COMMON GASTROINTESTINAL DISORDERS

Acute Gastrointestinal Bleeding

Upper Gastrointestinal Bleeding Lower Gastrointestinal Bleeding

Intestinal Obstruction and lleus

Small Bowel Obstruction Colonic Obstruction

llie us

Acute Pancreatitis

Etiology

Pathophysiology

Clinical Presentation

Assessment

Complications

Management

Hepatitis

Etiology

Pathophysiology

Assessment

Management

Complicarkins of Live, Disease

Cirrhosis

Hepatic Encephalopathy

Hepotorenal Syndrome

Spontaneous Bacterial Peritonitis

OBJECTIVES

Based on the content in this chapter, the reader should be able to:

• Examine the pathophysiological concepts that help define acute

gastrointestinal bleeding, obstruction and ileus, acute pancreatitis, hepatitis,
and cirrhosis.

• Compare and contrast the pertinent history, physical examination, and

diagnostic study findings for acute gastrointestinal bleeding, obstruction and
ileus, acute pancreatitis, hepatitis and cirrhosis.

• Discuss laboratory studies that are useful in the diagnosis and management
of acute gastrointestinal bleeding, obstruction and ileus, acute pancreatitis,
hepatitis, and cirrhosis.

• Analyze the similarities and differences in caring For patients with acute
gastrointestinal bleeding, obstruction and ileus, hepatitis, and cirrhosis.

• Explore the nursing role in assessing, managing, and evaluating a plan of

care for patients with acute gastrointestinal bleeding, obstruction and ileus,
acute pancreatitis, hepatitis, and cirrhosis.
ACUTE GASTROINTESTINAL BLEEDING

Acute gastrointestinal bleeding is a common, and potentially lethal, medical

emergency seen in people admitted to the intensive care unit (ICU). There are
500,000 hospital admissions each year in the United States as a result of acute
gastrointestinal bleeding.’ The 10% mortality rate associated with acute
gastrointestinal bleeding has remained constant over the past half century despite
advances in diagnosis and treatment.” The cause of death is rarely from
exsanguinations but rather from the exacerbation of other medical illnesses.
Prompt recognition and treatment of the patient experiencing an acute
gastrointestinal bleed requires a team approach.

Acute gastrointestinal bleeding is differentiated into upper and lower

gastrointestinal bleeding. ‘The ligament of Treitz at the junction of the duodenum
and jejunum is the anatomic division between the upper and lower gastrointestinal
tracts. An upper gastrointestinal bleed occurs from a source in the esophagus,
stomach, or duodenum. A lower gastrointestinal bleed occurs from, a source in the
jejunum, ileum, colon, or rectum.

UPPER GASTINTESTINAL BLEEDING

Etiology

The possible causes of acute upper gastrointestinal bleeding are listed in Box 41
LA complete discussion of this list is beyond the scope of this chapter. The most
commonly seen causes of acute gastrointestinal bleeding in the ICU are discussed.
Upper Gastrointestinal Bleeding
Esophageal Source
• Varices
• Esophagitis
• Ulcers
• Tumors
• Mallory-Weiss tears
Gastric Source
• Peptic ulcers
• Gastritis
• Tumors
• Angiodysplasia
• a Dieulafoys lesions
Duodenal Source
• Peptic ulcers
• Angiodysplasia
• Crohn’s disease
• Meckel’s diverticulum
Lower Gastrointestinal Bleeding
• Mal[gnant tumors
• Polyps
• Ulcerative colitis
• Crohn’s disease
• lschemic colitis
• Infectious colitis
• Angiodysplasia
• Diverticulosis
• Hemorrhoids
• • Massive upper gastrointestinal hemorrhage

Peptic Ulcer Disease

Peptic ulcer disease, which includes both gastric and duodenal ulcers,
accounts for approximately 50% of acute upper gastrointestinal bleeding. The
epithelial cells of the gastrointestinal mucosa are protected from the potentially
damaging effects of gastric secretions, medications, alcohol, and bacteria by
several protective mechanisms. These cells secrete nucins, phospholipids, and
bicarbonate that create a pH gradient between the acidic gastric lumen and the cell
surface. Prostaglandins enhance this mucosal protection by increasing mucosal
secretion, increasing bicarbonate production, maintaining mucosal blood flow, and
enhancing the resistance of gastrointestinal cells to injury. In addition, the tight
junctions of the epithelial cells resist diffusion. When these protective factors are
overwhelmed by aggressive factors, the integrity of the gastric or duodenal
mucosal is interrupted, which can result in peptic ulcer disease. Bleeding from
peptic ulcer disease occurs when the ulcer erodes into the wall of a blood vessel.
1’he primary risk factor for peptic ulcer disease is infection with the bacterium
Helicobacter pylori. H. pylon infection has been associated with 90% of duodenal
ulcers and 75% of gastric ulcers. H. pylon is a gram-negative, spiral, flagellated
rod that colonizes the mucus layer overlying the gastric epithelium. The flagellum
of H. pylon facilitates the bacterium’s ability to move and adhere to the mucus
layer. H. pylon produces urease, which converts urea to ammonia and carbon
dioxide. The ammonia buffers the acid surrounding the bacterium, creating a more
hospitable environment that allows the bacterium to thrive in the acidic stomach.
H. pylon infection predisposes the mucosa to damage by disrupting the mucus
layer, liberating enzymes and toxins, and adhering to the epithelium. Inflammation
is furthered by a host immune response. This chronic inflammation usually results
in an asymptomatic chronic gastritis. However, in some instances ulceration
develops.
In the absence of H. pylon infection, the ingestion of aspirin or nonsteroidal anti-
inflammatory drugs (NSAIDs) account for most cases of peptic ulcer disease. The
ingestion of aspirin and NSAJDs may directly injure the mucosal layer. Ingestion
enhances mucosal permeability and allows back-diffusion of acid. Systemic effects
of chronic aspirin or NSAID use include inhibition of prostaglandin synthesis by
the gastroduodenal mucosa, which decreases mucus and bicarbonate production, as
well as mucosal blood flow. This alteration in mucosal cytoprotection may lead to
the development of an ulcer. Cigarette smoking may also predispose to peptic ulcer
disease, and is linked to prolonged healing rates and high ulcer reoccurrence.
Stress-Related Erosive Syndrome
Stress-related erosive syndrome, also called erosive gastritis, stress ulceration, and
hemorrhagic gastritis, is a common cause of acute gastrointestinal bleeding in
critically ill patients. Stress ulcers are different from the ulcers of peptic ulcer
disease; they tend to be more numerous, more shallow, and more diffuse. These
ulcers may develop in the stomach, duodenum, and esophagus within hours of
injury. They are usually shallow and cause oozing from superficial capillaries, but
may erode into the sub-mucosa and cause massive hemorrhage.
The risk for development of a stress ulcer depends on the severity and type of
illness (Box 41-2). The common feature of these risk factors is the relationship to
physiological stress. Decreased perfusion of the stomach mucosa is probably the
main mechanism of ulcer development. This contributes to impaired mucus
secretion, low mucosal pH, poor mucosal cell regeneration, and decreased
tolerance to acid gastric secretions. Acute gastrointestinal bleeding from stress-
related erosive syndrome is associated with a high mortality rate.

Risk Factors for Stress-Related Erosive Syndrome

φ Hypotension or shock
φ Coagulopathy
φ Respiratory failure requiring mechanical ventilation
φ Sepsis
φ Hepatic failure
φ Rena] failure
 φ Multiple or severe trauma
φ Burns over 35% of the total body surface area (TBSA)
φ Post—organ transplant status
φ Head or spinal cord injury
φ History of peptic ulcer disease or upper gastrointestinal bleeding
φ Prolongeti stay in intensive care unit ICU)

Esophageal Varices

Portal hypertension usually develops as a result of cirrhosis, from increased

resistance in the portal venous system caused by disruption of the normal liver
lobular structure. This resistance impedes blood flow into, through, and out of the
liver. In response to portal hypertension, collateral veins develop to bypass the
increased portal resistance in an attempt to return blood to systemic circulation. As
pressure rises in these veins, they become tortuous and distended, forming varicose
veins or varices.

Varices may develop in the esophagus, stomach, duodenum, colon,

tecmm, or anus. The most clinically significant site of varices is the
gastroesophageal junction because of the propensity of varices in this area to
rupture, resulting in massive gastrointestinal hemorrhage. Esophageal varices
account for 10% to 15% of all cases of acute upper gastrointestinal bleeding.’ In
patients with cirrhosis, 60% of upper gastrointestinal bleeds are the result of
varices. The mortality rate associated with variceal bleeding is 40%.’

Mallory-Weiss Tears

Mallory-Weiss tears account for approximately 10% to 15% of acute upper

gastrointestinal bleeds.’ Mallory- Weiss tears are lacerations that occur in the distal
esophagus, at the gastroesophageal junction, and the cardia of the stomach.
Bleeding from Mallory-\Veiss tears occurs when the tear involves the underlying
venous or arterial bed. Mallory-Weiss tears are strongly associated with hea7
alcohol use or recent binge drinking and a prior history of forceflil vomiting or
retching, or violent coughing. Patients with portal hypertension have an increased
risk of bleeding from Mallory-Weiss tears.

Dieulafay ‘s Lesions

Dieulafoy’s lesions are vascular malformations of unusually large submucosal

arteries, which lie in close contact with the mucosal surface. They can be found
anywhere in the gastrointestinal tract but are most likely to be found in the
proximal stomach. Because of the large size of the artery, bleeding from a
Dieulafoy’s lesion may be massive and recurrent. Vhen bleeding ceases, a
Dieulafoy’s lesion can be difficult to identify because there is no associated

ulcer

CLINICAL PRESENTATION

Regardless of the cause, patients with acute upper gastrointestinal bleeding have a
clinical presentation consistent with the amount of blood loss. Patients with
minimal loss may present with anemia and no further symptoms, whereas those
patients with rapid and severe loss may present with signs and symptoms of shock.
If blood loss is moderate, the sympathetic nervous system responds with a release
of the catecholamines epinephrine and norepinephrine, which initially cause an
increase in heart rate and peripheral vascular vasoconstriction in an attempt to
maintain an adequate blood pressure. In this setting, orthostatic changes may be
present (a decrease in blood pressure greater than 10 mm Hg with a corresponding
heart rate increase of
20 beats/minute in the sitting or standing position), Orthostatic hypotension
indicates blood loss of greater than 1,000 mL.

The patient’s response to blood loss depends on the amount and rate of blood loss,
his or her age, the degree of compensation, and the rapidity of treatlucnt. Xkmith
severe blood loss, signs and symptoms of shock appear. The release of
catecholamines triggers the blood vessels in the skin, lungs, intestines, liver, and
kidneys to constrict, thereby increasing the volume of blood flow to the brain and
heart. Because of the decreased flow of blood in the skin, the person’s skin is cool
to the touch. With decreased blood flow to the lungs, hyperventilation occurs to
maintain adequate gas exchange.

The classic hallmarks of gastrointestinal bleeding are hematemesis, hematochezia,

and melena. Patients with upper gastrointestinal bleeding usually present with
he,natemesis, the vomiting of fresh, unaltered blood or “coffeeground” material;
anelcna, the passage of black, tarry, sticl’ stool; or both. A patient who presents
with hematemesis is usually bleeding from a source above the ligament of Treitz.
Reverse peristalsis is seldom sufficient to cause hematemesis if the bleeding point
is below this area. The classic “coffee-ground” emesis associated with upper
gastrointestinal bleeds results from the partial decumposition of the blood from
contact with gastric secretions. Gastric acid converts bright red hemoglobin to
brown hematin, accounting for the coffee-ground appearance of the drainage.
Maroon or bright red blood results from profuse bleeding and little contact with
gastric juices.

Melena is black from the breakdown of the blood in transit and suggests a long
transit time througb the gastrointestinal tract. Melena is indicative of an upper
gastrointestinal bleed in 90% of cases. It may take several days after bleeding
cessation for melenic stools to clear. After an upper gastrointestinal bleed, stool
may remain henioccultpositive for 1 to 2 weeks. Hematochezia, the passage of
maroon or bright red blood, usually indicates bleeding from a lower
gastrointestinal source. Uncommonly, heniatochezia can occur in the setting of
massive, rapid he,norrhage from the upper gastrointestinal tract, where the large
amount of blood acts as a cathartic and result in rapid transit through the
gastrointestinal tract.

ASSESSMENT

History

Patients may present with hematemesis, he,natochezia, or melena suggestive of an

upper gastrointestinal bleed, or hematochezia suggestive of a lower gastrointestinal
bleed. A prompt, careful, focused history may suggest the underlying cause. A
history of epigastric pain, dyspcpsia, or a past medical history of peptic ulcer
disease is suggestive of peptic ulcer disease. A past medical history of
gastrointestinal bleeding should be elicited because 60% of upper gastrointestinal
bleeds rehleed from the same site.’ Heavy alcohol use increases the likelihood of
cirrhosis and bleeding from esophageal varices. Patients with a history of tobacco
use have a greater risk for duodenal ulcers. Underlying medical conditions may
suggest an underlying cause; patients with renal failure frequently bleed from
arteriovenous malformations. Vomiting, coughing, or retching before bleeding
suggests a Mallory-Weiss tear. Prior use 0fNSAJD5 or aspirin increases the risk of
gastroduodenal ulcers, and the likelihood of bleeding from these ulcers.

Physical Examination

The physical examination should be directed initially to the assessment of

hemodynamic stability. Tachycardia and orthostatic hypotension indicate
dehydration secondary to blood loss or vomiting. Orthostatic hypotension is
suggestive of a greater than 15% blood volume loss, and tachycardia usually
occurs when greater than 15% of blood volume is lost. If 40% of blood volume is
lost, hypovolemia may occur) Therefore, assessing for signs and symptoms of poor
tissue perfusion such as angina, cyanosis, and altered mental status is important. A
baseline electrocardiogram is critical in patients with known cardiac disease
because blood loss may precipitate cardiac ischemia. A loss of circulating blood
volume may result in decreased cerebral perfusion. The nurse should be alert to
signs of agitation or confusion, which may signal cerebral hypo-perfusion. The
abdomen should be assessed for bowel sounds; abdominal tenderness; the presence
of guarding, rigidity, abdominal masses; and the stigmata of liver disease. A
tender, board like abdomen is suggestive of peritonitis, possibly as a result of
perforation. A rectal examination is essential to assess for hematochezia and
melena.

Laboratory Studies

Laboratory studies can help determine the extent of bleeding, and can often
provide a clue to the etiology. comumom laboratory abnormalities for the patient
with acute gastrointestinal bleeding are listed in Box 41-3. The initial hematocrit
and hemoglobin may not accurately reflect initial blood loss because plasma
volume is lost in the same proportion as red blood cells. Within 24 to 48 hours of
the initial bleed, redistribution of plasma from the extravascular to the
intravascular space results in a decreased hematocrit. Fluids administered during
resuscitation contribute to the heniodilution. Leukocytosis and hyperglycemia may
reflect the body’s response to stress. Hypokalemia and hypernatremia may result
from loss through emesis. An elevated blood urea nitrogen (BUN) level reflects a
large protein load from the breakdown of blood. A high BUN-to-creatinine ratio
suggests an upper gastrointestinal source of bleeding.’ Coagulopathy with a
prolonged prothrombin time (P1) can indicatç liver disease or concurrent long-term
anticoagulant therapy. Thrombocytopenia may be present in patients with cirrhosis
and portal hypertension with splenomegaly. If large amounts of blood are lost,
metabolic acidosis occurs as a result of anaerobic metabolism. Severe blood loss
can result in hypoxemia because of decreased circulating hemoglobin with
impairment of oxygen transport to cells.

BOX 41-3
• a Decreased hemoglobin and hematocrit
• Mild leukocytosis and hyperglycemia
• a Elevated blood urea nitrogen IBUNI level
• a Hypernatremia
• Hypokalemia
• Prolonged prothrombin time (PT)/partial thromboplastin time (PET)
• a Thrombocytopenia a Hypoxemia

MANAGEMENT

Resuscitation

The initial management of any patient with an acute gastrointestinal bleed is

directed at fluid resuscitation to reverse the effects of blood loss. Supplemental
oxygen is provided to any patient with an acute gastrointestinal bleed to promote
oxygen saturation and transport. Intubation may be required for actively bleeding
patients at high risk of aspiration, those with a diminished mental status, and those
in respiratory distress. Patients with acute upper gastrointestinal bleeding should be
made NPO because urgent endoscopy or surgery may be required. A Foley catheter
is inserted to monitor urine output as an indication of the adequacy of fluid
resuscitation. All patients with hemodynamic instability, a drop in heanatocrit,
transfusion requirements greater than 2 units of packed red blood cells (PRBCs), or
active bleeding warrant an ICU admission.

Volume Resuscitation. Patients with acute gastrointestinal bleeding require

immediate intravenous (IV) access with at least two large-bore (14- to l6-gauge)
IV catheters or central access. A type and cross-match should be sent early in the
course of the bleed because blood losses of greater than 1,500ml require blood
replacement in addition to fluids. While awaiting cross-matched blood, Ringer’s
lactate or normal saline is infused to restore circulating volume and to prevent the
progression to hypovolemic shock. Packed red blood cells are often transfused to
reestablish the oxygen-carrying capacity of the blood. Other blood products, such
as platelets and clotting factors, are ordered according to results of laboratory tests
and the patient’s underlying condition. Calcium replacement may be necessary if
large numbers of banked red blood cells are transfused because the citrate in
banked blood products can bind calcium and lead to hypocalcaemia. A pulmonary
artery catheter or central venous catheter may be useful to help avoid over-
resuscitation in patients with underlying renal or cardiac disease. In patients with a
coagulopathy, vitamin K can be given in the form of phytonadione (Aqua
MEPHYTON), 10 mg intramuscularly or very slowly intravenously, in an attempt
to restore the PT to normal. Fresh frozen plasma is ordered to correct the
abnormality if rapid correction of the abnormality is warranted.

Rarely, vasoactive drugs are used until fluid balance is restored to maintain blood
pressure and perfusion to vital body organs. Dopamine, epinephrine, and
norepinephrine are drugs that may be ordered to stabilize the patient until
definitive treatment can be undertaken.
Nasogastric Intubation. A large-bore nasogastric tube is placed in all patients with
gastrointestinal bleeding to aspirate and lavage gastric contents. A nasogastric tube
documents the presence and activity of bleeding. The color of gastric aspirate is
prognostically significant. “Coffee ground” or black nasogastric drainage with
melenic stools indicates a slow bleed, and has a corresponding 9% mortality rate,
whereas bright red nasogastric drainage and bright red blood in the stools signify a
rapidly bleeding upper gastrointestinal source, with a corresponding mortality rate
of 30%.

A nasogastric tube is also useful for decompression and lavage. Lavage helps to
clear blood from the stomach, which assists in identifying the source of bleeding
during endoscopy. Iced lavage should be avoided because it is uncomfortable, fails
to control bleeding, can significantly decrease core body temperature, and can
trigger cardiac dysrhythmias. Lavage should be performed with tap water or saline
—250 to 500 mL is instilled through the nasogastric rube and then removed with a
syringe or by intermittent wall suction until gastric secretions are clear.
Nasogustric tubes are usually removed after lavage of stomach contents unless the
patient is actively bleeding o is experiencing severe nausea and vomiting, because
a nasogastric tube may injure the gastric mucosa and contribute to bleeding.

Acid-Suppressive Therapy. Patients with acute upper gastrointestinal bleeding are

often treated with acid- suppressive therapy to decrease the risk of recurrent
bleeding, particularly from peptic ulcers. The use of high- dose proton pump
inhibitors (omeprazole, lansoprazole, esomeprazole, pantoprazole, rabeprazole) to
maintain a gastric pH greater than 4 has been shown to be beneficial in this
setting.2 Acid-suppressive therapy with histamine (J-I,)-antagonistic drugs
(cimetidine, ranitidine, famotidine, nizatidine) may be used as prophylactic therapy
in patients at high risk for stress-related erosive syndrome.
Antacids are also ordered. Antacids act as a direct alkaline buffer and are
administered to control gastric pH. Sucralfate, a basic aluminum salt of sucrose
octasulfate. acts locally as a cytoprotective drug and can be ordered for stress-
related erosive syndrome prophylaxis.

Pharmacotherapy for Decreasing Portal Hypertension. Even before a bleeding

source is identified, decreasing portal pressure with vasopressin or octreotide
should be considered in patients for whom variceal hemorrhage is suspected.
Vasopressin (Pitressin) decreases portal hypertension by constriction of the
splanchnic arteries, with reduces blood flow. Vasopressin is administered through
a central line at a rate of 0.4 to 1 U/minute. Complications 0f vasopressin therapy
can limit its use. Vasopressin reduces coronary blood flow and increases blood
pressure, which increases oxygen demand, and causes coronary artery constriction,
which can potentially result in multiple cardiac dysrhythmias. Because vgsopressin
also reduces blood flow to the mesenteric circulation, bowel ischemia can develop.
To minimize these potential side effects, vasopressin should be given with
concomitant use of IV, sublingual, or topical nitroglycerin to minimize the
systemic effects.

Somatostatin is a natural polypeptide that lowers portal venous pressure by

Vasoconstriction of splanchnic circu Somatostatin causes selective
vasoconstriction of the splanchnic circulation and is associated with fewer
systemic side effects than vasopressin. IV infusion is necessarv because of its short
half-life.

Octreotide (Sandostatin) is a synthetic analog ofsomauastatin with similar

hemodynamic properties but a longer half-life. Octreotide causes a 25% decrease
in splanchnic blood flow and a 30% to 35% decrease in intravariceal pressure.3
Octreotide is usually given as a SO-pg IV holus followed by 50 pg/hour for 3 to 5
days. The effects of octreotide are similar to vasopressin with nitroglycerin
infusion without the impact on hemodynamic or cardiac output.

Definitive Diagnosis

After patients with acute upper gastrointestinal bleeding are resuscitated,

endoscopyis considered. Endoscopy can be performed urgently at the bedside and
is the procedure of choice for the diagnosis and potential treatment of acute upper
gastrointestinal bleeding. Endoscopy within 12 to 24 hours of the initial bleed has
the best results. Then endoscopy is performed soon after bleeding, it has 90% to
95% accuracy in diagnosis.’ Early endoscopy is essential in gastrointestinal
bleeding from esophageal varices because the treatment is different. Endoscopy
allows the identification 0f the site of the bleed because direct mucosal inspection
is possible. The endoscopic appearance provides prognostic value for the risk of
rebleeding based on the presence of stigmata of recent bleeding and the patient’s
hemodynamic status.’ Vital signs must be monitored closely during endoscopy.
The left lateral decuhitus position decreases the risk of aspiration from active
bleeding.

When diagnostic endoscopy is unsuccessful due to massive hemorrhage,

angiography can he used to define the site of bleeding or abnormal vasculature,
Angiography can detect bleeding rates as low as 0.5 to 1 ml/minute.4

Barium studies, such as an upper gastrointestinal series, are not 0f any value
in acute upper gastrointestinal bleeding. These studies lack therapeutic capability
and preclude endoscopy and angiography because of retained bariuni. Barium
studies are also often inconclusive if there are clots in the stomach or if there is
superficial bleeding.
Therapeutic Intervention

Endoscopy. In addition to its use in diagnosis, endoscopy is the procedure of

choice for the treatment of a gastrointestinal bleed. Multiple therapeutic options are
available, including injection sclerotherapy, thermal coagulation, the placement of
hemostatic clips, and endoscopic variceal ligation (EVL). The optimal technique
depends on multiple variables, including the type and appearance of the lesIon and
the experience of the endoscopist.

The primary methods of endoscopic control of upper gastrointestinal hemorrhage

from peptic ulcers include injection therapy and thermal methods. Injection therapy
consists of the injection of an agent such as epinephrine around and into the
bleeding vessel. Thermal methods include heater probe and bipolar electro
coagulation (where a probe is applied with pressure to heat and seal the bleeding
vessel).5 Hemostatic clips, called endodips, have also been used successfully to
ligate bleeding blood vessels within a lesion.

EVL is the treatment of choice for the treatment of variceal bleeding. In EVL, a
rubber band is placed endoscopically around the base of each varix. This causes
coagulative necrosis and sloughing of thrombosed varices. EVL can control acute
variceal bleeding in 90% of cases with a reduction in the rate of rebleeding to
30%.’ An alternative to EVL is sclerotherapy. Injection sclerotherapy involves
injecting the varices with a sclerosing agent to stop the bleeding. These agents
cause local tamponade and vasoconstriction, causing necrosis and eventual
sclerosis of the bleeding vessel. Acute hemostasis rates are similar to those with
EVL, but sclerotherapy is associated with a higher complication rate.

Angiography. Most cases of gastrointestinal bleeding resolve spontaneously or can

be controlled during endoscopy. However, those patients with persistent bleeding
may require angiography to control the source of bleeding. During angiography,
arterial gastrointestinal bleeding can be controlled by the infusion of intra-arterial
vasopressin or by the Embolization of the artery by an interventional radiologist. If
therapeutic endoscopy fails this is a useful therapeutic option, particularly in those
who are critically ill and poor surgical candidates.

lntra-arterial vasopressin causes a generalized vasoconstriction that produces a

rapid reduction in local blood flow. Patients should be monitored closely for
dysrhythmias and fluid retention with resultant hyponatremia. Repeat angiography
is performed after the initial infusion and the dose can then be titrated as needed.
Once bleeding is controlled, this infusion may be continued in the ICU for 24 to 36
hours and then tapered over 24 hours.4 Patients should have cardiac monitoring
during vasopressin therapy to watch for cardiac dysrhythnias. Nitroglycerin
patches or drips may be used to counteract any ischemic changes.

Embolization of a bleeding vessel consists of occluding the vessel with material

that can be either temporary or permanent. Biodegradable long-acting gelatin
sponges are commonly used. These sponges cause hemostasis on contact when
injected into the vessel. Steel coils, balloons, and silk thread can be used to block
an artery mechanically, resulting in permanent occlusion.

Balloon Tamponade. Variceal bleeding unresponsive to endoscopic therapy can be

temporarily controlled with balloon tamponade in 60% to 90% of cases.’ Most
esophagogastric tubes have two balloons, one for the stomach and one for the
esophagus, and a distal port for gastric drainage. The Sengstaken-Blakemore tube
is the most widely used (Fig. 41-1).

With the use of balloon tamponade, pressure is exerted on the cardia of the
stomach and against the bleeding varices. The tube is inserted to at least 50 cm to
ensure gastric intubation. The gastric balloon is then slowly inflated with 250 to
300 ml of air, and gentle traction is applied, until the gastric balloon fits snugly
against the cardia of the stomach. Position is then confirmed by x-ray. Traction is
then placed on the tube where it enters the patient by means of a piece of sponge
rubber, as shown in Figure 41-1, or by traction fixed to a head helmet device or the
foot of bed. If chest pain occurs, the gastric balloon must be deflated immediately
because it may have shifted into the esophagus.

If bleeding continues, the esophageal balloon is inflated to a pressure of 25 to 40

mm Hg and maintained at this pressure for 24 to 48 hours. Although pressure for
longer than 24 hours may be needed to control bleeding, it can cause edema,
esophagitis, ulcerations, or perforation of the esophagus. After bleeding is
controlled, the balloon is maintained and inflated for no longer than 12 to 24 hours
to decrease the risk of gastric ischemia and necrosis. Unfortunately, rebleeding
often occurs after balloon deflation unless additional therapeutic measures are
taken.

A nasogastric tube should be placed in patients with a Sengstaken-Blakemore tube

to aspirate oral and nasopharyngeal secretions that collect above the esophageal
balloon, preventing aspiration of these secretions into the lungs. The Minnesota
esophagogastric tamponade tube (see Fig. 41-1) has a suction port above the
esophageal balloon in addition to the usual ports (two balloon, one gastric suction)
of the Sengstaken-Blakemore tube. Nursing interventions for the patient with an
esophageal tamponade tube are given in Box 4 1-4.

Transjugular Intrahepatic Portosystemic Shunt. A transjugular intrahepatic

portosystemic shunt (TIPS) is a radiologic procedure that creates an intrahepatic
shunt in an attempt to decrease portal pressure. The placement of TIPS may be
considered if other methods of managing esophageal varices fail.

Surgery. In the era of endoscopic therapy and proton pump inhibitors, surgery is
rarely used for the control of gastrointestinal bleeding. The indications for surgical
intervention are severe hemorrhage unresponsive to initial resuscitation, massive
bleeding that is immediately life-threatening, unavailable or failed endoscopic
therapy perforation, obstruction, suspicion of malignancy, or continued bleeding
despite aggressive medical therapies.

Surgical options for a bleeding peptic ulcer depend on the age and the condition of
the patient, as well as on the location, size, and anatomy of the bleeding source.
Emergency surgery of a bleeding duodenal ulcer may be a simple suturing (e.g.,
oversew) of the ulcer. Bleeding duodenal ulcers can also be treated using one of
the following procedures:

• Truncal vagotomy and pyloroplasty with suture ligation of the ulcer

• Truncal vagotomy and antrectomy with resection or suture ligation of the

ulcer

• Proximal gastric vagotomy with duodenotomy and suture ligation of the

ulcer

Bleeding gastric ulcers are commonly treated with one of the following
procedures:

• Truncal vagotomy and pyloroplasty with wedge resection of the ulcer

• Antrectomy with wedge excision of the proximal ulcer

• Distal gastrectomy with or without truncal vagotonw

 • Wedge resection of the
ulcero

A vagotomy involves
severing the vagus nerve, which
innervates the gastric cells. This
results in decreased gastric acid
secretion. A truncal (gastric)
vagotomy selectively cuts the
vagus distribution to the
stomach. A pyloroplasty is
necessary in conjunction with the
vagotomy because denervation of
the vagus nerve affects gastric
motility. A pyloroplasty allows
for continued gastric emptying.
An antrectomy removes acid-
producing cells in the stomach. A
Biliroth I procedure includes a
vagotomy and antrectomy with
anastoinosis of the stomach to
the duodenum. A Biliroth TI
procedure involves a vagotomy, resection of the antrum, and anastomosis of the
stomach to the jejunum (Fig. 41-2). A gastric perforation can be surgically treated
by simple closure or use of a patch to cover the mucosal hole.

Figure 41-1 Comparison of two types of esophageal tamponade tubes. (A) The
Sengstaken-Blakemore tube is the best known. An additional tube must be placed
in the proximal esophagus. (B) The Minnesota esophagogastnc tamponade tube
includes an esophageal aspirate lumen.

• Explain the purpose of the tube and the procedure to the patient

• Lubricate and chill the tube as directed by the manufacturer. Identify and
label the lumens of the tube.

• Check the patency of each lumen before insertion of the tube. Lavage the
patients stomach before insertion of the tube. Monitor the patient while the
physician inserts the tube. Elevate the head of the bed to 30 degrees to
prevent reflux. When a Sengstaken-Blakemore tube is in place, perform
oropharyngeal suction frequently to prevent aspiration, or place a second
nasogastric tube if ordered above the esophageal balloon to control
secretions and prevent aspiration

• Suction the esophageal port when a Minnesota tube is used. Maintain

nalloon pressure and traction.

• Maintain balloon position

• Clean and lubricate the patient’s nostrils frequently to prevent tube-caused

pressure areas.

• • Irrigate the nasogastric port every 2 hours to ensure patency and to keep
the stomach empty.

• Teach the patient to avoid coughing or straining, which increases intra-

abdominal pressure and predisposes to further bleeding.

• Have a second nasogastric tube, suction, and scissors available at the

 bedside.

• If the gastric balloon ruptures, the tube can rise into the nasooharynx.
Obstructing the airway. If this occurs, cut the tube immediately to deflate the
balloon rapidly.

• Cut and remove the tube whenever there is a question respiratory

insufficiency or aspiration

• Restrain the patient’s arms if the patient is at risk for pulling out the tube.
Agitation, confusion, and restlessness are risk factors.

• Assess for complications, including rupture or deflation of the balloon,

pulmonary aspiration, and esophageal rupture.

Surgical decompression of portal hypertension can be used in patients with

esophageal or gastric varices that are unresponsive to medical and endoscopic
therapy. In this surgery, a portosystemic shunt is created, connecting the portal
vein and the inferior vena cava to divert blood flow into the vena cava to decrease
pressure.

Medical Management. Once bleeding is controlled, management focuses on

treating the underlying cause of the acute upper gastrointestinal bleeding. For
patients with peptic ulcer disease, eradication of H, pylon and elimination of
NSAID use increases the healing rate and markedly reduces the recurrence of a
rebleed. Esophageal varices can be obliterated in subsequent endoscopy sessions,
and beta-blockade with propanolol (Inderal) or nadolol (Corgard) can be instituted
to decrease the rebleeding rate. The dose should be titrated to achieve a 25%
decrease in resting heart rate or a heart rate around 60 beats/minute as the desired
end point. Cessation of alcohol ingestion is imperative. See Box 41-5 for nursing
interventions in the care of the patient with acute gastrointestinal bleeding.

figure 41—2 (A) The Billroth I procedure induces a vagotomy and

antrectomy with anastomosis of the stomach to the duodenum. (B) The Billroth II
procedure includes a vagotomy, antrectomy, and anastomosis of the stomach to the
jejunum

Lower Gastrointestinal Bleeding

ETIOLOGY

Common causes of lower gastrointestinal bleeding are listed in Box 41-1. Most
cases of acute lower gastrointestinal bleeding that require ICU admission result
from diverticulitis or angiodysplasia, although bleeding from neoplasm, colitis,
inflammatory bowel disease, and hemorrhoids is also seen.

Diverticulosis

Daverticula are saclike protrusions in the colon wall that usually develop at
the point where arteries penetrate the colon wall. These vessels are separated from
the bowel lumen only by the mucosa and are subsequently prone to injury.
Diverticular bleeding accounts for 30% to 50% of all cases of acute lower
gastrointestinal bleeds.9 In the elderly, colonic diverticula account for 42% to 55%
of all cases of acute lower gastrointestinal bleeding.’ 0 Diverticular bleeding may
be massive, resulting in hemorrhage. Risk factors for diverticular bleeding include
a diet low in fiber, aspirin and NSAID use, advanced age, and constipation.

• Maintain a patent airway, elevate the head of the bed, and have suction
available at the bedside to prevent aspiration of emesis or blood.

• Administer oxygen therapy to treat hypoxia that may result from decreased
hemoglobin levers.

• Monitor pulse oximetry.

• Assess and document signs and symptoms of shock. such as restlessness:

diminished peripheral pulses: or cool, pale, or moist skin. Assess and document
vital signs, urinary output, hemodynamic values, and oxygen saturation (Sao2).

• Assess and document electrocardiographic monitoring and heart, lung, and

bowel sounds.

• Assist with the placement of a central venous pressure catheter or a

pulmonary artery catheter.

• Monitor and document central venous pressure (CVP). pulmonary artery

pressure (PAP), pulmonary artery wedge pressure (PAWP), cardiac output, and
systemic vascular resistance (SVR),

• Maintain IV access and administer IV fluids and blood products as ordered.

• Insert a nasogastric tube and lavage as ordered.

• Monitor gastric PH: consult with physician about specific pH range and
antacid administration.

• Administer antisecretory medications as ordered to reduce gastric acid

secretion.

• Administer vasopressin or octreotide as ordered

• Maintain accurate intake and output every 1 to 2 hours and PRN.

• Record urine, nasogastric drainage, and emesis

• Monitor electrolytes, which may be lost with fluids or altered due to fluid
shifts, and report abnormal values

• Monitor hemoglobin, hematocrit, red blood cell count. prothrombin time

(PT), partial thromboplastin time (PU), and blood urea nitrogen BUN) level and
report abnormal values.

• Provide mouth care as needed.

• Explain all procedures to the patient.

• Prepare the patient for diagnostic procedures and therapeutic interventions.

• Monitor the patient for potential complications of endoscopy or

colonoscopy, which include perforation, sepsis, pulmonary aspiration, and
induced bleeding.

• Teach the patient the importance of seeking medical intervention if signs or

symptoms of bleeding recur
 • Encourage smoking cessation and avoidance of alcohol

If lower gastrointestinal bleeding is chronic, patients may present with iron-

deficiency anemia and symptoms related to the anemia, such as weakness, fatigue,
or dyspnea on exertion. Massive bleeding from hemorrhoids is rare but can occur
in patients with rectal varices from portal hypertension.

ASSESSMENT

History

Relevant findings in the past medical history include abdominal surgery; a

previous bleeding episode; peptic ulcer disease; inflammatory bowel disease;
radiotion to the abdomen or pelvis; or cardiopulmonary, renal, or liver disease.
Knowledge of the patient’s current medications and the existence of any allergies
can also assist in diagnosis. A history of associated symptoms, including
abdominal pain, fever, rectal urgency, renesmus, weight loss, a change in bowel
habits, and the color and consistency of the stool should be elicited. The age of the
patient may give a clue to diagnosis because the risk of bleeding from diverticula
and angiodysplasia increases with age.

Physical Examination

The physical examination is often unremarkable. Viral signs are closely monitored
to assess for hemodynamic instability. A palpable mass may reveal a neoplosm. A
rectal examination is essential to assess for hematochezia and melena and exclude
the possibility of bleeding hemorrhoids, which can occasionally present as a
hemorrhage.

Laboratory Studies
The initial laboratory studies include a complete blood count, serum electrolytes,
BUN and creatinine levels, and P1 and partial thromboplastin time (PTI’). Type
and cross-match is mandatory before red blood cell transfusion, as in acute upper
gastrointestinal bleeding.

MANAGEM E NT

Resuscitation

The management of acute lower gastrointestinal bleeding requires aggressive fluid

resuscitation as described for acute upper gastrointestinal bleeding. Patients with
hematoeliezia should have a nasogastric tube inserted to exclude an upper
gastrointestinal source of bleeding because 10% of suspected lower gastrointestinal
bleeding occurs from tipper gastrointestinal sources.’ The presence of bloody
aspirate confirms an upper gastrointestinal source of bleeding. However, the
absence of blood does not exclude an upper gastrointestinal source because
bleeding from a site in the duodenum may riot reflux into the stomach. Nasogastric
aspirate that reveals bile without blood is unlikely in bleeding from an upper
gastrointestinal source. Once it is determined that bleeding is coming from a lower
gastrointestinal source, colonoscopy is the procedure of choice for both diagnosis
and treatment.

Definitive Diagnosis

Endoscopy. Colonoscopy is the test of choice for the evaluation of lower

gastrointestinal bleeding. Colonoscopy has a diagnostic accuracy of 70% to 80% in
patients with lower gastrointestinal bleeding.’’ Other advantages of colonoscopy
are the ability to precisely locate the source of the bleeding, the ability to take
biopsies, and the potential for therapeutic intervention. Before colonoscopy, the
colon needs to be cleansed with 4 L of polyethylene glycol solution given orally or
by nasogastric tube until the waste is clear. For those patients in whom bleeding
has stopped, it is reasonable to perform colonoscopy on an elective rather than
emergent basis. If a source of bleeding is identified during colonoscopy,
therapeutic options include thermal coagulation or injection with epinephrine or
other sclerosants, as discussed previously. Upper endoscopy should be performed
if colonoscopy is unable to distinguish a lower gastrointestinal source.

Radionucleatide Imaging. When colonoscopy fails to identify a bleeding source,

radionucleotide scanning can detect bleeding that occurs at rates of 0.1 to 0.5 ml/
minute. This is more sensitive than angiography but less specific than either
colonoscopy or a positive angiogram. The two types of scanning available are the
technetium (“Tc)—sulfur colloid and 9’Tc pertechnetate—labeled autologous red
blood cells. Unfortunately, both of these techniques provide poor localization
because of the penstrIde action of the bowel. However, these scans may be useful
before angiography because those patients with a negative scan are likely to have
negative angiograms.

Angiography. Angiography is reserved for patients with massive, ongoing bleeding

where endoscopy is not an acceptable option, or in the case of recurrent or
persistent bleeding from a source not identified on colonoscopy.

Angiography requires the active blood loss of 0.5 to 1.5 mL/ minute to visualize a
bleeding site.6 A positive angiograrn is associated with a high likelihood for
surgical intervention. When an active source is identified, arteriographic
intervention with intra-arterial vasopressin or ernholization maybe used. The
critical care nurse must be aware of the potential complications associated with
arteriography, which include allergy to contrast, contrast-induced renal failure,
bleeding from the arterial puncture site, and even embolism from thrombus.
Surgical Intervention

Surgical management of lower gastrointestinal bleeding is less likely to be an

emergent procedure. An exploratory laparotomy to identify the source of the
bleeding is often performed. A segmental bowel resection with a primary
anastomosis is often done for definitive treatment of lower gastrointestinal
bleeding. In patients who are unstable, a stoma and mucus fistula may be created.
In those patients with severe lower gastrointestinal bleeding without a localized
source, a blind total collection may be the operative choice. Surgical management
of diverticular bleeding is indicated if bleeding is not controlled with endoscopic or
angiographic means or in patients with recurrent bleeding from the same segment.

INTESTINAL OBSTRUCTION AND.WEUS

Intestinal obstruction occurs when the passage of intestinal contents through the
lumen is impaired. This can result from either mechanical (anatomical) or
nonmechanical causes. Ileus is the failure of passage of intestinal contents in the
absence 0f mechanical obstruction. Jntestinal obstruction is classified as either
partial or complete, depending on the degree of obstruction. In a simple obstruction
there is no ischemia, whereas in cases of strangulated obstruction, ischemia is
present. A closed-loop obstruction describes a mechanical obstruction with a
proximal and distal occlusion of the affected intestinal segment.

Bowel obstruction can occur in both the small and large bowel. The small bowel is
most commonly affected, with the ileum as the most common site of obstruction.
Large bowel obstruction accounts for only 15% of cases of bowel obstruction and
the sigmoid colon is the most common site of obstruction. The location of the
obstruction, the degree of obstruction, and the presence of ischemia are important
distinctions because treatment varies. Prompt recognition of bowel obstruction is
important for the critical care nurse because intestinal obstruction can progress to
bowel strangulation, infarction, and perforation and result in potentially life-
threatening peritoneal and systemic infection. The mortality rate associated with a
strangolated obstruction is 30%.i2

The causes of mechanical obstruction are varied and classified as extrinsic,

intrinsic, and intraluminal (Box 41-6). Extrinsic lesions occur outside of the bowel.
Examples of extrinsic lesions are adhesions, hernias, volvulus, and masses.
Intrinsic lesions extend into the bowel wall. Diverticulitis, neoplasms, and
radiation enteritis are examples of intrinsic lesions.