Esophageal Diverticulum and Cancer

Esophageal Diverticulum

• An outpouching of the mucosa of the esophagus
• Two types: Pulsion and Traction

Pulsion

• Weakness through the muscle wall of the esophagus

Traction

• Pulling outward of the esophageal wall due to scarred/enlarged peri-bronchial lymph node

Signs and Symptoms of Esophageal Diverticulum

• Dysphagia
• Fullness in the neck
• Regurgitation
• Tracheal irritation
• Coughing/belching

Interprofessional Collaborative Management for Patients with Esophageal Diverticulum

• Blenderized food
• Antacids as ordered.
• Small frequent feedings
• Backrest for several hours after eating
• Avoid irritating foods
• Surgery
• Care of the client with Chest Tubes during the postop period

Cancer of the Esophagus

• Lower 2/3 of the esophagus is most commonly affected.

Predisposing Factors for Esophageal Cancer

• Alcohol
• Smoking

Additional Esophageal Cancer Factors

• Avoid tobacco, salicylates, phenylbutazone
• Spicy foods
• Poor oral hygiene
• Family history
• Obesity
• Drinking large volume of hot tea

Collaborative Management of Esophageal Cancer

• Surgery: Esophagogastrectomy and Gastrostomy feedings

Hiatal Hernia

• Two types: sliding hiatal hernia and para-esophageal / rolling hiatal hernia

Sliding Hiatal Hernia

• The protrusion of the esophagogastric junction into the thoracic cavity and back into the abdominal cavity in relation to position changes
• Stomach slides up in a recumbent position and slides down in an upright position

Primary Cause of Sliding Hiatal Hernia

• Muscle weakness in the esophageal hiatus
• This may be due to aging, congenital muscle weakness, obesity, trauma, surgery, or prolonged increases in intraabdominal pressure

Para-Esophageal Hernia

• Protrusion of the fundus of the stomach and the greater curvature into the thorax next to the esophagus and is due to anatomic defect
• Gastric junction remains below the diaphragm

Clinical Manifestations of Hiatal Hernia

• Heartburns due to gastroesophageal reflux
• Dysphagia and odynophagia due to the compression of the esophagus
• Dyspnea due to compression of the lungs
• Abdominal pain due to compression of the protruding portion of the stomach
• Nausea and vomiting due to stimulation of sensitive structures in the stomach
• Gastric distention, belching, and flatulence due to accumulation of gas in the stomach and abdomen

Interprofessional Collaborative Management for Patients with Hiatal Hernia

• Medications:
  • Antacids relieve heartburn
  • Antiemetics to relieve nausea and vomiting
  • Histamine H2 receptor antagonists to suppress secretion of gastric acid
  • Proton pump inhibitors to suppress gastric acid secretion
• Avoid drugs that lower LES pressure to prevent gastroesophageal reflux
  • Drugs to be avoided: anticholinergics, Xanthine derivatives, calcium channel blockers, and diazepam.

Nursing Interventions for Hiatal Hernia

• Relieve pain by administering antacids
• Modify diet:
  • High protein diet enhances LES pressure and prevents esophageal reflux
  • Small frequent feedings prevents gastric distention and further protrusion of the stomach into the thoracic cavity
  • Instruct the patient to eat slowly and chew food properly to reduce gastric motility
  • Avoid foods and beverages that decrease LES pressure, like fatty foods, cola beverages, coffee, tea, chocolate, and alcohol
  • Assume an upright position after eating for 1 to 2 hours, preventing protrusion of the stomach into the thoracic cavity and preventing reflux
  • Avoid eating at least 3 hours before bedtime to prevent night time reflux
  • Reduce body weight, if obese, to reduce intraabdominal pressure
• Lifestyle Changes:
  • Elevate the head of the bed
  • Avoid factors that increase abdominal pressure
  • Avoid cigarette smoking
• Surgery:
  • Nissen fundoplication or gastric wrap-around

Peptic Ulcer Disease (PUD)

• An impairment of the mucosa and deeper structures of the esophagus, stomach, duodenum, or jejunum
• Helicobacter pylori infection is the cause

Helicobacter Pylori Infection

• Usually due to eating raw or improperly cooked meat
• Combination of hydrochloric acid (HCl) and pepsin serves as aggressor to GI mucosa, and increased secretion of HCl and pepsin may be caused by stress and stimulants
• Mucus secretion of the GI tract serves as a protector, and decreased mucus secretion may be caused by decreased blood flow and the presence of irritants in the GI tract

Predisposing Factors for Peptic Ulcer Disease

• Stress triggers the sympathetic nervous system (SNS); prolonged stress exhausts SNS and activates the parasympathetic nervous system (PNS)
• Nicotine stimulates increased HCl secretion and causes vasoconstriction, irritation, and damage to the GI mucosa
• Alcohol irritates the GI mucosa and causes vasoconstriction.
• Beer increases gastric acid secretion
• Caffeine stimulates increased HCl secretion and causes vasoconstriction
• Aspirin (ASA), Nonsteroidal anti-inflammatory drugs (NSAIDs), and steroids are ulcerogenic
• Gastritis leads to increased HCl secretion and mucus ulceration

Zollinger-Ellison Syndrome

• Caused by a pancreatic tumor (gastrinoma) that stimulates increased gastrin secretion, which in turn stimulates increased hydrochloric acid secretion
• Multiple areas or ulceration in the GI tract occur
• Irregular, hurried meals leads to increased gastric motility and increased HCl secretion
• Fatty, spicy, highly acidic foods are stimulants that increase HCl secretion and irritants to the GI mucosa
• Type A Personality (Stress Personality) characterized by overconscientiousness, perfectionism, "workaholism," inability to concentrate, parsimoniousness, very punctual has increased gastric motility and HCl secretion
• Type O Blood has higher pepsinogen levels; pepsin, in combination with HCl, acts as aggressor to the GI mucosa
• Genetics affect parietal cell mass

Gastric Ulcers

• Also called "poor man's" or "laborer's" ulcer because the stomach is usually empty
• 20% incidence
• Affects those who are 50 years old and above and malnourished
• Increased back diffusion of HCl into gastric mucosa
• Normal gastric emptying rate and normal HCl secretion

Duodenal Ulcers

• Also called "executive" ulcer because it is primarily stress-related
• 80% incidence
• Affects those who are 25 to 50 years of age and usually well-nourished
• Increased HCl secretion

Characteristics of PUD

• Both are characterized by dull, aching, gnawing epigastric pain
• Gastric ulcer pain radiates to the left side of the abdomen and is experienced ½ to 2 hours after eating; not relieved by food intake
• Duodenal ulcer pain radiates to the right side of the abdomen and is experienced 3 to 4 hours after eating; pain is relieved by food intake
• Gastric ulcer manifestations include nausea, vomiting, and hematemesis
• Duodenal ulcer manifestations include melena (black, tarry stools)

PUD Complications

• Hemorrhage and hypovolemic shock
• Perforation
• Peritonitis

Collaborative Management for Patients with Peptic Ulcer Disease

• Medications
  • Antacids neutralize HCl and should be administered 1 to 2 hours after eating
  • Cimetidine may cause mental confusion, agitation, psychosis, depression, anxiety, disorientation, anti-androgenic effects
  • Administer Cimetidine and antacids 1 hour apart from each other
• Cytoprotective Drugs:
  • Coat ulcers and enhance prostaglandin synthesis
  • Administer the medication on an empty stomach 30 to 60 minutes before meals
  • Administer Sucralfate at least 60 minutes apart from the antacid
• Prostaglandin Analogues:
  • Replace gastric prostaglandin and suppress secretion of gastric acid
  • Contraindicated in pregnancy
• Proton Pump Inhibitors (PPI's):
  • Suppress gastric acid secretion
  • Common side effects include headache, diarrhea, abdominal pain, and nausea
• Anticholinergics:
  • Reduce gastric motility and hydrochloric acid secretion
• Helicobacter Pylori drug treatment
  • Advise client to avoid alcohol to prevent disulfiram-like manifestations
  • Tetracycline is teratogenic and contraindicated in pregnancy

Surgical Interventions for Peptic Ulcer Disease

• Vagotomy - resection of the vagus nerves
• Pyloroplasty - surgical dilatation of the pyloric sphincter
• Antrectomies - surgical resection of 50% of the distal part of the stomach followed by anastomosis with the duodenum or jejunum:

Billroth I

• Gastroduodenostomy
• Anastomosis of the gastric stump with the duodenum and is indicated in gastric ulcer

Billroth II

• Gastrojejunostomy
• Anastomosis of the gastric stump with the jejunum; the duodenum is bypassed and is indicated in doudenal ulcer
• Subtotal Gastrectomy

Nursing Interventions for Peptic Ulcer Disease

• Relieve pain by administering antacid
• Encourage patient to promote a healthy lifestyle Patient Diet:
• May eat anything that can be tolerated when asymptomatic
• Liberal bland diet is recommended during exacerbation
• Avoid hot, spicy, and highly seasoned foods
• Eat slowly and chew food properly
• Small, frequent feedings during exacerbation
• Avoid: fatty foods, coffee, tea, chocolate, cola drinks, spices, red/black pepper, alcohol
• Avoid alcohol (these are irritants and stimulants), bedtime snacks, binge eating and large quantities of milk

Pre Op Care after Undergoing Gastric Surgery

• Provide psychosocial support
• Teach the client DBCT exercises
• Surgery involves a high abdominal incision, so the client is at risk to develop respiratory complications Provide Nutritional Support
• Inform the client and his family on postop measures
• Promote patent airway and ventilation, prevent atelectasis and hypostatic pneumonia, and place client in semi-Fowler's position

Additional Care after Undergoing Gastric Surgery

• Reinforce DBCT exercises and incentive spirometry
• Administer analgesic before activities
• Splint incision when patient coughs and encourage early ambulation
• Promote adequate nutrition – NPO until peristalsis returns
• Monitor for early satiety and regurgitation
• Eating less food at a slower pace
• Monitor weight regularly
• Prevent potential complications and monitor nasogastric tube drainage
• Prevent unnecessary irrigation or repositioning of the NGT

Dumping Syndrome

• Group of unpleasant vasomotor and GI symptoms caused by rapid emptying of gastric content into the jejunum, resulting in shock-like manifestations

Pathophysiology of Dumping Syndrome

• Rapid emptying of hypertonic food from the stomach to the jejunum causes fluid shift from the bloodstream to the jejunum, resulting in shock-like manifestations

Signs and Symptoms of Dumping Syndrome

• Occur 5 to 30 minutes after eating and include weakness, tachycardia, dizziness, diaphoresis, pallor, feeling of fullness or discomfort, nausea, abdominal cramps, and diarrhea
• Occur 2 to 3 hours after eating; initially, hyperglycemia occurs that leads to hypoglycemia

Collaborative Management for Patients with Dumping Syndrome

• Slow down emptying of gastric content
• Eat in a lying/recumbent position
• Place the patient in the left side-lying position after a meal
• Give small, frequent feedings
• Provide high-protein diet
• Limit carbohydrates
• Take fluid after meals or in-between meals and avoid very hot and very cold foods and beverages
• Administer anticholinergic or antispasmodic 30 minutes before meals

Marginal Ulcers

• Gastric acids come in contact with the area of anastomosis with duodenum or jejunum

Alkaline Reflux Gastritis

• Caused by a reflux of duodenal contents

Vitamin B12 Deficiency

• Partial or total loss of the intrinsic factor secreted by the parietal cells of the stomach

Viral and Bacterial Infections: Gastroenteritis

• Inflammation of the stomach and intestinal tract that primarily affects the small bowel

Risk Factors for Gastroenteritis

• Pathogens that cause GI disease are transmitted by fecal-oral route from person to person and contaminated food and water
• Bacterial sources of contaminated foods are eggs, raw or undercooked meat, and chicken
• Outbreaks of food-borne viral infections are almost entirely caused by fecal-contaminated shellfish
• Additional causes include unpasteurized milk, apple juice, ice cream, vibro cholerae, shigella bacilli and staphylococcus aureus

Clinical Manifestations of Gastroenteritis

• Diarrhea, abdominal pain and cramping, nausea and vomiting, fever, anorexia, abdominal distention, tenesmus, borborygmi, and stool tests positive for leukocytes

Health Promotion for Avoiding Gastroenteritis

• Good handwashing technique after defecation and before handling food
• Available vaccinations against bacterial and viral gastroenteritis
• Cleanliness and sanitation along with proper food handling, preparation and storage techniques
• Avoid antibiotics
• Follow practices for safe food
• Self-manage manifestations

Appendicitis

• Inflammation of the vermiform appendix caused by obstruction of the appendix by fecalith, foreign bodies, or infection
• Other causes are low fiber diet, high intake of refined carbohydrates, kinking of the appendix, swelling of the bowel wall

Clinical Manifestations of Appendicitis:

• Acute abdominal pain in the epigastric or umbilical region that usually starts
• Anorexia, nausea, and vomiting
• Rigid abdomen and guarding
• Rebound tenderness
• Psoas sign
• Obturator sign
• Rovsing's sign
• Dunphy's sign
• Fever and leukocytosis
• Decreased or absent bowel sounds

Collaborative Management for Patients with Appendicitis

• Bed rest to reduce peristalsis and prevent rupture of the appendicitis
• Maintain NPO
• Relieve pain with cold application over the abdomen;
• Avoid factors that increase peristalsis: heat application, laxatives, and enemas
• Maintain fluid and electrolyte balance, control infection, surgery

If Appendicitis Ruptured

• The client may experience peritonitis, and a Penrose drain is inserted and the nurse should place the client in semi-Fowler's position to promote drainage

Peritonitis

• Inflammation of the peritoneum caused by: Ruptured appendicitis, perforated peptic ulcer, diverticulitis, pelvic inflammatory disease, urinary tract infection, trauma, bowel obstruction, bacterial invasion

Peritonitis Problems

• Adhesions, abscess formation, intestinal obstruction, and hypovolemia:
• Ineffective peristalsis because: Fluid shifts into the abdominal cavity and the bowel, distends with gas and fluid

Clinical Manifestations of Peritonitis

• Abdominal pain and tenderness, abdominal guarding and rigidity, abdominal distention, paralytic ileus, fever, elevated wbc, nausea and vomiting, and signs of early shock

Collaborative Management for Patients with Peritonitis

• Monitor vital signs, provide a nasogastric tube, and bed rest in semi-Fowler's position
• Encourage deep breathing
• Peritoneal lavage is often ordered
• Insertion of drainage tubes and also fluids, electrolytes and colloid replacement are needed
• Antibiotics

Diverticulitis

• Acute inflammation and infection caused by trapped fecal material and bacteria in an outpouching

Diverticulum

• Single outpouching of the mucosal lining
• Diverticula (diverticulosis) are multiple outpouchings of the mucosal lining
• The most common cause of diverticulitis is low fiber diet
• Pathophysiology: Low fiber diet causes low fecal volume causing a need for increased contractions which decreases muscle strength in the colon causing herniations

Clinical Manifestations of Diverticulitis

• Crampy abdominal pain in the left, lower quadrant, chronic constipation, episodes of diarrhea, low grade fever, nausea and vomiting, abdominal distention and tenderness, occult bleeding

Collaborative Management for Patients with Diverticulitis

• High fiber diet to increase bulk of the feces and promote peristalsis, liberal fluid intake, avoid nuts and seeds, and bulk-forming laxatives
• During an acute episode: Bed rest, NPO, clear liquids
• Avoid high fiber foods to prevent further irritation of the colonic mucosa
• IV fluids, antibiotics, antispasmodic/anticholinergics, NGT insertion.
• Weight reduction, if obese