The Digestive System Also known as the gastrointestinal (GI) tract or the alimentary system, it is responsible for breaking down the complex food into simple nutrients the body can absorb and convert into energy. This process is known as digestion.

Major GI Function Organs Mouth Pharynx Esophagus Stomach Small intestine Large intestine

Accessory GI Organs Liver Gallbladder Pancreas

Figure 24-1 The gastrointestinal tract and accessory organs of digestion. (Source: Pearson Education/PH College)

Mouth Teeth chew and grind food into smaller parts Moistened with saliva for tasting, chewing, and swallowing

Pharynx Muscles that propel the food from the mouth

Esophagus Carries food through peristalsis Cardiac/lower esophageal sphincter Closes after food leaves esophagus

Figure 24-2 Structures of the stomach and duodenum, including the common bile duct and pancreatic duct. The relationship of the pancreas and gallbladder to the stomach also are shown.

Stomach Holds the food Pyloric sphincter: controls the emptying of the stomach

Small Intestine Approximately 20 to 25 feet long and is responsible for absorbing nutrients from the chyme (semi-liquid mass of partially digested food). Small intestine divided into: duodenum (first 10-12 inches); jejunum (the middle 8-10 feet) and the ileum (the distal 12 feet).

Large Intestine Begins at ileocecal valve, terminates at the anus 5 feet long Includes the appendix Nutrients absorbed and indigestible materials eliminated

Large Intestine Also known as the colon, the large intestine is responsible for absorbing water, electrolytes, and salts. The last 5 inches of the large intestine comprise the rectum. The distal end of the rectum forms the anal canal composed of muscles that control defecation. The opening to the anal canal is called the anus.

Large Intestine (continued) Parts: Ascending Transverse Descending Sigmoid colon Rectum

Liver Largest gland in the body Located in the right side of the abdomen Has four lobes Encased in a fibrous capsule Hepatocytes produce bile, which aids in digestion

Gallbladder Stores bile Located on the inferior surface of the liver

The liver, gallbladder, common bile duct, and sphincter of Oddi.

Pancreas Gland located between the stomach and small intestines Exocrine and endocrine functions Produce pancreatic juice to neutralize food Produce enzymes to digest food

Digestion Mouth The upper opening of the GI tract Lined by mucous membranes The teeth chew and grind food into smaller parts Saliva (produced by the salivary glands) moistens food for tasting, chewing, and swallowing

Mouth Digestive process starts here Enzymes in saliva begin the food breakdown Amylase Lysozyme

Digestion Pharynx Muscles here move the food into the esophagus Carries the food to the stomach through peristalsis

Stomach Mechanical digestion in the stomach mixes partially digested food with gastric juices to produce chyme

Nervous System Parasympathetic nervous system signals vagus nerve to increase gastric secretions in response to food Emotions (anxiety/stress) reduce gastric secretions and motility

Small Intestine Location where food is chemically digested and most absorbed Enzymes break down carbohydrates, proteins, and fats Pancreatic buffers neutralize the stomach acid

Small Intestine (continued) Microvilli enhance absorption Most of food, water, vitamins, and minerals are absorbed here into the blood or lymph

Liver Digestive functions: Metabolize carbohydrates, proteins, and fats Synthesize plasma proteins and enzymes Store blood, vitamins, and minerals Produce and secrete bile

Pancreas Produces enzymes for digestion Secretion is controlled by the vagus nerve and the hormones secretin and cholecystokinin Lipase promotes fat breakdown and absorption Amylase digests starch

Pancreas (continued) Trypsin, chymotrypsin, and carboxypeptidase digest protein Nucleases, which digest nucleic acids, are also present

Large Intestine Major function: eliminate indigestible food Absorbs water, salts, and vitamins forming it into feces or stool Feces move with peristalsis Goblet cells secrete mucus to aid with defecation Defecation reflex: sigmoid colon walls contract and anal sphincter relaxes

Nutrients Carbohydrates Proteins Fats Vitamins Minerals Water

Carbohydrates Simple sugars Milk Sugar cane Sugar beets Honey fruits Complex starches Grains Legumes Root vegetables

Proteins Complete proteins (all essential AA) Plant proteins Legumes Eggs Milk Milk products Meat Fish Poultry Plant proteins Legumes Nuts Grains Cereals Vegetables

Additional Nutrients Fats Saturated fats Unsaturated fats Vitamins Minerals Water

Assessment for Clients with GI Complaints

Health History Current complaints, food intolerance Appetite, heartburn, nausea, vomiting Abdominal discomfort, diarrhea, constipation Weight changes Food allergies Pattern and amount of daily food intake

Health History Teeth, mouth, ability to chew, swallow, dentures Change in stool frequency, amount, color, caliber Medications Chronic diseases Previous surgeries

Physical Examination Overall health status Skin color, hair, nails Height and weight Inspect mouth, teeth, tongue Swallow

Physical Examination Inspect abdomen, observe skin, peristalsis Auscultate bowel sounds Percuss the abdomen Palpate the abdomen

Laboratory Tests Serum albumin and total protein Serologic H. pylori testing Stool specimen Liver function tests Pancreatic function tests

Diagnostic Tests Gastric analysis Urea breath test Ambulatory pH monitoring Esophageal manometry Paracentesis

Gastric Analysis Gastric analysis consists of a series of tests used to analyze the contents of the stomach. The complete series involves: A- collecting residual gastric fluid from a fasting patient B- collecting basal secretions every 15 minutes for four hours C- intramuscular administration of a drug that stimulates gastric acid output D- collecting stomach secretions every 15 minutes for 90 minutes Instruct client to abstain from food, fluids, smoking, chewing gum, and some medications for 8 to 12 hours before the test Insert NG tube and collect samples

Urea Breath Test is a rapid diagnostic procedure used to identify infections by Helicobacter pylori, a spiral bacterium implicated in gastritis, gastric ulcer, and peptic ulcer disease. It is based upon the ability of H. pylori to convert urea to ammonia. Instruct client to abstain from food and fluids for 4 hours prior to the test Instruct client to abstain from antacids, bismuth sulfate, antibiotics, and Prilosec for 2 weeks prior to the test

More Diagnostic Tests Ambulatory pH Monitor: is a way for the doctor to see how much acid is backing up into the esophagus over a 24-hour period. The test involves placing a small catheter in the esophagus.  The catheter is connected to a small recording device called a Digitrapper. Instruct client how to care for the electrode and data recorder Esophageal Manometry: is a test to assess motor function of the Upper Esophageal Sphincter (UES), Esophageal body and Lower Esophageal Sphincter (LES). Instruct client to abstain from food and fluids up to 8 hours prior to the test Assist with insertion of the tube Paracentesis: is a medical procedure involving needle drainage of fluid from a body cavity, most commonly the peritoneal cavity in the abdomen.

Diagnostic Imaging Procedures Ultrasonography Radiologic Studies

Gastroesophageal Reflux Disease (GERD) 1. Definition a. Gastroesophageal reflux is the backward flow of gastric content into the esophagus. b. GERD common, affecting 15 – 20% of adults c. 10% persons experience daily heartburn and indigestion d. Because of location near other organs symptoms may mimic other illnesses including heart problems

Gastroesophageal Reflux Disease (GERD) 2. Pathophysiology a. Gastroesophageal reflux results from transient relaxation or incompetence of lower esophageal sphincter, sphincter, or increased pressure within stomach b. Factors contributing to gastroesophageal reflux 1.Increased gastric volume (post meals) 2.Position pushing gastric contents close to gastroesophageal juncture (such as bending or lying down) 3.Increased gastric pressure (obesity or tight clothing) 4.Hiatal hernia

Gastroesophageal Reflux Disease (GERD) c.Normally the peristalsis in esophagus and bicarbonate in salivary secretions neutralize any gastric juices (acidic) that contact the esophagus; during sleep and with 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. Heartburn after meals, while bending over, or recumbent b. May have regurgitation of sour materials in mouth, pain with swallowing c. Atypical chest pain d. Sore throat with hoarseness e. Bronchospasm and laryngospasm

Gastroesophageal Reflux Disease (GERD) 4. Complications a. Esophageal strictures, which can progress to dysphagia b. Barrett’s esophagus: changes in cells lining esophagus with increased risk for esophageal cancer 5. Collaborative Care a. Diagnosis may be made from history of symptoms and risks b. Treatment includes 1.Life style changes 2.Diet modifications 3.Medications

Gastroesophageal Reflux Disease (GERD) 6. Diagnostic Tests a. Barium swallow (evaluation of esophagus, stomach, small intestine) b. Upper endoscopy: direct visualization; biopsies may be done c. 24-hour ambulatory pH monitoring d. Esophageal manometry, which measure pressures of esophageal sphincter and peristalsis e. Esophageal motility studies

Gastroesophageal Reflux Disease (GERD) 7. Medications a. Antacids for mild to moderate symptoms, e.g. Maalox, Mylanta, Gaviscon b. H2-receptor blockers: decrease acid production; given BID or more often, e.g. cimetidine, ranitidine, famotidine, nizatidine c. Proton-pump inhibitors: reduce gastric secretions, promote healing of esophageal erosion and relieve symptoms, e.g. omeprazole (prilosec); lansoprazole (Prevacid) initially for 8 weeks; or 3 to 6 months d. Promotility agent: enhances esophageal clearance and gastric emptying, e.g. metoclopramide (reglan)

Gastroesophageal Reflux Disease 8. Dietary and Lifestyle Management a. Elimination of acid foods (tomatoes, spicy, citrus foods, coffee) b. Avoiding food which relax esophageal sphincter or delay gastric emptying (fatty foods, chocolate, peppermint, alcohol) c. Maintain ideal body weight d. Eat small meals and stay upright 2 hours post eating; no eating 3 hours prior to going to bed e. Elevate head of bed on 6 – 8 blocks to decrease reflux f. No smoking g. Avoiding bending and wear loose fitting clothing

Gastroesophageal Reflux Disease (GERD) 9. Surgery indicated for persons not improved by diet and life style changes a. Laparoscopic procedures to tighten lower esophageal sphincter b. Open surgical procedure: Nissen fundoplication 10. Nursing Care a. Pain usually controlled by treatment b. Assist client to institute home plan

Hiatal Hernia 1. Definition Increased intra-abdominal pressure a. Part of stomach protrudes through the esophageal hiatus of the diaphragm into thoracic cavity b. Predisposing factors include: Increased intra-abdominal pressure Increased age Trauma Congenital weakness Forced recumbent position

Hiatal Hernia c. Most cases are asymptomatic; incidence increases with age d. Sliding hiatal hernia: gastroesophageal junction and fundus of stomach slide through the esophageal hiatus e. Paraesophageal hiatal hernia: the gastroesophageal junction is in normal place but part of stomach herniates through esophageal hiatus; hernia can become strangulated; client may develop gastritis with bleeding

Hiatal Hernia 2. Manifestations: Similar to GERD 3. Diagnostic Tests a. Barium swallow b. Upper endoscopy 4. Treatment a. Similar to GERD: diet and lifestyle changes, medications b. If medical treatment is not effective or hernia becomes incarcerated, then surgery; usually Nissen fundoplication by thoracic or abdominal approach Anchoring the lower esophageal sphincter by wrapping a portion of the stomach around it to anchor it in place

Impaired Esophageal Motility 1. Types a. Achalasia: characterized by impaired peristalsis of smooth muscle of esophagus and impaired relaxation of lower esophageal sphincter b. Diffuse esophageal spasm: nonperistaltic contraction of esophageal smooth muscle 2. Manifestations: Dysphagia and/or chest pain 3. Treatment a. Endoscopically guided injection of botulinum toxin Denervates cholinergic nerves in the distal esophagus to stop spams b. Balloon dilation of lower esophageal sphincter May place stents to keep esophagus open

Gastritis 1. Definition: Inflammation of stomach lining from irritation of gastric mucosa (normally protected from gastric acid and enzymes by mucosal barrier) 2. Types a. Acute Gastritis 1.Disruption of mucosal barrier allowing hydrochloric acid and pepsin to have contact with gastric tissue: leads to irritation, inflammation, superficial erosions 2.Gastric mucosa rapidly regenerates; self-limiting disorder

Gastritis 3. Causes of acute gastritis a. Irritants include aspirin and other NSAIDS, corticosteroids, alcohol, caffeine b. Ingestion of corrosive substances: alkali or acid c. Effects from radiation therapy, certain chemotherapeutic 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 a. Mild: anorexia, mild epigastric discomfort, belching b. More severe: abdominal pain, nausea, vomiting, hematemesis, melena c. Erosive: not associated with pain; bleeding occurs 2 or more days post stress event d. If perforation occurs, signs of peritonitis

Gastritis 6. Treatment a. NPO status to rest GI tract for 6 – 12 hours, reintroduce clear liquids gradually and progress; intravenous fluid and electrolytes if indicated b. Medications: proton-pump inhibitor or H2-receptor blocker; sucralfate (carafate) acts locally; coats and protects gastric mucosa c. If gastritis from corrosive substance: immediate dilution and removal of substance by gastric lavage (washing out stomach contents via nasogastric tube), no vomiting

Chronic Gastritis 1. Progressive disorder beginning with superficial 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 Parietal cells normally secrete intrinsic factor needed for absorption of B12, when they are destroyed by gastritis pts develop pernicious anemia

Chronic Gastritis 3. Type B: more common and occurs with aging; caused by chronic infection of mucosa by Helicobacter pylori; associated with risk of peptic ulcer disease and gastric cancer

Chronic Gastritis Lack of B12 affects nerve transmission 4. Manifestations a. Vague gastric distress, epigastric heaviness not relieved by antacids b. Fatigue associated with anemia; symptoms associated with pernicious anemia: paresthesias Lack of B12 affects nerve transmission 5. Treatment: Type B: eradicate H. pylori infection with combination therapy of two antibiotics (metronidazole (Flagyl) and clarithomycin or tetracycline) and proton–pump inhibitor (Prevacid or Prilosec)

Chronic Gastritis Collaborative Care a. Usually managed in community b. Teach food safety measures to prevent acute gastritis from food contaminated with bacteria c. Management of acute gastritis with NPO state and then gradual reintroduction of fluids with electrolytes and glucose and advance to solid foods d. Teaching regarding use of prescribed medications, smoking cessation, treatment of alcohol abuse

Chronic Gastritis Diagnostic Tests a. Gastric analysis: assess hydrochloric acid secretion (less with chronic gastritis) b. Hemoglobin, hematocrit, red blood cell indices: anemia including pernicious or iron deficiency c. Serum vitamin B12 levels: determine pernicious anemia d. 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: a. Deficient Fluid Volume b. Imbalanced Nutrition: Less than body requirements

Peptic Ulcer Disease

Definition A circumscribed ulceration of the gastrointestinal mucosa occurring in areas exposed to acid and pepsin and most often caused by Helicobacter pylori infection. (Uphold & Graham, 2003)

Peptic Ulcer Disease (PUD) Definition and Risk factors a. Break in mucous lining of GI tract comes into contact with gastric juice; affects 10% of US population b. Duodenal ulcers: most common; affect mostly males ages 30 – 55; ulcers found near pyloris c. Gastric ulcers: affect older persons (ages 55 – 70); found on lesser curvature and associated with increased incidence of gastric cancer d. Common in smokers, users of NSAIDS; familial pattern, ASA, alcohol, cigarettes

Peptic Ulcer Disease (PUD) 2. Pathophysiology a. Ulcers or breaks in mucosa of GI tract occur with 1.H. pylori infection (spread by oral to oral, fecal-oral routes) damages gastric epithelial cells reducing effectiveness of gastric mucus 2.Use of NSAIDS: interrupts prostaglandin synthesis which maintains mucous barrier of gastric mucosa b. Chronic with spontaneous remissions and exacerbations associated with trauma, infection, physical or psychological stress

Peptic Ulcers: Gastric & Dudodenal

Peptic Ulcer Disease Ulcer development Lower esophagus Stomach Duodenum 10% of men, 4% of women

Compare and Contrast the symptoms of Duodenal and Gastric Ulcers Burning upper abd, pain 1-3 hrs after meals Worse pain when stomach empty Bleeding occurs with deep erosion Hematemesis Melena Relieved by food but pain may persist even after eating Anorexia, wt loss, vomiting Infrequent or absent remissions Small % become cancerous Severe ulcers may erode through stomach wall 79

Subjective Data Pain—”gnawing”, “aching”, or “burning” Duodenal ulcers: occurs 1-3 hours after a meal and may awaken patient from sleep. Pain is relieved by food, antacids, or vomiting. Gastric ulcers: food may exacerbate the pain while vomiting relieves it. Nausea, vomiting, belching, dyspepsia, bloating, chest discomfort, anorexia, hematemesis, &/or melena may also occur. nausea, vomiting, & weight loss more common with Gastric ulcers

Objective Data Epigastric tenderness Guaic-positive stool resulting from occult blood loss

Diagnostic Plan Stool for fecal occult blood Labs: CBC (R/O bleeding), liver function test, amylase, and lipase. H. Pylori can be diagnosed by urea breath test, blood test, stool antigen assays, & rapid urease test on a biopsy sample. Upper GI Endoscopy: Any pt >50 yo with new onset of symptoms or those with alarm markings including anemia, weight loss, or GI bleeding. Preferred diagnostic test b/c its highly sensitive for dx of ulcers and allows for biopsy to rule out malignancy and rapid urease tests for testing for H. Pylori. Rapid urease tests are considered the endoscopic diagnostic test of choice. The presence of H pylori in gastric mucosal biopsy specimens is detected by testing for the bacterial product urease. Three kits (CLOtest, Hpfast, Pyloritek) are commercially available, each containing a combination of a urea substrate and a pH sensitive indicator. One or more gastric biopsy specimens are placed in the rapid urease test kit. If H pylori are present, bacterial urease converts urea to ammonia, which changes pH and produces a color change

Peptic Ulcer Disease Treatment Rest and stress reduction Nutritional management Pharmacological management Antacids (Mylanta) Neutralizes acids Proton pump inhibitors (Prilosec, Prevacid) Block gastric acid secretion

Peptic Ulcer Disease Pharmacological management Histamine blockers (Tagamet, Zantac, Axid) Blocks gastric acid secretion Carafate Forms protective layer over the site Mucosal barrier enhancers (colloidal bismuth, prostoglandins) Protect mucosa from injury Antibiotics (PCN, Amoxicillin, Ampicillin) Treat H. Pylori infection

Peptic Ulcer Disease NG suction Surgical intervention Minimally invasive gastrectomy Partial gastric removal with laproscopic surgery Bilroth I and II Removal of portions of the stomach Vagotomy Cutting of the vagus nerve to decrease acid secretion Pyloroplasty Widens the pyloric sphincter

Peptic Ulcer Disease Surgical Therapy A. Billroth I Procedure B. Billroth II Procedure Fig. 40-16

Billroth I

Billroth II

Peptic Ulcer Disease (PUD) 4. Complications a. Hemorrhage: frequent in older adult: hematemesis, melena, hematochezia (blood in stool); weakness, fatigue, dizziness, orthostatic hypotension and anemia; with significant bleed loss may develop hypovolemic shock b. Obstruction: gastric outlet (pyloric sphincter) obstruction: edema surrounding ulcer blocks GI tract from muscle spasm or scar tissue 1.Gradual process 2.Symptoms: feelings of epigastric fullness, nausea, worsened ulcer symptoms

Peptic Ulcer Disease c. Perforation: ulcer erodes through mucosal wall and gastric or duodenal contents enter peritoneum leading to peritonitis; chemical at first (inflammatory) and then bacterial in 6 to 12 hours 1.Time of ulceration: severe upper abdominal pain radiating throughout abdomen and possibly to shoulder 2.Abdomen becomes rigid, boardlike with absent bowel sounds; symptoms of shock 3.Older adults may present with mental confusion and non-specific symptoms

Peptic Ulcer Disease Nursing Management Overall Goals Comply with prescribed therapeutic regimen Experience a reduction or absence of discomfort related to peptic ulcer disease

Peptic Ulcer Disease Nursing Management Overall Goals (cont.) Exhibits no signs of GI complications Have complete healing Lifestyle changes to prevent recurrence

Peptic Ulcer Disease Nursing Implementation Health Promotion Identify patients at risk Early detection and ↓ morbidity Encourage patients to take ulcerogenic drugs with food or milk Teach patients to report symptoms related to gastric irritation to health care provider

Peptic Ulcer Disease Nursing Implementation Acute Intervention Patient generally complains of ↑ pain, nausea, vomiting, and some bleeding May be maintained on NPO status for a few days, have NG tube inserted, fluids replaced intravenously Physical and emotional rest are conducive to ulcer healing

Peptic Ulcer Disease Nursing Implementation Hemorrhage Changes in vital signs, ↑ in amount and redness of aspirate signal massive upper GI bleeding ↑ amount of blood in gastric contents ↓ pain because blood helps neutralize acidic gastric contents Keep blood clots from obstructing NG tube

Peptic Ulcer Disease Nursing Implementation Perforation Sudden, severe abdominal pain unrelated in intensity and location to pain that brought patient to hospital

Peptic Ulcer Disease Nursing Implementation Perforation (cont.) Indicated by a rigid, boardlike abdomen Severe generalized abdominal and shoulder pain Shallow, grunting respirations

Peptic Ulcer Disease Nursing Implementation Perforation (cont.) Ensure any known allergies are reported on chart Antibiotic therapy is usually started Surgical closure may be necessary if perforation does not heal spontaneously

Irritable Bowel Syndrome (IBS) (spastic bowel, functional colitis) Definition a. Functional GI tract disorder without identifiable cause characterized by abdominal pain and constipation, diarrhea, or both b. Affects up to 20% of persons in Western civilization; more common in females

Irritable Bowel Syndrome (IBS) (spastic bowel, functional colitis) Pathophysiology a. Appears there is altered CNS regulation of motor and sensory functions of bowel 1.Increased bowel activity in response to food intake, hormones, stress 2.Increased sensations of chyme movement through gut 3.Hypersecretion of colonic mucus b. Lower visceral pain threshold causing abdominal pain and bloating with normal levels of gas c. Some linkage of depression and anxiety

Irritable Bowel Syndrome (IBS) (spastic bowel, functional colitis) Manifestations a. Abdominal pain relieved by defecation; may be colicky, occurring in spasms, dull or continuous b. Altered bowel habits including frequency, hard or watery stool, straining or urgency with stooling, incomplete evacuation, passage of mucus; abdominal bloating, excess gas c. Nausea, vomiting, anorexia, fatigue, headache, anxiety d. Tenderness over sigmoid colon upon palpation 4. Collaborative Care a. Management of distressing symptoms b. Elimination of precipitating factors, stress reduction

Irritable Bowel Syndrome (IBS) (spastic bowel, functional colitis) 5. Diagnostic Tests: to find a cause for client’s abdominal pain, changes in feces elimination a. Stool examination for occult blood, ova and parasites, culture b. CBC with differential, Erythrocyte Sedimentation Rate (ESR): to determine if anemia, bacterial infection, or inflammatory process c. Sigmoidoscopy or colonoscopy 1.Visualize bowel mucosa, measure intraluminal pressures, obtain biopsies if indicated 2.Findings with IBS: normal appearance increased mucus, intraluminal pressures, marked spasms, possible hyperemia without lesions d. Small bowel series (Upper GI series with small bowel-follow through) and barium enema: examination of entire GI tract; IBS: increased motility

Irritable Bowel Syndrome (IBS) (spastic bowel, functional colitis) Medications a. Purpose: to manage symptoms b. Bulk-forming laxatives: reduce bowel spasm, normalize bowel movement in number and form c. Anticholinergic drugs (dicyclomine (Bentyl), hyoscyamine) to inhibit bowel motility and prevent spasms; given before meals d. Antidiarrheal medications (loperamide (Imodium), diphenoxylate (Lomotil): prevent diarrhea prophylactically e. Antidepressant medications f. Research: medications altering serotonin receptors in GI tract to stimulate peristalsis of the GI tract

Irritable Bowel Syndrome (IBS) (spastic bowel, functional colitis) Dietary Management a. Often benefit from additional dietary fiber: adds bulk and water content to stool reducing diarrhea and constipation b. Some benefit from elimination of lactose, fructose, sorbitol c. Limiting intake of gas-forming foods, caffeinated beverages 8. Nursing Care a. Contact in health environments outside acute care b. Home care focus on improving symptoms with changes of diet, stress management, medications; seek medical attention if serious changes occur

Peritonitis Definition a. Inflammation of peritoneum, lining that covers wall (parietal peritoneum) and organs (visceral peritoneum) of abdominal cavity b. Enteric bacteria enter the peritoneal cavity through a break of intact GI tract (e.g. perforated ulcer, ruptured appendix)

Peritonitis Causes include: Ruptured appendix Perforated bowel secondary to PUD Diverticulitis Gangrenous gall bladder Ulcerative colitis Trauma Peritoneal dialysis

Peritonitis Pathophysiology a. Peritonitis results from contamination of normal sterile peritoneal cavity with infections or chemical irritant b. Release of bile or gastric juices initially causes chemical peritonitis; infection occurs when bacteria enter the space c. Bacterial peritonitis usually caused by these bacteria (normal bowel flora): Escherichia coli, Klebsiella, Proteus, Pseudomonas d. Inflammatory process causes fluid shift into peritoneal space (third spacing); leading to hypovolemia, then septicemia

Peritonitis 3. Manifestations a. Depends on severity and extent of infection, age and health of client b. Presents with “acute abdomen” 1.Abrupt onset of diffuse, severe abdominal pain 2.Pain may localize near site of infection (may have rebound tenderness) 3.Intensifies with movement c. Entire abdomen is tender with boardlike guarding or rigidity of abdominal muscle

Peritonitis d. Decreased peristalsis leading to paralytic ileus; bowel sounds are diminished or absent with progressive abdominal distention; pooling of GI secretions lead to nausea and vomiting e. Systemically: fever, malaise, tachycardia and tachypnea, restlessness, disorientation, oliguria with dehydration and shock f. Older or immunosuppressed client may have 1.Few of classic signs 2.Increased confusion and restlessness 3.Decreased urinary output 4.Vague abdominal complaints 5.At risk for delayed diagnosis and higher mortality rates

Peritonitis 4. Complications a. May be life-threatening; mortality rate overall 40% b. Abscess c. Fibrous adhesions d. Septicemia, septic shock; fluid loss into abdominal cavity leads to hypovolemic shock 5. Collaborative Care a. Diagnosis and identifying and treating cause b. Prevention of complications

Peritonitis 6. Diagnostic Tests a. WBC with differential: elevated WBC to 20,000; shift to left b. Blood cultures: identify bacteria in blood c. Liver and renal function studies, serum electrolytes: evaluate effects of peritonitis d. Abdominal xrays: detect intestinal distension, air-fluid levels, free air under diaphragm (sign of GI perforation) e. Diagnostic paracentesis 7. Medications a. Antibiotics 1.Broad-spectrum before definitive culture results identifying specific organism(s) causing infection 2.Specific antibiotic(s) treating causative pathogens b. Analgesics

Peritonitis 8. Surgery a. Laparotomy to treat cause (close perforation, removed inflamed tissue) b. Peritoneal Lavage: washing out peritoneal cavity with copious amounts of warm isotonic fluid during surgery to dilute residual bacterial and remove gross contaminants c. Often have drain in place and/or incision left unsutured to continue drainage

Peritonitis 9. Treatment a. Intravenous fluids and electrolytes to maintain vascular volume and electrolyte balance b. Bed rest in Fowler’s position to localize infection and promote lung ventilation c. Intestinal decompression with nasogastric tube or intestinal tube connected to suction 1. Relieves abdominal distension secondary to paralytic ileus 2. NPO with intravenous fluids while having nasogastric suction

Peritonitis 10. Nursing Diagnoses a. Pain b. Deficient Fluid Volume: often on hourly output; nasogastric drainage is considered when ordering intravenous fluids c. Ineffective Protection d. Anxiety 11. Home Care a. Client may have prolonged hospitalization b. Home care often includes 1. Wound care 2. Home health referral 3. Home intravenous antibiotics

Client with Inflammatory Bowel Disease Definition a. Includes 2 separate but closely related conditions: ulcerative colitis and Crohn’s disease; both have similar geographic distribution and genetic component b. Etiology is unknown but runs in families; may be related to infectious agent and altered immune responses c. Peak incidence occurs between the ages of 15 – 35; second peak 60 – 80 d. Chronic disease with recurrent exacerbations

Inflammatory Bowel Disease

Ulcerative Colitis Pathophysiology 1. Inflammatory process usually confined to rectum and sigmoid colon 2. Inflammation leads to mucosal hemorrhages and abscess formation, which leads to necrosis and sloughing of bowel mucosa 3. Mucosa becomes red, friable, and ulcerated; bleeding is common 4. Chronic inflammation leads to atrophy, narrowing, and shortening of colon

Ulcerative Colitis Manifestations 1. Diarrhea with stool containing blood and mucus; 10 – 20 bloody stools per day leading to anemia, hypovolemia, malnutrition 2. Fecal urgency, tenesmus, LLQ cramping 3. Fatigue, anorexia, weakness

Ulcerative Colitis Complications 1. Hemorrhage: can be massive with severe attacks 2. Toxic megacolon: usually involves transverse colon which dilates and lacks peristalsis (manifestations: fever, tachycardia, hypotension, dehydration, change in stools, abdominal cramping) 3. Colon perforation: rare but leads to peritonitis and 15% mortality rate 4. Increased risk for colorectal cancer (20 – 30 times); need yearly colonoscopies 5. Abcess, fistula formation 6. Bowel obstruction 7. Extraintestinal complications Arthritis Ocular disorders Cholelithiasis

Ulcerative Colitis Diet therapy Goal to prevent hyperactive bowel activity Severe symptoms NPO TPN Less severe Vivonex Elemental formula absorbed in the upper bowel Decreases bowel stimulation

Ulcerative Colitis Diet therapy Significant symptoms Low fiber diet Reduce or eliminate lactose containing foods Avoid caffeinated beverages, pepper, alcohol, smoking

Ulcerative Colitis Ostomy 1. Surgically created opening between intestine and abdominal wall that allows passage of fecal material 2. Stoma is the surface opening which has an appliance applied to retain stool and is emptied at intervals 3. Name of ostomy depends on location of stoma 4. Ileostomy: opening in ileum; may be permanent with total proctocolectomy or temporary (loop ileostomy) 5. Ileostomies: always have liquid stool which can be corrosive to skin since contains digestive enzymes 6. Continent (or Kock’s) ileostomy: has intra-abdominal reservoir with nipple valve formation to allow catheter insertion to drain out stool

Ulcerative Colitis Surgical Management 25% of patients require a colectomy Total proctocolectomy with a permanent ileostomy Colon, rectum, anus removed Closure of anus Stoma in right lower quadrant In selected patients an ileoanal anastamosis or ileal reservoir to preserve the anal sphincter J-shaped pouch is created internally from the end of the ileum to collect fecal material Pouch is then connected to the distal rectum

Proctocolectomy

Ulcerative Colitis Surgical management Total colectomy with a continent ileostomy Kock’s ileostomy Intra-abdominal pouch where stool is stored untile client drains it with a catheter

Kocks pouch

Ulcerative Colitis Surgical management Total colectomy with ileoanal anastamosis Ileoanal reservoir or J pouch Removes colon and rectum and sutrues ileum into the anal canal

Ulcerative Colitis Home Care a. Inflammatory bowel disease is chronic and day-to-day care lies with client b. Teaching to control symptoms, adequate nutrition, if client has ostomy: care and resources for supplies, support group and home care referral

Ulcerative Colitis Treatment Medications similar to treatment for Crohn’s disease

Ulcerative Colitis Nursing Care: Focus is effective management of disease with avoidance of complications Nursing Diagnoses a. Diarrhea b. Disturbed Body Image; diarrhea may control all aspects of life; client has surgery with ostomy c. Imbalanced Nutrition: Less than body requirement d. Risk for Impaired Tissue Integrity: Malnutrition and healing post surgery e. Risk for sexual dysfunction, related to diarrhea or ostomy

Crohn’s Disease (regional enteritis) Pathophysiology 1. Can affect any portion of GI tract, but terminal ileum and ascending colon are more commonly involved 2. Inflammatory aphthoid lesion (shallow ulceration) of mucosa and submuscosa develops into ulcers and fissures that involve entire bowel wall 3. Fibrotic changes occur leading to local obstruction, abscess formation and fistula formation 4. Fistulas develop between loops of bowel (enteroenteric fistulas); bowel and bladder (enterovesical fistulas); bowel and skin (enterocutaneous fistulas) 5. Absorption problem develops leading to protein loss and anemia

Crohn’s disease

Crohn’s Disease (regional enteritis) Manifestations 1. Often continuous or episodic diarrhea; liquid or semi-formed; abdominal pain and tenderness in RLQ relieved by defecation 2. Fever, fatigue, malaise, weight loss, anemia 3. Fissures, fistulas, abscesses

Crohn’s Disease (regional enteritis) Complications 1. Intestinal obstruction: caused by repeated inflammation and scarring causing fibrosis and stricture 2. Fistulas lead to abscess formation; recurrent urinary tract infection if bladder involved 3. Perforation of bowel may occur with peritonitis 4. Massive hemorrhage 5. Increased risk of bowel cancer (5 – 6 times)

Crohn’s Disease (regional enteritis) Collaborative Care a. Establish diagnosis b. Supportive treatment c. Many clients need surgery Diagnostic Tests a. Colonoscopy, sigmoidoscopy: determine area and pattern of involvement, tissue biopsies; small risk of perforation b. Upper GI series with small bowel follow-through, barium enema c. Stool examination and stool cultures to rule out infections d. CBC: shows anemia, leukocytosis from inflammation and abscess formation e. Serum albumin, folic acid: lower due to malabsorption

Crohn’s Disease (regional enteritis) Medications: goal is to stop acute attacks quickly and reduce incidence of relapse a. Sulfasalazine (Azulfidine): salicylate compound that inhibits prostaglandin production to reduce inflammation b. Corticosteroids: reduce inflammation and induce remission; with ulcerative colitis may be given as enema; intravenous steroids are given with severe exacerbations c. Immunosuppressive agents (azathioprine (Imuran), cyclosporine) for clients who do not respond to steroid therapy alone Used in combination with steroid treatment and may help decrease the amount of steroid use

Crohn’s Disease d. New therapies including immune response modifiers, anti-inflammatory cyctokines e. Metronidazole (Flagyl) or Ciprofloxacin (Cipro) For the fistulas that develop f. Anti-diarrheal medications

Crohn’s Disease (regional enteritis) Dietary Management a. Individualized according to client; eliminate irritating foods b. Dietary fiber contraindicated if client has strictures c. With acute exacerbations, client may be made NPO and given enteral or total parenteral nutrition (TPN) Surgery: performed when necessitated by complications or failure of other measures removal of diseased portion of the bowel

Crohn’s Disease a. Crohn’s disease 1. Bowel obstruction leading cause; may have bowel resection and repair for obstruction, perforation, fistula, abscess 2. Disease process tends to recur in area remaining after resection