High-Risk Newborns and Child During Illness and Hospitalization - Pediatric Nursing

Marcelo Q. Buenavista Jr.
HIGH RISK NEWBORN

 HighRisk Neonates  a newborn
regardless of gestational age or birth
weight, who has a greater-than-average
chance of morbidity or mortality because
of conditions or circumstances
superimposed on the normal course of
events associated with birth and the
adjustment to extrauterine existence.
HIGH RISK NEWBORNS
 Encompasses human growth and development
from the time of viability – 28 days following birth
and includes threat to life and health that occur
during the prenatal, perinatal, and postnatal
periods.
 Viability– gestational age at which survival

outside the uterus is believed to be possible, or
as early as 23 weeks of gestation.
CLASSIFICATION OF HIGH-RISK
NEWBORN
 Birth Weight
 Gestational Age – preterm/post term
 Predominant Physiologic Factors –
associated with state of maturity; chemical
disturbances (hypoglycemia,
hypocalcemia); consequences of
immature organ systems (hypothermia,
Respiratory Distress Syndrome,
CLASSIFICATION ACCORDING
TO SIZE
 Low Birth Weight – less than 2500g
regardless of gestational age
 Moderately Low Birth Weight – birth
weight is between 1501g to 2500g.
 Very Low Birth Weight – birth weight is
less than 1500g.
 Extremely Low Birth Weight – birth weight
less than 1000g.
TO SIZE
 Appropriate for Gestational Age (AGA) –
birth weight falls between the 10th and 90th
percentile
 Small for Gestational Age (SGA) – birth
weight falls below the 10th percentile
 Large for Gestational Age (LGA) – birth
weight falls above the 90th percentile
TO GESTATIONAL AGE
 Premature Infant – born before the
completion of 37 weeks of gestation,
regardless of birth weight
 Full-Term Infant – born between the
beginning of the 38 weeks and the
completion of the 42 weeks of gestation
 Postmature Infant – born after 42 weeks of
gestational age, regardless of birth weight
PRETERM INFANTS
 An infant born before term (</=36 weeks);
premature or preterm
 A low birth weight infant: </=1300-2000g
(Philippine Standards) (,2.5kg)
 Born before complete maturity; born
before body and organ system have
completely matured.
 PRETERM: refers to pregnancy (PT
labor); PREMATURE: to describe a baby
PRETERM INFANTS
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
 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
 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
 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
 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
 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
 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
Protein (used by the body) Unconjugated Bilirubin
liver
Bilirubin detched from albumin through enzyme glucoronyl transferase + glucoronic acid
Conjugated Bilirubin
Excreted into Bile (feces and urine)

HYPERBILIRUBINEMIA
PATHOPHYSIOLOGY:
 Result from increased unconjugated/
conjugated bilirubin
 Bilirubin – one of the breakdown products of
hgb from RBC destruction
 Unconjugated Bilirubin – insoluble, bound to
albumin
 Intestines – (+) bacterial action – reduces
conjugated bilirubin
 Urobilinogen – pigment that gives stool its
characteristic odor.
HYPERBILIRUBINEMIA
COMPARISON OF MAJOR TYPES OF
UNCONJUGATED HYPERBILIRUBINEMIA
PHYSIOLOGIC BREAST- BREAST MILK HEMOLYTIC
JAUNDICE FEEDING- JAUNDICE DISEASE
ASSOCIATED (LATE ONSET)
JAUNDICE
(EARLY ONSET)
CAUSE:
Immature hepatic Decreased milk Possible factors is Blood antigen
function + increased intake related to breast milk that incompatibility
bilirubin load from fewer calories prevent bilirubin causes hemolysis of
RBC hemolysis consumed by infant conjugation large # of RBCs.
before mother’s milk Less frequent Liver unable to
is well established; stooling conjugate & excrete
enterohepatic excess bilirubin
shunting from hemolysis
HYPERBILIRUBINEMIA
COMPARISON OF MAJOR TYPES OF UNCONJUGATED
HYPERBILIRUBINEMIA
JAUNDICE
(EARLY ONSET)
ONSET:
After 24 hours 2nd – 4th day 5th – 7th day During 1st 24 hrs
(preterm infants, (levels increase
prolonged) faster than
5mg/ml/day)
PEAK:
75 – 90 hours 3rd – 5th day 10th – 15th day Variable
DURATION:
Declines on 5th-7th Variable May remain Dependent on
day jaundiced x 3-12 severity &
weeks or more treatment
HYPERBILIRUBINEMIA
HYPERBILIRUBINEMIA

JAUNDICE
(EARLY ONSET)
THERAPY:
Increase frequency Frequent (10- Increase frequency Monitor TcB/TSB
of feedings & avoid 12x/day) of breast feeding; level.
supplements. breastfeeding, avoid use no Perform risk
Evaluate stooling glucose water, supplementations assessment
pattern. water supplements (glucose water); POST NATAL –
or formula. cessation of
Monitor phototherapy;
Evaluate stooling breastfeeding not
Transcutaneous administer IVIG per
pattern; stimulate as recommended.
Bilirubin (TcB)/ protocol; if severe,
Total Serum needed. Perform risk perform exchange
Bilirubin (TSB) assessment. transfusion.
HYPERBILIRUBINEMIA
HYPERBILIRUBINEMIA
JAUNDICE
(EARLY ONSET)
THERAPY:
Perform risk Use phototherapy if Consider PRENATAL –
assessment. bilirubin level performing transfusion (fetus)
Use phototherapy if increases additional Prevent sensitization
bilirubin level significantly (17- evaluations: G6PD, (Rh Incompatibility)
increases 22mg/dl) or direct and indirect of Rh-negative
significantly significant serum bilirubin, mother with Rhig
(>5mg/dl/day) or hemolysis is family history & (Rhogam)
significant present. others as
hemolysis is necessary.
present.
HYPERBILIRUBINEMIA
HYPERBILIRUBINEMIA
BREAST-FEEDING- BREAST MILK HEMOLYTIC DISEASE
ASSOCIATED JAUNDICE JAUNDICE
(EARLY ONSET) (LATE ONSET)
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:
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:
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
 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
 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
 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
 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
 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)
AGE CONSIDER PHOTOTHERAPY EXCHANGE EXCHANGE

(HOURS) PHOTOTHERAPY TRANSFUSION IF TRANSFUSION
INTENSIVE AND INTENSIVE
PHOTOTHERAPY PHOTOTHERAPY
FAILS
24 --- --- --- ---
25-48 >/= 12 (170) >/= 15 (260) >/= 20 (340) >/= 25 (430)
48-72 >/= 15 (260) >/= 18 (310) >/= 25 (430) >/= 30 (510)
>72 >/= 17 (290) >/= 20 (340) >/= 25 (430) >/= 30 (510)

HYPERBILIRUBINEMIA
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
Evidence of jaundice that appears before infant is

24 hrs of age – indication for assessing bilirubin
levels
HYPERBILIRUBINEMIA
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
 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
 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
Side effects: loose greenish stools transient skin

rashes, hypothermia, Increase BMR, DHN,
electrolyte imbalance (hypocalcemia), priapism
HYPERBILIRUBINEMIA
 PHOTOTHERAPY:
 Informed consent prior to treatment
 Oily lubricants/lotions not used – “frying effect”
 Full-term newborn – additional fluid volume to compensate
for fluid loss
 Meticulous skin care
 Rebound effect – after phototherapy is permanently
discontinued  subsequent increase in serum bilirubin level;
transient
 “Bronze Baby Syndrome” – serum, urine, skin turn grayish
brown hours after infant is placed under light
 Due to retention of bilirubin breakdown product of phototherapy
(copper prophyrin)
 Infants with elevated B2 level & some degree of cholestasis
 Resolves after discontinuation of phototherapy
RESPIRATORY DISTRESS
SYNDROME (RDS)
 Condition of surfactant deficiency & physiologic immaturity of thorax
 Seen almost exclusively in preterm infants; seen in infants <32 wks
AOG
 A disease related to developmental delay in lung maturation
 Also associated with multifetal pregnancies, infants of diabetic
mothers, Caesarean Section delivery, delivery before 37 weeks
AOG, low birth weight, precipitous delivery, cold stress, asphyxia,
history of previous RDS
 Rare in drug-exposed infants or those who have been exposed to
chronic intrauterine stress (HPN, preeclampsia)
 RDS of nonpulmonary origin in Newborn: sepsis, cardiac defects,
exposure to cold, airway obstruction, IVH, hypoglycemia, metabolic
acidosis, acute blood loss, drugs.
SYNDROME (RDS)
 PATHOPHYSIOLOGY
Deficient Surfactant
Collapse of Alveoli
Great deal of effort to reexpand the alveoli with each breath
Exhaustion
Fewer and fewer alveoli opens
Atelectasis
Hypoperfusion to the lung tissue
Hypoxemia and hypercapnia

SYNDROME (RDS)
 PATHOPHYSIOLOGY
 Preterm – born before lungs are fully
prepared for gas exchange (critical factor in
RDS)
 Combination of structural and functional
immaturity of lungs
 (+) fetal respiratory activity before birth: lungs
have feeble respiratory movements, fluid
excreted thru alveoli
SYNDROME (RDS)
 PATHOPHYSIOLOGY
 Finalunfolding of alveolar septa (increase
surface area of the lungs) occurs on last
trimester of pregnancy
Preterms are born with underdeveloped and uninflatable alveoli
Limited pulmonary blood flow
Collapsed lungs
Increased pulmonary vascular resistance
Fetal blood shunted from lungs by ductus arteriosus and foramen ovale
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
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
SYNDROME (RDS)
 PATHOPHYSIOLOGY
Inadequate pulmonary perfusion and ventilation
Hypoxemia and hypercapnia
Markedly reactive pulmonary arterioles and thick

Muscular layer decreased oxygen concentration
Decreased oxygen tension + decreased blood pH
Vasospasm in pulmonary arterioles
Increased PVR
Intrapulmonary shunting
Anaerobic glycolysis
Metabolic acidosis, cyanosis

SYNDROME (RDS)
 PATHOPHYSIOLOGY
 (+) pulmonary edema – impaired gas exchange
 (+) pulmonary interstitial emphysema –
overdistention of distal airways
MAJOR FACTORS IN RDS
CAUSE EFFECT
Increased surface tension of alveoli Alveolar collapse, atelectasis, increased
(surfactant deficiency) difficulty in breathing
Impaired gas exchange Hypoxemia, and hypercapnia with
respiratory acidosis
Increased pulmonary vascular resistance Hypoperfusion of pulmonary circulation
Hypoperfusion (with hypoxemia) Tissue hypoxia & metabolic acidosis
Increased transudation of fluid into lungs Hyaline membrane formation; impaired gas
exchange
SYNDROME (RDS)
 CLINICAL MANIFESTATIONS:
 Respiratory Signs and Symptoms:
 Tachypnea (80-120/min) initially : dyspnea
 Pronounced intercostals and/or substernal retractions
 Fine inspiratory crackles ; audible expiratory grunt
 Flaring of external nares
 Cyanosis / pallor
 As disease progresses
 Apnea ; flaccidity ; absent spontaneous movement
 Unresponsive ; diminished breath sounds ; mottling
 Severe disease: shock-like state
 Decreased cardiac output and bradycardia
 Low systemic BP
SYNDROME (RDS)
 EVALUATION:
 Blood glucose test
 Chest x-ray with fine, diffuse, recticogranular
or “ground glass appearance and air
bronchogram
 Arterial blood gas (ABGs) ; pulse oximetry
and carbon dioxide monitoring, pulmonary
function tests
SYNDROME (RDS)
 EVALUATION:
 Prenatal diagnosis:
 Problems like maternal diabetes – delay fetal lung maturation
 Antenatal administration of glucocorticoids – enhance fetal lung
maturation
 Lecithin
/ sphingomyelin ratio (L:S ratio) : relationship
between these 2 lipids during gestation
 L:S = 2:1
 “Shake/ bubble test” – stable foam bubbles form when
amniotic fluid is shaken in presence of ethanol
 Tap Test – abundant bubbles appear in test tube of amniotic
fluid with 6N – HCL and diethyl ether
 TDx fetal lung maturity assay
SYNDROME (RDS)
 TREATMENT / MANAGEMENT:
 Immediate establishment of adequate oxygen and ventilation
and supportive measures required for a preterm, prevent further
complications
 SUPPORTIVE MEASURES:
 Maintain adequate ventilation and oxygen
 Maintain acid-base balance
 Maintain neutral thermal environment
 Maintain adequate tissue perfusion and oxygen
 Prevent hypotension
 Maintain adequate hydration and electrolyte status
 NUTRITION: parenteral therapy during 1st phase of disease
 Nipple and gavage feedings are contraindicated – causes increase
RR, prone to aspiration
 Enteral substrate to infant with transient hypoxia – increase risk
Necrotizing Enterocolitis
SYNDROME (RDS)
 EXOGENOUS SURFACTANT REPLACEMENT (via ET Tube)
 Decrease oxygen requirements and mean airway pressure (MAP)
 Improves blood gas values & ventilator settings
 Decrease incidence of pulmonary air leaks
 Decrease deaths from RDS
 Decrease mortality rate
 COMPLICATIONS: pulmonary hemorrhage, mucous plugging
 Given at birth via endotracheal (ET) tube directly into infants trachea
 NURSING RESPONSIBILITIES:
 Assist in delivery of the product, collection, and monitoring of ABG’s,
scrupulous monitoring of oxygen with pulse oximetry
 Assess infant’s tolerance of procedure
 Delay suctioning for an hour or so to allow maximum effects to occur
SYNDROME (RDS)
 OXYGEN THERAPY
 Aggressive respiratory support: Oxygen, continuous positive
airway pressure (CPAP), intubation, mechanical ventilation
 Goals of Oxygen therapy: provide adequate oxygen to
tissues
 Prevent lactic acidosis resulting from hypoxia
 Avoid negative effects of oxygen barotrauma / toxicity
 Gas should be warmed before entering respiratory tract

 Oxygen can be supplied via plastic hood
 If oxygen saturation of blood cannot be maintained at
satisfactory level and PaO2 rises  ventilatory assistance
SYNDROME (RDS)
METHOD DESCRIPTION HOW PROVIDED
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
SYNDROME (RDS)
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
Synchronized Intermittent Mechanically delivered breaths Patient-triggered infant

Mandatory Ventilation are synchronized to the onset of ventilator with signal
(SIMV) spontaneous patient breaths; detector and
assist/control mode facilities full assist/control mode;
inspiratory synchrony; involves endotracheal tube
signal detection of onset of
spontaneous respiration from
abdominal movement, thoracic
impedance, airway pressure, or
flow changes
SYNDROME (RDS)
Volume Guarantee Delivers predetermined volume Volume guarantee
Ventilation of gas using an inspiratory ventilator with flow
pressure that varies according sensor; endotracheal
to infant’s lung compliance tube
(often used in conjunction with
SIMV)
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
SYNDROME (RDS)

High-Frequency Jet Uses separate, parallel, May be used alone or with
Ventilation (HFJV) low compliant circuit and low-rate IMV; endotracheal
injector port to deliver tube
small pulses or jets of
fresh gas deep into airway
at rates between 250 and
900 breaths/min
SYNDROME (RDS)
 COMPLICATIONS OF POSITIVE PRESSURE
VENTILATION:
 Increased incidence of air leaks that produce complications:
 Pulmonary Interstitial Emphysema
 Pneumothorax
 Pneumomediastinum
 Associated with Intubation:

 Nasal/tracheal/pharyngeal perforation
 Stenosis; inflammation
 Palatal grooves; subglottic stenosis
 Tube obstruction and infection
SYNDROME (RDS)
 INHALED NITRIC OXIDE (NO): for newborn with conditions that
cause persistent pulmonary HPN, pulmonary vasoconstriction,
subsequent acidosis, and severe hypoxia
 Colorless, highly diffusible gas: cause smooth muscle relaxation and
reduce pulmonary vasoconstriction and subsequent pulmonary HPN
when inhaled into lungs
 Administered through ventilator circuit and blended with oxygen
 Attaches readily to hemoglobin and deactivated so that systemic
vasculature is not affected
 Toxic in large quantities
 Mucus may collect I respiratory tract as a result of infant’s
pulmonary condition  interferes with gas flow and obstruct
passages
 Catheter inserted gently but quickly; intermittent suctioning (limited
to <5secs)
 FiO2 increased by 10% before suctioning
SYNDROME (RDS)
 Most advantageous position for facilitating an
infant’s open airway are on the side with head
supported in alignment by small folded
blanket
Back position – keep neck slightly extended
 Head in “sniffing” position
 Inspection of skin – position changes and use
of water pillows (prevents skin breakdown)
 Mouth care
SYNDROME (RDS)
 TRANSIENT
TACHYPNEA OF THE
NEWBORN (RDS TYPE 2)
 Delayed resorption of fetal lung fluid;
decrease lung compliance
 Management: Oxygen therapy
 Signs and symptoms similar to RDS 1
(hyaline membrane disease) but resolves 48-
72 hrs.
SEPSIS / SEPTICEMIA
 Generalized bacterial infection in the
bloodstream
 Newborns are highly susceptible to infection as
a result of diminished nonspecific (inflammatory)
& specific (humoral) immunity: impaired
phagocytosis, delayed chemotactic response,
minimal/absent IgA & IgM, decreased
complement levels
 High-Risk Infant 4x greater chance; males >
females
SEPSIS / SEPTICEMIA
 RISK FACTORS:
 Prematurity
 Congenital Anomalies
 Acquired injuries that disrupt the skin, mucous
membranes
 Invasive procedures – IV lines, ET tubes
 Administration of TPNs
 Nosocomial exposures – NICU
 Infant born after a difficult or traumatic labor &
delivery
SEPSIS / SEPTICEMIA
 PATHOPHYSIOLOGY:
 Premature withdrawal of placental barrier –
leaves infants vulnerable to viral, fungal,
bacterial, parasitic infections
 Early birth interrupts transplacental
transmission of passive immunity (IgG)
Preterms – low IgG; IgA & IgM not transferred to
fetus
SEPSIS / SEPTICEMIA
 SOURCES OF INFECTION:
 Acquired prenatally across placenta from
maternal blood stream or during labor from
ingestion or aspiration of infected amniotic
fluid
Prolonged rupture of membranes – maternal-fetal
transfer of pathogenic organisms
Transplacental transfer of CMV, toxoplasmosis,
syphilis can occur
SEPSIS / SEPTICEMIA
 Early Sepsis (< 3days) – acquired in perinatal period
 Direct contact with organisms from maternal GIT & GUT
 Group B streptococcus (GBS), E. Coli
 H. influenza, coagulase-negative staphylococci – Very Low
Birth Weight infants
 Gonococci, Candida albicans, Herpes Simplex Virus II,
Listeria organism, Chlamydia
 Late Sepsis (1-3 weeks after birth) – nosocomial
 Staphylococci,Kleibsiella, enterococci, Pseudomonas
 Coagulase-negative staphylococci – Extremely Low Birth
Weight, Very Low Birth Weight Infants
SEPSIS / SEPTICEMIA
 Bacterial Invasion: umbilical stump, mucous
membranes of the eyes, nose, pharynx, ear;
internal systems (respiratory, nervous,
urinary, GIT)
 Postnatal Infection: cross-contamination from
other infants, personnel, object in the
environment
SEPSIS / SEPTICEMIA
 SIGNS AND SYMPTOMS:
 Systemic Infections – subtle, vague, nonspecific
 General: Fever, Temperature instability; “not doing
well”; poor feeding, edema
 GI System: poor feeding, abdominal distention;
vomiting; diarrhea/ decreased stooling;
Hepatomegaly, hemoccult-positive stools
 Respiratory System: irregular respirations,
Apnea/tachypnea; dyspnea, retractions; flaring,
grunting; cyanosis
 Renal System: Oliguria
SEPSIS / SEPTICEMIA
 Cardiovascular System/ Circulatory: Pallor/ cyanosis/
mottling, cold clammy skin; hypotension; irregular
heartbeat : Tachycardia/ Bradycardia, edema
 CNS: diminished activity – lethargy, hyporeflexia,
coma
 Increased activity – irritability, tremors, seizures
 Full fontanelle, High-pitched cry, increased/ decreased tone,
abnormal eye movements
 Hematologic System: Jaundice, splenomegaly, pallor,
petechiae, purpura, ecchymosis
SEPSIS / SEPTICEMIA
 DIAGNOSIS:
 Based on suspicion of presenting clinical signs and
symptoms
 Laboratory and radiographic examination – definitive
diagnosis
 Blood/urine/ CSF cultures – 10% will have negative cultures
 CBC: anemia, leukocytosis/ leucopenia
 Leucopenia – ominous sign
 C-reactive protein serial measurements
 Chest x-ray
 Lumbar puncture if < 28 days old, and if with altered mental
status or meningeal signs
SEPSIS / SEPTICEMIA
 THERAPEUTIC MANAGEMENT:
 SUPPORTIVE THERAPY: Circulatory, respiratory
 Respiratory distress/ hypoxia : Oxygen therapy
 IVF regulation
 Correct electrolytes and acid-base balance
 NPO temporarily
 Blood transfusions for anemia and shock
 Vital signs, thermoregulation
 Aggressive
administration of antibiotics,
immunotherapy
 Antibiotics X7-10 days if cultures are positive, discontinue in
3 days if culture is negative & infant is asymptomatic (thru IV
infusion)
 Antifungal/ antiviral therapies
SEPSIS / SEPTICEMIA
 PROGNOSIS
 Variable
 ELBW/ VLBW infants: Early onset sepsis 
severe neurologic & respiratory sequelae
 Late-onset sepsis & meningitis: poor outcome
SEPSIS / SEPTICEMIA
 NURSING CONSIDERATIONS:
 Recognize existing problem: “something is wrong”
 Awareness of potential modes of infection
transmission
 Knowledge of the side effects of specific antibiotic &
proper regulation & administration of drug are vital
 Prolonged antibiotic therapy – (+) growth of resistant
organisms & superinfection from fungal/ mycotic agents
(Candida albicans)
 Nystatin oral suspension swabbed on oral mucosa –
prophylaxis
 Avoid fully flexed position for obtaining spinal fluid.
SEPSIS / SEPTICEMIA
 Continual cardiorespiratory & pulse oximetry
monitoring provides an ongoing assessment of
infant’s condition
 Decrease additional physiologic or environmental
stress
 Thermoregulated environment
 Anticipate potential problems – dehydration, hypoxia
 Precautionary measures: proper hand washing, use
disposable equipment
 Properdisposal of excretions (vomitus, stool)
 Adequate housekeeping
 Observe for signs of complications – meningitis,
septic shock
NECROTIZING ENTEROCOLITIS
 Acute inflammatory disease of the bowel
 Seen primarily in premature infants,
although, described in full-term neonates
as well
 Occurs several weeks after birth
 ETIOLOGY:
 PreciseCause: unknown
 Prematurity: risk factor
 ETIOLOGY:
3 FACTORS THAT PLAY ROLE IN
DEVELOPMENT OF NEC:
Intestinal Ischemia – vascular compromise on GIT
Diminished Blood Supply
Cell death
No secretion of protective, lubricating mucus
Thin unprotected wall attacked by proteolytic enzyme
Bowel wall swell and break down
Unable to synthesize IgM, mucosa permeable to toxins
Gas-forming bacteria invasion

(+) pneumatosis intestinalis (air in submucosa / subserosa)
 ETIOLOGY:
3FACTORS THAT PLAY ROLE IN DEVELOPMENT
OF NEC:
 Colonization by pathogenic bacteria
 Substrate (formula feeding) in intestinal lumen – stress on
ischemic bowel

 Nonspecific Clinical Signs:
 Lethargy, poor feeding, hypotension
 Vomiting, oliguria, hypotension
 Unstable temperature, jaundice
 Specific Signs:
 Distended (often shiny) abdomen; blood in stools/gastric
content
 Gastric retention; bilious vomitus
 Localized abdominal wall erythema/ induration
 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)
 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
 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
 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
 Inadequate nutritional knowledge – cultural confusion (immigrant

to USA); cognitive impairments
 Family Stress – overwhelming involvement with another

chronically ill child
 Financial, marital, excessive parenting & employment
responsibilities
 Single parent employed full time, depression, substance abuse,
acute grief
FAILURE TO THRIVE
 Psychosocial
factors – maternal depression,
Munchausen syndrome by proxy, child temperament
 Feeding resistance – oral tactile hypersensitivity

 Infantreceiving nonoral nutritional therapy early in life or
exclusively fed with feeding tubes
 Insufficient
breast milk – fatigue, poor release of milk,
breast surgery augmentation, lack of maternal
confidence / support.
FAILURE TO THRIVE
 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
 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
 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
 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
 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
 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
 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
Allowfor catch up growth

Restore optimum body composition
FAILURE TO THRIVE
Educate parents/ primary caregivers regarding
child’s nutritional requirements & appropriate
feeding methods
 Step-by-step directions for formula preparations, written
schedule of feeding times
 Juices should be avoided in children with growth failure
until adequate weight gain has been achieved (should
not exceed 4oz/day)
 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
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
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
NEWBORN
Fetal RBCs (with antigens foreign to mother)
Enters maternal circulation
Mother produces anti-Rh antibodies
 Isoimmunization – no effect on 1st pregnancy

Initial
sensitization to Rh antigens rarely occurs
before the onset of labor
With increased risk of fetal blood transferred to
maternal circulation during placental separation,
maternal antibody production is stimulated.
NEWBORN
Subsequent pregnancy with Rh (+) fetus
Previously formed maternal antibodies to Rh (+) blood cells enter fetal circulation
Attack and destroy fetal RBCs
 Factors that increase incidence of

transpalcental hemorrhage & subsequent
isoimmunization:
Multiple gestation, abruptio placenta, placenta
previa, manual removal of placenta, cesarean
delivery
NEWBORN
Fetus compensate for hemolysis and anemia
Increase rate of erythropoiesis
(+) erythroblasts in circulation
Erythroblastosis fetalis
 Sensitization
may occur during 1st pregnancy
if woman had previously received an Rh (+)
blood transfusion
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
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
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
NEWBORN
Antibodies in plasma of 1 blood group (except type AB)

+ Antigens of a different blood group
= agglutination (clumping)
hemolysis
Release large amounts of bilirubin into circulation

NEWBORN
 Mostcommon: mother – type O and infant –
type A or B
Naturally occurring anti-A or anti-B antibodies
Present in maternal circulation cross placenta
Attack fetal RBC
Hemolysis (less severe than Rh incompatibility)
 Mayoccur in 1st pregnancy and subsequent

pregnancy.
NEWBORN
POTENTIAL MATERNAL-FETAL ABO
INCOMPATIBILITIES
MATERNAL BLOOD INCOMPATIBLE FETAL

GROUP BLOOD BROUP
O A or B
B A or AB
A B or AB
NEWBORN
 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
NEWBORN
 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
NEWBORN
 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
NEWBORN
 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
NEWBORN
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
NEWBORN
 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
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
NEWBORN
 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
NEWBORN
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)
 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)
 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)
 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)
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)
 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
 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
 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 – observed during periods of REM sleep
 Precipitated/ worsened by a variety of factors:
 Infection
 Intracranial hemorrhage
 PDA
 Secondary causes: investigated in infants with new-

onset apnea or when there’s significant change in
frequency or severity of apneic episodes
 Apnea in full-term: consider secondary cause
 POSSIBLE CAUSES OF APNEA OF PREMATURITY:
 Prematurity
 Airway obstruction with mucus or milk, or poor positioning
 Anemia, polycythemia
 Dehydration
 Cooling / overheating
 Hypoxemia
 Hypercapnia / hypocapnia
 Hypoglycemia, hypocalcemia, hyponatremia
 Sepsis, meningitis
 Seizures
 Increased vaga tone (in response to suctioning nasopharynx, gavage
tube insertion, reflux of gastric contents, endotracheal intubation)
 CNS depression – pharmacologic agents
 Intraventricular hemorrhage (IVH)
 Patent ductus arteriosus (PDA), congestive heart failure (CHF)
 Depression following maternal obstetric sedation
 Respiratory distress – pnemonia, inborn errors of metabolism
(hyperammonemia), congenital defects of upper airways
 Persistent apneic spells
 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
 TREATMENT:
 Nasal continuous positive airway pressure
(NCPAP) and intermittent positive pressure
ventilation
CPAP acts to maintain airway patency
More effective for obstructive/ mixed apnea
 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
 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
 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
 YOUNG INFANT’S RESPONSE TO PAIN: <6 months

 Generalized response of rigidity, thrashing
 Loud crying
 Facial expressions of discomfort – most consistent indicator
of stress
 No understanding of the relationship between stimuli and
subsequent pain.
MAJOR STRESSORS OF
HOSPITALIZATION
 OLDER INFANT’S RESPONSE TO PAIN: (6months – 1year)
 Withdrawal from painful stimuli
 Loud crying
 Facial grimace
 Physical resistance
 YOUNG CHILD’S RESPONSE TO PAIN: (toddlers)

 Loud crying; screaming
 Verbalization, “ow”, “ouch”, “it hurts”
 Thrashing of limbs
 Attempts to push away stimulus
 Uncooperative; needs restraints
 Clings to parent, nurse, or other significant person
 Request emotional support
MAJOR STRESSORS OF
HOSPITALIZATION
 SCOOL-AGE CHILD’S RESPONSE TO PAIN
Stalling
behavior – “wait a minute”, “I’m not ready”
Muscle rigidity
May use all behaviors of young child
 ADOLESCENT’S RESPONSE TO PAIN

Less vocal protest, less motor activity
Increased muscle tension and body control
More verbalization (“It hurts”, You’re hurting me!”)
INDIVIDUAL RISK FACTORS
THAT INCREASE VULNERABILITY
TO STRESSES OF
HOSPITALIZATION
 “Difficult”temperament
 Lack of fit between child and parent
 Age (especially between 6 months and 5 years
old)
 Male gender
 Below average intelligence
 Multiple and continuing stresses (ex. Frequent
hospitalizations)
BENEFICIAL EFFECT OF
HOSPITALIZATION
 Recovery from illness
 Increase coping skills
 Master stress and feel competent in

coping
 New socialization experiences

PREVENTING OR MINIMIZING
SEPARATION
 Primary nursing goal
 Especially for children < 5 years old
 Family-centered care
 Parents are not “visitors”
 Familiar items from home

NORMALIZING THE HOSPITAL
ENVIRONMENT
 Maintain child’s routine, if possible
 Time structuring
 Self-care (age appropriate)
 School work
 Friends and visitors

PREVENTING OR MINIMIZING
FEAR OF BODILY INJURY
 Allchildren fear bodily injury from mutation,
bodily intrusion, body-image change, disability,
or death.
 Preparation of children for painful procedures
decreases their fears.
 Use of bandages
 Repeatedly stress the reason for a procedure
 Adolescents may express concern about the
actual procedure but more anxious about the
resulting scar.
PAIN FACTS AND FALLACIES
 FACT: Children are under treated for pain.
 FACT:Analgesia is withheld for fear of the child

becoming addicted
 FALLACY: Analgesia should be withheld

because it may cause respiratory depression in
children
 FALLACY: Infants do not feel pain.

PRINCIPLE OF PAIN
ASSESSMENT IN CHILDREN:
QUESTT
 Question the child.
 Use pain rating scale.
 Evaluate behavioral & physiologic changes.
 Secure parent’s involvement.
 Take the cause of pain into account.
 Take action and evaluate result.
 Question the child – verbal & description of pain. Ask child to

point where it hurts.
 Use of Pain Rating Scale – provide a quantitative self-reporting
measure of pain.
PAIN RATING SCALES
 Not
all pain rating scale are reliable or
appropriate for children
 Should be age appropriate
 Consistent use of same scale by all staff.
 Familiarize child with scale

PAIN RATING SCALE
F.L.A.C.C (FACE, LEGS, ACTIVITY, CRY, CONSOLABILITY
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
 CONTAGION – perceives cause of illness as

proximity between 2 events that occur by
magic
CONCEPT OF ILLNESS
 CONCRETE OPERATIONAL THOUGHT
(7-10years)
 CONTAMINATION – perceives cause as a
person, object, or action external to the child
that is “bad” or “harmful” to the body
 INTERNALIZATION – perceives illness as

having an external cause but as being located
inside the body
CONCEPT OF ILLNESS
 FORMAL OPERATIONAL THOUGHT
(13yrs & above)
 PHYSIOLOGIC – perceives cause as
malfunctioning or nonfunctioning organ or
process; can explain illness in sequence of
events
 PSYCHOPHYSIOLOGIC – realizes that

psychologic actions and attitudes affect health
and illness.

High-Risk Newborns and Child During Illness and Hospitalization - Pediatric Nursing

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High-Risk Newborns and Child During Illness and Hospitalization - Pediatric Nursing

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Marcelo Q. Buenavista Jr.

HIGH RISK NEWBORN

 Viability– gestational age at which survival

Protein (used by the body) Unconjugated Bilirubin

Excreted into Bile (feces and urine)

PHYSIOLOGIC BREAST- BREAST MILK HEMOLYTIC

AGE CONSIDER PHOTOTHERAPY EXCHANGE EXCHANGE

25-48 >/= 12 (170) >/= 15 (260) >/= 20 (340) >/= 25 (430)

48-72 >/= 15 (260) >/= 18 (310) >/= 25 (430) >/= 30 (510)

>72 >/= 17 (290) >/= 20 (340) >/= 25 (430) >/= 30 (510)

Evidence of jaundice that appears before infant is

Side effects: loose greenish stools transient skin

Great deal of effort to reexpand the alveoli with each breath

Fewer and fewer alveoli opens

Hypoperfusion to the lung tissue

Hypoxemia and hypercapnia

Limited pulmonary blood flow

Increased pulmonary vascular resistance

Hypoxemia and hypercapnia

Markedly reactive pulmonary arterioles and thick

Decreased oxygen tension + decreased blood pH

Vasospasm in pulmonary arterioles

Metabolic acidosis, cyanosis

 Gas should be warmed before entering respiratory tract

Synchronized Intermittent Mechanically delivered breaths Patient-triggered infant

METHOD DESCRIPTION HOW PROVIDED

 Associated with Intubation:

No secretion of protective, lubricating mucus

Thin unprotected wall attacked by proteolytic enzyme

Bowel wall swell and break down

Unable to synthesize IgM, mucosa permeable to toxins

Gas-forming bacteria invasion

 SIGNS AND SYMPTOMS:

 Inadequate nutritional knowledge – cultural confusion (immigrant

 Family Stress – overwhelming involvement with another

 Feeding resistance – oral tactile hypersensitivity

Allowfor catch up growth

Enters maternal circulation

Mother produces anti-Rh antibodies

 Isoimmunization – no effect on 1st pregnancy

Attack and destroy fetal RBCs

 Factors that increase incidence of

Increase rate of erythropoiesis

(+) erythroblasts in circulation

Antibodies in plasma of 1 blood group (except type AB)

Release large amounts of bilirubin into circulation

Attack fetal RBC

Hemolysis (less severe than Rh incompatibility)

 Mayoccur in 1st pregnancy and subsequent

MATERNAL BLOOD INCOMPATIBLE FETAL

 Secondary causes: investigated in infants with new-

 YOUNG INFANT’S RESPONSE TO PAIN: <6 months

 YOUNG CHILD’S RESPONSE TO PAIN: (toddlers)

 ADOLESCENT’S RESPONSE TO PAIN

 Increase coping skills

 Master stress and feel competent in

 New socialization experiences

 Especially for children < 5 years old

 Parents are not “visitors”

 Familiar items from home

 Self-care (age appropriate)

 Friends and visitors

 FACT:Analgesia is withheld for fear of the child