William J. Klish
Because the liver has systemic and portal circulations, the infrequency of liver abscess in infants and children is surprising. The low incidence is partly attributable to the extensive network of reticuloendothelial cells that line the sinusoids and are capable of clearing bacteria. Early use of antibiotics and improved medical and surgical care have reduced the liver’s exposure to bacteria and account for the infrequency of this disorder.
The exact incidence of hepatic abscess in children is unknown. Dehner and Kissane reported a 0.38% incidence at autopsy in patients younger than 15 years. In this large series studied from 1917 to 1967, 41% of the patients were younger than 2 years and 67% were 2 to 5 years of age. The incidence was estimated to be 3 per 100,000 admissions to a large pediatric hospital. In another review, the incidence was 25 per 100,000 pediatric hospital admissions. These findings suggest an increase in the incidence of this disorder, which may be related to the use of advanced diagnostic techniques. The prolonged lifespan of patients with primary and secondary immune defects could also account for the number of older children with pyogenic liver abscess.
Pyogenic liver abscess does occur in neonates and accounts for 0.026% of admissions to a neonatal intensive care unit in one study. No definite sex predilection is seen except that patients with chronic granulomatous disease, which is more frequently seen in boys, have an increased risk of developing liver abscess.
Infectious agents may reach the liver by direct invasion from contiguous structures, through the portal vein, by systemic (hematogenous) bacteremia, or by direct inoculation during surgery or through traumatic events. Cases in which the mode of transmission is obscure are described as cryptogenic.
Systemic bacteremia with hematogenous spread to the liver through the hepatic artery appears to be the most common source of liver abscess in children. In the series of Dehner and Kissane, the hematogenous route was responsible for 78% of the cases.
The portal system is the second most common route by which bacteria may reach the liver, and this route accounts for most cases of hepatic abscess in neonates. Among newborns, solitary liver abscess (usually due to gram-negative organisms) has been reported as a complication of umbilical venous catheterization or omphalitis. Prematurity and necrotizing enterocolitis are other important predisposing factors in neonates.
Portal vein inflammation and bacteremia can be associated with infections of the abdominal cavity. Appendicitis, perirectal abscess, Crohn disease, ulcerative colitis, and omphalitis are possible sources of portal vein sepsis. Liver abscess in Crohn disease may be secondary to seeding of the mesenteric vessels with portal bacteremia from the inflamed loops of bowel.
Direct extension of infection from contiguous structures accounts for 11% of the liver abscesses in children. Ascending cholangitis is a frequent complication of hepatic portoenterostomy in patients with biliary atresia and may lead to abscesses of the liver in these patients. Liver abscesses also may develop after liver transplantation, especially if technical problems with vascular supply or biliary drainage occur. Hepatic artery thrombosis can be a significant risk factor.
Penetrating and nonpenetrating trauma to the liver may lead to liver abscesses, presumably from the proliferation of bacteria within the localized hematomas or biliary collection that may result from trauma. This mode of infection is rare in children.
Cryptogenic hepatic abscesses have been reported in children with fever of unknown origin and account for a small percentage of patients. Hepatic abscesses also have been reported in patients with cat-scratch disease.
An increased incidence of hepatic abscess is found in immunocompromised children. Children with chronic granulomatous disease and acute leukemia are at increased risk. The pathophysiology may be related to chronic, low-grade intestinal infection or the small number of viable granulocytes and monocytes. Patients being treated with corticosteroids are at risk because of suppression of the natural host defenses.
Pyogenic liver abscess has been reported as a complication of anaerobic bacterial invasion of hepatic infarcts in patients with sickle cell anemia. These patients have other abnormalities that may contribute to their increased risk, such as splenic dysfunction and increased gut permeability to certain bacteria from microinfarcts.
Liver abscesses can result from infection of central parenteral nutrition catheters or ventriculoperitoneal shunts. Biliary tract disease predisposes the patient to the development of multiple liver abscesses, and portal vein inflammation usually results in a single abscess. Solitary abscess is most common in the right lobe of the liver.
Staphylococcus aureus was the most common pathogen seen in 44%, enteric organisms in 25%, and anaerobes in 10% of the cases in a review of 96 children with pyogenic liver abscess. Gram-negative organisms such as Escherichia coli, Aerobacter, Pseudomonas, Proteus, and Klebsiella species have been isolated frequently from liver abscesses in neonates. With improvement in culture techniques, anaerobes (e.g., Actinomyces, Fusobacterium, and Bacteroides species) and mycobacteria (i.e., typical and atypical species in patients infected with human immunodeficiency virus) have been identified in children. Fungi, especially Candida albicans, have been isolated from liver abscesses in neonates and leukemic patients on total parenteral nutrition. Entamoeba histolytica is a well-known cause of liver abscess. Liver abscess due to Mycobacterium tuberculosis and M. avium intracellulare can be the presenting infection in patients with acquired immunodeficiency syndrome.