HISTORY AND INTRODUCTION

The perforation of duodenal ulcer is one of the commonest abdominal

surgical emergencies met with in this part of the country, more so in southern

rice eating belt. The incidence of duodenal ulcer perforation is found to be

increasing. Nowadays varied views are put forth regarding its treatment.

The History of our knowledge of peptic ulcer was reviewed by Jordan in

1985. Rawlingson is credited with the 1st published report of a perforated

gastric ulcer in 1727. The first published report of a perforated duodenal ulcer

was by Hambergeri in 1746. Although Muralto described a perforated duodenal

ulcer in 1688. A report of this case by Lenepneau did not occur until 1839.

The frequency of peptic ulceration increases steadily with age:

therefore apparent rarity of the disease before twentieth century was due to

the generally short life expectancy at that time. In 1857 Brinton was able to

collect only 234 reported cases of perforated ulcer, all gastric. During the next

100 years there was an increase in the prevalence of peptic ulceration

especially duodenal ulcers. Illing worth and his colleagues showed that the

incidence of perforated ulcer in Glasgow doubled between 1924 and 1938

and similar rise was observed in other cities in Great Britain.

Braun, Von Mikulicz, Von Herber, Moynihan, Cleave, C.W. Mayo,

Zacharycope, Rodney Maingot, De Bekey and others have thrown much light

in this subject with their inexhaustible and vast experience and helped one to

avoid usual pitfalls in the management of duodenal. Ulcer perforation. It is

well said “more experience in the causalities. A person is the better surgeon,

he is to deal with Abdominal emergencies.

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Since the first report of successful operation for X the perforated

duodenal ulcer (Dean 1894) by simple closure, the treatment of this

catastrophic abdominal emergency remained the same till today.

Many follow-up studies between 1945 to 1965 indicated that simple

suture of perforated duodenal ulcer often fall short of being the ideal treatment

(IIIing worth et al, 1946; Avery – Jones and Doll, 1953; Gilmour, 1953;

Hadfield and Hatkins, 1964; Harbecht and Hamilton 1960). Poor results either

troublesome dyspepsia or other complications that necessitated further

surgical treatment were found in 50-70% patients.

Griffin and Organ (1976) in a study of natural history of perforated

duodenal ulcer treated by suture placation found that only 17 in 120 patients

(14%) were asymptomatic in the long term follow-up.

Henessy and associates (1076) in Australia, showed x that almost 90%

of the cases subsequently suffered from dyspepsia. They also found that one

patient in five bled during follow-up, one in eight developed pysoric stenosis

and one in eleven perforated again.

On reviewing the literature on duodenal ulcer perforation, I chose this

topic for my dissertation work in consultation with my professors and assistant

professors.

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SURGICAL ANATOMY OF STOMACH AND DUODENUM 1,2,3,4

STOMACH:

It is the largest dilatation of the gut and lies between the esophagus

and duodenum. It lies in the upper part of the abdomen beneath the

diaphragm and mainly to the left of the midline. It has got two surfaces, i.e.

anterior and posterior and two curvatures, i.e. lesser and greater.

The stomach can be divided into fundus, body and antrum. The fundus

is the dome of the stomach to the left and superior to the oesophagogastric

junction. An angulation at the midline of the body, approximately 5-6 cm.

proximal to the pylorus on the lesser curvature is called the incisura angularis.

The body of the stomach is the area between the fundus and line drawn from

the incisura angularis to the greater curvature. The gastric anturm is the area

distal to the line and proximal to the pylorus. The pylorus is a thick ring of

muscle and is externally marked by the vein of Mayo.

The oesophagogastric junction, the cardia, is located just to the left of

the tenth thoracic vertebra and the gastro duodenal junction, the pylorus, is

located to the right of the midline at about the inter space between the first

and second lumbar vertebrae (transpyloric plane). The superior margin of the

stomach between the cardia and pylorus (12-14 cm) is the lesser curvature,

which is suspended from the liver by the gastrohepatic ligament. The inferior

and lateral convex border of the stomach is the greater curvature, which is

about 3 times as long as the lesser curvature. Gastrocolic ligament is

suspended from the major protion of the greater curvature.

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Relations:

Anterosuperior surface; it is in contact with the left lobe of the liver and

under surface of the diaphragm and some times to the anterior abdominal

wall. Posteroinferior surface; it is related to many structures forming ‘stomach

bed’ viz., spleen, left adrenal, left kidney, splenic flexure of colon, anterior

surface of the pancreas, upper surface of transverse mesocolon, splenic

artery, portal vein and part of the diaphragm.

BLOOD SUPPLY:

The stomach is endowed with copious blood supply through the

branches of coelian axis. The left and right gastric arteries supply the area of

lesser curvature. The left gastric artery arises from celiac axis and the right

gastric artery is a branch of hepatic artery. The right and left gastro epiploic

arteries supply the area of greater curvature. The right is the branch of gastro

duodenal artery and left is from splenic artery. The splenic artery supplies the

area of fundus through its short gastric arteries. The gastro duodenal artery

sends branches to the area of pylorus.

VENOUS DRAINAGE: The veins accompany arteries and drain into portal

vein either directly of indirectly through splenic or superior mesenteric veins.

LYMPHATIC DRAINAGE

For the purpose of description of lymphatic drainage, the stomach is

divided into three lymphatic areas. It is divided by an imaginary line in its long

axis, 2/3rd of the stomach is further divided by an imaginary transverse line at

the junction of its upper 1/3rd with lower 2/3rd.

(1) The lymphatics of upper right 2/3rds of the stomach along the lesser

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Curvature drain into the superior gastric group of nodes which include

paracardiac nodes around the oesophagogastric junction. The supra pyloric

nodes receive lymph from the lesser curvature belong to the inferior gastric

group and subpyloric group. The receive lymph from the left lower 2/3rds of the

stomach along the greater curvature. 3) The lymphatics from the left upper

1/3 of the stomach drain into the pacreaticoleinal group. Efferents from all

three groups drain into celiac lymph nodes around the celiac trunk in front of

the aorta.

NERVE SUPPLY:

The stomach derives its parasympathetic (secretomotor) nerve supply

from both the vaginas the anterior and posterior gastric nerves which are

derived from the left and right vagi respectively. The sympathetic nerve

supply is derived from celiac plexus and accompany the arteries.

The left vagus passes into the abdomen in front of the esophagus an

anterior vagus nerve and supply the anterior wall of stomach. It sends

branches to the liver and gall-bladder. The nerve usually divides into

branches at a point 5-7cms. Proximal to the pylorus and supply the pyloric

antrum (Crow’s foot). These terminal branches are preserved in highly

selective vagotomy. This nerve supplies the acid-pepsin secreting areas of

the stomach.

The right vagus passes through the oesophageal hiatus behind the

esophagus as posterior vagus nerve and supplies posterior wall of the

stomach which sends branch to the celiac axis.

The criminal nerve of Grassi is the name given to the branch or

branches of posterior vagus that arises at or above the level

gastrooesophageal junction and supply the fundus of stomach. It has got an

important role in the etiology of the recurrent peptic ulcer, when it is not

divided.

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These nerves play major role in intermittent propulsion of gastric

contents by the antrum through the pyloric canal into the duodenim.

STRUCTURE:

The wall of the stomach is composed of four layers, viz. mucosa,

submucosa, muscle layer and serosa.

The serosal layer (visceral peritoneum) completely invests the stomach

except at its curvatures where it passes as double layer as hepatico gastric

ligament from lesser curvature and gastro colic ligament from greater

curvature and gastro splenic ligament from the left border of the fundus. The

muscular coat has got 3 layers, viz., outer longitudinal, middle circular and

inner oblique layers. The submucosa is a loose areolar tissue situated in

between the mucosa and muscular coats which allows free mobility of

mucosa over the muscular later. The mucosa of the stomach is smooth and

red. It is thrown into longitudinal folds which disappear when the stomach is

greatly distended. Mucosal architecture varies with the area of stomach. The

fundic mucosa consists of deep tubular glands lined superficially with

epithelial cells and containing in the deeper portions, characteristic parietal

cells and chief cells with occasional argentaffin cells. The pyloric and antral

mucosa consists of branching tubules lined predominantly with mucous cells

and gastric cells.

Several types of cells present in the mucosa of stomach with specific

functions.

Parietal Cells - Secretion of Hydrochloric acid and intrinsic factor.

Chief Cells - Synthesize and secrete pepsinogen.

Goblet cells - Secrete mucus.

Epithelial Cells - Probably secrete extra cellular fluid (non-parietal

Secretion)

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Gastrin Cells - Synthesize store and secrete somatostatin.

Mast Cells - Store heparin, histamine and other vasoactive

substances within granules.

Argentaffin Cells - May Synthesize and store enteroglucagon and

other peptide hormones.

The junction between antral and fundic mucosa cannot be

differentiated on Gross inspection but application of PH indicator to the

mucosal surface after the stimulation of gastric secretion will quickly and

clearly differentiate the proximal acid secreting mucosa from the distal neutral

antrum.

DUODENUM:

The duodenum begins at the pylorus and ends at the duodenojejunal

junction just to the left of the second lumbar vertebra making a ‘C’ shaped

curve. It is the first part of the intestine and is developed from foregut and

midgut so it has got dual blood supply.

It is divided into four parts:

First or Superior part (5 cms)

Second or descending part (8 cms)

Third or transverse part (10 cms)

Fourth or ascending part (2.5 cms)

Proximal first part of the duodenum is slightly dilated and called

‘duodenal bulb’ the mucosa of which is characterized by lack of plicae

circulates. The common bile duct enters the pancreas immediately posterior

to the duodenal bulb and lies within the head of the pancreas. This and the

main pancreatic duct open on to the media wall of the mid portion of the

second part of the duodenum at the ampulla of water. The superior

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mesenteric vessels emerge from behind the pancreas to cross over the third

part of duodenum. The fourth part ascends to the duideno-jenunal flexure,

which is suspended from the posterior body wall by the ligament of Treitz.

BLOOD SUPPLY:

The duodenum receives its blood supply through the branches of

arteries of foregut and midgut, from two sources; 1) Coeliac axis and

2) Superior mesenteric artery. They are

a) right gastric artery-branch of the common hepatic artery.

b) superior pancreatico-duodenal artery-a branch of gastro duodenal

artery.

c) Inferior pancreaticoduodenal artery – a branch of superior mesenteric

artery.

VENOUS DRAINAGE:

The veins accompany the arteries and drain into the portal system via

the splenic and superior mesenteric veins.

NERVE SUPPLY:

The autonomous supply comes from the celiac plexus. The

parasympathetic fibres are secretomotor and motor to the smooth muscles.

Sympathetic fibres are inhibitory to the glands and muscles.

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GASTRIC PHYSIOLOGY IN RELATION TO PEPTIC ULCER 5,6,7

The development of ulcer or the resistance to ulceration is determined

by the balance between aggressive factors (including secreted gastric acid

and pepsin) and those factors that comprise mucosal resistance to ulceration.

I. AGGRESSIVE FACTORS: ACIDS AND PEPSINS:

a) Hydrochloric Acid: Pariental cells secrete hydrocholoric acid (150

meq./ lit.), which can reduce gastric pH to 1.0 or less.

The pariential cell has multiple receptor sites on the cell membrance.

The maximal stimulation of cell may be achieved only when all the sites are

occupied (Grossman and Konturck). The cell is probably stimulated by five

chemical agents, viz, i) Acetylcholine, released from cholinergic nerve

endings, ii) Gastrin from G-Cells of antrum and duodenum, iii) Intestinal phase

hormone, iv) digested protein, v) Histamine from stores lying free within fundic

mucosa.

Parietal cells secrete hydrogen ions at a concentration of three million

times more than that found in blood. With each increase in hydrogen ion

secretion, there is a reciprocal decrease in sodium ion secretion. For each

hydrogen ion secreted into gastric Lumen, one bicarbonate ion is released

into the gastric venous circulation accounting for the alkaline tide, a direct

reflection of the magnitude of gastric hydrogen ion secretion.

The final step in hydrogen ion secretion is accomplished by a proton

pump mechanism involving a specific hydrogen – potassium adenosine

triphosphatase (H+, K+ - ATPase) located in the microvillous membrance.

This H+, K+ - ATPase exchanges hydrogen for potassium across microvillous

membrane.

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b) Pepsinogen: It is synthesized in the chief cells and stored as visible

granules. Cholinergic stimuli, gastrin and secretin are potent pepsinogogues.

The precursor zymogen is activated when pH falls below 5.0 Pepsin cleaves

peptide bonds, especially those containing phenyl alanine, tyrosine and

leucine. Its optimally pH is about 2.0 Its activity is abolished at pH 5.0. The

pepsin is irreversibly denatured at pH 8.0. The proteolytic effects of pepsins

in connection with the corrosive properties of secreted gastric acid are integral

components in the tissue injury which produces peptic ulceration.

William Beamount in 1822 identified the pepsin and its proteolytic

actions and studied the pathogenesis of peptic ulcer. He said “No, acid, No

peptic Ulceration.”

II. MUCOSAL DEFENCE:

The precise mechanisms whereby normal stomach and duodenum

resist the corrosive effects of acid pepsin have not been completely defined.

The potential contributions to mucosal defense are i) Gastric mucus, ii)

Bicarbonate ions, iii) Gastric mucosal barrier iv) normal mucosal blood flow

and v) prostaglandins.

GASTRIC MUCUS: It is secreted by gastric mucus cells located on the

surface of the gastric mucosal epithelium and in gastric glands. Mucus

secretion is enhanced by mechanical or chemical irritation and by cholinergic

stimulation. It is present in gastric juice in a soluble phase and as insoluble

mucus gel layer, approximately 0.6mm in thickness, which coates the

mucosal surface of the stomach. Normally the mucus gel is secreted

constantly by gastric mucus epithelial cells and is continuously solubilized by

pepsins secreted into the gastric lumen.

Gastric mucus is a large polymeric protein containing four sub-units

connected by disulfide bridges. Depolymerization of the glycoprotein submits

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of mucus by peptic digestion or disruption of disulfide bonds, renders the

glycoprotein incapable of forming or maintaining the gel state. When intact

this mucus gel serves as an unstirred water layer which shows ionic diffusion

but is much more impermeable to penetration by macromolecules such as

pepsins. Pepsin molecules secreted into the gastric lumen are deprived

reentry by the intact mucus gel, there by potentially protecting mucosal cells

from proteolytic injury. Gastric mucus gel thickness is increased by

administration of prostaglandins of the E series and reduced by NSAIDs

including aspirin.

Bacarbonate ions, secreted by non parietal gastric epithelial cells, enter

the mucus gel, contributing to the development of a microenvironment in the

gel with a substantial hydrogen ion gradient between the zone of gel facing

the gastric lumen (more acid pH2) and the zone in contact with the gastric

mucosal cells (more alkaline pH7) .

Gastric bicarbonate secretion is stimulated by calcium, prostaglandin of

the E and F series and cholinergic agents. It is inhibited by NSAIDs including

aspirin, acetazolamide alpha-adrenergic agents and ethanol.

Gastric mucosal barrier: Normally the gastric luminal epithelial cell surfaces

and inter cellular tight junctions provide almost completely impermeable

barrier to back diffusion of hydrogen ions from the lumen. This barrier is an

important component of mucosal resistance to acid peptic injury. The barrier

can be interrupted by bile acids, salicylates, ethanol and weak organic acids,

thereby permitting back-diffusion of hydrogen ions from lumen to gastric

tissues.

Normal mucosal Blood flow: Maintenance of normal mucosal blood flow is

an essential component of mucosal resistance to injury. Decreased mucosal

blood flow, accompanied by back diffusion of luminal hydrogen ions is

important in producing gastric mucosal damage.

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Prostagladins: Are present in abundant quantities in the gastric mucosa.

They stimulate secretion of gastric mucus and gastric and duodenal mucosal

bicarbonate. They participate in the maintenance of gastric mucosal blood

flow in the integrity of gastric mucosal barrier and in epithelial cell renewal in

response to mucosal injury.

ELECTRICAL ACTIVITY OF STOMACH:

An electrical pacemaker is situated in the fundal musculature near the

greater curvature. Regular (3/min) electrical impulses arise from this area and

pass towards the pylorus in the outer longitudinal layer. Every impulse is not

always followed by a peristaltic contraction, but the impulses determine the

maximal peristaltic rate.

Peristaltic contractions are more forceful in the antrum than the body

and travel faster as they progress distally. Gastric chime is forced in to the

funnel shaped antral chamber by peristalsis. About 5 - 15ml enter the

duodenum with each gastric peristaltic wave.

The volume of the empty gastric lumen is only 50 ml. by a process

called ‘receptive relaxation’ the stomach can accommodate about 1000 ml.

Before intraluminal pressure begins to raise. This process is an active process

mediated by vagal reflexes and abolished by vagotomy.

REGULATION OF ACID SECRETION:

a) Stimulation: Pavlov observed that food stimulation of gastric secretion

could be effected by a stimulus from the head or the stomach and later it was

found that stimuli might arise in the intestine.

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For descriptive purposes the process the process is divided into three

phases, 1) Cephalic Phase, 2) Gastric phase, 3) Internal phase.

Cephalic Phase: is stimulate by the sight or smell or chewing of food,

mediated via the vagus nerves.

Gastric Phase: is stimulated by the presence of food in stomach mediated by

the hormone – gastrin.

Intestinal phase: is stimulated by the presence of food in the small intestine.

The nature of the humoral agent of intestinal stimulation of gastric secretion

has not been fully identified.

b) Inhibition: There are two inhibitory mechanisms operating on the gastric

secretion. 1) Antral inhibition, 2) Intestinal inhibition

Antral inhibition: It is apparently due to passive removal of the gastrin

stimulus. Antral acidification suppresses the release of gastrin. At pH below

2.5 in the antrum, the gastrin release is inhibited regardless of stimulus.

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INCIDENCE

It is rather impossible to make a correct statement of the incidence of

the duodenal ulcer because there have been and indeed continue to be

changes from year to year. Two hundred years ago the disease was

practically rare and only became common in the 20th century.

It is even more difficult to assess the liability of peptic ulcer to perforate.

De Bakey has reviewed 33,439 cases of gastroduodenal ulcers in which 4410

perforations are noted, an incidence of 13.3 percent, Bager (1929) found that

perforation occurred in 18.1 percent of 9475 cases of peptic ulcer.

In the mid nineteenth century perforation was rare. Brinton (1957) was

able to collect only 234 cases of perforations of peptic ulcer. During the next

hundred years there was a progressive increase in its frequency but there is

ample evidence that since about 1955 there has been a steady decline in its

incidence. Dark and Mac Arthur (1983) reported that in South West Scotland,

the incidence has fallen from 21.6 per 100,000 population during the period

1946 through 1965 to 14.6 per 100,000 during 1975 through 1980 8.

AGE: 75 percent of perforated ulcers occur in the third to fifth decade of life.

It is very rare below the age of 16 years.

Johnson and Rintoul (1972) reviewed the literature and collected 118

cases of perforated duodenal ulcers in neonates, infants and children of which

only 50 survived.

The incidence in relation to age in women would appear to be similar to

that seen in men.

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SEX: Perforated peptic ulcer is more common in men that in women. There

is gradual decrease in the male to female ratio possibly due to the increasing

tendency for women to take on the responsibilities and occupations

traditionally associated with men. In addition in recent years a Mackay and

Mackay (1976) in which the ratio has fallen top 4:1. in the year 1988 the ratio

has still fallen down to 2:1.

OCCUPATION: It is commonly stated that perforation is more likely to occur

in those engaged in heavy manual work. Weir (1960) reviewed 1390 cases in

the 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.

SEASON: There is an increase in ulcer symptoms and in ulcer perforation in

the Winter.

Bodhe (1975) studied 986 cases of perforated peptic ulcers that

occurred in the Poona district of Maharastra in India between 1958 and 1972.

he found that high water vapour pressure coincided with periods of high

incidence. The highest incidence occurred with high water vapour pressure

and low temperature.

GEOGRAPHY: There are great variations in the incidence of perforations in

various parts of the world. It is particularly common in Western civilization

and practically unknown among were more primitive population such as Bantu

in the South Africa.

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ETIOLOGY

Hyper motility and hyperacidity are two important factors which

promote perforation of Peptic ulcer (James 1948).

The perforation is a rapid process even in chronic ulcers and is due to

the sudden sloughing of an un-supported portion of the floor of the ulcer.

Probably due to impairment of blood supply by endarteritis.

The best explanation for this condition is that the ulceration results from

a relative or absolute excess of acid-peptic gastric secretions. Several

arguments support this view.

The average patient with duodenal ulcer has higher rates of gastric

acid secretion than an ulcer free subject of the same age and sex in the

general population.

The temporary reduction of gastric acidity by buffers alleviates the

symptoms of duodenal ulceration, and healing of the ulcer follows permanent

reduction of acidity by surgical means. However, some aspects of the

relationship between acid output and duodenal ulcerations remain unclear.

Suggesting that some factors other than acid peptic activity may intervene.

a) Role of pepsin: Its role is important since that tissue destruction,

characteristic of ulcero – genesis required peptic activity. Yet pepsin cannot

be considered separately from the acid in ulcerogenesis. Pepsin is active only

in the acid / H. The longer the gastric outlet zone pH remains within the range

where pepsin is active, the longer will the duodenal mucosa remain exposed

to the proteolytic action of the pepsin. Thus gastric acid and pepsin operate in

concert, not only in the degradation of dietary proteins but also in the mucosal

destruction.

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b) Role of Gastric Hyperacidity 9:

i) Excessive neural stimulation of gastric secretion: It has been

suggested that increased vagal impulses of subconscious origin may cause

hyper secretion accompanying duodenal ulcer. This theory based on the well

known fact that vagatomy, when complete, abolishes gastric hyper secretion.

ii) Excessive hormonal stimulation of gastric secretion: Recent studies

suggest that serum gastrin levels may reach higher levels than those in the

normal subjects in response to vagal stimulation. At present, the role of

gastrin output in the etiology of the common variety of duodenal ulcer remains

unclear except in Zollinger Ellison Syndrome.

iii) Impairment of Physiologic mechanism responsible for gastric

inhibition: Patients with duodenal ulcer appear to have a normal drop in

gastric secretion upon acidification of the antrum or duodenum. However

gastric emptying is more rapid in patients with a duodenal ulcer than in ulcer

free subjects. This coupled with an augmented acid output, should have an

adverse effect on the duodenal mucosa. This theory has least experimental

support.

iv) Excessive capacity to produce acid: It has been shown that the

stomachs of patients with duodenal ulcer contain more parietal cells than

those of normal individuals. This is viewed as a genetically inherited trait, in

turn responsible for hyper secretion and duodenal ulcer production. It is also

thought that the hyperplasia of parietal cells is in response to an unknown

stimulus.

Cox counted the pariental cell mass in cadavers. The average cells in

subjects with duodenal ulcer is double the normal. The average there should

of parietal cell mass is 1 x 109 below which the duodenal ulcer was not found.

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c) Genetic and Blood Groups:

There is definite evidence that chronic ulcers occur in families.

Moreover, persons of blood groups ’O’ are about three times more likely to

develop a peptic ulcer than are persons of other blood groups. It seems

possible that the ABO genes may modify the size of the parietal cell mass.

d) Neurogenic theory:

Stimulation of vagus results in gastric hyper secretion and hypermotility.

Stress and anxiety may be a cause of duodenal ulcer and if so, may exert

their effect via the vagus.

e) Endocrine:

The effects of emotional as well as well as physical stress are

hormonally transmitted to the stomach via the pituitary adreno-cortical axis.

There are specific endocrine disorders which may be associated with sever or

intractable ulceration. These include (i) Zollinger Ellison Syndrome where a

non-betacell tumor secreting gastrin occurs in the pancreas, (ii) The multiple

adenoma. Syndrome-where adenomas occur in the pituitary, adrenal,

pancreatic and parathyroid glands, (iii) Hyper parathyroidism.

f) Accessory causes:

Drugs: Drugs such as phenylbutazone, indomethacin, aspirin and

corticosteroids decrease the efficiency of mechanisms that protect the gastric

and duodenal mucosae against acid.10,11

a) Inadequate Mastication

b) Smoking (Exclusive)

c) Alcohol

d) Irregular Meals

e) Vit. Deficiency

conclusively, smoking delay healing and promotes recurrence of a previously

healed ulcer.

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g) Infection:

Helicobacter Pylori a spirochaetal bacterium exists in the antrum and

duodenum deep to the mucosal layer. Ability to split urea with formation of

ammonia consequential local rise in pH has been blamed for causing

epithelial cellular damage and ulceration.

If organisms are removed by anotibiotics (Metronidazole) or Bismuth

salts (Tripotassium, Dicitrato Bismuthate) the recurrent ulcer rate is reduced.

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PATHOLOGY

Acute perforation may occur in acute or chronic duodenal ulcers. In

Desmond series (1962), 30 percent of 609 perforated duodenal ulcers were

acute i.e. there was no antecedent history of peptic ulcer and at operation the

first part of duodenum was mobile (with absence of fibrosis) and only a small

perforation was found on its anterior wall. There may be oedema and swelling

around the ulcer that has the appearance of chronicity. These should be

classified as chronic ulcers and if they are treated by simple suture a high

proportion of the patients develop symptoms of chronic ulceration.

Duodenal ulcers that perforate into the general peritoneal cavity are

situated on the anterior or anterosuperior wall of duodenum or at the

pyloroduodenal junction.

About 90% of duodenal ulcers occur in the first part of duodenum.

Generally within a few centimeters of the pyloric ring. The anterior wall of the

first part of the duodenum is more often affected than is the posterior wall.

i) The simplest explanation for the occurrence of duodenal ulcer is

excess gastric acid that strikes the duodenaol mucosa eroding and inflaming it

and producing duodenitis and ulceration. Almost all peptic ulcers occur on or

near the mucosal boundary (Oi and Samorai, 1959). Peptic ulcers occur only

in relation to certain muscular bundles possibly at the point of severe kinetic

strain (Oi and Samorai, 1969). The Oi dual control theory explain the fact that

duodenal ulcers are almost invariably sited just distal to the pyloroduodenal

mucosal boundary.

ii) Traction on the stomach, at laparotomy, may produce pale area on the

anterior duodenal wall and thus this area is ususal site for the duodenal wall

and thus this area is usual site for the duodenal ulcer (Mayo – 1908).

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Distention by meal may thus cause is in duodenal tissue tension with

submucosal ischaemia and localized susceptibility to attack by acid and ulcer

production.

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

site of perforation was found to be on the anterior wall in 92 percent, on the

posterior wall in 2 persons and on or about the pyloroduodenal junction

(classified as duodenal ulcers) in 6 percent.

The size of the perforation in a duodenal ulcer varies from 3 mm to

over 1 cm. in diameter. The larger the perforation and the older the patient.

The higher the morbidity and mortality.

APPEARANCE OF ULCER:

The base of all peptic ulcers is smooth, and clean, owing to peptic

digestion of any exudates. At times, thrombosed or even patent vessels that

provided the source of fatal haemorrhage project in to the base. Underlying

scarring causes puckering of the surrounding mucosa, so that the mucosal

folds radiate out from the crater in spoke like fashion. This gives a valuable

clue to the location of lesion for surgeon, pathologist and radiologist alike.

HISTOLOGICAL APPEARANCE:

It varies with the activity, chronicity and amount of healing. In the stage

of active necrosis, four zones are classically demonstrable.

1) The base and margins have a superficial thin layer of necrotic

fibrinoid debris not visible to the naked eye.

2) Beneath this layer is the zone of active non specific cellular infiltrate

with neutrophils predominating.

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3) In the deeper layers especially in the base of the ulcer, there is

active granulation tissue infiltrated with mono-nuclear leucocytes

and The granulation tissue rests on a more solid fibrous or

collagenous scar.

The arteries in the neighbourhood show evidence of endarteritis

obliterans. Often there are no nerves in the floor of the ulcer but always many

in the edge. The terminations of these nerves are bulbous, skin to those in an

amputation stump (kinsella). At the margin of the ulcer there may be epithelial

proliferation and down growths of glandular tissue. Which are some times

mis-interpreted as indicating a carcinomatous change (New comb).

Immediately after the perforation has occurred, chemical peritonitis

develops as a result of the irritant action of the contents of the duodenum and

stomach.

PATHOLOGY OF PERITONITIS:

The peritoneum consists of layer of flattended mesothelial cells

supported by small amount of connective tissue. On the connective tissue,

there are rich plexuses of capillaries, lymphatics, blood vessels and nerves.

The normal peritoneal fluid contains majority of mono-nuclear histiocytes with

many lymphocytes and few polymorphonuclear and eosinophills (Dixon and

Fixford).

These cells indicate whether the intestinal distension postoperatively is

due to peritoneal infection of merely as a result of atony of the bowel. In the

former case polymorphonuclear cells (80-905%) and in the later mono-nuclear

cells predominate.

In acute peritonitis the rapid absorption of bacterial toxins and toxic

products constitutes one of the gravest dangers of the disease. The

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semipermeable character of the peritoneum and its vast surface area have

been utilized in the treatment of reversible renal injuries. It has a surface area

of 22,000 sq. cms. As compared with 15,000 sq. cms. In the glomeruli. It can

be made to play the part of a dialyzing membrane similar to the cellophane in

the artificial dialysis. Patients have been maintained in good condition by

peritoneal dialysis for as long as 25 days after onset of uraemia (Kelly and

Best).

The omentum is a specialized part of the peritoneum which deserves

special mention. It has marked absorptive powers and plays important role in

the removal of bacteria and foreign substances.

Infection may reach the peritoneal cavity in the following ways.

i) Direct Infection

Via perforation of part of gastrointestinal tract.

Through the penetrating would of abdominal wall.

Post operative infections.

ii) Local Extension

From the inflamed intraperitoneal organs, i.e. appendicitis, Cholecystitis,

Diverticulitis etc.

Transmigration through damaged gut wall, i.e., unrelieved intestinal

obstruction

Through fallopian tubes

Part of general septicemia.

BACTERIOLOGY 12

Bacteria from alimentary canal

In majority of times the bacteria causing peritonitis are derived from the

alimentary canal. Usually the infection is caused by two or more strains. The

commonest organisms are E.Coli, anerobic and aerobic streptococci and the

23

bacteroides. Less frequently clostridium welchii are responsible. Very rarely

klebsicella pneumoniae and proteus are found.

Bacterioides

These are the predominant organisms in the lower intestine where they

greatly out number E. Coli. These gram negative non-sporing organisms

normally escape detection, because they are strictly anerobic and slow to

grow on culture media unless there is adequate CO2 tension in the anaerobic

apparatus (W.A. Gillepsie.).

Bacterioides not from Alimentary Canal

Examples of peritonitis due to gonococcus, Beta haemolytic

streptococcus, peumococcus and Mycobacterium tuberculosis.

CHANNELS OF SPREAD OF INFECTION

1) The bacteria may spread over the surface of the peritoneum by the

movement of bowel. This is prevented mainly by the cessation of

peristaltic activity of the bowel a protective physiological response to

any infection.

2) The bacteria may spread rapidly and extensively along the lymphatics

in the subperitoneal connective tissue. This is seen in the

streptococcal peritonitis.

FACTORS WHICH FAVOUR LOCALISATION OF PERITONITIS

1. Anatomical Factors: The peritoneal sac is divided into two (a) Pelvic

part, and b) The peritoneal cavity proper. The latter is divided into i)

Subphrenic space ii) Supra colic space and iii) infra colic space. The

infracolic space is again divided in to left and right compartments by the root

24

of mesentery and coils of intestine and bodies of the vertebrae. Each

compartment communicates freely with the pelvis.

When the supracolic compartment over flows as it is often the case

when a duodenal ulcer perforates. It does so over the colon in to the right

infra colic compartment and so through the right paracolic gutter to the right

iliac fossa.

2) Pathological Factors: The inflamed peritoneum loses its glistening

appearance and becomes reddened and velvety. There is outpouring of

exudates which later on become thick. The flakes of fibrin appear and cause

coils of intestine to become adherent to one another and to the parities. The

peristalsis is retarded in the affected coils and this helps in preventing the

spread of infection. The greater omentum by enveloping and becoming

adherent to inflamed structures often forms a substantial barrier to the spread

on infection.

FACTORS WHICH TEND TO CAUSE DIFFUSE PERITONITIS

1) The prime factor in peritonitis is whether it develops rapidly or slowly. If

a duodenal ulcer perforates before the natural defenses have had time

to come in to action. Where there is a gush of duodenal and stomach

contents in to the peritoneal cavity that spreads over a large area

almost peritonitis develops rapidly.

2) The ingestion of food or even water by stimulating peistalsis hinder

localization, violent peristalsis occasioned by the administration of

purgative or an enema causes a wide spread distribution of an

infection, that would other wise have been localized.

3) The virulence of the infective organism is high, the localization of

infection becomes difficult or impossible.

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PATHOLOGY OF PAIN

The abdominal and thoracic viscera and insensitive to the several

types of stimuli. The insensibility of alimentary tract to ordinary forms of

stimulation commences in the lower or middle of the esophagus and extends

as far as the commencement of anal canal. The intestines, the liver and the

pancreas etc., can be cut, burned or pinched without arousing immediate

sensation.

CONCEPT OF REFERRED PAIN ACCORDING TO ROSS AND MAKINZE:

Rose theory postulated that pain from abdominal viscera was of two

types. 1) Referred (somatic) pain, 2) True visceral or splanchnic pain.

Meckinze believed that afferent autonomic impulses arising in a

diseases organ, though temselves are incapable of arousing any sensation,

would upon entering the spinal cord set u an “irritable focus” with the result,

the cells accustomed to receive impulses from the corresponding somatic

area were excited. Thus the impulses from the viscera spread or irradiated on

to the cells of the corresponding somatic centers. In this way spontaneous

plain in the superficial structures remote from the disease organ in thus

explained. Meckinze spoke of these reactions as “Viscero sensory reflexes”.

The referred motor reactions in the form of muscle gaurding as “Viscero motor

reflexes”.

Adequate stimulus for True Visceral Pain:

Hurst (1911) from his investigations concluded that tension is the only

adequate stimulus for visceral pain fibres. Distension of hollow viscus e.g.

stomach, intestines, gall bladder etc., give rise to pain as a result of stretch

stimulus applies to the nerve terminals in its walls.

26

The diffuse character of the pain in contrast to the accurate localization

of cutaneous stimulation can be accounted for by i) existence of relatively few

afferent fibres in deep structures. ii) Lack of experience and training in

localization of sensation from viscera. iii) Impressions from the internal organ

do occur but their localization if not aided by sight as in the case of more

superficial sensations.

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CLINICAL ASPECTS OF DUODENAL ULCER PERFORATION

TYPES OF PERFORATION:

1) Acute: The ulcer perforates and the general peritoneal cavity

becomes flooded with duodenal and gastric contents. This is the most

common presentation.

2) Sub-acute: In this case, only a circumscribed areas of the peritoneal

activity becomes contaminated by the leakage (leaking peptic ulcer). Such

localization depends upon i) the limited size of perforation, ii) The emptiness

of stomach iii) adhesions around the ulcer and iv) The plugging of the opening

shortly after perforation either by omentum of a neighbouring viscus.

3) Chronic: When an ulcer perforates but the area is walled off by

adhesions or by viscera such as liver, colon or omentum, a chronic abscess

may from and give rise to considerable with an abdominal with an abdominal

mass and/or sign of Subphrenic abscesses.

CLINICAL MAINFESTATIONS: 13,14,15

Acute perforation: A history of peptic ulceration is not necessarily of

importance in the diagnosis of acute perforation. Only about 50 percentage of

patients with perforated to ulcer give history of symptoms suggestive f chronic

peptic ulcer, the acute episode. Carefully questioning after recovery,

however, increases this number to about 70 percentage. 15% of patients

given a short history with symptoms for 1 or 2 weeks prior to perforation. The

remaining 15 give no history of ulcer at all.

From the moment of perforation, the clinical course can be divided into

three stages, each of variable duration.

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1) The primary stage or stage of peritoneal irritation

2) The secondary stage or stage of peritoneal reaction.

3) The tertiary stage or stage of bacterial peritonitis.

Primary Stage

This stage follows immediately upon perforation. The symptoms which

arise with dramatic suddenness are due to intense irritation of peritoneum by

the escape of duodenal and gastric contents into the peritoneal cavity

(Chemical Peritonitis). This stage usually lasts for about 6 hours or so

depending on the size of perforation and emptiness of the stomach. Usually

the patient is suddenly seized with burning pain over the epigastrium often

referred to the tip of the right shoulder. In some cases, the pain gravitates

down along the right paracolic gutter in to the right iliac fossa similating the

acute appendicitis. Some times the patient may go in to transient neurogenic

shock with lived appearance.

On examination, at this stage, a little change will be observed in pulse,

4 respiraton and temperature. Patient may vomit once or twice but not

frequently. The patient will be motionless with muscle guard over upper half

of the right rectus muscle or some times with generalized guarding of the

abdomen.

Secondary Stage

The duration of this stage is variable, but rarely exceeds 6 hours. The

pain becomes less severe and called the stage of delusion. The general

condition will improve, patient feels better, extremities become warmer,

temperature becomes normal or slightly raised, pulse rate increases,

respiration is hurried, and patient feels thirsty. The patient is afraid of moving

for fear of aggravating the pain.

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In this stage, most of the errors in diagnosis occur. The abdominal

physical signs leave no room for doubt. The tenderness and rigidity are still

resent to a marked degree. The pelvic peritoneum is markedly tender on

rectal examination. On auscultation, the abdomen is silent. Two other

features may be added i.e. shifting dullness and obliteration of liver dullness.

One of the most reliable diagnostic procedures in acute perforated

duodenal ulcer is the X-ray demonstration of pneumoperitoneum. This is

present in 80% cases of perforations. It must be emphasized however that

negative X-ray finding does not exclude a diagnosis of perforation.

Tertiary Stage

This stage does not usually supervene until 12 or more hours after

perforation. The mortality will be higher. The clinical picture in this stage is

essentially the same as that of a generalized bacterial peritonitis from any

cause. The pain becomes less severe. Vomiting is frequent and hiccoughs

present. Dehydration and electrolytic depletion become some evident due to

sweating, vomiting, exudation of fluid in to peritoneal cavity and outpouring of

fluid in to distended paralyzed intestine. Patient complaints of increased

thirst. Urine output usually ceases, fever is present usually about 380 C.

Tongue is dry, pulse rate steadily raises and tready. Respiration remains

shallow and rapid. Blood pressure starts falling indicating hypovalemic shock

with circulatory failure. The characteristic picture of intestinal obstruction due

to paralytic ileus with effortless regurgitation of dark colored fluid and

meteorism takes 36 to 48 hours to develop.

The patient may either drift in to delirium followed by coma or may

remain conscious to the end. Death usually takes place some 4-5 days after

perforation.

30

DIAGNOSIS:

In 95% of cases the diagnosis will not be difficult. It is usually

diagnosed by clinical examination and aided by plain X-ray abdomen in erect

posture to demonstrate pneumoperitoneum. The existence of concomitant

disease may cause confusion. It is not rare for a perforation to occur in a

patient who is under treatment in medical wards for some other problem like

cardiac or pulmonary disease. The physician should be alert and suspicious

and surgeon should think of the possibility of duodenal ulcer during the

treatment of some other disorder. The diagnosis of perforated duodenal ulcer

should be made as follows.

1) To decide whether the condition is of acute abdominal one or not, by

eliciting the four signs which may prove helpful in general way.

a) The Pointing Test: The patient is asked to point to the site of pain. If

this proves to be the site of localized tenderness in right iliac fossa it goes in

favour of acute appendicitis, in right hypochondrium, or generalized goes, in

favour of duodenal ulcer perforation with peritonitis.

b) The Cough Test: The patient is asked to cough, and if pain is felt it

suggests an inflammatory process at the site of pain.

c) Rebound Tenderness: (Release sign, or Blumberg Sign) Having

palpated the suspected are as deeply as circumstances allow, the palpating

hand is withdrawn suddenly and completely. As a result of this abrupt

removal of the pressure that was applied slowly and gently, but with

increasing firmness, the stretched abdominal musculature springs back in to

lace, carrying with it attached peritoneum, which if inflamed, causes the

patient to wince or in many instances to cry out in pain. This sign is employed

over any part of abdomen suspected of harbouring an inflamed focus, where

there is doubt about the presence of early peritonitis. It is quite unnecessary

with undoubted involuntary rigidity.

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d) The bed shaking Test: (Bapat Test) If still in doubt whether early

peritonitis is present, the bed is shaken. This will cause pain at the site of

inflammation.

2) CLINICAL FEATURES:

Having confirmed that the case is of acute abdominal condition, by

doing above tests, the perforation of duodenal ulcer is diagnosed by noting

the following clinical features.

Pulse: For the first six hours, the pulse rate is often practically unaltered.

The gravity of the prognosis varies directly with the pulse rate. The great

majority of patients diagnosed and treated correctly recover which the pulse

still is under 100 percent/minute. As the pulse rate raises the outlook

becomes gloomy.

Temperature: It is likely to be subnormal due to shock. When bacterial

peritonitis sets in the temperature rises.

ABDOMINAL EXAMINATION 15

INSPECTION: The patient will be motionless with retraction of the

epigastrium. This retraction of the abdomen is due to muscular contraction of

the diaphragm and anterior abdominal wall. As time passes this sign is lost.

The abdominal muscles are held so rigidly that respiration is almost entirely of

the thoracic type.

PALPATION: Board – like rigidity is characteristic and cardinal sign of

peritonitis. With the onset of diffuse peritonitis and consequent distension,

rigidity passes off to a varying degree. There will be diffuse tenderness all

over the abdomen in late stage.

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PERCUSSION: The absence of liver dullness in the mid axillary like is very

fair evidence of gas in the peritoneal cavity. Shifting dullness will be present

indicating the presence of free fluid in abdomen.

AUSCULTATION: The abdomen is invariably silent in peritonitis. But in early

perforation with minimal peritoneal contamination the bowel sounds may be

heard.

RECTAL EXAMINATION: Some times tenderness can be detected in

rectovesical / Douglas Pouch.

INVESTIGATION: To aid in the diagnosis plain X-ray of the abdomen for sub-

phrenic regions in sitting and left lateral positions are helpful for the diagnosis

of perforation.

TECHNIQUE OF X-ray: The skiagram of posteroanterior and left lateral

views of the abdomen are taken after keeping the patient for 20 minutes in

sitting posture (Olson and Nagore 1946).

When a negative radiological evidence is obtained, about 20 to 30 cc of

air is injected in to the stomach through Ryle’s tube and the X-ray is repeated

(De-bakey, 1940).

X –ray should be taken only after complete aspiration of the gas and

food material from the stomach as the mucus or food material may block the

leak and hence results in absence of subphrenic gas shadow (peter job stran,

1955 and locle, 1951).

Some times small sub-phrenic gas shadow is better visualized in the X-

ray of the chest than X-ray of abdomen (Maynaurd and Prigot, 1961).

Sub – phrenic gas shadow is a crescent in shape, seen between the

diaphragm and the liver on right side and between it and stomach on the left.

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Sub- phrenic gas may absent in cases of: 1) Dry perforation, 2)

Preliminary gastric aspiration is not done, 3) Patient is not kept in sitting

posture for 20 minutes prior to X-ray, 4) Patient is uable to hold breath at the

time of X-ray.

Leur (1949) has shown that the mortality rate was less in cases with no

gas shadow (14.8%) when compared with those of positive gas shadow

(22.8%), but the prognosis cannot always be judged by the amount of gas

seen under the diaphragm (Stead, 1951).

Herman Taylor (1946) made a routine, in his conservative line of

treatment of perforation, of taking daily X-ray of the abdomen to be compared

with the previous films. An increase in the column of air after second day or

persistent failure to diminish the air, necessitates the laparotomy.

DIFFERENTIAL DIAGNOSIS 16

It falls in to two main categories.

i) Acute Medical Conditions

1) Acute Thoracic condition i.e. acute diaphragmatic pleurisy, Lobar

pneumonia, acute pericarditis, myocardial infarction etc.

2) Food poisoning 3) Gastric crisis of tabes dorsalis

4) Acute alcoholism 5) Meningitis

6) Pre-eruptive stage of Herpes zoster 7) Acute gastritis

8) Acute porphyria

ii) Acute surgical conditions

1) Acute appendicitis 2) Acute pancreatitis

3) Acute intestinal obstruction 4) Acute cholecystitis

5) Mesenteric thrombosis 6) Ruptured ectopic pregnancy

7) Peritonitis from other causes 8) Spontaneous rupture of esophagus

9) Dissecting aneurysm of aorta

34

MANAGEMENT

The straight forward logic of “Where there is hole, close it” has always

appealed to surgeons and fits with the general principles, that the continuing

leakage causes the development of bacterial peritonitis. Thus laparatomy and

closure remains the mainstay of treatment.

Being a common problem, the treatment of perforated duodenal ulcer

demands through planning (R.K. Sen, 1959). So no single method of

treatment is appropriate for every patient with a perforated duodenal ulcer.

The methods of treatment include

I) Surgical Management

a) Simple closure with omental graft

b) Definitive surgery with simple closure

1) Simple Closure + Gastrojejunostomy + Vagotomy

2) Simple Closure + Gastrojejunostomy

3) Simple Closure + Partial Gastrectomy

4) Simple Closure + Antrectomy + Vagotomy

5) Simple Closure + Pyloroplasty + Vagotomy

c) Laparoscopic closure.

II) Non Surgical Management

Conservative treatment

Whatever method of treatment is used, once the diagnosis of

perforated duodenal ulcer has been firmly made, the following measures have

been adopted while arrangements are being made for immediate operation.

35

Pre-operative Management

It is mandatory to resuscitate the patient prior to the operation, to bring

the patient to the normal physiological state as far as possible.

This regime may take 2-3 hours, but if the patient had bleeding in

addition to perforation, it is essential to operate earlier after vigorous

resuscitation and necessary blood transfusion.

The regime is as follows:

i) Better to treat the patient in supine position. If the patient is in shock,

foot end of the bed should be raised.

ii) Patient anxiety and pain should be relieved by sedation as soon as the

diagnosis is confirmed.

iii) Nasogastric aspiration is established

iv) No fluids should allowed by mouth

v) Intravenous lines should be secured. Fluid and electrolyte imbalance

should be corrected by saline and glucose or depending upon the pre

operative electrolyte levels of the blood.

vi) Blood grouping and cross matching should be done, especially when

the patient is anaemic.

vii) If the patient is not able to pass the urine and the bladder is distended,

catheterization should be done under aseptic conditions.

viii) Monitoring of vital data i.e. pulse rate, blood ressure, respiratory rate

and the temperature at half hourly intervals.

ix) Fluid intake output charts should be maintained

x) Administration of broad spectrum antibiotics

xi) Preparation of the abdomen is postponed till the patient is revived from

shock.

36

Surgical Management : In most however, operative treatment is indicated in

the form of definitive treatment to cure the ulcer, of simple closure of the

perforation.

Simple closure of the perforation remains the standard treatment even

to-day but in selected cases curative treatment like gastroduodenal resection,

vagotomy with or without drainage procedure may be indicated.

Simple Closure: There are two methods of simple closure.

a) Celline Jone (1929) method: A series of interrupted sutures are

placed across the perforation and a tag of omentum is pulled beneath

this arch of sutures before they are tied.

b) Graham’s Method (1937): In which the interrupted sutures are tied

and omentum is pulled in between the long ends of the sutures which

are tied again.

Bennet (1986) first suggested that where the perforation is large and

difficult to suture owing to the friability of the parts, omentum could be used to

plug the defect.

INDICATIONS: as suggested by Stead (1951)

i) Failure of conservative treatment.

ii) Persistent, recurrent pain after 6 hours of vigorous aspiration.

iii) Increase in tenderness and rigidity of abdomen.

iv) Associated Pyloric stenosis and haemorrhage

v) The patient is brought to the hospital late for surgery, usually 24 hours

after perforation.

vi) The patient is aged

37

vii) The general condition is poor, i.e. anaemic, shock has not been

improved even after vigorous treatment or associated with cardiac and

pulmonary diseases.

viii) Gross contamination of peritoneal cavity.

ix) The operation presents with great technical difficulties, e.g. obese

patients etc.

x) The surgeon has had but little experience in abdominal surgery.

xi) As a routine operative treatment

ADVANTAGES:

I) It is simple operation

ii) It needs no special technique and is performed in short time

iii) Peritoneal toilet is done

iv) Drainage of peritoneal cavity is done as and when necessary

v) Inspection of abdominal viscera with special reference to the lesion

bearing area and closure of perforation and Diagnosis is also

confirmed.

DISADVANTAGES:

The main disadvantage is its poor long term results. A high proporation

of patients treated by simple closure of perforated duodenal ulcer develop

further complications of the ulcer within five years and some of these

complications for e.g. hemorrhage, Reperforation or pyloric stenosis – prove

fatal.

i) It is not the treatment of duodenal ulcer

ii) Recurrence of perforation, haemorrhage and stenosis

iii) Recurrence of ulcer symptoms

38

iv) The strain of patients in subjecting themselves to second operation

either for the Reperforation or duodenal ulcer treatment.

v) The operative mortality associated with this method of treatment

averages to about 7 percent with a range of 2-20 percent (Recent

advances in Surgery, series 10, 387)

DETAILS OF OPERATIVE PROCEDURE:

i) Pre-operative resuscitation: is mandatory to make the surgery much

safer to the patient and prevent many of the possible postoperative

complications. Post operative recovery will be smooth, wound healing

is more certain and

infection is less likely. It is done as mentioned earlier.

ii) Anaesthesia: General anesthesia with cuffed oral endotracheal tube

intubation under pentathol sodium induction is preferred. Later

maintained with nitrous oxide and oxygen.

iii) Operative Procedure: Abdomen is opened by classical upper right

paramedian rectus displacing or splitting incision, which carries the

advantage of extensibility, accessibility and safety.

Bailey points out that in 10% cases, a muffled pop of escaping gas can

be heard on opening the peritoneum. The free fluid is sucked or moped up

with moist packs. The stomach is held near the greater curvature with a moist

pack and search for perforation should be started with another mop in the left

hand to wipe the stomach and duodenum.

If the perforation is found it is closed by either of the methods

described above. Peritoneal toilet is given with normal saline thoroughly. A

corrugated rubber drain is kept through the right flank into the peritoneal

cavity, i.e. Morrison’s Pouch. Abdomen is closed in layers after securing

complete homeostasis.

39

Post-operative Management: The treatment should include

1. Nasogastric aspiration 2. Antibiotics

3. Sedation 4. I.V. Fluids

5. Monitoring of vital data 6. Vitamins and oral fluids

7. Breathing exercise 8. Movement of limbs

9. Sutures are removed after 7 days

Post-operative Complications

1. Paralytic ileus 2. Pulmonary complications

3. Thrombophlebitis 4. Would infection

5. Sub- Phrenic abscess 6. Burst abdomen

7. Incisional Hernia

II) DEFINITIVE SURGERY WITH SIMPLE CLOSURE

Performing definitive surgery along with simple closure of duodenal

ulcer perforation is becoming immensely popular these days.

In 1902 Keatly performed first definitive surgery for duodenal ulcer

perforation. Habener (1919) followed it up Yudin (1937) popularized the

method with a mortality of 9% in 937 cases. Lowdon (1952) done it without

any mortality.

H. Stuart Iron Jr. from Pennsylvania reports 77 partial gastrectomies

from the veteran administration hospital series with gratifying results. He laid

down certain requirements before definitive surgery for duodenal ulcer

perforation is undertaken. They are

i) Hospital facilities must exist with trained operation theater staff and

assistants.

40

ii) The surgeon should be qualified and competent to do major gastric

surgery.

iii) The Patient should be in good general condition and adequate

preoperative hydration.

iv) Perforation of less than 12 hours duration.

v) History suggestive of peptic ulcer diseases for years.

vi) The ulcer which has perforated previously.

vii) The perforation is associated with other complications like haemorrhage

and obstruction.

viii) Emergency qualified anesthetist and blood bank facilities should be

available.

Thus the treatment of patients with perforated duodenal ulcer and

peritonitis required surgical sagacity. The tactics to be employed will depend

upon the patient (how fir? how old?, how fat ?, how long perforated?) and not

the least the surgeon (how experienced?).

Indications:

1) Patient with chronic ulcer history

2) Young patients.

3) Perforation admitted within 8-12 hours period without

established bacterial peritonitis and electrolyte imbalance.

4) Ulcer perforation with pyloric stenosis.

5) Ulcer perforation with haemorrhage.

6) Re-perforation of ulcer which was treated earlier by simple

closure.

41

Advantages:

1) Curative procedure for duodenal ulcer.

2) Safely done in selected cases.

3) Least incidence of recurrent dyspepsia

4) Least incidence of further gastric operation

5) Good clinical results.

Disadvantages:

1. When the patient come 24-48 hours after perforation with

established peritonitis and fluid and electrolyte balance, definitive

surgery cannot be done.

2) Opening in lesser cavity of peritoneum and introduction of infection

right upto the mediastinum leading to mediastinitis and high

mortality.

3) It takes quite a long time than simple closure, to be performed.

Gastro jejunostomy and vagatomy:

Under general endotracheal anesthesia, the abdomen is opened by

right paramedian or midline incision. The free fluid is sucked out. The

perforation is located. It is closed in a classical way. Then the

gastroesophageal junction is exposed by displacing the liver with Deaver’s

retractor and pulling the stomach downwards. The peritoneum over the

esophagus is divided. The anterior vagus is identified, clamped, cut and

ligated. Similarly the posterior vagus is identified, clamped, cut and ligated.

Similarly the posterior vagus also is divided and ligated.

The stomach is brought out through the transverse mesocolon and

anastomosed to jejunum in four layers. Through peritoneal lavage given and

42

corrugated rubber drain kept in right flank, complete haemostasis secured,

the abdomen is closed in layers.

Conservative Management 21

The potentiality of non-operative management of perforated duodenal

ulcer was first pointed out by Wangenstein in 1934.

If the surgical intervention is with held and conservative treatment is

undertaken, one of the three results may be expected.

1) The abdominal tenderness and rigidity may gradually abate and

the perforation closes.

2) A localized abscess perigastric or sub-phrenic may form.

3) The patient may die of septic peritonitis.

Indications

1) In early acute case when the diagnosis is in doubt.

2) When the patient is poor operative risk patient

3) In some cases of sub-acute perforations

4) When the patient is seen for the first time some days after

perforation and with sufficient evidence that the infection is

localized.

The chief objections to the non operative treatment.

1) Uncertainity or error in the diagnosis: first of all, the diagnosis of

perforated duodenal ulcer must not be in doubt, yet such certainity of

diagnosisis hard to achieve.

43

2) The site of perforation is un known: Acute perforated gastric ulcers

result in high death rate than do perforations of duodenal ulcers when

conservative management is employed.

3) The possibility of treating a perforated gastric carcinoma.

4) It denies surgeon the opportunity, which is afforded by surgical

treatment to perform “toilet” of peritoneal cavity and so intraperitoneal

abscesses are more common.

5) It makes great demand on the time of nursing and medical staff than

does surgical treatment.

Conservative treatment should be abandoned 1) if the diagnosis

remains uncertain for 6 hours or more, 2) If the patient has x-ray evidence of

gastric ulcer or gives a history of previous operation, 3) If no improvement is

seen after a trial of aspiration treatment. The abdominal exploration should be

carried out without delay.

Conservative treatment consists of 1) Continuous effective gastric

aspiration, 2) Adequate intravenous fluids and electrolytes administration,

3) Antibiotics, 4) Sedation, 5) Monitoring vital data, 6) No fluids are permitted

by mouth for the first 48 hours.

Conservative treatment in selected cases gives good results, but most

of the surgeons agree that early operative treatment is preferable.

Laparoscopic closure of duodenal ulcer perforation:

In recent days quite a good no. of studies proved that with skilled

surgeon the procedure is equally beneficial and effective to open closure of

duodenal ulcer perforation22.

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PROGNOSIS 23,24

1. The amount of the nature of fluid in the stomach at the movement of

perforation. The fuller the stomach and the stomach and the amount of

free fluid and gas in the peritoneal cavity, the worst is the prognosis.

2. The size perforation: The larger the perforation, the poorer the

prognosis (Anseline, 1977).

3. The age of the patient: Under the age of 60 years the mortality is

negligible, but with each increasing year of age the prognosis worsens.

4. The position of ulcer; The anterior ulcers over the duodenum perforate

and present with peritonitis and the posterior ulcer penetrate the

pancreas and some times present with haemorrhage.

5. Associated diseases; A high proportion of older patients will have

serious diseases such as hypertension, or cardiovascular and

pulmonary conditions and will thus be less able to with stand the

perforation and associated operation.

6. The time factor; The time that has elapsed between perforation and

treatment is one of the most important factors in prognosis. The longer

the interval between the rupture and the operation, the higher the

mortality after 12 hours the death rate rises steeply.(Sirinek,1981).

7. Associated haemorrhage; It considerably prejudices the patients

recovery.

8. The pre-operative and post-operative management; The marked

reduction in overall mortality is due to the following:

a) Improved methods of pre operative treatment.

b) Improved methods of anaesthesia, especially muscle relaxants

and positive pressure pulmonary ventilation.

c) Better post operative management, particularly greater control

over infection by antibiotics.

d) Improved operative technique and the adoption of more radical

approach, to the treatment of perforated ulcer.

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49

50

51

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PHOTOGRAPHS

Blood supply of Stomach and Duodenum

Nerve supply of Stomach and Duodenum

82

83

X-Ray Erect abdomen showing gas under diaphragm

Operative view of Duodenal Ulcer Perforation

Closure of Duodenal Ulcer Perforation with Omental patch

84

Laparoscopic view of Duodenal Ulcer Perforation

Laparoscopic closure of Duodenal Ulcer Perforation

85

ANALYSIS OF DATA

The duodenal ulcer perforation is a very serious condition and

invariably fatal if not properly managed.

The following chart is the percentage of the duodenal perforation

associated with peritonitis among the total number of cases admitted in

surgical wards, in MGM hospital, Warangal during the years 2007-2008 and

upto October 2009 respectively.

Table – 1

YEAR

Total No. of cases

admitted in MGMH,

Wgl

Total number of cases

admitted in surgical wards

Total No. of duodenal

ulcer perforations

Percentage %

2007 23,016 3369 94 2.79%

2008 23,276 3458 96 2.78%

2009(upto Oct.)

24,133 3391 102 3%

Table -2

Total No. of surgical emergencies in surgery

department during January 2007 through December 2008

Total No. of duodenal ulcer perforations

Percentage

1264 190 15.03%

86

Table -3

The perforation of duodenal ulcer was the third common surgical

problem in MGM Hospital ,Warangal.

Sl.No.

Surgical ProblemsNo. of cases

Percentage

1 Acute appendicitis 719 56.88 %

2 Intestinal obstruction(including obstructed hernia )

229 18.12%

3 Perforated duodenal ulcer 190 15.03 %

4 Peritonitis excluding duodenal ulcer perforation

70 5.54 %

5 Others 56 4.43 %

Total No. of cases 1264 100 %

Table -4

Age wise distribution of duodenal ulcer perforation in MGM Hospital

Warangal figures from 1-6-2007 through 31-12-2008 among the 100 cases

studied.

Age group in yearsTotal number

of patients

1-10 Nil

11-20 4

21-30 22

31-40 19

41-50 35

51-60 18

61 and above 2

Total 100

In our 100 cases studied the youngest patient of duodenal ulcer

perforation was 11 years old and the oldest was 70 years old. Duodenal ulcer

perforation is more common in the 5th decade 76% of our cases are in the age

group of 20 -49 years.

87

Table -5

Sex distribution of duodenal ulcer perforation during the period from

1-6-2007 through 31-12-2008 from 100 cases studied.

Total number of cases

Male Female

100 94 6

The male: Female ratio of duodenal ulcer perforation from the above statistics

is 16 : 1.Thus the incidence of duodenal ulcer perforations is more common in

males than in females

In 100 cases studied during the period from 1-6-2007 through

31-12-2008 the incidence of duodenal ulcer perforation is common in patients

belonging to the blood group “O”.

Table – 6

Blood group Rh factorTotal No. of

casesO + 52

A + 10

B + 14

AB + 24

Size of perforation: In majority of cases the size of the perforation is usually

less than 5 mm.

88

The following are the various sizes noted in the 12 cases presented in

the dissertation.

Case No. 1 2 3 4 5 6 7 8 9 10 11 12Size of duodenal ulcer perforation

3mm 5mm 4mm 15mm 5mm 10mm 10mm 3mm 3mm 10mm 3mm 4mm

In 12 studied cases, the size of duodenal ulcer perforation is less than

5 mm in 66.66% of cases. In 100 cases studied in MGM Hospital during

1-6-2007 through 31-12- 2008 the size of perforation is less than 5 mm in

80% of cases.

89

DISCUSSION

A clinical study of perforated duodenal ulcer was done during the

period of one and half years from 1-6-2007 through 31-12-2008, 2008 in

M.G.M. Hospital, Warangal.

Incidence: The incidence of perforation of duodenal ulcer in relation to total

number of admissions into the department of surgery at MGM Hospital has

been worked out to be 2.79 % during the period of study.

The incidence in relation to the total number of surgical emergency

operations has been worked out to be 15.03 %which is the third commonest

emergency at M.G.M. Hospital, Warangal.

The incidence at M.G.M Hospital is found to be gradually decreasing

on retrospective study. The incidence of duodenal ulcer perforation in 1994

was 26.6 % and in 1996 it was 16.6 % and in 1999-2000 it was 2.6%.

There is no single reason clear to explain the fall in the incidence of

duodenal ulcer perforation. It appears to be due to multiple reasons eg.,

Increased awareness on part of the patients in using drugs at the proper

time. Better patient compliance for the use of drugs like antacids and H2

receptor antagonists, proton pump inhibitors and of late Helicobactor Pylori

treatment. In addition to these as at many peripheral centres surgery for

duodenal ulcer perforations is taken up and the case incidence at MGM

Hospital has come down. It may be probably because of more private

hospitals coming up in Warangal district during recent times.

The incidence of perforation is variable not only in different countries

but in different regions of the same country. In UK reports by Watkins et aland

in USA reports by gustavsson et al have not shown any change. In the United

90

States Kurata et al have reported reduction while Scheeres et alhave reported

increased incidence. In Indian literature however such comparative study not

available.

Age Distribution : The youngest patient in our study was 11 years old and

the oldest was 70 years old. Duodenal ulcer perforation was more common in

the 4th decade.76 % of our cases are in the age group of 20 to 49 years.

The peak incidence of perforation duodenal ulcer as reported by A.K.

Dev, S. Paul N.Battacharjee and J.Roychoudary from dept. of surgery, north

Bengal Medical College and hospital, Siliguri from West Bengal India was in

the age of 46-55 years Rains and Ritchie reported similar age incidence.

Sex: There is significant male preponderence in the incidence of duodenal

ulcer perforation .The male :female ratio is 16:1 Male: female ratio ranged

from 2.5 to 1 to 10 to 1 in the study conducted by Ezra Steiger, MD and

Auram M.Cooper man MD considerations in the management of perforated

peptic ulcers.

Blood group: The incidence of duodenal ulcer perforation is common in

patients who are having blood group “O”. They represent 52 % of the cases

studied during the period from 1-6-2007 through December 2008.This finding

is consistent with reports in the literature.

Past history of peptic ulcer: There was past history of peptic ulcer

symptoms of variable duration ranging from 4 months to 12 years in 62 % of

the cases studied in MGM Hospital from 1-6-2007 through 31-12-2008.In 38

% of the cases of duodenal ulcer perforation there was no history of peptic

ulcer. This percentage is similar to the study done by Erza Steiger (M.D.)and

Avram M.cooperman M.D.(Surgical clinic’s of North America vol 56 No.6

December 1976)where 30 to 50 % of patients with perforated duodenal ulcers

had no history of duodenal ulcer disease in the past.ref.no.(25)

91

Strong & Spencer

S.R. Seelay

Glen and Harrison

P.K. Sen

Present study in M.G.M.

Hospital

Year 1950 1952 1952 19451-6-2007 to 31-12-2008

Past history of peptic ulcer percentage

7 % 27 % 12 % 47 % 62 %

Personal History : 58 % of the cases are habituated to smoking ranging

from five years to 30 years .72 % of the cases of duodenal perforation during

the period 1-6-2007 through 31-12-2008 are addicted to alcohol. In 90 % of

the patients take mixed diet with plenty of chillies and spices. History of stress

and strain were present in 85 % patients.

Rice is the commonest staple diet of our patients, all are used to

consume chillies and addicted to alcohol and smoking. It can be inferred that

the use of plenty of chillies predisposes to the development of chronic

duodenal ulcer and a precipitating factor for the duodenal ulcer perforations.

30 to 50 % of patients with perforated duodenal ulcer have no history

of duodenal ulcer disease in the past or ingestion of alcohol or salicylates.

(Surgical clinic’s of North America –vol 56 No.6 December 1976).

Past history of the use of NSAID was present only in 3 % of the 100

duodenal ulcer perforation cases studied in MGM Hospital during the period

from 1-6-2007 through 31-12-2008.history of taking NSAID is not so important

as an etiological factor in our cases.

The NSAID is the main predisposing factor in the west (44 % in Irvin

series) where as in India it is not so as quoted by Dr. S.H. Kulkarni and

Dr.A.Y.Kashirsagar.

Family History of peptic ulcer was present in 35 % of the cases of duodenal

ulcer perforation in M.G.M. Hospital Warangal.

92

Treatmant history :Among the patients of perforated duodenal ulcer with

past history of peptic ulcer disease during the study period 1-6-2007 through

31-12-2008 80 % of patients have taken medical treatment antacids ,H 2

receptor blockers ,proton pump inhibitors etc., for relief of peptic ulcer

symptoms. All of them have taken irregular treatment. The faulty patient’s

compliance seems to be important factor in non healing of ulcer and with

tendency for perforation.

Diagnosis: In all cases diagnosis was made on detailed history and clinical

examination. It is aided by taking plain x-ray in erect posture which revealed

pneumo peritoneum. In 86 % of cases studied during period from 1-6-2007

through 31-12-2008.

Obliteration of liver dullness was present in 76 % to 86 % of our cases.

Shock on admission: 15 % of cases of perforated duodenal ulcer were in

shock at the time of admission.

Operative findings: Quantity of peritoneal fluid aspirated is from 100 to 300

ml in 10 % of the cases studied from 1-6-2007 through 31-12-2008.In 90 % of

cases the quantity of peritoneal fluid varied from 500 ml to 5 litres.

Size of perforation : In 100 cases studied in MGM Hospital Warangal

during the period from 1-6-2007 through 31-112-2008 the size of the

perforation noted was less than 5 mm in 80 % of cases .In 20 % of the cases

the size of perforation was more than 5 mm.

Site of perforation: In 100 cases studied in MGM Hospital Warangal, the

perforation was present in the anterior wall of the first part of duodenum.

Kozol and Meyer (1962) recorded 92% of duodenal ulcer perforations

in the anterior wall of first part of duodenum, 2 % in the posterior wall and 6%

at about pyloro duodenal junction.

93

Operative treatment : In the 100 cases studied during the period from 1-6-

2007 through 31-12-2008 ,96 % of cases were treated with simple closure of

perforation ,sealed with patch of omentum ,2-0 catgut chromic or 2-0 mersilk

was used for closure. Thorough peritoneal toilet was given and corrugated

rubber drain or abdominal drains kept in one or both flanks and the wound is

closed in layers. In 2 % of cases the duodenal ulcer perforation was found to

be sponateousely closed with omentum. In these cases peritoneal toilet was

done and drains were kept wound closed in layers. In the 2 % of cases only

bilateral flank drains were kept under local anaesthesia as the general

condition of the patient is poor with severe shock, and or associated with

cardio vascular disease or renal failure and hence could not perform a

laporotomy for closure of duodenal ulcer perforation.

POST OPERATIVE COMPLICATIONS:

The following are the post operative complications among the 100

cases studied during 1-6-2007 through 31-12-2008 at MGM Hospital

Warangal.

Post operative complications

Percentage of cases

Wound infection 20 %

Stich abscess 10 %

Prolonged ileus 10 %

Pneumonia 5 %

Septicemia 10 %

Wound dehiscence 7 %

Pelvic abscess 3 %

Post operative fever 21 %

94

In the study done by AK Dev, S.Paul, N.Battacharjee and J.Roy

Choudary (Dept. of Surgery North Bengal Medical College ) from West Bengal

(Indian Journal of Surgery 1994: 56 (5) 222-227 - 158 cases were studied.

One or more major post operative complications were present in 41 % of the

cases.26

Post operative

complications

No.of cases

(A.K.Dev et al )

Present study ( MGM

HOSPITAL )

Prolonged ileus 6.96 % 10 %

Pneumonia 6.33 % 5 %

Pleural effusion 3.8 % -

Wound dehiscence 2.53 % 7 %

Septicemia 3.8 % 10 %

Deep vein thrombosis 2.53 % -

Sub phrenic abscess 2.53 % -

Upper GI bleeding 1.9% -

Myocardial infarction 1.9 % -

Cerebro vascular

accident

0.63 % -

Time factor: The time that has elasped between perforation and the

treatment is one of the most important factors in prognosis .The longer the

interval the higher the morbididty and mortality.After 12 hours of dodenal

ulcer perforation death rate rises steeply as quoted by Dr.Rodney Maingot.

95

Time factor between perforation and operation

The time factor between perforation and operation among the 12

presented cases in the dissertation.

Hours elapsed before operation

No.of cases Recovered

No.of cases Dead

Total Mortality

Under 6 hours - - - -

7-12 hours 3 Nil 2 Nil

13-18 hours Nil Nil Nil Nil

19-24 hours 1 Nil 1 Nil

Over 24 hours 8 Nil 8 nil

In the 12 cases presented no death occurred even 72 hours after

duodenal ulcer perforation. In the present study most of the patients have

reported sufficiently late from 18-24 hours or more after the onset of pain ,yet

except in few cases who were moribund at the time of admission, no

significant mortality is observed.

Hospital stay: In our study 86 % of the patients stayed in the hospital for a

period of 7-15 days the average stay being 11 days only.6 % of patients

stayed for about one to one and half months period because of postoperative

complications.

MORTALITY:

Sex: The mortality is more in men than in Women Christopher Wastell in his

series has recorded that out of 80 females only one died (1.25 %)and out

of 453 males there were 41 (9%) deaths.

96

Total number of deaths during the study period in males and females is

as follows.

Male Female

Total No. of patients 94 6

Total No. of dead

Patients

7 2

Mortality rate is found to be 7.44% in males and 33.33 5 in females in

the present study. This is because of lower incidence of the problem in

females when compared to males.

At MGM Hospital Warangal the mortality rate is 6% in duodenal ulcer

perforation cases during the period from 1-6-2007 through 31-12-

2008.Mortality rate was 14 % in a study conducted at MGM Hospital in the

year 1994.

The duodenal ulcer perforation is a very serious condition and

invariably fatal if not properly managed.

Mortality for simple closure for simple duodenal perforation was 5 % in

a study of 171 cases of perforated duodenal ulcers done by A.K.Dev, .S.Paul,

N.Bhattacharjee and J.Roy Chowdary, Dr. S.H.Kulkarni and A.Y.Kshirsagar

study on simple closure of perforated duodenal ulcer, the mortality was 7.5

%.27

The mortality noted in the present study is similar to that studied by the

workers in other parts of the country as mentioned above.

97

98

CONCLUSIONS

1. A general survey of surgical anatomy, Physiology and Pathology of

stomach has been presented.

2. A general survey of etiology and pathogenesis of acute duodenal ulcer

perforation has been made.

3. A detailed study and analysis of the duodenal ulcer perforations during

the period from 1-6-2007 through 31-12-2008 about 100 cases from

MGM Hospital has been made.

4. Of the 100 cases of duodenal ulcer perforations in the prospective

study, 12 cases are here by presented for the purpose of dissertation.

5. The incidence of duodenal ulcer perforation at MGM Hospital,

Warangal has been worked out to be 2.7%.

6. Dodenal ulcer perforation is commonly seen in 5th decade of life.76 %

of the cases in the age group of 20 to 49 years.

7. The youngest patient of duodenal ulcer perforation was 11 years old

and the oldest patient was 70 years old.

8. It is predominently seen in male population. Male: Female ratio is 16:1.

9. Duodenal ulcer perforation is more commonly seen in people who are

having blood group “O“ constituting 52 % of the total.

10. Past history of peptic ulcer was present in 62 % of cases of duodenal

ulcer perforation.

11. 58 % of the cases are addicted to chronic smoking and 72 %of the

cases are addicted to alcohol.

99

12. Family history of peptic ulcer was present in 35 % of the cases of

duodenal ulcer perforation.

13. 90 % patients consume diet with plenty of chillies and spices.

14. Out of 62% of cases with past history of duodenal ulcer, 80% of

patients had taken medical treatment with antacids and H 2 receptor

blockers, proton pump inhibitors drugs irregularly.

15. In the all the cases the diagnosis was made on clinical history and

physical examination of abdomen and aided by plain X-ray abdomen in

erect posture which showed pneumom peritoneum in 86 % of cases of

duodenal ulcer perforations.

16. Obliteration of liver dullness was present in 76 % to 86 % of our cases.

17. 15 % of the cases of perforated duodenal ulcer were in shock at the

time of admission.

18. The size of perforation is less than 5 mm in 80 % of cases. In only 2

cases the size was more than 10 mm, in 18 % of cases the size was 5

to 10 mm.

19. The site of perforation in all cases is present on the anterior wall of first

part of duodenum.

20. History of taking NSAID is not so important an etiological factor in our

study.

21. In 98 % of the cases, the operative procedure adopted is simple

closure of the perforation the omental patch.

22. The longer the time interval between perforation of duodenal ulcer and

the operation, morbidity and mortality high.

23. During the post operative period 90 % of patients recovered from

paralytic ileus with in 48 hours.

100

24. Post operative complications are seen in 24 % of cases.

25. The average hospital stay after surgery for dudenal ulcer perforation

was 11 days.

26. At MGM Hospital, Warangal 100 cases of duodenal ulcer perforation

studied from 1-6-2007 through 31-12-2008, the mortality rate is 6 %.

27. There is marked reduction in the overall mortality at MGM Hospital

Warangal compared to previous studies.

101

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