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INCIDENCE:
Highest among low socio economic class
Largest # of admission to NICU
12% of all pregnancies
Multiple pregnancies
PIH
Placental problems
PRETERM INFANTS
CAUSES:
UNKNOWN
MATERNAL FACTOR
Malnutrition
Preeclampsia (toxemia of pregnancy)
Chronic Medial illness (Cardiac/kidney disease/DM)
Infection (UTI, vaginal infection)
Drug Use (coccaine, tobacco, alcohol)
Abnormal structure of the uterus
Previous PT Births
PRETERM INFANTS
CAUSES:
PREGNANCY
Hypertension
Incompetent Cervix
Placental Previa/ Abruptio Placenta
PP.OM, poly/oligohydramnios
FETUS
Chromosomal abnormalities
Intrauterine Infection
Anatomic Abnormalities
IUGR, multiple gestations
PRETERM INFANTS
DIAGNOSTIC EVALUATION:
Appraisal is made as soon as possible after
admission to the nursery.
HEAD – head circumference is large in comparison
with chest (reflects cephalocaudal direction of growth)
The fontanels are small and bones are soft
Soft cranium subject to characteristic nonintentional
deformation, “preemie head”
Absent eyebrows, eyes closed, and ears are poorly
supported by cartilage (soft and pliable)
Bones of skull and ribs – soft
Very small and appear scrawny – less subcutaneous
fat (skin is wrinkled)
PRETERM INFANTS
DIAGNOSTIC EVALUATION:
SKIN – bright pink (often transluscent) with small
blood vessels
Smooth and shiny (may be edematous) with small blood
vessels clearly visible underneath thin epidermis
Fine lanugo hair abundant over body, sparse, fine &
fuzzy on head
Soles and palms – minimal creases
Harlequin color – Skin color changes when preterm
infant is moved; upper half or one side of the body is
pale or one side of the body is red.
Small breast bud size with underdeveloped nipples
Male Infants – few scrotal rugae, undescended testes
PRETERM INFANTS
DIAGNOSTIC EVALUATION:
Labia and clitoris are prominent in females
Posture - complete relaxation with marked flexion and abduction
of the thighs; random movements are common with slightest
stimulus
Activity – Inactive and listless
Extremities maintain an attitude of extension and remain in any
position in which they are placed.
Reflexes – partially developed
Sucking absent, weak or ineffectual; swallow, gag, cough reflexes –
ABSENT
Temperature instability – Heat regulation poorly developed in the
preterm infant because of poor development of CNS
Increased susceptibility to infection
PRETERM INFANTS
DIAGNOSTIC EVALUATION:
Respirations are not efficient because of muscular weakness of
lungs and rib cage and limited surfactant production;
Retraction at xiphoid is evidence of air hunger
Infants should be stimulated if apnea occurs
HMD/RDS, chronic lung disease, BPD, apnea of prematurity
Greater tendency toward capillary fragility in the preterm infant
Red and white blood cell counts are low with resulting anemia during
first few months of life.
Neuro – Higher incidence of intracranial hemorrhage in the
preterm infant
Muscle twitching, convulsions, cyanosis, abnormal respirations, and
a short shrill cry
Cerebral palsy, visual-motor deficits, altered intellectual functions
PRETERM INFANTS
DIAGNOSTIC EVALUATION:
GIT: Nutrition is difficult to maintain – because of weak sucking
and swallowing reflexes, small capacity of stomach, and slow
emptying time of the stomach
Renal: Reduced glomerular filtration rate results in decreased
ability to concentrate urine and conserve fluid.
Higher ECF – vulnerable to fluid and electrolyte imbalance
Cardio: (+) murmur
More susceptible to biochemical alterations – hyperbilirubinemia,
hypoglycemia
The greater degree of immaturity, the greater the degree of
potential disability.
PRETERM INFANTS
THERAPEUTIC MANAGEMENT:
Team approach: neonatologist, advance
practice nurse, nurse staff, respiratory
therapist
Incubator, IV lines, Oxygen therapy
PREVENTION:
PRENATAL CARE: key factor
Good nutrition and education
ID mothers at risk
Educate on symptoms of PT labor
Avoid heavy/repetitive work or standing long
periods of time
PRETERM INFANTS
THERAPEUTIC MANAGEMENT:
TREATMENT:
Oxygen, IVF
Umbilical catheterization – IVF, meds, bld
extraction
X-ray
Special feedings of breastmilk/formula
Medications
Kangaroo care – shorter stay in NICU
PRETERM INFANTS
THERAPEUTIC MANAGEMENT:
DISCHARGE:
Usually stay
in hospital until reach pregnancy due
date depending on their condition
GOALS:
Serious illness resolved
Stable temperature
Taking all feedings by breast/bottle
No recent apnea/bradycardia
Parents are able to provide care (meds and feedings)
Prior to discharge: eye examination, follow up visits
PRETERM INFANTS
NURSING CARE:
IMPLEMENTATION:
Maintain airway; check respirator function if employed;
position to promote ventilation; suction when necessary;
maintain temperature of environment; administer oxygen only
if necessary
Observe for changes in respirations, color, and vital signs
Check efficacy of Isolette: maintain heat, humidity, and
oxygen concentration; monitor oxygen carefully to prevent
retrolental fibroplasias
Maintain aseptic technique to prevent infection
Adhere to the techniques of gavages feeding for safety of the
infant
PRETERM INFANTS
NURSING CARE:
IMPLEMENTATION:
Observe weight-gain patterns
Determine blood gases frequently to prevent
acidosis
Institute phototherapy by letting them verbalize and
ask questions to relieve anxiety
Provide flexible and liberal visiting hours for
parents as soon as possible
Allow parents to do as much as possible for the
infant after appropriate teaching
Arrange follow-up before and after discharge by a
visiting nurse or a Barangay Health Worker
POST MATURE INFANTS
After42 weeks AOG/ 294 days past 1st day of
mother’s LMP; regardless of birth weight
Post term, post maturity, prolonged pregnancy,
post datism
INCIDENCE:
7% (3.5-15%) OF ALL PREGNANCIES
CAUSES: unknown
History of >/= 1 previous post term pregnancies &
miscalculated due date (not sure of LMP)
POST MATURE INFANTS
FETAL RISK:
Progressive placental dysfunction – placenta
(supplies nutrient & oxygen) ages toward the end of
pregnancy --- may not function efficiently
Amniotic fluid volume decreases, fetus may stop
gaining weight/ weight loss
Decreased amniotic fluid may lead to cord compression
during labor
Increased risk of MAS and hypoglycemia
Increasing size (mainly length) & hardening of skull
may contribute to CPD
GREATEST RISK: during stresses of labor & delivery
especially in infants of primigravidas.
POST MATURE INFANTS
CHARACTERISTICS OF INFANTS (1-3wks of
AGE):
Absent lanugo, little if any vernix caseosa, abundant
scalp hair, overgrown nails
Dry, peeling skin (cracked, parchmentlike &
desquamating)
Wasted physical appearance (reflects intrauterine
deprivation)
Minimal fat deposit (depleted subcutaneous fat) –
thin, elongated appearance
Meconium staining – seen in skin folds w/ vernix
caseosa
Visible creases palms/ soles
POST MATURE INFANTS
DIAGNOSIS: P.E
UTZ, non-stress testing, estimate amniotic fluid
volume
MANAGEMENT:
Check respiratory problems related to meconium
Blood test for hypoglycemia
PREVENTION:
Accurate due date and UTZ
Cesarean section/ induction of labor - recommended
HYPERBILIRUBINEMIA
Refers to excessive level of accumulated
Bilirubin in the blood
JAUNDICE or ICTERUS – yellowish
discoloration of skin, sclera, nails
Relatively benign but it can also be
pathologic
HYPERBILIRUBINEMIA
PATHOPHYSIOLOGY:
RBC DESTRUCTION
Globin Heme
liver
Bilirubin detched from albumin through enzyme glucoronyl transferase + glucoronic acid
Conjugated Bilirubin
DURATION:
Declines on 5th-7th Variable May remain Dependent on
day jaundiced x 3-12 severity &
weeks or more treatment
HYPERBILIRUBINEMIA
COMPARISON OF MAJOR TYPES OF UNCONJUGATED
HYPERBILIRUBINEMIA
THERAPY:
If phototherapy is instituted, May include home phototherapy PRENATAL – If mother is
evaluate benefits & harm of with a temporary (10-12hr) breastfeeding, assist with
discontinuation of a
temporarily discontinuing maintenance & storage of milk;
breastfeeding; a subsequent
breastfeeding; additional TSB may be drawn to evaluate a
may bottle-feed expressed milk
assessments may be required. drop in serum levels. as appropriate to therapy.
Assist mother with maintaining Assist mother with maintenance Minimize maternal-infant
milk supply, feed expressed milk of milk supply & reassurance separation & encourage
as appropriate. regarding her milk supply and contact as appropriate.
therapy.
After discharge, follow up
Use formula supplements only at
according to hour of discharge.
practitioner’s discretion.
HYPERBILIRUBINEMIA
POSSIBLE CAUSES:
PHYSIOLOGIC (DEVELOPMENTAL)
FACTORS (PREMATURITY):
Physiologic
Jaundice / Icterus Neonatorum – most
common cause; no pathologic process
2 PHASES: term infants
1ST phase – Bilirubin: 6mg/dl on 3rd DOL
decreased to 2-3mg/dl by 5th day
2nd phase – Steady plateau without
increase/decrease level 12th-14th day: levels
decresed to normal (1mg/dl)
Pattern varies according to racial group, method of
feeding, gestational age
PRETERM: Bilirubin – 10-12mg/dl at 4-5days
slowly decrease by 2-4 weeks.
HYPERBILIRUBINEMIA
POSSIBLE CAUSES:
PHYSIOLOGIC (DEVELOPMENTAL)
FACTORS (PREMATURITY):
Mechanisms Involved:
NB produce 2x as much bilirubin as do adults due to
higher concentrations of circulating RBC & shorter life
span of RBC (70-90days)
Liver’s ability to conjugate bilirubin reduced – due to
limited production of glucoronyl transferase
Lower plasma binding capacity for bilirubin because of
lower albumin concentrations than other children.
HYPERBILIRUBINEMIA
POSSIBLE CAUSES:
PHYSIOLOGIC (DEVELOPMENTAL)
FACTORS (PREMATURITY):
Primary Mechanism : enterohepatic
circulation/shunting
Normally: Conjugated bilirubin urobilinogen (excreted)
Sterile & less motile NB bowel is less effective in
excreting urobilinogen
Conjugated bilirubin thru B-glucoronidase
converted back to unconjugated bilirubin
reabsorbed by intestinal mucosa liver
HYPERBILIRUBINEMIA
POSSIBLE CAUSES:
An association with breast feeding or breast milk
BREASTFEEDING JAUNDICE – early onset
Begins at 2-4days of age; 12-13% of Breastfeeding infants
Related to process of breastfeeding, results from decreased
caloric & fluid intake by Breastfeeding infants before milk supply
is well-established (fasting is associated with decrease hepatic
clearance of bilirubin)
Feeding (+) peristalsis more rapid passage of meconium
decreased amount of reabsorption of unconjugated
bilirubin
Feeding introduces bacteria to aid in reduction of bilirubin
to urobilinogen
Colostrums, natural cathartic, facilitates meconium
evacuation
HYPERBILIRUBINEMIA
POSSIBLE CAUSES:
An association with breast feeding or breast
milk
BREAST MILK JAUNDICE – late onset
Onset: 4th-7th day of age; 12-13% of Breastfeeding
infants
Rising levels peak at 2nd week gradually diminish
May remain jaundiced x 3-12 weeks or more infants
are well
May be caused by factors in BM (pregnanediol, fatty
acids, B-glucorinidase) that either inhibit conjugation or
decrease excretion of bilirubin
Less frequent stooling by Breastfeeding infants may
allow for extended time for reabsorption of bilirubin from
stools
HYPERBILIRUBINEMIA
POSSIBLE CAUSES:
Excess production of bilirubin – Hemolytic
disease, biochemical defects, bruises
Hemolytic disease – blood antigen incompatibility –
hemolysis of RBC ; liver unable to conjugate &
excrete excess bilirubin from hemolysis
Onset: 1st 24 hours (levels increase faster than
5mg/dl/day)
Treatment: Postnatal – phototherapy ; exchange
transfusion – severe
Prenatal – transfusion (fetus) ; Rhogam
HYPERBILIRUBINEMIA
POSSIBLE CAUSES:
Disturbed capacity of liver to secrete
conjugated bilirubin – enzyme deficiency, bile
duct obstruction
Combined overproduction & undersecretion –
sepsis
Some disease states – hypothyroidism,
galactosemia, infant of a diabetic mother
Genetic predisposition to increase production
– Native Americans, Asians
HYPERBILIRUBINEMIA
CLINICAL MANIFESTATIONS
Jaundice – most obvious sign
Yellowish discoloration: sclera, nails, skin
If it appears within 1st 24 hours: hemolytic disease
of Newborn, sepsis, maternally-derived diseases
(DM, infections)
Appears on 2nd or 3rd day, peaks on 3rd – 4th day,
declines on 5th – 7th day: physiologic jaundice
(varies according to ethnicity)
Intensityof jaundice is not always related to
the degree of hyperbilirubinemia
HYPERBILIRUBINEMIA
DIAGNOSTIC EVALUATION
Serum Bilirubin (B1: 0.2-1.4mg/dl)
Jaundice appears at >5mg/dl
Evaluation based on:
Timing of appearance of clinical jaundice
Gestational age at birth
Age in days since birth
Family history including maternal Rh factor
Evidence of hemolysis
Feeding method
Infant’s physiologic status
Progression of serum bilirubin levels
HYPERBILIRUBINEMIA
DIAGNOSTIC EVALUATION
Indicators of physiologic jaundice – warrants further
investigation as to the cause of jaundice
Clinicaljaundice within 24 hrs. of birth
Persistent jaundice over 2 weeks in full-term, formula fed
infant
Total serum bilirubin levels 12.9mg/dl (term infant) or over
15mg/dl (preterm); upper limit for breastfeeding infant –
15mg/dl
Increase serum bilirubin >5mg/dl/day
Direct bilirubin (B2) 1.5-2mg/dl
Total serum Bilirubin – over 95th percentile for age (in hours)
on hour-specific risk nomogram
HYPERBILIRUBINEMIA
DIAGNOSTIC EVALUATION
Transcutaneous Bilirubinometry – noninvasive
monitoring of bilirubin via cutaneous
reflectance mechanisms; allow for repetetive
estimations of bilirubin
Hour-specific Serum Bilirubin Levels – predict
newborn at risk for rapidly rising levels
Recommended by AAP for monitoring healthy
Newborn >35wks AOG before discharge from
hospital
Carbon monoxide indices in exhaled breath –
CO is produced when RBC is broken down
HYPERBILIRUBINEMIA
COMPLICATIONS
BILIRUBIN ENCEPHALOPATHY/
KERNICTERUS – unconjugated bilirubin
highly toxic to the neurons
Syndrome of severe brain damage due to
deposition of unconjugated bilirubin in brain cells
(extremely high B1 level increase crosses the
blood-brain barrier)
KERNICTERUS – yellow staining of brain
cells that may result in bilirubin
encephalopathy
HYPERBILIRUBINEMIA
COMPLICATIONS
FACTORS THAT CONTRIBUTE TO
BILIRUBIN NEUROTOXICITY:
Serum bilirubin alone do not predict the risk of
brain injury
Metabolic acidosis
Low serum albumin level
Intracranial infections (meningitis)
Abrupt increase in BP
Conditions that increase metabolic demands for
oxygen and glucose – fetal distress, hypoxia,
hypothermia, hypoglycemia
HYPERBILIRUBINEMIA
COMPLICATIONS
SIGNS OFCNS DEPRESSION/
EXCITATION:
Prodrome: decreased activity, lethargy, irritability,
hypotonia, seizures
Athetoid CP, mental retardation, deafness
Those who survived: NEUROLOGIC DAMAGE
Mental retardation, ADHD, delayed/ abnormal motor
movements (ataxia, athetosis), behavior disorders,
perceptual problems, sensorineural hearing loss
HYPERBILIRUBINEMIA
THERAPEUTIC MANAGEMENT
Phototherapy – main form
Exchange transfusion – reduce high bilirubin levels
that occur with hemolytic disease
Phenobarbital – hemolytic disease; effective when
given to mother several days before delivery
Promotes hepatic glucoronyl transferase synthesis
increases bilirubin conjugation & hepatic clearance of
pigment in bile
Promotes protein synthesis – increase albumin for more
bilirubin binding sites
Heme-oxygenase inhibitors – decrease bilirubin
production
HYPERBILIRUBINEMIA
THERAPEUTIC MANAGEMENT
Early initiation of feedings & frequent
breastfeeding – promotes increased intestinal
motility, decreases enterohepatic shunting,
establish normal bacterial flora in the bowel
excrete B2
Frequent breastfeeding every 2 hrs
Avoid glucose water, formula or water
supplementation
HYPERBILIRUBINEMIA
THERAPEUTIC MANAGEMENT
Phototherapy – application of fluorescent light
(bili light) to infant’s exposed skin
Light promotes bilirubin excretion by
photoisomerization (alters structure of bilirubin to a
soluble form – lumirubin) for easier excretion
Blue Light – more effective in reducing bilirubin but
alters the color of the infant
Fluorescent bulbs with spectrum 420-460nm
preferred
Infant skin is fully exposed
HYPERBILIRUBINEMIA
THERAPEUTIC MANAGEMENT
Phototherapy – application of fluorescent light (bili light) to
infant’s exposed skin
Rapidly rising bilirubin/ critical level – double intensive phototherapy
Conventional overhead lamps while infant is lying on fiber optic blanket
BEST RESULT: occur within 1st 24-48hrs of treatment
Fiberoptic blanket/panel – light generating illuminator
blanket delivers therapeutic light consistently & continuously to infant &
achieve same photoisomerization as conventional phototherapy
For home phototherapy, permits more infant-parent interaction, better
temperature control
Eliminates the need for eye patches
SPECIAL CAUTION: plastic pad must completely be covered to
prevent exposing fragile skin of extremely immature/compromised
infant to fiberoptic blanket (dermal injury)
When blood is drawn, phototherapy lights are turned off, blood is
transported in covered tube to avoid false reading as a result of
bilirubin destruction in test tube.
HYPERBILIRUBINEMIA
MANAGEMENT OF HYPERBILIRUBINEMIA IN HEALTHY TERM
NEWBORN
TSB LEVEL (mg/dl/mmol/L)
PROGNOSIS:
Early recognition prevents brain damage
Bilirubin encephalopathy: athetosis,
sensorineural hearing loss, paralytic gaze
palsy, gaze abnormalities, delayed motor
skills, dental enamel hypoplasia
HYPERBILIRUBINEMIA
NURSING CONSIDERATIONS
ASSESSMENT
Observe for evidence of jaundice at regular
intervals
Observe color from head-toe, color of sclera & mucous
membranes
Apply direct pressure to skin especially bony
prominences (tip of nose or sternum) blanching
allow yellow stain to be more pronounced
Dark-skinned – color of sclera, conjunctiva, oral mucosa
Observe natural daylight
NURSING CONSIDERATIONS
Phototherapy – nude under light source,
repositioned frequently to expose all body surface
areas to light
Frequentbilirubin determination – every 6-12hrs (visual
assessment is no longer considered valid)
HYPERBILIRUBINEMIA
NURSING CONSIDERATIONS
PHOTOTHERAPY:
PRECAUTIONS:
Eye Shield – opaque mask to prevent exposure to light
Properly sized, correctly positioned without occluding the nares
Infant’s eyelids are closed before mask is applied, corneas may
become excoriated
Eyes checked every shift for discharge, excessive pressure on lids,
corneal irritation
Removed during feedings
Infants in open crib must have a protective plexiglass shield
between them & fluorescent lights to minimize amount of
undesirable UV lights reaching skin & protect them from
accidental bulb breakage
Temperature monitored
Maintain in flexed position w/ rolled blankets alongside body
HYPERBILIRUBINEMIA
NURSING CONSIDERATIONS
PHOTOTHERAPY:
ACCURATE CHARTING:
Times that phototherapy is started and stopped
Proper shielding of the eyes
Type of fluorescent lamp
Number of lamps
Distance between surface of lamps & infant (not <18 in)
Use of phototherapy in combination with an incubator or
open bassinet
Photometer measurement of light intensity
Occurrence of side effects
Collapse of Alveoli
Exhaustion
Atelectasis
Collapsed lungs
Fetal blood shunted from lungs by ductus arteriosus and foramen ovale
RESPIRATORY DISTRESS
SYNDROME (RDS)
PATHOPHYSIOLOGY
Rib Cage: weak and compliant
Fetal chest highly compliant because of predominance of
cartilage; diaphragm is prone to fatigue
Fetal Lungs deficient in surfactant due to immaturity
of surfactant producing type 2 alveolar cells
Surfactant – 1st produced at 24 wks AOG, type 2 cells do not
fully mature until about 36 wks AOG
Reduces surface tension of fluids that line the alveoli &
respiratory passages uniform expansion and maintains lung
expansion
RESPIRATORY DISTRESS
SYNDROME (RDS)
PATHOPHYSIOLOGY
Deficient surfactant – unequal inflation of alveoli on
inspiration, collapse of alveoli of end expiration
Without surfactant – infants unable to keep lungs
inflated, exerts great effort to reexpand the alveoli
exhaustion atelectasis
RESPIRATORY DISTRESS
SYNDROME (RDS)
PATHOPHYSIOLOGY
Inadequate pulmonary perfusion and ventilation
Increased PVR
Intrapulmonary shunting
Anaerobic glycolysis
CONVENTIONAL
METHODS
Continuous Positive Airway Provides contrast distending Nasal prongs, endotracheal
Pressure (CPAP) pressure to airway in tube, face mask, nasal
spontaneously breathing cannula
infant.
Positive End-Expiratory Provides increase end- Endotracheal intubation, and
Pressure (PEEP) expiratory pressure during either volume-limited or
expiration and between pressure-limited ventilator
Mandatory breaths which
prevents alveolar collapse;
maintains residual airway
pressure
RESPIRATORY DISTRESS
SYNDROME (RDS)
TREATMENT / MANAGEMENT:
METHOD DESCRIPTION HOW PROVIDED
Intermittent Mandatory Allows infant to breath Endotracheal
Ventilation (IMV) spontaneously at own rate but intubation and
provides mechanical cycled ventilator
respirations and pressure at
regular preset intervals
ALTERNATIVE
METHODS
High frequency Oscillation Application of high-frequency, Variable-speed piston
(HFO) low-volume, sine wave flow pump (or loudspeaker,
oscillations to airway at rates fluidic oscillator) ;
between 480 and 1200 endotracheal tube
breaths/min
RESPIRATORY DISTRESS
SYNDROME (RDS)
TREATMENT / MANAGEMENT:
ETIOLOGY:
PreciseCause: unknown
Prematurity: risk factor
NECROTIZING ENTEROCOLITIS
ETIOLOGY:
3 FACTORS THAT PLAY ROLE IN
DEVELOPMENT OF NEC:
Intestinal Ischemia – vascular compromise on GIT
Diminished Blood Supply
Cell death
DIAGNOSIS:
Abdominal x-ray: Sausage-shaped dilation of intestine
distended loops of bowel; “pneumatosis
intestinalis” --- “soapsuds” or bubbly appearance of
thickened bowel wall & ultralumina;
Air in portal vein; free air under the diaphragm (perforation)
NECROTIZING ENTEROCOLITIS
DIAGNOSIS:
Occult blood in the stool
Blood culture – bacteremia / septicemia
CBC: anemia, leucopenia/ leukocytosis
Metabolic acidosis, electrolyte imbalance
TREATMENT:
Begins with prevention
NPO x 24-48 hours – infants who have suffered birth
asphyxia, ELBW, VLBW infants
Breast milk
Minimal enteral feedings – trophic feeding, GIT priming
NECROTIZING ENTEROCOLITIS
TREATMENT:
Confirmed NEC:
Discontinue all oral feedings
Place NGT – for decompression
IV fluids; IV antibiotics
Surgery in extreme cases
PROGNOSIS:
Sequelae of surgical intervention: shirt-gut syndrome,
colonic stricture with obstruction, fat malabsorption,
failure to thrive
NECROTIZING ENTEROCOLITIS
NURSING CONSIDERATIONS:
Prompt recognition of early warning signs of NEC: abdominal
distention, absent bowel sounds
Measure abdominal girth, residual gastric contents before feedings,
listen for presence of bowel sounds
Vital signs including blood pressure
Avoid rectal temperatures (danger of perforation)
Avoid pressure on distended abdomen
Infants are left undiapered & positioned supine or on the side
Conscientious attention to nutritional and hydration needs,
administration of antibiotics
Oral feedings: started 7-10 days after diagnosis & treatment using
human milk, elemental formula
Sterile water may be given initially
Strict hand washing
FAILURE TO THRIVE
Sign of inadequate growth resulting from inability
to obtain or use calories required for growth
No universal definition
Common parameter: WEIGHT, sometimes
height that falls below 5th percentile for child’s
age
Weight for age (height) z value of less than -2.0
Weight curve (loss) that crosses >2 percentile
lines on National Center for Health Statistics
(NCHS) growth after previous achievement of a
stable growth pattern.
FAILURE TO THRIVE
3 GENERAL CATEGORIES:
Organic Failure to Thrive
Physical Cause
Congenital heart defects, neurologic lesions, cerebral palsy,
microcephaly
Chronic renal failure, gastroesophageal reflux
Malabsorption syndrome, endocrine dysfunction
Cystic fibrosis, acquired immunodeficiency syndrome (AIDS)
Nonorganic Failure to Thrive (NFTT)
Unrelated to disease
Result of psychosocial factors – inadequate nutritional information by
parent
Deficiency of maternal care of disturbance in maternal-child attachment
Disturbance in child’s ability to separate from parent leading to food
refusal to maintain attention
Idiopathic Failure to Thrive – unexplained by usual organic and
environmental etiologies but may also be classified as NFTT.
FAILURE TO THRIVE
Some experts suggest that classifications are
too simplistic because most cases of growth
failure have mixed causes.
FTT be classified according to pathophysiology for the
following categories:
Inadequate Caloric Intake
Incorrect formula preparations
Neglect, food fads
Excessive juice consumption
Poverty
Behavioral problems affecting eating
CNS problems affecting intake
FAILURE TO THRIVE
Inadequate absorption
Cysticfibrosis, celiac disease, vitamin/ mineral
deficiencies, biliary atresia, hepatic disease
Increase metabolism
Hyperthyroidism,
congenital heart defects, chronic
immunodeficiency
Defective utilization
Trisomy21 or 18, congenital infection, metabolic storage
diseases
FAILURE TO THRIVE
ETIOLOGY – multifactorial
Infantorganic disease
Dysfunctional parenting behaviors
Subtle neurologic/ behavioral problems
Disturbed parent-child interactions
FACTORSLEADING TO INADEQUATE
FEEDING OF INFANT
Poverty – dilute formula to extend available
supply; no insurance
No primary care practitioner; homelessness
FAILURE TO THRIVE
Health or childbearing beliefs – fad diets, excessive concern with
obesity, hypercholesterolemia, nursing caries
Strict use of scheduled feedings
Inappropriate food source; excessive juice intake
Insufficient
breast milk – fatigue, poor release of milk,
breast surgery augmentation, lack of maternal
confidence / support.
FAILURE TO THRIVE
CLINICAL MANIFESTATIONS:
Growth Failure – 5th percentile in weight only or weight and
height
Developmental delays – social, motor, adaptive, language
Apathy
Poor hygiene
Withdrawn behavior
Feeding/ eating disorder: vomiting, anorexia, pica, rumination
No fear of strangers (stage when stranger anxiety is normal)
Avoidance of eye contact
Wide-eyed gaze & continual scan of environment (radar gaze)
Stiff & unyielding or flaccid & unresponsive
Minimal smiling
FAILURE TO THRIVE
DIAGNOSTIC EVALUATION:
Evidence of growth retardation & caloric deprivation
Anthropometric measurements
Onset of FTT is fairly recent: weigh (not height) is below accepted
standards (5th percentile)
Long standing FTT: height and weight depressed; chronic
malnutrition
Complete health and dietary history --- history of food consumed
over 3-5 day period
Child’s activity level, perceived food allergies, dietary restrictions
P.E for evidence of organic causes, developmental assessment
Family assessment – parental height, household organizations &
mealtime behaviors & rituals
Rule out organic causes
Lead toxicity, anemia, stool-reducing substance, occult blood, ova,
parasites
Alkaline phospatase, zinc levels
FAILURE TO THRIVE
THERAPEUTIC MANAGEMENT:
Directed as reversing the malnutrition & underlying
cause
Goal: provide sufficient calories to support “catch up”
growth
Treat any coexisting problems
Multidisciplinary team: physician, nurse, dietitian,
gastroenterologist, child-life specialist, social worker
or mental health professional
Relieve any additional stresses on family – referrals to
welfare agencies or supplemental food programs
FAILURE TO THRIVE
THERAPEUTIC MANAGEMENT:
Family therapy
Behavior modification
Hospitalization indications:
Evidence (anthropometric) of severe acute malnutrition
Child abuse / neglect
Significant dehydration
Caretaker substance abuse or psychosis
Outpatient management that does not result in weight gain
FAILURE TO THRIVE
NURSING CONSIDERATIONS:
Accurate assessment of initial weight & height
and daily weight & recording of all food intake
Feeding behavior is documented & parent-
child interaction during feeding
Feeding checklist
Should be placed in a room with noninfectious
children of similar age
Structure feeding environment to encourage
eating
FAILURE TO THRIVE
NURSING CONSIDERATIONS:
The child
May exhibit altered behavioral interactions
Display intense interest in inanimate objects (toys) but less in
social interactions
Watchful of people at a distance but become distressed as
others come closer
Dislike being touched or held & avoid face-to-face contact;
when held they protest briefly on being put down& apathetic
when left alone
History of difficulty in feeding, vomiting, sleep disturbance,
excessive irritability
Crying during feedings, hoarding food in mouth, rumination
after feeding, refusing to switch from liquids to solids,
aversion behaviors (turning from food, spitting)
Difficult temperament or passive, sleepy, lethargic infant who
does not wake up for feedings
FAILURE TO THRIVE
NURSING CONSIDERATIONS:
The parent
Increased risk for altered parent-infant interactions
because:
Isolationand social crisis
Inadequate support systems
Poor / absent parenting role models when they were
children
Lack of education, physical/ mental health
problems
Physical
and sexual abuse, depression, drug
dependence, immaturity
FAILURE TO THRIVE
NUTRITIONAL MANAGEMENT:
4 Primary Goals in Nutritional management of
FTT:
Correct nutritional deficiencies & achieve ideal
weight for height
Increase caloric intake in formula fed infants:
supplements like Polycose, medium chain triglycerides
may be added slowly – in 2kcal/oz increments q2-3 days
to yield up 28-30 kcal/oz
Carbohydrate additives (8 kcal/tsp)
FAILURE TO THRIVE
NUTRITIONAL MANAGEMENT:
Rice cereal & vegetable oil
Multivitamin supplementation – zinc and iron
Breast-fed infants: add 1 tsp of 24 kcal/oz formula to 3 oz
breast milk
Toddlers: high caloric milk (PediaSure)
Fruit juices – minimized in infants < 6 months
Extreme cases: tube feedings or IV therapy
Family-system approach
HEMOLYTIC DISEASE OF THE
NEWBORN
Erythroblastosisfetalis
Hyperbilirubinemia in 1st 24 hrs of life
Abnormally rapid rate of RBC destruction
Anemia caused by this destruction (+)
production of RBCs increased # cells
for hemolysis
Major causes: isoimmunization (primarily
Rh) & ABO incompatibility
HEMOLYTIC DISEASE OF THE
NEWBORN
Blood Incompatibility
Antigen / Agglutinogens – substance capable of
producing an immune response if recognized by the
body as foreign
Antigens + Antibodies = agglutination (clumping)
Antibodies in plasma of 1 blood group (except AB
group – no antibodies) produce agglutination when
mixed with antigens of a different blood group
ABO blood group system – antibodies occur naturally
Rh system - isoimmunization
HEMOLYTIC DISEASE OF THE
NEWBORN
1. Rh Incompatibility
The presence of naturally occurring Rh
factor determines the blood type.
Rh (+) – presence of antigen
Rh (-) – absence of antigen
No problems occur when Rh blood type are
same in both mother and fetus or if mother
is Rh (+) and infant is Rh (-).
Mother Rh (-) and Infant Rh (+) : problem
HEMOLYTIC DISEASE OF THE
NEWBORN
Fetal RBCs (with antigens foreign to mother)
Previously formed maternal antibodies to Rh (+) blood cells enter fetal circulation
Erythroblastosis fetalis
Sensitization
may occur during 1st pregnancy
if woman had previously received an Rh (+)
blood transfusion
HEMOLYTIC DISEASE OF THE
NEWBORN
No sensitization: if there’s strong placental barrier
which prevents transfer of fetal blood into maternal
circulation
10-15% of sensitized mothers: no hemolytic reaction in
Newborn
Some Rh (-) women even though exposed to Rh (+) fetal
blood are unable to produce antibodies to foreign antigen
Most severe form: hydrops fetalis
Fetal hypoxia, cardiac failure, anasarca, effusions (pleural,
pericardial, peritoneal)
Stillborn or in severe respiratory distress
Early
intrauterine detection: ultrasound, fetal blood
sampling
Management: fetal blood transfusions
HEMOLYTIC DISEASE OF THE
NEWBORN
2. ABO Incompatibility
Major blood group antigens of fetus are
different from those of the mother
Major blood groups: A, B, AB, O
Presence / absence of antibodies & antigens
determines whether agglutination will occur
HEMOLYTIC DISEASE OF THE
NEWBORN
ABO RELATIONSHIP OF ANTIGENS / ANTIBODIES &
DONOR- RECIPIENT COMPATIBILITY
RBC
COMPATIBILITY
BLOOD GROUP GENOTYPE RBC PLASMA AS DONOR AS
(PHENOTYPE) ANTIGENS ANTIBODIES TO TYPE RECIPIENT
FROM
TYPE
A AA, AO A B AB, A O, A
B BB, BO B A AB, B O, B
AB AB A&B NONE AB O, A, B, AB
O OO NONE A&B AB, A, B, O O
HEMOLYTIC DISEASE OF THE
NEWBORN
hemolysis
B A or AB
A B or AB
HEMOLYTIC DISEASE OF THE
NEWBORN
CLINICAL MANIFESTATIONS:
Anemia (hemolysis of RBCs) jaundice on 1st 24 hours; serum bilirubin
elevated (result from liver’s inability to conjugate & excrete excess
bilirubin)
Hepatosplenomegaly, varying degrees of hydrops, sign of hypovolemic
shock
Hypoglycemia – due to pancreatic cell hyperplasia
DIAGNOSTIC EVALUATION:
Genetic testing
Chorionic Villus Sampling – determine fetal group and type can lead
to abortion
Amniocentesis – fetal blood type can lead to infection or leaking
Ultrasonography – allow early treatment; used to check amniotic fluid
and condition of the placenta
Indirect Coombs Test – evaluate rising anti Rh antibody titers in maternal
circulation; done Rh (-) mothers; 1st prenatal visit
Direct Coombs Test – detect antibodies attached to the circulating
erythrocytes of affected infants ; done to baby; to determine how
extensive is the hemolysis
HEMOLYTIC DISEASE OF THE
NEWBORN
THERAPEUTIC MANAGEMENT:
Postnatal therapy: phototherapy for mild cases,
exchange transfusion for severe cases
Prevention of Rh isoimmunization: Rho immune
globulin (Rhogam)
Human gamma globulin concentrate of anti-D to all
unsensitized Rh (-) mothers after delivery or abortion of an
Rh-positive infant or fetus
Destroys (by phagocytosis & agglutination) fetal RBCs
passing into maternal circulation before they can be
recognized by mother’s immune system immune response
is blocked, anti-D antibodies & memory cells not formed
HEMOLYTIC DISEASE OF THE
NEWBORN
THERAPEUTIC MANAGEMENT:
Must be administered to unsensitized mothers within 72
hours (possibly as long as 3-4 weeks) after the 1st delivery or
abortion & repeated after subsequent ones
Administration of RhIg at 26-28 weeks AOG reduces risk of
Rh isoimmunization
Administered thru IM to Rh (-) sensitized women, never to
newborn or father
Intravenous immunoglobulin (IVIG) – decreased
severity of RBC destruction (hemolysis) in HDN &
subsequent development of jaundice
Attacks maternal cells that destroy neonatal RBCs, slows
down the progression of bilirubin production
Used in conjunction with phototherapy; decreased necessity
for exchange transfusion
HEMOLYTIC DISEASE OF THE
NEWBORN
THERAPEUTIC MANAGEMENT:
Intrauterine transfusion – infuse blood into umbilical
vein of fetus
Infuse Rh O-negative packed RBCs to raise fetal hematocrit
to 40-50% every 2 weeks until fetus reaches 37-38 weeks
Exchange transfusion – infant’s blood removed in
small amounts (5-10ml at a time) & replaced with
compatible blood (Rh – negative blood)
Removes sensitized RBCs, lowers serum bilirubin, corrects
anemia, prevents cardiac failure
Indications:
Rapidly increasing bilirubin level, hemolysis despite intensive
phototherapy
Infant born with hydrops fetalis or sign or cardiac failure
HEMOLYTIC DISEASE OF THE
NEWBORN
THERAPEUTIC MANAGEMENT:
Fresh whole blood typed & crossmatched to
mother’s serum
Amount of donor blood is double the blood volume
of infant (85ml/kgBW) but not >500ml
Sterile surgical procedure: catheter umbilical
vein inferior vena cava
5-10
ml withdrawn within 15-20 secs same volume x
60-90 secs
HEMOLYTIC DISEASE OF THE
NEWBORN
THERAPEUTIC MANAGEMENT:
ABO INCOMPATIBILITY
Early detection & implementation of phototherapy
(+) jaundice within 1st 24 hours, increased serum
bilirubin levels, RBC spherocytosis, increased
ESR: diagnostic of ABO incompatibility
IVIG + phototherapy
Exchange transfusion – not commonly required
except when phototherapy fails to decrease
bilirubin concentration
HEMOLYTIC DISEASE OF THE
NEWBORN
PROGNOSIS:
Severe anemia: result in stillbirth, shock,
congestive heart failure, pulmonary/ cerebral
complications (cerebral palsy)
With early detection & intrauterine treatment –
erythroblastic Newborn rare, exchange
transfusions for the conditions less common
HEMOLYTIC DISEASE OF THE
NEWBORN
NURSING CONSIDERATIONS:
Initial nursing responsibility – recognizing jaundice
Thru prenatal & perinatal history
Exchange transfusion: prepare infant and family
assist practitioner with procedure
Document blood volume exchanged: amount of blood
volume withdrawn & infused, time of each procedure,
cumulative record of total volume exchanged
Vital signs monitored
(+) signs of cardiac/ respiratory problems: procedure stopped
temporarily & resumed once stable
Observe for transfusion reaction
HEMOLYTIC DISEASE OF THE
NEWBORN
NURSING CONSIDERATIONS:
Attention on thermoregulation
Hypothermia – increase oxygen and glucose
consumption metabolic acidosis; (-) binding capacity
of albumin & bilirubin & hepatic enzyme reaction
kernicterus
Hyperthermia – damages donor’s RBC, increase free K+,
predisposes infant to cardiac arrest
Performed with infant under radiant warmer, with
sterile drapes, blood is warmed
After procedure: nurse inspects umbilical vein (for
bleeding), catheter may remain in place
SUDDEN INFANT DEATH
SYNDROME (SIDS)
Sudden death of infant < 1 years old
Unexplained after a complete mortem examination,
including an investigation of death scene & review of
case history
3rd leading cause of death in children between 1 month –
1 year ; increased incidence in winter
Incidence: 0.65:1000 live births (1999); males > females
Peak age: 2-4 months; 95% occur by 6 months
Time of death: during sleep
Racial: Native Americans, African Americans, Hispanics
Lower socioeconomic class
SUDDEN INFANT DEATH
SYNDROME (SIDS)
Risks:Preterm especially low birth weight;
multiple births (2nd twin, male twin & small-
for-date twin)
Newborn with low APGAR score
Infants with CNS disturbances & respiratory
disorder (bronchopulmonary dysplasia/
chronic lung disease)
Increased birth order (subsequent siblings as
opposed to 1st born child)
Infants with recent history of mild illness
SUDDEN INFANT DEATH
SYNDROME (SIDS)
Sleep in prone position
Cause oropharyngeal obstruction or affect thermal balance
or arousal state
Rebreathing of carbon dioxide by prone infant & impaired
arousal from active & quiet sleep
Side-lying position no longer recommended – tends to turn to
prone position
Use of soft bedding – not able to move their heads to
the side suffocation and lethal rebreathing
Overheating (thermal stress); co-sleeping with adult
especially on sofa
Adult beds/ sofas are not designed for infants & may carry
risk of accidental entrapment & suffocation
SUDDEN INFANT DEATH
SYNDROME (SIDS)
Lower incidence in breast-fed infants – pacifier
may be protective against SIDS
Maternal risk: young age, cigarette smoking
especially during pregnancy
Poor prenatal care, substance abuse (heroin,
methadone, cocaine)
12% of all SIDS death could be prevented with
prenatal smoking cessation
Maternal smoking decreases infant’s ability to arouse to
auditory stimuli in mothers who smoke prenatally.
SUDDEN INFANT DEATH
SYNDROME (SIDS)
ETIOLOGY:
Unknown
Hypothesis:related to brainstem abnormality in
neurologic regulation of cardiorespiratory control
Abnormalities: prolonged sleep apnea, increased frequency
of brief inspiratory pauses, excessive periodic breathing,
impaired arousal responsiveness to increase carbon dioxide
or decrease oxygen
Sleep apnea is not the cause of SIDS; genetic predisposition
has been postulated as the cause
Autopsies:
pulmonary edema & intrathoracic
hemorrhages
Should be performed on all infants suspected of dying of
SIDS
SUDDEN INFANT DEATH
SYNDROME (SIDS)
INFANTS AT RISK FOR SIDS:
Infants with 1 or more ALTEs requiring
cardiopulmonary resuscitation (CPR) or vigorous
stimulation
Preterm infants who continue to have apnea at the
time of hospital discharge
Siblings of 2 or more SIDS victim
Infants with certain types of disease or conditions –
central hypoventilation
Home monitoring and/or use of respiratory stimulant drugs
recommended
No diagnostic tests exist to predict which infants will survive
SUDDEN INFANT DEATH
SYNDROME (SIDS)
NURSING CONSIDERATIONS:
Educate families in prevention of SIDS
Risk of prone sleeping position in infant births – 6 months
Use of appropriate beddings, parental smoking around infant
and dangers of sharing an adult bed with infant
Post partum discharge planning, newborn discharge
teaching and newborn-care classes
Follow-up visits, well-baby clinic visits, immunization
visits
Discuss infant sleep position
SUDDEN INFANT DEATH
SYNDROME (SIDS)
NURSING CONSIDERATIONS:
Psychologic intervention – loss of child
Practices that may reduce the risk of SIDS
Avoid smoking during pregnancy and near the
infant
Encouraging supine sleeping position
“back to sleep”
Avoid soft, moldable mattresses, blankets, pillows
No pillows/ quilts, stuffed toys, towels
Discouragingbed sharing
Encourage breastfeeding
SUDDEN INFANT DEATH
SYNDROME (SIDS)
NURSING CONSIDERATIONS:
Avoid overheating during sleep
Infants should wear light-clothing, comfortable room
temperature
Infant’shead position should be varied to prevent flattening
of the skull
Use of pacifier – protective against occurrence of SIDS;
naptime and bedtime, no sweetened coating
Finding the infant
it’s
always the mother who finds child dead in crib
Child is in disheveled bed w/ blankets over head, huddled in
1 corner
SUDDEN INFANT DEATH
SYNDROME (SIDS)
NURSING CONSIDERATIONS:
Frothy, blood-tinged fluid fills the mouth & nostrils,
lying face down in secretions (bled to death)
Diaper is wet and full of stool – cataclysmic type of
death
Parents must deal with his/her initial shock, panic,
grief
Compassionate, sensitive approach to family
SUDDEN INFANT DEATH
SYNDROME (SIDS)
NURSING CONSIDERATIONS:
Arriving at emergency department
No attempt at resuscitation
Parents are asked only factual questions – when
they found the infant, how he/she looked
No misguided statements: “this looks like suffocation”
(guilt)
Discuss possible autopsy
Compassionate care – allow them to say good-bye
to their child
APNEA OF PREMATURITY (AOP)
Preterm infants; rare: full-term
Apneic spells increase in prevalence the younger the gestational
age
1/3 infants <33 weeks AOG, >1/2 healthy infants < 30 weeks AOG
Resolves as infant reaches 37 weeks postmenstrual age
Preterms are periodic breathers – periods of rapid respirations
separated by periods of very slow breathing, often short periods with
no visible or audible respirations
Apnea – extension of periodic breathing
Lapse of spontaneous breathing for 20 seconds or longer, that may
or may not be followed by bradycardia, oxygen desaturation and
color change
Temporary apnea - <15-20 seconds
Pathologic apnea - > 20 seconds
APNEA OF PREMATURITY (AOP)
Classification according to origin:
Central Apnea – absence of diaphragmatic and other
respiratory effort
Occurs when CNS does not transmit signals to the
respiratory muscle
Obstructive Apnea – air flow ceases because of upper
airway obstruction yet chest or abdominal wall
movement is present
Mixed Apnea: combination of central and obstructive
apnea
Most common apnea seen in preterm infants
APNEA OF PREMATURITY (AOP)
PATHOPHYSIOLOGY:
Reflects the immature and poorly refined neurologic
and chemical respiratory control mechanism in
premature infants
Not responsive to hypercarbia and hypoxemia, have
fewer dendritic associations than those of more
mature infants
Respiratory reflexes less mature – contributing factor
in etiology
Weakness of muscles of thorax, diaphragm and
upper airway – contribute to apneic episodes
APNEA OF PREMATURITY (AOP)
PATHOPHYSIOLOGY:
Apnea – observed during periods of REM sleep
Precipitated/ worsened by a variety of factors:
Infection
Intracranial hemorrhage
PDA
TREATMENT
Observe for apnea
Check for thermal stability
Administration of methylxanthines (theophylline, aminophylline
or caffeine)
Reduce frequency of primary apnea-bradycardia spells in newborn
CNS stimulants to breathing
Observe for symptoms of toxicity
Caffeine – fewer side effects ; once daily dosing
Monitor weight and urine output
APNEA OF PREMATURITY (AOP)
TREATMENT:
Nasal continuous positive airway pressure
(NCPAP) and intermittent positive pressure
ventilation
CPAP acts to maintain airway patency
More effective for obstructive/ mixed apnea
APNEA OF PREMATURITY (AOP)
NURSING CONSIDERATION:
Monitor respiration and heart rate routinely in all preterm infants
Observe for presence of respirations
Observe color
Provide gentle tactile stimulation – rubbing the back/ chest
gently, turning infant to supine position
If tactile stimulation fails to reinstitute respiration – flow by
oxygen and suctioning of nose and mouth
Apply artificial ventilation with bag-valve mask and with sufficient
pressure to lift rib cage
If breathing does not begin
Raise chin gently to open airway
Infant is never shaken
APNEA OF PREMATURITY (AOP)
NURSING CONSIDERATION:
After breathing is restored: assess for and manage any
precipitating factors (temperature instability, abdominal
distention, ambient oxygen) – use pulse oximetry
Record episodes of apnea - # apneic spells, appearance during
and after the episode, did infant self-recover or whether tactile
stimulation or other measures were done to restore breathing.
Investigate possible cause of apneic episode
Observe for signs of theophylline or caffeine toxicity; tachycardia
(rate 180-190/ min) and later, vomiting, restlessness, irritability
Assess skin (with NCPAP) for breakdown, irritation, and nasal
septum
AUTISTIC SPECTRUM
DISORDER (AUTISM)
Complex developmental disorder of brain
function accompanied by intellectual and
behavioral deficits
Manifested during early childhood: 18-36
months of age
1-2 in 500 children; males > females
(females more severely affected)
Not related to socioeconomic level, race,
parenting style
AUTISTIC SPECTRUM
DISORDER (AUTISM)
ETIOLOGY
Unknown
Multiple biologic causes
Abnormal EEG, epileptic seizures, delayed development of hand
predominance, persistence of primitive reflexes, metabolic
abnormalities (increased serotonin), hypoplasia of vermis of
cerebellum
Increased in twins
High risk of recurrence of ASD in families with one affected child
Not caused by thimerosal-containing vaccines
Associated with fragile X syndrome, tuberous sclerosis,
metabolic disorder, fetal rubella syndrome, H. influenza
meningitis, structural brain anomalies
Perinatal events: higher incidence of maternal uterine bleeding
during pregnancy
Lower incidence of maternal vaginal infections during pregnancy
Decreased maternal use of contraceptives
Higher incidence of neonatal hyperbilirubinemia
AUTISTIC SPECTRUM
DISORDER (AUTISM)
CLINICAL
MANIFESTATIONS AND
DIAGNOSTIC EVALUATION:
Hallmark: inability to maintain eye contact with
another person
Display limited functional play and may interact with
toys in an unusual manner
Deficits in social development: primary feature of
illness
Majority have some degree of mental retardation
Females tend to have very low intelligence scores
Savants – children with ASD who excel in particular
areas: art, music, memory, mathematics, perceptual
skills (puzzle building)
AUTISTIC SPECTRUM
DISORDER (AUTISM)
Speech and language delays
Immediate evaluation of any child who does not
display such language skills as babbling or
gesturing by 12 months, single word by 16 months,
2-word phrases by 24 months
Sudden deterioration in extant expressive speech
is also a red-flag event for further evaluation
AUTISTIC SPECTRUM
DISORDER (AUTISM)
DIAGNOSTIC CRITERIA FOR ASD:
Total of 6 (or more) items from (1), (2), (3) with at
least two from (1), and one each from (2) & (3)
(1) Qualitative impairment in social interaction, as manifested
by at least 2 of the following:
Marked impairment in use of multiple nonverbal behaviors such
as eye-to-eye gaze, facial expression, body postures, &
gestures to regulate social interaction
Failure to develop peer relationships appropriate to
developmental level
A lack of spontaneous seeking to share enjoyment, interests, or
achievements w/ other people (ex. By a lack of showing,
bringing, or pointing out objects of interest)
Lack of social/ emotional reciprocity
AUTISTIC SPECTRUM
DISORDER (AUTISM)
(2) Qualitative impairments in communication as
manifested by at least 1 of the following:
Delay in, or total lack, of the development of spoken
language (not accompanied by an attempt to
compensate through alternative modes of
communication such as gesture or mime)
In individuals w/ adequate speech, marked impairment in
the ability to initiate or sustain a conversation with others
Stereotyped and repetitive use of language or
idiosyncratic language
Lack of varied, spontaneous, make-believe play or social
imitative play appropriate to developmental level
AUTISTIC SPECTRUM
DISORDER (AUTISM)
(3) Restricted repetitive and stereotyped patterns of behavior, interests
& activities, as manifested by at least 1 of the following:
Encompassing preoccupation with one or more stereotyped and
restricted patterns of interest that is abnormal either in intensity or focus
Apparently inflexible adherence to specific, nonfunctional routines or
rituals
Stereotyped & repetitive motor mannerisms (ex. Hand or finger flapping
or twisting, or complex whole-body movements)
Persistent preoccupation w/ parts of objects
Delays or abnormal functioning in at least 1 of the following
areas with onset before age 3 years
Social interaction
Language as used in social communication
Symbolic or imaginative play
The disturbance is not better accounted for by Rett disorder or
childhood disintegrative disorder
AUTISTIC SPECTRUM
DISORDER (AUTISM)
PROGNOSIS:
Severely disabling condition
Some improve with acquisition of language skills &
communication w/ others
Some achieve independence, but most require
lifelong adult supervision
Aggravation of psychiatric symptoms – ½ children
during adolescence, w/ girls having tendency for
continued deterioration
Most favorable for children who develop
communicative speech by age, years & have an IQ
higher than 50 at time of diagnosis
AUTISTIC SPECTRUM
DISORDER (AUTISM)
NURSING CARE MANAGEMENT:
No cure for ASD but there are numerous therapies
Highly structured & intensive behavior modification
programs
Promote positive reinforcement, increase social
awareness of others, teach verbal communication
skills and decrease unacceptable behavior
Provide a structured routine for the child to follow –
key management in ASD
AUTISTIC SPECTRUM
DISORDER (AUTISM)
NURSING CARE MANAGEMENT:
Hospitalized child with ASD: dcrease stimulation
Place child in private room
Avoid extraneous auditory & visual distraction
Encourage parents to bring in possessions to which child is
attached
Minimum holding & eye contact
Care must be taken when performing procedures,
administering meds, feeding these children – may swallow
thermometer, gags when eating
Family support - counseling
MAJOR STRESSORS OF
HOSPITALIZATION
SEPARATION ANXIETY
Middle
infancy – preschool age
STAGES:
PROTEST PHASE:
Cry and scream
Cling to parent
Avoids/ rejects contact with strangers
Verbally and physically attack strangers
Attempts to escape and find parents
MAJOR STRESSORS OF
HOSPITALIZATION
DESPAIR PHASE:
Crying stops, evidence of depression
Less active
Uninterested in food
Withdraws from others
Child’s physical condition may deteriorate from refusal to
eat, drink, or move
DETACHMENT PHASE:
Denial;resignation and not contentment
Child becomes more interested in the surroundings
Forms new but superficial relationship
May have serious attachment to parent after separation
MAJOR STRESSORS OF
HOSPITALIZATION
LOSS OF CONTROL
INFANTS
Trust
Consistent, loving caregivers
Attempts to control their environment through emotional
expressions
TODDLERS
Autonomy
When their egocentric pleasures meet with obstacles, they
react with negativism
Results from altered routines and rituals
MAJOR STRESSORS OF
HOSPITALIZATION
PRESCHOOLERS
Suffer loss of control by physical restriction, altered
routines, and enforced dependency
Egocentric and magical thinking typical of age
May view illness and hospitalization as punishment
for misdeed
PREOPERATIONAL THOUGHT – explanations
are understood only in terms of real events
TRANSDUCTIVE REASONING – deduct from the
particular to particular, rather than from the specific
to the general
MAJOR STRESSORS OF
HOSPITALIZATION
SCHOOL AGE
Striving for independence and productivity
Altered family roles, physical disability, fears of death,
abandonment, permanent injury, loss of peer acceptance,
lack of productivity
Boredom
ADOLESCENTS
Struggle for independence, self assertion and liberation –
personal identity
Separation from peer group
May respond with anger, frustration
Voluntarily isolate themselves from age mates until they can
feel they can compete
Need for information about their condition
MAJOR STRESSORS OF
HOSPITALIZATION
FEARS OF BODILY INJURY AND PAIN
Common fear among children
May persist into adulthood and result in avoidance of
needed care
Family-centered care
Time structuring
School work
0 1 2
FACE No particular Occasional grimace Frequent to constant
expression or smile or frown, withdrawn, frown, clenched jaw,
disinterested quivering chin
LEGS Normal, relaxed Uneasy, restless, Arched, rigid or
position, moves tense, shifting back jerking
ACTIVITY
easily and forth
CRY No cry (awake or Moans, whimpers, Crying steadily,
asleep) occasional screams or sobs,
complaint frequent complaints
CONSOLABILITY Content, relaxed Reassured by Difficult to console
occasional touching, or comfort
hugging or talking to
CHILDREN’S DEVELOPMENTAL
CONCEPT OF ILLNESS
PREOPERATIONAL THOUGHT
(2-7years)
PHENOMENISM – perceives an external,
unrelated, concrete phenomenon as cause of
illness