Anatomy and Physiology

Peritoneal fluid formation is a dynamic process that is maintained in a delicate equilibrium, dependent on factors of production and absorption, as well as the integrity of the peritoneal membrane and the lymphatic drainage system. There is a constant exchange of fluid and proteins between the plasma and peritoneal cavity, and this fluid equilibrium is controlled by osmotic and hydrostatic pressures within the hepatic and mesenteric capillaries. Under the influence of these pressures, 40% to 80% of intraperitoneal fluid is exchanged with the plasma every hour. The lymphatic system is responsible for the removal of interstitial fluid. Ascites arises when the net transfer of fluid from the peritoneal capillary bed (hepatic and mesenteric capillaries) to the peritoneal cavity occurs at a rate that overcomes the drainage capacity of the lymphatics, leading to accumulation of peritoneal fluid.

Blood reaches the hepatic capillaries via the portal vein and hepatic artery, which perfuse the hepatic sinusoids. The liver has a low sinusoidal pressure (2 mm Hg). Under normal conditions, lymph produced at the sinusoidal level enters the space of Disse and exits the liver by way of the transdiaphragmatic lymphatic vessels to the thor­acic duct. The sinusoidal membrane is highly permeable to albumin; thus the protein concentrations of hepatic lymph and plasma are nearly the same, thereby limiting any significant osmotic gradient.

Blood from the intestinal mesenteric capillaries drains into the portal vein via the mesenteric veins ( Figure 17-1 ). The mean mesenteric capillary pressure is around 20 mm Hg. The mesenteric capillary membrane is relatively impermeable to albumin such that the protein concentration of mesenteric lymph is one-fifth that of plasma. This resulting osmotic gradient favors the return of interstitial fluid into the capillary. The lymph that is produced drains from regional lymphatics into the thoracic duct; the rate is 800 to 1000 mL per day in the adult.

Ascites Formation.

Hepatic lymph is formed by filtration of sinusoidal plasma into the space of Disse. It drains from the liver via the transdia­phragmatic lymphatic vessels to the thoracic duct. The sinusoidal endothelium is highly permeable to albumin; there is normally no significant osmotic gradient across the sinusoidal membrane. Intestinal lymph drains from regional lymphatics into the thoracic duct. The mesenteric capillary membrane is relatively impermeable to albumin; there is a significant osmotic gradient that promotes the return of interstitial fluid into the capillary lumen. Ascites occurs when the net transfer of fluid from blood vessels to lymphatic vessels exceeds the drainage capacity of the lymphatics; fluid leaks through the hepatic capsule and, to a lesser extent, the intestine. IVC, Inferior vena cava; a., artery; v., vein.

(Adapted from Dudley (1992), with permission. )

Overall, intraperitoneal fluid accumulation occurs as a result of various mechanisms, which include increased capillary hydrostatic pressure or decreased colloid osmotic pressure within the hepatic and splanchnic vascular bed, increased permeability of peritoneal capillaries, and direct leakage of fluid into the peritoneal cavity. The pathophysiology of ascites varies depending on etiology and can be categorized as cirrhotic or noncirrhotic ascites.

Noncirrhotic Ascites

Noncirrhotic ascites can result from processes that cause peritoneal inflammation, portal venous or lymphatic obstruction, defects in the lymphatic system, or rupture of intra-abdominal viscus. Most commonly, ascites can arise from hepatic, gastrointestinal, and renal diseases, which lead to a decreased effective arterial blood volume with secondary activation of the central nervous sympathetic adrenergic system, the renin-angiotensin-aldosterone system, and vasopressin, leading to renal sodium and water retention. In nephrotic syndrome, hypoalbuminemia increases the movement of plasma into the interstitium. Peripheral edema is seen in ascites resulting from only hypoalbuminemia. In heart failure, hepatic congestion increases portal venous pressure. Prehepatic portal hypertension can also result from congenital anomalies of the portal vein.

Processes that cause peritoneal inflammation such as infections or malignancies can result in increased capillary permeability, with subsequent leakage of fluid into the peritoneum leading to increased colloid osmotic pressure of the intraperitoneal fluid. Ascites can also arise from a chemical peritonitis leading to pancreatic and bile-induced ascites. Chylous ascites results from disruption of the abdominal lymphatics. Perforated abdominal viscera results in peritoneal fluid accumulation, as does blunt trauma

Cirrhotic Ascites

Ascites is the most common complication in patients with cirrhosis and develops as a consequence of three main interrelated pathophysiologic processes: portal hypertension, vasodilation, and hyperaldosteronism. Peripheral arterial vasodilation secondary to portal hypertension is hypothesized to be the central event in the pathogenesis of cirrhotic ascites formation ( Figure 17-2 ). This circulatory dysfunction induced by splanchnic arterial vasodilation results in two different phenomena: (1) an increase in hepatic capillary pressure from increased blood flow into the splanchnic microcirculation that leads to peritoneal fluid accumulation; and (2) impairment of renal function, which leads to sodium and water retention.

Peripheral arterial vasodilation hypothesis of ascites formation.

(*Adapted from Arroyo V, N.M. Ascites and spontaneous bacterial peritonitis. In: Schiff ER, Maddrey WC, editors. Schiff’s diseases of the liver . S.M. Philadelphia: Lippincott WIlliams & Wilkins; 2007. p. 527–67.)

In cirrhosis, distortion of the vascular architecture from fibrosis and an increase in intrahepatic vascular tone leads to increased resistance to portal flow and the development of portal hypertension, collateral vein formation, and shunting of blood to the systemic circulation. Hepatic endothelin-1, a potent vasoconstrictor, modulates intrahepatic resistance in portal hypertension caused by cirrhosis. In response to this increased vascular tone, hepatic stellate cells acquire receptors for endogenous vasoactive peptides. Normal portal venous pressure is roughly 5 mm Hg higher than the inferior vena cava pressure and portal hypertension is defined as a hepatic venous-portal pressure gradient of more than 10 mm Hg. This increased hydrostatic pressure gradient across the splanchnic circulation results in increased lymph formation. Ascites develops when hepatic lymph production exceeds drainage and seeps through the hepatic capsule into the peritoneum.

Concurrently, production of local vasodilators such as nitric oxide is increased, which leads to splanchnic arterial vasodilation. Early in cirrhosis, the effects of splanchnic arterial vasodilation on effective arterial blood volume are compensated by a hyperdynamic circulation with increases in plasma volume and cardiac output. With advanced cirrhosis, cardiac output decreases with progression of splanchnic vasodilation and arterial pressure falls owing to a marked decrease in effective arterial blood volume. The renal juxtaglomerular apparatus senses this effective hypovolemia with resultant homeostatic activation of vasoconstrictor and antinatriuretic factors to maintain arterial pressure. Activation of the renin-angiotensin-aldosterone system increases sympathetic nervous activity and antidiuretic hormone secretion, which results in sodium and free water retention with expansion of plasma volume, leading to ascites. Urine sodium excretion is very low, often less than 5 mEq/day. However, the vasoconstrictive effect of angiotensin is blunted in cirrhosis, and unopposed splanchnic arterial vasodilation perpetuates a continued effective hypovolemic response that results in ascites formation.

In decompensated cirrhosis, a hyperdynamic circulatory state exists, with an expanded blood volume, increased cardiac output, tachycardia, wide pulse pressure, and peripheral dilation. Hepatocellular synthetic dysfunction can lead to hypoalbuminemia, which decreases the osmotic gradient and contributes to ascites formation. Peripheral edema occurs when increased abdominal pressure from ascites increases inferior vena cava pressure, producing an increase in hydrostatic pressure in the capillaries of the lower extremities.

Congenital Ascites

Congenital ascites can present as an isolated finding or as a complication of hydrops ( Figure 17-4 ). With congenital ascites, it is important to make this distinction because management and prognosis varies by etiology. Although only a small number of cases have been reported, isolated ascites appears to carry a better prognosis with a higher survival rate (52%) compared to ascites associated with other anomalies (43%) or hydrops (33%). Age at diagnosis appears to be a reasonable prognostic indicator, with a lower mortality rate associated with later onset of congenital ascites. Many cases of isolated ascites resolve spontaneously, but isolated ascites may also be a harbinger of impending hydrops fetalis.

Congenital ascites from hydrops.

Imaging from 4-month-old infant with hydrops. (A) Abdominal x-ray demonstrating classic radiographic features of ascites including bulging of the flanks and centralization of the bowel. (B) Transverse ultrasound image showing large amount of simple ascites with septations (arrows).

Most commonly, congenital ascites is associated with immune and nonimmune hydrops fetalis, with Rh incompatibility formerly being a leading cause of fetal ascites. Isolated ascites, defined as fluid accumulation in the peritoneal cavity only, occurs less commonly, accounting for up to one-third of all cases. With the introduction of high-resolution ultrasonography, an underlying etiology can be identified in more than 95% of cases of congenital ascites. Causes of isolated congenital ascites include gastrointestinal, genitourinary, cardiac, and metabolic abnormalities, as well as congenital infections and chyloperitoneum ( Box 17-1 ).

Bowel perforation with subsequent meconium peritonitis is the most commonly reported gastrointestinal cause of isolated congenital ascites. Other gastrointestinal abnormalities associated with ascites include bowel obstruction due to intrauterine intussusception, malrotation, or jejunal atresia as well as primary intestinal lymphangiectasia and omphalocele. Hepatic causes include biliary atresia, ductal plate malformation, neonatal iron storage disease, and inborn errors of metabolism. These metabolic causes include many types of lysosomal storage disorders such as Niemann-Pick Type C, Gaucher’s disease, and GM-1 gangliosidosis, as well as Wolman disease, sialic acid storage disease, and Sly disease. In severe forms, hepatosplenomegaly may be present in infancy, which can be the initial presenting sign in select instances. Some inborn errors of metabolism are also associated with nonimmune fetal hydrops.

Genitourinary causes of congenital ascites include hydronephrosis, multicystic kidney, cloacal dysgenesis, hydrometrocolpos, and urinary obstruction with subsequent perforation. Cardiac anomalies that lead to cardiac failure and resultant increased hepatic pressure can cause isolated ascites, including structural abnormalities and dysrhythmias. Congenital infections account for 8% to 11.5% of isolated congenital ascites and can lead to ascites by causing intestinal perforation or by inducing anemia, and resulting high-output cardiac failure. Infections that cause ascites include syphilis, parvovirus B19, cytomegalovirus, and toxoplasmosis. Other causes of congenital ascites include chromosomal abnormalities, pulmonary anomalies, hemolytic anemia chyloperitoneum, neoplasms, and fetal abuse.

Ascites in Infancy and Childhood

The causes of childhood ascites are numerous and ascitic fluid analysis can help differentiate these. Clinical differentiation between transudate and exudate is indicative of the underlying pathophysiology and directs management. The etiology of ascites in children also varies by age; ascites that occurs in the neonate ( Box 17-2 ) often results from a persistence of fetal ascites and causes of congenital ascites should be considered.

In the infant, a chemical peritonitis from meconium, bile, or vaginal secretions can be seen during the first few months of life. Spontaneous perforation of the biliary tree typically occurs between 4 and 12 weeks of age. The most common sites of perforation are at the anterior of the common bile duct or at the junction of the gallbladder and the cystic duct. It is hypothesized that embryologic weakness of the bile duct wall results in diverticulum, focal ischemia, and ultimately perforation. Most infants present clinically with jaundice that is oftentimes thought to be physiologic. Perforation is suspected with prolonged neonatal jaundice in combination with acholic stools and ascites. Hyperbilirubinemia without significant increase in aminotransferase levels is the common laboratory finding. Ultrasound may show fluid around the gallbladder without bile duct dilation, and biliary leakage can be demonstrated by hepatobiliary iminodiacetic acid scanning, both suggesting perforation. Definitive diagnosis depends on the demonstration of bile-stained fluid observed at paracentesis or laparotomy. Treatment requires prompt surgical intervention with intraoperative cholangiography, drainage of ascites, and surgical correction with cholecystostomy or T-tube drainage.

Genitourinary anomalies leading to ascites occur more commonly early in infancy. An aseptic peritonitis from vaginal secretions can be seen in neonates. Ascites arises from a mechanical obstruction of vaginal outflow, typically from an imperforate hymen or vaginal atresia. This obstruction causes genital secretions to seep into the peritoneal cavity by way of the fallopian tube, resulting in a fibrinous inflammation that covers the peritoneum. Urethral obstruction from hydrometrocolpos is also seen. Diagnosis relies on radiographic studies showing separation of bowel loops by free fluid and cystourethrography showing lateral displacement of the ureters and hydronephrosis from urethral obstruction. Treatment consists of drainage and relief of the vaginal obstruction, but prognosis is poor.

Uroascites accounts for nearly 30% of ascites in the neonate. Most cases of neonatal uroascites result from obstructive uropathy due to posterior urethral valves, but ureterocele, lower ureteral stenosis, and ureteral atresia have also been implicated. Complex urinary anomalies such as persistent cloaca can result in ascites in the absence of perforation as urine refluxes into the peritoneum via the genitourinary tract. Rupture of the bladder also leads to uroascites, which can occur with­out a demonstrable anatomic urinary obstruction or iatrogenically, following catheterization. In obstructive uropathy, rupture of the urinary system and resulting uroascites provide decompression and better renal function.

In uroascites, the peritoneal membrane “autodialyzes” the intraperitoneal urine, resulting in a characteristic serum biochemical profile of marked hyponatremia, hyperkalemia, and elevated serum creatinine levels.

Other causes of ascites in the neonate include gastrointestinal, neoplastic, and iatrogenic causes. Umbilical vein catheters can result in total parenteral nutrition ascites if it erodes through the liver or perforates the peritoneum. These catheters can also lead to uroascites by eroding through the bladder or causing rupture of a patent urachus.

Hepatocellular diseases may result in ascites, but often occur with the onset of cirrhosis later in childhood. Cirrhosis is the most common cause of hepatic ascites in infants and children and may be caused by a number of underlying conditions including α1-antitrypsin deficiency, biliary atresia, congenital hepatic fibrosis, neonatal or viral hepatitis, inborn errors of metabolism, and storages diseases ( Box 17-3 ). With severe hepatic disease, cirrhotic ascites develops and children will often have signs of portal hypertension including possibly hepatosplenomegaly and varices. Ascites with hepatomegaly may also result from obstruction of the hepatic vein, or Budd-Chiari syndrome.

Pancreatic ascites should be considered in cases of intractable ascites and typically results from trauma or congenital obstruction of the pancreatic duct leading to acute pancreatitis. Diagnosis of pancreatic ascites can be a challenge because amylase levels may be normal or only slightly elevated in infants with pancreatitis due to a delay in pancreatic isoamylase production. The exact mechanism of pancreatic ascites is unclear, but it has been proposed that disruption of the pancreatic duct leads to leakage of pancreatic fluid into the peritoneum, resulting in chemical peritonitis. Pseudocyst formation may occur, although technically a pancreatic pseudocyst is a separate entity in which the body walls off the pancreatic leak. In adult studies, up to half of patients with pancreatic ascites have a concomitant leaking pseudocyst. Alternative mechanisms of pancreatic ascites formation include a coincidental occurrence of pancreatitis with another reason for ascites or an increased amylase level due to renal failure and decreased renal clearance. Ascitic fluid analysis is integral in diagnosis, with a high concentration of amylase (>1000 IU/L) and protein (3 g/dL) and a low serum-to-ascites albumin gradient being supportive of pancreatic ascites. Endoscopic retrograde cholangiopancreatography can be used to identify the site of disruption and help determine management strategies. Most cases of pancreatic ascites may be self-limiting and require no treatment. However, ascites is also an independent predictor of severity of pancreatitis and pseudocyst formation. In one study, the mortality rate in individuals with acute pancreatitis and ascites was 40%; the ascites-to-serum amylase ratio (>1) was 83% sensitive and 92% specific as a predictor of death.

Chylous ascites is an infrequent cause of ascites that occurs more often in older children. It results from either obstruction of lymphatic drainage or secondary to trauma. Although only sporadic case reports exist in the literature, chylous ascites appears to be twice as common in males. Obstruction of lymphatic drainage from congenital malformations or a neoplasm may lead to direct leakage of chyle through a lymphoperitoneal fistula or by exudation of chyle through lymphatics without evidence of fistula. Cirrhosis has infrequently led to chylous ascites from hydrostatic hypertension within the lymph vessels leading to rupture. Other causes of chylous ascites include trauma or surgical procedures in the retroperitoneal region, such as a splenorenal shunt, with resultant disruption of lymphatic vessels as well as certain infections including tuberculosis. It been estimated that 10% of all chylous ascites is related to child abuse. Only 10% of patients with chylous ascites will have concomitant lymphedema, which can complicate the clinical diagnosis. Clinical signs, such as muscle wasting and respiratory distress from an associated chylothorax or pneumonitis, can be seen in other causes of ascites. Ascitic fluid analysis allows for differentiation from other causes of ascites, as characteristics of chylous ascites include a “milky” appearance, a specific gravity greater than 1.012, an alkaline pH, a negative culture, and the presence of fat globules. A secondary hypogammaglobulinemia due to loss of globulins in lymph can also be seen; consequently, intercurrent bacterial infections may occur frequently. In the absence of an identified etiology, management is typically conservative consisting of supportive care and a low-fat diet, which can reduce the rate of ascites formation.

There are many miscellaneous causes of ascites in children. Ascites can develop as a result of cardiac abnormalities that lead to right heart failure or from a constrictive pericarditis. Ventriculoperitoneal shunts can cause ascites as a result of a variety of shunt-related complications including subclinical bacterial peritonitis, immune reaction, high protein content, and seeding of the peritoneum by tumor. Intra-abdominal neoplasms associated with ascites include lymphoma, Wilms’ tumor, renal clear cell sarcoma, germ cell tumors, malignant peritoneal mesothelioma, ovarian tumors, and peritoneal seeding of neuroblastoma. Other miscellaneous causes of ascites in children include chronic eosinophilic ascites, hemorrhagic ascites due to Henoch-Schönlein purpura, and vitamin A intoxication, systemic lupus erythematous, hypothyroidism, and certain infections. In developed countries, appendicitis is a common cause of ascites, whereas tuberculosis and salmonella organisms are more commonly causative agents in developing countries.

Congenital Ascites

Congenital ascites can present as an isolated finding or as a complication of hydrops ( Figure 17-4 ). With congenital ascites, it is important to make this distinction because management and prognosis varies by etiology. Although only a small number of cases have been reported, isolated ascites appears to carry a better prognosis with a higher survival rate (52%) compared to ascites associated with other anomalies (43%) or hydrops (33%). Age at diagnosis appears to be a reasonable prognostic indicator, with a lower mortality rate associated with later onset of congenital ascites. Many cases of isolated ascites resolve spontaneously, but isolated ascites may also be a harbinger of impending hydrops fetalis.

Congenital ascites from hydrops.

Imaging from 4-month-old infant with hydrops. (A) Abdominal x-ray demonstrating classic radiographic features of ascites including bulging of the flanks and centralization of the bowel. (B) Transverse ultrasound image showing large amount of simple ascites with septations (arrows).

Most commonly, congenital ascites is associated with immune and nonimmune hydrops fetalis, with Rh incompatibility formerly being a leading cause of fetal ascites. Isolated ascites, defined as fluid accumulation in the peritoneal cavity only, occurs less commonly, accounting for up to one-third of all cases. With the introduction of high-resolution ultrasonography, an underlying etiology can be identified in more than 95% of cases of congenital ascites. Causes of isolated congenital ascites include gastrointestinal, genitourinary, cardiac, and metabolic abnormalities, as well as congenital infections and chyloperitoneum ( Box 17-1 ).

Bowel perforation with subsequent meconium peritonitis is the most commonly reported gastrointestinal cause of isolated congenital ascites. Other gastrointestinal abnormalities associated with ascites include bowel obstruction due to intrauterine intussusception, malrotation, or jejunal atresia as well as primary intestinal lymphangiectasia and omphalocele. Hepatic causes include biliary atresia, ductal plate malformation, neonatal iron storage disease, and inborn errors of metabolism. These metabolic causes include many types of lysosomal storage disorders such as Niemann-Pick Type C, Gaucher’s disease, and GM-1 gangliosidosis, as well as Wolman disease, sialic acid storage disease, and Sly disease. In severe forms, hepatosplenomegaly may be present in infancy, which can be the initial presenting sign in select instances. Some inborn errors of metabolism are also associated with nonimmune fetal hydrops.

Genitourinary causes of congenital ascites include hydronephrosis, multicystic kidney, cloacal dysgenesis, hydrometrocolpos, and urinary obstruction with subsequent perforation. Cardiac anomalies that lead to cardiac failure and resultant increased hepatic pressure can cause isolated ascites, including structural abnormalities and dysrhythmias. Congenital infections account for 8% to 11.5% of isolated congenital ascites and can lead to ascites by causing intestinal perforation or by inducing anemia, and resulting high-output cardiac failure. Infections that cause ascites include syphilis, parvovirus B19, cytomegalovirus, and toxoplasmosis. Other causes of congenital ascites include chromosomal abnormalities, pulmonary anomalies, hemolytic anemia chyloperitoneum, neoplasms, and fetal abuse.

Ascites in Infancy and Childhood

The causes of childhood ascites are numerous and ascitic fluid analysis can help differentiate these. Clinical differentiation between transudate and exudate is indicative of the underlying pathophysiology and directs management. The etiology of ascites in children also varies by age; ascites that occurs in the neonate ( Box 17-2 ) often results from a persistence of fetal ascites and causes of congenital ascites should be considered.

Box 17-2

Etiology of Ascites in Neonates

SAAG > 1.1 (Transudate)

• •
  

  Portal hypertensive (Cirrhotic)

  
  
  
  
  • •
    

    Hepatobiliary disorders

    
    
    
    
    • •
      

      Cirrhosis

      
      
      
      
      • •
        

        Biliary atresia

        
        
      • •
        

        α1-antitrypsin deficiency

      
      
      
      
    • •
      

      Inborn errors of metabolism

      
      
    • •
      

      Viral hepatitis

      
      
    • •
      

      Congenital hepatic fibrosis

      
      
    • •
      

      Hepatic venous occlusion

      
      
      
      
      • •
        

        Budd-Chiari

        
        
      • •
        

        Veno-occlusive disease

      
      

    
    
    
    
  • •
    

    Prehepatic

    
    
    
    
    • •
      

      Portal venous malformations or thrombosis

      
      
    • •
      

      Schistosomiasis

    
    
    
    
  • •
    

    Cardiac

    
    
    
    
    • •
      

      Arrhythmia

      
      
    • •
      

      Right-sided heart failure from structural abnormalities

    
    

  
  

SAAG < 1.1 (Exudate)

• •
  

  Noncirrhotic

  
  
  
  
  • •
    

    Nephrotic syndrome

    
    
  • •
    

    Protein-losing enteropathy

    
    
  • •
    

    Malnutrition and malabsorption

    
    
  • •
    

    Gastrointestinal disorders

    
    
    
    
    • •
      

      Meconium peritonitis

      
      
    • •
      

      Intestinal malrotation

      
      
    • •
      

      Intestinal atresia

      
      
    • •
      

      Intestinal perforation

      
      
    • •
      

      Acute appendicitis

    
    

  
  
  
  
• •
  

  Infectious

  
  
  
  
  • •
    

    Congenital infections

    
    
    
    
    • •
      

      CMV, syphilis, toxoplasmosis, parvovirus

    
    
    
    
  • •
    

    Fungal infections

  
  
  
  
• •
  

  Neoplasm

  
  
  
  
  • •
    

    Myeloproliferative disorder

    
    
  • •
    

    Ruptured hepatic mesenchymal hamartoma

    
    
  • •
    

    Myofibromatosis of the ovary

    
    
  • •
    

    Secondary malignant infiltration

  
  

Other Fluids

• •
  

  Pancreatic ascites

  
  
• •
  

  Biliary ascites

  
  
  
  
  • •
    

    Spontaneous bile duct perforation

  
  
  
  
• •
  

  Chylous ascites

  
  
• •
  

  Genitourinary disorders

  
  
  
  
  • •
    

    Obstructive uropathy

    
    
  • •
    

    Posterior urethral valves

    
    
  • •
    

    Ureterocele

    
    
  • •
    

    Lower ureteral stenosis

    
    
  • •
    

    Ureteral atresia

    
    
  • •
    

    Imperforate hymen

  
  
  
  
• •
  

  Parenteral nutrition extravasation

  
  
• •
  

  Iatrogenic

  
  
  
  
  • •
    

    Bladder injury from catheterization

    
    
  • •
    

    Ruptured corpus luteum cyst

  
  
  
  
• •
  

  Mesenteric cyst

  
  
• •
  

  Pseudo-ascites

  
  
  
  
  • •
    

    Small bowel duplication

  
  

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