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) • • • • 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 • • • • 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 • • • • • • 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 • • • • 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 o o o o o 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 • • • • • • • • • 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