific therapy
HRS in absence of prerenal azotemia = indication to consider liver transplantation

Hyponatremia

Severe (serum Na <130 mEq/L): fluid restrict to 1.5 L/day
Tolvaptan (V2-receptor antagonist) may transiently raise serum Na but has no overall survival benefit and carries hepatotoxicity risk - not routinely approved; short-term use as bridge to transplant only

Hepatic Encephalopathy

Cumulative survival: 20-40% at 1 year, 15% at 3 years once encephalopathy develops

Hepatic Hydrothorax

Ascitic fluid tracking through diaphragmatic defects, usually into the right pleural space

Special Fluid Characteristics

Type	Appearance	Protein	SAAG	Notes
Cirrhotic	Straw-colored	Low	≥1.1	Commonest
Cardiac	Light yellow	Low (<25 g/L)	≥1.1	Low specific gravity
Malignant	Dark yellow/blood-stained	High (>25 g/L)	<1.1	Cytology positive
TB	Straw/turbid	High	<1.1	Lymphocytic predominance
Chylous	Milky	High	<1.1	Triglycerides >200 mg/dL
Pancreatic	Variable	High	<1.1	Amylase very elevated
Meigs'	Straw	Variable	Variable	Resolves with ovarian fibroma resection

Sources: Harrison's Principles of Internal Medicine, 22E | Sleisenger and Fordtran's Gastrointestinal and Liver Disease | Yamada's Textbook of Gastroenterology, 7th Ed. | Goldman-Cecil Medicine | Bailey and Love's Short Practice of Surgery, 28th Ed. | Rosen's Emergency Medicine

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