The differential diagnosis of cystic lesions of the liver includes bilomas, abscesses, parasitic disease, simple cysts, polycystic liver disease, biliary cystadenoma, and cystadenocarcinoma.¹ The disease spectrum includes infectious, traumatic, congenital, and neoplastic hepatic lesions, which are relatively uncommon. Although significant improvements have been made in the diagnosis, treatment, and outcome of many of these cystic hepatic lesions, controversy continues regarding the best treatment option. Many classification systems exist for these lesions; however, the one used in this chapter is presented in Table 56-1.

The first description of a hepatic abscess is credited to Hippocrates in the year 4000 BC. Ochsner’s classic 1938 paper² described this disease as one that occurred in young males with pylephlebitis, usually due to appendicitis, and resulting in liver abscess. At that time, pyogenic liver abscesses carried a case-fatality rate of 77%,² and open surgical drainage remained the treatment of choice for many years. In 1953, McFadzean and associates³ in Hong Kong advocated closed aspiration and antibiotics for treatment of solitary pyogenic liver abscess; however, this treatment did not gain widespread acceptance until imaging advancements in the 1980s allowed for precise localization and a percutaneous approach to treatment. In recent decades, the predominant etiology of pyogenic liver abscess has changed from pylephlebitis to a biliary origin, and more recent reports from Asia and the United States have noted an increase in incidence of cryptogenic liver abscesses. Fortunately, advanced imaging techniques and improved therapeutic modalities have decreased the case-fatality rate for this disease to 6% to 26%.^4,5

Etiology

Kupffer cells act as a filter for the clearance of microorganisms in the liver. These organisms reach the liver through the bloodstream, biliary tree, or direct extension. Abscesses occur when normal hepatic clearance mechanisms fail or the system is overwhelmed. Parenchymal necrosis and hematoma secondary to trauma, obstructive biliary processes, ischemia, and malignancy also promote invasion of microorganisms.

In order to appropriately treat the abscess, source control is required. Six distinct categories have been identified as potential sources: (1) bile ducts, causing ascending cholangitis; (2) portal vein, causing pylephlebitis from appendicitis or diverticulitis; (3) direct extension from a contiguous disease; (4) trauma due to blunt or penetrating injuries; (5) hepatic artery, due to septicemia; and (6) cryptogenic^6,7 (Fig. 56-1).

Biliary disease accounts for 35% to 40% of all pyogenic liver abscesses, and 40% of pyogenic liver abscesses of biliary origin are related to an underlying malignancy.⁸ Obstruction of the biliary tree is the norm, and cholangitis is present in up to one-half of these patients.⁹ Intrahepatic stones and related biliary stricture are predominant in Eastern series, whereas malignant biliary obstruction is more common in the West.⁷ Any manipulation of the biliary tree—namely cholangiography, percutaneous transhepatic stents, endoscopic stent placement, and biliary-enteric anastomoses—also predisposes patients to cholangitis and pyogenic liver abscess. Malignancy contributes to poor nutrition and immunosuppression, potentiating the whole process.

Intestinal pathology is responsible for 20% of all pyogenic liver abscesses. Transient bacteremia due to bacterial translocation or frank gastrointestinal perforation causes overwhelming numbers of microorganisms to spread via the portal venous system to the liver. In the preantibiotic era, 43% of Ochsner’s 622 patients seeded the liver through the portal vein, and appendicitis was the most common source (34%).² Today, appendicitis accounts for only 2% of all pyogenic liver abscesses. Diverticulitis, perforated colon cancers, and abscesses elsewhere in the abdomen and pelvis remain common causes of pyogenic liver abscesses. Primary and metastatic liver tumors may also become colonized with enteric flora.

Contiguous extension of gangrenous cholecystitis, perforated ulcers, and subphrenic abscesses also is a reported source for pyogenic liver abscess. In addition, liver trauma causes parenchymal necrosis and clot, which creates an ideal milieu for the seeding and proliferation of microorganisms and subsequent abscess formation. Microorganisms can then seed these areas of necrosis through intraoperative contamination, biliary-enteric anastomoses, external drains involving the biliary tree, or percutaneous drains placed near the site of trauma or ablation.

Arterial embolization of bacteria via the hepatic artery causes approximately 12% of pyogenic liver abscesses. Intravenous drug abuse accounts for most of these cases, but hepatic artery chemoembolization or particle embolization as well as umbilical artery catheterization also have been cited. Liver abscess formation has been described as a complication in less than 5% of hepatic transarterial embolizations and less than 1% of tumor ablations. Arterial embolization also can occur from distant infection in the heart, lungs, kidneys, bones, ears, and teeth.⁸

Cryptogenic abscesses occur in 10% to 45% of patients, depending on the aggressiveness of investigation used to define the source.^8,10 Patients with cryptogenic abscesses usually have comorbidities such as diabetes, immunosuppression, or malignancy. Abscesses in these patients tend to be solitary and usually contain a single anaerobe.

Incidence

Pyogenic liver abscess affected 5 to 13 patients per 100,000 admissions prior to 1970 and accounts for approximately 15 cases per 100,000 admissions today. Seeto and Rocky¹¹ reported an incidence nearly two fold that of earlier reports (22 per 100,000). This rising incidence is attributed to a more aggressive management approach to hepatobiliary and pancreatic cancers as well as major improvements in diagnostic imaging.^7,12

Predisposing Factors

Pyogenic liver abscesses occur more frequently in adults with comorbid conditions including diabetes mellitus, cirrhosis, pancreatitis, inflammatory bowel disease, pyelonephritis, and peptic ulcer disease. Solid organ cancers, as well as lymphoma and leukemia, are present in 17% to 36% of patients with liver abscesses.⁸ Branum and associates¹³ reported an increased incidence in patients with underlying malignancy and immunosuppression. Civardi and colleagues¹⁴ and Lambiase and coworkers¹⁵ have reported series of patients with liver abscesses and underlying acquired immune deficiency. The combination of chemotherapy and steroid use is thought to be responsible in these cases.

In addition to comorbidities, age plays a role in the development of pyogenic liver abscess. The age of patients with pyogenic liver abscess has increased since 1938. This disease has now become a disease of the middle-aged and elderly, with a reported mean age of 47 to 65 years. Older patients are more likely to have a biliary etiology or underlying malignancy, whereas younger patients are more likely to be alcoholic males with a cryptogenic origin. Polymicrobial or anaerobic infections with multidrug-resistant organisms, a pleural effusion, inappropriate initial antibiotic selection, and a greater severity of illness on admission occur more frequently in older patients. Underlying malignancy is more prevalent in older patients and is a risk factor for developing anaerobic infections. Age and an Acute Physiology and Chronic Health Evaluation II (APACHE II) score ≥15 on admission are risk factors for case fatality in older patients. The case-fatality rate in older patients is related to host conditions, rather than characteristics of the abscess itself. Clinicians should apply an aggressive approach for older patients exhibiting a poor response to primary treatment, particularly in those with a greater severity of illness on admission.¹⁶

In children, pyogenic liver abscesses tend to occur in the setting of host-defense abnormalities or immune disorders. Complement deficiencies, chronic granulomatous disease, leukemia, and other malignancies place these children at increased risk for liver abscess. Hepatic abscesses also are seen in sickle cell anemia, congenital hepatic fibrosis, polycystic liver disease, and after liver transplantation (Table 56-2).⁸

Pathology

The source of the liver abscess is predictive of the number, location, and size of the abscess affecting a given patient. In general, portal, traumatic, and cryptogenic hepatic abscesses are solitary and large, whereas biliary and arterial abscesses are multiple and small. Huang and associates⁷ reported that 63% of patients had abscesses involving the right lobe, 14% had abscesses involving the left lobe, and 22% had bilobar disease. The number of bilateral and multiple abscesses has increased as more patients present with a biliary etiology. Bilateral disease may be seen in 90% of patients with an arterial or biliary source. In contrast, those with intra-abdominal infections frequently present with right lobe abscesses due to preferential flow from the superior mesenteric vein. Fungal abscesses are usually multiple, bilateral, and miliary.⁸

Bacteriology

Diagnostic confirmation of a pyogenic liver abscess involves aspiration of the abscess itself and obtaining blood cultures that are positive. Abscess cultures are positive for growth in the majority of cases (80%-97%), whereas blood cultures are positive in only 50% to 60% of cases.^11,14 Escherichia coli, Klebsiella species, enterococci, and Pseudomonas species are the most common aerobic organisms cultured, whereas Bacteroides species, anaerobic streptococci, and Fusobacterium species are the most common anaerobes.¹² Huang and colleagues⁷ cited the increased use of indwelling biliary stents as the cause of an increasing incidence of Klebsiella, streptococcal, staphylococcal, and pseudomonal species in liver abscesses. They also noted the presence of fungi in 22% of cultures taken between 1973 and 1993 compared to only 1% between 1952 and 1972. Broad-spectrum antibiotic use in the treatment of cholangitis was thought to be the causative factor. Candida fungal abscesses also are found in cancer patients who have undergone cytotoxic chemotherapy. Mycobacterium tuberculosis is a common infecting organism in acquired immunodeficiency syndrome⁹ (Table 56-3).

The species of microorganism found in a hepatic abscess is related to the source. The biliary tree gives rise to abscesses predominantly comprised of E coli and Klebsiella. E coli, enterococci, and anaerobes are the main organisms recovered from abscesses related to the intestinal tract. Anaerobes are the usual microorganisms found in cryptogenic liver abscesses in Western countries. Negative cultures may relate to poor anaerobic culture technique or the use of broad-spectrum antibiotics prior to abscess drainage. In series where careful attention is paid to anaerobic organism recovery, anaerobes may be detected in 10% to 17%, most often Bacteroides fragilis.¹⁷ If suspected bacterial cultures are repeatedly negative, amebic and parasitic organisms must be considered because they are difficult to identify by routine staining and culture techniques.⁸

Klebsiella pneumoniae is the number 1 pathogen found in pyogenic liver abscesses in Taiwan and Korea and usually occurs in a monobacterial, as opposed to mixed bacterial, setting. Investigation into the K antigen serotype revealed that the K1 serotype accounts for 60% of K pneumoniae strains causing liver abscess in these countries. In contrast, this particular serotype is rarely found in clinical isolates from Western countries. In Taiwan and Korea, the average age to develop a K pneumoniae liver abscess is 55 to 60 years. These abscesses are twice as likely to be diagnosed in men than in women and are much more likely to be cryptogenic in origin (64%). Diabetes is a known risk factor for developing K pneumoniae liver abscess and is a significant risk factor for embolic complications, especially endophthalmitis.^17,18

Diagnosis

The clinical presentation of pyogenic liver abscess is usually subacute and nonspecific, leading to delays in presentation, diagnosis, and treatment. In Seeto and Rocky’s review¹¹ of 142 patients with pyogenic liver abscesses, the classic triad of fever, jaundice, and right upper quadrant tenderness was present in less than 10% of patients overall.

Clinical Presentation

Most patients have fever (92%), and 50% have abdominal pain, but only half have pain in the right upper quadrant. Diarrhea occurs in less than 10% of patients. The liver may be tender (65%) and enlarged (48%), and the patient may appear jaundiced (54%). Other nonspecific complaints include malaise, anorexia, and nausea. If the diaphragm is involved, pleuritic chest pain, cough, or dyspnea may occur. If the abscess ruptures, peritonitis and sepsis may be presenting features^7,9,11 (Table 56-4).

Laboratory Evaluation

Leukocytosis is present in 70% to 90%, an elevated alkaline phosphatase in 80%, and an elevated bilirubin and transaminases in 50% to 67% of patients. Anemia, hypoalbuminemia, and prolonged prothrombin time are seen in 60% to 75% of patients.^7,9,11,12

Radiology

Plain films such as chest radiographs are abnormal in 50% of patients. Findings may include an elevated right hemi­diaphragm, a right pleural effusion, and/or right lower lobe atelectasis. Abdominal films may show hepatomegaly, air-fluid levels in the presence of gas-forming organisms, or portal venous gas if pylephlebitis is the source (Fig. 56-2). Ultrasound will distinguish solid from cystic lesions and is cost-effective and portable. Ultrasound (US) is 80% to 95% sensitive but has limited utility in the morbidly obese and in lesions that are located under the ribs or located in an inhomogeneous liver.

Computed tomography (CT) is more sensitive (95%-100%) than US in detecting hepatic abscesses. On CT examination, an abscess is of lower attenuation than the surrounding liver, and the wall of the abscess may enhance with intravenous contrast administration. Lesions are detectable to around 0.5 cm with CT and are not limited by shadowing from ribs or air. CT and US may be used to evaluate and potentially treat the source of infection by percutaneous drainage (Figs. 56-3 and 56-4). Radionuclide scanning with technetium-99m is no longer used and has been completely replaced by CT and US. However, cholangiography, usually through an indwelling biliary stent, may visualize the abscess (Fig. 56-5).

Treatment

The appropriate treatment for pyogenic liver abscesses requires treatment of the abscess itself and concomitant treatment of the source. Drainage of a pyogenic abscess is essential for cure in most cases. Although antibiotics alone may be curative, these patients have a higher risk of failure and complications such as abscess rupture. Percutaneous transhepatic drainage is a relatively low-risk and successful treatment method for both polymicrobial liver abscesses and K pneumoniae liver abscesses.¹⁷ Steps in management include antibiotic administration, radiologic confirmation by US or CT, and drainage. Exceptions to this strategy include multiple small abscesses and miliary fungal abscesses. These abscesses are treated with intravenous antibiotics and antifungals, respectively, without a drainage procedure.

ANTIBIOTICS

After confirmatory imaging with US or CT, abscesses are aspirated, blood cultures are drawn, and broad-spectrum intravenous antibiotics are administered until sensitivities allow a more selective antibiotic choice. Serologic testing also should be performed if an amebic abscess is suspected.⁹

Classic antibiotic regimens include an aminoglycoside, clindamycin, and either ampicillin or vancomycin. However, E coli, K pneumoniae, and other Enterobacteriaceae have developed up to 30% resistance to these antibiotics. Fluoroquinolones can replace aminoglycosides, and metronidazole can be used instead of clindamycin, especially if an amebic source is suspected. Single-agent therapy with ticarcillin-clavulanate, imipenem-cilastatin, or piperacillin-tazobactam also is acceptable.¹² Recent reports advise a third-generation cephalosporin and metronidazole or piperacillin-tazobactam as the initial regimen of choice. Carbapenems are recommended when extended-spectrum β-lactamase–producing strains are isolated. Treatment used to be given for 4 to 6 weeks; however, many studies now document success with only 2 weeks of antibiotic therapy.⁸ Empiric antibiotics should include anaerobic coverage in older pyogenic liver abscess patients, particularly in the setting of malignancy.¹⁶

For patients with a K pneumoniae liver abscess, ampicillin alone is not recommended. In addition, metronidazole is ineffective against aerobic organisms, and regimens containing first-generation cephalosporins have been shown to be inferior in treatment of K pneumoniae liver abscess. Thus, a broad-spectrum penicillin, such as piperacillin-tazobactam, or a second- or third-generation cephalosporin is preferred for patients with K pneumoniae liver abscess.¹⁷

Antibiotics alone have an 80% success rate for solitary abscesses with a diameter <5 cm.¹⁹ In a series of 107 patients with unilocular hepatic abscesses of <3 cm, treatment with antibiotics alone had a 100% success rate. In the setting of multiple abscesses <1.5 cm in size and no concurrent surgical disease, patients may be treated with intravenous antibiotics alone. However, multiple small abscesses frequently imply biliary tract disease and may require biliary drainage for source control. Similarly, fungal abscesses are miliary in nature and not amenable to percutaneous or surgical drainage.

ANTIFUNGALS

Candidal liver abscess is a rare disease reported most commonly in patients with hematologic malignancies during periods of neutropenia resolution. Most of the candidal liver abscesses in patients with hematologic malignancies are a manifestation of disseminated candidiasis and have high mortality rates. They also can be acquired by fungemia from the portal vein or an ascending retrograde infection from the biliary tree. In patients with hematologic malignancies, the yield of positive culture is often less than 50%, with the diagnosis usually based on microscopic examination or histopathology from deep tissues. Higher doses of amphotericin B (2-9 g) are recommended by most experts because a cumulative dose of <2 g correlated with residual lesions at autopsy. Cases of hepatosplenic candidiasis have been successfully treated with fluconazole. Symptoms improved at 3 to 8 weeks, but resolution of the lesions on CT scan was noted after at least 1 month of fluconazole.²⁰

Candida glabrata often has reduced susceptibility to both azoles and amphotericin B, and opinions on best therapy are divided. Both Candida krusei and C glabrata appear susceptible to caspofungin, and this agent may be a good alternative. Although fungemia due to C glabrata has been treated successfully with fluconazole (6 mg/kg/d), many experts prefer amphotericin B deoxycholate (>0.7 mg/kg/d). On the basis of pharmacokinetics predictions, fluconazole (12 mg/kg/d; 800 mg/d for the 70-kg patient) may be a suitable alternative, particularly in less critically ill patients.²¹

ASPIRATION AND PERCUTANEOUS CATHETER DRAINAGE

Needle aspiration and percutaneous catheter drainage of liver abscesses have similar mortality rates; however, recurrence rates and the requirement for surgical intervention may be greater in those who undergo aspiration alone.¹¹ Needle aspiration is less invasive, less expensive, and avoids all of the complications associated with catheter care. Giorgio and colleagues²² reported a series of 115 patients with a 98.3% success rate for needle aspiration, no mortality, and no procedure-related morbidity. A randomized controlled trial by Rajak et al²³ in 1998 compared percutaneous needle aspiration to catheter drainage and also found no major complications and no deaths. They did, however, report only 60% success with needle aspiration versus a 100% success rate with catheter drainage.²³ The highest rate of recurrence (15%) occurred in patients with biliary tract disease and obstructive lesions, whereas the recurrence rate with cryptogenic abscesses was less than 2%. This observation suggests that the underlying lesion should influence the type of therapy chosen. Another option that is infrequently employed is repeated aspiration.

Patients in whom percutaneous drainage is not appropriate include those with (1) multiple large abscesses; (2) a known intra-abdominal source that requires surgery; (3) an abscess of unknown etiology; (4) ascites; and (5) abscesses that would require transpleural drainage.⁶ An example of a patient managed by percutaneous drainage is provided in Figure 56-6.

SURGICAL DRAINAGE

Surgical drainage was the widely accepted treatment for liver abscesses for many years following Ochsner’s 1938 report.² Right-sided abscesses were drained extraperitoneally via a 12th rib resection to avoid contamination of the peritoneal cavity. With the advent of systemic antibiotics, transperitoneal surgical exploration also was considered a safe surgical approach. Advantages of the transperitoneal approach include the ability to: (1) treat the inciting pathology in the remainder of the abdomen/pelvis; (2) gain access and exposure of the entire liver for evaluation and treatment; and (3) access the biliary tree for cholangiography and bile duct exploration.

Since the 1980s, treatment has shifted to a less invasive approach utilizing percutaneous needle aspiration or catheter drainage to treat pyogenic abscesses. Surgical drainage is currently reserved for patients who have failed nonoperative therapy, those who need surgical treatment of the underlying source, those with multiple macroscopic abscesses, those on steroids, or those patients with concomitant ascites.⁷

Complications

Up to 40% of patients develop complications from pyogenic liver abscesses, with the most common being generalized sepsis. In addition to sepsis, morbidity can include pleural effusions, empyema, and pneumonia. Abscesses also may rupture intraperitoneally, which is frequently fatal. Usually, however, the abscess does not rupture, but develops a controlled leak resulting in a perihepatic abscess. Pyogenic abscesses also may cause hemobilia and hepatic vein thrombosis.⁸

Bacteremia is extremely common (95%) in K pneumoniae liver abscesses as opposed to other types of pyogenic liver abscesses (50%). As a result, end-organ seeding and distant abscesses are common. Extrahepatic abscesses occur in 7% to 12% of patient with K pneumoniae liver abscesses, with the most commonly reported organ being the eye. Endophthalmitis occurs in to 6% to 61% of cases and commonly occurs after liver abscess drainage. Disseminated intravascular coagulation, septic pulmonary emboli, and acute renal failure are also well-documented complications of K pneumoniae liver abscess.¹⁷

Outcome

Between the 1950s and 1990, mortality rates varied from as low as 11% to as high as 88%.⁶ High mortality rates came from delay or failure to diagnose the abscess, failure to detect smaller intrahepatic abscesses, ineffective surgical drainage, lack of source control, associated malignancy, immune insufficiency, or other major comorbid conditions. No general consensus has been reached regarding risk factors due to the variability of the patient population being studied (Table 56-5).

The prognosis for K pneumoniae is better than for other pyogenic liver abscesses with respect to mortality (6%-17%) and disease relapse. Prognosticators for mortality in K pneumoniae liver abscess are abscess >5 cm, concomitant sepsis, intrahepatic gas formation, APACHE III score >40, delayed/inadequate abscess drainage, use of antimicrobials alone, thrombocytopenia, and diabetes.¹⁷ The main concern in this type of liver abscess is no longer mortality, but catastrophic disability due to irreversible ocular or neurologic complications. The K pneumoniae genotype K1 is a pathogen capable of causing septic ocular or central nervous system complications from pyogenic liver abscess independent of host underlying diseases.¹⁸ The outcome for patients who develop endophthalmitis is grim because despite rapid intervention, visual acuity outcome is poor.¹⁷

Amebic liver abscess is caused by the parasitic protozoan Entamoeba histolytica. The disease was described in association with blood and mucus diarrheal stools in the 5th century BC by Hippocrates and other practitioners. In 1890, Sir William Osier described the first North American case when, after an attack of dysentery while in Panama, a physician’s stool and abscess fluid were both found to contain amebae. Councilman and LaFleur of Johns Hopkins Hospital went on to detail the pathogenic role of amebae and coined the terms “amebic dysentery” and “amebic liver abscess” in 1891.²⁴ Amebic liver abscess is the most common extraintestinal form of invasive amebiasis, and an estimated 100,000 people succumb to this disease each year.²⁵

Etiology

Three species of ameba mainly infect humans. Entamoeba dispar is associated with an asymptomatic carrier state and not with disease. Entamoeba moshkovskii has been associated with mild gastrointestinal discomfort. E histolytica is responsible for all forms of invasive disease. The life cycle involves cysts, invasive trophozoites, and fecally contaminated food or water to initiate the infection.^26,27 Fecal-oral transmission occurs; the cyst passes through the stomach into the intestine unscathed, and pancreatic enzymes start to digest the outer cyst wall. The trophozoite is then released into the intestine and multiplies there. Normally, no invasion occurs, and the patient develops amebic dysentery or becomes an asymptomatic carrier. In a small number of cases, the trophozoite invades through the intestinal mucosa, travels through the mesenteric lymphatics and veins, and begins to accumulate in the hepatic parenchyma, forming an abscess cavity. Liquefied hepatic parenchyma with blood and debris gives a characteristic “anchovy paste” appearance to the abscess.¹²

Incidence

Worldwide, an estimated 500 million people are carriers of E histolytica or E dispar, 50 million people have active disease, and 50,000 to 100,000 die annually. The vast majority of these infections are acquired in the developing world. Amebiasis is common in Africa, Indochina, and Central and South America. Up to 5% of diarrheal illness in Mexico is due to Entamoeba disease.²⁶ The overall prevalence in the United States is 4% per year. High-risk groups in the United States include sexually active homosexual men, immigrants, tourists who travel to endemic areas, institutionalized people, and those with HIV.²⁸ Children also have been known to infect entire families. Amebiasis follows a bimodal age distribution. One peak is at age 2 to 3 years, with a case-fatality rate of 20%, and the second peak is at >40 years, with a case-fatality rate of 70%.²⁶ Those living in developing countries have a greater risk and an earlier age of infection than do those in developed regions. Low socioeconomic status and unsanitary conditions are significant independent risk factors for infection.²⁸ Amebic liver abscess is 10 times as common in men as in women and is a rare disease in children.²⁷ The reason for this vast difference between the sexes is not clear. Greater alcohol consumption among men, which may impair Kupffer cellular function as well as cellular and humoral immune response, and the potentially protective effects of hormones and iron deficiency anemia in menstruating women have been proposed to play a role.

Pathology

Roughly 90% of people who become infected with E histolytica are asymptomatically colonized, and factors that control the invasiveness of this organism are not completely understood. E histolytica cysts can last for days in a dried state at temperatures of 30°C. These cysts are resistant to the effects of gastric acid pH, but become stimulated to form trophozoites in the alkaline pH of the bowel. Trophozoites are found in the colon and in the feces of humans and mammals. Humans become reservoirs, and transmission occurs by ingesting food and water contaminated with amebic cysts, or occasionally through person-to-person contact. Incubation takes 1 to 4 weeks. Left untreated, asymptomatic individuals may shed cysts for many years.

The reasons why only a small portion of the colonized people will develop invasive disease are not fully understood. Virulence factors of the parasite (eg, the amount of secreted cysteine proteinases, phospholipases, hemolysins, and amebapores) and the host’s immune status are the most likely factors. Invasive amebiasis can include anything from amebic dysentery to metastatic abscesses. The most common form of the invasive disease is colitis. The majority (70%-80%) of patients experience a gradual onset of symptoms with worsening diarrhea, abdominal pain, weight loss, and stools containing blood and mucus. Trophozoites invade and induce apoptosis in colonic mucosa, resulting in “buttonhole” ulcers with undermined edges. Trophozoites are actually found in the edge of the ulcers.

The most common extraintestinal site of amebiasis is the liver, occurring in 1% to 7% of children and 50% of adults (usually males) with invasive disease.²⁶ Trophozoites reach the liver through the portal system, causing focal necrosis of hepatocytes and multiple microabscesses that coalesce into a single abscess. The central cavity of the lesion contains a homogenous thick liquid that is typically red/brown and yellow in color and similar to anchovy paste in consistency.²⁹

Diagnosis

The definitive diagnosis of amebic liver abscess is by detection of E histolytica trophozoites in the pus and by finding serum antibodies to the ameba.²⁹ The differential diagnosis should include pyogenic liver abscess, necrotic adenoma, and echinococcal cyst.

CLINICAL PRESENTATION

Ninety percent of amebic liver abscesses occur in young adult males. The presentation may be acute, with fever and right upper quadrant (RUQ) pain, or subacute, with weight loss and, less frequently, fever and abdominal pain. The usual case of amebic liver abscess does not present with concurrent colitis, but patients may have had dysentery within the past year. Alcohol abuse is common.³⁰ Eighty percent of patients with amebic liver abscess present with symptoms that develop within 2 to 4 weeks, including fever, cough, and a dull aching pain in the RUQ or epigastrium. Diaphragmatic involvement causes right-sided pleural pain or pain referred to the shoulder. Gastrointestinal symptoms of nausea, vomiting, abdominal cramping, abdominal distention, diarrhea, and constipation occur in 10% to 35%. Hepatomegaly with point tenderness over the liver or subcostal region is common²⁷ (Table 56-6). In contrast to pyogenic liver abscesses, amebic liver abscesses are more likely to occur in males under 50 years old who have immigrated or traveled to a country where the disease is endemic. The patient also will not be jaundiced or have biliary disease or diabetes mellitus²⁷ (Table 56-7).