There Are Many Potential Causes of Liver Abscesses
There Are Many Potential Causes of Liver Abscesses
There Are Many Potential Causes of Liver Abscesses
Bacteroides
Enterococcus
Escherichia coli
Klebsiella
Staphylococcus
Streptococcus
Symptoms
Chalk-colored stool
Dark urine
Fever, chills
Loss of appetite
Nausea, vomiting
Pain in right upper abdomen (more common) or throughout the abdomen (less common)
Unintentional weight loss
Weakness
Yellow skin (jaundice)
Abdominal CT scan
Abdominal ultrasound
Blood culture for bacteria
Liver biopsy
Liver enzymes (liver function tests) and bilirubin
White blood cell count
Treatment
Treatment usually consists of surgery or going through the skin with a needle or tube (percutaneous) to
drain the abscess. Along with this procedure, you will receive long-term antibiotic therapy (usually 4 - 6
weeks). Sometimes antibiotics alone can cure the infection.
Outlook (Prognosis)
Even with treatment this condition can be life-threatening in 10 - 30% of patients. The risk is higher in
people who have many abscesses.
Possible Complications
Life-threatening sepsis can develop.
Prevention
Prompt treatment of abdominal and other infections may reduce the risk of developing a liver abscess.
Many cases are not preventable.
Alternative Names
Medication
Until cultures are available, the choice of antimicrobial agents should be directed toward the most
commonly involved pathogens. Regimens using beta-lactam/beta-lactamase inhibitor combinations,
carbapenems, or second-generation cephalosporins with anaerobic coverage are excellent empiric
choices for the coverage of enteric bacilli and anaerobes. Metronidazole or clindamycin should be added
for the coverage of Bacteroides fragilis if other employed antibiotics offer no anaerobic coverage.
Amebic abscess should be treated with metronidazole, which will be curative in 90% of cases.
Metronidazole should be initiated before serologic test results are available. Patients who do not respond
to metronidazole should receive chloroquine alone or in combination with emetine or dehydroemetine.
Systemic antifungal agents should be initiated if fungal abscess is suspected and after the abscess has
been drained percutaneously or surgically. Initial therapy for fungal abscess is currently amphotericin B.
Lipid formulations may offer some benefit in that the complexing of drug to lipid moieties allows for
concentration in hepatocytes. Further investigation is required for definitive proof. Cases of successful
fluconazole treatment after amphotericin failure have been reported; however, its use as an initial agent is
still being studied.
Ultimately, the organisms isolated and antibiotic sensitivities should guide the final choice of
antimicrobials.
Duration of treatment has always been debated. Short courses (2 wk) of therapy after percutaneous
drainage have been successful in a small series of patients; however, most series have reported
recurrence of abscess even after more prolonged courses. Currently 4-6 weeks of therapy is
recommended for solitary lesions that have been adequately drained. Multiple abscesses are more
problematic and can require up to 12 weeks of therapy. Both the clinical and radiographic progress of the
patient should guide the length of therapy.
Antibiotics
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context
of the clinical setting.
A liver abscess occurs when bacteria or protozoa destroy hepatic tissue, producing a cavity,
which fills with infectious organisms, liquelled liver cells, and leukocytes. Necrotic tissue
then walls off the cavity from the rest of the liver. Liver abscess occurs equally in men and
women, usually in those over age 50. Death occurs in 15% of affected patients despite
treatment.
Underlying causes of liver abscess include benign or malignant biliary obstruction along with
cholangitis, extrahepatic abdominal sepsis, and trauma or surgery to the right upper
quadrant. Liver abscesses also occur from intra-arterial chemoembolizations or cryosurgery
in the liver, which causes necrosis of tumor cells and potential infection.
The method by which bacteria reach the liver reflects the underlying causes. Biliary tract
disease is the most common cause of liver abscess. Liver abscess after intra-abdominal
sepsis (such as with diverticulitis) is most likely to be caused by hematogenous spread
through the portal bloodstream. Hematogenous spread by hepatic arterial flow may occur in
infectious endocarditis.
The organisms that predominate in liver abscess are gram-negative aerobic bacilli,
enterococci, streptococci. and anaerobes. Amebic liver abscesses arc caused by E.
histolytica.
The clinical manifestations of a liver abscess depend on the degree of involvement. Some
patients are acutely ill; in others, the abscess is recognized only at autopsy, after death
from another illness.
The onset of symptoms of a pyogenic abscess is usually sudden; in an amebic abscess, the
onset is more insidious. Common signs include abdominal pain, weight loss, fever, chills,
diaphoresis, nausea, vomiting, and anemia. Signs of right pleural effusion, such as dyspnea
and pleural pain, develop if the abscess extends through the diaphragm. Liver damage may
cause jaundice.
Diagnosis for Liver Abscess
Ultrasonography and computed tomography (CT) scan with contrast medium can accurately
define intrahepatic lesions and allow assessment of intra-abdominal pathology.
Percutaneous needle aspiration of the abscess can also be performed with diagnostic tests
to identify the causative organism. Contrast-aided magnetic resonance imaging may
become an accurate method for diagnosing hepatic abscesses.
Antibiotic therapy, along with drainage, is the preferred treatment for most hepatic
abscesses. Pereutaneous drainage, either with ultrasound or CT guidance, is usually
sufficient to evacuate pus. Surgery may be performed to drain pus in unstable patients with
continued sepsis (despite attempted non surgical treatment) and for patients with persistent
fevers (lasting longer than 2 weeks) after percutaneous drainage and appropriate antibiotic
therapy. A common combination is ampicillin, an amino glycoside, and either metronidazole
or clindamycin. Third-generation cephalosporins can be substituted for the aminoglycosides
in patients at risk for renal toxicity. When the causative organisms are identified, the
antibiotic regimen should be modified to match the patient's sensitivities. I.V. antibiotics
should be administered for 14 days and then replaced with oral preparations to complete a
6 week course. Surgery is reserved for bowel perforation and rupture into the pericardium.
1. Provide supportive care, monitor vital signs (especially temperature), and maintain fluid
and nutritional intake.
2. Administer anti-infective's and antibiotics as necessary, and watch for possible adverse
effects. Stress the importance of compliance with therapy.
5. Prepare the patient for I.V antibiotic administration as an outpatient with home care
support.