MODULE 13

ACUTE GASTROINTESTINAL BLEEDING

Upper GI Bleeding
Bleeding from the upper gastrointestinal (GI) tract is a medical emergency associated
with morbidity, mortality, and costly care. Prompt and decisive treatment is essential to
improve outcomes. Upper GI bleeding is 4 times more common than lower GI bleeding.
An acute upper GI bleed is suspected when patients present with syncope, hypotension,
or abdominal tenderness, and report melanic stool, hematochezia, and blood or coffee-
ground emesis. In addition to anemia, laboratory values typically show an elevation of
the blood urea nitrogen (BUN) to creatinine ratio(> 20:1). Although bleeding stops
spontaneously in 80% to 90% of cases, patients presenting with sudden blood loss are
at risk for hypotension, decreased tissue perfusion, and reduced oxygen-carrying
capability. Many organ systems may be adversely affected.

Acute upper GI bleeding has a mortality of 6% to 15% and a high rate of reoccurrence.
Many patients with bleeds are rebleeding from a previous upper GI tract lesion. A poor
prognosis with upper GI bleeding is associated with age above 65, shock, overall poor
health, active bleeding at the time of presentation, elevated creatinine or transaminases,
onset of bleeding during hospitalization, and initial low hematocrit. Death is typically not
a direct result of blood loss, but is related to age and comorbidities.
Lower GI bleeding
In contrast to upper GI bleeding, lower GI bleeding is defined as bleeding that originates
distal to the ligament of Treitz and unlike upper GI bleeding has a lower morbidity and
mortality. In fact, the bleeding resolves spontaneously in the vast majority of patients and
the mortality rate is less than 5%. Distinguishing upper versus lower GI bleeding by
origin is an important consideration because a rapid upper GI bleed may present as the
presence of blood in the lower GI tract.

Lower GI bleeding is a common disorder in older adults and may be associated with a
host of conditions including infection, hemorrhoids, cancer, diverticulitis, or vascular
anomaly. Regardless of the source, lower GI bleeding typically presents as
hematochezia. Bleeding sources within the left side of the colon often result in the
presence of bright red blood whereas those from the right colon may be mixed with stool
and present as a darker shade of red.

Common Sources Of Upper Gastrointestinal Bleeding

Peptic Ulcer Disease
- Gastric Ulcer
- Duodenal Ulcer

Varices
- Esophangeal
- Gastric

Pathologies of the Esophagus

- Tumors
- Mallory-Weiss Syndrome
- Inflammation
- Ulcer
Pathologies of the Stomach
- Cancer
- Erosive Gastritis
- Helicobacter Pylori Infection
-Tumors

Pathologies of the Small Intestine

- Peptic Ulcers
- Angiodysplasia
- Aortoenteric Fistula

ETIOLOGY, RISK FACTORS, AND PATHOPHYSIOLOGY

Peptic Ulcer Disease
 Is the most common cause of upper GI bleeding.
 Fifty-five percent of patients with gastric ulcers and 39% of patients with
duodenal ulcers are hospitalized for acute bleeds.
 The pathogenesis of peptic ulcer disease is related to hypersecretion of gastric
acid, coupled with impaired GI tract mucus secretion. Normally, mucus protects
the gastric wall from the erosive effects of acid. Peptic ulcers occur in the
stomach and the duodenum and are characterized by a break in the mucosal
layer that penetrates the muscularis mucosa (innermost muscular layer),
resulting in bleeding.
 Peptic ulcers are more prevalent in those with a history of alcohol abuse,
smoking, chronic renal failure, and nonsteroidal anti-inflammatory drug (NSAID)
use.
 Infection of the mucosa by Helicobacter pylori, an organism naturally found in the
GI tract, is strongly correlated with 90% to 100% of duodenal ulcers and 60% to
100% of gastric ulcers.
 However, the increased availability of over-thecounter NSAIDs also contributes
to the high prevalence of the condition despite advances in medical
management.
 Of note, many peptic ulcers are asymptomatic and patients can present with a
bleeding ulcer without previous GI symptoms.
Gastroesophageal Varices
 Develop when there is increased pressurein the portal venous system of the
liver.
 If blood cannot flow easily through the liver because of obstructive disease, it is
diverted to collateral channels. These channels are normally the low-pressure
vessels found in the distal esophagus (esophageal varices), the veins in the
proximal stomach (gastric varices), and in the rectal vault (hemorrhoids).
 Acute upper GI hemorrhage occurs when esophageal and/or gastric varices
rupture from increased portal vein pressure (portal hypertension).
 Esophagogastric varices do not generally bleed until the portal pressure exceeds
12 mm Hg.
 Portal hypertension is most commonly caused by primary liver disease, liver
trauma, or thrombosis of the splenic, mesenteric or portal veins. Massive upper
GI hemorrhage is associated with variceal bleeds.
Mallory-Weiss syndrome
 Is a linear, nonperforating tear of the gastricmucosa near the gastroesophageal
junction.
 The tear is the result of intra-abdominal pressure changes in the stomach that
occur with forceful vomiting.
 Alcohol abuse and inflammatory conditions of the stomach and esophagus are
associated with this disorder.
 Classically, these tears occur in alcoholic patients who experience intense
retching and vomiting associated with binge drinking.
 However, they may also occur in any patient with a history of repeated emesis
and other scenarios where the intra-abdominal pressure is suddenly increased.

Angiodysplasia
  Refers to abnormal superficial blood vessels in the GI tract that are prone to
bleeding.
 These abnormal vessels are associated with increased age.
 The potential for the malformed vessels to bleed is exacerbated with aortic
stenosis, chronic renal disease, liver disease, and Von Willebrand disease.
 This condition is commonly encountered in the outpatient setting and rarely
requires admission to the intensive care unit (ICU).

Erosive Gastritis
 Describes gastric lesions that do not penetrate the muscularis mucosa.
 These are also referred to as stress ulcers.
 Stress-related ulcers occur frequently in hospitalized patients.
 Patients with respiratory failure and coagulopathies have an increased risk of
bleeding from the ulcers.
 The onset of bleeding is sudden and is often the first symptom.
 However, the bleeding is often minimal and self-limited.
 The causes of gastritis are multifactorial, but are most commonly associated with
NSAID use, steroid intake, alcohol abuse, and physiologic conditions that cause
severe stress (eg, trauma, surgery, burns, radiation therapy, severe medical
problems).
 Alcohol and NSAIDs are known to directly disrupt the mucosal defense
mechanisms of the stomach.

Use of NSAIDs is particularly problematic in older adults and contributes to the

increased incidence of symptomatic acute upper GI bleeding in this population. In the
critical care population, particularly patients with neurological or burn injuries, Cushing
and Curling stress ulcers may be identified. However, they are rare and only occur in
1.5% of this population.

Regardless of the etiology, upper GI bleeding resulting in a significant and sudden loss
of blood volume is associated with decreased venous return to the heart, and therefore a
decrease in cardiac output (CO). The decrease in CO triggers the release of epinephrine
and norepinephrine, causing intense vasoconstriction and tissue ischemia. In addition,
aldosterone and antidiuretic hormones are released, resulting in sodium and water
retention. The clinical signs and symptoms of upper GI hemorrhage are directly related
to the effects of the decrease in CO and the vasoconstriction response typically seen in
hypovolemic shock.

CLINICAL PRESENTATION
History
Individuals may have a history of peptic ulcer disease, tobacco abuse, alcohol abuse,
liver disease, severe physiologic stress, NSAID use, and anticoagulation or antiplatelet
therapy. Older adults are at great risk for GI bleeding.
Signs and Symptoms
The response to blood loss depends on the rate and amount of blood loss, patient’s age,
overall health status, and the timing of the initial resuscitation. Specific signs and
symptoms may include:
 Hematemesis (bright red blood or coffee ground emesis)
 Melena (black tarry stools)
 Hematochezia (red or maroon stools)
 Nausea and/or early satiety
 Epigastric pain
 Abdominal distension or bloating
 BSs increased or decreased
 Hypotension ( orthostasis suggests 30% blood volume loss) and altered
hemodynamic values
 Rapid, deep respirations
 Tachycardia
 Fever
 Cold, clammy skin
 Dry mucous membranes
 Decreased pulses
 Weakness
 Decreased urine output
 Anxiety
 Mental status changes
 Restlessness
 Electrocardiographic (ECG) changes consistent with ischemia (eg, ST-segment
elevation, arrhythmias)

Diagnostic Tests
 Hematocrit may be normal initially, then decreased with fluid resuscitation and
blood loss. The hematocrit may not accurately reflect the actual volume of blood
loss because of hemodilution and movement of extravascular fluid. The
hematocrit decreases as extravascular fluid enters the vascular space in an
attempt to restore volume. This process continues for 24 to 72 hours.
 Hemoglobin may also be normal initially, then decreased with fluid resuscitation
and blood loss. It is considered slightly more reliable than hematocrit.
 White blood cell count is elevated due to inflammation.
 Platelet count may be decreased depending on the amount of blood loss.
 Serum sodium is usually elevated initially due to hemoconcentration.
 Serum potassium is usually decreased with vomiting.
  Serum BUN is mildly elevated.
 Serum creatinine is elevated.
 Serum lactate is elevated with severe bleeding.
 PT is usually decreased.
 Activated partial thromboplastin time (aPTT) is usually decreased.
 Arterial blood gases show respiratory alkalosis (early), then later metabolic
acidosis with severe shock and hypoxemia.
 Gastric aspirate shows normal or acidotic pH and is guaiac positive.

Principles of Management for GI Bleeding

The fundamental goal of initial treatment is volume resuscitation. The management of
the patient with acute GI bleeding focuses on hemodynamic stabilization, identification of
the bleeding site, and initiation of definitive medical or surgical therapies to control or
stop the bleeding. Measures to decrease anxiety in this patient population are also
indicated due to the severity and sudden onset of GI bleeding but sedatives are used
sparingly if at all, particularly in patients with liver impairment.

Hemodynamic Stabilization
The initial assessment of the patient with GI bleeding begins with a physical examination
in which vital signs and mental status are the most reliable indicators of the amount of
blood lost. In the presence of hemodynamic instability, resuscitation begins. In addition
to vital signs and physical assessment, risk stratification tools and laboratory findings
help determine the severity of the bleed. The Glasgow Blatchford, Rockall and AIMS65
scores can be used to predict risk of complications. The Glasgow Blatchford score
incorporates measures of BUN, Hgb, systolic BP, pulse, melena, syncope, liver disease,
and/or heart failure while the Rockall includes age, shock, and morbidity. The Rockall
score does have a secondary set of elements (age, shock, comorbidity, diagnosis, and
stigmata of recent bleed) that can be reviewed post-endoscopy to further delineate risk.
The AIMS65 score is used preprocedure and consists of five factors including albumin,
INR, mental status, systolic BP, and age. The use of a risk assessment tool to stratify
bleeding and associated mortality is recommended by several consensus groups.
Additionally, meta-analyses demonstrate that factors such as active bleeding,
hemoglobin less than 10 g/dL, systolic blood pressure less than 100 mm Hg,
tachycardia, ulcer size more than 1 to 3 cm, and ulcer location (in the lesser gastric
curvature or posterior duodenal bulb) are associated with poor patient outcomes.
1. Monitor and record cardiovascular status (blood pressure, heart rate including
orthostatic changes), hemodynamic indices, and peripheral pulses
2. Insert at least two large-bore intravenous (IV) catheters and begin fluid resuscitation
with crystalloid solution (eg, normal saline or lactated ringer solution). Administer fluids
to maintain mean arterial pressure (MAP) around 65 mm Hg or higher.
3. Administer supplemental oxygen and monitor respiratory function. Airway protection
with endotracheal intubation to prevent aspiration is indicated in patients with ongoing
hematemesis or altered mental status.
4. Obtain blood for measurement of hematocrit, hemoglobin, and clotting studies, as well
as for a type and cross-match for packed red blood cells (PRBCs). A Hgb less than 7 to
8 g/dL is considered a marker for transfusion. If the patient also has a history of unstable
coronary artery disease or comorbid conditions, a higher threshold is typically used. In
patients receiving multiple transfusions, monitoring ionized calcium levels is required as
citrate, contained in the transfused blood, may lower calcium. Estimates for the amount
of blood volume lost are most reliably guided by vital sign values and physical
assessment.
5. Administer prescribed IV colloids, crystalloids, or blood products until the patient is
stabilized. After the administration of crystalloid fluids, blood products may be
considered during the initial resuscitation if the hemodynamic response is poor. PRBCs
are used to rapidly increase the hematocrit while providing less volume compared to
infusions of whole blood. However, whole blood may be desired with severe hemorrhage
as it provides more volume and also includes both plasma and platelets. Each unit of
PRBC increases the hematocrit by 2% to 3% and improves gas exchange. It may take
up to 24 hours after blood is administered for changes to be reflected in the hematocrit
values, especially if large amounts of crystalloid solutions were administered during the
resuscitation period.
6. Monitor coagulation studies (eg, prothrombin time/ partial thromboplastin time
[PT/PTT], platelet count, and fibrinogen) to determine if transfusions of platelets or
clotting factors will benefit the patient.
7. Monitor fluid balance and renal function (intake and output, daily weight, BUN,
creatinine, and hourly urine output). An elevated BUN:creatinine ratio may indicate poor
renal perfusion but also occurs when blood is absorbed in the duodenum.
8. Insert a gastric tube if bleeding is massive (> 40% of blood volume) to assess the rate
of bleeding and minimize the potential risk of aspiration. Placement of a gastric tube in
the presence of varices is somewhat controversial and practices vary between
institutions. Use of gastric lavage is no longer used routinely to minimize bleeding. Some
institutions use room temperature saline lavage to clear the stomach prior to endoscopy.
Iced saline is no longer used as it lowers core temperature.
9. Position the patient with backrest elevation 30° to 45° to minimize aspiration
associated with hematemesis.
10. Monitor temperature and maintain normothermia. Rapid fluid resuscitation,
particularly with blood products, can lead to hypothermia which interferes with
coagulation. Warming of fluids may be required to prevent hypothermia, if traditional
measures are insufficient.
11. Administer medications such as IV octreotide and PPis.
12. Prepare for urgent endoscopic therapy in patients with high risk clinical features such
as history of varices, bright red emesis, or Class III or IV hemorrhage. These patients
may have improved outcomes when endoscopy is performed within 12 hours. Critically ill
patients with active bleeding or altered mental status may be electively intubated to
facilitate endoscopy and reduce aspiration risk. In patients at lower risk, endoscopy is
usually performed within 24 hours of admission.

Identify the Bleeding Site

Although the history and physical examination are used to differentiate between upper
and lower GI bleeding, endoscopic examination is required to determine the exact site of
bleeding and to direct future therapy. Endoscopy allows early direct visualization of the
upper GI tract during resuscitation measures.

1. Provide prokinetic agents, if required. The presence of blood in the upper GI tract can
impede visualization of the site of bleeding. Prokinetic agents facilitate gastric emptying
of retained blood and may be administered prior to endoscopy. Meta-analyses
demonstrate that when erythromycin is administered pre-endoscopy, visibility is
improved and the need for a repeat procedure is reduced.
2. Administer sedation (eg, midazolam) sparingly and institute monitoring protocol.
3. Elevate the head of the bed to a 30° angle (if tolerated) and if intubated, maintain
endotracheal tube (ET) cuff pressure to prevent aspiration.
4. Position the patient in a left lateral decubitus position, which facilitates scope
placement, and helps to prevent aspiration of GI contents during endoscopy. Have oral-
tracheal suction available at the bedside before the procedure begins.
5. Monitor for cardiac ischemia during the procedure (eg, draw troponin, arrhythmias).

Institute Therapies to Control or Stop Bleeding

Definitive therapies to treat the bleeding depend on the cause. Administration of PPIs is
routine for patients in whom an ulcer is suspected. The PPIs quickly neutralize acids and
elevate gastric pH levels, which results in stabilization of the blood clot. An acidic
environment will inhibit platelet aggregation and lyse an already formed clot.

In nonvariceal upper GI bleeding, endoscopic treatment is the modality of choice

because it is the most effective method to control acute ulcer bleeding, prevent
rebleeding and it is relatively safe procedure. Although individual studies have been too
small to show significant advantage for endoscopic therapy in reducing mortality, a
meta-analysis indicates that endoscopic therapy prevents not only rebleeding but also
death. While endoscopy carries a risk for complications including GI perforation,
precipitation of bleeding, aspiration, cardiac or respiratory compromise, and missed
lesions, these rarely occur.

A variety of interventions are used via endoscopy and include ablative or coagulation
therapy (laser, monopolar, bipolar, or multipolar electrocoagulation, and heater probe),
pharmacologic therapy also known as sclerotherapy, and mechanical and combination
therapies. Pharmacologic treatments are easy to use, inexpensive, and available in most
settings. The goal is to control bleeding by tamponade, vasoconstriction, and/or an
inflammatory reaction after the injection of the selected agent. A saline injection will
compress the vessels. Epinephrine provides local tamponade, vasoconstriction, and
improved platelet aggregation to promote hemostasis. It is the agent of choice in the
United States to rapidly control the bleeding site. However, its effects will only last for 20
minutes and therefore is used in combination with an additional more durable thermal or
mechanical treatment.

Thermal coagulation methods such as electrocautery and argon plasma coagulation are
examples of ablative treatments and are equally effective. Bleeding vessels can also be
mechanically compressed using metallic clips, endoloops, or rubber band ligation.
Metallic hemoclips are the mechanical treatment of choice and are shown to be as
effective as other endoscopic techniques. Combination therapy with epinephrine
injection has become the standard treatment for actively bleeding ulcers. Adding a
second endoscopic treatment, either an ablative therapy or endoclips, significantly
reduces the rate of recurrence, need for surgery, and mortality. It is no longer
recommended to use epinephrine alone. If the patient rebleeds, a second attempt with
endoscopic control may be considered before surgical intervention or
angiographyguided intervention. Rebleeding is more common in patients with variceal
bleeds and is highest initially after admission and for the first 24 hours.

Treatment of a Mallory-Weiss tear is supportive therapy. Bleeding episodes are self-

limited and the mucosa heals spontaneously within 72 hours in 90% of patients.

Today significant bleeding from stress gastritis is rarely encountered. Critically ill patients
with a history of gastritis, or those at risk for developing stress-related GI injury, benefit
from prophylactic acid-suppressive therapy and from early enteral feeding to prevent
bleeding. Invasive intervention is rarely required.

In patients with variceal bleeding, pharmacologic treatment to reduce portal hypertension

may be considered as preparations are underway for emergent endoscopy.
Somatostatin or its analogue octreotide are the vasoactive agents of choice. Continuous
IV infusion of these agents can temporarily control bleeding so that resuscitation,
diagnostic, and therapeutic measures can be completed. Both sclerotherapy and
variceal banding or ligation are used during endoscopy to control variceal bleeding.
Currently, balloon tamponade (Sengstaken-Blakemore [S-B] tube) is reserved for
patients with massive hemorrhage. Once bleeding is controlled, more definitive therapies
can be used.

Treatment of esophageal and gastric varices will also include antibiotic prophylaxis for
spontaneous bacterial peritonitis (SBP) in patients with cirrhosis. A third generation
cephalosporin or fluoroquinolone is indicated, as bacteremia is often present in patients
with variceal bleeding. Studies demonstrate that administering antibiotics to cirrhotic
patients prior to endoscopy decreases infections and mortality.

1. Monitor for complications of endoscopic therapy and/or the sclerosing agents used to
treat the ulcer or varix. Complications may include fever and pain due to esophageal
spasm, motility disturbances of the esophageal sphincter, and perforation. Systemic
complications of endoscopic therapy and/ or sclerosing agents also may occur and
predominantly affect the cardiovascular and respiratory systems. Cardiovascular effects
include heart failure, heart block, mediastinitis, and pericarditis. Respiratory effects
include aspiration pneumonia, atelectasis, pneumothorax, embolism, and acute
respiratory distress syndrome.
2. Institute pharmacologic therapies as prescribed totreat peptic ulcer disease or
gastritis. The most common pharmacologic agents and their actions are reviewed in
Table 14-4. PPis are the drug of choice for the management of patients with nonvariceal
bleeding. They provide a more durable and sustained acid suppression than histamine
receptor antagonists. Treatment with PPis is shown in randomized clinical trials to lead
to a decrease in recurrent bleeding because of ulcer disease, need for transfusions,
surgery, and the length of hospital stay. The traditional use of high dose continuous IV
PPis for 3 days after successful endoscopic treatment for active bleeding continues (80
mg esomeprazole bolus, 8 mg/h continuous infusion). Yet, newer meta-analyses
demonstrate the same benefits with IV BID dosing of 40 mg, until the patient is able to
take oral medications. Oral PPis are commonly recommended for months after an upper
GI bleeding episode to allow for healing of the mucosa. Their use is especially beneficial
in patients who use chronic NSAIDs or who have had H. pylori infection.

3. Administer pharmacologic therapies as prescribed to treat variceal bleeding (Table

14-5). Pharmacologic agents exert their effect by constricting splanchnic blood flow and
thereby reducing portal pressure.
4. Use intra-aortic balloon pump therapy as determined by a provider to achieve
temporary vascular control in patients in shock. This therapy optimizes blood pressure,
increases aortic diastolic pressure, increases coronary flow, and allows time for rapid
resuscitation. 5. Assist with the insertion of a tamponade tube, most commonly the S-B
tube (Figure 14-5), to emergently control bleeding so that endoscopy can be performed.
Other tamponade tubes exist but the characteristics are similar to the S-B tube; thus only
the S-B tube is discussed here. Endotracheal intubation is performed prior to tube
placement to prevent aspiration.

The S-B tube has both esophageal and gastric balloons. The gastric balloon is inflated
first (placement is verified by x-ray if time allows) and is pulled tautly against the junction
of the stomach and esophagus to prevent migration of the esophageal balloon upward
into the airway. The esophageal balloon is inflated once the gastric balloon is
appropriately placed. Both balloons are maintained at specific pressures to ensure
accurate placement and tamponade. Esophageal suction is maintained to prevent
aspiration while the S-B tube is in place. Some tubes have a port for this and others do
not in which case an additional suction tube is inserted. Constant tension is maintained
on the S-B tube via weights or the use of a helmet to which the tube is attached to
prevent slipping of the tubes into the stomach. Gastric balloon rupture can cause the
esophageal balloon to migrate upward. This is an emergency and thus scissors are kept
at the bedside to cut and remove the tube if necessary.
Monitor for other complications of this double (gastric and esophageal) balloon tube,
including, but not limited to, pulmonary aspiration, rupture of the esophagus, asphyxia,
and erosion of the esophageal or gastric wall. Rebleeding is common after deflation or
removal of the tamponade tube. Refer to AACN's procedure manual or institutional
policies and procedures for specific details of placement, management, and monitoring
of the S-B tube.

Shunt Procedure to Control Bleeding

When severe variceal bleeding cannot be controlled with endoscopic intervention,
emergent portal decompression is achieved with the percutaneous transjugular
intrahepatic portosystemic shunt (TIPS).

In the TIPS procedure, a stent is used to create a shunt between the hepatic vein and a
branch of the portal vein. This decreases the pressure in the portal vein (decreases
portal pressure) and subsequently on the varices to prevent rupture and bleeding.

The advantage of the TIPS procedure is that it is less invasive than surgery because the
portal circulation is accessed via the right jugular vein. Contraindications to TIPS include
severe-progressive liver failure, severe encephalopathy, polycystic liver disease, and
severe right heart failure. Complications of the TIPS procedures include puncture of the
biliary system, bleeding, infection, and clotting of the stent and stenosis. Postprocedural
systemic failure (septic shock, renal failure) and hepatic encephalopathy are also
associated complications.

Nursing management of the patient undergoing TIPS includes:

1. Monitor blood pressure, ECG, and pulse oximetry throughout the procedure.
2. Administer preprocedure antibiotic coverage for gram-negative organisms as
prophylaxis for sepsis.
3. Provide IV sedation.
4. Provide pain medication (eg, fentanyl). Certain parts of the procedure, such as balloon
dilation of the intrahepatic tract, can be painful.
5. Have lidocaine and atropine available to manage potential complications of the
procedure. Due to the proximity of the hepatic vein to the right ventricle of the heart,
ventricular ectopy can be induced during the procedure.
6. Have crystalloids, vasopressors, PRBCs, and fresh frozen plasma readily available to
manage hypotension from sepsis, bleeding, or sedation.
7. Have continuous and intermittent suction ready to manage bleeding and airway
patency.

An alternative to TIPS available at some institutions is the balloon-occluded retrograde

transvenous obliteration (BRTO) procedure. The procedure involves the occlusion of
blood flow to varices by inflating a balloon catheter and instilling a sclerosing agent. The
procedure results in a blockage of blood to the varix and the shunting of blood through
healthier veins. Further research is needed on the long-term results and effectiveness of
BRTO.

Surgical Therapies to Stop Bleeding

Surgery is less common today and is reserved for patients with refractory disease or
complications. Patients who experience life-threatening massive bleeding or who
continue to bleed despite aggressive medical therapies are candidates for surgery.
Surgical therapies include gastric resections such as antrectomy, partial gastrectomy,
vagotomy, or combination procedures. An antrectomy or gastrectomy may be performed
to decrease the acidity of the duodenum or stomach by removing gastric-acid secreting
cells. A vagotomy decreases acid secretion in the stomach by dividing the vagus nerve
along the esophagus. Combination procedures are common and one example is the
Billroth I, which is a vagotomy and antrectomy with anastomosis of the stomach to the
duodenum. A Billroth II consists of a vagotomy, resection of the antrum, and
anastomosis of the stomach to the jejunum (Figure 14-6). The latter is preferred over the
Billroth I because it does not present the risk for dumping syndrome. Gastric perforations
can be treated by simple closure.
Nursing considerations for patients undergoing surgery to treat GI bleed include:
1. Monitor for fluid and electrolyte imbalances postoperatively due to intraoperative fluid
loss and the drains inserted to decompress the stomach or to drain the surgical site.
2. Provide for adequate nutrition to promote wound healing.
3. Monitor the appearance of the incision and surrounding tissue.
4. Document and report all wound drainage ( color, amount, odor) and complaints of
pain or tenderness.
5. Culture any suspicious drainage.
6. Monitor white blood cell count and temperature trends.

Reducing Anxiety
1. Encourage communication with a calm, interested, and centered approach. If the
patient is intubated, consider written communication or use of a communication board.
2. Encourage the patient to identify and use coping skills used in past difficult situations.
These may include family presence, watching TV, listening to music, or relaxation
techniques to alleviate anxiety.
3. Offer appropriate reassurance, facts, and information as requested by the patient or
family. Explain the ICU routine and procedures to the patient or family. Present
information in terms that the patient or family can understand. Repeat and rephrase the
information as necessary. Allow time for questions.
4. As appropriate, help the patient establish a sense of control. Assist the patient to
make distinctions among those things he or she can control ( eg, bath time, visitor
preferences) and those things that cannot be controlled ( eg, need for vasopressors and
monitoring equipment).
5. Guide the patient to use relaxation exercises and other diversion strategies to
decrease anxiety.