Basics
Description
- Ascites is defined as a pathologic accumulation of intraperitoneal fluid.
- Peritoneal fluid formation is a dynamic process of production and absorption.
- In children, ascites is usually the result of liver or renal disease.
- In adults, ascites is most often due to portal hypertension from cirrhosis.
- Ascites is the most common of the three major complications of cirrhosis; the other two complications of cirrhosis are hepatic encephalopathy and variceal hemorrhage.
Pathophysiology
- Normal circulation
- Blood enters the liver from the hepatic artery and portal vein, perfuses the hepatic sinusoids, and exits the liver via the hepatic veins.
- Hepatic lymph, formed by the filtration of sinusoidal plasma into the space of Disse, drains from the liver via the transdiaphragmatic lymphatic vessels to the thoracic duct.
- Hepatic lymph is isosmotic to plasma, as the sinusoidal endothelium is highly permeable to albumin.
- In the intestine, the mesenteric capillary membrane is impermeable to albumin. The osmotic gradient favors the return of interstitial fluid/lymph into the capillary.
- Intestinal lymph from regional lymphatics combines with hepatic lymph in the thoracic duct.
- Portal hypertension
- Ascitic fluid production is due to a net transfer of fluid that exceeds the drainage capacity of the lymphatics.
- Cirrhotic ascites results from three pathophysiologic process:
- Portal hypertension
- Vasodilation: mediated predominantly by nitric oxide
- Hyperaldosteronism: Decreased effective volume sensed by the kidneys stimulate the renin-angiotensin-aldosterone system, leading to increased sympathetic activity and antidiuretic hormone secretion.
- Noncirrhotic ascites can be the result of the following:
- Proteinaceous material produced by malignant cells or by inflammation of visceral and/or parietal peritoneum: peritoneal carcinomatosis, tuberculous ascites
- Obstruction of lymphatic flow by mass, tumor, or external pressure
- Impaired portal flow: right-sided heart failure, Budd-Chiari syndrome, portal venous malformations
- Decreased effective arterial blood volume: heart failure
- Decreased oncotic pressure/ hypoalbuminemia: nephrotic syndrome, protein-losing enteropathy, severe malnutrition
- Primary (congenital) abnormalities of the lymphatics, metabolic disorders (lysosomal storage diseases including sialidosis, Wolman disease, GM1 gangliosidosis, Gaucher disease, and Niemann-Pick type C)
- Rupture of intra-abdominal viscus or peritoneal/mesenteric cyst, bowel perforation, ureteral rupture
Etiology
Accumulation of fluid occurs with the following:
- Inflammatory conditions (e.g., mesenteric adenitis, tuberculosis, pancreatitis, secondary to inflammation of visceral, and/or parietal peritoneum)
- Portal hypertension or obstruction of portal vein flow and/or lymphatic flow by mass, tumor, or external pressure; tumors of abdominal viscera, retroperitoneum, thorax, or mediastinum (often characterized by chylous ascites)
- Infectious processes: abscess, tuberculosis, Chlamydia infection, schistosomiasis
- Gastrointestinal: infarcted bowel/perforation, pancreatitis, ruptured pancreatic duct, parenchymal liver disease
- Gynecologic: ovarian tumors, torsion, or rupture
- Renal: nephrotic syndrome, obstructive uropathy, perforated urinary tract, peritoneal dialysis
- Cardiac: CHF, constrictive pericarditis, inferior vena cava web
- Neoplastic: lymphoma, neuroblastoma
- Miscellaneous: systemic lupus erythematous, eosinophilic ascites, chylous ascites, hypothyroidism, ventriculoperitoneal shunt
Diagnosis
History
- The etiology for acute decompensation in hepatocellular function (e.g., massive bleeding, sepsis, superimposed infections) should be investigated.
- Weight gain
- Use of umbilical catheters in newborn period (increased risk of portal vein thrombosis)
- Evidence of chronic liver disease
- Respiratory distress
- Exposure to hepatotoxins
- Developmental delay or growth failure suggestive of metabolic disease
Physical Exam
- Vital signs:
- Increased heart rate (increased cardiac output)
- Lower blood pressure seen in cirrhotics
- General appearance: cachexia
- Abdominal exam
- Protuberant abdomen, bulging flanks (fluid wave or shifting dullness)
- Caput medusae, umbilical hernia,
- Dullness to percussion
- Peritoneal signs
- Abdominal pain
- Splenomegaly
- Auscultation of the pericardium: pericardial friction rub (pericarditis), cor pulmonale
- Neurologic exam: hepatic encephalopathy
- Skin
- Jaundice
- Spider angioma
- Palmar erythema
- Scratch marks
- Striae
- Xanthomas
- Extremities
Diagnostic Evaluation
Laboratory
- Complete blood count
- Electrolytes
- Liver test: transaminases, prothrombin time/international normalized ratio, total protein, albumin, total and fractionated bilirubin
- Amylase and lipase (to exclude pancreatitis)
- Creatinine and blood urea nitrogen
- Fluid cultures: blood, urine, ascitic fluid
- Urinalysis
- Specific testing for etiologies of ascites from chronic liver disease and other causes as deemed appropriate
Imaging
- Ultrasound of the abdomen with Doppler study
- Study of choice to differentiate between free and loculated fluid collection and the presence of intra-abdominal masses
- Can evaluate patency of hepatic and portal vasculature and directionality of flow
- Plain radiography (centralized bowel loops)
- Abdominal computed axial tomography
- Abdominal magnetic resonance imaging
Abdominal Paracentesis
- Ascitic fluid analysis is essential:
- Cell count and differential
- Albumin, total protein
- Culture, Gram stain
- Glucose (low in infection)
- Lactate dehydrogenase concentration (high in infection, bowel perforation, or tumor)
- Other optional tests include amylase (high in perforated viscus or pancreatitis), triglycerides (high in chylous ascites), and cytology (peritoneal carcinomatosis).
- Serum to ascites albumin gradient (SAAG)
- (Serum albumin) - (ascites albumin)
- Blood and ascitic fluid analysis should be obtained on same day.
- SAAG ≥1.1 g/dL suggests presence of portal hypertension.
- If SAAG <1.1 g/dL, suspect other causes.
Differential Diagnosis
- Organomegaly: enlarged liver or spleen
- Mesenteric cyst or ovarian cyst: does not have shifting dullness when position is changed
- Bowel obstruction
- Cancer
- Heart failure
- Nephrotic syndrome
Treatment
- The management of the ascites should be directed toward the underlying etiology.
- Benefits of treatment of ascites should always be weighed against risks and complications of treatment.
- Mobilization of cirrhotic ascitic fluid is best accomplished by creating a negative sodium balance and then maintaining the balance.
- In patients with cirrhosis, causes of decompensation should be sought, such as sodium and fluid overload, infection, esophageal hemorrhage, spontaneous bacterial peritonitis.
- In adults, dietary sodium intake is restricted to 44-88 mEq (1-2 g/24 h) or approximately 17-35 mEq (0.4-0.8 g) per thousand calories.
- In pediatrics, restricting dietary sodium intake is recommended: diet with no extra salt to a maximum 2 mEq/kg/24 h (to be balanced against palatability of food and nutritional needs).
- Water is only restricted in patients with profound hyponatremia (<125 mEq/L): 50-75% of maintenance requirements.
- Goal of diuretic therapy is reduction of bodyweight by 0.5-1% daily until ascites is resolved.
- Spironolactone (PO)
- Most effective single diuretic, as it counteracts the hyperaldosteronism present in cirrhotic ascites
- Acts on the distal collecting system, hence, inhibits reabsorption of 2% of filtered sodium
- Bioactive metabolites have long half-lives, hence, need >5 days to achieve steady state.
- Start at 2-3 mg/kg/24 h as a single morning (max 100 mg initial dose). In adults, typical starting dose is up to 100 mg/24 h and can be increased to max 400 mg/24 h.
- Most effective in combination with furosemide
- Adequacy of spironolactone therapy can be monitored with urinary sodium excretion (desired >50 mEq/L). If no response, furosemide is added.
- Furosemide (PO)
- Loop diuretic: can increase sodium excretion by 30%
- Start at 1 mg/kg (max initial dose 40 mg), may increase every few days if needed.
- Adults maintain ratio of 100 mg of spironolactone to 40 mg of furosemide to maintain eukalemia (max 400 mg spironolactone to 160 mg of furosemide daily)
- When diuretics are used, urine output and serum electrolytes should be closely monitored to prevent prerenal azotemia and decreased effective blood flow to the kidneys.
- Albumin: Supplementation may aid fluid mobilization if albumin is <2.5 g/dL (use 1 g/kg of 25% albumin until level >2.5 g/dL).
- Refractory ascites: Diuretic-refractory ascites derives from a lack of response to dietary sodium restriction and maximal diuretic therapy. Treatment options are the following:
- Therapeutic abdominal paracentesis (large-volume paracentesis) is used in adults with refractory ascites.
- In children, this approach is used to relieve respiratory distress or other sequelae of rapidly increasing intra-abdominal pressure.
- Paracentesis of volumes >1 L should be accompanied by IV infusion of 25% albumin during the procedure.
- Transjugular intrahepatic portosystemic shunting may be valuable in cases where portal hypertension is felt to be the underlying etiology of ascitic accumulation.
- Orthotopic liver transplantation is the only curative therapy for refractory ascites from liver disease and the only definitive treatment that has been shown to improve survival.
- When diuretics are used, urine output and serum electrolytes should be closely monitored to prevent prerenal azotemia and decreased effective blood flow to the kidneys.
Alert
- Ultrasonography should be the initial diagnostic imaging of choice for evaluation of ascites.
- With congenital ascites, evaluate for lysosomal storage diseases.
- Diagnostic paracentesis is crucial in the evaluation of new-onset ascites.
- Calculate SAAG to differentiate between portal hypertension and other causes.
- In patients with liver disease and new-onset ascites, evaluate for etiologies to explain acute decompensation.
Prognosis
- Development of ascites in the setting of cirrhosis is a landmark in the natural history of cirrhosis: 15% of adult patients succumb in 1 year and 44% in 5 years.
- Liver transplantation dramatically improves survival.
- Prognosis depends on etiology of ascites: nephrotic syndrome (ascites will regress as proteinuria clears), infection, hepatic decompensation (prognosis improves if able to reverse cause of liver injury).
Complications
- Spontaneous bacterial peritonitis (SBP)
- Spontaneous ascitic fluid infection: Infection of the peritoneal fluid may occur in the absence of secondary cause (e.g., bowel perforation or intra-abdominal abscess).
- Fever, irritability, abdominal tenderness, and distention are common signs, vomiting and diarrhea may occur.
- Abdominal paracentesis must be performed and ascitic fluid must be analyzed before a confident diagnosis of ascitic fluid infection can be made. The blood culture bottle should be injected with peritoneal fluid at the bedside in order to increase the culture yield.
- Diagnosis: ascitic fluid absolute polymorphonuclear leukocytes ≥250 cells/mm3 without evidence of an intra-abdominal process
- Bacterial organisms commonly identified are the following: Streptococcus pneumoniae, Escherichia coli, Klebsiella pneumoniae, enterococci, and Haemophilus influenzae.
- Broad-spectrum antibiotics with gram-negative coverage such as third generation cephalosporin can be used until identification of bacterial pathogen allows narrower coverage.
- Prophylaxis for recurrent SBP has been recommended in certain situations.
- Other complications:
- Respiratory distress from decreased lung volume and diaphragmatic limitation: hepatic hydrothorax (large symptomatic pleural effusion that occurs in a cirrhotic patient in the absence of primary cardiopulmonary disease), abdominal wall hernias with rupture, tense ascites with leakage (especially after paracentesis)
- Conservative management consists of appropriate initial therapy for most of these except hernia rupture, which requires surgical reduction.
Additional Reading
- European Association for the Study of the Liver. EASL clinical practice guideline on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol. 2010,53(3):397-417. [View Abstract]
- Griefer MJ, Murray KF, Colleti RB. Pathophysiology, diagnosis, and management of pediatric ascites. J Pediatr Gastroenterol Nutr. 2011;52(5):503-513. [View Abstract]
- Hou W, Sanyal AJ. Ascites: diagnosis and management. Med Clin North Am. 2009;93(4):801-817. [View Abstract]
- Runyon BA. Management of adult patients with ascites due to cirrhosis: update 2012. Hepatology. 2013(6):2087-2107. [View Abstract]
Codes
ICD09
- 789.59 Other ascites
- 789.51 Malignant ascites
- 014.00 Tuberculous peritonitis, unspecified
ICD10
- R18.8 Other ascites
- R18.0 Malignant ascites
- A18.31 Tuberculous peritonitis
SNOMED
- 389026000 Ascites (disorder)
- 236005001 Malignant ascites (disorder)
- 236004002 Hepatic ascites (disorder)
- 4501007 Tuberculous ascites (disorder)
FAQ
- Q: What etiologies are likely in cases of congenital ascites?
- A: Lysosomal storage disorders and/or other metabolic diseases should be excluded. If hepatic function is impaired, causes of neonatal liver failure should also be investigated.
- Q: What is the best test to discriminate the type of ascites?
- A: Analysis of the peritoneal fluid collected by abdominal paracentesis is required for this purpose. The SAAG is helpful to discriminate ascites due to portal hypertension from other etiologies.
- Q: Where does the word "ascites" come from?
- A: It is thought that the word ascites is derived from the Greek word "askos" which refers to a container of wine or a wineskin.