Surgery for Peptic Ulcer Disease

CHAPTER

Surgery for Peptic Ulcer Disease Abubaker Ali* 

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  Bestoun H. Ahmed 

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  Michael S. Nussbaum

G

astroduodenal peptic ulcer disease (PUD) is a common problem with significant geographic variation in prevalence. In Western countries the incidence of PUD has steadily declined. Recent populationbased studies have shown a prevalence rate of 4% with 20% of patients having asymptomatic ulcers.1 In developing countries, the prevalence is much higher. In a recent population-based study from China, 17.2% of the population had endoscopically documented duodenal or gastric ulcers; however, more than 70% of these patients were asymptomatic. Such variations are likely related to the prevalence of Helicobacter pylori, smoking, and use of ulcerogenic drugs, such as nonsteroidal antiinflammatory drugs (NSAIDs). In a systematic review of the literature covering developed countries, the annual incidence of PUD ranged from 0.1% to 0.19% for physician-diagnosed PUD and 0.01% to 0.17% when based upon hospitalized patients.1 In a 1996 Veterans Affairs study the prevalence of PUD in H. pylori–positive patients was found to be 2%.2 In the United States, there has been a decrease in the prevalence and number of hospitalizations for PUD. Between 1993 and 2006 the rate of PUD-related admissions decreased by 30%, with a larger decrease in duodenal ulcer–related admissions than gastric ulcers. Such preferential decreases in duodenal versus gastric ulcer disease likely relate to testing for H. pylori and introduction of more potent and successful therapeutic regimens.3 The advent of histamine H2-receptor antagonists (H2 blockers) in the 1970s was responsible for an initial 40% decrease in incidence of ulcer operations. The later development of proton pump inhibitors (PPIs) in the late 1980s led to further acid reduction and faster, more efficient healing of active ulcer disease. The development of PPIs has not only influenced elective medical management but also has had an effect in the emergency setting. When combined, PPIs and endoscopic treatment have further decreased the need for emergency operation. PUD complications include bleeding, perforation, and gastric outlet obstruction. There has been a significant downward trend in the incidence of these complications. Although older studies demonstrated a stable or even an increase in the number of patients admitted with one of these complications, recent studies demonstrated that the rate of perforation and bleeding has been decreasing in the United States.4 Complications of PUD vary depending on the geographic location, with bleeding being the most common in the United States, whereas obstruction may be more common in other locations in the world.5,6 Risk factors for peptic ulcer complications and their recurrence included NSAID and/or acetylsalicylic acid use, H. pylori infection, and ulcer size greater than or *Supported by a grant from the Foundation for Surgical Fellowships.

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equal to 1 cm. PPI use has reduced the risk of peptic ulcer hemorrhage.7 Current indications for surgical intervention are as follows: 1. Protracted bleeding despite endoscopic therapy. Bleeding is the most common complication of PUD in the United States, with an incidence of approximately 100 per 100,000 population. 2. Perforation is the second most common with an annual incidence of 11 operations per 100,000 population. Perforations are associated with the highest rate of mortality.5 3. Obstruction occurs as a consequence of scarring following healing of prepyloric and/or duodenal ulcers. 4. Intractability despite maximum medical therapy is an uncommon indication for operation. 5. Inability to rule out cancer when an ulcer remains despite treatment and negative endoscopic biopsies. This is of particular importance with gastric ulcers. The goals of surgical procedures are to 1. Permit ulcer healing 2. Prevent or treat ulcer complications 3. Address the underlying ulcer etiology 4. Minimize postoperative digestive consequences No single procedure satisfies all of these objectives. To choose the best operation, the surgeon must consider the characteristics of the ulcer (location, chronicity, type of complication), the likely etiology (acid hypersecretion, drug induced, possible role of H. pylori), the patient (age, nutrition, comorbid illnesses, condition on presentation), and the operation (mortality rate, side effects). In some respects, all ulcer operations represent a compromise: The morbidity of ulcer disease is replaced by the morbidity of the operation. Finally, surgeon experience must play a role in the choice of operation; nowadays, most surgical residents complete their training with little experience with the more complex procedures. Undoubtedly this influences their choices for both elective and emergent operations.

HISTORY OF SURGICAL TREATMENT OF PEPTIC ULCER DISEASE PHYSIOLOGIC DISCOVERY Initial operations for ulcer disease were based on local control without a good understanding of the physiology involved. As the physiology of digestion and acid production was delineated, the operations changed and were subsequently shifted toward addressing the current understanding of the cause of PUD. Benjamin Brodie, an English physiologist and surgeon, in 1814, described the vagus nerves and their connection

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Surgery for Peptic Ulcer Disease  CHAPTER 59 

ABSTRACT Gastroduodenal peptic ulcer disease (PUD) is a common problem with significant geographic variation in prevalence. In Western countries, the incidence of PUD has steadily declined and the prevalence is much higher in developing countries. Such variations are likely related to the prevalence of Helicobacter pylori, smoking, and the use of ulcerogenic drugs, such as nonsteroidal antiinflammatory drugs. The advent of histamine H 2-receptor antagonists (H2 blockers) in the 1970s and the development of proton pump inhibitors (PPIs) in the late 1980s led to further acid reduction and faster, more efficient healing of active ulcer disease. The combined use of PPIs and endoscopic treatment has further decreased the need for emergency operation. PUD complications include bleeding, perforation, and gastric outlet obstruction. There has been a significant downward trend in the incidence of these complications. Complications of PUD also vary depending on the geographic location. Bleeding is the most common in the United States, and obstruction may be more common in other locations in the world. The goals of surgical procedures are to permit ulcer healing, prevent or treat ulcer complications, address the underlying ulcer etiology, and minimize postoperative digestive consequences.

KEYWORDS Peptic ulcer disease, gastric ulcer, duodenal ulcer, antrectomy, pyloroplasty, Billroth, vagotomy, Helicobacter pylori, nonsteroidal antiinflammatory drugs (NSAIDs), Roux-en-Y, proton pump inhibitor, giant duodenal ulcer, marginal ulcer, gastrojejunostomy, gastroenterostomy

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with the production of gastric acid. Then in 1822, William Beaumont, an army surgeon, cared for Alexis St. Martin, a man who sustained a shotgun wound to the abdomen. Beaumont treated his wound but expected him to die; however, the patient survived and was left with a gastrocutaneous fistula. In 1825 Beaumont began to study the patient’s digestive process by tying food to a string and inserting it through the fistula into the stomach and observe how it had been digested. He also studied the gastric fluid from the fistula. In 1833 Beaumont published his findings as Experiments and Observations on the Gastric Juice, and the Physiology of Digestion.8 The discovery of the three separate, yet related, phases of gastric secretion and its involvement in the consumption and digestion of a meal defined the surgical treatment of PUD. The cephalic, gastric, and to a lesser extent the intestinal phases are examples of physiologic discovery molding surgical practice. Ivan Pavlov, a Russian physiologist and physician, described the cephalic phase of gastric secretion. Through his physiologic studies with dogs, Pavlov showed that stimulation of the vagus nerves resulted in the secretion of gastric acid. His discovery earned him the 1904 Nobel Prize in Physiology and Medicine. The gastric or antral phase of secretion revolves around the work of the physiologist John Edkins, who injected an extract of pyloric mucus membrane “activated by hydrochloric acid or boiling” into the jugular vein of cats. He noted a marked increase in the gastric acid and pepsin secretion. In 1905 he named the active agent “gastrin.” Further study led to the understanding that gastric distention stimulates the release of gastrin from the antrum, resulting in the release of gastric acid.9 This knowledge was applied directly to the treatment of PUD and became the basis for antrectomy. The intestinal phase of gastric secretion refers to specific situations when a food bolus, which has not been exposed to gastric acid, comes in contact with the duodenal mucosa. In this situation the stomach is stimulated to secrete acid. Physiologically, food boluses are acidified and upon contact with the duodenal mucosa stimulate an inhibitory response.

SURGICAL TREATMENT In 1881 the Prussian surgeon, Ludwik Rydygier, performed the first successful resection for a gastric ulcer.10 In the early 1900s the standard operation performed for the treatment of gastric and duodenal ulcers was either a pyloroplasty without vagotomy or a gastroenterostomy. These operations were performed regardless of the presence or absence of obstructive symptoms, and many patients had resolution of their symptoms. Gastroenterostomy soon surpassed pyloroplasty as the treatment of choice. Charles Mayo presented the Mayo Clinic data on gastroenterostomy for treatment of both gastric ulceration and duodenal ulceration. His data from 647 patients with gastric ulcers showed a mortality rate of 3.2% after gastroenterostomy and less than 2% in the 2734 patients with duodenal ulceration.11 Eventually, recurrence rates and marginal ulcer formation were recognized, and surgical management began to change. Gastric resection gained favor, and the use of gastroenterostomy alone declined. In 1941 the Mayo Clinic data on the use of subtotal gastrectomy in the treatment of

benign gastric ulcer were presented. The data showed a mortality rate of only 2.2% and that other, previously used operations were being performed with much less frequency.10 In 1921 Andre Latarjet described the anatomy of the vagus nerves and applied that knowledge clinically by performing an anatomically complete vagotomy for dyspepsia. Subsequently, he observed postoperative issues with inadequate gastric emptying and included a gastrojejunostomy.12 Despite the improved understanding in vagal anatomy and physiology, therapeutic vagotomy remained an obscure treatment option for PUD. Lester Dragstedt, a physiologist and surgeon at the University of Chicago and later at the University of Florida, was paramount in the development of vagotomy for the treatment of peptic ulcers. Through his animal research, he elucidated the role of acid hypersecretion in the development of ulcers and stated “pure gastric juice as it is secreted by the fundus of the stomach has the capacity to destroy and digest all living tissue, including the wall of the jejunum, duodenum, and even the stomach itself.”13,14 Despite his understanding of the physiology, he was reluctant to perform a vagotomy on a human because he was unsure that a person could withstand the operation. However, in 1943 he managed a 35-year-old man with ulcer disease who had failed medical therapy. The patient was offered a subtotal gastrectomy and the patient promptly declined. The patient stated that both his father and his brother had undergone subtotal gastrectomies and that his father had died and his brother was miserable as a result of the operation.12,15 Dragstedt performed a bilateral vagotomy through a left thoracotomy. The patient had immediate relief of his symptoms postoperatively. By 1945 Dragstedt had performed vagotomies on 60 patients and, as other surgeons had noted, he began to see postvagotomy “pyloric stenosis.” Although he initially performed a drainage operation only for patients who were symptomatic from the impaired gastric emptying, he later modified his operation and performed abdominal truncal vagotomies (TVs) with a pyloroplasty concomitantly (Fig. 59.1). Vagotomy and drainage was gradually accepted because of its relatively equal results in regard to resolution of symptoms and a lower mortality when compared with resective procedures. Dragstedt considered his vagotomy surgical technique “the most important contribution of his career.” George Crile reported the Cleveland Clinic data: gastrectomy was associated with an ulcer recurrence rate and a mortality rate approximately three times higher than that in the vagotomy group.16 Goligher et al. compared vagotomy and pyloroplasty with other operations for duodenal ulceration and found that vagotomy and pyloroplasty had a recurrence rate at 2 years of 6.3%, vagotomy and enterostomy of 3.6%, whereas gastric resection had 0% recurrence. The surgical dictum of the time was that the treatment of ulcer disease was directed at reducing acid secretion. Vagotomy was used to eliminate the cephalic phase of acid secretion, which was considered to be the major contributor in duodenal ulceration. Antrectomy was the solution to eliminating the gastric phase of acid secretion, considered to be a major cause of gastric ulceration. Incorporating both vagotomy and antrectomy would

Surgery for Peptic Ulcer Disease  CHAPTER 59 

Right (posterior) vagus

Hepatic division Celiac division

Truncal vagotomy

Selective vagotomy

Crow's foot

Proximal gastric vagotomy

FIGURE 59.1  Schematic representation of the three standard forms of vagotomy. (From Sleisenger MH, Fordtran JS. Operations for peptic ulcer disease and early postoperative complications. In: Sleisenger MH, Fordtran JS, eds. Gastrointestinal Disease. 5th ed. Philadelphia: Saunders; 1993.)

effectively reduce, if not eradicate, acid production, thus continuing the “no acid, no ulcer” dogma of the time, and eradicated the need for a drainage procedure. Hubert et al. from the Mayo Clinic presented their results for vagotomy with antrectomy with a mean 17-year follow-up. They showed an operative mortality rate of 1.1% and an ulcer recurrence rate of 0.7%; the incidence of major postoperative complications was less than 1%.17 Extensive controversy revolved around the decision to perform a vagotomy and pyloroplasty versus a vagotomy with antrectomy. The idea that the two procedures both had a place in the treatment of ulcer disease was gradually accepted. At the time it was well established that for recurrent disease the optimal operation was vagotomy with resection. It was believed that, although both operations had equivalent results as to resolution of symptoms, vagotomy with antrectomy was associated with a lower recurrence rate, whereas vagotomy with drainage was associated with a lower mortality rate. The selective vagotomies (SVs) were thought to be the answer to the question of how to decrease acid secretion and at the same time limit the known and occasionally debilitating postoperative morbidity of the previously discussed operations. The basis behind the more SVs was

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the work done by Griffith and Harkins in 1957. They showed that fibers originating from the vagal trunks along the lesser curvature of the stomach innervate small groupings of parietal cells and as they approach the pylorus, they have a primary motor function. The goal of selective gastric vagotomy (SGV), first performed in the 1960s, was to limit the side effects encountered with other operations. However, gastric stasis was still a factor. In response to the motor denervation, a pyloroplasty or other drainage procedure was needed. Siim et al. followed 105 patients for up to 13 years and showed satisfactory resolution of symptoms in only 77% of those with low-grade ulcerations. In the individuals with high-grade/severe ulcer disease, only 19% had good results. In addition to the poor clinical results, there was a 15% recurrence rate. Ultimately, they concluded that “selective gastric vagotomy has no place in elective treatment.”18 Proximal gastric vagotomy (PGV), also referred to as a parietal cell vagotomy or highly SV, does not affect the distal motor function and thus does not impede gastric emptying. In the 1970s PGV became the most popular operation for elective treatment of PUD because of its lower mortality and morbidity rates and the omission of a drainage procedure.18 van Heerden et al. reported the data on 223 patients from 1973 to 1977 at the Mayo Clinic. With a 39-month mean follow-up, the incidence of postoperative adverse effects was less than 3%, with 0% deaths and a 4.9% recurrence rate. At the end of their study, they concluded that “proximal gastric vagotomy is an effective, safe, and satisfactory option.”19 Hoffmann et al. compared TV to SGV and PGV in a randomized controlled study of 248 patients with an 11- to 15-year follow-up. They found recurrence rates of 28.5% (TV), 37.4% (SGV), and 39.3% (PGV). Although there was a trend with lower recurrence in the TV group, the difference between the three groups failed to show statistical significance. Overall, the patient satisfaction for the three groups was similar, with approximately two-thirds of the patients being satisfied. The findings led to the conclusion that “none of the three forms of vagotomy can be recommended as the standard operative treatment.”20 As the discovery of H2 blockers and PPIs emerged, surgical indications decreased. The improved understanding of the pathogenesis of ulcer disease with the discovery of H. pylori and understanding the impact of NSAIDs further decreased the need for operation. Management became primarily medical in nature, with operation reserved for the emergency treatment of bleeding and perforation. This chapter discusses elective operations for intractable peptic ulcers and emergency procedures for complications.

PATHOPHYSIOLOGY OF PEPTIC ULCER DISEASE The decades of surgical therapy dominating the treatment of PUD have been followed by a period of potent acidreducing medication use that has now been replaced with a short-term regimen targeting the elimination of H. pylori infection. Discussions of the best operation have been

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BOX 59.1  Classification of Gastric and Duodenal Ulcers Helicobacter pylori infection Drug induced Nonsteroidal antiinflammatory drugs Low-dose aspirin Acid hypersecretory state Zollinger-Ellison syndrome Retained gastric antrum Anastomotic ulcer following gastric surgery Severe physiologic stress Tumors

replaced with a discussion of the best drug combination to treat the various manifestations of both gastric and duodenal peptic ulceration. A 10-day to 2-week course of drug therapy directed against H. pylori has an ulcer recurrence rate equivalent to TV with pyloroplasty. Although emergency operations for both peptic ulcer bleeding and perforation are still occasionally required, even their incidences are on the wane.21 The introduction of histamine H2-receptor antagonists in 1977 radically changed the need for elective surgical therapy of PUD. Yet, it was the discovery of the association of Campylobacter pyloridis (renamed H. pylori in 1989) with peptic ulceration by Warren and Marshall in 1982 that truly revolutionized our understanding of ulcer pathogenesis and its treatment.22 They received the Nobel Prize for this work in 2005. Epidemiology studies revealed a strong association between H. pylori infection and both gastric and duodenal ulcer disease. Treatment of the infection resulted in long-term cure of peptic ulcers. Despite the development of potent antisecretory drugs and treatment for H. pylori infection, PUD remains an important clinical problem because of the widespread use of NSAIDs. The cause of peptic ulcers is complex and multifactorial, as they result from the interplay of the effects of gastric acid and pepsin and the gastric mucosal barrier. Any entity that either increases acid and pepsin secretion or weakens the mucosal barrier can result in ulcers (Box 59.1).

HELICOBACTER PYLORI AND PEPTIC ULCER DISEASE H. pylori is the most common chronic bacterial infection in humans. Once acquired, infection persists and may or may not produce gastroduodenal disease. A number of factors determine whether H. pylori infection causes disease: the pattern of histologic gastritis induced; changes in homeostasis of gastrin and acid secretion; gastric metaplasia in the duodenum; interaction of H. pylori with the mucosal barrier; and the strain of H. pylori present. There is a great deal of variation in the virulence of different strains of H. pylori. Some genotypes of H. pylori appear to be particularly toxic and are more common in patients with peptic ulcers. These are vacA and cagA positive.23 There is also a genetic predisposition to acquire H. pylori infection. H. pylori colonizes the entire gastric epithelium. However, the severity of the chronic mucosal inflammation

is variable and the resultant clinical scenario is dependent on the distribution of the inflammation. The incidence of H. pylori in the setting of gastric ulcers is between 80% and 90% and up to 100% in the setting of duodenal ulcers.24 In patients with duodenal ulcer, density of infection and severity of inflammation are greatest in the distal antral region with sparing of the acid-secreting body mucosa. After H. pylori eradication, the gastric mucosal changes revert to normal. In gastric ulcers, the body and antrum are affected to a similar degree. In this case, gastric acid secretion can be decreased because of the more severe involvement of the parietal cell region. In response to the same stimulation with gastrin, duodenal ulcer patients with H. pylori produce more acid than infected patients without ulcers. This may result from an impaired acid-secreting ability of the nonulcer H. pylori-infected patient’s more diseased acidsecreting fundus mucosa. Increased gastric acid can lead to the development of gastric metaplasia in the duodenal bulb. This is a necessary forerunner to colonization of the duodenal epithelium with H. pylori, because H. pylori exclusively binds to the gastric epithelium. The metaplastic, H. pylori-colonized, duodenal epithelium then becomes more susceptible to acid and pepsin effects and ulceration. After the eradication of H. pylori infection, gastric metaplasia in the duodenum does not revert to normal, but with the elimination of the infection, the risk of ulcer recurrence is eliminated.24 H. pylori infection impairs the negative feedback of gastrin release by somatostatin secreted by antral D cells. Somatostatin causes inhibition of gastrin release through a paracrine effect. Production of alkaline ammonia by the bacteria on both the surface epithelium and in the antral glands prevents the D cells from properly interpreting the level of acid present. This leads to improperly low levels of somatostatin, and thus loss of gastrin inhibition. Chronic hypergastrinemia caused by H. pylori exerts a trophic effect and hyperplasia of the acid-secreting parietal cells.25 Infection with H. pylori also interferes with the neural connections between the antrum and fundus that downregulate acid production. This impaired neural control, coupled with hypergastrinemia, leads to further increases in acid production. With H. pylori eradication, the hypergastrinemia rapidly resolves. Resolution of acid hypersecretion occurs much more slowly.26 The inflammatory response caused by H. pylori infection of the gastric mucosa leads to cytokine production, mainly, interleukin (IL)-8.27 IL-8 acts as a potent chemotactic and attracts neutrophils and acute inflammatory cells into the submucosa. Other cytokines include IL-17 and IL-18. In a recent animal model, increased serum level of IL-17 was found to correlate with severity of gastritis; this correlation was not observed with changes in serum level of IL-8 and IL-18.28 Complex interactions occur between H. pylori and host defense mechanisms that affect the occurrence of peptic ulceration. Duodenal ulcers appear to be predominantly related to increased acid production, whereas in gastric ulceration, defense mechanism breaches appear to prevail. Despite these differences in mechanisms, H. pylori eradication effectively cures PUD and prevents relapses. In

Surgery for Peptic Ulcer Disease  CHAPTER 59 

addition, the rate of ulcer healing is accelerated if antibiotics effective against H. pylori are given in addition to drugs that suppress acid.

NONSTEROIDAL ANTIINFLAMMATORY DRUGS AND ULCER DISEASE NSAIDs increase the risk of peptic ulcers. NSAIDs are the most commonly identified risk factor for peptic ulcer bleeding, especially in older adults; the risk is drug specific and dose dependent. NSAIDs decrease the mucosal defense by suppression of prostaglandin synthesis in gastric and duodenal mucosa.29 Controlled trials with cyclooxygenase-2 (COX-2)-selective inhibitors have demonstrated a reduction in the risk of gastroduodenal ulcers and their associated complications.30 The presence of gastric acid contributes to NSAID injury by converting superficial mucosal lesions to deeper ulcers. In addition, acid interferes with platelet aggregation and impairs ulcer healing. 31 Acid suppression is the mainstay in the therapy of NSAID-associated ulcer disease. Risk factors that influence PUD in NSAID users include history of ulcer; advancing age; high-dose NSAIDs; steroids; aspirin; anticoagulants; and H. pylori infection.32 The use of COX-2 inhibitor and PPI can significantly reduce complications associated with NSAID intake.

LOW-DOSE ASPIRIN AND ULCER DISEASE Even at very low doses (75 mg daily), aspirin decreases gastric mucosal prostaglandin levels and can cause significant gastric lesions. The effect of aspirin is dose dependent, and ulcer complications are twofold to fourfold higher in patients taking 75 to 300 mg daily compared with controls.33 PPIs, given with low-dose aspirin, can significantly decrease the risk of developing peptic ulceration.34

ACID HYPERSECRETORY STATES AND ULCER DISEASE Both Zollinger-Ellison (ZE) syndrome as a consequence of gastrinoma, and retained gastric antrum after antrectomy with gastrojejunal anastomosis (so-called retained excluded antrum) result in peptic ulceration secondary to high levels of gastrin secretion. In cases of retained excluded gastric antrum, the residual gastric antral tissue is constantly bathed in a fluid with a high pH (nonacid), resulting in continuous secretion of gastrin. Fortunately, because of the infrequency of antrectomy in current surgical practice, this clinical situation is rarely encountered. In both disease states, high levels of serum gastrin result in gastric acid hypersecretion and resultant peptic ulceration. Serum gastrin elevations are also seen in chronic atrophic gastritis as a consequence of the lack of gastric acid secretion (typically achlorhydria) causing chronic G-cell stimulation.

SEVERE SYSTEMIC DISEASE (STRESS ULCER) The pathophysiology of stress ulceration is multifactorial and undefined. A breakdown of the gastroduodenal mucosal barrier, often a result of severe physiologic stress and splanchnic hypoperfusion, combined with gastric acid may lead to ulceration and bleeding. After splanchnic perfusion is restored, a reperfusion injury can further

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BOX 59.2  Risk Factors for Stress Ulcer–Related Bleeding Respiratory failure requiring mechanical ventilation >48 h Coagulopathy or anticoagulation Acute renal insufficiency Acute hepatic failure Sepsis Hypotension Brain or spinal cord injury History of gastrointestinal bleeding Low intragastric pH Burn involving >35% of body surface area Major operation (>4 h) High-dose corticosteroids (>250 mg/day hydrocortisone or equivalent)

exacerbate the condition. It can develop within hours in critically ill patients, typically starting in the fundus and spreading distally. Prior to the development of effective medical therapy to reduce or eliminate gastric acid, this was a feared and highly lethal condition, often requiring total or near-total gastrectomy for control in extremely ill patients. Even with such heroic measures, mortality was extremely high. With the advent of histamine H2-receptor antagonists and PPI therapy, the primary goal of stress ulcer therapy has been to prevent clinically important bleeding by identifying those patients at risk for the development of stress ulceration (Box 59.2) and administering appropriate prophylactic measures. Fortunately, acid-reducing medication effectively prevents significant bleeding in nearly all patients at risk for stress ulceration. Esophagogastroduodenoscopy (EGD) is the first line of intervention. It aids with the diagnosis. However, treatment is usually unsuccessful secondary to the diffuse nature of the bleeding. Angiography should be considered in patients who fail endoscopic intervention. Angiography can facilitate embolization of the bleeding vessel(s), which is usually the left gastric artery, or can help reduce the rate of bleeding by selective vasopressin infusion. Operative intervention is considered as the last resort in patients.

INDICATIONS FOR THE SURGICAL TREATMENT OF PEPTIC ULCER DISEASE ELECTIVE OPERATION FOR INTRACTABLE DUODENAL ULCER DISEASE The treatment of PUD has undergone a significant change. The previous use of elective surgical means to treat PUD has faded into history, and medical therapy has moved to the forefront of current treatment. Elective surgical procedures for PUD are limited these days to patients with gastric outlet obstruction because of long-standing, untreated or poorly treated ulcer disease. These patients are rare, and many are treatable with endoscopic dilation with or without stenting. In a meta-analysis including 2102 patients with PUD, the 12-month ulcer remission rates for gastric and duodenal ulcers were significantly higher in patients who were successfully eradicated of H. pylori infection when compared

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with those with a persistent infection (97% and 98% vs. 61% and 65%, respectively).35 H. pylori eradication even without concurrent acid suppression therapy heals greater than 85% of duodenal ulcers.36 Confirmation of H. pylori eradication should be strongly considered for all patients receiving treatment because of the availability of accurate, relatively inexpensive, and noninvasive tests. All patients with duodenal ulcer(s) should receive antisecretory therapy to facilitate ulcer healing; however, the duration of therapy will vary depending upon ulcer characteristics, risk factors for recurrent PUD, and the presence of ulcer complications. In patients with uncomplicated duodenal ulcer who test positive for H. pylori, PPI, given for 10 to 14 days, along with the antibiotic regimen to eradicate H. pylori, is usually adequate to induce healing, and additional PPI therapy is not needed as long as they are asymptomatic following therapy.37 Thus medical therapy for duodenal ulcer has shifted away from an antisecretory/antacid or surgical approaches to an antimicrobial strategy. Most peptic ulcers respond to medical treatment. However, in some individuals the ulcer is either refractory to conventional therapy or recurs following successful initial treatment. A refractory peptic ulcer is defined as an endoscopically proven ulcer greater than 5 mm in diameter that does not heal after 12 weeks of treatment with a PPI. On the other hand, a recurrent peptic ulcer is defined as an endoscopically proven ulcer greater than 5 mm in diameter that develops within 12 months following complete ulcer healing documented by repeat endoscopy. Prior to labeling the ulcer disease as intractable, it is important to rule out the following: • Cancer by performing endoscopy with adequate biopsy of the ulcer edge and base. • Gastrinoma by measuring fasting serum gastrin. • Total serum calcium should be measured to screen for hyperparathyroidism. • Ulcerogenic medication (e.g., NSAIDs, aspirin). • Persistent H. pylori infection by undergoing additional tests to confirm eradication. Ideally patients should be off of the PPI for at least 2 weeks to reduce false-negative results.38 • Chronic smoking, although smoking does not appear to be a risk factor for ulcer relapse after H. pylori has been eradicated. After these have been ruled out and when operative intervention is being considered, the strategy continues to be based on reduction of acid secretion. Gastric distention is an important stimulant of gastrin release by G cells, which are mainly located in the antrum; thus decompressing the stomach in patients with bleeding ulcers and gastric outlet obstruction secondary to ulcer is important to reduce gastrin and hence acid release. Acid release can surgically be reduced by dividing the vagus (cephalic phase), and eliminating hormonal stimulation from the antrum (gastric phase). Each of these maneuvers has consequences in terms of the normal physiology of the upper gastrointestinal tract that tend to be amplified when the procedures are combined, such as with vagotomy and antrectomy. In the past, the choice of operation involved weighing the risk of recurrent ulceration with the possibility of postoperative complications and long-term sequelae (postgastrectomy syndromes). This decision

dilemma prompted a large number of trials comparing these procedures in the surgical literature. Improvements in medical therapy, particularly treatment of H. pylori, have markedly reduced the risk of ulcer recurrence, rendering much of these data obsolete. Thus surgical decision-making has become confusing with little quality data available from the post–H. pylori era. The choices for surgical intervention for intractable duodenal ulcer disease include either a vagotomy with or without a drainage procedure or with a gastric resection.

VAGOTOMY The rationale for vagotomy is the elimination of direct cholinergic stimulation of gastric acid secretion. The released acetylcholine stimulates acid secretion via a specific receptor on the parietal cell. Vagotomy also renders the acid-producing parietal cells less responsive to histamine and gastrin. The distal portion of the anterior and posterior trunks send branches to the antrum and pylorus that serve a primarily motor function. Gastric motility is affected by the antral and pyloric branches of the vagus that stimulate peristaltic activity of the antrum and relaxation of the pylorus. The celiac branch of the posterior vagus mediates small intestine motility, whereas the hepatic branch mediates bile flow and gallbladder motility. TV results in a variety of physiologic alterations in the stomach. Acid secretion is drastically reduced because of diminished cholinergic stimulation of parietal cells, and the cephalic phase of gastric secretion is essentially eliminated. There is a 75% decrease in basal acid secretion and a 50% decrease in maximum acid output. The increased intraluminal stomach pH leads to elimination of the negative feedback on gastrin secretion; therefore, this results in increased serum gastrin levels and gastrin cell hyperplasia. As a result of loss of reflex relaxation of the gastric fundus, there is rapid emptying of liquids. Similarly, TV affects distal gastric motility, resulting in difficulty in emptying solids. Because of the latter alterations, approximately 20% to 30% of patients develop gastric atony, which leads to stasis and chronic abdominal pain and distention. For that reason, it is recommended that after a TV patients should undergo a drainage procedure to counteract the nonrelaxing pylorus, which acts as an obstruction. The various drainage procedures available are discussed later. There are four types of vagotomy to consider: truncal, selective, proximal gastric, and supradiaphragmatic. Truncal and proximal gastric are commonly used to treat PUD, whereas selective and supradiaphragmatic vagotomies are used infrequently.

TRUNCAL VAGOTOMY TV (see Fig. 59.1) involves division of the anterior and posterior vagal trunks after they emerge below the diaphragm. The first step is to incise the peritoneal covering of the gastroesophageal junction. The peritoneum is opened horizontally, from the lesser curvature to the cardiac notch at the greater curvature. The surgeon uses thumb and right index finger for blunt dissection to encircle the esophagus. A Penrose drain is placed around the lower esophagus to place more effective downward traction on the gastroesophageal junction. When encircling

Surgery for Peptic Ulcer Disease  CHAPTER 59 

the esophagus, the surgeon stays wide of the esophagus to prevent inadvertent entry into the lumen and to include the vagal trunks. In the course of this maneuver, the posterior vagal trunk usually will be palpated as a taut cord anterior to the aorta. A single anterior vagal trunk is usually identified in the anterior midportion of the esophagus, 2 to 4 cm above the gastroesophageal junction. It is not uncommon for vagal fibers to be distributed among two or three smaller cords at this level. These trunks are individually lifted up, and 2- to 4-cm segments of each are separated from surrounding tissues. A 1- to 2-cm length of nerve is resected and a clip is applied to the cut ends of the nerve. The “criminal nerve” of Grassi also may be identified wrapping around the cardiac notch from its origin in the posterior trunk and is a common cause of incomplete vagotomy. The posterior vagal trunk is usually identified along the right edge of the esophagus. If the anterior vagus has already been divided, the esophagus is more mobile. This mobility allows downward traction on the gastroesophageal junction, causing the posterior vagus to “bowstring” and making it easier to identify. A 2- to 4-cm segment is separated from surrounding tissues, its margins marked with clips, and resected. The resected portions of the anterior and posterior vagal trunks should be sent to pathology for frozen section. This procedure completely denervates the stomach and eliminates vagal innervation to the pancreas, small intestine, proximal colon, and hepatobiliary tree. Although this procedure significantly reduces acid secretion, it also markedly alters gastric motility. As discussed earlier, some form of gastric emptying procedure should be performed.

SELECTIVE VAGOTOMY The SV procedure (see Fig. 59.1) was developed in an attempt to decrease the incidence of postvagotomy diarrhea and ameliorate the increased incidence of gallbladder stasis, which may lead to increased gallstone formation. The vagal fibers are divided distal to the takeoff of the hepatic branch(es) from the anterior vagus and the celiac branch(es) from the posterior vagus. This procedure is technically more demanding than TV and requires a more careful and meticulous dissection. This technique spares vagal innervation to the gallbladder and intestine while completely denervating the stomach. Because the vagal pyloric innervation is also eliminated, a drainage procedure is still required. The primary reason for the development of this technique was its presumed lower side-effect profile. However, a prospective randomized study failed to show substantial benefit for SV over TV. 8 The incidence of diarrhea following an SV was no different when compared with TV. The introduction of PGV with its lower side-effect profile and the elimination of the need for a drainage procedure resulted in a limited use of SV as a therapeutic option.

PROXIMAL GASTRIC VAGOTOMY PGV is also known as parietal cell vagotomy and highly SV (see Fig. 59.1). The rationale for PGV is to eliminate the vagal stimulation to the acid-secreting portion of the stomach without interrupting motor innervation to the antrum and pylorus. The operation involves severing all

679

branches of the vagus nerve along the lesser curvature that innervate the corpus and fundus of the stomach, while preserving the hepatic and celiac branches, as well as the distal vagal branches extending to the antrum and pylorus. The end result of this procedure is the same reduction in acid secretion that occurs after TV (basal and stimulated acid secretion are reduced by more than 75% and 50%, respectively) but without the troublesome stasis and gastric atony. Because the distal motor nerves are preserved, emptying of solids is normal; however, the nerves affecting receptive relaxation are divided, and some rapid emptying of liquids may occur. The alteration in liquid emptying is usually minimal. This procedure is associated with the lowest morbidity rate of all vagotomy procedures and became the operation of choice in many centers despite a reported ulcer recurrence rate of between 5% and 20%. A meta-analysis of 12 trials confirmed that PGV has the highest recurrence rate when compared with TV with pyloroplasty, but fewer long-term side effects.39 PGV also has been compared with TV in a randomized trial, in which it was shown to have a lower incidence of dumping syndrome and weight loss. Although the ulcer recurrence rates were higher with PGV, this was not significant when prepyloric ulcers (for which PGV is not an adequate operation) were excluded.40 PGV is a complex and lengthy procedure, and, to help to simplify the procedure, several variations have been described. They usually consist of a posterior TV and a more selective ablation of the anterior vagal fibers to the gastric fundus and body. Hill and Baker performed a posterior TV with an anterior PGV (Hill-Baker procedure). Taylor combined the posterior TV with anterior lesser-curve seromyotomy (Taylor procedure). Randomized studies confirm the superiority of the Taylor procedure to TV41 and document equal outcomes to PGV with a shorter operative time.42 With the decreased incidence of elective ulcer surgery, such operations are not commonly used. However, such approaches are popular for laparoscopic treatment of ulcer disease.

SUPRADIAPHRAGMATIC VAGOTOMY This procedure is performed primarily for patients for whom attempts at complete vagotomy via an abdominal approach have failed; it is thought that further attempts to find the missed trunks in the reoperated abdomen may be difficult, and thus a thoracic approach is advised. This operation involves performing a thoracotomy or thoracoscopy, identifying the two large nerve trunks, and performing a TV.

DRAINAGE PROCEDURES Any patient who undergoes a truncal, selective, or supradiaphragmatic vagotomy should undergo a drainage procedure to facilitate gastric emptying. Drainage procedures fall into two categories: pyloroplasties and gastrojejunostomy (Fig. 59.2). Pyloroplasty is the preferred approach because it perpetuates the original anatomy, is a simple procedure, and is associated with less bile reflux than gastrojejunostomy. More than 90% of all drainage procedures currently performed are variations of pyloroplasty.

680

SECTION II  Stomach and Small Intestine

Gastrojejunostomy

Jaboulay Gastroduodenostomy

Heineke-Mikulicz Pyloroplasty

Finney Gastroduodenostomy

FIGURE 59.2  Drainage procedures used with truncal or selective vagotomy. (From Matthews JB, Silen W. Operations for peptic ulcer disease and early operative complications. In: Sleisenger MH, Fordtran JS, eds. Gastrointestinal Disease. 5th ed. Philadelphia: Saunders; 1993.)

PYLOROPLASTY Heineke-Mikulicz Pyloroplasty In 1888 the Heineke-Mikulicz procedure (see Fig. 59.2) was described independently by two surgeons, Heineke and Mikulicz. The technique is popular because it is technically straightforward, applicable to many clinical ulcer scenarios, and associated with few complications. The Heineke-Mikulicz pyloroplasty is the most commonly performed drainage procedure, and when conducted carefully and in a technically sound fashion, obstruction or leakage is rare. Patients who are candidates for this procedure include those who have a mobile, uninvolved anterior pylorus; those who have no evidence of a severely distorted or edematous pylorus; and those with small, minimally deforming pyloric perforations (massive perforations make pyloroplasty difficult and somewhat treacherous). The procedure may be performed using a single- or double-layer closure. After the pylorus is identified and the duodenum is mobilized with a Kocher maneuver, two traction sutures are placed in the anterior surface of the pylorus at the 12 and 6 o'clock positions; efforts should be made to include the pyloric vein of Mayo in these sutures, which is typically found in the inferior-anterior position on the pylorus (the vein may be used as a marker to identify the pylorus location, which is especially useful during laparoscopic procedures) to partially control the subsequent bleeding. The sutures are elevated, placing gentle tension on the anterior surface of the pylorus. A full-thickness longitudinal (horizontal) incision through the anterior wall of the pylorus (thus interrupting the circular muscle of the sphincter) is made, starting on the

anterior surface of the stomach 2 to 3 cm proximal to the pylorus and extending through the pylorus and approximately the same distance onto the anterior surface of the duodenum. In the presence of marked deformity, it may be advisable to incise the midportion of the duodenum and then one can use a curved clamp, such as a hemostat, directed up through the constricted pyloric canal as a guide. Traction on the angle sutures draws the longitudinal incision apart until it becomes diamond shaped; with the pylorus widely open one can ensure that there is no evidence of obstruction. The longitudinal incision is then closed in a transverse fashion. Typically this is done in either a two- or one-layer fashion (Fig. 59.3). The goal is complete inversion with good serosato-serosa approximation. Care is taken not to narrow the lumen by incorporating too much tissue into the closure. The thumb and index finger are used to palpate the newly formed lumen by invaginating the gastric and duodenal walls on each side of the transverse closure. Finney Pyloroplasty The Finney pyloroplasty (Fig. 59.4; see also Fig. 59.2) is indicated in the setting of extensive scarring and narrowing of a significant portion of the duodenal bulb, making a Heineke-Mikulicz pyloroplasty untenable. The pylorus is identified and mobilized with a generous Kocher maneuver. Traction sutures are placed along the pylorus as described for the Heineke-Mikulicz pyloroplasty. Then a single inverted U- or V-shaped incision is made though the prepyloric antrum, the pylorus, and the first part of the duodenum for a distance of approximately 7 cm in each direction. The reconstruction starts at the pylorus, in the middle of the incision, along the incised inferior aspect. The inferior leaf of the stomach is sutured to the inferior leaf of the anterior duodenal wall and continues to the extent of the incisions laterally on the stomach and duodenum. This is done with a running absorbable suture, and after the inferior leaflet has been approximated to the extent of the incision, it is continued back toward the pylorus, approximating the superior leaflets in the same fashion. A layer of Lembert sutures is then placed to invert the inner layer. The use of this drainage procedure makes a larger lumen possible but is more technically demanding compared with the Heineke-Mikulicz technique, involving a great deal more suturing, and has greater potential for complications. Jaboulay Gastroduodenostomy The Jaboulay drainage procedure (Fig. 59.5; see also Fig. 59.2) is the only one of the three described here that does not transect the pyloric muscle. The procedure involves an anastomosis of the distal stomach to the first and second portions of the duodenum, thus bypassing the pylorus. The procedure is indicated primarily for the severely scarred or deformed pylorus or duodenal bulb that would be too difficult and treacherous to incise. After carrying out a very extensive Kocher maneuver with thorough mobilization of the second and third portions of the duodenum, an area of the duodenum distal to the stenotic/scarred area is chosen, as is an area of the distal stomach just proximal to the pylorus. The duodenum is rolled anteriorly onto the stomach, and a posterior row

681

Surgery for Peptic Ulcer Disease  CHAPTER 59 

Traction suture Divided pylorus

Serosal sutures Heineke-Mikulicz

Kocher mobilization

Traction suture

1

Inverting suture

2

3

FIGURE 59.3  Schematic representation of Heineke-Mikulicz pyloroplasty. While lifting up on the traction sutures, a longitudinal incision is made through the pyloric muscles and extended 2 to 3 cm proximally into the stomach and distally into the duodenum (part 1). If the duodenum is soft, pliable, and minimally deformed, a running closure of the inside layer is begun with absorbable suture in an inverting fashion (part 2). An outside layer of Lembert silk sutures in an interrupted fashion completes the procedure (part 3). (From Zollinger RM. Atlas of Surgical Operations. New York: Macmillan; 1975.)

Traction suture Finney Divided pylorus Serosal sutures

Mucosal suture

4

5

FIGURE 59.4  Schematic of the Finney pyloroplasty. After the careful exploration, closure is initiated by using absorbable suture to begin a running closure (part 4). A final, interrupted row of silk sutures is then placed in Lembert fashion to complete the pyloroplasty (part 5). (From Zollinger RM. Atlas of Surgical Operations. New York: Macmillan; 1975.)

of Lembert sutures are placed. Two separate incisions are made through the previously chosen sites on the prepyloric antrum and the first portion of the duodenum. The posterior inner layer of the gastroduodenal anastomosis is completed with a continuous full-thickness absorbable suture; the anterior inner layer is completed with a continuous inverting Connell suture. Finally, anterior Lembert interrupted sutures are placed. The anastomosis can also

be performed in a single layer. Use of the Jaboulay procedure has been associated with increased bile reflux as the anastomosis is close to the ampulla of Vater.

GASTROJEJUNOSTOMY Gastrojejunostomy (see Fig. 59.2) was first performed alone in 1881 and was plagued by two problems: marginal ulcers (because no vagotomy was performed) and vomiting,

682

SECTION II  Stomach and Small Intestine

Angle suture

Jaboulay

Intact pylorus

Intact pylorus

Ulcer

Duodenal incision

6

Stomach incision

Serosal sutures

7

FIGURE 59.5  Schematic of the Jaboulay gastroduodenostomy. Equal-size incisions are made in the distal stomach and proximal duodenum approximately 4 to 5 cm in length (part 6). A final anterior, outside layer of interrupted Lembert silk sutures is then placed to complete the gastroduodenostomy (part 7). (From Zollinger RM. Atlas of Surgical Operations. New York: Macmillan; 1975.)

which was thought to be caused by kinking with an excessive length of the afferent limb of jejunum. The two problems have been overcome with the addition of vagotomy and construction of a shorter afferent jejunal segment. Gastrojejunostomy is most commonly indicated as a drainage procedure when there is duodenal obstruction and the duodenal bulb is so scarred, inflamed, and edematous that pyloroplasty is not safe or is excessively technically demanding. This is also the drainage procedure of choice when vagotomy and drainage is being performed laparoscopically. The jejunum, unlike the duodenum, lacks Brunner glands that secrete alkaline solution and protect against stomach pH. Therefore, historically, vagotomy was highly recommended as an adjunct when performing a gastrojejunostomy as a drainage procedure in the treatment of PUD. This was mainly to reduce the incidence of marginal ulcers; however, in the era of PPIs, we have learned that lifelong PPI can significantly reduce this complication without the morbidity associated with vagotomy.43 Older patients with achlorhydria and atrophic gastritis make little acid, and a vagotomy may not be necessary, especially in the setting of malignant obstruction. A variety of postgastrectomy complications may occur after pyloroplasty or gastroenterostomy, including dumping, diarrhea, alkaline reflux gastritis, anemia, and marginal ulceration. These may be seen in up to 50% of patients after operation on a temporary basis, but they resolve within 6 to 8 months in most, and only 5% to 7% of patients have a persistent, symptomatic postoperative complication such as dumping.

GASTRIC RESECTION PROCEDURES Although subtotal gastrectomy was used for the treatment of duodenal ulcer disease in the past, currently it is most commonly used for gastric ulcer and distal gastric malignancies. A more common gastric resection performed for intractable duodenal ulcer is antrectomy (40% distal gastrectomy) that is combined with a TV or an SV. The simultaneous effects of vagotomy and antrectomy remove both the cholinergic and gastrin stimulus to acid secretion. Basal acid secretion is virtually abolished and stimulated secretion is reduced by nearly 80%. After antrectomy, gastrointestinal continuity must be restored by some form of reconstruction. The remnant is anastomosed either to the duodenum (Billroth I [B I]) or, after closing the duodenal stump, to the jejunum distal to the ligament of Treitz (Billroth II [B II]) (Fig. 59.6). B I reconstruction has several theoretical advantages: 1. Restoring normal GI continuity 2. Leaving specialized duodenal mucosa next to the gastric mucosa 3. Avoiding problems with an afferent and efferent limb 4. Allowing easier performance of endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic examination of the bowel 5. Reduced incidence of gastric cancer in the remnant stomach.44 Despite the theoretical physiologic advantages, no important functional differences have ever been demonstrated between these reconstructions. Although studies show a larger fecal fat loss following a B II procedure,

683

Surgery for Peptic Ulcer Disease  CHAPTER 59 

this is unlikely to be of any significance. The difference in cancer risk is real but significant only after a long follow-up period (>15 years).45,46 The choice is typically based on the degree of scarring of the duodenum and the ease with which the duodenum and gastric remnant can be brought together. Several variations of the B I and B II operations have been described, and these are summarized in Figs. 59.7 and 59.8. Both Billroth reconstructions can lead to bile reflux, which can result in disabling symptoms. To avoid such complications, some favor a Roux-en-Y reconstruction. The long-term results (12 to 21 years) of a study in which patients were randomized to B II or 60-cm Roux-en-Y reconstruction confirm improved patient satisfaction and endoscopic appearance of the esophagus and the gastric remnant after Roux-en-Y reconstruction.47 Unfortunately, the Roux-en-Y reconstruction can be plagued with a Roux stasis syndrome. Studies show that the Braun variation of B II (see Fig. 59.8) has a lower incidence of bile reflux; consequently, some authors recommend this as the standard reconstruction technique.48 However, other authors promote the “uncut” Roux-en-Y reconstruction49 (Fig. 59.9).

Billroth I

Billroth II

FIGURE 59.6  Reconstruction techniques after partial gastrectomy: Billroth I gastroduodenostomy and Billroth II gastrojejunostomy. (From Matthews JB, Silen W. Operations for peptic ulcer disease and early operative complications. In: Sleisenger MH, Fordtran JS, eds. Gastrointestinal Disease. 5th ed. Philadelphia: Saunders; 1993.)

A

B

C

D

PARTIAL GASTRECTOMY WITH BILLROTH I RECONSTRUCTION An antrectomy removes the acid-secreting portion of the stomach, which contains the G cells that are responsible for secreting gastrin. To adequately remove all the G cells, 35% of the distal stomach should be removed. This correlates to removing 45% of the lesser curve (approximately 7 cm from the pylorus); the incisura is a reasonable proximal margin along the lesser curve. Fifteen percent of the distal greater curve should be removed; this correlates to the terminal portion of the right gastroepiploic artery. First, the greater curvature is mobilized along its distal portion by incising the gastrocolic ligament in an avascular plane. The dissection begins at the pylorus with ligation of the right gastroepiploic artery and proceeds cephalad along the greater curvature. It is important to take special care to avoid injury to the mesocolon and middle colic artery (Fig. 59.10). The dissection should be carried approximately 1 cm past the pylorus if a B I reconstruction is anticipated. If B II is anticipated, the dissection need only be carried far enough to comfortably place the transverse linear stapler past the pylorus or to close the duodenum by a handsewn technique. Next, the lesser curvature is mobilized (Fig. 59.11). The flimsy tissues of the lesser omentum are divided along the lesser curvature starting at the incisura and working toward the pylorus. The right gastric artery is divided and ligated. The posterior wall of the duodenal bulb is then carefully dissected off the pancreas. A Kocher maneuver should be performed prior to distal gastrectomy to minimize tension on the anastomosis. For handsewn gastroduodenostomy reconstruction first, the lower portion of the gastric staple line is removed. The length of the staple line to be removed is the same as the width of the duodenal stump. The duodenum and the stomach are then apposed through the placement of a posterior serosal layer of interrupted silk sutures (Fig. 59.12). An inner mucosal closure is initiated with a continuous absorbable suture (Fig. 59.13). The mucosal suture continues anteriorly (Fig. 59.14). Finally, an anterior serosal layer is placed with interrupted silk seromuscular sutures (Fig. 59.15).

E

F

G

H

I

FIGURE 59.7  Variations of Billroth I reconstructions. (A) Billroth (1881). (B) Billroth (1881). (C) Kocher (1890). (D) Kutscha-Lissberg (1925). (E) v. Haberer (1920). (F) v. Haberer (1920), Finney (1923). (G) Winkelbauer (1927). (H) Schoemaker (1911). (I) Harkins, Nyhus (1960). (From Siewert JR, Bumm R. Billroth I gastrectomy. In: Baker RJ, Fischer JE, eds. Mastery of Surgery. Philadelphia: Lippincott Williams & Wilkins; 2001.)

684

SECTION II  Stomach and Small Intestine

B

A

C

F

E

D

H

G

J

I

K

FIGURE 59.8  Variations of Billroth II reconstruction. (A) Billroth II. (B) Kronelin. (C) von Eiselberg. (D) Braun. (E) Roux. (F) Roux-en-Y. (G) Ploy and Reichel. (H) Finsterer-Hofmeister. (I) Balfour. (J) Moynihan. (K) Tanner. (From Wastell C, Davis PA. Billroth II gastrectomy. In: Baker RJ, Fischer JE, eds. Mastery of Surgery. Philadelphia: Lippincott Williams & Wilkins; 2001.)

For a stapled gastroduodenostomy, a gastrotomy is created with electrocautery on the anterior surface of the stomach at least 3 cm proximal to the staple closure (Fig. 59.16). The end-to-end stapling device, without the anvil, is passed into the anterior gastrotomy with the rod advancing through the posterior gastric wall, again 3 cm proximal to the stapled edge. The anvil is introduced into the duodenum after placement of a purse-string suture in the end of the duodenum (Fig. 59.17). The end-to-end anastomotic (EEA) stapler is closed, fired, and withdrawn.

The anastomosis is inspected to ensure adequate hemostasis. The anvil is then removed and checked to ensure that tissue doughnuts from both the duodenum and the stomach are present. The gastrotomy is closed by the application of a TA stapling device or sutured closed in two layers (Fig. 59.18). Laparoscopic partial gastrectomy with B I reconstruction has been described using many different surgical techniques. It can be performed using linear or end-to-end stapling devices depending on the surgeon’s preference and mobility of the duodenum.

Surgery for Peptic Ulcer Disease  CHAPTER 59 

Enteroenterostomy Stapled closure

685

Blunt dissection of avascular plane between stomach and pancreas

Ligation of right gastroepiploic artery

FIGURE 59.10  The gastrocolic omentum is dissected from the

60 cm

stomach. The dissection begins at the pylorus with ligation of the right gastroepiploic artery and proceeds cephalad along the greater curvature. The posterior antrum is then separated from the anterior pancreas and base of the transverse mesocolon by division of fine connective tissue attachments. (From Jones RS. Gastric resection: Billroth I anastomosis. In: Sabiston DC Jr, ed. Atlas of General Surgery. Philadelphia: Saunders; 1994:263.)

FIGURE 59.9  “Uncut” Roux-en-Y reconstruction after partial gastrectomy. A jejunoduodenostomy with a 60-cm efferent limb is constructed. The afferent limb is occluded with a staple line. (From van Stiegmann G, Goff JS. An alternative to Roux-en-Y for treatment of bile reflux gastritis. Surg Gynecol Obstet. 1988;166:69.)

Posterior row of seromuscular sutures in place Proximal duodenum

FIGURE 59.12  For gastroduodenostomy reconstruction, the FIGURE 59.11  The gastrohepatic ligament is incised, and the lesser curvature is dissected. The right gastric vessels are ligated close to the stomach. In patients with pyloric inflammation, care must be taken to avoid injury to both the hepatic artery and the common bile duct. (From Sedgewick C. Gastrectomy. In: Braasch JW, Sedgewick CE, Veidenheimer MC, Ellis FH Jr, eds. Atlas of Abdominal Surgery. Philadelphia: Saunders; 1991:37.)

duodenum and the inferior gastric staple line are apposed through the placement of a posterior serosal layer of interrupted silk sutures. (From Jones RS. Gastric resection: Billroth I. In: Sabiston DC Jr, ed. Atlas of General Surgery. Philadelphia: Saunders; 1994:267.)

686

SECTION II  Stomach and Small Intestine

Second row of sutures (through all layers)

FIGURE 59.13  An inner mucosal closure is initiated with a continuous absorbable suture. (From Jones RS: Gastric resection: Billroth I. In: Sabiston DC Jr, ed. Atlas of General Surgery. Philadelphia: Saunders; 1994:268.)

FIGURE 59.15  An anterior serosal layer is placed with interrupted silk seromuscular sutures. (From Zinner MJ. Atlas of Gastric Surgery. New York: Churchill Livingstone; 1992. After Gloege. In: Soybel DI, Zinner MJ: Stomach and duodenum: operative procedures. In: Zinner MJ, Schwartz SI, Ellis H, eds. Maingot’s Abdominal Operations. Stamford, CT: Appleton and Lange; 1997:1105.)

Opening gastrotomy for EEA stapler

FIGURE 59.14  The mucosal suture continues anteriorly. (From Zinner MJ. Atlas of Gastric Surgery. New York: Churchill Livingstone; 1992. After Gloege. In: Soybel DI, Zinner MJ: Stomach and duodenum: operative procedures. In: Zinner MJ, Schwartz SI, Ellis H, eds. Maingot’s Abdominal Operations. Stamford, CT: Appleton and Lange; 1997:1105.)

PARTIAL GASTRECTOMY WITH A BILLROTH II RECONSTRUCTION Antrectomy is carried out as described previously. The proximal end of the stomach is divided with a TA 90 stapling device or can also be accomplished with two applications of a gastrointestinal anastomotic (GIA) stapling device. The proximal duodenum is divided with care to avoid injury to the common bile duct. The duodenal closure can be reinforced with interrupted 3-0 silk sutures. The gastric staple line is oversewn superiorly with either

FIGURE 59.16  For a stapled gastroduodenostomy, a gastrotomy is created with electrocautery on the anterior surface of the stomach at least 3 cm proximal to the staple closure. EEA, End-to-end anastomotic. (From Siegler HF. Gastric resection: Billroth I anastomosis [stapler]. In: Sabiston DC Jr, ed. Atlas of General Surgery. Philadelphia: Saunders; 1994:274.)

continuous or interrupted suture (Fig. 59.19). Traction sutures are useful to steady the remnant within the operative field. A proximal loop of jejunum is chosen and apposed to the stomach. The jejunum can be delivered through an incision in the transverse mesocolon or anterior to the transverse colon. As long as the anastomosis will

Surgery for Peptic Ulcer Disease  CHAPTER 59 

Arm of stapler penetrating posterior stomach 2 to 3 cm from stapled transection

687

TABLE 59.1  Ulcer Recurrence Rates for the Three Common Acid-Reducing Procedures

Surgical Procedure Truncal vagotomy with drainage Truncal vagotomy with antrectomy Proximal gastric vagotomy

Ulcer Recurrence Rate (%)

Risk of Side Effects

10 2 15

Highest High Low

PARTIAL GASTRECTOMY WITH A ROUX-EN-Y RECONSTRUCTION

Securing duodenum over anvil of stapler

FIGURE 59.17  The end-to-end stapling device, without the anvil, is passed into the anterior gastrotomy with the rod advancing through the posterior gastric wall, again 3 cm proximal to the stapled edge. The anvil is introduced into the duodenum after placement of a purse-string suture with an automatic device. The end-to-end anastomotic stapler is closed, fired, and withdrawn. (From Siegler HF. Gastric resection: Billroth I anastomosis [stapler]. In: Sabiston DC Jr, ed. Atlas of General Surgery. Philadelphia: Saunders; 1994:275.)

not be under tension, the antecolic position will permit emptying as effective as the retrocolic anastomosis. For malignant disease, some surgeons favor an antecolic anastomosis to avoid disease recurrence and subsequent gastric outlet obstruction. If a retrocolic position is chosen, the window in the transverse mesocolon should be closed following construction of the anastomosis to prevent kinking and obstruction of the jejunal limbs. Interrupted sutures are placed in seromuscular fashion between the posterior gastric wall and the antimesenteric border of the jejunum (Fig. 59.20). Matching incisions are made with electrocautery in the jejunum and stomach, with the latter involving partial excision of the stapled gastric closure (Fig. 59.21). The posterior full-thickness suture line is initiated with a continuous suture of absorbable material on a double arm. Corner sutures include the anterior gastric wall, the posterior gastric wall, and the jejunum. The inner layer, full-thickness suture is continued along the length of the anterior aspect of the anastomosis. An anterior layer of interrupted silk sutures completes the anastomosis (Fig. 59.22). For stapled gastroenterostomy, the jejunal limb is placed next to gastric stapled line. Traction sutures are placed. A linear stapler is placed through a small gastrotomy and small enterotomy to create gastrojejunostomy. The enterotomy sites are closed either by TA stapler or handsewn. Similar to the open technique, a laparoscopic partial gastrectomy and B II reconstruction procedure is conducted in the same order as previously described.

After antrectomy and duodenal closure, reconstruction with the Roux-en-Y gastrojejunostomy is performed by dividing the jejunum approximately 40 cm distal to the ligament of Treitz. The mesentery is divided in a straight line down to the origin to allow more mobility of the Roux limb. A 50- to 70-cm Roux limb is created and a side-to-side jejunojejunal anastomosis is constructed. The mesenteric defect is closed using a running 2-0 silk suture to prevent internal hernias. A mesocolic window large enough to accommodate the Roux limb is created to the left of the middle colic vessels. The Roux limb is then advanced through the window up to the proximal stomach. Care must be taken not to twist the mesentery of the Roux limb when performing this maneuver. Alternatively the Roux limb may be placed in an antecolic position. The gastrojejunostomy can be performed via handsewn, an EEA- or a side-to-side linear-stapled anastomosis.

CHOICE OF OPERATION FOR INTRACTABLE DUODENAL ULCER As can be seen from the earlier descriptions, a variety of surgical operations are available for patients with intractable duodenal ulcer. Reliable data on the results of the various procedures for duodenal ulcer were generated by a series of trials during the latter half of the 20th century. Published series generally used different criteria for patient selection and for estimating the incidence of side effects. Table 59.1 summarizes the data on the three most commonly performed procedures: TV and antrectomy, TV and drainage, and PGV. Mortality and early morbidity were highest for the resection procedures and lowest for PGV, which avoids opening the gastrointestinal tract. Recurrence rates were significantly lower for vagotomy, and antrectomy. TV with pyloroplasty is virtually never indicated as an elective procedure because it has both the disadvantages of a high incidence of postgastrectomy complications and a high ulcer recurrence rate (10% to 15%). Historically, an important factor when considering the choice of operation was the ulcer recurrence rate. However, with identification of H. pylori, it is believed that recurrences are for the most part eliminated, although no data in this setting have yet been generated. Because of this, PGV, which is associated with fewer postoperative sequelae, is the preferred acid-reducing procedure in patients with intractable ulcer symptoms. One trial randomized 248

688

SECTION II  Stomach and Small Intestine

Trimming excess tissue from stapled gastrotomy

Completed gastrojejunostomy

FIGURE 59.18  The anastomosis is inspected to ensure adequate hemostasis. The anvil is then removed and checked to ensure that tissue doughnuts from both the duodenum and the stomach are present. The gastrotomy is closed by the application of a TA stapling device. (From Siegler HF. Gastric resection: Billroth I anastomosis [stapler]. In: Sabiston DC Jr, ed. Atlas of General Surgery. Philadelphia: Saunders; 1994:276.)

current experience with this more complex procedure is limited.

GIANT DUODENAL ULCER

FIGURE 59.19  The gastric staple line is oversewn superiorly. (Modified from Townsend CM, Evers BM. Atlas of General Surgical Techniques. Philadelphia: Elsevier; 2010; [Fig. 27.6B and C].)

patients with stable PUD to TV and drainage, SV and drainage, or PGV. At 11 to 15 years after surgery, PGV was associated with reductions in the incidence of severe postvagotomy symptoms, such as dumping, diarrhea, and dyspepsia. Interestingly, this study did not show a significant difference in the ulcer recurrence rates among the three groups.20 Although this would more strongly favor PGV,

Giant duodenal ulcer (GDU) is defined as a duodenal ulcer that is benign and measures at least 2 cm in diameter. The size of the ulcer makes it difficult to treat because the ulcer, by definition, involves the full circumference of the duodenal wall, leading to scarring and deformity of the duodenal bulb. GDU is seen in up to 1% to 2% of all duodenal ulcer.47 When compared with standard-size duodenal ulcers, GDUs are less often associated with H. pylori infection, and NSAID use plays a more prominent role.50 Patients usually present with epigastric pain that can radiate to the back, particularly when the ulcer penetrates into the pancreas. In complicated cases, patient can present with a combination of bleeding, perforation, and/or obstruction. Diagnosis is established via upper endoscopy. It is important to measure the ulcer so as not to misdiagnose it as a simple peptic ulcer. The ulcer usually involves more than 50% of the duodenal bulb circumference. It is essential to rule out cancer as the cause of ulcer formation with biopsy in the setting of GDUs, because the risk of malignancy in such a setting is approximately 19%.47 The first line of treatment for an uncomplicated GDU after ruling out cancer is PPI with eradication of H. pylori and discontinuation of NSAIDs. It is very important to confirm H. pylori eradication through a noninvasive test such as urea breath test and repeat endoscopy to confirm healing in 8 to 12 weeks. If the ulcer is partially healed,

Surgery for Peptic Ulcer Disease  CHAPTER 59 

689

Site of jejunal opening for stapler

Electrocautery used to open stomach for stapled gastrojejunostomy 1 cm from oversewn stapled edge of stomach

FIGURE 59.20  A proximal loop of jejunum is apposed to the stomach. Interrupted sutures are placed in seromuscular fashion between the posterior gastric wall and the antimesenteric border of the jejunum. (From Jones RS. Gastric resection: Billroth II. In: Sabiston DC Jr, ed. Atlas of General Surgery. Philadelphia: Saunders; 1994:284.)

Proximal jejunum

A

B

FIGURE 59.22  (A) The mucosal suture is continued along the FIGURE 59.21  Matching incisions are made in the jejunum and stomach, with the latter involving partial excision of the stapled gastric closure. The posterior mucosal closure is initiated with a continuous suture of absorbable material. Corner sutures include the anterior gastric wall, the posterior gastric wall, and the jejunum. (From Zinner MJ. Atlas of Gastric Surgery. New York: Churchill Livingstone; 1992. After Gloege. In: Soybel DI, Zinner MJ: Stomach and duodenum: operative procedures. In: Zinner MJ, Schwartz SI, Ellis H, eds. Maingot’s Abdominal Operations. Stamford, CT: Appleton and Lange; 1997:1112.)

length of the anterior aspect of the anastomosis. (B) An anterior layer of interrupted silk sutures completes the anastomosis.

690

SECTION II  Stomach and Small Intestine

medical treatment should continue for another 8 to 12 weeks, with repeat endoscopy afterward to confirm complete healing. Because of the large, penetrating nature of these ulcers, when not recognized and treated promptly, complications such as hemorrhage and perforation can occur, resulting in high rates of morbidity and mortality. Operative intervention for GDU is indicated for patients who present with 1. Hemorrhage in spite of maximum endoscopic intervention 2. Perforation 3. Gastric outlet obstruction 4. Intractability or recurrent disease in spite of maximum medical therapy The chronic inflammatory changes associated with this condition often make the operations technically challenging. A definitive acid-reducing operation should be performed in addition to removing the involved duodenum whenever possible. If the inflammation and edema of the duodenum is not a factor, a B I reconstruction can occasionally be performed. However, dissection and anastomosis can be hazardous, and it is best to leave the ulcer bed in situ and perform a B II. In such cases, duodenal stump leak is a major source of morbidity and mortality postoperatively. The use of a duodenostomy tube is known to be a safe and effective means in dealing with a difficult duodenal stump. This involves insertion of a tube through the second portion of the duodenum to encourage formation of a controlled fistula; by doing so, this takes off the pressure from the stump and allows healing. In situations in which the duodenum is scarred to the pancreatic capsule, a Nissen closure can be performed. This is performed by first transecting the duodenum. The duodenal stump is then anastomosed to the pancreatic capsule or duodenal wall left in place on the pancreatic capsule. Another way of dealing with a difficult duodenal stump is to perform a Bancroft closure. In this method of duodenal stump closure, the stomach is transected proximal to the pylorus, where tissue is less fibrotic. The gastric mucosa in the duodenal stump is then dissected away from the submucosa into the duodenum. This is secured with a purse-string suture, and the seromuscular layer is closed over the stump.

RECURRENT PEPTIC ULCER DISEASE Supradiaphragmatic vagotomy is used almost exclusively for the treatment of ulcer recurrence after previous acidreducing surgery that included vagotomy. The most common cause for ulcer recurrence after an acid-reducing procedure is an incomplete vagotomy. Attempting to find the missed nerve through the densely scarred upper abdomen is fraught with difficulty and can be hazardous. Transthoracic TV may be successfully used. The procedure can now be performed with minimally invasive thoracoscopic techniques.

LAPAROSCOPIC SURGERY An increasing number of reports indicates the feasibility of laparoscopic and robotic assisted approaches to operations for PUD. When performing a laparoscopic partial gastrectomy, the abdomen is entered at the left subcostal area using an optical trocar. The camera port is placed

FIGURE 59.23  Laparoscopic anterior seromyotomy as part of the Taylor procedure. (From Dubois F. New surgical strategy for gastroduodenal ulcer: laparoscopic approach. World J Surg. 2000;24:270.)

approximately 15 cm from the xiphoid process, slightly to the left of the midline. A 12-mm trocar is used for the surgeon’s right hand to accommodate a linear stapler. A third 5-mm trocar is placed in the right subcostal area. After placing the patient in steep reverse Trendelenburg position, a liver retractor is placed via a 5-mm incision in the subxiphoid area. This will elevate and retract the left lateral segment of the liver. The first portion of the duodenum is mobilized and divided using a laparoscopic stapler. The staple line can be reinforced with suture or staple-buttressing material at the surgeon’s discretion. The proximal stomach is divided using a laparoscopic stapler. Reconstruction is then performed either with a B II gastrojejunostomy or a Roux-en-Y gastrojejunostomy. Although most open procedures have been attempted laparoscopically, including the more difficult PGV, the Taylor procedure (anterior seromyotomy with posterior TV) appears to be the simplest option (Fig. 59.23). The Taylor procedure was reported in 1982 as an open procedure. Although the open approach is not widely performed, the technique is very suitable for a laparoscopic procedure. This procedure starts with a posterior TV followed by a seromyotomy that should start approximately 6 cm proximal to the pylorus. The circular muscle is incised 1.5 cm from the lesser curve and the muscle fibers divided using a hook coagulator. The dissection is continued caudally as far as the gastroesophageal junction. Along the length of the myotomy all of the circular muscle fibers are divided. It is not necessary to divide the deeper thin layer of the oblique muscle. Air is injected through a nasogastric tube to make sure there are no leaks. The

Surgery for Peptic Ulcer Disease  CHAPTER 59 

seromyotomy is then closed with an overlapping running suture.51

ELECTIVE OPERATION FOR INTRACTABLE GASTRIC ULCER DISEASE Although both gastric and duodenal ulcers are peptic lesions, fundamental differences between these entities affect surgical strategy. The most important difference is that gastric ulcers more commonly may harbor malignancy and thus must be excised or generously biopsied. Acid hypersecretion, which is important in pathogenesis of duodenal ulcers, does not have a role in pathogenesis of many gastric ulcers. In 1965 Dr. H.D. Johnson published a classification system that subsequently was adopted and, with little modification, is still currently in use. In his 1965 paper, he discusses Dragstedt’s theory that the cephalic phase of acid secretion is responsible for duodenal ulceration and that the gastric phase was responsible for gastric ulceration. He observed that his theory disregards the findings that less than half of patients with gastric ulcers are acid hypersecreters. He argues for a multifactorial pathogenesis for ulcers beyond the hypersecretion of gastric acid.52 The Johnson classification system, which is based upon anatomic location and acid-secretory potential, provides a useful basis for considering operative treatment of gastric ulcer (Table 59.2 and Fig. 59.24).

are now outdated because of the high ulcer recurrence rates.56 Addition of a TV to gastric resection offers no additional benefit to the patient.57 Low recurrence rates (5%) and excellent symptomatic relief are usually achieved with a distal gastrectomy alone.

TYPE II GASTRIC ULCER Type II gastric ulcers occur in the pyloric channel synchronously with ulceration in the duodenum or metachronously with scarring in the duodenum. Therefore patients presenting with a pyloric channel ulcer and history of duodenal ulcer classifies the gastric ulcer as type II and should be treated as such. They tend to be large, deep ulcers with poorly defined margins. They frequently occur in younger men and are associated with increased acid secretion. Preoperative endoscopic examination of such ulcers must include biopsy of the lesion to rule out an underlying malignancy. Treatment is similar to duodenal ulcer, with vagotomy and antrectomy as the preferred approach. PGV alone in type II gastric ulcer is

Type I lesser curve

TYPE I GASTRIC ULCER Type I ulcers are the most common form and are responsible for up to 60% of gastric ulcers. These typically occur along the lesser curvature at the junction of the fundic and antral mucosa near the area of the incisura and occur in the setting of acid hyposecretion. Distal gastrectomy with B I or II reconstruction is recommended for most patients because this approach removes the ulcer and the diseased antrum. Partial gastrectomy also eliminates the risk of missing a malignancy associated with a biopsy and reduces the acid secretory potential. Another option is to perform distal gastrectomy with Roux-en-Y gastrojejunostomy; as compared with B I and II, there is decreased dumping syndrome and patients do not get bile reflux gastritis.53,54 However, patients who undergo Roux-en-Y reconstruction are at higher risk of delayed gastric emptying. A randomized study evaluating patients who underwent B I versus Roux-en-Y reconstruction following distal gastrectomy for cancer found no difference in long-term quality of life.55 Earlier recommendations of performing a biopsy of the ulcer combined with vagotomy and drainage

691

Type II combined gastric and duodenal

Type IV juxtoesophageal

Type III prepyloric

Type V drug related

TABLE 59.2  Modified Johnson Classification of Gastric Ulcers Type

Location

Acid Secretion

I II III IV

Lesser curvature Body of stomach and duodenum Prepyloric (within 2–3 cm of pylorus) High on lesser curve, near gastroesophageal junction Anywhere, induced by medication

Low High High Low

V

Low

FIGURE 59.24  Classification of gastric ulcers based on their anatomic location. (From Matthews JB, Silen W. Operations for peptic ulcer disease and early operative complications. In: Sleisenger MH, Fordtran JS, eds. Gastrointestinal Disease. Philadelphia: Saunders; 1993.)

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SECTION II  Stomach and Small Intestine

discouraged because it leaves the gastric ulcer behind, which can harbor malignancy.

or nonresective procedures in which the ulcer itself is not excised, the Kelling-Madlener procedure, or vagotomy with pyloroplasty, which has a high ulcer recurrence rate. The risk of malignant transformation or missed malignancy (despite biopsies) is small but real, and thus the nonresective procedures are not recommended in this setting. Although there is no consensus in the literature, some have suggested that for ulcers 5 cm below the cardia, the Pauchet procedure should be used, whereas for those lesions within 2 cm of the cardia, the Csendes procedure should be attempted (see Fig. 59.25).59 The Csendes procedure involves a near-total gastrectomy and a Rouxen-Y esophagogastrojejunostomy for reconstruction. The principle of this operation is to remove the high gastric ulcer such that the circumference of the esophageal mucosa remains intact.

TYPE III GASTRIC ULCER Type III ulcers are prepyloric or pyloric channel ulcers. They occur in the setting of increased acid secretion and are also approached in a manner similar to duodenal ulcer and type II gastric ulcer. Type III ulcers are particularly resistant to both medical therapy and PGV, with recurrence rates ranging from 16% to 44% in various series.39 This finding, plus the observation that these lesions may harbor gastric malignancy, makes vagotomy and antrectomy the most prudent approach. Early consideration for surgical referral is advisable for resistant ulcers or those that present with obstructive symptoms. Ulcers associated with acid hypersecretion are responsible for approximately 45% of gastric ulcer disease, with type II accounting for 25% and type III for 20%.

TYPE V GASTRIC ULCER These lesions can occur anywhere in the stomach and are induced by the use of medications, such as NSAIDs. Prophylactic regimens that have been shown to dramatically reduce the risk of ulcers, especially if the NSAID treatment cannot be stopped, include the use of PPI and/or prostaglandin analogue.60,61 A definitive antisecretory operation (TV and antrectomy) should be considered if medical treatment fails or if the NSAID treatment cannot be stopped.

TYPE IV GASTRIC ULCER Type IV gastric ulcer is distinguished by its anatomic location high along the lesser curvature, close to the gastroesophageal junction. Antral mucosa may extend to within 1 to 2 cm of the gastroesophageal junction; thus type IV ulcers may simply represent a subset of type I gastric ulcer. Type IV ulcers are associated with gastric hyposecretion and present early with dysphagia and reflux. Large ulcer size, the degree of surrounding inflammation, and proximity to the gastroesophageal junction render operative management difficult and potentially dangerous. If the integrity of the distal esophagus can be ensured, subtotal gastric resection (including the ulcer bed) is considered optimal. However, lesions close to the cardia pose a particular challenge, and, to help to avoid a total gastrectomy and an esophageal anastomosis, other surgical approaches have been described. Such alternatives include the Schoemaker procedure (a modification of B I resection with tube-shaped resection of high gastric ulcers and anastomosis of the duodenum to the greater curvature side of the stomach; see Fig. 59.7), the Pauchet procedure,58 a modification of the Schoemaker procedure that involves a lower gastrectomy and excision of the ulcer (Fig. 59.25),

A

B

GASTRIC OUTLET OBSTRUCTION More than half of gastric outlet obstruction cases are caused by malignant disease rather than by chronic PUD. Consequently, a careful work-up with biopsy should be done to clarify the diagnosis. Gastric outlet obstruction represents 5% to 8% of ulcer-related complications and results in an estimated 2000 operations per year in the United States.62 Patients with gastric outlet (pyloric) obstruction because of a duodenal ulcer typically present with symptoms of gastric retention, including early satiety, bloating, indigestion, anorexia, nausea, vomiting, epigastric pain, and weight loss. They are frequently malnourished and dehydrated and have a metabolic alkalosis, which are factors that increase the operative risk. Operation in these

C

FIGURE 59.25  Operations for a type IV gastric ulcer. (A) Pauchet procedure. (B) Kelling-Madlener procedure. (C) Csendes procedure (esophagogastrojejunostomy). (Modified from Seymour NE. Operations for peptic ulcer and their complications. In: Feldman M, Scharschmidt BF, Sleisenger MH, eds. Gastrointestinal Disease. Philadelphia: Saunders; 1998.)

Surgery for Peptic Ulcer Disease  CHAPTER 59 

cases is almost never emergent and should be performed only after the patient has been stabilized and nutritional and electrolyte abnormalities have been corrected. Nasogastric decompression is helpful in decreasing gastric atony and hastening the time to resumption of postoperative oral intake. Nevertheless, operation is generally indicated if obstruction fails to resolve despite 48 to 72 hours of adequate intravenous fluid replenishment, antisecretory therapy, and nasogastric tube decompression. In a less acute setting in which the obstruction is incomplete, balloon dilation of the scarred pylorus may be attempted. Approximately 65% of patients experience sustained relief, but many require more than one dilation session. In patients who fail endoscopic dilation, operation is a reasonable option. The most serious complication of dilation is a perforation. Whenever balloon dilation is being attempted, it is important to rule out an underlying malignancy. TV with antrectomy is the ideal procedure for this condition. Placement of a feeding jejunostomy tube at the time of operation is usually recommended, both because of preoperative malnutrition and because the chronic gastric outlet obstruction predisposes to delayed postoperative gastric emptying. Furthermore, addition of either a retrograde jejunogastrostomy or gastrostomy tube is also beneficial. As a result of the extensive scarring present in the duodenum, pyloroplasty of various types are usually not possible. The Jaboulay side-to-side duodenoplasty may be used in this setting. In one report of 19 patients treated with this procedure combined with PGV, there was a high degree of patient satisfaction (100% modified Visick grade I or II), universal weight gain, and no operative mortality or ulcer recurrence at mean followup of 31 months.63 However, these benefits have not been noted in all reports. One trial randomized 90 consecutive patients with gastric outlet obstruction secondary to duodenal ulcer to PGV with gastrojejunostomy, PGV with Jaboulay duodenoplasty, or SV with antrectomy. Although there were no differences in the postoperative course or the reduction in gastric acid secretion, both PGV with gastrojejunostomy and SV with antrectomy produced a superior clinical result to PGV with Jaboulay pyloroplasty.64 Although the need for pyloric reconstruction or bypass would theoretically negate several advantages of PGV over other options, preservation of antropyloric innervation may preserve controlled gastric emptying and minimize bile reflux.65 In the past, simple gastrojejunostomy was not recommended because of a nearly 50% recurrence rate of ulcer disease.66 It should be noted that these data preceded the era of effective acid-reducing medication. With the increased adaptation of minimally invasive approaches, gastrojejunostomy with either vagotomy or lifelong proton pump inhibitor medication has gained resurgence in the management of gastric outlet obstruction. The role of H. pylori in the pathogenesis of gastric outlet obstruction has also been evaluated. Studies show that the incidence of H. pylori infection in this population is low (33% to 57%).62 However, in those infected with the organism, eradication therapy and balloon dilation may result in long-term symptomatic relief and alleviate the need for operation. In general, operation should be

693

the standard of therapy in this group (in particular, H. pylori–negative patients) until further studies define the role of nonoperative therapy in the H. pylori–positive patients.

EMERGENCY OPERATION FOR COMPLICATED PEPTIC ULCER DISEASE Approximately two-thirds of operations for complicated PUD are required because of bleeding and approximately one-third are because of perforations.21 Emergency operations for complicated PUD are most often performed in older adults and the sick. Patients may present with bleeding, perforation, or obstruction. The objectives of operation in these cases are to 1. Deal with the complication that necessitated surgical intervention 2. Reduce the risk of future ulcer recurrence 3. Perform a safe, quick, and effective operation 4. Minimize long-term effects on the gastrointestinal tract 5. Establish the H. pylori status of the patient The major intraoperative dilemma is whether to proceed with a definitive antiulcer operation (to reduce the risk of recurrence) in addition to addressing the specific ulcer complication. This issue has received considerable attention over the past several decades but remains unsettled. Shifting ulcer epidemiology, recognition of the role of H. pylori, and improvements in medical therapy have confused this issue considerably, and the decision must be individualized. However, studies show a trend toward favoring of less complex procedures in the setting of emergencies (patching or oversewing of ulcers) and of avoiding vagotomy or gastric resections.67 Omission of an acid-reducing ulcer procedure carries a risk of recurrent ulcer symptoms and complications; this risk is variable in the literature but not negligible. Evidence suggests that this risk may be considerably reduced by treatment for H. pylori postoperatively but obviously only if the patient is H. pylori positive. Unfortunately, there is no reliable, rapid test for H. pylori at the time of operation to help guide this decision making. A definitive procedure is always more appropriate in the setting of NSAIDs, especially if the patient is unlikely to be able to stop the treatment because of an underlying medical condition. A definitive procedure is also recommended if patient has been on antisecretory therapy and developed an ulcer complication despite acid suppression. On the other hand, inclusion of an acid-reducing ulcer procedure may result in serious gastrointestinal sequelae in patients who may not have required the intervention. Definitive operation is generally avoided during emergency procedures with major underlying medical illness or intraoperative hemodynamic instability.

BLEEDING Two-thirds of the emergency operations performed for PUD are carried out for uncontrolled hemorrhage. However, as endoscopic abilities improved, the indication for surgical treatment continued to decrease. As the indications for surgical interventions have changed dramatically, so have the operations. Eighty to 85% of bleeding

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SECTION II  Stomach and Small Intestine

TABLE 59.3  The Forrest Classification for Endoscopic Findings and Rebleeding Risks Classification

Rebleeding Risk

Grade Grade Grade Grade Grade Grade

High High High Intermediate Low Low

Ia: active, pulsatile bleeding Ib: active, nonpulsatile bleeding IIa: nonbleeding visible vessel IIb: adherent clot IIc: black dot III: no signs of recent bleeding

ulcers stop bleeding spontaneously.66 Of the remaining patients, 85% to 95% can be effectively treated by endoscopic means.68,69 Currently many surgeons choose a limited surgical approach followed by medical management instead of the historical aggressive resections and gastric denervation procedures. Most patients who present with a bleeding upper gastrointestinal lesion have an endoscopic examination of the stomach, the first and second part of the duodenum. This procedure enables identification of the site of bleeding and allows therapeutic attempts at stopping the bleeding. Despite endoscopic advances, the mortality rate following ulcer bleeding has remained stable at 5% to 10%. Indeed, recent epidemiologic data suggest that the incidence and mortality rate of bleeding duodenal ulcers may be increasing in older women.3 However, an estimated 10% to 20% of patients admitted with bleeding peptic ulcers fail medical therapy and require urgent surgical intervention. Thus the ability to predict the risk of rebleeding is important to the endoscopist and the surgeon because this permits closer monitoring of high-risk patients and early involvement of the surgical team in their management. High recurrent bleeding rates are associated with a spurting vessel, a visible arterial vessel in the ulcer bed, adherent clot, or a large ulcer bed. The Forrest classification was developed in an attempt to assess the risk of rebleeding based on endoscopic findings (Table 59.3). Of those patients who have recurrent bleeding, a second endoscopic attempt at control of bleeding will fail in 25%, requiring an emergency operation. This has stimulated some debate as to the timing of operation for a bleeding peptic ulcer and the role of a second attempt at endoscopic therapy. Randomized prospective studies have shown no increase in mortality rate in patients who undergo a second therapeutic endoscopy versus surgery after the first failed endoscopy. Consequently, most clinicians would encourage a second attempt at endoscopic control.70 Current indications for operation for peptic ulcer hemorrhage include 1. Hemodynamic instability despite vigorous resuscitation (>4 units or >6 units taking into consideration the patient’s age, with more transfusion tolerated for the younger patient) 2. Failure of endoscopic techniques to arrest hemorrhage 3. Recurrent hemorrhage after initial stabilization (with up to two attempts at obtaining endoscopic hemostasis) 4. Shock associated with recurrent hemorrhage 5. Continued slow bleeding with a transfusion requirement exceeding 3 units per day 6. GDU

Secondary or relative indications include a rare blood type or difficult crossmatch, refusal of transfusion, shock on presentation, advanced age, severe comorbid disease, and bleeding chronic gastric ulcer. The surgical threshold may have to be lowered in elderly patients who poorly tolerate prolonged resuscitation, large-volume transfusion, and periods of hypotension. The mortality rate for bleeding PUD is approximately 6%, with most patients dying of non–bleeding-related causes, such as multiple organ system failure. Thus further improvements in endoscopic or pharmacologic therapy are unlikely to lower the mortality rate, and our focus should be on appropriate management of these patients to avoid organ failure.71 Operation for Bleeding Duodenal Ulcer The first priority during an emergency operation for a bleeding duodenal ulcer is control of the bleeding site. If EGD has failed to identify the source of hemorrhage, a longitudinal pyloroduodenotomy is necessary to inspect the duodenal bulb and gastric antrum. The gastroduodenal artery is the usual source of bleeding, which should be controlled by placement of suture ligatures. After the bleeding has been addressed, a definitive acid-reducing operation may be performed. With the identification of H. pylori, the utility of a vagotomy has been questioned. However, the data suggest that, even in the era of H. pylori and our ability to eradicate it, a TV perhaps should be performed in those patients with a bleeding duodenal ulcer. There are several reasons for this recommendation: 1. Only 40% to 70% of patients with a bleeding duodenal ulcer are positive for H. pylori. 2. H. pylori testing in the setting of an acute hemorrhage is less reliable, with the CLO (Campylobacter-like organism) test having a false-negative rate of 18% versus 1% in those not actively bleeding.72 3. If an acid-reducing procedure is not performed, up to 50% of patients are at risk of recurrent bleeding. 4. Conflicting evidence that H. pylori treatment changes the risk of recurrent bleeding. Our inability to determine the H. pylori status in the case of acute bleeding and the lack of evidence that treatment of H. pylori alters the risk of rebleeding reinforces the need to perform an acid-reducing operation at the time of initial operation; however, if the patient is unstable, addition of an acid-reducing procedure to the hemorrhage control aspect of the operation adds to the operative time and should be avoided. In the latter case, postoperative long-term PPI therapy and eradication of H. pylori is the more appropriate course of action. Because it is simple to open the pylorus in a longitudinal fashion, TV with pyloroplasty is the most frequently used operation for bleeding duodenal ulcer. In most cases the bleeding will be localized in the first part of the duodenum and the bleeding vessel can be controlled at the time through the pyloroplasty incision. Upon entering the duodenum, the duodenal mucosa is inspected for any evidence of active bleeding, ulceration, or induration. If active bleeding is encountered, this is controlled by digital pressure. This controls the bleeding and gives time for fluid resuscitation of the patient. The bleeding vessel is then ligated. This vessel is often the gastroduodenal artery,

Surgery for Peptic Ulcer Disease  CHAPTER 59 

695

permits excision and histologic evaluation of the ulcer to rule out malignancy. In high-risk patients or in case of ulcers that are due to high acid secretion (types II and III), a vagotomy may be added.

PERFORATION

FIGURE 59.26  Technique of suture control of a bleeding duodenal ulcer. After a longitudinal pyloric incision and identification of the bleeding vessel, figure-of-eight sutures are placed at the cephalic and caudal aspects of the ulcer deep enough to occlude the gastroduodenal artery. An additional U stitch is placed to control small transverse pancreatic branches from the main vessel. (From Debas HT, Mulvihill SJ. Complications of peptic ulcer. In: Zinner MJ, Schwartz SJ, Ellis H, eds. Maingot’s Abdominal Operations. Stamford, CT: Appleton & Lange; 1997.)

which can be ligated both through the lumen as well as extraluminally. This vessel at the level of the posterior duodenal wall has a T or three-vessel junction. It is important to suture ligate the gastroduodenal artery superiorly and inferiorly, followed by ligation of the medial transverse pancreatic branches using a U stitch (Fig. 59.26). Care should be taken to avoid injury to the common bile duct during suture placement. If no bleeding is encountered upon opening the lumen, the mucosa should be carefully inspected for an ulcer. If identified, the ulcer base should be cleaned to help to identify a visible vessel, which if seen should be ligated. In situations in which no active bleeding is seen, it is important to carry out a careful inspection of the mucosa, looking for other potential bleeding ulcers, even if a nonbleeding ulcer is identified. This inspection can be done by manual palpation of the lumen using a finger. In cases in which the preoperative endoscopy failed to identify a specific location, it is reasonable to start with a duodenotomy, which can be extended proximally or distally to allow further exploration. On occasion, a second gastrotomy near the esophageal junction is needed to inspect the proximal stomach. After gaining control of the bleeding, the pyloroplasty is performed. Most often this is done as a Heineke-Mikulicz pyloroplasty. Performing a TV then completes the procedure. Bleeding Gastric Ulcer For bleeding gastric ulcers, distal gastrectomy with ulcer excision and B I or II reconstruction is preferred. This

Smoking and NSAIDs are important etiologic factors for ulcer perforations, and epidemiologic studies have documented an increasing rate of perforation, particularly in older women. The outcome of patients presenting with a perforated ulcer depends on the following: 1. Time delay to presentation and treatment—data suggest increasing delays for surgical treatment, in part as a consequence of more extensive diagnostic work-up 2. Site of perforation—gastric perforation is associated with a poorer prognosis 3. Patient’s age—older patients who often have associated comorbidities have a worse outcome 4. Presence of hypotension at presentation (systolic blood pressure <100 mm Hg) Recent studies comparing nonoperative treatment with surgical treatment in perforated PUD showed no decrease in morbidity or mortality with surgical treatment in carefully selected groups of patients. The nonoperative approach should be considered only if a water-soluble contrast study has confirmed that the ulcer is sealed with no extravasation of contrast into the peritoneal cavity. Such patients should be followed closely with regular physical exams and, if their abdominal exam or laboratory findings indicate progressive sepsis, they should undergo prompt operation. This approach is generally used for individuals who have a perforation of greater than 24 hours’ duration, are stable, and often have significant comorbidities that increase the risk of surgical intervention. It should be noted that, although this approach is often used for the older patient with comorbidities, studies show that the risk of nonoperative treatment failure is highest in older adults and thus close observation of such patients is recommended. Because perforated gastric ulcers have a higher rate of reperforation and complications, nonoperative therapy in situations in which the source of the perforation is known to be gastric is not recommended. Perforated Duodenal Ulcer An acute perforation is estimated to occur in 2% to 10% of patients with a duodenal ulcer. Operation for this indication should be directed at closing the perforation and cleansing the abdomen of debris. This can be done either as an open procedure or laparoscopically. There appears to be little difference in outcome between the two techniques. Surgeons have traditionally performed either simple patch closure or TV with pyloroplasty (incorporating the perforation). The natural history of those treated by a simple repair has been documented in a paper that followed the course of 122 such patients over a 25-year period. In total, 48% of the original study population required further ulcer treatment in the form of prolonged medical therapy or further surgery.74 Consequently, a TV with pyloroplasty had been recommended as the minimal therapy required. A study reported the outcomes in 159 patients who were followed more than

696

SECTION II  Stomach and Small Intestine

10 years after vagotomy with pyloroplasty for perforated duodenal ulcer.75 The perioperative mortality was 5.5%, ulcers recurred in 8.8%, and postoperative digestive sequelae, notably diarrhea and dumping, developed in 16%. Nevertheless, the overall results were good to excellent in almost 90% of cases. PGV with patch closure does at least as well. Boey et al., in a prospective study of 101 patients randomized to simple closure, TV with pyloroplasty, or PGV, showed 39-month recurrence rates of 63.3%, 11.8%, and 3.8%, respectively. The operative time was significantly more for the PGV, but there were no mortalities in any group. However, the study excluded older adults (older than age 70 years) and patients with preoperative shock; this may account for the low mortality rates.76 Another randomized study by the same group, comparing PGV with simple closure, documented recurrence rates of 10.6% and 36.6% (half requiring surgical intervention) at 3 years. Again there was a sample bias in the group because the unstable and older patients were excluded.77 Another series of 107 patients with perforated pyloroduodenal ulcers documented minimal morbidity, low mortality, and excellent patient satisfaction for omental patching and PGV, with a recurrence rate of 3.7% for duodenal ulcer; the recurrence rate for pyloric and prepyloric ulcer was substantially higher at 16%.78 Chronic pyloroduodenal scarring is considered a relative contraindication to PGV in this setting because it may be associated with delayed gastric emptying after surgery. With the identification of H. pylori, the ideal surgical approach has again been questioned. A study showed that 81% of patients with a perforated duodenal ulcer

are H. pylori positive. In this study, all patients underwent a simple closure of the perforation. The H. pylori-positive patients were then randomized postoperatively to a 4-week course of PPIs alone versus H. pylori eradication therapy. The ulcer recurrence rate at 1 year was 5% in the H. pylori-eradicated group versus 38% in the PPI-treated group, as determined by repeat endoscopy. Notably, the 5% recurrence rate is equivalent to the recurrence rate for those who undergo a definitive antiulcer procedure.79 These data provide good evidence for the practice of simple closure of perforated duodenal ulcers in the acute setting. However, at the time of operation, the H. pylori status of the patient is often unknown and, in the absence of a reliable intraoperative test, the merits of a definitive antisecretory procedure have to be considered. This may be particularly important in those patients with a previous history of peptic ulcer operation, H. pylori eradication, chronic ulcer symptoms despite use of PPIs, or those on NSAIDs in whom this therapy cannot be discontinued. In general, simple patch closure is appropriate for patients with 1. Acute NSAID-related perforation (provided that the drugs can be discontinued postoperatively) and for patients who have never been treated for PUD but who can be treated with PPIs and H. pylori eradication 2. Perforation in the setting of ongoing shock, delayed presentation, considerable comorbid disease, or marked peritoneal contamination Fig. 59.27 summarizes the recommended approach to a perforated duodenal ulcer. To perform the patch procedure, a midline laparotomy is performed and the

Perforated duodenal ulcer

Perforation >24 hrs and contrast study confirms sealed perforation

Yes

Conservative therapy

No

Recent onset of ulcer symptoms

Long ulcer history/previous Helicobacter pylori treatment

Is the patient stable? No Yes Omental patching

FIGURE 59.27  Treatment algorithm for surgery for perforated duodenal ulcers. HSV, Highly selective vagotomy.

Omental patching with truncal vagotomy and pyloroplasty or omental patching with HSV

Omental patching, H. pylori testing and treatment

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FIGURE 59.29  The omentum, which has been mobilized on a vascular pedicle, is secured in place with sutures tied loosely enough to prevent tissue strangulation. This technique allows effective closure of the perforation without narrowing the duodenal lumen. (From Baker RJ. Perforated duodenal ulcer. In: Baker RJ, Fischer JE, eds. Mastery of Surgery. Philadelphia: Lippincott Williams & Wilkins; 2001.)

FIGURE 59.28  Perforated duodenal ulcers. Repair is begun by placing sutures through the full thickness of the bowel wall in two steps. This allows the use of smaller, tapered needles, and reduces the risk of inadvertent penetration of the posterior duodenal wall. (From Baker RJ. Perforated duodenal ulcer. In: Baker RJ, Fischer JE, eds. Mastery of Surgery. Philadelphia: Lippincott Williams & Wilkins; 2001.)

intraabdominal organs are inspected. The presence of bilious fluid in the peritoneal cavity suggests an upper gastrointestinal perforation. After a duodenal perforation has been confirmed, pads are placed around the perforation to contain any further spillage. Next, 3-0 silk or polydioxanone sutures are placed across the perforation. Usually three to four sutures are needed. It is important to take bites of appropriate length (0.5 to 1 cm) to prevent the sutures cutting through the inflamed duodenal tissue. To ensure bites that are full thickness, it is recommended that one pass the needle through the wall of duodenum on one side of the ulcer, retrieving the needle through the perforation, and then passing it through the wall on the other side of the perforation (Fig. 59.28). These sutures should not be tied to approximate the ulcer; rather, the adjacent omentum should be mobilized on an intact vascular pedicle and brought up. The sutures are tied over this omental pedicle to secure this in place. These sutures should not be tied too tightly, to avoid strangulation of the omental patch (Fig. 59.29). Sewing the ulcer closed before placing the omental pedicle over

Omentum Space between duodenal serosa and omentum Ulcer perforation plugged with omentum Duodenum

A

B

FIGURE 59.30  When the sutures are initially tied to approximate the edges of the ulcer and the omentum is placed above those knots (A), there is less intimate apposition of the duodenal serosa to the omentum. By performing the procedure as described, the omentum plugs the hole (B) and is closely applied to the serosa, ensuring watertight closure. (From Baker RJ. Perforated duodenal ulcer. In: Baker RJ, Fischer JE, eds. Mastery of Surgery. Philadelphia: Lippincott Williams & Wilkins; 2001.)

the perforation is discouraged because it reduces the surface contact of the omentum with the duodenal mucosa (Fig. 59.30). Following closure of the ulcer, a thorough irrigation of the peritoneal cavity should be done with warm saline irrigation. Drains are not needed, and their

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use is discouraged because it tends to create a negative suction vacuum that can interfere with the repair. There is a growing body of literature on laparoscopic suture patch repair, as well as laparoscopic sutureless techniques using fibrin glue to repair the perforated ulcer. These studies have demonstrated the feasibility of minimally invasive approaches.80 A comparison of primary open and the laparoscopic approach showed similar postoperative morbidity and mortality.81 However, patients who were treated laparoscopically had a significantly shorter hospital stay.80 The conversion rates for such laparoscopic procedures have been between 15% and 20%. Factors that necessitated conversion from a laparoscopic approach included generalized peritonitis, Mannheim peritonitis index greater than 21, and a perforation located posteriorly.81 The presence of shock on admission is a risk factor for severe postoperative complications and generally an open approach is preferable in these patients. There are no absolute contraindications for the laparoscopic approach. To perform laparoscopic repair of a duodenal ulcer, the patient should be supine. The operating surgeon can stand either on the patient’s left or between the patient’s legs, with the patient placed in split leg position. The patient is then placed in reverse Trendelenburg position. Initially, a diagnostic laparoscopy is performed. After the ulcer size is carefully measured with reference to the 5-mm–diameter working laparoscopic instrument, the perforation is patched in similar fashion as described for the open approach with polydioxanone, polyglactin, or silk sutures. The perforation is closed by intracorporeal or extracorporeal knotting (depending on the surgeon preference) with an omental patch (omentopexy) directly applied to the perforation site. This approach avoids tension on the inflamed ulcer margin and cutting through the tissue. It is critical during the process to avoid anchoring the posterior duodenal wall. This can be avoided by pulling the needle through the perforation and reinserting it through the perforation to complete the next half of the stitch. It is important when tying the knots down to pay attention so as not to strangulate the omental pedicle. A leak test can be performed via a nasogastric tube; however, this step is not necessary. Suctioning of the peritoneal fluid is then performed with special attention directed to potential spaces for fluid collection. The fluid collected can be sent for Gram stain and culture in case the patient develops an abscess during recovery; however, this should not extend antibiotic coverage beyond 24 hours. Some surgeons advocate the performance of lavage of the abdominal cavity using 3 to 5 L of warm normal saline with the patient in various positions. Drains are not necessary. Perforated Gastric Ulcer A perforated gastric ulcer carries a greater overall mortality that ranges from 10% to 40%, and increases significantly with age (>65 years).82 There has been debate in cases of perforated types I and IV gastric ulcers over whether to perform a partial gastrectomy or proceed with a simple patching of the perforation. Partial gastrectomy is the preferred approach unless the patient is at unacceptably high risk because of advanced age, comorbid disease, intraoperative instability, or severe peritoneal soilage.83

Even in patients in this high-risk group, who may present with shock, there is increasing evidence that definitive operation can be tolerated as well as the simpler and quicker patching technique.84,85 Consequently, it is recommended that patients with a perforated type I gastric ulcer undergo a partial gastrectomy unless the patient is unstable with significant comorbidities. Biopsy and patch closure may be an appropriate approach for treatment of a high type IV ulcer, where a more extensive resection may lead to total gastrectomy in a critically ill patient. Because the pathophysiology of such ulcers does not involve acid hypersecretion, an acid-reducing procedure is not required. Whenever possible, the ulcer should be excised and the stomach closed. It is important to perform an adequate four-quadrant biopsy of ulcers that are not excised followed by patch closure.86 For type II ulcers, the treatment algorithm should be similar to that for perforated duodenal ulcers because the pathophysiology of the disease is very similar. This means that the ulcers should be patched, H. pylori status of the patient determined with an intraoperative biopsy, and the patient treated appropriately. In addition, it is important to obtain an intraoperative biopsy to rule out malignancy that can be associated with such gastric ulcers. Similar to a perforated duodenal ulcer, a definitive operation is not required unless the patient has a history of recurrent ulcer disease and has been previously treated for H. pylori. In circumstances in which a definitive procedure is deemed appropriate, a PGV or a TV with drainage should be considered. Type III ulcers are also thought to have a similar pathogenesis to duodenal ulcers; however, their treatment in the case of an acute perforation deserves particular attention. Patch repair of such prepyloric ulcers is associated with a high incidence of gastric outlet obstruction,86 and PGV is associated with a high recurrence rate for these ulcers. Therefore antrectomy with vagotomy is the best surgical approach in this setting. Fig. 59.31 summarizes the proposed surgical approach to a perforated gastric ulcer. Gastric ulcers can be managed laparoscopically as described previously for duodenal ulcers; however, these patients should have a follow-up EGD to rule out cancer as the cause of the ulcer.

ACKNOWLEDGMENTS The authors acknowledge these authors of chapters from the seventh edition of Shackelford’s Surgery of the Alimentary Tract: Tavakkolizadeh A, Ashley SW. Operations for peptic ulcer. In: Yeo CJ, McFadden DW, eds. Shackelford’s Surgery of the Alimentary Tract. Vol. I. 7th ed. Philadelphia: Elsevier; 2013:701-719. Postier RG, Havron WS III. Vagotomy and drainage. In: Yeo CJ, McFadden DW, eds. Shackelford’s Surgery of the Alimentary Tract. Vol. I. 7th ed. Philadelphia: Elsevier; 2013:720-730. Ben-David K, Caban AM, Behrns KE. Gastric resection and reconstruction. In: Yeo CJ, McFadden DW, eds. Shackelford’s Surgery of the Alimentary Tract. Vol. I. 7th ed. Philadelphia: Elsevier; 2013:731-748.

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Perforated gastric ulcer

Long ulcer history/ previous Helicobacter pylori treatment

Recent onset of ulcer symptoms

Is the patient stable?

Omental patching, biopsy of ulcer and H. pylori testing and treatment. For type III ulcer recommend antrectomy and truncal vagotomy

No Yes

Omental patching, biopsy of ulcer, and H. pylori testing and treatment Type I and IV: Partial gastrectomy or omental patching Type II: Truncal vagotomy and antrectomy or patching Type III: Truncal vagotomy and antrectomy

FIGURE 59.31  Recommended treatment algorithm for surgical management of perforated gastric ulcers.

REFERENCES 1. Sung JJ, Kuipers EJ, El-Serag HB. Systematic review: the global incidence and prevalence of peptic ulcer disease. Aliment Pharmacol Ther. 2009;29(9):938-946. 2. Anand BS, Raed AK, Malaty HM, et al. Low point prevalence of peptic ulcer in normal individuals with Helicobacter pylori infection. Am J Gastroenterol. 1996;91(6):1112-1115. 3. Groenen MJ, Kuipers EJ, Hansen BE, Ouwendijk RJ. Incidence of duodenal ulcers and gastric ulcers in a Western population: back to where it started. Can J Gastroenterol. 2009;23(9):604-608. 4. Bashinskaya B, Nahed BV, Redjal N, Kahle KT, Walcott BP. Trends in peptic ulcer disease and the identification of Helicobacter pylori as a causative organism: population-based estimates from the US nationwide inpatient sample. J Glob Infect Dis. 2011;3(4):366370. 5. Wang YR, Richter JE, Dempsey DT. Trends and outcomes of hospitalizations for peptic ulcer disease in the United States, 1993 to 2006. Ann Surg. 2010;251(1):51-58. 6. Irabor DO. An audit of peptic ulcer surgery in Ibadan, Nigeria. West Afr J Med. 2005;24(3):242-245. 7. Lau JY, Sung J, Hill C, Henderson C, Howden CW, Metz DC. Systematic review of the epidemiology of complicated peptic ulcer disease: incidence, recurrence, risk factors and mortality. Digestion. 2011;84(2): 102-113. 8. Beaumont W. Nutrition classics. Experiments and Observations on the Gastric Juice, and the Physiology of Digestion. By William Beaumont, Plattsburgh. Printed by F. P. Allen. 1833. 9. Modlin IM, Kidd M, Marks IN, Tang LH. The pivotal role of John S. Edkins in the discovery of gastrin. World J Surg. 1997;21(2):226-234. 10. Paulino F, Netto AP. Evolution of the surgical treatment of duodenal ulcer. Rev Assoc Med Bras. 1963;9:268-272. 11. Herrington JL Jr. Gastroduodenal ulcer. Overview of 150 papers presented before the Southern Surgical Association 1888-1986. Ann Surg. 1988;207:754-769. 12. Modlin IM, Darr U. The centenary of Lester Dragstedt—fifty years of therapeutic vagotomy. Yale J Biol Med. 1994;67(3-4):63-80. 13. Gustafson J, Welling D. “No acid, no ulcer” 100 years later: a review of the history of peptic ulcer disease. J Am Coll Surg. 2010;210: 110-116. 14. Dragstedt LR. Vagotomy for gastroduodenal ulcer. Ann Surg. 1945;122: 973-989. 15. Woodward ER. The history of vagotomy. Am J Surg. 1987;153(1):9-17. 16. Stempien SJ, Temkin E, Dagradi A. Duodenal ulcer; gastrectomy versus vagotomy with accessory procedures. Calif Med. 1956;84(3): 168-171.

17. Hubert JP Jr, Kiernan PD, Beahrs OH, ReMine WH. Truncal vagotomy and resection in the treatment of duodenal ulcer. Mayo Clin Proc. 1980;55:19-24. 18. Siim C, Lublin HK, Jensen HE. Selective gastric vagotomy and drainage for duodenal ulcer: a 10-13-year follow-up study. Ann Surg. 1981;194(6):687-691. 19. van Heerden JA, Kelly KA, Dozois RR, et al. Proximal gastric vagotomy. Initial experience. Mayo Clin Proc. 1980;55(1):10-13. 20. Hoffmann J, Jensen HE, Christiansen J, Olesen A, Loud FB, Hauch O. Prospective controlled vagotomy trial for duodenal ulcer. Results after 11–15 years. Ann Surg. 1989;209(1):40-45. 21. Zittel TT, Jehle EC, Becker HD. Surgical management of peptic ulcer disease today—indication, technique and outcome. Langenbecks Arch Surg. 2000;385(2):84-96. 22. Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1984;1(8390): 1311-1315. 23. Rauws EA, Tytgat GN. Cure of duodenal ulcer associated with eradication of Helicobacter pylori. Lancet. 1990;335(8700):1233-1235. 24. Kokoska ER, Kauffman GL Jr. Helicobacter pylori and the gastroduodenal mucosa. Surgery. 2001;130(1):13-16. 25. Graham DY, Go MF, Lew GM, Genta RM, Rehfeld JF. Helicobacter pylori infection and exaggerated gastrin release. Effects of inflammation and progastrin processing. Scand J Gastroenterol. 1993;28(8): 690-694. 26. McColl KE, Gillen D, El-Omar E. The role of gastrin in ulcer pathogenesis. Baillieres Best Pract Res Clin Gastroenterol. 2000;14(1):13-26. 27. Kim JM, Kim JS, Jung HC, Oh YK, Kim N, Song IS. Inhibition of Helicobacter pylori-induced nuclear factor-kappa B activation and interleukin-8 gene expression by ecabet sodium in gastric epithelial cells. Helicobacter. 2003;8(5):542-553. 28. Zhao YR, Zhou Y, Lin G, Hu WJ, Du JM. Association between IL-17, IL-8 and IL-18 expression in peripheral blood and Helicobacter pylori infection in mongolian gerbils. Jundishapur J Microbiol. 2015;8(8):e21503. 29. Wallace JL. Prostaglandins, NSAIDs, and gastric mucosal protection: why doesn’t the stomach digest itself? Physiol Rev. 2008;88(4):1547-1565. 30. Lanas A, Baron JA, Sandler RS, et al. Peptic ulcer and bleeding events associated with rofecoxib in a 3-year colorectal adenoma chemoprevention trial. Gastroenterology. 2007;132(2):490-497. 31. Wallace JL, McKnight GW. The mucoid cap over superficial gastric damage in the rat. A high-pH microenvironment dissipated by nonsteroidal antiinflammatory drugs and endothelin. Gastroenterology. 1990;99(2):295-304. 32. Melcarne L, Garcia-Iglesias P, Calvet X. Management of NSAIDassociated peptic ulcer disease. Expert Rev Gastroenterol Hepatol. 2016;10(6):723-733.

700

SECTION II  Stomach and Small Intestine

33. Weil J, Colin-Jones D, Langman M, et al. Prophylactic aspirin and risk of peptic ulcer bleeding. BMJ. 1995;310(6983):827-830. 34. Scheiman JM, Herlitz J, Veldhuyzen van Zanten SJ, et al. Esomeprazole for prevention and resolution of upper gastrointestinal symptoms in patients treated with low-dose acetylsalicylic acid for cardiovascular protection: the OBERON trial. J Cardiovasc Pharmacol. 2013;61:250-257. 35. Leodolter A, Kulig M, Brasch H, Meyer-Sabellek W, Willich SN, Malfertheiner P. A meta-analysis comparing eradication, healing and relapse rates in patients with Helicobacter pylori-associated gastric or duodenal ulcer. Aliment Pharmacol Ther. 2001;15:1949-1958. 36. Lam SK, Ching CK, Lai KC, et al. Does treatment of Helicobacter pylori with antibiotics alone heal duodenal ulcer? A randomised double blind placebo controlled study. Gut. 1997;41(1):43-48. 37. Gisbert JP, Pajares JM. Systematic review and meta-analysis: is 1-week proton pump inhibitor-based triple therapy sufficient to heal peptic ulcer? Aliment Pharmacol Ther. 2005;21(7):795-804. 38. Chey WD, Spybrook M, Carpenter S, Nostrant TT, Elta GH, Scheiman JM. Prolonged effect of omeprazole on the 14C-urea breath test. Am J Gastroenterol. 1996;91(1):89-92. 39. Chan VM, Reznick RK, O’Rourke K, Kitchens JM, Lossing AG, Detsky AS. Meta-analysis of highly selective vagotomy versus truncal vagotomy and pyloroplasty in the surgical treatment of uncomplicated duodenal ulcer. Can J Surg. 1994;37:457-464. 40. Jordan PH Jr, Thornby J. Twenty years after parietal cell vagotomy or selective vagotomy antrectomy for treatment of duodenal ulcer. Final report. Ann Surg. 1994;220(3):283-293; discussion 293-296. 41. Taylor TV, Lythgoe JP, McFarland JB, Gilmore IT, Thomas PE, Ferguson GH. Anterior lesser curve seromyotomy and posterior truncal vagotomy versus truncal vagotomy and pyloroplasty in the treatment of chronic duodenal ulcer. Br J Surg. 1990;77(9):1007-1009. 42. Oostvogel HJ, van Vroonhoven TJ. Anterior lesser curve seromyotomy with posterior truncal vagotomy versus proximal gastric vagotomy. Br J Surg. 1988;75(2):121-124. 43. Coblijn UK, Lagarde SM, de Castro SM, Kuiken SD, van Tets WF, van Wagensveld BA. The influence of prophylactic proton pump inhibitor treatment on the development of symptomatic marginal ulceration in Roux-en-Y gastric bypass patients: a historic cohort study. Surg Obes Relat Dis. 2016;12(2):246-252. 44. Tersmette AC, Offerhaus GJ, Tersmette KW, et al. Meta-analysis of the risk of gastric stump cancer: detection of high risk patient subsets for stomach cancer after remote partial gastrectomy for benign conditions. Cancer Res. 1990;50(20):6486-6489. 45. Moller H, Toftgaard C. Cancer occurrence in a cohort of patients surgically treated for peptic ulcer. Gut. 1991;32(7):740-744. 46. La Vecchia C, Negri E, D’Avanzo B, Moller H, Franceschi S. Partial gastrectomy and subsequent gastric cancer risk. J Epidemiol Community Health. 1992;46:12-14. 47. Rathi P, Parikh S, Kalro RH. Giant duodenal ulcer: a new look at a variant of a common illness. Indian J Gastroenterol. 1996;15(1):33-34. 48. Vogel SB, Drane WE, Woodward ER. Clinical and radionuclide evaluation of bile diversion by Braun enteroenterostomy: prevention and treatment of alkaline reflux gastritis. An alternative to Roux-en-Y diversion. Ann Surg. 1994;219(5):458-465; discussion 465-466. 49. Park JY, Kim YJ. Uncut Roux-en-Y reconstruction after laparoscopic distal gastrectomy can be a favorable method in terms of gastritis, bile reflux, and gastric residue. J Gastric Cancer. 2014;14(4):229-237. 50. Fischer DR, Nussbaum MS, Pritts TA, et al. Use of omeprazole in the management of giant duodenal ulcer: results of a prospective study. Surgery. 1999;126(4):643-648; discussion 648-649. 51. Croce E, Olmi S, Russo R, Azzola M, Mastropasqua E, Golia M. Laparoscopic treatment of peptic ulcers. A review after 6 years experience with Hill-Barker’s procedure. Hepatogastroenterology. 1999; 46(26):924-929. 52. Johnson HD. Gastric ulcer: classification, blood group characteristics, secretion patterns and pathogenesis. Ann Surg. 1965;162(6):996-1004. 53. Csendes A, Burgos AM, Smok G, Burdiles P, Braghetto I, Díaz JC. Latest results (12–21 years) of a prospective randomized study comparing Billroth II and Roux-en-Y anastomosis after a partial gastrectomy plus vagotomy in patients with duodenal ulcers. Ann Surg. 2009;249(2):189-194. 54. Nunobe S, Okaro A, Sasako M, et al. Billroth 1 versus Roux-en-Y reconstructions: a quality-of-life survey at 5 years. Int J Clin Oncol. 2007;12(6):433-439. 55. Nakamura M, Nakamori M, Ojima T, et al. Randomized clinical trial comparing long-term quality of life for Billroth I versus Roux-en-Y

reconstruction after distal gastrectomy for gastric cancer. Br J Surg. 2016;103(4):337-347. 56. Duthie HL, Moore TH, Bardsley D, Clark RG. Surgical treatment of gastric ulcers. Controlled comparison of Billroth-I gastrectomy and vagotomy and pyloroplasty. Br J Surg. 1970;57(10):784-787. 57. McDonald MP, Broughan TA, Hermann RE, Philip RS, Hoerr SO. Operations for gastric ulcer: a long-term study. Am Surg. 1996;62(8): 673-677. 58. Lewis A, Qvist G. Operative treatment of high gastric ulcer with special reference to Pauchet’s method. Br J Surg. 1972;59(1):1-4. 59. Csendes A, Braghetto I, Calvo F, et al. Surgical treatment of high gastric ulcer. Am J Surg. 1985;149(6):765-770. 60. Lai KC, Lam SK, Chu KM, et al. Lansoprazole for the prevention of recurrences of ulcer complications from long-term low-dose aspirin use. N Engl J Med. 2002;346(26):2033-2038. 61. Lai KC, Lam SK, Chu KM, et al. Lansoprazole reduces ulcer relapse after eradication of Helicobacter pylori in nonsteroidal anti-inflammatory drug users—a randomized trial. Aliment Pharmacol Ther. 2003;18(8): 829-836. 62. Gibson JB, Behrman SW, Fabian TC, Britt LG. Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection. J Am Coll Surg. 2000;191(1):32-37. 63. Dittrich K, Blauensteiner W, Schrutka-Kolbl C, Hoffer F, Armbruster C, Vavrik J. Highly selective vagotomy plus Jaboulay: a possible alternative in patients with benign stenosis secondary to duodenal ulceration. J Am Coll Surg. 1995;180(6):654-658. 64. Csendes A, Maluenda F, Braghetto I, Schutte H, Burdiles P, Diaz JC. Prospective randomized study comparing three surgical techniques for the treatment of gastric outlet obstruction secondary to duodenal ulcer. Am J Surg. 1993;166(1):45-49. 65. Donahue PE, Griffith C, Richter HM. A 50 year perspective upon selective gastric vagotomy. Am J Surg. 1996;172:9-12. 66. Stabile BE, Passaro E Jr. Surgery for duodenal and gastric ulcer disease. Adv Surg. 1993;26:275-306. 67. Smith BR, Wilson SE. Impact of nonresective operations for complicated peptic ulcer disease in a high-risk population. Am Surg. 2010;76(10):1143-1146. 68. Kapetanakis AM, Kyprizlis EP, Tsikrikas TS. Efficacy of repeated therapeutic endoscopy in patients with bleeding ulcer. Hepatogastroenterology. 1997;44(13):288-293. 69. Wang BW, Mok KT, Chang HT, et al. APACHE II score: a useful tool for risk assessment and an aid to decision-making in emergency operation for bleeding gastric ulcer. J Am Coll Surg. 1998;187(3): 287-294. 70. Lau JY, Sung JJ, Lam YH, et al. Endoscopic retreatment compared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl J Med. 1999;340(10):751-756. 71. Lanas A. Editorial: upper GI bleeding-associated mortality: challenges to improving a resistant outcome. Am J Gastroenterol. 2010;105(1): 90-92. 72. Behrman SW. Management of complicated peptic ulcer disease. Arch Surg. 2005;140(2):201-208. 73. Deleted in review. 74. Griffin GE, Organ CH Jr. The natural history of the perforated duodenal ulcer treated by suture plication. Ann Surg. 1976;183: 382-385. 75. Robles R, Parrilla P, Lujan JA, et al. Long-term follow-up of bilateral truncal vagotomy and pyloroplasty for perforated duodenal ulcer. Br J Surg. 1995;82(5):665. 76. Boey J, Lee NW, Koo J, Lam PH, Wong J, Ong GB. Immediate definitive surgery for perforated duodenal ulcers: a prospective controlled trial. Ann Surg. 1982;196(3):338-344. 77. Boey J, Branicki FJ, Alagaratnam TT, et al. Proximal gastric vagotomy. The preferred operation for perforations in acute duodenal ulcer. Ann Surg. 1988;208(2):169-174. 78. Jordan PH Jr, Thornby J. Perforated pyloroduodenal ulcers. Long-term results with omental patch closure and parietal cell vagotomy. Ann Surg. 1995;221(5):479-486; discussion 486-488. 79. Ng EK, Lam YH, Sung JJ, et al. Eradication of Helicobacter pylori prevents recurrence of ulcer after simple closure of duodenal ulcer perforation: randomized controlled trial. Ann Surg. 2000;231(2): 153-158. 80. Byrge N, Barton RG, Enniss TM, Nirula R. Laparoscopic versus open repair of perforated gastroduodenal ulcer: a National Surgical

Surgery for Peptic Ulcer Disease  CHAPTER 59  Quality Improvement Program analysis. Am J Surg. 2013;206(6):957-962; discussion 962-963. 81. Muller MK, Wrann S, Widmer J, Klasen J, Weber M, Hahnloser D. Perforated peptic ulcer repair: factors predicting conversion in laparoscopy and postoperative septic complications. World J Surg. 2016;40(9):2186-2193. 82. Hewitt PM, Krige J, Bornman PC. Perforated gastric ulcers: resection compared with simple closure. Am Surg. 1993;59(10):669-673. 83. McGee GS, Sawyers JL. Perforated gastric ulcers. A plea for management by primary gastric resection. Arch Surg. 1987;122(5):555561.

701

84. Hodnett RM, Gonzalez F, Lee WC, Nance FC, Deboisblanc R. The need for definitive therapy in the management of perforated gastric ulcers. Review of 202 cases. Ann Surg. 1989;209(1):36-39. 85. Di Quinzio C, Phang PT. Surgical management of perforated benign gastric ulcer in high-risk patients. Can J Surg. 1992;35(1):94-97. 86. Turner WW Jr, Thompson WM Jr, Thal ER. Perforated gastric ulcers. A plea for management by simple closures. Arch Surg. 1988;123(8): 960-964.