Transcript PERFORATED PEPTIC ULCER

PERFORATED PEPTIC ULCER
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
- Meckel’s 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
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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
60–70), chronically ill patients often (40–50%) 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 70–92% 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 40–50% 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.
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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
40–50% 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 selfsealing.
• 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 nonrandomised 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 surgeondependent.
• 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.
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Until further clinical trials are performed in relevant
population groups we will not know the definitve answer.
Therapy for H. pylori
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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
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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
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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
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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
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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
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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
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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