Upper GI Problems PDF

Upper GI Problems Nausea and Vomiting: Nausea: Feeling of discomfort in epigastric area; feeling like you need to vomit Vomiting: Action of “throwing up” or emesis; Forceful ejection of food and secretions Pathophysiology: ○ Stimuli from GI tract, kidneys, heart, or brian send...

Upper GI Problems Nausea and Vomiting: Nausea: Feeling of discomfort in epigastric area; feeling like you need to vomit Vomiting: Action of “throwing up” or emesis; Forceful ejection of food and secretions Pathophysiology: ○ Stimuli from GI tract, kidneys, heart, or brian send impulses via afferent pathways to receptors in the medulla (vomiting center) to initiate vomiting reflex ○ Chemoreceptor trigger zone (CTZ) in the brainstem responds to stimuli from drugs, toxins, and motion; activates ANS SNS -> tachycardia, tachypnea, diaphoresis PNS -> relaxes LES, increased gastric motility, increased saliva Causes: GI disorders/infections, CNS disorders, CV problem, pregnancy, endocrine/metabolic, medications, anesthesia, chemo, psychological factors, motion Manifestations ○ Anorexia ○ Weight Loss ○ Prolonged: Fluid and electrolyte imbalances Metabolic acidosis/alkalosis Acidosis - loss of HCl acid with vomiting of small intestine contents (less common) Alkalosis - loss of gastric HCl Decreased blood volume Circulatory failure Assessment ○ subjective/objective data Last bowel movment? Is this normal for you? Has anything changed with your bowel movments? ○ Identify high-risk patients ○ Determine precipitating factors ○ Describe contents of emesis ○ Describe color and characteristics of emesis Bright red blood = active bleeding Coffee-ground color = gastric bleeding ○ Identify timing/recurrent episodes of n/v Recurring episodes of n/v with fatigue lasting a few hours to up to 10 days = cyclic vomiting syndrome Treatment/Nursing considerations: ○ Identify and treat cause ○ SYMPTOM RELIEF Anticholinergic: Scopolamine patches Antihistamines: Hydroxyzine Serotonin Antagonists: Ondansetron (Zofran) Phenothiazines: Chlorpromazine, promethazine, metoclopramide, Reglan (CNS side effects) Antiemetic drugs - can CNS side effects: confusion, falls During hospital visit; patient is having issues with keeping food down;  ○ NPO ○ IV Fluids ○ NGT ○ Monitor I/O, assess for dehydration ○ Aspiration precautions ○ Dietary consult if needed Outcomes ○ Minimal or no N/V ○ Electrolytes within normal limits (WNL) ○ Maintain adequate fluid and nutrient intake Gastroesophageal Reflux Disease(GERD): Chronic mucosal damage d/t reflux of stomach acid into the esophagus (most common upper GI) ○ Gastric contents come up esophagus, can cause pain, discomfort, esophageal problems Patho: ○ Gastric contents are acidic, overwhelm the esophagus defenses, and causes irritation and inflammation ○ Primary factor: incompetent lower esophageal sphincter (LES) Caused by food, drugs, obesity, hiatal hernia Medication induced esophagitis - NSAIDs and K+ Clinical Manifestations ○ Heartburn (pyrosis) - most common s/s Burning, tight sensation under lower sternum spread into throat or jaw May mimic angina but relieved with antacids ○ Dyspepsia Pain/discomfort in upper abdomen ○ Regurgitation Hot, bitter, or sour, liquid in mouth or throat ○ **may complain of cough at night** Complications ○ Esophagitis: ulcerations lead to scar tissue, stricture and dysphagia-difficulty swallowing ○ Barrett’s Esophagus: replacement (metaplasia) of esophageal cells; increases risk for cancer ○ Respiratory: cough, bronchospasm, laryngospasm, aspiration into respiratory systems, chronic bronchitis, pneumonia (gastric secretions irritate upper airway, aspiration) ○ Dental erosion of posterior teeth Diagnostic studies ○ Upper GI endoscopy**hallmark dx for ANY upper GI issue** ○ **most often diagnosed using symptoms ○ barium swallow ○ Manometric studies - esophageal pressure and motility function ○ PH monitoring when no evidence of inflammation ○ Radionuclide studies - reflux of gastric contents and esophageal clearance Treatment/Nursing Considerations: ○ Lifestyle modifications Low-fat diet, small meals Avoid alcohol, caffeine, and smoking *Upright position 2-3 hrs after meals Avoid tight clothing at the waist or bending over after eating  Weight reduction Avoid eating 3 hrs before bed HOB - semi-fowlers Coping with stress, weight management, increased physical activity Drug Therapy ○ PPIs: “prazole” -> #1 DRUG for GERD Decrease HCl secretion and irritation Decreased incidence of strictures; take before 1st meal Adverse s/e with with prolonged use: decreased bone density, kidney disease, vitamin B12 deficiency, risk of dementia ○ H2 receptor blockers: “tidines” (pepcid, cimetidine, famotidine) Decrease HCl secretion and irritation Onset 1 hour duration up to 12 hours Oral, IV. combined with antacid ○ Prokinetics: metoclopramide (Reglan) Extrapyramidal effects (tremor and dyskinesia) CNS (anxiety and hallucinations) ○ Antacids (tums, AlkA-Seltzer) Neutralize acid Provides quick relief for mild, intermittent symptoms Short duration: 1-3 hours after meals and at bedtime Cautious use with older adults, cirrhosis, HTN, and renal pts, due to increased Na+ Nursing and Interprofessional Management ○ Surgical therapy: Nissen Fundoplications:Fundus wrapped around back side of esophagus, secured with sutures to anchor LE below diaphragm Reduces reflux and enhances LES function in those with complications or persistent symptoms ○ Nutritional Therapy Avoid foods that decrease LES pressure: chocolate, fatty food, peppermint, coffee, tea Avoid irritating foods and soda: spicy foods, acidic foods Avoid milk and eating before bedtime Encourage small meals and fluids between meals Hiatal Hernia: Herniation of part of the stomach into the esophagus through an opening (hiatus) in the diaphragm. Etiology and patho ○ Structural: weakened muscle in the diaphragm and esophagogastric opening occurs with aging ○ Increased abdominal pressure ○ Two types Sliding: part of stomach slides thru opening in the diaphragm Rolling: fundus rolls up and creates a fixed pocket; medical emergency! Clinical Manifestations: similar to GERD ○ Heartburn (pyrosis) ○ Dyspepsia ○ Regurgitation ○ Chest pain Complications: GERD, esophagitis, ulcers, stenosis, strangulation, aspiration Diagnostic studies: same as GERD = endoscopy OR barium swallow Nursing and Interprofessional Management ○ Conservative : Reduce intra abdominal pressure -> don’t wear tight clothes, belts, decrease weight, don’t bend over ○ Surgical: optimize LES pressure, prevent movement of the gastroesophageal junction Reduce hernia Herniotomy Fundoplication-top part of stomach is folded and sewn to LES Gerontologic considerations: ○ Incidence increases with age ○ Drug concerns: decrease LES pressure (nitrates CCB, antidepressants) ○ May be asymptomatic First sign may be severe - esophageal bleeding or respiratory complications from aspiration ESOPHAGEAL DIVERTICULA Sac-like outpouchings of one or more layers Three main areas ○ Above upper esophageal sphincter ○ Near esophageal midpoint ○ Above LES Symptoms ○ Dysphagia ○ regurgitation ○ Chronic cough ○ Food trapped in pouches causes sour taste and smell ○ Complications: Perforation of esophagus, malnutrition, aspiration Diagnosis: endoscopy or barium studies  Treatment ○ Dietary modifications ○ Surgery or endoscopic procedures ESOPHAGEAL STRICTURES Narrowing of the esophagus; most often from GERD Manifestations: ○ Dysphagia ○ Regurgitation ○ Weight loss Treatment ○ Dilation with bougies or balloons using endoscopy or fluoroscopy ○ Surgical excision with temporary or permanent gastrostomy PEPTIC ULCER DISEASE (PUD) Erosion of GI mucosa from HCl acid and pepsin ○ Susceptible ares: lower esophagus, stomach, duodenum, Subtypes: classified by degree and duration of mucosal involvement and by location ○ Acute: Superficial erosion and minimal inflammation ○ Chronic: Erosion of muscular wall with formation of fibrous tissue, present continuously for many months intermittently throughout a lifetime Classified by locations, gastric or duodenal ○ Gastric: (antrum - lower part of stomach) Prevalent in females >50 years Increased obstruction Risk factors: H.pylori, bile reflux High recurrence signs/symptoms: Burning or gaseous pain Pain at 1-2 hours after meal**different from duodenal ○ Food worsens the pain Perforation: the first symptoms in some patients; causes peritonitis ○ Duodenal: Prevalent for ages 35-45 Etiology: H. pylori High risk factors: COPD, Cirrhosis, Pancreatitis, Zollinger-Ellison syndrome: digestive disorder that results in too much gastric acid **Constant phases of appearances and disappearances signs/symptoms Burning or cramping across the mid-epigastric line or back; under the xiphoid process Pain at 2-5 hrs after eating - Duodenum is further down the GI tract Pain relief w/ antacids  Risk factors ○ H.pylori ○ Transmission: from family to child (ora-oral or fecal-oral) ○ Bacteria produce urease - increased gastric secretion, tissue damage ○ Medication induced NSAIDS; especially with corticosteroids or anticoagulants ○ Lifestyle - alcohol, smoking, coffee, psychological distress/depression Diagnostic Studies ○ Endoscopy gives direct visualization; most accurate ○ Barium contrast ○ Obtain specimens for H.pylori ○ Labs: CBC, Liver enzymes, serum amylase ○ Stool sample to Test for blood - may appear black/tarry ○ Emesis - coffee ground in appearance Interprofessional Management ○ Treatment goal = decrease acid in stomach(PPI)and enhance the mucosal defenses ○ Conservative care: Adequate rest, drug therapy, smoking cessation, diet modifications long-term follow-up care Pain management. NO NSAIDS or ASPIRIN for 4-6 weeks unless administered with PPI, H2RB, or misoprostol. ○ Medications: PPIs(proton pump inhibitors)**first like for peptic ulcer disease Reduces gastric acid secretions Used with ABX to treat H. Pylori Adherence to abx, report recurrence of pain or blood in vomit or stool Sucralfate Protects esophagus, stomach, and duodenum Give 1 to 2 hours before or after antacids Antibiotics 14 days of penicillin with PPI Metronidazole is used of allergy to PCN ○ Nutritional Therapy AVOID CAFFEINE AND ALCOHOL ○ Complications Bleeding, perforation, gastric outlet obstructions Emergency situation with surgical intervention GI bleeding, duodenal Most lethal - perforation ○ Gi contents spill into the peritoneal cavity. Sudden, severe abd pain radiates to back and shoulders; no relief with food or antacids. ○ If untreated, bacterial peritonitis occurs in 6--12 hrs Can lead to sepsis ○ Immediate focus - stop spillage and restore blood volume ○ Nursing Implementation Acute care: NPO, NGT, VS, monitor for shock, I&O, monitor labs, manage pain Gastric content analysis, check pH, blood or bile  ○ Diagnostics H&P, Upper Gi endoscopy w/biopsy, CBC, liver enzymes, amylase, tumor markers, stool occult Gastric Surgery: can be used to treat stomach cancer, polyps, perforation, chronic gastritis, PUD Partial gastrectomy ○ Gastroduodenostomy- Billroth I Removal of the distal ⅔ of stomach with anastomosis(fusing of stomach to duodenum) ○ Gastrojejunostomy-Billroth II Removal of the distal ⅔ of stomach with anastomosis(fusing of stomach to jejunum) ○ Gastrectomy: Total removal stomach (anastomosis of esophagus to jejunum) ○ Vagotomy: total or selective; sever vagus nerve; decreases gastric acid secretion ○ Pyloroplasty Enlargement of pyloric sphincter Gastric Surgery Complications: Hemorrhage Dumping Syndrome: - direct result of surgical removal of a large part of stomach and pyloric sphincter ○ Gastric chyme enters the small intestine as a large hypertonic bolus and pulls fluid into the bowel lumen causing decreased plasma volume, distention of the bowel lumen, and rapid transit within 15-30 mins of eating ○ signs/symptoms: Weakness, Sweating, Palpitations, Dizziness, Cramping, Increased bowel sounds(borborygmi), Defecation urge ○ Lasts about 1 hour, reduced with short rest periods after eating ○ Treatment: Reduced with rest after eating: tell patient to lay down for at least 30 min after eating; slows down digestion Post op complications: ○ Postprandial hypoglycemia: low BG after eating.. Uncontrolled high carbohydrate bolus enters small intestine causing excess insulin and resulting hypoglycemia 2 hours after eating Sweating, weakness, confusion, palpitations, tachycardia, anxiety ○ Bile reflux gastritis (after reconstruction or removal or pylorus) Bile reflux causes damage to gastric mucosa, chronic gastritis, and PUD  Epigastric distress temporarily relieved with vomiting Administer CHOLESTYRAMINE before or with meals Binds to bile salts thus decreasing amount of reflux Nursing Management: Gastric Surgery ○ ***Prevent infection ○ Monitor for complications Respiratory comp.(dyspnea, chest pain, cyanosis) ANASTOMOSIS LEAK Tachycardia Fever Abdominal pain REQUIRES IMMEDIATE TREATMENT TO PREVENT SEPSIS & DEATH ○ Hemorrhage: VS, NG aspirate contents(check for blood) ○ NGT for decompression; reduces pressure to suture line; decreases edema and inflammation Observe gastric aspirate: color, amount odor Blood drainage expected for 2-3 hrs (report excess > 75ml/hr) Monitor for clots/obstruction Nursing Management: Nutrition Therapy ○ **reduced stomach size means reduced meal size! ○ Small, frequent meals(6 meals) ○ No fluids with meals, chew thoroughly (takes up space for food) ○ Avoid simple sugars and extreme food temps ○ Avoid hypoglycemia GASTRITIS Inflammation of gastric mucosa ○ Acute or chronic ○ Diffuse or localized Patho: Breakdown in gastric mucosal barrier allowing HCL acid and pepsin to diffuse back into mucosa resulting in edema and possible bleeding Risk Factors: ○ NSAID-induced : female, > 60, hx of PUD, Anticoagulants, NSAIDs, chronic disorders ○ Diet related: binge-drinking alcohol, spicy irritating foods - tomatoes, chocolate, ○ Genetic: autoimmune gastritis ○ H. Pylori ○ Diseases: autoimmune gastritis, burns, crohn’s, hiatal hernia, stress, bile reflux, sepsis, shock Clinical Manifestations ○ Acute Anorexia, N/V, epigastric tenderness, feeling of fullness Bleeding with alcohol use may be only symptom Self-limiting - lasts from a few hours to a few days ○ Chronic Pernicious anemia: gastric mucosa is damaged so it does not secrete intrinsic factor  Nursing Management ○ Acute Gastritis Identify & Eliminate causes Supportive care; NPO, IV FLUIDS, ANTIEMETICS, MONITOR FOR DEHYDRATION Severe; NGT to monitor for bleeding, empty stomach Risk for bleeding Monitor VS, heme test for vomiting Drugs: PPIs or H2 receptor blockers ○ Chronic gastritis ABX FOR H. Pylori Cobalamin (B12) for pernicious anemia Lifestyle: No smoking/alcohol/drugs; 6 small meals per day, non irritating foods UPPER GI BLEEDING Hematemesis: bloody vomitus ○ Bright Red: arterial blood loss ○ Coffee ground: digested blood Melena: Black Tarry stools from upper GI source Occult:Guaiac test blood in gastric secretions, vomitus or stool Causes: (can be difficult to identify) ○ Stomach and duodenal H.pylori and NSAIDS Corticosteroids Cancer Gastritis polyps ○ Esophageal origin Chronic esophagitis, Mallory Weiss tear or esophageal varices Varices: swollen veins in esophageal tract (medical 911!!) Diagnostics ○ ENDOSCOPY IS GOLD STANDARD ○ Angiography - pt cannot be high-risk or unstable ○ CBC - Hgb & Hct ○ BUN - GI tract bacteria breakdown protein ○ Vomitus and stool occult Interprofessional Management ○ Massive GI Bleed >1500 ml blood loss ○ ASSESS FOR SHOCK = tachycardia, weak pulse, low BP, cool extremities, prolonged cap refill, apprehension ○ Monitor urine output hourly: monitoring kidney function ○ Hemodynamic monitoring - blood flow and BP in CV system ○ Oxygen - increased blood O2 sat ○ Assess FOR PERFORATION AND PERITONITIS - tense, rigid abdomen, bowel sounds ○ Administer IV fluids ○ Blood transfusions EMERGENCY ASSESSMENT AND MANAGEMENT Endoscopy Therapy- FIRST LINE MGMT within 24 hours to determine treatment or surgery ○ Goal = coagulate or thrombose bleed ○ clips/bands - compress vessel ○ Cauterization ○ Injection (epi or alcohol) ○ Balloon tamponade Surgical Therapy ○ Site identified ○ Requires more than 2000 ml blood or shock Drug therapy: ○ PPIs ○ Antacids