Constance W. Lee
George A. Sarosi Jr.
Presentation
A 70-year-old man presents to the emergency department (ED) with a 1-hour history of generalized abdominal pain that began abruptly and now radiates to both shoulders. The patient has a prior history of peptic ulcer disease but is not currently on acid-suppression therapy. He is also on low-dose aspirin for peripheral vascular disease. He has never had an abdominal surgery. He has no known drug allergies. He does not smoke tobacco or drink alcohol.
On physical examination, his temperature is 36.5°C, heart rate is 100, blood pressure is 125/70, and his abdomen is diffusely tender to palpation.
Differential Diagnosis
The differential diagnosis for this patient includes the following: perforated hollow viscus secondary to peptic ulcer disease (PUD), carcinoma, gastrinoma, mesenteric ischemia, small bowel obstruction, Crohn’s disease, and Boerhaave’s syndrome; pancreatitis, appendicitis, diverticulitis, ruptured abdominal aortic aneurysm, ruptured ectopic pregnancy, pneumonia, pulmonary infarction, and renal or biliary colic.
Peptic ulcers are most frequently found in the stomach and duodenum. They are most often associated with Helicobacter pylori infection or the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin. Risk factors for the development of NSAID-related ulcers include advanced age, history of prior ulcer, serious systemic illness, concomitant use of anticoagulants or corticosteroids, and high NSAID doses. Less common causes of PUD include gastrinoma, systemic mastocytosis, carcinoma, sarcoidosis, Crohn’s disease, and carcinoid syndrome.
Ulcer complications include perforation, obstruction, and bleeding. In a review of 88 patients with a perforated peptic ulcer, the most common location of perforation was the duodenal bulb (62%), followed by the pyloric region (20%), and then the gastric body (18%). Ulcer perforation is associated with prior history of ulcer disease and use of NSAIDs. In the setting of NSAID therapy, the risk factors associated with ulcer perforation include a history of prior ulcer, age >60 years, and the concomitant use of steroids, anticoagulants, selective serotonin reuptake inhibitors, or alendronate.
The classic clinical presentation of a perforated peptic ulcer has been described as a three-stage process:
1. Early (onset to 2 hours): The abdominal pain begins abruptly, with the patient often being able to remember the exact time the pain started. The pain may first localize to the epigastrum but quickly becomes generalized. The pain may radiate to the shoulders if the diaphragm is irritated. On examination, the patient may be tachycardic, have a low body temperature, and the abdomen is tender to palpation.
2. Intermediate (2 to 12 hours): The patient may report an improvement in pain. However, on physical exam the patient often displays increased pain with movement, and the abdominal wall is rigid. In addition, there may be significant pain with palpation of the hypogastrum and right lower quadrant secondary to drainage of enteric contents from the perforation.
3. Late (after 12 hours): The patient may complain of increased pain and fevers, signs of hypovolemia, and abdominal distension. Although the patient may vomit during any stage, it is most common at this stage.
Workup
It is important to quickly diagnose a perforated peptic ulcer because the prognosis is good if treatment is provided within the first 6 hours, whereas delayed treatment beyond 12 hours is associated with decreased survival and increased morbidity.
Imaging Studies
An upright chest x-ray or an abdominal x-ray may reveal the presence of intraperitoneal free air. A computed tomography (CT) scan may also be used to identify intraperitoneal free air or free fluid. However, approximately 10% to 20% of patients with a perforated duodenal ulcer will not have direct findings of perforation. If free air is present, no other test is required to confirm the diagnosis. An upper GI study or an abdominal CT scan with water-soluble contrast may demonstrate the leak if free air is not present and a confirmatory test is required for diagnosis.
Laboratory Studies
Laboratory studies are not necessary for the diagnosis of a perforated duodenal ulcer. However, they contribute to the complete evaluation and appropriate management of the patient. A basic metabolic panel will guide fluid and electrolyte resuscitation. A complete blood count may demonstrate leukocytosis with a left shift in a patient with a perforated ulcer. A serum gastrin level may assist in the diagnosis of gastrinoma, though the result of the test will likely not return in time to influence the operative strategy. Given that H. pylori infection is present in 70% to 90% of duodenal ulcers and 30% to 60% of gastric ulcers, patients with peptic ulcer disease should be tested. Noninvasive testing for H. pylori infection includes urea breath testing, stool antigen testing, and serology. Ideally, H. pylori infection is identified preoperatively, as it can influence operative strategy. A monoclonal stool antigen test is available that has 94% sensitivity, 97% specificity, and may be performed in about an hour. There is also a rapid stool antigen test for the diagnosis of H. pylori that can be done in 5 minutes. However, its sensitivity and specificity have been shown to be 76% and 98%, respectively.
In our scenario, the patient’s presenting signs and symptoms, combined with his risk factors place the diagnosis of a perforated peptic ulcer high on the list of differential diagnoses. An upright chest x-ray demonstrates free intraperitoneal air. A stool antigen test is positive for H. pylori infection. The ED physician consults general surgery, starts fluid resuscitation, initiates nasogastric decompression, places a Foley catheter, and administers omeprazole, ampicillin, metronidazole, ceftriaxone, and fluconazole.
Diagnosis and Treatment
The medical/nonoperative management of a perforated peptic ulcer includes fluid resuscitation, nasogastric decompression, acid suppression, and empiric antibiotic therapy for coverage of enteric gram-negative rods, oral flora, anaerobes, and fungus. In the setting of a perforated duodenal ulcer without peritonitis, the application of a nonoperative management strategy has been proposed, especially for patients at high risk for operative complications. However, delaying the surgical repair of a perforated peptic ulcer more than 12 hours after presentation has been associated with increased morbidity and mortality. Furthermore, a randomized trial of nonoperative treatment for perforated peptic ulcers by Crofts et al. demonstrated that patients over 70 years of age were less likely to improve with conservative management. Operative management is the preferred treatment strategy in most patients, especially the elderly.
In our clinical scenario, you evaluate the patient 2 hours after the start of the symptoms, at which time the patient notes an improvement in generalized pain. However, on examination the heart rate is 110, the blood pressure is 90/50, and the abdomen is rigid, with the patient more sensitive to changes in position. You decide to proceed to the operating room for management of this problem. On exploration of our patient you identify a 1 cm anterior duodenal perforation.
Surgical Approach
Elective operations for peptic ulcer disease have become uncommon with the successful medical management of acid and H. pylori infection. However, surgical management is almost always indicated for a perforated ulcer, especially when the patient is hemodynamically unstable, has signs of peritonitis, or has evidence of free contrast extravasation on imaging. Although operative treatment is the appropriate plan, the patient should receive fluid resuscitation and antibiotic treatment while preparing the operating room. It should be noted that emergency surgery for peptic ulcer perforation has up to 30% risk of mortality. The presence of comorbid disease has been shown to increase mortality. Furthermore, in patients requiring emergency surgery, variables identified as being independently associated with mortality include age, American Society of Anesthesiologists (ASA) class, shock on admission, hypoalbuminemia on admission, preoperative metabolic acidosis, and an elevated serum creatinine.
Surgical Procedure(s) for the Management of Perforated Duodenal Ulcers
1. Omental patch repair (Table 1): The safest technique for the management of a perforated duodenal ulcer, especially in the setting of delayed repair (>24 hours after presentation), hemodynamic instability, or significant intra-abdominal contamination is a patch repair with an omental pedicle. This technique combined with the appropriate medical therapy is likely sufficient in the case of a patient with a history of H. pylori infection or NSAID use.
TABLE 1. Key Technical Steps to Maneuvers in Oversewing a Bleeding Duodenal Ulcer
The repair may be performed laparoscopically or open. The perforation is repaired by taking a seromuscular bite from one side of the perforation, taking a bite of omentum, followed by another seromuscular bite from the other side of the perforation, and then tying to fix the omental pedicle in place. Typically, three to four sutures are required to secure the patch. Follow the repair by irrigation of the peritoneal cavity with large volumes of warm saline.
Pitfalls
• The optimal repair of duodenal ulcer perforations >2 cm can be challenging, and the omental patch repair may be associated with increased risk of failure. Performing a definitive repair has been suggested, as have less standard repairs, including tube duodenostomy.
• On exploration, the omentum, liver, or gallbladder may have already “patched” the perforation, in which case the surgeon must decide whether to remove the natural patch and surgically repair the defect, or to simply irrigate the peritoneal cavity.
• If the ulcer perforation is located at the distal end of the pyloric channel, the duodenum may need to be mobilized to provide adequate exposure of the defect.
2. A definitive ulcer procedure may be performed if the patient is hemodynamically stable, has minimal intra-abdominal contamination, and either (1) has a history of PUD with unknown H. pylori status or (2) is unable to stop NSAID therapy.
a. Truncal vagotomy and pyloroplasty (drainage) (V&D) (Table 2): A truncal vagotomy reduces basal acid secretion by 80% and stimulated acid secretion by 50%. It reduces acid secretion by preventing direct cholinergic stimulation for acid secretion and by decreasing the response of parietal cells to histamine and gastrin. Unfortunately, a truncal vagotomy also damages the stomach’s receptive relaxation and antral grinding, in addition to the pyloric sphincter’s coordination required for gastric emptying. To compensate for these changes, a pyloroplasty is performed to facilitate stomach drainage. The benefit of V&D is that it is safe and may be done relatively quickly. The drawbacks of the procedure are that 10% of patients later report diarrhea or dumping syndrome, and 10% have a recurrent ulcer.
TABLE 2. Truncal Vagotomy and Pyloroplasty Key Points
Procedure: Access the esophageal hiatus by dividing the left triangular ligament and retracting the left lateral lobe of the liver. Open the peritoneum overlying the esophagus by dividing the lesser omentum and the esophagophrenic ligament. Use blunt dissection between the esophagus and the adjacent crux to allow two fingers behind the esophagus. Careful dissection is critical to avoid iatrogenic esophageal perforation. Downward traction on the gastroesophageal junction facilitates identification of the vagus nerve. Identify the anterior and posterior vagal trunks, dissect them from the esophagus, and then transect them (Figure 2). Mark the transected vagal margins with hemoclips and send biopsies of both nerves to pathology to confirm that the transected structures were nerves. Note that the criminal nerve of Grassi coming off the posterior vagus trunk can be missed if the vagotomy is performed lower on the esophagus; to avoid this, complete circumferential dissection of the distal 6 cm of the esophagus ensures division of these nerve fibers.
A Heinecke-Mikulicz pyloroplasty is performed by mobilizing the second part of the duodenum using a Kocher maneuver. Then a 5 cm incision is made from the antrum, over the pyloric sphincter, and onto the proximal duodenum. Place seromuscular tacking sutures to the cephalad and caudad ends of the incision to facilitate the transverse closure of the wound (Figure 1). The incision is closed in one or two layers. If closed in two, start with an inner layer of full-thickness interrupted absorbable sutures, followed by a seromuscular layer of Lembert sutures. Alternatively, a stapled closure may be performed using a TA-55 stapler containing 4.8 mm staples. Note that if the duodenum is severely scarred or inflamed, then a gastrojejunostomy may be used in place of a pyloroplasty.
FIGURE 1 • Pyloroplasty. (Figure 46.2 in Mulholland MW. Gastroduodenal ulceration. In: Mulholland MW, Lillemoe KD, Doherty GM, et al., eds. Greenfield’s Surgery: Scientific Principles and Practice. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2006:722–735).
Pitfalls
• Failure to perform careful esophageal dissection and injuring/perforating the esophagus
• Forgetting to perform biopsies of the vagal nerves for confirmation of the appropriate resection of nerve tissue
• Causing splenic injury when applying traction on the stomach
• Causing a postoperative hiatal hernia from not repairing defects at the esophageal hiatus at the time of vagotomy
b. Vagotomy and antrectomy (Table 3): The combination of the vagotomy and antrectomy eliminates basal acid secretion and decreases stimulated acid secretion by 80%. The benefits of a vagotomy with antrectomy are that the procedure may be applied to a variety of situations, and that the ulcer recurrence rate is very low. The disadvantages are that the operative mortality is higher than with V&D or highly selective vagotomy (HSV), and that there may be complications associated with the subsequent Billroth I or Billroth II reconstructions. In the modern era, the antrectomy should be reserved for healthy/stable patients with refractory ulcer disease and/or anatomic indications (e.g., large antral gastric ulcers, pyloric scarring).
TABLE 3. Antrectomy
Procedure: The vagotomy proceeds as described above.
The antrectomy is begun by separating the distal half of the greater curvature by dissecting the greater omentum from the proximal half of the transverse colon, carefully isolating and ligating the branches from the gastroepiploic arcade. Then the posterior wall of the first part of the duodenum is dissected from the pancreas. The gastrohepatic ligament is divided proximally along the lesser curvature and the left gastric vessels along the lesser curvature are ligated and divided. The stomach is divided with the goal to remove all the antral mucosa. The upper margin of the antrum may be approximated by identifying the halfway point on the lesser curvature between the gastroesophageal junction and the pylorus. The stomach is divided with a GIA-style linear stapler using 4.8 mm staples. Next, the right gastric artery is identified above the pylorus, ligated, and divided. To facilitate manipulation of the duodenum, dissect approximately 1.5 cm of the posterior duodenum off of the pancreas. Divide the duodenum just distal to the pylorus with a GIA-style linear stapler. Send a frozen section biopsy of the margin of duodenal stump to confirm the presence of duodenal Brunner’s glands to avoid retained antrum. Following the antrectomy, either a Billroth I gastroduodenal anastomosis or a Billroth II gastrojejunostomy is constructed. A Billroth I requires at least 1 cm of healthy duodenum and in the case of significant scarring it is difficult to perform. A Billroth II is the default reconstruction and can almost always be performed. For a Billroth I reconstruction, the staple line of the transected duodenum is excised and an end-to-end gastroduodenal anastomosis is performed in two layers. The inner layer consists of full-thickness continuous sutures. The outer layer consists of interrupted seromuscular Lembert sutures. A crown stitch is placed at the “angle of sorrow” of the gastroduodenal anastomosis. If a Billroth II is to be constructed, then the duodenal stump is closed in two layers. The Billroth II gastrojejunostomy is begun by choosing a loop of proximal jejunum and bringing it antecolic or retrocolic to the stomach. If a retrocolic approach is chosen, care must be taken to close the mesenteric defect to reduce the risk of a future internal hernia. The jejunum is aligned along the gastric pouch and a two-layered gastrojejunostomy is performed. A crown stitch is placed at the “angle of sorrow” at the medial margin of the gastrojejunal anastomosis. Any exposed staples from the antrectomy should be oversewn.
Pitfalls
• Incomplete removal of the antrum increases the risk of developing a marginal ulcer.
• For the Billroth II reconstruction, it is important to properly close the duodenal stump to prevent future leaks that could be complicated by fistula formation or pancreatitis.
• Splenic injury may occur secondary to downward traction on the greater curvature of the stomach.
c. Parietal cell/proximal vagotomy (Table 4) (Figure 2): The goal of the parietal cell vagotomy is to eliminate vagal stimulation of the acid-secreting portion of the stomach, while retaining motor innervation to the antrum and pylorus. The receptive relaxation of the stomach is still affected by this procedure, and liquid emptying from the stomach is accelerated, but solid emptying is normal. This procedure reduces the basal acid secretion by 75% and the stimulated acid secretion by 50%. The HSV has low mortality (risk < 0.5%) and morbidity but has a high ulcer recurrence rate especially with inexperienced surgeons.
TABLE 4. Parietal Cell Vagotomy Key Points
FIGURE 2 • Truncal and proximal vagotomy. (Figure 46.1 in Mulholland MW. Gastroduodenal ulceration. In: Mulholland MW, Lillemoe KD, Doherty GM, et al., eds. Greenfield’s Surgery: Scientific Principles and Practice. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2006:722–735).
Procedure: The initial exploration is as described for truncal vagotomy. The anterior nerve of Latarjet, which is the termination of the left vagus nerve, is identified and encircled. Then the lesser sac is examined for adhesions to the pancreas and then entered by dividing the gastrocolic ligament, while preserving the gastroepiploic arcade. Next, the lesser omentum is divided from the lesser curvature between the incisura angularis and the cardia, by dividing all of the blood vessels and nerves that enter the lesser curvature. The dissection begins just proximal to the crow’s foot of the nerve of Latarjet and proceeds proximally along the lesser curvature to the left side of the gastroesophageal junction. The neurovascular branches should be ligated with 3-0 or 4-0 silk sutures and divided. Then the stomach is reflected upward and the posterior denervation is conducted in a similar manner. Then the nerve fibers and blood vessels on the lower 5 to 7 cm of the esophagus must be dissected and ligated.
Pitfalls
• Recurrent ulcers may be the consequence of an inadequate proximal vagotomy.
• Careful dissection around the lesser curvature of the stomach is important to decrease the risk of injury to the lesser curve.
Special Intraoperative Considerations
Laparoscopic repair: Omental patch repair of ulcers <1.0 cm may be performed by either an open or laparoscopic approach. A randomized controlled trial of 121 patients with perforated peptic ulcers reported that the laparoscopic group had significantly lower analgesic requirements, postoperative hospital length of stay, and returned to work significantly earlier than the open group. There were no significant differences between the two groups in mortality, incidence of reoperation, or postoperative intra-abdominal fluid collections.
Giant perforated ulcers: There is no standard management for giant perforated ulcers (>2 to 3 cm). Recommendations for repair have included omental patch, controlled tube duodenostomy, jejunal pedicled graft, jejunal serosal patch, free omental plug, partial gastrectomy, and pyloric exclusion. The choice of repair will be influenced by the patient’s status, the size of the perforation, the degree of intraperitoneal contamination, and the surgeon’s experience.
Posterior perforation: Spontaneous posterior perforation of a duodenal ulcer is rare. A definitive ulcer operation is typically undertaken, though there is no standard treatment.
Perforated gastric cancer: Though perforation is a rare complication (<1%) of gastric cancer, a biopsy and frozen section should be taken during surgery for all gastric perforations. Options for the surgical repair of a perforated gastric cancer include omental patch, emergency gastrectomy, and a two-stage radical gastrectomy.
Perforation at the gastroesophageal junction: The operative approach to perforation of an ulcer located next to the esophagogastric junction may include a subtotal gastrectomy to include the ulcer with a Roux-en-Y esophagogastrojejunostomy or a vagotomy with antrectomy.
Postoperative Management
H. pylori infection should be treated with triple therapy for 10 to 14 days; a common treatment regimen is clarithromycin, amoxicillin, and omeprazole. Following treatment conclusion, H. pylori eradication should be confirmed. Patients should receive counseling regarding NSAID use.
Postoperative complications include the following:
1. An early ulcer recurrence with leak is often treated with reexploration and may require gastric resection to adequately repair.
2. An uncontained leak after omental patch may require reexploration and gastric resection with a Billroth II.
3. Subphrenic and subhepatic abscesses are associated with a surgery delay >12 hours.
4. A patient should be evaluated for duodenal obstruction if gastric emptying is not normal by the eighth postoperative day.
5. Wound infection
6. Pneumonia
7. Pancreatitis
In patients following a definitive ulcer surgery there are also the following risks:
1. Diarrhea following truncal vagotomy occurs in 5% to 10% of patients. It typically occurs 1 to 2 hours following a meal. This problem usually resolves without intervention. Persistent symptoms may be improved by cholestyramine and/or loperamide. If medical therapy does not improve symptoms, a surgical option includes placement of a reversed jejunal interposition placed 100 cm distal to the ligament of Treitz.
2. Dumping syndrome occurs in 5% to 10% of patients following distal gastrectomy, pyloroplasty, or pyloromyotomy. It is classified as either early dumping, occurring within 30 to 60 minutes of eating; or late dumping, occurring 2 to 3 hours following a meal. Symptoms of early dumping include fatigue, facial flushing, lightheadedness, diaphoresis, palpitations, cramping abdominal pain, nausea, vomiting, and diarrhea. Symptoms of late dumping are typically limited to vasomotor symptoms. Treatment of these symptoms with dietary manipulation is often successful. Octreotide may be useful in severe cases. Octreotide, administered prior to meals, has been shown to improve both gastrointestinal and vasomotor symptoms. Remedial surgery is an option for patients with dumping symptoms resistant to medical management; however, this approach is typically not used because most patients do eventually respond to conservative therapy.
3. Following elimination of the pyloric sphincter bile can reflux into the stomach. Alkaline reflux gastritis develops in 2% of patients. It is characterized by epigastric pain and nausea that is provoked by meals. Medical therapy with cholestyramine may improve symptoms. Cases resistant to medical management may be treated surgically with a Billroth II gastrojejunostomy with Braun enteroenterostomy, Roux-en-Y gastrojejunostomy, or a Henley loop.
4. Early satiety with epigastric fullness and emesis with meals may develop secondary to gastric stasis, having a small gastric remnant, or from postsurgical atony. Atony may be confirmed with a solid food emptying test and then treated with a prokinetic agent, or if that fails, gastric pacing or completion gastrectomy. Symptoms of a small gastric remnant typically improve with small frequent meals.
5. Following Billroth II construction, the limb may become obstructed and cause afferent and efferent loop syndromes. Afferent loop syndrome is characterized by postprandial epigastric pain and non-bilious vomiting that is relieved following bilious vomiting. Efferent loop syndrome is characterized by epigastric pain, distention, and bilious vomiting. Both syndromes are treated with a surgical approach.
TAKE HOME POINTS
· Early diagnosis and operation are associated with improved outcome.
· It is important to identify prior NSAID use.
· It is important to identify H. pylori infection.
· Surgical goals are to control the perforation and lavage the abdominal cavity.
· Although rarely required, definitive ulcer operation may be required in select patients.
· Gastric perforation should prompt consideration of underlying gastric cancer.
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