Nursing Care of the Pediatric Individual with a

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Nursing Care of the Pediatric Individual with a
Respiratory Disorder
Etiology and pathophysiology differences in children
How would each of these differences in children affect their airway?
 Tongue is larger in proportion to mouth
 Airway has larger amount of soft tissue than adult
 Cricoid cartilage encircles airway until middle school age
 Larynx is 2-3 cervical vertebrae higher
 Lungs have fewer alveoli at birth than at one year
 Chest wall is less rigid and softerv
 Mucous membranes lining are more loosely attached
Assessment of Respiratory status:
Indications of respiratory distress
a. Breath sounds
 expiratory grunting
 inspiratory stridor
 wheeze, crackles
 consolidation
 evaluation by Respiratory Therapy
b. Pattern of respiration rate – tachypnea gasping and/or irregular
respirations. Tachypnea = 1 ½ x normal rate or more
c. Bradycardia or Tachycardia (depends on the condition)
d. Flaring nostrils
e. Retractions - the amount of accessory muscle use correlates with
the work of breathing. Increased muscle use indicates increased
distress. Retractions can be noted in subcostal, substernal, intercostals
areas of the chest.
f. Change of behavior
 listless
 difficulty feeding
g. oxygenation
 cyanosis – noted in mucous membrane &/or skin
 O2 sat monitor more objective read for oxygenation if aware of errors
in measurement
 review O2 therapy pgs 975-979
h. Increased blood pressure followed by decreased blood pressure
Therapeutic Interventions and Nursing Care

Medication Therapy:
o Antibiotics
1. check cultures at 24,48,72 hours
2. check sensitivities
3. Isolation until 24 of antibiotics
o Respiratory treatments; CPT, Nebulizations
1. Respiratory drugs : ie: albuterol, azmacort, pulmozyme
2. What is the nurses responsibility in regard to these drugs?

Nursing Care:
1. Assess respiration rate, describe sounds, chest movement
2. Positioning – high fowlers, orthopneic
3. Oxygen Therapy - The O2 setup needs humidification or the nares may
become dry and bleed. If it was not humidified Respiratory Therapy
may be called.
4. Fluid maintenance

NPO, or small freq feedings dependent on respiratory rate.
5. Temperature control

Normal temperature for an infant is 97.8 – 98.8.

If hypothermic it increases metabolism, hypoglycemia, puts at risk for
apnea or bradycardia, as well as may indicate the infant is septic. So
a low temp is just an important as an elevated temperature.
6. Organize care
7. Observation for complications
8. Apnea monitor

What do you need to check on this equipment?

Delay set 20 sec, alarms on
__________________________________________________
Otitis Media:
Etiology and Pathophysiology:
A common complication of an acute respiratory infection that occurs when edema of
the upper respiratory structures traps the infection in the middle ear.
Infants and young children’s Eustachian tubes are wide, short and straight and lie in a
relatively horizontal plane.
Assessment of Acute Otitis Media
1. Severe pain in the ear caused by pressure of fluid
2. Fever – hyperthermia is possible
3. Irritability
4. Anorexia
5. Continued symptoms of infections
6. Decreased light reflex of tympanic membrane
7. Red bulging tympanic membrane upon otoscopy
Therapeutic Interventions / Treatment:
 Medication Therapy
1. Antibiotics if a bacterial cause is present:
 Amoxil
 Ceclor
 Bactrim
 Cefzil
2. Antipyretics for the fever
3. Analgesics for the pain

Nursing Care
1. Alleviate the pain by administering Acetaminophen
2. Elevate the head of the bed
3. Position child with affected side on heating pad
4. Family teaching
Serous OTM:
Etiology and Pathophysiology:
Serous otitis media is when there is fluid (effusion) behind the tympanic membrane.
Serous otitis media occurs when one function is compromised:
1. Obstruction by adenoids or inflammation
2. Complication of purulent OTM
3. Altitude changes
4. Large amounts of secretion in middle ear
Assessment:
Signs and Symptoms:
1. Hearing loss
2. Intermittent pain
3. Drainage – yellow, green, purulent, foul-smelling
4. Fluid lines and bubbles present on otoscopy
Diagnostic tests
 Tympanogram
Therapeutic Interventions and Nursing Care:
 Surgical Intervention
1. Tympanostomy tubes to provide aeration and pressure
equalization
2. Lasts approximately 6 months – rejected spontaneously

Medication Therapy
1. Antibiotic ear drops
2. Analgesic ear drops

Nursing Interventions
1. Teaching with Tubes:
 Call MD if decrease hearing, increased ear drainage, increased pain,
fever, bleeding
 Use ear plugs when in water unless indicated otherwise by the MD
 Heat to ear
 Assess motor and language development
Tonsillitis and Adenoiditis:
Etiology and Pathophysiology:
Infection and inflammation of the palatine tonsils and adenoids. Caused by Group A
beta-hemolytic strep and viruses.
Assessment:
Tonsillitis

Fever

Persistent or recurrent sore throat

Anorexia

General malaise

Difficulty in swallowing, mouth breather, foul odor breath

Enlarged tonsils, bright red, covered with exudate
Adenoiditis

Stertorous breathing – snoring, nasal quality speech

Pain in ear, recurring otitis media
Diagnostic tests:
Rapid strep test
Culture
Therapeutic Interventions / Treatment:

Surgery:
Indications for surgery:
1. Repeated episodes of tonsillitis – infection
2. Difficulty in swallowing
3. Interference with breathing from enlarged tonsils and
adenoids
4. Blocked Eustachian tube – chronic otitis media
**Surgery performed only when absolutely necessary – tonsils are
thought to have important protective immunologic functions

Nursing Interventions:
Preoperative Management:
1. Take samples for blood tests:
 CBC
 Hgb, Hct,
 Bleeding and Clotting time
 serologic tests
 throat culture
2. Obtain complete health history, including history of allergies
3. If patient is a child, provide emotional support (Skippy program)
4. Provide routine preoperative care
Postoperative Management:
1.
Maintain in prone or Sims’ position until fully awake to facilitate drainage of
secretions and prevent aspiration. Then change to semi-Fowler’s position
2.
Avoid suctioning and coughing to prevent hemorrhage
3.
Observe for:
a. Frequent swallowing
b. Vomiting of blood
c. Risk for bleeding is in first 24 hours and again between 7-10 days
4.
Provide ice collar
5.
Encourage fluids
6.
Encourage cold fluids, Popsicles, ice chips
7.
Avoid use of citrus juices, milk, hot liquids
8.
Do not use straws
Discuss Discharge Teaching.

Medication Therapy
Administer Tylenol for pain (as ordered)
Croup and epiglotitis:
Etiology and Pathophysiology:
1. Croup is an inflammation of the upper airway, vocal cords,
subglottic tissue, trachea, bronchi, and bronchioles. Obstruction
of airway by edema and exudate.
2. Epiglotitis is an acute bacterial infection usually due to h-flu. It
is severe and rapidly progressive. The signs of respiratory
obstruction develop quickly.
Assessment:
1. Croup – gradual onset with several days of URI then progresses to
onset of cough, increased number of attacks at night, barking cough
with inspiratory stridor, mild elevation of temp (102), hoarseness,
rhinorrhea, sore throat.
2. Epiglotitis – very rapid onset inspiratory stridor, cough, muffled
voice, croaking frog-like inspiration, sore throat,
“4 D’s”
1. Drooling
2. Dysphagia – difficulty swallowing
3. Dysphonia – difficulty talking. Muffled voice
4. Distress inspiratory efforts - stridor, croaking frog-like
inspiration.
Comparison:
Croup
Viral
Slowly progressive
Low grade fever
Hoarseness
Stridor
Epiglottitis
Bacterial (usually H influenza)
Rapidly progressive
High fever
Dysphagia
Stridor (aggravated when
supine)
Therapeutic Interventions and Nursing Care:
For both disorders:
 Observe for signs of respiration distress, degree and location of retractions,
nasal flaring, inspiratory stridor, increasing restlessness.
 Report to Dr.:
a. Tachypnea – respirations > 60
b. Tachycardia – heart rate > 160
c. Elevated temperature - > 101
Considerations for Croup:
 Cool mist tent, monitor O2
 Teach mist from shower 15-20 minutes
 Considerations for Epiglottitis
Considerations for Epiglottitis:
 The child must never be alone.




No tongue blade it may cause laryngospasm and occlude the airway.
Endotracheal tube, tracheostomy / resuscitation set at bedside.
Corticosteroids (dexamethasone), and/or racemic epinephrine
Antibiotics
Bronchiolitis:
Etiology and Pathophysiology:
Lower respiratory tract infection usually caused by rhino syncytial virus (RSV). Affects
infants 2-6 months olds primarily. Infection of bronchial mucosa leads to obstruction
of small to medium airways, untreated usually lasts 7-14 days.
Assessment:
Clinical Manifestations:
1. Starts out with a upper respiratory infection - nasal stuffiness, cough, fever.
2. As illness progresses – lower respiratory tract becomes involved - inspiratory
and expiratory wheezing, tachypnea.
3. Severe respiratory distress develops – retractions, cyanosis, diminished breath
sounds
Diagnostic tests.
1. RSV wash
Therapeutic Interventions and Nursing Care:
 Medication Therapy
1. Bronchodilators
2. Steroids
3. Beta-antagonists
4. Prevention is with:
 Respigam – Intravenous RVS immune globulin
 palivizumab (Synagis)- given IM. It is a monoclonal antibody
These treatments are expensive so it is given mainly to high-risk children
for 5 consecutive months during the winter to prevent RSV.

Nursing Care
1. Humidified oxygen therapy by hood or face tent, mask or nasal
cannula.
2. Give supportive respiratory care
3. Hydration with intravenous or oral fluids
4. Follow Droplet and Contact precautions because RSV can live on
inanimate objects for up to 7 hours.
Apnea:
Delay of breathing over 20 seconds.
1. Assessment / Clinical Manifestations
1. Cessation of breathing for > 20 seconds
2. Cyanosis
3. Marked pallor
4. Hypotonia
5. Bradycardia
2. Diagnostic tests:
R/O seizures with EEG
R/O Gastroesophageal reflux
R/O RSV
2. Therapeutic Interventions and Nursing Care:
1. Apnea monitor if documented apnea
2. Teaching CPR
Sudden Infant Death Syndrome:
Definition:
The sudden death of an infant during sleep.
Etiology:
Association between SIDS and the following risk factors:
 Race – most common in native American infants
 Gender – more common in males
 prone sleeping
 exposure to tobacco / passive smoke
 soft sleeping surfaces; use of pillows and quilts with bedding
 bed sharing with others
 overheating due to excessive blankets, clothing on infant, room
temperature
Assessment:
1. Largest single cause of death after neonatal period.
2. Peak incidence 2 to 4 months
Therapeutic Interventions and Nursing Care:

Nursing Interventions
1. Teaching
2. Prevention: teach parents to place infant on back to sleep
3. Support of parents – help work through feelings of guilt and loss
4. Refer to National Foundation for Sudden Infant Death
Asthma/Reactive Airway Disease/RAD: Asthma
Etiology and Pathophysiology:
1. Obstructive airflow limitation due to:
 Mucosal edema - membranes that line airways
 Increased capillary permeability - WHY? Responding to airway irritation, mast
cells release substances that act upon airways)
 Bronchospasm (bronchoconstriction)
 Mucus plugging (thicker) causes
2. Increased airway resistance
3. Decreased flow rates – there is limit of airflow into and out of lungs. Oxygen and
carbon dioxide exchange and tissure oxygenation are diminished.
4. Increased work of breathing
5. Progressive decrease in tidal volume approaches dead space
6. Arterial pH abnormalities include:
 Respiratory alkalosis (early) WHY? or acidosis (late) increase co2

Metabolic acidosis - from hypoxemia, work of breathing
Since small children have relatively more small airways and mucus glands, their
airway obstruction tends to be due to edema, mucus plugging and cellular infiltrates
and responds slowly to treatment. Because of this, they are more likely to require
hospitalization for asthma attacks.
Triggers / Precipitating and aggravating factors of RAD.
1. Allergens – food, animals, mold spores, pollen, insects, infections agents
(viruses, fungi), drugs
2. Irritants – paint odors, hair sprays, perfumes, chemicals, air pollutants,
tobacco smoke, cold air, cold water, positive ions
3. Weather changes
4. Infections – viral respiratory pathogens, fungi, mycoplasma bacteria (rare;
pertussis)
5. Gastroesophageal reflux
6. Allergic rhinitis, sinusitis and upper airway inflammation
7. Nonallergic hypersensitivity – aspirin, NSAID, metabisulfites, tartrazine (FD & C
yellows #5) (?)
8. Exercise
9. Sleep or nocturnal asthma
There usually is some combination of factors.
Assessment:
1. Asthma Score:
0
1
2
PaO2 or
Cyanosis
70-100 (RA)
None
<70 (RA)
in RA
<70 40% FiO2
in 40% FiO2
Inspiratory breath
sounds
Normal
Unequal
Decreased or
absent
Accessory muscle
use
None
Moderate
Maximal
Expiratory
wheezing
None
Moderate
Marked or
Absent
Cerebral function
Normal
Depressed,
agitated
Coma
2. Peak Expiratory Flow Rate (PEFR)
Peak flow meter is used to:
 Assess lung volume
 Predict a possible oncoming attack – if % is low, may indicate an asthma
attach is approaching.
 Assess the effectiveness of respiratory treatments
Diagnostic Testing:
 Spirometer
Goals:
1. Prevent/control chronic symptoms
2. Monitor peak expiratory flow rate (Peak Flow) and treat accordingly
3. Prevent exacerbations, maintain normal pulmonary function
4. Relieve and minimized exacerbations
5. Maximize compliance to therapeutic regimen
Therapeutic Interventions / Treatment:
 Medication Therapy
I. Reliever or Rescue Medications
 Short acting beta agonists (albuterol)
o Relax smooth muscle in airway
o Used before inhaled steroid
o Drug of choice for therapy is metered-dose inhaler or nebulizer
o Goal is not use on a regular basis > 1 canister per month
o Assess for effectiveness – decrease in wheezing, retractions,
respiratory rate decreases, increase in peak flow
o Side effects – excitement and nervousness, GI distress, tachycardia.
 Corticosteroids – Prednisone (Prelone)
o Used to diminish airway inflammation and obstruction
o Used for short term therapy
 Anticholinergic agents (atrovent)
o Inhibits bronchoconstriction and decreases mucus production
II. Controller/Preventer Medications
 Mast-cell inhibitors – Cromolyn / Tilde
o Non steroidal
o Decrease inflammatory cells, inhibits release of histamine

Leukotriene modifiers: Accolade, Singulair
o Reduces inflammation cascade responsible for airway inflammation.
 Inhaled steroids: Most effective anti-inflammatory therapy for
persistent asthma
o Advair, Pulmicort, Flobid or flovent, beclovent, aerobid,
azmacort
o Inhaled steroids side effects: candidia, hoarseness, systemic
effects: growth, bone mineralization, immune function
Considerations of inhaled meds
 Always use a spacer with metered dose inhalers (MDI)
 Check proper spraying and inhalation
 Rinse mouth after each use
Therapeutic Interventions and Nursing Care:
 Daily
1. Allow to sit in high fowlers or orthopneic position
2. Assessment PEAK FLOW
3. Use controller meds
 Exacerbations
1. Assessment PEAK FLOW, respiratory status, sounds, rate, accessory muscle
use, air movement (asthma score)’
2. Rapid institution of reliever therapy
3. Frequent reassessment
4. Assurance of clinical improvement with PEAK FLOW and respiratory status
improved
Discuss Discharge Teaching.
 Discuss assessment of the environment for precipitating factors
o remove possible triggers if possible
 Assess Peak Flow expiratory flow rate with meter, before and after treatment to
assess response
 Assess respiratory status
 Evaluate and re-teach about Respiratory meds and proper inhalation
o Aerosol bronchodilators, adrenergics, anticholinergics, steroids
 When to seek EMERGENCY CARE
 Hydration
 Exercise: Recommend swimming to increase lung capacity, less irritating to
airway or stop start activities, RT before exercise, breathing exercises
 Psych support to decrease anxiety, no sedatives
 Show movie and give out pahphlet, advise when should see health care provider
the next time.
Cystic Fibrosis:
Etiology and Pathophysiology:
Inherited medallion recessive of exocrine gland from both parents. A dysfunction of
exocrine glands including mucous, salivary and sweat producing glands. The thick
tenacious mucous leads to altered functioning of the respiratory system, pancreas,
liver, intestine, reproductive system, and sweat glands.
A. Respiratory System
 accumulation and retention of thick mucus in the airways =
 viscosity.
 Inflammation = further obstruction
  infections WHY?= thick mucous secretions that stay in the respiratory
track increase risk for pathogen invasion
 Chronic lung infections and airway obstruction lead to bronchial destruction
and bronchiectasis (a lung condition characterized by irregular dilation and
destruction of bronchial walls).
 Atelectasis and pneumothorax
B. Pancreas
Obstruction of the pancreatic ducts by mucous which inhibits the flow of
pancreatic enzymes - trypsin, lipase, and amylase to the duodenum. Eventually
the pancreas becomes fibrotic.
C. Intestine/ Gastrointestinal tract
 With blockage of enzymes being release, there is a decrease in the breakdown
of food leading to decrease absorption of nutrients.
 There is malabsorption of fats causing steatorrhea (fatty, foul smelling bulky
stools)
 Mucus accumulation may lead to bowel obstruction
 Meconium ileus happens in 10-15%.
 Rectal prolapse and intussusception are not common
D. Reproductive System
 99% of males sterile due to mucus obstruction; females have decrease
fertility due to thick cervical secretions.
Assessment:
Clinical Manifestation:
1. Chronic respiratory infections is the hallmark of CF.
 Cough
 Sputum production – blood streaked, hemoptysis.
 Barrell chest
 Increased respirations
 Clubbing of fingers – chronic hypoxia
 Cyanosis
2. Failure to Thrive - despite high caloric intake, they are small in stature because
burn up calories just breathing.
3. Steatorrhea (frothy, foul smelling, undigested food
4. Absence of meconium stool in the first 24 hours after delivery.
Diagnostic tests:
a. Sweat test: Increased levels of Chloride
o Normal < 40 mEq/L.
o CF 40-60 mEq/L Diagnostic > 60 mEq/L. . Usually 3-5 X’s higher
b. Pancreatic enzymes via stool cultures: Trypsin absent in 80% of children
with cystic fibrosis. Lipase and amylase also absent.
Therapeutic Interventions / Treatment:
Mainly managed at home but brought into the hospital for “tune-ups”. Chest
physiotherapy, IV antibiotics, nutritional boost.

Diet Therapy
Nutritional Goal – to increase weight, formed non-greasy stool
1. Pancreatic enzymes:
 Viokase or Ultrace – comes in a powder or delayed-release capsules.
These are given prior to or with all meals and snacks. Sprinkled on the
food. Dosage is regulated by evaluation of the stool.
2. Water-soluble vitamins
o Fat-soluble vitamins A, D, K, E, in watermiscible form
3. Diet high in calories and protein and low in fat. Supplement with shakes
4. Maintain Na balance (when sweating and ill)

Nursing Care
a. Respiratory Goal – removal of secretions AEB loose productive cough,
Adequate hydration, decreased infections, no retractions or stridor
o Aerosol inhalation – before physiotherapy.
o
o
o
o
o
Chest physiotherapy - Postural drainage; CPT helps prevent respiratory
infections (vest called Thairapy vest) vibration and loosens secretions
so child can remove them.
Physical exercise
Antibiotics
Expectorant
Additional immunizations for pneumococcus and yearly for influenza
** do not give antihistamines or antitussives.
b. Parental Education Goal – Acceptance of illness, and positive adaptation as
evidence by verbalization of feelings, verbalization of medical regime, making
and keeping doctor appointment
o Explain disease, and reasons for therapeutic regime
o Demonstrate respiratory therapy techniques
o Explain the care and proper use of equipment in the home
o Inform parents of parental support groups, cripple children’s provides
some financial aid
o Encourage normal family routine as much as possible
o Parents need genetic counseling if they want more children
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