1. Nursing Care of Patients WithUpper GI Disturbances
Nursing Management II
When we talk about upper GI disturbances we usually are discussing structures and disease processes including the mouth, the esophagus, the stomach, and the duodenum. We will be covering the topics found in your readings which included GERD, achalasia, hiatal hernia, gastritis, peptic ulcer disease and cancers of the esophagus and the stomach.

2. Knowing Gastroesophageal Reflux
Backward flow of the gastric contents into the esophagus
Heartburn is hallmark symptom
Pressure differences between stomach and lower esophagus
Contributing factors
Increased gastric volume
Positioning (bending over, lying down)
Obesity
Tight clothing
Hiatal hernia
Causes: Transient relaxation of the lower esophageal sphincter
Incompetent lower sphincter
Increased pressure within the stomach
Factors contributing
Increased volume after a large meal
Positioning which allows acids to remain close to gastroesophageal junction
Increased gastric pressure obesity or wearing tight clothing
What is in gastric juices? Acid, pepsin, bile and all are corrosive!
Normally esophageal peristalsis along with salivary bicarbonate clear the esophagus of refluxed gastric secretions.
Results
Esophageal mucosa can become damaged by gastric juices that can cause an inflammatory response.
Prolonged exposure can result in esophagitis.
Superficial ulcers may develop and the mucosa may begin to bleed.
If this is not treated, the esophagus can become scarred and sometimes strictures can develop.

3. Manifestations of GERD
Have you ever had heartburn???
Regurgitation into the esophagus and sometimes regurgitation of sour material into mouth. Can also have difficulty swallowing or pain with swallowing.
Atypical chest pain (beware that cardiac pain many times cannot be differentiated from heartburn)
Belching
Sore throat
Aspiration of gastric contents can cause hoarseness or respiratory symptoms

4. Complications with the Esophagus
Esophageal strictures
Barrett’s esophagus
Barrett’s esophagus has changes in the cells lining the esophagus
Also places the client at an increased risk for esophageal cancer! Adenocarcinoma is commonly associated with Barrett’s esophagus.
Esophageal cancer – rare in the US. High mortality rate because of late diagnosis.
Squamous cell is the most common.
Most common symptom is progressive dysphagia.
Manifestations include weight loss, regurgitation, chest pain, anemia, GERD – like symptoms, anorexia, persistent cough.
Diagnostic tests include – barium swallow, esophagoscopy, chest x-ray, CBC, liver function tests
Health promotion – dangers of cigarette smoking, and alcohol consumption.
Nursing Diagnosis:
Impaired swallowing – Aspiration precautions, positioning
Imbalanced Nutrition: Less than Body Requirements fluid monitoring, nutrition management
Fear/ Anticipatory Grieving
Risk for Ineffective Airway clearance – coughing and deep breathing, enteral tube placement, avoid overdistention
Treatment
Surgery
Radiation
Chemotherapy

5. Knowing Achalasia
Impaired esophageal motility that causes dysphagia or even chest pain.
Unknown etiology
Impaired peristalsis of the smooth muscle of the esophagus combined with impaired relaxation of lower esophageal sphincter
Gradual increasing dysphagia with foods that are solid and liquid
Manifestations:
Fullness in chest with meals
Chest pain
Cough developing at night
Diffuse esophageal spasms (chest pain can be severe!)
Treatment:
Endoscopically guided injection of botulinum toxin in lower esophageal sphincter
Balloon dilatation of lower esophageal sphincter
Laparascopic myotomy (incision into muscle of the LES) which reduces pressure and reduces symptoms

6. Knowing Hiatal Hernias
The stomach protrudes thru the esophageal hiatus of the diaphragm into the thoracic cavity. There are different types and if treatment of symptoms does not present relief, surgery can be done. Post op care is similar for that of abdominal or thoracic surgery clients.
Many individuals are without symptoms
fullness, reflux heartburn, occult bleeding, chest pain, dysphagia, belching, indigestion
Nursing Care: Chocolate or mint increases pressure
Avoid spicy foods
No tight clothing
Weight reduction
Small frequent meals
Elevate the HOB 6-8Inches
Avoid eating three hours before bed

7. Knowing Gastritis: Acute and Chronic
Manifestations of Acute:
Anorexia
Pain, nausea, vomiting
Melena or hematemesis
Belching
Manifestations of Chronic:
Asymptomatic or vague symptoms
Once atrophied, then digestive
and gastric emptying problems
Fatigue
Anemia
B12 deficiency may exist
H. pylori
Acute: disruption of mucosa due to a local irritant. (ASA, NSAIDS, corticosteroids, alcohol, caffeine or foods contaminated with bacteria) Iatrogenic causes include radiation, and administration of certain chemo drugs) Disruption allows HCL and pepsin to come into contact with gastric tissue, resulting in irritation, inflammation, and superficial erosions.
The mucosa rapidly regenerates and limits the disorder when the problem is resolved and healing has occurred. Usually self-limited and resolves within a couple of days.
Erosive: severe form of acute gastritis; also known as stress-induced gastritis.
Complication of other life threatening illness like shock, trauma, surgery, sepsis, burns or a head injury.
Ischemia of the gastric mucosa either from vasoconstriction and tissue injury from acid. Leads to multiple gastric tissue erosions. Keeping the gastric pH greater than 3.5 can help in prevention.
Many times you will see on the patients we care for that they are placed on GI prophylaxis. May have painless GI bleeding
Chronic:
progressive disorder;
starts with superficial inflammation
gradually leads to a more debilitating condition that atrophies the gastric tissue.
Type A may have an autoimmune component
Type B is the most common form of chronic gastritis.
Incidence increases with age and is almost 100% in people over the age of 70.
Caused by H. pylori infection that inflames the gastric mucosa and causes infiltration of neutrophils and lymphocytes; the outer layer thins and atrophies and provides a less effective barrier against the autodigestive properties of HCL and pepsin.
Increased risk for peptic ulcer disease

8. Medications Proton pump inhibitors H 2 receptor blockers Anti-ulcer
Promotility agents
Antacids
Clients testing + for H. pylori will be placed on combination antibiotic and PPI therapies
Proton Pump Inhibitors: Inhibit the hydrogen – potassium pump, reduce gastric acid secretion
Prevacid
Prilosec
Protonix
Aciphex
Administer before breakfast
Do not crush
Monitor liver functions
Avoid cigarette smoking and irritants
Report signs of bleeding
H2 antagonists – reduce acidity of gastric juices by blocking the ability of histamine to stimulate acid secretion by the gastric parietal cells
Tagamet
Pepcid
Zantac
Axid
Do not give an antacid within 1 hour
Do not mix with other drugs
Rapid IV injection may cause dysrhytmias and hypotension
Long term use can lead to gynecomastasia and impotence in men, breast tenderness in women
Anti-Ulcer- reacts with gastric acid to from a thick paste which adheres to damaged mucosa protects and promotes healing
Carafate
Administer on an empty stomach
Do not crush or chew
Increase intake of fluids and fiber to prevent constipation.
Promotility: Acts on CNS to stimulate motility and emptying
Reglan – give 30 minutes before meals or at bedtime
Do not administer if obstruction, bleeding, history of seizures, pheochromocytoma or Parkinson’s
Monitor for extrapyramidal side effects – difficulty speaking, or swallowing, loss of balance, gait disturbances, twitching or twisting
Or tardive dyskinesia: rhytthmic facial movement, lip smacking, tongue rolling
May be given undiluted IV push over 1 – 2 minutes
Antacids – Buffer or neutralize gastric acid
May interfere with absorption of other drugs take 1 – 3 hours after meals, 2 hours before or 1 hour after other meds.

9. Upper Endoscopy
Modern scopes allow photographs to be taken to document findings.
Also called esophagogastroduodenoscopy (EGD)

10. Commonly Used Diagnostic Test
Allows direct visualization of the esophagus
Can also biopsy
Uses conscious sedation
Culture for H. pylori (bacteria linked to chronic gastritis & peptic ulcer disease)
Nursing implications:
no special prep for EGD – schedule 2 days after barium studies,
Keep NPO
Education on procedure and what to expect after
Informed consent signed
Remove dentures, glasses, and provide mouth care before testing
Nurses assisting with the procedure will monitor VS, pulse ox, LOC, GCS score
Educate after procedure on when to notify the physician
Difficulty swallowing, bleeding, epigastric pain, shoulder pain, chest pain, black stools

11. Common Nursing Diagnosis
Imbalanced Nutrition Less than Body Requirements
Pain
Ineffective Health Maintenance
Others may include:
Deficient Fluid volume with acute gastritis
Risk for Ineffective Airway Clearance post op esophageal cancer
Fear- Cancer
Anticipatory Grieving- Cancer

12. Knowing Peptic Ulcer Disease
Peptic Ulcers may occur in the esophagus, stomach or duodenum
Duodenal most common.
Gastric more often affect older adults
Risk Factors
H Pylori Infection
Use of NSAIDS
Cigarette Smoking
Family History
Peptic ulcer disease – break in the mucous lining of the GI tract

13. Peptic Ulcers
Gastric Ulcer
Duodenal Ulcer

14. Manifestations and Complications
Pain is classic symptom
Complications
Hemorrhage
Gastric Outlet obstruction
Perforation
Pain usually occurs when the stomach is empty.
Classic pain- food- relief pattern. May also have heart burn or regurgitation
Presentation less clear in older adult vague abdominal discomfort, chest pain, weight loss, anemia
Hemorrhage in % Symptoms of anemia
Gastric outlet obstruction secondary to edema surrounding the ulcer
Most lethal complication is perforation leading to peritonitis.
Zollinger Ellison is peptic ulcer caused by gatrinoma or gastin secreting tumor of pancreas, stomach or intestines.
Symptoms are pain and may have steattorhea.

15. Collaborative Care Diagnostics Upper GI Gastroscopy H. Pylori Testing
Biopsy Urease test
Urea breath test
Biopsy urease – specimen placed in gel If H. Pylori is present the urease produced by H. Pylori changes the gel color
Urea breath test - radiolabeled urea used bacteria converts to ammonia and carbon dioxide that can be measured when the patient exhales. Also used to evaluate treatment.

16. Collaborative Care Treatments Dietary management Surgery
Management of complications
Medications
Eradicate H. Pylori
Decrease gastric acid content
Agents that protect the mucosa
Combination two antibiotics plus bismuth or proton pump inhibitors. Erythromycin or Tetracycline.
Prostaglandin analogs misoprostal promotes healing by stimulating mucous and bicarb secretions. And inhibiting

17. Knowing Stomach Cancer
Risk Factors
H. Pylori Infections
Genetic Predisposition
Chronic Gastritis
Pernicious anemia
Gastric polyps
Carcinogenic factors in the diet such as
smoked food and nitrates
Adenocarcinoma is the most common form
Most frequently found in the distal portion
Metastasize early because of lymph and blood supply
Usually find mets to liver, lungs, ovaries, and peritoneum
Few symptoms usually advanced at time of diagnosis may have vague feelings of fullness, early satiety no appetite, often look cachectic. May have blood in stool.
Prognosis is poor

18. Collaborative Care Diagnostics Surgery Partial gastrectomy
Billroth I (duodenum)
Billroth II (jejunum)
Total gastrectomy
Postoperative Nursing Care
CBC, Upper GI, endoscopy
Complications
Dumping Syndrome- common complication undigested food bolus rapidly enters the duodenum or jejunum water is pulled in because hypertonicresulting in increasing intestinal motility.
Symptoms occur within 30 minutes of eating
Treatment: small frequent meals, increase protein and fat, decrease carbs, semirecumbent after meals may get antispasmodics and sedatives.
Second complication is B12 deficiency pernicious anemia
Poor absorption of calcium and weight loss.
May require insertion of feeding tubes.
In addition to surgery may have chemo and or radiation.