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KEYWORDS
Gastroduodenal Perforation Ulcer-reducing surgery
KEY POINTS
The most common cause of gastroduodenal perforation is peptic ulcer disease.
Nonoperative management can be considered in patients with minimal symptoms who
are younger than 70 years.
Abdominal washout, ulcer biopsy, and omental patch are appropriate in most
circumstances.
Acid-reducing surgery is indicated in patients who have a history of failed medical therapy.
CAUSE
The most common cause of gastroduodenal perforation is ulcer disease
Ulcer disease may be secondary to acid hypersecretion, H pylori infection, or
from medications (steroids, nonsteroidal antiinflammatories)
Other causes include trauma, neoplasm, foreign body ingestion, or iatrogenic
(endoscopic procedures).
Blunt trauma resulting in gastroduodenal perforation is rare, comprising only
5% of blunt hollow viscous injuries.
Malignant perforations may be secondary to necrotic tumor in the stomach or
duodenum that perforates or from an obstructing tumor, leading to proximal
dilation and perforation.
Foreign bodies may cause perforation from direct injury to the stomach or
duodenum or as a result of luminal obstruction.1
Department of Surgery, University of Utah, 50 North Medical Drive, Salt Lake City, UT 84132,
USA
E-mail address: r.nirula@hsc.utah.edu
PRESENTATION
Sudden onset of severe epigastric and right upper quadrant abdominal pain in
patients with a history of gastroesophageal reflux is common among those
with peptic ulcer disease perforations.
Peritonitis may be minimal in the case of contained leaks.
Mental status changes and septic shock (fever, hypotension, tachycardia) may
be observed in diffuse leakage of the perforation.
DIAGNOSIS
Leukocytosis, metabolic acidosis, and hyperamylasemia may be present but are
not sensitive.
Upright chest radiograph may show free air.
Computed tomography (CT) with enteral contrast shows free air, free fluid,
mesenteric fat stranding, and bowel wall thickening and may localize the site
of perforation. Early CT scans after traumatic injury may be falsely negative in
up to 12% of cases.3
MANAGEMENT
Nonoperative Management
Approximately half of the perforations spontaneously seal, which raises the question
as to whether these patients can be managed nonoperatively. The difficulty is identi-
fying those patients who have sealed without compromising the outcomes for those
who have not sealed while one observes them for signs of clinical deterioration.4 Fac-
tors mandating surgical management include shock and generalized peritonitis. Risk
factors that have been associated with failure of nonoperative management include
age greater than 70 years, symptoms of greater than 24 hours, and lack of improve-
ment after 12 hours of conservative therapy. Conservative therapy includes showing
that there is no free extravasation of contrast and that the leak is confined either by
CT or gastroduodenography. Once this information is verified, a nasogastric tube
Gastroduodenal Perforation 33
Operative Management
Patients who have free perforation, shock, generalized peritonitis, or progressive
symptoms should undergo surgery. The decision to perform an acid-reducing opera-
tion is made based on the patient’s history. Those patients who have perforated
despite antacid therapy and H pylori eradication or who require ulcerogenic medica-
tions such as steroids should undergo an acid-reducing operation. For those who
have not received adequate medical therapy, ulcer biopsy for gastric ulcers, omental
patch, and abdominal washout followed by medical therapy provide acceptably low
ulcer recurrence rates, of less then 10%.6–8
In patients who have failed medical therapy and are hemodynamically stable, there
are several antacid operations, each with its merits: truncal vagotomy with pyloro-
plasty, truncal vagotomy with antrectomy, and either a Bilroth I or Bilroth II reconstruc-
tion, or highly selective vagotomy. These operations should generally be reserved for
ulcers that are related to acid hypersecretion, which include prepyloric ulcers or
gastric ulcers within the body that occur in conjunction with duodenal ulcers. The
choice of which operation to perform needs to take into account the location of the
perforation and the ability to achieve closure along with the risk for ulcer recurrence
balanced by the risk of complications related to the operation. Vagotomy and antrec-
tomy carries the lowest risk for ulcer recurrence, at approximately 2%, whereas vagot-
omy and pyloroplasty carries a recurrence rate of 5%, and 10% to 20% for highly
selective vagotomy.9,10
Closure of gastric perforations can typically be easily performed, because of the
mobility and redundancy of the stomach, which can then be reinforced with an
omental patch. Duodenal perforations frequently cannot be primarily closed unless
they are small without causing duodenal narrowing. Therefore, an omental or jejunal
serosal patch may be necessary. If the integrity of the repair is in question, the right
upper quadrant should be drained in anticipation of a duodenal fistula and a gastro-
stomy tube for drainage, and a jejunal feeding tube should be placed. In patients
who are hemodynamically normal, this procedure may be performed laparoscopically.
If the perforation is proximal and an antacid operation is being performed, then, the
ulcer may be resected if the remaining duodenal stump is not indurated, and the
resection can be performed without injury to the ampulla.
REFERENCES
5. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of
complicated intra-abdominal infection in adults and children: guidelines by the
Surgical Infection Society and the Infectious Diseases Society of America. Clin
Infect Dis 2010;50(2):133–64.
6. Wong BC, Lam SK, Lai KC, et al. Triple therapy for Helicobacter pylori eradication
is more effective than long-term maintenance antisecretory treatment in the pre-
vention of recurrence of duodenal ulcer: a prospective long-term follow-up study.
Aliment Pharmacol Ther 1999;13(3):303–9.
7. Axon AT, O’Morain CA, Bardhan KD, et al. Randomised double blind controlled
study of recurrence of gastric ulcer after treatment for eradication of Helicobacter
pylori infection. BMJ 1997;314(7080):565–8.
8. Graham DY, Lew GM, Klein PD, et al. Effect of treatment of Helicobacter pylori
infection on the long-term recurrence of gastric or duodenal ulcer. A randomized,
controlled study. Ann Intern Med 1992;116(9):705–8.
9. Busman DC, Volovics A, Munting JD. Recurrence rate after highly selective
vagotomy. World J Surg 1988;12(2):217–23.
10. Sawyer JL, Scott HW Jr. Selective gastric vagotomy with antrectomy or pyloro-
plasty. Ann Surg 1971;174(4):541–7.