Medical management includes nil per os (NPO) status, NG tube decompression, intravenous fluid rehydration, and antisecretory therapy via proton pump inhibitors (PPI) or histamine receptor type 2 (H₂) blockers infused intermittently or continuously [10, 13]. Normal saline is the preferred initial crystalloid for resuscitation [9, 10]. Lost potassium needs to be replaced. To this end, serial monitoring of electrolytes and acid–base status is advisable. Serum gastrin levels may be obtained if concern for gastrinoma is present; however, use of antisecretory agents may interfere with test results [9]. Parenteral nutrition may also be indicated after initial resuscitation [10]. Nonsteroidal anti-inflammatory drugs (NSAIDs) should be stopped. Once initial resuscitation is completed, consideration should be given to performing esophagogastroduodenoscopy (EGD). A complementary UGI study or CT scan may also be performed once resuscitation is well under way [10].

The role of H. pylori in GOO is unclear. Reported rates of H. pylori positivity are between 33 and 47% in small studies [4, 21]. Nevertheless, testing for H. pylori should be performed, as its presence may predict successful balloon dilation decreased ulcer complication rate [21]. It has been noted that patients without H. pylori infection have a more severe ulcer diathesis. [21] It is hypothesized that patients without H. pylori infection may have chronic scarring that is less amenable to balloon dilation [21]. H. pylori infection can be diagnosed with a rapid urease breath test or on pathologic examination of samples [21]. While readily available, stool antigen testing and serologic testing are considered less accurate indicators of active infection [30]. If testing is positive, then eradication therapy should be commenced; this can be intravenous until enteral access is achieved. A variety of treatment regimens for H. pylori are available, including omeprazole, amoxicillin, and clarithromycin [21]. Of note, there are several case reports demonstrating resolution of GOO with H. pylori treatment, without recurrent GOO [8, 31]. These studies concluded that GOO associated with PUD is primarily because of edema and spasm and not cicatrization of the pyloric canal, and hence recommend prolonging a trial of medical management to 2 weeks, before proceeding with interventional techniques [8 , 31].

Medical management alone is generally favored in patients with first episodes of acute obstruction. Edema and gastritis are seen on endoscopy. This generally resolves quickly [9]. However, follow-up endoscopy is recommended to confirm H. pylori eradication and resolution of obstruction [9]. GOO unresponsive to medical therapy continues to be a problem in a small percentage of patients with PUD and is the main indication for surgery in a small percentage of patients requiring surgery for PUD [32]. Failure of medical management can be addressed via endoscopic/fluoroscopic balloon dilatation or surgery. The exact role of endoscopic balloon dilatation is still being defined. Surgery is recommended if there is concern for malignancy.

The primary therapeutic endoscopic modality for PUD-associated GOO is endoscopic balloon dilation (Table 18.1). It was first described by Benjamin et al., who used the principles of balloon catheter dilation in angiography to successfully perform through the scope (TTS) balloon dilation of a stenotic pylorus in a patient with GOO and acute myocardial infarction. Presently, balloon dilation is commonly done endoscopically; however the addition of fluoroscopy, with the use of contrast medium for balloon inflation, facilitates the procedure and may make it safer [21, 33]. Balloon dilation can also be performed under fluoroscopic guidance alone.

Several factors need to be considered prior to embarking on balloon dilation. First, malignancy needs to be excluded. This may be done via a combination of endoscopy with biopsy and CT scan. When endoscopy is done for PUD-associated GOO, multiple and perhaps repeat or jumbo biopsies should be taken to exclude malignancy [28, 29]. Second, in patients with H. pylori infection, both eradication therapy and balloon dilation appear necessary to decrease the risk of recurrent GOO [4]. Third, long-term antisecretory/antacid therapy will also be needed to decrease the recurrence rate [4, 5, 20]. Fourth, while generally effective initially, endoscopic balloon dilation has a high recurrence rate [10, 11]. Greater than 80% of patients treated with balloon dilation will eventually require surgical intervention [10].

Once the decision has been made to perform balloon dilation, the size of the balloon must be carefully considered, as smaller balloons are associated with higher recurrence rates, whereas larger balloons (greater than 15 mm diameter) are associated with an increased perforation risk [21, 33, 34]. In deciding upon balloon size, it should be recalled that the normal adult pyloric canal diameter is about 15 mm [35].

Given the remarkable efficacy of PPI, H. pylori eradication therapy, and NSAID avoidance, the role of a major surgical resection and/or vagal resection for complicated PUD has become less clear [17]. While this may be in part because endoscopic and interventional radiologic techniques are comparatively recent inventions, the need for salvage surgical intervention if other therapies fail or to treat complications of other interventions cannot be argued [4, 37]. Surgery appears to be the gold standard against which all others are judged. For patients with recurrent symptoms after two balloon dilations, and/or those who are H. pylori negative, surgical evaluation is suggested [4]. The goals of surgery are to eliminate long-term antiulcer medication use and cure the GOO with a single procedure [5]. Given gastric dysmotility with chronic GOO, consideration can be given to placement of a jejunal feeding tube and decompressive gastrostomy [38].

While both laparoscopic and open surgical intervention is used, the trend has been towards a greater role for laparoscopic surgery in the management of GOO. Often cited reasons for favoring a laparoscopic over an open approach include less pain, less immobility, shorter hospital length of stay, smaller wounds, and a quicker return to activities of daily living [44]. While laparoscopic HSV with gastrojejunostomy may also be considered, the literature primarily promulgates truncal vagotomy with gastroenterostomy. Hence, this technique will be discussed. A retrospective study of 21 GOO patients comparing laparoscopic with open truncal vagotomy and gastrojejunostomy noted that laparoscopic surgery was associated with significantly reduced operating time, intraoperative blood loss, time to flatus, time to tolerance of semisolid diet, length of hospital stay [42]. While laparoscopic equipment costs more, these costs are generally believed to be offset by the shorter hospital stay [44]. In considering laparoscopic procedures, while intervention may be done purely laparoscopically, there are also a variety of laparoscopically assisted techniques which may offer some element of patient safety, especially for those who are not expert laparoscopic surgeons. In this regard, a 2005 study of 18 patients with GOO who underwent laparoscopic truncal vagotomy followed by an extracorporeal antecolic posterior gastrojejunostomy reported no mortality, no conversions, and a median hospital stay of 6 days [45]. This study noted a 16% incidence of postvagotomy diarrhea, which is slightly higher than that commonly reported. Similarly, extracorporeal antecolic anastomosis was performed in a study of 18 patients undergoing laparoscopic-assisted gastrojejunostomy with truncal vagotomy for cicatrizing duodenal ulcer with GOO [22]. This study also noted that no patient required conversion to a fully open procedure, no mortality, but one patient had an anastomotic leak requiring laparotomy. With a mean follow-up of 22.8 months, none of the patients developed recurrent obstruction.

The general principles of HSV, as described in a standard surgical text, is briefly discussed [46]. The dissection is started at a point approximately 7 cm proximal to the pylorus, on the lesser curvature. The vagal nerve fibers distal to this point are preserved. The nerves of Latarjet are identified and encircled with vessel loops. The nerves emanating from the nerves of Latarjet along the lesser curvature along with associated blood vessels are ligated and divided. Dissection proceeds proximally to the esophagus, first dividing the anterior layer of nerves, followed by an irregular intermediate layer of nerves, and then the posterior layer of nerves. Finally, the esophagogastric junction is mobilized and branches to the stomach including the criminal nerve of Grassi, a branch of the posterior vagus nerve that supplies the cardia and can originate high in the mediastinum, are divided (Fig. 18.4). This generally involves clearing the distal 5 cm of the esophagus of vagal nerve fibers. A gastrojejunostomy is then performed near the antrum to the posterior wall of the stomach, along the greater curvature of the stomach using a gentle loop of jejunum [41].

The technique, as described by several authors, follows [39, 43, 45]. The patient is placed in reverse Trendelenburg, in the Lloyd-Davis position, with the operating surgeon standing between the patient’s legs. The peritoneal cavity is insufflated with carbon dioxide and several additional ports are inserted. The left lobe of the liver is retracted medially; subsequently the esophagus is identified by palpation of the previously placed nasogastric tube. The phrenosesophageal ligament is divided. The anterior vagus nerve is identified, clipped proximally and distally, transected, and the intervening segment is submitted for frozen section pathologic confirmation. Attention is then directed to the posterior vagus nerve; dissection in the peri-esophageal region between the right crus and esophagus facilitates exposure; again the main trunk is clipped and divided, and the intervening segment is submitted for frozen section pathologic analysis [39]. It is important not to carry the dissection too far towards the liver or too low over the gastric fundus [43]. A search is then made for additional branches of the vagus nerve, including the criminal nerve of Grassi [39, 43]. At least 5 cm of the distal esophagus is cleared of vagal fibers [39]. While the principles of laparoscopic vagal resection are the same as those in open surgery, with its magnified view, caution must be exercised to ensure that longitudinal esophageal muscles are not mistaken for the vagal nerves [43]. Gastrojejunostomy is performed using a loop of the jejunum that gives the shortest afferent loop, generally 30–40 cm from the ligament of Treitz [39, 43]. Ultrasonic dissection may be used to create the gastrostomy and jejunostomy [39]. The gastroenteric anastomosis can be completed intracorporeally or extracorporeally, using a gastrointestinal anastomosis stapling device or suture (Fig. 18.5). The opening at the anastomosis is then closed with suture or a stapler. All fascial incisions greater than 5 mm in diameter should be closed, unless a radially dilating type port is used. A radially dilating port may allow a slightly larger fascial incision to be left open.

In conclusion, while PUD-associated acute GOO often resolves with conservative measures, chronic GOO will generally require intervention. While the role of H. pylori in GOO is unclear, infection must be assessed and eradication therapy administered if it is found. Antisecretory medications are administered and malignancy must be excluded. Depending on patient preference and in poor-risk surgical candidates, it appears reasonable to offer a trial of endoscopic balloon dilation as it provides a rapid relief of symptoms and has a favorable safety profile, with the understanding that there is a high long-term recurrent GOO risk and long-term antisecretory therapy will be needed. In good-risk patients who are H. pylori negative, fail endoscopic treatment, wish to avoid long-term antisecretory medication treatment, or desire definitive treatment, surgical intervention should be performed. In deciding amongst the myriad of operations, one algorithm to consider is to perform vagotomy and antrectomy in the patient with a gastric ulcer with good performance status and simple anatomy. If the gastric ulcer patient has a limited performance status, then vagotomy with gastroenterostomy should be performed. If the patient has a duodenal ulcer, consider performing HSV with drainage or truncal vagotomy with drainage. While either technique can be performed laparoscopically, there is presently very little literature available on laparoscopic HSV with drainage for GOO. The decision between the two would depend on the surgeon’s familiarity with the procedures; it has been reported that surgeons today may have limited operative experience with GOO [48]. Additional factors to guide decision-making are informed consent from the patient, regarding side effects from surgery and risk of recurrent ulceration. As previously discussed, HSV with drainage has fewer side effects but a higher risk of recurrent PUD than truncal vagotomy with drainage.

Several local and systemic inflammatory conditions can also cause GOO. Local conditions include acute and chronic pancreatitis, pancreatic pseudocyst, and obstruction secondary to cholecystoduodenal fistula with calculous cholecystitis (Bouveret’s syndrome) [9, 49, 50]. Systemic inflammatory conditions include Crohn’s disease. While gastroduodenal involvement in Crohn’s disease is rare, with an incidence of about 5%, stenosis was noted in 78% of 54 patients in a small series of patients with gastroduodenal disease [51]. Other conditions include Behcet’s disease and systemic lupus erythematosus [9]. Finally, eosinophilic gastroenteritis can result in intestinal obstruction due to muscular infiltration with eosinophils [15].