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SURGICAL WEBSITES BREAST DISEASE LIVER ABSCESS Anatomy of liver SURGICAL WEBSITES KIDNEY SURGERY POSTGRADUATE SURGERY LINKS
BREAST DISEASE Breast cancer Breast lump Breast awareness Breast calcifications Breast cysts Breast pain Duct ectasia Fat necrosis Fibroadenoma Hyperplasia Intraductal papilloma Phyllodes tumour Sclerosing adenosis
LIVER ABSCESS Anatomy of liver Physiology of liver Method of examination of liver Haematology of liver disease. Amoebic liver abscess .Pyogenic liver abscess. Percutaneous needle aspiration of liver abscess. Case study. Result Result continued Discussion
CHOLECYSTECTOMY Introduction Historical Review Anatomy of Gallbladder Physiology of Gallbladder Physiologic effects of pneumoperitoneum Pathology of Gallbladder Investigations Pre- operative preparation of laparoscopic cholecystectomy Contraindications Treatment modalities for gallstones. Anaesthesia
INGUINAL HERNIA HOW SURGICAL OPERATION IS DONE THYROID EXAMINATION MANAGEMENT OF SEVERELY INJURED PATIENT SEPSIS AND MULTIPLE ORGAN FAILURE CHEST TRAUMA BRONCHOGENIC CARCINOMA TETANUS AND ANAEROBIC INFECTIONS
AMOEBIC LIVER ABSCESS AMOEBIC LIVER ABSCESS
EPIDEMIOLOGY
Amoebic liver abscess is more common than pyogenic liver abscess on a global scale.
Colonic amoebae have a worldwide distribution, but hepatic amoebiasis is a disease of the tropics. Endemic areas are South- East Asia, Africa, Mexico, Venezuela and Colombia. It is common in under developed countries, more so amongst the population with low socio-economic status, living in congested localities with poor sanitation.
Amoebiasis being more common in the developing countries, often there are no teaching institutions or academically interested personnel with necessary equipment to confirm the diagnosis in these areas. Thus a lot of clinical material on amoebic liver abscess from these regions goes unreported.
In developed countries the incidence of amoebiasis and hence amoebic liver abscess has gone down. Amoebic liver abscess and colitis have become almost non-existent in Alaska and Canada. In Canada, amoebic infection is encountered only in small patches of population migrated from endemic areas.
In United States, the incidence of amoebic infection has decreased considerably. Except for Massachusetts there are no reports of amoebic liver abscess from the northern states. Amoebiasis itself and amoebic liver abscess are still prevalent in the states of Louisiana, Texas and Arkansas, but there incidence is now falling.
In Mexico the incidence is still high. Amoebiasis is still common in Guatemala, Costa Rica and Panama but reports on amoebic liver abscess are very few. The problem of amoebic liver abscess is non existent in European Countries.
From African countries except South Africa there are hardly any reports on liver abscess.
Asia harbours many countries of the third world and it is not surprising that amoebiasis and even amoebic liver abscess are found in abundance in this continent, especially in the South east Asian countries Cases are reported from India and Pakistan in local as well as international literature. The other South East Asian countries where amoebiasis seems to be common are Malaysia, Korea, Taiwan and Pakistan. The features of the common ‘Third-World’ disease should be well known to all surgeons where ever they practice in view of the rapidity with which people can now travel from country to country 40.
In temperate climates, symptom-less carriers of toxic strains are found but colonic ulcers are not seen. It is frequent commensal in homosexual men.
In the tropics the new arrival is heavily exposed. Spread of infection by faeces is easier when sanitation is poor. Locals are less prone to hepatic amoebiasis than Europeans, presumably by the partial immunity induced by the repeated contact. An amoebic liver abscess has a variety of presentations but only the recognised and well established features are discussed here.
Age
Although amoebic liver abscess can develop at any age, it is more frequently encountered in the adult life with highest incidence occurring in the fourth decade of life 41. The disease is rare at the two extremes of life.
Sex
Amoebic liver abscess is far more common in males than in females.
Race / Travel history
Common in population of tropical and sub tropical areas. Multiple abscesses are frequent in such areas as Mexico and Taiwan. Note must be made of any residence or illness suffered in tropical or sub tropical areas.
Diarrhoea and dysentery
Hepatic amoebiasis has been recorded after the primary bowel infection. Amoebic dysentery and the cyst in the stool of may be present in the patients with hepatic amoebiasis.
Other predisposing factors
Alcoholism and use of steroids can predispose to the hepatic amoebiasis leading to abscess formation. It is also described as a rare complication of pregnancy 42. Use of corticosteroids can convert amoebiasis into hepatic amoebiasis leading to abscess formation 43. In a study by Fujihara and his colleagues carried out in Japan, amoebic liver abscess has been reported in patients suffering from syphilis and in homosexual 44. Liver abscesses can occur in association to Crohn's disease in its initial phases 45.
LIFE CYCLE OF ENTAMOEBA HISTOLYTICA
The latent period between the intestinal infection and hepatic involvement has not been explained. Entamoeba histolytica exists in a vegetative form and as cysts, which survive outside the body and are highly infectious. The cystic form passes unharmed through the stomach and small intestine and changes into the vegetative, trophozoite form in the colon. Here, it invades the mucosa, forming flask-shaped ulcers. Amoebae are carried to the liver in the portal venous system. Occasionally, they pass through the hepatic sinusoids into the systemic circulation with the production of abscesses in lung and brain.
Amoebae multiply and block small intra-hepatic portal radicles with consequent focal infarction of liver cells. They contain a proteolytic enzyme, which destroys the liver parenchyma. The lesions produced are single or multiple and of variable size.
The amoebic abscess is usually about the size of an orange. The most frequent in the right lobe, just below the diaphragm. The centre consists of a large necrotic area, which has liquefied into thick, reddish brown pus. This has been likened to be anchovy or chocolate sauce. It is not strictly pus because it is produced by lysis of liver cells. Fragments of liver tissue may be recognised in it. Initially the abscess has no well defined wall, but merely shreds of shaggy necrotic liver tissues. Histologically, the necrotic areas consist of degenerative liver cells, leukocytes, red blood cells, connective tissues strands and debris. Amoeba may be identified in the scrapings of the walls.
Small lesions heal with scars, but larger abscess show a chronic wall of connective tissue of varying age. Many factors determine the balance between healing and progression. The virulence of the infecting organism and the resistance of the host must play a part. Secondary bacterial infection occurs in about 20%. The pus then becomes yellow and foul smelling. Various stages of life cycle are shown in figure 21 to 25.
THE PROCESS OF ABSCESS FORMATION
How these unicellular organisms produce such large sized abscesses is another unsolved puzzle. Various workers have put forth direct and indirect evidences in support of various possibilities. Infarction, enzymatic hydrolysis and immunological reaction either independently or in combination may bring about the formation of an abscess.
Infarction
Some workers believe that trophozoites reach small portal radicles in large number and set up a thrombus formation which give rise to an infarct. The wall of the vessel is destroyed and amoeba come out and probably fed on the products of cytolysis. They may then enter other open portal radicles and the process may be repeated. Many workers have found thrombosed radicles of the portal vein in the walls of the abscess. Some have found amoebae entangled in the thrombus. Lesions resembling an infarct have been found in the wall of a liver abscess and appear as a dark, reddish brown wedge shaped with sharp demarcated borders. On microscopic examination they have a moth eaten appearance due to multiple small abscess 1-3 mm in diameter, extending from the portal triad into the liver substance of the liver. The portal vein radicles had undergone dissolution but the hepatic artery and the bile duct branches of the triad were normal.
Enzymatic dissolution
The Entamoeba Histolytica produces enzymes and thus theoretically it can produce hydrolytic dissolution of the liver tissue. The first clue to the possibility of chemical action on the tissue by Entamoeba Histolytica came from the fact that in its tissue section clear ‘halo’ like areas are seen around the amoebae. Histology examination shows a pattern of diffuse lyric necrosis and toxic oedema.
Liver amoeba trophozoites or even their saline extract can produce digestion of thin gelatine films. Attempts to identify the enzymes have been made by many workers. trophozoites could produce an enzyme with trypsin like activity. This can bring about dissolution of gelatin, casein, fibrin, haemoglobin and suspensions of epithelial cells. As this enzyme is effective over a wide range of pH i.e. 5.0-8.0 it can also be effective in liver. Pepsin like activity of Entamoeba Histolytica trophozoites was also discovered. The trophozoites do not seem to produce any enzyme.
For producing very large lesion like the once seen in clinical practice, either the amoebae have to be present in large number or some spreading factor like hyaluronidase has to assist.
On electron microscopic examination, the Entamoeba Histolytica trophozoite does not show any separate vacuoles containing the enzymes. The entire trophozoite is envoloped in a fuzzy coat. The cytotoxic effect of the release of enzymes can be seen after direct contact with the cells or from a distance.
Entamoeba Histolytica can bring about complete destruction of the polymorphs. The actual death of these cells is preceded by a stage of degranulation. The destructive effect of the enzymes secreted by the Entamoeba Histolytica is increased by hydrolytic enzymes released by the inflammatory cells due to action of Entamoeba Histolytica on them.
Phagocytosis
The amoebae have been shown to use phagocytosis and pinocytosis as mode of tissue damage.
PATHOLOGY
GROSS EXAMINATION
The liver is usually enlarged and weighs more than normal. The lobe which is seat of infection is enlarged, however generalised enlargement could be present. The generalised enlargement is due to oedema and congestion, produced by pressure on draining venous channels.
When the abscess is superficial, it forms a bulge on the surface of the organ. Sometimes there may be thin strands of adhesions on the surface even in the absence of a rupture. Right lobe is affected more commonly as compared to the left. It is because the right lobe receives the blood from the caecum, ascending colon and right half of transverse colon, where the amoebic involvement is more common. The appearance of the cut section varies according to the stage in which the abscess is seen.
Very early stage.
Acutely formed amoebic abscess.
Chronic abscess
Healing stage
In the initial stage, cell death occurs but the entire dissolution and liquefaction is not complete. Hence the affected area appears dark coloured, softened and well demarcated from the surrounding normal tissue. As the contents are not liquid, these may be termed as solid abscesses. Lesion of a similar description can be found just beyond the spreading border of a well established amoebic abscess.
An abscess of a recent onset has a distinct central liquefied area. The cavity may be round oval or branching. The wall of the abscess may be shaggy, i.e. shreds of non viable tissue are seen to hang loose from the walls. Just outside this wall is a rim of dark coloured congested liver tissue. The area slowly merges with the normal tissue without any capsule to separate into two parts.
The only distinct difference between acute and chronic abscess is that in the latter the body has had time to wall off from the lesion by producing a layer of fibrous tissue around it
If an abscess heals without being aspirated, the liquid contents may dry up and are described to look like ‘putty’. Rarely, these lesions may get calcified.
MICROSCOPIC EXAMINATIONS
The microscopic details also differ depending upon the age of lesion.
Very early lesion
These lesions still have resemblance to the liver architecture. The connective tissue may not be completely destroyed, but the hepatocytes show all the signs of death. The affections of the liver cell is more marked towards the centre of the lobule as compared to the periphery.
Recently formed and / chronic abscess
In a well-formed abscess the central zone is a cavity filled with thick liquid which is not true pus. Surrounding the necrotic area is a layer in which the hepatocytes are compressed, and tend to lie in cords, parallel to the wall of the abscess cavity. Sinusoids may appear congested and hyper-cellular. There are few changes at the portal triad. The portal vein radicles are maximally affected. Some of them show slight inflammatory changes in their wall other show thrombosis with Entamoeba histolytica caught in the thrombus. Occasionally some portal vein radicles are totally necrosed (probably by the enzymatic action of Entamoeba Histolytica). The branches of the hepatic artery are normal. In some cases specially those with jaundice, inspection of bile is noted. Fibrosis and bile duct proliferation may occur.
In general there is a paucity of inflammatory cells. When present they are in maximum number in portal triad. Monocytes and lymphocytes are observed more commonly than polymorphs. Whenever there is secondary infection, the polymorphs dominate the scene. Beyond this area there is a lot of spreading activity, the extension occurs radically. In this region there are a lot of trophozoites of Entamoeba Histolytica with evidence of multiplication of the parasite. The older lesion is walled off from the surrounding normal tissue by a distinct band. The thickness of this wall probably depends on the age of the lesion. The wall is composed of reticule fibres, fibroblast and collagen fibres. The thicker walls have thick band of collagen.
Beyond the fibrous wall, the liver appears normal. Some workers have noticed fatty change and altered staining pattern much beyond the site of abscess. The altered liver functions are due to hepatolysis in localised area (the abscess) and hepatic damage. Multiple small satellite abscesses are also found in this region. Finally compression of the intrahepatic duct has been observed. Thrombosis of small branches of hepatic veins has been recorded. This may also be responsible for congestion around the amoebic abscess 46.
Repair and healing
The abscess cavity may shrink within two to three days. Complete resolution of the abscess takes two weeks to eight months. Active regeneration is noted and can be seen even during acute phase. Periportal fibrosis of various degrees is also observed. For some unexplained reasons fibrosis seems to be a self limiting process in patients with liver abscess. Rarely does the fibrous tissue undergo calcification.
PUS OF LIVER ABSCESS
Demonstration of the pus is one of the criteria for making a definitive diagnosis of liver abscess. Some facts about the characteristics of the pus are mentioned below.
COLOUR:
The colour has been described as “like anchovy sauce”. It is worth remembering that anchovy sauce like pus is not always amoebic. It is not typical of amoebic liver abscess and has been over stressed in the past.
The pus is usually chocolate coloured or pinkish brown. However, the pus of different colours has been aspirated from patients in whom the diagnosis of amoebic liver abscess was confirmed by various other methods such as surgery, post mortem examination, serological tests and therapeutic response. The colour may be dirty yellowish. (like pus else where) or it may even be ivory (creamy white), grey or greenish. Very often in the same patient, the initial colour of the pus changes as the aspiration proceeds. Often specks of blood or necrotic tissues are seen floating in the pus. Also the colour changes to a darker shade after it is exposed to air for some time.
The red brown hue may be derived from the necrosed liver tissue or due to admixture of blood. As the abscess is actually formed by the liquefaction of the necrotic tissue, either of these possibilities may be correct. Previously it was believed that pus appears yellowish only if there is secondary infection, but some workers have found thin yellow pus even in the absence of secondary infection. This is more common in patients having a chronic amoebic liver abscess.
Greenish colour of pus may be due to admixture of bile. There is a direct communication between the abscess cavity and the bile ductules. It is a common observation that on successive aspirations the nature of the pus changes. It becomes thinner, clearer and its colour changes from brownish pink to greenish yellow. It is possible that in the past in some of these patients, secondary infection by anaerobic bacteroids was missed, because routine culture for these organisms was not done. Thus, the pus was wrongly labelled as sterile.
ODOUR
The pus is usually odourless except when secondarily infected. Some authors have described a musty smell.
CONSISTENCY
The pus is usually very thick in consistency. So often it is felt that similarity between amoebic pus and anchovy sauce is more in consistency than in the colour. In fact sometimes it is described as a “paste”. If serial aspirations are done, the consistency of the pus becomes much thinner, and it can be aspirated more easily. The explanation for this is not forthcoming.
VISCOSITY:
Paul has compared the viscosity of amoebic pus to that of thick lubricating oil. Some clinicians feel that if pus is not removed it again becomes semisolid or like ‘putty’. This stage can only be seen after cure takes place with medical therapy (without aspiration).
QUANTITY:
The quantity of the pus will naturally vary according to the size of the abscess. There are reports in the literature that three and a half litres of pus having being removed at a single tapping. Often the pus is under pressure and comes out in a gush, especially on initiating the tap.
MICROSCOPIC EXAMINATION OF PUS:
On microscopic examination the pus may show deformed of dead hepatocytes, debris, RBCs and a few polymorphs. The trophozoites of the Entamoeba Histolytica are usually present in the wall of the abscess. Hence it is not surprising that many authors report their total absence or very low incidence, on examination of the pus. However when the pus is examined carefully, they are found in 15-25% of the cases. The organism is more likely to found in the terminal part of the aspirate. Samples should be obtained in small containers at intervals during aspiration. Thus the last fraction which is usually mixed with blood and is most likely to contain amoebae will not be diluted by the main mass of the aspirate.
It is interesting to note that examination of the exudate a few days after open drainage, may reveal the organisms much more readily. Whether this reappearance of the amoebae in the aspirate is due to changes in the oxygen availability, pressure levels or vascularity, is not known.
MICROBIOLOGY OF THE PUS:
The pus is usually sterile but secondary infections can occur, the rate varying from 8-25%. This was more common when open surgical drainage of the abscess was carried out. Infections occurs more commonly on successive aspirations. Culture of the pus for aerobic and anaerobic organism will also help to identify the organism responsible for the secondary infection. Cocci, E. Coli, para colon and proteus bacilli have been cultured from amoebic pus. In some studies anaerobic bacteroides have been isolated in as many as 26% cases. If facilities are available, culture for E. Histolytica may be asked for. Superadded infection with Kl. Pneumoniae has been reported 47. In a study by Hayat et al the superadded infection with Salmonella, Staff aureus and E. coli has also been reported48.
IMMUNOLOGY OF THE PUS:
It hardly surprising that immunological tests of the pus show the presence of the amoebic antigen. This test can be of greater diagnostic significance and explain the coarse clumpy character of anchovy sauce type of aspirate. The aspirated material by Feulgem method and demonstrated the presence of D.N.A. material.
Pus may be simulated by the following:
1. Fluid aspirated from the Hepatoma –it is thick bloody opaque. A careful microscopic examination may show malignant cells.
2. Fluid aspirated inadvertently from a liver cyst. This could be brownish red, but is absolutely clear. There are no floating particles.
3. Haemangioma of liver if aspirated inadvertently will show blood.
4. Vascular tumours following oral contraceptives would show bloody fluid.
HISTORY AND CLINICAL EXAMINATION
HISTORY
Detailed history of the patient is very important in diagnosis and management of the patient. History of travel is of particular importance.
CLINICAL FEATURES
Onset of disease
Patient presents with an acute onset of less than weeks duration of illness usually gradual. In practice one sees three types of onset-
Acute
Sub-acute
Chronic.
The majority presents with a sub-acute type of onset of a few weeks duration. Duration of the history has little clinical significance and is not an indicator of prognosis.
Symptoms
The patient looks ill with a peculiar sallowness of skin. Majority of the patients present with pain and fever. Patients with fever, abdominal pain, and tender hepatomegaly should be subjected to ultrasound scan for early detection of liver abscess 49. Few cases are asymptomatic and are discovered when complications occur which could be local or symptomatic.
Systemic symptoms
Fever
The incidence of fever in liver abscess is 70%. The onset is with rigors and sweating. It is the most frequent symptom 50. Fever is intermittent, it rarely exceeds 40ºC. Deep abscesses may present simply as fever without signs referable to the liver. In chronic liver abscess the fever is often low grade, develops more gradually and may be the only symptoms for weeks. In such cases sweating is less pronounced and rigor may not occur.
Acute cases with high fever and right basal pulmonary signs may be wrongly diagnosed as right basal pneumonia. Cases in which fever lasts for several weeks may often be misdiagnosed as enteric fever or tuberculosis.
Other systemic symptoms
Weakness may appear early in the amoebic liver abscess but is very prominent in advance cases. A feeling of lassitude and fatigue may be present in sub-acute and chronic forms of the disease. Other symptoms like weight loss are always present, particularly if the duration of illness is more than two weeks. Where the illness extends over several months, the weight loss may exceed one-third of lean body mass so these cases are often misdiagnosed as carcinoma of the liver.
Cough is another common symptom. It is usually dry and unproductive. Liver abscess with basal pulmonary signs may also give rise to breathlessness. Sometimes patients suffer from hiccough. Other symptoms are anorexia nausea and vomiting. Jaundice is unusual and if present mild. Bile duct compression with large and multiple abscesses may lead to jaundice as a presentation.May present with recurrent haemorrhage of the upper GI 51.
Local symptoms
Pain
Pain in the liver area may commence as a dull ache, later becoming sharp and stabbing. If the abscess is near the diaphragm, there may be referred shoulder pain accentuated by deep breathing or coughing. Postural changes make the pain worse. The patient tends to lean to the left side; this opens up the right intercostal spaces and diminishes the tension on the liver capsule. The pain increases at the night.
Signs
Swelling
A swelling may be visible in the epigastrium or bulging the incostal spaces.
Hepatomegaly
There may be generalised enlargement of the liver, enlargement of the right lobe and of left lobe, or only upward enlargement of left or right lobe, enlargement in horizontal plane towards the left hypochondrium, posterior enlargement or rarely no enlargement at all.
The edge is usually ill defined, rounded and soft. Often the edge is difficult to feel because of localised rigidity and guarding in the right hypochondrium. Rarely compensatory hypertrophy of the liver in the area around a large abscess cavity may lead to a certain amount of irregularity and even nodularity making differentiation from malignancy difficult.
Hepatic tenderness
Hepatic tenderness is virtually constant. It may be elicited over a palpable liver edge or by the percussion over lower right chest wall. It may be diffused or localised. Point of maximum tenderness is helpful in deciding the site of entry for abscess drainage.
The spleen is not enlarged. The lung may show consolidation over the right lower zone, pleurisy or a pleural effusion. Pleural fluid may be blood stained.
Examination of the faeces.
Cyst and vegetative forms are rare.
Clinical features and complications are shown in figure 26 to 28.
IMMUNOLOGICAL / SEROLOGICAL TESTS
The humoral system usually functions to protect an individual from a particular infection. The immune sera neutralise the growth of Entamoeba Histolytica. they also exert direct cytolytic effect on the trophozoites (require complement for this effect). The antigen (amoeba) is present in the liver. The antibodies are produced and antigen-antibody reaction takes place in the liver. Severe hepatolysis by the action of this enzyme system. To prove this hypothesis, studies like immunofluorescent staining for identifying the presence of complement in the livers with amoebic abscesses will have to be done.
The role of cell-mediated immunological system has also been tested. Test to show presence of migration inhibition factor have been found to positive. Test for observing blast transformation have been carried out in patients suffering from amoebic liver abscess. Lesser number of cells are transformed to blast stage in patients with amoebic liver abscess. After the acute stage of the disease (amoebic liver abcess) passes off, the blast transformation returns to a stage comparable with that in normal. B cells are found during the active process of the disease in response to the destruction of the hepatocytes. The cell mediated immune response seems to render protection only after the acute stage passes away.
Serological tests remain positive for some time after clinical cure. However an amoebic abscess is unlikely to be present if serological tests are negative. The indirect haemagglutination test is sensitive and valuable in community surveys 52. An ELISA is sensitive for serum diagnosis and useful for stools and for aspirates from liver abscess. Diagnosis of amoebic liver could be confirmed by serology 53.
BIOCHEMICAL TESTS
In the chronic cases, serum alkaline phosphatase values are usually about twice normal. Increases in transaminases are found only in those who are acutely ill or with severe complications. A rise in serum bilirubin is unusual except in those who are acutely ill or with severe complications. A rise in serum bilirubin is unusual except in those with superinfections or rupture into the peritoneum.
RADIOLOGICAL FEATURES
Chest radiographs show a high right diaphragm, obliteration of the costo-phrenic and cardio-phrenic angles by adhesions, pleural effusions or right basal pneumonia. Perpendicular string like adhesions may pass from the diaphragm to the lung base. A right lateral abscess may cause widening of the intercostal space. A central or inferior abscess may show few signs. The liver shadow may be enlarged with a raised immobile right diaphragm. The abscess commonly causes a bulge in the antero-medial part of the right diaphragm.
An abscess in the left lobe of the liver may show a crescentic deformity of the lesser curve of the stomach.
Ultrasound is most useful in diagnosis and in following progress. CT shows the abscess with somewhat irregular edge and lower attenuation than the surrounding liver. It is more sensitive than the ultrasound for small abscesses. It is particularly useful for showing extra-hepatic involvement, for instance in the lung. MRI can be used for diagnosis and to follow the treatment. Liquefaction of the cavity may show as early as 4 days after starting treatment.
DIAGNOSTIC CRITERIA
1. History of residence in endemic area.
2. An enlarged tender liver in young male.
3. Response to metronidazole.
4. Leucocytosis without anaemia in those with short history, and marked leucocytosis and anaemia with long history.
5. Elevation of right hemi diaphragn in xray chest..
6. Scanning shows a filling defect.
7. A positive amoeba indirect haemagglutination test.
Mehnaz and Ali in their study of thirty eight cases based their diagnosis on clinical presentation, ultrasound examination, detection of Entamoeba Histolytica trophozoite in the aspirate and response to therapy 54.
COMPLICATION
Two thirds of ruptures are intra-peritoneal and one-third intra thoracic. Rupture into the lungs or pleura. The patient coughs up pus, develops pneumonitis or lung abscess. Thoracic amoebiasis characteristically presents as a febrile illness with cough, chest pain and point tenderness in an intercostal space or the right upper quadrant of the abdomen. Haemoptysis, diarrhoea and dysentry are uncommon. The most important factor in the recognition is the awerness of the possibility of the lesion. Chest radiography and serology help in the diagnosis 55.
Rupture into the pericardium is a complication of amoebic abscess in the left lobe. Intra-peritoneal rupture results in acute peritonitis 56. If the patient survive the initial effect, long term results are good. Abscesses of the left lobe may perforate into lesser sac. Rupture into portal vein. Bile ducts or gastrointestinal tract is rare. Secondary infection is suspected if prostration is particularly great, and fever and leucocytosis high. Aspiration reveals yellowish pus and culture reveals the causative organism. Perforation should be suspected in-patients with liver abscess developing severe abdominal pain and signs of peritonitis 57.
In a study carried out at Karachi, Abbas and his colleagues has described that syndrome of inappropriate secretion of antidiuretic hormone (SIADH) can be found in the patients suffering with amoebic liver abscess 58. Reactive arthritis is associated with amoebic liver abscess 59.
TREATMENT
Metronidazole, 750mg three times a day for 5-10 days but the treatment can be continued if required. An intravenous preparation is available. Therapy with potent tissue amoebicidal drugs such as metronidazole is optimally effective in treating amoebic liver abscess, and in uncomplicated cases 60. The time to defervescence is 3-5 days.
The time taken for the abscess to disappear depends on its size and varies from 10 –300 days. There is advantage of metronidazole with needle aspiration over metronidazole alone. Mohsin et al have state that prolongation of the disease may increase the risk of complication and can make the management difficult 61. Aspiration may be necessary with very large abscesses or where there is lack of response to 5 days of metronidazole treatment; if possible it should be done under ultrasound or CT guidance. The needle should be at least 10 cm long of 1-2 mm diameter and with a fitted stilette. A tense abscess in the left lobe that is likely to rupture into the peritoneum demands aspiration or open surgical drainage. Recurrent large abscesses also require open surgical drainage. Percutaneous catheter drainage has been advocated in cases of resistant cases 62. Amoebicidal therapy is effective in the treatment of both un-ruptured and extrahepatic rupture of amoebic liver abscess. Open surgical drainage is mandatory for extrahepatic rupture of liver abscess. Surgery is required if secondary complications develop 63.
A course of a luminal amoebicide such as diloxanide furoate (500 mg three times a day for 10 days) or iodoquinol (650 mg three times a day for 20 days) should be given to cover amoeba in gut.
MAIN OUTCOME MEASURES:
Response to the management not only confirms the diagnosis but inadequate response not only indicates inaccurate treatment but also dictates the need of alteration in the management offered. The observation of the patient is of prime importance if the patient is managed on conservative lines or by minimally invasive means. Sharma has outlined a few clinical parameters for measurement of outcome of the management which includes abdominal pain, fever, anorexia, hepatomegaly, erythrocyte sedimentation rate, serum aspartate, alanine aminotransferase and alkaline phosphatase values 64.
PROGNOSTIC FACTORS
The prognosis of the amoebic liver abscess need to be determined to decide whether aggressive intervention therapy should be used. A bilirubin level of greater than 3.5mg/dl, encephalopathy, volume of abscess cavity, hypoalbuminaemia (serum albumin level less than 2.0gm/dl) and the number of abscesses are the independent risk factors for mortality 65. The duration of the symptoms and type of treatment used can affect mortality.
Washington, DC Registry
Last modified: Friday, 22-Jul-2005 08:33:56 EDT |
