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adequate airway prior to any procedure.
EGD is the most important assessment tool since it
can be both diagnostic and therapeutic.
Treat patients with a PPI and evaluate for
H. pylori
infection.
EGD is a reasonable approach for patients who
rebleed and are not profoundly unstable.
Angiographic embolization is an option for patients
who fail endoscopic therapy or have
contraindications to surgery, but this option must be
readily available.
The operative approach should focus on cessation of
bleeding followed by an acid reduction procedure, if
appropriate.
SELECTED READINGS
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.
Elmunzer BJ, Young SD, Inadomi JM, et al. Systematic review of the
predictors of recurrent hemorrhage after endoscopic hemostatic therapy
for bleeding peptic ulcers. Am J Gastroenterol. 2008;103:2625–2632.
Katschinski B, Logan R, Davies J, et al. Prognostic factors in upper
gastrointestinal bleeding. Dig Dis Sci. 1994;39:706–712.
Lau JY, Sung JJ, Lam YH, et al. Endoscopic retreatment compared with
surgery in patients with recurrent bleeding after initial endoscopic control
of bleeding ulcers. N Engl J Med. 1999;340:751–756.
Lau JY, Sung JJ, Lee KK, et al. Effect of intravenous omeprazole on
recurrent bleeding after endoscopic treatment of bleeding peptic ulcers.
N Engl J Med. 2000;343:310–316.
Leontiadis GI, Sharma VK, Howden CW. Systematic review and meta-
analysis of proton pump inhibitor therapy in peptic ulcer bleeding. BMJ.
2005;330:568.
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Marmo R, Rotondano G, Piscopo R, et al. Dual therapy versus
monotherapy in the endoscopic treatment of high-risk bleeding ulcers: a
meta-analysis of controlled trials. Am J Gastroenterol. 2007;102:279–
289.
Vergara M, Calvet X, Gisbert JP. Epinephrine injection versus epinephrine
injection and a second endoscopic method in high risk bleeding ulcers.
Cochrane Database Syst Rev. 2007;CD005584.
Zittel TT, Jehle EC, Becker HD. Surgical management of peptic ulcer
disease today–Indication, technique and outcome. Langenbecks Arch
Surg. 2000;385:84–96.
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18
Perforated Duodenal Ulcer
CONSTANCE W. LEE and GEORGE A. SAROSI
Jr.
Presentation
A 70-year-old man presents to the emergency
department (ED) with a 1-hour history of generalized
abdominal pain that began abruptly and now radiates to
both shoulders. The patient has a prior history of peptic
ulcer disease but is not currently on acid-suppression
therapy. He is also on low-dose aspirin for peripheral
vascular disease. He has never had an abdominal
surgery. He has no known drug allergies. He does not
smoke tobacco or drink alcohol.
On physical examination, his temperature is 36.5°C,
heart rate is 100, blood pressure is 125/70, and his
abdomen is diffusely tender to palpation.
Differential Diagnosis
The differential diagnosis for this patient includes the
following: perforated hollow viscus secondary to peptic
ulcer disease (PUD), carcinoma, gastrinoma, mesenteric
ischemia, small bowel obstruction, Crohn’s disease, and
Boerhaave’s syndrome; pancreatitis, appendicitis,
diverticulitis, ruptured abdominal aortic aneurysm, ruptured
ectopic pregnancy, pneumonia, pulmonary infarction, and
renal or biliary colic.
Peptic ulcers are most frequently found in the stomach
and duodenum. They are most often associated with
Helicobacter pylori
infection or the use of nonsteroidal antiinflammatory drugs (NSAIDs), including aspirin. Risk
factors for the development of NSAID-related ulcers include
advanced age, history of prior ulcer, serious systemic
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illness, concomitant use of anticoagulants or
corticosteroids, and high NSAID doses. Less common
causes of PUD include gastrinoma, systemic mastocytosis,
carcinoma, sarcoidosis, Crohn’s disease, and carcinoid
syndrome.
Ulcer complications include perforation, obstruction,
and bleeding. In a review of 88 patients with a perforated
peptic ulcer, the most common location of perforation was
the duodenal bulb (62%), followed by the pyloric region
(20%), and then the gastric body (18%). Ulcer perforation is
associated with prior history of ulcer disease and use of
NSAIDs. In the setting of NSAID therapy, the risk factors
associated with ulcer perforation include a history of prior
ulcer, age >60 years, and the concomitant use of steroids,
anticoagulants, selective serotonin reuptake inhibitors, or
alendronate.
The classic clinical presentation of a perforated peptic
ulcer has been described as a three-stage process:
1. Early (onset to 2 hours): The abdominal pain begins
abruptly, with the patient often being able to
remember the exact time the pain started. The pain
may first localize to the epigastrum but quickly
becomes generalized. The pain may radiate to the
shoulders if the diaphragm is irritated. On
examination, the patient may be tachycardic, have a
low body temperature, and the abdomen is tender to
palpation.
2. Intermediate (2 to 12 hours): The patient may report
an improvement in pain. However, on physical exam
the patient often displays increased pain with
movement, and the abdominal wall is rigid. In
addition, there may be significant pain with palpation
of the hypogastrum and right lower quadrant
secondary to drainage of enteric contents from the
perforation.
3. Late (after 12 hours): The patient may complain of
increased pain and fevers, signs of hypovolemia, and
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increased pain and fevers, signs of hypovolemia, and
abdominal distension. Although the patient may vomit
during any stage, it is most common at this stage.
Workup
It is important to quickly diagnose a perforated peptic ulcer
because the prognosis is good if treatment is provided
within the first 6 hours, whereas delayed treatment beyond
12 hours is associated with decreased survival and
increased morbidity.
Imaging Studies
An upright chest x-ray or an abdominal x-ray may reveal the
presence of intraperitoneal free air. A computed
tomography (CT) scan may also be used to identify
intraperitoneal free air or free fluid. However, approximately
10% to 20% of patients with a perforated duodenal ulcer
will not have direct findings of perforation. If free air is
present, no other test is required to confirm the diagnosis.
An upper GI study or an abdominal CT scan with watersoluble contrast may demonstrate the leak if free air is not
present and a confirmatory test is required for diagnosis.
Laboratory Studies
Laboratory studies are not necessary for the diagnosis of a
perforated duodenal ulcer. However, they contribute to the
complete evaluation and appropriate management of the
patient. A basic metabolic panel will guide fluid and
electrolyte resuscitation. A complete blood count may
demonstrate leukocytosis with a left shift in a patient with a
perforated ulcer. A serum gastrin level may assist in the
diagnosis of gastrinoma, though the result of the test will
likely not return in time to influence the operative strategy.
Given that
H. pylori
infection is present in 70% to 90% of
duodenal ulcers and 30% to 60% of gastric ulcers, patients
with peptic ulcer disease should be tested. Noninvasive
testing for
H. pylori
infection includes urea breath testing,
stool antigen testing, and serology. Ideally,
H. pylori
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infection is identified preoperatively, as it can influence
operative strategy. A monoclonal stool antigen test is
available that has 94% sensitivity, 97% specificity, and may
be performed in about an hour. There is also a rapid stool
antigen test for the diagnosis of
H. pylori
that can be done
in 5 minutes. However, its sensitivity and specificity have
been shown to be 76% and 98%, respectively.
In our scenario, the patient’s presenting signs and
symptoms, combined with his risk factors place the
diagnosis of a perforated peptic ulcer high on the list of
differential diagnoses. An upright chest x-ray demonstrates
free intraperitoneal air. A stool antigen test is positive for
H.
pylori
infection. The ED physician consults general surgery,
starts fluid resuscitation, initiates nasogastric
decompression, places a Foley catheter, and administers
omeprazole, ampicillin, metronidazole, ceftriaxone, and
fluconazole.
Diagnosis and Treatment
The medical/nonoperative management of a perforated
peptic ulcer includes fluid resuscitation, nasogastric
decompression, acid suppression, and empiric antibiotic
therapy for coverage of enteric gram-negative rods, oral
flora, anaerobes, and fungus. In the setting of a perforated
duodenal ulcer without peritonitis, the application of a
nonoperative management strategy has been proposed,
especially for patients at high risk for operative
complications. However, delaying the surgical repair of a
perforated peptic ulcer more than 12 hours after
presentation has been associated with increased morbidity
and mortality. Furthermore, a randomized trial of
nonoperative treatment for perforated peptic ulcers by
Crofts et al. demonstrated that patients over 70 years of
age were less likely to improve with conservative
management. Operative management is the preferred
treatment strategy in most patients, especially the elderly.
In our clinical scenario, you evaluate the patient 2 hours
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after the start of the symptoms, at which time the patient
notes an improvement in generalized pain. However, on
examination the heart rate is 110, the blood pressure is
90/50, and the abdomen is rigid, with the patient more
sensitive to changes in position. You decide to proceed to
the operating room for management of this problem. On
exploration of our patient you identify a 1 cm anterior
duodenal perforation.
Surgical Approach
Elective operations for peptic ulcer disease have become
uncommon with the successful medical management of
acid and
H. pylori
infection. However, surgical management
is almost always indicated for a perforated ulcer, especially
when the patient is hemodynamically unstable, has signs of
peritonitis, or has evidence of free contrast extravasation
on imaging. Although operative treatment is the
appropriate plan, the patient should receive fluid
resuscitation and antibiotic treatment while preparing the
operating room. It should be noted that emergency surgery
for peptic ulcer perforation has up to 30% risk of mortality.
The presence of comorbid disease has been shown to
increase mortality. Furthermore, in patients requiring
emergency surgery, variables identified as being
independently associated with mortality include age,
American Society of Anesthesiologists (ASA) class, shock
on admission, hypoalbuminemia on admission,
preoperative metabolic acidosis, and an elevated serum
creatinine.
Surgical Procedure(s) for the Management of
Perforated Duodenal Ulcers
1.
Omental patch repair
(Table 1): The safest technique
for the management of a perforated duodenal ulcer,
especially in the setting of delayed repair (>24 hours
after presentation), hemodynamic instability, or
significant intra-abdominal contamination is a patch
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repair with an omental pedicle. This technique combined
with the appropriate medical therapy is likely sufficient in
the case of a patient with a history of
H. pylori
infection
or NSAID use.
TABLE 1. Key Technical Steps to Maneuvers in Oversewing a Bleeding
Duodenal Ulcer
The repair may be performed laparoscopically or open.
The perforation is repaired by taking a seromuscular bite
from one side of the perforation, taking a bite of omentum,
followed by another seromuscular bite from the other side
of the perforation, and then tying to fix the omental pedicle
in place. Typically, three to four sutures are required to
secure the patch. Follow the repair by irrigation of the
peritoneal cavity with large volumes of warm saline.
Pitfalls
• The optimal repair of duodenal ulcer perforations >2 cm
can be challenging, and the omental patch repair may
be associated with increased risk of failure. Performing
a definitive repair has been suggested, as have less
standard repairs, including tube duodenostomy.
• On exploration, the omentum, liver, or gallbladder may
have already “patched” the perforation, in which case the
surgeon must decide whether to remove the natural
patch and surgically repair the defect, or to simply
irrigate the peritoneal cavity.
• If the ulcer perforation is located at the distal end of the
pyloric channel, the duodenum may need to be
mobilized to provide adequate exposure of the defect.
2. A definitive ulcer procedure may be performed if the
patient is hemodynamically stable, has minimal intra-
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abdominal contamination, and either (1) has a history of
PUD with unknown
H. pylori
status or (2) is unable to
stop NSAID therapy.
a.
Truncal vagotomy and pyloroplasty (drainage) (V&D)
(Table 2): A truncal vagotomy reduces basal acid
secretion by 80% and stimulated acid secretion by
50%. It reduces acid secretion by preventing direct
cholinergic stimulation for acid secretion and by
decreasing the response of parietal cells to histamine
and gastrin. Unfortunately, a truncal vagotomy also
damages the stomach’s receptive relaxation and
antral grinding, in addition to the pyloric sphincter’s
coordination required for gastric emptying. To
compensate for these changes, a pyloroplasty is
performed to facilitate stomach drainage. The benefit
of V&D is that it is safe and may be done relatively
quickly. The drawbacks of the procedure are that
10% of patients later report diarrhea or dumping
syndrome, and 10% have a recurrent ulcer.
TABLE 2. Truncal Vagotomy and Pyloroplasty Key Points
Procedure:
Access the esophageal hiatus by dividing
the left triangular ligament and retracting the left
lateral lobe of the liver. Open the peritoneum overlying
the esophagus by dividing the lesser omentum and
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the esophagophrenic ligament. Use blunt dissection
between the esophagus and the adjacent crux to
allow two fingers behind the esophagus. Careful
dissection is critical to avoid iatrogenic esophageal
perforation. Downward traction on the
gastroesophageal junction facilitates identification of
the vagus nerve. Identify the anterior and posterior
vagal trunks, dissect them from the esophagus, and
then transect them (Figure 2). Mark the transected
vagal margins with hemoclips and send biopsies of
both nerves to pathology to confirm that the
transected structures were nerves. Note that the
criminal nerve of Grassi coming off the posterior
vagus trunk can be missed if the vagotomy is
performed lower on the esophagus; to avoid this,
complete circumferential dissection of the distal 6 cm
of the esophagus ensures division of these nerve
fibers.
A Heinecke-Mikulicz pyloroplasty is performed by
mobilizing the second part of the duodenum using a
Kocher maneuver. Then a 5 cm incision is made from
the antrum, over the pyloric sphincter, and onto the
proximal duodenum. Place seromuscular tacking
sutures to the cephalad and caudad ends of the
incision to facilitate the transverse closure of the
wound (Figure 1). The incision is closed in one or
two layers. If closed in two, start with an inner layer of
full-thickness interrupted absorbable sutures, followed
by a seromuscular layer of Lembert sutures.
Alternatively, a stapled closure may be performed
using a TA-55 stapler containing 4.8 mm staples.
Note that if the duodenum is severely scarred or
inflamed, then a gastrojejunostomy may be used in
place of a pyloroplasty.
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