Добавил:
Sekretar
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_615_Библиотеки_им_академика_М_И_Перельмана
.pdf
ESOPHAGUS
https://t.me/med1917
77
hemodynamically stable without signs of sepsis or multiorgan failure, the patient is admitted to the surgical critical care unit for 48 to
72 hours of observation. Patients should be maintained NPO with
the head of the bed elevated, started on 72 hours of broad-spectrum
antibiotics and a PPI, and, dependent on premorbid nutritional status, considered for parenteral nutritional support. Repeat imaging is
obtained in 72 to 96 hours. If this demonstrates no evidence of free
perforation, a liquid diet may be initiated. It is important to remember that these patients require close observation to ensure that they
continue to meet nonoperative criteria. Should the patient’s clinical
condition deteriorate as evidenced by the development of fever, leukocytosis, tachypnea, tachycardia, or mental status changes, repeat
imaging and possible endoscopy are indicated.
Endoscopic Stenting with Thoracoscopic Mediastinal
and Pleural Drainage
For patients with evidence of free contrast extravasation into the
mediastinum, endoscopic covered stent placement or endoluminal
clipping to attempt to seal the perforation can be performed as an
alternative to open surgical repair. It is vital to remember that this
approach does not address the associated mediastinal and possible
pleural contamination. For this reason, early video-assisted thoracoscopic surgery (VATS), performed either immediately after stent
placement or within 1 to 2 days following the procedure, is generally
required for debridement and drainage of the mediastinum and
pleural cavity. At the conclusion of the VATS procedure, depending
on the degree of contamination, at least one chest tube is left in the
pleural space, and another (often a Blake drain) is left adjacent to the
esophagus. Typically, a contrast esophagram is performed 48 hours
after stent placement to determine if sealing of the esophageal perforation has occurred. If there is no evidence of extravasation, a clear
liquid diet can be started and advanced to full liquids. It is advisable
to leave the tube in place adjacent to the esophagus while the liquid
diet is being initiated to monitor the character of the output as well as
the patient’s clinical condition. On the other hand, if the esophagram
shows extravasation of contrast around the stent into the mediastinum or the drainage character changes after liquids are begun, the
patient should be returned to NPO status and will require placement
of a jejunostomy tube.
In their study, Ben-David et al. showed encouraging results in 76
patients with esophageal perforation (majority iatrogenic or spontaneous) managed with endoscopically placed metallic covered stents
in addition to laparoscopic or VATS drainage and enteral feeding
access placement. All patients were treated within 24 hours of initial
presentation, and perforation occlusion was confirmed within 48
hours after stent placement in 68 patients (89.5%). Additionally, no
need for an open esophageal procedure was required, avoiding the
morbidity of a more invasive operation. However, stent placement
was not without complications, with an almost 40% migration rate
requiring additional intervention within the first week of placement.
The ideal time for esophageal stent removal remains controversial
and may depend on the size of the perforation. Some studies have
shown adequate healing within 10 days for small perforations, while
this process may take up to 8 weeks for larger defects. Ben-David et
al. showed a mean length of 36 days from initial placement to final
stent removal. In practice, waiting between 4 and 6 weeks, depending
on the size of the perforation, is reasonable. Imaging confirmation of
perforation healing with an esophagram should be obtained following stent removal before a liquid diet is initiated. If the perforation
has not healed at the time of stent removal, the stent can be replaced
for another 4 to 6 weeks.
Endoscopic Techniques
The use of endoluminal stents for the management of esophageal
perforations is not a new concept, and in fact the most used self-expanding metal stents (SEMS) have been available since the 1990s.
Technology improvement with better deployment mechanisms have
also increased their use. The development of covered stents with different polymers has increased the technical and clinical success of the
management of esophageal perforations and, at the same time, has
decreased the rate of stent-related complications. Esophagogastroduodenoscopy (EGD) is performed to localize the defect, determine
the extent of the perforation, and identify anatomic landmarks and
other esophageal abnormalities. Under direct vision and with the
concomitant use of fluoroscopy, a careful assessment of the landing
zones and the desired diameter and length of the stent is conducted.
Once this assessment is completed, the landmarks for the proximal
and distal extent of the stent are marked with radio-opaque markers
under fluoroscopy. A guidewire is then introduced under fluoroscopy. Figure 3 shows an endoscopic view of a perforation and subse-
quent stent placement. Ideally, the stent deployment will successfully
cover the perforation on the first attempt, however the stent can be
endoscopically repositioned to achieve complete coverage of perforation if needed. If there is evidence of incomplete radial deployment,
a balloon dilation may be performed to attain complete contact
between the stent and esophageal mucosa. An NGT can be placed
under direct vision for gastric decompression in the acute setting. An
anteroposterior and lateral chest x-ray should be obtained after stent
placement to have a baseline for its location and facilitate further
assessment of adequate positioning. As noted, a contrast esophagram
should be obtained 48 hours after stent placement before liquids are
begun. Figure 4 shows a SEMS in adequate position without evidence
of contrast extravasation.
Stent complications include migration, bleeding, erosion, and tissue overgrowth, among others. Migration is the most common complication reported in about 8% to 40% of cases, with less migration
rates reported with the use of metallic stents compared with plastic
stents. Some studies have reported endoscopic suturing or clipping to
secure the stent and prevent migration with favorable results.
Endoscopic suturing or clip placement may also be used to
attempt to primarily repair small, early perforations. Previous reports
demonstrate higher rates of closure, with an average defect size of 8
mm and higher failure rates when the lesion is greater than 13 mm.
EGD is performed, and the esophageal defect is identified to confirm
healthy mucosal edges for adequate clip placement. Through-thescope clips can be used for defects less than 1 cm, and an over-thescope clip system can be used for larger lesions. Suction can be used
to help approximate the lesion edges and aid with better clip deployment. Even though acceptable results have been reported in the
literature, this technique is not commonly used given that patients
usually present with a more advanced disease process requiring more
aggressive interventions.
Open Repair
Currently, little data exist to guide surgeons as to whether to proceed with an open repair or choose stent placement with pleural/
mediastinal drainage. Elderly patients and those with multiple
medical comorbidities are likely better served with the endoscopic/
thoracoscopic approach. Although the likelihood of success of an
open repair diminishes over 24 hours from the perforation event,
several reports describe successful repairs being performed for
perforations beyond the 24-hour mark. Following initial resuscitation efforts, patients who remain hemodynamically labile may
still undergo successful repair, although a less invasive approach
has obvious advantages in these patients. Ultimately, the decision
is left to surgeon judgment and experience of the surgeon and his
or her team with each approach. If open repair is chosen, it is critical to identify the location of the perforation to guide the surgical
approach. This may require performance of endoscopy in the operating room before incision. Whenever feasible, two-layer closure
should be performed and reinforced with a pedicled buttress. In
cases of delayed perforation, single-layer closure may be all that is
possible.
78 MANAGEMENT OF ESOPHAGEAL PERFORATION
AB
https://t.me/med1917
A B
FIG. 3 Endoscopic treatment of esophageal perforation. (A) Endoscopic view of a perforation in the middle third of the esophagus (arrow). (B) Endoscopic
view of the stent in place. (From Chirica M, Champault A, Dray X, etal. Esophageal perforations. J Visc Surg. 2010;147[3]:e117–e128.)
FIG. 4 Esophagram. (A) Esophageal stent in adequate position covering a
prior perforation. (B) Stent in place without evidence of contrast extravasation.
Thoracic Perforations
Perforations of the upper and middle thirds of the esophagus are
best approached through a right posterolateral thoracotomy via
the fourth or fifth intercostal space. The intercostal muscle (ICM)
within the interspace is harvested at this time using electrocautery
to ultimately buttress the repair. The cautery tip is positioned near
parallel with the surface of the superior rib to avoid injury to the
neurovascular bundle. The ICM is freed from the rib to the level of
the lumbar-dorsal fascia. Care must be taken to identify this landmark because further dissection risks injury to the intercostal vessels.
The ICM flap is transected anteriorly after ligating or clipping the
anterior aspect of the muscle to prevent bleeding. Next, the pleura is
opened in the area of the perforation, and the esophagus is dissected
enough to obtain clear visualization of the perforation. The edges of
the perforation should be debrided to determine the full extent of
the injury. Of note, the mucosal injury may extend a greater distance
than the visualized muscular injury. The esophageal mucosa is closed
with running or interrupted absorbable suture (4-0 Vicryl or PDS),
and the muscularis is closed with interrupted 3-0 silk sutures. The
pleural side of the ICM flap is then placed in contact with the repair
and secured to the muscle layer of the esophagus with multiple interrupted silk sutures. Pleural and mediastinal drainage tubes are placed
at the conclusion of the operation.
Perforations of the lower third of the esophagus should be
approached through a left posterolateral thoracotomy in the seventh
or eighth intercostal space. Although an ICM flap is generally used as
a buttress, a diaphragmatic flap is also an option. A posteriorly based
full-thickness diaphragmatic flap of adequate length and width can
be mobilized to reach the area of primary repair. The flap is secured
to the esophageal muscle with interrupted silk sutures to cover the
repair. The diaphragm then is closed primarily with nonabsorbable
suture. Advantages of diaphragmatic flap use include its, thickness,
ease, and extent of mobility.
Cervical Perforations
The preferred method of exposure for cervical esophageal perforation is a left-sided neck incision along the anterior border of the
sternocleidomastoid muscle (SCM). It may be necessary to ligate the
middle thyroid vein for improved exposure. The trachea and thyroid
gland are retracted medially for exposure of the esophagus (Fig. 5).
The retroesophageal space is entered bluntly along the prevertebral
fascia, with care taken to preserve the recurrent laryngeal nerve.
Blunt dissection should be continued down to the posterior mediastinum to drain all fluid collections. If the perforation is identified, the
defect is repaired primarily as described earlier. A strap muscle can
be used to buttress the repair. If the defect is not clearly identified,
closed drainage of the area is performed.
Abdominal Perforations
Patients with abdominal esophageal perforation and uncontained
leak should be taken to the operating room for primary repair.
FIG. 5 Cervical esophagus exposure. Incision
Omohyoid remnant
https://t.me/med1917
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/med1917
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, etal. 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, etal. 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, etal. 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/med1917
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/med1917
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/med1917
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/med1917
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/med1917
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, etal (eds), 11th ed. McGraw Hill.
Schroder VT, Pappas TN, Vaslef SN, etal. 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, etal. Perforated peptic ulcer. Lancet.
2015;386:1288–1298.
Sverden E, Mattsson F, Lindstrom D, etal. 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/med1917
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)
• Fecalantigentest
• Ureabreathtest
• Esophagogastroduodenoscopyandbiopsy
• Rapidureasetest
• Histology
• Culture
• Molecularreal-timepolymerasechainreaction(RT-PCR)
Some Common Helicobacter Treatment
Regimens (10–14 Days)
• Clarithromycintripletherapy(PPI,clarithromycin,amoxicillin,
or metronidazole)
• Bismuthquadrupletherapy(PPI,bismuth,tetracycline,
nitroimidazole)
• Sequentialtherapy(PPIandamoxicillinfor5–7days,andthen
a PPI, clarithromycin, and nitroimidazole for 5–7 days)
• Hybridtherapy(aPPIandamoxicillinfor7days,andthena
PPI, amoxicillin, clarithromycin, and nitroimidazole for 7 days)
PPI, Proton pump inhibitor.
Соседние файлы в папке Библиотека им академика М.И. Перельмана