Hepatic Abscesses

Hepatic AbscessesHepatic abscesses may be bacterial, parasitic, fungal in origin. In the USA, pyogenic abscesses are the most common, followed by amebic abscesses. Unless otherwise indicated, the remarks in this section refer to bacterial abscesses.

Cases are about evenly divided between those with a single abscess and those with multiple abscesses. About 90% of right lobe abscesses are solitary, while only 10% of left lobe abscesses are solitary.

The development of a hepatic abscess follows a suppurative process elsewhere in the body. Many abscesses are due to direct spread from biliary infections such as protracted cholangitis. About 40% of patients have an underlying malignancy. Other cases develop after generalized sepsis from bacterial endocarditis, renal infection, or pneumonitis. In 25% of cases, no antecedent infection can be documented (“cryptogenic” abscesses). Rare causes include secondary bacterial infection of an amebic abscess, hydatid cyst, or congenital hepatic cyst.

Escherichia, Klebsiella, bacteroides, enterococci (eg, Streptococcus faecalis), anaerobic streptococci (eg, Peptostreptococcus), and microaerophilic streptococci are most common. Staphylococci, hemolytic streptococci, or other gram-positive organisms are usually found.

Clinical Findings

Symptoms and Signs of Hepatic Abscesses

When liver abscess develops in the course of another intra-abdominal infection such as diverticulitis, it is accompanied by increasing toxicity, higher fever, jaundice, and a generally deteriorating clinical picture. Right upper quadrant pain and chills may appear.

In other cases, the diagnosis is much less obvious, since the illness develops insidiously in a previously healthy person. In these, the first symptoms are usually malaise and fatigue, followed after several weeks by fever.

The course of fever is often erratic, and spikes to 40–41 °C are common. Chills are present in about 25% of cases. The liver is usually enlarged, may be tender to palpation. If tenderness is severe, the condition may be confused with cholecystitis.

Jaundice is unusual in solitary abscesses unless the patient’s condition is worsening. Jaundice is often present in patients with multiple abscesses and primary disease in the biliary tree and in general is a bad prognostic sign.

Laboratory Findings

Leukocytosis is present in most cases and is usually over 15,000/L. A small group of patients, usually the most seriously ill, may fail to develop leukocytosis. Anemia is present in most. The average hematocrit is 33%.

Serum bilirubin is usually normal except in patients with multiple abscesses or biliary obstruction or when hepatic failure has supervened. Alkaline phosphatase is often elevated even in the presence of a normal bilirubin.

Imaging Studies

X-ray changes present in the right lung in about one-third of cases consist of basilar atelectasis. The right diaphragm may be elevated.

Plain films of the abdomen are usually normal. In a few patients, an air-fluid level in the region of the liver reveals the presence and location of the abscess. Distortion of the contour of the stomach on upper gastrointestinal series may be seen with large abscesses involving the left lobe.

Ultrasound and CT scans have the added advantage of being able to demonstrate abscesses or neoplasms elsewhere in the abdomen. The radioisotope liver scintiscan is able to demonstrate most liver abscesses but is nonspecific, gives little other useful information, and is therefore not helpful.

Differential Diagnosis

In many cases, early findings may be so vague that hepatic abscess is not even considered. The multiple other causes of malaise, weight loss, anemia would enter into the differential diagnosis. With spiking fevers, one must consider all the causes of fever. Failure to entertain the idea of hepatic abscess and to obtain the necessary scans leads to most errors in diagnosis.

Once imaging tests have demonstrated the abscess, the responsible organisms must be identified. Amebiasis should be considered in cases of a solitary abscess. Compared with amebic abscesses, pyogenic l abscesses are seen more often in patients with jaundice, pruritus, sepsis, a palpable mass, and elevated bilirubin and alkaline phosphatase levels. Patients with amebic abscesses more often have been to an endemic area and have abdominal pain, diarrhea, hepatomegaly, and positive serologic tests for amebiasis.


Intrahepatic spread of infection may create multiple additional abscesses and is responsible for some failures after treatment of an apparently solitary abscess. As the untreated abscess expands, rupture may occur into the pleural or peritoneal cavity, usually with catastrophic results. Septicemia and septic shock are common terminal complications of diffuse hepatic infection. Hepatic failure may develop in addition to uncontrolled sepsis, or it may predominate over signs of infection.

Hemobilia may follow bleeding from the vascular wall into the abscess cavity. In this case, hepatic artery embolization or ligation may be required to control bleeding.

Treatment of Hepatic Abscesses

Antibiotics should be started promptly. Initial coverage, before culture results are available, should be adequate for E. coli, bacteroides, enterococci, and anaerobic streptococci and consequently would usually include an aminoglycoside, clindamycin, metronidazole, ampicillin. The regimen may be modified later according to the results of cultures.

Whether the patient has a single abscess or multiple abscesses, this is usually the most appropriate initial therapy. The catheters can be removed in 2 weeks after output becomes nonpurulent and scant.

In about 40% of patients, the catheters do not drain well following initial placement and must be repositioned. The principal advantage of percutaneous drainage is lower morbidity (not lower mortality). It is easier to provide thorough drainage surgically, so when difficulties are encountered with percutaneous drainage, laparotomy should be performed promptly. Surgical intervention is more often necessary in cases of multiple, loculated collections or when the abscess cavity contains a large amount of necrotic debris. In such cases, open debridement should be considered. Rarely, multiple abscesses are confined to a single lobe and can be cured by lobectomy. Biliary obstruction or other causes of sepsis must also be corrected.


The overall mortality rate of 15% is more closely related to the underlying disease than to any other factor. The mortality rate is about 40% in patients with malignant disease. Pleural effusion, leukocytosis over 20,000/L, hypoalbuminemia, and polymicrobial infection correlate with a poor outcome. In the USA, whether the abscess is solitary or multiple no longer has a major influence on survival, but where benign biliary disease remains a major cause of this disease, multiple hepatic abscesses are associated with a worse prognosis. Death is rare in patient with a cryptogenic liver abscess.

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