CLINICAL STUDY OF LIVER ABSCESS
IN ALCOHOLIC AND NON ALCOHOLIC PATIENTS AT
MADRAS MEDICAL COLLEGE
Dissertation Submitted for
MS DEGREE (BRANCH I) GENERAL SURGERY MAY 2018
THE TAMILNADU DR.M.G.R MEDICAL
UNIVERSITY CHENNAI – 600 032.
MADRAS MEDICAL COLLEGE, CHENNAI
MAY - 2018
BONAFIDE CERTIFICATE
Certified that this dissertation is the bonafide work of
Dr.N.BALAMURUGAN on “CLINICAL STUDY OF LIVER
ABSCESS IN ALCOHOLIC AND NON ALCOHOLIC
PATIENTS” during his M.S. (General Surgery) course from march
2017 to august 2017 at the Madras Medical College and Rajiv Gandhi
Government General Hospital, Chennai – 600003.
Prof. DR.R.A.PANDYARAJ, MS,FRCS,FMAS,FICS,FIMSA,FIAGES,FALS (LAP), FMMC
Director Institute of General Surgery Madras Medical College & Rajiv Gandhi Government General Hospital, Chennai – 600 003.
Prof. Dr. R.LAKSHMANA KUMAR, MS Professor of General Surgery Institute of General Surgery Madras Medical College & Rajiv Gandhi Government General Hospital, Chennai-600003
Dr.R.NARAYANABABU M.D,DCH, DEAN,
Madras Medical College & Rajiv Gandhi Government General Hospital, Chennai – 600 003.
ACKNOWLEDGEMENT
I would like to express my deep sense of gratitude to the DEAN, Madras
Medical College and Prof. DR. R.A.PANDYARAJ, Director, Institute of General
Surgery , MMC & RGGGH, for allowing me to undertake this study on “Clinical
Study of Liver Abscess In Alcoholic And Non Alcoholic Patients
In Madras Medical College”
I was able to carry out my study to my fullest satisfaction, thanks to guidance,
encouragement, motivation and constant supervision extended to me, by my beloved
Unit Chief Prof. Dr. R.LAKSHMANA KUMAR, M.S. Hence my profuse thanks are
due for him.
I am bound by ties of gratitude to my respected Assistant Professors,
Dr.Krishnamoorthy M.S, Dr.Sabarigiriesan M.S, Dr.Kalyankumar M.S, in
general, for placing and guiding me on the right track from the very beginning of my
career in Surgery till this day. I would be failing in my duty if I don’t place on record
my sincere thanks to those patients who inspite of their sufferings extended their
fullest co-operation.
I am fortunate to have my postgraduate colleagues, for their invaluable
suggestions, relentless help for shouldering my responsibilities.
DR. N.BALAMURUGAN
DECLARATION
I, certainly declare that this dissertation titled “CLINICAL STUDY OF
LIVER ABSCESS IN ALCOHOLIC AND NON ALCOHOLIC PATIENTS”,
represent a genuine work of mine . The contributions of any supervisors to the
research are consistent with normal supervisory practice, and are acknowledged.
I, also affirm that this bonafide work or part of this work was not submitted by
me or any others for any award, degree or diploma to any other university board,
neither in India or abroad. This is submitted to The Tamil Nadu Dr.MGR Medical
University, Chennai in partial fulfillment of the rules and regulation for the award of
Master of Surgery Degree Branch 1 (General Surgery).
DATE: Dr.N.BALAMURUGAN
ABBREVIATIONS
A:G ratio
ALA
ALP
ASP
AST
B/L PE
C/I
c/s
CT
CxR
E.coli
E.dispar
E.Histolytica
HA
HIV
K.pneumoniae
LFT
MRI
No.
PA
PCD
Albumin : Globulin ratio Amoebic liver abscess Alkaline phosphatase Aspiration Aspartate Amino Transferase Bi-Lateral Pleural Effusion Contra Indication Culture and sensitivity Computed Tomography Chest X-ray Escherichia coli Entamoeba dispar Entamoeba histolytica Haemeagglutination Human Immuno deficiency Virus Klebsiella pneumoniae Liver function tests Magnetic Resonance Imaging Number Postero anterior Percutaneous catheter drainage
PLA Pyogenic liver abscess
PNA Percutaneous needle aspiration
PT Prothrombin time
RPEF Right Pleural Effusion
RBS Random Blood Sugar
Sec Seconds
SGOT Serum Glumatyl Oxalo Aceteate Transaminase
SGPT Serum Glumatyl Phenylalanine Transaminase
Staph.aureus Staphylococcus aureus
US Ultrasound
USG Ultrasonography
WBC White Blood Corpuscles
CONTENT
S.NO TITLE PAGE.NO
1 INTRODUCTION 1
2 AIMS AND OBJECTIVE 2
3 REVIEW OF LITERATURE 3
4 MATERIALS AND METHODS 61
5 RESULTS 62
6 DISCUSSION 80
7 CONCLUSION 86
8 BIBLIOGRAPHY 89
9 ANNEXURE 96
10 MASTER CHART 106
1
INTRODUCTION
Liver abscess is a common condition in India. India has 2nd highest incidence
of liver abscess in the world. Liver abscesses are caused by bacterial, parasitic and
fungal infection.
Pyogenic abscesses account for three fourth of hepatic abscess in developed
countries. While amoebic liver abscess cause two third of liver abscess in developing
countries2.
Amoebiasis is now the third most common cause of death from parasitic disease.
The World Health Organisation reported that Entamoeba Histolytica causes
approximately 50 million cases and 100,000 deaths annually.3 The vast majority of
these infections are all acquired in the developing world. In a country like India,
majority of population lives below poverty line, basic sanitary facilities are lacking.
This coupled with overcrowding, urban slums and also outdoor unhygienic eating
habits sets the stage for communicable diseases like amoebiasis.
Liver abscess continues to be condition with considerable mortality in our country.
Locally made alcoholic drinks like arrack may be the routes of faeco-oral
transmission of amoebic cysts.
Primary prevention by improving sanitation, health education, early diagnosis
and prompt treatment may result in lowering mortality / morbidity associated with the
disease.
This study has tried to delineate clinical profile, risk factors and management
strategies of liver abscesses.
2
AIM AND OBJECTIVES OF STUDY 1) To correlate incidence of liver abscess in Alcoholic and non alcoholic Patients.
2) spectrum of clinical presentations.
3) To evaluate the efficacy of ultrasonography.
4) To assess outcome of various treatment
3
REVIEW OF LITERATURE
♣ AMOEBIC LIVER ABSCESS
HISTORY
The first mention of blood and mucus diarrhea is found in the Sanskrit
document Bhrigu-samhita, dated 3000 BC.4 The association of ‘ball-like’
abdominal masses with this condition has also been recorded and is thought to
be indicative of co-existing hepatic abscess.
The occurrence of a similar syndrome in different parts of the world is
recorded in the writings of Hippocrates (5th century BC), Roman
physicians, and practitioners in the middle ages.5
Open drainage of liver abscesses with insertion of setons into the
abscess cavity were advocated by Ballingall, but the technique fell into
disrepute because it is highly associated mortality due to sepsis. Twenty-six
such tropical abscesses in association with dysentery were described in series
of autopsy in 1828 by Amesley in Bombay.2
In his 1875 a case report describing a fatal case of amoebic colitis in a
Russian peasant who had migrated to St. Peterburg from within the Arctic
circle, Lesch found motile amoebae in the mucus clots of his patient’s faeces
and demonstrated during autopsy that the terminal ileum and colon had
submucosal invasion by amoeba.5
Medical treatment for amoebic colitis has been described since ancient
times. A plant alkaloid called concessine was advocated in the Ayurveda, has
been found to kill E. histolytica in culture.
4
♣ EMBRYOGENESIS
Differentiation (vertical arrows) and induction (horizontal arrows) in the development of liver cords and sinuses in the embryo.
1. The earliest appearance of the liver primordium occurs on Day 22 after conception.
Day 24, the hepatic diverticulum is growing into the transverse septum.
2. The vitelline and umbilical veins divide into a plexus of vessels, and the
invading endoderm cells move into these spaces around and between them.
3. Day 32, most of the blood flow from the umbilical veins has been trapped by the
parenchyma that surrounds the venous channels which later become the liver
sinusoids.
4. The right umbilical vein regresses in the sixth week. The left vein carries placental
blood to the fetus upto birth.
5. Day 51, the intrahepatic veins have nearly attained the normal adult distribution and
segmentation.
6. Growth of the liver makes it to bulge out of the transverse septum so that the
liver becomes a truly abdominal organ lying in the ventral mesentery.
7. The intrahepatic bile ducts are believed to differentiate from hepatic cells and join the
extrahepatic duct system secondarily.
8. By the ninth week, the liver embraces as much as 10% of body volume. Its
relative size decreases to 5% by term.
9. Initially the left lobe is larger than right lobe. Between birth and adulthood, the
right lobe increases in size at the expense of the left lobe, which undergoes some
peripheral degeneration.
5
♣ ANATOMY OF LIVER:
• Liver is a large, solid, wedge shaped gland which occupies entire right
hypochondrium, the greater part of the epigastrium and part of the left
hypochondrium upto the left lateral plane.
• It is the largest gland of the body and contributes to 2% of the total body weight.
• Weighs 1.6kg in male and 1.3kg in female
• It has five surfaces:
Anterior
Posterior
Superior
Inferior and
Right
• It is divided into right and left lobe anteriorly by falciform ligament and superiorly,
by the fissure of ligamentum teres, inferiorly by the fissure for ligamentum venosum
posterioly.
• Right lobe is very much larger than the left lobe and forms five sixth of the liver and
also presents the caudate and quadrate lobe.
• Porta hepatis is a deep , transverse fissure situated on the inferior surface of the right
lobe.
• Portal vein , the hepatic artery and hepatic plexus of nerves enter the liver through the
porta hepatis while right and left hepatic ducts and few lymphatics leave it.
6
HEPATIC SEGMENTS
On the basis of intrahepatic distribution of the hepatic artery, portal vein and biliary
ducts, liver is divided into right and left hemilivers by Cantlie’s Line.
Further divided into total of eight segments i.e. Couinauds Segments.
Each segments have their own hepatic artery branch and biliary tree.
BLOOD SUPPLY:
Blood flow is 25% of total cardiac output.
80% is derived from portal vein.
20% is derived from hepatic artery.
Before entering the liver both hepatic artery and portal vein divide into right
and left branches.
Within the liver they redivide into segmental vessels, which further divide to
form interlobular vessels, which run in portal canals.
LYMPHATICS OF LIVER
Superficial lymphatics terminate in:
Caval
Hepatic
Paracardial and
Coeliac lymph node.
Deep lymphatics terminate in:
Supra diaphragmatic and
Hepatic lymph node.
7
NERVE SUPPLY
• Liver receives its nerve supply from hepatic plexus which contains
both sympathetic and parasympathetic( vagal plexus).
HISTOLOGY:
• Each segment is made up of a multiple smaller units known as hepatic lobule.
• Each lobule appears to be made up of cords of liver cells that is separated by
sinusoids.
• Along the periphery of each lobule, there are portal canals.
• Each portal canal contains:
a) A branch of the portal vein
b) A branch of the hepatic artery
c) An interlobular bile duct.
• These three structures collectively form a portal triad.
• Blood from the branch of the portal vein and from the branch of the hepatic artery, enterthe sinusoids at the periphery of the lobule and passes towards its centre.
• Here the sinusoids open into a central vein that occupies the centre of the
lobule.
• In contrast, the flow of bile is in the opposite direction along the biliary canaliculi into the terminal bile ductules and subsequently into the interlobular bile ducts located in the portal tracts.
• The sinusoids are lined by an endothelium in which there are numerous pores.
• Interspersed amongst the endothelial cells there are hepatic macrophages i.e
kupffer cells.
• The surface of the liver cell are separated from the endothelial lining of the sinusoid by a narrow perisinusoidal space of disse, which contains stellate cells.
8
• These stellate cells play a vital role in the storage and metabolism of vitamin
A and are transformed into collagen producing myofibroblasts when there is
inflammation of the liver
TABLE 1 : PHYSIOLOGICAL FUNCTIONS OF LIVER:
Principal Functions of the Liver.
1. Formation and secretion of bile
2. Nutrient and vitamin metabolism
a. Glucose and other sugars
b. Amino acids
c. Lipids
d. Fatty acids
e. Cholesterol
f. Lipoproteins
g. Fat-soluble vitamins
h. Water-soluble vitamins
3. Inactivation of various substances
a. Toxins
b. Steroids
c. Other hormones
4. Synthesis of plasma proteins
a. Acute-phase proteins
b. Albumin
c. Clotting factors
d. Steroid-binding and other hormone-binding proteins
5. Immunity a. Kupffer cells
9
TABLE 2 : TESTS OF LIVER FUNCTION
TESTS FUNCTION Serum Bilirubin Uptake, conjugation, and excretion of bile
Serum Alkaline Phosphatase Cholestasis and biliary obstruction
Serum GGT Cholestasis and biliary obstruction,
alcohol use Transaminases (AST and ALT) Hepatocyte Necrosis
Prothrombin Time Protein Synthesis
Albumin Protein Synthesis
Aminopyrine Breath Test Microsomal function
Antipyrine clearance Microsomal function
Caffeine clearance Microsomal function
Lidocaine clearance Microsomal function
Galactose elimination capacity Cytosolic function
Indocyanine Green Clearance Hepatic perfusion and anion excretion
Sulfobromopthalein clearance Hepatic perfusion and anion excretion
Tc-GSa scan Function hepatocyte mass
10
EPIDEMIOLOGY
Worldwide, amoebiasis is the 3rd most common parasitic cause of
death.9 It is classically defined as infection with E. histolytica with or without
overt clinical symptoms. E. histolytica was thought to be ubiquitous in
distribution in both the temperate and tropical countries with an estimated
12% global incidence of infection.
It is now recognized that a number of these individuals may harbour E.
dispar and not E.histolytica. Together these two organisms are now thought to
infect 10% of the world’s population, with E. dispar infection being 10-fold
more common than E. histolytica.
Among those infection with E. histolytica, 50 million persons develop
invasive amebiasis (colitis and hepatic abscess) resulting in 1,00,000 deaths
annually (1985).3
High risk groups include immigrants and travelers from endemic
zones, residents of institutions-especially mentally retarded individuals, , low
socioeconomic groups and male promiscuous homosexuals. It may be
important to note that here traveler’s diarrhea is rarely caused by E. histolytica,
which usually occurs only after a long stay – usually over 1 month in an
endemic area. Furthermore, the observation, that male homosexuals despite a
high incidence of infection; may rarely get invasive disease in temperate
climates is probably because of the usual organism harboured is the
morphologically indistinguishable E. dispar.10
11
PYOGENIC LIVER ABSCESS
Incidence
In 1938, Ochsner and DeBakey published what was then the largest
series of pyogenic abscess in the literature about 139 cases of amoebic abscess
and 47 cases of pyogenic abscess.
Pyogenic liver abscess (PLA) was seen to be a affecting young
patients, predominately with pyelophlebitis secondary to a acute appendicitis.
If left untreated, this condition was invariably become fatal. The median age of
patients with PLA was found to be the third decade. Many subsequent series
have been describing the changes in the clinical patterns of hepatic abscess.
With the effective treatment of such conditions (appendicitis, other acute
colonic diseases), there had been a shift in the aetiology and age distribution
of patients presenting with hepatic abscess.
Numerous studies have also subsequently reported biliary tract disease
to be the most frequent underlying lesion associated with PLA, with a peak
incidence in the seventh and eight decades .11,12
Studies from postmortem series have been constant. An early report in
1901 recorded an incidence of 0.45% among 17204 autopsies (Kobler 1901)
whereas a similar series in 1960 showed an incidence of 0.59%.11
The reduction of pyelophlebitis related PLA would account for a
proportional increase in the numbers of cryptogenic PLA. However, it remains
possible that there has been a recent true increase in the incidence of primary
cryptogenic PLA.9,13
12
ETIOPATHOGENESIS:
AMOEBIC LIVER ABSCESS
Figure 1 : E.histolytica Cycle
The organism
The protozoan E. histolytica belongs to subphylum Sarcodina (whose
motility depends on pseudopodia), the supercalss Rhizopoda and the order
Amoebida.
The genus Entamoeba includes the species E. histolytica, E. bartmanni
(a noninvasive ‘small race’ with cysts <10 um in diameter), Entamoeba. coli,
E.polecki (infects pigs) and E. moshkovski (a free-living non-pathogenic form
which isfound in sewage).
Except for E. histolytica, the other species are considered as non-pathogenic.
With the discovery of E. dispar, the identification of E. histolytica on
morphology has become unreliable.
13
The presence of ingested erythrocytes is seen only with E. histolytica.
The two species have now been characterized by the study of zymodemes
(patterns of electrophoretic mobility of isoenzymes) and the genetic
differences using RNA and DNA probes, and the use of polymerase chain
reaction amplification.
E. histolytica has two forms : Trophozoite and cyst. The trophozoites
areuninucleate, facultative anerobes with a double-layered limiting membrane
surrounded by a fuzzy, external 20-30 m glycocalyx. With the emerging
concepts of virulence, it appears that only certain strains of E. histolytica are
capable of tissue invasion and contact lysis of cells.14
Cysts of E. histolytica are quadrinucleate. These cysts, measuring 8-
20mm, are an important identifying feature, and constitute the infective form
of the organism.
They are responsible for the faecal-oral transmission via food, water or
direct person-to-person contact.
After ingestion, the quadrinucleate cysts reach the intestinal tract,
where they develop into a metacystic stage and undergo an additional nuclear
division; thus, eight new uninucleate trophozoites emerge to complete the life
cycle.
Cysts survive up to 45 minutes in faecal material lodged under the
finger-nails and up to 1 month in soil at 10oC. They remain infective in fresh
water, sea water and sewage but are rapidly destroyed by drying, 200 p.p.m. of
iodine and heat above 68oC. These are not killed by chlorination used to
purify ordinary drinking water.15
14
TABLE – 3 : DISTINGUISHING FEATURES OF VIRULENT AND NON-
VIRULENT AMOEBAE
Characteristics Virulent strains Non-virulent strains
Size (um) 20 - 60 (um) 7 – 30(um)
Negative surface charge Less More
Concanavalin A receptors Present Absent
Effect of PMNs and tissue Lethal 3000 PMNs/Eh Susceptible to PMNs
culture cells
Human serum complement Resistant Susceptible
Host factors
The human host represents the major reservoir although cross-infection from
animals particularly monkeys and rodents has been postulated. Interperson
transmission occurs via files and handles, and by sewage contamination of water
sources. Male homosexuals also transmit the disease, but usually harbour non-
pathogenic E. dispar.
Again, for the reasons not completely understood, menstruating women are
protected against invasive infection. Breast-fed children also have a low incidence
of invasion, and this has been postulated to be due both to the presence of
protective IgA in the immune mother’s milk and to the low iron content of milk.
Elderly individuals with the underlying diseases, and patients with depressed
immunity due to malnutrition or corticosteroid therapy, are also prone to invasion
by amoebae.
The natural resistance of menstruating women is lost in pregnancy.15
In Mexican Mestizo population the presence of HLA DR3 and complement
type SCO1 in both adults and children constitutes the primary independent risk
factor for the development of amoebic liver abscess, irrespective of the age or sex.
15
PATHOGENESIS
E. histolytica reaches the liver via the portal blood-evidence for
directextension and spread along lymphatics being lacking.
Agent-host interactions resulting in the production of such large abscesses are
postulated to be due to: Infarction, Enzymatic hydrolysis, and Immunological
reactions.
While small infarcts due to small vessel occlusion by amoebae have
been demonstrated, these may only be very early lesions.16
Cell-free extracts of E. histolytica are known to contain material toxic
to mammalian cells, and include proteases, glycosidases, phospholipase,
hemolysins and a pore forming protein.
However, enzymatic hydrolysis, probably one of the major mechanism
involved, occurs not because of released exotoxin by the amoebae, but owing
to a more complex sequence of events. All the amoebic enzymes are inhibited
by serum and they require direct contact to exert any effect on host tissue.
Adherence, followed by cytolysis, is followed in turn by amoebic phagocytosis
of the dead target cell. A current hypothesis of amoebic contact-development
cytolysis is as follows:17
Amoebae adhere to target cells by means of an adhesin. These
compounds are soluble lectins they are susceptible to inhibition by N-acetyl-
D-galactosamine.
Adherence initiates a calcium ion-dependent membrane perturbation
and amoebic microfilament function. Amoebic phospholipase A is activated
first.
Amoebic lyso compounds toxic to cell membranes are then released.
The poreforming protein, which acts on cells in a manner akin to complement,
16
and finally results in colloid osmotic lysis of the cell, may be the final toxic
Immunological reactions to E. histolytica are both cellular and humoral. While
it has not been finally established as to which one is responsible for limiting
invasion by amoebae, immunity against recurrent disease does develop. In
Amoebic liver abscess Recurrence is very rare-with only 0.29% recurrence
among 1021 patients followed for 5 years in Mexico.17
Among the various humoral mechanisms,the most important is the
natural protection afforded by circulating complement. E. histolytica is
susceptible to complement in the serum of both healthy and immune
individuals. However, complement, cannot prevent invasion, as it is not
present in gut mucosal secretions. Also, strains resistant to complement
develop over time when exposed in vitro, and complement resistance –
probably mediated by a 170kD submit of the adhesive lectin – one of the
characteristic features of the pathogenic zymodemes.
Between 81% to 100% of patients with invasive colonic amoebiasis
develop specific circulating IgG antibodies, and this response lasts for 2-11
years. There is, however, no positive correlation between this response and
invasive infection.
Amoebae have been shown to aggregate, ingest and shed human
antibodies,and invasive amoebiasis can occur in the presence of high titres.14
Similarly, among the cellular mechanisms, neutrophils are particularly very
much ineffective against E. histolytica, and are immediately lysed by the
virulence of the parasite. This result in the release of toxicenzymes of
neutrophil and such enzymes may further increase the local tissue destruction
in amoebic liver abscess.
17
There is an experimental evidence that liver cell necrosis is increased
when neutrophils are present along with E. histolytica.
Lymphocytes and macrophages appear to be the important effector
cells with activity against E. histolytica, the evidence being :
1. Lymphocytes (and lymphocyte supernatants) from patients recently cured
of amoebic liver abscess are cytotoxic to amoebic trophozoites.
Lymphocytes from normal controls are, however, phagocytosed by
E.histolytica.
2. Antimacrophage and antilymphocytes globulin, splenectomy,neonatal
thymectomy and steroid therapy results in enhanced formation of amoebic
liver abscesses in animal models.
3. Non-specific activators like concanavalin A (a classic T cell mitogen) and
phytohaemagglutinin appear to activate the macrophages, in contrast to
immune serum, thereby indicating an antibody-independent process.
4. Both oxidative and non-oxidative effector mechanisms of macrophages are
operative in the destruction of amoebae.
5. Lymphocytes of the T cells phenotype T8 are responsible for amoebicidal
activity.
Amoebic protein is capable of causing a marked T cell proliferative
response similar to concanavalin A, and appears to be important in the afferent
limb of cell mediated immunity.
18
PATHOLOGY:
Irrespective of the mechanism involved, liver cells will undergo liquefaction
necrosis starting in the centre and then spreading to peripherally and produce a cavity
filled with blood and liquefied liver tissue. The appearance of this pus is typically
described as like ‘anchovy sauce’, and it has no odour. Secondary infectionoccurs
very rarely spontaneously, but may changethe consistency and colour of the pus, and
certainly its odour too. With centrifugal extension the abscess soon comes to lie just
adjacent to Glisson’s capsule, which is resistant to the amoebae. Similarly, the abscess
cavity is criss-crossed by biliary portal and vascular structures which, because of their
intrahepatic covering of Glisson’s capsule, are resistance to the process of liquefaction
necrosis.
Fig. 2 : Variable appearance of fluid aspirated from a single amoebic liver abscess. Far left: initial aspirate, straw coloured but tinged with bile. Middle: mid aspirate
creamish in color. Far right: typical ‘Anchovy sauce’ from terminal aspirate.
Amoebae are identifiable in the spreading margin of the abscess, and under the
capsule. The abscess wall is typically ill-defined with a minimal host response of
fibrous tissue. Mature abscess may, however develop a fibrous wall and may even
calcify. In the completely treated case, complete resolution is the rule, but may take
longer time between 6 months to 2 years – longer usually than the time for pyogenic
abscesses to resolve.18
19
PYOGENIC LIVER ABSCESS
Etiology
Pyogenic liver abscess results from bacterial infection of the liver parenchyma and
subsequent infiltration, with an area of hepatic necrosis may result. Even if these areas
are initially sterile, bacterial seeding may subsequently occur resulting in the formation
of liver abscess. There may also be a much significant delay between the initial trauma
and the development of liver abscess, thereby adding to the diagnostic difficulty. Liver
abscess may also coexist with other forms of hepatic injury, for example; arterial
pseudoaneurysm. A very high index of suspicion is therefore required, together with an
high awareness of the other possible complications of liver trauma.19
In all series, there remain a group of patients where no underlying cause of liver
abscess in identified. In recent series such as cryptogenic abscesses have accounted for
between 20 and 45% of hepatic abscess.9,20. By definition, these patients have usually
undergone abdominal USG and CT. Computed tomography in particular has a very
high sensitivity for abdominal mass lesions associated with intraabdominal sepsis. It
therefore seems unlikely that unrecognized biliary tact disease or other sources of
intra-abdominal sepsis could account for cryptogenic PLA. A many number of possible
mechanisms have been proposed to account for the formation of cryptogenic liver
abscess.
These include the failure to diagnose or the resolution of an infective process within
the abdomen, spontaneous intrahepatic thrombosis and infarction, unrecognized
trauma or the presence of unrecognized hepatic cysts or hydatid disease. Portal
infection is then thought to result in bacterial seeding and the generation of hepatic
abscess.22
It has been suggested that all the patients with a diagnosis of cryptogenic liver
abscess should undergo full biliary and gastrointestinal evaluation. However, in the
20
absence of any specific symptoms or signs, data from recent series would not
appear to support this view.
Branum et al (1990)13 performed open surgical drainage in 16 of 20 patients
with cryptogenic liver abscess. Despite full operative evaluation, there remained no
identified cause for hepatic abscess in each of these patients.
The etiology of pyogenic liver abscess may be categorized according to
the route by which infecting organisms gain access to the liver. Hepatic abscess
may arise as the result of biliary obstruction and subsequent cholangitis. This may
result in formation of single or multiple macroscopic abscess collections. Acute
suppurative cholangitis is a condition that generally associated with small, multiple
and bilateral abscesses reflecting the uniform distribution of infecting organisms
throughout the biliary tree.
Ascending infection via the biliary system is now the single most identified
cause of pyogenic liver abscess, accounting for approximately one-half of all
cases.23,24
Liver abscess may also occur following biliary tract surgery, particularly
procedures that involve biliary enteric anastomosis. 25
Portal vein pyelophlebitis is now a very less frequent identified cause
of liver abscess, though this may still account for up to 20% of cases. The primary
sources of such abscesses include, pancreatitis, inflammatory bowel disease, acute
diverticulitis, perforated viscus or any other source of intra-abdominal or pelvic
abscess. In the neonatal period, liver abscess may occur following umbilical vein
sepsis.
21
TABLE 4 : THE ETIOLOGY OF PYOGENIC LIVER ABSCESS HUANG ET
AL 1996 CHU ET AL 199620
Huang et al 1996 Chu et al
1996 1952-1972 1973-1993 1984-1995
(n=80) (n=153) (n=83)
(%) (%) (%)
Biliary 51 60 51
Benign 27 18 45
Malignant 24 02 06
Cryptogenic 20 15 45
Portal vein 13 07 01
Direct extension 10 03 0
Trauma 5 5 0
Hepatic artery 1 10 2
Factors associated with liver abscess after biliary tract surgery
Anastomotic stricture (benign or malignant).
Foreign body (biliary stent, silk suture, sump syndrome).
Intrahepatic bile duct stricture.
Excluded bile duct segment (with external fistula).
Common duct stones.
Intrahepatic stones.
Vascular injury (hepatic arterial or portal venous).
Altered gastrointestinal flora (achlorhydria, duodenal diverticulum).
22
Bacterial seeding via the hepatic artery is a further recognized cause of liver
abscess. This may occur in subacute bacterial endocarditis or in other conditions
associated with systemic bacteremia such as pneumonia, osteomyelitis, urinary
sepsis or following intravenous drug abuse.
Hepatic artery catheterization may also be complicated by the formation of
liver abscess.
Bacterial seeding may occur in the context of deficiencies of the host defenses.
Branum et al (1990)13 have noted that there is an increase in the number of
patients with underlying solid tumors or hematological disease.
Children with chronic granulomatous disease or other disorders of
granulocyte function may also present with liver abscess, most commonly due to
organisms such as Staphylococcus aureus. Other authors have reported liver
abscess in patients with the acquired immune deficiency syndrome.26
Liver abscess may also result from the direct extension of infection
into the liver. This may occur with infection involving the subphrenic or pleural
space,gallbladder, or when gastric or intestinal perforation occurs directly into the
liver.
23
TABLE – 5 : PATHOGENESIS OF PYOGENIC LIVER ABSCESS BY
ETIOLOGY
Etiology Source of infection Distribution Primary microorganisms
Biliary system Cholangitis,biliary Both lobes, Single species, gram (-)
obstruction multiple aerobes and anaerobes
Ecoli
Portal circulation Intra-abdominalinfection Right lobe > left Polymicrobial, enteric
multiple or single aerobes and anaerobes
Efaecalis, Ecoli, B
fragilis
Liver metastasis Area of B fragilis metastasis
Arterial Bacteremia, systemic Both lobes, Single species, gram
circulation infection multiple (+)aerobes S aureus,
Spyogenes
Trauma Direct exposure,necrosis Area of injury Single species gram
(+)aerobes S aureus,
Spyogenes
Direct extension Cholecystitis, perforated Adjacent area Single species, gram (-
ulcer )aerobes E coli
Cryptogenic Unknown Right lobe > left Single species,
anaerobic B fragilis
Pathology
The etiology of a Hepatic abscess serves as the best predictor of the
number, location and size of abscesses affecting a given patient.
Generally, portal, cryptogenic and traumatic hepatic abscesses are
solitary and large, while biliary and arterial abscesses are multiple and small.
24
Overall, pyogenic liver abscesses highly localize to the right hepatic lobe in
65% of cases, with the majority of these being solitary. The left lobe is rarely involved
in 12% of cases, with 23% of patients having bilateral abscesses.
The number of multiple and bilateral abscesses has increased as more patients present
with a biliary etiology. Bilateral disease occurs in 90% of the cases with a biliary or
arterial source of infection, distributing along the terminal branches of the portal triad.
In contrast, hepatic abscesses resulting from the intra-abdominal infectious
sources have a more propensity to develop in the right hepatic lobe, a process that may
be explained by the preferential blood flow from the superior mesenteric vein to right
lobe.
Fungal hepatic abscesses are most often multiple, bilateral, and miliary in nature.
Microbiology
The pyogenic nature of PLA is usually confirmed by microbiological culture.
This involves aspiration of the liver abscess together with blood
culture. Abscess cultures are more likely to be positive than the blood cultures.
Positive abscess cultures are found around 80 to 97% of thecases, whereas
blood cultures are positive in around 50 to 60% of the cases.9,14,27.
In western countries, Escherichia coli is the most frequent organism isolated,
in oriental series, Klebsiella pneumoniae may be the predominant
organism.28,29
Other aerobic Gram-negative bacteria are frequently isolated including
Proteus spp, Enterococci, Enterobacter spp Pseudomonas aeruginosa and
Citrobacter spp.Bacteroides fragilis is the most common anaerobe,though
other Bacteroides, anaerobic streptococci andClostridia spp may also be
found.
25
TABLE – 6 : MICROBIOLOGICAL FINDINGS OF ABSCESS AND BLOOD
CULTURES
Organism Seeto and Seeto and Stain et al 1991 Rockey 1996 Rockey 1996
Stain et al 1991
Organism Abscess (%) Blood (%) Abscess (%) Blood
(%)
Escherichia 35 15 14 07
Klebsiella 28 13 12 10
pneumoniae sp
Enterococci 15 10 3 -
Pseudomaonas sp 12 4 1 1
Citrobacter sp 7 1 2 2
Proteus sp - - 2 1
Enterobacter - - 1 -
Serratia - - 1
Diphtheroids 7 8
Streptococci - -
Alpha / Viridans 14 7 6 2
Beta - - 6 2
Delta - - 3 1
Staphylococci 12 9 2 1
Other GNRs 10 3 - -
Other aerobes 6 2 - -
Bacteroides sp 18 6 7 8
Fusobacterium 7 3 1 2
Peptostreptococcus 7 2 - -
Lactobacillus 1 1 - -
Other anaerobes 4 6 - -
Microaerophilic - - - -
Streptococci 7 8 7 3
Candida - - 2 -
26
TABLE - 7 : ORGANISMS ISOLATED FROM PYOGENIC LIVER
ABSCESSES
Category of organism % of Patients
-
GRAM-NEGATIVE AEROBES
Escherichia coli 50-70
Klebsiella pneumoniae 18
Proteus 10
Enterobacter 15
Serratia Rare
Morganella Rare
Actinobacter Rare
-
GRAM-POSITIVE AEROBES
Streptococcal species 30
Enterococcus faecalis 20
B-Streptococci 10
A-Streptococci -
Staphylococcal species 15
40-50
ANAEROBES
Bacteroides species 24
Bacteroides fragilis 10
Fusobacterium 10
Peptostreptococcus 5
Clostridium 5
Antinomyces Rare
26
FUNGAL
7
STERILE
27
Microaerophilic streptococci have been shown to be the important
components of liver abscesses. In one series, these organisms were identified in
81% and 86% of positive abscess and blood cultures respectively.30
Other Gram positive organisms such as Group A streptococci and
Staphylococcus aureus account for the remainder of isolates. Causative organisms
tend to vary according to the underlying aetiology of liver abscess.
Abscesses secondary to pyelophlebitis and cholangitis are frequently
polymicrobial and usually involve Gram-negative organisms and anaerobic
bacteria.
Systemic bacteremia commonly causes infection with a single
organism, often Staphylococcus aureus, streptococci or other aerobic Gram-
negative organisms.
These organisms are more likely to cause liver abscess following
trauma. Staphylococcus aureus is the predominant organism isolated from hepatic
abscessesin children.
Hepatic abscess in childhood usually occurs as a result of chronic
granulomatous disease, haematological malignancy, or immunosuppression.
The main reasons for negative cultures probably related to poor anaerobic culture
technique or the use of broad-spectrum antibiotics prior to abscess drainage.
Rubin et al (1974)31 analyzed culture techniques in 50 patients with
pyogenic liver abscess. If culture techniques were adequate, 55% of samples grew
anaerobic bacteria.
However, if culture techniques were considered inadequate, only 8%
of samples yielded anaerobes. In the series reported by Sabbaj et al (1972).32 45%
of cultures obtained from hepatic abscesses were found to be anaerobic.
28
In this study, specimens were immediately placed under anaerobic
conditions and promptly cultured using a variety of selective media. Aerobic
organisms.
Were most commonly recovered as pure isolates whereas in case of anaerobic
organisms which are more likely to be cultured in combination with aerobes. This
would also suggest that many abscess contain anaerobes that are not isolated by
routine culture techniques.
Recently pyogenic liver abscess secondary to Klebsiella pneumoniae
has emerged as a distinct clinical entity in diabetic patients in a study.33
This would appear to be the only one factor though, as 25% of patients
with K.pneumoniae liver abscess do not have diabetes.
An increase in the number of patients with haematological malignance
has contributed to the emergence of fungal abscesses.34
Patients with fungal abscesses have almost always undergone
cytotoxic chemotherapy.
Hepatic abscess may be used by mycobacteria, though it is extremely
rare. However, of the few patients with acquired immunodeficiency syndrome
presenting with liver abscess, mycobacterium tuberculosis is a common infecting
organism.26
29
AMOEBIC LIVER ABSCESS CLINICAL PRESENTATION & LABORATORY INVESTIGATIONS
The symptoms and signs of amoebic liver abscess vary according to the
location of the abscess and the gravity of the illness.
Less than 30% of patients have active diarrhoea during any time before
presentation, even though intestinal infection by E. histolytica must have occurred.
A concomitant liver abscess is found in one third of patients with amoebic colitis.
Amoebic liver abscess occurs ten times more common in males.
While the peak incidence is between 20 and 60 years worldwide, it is
predominantly a disease of young adult males. Children, especially neonates,
pregnant women and women in the postpartum period have very much increased
risk of severe disease and death. Treatment with steroids, malnutrition and ,
malignancy are other risk factors for severe disease.35
Typically, the onset is abrupt, with pain located in the right
hypochondrium being the chief complaint. The pain may radiate to the right
shoulder and scapular areas, and increase with the movements of coughing, deep
breathing and walking.
If the abscess is located in the left lobe, the pain may be epigastric,
precordial or retrosternal and may radiate to the left shoulder. An abscess located
in the inferior aspect of the liver may present like signs of peritonitis due to any
upper abdominal cause.
The second most common feature is fever between 38 and 40oC, this is
seen virtually in all patients. Other less common symptoms include anorexia,
nausea, vomiting and an acute colitic illness. Occasionally the presentation is
insidious, last for 2 or more weeks and in such patients there will be significant
weight loss may occur.
Physical examination reveals a tender, generalized and soft
hepatomegaly which is usually accompanied by overlying muscle guarding,
30
intercostals tenderness and occasionally, increased warmth and subcutaneous
edema.
Mild jaundice is often seen, though only in 5-8% of cases is it a prominent feature.
In its commonest location – the right posterior superior surface – amoebic liver
abscess is mostly accompanied by right basal lung signs.
A pericardial rub may occur in association with left-side abscess.
Signs of hepatic failure, splenomegaly and , ascites are rare.
Clinically, the usual differential diagnoses include pyogenic liver abscess,
acute cholecystitis and hepatitis due to viral or other cause,.
With atypical presenation, liver hydatid or simple cysts hepatocellular
carcinoma, may be considered.
Haematological investigations in amoebic liver abscess usually reveal
leucocytosis (12000-30000 cells/ mm3) without eosinophilia.
Mild anemia may occur in one half of patients, although in young male
alcoholics, hemoglobin may be normal or raised.
Liver function tests show moderate raise of alkaline phosphatase, direct
bilirubin and transaminase levels.
The most common abnormality is an increased prothrombin time.
Chest radiography typically shows elevation of the right dome of the diaphragm
with an anterior bulge on the lateral view, atelectasis of the right lung and pleural
effusion.
The liver shadow on plain abdominal film is diffusely enlarged, and is
usually featureless.
Gas in the biliary tree or liver parenchyma indicates a pyogenic process
unless there is communication of the hepatic abscess cavity with the lung or
hollow viscus.36
31
TABLE 8: CLINICAL PRESENTATION & LABORATORY
INVESTIGATIONS
SYMPTOM % of Amoebic Abscesses
Pain 90
Fever 87
Nausea and vomiting 85
Anorexia 50
Weight loss 45
Malaise 25
Diarrhea 25
Cough or pleurisy 25
Pruritus <1
SIGN
Hepatomegaly 85
Right upper quadrant tenderness 84
Pleural effusion or rub 40
Right upper quadrant mass 12
Ascites 10
Jaundice 5
LABORATORY DATA
Increased alkaline phosphatise 80
WBC count >10,000/mm3 70
Hematocrit <36% 49
Albumin <3 g/dL 44
Bilirubin >2 mg/Dl 10
32
DIAGNOSTIC INVESTIGATIONS:
Ultrasonography
Though simple, inexpensive and quick to perform, with a diagnostic accuracy
of 90%,35 interpretation of ultrasonographic findings against the clinical background
and confirmation by serological tests is required to avoid major errors in diagnosis.
Abscesses are usually located peripherally in contact with the liver capsule and
vary from 2 to 21 cm in size (mean 7.75cm). The outline is round, oval or lobulated.
The abscess, though clearly defined from the surrounding normal liver
parenchyma with distal sonic enhancement, rarely has rim echoes that can be
interpreted as an abscess wall.
The contents of the abscess cavity are usually hypoechoic and non-
homogenous, with the internal echoes increasing at high gain and decreasing or
almost absent at normal gain.
In 78-80% of cases the abscess occurs singly and in the right lobe, 10% are in
the left lobe, and the rest multiple. In up to 6% of cases the abscess may be located in
the caudate lobe.
The mean resolution time is 7 months, and in 70% of patients the
ultrasonographic findings persist for 6 months or more.
This must be taken into account when evaluating treatment responses, for
which, serial scanning is unwarranted in patients with clinical improvement.
While pyogenic liver abscesses tend to resolve earlier, with 50% resolving in 2
months and 90% within 4 months.
33
Amoebic liver abscess acquire a more echogenic and fibrous wall in 8-16
weeks and begin to resemble but should be differentiated from an encapsulated tumor.
With time, resolution may be complete or result in a small residual cystic
cavity that resembles a simple cyst of the liver.37
TABLE 9 : ULTRASOUND CHARACTERSTICS OF LIVER ABSCESSESS72
FINDINGS DURATION OF CLINICAL NUMBER OF ILLNESS (WEEKS) ABSCESSES
Wall Echo poor wall 1 - 3 32
Fine echogenic rim 4-6 28
Thick echogenic wall 8 - 12 4
Contents
Mixed hyper- and 1 - 3 22 hypoechoic pattern
Homogenous hypoechoic 4 - 8 30 pattern
Mixed hypo- and anechoic 8 - 16 12 pattern
Echogenic nodules 4 – 12 15
TABLE 10 : EVOLUTION AND HEALING OF AMOEBIC LIVER ABSCESS72
ULTRASOUND DURATION OF ABSCESS CHARACTERISTICS
Echo-poor wall with heterogenous echo 2 to 3 weeks pattern
Fine echogenic rim with homogenous 4 to 8 weeks hypoechoic pattern
Echogenic nodules 4 to 2 weeks
Thich ecogenic wall with anechoic areas 8 to 16 weeks
Complete healing 3 to 6 months
34
o Computed tomography
Especially in the acute situation, a computed tomography (CT) scan
does not add to the diagnostic accuracy of ultrasound except in the evaluation
of imminent rupture of abscess.
In the atypical or chronic case it may be of value-showing better rim
enhancement with contrast in pyogenic liver abscess, and high CT density of
the contents in necrotic liver tumors.
o Magnetic resonance imaging
While current evidence is that magnetic resonance imaging is not
significantly superior to CT in diagnosis of amoebic liver abscess, it may be
useful in follow up of a treated cases, and in differentiating it from a hepatic
neoplasm.
Untreated amoebic liver abscess, show up as heterogeneous abscess
cavities that appear hypointense on T1- weighted and hyper-intense on T2-
weighted images.
Incomplete hyperintense rings can be seen at the abscess margin.
Reparative tissue changes are seen as early as 4 days after treatment
and indicate a favourable response. Evidence of haemorrhage would show up
on MRI, but the iron deposition is not typically in the periphery as in the case
of a hematoma.
o Angiography
Rarely required in the diagnosis of a straightforward amoebic liver
abscess, angiography may be necessary in a case where carcinoma is difficult
to exclude.
35
Typically, and in contrast to a neoplasm, it reveals a hypovascular or
avascular mass displacing the hepatic artery branches.
The venous phase images may likewise show displacement of the
portal vein branches, but may on occasion show a block of the portal vein.
o Gallium Scanning
Gallium scanning helps in the differentiation of amoebic from
pyogenic abscess. Amoebic abscesses, lacking in neutrophils, appear as cold
spots while pyogenic lesions are seen as warm spots.
However, owing to the long time taken in performing the scan and the
relative safety and speed of diagnostic aspiration, the role of gallium scan is
limited. It may be particularly useful in the differentiation between amoebic
and pyogenic abscess.
o Amoebic serology38 :
Patients with amoebic liver abscess virtually always (90-95%) have
serum antiamoebic antibodies.
They can be demonstrated using either indirect hemagglutination
(IHA) or counterimmunoelectrophoresis (CIE), which are similar in
sensitivity.
The enzyme-linked immunosorbent assay (ELISA) technique is also
highly sensitive and widely available.
Recent developments of this method have results in rapid and accurate
diagnosis – the test being completed in 35 minutes.
36
Antibody response is directly related to the duration of illness. It may
be negative during the first week after onset. Titres reach a peak by the second
and third months, decreasing to lower, but still detectable levels by 9 months.
Problems with interpreting serology results occur in endemic areas where
widespread amoebic colonic infection can result in high titres without invasive
colonic or hepatic amoebiasis. Its chief value lies in differentiating amoebic
from pyogenic liver abscess and from hepatocellular carcinoma.
ELISA or haemagglutination assay cannot differentiate acute from
remote infection in endemic areas. CIE and gel diffusion methods are less
sensitive but may be more helpful in the diagnosis of current infection in
endemic areas, as the results become negative 6 to 12 months after acute
infection. Efforts are on to identify antigens specific for acute infection.17
TEST PRINCIPLE38: (ELISA IgG Antibodies detection)
Purified antigens are coated to a microwell plate. Antibodies in the
patient samples bind to the antigens and are determined during the second step by
using enzyme-labelled Protein A (the conjugate). The enzyme converts the
colourless substrate (urea peroxide/TMB) to a blue end product. The enzyme
reaction is stopped by adding sulphuric acid and the colour of the mixture
switches from blue to yellow at the same time. The final measurement is carried
out at 450 nm on a photometer using a reference wavelength ≥ 620 nm.
37
Specimen collection and storage
The test has been developed for testing human serum samples. After blood collection,
the blood should be separated from blood clots as soon as possible in order to prevent
haemolysis. The serum which was separated aseptically was stored at 2-8oC until they are
tested. Haemolytic, icteric or turbid samples were not used, as it can lead to false results.
Test Procedure:
1. Bring the microwell plate PLATE and reagents to room temperature (20 – 25 o C)
2. Dilute the wash buffer WASH with distilled water 1:20.
3. Dilute the serum samples with the sample buffer DILUENT 1:50.
4. Place enough wells for positive control , negative control (in double determination),
and samples in the frame plate.
5. Pipette 100 microl positive control CONTROL + , negative control CONTROL – or
sample into the wells.
6. Incubate at room temperature (20 -25 o C) for 15 minutes.
7. Empty the microwell plate and then wash it 5 times with 300 microl diluted wash
buffer.
8. Place 50 microl (or 1 drop) substrate SUBSTRATE and chromogen CHROMOGEN
in each of the wells.
9. Incubate at room temperature (20 – 25 o C) for 15 minutes.
10. Add 50 microl (or 1 drop) stop reagent STOP.
11. Carry out a photometric measurement at 450 nm.
Figure 33 : Amoebic
38
c Serology (ELISA) TTest Proceddure
39
Evaluation and interpretation
Calculating the sample index
1. The average absorbance is calculated for the negative control.
2. 0.150 is added to the average absorbance. This yields the cut-off for the test.
3. The sample index is obtained by dividing the absorbance for the sample by the
cut-off.
For example:
Negative control 1 O.D. = 0.115
Negative control 2 O.D. = 0.125
Sample O.D. = 0.508
cut-off = 0.115 + 0.1252 + 0.150 = 0.270 2
Sample index = 0.5080.270 = 1.88
TABLE 11: EVALUATING THE SAMPLE INDEX
Negative Equivocal Positive
Sample Index < 0.9 0.9 -1.1 > 1.1
Limitations of the method
® RIDASCREEN E. histolytica IgG EIA detects IgG antibodies against
Entamoeba histolytica. and should be carried out in cases of suspected Amoebiasis.
The results obtained must always be interpreted in combination with the clinical
picture and other diagnostic findings.
Antibody signals are dependent on the localization of the parasitosis and may
vary from patient to patient.
40
If the amoebae findings in the stools are positive, a positive antibody
determination will mean that E. histolytica can be identified in the strict sense as the
cause of the clinical symptoms.
In cases of suspected extraintestinal dispersal of the parasite, a positive
antibody determination can indicate amoebiasis, even if the stool findings are
negative; the findings should be con-firmed by clinical symptoms and other diagnostic
methods.
RIDASCREEN® E. histolytica IgG 04-07-23
A negative result does not necessarily rule out the possibility of amoebiasis.
During the early stages of the infection, the number of antibodies may be so small that
the test yields a negative or equivocal result. In cases of suspected amoebiasis based
on the case history, another serum sample should be tested after a few days. A
positive result does not rule out the presence of another infectious pathogen
TABLE 12: SENSITIVITY AND SPECIFICITY IN COMPARISON
WITH TWO OTHER COMMERCIAL ELISAS
IgG
Sensitivity 100.0%
Specificity 95.6%
41
PYOGENIC LIVER ABSCESS
DIAGNOSIS
Clinical features & Laboratory Investigations.
The clinical presentation of PLA is often sub-acute.
Symptoms may have been present for many weeks prior to hospital admission.
In addition, diagnosis is often delayed for several days following
hospital admission.
Fever is the most frequent and consistent presenting symptom.
Abdominal pain is also a frequent complaint, though this is not
necessarily localized to the right upper quadrant. Many patients also complain
of a variety of non-specific symptoms such as malaise, anorexia, nausea,
vomiting and weight loss.
Diaphragmatic involvement may also result in pleuritic type pain and
symptoms of cough and dyspnoea are not infrequent. Occasionally patients are
admitted with sepsis syndrome or with peritonitis secondary to intraperitoneal
rupture of hepatic abscess. Rarely a hepatic abscess may rupture into the right
pleural space or pericardium.
Other than fever, right upper quadrant tenderness and or hepatomegaly
are the most common physical findings.
Seeto & Rockey (1996)9 found that 60% of patients had one or both
these physical signs. However, only approximately one-third of patients were
found to have the classic findings of fever and right upper quadrant
tenderness.
Jaundice was present in approximately 20% of patients and this was
suggestive to underlying biliary tract disease.
42
Chest signs, specifically related to the right lung base were present in
25% of patients in this series.
Almost all patients with pyogenic liver abscess have abnormal
haematological and liver function tests. Leukocytosis is noted in
approximately 70 to 90% of patients.
Many patients are also found to be anaemic and this usually reflects the
presence of chronic disease or a prolonged sub-acute presentation.
Erythrocyte sedimentation rate (ESR) is almost always elevated.
The most frequent liver function test abnormality observed in patients
with hepatic abscess is an elevated alkaline phosphatase. This is seen in
approximately 80% of patients.
Bilirubin is elevated in 20 to 50% of patients. Transaminases are also
abnormal in up to 60% of patients. Hypoalbuminemia is observed in
approximately 70% of patients and mild elevations of prothrombin time are
also frequently seen.
43
TABLE – 13 : SYMPTOMS AND SIGNS OF PYOGENIC LIVER ABSCESS9
Symptoms No. of patients Percentage
Fever 95 79
Chills 73 60
Abdominal pain 67 55
Nausea 45 37
Vomiting 36 30
Weight loss 34 28
Pleuritic chest pain 25 21
Cough or dyspnea 25 21
Diarrhea 24 20
Abdominal distention 6 5 Signs - -
Admitting temperature - -
> 38.5 54 39
37.5 – 38.4 34 24
Tender right upper quadrant 61 43
Hepatomegally 39 28
Abnormal chest findings 39 28
Jaundice 29 28
Guarding, rebound or 24 17
Murphy’s sign
Tender epigastrium 21 15
Abdominal distention 18 13
Ascites 6 4
44
Diagnostic imaging
Plain abdominal and chest radiographs are now used less frequently in
the assessment of patients with hepatic abscess, though they may still be of
diagnostic value. Chest radiographs are abnormal in approximately 50% of patients
presenting with hepatic abscesses. Changes suggestive of sub-diaphragmatic
pathology include an elevated right hemidiaphragm, a right pleural effusion and
right lower lobe atelectasis.
Similar findings are occasionally found in the left thoracic cavity, if the
abscess involves the left hepatic lobe. Abdominal films may show evidence of
hepatomegaly. If gas-forming organisms are present within the abscess, an air fluid
level may be seen. Air within an unoperated biliary tree may also be demonstrated,
confirming the diagnosis of cholangitis. Rarely portal venous gas may be seen on an
abdominal X-ray, confirming pyelophlebitis. Portal venous gas appears as branching
linear lucencies along the peripheral portion of the liver. Air within the biliary tree
tends to be seen more centrally. However, it is rarely possible to make this
distinction on the basis of plain film appearances alone and US or CT are usually
required.
Fig 4. : CXR showing an air fluid level within a large right lobe abscess. Elevation of
right hemi diaphragm and a loculated pleural effusion are also noted
45
TABLE 14 : DIAGNOSTIC RADIOLOGIC TECHNIQUES FOR
DIAGNOSIS OF PYOGENIC LIVER ABSCESS
ULTRASONOGRAPHY AND CT SCANNING
Abdominal US and CT both have major roles to play in the diagnosis
and management of patients with pyogenic liver abscess. Ultrasonography
shows pyogenic abscesses to be round or oval areas that are usually less
echogenic than the surrounding liver. Computed tomography shows hepatic
abscesses to be of lower attenuation than the surrounding liver.
The administration of intravenous contrast also results in intense
enhancement of the abscess wall. Ultrasound is particularly useful in
distinguishing solid from cystic lesions; it is cost effective, readily available
and has the advantage of being portable. However, ultrasound has a number of
limitations.
Ultrasound has a sensitivity of 80 to 95% for the detection of hepatic abscess.
46
Computed tomography may visualize hepatic collections as small as
0.5 cm and CT may more easily identify multiple small abscesses. Computed
tomography has been shown to be slightly more sensitive than US, with a
sensitivity of 95 to 100%.39,13,27,29,24,9. Both CT and US have the added
advantage of being able to detect other biliary and abdominal pathology.
Computed tomography is particularly sensitive for the detection of abdominal
mass lesions such as complicated appendicitis or diverticulitis. Seeto and
Rockey (1996)9 found that, for non cryptogenic hepatic abscess, CT scan was
able to identify the underlying cause in 69% of patients.
However, in addition to establishing the diagnosis, the main advantage
of these imaging modalities is that they facilitate definitive treatment by way
of US or CT guided aspiration or drainage.
Radionuclide scanning with 99mTc was the first form of imaging that
reliably detected mass lesions within the liver. This technique has a sensitivity
of approximately 80% for the detection of liver abscess.39 However, its role in
the detection of hepatic abscess has now been completely replaced by US and
CT.
Angiography is now also rarely used in the diagnosis of hepatic abscess.
Magnetic resonance has recently been used for the detection of hepatic
abscess.
47
MANAGEMENT STRATEGIES:
AMOEBIC LIVER ABSCESS
The management of amoebic liver abscess varies from conservative (medical)
management, needle aspiration, pigtail catheter drainage to open drainage depending
on various criteria. Amoebic liver abscess, undiagnosed and untreated, had a very
high mortalty rate, of almost 100%. With early diagnosis and prompt institution of
specific therapy, the prognosis is excellent and the mortality is extremely low. The
treatment and diagnosis of amoebic liver abscess has been changed dramatically over
the last three decades due to the availability of newer improved amoebicidal agents,
newer imaging modalities and guided percutaneous aspiration and catheter drainage
techniques and improved anaesthetic, surgical, and postoperative management in
cases of ruptured amoebic liver abscess.
Before 1900, the treatment of amoebic liver abscess was primarily of free
incision and drainage. But that procedure was associated with high morbidity and
mortality rate was reported to be at least 60%. Thus the treatment of amoebic liver
abscess shifted to more towards the closed aspiration with the view , to avoid
secondarily bacterial contamination of abscess cavity. The open drainage of abscess
was done only in large amoebic liver abscess and of long duration. Closed aspiration
was indicated in amoebic liver abscess as late studies suggested that living amoebae
was found in the walls of undrained tropical abscess, two thirds of the tropical
abscesses were free from bacteria when opened, and that amoebae of liver abscesses
were rapidly killed by weak solutions of quinine. The open drainage used to be done
in cases of suspected amoebic live abscess, if on microscopic examination of pus
(aspirated from abscess) shows bacteria, otherwise repeated aspiration and injection
used to be the treatment of amoebic liver abscess.
48
The rule, then, is to aspirate all liver abscess cases unless the pus is pointing at
the surface, and many cases are cured in this way without exposure to the risks of
incision. If incision subsequently becomes necessary, the previous aspiration of the
abscess is not found to prejudice the patient's chance ofrecovery.40
As early as 1935, Ochsner and De-Bakey advocated the following three principles of
treatment41.
Every case of suspected amoebic liver abscess should be given a course of
amoebicidal drug therapy before any other procedure is used, unless rupture of
the abscess appears imminent.
If evacuation of pus is necessary, aspiration and preliminary administration of
amoebicidal drugs is the procedure of choice.
Open drainage of the abscess should be reserved for the relatively few cases of
secondarily infected abscesses.
Thus, the management of uncomplicated amoebic liver abscess includes
conservative, needle aspiration, pigtail catheter drainage and open drainage depending
on the patients clinical features. Since ages the amoebic liver abscess has been known,
the treatment of amoebic liver abscess has been a matter of debate. With major
consensus, the mainstay of treatment has been medical since ages while closed
drainage versus open drainage has been a matter of hot debate till now.
49
Earlier surgical drainage was indicated in the following conditions:
Patients not responding to medical treatment in spite of repeated needle aspiration
or antiamoebic therapy.
Presence of more than one abscess cavity.
Doubt in diagnosis, or of the presence of a coexisting carcinoma or cirrhosis.
Lesions pointing below the costal margin, for fear of complications that may
result from needling of neighboring viscera, and abscesses of the left lobe liver
presenting as epigastric masses.
Patients presenting with complications such as peritonitis, empyema thoracis,
abscess bulging through the abdominal wall, pericarditis, hemobilia, obstructive
jaundice, and metastatic abscess.
Thrombosis of portal vein or inferior vena cava or fistulous connection with
hepatic ducts; and
Recurrent or refractory abscesses.
Role of Aspiration
In the era before ultrasonography became widely available, aspiration
of the typical ‘anchovy sauce’ pus from the liver was often considered vital to
confirm the diagnosis of amoebic liver abscess. Nowadays, ultrasound-guided
aspiration is often justified on the basis that the diagnosis will then be ‘more
certain’ or that the abscess can be ‘aspirate to dryness’ at the time of
diagnostic aspiration. The controversy about routine aspiration of
uncomplicated amoebic liver abscess remains unresolved.
50
Aspiration is therefore, now regarded as generally superfluous in the
management of amoebic liver abscess, and should be reserved for situation when :
♣ Amoebic serology is inconclusive, delayed, or unavailable and the main differential
diagnosis is a pyogenic liver abscess.
♣ A therapeutic trial with antiamoebic drugs is deemed inappropriate (as in
pregnancy).
♣ There is suspicion of secondary infection of the liver abscess. This is estimated to
occur in 15% of cases.
♣ When fever and pain persist for more than 3 to 5 days after starting appropriate
therapy, aspiration may provide symptomatic relief.
♣ In extremely large abscesses (>5cms and volume >200cc) where rupture is
suspected to be imminent, especially when pericardial rupture from a left lobe
abscess appears likely.
♣ Single aspiration may be sufficient for diagnostic purposes, but when performed as
part of therapy is likely to be inadequate. When more than one aspiration is
required, the placement of a percutaneous drain is probably indicated to reduce the
risk of recurrence.43
51
CHEMOTHERAPY: TABLE 15 : MEDICAL TREATMENT OF AMOEBIC LIVER ABSCESS
ADULT
DRUG DOSAGE ADVANTAGES SIDE EFFECTS
Metronidazole44 750 mg tid x 7-10 Achieves high
Half life is 8 hours. Headache (10%), days concentration in
High liver with small dizziness, nausea,
And 30-35mg/kg amounts of drug, anorexia, Heavy coating concentrations in
body wt. in three absorbs rapidly, of tongue, brownish liver, stomach,
divided doses for rapidly excreted urine, metallic taste, kidney, intestine,
10 days in without cumulative ataxia(<1%), seizures, crosses placental
children effect. paraesthesias, peripheral and blood brain
reaction with alcohol. barriers.
Tinidazole 2gm/day divided
similar Similar tid x 3 days
Emetine More effective
against trophozoites
Hydrochloride
1mg/kg/day (max. Regional Myositis, 45,46(Used where than cysts, mainly
rapid clinical 60 mg/day) for no concentrated in
CVS – hypotension, liver. Tissues level
response is more than 10 persists for 40-60 tachycardia, chest pain ,
required or days. days after dyspnoea, ecg changes.
Metronidazole
termination of
response is poor)
treatment
Chloroquine
1 gm (600 mg
C/I in patients with base) per day for
phosphate 46(used 2 days followed retinopathy and in
in recurrent or by 500 mg (300 psoriasis
resistant cases) mg base) per day Other side effects – G.I.
52
for 2-3 weeks
upset, headache, visual
disturbances and pruritis.
Effect in cyst
passers therefore
Flatulence, nausea, Diloxanide furoate 500 mg tid x 10
used for treatment
of asymptomatic vomiting, pruritis,
days carriers, family urticaria
members and
intimate contacts of
patients diagnosed
liver abscess
Parmomycin 25-35 mg/kg/day G.I. upset (1-10%),
divided tid x 7 headache, vertigo,
days eosinophilia, rash
Iodoquinol
650 mg tid x 10 Optic neuritis with long
days
term use.
53
Therapeutic strategy
Metronidazole is administered as a single drug after diagnosis, with
concomitant correction of hypoprothrombinemia, hypoproteinemia and anemia. If
dramatic improvement in 48-72 hours is noted, no other therapy other than the
complete course of metronidazole is required. A luminal agent such as Diloxanide
furoate (500 mg p,o, t.i .d. x 10 days) or Paromomycin (30 mg/kg/day in 3 doses x
10 days) must be administered following metronidazole therapy for the eradication
of intestinal infection as a part of the complete treatment.
In patients who do not respond satisfactorily, emetine or
dehydroemetine is added. Evidence of pulmonary, peritoneal or pericardial
extension is a indication for aspiration of the liver abscess with an intercostal tube
or catheter drainage into a closed-circuit collection system. Failure to adequately
control the abscess by these means – increasing signs or peritonitis, fistulization
into a hollow viscus or secondary infection with septicaemia constitutes an
indications for laparotomy.47
PREVENTION
Modern biologic techniques have helped to characterize amoebic antigents which
show great promise towards the development of a vaccine. These antigens include:
o Serine rich Entamoeba histolytica protein (SREHP) o A 170 kD subunit of Gal / Gal Nae binding lectin and o A 29 kD cysteine rich protein
Recombinant vaccines based on these antigens have been successfully used in
animal models of amoebiasis. Attempts an: now afoot to fuse these antigens with
the relevant subunits of cholera toxin and salmonella species to develop an oral
combination 'enteric pathogen' vaccine.
54
PYOGENIC LIVER ABSCESS:
Once a diagnosis of hepatic abscess is suspected, broad spectrum intravenous
antibiotics should be started. The diagnosis of hepatic abscess should be confirmed by
the aspiration of pus at the time of US or CT scan. Antibiotic therapy can be adjusted,
once the results of abscess cultures are available. Blood should also be sent for
culture. Specimens should be cultured for acid-fast bacilli and fungi and this is
particularly the case if there is a clinical suspicion of mycobacterial or fungal
infection or if patients are immunosuppressed. Empirical antibiotic therapy should
include effective cover against aerobic Gram-negative bacteria, streptococci and
anaerobic bacteria. Appropriate antibiotic combinations would include ampicillin, and
aminoglycoside and metronidazole or a third generation cephalosporin such as
cefotaxime together with ampicillin and metronidazole, alternatively a carbapenem
55
antibiotic such as imipenem or meropenem may be used. Metronidazole will also be
therapeutic for patients with amoebic liver abscess. All patients, at risk of amoebic
liver abscess should also undergo serological testing. The duration of antibiotic
treatment will vary according to the clinical setting. However, antibiotic penetration
into abscess cavities is often poor and 2 weeks of intravenous antibiotics are usually
recommended. Appropriate oral antibiotics are then usually continued for a further 4
weeks.
Extraperitoneal drainage was recommended so as to avoid contamination of
the peritoneal cavity. This was usually achieved via a posterior approach through the
bed of the twelfth rib. However, with the availability of modern antibiotics,
transperitoneal drainage may now be performed safely and this approach has the
advantage of allowing full laparotomy and assessment of any underlying
intraabdominal pathology. For patients with a known source of infection within the
abdomen or biliary system, definitive surgery may be performed, followed by abscess
drainage.
However , Bertel et al (1986)48 published a series of 39 patients with pyogenic
hepatic abscess: 23 patients were treated surgically, 16 patients underwent
percutaneous drainage. Three of the percutaneously treated group required surgical
drainage due to viscous abscess contents. However, the majority of patients were
successfully treated. Mortality was 17% in the surgical group and 13% in the
percutaneously drained group.
Wong (1990)49 described 21 patients with pyogenic liver abscess treated by
percutaneous drainage. This was successful in 85% of patients with a mortality of less
than 10%. Contraindications to catheter drainage include the presence
56
of ascites, coagulopathy and proximity to vital structures. Unfortunately, there are no
randomized controlled trials comparing surgical and percutaneous drainage and raw
comparisons between these two groups will inevitably be subject to selection bias.
However, many authors have since confirmed the safety and efficacy of percutaneous
aspiration or drainage and this is now considered the treatment of choice for patients
presenting with hepatic abscess.50 Surgery should now be reserved for patients with
an identified intraabdominal source of sepsis in which a concomitant surgical
procedure is planned or for patients who fail to respond to percutaneous treatment.
In 1996, Seeto and Rockey reported a series of 142 patients admitted between
January 1979 and December 1994, Percutaneous drainage was successful in 90% of
these patients.
TABLE –16 : THE TREATMENT OF PYOGENIC LIVER ABSCESS
Success Mortality Complications
Surgery PNA PCD Surgery PNA PCD Surgery PNA PCD (%) (%) (%)
Seeto and 61 58 77 13 6 6 - - -
Rockey 1979- (n=23) (n=17) (n=70) 1994 (1996)
Branum et al 81 - 83 9.5 - 25 48 - 71 1970- (n=28) (n=18) 1986(1990)
Rintoul et al 100 - 60 0 - 33 0 - 40 1989- (n=1) (n=15) 1993(1996)
Stain et al 66 79 83 0 2 0 0 7 4
1984- (n=3) (n=29) (n=23) 1990(1991)
Karatassas 69 60 - 43 - 0 - - 1980- (n=14) (n=18) 1987(1990)
57
THE TREATMENT OF PYOGENIC LIVER ABSCESS
There remains some controversy regarding the respective roles of
percutaneous catheter drainage (PCD) and percutaneous needle aspiration (PNA) for
the treatment of patients with liver abscess. It has recently been suggested that
percutaneous aspiration may be preferable to catheter drainage. The main advantages
of needle aspiration over catheter drainage are the fact that it is less invasive, less
expensive and needle aspiration avoids the problems related to follow-up catheter care
or loss of catheter position.
However, incomplete evacuation of the abscess cavity or rapid reaccumulation
of abscess contents following percutaneous aspiration were considered indications for
continuous catheter drainage. Percutaneous needle aspiration appears to be less
effective than PCD, though both procedures were shown to be safe with no major
complications and no deaths.51
. Abscess communication with the intrahepatic biliary tree does not prevent
abscess collections being successfully treated by percutaneous drainage. Studies have
shown that, in the absence of biliary obstruction, abscesses with intrahepatic biliary
communication are treated with equal efficacy by percutaneous drainage, though the
period of abscess drainage may be prolonged.52 This is in contrast to patients with
extrahepatic biliary communication when surgery and biliary diversion are usually
required.
Liver resection is occasionally required for patients with pyogenic liver
abscess. The indication for this is usually hepatolithiasis or intrahepatic biliary
stricture. In other patients, hepatic destruction may be so severe that they are best
served by liver resection. Clearly risks are involved as manipulation may produce a
life-threatening bacteremia. It is therefore recommended that, following ligation of the
58
vascular inflow, the involved hepatic vein should be ligated before parenchymal
dissection is carried out.
Laparoscopic drainage is an attractive alternative for patients requiring open
surgical drainage.53 The advantages of laparoscopic surgery in terms of reduced
analgesia requirements, reduced morbidity, faster postoperative recovery and shorter
hospital stay compared to laparotomy are well documented. Laparoscopic localization
of liver abscess may be more difficult than at open surgery due to lack of tactile
feedback. However, aspiration with a long endoscopic or spinal needle may aid
localization. Laparoscopic US is also likely to be useful in this respect.
A number of following studies have attempted to identify factors that are
predictive of poor outcome.
TABLE – 17 : PYOGENIC LIVER ABSCESS : FACTORS PREDICTIVE OF
MORTALITY
Lee et al Mishingeret al Chou et al(1994)
Chu et al Huang et al
(1991) (1994) (1996) (1996)(1973-1993)
Clinicaljaundice Bilirubin >1.5g/dL Age > 60 Female gender Multipleabscesses
Pleuraleffusion Leukocytosis>15.000/mm3 Gas forming
Rupture of abscess Malignancy
abscess
Bilobarabscess Haemoglobin<11 g/dL Rupture of abscess Emergency
Jaundice
laparotomy
Albumin <2.5 APACHE II Bilobar abscess Malignancy Hypoalbuminemia
g/Dl
Bilirubin >2 Malignancy Clinical sepsis Hyperglycemia Leukocytosis
mg/dL
AST >100 IU/L Bilirubin >2 mg/dL Hyperbilirubinemia Bactermia
Alkaline Urea nitrogen >20 Elevated prothrombin
phosphatase >150 Septic shock
IU/L mg/dL time
Leukocytosis >20 Creatinine Elevated APTT
000/mm3
>2mg/dL
AST > 100 IU/L
Albumin <2.5 g/dL
59
OUTCOME
The last 60 years have seen a continued improvement in the prognosis of
patients with pyogenic liver abscess. In the preantibiotic era, prior to the introduction
of surgical drainage, pyogenic hepatic abscess was almost always fatal. With the
introduction of surgical drainage and systemic antibiotics and widespread availability
of Ultrasonography and CT scan facilitated earlier diagnosis and the development of
percutaneous methods of drainage resulted in lower mortality. Following studies
shows mortality rate .
TABLE 18 : MORTALITY RATE
STUDIES MORTALITY
Miedema % Dineen (1984) 50%
John Hopkins series (1952-1972) 65%
(1972-1993) 31%
Branum et al (1990) 19%
Seeto & Rockey (1996) 11%
The incidence of pyogenic liver abscess appears to be increasing. This is in
part due to a more aggressive approach to the treatment of patients with hepatobiliary
and pancreatic malignancy and the increasing use of cytotoxic drugs. Uncomplicated
pyogenic liver abscess is now a disease with a good prognosis.
This is illustrated by the fact that patients with cryptogenic liver abscess may
have a mortality as low as 2%.9 Factors such as delayed presentation and delayed
diagnosis may both contribute to poor outcome. However, the major factor now
contributing to mortality in patients with pyogenic liver abscess is the severity of the
underlying disease and in particular the presence of malignancy.
It is the management of these patients that will continue to provide a clinical
challenge in the future.
60
COMPLICATIONS OF LIVER ABSCESS54,55,46
Communication or extension of liver abscesses occur into neighboring cavities
and organs – the peritoneum, viscera and large vessels on one side of the diaphragm
and the pleura, bronchi, lungs and pericardium on the other.
TABLE 19 : COMPLICATIONS OF LIVER ABSCESS
COMPLICATIO FEATURES USG/CT MANAGEMENT NS SCAN
AMOEBIC LIVER ABSCESS 1. Secondarily Most common, features - Aspiration and
Infected of Peritonitis Drainage (10.0%) 2. Peritoneal or Incidence of spontaneous Shows Laparotomy and
Visceral rupture – 2.7 – 17%of Perihepatic drainage or involvement cases. collection Laparoscopy drainage (Ruptured) Presentation: Abdominal but difficult - Appearance as tan – (18 – 70%) Pain, Mass or to say coloured bulge on the Generalised Distension, whether it surface. Tender Hepatomegaly, is a actual Mortality rate (12% - Intercostal Tenderness, leak or 50%) Right Basal Lung Signs, reactive Clinical Jaundice and from sudden bloody diarrhoea abscess (Colonic Rupture) and cavity. Haemetmesis (Hepatogastric fistula) 3. Thoracic or Presented as Sympathetic Pleural Thoracentesis, rarely
Pleuropulmonary straw coloured right effusion Pulmonary involvement sided effusion, rupture Decortication, into pleural cavity, Postural Drainage, bronchial tree – bronchodilators and Dyspnoea, dry cough, anti-amoebic drugs – Right basal crepitations, Metronidazole. Or a pleural rub combined approach. 3. Pericardial Abscess of Left lobe Pericardial Pericardiocentesis +
involvement more prone for this thickening Liver abscesss complications. or Aspiration followed May range from Pericardial by Antiamoebic drugs Pericardial effusion to effusion Pericardial Tamponade
61
MATERIALS AND METHODS
This study was conducted in RAJIV GANDHI GOVT GENERAL HOSPITAL,
CHENNAI during the period of March 2016- August 2017.
INCLUSION CRITERIA Liver abscess in alcoholic and nonalcoholic patients, who are admitted in
Institute of General Surgery, Rajiv Gandhi Government General Hospital, Chennai
EXCLUSION CRITERIA 1) Age <18 years
2) Liver abscess in Malignancy.
3) Traumatic liver abscess
MODE OF EVALUATION
Patient data collected from all patients admitted in General Surgery
department, Rajiv Gandhi Government General Hospital, Chennai. Detailed history of
patient will be entered in proforma.
Complete haemogram , LFT, Prothrombin time, urea, creatinine will be sent immediately on presentation.
Preliminary Ultrasound of Abdomen and Pelvis done on the same day of
presentation. CECT done if needed.
Treatment of patient done based on patient condition according to hospital
protocol.
Patient planned for surgery informed consent taken.
STATISTICS
Proportion (%) of various outcomes of liver abscess studied and tabulated below.
th
The me
he oldest pa
02468
1012141618
TABL
U
31
41
A
T
ean age of p
atient is 68 y
Upto 30 yrs
8
R
LE NO: 20
Age
Upto 30 yrs
1 - 40 yrs
1 - 50 yrs
Above 50 yrs
otal
Figu
presentation
years of age
31 - 40 y
14
Age
62
RESULTS
0. AGE D
Freq
s
re 5: Age D
n is 41.66, t
e
yrs 41 - 5
4
distribu
S
DISTRIBU
quency Pe
8
14
17
11
50
Distribution
the younges
50 yrs Ab
17
ution
UTION
ercent
16.0
28.0
34.0
22.0
100.0
n
st patient is
bove 50 yrs
11
18years of
age and
Li
Gender
Female
Male
Total
iver abscess
TABLE
Frequen
Fig
is more com
90%
63
NO:21 G
ncy Perce
5 10
45 90
50 100
gure 6: Gen
mmon in male
10%
%
GENDER
Female M
GENDER
ent
Valid
Percen
0.0 10.0
0.0 90.0
0.0 100.0
nder
es 90% than
%
Male
nt
Cumulat
Percen
0 1
0 10
0
females (10
tive
nt
10.0
00.0
%)
A
Out
TAB
Abdominal
pain
Absent
Present
Total
of 50 patien
BLE NO:2
Frequen
F
nts 31 patien
62%
AB
64
22 ABDOM
ncy Perce
19 38
31 62
50 100
Figure 7: A
nt (62%) had
DOMINAL
Absent P
MINAL P
ent
Valid
Percen
8.0 38.0
2.0 62.0
0.0 100.0
Abdominal
d abdominal p
38%
L PAIN
Present
PAIN
nt
Cumulat
Percen
0 3
0 10
0
Pain
pain.
tive
nt
38.0
00.0
Out
Feve
Fever
Absent
Present
Total
of 50 of pati
er is the mos
TABLE
Frequen
ients 37 patie
st common sy
74%
A
65
E NO:23 F
ncy Perce
13 26
37 74
50 100
Figur
ents had feve
ymptoms.
FEVER
Absent Pre
FEVER
ent
Valid
Percen
6.0 26.0
4.0 74.0
0.0 100.0
e 8: Fever
er. That is 74
26%
esent
nt
Cumulat
Percen
0 2
0 10
0
4% patients h
tive
nt
26.0
00.0
had fever.
Out
Icterus
Absent
Present
Total
t of 50 patie
TABLE
Frequen
ents studied
24%
I
A
66
NO:24 IC
ncy Perce
38 76
12 24
50 100
Figure 9:
only 12(24
ICTERUS
Absent Pre
CTERUS
ent
Valid
Percen
6.0 76.0
4.0 24.0
0.0 100.0
Icterus
4%) patients
76%
S
esent
nt
Cumulat
Percen
0 7
0 10
0
s had icterus
tive
nt
76.0
00.0
s.
He
32% of pati
0.0
10.0
20.0
30.0
40.0
50.0
60.0
70.0
80.0
TAB
epatomegaly
NO
YES
Total
ients had he
BLE NO:2
y Frequen
Figu
epatomegaly
68.0
NO
HEP
67
25 HEPA
ncy Perce
34 68
16 32
50 100
ure 10: Hep
y other pati
PATOMEG
Series1
TOMEGA
ent
Valid
Percen
8.0 68.0
2.0 32.0
0.0 100.0
patomegaly
ents had no
GALY
ALY
nt
Cumulat
Percen
0 6
0 10
0
y
ormal liver s
32.0
YES
tive
nt
68.0
00.0
span.
A
Out of 50 p
alcoholics.
TA
Alcoholism
Absent
Present
Total
patients 35 (
No female
ABLE NO
Frequen
Figur
(70%) patie
e was alcoho
70%
ALC
A
68
O:26 ALC
ncy Perce
15 30
35 70
50 100
re 11: Alcoh
ents were al
olics.
%
COHOLI
Absent Pre
COHOLIS
ent
Valid
Percen
0.0 30.0
0.0 70.0
0.0 100.0
holism
lcoholics an
30%
SM
esent
SM
nt
Cumulat
Percen
0 3
0 10
0
nd 15 (30%)
tive
nt
30.0
00.0
) patients wwere non
Out of 50 p
ALTE
TAB
Serum bi(mg%
<1.>1.
patients 13(
ERED LIV
LE NO:2
ilirubin %)
2 2
Figu
(26%) patie
26%
Seru
69
VER FUN
27 SERUM
Frequenc
37 13
re 12: Seru
ent had jaun
um bilir<1.2 >1.
NCTION
M BILIRU
y Pe
um Bilirubi
ndice.
7
ubin.2
TEST
UBIN
ercent
74 26
in
74%
SGOT( NO
YE
To
2
4
6
8
(>40IU/ML)O
ES
otal
0.0
20.0
40.0
60.0
80.0
TABL
) Frequ
Fig
NO
72.0
70
E NO:28
uency Pe36
14
50
gure 13: SG
SGOT
Series1
SGOT
ercent P72.0
28.0
100.0
GOT
YES
28.0
Valid Percent
C
72.0
28.0
100.0
Cumulative Percent
72.0
100.0
SGPT
2
4
6
8
T(>40IU/M
NO
YES
Total
0.0
20.0
40.0
60.0
80.0
TABL
ML) Freque
Fig
NO
74.0
71
LE NO:29
ency Perc
37 7
13 2
50 10
gure 14: SG
SGPT
Series1
SGPT
cent
Val
Perc
74.0 7
26.0 2
00.0 10
GPT
YES
26.0
id
ent
Cumu
Per
74.0
26.0
00.0
ulative
cent
74.0
100.0
72
TABLE NO:30 GGT
GGT(>30IU/L) FREQUENCY PERCENT
YES
NO
TOTAL
33
17
50
66
34
100
Figure 15: GGT
66%
34%
0
10
20
30
40
50
60
70
GGT(>30IU/L)
GGT
YES NO
AL
0.0
10.0
20.0
30.0
40.0
50.0
60.0
70.0
LP RAISED
NO
YES
Total
0
0
0
0
0
0
0
0
TABL
Frequ
Figure
NO
64.0
AL
73
LE NO:31
uency Perc
32
18
50 1
e 16: ALP R
LP RAISED
1 ALP
cent
Va
Perc
64.0
36.0
00.0 1
Raised
YES
36.0
alid
cent
Cum
Pe
64.0
36.0
00.0
mulative
ercent
64.0
100.0
S.ALBU
N
0
20
40
60
80
100
TAB
UMIN(<3MG
NO
YES
Total
0.0
0.0
0.0
0.0
0.0
0.0
BLE NO:3
G/ML) Fr
Figur
NO
88.0
S.A
74
32 SERUM
requency P
44
6
50
re 17: S.Alb
ALBUM
M ALBU
Percent P
88.0
12.0
100.0
bumin
YES
12.0
MIN
UMIN
Valid
Percent
Cu
88.0
12.0
100.0
umulative
Percent
88.0
100.0
PT(>
Liver func
SGOT wa
SGPT was
ALP was r
GGT was
S.albumin
PT was inc
TABLE
>20SEC)
NO
YES
Total
ction test wa
s raised in 2
s raised in 2
raised in 36
raised in 66
n was decrea
creased in 1
E NO:33
Frequ
Figur
as done in a
28% of pati
26% 0f patie
6% of patien
6% of patien
ased in 14%
14% of patie
14
75
PROTHR
uency Pe
43
7
50
re 18: Prot
all 50 patien
ent
ent
nt
nt
% of patient
ent
8
4%
PT
NO YES
ROMBIN
ercent
V
P
86.0
14.0
100.0
hombin Ti
nts
6%
S
N TIME
Valid
Percent
C
86.0
14.0
100.0
me
Cumulative
Percent
86.0
100.0
LOBE I
Bot
Lef
Rig
Tot
U
TAB
INVOLVED
th
ft
ght
tal
ULTRAS
BLE NO:3
D Frequ
Figure
70%
LOB
76
SOUND F
34 LOBE
uency Pe
8
7
35
50
19 : Lobe I
1
E INVOL
B L R
INDINGS
E INVOLV
ercent
V
P
16.0
14.0
70.0
100.0
Involved
6%
14
LVED
R
S
VED
Valid
Percent
C
16.0
14.0
70.0
100.0
4%
Cumulative
Percent
16.0
30.0
100.0
NO. O
M
Si
T
TAB
OF ABSCES
Multiple
ingle
otal
BLE NO:35
SS Freque
Figure 2
76%
SINGL
M
77
5 NUMBER
ency Perc
12
38
50 1
20: Single /
LE/MUL
Multiple Si
R OF ABSC
cent
Va
Perc
24.0 2
76.0 7
00.0 10
Multiple
24%
LTIPLE
ingle
CESS
lid
cent
Cum
Per
24.0
76.0
00.0
mulative
rcent
24.0
100.0
S
Usg was doIsolated RigIsolated LeBoth lobes 76% pts ha24% pts ha 68% pts ha32% pts ha
TAB
SIZE(CM) <5
>5
Total
one in all caght lobe wa
eft lobe was involved in
ad single absad multiple a
ad abscess siad abscess si
68
BLE NO:3
Frequ
F
ases as involved
involved inn 16% of ca
scess abscesses
ize >5cm ize <5cm
8%
S
78
36 SIZE O
uency Per16
34
50
Figure 21: S
in 70% of cn 14% of cases
SIZE/cm
<5 >5
OF ABSC
rcent V
Pe32.0
68.0
100.0
Size / cm
cases ases
32%
m
CESS
Valid ercent
CuP
32.0
68.0
100.0
umulative Percent
32.0
100.0
R
W
1
CO
LA
PIG
DR
Tot
Regarding tr
While 52% o
14% of pts
0
5
10
15
20
25
30
Treatment
ONSERVAT
APARATOM
GTAIL
RAINAGE
tal
reatment 34
of pts liver
underwent
CONSERVA
TABLE N
Freq
TIVE
MY
Fi
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ATIVE LA
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quency Pe
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APARATOMY
REATME
EATMENT
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Val
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14.0 1
52.0 5
100.0 10
reatment
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gtail cathete
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PIGTAIL D
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34.0
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52.0
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DRAINAGE
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34.0
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80
DISCUSSION
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%.1
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 liver abscess has remained relatively unchanged. Untreated, this infection remains
uniformly fatal.
The changing scenario in incidence, diagnostic methods, treatment
&complications associated with liver abscess due to increasing percentage of
alcoholics. the current serious problem in our country, has inspired me in doing an
indepth study, regarding Liver Abscess, which assumes more importance in our country
where rural population constitutes approximately 70% and therefore it mandates,
appropriate & realistic guidelines to be drawn up for early diagnosis and change in
management strategies, in order to reduce the morbidity and mortality associated with
it.
The collected data were analysed with IBM.SPSS statistics software 23.0
Version. To describe about the data descriptive statistics frequency analysis,
percentage analysis were used for categorical variables and the mean & S.D were used
for continuous variables.
81
AGE AND SEX INCIDENCE
Most of the patients who presented with Liver Abscess were in the middle age
with patients in third to fifth decade accounting for 71.0% of the cases. Mean age of
presentation is 42yrs, which is comparable to other Studies.
Studies Mean Age[ in years]
Shyam Mathur56 20 – 45 years (32.5 years)
Khee Siang Chang, Chin Ming57 47.6 years
Antonio Grorgia58 16 – 78 years ( 45.3 years)
Present study 18 – 68 years (42 years)
Studies Male Female
Shyam Mathur56 90.0 % 10.0%
Indian Journal Of Surgery200259 96% 04%
Present study 90.0% 10.0%
Present study shows a very high incidence of Liver Abscess in males [90.0%] as seen
in other Indian studies like Shyam Mathur [90.0%] and Indian Journal Of Surgery [96.0%]
SYMPTOMS & SIGNS
Most of the patients who presented in this series presented with Fever
[74.0%], abdominal pain(62.0%) which was more significant as compared to other
studies listed below.
Fever (74.0%), Hepatomegaly (32.0%) was common presentation in our
series and was comparable to the studies listed below but icterus (32.0%) was more
common clinical presentation compared to study done by Hyo Min Yoo et al (7.0%)
82
SYMPTOMS Hyo Min Khee Siang, Shyam Present Series
Yoo et al60 Ching Ming Mathur
Pain in Abdomen 85.0% 57.0% 80.0% 62.0% Fever 71% 97.2% 70.0% 94.0% SIGNS
Hepatomegaly 41.0% - - 32.0% Icterus 7.0% - - 76.0%
ALCOHOLISM IN CASES OF LIVER ABSCESS
Study Alcoholism Shyam Mathur et al 70%
Present Series 70.0%
Alcoholism was found to be the most consistent etiological factor in this study
of liver abscess. 70% of the cases of this study were found to be alcoholics as
compared to other study by Shyam Mathur et al where 70% of the cases were
alcoholic which concludes Alcoholism has a strong association with liver abscess
patients.
83
ANALYSIS OF LABORATORY
INVESTIGATIONS
Labarotary Investigations Hyo Min Yoo et al Present Series
Alkaline Phosphatase 55% 36.0%
(>115 IU/L) Albumin (<3.0gm/dl) 68% 12.0%
Prothrombin Time (>20 14% 14.0%
sec)
The above table shows that following Lab. Investigations Raised Alkaline
Phosphatase, Raised GGT was found in most of Alcoholic liver abscess patients.
Hypoalbuminaemia, Raised Prothrombin Time are the most important Laboratory
Investigations in Diagnosing Liver Abscess.
Present series showed trends similar to those of other study listed above
but Raised Alkaline Phosphatase Levels was the single most common Labarotory
abnormality in our study for Diagnosis of Liver abscess.
USG FINDINGS OF LIVER ABSCESS
Chaturbhul World J
Hyo Min Lal Rajak Gastroenterol Present
Lobar Distribution et al65
2008 April 7;
Yoo et al Series
14(13): 2089-
2093
Solitary abscess 89.0% 84.0% 76.29% 76.0%
Right lobe abscess 69.0% 72.0% 74.12% 70.0%
Left lobe abscess 20.0% 12.0% 14.28% 14.0%
Multiple abscess 11.0% 20.0% 23.7% 24.0%
84
Size of liver abscess
(cms)
<5cms 45.0% - 34.16% 32.0%
>5cms 55.0% - 65.83% 68.0%
Ultrasound abdomen was done to all patients in this study and various findings
were analysed.
Solitary abscess was seen in 76.0% of cases & Multiple abscesses were seen in
24.0% cases comparable to other Studies
Right lobe involvement (70.0%) was comparable to other studies listed above
but isolated left lobe involvement was 14% in our study as compared to other study
Hyo Min Yoo et al (11.0%) and Chaturbhul Lal Rajak et al (20.0%) & World J
Gastroenterol 2008 April 7; 14(13): 2089-2093 (23.7%)
85
ANALYSIS OF TREATMENT
Treatment Modality Hyo Min Yoo et al Present Series Surgical 21.0% 14.0%
Open Laparotomy 21.0% 14.0% Aspiration 79.0% - Pigtail Catheter Drainage - 52.0%
Conservative (Antibiotics - 34.0%
Only)
Controversies in the management of liver abscess still exist. Surgical drainage
of liver abscess has been an accepted therapy for decades. The diagnosis and
treatment of liver abscess has changed due to advances in imaging techniques.
7/50 Patients (14%) underwent laparotomy compared to 21.0% Hyo Min et al
study.
26/50 patients (52.0%) underwent pigtail catheter drainage under ultrasound
guided compared to Hyo Min et al study no patient underwent pigtail drainage.
17/50 patients (34.0%) whose abscess size was <5ml underwent conservative
(medical) management compared to Hyo Min et al study no concept of conservative
management.
86
CONCLUSION
Liver abscess is a very common condition in India. India has 2nd highest incidence of
liver abscess in world.
Liver abscesses occurred most commonly between 30-60 years
Most of the cases had an acute presentation
Males were affected more than females.
Pain abdomen was the most consistent symptom
Fever being the most common occurring symptom
Alcohol consumption was the single most important etiological factor for causation of
liver abscesses.
Alkaline phosphatase is the most consistently elevated among all Liver Function
Tests.
Raised Alkaline phosphatise level, Raised SGOT,SGPT,GGT, Hypoalbuminaemia,
Prolonged Prothrombin time were considered as the predictive factors of complicated
(Ruptured) liver abscess in this study..
Liver abscess usually present as a solitary abscess most commonly in the right lobe of
liver.
All cases of liver abscesses do not require invasive management.
Multiple small abscesses and solitary abscess of volume < 5cm can be managed
successfully on conservative antimicrobial therapy alone but recurrence rate was high.
Ultrasound Guided Pig Tail Catheter drainage procedure is a safe and effective
method of liver abscess management in abscesess size >5cm unrupturred.
Laparotomy and Drainage remains the standard of care in ruptured liver abscess into
the peritoneal cavity in this study, as we had no recurrence and mortality associated
with it.
87
SUMMARY
A clinical study of liver abscesses was chosen as this is a fairly commonly
disease in this part of the country. An attempt was made in this study to define the
various symptom complex, modes of presentation, methods used in diagnosis,
treatment options of liver abscesses.
The following observations were made in the present study: Mean age of preseFever being the most commonly occurring symptom in 74.0% of cases.
Fever being the most commonly occurring symptom in 74.0% of cases.
Pain abdomen was the most consistently occurring symptom present in 62%cases
Hepatomegaly was present in 32% of cases, icterus was found in 76% of the cases,
This study found the Alcohol as the single most consistent etiological factor in
all patients of liver abscess. 70.0% of cases consumed alcohol. Thus it may seem
likely that alcoholism may predispose to formation of liver abscesses.
Laboratory investigations were analysed. Alkaline phosphatase (64%)
was the single most consistent liver function test to be abnormal in cases of liver
abscesses. Hypoalbuminemia was noted in 12% of cases, Prolonged Prothrombin time
(>20 sec) in 14% cases and raised SGOT (28%) & SGPT (26%), GGT (66%).
Alkaline phosphatase level (>300 IU/l), Hypoalbuminaemia
(<3.0mg/dl), Prolonged Prothrombin time (>20 sec) were considered as the predictive
factors of complicated (Ruptured) liver abscess in our study.
Ultrasonography revealed solitary abscess in 76.0% and multiple
abscesses in 24.0%. Isolated right lobe abscess was seen in 70.0% and left lobe
abscess in 14%. Both lobe involvement was seen in 16.0% of cases. Number of cases
with abscess volume size <5cms was 32% and those with size >5cms was 68%.
88
Out of the total 50 cases in this study, cases who had multiple small abscesses
and solitary abscesses < 5ml were managed conservatively. 17/50 (34.0%) were
managed conservatively.
While 26/50(52.0%) cases underwent Pig-Tail Catheter Drainage
Rest 7/50 (14.0%) required Laparotomy and Drainage and for ruptured liver abscess.
89
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INFORMATION SHEET
We are conducting a study on “ CLINICAL STUDY OF LIVER ABSCESS ”
among patients attending Rajiv Gandhi Government General Hospital, Chennai
The purpose of this study is to assess
We are selecting certain cases and if you are found eligible, we may be using
clinical profile, lab test reports and radiological reports for study purposes which does
not affect your final report or management.
The privacy of the patients in the research will be maintained throughout the
study. In the event of any publication or presentation resulting from the research, no
personally identifiable information will be shared.
Taking part in this study is voluntary. You are free to decide whether to
participate in this study or to withdraw at any time; your decision will not result in
any loss of benefits to which you are otherwise entitled.
The results of the special study may be intimated to you at the end of the study
period or during the study if anything is found abnormal which may aid in the
management or treatment.
Signature of Investigator Signature of Participant / Guardian
Date : Place:
PATIENT CONSENT FORM
Study Detail :
Study Centre : Rajiv Gandhi Government General Hospital, Chennai.
Patient’s Name :
Patient’s Age :
Identification Number :
Patient may check (☑) these boxes
The details of the study have been provided to me in writing and explained to me in my own language ❏
I understand that my participation in the study is voluntary and that I am free to withdraw at any time without giving reason, without my legal rights being affected. ❏
I understand that sponsor of the clinical study, others working on the sponsor’s behalf, the ethical committee and the regulatory authorities will not need my permission to look at my health records, both in respect of current study and any further research that may be conducted in relation to it, even if I withdraw from the study I agree to this access. However, I understand that my identity will not be revealed in any information released to third parties or published, unless as required under the law. I agree not to restrict the use of any data or results that arise from this study. ❏
I agree to take part in the above study and to comply with the instructions given during the study and faithfully cooperate with the study team and to immediately inform the study staff if I suffer from any deterioration in my health or well being or any unexpected or unusual symptoms. ❏
I hereby consent to participate in this study. ❏
I hereby give permission to undergo complete clinical examination , biochemical and radiological tests ❏
Signature of Investigator Signature/thumb impression Study Investigator’s Name: Patient’s Name and Address: DR.N.BALAMURUGAN
Urkund Analysis Result Analysed Document: BALAMURUGAN THESIS.docx (D31220728)Submitted: 10/11/2017 3:42:00 PM Submitted By: [email protected] Significance: 2 %
Sources included in the report:
prem dissertation final rough.doc (D31083063) http://emedicine.medscape.com/article/183920-overview https://link.springer.com/article/10.1007/s15010-011-0157-x http://onlinelibrary.wiley.com/doi/10.1111/j.1365-3156.2004.01246.x/full
Instances where selected sources appear:
9
U R K N DU
CERTIFICATE – II
This is to certify that this dissertation work titled “CLINICAL STUDY
OF LIVER ABSCESS IN ALCOHOLIC AND NON ALCOHOLIC
PATIENTS” of the candidate Dr.N.BALAMURUGAN with Registration
Number 221511003 for the award of M.S. in the branch of GENERAL
SURGERY. I personally verified the urkund.com website for plagiarism
Check. I found that the uploaded thesis file contains from introduction to
conclusion pages and result shows 2 percentage of plagiarism in the
dissertation.
Guide & Supervisor sign with Seal.
PROFORMA
NAME OF THE PATIENT :
AGE / SEX :
IP/OP NUMBER :
OCCUPATION :
ADDRESS :
CONTACT NUMBER :
CARE GIVER :
CHIEF COMPLAINTS:
PRESENTING ILLNESS:
1. JAUNDICE :
2. ABDOMINAL DISTENSION :
3. ABDOMINAL PAIN :
4. FEVER :
5. ALTERED SENSORIUM :
6. BLEEDING MANIFESTATION :
7. VOMITING :
8. LOSS OF WEIGHT :
PAST HISTORY:
1. DIABETES MELLITUS :
2. SYSTEMIC HYPERTENSION :
3. CHRONIC KIDNEY DISEASE :
4. CORONARY ARTERY DISEASE :
5. HYPOTHYROIDISM :
6. SEIZURE DISORDER :
7. TRAUMA :
TREATMENT HISTORY:
1. ANTIEPILEPTIC THERAPY :
2. ANTIRETROVIRAL THERAPY :
3. TREATMENT FOR CIRRHOSIS :
4. VASOPRESSIN THERAPY :
PERSONAL HISTORY:
SMOKING :
ALCOHOL :
TEMPERATURE :
PULSE RATE :
BLOOD PRESSURE :
SYSTEMIC EXAMINATION:
CVS :
RS :
ABDOMEN :
CNS :
INVESTIGATIONS:
WBC :
HB :
HCT :
PLATELET :
SERUM UREA :
SERUM CREATININE :
TOTAL BILRUBIN :
DIRECT BILRUBIN :
SGOT :
SGPT :
GGT :
ALT :
SERUM PROTIEN :
SERUM ALBUMIN :
PROTHROMBIN TIME :
USG ABDOMEN :
KEY TO MASTER CHART
- - Absent
+ - Present
ALP - Alkaline Phosphatase R - Right lobe
L - Left lobe
B - Both lobes
Hb - Hemoglobin
PT - Prothrombin time SGOT - Serum glutamic-oxaloacetic transaminase SGOT - Serum glutamic-pyruvic transaminase GGT - Gama glutamyl transferrase S.Albumin - Serum Albumin
MASTER CHART
S.NO NAME AGE SEXABDOMINAL PAIN FEVER ALCHOLISM ICTERUS
HEPATOMEGALY HB% WBC BILIRUBIN ALP RAISED
S.ALBUMIN (<3MG/ML)
SGOT (>40IU/ML)
SGPT (>40IU/ML)
GGT (>30IU/L) PT(>20SEC)
LOBE INVOLVED
SINGLE/ MULTIPLE SIZE(CM) TREATMENT
1 KUPPUSAMY 54 M + + + - NO 10.4 14000 0.5 NO NO YES NO YES NO R S <5 CONSERVATIVE
2 RAJA 25 M + + - - NO 11 13700 0.2 NO NO YES NO NO YES R S >5 PIGTAIL DRAINAGE
3 VINAYAGAM 51 M - - + - NO 11.8 8600 0.7 NO NO NO NO YES NO R S <5 CONSERVATIVE
4 MANIVEL 44 M + + + + YES 12.2 13100 4.5 NO NO YES YES YES NO R M >5 LAPARATOMY
5 FAZHIL 56 M - + + - NO 10.3 11500 0.5 YES NO NO NO YES NO L S >5 PIGTAIL DRAINAGE
6 VETRI 35 M + + + - YES 10.8 13000 0.6 NO NO NO NO YES NO R S <5 CONSERVATIVE
7 HARI 28 M + + + - YES 10.5 14800 0.3 NO NO NO NO YES YES R S >5 PIGTAIL DRAINAGE
8 RANGANATHAN 47 M - + - + NO 7.8 7000 5.2 YES NO YES NO NO NO R M >5 LAPARATOMY
9 SAMYKANNU 55 M + - + - NO 10.6 12300 0.6 NO NO NO NO YES NO L S <5 CONSERVATIVE
10 VIVEKANANDHAN 45 M + + + - YES 10.5 10700 0.7 NO NO NO NO NO NO R S >5 PIGTAIL DRAINAGE
11 GOVINDASAMY 68 M - + - - NO 10.2 1130 0.6 NO NO NO NO YES NO R S <5 CONSERVATIVE
12 RAJKAMAL 43 M + + + + NO 10.2 12300 4.8 NO NO YES YES YES NO B M >5 LAPARATOMY
13 AMUL 46 F - + - - YES 10.1 12500 0.7 YES NO NO NO NO NO R S >5 PIGTAIL DRAINAGE
14 KALAIYARASAN 53 M + + + - NO 10.7 13100 0.8 NO NO NO NO YES NO L S <5 CONSERVATIVE
15 NARAYANAN 42 M - - + - NO 10.5 14200 1.9 NO YES NO YES YES YES B M >5 PIGTAIL DRAINAGE
16 KARTHICK 38 M + + + - NO 11.3 13400 0.5 YES NO NO NO YES NO R S >5 PIGTAIL DRAINAGE
17 RENUKA 55 F - + - - NO 11.7 12500 0.8 NO NO NO NO NO NO L S <5 CONSERVATIVE
18 KANNISAMY 46 M + + + - YES 11.1 15400 0.8 YES NO NO YES YES NO R M >5 LAPARATOMY
19 JOTHY 36 F + + - - NO 7.8 12800 0.7 YES NO NO NO NO NO R S >5 PIGTAIL DRAINAGE
20 STALIN 45 M - - + - NO 10.7 13000 0.7 YES NO NO YES YES NO R S <5 CONSERVATIVE
21 BASHA 32 M + + + - YES 10.1 11200 0.3 YES NO NO NO YES NO R S <5 CONSERVATIVE
22 RAJA 42 M - + - + NO 10.4 12500 4.2 NO NO YES YES NO NO R M >5 LAPARATOMY
23 THAMSEEN 55 M + - + - NO 9.6 13000 0.6 YES YES NO NO YES NO R S >5 PIGTAIL DRAINAGE
24 PONNAIYAN 35 M - - + - YES 11.2 12400 1.6 YES YES NO NO YES NO R S <5 CONSERVATIVE
25 DHANASEKAR 24 M + + + - NO 11 11000 0.4 NO NO NO NO NO NO R S >5 PIGTAIL DRAINAGE
26 ANBARASI 35 F + + - - YES 10.6 8000 0.4 NO NO NO NO NO NO R S >5 LAPARATOMY
27 VIJAY 23 M + - + - NO 10.3 12800 0.7 NO NO NO NO YES NO L S <5 CONSERVATIVE
28 MUNIYAN 46 M - + + + NO 10.7 19000 7.4 YES NO YES YES YES YES B M >5 PIGTAIL DRAINAGE
29 KATHAMUTHU 49 M + - + - NO 9.1 10500 0.4 NO NO NO NO YES NO R S >5 PIGTAIL DRAINAGE
30 LANKARAM 39 M - + + + YES 10.8 11000 2.1 NO NO YES YES YES YES B M >5 PIGTAIL DRAINAGE
31 RAJESH 48 M + - + - NO 11.4 13400 0.5 YES NO NO NO YES NO R S <5 CONSERVATIVE
32 PRATHAP 36 M - + - - YES 10.7 13100 0.6 NO YES NO NO NO NO R S <5 CONSERVATIVE
33 SURYA 55 M + + + - NO 11.5 12700 0.3 NO NO NO NO YES NO R S >5 PIGTAIL DRAINAGE
34 MATHIALAGAN 45 M + - + + NO 11.3 12500 2.5 NO NO YES YES YES NO B M >5 LAPARATOMY
35 BABU 37 M + + - - YES 10.5 13000 0.5 YES NO NO NO NO NO R S >5 PIGTAIL DRAINAGE
36 NOOR BASHA 32 M - + - - NO 10.8 13400 0.6 NO NO NO NO NO YES R S >5 PIGTAIL DRAINAGE
37 SENTHIL 26 M + + + + NO 10.3 9000 2.8 YES YES YES YES YES NO B M >5 PIGTAIL DRAINAGE
38 MOHAN 48 M - + - - YES 10.6 10700 0.5 YES NO NO NO NO NO R S >5 PIGTAIL DRAINAGE
39 ANTONY 33 M + + + - NO 10.1 12800 0.6 NO NO NO NO NO YES R S >5 CONSERVATIVE
40 PONMANI 27 F - + - + NO 9.6 12600 2.7 NO YES YES YES NO NO B M >5 PIGTAIL DRAINAGE
41 RAMKUMAR 45 M - + + - NO 10.2 13400 0.8 NO NO NO NO YES NO R S <5 CONSERVATIVE
42 DANDAPANI 37 M + + + - YES 10.6 7000 0.8 NO NO NO NO YES NO L S >5 PIGTAIL DRAINAGE
43 SAKTHIVEL 46 M + + + + NO 8.6 13500 2.3 YES NO YES YES YES NO R S >5 PIGTAIL DRAINAGE
44 KARIYAN 58 M + - + - NO 9.2 14300 0.7 NO NO NO NO YES NO R S >5 PIGTAIL DRAINAGE
45 RAMESH 18 M - + + + YES 11.4 12700 3.3 NO NO NO NO YES NO R S <5 CONSERVATIVE
46 CHANDRU 35 M + + - - NO 10.4 11300 0.4 NO NO NO NO NO NO R S >5 PIGTAIL DRAINAGE
47 ARIUDAINAMBI 43 M + - + + YES 10.7 13800 2.9 YES NO YES YES YES NO B M >5 PIGTAIL DRAINAGE
48 VELMURUGAN 28 M + - + - NO 11.5 13500 0.5 NO NO NO NO YES NO R S <5 CONSERVATIVE
49 SIVARUBAN 58 M - + - - NO 11.3 9000 0.7 NO NO YES NO NO NO L S >5 PIGTAIL DRAINAGE
50 JANA 36 M + + + - NO 10.4 12300 0.5 YES NO NO NO YES NO R S >5 PIGTAIL DRAINAGE