Gastro-Esophageal Reflux Disease
GENERAL OBJECTIVE: On completion of the seminar students will acquire in depth knowledge regarding gastroesophageal reflux disease, gain skills in identifying & managing the conditions and develop a positive attitude about nurse’s role. SPECIFIC OBJECTIVES: On completion of seminar students will be able to * Define gastro oesophageal reflux disease * Enlist the risk factors for GERD * Explain the pathophysiology of GERD * List down clinical manifestations GERD * Describe the management of GERD. * Enlist the complications of GERDINTRODUCTION
Gastro oesophageal reflux disease is a common, lifelong condition that requires long term treatment. GERD is the most common upper GI problem seen in adults. Some degree of gastro oesophageal reflex is normal in both adults ; children. Excessive reflux may occur because of an in competent lower oesophageal sphincter, pyloric stenosis or a motility disorder. Many patients have (NERD) Non erosive reflux disease show no sign of oesophageal inflammation. DEFINITIONS 1. Gastro oesophageal reflux disease is a condition in which gastric recreations reflux into oesophagus. (Linda s.
William, 2003) 2. GERD entails the reflux of gastric ; duodenal contents through the lower oesophageal sphincter (LES) into the oesophagus to cause symptoms or injury to oesophageal, oropharyngeal or respiratory tissues. (Neil R. Floch, 2010) 3. GERD is a heterogeneous syndrome resulting from oesophageal reflux. (Phipps, Monnahon, 2003) 4. GERD is a syndrome with clinically significant symptomatic condition or histopathology alteration secondary to reflux of gastric contents into the lower oesophagus. (Lewis, heitkemper,2004) INCIDENCE GERD is a common disorder in adults.
There are no documented genders or cultural patterns associated with reflux but older adults experience decreased esophageal peristalsis and a higher incidence of hiatal hernia which together increase the likelihood of reflux in this population. ETIOLOGY There is no single cause of GERD . Several factors or combination of factors can be involved. It results when the defences of lower oesophagus are overwhelmed by the reflux of acid gastric contents into oesophagus. The LES is the anti reflux barrier. PREDISPOSING FACTORS: * Hiatal hernia: which displaces LES into the thorax * Incompetent LES Decreased oesophageal clearance resulting from impaired oesophageal motility or gastric motility( auto immune disorders, neuromuscular disease, endocrine disorders, DM) A number of environmental and physical factors appear to influence GERD such as: * Intake of fatty foods, chocolate ,coffee, cola, nicotine * Drugs such as calcium channel blockers, theophylline ; possibly NSAIDs * Cigarette smoking * Elevated levels of estrogen and progesterone Condition that elevate intra abdominal pressure: * Obesity * Pregnancy * Heavy lifting Reflux is much more common after a meal.
Genetic factors may also be considered. PATHOPHYSIOLOGY Normally a high pressure zone exists in the region of gastric oesophageal sphincter (LES). High pressure prevents reflux but permits the passage of food and liquids. When there is relaxation of LES , pressure decreases and reflux of stomach contents into lower oesophagus occurs. Delayed gastric emptying may also contribute to reflux by increasing gastric volume and pressure. Decreased salivation ; buffering from salivary bicarbonate may contribute to impaired clearing of acid reflux from the oesophagus.
The reflux most often consists of HCL or gastric acid (enzyme pepsin) and duodenal contents containing bile acid and pancreatic juice. These are all corrosive to oesophageal mucosa. Frequent or prolonged reflux results in inflammation of oesophageal mucosa (oesophagitis) the degree of inflammation depends on amount and composition of gastric reflux and on ability of oesophagus to clear acid content. GERD may be present at one of 3 levels – NERD, erosive esophagitis ; barretts oesophagus Pathologic GERD is defined as reflux of acid (ph ;4) and evidence of abnormalities such as pathologic biopsies of erosive oesophagitis.
GERD develops when frequent episodes of reflux breakdown the mucosal barrier and initiate an inflammatory response. An inflamed oesophagus gradually loses its ability to clear refluxed material quickly ; efficiently ; duration of each episode gradually lengthens. Repeated episodes of inflammation ; healing can gradually produce a change in epithelial tissue that makes it more resistant to acid. However the presence of this new tissue termed Barrett’s epithelium is also associated with high risk of adenocarcinoma. Over time fibrotic changes can also occur and produce oesophageal stricture.
CLINICAL MANIFESTATIONS * Dyspepsia : also known as heart burn is the main symptom of GERD. The pain is described as a substernal burning sensation that tends to move up & down the chest in a wavelike fashion. If heart burn is severe pain may radiate to the neck or jaw or may be referred to the back. The pain typically worsens when the patient bends over strains or lie down. With severe GERD the pain occurs after each meal & last for 20mt to 23 hours. Patients usually obtain prompt relief by drinking fluids, taking antacids or maintaining an upright posture. Regurgitation: (effortless backflow of food or gastric contents) if the fluid reaches the level of pharynx he or she notes a sour or bitter taste in the mouth. The danger of aspiration is increased if regurgitation occurs when patient is lying down. * Nausea ,vomiting * Coughing ,hoarseness or wheezing at night * Water brash(hyper salivation) * Dysphagia ,odynophagia(chronic GERD) * Epigastric pain * Belching(eructation) and bloating after eating * Flatulence ,nausea * Pyrosis(retrosternal burning) * Globus feeling of something in back of throat * pharyngitis dental caries(rare cases) ASSESSMENT & DIAGNOSTIC EVALUATION * Complete history and physical examination * Endoscopy (esophagastrodeudenoscopy) or barium swallow to evaluate damage to oesophageal mucosa * Ambulatory 12 to36hr oesophageal ph monitoring is used to evaluate the degree of acid reflux. This test involves placing a small catheter through the nose into the distal oesophagus. The patient is asked to keep a diary of activities & symptoms and ph is continuously monitored & recorded. It is useful in monitoring patients with atypical symptoms. Oesophageal manometry : motility testing ,it is not commonly used. In this water filled catheters are inserted into the patient’s nose or mouth slowly withdrawn while measurements of LES ; peristalsis are recorded. Bilirubin monitoring (bilitec) is used to measure bile reflux patterns as exposure to bile can cause mucosal damage. MANAGEMENT The purpose of treatment of esophagitis and prevention of complications such as stricture or barrettes oesophagus. Most patients with GERD can be successfully managed by nutritional therapy, life style modifications and drug therapy.
The most important role of nurse is patient and family education Life style modifications: the patient with GERD is taught to avoid factors that aggravate symptoms. Particular attention is given to drugs and diet. Patient who smoke are encouraged to stop.. Cigarette smoking has been associated with decreased acid clearance from the lower oesophagus. Patient teaching * The patient is instructed to eat a low fat diet, to avoid caffeine, tobacco, beer ,milk, foods containing pepper mint or spear mint and carbonated beverages * To avoid eating or drinking 2hrs before bed time To maintain normal body weight * To avoid tight fitting clothes * To elevate the head of bed on 6-8inch(15-20cm) blocks to elevate the upper body on pillows * Remind the patient to eat 4-6 small meals each day rather than 3 large meals * Teach the patient to be in right side lying position to decrease effects of night time episode of reflux. Drug therapy: Some drugs lower LES pressure and cause reflux such as oral contraceptives, anti cholinergic agents, sedatives, NSAIDS (e. g. ibuprofen) nitrates and Calcium channel blocker.
The possibility of eliminating those drugs causing reflux should be explored with the health care provider. Drug therapy for GERD includes three major types Antacids, histamine blockers, and proton pump inhibitors * Inhibit gastric acid reaction * Accelerate gastric emptying * Protect the gastric mucosa Antacids: Aluminium or magnesium salts(Mylante,Macilox)30ml orally between meals and as needed throughout the day and at bedtime Increases pH of gastric contents Histamine Receptor antagonists * cimetidine 300mg orally four times daily or 900-1200mg orally at bedtime * Ranitidine 150mg orally twice daily Famotidine 40mg orally daily or 20 mg orally twice daily Prokinetic drugs * Metoclopramide (Reglan)10 mg orally 3-4 times Proton pump inhibitor * Omeprazole 20-30 mg orally daily * Lansoprazole 15mg orally * Rabeprazole 60 mg NURSING ASSESSMENT For nonemergency symptoms, a complete health history may reveal the nature of the oesophageal disorder. The nurse asks about the patients appetite. Has it remained the same, increased or decreased? Is there any discomfort with swallowing? Does the change in position affect the discomfort?
The patient is asked to describe the pain. Does anything aggravate it? Are there any other symptoms that occur regurlarly,such as regurgitation, nocturnal regurgitation, eructation(belching),heartburn,substernal pressure, a sensation that food is sticking in the throat, a feeling of fullness after eating a small amount of food,nausea,vomiting or weight loss? History also includes questions about past or present causative factors, such as infections and chemical,mechanical,or physical irritants, alcohol and tobacco use, and the amount of daily food intake.
The nurse determines whether the patient appears emaciated and auscultates the patient’s chest to assess for pulmonary complications. NURSING DIAGNOSIS Based on the assessment data, the nursing diagnosis may include the following * Acute pain related to difficulty swallowing, ingestion of an abrasive agent, tumour or frequent episodes of gastric reflux. * Imbalanced nutrition, less than body requirements, related to difficulty swallowing. * Deficient knowledge about the oesophageal disorder, diagnostic studies, medical management, surgical intervention, and rehabilitation. Risk for aspiration related to difficulty swallowing or to tube swallowing. PLANNING AND GOALS The major goals for the patient may include attainment of adequate nutritional intake, avoidance of respiratory compromise from aspiration, relief of pain, and increased knowledge level. NURSING INTERVENTIONS 1. Encouraging adequate nutritional intake The patient is encouraged to eat slowly and to chew all food thoroughly so that it can pass easily into the stomach. Small, frequent feedings of non-irritating foods are recommended to promote digestion and to prevent tissue irritation.
Sometimes liquid swallowed with food helps the food pass through the oesophagus, but usually liquids should be consumed between meals. Food should be prepared in an appealing manner to help stimulate the appetite. Irritants such as tobacco and alcohol should be avoided. A baseline weight is obtained, and daily weights are recorded. The patient’s intake of nutrients is assessed. 2. Decreasing Risk Of Aspiration The patient who has difficulty swallowing or difficulty handling secretions should be kept in at least a semi-Flower’s position to decrease the risk of aspiration. . Relieving Pain Small, frequent feedings (six to eight per day are recommended because large quantities of food overload the stomach and promote gastric reflux. The patient is advised to avoid any activities that increase pain and to remain upright for 1 to 4 hours after each meal to prevent reflux. The head of the bed should be placed on 4-8 inch (10-20 cm) blocks. Eating before bedtime is discouraged. The patient is advised that excessive use of over the counter antacids can cause rebound acidity. 4. Providing Patient Education
The patient is prepared physically and psychologically for diagnostic tests, treatments and possible surgery, The principle nursing interventions include reassuring the patient and explaining the procedures and their purpose. BIBLIOGRAPHY * Lewis, Heitkemper, Dirksen. (2004). Medical surgical nursing. (6th Edition). St. Lewis : Mosby Publishers. PP(895-898) * Brunner, Suddarth( 2009). Medical Surgical Nursing(10th ed) Philadelphia PP1789-1790). * Ignatavicuis, Workman(2010). Medical Surgical Nursing. (2010) St. Lewis.. Saunders Elsevier PP(776-779) * Sands, Phipps, Etal (2003).
Medical Surgical Nursing (7th Edition). St. Lewis. Mosby Publishers PP(1771-1775) * Joyce,M ,Black. Medical Surgical Nursing. .(7th edn)vol2. Saunders publishers. pp(1871-1873) INTRODUCTION Peptic Ulcer disease is an extremely common health problem that has undergone dramatic shifts in incidence and prevalence over the last century. The importance of this disease is reflected in the Healthy People 2010 objective to reduce hospitalizations caused by PUD in the United States from the baseline of 71 per 100,000 to a target of 46 per 100,000 populations. DEFINITION A.
Peptic Ulcer Disease (PUD) is a condition characterized erosion of the G1 mucosa resulting from the digestive action of HCL acid and pepsin. (Lewis, Heitkemper (2007) B. A peptic ulcer is an excavation(hollowed-out area)that forms in the mucosal wall of the stomach ,in the pylorus(the opening between the stomach and the duodenum)in the duodenum or oesophagus (Brunner and Suddarth 2010) C. A peptic ulcer is a mucosal lesion of the stomach or duodenum. PUD results when the mucosal defences become impaired and no longer protect the epithelium from the effects of acid and pepsin. Ignatavicius 2009) D. PUD is a break in the continuity of oesophageal gastric or duodenal mucosa. (Luckmann. 2008) TYPES Peptic ulcers can be classified as acute or chronic depending on the degree and duration of mucosal involvement and gastric or duodenal according to location. a. Acute ulcer is associated with superficial erosion and minimal inflammation. It is of short duration and resolves quickly when the cause is identified and removed. b. Chronic ulcer is one of long duration, eroding through the muscular wall with the formation of fibrous tissue.
It is present continuously for many months or intermittently throughout the person’s life time. ETIOLOGY * Helicobacter Pylori is the causative agent of peptic ulcer in 90%of cases, this may be acquired through food and water. * Chronic NSAID use leads to peptic ulcer. RISK FACTORS * Smoking: Current smokers are twice as likely as non smokers to develop ulcers. * Alcohol, caffeine, wine, beer are all risk factors. These are all known to be secreatgogues for acid reaction. * Tea, coffee, cola, milk and spices are all identified as potent secretagogues. * Steam has also been showed to increase the risk. The presence of chrons disease, zollinger Ellison syndrome and hepatic and biliary diseases also increases the risk of ulcer formation. * Familial tendency may also be a significant predisposing factor. * People with blood group O are more susceptible to peptic ulcer than those with blood type A, B or AB. * There is also an association between peptic ulcer and chronic pulmonary disease or chronic renal disease. PATHOPHYSIOLOGY Peptic ulcer occurs mainly in the gastro duodenal mucosa because this tissue cannot withstand the digestive action of gastric acid and pepsin.
The erosion is caused by the increased concentration or activity of acid-pepsin or by decreased resistance of the mucosa. The stomach is normally protected from auto digestion by the gastric mucosal barrier. A damaged mucosa cannot secrete enough mucosa to act as a barrier against hydrochloric acid. The use of NSAIDs inhibits the secretion of the mucus that protects the mucosa. Patients with duodenal ulcer tend to secrete more acid than normal or decreased levels of acid. Damage to gastro duodenal mucosa results in decreased resistance to bacteria and thus infection from pylori bacteria may occur.
Acid Secretion:-It is controlled by endocrine, neural and paracrine factors. Gastric acid is secreted by parietal cells of the fundus of stomach in response to: * Gastrin * acetylcholine, which is secreted by cholinergic activation of the vagus * Histamine which is found in cells throughout the gastric mucosa. There are two types of cellular receptor to histamine. Histamine H1 receptors-mediate smooth muscular contraction and capillary dilatation. Histamine H2 receptors-mediate secretion of hcl acid. Mucosal defences:-The entire stomach and duodenum are covered by a worm thick layer of gel like mucus that is 45%water 25%glycoproteins.
This layer is continuously both degraded and replaced. The gel protects the mucosa against shearing and mechanical injury, assists in transport of food particles, retains water near the mucosa and blocks the back diffusion of hydrogen ion. The epithelial cells secrete bicarbonate into the mucous layer which helps maintain a neutral pH immediately adjacent to mucosa. When minor injury occurs the epithelium is capable of quick repair by creating a “cap” of mucus and fibrin that raises the mucosal pH and repair the damage.
An adequate mucosal blood flow at a normal Ph is critical to support of mucosal epithelial cell function. Zollinger Ellison Syndrome is an ulceration syndrome which has several peptic ulcers or an ulcer that is resistant to standard medical therapy. Stress ulcer is the term given to the acute mucosal ulceration of the duodenal or gastric area that occurs after physiologically stressful events, such as burns, shock, severe and multiple organ traumas. These are most common in ventilation dependent patients after trauma or surgery.
Fiberoptic endoscopy within 24 hours of trauma or surgery reveals shallow erosions of the stomach wall; by 72 hours multiple erosions are observed. As the stressful conditions continue the ulcers spread. The patient recovers the lesions are reversed. This is a typical pattern of stress ulceration. Cushing’s ulcer and Curling’s ulcer are two other forms of gastric ulcer. Cushing ulcers are common in patients with head injury and brain trauma. They may occur in the oesophagus, stomach or duodenum and are usually deeper and more penetrating than stress ulcers.
Curling’s ulcer is frequently observed about 72 hours after extensive burns and involves the antrum or the duodenum. ASSESSMENT AND DIAGNOSTIC FINDINGS 1) A physical examination may reveal pain, epigastric tenderness, or abdominal distension, History collection- collect regarding NSAID use. 2) Endoscopy is the preferred procedure because it allows direct visualization of the inflammatory changes, ulcers and lesions. Through endoscopy a biopsy of gastric mucosa and of any suspicious lesions. 3) A barium study of the upper G1 tract may reveal an ulcer. ) Histologic examination of a tissue specimen obtained by a biopsy determines H. pylori infection and rapid weak test. 5) Serologic testing of antibodies against H. pylori antigen. 6) Stool antigen test and urea breath test. 7) Laboratory findings of hypochromic anaemia and occult blood in stools indicate bleeding. * CBC,urinalysis ,liver Enzyme studies helps to determine any liver problems that may complicate PUD treatment. * Serum Amylase determination is done to determine pancreatic function when posterior duodenal ulcer penetration of the pancreas is suspected. Gastric analysis to determine the presence of a possible Zollinger Ellison syndrome. Elevated serum gastric levels combined with elevated gastric acid secretion levels are suggestive of gastrinoma. MANAGEMENT The regimen consists of adequate rest, dietary modifications, drug therapy, elimination of smoking, surgical intervention, long term follow up care. The aim of treatment is to decrease gastric acidity, enhance mucosal defence mechanism and minimize the harmful effects on mucosa. Pharmacologic Therapy
Most commonly used therapy is combination of antibiotics, proton pump inhibitors and bismuth salts that suppress or eradicate H. pylori infection. Recommended therapy for 10-14 days includes triple therapy with two antibiotics e. g. metronidazole (flagyl) or amoxicillin or clarithromycin (biaxin) plus proton pump inhibitor e. g. lansoprazole, omeprazole or rabeprazole. OR Quadruple Therapy Two antibiotics (metronidazole and tetracycline) plus a proton pump inhibitor and bismuth salts. Research is being conducted to develop a vaccine against H. pylori. Kabir 2007) * Histamine-2 H2receptor antagonists and proton pump inhibitors are used to treat NSAID induced ulcers. * Antisecretory drugs for ulcer healing H2 Receptor Antagonists * Nizatidine 150mg bid or 300mg at bedtime * Ranitidine 150mg bid or 300mg at bedtime * Cimetidine 400mg bid or 800mg at bedtime * Famotidine 20mg bid or 40mg at bedtime Should be used for 6 weeks for duodenal ulcers and 8 weeks for gastric ulcer. Proton Pump Inhibitors (PPI) * Omeprazole 20 mg daily * Lansoprazole 30mg daily * Rabeprazole 20 mg daily * Pantoprazole 40mg daily
Should be used for 4 weeks for duodenal ulcer and 6 weeks for gastric ulcer. Healing occurs in 90%of patients who are compliant with therapy. Antisecretory and cytoprotective: Misoprostol Cytoprotective: Sucralfate, bismuth subsalicylate Antacids: as adjunct therapy for PUD. They increase gastric Ph by neutralizing hydrochloric acid. * Aluminium Carbonate * Aluminium Phosphate * Magnesium Oxide * Aluminium hydroxide Mixtures of Aluminium Hydroxide and Magnesium Salts * Gelusil and GeluSil M * Delcid * Mylanta Mixtures of Calcium Carbonate and Aluminium and Magnesium Hydroxides * Camalox ducon Patients at risk for stress ulcers may be treated prophylactically with IV H2 receptor antagonists and cytoprotective agents (e. g. misoprostol, sucraflate) because of the risk of upper G1 tract haemorrhage. Anticholinergic drugs are used occasionally only. These drugs decrease cholinergic (vagal) stimulation of Hcl acid. Other drugs are Tricyclic anti depressants e. g. Imipramine, doxepine, and serotonin reuptake inhibitors may contribute to overall pain relief through their effect on afferent pain fiber transmission. Stress Reduction and Rest
Reducing environmental stress requires physical and psychological modifications on patients past and family members. A hectic life style and an irregular schedule may aggravate symptoms and interfere with regular meals taken in relaxed settings along with administration of medications. Biofeedback, hynoris, behaviour modification, massage or acupuncture may be helpful. Smoking Cessation Studies have shown that smoking decreases the secretion of bicarbonate from the pancreas into the duodenum resulting in increasing acidity of the duodenum. Research indicates that continued smoking inhibit ulcer repair (suzalai ct. l 2006). Therefore patient is encouraged to stop smoking. Dietary Modification The goal is to avoid oversecretion of acid and hyper motility in the G1 tract. These can be minimised by avoiding extremes of temperature of food and beverages and overstimulation from consumption of meat extracts, alcohol, coffee and other caffeinated and diets rich in milk and cream. In addition an effort is made to neutralise acid by eating three regular meals a day. The patient eats foods that are tolerated and avoid those that produce pain. SURGICAL MNAGEMENT
Surgery is usually recommended for patients with intractable ulcers, life threatening haemorrhage, perforation or obstruction and for those with Zollinger Ellison Syndrome that is unresponsive to medications. * Vagotomy with or without pyloroplasty: Severing of the vagus nerve decreases gastric acid by diminishing cholinergic stimulation to the parietal cells making them less responsive to gastrin. May be performed via open surgical approach, laparoscopy or thoracoscopy. Pyloroplasty: Longitudinal incision is made into the pylorus and transversely stsred closed to enlarge the outlet and relax the muscle. Truncal Vagotomy: Severs the right and left vagus nerves as they enter the stomach at the distal part of the oesophagus. This is used commonly to decrease acid secretions and reduce gastric and intestinal motility. * Selective Vagotomy: consists of cutting the nerve at a particular branch of the vagus nerve resulting in denervation of only a portion of the stomach such as the antrum or parietal cell mass. * Proximal (parietal cell) gastric vagotomy: Denervates acid secreting parietal cells but preserves vagal innervation to the gastric antrum and pylorus. * Antrectomy
Billroth 1 (Gastro Duodenostomy): Removal of the lower portion of the antrum of the stomach (which contains the cells that secrete gastrin) and anastomosis of the gastric stump to the duodenum. Billroth 2 (Gastro jejunostomy): Removal of lower portion (antrum) of stomach and anastomosis to jejunum. FOLLOW UP CARE Recurrence of PUD within 1 year may be prevented with prophylactic use of H2 receptor antagonists taken at a reduced dose. Only those with two or three recurrences per year, those who have had a complication such as bleeding or gastric outlet obstruction, or who are candidates for gastric surgery require maintenance therapy.
The likelihood of recurrence is reduced if the patient avoids smoking, coffee, caffeinated beverages, and alcohol . POSTOPERATIVE COMPLICATIONS * Dumping syndrome is associated with meals having a hyperosmolar composition * Postprandial hypoglycaemia: uncontrolled gastric emptying of a bolus of fluid high in carbohydrate into the small intestine * Bile reflux gastritis :prolonged contact of bile especially bile salts causes damage to gastric mucosa COMPLICATIONS Perforation and Penetration: Perforation is the erosion of the ulcer through the gastric serosa into peritoneal cavity without warning * Penetration is erosion of the ulcer through the gastric serosa into adjacent structures such as the pancreas, biliary tract or gastro hepatic omentum. Symptoms include back and epigastric pain not relieved by medications. Signs and symptoms of perforation: Sudden, severe upper abdominal pain (persisting and increasing in intensity). Pain may be referred to the shoulder especially right shoulder (phrenic nerve irritation) * Vomiting Collapse * Extremely tender and rigid(broad like abdomen) * Hypotension and tachycardia, indicating shock. Pyloric Obstruction also called gastric outlet obstruction occurs when the area distal to the pyloric sphincter becomes scarred and stammered from spasm or oedema or from scar tissue that forms when an ulcer alternately heals and breakdown. The patient may have nausea or vomiting, constipation, epigastric fullness of stomach and later weight loss. NURSING MANAGEMENT Assessment The nurse asks the patient to describe the pain and the methods used to relieve it (e. . food, antacids). The patient usually describes peptic ulcer pain as burning or yawning; it occurs about two hours after a meal and frequently awakens the patient between midnight and 3 am. If the patient reports a recent history of vomiting, the nurse determines how often emesis has occurred and notes important characteristics of the vomitus; is it bright red, does it resemble coffee grounds, or is there undigested food from previous meals? Has the patient noted any bloody or tarry stools? Lifestyle and habits are other concerns as well.
The nurse inquires about the patient’s level of anxiety and his or her current perception of stressors. The nurse assesses the patient’s vital signs and reports tachycardia and hypotension, which may indicate anaemia from GI bleeding. The stool is tested for occult blood, and a physical examination, including palpation of the abdomen for localized tenderness, is performed. NURSING DIAGNOSIS Based on the assessment data, the patient’s nursing diagnosis may include the following * Acute pain related to the effect of gastric acid secretion on damaged tissue. Anxiety related to an acute illness. * Imbalanced nutrition related to changes in diet. * Deficient knowledge about prevention of symptoms and management of the condition. Collaborative Problems or Potential Complications Potential complications may include the following: * Haemorrhage * Perforation * Penetration PLANNING AND GOALS The goals for the patient may include relief of pain, reduced anxiety, maintenance of nutritional requirements, knowledge about the management and prevention of ulcer recurrence, and absence of complications.
NURSING INTERVENTIONS Relieving Pain Pain relief can be achieved with prescribed medications. The patient should avoid aspirin, foods and beverages that contain caffeine, and decaffeinated coffee . In addition meals should be eaten at regularly paced intervals in a relaxed setting. Some patients benefit from learning relaxation techniques to help manage stress and pain. Reducing Anxiety The nurse assesses the patient’s level of anxiety. Patients with peptic ulcers are usually anxious, but their anxiety is not always obvious.
Appropriate information is provided at the patient’s level of understanding, all questions are answered and the patient is encouraged to express fears openly. Explaining diagnostic tests and administering medications as scheduled also help to reduce anxiety . The nurse interacts with the patient in a relaxed manner, helps identify stressors, and explains various coping techniques and relaxation methods, such as biofeedback, hypnosis, or behaviour modification. The patient’s family is also encouraged to participate in care and to provide emotional support. Maintaining Optimal Nutritional Status
The nurse assess the patient for malnutrition and weight loss. After recovery from an acute phase of peptic ulcer disease, the patient is advised about the importance of complying with the medication regimen and dietary restrictions. Monitoring and Managing Potential Complications: Haemorrhage, perforation RESEARCH STUDIES Prophylactic aspirin and risk of peptic ulcer bleeding Abstract Objective: To determine the risks of hospitalisation for bleeding peptic ulcer with the current prophylactic aspirin regimens of 300 mg daily or less. Design: A case-control study with hospital and community controls.
Setting: Hospitals in Glasgow, Newcastle, Nottingham, Oxford, and Portsmouth. Subjects: 1121 patients with gastric or duodenal ulcer bleeding matched with hospital and community controls. Results: 144 (12. 8%) cases had been regular users of aspirin (taken at least five days a week for at least the previous month) compared with 101 (9. 0%) hospital and 77 (7. 8%) community controls. Odds ratios were raised for all doses of aspirin taken, whether compared with hospital or community controls (compared with combined controls: 75 mg, 2. 3 (95% confidence interval 1. 2 to 4. ); 150 mg, 3. 2 (1. 7 to 6. 5); 300 mg, 3. 9 (2. 5 to 6. 3)). Results were not explained by confounding influences of age, sex, prior ulcer history or dyspepsia, or concurrent non-aspirin non-steroidal anti-inflammatory drug use. Risks seemed particularly high in patients who took non-aspirin non-steroidal anti-inflammatory drugs concurrently. Conclusion: No conventionally used prophylactic aspirin regimen seems free of the risk of peptic ulcer complications. CONCLUSION Any portion of the GI tract that comes into contact with gastric secretions is susceptible to ulcer development.
If not treated properly it can become a chronic disease BIBLIOGRAPHY * Lewis, Heitkemper, Dirksen. (2004). Medical surgical nursing. (6th Edition). St. Lewis: Mosby Publishers. PP(895-898) * Brunner, Suddarth (2009). Medical Surgical Nursing (10th ed) Philadelphia PP1789-1790). * Ignatavicuis, Workman (2010). Medical Surgical Nursing. (2010) St. Lewis. Saunders Elsevier PP(776-779) * Sands, Phipps, Etal (2003). Medicasl Surgical Nursing (7th Edition). St. Lewis. Mosby Publishers PP(1771-1775) * Joyce,M ,Black. Medical Surgical Nursing. (7th edn)vol2. Saunders publishers. pp(1871-1873)