SECOND SEMESTER 2008 – 2009

LECTURE:

ACTIVITIES

1. Group Reporting

a. Anatomy and Physiology

b. Assessment
c. Physical Examination
d. Diagnostic Test
e. Stomatitis
f. Diverticulosis
g. Cholelithiasis

2. Assignment

a. Journals
• Client’s with lip / cleft palate
• Client’s with hiatal hernia
• Client’s with ulcers
• Client’s with cystic fibrosis
• Client’s with diabetes
b. Nursing Care Plans

3. Quizzes / Unit Exam

a. 15 items per meeting

b. 50 items unit exam.

4. Graded Recitation

a. Esophageal Atresia / Fistula

b. GERD
c. Intestinal Obstruction
• Pyloric Stenosis
• Hirshprung Disease
• Intussusception

d. Hypothyroidism / Hyperthyroidism
e. Addison / Cushing
 COURSE SYLLABUS
I. COURSE TITLE: NCM 103 - A

II. COURSE CONCEPT: Alteration in ENDOCRINE and METABOLISM

III. OBJECTIVE: At the end of 20 hrs, the student will be able to acquire the
knowledge, skills and attitude relevant to the care of clients with nursing problems
related to metabolism and endocrine. The students will also be able to utilize the
nursing care process in prioritizing the needs of clients with disturbances in
metabolism and endocrine.

IV. COURSE DESCRIPTION: This course deals with the principles and
techniques of nursing management of general problems of the sick client in all stages
of development in the institution or community. Emphasis is placed on the
application of the nursing process considering further the psychological,
pathophysiological aspects and the client’s needs and problems.

V. TIME ALLOTMENT: 20 Hours (4 Hrs. / meeting)

VI. METHODOLOGY: Interactive lecture

Simulation
Case analysis

VII. COURSE OUTLINE:

A. Anatomy and Physiology of GI System

B. Assessment of GIT
1. History
2. Physical Examination

C. Laboratory / Diagnostic Test

1. Laboratory Examinations 5. Ultrasonography
2. Radiographic Tests 6. Exfoliative Cytology
3. Endoscopy 7. Computed Tomography
4. MRI
D. Disorders of GI System / Endocrine
1. Cleft lip / Palate
2. Stomatitis
3. Esophageal Atresia / Fistula
4. Hiatal Hernia
5. Gastroesophageal Reflux
6. Ulcers
7. Intestinal Obstruction

i. Pyloric Stenosis
ii. Hirshprung Disease
iii. Intussusception

8. Diveticulosis
9. Elimination

i. Anorectal abnormalities
a. Hemorroids
b. Imperforate anus

10. Hepatic Disorders

i. Hepatitis
ii. Cholelithiasis
iii. PKU

11. Exocrine Disorder

i. Cystic Fibrosis

12. Endocrine Disorders

i. Hypothyroidism
ii. Hyperthyroidism
iii. Addison
iv. Cushing
v. Diabetes
 The Digestive System
Care of Clients
with Problems in Metabolism

Functions of the GI System

• 1. Convert ingested nutrients and fluids so that they can be assimilated into the
body for nourishment of tissue.
• 2. Store and then excrete solid waste residue of the tract.

• The Gastrointestinal System is a 23- to 26 foot pathway for food, water, vitamins
and minerals for which has the primary function of breaking down food products
that can fuel the body as a source of energy.

3 Main Processes of the Gastrointestinal System

• 1. Digestion: the mechanical and chemical breakdown of food into amino acids,
glucose and fatty acids for usage of the body’s cellular functions.
• 2. Absorption: the passage of digested food products (i.e., essential nutrients)
from the lumen of the gastrointestinal tract into the blood and the lymphatic
system.
• 3. Metabolism: use of the basic food products by the cell.

Gastro-intestinal System

• The gastrointestinal system consists of the mouth, the pharynx or throat,

esophagus, stomach, and small and large intestines.
• Accessory Organs are the teeth and salivary glands in the mouth, the liver,
gallbladder, and pancreas.
• Mouth---bite, chew, swallow
• Pharynx and esophagus----transport
• Stomach----mechanical disruption; absorption of water & alcohol
• Small intestine--chemical & mechanical digestion & absorption
• Large intestine----absorb electrolytes & vitamins (B and K)
• Rectum and anus---defecation

Secretions of the Gastrointestinal System

• 1. Exocrine secretions: prepare food for absorption by diluting osmolality of
plasma (isotonic in nature), altering the ph for the purpose of hydrolysis, and
hydrolyzing complex foods. It also protects the mucosa from physical and
chemical irritants.

• 2. Endocrine secretions: critical in the control and coordination of secretory and

motor activities involved in the digestion and absorption of food.
 • Microflora or indigenous bacteria exist throughout the G.I. tract. This protects the
host from pathogens if maintained to a normal level.

Onset of Digestion

Process of Chewing or Mastication

1. The salivation reflex is stimulated just by the sight, smell,
or tasting food. About 1.5 liters of saliva is secreted daily
by the 3 pairs of glands – parotid, submaxillary, and
sublingual glands.

2. Saliva contains the enzyme ptyalin, or salivary amylase,

which begins the digestion of starches.
Swallowing
Upon swallowing, the epiglottis moves to cover the tracheal opening and
prevent swallowing

Esophageal Peristalsis
A reflex action into the upper esophagus propels the bolus of food
contracting in a rhythmic sequence toward the stomach. The process of esophageal
peristalsis simultaneously relaxes the esophageal sphincter to permit this movement
of food to the stomach.

Stomach
The stomach produces acidic fluid called the hydrochloric acid. Its purpose is
to further breakdown food into a more absorbable component and to aid in the
destruction of ingested bacteria.

1. The enzyme pepsin, initiates protein digestion.

2. Intrinsic factor is also secreted by the gastric mucosa which combines
with dietary vitamin B12 so that it can be absorbed in the ileum. The absence of this
intrinsic factor results to pernicious anemia.

Peristalsis in the Stomach

Peristalsis in the stomach (about half hour to several hours) propels food to
the pylorus. The pyloric sphincter contracts to allow food to move towards the small
intestines. Food mixed with gastric secretions is called chyme. Gastric secretions and
motility is governed by hormones, neuroregulators, and local regulators.
Small Intestines
Upon reaching the duodenum, accessory organs contribute to the secretions
encountered by food therein:
1. Pancreas: secretes alkaline ph, high in concentrations of bicarbonate, to
neutralize the acid entering the duodenum from the stomach. Digestive enzymes
involved from the pancreas are:
a. Trypsin: digests proteins.
b. Amylase: digests starch.
c. Lipase: digests fats.
2. Liver: secretes bile which emulsifies fats.
3. Gallbladder: stores bile secreted by the liver that will aid in the digestion and
absorption of fats.

• Small, fingerlike projections called villi are present in the entire intestines that
produce the digestive enzymes and absorb nutrients from food. Absorption is the
primary function of the small intestines which begins in the jejunum by active
transport and diffusion across the intestinal wall.

Large Intestines
• After four hours of eating, waste residuals are passed in the terminal ileum into the
proximal portion of the colon through the ileoceccal valve. Bacteria make up a major
component of its contents which are neutralized by electrolyte secretions and mucus.
• Controlled by the autonomic nervous system (parasympathetic nerve fibers as a spinal
reflex), defecation is elicited by the relaxation of the external anal sphincter.

The path of food:

oral cavity/teeth/

oropharyn

esop

stom

small intesti
ASSESSMENT OF GIT

• Health History
– Demographic Data (age, sex)
– Personal & Family History
– Diet History: indicates or reveal changes or patterns of eating that reflect
characteristics symptoms or disorders
– Chief Complaint
• Onset
• Duration and frequency
• Quality & characteristics
• Severity and factors that aggravate complaint
• Location, spread and radiation
• Precipitating Factors
• Relieving Measures / factors
• Treatment measures
• Associated Symptoms
• Setting

• Cont on Health History

– Family History
– Medical history
– Major illness and hospitalization
– Medications
– Allergies
– Psychosocial history and lifestyle
– Spiritual
• Physical Examination/Review of Systems
A. Assessing the oral cavity
B. Assessing the abdomen
• Inspection
• Palpation
• Percussion
• Auscultation
C. Assessing the anus and rectum
DIAGNOSTIC TESTS

• Laboratory Tests
– CEA ( Carcinoembryonic Antigen)
• (+) colorectal Ca
• X heparin for 2 days
• Specimen by venipuncture
– Exfoliative Cytology
• Detect malignant cells
• Written consent
• Liquid diet
• UGI : NGT insertion
• LGI : laxative; enema
• Cells are obtained from saline
• Lavage – NGT / Proctoscope

Fecal Analysis
– Stool for Occult Blood (Guaiac Stool Exam)
• Detect G.I. Bleeding
• fiber diet 48 – 72 hours
• X red meats, poultry, fish, turnips, horseradish
• Withold for 48 hrs: Iron, Steroids, Indomethacine, Colchicine
• 3 stool specimen ( 3 successive days)
– Stool for Ova and Parasites
• Send fresh, warm stool specimen
– Stool Culture
• Sterile test tube / cotton – tipped applicator
– Stool for Lipids
• Assess steatorrhea
• fat diet, No alcohol ( 3 days )
• 72 hour stool specimen ( store on ice )
• X mineral oil, neomycin SO4
 LABO
• Gastric Analys
Analy
– Measures s
RADIOGRAPHIC TESTS

– NPO for 12
• Scout Film / Flat Plate of the Abdomen
– Plain X – ray of the abdomen
– X belts / jewelries

• UGIS ( Barium Swallow)

– NGT is inse
– To visualize the esophagus, stomach, duodenum and jejunum
– NPO for 6 – 8 hours
– Barium Sulfate (BaSO4) per orem

– After the procedure:

• Laxative
– Gastric con
– X – rays taken on standing, lying position

minutes to
• Increase fluid intake
• Inform client that the stool is white for 24 – 72 hours
• Observe for Ba impaction : distended abdomen, constipation

• LGIS (Ba Enema)

– To visualize the colon
– Low residue / clear liquid diet for 2 days
– Laxative for cleansing the bowel
– Suppository / cleansing enema in A.M.
– BaSO4 per rectum
↑HCL
↑HCL:: Zolling
Zollin
Dou
– Care after the procedure – same as UGIS

Do
ENDOSCOPY

• UGI Endoscopy
– Direct visualization of esophagus, stomach, and duodenum
– Obtain written consent
– NPO for 6 – 8 hours
– Anticholinergic (AtSO4) as ordered
– Sedatives, narcotics, tranquilizers
• E.g. Diazepam, Meperidine HCl
– Remove dentures, bridges
– Local spray anesthetic on posterior pharynx – instruct : X swallow saliva
– After the procedure
• Side – lying position
• NPO until gag reflex returns (2 – 4 hrs)
• NSS gargle; throat lozenges
• Monitor VS
• Assess : bleeding, crepitus (neck), fever, neck / throat pain,
dyspnea, dysphagia, back / shoulder pain
• Advise to avoid driving for 12 hours if sedative was used.

• LGI Endoscopy
– Proctosigmoidoscopy (sigmoid, rectum)
• Clear liquid diet 24 hours before
• Administer cathartic / laxative as ordered
• Cleansing enema
• Knee – chest / lateral position
• After the procedure
– Supine position for few minutes
– Assess for signs of perforation
• Bleeding
• Pain
• Fever
– Hot sitz bath for discomfort
– Colonoscopy
• Sedation
• Position : left side, knees flexed
• After the procedure:
– Monitor VS (note for vasovagal response)
– Assess for signs and symptoms of perforation.
• Ultrasonography
– NPO for 8 – 12 HOURS
– Laxative as ordered (↓ bowel gas)

• Magnetic Resonance Imaging

 – Non-invasive producing cross sectional images of soft tissues and blood
vessels using magnetic fields.
– C/I: pacemakers, aneurysm clips, or orthopedic screws
– NPO 6h before
– Instruct to lie still for 60-90 minutes.
– Remove all jewelries

Disturbances in Metabolism
CLEFT LIP / PALATE
• A congenital anomaly that occurs as a result of failure of soft tissue or bony
structure to fuse during embryonic development.

• The defects involve abnormal openings in the lip or palate that may occur
unilaterally or bilaterally and are readily apparent at birth

• Cleft lip occurs with or without cleft palate.

• Cleft lip results from the incomplete fusion of the embryonic primitive oral cavity
structures on the 7th week of gestation.
 indentation of the lip to the extent of a deep and wider fissure to the
nostril
 unilateral or bilateral which may or may not be associated with cleft
palate. Dental anomalies are common.

• Cleft palate is the failure of the primary and secondary palatine plates to fuse
during embryonic development from the 7th to the 12th week of gestation.
 It may involve the soft palate only to the extent of the hard palate, or
occurring only in the midline of the posterior palate, but also to the extent
to the nostril on one or both sides.

• Causes include:
a. Multifactorial Inheritance
b. Chromosomal Anomalies
c. Environmental Factors or Teratogens

• TYPES
A. Notch in vermillon border
B. Unilateral CL and CP
C. Bilateral CL and CP
D. Cleft Palate
ASSESSMENT
1. Cleft lip can range from a slight notch to a complete
separation from the floor of the nose.
2. Cleft palate can include nasal distortion, midline or bilateral
cleft and variable extension from the uvula and soft and hard
palate.
-obviously visible at birth; assess the location and extent of the defect
during crying; palpate the palate with gloves during newborn assessment

Diagnosis
a. Preoperatively
i. Imbalanced nutrition (less than body requirements) related to physical defect.
ii. Risk for impaired parenting related to infant with highly visible defect.

b. Postoperatively
i. Potential for trauma of the surgical site related to the surgical
procedure compromised swallowing.
ii. Interrupted family processes related to the child with physical defect.

Cleft Lip &

Palat
• Planning
Intervention
•Cleft lip : surgical repair
• 1. Assess the ability to suck, swallow, handle normal secretions and breathe
without distress.
• 2. Assess fluid and calorie intake daily and monitor weight.
palate on the first week o
• 3. Modify feeding techniques; plan to use specialized feeding techniques,
obturators and special nipples and feeders.
• 4. Hold the child in an upright position and direct the formula to the side and
several staggered suture line
back of the mouth to prevent aspiration; feed small amounts gradually and
burp frequently.

notching of the lip from retra

• 5. Position on side after feeding.
• 6. Keep suction equipment and bulb syringe at bedside.
• 7. Encourage breast feeding if appropriate.

and to lengthe
 • 8. Teach the parents special feeding or suctioning techniques.
• 9. Teach the parents the ESSR method of feeding.
• 10.encourage the parents to describe their feelings related to the deformity

MANAGEMENT

• A. CHEILOPLASTY : ideally 6 -12 weeks old

• B. PALATOPLASTY : ideally 12 -18 months

• a. Preoperatively
• Consumption of adequate caloric needs.
• - hold the infant’s head in an upright position, use special nipples
or other feeding devices, direct the formula to the back of the mouth to prevent
aspiration.
• -frequently burp: tendency to swallow more air.
• - breastfeeding is possibly accomplished by using a breast pump
first, positioning the nipple and stabilizing it well at the back of the oral cavity of
the infant so that the tongue’s action can facilitate expression of milk.

ESSR METHOD OF FEEDING

• Enlarge the nipple
• Stimulate the suck reflex
• Swallow
• Rest to allow the child to finish swallowing what is left in the mouth.

b. Postoperatively

1. CLEFT LIP REPAIR

• a. A lip protector device may be taped securely to the cheeks to prevent
trauma to the suture line.
• b. Position the child on the side lateral to the repair or on the back; to
avoid the prone position to prevent rubbing of the surgical site on the mattress
• c. After feeding, cleanse the suture line of formula or serosanguineous
drainage with a cotton tipped swab dipped in saline; apply antibiotic ointment if
prescribed.
•
2. CLEFT PALATE REPAIR
• a. Child is allowed to lie on the abdomen.
• b. Feedings are resumed by bottle, breast or cup.
• c. Oral packing may be secured to the palate.
• d. Do not allow the child to brush his or her teeth.
• e. Instruct the parents to avoid offering hard food items to the child, such as
toast or cookies.
• SOFT ELBOW OR JACKET RESTRAINTS MAY BE USED (CHECK AGENCY
POLICIES AND PROCEDURES) TO KEEP THE CHILD FROM TOUCHING
THE REPAIR SITE; REMOVE RESTRAINTS ATLEAST EVERY 2 HOURS TO
ASSESS THE SKIN INTEGRITY AND ALLOW FOR EXERCISING THE ARMS.
• AVOID CONTACT WITH SHARP OBJECTS NEAR SURGICAL SITE.
• AVOID THE USE OF ORAL SUCTION OR PLACING OBJECTS IN THE
MOUTH SUCH AS A TONGUE DEPRESSOR, THERMOMETER, STRAWS,
SPOONS, FORKS, OR PACIFIERS.
• 6. PROVIDE ANALGESICS FOR PAIN.
• 7. INSTRUCT THE PARENTS IN FEEDING TECHNIQUES AND IN THE CARE
OF THE SURGICAL SITE.
• Instruct the parents to monitor for signs of infection at the surgical site, such as
redness, swelling or drainage.
• 9. Encourage the parents to hold the child.
• 10. Initiate appropriate referrals for speech impairment or language based
learning difficulties.

 OBJ 1: Will experience no trauma on the site of operation.

• 1. Position:
– Cleft lip repair (cheiloplasty): avoid prone position (supine position and
side lying is recommended)
– Cleft palate: lie on his abdomen.

• 2. Restraint
– -Cleft lip will use a protective device on the suture line and elbow
restraints to prevent him from rubbing the site. Remove the restraints
every 2 hours to allow opportunity for cuddling and body contact.

• 3. Avoid oral suctioning or placing objects in the mouth (like tongue depressors,
thermometer, straw, etc.).

 OBJ 2: Will consume adequate caloric needs.

1. Administer diet appropriate for age.
2. Involve the parents in choosing the best feeding method since it will be them who
will assume the feeding responsibility at home.
3. Feed in sitting position to prevent aspiration.

 OBJ 3: Will receive adequate support from the family.

• Encourage parents to hold their child. Referrals to speech therapists to evaluate
the needs of the child and to guide the parents for activities that will promote
speech development.
• The ultimate goal is the development of a healthy personality and self-esteem.
 NURSING DIAGNOSIS
• 1.Alteration in Nutrition : Less than body requirements
• 2. Risk for Infection
• 3. Ineffective Breastfeeding
• 4. Altered parent – infant attachment / Risk for altered parenting
• 5. Post Op; Risk for trauma of surgical site.
• 6. Pain

Evaluation
1. A home care nurse provides instructions to the mother of an infant with cleft palate
regarding feeding. Which statement if made by the mother indicated a need for further
instructions?
• a. “I will use a nipple with a small hole to prevent choking.”
• b. “I will stimulate sucking by rubbing the nipple on the lower lip.”
• c. “I will allow the infant time to swallow.”
• d. “I will allow the infant to rest frequently to provide time for swallowing
what has been placed in the mouth.”

Rationale: The mother is taught the ESSR method of feeding the child with a cleft
palate: enlarge the nipple, stimulate the sucking reflex, swallow and rest to allow the
infant to finish swallowing what has been placed in the mouth. (Saunders)

2. An infant has just returned to the nursing unit following a surgical repair of a cleft lip
located on the right side of the lip. The nurse places the infant in which most appropriate
position?
• a. On the right side
• b. On the left side
• c. Prone
• d. Supine

Rationale: After cleft lip repair the infant should be positioned supine or on the side
lateral to the repair to prevent the contact of the suture lines with the bed lines.
Placing the infant on the left side rather than supine immediately after surgery is
best to prevent the risk of aspiration if the infant vomits. (Saunders)
STOMATITIS
Inflammation of the oral cavity
Causes:
1. Mechanical Trauma - injury, jagged teeth, cheek biting, mouth breathing
2. Chemical Trauma – drugs given to cancer pts., foods, drinks, sensitivity
to mouthwashes or toothpaste
Complications:
• 1. Infections 3. Bacteria
• 2. Viruses 4. Yeast or Fungus
Classification:
• 1. Primary – canker sore, herpes simplex
• 2. Secondary – decreased resistance, opportunistic infections
• * systemic disorder like : allergies, bone marrow disorders,
nutritional disorders, immunodeficiency, chemo therapy
, radiation or immunosuppressive
Signs and Symptoms:
• 1. small vesicles or erupted vesicles (sore)
• 2. shallow ulcer
• 3. tongue with heavy white coating
• 4. foul breath odor
• 5. pain
Intervention:
• 1. Nursing History to prevent recurrence
• Remove cause.
• 2. Care of lesion
• Frequent, soothing oral hygiene measures.
• 3. Lip Balm
• 4. Saline solution, 50% Hydrogen peroxide or NA HCO on cotton swabs, swish
every 2 – 4 hours
• 5. Adequate nutrition and balanced food
• 6. Mechanical soft diet at room temperature.
• 7. Vitamin C
• 8. Apply topical oral medications (Hydrocortisone, Antibiotics).
• 9. Avoid hot spicy, salty, acidic or abrasive foods.
 Manifestations
common Stom
Type Causes Manifesta
Cold sore Herpes Initial bur
fever blister Simplex Virus
• Diagnosis: Altered oral mucous membrane: r/t traumatic conditions, infections Clustered

Evaluation lip or oral

• 1. The nursing diagnosis is Acute Pain related to altered oral mucous membrane
Aphthous Unknown, Well circu
and ulcerations for a client with Vincent’s angina. To wash the mouth, the client
should be instructed to use
•
• ulcer (canker
a. a commercial mouthwash.
b. Dakin’s solution. may be type of erosions
•
• sore,ulcerative
c. saline mouth rinses.
d. half-strength peroxide. Herpes virus center en
stomatitis Less than
Candidiasis Candida Creamy w
(Thrush) Albicans patches
Red, eryt

Tracheoesophageal Fistula and Esophageal Atresia

Necrotizing Infection with Acute gin
ulcerative spirochetes and necro
A. DESCRIPTION

• TEF and EA are malformations that are caused by the defective separation,
incomplete fusion of the tracheal folds following this separation, or altered
cellular growth during the embryonic development of the 4th and 5th weeks of
gestation.
• The danger→Mthe proneness to aspiration, pneumonia and severe respiratory
distress
• 1. The Esophagus terminates before it reaches the stomach or a fistula is present
that forms an unnatural connection with the trachea.
• 2. The condition causes oral intake to enter the lung or a large amount of air enter
the stomach, and choking, coughing and severe abdominal distention can occur.
• 3. Aspiration pneumonia and severe respiratory distress will develop, and death
will occur without surgical intervention.
• 4. Treatment includes maintenance of a patent airway, prevention of pneumonia,
gastric or blind pouch decompression, supportive therapy and surgical repair

B. ASSESSMENT
• 1. Frothy saliva in the mouth and nose and drooling
• 2. The “3 C’s” – coughing and choking during feedings and unexplained cyanosis
• 3. Regurgitation and vomiting
If fed, swallows normally but may gag and cough then fluid returns to the
nose and mouth
• 4. Abdominal distention with air
• 5. Inability to pass a small – gauge ( such as a No. 5 French) orogastric feeding
tube via the mouth into the stomach.
• Becomes apneic and cyanotic because of aspiration of the formula

C. DIAGNOSIS
• Ineffective airway clearance related to abnormal opening between the esophagus
and trachea, obstruction to swallowing
• Impaired swallowing related to mechanical obstruction
• Risk for injury related to surgical procedure
• Interrupted family processes related to the child’s physical defect

D. PLANNING AND IMPLEMENTATION

OBJ 1: Will maintain patent airway.
 Place on NPO.
 Hook on IVF.
 Position to facilitate drainage of secretions and prevent aspiration.
 Insertion of double lumen catheter to the upper esophageal pouch attached to a
suction machine to allow removal of fluids that can be aspirated to the lungs.
 Administration of broad spectrum antibiotics.
 Respiratory assessment, airway management, thermoregulation, fluid and
electrolyte management.

OBJ 2: Will meet caloric needs.

 Provide parenteral nutritional support.
 Administer gastrostomy feedings.
 Provide non-nutritive sucking by giving the infant an oral pacifier.

OBJ 3: Will not experience trauma to the operative site.

 Suction only with a catheter premeasured to a distance that will not reach the
surgical site to prevent trauma.
 Series of surgical procedures requiring thoracotomy, ligation of the TEF, and an
end-to-end anastomosis of the esophagus are done.
 Care includes returning to the radiant warmer; double lumen catheter attached to
low suction or gravity drainage, parenteral nutrition, and gastrostomy tube is
drained until the infant can tolerate feedings.
 Waiting for esophageal anastomosis to heal before initiation of gastrostomy
feedings.
 Oral feedings initiated beginning with sterile water followed by frequent
breastfeeding or formula-feeding.

OBJ 4: Will be prepared for home care.

 Instruct parents with the skills and needed observation for discharge:
– proper positioning;
– signs of respiratory distress;
– notify physician if the infant is manifesting the symptoms of refusal to eat,
– dysphagia, and increased coughing;
– Infant CPR, care of gastrostomy and esophagostomy.

E. INTERVENTIONS PREOPERATIVELY
• 1. Infant may be placed in an incubator or radiant warmer in which humidified
oxygen is administered (incubation and mechanical ventilation may be necessary
if respiratory distress occurs).
• 2. Maintain an NPO status.
• 3. Maintain IV fluids as prescribed.
• 4. Suction accumulated sections from the mouth and pharynx
• 5. A double lumen catheter is placed into the upper esophageal pouch and
attached to intermittent or continuous low suction to keep the pouch empty of
secretions; it is irrigated with normal saline as prescribed to prevent clogging.
• 6. Maintain in an upright position to facilitate drainage and to prevent aspiration
of gastric secretion.
• 7. A gastrostomy tube may be placed and is left open so that air entering the
stomach through fistula can escape, minimizing the danger of regurgitation.
• 8. Administer broad-spectrum antibiotics as prescribed because of the high risk
for aspiration pneumonia.
D. INTERVENTIONS POSTOPERATIVELY

• 1. Monitor respiratory status

• 2. Maintain IV fluids, antibiotics, and parenteral nutrition as prescribed.

• 3. Monitor intake and output and weight daily.

• 4. Inspect surgical site

• 5. Provide care to the chest tube if in place.

• 6. Assess for signs of pain

• 7. Assess for dehydration and possible fluid overload.

• 8. Monitor for anastomotic leaks as evidenced by purulent chest drainage,

increased temperature and an increased white blood cell count.

• 9. The double lumen catheter is attached to low suction.

• 10. If a gastrostomy tube is present, it is attached to gravity drainage until the

infant can tolerate feedings (usually the fifth to seventh day postoperatively).

• 11. Before oral feedings and removal of the chest tube, a barium swallow is
performed to verify the integrity of the esophageal anastomosis.

• 12. Before feeding, the gastrostomy tube is elevated and secured above the level
of the stomach to allow gastric secretions to pass to the duodenum and swallowed
air to escape through the open gastrostomy tube.

• 13. Feedings through the gastrostomy tube may be prescribed until the
anastomosis is healed.

• 14. Oral feedings are began with sterile water, followed by frequent small
feedings of formula.

• 15. The gastrostomy tube may be removed before discharge or may be maintained
for supplemental feedings at home.

• 16. If the infant is awaiting esophageal replacement a cervical esophagostomy

may be performed.

• 17. Assess cervical esophagostomy site for redness, breakdown or exudate

(continued discharge or saliva can cause skin breakdown); remove drainage
 frequently and apply a protective ointment, a barrier dressing, and/or a collection
device.

• 18. If the infant is awaiting esophageal replacement, nonnutritive sucking is

provided by a pacifier, infants who remain NPO for extended periods and have
not received oral stimulation frequently may have difficulty eating by mouth after
surgery and develop oral hypersensitivity and food aversion.

• 19. Instruct the parents in the techniques of suctioning, gastrostomy tube care and
feedings, and skin site care as appropriate

• 20. Instruct parents to identify behaviors that indicate the need for suctioning,
signs of respiratory distress, and signs of a constricted esophagus (poor feeding,
dysphagia, drooling or regurgitated undigested food).

Evaluation

A clinic nurse reviews the record of an infant seen in the clinic. The nurse notes
that a diagnosis of esophageal atresia with tracheoesophageal fistula is
suspected. The nurse expects to note which most likely sign of this condition
documented in the record?
• A. Severe projectile vomiting
• B. Coughing at night time
• C. Choking with feedings
• D. Incessant crying

Rationale: Any child who exhibits the 3’C s – coughing, and choking with
feedings and unexplained cyanosis – should be suspected of TEF. Options A, B,
D are not specifically associated with TEF.
HIATAL HERNIA

A. Description

• 1. A Hiatal Hernia also known as esophageal or diaphragmatic hernia.

• 2. A portion of the stomach herniates through the diaphragm and into the thorax.
• Protrusion in the portion of the stomach through the hiatus of the diaphragm and
into the thoracic cavity.
• 3. Herniation results from weakening of the muscles of the diaphragm and is
aggravated by factors that increase abdominal pressure such as pregnancy, ascites,
obesity, tumors and heavy lifting.
• 4. Complications include ulceration, hemorrhage, regurgitation and aspiration of
stomach contents, strangulation, and of the stomach in the chest with possible
necrosis, peritonitis and mediastinitis.
•
B. Types

1. Sliding Hiatal Hernia: stomach and esophagus slip up into the chest.
• Causes:
– Muscle weakness in the esophageal hiatus:
• Aging process
• Congenital muscle weakness
• Obesity
• Trauma
• Surgery
• Prolonged increases in intraabdominal pressure
2. Paraesophageal / Rolling Hernia
– The gastric junction remains below the diaphragm, but the fundus of the
stomach and the greater curvature rolls into the thorax next to the
esophagus
– Cause : anatomic defect
–
C. Assessment
• 1. Heartburn due to gastroesophageal reflux
• 2. Regurgitation or vomiting
• 3. Dysphagia / odynophagia
• 4. Feeling of fullness, Gastric distention, belching, flatulence
• 5. Dyspnea
• 6. Abdominal pain
• 7. Nausea and vomiting
D. Interventions
• 1. Medical and surgical management is similar to that for GERD.
• 2. Provide small frequent meals and minimize the amount of liquids.
• 3. Advise the client not to recline for 1 hour after eating
• 4. Avoid anticholinergics, which delay stomach emptying.

E. COLLABORATIVE MANAGEMENT
Medications
– Antacids
– Antiemetics
– Histamine Receptor Antagonists
– Gastric Acid Secretion Inhibitors
AVOID:
• Anticholinergics
• Xanthine derivatives
• Ca – channel blockers
• Diazepam
These drugs lower the LES pressure

NURSING MANAGEMENT

• Relieve pain
– Antacids
• Modify diet
– High CHON diet to enhance LES pressure
– Small frequent feedings ( 4 to 6 )
– Eat slowly and chew food properly

• Modify diet
– Avoid :
• Fatty foods
• Cola beverages
• Coffee
• Tea
• Chocolate
• Alcohol
These foods and beverages decrease LES pressure
– Assume upright position before and after eating (1-2 hrs.)
– X eat at least 3 hrs. before bedtime to prevent night-time reflux
– X evening snacks
– Reduce BW if obese

• Promote lifestyle changes

 – Elevate HOB 6 to 12 in. for sleep
– X factors that increase intraabdominal pressure
• Use of constrictive clothing
• Straining
• Heavy lifting
• Bending, stooping
• Coughing
– X smoking (causes rapid and significant drop in LES pressure)
–
SURGERY

 Nissen Fundoplication (gastric wrap – around)

Preop Care
– Teach on DBCT exercises, incentive spirometry to prevent postop
respiratory complications
– Inform on possible postop contraptions:
• Chest tube
• NGT

POSTOP CARE

• Facilitate AW clearance
• Semi – Fowler’s position
• Reinforce DBCT exercises, incentive spirometry, chest physiotherapy

• Facilitate swallowing
– A large NGT is inserted to prevent the fundoplication from being made
too tightly
– Drainage from NG tube turns to yellowish green within first 8 hrs, postop
– Oral fluids after peristalsis returns; near normal diet within 6 weeks
– Small, frequent meals
– Maintain upright position
– Avoid gas- forming foods
– Frequent position changes and early ambulation to clear air from the GI
tract
– Report for persistent dysphagia and gas pain

Evaluation
In a patient with hiatal hernia, the nurse will most probably observe the patient
to:
• A. have the abdomen bulge when coughing and sneezing.
• B. experience substernal pain when eating
• C. have loss of appetite and abdominal cramps.
• D. have intolerance for fatty foods and cold fluids.

Rationale:

Gastroesophageal Reflux Disease (GERD)

A. Description
• 1. Gastroesophageal reflux is a backflow of gastric contents into the esophagus as a
result of relaxation or incompetence of the lower esophageal or cardiac sphincter.
• Return of gastric and duodenal contents into the esophagus
• 2. Complications include esophagitis, esophageal strictures, aspiration of gastric contents
and aspiration pneumonia.
• 3. Most infants with gastroesophageal reflux have a mild problem that improves in about
1 year and requires only medical therapy.

B. Etiology: due to an incompetent lower esophageal sphincter, pyloric stenosis or

a motility disorder
– may be associated with obesity, pregnancy, caffeine, chocolate, high fat
food ingestion and hiatal hernia
• If not treated, it may lead to Barrett’s esophagus, a condition which may lead to
esophageal cancer

C. Assessment
– Dyspepsia
– Dysphagia
– Pyrosis
– Regurgitation
– Hypersalivation

GASTROESOP
DISEAS
• B. Assessment
•
D. Planning- Nursing Diagnosis 1. Passive regurgitation
emesis
• 2. Poor weight gain
 – Acute pain related to tissue trauma
– Imbalanced nutrition, less than body requirement related to excess intake
–
E. Treatment
• 1. Diet
• 2. Positioning
• 3. Medications
• 4. Surgery: performed when severe complications occur

F. Intervention
– Avoid giving anticholinergic- delays gastric emptying
– Prepare the patient for surgery
– Patient education
– Diet- low fat, high fiber
– Avoid caffeine, tobacco, carbonated beverage, spicy food- decreases lower
esophageal sphincter tone and cause esophageal irritation
– Avoid eating and drinking 2 hours before bedtime
– Elevate the bed on 6 to 8 inch blocks to prevent back flow
– Administer prokinetic medication, antacids, histamine H2-receptor
antagonists, proton pump inhibitors as prescribed
– Maintain normal weight.
– Avoid tight clothes- obesity and wearing of tight clothing causes increase
abdominal pressure forcing the food back.

– 1. Assess amount and characteristics of emesis.

– 2. Assess the relation of vomiting to the times of feedings and infant activity.
– 3. Monitor breath sounds before and after feedings.
– 4. Place suction equipment at the bedside.
– 5. Monitor intake and output.
– 6. Monitor for signs and symptoms of dehydration.
– 7. Maintain IV fluids as prescribed.

G. Positioning: Place child in the flat prone position or the head- elevated prone
position following feedings and at night.

H. Diet
– 1. Provide small, frequent feedings to decrease the amount of regurgitation;
nasogastric tube feedings are indicated if severe regurgitation and poor growth are
present
– 2. For infants, thicken formula by adding 1 table spoon of rice cereal per 6 oz of
formula and crosscut the nipple; monitor for coughing during feeding.
– 3. Breast- feeding may continue, and the mother may provide more frequent
feeding times or express milk for thickening with rice cereal.
– 4. Burp the infant frequently when feeding and handle the infant minimally after
feeding.
– 5. For toddlers, feed solids first, followed by liquids.
– 6. The parents are instructed to avoid feeding the child fatty foods, chocolate,
tomato products, carbonated liquids, fruit juices, citrus juices and spicy foods.
– 7. Avoid vigorous play after feeding and avoid feeding just before bedtime.

I. Medications
• 1. Administer antacids and histamine receptor antagonists as prescribed to
reduce the amount of acid present in gastric secretions and to prevent esophagitis.
• 2. Administer prokinetic agents to accelerate gastric emptying and decrease
reflux.
• 3. Administer acetaminophen (Tylenol) as prescribed to relieve reflux pain.

J. Surgery
• 1. If surgery is prescribed, it will require a procedure known as Fundoplication,
in which a wrap to the stomach fundus is made around the distal esophagus
(restores the competence of the lower esophageal sphincter)
• 2. A gastrostomy may be performed at the same time as the fundoplication for
decompression of the stomach postoperatively.
• 3. Fundoplication may be combined with pyloroplasty in children with
gastroesophageal reflux who also have delayed gastric emptying.
• 4. Postoperative care is similar to that for other types of abdominal surgery.
• 5. Instruct parents in the potential postoperative problems, such as bloating
symptoms or discomfort after consuming large, solid meals.

Evaluation
A nurse is instructing a patient about gastroesophageal reflux disease (GERD). Which
of the following instruction should the nurse stress?
• A. reduce intake of caffeine beverages
• B. eat three large meals a day
• C. drink milk as a bedtime snack
• D. take antacids directly after a meal
Peptic Ulcer Disease
• Peptic ulcer is a break in the gastric or duodenal mucosa that arises when the
normal mucosal defensive factors are impaired or are overwhelmed by aggressive
luminal factors such as acid and pepsin. By definition, ulcers extend through the
muscularis mucosae and are usually over 5 mm in diameter.

Description
• 1. It is ulceration in the mucosal wall of the stomach, pylorus, duodenum, or
esophagus in portions that are accessible to gastric secretions; erosions may
extend through the muscle.
• 2. The ulcer may be referred to as gastric, duodenal or esophageal depending
on its location.
• 3. The most common peptic ulcers gastric ulcers and duodenal ulcers.

PEPTIC UL
 I mpairment of the muc
the esophagus, stomac
 With remissions and ex
PREDISPOSING FACTORS

• Cause : Unknown
• Stress
– PNS → gastric motility, HCl
• Cigarette smoking

• Theory
– Stimulant ; Vasoconstrictor
• Alcohol
– Irritant; vasoconstrictor; beer gastric acid secretion
• Caffeine

HCl
HCl++Pepsin
Pepsin
(Aggressor)
(Aggressor)
 – Stimulant ; vasoconstrictor
• Drugs
– ASA
– NSAIDs
– Steroids
• Gastritis
– HCl; mucous ulceration
• Infection
– Campylobacter/ H. Pylori

PREDISPOS

• Zollinger – Ellison
• Irregular, hurried meals (stressful)
• Fatty, spicy, highly acidic foods, (stimulants, irritants)
• Type A personality
– “stress personality”
• Type O blood
– pepsinogen levels → PEPSIN
Pancr
(gas
• Genetics
– in parietal cell mass → acid secretion

Gastric ulcers
• Ulcer involves ulceration of the mucosal lining that extends to the submucosal
layer of the stomach.
Duodenal ulcers

↑ Gast
• Is a break in the mucosa of the duodenum.
• Gastric ulcers
• Predisposing factor
• 1. Stress
• 2. smoking
• 3. use of corticosteroids
• 4. NSAIDs
• 5. alcohol
• 6. history of gastritis
• 7. a family history of gastric ulcers or infection with H.pylori

• Duodenal ulcers
• Risk factor and causes
• 1. alcohol
• 2. smoking
• 3. stress
• 4. caffeine
• 5. use of aspirin, cortocosteroids and NSAIDs
• 6. infection with H.pylori
•

DIFFERENCE BETWEEN G

GASTRI C ULCER
• “poor man’s” ulcer
• “laborer’s ulcer
Complications

Gastric ulcers Duodenal ulcers

1. hemorrhage 1. bleeding

• 20 % incidence
2. perforation 2. perforation
3. pyloric obstruction 3.gastric outlet obstruction and intractable disease

• 50 years and above

 DIFFERENCE BETWEEN G

GASTRI C ULCER
• dull, aching , g
• radiates to left
Gastric ulcers
• Assessment
•
• ½ to 2 hrs. p.c.
1. gnawing, sharp pain in or left of the midepigastric region 1 to 2 hours after
eating
• 2. hematemesis
•
• X relieved by food
3. nausea and vomiting

Duodenal ulcers
• Assessment
• 1. burning pain in the midepigastric area 2 to 4 hours after eating and during the
night
• 2. melena
• 3. pain that is often relieved by eating

• nausea and vomiting, hemateme

Gastric ulcers
• Interventions
• 1.common
Monitor VS and for signs of bleeding
• 2. Administer small frequent bland feedings during the active phase
• 3. Administer histamine H2 receptor antagonist
•
• • complications
4. Administer antacids
5. Administer anticholinergics
• 6. Administer mucosal barriers
• – hemorrhage
7. Administer prostaglandins

– perforation
– peritonitis
Duodenal ulcers
• Interventions
• 1. Monitor VS
• 2. Perform abdominal assessment
• 3. Instruct the client in a bland diet with small frequent meals
• 4. Provide for adequate rest
• 5. Encourage the cessation of smoking
• 6. Avoid alcohol intake, caffeine, use of aspirin, corticosteroids and NSAIDs
• 7. Administer antacids
• 8. Administer histamine H2 receptor antagonist

COLLABORATIVE MANAGEMENT
• Medications
– Antacids
 Neutralize HCl
 Taken 1 to 2 hrs. p.c.
 Amphogel (AL – OH)
 Basaljel (AL – Carbonate)
 Maalox (AL – Mg – OH)
 Gaviscon (AL – Mg – Trisilicate)
 Milk of Magnesia (Mg – OH)
 Riopan (Magaldrate)
 Alka – 2 (Calcium carbonate)
• Tums (Calcium carbonate)
• Rolaids (Calcium carbonate)
• Mylanta (AL – Mg – OH with Simethicone)
• Maalox plus Gelusil (AL – Mg – OH with Simethicone)
• Magnesium based → diarrhea
• Aluminum – based → constipation

• Histamine (H2) receptor antagonists

 Reduces HCl secretion
 Taken with meals
 Tagamet (Cimetidine)
 Zantac (Ranitidine)
 Pepcid (Famotidine)
 Axid (Nizatidine)
 Side effects
 Diarrhea
 Abdominal cramps
 Confusion
 Dizziness
 Weakness
  Cimetidine – antiandrogenic (gynecomastia, ↓ libido, impotence)

• Cytoprotective
 Coats ulcer
 prostaglandin synthesis
 Taken on an empty stomach (30 – 60 mins. before meals)
 Eg., Carafate (Sucralfate)

SURGERY
• Vagotomy
– Resection of the vagus nerve
– Decrease cholinergic stimulation
↓
↓ HCl secretion
↓Gastric motility
• Pyloroplasty
– Surgical dilatation of the pyloric sphincter
– Improves gastric emptying of acidic chyme

• Antrectomies
– Removal of 50% of the lower part of the stomach
– Types
• Billroth I (Gastroduodenostomy)
• Billroth II (Gastrojejunostomy)
– The duodenum is bypassed to permit the flow of the bile

• Subtotal Gastrectomy
– Removal of 75% of the distal stomach with Billroth I or II repair

NURSING MANAGEMENT
• Relieve pain
– Take prescribed medications as ordered
• Promote a healthy lifestyle
– Diet
• Liberal bland diet during exacerbation
• Eat slowly and chew food properly
• Small, frequent feedings during exacerbation
• Avoid the following:
– Fatty foods
– Coffee, tea, cola drinks, chocolate
– Spices, red /black pepper
– Alcohol
– Bedtime snacks
– Binge eating
– Large quantities of milk (400 mls/day is allowed)
 – Quit smoking
– Coping
• Stress Therapy
– Recreation and hobbies
– Regular pattern of exercise
– Stress reduction at home and at work

Evaluation
A 65 year old is admitted to the hospital with peptic (Duodenal) ulcer. The discomfort
that most probably led this patient to seek health care is epigastric pain that is relieved
by:
• a. eating c. physical activity
• b. resting d. voiding
Intestinal Obstruction

Hypertrophic Pyloric Stenosis (HPS)

Description
• 1. Hypertrophy of the circular muscles of the pylorus causes narrowing of the
pyloric canal between the stomach and the duodenum.
• 2. The stenosis usually develops in the first few weeks of life, causing projectile
vomiting, dehydration, metabolic alkalosis and failure to thrive.
• HPS occurs when the circumferential muscle of the pyloric sphincter becomes
thickened which results to the elongation and narrowing of the pyloric channel.
• As a compensatory mechanism→ obstruction, dilatation, hypertrophy and
hyperperistalsis of the stomach occurs.
• It is not a congenital disorder but rather is a result of the dysfunction in the local
innervation of the involved muscle.

Assessment
1. Vomiting that progresses from mild regurgitation of non-bilous to forceful and
projectile and usually occurs after feeding.
2. Signs of dehydration as a result of persistence of vomiting and malnutrition can
occur.
3. Vomitus contains gastric contents such as milk or formula, may contain mucus,
may be blood tinged and does not usually contain bile.
4. The child exhibits hunger and irritability
5. Palpable olive-shaped mass in the epigastrium just to the right of the umbilicus
6. Peristaltic waves are visible from left to right across the epigastrum during or
immediately following a feeding.
7. Electrolyte imbalances can occur.
8. Metabolic alkalosis can occur.

Interventions
• 1. Monitor Vital signs
• 2. Monitor for intake and output and weight.
• 3. Monitor for signs of dehydration and electrolyte imbalances.
• 4. Prepare the child and parents for pyloromyotomy if prescribed

IMPLEMENTATION
Preoperatively: monitor VS, I & O, signs of dehydration and metabolic alkalosis,
and preparation of the child and parents for pyloromyotomy.

• Therapeutic Management: Pyloromyotomy or the Fredet-Ramstedt

procedure
PYLOROMYOTOMY
• 1. Description: An incision through the muscle fibers of the pylorus that
may be performed by laparoscopy.
• 2. Interventions preoperatively
• a. Monitor hydration status by daily weights, intake and output, and
urine for specific gravity.
• b. Correct fluid and electrolyte imbalances; administer fluids
intravenously as prescribed for rehydration.
• c. Maintain NPO status
• d. Monitor the number and character of stools
• e. Maintain patency of the nasogastric tube placed for stomach
decompression.
– Preoperatively: must correct dehydration and metabolic alkalosis with
parenteral fluid and electrolyte administration. Stomach is decompressed
with NG tube.
• 3. Interventions postoperatively
• Monitor for postoperative vomiting during the 24 to 48 hour.
• Administer IVF and medications.
• Assess response to stress of surgery and pain.
• Maintain patency of NG tube and institute feedings once tolerated at frequent
intervals and in small quantities.
• Monitor operative site for signs of infection.

• a. Monitor intake and output.

• b. Maintain IV fluids until infant is taking and retaining adequate amounts
by mouth.
• c. Begin small, frequent feedings of glucose, water, or electrolyte solution 4
to 6 hours postoperatively as prescribed; advance the diet to formula 24
hours postoperatively as prescribed.
• d. Gradually increase amount and interval between feedings until a full
feeding schedule is reinstated, usually by 48 hours postoperatively
• e. Feed the infant slowly, burping frequently; handle the infant minimally
after feedings
• f. Monitor for abdominal distention.
• g. Monitor the surgical wound and for signs of infection.
• h. Instruct parents about wound care and feeding.
– Postoperatively: feedings initiated at 4-6 hours post-op beginning with
glucose, water or electrolyte solution. Formula is started on the 24th hour.

• Nursing Considerations
Goal of care is the establishment of diagnosis, careful regulation of
fluid therapy, and reestablishment of normal feeding patterns.
Intussusceptions
Description
• 1. Intussuseption is telescoping of one portion of the bowel into another portion.
• Is the telescoping of the proximal portion of the bowel into a more distal
segment, pulling the mesentery accompanying it.
• mesentery gets compressed and angled
• Leads to lymphatic and venous obstruction.

• 2. The condition results in an obstruction to the passage of intestinal contents.

• Common sites
– ileoceccal valve (ileocolic), invagination of the ileum into the ceccum;
ileoileal, telescoping of one part of the ileum to its other section; and
colocolic, when one part of the colon invaginates into its other part.

Assessment
• 1. Colicky abdominal pain that causes the child to scream and draw the
knees to the abdomen.
• 2. Vomiting of gastric contents.
• 3. Bile – stained fecal emesis.
• 4. Currant jelly – like stools containing blood and mucus.
• 5. Hypoactive or hyperactive bowel sounds.
• 6. Tender distended abdomen, possibly with a palpable sausage shaped
mass in the upper right quadrant.
•
– sudden onset of crampy abdominal pain that causes the child to
inconsolably cry and draw his knees up to the chest
– bilious vomiting as lethargy increases
– Classic triad:
- Pain
- Palpable sausage-shaped abdominal mass
- Currant jelly-like stools
– sepsis
– demonstrated obstruction as seen in the barium enema

Management

a. nonsurgical: hydrostatic reduction by barium enema. Not recommended if

the symptoms of shock and perforation are evident.
b. Surgical: manual reduction of the invagination and if necessary, resection
of the necrotic intestine.
 Interventions
1. Monitor for signs of perforation and shock as evidenced by fever, increased
heart rate, changes in level of consciousness or blood pressure, and
respiratory distress and report immediately.
2. Prepare for hydrostatic reduction if prescribed ( not performed if signs of
perforation or shock occur ).
a. Antibiotics, IV fluids, and decompression via nasogastric tube may be
prescribed.
b. Monitor for the passage of normal brown stool, which indicates that the
intussuseption has reduced itself.
3. After hydrostatic reduction, do the following;
a. Monitor for the return of normal bowel sounds, for the passage of barium,
and the characteristics of stool.
b. Administer clear fluids and advance the diet gradually as prescribed.
4. If surgery is required, postoperative care is similar to that following any
abdominal surgery.

Evaluation
A nurse admits a child to the hospital with a diagnosis of pyloric stenosis.
On admission assessment, which data would the nurse expect to obtain when
asking the mother about the child’s symptoms?
• 1. Vomiting large amounts of bile
• 2. Watery diarrhrea
• 3. Increased urine output
• 4. Projectile vomiting
Rationale
Clinical manifestations of pyloric stenosis include projectile vomiting, irritability,
hunger, and crying, constipation, and signs of dehydration, including decrease in
urine output.

Evaluation
A nurse is preparing to care for a child with a diagnosis of intussusception.
The nurse reviews the child’s record and expects to note which symptom of this
disorder documented?
• 1. Bright red blood and mucus in the stools.
• 2. Profuse projectile vomiting
• 3. Watery Diarrhea
• 4. Ribbonlike stools
Rationale
The child with intussusception classically has severe abdominal pain that is crampy
and intermittent, causing the child to draw in the knees to the chest. Vomiting may
be present but is not projectile. Bright red blood and mucus are passed through the
rectum and commonly are described as currant jelly stools. Watery diarrhea and
ribbonlike stools are not manifestations of this disorder.
Hirschsprung Disease (Congenital Aganglionic
Megacolon)
Description
• 1. A congenital anomaly also known as congenital aganglionosis or megacolon.
• 2. The disease occurs as the result of an absence of ganglion cells in the rectum
and upward in the colon.
• 3. The disease results in mechanical obstruction from inadequate motility in an
intestinal segment.

• The involved portion of the intestine has no ganglion cells; thus, no

functional rectosphincteric reflex and with an abnormal microenvironment
of the affected intestine.

• 4. The disease may be a familial congenital defect or may be associated with other
anomalies, such as Down syndrome and genital urinary abnormalities.
• 5. A rectal biopsy demonstrates histologic evidenced of the absence of ganglionic
cells.
• 6. The most serious complication is enterocolitis; signs include fever, sever
prostration, gastrointestinal bleeding, and explosive watery diarrhea.
• 7. Treatment for mild or moderate diarrhea is based relieving the chronic
constipation with stool softeners and rectal irrigations; however, most children
require surgery.
• 8. Treatment for moderate to sever disease involves a two- step surgical
procedure.
• 9. Initially, in the neonatal period, a temporary colostomy is created to relieve
obstruction and allow the normally innervated, dilated bowel to return to its
normal size.
• 10. A complete surgical repair is performed when the child weighs about 9 kg ( 20
pounds) via a pull through procedure to excise portions of the bowel; at this time
the colostomy is closed.
Assessment:
(+) Rectal biopsy,
(+) anorectal manometry: catheter inserted into the rectum which records the reflex
pressure of the internal sphincter, for which does not relax

Clinical symptoms are –

a. Newborn: abdominal distention, bilious vomiting, constipation, and failure to
pass meconium within the first 48 hours of life
b. Older infants: chronic constipation, passage of ribbon-like foul smelling stools,
abdominal distention, with a history of unable to pass meconium in the first 48 hours
of life
• 1. Newborn infants
• a. Failure to pass meconium stool
• b. Refusal to suck
• c. Abdominal distention
• d. Bile – stained vomitus
Older children: with the history of previous gastrointestinal dysfunction, failure to
thrive, or chronic constipation
• 2. Children
• a. Failure to gain weight and delayed growth
• b. Abdominal distention
• c. Vomiting
• d. Constipation alternating with diarrhea
• e. Ribbonlike and foul smelling stools.

Interventions: Medical management

• 1. Dietary management
• 2. Stool softeners
• 3. Daily rectal irrigations with normal saline to promote adequate elimination
and prevent obstruction.
Surgical management: preoperative interventions
• 1. Assess bowel function and administer bowel preparation as prescribed.
• 2. Maintain NPO status.
• 3. Monitor hydration and fluid and electrolyte status; provide fluids
intravenously as prescribed for hydration
• 4. Administer antibiotics as prescribed to clear the bowel of bacteria.
• 5. Monitor intake and output and weight
• 6. Measure abdominal girth
• 7. Avoid taking the temperature rectally
• 8. Monitor respiratory distress associated with abdominal distention.
 Postoperatively
• 1. Monitor vital signs, avoiding taking the temperature rectally.
• 2. Measure abdominal girth.
• 3. Assess surgical site for redness, swelling, and drainage.
• 4. Assess the stoma if present for bleeding or skin breakdown (stoma should be
pink and moist).
• 5. Assess anal area for the presence of stool, redness or discharge.
• 6. Maintain NPO status until bowel sounds return or flatus is passed; bowel
sounds usually return within 48 to 72 hours.
• 7. Maintain the nasogastric tube to allow intermittent suction until peristalsis
returns.
• 8. Maintain IV fluids until the child tolerates appropriate oral intake; begin the
diet with clear liquids, advancing to regular as tolerated and as prescribed.
• 9. Assess for dehydration and fluid overload.
• 10. Monitor intake and output and weight.
• 11. Assess for pain and provide comfort measures as required.
• 12. Provide the parents with instruction regarding colostomy care and skin care.
• 13. Teach the parents about the appropriate diet and the need for adequate fluid
intake.
Therapeutic Management:
• Primary Pull-through (1-stage procedure)
• 2 – stage surgical management:
i. Temporary ostomy to relieve obstruction and to allow the normal bowel
to return to normal size.
ii. Corrective Surgery: Soave Endorectal Pull-through Procedure when
the child weighs 9kg.
• it involves pulling the end of the normal bowel through the
muscular sleeve of the rectum, from which the aganglionic portion
was removed.
Evaluation
A clinic nurse reviews the record of a 3 week old infant and notes that the physician
has documented a diagnosis of suspected Hirschsprung’s disease. The nurse reviews
the assessment findings documented in the record, knowing that which symptom
most likely led the mother to seek health care for the infant?
• 1. Diarrhea
• 2. Projectile vomiting
• 3. Regurgitation
• 4. Foul smelling ribbonlike stools
Rationale
Chronic constipation beginning in the first month of life and resulting in pelletlike
or ribbon stools that are foul smelling is a clinical manifestation of this disorder.
Delayed passage or absence of meconium stool in the neonatal period is the cardinal
sign. Bowel obstruction, especially in the neonate period, abdominal pain and
distention, and failure to thrive are also clinical manifestations
DIVERTICULITIS

Description
• 1. Diverticulosis
• a. Diverticulosis is an outpounching or herniation of the intestinal mucosa,
commonly in the colon.
• b. The disorder can occur in any part of the intestine but is most common in
the sigmoid colon

• 2. Diverticulitis
• a. Diverticulitis is the inflammation of one or more diverticula that results
when a diverticulum perforates.
• b. A perforated diverticulum can progress to intraabdominal perforation with
generalize peritonitis.
• c. It is acute inflammation and infection caused by trapped fecal material and
bacteria

• 3. Diverticula / diverticulosis are multiple outpouchings

• Cause
– low fiber diet

PATHOP
Low fecal vol

I ncreased intra

Decreased m
the c
ASSESSMENT
• 1. Left lower quadrant abdominal pain that increases with coughing, straining
or lifting.
• 2. Elevated temperature /Low - grade fever
• 3. Nausea and vomiting
• 4. Flatulence
• 5. Cramplike pain
• 6. Abdominal distention and tenderness
• 7. Palpable tender rectal mass
• 8. Blood in the stools /Occult bleeding
• Chronic constipation with episodes of diarrhea
• Signs and symptoms of peritonitis due to development of abscess or perforation

Interventions
• 1. Provide bed rest during the acute phase.
• 2. Maintain NPO status or provide clear liquids during the acute phase as
prescribed.
• 3. Introduce a fiber- containing diet gradually, when the inflammation has
resolved.
• 4. Administer antibiotics, analgesis and anticholinergics to reduce bowel spasms
as prescribed.
• 5. Instruct the client to refrain from lifting, straining, coughing, or bending to
avoid increased intraabdominal pressure.
• 6. Monitor for perforation, hemorrhage, fistulas and abscesses.
• 7. Instruct the client to increase fluid intake to 2500 to 3000 ml daily, unless
contraindicated.
• 8. Instruct the client to avoid gas-forming foods or foods containing indigestible
roughage, seeds or nuts because these food substances become trapped in
diverticula and cause inflammation.
• 9. Instruct the client to consume a small amount of bran daily and to take bulk
forming laxatives as prescribed to increase stool mass.
• 10. Instruct the client to avoid high fiber foods when inflammation occurs
because these foods will irritate the mucosa further.

COLLABORATIVE MANAGEMENT
• High fiber diet
• Liberal fluid intake of 2,500 to 3,000 mls./day
• Avoid nuts and seeds which can become trapped in the diverticula
• Bulk – forming laxatives
• During an acute episode:
– Bed rest
– NPO, then clear liquids to rest the bowel
– X other foods to prevent further irritation of the mucosa
– IVF’s, antibiotics, analgesics, anticholinergics (Pro – Banthine)
– NGT insertion to relieve distention
• Weight loss to reduce intraabdominal pressure
Surgical Intervention
• 1. Colon resection with primary anastomosis is one option.
• 2. Temporary or permanent colostomy may be required for increased bowel
inflammation.

Evaluation

Rationale
ELIMINATION
ANORECTAL ABNORMALITIES

a. HEMMORRHOIDS

Description
• 1. Hemorrhoids are dilated varicose veins of the anal canal.
• 2. Hemorrhoids may be internal, external or prolapsed.
• Types are:
– Internal hemorrhoids- lie above the anal sphincter and cannot be seen
upon inspection of the peri-anal are
– External hemorrhoids- lie below the anal sphincter can be seen on
inspection
– Prolapsed hemorrhoids can become thrombosed or inflamed
• 3. Internal hemorrhoids lie above the anal sphincter and cannot be seen on
inspection of perianal area.
• 4. External hemorrhoids lie below the anal sphincter and can be seen on
inspection.
• 5. Prolapsed hemorrhoids can become thrombosed or inflamed.
• 6. Hemorrhoids are caused from portal hypertension, straining, irritation,
increased venous or abdominal pressure.

Precipitated by
– constipation,
– portal hypertension,
– straining/ irritation,
– pegnancy or increased venous or abdominal pressure
– persistently elevated venous pressure within the hemorrhoidal plexus

Assessment

• 1. Bright red bleeding with defecation

• 2. Rectal Pain / Anal pain
• 3. Rectal Itching / Pruritus
• 4.Protrusion of varicosities around the anus
• 5.Rectal bleeding and mucus discharge
Management of Hemorrhoids
• Diet- high- fiber diet and fluids to promote bowel movement without straining
• Administer stool softener as prescribed
• Apply cold packs to the anal/rectal area followed by sitz baths as prescribed
• Prepare for surgery- cryosurgery, hemorrhoidectomy
• Prepare for sclerotherapy, endoscopic ligation
• Apply witch hazel soaks and topical anesthetics as prescribed
.
Endoscopic procedures
• 1. Sclerotheraphy
• 2. Endoscopic ligation

Surgical procedures
• 1. Cryosurgery
• 2. Hemorrhoidectomy

Postoperative interventions
• 1. Assist the client to a prone or side lying position to prevent bleeding.
• 2. Maintain ice packs over the dressing as prescribed until the packing is
removed by the physician.
• 3. Monitor urinary retention.
• 4. Administer stool softeners.
• 5. Instruct the client to increase fluids and high fiber foods.
• 6. Instruct the client to limit sitting to shorts periods of time.
• 7. Instruct the client in the use of sitz baths 3 to 4 times a day as prescribed.

Planning- Nursing Diagnosis

– Constipation related to fear of pain on defecation
– Pain related to inflammation

Evaluation

Rationale
b. IMPERFORATE ANUS
Description: Incomplete development or absence of the anus in its normal position
in the perineum.
• Is an anorectal malformation without the obvious opening or there is an
absence of anus in its normal position in the perineum.

Assessment
a. absent or stenosis of the anal rectal canal
b. failure to pass meconium stool
c. flat perineum and the absence of a midline intergluteal groove
d. presence of meconium in the urine
e. Presence of an anal membrane
f. External fistula to the perineum or genitourinary system

Interventions
• 1. Determine patency of the anus
• 2. Monitor for the presence of stool in the urine and vagina and report
immediately.

Implementation
a. Therapeutic Management:

Posterior Sagittal Anorectoplasty

- common surgical repair of anorectal malformations among infants
approximately after a month on initial colostomy.

b. Nursing Intervention

i. Assist in the identification of anorectal malformation.

ii. Provide preoperative care for diagnostic procedures, GI compression
and IV fluids.
iii. Irrigate the distal stoma to prevent contamination of the operative site.
iv. Postoperative care of anoplasty involves maintaining appropriate skin
care, management of pain, IV fluids and administration of antibiotics.

c. Interventions Postoperatively
1. Monitor the skin for signs of infection.
2. Position side- lying with legs flexed or in prone position to keep
the hips elevated to reduce edema and pressure on the surgical site.
3. Keep the surgical incision clean and dry, and monitor for redness,
swelling and drainage.
4. Maintain NPO status and nasogastric tube if in place.
5. Maintain IV fluids until gastrointestinal motility returns.
6. Provide colostomy care if present as prescribed.
7. A fresh colostomy stoma will be red and edematous, but this should decrease
with time.
8. Instruct the parents to perform anal dilation if prescribed to achieve and maintain
bowel patency.
9. Instruct the parents to use only dilators supplied by the physician and a water-
soluble lubricant and to insert the dilator no more than 1 to 2 cm into the anus to
prevent damage to the mucosa.

Evaluation
Rationale
 HEPATITIC DISORDERS

A. HEPATITIS
Description
• 1. An inflammation of the liver caused by a virus, bacteria or exposure to
medications or hepatotoxins.
• 2. The goal of treatment include resting the inflamed liver to reduce metabolic
demands and increasing the blood supply, thus promoting cellular regeneration
and preventing complication.
Types are:
• Toxic hepatitis
• Viral hepatitis
Types of Viral Hepatitis
1. Hepatitis A virus (HAV), infectious hepatitis
2. Hepatitis B virus (HBV), serum hepatitis
3. Hepatitis C virus (HCV), non A, non B hepatitis, or
posttransfusion hepatits
4. Hepatitis D virus (HDV), delta agent hepatitis
5. Hepatitis E virus (HEV), enterically transmitted or
epidemic non A, non B hepatitis
6. Hepatitis G virus (HGV), non A, non B non C hepatitis

Toxic Hepatitis
Etiology
• Drugs, alcohol, industrial toxin, poisonous chemicals
Assessment
anorexia, N/V
lethargy
icterus
hepatomegaly
Collaborative management
• Patient education
• Rest
• Maintain FE balance
• Promote well-balance diet
• Identify toxic agent and eliminate it
• Gastric lavage
•
Viral Hepatitis
General Consideration
1. Hand washing by all person
2. Feces, urine, blood and other body fluid precaution
3. Contaminated needles and other instruments that came in contact with
infected body fluids should be handled with great care and properly
discarded
4. Practice “Universal Precaution” in all clients
5. Do not recap needles
6. Proper sterilization of equipments

Preventive Measures in Person Infected with Hepa Virus

• In Hep A & E, enteric precaution should be implemented
• For clients with HepaType B,C,D body fluid precaution should be
observed
• Instruct client with hepatitis not to donate blood
• Advise client with Hepa B, C, D not to have intimate sexual contact

Stages of viral hepatits

1. Preicteric phase (prodromal phase)

The first stage of hepatitis preceding the appearance of jaundice
• last for 1 week

Assessment
• 1.Preicteric stage
• a. Flulike sypmtoms; malaise, fatigue
• b. Anorexia, nausea , vomiting, diarrhea
• c. Pain; headache, muscle aches, polyarthritis
• d. serum bilirubin and enzyme levels are elevated
fever, chills, arthralgia, RUQ tenderness, hepatomegaly, lymphadenopathy

2. ICTERIC PHASE
The second stage of hepatitis, which includes the appearance of jaundice and
associated symptoms such as elevated bilirubin levels, dark or tea colored urine, and
clay colored stools.

• Starts with onset of jaundice

• Reaches intensity in 2 wks, last from 4-6 weeks
Assessment: progression of symptoms
• a. Jaundice
• b. Pruritus
• c. Brown colored urine
• d. Lighter colored stools
• e. Decrease in preicteric phase symptoms
3. Post-icteric phase
The convalescent stage in which the jaundice decreases and the color of the urine
and stool return to normal.
• Disappearance of jaundice
• Last for several weeks up to 4 months
Assessment
• a. Increased energy level
• b. Subsiding pain
• c. Minimal to absent gastrointestinal symptoms
• d. Serum bilirubin and enzyme levels returned to normal

Laboratory assessment
• 1.Alanine aminotransferase: elevated to more than 1000 milliunits/ml and may
rise to as high as 4000 milliunits/ml
• 2. Aspartate aminotransferase: may rise to 1000 to 2000 milliunits/ml
• 3. Alkaline phophatase levels: may be normal or mildly elevated
• 4. Total bilirubin levels: elevated in serum and urine

HEPATITIS A
• A. Description
• 1. Formerly known as infectious hepatitis.
• 2. Commonly seen during the fall and early winter
• B. Individuals at increased risks
• 1. Commonly seen in young children
• 2. Individuals in institutionalized settings
• 3. Health care personnel
• C. Transmission
• 1. Fecal oral route
• 2. Person to person contact
• 3. Parenteral
• 4.Contaminated fruits, vegetables, or uncooked shelfish
• 5. Contaminated water or milk
• 6. Poorly washed utensils
• D. Incubation period
• 1. Incubation period is 2 to 6 weeks
• 2. Infectious period is 2 to 3 weeks before and 1 week after development of
jaundice.
• E. Testing
• 1. Infection is establish by the presence of HAV antibodies ( anti- HAV ) in the
blood.
• 2. Immunoglobulin m (IgM) and IgG are normally present in the blood and
increased levels indicate infection and inflammation.
• 3. Ongoing inflammation of the liver is evidenced by the presence of elevated
IgM antibodies, which persist in the blood for 4 to 6 weeks.
• 4. Previous infection is indicated by the presence of elevated IgG antibodies.
• F. Prevention
• 1. Strict hand washing
• 2. Stool and needle precaution
• 3. Treatment of municipal water supply
• 4. Serological screening of food handlers
• 5. Hepatits A vaccine (Havrix)
• 6. Immune globulin: For individuals exposed to HAV who have never received
the hepatitis A vaccine; administer immunoglobulin during the period of
incubation and within 2 weeks of exposure.
• 7. Immunoglobulin is recommended for household members and sexual contacts
of individuals with hepatitis A.
• 8. Preexposure prophylaxis with immunoglobulin is recommended to individuals
traveling to countries with poor or uncertain sanitation conditions.

HEPATITIS B
• A. Description
• 1. Hepatitis B is nonseasonal
• 2. All age groups are affected.
• B. Individuals at increased risks
• 1. Drug addicts
• 2. Clients undergoing long term hemodialysis
• 3. Health care personnel
• C. Transmission
• 1. Blood or body fluid contact
• 2. Infected blood products
• 3. Infected saliva or semen
• 4. Contaminated needles
• 5. Sexual contact
• 6. Parenteral
• 7. Perinatal period
• 8. Blood or body fluids contact at birth
• D. Incubation period: 6 to 24 weeks
• E. Testing
• 1. Infection is establish by the presence of hepatitis B antigen antibody systems
in the blood
• 2. Presence of hepatitis B surface antigens (HBsAg) in the serological marker
to establish the diagnosis of Hepatitis B
• 3. The client is considered infectious if these antigens are present in the blood.
• 4. If the serological marker (HBsAg) is present after 6 months, it indicates a
carrier state or chronic hepatitis.
• 5. Normally the serological marker (HBsAg) level declines and disappears after
the acute hepatitis B episode
• 6. The presence of antibodies to HBsAg (anti-HBs) indicates recovery and
immunity to hepatitis B.
• 7.Hepatitis B early antigen (HBeAG) is detected in the blood about 1 week after
the appearance of HBsAg and its presence determines the infective state of the
client.
• F. Complications
• 1. Fulminant hepatitis
• 2. Chronic liver disease
• 3. Cirrhosis
• 4. Primary hepatocellular carcinoma
• G. Prevention
• 1. Strict hand washing
• 2. Screening of blood donors
• 3. Testing of all pregnant women
• 4. Needlle precaution
• 5. Avoiding intimate sexual contact if test for hepatitis B surface antigen (HBsAg)
is positve in a person.
• 6. Hepatitis B vaccine: Engerix – B, Recombivax HB
• 7. Hepatitis B immune globulin is for individuals exposed to HVB through sexual
contact or through the percutaneous or transmucosal routes, who have never had
hepatitis B and have never received hepatitis B vaccine.

HEPATITIS C
• A. Description
• 1. Hepatitis C virus infection occurs year round.
• 2. Infection can occur in any age group
• 3. Infection with HCV is common among drug abusers and is the major cause of
posttranfusion hepatitis.
• 4. Risk factors are similar to those for HBV because hepatitis C also is
transmitted parenterally.
• B. Individuals at increased risk
• 1. Parenteral drug users
• 2. Clients receiving frequent transfusions
• 3. Health care personnel
• C. Transmission: Same as for HBV; primarily through blood.
• D. Incubation period: 5 to 10 weeks
• E. Testing Anti-HCV is the antibody to HCV and is most accurate in
detecting chronic states.
• F. Complications
• 1. Chronic liver disease
• 2. Cirrhosis
• 3. Primary hepatocellular carcinoma
• G. Prevention
• 1. Strict hand washing
• 2. Needle precautions
• 3. Screening of blood donors
HEPATITS D
• A. Description
• 1. Hepatitis D is common in the Mediterranean and Middle Eastern areas.
• 2. Hepatitis D occurs with Hepatitis B and may cause infection only in the
presence of active HBV infection.
• 3. Coinfection with the delta agent intensifies the acute symptoms of hepa B
• 4. Transmission and risk of infection are the same as for HBV, via contact with
blood and blood products.
• 5. Prevention of HBV infection with vaccine also prevents HDV infection
because HDV depends on HBV replication
• B. High – Risk individuals
• 1. Drug users
• 2. Clients receiving hemodialysis
• 3.Clients receiving frequent blood transfusion
• C. Transmission: Same as for HBV
• D. Incubation period: 7 to 8 weeks
• E. Testing: Serological HDV determination is made by detection of the
hepatitis D (HDAg) antigen early in the course of the infection and by
detection of anti HDV antibody in the later disease stage.
• F. Complications
• 1. Chronic liver disease
• 2. Fulminant hepatitis
• G. Prevention: Hepatitis D must coexist with Hepatitis B, the precautions
that help prevent hepatitis B are also useful in preventing delta hepatitis.

HEPATITIS E
• A. Description
• 1. Waterborne virus
• 2. Prevalent in areas where sewage disposal is inadequate or where communal
bathing in contaminated rivers is practiced.
• 3. Risk of infection is the same as for
• HAV
• 4. Infection with HEV presents as a mild disease except in infected women in
the third trimester of pregnancy, with whom the mortality rate is high.
• B. Individuals with increased risk
• 1. Travelers to countries that have a high incidence of Hepatitis E such as India,
Burma (Myanmar), Afghanistan, Algeria and Mexico.
• C. Transmission: Same as for HAV
• D. Incubation period: 2 to 9 weeks
• E. Testing: Specific serological tests for HEV include detection of IgM and
IgG antibodies to heaptitis E (anti-HEV).
• F. Complications
• 1. High mortality rate in pregnant women
• 2. Fetal demise
• G. Prevention
• 1. Strict hand washing
• 2. Treatment of water supplies and sanitation measures.

HEPATITIS G
• A. Hepatitis G is non A, non B, non C hepatitis.
• B. Antibodies are absent
• C. Risk factors are similar to those for C
• D. Hepatitis G virus has been found in some blood donors, IV drug users,
hemodialysis clients, and clients with hemophilia; however, hepatitis G virus does
not appear to cause significant liver disease.

Collaborative Management
• Promote rest
• Maintenance of food and fluid intake
• 3,000 ml/day of fluids, I & O and wt monitoring
• Well-balance diet, fruit juices and carbonated beverage
• Fat restriction
• Avoid alcoholic beverage
• Prevention of injury/bleeding precaution
• Monitor PT, hct, hgb
• Avoid parenteral injections
• Apply pressure on injection sites for 5 min
• Monitor urine, stool, skin petechiae, administer Vit K as
ordered
• Provision of comfort measures
• Relieve pruritus
• Provide comfortable environment

Diagnostic Tests for GB Function

• Ultrasound of the gall bladder
• Cholecystography
Oral cholecystography
IV cholecystography
• Preparation for oral cholecystography
• Fat free dinner, then NPO for 2 hrs
• Contrast medium/oral, take 1 tab q 5 min x 6 or 12 tabs
• 1 glass of water only for entire tablets
• NPO for 10 hrs, then X ray is taken in AM
• High fat meal to stimulate contraction
• Series of x rays are taken
• Poor visualization of GB indicates obstruction
• Cholangiography
• X ray visualization of the bile ducts following administration of contrast
medium
• Preparation
• Assess for iodine allergy
• Drink ample fluids after dye administration
• IVF if client is unable to drink fluids
• Care after the procedure
• Assess for delayed hypersensitivity reaction
• Burning sensation on voiding is felt due to excretion of dye
• Poor x ray visualization indicates biliary obstruction

Evaluation
Rationale
B.CHOLELITHIASIS

Cholelithiasis is stone formation in the GB

Cholecystitis is inflammation of the GB
Cause: unknown
1. Cholesterol stones
• Risks Factors
• a. obesity
• b. middle age
• c. female gender
• d. American Indian ancestry
• e. gallbladder, pancreatic or ileal disease
2. Pigmented stones
• Risks Factors
• a. cirrhosis

Predisposing factors
female fat
forty fair complexion
fertile

• Theories
– Metabolic factors
– Biliary stasis
– Inflammation
• Composition of Gall stone
• cholesterol
• bile salts
• Ca
• bilirubin
• protein

Clinical manifestations
• 1. Abdominal pain and jaundice (cardinal symptoms)
• 2. heartburn
• 3. flatulence
• 4. epigastric discomfort
• 5. food intolerances particularly to fats and cabbage
 Assessment

• Decreased fat emulsification

fat intolerance anorexia, N/V
flatulence steatorrhea
• Inflammation
pain (RUQ), fever, leukocytosis
• Decreased bile flow in colon
acholic stool, poor absorption of fat soluble vit
• Increased serum bilirubin
jaundice, pruritus, tea-colored urine
• Infection
cholecystitis, pancreatitis

Evaluation and treatment

• 1. Diagnosis is based on the history, physical examination and radiographic
evaluation
• 2. An oral cholecystogram usually outlines the stones
• 3. Intravenous cholangiography is used to differentiate cholelithiasis from other
causes of extrahepatic biliary obstruction if the cholecystogram is negative.
• 4. Endoscopic or percutaneous cholangiography is also a diagnostic option.
• 5. Laparoscopic cholecystectomy is the preferred treatment for gallstones that
cause obstruction and inflammation.
• 6. Alternative treatments are the administration of drugs that dissolve the stones
and ultrasonic lithotripsy.

Collaborative Management
Postop Care
1. Low or semi-fowler’s position
2. NGT for decompression
3. DBCT
4. Diet: low fat for 2-3 months
5. Ambulation after 24 hrs post op
6. T tube if with CBD exploration
Purpose is to drain bile
Drainage:
• Brownish red for 1st 24 hrs
• 300-500 ml of bile drainage for 1st 24 hrs
• Drainage bottle should be placed in bed at level of incision
to drain excess but not all of the bile

Evaluation
Rationale
C.PKU
• Is an inborn error of metabolism characterized by the inability of the
body to convert the essential amino acid phenylalanine to tyrosine
• Is a genetic disorder that results in central nervous system damage from
toxic levels of phenylalanine in the blood
• An autosomal recessive disorder
• Characterized by blood phenylalanine levels greater than 8mg/dl (normal
level is less than 2mg/dl 2 to 5 days after birth

• It is the inherited autosomal recessive trait in which there is no enzyme needed to

metabolize the essential amino acid, phenylalanine.
• There is no hepatic enzyme, phenylalanine hydroxylase which normally converts
phenylalanine to tyrosine. Thus, there is accumulation of phenylalanine in the
blood and the urine excretes high amounts of its metabolites, phenyl acids.

Assessment
a. musty-odor of urine due to phenol ketones, phenylpyruvic acid
b. the non-production of tyrosine gives the following symptoms:
• i. blond hair, blue eyes, and fair skin (since the absence of tyrosine
do not form melanin)
• ii. mental retardation (since the absence of tyrosine which is
involve in the production of neurotransmitters, thus, affecting the development of
the brain and the CNS)
• iii. symptoms of failure to thrive (like vomiting and irritability)
• iv. hyperactivity
• v. unpredictable schizoid behaviour patterns
• 1. In all children
• a. digestive problems and vomiting
• b. seizures
• c. musty odor of the urine
• d. mental retardation

• 2. In older children
• a. Eczema
• b. Hypertonia
• c. Hypopigmentation
• d. Hyperactive behavior
 Diagnosis
• Newborn Screening Test: Guthrie blood test with a greater than 4 mg/dl result
• a. The major treatment regimen in the management of phenylketonuria (PKU) is
the restriction of dietary protein.
The maintenance of serum phenylalanine levels between 2-8mg/dl by a dietary
phenylalanine intake of 20-30 mg per kg body weight is observed.
Nursing responsibility is geared to providing instruction to parents regarding this
restriction. Foods like meat and dairy products are either eliminated or restricted.
• b. Referral to a registered nutritionist is advocated to render practical suggestions
regarding food selection and preparation.
•
c. Computer, voice activated calculator, cards, or colored beads keep tract of the
daily recommended allowance of phenylalanine foods.
d. The use of blender or mixer to dissolve the lumpy and distinctive odour of the
formula. Add orange Tang, fruit flavoured powdered punch, or strawberry or chocolate
Quik to camouflage the taste of the formula, especially in older children.
• e. Provide family support.

Interventions
• 1. Screening of newborn infants for phenylalanine; the infant should have begun
formula or breast milk feeding before specimen collection.
• 2. If initial screening is positive, a repeat test is performed and further diagnostic
evaluation is required to verify the diagnosis.
• 3. Rescreen infants by 14 days of age if the initial screening was done before 48
hours of age.
• 4. If phenylalanine is diagnosed, do the following:
• a. Restrict phenylalanine intake; high protein foods (meats and dairy products)
and aspartame are avoided because they contain large amount of phenylalanine
• b. Monitor physical, neurological, and intellectual development
• c. Stress the importance of follow up treatment
• d. Encourage the parents to express feelings about the diagnosis and the risk of
phenyketonuria in future children

EVALUATION
RATIONALE
EXOCRINE: CYSTIC FIBROSIS

Description
• 1. Is a chronic multisystem disorder (autosomal recessive trait disorder)
characterized by exocrine gland dysfunction.
• 2. The mucus produced by the exocrine glands is abnormally thick, causing
obstruction of the small passageways of the affected organs.
• 3. The most common symptoms are pancreatic enzyme deficiency caused by
duct blockage, progressive chronic lung disease associated with infection, and
sweat gland dysfunction resulting in increased sodium and chloride sweat
concentrations.
• 4. An increase in sodium and chloride in sweat and saliva forms the basis for the
most reliable diagnostic test, the sweat chloride test.

• Genetic illness that affects the exocrine (mucus producing) glands involving
multi-systems.
• inherited autosomal recessive trait: from the defect of both parents’ genes with an
incidence of 1:4
• Most common among Caucasians.
• Defect in the gene cystic fibrosis transmembrane regulator (CFTR) which codes
proteins related to the family of membrane-bound glycoproteins. This regulates
chloride and sodium channels in the epithelial cells.
• The defect causes abnormal transport across the epithelium which owes to the
manifestations of increased viscosity of the airway mucus, abnormal mucociliary
pancreatic ducts and acini are obstructed and are filled with thick mucous.
Enzymes trypsin, chymotrypsin, lipase and amylase do not reach the intestines;
thus, impairing digestion.
• Bile acids that digest fats are as well interrupted. Malabsorption becomes evident
in the stools.
• The obstruction of thick intestinal secretions lead to meconium ileus or when the
cecum is obstructed, could lead to the distal intestinal obstruction syndrome
(DIOS).
• clearance and lung disease.

– Prolapse of the rectum which is related to the large, bulky stools,

malnutrition and increase in intraabdominal pressure secondary to exertion
during paroxysmal cough.
– The obstruction of intrehepatic biliary tract leads to biliary cirrhosis.
• In the sweat glands and saliva, secretions become rich in sodium and chloride
content which are highly lost, especially during hot weather, fever or exertion.
Respiratory system
• 1. Symptoms are produced by the stagnation of mucus in the airway, leading to
bacterial colonization and destruction of lung tissue.
• 2. Emphysema and atelectasis occurs as the airways become increasingly
obstructed.
• 3. Chronic hypoxemia causes contraction and hypertrophy of the muscle fibers
in the pulmonary arteries and arterioles, leading to pulmonary hypertension and
eventual cor pulmonale.
• 4. Pneumothorax from ruptured bullae and hemoptysis from erosion of the
bronchial wall through an artery occur as the disease progresses.
• 5. Other respiratory symptoms include the folowing
• a. wheezing and dry non productive cough.
• b. Dyspnea
• c. Cyanosis
• d. Clubbing of the fingers and toes
• e. Repeated episodes of bronchitis and pneumonia

Gastrointestinal system
• 1. Meconium ileus in the neonate.
• 2. Intestinal obstruction (distal intestinal obstructive syndrome) caused by thick
intestinal secretions; signs include pain, abdominal distention, nausea and
vomiting.
• 3. Steatorrhea (frothy, foul smelling stools).
• 4. Deficiency of the fat soluble vitamins A, D, E and K, which causes easy
bruising and anemia.
• 5. Malnutrition and failure to thrive; demonstration of hypoalbumenimia from
diminished absorption of protein, resulting in generalized edema.
• 6. Rectal prolapsed that can result from the large, bulky stools, and lack of the
supportive fat pads around the rectum.

Integumentary system
1. Abnormally high concentrations of sodium and chloride in sweat.
2. Parents reporting that the infant tastes “ salty “ when kissed.
3. Dehydration and electrolyte imbalances, especially during
hyperthermicnconditions.

Reproductive system
1. Cystic fibrosis can delay puberty in girls.
2. Fertility can be inhibited by highly viscous cervical secretions, which act as a
plug and block sperm entry.
3. Males are usually sterile, caused by the blockage of the vas deferens by
abnormal secretions or by failure of normal development of duct structures.
 Assessment
• failure to thrive symptoms:
– a. pancreatic enzyme deficiency resulting from duct blockade
• Abdominal distention, vomiting, failure to pass stools, steatorrhea,
and rapid development of dehydration and electrolyte imbalance.
• mecolium ileus, impacted feces, DIOS, passage of foul and frothy
large, loose stools with normal frequency or chronic diarrhea of
unformed stools.

b. progressive chronic obstructive lung disease related to infection and intestinal

obstruction
-wheezing respirations and a dry, non-productive cough.

-If with infection, fever and dyspnea with mucoid impactions

-Barrel-chested; cyanosis, clubbing of the fingers and toes.
c. sweat gland dysfunction.
-taste “salty” when kissed;
-thin extremities, sallow skin, wasted buttocks
d. others
-hyperglycemia, glucosuria, polyuria, weight loss
-sterility in males
-obstructive jaundice
-hypoproteinenia/anemia
-hyponatremia

Diagnostic tests
1. Quantitative sweat chloride test
2. Chest x-ray film reveals atelectasis and obstructive emphysema.
3. Pulmonary function tests provide evidence of abnormal small airway function.
4. Stool/ fat and/ or enzyme analysis: A 72 hour stool sample is collected to check
the fat and/ or enzyme (trypsin) content (food intake is recorded during the
collection).

Management:
• Ensure adequate nutrition for growth
i. Ensure the replacement of pancreatic enzymes (administered with meals so that they
are mixed with food at the duodenum)
ii. Nourishment with a well-balanced, high protein, high calorie diet.
iii. Supplement zinc and iron supplements and water-soluble and fat-soluble vitamins.
iv. Adequate fluids (like Gatorade or Exceed) which has adequate electrolytes and salt
supplementation especially during hot weather and febrile episodes.
Interventions
1. Respiratory system
• a. Goals and treatment include preventing and treating pulmonary infection by
improving aeration, removing secretions, and administering antimicrobial
medications.
• b. Chest physiotherapy (am and pm)
• c. Bronchodilator medication by aerosol opens the bronchi for easier
expectoration.
• d. Use of flutter mucus clearance device
• e. Use of a ThAIRapy vest device
• f. Administration of recombinant human deoxyribonuclease (DNase).
• g. Administer oxygen and antibiotics.

2. Gastrointestinal system
• a. The goal of treatment for pancreatic insufficiency is to replace pancreatic
enzymes.
• b. Encourage a well balanced, high protein, high caloric diet; multivitamins and
vitamin A, D, E and K are also administered.
• c. Assess weight and monitor for failure to thrive.
• d. Monitor for constipation and intestinal obstruction.

Evaluation
Rationale
 ENDOCRINE

Diabetes Mellitus

• Is a chronic disorder of impaired carbohydrate, protein and lipid metabolism that

is caused by a deficiency of insulin?
• A deficiency of insulin results in hyperglycemia
Diabetes is a chronic metabolic disorder in which the body
cannot metabolize carbohydrates, fats, and proteins
because of a lack of, or ineffective use of,the hormone
insulin. Diabetes is classified into three primary types that
are different disease entities but share the symptoms and
complications of hyperglycemia (High blood glucose).
Impaired glucose tolerance, formerly known as"borderline
diabetes" is a degree of hyperglycemia that may precede
type 2 diabetes.

Type I (previously called insulin dependent diabetes mellitus (IDDM) or

juvenileonsetdiabetes)

• Is nearly absolute deficiency of insulin; if insulin is not given, fats are

metabolized, resulting in ketonemia (acidosis)

A. Causes

1. Genetic predisposition.
2. Environmental exposure: virus, toxin, stress.
3. Autoimmune reaction: beta-cells that produceinsulin in the pancreas
are destroyed.
When 80-90% of the beta-cells are destroyed,overt symptoms occur.

B. Characteristics

1. Usually occurs before 30 years of age, butcan occur at any age.

Peak incidence
occurs during puberty, around 10-12 yearsof age in girls and 12-14
years in boys.*
2. Abrupt onset of signs and symptoms ofhyperglycemia: increased
thirst and hunger,
frequent urination, weight loss, and fatigue.
3. Ketosis prone.

C. Treatment
1. Insulin by injection with syringes or pumps
2. Diet
3. Exercise
4. Education
5. Monitoring

Type II
• Is a relative lack of insulin or resistance to the action of insulin; usually insulin is
sufficient to stabilize fat and protein metabolism but not to deal with carbohydrate
metabolism.
II. Type 2 (previously called non-insulindependentdiabetes mellitus, NIDDM, or
adult-onset diabetes)

A. Causes
1. Insulin resistance: unable to utilize insulin that the body makes
because of cell-receptor
defect; glucose is unable to be absorbed into cells for fuel.
2. Decreased insulin secretion: pancreas does not secrete enough
insulin in response to
glucose levels.
3. Excess production of glucose from the liver: result of defective
insulin secretory response; dawn phenomenon (see glossary) is an
example.

B. Characteristics
1. Usually occurs after 30 years of age, but is now occurring in children
and adolescents.
2. Increased prevalence in some ethnic groups, e.g., African
Americans, Hispanic/Latino,
Native Americans , Asian Americans, and Pacific Islanders.
3. Strong genetic predisposition.
4. Frequently obese.
5. Not prone to ketoacidosis until late in course or with prolonged
hyperglycemia.
6. May or may not have symptoms of hyperglycemia.
7. May also have extreme tiredness, blurred vision, delayed healing,
numbness and
tingling of hands and feet, recurring yeast infection.
8. Children between the ages of 10-19 that have one or more of the
following are at an
increased risk:
• Family history
• Member of certain ethnic populations listed above in
B.2.
• Overweight
 • Sedentary lifestyle
• Pre-puberty.
• Signs of insulin resistance or conditions associated with
insulin resistance
(acanthosis nigricans [dirty-neck syndrome], hypertension [high blood
pressure], dyslipidemia [lipoproteins inbalance], polycystic ovarian
syndrome [PCOS]).

C. Treatment
1. Diet/weight management
2. Exercise/increase physical activity
3. Oral hypoglycemic/antihyperglycemic agents, insulin sensitizers, or
insulin
4. Education
5. Monitoring
6. Treatment of comorbid conditions (e.g., hypertension, lipid
abnormalities)

Gestational Diabetes Mellitus (GDM)

A. Causes
1. Insulin resistance due to pregnancy
2. Genetic predisposition

B. Characteristics
1. Carbohydrate intolerance during pregnancy identified via 1-hour
screen using a 50-g oral glucose load (performed between 24th and
28th week of gestation unless otherwise
indicated). If the 1-hour screen for glucose is >140 mg/dl (>7.8
mmol/l), a full diagnostic
100-g, 3-hour oral glucose tolerance test
(OGTT) is indicated.

C. Treatment
1. Diet: provide adequate calories without Hyperglycemia or ketonemia
2. Exercise: program that does not cause fetal distress, contractions, or
hypertension (>140/ 90 mmHg).
3. Insulin: if unable to consistently maintain blood glucose <95 mg/dl
fasting (<5.3 mmol/l) and <140 mg/dl (<7.8 mmol/l) 1 hour
postprandial and <120 mg/dl (<6.7 mmol/l) 2 hours postprandial.

D. Monitoring
1. Blood glucose: required to determine effectiveness of treatment and
possible need for
insulin. Glucose should be checked fasting and 1-2 hours postprandial.
2. Ketones: test for ketones using first morning urine sample. Presence
of ketones may
indicate starvation rather than hyperglycemic ketosis.

Macrovascular complications
• 1. Coronary artery disease
• 2. Cardiomyopathy
• 3. Hypertension
• 4. Cerebrovascular disease
• 5. Peripheral vascular disease
• 6. Infection

Microvascular complications
• 1. Retinopathy
• 2. Nephropathy
• 3. Neuropathy

Assessment
• 1. Polyuria, polydipsia, polyphagia (more common in type I)
• 2. Hyperglycemia
• 3. Weight loss (common in type I rare in type 2
• 4. Blurring of vision
• 5. Slow wound healing
• 6.Vaginal infections
• 7. Weakness and paresthesia
• 8. Signs of inadequate circulation to the feet
• 9. Signs of accelerated atherosclerosis (renal, cerebral, cardiac, peripheral)

HYPOTHYROIDISM

Description
• a. Hypothyroidism is a hypothyroid state resulting from a hyposecretion of the
thyroid hormones T4 and T3.
• b. Hypothyroidism is characterized by a decreased rate of body metabolism
Assessment
• a. Lethargy and fatigue
• b. Weakness, muscle aches, paresthesia
• c. Intolerance to cold
• d. Weight gain
• e. Dry skin and hair
• f. Loss of body hair
• g. Bradycardia
• h. Constipation
• i. Generalized puffiness and edema around the eyes and face
• j. Forgetfulness and loss of memory
• k. Menstrual disturbances
• l. Cardiac enlargement, tendency to develop congestive heart failure.

Intervention
• a. Monitor vital signs including heart rate and rhythm.
• b. Administer thyroid replacement; levothyroxine sodium (Synthroid) is most
commonly prescribed.
• c. Instruct the client about thyroid replacement therapy
• d. Instruct the client in low calorie, low cholesterol, and low saturated fat diet.
• e. Assess the client for constipation; provide roughage and fluids to prevent
constipation.
• f. Provide a warm environment for the client.
• g. Avoid sedatives and narcotics because of increased sensitivity to these
medications
• h. Monitor for overdose of thyroid medications, characterized by tachycardia,
restlessness, nervousness and insomia
• i. Instruct the client to report episodes of chest pain immediately.

• MYXEDEMA COMA

Description
• a. Is a rare but serious disorder that results from persistently low thyroid
production?
• b. Coma can be precipitated by acute illness, rapid withdrawal of thyroid
medication, anesthesia and surgery, hypothermia, or the use of sedatives and
narcotics.

Assessment
• a. Hypotension
• b. Bradycardia
• c. Hypothermia
• d. Hyponatremia
• e. Hypoglycemia
• f. Respiratory failure
• g. Coma

Interventions
• a. Maintain a patent airway.
• b. Administer IV fluids as prescribed.
• c. Administer levothyroxine sodium (Synthroid) intravenously as prescribed.
• d. Administer glucose intravenously as prescribed.
• e. Assess client’s temperature frequently
• f. Monitor blood pressure
• g. Keep client warm
• h. Monitor for changes in mental status.
• i. Monitor electrolytes and glucose level.

HYPERTHYROIDISM
Description
• a. Is a hyperthyroid state resulting from hypersection of thyroid hormone (T3
and T4).
• b. It is characterized by an increased rate of body metabolism
• c. A common cause is Grave’s disease, also known as toxic diffuse goiter.
• d. Clinical manifestation is referred to as thyrotoxicosis.

Assessment for hyperthyroidism caused by Grave’s disease

• a. Enlarge thyroid gland (goiter)
• b. Palpitations, cardiac dysrhythmias, such as tachycardia or atrial fibrillation
• c. Protruding eyeballs (exophthalmos) possibly present.
• d. Hypertension
• e. Heat intolerance
• f. Diaphoresis
• g. Weight loss
• h. Diarrhea
• i. Smooth, soft skin and hair
• j. Nervousness and fine tremors of hands
• k. Personality changes
• l. Irritability and agitation
• m. Mood swings

Interventions
• a. Provide adequate rest
• b. Administer sedatives as prescribed
• c. Provide a cool and quiet environment
• d. Obtain weight
• e. Provide a high calorie diet
• f. Avoid the administration of stimulants
• g. Administer antithyroid medication (propylthiouracil – PTU) that block
thyroid synthesis as prescribed
• h. Administer iodine preparations that inhibit the release of thyroid hormone as
prescribed.
• i. Administer propranolol ( Inderal) for tachycardia as prescribed
• j. Prepare the client for radioactive iodine therapy, as prescribed, to destroy
thyroid cells.
• k. Prepare the client for thyroidectomy if prescribed.

• THYROID STORM
• 1. Description
• a. It is an acute and life threatening condition that occurs in a client with
uncontrollable hyperthyroidism.
• b. It can occur from manipulation of the thyroid gland during surgery and the
release of thyroid hormone into the bloodstream; it also can occur from severe
infection and stress.
• c. Antithyroid medications, Beta blockers, glucocorticoids, and iodides are
administered to the client before thyroid surgery to prevent its occurrence.

Assessment
• a. Elevated temperature
• b. Tachycardia
• c. Systolic hypertension
• d. Nausea, vomiting and diarrhea
• e. Agitation, tremors, restlessness, confusion and seizures as the condition
progresses.
• g. delirium and coma

Interventions
• a. Maintain a patent airway and adequate ventilation.
• b. Administer antithyroid medications, sodium iodide solution, propranolol
(Inderal), and glucocorticoids as prescribed
• c. Monitor vital signs
• d. Monitor continually for cardiac dysrhythmias.
• e. Administer nonsalicylate antipyretics as prescribed ( salicylates increase free
thyroid hormone levels)
• f. Use a cooling blanket to decrease temperature as prescribed.

THYROIDECTOMY

Description
• a. Removal of the thyroid gland
• b. Performed when persistent hyperthyroidism exists

Preoperative interventions
• a. Obtain vital signs and weight
• b. Assess electrolyte levels
• c. Assess for hyperglycemia and glycosuria
• d. Instruct the client in how to perform coughing and deep breathing exercises
and how to support the neck in the postoperative period when coughing and
moving.
• e. Administer antithyroid medications, sodium iodide solution, propranolol
(Inderal), and glucocorticoids as prescribed to prevent the occurrence of thyroid
storm.

Postoperative Interventions
• a. Monitor for respiratory distress
• b. Have a tracheostomy set, oxygen ans suction at bedside.
• c. Maintain client in semi fowler position.
• d. Monitor surgical site for edema and for signs of bleeding; check dressing
anteriorly and at the back of the neck.
• e. Limit client talking and assess level of haorseness.
• f. Monitor for laryngeal nerve damage, as evidenced by respiratory obstruction,
dysphonia, high pitched voice, stridor, dysphagia, and restlessness.
• g. Monitor for signs of hypocalcemia and tetany, which can be due to trauma to
the parathyroid.
• h. Prepare to administer calcium gluconate as prescribed for tetany.
• i. Monitor for thyroid storm.
ADDISON’S DISEASE
Description
• a. Addison’s disease is hyposecretion of adrenal cortex hormones
( glucocortocoid and mineralocorticoids).
• b. The condition is fatal if left untreated.

Assessment
• a. Lethargy, fatigue and muscle weakness
• b. Gastrointestinal disturbances
• c. Weight loss
• d. Menstrual changes in women; impotence in men
• e. Hypoglycemia
• f. Hyperkalemia
• g. Postural hypotension
• h. Dehydration
• i. Emotional disturbances

Interventions
• a. Monitor vital signs, particularly blood pressure, weight, intake and output.
• b. Monitor blood glucose and potassium level.
• c. Administer glucocorticoid and mineralocorticoid medications as prescribed.
• d. Observe for Addisonian crisis caused by stress, infection, trauma, or surgery.

Client education
• a. Avoid individuals with an infection.
• b. Diet: High protein and carbohydrate; normal sodium intake.
• c. Avoid strenuous exercise and stressful situations.
• d. Need for lifelong glucocorticoid therapy.
• e. Avoid over the counter medications.
• f. Wear a Medic Alert bracelet.

ADDISONIAN CRISIS
Description
• a. A life threatening disorder caused by acute adrenal insufficiency.
• b. Crisis is precipitated by stress, infection, trauma, or surgery.
• c. It can cause hyponatremia, hyperkalemia, hypoglycemia and shock.

Assessment
• a. Severe headache
• b. Severe abdominal, leg and lower back pain
• c. Generalized weakness
• d. Irritability and confusion
• e. Severe hypotension
• f. Shock
Interventions
• a. Prepare to administer glucocorticoids intravenously as prescribed;
hydrocortisone sodium succinate (solu-cortef) usually is prescribed initially.
• b. Following resolution of the crisis, administer glucocorticoid and
mineralocorticoid orally as prescribed.
• c. Monitor vital signs, particularly blood pressure
• d. Monitor neurological status, noting irritability and confusion.
• e. Monitor intake and output.
• f. Monitor laboratory values, particularly the sodium, potassium and blood
pressure.
• g. Administer IV fluids as prescribed to restore electrolyte balance.
• h. Protect the client from infection.
• i. Maintain bed rest and provide a quiet environment.
CUSHING’S SYNDROME

Description
• a. Cushing’s syndrome is a condition resulting from the hypersecretion of
glucocorticoids from the adrenal cortex.
• b. Cushing’s syndrome can be caused by an increased pituitary secretion of
ACTH, a pituitary adenoma, or an adrenal adenoma.

Assessment
• a. Truncal obesity with thin extremities.
• b. Moonface
• c. Buffalo hump
• d. Supraclavicular fat pads
• e. Generalized muscle wasting and weakness
• f. Fragile skin that easily bruises.
• g. Reddish purple striae on the abdomen and upper thighs.
• h. Hirsutism (masculine characteristics in female)
• i. Hypertension
• j. Elevated blood glucose, sodium and white blood cell counts.
• k. Decreased calcium and potassium levels.

Interventions
• a. Monitor vital signs, particularly blood pressure
• b. Monitor intake and output and weight
• c. Monitor laboratory values, particularly the blood glucose, white blood cells,
sodium, potassium and calcium levels.
• d. Provide good skin care.
• e. Allow the client to discuss feelings related to body appearance.
• f. Administer chemotherapy agents as prescribed for inoperable adrenal
tumors.
• g. Prepare the client for radiation as prescribed if the condition results from a
pituitary adenoma.
• h. Prepare the client for removal of pituitary tumor (hypophysectomy,
transphenoidal adenectomy) if the condition results frim increased pituitary
secretion of ACTH.
• i. Prepare the client for adrenalectomy if the condition results from an adrenal
adenoma; glucocorticoid replacement may be required following adrenalectomy.