G A S T R O I N T E S T I N A L S Y S T E M A. INTRODUCTORY CONCEPT Assessing Clients with Nutritional and Gastrointestinal Disorders BACKGROUND ANATOMY AND PHYSIOLOGY A. Digestive organs 1. Mouth (oral, buccal cavity) a. Struct Structur ures: es: lips lips,, cheeks cheeks,, tongue tongue,, teeth teeth b. Processes: • Food is chewed and mixed with saliva to form a mass or bolus • Saliva from salivary glands facilitates taste and provides enzymes which initiate chemical breakdown of starches 2. Pharynx a. Struct Structur ures: es: oropha oropharyn rynx, x, laryng laryngoph ophar arynx ynx b. Processes • Provide passagewa passageways ys for food, fluids, air • Pharyngeal mucosa produces fluid to facilitate passage of bolus as it is swallowed • Muscles of pharynx move bolus to esophagus through peristalsis 3. Esophagus: passageway for food from pharynx to stomach a. Structur tures: • Epiglottis: flap of cartilage over top of larynx that prevents food from entering larynx during swallowing • Gastroesophageal Gastroesophageal sphincter: closure of esophagus at cardiac orifice of stomach b. Proce Process: ss: Food Food passe passes s from from pha pharyn rynx x to stomac stomach h 4. Stomach a. Regions Regions of stoma stomach: ch: cardiac, cardiac, fundus, fundus, body, body, pylorus pylorus b. Stru Struct ctur ures es:: Stom Stomac ach h li lini ning ng • Gastric glands produce gastric juice • Mucous cells: produce alkaline mucus to protect stomach lining • Zymogenic cells: produce pepsinogen (inactive form of pepsin) • Parietal cells: secrete 2 substances: • Hydrochloric acid: bactericidal; bactericidal; acts in protein digestion • Intrinsic factor: needed for absorption of vitamin B12 in small intestine • Enteroendocrine Enteroendocrine cells: secrete gastrin (regulates secretion and motility), histamine, endorphins, serotonin, somatostatin c. Innervation • Secretory activity regulation regulation • Vagus nerve (parasympathetic) increases secretory activity • Stimulation of sympathetic nerves decreases secretory activity • Secretory activity has 3 phases • Cephalic phase: phase: preparation preparation for digestion; triggered by sight, odor, taste, taste, or thought of food • Gastric phase: phase: begins when food enters stomach; stomach; more gastric juice and hydrochloric hydrochloric acid secreted • Intestinal phase: initiated by partially digested food entering small intestine; continued gastric secretion d. Processes: • Acts as storage reservoir for food • Continues mechanical mechanical breakdown of food • Begins process of protein digestion • Mixes food with gastric juices into thick fluid: chyme • Connects esophagus and small intestine • Pyloric sphincter controls emptying of stomach into duodenum • Empties completely in 4 – 6 hours post normal meal • Large volumes speed process • Solid and fats slow process 5. Small Intestine a. Regi Region ons s of sma small ll int intes esti tine ne::
Duodenum (pancreatic enzymes and bile enter) • Jejunum • Ileum b. Structures • Circular folds of mucosa and submucosa • Villi • Microvilli provide large surface area c. Processes • Connects stomach (at pyloric sphincter) to large intestine (at ileocecal junction) • Peristalsis Peristalsis moves contents • Production of secretin and cholecystokinin when chyme enters stimulating • Pancreatic enzymes and bile to enter at duodenum • Chemical digestion of foods by enzymes • Amylase acts on starches • Trypsin and chymotrypsin chymotrypsin act act on proteins • Lipases act on lipids • Bile salts emulsify triglycerides • Intestinal enzymes continue to further break down starches and proteins • Absorption of almost all food products, water, vitamins and most electrolytes; (i.e. 10 L of fluid enters small intestine; < 1L reaches large intestine daily) B. Accessory Digestive Organs 1. Liver a. Structure: • Four lobes: right, left, caudate, quadrate • Encased in fibroelastic capsule • Tissue as lobules, lobules, plates plates of hepatocytes hepatocytes • Each lobule communicates with branch of hepatic artery, branch of hepatic portal vein, bile duct • Sinusoids, blood-filled spaces are within lobules • Kupffer cell line sinusoids and remove debris from blood b. Processes • Synthesis of • Plasma proteins and clotting factors • Fats from carbohydrates and proteins for energy or as adipose tissue • Phospholipids and cholesterol for production of bile salts, steroids, plasma membranes • Responds to glucose levels in blood • Releases glucose in response to hypoglycemia • Stores glucose as glycogen or fat in response to hyperglycemia hyperglycemia • Stores • Blood and releases stored blood during hemorrhage • Iron as ferritin (needed in production of red blood cells) • Fat soluble vitamins • Converts amino acids to carbohydrates • Metabolizes bilirubin • Lessens toxicity of chemicals, foreign molecules, hormones • Secretes bile: needed for emulsification and absorption of fats 2. Gallbladder • Structure • Small sac on inferior surface of liver • Connected to cystic duct which is joined to hepatic duct forming common bile duct: pathway for bile from liver to small intestine • Processes • Concentration and storage of bile • Secretion of bile into cystic duct to enter duodenum at sphincter of Oddi when fatty food enters duodenum •
3. Pancreas (Exocrine portion) • Structure: Acini, i.e. secretory cells drain into pancreatic duct, which joins the common bile duct • Processes • Secretion of pancreatic juice containing enzymes amylase, lipase, trypsin, chymotrypsin • Alkaline pancreatic pancreatic juice neutralizes acidic chyme to optimum pH for digestion and absorption of food C. Metabolism • Biochemical reaction occurring at cellular level, which produces and provides energy to maintain life • Metabolic reactions are either anabolic or catabolic • Anabolic processes involve simple molecules combining to build more complex structures, i.e. amino acids bind to form proteins • Catabolic processes involve the breakdown of complex structures to simpler forms, i.e. breakdown of carbohydrates releasing ATP, energy molecule necessary for cellular activity • Kilocalorie • Measurement Measurement of energy value of food • Amount of heat energy needed to raise temperature of 1 kilogram of water 1 degree centigrade D. Catego Categorie ries s of nutr nutrien ients ts 1. Carbohydrates Carbohydrates a. Primary Sources: Sources: plant foods: sugars (milk, fruits) fruits) and starches (grains, (grains, root vegetables) b. Energy value: 4 kcal per gram; excess converted to glycogen or fat c. Recommended daily intake: 125 – 175 gm (mostly complex) d. Body function: converted to glucose for cellular function e. Deficiency: over time tissue wasting since protein and fats are broken down and metabolic acidosis could result 2. Proteins a. Primary Sources • Complete (all essential amino acids): animal products • Incomplete (lack some amino acids): plant sources: legumes, nuts b. Energy value: 4 kcal per gram c. Recommended daily intake • Male: 56 gm • Female 45 gm • Additional needed with growth, pregnancy, pregnancy, tissue repair and healing d. Body function: building body tissues, enzymes, hormones, hemoglobin 3. Fats a. Source • Saturated fats: animal products, coconuts • Unsaturated fats: seeds, nuts, vegetable oil; cholesterol: meats, milk products, egg yolks b. Energy value: 9 kcal per gram c. Recommended daily intake • 30% or less of daily caloric intake • < 10% saturated fat • Cholesterol no more than 250 mg c. Body function • Fatty acids are essential for body cell membranes for some substances, including hormones • Concentrated source of cell fuel d. Deficiency: excessive weight loss and skin lesions 4. Vitamins a. Essential organic compounds facilitate body’s use of nutrients b. Categories: • Fat Soluble: A, D, E, K which are produced or stored in body and can reach toxic levels a. Vitamin A: needed for vision, skin and mucous membrane integrity b. Vitamin D • Needed for calcium homeostasis
Body produces: formed by sunlight action in skin • Additive to milk c. Vitamin E: antioxidant d. Vitamin K • Needed for clotting proteins by the liver • Body produces: synthesized by bacteria in large bowel • Water Soluble: B vitamins and C which are excreted and seldom reach toxic levels a. Vitamin B1 (Thiamin) needed for function of heart, muscles, nerves b. Vitamin B2 (riboflavin) needed to utilize other nutrients c. Vitamin B6 (pyridoxine) needed for protein metabolism d. Vitamin B12 (cyanocobalamin) (cyanocobalamin) • Essential for red blood cell formation • Not found in any plant foods e. Vitamin C (ascorbic acid) • Antioxidant • Needed for healing wounds • Found in citrus fruits, vegetables vegetables f. Niacin (nicotinamide) needed for carbohydrate and fat metabolism g. Biotin needed for catabolism of fatty acids and carbohydrates carbohydrates h. Pantothenic acid needed for steroid, heme synthesis i. Folic acid (folacin) needed for formation of red blood cells, health of nervous system 5. Minerals • Necessary Necessary for maintenance maintenance of body’s structures and functioning • Major minerals needed include: calcium, phosphorus, potassium, sulfur, sodium, chloride, magnesium • Trace elements elements (necessary (necessary in small small amounts) include: include: iron, iodine, copper, copper, zinc, selenium selenium •
HEALTH ASSESSMENT INTERVIEW: SUBJECTIVE DAT A • Record presence of any problems client relates to nutrition, digestion, discomfort in eating, bowel function • Follow with specific questions related to anorexia, nausea, vomiting, diarrhea or constipation • Address specifically specifically any changes in weight or appetite, or changes in functioning • Ask client to describe typical dietary intake over 24 hour period; include beverages and water • Ask client if taking any vitamins, herbal supplements • Address alcohol intake • Address intake of fluids especially those with sugar and/or caffeine • Record presence of any food allergies of intolerance to foods • Ask client to describe a healthy diet and assess the individual’s individual’s diet • Ask about health history including surgeries surgeries or diseases of gastrointestinal gastrointestinal system or metabolism (diabetes mellitus), dental history PHYSICAL ASSESSMENT A. Includes techniques of inspection, auscultation, auscultation, percussion, and palpation B. Palpation is performed last to avoid problems with assessment of bowel sounds or causing pain C. Parts 1. Anthropometric assessment: obtain measurement and compare to standards a. Weigh client and compare to ideal body weight (IBW) • 10 – 20% 20% < IBW: malnutrition • 10% > IBW: overweight • 20% > IBW: obese b. Measure Triceps Skinfold Thickness (TST) • Readings 10% or more below standards: malnutrition malnutrition • Readings 10% or more above standards: obesity c. Measure Midarm circumference (MAC) • Decreased with malnutrition malnutrition • Increased with obesity
d. Calculate Midarm Muscle Circumference (MAMC) MAMC < 90% standard: standard: mild mild malnutrition malnutrition • MAMC < 90% standard standard moderate malnutrition • MAMC < 90% severe malnutrition 2. Oral assessment: examiner must wear gloves a. Abnormal findings of the lips • Cheliosis: painful lesions at corners of mouth associated with riboflavin or niacin deficiency • Clear vesicles or cord sore with herpes simplex 1 b. Abnormal findings of the tongue • Moisture: vertical fissures with dehydration • Color: bright red with folic acid, B12, iron deficiency; deficiency; Black and hairy hairy with post antibiotic therapy c. Abnormal findings of the buccal mucosa • Leukoplakia (small white patches) possibly pre-malignant • Reddened, dry, or swollen as with stomatitis • White cheesy patches that bleed when scraped as with candidiasis d. Abnormal findings of the teeth and gums • Excessive cavities, plaque on teeth • Swollen, bleeding bleeding gums: periodontal disease, disease, vitamin vitamin C deficiency e. Abnormal findings of the throat and tonsils: red swollen with white spots as with acute infections f. Abnormal findings of the breath • Foul odor: significant for poor hygiene, liver disease, respiratory respiratory infections • Fruity, sweet odor: as with ketoacidosis • Acetone odor: uremia 3. Abdominal assessment assessment a. Abnormal findings upon inspection • Generalized Generalized abdominal distention: obesity, gas retention • Generalized Generalized abdominal distention with eversion of umbilicus: could signify ascites, presence of tumor(s) • Lower abdominal distention: as with pregnancy, ovarian mass, distended bladder • Sunken abdomen: malnutrition or muscle replacing fat • Striae (stretch marks): conditions with rapid weight gain • Spider angiomas: could signify liver disease • Dilated veins: indicate possible hepatic problem • Increased pulsation: could indicate aortic aneurysm b. Abnormal findings upon auscultation auscultation • Absent bowel sounds: post surgery, late bowel obstruction, peritonitis • Borborygmus (hyperactive or growling bowel sounds): diarrhea, early bowel obstruction • Bruit: restricted blood flow • Venous hum over liver: as with liver cirrhosis • Friction rub: inflammation of spleen or liver c. Abnormal findings upon percussion: Dullness is heard where bowel is displaced with fluid, tumors, or filled with fecal mass d. Abnormal findings upon palpation 1. Do not use deep palpation with clients with a pulsatile abdominal mass, risk for hemorrhage, renal transplant, or polycystic kidneys 2. Findings • Abdominal pain with involuntary muscle spasms could signify peritoneal peritoneal irritation • Abnormal masses, as with aortic aneurysm, tumors, distended bowel or bladder • Boardlike abdomen: perforated bowel • Rebound tenderness: signifies peritoneal irritation 3. Specific areas • Right upper quadrant pain: acute cholecystitis • Upper middle abdominal pain: acute pancreatitis • Right lower quadrant pain: acute appendicitis • Left lower quadrant pain: acute diverticulitis •
4. Palpation of liver • Enlargement Enlargement with smooth tender edge: hepatitis, venous congestion • Enlargement, nontender: malignancy • Sharp pain on inspiration inspiration and client stops inspiring (Murphy’s sign): inflammation of gallbladder B. COMMON HEATH PROBLEMS (UPPER GI) I: PEDIATRICS P Y L OR I C S T E N O S I S narrowing of the pyloric sphincter at the outlet of the stomach. stomach. A. Description: Pyloric stenosis is the narrowing B. Etiology: The exact cause is unknown; unknown; however, heredity may play play an important role. Pathophysiology: C. a. The pylorus pylorus narrows because of progressive progressive hypertrophy hypertrophy and hyperplasia hyperplasia of the circular circular pyloric muscle. muscle. The muscle may grow grow to twice its size. b. This leads leads to obstruction of the pyloric sphincter, wit subsequent subsequent gastric gastric distention, dilatation, and hypertrophy. D. Assessment Findings: a. No abnorma abnormall signs signs in the first first weeks weeks after after birth birth (usual (usually) ly) b. Regurgitation Regurgitation or nonprojectile nonprojectile vomiting vomiting beginning beginning by 3 weeks of age; emesis emesis is not not bile stained and contains only gastric contents bt may be blood tinged. c. Vomiting increases increases in frequency frequency and force force over the next 1 to 2 weeks weeks until most of ingested ingested food is expelled through projectile vomiting. d. No signs signs of anorex anorexia; ia; good good appetite appetite and and feeding feeding habits habits e. No evid eviden ence ce of pain pain f. Weight loss g. Upper Upper abdo abdomin minal al dist distent ention ion h. Palpable olive-shaped olive-shaped mass in the epigastrium epigastrium just to the right of the umbilicus umbilicus i. Visi Visible ble gastric gastric perist peristalti altic c waves movin moving g from left to right right across across the epigas epigastriu trium m j. Decreased Decreased frequency and and volume of stools stools k. Signs Signs of malnut malnutrit rition ion and and dehydra dehydratio tion n E. Nursing management a. Monitor Monitor feeding feeding pattern pattern and the associa association tion between between feeding feedings s and vomiting vomiting b. Ass Assess ess the the amount, amount, charac character, ter, and and frequen frequency cy of emesis emesis c. Promote adequate hydration. Administer IVF, as prescribed, to replenish potassium and correct alkalosis d. Prev Preven entt asp aspir irat atio ion n i. Feed Feed the the infa infant nt slo slowl wly y ii. ii. Burp Burp the the infan infantt frequ frequent ently ly iii. Position Position the infant infant in the high-fow high-fowler’ ler’s s position position on the right side side after feedin feedings gs e. Provi Provide de post post-op -opera erativ tive e care care f. Prov Provid ide e fami family ly teac teachi hing ng TRACHEOESOPHAGEAL FISTULA
II: ADULT G A S T R O E S O P H A G E A L R E F L U X D I S E A S E (GERD) 1. Definition • Gastroesophageal Gastroesophageal reflux is the backward flow of gastric content into the esophagus. • GERD common, affecting 15 – 20% of adults • 10% persons experience daily heartburn and indigestion • Because of location near other organs symptoms may mimic other illnesses including including heart problems 2. Pathophysiology a. Gastroesophageal Gastroesophageal reflux results from transient transient relaxation or incompetence incompetence of lower lower esophageal esophageal sphincter, sphincter, or increased pressure within stomach b. Factors Factors contribut contributing ing to gastroes gastroesophag ophageal eal reflux reflux • Increased gastric volume (post meals)
Position pushing gastric contents close to gastroesophageal gastroesophageal juncture (such as bending or lying down) • Increased gastric pressure (obesity or tight clothing) • Hiatal hernia c. Normally the peristalsis peristalsis in esophagus esophagus and and bicarbonate bicarbonate in salivary salivary secretions neutralize any gastric juices (acidic) that contact the esophagus; during sleep and with gastroesophageal gastroesophageal reflux esophageal mucosa is damaged and inflamed; prolonged exposure causes ulceration, friable mucosa, and bleeding; untreated there is scarring and stricture 3. Manifestations a. Heartbur Heartburn n after after meals, meals, while while bending bending over, over, or recum recumbent bent b. May have have regurgi regurgitatio tation n of sour mater materials ials in in mouth, mouth, pain with with swallow swallowing ing c. Atyp Atypic ical al ches chestt pai pain n d. Sore Sore thr throa oatt with with hoa hoars rsen enes ess s 4. Complications a. Esophage Esophageal al strict strictures ures,, which which can can progr progress ess to to dysphag dysphagia ia b. Barrett’s esophagus: esophagus: changes in cells lining esophagus with increased increased risk risk for esophageal esophageal cancer 5. Collaborative Care a. Diagnosi Diagnosis s may be made made from from histo history ry of symptoms symptoms and and risks risks b. Trea Treatm tmen entt inc inclu lude des s • Life style changes • Diet modifications modifications • Medications c. Surgery Surgery may may be indicat indicated ed for clients clients with with serious serious compl complicat ications ions 6. Diagnostic Tests a. Barium Barium swallow swallow (eval (evaluati uation on of esophag esophagus, us, stomach stomach,, small small intestine intestine)) b. Upper Upper endos endoscopy: copy: direct direct visualiz visualization ation;; biopsie biopsies s may may be done c. 24-hou 24-hourr ambula ambulator tory y pH monito monitorin ring g d. Esophage Esophageal al manometry manometry,, which measure measure pressur pressures es of esophageal esophageal sphincter sphincter and and peristalsi peristalsis s 7. Medications a. Antacids Antacids for mild to moder moderate ate symptom symptoms, s, e.g. Maalox, Maalox, Mylant Mylanta, a, Gavisc Gaviscon on b. H2-recep H2-receptor tor blocker blockers: s: decrease decrease acid produ production ction;; given BID BID or more more often, often, e.g. cimeti cimetidine dine,, ranitidine, famotidine, nizatidine c. Proton-pu Proton-pump mp inhibitors: inhibitors: reduce reduce gastric gastric secretion secretions, s, promote promote healing healing of esophage esophageal al erosion erosion and relieve symptoms, e.g. omeprazole (prilosec); lansoprazole lansoprazole (Prevacid) initially for 8 weeks; or 3 to 6 months d. Promotili Promotility ty agent: enhances enhances esophagea esophageall clearance clearance and gastric gastric emptying, emptying, e.g. metoclopr metoclopramid amide e (reglan) 8. Dietary and Lifestyle Management a. Eliminat Elimination ion of acid acid foods foods (tomat (tomatoes, oes, spicy spicy,, citrus citrus foods, foods, coffee coffee)) b. Avoiding Avoiding food which which relax relax esophageal esophageal sphinct sphincter er or delay gastri gastric c emptying emptying (fatty (fatty foods, chocolate, peppermint, alcohol) c. Main Mainta tain in idea ideall bod body y wei weigh ghtt d. Eat small small meals meals and stay stay upright upright 2 hours post post eating; eating; no eating eating 3 hours prior prior to going going to bed e. Elev Elevat ate e hea head d of of bed bed on 6 – 8 ″ blocks to decrease reflux f. No smoking g. Avoiding Avoiding bending bending and wear loose fitting fitting clothi clothing ng 9. Surgery indicated for persons not improved by diet and life style changes a. Laparosc Laparoscopic opic procedu procedures res to tighten tighten lower lower esopha esophageal geal sphin sphincter cter b. Open surgica surgicall procedur procedure: e: Nissen Nissen fundoplic fundoplicatio ation n 10. Nursing Care a. Pain Pain usua usually lly cont control rolled led by by treat treatmen mentt b. Assis Assistt clien clientt to instit institute ute home home plan plan •
DIVERTICULAR DISEASE 1. Definition • Diverticula are saclike projections projections of mucosa through muscular layer of colon mainly in sigmoid colon
Incidence increases with age; less than a third of persons with diverticulosis develop symptoms 2. Risk Factors • Cultural changes in western world with diet of highly refined and fiber-deficient fiber-deficient foods • Decreased activity levels • Postponement of defecation 3. Pathophysiology • Diverticulosis is the presence of diverticula which form due to increased pressure within bowel lumen causing bowel mucosa to herniate through defects in colon wall, causing outpouchings • Muscle in bowel wall thickens narrowing bowel lumen and increasing intraluminal pressure • Complications of diverticulosis include hemorrhage and diverticulitis, diverticulitis, the inflammation of the diverticular diverticular sac • Diverticulitis: Diverticulitis: diverticulum in sigmoid sigmoid colon irritated with undigested undigested food and bacteria forming a hard mass (fecalith) that impairs blood supply leading to perforation • With microscopic perforation, inflammation inflammation is localized; more extensive perforation perforation may lead to peritonitis or abscess formation 4. Manifestations • Pain, left-sided, mild to moderate and cramping or steady • Constipation or frequency of defecation • May also have nausea, vomiting, low-grade fever, abdominal distention, tenderness and palpable LLQ mass • Older adult may have vague abdominal pain 5. Complications • Peritonitis • Abscess formation • Bowel obstruction • Fistula formation • Hemorrhage 6. Collaborative Care: Care : Focus is on management of symptoms and complications 7. Diagnostic Tests • Abdominal Xray: detection of free air with perforation, perforation, location of abscess, fistula fistula • Barium enema contraindicated contraindicated in early diverticulitis diverticulitis due to risk of barium leakage into peritoneal cavity, but will confirm diverticulosis • Abdominal CT scan, sigmoidoscopy or colonscopy used in diagnosis of diverticulosis • WBC count with differential: leukocytosis with shift to left in diverticulitis • Hemocult or guiac testing: determine presence of occult blood 8. Medications • Broad spectrum antibiotics against gram negative and anaerobic bacteria to treat acute diverticulitis, diverticulitis, oral or intravenous route depending on severity of symptoms • Analgesics for pain (non-narcotic) • Stool softener but not cathartic may be prescribed (nothing to increase pressure within bowel) 9. Dietary Management • Diet modification may decrease risk of complications • High-fiber diet (bran, commercial bulk-forming products such as psyllium seed (Metamucil) or methycelluose) • Some clients advised against foods with small seeds which could obstruct diverticula 10. Treatment for acute episode of diverticulitis diverticulitis • Client initially NPO with intravenous fluids (possibly TPN) • As symptoms subside reintroduce reintroduce food: clear liquid liquid diet, to soft, low-roughage diet psyillium psyillium seed products to soften stool and increase bulk • High fiber diet is resumed after full recovery 11. Surgery • Surgical intervention indicated indicated for clients with generalized peritonitis or abscess that does not respond to treatment • With acute infection, 2 stage Hartman procedure done with temporary colostomy; re-anastomosis performed 2 – 3 months later •
12. Nursing Care: Health promotion includes teaching high-fiber foods in diet generally, generally, may be contraindicated contraindicated for persons with known conditions 13. Nursing Diagnoses • Impaired Tissue Integrity, gastrointestinal • Pain • Anxiety, related to unknown outcome of treatment, possible surgery 14. Home Care • Teaching regarding regarding prescribed prescribed diet, fluid intake, intake, medications medications • Referral for home health care agency, if new colostomy client PEPTIC ULCER DISEASE 1. Definition and Risk factors Break in mucous lining of GI tract comes into contact with gastric juice; affects 10% of US population Duodenal ulcers: most common; affect mostly males ages 30 – 55; ulcers found near pyloris Gastric ulcers: affect older persons (ages 55 – 70); found on lesser curvature and associated with increased incidence of gastric cancer Common in smokers, users of NSAIDS; familial pattern 2. Pathophysiology Ulcers or breaks in mucosa of GI tract occur with • H. pylori infection (spread by oral to oral, fecal-oral routes) damages gastric epithelial cells reducing effectiveness of gastric mucus • Use of NSAIDS: interrupts prostaglandin prostaglandin synthesis which maintains mucous barrier of gastric mucosa Chronic with spontaneous remissions and exacerbations exacerbations associated with trauma, infection, physical or psychological stress 3. Manifestations Pain is classic symptom: gnawing, burning, aching hungerlike hungerlike in epigastric region possibly radiating radiating to back; occurs when stomach is empty and relieved by food (pain: food: relief pattern) Symptoms less clear in older adult; may have poorly localized discomfort, dysphagia, dysphagia, weight loss; presenting symptom may be complication: GI hemorrhage hemorrhage or perforation of stomach or duodenum 4. Complications • Hemorrhage: frequent in older adult: hematemesis, melena, hematochezia hematochezia (blood in stool); weakness, fatigue, dizziness, orthostatic hypotension and anemia; with significant bleed loss may develop hypovolemic shock • Obstruction: gastric outlet obstruction: edema surrounding ulcer blocks GI tract from muscle spasm or scar tissue • Gradual process • Symptoms: feelings of epigastric epigastric fullness, nausea, worsened ulcer symptoms • Perforation: ulcer erodes through mucosal wall and gastric or duodenal contents enter peritoneum leading to peritonitis; peritonitis; chemical at first (inflammatory) (inflammatory) and then bacterial in 6 to 12 hours • Time of ulceration: ulceration: severe severe upper abdominal abdominal pain radiating radiating throughout throughout abdomen and and possibly to shoulder • Abdomen becomes rigid, boardlike with absent bowel sounds; symptoms of shock • Older adults may present with mental confusion and non-specific symptoms 5. Zollinger-Ellison syndrome • Peptic ulcer disease caused by gastrinoma (tumor in pancreas, stomach, or intestine which secretes gastrin) • Excess gastric acid leads to ulceration and often bleeding and perforation • Excess hydrochloric acid production also leads to diarrhea and steatorrhea (excess (excess fat in stools) 6. Collaborative Care • Elimination of H. pylori • Prevention of or treatment of ulcers from NSAIDS use 7. Diagnostic Tests • Upper GI series detects up to 90% of ulcers • Gastroscopy: visualization visualization of esophageal, esophageal, gastric, and duodenal mucosa for ulcers, perform biopsies • Tests for H. pylori pylori
Biopsy urease test on specimen biopsy • Urea breath test (non-invasive) (non-invasive) • Serologic testing • Gastric analysis: analysis of stomach contents aspirated through naso-gastric tube; diagnosis of Zollinger-Ellison Zollinger-Ellison syndrome 8. Treatment a. Medications • Control of H. pylori with combination therapy of two antibiotics and proton-pump inhibitors inhibitors or bismuth subsalicylate subsalicylate • Stop NSAID use or add twice a day proton-pump inhibitors b. Specif Specific ic medi medica catio tion n inter interven ventio tions ns • Proton-pump inhibitors often heal ulcers in 4 weeks • Histamine-2 blockers blockers are used for 8 weeks or longer to heal ulcers and can interact with other medications • Sulcralfate: Sulcralfate: binds to ulcer base base forming protective barrier barrier • Bismuth compounds (including Pepto-Bismol) stimulate mucosal bicarbonate bicarbonate and prostaglandin prostaglandin production to heal ulcers; antibacterial against H. pylori • Prostaglandin Prostaglandin analogs (misoprostol): (misoprostol): prevent NSAID-induced NSAID-induced ulcers ulcers • Antacids: rapid relief of ulcer symptoms; need to be taken frequently and not with other medications, medications, inexpensive c. Diet Dietar ary y Mana Manage geme ment nt • Maintain good nutrition: balanced meals at regular intervals • Limited alcohol intake; stop smoking d. Surgery Surgery no longer longer part part of treatment, treatment, but but may see clien clients ts who have have had surgica surgicall treatment treatment in past and may have long-term complications e. Treat Treatmen mentt of comp complic licati ation on hemor hemorrh rhage age • Restore and maintain circulation with intravenous intravenous fluids and/or blood transfusions • Gastroscopy with interventions to control bleeding (laser, electrocautery, sclerosing sclerosing agents) • Maintain NPO status with nasogastric tube; antacids per nasogastric tube and intravenous H2receptor blockers • Surgery may be indicated if medical treatment does not control bleeding f. Treatmen Treatmentt of complica complication tion gastric gastric outle outlett obstruc obstruction tion • Gastric decompression with nasogastric suction, intravenous and electrolyte replacement • Intravenous H2 receptor blockers • Endoscopy for balloon dilation of gastric outlet • Surgery if other methods are not successful g. Treat Treatmen mentt of compli complica catio tion n perfor perforati ation on • Gastric decompression with nasogastric suction, intravenous and electrolyte replacement • Fowler’s or semi-Fowler’s semi-Fowler’s positioning • Aggressive intravenous antibiotic therapy • Laparoscopic or open laparotomy to close perforation 9. Nursing Diagnoses • Pain: clients should eliminate any food found to precipitate precipitate pain • Sleep Pattern Disturbance: related to ulcer pain • Imbalanced Nutrition: Less than body requirements: six small meals may be more effective in avoiding symptoms • Deficient Fluid Volume: prevent hypovolemic shock and allow adequate replacement replacement for nasogastric nasogastric drainage with intravenous intravenous fluids and electrolytes 10. Home care involves teaching clients medication regimens and an action plan, including recognition of complications and to seek medical assistance for complications •
GASTRITIS Gastritis 1. Definition: Inflammation Inflammation of stomach lining from irritation of gastric mucosa (normally protected from gastric acid and enzymes by mucosal barrier) 2. Types
a. Acut Acute e Gast Gastri riti tis s 1. Disruption of mucosal barrier allowing hydrochloric hydrochloric acid and pepsin to have contact with gastric tissue: leads to irritation, irritation, inflammation, superficial erosions 2. Gastric mucosa rapidly regenerates; self-limiting disorder 3. Causes of acute gastritis a. Irritants include aspirin and other other NSAIDS, NSAIDS, corticosteroids corticosteroids,, alcohol, alcohol, caffeine caffeine b. Ingestion Ingestion of corrosiv corrosive e substan substances: ces: alkal alkalii or acid acid c. Effects Effects from radiati radiation on therapy, therapy, certain certain chemothe chemotherape rapeutic utic agents agents 4. Erosive Gastritis: form of acute which is stress-induced, complication of life-threatening condition (Curling’s ulcer with burns); gastric mucosa becomes ischemic and tissue is then injured by acid of stomach 5. Manifestations Manifestations • Mild: anorexia, mild epigastric discomfort, belching • More severe: abdominal pain, nausea, vomiting, hematemesis, hematemesis, melena • Erosive: not associated with pain; bleeding occurs 2 or more days post stress event • If perforation occurs, signs of peritonitis 6. Treatment • NPO status to rest GI tract for 6 – 12 hours, reintroduce clear liquids gradually and progress; progress; intravenous fluid and electrolytes if indicated • Medications: Medications: proton-pump inhibitor or H2-receptor blocker; sucralfate sucralfate (carafate) acts locally; coats and protects gastric mucosa • If gastritis from corrosive substance: immediate dilution and removal of substance by gastric lavage (washing out stomach contents via nasogastric tube), no vomiting b. Chro Chroni nic c Gastr Gastrit itis is 1. Progressive disorder beginning with superficial inflammation inflammation and leads to atrophy of gastric tissues 2. Type A: autoimmune component and affecting persons of northern European descent; loss of hydrochloric acid and pepsin secretion; develops pernicious anemia 3. Type B: more common and occurs occurs with aging; cause caused d by chronic infection infection of mucosa by Helicobacter Helicobacter pylori; pylori; associated with risk of peptic ulcer disease and gastric cancer 4. Manifestations Manifestations • Vague gastric distress, epigastric heaviness not relieved by antacids • Fatigue associated with anemia; symptoms associated associated with pernicious anemia: paresthesias paresthesias 5. Treatment: Type B: eradicate H. pylori pylori infection with combination combination therapy of two antibiotics (metronidazole and clarithomycin or tetracycline) and proton–pump inhibitor 3. Collaborative Care • Usually managed in community • Teach food safety safety measures to prevent acute acute gastritis from food contaminated contaminated with bacteria bacteria • Management of acute gastritis with NPO state and then gradual reintroduction of fluids with electrolytes and glucose and advance to solid foods • Teaching regarding regarding use of prescribed medications, medications, smoking cessation, cessation, treatment treatment of alcohol abuse abuse 4. Diagnostic Tests • Gastric analysis: assess hydrochloric acid secretion (less with chronic gastritis) • Hemoglobin, hematocrit, red blood cell indices: anemia including pernicious or iron deficiency • Serum vitamin B 12 levels: determine pernicious anemia • Upper endoscopy: visualize mucosa, identify areas of bleeding, obtain biopsies; may treat areas of bleeding with electro or laser coagulation or sclerosing agent 5. Nursing Diagnoses: • Deficient Fluid Volume Imbalanced Nutrition: Less than body body requirements requirements CHOLELITHIASIS / CHOLECYSTITIS Cholelithiasis Cholelithiasis and Cholecystitis 1. Definitions • Cholelithiasis: Cholelithiasis: formation of stones (calculi) within the gallbladder or biliary duct system • Cholecystitis: inflammation inflammation of gall bladder • Cholangitis: inflammation inflammation of the biliary biliary ducts
2. Pathophysiology a. Gall Gallst ston ones es for form m due due to • Abnormal bile composition • Biliary stasis • Inflammation of gallbladder gallbladder b. Most gallsto gallstones nes are compose composed d primarily primarily of bile (80%); (80%); remaind remainder er are composed composed of a mixture mixture of bile components c. Excess Excess cholester cholesterol ol in bile is associa associated ted with obesity obesity,, high-chole high-cholester sterol ol diet and drugs drugs that lower lower cholesterol levels d. If stones stones from gallblad gallbladder der lodge lodge in the cystic cystic duct duct • There can be reflux of bile bile into the gallbladder gallbladder and liver • Gallbladder has increased pressure leading to ischemia and inflammation • Severe ischemia can lead to necrosis of the gall bladder • If the common bile duct is obstructed, pancreatitis pancreatitis can develop 3. Risk factors for cholelithiasis • Age • Family history, also Native Americans and persons of northern European heritage • Obesity, hyperlipidemia • Females, use of oral contraceptives • Conditions which lead to biliary biliary stasis: pregnancy, pregnancy, fasting, prolonged parenteral parenteral nutrition • Diseases including cirrhosis, ileal disease or resection, sickle-cell anemia, glucose intolerance 4. Manifestations of cholelithiasis • Many persons are asymptomatic • Early symptoms are epigastic fullness after meals or mild distress after eating a fatty meal • Biliary colic (if stone is blocking cystic or common bile duct): steady pain in epigastric or RUQ of abdomen lasting up to 5 hours with nausea and vomiting • Jaundice may may occur if there there is obstruction obstruction of common bile bile duct 5. Manifestations of acute cholecystitis • Episode of biliary colic involving RUQ pain radiating to back, right scapula, or shoulder; the pain may be aggravated by movement, or deep breathing and may last 12 – 18 hours • Anorexia, nausea, and vomiting • Fever with chills 6. Complications of cholecystitis • Chronic cholecystitis occurs after repeated attacks of acute cholecystitis; often asymptomatic • Empyema: collection of infected infected fluid within gallbladder gallbladder • Gangrene of gall bladder with perforation leading to peritonitis, abscess abscess formation • Pancreatitis, liver damage, intestinal obstruction 7. Collaborative Care • Treatment depends depends on the acuity acuity of symptoms and client’s health status status • Clients experiencing experiencing symptoms are usually treated with surgical removal of the stones and gallbladder 8. Diagnostic Tests • Serum bilirubin: conjugated bilirubin bilirubin is elevated with bile duct obstruction obstruction • CBC reveals elevation in the WBC as with infection and inflammation • Serum amylase and lipase are elevated, elevated, if obstruction of the common bile duct has caused pancreatitis • Ultrasound of gallbladder: identifies presence of gallstones • Other tests may include flat plate of the abdomen, oral cholecytogram, gall bladder scan 9. Treatment • Treatment of choice choice is laparoscopic laparoscopic cholecystectomy cholecystectomy • If surgery is inappropriate due to client condition • May attempt to dissolve the gallstones with medications • Medications are costly, long duration • Stones reoccur when treatment is stopped 10. Laparoscopic cholecystectomy
Minimally invasive procedure procedure with low risk of complications; required hospital stay< 24 hours. • Learning needs of client and family/caregiver include pain control, deep breathing, mobilization, incisional care and nutritional/fluids nutritional/fluids needs • Client is given phone contact for problems 11. Some clients require a surgical laparotomy (incision inside the abdomen) to remove gall bladder • client will have nasogastric nasogastric tube in place post-operatively post-operatively and require several several days of hospitalization • If exploration of the common bile duct is done with the cholecystectomy, the client may have a Ttube inserted which promotes bile passage to the outside as area heals 12. Clients with cholelithiasis and cholecystitis prior to surgery can avoid future attacks by limiting fat intake 13. Nursing Diagnoses • Pain • Imbalanced Nutrition: Less than body requirements • Risk for Infection •
LIVER CIRRHOSIS 1. Definition • End state of chronic liver disease • Progressive and irreversible • Tenth leading cause of death death in U.S. 2. Pathophysiology • Functional liver tissue gradually destroyed and replaced with fibrous scar tissue • As hepatocytes are destroyed, metabolic functions are lost • Blood and bile flow within liver is disrupted • Portal hypertension develops 3. Alcoholic cirrhosis (Laennec’s cirrhosis) • Alcohol causes metabolic changes in liver leading to fatty infiltration (stage in which abstinence from alcohol could allow liver to heal) • With continued alcohol abuse, inflammatory cells infiltrate liver causing necrosis, fibrosis and destruction of liver tissue • Regenerative nodules form, liver shrinks and is nodular • Malnutrition commonly present 4. Biliary cirrhosis: Bile flow is obstructed and is retained within liver causing inflammation, fibrosis and regenerative nodules to form 5. Posthepatic cirrhosis: Chronic hepatitis B or C and unknown cause leads to liver shrinkage and nodule formation with extensive liver cell loss and fibrosis 6. Manifestations • Early: liver enlargement and tenderness, dull ache in RUQ, weight loss, weakness, anorexia, diarrhea or constipation • Progresses to impaired metabolism causing bleeding, ascites, gynecomastia in men, infertility in women, jaundice, neurological changes, ascites, peripheral edema, anemia, low WBC and platelets 7. Complications • Portal hypertension: hypertension: shunting of blood to collateral blood vessels vessels leading to engorged veins in esophagus, rectum and abdomen, ascites • Splenomegaly: Splenomegaly: anemia, leucopenia, thrombocytopenia • Ascites: accumulation accumulation of abdominal fluid rich in protein; hypoalbuminemia, sodium and water retention • Esophageal varices varices:: thin walled dilated veins in esophagus which may rupture leading to massive hemorrhage • Hepatic encephalopathy: encephalopathy: from accumulated accumulated neurotoxins in blood; ammonia produced in gut is not converted to urea and accumulates in blood; medications may not be metabolized and add to mental changes including personality changes, slowed mentation, asterixis (liver flap); progressing progressing to confusion, disorientation disorientation and coma
Hepatorenal syndrome: syndrome: renal failure failure with azotemia 8. Collaborative Care: Holistic care to client and family addressing physiologic, psychosocial, spiritual needs 9. Diagnostic Tests • Liver function tests (ALT, AST, alkaline phosphatase, phosphatase, GGT); elevated, but not as high as with acute hepatitis • CBC and platelets: anemia, leucopenia, leucopenia, thrombocytopenia • Prothrombin time: prolonged (impaired coagulation due to lack of Vitamin K) • Serum electrolytes: deficiencies in sodium, potassium, phosphate, magnesium • Bilirubin: elevated • Serum albumin: hypoalbuminemia hypoalbuminemia • Serum ammonia: elevated • Serum glucose and cholesterol • Abdominal ultrasound: evaluation of liver size and nodularity, ascites • Upper endoscopy: diagnose and possibly treat esophageal varices • Liver biopsy: may be done to diagnose cirrhosis; cirrhosis; may be deferred if bleeding times are elevated elevated 10. Medications • Medications are used to treat complications and effects of cirrhosis; all liver toxic drugs (sedatives, hypnotics, acetaminophen) acetaminophen) and alcohol must be avoided • Diuretics: Spironolactone (Aldactone) (Aldactone) (works against increased aldosterone aldosterone levels), furosemide furosemide (Lasix) • Medications to decrease manifestations manifestations of hepatic encephalopathy encephalopathy by reducing number of ammonia forming bacteria in bowel and to convert ammonia to ammonium which is excreted in stool; Lactulose, Neomycin • Beta-blocker nadolol (Corgard) (Corgard) with isosorbide mononitrate (Ismo, Imdur) used to prevent esophageal varices from rebleeding • Ferrous sulfate and folic acid to treat anemia • Vitamin K to reduce risk of bleeding • Antacids to decrease risk of acute gastritis • Oxazepam (Serax) benzodiazepine benzodiazepine antianxiety/sedative drug not metabolized by liver; used to treat acute agitation 11. Treatment: Dietary and and fluid management • Fluid and sodium restrictions based on response to diuretic therapy, urine output, electrolyte values • Protein: 75 – 100 grams per day; unless client has hepatic encephalopathy (elevated ammonia ammonia levels),then levels),then 60 – 80 gm/day • Diet high in carbohydrates, carbohydrates, moderate in fats or as total parenteral parenteral nutrition (TPN) • Vitamin and mineral supplements; deficiencies often include B vitamins, and A, D, E, magnesium 12. Treatment: Complication management • Ascites and associated respiratory distress; Paracentesis • For bleeding esophageal varices • Restore hemodynamic stability with fluids, blood transfusion and fresh frozen plasma (contains clotting factors) • Control bleeding with vasoconstrictive vasoconstrictive medications: somatostatin or octreotide, vasopressin vasopressin • Upper endoscopy to treat varices with banding (variceal ligation or endoscopic sclerosis) • Balloon tamponade, if bleeding not controlled or endoscopy unavailable unavailable as short term measure: multiple-lumen naso-gastric naso-gastric tube such as Sengstaken-Blakemore tube or Minnesota tube which have gastric and esophageal balloons to apply tension to control bleeding • Insertion of transjugular intrahepatic intrahepatic portosystemic shunt (TIPS), a short-term measure to control portal hypertension (varices and ascites); using a stent to channel blood between portal and hepatic vein and bypassing liver (increases risk for hepatic encephalopathy) • Surgery: liver transplant; contraindications include malignancy, malignancy, active alcohol or drug abuse, poor surgical risk 13. Nursing Care •
Health promotion includes education about relationship of alcohol and drug abuse with liver disorders; avoidance of viral hepatitis • Home care includes teaching family to participate participate in disease management, management, possible hospice care 14. Nursing Diagnoses • Excess Fluid Volume • Disturbed Thought Processes: Early identification of encephalopathy encephalopathy and appropriate appropriate interventions, i.e. client safety, avoidance of hepatoxic medications, low-protein diet, medications to treat • Ineffective Protection: Risks associated with impaired coagulation, esophageal varices, acute gastritis • Impaired Skin Integrity: Bile deposits on skin cause severe pruritis; topical treatments • Imbalanced Nutrition: Less than body requirements •
PANCREATITIS 1. Definition • Inflammation of pancreas characterized by release of pancreatic enzymes into pancreatic tissue itself leading to hemorrhage and necrosis • Mortality rate is 10%; • Occurs as acute or chronic in form 2. Risk factors • Alcoholism • Gallstones 3. Acute Pancreatitis a. Path Pathop ophy hysi siol olog ogy y • Interstitial pancreatitis: pancreatitis: milder form leading to inflammation and edema of pancreatic pancreatic tissue; often self-limiting self-limiting • Necrotizing pancreatitis: pancreatitis: inflammation, inflammation, hemorrhage, hemorrhage, and necrosis of pancreatic pancreatic tissue • Exact cause is unknown; gallstones can cause bile reflux activating pancreatic pancreatic enzymes; alcohol causes duodenal edema, obstructing pancreatic outflow • Other factors are trauma, surgery, tumors, infectious agents • With pancreatitis, pancreatitis, large volume of fluid shifts from circulation into retroperitoneal retroperitoneal space, peripancreatic space, abdominal cavity b. Mani Manife fest stat atio ions ns • Abrupt onset of continuous severe epigastric and abdominal pain, radiating to back and relieved somewhat by sitting up and leaning forward; initiated by fatty meal or alcohol intake • Nausea and vomiting • Abdominal distention and rigidity • Decreased bowel sounds • Hypotension • Fever, cold and clammy skin • 24 hours later: jaundice; • 3 – to 6 days: retroperitoneal retroperitoneal bleeding, bruising in flanks (Turner sign) or around umbilicus (Cullen’s sign) c. Comp Compli lica cati tion ons: s: Intravascular volume depletion leads to • Acute tubular necrosis and renal failure: 24 hours post • Acute respiratory respiratory distress syndrome (ARDS): 3 – 7 days post • Local complications of pancreatic necrosis, abscess, pseudocysts, pancreatic ascites 4. Chronic Pancreatitis a. Back Backgr grou ound nd • Characterized Characterized by gradual destruction of functional pancreatic pancreatic tissue • Irreversible Irreversible process • Primary risk is alcoholism • 10 – 20% idiopathic b. Path Pathop ophy hysi siol olog ogy y: Pancreatic ducts and flow of pancreatic juices is blocked leading to recurrent inflammation inflammation with fibrosis and loss of exocrine function c. Mani Manife fest stat atio ions ns
Recurrent episodes of epigastric and LUQ abdominal pain radiating to back, pain lasts from days to week with increased frequency • Anorexia, nausea and vomiting, weight loss, flatulence, constipation, and steatorrhea (fatty, frothy, foul-smelling stools) d. Comp Compli lica cati tion ons s • Malabsorption, Malabsorption, malnutrition, malnutrition, peptic ulcer disease • Pancreatic pseudocyst pseudocyst or abscess, stricture of common bile duct • Diabetes mellitus • Increased risk for pancreatic cancer • Risk of narcotic addiction 5. Collaborative Care • Acute pancreatitis is usually a mild, self-limiting disease with care focused on eliminating causative causative factors, reducing pancreatic secretions, supportive care • Severe necrotizing pancreatitis requires intensive care management • Chronic pancreatitis focuses on pain management and treatment of malabsorption and malnutrition 6. Diagnostic Tests a. Labo Laborratory ory tes tests • Serum amylase: 2 -3 times normal in 2 – 12 hours with acute; returns to normal in 3 – 4 days • Serum lipase: rises and remains elevated 7 – 14 days • Serum trypsinogen: elevated with acute; decreased with chronic • Urine amylase: rises with acute • Serum glucose: transient elevation with acute • Serum bilirubin and alkaline phosphatase: may be increased with compression of common bile duct with acute • Serum calcium: hypocalcemia with acute • CBC: elevated white blood cells count count • BUN, Creatinine: monitor renal function b. Ultrasou Ultrasounds nds to diagnos diagnose e gallston gallstones, es, pancre pancreatic atic mass mass,, pseudocys pseudocystt c. CT scan to to identify identify pancreat pancreatic ic enlargem enlargement, ent, fluid fluid collecti collections, ons, areas areas of necrosi necrosis s d. Endoscopi Endoscopic c retrograde retrograde cholangiopa cholangiopancre ncreatog atography raphy (ERCP) (ERCP) diagnose diagnose chronic pancreati pancreatitis tis (acute pancreatitis can occur after this procedure) e. Endo Endosc scop opic ic ultr ultras asou ound nd f. Percutan Percutaneous eous fine-nee fine-needle dle aspirat aspiration ion biopsy biopsy to differentia differentiate te between between chronic chronic pancrea pancreatitis titis and and malignancy 7. Treatment a. Acute Acute pancreati pancreatitis tis is supportiv supportive e and includes includes hydrati hydration, on, pain control, control, and and antibiotics antibiotics b. Chronic Chronic pancreat pancreatitis itis include includes s pain managem management ent without without causing causing drug drug dependence dependence c. Medi Medica cati tion ons s may may incl includ ude e • Pancreatic enzyme supplements to reduce steatorrhea • H2 blockers or proton pump inhibitors to decrease gastric gastric secretions • Octreotide (sandostatin) to suppress pancreatic secretion d. Flui Fluid d and and diet dietar ary y mana manage geme ment nt • Initially client is NPO usually with nasogastric suction, intravenous fluids and possibly total parenteral parenteral nutrition • Oral food and fluids begun as condition resolves • Low fat diet and no alcohol e. Surg Surger erie ies s incl includ ude e • Blocked gallstones may be removed endoscopically • Cholecystectomy for cholelithiasis cholelithiasis • Drainage procedures or resection of pancreas may be needed 8. Nursing Diagnoses • Pain • Impaired Nutrition: Less than body requirements • Risk for Deficient Fluid Volume •
9. Home Care: Care : Client and family teaching to include prevention of future attacks including abstinence from alcohol and smoking; low fat diet; monitoring for signs of infection (as with abscess formation) C. COMMON HEALTH PROBLEMS (LOWER GI) I: PEDIATRICS CONGENITAL AGANGLIONIC MEGACOLON / HIRSCHSPRUNG DISEASE Congenital Aganglionic Megacolon / Hirschsprung Hirschsprung disease 1. Desc Descri ript ptio ion: n: • Hirschsprung Hirschsprung disease is a congenital anomaly characterized characterized by the absence of the nerves to a section of the intestine. It results in mechanical mechanical intestinal obstruction obstruction due to inadequate motility in an intestinal segment. • It is least four times more common in boys than in girls is seen more commonly in children with Down Syndrome • It can be acute and life-threatening life-threatening or chronic. 2. Etio tiology • Hirschsprung Hirschsprung disease is believe to be a familial, congenital defect • It results from failure of the craniocaudal migration of ganglion nerve cell precursors along the GU tract between the 5 th and 12th weeks of gestation 3. Path Pathop ophy hysi siol olog ogy y • Absence of Autonomic parasympathetic parasympathetic ganglion cells in one segment of the colon causes lack of innervation in that segment • Lack of innervation leads to absence of propulsive movements, causing accumulation of intestinal contents and distention of the bowel proximal to the defects • Enterocolitis, inflammation inflammation of the small bowel and colon, is the leading cause of death in children with Hirschsprung Hirschsprung disease. It occurs as a result of intestinal intestinal distention and ischemia secondary secondary to bowel wall distention. 4. Asse Assess ssme ment nt find findin ings gs • Newborn: failure to pass meconium, meconium, reluctance to ingest fluids, fluids, abdominal distention, and bilebilestained emesis • Infants: failure to thrive, constipation, constipation, abdominal abdominal distention, vomiting, and episodic episodic diarrhea • Older children: Anorexia, chronic chronic constipation, foul-smelling and ribbon-like ribbon-like stools, abdominal distention, visible peristalsis, peristalsis, palpable fecal mass, malnourishment malnourishment or poor growth, signs of anemia, and hypoproteinemia 5. Nurs Nursin ing g Manag Managem emen entt • Assess for, and promptly report, any signs of Enterocolitis • Promote adequate hydration • Assess bowel functioning a. Assess Assess passage passage of mecon meconium ium in neonates neonates b. Note and record the frequency and characteristic characteristics s of stools in infants infants and older older children children c. Periodic Periodically ally measure measure abdomina abdominall girth to assess for increa increasing sing distenti distention on • Promote adequate nutrition according to the child’s age and nutritional requirements • Administer enemas, as prescribed to relieve constipation • Avoid taking temperatures rectally because of the potential for damaging frail mucosa • Administer prescribed medications, which may include: a. Systemic Systemic antibio antibiotics tics given given with enemas enemas to reduce reduce intestin intestinal al flora b. Stool softeners softeners to relie relieve ve constipa constipation tion • Decrease discomfort due to abdominal distention a. Eleva Elevate te the the head head of the bed b. Change Change the the child’s child’s position position frequentl frequently y c. Assess Assess for any any respirato respiratory ry difficult difficulty y associate associated d with distent distention ion • Support the child and parents • Prepare the child and the parents for procedures and treatments • Educate the child and family
CELIAC DISEASE 1. Chronic malabsorption disorder due to sensitivity sensitivity to gluten, protein found in wheat, rye, barley, oats; commonly affects Caucasians of European descent 2. Intestinal mucosa is damaged by immune response; there is loss of the absorptive surface 3. Manifestations: abdominal bloating and cramps, diarrhea, and steatorrhea; leading to anemia, delayed maturity, symptoms associated with nutritional deficiencies; potential complications are GI malignancies malignancies and intestinal lymphoma 4. Gluten free diet causes manifestations to resolve; treat nutritional deficiencies I R R I T A B L E B O W E L S O U N D S (IBS) (S P A S T I C B O W E L , F U N C T I O N A L C O L I T I S ) 1. Definition • Functional GI tract disorder without identifiable cause characterized characterized by abdominal pain and constipation, diarrhea, diarrhea, or both • Affects up to 20% of persons in Western civilization; civilization; more common in females 2. Pathophysiology • Appears there is altered CNS regulation regulation of motor and sensory functions of bowel • Increased bowel activity in response to food intake, hormones, stress • Increased sensations sensations of chyme movement through gut • Hypersecretion Hypersecretion of colonic mucus • Lower visceral pain threshold causing abdominal pain and bloating with normal levels of gas • Some linkage of depression and anxiety 3. Manifestations • Abdominal pain relieved by defecation; may be colicky, occurring in spasms, dull or continuous • Altered bowel habits including frequency, hard or watery stool, straining or urgency with stooling, incomplete evacuation, passage of mucus; abdominal bloating, excess gas • Nausea, vomiting, anorexia, fatigue, headache, anxiety • Tenderness over over sigmoid colon colon upon palpation palpation 4. Collaborative Care • Management of distressing symptoms • Elimination of precipitating factors, stress reduction 5. Diagnostic Tests: to find a cause for client’s abdominal pain, changes in feces elimination • Stool examination for occult blood, ova and parasites, culture • CBC with differential, differential, Erythrocyte Sedimentation Rate (ESR): to determine if anemia, bacterial infection, or inflammatory process • Sigmoidoscopy or colonoscopy • Visualize bowel mucosa, measure intraluminal pressures, obtain biopsies if indicated • Findings with IBS: normal appearance increased mucus, intraluminal pressures, marked spasms, possible hyperemia without lesions • Small bowel series (Upper GI series with small bowel-follow through) and barium enema: examination of entire GI tract; IBS: increased motility 6. Medications • Purpose: to manage symptoms • Bulk-forming laxatives: laxatives: reduce bowel spasm, normalize bowel movement in number and form • Anticholinergic Anticholinergic drugs (dicyclomine (Bentyl), hyoscyamine) hyoscyamine) to inhibit bowel motility; given before meals • Antidiarrheal Antidiarrheal medications (loperamide (Imodium), diphenoxylate diphenoxylate (Lomotil): prevent diarrhea prophylactically • Antidepressant Antidepressant medications • Research: medications medications altering serotonin receptors in GI tract 7. Dietary Management • Often benefit from additional dietary fiber: adds bulk and water content to stool reducing diarrhea and constipation • Some benefit from elimination elimination of lactose, fructose, sorbitol • Limiting intake of gas-forming foods, caffeinated beverages 8. Nursing Care
Contact in health environments outside acute care • Home care focus on improving symptoms with changes of diet, stress management, management, medications; seek medical attention if serious changes occur 9. Nursing Diagnoses • Constipation • Diarrhea • Anxiety • Ineffective Coping •
II: ADULT PERITONITIS 1. Definition • Inflammation of peritoneum, lining that covers wall (parietal peritoneum) and organs (visceral peritoneum) of abdominal cavity • Enteric bacteria enter the peritoneal cavity through a break of intact GI tract (e.g. perforated ulcer, ruptured appendix) 2. Pathophysiology • Peritonitis results from contamination of normal sterile peritoneal cavity with infections or chemical irritant • Release of bile or gastric juices initially causes chemical peritonitis; infection occurs when bacteria enter the space • Bacterial peritonitis usually caused by these bacteria (normal bowel flora): Escherichia coli, Klebsiella, Proteus, Pseudomonas • Inflammatory process causes fluid shift into peritoneal space (third spacing); leading to hypovolemia, then septicemia 3. Manifestations • Depends on severity and extent of infection, age and health of client • Presents with “acute abdomen” • Abrupt onset of diffuse, severe abdominal pain • Pain may localize near site of infection (may have rebound tenderness) • Intensifies with movement • Entire abdomen is tender with boardlike guarding or rigidity of abdominal muscle • Decreased peristalsis peristalsis leading to paralytic ileus; bowel sounds are diminished or absent with progressive progressive abdominal distention; pooling of GI secretions lead to nausea and vomiting • Systemically: Systemically: fever, malaise, tachycardia tachycardia and tachypnea, restlessness, restlessness, disorientation, oliguria with dehydration and shock • Older or immunosuppressed client may have • Few of classic signs • Increased confusion and restlessness • Decreased urinary output • Vague abdominal complaints • At risk for delayed diagnosis and higher mortality rates 4. Complications • May be life-threatening; mortality rate overall 40% • Abscess • Fibrous adhesions • Septicemia, septic shock; fluid loss into abdominal cavity leads to hypovolemic shock 5. Collaborative Care • Diagnosis and identifying and treating cause • Prevention of complications 6. Diagnostic Tests • WBC with differential: differential: elevated WBC WBC to 20,000; shift to left • Blood cultures: identify bacteria in blood • Liver and renal function studies, serum electrolytes: evaluate effects of peritonitis
Abdominal xrays: detect intestinal distension, air-fluid levels, free air under diaphragm (sign of GI perforation) • Diagnostic paracentesis 7. Medications • Antibiotics • Broad-spectrum Broad-spectrum before definitive culture results identifying specific organism(s) causing infection • Specific antibiotic(s) treating causative pathogens • Analgesics 8. Surgery • Laparotomy to treat cause (close perforation, removed inflamed tissue) • Peritoneal Lavage: washing out peritoneal cavity with copious amounts of warm isotonic fluid during surgery to dilute residual bacterial and remove gross contaminants contaminants • Often have drain in place and/or incision left unsutured to continue drainage 9. Treatment • Intravenous fluids and electrolytes to maintain vascular volume and electrolyte balance • Bed rest in Fowler’s position to localize infection and promote lung ventilation • Intestinal decompression decompression with nasogastric tube or intestinal tube connected to suction • Relieves abdominal distension secondary to paralytic ileus • NPO with intravenous fluids while having nasogastric suction 10. Nursing Diagnoses • Pain • Deficient Fluid Volume: often on hourly output; nasogastric drainage is considered when ordering intravenous fluids • Ineffective Protection • Anxiety 11. Home Care • Client may have prolonged hospitalization • Home care often includes • Wound care • Home health referral • Home intravenous antibiotics •
INTESTINAL OBSTRUCTION 1. Definition • May be partial or complete obstruction • Failure of intestinal contents to move through the bowel lumen; most common site is small intestine • With obstruction, gas and fluid accumulate proximal to and within obstructed segment causing bowel distention • Bowel distention, vomiting, third-spacing leads to hypovolemia, hypokalemia, hypokalemia, renal insufficiency, shock 2. Pathophysiology a. Mechanical 1. Problems outside intestines: intestines: adhesions (bands of scar tissue), hernias 2. Problems Problems within within intesti intestines: nes: tumors, tumors, IBD IBD 3. Obstruct Obstruction ion of intestina intestinall lumen (parti (partial al or complete) complete) • Intussusception: Intussusception: telescoping bowel • Volvulus: twisted bowel • Foreign bodies • Strictures b. Functional 1. Failure of peristalsis peristalsis to move intestinal intestinal contents: contents: adynamic ileus ileus (paralytic (paralytic ileus, ileus) due to neurologic or muscular impairment 2. Accounts Accounts for most bowel bowel obstru obstruction ctions s 3. Caus Causes es incl includ ude e
Post gastrointestinal gastrointestinal surgery • Tissue anoxia anoxia or peritoneal peritoneal irritation irritation from hemorrhage, hemorrhage, peritonitis, peritonitis, or perforation perforation • Hypokalemia • Medications: narcotics, anticholinergic drugs, antidiarrheal antidiarrheal medications • Renal colic, spinal cord injuries, uremia 3. Manifestations Small Bowel Obstruction a. Vary Vary depend depend on level level of obstructio obstruction n and speed speed of devel developmen opmentt b. Cramping Cramping or colic colicky ky abdomina abdominall pain, inter intermitte mittent, nt, intensi intensifyin fying g c. Vomiting • Proximal intestinal distention stimulates vomiting center • Distal obstruction vomiting may become feculent d. Bowel sounds • Early in course of mechanical mechanical obstruction: borborygmi and high-pitched tinkling, may have visible peristaltic waves • Later silent; with paralytic ileus, diminished or absent bowel sounds throughout e. Sign Signs s of of deh dehyd ydra rati tion on 4. Complications • Hypovolemia and hypovolemic shock can result in multiple organ dysfunction (acute renal failure, impaired ventilation, death) • Strangulated Strangulated bowel can result in gangrene, perforation, perforation, peritonitis, possible septic shock • Delay in surgical intervention leads to higher mortality rate 5. Large Bowel Obstruction • Only accounts for 15% of obstructions • Causes include cancer of bowel, volvulus, diverticular disease, inflammatory inflammatory disorders, fecal impaction • Closed-loop obstruction: competent ileocecal valve causes massive colon dilation • Manifestations: Manifestations: deep, cramping pain; severe, continuous pain signals bowel ischemia and possible perforation; localized tenderness tenderness or palpable mass may be noted 6. Collaborative Care • Relieving pressure and obstruction • Supportive care 7. Diagnostic Tests a. Abdominal Abdominal Xrays Xrays and and CT scans scans with with contr contrast ast media media • Show distended loops of intestine with fluid and /or gas in small intestine, confirm mechanical obstruction; indicates free air under diaphragm • If CT with contrast media meglumine diatrizoate (Gastrografin), (Gastrografin), check for allergy to iodine, need BUN and Creatinine to determine renal function b. Laborator Laboratory y testing to evaluate evaluate for presenc presence e of infection infection and electrolyte electrolyte imbalan imbalance: ce: WBC, Serum Serum amylase, osmolality, electrolytes, arterial blood gases c. Barium Barium enema enema or colonosco colonoscopy/s py/sigmoi igmoidosco doscopy py to identify identify large large bowel bowel obstructi obstruction on 8. Gastrointestinal Decompression • Treatment with with nasogastric nasogastric or long intestinal intestinal tube provides provides bowel rest and removal removal of air and fluid • Successfully relieves many partial small bowel obstructions 9. Surgery a. Treatmen Treatmentt for complete complete mechanica mechanicall obstructions obstructions,, strangulate strangulated d or incarcer incarcerated ated obstructi obstructions ons of small bowel, persistent incomplete mechanical obstructions b. Preo Preope pera rati tive ve care care • Insertion of nasogastric tube to relieve vomiting, abdominal distention, distention, and to prevent aspiration of intestinal contents • Restore fluid and electrolyte balance; correct acid and alkaline imbalances • Laparotomy: inspection of intestine and removal removal of infarcted or gangrenous tissue tissue • Removal of cause of obstruction: adhesions, tumors, foreign bodies, gangrenous portion of intestines and anastomosis or creation of colostomy depending on individual case 10. Nursing Care • Prevention includes healthy diet, fluid intake • Exercise, especially especially in clients with recurrent small bowel obstructions •
11. Nursing Diagnoses • Deficient Fluid Volume • Ineffective Tissue Perfusion, gastrointestinal gastrointestinal • Ineffective Breathing Pattern 12. Home Care • Home care referral as indicated • Teaching about about signs of recurrent recurrent obstruction obstruction and seeking seeking medical attention
