Transcript Nursing Care of Patients with Alterations in the GI tract

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
Stomach
Function:
Parietal cells secrete HCL acid and intrinsic factor, which absorbs
B 12, without it, what anemia can occur?
Chief cells secrete Pepsinogenpepsin
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–
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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- CA199 and CEA, used to
monitor for cancer in the
GI tract
• Ca- decreased in
malabsorption
• K – decreased with
vomiting, diarrhea
• Xylose absorptiondecreased indicates
possible malabsorption in
the small intesting
• Stool for Occult blood
• Stool for ova and
parasite- infection
• Stool for fecal fatincreased with Crohn’s
disease and
malabsorption
Radiology
• Abdominal films- air in bowel and
masses
• Upper GI and small bowelpharynx 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:
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–
–
–
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, Badrenergic 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
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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 backdiffusion 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
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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
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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:
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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, tenesmusuncontrolled 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.