COMMON

DISORDE
RS IN
CHILDREN
RESPIRATORY
DISORDERS
 ACUTE NASOPHARYNGITIS
(CORYZA)
 Most frequent infectious disease in
children
 Average of 10-12 colds/ year

 Incubation period- 2-3 days

ETIOLOGIC AGENT:
ETIOLOGIC AGENT:
1. rhinovirus-most common cause
2. coxsackie virus -
3. respiratory syncitial virus (major
etiologic agent)
4. adenovirus
5. parainfluenza/ influenza virus
 SIGNS AND SYMPTOMS
1. nasal congestion
2. watery rhinitis
3. low grade fever
4. mucus membrane is edematous
5. cervical lympnode may be swollen and
palpable
6. body malaise
 PATHOPHYSIOLOGY
 initial pathology is submucosal
edema of nasal mucosa followed by
shedding of ciliated epithelial
cells( 5th day) nasal mucopurulent
discharge, then release of interferon
(play major role in recovery)
 TREATMENT
 Common colds is self-limiting
 supportive care
 relief of nasal obstruction - use of
isotonic saline drops and aspiration
 antipyretic or analgesic agents
 antitussive is sometimes used for
persistent cough
 Streptococcal pharyngitis:
> caused by group A beta-hemolytic
streptococcus (GABS)
> can lead to cardiac and kidney damage
> more severe than viral infection

Signs and symptoms:

1. marked erythema of the back of throat and
palatine tonsils
2. tonsils are enlarged and (+) white exudates in
the tonsillar crypts
3. high grade fever
4. difficulty swallowing
Dx:
throat swab and culture
 TREATMENT
1. antibiotics- 10 days course of oral
antibiotics (pen G or
clindamycin)
2. high fluid intake
3.relief of pain
COMPLICATION:
1. Rheumatic fever
2. Glomerulonephritis
 TONSILLITIS
- term commonly used to refer to infection and
inflammation of palatine tonsils
palatine tonsils - located on both side of
pharynx
Adenitis - refers to infection and inflammation of
the adenoids ( pharyngeal) tonsils
adenoids - located in the nasopharynx
Tubal tonsils - located at entrance to the
Eustachian tube
lingual tonsils - located at base of tongue
SIGNS AND SYMPTOMS

1. difficulty of swallowing
2. fever
3. lethargy
4. mouth breathing (post pharyngeal)
5. difficulty hearing (Eustachian tube)
6. halitosis
7. sleep apnea
 ETIOLOGY
 <3 years old - often viral
 school age children
 TREATMENT
1. antipyretic
2. analgesics
3. Antibiotics ( 10 day course - usually
penicillin but may be erythromycin if allergic
to penicillin) is prescribed for bacterial
infections to prevent the complication of
rheumatic fever.
4. Surgical – tonsillectomy with adenoidectomy
Post –op Care:
1.Observe for, & report unusual
bleeding ( frequent swallowing)
2. Help prevent bleeding by
discouraging the child from coughing
& clearing the throat.
3. Position the child on the side or the
abdomen to facilitate drainage from
the throat
4.Provide appropriate teaching . Instruct
the child & parents to:
a.Observe activity restrictions,
including when the child can return
to school.
b. Avoid persons with known infections
c. Avoid acidic & other irritating foods
d. Monitor the child for bleeding,
especially immediately
postoperatively& 5 to 10 days post
op when tissue sloughing occurs.
 INDICATION

1. chronic tonsillitis (not done if

inflamed
because may spread infection)
2. Recurrent tonsillitis (4-6x/year)
3. Sleep apnea

Nursing diagnosis: pain related to

surgical procedure
NOSEBLEED
MANAGEMENT

1. keep pt in upright position with head tilted

slightly forward to minimize the amount of
blood pressure in nasal vessels, keep blood
moving forward not back to nasopharynx
2. apply pressure to the side of the nose with
your fingers
3. keep the child quiet and stop
crying because crying increases
pressure in the blood vessels of
the head and prolonged bleeding
4. control of bleeding, can give
epinephrine
(1:1000) to constrict blood
vessels
5. can put nasal packing for
continuous pressure
 CROUP (LTB)
Acute
Laryngotracheobronchitis)
- Inflammation & narrowing of the larynx, trachea,
and major bronchi. Most common form of croup &
usually affects children younger than 5 years old.
- one of the most frightening diseases of early
childhood for both parents and children. Tends
to occur at night & recur with respiratory tract
infections.
- common cause is viral infection usually
parainfluenza virus, influenza virus.
 signs and symptoms
1.Gradual onset from upper respiratory
tract infection , which progresses to
signs of distress.
2. Hoarseness
3. low grade fever
4. barking cough at night
5. inspiratory stridor
6. Retractions
7.Severe respiratory distress
8. Restlessness& Irritability
9. Wheezing, rales, rhonchi, & localized
areas of diminished breath sounds

MANAGEMENT
- Assess for airway obstruction by evaluating
respiratory status. Note color, respiratory effort,
evidence of fatigue, & VS.
 provide warm, moist environment-give o2 to
alleviate hypoxia
 Keep emergency equipment ( tracheostomy &
intubation tray) near the bedside.
 give corticosteroids & epinephrine (nebulizer) -
reduce inflammation and bronchodilation
 intravenous hydration

Nursing dx: Ineffective airway clearance related to

edema
Health Teachings
1.When the child awakens with a
barklike cough, tell the parents to
place the child in the bathroom & to
run hot water to produce steam.
2.Instruct the parents to stay in the
bathroom with the child to prevent
accidental injury.
 Epiglotitis
>an acute , severe inflammation of
the epiglottis.( flap of tissue that
covers the opening to larynx to
keep out food and fluids)
> it is considered an emergency
because the swollen epiglottis can’t
rise and allow the airway to open.
> This emergency situation occurs
most commonly in children between
3 and 6 years of age.
Causes:
1. Bacterium H-Influenza type b
2. pneumococci, streptococci -
most common cause
3. echovirus
4.respiratory syncitial virus
Sign and symptoms:
1. begins as mild URTI
2. restlessness & anxiety
3. hyperextension of the neck,
drooling, & severe sore throat with
refusal to drink
4 rapid, thready pulse
5. characteristic “tripod:
position: child sits in upright
position, with chin thrust out &
tongue protruding.
6. sudden onset of high fever,
lethargy, & dyspnea & dysphygia
7. Red & inflamed throat with
 NURSE ALERT!!! “ Never
illicit gag reflex-may cause
complete obstruction”

Laboratory findings:
1. leukocytosis ( 20,000-
30,000 mm3)
MANAGEMENT:
1.Closely monitor respiratory status to
ensure patent airway. If a child presents
with sx of epiglottitis, ensure that
appropriate personnel perform a throat
examination & that emergency
equipment is at hand.
2. Prepare for emergency hospitalization
= after dx is confirmed, an
endotracheal intubation or
tracheostomy is performed to maintain
a patent airway. Swelling usually
3. After the child is intubated, monitor
closely & maintain a patent airway by
suctioning as needed& providing
oxygen therapy as prescribed.
4. Administer prescribed medications
( antibiotics, anti-inflammatories.)
5. Recommend that all children receive
H. Influenzae type B ( Hib) conjugate
vaccine beginning at 2 months of age,
because H.Influenzae is the most
common cause of epiglottitis.
. Provide warm, moist environment
7

8. o2 therapy
9. Intravenous therapy
 Asthma
> chronic, reversible , obstructive airway disease,
characterized by wheezing. It is caused by
smooth muscle spasm w/ hypertrophy of the
bronchial tubes, or swelling of the bronchial
mucosa, after exposure to various stimuli.
 Hypersecretion of mucus

 Most common chronic disease in childhood.

Most children experience their first sx by 5yo
 exercise, nocturnal occurrence, seasonal, hx of
allergy, stress
Etiology:
1.Commonly results from
hyperresponsiveness of the
trachea & bronchi to irritants.
Common irritants include:
1.Allergens = dust mites, molds,
animal danders
2. Viral infections
3. Irritants = air pollution, smoke,
perfumes, laundry detergents
4. Certain foods ( food additives,
5. Rapid changes in environmental
factors
6. Exercise
7. Psychological stress
Pathophysiology:
* Release of inflammatory mediators
from bronchial mast cells,epithelial cells,
& macrophages >>> activation of
inflammatory cells >>>bronchial spasm
>>> inflammation >>> edema of the
mucosa >>> production of thick
mucus>>> inc. airway resistance
>>>closure of airways >>>dyspnea &
wheezing
Dx:allergy skin test, pulse
oximetry, peak flow meter
 Clinical Assessment of
Asthma
MILD MOD SEVERE
breathless walking talking at rest
talks in sentences Phrases words
Alertness may be usually agitated
agitated agitated
RR Inc inc >30
accessory (-) (+) (+)
wheeze audible audible audible w/o
steth
pulse <100 100-120 >120
 Intermittent Mild Moderate Severe
Persistent Persistent Persistent

Am sx < 1x/wk >1x/wk Daily; aff Daily; dec

activ activ
Pm sx </= 2x/mo >/= 2x/mo >1x/wk > 1x/wk
Management
 B2 agonists ( Bronchodilators),

Theophylline, Steroids( anti

inflammatories), Cromolyn Na, O2
 Orthopneic position

 Monitor VS, hydration

 Adequate nutrition and non

allergenic diet
 Environmental modification

 Health education
 Status Asthmaticus
 Progression of acute, severe, prolonged
asthma attack unresponsive to therapy
 Preceding upper respiratory tract
infection, allergen, cigarette smoke
 HR and RR inc, dec breath sounds,
cyanosis
Mx: cont B2 agonist and IV steroid, O2,
coughing, fluids, monitor I and O
 Sudden Infant Death
Syndrome
>sudden, unexpected death of any infant for
>sudden, unexpected death of any infant for
whom a postmortem exam fails to determine
the cause of death
> Death occurs during sleep
>most common cause of death (1 mo-1 year
old, peaks 2-4 mos)
 Preterm / infants with apneic episodes, with
prenatal drug exposure, siblings of infants
who died of SIDS, exposed to smoking,
infants of adolescent mothers, infants of
closely spaced pregnancies, underweight
 the victim seems healthy
 sleeping on prone position
 Theories of causation: abnormalities in the
brain and metabolic disorder
Maternal risk factors - cigarette smoking
during pregnancy, maternal age < 20 yo,
poor prenatal care, low weight gain,
anemia, use of illegal drugs and alcohol,
low socioeconomic status

Newborn risk factors – cyanosis,

tachycardia, respiratory distress,
irritability, hypothermia, poor feeding
Nsg Dx:
Dysfunctional grieving r/t loss of a
child

Management
 assist psychologically - intense
grief and guilt for parents
Gastrointestinal
Disorders
 Cleft Lip and Palate
 failure of fusion of maxillary
and median nasal process
 hereditary

 unilateral/bilateral

 males

Mx: surgery - Cheiloplasty

 Rule of 10’s-10 wks,
10 lbs, Hgb 10 gm
Gastrointestinal
anomalies
 MX : Surgical repair ( Cheiloplasty)
 LIP : 6 weeks – 12 weeks
 PALATE : 12-18 months

 PREOP = feed upright / burp frequently

use large holed nipple
 POSTOP = Position : on side / use cup/ avoid
straw. ELBOW restraint, give water after
each feeding to clean suture line .
 Cleft Palate
 midline opening of
palate
 usually w/ Cleft lip
 Female
 surgery 12-18 mos -
allow anatomic
changes <1 yo ie
formation of palatine
arch and tooth buds
Ndx:
 Risk for imbalanced nutrition, less than
body requirements r/t feeding problems
 Risk for ineffective airway clearance r/t
oral surgery
 Risk for infection during post op period
Nursing mx:
 Adequate nutrition; sips of fluid btw feeding in semi-
upright position; use rubber tipped syringe
 Direct the formula away from the cleft & toward the
side & back of the mouth to prevent aspiration.
 Provide special nipples or feeding devices ( ex. Soft
pliable bottle with soft nipple with enlarged
opening)
 Feed the infant slowly & burp frequently to prevent
excessive swallowing of air & regurgitation.
 Prevent ear and upper respiratory tract infection
 Address body image and speech concerns
 Reassurance to parents
Pre-op:
1.Surgical correction of the cleft lip
usually occurs at 1-3 mos. Repair of
the cleft palate is usually performed
between 6-18 mos. Repair of the cleft
palate may require several stages os
surgery as the child grows.
2. Early correction of the CL enables
development of more normal speech
pattern
3. Delayed closure or large defects may
require the use of orthodontic
appliances
 Nursing Care
Postop
 monitor respiratory distress d/t edema, hemorrhage
 Use mist tent , if prescribed, to minimize edema,
liquefy secretions & minimize distress.
 Suction mucus and blood gently
 dropper feeding 1st 3 weeks; regular feeding after
 Use elbow restraints to maintain suture line
integrity. Remove them every 2 hours
 Position side lying or back in cleft lip to avoid
injury to the operative side; prone in cleft palate to
facilitate drainage.
Tracheoesophageal Fistula
 Gastrointestinal
anomalies
Esophageal atresia / tracheoesophageal atresia

 EA is a condition in which the

proximal and distal portions of
the esophagus do not
communicate.
 TEF is an abnormal
communication between the
trachea and esophagus
> Communication of the esophagus
and trachea
> maternal hydramnios and
prematurity
S/sx:coughing, choking, cyanosis,
dyspnea, excessive secretion,
abdominal distention

Dx: Ba swallow
 Nursing care
Preop
 Suction regularly
 Elevate the head
 Gastrostomy feeding
 hydration
 O2

Postop
1. Observe for respiratory distress
2. Proper positioning –avoid hyperextension
of neck
3. Continue suction
4. Prevent wound infection
5. Provide pacifier
Hirschprung’s Disease
Hirschsprung disease ( Aganglionic
Megacolon) – is a congenital anomaly
characterized by absence of
nerves( innervation) to a section of the
intestines ( usually the rectosigmoid)
4x more common in boys ( esp. with
Down’s syndrome)
It can be acute & life threatening or
chronic
familial, congenital
No peristalsis in the affected area.
Pathophysiology:
1. Absence of ganglion cells in one segment
of the colon >>> lack of innervation >>>
absence of propulsive movements >>>
accumulation of intestinal contents &
distention of the bowel proximal to the
defect >>> enterocolitis ( inflammation of
the small bowel & colon – leading cause of
death in children with hirschsprung)
S/SX:
1.Newborns – failure to pass
meconium, reluctance to ingest
fluids, abdominal distention, bile
stained emesis.
2. Infants – failure to thrive,
constipation, abdominal distention,
vomiting& episodic diarrhea
3. Older children – anorexia, chronic
constipation, foul smelling & ribbon
like stools, abdominal distention,,
Rectal exam reveals a rectum empty
of stool, a tight anal sphincter, & stool
leakage.
Ominous sign signifying enterocolitis
include explosive, bloody diarrhea,
fever, & severe prostration.
DX : > Barium enema reveals
megacolon
> Rectal biopsy reveals absence of
ganglionic cells which confirms the
diagnosis.
Preop Nursing Care
1. Daily cleansing enemas w/ 0.9% NaCl
*Tap/hypotonic water will cause cardiac
congestion or cerebral edema
2. Manual dilatation of the anus
2. Minimal residue diet w/ vitamin supplementation
3. Position semi fowlers to relieve dyspnea from
distended abdomen
Postop
1. Observe for abdominal distention
2. Small frequent feedings after NGT removal
3. Colostomy care
4. Assist parents to cope with children’s feeding
problems
Surgery is done in 3 Stages:
1.Temporary colostomy before definitive
surgery to allow the bowel to rest & the
child to gain weight.
2. Reanatomosis by means of
abdominoperineal pull-through about 9-
12 mos later.
3. Closure of the colostomy about 3 mos
after the pull through procedure.
Intussusception
Intussusception - invagination
or telescoping of one portion of the
intestine into an adjacent portion,
causing obstruction.
One of the most frequent causes of
intestinal obstruction in children ages
3 mos to 5 yrs, most commonly bet 3-
12 mos of age.
If tx is delayed for longer than 24 hrs,
bowel strangulation may occur,
leading to necrosis, hemorrhage,
Cause: > unknown
> maybe associated with viral
infections, intestinal polyps,lymphoma
Pathophysiology:
Invagination because of
hyperperistalsis in an intestinal
segment usually the ileocecal valve
>>>peristalsis continues to pull the
invaginated segment along the bowel
>>> intestinal edema >>>obstruction
occur >>> blood supply is cut off
Ndx:
 Pain r/t abnormal abdominal peristalsis
 Risk for deficient fluid volume r/t bowel
obstruction
DX:
 Barium enema for dx & therapeutic
treatment tool ( reduction by
hydrostatic pressure)
 Sonogram reveals “ coiled spring “

MX: surgery
S/Sx:
1.Severe paroxysmal abdominal pain,
causing the child to scream & draw
his knees to the abdomen.
2. Vomiting of gastric contents
3. Tender, distended abdomen with
palpable sausage shaped mass.
4. “ Currant jelly stools”containing
blood & mucus
5. Bile stained or fecal emesis, &
 Nursing Care

1. Provide comfort measures -

pacifier for infants

2. NPO

3. Adequate hydration via IV therapy

4. Promote parent-infant bonding

Pyloric Stenosis
Pyloric Stenosis – is the narrowing of
the pyloric sphincter at the outlet of the
stomach d/t hypertophy or hyperplasia.
> Common in males
Cause: unknown ; may be hereditary
Pathophysiology:
Pylorus narrows bec of hyperplasia/
hypertrophy>>>obstruction of the
pyloric sphincter >>>gastric distention
>>> dilatation >>>hypertrophy
S/SX:
1.Projectile vomiting
2. Non bile stained emesis
3. No signs of anorexia, good appetite
& feeding patterns.
4. No evidence of pain, weight loss,
upper abdominal distention
5. Palpable olive shaped mass in the
epigastrum (RUQ) just to the right of
the umbilicus.
6. Visible gastric peristalsis moving
from left to right across the epigastrum.
7. Decreased frequency & volume of
stools.
8. Signs of malnutrition & dehydration
DX: x-ray “ string sign”, Endoscopy
MX: Surgery ( pyloromyotomy) fredet
ramstedt procedure
Ndx:
 Risk for deficient fluid volume r/t
inability to retain food
 Risk for infection at site of surgical
incision r/t danger of contamination
from feces d/t proximity of incision
to diaper area
 Nursing care
 Hydration
 Pacifier

 may give thickened feedings on upright position

then NPO just before surgery
 Monitor I and O, weight, and vomiting

Postop
1. dropper feeding 4-6 hrs after surgery 45 min- 1 hr
duration; oral rehydration soln then half strength
breastmilk/formula at 24 hr interval
2. Side lying position
3. Monitor weight and return of peristalsis
4. Wound care
5. Pacifier for oral needs
 Diaphragmmatic Hernia

 Herniation of intestinal
content into the
thoracic cavity
 Left side
 S/sx:respiratory
difficulty, cyanosis,
retractions, (-) breath
sounds affected side,
scaphoid abdomen
 Cx: pulmonary HPN
 Mx:’E’ surgery
Ndx:
Risk for ineffective airway
clearance r/t displaced bowel
Risk for imbalanced nutrition, less
than body requirements, r/t NPO
status
 Nursing Care
Preop
 Elevate head

 Low intermittent suction

Postop
1. Semi-fowlers

2. Maintain warm, humidified envt – lung

fluid drainage
3. Suction prn

4. Chest pptx

5. NPO – prevent pressure on diaphragm

 Celiac Disease/Gluten
sensitive enteropathy/Celiac
sprue
 Malabsorption syndrome that occurs when
the mucosa of the proximal small intestine
is sensitive to gluten. (wheat, rye, oats,
barley)
 inability to absorb fat, thus steatorrhea, def
fat soluble vitamins, malnutrition and
distended abdomen
 S/Sx appears bet 1-5 yo after introduction
of gluten in the diet.
 S/sx:diarrhea, wt loss, anorexia, irritable,
anemic (Fe deficiency)
Pathophysiology:
Intolerance for or inability to digest gluten
>>>accumulation of the amino acid
glutamine>>>toxic to intestinal mucosal
cell>>> intestinal villi atrophy
>>>reduction of absorptive surface of the
small intestine.
 CELIAC CRISIS (due to ingestion of gluten,
infections, prolonged fasting) = acute vomiting and
diarrhea & may lead to F & E imbalance & rapid
dehydration.
 Dx: Biopsy of the jejunum reveals the mucosal
surface with hyperplastic villus atrophy. ( Definitive
diagnosis of celiac disease). This characteristic
lesion return to normal after dietary restriction of
gluten which helps confirm the dx.

 Mx: hydration, gluten free diet, vitamin & Fe

supplementation , avoid cereals, bread, cake,
cookies, spaghetti, pizza, instant soup, some
chocolates, some ice cream, donuts, pies, hotdogs,
Foods allowed:
1.Meats: beef, pork, poultry & fish
2. Eggs
3. Milk & dairy products: milk, cheese,
cream
4. Fruits & veg: all
5. Grains: rice, corn, gluten free wheat
flour, corn flakes, corn meal &
gluten free pre-cooked cereals
Endocrine
Disorders
 Cystic Fibrosis
 Autosomal recessive
 Chronic multisystem disorder of the
exocrine glands characterized by
abnormally thick pulmonary
secretions.
 Affects lungs, pancreas, intestines
and sweat glands, salivary glands,
reproductive tract.
S/SX: GI - meconium ileus, rectal
prolapse,( most common GI sign); loose,
bulky, fatty stools (steatorrhea,)
malnutrition ( vit ADEK deficiency),
failure to thrive; marked tissue wasting;
distended abdomen thin extremities.
Respiratory –wheezing, recurrent
infection,cough, dyspnea, clubbing,
cyanosis, atelectasis, generalized
obstructive emphysema, chronic
sinusitis, bronchitis, ear, nose, throat
problems.
Reproductive –
Female – delayed puberty & decreased
fertility ( from decreased viscosity of
cervical mucus which blocks the entry
of sperm)
Male – infertile, sterility is due to
blockage of the vas deferens with
abnormal secretions.
Cardiovascular – Cor Pulmonale, right
sided heart enlargement, CHF d/t
obstruction of pulmonary flow
S/SX of hyponatremia – rapid IV
Integumentary –
> Increased concentrations of
sodium & chloride in sweat; parents
report “salty” taste when they kiss their
babies.
> Failure to thrive may result in
hypoalbuminuria, which causes edema.
Dx: > “Sweat test” (Chloride 2-5x the
normal), > absence of
pancreatic enzymes, >immunoreactive
trypsinogen in blood
> stool analysis – steatorrhea
> xray – patchy atelectasis &
generalized obstructive emphysema.
Mx: chest physiotherapy, antibiotics,
pancreatic enzymes, vitamins, lung or
pancreas transplant
 Nursing Care

1. Hi calorie, Hi CHON, moderate fat

diet
2. Nebulization and physiotherapy
3. Frequent Position changes when in
bed
4. Oral care
5. Adequate rest and comfort
 Musculoskeletal
Anomalies
 Congenital club foot
 clubfoot, or talipes equinovarus is a birth
defect .
 The foot is twisted in (inverted) and down.
 Mgt : long leg cast q2 wks 6-12 weeks
 Denis browne splint (bar shoe)

surgical correction- 3-6 mos

 Congenital Hip Dysplasia

 Imperfect hip
development
affecting femoral
head and
acetabulum
 Female
 Unilateral more
common
A. Lower right leg
 Inc frequency w/
breech delivery B. asymmetric skin
fold
Etiology: Unknown
Possible Causes:
a. Abnormal Development of the
joint caused by:
> Fetal position
> Genetic factors
b. Abnormal relaxation of the
capsule & ligaments of the joint
caused by hormonal factors.
c. Environmental factors such as
breech delivery
S/sx:
 limited abduction of affected hip

 shortening of leg on affected side

( Galeazzi / Allis sign )
 asymmetric thigh and gluteal folds

 buttocks on affected side will flatten

on prone
 pelvis dips on normal side when
standing on affected leg
( Trendelenburg )
 palpable click ( Ortolani’s click)
. Leg length Inequality with unilateral
complete dislocation.
. Delayed walking
. Limp
> Trunk dips when the child puts
weight on his involved leg.
> Waddling gait is observed in
children with bilateral dislocation.

Mx: maintaining hip in abduction

traction and casting
Treatment:
Goal: To restore as closely as possible
anatomic alignment of the hip while
maintaining pain-free function. Early
recognition is the key to successful
treatment.
1. Tx varies with age & extent of the
defect.
2. Early Stage ( Birth – 3 months)
a. Reduction by gentle
manipulation.
b. Splinting the hip by means of
 3. Later Stages ( 3-18 months)
a. Preliminary traction
b. Closed reduction
c. Immobilization in a hip spica
cast or splint or Pavlik harness
4. Older child ( 18 mos – 4 yrs
old)
a. Preliminary traction
b. Possible need for open
reduction or osteotomy.
c. Immobilization in a hip spica
 some splinting devices used for
DDH
principle: normal development of the femoral
head and the acetabulum depends on
reestablishing a normal acetabulofemoral
relationship that is sufficiently stable to permit early
motion
von Rosen
splint

Pavlik harness Frejka splint

 Spina Bifida
 Collective term for all SC disorders

Spina Bifida Occulta – posterior laminae fail to fuse

- dimpling, abnormal tufts of hair

Meningocoele - meninges herniate through unformed

vertebrae; protrusion covered by a layer of skin
- usually occurs in the lumbar region
- protrusion is covered by a skin layer or only the clear
dura mater
Myelomeningocoele – SC and meninges
protrude through the vertebrae defect
- absent motor and sensory function
- flaccidity, lack of sensation in LE
- loss of bowel and bladder control
- may be accompanied by hydrocephalus

Dx: sonography
NEURO
 HYDROCEPHALUS
 Types of Hydrocephalus?
1. Congenital hydrocephalus -is present at birth
and may be caused by environmental influences during fetal
development or by genetic factors.
2. Acquired hydrocephalus -develops at the time of
birth or at some point afterward. This type of hydrocephalus can
affect individuals of all ages and may be caused by injury or
disease.
3. Communicating hydrocephalus -occurs when
the flow of cerebrospinal fluid (CSF) is blocked after it exits the
ventricles . the CSF can still flow between the ventricles, which
remain open

4. Non-communicating hydrocephalus-also called

"obstructive" hydrocephalus -- occurs when the flow
of CSF is blocked along one or more of the narrow
pathways connecting the ventricles.
 Hydrocephalus
S/sx: head enlargement, ant fontanel
wide and bulging, scalp veins
dilated, broad forehead, sclera
shows above iris, brisk tendon
reflexes, spasticity, irritability,
lethargy, poor appetite, cracked pot
sound on percussion
Cardiovascular
Disorders
 Congenital Heart Defects
-CHD are structural defects of the
heart, great vessels, or both that
are present at birth.
-Children with CHD are more likely
to have associated defects such as
tracheoesophageal fistula.
- CHD is second only to prematurity
as a cause of death in the first year
of life.
1.Acyanotic Heart Disease – conditions
that interfere with normal blood
flow through the heart either by
slowing it down or by
L R shunt
high pressure to low pressure
oxygenated to unoxygenated blood

2. Cyanotic Heart Disease – allow

unoxygenated blood into the
systemic circulation
R L shunt
 4 Classifications of Congenital Heart Defects:

1. Defects with increased pulmonary blood

flow:
a. Atrial Septal Defect (ASD)
b. Ventricular Septal Defect (VSD)
c. Patent Ductus Arteriosus (PDA)
2. Defects with Decreased pulmonary blood
flow:
a. Tetralogy of Fallot (TOF)
b. Tricuspid Atresia ( TA)
3. Obstructive Defects:
a. Coarctation of the Aorta ( COA)
b. Aortic stenosis ( AS)
c. Pulmonic stenosis ( PS)
4. Mixed Defects:
a. Transposition of the Great Vessels
( TOGV)
b. Truncus Arteriosus
c. Hypoplastic left Heart Syndrome (
HLHS)
 ACYANOTIC HEART DISEASE
1. Atrial Septal Defect
 Opening between 2 atria
 Atrial septal tissue does not fuse
properly during embryonic
development
 S/sx: cyanosis(CHF), dyspnea on
exertion, fatigue, failure to
thrive, split S2
 Mx: surgery 1-3 yo
 Cx: endocarditis, heart failure
 Postop: monitor arrhythmia,
administer antibiotics
Pathophysio:
Pressure is higher in the left atrium than
the right >>>blood shunts from the left
to the right >>>RV & pulmonary artery
enlarge ( they are handling more blood).
Notes:
>Most infants are asymptomatic until
early childhood; many defects close
spontaneously by 5 yo.
DX: Echocardiography –reveals enlarged
right side of the heart & inc. pulmonary
circulation.
2. Ventricular Septal Defect
Opening in ventricular

septum, most common
 S/sx: respi infections, failure
to thrive, dyspnea, fatigue,
pansystolic murmur
 Mx:close spontaneously
otherwise surgery <2 yo
 Cx:pulmonary HPN,
endocarditis, heart failure
 Postop: monitor arrhythmia,
administer antibiotics
Ventricular septal defect
 Sometimes called a hole in the heart
 most common congenital heart defect
 occurs when the septum, the muscular wall separating the
right and left ventricles, fails to fully form
 The hole allows oxygen-rich blood to leak from the left
ventricle into the right ventricle, instead of moving into the
aorta and on to the body.
 Too much blood may flood the lungs.
 This defect can lead to heart failure, excessive blood
pressure in the lungs (pulmonary hypertension), infections
of the heart (endocarditis), irregular heartbeats
(arrhythmias) and delayed growth.
 Small holes may heal on their own or cause no symptoms.
Larger holes may require surgical repair by stitching
together or covering with a patch.
Congenital Heart
Defect
3. Patent Ductus Arteriosus
Aorta to pulmonary artery


 Fetal ductus arteriosus fails to

close after birth
 Common in prematurity, high
altitude, maternal rubella
 females
 S/sx:clubbing, dyspnea, “machine
like murmur” (2nd-3rd ICS)
 Cx:heart failure, endocarditis,
pulmonary artery stasis/HPN
 Mx:Indomethacin, surgery/2-3yo
Patent ductus arteriosus
 Before birth, a temporary blood vessel called
the ductus arteriosus connects the pulmonary
artery and the aorta.
 This allows blood to bypass the lungs because
oxygen is delivered to the fetus through the
placenta and umbilical cord.
 The temporary vessel normally closes within a
few hours or days of birth since the lungs take
over.
 If it remains open (patent), some blood that
should circulate through the body is
misdirected to the lungs.
 This defect can cause heart failure or
endocarditis. In infants, it can be closed with
medications. In older children and adults,
plugs, coils or surgery can be used to close the
vessel.
Congenital Heart
Defect
 CYANOTIC HEART DISEASE
1. Tetralogy of Fallot
 Localized narrowing of
the aorta.
 TOF consists of 4
major anomalies:
 1. VSD
 2. Right Ventricular
Hypertrophy
 3. Pulmonic Stenosis
 4. Aorta overriding the
VSD
Tetralogy of Fallot
 This defect is a combination of four (tetralogy)
congenital abnormalities. The four defects
typically are ventricular septal defect (VSD),
pulmonary stenosis, a misplaced aorta and a
thickened right ventricular wall (right
ventricular hypertrophy).
 They usually result in an insufficient amount of
oxygenated blood reaching the body.
 Complications of tetralogy of Fallot (fuh-LOE)
include cyanosis — sometimes called "blue baby
syndrome," since the lips, fingers and toes may
have a bluish tinge from lack of oxygen — as
well as poor eating, inability to tolerate
exercise, arrhythmias, delayed growth and
development, and stroke.
 Surgical repair of the defects is required early
in life.

 Tet spells- irritability, pallor and blackouts or

convulsions,
Pathophysio:
PS impedes flow of blood to
lungs>>>inc pressure in the rt
ventricle ( causes
hypertrophy)>>>forces deoxygenated
blood thru the septal defect to the left
ventricle >>>overriding aorta receives
blood from both rt & left ventricles.
S/sx: 1.Acute episodes of cyanosis ( “
Tet spells”). Tet spells are
characterized by irritability, pallor &
blackouts or convulsions.
 Cyanosis occuring at rest as PS
worsens
 clubbing, exertional dyspnea,
fainting, fatigue slowness due to
hypoxia
 Squatting,( a characteristic posture
of older children that serves to decrease the
return of poorly oxygenated venous blood from the
lower extremities & to increase systemic vascular
resistance, which increases pulmonary blood flow &
DX: Echocardiography – shows enlarged
rt chamber & dec in pulmonary artery
size
> Cardiac catheterization &
Angiography – allows definitive
evaluation
Cx: thromboembolism,CVA
Mx: 1. Surgical repair when infant is 1
yo
Blalock Taussig: anastomose SC
and pulmonary artery
- avoid BP and venipuncture in right
arm
 2. Tricuspid
Atresia
- Tricuspid valve fails to develop
-Without the tricuspid valve, there is no
communication between the right atrium
& the right ventricle
-Involves complete mixing of oxygenated
& unoxygenated blood on the left side
of the heart resulting in pulmonary
obstruction. Blood flows thru a patent
foramen ovale to the left side of the
heart & thru the VSD, to the right
ventricle & to the lungs.
S/S:
1.Cyanosis in NB
2. Chronic hypoxia, clubbing in older
children
DX:
Echocardiography
MX:
1.Palliative procedures such as
pulmonary to systemic artery
anastomosis ( for children w/ CHF)
2. Corrective surgery may be performed
Mixed Defects
1. Transposition of the Great
Vessels
 Pulmonary artery leaves
the L ventricle, Aorta
exits the right ventricle.
 No communication bet
systemic & pulmonary
circulations
 This defect results in 2
separate circulatory
patterns. Rt heart –
systemic circulation Left
heart – pulmonary
circulation.
Transposition of the great vessels/
arteries:
 With this defect, the positions of the aorta and
the pulmonary artery (the great arteries) are
reversed (transposed).
 The aorta arises from the right ventricle instead
of the left and the pulmonary artery arises from
the left ventricle instead of the right.
 This creates a circulatory pattern that prevents
nourishing oxygenated blood from reaching the
body.
 This condition would quickly be fatal to a
newborn except it's generally accompanied by
another defect — commonly a septal defect or
patent ductus arteriosus — that does allow
oxygen-rich blood to get to the body. Surgical
repair is usually necessary shortly after birth.
** To sustain life, the child must have
an associated defect ( VSD, ASD,
PDA)- which permits oxygenated
blood into the systemic circulation,
but cause increased workload.
S/SX:
1.In infants w/ no associated defects,
severe respiratory depression &
cyanosis
2. In infants w/associated defects, less
cyanosis but may have sx of CHF
Mx: PGE for PDA, Balloon catheter to
create ASD, Arterial switch procedure-
Total Anomalous Pulmonary
Venous Return

 Pulmonary v. drain
to SVC or R atrium
 PDA or foramen
ovale essential
 S/sx :cyanosis,
fatigue
 CX: R heart failure
 Mx: PGE, surgery
Truncus arteriosus
Truncus arteriosus
 This is a defect in which the normally distinct
pulmonary artery and aorta merge into one single
great vessel (truncus) arising from the right and left
ventricles.
 In addition, there's usually a large ventricular septal
defect, essentially turning the right and left
ventricles into a single chamber.
 This allows oxygenated and unoxygenated blood to
mix. Too much blood may flow to the lungs, flooding
them and making it difficult to breathe.
 It can also result in life-threatening pulmonary
hypertension. Surgery is needed to close the septal
defect with a patch and to separate the pulmonary
arteries from the trunk.
 A conduit is placed to connect the right ventricle to
the pulmonary artery. Because the conduit doesn't
grow with the child, repeat surgery may be
necessary over time.
Hypoplastic left heart syndrome
Hypoplastic left heart syndrome
 In this condition, the left side of the heart is
underdeveloped (hypoplastic), including the aorta,
aortic valve, left ventricle and mitral valve.
 As a result, the body doesn't receive enough
oxygenated blood. In the first few days after a baby is
born, the ductus arteriosus remains open (patent),
allowing normal circulation, so the baby may seem fine
initially.
 But when the ductus arteriosus naturally closes, signs
and symptoms begin, including a bluish cast to the skin
from lack of oxygen, difficulty breathing and poor
feeding. This condition may be accompanied by an atrial
septal defect.
 Treatment options for this life-threatening condition are
a heart transplant or a multistage surgical procedure
done during the first few years of life.
Atrioventricular canal defect
Atrioventricular canal defect
 This is a combination of defects, including a
large hole in the center of the heart and a
single common valve instead of the separate
tricuspid and mitral valves.
 Also called atrioventricular septal defect, this
defect is classified by whether it's only partial,
involving only the upper chambers of the
heart, or complete, in which blood can travel
freely among all four chambers of the heart.
 Both forms allow extra blood to circulate to the
lungs, causing the heart to enlarge. The
condition is often associated with Down
syndrome. Infants may also have trouble
breathing and not grow well.
 Surgery is often done in infancy to close the
hole and reconstruct the valves.
Obstructive Defects
 1. Coarctation of the Aorta
 males
 Constriction of aorta

 S/sx: asymptomatic HPN,

irritability, headache,
epistaxis, dyspnea, bounding
UE pulses, higher BP in upper
extremities, dec femoral and
distal pulses,systolic murmur
 Cx:chronic HPN
 Mx:surgery 2 yo
 Postop: monitor abdominal
pain, antihypertensives
Coarctation of the aorta
 This is a narrowing (coarctation), or constriction,
in a portion of the aorta.
 Coarctation forces the heart to pump harder to
get blood through the aorta and on to the rest of
the body.
 This defect can cause several life-threatening
complications, including severe hypertension,
aortic aneurysm, dissection or rupture,
endocarditis, brain hemorrhage, stroke, heart
failure and premature coronary artery disease.
 Repair is typically recommended before age 10,
either by surgically removing the affected portion
or widening it through balloon angioplasty and
placement of a stent.
Aortic stenosis

 defect that narrows or obstructs the

aortic valve opening, making it difficult
for the heart to pump blood into the
aorta.
 Mild cases may not have symptoms
initially, but they can worsen over time.
 The defect can cause heart enlargement,
left-sided heart failure, arrhythmias,
endocarditis and fainting.
 Treatment includes surgical repair or
replacement of the valve or, in young
children, widening through balloon
valvuloplasty
 2. Aortic Stenosis
-Involves an obstruction of the
ventricular outflow of the blood
S/SX: faint pulse, hypotension,
tachycardia, poor feeding, exercise
intolerance, chest pains
DX; ECG, Echocardiography reveals left
ventricular hypertrophy.
MX:
-Surgical aortic valvutomy or prosthetic
valve replacement.
Pulmonary stenosis
 the flow of blood from the right
ventricle to the pulmonary
artery is obstructed by
narrowing at the pulmonary
valve.
 When there's an obstruction
(stenosis), the right ventricle
must pump harder to get blood
into the pulmonary artery.
 The defect may occur along with
other defects, such as
thickening of the muscle of the
right ventricle immediately
below the valve.
 in many cases, pulmonary stenosis is mild and
doesn't require treatment. But because it can
cause heart failure, arrhythmias or enlargement
of the right heart chambers, surgery may be
necessary to repair the stenosis or replace the
valve.
 Special balloons to widen the valve (balloon
valvuloplasty) may also be used.
 Kawasaki Disease/
Mucocutaneous Lymph Node
Syndrome
 Before puberty, peaks 4 yo

 S/sx:spiking fever x 5 days, bilateral conjunctivitis,

reddened pharynx, dry lips, strawberry tongue,
cervical lymphadenopathy, peripheral edema,
erythema and desquammation, truncal rash, arthritis
 Patho: Respi infection immune complex systemic
vasculitis
 Unwanted Cx: aneurysm and MI
 Dx:clinical
 Mx: Salicylates and Immunoglobulins given via IV
KAWASAKI
Other Measures:
Protect edematous areas
Record intake and output
Offer soft food
Administer prescribed medication
 Rheumatic
Fever
 Autoimmune
J. N. E. S.
 Grp A Beta hemolytic
strep
 6-15 yo, peaks 8 yo
 1-3 wks after untreated
infection
 Dx: 5 major criteria –
polyarthritis, carditis,
subcutaneous nodules,
erythema marginatum,
sydenham’s chorea
minor – fever,
polyarthralgia, hx of RF,
inc ESR, antecedent strep
infection
S/SX:
1.Carditis – sx include tachycardia,
cardiomegaly, murmur, muffled heart
sounds, precordial pain.
2.Polyarthritis – consists of swollen, hot,
painful joints
3.Syndenham Chorea or St. Vitus dance –
demonstrated by sudden, aimless,
irregular movements of the
extremities, involuntary facial
grimaces, speech disturbances.
4. Erythema marginatum – clear
centered,transitory, nonpruritic
MX:
1.Child may receive monthly injections of
benzathine penicillin, 2 daily oral doses
of penicillin ( to prevent recurrent
streptococcal infections
CX:= Mitral valve insufficiency & myocarditis
To diagnose: = either 2 major or I major 2
minor criteria present
Nursing Care
 Monitor vital signs

 Provide adequate nutrition

 Promote safety to prevent chorea

related injuries
 Acute Glomerulonephritis

 Inflammation of glomeruli or kidney

 Follows infection with strep 10-14 days
 5-10 yo
 Males
S/sx:sudden onset of edema and hematuria,
proteinuria, hypertension

Dx: urinalysis and 24 hour urine

hypoalbuminemia
inc ESR, BUN, Crea, antistreptolysin O
Mx: semi fowlers
diuretics, antibiotics
O2
antihypertensives

Nsg Care:
quiet play activities
diet – normal CHON, mod salt restriction,
fluid restriction
daily weight and output
 Nephrotic Syndrome

 Altered glomerular
permeability(autoimmune);
inc permeability to albumin
 3 yo
 Males
 Minimal change syndrome

S/sx: proteinuria, edema-

periorbital area,
hypoalbuminemia,
hyperlipidemia

Dx:urinalysis and 24 hr
CHON, inc ESR
Mx:steroids, immunosupressant

NDx: Risk for decreased fluid volume r/t CHON

and fluid loss
Imbalanced nutrition: less than BR r/t CHON
and fluid loss

Nsg care:
Adequate nutrition
proper diet – dec salt
Weigh daily, monitor I and O
Protect edematous areas
Administer prescribed drugs
Health teaching
 Wilm’s Tumor

 Malignant tumor of the kidney

 Associated with other anomalies
 6 mos-5 yo, peaks 3-4 yo
 Good prognosis
 S/sx:abdominal mass, hematuria, low grade
fever, anemia, wt loss
 Dx: CT scan
 Mx: Nephrectomy, radiotherapy
avoid abdominal palpation
 Acute
Glomerulonephritis
 Inflammation of glomeruli or kidney
 Follows infection with strep (10-14 days)
 5-10 yo, peak 6-7 yo
 Males
 Etiology : GABS ( Group A Beta Hemolytic
Streptococcus) Poststreptococcal infection
( usually of the skin- impetigo or upper
respiratory tract.
S/SX: >history of infection about 10 –
14 days before the onset of sx.
>irritablity, fatigue & lethargy
>anorexia, pallor , hypertension
> sudden onset of edema ( peri-
orbital) and hematuria ( urine
is brown (tea or cola colored)

Dx: urinalysis and 24 hour urine

mild hypoalbuminemia
inc ESR, BUN, Crea,
antistreptolysin O
Mx: semi fowlers
diuretics, antibiotics, O2
antihypertensives – calcium channel
blockers, B- blockers, ACE inhibitors
( Angiotensin converting enzyme)
Nsg Care:
quiet play activities
diet – normal CHON, mod salt
restriction, fluid restriction
daily weight and output
 Nephrotic Syndrome
 Altered glomerular
permeability(autoimmune);
inc permeability to albumin
 3 yo
 Males
 Minimal change syndrome

S/sx: proteinuria, edema-

periorbital area, significant
hypoalbuminemia,
hyperlipidemia
Dx:urinalysis and 24 hr CHON,
inc ESR
Mx: steroids, immunosupressant
NDx: Risk for decreased fluid volume r/t
CHON and fluid loss
Imbalanced nutrition: less than BR r/t
CHON and fluid loss

Nsg care:
Adequate nutrition, proper diet – dec salt
Weigh daily, monitor I and O
Protect edematous areas
Administer prescribed drugs
Health teaching
 Wilms tumor( nephroblastoma)
 is the fifth most common pediatric
malignancy and the most common renal
tumor in children.
 NURSE : post a sign DO NOT PALPATE THE
ABDOMEN on the bed

 Osteogenic Sarcoma(osteosarcoma)
 A cancer of the bone that usually affects
the large bones of the arm or leg.
 common site : epiphyseal plate of the long
bones (femur)
 It occurs most commonly in young people
and affects more males than females.

Atopic
2 mos-3 yo
Dermatitis
 R/t food allergy
S/sx: papular and vesicular
skin eruptions w/ erythema,
pruritus, dry,flaky scales
upon healing
Mx: reduce allergen, topical
steroids
NDx: Impaired skin integrity
r/t eczematous lesion
Nsg care: Reduce allergen
Prevent skin dryness and
pruritus
Protein Energy Malnutrition
Marasmus Kwashiorkor
Low calorie, low CHON Low CHON
0-2 yo 1-3 yo
(-) edema (+) edema
Wasting variable
“all skin and bone”
Growth retardation
(+) growth retardation
variable
Apathetic, quiet Irritable, moaning
Good appetite Poor appetite
Infrequent skin/hair (+) skin and hair
changes changes
Anemia uncommon (+) anemia