Focal inflammatory diseases of the liver
Introduction
Hepatic abscess is defined as a localized collection of purulent material in liver with associated destruction of hepatic parenchyma and stroma [1]. The incidence of liver abscess is low compared to that of other focal liver lesions. Early diagnosis of these lesions has important prognostic and therapeutic implications [1], [2], [3]. An abscess may be either pyogenic, amebic or fungal in origin. In developed countries most abscesses are pyogenic. However on a worldwide basis Entamoeba histolytica is the most commonly encountered organism. Uncommonly abscess from actinomycosis or mycobacterium may also occur. Fungal abscess is most often seen in immunosuppressed patients and most often caused by Candida albicans. Distinction between the causative agents has vital importance with regard to the prognosis and the preferred therapeutic approach. Pyogenic abscess is treated with percutaneous drainage and antibiotic therapy whereas amebic and fungal abscesses should not be initially drained. Instead amebic abscess is treated with metronidazole and fungal abscess is treated with antifungal agents such as amphotericin and no drainage is usually needed [1], [4], [5].
Hepatic abscess can be classified into four main categories according to their origin: portal, biliary, arterial and direct extension. Portal venous system is one of the most common way of spread especially for pyogenic and amebic abscesses. Localized collections in the abdomen such as diverticulitis and appendicitis may first spread into superior or inferior mesenteric vein then into the main portal vein and liver. An aggressive early operation in patients with suspected appendicitis led to a marked reduction in the number of complicating liver abscesses. Biliary seeding is seen in cases of cholangitis with or without accompanying biliary obstruction. Hepatic arterial seeding is the usual mode of spread for fungal abscesses and in patients with septicemia. Although rare, hepatic abscesses secondary to direct extension from a contigious infection or a penetrating trauma is also encountered [6]. Abscesses can be characterized according to their stage of evolution, regardless of the etiology [1]. Within the first 10 days of infection, necrosis with small areas of liquefaction is predominant. At 10–15 days,which is the subacute phase, necrotic cellular debris starts to be resorbed and liquefaction starts to predominate. In the chronic phase (after 15 days) only a small amount of necrotic debris is evident centrally surrounded by a thick fibrous wall. Later on calcification may form in the thick wall of the abscess [4], [7]. The radiological appearance of an abscess is variable depending on the pathological stage of the infection.
Section snippets
Pyogenic abscesses
Pyogenic liver abscesses most commonly occur in older patients with cancer, biliary disease, trauma, bacteremia and history of prior surgery [3], [8], [9], [10], [11]. In the preantibiotic era, appendicitis was the most common cause of hepatic abscesses. Solitary hepatic abscesses are often cryptogenic with no obvious predisposing etiology [11], [12]. Nearly half of pyogenic liver abscesses are polymicrobial. E. coli is the most common causuative organism. Anaerobic bacteria like Clostridia and
Ultrasonography
On US, pyogenic abscesses have variable appearance depending on the morphology and content of the lesions. They are often hypoechoic; however depending on the distribution of necrotic debris they may be focally echogenic, diffusely echogenic or they may contain fluid-debris levels. The very intensely echogenic lesions are due to the presence of air within the abscess cavity [21]. Sonographically liver abscesses often have irregular walls with poor deffinition. Thicker walls are seen in chronic
Amebic liver abscess
Amebiasis is a worldwide health problem with 10% of the world population infected with E. histolytica [35]. Invasive amebiasis may be confined to the intestinal tract or may spread by direct extension and/or hematogenous disemination [36]. Amebic liver abscess is the most common extraintestinal complication of amebiasis and occurs in approximately 8.5% of all patients with amebic infection. Variability in clinical presentation, a low index of suspicion for amebic infection, difficulty in
Ultrasonography
US has led to early diagnosis of amebic abscess. Classical US findings were described by Ralls et al. (1) Absence of significant wall echoes; (2) round or oval shape; (3) lower echogenicity than normal liver with fine, homogenous low-level internal echoes at high gain; (4) contiguity with the liver capsule, and (5) distal acoustic enhancement (Fig. 4A) [41], [42]. However only one third of patients with amebic abscess showed all five features – a pattern suggestive but not pathognomonic of
Candidiasis
Fungal infection of the liver and spleen occur in individuals with compromised host defense mechanisms. Upto 40% of patients with hematopoietic malignancy develop fungal infection [48], [49], [50]. Most hepatic fungal abscesses are caused by Candida albicans [51]. Involvement of the liver with Candida has been demonstrated in 50–75% of patients with acute leukemia and 50% of those with lymphoma at autopsy [48], [52], [53]. Aspergillus, cryptococcus, histoplasmosis, and mucormycosis are less
Ultrasonography
On US, Pastakia et al. described four different patterns for hepatic microabscesses from Candidiasis: (1) discrete hypoechoic nodule (most common form); (2) bull’s eye configuration (central echogenic nidus surrounded by a hypoechoic rim); (3) discrete echogenic focus with variable degrees of acoustic shadowing; (4) wheel within a wheel appearance [57]. None of these patterns are specific for Candidiasis and may occur in lymphoma, leukemia, Kaposi’s sarcoma and metastatic disease [58].
Computed tomography
CT is
Tuberculosis
Hepatic tuberculosis is commonly associated with miliary tuberculosis and found in 80–100% of autopsied patients with disseminated pulmonary tuberculosis [66]. Hepatic tuberculosis develops under micro- or macronodular forms. The micronodular form of hepatic involvement is observed in the miliary form of pulmonary tuberculosis and is usually noted as moderate hepatomegaly [67], [68]. On US, micronodular form of hepatic involvement may show diffuse hyperechogenicity, the ‘bright liver’ pattern
Hydatid disease
Hydatid disease caused by Echinococcus granulosus is an endemic disease in some parts of the world where sheep herding is a common occupation. The highest incidence is seen in the Middle-East, Mediterranean, Latin American countries, and Australia [80]. The life-cycle typically involves two hosts. The definitive host is a carnivore, – usually a dog – in the gut of which the adult worm lives and sheds its ‘eggs’ in the host feces. The intermediate host is a herbivore – cattle, sheep, goats, and
Imaging
US, CT and MR are used as screening modalities for the diagnosis of hydatid cysts. Although the diagnosis of hydatid disease has been facilitated with cross-sectional imaging modalities, some cysts may still present a diagnostic dilemma.
Hepatic fascioliasis
Fasciola hepatica is a trematode that affects herbivorous animals, mostly sheep and cattle. Man is an accidental host during the life cycle of the parasite and infected after ingestion of watercress, contaminated water, raw fish or contaminated cattle or sheep liver. When the metacercaria hatches in the intestine, immature fluke penetrates the intestinal wall and migrates through the peritoneal cavity. Then, it penetrates Glisson’s capsule and enters liver parenchyma. This is the first stage of
Ascariasis
Ascaris roundworm is endemic in Far East, Russia, Latin America and Africa and infests one quarter of the world’s population. The adult worm lives mainly in the jejunum and may move from duodenum to common bile duct. Then it may enter the gallbladder or intrahepatic bile ducts. Biliary complications are often seen in children in highly endemic areas. US is the method of choice for suspected biliary ascariasis [111], [112]. Worms are usually seen in the main bile duct and/or gallbladder. On real
Schistosomiasis
Schistosomiasis is a parasitic disease caused by S. mansoni, S. hematobrium, and S. japonicum. The schistosomes live in the bowel lumen and lay eggs in the mesenteric veins. The egss may embolize to portal vein where they cause a granulomatous reaction, causing fibrosis and presinusoidal portal hypertension. The inflammation involves the portahepatic and does not invade the lobules so the architecture is not destroyed.
On US, the liver shows an area of increased echogenicity at the porta hepatis
Sarcoidosis
Hepatic involvement with sarcoidosis is not uncommon, and sarcoidosis is reported as the most common cause of hepatic granulomas [118]. The changes are mostly seen in periportal location rather than intraparenchymally and result in portal hypertension. US usually can not show hepatic focal sarcoid lesions although heterogenous and/or increased echogenicity with organ enlargement has been reported [119], [120]. CT scan shows diffuse hepatosplenomegaly but focal hepatic lesions were detected in
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Chapter 73 - Amebiasis and other parasitic infections
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2012, Blumgart's Surgery of the Liver, Biliary Tract and PancreasAbdominal MRI advances in the detection of liver tumours and characterisation
2007, Lancet OncologyCitation Excerpt :A dual-contrast MRI examination combining gadolinium and SPIO-enhanced imaging could be the most accurate magnetic resonance technique for detection of hepatic tumours.46 MRI can classify different liver lesions more accurately than multidetector CT.4,35 In patients with cancer, incidental liver cysts, haemangiomas, focal nodular hyperplasia, adenomas, and other benign hepatic diseases are easily depicted and correctly identified by combination of the information from the comprehensive liver magnetic resonance examination.47–52 Every benign liver lesion has a characteristic appearance on T1-weighted, T2-weighted, diffusion imaging, and dynamic gadolinium-enhanced and SPIO-enhanced MRI.