GI disorders

feeling of discomfort in the epigastrium with a conscious desire to vomit

the forceful ejection of partially digested food and secretions (emesis) from the upper GI tract. Vomiting isa complex act that requires the closure of the glottis, deep inspiration with contractions of the diaphragm in the inspiratory position, closure of the pylorus, relazation of the stomact and lower esophageal sphincter, and contraction of the abdominal muscles with increasing intrabdominal pressure.

• pregnancy, infection, central nervous system disorders (meningitis, tumor), cardiovascular problems (MI, heart failure), metabolic disorders (DM, Addison's disease, renal failure), side effects of drugs (chemotherapy, opioids, digitalis), and psychological factors (stress, fear)
• Vomiting can also occur when the GI tract becomes overly irritated, excited or distended. It is a protective mechanism to rid the body of spoiled or irritating foods and liquids.
• Sympathetic activation produces tachycardia, tachypnea, and diaphoresis.
• Parasympathetic stimulation causes relaxation of the lower esophageal sphincter, an increase in gatric motility, and a pronounced increase in salivation.

• Nausea is subjective. Anorexia (lack of appetite) usually accompanies nausea.
• Dehydration can occur when n/v occurs over a long period of time.
• As vomiting persists, there may be electrolyte imbalances, loss of ECF volume, decreased plasma volume, and eventuallyy circulatory failure.
• Metabolic alkalosis can result from loss of gastric hydrochloric acid.
• To prevent aspiration, put the patient in a semi-Fowler's or side-lying position.

• Determine and treat the underlying cause.
• Emesis containing partially digested foods several hours after a meal is indicative of gastric outlet obstruction or delayed gastric emptying. The presence of bile may suggest obstruvtion o the ampulla of Vater.
• Vomitus with a coffee ground appearance is indicative of gastric bleeding where blood changes to dark brown as a result of its interaction with HCl acid. Bright red blood indicates active bleeding.
• Mallory-Weiss tear: disruption of the mucosal lining near the esophageal-gastric junction. Can occur in esophageal varices or duodenal ulcer of neoplasm.
• Early morning vomitus is ommon in pregnance. Emotional stressors may elicit vomiting durng or immediately before eating.

• patient with severe n/v may required IV fluid therapy with electrolyte and glucose replacement until able to tolerate oral intake.
• Once the symptoms have subsided, oral nutrition beginning with clear liquids is started.
• Hot/cold liquids are hard to tolerate.
• Room temperature, carbonated beverages are easier to tolerate when the carbonation is gone and warm tea as well.
• Dry toast and crackers may alleviate feelings of nausea.
• Sipping water (5-15mL) ever 15-20 minutes is usually better tolerated than drinking a large amount.
• Broth and gatorade are hgih in sodium to administer with caution.
• As the patient improves, provide a diet high in carbohydrates and low in fatty foods. Baked potato, plain gelatin, cereal with milk and sufar, and hard candy are ideal.
• Coffee, spicy foods, highly acidic foods, and food with strong odor are often poorly tolerated.
• Patients should eat slowly to prevent overdistention of the stomach.

experience minimal or no n/v; maintain normal electrolyte levels and hydration status, and; return to a normal pattern of fluid balance and nutrient intake.

• Acute care:
• Maintain NPO status and give IV fluids until a diagnosis is confirmed.
• NG tube with suction may be necessary for the patient with persistent vomiting., as well as when a bowel obstruction or paralytic ileus is suspected. Secure the NG tube to prevent its movement in the nose and back of the throat bc this can stimulate n/v

Deficient fluid volume rt to prolonged vomiting and inability to ingest or digest foods amb decreased urine, decreased urine concentration, increased pulse, hypotension (postural), decreased intake, decreased skin turgor, dry skin and mucus membranes.

Imbalanced nutrition-less than body requirements rt to nausea and vomiting amb lack of interest or aversion to food, perceived or actual inabiluty to ingest foods, weight loss.

chronic symptoms or mucosal damanfe secondary to reflux of gastric contents into the lower esophagus. GERD is the most common upper GI problem seen in adults.

• Heartburn (pyrosis): a burning, tight sensation felt intermittently beneath the lower sternum and spreading upward to the throat or jaw.
• Dyspepsia: pain or discomfort centered in the upper abdomen (mainly in or around the midline as opposed to the right or left hypochondrium).
• Hypersalivation (water brash) may also be reported
• Complaints of noncardiac chest pain are more common in older adults with GERD.
• other symptoms may include wheezing, coughing, and dyspnea. Nocturnal discomfort that disturb sleep patterns.
• Hoarseness, sore throat, a globus sensation (sense of a lump in the throat), and choking may also occur.
• Regurgitation is another common symptom of GERD.
• Persistent reflux that occurs more than twice a week is considered GERD.
• May be relieved with milk, antacids or water.

• Esophagitis: inflammation of the esophagys. Repeated esophagitis may cause scar tissue formation and decreased distensibility (esophageal stricture) This may also result in dysphagia.
• Barrett's esophagitis: (esophageal metaplasia-metaplasia is the reversible change from one type of cell to another and is generally caused by an abnormal stimulus). The flat epithelial cells in the distal esophagus change to columnar epithelial cells. Considered a precancerous lesion that increases the patient's risk for esophageal adenocarcinoma. Signs and symptoms can range from none to mild bleeding and perforation.
• Respiratory complications include: cough, bronchospasm, larygospasm, and cricopharyngeal spasm. Due to irritation of the upper ariway by gastric secretions.
• Asthma, chronic bronchitis, and pneumonia may develop from aspiration of gastric contents into the respiratory system.
• Dental erosion may occur from acid reflux into the lungs.

• Nutritional: (Table 42-7, p 972)
• Fatty foods decrease LES pressure and the rate of gastric emptying. Teach pt to avoid such foods like chocolate, peppermint, tomatoes, coffee and tea bc they predispose to reflux.
• Avoid milk, especially at bedtime bc it increase gastric secretion.
• Small frequent meals help prevent overdistention of the stomach.
• Avoid late meals and nocturnal snacking. Take fluids, rather than food between meals to reduce distention.
• Saliva production can be increased by chewing gum and oral lozenges, which may help with mild symptoms of GERD.
• Drug therapy:
• focuses on decreasing volume and acidity of reflux, improving LES function, increasing esophageal clearance, and protecting esophageal mucosa.
• Proton pump inhibitors and histamine receptor blockers are the most common an effective treatments of symptomatic GERD.
• Surgical: antireflux surgery is reserved for those patients with complications of reflux including esophagitis, intolerance of medications, stricture, Barrett's metaplasia, and persistence of severe symptoms.
• Endoscopic: endoscopic mucosal resection, photodynamic therapy, cryotherapy, and radiofrequency ablation.

• Teaching Table 14-10 p974
• Head of bed is elevated at 30 degrees.
• For 2-3 hours following a meal the patient should not be supine.
• Avoid food and activities that cause reflux
• Continue meds according to symptom severity
• Headache is the most common complaint of patients taking a PPI.
• Antacids with aluminum can cause constipation, whereas those with magnesium can cause diarrhea.
• Side effects of metoclopramide include restelessness, anxiety, insomnia, and hallucination.
• Avoid gas forming foods such as gastric distention.

herniation of a portion of the stomach into the esophagus through an opening, or hiatus in the diaphragm. Common in older adults and occur more often in women than in men.

Sliding: the junction of the stomach and esophagus is above the hiatus of the diaphragm, and a part of the stomach slides through the hiatal opening in the diaphragm. Occurs when patient is supine and usually goes back into the abdominal cavity when the patient is standing upright. Most common.

Paraesophageal or rolling: Esophagogastric junction remains intact, but the fundus and the greater curvature of the stomach roll up trhough the diaphragm, forming a pocket alongside the esophagus. Acute paraesophageal hernia is a medical emergency.

• Can be asymptomatic. Similar to people with GERD
• Heartburn, especially after a meal or afer lying supine, is a common symptom.
• Bending over may cause severe burning pain, which is relieved by sitting or standing.
• Precipitating factors: large meals, alcohol, and smoking. Nocturnal symptoms of heartburn are common, especially if the person as eaten before lying down.
• May experience dysphagia.

GERD, esophagitis, hemorrhage from erosion, stenosis (narrowing of the esophagus), ulcerations of the herniated portion of the stomach, strangulation of the hernia, and regurgitation with tracheal aspiration.

• Conservative therapy:
• reduction of intraabdominal pressure-eliminating constricting garmets, avoiding lifting and straining, eliminating alcohol and smoking, elevating HOB, reducing body weight if overweight, and use of antisecretory agents and antacids.

• Surgical therapy:
• reduction of the herniated stomach into the abdomen
• herniotomy-excision of hernia sac
• herniorraphy-closure of hiatal defect
• antireflux procedure
• gastropexy-attachment of the stomach subdiaphragmatically to prevent reherniation.

Goals: reduce the herna, provide an acceptable LES pressure, and prevent movement of the gastroesophageal junction.

• Obvious bleeding:
• Hematemesis-bloody vomitus appearing as fresh, bright red blood or coffee ground appearance (dark, grainy digested blood)
• Melena-black tarry stools caused by digestion of blood in the GI tract; black appearance is presence of iron.

Occult bleeding: small amounts of blood in gastric secretions, vomitus or stools detectable only by guaiac test.

Causes of Upper GI bleed table 42-13 p 981

• Endoscopic therapy: performed within first 24 hours of bleeding is important for diagnosis, as well as determination of the need fo surgical intervention.
• Goal of endoscopic hemostasis is to coagulate or thrombose the bleeding vessel. Useful in patients with severe gastritis, Mallory-Weiss tear, esophageal and gastric varices, bleeding, peptic ulcers, and polyps.

Surgical therapy: indicated when bleeding continues regardless of the therapy provided and when the site of bleeding as been identified. Pts may have massive hemorrhage five years after first bleeding episode. Surgical therapy may be necessary when the patient continues to bleed after rapid transfusion of up to 2000mL of whole blood or remains in shock after 24 hours.

• Drugs are used to decrease bleeding, decrease HCl acid secretion, and neutralize HCl acid that is present.
• Antacids: neutralize acid and maintain gastric pH
• H2-receptor blockers: Inhibits action of histamine at H2 receptors on parietal cells and decrease HCl acid secretion.
• Proton Pump Inhibitors: Suppress gastric secretions

• Signs and symptoms of shock include low BP, rapid, weak pulse, increased thirst, cold, clammy skin, and restlessness. Assess vital signs every 15-30 minutes.
• Check for abdomen distention, guarding and peristalsis.

• Health promotion:
• History of chronic gastritis or peptic ulcer disease. Patients with cirrhosis and those with previous upper GI bleed from varices are high risk of another incident.
• Avoid gastric irritants, such as alcohol and smoking, increased stress and take only prescribed medications.
• Aspirin, corticosteroids and NSAIDs can increase chances of GI bleed. Take with meals or snacks to lessen irritation.

• Acute care:
• Maintain IV line for fluid or blood replacement.
• Observe older adult for fluid overload when receiving IV supplementation.
• Closely monitor pts' vital signs especially when they have a hx of cv disease because dysrhythmias can occur. Keep HOB elevated for comfort and prevention of aspiration.
• Assess stools for blood. Black tarry stools are indicative of prolonged bleeding. Bright red or maroon colored stools (hematochezia) are usually from a source in the lower bowel.
• Monitor the lab studies.
• When oral nourishment is begun, observe the patient for symptoms of n/v.

• Ambulatory and home care:
• Ulcer disease, drug or alcohol abuse, and liver and respiratory disease can all result in upper GI bleeding.
• Eliminate smoking and alcohol consumption.
• Recognize signs and treatment of acute hemorrhage

• Decreased cardiac output rt loss of blood
• Deficient fluid volume rt acute loss of blood and gastric secretions.
• Ineffective tisue perfusion rt los of circulatory volume

• penetrating lesion (associated with deformity or duodenal bulb from healing of recurrent ulcers)
• located in the first 1-2 cm of the duodenum
• Gastric secretions are increased
• Incidence is greater im ne, but increasing in postmenopausal women. Peak age is 35-45 yrs. Associated with psychological stress. Increased with smoking, drug and alcohol use. Aossictaed with other dieases such as COPD, pancreatic disease, hyperparathyroidism, and chronic renal failure)
• Manifestations include burning, cramping, pressure-like pain across midepigastrium and upper abdomen, back pain with posterior ulcers. Pain occurs 2-4 hours after meals and midmorning, midafternoon, middle of the night, periodic and episodic.
• Pain relief with antacids and food, occasional n/v
• Recurrence is high
• Complications include hemorrhage, perforation, and obstruction.

• Superficial, smooth margin, round, oval or cone shaped.
• Predominately in the antrum, also in the body and fundus of the stomach
• Gastric secretion is normal to decreased
• Incidence-peak age is 50-60 yes, more common in pts of lower socioeconomic status, increased with smoking, drug (NSAIDs) and alcohol use, increased with incompetent pyloric sphincter and bile reflux
• manifestionas-burning or gaseous pressure in high left epigastrium and back and upper abdomen. Pain occurs 1-2 hours after meals, if penetrating ulcer aggravated by food. Occasional n/v
• Recurrence is high
• Complications-hemorrhage, perforation, gastric outlet obstruction and intractability

• is a condition characterized by erosion of the GI mucosa resulting from the digestive action of HCl acid and pepsin. Any portion of the GI tract that comes into contact with gastric secretions is susceptible to developing ulcers.
• Causes:
• H. pylori
• chronic gastritis
• ulcerogenic drugs such as aspirin and NSAIDs
• High alcohol intake, coffee and psychological distress
• Infection with herpes and CMV in immunocompromised patients

Gastric vs duodenal ulcers p 987 table 42-18

• Dyspepsia associated with gastric ulcers is located high in the epigastrium and occurs about 1-2 hours after meals. Pain is described as burning or gaseous. If ulcer has eroded through the gastric mucosa, food tends to aggravate tather than alleviate pain.
• Duodenal ulcer symptoms tend to occur 2-5 hours after a meal. Pain is described as burning or cramplike. Found in the mid-epigastric region beneath the xiphoid process. Duodenal ulcers also produce back pain. Antacids alone or with H2-receptor blockers, as well as food neurtalize the acid to provide relief.
• Silent peptic ulcers tend to occur most commonly in older adults and those taking NSAIDs.

• Hemorrhage-more common in duodenal ulcers
• Perforation-most dangerous. Most common in duodenal ulcers, but most deadly in gastric ulcers. Sudden severe upper abdominal pain that radiates to the back and is not relieved by food and antacids.
• Gastric outlet obstruction-result of edema, inflmmation or pylorospasm as well as fibrous scar tissue formation. Relief may be obtained by belching or self-induced vomiting.

• Adequate rest, drug therapy, smoking cessation, dietary modification and long term follow up care.
• Aim is to decrease gastric acidity, and enhance mucosal defense mechanisms.
• Endoscopic examination is the most accurate method to monitor for ulcer healing, whih may take up to 3-9 weeks. Pain may disappear in 3-6 days.
• Discontinue aspirin and nonselective NSAIDs.
• Drug therapy p 991
• Acute exacerbation is accompanied by bleeding, increased pain and discomfort, and nausea and vomiting. Treatment similar to upper GI bleed.
• Perforation-stop spillage of gastric or duodenal contents into the peritoneal cavity and restore blood volume. NG tube is inserted to provie continuous aspiration and gastric decompression to halt spillage through the perforation. Lactated ringers and albumin solutions replace circulating blood volumes.
• Gastric outlet obstruction-decompress the stomach, correct any existing fluid and electrolyte imbalances, and improve the patient's general state of health.

• Patients who are taking ulcerogenic drugs such as aspirin or NSAIDs are at risk for PUD. Encourage to take with food.
• For acute exacerbation: patient may be NPO for a few days, have an NG tube inserted and connected to intermittent suction, and have IV fluid replacement. Regular mouth care, and lubrication of the nares facilitates breathing and decrease soreness.
• Obtain lab results to assess for fluid loss.
• Hemorrhage: changes in vitals and an increase in amount of redness of the aspirate often signal massive GI bleed. Maintain patency of NG tube so that blood clots do not obstruct the tube. Similar to interventions of GI bleed.
• Perforation: rigid boardlike abdomen, abdomen and shoulder pain, drawing up of knees, and shallow grunting respirations. Stop all oral or NG drugs and feeding. Administer IV fluids to replace depleted plasma volume. Antibotic therapy begin when perforation is confirmed.
• Gastric outlet obstruction: Constant NG aspiration of stomach contents can help relive symptoms. Allows edema and inflammation to subside and permit nomral flow of gastric contents through the pylorus. Check patency of NG, regular irrigations. Reposition pt from side to side so the tube tup is not constantly lying against the mucosal surface.
• Teaching table 42-24 p 996

• Partial gastrectomy with removal of the distal two thirds of the stomach and anastomosis of the gastric stump to the duodenum is called gastrodudenostomy or Billroth I operation.
• Partial gastrectomy with removal of the distal two thirds of the stomach and anastomosis of the gastric stump to the jejunum is called a gastrojejunostomy of Billroth II operation.
• Vagotomy is the severing of the vagus nerve, either totally (truncal) or selectively. Selective vagotomy results in denervatin of only a portion of the stomach or the parietal cell mass (highly selective vagotomy). These procedures are done to decrease gastric secretions.
• Pyloroplasty consists of surgival enlargement of the pyloric sphincter to facilitate the easy passge of contents from the stomach. It is commonly done after vagotomy or to enlarge an opening that has been constricted from scar tissue. A vagotomy decrease gastric motility and subsequently, gastric emptying. A pyloroplasty accompanying vagotomy increase gastric emptying.

Nutritional therapy: drink fluids with meals. Dry foods with a low carb content and moderate protein and fat content are better tolerated initially. Limit sugar intake to avoid postpranfial hypoglycemic reactions. Take fluids between meals, plan rest periods of at least 30 minutes after each meal.

• Dumping syndrome: direct result of surgical removal of a large portion of the stomach and the pyloric sphincter. Associated with meals having a hyperosmolar composition. Onset of symptoms occur within 15-30 minutes after eating. Generalized weakness, sweating, palpitations and dizziness are attributed to the sudden decrease in plasma volume. Abdominal cramps, hyperactive intestinal peristalsis
• (borborygmi) and the urge to defecate also occur. Last no longer than an hour after meals.

Postprandial hypoglycemia: variant of dumping syndrome because it is result of uncrontrolled gastric emptying of a volus of fluid high in carbohydrate into the small intestine. Results in hyperglycemia and the release of excessive amounts of insulin into the circulation. Symptoms include sweating, weakness, mental confusion, palpitations, tachycardia and anxiety. occur two hours after eating.

Bile reflux gastritis: gastric surgery that involves the pylorus, either reconstruction or removal, can result in reflux of bile into the stomach. Prolonged contact with bile causes damage to the gastric mucosa and chronic gastritis and recurrence of PUD. Symproms are continuous epigastric distress that increases after meals. Vomiting relieves distress. Bile salts are the source of gastric irritation in this condition.

• Preoperative:
• help the patient and family by clarifying and interpreting their questions. Make sure the instructions are clear on what to expect after surgery, like pain and comfort measures. The surgeon should provide necessary information about the procedure and the expected outcome.
• Postoperative:
• Observe the color, amount and odor of gastric aspirate. Usually bright red at first, with a gradual darkening within 24 hours and then yellow-green within 36-48 hours.
• Check patency of NG tube-clogging can lead to distention. and can rupture the sutures, cause leakage of gastric contents, hemorrhage, and possibly abcess.
• Observe for signs of decreased peristalsis, including distention and abdominal discomfort.
• Encourage to splint area with pillow.

Pernicious anemia: due to loss of intrinsic factor, which the parietal cells produce. May be a longterm complication of total gastrectomy and may occur after partial gastrectomy. Patient may require cobalmin depending on the amount of parietal cell mass removed. Give IM B12 shot if their is a chance of anemia.

• adenocarcinoma of the stomach wall. Probably begins with a nonspecific mucosal injury as a result of infection (H. pylori), autoimmune-related inflammation, repeated exposure to irritants, such as bile, antiinflammatory agents, or tobacco use.
• Other predisposing factors include atrophic gastritis, pernicious anemia, adenomatous polyps, hyperplastic polyps, hypertrophic hastropathy and achloryhydria. Smoking and obesity both increase the risk. Stomach cancer is most likely to develop in a pt who has had a gastrectomy for PUD.
• associated with diets containing smoked foods, salted fish and meat, and pickled vegetables.
• Whole grains and fresh fruits and vegetables are associated with reduced rates of stomach cancer.

• unexplained weight loss, lack of appetite, indigestion, abdominal discomfort or pain, s/s of anemia.
• Anemia is common, and is caused by chronic blood loss as the lesion erodes through the mucosa or as a result of pernicious anemia (due to loss of intrinsic factor).
• Person appears pale, weak and complains of fatigue, weakness, dizziness, and in extreme cases shortness of breath.
• A mass can be felt in the epigastrium. Supraclavicular lymph nodes that are hard and enlarged are suggestive of metastasis via the thoracic duct.
• Presence of ascites is a poor prognostic sign.

• Treatment of choice is surgical removal of the tumor.
• Preoperative management focuses on correction of nutritional deficits and treatment of anemia. Transfusion of packed RBCs correct anemia.

• Surgical therapy:
• For patients with lymph-node negtive stomch cancer, surgery alone results in a 75% 5 year survival rate.
• For patients with lymph-node positive cancer the rate is 10-50%.
• Survival rates are less when organs adjacent to the stomach show evidence of invasion at the time of emergency.

• Adjuvant therapy:
• Surgical resection followed by fluorouracil (5-FU) and radiotherapy or preoperative and postoperative epirubicin, cisplatin, and continuous infusion fluorouracil without radiotherapy.
• Radiation may be used as a palliative measure to decrease tumor mass and provide temporary relief of obstruction.
• Neo adjuvant chemotherapy and chemoradiotherapy maybe used preoperatively to decrease complication. Postoperatively, chemotherapy and chemoradiation may be used to reduce the rate of recurrence.

• Health promotion:
• Early detection, and encourage diagnostive evaluation for people with positive family history.

• Preoperative care:
• Treat malnutrition in patient undergoing surgery.
• Blood replacement

• Postoperative:
• Similar to those who undergo Billroth I and II.
• IV replacement of vitamins C, D, and K and the B-complex vitamins and replacement of cobalmin.
• Provide detailed instructions, reassure the patient and ensure the completion of the designated number of treatments for radiation therapy.
• Teach about skin care, need for nutrition and fluid intake and appropraite use of antiemetic drugs.

• Ambulatory and home care:
• Relief of pain and comfort measure.
• Teach wound care
• List of community resources.
• Home health nurse

• Imbalanced nutrition-less than body requirements rt inability to ingest, digest and absorb nutrients.
• Activity intolerance rt generalized weakness, abdominal discomfort, and nutritional discomfort.
• Acute pain
• Anxiety

passage of at least three loose or liquid stools per day. May be acute of chronic. Chronic if it lasts longer than 4 weeks.

• Ingestion of infectious organisms is the primary cause of acute diarrhea.
• Clostridium difficile impair absorption by destroying cells and producing inflammation in the colon.
• Organisms enter body by eating contaminated food, or drinking contaminated waer.
• Susceptibility depends on genetics, gastric acidity, intestinal microflora, and immunocompetenece.
• Some antibiotics kills off the normal flora making people more susceptible to pathogenic organisms.
• Most infectious diarrhea in the US is caused by viruses.
• E. coli is the most common cause of bloody diarrhea in the US. It is transmitted by inadequately cooked meat, or fruits and vegetables exposed to contaminated manure.

• Acute diarrhea most commonly results from infection. Bacterial infection may cause inflammation, and systemic infections (fever, headache, malaise) in addition to n/v abdominal cramping and diarrhea.
• Liquid stools also lead to perianal skin irritation. Leukocytes, blood and mucus may be present in the stool depending on the causative agent.
• Acute diarrhea is self limiting in adults
• People may remain contagious for 2 weeks or more even after recovering from a viral infection.

Severe diarrhea produce life-threatening dehydration, electrolyte disturbances (hypokalemia), and acid-base imbalances.

• C. diff causes mild to severe diarrhea, abdominal cramping and fever. It can progress to fulminant colitis and intestinal perforation.
• Hospitalized patients who receive antibiotics are particularly susceptible to diarrhea
• Pts with C.diff may also develop paralytic ileus or toxic megacolon and require colectomy.
• Elderly are particularly susceptible to C. diff
• Chronic diarrhea can result in malabsorption and ultimately malnutrition.

• Treatment depends on cause
• Food and medications that cause diarrhea should be avoided.
• Prevent transmission, fluid and electrolyte replacement, and resolution of diarrhea. Oral solutions containing glucose and electrolytes (Gatorade and Pedialyte) may be sufficient to replace loss from mild diarrhea, but parenteral administration of fluids, electrolytes, vitamins and nutrition is necessary when losses are severe.
• Antidiarrheal agents are given to coat and protect mucus membrans, absorb irritating substances, inhibit GI motility, decrease intestinal secretions and decrease CNS stiumlation of the GI tract. Table 43-2 p 1008 Drug therapy

• Spores can survive up to 70 days on objects inluding commodes, telephones, thermometers, etc
• Transmitted from HCP who do not adhere to infection control precautions.
• Flagyl or vancomycin is given to treat the infections.
• Flagyl is is the first line of treatment in mild disease becase oral vancomycin is expensive and because of VRE.
• Probiotics and stool transplantation may also be used.

• Hand hygiene
• Teach proper food handling, cooking and storage
• C. diff is not eliminated by alcohol. Symptomatic C. diff patients must be placed in isolation.
• Goals include:
• No transmission of microorganism causing the infectious diarrhea
• cessation of diarrhea and resumption of normal bowel patterns
• normal fluid and electrolyte and acid-base balance
• normal nutritional status
• no perianal skin breakdown

• a decrease in frequency of bowel movements from what is normal for the individual.
• Also includes difficult to pass stools, a decrease in stool volume, and or retention of feces in the rectu,
• Reduction in stool output may also be an indication of bowel obstruction produced by tumor

• Common causes include insufficient dietary fiber, inadequate fluid intake, decreased physical activity, and ignoring the urge to defecate.
• Constipation may also occur in disease that slow GI transit, and hamper neurologic function such as DM, Parkinsons and MS.
• Some medications may cause constipation as an adverse effect as well

• Stools are absent, hard, dry, and difficult to pass.
• Abdominal distention, bloating, increased flatulence, and increase rectal presure may alos be present.
• Hemorrhoids are also common. They result from venous engorgement caused by repeated Valsalva maneuvers (straining) and venous compressions from hard impacted stools.
• Valsalva maneuver may cause complications in heart failure, cerebral edema, HTN and CAD bcause it increases both intraabdominal and intrathoracic pressures and reduces venous return to the heart.
• Obstipation: severe constipation when no gas or stool is expelled or fecal impaction secondary to constipation, colonic perforation may occur.
• Rectal mucosal ulcers and fissures may occur. Diverticulosis is another complication.

• Laxative or enema depends on severity of the constipation.
• Drug therapy Table 43-5 p 1013
• Enemas are fast acting and beneficial for immediate treatment, but may cause inflammation of the muscoa or lead to water inflammation or electrolyte imbalances
• Glycerin suppositories
• Dietary fiber is found in plant foods such as fruits and vegetables, and grains. Wheat bran and prunes are especially effective for preventing and treating constipation (High fiber foods Table 43-6 p 1014)
• Fluid intake of 2000mL a day is important, unless contraindicated in pts with cardiac disease or renal insufficiency.

• Teaching guide Table 43-8 p 1015
• increase intake of fiber and fluids
• increase physical activity
• pass soft, formed stools
• no complications such as bleeding hemorrhoids

• Place pt in sitting position for defecation.
• Teach pt to establish a regular time to defecate and not to suppress the urge to defecate. The use of laxative and eneams to achieve fecal elimination is discouraged.

• chronic inflammation of the GI tract, characterized by periods of remission interspersed with periods of exacerbation.
• Either Crohn's disease or ulcerative colitis Table 43-14 p 1023

• Onset is teens to mid 30s
• bloody diarrhea is common
• Abdominal cramping is present
• Fever occurs only in acute attacks
• Weight loss is rare
• Rectal bleeding is common
• Tenesmus is also common
• Malabsorption and nutritional deficiencies is minimal
• increased stool output, increased bleeding, and systemic symptoms in moderate disease
• In severe disease, diarrhea is bloody, contains mucus, and occurs 10-20 times a day. In addition, weight loss greater than 10% of total body weight, anemia, tachycardia, and dehydration are present.
• Starts in rectum and spreads in a continuus pattern up to the colon.
• Continuous areas of inflammation
• Involves the mucosa and submucosa.
• Pseudopolyps are common
• Small bowel involvement is minimal

• Onset is tenns to mid 30s
• Genetic
• Diarrhea, abdominal cramping pain, fever, and severe weightloss are common.
• Rectal bleeding is infrequent
• Malabsorbption and nutritional deficiencies are common
• Occurs anywhere along the GI tract in hracteristic skip lesions. Most common in terminal ileum.
• Healthy tissue is interspersed with areas of inflammation. Involves entire thickness of bowel wall (transmural)
• Granulomas and cobblestoning of mucosa are common. Small bowel involvement is also common

• Table 43-15 p 1025
• Hemorrhage may lead to anemia.
• Nutritional problems more common in Crohn's disease when the terminal ileum is involved.
• Pts with longstanding ulcerative colitis are at risk for colorectal cancer, and those with Crohn's are at risk for small intestine cancer.
• Some people with IBD suffer from arthritis, ankylosing spondylitis, eye inflammation, and skin lesions due to circulating products of inflammation.
• Kidney stones
• thromboembolism
• Primary sclerosing cholangitis which can lead to liver failure and gallstones

Ulcerative colitis: perforation (bc of megacolon) is common. Toxic megacolon is relatively more common. Increased incidence of carcinoma after 10 yrs of disease. Cure with colectomy.

Crohn's disease: Fistulas, strictures, anal abcesses, perforation (bc inflammation involves entire bowel wall). Carcinoma involving the small intestines is increased; colon is increased, but not as much with ulcerative colitis. Recurrence after surgery is common at site of anastomosis.

• More common with ulcerative colitis.
• Colonic dilation

• rest the bowel
• control the inflammation
• combat infection
• correct malnutrition
• alleviate stress
• provide symptomatic relief
• improve quality of life

• Drug therapy: aminosalicylates; antimicrobials; corticosteroids, immunosuppresants; biologic and targeted therapy.
• Aminosalicylates and antimicrobials are used first
• Table 43-17 p 1026

• Surgical therapy:
• Crohns disease-strictureplasty. Reserved for emergency situations (excessive bleeding, obstructions, periotonitis) or when medications have failed.

Ulcerative colitis: total colectomy with rectal mucosal stripping and ileoanal reservoir; total proctocolectomy with permanent ileostomy; total proctocolectomy with continent ilesotomy (Kock pouch)

• drainage of abdominal abcess
• failure to respond to conservative therapy
• Fistulas
• inability to decrease corticosteroids
• intestinal obstruction
• massive hemorrhage
• perforation
• severe anorectal disease
• suspicion of carcinoma

• Check stoma
• Ileostomy output initially may be as high as 1500 to 2000mL per 24 hours. Observe pt for signs of hemorrhage, abdominal abcess, small bowel obstruction, dehyrdation.
• remove NG when bowel function returns
• Teach kegal exercises-but not during postop period.
• Perianal care

• 1. emotional support-radical change in body image
• 2. patient and caregiver teaching about stomay care and the ostomy

• Preoperative:
• 1. psychological preparation
• 2. selection of a flat site on the abdomen that allows for secure attachment of the collection bag.
• 3. selection of the stoma site that will clearly be visible to the patient and is appropriate for clothing and activities.
• WOCN recommends that an experienced, educated, and competent clician select the site

delegation decisions Ostomy care p 1044

• assessment of stoma (43-28 p 1041). Stoma should be pink.
• Dusky blue indicates ischemia
• brown-black indicates necrosis
• Assess and document stoma color every 4 hours
• Mild to moderate swelling for the first 2-3 weeks after surgery.
• Colostomy functions when peristalsis has been adequately restored.
• One piece system-allows has the skin barrier attached
• The two piece system allpws removal of the pouch without removal of the skin barrier. The skin should be washed with plain water or mild soap, rinsed with warm water and dried thoroughly before barrier is applied.
• Apply open ended, transparent plastic, odor-proof pounch to observe the stoma and collect the drainage.
• Ensure that the pt can perfrom a pouch change, provide appropriate skin care, control odor and care for the stoma and identiy s/s of complications.
• Ostomy self care table 43-29 p 1042

• in the ascending and transverse colon has semi-liquid stools.
• in sigmoid or descending colon has semi formed or formed stools.
• Colostomy irrigations may be used to stimulate emptying of the colon. Regularity is only possible when the stoma is in the distal colon or rectum.

• Drainage pouch isusually worn for 4-7 days before being changed unless leakage occurs
• Observe for s/s of fluid and electrolyte imbalances, particularly sodium, potassium, and fluid deficits.
• In the first 24-48 hours after surgery the amount of drainage from the stoma may be negligible.
• Increase fluid intake to 2-3L a day. May also need to ingest additional sodium.
• Low fiber diet is ordered initially and introduced gradually. Goal is to return to normal postsurgical diet.
• Stoma may bleed easily when touched due to its high vascularity.

Nutritional therapy 43-30 p 1044

Diverticula: saccular dilations or outpouchings of the mucosa that develop in the colon at points whenre the vasa recta penetrate the circular muscle layer

Diverticulosis: multiple noninflamed diverticula

Diverticulitis: inflammation of the diverticula, resulting in perforation into the peritoneum

• Clinically, diverticular disease covers a spectrum from asymptomatic, uncomplicated diverticulosis to diverticulitis with complications such as perforation, abscess, fistula and bleeding.
• May occur at any point within the GI tract but are most commonly found in the sigmoid colon.

• Diverticulosis typically has no symptoms. Those with symptoms have abdominal pain, bloating, flatulence, and/or changes in bowel habits.
• Diverticulitis abdominal pain is localized around the colon in the left, lower quadrant. Sometimes fever, leukocytosis, and a palpable abdominal mass. Complications include perforation, peritonitis, abscess, and fistula formation, obstruction and bleeding. Obstruction is most common.

• high fiber diet and decreased intake of fat and red meat are recommended in preventing diverticular disease
• Nuts and popcorn may protect against diverticulitis.
• weight reduction is important for obese people
• increased intrabdominal pressure should be avoided, such as straining at stool, vomiting, bending, lifting, and tight restrictive clothing

In acute divertilitis, the goal is to let the colon rest and the inflammation subside. Clear liquid diet with broad spectrum antibiotics (Flagyl). May be NPO.

Surgery is reserved for people with complications such as abcess or obstruction that cannot be managed medically. Usually resetion of the invovled colon with either a primary anastomosis if adequate bowel cleansing is feasable or temporary diverity colostomy.

occurs when intestinal contents cannot pass through the GI tract. May occur in the small intestine or colon and can be partial or complete

a detectable occlusion of the intestinal lumen. Mostly occur in the small intestine. Surgical adhesion is the most common cause of small bowel obstruction and can occur within days of surgery or several years later. Hernias and tumors are the next most common cause.

Carcinoma is the most common cause of large bowel obstructions, followed by volvulus and diverticular disease.

result from neuromuscular or vascular disorder.

• Paralytic (adynamic) ileus: lack of intestinal peristalsis and the presence of no bowel sounds is the most common form of nonmechanical obstruction.
• Paralytic ileus can also be caused by peritonitis, inflammatory responses, electrolyte abnormalities, and thoracic and spinal fractures.

Pseudo obstructions is an apparent mechanical obstruction of the intestine without demonstration of obstruction by radiologic methods. Collagen vascular disease and neurologic endocrine disorders may cause pseudo obstruction, but at the time be unknown.

rare and occur as a result of interference with the blood supply to a portion of the intestins. Most common cause is emboli, and atherosclerosis of the mesenteric arteries. This is a surgical emergency.

• nausea, vomiting, poorly localized abdominal pain, abdominal distention, inability to pass flatus, obstipation and s/s of hypovolemia
• proximal small intestine obstruction develop n/v
• vomiting from more distal obstructions of the small intestines is more gradual in onset. and the vomitus may be orange-brown and foul smelling like feces.
• vomiting relieves abdominal pain in proximal intestinal obstructions.
• Persistent, colicky abdominal pain is seen in pts with lower intestinal obstructions.
• Mechanical obstruction pain comes and goes in waves
• Abdominal distention is marked in lower intestinal obstructions.
• Auscultation of bowel sounds reveals high-pitched sounds above the area of the obstructions
• Table 43-20 p 1032

• NPO status
• insertion of NG tube
• IV fluid rescusitation with either normal saline or lactated ringers, additional potassium to IV fluids after renal function is verified
• Analgesics for pain control.
• If obstruction doesnt improve within 24 hours, surgery is perfomed and may involve a simple resectioing of the obstructed segment of the bowel and anastomosing the reaming healthy bowel back together. Partial or total colectomy, colostomy, or ileostomy may be required when extensive obstruction or necrosis is present.
• Colonoscope can be used to remove polyps, dilate strictures, and remove and destory tumors with a laser.

• prevent fluid and electrolyte imbalances
• recognition of complications (hypovolemic shock and bowel strangulation)
• Record onset, frequency, color, odor and amount of vomitus.
• Auscultate for bowel sounds and document
• Note any muscle guarding and rebound tenderness which are signs of peritoneal irritation and are indiciative of strangulation.
• look closely for signs of dehydration .
• Administer IV fluids as ordered.
• Monitor serum electrolytes closely.
• pt with high intestinal obstruction is at greater risk of metabolic alkalosis; pt with low intestinal obstruction is a greater risk of metabolic acidosis.
• Proper care of NG tube

• the accumulation of hardened feces in the rectum or sigmoid colon that cannot be expelled. Incontinence occurs as liquid stool seeps around the mass of hardned feces. Fecal incontinence caused by fecal impaction is a common problem in older adults with limited mobility. Constipated individuals tend to strain during defecation: straining contributes to incontience because it weakens the pelvic floor muscles.
• Anorectal surgery (hemorrhoidectomy, colectomy) can damage the sphincters and pudendal nerves. Irradiation for prostate cancer decreases rectal compliance. Neurological conditions such as stroke, spinal cord injurty and MS and diabetic neuropathy can also interfere with defecation.

Causes Table 43-4 p 1011

• Bowel retraining
• bisacodyl (Dulcolax), glycerin suppository or a small phospahte enema may be administered 15-30 minutes before the usualy evacuation time. These preparations stimulate the anorectal reflex. Once a regular pattern is established, these are discontinued.
• Incontinence briefs
• maintaining skin integrity
• Avoid foods such as caffeine that aggravate symptoms.

• Rectal examination can reveal the anal canal muscle tone and contraction strength of the external sphincter as well as detect internal prolapse, rectocele, hemorrhoids, fecal impaction and massess.
• If the impaction is higher in the colon, an abdominal x-ray or a computed tomography (CT) scan may be helpful.
• Fecal incontinence from fecal impaction usually resolves after manial disimpaction of the hard feces and cleansing enemas.
• To prevent recurrence-bowel management program inclued regular defecation practices, a high fiber diet and increased fluid intake.
• Damage to the anal sphincers may require surgical repair.

• Proton pump inhibitors (PPI)
• Antisecretory to treat peptic ulcer disease and GI bleeding
• Useful for duodenal ulcers, gastric ulcers, acute gastritis (corrosive, erosive, and hemorrhage)
• Also used with antibiotics to treat ulcers caused by H. pylori.

• Suppresses gastric secretion by inhibiting H+, K+ ATPase enzyme system in gastric parietal cells; inhibits the gastric acid pump which is necessary for secretion of HCl acid.
• Side effects: headache, nausea, diarrhea, abdominal pain, fatigue, dizziness. Long term, may cause hypomagnesiumia and may increase the risk of fractures of hip, wrist and spine
• Depressed vitamin b12 absorption may also occur because the body uses gastric acid to release B12 from food particles

• most commonly caused by pernicious anemia.
• Loss of intrinsic factor. IF is required for cobalamin (extrinsic factor) absorption.
• Most common in people who have GI surgery, patients who had a small bowel resection involving the ileum, and patients with Crohn's disease, ileitis, celiac diseas, diverticuli of the small intestine and/or chronic atrophic gastritis.

• Increased risk of serious GI adverse events (especially in elderly) including bleeding, ulceration and perforation.
• NSAIDs, except aspirin have been linked to higher risk for increased CV events such as MI, stroke and heart failure.
• inhibit enzyme cyclooxygenase (COX), the enzyme that converts arachidonic acid into prostaglandins. Inhibition of COX-1 may have many untoward effects such s bleeding, renal dysfunction, GI irritation and ulceation due to COX mediation of inflammation.
• NSAIDs should be limited in those at high risk for adverse effects, including the elderly, pt with history of peptic ulcer disease.
• If used in pts with increased risk of GI bleeding, should have concomitant therapy with misoprotol or a PPI. Should not be administered with aspirin as the risk for bleeding and GI adverse effects are increased.

cimetidine, ranitidine, famotidine, and nizatidine are used in PUD, GERD and upper GI bleeding treatment.

• Duodenal ulcer, gastric ulcer, esophagitis, acute gastritis (especially hemorrhagic).
• Inhibits action of histamine at H2 receptors on parietal cells and decreased HCL acid secretion

• H2 blocker used to treat ulcers and GERD
• heart burn relief
• can be given IV

used to control diarrhea by inhibiting peristalsis, delaying transit, increasing absorption of fluid from the stools.

defined as nutrition (nutritionally balanced liquefied food or formula) provided through the GI tract via a tube, catheter, or stoma that delived nutrients distal to the oral cavity.

Indications: anorexia, orofacial fractures, head and neck cancer, neurological or psychiatric conditions that prevent oral intake, extensive bruns, critical illnesses and those receiving chemotherapy or radiation therapy.

Common delivery is through continuous infusion by pump, intermittent infusion by gravity, intermitten bolus by syringe, and cyclic feedings by infusion pump.

Nasogastric is the most commonly used for short term feedings.

• long, small in diameter, soft and flexible thereby decreasing the risk of mucosal damage from prolonged placement.
• More easily clogged bc of small diameter.
• More difficult to use for checking residual volumes.
• Dislodged by vomiting, coughing and can become knotted or kinked in the GI tract.
• Be sure to flush tube before and after drug administration.

• requires EN for an extended period of time
• for pts with chronic reflux.
• reduce risk for aspiration
• pt must have intact unobstructed GI tract and the esophageal lumen must be wide enough to pass the nedoscope for PEG tube placement.
• Requires to sedation to place.
• EN can be started within 24-48 hours after placement without waiting for flatus or bowel movement and within two hours of PEG tube.

• Table 40-12 p 933
• Vomiting and aspiration: improper placement, delayed gastric emptying, increase residual volume

Diarrhea: feeding too fast, medications, low-fiber formula, tube moving distally, contamination of formula.

Constipation: formula components, poor fluid intake, drugs, impaction

Dehydration: excessive diarrhea, vomiting, poor fluid intake, high protein formula, hyperosmotic diuresis