Scandinavian Journal of Surgery 99: 73–77, 2010
Gastroduodenal perforation: Maximal or minimal
intervention?
F. Y. Lui, K. A. Davis
Section of Trauma, Surgical Critical Care and Surgical Emergencies,
Yale University Department of Surgery, New Haven, CT, U.S.A.
Key words: Peptic ulcer; perforation; Helicobacter pylori; peritonitis; emergency surgery; nonoperative
management
Introduction
Over the last quarter century, a paradigm shift has
occurred in the surgical management of critically ill
and injured patients across a variety of surgical dis-
eases. The advent of minimally invasive techniques,
angiographic interventions, and the increasing use of
both nonoperative management and damage control
surgery has prompted the careful assessment of the
risks and benefits of aggressive surgical intervention
in critically ill patients, who may not be able to toler-
ate the associated physiologic costs.
The medical management of peptic ulcer disease
has undergone a major revolution, with the develop-
ment of anti-secretory medications including hista-
mine 2 receptor blockers (H2RBs) and proton pump
inhibitors (PPIs). The additional recognition that pep-
tic ulceration is an infectious disease and treatment
for Helicobacter pylori infection has further improved
outcomes (1). Despite this, the incidence of surgery
for gastroduodenal perforation has remained stable
or increased over the past two decades. This may in
part be due to increased use of non-steroidal anti-
inflammatory medications and/or aspirin, especially
in elderly patients in whom surgical intervention may
be increasing.
The gold standard for the management of gas-
troduodenal perforation has traditionally been open
exploration with surgical repair in association with
an acid reducing procedure. While excellent results
can be achieved in stable patients in good condition,
surgery in elderly patients and those in extremis has
Correspondence:
Kimberly A. Davis, M.D.
Section of Trauma, Surgical Critical Care
and Surgical Emergencies
Yale University Department of Surgery
330 Cedar Street, BB 310
PO Box 208062
New Haven, CT 06520-8062, U.S.A.
Email: kimberly.davis@yale.edu
been associated with high morbidity and mortality
(2). With the advent of increasingly successful medi-
cal management for hyperacidity, the need for surgi-
cal acid reducing procedures has declined signifi-
cantly. Excellent results can be obtained with less
aggressive, non-resectional surgical intervention. Tra-
ditionally performed via an open approach, the use
of minimal access techniques has become increas-
ingly frequent, resulting in similar outcomes to open
surgery, with decreased perioperative pain. Addi-
tionally, nonoperative management has become more
frequent in hemodynamically normal patients with
minimal abdominal and systemic symptoms (3, 4).
Nonoperative management in otherwise healthy pa-
tients has yielded good results, but its use in those
who are poor surgical candidates due to severe co-
morbidities has not been formally examined.
Incidence and etiology
Ulcer disease remains the most common cause of gas-
troduodenal perforation, with an incidence between
2% and 10% in patients with ulcers (5). Infection with
Helicobacter pylori has been clearly implicated in the
development of gastric and duodenal ulcers, and re-
sponds well to antimicrobial therapy. Despite success
in decreasing the recurrence rate of peptic ulcers
through treatment with antimicrobials, H2 receptor
blockers and proton pump inhibitors, the frequency
of peptic ulcer complications requiring surgical inter-
vention has increased, especially in elderly patients
(1). The use of aspirin (ASA) and/or non-steroidal
anti-inflammatory medications (NSAID) has been
clearly shown to increase the incidence of peptic ulcer
disease in a dose dependent manner. It is likely that
the increased frequency of complications related to
peptic ulcers is related to the increased use of these
medications in this population (6, 7).
Other causes of gastroduodenal perforation are
traumatic, neoplastic, foreign body ingestion, and
those that occur as a result of a diagnostic or thera-
74 F. Y. Lui, K. A. Davis
Table 1
Causes of gastroduodenal perforation.
Nontraumatic
 Gastric ulcer
  Duodenal ulcer
 Obstruction
  Ischemia
  Malignancy
Traumatic
  Iatrogenic
  Foreign body
  Violence
Table 2
Boey score.
Concomitant severe medical illness
Preoperative shock
Duration of perforation > 24 hours
Score: 0–3 (Each factor scores 1 point if positive)
Table 3
Boey score and outcomes.
Risk score Mortality (OR) Morbidity (OR)
1 08%  (2.4) 47%  (2.9)
2 33%  (3.5) 75%  (4.3)
3 38%  (7.7) 77%  (4.9)
Adapted from Lohsiriwat V, Prapasrivorakul S, Lohsiriwat D. Per-
forated peptic ulcer: clinical presentation, surgical outcomes, and
the accuracy of the Boey scoring system in predicting postopera-
tive morbidity and mortality. World J Surg. 2009 Jan;33(1):80–65.
peutic intervention (iatrogenic). Traumatic injury to
the stomach and duodenum causing perforation is
rare, comprising only 5.3% of all blunt hollow organ
injuries, but is associated with a complication rate of
27% to 28% (8). Perforations from malignancy can
result from obstruction and increased luminal pres-
sure, or from successful treatment and response to
chemotherapy and involution of a previously trans-
mural tumor (9). Foreign bodies, ingested either in-
tentionally or accidentally can cause perforations,
either through direct injury or as a result of luminal
obstruction (10, 11) (Table 1)
Iatrogenic injury is a rising cause of gastroduode-
nal perforation. The increasing use of esophagoduo-
denoscopy for diagnosis and therapy is associated
with an increase in procedure related perforations
(12). Gastroduodenal perforation has also been re-
ported as a complication of a variety of abdominal
procedures including inferior vena cava filter place-
ment (13, 14), ERCP (15 16), and biliary stents (17).
Outcomes
When diagnosed promptly and treated expediently,
outcomes are excellent. Mortality rates range from 6
to 14% in recent studies (18, 19, 20). Poor outcomes
have been associated with increasing age, major me-
dial illness, pre-operative hypotension (21), and de-
lays in diagnosis and management (greater than 24
hours) (22). With improvements in resuscitation, hy-
potension may no longer be a significant prognostic
indicator (23). Advanced age (greater than 70 years)
is associated with a higher mortality with rates of
approximately 41% (24, 25).
Several scoring systems including the Boey scoring
system (22) (Table 2 and 3) and the Mannheim Peri-
tonitis Index (MPI) (26) have been used to risk stratify
patients and predict outcomes of patients with perfo-
rated peptic ulcer. The Boey score is the most com-
monly and easily implemented of these scoring sys-
tems, and accurately predicts perioperative morbidity
and mortality.
Morbidity is common after perforation, with rates
ranging from 17% to 63% (27, 28). Pulmonary and
wound infections are the most common postopera-
tive infections. Fungal infections after perforation are
fairly common (between 13 and 37%) and when iden-
tified are associated with significant mortality (up to
21.7%) (29, 30).
Diagnosis
Prompt diagnosis of gastroduodenal perforation re-
quires a high index of suspicion based on history and
clinical examination. A history of intermittent abdom-
inal pain or gastroesophageal reflux is common. Ad-
ditionally, known peptic ulcer disease that has been
inadequately treated or with ongoing symptoms and
sudden exacerbation of pain can be an indication of
perforation. A history of recent trauma or instrumen-
tation followed by pain and tenderness should alert
the clinician to the potential for injury. Patients with
gastroduodenal perforation usually present with ab-
dominal pain and peritoneal irritation from leakage
of acidic gastric contents. However, physical exami-
nation findings may be equivocal, and peritonitis
may be minimal or absent, particularly in patients
with contained leaks (31). Patients in extremis may
also present with altered mental status, further com-
plicating an accurate physical examination. Labora-
tory studies are not useful in the acute setting as they
tend to be nonspecific, but leukocytosis, metabolic
acidosis, and elevated serum amylase may be associ-
ated with perforation (31).
Free air under the diaphragm found on an upright
chest X-ray is indicative of hollow organ perforation
and mandates further work-up and/or exploration.
In the setting of an appropriate history and peritoni-
tis on examination, free air on X-ray is sufficient to
justify exploration. In patients without pneumoperi-
toneum on admission chest radiograph should be
evaluated with computed tomography (CT) scanning
with oral contrast.
The increased use of CT scans has greatly improved
our ability to detect perforation. Suspicious findings
on CT scan include unexplained intraperitoneal fluid,
pneumoperitoneum, bowel wall thickening, mesen-
teric fat streaking, mesenteric hematoma and extrava-
sation of contrast (32, 33). However, up to 12% of
 Gastroduodenal perforation: maximal or minimal intervention?
patients with traumatic perforations may have a nor-
mal CT scan.
In the setting of trauma, diagnostic peritoneal la-
vage (DPL) has essentially been replaced by the fo-
cused assessment by sonography for trauma (FAST),
which lacks specificity for hollow organ perforation
(34, 35). Victims of penetrating trauma with signs of
peritonitis merit surgical exploration without further
diagnostic workup. In blunt trauma patients, and in
penetrating trauma patients without peritonitis, in
whom the trajectory of the missile may be unclear, CT
scanning of the abdomen and pelvis with oral and
intravenous contrast remains the standard of care.
Management
It is estimated that approximately half of perforations
will seal themselves. Therefore, in a select popula-
tion, nonoperative management of the perforated
ulcer is a reasonable option. The onset of symptoms
of less than 24 hours, mild abdominal pain with min-
imal peritoneal irritation, hemodynamic stability and
an absence of systemic signs of sepsis in a patient
under the age of 70 are all indications for a trial of
nonoperative management (36, 37). Imaging studies,
most commonly CT of the abdomen, but occasionally
gastroduodenography with a water soluble contrast,
should be performed to identify any contrast extrava-
sation. Patients with contained perforations, and
those without free contrast extravasation, are candi-
dates for nonoperative management. Nasogastric
tube decompression, fluid resuscitation, administra-
tion of a proton pump inhibitor, thromboembolic pro-
phylaxis and appropriate antimicrobial therapy
should result in clinical improvement in a patient’s
symptomatology within 12 hours (36, 37). However,
it has been clearly demonstrated that observation pe-
riods of longer than 12 hours without improvement
worsen the outcomes from perforated peptic ulcers,
and should be avoided (38–40). Patients with hemo-
dynamic instability, onset of symptoms longer that 24
hours in duration, those with peritonitis on physical
examination and those with systemic signs of sepsis
should be surgically explored. Additionally, patients
who are age 70 or greater are less likely to respond to
nonoperative management, and should be considered
for early operative intervention (37). Mortality rates
between 0% and 8% have been reported for nonop-
erative management as opposed to 3–9% for emer-
gency ulcer surgery (41–43). Complication rates of
nonoperative management are significant, occurring
in 13–73% of patients, and encompass septic shock,
multisystem organ failure, intra-abdominal abscesses,
delayed surgical management and delayed abdomi-
nal closure (41). However, little data exists in the
modern era of PPI use and Helicobacter pylori eradica-
tion. Bucher et al. demonstrated that in their series of
PPI treated patients, a mortality of 11% and a morbid-
ity of 16% could be achieved (44)..
Failure of nonoperative management, defined as
increasing abdominal symptoms, fever or worsening
leukocytosis, should prompt urgent surgical inter-
vention. Most perforated peptic ulcers are located in
75
the first part of the duodenum (35–65%), with 25–45%
located in the pylorus and 5–25% located in the stom-
ach (45–48). In the era of H. pylori therapy and acid
reducing medications, up to 90% of perforations may
be treated with simple closure with or without omen-
tal patch (Graham patch). Definitive ulcer surgery is
no longer required in the majority of patients, as re-
currence rates have dropped dramatically with post-
operative medical therapy (49–53). For gastric ulcers,
excision of the ulcer for pathologic examination re-
mains an important surgical tenet, to rule out the
possibility of perforated gastric malignancy (36, 37,
39, 54). Formal gastric resection with reconstruction
(Billroth I, Billroth II, Roux-en-Y) with or without
vagotomy is rarely required, and is used in less than
10% of cases (40, 45–47, 51). In patients with a recent
(< 12 hr) perforation with a history of chronic ulcer
disease and prior failed medical therapy, a definitive
ulcer operation may be indicated (55–57).
Minimally invasive surgical techniques have
gained in popularity, as several reports demonstrate
equivalent outcomes to open surgery (58–67). In fact,
the laparoscopic approach appears feasible in most
cases, with a conversion rate to open surgery of less
than 25% (54, 58–67). Although operative times are
generally longer, there appears to be no difference in
the open vs. laparoscopic approaches, except poten-
tially in decreased postoperative pain (58, 60, 61,
64–66). Patients with large perforations, perforations
in the posterior location, or patients with significant
medical comorbidities are considered to have relative
contraindications to the laparoscopic approach, and
should be considered for open surgery (54, 58, 62,
66).
Emergency operations for perforated peptic ulcer
disease results in a mortality of 6–30% (38, 39, 45–47,
51, 60, 70). Perioperative shock, renal failure, delayed
operative intervention > 12 hours, significant co-mor-
bidities, advanced age, cirrhosis and immunocom-
promise have all been identified as risk factors for
adverse outcome (38, 40, 45, 46, 67, 68). In fact, delays
of greater than 12 hours result in a three-fold increase
in mortality, while delays of 24 hours are associated
with a nine-fold increase in mortality (38, 40). The
presence of underlying cardiovascular or pulmonary
disease, or diabetes mellitus, identified in approxi-
mately 50% of all patients with perforation, is associ-
ated with a mortality of up to 50%. Advanced age,
particularly age greater than 70 years, dramatically
increases mortality (45, 46). Additionally, the mortal-
ity appears to be related to the location of the inciting
ulcer, as gastric ulcers have a two- to three-fold in-
crease in mortality relative to duodenal ulcers (38–40,
46, 47, 51). The need for gastric resection increases
this risk relative to simple closure (40).
Traumatic perforations of the stomach and duode-
num can be the result of both blunt and penetrating
mechanisms of injury. Generally, these can be man-
aged with simple suture repair, without the need for
resection. However, in large devitalizing blunt
wounds of the second and third portions of the duo-
denum, resection with reconstruction may be re-
quired. Perforations related to neoplasm generally
require formal resection for management.
76 F. Y. Lui, K. A. Davis
Postoperative morbidity is generally infectious,
with pneumonia as the most common complication
(up to 30%), followed by superficial and deep surgi-
cal site infections (46, 47). In the elderly, perioperative
cardiovascular morbidity is increased (46, 47, 67).
Summary
With modern improvements in resuscitative care and
acid suppressive therapy with PPI’s, a less aggressive
operative approach has been shown to be effective in
the management of gastroduodenal perforation. In
the majority of cases, simple closure with or without
omental patch combined with optimal medical man-
agement including acid suppression and antibiotic
therapy for H. pylori is appropriate. Resectional ther-
apy, including an acid reducing procedure, is unnec-
essary in most patients, and should be reserved for
those patients who have failed prior medical therapy.
Surgery may be performed either using open or lap-
aroscopic techniques with equivalent outcomes. In a
small subset of patients who present with minimal
symptoms, contained perforations, and without sys-
temic derangements, nonoperative management is an
option, but requires close observation and a low
threshold for surgical intervention if clinical deterio-
ration occurs.
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Received: May 4, 2010