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Authors:
David W Mercer, MD
Matthew R Goede, MD
Section Editor:
David I Soybel, MD
Deputy Editor:
Wenliang Chen, MD, PhD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Mar 2017. | This topic last updated: Sep 01, 2015.
INTRODUCTION Stress ulcers were once a major cause of morbidity and mortality in
critically ill patients. However, with the advent of ulcer prophylaxis and improved critical care,
surgical intervention is only necessary for a small number of patients with life threatening
hemorrhage or perforation from stress ulcers [1].
The nonsurgical management, indications for surgery, and surgical management of patients
with stress ulcers are reviewed here. The epidemiology, pathogenesis, clinical
manifestations, and prophylaxis of stress ulcers, as well as the nonsurgical treatments of
upper gastrointestinal bleeding are discussed elsewhere. (See "Stress ulcer prophylaxis in
the intensive care unit" and "Approach to acute upper gastrointestinal bleeding in adults".)
The surgical treatment of peptic ulcer disease (not stress ulcer disease) is presented
separately. (See "Surgical management of peptic ulcer disease".)
Stress gastritis erosions can be identified within hours following injury and occur nearly
universally (in the absence of prophylaxis) following severe shock [5]. These erosions appear
as wedge-shaped mucosal hemorrhages with necrosis of the superficial mucosal cells. If
these erosions continue to progress and extend into the submucosa, significant and life-
threatening bleeding may arise. The pathogenesis of stress gastritis is presented elsewhere.
(See "Stress ulcer prophylaxis in the intensive care unit", section on 'Pathophysiology'.)
INITIAL MANAGEMENT Despite almost universal use of ulcer prophylaxis, some critically
ill patients still develop stress ulcers, and a small number of them may develop clinically
significant bleeding. The clinical manifestations and diagnosis of stress ulcers are discussed
elsewhere. (See "Stress ulcer prophylaxis in the intensive care unit".)
When patients are diagnosed with bleeding stress ulcers, they should be promptly
resuscitated with intravenous fluid or blood products. Any coagulopathy is corrected. A
nasogastric tube should be inserted to remove gastric blood and irritants such as acid, bile,
or pancreatic secretions, which may cause further injury to the gastric mucosa. An
intravenous proton pump inhibitor should be administered, and broad-spectrum antibiotics
should be given to septic patients. Underlying sepsis is an important cause of stress ulcers.
Thus, in patients with sepsis, appropriate antibiotic coverage and source control are required
for adequate ulcer healing. (See "Evaluation and management of suspected sepsis and
septic shock in adults".)
Endoscopy is usually the first-line therapy for patients with bleeding stress ulcer disease,
both for diagnosis and treatment. Depending upon local expertise, angiographic interventions
can also stop bleeding from stress ulcers.
Data from mixed trauma patients with massive transfusion requirements indicate that
patients with acute traumatic coagulopathy appear to benefit from receiving transfusions of
packed red blood cells, FFP or similar products (eg, PF24), and platelets in ratios
approaching 1:1:1 [8,9]. Although still controversial, these data may be applicable to patients
with life-threatening bleeding from stress gastritis.
Vasopressin has to be used with extreme caution in patients with a history of ischemic heart
disease, as it may precipitate acute coronary events. (See "Angiographic control of
nonvariceal gastrointestinal bleeding in adults".)
INDICATIONS FOR SURGERY Although most of the bleeding from stress ulcers can be
treated nonoperatively, there remains a small subset of patients who either do not respond to
nonsurgical management, rebleed after repeated nonsurgical interventions, or develop a
perforation. Alternatively, patients may be too unstable to undergo nonsurgical interventions.
For those patients, prompt surgical intervention is indicated because it provides the only
chance of survival.
Refractory bleeding Surgical intervention may be indicated in two different clinical
scenarios involving bleeding from stress ulcers.
Gastrointestinal perforation Compared with patients who have superficial ulcers from
trauma, shock, or sepsis, patients with Cushings and Curlings ulcers are more susceptible
to gastrointestinal perforations, as these two types of stress ulcers tend to be deep and
cause extensive necrosis [3,17].
Because Cushings or Curlings ulcers can cause extensive necrosis of the gastric wall
before perforation occurs, more extensive gastric resection (like a subtotal gastrectomy, with
a delayed anastomosis until the patient has stabilized) may be required to treat a gastric
perforation caused by stress ulcers than a gastric perforation caused by type 1 gastric peptic
ulcers. (See 'Gastric resection procedures' below and "Surgical management of peptic ulcer
disease", section on 'Type I gastric ulcer'.)
Establish two large bore (14 or 16 gauge) peripheral intravenous lines for volume
infusion. In addition, insert an arterial line and either a central venous or pulmonary
arterial catheter for hemodynamic monitoring and vasopressor administration.
Heat the operating room to an appropriate temperature (usually 85 degrees
Fahrenheit); cold operating room air temperatures can exacerbate hypothermia and
therefore coagulopathy.
Ensure that blood products (typed and cross-matched packed red blood cells, fresh
frozen plasma, and platelets) are readily available.
Have adequate numbers of fluid warmers and rapid infusers readily available.
Use pneumatic compression devices for prophylaxis against venous
thromboembolism. (See "Prevention of venous thromboembolic disease in surgical
patients".)
Give antibiotic prophylaxis prior to incision in patients who are not already receiving
antibiotics. (See "Antimicrobial prophylaxis for prevention of surgical site infection in
adults".)
SURGICAL ANATOMY The stomach resides in the left upper quadrant of the abdomen.
Anteriorly, it is contained by the chest and abdominal walls, and usually a large portion is
covered by the left lateral segment of the liver. Superiorly and posteriorly, it is confined by the
diaphragm. The spleen occupies its position superiorly and laterally to the greater curvature.
The pancreas resides in the lesser sac, posterior to the stomach. Inferiorly, the stomach is
bordered by the transverse colon. The stomach is fixed at the gastroesophageal junction and
the pylorus (figure 1). However, between these two points the stomach is mobile, which
assists in its ability to distend.
The most proximal portion of the stomach that attaches to the intraabdominal esophagus is
the cardia. Between the esophagus and the cardia is the lower esophageal sphincter. The
highly distensible fundus is distal to the cardia and is bordered by the angle of His, which
forms between the left edge of the esophagus and the fundus, the diaphragm superiorly, and
the spleen laterally. Continuing distally is the body of the stomach. This is the largest portion
of the stomach and contains the majority of the parietal cells. The body is defined from the
antrum by the angularis incisura, at which point the lesser curvature of the stomach acutely
angles towards the right. The pylorus then lies between the antrum of the stomach and the
first portion of the duodenum.
Blood supply Most of the blood supply to the stomach arises from the celiac artery
(figure 2). Four vessels supply the majority of the stomach. The left and right gastric arteries
supply the lesser curvature. The left and right gastroepiploic arteries supply the greater
curvature. The largest artery to the stomach is the left gastric artery. In 15 to 20 percent of
patients, an aberrant left hepatic artery originates from the left gastric artery. This is of
special surgical significance because if the left gastric artery is ligated or embolized
proximally to the take off of an aberrant left hepatic artery, it may lead to ischemia of the left
lobe of the liver.
The stomach also has a rich collateral circulation. A substantial amount of the circulation to
the proximal stomach can be provided by the inferior phrenic arteries. The short gastric
arteries arising from the splenic circulation can supply much of the greater curvature. This
rich collateral circulation is what allows the stomach to survive if gastric devascularization is
attempted to control catastrophic bleeding.
The venous drainage from the lesser curvature is through the left gastric vein (also known as
the coronary vein) and the right gastric vein, which both drain into the portal vein. The left
gastroepiploic vein drains into the splenic vein and the right gastroepiploic vein drains into
the superior mesenteric vein.
Vagal innervation The sympathetic innervation of the stomach is from the celiac plexus.
The parasympathetic innervation of the stomach is from the vagus nerve (figure 3). The
vagus nerve arises in the vagal nucleus in the brain, travels through the carotid sheath in the
neck, and then enters the mediastinum where it divides into numerous branches around the
esophagus. At the level of the diaphragmatic hiatus, those vagal branches then coalesce into
the left (anterior) and right (posterior) vagus nerves. The left vagus nerve branches to give off
the hepatic branch and the anterior nerve of Latarjet, which courses down the lesser
curvature of the stomach. The first branch off of the right vagus nerve is the criminal nerve of
Grassi. The criminal nerve of Grassi is of particular interest because if it is not divided,
recurrent ulcers can develop. The right vagus nerve continues to travel down the lesser
curvature of the stomach, giving off branches to the celiac plexus along the way.
In order to perform a truncal vagotomy, both left and right vagus nerves are divided above
the hepatic and celiac branches. A selective vagotomy divides below these branches, which
preserves the hepatic and pyloric branches.
SURGICAL APPROACH Surgery for stress ulcer disease can be challenging because
patients are often ill from both their underlying disease processes (eg, sepsis), as well as
acute hemorrhagic shock. For bleeding patients who are acidotic, hypothermic, or
coagulopathic, a staged surgical approach appears safer [18].
The initial stage of the operation is usually done with the primary goal of bleeding control
[19,20]. Once that is achieved, the second stage of the operation needs to be tailored to
each individual patient based on their hemodynamic stability. Stable patients go on to have a
vagotomy and pyloroplasty before abdominal closure, while unstable patients are sent back
to the intensive care unit for further resuscitation with an open abdomen. More elaborate
procedures such as gastrectomy or gastric devascularization are now rarely used because of
the high morbidity and mortality associated with them.
Abdominal incision and exploration A long midline incision is recommended for its
versatility and expediency. The entire abdomen is then quickly but systematically explored to
exclude any pathology including bleeding, perforation, infection, obstruction, or tumor. The
focus of the surgeon is then directed towards the stomach.
In stress gastritis, the bleeding sources often reside high along the lesser curvature close to
the esophagogastric junction [21]. Therefore, the initial gastrotomy needs to be made high
enough to allow for eversion and close inspection of the flattened rugal folds of the upper
stomach [22] (figure 4). A counter incision in the form of a longitudinal gastroduodenostomy
can be made across the pylorus after a Kocher maneuver to mobilize the duodenum. This
would allow for inspection of the distal stomach, pyloric channel, and proximal duodenum.
Stable patients In patients who are hemodynamically stable after incision, exploration,
and oversewing of bleeders, a vagotomy and pyloroplasty can be added, followed by closure
of the abdomen.
Patients may be returned to the operating room when hemodynamically stable for vagotomy
and pyloroplasty (or other drainage procedure), followed by abdominal closure (usually within
24 to 48 hours) [18].
Specific techniques of partial gastrectomy are also discussed elsewhere. (See "Partial
gastrectomy and gastrointestinal reconstruction".)
Subtotal or total gastrectomy Subtotal and total gastrectomy are rarely performed now
that proton pump inhibitors are in widespread use. However, in the past, a subtotal
gastrectomy or even total gastrectomy was performed in dire circumstances to control
bleeding. Unfortunately, patients requiring a subtotal gastrectomy had a mortality
approaching 80 to 100 percent [29,32]. If performed, most surgeons would advocate for a
delayed anastomosis after the gastrectomy, allowing the patient to be resuscitated out of
shock before performing a definitive anastomosis 24 to 48 hours later, analogous to damage
control laparotomies in trauma patients.
During gastrectomy, leaving a cuff of proximal stomach on the esophagus may be desirable,
because an esophageal-jejunal anastomosis is associated with a higher leak rate than a
gastro-jejunal anastomosis. Before using any mechanical stapling device, the surgeon must
remember to call for removal of the nasogastric tube to avoid the disastrous complication of
entangling the tube by the staple line. A more detailed discussion on total gastrectomy and
reconstruction is contained elsewhere. (See "Total gastrectomy and gastrointestinal
reconstruction".)
Following operative intervention, the patient is returned to the intensive care unit to continue
resuscitation and medical management:
Treatment with intravenous proton pump inhibitors is continued if any part of the
stomach remains.
Antibiotics and antifungal medications are continued.
Normothermia needs to be maintained.
Coagulopathy needs to be controlled.
As noted above, the initially unstable patient may be returned to the operating room in
24 to 48 hours if hemodynamically stable for definitive procedure, anatomical
restoration, and abdominal closure. (See 'Unstable patients' above.)
Enteral feeding can commence when the patient is weaned down on vasopressors,
provided that a feeding tube is placed distal to an anastomosis.
A water soluble contrast upper gastrointestinal series should be performed to rule out
a leak in those patients undergoing gastrectomy prior to starting oral intake.
FOLLOW-UP CARE Patients who have bleeding control by simple oversewing of the
ulcerations, endoscopic therapy, or angiographic intervention only will likely require proton
pump inhibitors for several months. During this period, the gastric mucosa remains friable,
and may take a significant amount of time to heal completely. However, those patients who
also underwent vagotomy do not require antisecretory therapy because vagotomy
substantially reduces gastric acid secretion.
Long-term continuation of the proton pump inhibitor after ulcer healing is complete is
controversial. Once acute shock has resolved and patients recover from their underlying
illness, the nidus for stress ulceration has been removed as has the need for long-term
antisecretory therapy.
Patients who have had gastric resection and reconstruction can develop complications
including osteoporosis, iron deficiency anemia, pernicious anemia, and malnutrition. These
issues are discussed elsewhere in detail. (See "Bariatric surgery: Postoperative nutritional
management".)
Thus, it is not surprising that patients who develop overt bleeding from stress ulcers continue
to have a poor prognosis, with mortality rates ranging from 30 to 70 percent. Those who
require surgical intervention have mortality rates in excess of 50 percent [29]. Rebleeding
rates following surgical interventions vary depending on the series examined, ranging from
20 to 40 percent [29].
Surgical intervention also carries the additional risks of anastomotic leak, surgical site
infections, and abdominal wall hernia.
Superficial stress ulcers can occur after physical trauma, shock, hemorrhage, and
sepsis. They can cause major morbidity and mortality in critically ill patients because of
the risk of bleeding. In addition, patients with two other forms of stress ulcers, Cushings
ulcer (following head trauma or brain surgery) and Curlings ulcer (following significant
burn), are also susceptible to gastrointestinal perforations. (See 'Introduction' above.)
For patients diagnosed with bleeding stress ulcers, resuscitative efforts start with
intravenous proton pump inhibitors, volume repletion, and correction of coagulopathy.
Antibiotics are given to patients with underlying sepsis. A nasogastric tube is inserted for
gastric lavage and decompression. Endoscopy or angiography can be used as first-line
therapy to localize the bleeding sources and stop them if possible. (See 'Initial
management' above.)
Surgical consultation is indicated for severe bleeding causing hemodynamic instability,
free gastrointestinal perforation, or refractory bleeding compromising comorbid medical
conditions. (See 'Indications for surgery' above.)
For patients with a bleeding stress ulcer, the goal of the surgery is to control bleeding.
We typically make a long gastrotomy high on the anterior wall of the stomach in order to
identify and oversew all bleeders. A truncal vagotomy with pyloroplasty could be added
if the patients condition permits. Gastric resection and devascularization procedures are
rarely performed and are usually reserved for reoperations for stress ulcer bleeding, or
for patients who present with a gastric perforation. (See 'Surgical approach' above.)
After bleeding control, the abdomen can be left open to expedite the surgery and to
prevent abdominal compartment syndrome in unstable patients. These patients are
promptly returned to the intensive care unit for further resuscitative efforts before being
brought back in 24 to 48 hours for second look, anatomical restoration, and abdominal
closure. (See 'Postoperative care' above.)
Following surgical intervention, patients frequently require continued proton pump
inhibitors for acid suppression and/or nutritional supplements dictated by the specific
procedure they undergo. (See 'Follow-up care' above.)
Patients who develop overt bleeding or perforation from stress ulcers continue to have
a poor prognosis, with mortality rates ranging from 30 to 70 percent. Those who require
surgical intervention have mortality rates in excess of 50 percent. Much of the morbidity
and mortality are attributed to the patients underlying disease processes.
(See 'Morbidity and mortality' above.)
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