ABSCESSO HEPTICO AMEBIANO PDF
Estes resultados mostram que o teste de ELISA foi de maior sensibilidade (% i de sensibilidade) no diagnóstico do abscesso hepático amebiano, quando. Chaves L.C. Abscesso Amebiano do Fígado, Dissertação (Mestrado em Cirurgia Moraes L.A. Estudo clínico de casos de abscesso hepático amebiano do. do CA um caso clínico. Palavras Chave. Abcesso hepático amebiano · CA · CA Resumo. Introduçao: O abcesso amebiano é a.
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Amebiasis can be considered the most aggressive disease of the human intestine, responsible in its invasive form for clinical syndromes, ranging from the classic dysentery of acute colitis he;tico extra-intestinal disease, with emphasis on hepatic amebiasis, unsuitably named amebic liver abscess. Found worldwide, with a high incidence in India, tropical regions of Africa, Mexico and other areas of Central America, it has been frequently reported in Amazonia.
The trophozoite reaches the liver through the portal system, provoking enzymatic focal necrosis of hepatocytes and multiple micro-abscesses that coalesce to develop a single lesion whose central cavity contains a homogeneous thick liquid, with typically reddish brown and yellow color similar to “anchovy paste”.
Amebiqno upper quadrant pain, fever and hepatomegaly are the predominant abscessk of hepatic amebiasis. Jaundice is reported in cases with multiple lesions or a very large abscess, and it affects the prognosis adversely. Besides chest radiography, ultrasonography and computerized tomography have brought remarkable contributions to the diagnosis of hepatic abscesses.
The conclusive diagnosis is made however by the finding of Entamoeba histolytica trophozoites in the pus and by the detection of serum antibodies to the amoeba. During the evolution of hepatic amebiasis, in spite of the availability of highly effective drugs, some important complications may occur with regularity and are a result of local perforation with extension into the pleural bascesso pericardium cavities, causing pulmonary abscesses and purulent pericarditis, respectively The ruptures into the abdominal cavity may lead to subphrenic abscesses and peritonitis.
The treatment of hepatic amebiasis is made by medical therapy, with metronidazole as the initial drug, followed by a luminal amebicide. In patients with large abscesses, showing signs of imminent rupture, and especially those who do not respond to medical treatment, a percutaneous drainage must be performed with either ultrasound or heeptico tomography guidance.
Surgical drainage by laparotomy is reserved to patients with secondary heptick. Entamoeba histolyticahepatic ameabiasis. Amebiasis is the most aggressive protozoal disease that heptoco the human bowel, considered the second or third leading cause of death amongst the parasitic diseases, surpassed only by malaria and schistosomiasis.
In spite of the great number of asymptomatic patients infected by Entamoeba dispar or even amebianl some strains of Entamoeba histolytica that remain in the luminal surface of the bowel, amebiasis in its invasive form, is responsible for enteric syndromes, ranging from frank dysentery to fulminant colitis, which heptiico highly lethal. Once through the bowel wall, trophozoites invade the portal circulation and disseminate systemically, reaching the liver to cause hepatic amebiasis.
Reported in the metropolitan regions of developing countries, hepatic amebiasis is endemic in Thailand, India, Egypt and South Africa, with high mortality rates . In Mexico, a national serosurvey demonstrated that 8. In Brazil, though there is lack of national reports, the incidence of hepatic amebiasis differs from one region to another, being uncommon in the south and prevalent in the north [3,4].
In this region hepatic amebiasis is very important and amebinao high frequency has been reported by different investigators  Table 1. Until now, it remains unclear why hepatic amebiasis is more common in asbcesso than heptixo women.
Individuals in the fourth and fifth decades of life are most commonly afflicted. The trophozoite may remain confined to the intestinal lumen as a simple hepico, feeding on bacteria and cellular debris. Sometimes, however, depending on the genetic and immunoenzymatic profile, and the parasite’s asbcesso to produce proteolytic enzymes and to resist to complement-mediated lysis, the trophozoite becomes virulent, and starts its invasion of the intestinal mucosa.
It can then establish persistent extra-intestinal infection throughout the portal veins radicles, most commonly in the liver . In regions where amebiasis is endemic, a variety of conditions, including climate conditions, overcrowding, ignorance, poverty, malnutrition, suboptimal sanitation, impaired cellular and humoral immunity, play an important role in this exacerbation .
Following depression of the protective mucus blanket, trophozoites attach to the cells of interglandular epithelium and, with the aid of proteolytic enzymes that degrade elastin, collagen and fibronectin, especially cysteine proteinase, phospholipase and hemolysin , they invade the colonic epithelium by disruption of the extra cellular matrix.
The first signal of colonic aggression may be manifested as a non-specific thickening of the mucosa or by pinhead-size micronodules, visible by sigmoidoscopy. Peptide-mediated lysosome enzymes released by the lysed polymorphonuclear leucocytes and monocytes, contribute to the destruction of host tissue and extend the lesion. The trophozoites invade the submucosa and spread out laterally, creating the classic flask-shaped amebic ulcer  Figure 1.
Histopathology shows necrotic areas and vascular congestion. There is little inflammation in contrast with the extension of the lesion. The amoebas may be found in the surface layer of the ulcers or in adjacent sites .
Invading the small vessels of submucosa, the trophozoites gain access to the superior mesentery, and disseminating throughout the blood stream, they reach the portal system to cause microembolus and infarction of small vascular branches. Resisting complement-mediated lysis, the trophozoites pass to the liver, causing areas of focal necrosis. Amebic lysis of neutrophils at the edge of the lesion, releases mediators, and this leads to hepatocyte death, extending the damage to distant hepatic cells and increasing the number of small lesions that coalesce to develop a larger hepatic lesion, which is unsuitably named the amebic abscess.
The content of its central cavity is a thick, clotty exudate. This is generally homogeneous, and varies in color, ranging from creamy-white to dirty brown and pink, similar to “anchovy sauce”  Figure 2. This material is almost always sterile, except when a secondary infection has occurred, allowing differential diagnosis from a pyogenic abscess.
The amebae can be found at the edge of the lesion, but are rarely detected in the pus or within the abscess cavity itself . The hepatic lesion is usually solitary, and most frequently is located in the right lobe, situated contiguously with the liver capsule.
This may be explained by the larger volume of the right lobe, which receives most of the venous drainage from the right colon, a segment of the bowel frequently affected by intestinal amebiasis .
The amebic lesions of the left lobe are less common, and multiple abscesses may occur in advanced cases of amebiasis. The clinical manifestations of hepatic amebiasis are so typical that they might suggest the diagnosis in the areas where it is prevalent, such as in Amazonia. Some days or months after the onset of classic dysentery, or as usually happens, without any symptoms or a history of intestinal amebiasis, the clinical features begin to appear.
Despite the size and the site of the hepatic lesion, the most common symptoms are fever, pain and hepatomegaly. It is often very high, continuous or intermittent and accompanied by chills, weakness and profuse perspiration.
In chronic forms the fever is low and develops more gradually, without chills or sweating. It starts as a feeling of heaviness, and then becomes a sharp pain that increases according to the position of the body, compelling the patient to find relief in bed by turning to the opposite side of the lesion.
In abscesses of the right lobe the pain is felt in the right hypochondria, in the right subcostal area or in the cystic point, and may radiate to the shoulder, right side of the neck or the back.
In abscesses of the left lobe, the abscssso is located in the epigastria and left hypochondria and radiates to the left back and left scapular regions. Besides these prevailing symptoms, patients may also abscess of malaise, nausea, vomiting, anorexia and weight loss. In some patients, when diarrhea is absent sigmoidoscopy may show the amebic ulcers .
Its appearance suggests the existence of large or multiple abscesses, bacterial infection and derangement of hepatic function . The presence of jaundice may worsen considerably the prognosis.
Dry cough, chest pain and decreased breath may be due to pleuropulmonary extension of the inflammatory process in the lesions of the superior amebuano. Hepatomegaly is the most important physical sign in hepatic amebiasis. The enlargement of the liver varies with the size and the site of the lesion.
There may be a generalized enlargement, downward enlargement or upward enlargement of the right or left lobe, compressing the diaphragm. In this situation there is a decrease in the ability to breathe, and the patient complains hepticoo dyspnea. In the larger abscesses, a mass or a lump may sometimes be seen in the right hypochondria or epigastria anebiano Figure 4. In the abscesses of the left lobe, the mass is palpable at the left hypochondria. The tenderness may be abcsesso or localized.
In cases with severe tenderness, the patient avoids the palpation, abscessi before the examiner reaches the affected area. After the old days of splenoportography and less sensitive tests, the non-invasive imaging procedures, including ultrasonography, computerized tomography, magnetic resonance imaging and, principally serology, have dramatically improved the clinician’s ability ueptico promptly diagnosis hepatic amebiasis and quickly start treatment.
Among the hepptico findings, the blood count reveals a mild degree of anemia that may be either normochromic or hypochromic. In the majority of cases, a mild to moderate leukocytosis is present, with an average white blood cell count of 16, In patients with multiple abscesses, or bacterial infection, the leukocytosis may be severe, accompanied by neutrophilia, with an increased percentage of immature forms similar to a leukemoid reaction .
The recovering of trophozoites and cysts of Entamoeba histolytica in feces of patients with hepatic amebiasis strengthens the hypothesis of amebic heotico. Liver function tests are not very helpful, presumably because too little liver tissue is affected. A moderate elevation of alkaline phosphatase, as well as hypoalbuminemia and transaminases, would suggest the possibility of a large abscess .
In imaging studies, an elevation of the right hemidiaphragm in chest radiography is a common find when there are lesions of the right lobe Figure 5. In lesions of the left lobe, the elevation is seen on the opposite side .
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Ultrasonography is the most widely used initial imaging procedure indicated for patients with a history and symptoms of hepatic amebiasis. In addition to its low cost and accessibility, it has the ability to rapidly detect hepatic lesions at the different stages of the disease, determining their number, size and exact position Figure 6. It may even differentiate a solid tumor from an abscess and a biliary tract disease from a lesion.
It is also very helpful in guiding percutaneous catheter liver drainage and in following the course of infection and its clinical resolution [24,25]. At ultrasonography the amebic hepatic lesion abcesso to be round or oval, hypoechoid, with well-defined margins Figure 6.
The abdominal CT scan is another valuable imaging procedure, with greater resolution and sensitivity in detecting hepatic lesions, especially the smaller ones, which is useful for early diagnosis .
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In the CT scan, an amebic abscess usually appears as a rounded, well-defined, low-density lesion, with an homogeneous septated cavity, and with considerable fluid Figure 7. In spite of the important support provided by imaging studies, the definitive confirmation of hepatic amebiasis is based on a demonstration of Entamoeba histolytica trophozoites in the aspirated pus, or more frequently from the necrotic material obtained by needle biopsy of the edge or the bottom of the lesion.
Nevertheless, the ameba will be found in only a small percentage of cases. Considering the humoral immune response to Entamoeba histolyticaserology has become a valuable tool for diagnosis, detecting specific circulating antibodies against the invasive forms, and indicating the etiology with a reasonable margin of safety, and therefore differentiating hepatic amebiasis from a pyogenic abscess .
Indirect immunofluorescence is also very helpful, giving values higher than 1: Because of the low positivity of microscopic diagnosis, antigen detection can be an essential adjunct method. Recent studies indicate improved sensitivity and specificity of fecal antigen assays for invasive strains, with the use of monoclonal antibodies that can distinguish between Entamoeba histolytica and Entamoeba dispar .
Unfortunately this test is not yet available commercially. Despite a similarity with several diseases such as hepatoma, acute cholecystitis, parasitic cysts, subphrenic and pulmonary abscesses provoked by bacteria, the differential diagnosis of hepatic amebiasis must be established principally against pyogenic abscess [30,31].
Although epidemiological information may show the patient to be from an area endemic for amebiasis, acute onset of fever, abdominal pain and hepatomegaly are common to both amebic and pyogenic abscesses, and laboratory findings and the images obtained from radiography, ultrasonography and CT scan studies, are not decisive for determining an absolute difference between amebic and pyogenic abscesses.
In spite of the availability of effective drugs, complications may be found with regularity during the course of hepatic amebiasis. Its appearance depends on the size, number and localization of the lesions, and they may interfere unfavorably with the prognosis of the disease. Firstly, the liver is prone to bacterial invasion due to its anatomical location and function.
Since most of the blood supply from the large gut drains into the right lobe of the liver through the portal system, translocated organisms, such aerobic and anaerobic Enterobacteriaceae, may reach the hepatic sinusoids, being phagocytized most of the time.
When the mononuclear-macrophage system is unable to destroy the invaders, they subsequently inflict cellular injury and secondary bacterial infection, producing clinical symptoms of severe illness that are distinct from those of amebic abscess . There is the risk of sepsis, needing prompt diagnosis and therapy with antibiotics.
Repeated liver aspirations without appropriate technique and asepsis may also be responsible. Under these circumstances Staphylococcus aureus is the principal invader .
The spreading of the amebic lesion to adjoining structures, involving a contiguous mechanism, is a frequently reported complication. The close vicinity of the diaphragm to the superior surface of the hepatic lesion may lead to inflammatory reactions of the diaphragm itself, subphrenic space, pleura, lungs and pericardium ameiano.
Clinically this can result in atelectasis, pleuritis, empyema and pulmonary condensation.