Ascites

Overview

Definition and epidemiology

• Accumulation of fluid within the peritoneal cavity

• Associated with increased mortality in cirrhotic patients
  • Episodic ascites → 50% 3-year mortality
  • Refractory ascites → 50% 1-year mortality
• 5% of patients will have more than one cause.

Etiology

• Portal hypertension
  • Cirrhosis is the most common cause (80% of cases).
  • Hepatitis (without cirrhosis)
  • Hepatic veno-occlusive disease (Budd-Chiari syndrome)
  • Heart failure
  • Constrictive pericarditis
  • Hemodialysis
• Hypoalbuminemia
  • Nephrotic syndrome
  • Enteropathy
  • Malnutrition
• Peritoneal disease
  • Malignancy
  • Infection 
  • Peritoneal dialysis
• Other
  • Chylous ascites
  • Pancreatic duct injury
  • Myxedema
  • Hemoperitoneum
  • Vasculitis

Pathophysiology

Ascites is caused by an osmotic and/or hydrostatic pressure imbalance often secondary to:

• Portal hypertension (most common)
• Non-portal hypertension
  • Hypoalbuminemia
  • Malignancy 
  • Infection

Portal hypertension-related ascites:

• ↑ Pressure in the portal vein → ↑ hydrostatic pressure in the downstream hepatic vessels → fluid shift from the intravascular space to the peritoneal cavity
• ↑ Splanchnic vasodilation and blood pooling → ↓ arterial volume → ↓ renal blood flow → renin-angiotensin-aldosterone system (RAAS) activation → sodium and water retention

Non-portal hypertension–related ascites:

• Hypoalbuminemia: ↓ oncotic pressure in the vessels → ↓ intravascular osmotic gradient → fluid shift from the intravascular space to the peritoneal cavity
• Malignancy: blockage of lymphatic channels and ↑ vascular permeability
• Infection: ↑ vascular permeability

Clinical Presentation

Symptoms

• Abdominal distension 
• Weight gain
• Abdominal discomfort
• Dyspnea
• Early satiety
• Time course of symptoms will vary depending on the etiology.

Physical exam

• Abdominal distension: may be associated with umbilical eversion
• Shifting dullness 
  • Change of resonance (from dull to tympanic) when patient changes from supine to lateral decubitus position
  • Approximately 1.5 L of fluid must be present to be detected by this method.
• Fluid wave test 
  • Wave produced by tapping 1 side of the abdomen in a patient in the supine position 
  • This fluid wave will be transmitted to the other side of the abdomen via the ascitic fluid.
• Evidence for the underlying etiology:
  • Liver disease:
    • Hepatosplenomegaly
    • Jaundice and scleral icterus
    • Spider angiomata
    • Palmar erythema
    • Caput medusae
  • Heart failure:
    • Crackles
    • Jugular venous distension
    • Peripheral edema
  • Malignancy:
    • Weight loss
    • Virchow’s node (enlarged left-sided supraclavicular lymph node)

Diagnosis

Initial steps

• Ultrasound
  • Best initial test
  • Sensitive for detecting ascitic fluid (can detect > 30 mL)
  • Can evaluate for liver pathology
• Diagnostic paracentesis is indicated for:
  • New-onset ascites
  • Large, worsening ascites 
  • Suspected spontaneous bacterial peritonitis (SBP)
• Computed tomography (CT)
  • Not the diagnostic test of choice, but can also demonstrate ascites
  • Useful in evaluating for underlying causes (e.g., malignancy)

Analysis of the ascitic fluid

The next step requires analysis of the ascitic fluid.

• Appearance and color
  • Bloody → trauma, malignancy
  • Milky → chylous, pancreatic
  • Turbid → possible infection
• Cell count and differential
  • < 250 polymorphonuclear leukocytes (PMN)/mm³ → no peritonitis
  • > 250 PMN/mm³ → peritonitis
• Albumin
  • Calculate the serum ascites albumin gradient (SAAG) 
  • (Serum albumin level) – (ascitic albumin level)
    • > 1.1 g/dL → suggests portal hypertension
    • < 1.1 g/dL → unrelated to portal hypertension
• Lactate dehydrogenase (LDH) and cytology → malignancy
• Gram stain, microbial culture, and glucose → infectious ascites
  • Acid-fast bacilli smear and culture → if tuberculosis is suspected
• Triglycerides → chylous ascites
• Amylase → pancreatic ascites
• Total protein
  • Previously used to determine if the fluid was an exudate or transudate
  • Now replaced by the SAAG

Other helpful laboratory investigations for a potential etiology

• Complete blood count
  • Pancytopenia → cirrhosis 
  • Leukocytosis → infection
• Liver function tests → liver disease, congestive hepatopathy from heart failure
• Albumin → hypoalbuminemia seen in cirrhosis and nephrotic syndrome
• Coagulation tests → cirrhosis
• Brain natriuretic peptide → heart failure
• Thyroid-stimulating hormone → myxedema
• 24-hour urinary protein → nephrotic syndrome

Management

Conservative management

• Sodium restriction (< 2 g/day)
• Treat the underlying etiology.
• Diuretic therapy
  • Furosemide
  • Spironolactone

Invasive management

• Therapeutic paracentesis
  • Rapid symptom relief
  • Used if ascites is refractory to conservative measures
  • Albumin infusion is needed if > 5 L of ascites is removed.
    • Prevents large intravascular fluid shifts, kidney injury, and electrolyte abnormalities
• Transjugular intrahepatic portosystemic shunt (TIPS)
  • Creates a connection between the portal and systemic circulations to reduce portal hypertension
  • For patients with ascites refractory to the above measures
• Consideration for liver transplantation for cirrhosis patients with refractory ascites

Management algorithm

The figure below summarizes how to approach treatment in a patient with ascites:

Complications

Spontaneous bacterial peritonitis

• Common and potentially fatal bacterial infection of ascitic fluid
• Symptoms:
  • Fever
  • Abdominal pain 
  • Hypotension
  • Encephalopathy 
• Diagnosis:
  • Paracentesis with PMN > 250 cells/mm³ in the ascitic fluid
  • Most often caused by aerobic gram-negative organisms (Escherichia coli)
• Treatment:
  • Intravenous (IV) cefotaxime or ceftriaxone 
  • IV albumin decreases mortality by lowering the risk of acute renal failure.
• Prophylaxis is considered in patients with:
  • Gastrointestinal (GI) bleed: ceftriaxone or norfloxacin
  • Prior episodes of SBP: long-term therapy of norfloxacin or trimethoprim-sulfamethoxazole (TMP-SMX)

Hepatic hydrothorax

• Pleural effusion development in cirrhosis patients
• Likely due to the passage of ascites into the pleural space through defects in the diaphragm
• Symptoms:
  • Dyspnea
  • Non-productive cough
  • Pleuritic chest pain
• Diagnosis:
  • Pleural effusion may be seen on chest X-ray.
  • Thoracentesis can confirm the diagnosis.
    • Transudate
    • Low PMN count rules out spontaneous bacterial empyema.
    • Rule out other causes.
• Treatment:
  • Similar to ascites (sodium restriction, diuretics)
  • Refractory hydrothorax
    • Thoracentesis
    • TIPS
    • Liver transplant consideration

Umbilical hernia

• Soft bulge near the umbilicus 
  • Due to protrusion of bowel or fatty tissue through the abdominal wall 
  • Results from increased abdominal pressure secondary to ascites
• Occurs in 20% of patients with ascites
• Typically asymptomatic
• Incarceration should be considered if the hernia becomes painful and is unable to be reduced.
• Treatment
  • Management of ascites
  • Surgical repair

Risks associated with repeated paracentesis

• Hypovolemia
• Acute kidney injury 
• Bleeding
• Bowel perforation
• Electrolyte imbalances
• Infection

Differential Diagnosis

• Obesity: abnormal and excess fat deposition, which presents a risk to the patient’s health. Locations of fat accumulation can vary from person to person. Abdominal obesity can give the appearance of abdominal distension. Calculating the patient’s body mass index (BMI) and evaluating the history can give clues to the diagnosis. In addition, imaging will not demonstrate ascites. Treatment focuses on lifestyle modifications.
• Ovarian cyst: most commonly presents as an asymptomatic mass in women. These cysts may be physiologic, malignant, or benign. Patients may have pelvic pain, bloating, and abdominal distension (if significantly enlarged). Diagnosis is with pelvic exam and ultrasound, which will differentiate an ovarian cyst from ascites. Treatment depends on the type of cyst; may require surgery if the cyst is large or there is concern for malignancy. 
• Small bowel obstruction: disruption of the normal flow of intraluminal contents in the bowel; may be functional or mechanical. Patients may have abdominal pain, distension, and vomiting. Exam will show tympany to percussion instead of the shifting dullness in ascites. Diagnosis is by clinical history or abdominal X-ray, which will show dilated bowel loops and air-fluid levels. Treatment includes nasogastric decompression, intravenous fluids, and, sometimes, surgery.
• Kwashiorkor: a type of severe acute malnutrition most commonly seen in children of resource-limited countries (though it can also occur in older adults). Exam findings include abdominal distension, anasarca, bradycardia, and hypotension. The history and evidence of severe wasting will point to the diagnosis and differentiate it from possible causes of ascites. Treatment includes nutritional support and close monitoring for re-feeding complications.
• Pregnancy: period of fetal development in a woman’s uterus. Uterus expansion will increase abdominal size. Diagnosis is made through measurement of human chorionic gonadotropin (hCG) and confirmed with ultrasound, which differentiates it from ascites.