Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_616_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
30.08.2026
Размер:
66 Мб
Скачать
FIG. 5 Cervical esophagus exposure. Incision
Omohyoid remnant
https://t.me/medicina_free
is made over the anterior border of the sterno­cleidomastoid muscle. If necessary, the middle thyroid vein and inferior thyroid artery can be ligated. Medial retraction of the trachea and thyroid gland is performed to help expose the esophagus. (From Cooke DT, Lau CL. Primary repair
of esophageal perforation. Op Tech Thor Cardiovasc Surg. 2008;13[2]:126–137.)
Trachea
Esophagus
Carotid a.
ESOPHAGUS
Stump of middle thyroid v.
79
Perforations of the abdominal esophagus can be approached via an upper midline incision. Once debrided, the perforation should be closed primarily and buttressed with omentum or, more commonly, a fundoplication.
Nutritional Management Following Repair
Traditionally, following transthoracic repair, patients were immedi­ately repositioned for a laparotomy and underwent placement of a gastrostomy tube for gastric decompression and a jejunostomy tube for nutritional access. This has become less commonly performed over time. If patients are requiring inotropic support following the repair, spending extra time in the operating room to place these tubes is not warranted. Furthermore, if the repair is successful, oral nutrition may be able to be started within 1 week, obviating the need for the feeding tube. To promptly begin nutritional support, as an alternative to a surgical feeding tube, a Dobhoff tube may be placed at the time of the repair under direct vision before the repair has been completed. The tube can then be advanced to a post-pyloric position postop­eratively to allow early initiation of enteral feeding. An NGT could also be placed at this same time to allow for gastric decompression if the surgeon feels this is necessary. Early initiation of total paren­teral nutrition is another option. Regardless of the initial nutritional strategy, an esophagram is obtained approximately 5 to 7 days after surgery depending on the patient’s condition. If no leak is identified, liquids may be started and slowly advanced to a soft diet. If there is a persistent leak, this may be managed with subsequent stent placement, which may seal the leak. If the leak persists following stent placement, the patient will require jejunostomy tube placement as several weeks or more will likely be required for healing of the perforation. Although it can be difficult to maintain patience, ultimate healing is still very likely to occur following adequate mediastinal debridement, appropri­ate antibiotic therapy, and good nutritional support.
Resection with Diversion
Although every attempt should be made to preserve the patient’s esophagus, there are rare instances in which this is not possible. These include long (generally >6 cm) perforations that are not amenable to stenting, a large segment of devitalized esophagus, which generally is
seen with long delays in diagnosis, or perforated cancers that cannot be stented because of the size of the perforation or tumor. In stable patients, when large defects are encountered, options like stenting followed by operative coverage of the defect with biodegradable mesh and a muscle flap, such as the serratus anterior or latissimus dorsi, can be considered. Although the healing process will take months, an intact, functional esophagus is still possible. Previous reports have described use of a T-tube to create a controlled esophageal fistula for management of very large defects. This is often cumbersome to care for postoperatively and has generally been abandoned. When repair is deemed not to be possible, esophageal exclusion is recommended over resection and immediate reconstruction. The risk of anasto­motic failure in patients who are hemodynamically unstable and/or have significant mediastinal contamination is very high.
Once the decision has been made to perform an esophageal exclusion procedure, the esophagus should be mobilized as much as possible in the chest. The esophagus is dived as far distally as possi­ble near the gastroesophageal junction with a 45-mm stapler. After the chest is closed, the patient is then turned to the supine position. A left-sided neck incision is made along the anterior border of the SCM, as described for cervical esophageal perforations. The esoph­agus should be dissected circumferentially with care taken to avoid injury to the recurrent laryngeal and vagus nerves. Once mobilized from the prevertebral fascia and posterior mediastinum, the esoph­agus is elevated into the wound. It is vital to preserve as much viable esophagus as possible to aid in future reconstruction. After the esophagus has been transected, it is tunneled subcutaneously onto the left chest, and an end esophagostomy is created. A jejunostomy tube is then placed. If the surgeon wishes to place a gastrostomy tube for gastric decompression, care must be taken not to compromise the use of the stomach as a conduit for later reconstruction.
Special Situations
Malignancy
When esophageal perforation involves a malignancy, consideration must be given to the treatment of both problems. If drainage is ade­quate, placement of an esophageal stent to control contamination is favored, reserving resection and anastomosis for a later time. If the
80 MANAGEMENT OF ESOPHAGEAL PERFORATION
https://t.me/medicina_free
patient is found to have massive contamination with hemodynamic instability not amenable to stent placement, resection, cervical esophagostomy, tube placement, and gastrostomy should be consid­ered as described earlier.
Achalasia
Patients with a known diagnosis of achalasia with perforation require special consideration. These patients may experience esophageal perfo­ration during pneumatic dilation, at the time of myotomy, or with other previously mentioned mechanisms. Because of the elevated intralumi­nal pressure proximal to the esophageal sphincter, healing of the repair often is precluded. Following repair of the perforation, these patients require myotomy for adequate healing. The myotomy should be per­formed on the opposite side of the esophagus from the perforation.
S u g g e S t e d R e a d i n g S
Abbas G, Schuchert MJ, Pettiford BL, etal. Contemporaneous management
of esophageal perforation. Surgery. 2009;146(4):749–755; discussion 755–756.
Axtell AL, Gaissert HA, Morse CR, et al. Management and outcomes of
esophageal perforation. Dis Esophagus. 2022;35(1):doab039.
Ben-David K, Behrns K, Hochwald S, etal. Esophageal perforation manage-
ment using a multidisciplinary minimally invasive treatment algorithm. J Am Coll Surg. 2014;218(4):768–774.
Fadoo F, Ruiz DE, Dawn SK, Webb WR, Gotway MB. Helical CT esophagog-
raphy for the evaluation of suspected esophageal perforation or rupture. AJR Am J Roentgenol. 2004;182(5):1177–1179.
Kaman L, Iqbal J, Kundil B, Kochhar R. Management of esophageal perfora-
tion in adults. Gastroenterology Res. 2010;3(6):235–244.
Kamarajah SK, Bundred J, Spence G, Kennedy A, Dasari BVM, Griffiths EA.
Critical appraisal of the impact of oesophageal stents in the management of oesophageal anastomotic leaks and benign oesophageal perforations: an updated systematic review. World J Surg. 2020;44(4):1173–1189.
Norton-Gregory AA, Kulkarni NM, O’Connor SD, Budovec JJ, Zorn AP,
Desouches SL. CT Esophagography for evaluation of esophageal perfora­tion. Radiographics. 2021;41(2):447–461.
Rausa E, Asti E, Aiolfi A, Bianco F, Bonitta G, Bonavina L. Comparison of
endoscopic vacuum therapy versus endoscopic stenting for esophageal leaks: systematic review and meta-analysis. Dis Esophagus. 2018;31(11).
Schweigert M, Sousa HS, Solymosi N, etal. Spotlight on esophageal perfora-
tion: A multinational study using the Pittsburgh esophageal perforation severity scoring system. J Thorac Cardiovasc Surg. 2016 Apr;151(4):1002–
1009.
Watkins JR, Farivar AS. Endoluminal therapies for esophageal perforations
and leaks. Thorac Surg Clin. 2018;28(4):541–554.
S
https://t.me/medicina_free
Benign Gastric Ulcer
Daniel T. Dempsey, MD, MBA
enign gastric ulcer is a discrete macroscopic wound in the lumi­nal surface of the stomach, extending into the submucosa or
B
muscularis propria and rarely to the serosa of the organ. It is gener­ally believed to start as a mucosal defect that remains unrepaired and deepens because of an imbalance between gastric mucosal defenses and aggressive luminal forces, primarily acid and pepsin. The early natural history of benign gastric ulcer is poorly understood, but most patients presenting to a surgeon with this problem are believed to have had the ulcer for weeks or months or even years. However, gastric ulcers related to drugs (nonsteroidal antiinflammatory drugs [NSAIDs] or cocaine) or stress may form and create clinical prob­lems more rapidly. Most gastric ulcers are caused by (or strongly associated with) Helicobacter pylori infection, NSAID use (including aspirin), smoking, or physiologic or psychological stress. There are undoubtedly other factors that play a role in ulcer formation and healing, such as abnormalities in locoregional gastric blood flow, gastroduodenal motility, or duodenogastric reflux.
It is likely that microscopic defects occur commonly in the surface epithelial layer of the gastric mucosa. These are repaired by a process of rapid restitution, restoring an intact layer of surface epithelial cells (SECs). Numerous mucosal defenses are necessary for this local healing process to occur, lest luminal acid and pepsin enter the lamina propria, causing further tissue damage. The mucus secreted by the SECs forms a physiologic bandage over the denuded mucosa, while healthy SECs move in from the periphery to recon­stitute an intact epithelial layer. Mucosal blood flow is augmented during this process. Prostaglandins are important mediators. The causes of gastric ulcer described above interfere with these muco­sal defenses. NSAIDs and aspirin block prostaglandin production. Smoking decreases mucosal blood flow. Helicobacter causes chronic mucosal inflammation, priming the lamina propria with inflamma­tory cells and mediators, which interfere with local defenses. These inflammatory cells are probably upregulated when the mucosal layer breaks, exposing them to acid and pepsin. Helicobacter infection also interferes with acid and gastrin secretion. Severe physiologic or psychologic stress can interfere with mucosal blood flow, gastric motility, and acid secretion.
TYPES OF BENIGN GASTRIC ULCER
Johnson initially defined three types of gastric ulcer (Fig. 1). Type 1 ulcers are the most common benign gastric ulcer. They typically occur at or near the angularis incisura on the lesser curvature of the stomach where the parietal cell containing body transitions to the gastric antrum (locus minoris resistentiae). Type 1 gastric ulcers are
not associated with gastric acid hypersecretion, and thus vagotomy has not traditionally been part of the surgical treatment. Type 2 ulcers usually occur in the distal stomach and are associated with duodenal ulcer disease, either active or chronic. Type 3 ulcers occur in the prepyloric region. Pathophysiologically, type 2 and 3 gastric ulcers are believed to resemble duodenal ulcers, and thus truncal vagotomy to ameliorate acid hypersecretion has been part of the surgical treatment. Recently two additional types of gastric ulcer have been described, resulting in a “modified Johnson classification” (Table 1). Type 4 gastric ulcer occurs high on the lesser curvature near the gastroesophageal (GE) junction. Excision of type 4 ulcers may get close to the esophagus, requiring Roux reconstruction (Csendes operation). Type 5 gastric ulcers are believed to be drug induced and typically occur toward the greater curvature, making them amenable to simple wedge resection. Neither type 4 nor 5 gas­tric ulcers are believed to be associated with acid hypersecretion, so vagotomy is probably unnecessary.
SURGICAL OPTIONS FOR GASTRIC ULCER
When operating on a patient with gastric ulcer, the choice of opera­tion depends on a variety of technical and clinical factors, which will be discussed further below. Fundamentally, operations for gastric ulcer fall into two categories: those that excise the ulcer and those that do not (Table 2). If the ulcer is not excised, it must be biopsied to rule out cancer. Formal gastric resection with anastomosis is avoided in unstable patients. Before embarking on resection, it is prudent to assess during surgery whether the ulcer involves the pancreas, portal triad, or celiac artery or branches. For low-risk patients with distal gastric ulcers, distal gastrectomy with (type 2 and 3 ulcers) or without (type 1 ulcers) truncal vagotomy is the treatment of choice. Reconstruction consists of Billroth 1 gastroduodenostomy or Billroth 2 gastrojejunostomy (Fig. 2). The latter may be preferred when there is concomitant duodenal ulcer disease (type 2 gastric ulcer). With both types of reconstruction, we prefer to do the anas­tomosis to the greater curvature side of the gastric remnant. Roux reconstruction is much preferred with small gastric remnants when the gastrojejunostomy is close to the GE junction, but it should be avoided with large gastric remnants. For low-risk patients with high gastric ulcers (type 4), distal subtotal gastrectomy and in-continuity excision of the high lesser curvature ulcer can be considered, with reconstruction via Roux-en-Y esophagogastrojejunostomy (Csendes procedure) if resection encroaches on the gastric cardia (Fig. 3). For type 4 ulcers that are more distally located (or type 1 ulcers that are unusually proximal), a more limited distal gastric resection and lesser curvature extension can be performed, with reconstruction by gastrojejunostomy (Billroth 2 or Roux) (Pauchet procedure). Simple wedge resection is a good option for type 5 gastric ulcers, but it is difficult to perform for prepyloric ulcers (type 2 and 3), juxtacardial
81
gastric an
https://t.me/medicina_free
82 BENIGN GASTRIC ULCER
Type I
lesser
curve
Type II
combined
juxtoesophageal
FIG. 1 Types of gastric ulcer. (From Matthews JB, Silen W. Operations for pep-
tic ulcer disease and early operative complications. In: Sleisenger MH, Fordtran JS, eds. Gastrointestinal disease. Philadelphia: Saunders; 1993.)
d
duodenal
Type IV
drug related
Type III
prepyloric
Type V
TABLE 1 Modified Johnson Classification
Type Location Acid Hypersecretion
I Lesser curvature, incisura No II Body of stomach, incisura, and
duodenal ulcer (active or
healed) III Prepyloric Yes IV High on lesser curve, near gas-
troesophageal junction V Anywhere (medication induced) No
Yes
No
TABLE 2 Choice of Operation for Gastric Ulcer
by Type*
Gastric Ulcer Type Option 1 (Resect Ulcer) Option 2 (Biopsy Ulcer)
1 Distal gastrectomy Vagotomy and drainage
(with or without wedge excision)
2 Distal gastrectomy and
Vagotomy and drainage
vagotomy
3 Distal gastrectomy and
Vagotomy and drainage
vagotomy
4 Csendes or Pauchet
procedure
Kelling-Madlener
procedure, or vagotomy and drainage
5 Wedge resection Patch/oversew
*Simple patch or oversew with biopsy is a reasonable option for all types of gastric ulcer in unstable patients.
INDICATIONS FOR OPERATION
Most patients with benign gastric ulcer never see a surgeon. They present to primary care or gastrointestinal (GI) practices or emer­gency departments, with complaints of upper abdominal pain, nausea, vomiting, or iron deficiency anemia. These complaints are evaluated with upper endoscopy with or without upper GI radiol­ogy. If a gastric ulcer is diagnosed, it is aggressively biopsied to rule out gastric cancer. If biopsy and cytology specimens are benign, the patient is treated with acid suppression, and the causative factors discussed above (H. pylori, NSAIDs, smoking) are eliminated if possible. Then the upper endoscopy is repeated in 2 to 3 months to document ulcer healing and to perform repeat biopsy. With this approach, the likelihood of misdiagnosing a gastric adenocarcinoma or lymphoma as a benign gastric ulcer is 1%.
If helicobacter is eradicated, NSAID and aspirin use is stopped, and smoking is eliminated, almost all gastric ulcers will heal with a 2- to 3-month course of proton pump inhibitor therapy, and recurrence or nonhealing is unusual. But, if helicobacter infection, NSAID or aspirin use, or smoking persists, recurrent gastric ulcer is the rule after the cessation of acid suppression. It is doubtful that definitive operation can completely nullify this fact, although recurrence of peptic ulceration (gastric or marginal ulcer or both) may be delayed after operation. For optimal results after operation for gastric ulcer, it is very important to strive for and document after surgery the absence of helicobacter infection, NSAID use, and smoking. Vagotomy or long-term acid suppressive medication may prevent recurrent peptic ulcer in some patients, and clearly patients having operation for gastric ulcer who require long-term NSAIDs or aspirin should receive long-term acid-suppressive medication. Selective COX-2 inhibitors should be considered in patients with ulcers requiring NSAIDs because these may have a lower risk of peptic ulceration.
ulcers (type 4), and ulcers on the lesser curvature. For type 2 and 3 gastric ulcers that are left in situ, truncal vagotomy and gastro­jejunostomy (with ulcer biopsy) may be a reasonable alternative to distal gastric resection. Similarly, for type 4 gastric ulcers, distal gastrectomy without ulcer excision (but with ulcer biopsy) can be considered (Kelling-Madlener operation).
PERFORATED GASTRIC ULCER
The most common indication for operation in benign gastric ulcer is perforation. Patients with gastric ulcer perforation present with acute abdominal pain and tenderness, usually with signs of peri­toneal irritation (i.e., rebound tenderness and referred rebound tenderness). Because of the severity and acuteness of the symptoms, these patients most commonly present to the emergency department
STOMACH
BA C
https://t.me/medicina_free
FIG. 2 Three types of reconstruction after distal gastrectomy. (A) Billroth I: A gastroduodenostomy is performed toward the greater curvature.
(B) Billroth II: A gastrojejunostomy is created to reestablish the alimentary transit. Several variations may be observed in this type of reconstruction. (C) Roux-en-Y: To prevent biliopancreatic reflux into the stomach, a 50-cm to 60-cm Roux limb is anastomosed to the stomach with the biliopancreatic
limb brought in 50 to 60 cm distal to the gastrojejunostomy. (Modified from Ginsburg GG, Kochman ML, Norton ID, Gostout CJ. Clinical gastrointestinal endoscopy. 2nd ed. Philadelphia: Elsevier, 2011.)
83
FIG. 3 Operations for a type 4 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.)
where computed tomography (CT) scanning reveals free intraperito­neal air, usually with free fluid as well. If water-soluble oral contrast has been administered, the scan often reveals extravasation from the stomach. Gastric wall thickening is difficult to evaluate on CT if the stomach is collapsed. Simple upright chest radiography usually shows free air under the diaphragm, but this classic radiologic find­ing may be absent in 20% of patients with perforated gastric ulcer.
Intravascular volume depletion is the rule, so fluid resuscitation begins with 1 to 2 L of isotonic fluid. Induction of general anesthesia in the patient with severe hypovolemia may result in cardiovascular collapse and cardiac arrest. Intravenous antibiotics (cefazolin and fluconazole) are administered. Careful insertion of a nasogastric (NG) tube before surgery for gastric decompression is prudent, espe­cially if water-soluble oral contrast has recently been administered
or if imaging shows gastric distention. Operation is planned to occur usually within 2 hours of presentation. Rarely, nonoperative treatment is indicated if the patient is clinically stable, without signs and symptoms of sepsis, and with good radiologic evidence that the perforation has sealed.
Operation may be done open or laparoscopically. Copious irri­gation of the soiled peritoneal cavity is performed with 5 to 10 L of warm saline. The entire anterior surface of the stomach is inspected. If no perforation is seen, the lesser sac is entered through the gastro­colic omentum and irrigated and the posterior stomach inspected. If still no perforation is found, it may be along the greater or lesser cur­vatures. If the patient is hemodynamically unstable or a poor opera­tive risk, the perforated gastric ulcer should be biopsied and closed, either with a Graham (omental) patch or with a wedge resection of
84 BENIGN GASTRIC ULCER
https://t.me/medicina_free
TABLE 3 Choice of Operation for Gastric Ulcer by Indication
Indication Option 1 Option 2 Option 3
Perforation Patch or wedge excision Patch or wedge excision with vagotomy and
drainage Bleeding Oversew or wedge excision Oversew with vagotomy and drainage Distal gastrectomy* Obstruction Vagotomy and distal gastrectomy Vagotomy and gastrojejunostomy Nonhealing/Intractability Distal gastrectomy (with vagotomy for
type 2 and 3)
*Consider addition of vagotomy for type 2 and 3 gastric ulcer.
Wedge excision with vagotomy and drainage
Distal gastrectomy*
TABLE 4 Rockall Score to Assess Rebleeding and Mortality Risk in Upper Gastrointestinal Bleeding
Variable 0 Points 1 Point 2 Points 3 Points
Age (yr) <60 61–79 >80 Shock None P >100; BP >100 systemic BP <100 systemic Comorbidity None CHF, ASCVD, COPD Renal or liver failure; metastatic cancer Diagnosis Mallory-Weiss All other GI cancer Bleeding stigmata None Visible vessel, active bleeding
ASCVD, Atherosclerotic cardiovascular disease; B P, blood pressure; CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; GI, gastrointestinal; P, pulse.
the ulcer (Table 3). The latter is appropriate for perforations that occur along the greater curvature, or on the anterior or posterior sur­face of the proximal stomach. In the low-risk patient who is hemody­namically stable, definitive operation can be considered, either distal gastrectomy, including the ulcer in the specimen (vagotomy should be considered for type 2 and type 3 ulcers), or vagotomy and drain­age with ulcer biopsy and closure for inconveniently located ulcers (high juxtacardiac ulcers, peripyloric ulcers with scarred duodenum or inflammatory mass). Giant (>2 cm) perforated gastric ulcers may be too big to securely patch with omentum and thus may require resection. If resection is deemed hazardous, it may be possible to achieve closure by anastomosing the perforation to a Roux limb (mucosa to mucosa). Before closure of the abdomen, the NG tube is positioned appropriately in the stomach and secured to the nose. We test the repair with both air insufflation and methylene blue via the NG tube. If postoperative reinsertion of the prematurely pulled NG is deemed a risk to the ulcer repair or suture line, it should be sutured or “bridled” to the nose before leaving the operating room. After surgery antibiotics are continued until the patient is fever free with a normal white blood cell count. Once GI function has returned, gas­trografin swallow is performed before the initiation of a liquid diet. Leakage at the repair site is managed without surgery, if adequately drained and the patient is doing well. Otherwise, early reoperation is necessary, the primary goal of which is to achieve adequate drainage of the leak, and enteral access for proximal decompression (e.g., gas­trostomy) and feeding distally (e.g., jejunostomy).
BLEEDING GASTRIC ULCER
Although still a common reason for hospitalization, bleeding gastric ulcer is increasingly less common as an indication for operation. This is likely due to the increasing effectiveness of medical and endoscopic treatment for bleeding gastric ulcer. The most common cause of GI bleeding in hospitalized patients is peptic ulcer, and annually in the United States a few thousand patients die of peptic
ulcer bleeding. About half of these patients succumb to bleeding gastric ulcer. Essentially all the deaths from bleeding ulcer occur in patients with risk factors for persistent or recurrent bleeding. Thus, it is important to identify this high-risk group, which represents about one-quarter of patients admitted to the hospital with bleeding peptic ulcer. Risk assessment tools have been developed for this, such as the Rockall score (Table 4). None of these tools can predict with 100% accuracy who does and does not have a life-threatening ulcer bleed, but they are useful as guides. Patients with a Rockall score of 0 to 1 are very unlikely to have a life-threatening GI hem­orrhage, whereas patients with a score from 9 to 11 may very well succumb to the bleed. In general, patients at high risk present with hematemesis, hypotension, or the requirement for multiple units of blood transfusion. These patients require early surgical consulta­tion. Urgent upper endoscopy often shows high-risk endoscopic fea­tures, such as active bleeding or visible vessel in the ulcer base. Such patients should have endoscopic hemotherapy consisting of cautery, injection of epinephrine, and application of clips. Intravenous acid suppression and fluid resuscitation are important. Rebleeding can usually be managed with repeat endoscopic therapy, but angiogra­phy with possible embolization should also be considered. In the occasional patient in whom these modalities fail, operation should be considered. In general, candidates for operation for bleeding gastric ulcer have been transfused more than a few units of blood, have recurrent or refractory hemorrhagic shock, or have ulcer ero­sion into a large artery such as the left gastric or splenic artery. The operative mortality rate is around 25%.
Biopsy and oversewing of the bleeding ulcer is the appropriate operation for high risk or hemodynamically unstable patients. Wedge resection should be considered for bleeding ulcers on the greater curvature or free wall of the proximal stomach. Formal resec­tion should be reserved for good risk and hemodynamically stable patients. Rebleeding is more common when the ulcer is not resected, but ultimate hospital mortality is similarly high in patients who are initially managed with oversewing and those initially managed with
STOMACH
https://t.me/medicina_free
85
resection. Postoperative bleeding might respond to angiographic embolization.
OBSTRUCTING GASTRIC ULCER
The most common cause of gastric outlet obstruction in the adult patient is cancer (pancreatic, duodenal, or gastric). So, when consid­ering operation for obstructing distal gastric ulcer, the surgeon must ask whether the patient might have malignant obstruction. Whereas upper endoscopy, biopsy, contrast radiography, endoscopic ultra­sound, CT, or magnetic resonance imaging may all be reassuring that the obstruction is benign, misdiagnosis, although rare, remains a real possibility. The classic operation for obstructing gastric ulcer is vag­otomy and distal gastrectomy, but vagotomy and gastrojejunostomy may be an acceptable alternative. The latter procedure has a lower operative mortality risk, and, in the event of severe dumping, the gas­trojejunostomy is potentially reversible if gastric outlet patency can be maintained. However, distal gastrectomy confirms the absence of cancer. Vagotomy should be performed because obstructing gastric ulcers are likely to be Johnson type 2 or 3 lesions.
NONHEALING GASTRIC ULCER (INTRACTABILITY)
Operation for nonhealing gastric ulcer should be unusual today because our understanding of ulcer pathophysiology is more com­plete than ever. Acid suppression, eradication of helicobacter, elim­ination of NSAIDs, and smoking cessation should heal the ulcer. So why would the gastric ulcer persist? Could it be cancer? Is the patient noncompliant? Is there unrecognized gastric stasis or enterogastric reflux? Are there important factors in ulcer pathogenesis that we have not discovered yet? These are all important questions for the surgeon to consider before operating on a patient for nonhealing gastric ulcer. Furthermore, it must be recognized that patient non­compliance and unknown pathophysiologic factors may predispose to ulcer recurrence or poor functional results after gastrectomy for nonhealing ulcer. This may be particularly problematic in thin patients who are easy to operate on but who have insufficient nutri­tional reserves in the event of a poor functional outcome.
In the event that operation for nonhealing ulcer is necessary, the ulcer should be excised either with distal gastrectomy or wedge resection. This both excludes cancer and resects the vulnerable part of the stomach. If distal gastrectomy, the classic operation, is performed, then vagotomy should be added for type 2 and 3 gastric ulcers. If the ulcer is wedged out, then vagotomy and drainage should be added.
MARGINAL AND RECURRENT ULCER
Ulcers that occur at or near the gastroenterostomy are termed mar­ginal ulcers. They may occur on either side of the anastomosis. When
on the distal side, they are generally believed to be due to acid/peptic injury to small bowel mucosa, which is ill equipped to defend itself against unbuffered gastric juice. This occurs more commonly in Roux gastrojejunostomy because the anastomosis is devoid of the buffering effects of duodenal contents, which help protect a Billroth 2 anastomosis. When on the proximal side of the anastomosis, the ulcer is generally thought to be due to ischemia, stasis, foreign body (suture), bile reflux, or the circumstances that led to the gastric ulcer in the first place (recurrent ulcer). Marginal ulcer complicates Roux­en-Y gastric bypass in about 8% of patients, and presently this is the most common cause of marginal ulcer, which may also complicate gastrojejunostomy for cancer or ulcer.
The medical treatment of marginal ulcer is identical to gastric ulcer: acid suppression, eradication of helicobacter, elimination of
NSAIDs, and smoking cessation. Indications for operation are also identical to those for gastric ulcer: perforation, bleeding, obstruction, and intractability. The realization that reoperation for recurrent or marginal ulcer puts the patient at increased risk (and closer to total gastrectomy) underscores the importance of patient education and good management after the first ulcer operation, which includes minimizing the risk factors for ulcer recurrence. In addition to elim­ination of helicobacter, NSAIDs, and smoking, we consider every patient who has had an operation for gastric ulcer a candidate for lifelong acid suppression, unless the patient has had a vagotomy.
Perforated marginal ulcer may be treated with simple patch clo­sure, which is certainly appropriate in high-risk and unstable patients. It may also be the preferred treatment in patients with Roux-en-Y gastric bypass because resection may necessitate esophagojejunos­tomy. In stable low-risk patients with perforated gastrojejunostomy after distal gastric resection, resection of the anastomotic region (segmental jejunal resection with additional gastrectomy) is pre­ferred. The addition of truncal vagotomy may be considered. If the remaining gastric remnant is 30% or less, reconstruction should be Roux gastrojejunostomy to avoid bile reflux esophagitis. If the remaining remnant is larger than 30%, reconstruction should be via Billroth 1 or 2 technique to minimize recurrence of marginal ulcer­ation. If the original operation was a simple loop gastrojejunostomy, consideration may be given to reversal (if the gastric outlet is patent) or distal gastrectomy with Billroth 1 or 2 reconstruction.
Bleeding marginal ulcer can usually be managed without surgery with the help of endoscopic hemostatic techniques or angiographic embolization, unless the ulcer has eroded into a named visceral vessel such as the splenic, left gastric, or middle colic artery. Those patients requiring emergency operation may have torrential bleeding and often present with a less impressive “herald bleed.” Whereas gastroenterotomy and transluminal oversewing of the bleeding vessel may prove adequate, resection of the anastomotic region may be expeditious and safer. Postoperative angiographic embolization might complement the operation. Marginal ulcers associated with obstruction or intractability should be treated with elective resection of the anastomosis, followed by Roux or Billroth reconstruction, depending on how close the anastomosis is to the GE junction.
S u g g e S t e d R e a d i n g S
Abubaker A, Ahmed BH, Nussbaum MS. Surgery for peptic ulcer disease. In:
Yeo CJ et al, ed. Shackelford’s Surgery of the Alimentary Tract. 8th ed.; 2019. Byrge N, Barton RG, Enniss TM, Nirula R. Laparoscopic versus open
repair of perforated gastroduodenal ulcer: a National Surgical Quality
Improvement Program analysis. Am J Surg. 2013;206:957–963. Laine L. Upper gastrointestinal bleeding due to a peptic ulcer. NEJM.
2016;374:2367–2376. Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017;390:613–624. Lightner AL, Brunicardi FC. The management of benign gastric ulcers. In:
Cameron JL, Cameron AM, eds. Current Surgical Therapy. 12th ed.; 2017. Roses RE, Dempsey DT.Stomach, in Schwartz’s Principles of Surgery. In:
Brunicardi, etal (eds), 11th ed. McGraw Hill. Schroder VT, Pappas TN, Vaslef SN, etal. Vagotomy/drainage is superior to
local oversew in patients who require emergency surgery for bleeding
peptic ulcers. Annals of Surgery. 2014;259:1111–1118. Soreide K, Thorsen K, Harrison EM, etal. Perforated peptic ulcer. Lancet.
2015;386:1288–1298. Sverden E, Mattsson F, Lindstrom D, etal. Transcatheter arterial embolization
compared with surgery for uncontrolled peptic ulcer bleeding—a popula-
tion based cohort study. Annals of Surgery. 2019;269:304–309. Wang YR, Richter JE, Dempsey DT. Trends and outcomes of hospitalizations
for peptic ulcer disease in the United States, 1993 to 2006. Annals of
Surgery. 2010;251:51–58. Wilhelmsen M, Moller MH, Rosenstock S. Surgical complications after open
and laparoscopic surgery for perforated peptic ulcer in a nationwide
cohort. Br J Surg. 2015;102:382–387.
86 MANAGEMENT OF DUODENAL ULCERS
https://t.me/medicina_free
Management of Duodenal Ulcers
Daniel T. Dempsey, MD
INTRODUCTION
Duodenal ulcer is an acute or chronic localized wound of the duo­denal mucosa caused by acid/peptic injury. Superficial ulcers involve the submucosa; deeper ulcers involve the muscularis propria or the serosa and may penetrate posteriorly or perforate anteriorly. Common predisposing factors are Helicobacter pylori infection, use of nonsteroidal antiinflammatory drugs (NSAIDs) or aspirin, smok­ing, and stress. Less common causative factors include gastrinoma (Zollinger-Ellison syndrome), radiation, Crohn’s disease, cocaine, and gastroduodenal dysmotility. The most common symptoms of duodenal ulcer are abdominal pain, nausea, vomiting, and anemia.
The reasons for hospitalization resulting from duodenal ulcer are (in decreasing order) upper gastrointestinal (GI) bleeding, perfora­tion, obstruction, and intractability. Peptic ulcer is the most common cause of clinically significant upper GI bleeding requiring hospital­ization, but nowadays very few of these patients require operation. Currently the most common indication for operation in duodenal ulcer patients is perforation. Surgery for bleeding and obstruction is less common, and surgery for medically intractable duodenal ulcer is very uncommon. The operative (90-day) mortality rate for emer­gency peptic ulcer surgery is about 30%. After surgery for duodenal ulcer, recurrent ulcer can be minimized if all of the following condi­tions are met: eradication of H. pylori infection, diligent and perma­nent avoidance of NSAIDs and aspirin, and long-lasting abstention from smoking. If compliance with these management principles cannot be followed, eventual ulcer recurrence is likely. Testing for H. pylori infection should be performed in all patients with active peptic ulcer disease or a history of peptic ulcer disease unless previous cure of H. pylori infection has been documented. Testing should also be strongly considered if long-term aspirin or NSAIDs are required. All patients who test positive should be treated. Testing for H. pylori infection should be performed in all patients with peptic ulcer, mucosa-associated lymphoid tissue (MALT), early gastric cancer, and those on long-term aspirin or NSAID regimens (Box 1). With the appropriate 10- to 14-day multidrug regimen (which takes into account local antibiotic resistance and recent antibiotic usage) and patient compliance, H. pylori eradication will be confirmed in about 85% of patients who undergo a urea breath test, fecal antigen test, or endoscopic biopsy (H. pylori serology should not be used to test for cure of H. pylori infection). Consultation with a gastroenterologist or infectious diseases specialist with an interest and expertise in H. pylori treatment and cure should be considered.
If medically indicated, daily aspirin for cardiovascular prophy­laxis may be taken safely, provided a daily proton pump inhibitor (PPI) is also taken. It is not unreasonable to consider long-term PPI treatment (e.g., omeprazole 20 mg before breakfast) for all patients who have required hospitalization for duodenal ulcer unless a vag­otomy has been performed, particularly in patients for whom the above conditions cannot be assured. It is unclear whether definitive duodenal ulcer surgery (e.g., vagotomy and drainage; vagotomy and antrectomy [V/A]) is as effective in preventing ulcer recurrence as it was in the past. The acid suppressive effect of vagotomy may be no more profound than a properly taken PPI, but admittedly the former does not depend on patient compliance. Clearly, the concept that a more complex surgery is better should be used carefully and spar­ingly today in ulcer surgery, particularly during emergency surgery, which now is far more common than elective surgery. Gastrectomy
for duodenal ulcer should be avoided in thin or chronically malnour­ished patients.
MEDICAL MANAGEMENT OF DUODENAL ULCER
Most patients with duodenal ulcer are treated medically as outpa­tients and never seen by a surgeon. Typically, the diagnosis is made with esophagogastroduodenoscopy (EGD). Biopsy of duodenal ulcer is unnecessary, but gastric biopsies should be taken to rule out H. pylori infection. Medical management includes acid suppression with a PPI, diagnosis and treatment of H. pylori infection (present in up to 90% of duodenal ulcer patients), elimination of NSAIDs, smoking cessation, and (in the appropriate clinical setting) evaluation for gas­trinoma. Unless the patient has required hospitalization for an ulcer complication, long-term PPIs are not indicated. The obvious excep­tions are duodenal ulcer patients who require long-term NSAIDs, aspirin, or anticoagulants, all of whom require PPI ulcer prophylaxis.
Perforated Duodenal Ulcer
Duodenal ulcer perforation (Fig. 1), the most common indication for surgery, presents as an acute abdomen. The patient usually can pinpoint the onset of severe abdominal pain. There may or may not be a history suggestive of chronic duodenal ulcer. The longer surgery is delayed from the onset of perforation, the higher the mortality risk. On examination, the patient is very uncomfortable and loath to move. Tachycardia may be the only early vital sign abnormality. Fever and tachypnea then ensue, and hypotension is a late finding. The abdomen is rigid, and there is obvious peritonitis. Leukocytosis is common. Anemia suggests the possibility of a second, usually posterior, bleeding ulcer (“kissing ulcers”), which can be evaluated intraoperatively with direct inspection or EGD. An upright chest x-ray usually shows pneumoperitoneum (absent in 10% to 15% of cases). Computed tomography (CT) nearly always reveals extralu­minal air in the upper abdomen, often with free peritoneal fluid. The mortality risk of perforated duodenal ulcer in the modern era is high, up to 30% in some series. Although this may be caused in part by the frailty of the patient population affected, there is no doubt that delayed treatment increases mortality risk. Prompt fluid
BOX 1 Helicobacter pylori Tests
Tests for H. pylori (All Positive Patients Should Be Treated)
• Fecalantigentest
• Ureabreathtest
• Esophagogastroduodenoscopyandbiopsy
• Rapidureasetest
• Histology
• Culture
• Molecularreal-timepolymerasechainreaction(RT-PCR)
Some Common Helicobacter Treatment Regimens (10–14 Days)
• Clarithromycintripletherapy(PPI,clarithromycin,amoxicillin,
or metronidazole)
• Bismuthquadrupletherapy(PPI,bismuth,tetracycline,
nitroimidazole)
• Sequentialtherapy(PPIandamoxicillinfor5–7days,andthen
a PPI, clarithromycin, and nitroimidazole for 5–7 days)
• Hybridtherapy(aPPIandamoxicillinfor7days,andthena
PPI, amoxicillin, clarithromycin, and nitroimidazole for 7 days)
PPI, Proton pump inhibitor.
FIG. 1 Perforated duodenal ulcer.
https://t.me/medicina_free
resuscitation and intravenous (IV) antibiotics are important, but so is prompt surgery. Medical optimization, although necessary, should not be an excuse for prolonged delay in surgical treatment. In addi­tion to routine empiric broad-spectrum perioperative antibiotics, selective antifungal treatment may be considered in frail, immuno­suppressed, or hospitalized patients. Routine use of antifungal agents is not indicated. Rarely, a stable patient without peritonitis and with a radiologically documented sealed perforation may be cautiously managed nonoperatively. Laparotomy or laparoscopy with peritoneal washout (5 to 10 L) and omental patch closure of the perforation is the treatment of choice for most patients with a perforated duode­nal ulcer. Peritoneal fluid should be sent for culture and sensitivity (including fungal studies). Routine ulcer biopsy is not necessary but should be performed if there is any suspicion of malignancy. At least one closed-suction peritoneal drain is placed. Leakage at the repair site is not uncommon.
Omental Patching
Omental patching (Graham patching), a technique attributed to Dr. Roscoe Graham, is the most common method of perforated duodenal ulcer repair (Fig. 2). Typically, the hole in the duodenum is small (<1 cm) and is not repaired primarily before application of a well-vascularized tension-free piece of omentum. The duodenal tissue immediately adjacent to the perforation is friable, and attempts at primary closure often result in the sutures pulling through, enlarg­ing the hole considerably. Primary closure may also further narrow an already scarred gastric outlet. The omental patch is held in place by interrupted seromuscular Lembert sutures placed into healthy duodenum on either side of the perforation. We usually place two or three interrupted bridging sutures, lay the patch on, and then tie the sutures gently but snugly over the omental patch. This technique creates better apposition between the duodenum and the omentum than the technique of using the suture “tails” from a primary closure to secure the omentum (Fig. 3). If necessary, additional sutures may be placed circumferentially between the healthy duodenum and the omental patch. Once the patch is secure, the adequacy of the seal can be tested by submerging the site under irrigation fluid while injecting air and/or methylene blue into the nasogastric (NG) tube (which remains in place postoperatively), and a closed-suction peritoneal drain is placed.
Special Considerations for Large Ulcer Perforations
Large ulcer perforations (>2 cm) merit special considerations. They are difficult to securely close with the Graham patch technique described earlier, but primary repair of a large perforated chronic
STOMACH
FIG. 2 Graham patch of perforated duodenal ulcer. (From Townsend C.
Sabiston Textbook of Surgery, 21st ed. Philadelphia: Elsevier, 2021.)
2PHQWXP
6SDFHEHWZHHQ GXRGHQDOVHURVD DQGRPHQWXP
8OFHUSHUIRUDWLRQ
SOXJJHGZLWK
RPHQWXP
'XRGHQXP
FIG. 3 This technique creates better apposition between the omentum
and the duodenum. (From Yeo CJ. Shackleford’s Surgery of the Alimentary Tract. 8th ed. Philadelphia: Elsevier, 2019.)
87
duodenal ulcer is more prone to break down than primary repair of a similar-size acute duodenal laceration. And in the high-risk patient, an expeditious surgery is important. After peritoneal irrigation, the perforation is closed if possible with sutures or stapling, and the clo­sure is buttressed with omentum or a falciform ligament. If it can be done safely, a Kocher maneuver facilitates primary closure. Multiple drains are placed. If the large perforation cannot be closed primarily, it can be plugged with omentum or falciform, which is pulled into the perforation using double-armed sutures placed first in the plug and then “inside out” into the duodenum surrounding the perfora­tion (Fig. 4). Alternatively a loop of jejunum can be used as a serosal patch. Treatment of large perforations by direct intubation with or without an omental buttress is prone to ongoing leakage, but it can be used as a last resort or bailout procedure (Fig. 5). Multiple peritoneal drains are placed. In unstable patients, a damage control approach might be considered.
The fact that large perforated duodenal ulcers are hard to fix is indicated by the wide variety of (sometimes anecdotal) repair tech­niques. One useful ancillary procedure that has been evaluated with a retrospective controlled study is the triple-tube technique, which
88 MANAGEMENT OF DUODENAL ULCERS
https://t.me/medicina_free
FIG. 4 Technique to “pull” an omental patch into a large perforated
duodenal ulcer. (From Townsend C. Sabiston Textbook of Surgery. 21st ed. Philadelphia: Elsevier, 2021).
and quick, and we have never regretted using it in the setting of high­risk duodenal perforation. We much prefer this to lateral duode­nostomy or transpyloric intubation. For the most tenuous duodenal closures, we consider pyloric exclusion (pyloric closure with heavy absorbable suture and dependent loop gastrojejunostomy). One other option for repair of a large chronic duodenal perforation in a stable low-risk patient is a Roux-en Y duodenojejunostomy in which a tension-free two-layer anastomosis is created between the debrided duodenal opening and a Roux limb.
Definitive Ulcer Surgery
Definitive ulcer surgery can be considered in stable patients of low to medium risk (ASA 1 or 2) requiring emergency surgery for a perforated duodenal ulcer if there is a clinical history of duodenal ulcer, or if the perforation is large (>2 cm). Definitive surgery should not be performed if peritonitis is severe or well established (exu­dative). All of these contingencies (low-risk patient with a positive history or large perforation and without serious peritonitis) mean that the majority of patients with a perforated duodenal ulcer are not candidates for definitive ulcer surgery. Parietal cell vagotomy as a definitive ulcer surgery in this setting is largely of historical inter­est. Currently the two options for definitive surgery are (1) truncal vagotomy and gastrojejunostomy ([V/GJ] with or without temporary pyloric closure) after repair of perforation as described earlier; or (2) truncal V/A if the perforated duodenum can safely be resected with the antrum and a secure duodenal stump fashioned. If the ampulla is deemed to be at risk, a biliary Fogarty catheter can be advanced from above via the cystic duct or common bile duct. Resection should not be contemplated if a tenuous duodenal stump is likely or if injury to the ampulla or bile duct is an obvious possibility.
DJ
Gastrostomy
15 cm
Retrograde
duodenostomy
5 cm
Feeding
jejunostomy
FIG. 5 Triple tube technique for high-risk perforated duodenal ulcer.
should be considered in high-risk perforations, whether repaired as described earlier or with one of the more complex surgeries described later. This involves placement of a gastrostomy, antegrade feeding jejunostomy, and a retrograde jejunostomy tube that is passed into the duodenum for decompression. This technique is safe
Minimally Invasive Surgery
Minimally invasive surgery for perforated duodenal ulcer is now commonplace, and some studies suggest that the laparoscopic approach is superior to open operation. Laparoscopy confirms the diagnosis, including the size and location of the perforation and the severity of peritonitis. Thorough irrigation of the peritoneal cavity can readily be accomplished laparoscopically. Laparoscopic omental patch closure of the perforation is usually straightforward for the typ­ical small perforation. Even when conversion to open surgery is nec­essary, the laparotomy incision is smaller and optimally placed after laparoscopic evaluation. In the unlikely event that a definitive sur­gery is indicated, it can be performed either open or laparoscopically. Even a modest size perforation can be repaired laparoscopically, and vagotomy is straightforward for the minimally invasive surgeon with some foregut experience. A dependent loop gastrojejunostomy com­pletes the ulcer surgery. Two types of vagotomy may be considered: (1) the more traditional bilateral truncal vagotomy or (2) a modified Taylor procedure. The latter consists of posterior truncal vagotomy and division of the segmental vagal branches to the anterior stomach with preservation of the anterior innervation to the antropyloric region. This technique may facilitate gastric emptying.
Postoperative Management
Postoperative management for many perforated ulcer patients starts in the ICU with continued optimization of critical organ function, fluid management, and treatment of sepsis. The decision to remove the NG tube and initiate oral liquids is made on clinical grounds. Postoperative contrast study (fluoroscopy or CT) is usually per­formed to rule out ongoing leak and to demonstrate gastric empty­ing. Antibiotics are discontinued on postoperative day 5 unless there is obvious ongoing infection. Peritoneal drains are removed 24 hours after the initiation of oral liquids if drainage is benign and the patient is doing well. Reoperation is sometimes required for persistent leak­age from the perforation site or from abdominal wound dehiscence. Percutaneous drainage can be performed for localized infected fluid collections, but multiple fluid collections or extensive peritoneal fluid in the setting of sepsis may be a manifestation of uncontrolled