Managing Clients Experiencing Problems of the ▫ Low-residue diet 1-2 days b4 exam

Gastrointestinal ▫ Clear liquid diet day b4

I. Diagnostic Testing- Chapter 34 ▫ Laxative evening b4
A. Laboratory studies ▫ NPO after midnight
1. Serum proteins: ▫ Enemas till clear in AM
▫ Albumin, prealbumin, retinol-binding protein, & c. Nursing Care:
transferrin ▫ Always schedule barium enema BEFORE UGI
2. Total lymphocyte count (TLC) series exacuate barium first ….upi first mess up lgi
▫ Below 1800/mm3 suggests malnutrition d. Post-procedure: Encourage increased fluid &
3. Nitrogen Balance assess BM for elimination of barium
▫ Record all calories& all urine for 24 hours (4-6Gm) 9. Endoscopic Examination directly looking at
▫ Negative values indicate catabolic states or increased inner lumen
nutritional requirements a. Esophagogastroduodenoscopy (EGD) down
4. Carcinoembryonic Antigen (CEA)- “tumor marker” esphg 11 ;(
▫ Increased in colorectal cancer & inflammatory bowel b. Colonoscopy
disease c. Proctoscopy/Sigmoidoscopy
5. Fecal Analysis d. Small-bowel Enteroscopy
 Cultures 10. Esophagogastroduodenoscopy (EGD)- Direct
 Ova& parasites visualization of internal structures of upper GI using
 Occult Blood-guiac, Hemocult gastroscope & may obtain specimens
 Color a.Pre-procedure
 Blood on or within  NPO 8 hours prior to exam
 Lipids  Given a local anesthetic gargle or spray to numb
 Odor throatØnumb gag reflex
 Consistency  IV Midazolam (Versed) provides moderate sedation
6. Gastric Analysis & relieves anxiety
a. Measures secretion of HCl & Pepsin in the  Atropine may be given to decrease secretions
stomach  Glucagon Ø relax smooth muscle
b.Used to diagnose duodenal ulcer, Zollinger- b. Procedure
Ellison syndrome, gastric carcinoma, & pernicious  Position patient in left lateral position
anemia  Ongoing assessment of patient status
c.Two Parts: c. Post-procedure gag reflex
 Basal cell secretion test ▫ Assess LOC, V/S, sats, pain, signs of perforation,&
 Gastric acid stimulation test~how much gastric return of gag reflex
acid after med is given that would …. 4.4 not 11. Proctoscopy-Sigmoidoscopy- Endoscopic exam of
normalendocopy the anus, rectum,& sigmoid & descending colon
d. Dx prob more in mucous layer  Flexible scopes have replaced rigid scopes (that
 Markedly increased indicates Zollinger-Ellison could only visualize 10 inches) & can visualize
 Moderately elevated- Duodenal ulcer 16-20 inches
 â levels- gastric ulcer or cancer  Bowel prep: TWE or Fleet’s enema till clear
7. UGI watch how barium moves throughtrack  Dietary restrictions not necessaryØno t going far
a. Upper GI Study- Fluoroscopic& X-ray  Sedation usually not needed
examination of upper GI tract following  Position in Left lateral w/right leg bent & placed
instillation of radiopaque liquid (often Barium) anteriorly toward chest
b. Patient Education:  During procedure, monitor VS, skin color & temp.,
▫ Clear liquid diet w/NPO from midnight night before pain, & vagal response
▫ Usually withhold AM meds morning of exam  Post- Monitor for bleeding & signs of perforation
c. Follow-up 12. Colonoscopy - Direct visualization of large
▫ á fluids to facilitate evacuation of stool & barium intestine (anus, sigmoid, transcending, & ascending
▫ Make sure patient has eliminated barium colon) via colonscope
8. LGI study- Visualization of lower GI tract after  Can be used diagnostically or therapeutically
rectal installation of barium, “barium enema”  Preparation:
b. Bowel prep: o No asprinØâ/R bleed
 o Clear liquids starting at Noon b4 exam III. Meds for GI Problems
o Bowel Cleansing w. laxatives & enemas or more • See Table 37-1, p. 1206-07
commonly w. glycol electrolyte lavage solution • Antibx
(Go-Lytely, Colyte,& Nu-Lytely) orally over 3-4 ▫ Amoxicillin (Amoxil), Clarithromycin (Biaxin),
hours › high electrolyte17 Metronidazole (Flagyl), Tetracylcine
o loose stoolsliquid stools….pulls out all fluid from • AntiD*l
body too ▫ Bismuth subsalicylate (Pepto-Bismol)
 Procedure: • Histamine-2 (H2) receptor antagonists
 Obtain informed consent ▫ Cimetidine (Tagamet), Famotidine (Pepcid),
 Sedate w/opioid or sedative for moderate sedation Ranitidine (Zantac)
 Glucagon may be given to relax colon & â spasm • Proton pump inhibitors (PPIs)
▫ Esomeprazole (Nexium), Lansoprazole (Prevacid),
 Monitor V/S, color, skin temp., LOC, distention, vagal
Omeprazole (Prilosec), Pantoprazole (Protonix),
response (âP, rebound áP, sweaty pale), pain
Rabeprazole (AcidHex)
 Position on left side w/knees drawn toward chest;
• Prostaglandin E1 analog- cytoprotective agents
may have to change position during test to facilitate
▫ Misoprostol (Cytotec), Sucralfate (Carafate)
advancement of the scope
• Antacids- neutralize acid in stomach
d.Post-procedure:
▫ Aluminum compounds- aluminum hydroxide,
• Maintain on BR till fully alert
carbonate or phosphate
• May experience cramps d/t increased peristalsis 2nd
▫ Magnesium compounds- magnesium hydroxide
to air insufflated into bowel
(MOM) or magnesium oxide
• Assess for S & S of bowel perforation (bleeding, pain,
▫ Calcium compounds- calcium carbonate
distention, F*{100-101}) peritonitisØperfureated
▫ Sodium compounds- sodium bicarbonate
bowelinflam starts muscles hardlocalized where
• Anticholinergics- block action of PNS
perforation is 20 contents leakout inflam
• Cholinergics- enhance PNS
• Provide patient education verbally& in writing as
• Prokinetics
sedating meds have amnesic qualities
▫ Metoclopramide (Reglan), Cisapride (Propulsid)
• Should report any bleeding to MD
▫ PNSØactive during digestionØ enhance effect of PNS
or block (diarreah)
II. A & P Review of Esophagus-Stomach
▫ REGLANØ 25
• Lower esophageal sphincter LES) prevents gastric
fluid from entering esophagus. Affected by:
IV. Disorders of Esophagus & Stomach
▫ Muscle tone, innervation, intrabd pressure, gastric
A. Disorders of the Esophagus
distention, size of bolus, rate of eating
1. Dysphagia- difficulty swallowingØneuro. Muscles,
• Stomach cells:
obstruction,
▫ Parietal- produce HCl acid (activates pepsin) produce
▫ Mechanical obstructions
intrinsic factor (needed for Vit B12 absorption)
▫ Cardiovascular abnormalitiesØfluid prob
▫ Mucous cells- produce K+ & HCO3; protects stomach
▫ Neurological
from acid
2. Regurgitation- ejection of gastric juice into mouth
• Parts of stomach:
3. Odynophagia- pain w/swallowing (too big)
▫ Fundus (top), Body (middle),& Antrum (bottom)
narrowing, restrictions
▫ Body & fundus highly distensible
Triggered by cold or carbonated beverages or solid
▫ Contents empty from antrum through pyloris into
food passign through esophagus
duodenum
4. Dyspepsia or heartburn, “indigestion”- burning
midline in lower retrosternal area that radiates toward
• Innervation
neck
▫ PNS- Vagus; stimulates
5. Achalasia- á dysphagia; “something stuck in
▫ SNS- Celiac, mesenteric, & hypogastric ganglia;
throat”
inhibit
C. Gastroesophageal Reflux (GERD) midlife, ileus
▫ Auerbach plexus- Motor
isn’t tight anymore stomach contants È to esphoageas
▫ Meissner’s plexus- Sensory
erodesprelude to esoph cancer
• Secretions
1. Inappropriate relaxation of LES w/reflux of gastric
▫ Pepsin (pepsinogen), gastrin, gastric lipase, HCl acid
or duodenal contents into esophagus
▫ Breakdown food & mix w/secretions for digestion
 2 . Etiology: unknown don’t have a strong esph
musc. Pressure from stomach pushes fluid us
3. Assoc with:
 Altered innervation, displacement of the angle of the
gastroesophageal junction, & incompetent LES
 á intragastric pressure pushes contents up
4. R/FxØObesity, preg, tobacco use, high fat diet,
caffeine, & á estrogen & progesterone levels
5. Manifestations of GERD
 May mimic ♥ attack
 Pyrosis (burning in the esophagus)
 Dyspepsia
 Regurgitation
 Dysphagia
 Odynophagia
 Hypersalivation Øwatery In mouth b4 eruptation
 Esophagitis Øinflam
6. Management of GERD
a. Patient EducØConsume low-fat diet; avoid caffeine,
tobacco, OH, milk, foods containing peppermint, &
carbonated beverages; avoid intake 2 hrs before bed;
maintain healthy weight; avoid tight-fitting clothes; á
HOB
b. Meds:
 Antacids, H2 receptor antagonists(block
hydrochloric acid), Proton pump inhibitors, or
Prokinetic agents(food outa stomach faster
into33: …to reduce,…_
 Avoid anticholinergics(want GI syst to be used),
Ca-channel blockers, bisphosphonates, &
Theophyllin
c. Surgical management
▫ Nissen fundoplicationØ fudus around stomach&
support to illeus so theres less likey to have food back
u[
D. Barrett’s Esophagus r cell structure in llower part
of esph
1. Assoc w/untreated GERD
• Squamous cells of esophagus replaced by
columnar epithelium resembling stomach or intestines
• Lining is reddened rather than pink
2. Management:
▫ Monitor w/EGD
▫ Photodynamic therapy- laser ablation for surgical
risks
▫ Esophagectomy reduces risk for development of
adenocarcinoma
E. Gastritis- Inflam of the gastric or stomach mucosa
1. Acute meds that need to be taken w/ food bc
irritating to stomach
▫ Caused by dietary indiscretion, overuse of aspirin or
NSAIDS, excess OH, radiation therapy, ingestion of
strong acid or alkali, acute illness or traumatic injury
2. Chronic
▫ Caused by ulcers of the stomach, infect w/ H. pylori,
autoimmune diseases, excess caffeine, meds- NSAIDS,
bisphosphonate (Fosamax or Actonel), OH , smoking,
chronic reflux of pancreatic secretions & bile into
stomach
3. Pathophysiology
▫ Mucous membrane becomes edematous &
hyperemic; undergoes superficial erosion. Secretes less
gastric juice w/little acid & much mucus 
hemorrhageupper GI bleed (throw up blood) if not
blood in bm
▫ IF always bleeding Fe defiency 38 ;(:::
4. Manifestations of Gastritis
• Acute
▫ Rapid onset
▫ Abd discomfort, HA , lassitude, N*, anorexia, V*, &
hiccups
▫ Lasts hours to days
• Chronic
▫ Anorexia, heartburn after eating, belching, sour taste
in the mouth, N & V
▫ Some have only mild epigastric discomfort or
intolerance to spicy or fatty foods or slight pain relieved
by eating
▫ Evidence of malabsorp of B12
▫ Some have no sx Øbleeding until CBC shows
5. Management Gastritis
 Gastric mucosa repairs itself & patient recovers in
about 1 day
 Should refrain from OH & food until resolved
 Nonirritating diet recommended
 Persistent sx treated w/IVF, NG(tube suck out
gastric secretion, irritants rests system,
secretions that happen in GI), analgesics,
sedatives, antacids
6. Nursing Management- Gastritis
• Nursing Diagnoses
▫ Anxiety r/t treatment
▫ Imbalanced nutrition, less than body requirements
▫ Risk for imbalanced fluid volume r/t insufficient
intake & excessive loss 2nd to V*
▫ Health maintenance r/t insufficient knowledge about
dietary management & disease process
▫ Acute pain r/t irritated stomach mucosa
• Collaborative ProblemØRisk for complication:
Hemorrhage
7. Nursing Care
▫ Support client, use calm approach, explain all
procedures& treatment
▫ NPO until acute sx subside
▫ Monitor I & O, serum elects
 ▫ When sx subside, start w/ice chipsclear
liquidsfullsolids
▫ Evaluate response to diet
▫ Teach client to avoid caffeine, OH , & cigarette
smoking
▫ Assess for signs of dehydration
▫ Assess for signs of hemorrhagic gastritis
 Hematemesis, tachycardia, & hypotension
F. Peptic Ulcer Disease (PUD)
1. General Information
• May be gastric, duodenal, or esophageal
• An erosion & excavation in the mucosal wall; may
through muscle  leak into peritoneum
• Strikes people btwn 40-60 years old; rare in women
of childbearing age but after menopause rates for
women equal to men, estrogen protectice
• Almost always d/t infect w/H. pylori not stress &
anxiety as was once thought
• Excess secretion of HCl acid in the stomach also
contributes to formation of peptic ulcers
o Milk, pop, smoking, & OH á HCl secretion
o Stress & spicy foods may aggravate peptic ulcers
▫ * look up in book* Zollinger-Ellison syndrome (ZES)
Øsevere gastric ulsers extreme gastric (non)cancer in
pancreas
2. Pathophysiology of PUD
▫ Erosion results from action of gastric acid (HCl) &
pepsin caused by excess activity of these substances or
decreased resistance of the mucosa.
• 53 AggravatingØh pylori, NSAIDS not enteric
coated
• Impaired defenceØ ishchemia, shock, delayed gastric
empty,
• Stress ulcer-sepsis, ventilated Øinsult to body occurs
after physiologically stressful events (burns, shock,
sepsis, or multiple organ trauma)
▫ Most common in ventilator-dependent patients after
trauma or surgery
▫ Ulcerations begin within 24-72 hrs, spread as
condition continues,& resolve as patient recovers
• Cushing’s Ulcer- neuro in patients w/head injuries
or brain trauma; occurs in esophagus, stomach, or
duodenum
• Curling’s Ulcer- burn seen 72 hrs after extensive
burns in antrum of stomach or the duodenum
3. Manifestations of PUD come& go
Pain radiates to back, wet burps
▫ Sx last days, weeks, months & may disappear then
reappear; some are asymptomatic
▫ Dull, gnawing pain or burning sensation in the
midepigastric area or in the back
▫ Pyrosis (heartburn), V*, constipation, or D*,&
bleeding
▫ Sour eructation (burping) when stomach empty
▫ V* Ø obstruction of pyloric cant get from stomach
to duodemum may (not) precede N*
▫ Emesis often contains undigested food
▫ 15% experience bleeding
4. Management of PUD
• Combination of antibx, proton pump inhibitors, &
bismuth salts to suppress or eradicate H. pylori
• Recommend therapy for 10-14 days
o Triple therapy- two antibx (Flagyl or Amoxil &
Biaxin) plus a proton pump inhibitor (PPI)
o Quadruple therapy- two antibx, PPI, & bismuth
salts
o H2 receptor antagonists & PPI treat NSAID-
induced ulcers & ulcers not assoc w/ H. pylori
o See Table 37-3, p. 1211 for med regimens
• Rest, sedatives, tranquilizers prn for comfort
• MaintainØH2 receptor antagonists recommended
for 1yrØkeep from ulcer from coming back.
• Patients at risk for stress ulcers treated
prophylactically w/H2 receptor antagonists &
cytoprotective agents to decrease risk for upper GI
tract hemorrhage
• Stress reduction & rest
• Smoking cessation
• Dietary modificationØAvoid extreme food
temperatures, meat extracts, OH , coffee (even
decaffeinated), caffeinated beverages, diets rich in
milk & cream; eat 3 meals a day
5. Nursing Diagnoses
▫ Acute pain r/t action of acid on damaged mucosa
▫ Anxiety r/t acute illnessØthey think its something
severe
▫ Imbalanced nutrition r/t dietary changes
▫ Risk for Ineffective Health Maintenance r/t deficient
knowledge about prevention of sx & management of
condition
6. Collaborative Problems
▫ Hemorrhage
▫ PerforationØerodes through
▫ PenetrationØulcer erodes to musc wall spasms
▫ Pyloric obstruction (gastric outlet obstruction)Øfood
cant get outa stomach
G. Morbid Obesity
1. Definitions:
▫ BMI > 30 z Body weight > 100 # & > 2 x deal body
weight
2. Growing problem in US where 65% are
overweight
3. á/R for other health compØDiab, ♥ dis, stroke, htn,
gallbladder dis , arthritis, sleep apnea, & breathing prob
 4. Management of Obesity
▫ Conservative managØDiet & exercise-Limited success
▫ Pharmacologic tx options
▫ Excess …â … tell when there full. 1.10
 Sibutramine HCl (Meridia)- inhibits serotonin &  Psychological support
NE & â appetite
 May increase BP, cause dry mouth, insomnia,
HA , diaphoresis, & increased HR
 Orlistat (Xenical)- â absorb of fat zâ caloric intake I. Inflammatory Problems
by binding to gastric & pancreatic lipase to prevent
digestion of fats
 SE: á BM, gas w/oily discharge, â food
absorption, â bile flow, â absorption of vit  S&S: D*, abd pain, cramping, N-V, F*, anorexia,
 Rarely result in loss of more than 10% total
weight & low LT effectiveness
6. Surgical Management of Obesity
▫ Achieve weight loss Restricting intake, â absorpt,
or combo
▫ Duodem jejumum ileum Øall absorb certian things
better
 Roux-en-Y gastric bypass: restrictive &
malabsorptive
 Gastric banding: restrictiveØâ /R for vit dific
 Vertical-banded gastroplasty: restrictiveØmake
stomach smaller
 Biliopancreatic diversion & duodenal switch:
restrictive & malabsorptive
▫ Average weight loss is 61% of previous body weight at an uncoordinated way  good movmt of food
▫ Comorbid conditions such DM, htn, sleep apnea, &
dyslipidemia È
▫ Candidates must be carefully screened & counselled
▫ Less than body needs …..
7. Common Complications
 Bleeding
 Blood clots
 Bowel obstruction
 Incisional or ventral hernias
 Infects 2nd to leaks at anastomosis
 N d/t overfilling of pouch
 Dumping syndrome 2nd to consumption of simple
sugars
• Sensation of fullness, weakn, faintness, dizziness,
palpitations, diaphoresis, cramping pains, & D*
• Vasomotor sx occur 10-90 min after
eatingPallor, perspiration, palpitations, HA ,
feelings of warmth, dizziness, & even drowsiness
 r bowel fx (intestine not being used) : D*, constip,
steatorrhea
• Nutritional defic 2nd to malabsorp
8. Nursing Management
 Monitor for immediate post-operative complications
▫ Peritonitisnleak, stomal obstruction /ulcers,
atelectasis & pneum, thromboembolism, &
metabimbal
 After bowel sounds return & oral intake is resumed,
6 small feedings are provided
 Sip fluids btwn meals~  w/ meals to delay emptying
 Report excessive thirst or concentrated urine
 Long term S/EØá/R gallstones, nutritional defic, risk
for weight re-gain.
Management of Clients w/Bowel Problems: Chapter 38
A. Gastroenteritis & Dysentery
 Inflam of the stomach & intestinal tract affecting the
small bowel
distention, tenesmus, borborygmi (hyperactive
bowel sounds)
 Primarily caused by contaminated food & water;
transmitted by fecal-oral route
 Clostridium difficile (C. diff) is a bacterial
dysentery commonly seen in clients who have been
receiving large doses of antibx for extended time, kill
normal intestinal floraovergrowth C.diff
*hx w/ c. diffhx of antibx
▫ More & more common in hospitalized patients
▫ Generally resolves in 1-5 days but can be fatal to
the debilitated, older or very young patient
2. Treated w/F & E replacement
Irritable Bowel Syndrome disreg intestine spasms
 Common GI problem, occurring more in females
o Heredity, stress, depression-anxiety, á-fat diet,
food intol, OH , & smoking
 It is a disorder of intestinal motility r/t
neuroendocrine dysregulation, infect or irritation,
vascular or metabdisturbance
 Peristaltic waves affected at specific segments
 Altered peristaltic intensity
 No evidence of inflam or tissue changes in intestinal
mucosa
1. Management of IBS
2. GoalsØRelieve pain, regulate BMs, â stress
 Begins w/dietary restriction & gradual
reintroduction of foods while recording tolerance
 High fiber diet recommended
 Exercise program
 Pharmacologic agents:
o Bulk forming productsØ +fiber bulk to BM
o AntiD*l agents
o Antidepressants
o Anticholinergics
o Tegaserod (Zelnorm)
 Nursing Management IBS
Provide education
o Understanding of disease
o Good dietary habits o If perforation occurs, an abcess may form. May need
o Eat slowly at regular times antibx & a drain to empty abcess before performing
o Chew foods thoroughly appendectomy
o Limit fluid intake at meal time Nursing Care: (See Table 38-3, p. 1242)
o Adequate daily fluid intake o Manage pain, fluids, anxiety, nutrition, & infect
o  OH & smoking o May have NG tube(esp w. rupture or peritonitis) to
Malabsorp prevent paralytic ileus
 Inability of digestive tract to absorb necessary vits o Patient positioned in high fowlers
&/or nutrients o Morphine usually used for pain
 Conditions that lead to malabsorp: o Usually d/c in a day
▫ Mucosal (transport) disorders o If possible peritonitis, in surgery rinsed out, a drain is
▫ Infectious diseases left in place & will be kept longer for antibx &
▫ Luminal disorders monitoring
▫ Postoperative malabsorp Diverticular Disease
▫ Disorders r/t malabsorp of specific nutrients  Diverticulum- saclike herniations of the lining of the
 Manifestations: bowel that extends through a defect in the muscle layer
o D* or frequent, loose, bulky, foul-smelling stools & may occur anywhere in the small intestine but is most
w/increased fat content & often grayish in color common in the sigmoid colon
o Abd distention, pain, increased flatus, weakness,  Diverticulosis- multiple diverticula w/o inflam or sx.
weight loss, decreased sense of well-being Very common in developed countries & increases w/age.
o Malnutrition & signs of vitamin & mineral deficiency  Diverticulitis- food & bacteria retained in the
 Intervention aimed at underlying cause & diverticulum produce infect & inflam perforation or
supplements abscess formation
 Appendicitis o Sx  complicationsØabscess, fistula (abnormal tract)
 Inflam & edema of appendix formation, obstruction, perforation, peritonitis, &
 Most common reason for emergency abd surgery; hemorrhage
ages 10-30 years greatest incidence Pathophysiology
 Pathophysiology: o High intraluminal pressure, low volume in colon, & â
o Appendix becomes obstructed or twisted causing colon wall muscle strength  mucosa & sub-mucosal
inflam -> increased intraluminal pressure causes layers of the colon to herniate  inward pouch-
pain -> eventually fills w/pus. Can rupture& lead to muscular wall
generalized peritonitis. o Bowel contents accumulate in the diverticulum &
 Manifestations of Appendicitis decompose, causing inflam & infect
o Vague epigastric or periumbilical pain progresses o Can perforate causing irritability & spasticity of the
to RLQ pain McBurneys colon
o Low grade F* 99-100, if high peritonitis o Abscesses can develop & perforate. This can lead to
o N*, possible V* peritonitis & erosion of arterial blood vessels &
o Anorexia subsequent bleeding
o Pain at McBurney’s pointif goes away (repture) Manifestations
infect organ dumped out peritoneum o Chronic constipation often precedes development by
o Rebound tendernessnever press over inflame many years
organ o S & S are mild & include bowel irregularity
o Positive Rosving’s sign w/intervals of D & N, anorexia, & bloating or distention
o Ruptured Appy: Diffuse abd pain, distention, elevated o Large bowel may narrow w/fibrotic strictures,
temp.,& positive obturator test leading to cramps, narrow stools, constipation, or
**If constipated,  strain, avoid laxatives may cause obstruction
rupture o Weakness, fatigue, & anorexia are common
› Management of Appendicitis o Strictures impede progress of BMnarrow BM
o Surgery o If deverticulitis develops, there is an acute onset of
o IVF & antibx mild to severe pain in LLQ, w. N-V, áT, chills, &
leukocytosis
 o If untreated,  septicemia Øintest – vessles wrapped
around theminfection to blood stream
Complications
o Peritonitis- adb pain, rigid board-like abdomen, loss
of BS, & S&S of shocksepticemia
o Abscess formation- Tenderness, palpable mass, F*,
leukocytosis
o Bleeding- Massive rectal bleeding if erosion occurs
into arterial branch
 Management
o Usually Tx outpatient w/diet & meds
 Rest, analgesics, & antispasmodic meds
 Clear liquids until inflam subsides, then high-fiber,
low-fat diet recommended
 Antibx & bulk-forming laxatives prescribed
o Acute cases managed in the hospital
 NPO w/IVF
 NG to control V* or distention
 Broad spectrum antibx 7-10 days
 Opioids for pain (Demerol preferred)
 á oral intake as sx improve
 Low-fiber diet until infect relievedreturn to
áfiber
 Antispasmodics may be needed
 Bulk products, softeners, or suppositories › not –IT ▫
IS bc hard on inflame, edematous cant maintained
o Surgical management- See Fig. 38-3, p. 1244
o If complications occur -> emergency surgery
Procedures
o One-stage resection take out inflame sect attach
good end
 Inflamed area is removed & end-to-end
anastomosis is done
o Multiple-stage
 Performed when complications occur
 Diseased area is resected but no anastomosis done
 Both ends of bowel brought out & “double-barrel”
temporary colostomy formed
 When inflam/infect subside, may be reattached in ▫
separate procedure
1. Nursing care- see p. 1244-45
Peritonitis - An inflam of the peritoneum
▫ Usually d/t bacterial infect from diseases of the GI
tract, or in women, the reproductive organs
▫ Inflam & paralytic ileus (infect, inflame in inteste )
are the direct effects of infect
▫ Other common causes: spilling of gastric contants
peritoneum
o Appendicitis, perforated ulcers, diverticulitis, &
bowel perforation
o Also assoc w/abd surgery & peritoneal dialysis
▫ Pathophysiology of Peritonitis
o Contents from inflamed/infected abd organs leak
 abd cavity
o Bacterial proliferation occurs
o Tissue edema follows w/development of
exudative fluid in a short time
o Fluid in peritoneal cavity becomes turbid
w/proteins WBCs, cellular debris, & blood
o Fluid is lost from vascular into peritoneal cavity
o Causes GI hypermotility followed by paralytic ileus
▫ Manifestations Øâvolemia 2.10 
o Depends on location
o Early sx are d/t underlying cause
o Starts w/diffuse pain that becomes constant,
localized, & more intense near site of inflam
o Pain is exacerbated by movement
o Affected area extremely tender, distended,
w/muscle rigidity
o Rebound tenderness & paralytic ileus may be
present
o Corticosteroids or analgesics may mask pain
o N-V & â peristalsis
o áT (100-1) & P
o SOBØ fluid pressure
Management of Peritonitis
o Monitor for compl:
 Widespread infect leading to sepsis & shock
o Need fluid (manage like shock), colloid, &
electrolyte replacement
 Several liters of isotonic solution is
administered
o Analgesics & antiemetics for pain& N-V
o NG suction relieves distentionØrest bowel 2.13 
o Fluid in abd cavity can restrict lung expansion so
O2 per nasal cannula improves oxygenation
o Antibx in large doses
o Surgical treatment- remove infected material &
correct underlying cause
Nursing Management of Peritonitis
o Monitor for post-op complications
› Wound evisceration
 Sudden appearance of serosanguineous
drainage strongly suggests wound dehiscence
 Patient may c/o pain, tenderness, &
“something gave way”
› Abscess formation
▫ Often in ICU where BP monitored per arterial line &
CVP measured via pulmonary arterial wedge
pressure
o Measure UOP & I & O
o Evaluate fluid & electrolyte balance
o Position w/knees flexed
o Monitor output from surgical drains
 o Signs of improvement: T. & HR decrease,  Scar tissue & granulomas interfere w/peristalsis
Abdomen softens, BS return, & the presence of causing crampy abd pain
flatus,& BM  Abd tenderness & spasm exacerbated by eating
Inflammatory Bowel Disease  Weight loss & malnutrition
▫ Two chronic disorders: inflame within the bowel  Malabsorp leads to chronic D*
o Crohn’s (regional enteritis)  Steatorrhea (fatty stools)
o Ulcerative colitis  Other: arthritis, erythema nodosum,
o See Table for 38-4, p. 1247 for comparison conjunctivitis, & oral ulcers
▫ triggered by environmental agents (pesticides, food Ulcerative colitis
additives, tobacco, radiation)Triggeres  Usually presents w/exacerbations & remissions
autoimmune responseØ kills antibodies  LLQ pain
▫ Allergies & immune disorders also suggested as  D* w/rectal bleeding
cause  Intermittent tenesmus
▫ NSAIDs tend to exacerbate IBD  Pallor, anemia, & fatigue
▫ Pathophysiology of IBS both have  Anorexia, weight loss, F*, V*, & dehydration
exacerbation/remission  Urgent need to defecate
o Chron’s (Regional) large/small intest, all layers  Pass 10-20 liquid stools/day
of intest, areas of inflamed cellsØ separated by  Hypocalcemia develops
healthy bowels, (cobble stone), tissue fibrotic,  Other: Erythema nodosum, uveitis, arthritis, &
▫ Subacute & chronic inflam of bowel that extends liver disease
through all layers; usually affects distal ileum & › Potential Complications of IBS á/r cancer
sometimes ascending colon. Characterized by o Regional Enteritis
periods of remission& exacerabtions.
o Intestinal obstruction or stricture
 Begins w/edema & thickening of mucosa. Ulcers
o Perianal disease
appear in inflamed mucosa. These lesions are
o F & E imbalances
separated by normal tissue, taking on a “cobblestone”
appearance. o Malnutrition
 Fistulas, fissures, & abscesses formØchronesall o Fistula & abscess formation
layers of colon& sm intest o á/R for colon CA
 Granulomas occur in 50% of pts Ulcerative Colitis
 Bowel wall thickens, becomes fibrotic, & lumen o Toxic megacolon
narrows o Perforation
 Bowel loops can adhere to each other o Bleeding
a. Ulcerative Colitis large intest, submucosa layer, › Management of IBS
see bleeding from stool, continueous inflame, stick o Nutrition
together?,  Fluids îelec, low-residue, high-protein, high-calorie
 Affects superficial mucosa of the colon & diet w. supplm vits & Fe
characterized by multiple ulcerations, diffuse inflam, &  Avoid foods that exacerbate condition
shedding of eipthelium  Milk, cold foods, smoking
 Ulcers cause bleeding o Surgery
 Mucosa edematous & inflamed; lesions are o Total colectomy w/ileostomy
contiguous (one after the other)  Continent ileostomy- Kock pouchØmore liquid
 Cricks Abcesses form & infiltrate is seen in bigger volume
submucosa & submucosa w/clumps of neutrophils  Restorative proctocolectomy w/ileal pouch anal
found in the lumen of the cryps that line the mucosa anastomosis- procedure of choice (Fig. 38-5, p.
 Process usually begins in the rectum & spreadsd 1251)
proximally to involve the entire colon › Pharmacologic Management of IBS
 Eventually bowel narrows, shortens, & thickens o Sedatives, antiD*l, & antiperistaltic meds rest bowel
2. Manifestations of IBS o Aminosalicylates Ø sulfasalazine (Azulfidine) Ø mild
Regional Enteritis /Chrones or moderate cases
 Insidious onset w RLQ pain o Sulfa-free aminosalicylates (mesalamine [Asacol,
 May present w/exacerbations & remissions or Pentasa]) prevent & tx recurrences
progressive o Antibx (metronidazole (Flagyl) Ø 2nd infects
o Corticosteroids- tx severe & fulminant disease
 Stopping triggers disease, continuing leads to SE,
á/r infect, can’t protect
o Immunomodulators- alter immune response, didn’t
respond to meds
 Azathioprine (AZA), 6-mercaptopurine (6-MP),
methotrexate, cyclosporineØkills some inflame
triggers
 For patients who haven’t responded to other
therapies
Nursing Management of IBS
o See Nursing Process & Care Plan p. 1251-1258
o Education about diet& meds
o Refer to support groups
o Monitor nutritional & fluid status
o Promote balance of rest w/activity
o Healthy stress management
o Eliminate smoking
o TPN used when sx are severe
 High glucose levels can  áBS
 High in protein, low in fat & residue so digested
primarily in jejunum-> doesn’t stimulate intestinal
secretions so bowel continues to rest
 Note intolerance such as N-V, D*, or distention
Intestinal Obstruction- Blocks movement of contents
through GI tract
 Two types
o Mechanical
 Obstruction from pressure on intestinal wall
 Intussusception, polypoid tumors & neoplasms,
stenosis, strictures, adhesions (most common),
hernias, ,abscesses
o Fuctional (Neurogenic) cant get the message
 Musculature cannot propel contents forward
 Amyloidosis, muscular dystrophy, endocrine
disorders, & neurological disorders
 Can be temporary & result from manipulation of
the bowel during surgery
o Partial or Complete
o Vascular FactorsØblood is not supplied to a part of
intestine unable to perform norm peristaltic
fxischemicabd pain áWBC, T, peritonitis fx-
ápermleak bacteriashock.
Pathophysiology of Small Bowel Obstruction
(SBO)
▫ Obstruction coming from that decendsloosing
fluids  stim Gastric secterion â pressure  blood o
edema congestinartierial
bloodishemiadeathmore peritonitis 52.5 
▫ Intestinal contents, fluid, & gas accumulate above the
obstruction Distention & fluid retention reduces
absorption of fluids & stimulates more gastric
secretion -> increases pressure within intestinal
lumen-> decreases venous return, increases venous
pressure, & increases capillary permeability ->
causes edema & congestion-> reduced arterial flow
to bowel -> necrosis, & eventual rupture or
perforation of intestinal wall -> peritonitis
▫ Manifestations of Bowel Obstruction
o Initial symptom: crampy pain that is wavelike &
colicky
o May pass blood & mucus w/o fecal matter or flatus
o V* occursØclosest to the mouth downØempty
stomach contents bile jejunumfecal type
If obstruction is complete, peristaltic waves are initially
excessive & eventually reverse direction & move
contents up toward mouth
o First vomits stomach contents
o Then bile-stained contents (duodenum & jejunum)
o Eventually fecal-like contents of ileum
o DehydrationØThirst, drowsiness, malaise, aching ,
parched tongue & mucous membranes
o Abd distention (lower the obstruction, greater the
distention)
o Initially hyperactive BS auscultated proximal to
obstruction then become hypoactive or absent
o Dx made by X-ray or CT
› Management of Small Bowel Obstruction
o NG tube for decompression
o IVF to replace water, sodium, chloride, & K+
o Complete obstruction w/necrosis requires surgery to
remove necrotic section
› Nursing care:
 Manage NG suction & measure output; note
quality
 Assess for fluid & electrolyte imbalances
 Monitor nutritional status
 Note return of bowel sounds, flatus,& BM
 Monitor distention
 Monitor& manage pain
Large Bowel Obstruction Pathophysiology: less
dramatic than small › isn’t complete bc fecal
resorvior, distensible,
o Obstruction results in an accumulation of intestinal
contents, fluids, & gas proximal to obstruction
severe distention & perforation unless gas & fluid can
flow back through ideal valve
Even if complete may be undramatic if the blood
supply is not disturbed
o c. If the blood supply is cut off, intestinal
strangulation & necrosis occurs-> life-threatening
o Dehydration occurs more slowly b/c colon can
absorb its fluid contents & can distend to a size well o Passage of blood in stool 2nd most common symptom
beyond its normal size
o Adenocarcinoid tumors account for majority of cases ▫ Right-sided lesions: Dull abd pain & melena
Manifestations of Large Bowel Obstruct
o Sx develop & progress slowly
o Constipation only sx for months
o Shape of stool altered by obstructionØlrg growth in
colonsquishes
o Blood in stool from tumor or Fe defic anemia
o weakness, weight loss, & anorexia
o Eventually abd distended
o Loops of bowel may become visible through abd wall
o Crampy lower abd pain
o Few~Fecal V* eventually develops
o Sx of shock may occur
o DxØ X-ray, CT, or MRI
Management of Lg Bowel Obstruction
o Restore intravascular volume
o Correct electrolyte abnormalities
o NG Ø decompress bowel
o Colonoscopy may be performed to untwist &
decompress bowel
o May insert rectal tube
o Temporary or permanent colostomy may be needed o Supportive therapy
Nursing care:
o Monitor for worsening sx
o Provide emotional support & comfort
Colorectal Cancer
 Relatively common; 3rd most common site of new CA
cases & deaths in US
 A disease of Western cultures
 á/RØ age, family hx, those w. IBD or polyps
 Cause not known
▫ È screening – â deaths
▫ Early dx & prompt treatment could save almost 3 of 4 ▫ Caused by congenital absence of some or all of
persons
▫ 90% 5-year survival rate is detected early; survival
rates very low w/late diagnosis
▫ Unfortumately, most are asymptomatic for long
periods & seek health care only when they notice a
change in bowel habits or rectal bleeding
Pathophysiology of Colorectal CA
o 95% - adenocarcinoma lrg bowel obstruct, polyps
become malignant, clip to â Malignant (arising from
epithelial lining of intestine)
o May start as a benign polyp that becomes malignant-
> invades & destroys normal tissues-> extends into
surrounding structures
o Cells may migrate to other areas (often the liver)
▫ Manifestations of Colorectal CA
o Sx determined by location, stage, & fx of segment
o r in bowel habits
o Other: unexplained anemia, weight loss, & fatigue
▫ Left-sided lesions: Sx assoc w/obstruction ->Abd
pain & cramping, narrowing stools, constipation,
distention
o Bright-red blood in stool
▫ Rectal lesions: Tenesmus, rectal pain, feeling of
incomplete evacuation after BM, alternating *C & D*,
& bloody stools
Assessment & Dx
▫ Positive fecal occult blood
▫ Barium enema & endoscopic procedures reveal
abnormal tissue on biopsy & cytology smear
▫ Carcinoembryonic antigen (CEA)- Not highly
reliable, but elevations positive for CA
~With complete tumor excision, CEA returns to
normal within 48 hours& later elevations suggest
recurrence
▫ Most common complication is bowel obstruction
Management of Colorectal CA
▫ If obstruction present, treat that w/fluids & NG
▫ Tumor treatment depends on stage:
o Surgery to remove tumor
o Adjuvant therapy- typically delays tumor recurrence
& increases survival time
 Chemotherapy
 Radiation
 Immunotherpay
 Multimodal therapy
Hirschsprung’s Disease
 Most common cause of lower GI obstruction in
neonate
▫ Occurs in 1:5000 children w/4:1 ratio male : female
normal bowel ganglion cells, beginning at anus,
extending variable lengths
▫ DxØ barium enema
▫ S&S: Extremely dilated colon & chronic constipation,
fecal impaction, & overflow D*Øfecal matter goes
around obst.
▫ TxØ Surgically resect affected segment & reattach
healthy bowel
▫ Nursing: Encourage bonding, prepare 4
interventions, explain that colostomy will be
temporary
Pyloric Stenosis Narrowing of pyloric orifice, food 
stomachsmall intest.
 In children, excessive thickening of the pyloric
sphincter or átrophy & plasia of mucosa &
submucosa of pylorus is responsible
 TxØ w/revision of the muscles of the pylorus
▫ Celiac Disease Malabsorp or gluten-induced
enteropathy
o A sensitivity or immunologic response to protein,
especially protein found in grains
o When child ingests gluten, intestinal mucosa or villi
changes & prevents absorption of food into blood
o Children develop inability to absorb fat
 S & S:
o Cramp, abd pain, unable to absorb food, nutrients
cant  blood stream
o Steatorrhea (elim fat bc cant use) & defic in fat-
soluble vits (A, D, E, & K)
o Malnutrition, distended abdomen & possible rickets
o Hypoprothombinemia  loss of Vit K
o hypochormic anemia (Fe deficiency)
o â albuminemia Ø poor protein absorption
▫ Relatively rare condition, but needs early recognition
to prevent complications
▫ Affects children of northern European › inherited
illness
▫ different degrees of involvement
▫ á incidence in Down’s synd
 Treatment:
o Educated about following a gluten-free diet for life
o Prone to GI CA later in life if diet not followed
o Celiac crisis:
o When child develops any type of infect, a crisis of
extreme sx may occur
 Acute V & D
 Rapid F & E imbal Ø immediate, intensive therapy