Nursing Care of Patients with Alterations in the GI tract

C. Cummings RN,EdD

A & P of GI system

GI tract

• Hollow muscular tube, lumen surrounded by 4 tissue layers:– Mucosa- innermost, thin layer of smooth muscle

and exocrine cells– Submucosa- connective tissue– Muscularis- smooth muscle– Serosa- outermost, connective tissue

GI tract

• Function:– Secretion- secretes HCL acid, digestive enzymes– Digestion- mechanical and chemical, food is

broken down to chyme– Absorption- from GI tract to blood supply– Motility– Elimination

GI tract

• Nerve Supply– Intrinsic stimulation by myenteric plexus in smooth

muscle and submucosa plexus in inner layer– Autonomic system- Parasympathetic stimulation

by vagus nerve, connects with intrinsic system• Vagus-stimulates motor and secretory activity and

relaxes spinchters– Sympathetic system- thoracic and lumbar

splanchnic nerves slows movement, inhibits secretions and contracts spinchters

Nerves of GI tract

Mouth• Function:

– Mastication, taste, begin movement– Glands produce 1 L of saliva/day– Saliva contains mucin and salivary amylase with begins to break

down CHO– Oral preparatory phase- food is softened, made into a “bolus”

and tongue moves to the back of the mouth– Oral phase- tongue presses bolus against hard palate, elevates

the larynx and forces the food bolus to the pharynx, triggering swallowing

– Pharyngeal phase- soft palate elevates and seals nasal cavity, inhibits respirations and allows esophagus to open

– Esophageal phase- is when bolus enter at cricopharyngeal juncture, peristalsis now takes food to the stomach

– All this takes about 10 seconds !

Esophagus• Canal about 10 in long, passes through the center of the

diaphragm• Upper end is the upper esophageal sphincter, at rest it is

closed to prevent air from entering the esophagus• Lower end is the lower esophageal sphincter, it sits at the

gastroesophageal junction, at rest it is closed to prevent reflux of gastric contents, this is where GERD occurs

• Function- to propel food and fluids and prevent reflux• Mucous is secreted to move the food along• Cardiac sphincter of the stomach opens to allow the food to

enter

Stomach• Digestive and endocrine organ, in midline and LUQ• Four regions:

– Cardia- narrow part that is distal to the gastroesophageal junction

– Fundus- left above the GE junction– Body or corpus- largest area– Antrum- pylorus, is the distal portion and is separated from the

duodenum by the pyloric sphincter, prevents backflow from the duodenum

– Surface is covered in rugae or folds and have smooth muscle for motility

– Has intrinsic and extrinsic nerves

StomachFunction:

Parietal cells secrete HCL acid and intrinsic factor, which absorbs B 12, without it, what anemia can occur?

Chief cells secrete Pepsinogenpepsin Cephalic phase- sight, smell and taste of food, regulated by vagus,

begin secretory and contractile activity Gastric phase- G cells in the antrum secrete gastrin, which causes

HCL and pepsinogen to be released. HCL changes pepsinogen to pepsin, which digest proteins. Mucous and Bicarb are secreted to protect the stomach wall

Intestinal phase- chyme produced empties into the duodenum and causes distention, this produces secretin, which stops the acid production and gastric motility !

Stomach

Small Intestine

• Longest portion of the GI tract, 16-19 ft.• Made up of 3 sections:

– Duodenum- first 12” and is attached to the pylorus. The CVD and pancreatic duct join to form the ampulla of Vater and empty into the duodenum at the duodenal papilla. This surrounded by a muscle, called the Sphincter of Oddi

– Jejunum- middle 8 ft portion– Ileum- last 8-12 ft. The ileocecal valve separates the ileum form

the cecum of the large intestine– Inner lining is made up of intestinal villi and folds of mucosa and

submucosa for digestion.

Small Intestine

• 3 main functions:– Movement- mixing and peristalsis

• Moves chyme by segmental contractions and mixes with enzymes

– Digestion- enzymes produced by the intestinal cells make:

• Enterokinase, peptidases, lactase, maltase and sucrase• Help to digest, CHO, proteins and lipids

– Absorption- absorbs most of the nutrients from food, takes 3-10 hours for the contents to pass through

• Major organ for absorption

Small intestine

Large Intestine

• Ileocecal valve to the anus, 5-6’, lined with columnar epithelium tha thas absorptive and mucous cells.

• Cecum- is the beginning, dilated pouch like structure, appendix is attached to the base

• Colon has 4 divisions:– Ascending, transverse, descending and sigmoid

• Rectum- last 6-8” to the sphincter muscles and anus

Large Intestine

• Function:– Movement- segmental contractions, to allow time

for the water and electrolytes to be absorbed– Absorption- absorbs most of water and

electrolytes, reduces fluid volume of chyme and creates a more solid mass for elimination

– Elimination- 3-4 strong peristaltic contraction /day triggered by colonic distention in proximal large intestine to propel contents to rectum, until urge to defecate.

Nursing Assessment• Family history- GI disorders, cancer• Personal history- what kinds of things?• Diet history- anorexia, dyspepsia- what is that? What

should you question them on for diet history?• Health history- diarrhea, constipation, # and color of

stools, change in wt. or appetite• Abdominal pain-

– P- precipitating– Q-quality- how intense, severe, type– R-region or radiation– S- severity scale- 0-10– T-timing- when did it first occur, duration and frequency

Physical Assessment

• Abdomen:– Inspection- skin, symmetry, rashes, lesions, scars– Auscultation- all four quadrants, normally heard in

5-15 seconds, normal, hypoactive or hyperactive, listen 1 full minute. What is borborygmus? Why would bruits be heard? Why would there not be bowel sounds heard?

– Percussion- tympanic- air filled, dull- organ– Palpation- light and deep palpation, masses,

tenderness, look for guarding

Lab tests• CBC- anemia• Oncofetal antigens- CA19-

9 and CEA, used to monitor for cancer in the GI tract

• Ca- decreased in malabsorption

• K – decreased with vomiting, diarrhea

• Xylose absorption- decreased indicates possible malabsorption in the small intesting

• Stool for Occult blood• Stool for ova and

parasite- infection• Stool for fecal fat-

increased with Crohn’s disease and malabsorption

Radiology• Abdominal films- air in bowel and

masses• Upper GI and small bowel-

pharynx to duodenojejunal junction, barium swallow and SBFT– NPO 8 hours before, drink

barium, then lie, stand and turn in multiple directions to view movement of barium

– SBFT- drink more barium and view passage

– After drink fluids to pass barium

• Barium enema– Large intestine, done for

obstructions, masses, not done is perforated colon or fistulas

– Only clear liquids for 12-24 hours prior, NPO, given bowel prep like Golytely

– Insert rectal catheter with a balloon and give 500-1500 ml of barium and hold

– Can be uncomfortable, must take a laxative after

UGI exam

Diagnostic Tests• EGD- esophagogastroduodenoscopy• Visualize esophagus to duodenum, NPO prior, given versed

and fentanyl, maybe cetacaine to inhibit gag reflex, pass tube and visualize structures, can take biopsies

• Gag reflex may not return for 1-2 hours after, so no eating or drinking until then

• Colonoscopy- large bowel, take biopsies and remove polyps, have a bowel prep prior, given versed and fentanyl prior; Capsule enteroscopy is now done to visualize, apply a data recorder to the abdomen and the patient swallows the capsule

• Proctosigmoidoscopy- like colonoscopy, only a rigid tube, less invasive and does not require the cleansing of the colonoscopy

Colonoscopy

Case Study

• 72 year old male admitted with chest pain and nausea. He states that he awakens in the night with pain in his chest and nausea.

• What would you do first to evaluate his condition?

• What diseases could he have?• What kind of lab work would you like to

obtain?• What past medical history do you need?

Case Study• Your patient starts to

have hematemesis.• What does this mean?• Is this life-threatening?• What interventions

should be done?• What could have caused

this condition?

Case Study

• It is determined that your patient can be treated non-surgically. What medications would be given? (should have 3)

• What type of teaching would be done for prevention?

• If he needed surgery, what could have been done?

Esophageal Problems

• GERD- gastroesophageal reflux disease• Reflux causes esophageal mucosa to be irritated by the

effects of gastric and duodenal contents, results in inflammation

• Causes:– Inappropriate relaxation of the LES, sphincter tone is decreased– Irritation from refluxed material– Delayed gastric emptying, gastric volume or intra-abdominal

pressure is increased– Abnormal esophageal clearance

GERD

• Refluxed material has a pH of 1.5-2, whereas the esophagus normally has a pH of 6-8 erosive esophagitis, once inflammed, the mucosa can’t eliminate the material as quickly. This leads to increased blood flow and more erosion. Gastric acid and Pepsin cause the tissue injury.

• Can lead to Barrett’s epithelium- thicker, but can be cancerous, can also cause hemorrhage, aspiration pneumonia, asthma, laryngitis and dental deterioration.

GERD

GERD

• Physical Manifestations:– Dyspepsia- heartburn, substernal or retrosternal

burning that moves up and down in wavelike fashion, pain may radiate to neck or jaw or back, worsens when bends over, strains or lies on their back, occurs after meals and last 1-2 hours, helped by fluids and staying upright

– Regurgitation- food entering throat without nausea, watch for cough, hoarseness or wheezing

– Hypersalivation- water brash in response to reflux, fluid without sour or bitter taste

GERD • Physical Manifestations

– Dysphagia and Odynophagia- difficulty swallowing, esophagus may be narrowed by inflammation or tumor, odynophagia- means what?

– Chronic cough, mostly at night– Atypical chest pain– Belching and flatulence or bloating

• Diagnosis:– Endoscopy, 24 hour ambulatory pH monitoring- pass a

small tube into esophagus and monitor pH levels

GERD

• Nursing Diagnoses:– What diagnoses would apply to these patients?– 1.– 2.– 3.

• Interventions:– Diet therapy- what type of dietary modifications would be

appropriate? – Certain foods decrease LES pressure- chocolate, fat and mints.

Also, smoking and alcohol decrease– Spicy foods irritate the esophagus and Carbonated can increase

gastric pressure

GERD

• Lifestyle changes: – How should they sleep?– What things increase intra-abdominal pressure?

• Drug therapy:– Goal is to inhibit gastric acid secretion, accelerate

gastric emptying and protect the gastric mucosa– Antacids:

• Elevate the pH and deactivate pepsin, good for heartburn, take 1 hour before and 2-3 hr after a meal

• Name 2 antacids.

GERD

• Drug therapy:– Histamine Receptor Antagonists

• Decrease acid, help promote healing of the esophagus• Name 2 common ones sold OTC (generic ends in

“dine”)– Proton Pump Inhibitors

• Main treatment for GERD, long acting inhibition of gastric acid secretions by inhibiting protom pump of parietal cell, can reduce by 90%/ day

• Name 2 proton pump inhibitors (generic ends in “zole”)

GERD• Other therapies:

– Consider medications that may lower LES pressure- oral contraceptives, anticholinergics, sedative, tranquilizers, B-adrenergic agonists, nitrates and Ca channel blockers

– Prokinetic drugs- for emptying and peristalsis- metoclopramide (reglan)

– Endoscopic: • Enteryx procedure- spongy material in LES to tighten it Stretta

procedure- radiofrequency energy through needles to inhibit the vagus nerve

– Surgical:• Laparoscopic Nissen Fundoplication• Angelchik esophageal antireflux- anchors the LES in the abdomen

to increase sphincter pressure

Hiatal Hernia• Protrusion of stomach through the esophagus• Sliding or Rolling hernias• Symptoms are similar to GERD patient• Nonsurgical management is like GERD• Surgical:

– Lap Nissen Fundoplication- reinforces the LES, wraps a portion of the stomach around the distal esophagus to anchor it

– Post op- risk for bleeding, infection and respiratory complications

• Have an NGT, begin PO once BS return• Watch for gas-bloat syndrome and air swallowing

Nursing Diagnosis: GERD

• Impaired Nutrition: less than body requirements– What things can be done to improve their intake and decrease

pain?– What would be the expected outcomes?– How would you monitor their progress?

• Acute Pain r/t irritation of the esophagus– What interventions can be performed?

• Risk for aspiration r/t reflux of gastric contents– How can you determine that this does not occur?

Peptic Ulcer Disease

• Mucosal lesion of the stomach or duodenum• Peptic can be gastric or duodenal• PUD- gastric mucosal defenses become

impaired and they can no longer protect the epithelium from acid and pepsin

• Three main types of ulcers:– Gastric– Duodenal– Stress

Peptic Ulcers

Gastric Ulcers• Gastric mucosa is protected by mucous and bicarbonate

that maintain a normal pH on the gastric tissue and protects it from acid

• Gastromucosal prostaglandins increase the barrier’s resistance to ulceration by producing mucous

• Integrity is improved by a rich blood supply to the mucosa

• If there is a break in the mucosal barrier, HCL acid damages the epithelium. Gastric ulcers result from back-diffusion of acid or dysfunction of the pyloric sphincter.

Gastric Ulcers

• If the pyloric sphincter doesn’t function, bile backs up into the stomach, produces H+ ion back diffusion and mucosal inflammation

• Toxic agents and bile destroy the lipid plasma membrane of the mucosa. Delayed gastric emptying also affects. What drug can be given to improve emptying?

• Gastric Ulcers are deep and penetrating and usually are in the lesser curvature of the stomach, near the pylorus

Duodenal Ulcers• Occur in the first portion of the duodenum.• Deep lesions that penetrate through the mucosa and submucosa into

the muscle layer. The floor of the ulcer consists of a necrotic area on granulation tissue and surrounded by fibrosis

• High gastric acid secretion, pH levels are low for long periods• Protein rich meals, calcium and vagal excitation stimulate acid

secretion• Hypersecretion, rapid emptying of food from stomach reduces the

buffering effect of food and delivers a large acid bolus to the duodenum

• Inhibitory secretory mechanisms and pancreatic secretion may be insufficient to control the acid

• Many patients have H. pylori infection. H. pylori produces urease changes urea to ammonia, H+ ions released contribute to damage

Stress Ulcers

• Acute gastric mucosal lesions occurring after and acute medical crisis or trauma

• Associated with head injury, major surgery, burns, respiratory failure, shock and sepsis

• Bleeding is the principle manifestation• Multifocal areas often in the proximal portion

of the stomach and duodenum• Usually elevated HCL acid levels and hospital

stay longer than 11 days

Complications of Ulcers

• Hemorrhage:– 15-25% of patients with PUD, most serious

complication– Most often with gastric ulcers and elderly– After initial bleed, 40% have a recurrence if

untreated, especially if H. pylori untreated and no H2 antagonist

– Have Hematemesis- bleeding at or above the duodenojejunal junction

– Smaller amounts of bleeding are seen as melena, more often seen in duodenal ulcers, stool may appear black.

Complications of Ulcers• Perforation

– Gastric or duodenal may perforate or bleed– Stomach or duodenal contents can leak into the abdomen, acid

peptic juice, bile and pancreatic juice empty through the anterior wall of the stomach into the peritoneal cavity

– Sudden, sharp pain in midepigastric region and spread over the abdomen

– Amount of pain correlates with the amount and type of GI contents spilled

– Abdomen is tender, rigid and boardlike, go into a fetal position to decrease tension of abdomen

– Chemical peritonitis, bacterial septicemia and hypovolemic shock follow paralytic ileus and possible death

Perforated ulcer

Complications of Ulcers

• Pyloric obstruction– Small number of patients, vomiting caused by

stasis and gastric dilation– Obstruction occurs at the pylorus and is caused by

scarring, edema, and/or inflammation– Gastric outlet obstruction abdominal bloating,

nausea and vomiting– May go into metabolic alkalosis from loss of large

quantities of acid gastric juice (H+ and Cl-)– Hypokalemia may result from the vomiting

Complications of Ulcers

• Intractable disease– Disease may recur throughout life, stressors, inability to adhere

to therapy, no longer responds to management• Cause:

– Use of NSAID’s- break down the mucosal barrier and disrupt the protection by COX inhibition. Cause the depletion of prostaglandins, have a high rate of recurrence

– Drugs such as Theophylline, corticosteroids and caffeine stimulate HCL acid production

– H pylori infection is transmitted person to person– 50% of people with PUD have a first or second line relative with

PUD, usually the same type of ulcer

Physical Manifestations• Epigastric tenderness, midline between the umbilicus

and xiphoid process• May begin as hyperactive BS, then diminish if perforation• Dyspepsia- discomfort around the epigastrium, sharp,

burning or gnawing– Gastric- occurs in upper epigastrium with localization to the left

of the midline and may be relieved by food– Duodenal- located to the right of the epigastrium, occurs 90 min

to 3 hours after eating and awaken at night, may be aggravated by spicy foods, onions, alcohol, caffeine and ASA, NSAIDS

Physical Manifestations

• Vomiting may occur• Appetite is maintained, unless pyloric obstruction occurs• Fluid volume deficit, if bleeding, take orthostatic BPs• Watch for Hematemesis and melena• Monitor H & H• Dx- barium swallow and EGD• Test for H. pylori is IgG serologic testing and urea breath

testing

Nursing Diagnoses

• Name 5 diagnoses r/t PUD• 1.• 2.• 3.• 4.• 5.• What would be an expected outcome for this

disorder?

Nursing Interventions

• Drug Therapy– Goals: Provide pain relief, eradicate H. pylori, heal

ulcerations, prevent recurrence– Eliminate H. pylori- triple treatment:

• Bismuth product (pepto-bismol) or a a proton pump inhibitor and two antibiotics (metronidazole (Flagyl) and tetracycline or amoxicillin)

• May have to take medications 4 x’s/day for 14 days and often they don’t complete the series

Nursing Interventions

• Drug therapy:– Hyposecretory drugs- reduce gastric acid

secretions• Antisecretory agents- proton pump inhibitors, “zole”

ending, suppress H, K-ATP ase enzyme system of gastric acid production, can be given IV or PO

• H2 receptor antagonists- block histamine-stimulated gastric secretions, “dine” ending

• Prostaglandin analogues- reduce gastric acid secretion and enhance gastric mucosal resistance to tissue injury, Misoprostol (Cytotec) helps prevent NSAID induced ulcers, does cause uterine contraction and can not be given to pregnant women

Nursing Interventions• Antacids

– Buffer gastric acid and prevent formation of pepsin, heal duodenal ulcers

– Aluminum hydroxides and magnesium hydroxide, may affect those with renal impairment

– Take 2 hours after meals to reduce the H+ion load– Calcium carbonate (TUMS) is an antacid, but it triggers gastrin

release and causes a rebound acid secretion– Antacids can interact with other drugs- tetracycline, dilantin,

also may have a high sodium content• Mucosal Barrier fortifiers- sucralfate (Carafate) supplies

a protect coating by forming a complex with proteins, binds with bile acids and pepsin, should be given on an empty stomach and not within 1 hour of eating or taking antacids

Nursing Interventions

• Diet therapy– Bland diet may help to relieve symptoms– Food may help to neutralize acids, rebound may

follow when more acid is released– Avoid foods that stimulate gastric acid release– They are??– Yoga for stress relief, herbals, such as licorice and

vitamins may help

Gastrointestinal Bleeding

• What would be a nursing diagnosis for GI Bleeding?

• 1.• 2.• What would be the expected outcome and

how would you know that this was met?

GI bleeding

Gastrointestinal Bleeding

• Hypovolemia Management– Monitor vital signs and I&O, assess for bleeding

and vomiting, monitor CBC– Fluid and electrolyte replacement is necessary,

usually NSS or LR, may give PRBC’s or FFP– Watch for signs of shock, what are they??

• Bleeding reduction– Monitor labs, insert and NGT to decompress the

stomach, give an H2 blocker, may need gastric lavage, what is that??

Nursing Interventions for GI bleeding

• Endoscopic therapy– EGD, can do: – cautery on the bleeding sites – inject a sclerosing agent with diluted epipherine– Laser therapy– Clip the bleeding vessel

• Somastatin Analogue- Sandostatin may be used to suppress gastric acid secretion on parietal and chief cells, vasoconstricts the splanchnic arteries which reduce hemorrhage

Surgical management of GI bleeding

• MIG- minimally invasive gastrectomy- laproscopic to remove chronic gastric ulcer or treat hemorrhage, make several small incisions, may partially remove the stomach and/or vagotomy to control acid secretion

• Gastroenterostomy- creates a passage between the body of the stomach and jejunum, reduces motor activity in the pyloroduodenal area, diverts acid, a vagotomy may be done with it to decrease secretion. Can do truncal, selective or proximal. Billroth I- connect to duodenum, Billroth II connects to jejunum

• Pyloroplasty- widens the exit of the pylorus and empties the stomach

Billroth 1

Postop care for GI surgery

• NGT management• Monitor for complications of:

– Dumping syndrome- vasomotor symptoms, rapid emptying of gastric contents into the small intestine, shifts fluid into the gut and cause abdominal distention, 30 min after eating have vertigo, tachycardia, syncope, sweating, pallor, palpitations. 90 min later have excessive amount of insulin released, this dizziness, palpitations, diaphoresis and confusion

– Should eat smaller amounts, take less liquid with food, high protein and fat, low CHO diet, sandostatin may be given and pectin with food

Postop Care of GI surgery• Reflux gastropathy- bile reflux, when pylorus is

bypassed, bile in stomach and have abdominal discomfort and vomiting

• Delayed gastric emptying- usually resolves in 1 week, edema at the anastomosis or adhesions may occur, hypokalemia, hypoproteinemia and hyponatremia may also cause

• Afferent loop syndrome- duodenal loop is partially obstructed, pancreatic and biliary secretions fill the intestinal loop, it becomes distended painful contractions, bloating and pain 20-60 min after eating

Post op GI surgery

• Recurrent ulceration- occurs in 5% of patients, may have ulcers at the anastomosis

• Nutritional management:– Deficiencies of B12, folic acid and iron– Impaired Ca metabolism and reduced absorption of Ca and

vitamin D– Shortage of intrinsic factor, r/t the resection and rapid emptying

of the food– pernicious anemia- weak, anemic, atrophic glossitis- beefy

shiny tongue– Give back B12 and folic acid

Pernicious anemia

Irritable Bowel Syndrome

• Chronic GI disorder, with chronic or recurrent diarrhea, constipation, abdominal pain and bloating

• Spastic colon, impairment of the motor/sensory function diarrhea alternating with constipation

• Usually begin as a young adult• Stress, anxiety and familial factors may

predispose patient

IBS

• Assessment:– History of bowel pattern– Manning criteria- abdominal pain relieved by

defection, abdominal distention, sensation of incomplete evacuation of stool, presence of mucus with the stool

– Pain in LLQ and cramps, may be tenderness and air in bowels

– Dx- flexible sigmoidoscopy or colonoscopy if >40– Barium enema

IBS

• Interventions– Diet therapy- limit caffeine, alcohol, beverages

with sorbitol, take in fiber and bulk, 30-40 gm/day– Drug therapy:

• Bulk forming laxatives (Metamucil) • antidiarrheals (loperamide) • anticholinergics (bentyl)• antidepressants (elavil) • 5-HT4 agonists(Zelnorm) for prokinetic activity, imitates

serotonin to stimulate peristalsis– Stress management- relaxation techniques

Nursing Diagnoses

• Constipation r/t low residue diet and stress– What can be done to manage this?

• Diarrhea r/t increased motility of intestines– How can this be corrected or treated?

• What can be done to correct constipation and impaction?

• What role may analgesics play in constipation?

Colorectal Cancer• 95% are adenocarcinomas, most come from

adenomatous polyps • 2/3 occur in rectosigmoid region• Can metastasize through blood and lymph, liver most

common site with 15-30% spread there, can also go to the lungs, brain, bones and adrenals

• May form fistulas into bladder and vagina• Genetics- autosomal dominant disorder- familial

adenomatous polyposis only 1%, 100% malignant, usually starting at age 20. Also, hereditary nonpolyposis colorectal cancer- autosomal dominant, 10% of cancers, develop by age 45

Colorectal cancer

• 75% have no known cause• Age is a risk factor• Dietary- decreased bowel emptying time,

foods with carcinogens- red meat, fatty food, fried meats and fish, concentrated sweets

• High fat diet increases bile acid secretion and anaerobic bacteria

• Irritable bowel diseases• Third most common malignancy

Colorectal Cancer

Colorectal cancer

• Manifestations:– Rectal bleeding, anemia and change in stool– Gas pains, cramping or incomplete evacuation– Hematochezia- bright red blood when in rectum– Tumors can grow large when in upper abdomen,

mostly liquid stool, more pain when in lower– Tests- stool for occult blood, CEA, barium enema,

CT of abdomen– Colonoscopy or sigmoidoscopy

Colorectal cancer

• Nursing Diagnoses- Name 4 diagnoses, associated with colorectal cancer

• 1.• 2.• 3.• 4.• What would be the expected outcomes?

Colorectal cancer• Nonsurgical management:

– Duke’s staging classification• A- tumor has penetrated into, but not through the bowel wall• B- tumor has penetrated through the bowel wall• C-tumor has penetrated through the bowel wall and there is

lymph node involvement• D- tumor has metastasized to distant sites

• Radiation therapy• Drug therapy- chemotherapy IV 5-FU and leucovorin,

side effects are diarrhea, mucositis, leucopenia and mouth ulcers– Eloxatin, Camptosar, Avastin are also being used, along with

monoclonal antibodies- cetuximab

Colorectal cancer

• Surgical management:– Colon resection- removal of tumor and lymph

nodes– Colectomy- colon removal– Abdominal perineal resection- removes sigmoid

colon, rectum and anus, colostomy is performed– Colostomies may be ascending, descending,

sigmoid, transverse or double barreled– Stool returned depends on the site of the

colostomy

Colostomy

Colorectal cancer

• Postoperative Care:– Colostomy management

• What types of nursing diagnoses may accompany this procedure?

• How should the stoma appear?• Report any bleeding, breakdown of the sutures from

the wall and signs of ischemia or necrosis– Wound care management- JP drains, monitor for

infection– Fluid volume deficit and electrolyte imbalance

Colorectal cancer

• Teaching:– Colostomy care- what kinds of things should be

covered?– Dietary measures to control stool and gas, what

would they be?– Psychological adjustment to the colostomy, what

diagnosis relates to this?– Grief and family coping- what resources may be

needed?– Genetic testing if familial type

Intestinal Obstruction

• Partial or complete• Mechanical- bowel is physically obstructed by adhesions,

tumors• Nonmechanical- paralytic ileus or adynamic ileus,

neuromuscular distrubance- slow movement or backup• Contents accumulate at or above the obstruction

distention, peristalsis increases to aid movement, stimulates more secretions more distention edema of the bowel, increased capillary permeability

Intestinal Obstruction

• Plasma leaks into the peritoneal cavity and trapped fluid decreases the absorption of fluid and electrolytes into the vascular space reduced blood volume and electrolyte imbalances, can hypovolemic shock

• Can also lead to metabolic alkalosis if high and there is a loss of gastric acid, if low, metabolic acidosis occurs with the loss of alkaline fluids

• Bacterial peritonitis and septic shock can also occur from the release of endotoxins

Intestinal obstruction

Intestinal Obstruction

• Adhesions account for 45-60%, r/t scar tissue• Intussusception- telescoping bowel and

volvulus- twisting of the bowel• Paralytic ileus- decreased peristalsis from

trauma, toxin or autonomic, can result from surgery, MI’s, rib fracture, pneumonia, peritonitis and vascular insufficiency from heart failure or shock

Intestinal Obstruction

• Assessment:– History of symptoms and occurrence– Abdominal pain and cramping– Obstipation, vomiting with brown and foul

smelling– Borborygni above the obstruction, then absent– Abdominal distention and tympanic abdomen– Abdominal films and CT of abdomen– WBC elevated in some cases

Intestinal Obstruction

• Nonsurgical management:– NGT to decompress to LCS– Nasointestinal tubes- Miller-Abbott, mercury balloons and

migrate down the intestine by peristalsis, don’t irrigate with fluid- it will increase edema at the obstruction

– Fluid and electrolyte replacement- NPO, give NSS or LR, replace K

– Pain control- not normally given opioids, mask pain and peritonitis

– Antibiotics if suspect perforation• Surgical management:

– Exploratory laparotomy

Case Study

• 24 year old female admitted with frequent bloody diarrhea stools, weight loss and anemia.

• What do you suspect?• What labwork should you do?• What treatment may be needed?

Case Study• Your patient tells you that

the diarrhea has been occurring for months.

• How do you differentiate between U.C. and Crohn’s disease?

• What may be her treatment options?

Case Study• How do you help your

patient decide about a colostomy?

• If she does want a colostomy, what type of teaching needs to be done?

Chronic Inflammatory Bowel Disease

• Ulcerative Colitis and Crohn’s • Ulcerative Colitis:

– Remissions and exacerbations– Loose stools with blood and mucous 10-20/day– Poor absorption of nutrients and thickening of the

colon wall– Abdominal distention and cramping– Complications are: hemorrhage, perforation,

fistulas and nutritional deficiencies– May be familial tendency, inflammation r/t

response to normal flora

Ulcerative Colitis

Chronic Inflammatory Bowel Disease

• Crohn’s disease– Terminal ileum, patching involvement through all

layers of the bowel– Deep fissures and ulcers occur– 5-8 loose stools/day, rarely bloody– Complications are:

• Fistulas, nutritional deficiencies– Cause is thought to be mycobacterium

paratuberculosis, genetic predisposition

Crohn’s Disease

Garrard Crohn's story

Ulcerative Colitis

• Manifestations:– Abdominal pain, bloody diarrhea, tenesmus-

uncontrolled straining– Dx- barium enema

• Nursing Diagnoses:– Diarrhea r/t inflammation of the bowel– Acute and chronic pain– Imbalance nutrition: less than body requirements– Disturbed body image

Ulcerative Colitis

• Diarrhea management-– Drugs- salicylate compounds- Sulfasalazine

(Azulfidine) inhibits prostaglandins to reduce inflammation, also use Asacol, Pentasa

– Corticosteroids- Prednisone to decrease edema– Immunosuppressive- cyclosporine– Antidiarrheals– Monoclonal antibody- Remicade neutralizes the

activity of tumor necrosis factor and prevents toxic megacolon

Ulcerative Colitis

• Diet therapy:– NPO at first, then TPN, may have low fiber or low

residue, what foods would be included?• Surgical management:

– Total Proctocolectomy with permanent Ileostomy– Total colectomy with a continent ileostomy– Total colectomy with ileoanal anastomosis and

ileoanal reservoir or pouch• Postop- teaching for ostomy, pain control and

monitoring for GI bleeding and fluid volume deficit

Crohn’s Disease• Aggravated by bacterial infection, inflammation and

smoking• History of fever, abdominal pain and loose stools, weight

loss• Steatorrhea is common- fatty stools• Fistulas may occur between bladder and vagina• Drug therapy- same as UC, except may take

metronidazole if fistulas and imuran as an immunosuppressant

• Diet therapy- may be on TPN, supplements like ensure, vivonex

Crohn’s Disease

• Monitor for fistulas- infections, skin problems, malnutrition, fluid and electrolyte imbalances

• Fluid and electrolyte therapy- what would this entail?

• Name one antidiarrheal.• Surgical management:

– Bowel resections– Fistula repairs– Ileostomies may also be required to rest the bowel

or repair damaged areas.