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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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: drbala_vdm@yahoo.com 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