1%. Permanent symptoms of dumping are rare after proximal gastric vagotomy. The incidence of

diarrhea, which is presumably caused by denervation of the pylorus and small bowel and by elimination

of pyloric function, parallels the incidence of dumping after truncal vagotomy and antrectomy or

pyloroplasty. Persistent or disabling diarrhea is present in less than 1% of patients after proximal gastric

vagotomy.

Most prospective surgical series were reported in the era before the pathogenic role of H. pylori was

appreciated. With appropriate use of postoperative antimicrobials directed against H. pylori, ulcer

recurrence rates are currently much lower than historical standards. Although recurrence rates (without

H. pylori treatment) as low as 5% have been reported, a more generally accepted figure is 10%. This

rate is similar to that of reinfection with H. pylori after its successful eradication. The reported ulcer

recurrence rates after proximal gastric vagotomy can be adversely affected by the inclusion of

prepyloric and pyloric channel ulcers.

Hemorrhage

5 Hemorrhage is the leading cause of death associated with peptic ulcer, and the incidence of this

complication has not changed since the introduction of H2

-receptor antagonists. The lifetime risk of

hemorrhage for patients with duodenal ulcer who have not had surgery and who do not receive

continuing maintenance drug therapy approximates 15% at 5 years.15 Most hemorrhages occur during

the initial episode of ulceration or during a relapse, and patients who have hemorrhaged previously

have a higher risk of bleeding again. Continued or recurrent bleeding occurs in 20% to 30% of patients,

and when this happens, mortality varies between 10% and 40%. Patients with recurrent hemorrhage

and elderly patients are at greatest risk of death, and these two groups should be resuscitated

vigorously, investigated promptly, and treated aggressively.16,17

The contemporary risk of mortality from bleeding ulcer approximates 10% to 20%. Operative risk is

increased in patients who have shock at admission, recurrent bleeding, delay in operative intervention,

or coexisting medical illnesses. Surgical delay may lead to recurrent hypovolemia and, subsequently,

multisystem organ failure.

Upper gastrointestinal endoscopy is the appropriate initial diagnostic test when hemorrhage from

duodenal ulceration is suspected. Endoscopy can correctly determine the site and cause of bleeding in

more than 90% of patients. An ulcer should be accepted as the bleeding source only if it has one of the

stigmata of active or recent hemorrhage. Active hemorrhage is defined by an arterial jet, active oozing,

or oozing beneath an adherent clot. The signs of recent hemorrhage include an adherent clot without

oozing, an adherent slough in the ulcer base, or a visible vessel in the ulcer. The ability of these

endoscopic findings to accurately predict recurrent hemorrhage has been extensively validated.

Approximately 30% of patients who have stigmata of recent hemorrhage experience rebleeding, and

most of the patients who experience recurrent hemorrhage require emergency treatment. These

stigmata are not sufficiently accurate to be used alone as indications for surgery. Rather, they serve as a

warning that aggressive therapy is needed and close follow-up mandatory. The occurrence of

hypovolemic shock, rebleeding during hospitalization, and a posteroinferior location of the ulcer are

additional clinical features that have been associated with increased risks of recurrent bleeding. A recent

study suggests that rebleeding risk in excess of 30% justifies second-look endoscopy as a means to

anticipate, and thus preemptively treat, ulcers at highest risk of recurrent hemorrhage.18 The role of

gastric acidity as a cause for in-hospital rebleeding appears to be inconsequential, and reduction of acid

secretion by H2

-receptor antagonists or omeprazole is not sufficient to prevent recurrent hemorrhage.

The ability to visualize bleeding duodenal ulcers endoscopically has led to development of methods to

treat hemorrhage endoscopically. There are many different methods of endoscopic therapy, but the

most established consist of thermal coagulation, injection of alcohol, or sclerosants. Thermal

coagulation can be achieved by bipolar electrocoagulation or direct application of heat through a heater

probe. Injection of epinephrine into the base of the bleeding ulcer is also effective in control of ulcer

hemorrhage.

Proof of efficacy, in the form of lowered rebleeding rates and avoidance of operation, has been

convincingly demonstrated for all of these methods of endoscopic hemostasis. The analysis of reports of

endoscopic treatment of hemorrhage is complicated by the 70% rate of spontaneous, although

sometimes temporary, cessation of bleeding without intervention. In addition to endoscopic stigmata,

hemodynamic instability, need for continuing transfusion, red stool or hematemesis, age older than 60

years, and serious medical comorbidity are clinical features that mandate endoscopic therapy.

Rebleeding during hospitalization and the endoscopic findings of visible vessel, oozing, or bleeding

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associated with an adherent clot are other indications for endoscopic hemostasis. Ulcers with clean bases

require no treatment. Failure of endoscopic hemostasis is usually due to inaccessibility because of

scarring, to rapid active bleeding obscuring the endoscopic view, or to an adherent clot. Patients treated

endoscopically should be observed closely for further hemorrhage. Patients who rebleed within 72

hours of initial endoscopic control may be successfully retreated without increasing the risk of

mortality.19

The efficacy of endoscopy is dependent on timing. Early endoscopy correctly identifies patients at low

risk for recurrent hemorrhage and permits safe avoidance of hospitalization. Early endoscopy also

benefits high-risk patients by directing active hemostatic therapy. Patients treated in this way have been

demonstrated to have fewer episodes of rebleeding, lower rates of operation, and shorter

hospitalizations.

Table 45-3 lists situations in which operative intervention is appropriate. The need for emergency

surgery significantly increases surgical risks; mortality rates are increased approximately 10-fold.

Operative therapy should consist of duodenostomy with direct ligation of the bleeding vessel in the

ulcer base.

INDICATIONS/CONTRAINDICATIONS

Table 45-3 Situations in Which Operative Intervention is Appropriate

Postoperatively, patients should receive antibiotics directed against H. pylori. This treatment

paradigm is based on the observation that peptic ulcer hemorrhage recurs in 20% of patients in whom

H. pylori is not eradicated, whereas rebleeding is reduced to 3% in patients who receive H. pylori

eradication therapy (Algorithm 45-1).20 The studies that support this practice were not specifically

designed to evaluate postoperative hemorrhage, but the results are so definitive that they support this

application (Fig. 45-4).

Perforation

The lifetime risk for perforation in patients with duodenal ulceration who do not receive therapy

approximates 10%. In contrast, ulcer perforation is unusual if initial ulcer healing has been achieved.

Perforation of a duodenal ulcer is usually accompanied by sudden and severe epigastric pain. The

pain, caused by the spillage of highly caustic gastric secretions into the peritoneum, rapidly reaches

peak intensity and remains constant. Radiation to the right scapular region is common because of right

subphrenic collection of gastric contents. Occasionally, pain is sensed in the lower abdomen if gastric

contents travel caudally through the paracolic gutter. Peritoneal irritation is usually intense and most

patients avoid movement to minimize discomfort.

Physical examination reveals low-grade fever, diminished bowel sounds, and rigidity of the

abdominal musculature. Usually, upright abdominal radiographs reveal pneumoperitoneum, but up to

20% of perforated ulcers do not show free intraperitoneal air. Computed tomography of the abdomen is

very sensitive for demonstrating perforation if pneumoperitoneum is not demonstrated but perforation

is still suspected.

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Figure 45-4. Probability of freedom from recurrent hemorrhage according to posttreatment H. pylori status.

Algorithm 45-1. Treatment of bleeding duodenal ulceration.

Although occasional reports have described the nonoperative treatment of this complication,

perforation remains a strong indication for surgery in most circumstances. Laparotomy or laparoscopy

affords the opportunity to relieve intraperitoneal contamination and to close the perforation (Fig. 45-5).

Signs of antecedent duodenal ulceration, in terms of history of prior symptoms and anatomic evidence

of duodenal scarring, should be sought. A lack of antecedent symptoms is not protective. Reports

suggest that patients without antecedent symptoms are also at risk for recurrent ulceration. By 5 to 6

years, symptomatic ulcer recurrence in patients with acute ulcer perforation is similar to that for

patients with chronic disease. Before the role of H. pylori was appreciated, simple omental closure of

duodenal perforation resulting from chronic ulceration did not provide satisfactory long-term results; up

to 80% of patients so treated had recurrent ulceration, and 10% experienced reperforation if untreated.

Approximately four-fifths of all patients with perforation have H. pylori infestation and therefore are at

risk of recurrent disease.

The mortality of emergent ulcer operations is most clearly correlated with the following

circumstances: preoperative shock, coexisting medical illness, and presence of perforation for more than

48 hours.21 Mortality increases progressively with the number of prognostic variables present – the socalled Boey Score – being 0%, 10%, 45%, and 100% with zero to three positive. Mortality with

perforated peptic ulcer disease has also been correlated with the American Society of Anesthesiology

(ASA) score and the Peptic Ulcer Perforation (PULP) score.22

6 Current reports advocate omental patch closure only, often laparoscopically, with postoperative

1175

anti–H. pylori therapy. This approach presumes that most duodenal ulcers are caused by H. pylori, that

secure closure of the perforation can be obtained, and that further surgical therapy will be obviated by

the effects of medical therapy. Minimally invasive approaches are becoming standard practice.

Figure 45-5. Omental patching of perforated duodenal ulcer.

Three meta-analyses of surgical treatment of perforated peptic ulcer have compared open surgical

therapy with laparoscopic approaches.23–25 In terms of operative time, there is no clear superiority of

one approach over the other, but trials reported after 2001 have favored laparoscopic repair. While inhospital analgesic use is less in laparoscopically treated patients, the more important variable of hospital

length of stay was not significantly shorter for these patients. Overall rates of postoperative

complications were not statistically different between the two approaches. A lower rate of wound

infection in the laparoscopic group approached significance. Return to normal daily activities and work

favored the laparoscopic group. The pooled estimate of mortality favored laparoscopic repair. Thirtyday mortality risk approximates 15%.26 Septic complications, organ space infection, and prolonged

ventilation are leading causes of postoperative morbidity.27

Obstruction

Gastric outlet obstruction can occur acutely or chronically in patients with duodenal ulcer disease. Acute

obstruction is caused by edema and inflammation associated with ulcers in the pyloric channel and the

first portion of the duodenum. Pyloric obstruction is suggested by recurrent vomiting, dehydration, and

hypochloremic alkalosis due to loss of gastric secretions. Acute gastric outlet obstruction is treated with

nasogastric suction, rehydration, and intravenous administration of antisecretory agents. In most

instances, acute obstruction resolves with such supportive measures within 72 hours.

Repeated episodes of ulceration and healing can lead to pyloric scarring and a fixed stenosis with

chronic gastric outlet obstruction.

Upper endoscopy is indicated to confirm the nature of the obstruction and to exclude neoplasm.

Endoscopic hydrostatic balloon dilatation of pyloric stenoses can also be attempted at this time (Fig. 45-

6). Approximately 85% of pyloric stenoses are amenable to balloon dilatation. Only 40% of patients

with gastric stenoses have sustained improvement by 3 months after balloon dilatation. Recurrent

stenoses are presumably due to residual scarring in the pyloric channel. Thus, although pyloric

dilatation is occasionally palliative, in most cases operative correction is required.

Operative management of gastric outlet obstruction should be focused on relief of the anatomic

abnormality. Antrectomy has been used with success in this circumstance, with low ulcer recurrence

rates and with satisfactory restoration of gastric emptying.

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GASTRIC ULCER

Benign gastric ulcers are a form of peptic ulcer disease, occurring with one-third the frequency of

benign duodenal ulceration. In the United States, gastric ulcer is somewhat more common in men than

in women and occurs in a patient cohort approximately 10 years older than for duodenal ulceration.

Endoscopic Diagnosis

Upper gastrointestinal endoscopy is the preferred method for diagnosing gastric ulceration. The ulcer

base in benign disease is commonly smooth and flat and often covered by a gray, fibrous exudate. The

margin is usually slightly raised, erythematous, and friable. Differentiation of benign and malignant

gastric ulcers is reliably made only by histologic examination. Visual endoscopic differentiation of

benign from malignant ulcers is not reliable. All gastric ulcers should have multiple biopsies taken from

the perimeter of the lesion. The addition of lesional brushings to biopsy increases diagnostic accuracy to

approximately 95%.

Benign gastric ulcers may occur in any location in the stomach, but approximately 60% are located

along the lesser curvature proximal to the incisura angularis. Less than 10% of benign gastric ulcers are

located on the greater curvature. Virtually all gastric ulcers lie within 2 cm of the histologic transition

between fundic and antral mucosa. With increasing age, this mucosal transition zone moves proximally

along the lesser curvature. Movement of this transition zone is reflected by the greater prevalence of

proximal ulcers in elderly patients.

As with benign duodenal ulceration, H. pylori plays a central role in the pathogenesis of benign gastric

ulcers.28 Benign gastric ulcers associated with H. pylori respond to antibiotic therapy at a rate equivalent

to that of duodenal ulceration. The recurrence rate of ulcerations in these patients after H. pylori

eradication is equal to the rate of reinfection.

A strong association of benign gastric ulceration with the use of NSAIDs has been recognized.

Cigarette smoking is associated with development of gastric ulceration, and continued smoking impedes

medical therapy. Gastric and duodenal ulcers have been noted in patients receiving hepatic artery

chemotherapy in whom improper placement of the catheter permits perfusion of gastric and duodenal

mucosae. A variety of agents, including 5-fluorouracil, cisplatin, doxorubicin, and mitomycin C, have

been implicated.

Figure 45-6. Schematic representation of balloon dilatation of pyloric stenosis.

Therapy

The primary therapy for benign gastric ulceration in most patients is antimicrobial treatment of H. pylori

infection. The treatment protocols are similar to those used for benign duodenal ulceration. For many

patients, cessation of NSAID therapy is also required.

Indications for surgical treatment of gastric ulcer include hemorrhage, perforation, failure of a

recurrent ulcer to respond to medical therapy, and inability to exclude malignant disease.

For benign gastric ulcers, the elective operation of choice is usually a distal gastrectomy with

gastroduodenal (Billroth I) anastomosis. The ulcer should be included in the gastrectomy specimen.

With this approach, operative mortality rates of 2% to 3%, with ulcer recurrence rates of less than 5%,

have been reported. Because benign gastric ulcers are not associated with gastric acid hypersecretion,

1177

inclusion of vagotomy is not necessary.

The occurrence of a gastric ulcer near the gastroesophageal junction represents a difficult surgical

problem. When possible, the ulcer should be excised. This usually requires a distal gastrectomy with an

extension along the lesser curvature near the esophageal wall and reconstruction with

gastrojejunostomy.

Emergency operations performed for hemorrhage or perforation require ulcer excision. Distal

gastrectomy, performed with gastroduodenal reconstruction, is usually the procedure of choice.

Operative mortality rates average 10% to 20% in the presence of hemorrhage or perforation.

POSTGASTRECTOMY SYNDROMES

A number of syndromes have been described that are associated with distressing symptoms after gastric

operations performed for peptic ulcer or gastric neoplasm. The occurrence of severe postoperative

symptoms is fortunately low, perhaps 1% to 3% of cases, but the disturbances can be disabling. The two

most common postgastrectomy syndromes, categorized according to predominant manifestation, are

dumping and alkaline reflux gastritis.

Dumping

The term dumping denotes a clinical syndrome with both gastrointestinal and vasomotor symptoms. The

precise cause of dumping is not known but is believed to relate to the unmetered entry of ingested food

into the proximal small bowel after vagotomy and either resection or division of the pyloric sphincter.

Early dumping symptoms occur immediately after a meal and include nausea, epigastric discomfort,

borborygmi, palpitations, and, in extreme cases, dizziness or syncope. Late dumping symptoms follow a

meal by 1 to 3 hours and can include reactive hypoglycemia in addition to the aforementioned

symptoms.

Although a relatively large number of patients experience mild dumping symptoms in the early

postoperative period, minor dietary alterations and the passage of time bring improvement in all but

approximately 1%. The somatostatin analogue octreotide has been reported to improve dumping

symptoms when 50 to 100 mg is administered subcutaneously before a meal. The beneficial effects of

somatostatin on the vasomotor symptoms of dumping are postulated to be due to pressor effects of the

compound on splanchnic vessels. In addition, somatostatin analogues inhibit the release of vasoactive

peptides from the gut, decrease peak plasma insulin levels, and slow intestinal transit, all effects that

might be expected to ameliorate dumping symptoms. Octreotide administration before meal ingestion

has been shown to prevent changes in pulse, systolic blood pressure, and packed red cell volume during

early dumping and blood glucose levels during late dumping.

Alkaline Reflux Gastritis

The term alkaline reflux gastritis should be reserved for patients who demonstrate the clinical triad of

postprandial epigastric pain often associated with nausea and vomiting, evidence of reflux of bile into

the stomach, and histologic evidence of gastritis. One or more of these findings occur transiently in 10%

to 20% of patients after gastric resection, but they persist in only 1% to 2%.

The differential diagnosis for a patient with postoperative epigastric pain includes recurrent

ulceration, biliary and pancreatic disease, afferent loop obstruction, and esophagitis in addition to

alkaline reflux gastritis. Serum gastrin measurements should be determined to exclude Zollinger–Ellison

syndrome and retained gastric antrum. Endoscopic examination is essential to exclude recurrent ulcer.

Endoscopically, the gastric mucosa appears red, friable, and edematous. Gastric inflammation is

patchy and nonulcerative. Histologic examination shows mucosal and submucosal edema and infiltration

of acute and chronic inflammatory cells into the lamina propria. Glandular atrophy and intestinal

metaplasia are frequent accompaniments.

No perfect solution to alkaline reflux gastritis exists. H2

-receptor antagonists, proton pump inhibitors,

bile acid chelators, and dietary manipulations have not been demonstrated definitely to be beneficial.

The only proved treatment for alkaline reflux gastritis is operative diversion of intestinal contents from

contact with the gastric mucosa. The most common surgical procedure used for this purpose is a Rouxen-Y gastrojejunostomy with an intestinal limb of 50 to 60 cm constructed to prevent reflux of intestinal

contents (Fig. 45-7). This procedure is effective in eliminating bilious vomiting (nearly 100%), but

recurrent or persistent pain is reported in up to 30% of patients, and up to 20% of patients are troubled

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