The incidence of pyogenic liver abscess in developed countries has not changed appreciably over the past 50 years, being estimated at 8 to 16 cases/100000 admissions, with a prevalence at autopsy of 0.3 to 1.5 per cent. A slight male predominance of cases has remained during this period, and no ethnic group appears to be at increased risk (Table 1) 358.

What has changed over this time are the age of the patients and the underlying cause of the liver infection. Fifty years ago, the majority of patients were under the age of 40 and appendicitis was the leading cause of the disease; today the average age is between 43 and 60, with an increasing proportion of cases over age 60. This change corresponds to the finding that appendicitis has been replaced by biliary tract disease as the most common underlying aetiology. The increasing age of patients has been associated with an increased incidence of malignancy in patients with liver abscesses. In younger patients with liver abscess related to biliary tract disease the underlying process is usually benign, such as biliary tract calculi; in the elderly, malignancies invading or compressing the biliary tract are common.

Pyogenic liver abscesses may be divided into two general categories, based upon the size and distribution of the focal sites of inflammation, the acuity of clinical presentation, and the nature of the therapy that is required. Macroscopic abscesses are usually restricted to one lobe of the liver, are frequently single or confluent, present subacutely with symptoms of several days to weeks' duration, and require some form of primary drainage. Microscopic abscesses are multiple, widely distributed throughout the hepatic parenchyma, usually manifest themselves acutely over a few days, and require primarily medical therapy, with any surgery that is carried out being aimed at the underlying process, rather than the hepatic parenchymal inflammation.

Focal infection within the liver can be divided into six general categories, based upon the pathogenetic route by which infecting organisms were introduced into the liver (Table 2) 359.

Hepatic abscess may arise due to cholangitis whenever bile flow is obstructed. In general, total obstruction is associated with elevated pressure within the biliary tree, an acute septic course, and miliary microabscesses throughout the hepatic parenchyma—a process that has been termed ‘acute suppurative cholangitis’. Infection associated with less complete obstruction is associated with normal biliary tract pressure, a subacute course, and macroscopic abscesses.

Liver abscess may arise because of suppurative thrombophlebitis in the portal venous system that is secondary to such intra-abdominal inflammatory processes as appendicitis (the classical cause), diverticulitis, infected haemorrhoids, or any other cause of intra-abdominal or pelvic infection that impacts upon the portal venous system. A clinical curiosity which remains unexplained is that although portal vein bacteraemia is common in patients with inflammatory bowel disease, hepatic abscess is uncommon.

Two subcategories of liver abscess should be considered. Systemic bacteraemias may occasionally seed the liver, resulting in either macroscopic abscesses (usually in the setting of some form of antimicrobial therapy that permits the individual to survive, although not to be cured of the systemic process) or, more commonly, miliary microabscesses. Typically, such infections occur in children with such underlying conditions as chronic granulomatous disease, leukaemia, or other disturbances of granulocyte number or function, and are caused by such organisms as Staphylococcus aureus. In other patients the primary process affecting the hepatic artery is thrombosis, with hepatic injury then becoming superinfected with micro-organisms of local or systemic origin. With the increasing prevalence of liver transplantation, particularly in young children in whom the hepatic arterial anastomosis is especially vulnerable, this entity is becoming more common.

Both penetrating and non penetrating trauma to the liver can result in liver abscess formation. The common denominator is hepatic necrosis, intrahepatic haemorrhage, and intraparenchymal bile extravasation. Such areas of devitalized tissue commonly become infected, even if they are initially sterile, resulting in macroscopic abscesses. Prevention of this form of hepatic abscess is dependent upon an aggressive surgical approach to devitalized hepatic tissue, wide excision of such necrotic tissue being essential.

Contiguous sites of infection involving the gallbladder, subphrenic space, or pleural space and disease processes in which gastric or intestinal perforation occur directly into the liver can result in macroscopic hepatic abscesses. Malignancy is often present in patients with bowel perforation.

The aetiology of the liver abscess remains obscure in about 5 per cent of patients, even after extensive evaluation. Presumably, a minor injury to the liver renders such individuals susceptible to seeding by a transient bacteraemia. Other unusual causes of liver disease, such as cysts, intrahepatic malignancy, amoebic abscesses, and hydatid disease, may become secondarily infected, resulting in a pyogenic liver abscess. The common denominator, as in the post-traumatic cases, is the microbial seeding of a locus minoris resistentiae within the liver.

The majority of the organisms that invade the liver to cause hepatic abscesses are derived from the gastrointestinal tract: gastrointestinal flora account for more than 75 per cent of these abscesses (Table 3) 360. Polymicrobial infection occurs in 22 to 64 per cent of cases, usually involving both aerobic and anaerobic flora of gastrointestinal origin. Escherichia coli is the most common aerobic organism isolated from liver abscesses, being demonstrated in specimens from 35 to 45 per cent of patients, with Klebsiella pneumoniae being the second most frequent isolate in this category. Other aerobic Gram-negative bacteria, including Proteus spp., Enterobacter cloacae, Citrobacter spp., Pseudomonas aeruginosa, Morganella morganii, Serratia marsecens, and Acinetobacter and Eikenella spp. may also be isolated, usually in association with other gut flora. Those are particularly common in patients with biliary tract disease.

Anaerobic and microaerophilic organisms, either alone or in conjunction with aerobic organisms, are isolated from up to 60 per cent of pyogenic liver abscesses. Bacteroides fragilis (particularly spp. fragilis) is the most common anaerobe isolated, but such others as other Bacteroides spp., Fusobacterium spp., anaerobic streptococci, Clostridium spp., and Actinomyces spp. may be found on occasion. An important group of organisms are the microaerophilic streptococci, particularly Streptococcus milleri. If appropriate microbiological techniques are employed (especially the provision of an environment enriched with CO&sub2; microaerophilic streptococci may be found to be the most common causes of pyogenic liver abscess. S. milleri is especially virulent and likely to cause suppuration of the liver and other organs.

Other Gram-positive organisms account for less than 25 per cent of isolates. Staphylococcus aureus and group A streptococci occur most commonly after trauma and in children with the previously delineated granulocyte disorders. Seeding of the liver in these individuals usually is secondary to a systemic bacteraemia.

Focal candida infection of the liver and/or spleen has been reported in an increasing number and variety of patients, most notably in those undergoing chemotherapy for leukaemia or liver transplantation. In the leukaemic patient in particular a subacute–chronic entity that has been termed hepatosplenic candidiasis has been defined. This is characterized by persistent fevers and macroscopic abscesses due to Candida spp., most notably C. albicans and C. tropicalis. This process is usually initiated when the patient is neutropenic due to chemotherapy, presumably due to the entrance of the yeast into the portal vein through mucosal ulcerations induced by the chemotherapy. The abscesses and the clinical symptoms persist, however, even after haematological remission has been achieved.

Patients with microscopic liver abscesses usually have an acutely septic clinical presentation, with fever, rigors, and, not uncommonly, hypotension, as well as right upper quadrant discomfort that can be quite severe. Other manifestations depend upon the underlying condition producing the microabscesses: rapidly progressing jaundice in the presence of biliary tract disease, congestive heart failure if the systemic sepsis is associated with endocarditis.

In contrast, the clinical presentation of macroscopic liver abscesses is more subacute, developing over several days to weeks, with fever, night sweats, anorexia, weight loss, and malaise far more common than rigors and hypotension. Fever is present in 90 per cent of these patients, nausea, vomiting, and abdominal pain occur in 50 to 75 per cent, and symptoms such as pleurisy, diarrhoea, dyspnoea, and cough are seen in 5 to 25 per cent of patients.

Other than fever, abdominal tenderness, usually localized to the right upper quadrant, is the most common physical finding, being demonstrable in 50 to 75 per cent of affected individuals. Hepatomegaly is demonstrable in approximately 50 per cent of patients with macroscopic liver abscesses. Jaundice is uncommon, unless biliary obstruction is present.

Almost all patients with pyogenic hepatic abscesses have abnormal haematological and liver function tests. Leucocytosis, usually of a moderate extent, is noted in 70 to 80 per cent, an elevated ESR in at least 90 per cent, and anaemia in 50 to 65 per cent of patients with liver abscess. The most characteristic liver function test abnormality observed in patients with hepatic abscess is an elevated alkaline phosphate level, which is observed in more than 75 per cent of these individuals. An elevated serum bilirubin level is seen in 40 per cent of patients, with elevated transaminases being found in approximately 30 per cent. Other abnormalities that are not uncommon include a prolonged prothrombin time and a raised serum vitamin B&sub1;&sub2; level. Laboratory abnormalities associated with a poor prognosis include an elevated bilirubin and a serum albumin level of 2 g/dl.

Positive blood cultures are obtained in approximately 50 per cent of all patients. Although up to 65 per cent of abscesses are polymicrobial when aspirated pus is cultured from the liver, it is unusual to retrieve more than one organism from the blood cultures.

Chest radiographs are abnormal in about 50 per cent of patients, usually because the inflammatory process within the liver impinges on the diaphragm, producing a variety of ‘sympathetic’ responses. These include a right pleural effusion, right lower lobe atelectasis and pneumonitis, and elevation of the right hemidiaphragm. Occasionally, if a gas-forming organism is present in the abscess, air–fluid levels are discernible on chest or abdominal radiographs. Rarely, a liver abscess presents by discharging itself into the chest, with both clinical symptoms (cough, haemoptysis, dyspnoea) and chest radiographic appearances which reflect this.

Clinical suspicion of a liver abscess (either pyogenic or amoebic) is aroused when a patient has fever, right upper quadrant abdominal pain and tenderness, and abnormal liver function tests (Fig. 1) 1211. The differential diagnosis includes acute cholecystitis, cholangitis, subphrenic or subhepatic abscess, malignancy, and hepatitis.

Ultrasonography is the initial procedure of choice to assess a suspected liver abscess because it is non-invasive, 80 to 90 per cent accurate, and capable of delineating liver lesions as small as 2 cm in diameter. Ultrasound is more useful than computed tomography (CT) for distinguishing solid masses from cystic lesions. However, ultrasonography may miss lesions in the dome of the right liver lobe or multiple microscopic abscesses. Fatty infiltration can produce an echogenic liver, making detection of small abscesses difficult. Although some features of amoebic abscesses differ on ultrasound from those of pyogenic origin, the differences are not sufficient to permit a specific diagnosis.

Abdominal CT can detect intrahepatic collections as small as 0.5 cm in diameter and can be particularly useful in identifying multiple small abscesses or abscesses located near the hemidiaphragm. The diagnostic accuracy of CT is 90 to 95 per cent. Another advantage of CT is that it may identify other abdominal pathology responsible for the pyogenic liver abscess.

Although radionuclide scans of the liver have a sensitivity comparable to that of ultrasonography in detecting liver abscesses, nuclide scans have largely been replaced by ultrasonography and by CT, at least in part, because either sonography or CT allows the clinician to proceed directly to percutaneous aspiration for either diagnosis or therapy. Any material obtained by aspiration should be examined microscopically after Gram staining, cultured aerobically and anaerobically, and, if there is any suspicion clinically or epidemiologically, submitted for examination for Entamoeba histolytica trophozoites. Fungal and mycobacterial cultures should also be carried out, particularly in immunosuppressed patients.

The traditional approach to the therapy of pyogenic liver abscesses has been open surgical drainage of the abscess, correction, whenever possible, of the underlying pathology that led to the abscess, and a 4- to 6-week course of parenteral antibiotics (Fig. 2) 1212. Such antibiotics have usually included a &bgr;-lactam, an aminoglycoside, and either metronidazole or clindamycin (aimed at the anaerobic organisms), but treatment could be modified on the basis of microbiological results. Over the past decade, the majority of patients with macroscopic pyogenic abscesses have been managed with antibiotics and percutaneous drainage, thus avoiding more surgery in typically debilitated patients.

Percutaneous drainage is carried out under CT or ultrasound guidance, with the insertion of a pigtail catheter using the Seldinger technique. Samples are then withdrawn for microbiological examination, the abscess cavity is gently irrigated with saline, and the catheter is left in place to provide continuing drainage. More than one catheter may need to be placed to provide complete drainage. Such percutaneous aspiration and drainage does not correct the problem in 10 to 30 per cent of patients, and open drainage is then necessary. Failure to achieve drainage may be due to poor catheter placement, to the presence of a multiloculated abscess, to excessive viscosity of the abscess contents causing plugging of the drainage catheters, to thick abscess walls that do not collapse with drainage, and to inadequate anatomical localization of the abscess. Follow-up ultrasonography or CT scanning is necessary to ensure complete resolution of the process.

Percutaneous drainage is less likely to be of value when there are multiple abscesses, a known intra-abdominal source of infection that requires surgical correction, and abscess of unknown cause, ascites, or when the abscess requires a transpleural drainage route.

Patients with biliary tract disease, diverticulitis, and appendicitis as the source for their liver abscesses are better treated with open surgical drainage, than by percutaneous drainage. Guidelines other than those mentioned to recommend percutaneous or an open surgical approach to these patients are still being formulated.

Mortality rates of patients with macroscopic liver abscesses reported in the 1960s and early 1970s were 65 to 79 per cent. Recent studies have noted a marked improvement, with mortality rates being as low as 11 per cent. Such improvement is due to the widespread availability of ultrasonography and CT scanning and hence earlier diagnosis, and the utility of the percutaneous approach to drainage, especially in debilitated patients, who tolerate conventional surgery poorly. The major determinants of mortality are the nature of the underlying process causing the abscess, the anatomy of the intrahepatic infection, and the presence or absence of such comorbidity factors as cancer, diabetes, heart disease, and renal failure.

Entamoeba histolytica infection affects an estimated 10 per cent of the world's population, with the great majority of such infections occurring in people living in sub-Saharan Africa, the Indian subcontinent, Asia, and parts of Central and South America. In these endemic areas approximately 50 per cent of the population is infected, with 90 per cent or more being asymptomatic cyst passers. In more developed countries, amoebic infection occurs predominantly in immigrants or travellers returning from endemic areas, in sexually active male homosexuals, in residents of Indian reservations, and in people institutionalized for mental or emotional disability. The common denominator in these last groups is an increased opportunity for person-to-person spread via the faecal–oral route.

Amoebic liver abscess occurs in less than 10 per cent of individuals infected with this organism. Whereas amoebic infection of the liver is far less common than is pyogenic infection in the United States, in areas of the world such as India, amoebic abscesses are 3 to 5 times as frequent as pyogenic liver abscesses. The average age of patients with amoebic liver abscess is between 28 and 48 years, which is significantly younger than patients with pyogenic infection (Table 1) 358. Although infection rates are similar in men and women, there is a striking male predominance (up to 20:1) in patients who develop hepatic abscesses from amoebiasis. Particularly severe invasive disease occurs in patients with compromised cellular immunity, in young infants, in the malnourished, in pregnant women, and in patients receiving corticosteroids.

Amoebiasis is initiated by the ingestion of E. histolytica cysts. Once these cysts reach the small intestine, motile trophozoites are released and migrate to the colon, where they proliferate along with the resident bacterial flora. In most cases the organism becomes a commensal. There is some evidence that virulence of different strains can be correlated with a particular isoenzyme pattern of key enzymes which can be isolated from the trophozoites. Other important determinants of invasiveness probably include the inherent virulence of the organism, diet, the constituents of the bacterial flora of the gut, and both humoral and cell-mediated host resistance.

Once intestinal infection is established, amoebae may be carried to the liver via the portal vein. Within the liver these organisms multiply and block small intrahepatic portal radicals, causing focal infarction of hepatocytes. A proteolytic enzyme produced by the invading trophozoites causes coalescence of the invaded areas and abscess formation. Some authorities differentiate between so-called amoebic hepatitis and amoebic hepatic abscess, depending upon whether or not a macroscopic abscess has formed. We regard this differentiation as a difficult one, as this process might best be regarded as a continuum rather than as two separate entities.

At the time of clinical presentation, approximately 80 per cent of amoebic liver abscesses are solitary; 83 per cent of them are located in the right lobe of the liver, characteristically high in the dome subjacent to the diaphragm. The propensity for this site reflects the fact that venous return from the right side of the colon (amoebic infection having a particular impact on the caecum and right colon) into the portal vein is predominantly delivered to the right lobe of the liver. The juxtaposition of these abscesses to the diaphragm explain the common occurrence of thoracic symptoms in these patients. Discharge of amoebic hepatic abscesses into the subphrenic, pleural, and even into pericardial spaces is not uncommon, with frank rupture into the lung as an uncommon complication.

Amoebic abscesses can become extremely large, containing several litres of fluid that is classically described as ‘anchovy sauce’ but may be yellow or green. This fluid is primarily necrotic liver tissue and blood, with a paucity of inflammatory cells unless bacterial superinfection has occurred. Because bile appears to have a deleterious effect on amoebae, infection of the gallbladder and bile ducts does not occur.

Amoebic liver abscess has a more subacute presentation than that of pyogenic liver abscess. Symptoms typically evolve over a few weeks to months (as opposed to several days to weeks for a pyogenic process) before medical attention is sought. Initial symptoms are non-specific: fever, anorexia, night sweats, malaise, anorexia, nausea and vomiting, and weight loss. As the disease becomes established, right upper quadrant abdominal pain becomes a dominating symptom in at least two-thirds of these patients. Approximately 25 per cent of patients exhibit thoracic symptoms, such as pleurisy, non-productive cough, right shoulder pain, and/or hiccups as an important part of the symptom complex. Characteristically, simultaneous intestinal complaints such as dysentery or diarrhoea are not present. Uncommonly, patients may have a more acute presentation, suggesting an acute abdominal surgical emergency.

The patients typically appear chronically ill, with fever, abdominal tenderness, and hepatomegaly. Chest findings (râles, decreased breath sounds, dullness to percussion, impaired diaphragmatic movement) are observed in 50 per cent of patients. Jaundice is rare (less than 15 per cent of individuals).

Anaemia and an elevated erythrocyte sedimentation rate are present in at least 80 per cent of patients, as well as a moderate leucocytosis in 60 to 75 per cent. More extreme white blood cell responses suggest the presence of bacterial superinfection. Eosinophilia is not observed in patients with amoebic liver abscesses; if present, another explanation should be sought. Normal liver function tests do not exclude the diagnosis of an amoebic abscess, although slight to moderate elevations of the alkaline phosphatase, reduction in the serum albumin, and minimal changes in transaminase values are generally observed.

Positive blood cultures are obtained in up to 20 per cent of patients with amoebic abscess with secondary bacterial infection. Aspirated abscess fluid may also be culture positive for bacteria. Stool examination may reveal trophozoites or cysts in up to 25 per cent of patients.

The typical location of an amoebic abscess in the dome of the right lobe of the liver produces not only thoracic symptoms, but also abnormalities on chest radiograph: an elevated right hemidiaphragm, pleural effusion, and atelectasis are the most common.

In areas of the world free of endemic amoebiasis, serological testing is extremely useful in evaluating the patient for an amoebic liver abscess (Fig. 1) 1211. The indirect haemagglutination test is positive in 90 to 95 per cent of patients with an amoebic abscess, and in areas of low prevalence a positive result strongly suggests the presence of acute infection. False-negative tests are usually obtained early in the disease course. Levels of haemagglutinating antibodies remain elevated for many years after an episode of invasive disease, and the indirect haemagglutination test is therefore less useful in diagnosing acute disease in endemic regions, where 50 per cent of the general population may be seropositive. Levels of antibodies detectable by counterimmunoelectrophoresis and indirect immunofluorescence usually become undetectable within 6 months of acute infection; they may be more useful in evaluating patients in endemic areas.

Since amoebic abscesses, unlike most pyogenic liver abscesses, respond to antimicrobial therapy without drainage, a non-invasive approach to diagnosing amoebic infection is needed. In the patient with subacute disease in whom the problem is a diagnostic dilemma rather than a therapeutic emergency, amoebic serology should be performed and a therapeutic trial is initiated if the patient has an appropriate epidemiological history. If the patient is unstable, if there is reason to suspect a pyogenic component to the illness on the basis of clinical or epidemiologic findings, if the amoebic serology is negative, or if the patient has failed to respond clinically to several days of antiamoebic therapy, a percutaneous needle aspiration should be performed.

Most amoebic abscesses are cured with a regimen of metronidazole 750 mg orally or intravenously three times per day, for 10 days, followed by treatment with an agent that is effective in eradicating the cysts which may persist in the intestine after treatment with metronidazole (Fig. 3) 1213. Agents effective in the treatment of such luminal disease include iodoquinol 650 mg orally three times per day for 20 days, diloxanide furoate 500 mg orally three times per day for 10 days, or paramomycin 25 to 30 mg/kg.day orally in three divided doses for 7 days.

Most patients show a prompt therapeutic response to metronidazole, with defervescence and decreased abdominal pain within 3 or 4 days. This response is useful for differentiating amoebic and pyogenic abscesses in situations where serological testing is unavailable or uninterpretable. Fewer than 10 per cent of patients with amoebic liver abscess fail to respond to metronidazole therapy. Treatment in the non-responders is with dihydroemetine (1–1.5 mg/kg.day, maximum dose 90 mg/day intramuscularly for 5 days) plus chloroquine phosphate (600 mg base/day for 2 days, followed by 300 mg of chloroquine base orally daily for 2–3 weeks). This regimen should be followed by treatment with an agent active against luminal disease.

Considerable controversy surrounds the role of percutaneous drainage in the management of amoebic liver abscesses. Proposed indications for such drainage include liver abscesses in the left lobe of the liver, because of the risk of rupture into the pericardial sac, drainage of large abscesses to facilitate more rapid healing with chemotherapy, and lack of response to metronidazole therapy. However, because of the risk of introducing bacteria during catheter drainage, we reserve a drainage procedure for patients in whom the differentiation between pyogenic and amoebic infection is unclear, for acutely ill patients, for patients who have failed to respond to therapy, and for patients whose infection has spread into adjoining structures.

Treatment of an amoebic hepatic abscess is usually successful, mortality being associated only with delayed diagnosis or complications such as bacterial superinfection, or rupture into adjoining structures.

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