Faisal Aziz, MD,
Fellow in Vascular Surgery, Jobst Vascular
Center
Nothing to disclose.
Coauthor(s)
Jay A Yelon, DO, FACS,
Associate Professor of Surgery and
Anesthesiology, Program Director, Surgical Critical Care
Fellowship, New York Medical College; Chief, Division of
Trauma and Surgical Critical Care, Westchester Medical
Center
Nothing to disclose.
Specialty Editor(s)
Brian James Daley, MD, MBA, FACS, FCCP,
CNSC,
Professor, Associate Program Director,
Department of Surgery, Division of Trauma and Critical Care,
University of Tennessee Health Science Center College of
Medicine
Nothing to disclose.
Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
eMedicine Salary Employment
Paolo Zamboni, MD,
Professor of Surgery, Chief of Day Surgery
Unit, Chair of Vascular Diseases Center, University of
Ferrara, Italy
Nothing to disclose.
Chief Editor
John Geibel, MD, DSc, MA,
Vice Chairman, Professor, Department of
Surgery, Section of Gastrointestinal Medicine and Department
of Cellular and Molecular Physiology, Yale University School
of Medicine; Director of Surgical Research, Department of
Surgery, Yale-New Haven Hospital
AMGEN Royalty Other
Background
The treatment of peptic ulcer disease (PUD) that involves duodenal bulb and prepyloric ulcers continues to evolve because of recent advances in pharmacology, bacteriology, and operative techniques.
The first major change occurred after the introduction of H2-receptor antagonists for gastric acid suppression in the late 1970s, followed by proton pump inhibitors in the late 1980s.[1, 2] In addition, the discovery that Helicobacter pylori is present in 75-85% of these patients revolutionized the pathophysiologic understanding of peptic ulcer disease.
Elective peptic ulcer surgery has been virtually abandoned. In the 1980s, the number of elective operations for peptic ulcer disease dropped more than 70%, and emergent operations accounted for more than 80%.[3]
In 350 BC, Diocles of Carystos provided perhaps the first account of gastric ulceration. Marcellus Donatus of Mantua first described gastric ulcer at autopsy in 1586, and Muralto described duodenal ulcer at autopsy in 1688. In 1737, Morgagni described both gastric ulcer and duodenal ulcer at autopsy. In 1880, Rydygier resected a distal gastric cancer, and the patient died 12 hours later. Billroth was the first surgeon to successfully resect the distal stomach for distal gastric cancer. The continuity was reestablished with a gastroduodenostomy (Billroth I) using interrupted silk suture. In 1885, Billroth performed a successful distal gastrectomy and gastrojejunostomy (Billroth II) for gastric cancer. Rodman performed the first successful gastrectomy in the United States, in Philadelphia.
In 1886, Heineke performed the first pyloroplasty. In 1888, Johann von Mikulicz-Radecki performed the same operation. Their technique persists today as the Heineke-Mikulicz pyloroplasty. In 1892, Jaboulay described pylorus-preserving gastroduodenostomy. Shortly thereafter, Kocher described the mobilization of the duodenum that bears his name. In 1902, Finney from Baltimore described his pyloroplasty, a modification of the Jaboulay technique with the distal gastrotomy extended well into the duodenum, transecting the pylorus and closing with a gastroduodenostomy.
In the early decades of the 1900s, von Haberer and Finsterer touted subtotal gastrectomy as a treatment of gastric ulcer. In 1943, Dragstedt and Owen described transthoracic truncal vagotomy to treat peptic ulcer disease. Physicians recognized that some patients developed gastric stasis after this procedure, and transabdominal truncal vagotomy and drainage (eg, pyloroplasty, gastrojejunostomy) became a standard ulcer operation. In 1952, Farmer and Smithwick described good results with truncal vagotomy and hemigastrectomy for peptic ulcer. Vagotomy and antrectomy were described by Edwards and Herrington from Nashville in 1953. In 1957, Griffith and Harkins from Seattle described parietal cell vagotomy (highly selective vagotomy) for the elective treatment of peptic ulcer disease.
In the United States, the lifetime prevalence of peptic ulcer disease (PUD) is approximately 10%. One-year point prevalence is 1.8%. Annually, 4.5 million people are affected. Lifetime prevalence of perforation in patients with peptic ulcer disease is approximately 5%.
Internationally, the frequency varies among countries and is determined primarily by the association with H pylori and nonsteroidal anti-inflammatory drugs (NSAIDs).
Peptic ulcer disease (PUD) results from an imbalance of acid secretion and mucosal defenses that resist acid digestion. Moreover, studies have confirmed the strong association between gastric antral infection with H pylori and peptic ulceration. More than 90% of patients with peptic ulcer disease are infected with H pylori, and eradication of this infection not only heals most uncomplicated ulcers but also significantly decreases the likelihood of recurrent ulceration.
Most peptic ulcer disease not associated with H pylori is secondary to the use of NSAIDs. Steroid use, cigarette smoking, rapid gastric emptying, and defective duodenal acid defense mechanisms also contribute to the pathophysiology of peptic ulcer disease. Patients with high gastrin levels (eg, those with Zollinger-Ellison syndrome) are at increased risk of developing peptic ulcer disease and subsequent perforations. Importantly, although the frequency of ulcer disease in general has declined, the number of patients affected by bleeding and perforation has not changed significantly.[4]
Most gastric acid is produced by parietal cells, which are located in the fundus and body of the stomach. The acid is then secreted into a gastric pit, which is a common lumen for small groups of gastric glands located in the lamina propria of the gastric wall. Parietal cells (which secrete both hydrochloric acid and intrinsic factor), mucous cells, and chief cells (which secrete pepsinogen) comprise these gastric glands. Numerous tubular vesicular membranes thought to contain the proton-potassium-adenosine triphosphatase (H+-K+-adenosine triphosphatase [ATPase]) pump, or proton pump, are located inside a resting parietal cell.
Theoretically, when the cell is stimulated to secrete acid, these tubular vesicular membranes bind to the apical plasma membrane, substantially increasing the surface area of the microvilli. The proton pumps, now fused with the apical plasma membrane, can secrete hydrochloric acid directly into the lumen of the gastric pits.[5] Stimulating factors for parietal cells include histamine, acetylcholine, and gastrin.
Because many surgical procedures for peptic ulcer disease (PUD) entail some type of vagotomy, a discussion concerning the vagal innervation of the abdominal viscera is also appropriate. The left (anterior) and the right (posterior) branches of the vagus nerve descend along either side of the distal esophagus. As they enter the lower thoracic cavity, they can communicate with each other through several cross-branches that comprise the esophageal plexus. However, below this plexus, the 2 vagal trunks again become separate and distinct before the anterior trunk branches to form the hepatic, pyloric, and anterior gastric (also termed the anterior nerve of Latarjet) branches. The posterior trunk branches to form the posterior gastric branch (also termed the posterior nerve of Latarjet) and the celiac branch.
The parietal cell mass of the stomach is segmentally innervated by terminal branches from each of the anterior and posterior gastric branches. These terminal branches are divided during a highly selective vagotomy. The gallbladder is innervated from efferent branches of the hepatic division of the anterior trunk. Consequently, transection of the anterior vagus trunk (performed during truncal vagotomy) can result in a dilated gallbladder with inhibited contractility and subsequent cholelithiasis. The celiac branch of the posterior vagus innervates the entire midgut (with the exception of the gallbladder). Thus, division of the posterior trunk during truncal vagotomy may contribute to postoperative ileus.
Patients with perforated peptic ulcer disease (PUD) usually present with a sudden onset of severe, sharp abdominal pain. Most patients describe generalized pain; few present with severe epigastric pain. As even slight movement can tremendously worsen their pain, these patients assume a fetal position. Abdominal examination findings are usually consistent with generalized tenderness, rebound tenderness, guarding, and rigidity. However, the degree of peritoneal findings is strongly influenced by a number of factors, including the size of perforation, amount of bacterial and gastric contents contaminating the abdominal cavity, time between perforation and presentation, and spontaneous sealing of perforation.
These patients may also demonstrate signs and symptoms of septic shock, such as tachycardia, hypotension, and anuria. Not surprisingly, these indicators of shock may be absent in elderly or immunocompromised patients or in those with diabetes. Patients should be asked if retching and vomiting occurred before the onset of pain. Obtaining the medical history, especially for peptic ulcer disease, H pylori infection, ingestion of NSAIDs, or smoking, is essential in making the correct diagnosis.
Traditionally, perforated peptic ulcers have been treated surgically with urgent surgical repair, with or without an ulcer-curative operation, depending on the patient's hemodynamic status. However, several studies have demonstrated that perforated peptic ulcers can be treated nonoperatively. Each study has demonstrated different indications to operate; however, the general consensus is that any patient with a perforated peptic ulcer who has peritoneal signs should undergo exploratory laparotomy.
Wangensteen et al believed that, in a patient with perforation but without evidence of pneumoperitoneum, one can safely assume that perforation has sealed off on its own.[6] He advocated a nonoperative approach for such patients. However, he too agreed with operative treatment in patients with perforated ulcer and evidence of pneumoperitoneum. Berne and Donovan emphasized the use of a water-soluble upper GI study to demonstrate spontaneous sealing of the perforation.[7] They demonstrated that as many as 40% of perforated peptic ulcers had no evidence of leak on upper GI contrast study.
Berne and Donovan concluded that these patients can be observed safely as long as peritonitis does not develop.[7] Mortality rates were 6% and 3% in the operative and nonoperative groups, respectively. In 1998, in another study by Donovan et al, the authors proposed to divide the patients based on their H pylori infection status and recommended nonoperative treatment in all patients except those without H pylori infection and those in whom prior treatment of H pylori infection had failed.[8]
Despite strong arguments favoring nonoperative treatment of patients with perforated peptic ulcer disease (PUD), delaying the initiation of surgery more than 12 hours after presentation was demonstrated to worsen the outcome in patients with perforated peptic ulcer disease. Therefore, when definitely indicated, a laparotomy should be performed as soon as possible.[9]
The stomach is the dilated portion of the foregut between the esophagus and duodenum. The stomach is typically J shaped and located in the left upper quadrant and epigastrium, and its distal part can extend to the level of the umbilicus. The stomach is divided into a fundus, body, antrum, and pylorus (see the image below).
View Image
Anatomy of stomach.
The fundus is the part of the stomach that lies above the level of the gastroesophageal junction. The body extends from the fundus to the incisura angularis, which is most clearly observed during gastroscopy. The pyloric portion of the stomach consists of the antrum, which extends from the incisura angularis to the proximal limit of the pylorus. The pyloric canal is surrounded by a thick muscular wall that forms the pyloric sphincter. The pyloric canal is approximately 2.5 cm long, and the pyloroduodenal junction is identified by the presence of the prepyloric vein (vein of Mayo), which crosses its anterior surface.
The stomach possesses a lesser and a greater curvature. The lesser curvature extends from the right side of the esophagus to the level of the pylorus, and the lesser omentum (gastrohepatic ligament) is attached to it. Conversely, the greater curvature extends from the left of the esophagus, around the fundus, and to the right side of the pylorus. The upper part of the greater curvature attaches to the gastrosplenic ligament that contains the short gastric vessels, whereas the greater omentum extends from the lower portion of the greater curvature. The lesser sac forms the posterior relation of the stomach, also termed the bed of the stomach. Posteriorly, the relations include the diaphragm above and, from right to left, the pancreas, the splenic artery, the spleen, the left kidney, and the adjacent adrenal gland.
Because the stomach is derived from the foregut, its blood supply originates from the branches of the foregut artery, the celiac axis (see the image below).
View Image
Blood supply to stomach.
The left gastric artery that arises from the celiac axis and the right gastric artery that arises from the hepatic artery supply the lesser curvature and the adjacent surfaces. The greater curvature and the adjacent portion of the stomach are supplied by the left gastroepiploic artery, which arises from the splenic artery, and from the right gastroepiploic artery, which arises from the gastroduodenal branch of the hepatic artery.
The short gastric arteries arise from the splenic artery at the hilum, pass within the gastrosplenic ligament, and supply the fundus. The venous drainage of the stomach flows through the portal vein. The right and the left gastric veins enter the portal vein directly, the right gastroepiploic vein drains into the superior mesenteric vein, and the left gastroepiploic vein and the short gastric veins join the splenic vein. The lymphatic drainage follows the arteries and ultimately drains into the celiac lymph nodes.
The nerve supply of the stomach is derived from both the right and the left vagus nerve and the celiac plexus of sympathetic fibers that arise from the fifth, sixth, seventh, and eighth thoracic segments of the spinal cord (see the image below).
View Image
Vagal innervation of stomach.
Because of the rotation of the stomach during embryonic development, the left vagus lies anterior to the esophagus, whereas the right vagus lies posterior. The anterior vagus enters the abdomen anterior to the esophagus and gives off hepatic branches that travel in the lesser omentum to supply the liver and the gallbladder and a branch through the pyloric antrum. The anterior vagus nerve continues along the lesser omentum as the nerve of Latarjet and terminates approximately 5-7 cm proximal to the pylorus in several branches, described as the crow's foot.
The posterior (right) vagus nerve also lies between the leaves of the lesser omentum and follows a course along the lesser curvature posterior to the anterior vagus nerve as the nerve of Latarjet. In 90% of individuals, the posterior vagus nerve gives rise to the nerve of Grassi, which originates at the level of the gastroesophageal junction and supplies the gastric fundus. However, in as many as 20% of individuals, the nerve of Grassi originates above the hiatus. When truncal vagotomy is performed, this branch should be identified and divided to minimize recurrent ulceration.
CBC count (Leucocytosis with left shift is found in most cases.)
Serum gastrin levels: Gastrin levels greater than 1000 pg/mL are suggestive of gastrinoma.
H pylori infection testing
Serum H pylori antibody detection: Antibodies (immunoglobulin G [IgG]) to H pylori can be measured in serum, plasma, or whole blood. However, results from whole blood tests using finger sticks are less reliable.
Urea breath tests: Urea breath tests are used to detect active H pylori infection by testing for the enzymatic activity of bacterial urease. In the presence of urease produced by H pylori, labeled carbon dioxide (heavy isotope, carbon-13, or radioactive isotope carbon-14) is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled.
Fecal antigen tests: Fecal antigen testing is used to identify active H pylori infection by revealing the presence of H pylori antigens in stools. This test is more accurate than antibody testing and less expensive than urea breath tests.
Upright chest radiography or lateral abdominal decubitus radiography reveals evidence of free air (pneumoperitoneum).
Upper GI contrast study with water-soluble contrast: Extravasation of contrast is evidence of gastric perforation.
CT scanning is not used in the diagnosis of peptic ulcer disease. CT of the abdomen may demonstrate free air in the presence of a perforated ulcer. CT with oral contrast may also demonstrate extravasation of contrast in the presence of a perforated ulcer. If history and physical examination raise the possibility of perforation, upright chest radiography and an upper GI contrast study with water-soluble contrast are the diagnostic studies of choice. Do not perform CT scanning in this situation.
Gastric ulcers are classified according to the Johnson classification.
Type I gastric ulcers are typically located near the angularis incisura on the lesser curvature, close to the border between the antrum and the body of the stomach. Patients with type I gastric ulcers usually have typical or decreased gastric acid secretion.
Type II gastric ulcers are a combination of stomach and duodenal ulcers, and type III gastric ulcers are prepyloric. Both type II gastric ulcers and type III gastric ulcers are associated with normal or increased gastric acid secretion.
Type IV gastric ulcers occur near the gastroesophageal junction, and gastric acid secretion is normal or below normal.
Nonoperative treatment is the rational choice for a selected subgroup of patients who meet the criteria discussed in Indications. Treatment of these patients includes the following[10] :
Nasogastric decompression
Fluid resuscitation with replacement of fluid and electrolytes
Proton pump inhibitor
Broad-spectrum antibiotics
Initial treatment typically requires triple therapy with 2 antibacterial agents and an acid inhibitor, typically a proton-pump inhibitor (PPI). Drug regimens most often include 2 weeks of antibacterial therapy with 4 weeks of acid suppression.
Several second-line regimens are available for adults; a regimen of ranitidine, bismuth citrate, metronidazole, and tetracycline has an eradication rate similar to that of PPI with amoxicillin and metronidazole.
Omeprazole, furazolidone, and clarithromycin demonstrated a high eradication rate (90%) similar to that of standard Maastricht triple therapy (ie, omeprazole, amoxicillin, clarithromycin).
High eradication rates (85%) were also found with a 7-day course of levofloxacin, clarithromycin, and a PPI.
Indications to abandon nonoperative treatment in favor of surgery include the following:
Failure of symptoms to improve over 12-24 hours
Peritoneal signs and an increase in abdominal tenderness
Fluid resuscitation should be initiated as soon as the diagnosis is made. Essential steps include insertion of a nasogastric tube to decompress the stomach and a Foley catheter to monitor urine output. Intravenous infusion of fluids is begun, and broad-spectrum antibiotics are administered. In select cases, insertion of a central venous line or a Swan-Ganz artery catheter may be necessary for accurate fluid resuscitation and monitoring. As soon as the patient has been adequately resuscitated, emergent exploratory laparotomy should be performed.
Moller et al conducted a retrospective study on 398 patients undergoing emergency surgery for perforated peptic ulcer and found that ASA class, age, shock upon admission, preoperative metabolic acidosis, elevated creatinine level, and subnormal concentration of albumin upon admission are independently related to a 20-day mortality for these patients.[11]
The patient is placed in the supine position. A midline incision provides the most expeditious entry into the abdominal cavity. The incision can be extended to the symphysis pubis if necessary. Once the abdomen is entered, the stomach and duodenum are carefully examined to determine the site of perforation. If the anterior surface of the stomach and duodenum shows no abnormalities, the gastrocolic ligament is serially divided between clamps to allow entrance into the lesser sac and inspection of the posterior surface of the stomach. The choice of operative procedure depends on variables, such as the presence of shock, life-threatening comorbid conditions, the degree of contamination of the upper abdomen, the amount and duration of perforation, and whether the patient has a history of or currently has intraoperative evidence of chronic peptic ulceration.
In the presence of life-threatening comorbid conditions and severe intra-abdominal contamination, the safest technique for an acute anterior duodenal perforation is a simple closure with a Graham patch using omentum. Several full-thickness simple sutures are placed across the perforation using 2-0 or 3-0 silk sutures. A segment of omentum is placed over the perforation. The silk sutures are secured. If contamination of the upper abdomen is minimal and the patient is stable, a definitive ulcer procedure can be performed. For a perforated duodenal ulcer, this may include a highly selective vagotomy, a truncal vagotomy and pyloroplasty, or vagotomy and antrectomy.
For a perforated gastric ulcer, the procedure performed depends on the patient’s condition. If the patient is moribund, the ulcer is best excised by grasping it with multiple Allis clamps and using a GIA-60 linear stapler. Alternatively, the ulcer can be excised with electrocautery, and the defect is approximated with a 2-layer closure with inner continuous 3-0 absorbable sutures and outer interrupted Lambert sutures using 2-0 or 3-0 silk sutures. In a stable patient, the ulcer is excised and sent for frozen section analysis to exclude malignancy. For a benign gastric ulcer, a distal gastrectomy with either a Billroth I gastroduodenostomy or a Billroth II gastroduodenostomy is performed.
Truncal vagotomy and drainage
To obtain access to the esophageal hiatus, the left triangular ligament is sharply divided with electrocautery, and the left lateral lobe of the liver is carefully retracted or folded. A transverse incision is made in the peritoneum overlying the esophagus at the hiatus in the diaphragm. This opening is then widened on each side of the esophagus by sharply dividing the adjacent lesser omentum and the esophagophrenic ligament. Blunt dissection is continued until 2 or 3 fingers can be comfortably passed around the esophagus.
Using a large, right-angle Mixter clamp, a one-half-inch Penrose is passed around the esophagus. The anterior (left) vagal trunk is then sought. The anterior trunk is separated from the esophagus with the aid of a right-angle Mixter clamp or a nerve hook. The posterior vagus is usually felt as a stout cord lying behind and to the right of the esophagus. The nerve is carefully freed. After the vagal trunks are transected, the distal 5-6 cm of the esophagus must be cleared by meticulously dissecting and dividing all strands of nerve fibers, small blood vessels, and fascia.
The criminal nerve of Grassi, which is a branch of the posterior vagus to the fundus, must be sought diligently and divided in the usual fashion. After completion of this extensive periesophageal dissection, only the longitudinal esophageal fibers should be visible. Such meticulous dissection is essential to ensure complete vagotomy and subsequent low incidence of recurrent ulceration. If a selective vagotomy is to be performed, the hepatic branch of the anterior vagus nerve and the celiac division of the posterior vagus nerve are preserved.
The type of drainage procedure performed depends on the condition of the duodenum. Typically, a pyloroplasty is considered standard practice; however, if the duodenum is scarred and inflamed, a gastrojejunostomy is a suitable alternative.
Pyloroplasty
A Kocher maneuver is first performed to mobilize the second part of the duodenum. Two 2-0 silk stay sutures are placed at the superior and inferior aspects of the pylorus. A 6- to 10-cm transverse incision is made starting from the antrum and extending across the pylorus and into the first part of the duodenum. This incision is closed longitudinally with an inner layer of interrupted 3-0 absorbable sutures encompassing all layers, followed by a seromuscular layer of 3-0 silk Lembert sutures. Alternatively, a stapled closure can be performed. In this case, the edges of the incision are grasped in a longitudinal fashion with several Allis clamps. The incision is closed with a TA-55 stapler containing 4.8-mm staples.
Gastrojejunostomy
To construct a gastrojejunostomy, a loop of jejunum approximately 12-15 cm from the ligament of Treitz is first selected and brought through an opening in the transverse mesocolon, usually to the left of the middle colic vessels. The stoma should be placed in the prepyloric region or at the most dependent portion of stomach.
Using 3-0 silk, a posterior layer of seromuscular Lembert sutures is placed. Before the bowel is opened, noncrushing Doyen clamps are placed on both sides of the proposed anastomosis to occlude the jejunum. The area of the anastomosis is isolated with moist laparotomy pads in case spillage of jejunal contents occurs. In addition, the suction catheter must be readily available to contain any spillage. The stomach and the adjacent jejunum are opened. Using 3-0 absorbable sutures, the full-thickness inner layer is started posteriorly and completed anteriorly using inverting Connell sutures. An anterior seromuscular layer of interrupted 3-0 silk Lembert sutures is placed to complete the anastomosis.
For a stapled anastomosis, the jejunum is first aligned to the dependent portion of the stomach with 2-0 silk stay sutures at each end. A stab incision is made in the stomach and jejunum, and the anastomosis is performed using a GIA-60 stapling device. The staple line is inspected for hemostasis. The combined stab incision is closed with an inner layer of continuous 3-0 absorbable sutures and an outer layer of interrupted 3-0 silk Lembert sutures. Finally, the transverse mesocolon is carefully closed around the anastomosis to avoid herniation.
Billroth I and II gastrectomy
If antrectomy is to be performed as part of the antiulcer procedure, dissection is commenced along the distal half of the greater curvature. First, the greater omentum is separated from the proximal half of the transverse colon. Next, the branches from the gastroepiploic arcade to the greater curvature are divided and ligated. As this dissection proceeds toward the duodenum, the small, fragile vessels are ligated in continuity with 3-0 silk sutures and divided.
With gentle dissection, the posterior wall of the first part of the duodenum is freed from the pancreas and divided with a GIA-60 linear stapler. The right gastric artery is identified above the pylorus, divided, and ligated with 2-0 silk sutures. With electrocautery, the gastrohepatic ligament is divided proximally along the lesser curvature. Just proximal to the incisura angularis, the left gastric vessels lying along the lesser curvature are carefully isolated with a right-angle Mixter clamp. These vessels are individually ligated in continuity with 2-0 silk sutures and divided. Proximally, these vessels are suture ligated with 3-0 silk sutures. After the nasogastric tube is withdrawn proximally, the stomach is divided with a GIA-90 linear stapler.
If adequate length of supple duodenum is available, a Billroth I gastroduodenal anastomosis can be constructed. The staple line along the transected duodenum is sharply excised and hemostasis is controlled. A 2-layer anastomosis, with an outer layer of interrupted Lembert 3-0 silk sutures and an inner layer of full-thickness continuous 3-0 absorbable sutures, is performed. The gastric staple line from the lesser curvature is inverted with 3-0 silk interrupted Lembert sutures until the angle of sorrow of the gastroduodenal anastomosis is reached. A crown suture is placed there.
If a Billroth II gastrojejunostomy (Polya-Hoffmeister type) is to be constructed, a loop of proximal jejunum is selected and brought in an antecolic or retrocolic fashion toward the transected stomach. The loop of jejunum is aligned along the lower half of the gastric staple line with 3-0 silk stay sutures. For a hand-sewn anastomosis, a posterior layer of interrupted 3-0 silk Lembert sutures is placed, approximating the posterior wall of the stomach and jejunum. Noncrushing bowel clamps are placed on the small bowel. With electrocautery, a longitudinal enterotomy is made in the loop of jejunum, and the appropriate length of adjacent gastric staple line is sharply excised. An inner layer of continuous 3-0 absorbable sutures is placed. Finally, the anterior interrupted Lembert 3-0 silk sutures are placed to complete the anastomosis.
Next, the gastric staple line from the lesser curvature is inverted with 3-0 silk interrupted Lembert sutures until the angle of sorrow of the gastrojejunal anastomosis is reached. A corner crown suture is placed there. For additional security at this location, the adjacent jejunal wall can be used to cover the angle of sorrow. For a stapled Billroth II anastomosis, stay sutures are placed to hold the loop of jejunum adjacent to the gastric remnant. A small stab incision is made in the jejunum and at the adjacent posterior wall along the greater curvature of the stomach. The limbs of the GIA stapler are inserted and fired. At least 2 cm of posterior gastric wall is needed between the gastric staple line and the gastrojejunostomy to avoid necrosis.
Highly selective vagotomy
The position, incision, and initial exploration are as described for truncal vagotomy and pyloroplasty. First, the anterior nerve of Latarjet is identified, which may be observed leaving the gastroesophageal junction and running downward in the lesser omentum parallel to the lesser curvature and terminating at the incisura angularis (5-7 cm from the pylorus) as several branches resembling a crow's foot. These terminal branches and the branches from the nerve of Latarjet to the body of the stomach are accompanied by the blood vessels. The posterior vagal trunk also runs downward within the lesser omentum as the posterior nerve of Latarjet, and its course and distribution to the posterior aspect of the stomach are similar to those of the anterior nerve of Latarjet.
Before the anterior dissection is begun, inspect the lesser sac for adhesions to the pancreas that could be inadvertently avulsed during dissection, which can lead to bleeding. To enter the lesser sac, the gastrocolic ligament is sharply divided, but the gastroepiploic arcade is kept intact. Any avascular congenital adhesions between the stomach and pancreas are divided with electrocautery. A nasogastric tube is placed by the anesthesiologist and should be directed toward the antrum to be used to grasp the greater curvature and provide downward traction.
The dissection commences at the site just proximal to the crow's foot on the anterior aspect of the stomach. The objective is to divide the lesser omentum from the lesser curvature, between the incisura angularis and the esophagus, by dividing all the blood vessels and the accompanying nerves that enter the lesser curvature. The anterior layer of the lesser omentum, adjacent to the neurovascular bundle, is sharply incised. With the use of a fine Schnidt clamp, the neurovascular branches are carefully dissected, ligated in continuity with 3-0 or 4-0 silk sutures, and divided. This dissection proceeds proximally up along the lesser curvature until the left side of the gastroesophageal junction is reached.
Next, the stomach is turned upward, and, again, the nasogastric tube is used to grasp the greater curvature. The posterior denervation is conducted in a similar fashion. Attention is then turned to careful and meticulous dissection of the lower 5 cm of the esophagus, which involves ligating and dividing all blood vessels and nerve fibers entering the esophagus, particularly on its right lateral and posterior aspects. By dividing close to the wall of the upper stomach and lower esophagus, damage to the main vagal trunk and its celiac and hepatic branches is avoided.
The two critical components of achieving a successful, complete highly selective vagotomy include (1) completely separating the lesser curvature of the stomach from the lesser omentum, extending from the incisura angularis to the cardia, and (2) skeletonizing the lower 5-7 cm of the esophagus.
The nasogastric tube can be discontinued on postoperative day 2 or 3, depending on the return of GI function, and diet can be slowly advanced. Patients who are found to have H pylori infection should receive the appropriate antibiotic regimen. Patients with high serum gastrin levels should undergo an evaluation for Zollinger-Ellison syndrome. Patients should undergo upper endoscopy to evaluate the area of ulcer and healing of the perforation site 4-6 weeks after surgery.
Conservative treatment may be possible in 60% of patients. Approximately 30% of patients with perforated peptic ulcer disease (PUD) undergo surgery immediately. In the first group of patients, approximately 10% of patients fail to improve with conservative treatment and must undergo secondary surgery. Emergency operations for peptic ulcer perforation carry a mortality risk of 6-30%.[9] Factors that affect the prognosis include the following:
Shock at the time of admission
Renal insufficiency
Delaying the initiation of surgery more than 12 hours after presentation
Concurrent medical illness (eg, cardiovascular disease, diabetes mellitus)
Age older than 70 years
Cirrhosis
Immunocompromised state
Location of ulcer (Mortality associated with perforated gastric ulcer is twice that associated with perforated duodenal ulcer.)
Successful treatment of perforated peptic ulcer with the laparoscopic approach was first reported in 1990.[12] Since then, various institutions have used this technique to treat patients with perforated peptic ulcer. Studies have shown that the conversion rate from a laparoscopic approach to an open approach varies from 0-25%. Compared with the open approach, the following results were observed with the laparoscopic method:
Increased operative time
Reduced requirement for postoperative analgesia
Reduced time to return to a normal diet
Shorter hospital stay
Earlier return to work[13]
No difference was found in blood loss, stress response (as determined by endotoxemia, bacteremia, and inflammatory markers), postoperative gastric emptying, or morbidity or mortality.[14]
One prospective randomized trial has compared laparoscopic surgery with open surgery for perforated ulcer. The study found that the only difference between the two groups was a reduced need for analgesia and an increased operative time in the laparoscopic group.[15]
Another randomized control trial was conducted in 9 medical centers across the Netherlands.[16] A total of 109 patients with perforated peptic ulcers were randomized to laparotomy or laparoscopic procedure. Operating time in the laparoscopic group was significantly longer than the open group (75 min vs 50 min). Patients treated laparoscopically had significantly reduced pain when compared with patients who were treated by laparotomy. Hospital stay was 6.5 days for the laparoscopic group versus 8 days for the laparotomy group. The authors concluded that laparoscopic repair of perforated peptic ulcer is a safe procedure.
Vaidya et al have shown that the laparoscopic approach to perforated peptic ulcer is safe even in the case of delayed presentation (>24 h).[17] The only complication associated with laparoscopy is increased risk of port site infection.
Khelifi et al conducted a study on 160 patients with perforated duodenal ulcer and showed that laparoscopy is a safe surgical approach in cases of perforated duodenal ulcers.[18]
Contraindications for laparoscopic repair for perforated peptic ulcer include large perforations, a posterior location of the perforation, and a poor general state of health.
Elder JB, Deakin M. Gastric physiology. In: Wasell C, Nyhus LM, Donahue PE, eds. Surgery of the Esophagus, Stomach and Small Intestine. Boston: Little, Brown; 1995:420-424.
Wangensteen OH. Non-operative treatment of localized perforations of the duodenum. Proc Minn Acad Med. 1935;18:477-480.
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