Hepatic abscess
BACTERIAL:
Background:
Bacterial abscess of the liver is relatively rare. It has been described since the time of Hippocrates (400 BC), with the first published review by Bright appearing in 1936. In 1938, Ochsner's classic review heralded surgical drainage as the definitive therapy; however, despite the more aggressive approach to treatment, the mortality rate remained at 60-80%. The development of new radiologic techniques, the improvement in microbiologic identification, and the advancement of drainage techniques, as well as improved supportive care, have decreased mortality rates to 5-30%; yet, the prevalence of the condition has remained relatively unchanged. Untreated, this infection remains uniformly fatal.
The 3 major forms of liver abscess, classified by etiology, are as follows:
- Pyogenic abscess, which is most often polymicrobial, accounts for 80% of hepatic abscess cases in the United States.
- Amoebic abscess due to Entamoeba histolytica accounts for 10% of cases.
- Fungal abscess, most often due to Candida species, accounts for less than 10% of cases.
Pathophysiology:
The liver receives blood from both the systemic and portal circulations. Increased susceptibility to infections would be expected given the increased exposure to bacteria. However, Kupffer cells lining the hepatic sinusoids clear bacteria so efficiently that infection rarely occurs. Multiple processes have been associated with the development of hepatic abscesses.
- Appendicitis was traditionally the major cause of liver abscess. As diagnosis and treatment of this condition has advanced, its frequency as a cause for liver abscess has decreased to 10%.
- Biliary tract disease is now the most common source of pyogenic liver abscess (PLA). Obstruction of bile flow allows for bacterial proliferation. Biliary stone disease, obstructive malignancy affecting the biliary tree, stricture, and congenital diseases are common inciting conditions. With a biliary source, abscesses usually are multiple, unless they are associated with surgical interventions or indwelling biliary stents. In these instances, solitary lesions can be seen.
- Infections in organs in the portal bed can result in a localized septic thrombophlebitis, which can lead to liver abscess. Septic emboli are released into the portal circulation, trapped by the hepatic sinusoids, and become the nidus for microabscess formation. These microabscesses initially are multiple but usually coalesce into a solitary lesion.
- Microabscess formation can also be due to hematogenous dissemination of organisms in association with systemic bacteremia, such as endocarditis and pyelonephritis.
- Cases also are reported in children with underlying defects in immunity, such as chronic granulomatous disease and leukemia.
- Abscesses can result from fistula formation between local intra-abdominal infections. Of abscesses, 4% develop in this manner. Despite advances in diagnostic imaging, cryptogenic causes account for a significant proportion of cases; surgical exploration has impacted this minimally. These lesions usually are solitary in nature.
- Penetrating hepatic trauma can inoculate organisms directly into liver parenchyma, resulting in PLA.
- Nonpenetrating trauma results in localized hepatic necrosis, intrahepatic hemorrhage, and bile leakage due to disruption of canaliculi. The resulting tissue environment permits bacterial growth with resultant PLA. Lesions of this etiology typically are solitary in nature.
- PLA has been reported as a secondary infection of amoebic abscess, hydatid cystic cavities, and metastatic and primary hepatic tumors.
- It also has been a complication of liver transplantation, hepatic artery embolization in the treatment of hepatocellular carcinoma, and the ingestion of foreign bodies, which penetrate the liver parenchyma. Trauma and secondarily infected liver pathology account for a small percentage of liver abscess cases.
The right hepatic lobe is affected more often than the left by a factor of 2:1. Bilateral involvement is seen in 5% of cases. The predilection for the right lobe can be attributed to anatomic considerations. The right hepatic lobe receives blood from both the superior mesenteric and portal veins, whereas the left lobe receives inferior mesenteric and splenic drainage. It also contains a denser network of biliary canaliculi and, overall, accounts for more hepatic mass. Studies have suggested that a streaming effect in the portal circulation is causative.
Frequency:
The incidence of pyogenic liver abscess remained unchanged over the past 70 years. In the United States, the incidence of pyogenic liver abscess is estimated to be 8-15 cases per 100,000 population. This figure is considerably higher in countries where health care is not readily available. The male-to-female ratio is approximately 2:1 in recent studies, and the problem occurs most commonly in the fourth to sixth decade of life.
Aetiology:
Biliary disease accounts for 21-30% of reported cases. Extrahepatic biliary obstruction leading to ascending cholangitis and abscess formation is the most common cause and is usually associated with choledocholithiasis, benign and malignant tumors, or postsurgical strictures. Biliary-enteric anastomoses (choledochoduodenostomy or choledochojejunostomy) have also been associated with a high incidence of liver abscesses. Biliary complications (eg, stricture, bile leak) after liver transplantation are also recognized causes of pyogenic liver abscesses. Infection via the portal system (portal pyaemia). The infectious process originates within the abdomen and reaches the liver by embolization or seeding of the portal vein. With the liberal use of antibiotics for intra-abdominal infections, portal pyemia is now a less frequent cause of pyogenic liver abscesses but still accounts for 20% of cases.
Appendicitis and pylephlebitis are the predominant causes. However, any source of intra-abdominal abscess, like acute diverticulitis, inflammatory bowel disease, and perforated viscus, can lead to portal pyaemia and hepatic abscesses.
Haematogenous (via the hepatic artery): this infectious process results from seeding of bacteria into the liver in cases of systemic bacteremia from bacterial endocarditis, urinary sepsis, or following intravenous drug abuse.
Blunt or penetrating trauma and liver necrosis from inadvertent vascular injury during laparoscopic cholecystectomy are recognized causes of liver abscess.
Cryptogenic: no cause is found in approximately half the cases. However, the incidence is increased in patients with diabetes or metastatic cancer. Patients with repeated cryptogenic liver abscess should undergo biliary and gastrointestinal evaluation.
Pathophysiology:
Pyogenic bacteria can gain access to the liver by direct extension from contiguous organs or through the portal vein or hepatic artery. Hepatic clearance of bacteria via the portal system appears to be a normal phenomenon in healthy individuals; however, organism proliferation, tissue invasion, and abscess formation can occur with biliary obstruction, poor perfusion, or microembolization.
Microbiology:
The organisms isolated most often are included below. Most abscesses contain more than one organism and frequently are of biliary or enteric origin. Blood culture results are positive in 33-65% of cases, with positive results from abscess cultures reported in 73-100% of series. Escherichia coli is the most common organism isolated in western series, while Klebsiella pneumoniae has recently emerged as a common isolate in patients with diabetes in Taiwan.
The most common microorganisms isolated from blood and abscess cultures are as follows:
- E coli - 33%
- K pneumoniae - 18%
- Bacteroides species - 24%
- Streptococcal species - 37%
- Microaerophilic streptococci - 12%.
AMOEBIC:
Background:
Amoebic liver abscess is the most frequent extraintestinal manifestation of Entamoeba histolytica infection. This infection is caused by the protozoa E histolytica, which ascends the portal venous system. Amoebic liver abscess is an important cause of space-occupying lesions of the liver, mainly in developing countries. Prompt recognition and appropriate treatment of amebic liver abscess lead to improved morbidity and mortality rates.
Pathophysiology:
E histolytica exists in 2 forms. The cyst stage is the infective form, and the trophozoite stage causes invasive disease. People who chronically carry E histolytica shed cysts in their faeces; these cysts are transmitted primarily by food and water contamination. Rare cases of transmission via oral and anal sex or direct colonic inoculation through colonic irrigation devices have occurred. Cysts are resistant to gastric acid, but the wall is broken down by trypsin as it passes through the small intestine. Trophozoites are released and colonize the cecum. To initiate symptomatic infection, E histolytica trophozoites present in the lumen must adhere to the underlying mucosa and penetrate the mucosal layer. Liver involvement occurs following invasion of E histolytica into mesenteric venules. Amoebae then enter the portal circulation and travel to the liver where they typically form large abscesses. The abscess contains acellular proteinaceous debris, which is thought to be a consequence of induced apoptosis and is surrounded by a rim of amoebic trophozoites invading the tissue.
The right lobe of the liver is more commonly affected than the left lobe. This has been attributed to the fact that the right lobe is supplied predominantly by the superior mesenteric vein, whereas the left lobe is supplied by the splenic vein.
Frequency:
In the US: Amebic liver abscess is rare and currently is seen almost exclusively in immigrants or travelers. In 1994, 2,983 cases of amebiasis were reported to the Centers for Disease Control (CDC). The disease was removed from the National Notifiable Diseases Surveillance System in 1995. The overall prevalence of amebic infection can be as high is 4%. An estimated 4% of patients with amebic colitis develop an amebic liver abscess. An estimated 10% of the population is infected with Entamoeba dispar. Previously thought to be a nonpathogenic strain of E histolytica, this type of amoeba does not produce clinical symptoms even in the immunocompromised host.
Internationally: Worldwide, approximately 40-50 million people are infected annually, with the majority of infections occurring in developing countries. The prevalence of infection may be as high as 50% in less-developed areas. The highest prevalence is found in developing countries in the tropics, particularly in Mexico, India, Central and South America, and tropical areas of Asia and Africa.
AMH









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The development of new
The development of new radiologic techniques, the improvement in microbiologic identification, and the advancement of drainage techniques, as well as improved supportive care, have decreased mortality rates to 5-30%; yet, the prevalence of the condition has remained relatively unchanged. Untreated, this infection remains uniformly fatal.
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E histolytica exists in 2
E histolytica exists in 2 forms. The cyst stage is the infective form, and the trophozoite stage causes invasive disease. People who chronically carry E histolytica shed cysts in their feces; these cysts are transmitted primarily by food and water contamination. Rare cases of transmission via oral and anal sex or direct colonic inoculation through colonic irrigation devices have occurred. Cysts are resistant to gastric acid, but the wall is broken down by trypsin in the small intestine. Trophozoites are released and colonize the cecum. 70-630 To initiate symptomatic infection, E histolytica trophozoites present in the lumen must adhere to the underlying mucosa and penetrate the mucosal layer. 642-456 Liver involvement occurs following invasion of E histolytica into mesenteric venules. Amebae then enter the portal circulation and travel to the liver where they typically form large abscesses. The Gal/GalNAc lectin is an adhesion protein complex that sustains tissue invasion.1 The abscess contains acellular proteinaceous debris, which is thought to be a consequence of induced apoptosis2 and is surrounded by a rim of amebic trophozoites invading the tissue. 70-562 The right lobe of the liver is more commonly affected than the left lobe. This has been attributed to the fact that the right lobe portal laminar blood flow is supplied predominantly by the superior mesenteric vein, whereas the left lobe portal blood flow is supplied by the splenic vein.