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Nursing Care of Patients WithUpper GI Disturbances

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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.

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