prospective study of duodenal ulcer perforation and …

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE,

KARNATAKA.

“PROSPECTIVE STUDY OF DUODENAL ULCER

PERFORATION AND ITS MANAGEMENT”

By

Dr. SWAROOP S. M.B.B.S.

A dissertation submitted to the

Rajiv Gandhi University Of Health Sciences, Bangalore, Karnataka

In Partial fulfilment

of the regulations for the award of

MASTER OF SURGERY

IN

GENERAL SURGERY

Under the guidance of

Dr. G.C. RAJENDRA M.S.

PROFESSOR

DEPARTMENT OF SURGERY,

J.J.M. MEDICAL COLLEGE,

DAVANAGERE- 577004.

2016

I

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE,

KARNATAKA.

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled “PROSPECTIVE STUDY OF

DUODENAL ULCER PERFORATION AND ITS MANAGEMENT” has been

prepared by me after studying the cases admitted to C.G. Hospital and Bapuji

Hospital attached to J.J.M. Medical College, Davangere, under the direct guidance

and supervision of Dr. G.C. RAJENDRA M.S., Professor, Department of General

Surgery, J.J.M.Medical College, Davangere. It is submitted to the Rajiv Gandhi

University of Health Sciences, Bangalore, Karnataka, in partial fulfilment of its

regulations for the award of M.S. (GENERAL SURGERY) Degree.

I have not submitted this previously for the award of any Degree or Diploma

to any other University.

Place:

Date: (Dr. SWAROOP S.)

II

CERTIFICATE BY THE GUIDE

This is to certify that Dr. SWAROOP S. has prepared this dissertation entitled

“PROSPECTIVE STUDY OF DUODENAL ULCER PERFORATION AND ITS

MANAGEMENT” under my direct guidance and supervision at C.G. Hospital and

Bapuji Hospital attached to J.J.M. Medical College, Davangere, in partial fulfillment

of the regulations of Rajiv Gandhi University of Health Sciences, Bangalore,

Karnataka, for the award of M.S. (GENERAL SURGERY).

I have great pleasure in forwarding this dissertation to the Rajiv Gandhi

University Of Health Sciences, Bangalore, Karnataka.

PLACE:

DATE : Dr. G.C. RAJENDRA M.S.

Professor of General Surgery,

Department of Surgery,

J.J.M. Medical College,

Davanagere- 577004.

III

ENDORSEMENT BY THE HOD, PRINCIPAL/

HEAD OF THE INSTITUTION

This is to certify that Dr. SWAROOP S. has prepared this dissertation entitled

“PROSPECTIVE STUDY OF DUODENAL ULCER PERFORATION AND ITS

MANAGEMENT” in Department of Surgery, J.J.M. Medical College, Davangere,

under the guidance of Dr. G.C. RAJENDRA in partial fulfillment of the regulations

of Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka, for the award

of M.S. (GENERAL SURGERY).

Dr. R.L. CHANDRASHEKAR M.S. PROFESSOR AND HEAD,

DEPARTMENT OF SURGERY,

J.J.M. MEDICAL COLLEGE

DAVANGERE – 577 004.

Dr. MANJUNATH ALUR M.D., PRINCIPAL,

J.J.M. MEDICAL COLLEGE

DAVANGERE – 577 004.

DATE : / /2015

PLACE : DAVANGERE

DATE : / /2015

PLACE : DAVANGERE

IV

COPY RIGHT

DECLARATION BY THE CANDIDATE

I hereby declare that the Rajiv Gandhi University of Health Sciences,

Karnataka shall have the rights to preserve, use and disseminate this dissertation /

thesis in print or electronic format for academic / research purpose.

PLACE : DAVANGERE

DATE : / /2015 (Dr. SWAROOP S.)

Rajiv Gandhi University of Health Sciences, Karnataka.

V

ACKNOWLEDGEMENT

“True Gratitude is difficult to express in words”

It is my proud privilege to express my highest feeling of obligation and deep

sense of gratitude to my esteemed teacher and guide Dr. G.C. RAJENDRA, M.S.,

Professor, Department of Surgery, J.J.M. Medical College, Davangere, without whose

kind and able guidance and timely advice, this study would not have seen the light of

this day. I consider myself fortunate and extremely privileged for having him as my

guide.

I take this opportunity to express my deep sense of gratitude and sincere

thanks to Dr. R.L.CHANDRASEKHAR. M.S., Professor and Head of the Department

of surgery, J.J.M. Medical College, Davangere, who has been a constant source of

inspiration, has given valuable suggestions, support and encouragement throughout

the period of my postgraduate study.

My sincere thanks to my Professors and unit chiefs Dr. G.C. RAJENDRA,

Dr. M. SHIVAKUMAR, Dr. J.T. BASAVARAJ, Dr. R.M. SHEKHAR,

Dr. G.C. EDAGUNJI, Dr. DINESH M. GUNASAGAR, Dr. G. MANJUNATH

GOWDA, Dr. S.N. SOMASEKHAR, Dr. DEEPAK UDAPUDI, Dr.

JAGADEESH B.V.C. Department of Surgery, J.J.M. Medical College Davangere for

their valuable guidance.

I am extremely thankful to Professors, Dr. RUDRAIAH H.G.M.,

Dr.PRAKASH M.G, Dr. ANUP KUMAR M.C., Dr. PATIL VIRUPAKSHA

GOWDA, Dr., SUSRUTH .P. MARALIHALLI, Dr.MAHESH.K,

Dr.U.MAHENDRANATH PATIL for their guidance during the course of my study.

I also thank Associate and Assistant professors Dr VEERENDRA KUMAR

H.M, Dr. HARSHITH HEGDE, Dr.B.N.BASAVARAJ, Dr.NATARAJ.K.M.,

VI

Dr. KIRAN N.G., Dr BASAVARAJ .C for their professional guidance and

encouragement during my post-graduate course.

I infact have no words to express my deep sense of gratitude to all my teachers

for their valuable guidance, most enlightening constructive suggestions, constant

support and personal attention throughout the period of my post graduate course.

I like to extend my sincere thanks to the Superintendent, Chigateri General

Hospital and Bapuji Hospital, Davangere District for permitting me to conduct the

study and for giving necessary information.

My hearty thanks to Dr. MANJUNATH ALUR M.D., Dip.Diab, Principal,

J.J.M. Medical College, Dr. GURUPADAPPA, Director of postgraduate studies, for

permitting me to utilize the facilities available in the college and the hospitals for the

present study.

I also thank Sri. MAHESH .P.S., Librarian, and his colleagues for their

support for his valuable guidance in the analysis of my study throughout my P.G.

course.

I express my sincere thanks to my PARENTS DR. U.S. SUBBARAYA and

LATHA SUBBARAYA, my BROTHER Dr. SUDHARSHAN S. for their constant

support and encouragement.

I express my sincere thanks to my colleagues and friends for their constant

support and invaluable friendship.

I thank Mr. Bharath Kumar, Sri Maruthi DTP Centre, for the exquisite

layout, styling and printing of this dissertation.

My gratitude to patients for their participation in the study without which this

study would not have been possible.

VII

Above all I thank God for all that he has done for me and for having blessed

me to pursue the PG course in the most noble subject of the most noble profession i.e.

surgery.

PLACE : DAVANGERE

DATE : / /2015 (Dr. SWAROOP S.)

VIII

LIST OF ABBREVATIONS

CECT - Contrast Enhanced Computed Topography

DU - Duodenal Ulcer

PUD - Peptic Ulcer Disease

ZE - Zollinger Ellison

GIT - Gastro Intestinal Tract

NSAID - Non Steroidal Anti- Inflammatory Drugs

BP - Blood Pressure

CP - Crystalline Penicillin

CBD - Common Bile Duct

PGV - Proximal Gastric Vagotomy

EGD - Esophago Gastroduodenoscopy

MODS - Multi Organ Dysfunction Syndrome

PPI - Proton Pump Inhibitor

IV - Intra Venous

NG - Naso Gastric

PR - Per rectal

IX

ABSTRACT

BACKGROUND AND OBJECTIVE

Duodenal perforation is one of the most important complications of duodenal

ulcer. This study is done in an attempt to evaluate the age and sex incidence, various

etiologic factors and clinical manifestations of DU perforation. The various modalities

of treatment, postoperative complications and mortality, factors affecting these

complications, measures taken to prevent and treat these complications has been

studied extensively.

METHOD:

50 cases for this study were sourced from cases admitted to CG Hospital and

Bapuji Hospital, Davangere during August 2013 to June 2015, who were diagnosed to

be having duodenal perforation intraoperatively.

A proforma was used to collect relevant information from all the selected

patients. Patients were treated accordingly and regular follow up was done.

RESULTS:

Majority of patients in this study were of group 40-50years and 90% were

males and was commonly seen in manual labourers .Most of the perforations were in

first part of duodenum (86%).Open omental patch closure was done in majority of

patients (85.9%), laparoscopic closure in 2 cases, definitive procedures in 3 cases and

conservative management in one case. Complications were seen in 44% of patients,

most common being respiratory complications and only two patients died. The factors

which affected prognosis were age, duration, shock at presentation, comorbid

conditions, techniques used and postoperative management.

X

INTERPRETATION AND CONCLUSION:

Perforation is a life threatening complication of duodenal ulcer. It is common

in 5th

decade, in males, in smokers and alcoholics, in those who have long standing

duodenal ulcer and those with NSAID abuse.

Most of the patients presented late, which affected the prognosis. Initial

resuscitation is very important. Diagnosis is mainly by erect Xray abdomen.

Open omental patch closure is the commonest procedure done. With good

surgical expertise definitive ulcer surgery and laparoscopic closure can be done with

very less morbidity and mortality in stable patients.

Keywords: Duodenal ulcer; perforation; vagotomy; Omental patch; laparoscopic

closure; gastrojejunostomy.

XI

TABLE OF CONTENTS

PAGE NO.

1. INTRODUCTION 1-3

2. OBJECTIVES 4

3. REVIEW OF LITERATURE 5-85

4. MATERIALS AND METHODS 86-88

5. OBSERVATIONS AND RESULTS 89-115

6. DISCUSSION 116-124

7. CONCLUSION 125-126

8. SUMMARY 127-130

9. BIBLIOGRAPHY 131-138

10. PHOTOGRAPHS 139-140

11. ANNEXURES

ANNEXURE-I : PROFORMA 141-146

ANNEXURE-II: CONSENT FORM 147

ANNEXURE-III: MASTER CHART 148-152

XII

LIST OF TABLES

Sl.

No.

Tables Page

No.

1 AGE INCIDENCE 89-90

2 AGE VS POST OPERATIVE COMPLICATIONS 91

3 SEX INCIDENCE 92

4 SEASONAL INCIDENCE 93

5 OCCUPATIONAL INCIDENCE 94

6 CLINICAL SYMPTOMS 95

7 DURATION OF SYMPTOMS BEFORE PRESENTATION 97

8 DURATION OF SYMPTOMS VERSUS POST OPERATIVE

COMPLICATIONS

99

9 DURATION OF SYMPTOMS VERSUS MEAN DURATION

OF STAY IN HOSPITAL

99

10 HABITS 100

11 PAST HISTORY OF PEPTIC ULCER AND NSAID ABUSE 101

12 FEVER AND DEHYDRATION 102

13 BLOOD PRESSURE AND PULSE RATE 103

14 SIGNS ON PER ABDOMEN EXAMINATION 105

15 TOTAL LEUCOCYTE COUNT 105-106

16 ERECT X-RAY ABDOMEN AND WIDAL TEST 107

17 SITE OF PERFORATION 107

18 SIZE OF PERFORATION 108-109

19 SIZE OF PERFORATION vs MEAN DURATION OF STAY

IN HOSPITAL

109

XIII

20 TYPE OF TREATMENT 111

21 DURATION OF STAY IN HOSPITAL 112

22 TYPE OF SURGERY vs DURATION OF STAY IN

HOSPITAL

113

23 POST OPERATIVE COMPLICATIONS 114

24 FOLLOW UP 115

25 PEAK AGE INCIDENCE BY VARIOUS AUTHORS 116

26 MEAN AGE INCIDENCE BY VARIOUS AUTHORS 117

27 SEX INCIDENCE BY VARIOUS AUTHORS 118

28 DURATION OF SYMPTOMS BEFORE PRESENTATION

TO HOSPITAL BY OTHER AUTHORS

120

29 MORTALITY WITH SIMPLE CLOSURE AND DEFINITIVE

SURGERY BY OTHER AUTHORS

123

30 MEAN POST OPERATIVE STAY IN LAPAROSCOPIC

CLOSURE BY VARIOUS AUTHORS

124

XIV

LIST OF GRAPHS

Sl.

No.

Graphs Page

No.

1 AGE INCIDENCE 90

2 AGE VS POST OPERATIVE COMPLICATIONS 91

3 SEX INCIDENCE 92

4 SEASONAL INCIDENCE 93

5 OCCUPATIONAL INCIDENCE 94

6 CLINICAL SYMPTOMS 96

7 HABITS 100

8 PAST HISTORY OF DYSPEPSIA/PEPTIC ULCER 101

9 PAST HISTORY OF NSAID ABUSE 102

10 PULSE RATE 104

11 BLOOD PRESSURE 104

12 TOTAL LEUCOCYTE COUNT 106

13 SITE OF PERFORATION 108

14 POST OPERATIVE COMPLICATIONS 114

XV

LIST OF FIGURES

Sl.

No.

Graphs Page

No.

1 ANATOMY OF DUODENUM: PARTS AND RELATIONS 9

2 ARTERIAL SUPPLY OF DUODENUM 12

3 VENOUS DRAINAGE OF DUODENUM 14

4 DIAGRAMMATIC PRESENTATION OF DUODENAL

LYMPHATICS

14

5 TECHNIQUE OF TWO TUBE DRAINAGE 65

6 DIAGRAMMATIC REPRESENTATION OF TRIPLE TUBE-

OSTOMY TECHNIQUE

66

7 ERECT XRAY ABDOMEN SHOWING GAS UNDER

RIGHT DOME OF DIAPHRAGM

139

8 ERECT XRAY ABDOMEN SHOWING GAS UNDER LEFT

DOME OF DIAPHRAGM

139

9 ERECT XRAY ABDOMEN SHOWING GAS UNDER BOTH

DOMES OF DIAPHRAGM

139

10 ANTERIOR PERFORATION IN FIRST PART OF

DUODENUM

140

11 OPEN CLOSURE TECHNIQUE OF DU PERFORATION 140

12 LAPAROSCOPIC CLOSURE OF DU PERFORATION

(INTRACORPOREAL SUTURING)

140

Introduction

1

INTRODUCTION

Peptic ulcer is one of the most common health issues that affects mankind in

south India. Though lot of work has been done on the etiology of this condition, one

specific etiological agent cannot be incriminated in the causation of this particular

disease especially in our part of country. Peptic ulcer can be gastric ulcer or duodenal

ulcer.

Perforation is one of the important complications of peptic ulcer. As rightly

stated by Lord Moynihan “Perforation of gastric or duodenal ulcer is one of the most

serious and most overwhelming catastrophe that can befall a human being”.

The sudden release of duodenal contents into the peritoneal cavity through a

perforation leads to a devastating sequence of events which if not properly managed,

is likely to cause death.

Magnitude of the problem

The disease continues to have a substantial impact on our society‟s health care

system. Among abdominal emergencies, perforations of peptic ulcer are third in

frequency, acute appendicitis and acute intestinal obstruction being more common.

Prompt recognition of the condition is very important and only by early diagnosis and

treatment it is possible to reduce the still relatively high mortality.

It occurs slightly more frequent in men. Although 70% of ulcer patients are

between the ages of 25 and 64, the peak prevalence of complicated ulcer disease

requiring hospitalization is in the age group 65 to 74 years.

Although morbidity from PUD is decreasing in the west, the incidence of

perforated ulcer remains relatively constant. Perforated ulcers are decreasing in

incidence in younger age patients and are increasingly being observed in the elderly

and in women.

Introduction

2

Most duodenal ulcers perforate anteriorly. Elective surgery leads to 5 – 10%

of mortality while in emergency situation it goes to 20 – 30% and may be as high as

30% to 50% particularly in elderly.

There is decline in incidence of peptic ulcers and elective surgery for peptic

ulcers, which is attributed to the era of H2 blockers and proton pump inhibitors, which

provides symptomatic relief to patient. But the percentage of patients with perforation

has not declined, probably due to increased inadvertent use of NSAIDS,

corticosteriods and because of irregular use of H2

antagonist drugs.

The treatment of perforation still continues to be controversial. Just closure of

perforation may save life, but chance of recurrence of ulcer is too high and patient

may not turn up for a second curative surgery. So, there is a school of thought, which

recommends definitive surgery in a perforated peptic ulcer. This may to a certain

extent reduce the mortality and morbidity of the patient, because patients have to risk

a major surgery when the general condition is not good. On the other hand it saves the

patient of further surgery.

When acute or chronic duodenal ulcer perforates into the peritoneal cavity,

three components require treatment viz., the ulcer, the perforation and the resultant

peritonitis. The perforation and resultant peritonitis are immediate threats to the life,

the ulcer itself is not. The therapeutic priorities thus are treatment of peritonitis and

securing the closure of perforation, which may be achieved with surgical procedure.

Inspite of better understanding of disease, effective resuscitation and prompt

surgery under modern anesthesia techniques, there is high morbidity and mortality.

Hence, attempt has been made to analyse the various factors, which are affecting the

morbidity/mortality of patients with peptic ulcer perforations.

Introduction

3

The mortality increases with delay in surgery. The mortality rate when surgery

is performed within 6 hours of onset of pain approaches zero; from 6-12 hours the rate

is 5-10%, 12-24 hours it is 25% or higher and in the course of 3rd

day after, surgeries

are seldom successful. Hence it is said that “There is no intraabdominal catastrophe

where a successful outcome is more dependent upon early diagnosis and prompt

treatment (surgery)”.

Objectives

4

OBJECTIVES

1. To evaluate the age and sex incidence and to study etiologic factors for

duodenal ulcer perforation

2. To study the various clinical manifestations of duodenal ulcer perforation.

3. To study the various modalities of treatment of duodenal ulcer perforation.

4. To study postoperative complications and mortality.

Review of Literature

5

REVIEW OF LITERATURE

HISTORICAL REVIEW1,2

The knowledge of perforation dates back to over 2000 years remote past when

“Sushrutha”, the great Indian surgeon described it as “Parinamashula” giving the

relation of the food, pain and vomiting. Surgeons have attempted for 100years to cure

the peptic ulcer by reducing the secretion of acid and pepsin. History of surgery for

duodenal ulcer is a chronicle of their attempts to achieve this aim without producing

major disturbance to the functions of alimentary tract. Perforated duodenal ulcers, as a

disease entity has been known since 1670.

1726-George Hamberg, Germany described a duodenal ulcer.

1727-Christopher Rawlinson, England first described a case of perforated

peptic ulcer.

1793-Jacopo Penada, Italy first recorded a duodenal perforation.

1881-Ludwig Rydygier, performed a successful resection of a prepyloric

peptic ulcer.

1881-Theodor Billroth, Father of Surgical Audit and Father of Abdominal

surgery, performed the excision of distal part of the stomach with an

anastomosis of the gastric stump to the duodenum (Billroth I Surgery).

1886-Heineke, did the first pyloroplasty.

1888-Mikulicz redefined the pyloroplasty done by Heineke.

1893-Barling, of Great Britain, treated perforated ulcer by closure and

vigorous lavage of peritoneal cavity with large quantity of saline.

1893-Codivilla reportedly did the first gastrojejunostomy for a duodenal ulcer.

1896-Bennett suggested sealing a large perforation with omentum


6

1937-Cellian- Jones and Graham, popularized the effectiveness of omental

patch for perforation.

1943-Dragsted and Owens introduced bilateral truncal vagotomy.

1948-Franksson of Stockholm first reported selective vagotomy.

1965-Erik Amdrup performed highly selective vagotomy.

1970-Robin Warren reported an association between Helicobacter pylori,

gastritis and peptic ulcer perforation.

1985-Barry Marshall cultured Helicobacter pylori.

1985-Johansson B. Gilse H. described a laparoscopic technique for closure of

perforated duodenal ulcer.

1996-Halkic N. Pescatore P. and Gilleton combined both laproscopic –

endoscopic method using an omental plug for therapy gastroduodenal ulcer

perforation.

Perforation of duodenal ulcer is now a common complication. Second to

penetration. It was rare until the end of the 19th century, but since then its frequency

has increased progressively. Moreover, there was a curious change in incidence in the

19th century, most perforations were gastric perforations and the majority affected

women, especially girls aged from 10-28 years. By 1959, duodenal perforations

greatly exceeded gastric, men were affected more than women and most cases

occurring between 25-45 years.


7

ANATOMY3,4,5

The word Duodenum is a Latin corruption of the great word "dedekadaktulos"

meaning 12 fingers. About 300 B.C. Herophilus of Alexandria gave the name “Od

dodekadatulos” to the first part of intestine before it is thrown into folds. It was so

called, for it being as long as 12 fingers broad in those animals in which it was first

described (Finnleyson).

EMBRYOLOGY OF DUODENUM

The terminal part of the foregut and the cephalic part of the midgut form the

duodenum. The junction of two parts is directly distal to the origin of liver bud. As the

stomach rotates, the duodenum takes on the form of a C-shaped loop and rotates to

the right. This rotation, together with rapid growth of the head of the pancreas, swings

the duodenum from its initial midline position to the right side of the abdominal

cavity.

The duodenum and the head of the pancreas press against the dorsal body wall

and the right surface of the dorsal mesoduodenum fuses with the adjacent peritoneum.

Both layers subsequently disappear and the duodenum and the head of the pancreas

become fixed in a retroperitoneal positon. The entire pancreas thus obtains a

retroperitoneal position. The dorsal mesoduodenum disappears entirely except in the

region of the pylorus of the stomach, where a small portion of the duodenum

(duodenum cap) retains its mesentery and remains intraperitoneal.

During the second month, the lumen of the duodenum is obliterated by

proliferation of cells in its wall. However the lumen is recanalised shortly thereafter.

Since the foregut is supplied by the celiac artery and the midgut by the superior

mesenteric artery, the duodenum is supplied by branches of both arteries.

SURGICAL ANATOMY OF DUODENUM


8

The duodenum is the first, widest and most fixed part of small intestine. It is

about 10 inches in length. It has no mesentery and is partially covered with

peritoneum.

In extends from the pylorus to the duodenojejunal flexure forming a "C"

shaped curve whose concavity extends towards the left and upwards. This "C" shaped

curve is occupied by the head of pancreas. Since it forms a "C" shaped curve, the

beginning and the end of duodenum are close together. It lies on the posterior wall of

the abdomen above the level of the umbilicus and almost wholly in the right half of

the abdomen.

The duodenum begins at the pylorus, passes backwards upwards and to the

right 2.5 cm under cover of the posterior part of the quadrate lobe of the liver, to the

neck of the gall bladder varying slightly in directions. According to the degree of

distension of the stomach, it then makes a sharp curve (superior duodenal flexure) and

descends for about 7.5 cm in front of the medial part of right kidney, generally to the

level of the lower border of body of the 3rd lumbar vertebra lying medial to the

lateral plane. Here it makes a second bend (inferior duodenal flexure) and passes

almost horizontally from right to left across the vertebral column just above the level

of the umbilicus having a slight inclination upwards. It then ascends in front and to

the left of the abdominal aorta for about 2.5 cm and ends opposite the body of second

lumbar vertebra in the jejunum. At its union with jejunum it turns abruptly forwards,

forming the duodeno jejunal flexure which is situated 2.5 cm to the left of the medial

plane and below the transpyloric plane. The principal changes of direction in the "C

shaped curve are made use of, to divide the duodenum into four parts .


9

FIGURE 1: ANATOMY OF DUODENUM: PARTS AND RELATIONS


10

FIRST PART - THE SUPERIOR PART :

It is about 5 cm long and is the most mobile of the four parts. It begins at the

pylorus in the transpyloric plane about an inch to the right of median plane and passes

backwards and upwards in close relation with the liver and ends at the neck of the gall

bladder, where it bends sharply to become the second part.

SECOND PART - THE DESCENDING PART :

It is about 8-10 cm long, descends from the neck of the gall bladder along the

right side of the vertebral column as low as lower border of the body of the 3rd

lumbar vertebra. It is crossed by transverse colon. The parts above and below the

transverse colon are covered in front with peritoneum

THIRD PART - THE HORIZONTAL PART :

It is about 10 cm long, begins on the right psoas major muscle at the level of

the lower border of the 3rd

lumbar vertebra and passes horizontally towards the left,

across the inferior venacava and aorta and then bends upwards to become the 4th part.

FOURTH PART - THE ASCENDING PART

It is about 2.5 cm and it is the shortest part of the duodenum. It curves

upwards along the left side of the aorta and the head of pancreas, onto left psoas

muscle. It ends about 2.5 cm to the left of midline at the level of the second lumbar

vertebra by bending sharply forwards to form duodenojejunal flexure where it is

continuous with jejunum. Posteriorly it is related to the left ovarian artery in female

and the left renal vessels. Along its right border it gives attachment to the upper part

of the root of mesentery. To its left there are left kidney and ureter, above there is the

body of the pancreas, in front there is transverse mesocolon.


11

PERITONEAL RELATIONS :

First part :

The first inch of the first part of duodenum is entirely covered with

peritoneum except for a small part above and behind. The second inch is covered with

peritoneum only above and in front, where it is related to the liver and neck of gall

bladder. The first inch owing to its peritoneal relations is free to move and moves with

the stomach. The second inch is fixed firmly by areolar tissue to the structures behind

it.

Second part :

This part of duodenum has a very incomplete covering of the peritoneum,

covering only on parts of anterior surface, that are above and below the transverse

colon because the colon lifts the peritoneum off the greater part of it.

Third part :

The anterior and inferior surfaces of the 3rd

part are covered with peritoneum

except at its end where it is crossed by superior mesenteric vessels and the root of the

mesentery.

Fourth part :

This part of the duodenum is covered with peritoneum on the front and left

side only.

The terminal part of the duodenum and the duodenojejunal flexure are fixed

by a fibromuscular band termed the suspensory muscle of the duodenum, the

Ligament of Treitz which arises from the right crus of the diaphragm, close to the

right side of the esophagus.


12

FIGURE 2: ARTERIAL SUPPLY OF DUODENUM

The superior part of the duodenum as stated above is slightly mobile but the

rest is relatively fixed. Radiologically after a barium meal, the superior part of the first

part is seen as somewhat triangular homogeneous shadow called the "duodenal cap"


13

VARIATIONS IN FORM AND POSITION.

The curve of the duodenum varies with the position of the 3rd part, usually the

3rd part is nearly horizontal and 4th

part is vertical. But the third part may incline

upwards as it passes towards the left and lie in the line of the 4th

part. On account of

these variations the 3rd

and 4th

parts may be grouped together as the "inferior part',

sometimes there may be considerable variations not only in the position of the 1st part

owing to its mobility but the position of the whole of the duodenum in relation to the

vertebral column.

BLOOD SUPPLY :

Arterial supply: The arterial supply of duodenum is derived from the right gastric

artery, supraduodenual, right gastro epiploic, superior and inferior

pancreaticoduodenal arteries. The superior part of duodenum receives small branches

from the hepatic artery proper and similar vessels from gastroduodenal artery.

Surgical importance of arterial supply :

The surgical importance with regard to the arterial supply is that the area of

mucus coat supplied by the duodenal branch of hepatic artery is specially liable to the

formation of "duodenal ulcer'. This is thought to be due to the fact that the artery has

poor anastomosis with its neighbouring arteries.


14

FIGURE 3: VENOUS DRAINAGE OF DUODENUM

FIGURE 4: DIAGRAMMATIC PRESENTATION OF DUODENAL

LYMPHATICS


15

Venous supply: The veins end in the splenic, superior mesenteric and portal veins.

On table, the pre-pyloric veins of Mayo are helpful landmarks in distinguishing the

pyloric canal from the first part of duodenum.

NERVE SUPPLY

The sympathetic supply is from T9,10 and the parasympathetic is from vagus

nerves. It passes through coeliac and superior mesenteric plexus and accompany the

arteries.

LYMPHATIC DRAINAGE

The lymph vessels end in the nodes that lie between the duodenum and the

head of the pancreas from where the lymph is carried to coeliac and superior

mesenteric nodes.

STRUCTURE OF DUODENUM

The duodenal wall is composed of 4 layers:

1. Serous Coat

2. Muscular Coat

3. Submucous coat and

4. Mucous coat

The serous coat is formed by the visceral peritoneum and is incomplete.

The muscular coat is composed of outer layer of longitudinal fibres and an

inner layer of circular fibres as in other parts of intestine.

The submucous coat is peculiar in that it contains small compound glands

called "the duodenal glands" or “Brunners glands". These glands form an almost

continuous layer in the upper half of the duodenum and diminish progressively in the

lower half. The ducts pierce the lamina muscular mucosa and pass into the intestinal

glands of the mucous coat to open on the mucosal surfaces.


16

The mucous coat contain circular and longitudinal folds. The circular folds

begin about an inch from pylorus. The lower half of the second Part contains a

longitudinal fold near its posteromedial border. If this longitudinal fold is traced

upwards, it leads to a small round eminence called "The duodenal papilla". On the

summit of the papilla, there is a small opening which is the opening of the CBD and

pancreatic duct.


17

PHYSIOLOGY OF DUODENUM6,7,8

The functions of the duodenum can be studied under 3 headings :

1. Secretory functions

2. Motility of duodenum and

3. Absorption of duodenum

1. Secretory functions :

Exocrine secretion: The precise nature of Brunner's glands present an

unsolved problem since the secretion obtained from a pouch from the duodenum, in

which these glands are situated, must inevitably be mixed with the secretions coming

from the crypts of Lieberkuhn and cells of Villi which are also present. The secretion

is alkaline pH 8 to 8.2 and contain bicarbonate. The fluid is colourless and clear,

except for traces of amylase which converts starch to maltose. The regulation of

secretion from the Brunner's gland area has not been cleared. The only evidence that

these glands may be subjected to excitation from vagus nerve during the response to a

meal comes from acute experiments on decerebrate cats, in which it was shown that

prolonged stimulations of the thoracic vagus nerves caused a considerable flow of

mucoid juice. It was noted that atropine did not abolish this response.

It can be concluded that the secretions from Brunner‟s gland region has little

if any significant digestive functions as a source of intestinal enzymes, nor does it

seem likely that it contributes significantly to or neutralization of gastric contents as

they enter the duodenum.

Endocrine secretion of duodenum :

Secretin is normally present in the mucosa of the duodenum and upper jejunum. It is

liberated from the mucosa on the entry of acid into the duodenum and also on entry of

bile salts and fat.


18

Functions of secretin:

a. Inhibits acid secretion from parietal cells.

b. Stimulates bile secretion from the liver.

c. Stimulate bicarbonate secretion.

2. Motility of duodenum :

The advent of the radiotelemetering capsule which is swallowed, has for the

first time made it possible to obtain quantitative data from the alimentary tract without

the use of indwelling tubes. The small intestine exhibits a well-marked gradient of

activity as it is traced from the duodenum to the caecum. There are 2 principal types

of movements:

i. Rhythmic segmentation

ii. Peristalsis.

i) Rhythmic segmentation :

This type of activity is well studied by means of X-ray screening of the barium

filled intestines. It is not well developed in duodenum as compared to jejunum or

ileum. Segmentation is probably not under nervous control as it is not abolished by

the action of cocaine or its analogue.

ii) Peristalsis:

Propulsion of intestinal contents depends upon peristalsis. It is characteristic

of both intact and excised intestine that the waves are propagated always in a cranio-

caudal direction. Peristalsis is exhibited by the whole length of the intestine, but in

differing degree. In the duodenum at rest, small amplitude peristalsis which is

propagated so rapidly that food or barium is whisked round into the jejunum. This

high speed propagation is characteristic of the duodenum and measurement has shown

it to be of the order of 25 cm per second, or about tenfold faster than in the rest of the


19

small intestine. The peristalsis if fixed in the rate which it occurs, duodenum shows

waves occurring at the rate of 17-18 per minute, while jejunum and ileum show a

slower rate. Reverse peristalsis has been noted to occur in the duodenum during

nausea and vomiting. The peristaltic activity is under nervous control. The sensory

fibres arise mainly from the cells in the submucous plexus of Meissner. Their axons

make connections with mesenteric plexus of Auerbach. The mesenteric plexus

contain mainly the motor neurons innervating the muscle. The peristaltic reflex

depends on the integrity of the mucosa.

3. Absorption in duodenum :

Two factors decide the site at which absorption of different substances occur

in the small intestine. The first is the relationship between the rate of absorption and

upper intestinal motility. The second factor is the location of specific transport

mechanism in specific segments of intestine. Studies in both experimental animals

and in man have shown that the following substances are absorbed from the

duodenum ;

a) Glucose

b) Iron

c) Water soluble vitamins -Folic acid , riboflavin, pyridoxine, ascorbic

acid


20

PATHOLOGY9,10,11,12,13,14

PATHOGENESIS OF DUODENAL ULCER

All peptic ulceration arises because of an imbalance between the aggressive

action of acid, pepsin secretion and the normal defenses of the gastroduodenal

mucosa.

For duodenal ulcer, the major causal influence appears to be exposure of the

duodenal mucosa to excess amount of acid and pepsin.

Individual with total achlorhydria never develop duodenal ulcer.

Defect in the defense mechanism includes deficiencies in mucosal cell

removal, in mucous production in elaboration of bicarbonate and in production of

prostaglandin.

Irrespective of treatment, ulcer takes one of the courses during the period of its

progress:-

- Healing

- Chronicity

- Complications.

The complications of duodenal ulcer are:

I. Haemorrhage

II. Perforation

III. Cicatrical contraction

IV. Carcinomatous changes.

PATHOPHYSIOLOGY OF PERFORATION OF DUODENAL ULCER

Perforation is due to the sudden sloughing of an unsupported portion of an

ulcer, secondary to a slow process of devascularisation. The devascularisation is most

often progressive. It is easier to explain a blow out of the avascular floor of chronic


21

ulcer than to account for the sudden perforation of all components of the visceral wall

in acute ulcer.

Acute perforation may occur in acute or chronic duodenal ulcers and in over

95% of cases, the ulcer that perforates is of chronic variety. In acute perforation an

embolic phenomenon results in the formation of a disc shaped infarct. Localised

vasospasm has also been suggested as a cause. Auto digestion may be the final factor

to decide for perforation to occur.

In an acute perforation sudden rupture of the base of the duodenal ulcer takes

place with the result that the contents of the duodenum escape freely into general

peritoneal cavity. In certain instances the perforation might become sealed off and

then the spillage may be circumscribed.

Duodenal ulcer which perforates into the general peritoneal cavity are situated

on the anterior or antero-superior walls of the duodenum. Most commonly on the

anterior surface of first part of duodenum within an inch of the pylorus. Peptic ulcer

perforation is rare in 2nd and 3rd parts of duodenum.

But the possibility of a retroperitoneal perforation in the 2nd part of duodenum has

also been reported.

Of 211 cases of gastro duodenal perforation in the Charity hospital series, De

Bakey15

found 40% of perforations in the duodenal bulb, where in 44% were in the

lesser curvature. 95% of all cases of duodenal perforations were in the anterior wall of

duodenum. Perforations on the anterior surface of duodenum leads to widespread

peritoneal soiling. Localised adherence to the parietal peritoneum or omentum or

other structures (viscera) is unusual with anterior ulcers.

Posterior ulcers may cause free leakage into the lesser sac through the

Foramen of Winslow. But more often such ulcers penetrate the neighbouring


22

structures such as pancreas or liver to which they are adhered by local peritoneal

reaction.

An encircling ulcer penetrate into the pancreas in its posterior part, may

perforate in its anterior part. Two duodenal ulcers, an anterior one which has

perforated and a posterior penetrating are commonly found at surgery.When

haemorrhage coexists with perforation it is usually the posterior one which bleeds.

Rarely a posteriorly situated ulcer may perforate extra peritoneally and

extravasated fluid may collect in the region around the kidney. If the fluid tract

downwards still further a mass may appear in the right iliac fossa simulating an

appendicular abscess. The drainage of such abscess result in a duodenal fistula.

The size of the perforation varies from 3 mm - 1 cm in diameter. Perforation

of more than 2.5 cm have also been reported. In majority of cases the site of

perforation is obvious during surgery. The veins of Mayo always help to know

whether it is duodenal ulcer perforation or gastric ulcer perforation. In some cases the

anatomy of the pylorus and of the duodenal bulb may be greatly disturbed. It may be

impossible to identify the veins of Mayo which mark the division between duodenum

and stomach and the region may be so obscured by oedema and adhesions, that it may

be difficult to make sure whether the ulcer is pyloric, prepyloric or duodenal.

At operations or at autopsy in cases of perforated duodenal ulcer, the site of

perforation was found to be on the anterior wall of duodenum in 92%, on the

posterior wall 2% and on or about the pyloroduodenal junction (classified as

duodenal ulcer) in 6% of cases (Kozall and Meyer in 1960)26

.

Multiple perforations are described, but is extremely rare. Austin described a

patient with simultaneous perforations of gastric and duodenal ulcers. He collected


23

33 cases described to that date. In most instances, the second perforation may be

overlooked at surgery.

Immediately after the perforation has occurred, chemical peritonitis develops

as a result of the irritating action of the contents of the stomach and the duodenum.

The irritants being :

I. Acid

II. Biliary secretions

III. Pancreatic secretions

It is difficult to determine how long it takes for chemical peritonitis to

develop into frank bacterial peritonitis. Theoritically it should depend on:

i) Size of the perforation.

ii) Magnitude of the spillage.

iii) Reaction and composition of duodenal contents.

iv) General condition of the patient.

v) Capacity of resistance of the patient to infection.

When the duodenal contents are neutral or alkaline, the onset of septic

peritonitis can only be delayed for a few hours. When the escaped contents are

strongly acidic and actively bactericidal, the infection is considerably inhibited. The

bacteria are derived from many sources. The flora of the mouth and nasopharynx may

be swallowed.

The contents of the stomach and duodenum may be heavily infected in

conditions of chronic obstructions or large ulcer favouring the retention of many

organisms. Ingested food and drink again has variable bacterial content. Finally

infected small intestinal contents may regurgitate to the site of perforation. Then the


24

paralytic ileus with peritonitis becomes a marked feature, organisms therefore vary in

type and may include

a) Streptococci

b) Staphylococci

c) Coliform group

d) Candida species

e) Pneumococci.

Rarely an unusually specific organism, streptothrix may cause peritoneal

infections. Infection is unusual with gas forming organisms. In an average case it may

be assumed that during the first six hours, the peritonitis is less infective. When the

perforation has existed for more than 8 to 12 hours, fluid will be infective in

character. There is an immediate sudden and gross soiling of peritoneum after rupture.

Hyperemia, edema, exudation, fibrin deposition and pus formation occur in varying

degree according to the chemical nature of the fluid and type, virulence and number

of organisms. Davidson et al in 1930 studied 34 cases and found 75% positive culture

in the second 6 hours after perforation. Paralytic ileus and intestinal obstruction

supervene it, bacterial peritonitis sets in and then the clinical picture will be similar to

that in peritonitis from other causes.

According to Greco and Cashow in 1974 and Boey16

et al in 1982, more than

half the cultures of peritoneal fluid taken at the time of surgery for perforations were

sterile. Antacids and H2 antagonists raise the intragastric pH and thus may allow

bacterial growth. Contamination may be highest in patients who were taking these

drugs before perforation. Hamilton and Harbrecht (1967) and Kincanon et al have

demonstrated that the spillage is nearly sterile, furthermore that the culture taken at

surgeries performed even after 24 hours were often negative and less often grew


25

pathogens than at earlier surgeries. They also conclude that the magnitude of the

spillage does not influence the development of peritonitis. The preoperative use of

antibiotics may play a considerable part in this finding. It would appear that bacterial

peritonitis will supervene only in grossly neglected cases or in debilitated patients

with poor resistance to infection.

As a result of perforation, generalised and diffuse peritonitis develops in a

matter of few hours. The development of diffuse peritonitis can be considered in the

following three stages:

i) Early stage

ii) Intermediate stage

iii) Late stage

i) Early stage:

This is the stage of diffuse or spreading peritonitis. Pain which commences in

one part of abdomen at the time of onset of perforation becomes more widespread.

Later the patient develops vomiting, which becomes frequent and bile stained and

most often effortless. The patient lies supine with knees flexed. The temperature is

usually raised but in late fulminating cases it may be subnormal. A rising pulse rate

shown by recording an hourly pulse rate is an indication of that the peritonitis is

advancing. Peritonitis further leads on to the development of paralytic ileus, which

may be progressive. At the outset the peristaltic activity ceases as a normal response

to prevent dissemination, but afterwards the bacterial toxins prevent the normal

activity of the nerve plexuses. When the bowel begins to recover, the early feeble

peristaltic waves may not be able to overcome the obstructive effect of the newly

formed slender adhesions between the adjacent loops of intestines. This further leads

to quiescence of activity of intestinal musculature.


26

Further vomiting leads to loss of sodium chloride and also potassium, leading

to the fluid and electrolyte imbalance. Hypokalemia is also responsible for the

development of paralytic ileus. The development of paralytic ileus can be recognised

by

a) Distension of abdomen

b) Vomiting

c) Absence of normal intestinal peristaltic sounds on auscultation.

ii) Intermediate stage:

This stage develops after 72 hours after the onset of diffuse peritonitis. In

those cases which may improve, there will be fall in the pulse rate but in those cases

where no improvement occurs, the pulse rate continues to rise. The abdominal rigidity

may pass off and give place to increasing abdominal distension. The whole abdomen

will be acutely tender. The amount of fluid removed by gastric aspirations also

increases.

iii) Late stage :

If by 4th and 5th day after the occurrence of perforation, there is no

localisation of infection, the patient‟s condition becomes extremely grave. The whole

abdomen will be grossly distended. The pulse becomes rapid and thready. The eyes

will be sunken, the nose may appear pinched, the tongue will be dry and shrivelled.

The forehead and hands will be cold and clammy. This classical facies has been

described as "HIPPOCRATIC FACIES'. Finally the patient goes into a state of semi

consciousness which might lead to complete loss of consciousness and death. The

amount and nature of peritoneal fluid will have an important bearing upon the

prognosis. If there is more fluid, if it is thick and contains particles of food, the

outlook may be worse and mortality rate is higher.


27

Some perforations leak continuously and some are sealed off by fibrous and

omental adhesions. Few are sealed permanently by the natural methods alone. It is

possible that a limited volume of irritant and infected material is diluted and

neutralised by reactive peritoneal exudates rich in polymorphs and antibodies.

When large accumulations are found, the intestines which are submerged in

this turbid fluid are unable to form defensive adhesions or to limit the spread of

contamination.

If the perforation is small and the stomach is empty the perforation may be

sealed off or at best a localised abscess may form. When pus tracks up towards the

diaphragm a subphrenic abscess may develop. When it gets shut off in the pelvis a

localised pelvic abscess may result.


28

CLINICAL FEATURES9,12,13,14,17,18,38

Usually there is a previous history of dyspepsia and the patient may be

knowing from the earlier investigations that he has an ulcer. However, that a patient

suffering from perforation may be in no fit state to give an accurate history of

previous investigation. Such an information may only be obtained by further

questioning during convalescence. Rarely perforation may take place during a first

attack of acute ulceration.

An untreated patient passes through 3 clinical phases following perforation of

an ulcer, but the pathological process and clinical picture tend to overlap.

i) Stage of peritonism or primary stage.

ii) Stage of reaction or secondary stage.

iii) Stage of bacterial peritonitis or tertiary stage.

i) Stage of peritonism :

This stage follows immediately upon perforation and lasts for about 6 hours.

The symptoms which arise with dramatic suddenness, are due to the intense irritation

of the peritoneum by the escape of gastric and duodenal contents. This sudden and

violent irritation of the peritoneum produces the immediate reflex effect on the

circulatory and nervous system, commonly referred as primary neurogenic shock.

Usually however this state of so called shock is transient and most patients when first

seen in hospital will have relatively normal pulse and blood pressure, though they will

be in considerable distress. In the early stages nausea and vomiting are uncommon,

although retching may be troublesome.In addition to abdominal pain, there may be

referred pain over one or both shoulders as a result of diaphragmatic irritation.


29

On Examination :

It will be seen that the patient lies almost rigid and in supine position with his

legs drawn up and his hands held tensely to his side. He is afraid to move,as slightest

movement aggravates the pain. In few instances the patient may be extremely restless,

he may be curled up in bed in the position of flexion with his hands grasping

epigastrium. The face is pale with sweating and expression is one of anxiety or fear.

The extremities are pale, cold and moist with sweat.

The temperature during the primary stage may be subnormal, as low as 950 to

96 0

F or normal. Occasionally it is slightly raised. Respiratory rate is always

increased and respiratory excursion are shallow and thoracic in nature, owing to the

immobility of the diaphragm. On palpation the muscles are tensely rigid and board

like. This rigidity is universal and extends into the flanks. There is marked tenderness

and usually rebound tenderness which extends to all parts. In old people and

debilitated patients the rigidity may be less marked, but tenderness is not less marked.

The abdomen is often tympanic (from the escape of gas) on percussion, liver

dullness may be diminished or absent, but the sign is less reliable than its radiological

counterpart. The patients suffering is obviously so great that it is rarely justifiable to

elicit shifting dullness.

Sometimes the fluids escaping from a perforated duodenal ulcer may trickle

down the right paracolic gutter producing signs suggestive of acute appendicitis with

tenderness and rigidity limited to the right side of the abdomen. Tenderness may be

present on rectal examination. From the moment of perforation, the transition through

the primary stage to secondary stage is 2 to 6 hours, depending upon the site of

perforation and magnitude of peritoneal soiling. It is during this stage that the


30

spontaneous sealing off of the perforation occurs. If there is gross leakage of gastric

and duodenal contents the patient may pass rapidly to the stage of septic peritonitis.

Since the greatest chance of recovery depends on correct diagnosis at this

stage, greater attention should be paid to the early features of this catastrophe.

ii) Stage of reaction or secondary stage :

The length of this stage of reaction, although variable rarely exceeds 6 hours.

The pain which is most intense at the moment of perforation and during the peritoneal

irritation, tends to cease off somewhat during this stage. This is due to the dilution of

irritants by the peritoneal exudates. For this reason, the stage of reaction has

sometimes been called "stage of delusion or deceptive stage". There is, to all

appearances, a general improvement in the patient‟s condition. He will state that he

feels better and that he thinks the crisis has passed.

The sharp edge of the pain has been dulled. He feels warmer and his condition

has improved. He may still be sweating but the extremities are no longer chilled. The

temperature is normal or only slightly raised, the pulse shows little if any change in

rate. He will be thirsty and often asks for a drink. Though the symptoms may be

relieved, the signs will persist. On careful examination it will be seen that the alae

nasi are working vigorously.

The respirations are still shallow, laboured and costal in type, and the patient

lies completely motionless with knees drawn slightly upwards. The tenderness and

rigidity are still present to a marked degree. Two more physical signs appear during

this stage :

i) Shifting dullness and

ii) Obliteration of normal liver dullness in mid axillary line.


31

On auscultation, the abdomen is silent, PR examination in most of the cases

may reveal tenderness in rectovesical pouch in male and rectovaginal pouch in

female.If a plain X-ray of abdomen is taken in an erect posture, gas shadow may be

seen under right cupola of the diaphragm. However a negative X-ray finding do not

exclude a diagnosis of perforation.

iii) Stage of peritonitis :

The stage of peritonitis develops in from 6 to 12 hours after perforation. The

clinical picture is essentially same as that of a generalised bacterial peritonitis from

any other cause. Pain, although present is less severe, vomiting is now frequent while

hiccough may further distress the patient.

As a result of sweating, vomiting and outpouring of fluid into both the

peritoneal cavity and distended paralysed intestine, dehydration and electrolyte

depletions become more evident. Fever if present, the temperature is usually above

100 0F and the body is dry and flushed ,while the lips and tongue are dry and coated.

This stage is characterized by an anxious look and sunken eyes, and so called

"Hippocratic facies”.

The pulse rate steadily rises and become small and thready and the respiration

is shallow and rapid. The BP starts to fall, indicating that a hypovolemic shock with

circulatory failure has supervened. Examination of the abdomen will show certain

important differences between this and the preceding stage. The abdomen is distended

and the abdominal muscles are still "guarded", but no longer board like, they are

nevertheless tense enough, to limit the distension to some degree. Tenderness is still

generalised but the palpating hand is no longer resented. On auscultation,an

occasional "obstructive tinkle" is heard. The characteristic picture of intestinal


32

obstruction due to paralytic ileus with effortless regurgitation of dark feculent fluid

and meteorism takes 36 to 48 hours to develop.

The terminal stage is a complex clinical stage in which toxaemia, paralytic

ileus, oligaemia and hypovolemic shock with circulatory failure all contribute. The

patient is overwhelmed and a fatal outcome is inevitable. He may either drift into

delirium followed by coma or may remain acutely conscious till the end. Death

usually takes place some 4 to 5 days after perforation.

SUB ACUTE PERFORATION :

An ulcer may perforate and the perforations may seal rapidly before there is

spillage of gastric and duodenal contents into the general peritoneal cavity.There is

sudden onset of acute upper abdominal pain, often more severe in the right upper

quadrant.It may radiate to the back, to the precordium,to left scapular region.

Respiration will be shallow and deep inspiration may be associated with an abrupt

catch in the breath.

On examination there is local tenderness and rigidity but the rest of the

abdomen will be soft to palpate and non-tender. Unusually an x-ray film will reveal a

small amount of gas under the diaphragm. The condition closely mimics acute

cholecystitis. But there is no pyrexia and a history of chronic peptic ulceration may be

obtained. After an hour or two with bed rest, the pain will usually subside. Rarely the

tenderness and rigidity may extend and the signs of acute perforation develops.

CHRONIC PERFORATION:

When an ulcer perforates into area which is walled off by adhesions or by

adjacent viscera such a colon or greater omentum , into the omental sac, a chronic

abscess will form and will give rise to considerable confusion in diagnosis. As these

patients do not present with the signs and symptoms of peritonitis they are seldom


33

diagnosed as having perforated peptic ulcer. The common sites for abscess to form are

Morrison 's pouch, right infrahepatic subphrenic space. Usually the true diagnosis is

made only on exploratory laparotomy, performed to drain the abscess.

PERFORATION ASSOCIATED WITH HAEMORRHAGE :

The association of a perforation with massive haemorrhage is a grave but

fortunately a rare complication.

It may present in one of the 3 ways.

a) Haemorrhage and perforation occurring concomitantly.

b) Haemorrhage following a recently sutured perforation.

c) Perforation occurring during medical treatment for haemorrhage.

In most of these cases the ulcer is large and found deeply penetrating the

pancreas, the liver or the left gastric pedicle. The ulcer ruptures where it is relatively

unsupported but the bleeding arises from erosion of large vessel, such as the gastro-

duodenal, the splenic or left gastric artery. The clinical picture is that of acute

perforation of peptic ulcer with signs of haemorrhage. The patient is usually pale and

severely "shocked' with a rapid pulse and a low blood pressure.

This combination is very rare. Merse and Fuller found 5 out of 969 patients

had a grand slam of perforation, haemorrhage and obstruction.


34

AETIOLOGICAL FACTORS

The exact reasons for the perforation of duodenal ulcer are not certain.

The following aetiological factors help in considering this catastrophe:

i. Sex incidence

ii. Age incidence

iii. Occupational incidence

iv. Trauma

v. Seasonal incidence

vi. Geographic incidence and

vii. Perforation in association with well defined clinical states

Other factors are

a. Psychological and emotional factors

b. Relation to food

c. Iatrogenic (drug induced) perforation

d. Relation of blood groups

e. Environmental factors

f. Smoking and alcohol

g. Helicobacter Pylori infection

i) Sex incidence:

In a large series of cases in studies, the striking fact emerges that there is a

great preponderance of males over females. The male : female ratio in UK for DU fell

from 6:1 in 1958-62 to 2:1 in 1978 to 1982 and 2.5: 1 between 1974 and 84 at

Copenhagen in 1907 cases during this period.


35

But recent literature has shown increasing proportions of females, the cause of

this is difficult to determine, but in the last 40 years women have more and more

undertaken the tasks, responsibilities of men or even occupation of men and higher

proportions of them are heavy smokers. Thorsen et al19

studied during 2001 to 2010

and found that there was an equal gender distribution (52% were women), but women

were significantly older than men. In a study by Kuremu20

male/female ratio was

1.7:1. Dakubo21

reported that male to female ratio was 4.5:1 In a study by Nuhu22

male to female ratio was 4.8:1.

Although perforated duodenal ulcer is common in both sexes, undoubtedly a

higher proportion in females are gastric ulcers.

In males, nearly 83.6% are duodenal ulcer perforations whereas in 12% of

cases gastric ulcer perforations were found. The comparable figures in females being

70.6% and 25% respectively.

Since the beginning of the century, there is a steady increase in incidence of

perforations and this is commonly attributed to the increased psychological stress and

strain to which 21th century men are subjected to. But 21th century women were

equally subjected to same kind of stress and strain, yet it was interesting that the

increasing incidence of the perforation was confined to men. Perhaps the more

physical strains in males may be responsible for increased incidence of perforations

ii) Age incidence:

The age incidence in peptic ulcer perforation after the 2nd world war has

definitely shifted towards the older age group.

Although the acid secretion decreases with age, the incidence of duodenal

ulcer increases. The production of duodenal bicarbonate decreases with age,

suggesting that a breakdown in mucosal defense mechanisms may be responsible.


36

Before the war 75% of perforations occurred in the 3rd to 5th decades and 5% in the

first and second decade The highest incidence was found between 45 and 55 years.

Perforations very rarely may occur infants or in extreme old ages.

In a study in the UK, reported by Wilt et al, perforation rates of duodenal and

gastric ulcer were highest in patients more than 65 years of age.

Kuremu20

reported the mean age was 47 years. Dakubo21

reported that the

mean age of 40.9 years. Bin-Taleb23

found that an overall mean age of 39.08 years.

Nuhu22

reported that age range of 18-77 years and a mean age of 45.5 years. Sarath24

reported that the mean age of the patients was 44.5 years.

iii) Occupational incidence :

Since 1950 both gastric and duodenal ulcers have been more frequent in lower

socio economic groups in UK and USA. It is commonly stated that perforation is

more likely to occur in those engaged in heavy manual work .Lifting of weights and

strenuous exercise by causing a rise in intra abdominal pressure predisposes a patient

who is suffering from peptic ulcer for peforation.

Weir in 1900 in reviewing 1390 cases in North East Scotland found the

highest incidence in fishermen, farm labourers and heavy manual workers.

Less than half the numbers were in professional or sedentary occupation.

Kozoll and Meyers26

, in 1904 reported perforations reported incidence as

follows ;

Non-skilled 27.9%

Dependents 12.9%

Semi-skilled 14.5%

Skilled 11%

White collar worker 3.8%


37

It would appear that when a series is reported from “General hospital" which

has a high intake of many workers the incidence in the professional and sedentary

groups is low, whereas in a “private" practice the reverse is the case. But in India,

most of the perforated peptic ulcers are among the labour class particularly with

farmers and people of poor class. The reason for this is that the socioeconomic

conditions being poor in these class of people, they are more prone to develop

perforation. The general resistance of these individuals to state of stress and strains

will be much less as compared to middle and rich class of people.

iv) Trauma :

Trauma to the abdomen such as a forcible blow over the epigastric region may

precipitate perforation. Shaw analysing 389 cases of perforation reports that 8 patients

gave a definite history of trauma which was apparently responsible for the

perforation. But of these one patient gave the history of fall of a sac of cement upon

his abdomen, whereas the other one was hit by a moving belt and others gave history

of having received trauma by various other objects.

Most patients try to relate their acute pains to some possible casual incident

and occurrence of traumatic incident to the abdomen can sometimes be foremost in

their minds. John A. Shepherd states that trauma can rarely be provided except as a

final where the disaster was already imminent.

v) Seasonal Incidence :

Many writers have sought to show that there is an increase in ulcer symptoms

and in ulcer perforation in the winter. Jamieson72

states the incidence was uniform

throughout the spring and summer but dropped in the autumn, only to rise again to a

peak in winter. Debackey15

while reviewing 192 cases of acute gastroduodenal


38

perforations has made a mention that the highest incidence of perforations took place

during the month of December and January.

In India also greater number of perforations occur in November, December

and January months (Shanmukarao). This may be due to the work of the cultivators

being more during the winter season.

vi) Geographic incidence:

There are great variations in the incidence of perforations in various parts of

the world. It is common particularly among westernized civilization and practically

unknown among more primitive populations, such as Bantu in South Africa. When

primitive people move to and work in areas of western civilization and adopt western

dietary social habits they become more likely to develop peptic ulceration and

perforation.

In India the incidence is more in southern parts of the country. The staple diet

in south is rice with curry.

vii) Perforation of peptic ulcer in association with other clinical states :

The following well defined clinical states may be associated with perforation.

a . Burns

b. Neurological injury

c. Z.E. syndrome

d. Aortic aneurysm surgery

e. Cardiac transplantation

f. Renal transplantation


39

viii) Other factors

a) Emotional stress and psychological factors

It is a matter of common experience to observe that individuals who perforate

will admit recent worry or overwork. There was an apparent increase in incidence of

perforation during the London air raids which suggest the anxiety,trauma and

psychological stresses predisposed to perforation. Attempts have been made, most

notably by Stewards Winsor in 1942 and Illingworth27

in 1944 to link perforation with

psychic stress, especially in war time.

b) Relation to food

Beans found that nearly 90% perforate more than 2 hours after a meal and

only 105 immediately after food. Acute distensions immediately after food might be

expected as factor. But Debakey15

in his extensive survey suggests perforation is

unusual within 3 hours after a meal.

c) Iatrogenic perforations (drug induced):

It has been stated by various authors that if excessive doses of cortisone are

given to patients suffering from chronic duodenal ulcer, they may develop

manifestations of acute exacerbation and also perforation of duodenum.

Hydrocortisone, by their anti inflammatory property prevent fibrous tissue

formation at the site of ulcer and predisposes for the perforation. Also there is acidity

during cortisone therapy and cause perforation of peptic ulcer.

Spiro and Miles (1960) reported that peptic ulcer occur in about 5% of patients

with rheumatoid arthritis. But where such patients are treated with cortisone the

incidence raised to 12% and a significant number of these ulcers perforate. Dayton et

al in 1987 reported 161 ulcer perforations, associated with corticosteroid

administration.


40

Dakubo21

reported that ulcerogenic substance intake was found in 67%

patients and Horowitz28

found that 50% of patients with perforated duodenal ulcer had

a prior history of NSAIDs use.

Torab29

reported NSAIDs as one of the common risk factors for perforation.

Lanas30

found that use of aspirin was associated with 70% of upper gastrointestinal

perforations. Numerous studies demonstrated that NSAID users are at increased risk

of complications from three to fourfold compared to patients not on NSAIDs or

aspirin routinely. Ohene-Yeboah31

reported that some of these perforations were

associated with the intake of NSAIDS.

d) Blood groups

Clark (1985) reported the incidence of Duodenal ulcer perforation and

Gastric ulcer perforation in various ABO blood groups as :

Blood group O A B AB

DU perforation 49 45 40 20

Gastric ulcer perforation 5 1 3 1

e) Environmental factors :

During the last 50 years there is remarkable increase in the frequency of

incidence of peptic ulcer. This is attributed to alteration in environments, one's

reaction to such changed environments. The increase in "Wear and tear" of life in this

age of "rush and hurry" is the factor responsible for the ulcer to develop. The same

reasons also hold good for the occurrence of perforations.


41

f) Smoking and alcohol :

In a study by Svanes32

, on smoking and ulcer perforation, current smoking

increased the risk for ulcer perforation 10-fold in the age group 15–74 years No

increase in risk was found in previous smokers.

Andersen33

in the year 2000, assessed the association between smoking,

intake of alcohol and the risk of peptic ulcer perforation, and found that smoking

more than 15 cigarettes per day increased the risk of perforation more than 3-fold.

Drinking more than 2 litres of alcohol per week increased the risk of ulcer perforation.

In another study by Zangana34

sixty five percent of the cases were smokers. Stress and

smoking played a significant role in the occurrence of perforation in 83% of cases.

g) Helicobacter pylori infection

While H. pylori is well recognized as a causative factor in PUD, its exact role

in cases of perforated ulcer has not been established. Chowdhary35

reported on a

series of 45 patients, of which 15 had a perforated duodenal ulcer; none of these 15

patients had evidence of H. pylori infection. Reinbach36

also concluded that there was

no clear association between H. pylori infection and duodenal ulcer perforation. In

their series of patients with acute perforated duodenal ulcer, 47% of patients had

evidence of H. pylori infection, which was similar to the 50% rate in the control

group.

Results obtained by Tokunaga28

when evaluating H. pylori infection in

patients operated for duodenal ulcer showed that H. pylori infection was more

prevalent in perforated duodenal ulcer (92%) than hemorrhagic (55%) and stenotic

ulcer (45%).


42

DIAGNOSIS 9,11,12,13,14,18,39,40,43

There is no intra-abdominal catastrophe where a successful outcome more

dependent upon early diagnosis than duodenal ulcer perforation. In 95% of cases the

diagnosis presents little difficulty.

The diagnosis of perforated DU is by :

1. Careful history.

2. Examination of the patient both by general physical examination and

examination of abdomen.

3. Confirmation of diagnosis by necessary investigations.

DIFFERENTIAL DIAGNOSIS:

The most reliable guides to a correct diagnosis of perforated peptic ulcer are

provided by a suggestive history of previous dyspepsia, by the demonstration of gas

under the diaphragm and by the persistence of abdominal pain, rigidity and when

present shifting dullness and rectal tenderness. The conditions which may mimic

perforated peptic ulcer can be grouped as follows:

The differentiation falls mainly into 3 categories.

I. Intra abdominal conditions.

a. Acute gastric ulcer perforation.

b. Acute ileal perforation-Typhoid and non-specific

c. Acute appendicitis

d. Acute pancreatitis

e. Acute cholecystitis

f. Acute intestinal obstruction

g. Vascular accidents like mesenteric infarction or ruptured aneurysm.

h. Ruptured ectopic gestation.


43

i. Ruptured viscus as in perforated diverticulitis or after trauma or from a

foreign body.

j. Acute peritonitis from any other cause. (Rare type of perforated peptic

ulcer) peptic ulcer in a Meckel's diverticulum or an intestinal

duplication may perforate.

II. Intra thoracic conditions

a. Acute myocardial infarction;

b. Pneumonia.

c. Pleurisy

d. Acute pericarditis.

e. Spontaneous pneumothorax.

f. Emetic rupture of oesophagus.

III. Metabolic and neurological

Acute abdominal pain simulating perforation may occur in

a. Acute porphyria.

b. Diabetes mellitus.

c. Uraemia.

d. Hyperlipidaemia.

e. Acute poisonings of various kinds,

f. Neurologic disorders such as

i. Meningitis.

ii. Pre-eruptive stage of herpes.

iii. Multiple sclerosis.

iv. Neurosyphilis.


44

The conditions which mimic perforated peptic ulcer can be classified on the

grounds of "Emergency Surgery" required or not, into 3 groups :

I. Those in which surgery is essential:

a. Acute appendicitis.

b. Acute intestinal obstruction.

c. Ruptured or leaking aortic aneurysm.

d. Ruptured ectopic gestation.

e. Acute enteric perforations due to typhoid ulcer, paratyphoid and non-

specific ulcers.

f. Mesenteric infarction.

g. Ruptured viscus.

II. Conditions in which surgery is not essential but not harmful and may even be

alternative and satisfactory treatment.

a. Acute pancreatitis.

b. Acute cholecystitis.

c. Acute primary peritonitis.

III. Those conditions in which surgery is likely to be harmful.

a. Coronary thrombosis.

b. Diaphragmatic pleurisy

c. Pneumonia.

d. Acute non-specific mesenteric lymphadenitis.

e. Neurological conditions:

Herpes Zoster

Tabetic Crisis

Meningitis


45

Multiple sclerosis

f. Metabolic causes: Hyperlipidaemia, acute poisoning of various kinds.

g. Other causes of acute peritonitis which simulate perforation

like pelvic inflammatory diseases such as acute salpingitis, familial

mediterranean fever.

INVESTIGATIONS

The following investigations are usually performed , which help in diagnosing

perforated duodenal ulcer.

1. Routine investigations.

a) Hb % and haematocrit values

b) TC and DC

c) ECG in 12 leads

d) X-ray chest - PA view

e) Urine-Albumin, sugar, microscopy

2. Plain Erect X ray of abdomen

3. Upper gastro-intestinal study with gastrograftin series.

4. Ultrasonography and CECT Abdomen

5. Serum amylase estimation.

6. Urinary amylase estimation.

7. Diagnostic peritoneal aspiration.

8. Culture and sensitivity of peritoneal fluid.

9. Helicobacter Pylori Diagnosis


46

1) Routine investigations :

a) Estimation of Hb and Haematocrit values : According to Kozoll and Meyers25

,

significant number of perforated duodenal ulcer patients showed evidence of anaemia.

If the patient is severely anaemic, it has to be corrected. Some of the patients may

show haemo-concentrations which may be due to marked fluid loss into the peritoneal

cavity.

b) Total count and differential WBC counts: This investigation is not of much help

in earlier stages, but it certainly helps to exclude the possibility of other conditions

where there may be leucocytosis. In later stages of DU perforation when the

bacterial peritonitis set in, leucocytosis with polymorphonuclear leucocyte

predominance may be found.

c) ECG in 12 leads: This is very important in patients especially over the age of 40

years. It helps to exclude the conditions, where there will be characteristic ECG

changes which simulate DU perforation and to rule out underlying cardiovascular

disease in case of of DU perforation,

d) X-ray chest PAview : Routinely practiced for two reasons -

l) To exclude cardiothoracic conditions, which simulate DU

perforation.

2) To rule out the underlying cardiorespiratory diseases.

2) Plain X-ray of the abdomen41

This is of utmost importance to confirm the diagnosis of peptic ulcer

perforation and is extremely valuable in typical cases. Radiograph can be taken either

in erect posture or left lateral decubitus. Leroux (1951) believes that a straight x-ray

of the chest of a semi-recumbent patient is the best method of demonstrating

collection of gas, this method also reveals any pulmonary lesions.


47

Plain x-ray reveals the presence of air under the right cupola of the diaphragm

in about 70% of the cases. In order to get a positive finding radiologically it is

essential that patient should wait for 5 to 10 minutes in the erect posture or in the left

lateral decubitus. In the earlier stages of perforation, plain x-ray of abdomen may not

reveal the presence of air under the diaphragm. In such cases repeated x-rays should

be taken after waiting for one or two hours.

The air may also collect under the left cupola of the diaphragm. Since

normally the fundal gas shadow is seen on the left side it may be difficult to

distinguish the collection of air under the left dome. But if carefully observed, a

collection of air would be visualised well above the level of air shadow in the fundus

of the stomach.

In those cases where radiologically it is not be possible to confirm the

presence or absence of perforation, after aspirating gastric contents, 20 to 30 ml of air

can be injected into the stomach through the nasogastric tube, the patient lies on his

left side for few minutes then a radiograph is taken in the sitting or erect posture. In

these circumstances if a perforation is present the crescentic translucent area will be

seen under the right dome of diaphragm in a very high percentage of cases.

The presence of air under the right dome of the diaphragm is of both

diagnostic and prognostic importance. The amount of air collected may possibly give

a clue not only regarding the size of perforation but also regarding probable duration

of perforation. It also affords useful information regarding the line of treatment to be

adopted. In minimal collection of gas under the diaphragm, there is a chance for

conservative line of treatment till patient‟s general condition stabilises, whereas

emergency operative line of treatment is mandatory if huge collections of gas is

present.


48

Sometimes, x-ray of the abdomen is taken in supine positions, when the

patient is not in a position to stand or sit.

In supine position gas may be outlined lying free in the peritoneal cavity. A

careful watch is necessary to differentiate the gas shadow in the abdomen, which have

got a definite contour and characteristic of gastrointestinal tract.

Gas under the right dome of diaphragm may be missed if the x-ray taken is not

sufficiently high up at least upto the level of 7th or 8th costal cartilage. Free gas under

one or both halves of the diaphragm is not necessarily indicative of perforated

duodenal ulcer. Free gas under the diaphragm may be demonstrated in the following

conditions.

a) All small bowel ulcer perforations which include perforation of typhoid

ulcers, traumatic ulcers and non specific ulcers,

b) All large bowel ulcer perforations.

c) Perforations of gall bladder due to stones or due to trauma.

d) Interposition of either small bowel or large bowel between the dome of

the diaphragm and fundus of the stomach.

e) Liver abscess with gas forming organisms involving the upper most

portion of the liver in which gas bubbles may be demonstrated.

f) Surgical procedures ;

i. After recent laparotomy

ii. Peritoneoscopy

iii. Pneumoperitoneum - as a therapeutic measure in collapsing the

cavity in the lung in pulmonary tuberculosis.

iv. Rubin's test: to know the tubal patency in cases of infertility.


49

Cases have been studied in western countries where radiological evidence of

gas under the diaphragm was found particularly in ladies engaged chronically in

sweeping the floors. In such cases speculations have been made that an entry might

have occurred through the genital tract possibly facilitated by the knee-chest

exercises.

3. Upper gastrointestinal study with gastrograffin series :

This investigation is mainly to distinguish between gastric and duodenal

perforations. Moore (1955) has suggested the instillation of radio opaque material and

gastrograffin by the indwelling nasogastric tube. But pylorospasm may prevent the

entry of dye into the first part of duodenum,the commonest site of perforation. This

investigation is rarely justified as it is an invasive procedure and the general condition

of the patient usually will not permit this investigation.

4. Ultrasonography and CECT Abdomen41

:

Ultrasonography of abdomen was performed using a convex multi frequency

probe (3.5-5mHz). Evidence of intraperitoneal free fluid and of reduced intestinal

peristalsis was considered indirect evidence of perforation.

Because of classical presentation in most patients, CT-Scanning is rarely

required for diagnosis. However, patients with perforated duodenal ulcer who are on

steroid therapy or who are hospitalized for other abnormalities may develop occult

causes of abdominal pain and sepsis. CT-Scanning may be required to determine the

cause in occult abdominal sepsis.

5. Serum Amylase estimation :

Serum amylase estimation is one of the most used single means for

recognising certain acute abdomen cases especially acute pancreatitis. The normal

level of serum amylase as given by Burnett and Hers (1955) ranges from 62 to 70


50

units. The normal range according to Somogyi units is 80-150 units. The reason to

why serum amylase is increased in perforated duodenal ulcer is due to the escape of

pancreatic juice and absorption of its ferments. It must be emphasized that it is

exceptional to obtain very high levels of serum amylase in perforated peptic ulcers.

Apart from acute pancreatitis and perforated duodenal ulcer, the serum

amylase may be raised to a high level in small bowel obstructions, acute cholecystitis,

common bile duct stone with or without cholangitis. Other conditions in which serum

amylase level is elevated include acute alcoholism without pancreatitis, afferent loop

obstructions after gastrectomy, ectopic pregnancy, perforated duodenal diverticulum,

renal failure, carcinoma of the pancreas and mumps.

Of 31 cases of DU perforation described by Burnett and Hers (1955) 8 cases

were found to have values above 400 units. In case of duodenal ulcer perforation, the

highest level found was 3400 units.

There is no level of elevation of serum amylase which is absolutely

diagnostic of pancreatitis to the exclusion of perforation.

6. Urinary amylase estimation :

Estimation of the total amount of amylase in a 2 hour urine sample is accurate

than ,the simple measurement of the concentration of the enzyme in the urine, blood

or the serum lipase.

It is necessary to collect 24 hour sample of urine. Single sample of urine does

not permit an accurate estimation, as urinary amylase level fluctuates with normal

renal function, which may be impaired by hypotension and dehydration,

The normal values of urinary amylase (diastase) expressed are 35 units in 24

hour collection of urine and in casual specimen upto 50 units may be taken as normal.

After 12-24 hours it often rises to 100 units or more. Sometimes may be as high as


51

500 units. The urinary amylase level remains elevated after serum amylase level has

returned to normal. Later it too will decline usually to reach normality between 3rd

and 5th

day.

7. Diagnostic peritoneal aspiration :

Bile stained fluid is characteristic of perforated DU usually the fluid is turbid

and contains food particles and may be cloudy due to debris, mucus and some pus

later. The most important observation is the fluid was never acidic when tested with

litmus paper, the fluid was either neutral or alkaline.

The differential diagnosis for bile stained fluid :

i. Perforated duodenal ulcer.

ii. Perforated gastric ulcer.

iii. Perforated gall bladder.

iv. Perforated bile duct.

v. Spontaneous biliary peritonitis.

8. Culture sensitivity of peritoneal fluid :

A higher incidence of positive culture is obtained by collecting some of

peritoneal fluid or implantation in the culture medium, than when a swab dipped in

the exudate is submitted. For the first 10 hours, the cultures are often sterile because

of the bacteriostatic effect of hydrochloric acid from the stomach.

After 12 hours, inhibition due to the acid is no longer present, The following

organisms are often encountered, the first two being found most frequently.

a. Staphylococci.

b. Colon bacilli

c. Anaerobes

d. Streptococci


52

e. Pneumococci

f. Yeast cells

9. Diagnosis of Helicobacter Pylori12,42

:

The diagnosis of Helicobacter pylori infection is done by following different

methods:

i) Non invasive - a) Serology- ELISA.

b) Urea breath test.

ii) Invasive - a) Rapid urease test e.g. Eco, Pyloritek

b) Histology.

iii) Culture.

Serology: H-Pylori infection evokes both local and systemic immune

response. Serological tests can be done for detection of IgM, IgG, or IgA antibodies.

The systemic IgG response is the most commonly used parameter for this infection.

ELISA, using a commercial kit, has high sensitivity (100%) and specificity (up to

95%).

Urea breath test: This test is based on the production of urease by H- Pylori.

The patient ingests a solution of urea containing a labelled carbon atom. The

appearance of labelled carbon dioxide in the breath indicated the presence of

infection. The label used is either non-radioactive 13C or radioactive 14C.

Rapid urease test: This test depends on the ability of H-Pylori to produce the

enzyme urease, which hydrolyze urea to produce carbon dioxide and ammonium ions,

which change the colour of the pH indicator, pheno-red from yellow to red indicating

positive result.

Histology: H-Pylori can be identified on haematoxylin and eosin, modified

Giemsa and Ethin-stony silver stains.


53

Culture: This is the most difficult method for diagnosing the H-Pylori

infection. Successful growth of H-Pylori depends on laboratory expertise, timely

handling of specimens, use of appropriate media and incubation environment. Culture

facilities are absent in most of the centres in India.

PROGNOSIS 25,26,44

The prognosis depends on the following factors

a. The age and general condition of the patient

b. Sex

c. Time of occurrence.

d. Condition of the stomach: whether full or empty at the time of

perforation.

e. Size of perforation

f. Chronicity of perforation

g. Position of the ulcer

h. Associated haemorrhage

i. Associated diseases

j. The time taken for diagnosis of the condition.

k. The pre and postoperative management.

l. The line of treatment adopted, whether conservative or operative.

a) Age and general condition of the patient:

The prognosis is good in young adults and middle aged individuals when

compared to old people and children. After 60 years the prognosis worsens with each

year of age.


54

b) Sex :

The postoperative mortality is higher in men although the incidence of gastric

ulcer perforation is higher in men.

c) Time of occurrence of perforation :

The time which has elapsed between perforation and treatment is one of the

most important factors in prognosis. The longer the interval between the perforation

and the surgery, the higher the mortality. After 12 hours, the death rate rises steeply.

The "golden time" for treatment is between 6 and 12 hours after perforation. If the

perforation occurs in day time, better medical care can be obtained rather than in

perforation occurring at night particularly those residing at remote areas.

d) Condition of the stomach :

Fuller the stomach ,greater is the amount of free fluid and gas in peritoneal

cavity, the worse is the prognosis. If the perforation occurs in an empty stomach there

will be much less chance of spillage into the peritoneal cavity and the prognosis in

such cases is better than a perforation occurring in a full stomach.

e) The size of the perforation :

Smaller the perforation, lesser is the spillage into the peritoneal cavity and

better would be the prognosis.

f) Chronicity of ulcer :

It is exceptional for a patient with a perforated acute ulcer not to recover. The

great majority of the deaths occur when a chronic ulcer perforates (Bilmour 1953 and

Ddesmon 1962).


55

g) Position of the ulcer :

Prognosis is best with anterior ulcer perforation than with those occurring in

posterior ulcers. The higher the ulcer is situated on the lesser curvature, greater is the

post operative mortality (Kozoll and Meyer 1960)25

.

h) Associated haemorrhage :

Associated haemorrhage considerably prejudices the patient's chances

of recovery. The incidence is about 2% in studies by Slatu (1951) and Avery James et

al (1933). A more radical surgical approach and the substitutional partial gastrectomy

for simple suture has reduced the mortality considerably but this association is

probably the greatest factor in prognosis.

i) Associated diseases :

A higher proportion of older patients will have serious diseases such as

hypertension or cardiovascular and pulmonary conditions and will thus be less able to

withstand the rigors of perforation and its associated sugery.

Many will die of pulmonary or cardiac complications. Although recovery from the

perforation is "Pathologically" complete.

j) The efficiency of the local GP to diagnose the condition:

If the local practitioner who will be having the opportunity of seeing the

patient early, will be having sufficient time to diagnose the condition and refer the

patient to nearest possible surgical centre. Certainly patients will have better

prognosis when referred early than when the patient is seen late and mismanaged.

k) The pre and post operative management :

There is marked reduction in overall mortality in recent years and is due to the

following factors :


56

i. Improved methods of pre operative treatment especially gastric

suction, IV fluids,electrolyte replacement, antibiotic therapy and blood

transfusion.

ii. Improved methods of anaesthesia, especially muscle relaxants and

positive pressure pulmonary ventilation.

iii. Better post operative management, particularly greater control over

infection by antibiotics.

iv. Improved operative technique and the adoption of a more radical

approach to the treatment of perforated ulcer.

l) Line of treatment adopted :

Prognosis also depends on the line of treatment adopted either conservative or

operative. The results of operative line of treatment, is better than the conservative

treatment. The conservative one is a blind procedure, and can be adopted only in cases

where patients is not fit for anesthesia and risks outweigh benefits.


57

TREATMENT

In most hospitals, the treatment of perforation is operative. Although non-

operative management has had its strong advocates, most notably, Herman Taylor in

1957 and Donovan in 1979. Immediate surgery has the significant advantage of

enabling the surgeon to confirm the diagnosis, close the perforation, toilet the

peritoneal cavity and if feasible perform definitive ulcer surgery.

The following operative procedures have been described for the treatment of

perforated duodenal ulcer12,13, 40,43,45,46

:

l. Simple closure of perforation, or along with modifications such as the use of an

omental patch (Graham „s patch) has been the mainstay of surgical treatment of

perforation of duodenal ulcer in most centres.

2. Definitive ulcer surgeries for perforated duodenal ulcer;

a. Simple closure of perforation with drainage procedure like

gastroenterostomy with or without vagotomy.

b. Simple closure of perforation with pyloroplasty and vagotomy.

c. Simple closure with PGV.

d. Gastric resection with or without vagotomy.

3. Laparoscopic closure of perforation.

4. Combined laparoscopic- endoscopic method.

Pre-operative management :

It is mandatory that a short time be spent on resuscitation of the patient before

surgery. Precipitate surgery increases morbidity and mortality,whereas resuscitation

with restoration of fluid, electrolytes and blood with control of septicaemia, makes

surgery much safe and prevents possible complications.

The following regimen is suggested.


58

a) As soon as the presumptive diagnosis of perforation is made, pain should be

relieved by an appropriate dose of narcotic analgesic.

b) Large bore nasogastric tube should be passed and the stomach is emptied as

completely as possible.

c) Patient is kept nil per oral. Blood should be drawn for grouping and Rh

typing and a biochemical profile including serum amylase is done. An IV

fluid infusion should be commenced.

d) A catheter should be inserted, urinary retention is common in acute

peritonitis and it is also necessary to monitor the urine output closely.

e) It is advisable to obtain a chest X-ray and ECG. Cardio-vascular monitoring

appropriate to the condition of the patient should be instituted.

f) Antibiotics should have an appropriate spectrum for the aerobic and

anaerobic organisms commonly found in the GIT.

g) Consent for definite ulcer surgery should be obtained.

h) Preparation of the abdomen is better postponed until the patient is

anaesthetized.

i) If the patient is not immunized against tetanus, tetanus toxoid should be

given.

j) BP and pulse rate are recorded at half hourly interval.

1. SIMPLE CLOSURE OF PERFORATION TOGETHER WITH TECHNICAL

MODIFICATIONS SUCH AS THE USE OF OMENTAL PATCH

This surgery has been the mainstay of surgical treatment of perforation in most

centres and carries low mortality rate compared to other definitive surgical

procedures.


59

Heusner was the first to close a perforated ulcer successfully, after number of

failures by well known surgeons of that day, including Mikulicz-Radeki. Heusner

sutured a perforated gastric ulcer in the patient‟s home, the case being reported some

months later by Kriege in 1892. The first report of a successful surgery for perforated

duodenal was by Dean in 1894.

The first surgery consisted of simple closure of the perforation with two rows

of Lembert sutures, washing out the peritoneal cavity with warm water or antiseptic

lotions and inserting rubber or glass drainage tube down to the site of ulcer, to the

pelvis and sometimes to the loins.

Bonnett (1896) suggested that in some cases in which perforation was very

large and difficult to suture owing to the flexibility of the parts, omentum could be

used to plug the defect. Today it is found more satisfactory to introduce 3 interrupted

sutures, one at the top, one in the middle and one at the bottom of the perforation and

after bringing up a portion of the greater omentum and laying it over the defect, to tie

them in order to hold it in position. Cellan Jones(1929) and R.Graham(1937)

emphasized the simplicity and effectiveness of this procedure and advocated that it

never produced duodenal stenosis.

This procedure aims solely at warding off the immediate danger in a patient

who is seriously ill and whose life is threatened, while subjecting him to minimum

amount of operative trauma. The object is not to cure the ulcer, this can be deferred

to a later date. Nevertheless cure may be achieved in 85% by this simple technique if

the ulcer is acute and in 25% if it is of chronic ulcer. There are different reports by

various authors regarding this statistics. The controversy was well reviewed by Boey

et al16

in 1982. In their own patients they found after 3 years of follow up, the

cumulative recurrence free rates were 70.55% and 55.3% for the short pre-perforation


60

history and long pre-perforation history respectively. They also noted as did

Illingworth in 1946, that relapse after perforation closure was more frequent in

younger patients regardless of their duration of pre-perforation history.

Gilmour and saint (1932) reported a mortality of 4.7% while Houston (1946)

gives the Newcastle figures for 1943 as 184 cases with 8.2% mortality and for 1944 as

190 cases with 6.3% mortality. Avery Jones (1957) reported a mortality of 4.9% in

365 cases. Kingsburty and Pennoyer (1962) reports 12% mortality in 506 surgeries.

A collective review by Janet and Donaldson in 1972 of 1895 cases followed

up after simple closure for 1 to 26 years showed that 2/3 rd had subsequent symptoms

and that more than 1/3rd had subsequent definitive surgery. There is substantial

variation from study to study. When patients in whom the perforation is associated

with haemorrhage are treated by simple closure, the incidence of post-operative

haemorrhage is high, sometimes necessitating a second surgery in a few days.

Techniques of simple closure45,46,68,69

:

Surgery can be undertaken under general anaesthesia. Muscle relaxants have

added greatly to the performance of the surgeries and the peritoneal toilet and

simplifying wound closure. Premedication with morphine and atropine 0.6mg is ideal.

Incision :

The surgeon has a choice between two epigastric incisions, midline or

paramedian. The former is the most rapid method of entry. Moreover it is easy to

close and in a potentially infected area, it does not lay open the rectus sheath. On

opening the peritoneal cavity there is often an escape of gas, a sort of "hissing noise'

or "muffled pop' of escaping gas could be heard if listened carefully. This is

diagnostic of perforation of a hollow viscus.


61

Location of perforation :

The edges of the wound are gently retracted and the right lobe of the liver is

drawn upwards with a suitable retractor so also to bring the lesser curvature of the

stomach, pylorus and the first part of the duodenum into view. The stomach is drawn

down by applying gentle traction on the greater curvature with a moist abdominal

pack.

In most cases the perforation is readily seen (8 out of 10). It may be oval or

circular and punched out and of a variable diameter. In duodenal perforation the

escaping fluid is usually bile stained and somewhat frothy. The gut around the

perforation is infected and oedematous in many cases. In the acute ulcer the

duodenum is mobile, there are no adhesions. In large chronic ulcers the first part of

the duodenum seems to be part of a chronic inflammatory mass consisting of greater

omentum , pancreatic head, the lower portion of the stomach and sometimes the liver

and the hepatic flexure of the colon. In many of the cases ,perforation may be sealed

at the time of laparotomy and may not be obvious without a careful search.

Occasionally omentum, sometimes viscus or the anterior abdominal wall seals off the

hole and only separation of one or other of these structures will reveal perforation. If

the perforation is so obscured, gentle dissection with the finger will produce some

welling up of fluid and this reveals it.

A careful search should be made for a second perforation elsewhere and for

evidence of ulcer disease in other sites, such as posterior gastric ulcer that has

ruptured into the lesser sac. Occasionally, perforation of an ulcer of the 2nd part of the

duodenum may be unmasked by mobilization of the duodenum by Kocher's method.


62

For quick location of the perforation, when it is not found early, 30-60 ml. of

1% solution of methylene blue may be injected down the nasogastric tube and then

site of perforation becomes readily apparent.

Closure of perforation :

There are many ways of closing perforation. A question that has to be

considered is whether variations in the technique of closure itself may influence the

long term results. The frequency of complication of gastric outlet obstruction after

simple closure varies from 26% reported by Read and Ompson to 3% reported by

Playforth and McMahon.

According to a study reported by Thompson, gastric outlet obstruction was the

indication for surgery in almost half of their patients who underwent subsequent

definitive surgery. A study conducted by Balinger and Solanke showed that

techniques such on omental patch may also contribute to stenosis.

The perforation having been found, retraction of the abdominal wall and

traction upon the stomach are so arranged as to bring the perforation into best possible

view. Among the many ways of closing perforations, simple closure of perforation

with interrupted sutures is the ideal method.

The suture material used should be synthetic monofilament sutures, such as

'Polydioxanone' (PDS). The non absorbable material such as silk should be avoided,

because those materials cause silk ulcers, which may bleed and produce pain. The

term plication is used for simple closure method. The first stitch is taken above the

perforation, 2nd below the perforation and 3rd through the opening. Cutting out of the

sutures were prevented by taking considerable bite of the duodenal wall, which is

prone to occur especially in edematous tissues. The first and second stitches should be

tied and held in forceps before and centre stitch is drawn tight to complete the closure


63

of Perforation. The line of closure should now be reinforced with interrupted

seromuscular (Lembert) stitches which bury the previous suture line. The ends of one

or two of these sutures should be utilised to suture a tag of omentum over the closure.

In cases where in duration is so marked that all the stitches tend to cut out, then the

perforation is closed with the omentum alone. Omentum is plugged into the hole and

is secured so as to avoid narrowing the lumen of the bowel. In duodenal ulcer

perforation, the sutures should be placed in the long axis of the gut. If however, the

tissues are friable or the hole is larger and the sutures cut through, no hesitations

should be allowed in placing sutures in that axis, which permits the safest closure. It is

rare for actual stenosis to be caused by the surgery and it can always be treated by a

short circuit i.e., gastroenterostomy 7-10 days later, when the patient overcomes the

immediate danger. The aim of the surgery is to close the perforation securely.

Other methods of closure of perforation described are:

a) Dragging the omentum into perforation and plugging it into the ryles tube and

fixing the ryles tube.

b) Use of rectus muscle to seal the perforation

c) Use of jejunal serosal patch for closure of large perforations.

Peritoneal toilet :

It is often stated that the general condition of the patient improves

immediately, when the peritoneal fluid is aspirated. The exact mechanism is not

known.

The peritoneal toilet should be done meticulously as a fixed routine with the

use of suction.

i. A specimen of fluid should be taken in a sealed syringe for aerobic and

anaerobic cultures with immediate plating.


64

ii. The subphrenic spaces should be gently revealed drawing down the liver.

iii. The morrisons pouch and the right paracolic gutter sucked out.

iv. The intestine should be drawn up while the fluid is removed from the pelvis.

v. The spleen should be gently retracted medially and the left subphrenic area and

paracolic gutter sucked out.

vi. Swabbing with gauze should be minimal as it is traumatic to the inflamed

visceral peritoneum and may encourage the formation of adhesions.

vii. No attempt be made to remove fluid from amongst the coils of intestine, both

solid pieces of food or debris should be removed if found during these

manipulations.

The beneficial effect of irrigation of the peritoneal cavity was well reviewed

by HAU, who recommended irrigation with copious amounts of a crystalloid

solution. Adding antibiotics to irrigant has no advantage over systemic therapy.

DRAINAGE:

In most early perforations i.e., within 6 to 8 hours, provided that the exudate is

little in amount and is not markedly bile stained, it is advisable to close the peritoneal

cavity without drainage. In perforations beyond 6 to 8 hours where the exudate is

usually copious and may be frank pus, it is advisable to provide drainage either

through the main wound or through a separate incision in the right flank below the tip

of the 11th rib or making a suprapubic incision.

TWO TUBE DRAINAGE47

: Anil in his study of more than 200 cases

reported this novel technique.It is the method of aspiration of gastro-intestinal

secretions, in gastro-duodenal repairs. It comprises of ryles tube suction, at two

different levels of gastro intestinal tract, using two ryles tubes, first in the stomach,

conventionally aspirating gastric secretions and second negotiated just distal to


65

duodenal repair, aspirating pancreatic and biliary secretions, along with superfluous

gastric secretions, preventing leakage from site of repair during phase of healing and

thus facilitating healing process, minimizing post-operative flatuence, excessive

prolonged ryles tube aspirates, leaks and other complications associated with it.

FIGURE 5: TECHNIQUE OF TWO TUBE DRAINAGE

TRIPLE-TUBE-OSTOMY TECHNIQUE48

:

This is a novel technique tried in large duodenal ulcer perforations and in large

iatrogenic perforations. The perforated part is closed with omental patch as in

conventional method. Following repair of the perforated site, biliary drainage is

carried out by cholecystectomy, followed by insertion of a C-tube (6 Fr) into the

common bile duct through the cystic duct. The next step is identification of the

jejunum 5-15 cm distal to the Treitz ligament, and passage of a 4-mm tube through an

antimesenteric enterotomy in a retrograde manner into the junction of the second and

third portion of the duodenum. The tubing into the duodenum allows it to be

decompressed. In the final step, as a feeding jejunostomy, a 10-Fr catheter is passed


66

into the jejunum through an enterotomy in an antegrade manner. This 10-Fr catheter

enables early enteral nutrition. After a thorough lavage of the entire peritoneal cavity,

drains are placed at appropriate sites. This method avoids gastric and biliary

secretions at the site of perforation and facilitates healing process.

FIGURE 6: DIAGRAMMATIC REPRESENTATION OF TRIPLE TUBE-

OSTOMY TECHNIQUE

LOOKING FOR A SECOND PERFORATION :

It is worthwhile making a practice of looking for a second perforation. Several

examples of simultaneous perforation of two ulcers have been reported. If a second

perforation is found, it should be closed as is done for the first one.

CLOSURE OF THE ABDOMEN :

After meticulous haemostasis the abdominal incision is closed in layers. When

there is gross contamination of the wound it may be advisable to close the linea alba

and to use delayed primary closure of the skin wound.


67

2. DEFINITIVE ULCER SURGERY FOR PERFORATED DU16,24,39,49,50

An immediate definitive ulcer operation was advocated in the early part of this

century. Moynihan recommended closure of perforation and gastroenterostomy in

1901. Finsterer in 1910 urged the use of partial gastrectomy.

It has become apparent that substantial proportions of patients with simple

closure of perforations have continuing further serious trouble with their ulcer, have a

subsequent major ulcer complication or undergo subsequent definitive ulcer surgery.

The proportion suffering from these sequelae varies from centre to centre.

Illingworth et al27

reported a meticulous long term follow up study of 733

patients who had survived simple closure of a perforated ulcer. These investigations

showed that more than half of these patients had a severe relapse of their ulcer disease

within 5 years of perforation. A collective review by Janett and Donaldson of 1895

cases followed up after simple closure of perforation for 26 years showed that 2/3rd

had subsequent symptoms and that more than 1/3rd had subsequent definitive surgery.

The first prospective controlled trial of immediate definitive surgery versus

simple closure was reported by Boey et al16

with outstanding long term results in the

patients subjected to definitive surgery. Good results after definitive ulcer surgery for

perforation exclude high risk cases. Diathesis Robbs et al compared the natural

history of perforated ulcers with that of non-perforated group and found a definite

tendency for the perforated group to have more symptomatic relapses and a greater

subsequent definitive surgery. Sherlock and Holl-Allen studied patients whose

perforation occurred during medical therapy with Cimetidine and found that all

eventually required definitive surgery.

Illingworth et al27

and Sawyers et al42

have suggested that the duration of the

pre-perforation ulcer history is a reliable guide to prognosis after simple closure of


68

perforation. Conversely others do not agree with this. In their own patients they found

that, after 3 years of follow up, the cumulative recurrence free rates were 70.5 and

55.3% for the short preperforation history and long pre-perforation history groups,

respectively.

I. Definitive Indications :

i. The presence of a synchronous complicated second ulcer.

ii. Complications of previous ulcer.

iii. Perforation of an ulcer during anti-secretory treatment.

iv. When closure of stenosed duodenum or pylorus causes obstruction.

II. Relative indications :

i. A long pre-perforation ulcer history.

ii. A young patient.

iii. General condition being adequate for more extensive surgery.

iv. Moderate soiling of peritoneal cavity.

v. Recent perforation (within 12 hours).

An immediate definitive surgery is contraindicated if:

a) The patient is a poor risk because of major concurrent medical illness or shock

or because more than 24 hours has elapsed since perforation.

b) A surgeon experienced in vagotomy is not available, because perforation is

frequently an 'out of hour' emergency.

The different operative procedures are :

a. Simple closure of perforation with gastro-jejunostomy and vagotomy :

If the patient is young, general condition is good and the perforation is less

than 24 hours old, gastro-jejunostomy and total truncal vagotomy is the right choice

after closure of perforation. This procedure usually avoids the patient being subjected


69

to surgery again. The fears of mediastinitis following vagotomy have not been

fulfilled.

Another alternative to total truncal vagotomy is selective vagotomy in which

the hepatic and coeliac branches are preserved. This is a more difficult, tedious and

time consuming procedure and the efficacy of which is still under review.

The surgery of choice for perforation associated with stenosis is

gastrojejunostomy placed away from the site of perforation together with total truncal

vagotomy.

b) Pyloroplasty and vagotomy :

Pyloroplasty with vagotomy has been carried out successfully as an

emergency procedure in perforated duodenal ulcers.Pyloroplasty and vagotomy is the

method of choice in two situations:

i) When the perforation is very big and not possible to close by simple closure or by

omental patch and if the patient is young the surgery is completed by vagotomy

ii) When the perforation is associated with haemorrhage

Haemorrhage in association with perforation is usually due to a posterior wall

kissing or penetrating ulcer. It is often convenient to enlarge the perforation by

converting it into a pyloroplasty with an incision in the long axis. So that suture

ligation of the bleeding point in the posterior wall ulcer can be carried out. The

surgery may be completed by a truncal vagotomy.

Ernestoching and Rennie , Hamilton and Harbrecht reported 27 patients

operated with vagotomy and pyloroplasty in a series of 36 patients of duodenal ulcer

perforation with haemorrhage.

Walngekar, Bapt, Deshmukh from Bombay have reported 32 patients with

acute perforations of duodenal ulcer having been subjected to Pyloroplasty and


70

truncal vagotomy. They claim that management of perforated duodenal ulcer, either

by conservative or by simple closure technique, the basic causative pathology is

untouched, resulting in 85% developing symptoms within one year and 50%

undergoing definitive surgery in due course.

It is easier to convert the perforation into pyloroplasty and then add vagotomy

if the general condition permits. This procedure is less time consuming, easy, takes

care of the basic pathology lying behind the ulceration and gives long term results.

c. Simple closure of perforation with proximal gastric vagotomy (Highly Selective

Vagotomy or Parietal cell vagotomy) 52

:

This surgery denervates the acid-pepsin secreting mucosa but spares the

innervations of antrum and pylorus so that a drainage procedure is not required. It

carries least mortality of only 0.3%.The only disadvantage with PGV is high

recurrence rate of about 2-15% equal to total truncal vagotomy and drainage

procedure. PGV carries lowest incidence of side effects such as dumping syndrome,

bilious vomiting and distension. It can be argued that recurrence of ulcer after PGV is

easier to deal with than severe dumping and diarrhoea. It should be stressed that this

surgery is unpopular because many surgeons do not adopt this approach as total

truncal vagotomy with drainage procedure is popularly done in most of the centres.

Some authors including Jordon and Morrow , suggest that PGV be added to

simple closure whenever possible in all patients with perforated duodenal ulcer

because prediction of the post perforation course is unreliable.

Although many surgeons believe that the additional operating time involved in

a meticulous surgery such as PGV must have an adverse effect on the immediate

outcome of perforation and increase in mortality and morbidity has been indicated.


71

Few authors mention the complication of splenic injury during PGV in the

treatment of perforated duodenal ulcer.

Boey et al52

demonstrated that a PGV can be performed as effectively in an

emergency as in elective circumstances. It is clear, however that the success of PGV

depends on the experience of the surgeon.

If a definitive ulcer operation is deemed as an appropriate addition to simple

closure of a perforated duodenal ulcer, PGV is the procedure of choice,

d. Gastric resection with or without vagotomy :

The estimated risk of recurrence is least compared to other methods. It is less

than 1% for antrotomy and truncal vagotomy and 2-5% after truncal vagotomy and

partial gastrectomy. Whereas the recurrence rate for truncal vagotomy and drainage is

about 4-15%.

However, gastric resection carries the highest mortality. This surgery requires

an experienced surgeon. Perforation is frequently an 'out of hours' emergency and

surgery is performed by trainee surgeons.

Zachary and Keetley operated upon a large perforated ulcer situated near the

pylorus for which pyloroduodenectomy was performed . The patient made an

excellent recovery and in consequence Keetly advocated this procedure. However,

very few surgeons practice partial gastrectomy for perforated duodenal ulcer. Some

people advocated distal 2/3 rd gastrectomy at the time of occurrence of perforation

which is supposed to avoid further surgery or future complication.

Ernestoching and William Rennie , reported 21 patients having been treated

with 2/3rd partial gastrectomy being performed without any fatality .The same author

also reported 8 cases being treated with vagotomy and hemigastrectomy with good

results.


72

Partial gastrectomy is more radical procedure, which requires an experienced

surgeon, facilities must be ideal, patients general condition should be good.

As there are other methods which are safe, can be done by a trainee surgeon

with supervision and less time consuming, gastric resection is no longer

recommended for perforated DU.

Gastric resection is advocated (provided patients general condition is good) in

perforation associated with ZE syndrome. Perforation has been recorded in 23% cases

of ZE syndrome, according to Zollinger.

In summary, it may be said that whilst simple suture still remains the most

commonly employed method, radical treatment of perforated duodenal ulcer by

antrectomy plus vagotomy is justified in the hands of experienced surgeons.

There is no doubt that vagotomy plus a drainage procedure carried a lower

mortality than partial gastrectomy alone. Whenever definitive surgery is deemed an

appropriate addition to simple closure of perforation, PGV is the procedure of choice.

Many surgeons do not adopt PGV. Total truncal vagotomy with gastrojejunostomy or

pyloroplasty is still the most popular surgery.

Omental closure is indicated for perforations in poor risk patients and for acute

ulcer associated with drug ingestion or acute stress. H2 blockers,PPI and elective

surgery may be offered to patients who relapse after closure. Only in fit patients with

acute ulcer perforation, when an experienced surgeon is available, PGV is undertaken

as an ideal surgery.

Postoperative management :

The postoperative management plays a vital role in the final outcome of this

abdominal catastrophe. The adoption of a careful postoperative regime has led to a

considerable reduction in mortality and postoperative complications.


73

The important steps in the postoperative management are:

l. Position in bed :

The foot end of the bed is elevated, when returned to bed after surgery. This

position is maintained for 12-24 hours till the patients pulse and BP are stabilised. In

order to avoid the risk of vomitus being aspirated the patient should be placed in

semi-prone position till the conscious is regained. Old people are given propped up

position in order to allow maximum pulmonary ventilation in order to reduce future

pulmonary complication.

2. Sedation :

When the patient comes out of effects of anaesthesia, he may develop pain and

restlessness. Such cases may be effectively treated by intra muscular injection of 10

mg of morphine hydrochloride or 30 mg of pentazocine.

3. Fluid requirement :

Patient requires IV fluids therapy for the first 2 to 3 days. Dextrose, dextrose

saline and RL are administered intravenously. About 2.5 to 3 litres may be required in

the course of 24 hours. However, while calculating the fluid requirement for the day,

one must take into account of the condition of the patient, volume of nasogastric

aspiration, urine output, perspiration, associated respiratory diseases like chronic

bronchitis, pneumonia etc. Additional allowances of fluid are made depending upon

the individual requirement. Over hydration should be avoided.

4. Nasogastric aspiration :

The nasogastric aspiration should be started from the time of surgery and

should be continued at a regular interval of one to two hours. A correct record is kept

about the volume, colour and nature of the aspiration every time. When the bowel

sounds appear after 48-72 hours and the volume of aspiration goes on diminishin, the


74

nasogastric tube can be removed. However, if there is distension of abdomen even

beyond 72 hours and the volume of aspiration each time is increasing, one is justified

to keep the nasogastric tube as long as it is found necessary.

5. Antibiotics :

Initially either penicillin or ampicillin with metronidazole is given

parenterally. If the patient is allergic to penicillin or ampicillin, tetracycline

hydrochloride is substituted. If the peritoneal fluid is sent for c/s, further antibiotics

should be administered depending upon c/s report. Usually antibiotics are given for 5

days from the day of surgery.

6. H 2 antagonists and Proton pump inhibitors:

It is started parenterally immediately after the surgery.

7. Blood transfusion :

If the patient is anaemic or perforation is associated with severe haemorrhage,

blood transfusion may be advised.

8. Bowel action :

After 48-72 hours a small glycerine enema may be given to ensure bowel

movement. Drastic purgatives should be avoided.

9. Diet :

The oral feeds are started after the removal of nasogastric tube, after the

appearance of bowel sounds, if there is no vomiting and abdominal distension. The

diet is gradually increased through the stages of fluids into semisolids and gradually is

switched onto the normal diet. Protein and vitamins should be supplemented to ensure

quick recovery. It is the modern practice to regulate dietary progress by the needs and

reactions of the patient, rather than by arbitrary rules of olden days.


75

10. Exercises and period of bed rest :

During the recent years, the principles of early ambulation have become more

and more widely accepted. The patient is helped into chair by the 2nd or 3rd

postoperative day and after 3rd day he can gradually start walking with support.

Post-operative care after simple closure :

Explanation should be made to the patient that the perforation has been closed

but the underlying ulcer disease has not been treated.

Proton pump inhibitors should be administered intravenously and then orally

in full dosage as soon as the patient is able to take orally. However, the incidence of

perforation and bleeding ulcers were unchanged after the introduction of H2 receptor

antagonists in study from 1974 to 84. Patient should be discharged on full dosage of

PPI and arrangements should be made for a follow up endoscopy at 8 weeks to

ensure that ulcer healing has taken place. It is not sufficient to rely on the absence of

symptoms as an indication that ulcer healing has taken place. Mensberger reported

endoscopic follow up of perforated duodenal ulcer and found that 65% of patients

treated with omental patch and cimetidine therapy continued to have active ulcer

disease 4 to 12 weeks after perforation and 23% had no symptoms despite the

presence of active ulcer disease. Raimes and Devin, advised that patients receiving

maintenance treatment should be followed for atleast 6 months after healing. They

recommend that assessment should include endoscopy and suggested that relapse may

indicate the need for surgery.


76

3. LAPAROSCOPIC PROCEDURES 55,56,57,58,59

:

The scope of laparoscopic closure of perforation is rapidly expanding.

Perforated duodenal ulcer is often repaired by laparoscopic surgery with or without

sutures.

Laparoscopic closure of perforated duodenal ulcers was first described by

Nathansonet al. At the same time, Mouret et al reported the closure of perforated

ulcers using fibrin glue to seal the perforation with the omentum. A sutureless method

for laparoscopic treatment of ulcer is done using Gelatin sponge plug and fibrin

sealant.

The following advantages of Laparoscopic procedures have made it a safer

alternative:

a. Better visualization of the site of perforation as well as the other organs.

b. Better peritoneal toileting.

c. Early bowel recovery.

d. Early ambulation of the patient.

e. Decreased wound related complications in the short and long term.

f. Decreased hospital stay.

Various laparoscopic techniques have been attempted for the treatment of

perforated hollow viscera. These include stapled omental patch, gastroscopy

aided insertion of the ligamentum teres, or omental plug. Yet, these techniques

were either used only in small case series or tend to have high rates of re-

operation.


77

4. COMBINED LAPAROSCOPIC –ENDOSCOPIC METHOD60,61

Sole Endoscopic therapy (eg,mechanical clips) are not currently recommended

for the management of acute perforation in the setting of duodenal ulcer, for which

surgical closure is the usual approach. Closure of acute iatrogenic perforations with

endoscopically placed clips has been described. Because of the decreased tissue

compliance of a perforated peptic ulcer compared with acute iatrogenic perforations,

mechanical clips may be ineffective in the former case. Combined laparoscopic-

endoscopic approaches to closure of perforated duodenal ulcers have been described.

In some series, the role of endoscopy has been limited to the identification of the site

of perforation and the guidance of subsequent laparoscopic intracorporeal suture

repair with an omental patch.

POST OPERATIVE COMPLICATIONS:

Complications are likely to happen in high risk patients. The most common

complications are as follows :

1. Intraperitoneal abcess, usually subphrenic or pelvic.

2. Wound infection,

3. Gastric and duodenal fistulae,

4. Respiratory complications : Atelectasis sometimes preceding

pneumonia is common, a persistent basal effusion may require

treatment and this complication is an indication of sub diaphragmatic

sepsis.

5. Mediastinitis is a rare complication after vagotomy and thorough

peritoneal lavage. Antibiotics coverage should be given to prevent this

complication.


78

Hennessy reporting on 603 cases of perforated gastric and duodenal ulcer

found post-operative pneumonia in 42.9% of cases and intra abdominal abscess in

8.4% and wound infection in 31.9%.

Management of early perforation and leak:

- Priority towards fluid and electrolyte management.

- Nasogastric aspiration.

- H2 blockers.

- Antibiotics.

- Nutrition of the patient, ideally total parental nutrition (TPN) or feeding

jejunostomy

Causes of leak are:

- Old patients.

- Large perforation.

- Inadequate closure.

- Difficult closure with friable margin.

- Late presentation to hospital after perforation.

Leak are usually seen from 2nd to 5th postoperative day presenting as bilious

drain from the drain site.

Fistula may be high or low output. In case of high output fistula, where TPN

facilities are available, patients can be managed conservatively, feeding jejunostomy

can be added for enteral feeds. Trial can be given for 3weeks after which operative

treatment can be adopted.

Where TPN facilities are not available, ideally after resuscitation patient can

be taken up to surgery at an early stage to prevent further deterioration. In low output

fistula, conservative management is usually adopted.


79

Surgical management for fistula:

- Feeding jejunostomy.

- Use of serosal patch (Kobold &Thal) technique: The upper jejunum is used as

loop or Roux-en-y loop to occlude or patch the perforation. Duodenum mucosa

lines the serosa.

- Partial gastrectomy: In large perforation with friable margins where repair cannot

be done, it is ideal to proceed with partial gastrectomy with poly anastamosis.

- Conservative or nonoperative management: By passing Foley‟s catheter into the

drain wound and manipulating it into or near to the perforation can be converted

into a controlled fistula.

H2 Blockers: These drugs act by selectively blocking H2 receptors of parietal cells.

They have a dose dependent antisecretory potency. Their simple dosage schedules and

associated good therapeutic compliance.

Drugs: - Cimetidine: No more used.

- Ranitidine: 150mg Bid, after 4-6wks OD at night.

- Famotidine: 20-40mg OD.

- Roxatindine: 75mg OD.

- Nizatidine: 20mg Bd.

Proton pump inhibitors: These act by inhibiting the H+ / K+ ATP system on the

luminal side of the parietal cells. Action is long lasting and dose dependent. In dose of

20-40mg OD, it achieves almost 100% inhibition of intragastric acidity throughout

day and night.

Dosage: 20-40mg OD for 4-6weeks, followed by 10-20mg OD.


80

Mortality rate associated with perforation:

Although the mortality rate associated with perforated ulcer has declined over

the 50 years, it is still substantial because of the increasing number of elderly ill

patients with this problem.

Mortality rate varies from study to study. Kozoll and Meyer26

reported deaths

in 24% of 1904 patients with perforation at Cook County Hospital, Chicago. Hennesy

reported a mortality of 15.4% for gastric and duodenal ulcer perforation. Boey and

Wong51

reported an overall 4.7% mortality rate for perforated DU in HongKong

County Charity Hospitals with high proportion of elderly patients and of patients from

lower socio-economic group.

Boey and Wong53

defines significant risk factors in DU perforation as , a

major concurrent medical illness,preoperative shock and longstanding perforation

(more than 72 hours). In patients without any of these factors, the mortality rate was

0.4%. When one risk factor was present, the mortality rate was 4.2% raising to 6.7%

with all 3 risk factors present. Recent studies54

show that the mortality rate among the

elderly patients undergoing surgery for perforated PU is as high as 12-47%. In this

study, patients older than 65 years had a higher mortality rate when compared to

younger patients .

The other factors which increases the mortality rate are:

1. Position of the ulcer: Gastric ulcer perforation carry greater mortality than

DU perforation. The higher the ulcer greater is the risk of hemorrhage

2. Associated haemorrhage.

3. Age: Most include extreme age as a risk factor.


81

H-PYLORI INFECTION ERADICATION11,85

:

The key success factor in management of peptic ulcer is treatment of H-Pylori

infection, which has been widely advocated. Current regimens for eradication of H-

Pylori infection are quite diverse, not only in the combination of agents used but also

in dosage and duration of the treatment.

There are various regimens against H-Pylori

1. Dual drug therapy.

2. Triple drug therapy.

3. Quadruple drug therapy.

1. Dual drug therapy:

a. Proton pump inhibitor + clarithromycin/ amoxycillin.

b. Ranitidine + clarithromycin for 14 days. Not recommended due to its sub

optimal results.

2. Triple drug therapy:

a) Omeprazole 40mg OD + Clarithromycin 500mg BID For 7days+Metranidazole

400mg BID.

b) Omeprazole 40mg OD + Amoxycillin 500mg BID For 7days+ Clarithromycin

500mg BID.

c) Omeprazole 40mg OD + Amoxycillin 500mg BID For 7 –10 days+

Metranidazole 400mg BID.

d) Colloidal Bismuth Subcitrate 125mg QID For 14 days +Amoxycillin 500mg

BID + metranidazole 400mg BID.


82

3. Quadruple drug therapy:

Omeprazole 40mg OD + Collidal Bismuth Subcitrate 125mg For 7 days 4OD

+ Tetracycline 500mg TID + Metranidazole 400mg TID.

The Clarithromycin based regimens are much costlier than Amoxycillin based

regimens.

CONSERVATIVE LINE OF TREATMENT 24,62,63,64,65

:

Conservative line of treatment is justified in -

1. A high risk group of patients with perforation, who are likely to die and in whom

surgery is unlikely to be beneficial.

2. As an expectant measure when the diagnosis is uncertain in early acute cases.

3. In cases where perforation is a very small one i.e. a leaking ulcer with

correspondingly slight peritoneal reaction.

4. Sub acute perforation.

Non-operative treatment of these patients with modern methods such as CT

scanning, ultrasonography to monitor progress and in combination with percutaneous

aspiration of fluid collection and abscess deserves evaluation.

Of the many advocates of non-operative treatment Herman Taylor is a forceful

representative. Conservative treatment is based on assumption that clinical and

radiographic diagnostic methods are accurate, that leakage may be controlled by or

diminished by gastric suction, that electrolytes and fluid loss can be corrected and the

peritoneal infection is minimal in the early hours after perforation and can be

controlled by antibiotics. Taylor believes that this method facilitates natural healing

process, whereas suturing of perforation may make an ulcer become chronic and

intractable.


83

Most writers who advocate non-operative treatment emphasize the need for

close observation. Donoval et al advised the use of oral radio opaque contrast studies

to verify that sealing has taken place.

If medical line of treatment is undertaken and operative line is withheld one of

the 3 results may be expected .

a) The abdominal tenderness and rigidity may gradually disappear and the

perforation closes.

b) A localised abscess - perigastric, periduodenal, sub diaphragmatic may form.

c) The patient may die of septic peritonitis.

Details of conservative line of treatment :

1. Sedation : Having decided on non-operative treatment the patient should

receive not more than 16 mg. Morphine or Pentazocine 30 mg

intramuscularly.

2. Charts : As a routine the pulse rate, BP, respiratory rate recorded every hour

or half hourly in graphic form on a special chart. The temperature is recorded

4th hourly. A special antibiotic chart and an input and output charts are also

necessary.

3. Repeated radiograph : Is an essential part of the conservative line of

treatment. If the perforation becomes sealed off, this subdiaphragmatic

shadow slowly diminishes in size. Conversely, if the shadow has increased in

size, after the passage of the stomach tube of a good size, to allow the air in

the stomach and peritoneal cavity to escape, surgery should be performed

without delay.

4. Nasogastric tube aspiration : Nasogastric aspiration is the most important

part of conservative treatment. After the stomach has been emptied through a


84

wide bore tube, it is kept empty by intermittent or continuous nasogastric

aspiration through an indwelling nasogastric tube. Aspiration should be

continued until the flatus is passed and the volume of aspiration is 300ml or

less in 24 hours. No fluids are permitted by mouth for the first 48 hours.

5. Antibiotics : Should be started right from the time of admission and continued

for 5 to 7 days. CP 10 L 6th hourly or ampicillin 500mg 6th hourly with

metronidazole 500mg 8th hourly should be given parenterally. If the patient is

allergic to CP and Ampicillin, tetracycline should be given.It is necessary to

give parenteral vitamin preparations to prevent the staphylococcal enteritis in a

patient being treated by broad spectrum antibiotics.

6. H2 receptor antagonists and PPI: Injection pantaprazole should be started

from the time of admission, usually 40mg BD parenterally.

7. Simple drainage : In those cases where perforation may seal by fibrous

exudate, simple drainage of peritoneal fluid may be done by making an

incision over one or both flanks. This procedure can be carried out under local

anaesthesia. Simple drainage helps for the easy escape of peritoneal fluid and

also gas. By providing this simple drainage, further complications of the

development of residual abscess like subphrenic and pelvic abscesses may be

minimised.

Contraindications to the conservative line of treatment

Conservative line of treatment is contraindicated in

i. In fit for surgery patients

ii. Pyloric stenosis

iii. After a heavy meal

iv. In air swallowers.


85

Advantages of conservative line of treatment :

The period of convalescence and absence of work is shorter after conservative

than following operative line of treatment. However, this seems to be a small

consideration when weighed against the lessened anxiety and ensured results after a

simple closure of perforation.

Disadvantages and Dangers of conservative treatment ;

i. One cannot judge without surgery, whether the peritoneal contamination is or

is not excessive. Even if the stomach is kept empty, peritoneal contamination

can occur from regurgitation from the duodenum and jejunum.

ii. A perforated carcinoma of stomach cannot be diagnosed.

iii. There is a risk of leaving unoperated another condition requiring surgery.

iv. The incidence of lung complications is higher than with operative methods, as

also is the occurrence of intraperitoneal and subdiaphragmatic abscesses.

Prognosis after conservative treatment :

The medical management of peptic ulcer perforation was discussed in a most

comprehensive manner by Chamberlain, Heslpe et al and Herman Taylor . Taylor

67reported a mortality rate of 9.6% which should be contrasted with mortality

following simple closure and immediate partial gastrectomy. Seely and Campbell66

reported a collected series of 139 such cases with a mortality rate of 5%.

Materials & Methods

86

MATERIALS AND METHODS

The study was conducted in CG Hospital and Bapuji Hospital attached to

JJMMC, Davangere, from August 2013 to June 2015. During this period the number

of cases admitted and selected for analyzing the data was 50. These 50 cases were

studied thoroughly according to the proforma. The details of 50 patients were

arranged in the master chart for convenience of presentation.

The diagnosis was made on clinical findings supported by investigations like

plain x-ray abdomen in erect posture. In cases managed surgically, confirmation of

Duodenal Perforation was made on the operation table only.

A detailed history was taken when the condition of the patient is stable. In

critically ill patients, the patients were resuscitated and history was taken after the

patient was stabilized.

The hospital records were also reviewed to obtain appropriate epidemiological

information regarding age, sex, occupation, clinical presentation, duration of

symptoms, past history of chronic duodenal ulcer, investigations and mode of

treatment.

All the patients with suspected duodenal ulcer perforation were examined

thoroughly and base line findings were recorded, repeated examination of the patient

was done during resuscitation and till the diagnosis is confirmed. Tachycardia

associated with fever, tenderness in the epigastrium and abdominal rigidity pointed

towards the diagnosis of peritonitis.

All the patients are examined as per the proforma. Complete physical

examination was done, to rule out associated diseases.

The decision regarding the line of treatment and type of surgery to be

undertaken for each case was arrived after consideration of the following factors:

Materials & Methods

87

o Age of the patient

o General condition of the patient

o Evidence of shock

o Duration of perforation

o Associated medical illness- e.g. cardiac,respiratory

o Amount of peritoneal contamination

For selecting a case for definitive surgery most of the times general condition

of the patient taken up for surgery and also operative findings were taken into

consideration. In those cases, where both these conditions were satisfactory, definitive

surgery was performed, giving weightage to the choice of the surgeon.

Those patients who are young, hemodynamically stable, presenting early to

hospital, with no other co-morbid conditions laproscopic closure of perforation was

done. If there was a difficulty it was converted to open procedure.

Surgery was done to close the perforation in all the cases except where

condition of the patient was very poor (shock at the time of presentation) or when

patient himself refuses surgery. In that group conservative treatment was adopted.

Patients were followed up everyday with continuous bedside monitoring of

vital data in the immediate post operative period. Due attention was paid to note the

development of any complications. Suitable and appropriate treatment was instituted

from time to time according to the needs of the patients.

After satisfactory improvement patients were discharged from the hospital

with advice regarding the diet, rest, drugs to be taken and need for periodic checkup

and need to undergo EGD if symptoms persist.

Patients who came for regular followup were examined in detail.Patients were

advised necessary treatment and need to undergo EGD after 6 months to know the

Materials & Methods

88

presence or absence of ulcer.If present patients are counselled regarding need for

definitive ulcer surgery for the chronic duodenal ulcer.

After studying in detail 50 cases an extensive review of the available literature

was made and results are compared with that of other authors. Detailed analysis was

done and conclusions were drawn.

Observations & Results

89

OBSERVATIONS AND RESULTS

50 CASES OF DUODENAL PERFORATION

The observation is based on the analysis of the data pertaining to 50 cases.

This is summarized as follows:

AGE INCIDENCE:

In the present series of 50 cases of DU perforation the age varied from 16

years to 70 years, with the mean age of 48.24.The peak incidence was in 5th

decade,

i.e 40-49 years, which constituted 32percent of total number of cases. The incidence

of DU perforation is uncommon in adolescence, with only one case reported, who was

16years.

TABLE 1.1: AGE INCIDENCE (MEAN)

Age

N 50

Mean 48.24

Std. Deviation 12.95

Range 54.00

Minimum 16.00

Maximum 70.00


90

TABLE 1.2: AGE INCIDENCE (DISTRIBUTION)

Age Incidence

Age No. of patients Percent

< 20 yrs 1 2.0

20 - 29 2 4.0

30 - 39 9 18.0

40 - 49 16 32.0

50 -59 10 20.0

60 & Above 12 24.0

Total 50 100.0

GRAPH 1: AGE INCIDENCE

Postoperative complications increased with increase in age as per this study

with majority of complications occurring after 40years.This is mainly because of

associated co-morbid conditions of old age.

0.0

5.0

10.0

15.0

20.0

25.0

30.0

35.0

< 20 yrs 20 - 29 30 - 39 40 - 49 50 -59 60 & Above

Pe

rce

nta

ge

Age in years

AGE INCIDENCE


91

TABLE 2: AGE VS POST OPERATIVE COMPLICATIONS

POST OPERATIVE COMPLICATIONS

AGE NO. OF PATIENTS

<20 1

20-29 2

30-39 3

40-49 7

50-59 2

>60 7

GRAPH 2: AGE VS POST OPERATIVE COMPLICATIONS


92

SEX INCIDENCE:

In this present series of 50 cases, DU perforation is found to be more common

in males, with male to female ratio of 9:1. 45 out of 50 patients were males. The

majority of authors have reported that incidence is high in males when compared to

females. The high incidence in male can be explained on the basis of greater stress,

habits like alcohol and smoking in males.3

TABLE 3: SEX INCIDENCE

Sex No. of patients Percent

Male 45 90.0

Female 5 10.0

Total 50 100.0

GRAPH 3: SEX INCIDENCE

90

10


93

SEASONAL INCIDENCE:

In the present series, maximum incidence of DU perforation was seen during

January to March. i.e.36% of cases followed by October to December i.e 34% of

cases. It was lowest during July to September.

TABLE 4: SEASONAL INCIDENCE

Seasons No. of patients Percent

Jan - march 18 36.0

April-June 12 24.0

July-Sept 3 6.0

Oct-Dec 17 34.0

Total 50 100

GRAPH 4: SEASONAL INCIDENCE

0

5

10

15

20

25

30

35

40


94

OCCUPATIONAL INCIDENCE:

In this study it was found that majority of the cases were manual labourers.

Highest incidence was seen in coolies (40%) followed by farmers (16%), who

constituted the bulk of cases in this study.

TABLE 5: OCCUPATIONAL INCIDENCE

Occupation No. of patients Percent

Business 3 6.0

Coolie 20 40.0

Farmer 16 32.0

House wife 4 8.0

Self Employed 3 6.0

Student 1 2.0

Unemployed 3 6.0

Total 50 100.0

GRAPH 5: OCCUPATIONAL INCIDENCE

6.0

40

.0

32

.0

8.0

6.0

2.0

6.0

Occupational Incidence

Business

Coolie

Farmer

House wife

Self Employed

Student

Unemployed


95

CLINICAL SYMPTOMS:

In all the 50 cases studied, pain was the chief presenting symptom. The pain

was moderate to severe in intensity, usually started in epigastrium and right

hypochondrium, then with time most of the patients had diffuse tenderness.

Distension was present in all the cases except one female patient who

presented early, with just pain abdomen and vomiting.

Vomiting was seen in 90% of the patients and was projectile, bilious and

contained undigested food particles. None of them had hematemesis

None of the patients included in the study gave history of recent trauma to

abdomen.

TABLE 6: CLINICAL SYMPTOMS

Clinical Symptoms No. of patients Percent

PAIN

Present 50 100.0

Absent 0 0

DISTENSION

Present 49 98.0

Absent 1 2.0

VOMITING

Present 45 90.0

Absent 5 10.0

HISTORY OF TRAUMA

Present 0 0

Absent 50 100.0


96

GRAPH 6: CLINICAL SYMPTOMS

0

5

10

15

20

25

30

35

40

45

50

PAIN DISTENSION VOMITING HISTORY OFTRAUMA

No

. of

pat

ien

ts

Symptoms


97

DURATION OF SYMPTOMS BEFORE PRESENTATION:

In this study most of the patient presented late to hospital.The mean time

duration of presentation being 35.4hrs. Majority of the cases presented after 12hrs and

before 24hrs of the onset of symptoms(42%). Most of the patients were treated

initially in periphery before being referred here. The maximum duration was 96hours.

TABLE 7.1: DURATION OF SYMPTOMS BEFORE PRESENTATION

(MEAN)

DURATION (HRS)

N 50

Mean 35.40


Range 90.00

Minimum 6.00

Maximum 96.00

TABLE 7.2: DURATION OF SYMPTOMS BEFORE PRESENTATION

(DISTRIBUTION)

DURATION (HRS) No. of patients Percent

< 12 hrs 8 16.0

13 - 24hrs 21 42.0

25 - 48hrs 13 26.0

49 - 72hrs 6 12.0

>72 hrs 2 4.0

Total 50 100.0


98

It was found in this study that duration with which patient presents to hospital

has got relevance with post operative morbidity and mortality. It was found that only

12.5% of patients had post operative complications, when patient presented within 12

hours of onset of symptoms, as compared to 61.5% and 62.5% of patients having

complications when patient presented 25-48 hrs and more than 48hrs respectively.

The two deaths seen in this study, one managed conservatively presented

48hrs after the onset and another presented 72 hours after the onset, both died of

septicemia.


99

TABLE 8: DURATION OF SYMPTOMS VERSUS POST OPERATIVE

COMPLICATIONS

Duration of

symptoms(hours)

(N=49)

No. of

cases

Post operative complications

No

Complication

Complications Death

< 12 hrs 8 7(87.5) 1(12.5) 0

13 – 24hrs 21 15(71.4) 6(28.6) 0

25 – 48hrs 13 4(30.8) 8(61.5) 1(7.8)

> 48 hrs 8 2(25) 5(62.5) 1(12.5)

Total 50 28(56) 20(40) 2(4)

One more indicator of morbidity i.e. mean duration of stay in hospital also

showed that patients who presented before 12 hours of onset had lesser stay in

hospital (9.13 days) as compared to those who presented after 48hrs(12 days).

TABLE 9: DURATION OF SYMPTOMS VERSUS MEAN DURATION OF

STAY IN HOSPITAL

Mean duration of stay in hospital

Duration of onset of

symptoms (hours) (N=49)

No. of

patients Mean

Std.

Deviation

1 < 12 hrs 8 9.13 2.03

2 13 - 24hrs 21 9.43 1.83

2 25 - 48hrs 12 12.75 3.05

3 > 48 hrs 8 12.00 6.65

1 Vs 3, t=2.94, P<0.009


100

HABITS:

In this series it was found that smoking and alcohol has significant risk in DU

perforation. 40% of patients had significant history of consumption of alcohol and

smoking, 20% had alcohol history alone and 10 percent were smokers.

TABLE 10: HABITS

Habits No. of patients Percent

Only smoking 5 10.0

Only Alcohol 10 20.0

Smoking & Alcohol 20 40.0

No Habits 15 30.0

Total 50 100.0

GRAPH 7: HABITS


101

PAST HISTORY

In this series a significant relation to patients past history was noted. 58% of

the cases in this study had significant past history of dyspepsia and few were

diagnosed with peptic ulcer /duodenitis/ duodenal erosions on upper GI endoscopy.

34% of the patients had history of regular NSAID intake for chronic

osteoarthritis, low back ache and other conditions.

TABLE 11: PAST HISTORY OF PEPTIC ULCER AND NSAID ABUSE

No. of

patients

Percent

Past h/o dys /peptic ulcer

Present 29 58.0

Absent 21 42.0

NSAID abuse

Present 17 34.0

Absent 33 66.0

GRAPH 8: PAST HISTORY OF DYSPEPSIA/PEPTIC ULCER

29

21

Past H/O Dys/Peptic Ulcer

Present

Absent


102

GRAPH 9: PAST HISTORY OF NSAID ABUSE

GENERAL PHYSICAL EXAMINATION

On general physical examination 92% of the cases had normal temperature. 4

cases had raised temperature out of which two patients were in septicemia when they

presented. The fever can be attributed to septicemia in those cases.

90% of the cases were in moderate to severe dehydration when they presented

to our centre.

TABLE 12: FEVER AND DEHYDRATION

General Physical Examination No. of patients Percent

Fever

Present 4 8.0

Absent 46 92.0

Dehydration

Present 45 90.0

Absent 5 10.0

17

33

NSAID ABUSE

Present

Absent


103

BLOOD PRESSURE AND PULSE RATE:

In this study of 50 cases, the mean systolic blood pressure was 112mmHg and

mean diastolic blood pressure was 71.8mmHg. Out of 50 patients only 6 patients had

SBP <90mmHg (12%) and 12 patients had DBP <60mmHg ( 24%). Most of the

patients who were hypotensive were resuscitated with fluids. One patient did not

come out of shock , hence managed conservatively.

Most of the patients in this study were tachycardic at the time presentation.

The mean pulse rate being 102.24 bpm. 12% of the cases had pulse rate more than

120 and 38% of the cases had pulse rate 100 to 120bpm.

TABLE 13.1: BLOOD PRESSURE AND PULSE RATE(MEAN)

General Physical

Examination

N Mean

Std

Deviation

Range Minimum Maximum

SBP 50.0 112.0 16.0 72.0 80.0 152

DBP 50.0 71.8 11.6 40.0 50.0 90

PR (bpm) 50 102.24 12.05 52 76 128

TABLE 13.2: BLOOD PRESSURE AND PULSE RATE (DISTRIBUTION)

Parameters No. of patients Percent

PR

< 100 25 50.0

100 - 120 19 38.0

> 120 6 12.0

SBP

< 90 6 12.0

> 90 44 88.0

DBP

< 60 12 24.0

> 60 38 76.0


104

GRAPH 10: PULSE RATE

GRAPH 11: BLOOD PRESSURE

50.0

38.0

12.0

PR

< 100

100 - 120

> 120

0.0

10.0

20.0

30.0

40.0

50.0

60.0

70.0

80.0

90.0

Pe

rce

nta

ge o

f ca

ses


105

EXAMINATION OF ABDOMEN:

All 50 patients in this study had tenderness, guarding/rigidity, obliteration of

liver dullness and free fluid. The tenderness was diffuse in most of the cases with

guarding and rigidity predominantly in the upper abdomen.

TABLE 14: SIGNS ON PER ABDOMEN EXAMINATION

SIGNS NO. OF PATIENTS PERCENT

TENDERNESS 50 100%

GAURDING/RIGIDITY 50 100%

OB. OF LIVER DULLNESS 50 100%

FREE FLUID 50 100%

TOTAL COUNT

In this study the mean total count was 11805 which is on upper limit of

normal. 50% of the patients had leukocytosis (>11000 cells/ µL). Two patients had

leucopenia.

TABLE 15.1: TOTAL LEUCOCYTE COUNT (MEAN)

TC

N 50

Mean 11805.00


Range 29530.00

Minimum 3360.00

Maximum 32890.00


106

TABLE 15.2 : TOTAL LEUCOCYTE COUNT(DISTRIBUTION)

TC( cells/µL) No. of patients Percent

< 4000 2 4.0

4000 - 11000 23 46.0

>11000 25 50.0

Total 50 100.0

GRAPH 12: TOTAL LEUCOCYTE COUNT

4.0

46.0 50.0

0.0

10.0

20.0

30.0

40.0

50.0

60.0


107

INVESTIGATIONS:

All 50 patients in this study had erect x ray showing air under diaphragm.

Three patients in whom typhoid ileal perforation was suspected preoperatively, widal

test was done. All three were negative. Rest of the cases this test was not done.

TABLE 16: ERECT X RAY ABDOMEN AND WIDAL TEST

INVESTIGATIONS NO. OF PATIENTS PERCENT

ERECT XRAY ABDOMEN

FOR AUD

Present 50 100.0

Absent 0 0

WIDAL TEST

Not Done 47 94.0

Negative 3 6.0

SITE OF PERFORATION:

In 84% of the patients the perforation was found on the first part of duodenum.

In only 7 cases perforation was in second part. All the perforations were anteriorly

placed. In one patient exact site on duodenum could not be assessed as patient was

managed conservatively. Ultrasonography and clinical features suggested that the

perforation was duodenal in that one case.

TABLE 17: SITE OF PERFORATION

SITE

NO. OF

PATIENTS PERCENT

FIRST PART OF DUODENUM 42 86.0

SECOND PART OF DUODENUM 7 14.0


108

GRAPH 13: SITE OF PERFORATION

SIZE OF PERFORATION:

In the present series, the size of the perforation varied from 0.3 to 1.5 cm.

42% of the cases had perforation less than 1cm and 57% of cases more than 1 cm. The

mean size being 0.9cms. One case which was managed conservatively the size of

perforation couldnot be assessed.

TABLE 18.1 : SIZE OF PERFORATION(DISTRIBUTION)

Size of perforation ( cms) No. of patients Percent

Less than 1 21 42.9

More than 1 28 57.1

Total 49 100.0

86%

14%

SITE OF PERFORATION

FIRST PART OF DUODENUM SECOND PART OF DUODENUM


109

TABLE 18.2 : SIZE OF PERFORATION(MEAN)

Variables Mean

Standard

Deviation


Size of perforation

( cms)

0.9 0.4 1.3 0.3 1.5

The size of perforation is compared with the mean duration of stay in hospital

in an attempt to establish morbidity w.r.t size of perforation. However the results of

this analysis were found to be statistically insignificant. So no relation was found

between size of perforation and morbidity in this study.

TABLE 19: SIZE OF PERFORATION vs MEAN DURATION OF STAY IN

HOSPITAL

Mean Duration of stay in Hospital

Unpaired t

test

Size of perforation

(cms)

N Mean

Std.

Deviation

Less than 1 21 10.24 3.71 t= -0.62,

P<0.53, NS More than 1 28 10.89 3.57

TREATMENT:

Open Grahams omental patch closure was done in majority of the cases

(85.9%).Modifications are done in few cases whenever required. Closure was done

with atraumatic 2-0 Vicryl along the long axis of duodenum.

A novel method of omental patch closure with two tube drainage was tried in

one case, as patient presented late and peritoneal soiling was more. This was done in

view to avoid leak in postoperative period.


110

Laparoscopic omental patch closure was done in two cases using intra

corporeal suturing. It was done in young patients, who presented early and who were

hemodynamically stable.

The choice of definitive surgery was done depending on the age of the patient,

duration of perforation, size of perforation, associated medical illness and amount of

peritoneal contamination. One patient was subjected to B/L truncal Vagotomy with

Pyloroplasty and another patient was operated with Pyloroduodenotomy with

Pyloroplasty. Both the patients had a big 1.5 cm perforation on the anterior wall.

All cases were subjected to peritoneal lavage with warm normal saline. Chest

tube was placed in right paracolic gutter and subhepatic space. When there is gross

pelvic contamination and collection, an additional pelvic drain was placed.

Abdomen was closed in layers. Port sites were closed in laparoscopic

approach.

In the present series, only one patient was managed conservatively. Patient

presented after 48hrs and was in septic shock. Patient had associated pneumonitis and

diabetes mellitus. Patient did not recover from the shock even after aggressive

resuscitation. So decision was made to manage the patient conservatively which

consisted of nil by mouth, ryles tube aspiration, broad spectrum antibiotics, IV fluid

resuscitation, parenteral analgesics. Under local anesthesia, under ultrasound

guidance, bilateral flank drains were placed. Patient eventually died because of sepsis.


111

TABLE 20: TYPE OF TREATMENT

Procedure No. of patients Percent

Open Grahams omental patch closure 43 85.9

Laparoscopic omental patch closure 2 4.0

Bilateral truncal Vagotomy with Pyloroplasty

with omental patch

2 4.0

Omental patch closure with two tube drainage 1 2.0

Pyloroduodenotomy with pyloroplasty 1 2.0

Conservative management with bilateral flank

drain

1 2.1

Total 50 100.0

Post operative treatment consisted of nil by mouth, NG aspiration, IV fluids,

intermittent oxygen and nebulization if chest is bad, IV antibiotics, continuous

monitoring. Metronidazole with third generation cephalosporin was used in most of

the cases. Higher antibiotics were started if patient had increased counts, fever and

other respiratory conditions. Antibiotics were added as per culture and sensitivity

reports of the peritoneal fluid sample taken intraoperatively and sputum sample taken

post operatively.

By 3rd

or 4th

day once the aspiration quantity decreases and bowel sounds

return to normal, patient was started orally. In laparoscopic closure patient was started

orally within 2 days in both the cases. Drain was removed on 5th

post operative day in

most of the cases. Sutures were removed on 8th

or 9th

day if there is no infection.


112

DURATION OF STAY IN HOSPITAL:

In this study, the duration of stay in hospital was studied extensively in view

to establish relation between various parameters of the disease and the treatment

adopted. Duration of stay in cases of open omental patch closure was more when

compared to laparoscopic technique. Overall mean duration of stay in hospital was

10.6 days. Maximum was 23 days as patient had wound gaping which was sutured

secondarily. 50% of the open cases stayed for 10-15days. Two cases which were

operated laparoscopically stayed for 6 days. So laparoscopic closure has got lesser

postoperative morbidity.

TABLE 21.1: DURATION OF STAY IN HOSPITAL (MEAN)

Variables Mean

Std

Deviation


Duration of stay in hospital 10.6 3.6 17.0 6.0 23

TABLE 21.2: DURATION OF STAY IN HOSPITAL (DISTRIBUTION)

Duration of stay in hospital

Duration (In days) No. of patients Percent

< 10 22 44.9

10 - 15 23 46.9

> 15 4 8.2


113

TABLE 22: TYPE OF SURGERY vs DURATION OF STAY IN HOSPITAL

Procedure

Duration of stay in

hospital (In days)

Total < 10 10 - 15 > 15

Open omental patch closure 19 22 3 44

Laparoscopic omental patch closure 2 0 0 2

Definitive surgery 1 1 1 3

Total 22 23 4 49

COMPLICATIONS:

In this study 44% of patients had post operative complications. 28 cases had

uneventful post operative period, which included 2 laparoscopic closures and rest by

open technique.

Respiratory complications took the major share of complications (20%)

followed by wound infection (18%). Pneumonia was managed by chest x ray, sputum

analysis, suitable antibiotics, chest physiotherapy, nebulization, expectorants. Wound

infection was managed by regular dressing, pus for culture and sensitivity. Wound

gaping occurred in one case. Two cases who had septicemia died, out of which one

was managed conservatively. Biliary leak was not seen in any of the cases in this

study. Out of 49 operated cases one patient died and one patient who was managed

conservatively died.


114

TABLE 23: POST OPERATIVE COMPLICATIONS

Post-operative complications No. of patients Percent

No complications 28 56.0

Complications 22 44.0

COMPLICATIONS No. of patients

Basal pneumonia 11

Wound infection 9

Renal failure 1

Acute respiratory distress syndrome 1

Septicemia 2

Wound gaping 1

Death 2

GRAPH 14: POST OPERATIVE COMPLICATIONS


115

ADVICE ON DISCHARGE AND FOLLOW UP

Out of 50 patients studied in our series, 2 patients died. All 48 patients were

advised anti-H-pylori treatment with omeprazole, amoxycillin and metronidazole for

one week, followed by omeprazole 20mg OD for 3 months and follow up every

month. In the follow up of 3 months period only 16 patients out of 38 patients who

came for follow-up complained of pain abdomen, suggestive of peptic ulcer disease.

They were advised endoscopy and definitive surgery and put on medical line of

treatment. Out of 16, only 2 turned up for definitive surgery, inspite of proper advice

and postal communication.

TABLE 24 : FOLLOW UP

Follow-up No. of patients

Lost for follow up 10

Dyspepsia 16

Definitive Surgery in follow up 2

No symptoms 22

Discussion

116

DISCUSSION

Hollow viscus perforation is one of the commonest surgical emergencies.

Peptic ulcer perforation constitutes majority of these cases, out of which duodenal

ulcer perforation is the most common perforation seen in CG Hospital and Bapuji

Hospital attached to JJMMC, Davangere. Although incidence of surgery for peptic

ulcer diseases has reduced drastically with advent of proton pump inhibitors and H2

receptor antagonist, but incidence of surgery for perforation has not changed.

Age incidence:

Duodenal perforation is common in fifth and sixth decade with an

approximate incidence of 7 to 10 cases per 100,000 person-years70

. Previously peptic

ulcer was more common in 4th

decade and perforations were common in 4th

and 5th

decade. Previously, most patients were middle aged, with time, there has been a

steady increase in the age of the patients suffering this complication. DU perforation

is rare in young age.

Table 25:Peak age incidence by various authors

Authors Peak age in years

Turner71

( 1951 ) 30 – 40

James et al73

( 1961 ) 30 – 50

Jamieson72

( 1964 ) 20 – 35

Mishra et al74

(1982) 35 – 55

Weinganker 20 – 40

Present series 40– 50

Discussion

117

Table 26: Mean age incidence by various authors

Authors Mean age in years

Kuremu 20

(2002) 47

Dakubo et al 21

(2009) 40.9

Bin-Taleb et al 23

(2008) 39.08

Sarath et al24

(2009) 44.5

Nuhu et al 22

(2008) 45.5

Present series 48.24

In the present study the peak incidence is in 5th

decade, which is close to study

conducted by James et al. The mean age was 48.24. It can be seen from these tables

that there is a steady increase in age of peak incidence with time. Earlier studies had

peak incidence in 30-40 years, when compared to recent studies showing peak

incidence in 40-60 years age group. The youngest patient in our study was 16 years.

Sex incidence:

In our series 90% were males and 10% were females, and the male-female

ratio being 9:1. Perforation is more common in males than females, because males

were subjected to more stress and strain of life and predisposed to risky behaviour.

Sex hormone offer some security against perforation in females as claimed by

Debakay15

(1940).

Discussion

118

Table 27: Sex incidence by various authors.

Authors Male : female ratio

Jordan P H et al 75

( 1976 ) 8.1 : 1

S. R. Vyarahase et al (1977 ) 19 : 1

R.B. Satwakar et al ( 1978 ) 9 : 1

J. Boey et al 16

( 1982 ) 6.6 : 1

Primose N. John 13

(Bailey Love) 2 : 1

Ersumo et al 76

(2005) 7.2:1

Zangana et al 34

(2004) 8.5:1

Aman et al 77

(2008) 9:1

Present series 9 : 1

Seasonal incidence:

Many writers have depicted that there is an increase in ulcer symptoms and in

ulcer perforation in the winter. Jamieson72

states that incidence was uniform

throughout the spring and summer but dropped in the autumn, only to rise again to a

peak in winter. DeBakey15

while reviewing 192 cases of acute gastroduodenal

perforations has made a mention that the highest incidence of perforations took place

during the month of December and January.

In India also greater number of perforations occur in November, December

and January months (Shanmukarao). This may be due to the work of the cultivators

being more during the winter season.

In our study also similar results were obtained with 36% of cases occurring

from January to March, followed by 34% of cases from October to December.

Discussion

119

Occupational incidence:

It is believed that perforation of peptic ulcer occurs in those people who are

engaged in heavy manual labour. Weir78

(1960) in relatively 1390 cases in Scotland,

found highest incidence in fishermen, farm labourers and heavy manual workers. Less

than half the number had professional sedentary occupation.

In our series, it is noticed that perforations occurred in the patients belonging

to poor socioeconomic status and more so in the rural population, who are manual

workers (unskilled workers). 40% of patients were coolies who did unskilled heavy

manual work and 16% were farmers. It was very rare in people who had white collar

jobs and who were educated. This is probably because of early treatment for peptic

ulcers, lesser stress, lesser habits, hence less complications.

Habits:

Svanes. C and Fevang BT et al32

showed that chronic smoking increased the

risk of ulcer perforation to 10-fold in the age group of 15-74 years, and there was

highly significant dose-response relationship. The results were similar in men and

women and for gastric and duodenal ulcer perforation. They concluded that smoking

is a casual factor for ulcer perforation and accounts for a major part of ulcer

perforations in the population aged > 75 years.

Murty et al54

studied the risk factors for death in gastroduodenal

perforations.13 of the deceased were alcohol consumers, which was 21.31%. 7

deceased were smokers, which was 11.48%.

In our study 40% of patients had significant history of consumption of alcohol

and smoking, 20% had alcohol history alone and 10 percent were just smokers. One

patient who died had both smoking and alcohol history.

Discussion

120

Duration of symptoms before presentation to hospital:

Walgenbach S and Bernhard G (1992)79

analyzed that when time interval

between onset of acute symptoms and surgery was less than or equal to 24 hours

mortality rate is 12% and if more than 24 hours the mortality rate is 21%. The

mortality risk for a patient who is operated on more than 24 hours after the onset of

acute symptoms is 4.9 times to that of a patient operated within 24 hours.

So the interval between the time of perforation and surgery has a very strong

significance in deciding the mode of treatment i.e. type of surgery to be planned and

outcome of the disease79

.

Only 8% of patients reached the hospital within 12 hours after the onset of

symptoms. Most of our patients are from rural area, probably be the reason for the

delay. Most of the patients were treated initially in periphery before being referred

here. However majority of the patients made it to hospital within 24 hours probably

because of free ambulance facility round the clock.

Table 28: Duration of symptoms before presentation to hospital by other authors

Duration (in hours)

De Bakey Series15

(1940)

Bharati C Ramesh

et al49

(1996)

0 – 6 50.83% 12.00%

6- 12 13.02% 12%

12 – 24 4.73% 24%

>24 13.60% 64.00%

Discussion

121

Present Series

DURATION (HRS)

Per cent

< 12 hrs 16.0

13 - 24hrs 42.0

25 - 48hrs 26.0

49 - 72hrs 12.0

>72 hrs 4.0

Tsugawa K et al64

reviewed three risk factors: pre-operative shock, delay for

surgery over 24 hours and medical illness, and showed progressive rise in the

mortality rate with the increasing number of risk factors. Boey et al16

revealed

concurrent medical illness, pre-operative shock and delayed operation (>48 hours) as

significant risk factors that increase mortality in patients with perforated duodenal

ulcers .In the present study we reported that age, size of perforation, duration of

perforation, type of surgery are the risk factors for the outcome of perforated duodenal

ulcer.

The mortality and morbidity are increased whenever, perforations exceed 12

hours because of the peritoneal infection80

. In the presence of gross contamination,

late exploration (after 48 hours) carried a high mortality i.e. 50% (Boey John et al,

1982)16

. The importance of the peritoneal soilage and duration of perforation is

mentioned as a risk in the outcome of the perforation of duodenal ulcer (Donaldson ,

1970)46

.

It was found in this study that duration with which patient presents to hospital

has got relevance with postoperative morbidity and mortality. It was found that only

12.5% of patients had postoperative complications, when patient presented within 12

Discussion

122

hours of onset of symptoms, as compared to 61.5% and 62.5% of patients having

complications when patient presented 25-48 hrs and more than 48hrs respectively.

The two deaths seen in this study, one managed conservatively, presented

48hrs after the onset and another presented 72 hours after the onset, both died of

septicemia.

Patients who presented before 12 hours of onset had lesser mean post

operative stay in hospital (9.13 days) as compared to those who presented after 48hrs

(12 days).

Surgical management:

- Lawal OO et al81

(1998) advised the treatment of perforations in the majority of

patients was by simple closure or truncal vagotomy and pyloroplasty.

- Marauez R et al 82

revealed that simple closure remains the selected treatment in

the majority of patients who present with a perforated peptic ulcer (2000).

- Fombellids Deus et al 83

(1998) review of literature has revealed that the absence

of risk factors must lead to accomplish a definitive treatment through the resection

or the suture of the perforation followed by any type of vagotomy and eventually a

drainage operation.

- Tsugawa K64

reported that a simple closure and vagotomy is recommended for

perforated duodenal ulcers because of its low mortality and minimal stress, except

for cases with a giant perforation measuring over 20mm in diameter at the

perforation hole (2001).

- Bharati C Ramesh et al49

(1996) quotes that in perforated duodenal ulcer patients,

the definitive procedure (Truncal vagotomy with pyloroplasty) can be done as

safely as simple closure.

Discussion

123

- In the present study, we have done simple closure with omental patch in 44

patients, laparoscopic closure of perforation in 2 cases, definitive surgery in 3

patients and conservative management in 1 patient.

Mortality was nil in the group of the patients who underwent definitive

surgery and laparoscopic closure because it was done on selected patients who are

young and hemodynamically stable with minimal peritoneal contamination. Only one

case of open omental patch died out of 44 cases. Patient who was managed

conservatively died. The high mortality in conservative treatment was due to late

presentation, patients were toxic and hemodynamically unstable and were not fit for

surgery.

Table 29: Mortality with simple closure and definitive surgery by other authors

Authors

Mortality with simple

closure and omental

patch

Mortality with

definitive surgery

DeBakey Series15

(1940) 26.00% 13.40%

Sawyers et al series42

(1975) 6.70% 2.80%

Bharati C Ramesh et al49

(1996) 7.00% 4.00%

Present study (2015) 2.00% 0%

Laparascopic closure done in selected patients has got excellent results and

reduced post operative stay. Palanivelu et al57

reported that the mean post operative

stay of 5.8 days and no mortality and very low morbidity in the study. In the present

study the mean post operative stay was 6 days.

Discussion

124

Table 30: Mean Post Operative stay in laparoscopic closure by various authors

Authors

Mean post operative stay in laparoscopic

closure of DU perforation

Palanivelu et al 57

(2007) 5.8 days

Abdelaziem et al55

(2015) 4.5 days

Wadaani et al56

(2013) 75 ± 12.6 hours

Present study 6 days

Post operative Complications:

Basal pneumonitis and wound site infections are the major post operative

complications in various studies. Phillipo et al 84

in their study found that surgical site

infection (48.0%) was the most common post-operative complication. Smitha et al

found that respiratory complications and wound infection are the most common

complications in their study.

In our study respiratory complications were the most common complications

post operatively, followed by wound site infection. Patients operated with

laparoscopic closure did not have any complication. Only one patient who was

operated succumbed to death in our study.

Conclusion

125

CONCLUSION

A series of 50 cases of duodenal ulcer perforation were studied and analysed.

The cases were followed up for a variable period of 6 months to 2 years. The

following conclusions were made:

− Duodenal ulcer perforation is one of the most common abdominal emergencies.

− The perforation was common between age group of 40-50 years.

− Perforation was more common in males. Male to Female ratio was 9:1.

− Most of the patients were from rural area belonging to poor socioeconomic

status and were unskilled workers.

− Smoking and alcohol are precipitating factors for perforation and are factors

which increases morbidity in post operative period.

− Mortality rate in our study series was 4%.

− The duration of perforation more than 48 hours has increased morbidity and

mortality.

− Early diagnosis and prompt management of shock and septicemia is important

for better prognosis of patients.

− Total counts, blood pressure, respiratory rate and pulse rate help in assessing

the general condition of patient, need for aggressive resuscitation and proper

antibiotics.

− Definitive surgery can be done in fit patients, to avoid future second major

surgery.

− Laparoscopic closure is the procedure of choice in young patients who are

hemodynamically stable and has lesser post operative morbidity and mortality.

− Conservative management has highly unacceptable mortality and morbidity.

Conclusion

126

− Respiratory complications and wound site infection are the most common

complications following surgery.

− H-pylori eradication treatment is mandatory after simple closure of the

perforation to prevent recurrence of ulcer.

− Patients should be followed up and should be subjected to upper GI endoscopy

if patient is symptomatic.

− Definitive ulcer surgery is done if endoscopy shows duodenal ulcer.

− Even with the advent of newer modalities like laparoscopic, combined

laparoscopic-endoscopic technique, open surgery with omental patch closure is

the commonest procedure done. With good surgical expertise and good general

condition of patient, definitive ulcer surgery and laparoscopic closure can be

done with very less morbidity and mortality.

Summary

127

SUMMARY

In this series 50 cases of duodenal ulcer perforation were studied during the

period from August 2013 to June 2015, admitted in all units of General Surgery at

C.G Hospital and Bapuji Hospital, Davangere.

- DU perforation is one of the common life threatening acute abdominal emergency.

- The peak incidence was between 40-50 years and rare in adolescence. Youngest in

this study being 16years.

- Duodenal ulcer perforation was common in males than females (9:1). 90% were

males and 10% were females.

- Majority of patients were belonging to rural area with poor socioeconomic status

and were unskilled workers.

- The maximum incidence was in the months of November, December, January and

February.

- Majority (58%) of patients had significant past history of dyspepsia or peptic ulcer

disease.

- Many patients had significant( 34%) history of NSAID abuse

- Smoking and alcohol consumption were risk factors in most cases. It also

contributed to increased morbidity in post operative period.

- Sudden onset of abdominal pain, situated at epigastrium and right hypochondrium

was constant symptom and was present in all the patients in this study.

- Most of patients (42%) presented 12 to 24 hours after the onset of symptoms.

Only 8 patients presented within 12 hours.

- Vomiting and nausea was seen in majority of the cases(90%).

- General condition of majority of patients was satisfactory at the time of

admission. Most of them were normotensive at admission (88%)

Summary

128

- Generalised guarding and rigidity, obliteration of liver dullness, tenderness are

the important signs and were present in all the cases.

- Absence of bowel sounds is one of the early sign of perforative peritonitis.

- Absence of previous history of peptic ulcer showed not be considered as an

important criteria to rule out the possibility of peptic ulcer perforation, as sizeable

number of patients do not give positive history of chronic peptic ulcer.

- Presence of gas under the diaphragm confirms the diagnosis, but their absence

does not exclude the diagnosis. Most of the patients had air under right dome of

diaphragm and only 2 patients had air under both domes.

- The amount of air under the diaphragm was directly proportional to the size of

perforation and duration of perforation.

- Majority of the perforation was found in first part of duodenum(86%).

- The mean size of perforation was 0.9 cms.

- Resuscitation and preoperative management of the patient is as important as the

surgical procedure. The surgical management of peptic ulcer perforation was

mainly done by simple closure of perforation with omental patch(85.9%). In

patients without any contraindications for definitive surgery without any risk

factor were treated with vagotomy with gastrojejunostomy or pyloroplasty and

simple closure(6%).

- Laparoscopic closure has shown promising results w.r.t postoperative morbidity

and mortality. Mean duration of stay in hospital was 6 days.

- Patient selection is very important for definitive ulcer surgery and laparoscopic

closure of perforation.

Summary

129

- Two tube drainage was done in a case of a very big perforation with more

peritoneal soiling, to prevent leak from the site of closure and to increase the

healing.

- Only one patient was managed conservatively with bilateral flank drain as patient

did not come out of septic shock and was not fit for surgery. The patient died due

to septicemia and MODS.

- Only one patient who was brought to hospital in sepsis, died after surgery.

- In this study postoperative complications occurred in 44% of cases, most common

being respiratory complications and wound infection. Life threatening

complications like subdiaphragmatic abcess, mediastinitis, biliary leak are not

seen.

- Risk factors for surgery of perforated peptic ulcer was old age, duration of

perforation, size of perforation and presence of preoperative shock. However size

of perforation did not show statistically significant risk for morbidity in this study.

- Most of the patients responded well to broad spectrum antibiotics like

cephalosporin, metronidazole and amikacin.

- Very few patients were started with higher antibiotics in view of impending sepsis

and increased peritoneal soiling. Antibiotics were changed as per culture

sensitivity reports from the peritoneal fluid.

- Morbidity and mortality are negligible with definitive treatment. The patient in

which perforation was closed by simple closure with omental patch, anti H-pylori

treatment can be given for 7 days followed by PPI for 3 months. Recurrence of

symptoms occurs in significant number of patients (16 patients). Hence it must be

treated either by medical line of treatment or a definitive surgery. Upper GI

endoscopy must be advised in such patients with recurrence of symptoms. In this

Summary

130

study out of 16 who were advised EGD, only 2 patients turned up for definitive

surgery.

- Patients who underwent definitive surgery during follow up had no morbidity and

mortality.

- Surgery is the gold standard treatment for duodenal ulcer perforation as exact

pathology can be found and definitive surgery can be done.

- Drainage procedures like two tube technique/three tube technique are helpful in

large perforations. However large trials has to be done to validate the use of these

procedures.

- Conservative surgery should be considered only in patients who are not fit for

surgery.

- Laparoscopic closure if done by an experienced surgeon in selected patients has

got least morbidity and mortality.

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131

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Photographs

139

PHOTOGRAPHS

FIGURE 7 : ERECT XRAY

ABDOMEN SHOWING GAS UNDER

RIGHT DOME OF DIAPHRAGM

FIGURE 8: ERECT XRAY

ABDOMEN SHOWING GAS UNDER

LEFT DOME OF DIAPHRAGM

FIGURE 9 : ERECT XRAY ABDOMEN SHOWING GAS UNDER BOTH

DOMES OF DIAPHRAGM

Photographs

140

FIGURE 10 : ANTERIOR

PERFORATION IN FIRST PART OF

DUODENUM

FIGURE 11: OPEN CLOSURE

TECHNIQUE OF DU PERFORATION

FIGURE: 12 LAPAROSCOPIC CLOSURE OF DU PERFORATION (INTRA

CORPOREAL SUTURING)

Annexures

141

ANNEXURE I

PROFORMA

CASE NO:

Name: IP NO:

Age: UNIT:

Sex: WARD:

Religion:

Address:

Occupation:

DOA:

Date of operation:

Date of discharge/death:

PRESENTING HISTORY AND SYMPTOMS

1. COMPLAINTS

a) Pain abdomen: • Duration:

• Time of onset:

• Mode of onset:

• Site:

• Nature: Intermittent/ colicky/ dull aching/

continuous/vague/ radiating

• Intensity of pain: Mild / Moderate / Severe

• Radiation:

• Worsened by:

• Relieved by:

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142

b) Distension of abdomen:

• Mode of onset: With pain / After pain / Before pain.

• Duration:

c) Vomiting: • Duration:

• Frequency:

• Amount :

• Vomitus: Blood / Food particles / Bile / Faceal matter.

d) Diarrhea : Duration :

e) Malaena : Duration :

f) Constipation : Duration :

g) Fever : Intermittent / Continuous / Undulant / Duration:

h) Drugs taken : Steroids / Antihistamines / Aspirin / Analgesics

i) Other complaints :

2. PAST HISTORY

Pain abdomen: Site: Nature:

Associated symptoms and duration:

3. PERSONAL HISTORY

Food habits : vegetarian/ non-vegetarian / mixed

Spicy food : Likes very much / does not like / moderate

Food : rice / wheat / ragi : refined/ unrefined

Alcoholic : Chronic / Occasional / Non- alcoholic

Smoking : No. beedies/cigarettes per day Duration:

Occupation : Nature of work: Manual laborer / sedentary

Socio-economic status: Low/ middle / high.

Bowel & Bladder :

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143

4. FAMILY HISTORY :

History of peptic ulcer or perforation in family members

5. GENERAL EXAMINATION

General:

Appearance-

Nourishment –

Facies –

Built -

Hydration – Good / Dehydrated

Anemia / Jaundice / Cyanosis / Pedal edema /

Lympadenopathy

Other signs of shock: sunken eyes,cold extremities,oliguria

Vital Signs: a) Pulse: Rate- /min, Regularity & Volume b) B.P: c)Temp:

Respiration: a)Rate & Regularity: b) Type - Abdominal / Thoracic

6. EXAMINATION OF ABDOMEN

a) Inspection: Shape/ Movements of quadrants/ Respiratory movement-

Peristaltic movements-

Hernial orifices-

Skin-

Umbilicus-

Engorged veins-

b) Palpation : Tenderness and site of tenderness-

Rebound phenomenon-

Rovsing‟s sign:

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144

Liver/ Spleen/ Other masses

Muscular rigidity / guarding –

Distension-

Hernial orifices-

c) Percussion: Shifting dullness: Fluid thrill: Obliteration of liver dullness

d) Auscultation: Peristaltic sounds – Heard / Not heard / Borborygmi

e) Measurements:

f) Rectal examination:

SYSTEMIC EXAMINATION:

Cardiovascular system/ Respiratory system/ Nervous system/ Skeletal system

INVESTIGATIONS:

Hb%

Blood group

TC

BT ,CT

LFT

RBS:

Serum Amylase

Blood Urea: S. Creatinine:

Urine: Sug: Alb.: Micro:

Plain X-Ray of abdomen (erect): Air under the diaphragm:

Present / absent.

Bilateral / unilateral

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145

PROVISIONAL DIAGNOSIS/ PRE OPERATIVE DIAGNOSIS:

TREATMENT:

1) CONSERVATIVE TREATMENT: Reason for not operating:

2) OPERATIVE TREATMENT:

PRE OPERATIVE RESUSCITATION:

OPERATIVE NOTES: Date: Anesthesia:

Incision : On opening peritoneum:

Exudate: Color: Bloody / Bilious / Purulent

Amount-

Site, Size & No. Of Ulcers:

No. of perforations:

Size of perforation:

Other findings:

Procedure: Open/ laparoscopic

Simple closure with omental graft with peritoneal lavage.

Or any other procedures like partial gastrectomy

Or closure of perforation and bypass procedure.

Or drainage procedure only.

Material used for closure:

Method of drainage: Peritoneum:

Biliary and gastric secretions:

POST OPERATIVE DIAGNOSIS :

POST OPERATIVE TREATMENT :

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146

RESULT: Cured / Relived / Expired / Others

POST OPERATIVE FOLLOW-UP

1. Date of Ryle‟s tube removed:

2. Date of suture removal:

3. Immediate post operative complications:

DISCHARGE SUMMARY: Condition on discharge:

Advice on discharge:

FOLLOW UP :

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147

ANNEXURE-II

CONSENT FORM FOR SURGERY/ ANESTHESIA

I……………….Hosp. No……….in my full senses hereby give my complete

consent for……………..or any other procedure deemed fit which is a/and diagnostic

procedure/biopsy/transfusion/therapy to be performed on me/my………………

admitted in ward…………. Of age……… under any anaesthesia deemed fit. The

nature and risks involved in the procedure have been explained to me to my

satisfaction. For academic and scientific purpose, the procedure may be televised or

photographed.

Date : Signature / Thumb impression

Of Patient / Guardian

Name :

Designation:

Guardian

Relationship

Full Address

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148

ANNEXURE III

MASTER CHART

Annexures

149

Annexures

150

KEY TO MASTER CHART

GPE - GENERAL PHYSICAL EXAMINATION

M - MALE

F - FEMALE

BH - BAPUJI HOSPITAL

CH - CHIGATERI GENERAL HOSPITAL

C - COOLIE

F - FARMER

ST - STUDENT

UE - UNEMPLOYED

SE - SELF EMPLOYED

HW - HOUSE WIFE

B - BUSSINESS

H/O - HISTORY OF

NSAID - NON STEROIDAL ANTI INFLAMMATORY DRUGS

BP - BLOOD PRESSURE

PR - PULSE RATE

OB. - OBLITERATION

TC - TOTAL COUNT

AUD - AIR UNDER DIAPHRAGM

DUP - DUODENAL ULCER PERFORATION

HVP - HOLLOW VISCUS PERFORATION

GUP - GASTRIC ULCER PERFORATION

IP - ILEAL PERFORATION

X - CEFTRIAXONE

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151

XS - CEFTRIAXONE+SULBACTUM

M - METRONIDAZOLE

A - AMIKACIN

PT - PIPERACILLIN+TAZOBACTUM

ME - MEROPENEM

OF - OFLOXACIN

O - ORNIDAZOLE

D1 - FIRST PART OF DUODENUM

D2 - SECOND PART OF DUODENUM

CON+FD - CONSERVATIVE MANAGEMENT WITH BILATERAL

FLANK DRAIN

B/L TV+ PP+ OPC - BILATERAL TRUNCAL VAGOTOMY WITH

PYLOROPLASTY WITH OMENTAL PATCH

OPC - GRAHAMS OMENTAL PATCH CLOSURE

LAP OPC - LAPAROSCOPIC OMENTAL PATCH CLOSURE

OPC+TTD - OMENTAL PATCH CLOSURE WITH TWO

TUBE DRAINAGE

PD+PP - PYLORODUODENOTOMY WITH PYLOROPLASTY

WI - WOUND INFECTION

SEP - SEPTICEMIA

MI - MYOCARDIAL INFARCTION

RF+ARDS - RENAL FAILURE + ACUTE RESPIRATORY DISTRESS

SYNDROME

WG - WOUND GAPING

BP - BASAL PNEUMONIA

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LRTI - LOWER RESPIRATORY TRACT INFECTION

PPI - PROTON PUMP INHIBITOR

ND - NOT DONE

DYS - DYSPEPSIA

DS - DEFINITIVE SURGERY

** - NO COMPLAINTS

LFF - LOST FOR FOLLOW UP

prospective study of duodenal ulcer perforation and …

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