HIGH RISK

NEWBORN
• High Risk 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.
CLASSIFICATION ACCORDING 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
CLASSIFICATION ACCORDING TOGESTATIONAL
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
• [Link], 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
• After 42 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
HYPERBILIRUBINEMI
A
• 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
HYPERBILIRUBINEMI
A
HYPERBILIRUBINEMI
A
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)

HYPERBILIRUBINEMI
A
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.
 HYPERBILIRUBINEMI
A
COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
BREAST-FEEDING- BREAST MILK HEMOLYTI
JAUNDICE ASSOCIATE JAUNDICE CDISEASE
D JAUNDICE (LATE ONSET)
(EARLY
ONSET)
CAUSE:
Immature hepatic function Decreased milk intake Possible factors is breast Blood antigen
+ increased bilirubin load related to fewer calories milk that prevent incompatibility causes
from RBC hemolysis consumed by infant bilirubin conjugation hemolysis of large # of
before mother’s milk is Less frequent stooling RBCs.
well established; Liver unable to conjugate
enterohepatic shunting & excrete excess bilirubin
from hemolysis
 HYPERBILIRUBINEMI
A PHYSIOLOGIC
COMPARISON OF MAJOR TYPES OF UNCONJUGATED HYPERBILIRUBINEMIA
BREAST- BREAST MILK HEMOLYTI
JAUNDICE FEEDING- JAUNDICE C
ASSOCIATED (LATE ONSET) DISEASE
JAUNDICE
(EARLY ONSET)
ONSET:
After 24 hours (preterm 2nd – 4th day 5th – 7th day During 1st 24 hrs (levels
infants, prolonged) increase faster than
5mg/ml/day)

PEAK:
75 – 90 hours 3rd – 5th day 10th – 15th day Variable

DURATION:
Declines on 5th-7th day Variable May remain jaundiced x 3- Dependent on severity &
12 weeks or more treatment
HYPERBILIRUBINEMIA
PHYSIOLOGIC BREAST- BREAST MILK HEMOLYTIC DISEASE
JAUNDICE FEEDING- JAUNDICE
ASSOCIATED (LATE ONSET)
JAUNDICE
(EARLY ONSET)
THERAPY:
Increase frequency of Frequent (10-12x/day) Increase frequency of Monitor TcB/TSB level.
feedings & avoid breastfeeding, avoid breast feeding; use no Perform risk assessment
supplements. glucose water, water supplementations POST NATAL –
Evaluate stooling pattern. supplements or formula. (glucose water); phototherapy; administer
Monitor Transcutaneous Evaluate stooling pattern; cessation of IVIG per protocol; if severe,
Bilirubin (TcB)/ Total stimulate as needed. breastfeeding not perform exchange
Serum Bilirubin (TSB) recommended. transfusion.
Perform risk
assessment.
HYPERBILIRUBINEMIA
PHYSIOLOGIC BREAST- BREAST MILK HEMOLYTIC DISEASE
JAUNDICE FEEDING- JAUNDICE
ASSOCIATED (LATE ONSET)
JAUNDICE
(EARLY ONSET)
THERAPY:
Perform risk assessment. Use phototherapy if Consider performing PRENATAL – transfusion
Use phototherapy if bilirubin level increases additional evaluations: (fetus)
bilirubin level increases significantly (17-22mg/dl) G6PD, direct and indirect Prevent sensitization (Rh
significantly or significant hemolysis is serum bilirubin, family Incompatibility) of Rh-
(>5mg/dl/day) or present. history & others as negative mother with Rhig
significant hemolysis is necessary. (Rhogam)
present.
HYPERBILIRUBINEMI
A
BREAST-FEEDING- BREAST MILK JAUNDICE HEMOLYTIC DISEASE
ASSOCIATED JAUNDICE (LATE ONSET)
(EARLY ONSET)

THERAPY:
If phototherapy is instituted, evaluate May include home phototherapy with a PRENATAL – If mother is
benefits & harm of temporarily temporary (10-12hr) discontinuation breastfeeding, assist with
of a breastfeeding; a subsequent TSB
discontinuing breastfeeding; additional maintenance & storage of milk; may
may be drawn to evaluate a drop in
assessments may be required. serum levels.
bottle-feed expressed milk as
Assist mother with maintaining milk appropriate to therapy.
Assist mother with maintenance of
supply, feed expressed milk as milk supply & reassurance regarding Minimize maternal-infant separation
appropriate. her milk supply and therapy. & encourage contact as
After discharge, follow up according to Use formula supplements only appropriate.
hour of discharge. at practitioner’s discretion.
HYPERBILIRUBINEMI
A
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.
HYPERBILIRUBINEMI
A
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.
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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)
• Intensity of jaundice is not always related to the degree of
hyperbilirubinemia
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
DIAGNOSTIC EVALUATION
• Indicators of physiologic jaundice – warrants further investigation as to the
cause of jaundice
• Clinical jaundice 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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
COMPLICATIONS
• SIGNS OF CNS 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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
A
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.
HYPERBILIRUBINEMI
MANAGEMENT OF HYPERBILIRUBINEMIA IN HEALTHY TERM NEWBORN TSB LEVEL
A AGE CONSIDER
(mg/dl/mmol/L)
PHOTOTHERAPY EXCHANGE EXCHANGE
(HOURS) PHOTOTHERAPY TRANSFUSION IF TRANSFUSION AND
INTENSIVE 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)

HYPERBILIRUBINEMI
A
PROGNOSIS:
• Early recognition prevents brain damage
• Bilirubin encephalopathy: athetosis, sensorineural hearing loss, paralytic gaze
palsy, gaze abnormalities, delayed motor skills, dental enamel hypoplasia
HYPERBILIRUBINEMI
A
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
HYPERBILIRUBINEMI
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NURSING CONSIDERATIONS
• Phototherapy – nude under light source, repositioned frequently to expose all body
surface areas to light
• Frequent bilirubin determination – every 6-12hrs (visual assessment is no longer considered
valid)
HYPERBILIRUBINEMI
A
NURSING CONSIDERATIONS
• PHOTOTHERAPY:
• PRECAUTIONS:
• Eye Shield –
opaque
mask to
prevent
exposure to
light
• Properl
y sized,
correctl
y
positio
ned
withou
t
occludi
HYPERBILIRUBINEMI
A
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
• Side effects: loose greenish stools transient skin rashes, hypothermia, Increase BMR,
DHN, electrolyte imbalance (hypocalcemia), priapism
HYPERBILIRUBINEMI
A
NURSING CONSIDERATIONS
• 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.
RESPIRATORY DISTRESS 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

RESPIRATORY DISTRESS 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
RESPIRATORY DISTRESS SYNDROME
(RDS)
• PATHOPHYSIOLOGY
• Final unfolding 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
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

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

PATHOPHYSIOLOGY
• Pulmonary edema – impaired gas exchange
• Pulmonary interstitial emphysema – over distention of distal airways
MAJOR FACTORS IN RDS
CAUSE EFFECT
Iincreased surface tension of alveoli due to alveolar collapse, atelectasis
due to surfactant deficiency
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
RESPIRATORY DISTRESS 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
RESPIRATORY DISTRESS 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
RESPIRATORY DISTRESS 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
RESPIRATORY DISTRESS 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
RESPIRATORY DISTRESS SYNDROME
(RDS)
• TREATMENT / MANAGEMENT:
• 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
RESPIRATORY DISTRESS SYNDROME
(RDS)
• TREATMENT / MANAGEMENT:
• 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
RESPIRATORY DISTRESS SYNDROME
(RDS)
RESPIRATORY DISTRESS SYNDROME
(RDS)
 RESPIRATORY DISTRESS SYNDROME
(RDS) / MANAGEMENT:
• TREATMENT
METHOD DESCRIPTION HOW PROVIDED

CONVENTIONAL METHODS

Continuous Positive Airway Provides contrast distending Nasal prongs, endotracheal tube,
Pressure (CPAP) pressure to airway in spontaneously face mask, nasal cannula
breathing infant.

Positive End-Expiratory Pressure Provides increase end-expiratory Endotracheal intubation, and either
(PEEP) pressure during expiration and volume-limited or pressure-limited
between Mandatory breaths which ventilator
prevents alveolar collapse;
maintains residual airway pressure
 RESPIRATORY DISTRESS SYNDROME
(RDS) / MANAGEMENT:
• TREATMENT
METHOD DESCRIPTION HOW PROVIDED
Intermittent Mandatory Ventilation Allows infant to breath spontaneously at Endotracheal intubation and
(IMV) own rate but provides mechanical cycled ventilator
respirations and pressure at regular preset
intervals

Synchronized Intermittent Mechanically delivered breaths are Patient-triggered infant

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

ALTERNATIVE METHODS
High frequency Oscillation (HFO) Application of high-frequency, low- Variable-speed piston pump
volume, sine wave flow oscillations to (or loudspeaker, fluidic
airway at rates between 480 and 1200 oscillator) ; endotracheal tube
breaths/min
RESPIRATORY DISTRESS SYNDROME
(RDS)
ATMENT / MANAGEMEN T: DESCRIPTION
METHOD HOW PROVIDED
High-Frequency Jet Ventilation Uses separate, parallel, low May be used alone or with low-rate
(HFJV) compliant circuit and injector port to IMV; endotracheal tube
deliver small pulses or jets of fresh
gas deep into airway at rates
between 250 and 900 breaths/min
RESPIRATORY DISTRESS SYNDROME
(RDS)
• TREATMENT / MANAGEMENT:
• 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
RESPIRATORY DISTRESS SYNDROME
(RDS)
• TREATMENT / MANAGEMENT:
• 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
RESPIRATORY DISTRESS SYNDROME
(RDS)
• TREATMENT / MANAGEMENT:
• 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
RESPIRATORY DISTRESS 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
• SOURCES OF INFECTION:
• 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
• SOURCES OF INFECTION:
• 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
• SIGNS AND SYMPTOMS:
• 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
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
• NURSING CONSIDERATIONS:
• 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
• Proper disposal 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:
• Precise Cause: 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

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)
NECROTIZING
ENTEROCOLITIS
• ETIOLOGY:
• 3 FACTORS THAT PLAY ROLE IN DEVELOPMENT OF NEC:
• Colonization by pathogenic bacteria
• Substrate (formula feeding) in intestinal lumen – stress on ischemic bowel

• SIGNS AND SYMPTOMS:

• Nonspecific Clinical Signs:
• Lethargy, poor feeding, hypotension
• Vomiting, oliguria, hypotension
• Unstable temperature, jaundice
NECROTIZING
ENTEROCOLITIS
• SIGNS AND SYMPTOMS:
• 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)
NECROTIZING
ENTEROCOLITIS
NECROTIZING
ENTEROCOLITIS
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
• Cystic fibrosis, celiac disease, vitamin/ mineral deficiencies, biliary atresia, hepatic disease

• Increase metabolism
• Hyperthyroidism, congenital heart defects, chronic immunodeficiency

• Defective utilization
• Trisomy 21 or 18, congenital infection, metabolic storage diseases
FAILURE TO
THRIVE
• ETIOLOGY – multifactorial
• Infant organic disease
• Dysfunctional parenting behaviors
• Subtle neurologic/ behavioral problems
• Disturbed parent-child interactions

• FACTORS LEADING 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

• Infant receiving 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
• 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:
• Isolation and 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
• Allow for catch up growth
• Restore optimum body composition
FAILURE TO
THRIVE
• NUTRITIONAL MANAGEMENT:
• 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 OFTHE
NEWBORN
• Erythroblastosis fetalis
• 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 OFTHE
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 OFTHE
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 OFTHE
NEWBORN
• Isoimmunization – no effect on 1st pregnancy
Fetal RBCs (with antigens foreign to mother)
• Initial sensitization to Rh antigens rarely occurs befor e the onset of
Enters maternal circulation
• labor
With increased risk of fetal blood transferred to maternal circulation during placental
separation, maternal antibody production
Mother produces is stimulated.
anti-Rh antibodies
HEMOLYTIC DISEASE OFTHE
NEWBORN
• Factors that increa se Subsequent
incidencepregnancy with Rh (+) fetus
of transpalcental hem orrhage &
isoimmunization:
subsequent
Previously formed maternal antibodies to Rh (+) blood cells enter fetal circulation
• Multiple gestation, abruptio placenta, placenta previa, manual removal of place nta,
cesarean delivery
Attack and destroy fetal RBCs
HEMOLYTIC DISEASE OFTHE
NEWBORN Fetus compensate for hemolysis and anemia
• Sensitization may occur during 1st pregnancy if woman had previously
transfusion
received an Rh (+) bloodIncrease rate of erythropoiesis

(+) erythroblasts in circulation

Erythroblastosis fetalis
HEMOLYTIC DISEASE OFTHE
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 OFTHE
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 OFTHE
NEWBORN
ABO RELATIONSHIP OF ANTIGENS / ANTIBODIES & DONOR- RECIPIENT
COMPATIBILITY
RBC
COMPATIBILIT
BLOOD GROUP GENOTYPE RBC PLASMA ASYDONOR AS
(PHENOTYPE) ANTIGENS ANTIBODIES TO TYPE RECIPIENT
FROM
TYPE
A AA, AO A B AB, A O, A
B BB, AB, B O, B
AB BO AB B A AB O, A, B,
O OO A N AB
& O AB, A, B, O O
B N
N E
O A
HEMOLYTIC DISEASE OFTHE
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

HEMOLYTIC DISEASE OFTHE
NEWBORN
• Most common: 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

• May occur in 1st pregnancy andsevere

Hemolysis (less subsequent pregnancy.
than Rh incompatibility)
HEMOLYTIC DISEASE OFTHE
NEWBORN
INCOMPATIBLE FETAL BLOOD BROUP
O A or B

A or AB
B

B or

AB
A
HEMOLYTIC DISEASE OFTHE
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 OFTHE
NEWBORN
HEMOLYTIC DISEASE OFTHE
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 OFTHE
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 OFTHE
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 OFTHE
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 OFTHE
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 OFTHE
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 OFTHE
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 OFTHE
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
• Discouraging bed sharing
• Encourage breastfeeding
SUDDEN INFANT DEATH SYNDROME
(SIDS)
• NURSING CONSIDERATIONS:
• Avoid overheating during sleep
• Infants should wear light-clothing, comfortable room temperature
• Infant’s head 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
• 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
APNEA OF PREMATURITY
(AOP)
• 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
APNEA OF PREMATURITY
(AOP)
• CLINICAL MANIFESTATIONS:
• 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
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

• 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
•HOSPITALIZA TION
“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 OFBODILY
INJURY
• All children 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 expression Occasional grimace or Frequent to constant
or smile frown, withdrawn, frown, clenched jaw,
disinterested quivering chin
LEGS Normal, relaxed position, Uneasy, restless, tense, Arched, rigid or jerking
moves easily shifting back and forth
ACTIVITY
CRY No cry (awake or asleep) Moans, whimpers, Crying steadily, screams
occasional complaint or sobs, frequent
complaints
CONSOLABILITY Content, relaxed Reassured by occasional Difficult to console or
touching, hugging or comfort
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
CHILDREN’S DEVELOPMENTAL 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
CHILDREN’S DEVELOPMENTAL 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.