diagnosis and management of benign gastric and … · peptic ulcer disease epidemiology pud has an...

Scientifi c American SurgeryDOI 10.2310/7800.2003

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© 2014 Decker Intellectual Properties Inc

gastrointestinal tract and abdomen

D I A G N O S I S A N D M A N A G E M E N T O F B E N I G N G A S T R I C A N D D U O D E N A L D I S E A S E

Gentian Kristo, MD, and Thomas E. Clancy, MD*

The treatment of benign gastric and duodenal disease has changed in recent decades, refl ecting improved medical management of peptic ulcer disease (PUD) and a decreased need for surgical intervention. Although surgical therapy was the only effective option for PUD in the past, elective surgery is increasingly rare in recent decades. Operative therapy for PUD is largely reserved for urgent management of complications such as hemorrhage, bleeding, or perfora-tion or the management of obstruction from intractable disease. The shift away from acid-reducing operations to damage control procedures refl ects the remarkable success of medical management.

In this chapter, we focus primarily on the management of benign gastroduodenal disease, with a focus on the workup and management of PUD and consideration of relevant surgical techniques. The management of duodenal diverticu-lar disease is briefl y addressed. Additional gastroduodenal disease and procedures are considered elsewhere in the publication, including bariatric surgery, transduodenal approaches to the bile duct, cystgastrostomy for intractable pancreatic pseudocysts, and duodenal diverticularization for trauma.

Peptic Ulcer Disease

epidemiology

PUD has an overall point prevalence in the US population of 1.8%, with a lifetime incidence of 10%.1 The presence of Helicobacter pylori increases the incidence of ulcer to about 1% per year, a rate that is six- to 10-fold higher than for noninfected subjects.2

Advances in the medical management of PUD, including the use of effective acid-suppressing medications (e.g., histamine receptor antagonists and proton pump inhibitors [PPIs]) and the treatment of H. pylori, have led to a decrease in the incidence of PUD, the rates of hospitalization, and mortality. Despite these trends, PUD remains a signifi cant cause of morbidity and health care costs, with estimates of annual expenditures (excluding medication costs) of $5.65 billion in the United States. Although the need for elective surgical management of uncomplicated duodenal and gastric ulcers has steadily decreased in recent decades, the rate of emergent surgery for complicated PUD has remained unchanged, at 7% of hospitalized patients.3

pathophysiology

The relationship between gastroduodenal ulcers and gastric acid secretion has been recognized for decades and is

expressed in the dictum “no acid, no ulcer.” A contempo-rary viewpoint suggests that PUD results from an imbalance between factors damaging the gastroduodenal mucosa and those protecting the mucosa [see Table 1].4

The majority of gastric and duodenal ulcers are caused by three factors: H. pylori infection, nonsteroidal antiinfl am-matory drug (NSAID) use, and acid hypersecretory states (e.g., Zollinger-Ellison syndrome [ZES]). Most patients with gastroduodenal ulcers will be colonized with H. pylori, and recurrence of ulcers is common without treating the H. pylori infection. H. pylori, a gram-negative spiral organ-ism, is present in about half the world population, particu-larly in developing countries, where up to 20% of healthy volunteers will demonstrate infection. Infection of gastric epithelium is followed by gastric infl ammation, and the relationship between H. pylori and ulcer formation has been widely demonstrated.5 The presence of ulcers in just a small fraction of individuals with infection suggests the action of other etiologic factors causing ulceration.

NSAIDs cause injury via suppression of prostaglandin synthesis, which leads to impaired mucosal defense. NSAID use can result in a range of lesions, from superfi cial erosions to deeper ulcerations. Mucosal injury caused by NSAIDs is more common in the stomach than the duodenum. Cigarette smoking may impair ulcer healing and may increase the risk of H. pylori–related ulceration.6

presentation/clinical manifestations

Most patients with PUD present with mild pain, burning discomfort, tenderness in the epigastrium, or nausea. Clas-sically, the pain from a duodenal ulcer occurs 2 to 3 hours after a meal, is relieved temporarily with food or antacids, and at times awakens patients at night between about 11 pm and 2 am, when the circadian stimulation of acid secretion

* The authors and editors gratefully acknowledge the contribu-tions of the previous author, Stanley W. Ashley, MD, FACS, to the development and writing of this chapter.

Table 1 Factors Damaging and Protecting the Gastroduodenal Mucosa4

Damaging factorsGastric acidPepsinBile saltsHelicobacter pylori infectionNonsteroidal antiinflammatory drugs (NSAIDs)SmokingAlcoholStress

Protective factorsMucusBicarbonateEndogenous prostaglandinsGrowth factorsCell regenerationMucosal blood flow

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gastro diagnosis and management of benign gastric and duodenal disease — 2

sensitivity of 90 to 95% and a specifi city of 95 to 100%. Histologic examination of tissue samples remains the gold standard for determining the presence of H. pylori and can also provide additional information regarding the presence of gastritis, intestinal metaplasia, or mucosa-associated lymphoid tissue.

Routine culture of the gastric biopsy specimens for H. pylori is not recommended as it is relatively expensive, and diagnosis requires more time (3 to 5 days). However, the incidence of antimicrobial resistance is high in patients with refractory peptic ulcers, and they may benefi t from culture and antibiotic sensitivity testing.

treatment

The medical management of PUD includes treatment with drugs that reduce the production of gastric acid (antacids, histamine receptor antagonists, and most notably PPIs), create a protective coating over the ulcer craters to prevent further peptic damage (sucralfate), increase mucosal blood fl ow and the secretion of bicarbonate and mucus (prosta-glandin analogues such as misoprostol used in NSAID-induced ulcers), and treat H. pylori infection. In addition to drug therapy, general measures such as cessation of smoking and alcohol and discontinuation of NSAID use are recommended.

In patients infected with H. pylori, the current pharmaco-logic therapy consists mainly of a combination of PPIs and antibiotics against H. pylori [see Table 2]. Eradication of H. pylori infection has resulted in very high ulcer healing rates (90%) and decreased recurrence rates of approximately 2%, particularly in patients with a duodenal ulcer. Further-more, it also has a prophylactic effect on recurrent ulcer bleeding.13

is maximal. Gastric ulcer pain is often aggravated by meals. However, the classic symptoms described are neither sensi-tive nor specifi c and are present in only a small number of patients. Furthermore, the nature of presenting symptoms alone does not differentiate between benign ulcerations and gastric malignancy.

diagnosis

Given the low predictive value of the signs and symptoms of PUD, the diagnosis of uncomplicated peptic ulcers is diffi cult to make solely on a clinical basis.

The diagnosis of PUD is typically made by endoscopy and upper gastrointestinal (UGI) radiography. Endoscopy is the most accurate method of establishing the diagnosis of peptic ulcers, with a reported sensitivity of 92% and specifi city of 100%.7 In addition to identifying the ulcer and its features, location, and size, endoscopy provides an opportunity for biopsies to test for H. pylori and exclude malignancy and for therapeutic interventions for bleeding ulcers. Duodenal ulcers are most often benign and do not require routine biopsy. Multiple biopsies are indicated for all gastric ulcers as even lesions with a benign appearance harbor malignancy in 5 to 11% of cases.8,9

Given the advances in the use of endoscopy in recent decades, the role of radiographic UGI series in the diagnosis of PUD has decreased, leading to a parallel decline in techni-cal expertise. However, it can be useful when endoscopy is unavailable or in patients not eligible to undergo endoscopy. Diagnosis of peptic ulcer on UGI series requires demonstra-tion of barium within an ulcer niche, which is generally round or oval and may be surrounded by a smooth mound of edema.10,11 Secondary changes include folds radiating to the crater and regional deformities secondary to spasm, edema, and scarring [see Figure 1]. The accuracy of the UGI radiography varies with the technique being used; single-contrast techniques (using liquid barium only) may miss as many as 50% of duodenal ulcers, whereas double-contrast studies (using air and liquid barium) create a more detailed view of the stomach lining and can detect 80 to 90% of ulcers.10,11 When radiographic features suggestive of cancer are present, endoscopy with biopsies is warranted.

Routine laboratory tests are of limited value in evaluating patients with uncomplicated PUD. When ZES is suspected, a fasting serum gastrin level may be useful.

However, laboratory tests do play an important role in the diagnosis of H. pylori infection. The serologic determination of anti–H. pylori IgG antibodies in peripheral blood has high sensitivity (90 to 100%) but variable specifi city (76 to 96%). Serology is preferred for initial diagnosis when endos copy is not required. Urea breath testing has a sensitivity of 88 to 95% and a specifi city of 95 to 100% for establishing the presence of H. pylori infection12 and is the test of choice for confi rming successful eradication of the organism 4 to 6 weeks after the cessation of antibiotic treatment.

Although endoscopy is not indicated solely for the pur-pose of establishing the presence of H. pylori, gastric biopsy specimens can be used in the diagnosis of H. pylori by rapid urease test, histology, and bacterial culture [see Figure 2]. Rapid urease testing of the biopsy specimen is the preferred method when histopathology is not required because it is fast (results within hours), is less expensive, and has a

Figure 1 Upper gastrointestinal series in which double contrast (barium and air) is used, showing rounded collection of barium in an ulcer in the duodenal bulb of a patient presenting with dyspepsia (uncomplicated duodenal ulcer).


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Triple therapy with two antibiotics, amoxicillin and clar-ithromycin, and a PPI for a week is considered the H. pylori treatment of choice. However, given the recent increase in resistance to clarithromycin, quadruple therapy with a combination of a PPI, bismuth, metronidazole, and tetracy-cline for 10 to 14 days is recommended in areas with a

clarithromycin resistance over 15 to 20%.14 Maintenance therapy with a PPI after H. pylori eradication can signifi cantl y reduce ulcer recurrence15 and complications.16 Standard-dose maintenance PPI treatment should be prescribed for 4 weeks in patients with duodenal ulcers and for 8 weeks in patients with gastric ulcers.

In patients with PUD without evidence of H. pylori infec-tion or a history of NSAID use, further investigations are necessary to determine the etiology of the ulcer disease before establishing specifi c therapy.

management of complicated peptic ulcer disease

Although the vast majority of ulcer patients are success-fully managed medically, the role of surgical therapy for PUD is now largely reserved for the management of the acute complications of bleeding and perforation as well as for more chronic and refractory issues, such as gastric outlet obstruction and intractable PUD. The recognition that med-ical management successfully prevents ulcer recurrence in most patients has caused surgical management of compli-cated ulcer disease to evolve into a more minimalist strategy that favors damage control surgery for complications and only infrequently resorts to acid-reducing operations.17

A multidisciplinary approach is crucial in the treatment of patients with complicated PUD. Early collaboration between the gastroenterologist, the intensivist, and the sur-geon provides a great expertise for appropriate resuscita-tion, establishment of goals and limits for initial nonopera-tive therapy, and timely preoperative preparation.

Hemorrhage

UGI bleeding secondary to PUD has an overall incidence of about 60 per 100,000 individuals, increasingly related to NSAID use.18 The mortality associated with bleeding peptic ulcers remains high at 5 to 10%.19 Bleeding typically presents with hematemesis or melena, although hematochezia can

Figure 2 Gastric biopsy samples stained with hematoxylin and eosin demonstrating (a) chronic active gastritis with a few Helicobacter pylori organisms faintly seen in the lumen of a gland and (b) chronic active gastritis with H. pylori organ-isms more abundant, as shown in the circle.

Table 2 Commonly Used Regimens to Eradicate Helicobacter pylori

Triple therapyProton pump inhibitor, amoxicillin, clarithromycin

Proton pump inhibitor b.i.d. for 7–14 daysAmoxicillin, 1 g b.i.d. for 7–14 daysClarithromycin, 500 mg b.i.d. or t.i.d. for 7–14 days

Proton pump inhibitor, metronidazole, clarithromycinProton pump inhibitor b.i.d. for 7–14 daysMetronidazole, 500 mg b.i.d. for 7–14 daysClarithromycin, 500 mg b.i.d. for 7–14 days

Quadruple therapyProton pump inhibitor b.i.d. (or ranitidine, 150 mg orally

b.i.d.) for 10–14 daysBismuth subsalicylate, 525 mg q.i.d. for 10–14 daysMetronidazole, 250 mg orally q.i.d. for 10–14 daysTetracycline, 500 mg orally q.i.d. for 10–14 days

Levofloxacin-based triple therapyProton pump inhibitor b.i.d. for 10 daysLevofloxacin, 250–500 mg b.i.d. for 10 daysAmoxicillin, 1 g b.i.d. for 10 days

Sequential therapyClarithromycin-based sequential therapyProton pump inhibitor b.i.d. for 10 daysAmoxicillin, 1 g b.i.d. for the first 5 days followed byClarithromycin, 500 mg b.i.d. andTinidazole, 500 mg b.i.d. for the next 5 days

Levofloxacin-based sequential therapyProton pump inhibitor b.i.d. for 10 daysAmoxicillin, 1 g b.i.d. for the first 5 days followed byLevofloxacin, 250 mg b.i.d. andTinidazole, 500 mg b.i.d. for the next 5 days

a b


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also occur in cases of massive bleeding. The initial manage-ment of a patient with UGI bleeding starts with restoring hemodynamic stability and administration of an intrave-nous PPI. Early treatment with PPI promotes rapid healing, decreases the need for endoscopic treatment, and reduces rebleeding rates.20

After initial stabilization, patients should undergo endoscopy to identify the source of bleeding. In many cases, endoscopic therapy using contact thermal devices, hemo-clips, and/or combination therapy with epinephrine injec-tion will control bleeding, rendering surgical management unnecessary. Defi nitive surgical management is indicated if bleeding leads to hemodynamic instability, an extensive transfusion requirement (i.e., more than 6 units in 24 hours), or rebleeding after initial endoscopic hemostasis or when endoscopic therapy is unavailable.

Objective criteria for surgery must be determined on a patient-by-patient basis. Precise preoperative localization of the bleeding source is essential; a bleeding posterior duode-nal ulcer, for example, cannot be managed in the same way as hemorrhage from diffuse severe gastritis. Endoscopy should therefore be performed whenever possible.

Alternatively, if brisk bleeding prevents clear intraluminal visualization of a bleeding site, angiographic localization may be attempted. Furthermore, depending on local resource s and expertise, angiographic transarterial embolization can be considered following failed endoscopic hemostasis, particularly in high-risk surgical patients, as it reduces the recurrent bleeding and the need for surgery without increasing the overall mortality and leads to fewer complications.21

Perforation

Perforated peptic ulcer has an incidence of 1.5 to 7.8 cases per 100,000 population per year and a high mortality of approximately 15%. Perforations are most likely in elderly patients on chronic NSAID therapy. The perforation site usually involves the anterior wall of the duodenum (60%), antrum (20%), or lesser-curvature gastric ulcers (20%).22

Perforation of peptic ulcer remains largely a clinical diag-nosis. Initial symptoms include severe abdominal pain, worse in the epigastrium, often accompanied by nausea and vomiting. Patients typically present in distress with an acute abdomen. A chest x-ray that demonstrates free intraperito-neal air [see Figure 3] is all that is needed before the patient is taken to the operating room; the decision to proceed to operation should not be delayed by waiting for further images (e.g., computed tomographic [CT] scans). Surgical delay is a critical determinant of survival in perforated pep-tic ulcer; every hour of delay from presentation to surgery is associated with an adjusted 2.4% decreased probability of survival compared with the previous hour.23

When there is no free air on the plain fi lm and diagnostic uncertainty persists, an UGI series using water-soluble con-trast material may be helpful. Perforation is a contraindica-tion for endoscopy because air insuffl ation may disrupt a sealed perforation and increase spillage of gastrointestinal contents.

In well-selected cases, when there is evidence of contained perforation without free air in a hemodynamically normal patient without peritonitis, nonoperative management with

nasogastric drainage, intravenous PPIs, antibiotics, and serial abdominal examinations can be attempted. However, the decision to manage patients without surgery should undergo frequent reevaluations as failure of nonsurgical management is an indication for surgery.

Gastric Outlet Obstruction

Although, historically, PUD was the most common cause of gastric outlet obstruction, with an incidence of up to 90%,24 treatment for H. pylori and the introduction of PPIs have led to a signifi cant decrease in the incidence of ulcer-induced gastric outlet obstruction. Benign obstruction secondary to PUD requires surgical treatment in about 2,000 patients per year in the United States.25 PUD can lead to gastric outlet obstruction by causing acute infl ammatory swelling of the pyloric channel or chronic scarring associate d with fi brosis. Patients typically have a long history of peptic ulcer pain and present with early satiety, bloating, nausea, vomiting, and epigastric fullness. Patients with long-standing obstruction commonly present with progressive weight loss and malnutrition.

Gastric outlet obstruction can be confi rmed with UGI barium contrast radiography, which shows a markedly dilated stomach and delayed gastric emptying. After decompression of the stomach for 12 to 24 hours, endoscopy is performed to visualize the gastric outlet and perform

Figure 3 Upright chest x-ray showing air beneath the right hemi-diaphragm (pneumoperitoneum) of a patient presenting with an acute abdomen caused by a perforated duodenal ulcer.


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biopsies to rule out cancer. Nonoperative management of peptic gastric outlet obstruction with repeated endoscopic dilations and H. pylori eradication has been shown to have good long-term results and in 70 to 80% of cases can avoid subsequent surgical therapy.26,27 Patients with refractory obstruction require a surgical drainage procedure and treat-ment of the predisposing ulcer with an acid-reducing proce-dure. Typically, this will require a resection procedure such as antrectomy with reconstruction and vagotomy.

Intractable Peptic Ulcer Disease

Occasionally, patients present for surgery with refractory peptic ulcers. If a gastric ulcer has not healed after 12 weeks of optimal medical therapy, resection is indicated to rule out an occult gastric malignancy. In such cases, the preoperative workup should include endoscopic biopsies of the ulcer base and the surrounding gastric mucosa so that a preop-erative diagnosis of malignancy can be made if possible. In view of the concern about a possible gastric malignancy, it is reasonable to obtain a preoperative chest x-ray and a CT scan of the abdomen so as to detect possible nodal or distant metastases.

The fi rst step in the management of refractory duodenal ulcerations is a complete workup for the possible causes, such as gastrinoma, Crohn disease, lymphoma, and carci-noma. Once diseases with identifi able etiologies have been ruled out, maximal medical therapy should be instituted.

Highly selective vagotomy is the acid-reducing procedure of choice in patients with intractable PUD.

Surgical Procedures for Peptic Ulcer Disease

bleeding ulcers

For patients with bleeding duodenal ulcers, especially those with a fi rst ulcer who have not been on PPIs or other acid suppression therapy, ligation of the bleeding vessel and closure of the duodenum/pylorus with pyloroplasty may be suffi cient. Acid-reducing procedures such as truncal vagot-omy with pyloroplasty are rarely employed as primary therapy for PUD. However, such acid-reducing procedures do play a role in the emergency management of bleeding duodenal ulcers after oversewing the bleeding vessel, espe-cially in patients already on PPIs or patients at high risk for noncompliance with medical therapy.

Oversewing of Bleeding Ulcer, Pyloroplasty, and Vagotomy

Operative technique Step 1: ligation of bleeding vessel After a longitudinal incision across the pylorus, the ulcer bed is oversewn with fi gure-of-eight sutures placed at the cephalad and caudad portions of the ulcer to occlude the gastroduodenal artery. An additional U stitch is placed to control small transverse pancreatic branches [see Figure 4]. Care should be taken to avoid the underlying common bile duct (CBD).

Step 2: pyloroplasty The longitudinal incision is closed transversely in two layers (Heineke-Mikulicz pyloroplasty) [see Figure 5]. If substantial duodenal scarring is present, a tension-free Heineke-Mikulicz pyloroplasty may not be possible, and a side-to-side anastomosis between the distal stomach and the proximal duodenotomy may be preferable (Finney pyloroplasty) [see Figure 6].

Step 3: vagotomy Downward traction on the greater cur-vature of the stomach is essential to apply gentle tension to the esophagogastric junction and the proximal vagi. The left (anterior) vagus is best identifi ed by applying traction to the right and posteriorly so that the nerve can be traced into the posterior mediastinum. The main nerve trunk is clipped proximally and distally, and a 2 cm long segment is excised. The right (posterior) vagus is exposed by applying traction

Figure 4 Vagotomy and pyloroplasty: sutures. To control a bleeding duodenal ulcer, traction sutures are placed along the cephalad and caudad borders of a longitudinal incision across the pylorus. Figure-of-eight sutures are placed at the cephalad and caudad portions of the ulcer to occlude the gastroduodenal artery. An additional U stitch is placed to control small transverse pancreatic branches that may cause late bleeding. Care should be taken to avoid the underlying common bile duct.

Figure 5 Vagotomy and pyloroplasty. For a Heineke-Mikulicz pylo-roplasty, a full-thickness longitudinal incision is made that extends from a point 1 cm proximal to the pylorus to a point 1 to 2 cm distal to the pylorus. The incision is closed transversely in two layers. Superior and inferior stay sutures help align the incision for closure.


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Gallbladder

Pylorus

Inverted Incision

Duodenum

Duodenum

a

b

c

d

Figure 6 Finney pyloroplasty. If a tension-free Heineke-Mikulicz pyloroplasty is not feasible, a Finney pyloroplasty may be performed instead. (a) The distal stomach and the proximal duodenum are aligned with stay sutures; meticulous lysis of surrounding adhesions is essential. An inverted U-shaped incision is made. (b) The pyloroplasty is created in two layers. The posterior portion of the outer layer, consisting of seromus-cular Lembert sutures, is placed fi rst, followed by an inner layer constructed with a continuous full-thickness absorbable suture. (c) The anterior portion of the inner layer is closed with a continuous full-thickness suture. Some surgeons prefer a Connell suture at this site. (d) The anterior portion of the outer layer, consisting of silk Lembert sutures, is placed.

to the left and anteriorly. For a complete vagotomy, the distal esophagus must be skeletonized for approximately 5 cm [see Figure 7].

ulcer resection

Exploration for Bleeding Gastric Ulcers

Gastric ulcer bleeding is often self-limited and typically managed endoscopically with coagulation, injection, or

clipping bleeding vessels. The presence of active pulsatile bleeding or a visible vessel is predictive of a higher rate of rebleeding. Emergency operations for bleeding gastric ulcers should be tailored to the type of ulcer identifi ed. For patients with a bleeding gastric ulcer, the preferred approach is partial gastrectomy because of the risk of gastric malig-nancy. For patients who are at high risk because of advanced age, comorbid disease, or intraoperative instability, ulcer excision combined with truncal vagotomy and pyloroplasty


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is an option. Ulcer excision alone is associated with rebleed-ing in approximately 20% of patients.

Operative technique Step 1: anterior gastrotomy The stomach is opened through a longitudinal anterior gastro-tomy in the distal stomach or antrum and explored for a bleeding source.

Step 2: ulcer resection Resection of a type I (lesser curva-ture) or II/III (prepyloric ± duodenal) bleeding ulcer will require antrectomy or distal gastrectomy. Type IV ulcers (juxtaesophageal) require a more technically diffi cult resec-tion, including subtotal gastrectomy with upward extension to include the ulcer followed by Roux-en-Y reconstruction (Csendes procedure).28 Rarely, for severe bleeding, devascu-larization of the stomach with ligation of the left gastric artery can be performed while leaving the short gastric arcade intact. This can be accompanied by oversewing the ulcer. Vagotomy is usually not added in the absence of a failure of medical management.

Step 3: reconstruction Reconstruction via a gastroduode-nal anastomosis (Billroth I) [see Figure 8], a gastrojejunal anastomosis (Billroth II) [see Figure 9], or a Roux-en-Y gastro-jejunostomy must be tailored to the resection performed.

exploration for perforated ulcers

Omental Patch for Duodenal Perforation (Graham Patch)

Perforated duodenal ulcers are generally managed with an omental patch. With adequate acid suppression and

adequate treatment of H. pylori, symptoms of duodenal ulcer are unlikely to recur and vagotomy is usually not required. The 1-year recurrence rate after omental patching is substan-tially lower when both therapies are employed than when only a PPI is given (5% versus 38%).29

Operative technique Step 1: exploration The ulcer is identifi ed and débrided if possible.

Step 2: closure Primary closure is not attempted if the duodenal wall is overly edematous to avoid excess tension. The defect is plugged with a well-vascularized omental pedicle [see Figure 10].

Step 3: acid-reducing procedure A vagotomy is avoided if there is no history of PUD, if the patient is hemodynami-cally unstable, or if there is gross abdominal contamination to avoid dividing the peritoneum over the esophagus and exposing the mediastinum.

Antrectomy

The primary indication for gastric resection in the setting of PUD is chronic obstruction caused by scarring, typically from a pyloric channel ulcer. In addition, antrectomy may be required and may be the elective operation of choice for intractable type I, II, and III gastric ulcers, as well as a pri-mary emergency surgical option for perforated or bleeding gastric ulcers. A primary Billroth I gastroduodenostomy [see Figure 8] has been the preferred procedure, but surrounding scar tissue may limit the mobility of the duodenum, in which case, a Billroth II gastrojejunostomy [see Figure 9] may be required for a tension-free anastomosis. Antrectomy is typically combined with truncal vagotomy.

Operative technique Step 1: exposure The proximal border of the antrum on the greater curvature extends to a point between the pylorus and the fundus; on the lesser cur-vature, it extends to a point just above the incisura. Distally, the dissection is carried past the pylorus.

Step 2: division of stomach A gastrointestinal anastomosis (GIA) stapler is used to divide the stomach at the estimated borders of the antrum. The right gastroepiploic artery and vein are divided just distal to the pylorus. The duodenum is then divided distal to the pylorus with a transverse anastomosis (TA) stapler.

Step 3: reconstruction When feasible, a Billroth I recon-struction [see Figure 8] may be performed to maintain physiologic antegrade fl ow and avoids the complications associated with a Billroth II reconstruction [see Figure 9], such as afferent and efferent loop syndromes and duodenal stump leaks. A generous Kocher maneuver is necessary to minimize tension on the anastomosis [see Figure 11].

If a primary gastroduodenostomy is not possible, a Billroth II reconstruction [see Figure 9] is indicated. If the duodenum is not scarred or infl amed, simple staple closure will suffi ce; if closure proves diffi cult, a lateral duodenos-tomy tube may help decompress the stump. Alternatively, if the duodenum cannot be closed without signifi cant tension, closure may be accomplished around a red rubber or mush-room catheter. In addition, omental patch reinforcement of the duodenal stump may be desirable. The segment used for the anastomosis should be as short as possible while still being able to reach the stomach without tension;

Posterior Vagus

Anterior VagusDivided

Figure 7 Vagotomy and pyloroplasty. For the truncal vagotomy, the peritoneum over the esophagogastric junction is opened wide to afford exposure. Gentle downward traction is applied to the stomach to facili-tate identifi cation of the two vagus nerves. Surgical clips are applied to each nerve in turn, and a 2 to 3 cm nerve segment is removed between the clips. These segments should be inspected to confi rm removal of neural tissue.


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approximately 20 cm of proximal jejunum should be suffi -cient to serve as the afferent limb. Passing the jejunum through a retrocolic window places less tension on the mesentery than an antecolic approach does.

The gastrojejunostomy may be handsewn in two layers either to the posterior wall of the stomach or to the inferior portion of the excised staple line [see Figure 9]. Alternatively, the gastrojejunostomy may be created by means of stapling.

Some authors recommend the use of a Braun enteroenter-ostomy between the efferent and afferent limbs to reduce bile refl ux and decompress the duodenal stump [see

Figure 12a]. Staple closure of the afferent limb above the enteroenterostomy may also be performed to limit bile refl ux into the stomach; this measure creates a confi guration referred to as an uncut Roux-en-Y [see Figure 12b]. Entero-enterostomy at this site may also be performed on an emergency basis to treat afferent limb syndrome. Staple closure of the afferent limb may discourage bile refl ux, with the effect of limiting bile refl ux, gastritis, and esophagitis.30

Complications Following antrectomy, a number of potential complications must be anticipated and recognized.

a

b

Billroth I

Figure 8 Antrectomy: Billroth I reconstruction (gastroduo-denostomy). (a) The anastomosis is done in two layers. The inner layer is constructed by placing a continuous full-thickness suture. (b) The outer layer is constructed with silk Lembert sutures. The junction of the anastomosis and the gastric staple line has been referred to as the angle of sorrow, a term that refl ects the common complication of leakage at the intersection of suture or staple lines. This junction may be reinforced with additional Lembert sutures.

Figure 9 Antrectomy: Billroth II reconstruction (gastrojejunostomy). (a) The inferior portion of the gastric resection line is excised, along with a small wedge of the stomach. (b, c) A two-layer anastomosis is created, with an outer layer of Lembert sutures and an inner layer of full-thickness absorbable sutures. The upper gastric staple line may be oversewn with interrupted Lembert sutures.

a b c


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GonadalVessels

InferiorVena Cava

RenalVeins

HepatoduodenalLigament Common Duct

Node

Pancreas

SuperiorMesentericArtery

Duodenum

Aorta

Figure 10 Omental (Graham) patch. Three or four interrupted sutures are placed along the ulcer edge. If possible, the ulcer is closed primarily and reinforced with omentum. Primary closure may be diffi cult; in a true Graham patch, primary closure is not attempted, and omentum is used to cover the tissue defect.

Leakage from the duodenal stump necessitates prompt reoperation, washout, and drainage. The diagnosis of duodenal stump leakage is confi rmed by aspirating bilious fl uid from a right upper quadrant fl uid collection or by performing a technetium 99m–labeled hepatoiminodiacetic acid scan. Duodenal leaks can rarely be closed primarily. Duodenostomy may be indicated to further decompress the afferent limb and prevent continuous leakage. The goals are to create a controlled fi stula to the skin and to prevent the accumulation of biliary fl uid in the abdomen.

Delayed gastric emptying after gastrojejunostomy may occur and is generally managed conservatively. On rare occasions, reoperation is required for delayed anastomotic function.

Afferent limb obstruction may occur as a consequence of adhesions, internal herniation, volvulus, or a kink at the angle formed with the gastric remnant. Obstruction to out-fl ow of the afferent limb creates a closed-loop obstruction, with persistent secretion of bile and pancreatic fl uids into the loop. Correction of the obstruction may necessitate conversion to a Roux-en-Y reconstruction, shortening of the afferent limb, or a side-to-side enteroenterostomy with the efferent limb [see Figure 12].

Alkaline refl ux gastritis is one of the most common long-term complications of gastrectomy, developing in 5 and 15% of patients after gastric surgery.31 This complication is most

Figure 11 The Kocher maneuver refl ects the duodenum and the pancreatic head from the retroperi-toneum, allowing access to the infrahepatic inferior vena cava and to the distal common bile duct, the duodenum, and the pancreatic head.


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Figure 12 Braun enteroenterostomy. Antre-ctomy: Billroth II reconstruction (gastrojejunos-tomy). (a) A Braun enteroenterostomy facilitates decompression of the afferent limb in a Billroth II gastrojejunostomy. It may be done as either a sutured or a stapled anastomosis. (b) An option is to close the afferent limb above the enteroenter-ostomy with a transverse anastomosis stapler (so that the jejunal lumen is occluded but not divided). This confi guration, often referred to as an uncut Roux-en-Y, temporarily discourages, but does not prevent, refl ux of bile into the stomach.

the stomach, the left gastric vascular arcade is identifi ed, and all tissue between this arcade and the lesser curvature is divided and ligated. The dissection should proceed upward as far as the esophagogastric junction. The posterior branches are approached either by rotating the stomach or by proceeding directly through the lesser omentum [see Figure 13a].

Step 2: dissection of esophagogastric junction The distal esophagus is cleared of all nerve fi bers for a distance of approximately 5 cm above the esophagogastric junction. The posterior esophagogastric junction is exposed by means of gentle traction and slight rotation of the distal esophagus. Exposure is facilitated by downward traction provided by a Penrose drain placed around the esophagogastric junction. The dissection must stay close to the lesser curvature and the esophagus, avoiding the tissues to the right of the esophagus, where the main vagal trunks lie.

The left side of the distal esophagus must be manually stripped so that the so-called criminal nerve of Grassi [see Figure 13b] can be identifi ed and ligated.

Gastrinoma (Zollinger-Ellison Syndrome)

ZES has been estimated to cause 0.1 to 1% of PUD.35 It consists of hypergastrinemia, gastric acid hypersecretion, severe PUD, and non–b-islet cell tumors of the pancreas. Classically, ZES is associated with multiple duodenal ulcers, ulcers in unusual locations (beyond the fi rst portion of the duodenum; jejunum), or ulcers that fail to respond to standard therapy.

Patients with ulcers refractory to treatment with PPIs, those with ulcers in the distal dudodenum or jejunum, and those with recurrent ulcers despite treatment should be evaluated for ZES. In addition, patients with PUD who are not infected with H. pylori and who do not use NSAIDs should also be evaluated for ZES. The biochemical diagnosis

frequently associated with Billroth II reconstructions. Although refl ux is common, symptoms (e.g., epigastric pain, nausea, and bilious emesis) are relatively rare. Medical management is generally ineffective. If surgery is required, conversion of the Billroth II reconstruction to a Roux-en-Y reconstruction is indicated. In those patients who have a Roux-en-Y rather than a Billroth II reconstruction, the pre-ferred treatment is to divert alkaline contents to a location 45 to 60 cm beyond the gastric remnant.

Highly Selective Vagotomy

Acid-reducing operations such as vagotomy with antrec-tomy or vagotomy with pyloroplasty will provide relief from duodenal ulcers but may also be associated with signifi cant complications. Highly selective vagotomy (HSV), also referred to as parietal cell vagotomy, avoids vagal denervation of viscera other than the parietal cell mass while keeping the pylorus mechanically and functionally intact.32,33 HSV was found to reduce postvagotomy diarrhea and dumping dramatically; however, it was also found to be associated with a much higher rate of recurrent ulceration (greater than 10% at 5 years).34 Today, in an era character-ized by greatly improved medical management of PUD, most gastrointestinal surgeons rarely perform HSV, if at all.

In the current context, this procedure could be used to treat intractable ulcer disease in young patients (after ZES and other hypersecretory conditions are ruled out) or in patients noncompliant with PPI therapy. If the surgeon is not experienced with HSV, then in the emergency situation, a truncal vagotomy and pyloroplasty are adequate treatment.

Operative technique Step 1: dissection of anterior and posterior nerve branches to lesser curvature The distal branche s of the nerve of Latarjet are defi ned, with care taken to pre-serve the so-called crow’s foot, which is typically located near the incisura angularis, approximately 6 to 7 cm proxi-mal to the pylorus. Gentle downward traction is applied to

a b


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7 cm

a

Pyloric Nerves

Pyloric Branches

Hepatic Nerves

Posterior Vagus Nerve

Celiac Gangliaand Nerves

Anterior VagusNerve

Criminal Nerveof Grassi

Anterior Gastric Nerves

Greater PosteriorGastric Nerve

Greater AnteriorGastric Nerve

b

Figure 13 Highly selective vagotomy. (a) Anterior and posterior branches of the nerve of Latarjet to the lesser curvature are ligated and divided. The distal branches, comprising the so-called crow’s foot, are left intact. The posterior branches may be approached via the lesser omentum. (b) Note the criminal nerve of Grassi.


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is established by fi ndings of elevated fasting serum gastrin levels, reduced gastric pH, or increased basal acid output.

Patients should have PPI held for 1 week before measur-ing fasting gastrin as acid suppression with PPI will artifi -cially elevate the gastrin. H2 blockers should be held for 2 days. All patients with ZES will have a fasting gastrin greater than 100 pg/mL.

Demonstration of acid hypersecretion (in the presence of elevated gastrin) is also critical to make the diagnosis of ZES as achlorhydria could also lead to hypergastrinemia. Basal acid output greater than 15 mEq/hr is diagnostic, as is pH less than 2.3.

Elevations of serum gastrin levels of greater than 200 pg/mL above baseline after administration of secretin can confi rm ZES when the diagnosis is equivocal. Preopera-tively, ZES patients are treated with higher-than-normal doses of PPI, and imaging studies are undertaken in an attempt to localize the tumor. Somatostatin receptor scintig-raphy is the study of choice, with a sensitivity of 85%.36 Treatment of localized gastrinoma is surgical resection.

7 cm

Branchesto PylorusPreserved

Anterior Vagal Trunk

Posterior Vagal Trunk

Laparoscopic Treatment of Peptic Ulcer Disease

With the advent of minimal access techniques in recent decades, laparoscopy has become an accepted approach in the treatment of peptic ulcers. Numerous reports of laparo-scopic truncal vagotomy and HSV have been published over the past two decades. The laparoscopic versions of these procedures proceed in much the same way as the tradition-al open versions. In a laparoscopic HSV, the ultrasonic shears are frequently used to divide the anterior and poste-rior vagal branches to the lesser curvature from the crow’s foot to the esophagogastric junction. Mixed procedures that combine posterior truncal vagotomy with more selective anterior gastric denervation are common. In the Taylor pro-cedure [see Figure 14], an anterior seromyotomy is performed from the angle of His to the crow’s foot, and the seromuscu-lar layers are subsequently closed primarily.37 A variant of the laparoscopic Taylor procedure includes an anterior linear gastrectomy, in which a linear strip of the stomach wall is removed parallel to the lesser curvature with an

Figure 14 Taylor procedure. An anterior seromyotomy is performed from the angle of His to the crow’s foot, dividing all the branches of the anterior nerve of Latarjet. A posterior truncal vagotomy is also performed.


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endoscopic GIA stapler. This procedure seems to be func-tionally equivalent to HSV. The majority of the studies of laparoscopic vagotomy, however, have been individual case series that do not compare the laparoscopic approach with a traditional open approach. Undoubtedly, the scarce com-parative data refl ect the declining indications for vagotomy for intractable PUD. Thus, although laparoscopic HSV has been well described, it is by no means clear that it should be recommended over open HSV for those rare patients in whom this procedure is indicated.

With increasing laparoscopic expertise and advancement in equipment, laparoscopic repair of perforated duodenal ulcers has become more common.38 In experienced hands, the laparoscopic approach is considered as safe and effective as open Graham patch repair. The longer operating time associated with laparoscopic repair has no effects on the outcomes.39

Selecting patients who are good candidates for laparos-copy is very important. The laparoscopic repair is contrain-dicated in patients with prolonged perforation for more than 24 hours, shock on admission, and signifi cant systemic ill-ness (defi ned as American Society of Anesthesiologists grades III–IV).40

Laparoscopic procedures for perforation include either suture closure of the perforation followed by omental patch or omental patch alone and should be attempted only by surgeons with advanced laparoscopic skills. Intracorporeal knotting is preferred because extracorporeal suturing may cut through the friable edge of the duodenal perforation.41 The threshold for conversion to an open procedure should be low if the ulcers are particularly large or prove diffi cult to localize.

Laparoscopic duodenotomy and oversewing of the gastroduodenal and transverse pancreatic arteries for the bleeding duodenal ulcer have been shown to be technically feasible42 in select patients with slow-bleeding duodenal ulcers. However, the role of laparoscopic surgery for bleeding peptic ulcers is not yet established.

Duodenal Diverticula

Incidental duodenal diverticula are common. They are false diverticula, including only mucosa and submucosa. Most are located in the medial wall of the second portion of the duodenum, within 2 cm of the ampulla of Vater. Complications include ulceration and bleeding, compres-sion of the CBD with cholangitis or pancreatitis, and, in cases of perforation, abscess formation with peritonitis. CT scanning is useful for differentiating this condition from cholecystitis or pancreatitis.

Incidentally found duodenal diverticula should be left alone. In cases of vague abdominal complaints, duodenal diverticula are rarely the cause and are usually not resected in the absence of complications. When the duodenal diver-ticulum produces biliary obstruction, diverticulectomy is the appropriate procedure. In high-risk patients, endoscopic sphincterotomy or stenting can be performed. Diverticular bleeding may require endoscopic hemostatic therapies, angio-graphic embolization, or lateral duodenotomy followed by

direct suturing of the bleeding point. Diverticulitis is fi rst managed with antibiotics and bowel rest if no perforation has occurred. Perforation with abscess will require an operative procedure.

duodenal diverticulectomy

Operative Technique

When indicated, the main surgical options are simple diverticulectomy with drainage and transduodenal diver-ticulectomy (as described by Iida43). If the duodenum is free of infl ammation, the transduodenal approach is preferred because it minimizes the need for dissection of the diverticu-lum from the surrounding pancreas. However, if the diver-ticulum does not involve the pancreas, simple excision fl ush with the duodenal wall, followed by closure in two layers, may be suffi cient. The ensuing technical description focuses on transduodenal diverticulectomy.

Step 1: exposure and duodenotomy After a generous Kocher maneuver, the duodenum is opened by making a 4 cm longitudinal incision along the antimesenteric border, and the ampulla is either visualized or palpated. To identify the ampulla, it may be necessary to place a catheter into the CBD via a separate choledochotomy [see Figure 15a].

Step 2: diverticulectomy The orifi ce of the diverticulum is identifi ed, and the mucosa is inverted into the lumen of the duodenum. The neck of the diverticulum is transected 2 mm from the junction with the duodenal wall. The diver-ticular opening is then closed with interrupted seromuscular Lembert sutures of 3-0 silk and interrupted mucosal sutures of 4-0 polyglactin [see Figure 15b]. Inadvertent closure of the CBD may be prevented by inserting a catheter into the duct. The duodenum is closed in two layers, also with an inner layer of 4-0 polyglactin and an outer layer of seromuscular Lembert sutures of 3-0 silk. Closed-suction drainage adjacent to the duodenum is indicated.

If the duodenum is markedly infl amed, suture line break-down is likely, eventually leading to a duodenal fi stula. The area can be isolated by means of pyloric exclusion or antrec-tomy with Billroth II reconstruction. In addition, bile fl ow can be diverted by performing a choledochojejunostomy to a Roux-en-Y intestinal limb to prevent combined leakage of pancreatic fl uid and bile.

Diverticula arising from the third or fourth portion of the duodenum may be excised either primarily or via a trans-duodenal approach. Inverting the diverticulum without excising it is not recommended, because it may lead to duodenal obstruction.

Special case: perforated duodenal diverticulum In the setting of acute infl ammation, duodenotomy is avoided. Instead, the abscess is evacuated, and the diverticulum is excised along with just enough of the adjacent duodenal wall to ensure that only healthy tissue is left. If the resulting duodenal defect is large, either sleeve resection of the duodenum or drainage of the open duodenal defect into a Roux-en-Y jejunal limb may be required.


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a

b

Interrupted Sutures

Inverted Mucosa of Diverticulum

Catheter Exiting Ampulla

Orifice of Diverticulum

Duodenum

4 cmIncision

Catheter in CommonBile Duct

Figure 15 Duodenal diverticulectomy. (a) The duodenum is opened by making a 4 cm longitudinal incision along the antimesenteric border. The orifi ce of the diverticulum is identifi ed, and the mucosa is inverted into the lumen of the duodenum. To identify the ampulla, a catheter is placed into the common bile duct via a separate choledochotomy. (b) The neck of the diverticulum is transected 2 mm from the junction with the duodenal wall. The diverticular opening is then closed with interrupted seromuscular Lembert sutures of 3-0 silk and interrupted mucosal sutures of 4-0 polyglactin.

Financial Disclosures: Gentian Kristo, MD, and Thomas E. Clancy, MD, have no relevant fi nancial relationships to disclose. This chapter was previously authored by Stanley W. Ashley, MD, FACS, with disclosure made at the time of initial publication. This chapter has been reviewed, updated, and rereleased by the authors listed.

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Acknowledgments

Figures 1, 2, and 3 Courtesy of Edward A. Lew, MD, MPH.Figures 4 through 10, 12, and 13a Tom MooreFigure 11 Susan Brust, CMI. Revised and updated by Christine Kenney.Figures 13b, 14, and 15 Christine Kenney

diagnosis and management of benign gastric and … · peptic ulcer disease epidemiology pud has an...

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