PERFORATED PEPTIC ULCER PERFORATION DEFINITION It is the terminology used for perforation of duodenal ulcer or gastric ulcer or stomal ulcer. Otherwise all clinical features and management are similar. Perforation is common in duodenal ulcer Mortality is more in gastric ulcer perforation and perforation in elderly

1. en love da Homoeopathy
PERFORATED
PEPTIC ULCER

2. PERFORATED
PEPTIC ULCER

3. PERFORATEDPEPTICULCER
PERFORATION
DEFINITION
• It is the terminology usedfor
perforationof duodenal
ulcer or gastric ulcer or
stomal ulcer.
• Otherwise all clinical
features and management
are similar.
• Perforationis common in
duodenal ulcer
• Mortality is more in gastric
ulcer perforation and
perforationin elderly

4. DUODENALULCER
PERFORATEDDUODENAL
ULCER
• It is common in males (8:1)
between35–45years of age
group, but can occur in any
age group.
• In 80% of cases, thereis a
history of chronic DU.
• In 20% cases, it is silent
perforation.
• Perforationcan occur in
acuteulcers or in acute
presentation of a pre-
existing chroniculcer.
• Perforationmay be
precipitatedby steroids,
analgesics (NSAIDs),
alcohol, antimalarials.
• Overall incidence is 5%.
• Active ulcers perforate
commonly.
• Duodenal ulcer with H.
pylori infection causes
perforationmore
commonly, especially in
young individual
• NSAID-induced ulcer
causes perforation in
elderly.

5. • Mortality in perforated
duodenal ulcer is 10% (in
gastriculcer it is more—
20%).
STAGESOF PERFORATION
Stage of chemical peritonitis:
• Once perforationoccurs
↓
stomachcontents escape into
theperitoneal cavity
↓
The acidfromthe stomach
causes chemical peritonitis
↓
leading to severe painin
epigastric region, vomiting,
tenderness, guarding, rigidity,
tachycardia, sweating.
Stage of reaction (Stage of
illusion):
• Peritoneumsecretes lots of
fluid
↓
to neutralisethe escaped content
↓
and so temporarily the pain
reduces,

6. ↓
and the patient feels better.
↓
This phaselasts for about 6
hours.
Stage of diffusebacterial
peritonitis:
• After about six hours,
bacteria fromGIT
(escape) migrate from
the site of perforation
causing diffuse
peritonitis
CLINICALFEATURES
PAIN
• Severe persistent painin the
epigastriuminitially,
• later in the right side
abdomen(as the
inflammatoryfluidspills
along the right paracolic
gutter)
• and finally becomes
generalised.
• Painis of sudden in onset, is
due to contact of expelled
gastriccontents with the
parietal peritoneum.

7. • Painoftenradiates to right
scapular region.
• Painbecomes more on
movements
TENDERNESS
• Tenderness and rebound
tendernessis seen
(Blumberg sign) all over
the abdomen.
OTHERS
• Fever
• Vomiting
• Dehydration
• oliguria occurs.
• Patient is toxic, with
tachycardia, hypotension,
tachypnoea.
• Abdominal distension
occurs.
• Guarding and rigidity,
initially in the epigastrium
but later all overthe
abdomen
• Dullness over the flank
becauseof fluid.
• Obliteration of liver
dullness—as a result of
collection of escaped gas
under the diaphragm.

8. • Silent abdomenwith
absence of bowel
sounds.
• Tenderness felt on per
rectal examination.
• Oftenslow, small
perforationpresents
with subacute features,
but diffuse peritonitis
eventually sets in 24–48
hours.
• Sometimes fluid from
supracolicregion
↓
slowly trickles down along the
rightparacolic gutter
↓
and collects in right iliacregion
↓
causing painand tendernessin
RIF
↓
mimicking appendicitis.

9. • Terminal stage:
• Oliguria
• Septicaemia
• Shock
• Hippocratic facies
(sunkeneyes, cold
periphery and shallow
rapidbreathing, ill look)
• with MODS (Multiorgan
dysfunctionsyndrome).
INVESTIGATION
• Chest X-ray with abdomen
in erect posture (plainX-
ray):
• Shows gas under
diaphragmin 70% of
cases. In 30%of cases,
there is no gas under
diaphragm
• Ultrasoundabdomen
shows free fluidand often
gas.
• Blood urea, serum
creatinine, total count,
electrolytes, are helpful.

10. • CT scanabdomenis very
sensitive investigation
whenever there is absence of
gas under diaphragm. It
rules out other conditions
like pancreatitis.
Gastrograffinupper GI
studyalso confirms the
perforation.
DIFFERENTIAL DIAGNOSIS
• Acute appendicitis™
• Acute pancreatitis ™
• Acute cholecystitis ™
• Ruptured aortic aneurysm™
• Myocardial infarction™
• Mesentericischaemia™
• Pneumonia

11. TREATMENT
• Patient is advisedadmission.
• IV fluids—Ringer lactate,
normal saline, dextrose
saline.
• Antibiotics—Cefotaxime,
metronidazole, amikacin.
• Catheterisation.
• Ryle’s tube aspiration.
SURGERY
• Emergency laparotomy
through upper midline
incisionis done.
• All infected fluid is sucked
out.
• Perforationis identified
and closedwith
interrupted, horizontal
sutures using either silk or
vicryl.
• Omental patch is placed
before suturing—it is
called as Rosoe-Graham
Operation

12. • Peritoneal wash (toilet)
using 5–10litres of saline is
given.
• Drainis placedand
abdomenis closed, oftenif
required withtension
sutures.
GASTRICULCER.
PERFORATEDGASTRIC
ULCER
• Commonly ulcer in the
lesser curve near the antrum
perforates.
• Amount of gas escaped is
more than theperforated
DU.
• Malignancy shouldalways
be suspectedand so biopsy
fromthe edgeis a must.
• Mortality in gastriculcer
perforationis high (20%).

13. • Commonly they are
prepyloricin position.
• Primary closure with an
edge biopsyis commonly
used.
• Distal gastrectomy,
including ulcer area is
better optionif patient’s
general condition is
favourable.
• Posterior gastriculcer
perforationis often
difficult to diagnoseboth
clinicallyand
radiologically.
XRAY SIGNS
Different signs in X-ray in
perforation™
• Cupola sign—crescent
shaped radiolucencyunder
thediaphragm ™
• Riglers sign—visualisation
of bothaspects of the bowel
wall being outlinedby gas
on either side ™
• Inverted V sign—gas on
either sides of the falciform
ligament ™

14. • Football sign—collectionof
gas in the center of the
abdomenlike a foot ball ™
• Triangle sign—gas between
bowel loops
AETIOLOGY
• Common in people with
blood group O +ve.
• Stress, anxiety—‘hurry,
worry, curry’.
• Helicobacter pylori infection
is an important aetiology for
duodenal ulcer (90%).
• NSAIDs, steroids.
• Endocrine causes: Zollinger-
Ellison syndrome, MEN
syndrome,
hyperparathyroidism.
• Other causes:Alcohol,
smoking, vitamindefi
ciency.
• Dragstedt dictum: “No acid
– No ulcer

15. PATHOLOGY
• Ulcer occurs in the first part
of duodenum
↓
usually with in the first inch,
↓
involving the muscular layer
↓
Sites:
a. In the bulb (bulbar)—95%.
b. b. Post-bulbar (5%).
↓
Eventually it shows cicatrisation
causing pyloricstenosis.
↓
Serosaoverlying the site of
duodenal ulcer
↓
shows petechial haemorrhages
with speckled red dots
↓
appearing like sprinkled
cayenne pepper
↓
Microscopically, ulcer with
chronic inflammation
↓
withgranulation tissue

16. ↓
gastricmetaplasia of duodenal
mucosa, endarteritis obliterans
are visualised.
↓
Sometimes two opposing ulcers,
i.e. over anterior and posterior
surfaces of duodenumare
present and are called as kissing
ulcers.
↓
An anterior ulcer perforates
commonly, posterior ulcer bleeds
or penetrates commonly.
CLINICALFEATURES
• Water-brash, heartburn,
vomiting may be present.
• Melaenais more common,
haematemesis also can
occur.
• Appetiteis good and there is
gain in weight. It decreases
oncestenosis develops.
• Eats more frequently without
any restriction.
• Chronicduodenal ulcer can
be uncomplicatedor
complicated.

17. Gastric
ulcer
Duodenal
ulcer
Painafter
food intake
Painbefore
food intake
Periodicity
less
common
Periodicity
more
common
DIFFERENCE
• Differences between clinical
features of gastriculcer and
duodenal ulcer
Haemateme
sis more
common
Malaena more
common
Weight loss
occurs
Weight gain
occurs
Equal in
bothsexes
Common in
males

18. COMPLICATION
1. Pyloric stenosis: Due to
scarring and cicatrisation of
first part of the duodenum.
2. Bleeding (10%).
3. Perforation(5%). Both
acuteand chronic ulcers
can perforate. Anterior
ulcers perforate.
4. Residual abscess.
5. Penetrationto pancreas.
INVESTIGATION
Bariummeal X-ray
• shows deformedor absence
of duodenal cap (becauseof
spasm).
• Appearanceof ‘trifoliate’
duodenum is due to
secondary duodenal
diverticula
• whichoccurs as a result of
scarring of ulcer.

19. Gastroscopy
• reveals the type, location
of ulcer, narrowing if any.
• Biopsy also can be taken
to look for the presence of
Helicobacter pylori.
• Usually biopsies are
takenfromduodenum,
pylorus, antrum, body,
fundus, and confirmed
by rapidurease test or
C13 or C14breathtests.
• Estimationof serum
gastrin level, serum
calciumlevel.
DIFFERENTIAL DIAGNOSIS
• Carcinoma stomach
(pylorus)™
• Dyspepsia due to other
causes
• Hiatus hernia
• Oesophagitis
• Cholecystitis
• Chronicpancreatitis

20. Aim of therapy:
• To relieve symptoms; to
heal ulcer; to prevent
recurrence.
I. General measures:
• Avoid alcohol,
NSAIDs, smoking,
spicy foods
• Have more frequent
food.
II. Specific measures:
• Intragastric pH should be
maintainedabove 5.
• Drugs
1. H2 Blockers
2. Proton-pumpinhibitors
3. Antacids:
• Neutralises the HCl to form
water and salt and also
inhibits peptic activity.
• Aluminiumhydroxideand
magnesiumtrisilicate are
commonly used.
• Dose is 2 grams 2 hours
after food.

21. 4.Sucralfate
• It is an aluminiumsalt of
sulfatedsucrose
• whichprovides a protective
coat to ulcer crater thereby
promotes healing.
• It inhibits peptic activity.
5. Anti-Helicobacter pylori
regime:
• It is veryuseful, givenfor 7–
14 days—later the proton-
pump inhibitors are
continued.
• Triple or quadruple
(tetracycline, bismuth,
tinidazole, pantoprazole)
regimes are used
6. Colloidbismuth sulphateis a
good drug for ulcer
7. Misoprostol (200 mg tid) is
the only prostaglandin agonist
accepted

22. SURGERY
• Highlyselective vagotomy
(HSV).
• Selective vagotomy with
pyloroplasty(SV+ P).
• Truncal vagotomywith
gastrojejunostomy (TV + GJ).
• Posterior truncal vagotomy
with anteriorseromyo
tomy—Taylor’s operation.
• It can be done through
laparoscopy.
• Vagotomy with antrectomy
• Posterior truncal vagotomy
• Linear gastrectomy with
posterior truncal vagotomy
through laparoscopy.
REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

23. A
Special Thanks
To A Very
Special Doctor