Disturbances in Digestion
 Identifies the source and cause of bleeding
Gastrointestinal bleeding
 A bleeding symptom either in upper of lower GI
 Maybe obvious in emesis or stool or occult or
hidden
TYPES OF GI BLEEDING (LOCATION)
Upper GI bleeding  diarrhea
• bleeding in the upper gastrointestinal tract
arising from the esophagus, stomach or
duodenum.
• Coffee ground or black
Lower GI Bleeding
 Bleeding occurs in the colon, rectum, or anus
 presents hematochezia or melena
Pathophysiology and Etiology
 Trauma in the GI tract
 Erosions or ulcers
 Ruptured of an enlarged vein such as varicosity
(esophageal or gastric varices
 Inflammation such as esophagitis (cause by
acid), gastritis,
 Inflammatory bowel disease (ulcerative colitis
and Crohn’s
 Alcohol and drugs ( aspirin, NSAIDS and
cortecosteroids)
 Diverticular disease
 Hemorrhoids or fissures
Clinical Manifestations
Characteristic of blood
 Bright red: vomited from high esophagus
(hematemesis), rectum or distal colon
 Mixed with dark red: higher up in colon and
small intestine, mixed with stool
 Coffee Ground: esophagus, stomach, and
duodenum
 Melena (black tarry stool) excessive blood in the
stomach
Signs and Symptoms of Bleeding
Massive bleeding
 Acute, bright red hematemesis or large amount
of black tarry stool
 Rapid pulse, hypotension, hypovolemia and
shock
Subacute bleeding
 Intermittent/alternate melena or coffee ground
emesis
 Weakness, dizziness
Chronic Bleeding
 Intermittent appearance of blood
 Increased weakness, paleness or SOB
 Occult blood
Diagnostic Evaluation/test/Assessment
History
 Change in bowel pattern,
 Presence of pain or tenderness
 Recent intake of food and what kind(red beef),
 Alcohol consumption and medications taken
(aspirin or steroids, NSAIDS)
CBC
 Low hemoglobin, high hematocrit, low platelet
 High PT( 10-12 sec )and aPTT( 30-45sec); NV
Endoscopy and MRI or CT
Stool test- for occult blood
Nursing Diagnosis
 Fluid volume deficit related to blood loss
 Altered Nutrition: Less than body
requirement related to nausea, vomiting and
EMERGENCY INTERVENTION
 Patient remains on NPO
 IV lines and oxygen therapy
 Administer vasopressin and blood replacement
because severe bleeding is life threatening and to
treat shock
 Intra arterial vasopressin- to slow or stop
bleeding from diverticulum
 Surgical if indicated.
Nasogastric tube Intubation
 An NG tube should be in place for most patients
with acute or upper GI bleeding
 2-3 L of tap water lavage and if the aspirate
continues to be bloody, this indicate that the
patient is in active bleeding that requires
emergent intervention
Nursing Interventions
Attaining Normal Fluid Volume
 Maintain NG tube and NPO status to rest GI
tract and evaluate bleeding
 Monitor I and O to evaluate fluid status and
hydration
 Monitor VS
 Administer IV fluids,
 Assess signs of shock such as hypotension,
tachycardia, tachypnea (increase RR), decrease
urine output, change in mental status.
Attaining Balance Nutritional Status
 Weigh daily to monitor caloric status’
 TPN, to promote hydration and nutrition while
on NPO restriction
 Begin liquids if patient is no longer on NPO,
then DAT. DAT should be high in calorie, high
CHON. Frequent small feedings if indicated.,
Patient Education
 Instruct the patient to report signs of GI
bleeding such as melena, emesis that is bright
red or coffee ground color, rectal bleeding,
weakness, fatigue and SOB
Evaluation
 Fluid volume is maintained, hypovolemic shock
is prevented
 Patient verbalized no signs of bleeding
 Nutritional and body weight status is maintained
Complications
 Hemorrhage, Shock, Death
GASTRITIS
 Inflammation of the gastric or stomach mucosa
 It affects both sexes but more common in older
adults
TYPES OF GASTRITIS
ACUTE
 lasting several hours to few days
Causes
 severe form of acute gastritis is caused by
ingestion of strong acid or alkali that may
cause the mucosa to become gangrene or
possible for perforation. Scarring can occur
which results to Pyloric stenosis (narrowing or
tightening) or obstruction
 AG maybe develop in acute illnesses or major
traumatic injuries (Burns, severe infection,
hepatic,kidney or respiratory failure and major
surgery also known as Stress Related Gastritis
CLASSIFICATION OF ACUTE GASTRITIS
Based on pathologic manifestations present in the gastric
mucosa (Wehbi, et al.,2104)
Erosive Acute Gastritis
 most often cause by local irritants such as
aspirin and other NSAIDS (Naproxen, Voltaren,
Ibuprofen), alcohol consumption and gastric
radiation therapy (Grossman, & Porth, 2014,
Wehbi, et al.,2104NIDDK, 2015)
Non-Erosive Acute Gastritis
 most often caused by an infection with
Helicobacter Pylori (H. Pylori) (Wehbi, et
al.,2104)
 70% of individauls in US and other
industrialized countries are infected with H.
Pylori (CDC, 2016)
CHRONIC
 results from repeated exposure to irritating
agents or recurrent episodes of acute gastritis
Causes
 H. Pylori infection is the most common cause
(Marcus and Greenwald, 2014). Chronic H.
Pylori gastritis is implicated in the development
ofPUD, gastric adeno carcinoma, and gastric
mucosa associated with lymphoid tissue
lymphoma (Chin, et al.,2015)
 Chemical gastric injury (Gastropathy)- long
term use of NSAIDS and aspirin
 Autoimmune disease- Hashimoto thyroiditis,
Addison’s disease, Grave’s disease are also be
associated with Chronic Gastritis (Grossman and
Porth, 2014; Marcus and Greenwald, 2014)
PATHOPHYSIOLOGY
 Gastritis is characterized by Disruption of the
mucosal barrier that normally protects the
stomach from digestive juices (Hcl and pepsin)
are irritating agents (Aspirin, NSAID and H.
Pylori) comes in contact with the gastric mucosa
that resulted to inflammation.
 In Acute gastritis, the inflammation is usually
transient and self-limiting in nature.
Inflammation causes the gastric mucosa to
become edematous and hyperemic (congested
with fluid and blood) and to undergo superficial
erosion which will result to hemorrhage.
 In chronic gastritis, persistent and repeated
insults lead to chronic inflammation that leads to
atrophy or thinning of the gastric tissue.
(Grossman and Porth, 2014)
Clinical Manifestations
Acute Gastritis- rapid onset of symptoms that last
from a few hours to a few days
 Hiccups
 Anorexia
 Epigastric pain (rapid onset
 Dyspepsia (Indigestion)
 Nausea and vomiting
 Melena (black, tarry stools,) hematemesis
(blood in vomitus), hematochezia (bright red,
bloody stools)- Erosive gastritis ,Possible sign of
shock
Chronic Gastritis
 Belching
 Early satiety Anorexia
 Intolerance to fatty and spicy foods
 Nausea and vomiting
 Pyrosis/heartburn (Burning sensation in the
stomach and esophagus that moves up into the
mouth after eating
 Sour taste in mouth
 Epigastric pain relieves by eating
 Systemic: Fatigue and anemia
Diagnostic Test
 Upper Endoscopy and histologic examination
confirms the diagnosis. This visualized
inflammatory changes lesions or erosion and can
determine H.Pylori by biopsy
 Other non invasive test that can detect H. Pylori
is through serologic testing for antibodies
against H Pylori antigen, stool antigen test ,
Urea breath test
 CBC- to assess anemia as a result of hemorrhage
NURSING INTERVENTIONS
Independent
Promoting Optimal Nutrition
 No foods of fluids by mouth for a few days-
until acute symptoms subside to allow gastric
mucosa to heal. (Erosive)
 Monitor I and O and electrolytes (Na, K,
Chloride) if in IVF every 24 hrs. to detect any
imbalances and signs of DHN (minimum oral
fluid intake of 1.5 L/day
 Assess for signs of hemorrhagic gastritis such as
hematemesis, tachycardia and hypotension. All
stools should examine for the presence of occult
bleeding.
 Monitor VS and notify the primary provider or
the attending physician.

Dependent Nursing Interventions
Diet
 Ice chips followed by clear liquids after
symptoms subsides then solid foods as ordered.
 Advise Non-irritating food. high-fiber foods,
such as whole grains, fruits, vegetables, and
beans. low-fat foods, such as fish, lean meats,
and vegetables. Foods with low acidity,
including vegetables and beans.
 IV fluids if symptom persist just to maintain
hydration if bleeding persist. If IV 3L/day
 NG tube intubation
 Administer antacids. H2 receptors blockers,
PPI, Antibiotics
Pharmacological Therapy
ANTACIDS
 Neutralized gastric acid by increasing the in pH
the GI tract. Provide symptomatic relief but do
not heal esophageal lesions.
 Ex: Aluminum hydroxide (Amphogel),
Aluminum hydroxide and Magnesium hydroxide
(Maalox); Milk of magnesia
 Antacids containing both aluminum and
magnesium hydroxide balance the constipating
effects of ALUMINUM with the LAXATIVE
effects of MAGNESIUM
Nursing Responsibilities
 shake the suspension or chewable tablets chew
them thoroughly and drink half glass of water to
promote passage to the stomach
 Give antacids at least 1 hour from enteric coated
tablets
Histamine 2 receptor antagonist/H2 blockers
 Inhibit or decrease acid production by blocking
action of histamine on histamine receptors of
parietal cells of the stomach
 Ex: Cimetidine (Tagamet), Famotidine (Pepcid),
Ranitidine (Zantac)
PROTON PUMP INHIBITORS
 Block gastric acid secretions by inhibiting acid
pump in gastric parietal cells
 Treat erosive esophagitis and GERD
 Doudenal ulcer, Active gastric ulcer
 Eradicate H. Pylori infection
 Ex: Esomeprazole (Nexium), Lanzoprazole,
Omeprazole, Pantoprazole, Rabeprazole
NURSING RESPONSIBILITY
 Swallow the capsules whole and not to chew or
crush them
 Administer 1 hour before meal
 Avoid gastric irritants like alcohol, smoking,
aspirin, caffeine, NSAIDS
For CHRONIC GASTRITIS
 Modify the diet. Avoid carbonated and caffeine,
irritating foods
 Rest
 Reduce stress
 Avoid NSAIDS and alcohol
 Antacids, H2 blockers, PPI (NIDDK, 2015)
 Antibiotics- Metronidazole (Flagyl),
Amoxixillin, Clarithromicin, Tetracycline
 Bismuth salts (rare)
Metronidazole (Flagyl)
 MA: Antibacterial & anti protozoal that assist in
eradicating H. Pylori in gastric mucosa. It may
cause anorexia and metallic taste
 NC: Give with meals to decrease GI upset.
Avoid alcohol, it increases blood thinning
effects of warfarin
Amoxixillin,
 MA: Eradicated H pylori bacteria in gastric
mucosa
 NC: Should not be used in patients with
hypersensitivity to penicillin
Clarithromicin,
 MA: Eradicated H pylori bacteria in gastric
mucosa
 NC: may cause GI upset, headache and altered
taste, Can cause drug-drug interaction
Tetracycline
 MA: Eradicated H pylori bacteria in gastric
mucosa
 NC: may cause photosensitivity reaction, advise
the patient to use sunscreen
 May cause GI upset
 Caution in renal or hepatic impairment
 Avoid intake of milk and dairy products that
reduce effectiveness
 Do not take iron supplements, multivitamins,
calcium supplements, antacids, or laxatives
within 2 hours before or after taking
tetracycline. These products can
make tetracycline less effective in treating your
infection.
Bismuth salts (rare)
 MA: suppresses H. Pylori in the gastric mucosa
and assist in healing of ulcers
 NC: should be taken on an empty stomach. And
maygiven with antibiotics to eradicate the H
Pylori
RELIEVES PAIN
 Assess the level of pain
 Analgesics as ordered.
Heath Teachings
 Avoid taking NSAIDS and Aspirin
 Avoid or refrain from alcohol and food until
symptoms subside
 Avoid carbonated and caffeine drinks. Caffeine
is a CNS stimulant that increase gastric activity
and pepsin secretion
 Avoid smoking because nicotine reduces
secretion of pancreatic bicarbonate which
inhibits neutralization of gastric acid in the
duodenum (Lu et al., 2014)
 Enforce to the patient the importance of
completing medication regimen as prescribed to
eradicate H. Pylori infection
 Teach family members to how to administer
vitamin B 12 injection or make arrangement to
the primary provider in order to receive injection
. In gastritis or PUD, there is malabsorption of
Vitamin B 12
 Emphasized the follow up appointments with
primary provider.