Professional Documents
Culture Documents
1
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.
2
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.
3
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:
VENOUS DRAINAGE: The veins accompany arteries and drain into portal
vein either directly of indirectly through splenic or superior mesenteric veins.
LYMPHATIC DRAINAGE
(1) The lymphatics of upper right 2/3rds of the stomach along the lesser
4
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 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.
5
These nerves play major role in intermittent propulsion of gastric
contents by the antrum through the pyloric canal into the duodenim.
STRUCTURE:
6
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.
DUODENUM:
7
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:
VENOUS DRAINAGE:
The veins accompany the arteries and drain into the portal system via
the splenic and superior mesenteric veins.
NERVE SUPPLY:
8
GASTRIC PHYSIOLOGY IN RELATION TO PEPTIC ULCER 5,6,7
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.
9
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.
10
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.
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.
11
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.
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.
12
For descriptive purposes the process the process is divided into three
phases, 1) Cephalic Phase, 2) Gastric phase, 3) Internal phase.
13
INCIDENCE
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.
14
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.
15
ETIOLOGY
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.
16
b) Role of Gastric Hyperacidity 9:
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.
17
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:
18
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.
19
PATHOLOGY
Duodenal ulcers that perforate into the general peritoneal cavity are
situated on the anterior or anterosuperior wall of duodenum or at the
pyloroduodenal junction.
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).
20
Distention by meal may thus cause is in duodenal tissue tension with
submucosal ischaemia and localized susceptibility to attack by acid and ulcer
production.
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.
21
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.
PATHOLOGY OF PERITONITIS:
22
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).
i) Direct Infection
Via perforation of part of gastrointestinal tract.
Through the penetrating would of abdominal wall.
Post operative infections.
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.).
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.
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.
25
PATHOLOGY OF PAIN
Rose theory postulated that pain from abdominal viscera was of two
types. 1) Referred (somatic) pain, 2) True visceral or splanchnic 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.
27
CLINICAL ASPECTS OF DUODENAL ULCER PERFORATION
TYPES OF PERFORATION:
From the moment of perforation, the clinical course can be divided into
three stages, each of variable duration.
28
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
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.
29
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.
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.
30
DIAGNOSIS:
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.
31
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:
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.
ABDOMINAL EXAMINATION 15
32
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.
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.
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).
33
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).
DIFFERENTIAL DIAGNOSIS 16
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.
I) Surgical Management
Conservative treatment
35
Pre-operative Management
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.
ii) Patient anxiety and pain should be relieved by sedation as soon as the
diagnosis is confirmed.
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.
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.
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.
v) The patient is brought to the hospital late for surgery, usually 24 hours
after perforation.
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.
ix) The operation presents with great technical difficulties, e.g. obese
patients etc.
ADVANTAGES:
I) It is simple operation
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.
38
iv) The strain of patients in subjecting themselves to second operation
either for the Reperforation or duodenal ulcer treatment.
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.
39
Post-operative Management: The treatment should include
Post-operative Complications
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.
Indications:
2) Young patients.
41
Advantages:
Disadvantages:
42
corrugated rubber drain kept in right flank, complete haemostasis secured,
the abdomen is closed in layers.
Conservative Management 21
Indications
4) When the patient is seen for the first time some days after
perforation and with sufficient evidence that the infection is
localized.
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.
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.
44
PROGNOSIS 23,24
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.
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).
45
46
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49
50
51
52
53
54
55
56
57
58
59
60
61
62
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81
PHOTOGRAPHS
82
X-Ray Erect abdomen showing gas under diaphragm
83
Operative view of Duodenal Ulcer Perforation
84
Laparoscopic view of Duodenal Ulcer Perforation
85
ANALYSIS OF DATA
Table – 1
Total No.
Total number Total No. of
of cases
of cases duodenal Percentage
YEAR admitted in
admitted in ulcer %
MGMH,
surgical wards perforations
Wgl
2007 23,016 3369 94 2.79%
2008 23,276 3458 96 2.78%
2009
24,133 3391 102 3%
(upto Oct.)
Table -2
86
Table -3
Sl. No. of
Surgical Problems Percentage
No. cases
1 Acute appendicitis 719 56.88 %
2 Intestinal obstruction 229 18.12%
(including obstructed hernia )
3 Perforated duodenal ulcer 190 15.03 %
4 Peritonitis excluding duodenal ulcer 70 5.54 %
perforation
5 Others 56 4.43 %
Total No. of cases 1264 100 %
Table -4
Total number
Age group in years
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
Table -5
87
Sex distribution of duodenal ulcer perforation during the period from
1-6-2007 through 31-12-2008 from 100 cases studied.
Total number of
Male Female
cases
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
Table – 6
Total No. of
Blood group Rh factor
cases
O + 52
A + 10
B + 14
AB + 24
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 12
Size of
duodenal 3mm 5mm 4mm 15mm 5mm 10mm 10mm 3mm 3mm 10mm 3mm 4mm
ulcer
perforation
89
DISCUSSION
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.
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
Present
Strong & S.R. Glen and P.K. study in
Spencer Seelay Harrison Sen M.G.M.
Hospital
1-6-2007 to
Year 1950 1952 1952 1945
31-12-2008
Past history of
peptic ulcer 7% 27 % 12 % 47 % 62 %
percentage
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.
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.
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.
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.
The following are the post operative complications among the 100
cases studied during 1-6-2007 through 31-12-2008 at MGM Hospital
Warangal.
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
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
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 7 2
Patients
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
Distribution of Duodenal ulcer perforation
in Age Groups
40
35
30
No.of cases
25 Below 20 yrs
20 20-30yrs
15 30-40yrs
10 40-50yrs
5 50-60yrs
0 60-80yrs
Age Group
100 cases
50
40
No.of cases
30 O
A
20
B
10
AB
0
BLOOD
GROUPS
100 cases
98
CONCLUSIONS
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.
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.
19. The site of perforation in all cases is present on the anterior wall of first
part of duodenum.
22. The longer the time interval between perforation of duodenal ulcer and
the operation, morbidity and mortality high.
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.
101
BIBILOGRAPHY
11. Ulcer and anti inflammatory agents Mitchell W.S. et al., Br.M.J.1982
March.6.284.
102
17. Maingot’s abdominal operations 10thedition.Vol.I
23. Factors influencing the Mortality Morbidity perforated peptic ulcer Belma
Kocher; Suleyman Surmeli; Cem Solak; Journ. of Gastroenterology and
Hepatology;Pub05/10/2007.
103
28. Bailey & Love‘s short practice of surgery revised by Charles
V.mann,R.C.G.Russel; Normal S Williams,25th edition.
104