A shift in the Paradigm”

Peptic Ulcer Surgery: “A shift in the Paradigm”
Indications, Operations of Choice and Operative Technique
Dr. Hardeep Gill, FCS(ECSA) Trainee, FCS(SA) Trainee,
Groote Schuur Hospital, University of Cape Town, South Africa.
1. Introduction
2. Bleeding Peptic Ulcer
3. Perforated Peptic Ulcer
3.1. Epidemiology
3.2. Surgical management
3.2.1 Perforated Duodenal Ulcer
3.2.1.1. Simple patch closure
3.2.1.2. Laparoscopic repair of perforated peptic ulcer: first choice?
3.2.1.3. Conservative approach to duodenal ulcer perforations
3.2.1.4. Management of large perforated peptic ulcers
3.2.1.5. Failure of primary omental patching
3.2.1.6. Duodenal perforations associated with a bleeding (“kissing”) ulcer
3.2.1.7. Perforations associated with Gastric Outlet Obstruction (GOO)
3.2.1.8. Perforations with duodenal destruction and local organ penetration
3.2.1.9. Tube duodenostomy
3.2.2. Perforated Gastric Ulcer
4. Gastric Outlet Obstruction
5. non healing or recurrent ulcers
6. Conclusions
7. recommendations
8. References
1. Introduction
With the success of medical therapy, surgery has a very limited role in the management of peptic
ulcer disease (PUD). Helicobacter Pylori eradication has become the medical equivalent of
vagotomy, relegating definitive operations to the history chapters of surgical textbooks. (1)
Combinations of multiple antibiotics and acid reducing agents, usually PPIs, have been the
mainstay of these regimes. Cure rates of greater than 80% (intent to treat) are possible. (2)
Eradication of H.pylori infection can give long-term remission of ulcer disease; reduce
recurrence; prevent recurrent ulcer bleeding and resolve pyloro-duodenal stenosis in some cases.
(3) In light of this evidence general surgeons need to revise their indications for peptic ulcer
surgery and critically re-appraise the procedures performed for peptic ulcer disease. Elective
peptic ulcer surgery has been virtually abandoned. In the 1980s, the number of elective
operations for peptic ulcer disease dropped more than 70%, and emergent operations accounted
1
for more than 80% of these. (4) Currently, surgery for peptic ulcer disease is largely restricted to
the treatment of complications, particularly bleeding, perforation, and obstruction, while relying
on H.pylori eradication to prevent ulcer recurrence, and these will be the focus of this review.
The focus of surgical therapy is to manage the complication effectively and not necessarily to
cure the ulcer.
2. Bleeding Peptic Ulcer
Bleeding is the commonest complication of peptic ulceration. Endoscopic hemostasis is now
accepted as the first-line treatment in patients with non-variceal upper gastro-intestinal bleeding.
Endoscopy is an effective tool in the diagnosis, prognostication, and therapy of bleeding PUD
and has been shown in randomized studies to lead to a reduction in blood transfusion
requirements, to shortened intensive care unit and hospital stays, to a decreased need for surgery,
and a lower mortality rate.(5,6) Early endoscopy (within 24 hours of admission) has been shown
to reduce blood transfusion requirements and length of hospital stay. (7) Patients who are
hemodynamically stable with endoscopy revealing ulcers without high-risk stigmata may be
safely discharged home after endoscopy. (8) Patients with endoscopic stigmata indicating a high
risk of rebleeding, including adherent clots, visible vessels, and active arterial bleeding should all
undergo endoscopic therapy to achieve hemostasis and reduce the risk of rebleeding.(5,9,10)
Recurrent bleeding may occur in as many as 10% of patients despite endotherapy and the use of
high-dose proton pump inhibitors. (11, 12) In patients who rebleed after initial endoscopic
therapy, repeat endoscopic therapy is suggested before considering surgical or radiologic
intervention.
Several controlled trials have shown that endoscopic therapy using a variety of combined
techniques significantly reduces the need for blood transfusion and emergency surgical
intervention.(13) Similar results are reported with acid suppression, especially when gastric pH is
kept above 6 by using high dose proton pump inhibitor (PPI) therapy.
Further benefits have been shown when endoscopic therapy is combined with intravenous PPI
therapy. The combined therapy has now been endorsed by the British Society of
Gastroenterology, who have recommended intravenous PPI therapy with an initial dose of 80mg,
followed by a maintenance dose of 8mg per hour over 72 hour period. (14)The blanket use of
expensive PPI therapy has been challenged by a recent randomized study (15) showing that
smaller intravenous doses (20mg) of omeprazole administered after endoscopic therapy gave
results comparable to the recommended high dose PPI regimen when rebleeding, surgery and
mortality were analyzed. However the cost and availability of intravenous PPI therapy remain a
major consideration and should be restricted to high risk patients.
The independent pre-endoscopic predictors of rebleeding that are significant in at least two
separate studies are hemodynamic instability and comorbid illness. The independent endoscopic
predictors of rebleeding that are significant in at least two separate studies are active bleeding at
endoscopy, large ulcer size, posterior duodenal location, and lesser gastric curve location. (16 )
2
The benefit of early “second look” endoscopy and further injection if required has been debated
for some time. There is now an increasing body of evidence that this approach does not confer
benefit by further reducing the incidence of re-bleeding. (17,18 ) However the benefit of early
“second look” endoscopy is still valuable in selected cases where the initial endoscopy was
inadequate or demonstrated a Forrest I or IIA ulcer. Rebleeding can be handled effectively by
repeat endoscopic therapy or surgery: which to use should be based on the pre-existing
comorbidities of the patient. Pre-operative on table endoscopy is first done for an acute upper GI
bleed to exclude varices.
The role of surgery during acute bleeding is now restricted to patients with an exsanguinating
bleed or those in whom endoscopic therapy fails for technical reasons, or in patients who rebleed
after a second endoscopic attempt to control the bleeding.(14,19,20)
The preferred operation today for a bleeding duodenal ulcer is to under-run the bleeder with or
without a pyloroplasty.
For bleeding gastric ulcers, a gastrotomy with under-running of the bleeder with biopsy , or
depending on the site, local excision is recommended. If the source of bleeding cannot be
identified on gastroscopy, a gastrotomy commencing from the pre-pyloric region through the
pylorus to the first part of the duodenum should be done, and the incision extended in the
direction where the bleeding seems to be coming from. Gastrectomy is reserved for large
penetrating ulcers or when there is suspicion of a malignant ulcer. The move away from
definitive surgery has been vindicated by ulcer cure rates in excess of 90% in patients who have
had successful H.Pylori eradication therapy. (21-23) Patients who require long-term nonsteroidal anti-inflammatory drug (NSAIDS) therapy are advised to take PPI medication, or
alternatively use the safest NSAID available.
3. Perforated Peptic Ulcer
Perforation occurs in approximately 7% of patients hospitalized for peptic ulcer disease. (24)
Duodenal perforation tends to occur in the anterior wall while gastric ulcers may perforate
anteriorly or posteriorly. Concomitant haemorrhage should suggest the presence of a „kissing‟
ulcer (ulcers involving anterior and posterior duodenal walls simultaneously).
3.1. Epidemiology
Risk factors
NSAIDs, immunosuppression (esp. transplant patients on steroids), increasing patient age,
chronic obstructive lung disease, major burns, multi-organ failure and smoking
Gender and age of patients with perforated PUD
The percentage of women with duodenal ulcer perforations has increased almost threefold over
the last 45 years. The male to female ratio is now 2:1 (initially was 7:1). The mean age of women
with perforated duodenal ulcers is 10 years higher than for their male counterparts (25).
Localization
Perforations of duodenal ulcers are 7 times more common than perforated gastric ulcers in both
sexes in Western literature. However, in developing countries 74% of the perforations may be in
the pre-pyloric area.
Predicting morbidity and mortality
It is important to stratify patients into different categories based on the likelihood of morbidity
and mortality, so that high-risk patients can receive more appropriate treatment and greater
3
intensive care. Several risk scores exist for the prediction of outcomes in PUD example, Boey,
ASA, APACHE II and the Mannheim Peritonitis index ( 24-25).
The Boey scoring system (26) is among the common risk stratifications used because of its
simplicity and high predictive value for mortality in perforated peptic ulcers. Boey risk factors
include: pre-op shock (<100mmHg), perforation present for >24hours, associated medical comorbidities.
Each of these risk factors score 1 point to a maximum of 3 points with corresponding mortality
rates.
Boey scoring system
Risk factors
0
1
2
3
Mortality rates
0%
10%
45.5%
100%
The incidence of mortality of perforated PU is 5-10%. Mortality increases up to 50% if the
perforation has been present > 24 hours.
Classification of gastroduodenal ulcer perforation :
Type A: solitary prepyloric ulcer located anteriorly. Treatment of choice should be an open/
laparoscopic closure by suture with omentopexy and post-op endoscopic biopsy to identify
H.Pylori and to exclude malignancy.
Type B: perforated ulcer with a large defect. Excision and suture is necessary by open surgery.
Type C: complicated perforated ulcer with proximal duodenal destruction and penetration into
adjacent organs, often pancreas, for which resectional surgery may be indicated like Billroth I, II,
with Roux-en-Y or an atypical resection.
Regardless of the ulcer types, those patients that are critically ill and high risk can be offered
minimal surgical intervention by percutaneous peritoneal drainage which may significantly lower
the mortality in this selected patient group.(27)
Presentation
Classically: acute onset of severe epigastric pain with / without radiation to the shoulders.
Anxiety, fever, tachypnoea and tachycardia, generalized peritonitis, loss of liver dullness are also
present. These classic features may be absent in the very young/old, immunosuppressed,
quadriplegic and comatose patient.
Radiology: Free air on erect chest or left decubitus x-ray. This may not be visible in 30% cases
and a water-soluble contrast may facilitate the diagnosis.
Management
Resuscitation – with view to stabilization for anaesthesia and surgery:
Nasogastric tube, intravenous fluids, catheterize and monitor urine output
Analgesia, intravenous antibiotics, acid suppression, eradication therapy.
4
3.2. Surgical management
3.2.1 Perforated Duodenal Ulcer
The primary aim is to close the perforation, and decontaminate the peritoneal cavity.
3.2.1.1. Simple patch closure
The long debate, about the choice between simple patch closure and definitive surgery, has now
been settled in favour of patch closure combined with H.Pylori eradication. (27, 28) There is
conclusive evidence that the risk of recurrent ulceration is below 10% with this combination
therapy. Simple patch closure is also the treatment of choice for NSAID induced perforations
since PPI therapy provides effective ulcer protection in these patients.
3.2.1.2. Laparoscopic repair of perforated peptic ulcer: first choice?
The controversy about the surgical management of perforated peptic ulcers has now shifted to
the choice between open or laparoscopic closure. Several laparoscopic techniques have been
described, ranging from a simple stitch to the use of fibrin glue. Controlled studies have shown
that laparoscopic closure is associated with less postoperative analgesic requirements, a lower
incidence of respiratory infection, a lower median hospital stay and earlier return to normal
activity. (27-30)
A recent literature review has concluded that laparoscopic ulcer repair is safe even in patients
with prolonged peritonitis. (29) It is however technically demanding and requires a surgeon
experienced in laparoscopy. A remarkable difference in morbidity (14.35 in laparoscopic group
vs. 26.9% in open group) and mortality (3.6% vs 6.4%) should advocate laparoscopy as a
diagnostic and therapeutic tool. The overall conversion rate is around 12.4% (range 0-28.5%).
The most common reason for conversion was the size of the perforation, but by using a pedicled
omentoplasty, size might not necessarily be a reason to convert anymore. Other common reasons
for conversion include failure to locate the perforation, shock on admission (conversion rate 50%
vs. 8%) and time elapsed since perforation and presentation (33% vs. 0%). The reported series on
laparoscopic repair of perforated peptic ulcers comes from specialized centres and cannot be
recommended for general community practice where most of these patients are treated.
The new “stamp” method which consists of closure of the perforation by gluing a biodegradable
patch onto the outside of the stomach could, in the future, further improve the ease of
laparoscopic management.
Open simple patch closure remains the gold standard in the management of perforated peptic
ulcers and, when performed through a small midline incision, the outcome should be similar to
the laparoscopic approach.
3.2.1.3. Conservative approach to duodenal ulcer perforations
The feasibility of non-operative management for perforated peptic ulcers was first reported by
Taylor in 1951. Croft from Hong Kong in 1989 reported the first prospective randomized trial
comparing the outcome of non-operative treatment with that of emergency surgery in patients
with a clinical diagnosis of perforated peptic ulcer. (31)
Approximately half of the duodenal ulcers will have self-sealed by the time of admission. The
presence of self-sealing can be reliably established by a water-soluble contrast meal and followthrough. The spontaneous seal for a perforated duodenal ulcer is remarkably secure (only 2 out
of 152 re-leaked) and non surgical treatment should include nasogastric drainage, antibiotics, IV
PPIs and serial abdominal examinations.
5
If the signs of peritonitis are not beginning to resolve within 12 hours, the diagnosis of a selfsealed ulcer should be questioned. In patients with severe co-morbid disease preventing surgical
intervention, sump suction drains can be placed under local anaesthesia to the site of perforation
with an aim of creating an external fistula.
3.2.1.4. Management of large perforated peptic ulcers
Large perforations are between 1 and 3 cm in size; with giant perforations exceeding 3cm in size
occurring in only 2.5% of peptic ulcers. It should be stressed that large perforations may not be
suitable for simple patch closure. The leak rates with its attendant morbidity and mortality is high
in these patients. Different authors have recommended various surgical options as these large
perforations are particularly hazardous because of the extensive duodenal tissue loss and
surrounding tissue inflammation. (32)
These options include resection of the perforation bearing duodenum and the antrum in the form
of a partial gastrectomy with either a BI or BII anastomosis, or the more morbid procedure of
gastric disconnection in which an antrectomy, gastrostomy, lateral duodenostomy and feeding
jejunostomy are performed, with restoration of gastrointestinal continuity electively at 4 weeks.
Others have recommended conversion of the perforation into a pyloroplasty, or closure of the
perforation using a serosal jejunal patch or a pedicled jejunal graft. It is probably advisable
where possible to attempt the simplest closure technique. Omentopexy is still safe to perform in
perforations of up to 3cm. it is simple and avoids a major resection in an already compromised
patient. (33,34)
Omental plugging can be safely performed with giant perforated duodenal ulcers with indurated,
fibrotic, friable margins and seems to have a better long term outcome with regards to gastric
outlet obstruction when compared to omentopexy.
The technique of omental plugging is as follows:
The tip of the NG tube is guided through the perforation. The free edge of the omentum is then
sutured to the tip of the tube, which is then carefully withdrawn, pulling the plug of omentum
into the stomach. 5-6cm of omental plug is usually enough to occlude the perforation. The
omentum is then fixed with interrupted sutures taken between the omentum and the healthy
duodenum, approximately 3-4mm from the margins of the perforation.
An alternative approach described in critically ill patients with giant perforations, where a
resection would increase the patients‟ morbidity, is to perform a gastric partition,
gastrojejunostomy and simple closure of the perforated peptic ulcer. The gastric body partition
above the angular incisura is expected to avoid or minimize hypergastrinemia, as well as avoid
uncontrollable leakage from the site of ulcer repair. A tube duodenostomy is added for bile
drainage.
3.2.1.5. Failure of primary omental patching
Failure is defined as an early post-operative re-perforation, obstruction and or hemorrhage. A
more aggressive surgical procedure is then recommended, such as pyloroplasty or an antral
resection.
3.2.1.6. Duodenal perforations associated with a bleeding (“kissing”) ulcer
In this situation a pyloroplasty should be performed to allow undersewing of the posterior
bleeder. The pyloroplasty will then include closure of the perforation. Pyloroplasty options
6
include Jabulay, Finney or Heinecke-Mikulicz techniques. Alternatively, partial gastrectomy
may be considered as a definitive procedure.
pyloroplasties
3.2.1.7. Perforations associated with Gastric Outlet Obstruction (GOO)
If an element of GOO is suspected in a duodenal perforation it is safest to perform a
pyloroplasty, or consider simple omentopexy with a diverting gastrojejunostomy, before a partial
gastrectomy is considered. If post-operatively the patient develops GOO treatment options
include: pyloroplasty or antral resection; balloon dilatation; removable stent.
3.2.1.8. Perforations with duodenal destruction and local organ penetration
In situations with significant duodenal obstruction and local organ penetration any repair will be
difficult due to much inflammation and friable, fibrotic tissue edges. A higher than normal
duodenal leak rate must be anticipated. Various authors will advocate different techniques of
management from partial gastrectomy to gastric disconnection. Again, the simplest technique
possible should be advised: pyloroplasty or omentopexy or plugging with diverting
gastrojejunostomy. A Billroth I may provide a safe option than a Billroth II using a Horsley slit
technique. If a formal resection is unavoidable, be aware of the high risk of duodenal stump
blow-out and always leave a drain. In this situation some recommend a tube duodenostomy.
3.2.1.9. Tube duodenostomy
Duodenal stump leakage remains one of the most feared complications of gastric resection.
Despite good results reported with this technique it has not gained wide acceptance and is rarely
used. (35) It may be considered when surgical closure of the inflamed or scarred duodenum is
not safe after resection for chronic peptic ulcer disease, or when a duodenal stump leakage has
occurred following previous duodenal stump closure.
The technique is as follows: a soft 22F Pezzer catheter is inserted through the open end of the
duodenal stump to a depth of 4-5cm. the holes on the catheter tip may be widened to improve
drainage and also to make removal as atraumatic as possible. A purse string suture is then
invaginated into the lumen to keep the catheter in place. A viable omental pedicle may be
secured around the junction of the tube end and duodenum. A closed suction drain (JacksonPratt) is then left near the tube duodenostomy. Depending on the surgeon, the duodenostomy
7
tube stays in place between 10-21 days. The choice of the site of introduction of the catheter,
either through the lateral duodenal wall or the duodenal stump, is of great importance.
Conceptually these two techniques differ. Lateral duodenostomy through the 2nd part of the
duodenum is primarily used for intra-luminal decompression, but it has been shown that this
does not lead to a significant decrease in intra-duodenal pressures. End tube duodenostomy is an
effort to create a controlled duodenal fistula, and is employed when technical factors prevent
adequate surgical closure of the duodenal stump.
3.2.2. Perforated Gastric Ulcer
Distal gastrectomy was always considered the preferred surgical management of perforated
gastric ulcers. However, gastric ulcers are now curable by medical treatment, therefore omental
patch closure and ulcer excision are being increasingly employed as alternatives to gastrectomy.
The complication rate is significantly lower in patch closure patients than in both the
gastrectomy and ulcer excision groups. The focus of surgical therapy is to manage the
complication effectively and not necessarily to cure the ulcer. This makes simple operations such
as omentopexy and ulcer excision possible primary interventions for all, not just being confined
to elderly, unfit or unstable high-risk patients. Biopsy of perforated gastric ulcers is mandatory
due to the reported incidence of malignancy being between 3-14%. (36) Candida may also be an
associated pathogen. In addition, endoscopy should be performed post operatively to re-biopsy
and follow up persistent ulcers until healed. Considering the early and late morbidity associated
with gastrectomy, this procedure should be reserved for giant, penetrating or atypically situated
perforations that preclude a patch or excision and repair for technical reasons.
4. Gastric Outlet Obstruction
Gastric outlet obstruction (GOO) occurs in 6-8% of patients with duodenal ulcer disease. Before
the H.Pylori era most patients with outlet obstruction required surgical intervention, including
those who underwent endoscopic balloon dilatation. (37-39) The prevalence of H.Pylori varies
widely (33-91%) in reported series on GOO and the association appears to be less established
when compared with the other complications. (40)
Patients with gastric outlet obstruction are frequently malnourished, hypovolemic, and have
metabolic alkalosis. Operation is usually indicated if the obstruction fails to resolve after 72
hours with correction of fluid and electrolyte abnormalities, antisecretory therapy, and
nasogastric tube decompression.
Several reports have now shown that H.Pylori eradication with or without balloon dilatation can
successfully overcome GOO in the short to midterm, including patients who have an associated
fibrotic stricture. (41) However not all reports are favourable and there is increasing evidence
that NSAID users are less likely to respond. More data is required to assess the efficacy of
combining H.pylori eradication and endoscopic balloon dilatation of stenosis but, at present, it
would seem reasonable to try balloon dilatation before considering surgery.
The conventional treatment for GOO was vagotomy and a drainage procedure or alternatively
vagotomy and antrectomy. As with bleeding and perforated ulcers, in this situation definitive
operations have also become obsolete and addressing the obstruction is all that is needed after
successful eradication of H.Pylori. For “burnt-out” ulcers with residual fibrotic strictures a
8
pyloroplasty or Jaboulay gastroduodenostomy is all that is required. A more difficult question is
what to offer patients with persistent or recalcitrant penetrating ulcers despite successful H.Pylori
eradication. The reason why these ulcers fail to heal remains uncertain, but an important local
healing process may play an important role. Nevertheless, a limited distal resection with excision
or exclusion of the ulcer should be performed in these situations.
5. Non healing or recurrent ulcers.
The definition of a non-healing ulcer is failure to heal, after appropriate treatment, in two months
for DU or three months for GU. It must be said that these are rare, especially in the developing
world. A diagnostic dilemma in these cases has been observed. (43) H. pylori persistence or reinfection needs to be ruled out, as does Zollinger Ellison syndrome (a gastrinoma secreting
abnormally high levels of gastrin). Other aggravating factors - NSAIDS, smoking, alcohol - need
to be eliminated if possible. If the ulcer recurs, one option is long term PPI therapy. If there is
failure to heal on these, surgery becomes indicated. In GUs, particularly Type I, the standard
procedure has been the Bilroth I gastrectomy with excision of the ulcer. (44) Pre/peri-operative
biopsies should be performed to make sure the ulcer is not malignant and a larger resection not
required. For DUs, the modern options have been some form of vagotomy, truncal vagotomy
with drainage or highly selective vagotomy (parietal cell vagotomy) versus vagotomy and
antrectomy. (45) The latter procedure has an improved cure rate with increased side effects.
Recurrence of ulcer after surgery has long been a problem, often requiring more aggressive
surgery. (46)
6. Conclusions
With the discovery of H.Pylori, and the availability of effective acid suppressing drugs and
eradication therapy, one needs to question the validity and appropriateness of vagotomy and
gastrectomy and its numerous variations to control acid secretion. The present generation
surgeon is modestly trained and not equipped with the experience of elective gastric surgery.
Surgeons should therefore only intervene when complications of peptic ulceration present and
then too, should the surgery be tailored and kept to a minimum procedure. With perforation and
bleeding, the surgeon should allow for selective conservative treatment under appropriate
conditions, simple patching which may be performed via minimal access or more conventional
open surgery and, under-run a bleeding vessel when endoscopic haemostasis has failed. Early
surgery is still recommended in the elderly in view of the associated high morbidity and
mortality. The surgeon should leave acid control and eradication of H.Pylori to drug therapy.
Occasionally when operating for a bleeding ulcer or gastric outlet obstruction, a distal
gastrectomy may be necessary for scarring. But even here the resection should be limited and
undertaken for technical reasons and not for long term control.
In an editorial in the BMJ in 1991, appropriately titled “A requiem for vagotomy, despite the last
ditch efforts of surgeons”, John Alexander-Williams predicted that “vagotomy for ulcers will
soon go the way of vagotomy for tabes, made obsolete by the conquest of spiral organisms”.
These prophetic words have now become a reality. Surgeons should graciously accept their
9
diminishing role in the management of peptic ulcer disease, a role now confined, in the main, to
conservative surgery for complications - which ultimately is to the benefit of our patients. (42)
7. Summary and Recommendations:
GENERAL:
The major complications of peptic ulcer disease (PUD) include bleeding, perforation, and
gastric outlet obstruction.
The overall incidence of PUD has declined significantly, due to better medical therapy,
including proton pump inhibitors (PPI), regimens for eradication of Helicobacter
pylori, and improvements in endoscopic methods for control of hemorrhage. Surgery
for peptic ulcer disease is now typically confined to high risk patients.
Early surgical consultation for patients with complications of PUD is required to assure
stabilization of the patient, collaboration among services, and agreement on initial
nonoperative therapy.
BLEEDING:
Most patients with bleeding ulcers are treated with fluid resuscitation to correct
hypovolemia, blood transfusions as necessary, medical therapies, and endoscopic
intervention. Surgery is required when endoscopic techniques are unsuccessful or if the
patient is hemodynamically unstable or has continued bleeding.
The major endoscopic predictors of persistent or recurrent bleeding include
o
Active bleeding during endoscopy - 90 percent recurrence
o
Visible vessel - 50 percent recurrence
o
Adherent clot (in elderly patients particularly with large ulcers) - 25 to 30 percent
recurrence
Patients with actively bleeding peptic ulcers or ulcers with high-risk stigmata (such as a
visible vessel or adherent clot) should receive an intravenous proton pump inhibitor
(PPI) .
10
PERFORATION:
For patients with a perforated ulcer, initial management includes insertion of a
nasogastric tube, intravenous hydration, and broad spectrum antibiotics. Operation is
almost always indicated and the surgical approach will depend upon whether the ulcer
is duodenal or gastric.
GASTRIC OUTLET OBSTRUCTION:
For patients with gastric outlet obstruction, a simple drainage procedure is indicated if the
obstruction fails to resolve after 72 hours of nasogastric suction and intravenous PPI.
The indications for a definitive ulcer operation, which generally involves an acidreducing procedure (such as a truncal, selective, highly-selective, or parietal-cell
vagotomy), are now very limited.
Dr. Hardeep Gill, FCS(ECSA) Trainee, FCS(SA) Trainee,
Groote Schuur Hospital, University of Cape Town, South Africa.
8. References
1. Church NC, Palmer KR. Acute non-variceal upper gastrointestinal haemorrhage treatment.
In: McDonald J, Burroughs A, Feagan B, eds. Evidence Based Gastrology and Hepatology.
London: BMJ Books, 1999; 118-138.
2. Brian Ostrow MD, FRCSC. April: Peptic Ulcer Disease - the impact of Helicobacter pylori
on management in the developing world . SIA; April 2007
3. Javier P Gisbert, Sam Khorrami. Helicobacter pylori eradication therapy vs. antisecretory
non-eradication therapy (with or without long-term maintenance antisecretory therapy) for
the prevention of recurrent bleeding from peptic ulcer. November 2010
4. Gustavsson S, Kelly KA, Melton LJ 3rd, Zinsmeister AR. Trends in peptic ulcer surgery. A
population-based study in Rochester, Minnesota, 1956-1985. Gastroenterology 1988; 94:688.
5. Barkun A, Bardou M, Marshall JK. Consensus recommendations for managing patients with
nonvariceal upper gastrointestinal bleeding. Ann Intern Med 2003;139:843-57.
6. Spiegel BM, Vakil NB, Ofman JJ. Endoscopy for acute nonvariceal upper gastrointestinal
tract hemorrhage: is sooner better? A systematic review. Arch Intern Med 2001;161:1393404.
7. Lin HJ, Wang K, Perng CL, et al. Early or delayed endoscopy for patients with peptic ulcer
bleeding. A prospective randomized study. J Clin Gastroenterol 1996;22:267-71.
8. Lai KC, Hui WM, Wong BC, et al. A retrospective and prospective study on the safety of
discharging selected patients with duodenal ulcer bleeding on the same day as endoscopy.
Gastrointest Endosc 1997; 45:26-30.
11
9. Johnston JH. Endoscopic risk factors for bleeding peptic ulcer. Gastrointest Endosc
1990;36(Suppl):S16-20.
10. Bleau BL, Gostout CJ, Sherman KE, et al. Recurrent bleeding from peptic ulcer associated
with adherent clot: a randomized study comparing endoscopic treatment with medical therapy.
Gastrointest Endosc 2002;56:1-6.
11. Spiegel BM, Ofman JJ, Woods K, et al. Minimizing recurrent peptic ulcer hemorrhage after
endoscopic hemostasis: the cost-effectiveness of competing strategies. Am J Gastroenterol
2003;98:86-97.
12. Zed PJ, Loewen PS, Slavik RS, et al. Meta-analysis of proton pump inhibitors in treatment of
bleeding peptic ulcers. Ann Pharmacother 2001;35:1528-34.
13. Vergara M, Calvet X, Gisbert JP. Epinephrine injection versus epinephrine injection and a
second endoscopic method in high risk bleeding ulcers (Review) The Cochrane Library 2010,
Issue 2
14. British society of Gastroenterology Endoscopy Committee. Non-variceal upper gastrointestinal
haemorrage: Guidelines. Gut 2002; 51: suppl IV , iv1-iv 6.
15.Udd M, Miettien P, Palmu A, et al. Regular-dose verses high-dose omeprazole in peptic ulcer
bleeding – a prospective randomized double-blind study. Scand J Gastroenterol 2001; 12: 13321338.
16. B. Joseph Elmunzer, M.D. Systematic Review of the Predictors of Recurrent Hemorrhage
After Endoscopic Hemostatic Therapy for Bleeding Peptic Ulcers. Am J Gastroenterol
2008;103:2625–2632
17.Saeed ZA, Cole RA, Ramierez FC, et al. Endoscopic retreatment after successful initial
haemostasis prevents ulcer rebleeding : a prospective randomized trial. Endoscopy 1996; 28:288294.
18.Chiu PWY, Lam CYW, Lee SW, et al. Effect of scheduled second therapeutic endoscopy on
peptic ulcer rebleeding: a prospective randomized trial. Gut 2003; 52: 1403-1407.
19.Palmer K. Management of haematemesis and melaena. .Postgrad Med J 2004; 80: 399-404.
20Lau JYW, Sung JYW, Kim HS, et al. Endoscopic retreatment compared with surgery in patients
with recurrent bleeding after initial endoscopic control of bleeding ulcers. New Eng J Med 1999;
340: 751-756.
21.Graham DY, Hepps KS, Ramierez FC, Lew GM, Saeed ZA. Treatment of Helicobacter Pylori
reduces the rate of rebleeding in peptic ulcer disease. Scand J Gastroenterol 1993; 28:939.
22.Jaspersen D, Koerner T, Schoor W, Breenestuhl M, Raschka C, Hammer CH. Helicobacter
pylori irradication reduces the rate of rebleeding in ulcer haemorrhage. Gastrointest Endo 1995;
41:5.
23.Satander G, Gravelas RG. Antimicrobial therapy for Helicobacter pylori infection verses long
term maintenance anti-secretory treatment in the prevention of recurrent haemorrhage for peptic
ulcer: prospective non-randomised trial of 125 patients. Am J Gastroenterol 1996;91: 1549-1552.
12
24. Lohsiriwat et al. Perforated Peptic Ulcer: Clinical Presentation, Surgical Outcomes, and the
Accuracy of the Boey Scoring System in Predicting Postoperative Morbidity and Mortality.
World J Surg (2009) 33:80-85
25.Wysocki et al.changes in the localization of perforated peptic ulcer and its relation to gender
and age of the patients throughout the last 45 years. World Journal of Surgery 2011; April;
35(4): 811–816.
26.Boey J, et al. Risk stratification in perforated duodenal ulcers. A prospective validation of
predictive factors. Ann Surg 1987; 205:22–26.
27.Sauerland et al. laparoscopy for abdominal emergencies. Evidence based guidelines of the
European association for endoscopic Surgery. Surg Endosc 2006; 20: 14-29.
28.Bertleff et al. Laparoscopic correction of perforated peptic ulcer: first choice? A
review of
literature. Surg endosc 2010;24:6: 1231-1239.
29.Bertleff et al. randomized clinical trial of laparoscopic versus open repair of the perforated
peptic ulcer. The LAMA trial. Worl J surg 2009; 33: 7, 1368-1373
30.B Bertleff et al comparison of closure of Gastric perforation ulcers with biodegradable
lactide-glycolide-caprolactone or omental patches. JSLS: 2009 Oct–Dec; 13(4): 550–554.
31.Crofts TJ,Park KGM, Steele RJC et al. A randomized trial of non-operative treatment of
perforated peptic ulcer. NEJM 1989; 320:970-973.
32.Gupta et al. The management of large perforations of duodenal ulcers.
BMC Surg 2005; 5:15- 28.
33.Jani et al. omental plugging for large sized duodenal peptic perforations. A prospective
randomized study of 100 patients. South Med J. 2006 May;99(5):467-71
34.Shyu et al. gastric body partition for Giant Perforated Peptic Ulcer in Critically ill Elderly
patients. World J Surg 2006 ;30: 12, 2204-2207
35. Isik et al. a life saving but inadequatelt discussed procedure. Tube duodenostomy. Known
and unknown aspects. World J Surg 2007;31;8: 1616-1624.
36. Madiba et al. perforated gastric ulcers. Reappraisal of surgical options SAJS VOL 43, NO. 3,
august 2005
37.Hewitt PM, Kringe JE, Funnell IC, Wilson C, Bornman PC. Endoscopic balloon dilatation of
peptic pyloroduodenal strictures. J Clin Gastroenterol 1999;1:33-35.
38.Lau JYW, Chung SCS, Sung JJY, et al. Through-the-scope dilatation of pyloric stenosis: longterm results. Gastrointest Endosc 1996; 43:98-101.
39.Mista SP, Dwivedi M. Long term follow-up of patients undergoing balloon dilatation for benign
pyloric stenosis. Endoscopy 1996;28:552-554.
40.Rinaldi V, Zullo A, Diana F, de Francesco V, Pugliano F, Atilli AF. Duodenal stenosis may not
regress after eradication of Helicobacter pylori. J Clin Gastroenterol 1997; 24:288-289.
41.Borody TJ, Bampton P, Moont M, et al. Gastric outlet obstruction and Helicobacter pylori. Am J
Gastroenterol 1997; 92:1576-1577.
42.Alexander-Williams J, A requiem for vagotomy. Despite the last ditch efforts of surgeons. BMJ
1991; 302: 547-548.
(43) Guzzo JL, Duncan M, Bass BL, Bochicchio GV, Napolitano LM. Severe and refractory peptic
ulcer disease: the diagnostic dilemma: case report and comprehensive review. [Review] [42 refs].
Digestive
Diseases&
Sciences
50(11):1999-2008,
2005.
211
KB
(44) Wayne JD, Bell RH, Jr. Limited gastric resection. [Review] [42 refs]. Surgical Clinics of North
13
America;85(5):1009-20,vii,2005.396KB
(45) Donahue PE. Parietal cell vagotomy versus vagotomy-antrectomy: ulcer surgery in the modern
era. [Review] [28 refs]. World Journal of Surgery 24(3):264-9, 2000. 105 KB
(46) Turnage RH, Sarosi G, Cryer B, Spechler S, Peterson W, Feldman M. Evaluation and
management of patients with recurrent peptic ulcer disease after acid-reducing operations: a
systematic review. [Review] [85 refs]. Journal of Gastrointestinal Surgery 7(5):606-26, 2003;-Aug.
185 KB
14