OVERVIEW: What every practitioner needs to know
Are you sure your patient has a liver abscess? What are the typical findings for this disease?
Liver abscesses are relatively rare in children. Children who are immunosuppressed or those with primary immunodeficiency diseases (particularly those with defects in phagocytosis) are more susceptible. In developing countries malnutrition, sepsis and parasytic disease predispose to liver abscesses.
Although bacteria are often the cause of pyogenic liver abscesses, other pathogenic organisms such as fungi, amoeba, or parasites may also cause liver abscesses in certain clinical settings.
Typical findings for liver abscess include fever, abdominal pain, right upper quadrant tenderness and hepatomegaly. Less common manifestations include fatigue, weight loss, right shoulder pain, sepsis, and acute abdomen pain.
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What other disease/condition shares some of these symptoms?
Cholecystitis, cholangitis, Fitz-Hugh Curtis Syndrome, pneumonia, viral and bacterial hepatitis, and other intrahepatic abscesses share similar symptoms.
What caused this disease to develop at this time?
The pathogenesis of hepatic abcesses in children is multifactorial. Immunodeficiency, either primary or secondary (malnutrition) is a known predisposing factor. Prexisting biliary disease with resultant cholangitis is another risk factor. Trauma and preexisting intrabdominal sepsis or infection (appendiceal abcess, inflammatory bowel disease, Entamoeba Histolytica) may also result in intrahepatic abscess. Helminthic infection, such as that caused by toxicara canis, may also serve as a nidus for infection. Liver abscess may also occur as a result of infection with Bartonella Henselae via a feline vector. Finally, a significant proportion of hepatic abscesses are idiopathic. The majority of liver abscesses occur in the right lobe.
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
Laboratory studies are of limited use in making the diagnosis of liver abscess. Leukocytosis may be present, along with elevation of inflammatory markers such as C reactive protein and erythrocyte sedimentation rate. The serum albumin is often depressed, and anemia may be present. Serum transaminases are of limited use; only mild elevation may be present, along with mild elevation of serum alkaline phosphatase and bilirubin. However, it is important to emphasize that normal values do not rule out the presence of hepatic abcess. Specific serologic testing is often of use when parasitic agents (Entamoeba Histolytica, Echinococcus) or Bartonella Henselae are suspected.
Would imaging studies be helpful? If so, which ones?
Along with a high index of clinical suspicion, imaging studies are the mainstay of diagnosis. Ultrasound is most commonly used as a front line diagnostic tool, although sensitivity (80-95%) may be less than contrast enhanced computed tomography (CT) (>95%) or magnetic resonance imaging (MRI). Ultrasound may miss liver abscesses that are early in the course of development and lesions that occur in the dome of the liver. Radioisotope scanning (Gallium) has a sensitivity similar to that of ultrasonography, and is probably not indicated in most cases when liver abscess is suspected on clinical grounds.
Confirming the diagnosis
Definitive diagnosis of a pyogenic hepatic abscess rests upon percutaneous aspiration, with subsequent microscopic examination and culture of aspirated material. Although repeated needle aspiration may be employed, drainage via catheter placement under CT or ultrasound guidance is usual. Catheter withdrawal is performed after successful drainage, usually in 24-72 hours.
For ruptured lesions, or those inaccessible to percutaneous drainage, open surgical drainage may be required. Antibiotic treatment alone may be considered for small and/or multiple abscesses.
Antibiotic treatment duration is variable, but generally is at least 4-6 weeks. Undrained multiple abscesses may require even longer treatment courses. Finally, in regions known to have a high incidence of amebic abscesses, antibiotic treatment of lesions less than 5 cm in size for 4-5 days is probably indicated initially. Drainage should be reserved for those who do not improve clinically or in those patients in whom rupture of the abscess seems imminent.
If you are able to confirm that the patient has a liver abscess, what treatment should be initiated?
Patients believed to have a liver abscess should be placed upon empiric antibiotic therapy. Metronidazole, which provides coverage for both Entamoeba Histolytica and anerobes, should be combined with an anti-staphylococcal agent such as vancomycin. Gram negative coverage with a third generation cephalosporin, aminoglycoside, or other appropriate antimicrobial agent should also be provided initially.
Results of culture and microscopic examination of aspirated purulent material should guide longer term therapy, keeping in mind that polymicrobial infection may be present. In the appropriate clinical settings, serologies for entamoeba histolytica, echinococcus, and Bartonella Henselae may be obtained and, if positive, guide therapy. Although rare, tuberculosis should be considered. Finally, antifungal therapy may be required in the immunocompromised host.
Treatment duration is dependent upon etiologic agent, adequacy of drainage, and clinical response but rarely is less than 4 weeks and may extend to several months.
What are the adverse effects associated with each treatment option?
With needle aspiration, percutaneous drainage and open drainage, the success rate is 70-95% with complications including hepatic laceration, bleeding, bacteremia, sepsis, abscess rupture with peritonitis, and/or fistula formation. Conservative therapy (no drainage) may cause abscess rupture with peritonitis, sepsis, and/or portal vein thrombosis. These complications may occur even with appropriate drainage. Conservative therapy often requires a longer antimicrobial course.
What are the possible outcomes of a liver abscess?
While hepatic abscess remains a serious condition, mortality rates have fallen to less than 15% in children. Prognosis is less favorable in those with multiple abscesses.
A risk-benefit analysis of therapeutic options depends largely upon the clinical setting. For example, a previously well child with fever, recent exposure to a kitten, regional adenopathy and positive Bartonella henselae testing who is noted to have hepatosplenic abscesses on CT scanning would be treated differently than a child with leukemia and multiple small hepatic lesions, most likely attributable to fungal infection. Similarly, a child with recent travel to areas in which Entamoeba Histolytica is endemic, who now has a single intrahepatic lesion would be treated differently than a child status post penetrating abdominal trauma who presents with similar ultrasound findings.
What causes this disease and how frequent is it?
The predominant pathogen associated with pyogenic liver abscess in childhood in Staphylococcus aureus. Enteric gram negative organisms which predominate in adult series, account for approximately 30% of cases in childhood, with anaerobes found in approximately half that number. Bartonella Henselae, and, rarely tuberculosis and actinomycosis are other bacterial causes. Other causative organisms are noted above, and include Entamoeba Histolytica (1-7% of pediatric patients with amebiasis), Echinococcus granulosus, and, in immunocompromised patients, fungal infections such as that caused by Penicillium marneffei.
Pathogenesis in the usual patient is described above. Hepatic abscess formation may occur as a result of hematogenous seeding of organisms via the portal vein and hepatic artery. Organsims may also enter the hepatic parenchyma from an infected and often obstructed biliary system. Finally, direct innoculation may occur following penetrating trauma to the liver. In addition, hepatic abscess formation may occur after orthotopic hepatic transplantation, presumably as a result of immunosuppression combined with biliary disease and/or diminished blood flow to the transplanted organ.
The incidence of pyogenic liver abscess in childhood is difficult to accurately estimate, but varies in different parts of the globe. In the United States, incidence has been estimated at approximately 25 cases per 100,000 pediatric hospital admissions.
Genetic predisposition to hepatic abscesses may occur in patients with congenital immunodeficiencies including chronic granulomatous disease. Papillon-Leferve syndrome, or palmoplantar keratoderma with periodontitis associated with mutations in the Cathepsin C gene is also associated with hepatic abscess formation.
What is the evidence?
Novak, DA, Lauwyers, GY, Kradin, RL, Suchy, FJ, Sokol, RJ, Balistreri, WF. “Bacterial, parasitic and fungal infections of the liver”. 2007. pp. 871-896. (A well referenced review of usual and unusual pediatric hepatic infections including hepatic abscess.)
Mishra, K, Basu, S, Roychoudhury, S, Kumar, P. “Liver abscess in children”. World J Pediatr. vol. 6. 2010 Aug. pp. 210-6. (Current review.)
Srivastava, A, Yachha, SK, Arora, V, Poddar, U, Lal, R, Baijal, SS. “Identification of high-risk group and therapeutic options in children with liver abscess”. Eur. J. Pediatr. vol. 171. 2012 Jan. pp. 33-41. (Review of risk stratification and therapeutic options in pediatric hepatic abscess.)
Liu, CH, Gervais, DA, Hahn, PF, Arellano, RS, Uppot, RN, Mueller, PR. “Percutaneous hepatic abscess drainage: do multiple abscesses or multiloculated abscesses preclude drainage or affect outcome”. J Vasc Interv Radiol. vol. 20. 2009 Aug. pp. 1059-65. (This is a large study (149 patients) demonstrating the feasibility of percutaneous drainange even in those with multiple, complex hepatic abscesses.)
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