PERFORATED PEPTIC ULCER

DR. ANBIAR MANJAS, SP.B-KBD

DEFINITION
A peptic ulcer is a mucosal defect which
penetrates the muscularis mucosae and
muscularis propria

Produced by acid-pepsin aggression.

PEPTIC ULCER DISEASE
PUD
70-90% of ulcers are associated with Helicobacter
pylori a spiral-shaped bacterium that lives in the
acidic environment of the stomach.

Ulcers can also be caused or worsened by drugs such

as Aspirin, Plavix, NSAIDs
PEPTIC ULCER DISEASE
PUD

More peptic ulcers arise in the duodenum rather than in the

stomach.

About 4% of stomach ulcers are caused by a malignant tumor,

so multiple biopsies are needed to exclude cancer.

Duodenal ulcers are generally benign.

CLASSIFICATION

By Region/Location
-Stomach
-Duodenum
-Esophagus
-Meckels Diverticulum
MODIFIED JOHNSON CLASSIFICATION OF
PEPTIC ULCERS

Type I: Ulcer along the body of the stomach, most

often along the lesser curve at incisura angularis
along the locus minoris resistentiae.

Type II: Ulcer in the body in combination with

duodenal ulcers. Associated with acid
oversecretion.
MODIFIED JOHNSON CLASSIFICATION OF
PEPTIC ULCERS

Type III: In the pyloric channel within 3 cm of pylorus.

Associated with acid oversecretion.

Type IV: Proximal gastroesophageal ulcer

Type V: Can occur throughout the stomach. Associated with

chronic NSAID use .
SYMPTOMS

Usually, children and the elderly do not develop

any symptoms unless complications have arisen.
COMPLICATIONS
Upper digestive bleeding is the most common complication.

Sudden large bleeding can be life-threatening.

It occurs when the ulcer erodes one of the blood vessels, such
as the gastroduodenal artery.
COMPLICATIONS
Perforation often leads to catastrophic consequences.
Erosion of the gastro-intestinal wall by the ulcer leads to
spillage of stomach or intestinal content into the abdominal
cavity.
Perforation at the anterior surface of the stomach leads to
acute peritonitis, initially chemical and later bacterial
peritonitis. The first sign is often sudden intense abdominal pain.
Posterior wall perforation leads to pancreatitis; pain in this
situation often radiates to the back.
Perforation in the CBD- aerobilia, colangitis
COMPLICATIONS
Penetration is when the ulcer continues into
adjacent organs such as the liver and pancreas.
Gastric outlet obstruction - scarring and swelling
due to ulcers causes pyloric narrowing. Patient
often presents with severe vomiting.
Cancer is included in the differential diagnosis
(elucidated by biopsy), Helicobacter pilory as the
etiological factor making it 3 to 6 times more
likely to develop stomach cancer from the ulcer.
DIFFERENTIAL DIAGNOSIS OF EPIGASTRIC
PAIN
Peptic ulcer
Gastritis
Stomach cancer
Gastroesophageal reflux disease
Pancreatitis
Hepatic congestion
Cholecystitis
Biliary colic
Inferior myocardial infarction
Referred pain: pleuresy, pericarditis
Superior mesenteric artery syndrome
PERFORATED PEPTIC ULCER
The first report of a series of patients presenting with
perforation of a duodenal ulcer was made in 1817 by
Travers.

The earliest operative description was made by Mikulicz in

1884 but the first successful operation for a perforated
duodenal ulcer was not until 1894.
PPU patients - various treatment protocols:
- an expanded role for non-operative treatment,
- a developing role for laparoscopic surgery
- more precise identification of those patients
suitable for immediate definitive ulcer
management.
PATHOGENESIS AND EPIDEMIOLOGY
PPU
Perforation complicates DU about 1/2 as often as
bleeding
Most perforated ulcers are on the anterior surface of
the duodenum.

The patient population tends to be elderly (mean age

6070), chronically ill patients often (4050%) taking
ulcerogenic medication.
PATHOGENESIS AND EPIDEMIOLOGY
The fall in admissions for uncomplicated duodenal
ulcers noted since the 1970's is largely attributed to
the introduction of H2 antagonists.
In the third world the clinical picture is different:
a high male : female ratio (approximately 8 : 1),
younger age
a strong link with cigarette smoking.

In addition in the third world there is a high incidence

of patients who present late - accounting for the high
mortality (20%)
PATHOGENESIS AND EPIDEMIOLOGY
Helicobacter pylori is implicated in 7092% of all
PPU

The second most common cause of perforated

duodenal ulcer is the ingestion of NSADs.

The least common cause is pathologic hypersecretory

states, such as Zollinger-Ellison syndrome, although
these should be considered in all cases of recurrent
ulcer after adequate treatment.
PATHOGENESIS AND EPIDEMIOLOGY

In the modern treatment of PDU it must be born in mind

that appropriate treatment of H. pylori infection results in
eradication of the bacteria and healing of uncomplicated
ulcers in more than 90% of cases.

Therefore, in the majority of cases duodenal ulcer may be

regarded as a curable infectious disease or related to the
ingestion of an ulcerogenic drug.
DIAGNOSIS
The most characteristic symptom is the suddenness
of the onset of epigastric pain.

The pain rapidly becomes generalised although

occasionally it moves to the RLQ.

The patient stays still.

DIAGNOSIS
There may be a history of previous dyspepsia, previous or
current treatment for a DU, or ingestion of NSADs.
On examination the patient is in obvious pain.
Hypotension is a late finding as is a high fever.
The abdominal findings are characteristically described as
of board-like rigidity.
DIAGNOSIS
With time the patient may improve with dilution
of the duodenal contents by exudate from the
peritoneum but this is later replaced by the signs
and symptoms of bacterial peritonitis.

Once an ulcer perforates, the subsequent clinical

picture is influenced by whether or not the ulcer
self seals.
DIAGNOSIS
In approximately 4050% of cases the ulcer self-seals
with omentum or by fusion of the duodenum to the
underside of the liver between the gallbladder and the
falciform ligament.

This is important when one considers whether or not

laparotomy is indicated to deal with the perforation itself
as will be seen below.

On an erect Chest X Ray free air can be seen in about

80% of cases.
 DIAGNOSIS
In doubtful cases a water-soluble gastroduodenogram will show the
leak from the duodenum or its sealing.

This can be a useful test when one is considering non-operative

treatment or in the situation where the diagnosis is in doubt.
WHAT IS THE TYPICAL PRESENTATION IN
PATIENTS WITH PERFORATED PEPTIC ULCER?
Studies have shown that of patients presenting with
complicated peptic ulcer disease (PUD), nearly half have no
history of the disease.

In younger patients, severe abdominal pain, which may

radiate to the shoulder, may be the initial presentation.

In elderly patients, signs and symptoms may be minimal.

WHAT IS THE TYPICAL PRESENTATION IN
PATIENTS WITH PERFORATED PEPTIC ULCER?

Other reported symptoms were dyspepsia, anorexia,

nausea, and vomiting.

Duration of symptoms ranged from 4 hours to 10 days.

WHAT ROLE DO X-RAYS AND LABORATORY TESTS
PLAY IN THE DIAGNOSIS OF PERFORATED PEPTIC
ULCER?

Plain x-rays of the abdomen with the patient in the

upright position have been used in diagnosing perforated
ulcer. However, several case series have shown that in
30% to 50% of patients, the x-ray may be negative for
free air, particularly in the elderly.

Similarly, use of water-soluble contrast medium with an

upper gastrointestinal tract series or computed
tomography scan may increase the diagnostic yield.
HOW COMMON IS PERFORATED PEPTIC ULCER?
Thanks to effective medical management with H2 blockers and
proton pump inhibitors and the eradication of H. pylori, the incidence
of PUD and the hospitalization rate for treatment have decreased.
However, the rate of complicated PUD appears to be unchanged.

For example, there was a 39.3% decrease in the hospitalization

rate for PUD at Massachusetts General Hospital during the years
after the introduction of cimetidine.

During that same period of time, however, the incidence of

perforated peptic ulcer stayed the same.
RISK STRATIFICATION
Mortality from PPU is dependant upon the presence or
absence of several risk factors.
Individual risk can also be assessed by use of APACHE II.
Overall mortality is approximately 10% in most studies.
Those in whom the diagnosis is overlooked almost always die.
Risk factors affecting prognosis are:
delayed treatment (> 24 hours),
preoperative shock (BP < 100 mmHg),
concurrent serious medical illness.

When all three are present the mortality rises to 100%.

WHAT ARE THE RISK FACTORS FOR PUD AND
PERFORATION?

In recent years, patients presenting with perforated PUD

have tended to be:
elderly,
chronically ill,
taking one or more ulcerogenic drugs.
WHAT ARE THE POTENTIAL COMPLICATIONS
OF PERFORATED PEPTIC ULCER?
In most cases of perforation, gastric and duodenal content leaks
into the peritoneum.

This content includes gastric and duodenal secretions, bile,

ingested food, and swallowed bacteria.
The leakage results in peritonitis, with an increased risk of
infection and abscess formation.
Subsequent third-spacing of fluid in the peritoneal cavity due to
perforation and peritonitis leads to inadequate circulatory
volume, hypotension, and decreased urine output.

In more severe cases, shock may develop.

WHAT ARE THE POTENTIAL COMPLICATIONS
OF PERFORATED PEPTIC ULCER?
Abdominal distension as a result of peritonitis and
subsequent ileus may interfere with diaphragmatic
movement, impairing expansion of the lung bases.

Eventually, atelectasis develops, which may compromise

oxygenation of the blood, particularly in patients with
coexisting lung disease.
NON SURGICAL TREATMENT

In 1935 Wangensteen noted that ulcers are able to self

seal and reported on seven cases treated without
surgery.

In 1946 this observation was confirmed by Taylor and he

treated 28 cases without surgery with good success.

This was in the context of the high mortality and

morbidity associated with surgical management at the
time.
NON SURGICAL TREATMENT

Subsequent work showed that a water-soluble contrast

study could confidently demonstrate the presence of self-
sealing in 4050% of cases.

In 1989 a trial from Hong Kong by Crofts et al. showed

that non-operative treatment for PPU was accompanied
by a low mortality rate and was not associated with a
large number of complications when the
gastroduodenogram documented a sealed perforation .
In practical terms, when the diagnosis of a perforated
duodenal ulcer is established the patient is aggressively
resuscitated, nasogastric suction begun, and broad
spectrum antibiotic cover instituted.
If a tension pneumoperitoneum embarrasses respiration
this can be aspirated to release the pneumoperitoneum.
A gastroduodenogram is performed to confirm self-
sealing.
The peritonitis should resolve in 4 to 6 hours and if there is
continued major fluid loss after this time or if there are
progressive signs of peritonitis or increasing
pneumoperitoneum then surgical intervention is required
 NON SURGICAL TREATMENT
In the study by Crofts they carefully selected patients under the age of
70 who were haemodynamically stable, had been perforated for less
than 24 hours, and could be closely monitored.
Using these criteria 70% of patients were selected to be randomized to
be treated in this way.
Despite this encouraging report, and a number of other non-
randomised studies, non-operative treatment of PPU has not become
popular.
Non-operative management has not been widely adopted probably
due to problems with repeated review by senior surgeons, problems
with misdiagnosis, and the lack of opportunity to perform definitive
ulcer surgery.
 LAPAROSCOPIC SURGERY

The traditional management of a perforated duodenal ulcer has been

a Graham Omental Patch and a thorough abdominal lavage.
More recently this has been shown to be able to performed using a
laparoscope. The only proven advantage of the laparoscopic
technique appears to be decreased postoperative pain.
Operating times are longer compared to open techniques and
hospital time appears to be similar to conventional treatment.
This technique has not been subjected to any large prospective trials
and at present must not be considered as standard management.
IMMEDIATE DEFINITIVE SURGERY
Over the last one hundred years a number of attempts have been
made to improve upon the results of simple closure and lavage.
This has been in response to the large number of patients (25
85%) who continue to have symptoms attributable to their ulcer
diathesis after surgery.
The incidence of ulcer symptoms, in most studies, is related to
whether the ulcer is acute or chronic (history greater than 3
months) as judged by preoperative history.
Patients with chronic ulcer symptoms generally have a higher
incidence of subsequent recurrent ulcers. Up to 71% come to
require subsequent definitive surgery although in most studies the
figure is considerably less than this.
PATHOGENIC SURGERY
There is good evidence that, in the emergency situation, highly
selective vagotomy (proximal gastric, or parietal cell
vagotomy) combined with simple omental patch closure of the
perforation, in patients without the risk factors mentioned
above, is just as effective as that performed in the elective
setting (Grade C).

This is associated with a less than 1% mortality rate and a 4

11% ulcer recurrence rate. The success of this operation is
surgeon-dependent.
Truncal vagotomy with drainage has its advocates as an
expedient operation familiar to most surgeons.
IMMEDIATE DEFINITIVE SURGERY

Immediate definitive ulcer surgery has not gained widespread

popularity due to an unfounded feeling that it is associated with a
higher mortality than simple closure.
Many agree that an appropriate approach is to select only those
with a chronic history (> 3 months) and without preoperative risk
factors for immediate definitive surgery.
A major difficulty is defining preoperatively the patients who truly
have a chronic ulcer history as many patients are too unwell to give a
reliable history.
In addition, many ulcers have a silent ulcer history with as many as
70% of perforations occurring as the first manifestation of the ulcer
diathesis.
It must be recalled, however, that in the developed world the surgeon's major role in
the management of PPU will continue to be the performance of lifesaving operations
in elderly unfit patients
CONSERVATIVE TREATMENT

There has been a return to the use of simple omental patch closure since
the late 1970's with the introduction of post-operative H2 antagonists
and more recently Proton Pump Blockers.
Over the last 10 years this trend has only grown stronger due to the
discovery of the role of H. pylori in the pathogenesis of duodenal ulcer.
Given that H. pylori is able to be implicated in up to 90% of perforated
duodenal ulcers it would seem logical to utilise patch closure and
subsequent antibiotic treatment of the infectious agent saving definitive
surgical ulcer management for those who fail this regimen. This has
recently been tested in a randomiced controlled trial from Hong Kong
where it was found that simple dosure of duoderal ulcer perforation with
eradication of H. pylori resulted in ulcer healing in 78% of patients with
only a 48% recurrence rate at one year (Grade A).
CONSERVATIVE TREATMENT

The counter argument is that PPU patients represent a

subgroup of patients with a very vigorous ulcer diathesis
and simple closure of the ulcer and treatment of the
infecting organisms may not be adequate.

Until further clinical trials are performed in relevant

population groups we will not know the definitve answer.
 THERAPY FOR H. PYLORI
The most effective present first line regimen for eradicating H. pylori, with
approximately 90% eradication rates, is a combination of Bismuth, Metronidazole and
Amoxycillin or Tetracycline given for a period of 14 days with or without proton
pumpblocker (Grade A/B).
It is important to check for eradication, as resistance is developing to the first line
regimens, especially in the third world. Tests to confirm eradication include endoscopy
and biopsy and non invasive tests such as serology or breath testing for urea.
At present it would seem prudent to perform a post-operative endoscopy to confirm H.
pylori eradication, confirm the diagnosis, and to check ulcer healing.
If H. pylori is eradicated the risk of reinfection is low, in the order of 1% per year, and
the ulcer is likely to heal. If the ulcer heals there is no role for continuing with antisec-
retory drugs. If the patient needs to continue Non Steroidal Antiinflammatories the most
effective prophylactic drug is Misoprostol (Grade B).
TREATMENT

The present management of perforated duodenal ulcer is in flux. The great

debates of earlier in the century regarding simple patch closure versus
immediate definitive surgery have been complicated by the arguments for
and against laparotomy, the introduction of laparoscopy, and the discovery
of the role of H. pylori.
Faced with a patient with a perforated duodenal ulcer the surgeon should
bear in mind the role of non-operative treatment in the first instance. If this
option is selected the patient will require close vigilance and a readiness to
intervene at any moment that the patient shows signs of deterioration or
failure to progress satisfactorily (Grade A).
If operative management is considered to be indicated, the evidence at
present supports simple omental patch closure and lavage followed by
antibiotic treatment for H. pylori (Grade A). If the patient remains with an
ulcer after surgery and H. pylori eradication then a Highly Selective
Vagotomy should be performed after exclusion of a pathological
hypersecretory state (Grade C).
TREATMENT

In the rare case of a patient who has been investigated and found to be
negative for H. pylori , or who has been treated and then perforated,
immediate definitive ulcer surgery should be performed in the absence of
preoperative risk factors. If the surgeon is not experienced with Highly
selective vagotomy then in the emergency situation a Truncal Vagotomy and
Pyloroplasty is adequate treatment. If the patient perforates while taking
ulcerogenic drugs a simple closure and lavage should suffice.
As the ulcer diathesis in many patients is silent, ulcer healing and H. pylori
eradication should be confirmed by endoscopy.
Until a randomised prospective trial is performed the relative merits of the
treatment strategies outlined above will continue to be controversial.
In one series of cases reported by Werbin, a 50% mortality
rate was found in patients over age 70 with acute perforation
of a duodenal ulcer who presented more than 24 hours after
onset of symptoms. In this same series, patients who presented
early and were operated on within 24 hours of onset of
symptoms had 0% mortality.
In elderly patients with perforation, the ratio of female
patients is higher. A study by Kubler and colleagues found that
57% of patients age 60 and older with perforated peptic
ulcer were women. In this same study, 89% of patients
presented with perforated duodenal ulcer.
WHAT ARE THE TREATMENT OPTIONS FOR
PERFORATED PEPTIC ULCER?

Principles of conservative treatment include nasogastric suction, pain

control, antiulcer medication, and antibiotics. Nonsurgical treatment has
been recognized for a long time. The first major series was published by
Taylor nearly 50 years ago; it reported a mortality rate of 11% in the
nonsurgical treatment group, compared to 20% in the surgical group.
Since then, because of improvements in operative and postoperative care,
the mortality rate with surgical treatment of perforated peptic ulcer has
decreased to about 5%.
Croft and colleagues compared surgical and nonsurgical treatment of
perforated peptic ulcer in a randomized trial and concluded that an
initial period of nonoperative treatment may be prudent except in
patients over age 70. Careful observation is necessary during this period,
but it may obviate the need for emergency surgery in 70% of patients.
The mortality rate in this study was 5% in each group. Two-thirds of the
patients over age 70 required emergency surgery.
SURGERY
Several surgical techniques have been employed in the treatment of
perforated peptic ulcer.

These include conservative surgery with patching of the ulcer,

peritoneal lavage, and antiulcer medication,

Definitive surgery with truncal vagotomy, highly selective vagotomy, or

partial gastrectomy.

Some studies have reported a high rate of ulcer recurrence in the

conservative surgery group and have recommended definitive ulcer
surgery for perforation.
WHAT MEASURES CAN BE TAKEN TO DECREASE THE
RISK OF PEPTIC ULCER DISEASE AND
PERFORATION?

Nearly one third of patients presenting with perforated peptic

ulcer take NSAIDS.
Therefore, decreasing NSAID use is an important preventive
measure.
For patients who must take NSAIDs, concomitant use of a proton
pump inhibitor or misoprostol may decrease the risk of ulcer
formation.
Smoking cessation and abstinence from alcohol should also
decrease the risk of complicated PUD.
Maintaining a high index of suspicion for the disease,
particularly in elderly patients, will help clinicians diagnose
PUD early in its course, thus reducing morbidity and mortality.
DUMPING SYNDROME

20% after gastrectomy and vagotomy+drainage

Rapid empting of the hyperosmolar chyme in the intestine
Vasoactive hormone- serotonine, VIP
Abdominal colicky pain, nausea, vomiting
Small meals without carbohydrates
octreotide
POSTVAGOTOMY DIARRHEA

30% of patients
Rapid transit of unconjugated biliary saults from the
denervated biliary tree into the colon
Colestiramine binds the biliary saults
ALKALINE REFLUX GASTRITIS
2%
Persistent epigastric pain like a burn
Aggravated by meals
Chronic nausea
EDS/Tc scintigraphy
Ursodezoxicholic acid
Roux-en-Y anastomosis, draining the bile at 45-60 cm from gastro-
jejunal anastomosis
AFFERENT LOOP SYNDROME

After gastrojejunal anastomosis and gastro-jejunostomy

Mechanical obstruction of the aferent loop: twisting,
stenosis, adhesions,kinking
Epigastric pain
Epigastric distension
Non-bile stained vomiting
Distented afferent loop on Xray study or CT
Roux-en-Y
EFFERENT LOOP SYNDROME

Epigastric pain
Epigastric distention
Bile-stained vomiting
Mechanical cause
Roux-en Y
CARCINOMA OF THE GASTRIC STUMP
3%
Endoscopic screening for risk population
PERFORATED PEPTIC ULCER

50 years ago perforated peptic ulcer was a disease

of young men
Today it is a problem seen mainly in elderly women
Overall incidence for admission with peptic ulceration
is falling
The number of perforated ulcers remains unchanged
Sustained incidence possibly due to increased NSAID
in elderly
80% of perforated duodenal ulcers are H. pylori
positive
CLINICAL FEATURES

Most occur in patients with pre-existing dyspepsia

10% have no previous symptoms
Classic presentation is with:
Sudden onset epigastric pain
Rapid generalisation of pain
Examination shows peritonitis with absent bowel sounds
10% have an associated episode of melaena
10% have no demonstrable gas on an erect chest x-ray
If diagnostic doubt then water soluble contrast enema may confirm perforation
Can be associated with elevated serum amylase but not to same level as in
pancreatitis
MANAGEMENT

Most patients require surgery after appropriate resuscitation

Conservative management may be considered if significant co-
morbidity
More likely to fail if perforation is of a gastric ulcer
PREOPERATIVE PREPARATION

Fluid resuscitation with CVP or Swan Ganz monitoring

Analgesia

Antibiotics

Nasogastric intubation
CLASSIC OVERSEW
Oversew of ulcer first performed by Dean in 1894
Usually performed through an upper midline incision
Oversew perforation with omental patch
Use 2/0 synthetic absorbable.
Take 1 cm bites either side of ulcer
Thorough wash out and irrigation of peritoneal cavity
with 0.9% saline
If unable to find perforation open the less sac
CLASSIC OVERSEW
Remember that multiple perforations can occur
If closure secure and adequate toilet then a drain is not required
Prepyloric ulcer behave as duodenal ulcers
All gastric ulcers require biopsy to exclude malignancy
Definitive ulcer surgery probably not required
50% patients develop no ulcer recurrence
Postoperatively patients should receive H. pylori eradication therapy
OPERATIVE MORTALITY DEPENDS ON FOUR
MAJOR RISK FACTORS

Long period from perforation to admission

Increasing age

Coexisting medical disease

Hypovolaemia on admission