Diagnosis and Management of Benign Gastric and Duodenal Disease

gastrointestinal tract and abdomen DIAGNOSIS AND MANAGEMENT OF BENIGN GASTRIC AND DUODENAL DISEASE

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

The treatment of benign gastric and duodenal disease has expressed in the dictum “no acid, no ulcer.” A contempo- changed in recent decades, refl ecting improved medical rary viewpoint suggests that PUD results from an imbalance management of peptic ulcer disease (PUD) and a decreased between factors damaging the gastroduodenal mucosa and need for surgical intervention. Although surgical therapy those protecting the mucosa [see Table 1].4 was the only effective option for PUD in the past, elective The majority of gastric and duodenal ulcers are caused surgery is increasingly rare in recent decades. Operative by three factors: H. pylori infection, nonsteroidal antiinfl am- therapy for PUD is largely reserved for urgent management matory drug (NSAID) use, and acid hypersecretory states of complications such as hemorrhage, bleeding, or perfora- (e.g., Zollinger-Ellison syndrome [ZES]). Most patients with tion or the management of obstruction from intractable gastroduodenal ulcers will be colonized with H. pylori, disease. The shift away from acid-reducing operations to and recurrence of ulcers is common without treating the damage control procedures refl ects the remarkable success H. pylori infection. H. pylori, a gram-negative spiral organ- of medical management. ism, is present in about half the world population, particu- In this chapter, we focus primarily on the management of larly in developing countries, where up to 20% of healthy benign gastroduodenal disease, with a focus on the workup volunteers will demonstrate infection. Infection of gastric and management of PUD and consideration of relevant epithelium is followed by gastric infl ammation, and the surgical techniques. The management of duodenal diverticu- relationship between H. pylori and ulcer formation has been lar disease is briefl y addressed. Additional gastroduodenal widely demonstrated.5 The presence of ulcers in just a small disease and procedures are considered elsewhere in the fraction of individuals with infection suggests the action of publication, including bariatric surgery, transduodenal other etiologic factors causing ulceration. approaches to the bile duct, cystgastrostomy for intractable NSAIDs cause injury via suppression of prostaglandin pancreatic pseudocysts, and duodenal diverticularization synthesis, which leads to impaired mucosal defense. NSAID for trauma. 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 Peptic Ulcer Disease smoking may impair ulcer healing and may increase the risk epidemiology of H. pylori–related ulceration.6 PUD has an overall point prevalence in the US population presentation/clinical manifestations of 1.8%, with a lifetime incidence of 10%.1 The presence of Most patients with PUD present with mild pain, burning Helicobacter pylori increases the incidence of ulcer to about discomfort, tenderness in the epigastrium, or nausea. Clas- 1% per year, a rate that is six- to 10-fold higher than for sically, the pain from a duodenal ulcer occurs 2 to 3 hours noninfected subjects.2 after a meal, is relieved temporarily with food or antacids, Advances in the medical management of PUD, including and at times awakens patients at night between about 11 pm the use of effective acid-suppressing medications (e.g., and 2 am, when the circadian stimulation of acid secretion 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 Table 1 Factors Damaging and Protecting the cause of morbidity and health care costs, with estimates of Gastroduodenal Mucosa4 annual expenditures (excluding medication costs) of $5.65 Damaging factors billion in the United States. Although the need for elective Gastric acid surgical management of uncomplicated duodenal and Pepsin gastric ulcers has steadily decreased in recent decades, the Bile salts rate of emergent surgery for complicated PUD has remained Helicobacter pylori infection 3 Nonsteroidal antiinflammatory drugs (NSAIDs) unchanged, at 7% of hospitalized patients. Smoking Alcohol pathophysiology Stress The relationship between gastroduodenal ulcers and Protective factors gastric acid secretion has been recognized for decades and is Mucus Bicarbonate Endogenous prostaglandins * The authors and editors gratefully acknowledge the contribu- Growth factors tions of the previous author, Stanley W. Ashley, MD, FACS, Cell regeneration to the development and writing of this chapter. Mucosal blood flow

06/14 gastro diagnosis and management of benign gastric and duodenal disease — 2 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 Figure 1 Upper gastrointestinal series in which double contrast decades, the role of radiographic UGI series in the diagnosis (barium and air) is used, showing rounded collection of barium in of PUD has decreased, leading to a parallel decline in techni- an ulcer in the duodenal bulb of a patient presenting with dyspepsia cal expertise. However, it can be useful when endoscopy is (uncomplicated duodenal ulcer). unavailable or in patients not eligible to undergo endoscopy. Diagnosis of peptic ulcer on UGI series requires demonstra- sensitivity of 90 to 95% and a specifi city of 95 to 100%. tion of barium within an ulcer niche, which is generally Histologic examination of tissue samples remains the gold round or oval and may be surrounded by a smooth mound standard for determining the presence of H. pylori and can of edema.10,11 Secondary changes include folds radiating to also provide additional information regarding the presence the crater and regional deformities secondary to spasm, of gastritis, intestinal metaplasia, or mucosa-associated edema, and scarring [see Figure 1]. The accuracy of the UGI lymphoid tissue. radiography varies with the technique being used; single- Routine culture of the gastric biopsy specimens for contrast techniques (using liquid barium only) may miss as H. pylori is not recommended as it is relatively expensive, many as 50% of duodenal ulcers, whereas double-contrast and diagnosis requires more time (3 to 5 days). However, studies (using air and liquid barium) create a more detailed the incidence of antimicrobial resistance is high in patients view of the stomach lining and can detect 80 to 90% of with refractory peptic ulcers, and they may benefi t from ulcers.10,11 When radiographic features suggestive of cancer culture and antibiotic sensitivity testing. are present, endoscopy with biopsies is warranted. Routine laboratory tests are of limited value in evaluating treatment patients with uncomplicated PUD. When ZES is suspected, The medical management of PUD includes treatment with a fasting serum gastrin level may be useful. drugs that reduce the production of gastric acid (antacids, However, laboratory tests do play an important role in the histamine receptor antagonists, and most notably PPIs), diagnosis of H. pylori infection. The serologic determination create a protective coating over the ulcer craters to prevent of anti–H. pylori IgG antibodies in peripheral blood has high further peptic damage (sucralfate), increase mucosal blood sensitivity (90 to 100%) but variable specifi city (76 to 96%). fl ow and the secretion of bicarbonate and mucus (prosta- Serology is preferred for initial diagnosis when endos copy glandin analogues such as misoprostol used in NSAID- is not required. Urea breath testing has a sensitivity of 88 induced ulcers), and treat H. pylori infection. In addition to 95% and a specifi city of 95 to 100% for establishing the to drug therapy, general measures such as cessation of presence of H. pylori infection12 and is the test of choice smoking and alcohol and discontinuation of NSAID use for confi rming successful eradication of the organism 4 to are recommended. 6 weeks after the cessation of antibiotic treatment. In patients infected with H. pylori, the current pharmaco- Although endoscopy is not indicated solely for the pur- logic therapy consists mainly of a combination of PPIs and pose of establishing the presence of H. pylori, gastric biopsy antibiotics against H. pylori [see Table 2]. Eradication of specimens can be used in the diagnosis of H. pylori by rapid H. pylori infection has resulted in very high ulcer healing urease test, histology, and bacterial culture [see Figure 2]. rates (90%) and decreased recurrence rates of approximately Rapid urease testing of the biopsy specimen is the preferred 2%, particularly in patients with a duodenal ulcer. Further- method when histopathology is not required because it more, it also has a prophylactic effect on recurrent ulcer is fast (results within hours), is less expensive, and has a bleeding.13

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06/14 gastro diagnosis and management of benign gastric and duodenal disease — 3 a b

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 organisms more abundant, as shown in the circle.

Triple therapy with two antibiotics, amoxicillin and clar- clarithromycin resistance over 15 to 20%.14 Maintenance ithromycin, and a PPI for a week is considered the H. pylori therapy with a PPI after H. pylori eradication can signiﬁ cantly treatment of choice. However, given the recent increase reduce ulcer recurrence15 and complications.16 Standard- in resistance to clarithromycin, quadruple therapy with a dose maintenance PPI treatment should be prescribed for combination of a PPI, bismuth, metronidazole, and tetracy- 4 weeks in patients with duodenal ulcers and for 8 weeks in cline for 10 to 14 days is recommended in areas with a patients with gastric ulcers. In patients with PUD without evidence of H. pylori infection or a history of NSAID use, further investigations are Table 2 Commonly Used Regimens to Eradicate necessary to determine the etiology of the ulcer disease before establishing speciﬁ c therapy. Helicobacter pylori Triple therapy management of complicated peptic ulcer disease Proton pump inhibitor, amoxicillin, clarithromycin Although the vast majority of ulcer patients are success- Proton pump inhibitor b.i.d. for 7–14 days Amoxicillin, 1 g b.i.d. for 7–14 days fully managed medically, the role of surgical therapy for Clarithromycin, 500 mg b.i.d. or t.i.d. for 7–14 days PUD is now largely reserved for the management of the Proton pump inhibitor, metronidazole, clarithromycin acute complications of bleeding and perforation as well as Proton pump inhibitor b.i.d. for 7–14 days for more chronic and refractory issues, such as gastric outlet Metronidazole, 500 mg b.i.d. for 7–14 days obstruction and intractable PUD. The recognition that med- Clarithromycin, 500 mg b.i.d. for 7–14 days Quadruple therapy ical management successfully prevents ulcer recurrence in Proton pump inhibitor b.i.d. (or ranitidine, 150 mg orally most patients has caused surgical management of compli- b.i.d.) for 10–14 days cated ulcer disease to evolve into a more minimalist strategy Bismuth subsalicylate, 525 mg q.i.d. for 10–14 days that favors damage control surgery for complications and Metronidazole, 250 mg orally q.i.d. for 10–14 days 17 Tetracycline, 500 mg orally q.i.d. for 10–14 days only infrequently resorts to acid-reducing operations. Levofloxacin-based triple therapy A multidisciplinary approach is crucial in the treatment Proton pump inhibitor b.i.d. for 10 days of patients with complicated PUD. Early collaboration Levofloxacin, 250–500 mg b.i.d. for 10 days between the gastroenterologist, the intensivist, and the sur- Amoxicillin, 1 g b.i.d. for 10 days geon provides a great expertise for appropriate resuscita- Sequential therapy Clarithromycin-based sequential therapy tion, establishment of goals and limits for initial nonopera- Proton pump inhibitor b.i.d. for 10 days tive therapy, and timely preoperative preparation. Amoxicillin, 1 g b.i.d. for the first 5 days followed by Clarithromycin, 500 mg b.i.d. and Hemorrhage Tinidazole, 500 mg b.i.d. for the next 5 days Levofloxacin-based sequential therapy UGI bleeding secondary to PUD has an overall incidence Proton pump inhibitor b.i.d. for 10 days of about 60 per 100,000 individuals, increasingly related to Amoxicillin, 1 g b.i.d. for the first 5 days followed by NSAID use.18 The mortality associated with bleeding peptic Levofloxacin, 250 mg b.i.d. and ulcers remains high at 5 to 10%.19 Bleeding typically presents Tinidazole, 500 mg b.i.d. for the next 5 days with hematemesis or melena, although hematochezia can

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06/14 gastro diagnosis and management of benign gastric and duodenal disease — 4 also occur in cases of massive bleeding. The initial management of a patient with UGI bleeding starts with restoring hemodynamic stability and administration of an intravenous 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 injection 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 duodenal 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 Figure 3 Upright chest x-ray showing air beneath the right hemi- diaphragm (pneumoperitoneum) of a patient presenting with an acute Perforation abdomen caused by a perforated duodenal ulcer. 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 nasogastric drainage, intravenous PPIs, antibiotics, and patients on chronic NSAID therapy. The perforation site serial abdominal examinations can be attempted. However, usually involves the anterior wall of the duodenum (60%), the decision to manage patients without surgery should antrum (20%), or lesser-curvature gastric ulcers (20%).22 undergo frequent reevaluations as failure of nonsurgical Perforation of peptic ulcer remains largely a clinical diag- management is an indication for surgery. nosis. Initial symptoms include severe abdominal pain, worse in the epigastrium, often accompanied by nausea and Gastric Outlet Obstruction vomiting. Patients typically present in distress with an acute Although, historically, PUD was the most common cause abdomen. A chest x-ray that demonstrates free intraperito- of gastric outlet obstruction, with an incidence of up to neal air [see Figure 3] is all that is needed before the patient 90%,24 treatment for H. pylori and the introduction of PPIs is taken to the operating room; the decision to proceed to have led to a signifi cant decrease in the incidence of operation should not be delayed by waiting for further ulcer-induced gastric outlet obstruction. Benign obstruction images (e.g., computed tomographic [CT] scans). Surgical secondary to PUD requires surgical treatment in about delay is a critical determinant of survival in perforated pep- 2,000 patients per year in the United States.25 PUD can lead tic ulcer; every hour of delay from presentation to surgery is to gastric outlet obstruction by causing acute infl ammatory associated with an adjusted 2.4% decreased probability of swelling of the pyloric channel or chronic scarring associate d survival compared with the previous hour.23 with fi brosis. Patients typically have a long history of peptic When there is no free air on the plain fi lm and diagnostic ulcer pain and present with early satiety, bloating, nausea, uncertainty persists, an UGI series using water-soluble con- vomiting, and epigastric fullness. Patients with long- trast material may be helpful. Perforation is a contraindica- standing obstruction commonly present with progressive tion for endoscopy because air insuffl ation may disrupt a weight loss and malnutrition. sealed perforation and increase spillage of gastrointestinal Gastric outlet obstruction can be confi rmed with UGI contents. barium contrast radiography, which shows a markedly In well-selected cases, when there is evidence of contained dilated stomach and delayed gastric emptying. After perforation without free air in a hemodynamically normal decompression of the stomach for 12 to 24 hours, endoscopy patient without peritonitis, nonoperative management with is performed to visualize the gastric outlet and perform

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06/14 gastro diagnosis and management of benign gastric and duodenal disease — 5 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 treatment of the predisposing ulcer with an acid-reducing procedure. 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 preoperative 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. Figure 4 Vagotomy and pyloroplasty: sutures. To control a bleeding The ﬁ rst step in the management of refractory duodenal duodenal ulcer, traction sutures are placed along the cephalad and ulcerations is a complete workup for the possible causes, caudad borders of a longitudinal incision across the pylorus. Figure- such as gastrinoma, Crohn disease, lymphoma, and carci- of-eight sutures are placed at the cephalad and caudad portions of the noma. Once diseases with identiﬁ able etiologies have been ulcer to occlude the gastroduodenal artery. An additional U stitch is ruled out, maximal medical therapy should be instituted. placed to control small transverse pancreatic branches that may cause Highly selective vagotomy is the acid-reducing procedure late bleeding. Care should be taken to avoid the underlying common of choice in patients with intractable PUD. bile duct.

Surgical Procedures for Peptic Ulcer Disease Step 3: vagotomy Downward traction on the greater curvature of the stomach is essential to apply gentle tension to bleeding ulcers the esophagogastric junction and the proximal vagi. The left For patients with bleeding duodenal ulcers, especially (anterior) vagus is best identifi ed by applying traction to the those with a fi rst ulcer who have not been on PPIs or other right and posteriorly so that the nerve can be traced into the acid suppression therapy, ligation of the bleeding vessel and posterior mediastinum. The main nerve trunk is clipped closure of the duodenum/pylorus with pyloroplasty may be proximally and distally, and a 2 cm long segment is excised. suffi cient. Acid-reducing procedures such as truncal vagot- The right (posterior) vagus is exposed by applying traction 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, especially 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, Figure 5 Vagotomy and pyloroplasty. For a Heineke-Mikulicz pylo- a tension-free Heineke-Mikulicz pyloroplasty may not be roplasty, a full-thickness longitudinal incision is made that extends possible, and a side-to-side anastomosis between the distal from a point 1 cm proximal to the pylorus to a point 1 to 2 cm distal to stomach and the proximal duodenotomy may be preferable the pylorus. The incision is closed transversely in two layers. Superior (Finney pyloroplasty) [see Figure 6]. and inferior stay sutures help align the incision for closure.

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06/14 gastro diagnosis and management of benign gastric and duodenal disease — 6

a Pylorus

Gallbladder

Inverted Incision

Duodenum

c Duodenum

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 seromuscular 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 clipping bleeding vessels. The presence of active pulsatile distal esophagus must be skeletonized for approximately bleeding or a visible vessel is predictive of a higher rate 5 cm [see Figure 7]. of rebleeding. Emergency operations for bleeding gastric ulcers should be tailored to the type of ulcer identiﬁ ed. For ulcer resection patients with a bleeding gastric ulcer, the preferred approach is partial gastrectomy because of the risk of gastric malig- Exploration for Bleeding Gastric Ulcers nancy. For patients who are at high risk because of advanced Gastric ulcer bleeding is often self-limited and typically age, comorbid disease, or intraoperative instability, ulcer managed endoscopically with coagulation, injection, or excision combined with truncal vagotomy and pyloroplasty

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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- Posterior Vagus 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 hemodynamically unstable, or if there is gross abdominal contamination to avoid dividing the peritoneum over the esophagus and exposing the mediastinum. Anterior Vagus Divided 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- Figure 7 Vagotomy and pyloroplasty. For the truncal vagotomy, the mary emergency surgical option for perforated or bleeding peritoneum over the esophagogastric junction is opened wide to afford gastric ulcers. A primary Billroth I gastroduodenostomy [see exposure. Gentle downward traction is applied to the stomach to facili- Figure 8] has been the preferred procedure, but surrounding tate identifi cation of the two vagus nerves. Surgical clips are applied to scar tissue may limit the mobility of the duodenum, in which each nerve in turn, and a 2 to 3 cm nerve segment is removed between case, a Billroth II gastrojejunostomy [see Figure 9] may be the clips. These segments should be inspected to confi rm removal of required for a tension-free anastomosis. Antrectomy is neural tissue. typically combined with truncal vagotomy. is an option. Ulcer excision alone is associated with rebleed- Operative technique Step 1: exposure The proximal ing in approximately 20% of patients. border of the antrum on the greater curvature extends to a point between the pylorus and the fundus; on the lesser cur- Operative technique Step 1: anterior gastrotomy The vature, it extends to a point just above the incisura. Distally, stomach is opened through a longitudinal anterior gastro- the dissection is carried past the pylorus. tomy in the distal stomach or antrum and explored for a Step 2: division of stomach A gastrointestinal anastomosis bleeding source. (GIA) stapler is used to divide the stomach at the estimated Step 2: ulcer resection Resection of a type I (lesser curva- borders of the antrum. The right gastroepiploic artery and ture) or II/III (prepyloric ± duodenal) bleeding ulcer will vein are divided just distal to the pylorus. The duodenum require antrectomy or distal gastrectomy. Type IV ulcers is then divided distal to the pylorus with a transverse (juxtaesophageal) require a more technically diffi cult resec- anastomosis (TA) stapler. tion, including subtotal gastrectomy with upward extension Step 3: reconstruction When feasible, a Billroth I recon- to include the ulcer followed by Roux-en-Y reconstruction struction [see Figure 8] may be performed to maintain (Csendes procedure).28 Rarely, for severe bleeding, devascu- physiologic antegrade fl ow and avoids the complications larization of the stomach with ligation of the left gastric associated with a Billroth II reconstruction [see Figure 9], artery can be performed while leaving the short gastric such as afferent and efferent loop syndromes and duodenal arcade intact. This can be accompanied by oversewing the stump leaks. A generous Kocher maneuver is necessary to ulcer. Vagotomy is usually not added in the absence of a minimize tension on the anastomosis [see Figure 11]. failure of medical management. If a primary gastroduodenostomy is not possible, a Step 3: reconstruction Reconstruction via a gastroduode- Billroth II reconstruction [see Figure 9] is indicated. If the nal anastomosis (Billroth I) [see Figure 8], a gastrojejunal duodenum is not scarred or infl amed, simple staple closure anastomosis (Billroth II) [see Figure 9], or a Roux-en-Y gastro- will suffi ce; if closure proves diffi cult, a lateral duodenos- jejunostomy must be tailored to the resection performed. tomy tube may help decompress the stump. Alternatively, if the duodenum cannot be closed without signifi cant tension, exploration for perforated ulcers closure may be accomplished around a red rubber or mush- room catheter. In addition, omental patch reinforcement Omental Patch for Duodenal Perforation (Graham Patch) of the duodenal stump may be desirable. The segment used Perforated duodenal ulcers are generally managed with for the anastomosis should be as short as possible while an omental patch. With adequate acid suppression and still being able to reach the stomach without tension;

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Billroth I

Figure 8 Antrectomy: Billroth I reconstruction (gastroduodenostomy). (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. approximately 20 cm of proximal jejunum should be suffi - Figure 12a]. Staple closure of the afferent limb above the cient to serve as the afferent limb. Passing the jejunum enteroenterostomy may also be performed to limit bile through a retrocolic window places less tension on the refl ux into the stomach; this measure creates a confi guration mesentery than an antecolic approach does. referred to as an uncut Roux-en-Y [see Figure 12b]. Entero- The gastrojejunostomy may be handsewn in two layers enterostomy at this site may also be performed on an either to the posterior wall of the stomach or to the inferior emergency basis to treat afferent limb syndrome. Staple portion of the excised staple line [see Figure 9]. Alternatively, closure of the afferent limb may discourage bile refl ux, with the gastrojejunostomy may be created by means of stapling. the effect of limiting bile refl ux, gastritis, and esophagitis.30 Some authors recommend the use of a Braun enteroenterostomy between the efferent and afferent limbs to reduce Complications Following antrectomy, a number of bile refl ux and decompress the duodenal stump [see potential complications must be anticipated and recognized.

abc

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.

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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 Figure 10 Omental (Graham) patch. Three or four interrupted sutures are placed along the ulcer edge. If possible, the ulcer is closed primarily efferent limb [see Figure 12]. and reinforced with omentum. Primary closure may be diffi cult; in a Alkaline refl ux gastritis is one of the most common long- true Graham patch, primary closure is not attempted, and omentum is term complications of gastrectomy, developing in 5 and 15% used to cover the tissue defect. of patients after gastric surgery.31 This complication is most

Hepatoduodenal Ligament Common Duct Node

Pancreas

Renal Superior Veins Mesenteric Artery

Duodenum

Inferior Vena Cava

Gonadal Figure 11 The Kocher maneuver Vessels Aorta 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 (gastrojejunostomy). (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 enteroenterostomy 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. frequently associated with Billroth II reconstructions. the stomach, the left gastric vascular arcade is identifi ed, Although refl ux is common, symptoms (e.g., epigastric and all tissue between this arcade and the lesser curvature pain, nausea, and bilious emesis) are relatively rare. Medical is divided and ligated. The dissection should proceed management is generally ineffective. If surgery is required, upward as far as the esophagogastric junction. The posterior conversion of the Billroth II reconstruction to a Roux-en-Y branches are approached either by rotating the stomach reconstruction is indicated. In those patients who have a or by proceeding directly through the lesser omentum [see Roux-en-Y rather than a Billroth II reconstruction, the pre- Figure 13a]. ferred treatment is to divert alkaline contents to a location Step 2: dissection of esophagogastric junction The distal 45 to 60 cm beyond the gastric remnant. esophagus is cleared of all nerve fi bers for a distance of Highly Selective Vagotomy approximately 5 cm above the esophagogastric junction. The posterior esophagogastric junction is exposed by means Acid-reducing operations such as vagotomy with antrec- of gentle traction and slight rotation of the distal esophagus. tomy or vagotomy with pyloroplasty will provide relief Exposure is facilitated by downward traction provided by a from duodenal ulcers but may also be associated with Penrose drain placed around the esophagogastric junction. signifi cant complications. Highly selective vagotomy (HSV), The dissection must stay close to the lesser curvature and also referred to as parietal cell vagotomy, avoids vagal the esophagus, avoiding the tissues to the right of the denervation of viscera other than the parietal cell mass while esophagus, where the main vagal trunks lie. keeping the pylorus mechanically and functionally intact.32,33 The left side of the distal esophagus must be manually HSV was found to reduce postvagotomy diarrhea and stripped so that the so-called criminal nerve of Grassi [see dumping dramatically; however, it was also found to be associated with a much higher rate of recurrent ulceration Figure 13b] can be identifi ed and ligated. (greater than 10% at 5 years).34 Today, in an era character- ized by greatly improved medical management of PUD, Gastrinoma (Zollinger-Ellison Syndrome) most gastrointestinal surgeons rarely perform HSV, if at all. ZES has been estimated to cause 0.1 to 1% of PUD.35 It In the current context, this procedure could be used to treat intractable ulcer disease in young patients (after ZES consists of hypergastrinemia, gastric acid hypersecretion, b and other hypersecretory conditions are ruled out) or in severe PUD, and non– -islet cell tumors of the pancreas. patients noncompliant with PPI therapy. If the surgeon is Classically, ZES is associated with multiple duodenal ulcers, not experienced with HSV, then in the emergency situation, ulcers in unusual locations (beyond the fi rst portion of a truncal vagotomy and pyloroplasty are adequate treatment. the duodenum; jejunum), or ulcers that fail to respond to standard therapy. Operative technique Step 1: dissection of anterior and Patients with ulcers refractory to treatment with PPIs, posterior nerve branches to lesser curvature The distal branche s those with ulcers in the distal dudodenum or jejunum, and of the nerve of Latarjet are defi ned, with care taken to pre- those with recurrent ulcers despite treatment should be serve the so-called crow’s foot, which is typically located evaluated for ZES. In addition, patients with PUD who are near the incisura angularis, approximately 6 to 7 cm proxi- not infected with H. pylori and who do not use NSAIDs mal to the pylorus. Gentle downward traction is applied to should also be evaluated for ZES. The biochemical diagnosis

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7 cm

Anterior Vagus b Nerve Criminal Nerve of Grassi

Posterior Vagus Nerve

Anterior Gastric Nerves Celiac Ganglia and Nerves Hepatic Nerves Greater Posterior Gastric Nerve

Greater Anterior Gastric Nerve Pyloric Branches

Pyloric Nerves

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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06/14 gastro diagnosis and management of benign gastric and duodenal disease — 12 is established by fi ndings of elevated fasting serum gastrin Laparoscopic Treatment of Peptic Ulcer Disease levels, reduced gastric pH, or increased basal acid output. With the advent of minimal access techniques in recent Patients should have PPI held for 1 week before measur- decades, laparoscopy has become an accepted approach in ing fasting gastrin as acid suppression with PPI will artifi - the treatment of peptic ulcers. Numerous reports of laparo- cially elevate the gastrin. H blockers should be held for 2 scopic truncal vagotomy and HSV have been published over 2 days. All patients with ZES will have a fasting gastrin the past two decades. The laparoscopic versions of these greater than 100 pg/mL. procedures proceed in much the same way as the tradition- Demonstration of acid hypersecretion (in the presence of elevated gastrin) is also critical to make the diagnosis of ZES al open versions. In a laparoscopic HSV, the ultrasonic as achlorhydria could also lead to hypergastrinemia. Basal shears are frequently used to divide the anterior and poste- acid output greater than 15 mEq/hr is diagnostic, as is pH rior vagal branches to the lesser curvature from the crow’s less than 2.3. foot to the esophagogastric junction. Mixed procedures that Elevations of serum gastrin levels of greater than combine posterior truncal vagotomy with more selective 200 pg/mL above baseline after administration of secretin anterior gastric denervation are common. In the Taylor pro- can confi rm ZES when the diagnosis is equivocal. Preopera- cedure [see Figure 14], an anterior seromyotomy is performed tively, ZES patients are treated with higher-than-normal from the angle of His to the crow’s foot, and the seromuscu- doses of PPI, and imaging studies are undertaken in an lar layers are subsequently closed primarily.37 A variant of attempt to localize the tumor. Somatostatin receptor scintig- the laparoscopic Taylor procedure includes an anterior raphy is the study of choice, with a sensitivity of 85%.36 linear gastrectomy, in which a linear strip of the stomach Treatment of localized gastrinoma is surgical resection. wall is removed parallel to the lesser curvature with an

Posterior Vagal Trunk

Anterior Vagal Trunk

Branches to Pylorus Preserved

7 cm

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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06/14 gastro diagnosis and management of benign gastric and duodenal disease — 13 endoscopic GIA stapler. This procedure seems to be func- direct suturing of the bleeding point. Diverticulitis is fi rst tionally equivalent to HSV. The majority of the studies of managed with antibiotics and bowel rest if no perforation laparoscopic vagotomy, however, have been individual case has occurred. Perforation with abscess will require an series that do not compare the laparoscopic approach with operative procedure. a traditional open approach. Undoubtedly, the scarce comparative data refl ect the declining indications for vagotomy duodenal diverticulectomy for intractable PUD. Thus, although laparoscopic HSV has Operative Technique been well described, it is by no means clear that it should be recommended over open HSV for those rare patients in When indicated, the main surgical options are simple whom this procedure is indicated. diverticulectomy with drainage and transduodenal diver- 43 With increasing laparoscopic expertise and advancement ticulectomy (as described by Iida ). If the duodenum is free in equipment, laparoscopic repair of perforated duodenal of infl ammation, the transduodenal approach is preferred ulcers has become more common.38 In experienced hands, because it minimizes the need for dissection of the diverticu- the laparoscopic approach is considered as safe and effective lum from the surrounding pancreas. However, if the diver- as open Graham patch repair. The longer operating time ticulum does not involve the pancreas, simple excision fl ush associated with laparoscopic repair has no effects on the with the duodenal wall, followed by closure in two layers, outcomes.39 may be suffi cient. The ensuing technical description focuses Selecting patients who are good candidates for laparos- on transduodenal diverticulectomy. copy is very important. The laparoscopic repair is contrain- dicated in patients with prolonged perforation for more than Step 1: exposure and duodenotomy After a generous 24 hours, shock on admission, and signifi cant systemic ill- Kocher maneuver, the duodenum is opened by making a ness (defi ned as American Society of Anesthesiologists 4 cm longitudinal incision along the antimesenteric border, grades III–IV).40 and the ampulla is either visualized or palpated. To identify Laparoscopic procedures for perforation include either the ampulla, it may be necessary to place a catheter into the suture closure of the perforation followed by omental patch CBD via a separate choledochotomy [see Figure 15a]. or omental patch alone and should be attempted only by surgeons with advanced laparoscopic skills. Intracorporeal Step 2: diverticulectomy The orifi ce of the diverticulum knotting is preferred because extracorporeal suturing may is identifi ed, and the mucosa is inverted into the lumen of cut through the friable edge of the duodenal perforation.41 the duodenum. The neck of the diverticulum is transected The threshold for conversion to an open procedure should 2 mm from the junction with the duodenal wall. The diver- be low if the ulcers are particularly large or prove diffi cult ticular opening is then closed with interrupted seromuscular to localize. Lembert sutures of 3-0 silk and interrupted mucosal sutures Laparoscopic duodenotomy and oversewing of the of 4-0 polyglactin [see Figure 15b]. Inadvertent closure of the gastroduodenal and transverse pancreatic arteries for the CBD may be prevented by inserting a catheter into the duct. bleeding duodenal ulcer have been shown to be technically The duodenum is closed in two layers, also with an inner feasible42 in select patients with slow-bleeding duodenal layer of 4-0 polyglactin and an outer layer of seromuscular ulcers. However, the role of laparoscopic surgery for Lembert sutures of 3-0 silk. Closed-suction drainage bleeding peptic ulcers is not yet established. 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 Duodenal Diverticula area can be isolated by means of pyloric exclusion or antrec- Incidental duodenal diverticula are common. They are tomy with Billroth II reconstruction. In addition, bile fl ow false diverticula, including only mucosa and submucosa. can be diverted by performing a choledochojejunostomy to Most are located in the medial wall of the second portion a Roux-en-Y intestinal limb to prevent combined leakage of of the duodenum, within 2 cm of the ampulla of Vater. pancreatic fl uid and bile. Complications include ulceration and bleeding, compres- Diverticula arising from the third or fourth portion of the sion of the CBD with cholangitis or pancreatitis, and, in duodenum may be excised either primarily or via a trans- cases of perforation, abscess formation with peritonitis. duodenal approach. Inverting the diverticulum without CT scanning is useful for differentiating this condition from excising it is not recommended, because it may lead to cholecystitis or pancreatitis. duodenal obstruction. Incidentally found duodenal diverticula should be left alone. In cases of vague abdominal complaints, duodenal Special case: perforated duodenal diverticulum In the diverticula are rarely the cause and are usually not resected setting of acute infl ammation, duodenotomy is avoided. in the absence of complications. When the duodenal diver- Instead, the abscess is evacuated, and the diverticulum is ticulum produces biliary obstruction, diverticulectomy is excised along with just enough of the adjacent duodenal the appropriate procedure. In high-risk patients, endoscopic wall to ensure that only healthy tissue is left. If the resulting sphincterotomy or stenting can be performed. Diverticular duodenal defect is large, either sleeve resection of the bleeding may require endoscopic hemostatic therapies, angio- duodenum or drainage of the open duodenal defect into a graphic embolization, or lateral duodenotomy followed by Roux-en-Y jejunal limb may be required.

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Catheter in Common Bile Duct 4 cm Incision

Duodenum

Orifice of Diverticulum

Catheter Exiting Ampulla

Inverted Mucosa of Diverticulum

Interrupted Sutures

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 References relevant ﬁ nancial relationships to disclose. This chapter was previously authored 1. Aro P, Storskrubb T, Ronkainen J, et al. Peptic ulcer disease 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 in a general adult population: the Kalixanda study: a random listed. population-based study. Am J Epidemiol 2006;163:1025–34.

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39. Bertleff MJ, Halm JA, Lange JF, et al. Randomized clinical 43. Iida F. Transduodenal diverticulectomy for periampullary trial of laparoscopic versus open repair of the perforated diverticula. World J Surg 1979;3:103. peptic ulcer: the LAMA Trial. World J Surg 2009;33:1368–73. 40. Lunevicius R, Morkevicius M. Systematic review compar- ing laparoscopic and open repair for perforated peptic Acknowledgments ulcer. Br J Surg 2005;92:1195–207. 41. Palanivelu C, Jani K, Senthilnathan P. Laparoscopic management of duodenal ulcer perforation: is it advantageous? Figures 1, 2, and 3 Courtesy of Edward A. Lew, MD, MPH. Indian J Gastroenterol 2007;26:64–6. Figures 4 through 10, 12, and 13a Tom Moore 42. Martin I, O’Rourke N, Fielding G, et al. Laparoscopic under- Figure 11 Susan Brust, CMI. Revised and updated by Christine running of bleeding duodenal ulceration: a minimalist Kenney. approach to therapy. Aust N Z J Surg 1998;68:213–5. Figures 13b, 14, and 15 Christine Kenney

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