N 246 Health Alterations lll
Fall, 2010
Alterations in the GI System
Sandra Buckley, RN,MS
A & P of GI system
30 ft. long from mouth to anus.
Consists of mouth, esophagus, stomach, small
intestine, large intestine, rectum, anus.
Associated organs: liver, pancreas, gallbladder.
Organs covered by peritoneum (parietal:lines
abdominal cavity, visceral:covers organs), two folds of
peritoneum are mesentery (contains blood vessels and
lymph glands) and omentum (contains fat and lymph nodes)
Physiology
Innervated by parasympathetic, sympathetic and
intrinsic nervous system.
Parasympathetic:excitatory (increased peristalsis).
Sympathetic: inhibitory (decreased peristalsis).
Intrinsic (enteric): coordination of motor and
secretory functions-two nerve layers that lie between
mucosa, contribute to motor and secretory activities.
Circulation of GI system
Receives approximately 25-30% of cardiac
output. Major source from which blood can
be diverted during exercise or stress.
Venous blood draining the GI tract organs
empties into portal vein, which then perfuses
liver. Upper GI- blood from splanchnic artery,
small intestine-blood from branches of
hepatic and superior mesenteric
arteries.Large intestine-superior and inferior
mesenteric arteries.
Arteries of stomach, liver, spleen
Function/physiology of GI
Each part of system performs different
activities.
Ingestion and propulsion of food:
mouth, pharynx, esophagus.
Digestion and absorption: mouth,
stomach, small intestine.
Elimination: large intestine
Ingestion
Intake of food, impacted by:
appetite-desire to eat, center located in hypothalmus, factors
affecting;
(increasing appetite) hypoglycemia, empty stomach, decrease in
body temperature, sight, smell, taste of food.
(decreasing appetite) stomach distention, illness
(fever),hyperglycemia, nausea, vomiting, drugs, input from
higher brain centers.
Hormone Ghrelin; released from stomach mucosa to stimulate
appetite.
Hormone Leptin; released and involved in appetite suppression
Factors affecting GI tract
Emotions: stress, anxiety, happiness. May be
manifested by anorexia, epigastric and
abdominal pain, diarrhea, constipation, gas,
decreased satiety and increased consumption
(above caloric need).
Physical factors: diet, alcohol, caffeine,
cigarette smoking, drugs, fatigue, organic
diseases, metabolic factors.
Swallowing (deglutition)
Involve mouth pharynx and esophagus
Mouth-lips and oral (buccal) cavity, roof of
cavity is soft palate, contains teeth used in
chewing (mastication) and tongue. Taste
receptors; sides and tip of tongue (important
for speech and pushing food to back of
throat).
3 sets of salivary glands: parotid,
submixillary, sublingual-produces saliva
(contains salivary enzyme amylase)
Swallowing video
http://www.youtube.com/watch?v=Z7x
KYNz9AS0
http://www.youtube.com/watch?v=uxH
UUgLeNzk
Pharynx
Musculomembranous tube;
nasopharynx, orophrynx ( when food or water
present, stimulates swallowing reflex), laryngeal
pharynx
Secretes mucus, aids in swallowing
Epiglottis: lid of fibrocartilage that
closes over the larynx during
swallowing.
pharynx
Esophagus
Hollow, muscular tube ~ 10 inches long.
When swallowing: upper esophageal
sphincter (cricopharyngeal muscle) relaxes
and a peristaltic wave moves the bolus into
the esophagus. Muscular layers contract
(peristalsis) and propel food to stomach.
Lower esophageal sphincter (LES)- at distal
end of esophagus, remains contracted except
during swallowing, belching or vomiting.
Important barrier that prevents reflux.
Dyspepsia
Refers to host of upper abdominal or
epigastric symptoms such as pain,
discomfort, fullness, heartburn,
regurgitation or “indigestion”.
Etiology: drug intolerance, GI tract
dysfunction, pancreatic or biliary tract
disease.
Dyspepsia
Functional or nonulcer dyspepcia-most
common cause of chronic dyspepsia.
2/3’s of patients have no obvious
organic or biochemical cause for
symptoms that can be evidenced by
endoscopy.
Clinical findings: weight loss, vomiting,
dysphagia, melena, anemia.
GERD
Gastroesophageal reflux disease (GERD),not
a disease but a syndrome that results in
reflux of gastric secretions into esophagus.
Predisposing conditions: LES (incompetent
lower esophgeal sphincter), hiatal hernia,
decreased gastric emptying. Results in:
- irritation – pyrosis (heartburn),
-inflammation - esophagitis, hoarseness,
-difficulty swallowing – dysphagia.
Gerd-diagnosis
Upper GI x-ray with barium swallow
Esophageal endoscopy
Esophageal manometry
Ph monitoring
Barium swallow
Outlines the esophagus
Contrast is ingested
Gastrografin (water soluble contrast), and barium
Nursing care: educate and support pt.; signed
consent, allergy status to meds or contrast, need to
drink contrast, assume various positions on table,
NPO 8-12 hours before procedure, avoid smoking 12
after midnight. After procedure; take measures to
prevent contrast media impaction (fluids, laxatives),
stool may be white 72 hours post-test.
PT. education
Lifestyle changes
Dietary changes- alcohol, spices, chocolate,
broccoli, salmon, caffeine, smoking, mint, fat.
Medications-antacids(tums, maalox), H2
blockers (tegamet, pepsid), protein pump
inhibitors (nexium, Protonix), prokinetic
meds (metaclpromide)
Other esophageal disorders
Barrett’s esophagus-precancerous
lesion, requires annual tissue biopsy.
Esophagitis-due to chemical irritation
(dust, lye, temperature, ETOH abuse).
Achalasia-cardiospasm of lower portion
of esophagus muscle. Causes
obstruction and accumulation of food
and fluid.
Esohageal disorders
Esophageal cancer-rate is high in Asia,
low in U.S., but higher incidence in
African-Americans and men. Prognosis
poor. Clinical manifestations-similar to
GERD.
Esophageal strictures-caused by chronic
GERD or ingestion of caustic liquids.
Intervention-endoscopic dilation.
Esophageal varices
Dilated tortuous
veins in lower
portion of
esophagus.
Complication of
liver cirrhosis.
Bleeding varices
most life-threatening
complication of
cirrhosis.
Factors producing
irritation:
Alcohol, poorly
masticated food,acid
regurgitation,
increased abdominal
pressure (nausea,
vomiting, straining,
coughing).
stomach
Function is to store food, mix food with gastric
secretions, and empty contents into small intestine.
Absorbs only small amount of water, alcohol,
electrolytes and certain drugs.
Average length of time food in stomach:3-4 hours
Chief cells secret pepsinogen (antecedent of pepsinthe main enzyme of gastric juice which converts
proteins into peptones)
Parietal cells secrete hydrochloric acid, water and
intrinsic factor (increases absorption of vitamin B
complex)
stomach
Gastritis
Results from breakdown in normal
gastric mucosal barrier. May be acute or
chronic.
Type A-associated with autoimmune
disorder, Type B-associated with H.
Pylori.
Clinical manifestations similar to GERD,
often self-limiting.
Gastritis (continued)
Severe cases may require NPO, IV fluids, NG
for lavage.
When atrophy of cells occur, may result in
loss of intrinsic factor/decreased
RBC’s/anemia.
Tx- education,lifestyle modification,
assessment of severity,medication, surgical
interventions (gastrectomy,vagotomy or
pyloroplasty).
Medications- antacids,Zantac, Tagamet,
prilosec, prevacid
Pernicious anemia
Intrinsic factor produced by cells in gastric mucosa
Binds with ingested B12 (degraded by HCL) to form
complex that travels to small intestine for absorption.
B12 deficiency: anemia
Atrophic gastritis: common condition in older people,
damages cells of stomach, without healthy cells,
production of HCL and intrinsic factor is diminished.
Vitamin B12 deficiency caused by atrophic gastritis
and a lack of intrinsic factor is know as pernicious
anemia.
Hiatal Hernia
Herniation (bulging upwards) of a portion
of stomach through diaphragmatic opening.
Acid from stomach spills into unprotected
esophagus – irritation of mucus lining.
“choking feeling”, lump in throat, food
stoppage and regurgitation
More common in older adults and women.
Hiatal Hernia
Diagnositic studies: barium swallow,
endoscopy.
Collaborative care: administration of
medications (antacids, antisecretory
agents), avoidance of lifting and
straining, elimination of alcohol and
smoking, HOB elevation
Surgical Therapy (hiatal
hernia)
Objective to reduce reflux by enhancing
integrity of LES.
Procedures: valvuloplasties: also called
fundoplication, involves wrapping of
fundus of stomach around lower portion
of esophagus. Can be preformed
laproscopically. Prevents reflux in 90%
of patients.
Nursing management
Postop care: prevention of respiratory
complications, IV therapy, wound care,
education.
If NG present- maintain patency of tube,
dangerous to attempt to replace tube if
dislodged due to possibility of
perforation of surgical repair.
Upper GI Ulcers
Peptic ulcers- erosion of GI mucosa
mostly in Antrum an duodenum
Caused by the digestive action of
HCL acid & pepsin.
Acute (superficial)
Chronic (deep, longer healing)
Gastric or duodenal ( by location), but
different in etiology and incidence.
Physiology of Peptic ulcer disease
Mucosal defense system may be
impaired by: H. pylori, inadequate blood
flow, smoking ,NSAIDs
Compare gastric vs duodenal
Gastric - superficial, in
antrum/body of stomach
Common in women
and unskilled workers,
low socio-eco.
Burning, gas pressure
left epigastric, to back,
high abdominal.
Pain 1-2 hrs after
food intake.
Increased w/ smoking,
drugs and alcohol use
N/V, weight. loss
Duodenal-high end of
duodenum.
Common in men,
associated with psychic
stress, 80% of all ulcers
Burning, gnawing, midepigastric, to back, high
abdominal,pain 2-4 hrs
after meals, episodic,
middle of night.
Pain relief with antacids
and food intake, N/V.
Increased with alcohol,
Stress ulcers
Erosive gastritis caused by:
Transient GI ischemia (low blood supply)
with shock, severe injury, burns, surgery.
Low blood supply results in imbalance of acid
and mucus barrier- causing erosion.
Prevention: prophylactic meds:
antacid, Famotidine (Pepcid)
Complications of chronic ulcer
disease.
Hemorrhage, more common with
duodenal ulcers
Perforation, most lethal complication,
associated with peritonitis.
Gastric outlet obstruction-scaring and
atony of pylorus.
Systemic Acid Blockers
Histamine 2
Take any time of
day (x2), no food
restrictions
Zantac, Tagamet
(oldest, not for elderly/drug
interactions), pepcid
(IV, PO)
Proton Pump
inhibitors
Take in AM before
meal (30 min.)
Usually 1xday
Prilosec, Prevacid,
Protonex, Aciphex
Prilosec not indicated
for those on coumadin
Surgical interventions
ulcer disease
20% of ulcer pt’s require surgery, but
rarely performed now, usually resolved
with medications.
Procedures:
gastrectomy (billroth I or II)
vagotomy (cut vagus nerve to decrease gastic acid
secretion)
Pyloroplasty(pyloric dilatation)
Nursing interventions of Post-op
care
If NG present, maintain patency, nares care,
I&O, comfort, educational and emotional
support.
Surgical wound monitoring
Observe signs of bowel status: bowel sounds
present? r/o obstruction or bleeding)
Pain control (monitor, position change)
Post op teaching: diet, lifestyle risks and
changes
Dumping Syndrome
Results from reduced gastric capacity
after resection of most of the stomach and
pyloric sphincter.
Symptoms occur 15-30 min. after a meal,
feelings of weakness, sweating, palpitations,
dizziness
Due to large bolus of hypertonic fluid entering
intestine and fluid drawn into bowel, causes
distention of bowel.
Advise patient to lie down.
Postprandial hypoglycemia
Varian of dumping syndrome
Bolus of concentrated carbohydrate results in
hyperglycemia and excessive amounts of
insulin, occurs 2 hrs after meals.
Treatment-sugared fluids or candy to relieve
hypoglycemia. Then, limit amount of sugar
consumed with meal and eat small, frequent
meals.
Nutritional therapy related to
surgical intervention
Eliminate drinking fluids with meals
Dry foods with low carbohydrate
content (avoid high sugar diet)
Small meals
Rest after meals
Heliocobacter pylori bacterium
Promotes peptic ulcer formation
Acquired in childhood and common in adults
Gram-negative bacillus cultured in 1982
Prevalence of H. Pylori infection in duodenal
ulcer patients as high as 95-100%.
Treatment: triple Therapy (amoxicillin,
Biaxin,Prilosec)
H. Pylori and autoimmune
response
http://www.wnyc.org/shows/radiolab/e
pisodes/2009/09/25/segments/133980
c. Diff
http://www.nytimes.com/2010/07/13/s
cience/13micro.html?_r=2&ref=science
Upper GI hemorrhage
management
Upper GI hemorrhage is defined as loss of
more than 1500ml. Of blood, or 25% of blood
volume.
~200,000 hospital admissions year for UGI
bleed
Mortality rate 6-10%
Increased incidence of UGI bleed in older
adults, women r/t use of NSAIDs
Drug induced: aspirin, NSAIDs,
corticosteroids (get history!)
GI Hemorrhage-upper GI
Self-limiting in 85% of patients.
Originates from a number or sources:
-Peptic ulcer disease-accounts for ½ of
major upper GI bleeds.
-Portal hypertension-results in bleeding
Varices (most often esophageal),
accounts for 10-20% of hemorrhages.
Upper GI hemorrhage
Mallory-weiss tear-laceration of
gastroesophgeal junction, 5-10% of GI
hemorrhages, ~1/2 of patients report history
of heavy alcohol use or retching.
Vascular anomalies
Gastric neoplasm's
Erosive gastritis, usually superficial and
attributable to NSAID, aspirin, corticosteroids,
alcohol or stress.
Erosive esophagitis-due to chronic GERD
GI Hemorrhage
Obvious – hematemesis frank blood,
bright red or coffee- ground, ( dark
mahogany, grainy digested blood),
Melena- black, tarry stools
Hematochezia-stools containing bright red
blood.
Occult – not visible to the naked eye.
Presence of very small amount of blood in
mucus, gastric secretions or stool, detected
by guaiac test.
Esophageal varices
bleeding/hemorrhage control
Stabilize pt. and mange airway. IV
started (may include blood products).
Diagnosis determination
Endoscopic exam, lavage
Esophageal varices
management
Main goal is avoidance of bleeding and
hemorrhage.
Management of bleeding-medications
(vasopressin, nitroglycerin, b adrenergic
blockers), balloon tamponade,
sclerotherapy, ligation of varices, shunt
therapy
Causes: GI BLEED
In stomach & duodenum: erosion of bld.
Vessels in the lining due to:
peptic ulcer, stress ulcer,
hemorrhagic gastritis,
cancer, GI polyps, medications
Systemic disease: interfere with blood
clotting.
blood dyscrasias
leukemia
Nursing interventions
Stabilization, (don’t forget emesis basin!, universal
precautions) evaluation, vs q 15
min.,evaluate for signs of shock, lab
values, ABGs, U/A, guiac stool, IV fluid
replacement Assessment of
hemodynamic status, hematocrit, NG
tube placement, pharmacologic
intervention, use of O2 blood
replacement, endoscopy.
Cancer of stomach
7th leading cause of cancer mortality in
US.
Worldwide, 2nd most common form of
cancer, Japan and Costa Rica have
highest rates
More common in men
Signs and symptoms
Manifestations may exhibited by: pain,
anemia, ulcer disease, indigestion.
Detection difficult due to vagueness of
symptoms.
Diagnostic tests: analysis of blood, stool and
gastric secretions(histology), CEA test
(carcinoembryonic antigen), upper GI series,
endoscopy.
Surgery-gastrectomy as radiation and
chemotherapy not proven to be successful as
primary intervention.
Nausea and Vomiting
Feeling of discomfort with desire to vomit
(forceful ejection of food and secretions-emesis)
Related to slowing of gastric motility and
emptying, or if GI tract becomes irritated,
excited or distended.
Nausea is subjective usually accompanied by anorexia (lack
of appetite)
May result in dehydration, electrolyte imbalances,
decreased plasma volume, metabolic alkalosis,
weight loss, threat of aspiration (elderly, unconscious
or conditions that impair gag reflex)
N&V
Most common manifestation of GI
diseases
Protective mechanism
Fecal odor or bile (d. green) indicate
lower GI obstruction
Collaborative care
Emotional support
Nutritional therapy-IV
fluids, electrolyte
replacement, glucose, advance to clear liquids-full liquids.
NG tube to suction (decompression)
Dietary consult
Nursing diagnosis: imbalanced nutrition:
less than body requirements.
Gerontologic considerations
Increased risk of cardiac or renal
insufficiency, fluid/electrolyte
imbalances, increased susceptibility to
CNS side effects of antiemetic meds.
Caution with fluid replacement (monitor fluid
status: edema, BP, resp. status)
Alteration in LOC (increased risk for aspiration)
Medications/antiemetics
Easier to prevent than treat! Give
prophylactically.
Most cause sedation
Prokinetic-Reglan (aka metoclopromide, dopamine and
serotonin receptor blocker, increases upper GI motility)
Serotonin Receptor agonists-Zofran, Kytril,
Anzemet,( used for Chemo and induction of anesthesia)
Dopamine antagonists-Phenothiazines-Phenergan,
compazine, thorazine. Butyrophenones-Haldol
Diarrhea
Not a disease but a symptom
May be acute (infection, can be selflimiting) or chronic (2-4wks)
May result in explosive watery diarrhea,
tenesmus, cramping, abdominal pain.
Perianal skin irritation
Symptoms continue until the irritant or
causative agent is excreted.
Potential Consequences of diarrhea
Debilitating, life threatening
Dehydration
Electrolyte imbalances
Malabsorption and malnutrition
Major cause of death throughout world
(especially in children)
In 2009 diarrhea was estimated to have
caused 1.1 million deaths in people aged 5
and over and 1.5 million deaths in children
under the age of 5 (wikipedia)
diagnosis
History: travel, food ingestion (diet, food
allergies, lactose intolerance) medications,
surgery, family exposure, etc. (see previous chart)
Lab: WBC, anemia, iron and folate
deficiencies, elevated liver enzymes,
electrolyte disturbances. Stool: blood, mucus,
WBC’s, paracites (O&P), culture, fat content
Collaborative care
Based on cause and aimed at replacement of
fluid and electrolytes, decrease in number,
volume and frequency of stool.
Physical assessment: vs, weight, skin
breakdown, abdominal inspection
Oral replacement-water, solutions containing
glucose and electrolytes (mild)
Parenteral- fluids, electrolytes, vitamins,
nutrition (severe)
Antibiotics, antidiarrheals
Nursing implementation
Infection control
Pt support-emotional, fatigue,
embarrassment, pain
Hydration status, I&O, fluid
replacement
Normal nutritional intake
medications
Antibiotics-specific to organism, but may
cause inreased diarrhea by altering normal
GI flora (lactobacillus)
May be susceptible to Clostridium difficile
infection ( treated with Vancomycin, Flagyl)
Healthcare workers use vigilance regarding
transmission (isolation, hand friction, gloves)
Diarrhea etiology
(general classifications)
Diarrhea-infectious
Lower GI hemorrhage
Hematochezia usually present
Bleeding from small intestine or colon
Etiology: diverticulosis, most common
cause of lower GI bleed, ~40%. Present
in patients who are >50 with
hematochezia
Vascular ectasis-common in patients
over 70yrs old.
Lower GI hemorrhage
Neoplasms
Inflammatory bowel disease-ulcerative
colitis, often have diarrhea with varying
amounts of hematochezia. Symptoms:
abdominal pain, urgency and tenesmus.
-Tenesmus-spasmodic contraction of anal
sphincter with pain or persistent desire
to empty bowel or bladder.
-Anorectal disease-hemorrhoids, fissures.
Inflammatory Bowel disease
Crohn’s disease
Most often seen in
ileum, jejunum and
colon.
Abscesses or fistulas
may develop
Nonbloody diarrhea
and abdominal pain.
Not cured by surgery
Tx to rest bowel
Ulcerative colitis
Multiple abscess
develop
Bloody diarrhea and
abdominal pain
Tenesmus
Cure with colectomy
Tx to rest bowel
Diverticulosis and diverticulitis
Multiple outpouching of mucosa in colon.
Diverticulosis-multiple, noninflammed
diverticula, pt. often w/o symptoms
Diverticulitis-inflammation of diverticula in
sigmoid colon, due to retention of stool and
bacteria in diverticulum Associated with lack
of dietary fiber.
Pt. should not have BE or colonoscopy due to
possibility of perforation or peritonitis.
Ulcerative colitis
Inflammation and ulceration of colon and
rectum, multiple abscesses may develop
Higher incidence in women, age 15-25,
chronic disorder
Symptoms: bloody diarrhea and abdominal
pain.
Treatment-rest bowel, medications, diet,
surgery
Crohn’s disease
Inflammation of segments of GI tract,
most often ileum, jejunum and colon,
chronic disorder
Abscesses and fistulas may develop
Symptoms: diarrhea, fatigue, abdominal
pain, weight loss, fever.
Treatment-drug therapy, nutritional
therapy, surgery does not cure disease.
Cancer of colon and rectum
2nd most common cause of cancer death in
US. Diet is most important environmental
factor associated with colorectal cancer.
Symptoms: rectal bleeding, changes in bowel
habits, abdominal discomfort, occult bleeding.
Steady blood loss as it grows and ulcerates
Diagnostic studies
Digital rectal exam
Sigmoidoscopy, barium enema, CT
scan, lab tests (anemia).
Treatment-surgery, extent determined
by location and extent of cancer,
radiation , chemotherapy.
GI Inflammation & Infection
Acute abdomen – sudden onset
abd. pain
requiring prompt decision making.
Varied causes: trauma, ischemic
bowel, ulcers, PID, pancreatitis, GB,
ruptured gut, uterus, ovarian cysts,
peritonitis, perforations, bowel
obstruction.
Acute Abdomen dx and tx
Exploratory laparotomy –
“open, look & see”.
Diagnostic as well as a surgical
procedure.
Use to surgically remove (GB, appendix)
or surgically repair (ruptured abdominal
aortic aneurysm)
Trauma - abdominal
Blunt trauma – motor vehicle accident
Penetration injuries – gunshot, stab wounds
Both results in internal organ damage..
Trauma: signs and symptoms
See: contusions, abrasions, hematoma,
bruising,
Cullen’s sign, Turner’s sign.
hematuria, hematemesis
Feel: hard, distended abdomen
guarding, splinting.
Hear: absent or decreased bowel sounds.
Peritonitis
Local or generalized inflammation.
Primary causes: infections from blood,
cirrhosis w/ ascitis, genital tract organisms.
Secondary: ruptured appendix, blunt or
penetrating abdominal trauma, pancreatitis,
ruptured diverticulitis, peritoneal dialysis.
S/S: abd. pain, rebound tenderness, spasm
Pancreatitis
Mild edema to severe necrosis of the
pancreas.
More common in middle-aged men.
Common causes: alcoholism, GB disease
Less common causes: trauma, viral,
duodenal ulcer, pancreatic cysts, CF,
drugs (sulfas, thiazides steroids, NSAIDs)
Pancreatitis
Auto digestion of pancreas due to
reflux of bile acids into pancreatic duct.
as in post GI surgery,
post ERCP -
ERCP - Endoscopic retrograde
cholangio-pancreatography
Pancreatitis: manifestations
Abdominal pain – LUQ to mid epigastric,
radiate to back.
Deep, piercing, steady pain.
GI: pain aggravated by food, nausea not
relieved by vomiting, distended abd (ileus)
absent bowel sounds.
CV/resp . <BP, >HR, >RR, fever, crackles
Skin: jaundiced, flushed,
Pancreatitis: Dx & treatment
DX: elevated serum amylase, lipase
ERCP reveals gallstones
xrays of abd. Ultrasound
TX: NPO then high CHO, lo fat, hi
protein
Relieve pain and spasm
Meperidine, nitro, papaverine
Cholecystitis/Cholelithiasis
Cholecystitis commonly due to bile stones
Also caused by bacteria (e. coli,
streptococci, salmonella) from vascular or
lymphatic route or chemical in bile.
Cholelithiasis bile supersaturated with
cholesterol causing precipitation – stones.
Stones may migrate to cystic or CBD ducts
resulting in obstruction.
S/S indigestion, pain, fever, jaundice, N/V
Fluid Elect. Imbalances
from GI fluid loss (daily amts)
Salivary
glands
Stomach
Small
intestines
Pancrease
Liver, GB
1000 to
1500 ml
Enzyme-
Amylase
(ptyalin)
2500 ml
Pep’gen,hcl
Gastric juice Lipase,I fac
3000 ml
Amyl,lipase
peptidases
700 ml panc Tryp’gen,
reatic juice Amyl, lipase
1000 ml
Bile
bile
Initiates
CHO digest
Protein, fat
Cobalamin
CHO, fat
protein
Protein, fat
CHO
Fat
emulsion
Fluid losses from GI
Vomiting
Gastric/intestinal suctioning
Diarrhea
Ileostomy
Prolonged use of laxatives
enemas
Parenteral fluid/elect
replacement
Provide adequate fluid replacement.
Dietary consult. Calorie count.
Monitor labs: elect., glucose, albumin levels.
Monitor tube placement– gastric residual
output (grass green color), acid level, amount
Monitor temps, WBC, infection control ”wick”
via NG tube, frequent oral care, nasal care.
I & O- IV fluids, PEG/tube feeds, BM, ostomy
drainage.
IV fluids, electrolytes,
parenteral feedings:
Crystalloids- dextrose, Ringer’s lactate
Colloids – albumin
Bld products- packed RBC, leucocyte
poor blood, Fresh Frozen Plasma
Electrolytes- Kcl, Nacl
PPN - peripheral parenteral nutrition
TPN – total parenteral nutrition
Influencing factors GI
Environment: lifestyle, travel
Growth and development: childhood illness
, eating habits anorexia nervosa, bulimia
Diversity: home remedies, intolerances,
obesity, eating disorders, dietary
preferences
Sexuality: practices, slimming diets, exercise
Coping - stress response result in ulcer
formation or aggravation
c. Influencing factors
Aging:
Loss of appetite due: problems with gums,
teeth, loss sense of taste, smell, less saliva
Delayed esoph. emptying, incompetent LES,
< gastric motility,< emptying ,< HCL, I factor
< ability of liver to metabolize med/hormones
Constipation: name 7 causes
Pediatric Differences
GI system immature at birth
Gastric capacity – newborn – 10-20ml
1 wk.- 30-90, 1 mo.- 90-150, 1yr.- 210-360
Peristalsis greater in newborn – loose BM
Digestion occurs in duodenum
Enzymes are deficient until 4-6 months
Liver function immature.
Structural Defects:
Cleft lip, cleft palate- difficulty feeding.
Esophageal atresia (blind pouch) w/
tracheo-esophageal fistula.
Pyloric stenosis- obstructive hypertrophy of
the circular muscle around pyloric canal,
S/S: projectile vomiting, irritable, hungry.
Surgical correction –treatment of choice.
Disorders - GI Motility in Child
Gastroenteritis –inflammation of the
stomach & intestines accompanied by
vomiting, cramps and diarrhea
Kids in day care, poor housing sanitation
Average 5 yr old - 2 episodes/year
Cause- viral, bacterial, parasitic.
Risk for hypovolemic shock if untreated
due to severe dehydration.
Health History
Health Mgt: Smoking, alcohol,exposure,travel
Usual daily food and fluid intake, weight
gain/loss, food allergies, intolerances.
Measures (cultural) used to treat symptoms,
pain, diarrhea, nausea, vomiting, caregiver
Elimination pattern: frequency, time of day,
consistency
Activity/sleep pattern: How exercise affect GI,
been awakened by gas, heartburn.
Relationships, stress/coping, value/belief
patterns.
Assessment: syllabus outline
Nursing history: main complaint, pain,location
duration, aggravation by food or not.
Medical hx, family hx, meds, OTC drugs.
Physical exam: oral, dental, gum, breath odor
Abdomen: skin pigment, scars, striae, masses
pulsations, bruits, bowel sounds, peristalsis,
distention. Note location, quadrants, region.
Inspect, auscultate, percuss first, then
palpate. “Listen before you touch.”
Common alterations/disorders: chronic or
recurring.
Diagnostic Tests: prep and
care
Fiberoptics: EGD, ERCP- examines upper GI.
proctosigmoidoscopy colonoscopy- lower GI.
Xrays: barium swallow- esophageal study
Ultrasounds, CT scans, angiography
Lab tests: serum amylase, lipase
Stool- clay-colored, guaiac, ova/parasite
Gastric analyses- acidity and content
Paracentesis- removal ascitic fluid- dx and tx
Tube feeding
Types: gastrointestinal- short vs longterm
gastrostomy-differt insertion than PEG
Jejunostomy- do not check residuals.
Formulas: depending on alteration.
Precautions: aspiration, HOB 30 degrees,
stop feeding w/ patient turns, ? residuals
Infection: oral care, intubated, how often.
Prevent accidental displacement or removal.
Surgical Care
Vagotomy (reduce acid in peptic ulcer)
Billroth I, II (dumping syndrome)
Bowel resection (seminar)
Fecal diversions
colostomy
ileostomy
Nursing Diagnoses - GI
Impaired tissue integrity: chemical irritant
Altered elimination: diarrhea, constipation
Risk fluid volume deficit r/t vomiting,
diarrhea, gastric decompression, hemorrhage
Risk for infection/altered protection
Risk impaired peristomal skin integrity
Nursing Diagnoses: GI
Altered comfort: pain r/t tissue damage
inflammatory process
distention, nausea
Knowledge deficit r/t disease and
treatment
P.C. metabolic alkalosis/acidosis
P.C. low potassium, low/high sodium,
low magnesium
Interventions
Position: semi-fowlers, knee support
Activity: bedrest, BR privilege, commode
Pain mgt: assess and treat regularly.
Diet mgt: npo, ice chips, mouth care, liquids
Meds: a.c. p.c. crushed, via feeding tubes
GI tubes purpose:decompression/feeding
salem-sump - for decompression- low suction
levine, Keofeed or Dobhoff,
intestinal tubes (Miller, Abbot)
Outcome Criteria
Normovolemic status – vital signs stable
NO infection and injury, adequate blood
sugar, electrolytes, calories required.
Pain decreased.
Self-care, ADL, dressings.
Verbalize knowledge about cause and
rationale for treatment.
Discharge planning/teaching
Lifestyle modification: diet, activity,
weight and stress management,
relaxation techniques, OTC drugs.
Signs of exacerbation, infection
Wound, colostomy care, follow-up
Sexuality concerns
Support groups and com. resources
Legal and ethical issues
Withholding Treatment
26 yr old patient in a permanent vegetative
state, enteral tube fed, w/ 15th bladder
infection.
Should antibiotics be w/held? Feeding?
Family expressed concern that no heroic
measures be used to extend biologic life of
their daughter. They have been unwilling to
withdraw existing enteral nutrition.
Ethical and Legal Principles
Treatment maybe withheld if a competent
patient, refuses consent, if it is medically
futile or if the burden of it’s provision
outweighs the benefit.
If withholding treatment leads to death, the
underlying disease is the cause. Intervention
simply prolongs life.
Pt in a permanent vegetative state cannot be
cured of that brain damage. Any treatable comorbidities related to condition will not lead
to recovery from permanent vegetative state.
Bibliography
Medical-Surgical Nursing, 7th edition, Lewis,
Heitkemper, Dirksen, O’brian, Bucher.
Atlas of Human Anatomy, 4th edition, Netter
Pharmacology, 3rd edition, Kee and Hayes
Understanding Nutrition, 11th edition,
Whitney.