Upper GI
Problems
Chapter 41
Digestion and Absorption
 Digestion
 Absorption
GERD
Gastroesophageal reflux disease (not actually
a disease, but a syndrome)
Caused by reflux of gastric contents into lower
esophagus
Assessment: Risk factors contributing to GERD
o Incompetent LES – Primary
• Can be due to certain foods (caffeine, chocolate) and drugs (anticholinergics)
• Obesity increases risk
• Cigarette and cigar smoking can contribute to GERD
o Hiatal Hernia
o Delayed gastric emptying
Assessment: Signs and Symptoms
o Heartburn (pyrosis) (chest pain)
o Most common clinical manifestation
o Burning, tight sensation felt beneath the
lower sternum and spreading upward to
throat or jaw
o Felt intermittently
o Severe if more than 2x/week, wakes a
person from sleep, or associated with
dysphagia
o Dyspepsia
o Pain or discomfort centered in upper
abdomen
o Regurgitation
o Described as hot, bitter, or sour liquid
coming into throat or mouth
o Hypersalivation may also be reported
• Respiratory symptoms
o Wheezing
o Coughing
o Dyspnea
o Nocturnal coughing with loss of
sleep
• Otolaryngologic symptoms
o Hoarseness
o Sore throat
o Lump in throat
o Choking
• Diagnosis
• Generally based on symptoms and
response to treatment
• Can do endoscopy
Interventions: Nursing Management
Patient Education
oStress reduction techniques
oElevation of head of bed 30 degrees
oWeight reduction, if appropriate
oNot lying down for 2–3 hours after eating
oAvoid tight clothing
oAvoidance of late-night eating and milk at night
oSmall, frequent meals
oEvaluating effectiveness of medications
oObserving for side effects of medications
oDrink between meals
oAvoidance of factors that cause reflux
oStop smoking
oAvoid alcohol and caffeine
oAvoid acidic foods, high fat foods, chocolate,
peppermint
Interventions: Collaborative Care- Medications
Drug therapy (decrease volume and acidity of reflex, improve LES function, increase esophageal clearance, protect mucosa)
• Proton pump inhibitors (PPIs)
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Decrease acid secretion
Promote esophageal healing in 80% to 90% of patients
Example: omeprazole (Prilosec), Nexium
Headache: Most common side effect
• Histamine-2 receptor (H2R) blockers
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Decrease secretion of HCl acid
Reduce symptoms and promote esophageal healing in 50% of patients
Example: cimetidine (Tagamet)
Side effects uncommon
• Prokinetic drugs
• Promote gastric emptying
• Reduce risk of gastric acid reflux
• Example: metoclopramide (Reglan)
• Antacids
• Neutralize acid
Interventions: Collaborative Care
• Surgical therapy
• Nissen (and Toupe) fundoplication
• Failure of conservative therapy
• Medication intolerance
• Barrett’s metaplasia
• Esophageal stricture and stenosis
• Chronic esophagitis
Interventions: Nursing Management Post op
• Postoperative care
• Focus
• Prevention of respiratory complications
• Maintenance of fluid/electrolyte balance
• Prevention of infection
• Diet
• When peristalsis returns, only clear liquids given initially
• Solids added gradually
• Normal diet gradually resumed
• Patient must avoid gas-forming foods and must chew foods thoroughly
• Discharge teaching
• First month after surgery, patient may report mild dysphagia; should resolve after edema subsides
• Patient should report persistent symptoms such as heartburn and regurgitation
The recurrence rate may range from 10% to 30% over a 20-year period following surgery.
Evaluation: Complications
• Esophagitis
• Inflammation of esophagus
• Frequent complication
• Repeated exposure: esophageal stricture, resulting in
dysphagia
• Barrett’s esophagus (esophageal metaplasia)
• Replacement of normal squamous epithelium with
columnar epithelium
• Precancerous lesion
• Respiratory
• Potential for bronchospasm
• Asthma, bronchitis, and pneumonia (from aspiration)
• Dental erosion
• From acid reflux into mouth
• Especially posterior teeth
Assessment: Risk Factors
o Drugs
o Direct irritating effect on gastric mucosa
o NSAIDs, aspirin, corticosteroids
o Diet
o Alcohol, spicy food
o Microorganisms
o Helicobacter pylori
o Important cause of chronic gastritis
o Promotes breakdown of gastric mucosal
barrier
o Bacterial, viral, and fungal infections
o Mycobacterium, cytomegalovirus (CMV),
and syphilis
o Environmental factors
o Radiation, smoking
o Pathophysiologic conditions
o Burns, renal failure, sepsis
o Other factors
o Psychologic stress, NG tube
Assessment: Acute Gastritis Signs and Symptoms
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Anorexia
Nausea
Vomiting
Epigastric tenderness
Feeling of fullness
Hemorrhage
• Common with alcohol abuse
• May be only symptom
Assessment: Chronic Gastritis Signs and Symptoms
• Symptoms are similar to those of acute gastritis, although may be asymptomatic
• Loss of intrinsic factor can occur when acid-secreting cells are lost or nonfunctioning
• Essential for absorption of cobalamin (vitamin B12) (so have a cobalamin deficiency)
• B12 needed for RBC growth and maturation
• Pernicious anemia
• Neurological complications
Assessment: Diagnostic
o Often based on symptoms and history
o May do endoscopic examination with biopsy
o May check blood for anemia
Interventions
• Acute Gastritis
• Chronic Gastritis
• Focuses on evaluating and eliminating cause
• Cessation of alcohol intake
• Abstinence from drugs
• H. pylori eradication- antibiotics (amoxicillin
and clarithromycin) + PPI x 7-14 days
• Same as acute plus:
• Smoking cessation
• Pernicious anemia: cobalamin
supplements- lifelong
• Nonirritating diet
• Supportive care for nausea/vomiting
• NPO
• IV fluids
• Dehydration can occur rapidly
• Rest
• Antiemetic
NG tube, bleeding management for hemorrhage
Peptic Ulcer Disease
Erosion of GI mucosa resulting from digestive action of HCl acid and pepsin
Duodenal Ulcers
Account for ~80% of all peptic ulcers
Occur at any age and in anyone
o ↑ Between ages of 35 and 45 years
• H. pylori is found in 90% to 95% of patients
Risk factors- Associated with increased HCl acid
secretion
o Alcohol
o Cigarette smoking
o Caffeine
o Stress
Gastric Ulcers
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Higher mortality rate
Located primarily in antum
Peak age women > 50
Higher risk factorso H-pylori
o Bile reflux
o Medications- NSAIDS,
corticosteroids
o (also smoking and alcohol)
The risk factors are the same, but some point more toward one ulcer over the other
Assessment: Signs and Symptoms
Duodenal Ulcers
o Midepigastric region beneath
xiphoid process
o Back pain—if ulcer is located
in posterior aspect
o Food buffers and relieves
symptoms
o 2–5 hours after meals
o “Burning” or “cramp like”
o Tendency to occur, then
disappear, then occur again
o Antacids/food neutralize acid
and provide relief
Gastric Ulcers
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o
o
o
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Pain high in epigastrium
Food aggravates
1–2 hours after meals
“Burning” or “gaseous”
Food aggravates pain as ulcer
has eroded through gastric
mucosa
Assessment: Ulcer Diagnostic Studies
• Endoscopy- most accurate
• Biopsy for H- Pylori
• Barium contrast
• Laboratory analysis
• Blood H-Pylori
• CBC
• Urinalysis
• Liver enzyme studies
• Serum amylase determination
• Pancreatic function
• Stool examination
Interventions: Nursing and Collaborative Care
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Adequate rest
Drug therapy
Elimination of smoking and alcohol
Dietary modification
Long-term follow-up care
Stress management
NPO, NG tube placement
IV fluids
Surgical treatment in rare cases (remove section of affected bowel or stomach)
• Risk for dumping syndrome
• Cholestyramine (Questran) prevents reflux alkaline gastritis (reflux of bile into
stomach)
Interventions: Medications
• PPIs
• H2R blockers
• Antibiotics
• Antacids
• Anticholinergics
• Cytoprotective therapy
Evaluation: Complications
• Three major complications:
• Hemorrhage
• Perforation
• Gastric outlet obstruction
• All considered emergency situations
Perforation
• Signs and Symptoms
• Sudden, dramatic onset
• Initial phase (0–2 hours after perforation)
• Severe upper abdominal pain spreads throughout abdomen
• The pain radiates to the back and is not relieved by food or antacids.
• Tachycardia, weak pulse
• Rigid, board-like abdominal muscles
• Shallow, rapid respirations
• Bowel sounds absent
• Nausea/vomiting
• History of reporting symptoms of indigestion or previous ulcer
• Bacterial peritonitis may occur within 6–12 hours
Interventions
• Vital signs every 15-30 min
• Fluid replacement- priority
• 2 large bore IV’s (what type of fluid?)
• NPO
• NG tube is placed into stomach
o Continuous suction and decompression
o Placement of tube near to perforation site facilitates decompression – stop gastric spillage into
abdomen cavity
o ECG if patient has history of cardiac disease
o Broad-spectrum antibiotics
o Pain medication
o Open or laparoscopic repair
o Simple over sewing involves the least risk
o Excess gastric contents are suctioned from peritoneal cavity
Gastric Outlet Obstruction
• Signs and Symptoms
• Pain worsens toward end of day as stomach fills and dilates
• Vomiting is forceful/projectile (food from hours ago)
• Relief of discomfort obtained by belching or vomiting
• Constipation is a common complaint
• Dehydration, lack of roughage in diet
• Swelling in stomach and upper abdomen (distention)
• If stomach grossly distended, may be palpable
• Loud peristalsis
Gastric Outlet Obstruction
Interventions
o Correct any existing fluid and electrolyte imbalances
o Improve patient’s general state of health
o Decompress stomach- NG tube inserted in stomach, attached to continuous suction (residual volume
checked, <200ml resume clear liquids)
o Watch patient carefully for signs of distress or vomiting
o As residual obstruction ↓, solid foods added, and tube removed
o Pyloric obstruction: endoscopically treated with balloon dilations
o Surgery may be necessary to remove scar tissue (Billroth I and Billroth II)
Postoperative Interventions
• Nutritional Therapy
o Start as soon as immediate postoperative period has successfully passed
o Patient should be advised to reduce drinking fluid (4 oz) with meals
o Diet should consist of
o Small, dry feedings daily
o Low carbohydrates
o Restricted sugar with meals
o Moderate amounts of protein and fat
o Rest for 30 minutes after each meal
• Complications
o Dumping syndrome
o Postprandial hypoglycemia
o Bile reflux gastritis
Upper GI Bleed (UGIB)
• Severity depends on bleeding origin: venous, capillary, arterial
Obvious bleeding
• Hematemesis (bloody vomitus)
• Appears fresh, bright red blood or “coffee grounds”
• Melena (black, tarry stools)
• Caused by digestion of blood in GI tract
• Black appearance—due to iron
• Occult bleeding
• Small amounts of blood in gastric secretions, vomitus, or stools
• Undetectable by appearance
• Detectable by guaiac test
Nursing Assessment
• LOC
• VS
• Orthostatic (but not if it’s already low!)
• Every 15–30 minutes (more if indicated)
• Appearance of neck veins
• Skin color
• Capillary refill
• Abdominal distention, guarding, peristalsis
• Signs/symptoms of shock
• Low BP
• Rapid, weak pulse (if you can’t feel a central pulse, they are not perfusing…Start
CPR…)
• Increased thirst
• Cold, clammy skin
• Restlessness
Assessment: Diagnostic Studies
• Laboratory studies
• Complete blood cell count (CBC)
• Blood urea nitrogen (BUN) measurement
• Serum electrolyte measurements
• Prothrombin time, partial thromboplastin time
• Liver enzyme measurements
• ABG measurements
• Typing/crossmatching for possible blood transfusions
• Vomitus/stools
• Tested for the presence of gross and occult blood
• Urinalysis
• Specific gravity: indication of patient’s hydration status
Interventions: Emergency Management
• Fluid replacement
• IV lines
• Should be established for fluid and blood
replacement
• Preferably two IV lines
• 16- or 18-gauge catheter (large bore)
• Generally best to begin with an isotonic
crystalloid solution (lactated Ringer’s solution)
(LR vs. NS, the debate..)
• Use of supplemental O2 helps increase blood O2
saturation
• Indwelling urinary catheter (place in ICU only… )
• Accurate urine volume assessment
• CVP line to monitor patient’s fluid volume status (if
hemodynamically unstable)
• Blood replacement
• Type and Screen ASAP
• Whole blood, packed RBCs, and fresh
frozen plasma
• Used for replacement of lost volume in
massive hemorrhage
• Packed RBCs are preferred over whole
blood because of fluid overload and
immune reactions
Interventions: Nursing Management
• Hourly input/output
• What if patient is in fluid overload (lungs wet) and their blood pressure is low? See page 919, table 41.23
• If NG tube is inserted
• Keep in proper position
• Observe aspirate for blood
• Effectiveness of gastric lavage is questionable
Endoscopic hemostasis therapy
•
Surgical therapy
Primary tool for visualization and
diagnosis of an upper GI bleed
• Site of hemorrhage determines
choice of operation
•
Goal: to achieve coagulation or
thrombosis in bleeding artery
• Surgeon must consider age of
patient
•
Useful for gastritis, MalloryWeiss tear, esophageal and
gastric varices, bleeding peptic
ulcers, and polyps
• Mortality rates increase
considerably in patients older
than 60 years
Drug therapy
During acute phase, used to
•↓ Bleeding
•↓ HCl acid secretion
•Neutralize HCl acid that is
present
•Injection therapy with
epinephrine during endoscopy for
acute hemostasis
Interventions: Collaborative Care