Practice Essentials

Acute gastrointestinal bleeding is a potentially life-threatening abdominal emergency that

remains a common cause of hospitalization. Upper gastrointestinal bleeding (UGIB) is
defined as bleeding derived from a source proximal to the ligament of Treitz.

Signs and symptoms

Signs and symptoms of acute upper GI bleeding[1] include the following:

Hematemesis

Melena

Hematochezia

Syncope

Presyncope

Dyspepsia

Epigastric pain

Heartburn

Diffuse abdominal pain

Dysphagia

Weight loss

Jaundice

See Clinical Presentation for more detail.

Diagnosis

Workup includes the following:

Orthostatic blood pressure

Complete blood count with differential

Hemoglobin level
 Type and crossmatch blood

Basic metabolic profile, blood urea nitrogen, and coagulation profile

Calcium level

Gastrin level

Endoscopy

Chest radiography

Nasogastric lavage

Angiography (if bleeding persists and endoscopy fails to identify a bleeding site)

Computed tomography scanning and ultrasonography may be indicated for the evaluation of
the following[2] :

Liver disease with cirrhosis

Cholecystitis with hemorrhage

Pancreatitis with pseudocyst and hemorrhage

Aortoenteric fistula

See Workup for more detail.

Management

Treatment includes the following:

Secure the airway

Insert bilateral, 16-gauge (minimum), upper extremity, peripheral intravenous lines

Replace each milliliter of blood loss with 3 mL of crystalloid fluid

In patients with severe coexisting medical illnesses, pulmonary artery catheter

insertion for monitoring hemodynamic cardiac performance

Foley catheter placement for continuous evaluation of urinary output as a guide to

renal perfusion

Endoscopic hemostatic therapy for bleeding ulcers and varices

 Surgical repair of perforated viscus

For high-risk peptic ulcer patients, high-dose intravenous proton pump inhibitors

Indications for surgery in patients with bleeding peptic ulcers include the following:

Severe, life-threatening hemorrhage not responsive to resuscitative efforts

Failure of medical therapy and endoscopic hemostasis with persistent recurrent

bleeding

A coexisting reason for surgery (eg, perforation, obstruction, malignancy)

Prolonged bleeding, with loss of 50% or more of the patient's blood volume

A second hospitalization for peptic ulcer hemorrhage

See Treatment and Medication for more detail.

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Background
Acute gastrointestinal (GI) bleeding is a potentially life-threatening abdominal emergency
that remains a common cause of hospitalization. Upper gastrointestinal bleeding (UGIB) is
defined as bleeding derived from a source proximal to the ligament of Treitz.

The incidence of UGIB is approximately 100 cases per 100,000 population per year.[3]
Bleeding from the upper GI tract is approximately 4 times as common as bleeding from the
lower GI tract and is a major cause of morbidity and mortality. Mortality rates from UGIB are
6-10% overall.[3] (See Epidemiology, below.)

The diagnosis of and therapy for nonvariceal upper gastrointestinal bleeding (UGIB) has
evolved since the late 20th century from passive diagnostic esophagogastroduodenoscopy with
medical therapy until surgical intervention was needed to active intervention with endoscopic
techniques followed by angiographic and surgical approaches if endoscopic therapy fails.[4]
(See Workup and Treatment and Management, below.)

Variceal hemorrhage is not discussed in this article because the underlying mechanisms of
bleeding are different and require different therapies.

The underlying mechanisms of nonvariceal bleeding involve either arterial hemorrhage, such
as in ulcer disease and mucosal deep tears, or low-pressure venous hemorrhage, as in
telangiectasias and angioectasias. In variceal hemorrhage, the underlying pathophysiology is
due to elevated portal pressure transmitted to esophageal and gastric varices and resulting in
portal gastropathy. A bleeding ulcer is seen below. (See Etiology, below.)

Go to Pediatric Gastrointestinal Bleeding for complete information on this topic.

Ulcer with active bleeding.

In patients with UGIB, comorbid illness, rather than actual bleeding, is the major cause of
death. Comorbid illness has been noted in 50.9% of patients, with similar occurrences in
males (48.7%) and females (55.4%).

One or more comorbid illnesses have been noted in 98.3% of mortalities in UGIB; in 72.3%
of patients, comorbid illnesses have been noted as the primary cause of death.[5, 6] (See
Epidemiology and Prognosis, below.)

Significant comorbidities have become more prevalent as the patient population with UGIB
has become progressively older. In a retrospective chart review by Yavorski et al, 73.2% of
deaths occurred in patients older than 60 years.[6] (See Epidemiology and Prognosis, below.)

Rebleeding or continued bleeding is associated with increased mortality; therefore,

differentiating the patient with a low probability of rebleeding and little comorbidity from the
patient at high risk for rebleeding with serious comorbidities is imperative. (See Clinical
Presentation and Workup, below.)

Peptic ulcer disease and UGIB

Peptic ulcer disease (PUD) remains the most common cause of UGIB. In a literature review
involving more than 10,000 patients with UGIB, PUD was responsible for 27-40% of all
bleeding episodes.[7] High-risk patient populations at risk for PUD include those with a
history of alcohol abuse, chronic renal failure, and/or nonsteroidal anti-inflammatory drug
(NSAID) use.[8]
Peptic ulcer disease is strongly associated with Helicobacter pylori infection. The organism
causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and
duodenal mucosa, reducing mucosal defenses and increasing back diffusion of acid by
loosening tight cellular junctions. (Rates of H pylori infection are reportedly lower in patients
with complicated ulcer disease than in patients with uncomplicated ulcers. Hosking et al
reported a 71% incidence of H pylori infection in patients with bleeding duodenal ulcers;
patients with nonbleeding ulcers had an incidence of 93%.) This discrepancy may be due to
the decrease in sensitivity of biopsy in patients with ulcer bleeding.[9]

Eradication of H pylori been demonstrated to reduce the risk of recurrent ulcers and, thus,
recurrent ulcer hemorrhage after the initial episode. In fact, the proportion of UGIB cases
caused by peptic ulcer disease has declined,[10] a phenomenon that is believed to be due to the
use of proton pump inhibitors (PPIs) and H pylori therapy.

Duodenal ulcers are more common than gastric ulcers, but the incidence of bleeding is
identical for both. In most cases, the bleeding is caused by the erosion of an artery in the base
of the ulcer. In approximately 80% of patients, bleeding from a peptic ulcer stops
spontaneously.[7]

Initial endoscopic attempts to maintain hemostasis have a high failure rate. Bleeding vessels
larger than 1.5 mm in diameter are associated with an increased mortality rate due to the
difficulty of producing adequate hemostasis with thermal probes.

A minority of patients experience recurrent bleeding after endoscopic therapy, and these cases
are usually associated with risk factors for rebleeding. These factors include age older than 60
years, the presence of shock upon admission, coagulopathy, active pulsatile bleeding, and the
presence of cardiovascular disease. (The appearance of the ulcer at the time of endoscopy
provides important information regarding the risk of rebleeding.) These circumstances are
associated with a poorer prognosis and a higher mortality rate.[11]

Despite the dangers associated with a bleeding peptic ulcer, a study by Sung et al of 10,428
cases of such bleeding (in 9,375 patients) found that most patient deaths were not caused by
it.[12] Of the 577 deaths that occurred in the cohort, almost 80% resulted from other causes,
including multiorgan failure, pulmonary conditions, and terminal malignancy. The authors
concluded that the management of patients with peptic ulcers should focus not only on
hemostasis but also on lowering the risk of multiorgan failure and cardiopulmonary death.

Recurrent bleeding risk in peptic ulcers

Forrest et al were the first to classify the stigmata of hemorrhage from peptic ulcers. Based on
these classifications, the risk of recurrent bleeding can be predicted. The ulcers at highest risk
for rebleeding are those that involve active arterial bleeding or those with a visible,
protuberant, nonbleeding vessel in the base of the ulcer. The study not only correlated the
incidence of rebleeding with the stigmata of recent bleeding and the endoscopic appearance
of an ulcer, but also determined prognostic information regarding the need for surgery.
Mortality was also correlated.[13]

In patients with H pylori infection, the rate of recurrent bleeding is extremely low. This is
why documenting the presence of H pylori and aggressively treating the infection are
important.
Patients who are not infected with H pylori may require a subsequent acid-lowering surgical
procedure or long-term medical therapy for recurrent ulcer disease and bleeding.

Other causes of UGIB

Other major causes of UGIB are mucosal tears of the esophagus or fundus (Mallory-Weiss
tear), erosive gastritis, erosive esophagitis, Dieulafoy lesion, gastric cancer, and ulcerated
gastric leiomyoma.

Patients with chronic liver disease and portal hypertension are at increased risk for variceal
hemorrhage and portal gastropathy in addition to ulcer hemorrhage.

Rare causes of UGIB include aortoenteric fistula, gastric antral vascular ectasia, angiectasias,
and Osler-Weber-Rendu syndrome.

An aortoenteric fistula results from the erosion of the aortic graft into the bowel lumen,
usually the third or fourth portion of the duodenum. The result is a direct communication
between the aortic graft lumen and the bowel lumen. Most aortoenteric fistulas involve the
proximal aortic anastomotic suture line.

UGIB can also result from acute stress gastritis, a disease process characterized by diffuse
superficial mucosal erosions that appear as discrete areas of erythema.[13] The bleeding is
usually mild and self-limiting and rarely progresses to life-threatening hemorrhage.

In intensive care unit (ICU) patients, the incidence of clinically significant GI bleeding (eg,
hypotension, transfusion) from acute stress gastritis was found to be 1.5%.[14] Stress gastritis
and mucosal ulceration are historically associated with (1) head injuries with associated
elevations in intracranial pressure and (2) burn injuries. These stress ulcers are called Cushing
ulcers and Curling ulcers, respectively.

Angiodysplasia of the upper GI tract accounts for 2-4% of bleeding lesions.[7] The condition is
also a cause of lower GI bleeding in 6% of cases.[13] The lesion is a vascular malformation
that represents an abnormal dilation of mucosal and submucosal vessels.

Histologically, angiodysplasias are dilated, thin-walled vascular channels that appear

macroscopically as a cluster of cherry spots. When located in the upper GI tract, they most
commonly involve the stomach and duodenum. The lesions can be acquired or congenital, as
in hereditary hemorrhagic telangiectasia and Rendu-Osler-Weber syndrome.

The acquired angiodysplasias are commonly found in patients with chronic renal failure
requiring hemodialysis and with aortic valvular disease (especially aortic stenosis). Other
diseases, such as cirrhosis and von Willebrand disease, are associated with a higher frequency
of angiodysplasias. Most lesions are smaller than 1 cm in diameter and can be multiple in
66% of patients.[7]

Etiology

Ulcer-related UGIB
As previously mentioned, peptic ulcer disease is strongly associated with H pylori infection.
The organism causes disruption of the mucous barrier and has a direct inflammatory effect on
gastric and duodenal mucosa.

In cases of ulcer-associated UGIB, as the ulcer burrows deeper into the gastroduodenal
mucosa, the process causes weakening and necrosis of the arterial wall, leading to the
development of a pseudoaneurysm. The weakened wall ruptures, producing hemorrhage.

The flow through the vessel varies with the fourth power of the radius; thus, small increases
in vessel size can mean much larger amounts of blood flow and bleeding, with more severe
hypotension and more complications, especially in older patients.

Visible vessels usually range from 0.3-1.8 mm.

Exsanguinating hemorrhage has been reported from larger vessels. The larger vessels are
located deeper in the gastric and duodenal submucosa and serosa. Larger branches of the left
gastric artery are found high on the lesser curvature, while the pancreatoduodenal artery and
its major branches are located posteroinferiorly in the duodenal bulb.

Vomiting-related UGIB

During vomiting, the lower esophagus and upper stomach are forcibly inverted. Vomiting
attributable to any cause can lead to a mucosal tear of the lower esophagus or upper stomach.
The depth of the tear determines the severity of the bleeding. Rarely, vomiting can result in
esophageal rupture (Boerhaave syndrome), leading to bleeding, mediastinal air entry, left
pleural effusion (salivary amylase can be present) or left pulmonary infiltrate, and
subcutaneous emphysema.

Mallory-Weiss tears in UGIB

Mallory-Weiss tears account for 15% of acute upper GI hemorrhage.[7] Kenneth Mallory and
Soma Weiss first described the syndrome in 1929.[15] The massive UGIB results from a tear in
the mucosa of the gastric cardia.

This linear mucosal laceration is the result of forceful vomiting, retching, coughing, or
straining. These actions create a rapid increase in the gradient between intragastric and
intrathoracic pressures, leading to a gastric mucosal tear from the forceful distention of the
gastroesophageal junction.[16] In 80-90% of cases, this is a single, 1.75- to 2.5-cm mucosal
tear along the lesser curve of the stomach just distal to the gastroesophageal junction.[15]

Go to Mallory-Weiss Tear for complete information on this topic.

Acute stress gastritis in UGIB

Acute stress gastritis results from predisposing clinical conditions that have the potential to
alter local mucosal protective barriers, such as mucus, bicarbonate, blood flow, and
prostaglandin synthesis. Any disease process that disrupts the balance of these factors results
in diffuse gastric mucosal erosions.

This is most commonly observed in patients who have undergone episodes of shock, multiple
trauma, acute respiratory distress syndrome, systemic respiratory distress syndrome, acute
renal failure, and sepsis.

The principal mechanisms involved are decreased splanchnic mucosal blood flow and altered
gastric luminal acidity.

Dieulafoy lesions in UGIB

The Dieulafoy lesion, first described in 1896, is a vascular malformation of the proximal
stomach, usually within 6 cm of the gastroesophageal junction along the lesser curvature of
the stomach. However, it can occur anywhere along the GI tract. This lesion accounts for 2-
5% of acute UGIB episodes.[17]

Endoscopically, the lesion appears as a large submucosal vessel that has become ulcerated.
Because of the large size of the vessel, bleeding can be massive and brisk. The vessel rupture
usually occurs in the setting of chronic gastritis, which may induce necrosis of the vessel
wall. Alcohol consumption is reportedly associated with the Dieulafoy lesion.

In a review of 149 cases, the Dieulafoy lesion mostly occurred in men and mostly in those in
their third to tenth decade.[18]

NSAIDs in UGIB

NSAIDs cause gastric and duodenal ulcers by inhibiting cyclooxygenase, which causes
decreased mucosal prostaglandin synthesis and results in impaired mucosal defenses. Daily
NSAID use causes an estimated 40-fold increase in gastric ulcer creation and an 8-fold
increase in duodenal ulcer creation.[13]

Long-term NSAID use is associated with a 20% incidence in the development of mucosal
ulceration.[19] Medical therapy includes avoiding the ulcerogenic drug and beginning a
histamine-2 (H2)receptor antagonist or a proton pump inhibitor that provides mucosal
protection.

Epidemiology

Annually, approximately 100,000 patients are admitted to US hospitals for therapy for UGIB.

UGIB is a common occurrence throughout the world. In France, a report concludes that the
mortality from UGIB has decreased from about 11% to 7%; however, a similar report from
Greece finds no decrease in mortality. In a nationwide study from Spain, UGIB was 6 times
more common than lower GI bleeding.[20]
The incidence of UGIB is 2-fold greater in males than in females, in all age groups; however,
the death rate is similar in both sexes.[6]

The population with UGIB has become progressively older, with a concurrent increase in
significant comorbidities that increase mortality. Mortality increases with older age (>60 y) in
males and females.[19]

Prognosis
As previously mentioned, age older than 60 years is an independent marker for a poor
outcome in upper gastrointestinal bleeding (UGIB),[21] with the mortality rate ranging from
12-25% in this group of patients.

The American Society for Gastrointestinal Endoscopy (ASGE) grouped patients with UGIB
according to age and correlated age category to risk of mortality. The ASGE found a
mortality rate of 3.3% for patients aged 21-31 years, a rate of 10.1% for those aged 41-50
years, and a rate of 14.4% for those aged 71-80 years.[21]

Tthe following risk factors are associated with increased mortality, recurrent bleeding, the
need for endoscopic hemostasis, or surgery[11, 22] :

Age older than 60 years

Severe comorbidity

Active bleeding (eg, witnessed hematemesis, red blood per nasogastric tube, fresh
blood per rectum)

Hypotension

Red blood cell transfusion greater than or equal to 6 units

Inpatient at time of bleed

Severe coagulopathy

Patients who present in hemorrhagic shock have a mortality rate of up to 30%.

Diagnostic Considerations
In addition to the disorders listed in the Differentials section, below, diagnostic consideration
should be given to the following conditions in patients with symptoms of UGIB:

Gastric varices

Mallory-Weiss tear
 Neoplasm

Hemorrhagic gastritis

Dieulafoy lesion

Hemobilia

Pancreatic pseudoaneurysm

Aortoenteric fistula

Benign gastric tumors

Cardiac cirrhosis

Celiac sprue

Cholecystitis

Cirrhosis

Disseminated intravascular coagulation

Strongyloidiasis

Syncope

von Willebrand disease

Zollinger-Ellison syndrome

Dengue fever

Differential Diagnoses
Abdominal Aortic Aneurysm

Barrett Esophagus and Barrett Ulcer

Duodenal Ulcers

Esophageal Cancer

Esophageal Varices
 Esophagitis

Gastric Cancer

Gastric Outlet Obstruction

Gastric ulcer

Gastrinoma

Gastritis, Acute

NSAIDs in UGIB

NSAIDs cause gastric and duodenal ulcers by inhibiting cyclooxygenase, which causes
decreased mucosal prostaglandin synthesis and results in impaired mucosal defenses. Daily
NSAID use causes an estimated 40-fold increase in gastric ulcer creation and an 8-fold
increase in duodenal ulcer creation.[13]

Long-term NSAID use is associated with a 20% incidence in the development of mucosal
ulceration.[19] Medical therapy includes avoiding the ulcerogenic drug and beginning a
histamine-2 (H2)receptor antagonist or a proton pump inhibitor that provides mucosal
protection.

Approach Considerations
An electrocardiogram (ECG) should be ordered to exclude arrhythmia and cardiac
disease, especially acute myocardial infarction due to hypotension.
Esophagogastroduodenoscopy may increase the risk of arrhythmias.
Performing a troponin test may be useful in identifying patients with severe coronary
ischemia or atypical myocardial infarction.
Go to Imaging of Upper Gastrointestinal Bleeding and Imaging of Esophageal Varices
for complete information on these topics.

Assessment of hemorrhagic shock

As previously mentioned, patients who present in hemorrhagic shock have a mortality

rate of up to 30%. Hemorrhage may be classified based on the amount of blood loss,
as noted in the following table.[26]
Table 2. Estimated Fluid and Blood Losses in Shock (Open Table in a new window)

Class 1 Class 2 Class 3 Class 4

Blood Loss, mL Up to 750 750-1500 1500-2000 >2000
Blood Loss,% blood Up to 15% 15-30% 30-40% >40%
volume
Pulse Rate, bpm < 100 >100 >120 >140
Blood Pressure Normal Normal Decreased Decreased
Respiratory Rate Normal or Decreased Decreased Decreased
Increased
Urine Output, mL/h >35 30-40 20-30 14-20
CNS/Mental Status Slightly Mildly Anxious, Confused,

anxious anxious confused lethargic

Fluid Replacement, 3- Crystalloid Crystalloid Crystalloid and Crystalloid and

for-1 rule blood blood

This classification scheme aids in understanding the clinical manifestations of

hemorrhagic shock. In early class 1 shock, the patient may have normal vital signs,
even with a 15% loss of total blood volume. As the percentage of blood volume loss
increases, pertinent clinical signs, symptoms, and findings become more apparent.
Although early cardiovascular changes occur as blood loss continues, urine output, as
a sign of end organ renal perfusion, is only mildly affected until class 3 hemorrhage
has occurred.
 Bornman et al correlated the presence of shock (defined as a pulse rate >100 bpm or
SBP < 100 mm Hg) with the incidence of rebleeding rates after initial nonsurgical
intervention.[26] They found that rebleeding (a marker for increased mortality and need
for surgery) occurred in 2% of patients without shock, in 18% with isolated
tachycardia, and in 48% with shock.
Schiller et al determined that SBP is a sensitive clinical marker for helping to predict
mortality. They correlated mortality rates based on the patient's SBP at the time of
bleeding and found mortality rates of 8% for patients with SBP more than 100 mm
Hg, rates of 17% for SBP of 80-90 mm Hg, and rates of more than 30% for SBP less
than 80 mm Hg.
Unless the patient has evidence of shock, orthostatic testing should be performed to
assess and document a hypovolemic state. A positive tilt test finding is defined as an
SBP decrease of 10 mm Hg and a pulse rate increase of 20 bpm with standing
compared to the supine position. The ASGE survey was able to correlate orthostatic
changes with the incidence of mortality.[27] The mortality rate when orthostatic
changes are present is 13.6%, compared to 8.7% when they are absent.
Knopp et al studied the use of the tilt test in phlebotomized healthy volunteers and
found that a positive tilt test result consistently correlated with a blood loss of 1000
mL. This becomes extremely useful when evaluating patients with class 1
hemorrhagic shock.

THERAPY

Approach Considerations
The goal of medical therapy in upper gastrointestinal bleeding (UGIB) is to correct shock and
coagulation abnormalities and to stabilize the patient so that further evaluation and treatment
can proceed. High doses may reduce the need for endoscopic therapy (see treatment with
proton pump inhibitors).

Various methodologies have been proposed to quantitate rebleeding risk (eg, Rockall score,
Baylor score). These remain somewhat controversial in their application.

The 2008 Scottish Intercollegiate Guidelines Network (SIGN) guideline on the management
of acute upper and lower gastrointestinal bleeding recommends that an initial (pre-
endoscopic) Rockall score be calculated for all patients presenting with acute UGIB. In
patients with an initial Rockall score >0, endoscopy is recommended for a full assessment of
bleeding risk.[31]

Resuscitation of a hemodynamically unstable patient begins with assessing and addressing

the ABCs (ie, airway, breathing, circulation) of initial management. (Baradarian et al
demonstrated that early, aggressive resuscitation can reduce mortality in acute UGIB.[35] )

Patients presenting with severe blood loss and hemorrhagic shock present with mental status
changes and confusion. In such circumstances, patients cannot protect their airway, especially
when hematemesis is present. In these cases, patients are at increased risk for aspiration,
which is a potentially avoidable complication that can significantly affect morbidity and
mortality. This situation must be recognized early, and patients should be electively intubated
in a controlled setting.
Intravenous access must be obtained. Bilateral, 16-gauge (minimum), upper extremity,
peripheral intravenous lines are adequate for volume resuscitative efforts. Poiseuilles law
states that the rate of flow through a tube is proportional to the fourth power of the radius of
the cannula and is inversely related to its length.[19] Thus, short, large-bore, peripheral
intravenous lines are adequate for rapid fluid infusion.

According to the 2008 SIGN guideline, either colloid or crystalloid solutions may be used to
attain volume restoration prior to administering blood products.[31] A rough guideline for the
total amount of crystalloid fluid volume needed to correct the hypovolemia is the 3-for-1 rule.
Replace each milliliter of blood loss with 3 mL of crystalloid fluid. This restores the lost
plasma volume. Patients with severe coexisting medical illnesses, such as cardiovascular and
pulmonary diseases, may require pulmonary artery catheter insertion to closely monitor
hemodynamic cardiac performance profiles during the early resuscitative phase.

Once the ABCs have been addressed, assess the patient's response to resuscitation, based on
evidence of end organ perfusion and oxygen delivery.

A study published by Kaplan et al indicated that skin temperature upon physical examination
in combination with serum bicarbonate levels correlated well with the level of systemic
perfusion.[36]

Pulmonary artery catheters may be helpful to guide therapy. Foley catheter placement is
mandatory to allow a continuous evaluation of the urinary output as a guide to renal
perfusion. This labor-intensive management should be performed only in an ICU setting.

Once the maneuvers to resuscitate are underway, insert a nasogastric tube and perform an
aspirate and lavage procedure. This should be the first procedure performed to determine
whether the GI bleeding is emanating from above or below the ligament of Treitz. If the
stomach contains bile but no blood, UGIB is less likely. If the aspirate reveals clear gastric
fluid, a duodenal site of bleeding may still be possible.

In a retrospective review of 1190 patients, Luk et al found that positive nasogastric-tube

aspirate findings were 93% predictive of an upper GI source of bleeding.[37]

According to a study performed by the ASGE, however, a nasogastric-tube aspirate finding

can be negative even in the setting of a large duodenal bleeding ulcer. The study compared
nasogastric-tube aspirate findings with endoscopic findings of the bleeding source. [22] The
investigation revealed that 15.9% of patients with a clear nasogastric-tube aspirate, 29.9% of
patients with coffee-ground aspirate, and 48.2% of patients with red blood aspirate had an
active upper GI source of bleeding at the time of endoscopy.

A study correlated mortality with the color of the fluid from the nasogastric-tube aspirate and
the color of the stool.[2] As shown in the following table, the color of the nasogastric-tube
aspirate can be a prognostic indicator.

Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool on UGIB Mortality
Rate (Open Table in a new window)

Nasogastric Aspirate Color Stool Color Mortality Rate, %

Clear Brown or red 6
Coffee-ground Brown or black 8.2
Red 19.1
Red blood Black 12.3
Brown 19.4
Red 28.7

Go to Pediatric Gastrointestinal Bleeding for complete information on this topic.

Surgery

Primary surgical intervention should be considered in patients with a perforated viscus (eg,
from perforated duodenal ulcer, perforated gastric ulcer, or Boerhaave syndrome). In patients
who are poor operative candidates, conservative treatment with nasogastric suction and
broad-spectrum antibiotics can be instituted. Endoscopic clipping or sewing techniques have
also been used in such patients.

Emergency surgery in UBIG typically entails oversewing the bleeding vessel in the stomach
or duodenum (usually preoperatively identified by endoscopy), vagotomy with pyloroplasty,
or partial gastrectomy. Angiographic obliteration of the bleeding vessel is considered in
patients with poor prognoses.

Treatment-related contraindications and precautions

Contraindications to upper endoscopy include an uncooperative or obtunded patient, severe

cardiac decompensation, acute myocardial infarction (unless active, life-threatening
hemorrhage is present), and perforated viscus (eg, esophagus, stomach, intestine).

Contraindications to emergency surgery include impaired cardiopulmonary status and

bleeding diathesis.

Esophagogastroduodenoscopy may be more difficult or impossible if the patient has had

previous oropharyngeal surgery or radiation therapy to the oropharynx.

The presence of a Zenker diverticulum can make intubation of the esophagus more difficult.

Patients with Down syndrome are more sensitive to conscious sedation and should receive
much less sedation, or they should be monitored by an anesthesiologist and/or intubated
prophylactically prior to the procedure.

Hypotension may be exacerbated by sedation; therefore, patients who are unstable should be
given less sedation.

Patients with massive bleeding should be considered for intubation to reduce the increased
risk of aspiration. Such patients should be treated in an intensive care setting.

Ideally, the patient should be stabilized prior to endoscopy and abnormalities in coagulation
should be corrected. When this is not possible, the judgment of an experienced endoscopist is
vital.
PPIs
The relative efficacy of the PPIs may be due to their superior ability to maintain a gastric pH
at a level above 6.0, thereby protecting an ulcer clot from fibrinolysis. [38] Considering the
available data, the ideal pharmacologic therapy for patients with acute ulcer bleeding appears
to be an intravenous PPI whether the patient is NPO or not. This is confirmed in the 2008
SIGN guidelines, which recommend high-dose intravenous PPIs in patients with major peptic
ulcer bleeding or nonbleeding visible vessels after endoscopic bleeding control. [31]
Pantoprazole, lansoprazole, and esomeprazole are the only PPIs available as an intravenous
formulation in the United States; intravenous omeprazole is used in other countries.

Lao et al have demonstrated that high-dose intravenous omeprazole can accelerate the
resolution of stigmata of recent hemorrhage and reduce the need for endoscopic therapy.[39]

The suggested dosing of intravenous pantoprazole and esomeprazole is 80-mg bolus followed
by 8-mg/h infusion. The infusion is continued for 48-72 hours. This therapy has been shown
to be cost-effective by Barkun et al.[40] Laine et al has demonstrated that intravenous high-
dose lansoprazole, as well as orally administered high-dose lansoprazole, can maintain the
intragastric pH above 6.[41]

A meta-analysis of 24 randomized controlled trials that evaluated PPIs for bleeding ulcers
(with or without endoscopic therapy) found a significant reduction in the risk of rebleeding,
the need for repeat endoscopic hemostasis, and surgery. An improvement in mortality was
also seen in Asian trials and in patients with active bleeding or nonbleeding visible vessels.[42]

The 2010 international consensus guidelines on UGIB recommend the use of intravenous
PPIs in all patients with high-risk lesions post-endoscopic therapy; PPI therapy might
downgrade the lesion if given pre-endoscopy.{Ref53} The 2008 SIGN guideline agrees that
PPIs should not be used pre-endoscopy in patients presenting with acute UGIB.[31]

High-dose oral PPIs may be used in patients who do not have active bleeding or other high-
risk stigmata for recurrent bleeding (eg, a visible vessel, adherent clots); in such patients, the
risk of recurrent bleeding is low. The goal of treatment in these patients (following
resuscitation) should be directed at healing the ulcers and at eliminating precipitating factors
(eg, H pylori, NSAIDs).

The 2008 SIGN guideline recommends taking biopsy samples to test for H pylori at the initial
endoscopy procedure before starting PPI therapy. Biopsy specimens should be histologically
evaluated when the rapid urease test is negative.[31]

A combined analysis of 5 studies that evaluated oral dosing with PPI (with or without
endoscopic therapy) found a significant reduction in the risk of rebleeding and surgery.[43]

Endoscopy
Since the late 1980s, endoscopic techniques to achieve hemostasis for bleeding ulcers and
varices have continued to evolve. Endoscopy is now the method of choice for controlling
active ulcer hemorrhage.
Several randomized clinical trials and meta-analyses have demonstrated and supported the
idea that early endoscopic hemostatic therapy significantly reduces rates of recurrent
bleeding, the need for emergent surgery, and mortality in patients with acute nonvariceal
upper gastrointestinal bleeding (UGIB).

In the early history of endoscopy for UGIB, multiple published studies questioned the cost-
effectiveness of endoscopy in this setting, because it was unclear whether the outcome was
changed. In a setting in which 80% of patients respond to conservative medical management,
studies were hampered by type 2 errors because of the large number of patients needed to
demonstrate statistical significance.

In 1989, a National Institutes of Health (NIH) consensus conference on UGIB concluded that
effective therapy was needed in the presence of active bleeding or a visible vessel. The
conference affirmed that the treatment, when performed by an experienced endoscopist using
1 of 4 techniques (ie, injection of epinephrine or sclerosants, heater-probe coagulation,
bipolar electrode coagulation, laser coagulation), was proven effective by the published
evidence.

Three other techniques have since been developed: (1) endoscopic application of clips, (2)
use of banding devices, and (3) argon plasma coagulation. Aside from ulcer hemorrhaging,
other causes of gastrointestinal bleeding, including mucosal tears in the esophagus or upper
stomach due to vomiting (Mallory-Weiss tears), venous blebs, and vascular ectasias, can also
be treated with endoscopic coagulation.

The bleeding from gastric cancers and ulcers in leiomyomas does not usually respond to
endoscopic therapy; surgical or radiologic intervention is needed.

Much debate has focused on the significance of the nonbleeding visible vessel (ie, color, size,
diagnostic characteristics, risk of rebleeding) in ulcer hemorrhage. These matters became
clarified after the characteristics and significance of the visible vessel in the ulcer crater were
defined and the evidence for endoscopic therapy was established, demonstrating that patients
requiring therapy to control bleeding or rebleeding could be diagnosed and treated at the time
of the upper endoscopy.

Patients should be considered for upper endoscopy if blood loss from the upper
gastrointestinal tract is suspected.

The patient should undergo upper endoscopy prior to any operative intervention in order to
diagnose and localize the bleeding site. Most patients (85-90%) respond to endoscopic
therapy.

During the endoscopy, the patient is monitored according to analgesia and sedation guidelines
formulated by the American Society of Anesthesiology. The characteristics of the bleeding
lesion are noted, and appropriate therapy is applied when necessary for high-risk lesions or
active bleeding.

Urgent endoscopy
Urgent endoscopy is indicated when patients present with hematemesis, melena, or postural
changes in blood pressure. Cooper et al have demonstrated a lower rate of rebleeding and
shorter length of stay when endoscopy is performed within 24 hours of admission.[37, 44]

Early endoscopy

Cooper et al studied the effectiveness of performing an early endoscopy within the first 24
hours of an acute UGIB episode and found it to be associated with reductions in the length of
hospital stay, rate of recurrent bleeding, and need for emergent surgical intervention.[44]

According to the 2010 international consensus on nonvariceal upper gastrointestinal bleeding,

early endoscopy (within 24 hours of presentation) is appropriate for most patients with UGIB.
[45]
In a retrospective review involving more than 30,000 cases, Yavorski et al showed that the
mortality rates were more than twice as high for patients who did not undergo an early
endoscopic procedure than for those who did undergo the procedure early on (11.1% vs 5.2%,
respectively).

Endoscopic techniques

The following endoscopic techniques have been developed for achieving hemostasis[7] :

Injection of epinephrine or sclerosants

Bipolar electrocoagulation

Band ligation[46]

Heater probe coagulation

Constant probe pressure tamponade

Argon plasma coagulator

Laser photocoagulation

Rubber band ligation

Application of hemostatic materials, including biologic glue

Application of hemoclips or endoclips

Application of nanopowder (experimental)[47]

Treatment using a combination of endoscopic therapies has become more common. For
example, injection therapy can be applied first to better clarify the bleeding site, especially in
the actively bleeding patient, followed by the application of heater probe or bipolar (gold)
probe coagulation. Injection therapy can also be performed prior to endoscopic placement of
hemoclips.
According to the 2008 SIGN guideline, combinations of endoscopy with an injection of at
least 13 mL of 1:10,000 adrenaline, coupled with either a thermal or mechanical treatment,
are more effective than single modalities.[31]

The 2010 international consensus guidelines on UGIB recommend the use of endoscopic
clips or thermal therapy for high-risk lesions.[45] As another example, injection therapy is
useful prior to laser therapy to reduce the heat sink effect of rapidly flowing blood prior to
laser coagulation.

Heater probe coagulation

The heater probe consists of a resistor electrode enveloped by a titanium capsule and covered
by Teflon (to reduce sticking to the mucosa by the probe). The probe temperature rises to
250C (482F).

Bipolar electrocoagulation

The bipolar probe consists of alternating bands of electrodes producing an electrical field that
heats the mucosa and the vessel. The electrodes are coated with gold to reduce adhesiveness.
The probes are stiff in order to allow adequate pressure to the vessel to appose the walls and
thus produce coaptive coagulation when the electrical-field energy is transmitted. Careful
technique is required to heat-seal the perforated vessel.

Injection therapy

Injection therapy involves the use of several different solutions injected into and around the
bleeding lesion. The different solutions available for injection are epinephrine, sclerosants,
and clot-producing materials, such as fibrin glue.

The epinephrine used for injection is diluted (1:10,000) and injected as 0.5- to 1-mL aliquots.
Debate continues over whether the hemostatic effect of epinephrine is due to induced vessel
vasoconstriction and subsequent platelet aggregation or to the tamponade effect produced by
injecting the volume of drug into the tissue surrounding the bleeding lesion.

Epinephrine injection is often used to reduce the volume of bleeding so that the lesion can be
better localized and then treated with a coaptive technique (ie, heater probe, gold probe).

Combining epinephrine injections with human thrombin (600-1000 IU) reduces the risk of
bleeding.[3]

Although the epinephrine administered in injection therapy is absorbed into the systemic
circulation, this does not appear to have any adverse effects on hemodynamic status.

Injecting a volume of sterile isotonic sodium chloride solution and providing a tamponade
effect also leads to hemostasis, although not as effectively as does epinephrine.[3]

The sclerosant solutions used today include ethanol, polidocanol, and sodium tetradecyl
sulfate.
The sclerosants create hemostasis by inducing thrombosis, tissue necrosis, and inflammation
at the site of injection. When large volumes are injected, the area of tissue necrosis can
produce an increased risk of local complications, such as perforation. Combining the various
agents into a single injection has not been shown to be more beneficial than single-agent
therapy alone.[3]

The use of fibrin glue in injection therapy has been shown to be successful, with results
similar to those of epinephrine injections.[48]

Laser therapy

Laser phototherapy uses an Nd:YAG laser to create hemostasis by generating heat and direct
vessel coagulation. This is a noncontact thermal method. It is not as effective as coaptive
coagulation, because it lacks the use of compression to create a tamponade effect. [3] An
additional deterrent to its use is expense.

To perform laser coagulation, the area near the vessel is first injected with epinephrine to
reduce blood flow (reducing the heat-sink effect); then, the laser is applied around the vessel,
producing a wall of edema. Caution must be observed to avoid drilling into the vessel with
the laser, causing increased bleeding.

Hemostatic clips and endoclips

Hemostatic clips are available in the United States.

Modification of the delivery system has made clip placement much easier than it was in the
original model. With careful placement of the clip, closing the defect in the vessel is possible.
Usually, multiple clips are applied. They vary in the size and the strength of the clip. Four
models of hemoclips are available: QuickClip2, which is rotatable; Resolution Clip, which
can be reopened after closure; TriClip, which has 3 prongs; and InScope, which is a multiclip
applier with 4 endoclips. The Resolution Clip seems to be the current clip of choice by
experienced endoscopists.

Considering the available data, the efficacy of hemoclips is similar to that of thermal
coagulation methods.

One report, concerning 113 patients with major stigmata of ulcer hemorrhage, found no
difference between the use of hemoclips and photocoagulation with regard to hemostasis, 30-
day mortality, and the need for emergency surgery.[49] Patients randomized to the endoclip
group had significantly lower rebleeding rates (2% vs 21%). However, only 60% of active
bleeders were successfully treated with the heater probe, a rate much lower than in previous
reports.

A study of 80 patients found a higher rate of control of initial bleeding with the heater probe
compared with the Olympus endoclip (100% vs 85%).[50] Rebleeding rates were not
significantly different.

No significant differences in procedure duration, initial hemostasis, or rebleeding rates were

found in a study of 47 patients comparing combination therapy with epinephrine injection
plus monopolar electrocoagulation versus hemoclips.[51]
There are some clinical settings in which endoclips may be preferred over other hemostatic
methods. These include the treatment of ulcers in patients who are coagulopathic or who
require ongoing anticoagulation; in such patients, electrocoagulation will increase the size,
depth, and healing time of treated lesions. Endoclips may also be preferable in the retreatment
of lesions that rebleed after initial thermal hemostasis.

Ulcers on the lesser curvature, the posterior duodenum, or the cardia increase the difficulty of
clip deployment and clip failure rates.

Larger endoclips have advantages over smaller hemoclips for the hemostasis of chronic
ulcers and the closure of larger lesions.

Argon plasma coagulation

Argon plasma coagulation is a technique in which a stream of electrons flows along a stream
of argon gas. The coagulation is similar to monopolar cautery, with the current flow going
from a point of high current density (the point of contact of the gas with the mucosa) to an
area of low current density (the conductive pad on the patient's body). The current flows
through the body in an erratic path to the pad.

This monopolar cautery technique is similar to the laser technique in that energy is delivered
to the vessel for coagulation with apposition of the vessel walls. This technique was found to
not be effective for visible vessels larger than 1 mm. No animal models have been used for
ulcer hemorrhage to validate this technique.

Nanopowder

Nanopowder has been found to be effective in a small study using a porcine model of arterial
bleeding.[47] Further trails are awaited.

Endoscopic treatment decisions

The choice of treatment modality is influenced by the size of the vessel. Animal studies have
demonstrated that the heater probe and bipolar probe are effective for vessels as large as 2
mm in diameter.

Other techniques (eg, clips, band ligation) or a combination of techniques are needed for
larger vessels or vessels that are not approachable by the heater probe or bipolar probe.
(Surgical intervention should be considered when dealing with vessels larger than 2 mm in
diameter, discounting an enlargement due to the development of pseudoaneurysm.)

The 2008 SIGN guidelines recommend variceal band ligation in patients with confirmed
esophageal variceal hemorrhage. It can be combined with a beta blocker as secondary
prevention for esophageal variceal hemorrhage. For patients in whom band ligation is not
suitable, a combination of nonselective beta blocker and nitrate is recommended as secondary
prevention.[31]

Ulcers with an overlying clot

In the patient who has an ulcer with an overlying clot, attempting to remove the clot by target
washing is critical. Endoscopic removal of the clot by washing or cold snare has been
demonstrated to be effective in reducing the recurrence of bleeding.[52] (Cutting away the
adherent clot is somewhat controversial but is recommended based on study results from
experienced centers.)

The findings under the clot (eg, bleeding vessel, visible vessel, flat spot, clean base, examples
of which are seen in the images below) help to determine the therapy needed and improve
efficacy by allowing treatment to be applied directly to the vessel. (See the table below.)

Ulcer with active bleeding.

Ulcer with a clean base. Diagram of an ulcer with a clean

base. Ulcer with a flat spot.

Ulcer with an overlying clot. Ulcer with a visible vessel.

Diagram of an ulcer with a visible vessel.

Table 5. Ulcer Characteristics and Correlations (Open Table in a new window)

Ulcer Prevalence Rate, Rebleeding Rate, Surgery Rate, Mortality Rate,

Characteristics % % % %
Clean base 42 5 0.5 2
Flat spot 20 10 6 3
Adherent clot 17 22 10 7
Visible vessel 17 43 34 11
Active bleeding 18 55 35 11

If the clot cannot be removed by washing, then cutting away the clot using a cold snare can
be considered by experienced endoscopists.

Vigorous washing of the clot formed after therapy is useful in determining the adequacy of
coagulation. A combination of injection with heater probe or bipolar coaptive coagulation is
often used and has been shown to be more effective in patients with active bleeding.

The patient is monitored under the protocol for conscious sedation, also called analgesia and
sedation (ie, per the American Society of Anesthesiologists and the American Society for
Gastrointestinal Endoscopy guidelines).

Active bleeding and rebleeding

Attempting to control active bleeding using the recommended techniques with the
appropriate equipment or instituting appropriate therapy for a high-risk lesion is important.
The large-channel therapeutic endoscope should be used so that the 10-French thermal probe
can be employed for adequate coaptation.

Endoscopists should use the technique with which they have the most familiarity. The
endoscopy should not be started unless the endoscopist is equipped for any potential lesions
(eg, ulcer, varix, angioectasia, tear, tumor). The patient should be monitored for recurrent
bleeding and treated a second time if appropriate. A surgical consultation should be
considered for all patients with gastrointestinal hemorrhage.

The 2008 SIGN guidelines urge the consideration of transjugular intrahepatic portosystemic
stent shunts (TIPS) to prevent esophageal variceal rebleeding for patients in whom endoscopy
is contraindicated or has failed, and/or who are intolerant to pharmacological therapy,[31]

Rebleeding occurs in 10-30% of endoscopically treated patients. A second attempt at

endoscopic control is warranted. Some authorities have concerns about the perils of a second
esophagogastroduodenoscopy, which may result in delayed surgery, perforation, and
increased morbidity and mortality rates. However, this approach has been validated in a large,
randomized, controlled trial that showed decreased morbidity and mortality rates.[53]

Specific characteristics at endoscopy can predict rebleeding. Rebleeding occurs in 55% of

patients who have active bleeding (pulsatile, oozing), in 43% who have a nonbleeding visible
vessel, in 22% who have an ulcer with an adherent clot, and in 0-5% who have an ulcer with
a clean base.

At endoscopy, the prevalence rate for a clean base is 42%, for a flat spot is 20%, for an
adherent clot is 17%, for a visible vessel is 17%, and for active bleeding is 18%. (See the
images below.)

Freeman et al have described a pale, visible vessel that appears to have a very high risk for
rebleeding.[54] This must be differentiated from the presence of a clean ulcer base.

Good visualization is important. The uncleared fundal pool may obscure an ulcer, mucosal
tear, gastric varices, portal gastropathy, or tumor (eg, leiomyoma, adenocarcinoma,
lymphoma). Endoscopic therapy is recommended for ulcers at increased risk for rebleeding.

According to the 2008 SIGN guidelines, TIPS should be considered to prevent gastric
variceal rebleeding.[31]

Using a combination of techniques is prudent when re-treating the ulcer site because the first
therapy produced necrosis and weakening of the intestinal wall. Ulcers on the anterior surface
of the stomach and duodenum are at increased risk for perforation. Using injection as the first
step increases the thickness of the submucosal layer, thus providing an extra margin of safety.

Even operative techniques can have a significant rebleeding rate with significant mortality, as
noted in the study of Poxon et al. In this investigation, the rebleeding rate was 10% (80%
mortality for rebleeders) in patients who underwent a conservative surgical technique in
which the ulcer base was undersewn.[55] This more conservative approach was compared with
the standard surgical technique (ie, vagotomy and pyloroplasty or partial gastrectomy). The
comparison of the conservative approach with a standard gastrectomy resulted in similar
mortality rates, ie, 26% versus 19%, respectively, with no rebleeding after partial
gastrectomy.

Postendoscopic monitoring

Postoperatively, the patient is monitored for recovery from conscious sedation after
endoscopy and from general anesthesia after abdominal surgery. Monitor the patient's mental
status, vital signs, chest, cardiac, and abdominal findings to ascertain that the patient's clinical
status has stabilized and that no complications (eg, aspiration, perforation, recurrent bleeding,
myocardial infarction due to hypotension) have occurred. Monitor the hemoglobin level.

Bleeding Peptic Ulcer Treatment

Upper GI endoscopy is the most effective diagnostic tool for PUD and has become the
method of choice for controlling active ulcer hemorrhage. Failure of endoscopy to maintain
hemostasis is one of the indications to initiate surgical intervention, especially in high-risk
patients.

In a randomized, prospective trial that included 92 patients with recurrent peptic ulcer
bleeding after initial endoscopic therapy for hemostasis, patients who underwent a second
endoscopic attempt to control bleeding were found to have decreased transfusion
requirements, 30-day mortality rates, and duration of ICU stay in comparison with the
surgical group.[56]

With the exception of a patient in shock who has a life-threatening recurrent hemorrhage, this
study supports attempting another trial of endoscopy to control a bleeding ulcer.

Regardless of the endoscopic therapy, however, 10-12% of patients with acute ulcerous
hemorrhage require an operation as the definitive procedure to control the bleeding ulcer. In
most circumstances, the operation is performed emergently, and the associated mortality rate
is as high as 15-25%.

Medical therapy used in conjunction with endoscopy involves PPI administration. PPIs
decrease rebleeding rates in patients with bleeding ulcers associated with an overlying clot or
visible, nonbleeding vessel in the base of the ulcer.[57, 58] Consider transcatheter angiographic
embolization in patients who are poor surgical candidates. Because of the extensive collateral
circulation of the upper GI tract, ischemic complications are rare.

Surgical treatment

If 2 attempts at endoscopic control of the bleeding vessel are unsuccessful, avoid further
attempts (ie, because of increased rebleeding and mortality rates) and pursue surgical
intervention. The indications for surgery in patients with bleeding peptic ulcers are as
follows:

Severe, life-threatening hemorrhage not responsive to resuscitative efforts

Failure of medical therapy and endoscopic hemostasis with persistent recurrent

bleeding
 A coexisting reason for surgery, such as perforation, obstruction, or malignancy

Prolonged bleeding, with loss of 50% or more of the patient's blood volume

A second hospitalization for peptic ulcer hemorrhage

The operative treatment options for a bleeding duodenal ulcer historically include vagotomy,
gastric resection, and drainage procedures. Each specific operative option is associated with
its own incidence of ulcer recurrence, postgastrectomy syndrome, and mortality (as seen in
the table below). When making an intraoperative judgment on how to best manage the
bleeding ulcer, it is extremely important for the surgeon to be aware of these differences.[13]

Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operations for Duodenal
Ulcer (Open Table in a new window)

Recurrence Postgastrectomy Syndrome Mortality Rate,

Original Operation
Rate, % Rate, % %
Proximal gastric 10 5 0.1
vagotomy
Truncal vagotomy and 7 20-30 <1
drainage
Truncal vagotomy and 1 30-50 0-5
antrectomy

Billroth I or Billroth II

Truncal vagotomy and 5-10 50-60 0-5

antrectomy

Roux-en-Y

The 3 most common operations performed for a bleeding duodenal ulcer are as follows[7] :

Truncal vagotomy and pyloroplasty with suture ligation of the bleeding ulcer

Truncal vagotomy and antrectomy with resection or suture ligation of the bleeding
ulcer

Proximal (highly selective) gastric vagotomy with duodenostomy and suture ligation
of the bleeding ulcer
The purpose of the vagotomy is to divide the nerves to the acid-producing body and fundus of
the stomach. This inhibits the acid production that occurs during the cephalic phase of gastric
secretion. Although acid secretion is controlled, gastric motility and gastric emptying is
affected, as indicated in the following table.[13]

Table 7. Effects of Operations for PUD on Gastric Emptying and Motility (Open Table in a
new window)

Operation Antral Innervation Liquid Emptying Solid Emptying

Proximal gastric vagotomy Preserved Fast Normal
Truncal vagotomy Divided Fast Slow
Truncal vagotomy and drainage Divided Fast Fast
Truncal vagotomy and antrectomy Divided Fast Fast

Proximal vagotomy abolishes gastric receptive relaxation and impairs storage in the proximal
stomach. As a result, a more rapid gastric emptying of liquids occurs. A drainage procedure is
not required, because the innervation of the antrum and pylorus is still intact. Because of this,
the gastric emptying of solid food is not altered. The antropyloric mechanism still functions
normally and continues to prevent duodenogastric reflux.

In addition to having the same effects as a highly selective vagotomy in the proximal
stomach, a truncal vagotomy also has marked effects on distal gastric motor function. It
weakens distal gastric peristalsis, thus requiring the creation of a pyloroplasty to decrease the
resistance to outflow from the stomach.

Truncal vagotomy and suture ligation of a bleeding ulcer is a frequently used operation for
treating upper gastrointestinal bleeding (UGIB) in elderly patients with life-threatening
hemorrhage and shock. The procedure can be performed rapidly, minimizing the time spent in
the operating room under general anesthesia.

The principles of suture ligation of a duodenal bleeding ulcer that involves the
gastroduodenal artery require use of the 3-point ligation technique.

The gastroduodenal artery is ligated proximally and distally to the arterial bleeding site. The
third suture is a horizontal mattress placed to control hemorrhage from the transverse
pancreatic branch of the gastroduodenal artery. Failure to place this third stitch may result in
recurrent bleeding that requires another emergent laparotomy of the abdomen. Vagotomy
with antrectomy is reserved for patients whose conditions have failed to respond to more
conservative attempts at surgical intervention and for those with aggressive and recurrent
duodenal ulcer diathesis, such as gastric outlet obstruction.

When performing a highly selective vagotomy, the duodenostomy or the

pyloroduodenostomy is closed anatomically, preserving the normal pyloric sphincter muscle.
Most commonly, this operation is reserved for young, stable, low-risk patients. Although
long-term follow-up care is still necessary, the recurrent ulcer rate is less than 10% at a mean
follow-up of 3.5 years.[7]

Much of what is now known about the operations performed for bleeding duodenal ulcers
came from the era before the etiologic role for H pylori and NSAIDs in the development of
peptic ulcers was understood. Reducing gastric acidity has been proven to be beneficial, with
lower rebleeding rates when using high-dose omeprazole. [3] Although PPIs seem to have an
advantage, they have no affect on mortality.

The diagnosis of H pylori infection is important in the management of patients with a

complicated bleeding peptic ulcer. If a patient with a bleeding ulcer requires surgery, then
knowledge of the patient's H pylori status becomes pertinent, because it may help to guide the
decision to choose a particular surgical procedure, eg, simply oversewing the ulcer as
opposed to performing an antiulcer operation. Many studies support the decision to manage
the bleeding ulcer in conjunction with eradication of H pylori.

The 2008 SIGN guideline recommends testing for H pylori in patients with peptic ulcer
bleeding and a 1-week course of therapy prescribed for those who test positive. Three weeks
of continuous treatment should be given. In those who use NSAIDs, maintenance
antisecretory therapy should not persist after successful healing of the ulcer and H pylori
eradication.[31]

Bleeding Gastric Ulcer Treatment

The surgical management of bleeding gastric ulcers is slightly different from that of duodenal
ulcers, but the concepts are identical. The 3 most common complications of a gastric ulcer
that mandate emergent surgical intervention are hemorrhage, perforation, and obstruction.
The goals of surgery are to correct the underlying emergent problem, prevent recurrent
bleeding or ulceration, and exclude malignancy.

A bleeding gastric ulcer is most commonly managed by a distal gastrectomy that includes the
ulcer, with a gastroduodenostomy or a gastrojejunostomy reconstruction.

The common operations for the management of a bleeding gastric ulcer include (1) truncal
vagotomy and pyloroplasty with a wedge resection of the ulcer, (2) antrectomy with wedge
excision of the proximal ulcer, (3) distal gastrectomy to include the ulcer, with or without
truncal vagotomy, and (4) wedge resection of the ulcer only.

Types of gastric ulcers

The choice of operation for a bleeding gastric ulcer depends on the location of the ulcer and
the hemodynamic stability of the patient to withstand an operation. Five types of gastric
ulcers occur, based on their location and acid-secretory status.

Type 1 gastric ulcers are located on the lesser curvature of the stomach, at or near the incisura
angularis. These ulcers are not associated with a hypersecretory acid state.

Type 2 ulcers represent a combination of 2 ulcers that are associated with a hypersecretory
acid state. The ulcer locations occur in the body of the stomach in the region of the incisura.
The second ulcer occurs in the duodenum.

Type 3 ulcers are prepyloric ulcers. They are associated with high acid output and are usually
within 3 cm of the pylorus.
Type 4 ulcers are located high on the lesser curvature of the stomach and (as with type 1
ulcers) are not associated with high acid output.

Type 5 ulcers are related to the ingestion of NSAIDs or aspirin. These ulcers can occur
anywhere in the stomach.

Surgical management according to ulcer type

A vagotomy is added to manage type 2 or type 3 gastric ulcers.

Patients who are hemodynamically stable but have intermittent bleeding requiring blood
transfusions should undergo a truncal vagotomy and distal gastric resection to include the
ulcer for type 1, 2, and 3 ulcers.

In patients who present with life-threatening hemorrhage and a type 1, 2, or 3 ulcer, biopsy
and oversew or excision of the ulcer in combination with a truncal vagotomy and a drainage
procedure should be considered.

Patients with type 4 ulcers usually present with hemorrhage. The left gastric artery should be
ligated, and a biopsy should be performed on the ulcer. Then, the ulcer should be oversewn
through a high gastrotomy.

Rebleeding rates for the procedures that keep the ulcer in situ range from 20-40%.[13]

Gastric bleeding in the immediate postoperative period from recurrent PUD is initially best
managed by endoscopic or angiographic means. If reoperation is required, gastric resection is
usually indicated, because a repeat vagotomy is not reliable. A more definitive solution is
warranted.

According to the 2008 SIGN guidelines, patients with confirmed gastric variceal hemorrhage
require endoscopic therapy, preferably with cyanoacrylate injection.[31]

Stress Gastritis Treatment

Knowledge of the predisposing conditions for stress ulceration allows the clinician to identify
patients at risk for developing gastritis and GI bleeding. Treatment in this group of high-risk
patients should focus on prevention. This is best accomplished by treating the underlying
causes of ulceration.

Aggressive support of hemodynamic parameters ensures adequate mucosal blood flow. In

addition, several strategies have evolved to treat gastric luminal acidity. Histamine receptor
antagonists (HRAs) have proven to be the most effective at controlling stomach pH. Proton
pump inhibitors (PPIs) are superior to the HRAs at suppressing acid; however, their role in
stress ulceration prophylaxis is still being studied.[14]

Stress-related bleeding usually occurs 7-10 days after the initial insult but may manifest
sooner. Initially, endoscopy is the most important diagnostic tool. The acute superficial
erosions are multiple, begin in the fundus, and progress toward the antrum. Ninety percent of
patients stop bleeding with conservative medical therapy that includes NGT lavage and
gastric acidcontrolling medications to maintain the gastric luminal pH above 5.0.[15]

Endoscopic hemostasis is attempted using electrocoagulation, laser, or injection therapy.

Selective angiographic catheterization of the left gastric artery may be attempted with
selective infusion of vasopressin (48-72 h) or embolization using Gelfoam, coils, or
autologous clot to embolize the left gastric artery. Regardless of the angiographic technique
used, it is often unsuccessful because of the rich and extensive submucosal plexus and
collateral circulation within the stomach.

Surgical treatment

Surgical intervention becomes necessary if nonoperative therapy fails and blood loss
continues. The goals of operative treatment are to control bleeding and to reduce recurrent
bleeding and mortality. These patients are at extremely high risk, and the most expeditious
procedure is the best option.

Simply oversewing an actively bleeding erosion is sometimes effective enough to control the
bleeding. In the setting of life-threatening hemorrhage not amenable to endoscopic control,
gastric resection with or without vagotomy with reconstruction may be necessary.

The type of gastric resection depends on the location of the gastric erosions, ie, whether they
are proximal or distal. The options are antrectomy and subtotal, near total, or total
gastrectomy. Operative mortality rates range from 4-17%. [59] The choice of the initial
operation must be made with an understanding of the patient's condition, the amount and
location of gastric disease, and an accurate assessment of one's technical ability to rapidly and
safely perform a gastric resection. The trend has been to perform less surgery in general and
to minialize the type of surgical procedure performed.[60]

Managing the underlying insult causing the gastric stress ulcerations is also important. This
involves supportive measures to maintain acceptable hemodynamic parameters, to provide
adequate nutritional support in the critically ill patient, and to treat sepsis (if present).

Mallory-Weiss Syndrome Treatment

Distinguishing Mallory-Weiss syndrome from Boerhaave syndrome is critical. Although both
entities share a common pathogenesis, their management is completely different.

Boerhaave syndrome represents a full-thickness transmural laceration with perforation of the

esophagus. A Gastrografin swallow helps to confirm the presence of the perforation in most
cases, and prompt surgical intervention is necessary to prevent mediastinitis and sepsis.

On the other hand, surgical intervention in Mallory-Weiss syndrome is required to achieve

hemostasis in only 10% of cases.[15] The bleeding from a Mallory-Weiss tear spontaneously
ceases in 50-80% of patients by the time endoscopy is performed.[15]

For patients in whom bleeding is visualized at endoscopy, the endoscopic treatment options
are electrocoagulation, heater-probe application, hemoclips, epinephrine injection, or
sclerotherapy.
In a series published by Bataller et al, hemostasis was achieved in 100% of patients with
Mallory-Weiss tears by using endoscopic sclerotherapy with epinephrine (1:10,000) and 1%
polidocanol. Other nonoperative therapies are reserved for cases in which endoscopic
attempts at creating hemostasis have failed.

Other available options are angiographic intra-arterial infusion of vasopressin and

transcatheter embolization of branches of the left gastric artery using Gelfoam. Avoid the
balloon tamponade technique using the Sengstaken-Blakemore tube in this particular
circumstance, because this apparatus may extend the mucosal laceration into a transmural
laceration with perforation.[15]

Surgical intervention is indicated in patients with continued bleeding after failed attempts at
nonoperative therapies.

Bleeding from the gastroesophageal junction is visualized through an anterior gastrotomy.

Once the tear is localized, the bleeding is controlled by oversewing the lesion.

The overall mortality rates for patients who require emergent surgery is 15-25%, in contrast
to a mortality rate of 3% or less for patients whose bleeding stops by the time of the initial
endoscopy.[15]

Go to Mallory-Weiss Tear for complete information on this topic.

Posttreatment Monitoring and Care

The 2010 international consensus guidelines on UGIB state that selected low-risk patients
may be discharged immediately following endoscopy, but high-risk patients should remain
hospitalized for at least 72 hours.[45]

According to the 2008 SIGN guideline, patients with a post-endoscopic Rockall score of less
than 3 have a low risk of rebleeding or death and are candidates for early discharge and
outpatient follow up.[31]

The goal is to maintain the intragastric pH above 6 to maintain the clot. This is most easily
achieved by intravenous proton pump inhibitor (PPI) therapy. After the acute phase, 72 hours,
the coagulated vessel should be stable and the patient can be switched to oral therapy. If the
patient rebleeds or has ongoing bleeding, then repeat of endoscopic therapy would be
considered. If this is not successful, then interventional radiology is performed to clot the
bleeding vessel. If this fails, then surgery would be considered.

In the subsequent 48-72 hours after endoscopic therapy, the patient should receive acid-
suppressive therapy to maintain a high gastric pH (above 6). A high gastric pH can be
achieved by a continuous infusion of high-dose intravenous PPI therapy.

Patients who do not require endoscopic therapy and do not have other comorbidities should
be considered for discharge.
Patients who did not require endoscopic treatment should receive routine, oral dosing of a
PPI, ie, daily dosing prior to breakfast. Whether high-dose intravenous PPI therapy is
advantageous in this setting remains controversial.

Oral PPI therapy can be achieved with any of the oral PPI preparations.

Patients should be tested for H pylori either by histology of gastric biopsy specimens taken
on initial upper endoscopy or by serologic tests. If positive, H pylori therapy should be
instituted after the patient has been discharged and is in stable condition. Moreover, H pylori
eradication should be confirmed 4-6 weeks later in patients with UGIB. This can be done by
checking the stool for the H pylori antigen.

Tachyphylaxis may develop within 24 hours if H2-receptor antagonists are administered.

Data on acid suppression via oral PPI therapy in order to produce a reduction in rebleeding
are limited. High-dose intravenous PPI therapy appears to reduce rebleeding, but PPIs are not
currently approved by the US Food and Drug Administration (FDA) for such treatment. The
patient may be fed after recovery from local and intravenous anesthesia.

Some patients may require further endoscopic therapy. If repeat endoscopic therapy is
needed, the stomach will empty liquids without residue within 3 hours. The 2008 SIGN
guideline recommends repeat endoscopy and endotherapy within 24 hours when initial
endoscopic treatment is deemed suboptimal or in patients in whom rebleeding will likely be
life threatening.[31]

If the patient remains stable, the patient can then be started on therapy for ulcer healing.

The patient should continue oral therapy for ulcer disease noted on endoscopy or for ulcers
caused by cautery techniques during endoscopic therapy. The greatest risk for perforation is
usually within the first 48 hours after endoscopic therapy. Long-term acid suppression
therapy should be offered with either full-dose H2-receptor antagonists or low-dose PPIs to
prevent ulcer recurrence or its complications.[69]

Aspirin and NSAID therapies should be avoided in view of their adverse effect on platelet
aggregation and ulcer healing. However, according to the 2010 international consensus
guidelines, resumption of aspirin therapy in patients who require anticlotting prophylaxis
should not be delayed as cardiovascular risks outweigh the risk of rebleeding.[45]

The 2008 SIGN guidelines state that patients with healed bleeding ulcers who are negative
for H pylori require concomitant PPI therapy at the usual daily dose if NSAIDs, aspirin, or
COX-2 inhibitors are indicated.[31]

If patients must remain on NSAIDs or low-dose aspirin, secondary prophylaxis against

NSAID-induced ulcers should be given. According to the 2010 international consensus
guidelines on UGIB, postdischarge use of aspirin or NSAIDs requires cotherapy with PPI.[45]
Only lansoprazole (15 mg or 30 mg daily), [70] esomeprazole (20-40 mg daily), and
misoprostol (200 g 4 times daily)[71] are approved by the FDA for prophylaxis against
NSAID-induced ulcers.

The patient's hemoglobin value should be monitored to assess the efficacy of iron therapy as
an outpatient; further improvement should be noted. Erythropoietin analogues have been
shown to be effective in increasing the rate of hemoglobin production after ulcer hemorrhage.

Repeat endoscopy should be done in a few weeks in patients with gastric ulcers to document
ulcer healing and to exclude cancer.[72]

Medication Summary
Rebleeding is associated with increased morbidity and mortality; therefore, this is the major
goal of therapy.

As advised in the 2008 SIGN guidelines, patients with chronic liver disease who present with
acute UGIB should be started on antibiotic therapy.[31]

The use of H2-receptor antagonists has not been shown to be effective in altering the course
of UGIB. A meta-analysis concluded that there was a possible minor benefit with intravenous
H2 antagonists in bleeding gastric ulcers but no benefit in duodenal ulcers.[73]

The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer
hemorrhage, although only when not combined with aspirin therapy. Concerns have been
raised about an increase in myocardial infarction and stroke in patients taking selective
cyclooxygenase-2 inhibitors.

As demonstrated in the study by al-Assi et al, the combination of H pylori infection and
NSAID use may increase the risk of ulcer hemorrhage; however, the treatment of H pylori in
patients who are taking NSAIDs remains controversial.[1]

The 2008 SIGN guidelines clearly advocate the discontinuation of aspirin and NSAIDs in
patients who present with peptic ulcer bleeding. When ulcer healing and eradication of H
pylori are confirmed, aspirin and NSAIDs should only be resumed if there is a clear
indication for their use.[31]

Eradication of H pylori can reduce the risk of rebleeding. Current anti-H pylori regimens
include a variety of drug combinations. Typically, an antimicrobial agent is combined with an
H2-receptor antagonist or a PPI.

The treatment regimens approved by FDA have eradication rates for H pylori of 70-90%.[13]

Drugs used to treat H pylori infection include the following:

Omeprazole

Ranitidine bismuth citrate

 Bismuth subsalicylate

Lansoprazole

Proton Pump Inhibitors

Class Summary

PPIs inhibit gastric acid secretion by inhibition of the H +/K+/ATPase enzyme system in the
gastric parietal cells. IV therapy may be a useful adjunct via stabilization of the clot by
increasing intragastric pH. High-dose intravenous dosing is the norm; however, high-dose
oral therapy may be able to maintain the intragastric pH about 6 as well.[41]

View full drug information

Pantoprazole (Protonix intravenous formulation)

This agent suppresses gastric acid secretion by specifically inhibiting the H+/K+/ATPase
enzyme system at the secretory surface of gastric parietal cells. Use of the IV preparation has
been studied only for short-term use (ie, 7-10 d).

IV dosing has been approved by FDA for the treatment of gastroesophageal reflux disease
(GERD) that cannot be managed by oral medication.

The dosing has not been approved by FDA for the treatment of UGIB at present but has been
suggested in literature.

IV use should be limited to 2 settings: (1) when the patient is NPO and (2) after endoscopic
therapy, to maintain the gastric pH above 6 for clot stability.

Esomeprazole magnesium (Nexium intravenous formulation)

This agent suppresses gastric acid secretion by specifically inhibiting the H+/K+/ATPase
enzyme system at the secretory surface of gastric parietal cells. Use of the IV preparation has
been studied only for short-term use (ie, 7-10 d).

IV dosing has been approved by FDA for the treatment of gastroesophageal reflux disease
(GERD) that cannot be managed by oral medication.

The dosing has not been approved by FDA for the treatment of UGIB at present but has been
suggested in literature.

IV use should be limited to 2 settings: (1) when the patient is NPO, and (2) after endoscopic
therapy, to maintain the gastric pH above 6 for clot stability.