DISTURBAN

CES IN
INGESTION
 GASTROESOPHAGEAL REFLUX DISEASE

• Some degree of gastroesophageal

reflux (back-flow of gastric or
duodenal contents into the esophagus)
is normal in both adults and children.
Excessive reflux may occur because
of an incompetent lower esophageal
sphincter, pyloric stenosis, or a
motility disorder.
 Clinical manifestations symptoms

• Pyrosis (burning sensation n in the esophagus),

• Dyspepsia (indigestion),
• Regurgitation,
• Dysphagia or odynophagia (difficulty swallowing, pain on
swallowing),
• Hypersalivation, and esophagitis. The symptoms may mimic
those of a heart attack. The patient’s history aids in obtaining an
accurate diagnosis
 Assessment and diagnostic findings

• Diagnostic testing may include an endoscopy or barium

swallow to evaluate damage to the esophageal mucosa.
• Ambulatory 12- to 36-hour esophageal ph monitoring is
used to evaluate the degree of acid reflux.
• Bilirubin monitoring (bilitec) is used to measure bile
reflux patterns. Exposure to bile can cause mucosal
damage
 Nursing management

• Instruct the client to avoid factors that decrease lower

esophageal sphincter (les) pressure or cause esophageal
irritation, such as peppermint, chocolate, coffee, fried or
fatty foods, carbonated beverages, alcoholic beverages,
and cigarette smoking.
• Instruct the client to eat a low-fat, high-fiber diet and to
avoid eating and drinking 2 hours before bedtime and
wearing tight clothes; also, elevate the head of the bed
on 6- to 8-inch (15 to 20 cm) blocks.
• Avoid the use of anticholinergics, which delay stomach
emptying; also, nonsteroidal antiinflammatory
medications (nsaids) and other medications that contain
acetylsalicylic acid need to be avoided.
 Medical management

• If reflux persists, the patient may be given medications such

as
• Antacids or histamine receptor blockers.
• Proton pump inhibitors (medications that decrease the release of
gastric acid, such as lansoprazole [prevacid] or rabeprazole
[aciphex])
• Prokinetic agents, which accelerate gastric emptying. These agents
include bethanechol (urecholine), domperidone (motilium), and
metoclopramide (reglan).
 Surgical management

• Fundoplication (wrapping of
a portion of the gastric
fundus around the sphincter
area of the esophagus).
Fundoplication may be
performed by laparoscopy
 ACHALASIA
• absent or ineffective peristalsis of the
distal esophagus, accompanied by
failure of the esophageal sphincter to
relax in response to swallowing.
Narrowing of the esophagus just
above the stomach results in a
gradually increasing dilation of the
esophagus in the upper chest.
Achalasia may progress slowly and
occurs most often in people 40 years
of age or older.
 CLINICAL MANIFESTATIONS

• Difficulty in swallowing both liquids and solids.

• Sensation of food sticking in the lower portion of the esophagus
• As the condition progresses, food is commonly regurgitated,
either spontaneously or intentionally
• Chest pain and heartburn (pyrosis).
• Pain may or may not be associated with eating.
• Secondary pulmonary complications from aspiration of gastric
contents.
 Assessment and diagnostic findings
• X-ray studies show esophageal dilation above the narrowing
at the gastroesophageal junction.
• Barium swallow
• Computed tomography(ct) of the esophagus
• Endoscopy may be used for diagnosis
• Diagnosis is confirmed by manometry- a process in which
the esophageal pressure is measured by a radiologist or
gastroenterologist.
 Nursing management
• The patient should be instructed to eat slowly and to drink
fluids with meals.
• As a temporary measure, calcium channel blockers and
nitrates have been used to decrease esophageal pressure and
improve swallowing.
• Injection of botulinum toxin (botox) to quadrants of the
esophagus via endoscopy
 Surgical management
• Pneumatic (forceful) dilation or
surgical separation of the muscle
fibers to stretch the narrowed area
of the esophagus. The patient is
monitored for perforation.
Complaints of abdominal
tenderness and fever may be
indications of perforation.
• Esophagomyotomy usually is
performed laparoscopically,
either with a complete lower
esophageal sphincter myotomy
and an antireflux procedure or
without an antireflux procedure.
The esophageal muscle fibers
are separated to relieve the
lower esophageal stricture.
Medical Mgt:
 Medications – Nitrates, Nifedipine – to decrease LES pressure
 Forceful dilation of the LES by pneumatic dilators  a balloon is inserted
and inflated for 1 min., 2-3 times
- opens the sphincter and relieves the dysphagia

Nsg. Interventions:
 encourage pt. to drink fluids with meals and use the valsalva maneuver
(bearing down with a closed glottis) while swallowing  to help push the
food
 advise soft diet
 elevate head during sleeping to prevent regurgitation
 after esophageal surgery, monitor for signs of esophageal perforation as
evidenced by chest pain, shock, dyspnea and fever
 HIATAL HERNIA
• The esophagus enters the abdomen through an opening
in the diaphragm and empties at its lower end into the
upper part of the stomach.
• the opening in the diaphragm through which the
esophagus passes becomes enlarged, and part of the
upper stomach tends to move up into the lower portion
of the thorax. Hiatal hernia occurs more often in
women than men.
 Two types of hiatal hernias

• Sliding, or type I, hiatal hernia

occurs when the upper
stomach and the
gastroesophageal junction
(GEJ) are displaced upward
and slide in and out of the
thorax
• Paraesophageal hernia occurs
when all or part of the stomach
pushes through the diaphragm
beside the esophagus.
Paraesophageal hernias may be
further classified as types II, III,
or IV, depending on the extent of
herniation, with type IV having
the greatest herniation.
 Clinical manifestations
• The patient with a sliding hernia may have
• Heartburn,
• Regurgitation
• Dysphagia
• Often implicated in reflux.
• The patient with a paraesophageal hernia
usually feels a
• Sense of fullness after eating or may be
asymptomatic.
• Reflux usually does not occur, because the
gastroesophageal sphincter is intact.
 *THE COMPLICATIONS OF
HEMORRHAGE,
OBSTRUCTION, AND
STRANGULATION CAN OCCUR
WITH ANY TYPE OF HERNIA.
Assessment and diagnostic
findings
•X-ray studies
•Barium swallow
•Fluoroscopy.
 Nursing management

• Frequent, small feedings that can pass easily through the

esophagus
• Not to recline for 1 hour after eating, to prevent reflux or
movement of the hernia
• To elevate the head of the bed on 4- to 8-inch (10- to 20-
cm) blocks to prevent the hernia from sliding upward.
MANAGEMENT
• MEDICATIONS
• ANTACIDS
• ANTIEMETICS
• HISTAMINE RECEPTOR ANTAGONIST
• GASTRIC ACID SECRETION INHIBITOR

• AVOID; THESE DRUGS LOWERS THE LES (LOWER ESOPHAGEAL

SPHINCTER) PRESSURE:
• ANTICHOLINERGICS
• XANTHINE DERIVATIVES
• CA-CHANNEL BLOCKERS
• DIAZEPAM
 SURGICAL MANAGEMENT

• Surgery is indicated in about 15% of patients. Medical

and surgical management of a paraesophageal hernia is
similar to that for gastroesophageal reflux
• paraesophageal hernias may require emergency surgery
to correct torsion (twisting) of the stomach or other
body organ that leads to restriction of blood flow to
that area.
DISTURBAN
CES IN
DIGESTION
 NAUSEA AND VOMITING

• Nausea and vomiting are the most common

manifestations of gastrointestinal (GI) diseases.
Although nausea and vomiting can occur
independently, they are usually closely related and
treated as one problem.
• Nausea is a feeling of discomfort in the epigastrium
with a conscious desire to vomit.
• Vomiting is the forceful ejection of partially digested food
and secretions (emesis) from the upper GI tract.
• closure of the glottis, deep inspiration with contraction of the
diaphragm in the inspiratory position, closure of the pylorus,
relaxation of the stomach and lower esophageal sphincter
(LES), and contraction of the abdominal muscles with
increasing intraabdominal pressure. These simultaneous
activities force the stomach contents up through the
esophagus, into the pharynx, and out the mouth.
 CAUSES

•Nausea and vomiting occur in a wide

variety of GI disorders and in conditions
that are unrelated to GI disease
• Pregnancy
• Infection
• Central nervous system (CNS) disorders (e.G.,
Meningitis, tumor)
• Cardiovascular problems (e.G., Myocardial infarction,
heart failure)
• Metabolic disorders (e.G., Diabetes mellitus, addison’s
disease, renal failure)
• Postoperatively after general anesthesia
• Side effects of drugs (e.G., Chemotherapy,
opioids, digitalis)
• Psychologic factors (e.G., Stress, fear)
• And conditions in which the GI tract becomes
overly irritated, excited, or distended.
 Pathophysiology
• A vomiting center in the brainstem coordinates the multiple
components involved in vomiting. This center receives input
from various stimuli. Neural impulses reach the vomiting
center via afferent pathways through branches of the autonomic
nervous system. Receptors for these afferent fibers are located
in the GI tract, kidneys, heart, and uterus. When stimulated,
these receptors relay information to the vomiting center, which
then initiates the vomiting reflex.
• The chemoreceptor trigger zone (CTZ) located in the brainstem
responds to chemical stimuli of drugs, toxins, and labyrinthine
stimulation (e.G., Motion sickness). Once stimulated, the CTZ
transmits impulses directly to the vomiting center. This action
activates the autonomic nervous system, resulting in both
parasympathetic and sympathetic stimulation. Sympathetic
activation produces tachycardia, tachypnea, and diaphoresis.
Parasympathetic stimulation causes relaxation of the LES, an
increase in gastric motility, and a pronounced increase in
salivation.
 Clinical manifestations

• Nausea is a subjective complaint.

• Anorexia (lack of appetite) usually accompanies
nausea.
• Dehydration if it occur over a long period of time.
• As vomiting persists, the patient may have severe
electrolyte imbalances, loss of extracellular fluid
volume, decreased plasma volume, and eventually
circulatory failure.
• Metabolic alkalosis can result from loss of gastric
hydrochloric (HCl) acid.
• Weight loss resulting from fluid loss
 Nursing management
• Prevent aspiration, put the patient who cannot
adequately manage self-care in a semi-fowler’s or
side-lying position.
• Determine and treat the underlying cause of the
nausea and vomiting and to provide symptomatic
relief. Assess the patient for precipitating factors, and
describe the contents of the emesis.
 Medical management
• Antiemetics before determining the cause can mask the underlying
disease process and delay diagnosis and treatment.
• The serotonin (5-HTP)
• Receptor antagonists are effective in reducing cancer
chemotherapy–induced vomiting caused by delayed gastric
emptying and also the nausea and vomiting related to migraine
headache and anxiety
• 5-HT3 antagonists are also used in prevention and treatment of
postoperative nausea and vomiting.
• Dexamethasone (decadron) is used in the management of
both acute and delayed cancer chemotherapy– induced
emesis
• P/neurokinin-1 receptor antagonist, is used for the
prevention of chemotherapy-induced and postoperative
nausea and vomiting.
• Dronabinol (marinol) is an orally active cannabinoid that is
used alone or in combination with other antiemetics for the
prevention of chemotherapy-induced emesis.
 GASTRITIS

• Inflammation of the gastric or

stomach mucosa is a common GI
problem. Gastritis may be acute,
lasting several hours to a few days,
or chronic, resulting from repeated
exposure to irritating agents or
recurring episodes of acute gastritis.
 CAUSES
• Acute gastritis is often caused by
• Dietary indiscretion—the person eats food that is contaminated
with disease-causing microorganisms or that is irritating or too
highly seasoned.
• Overuse of aspirin and other nonsteroidal anti-inflammatory drugs
(nsaids),
• Excessive alcohol intake,
• Bile reflux
• Radiation therapy
• Ingestion of strong acid or alkali, which may cause
the mucosa to become gangrenous or to perforate.
• May be the first sign of an acute systemic infection.
• Sometimes associated with autoimmune diseases such
as pernicious anemia
 Clinical manifestations

• The patient • Headache,

*Some patients, however,
with acute • Lassitude, have no symptoms.
gastritis may • Nausea,
have • Anorexia,
• Abdominal • Vomiting,
discomfort, and
• Hiccupping.
 CHRONIC GASTRITIS
• Anorexia vomiting.
• Heartburn after • Evidence of
eating malabsorption of
• Belching vitamin b12
caused by
• Sour taste in the
antibodies
mouth
against intrinsic
• Nausea and factor.
 Assessment and diagnostic findings

• Gastritis is sometimes associated with

achlorhydria or hypochlorhydria (absence or
low levels of hydrochloric acid [HCl]) or with
hyperchlorhydria (high levels of HCl).
• Diagnosis can be determined by endoscopy,
• Upper GI radiographic studies
• Histologic examination of a tissue specimen obtained by
biopsy
• Other diagnostic measures for detecting H. Pylori include
serologic testing for antibodies against the H. Pylori antigen,
a 1-minute ultrarapid urease test, and a breath test.
 Nursing management
• The gastric mucosa is capable of repairing itself after a bout of
gastritis. As a rule, the patient recovers in about 1 day, although
the appetite may be diminished for an additional 2 or 3 days.
• Instruct the patient to refrain from alcohol and food until symptoms
subside.
• Nonirritating diet is recommended
• fluids may need to be administered parenterally.
• If bleeding is present, management is similar to the procedures used for
upper gi tract hemorrhage
 Medical management

• To neutralize acids, common antacids (eg, aluminum

hydroxide) are used
• To neutralize an alkali, diluted lemon juice or diluted
vinegar is used.
• If corrosion is extensive or severe, emetics and lavage are
avoided because of the danger of perforation and damage to
the esophagus
• Therapy is supportive and may include nasogastric (NG)
intubation, analgesic agents and sedatives, antacids, and
intravenous (IV) fluids.
• H. Pylori may be treated with antibiotics (eg, tetracycline or
amoxicillin, combined with clarithromycin) and a proton
pump inhibitor (eg, lansoprazole [prevacid]), and possibly
bismuth salts (pepto-bismol)
• Fiberoptic endoscopy may be necessary.
 Surgical management

• Gastrojejunostomy or
gastric resection may be
necessary to treat pyloric
obstruction, a narrowing
of the pyloric orifice.
 GASTRIC AND DUODENAL ULCERS
• A peptic ulcer is an excavation (hollowed-out area) that
forms in the mucosal wall of the stomach, in the pylorus
(opening between stomach and duodenum), in the
duodenum (first part of small intestine), or in the esophagus.
A peptic ulcer is frequently referred to as a gastric,
duodenal, or esophageal ulcer, depending on its location, or
as peptic ulcer disease. Erosion of a circumscribed area of
mucous membrane is the cause
Pathophysiology

Emotional Cigarette Genetic

Psychogenic Drugs Caffeine Alcohol Smoking Factors

Imbalance between Acid secretion and mucosal barrier

Autodigestion

Erosion
Painless

Ulceration Pain

N/V

Bleeding
 GASTRIC ULCERS

• Involves ulceration of the mucosal lining that

extends to the submucosal layer of the stomach.
ALSO CHARACTERIZED BY REFLUX INTO
THE STOMACH OF BILE CONTAINING
DUODENAL CONTENTS
OCCURS MORE OFTEN IN MEN, IN
UNSKILLED LABORERS, AND IN LOWER
SOCIOECONOMIC GROUPS; PEAK AGE 40 – 55
YEARS (OLDER AGE GROUP)
 Predisposing factors
• Stress ids • Alcohol
• Smoking • NSAIDS • History of gastritis
• Use of • Family history of gastric
corticostero ulcers
• Infection with H. Pylori
  
Clinical manifestations

• Gnawing, sharp pain in or to the left of the mid-

epigastric region occurs 30 to 60 minutes after a
meal (food ingestion accentuates the pain
• Hematemesis is more common than melena.
 Nursing management
• Monitor vital signs and for signs of bleeding.
• Administer small, frequent bland feedings during the active
phase.
• Client education about avoidance of the following
• Alcohol and substances that contain caffeine or
chocolate.
• Smoking.
• Aspirin or NSAIDS
 Pharmacological management

• Administer h2-receptorantagonists or proton pump

inhibitors as prescribed to decrease the secretion of
gastric acid.
• Administer antacids as prescribed to neutralize
gastric secretions.
• Administer anticholinergics as prescribed to reduce
gastric motility.
• Administer mucosal barrier protectants as prescribed
1 hour before each meal.
• Administer prostaglandins as prescribed for their
protective and antisecretory actions
 Managements during active bleeding

• Monitor vital signs closely.

• Assess for signs of dehydration,
hypovolemic shock, sepsis, and respiratory
insufficiency.
•Maintain NPO status and administer intravenous
(IV) fluid replacement as prescribed
•Monitor intake and output.
•Monitor hemoglobin and hematocrit.
•Administer blood transfusions as prescribed .
 Surgical managements

• Total gastrectomy: removal

of the stomach with
attachment of the esophagus
to the jejunum or duodenum;
also called
esophagojejunostomy or
esophagoduodenostomy
• Vagotomy: surgical
division of the vagus nerve
to eliminate the vagal
impulses that stimulate
hydrochloric acid secretion
in the stomach
• Gastric resection:
removal of the
lower half of the
stomach and usually
includes a
vagotomy; also
called antrectomy
• Gastroduodenostomy
: partial gastrectomy,
with the remaining
segment anastomosed
to the duodenum; also
called BILLROTH I
• Gastrojejunostomy: partial
gastrectomy, with the
remaining segment
anastomosed to the jejunum;
also called BILLROTH II
• Pyloroplasty:
enlargement of the
pylorus to prevent or
decrease pyloric
obstruction, thereby
enhancing gastric
emptying
SUMMARY OF NURSING MANAGEMENT OF THE
PATIENT UNDERGOING GASTRIC SURGERY
PRE – OP CARE
 TEACH DEEP BREATHING EXERCISES (HIGH
ABDOMINAL INCISION CAUSES RESPIRATORY
COMPLICATIONS).
 PROVIDE NUTRITIONAL SUPPORT  TPN
 INFORM ABOUT POST-OP MEASURES AND TUBES TO
ANTICIPATE
NASOGASTRIC TUBE
TPN UNTIL PERISTALSIS RETURNS
POST-OP CARE
 PROMOTE PATENT AIRWAY AND VENTILATION
 SEMI-FOWLER’S POSITION
 REINFORCE DEEP BREATHING AND COUGHING
EXERCISE, INCENTIVE SPIROMETRY
 ADMINISTER ANALGESIC BEFORE ACTIVITIES
 SPLINT INCISION BEFORE PATIENT COUGHS
 ENCOURAGE EARLY AMBULATION
• Assess bowel sounds.
• Monitor and suction as prescribed.
• Maintain npo status as prescribed for 1 to 3 days until
peristalsis returns.
• Progress the diet from npo to sips of clear water to 6 small
bland meals a day, as prescribed when bowel sounds return.
• Monitor for postoperative complications of hemorrhage,
dumping syndrome, diarrhea, hypoglycemia, and vitamin
b12 deficiency
SUMMARY OF NURSING MANAGEMENT OF THE
PATIENT UNDERGOING GASTRIC SURGERY
PROMOTE ADEQUATE NUTRITION
 NPO UNTIL PERISTALSIS RETURNS
 MEASURE DRAINAGE ACCURATELY (REDDISH FOR THE FIRST
12 HRS.)
 MONITOR FOR SIGN OF LEAKAGE OF ANASTOMOSIS, E.G.
DYSPNEA, PAIN, FEVER, WHEN ORAL FLUIDS ARE INITIATED
 SMALL, FREQUENT FEEDINGS
 MONITOR FOR EARLY SATIETY AND REGURGITATION
 EAT LESS FOOD AT A SLOWER PACE
 MONITOR WEIGHT REGULARLY
 PREVENT POTENTIAL COMPLICATIONS
 BLEEDING – FIRST 24 HOURS, 4TH TO 7TH DAY POST-OP DUE TO
NON-HEALING
 MONITOR NG DRAINAGE FOR BLOOD
 AVOID UNNECESSARY IRRIGATION OR REPOSITIONING OF THE
NGT
 MONITOR FOR SIGNS OF PERITONITIS:
 SEVERE ABDOMINAL PAIN, RIGIDITY FEVER
DUMPING SYNDROME
 DUODENAL ULCERS

• A duodenal
ulcer is a break
in the mucosa of
the duodenum
 Risk factors and causes

• Infection intake • Caffeine

with H. • Smoking • Use of aspirin
Pylori • Stress • Corticosteroids
• Alcohol • NSAIDS.
 Clinical manifestations

• Burning pain occurs in the mid-epigastric area 1½ to

3 hours after a meal and during the night (often
awakens the client)
• Melena is more common than hematemesis
• Pain is often relieved by the ingestion of food.
 Nursing management
• Monitor vital signs.
• Instruct the client about a bland diet, with small, frequent
meals.
• Provide for adequate rest.
• Encourage the cessation of smoking.
• Instruct the client to avoid alcohol intake; caffeine; and the
use of aspirin, corticosteroids, and NSAIDS.
 Medical management
• Administer medications to treat H. Pylori and antacids
to neutralize acid secretions as prescribed.
• Administerh2-receptorantagonistsorproton pump
inhibitors as prescribed to block the secretion of acid.
 Surgical interventions

Surgery is performed only if the ulcer is unresponsive

to medications or if hemorrhage, obstruction, or
perforation occurs.
 UPPER GASTROINTESTINAL BLEEDING
• ETIOLOGY AND PATHOPHYSIOLOGY
Although the most serious loss of blood from the upper GI
tract is characterized by a sudden onset, insidious occult
bleeding can also be a major problem. The severity of
bleeding depends on whether the origin is venous, capillary,
or arterial. Bleeding from an arterial source is profuse, and the
blood is bright red, indicating it has not been in contact with
gastric hcl acid secretion.
• In contrast, “coffee-ground” vomitus indicates that the blood
has been in the stomach for some time. A massive upper GI
hemorrhage is a loss of more than 1500 ml of blood or 25%
of intravascular blood volume. Melena (black, tarry stools)
indicates slow bleeding from an upper GI source. The longer
the passage of blood through the intestines, the darker the
stool color because of the breakdown of hemoglobin and the
release of iron.
 Causes
• PEPTIC ULCER. This is the most common cause of
upper GI bleeding. Peptic ulcers are sores that develop on the lining
of the stomach and upper portion of the small intestine. Stomach
acid, either from bacteria or use of anti-inflammatory drugs,
damages the lining, leading to formation of sores.
• Tears in the lining of the tube that connects your throat to your
stomach (esophagus). Known as MALLORY-WEISS TEAR, they
can cause a lot of bleeding. These are most common in people who
drink alcohol to excess.
• Abnormal, enlarged veins in
the esophagus
(ESOPHAGEAL
VARICES). This condition
occurs most often in people
with serious liver disease.
• Esophagitis. This
inflammation of the
esophagus is most commonly
caused by gastroesophageal
reflux disease (GERD).
• Drugs (aspirin, nsaids, and corticosteroids)
• Stress-related mucosal disease (srmd), also called
physiologic stress ulcers, occurs in patients who have had
severe burns or trauma or major surgery.
• Patients with coagulopathy and those who experience
respiratory failure resulting in mechanical ventilation for
more than 48 hours are at highest risk.
 Clinical manifestations
• Hematemes zia • Dyspepsia
is • Syncope • Epigastric pain
• Melena • Heartburn
• Presyncope
• Hematoche • Jaundice • Diffuse abdominal pain
• Dysphagia
• Weight loss
 Assessment and diagnostic findings
• Endoscopy is the primary tool for diagnosing the source (e.G.,
Esophageal or gastric varices, gastritis) of upper GI bleeding
• Angiography is used in diagnosing upper GI bleeding when endoscopy
cannot be done or when bleeding persists after endoscopic therapy.
• Laboratory studies include CBC, blood urea nitrogen (BUN), serum
electrolytes, prothrombin time, partial thromboplastin time, liver
enzymes, arterial blood gases (ABGS), and a type and crossmatch for
possible blood transfusions.
 Nursing management

• A complete history of events leading to the bleeding episode

is deferred until emergency care has been initiated.
• Physical examination should focus on early identification of
signs and symptoms of shock such as tachycardia, weak
pulse, hypotension, cool extremities, prolonged capillary
refill, and apprehension.
• Monitor vital signs every 15 to 30 minutes.
• Do a thorough abdominal examination, and note the presence or
absence of bowel sounds.
• Iv lines, preferably two, with a 16- or 18-gauge needle are placed for
fluid and blood replacement.
• The use of supplemental oxygen delivered by face mask or nasal
cannula may help increase blood oxygen saturation.
• Indwelling urinary catheter is inserted so that output can be accurately
assessed hourly.
• A central venous pressure line may be inserted for fluid volume status
assessment.
 Pharmacological management

• During the acute phase of upper GI bleeding, empiric

proton pump inhibitor (PPI) therapy with high-dose
IV bolus and subsequent infusion is often started
before endoscopy.
• Injection therapy with epinephrine (1:10,000 dilution)
during endoscopy is effective for acute hemostasis.
• PPIs or h2-receptor blockers are administered IV to decrease acid
secretion
• In patients with upper GI bleeding, somatostatin or its long-acting
analog octreotide (sandostatin) may be administered when endoscopy
is not available.
• After an initial bolus, somatostatin is used for 3 to 7 days, whereas
octreotide is given for 3 days after the start of bleeding.
 Endoscopic management

• The first-line
management of upper GI
bleeding is endoscopy
and endotherapy.
• The goal of endoscopic hemostasis is to coagulate or thrombose the bleeding
vessel. Several techniques are used, including
• thermal (heat) probe
• multipolar and bipolar electrocoagulation probe
• argon plasma coagulation (APC)
• neodymium:yttrium-aluminum-garnet (nd:yag) laser.
• Multipolar electrocoagulation and thermal probe are the two most commonly used
procedures. The heat probe coagulates tissue by directly applying a heating element
to the bleeding site. The APC is a noncontact coagulation that delivers monopolar
current to tissue.
• For variceal bleeding, other strategies include variceal ligation, injection
sclerotherapy, and balloon tamponade
 Surgical management

• Surgical intervention is indicated when bleeding continues regardless

of the therapy provided and when the site of the bleeding has been
identified. Surgical therapy may be necessary when the patient
continues to bleed after rapid transfusion of up to 2000 ml of whole
blood or remains in shock after 24 hours. The site of the hemorrhage
determines the choice of operation
 LOWER GASTROINTESTINAL BLEEDING

• Commonly abbreviated LGIB, is any form

of gastrointestinal bleeding in the lower
gastrointestinal tract
 Causes
• Diverticular disease. This
involves the development of
small, bulging pouches in the
digestive tract
(diverticulosis). If one or
more of the pouches become
inflamed or infected, it's
called diverticulitis
• Inflammatory bowel
disease (IBD). This includes
ulcerative colitis, which
causes inflammation and
sores in the colon and
rectum, and crohn's disease,
and inflammation of the
lining of the digestive tract
• Tumors. Noncanerous (benign) or
cancerous tumors of the esophagus,
stomach, colon or rectum can weaken
the lining of the digestive tract and
cause bleeding.
• Colon polyps. Small clumps of cells
that form on the lining of your colon
can cause bleeding. Most are harmless,
but some might be cancerous or can
become cancerous if not removed
• Hemorrhoids. These are
swollen veins in your anus
or lower rectum, similar to
varicose veins
• Anal fissures. These are
small tears in the lining of
the anus.
• Proctitis. Inflammation of
the lining of the rectum can
cause rectal bleeding.
 Clinical manifestations
• The clinical presentation of LGIB varies with the
anatomical source of the bleeding, as follows:
• Maroon stools, with LGIB from the right side of the
colon
• Bright red blood per rectum with LGIB from the left
side of the colon
• Melena with cecal bleeding
• The presentation of LGIB can also vary depending on the
etiology. A young patient with infectious or noninfectious
(idiopathic) colitis may present with the following:
• Fever
• Dehydration
• Abdominal cramps
• Hematochezia
• An older patient with diverticular bleeding or
angiodysplasia may present with painless bleeding
and minimal symptoms. Ischemic colitis, abdominal
pain, and varying degrees of bleeding are usually
observed in patients with multiple comorbidities such
as congestive heart failure (CHF), atrial fibrillation, or
chronic renal failure (CRF).
 NURSING MANAGEMENT

•*Same with upper GI bleeding

 Assessment and diagnostic findings

• Nonsurgical modalities used to diagnose LGIB

include the following:
• Colonoscopy
• Radionuclide scans
• Angiography
• Fiberoptic flexible colonoscopy is the initial diagnostic method of
choice in most patients who are hemodynamically stable.
Colonoscopy should be performed following a rapid bowel
preparation (“prep”) with volume cathartic agents. Angiography is
also performed if colonoscopy has failed to identify a bleeding site.
Rarely, exploratory laparotomy and intraoperative push enteroscopy
can be performed in truly hemodynamically unstable patients owing
to the speed and the volume of the bleeding
• Appropriate routine blood tests include the following:
• Complete blood cell (CBC) count
• Serum electrolytes levels
• Coagulation profile, including activated partial
thromboplastin time (APTT), prothrombin time (PT),
platelet count, and/or bleeding time (bleeding time is only
recommended in patients with bleeding disorders and in
those using antiplatelet agents)
• Patients who have experienced multiple episodes of LGIB
without a known source or diagnosis should undergo the
following:
• Elective mesenteric angiography
• Upper and lower endoscopy
• Meckel scanning
• Upper GI imaging series with small bowel assessment
• Enteroclysis
 Medical and surgical management

• The management of LGIB has three components, as

follows:
• Resuscitation and initial assessment
• Localization of the bleeding site
• Therapeutic intervention to stop bleeding at the site
• Resuscitation and initial assessment
• Initial resuscitation involves establishing large-bore
intravenous (IV) access and administration of normal
saline. The patient's blood loss and hemodynamic status
should be ascertained and, in cases of severe bleeding, the
patient may require invasive hemodynamic monitoring to
direct therapy.
• Hemostasis
Once the bleeding site is localized, nonsurgical therapeutic options
that may be considered include the following:
• Diverticular bleeding: colonoscopy with bipolar probe coagulation,
epinephrine injection, or metallic clips
• Recurrent bleeding: resection of the affected bowel segment
• Angiodysplasia: thermal therapy (eg, electrocoagulation, argon plasma
coagulation)
• Conservative management, including nothing by mouth (NPO) and IV
hydration in patients with ischemic colitis
• In patients in whom the bleeding site cannot be
determined, vasoconstrictive agents such as
vasopressin (pitressin) can be used. If
vasopressin is unsuccessful or contraindicated,
superselective embolization is useful.
END OF PRESENTATION
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