CH 94 THE NEWBORN INFANT

HISTORY IN NEONATAL PEDIATRICS

Neonatal history should
o Identify disabling dss that are amenable to preventive action
or treatment
o Anticipate conditions that may be of later importance
o Uncover factors that may explain pathologic conditions
PHYSICAL EXAMINATION OF THE NEWBORN INFANT
Initial examination
o Done asap
o For high-risk deliveries, perform in delivery room
Monitor every 30 min for 2 hours
o Temp
o Pulse (normal : 120-160 cpm)
o RR (normal: 30-60 bpm)
o Color
o Type of respiration
o Tone
o Activity
o Level of consciousness
Second examination
o More detailed exam performed within 24 hr of birth
Discharge examination
o Done if infant stays more than 48 hrs in the hosp
Blood pressure
o Done if infant

Appears ill

Has a heart murmur

Palpation of the abd or ausculatation of the heart performed 1 st
before other more disturbing manipulations
GENERAL APPEARANCE
Myoclonus (active) & convulsive twitching (quiet)
o Normal in neonates
Edema of the eyelids
o Irritation caused by admin of silver nitrate
Generalized edema
o Prematurity, hypoproteinemia 2ndary to severe
erythroblastosis fetalis, nonimmune hydropsm congenital
nephrosis, Hurler syndrome
Localized edema
o Suggests congenital malformation of lymphatic system
Localized edema confined to extremities of female infant
o Initial sign of Turner syndrome
SKIN
Acrocyanosis
o Harmless cyanosis of hands and feet
Mottling
o Gen circulatory instability assoc w/ serious illness or r/t
transient fluctuation in skin temp
Harlequin color change
o Division of body fr forehead to pubis into red & pale s
o Transient & harmless
Mongolian spots
o Bluish pigmentation over the buttocks
o Disappears in a year
o Common in 50% of black, native ame, Asian
Lanugo

o Fine , downy hair in preterm infants

o Covers scalp, brow and face of PT
Vellus
o Fine, downy hair in full-term infants
Localized cyanosis, icterus
ecchymosis
Blanching pallor upon pressure
none
premature
Thin skin
Delicate
Deep red

Extremely PT
Gelatinous
Bleeds and bruises
easily

postmature
Paler
Thicker skin

Cavernous hemangioma
o
Deep blue masses
o
Trap platelets and produce DIC

Tufts of hair over lumbosacral spine

o
Suggests spinal abnormalities

Ichthyosis congenital
o
Results to full-term infants having parchment-like skin
Erythema toxicum
Pustular melanosis
Benign rash
Benign lesion
Small, white, vesiculopustular papules on
Vesiculopustulare eru
erythematous base
Face, trunk, extremities
Chin, neck, back, ext
Contains eosinophil
neutrophil
Common in black neo
Lasts for 1 week
Lasts for 2-3 days

Amniotic bands
o
Disrupt skin, extremities, face, trunk
o
r/t amniotic memb rupture or vascular compromise w/
fibrous band formation

Excessive skin fragility

o
Ehlers-Danlos synd, Marfans, congenital arachnodactyly,
d/o of collagen synth
SKULL

Roundness of the head for

o
C/S delivery
o
Breech presentation

Cranial synostosis
o
Premature fusion of sutures
o
Identified by a

Hard, non-movable ridge over the suture

Abnormally shaped skull

Anterior fontanel
o
Normal : 20 +_ 10 mm
o
Enlarges if it is small in first few months of life

3rd fontanel
o
suggests trismoy 21 in premature infants

craniotabes
o
soft areas found in the parietal bones

d/t uterine compression in PT

o
if found in occipital bone

suggests

irregular calcification

wormian bone formation

skull in premature infants

o
suggests hydrocephaly

d/t larger brain growth in comparison to other organs

small fontanel suggests

o
microcephaly
o
craniosynostosis
o
congenital hyperthyroidism
o
wormian bones
large head suggests
o
hydrocephaly
o
storage dss
o
achondroplasia
o
cerebral gigantism
o
neurocutaneous syndrome
o
inborn error of metabolism
depression of skull
o
from prolonged exposure by bony pelvis
deformational plagiocephaly
o
d/t in utero positioning forces on the skull
o
manifested as

asymmetric skull and face

ear malalignment
o
assoc w/ torticollis & vertex positioning

FACE

Mobius syndrome
o
Symmetric facial palsy d/t absence of 7th nerve nucleus

Eyes
o
How to open eyes spontaneously?
1. Held infant up
2. Tip gently forward and backward

Whats the reason?

o
Result of labyrinthine and neck reflexes

retinal hemorrhages
o
d/t vacuum assisted deliveries (75%)
o
Resolves
most Infants (85%) - 2 wks
All infants - 4 wks
o
Pupillary reflex presemt after 28-30wk AOG
o
Iris inspected for colobomas and heterochromia
o
Cornea >1cm in diameter in FT w/ photobia and tearing
congenital glaucoma
o
Bilateral red reflex absence of cataracts & intraocular
pathology
o
Leukokoria (white papillary reflex) cataracts, tumor,
chorioretinitis, ROP, persistent hyperplastic primary
vitreous
Nose
o
Dislocation of nasal cartilage from vomerian groove
asymmetric nares
Mouth
- teeth in lower incisor position come out first dont
remove

Eipstein pearls

temporary accumulation of epithelial cells in hard

palate

retention cyst

seen on gums

disappear spontaneously

neonates dont have an active salivation

frenulum is normally short

dont cut

do cut if it interferes with feeding

throat is hard to see because of low arch of palate

tonsils are small
marble-sized buccal mass

d/t benign idiopathic fat necrosis

NECK

short

Congenital torticollis
o
Head to turn toward & face to turn away from affected
side
o
Plagiocephaly, facial asymm, hemihypoplasia develops if
unttt

Redundant skin or webbing in a femal intrauterine edema &

turner syndrome
CHEST

breast hypertrophy is common

o
milk may also be present but should not be expressed

asymm, erythema, induration & tenderness

o
suggest mastitis or breast abscess

Widely spaced nipples w/ a shield-shaped chest turner

syndrome
LUNGS

respiratory rate
o
count for 1 min, preferably when infant is asleep
o
normal value : 30-40 / min
o
rare is higher & fluctuates more rapidly in PT
o
consistently >60/min during pd of regular breathing

pulmonary, cardiac or metabolic dse (acidosis)

PT may breath w/
o
Cheyne-Stokes/periodic respiration or
o
Complete irregularity

Irregular gasping accomp by spasmodic movt of mouth & chin

impaired resp center

breathing is diaphragmatic
o
during inspiration

thorax is drawn inward

abdomen protrudes

labored respiration w/ retraction

o
respiratory distress synd
o
pneumonia
o
anomalies
o
mech disturbance of the lungs

grunting during expiration

o
serious cardiopulmo or sepsis

when benign grunting resolves bet 30-60min after birth

breath sounds are bronchovesicular

HEART

transitory murmurs closing ductus arteriosus

PR 90/min in relaxed sleep to 180/min in act

o
Restin HR in PT 140-150/min

premature infants may have sudden onset of sinus

bradycardia

palpate pulses in upper and lower extremities

o
to detect coarctation of aorta

Oscillometric method easiest and most accurate

noninvasive method available

ABDOMEN

Liver - palpable 2 cm below rib margin

kidney - determined on deep palpation

Gas in rectum on roentgenogram by 24H

abdominal wall
o
normally weak

diastasis recti and umbilical hernia are common

occurrence among black
o
renal pathology is the most common cause for neonatal
abdominal masses
o
Abd distention at birth obstruction or perforation of GIT
as a result of meconium ileus
o
Later distention lower bowel obstruction, sepsis,
peritonitis
o
scaphoid abdomen suggests diaphragmatic hernia
o
Abd wall defects produce

Omphalocele (thru umbilicus)

Gastroschisis (lateral to midline)

umbilical cord
o
omphalitis acute local inflamm of the periumbilical
tissue

may result in later portal HPN

o
consists of

2 arteries

presence of only one artery suggests renal

pathology

1 vein (AVA)
GENITALS

due to maternal hormones

o
enlargement and secretion of breast of both sexes
o
prominence of female genitals

with nonpurulent discharge

o
no intervention is needed

imperforate hymen result in hydrometrocolpos and lower

abd mass

N scrotum is large
o
Size inc by trauma of breech or by a transitory hydrocele

Prepuce is tight and adherent

Erection of penis is common

Most void by 12H, 95% PT and FT w/in 24H

ANUS

Some Passage of meconium w/in 1st 12H at birth

99% FT and 95% PT pass meconium w/in 48H

imperforate anus
o
assess by

inserting little finger gently

use rectal tube

o
passage of meconium does not rule out

could be d/t rectal-vaginal fistula

ROUTINE DELIVERY ROOM CARE

placed head downward

o
clear out secretions

do gentle suction

wiping palate and pharynx w/ gauze thrush, pterygoid

ulcers or tooth bud infection

if delivered by c/s section

o
stomach of infants would contain more fluid

emptied by gastric tube

if unnecessary , dont do suctioning

avoid tube placement! Coz predispose to future poor

experiences w/ pain

if infant has respiratory distress

o
place in a warmer
o
head is dependent

APGAR score
o
assesses newborn infants

requiring resuscitation

predict survival
o
not designed to predict neurologic outcome
1-min APGAR Score
5-, 10-, 15-, 20-min APGAR
scores
Identify need for
Indicates the probability of
immediate
successfully resuscitating an
resuscitation
infant

apgar score and umbilical artery blood pH

o
both predict neonatal death
o
apgar score

better predictor than umbilical artery pH

MAINTENANCE OF BODY HEAT

body surface area of a newborn

o
3x that of an adult

heat of newborn
o
4x that of an adult

Usual delivery room (20-25C)

Cumulative loss of 2-3C in deep BT after delivery

heat loss occurs through
1. convection
o
to cooler surrounding air
2. conduction
o
to colder materials, where the infant is placed
3. Radiation
o
From infant to other nearby cooler solid obj
4. evaporation
o
from moist skin and lungs

EXTREMITIES

spont or stimulated act suspect fracture or nerve injury

assoc w/ delivery

examing for polydactyly, syndactyly, abn dermatoglyphic

pattern s/a simian crease
NEURO

severe positional ddeformation & contractures

arthrogryposis

conditions that develop in infants upon heat compensation d/t

cold exposure
o
metabolic acidosis
o
hypoxemia
o
hypoglycemia
o
inc renal excretion of water and solutes

release of norepinephrine oxidation of brown fat

nonshivering thermogenesis
o
inc metabolic rate and oxygen consumption

dec response upon hypoxemia and hypoglycemia

Hypothermia most impt factor that impairs ability to respond
to asphyxia
skin-to-skin contact with mother
o
optimal method to maintain temperature in stable
newborn

ANTISEPTIC SKIN AND CORD CARE

cord cleaning done by

o
cleansing with warm water
o
use of mild nonmedicated soap soln
o
to avoid Staph infxn, do the ff

treat daily with bactericidal agent

or use bacitracin or triple dye with 2x alcoholswabbing

chlorhexidine washing for S. aureus epidemics

total body exposure to hexachlorophene

neurotoxic, thus contraindicated in LBW

OTHER MEASURES

eye-drops to prevent gonococcal infxn

o
use the ff

1% silver nitrate

best-proven therapy

alternatives:

erythromycin

tetracycline
o
also cover Chlamydia

povidone-iodine

one-time prohylactic

Vit K prophylaxis
o
given IM, 1 mg
o
not done

giving large doses

giving of mother d/t placental transfer

all lead to hemolysis

NB screening for:
o
Hypothyroidism
o
PKU
o
Galactosemia
o
Maple syrup urine dse
o
Homcystinuria
o
Biotinidase def
o
Adrenal hyperplasia
o
Hemoglobinopathy
o
CF
o
Tyrosinemia
o
Organic acid defects or aminoacidopathies

routine screening for hematocrit or blood glucose

o
not recommended

hearing impairment
o
universal screening is recommended
NURSERY CARE

nursery temp kept at 24C

infants temp
o
taken via axillary

normal: 36.4- 37 C
monitoring

1st 2-3 days - every 4 hrs

thereafter
- every 8 hrs

place supine to prevent sudden infant death syndrome

vernix shed during day 2-3 d

foreskin of male should not be retracted

o
circumcision is an elective procedure

inc risk of rehospitalization

o
early discharge
- <48 hours
o
very early discharge - <24 hours
o
early discharge requires ff up w/in 48H
table 94-3, p 680
o

DRUGS AND BREASTFEEDING

when fresh breast milk is fed by bottle bacteriologic eval of

stored milk w/in 24H

contraindications to breastfeeding
o
HIV infxn
o
human T-cell leukemia virus
o
cytomegalovirus
o
active TB (ttt < 2 wks)
o
hep B ( baby not received immune globuline and
vaccine)

table 94-6, p 682

table 94-5, p 681
CH42 FEEDING PROBLEMS DURING FIRST YEAR OF LIFE
OVERFEEDING
*If intake is excessive, the most frequent symptoms are
o
regurgitation
o
vomiting

supplementation should be avoided

dilutes protein, minerals, etc

REGURGITATION AND FEEDING

within limits, regurgitation is normal

to reduce, do the ff
o
placing infant on right side for short time after eating
o
head not lower than rest of the body
LOOSE OR DIARRHEAL STOOL

Stool from formula-fed infant is softer than formula-fed infants

diarrhea from overfeeding is unusual

COLIC
-it is a paroxysmal abdominal pain
-of intestinal origin
-presents with
o
severe crying
o
legs drawn upto abdomen
- may disappear with
o
passage of flatus or feces
o
holding infant upright or in a prone position
o
using heat pad

Ch95 High Risk Pregnancies

-

10-20% of pregnant women are identified as high-risk

by history alone

identifying high-risk pregnancies

1st step toward prevention

Those that inc likelihood of:
a. Abortion
b. Fetal death
c. Premature delivery
d. IUGR
e. Poor cardiopulmonary or metabolic transitioning at birth,
fetal or neonatal dse
f.
Congenital malformations
g. Mental retardation
h. Other handicaps
Factors r/t risk:
a. Ingestion of terartogenic drug in the 1st tri
b. Polyhydramnios

Genetic Factors
Chromosomal Abn
Congenital anomaly
Inborn errors of metabolism
Mental retardation
Any familial dse

e.

3.
-

Maternal Factors
lowest neonatal mortality rate occurs in

mothers receiving adequate prenatal care

20-30 yrs of age

Teenage pregnancies and >40 y.o. are at inc risk for:
a. IUGR
b. Fetal distress
c. Intrauterine death
Advanced maternal age fetal malformations
Maternal illness
Multiple pregnancies
Infections
Certain drugs
In vitro LBW and VLBW
1.

Factors assoc w/ PREMATURITY include biologic markers

s/a:
a. Cervical shortening
b. Genital infection
c. Fetal fibronectin in cervicovaginal secretions
d. Preterm PROM leading identifiable cause of
prematurity (30-40%)

2. POLYHYDRAMNIOS
> 2,000mL in the 3rd tri
Complicates 1-3%
UTZ criteria: amniotic fluid index >24cm
1. acute polyhydramnios assoc w/ delivery b4 28wks
2. chronic polyhydramnios

in 3rd tri by discrepancy in uterine size & AOG

when px has dysfxnal labor

abn large amt of amniotic fluid during labor

Assoc w/:
a. Premature labor
b. Abruption placentae
c. Multiple congenital anomalies
d. Fetal neuromuscular dysfunction

Obstruction of GIT that interferes w/ reabsorption of the

amniotic fluid
f.
Inc fetal urination or edema formation
In 60%, no cause is identified
Can be managed by:
a.
serial amniocentesis
b. by short-course maternal indomethacin if d/t excessive
fetal urination
indications for ttt:
a. acute maternal respiratory distress
b. threatened preterm labor
c. to provide time for admin of corticosteroids for fetal lung
maturity
OLIGOHYDRAMNIOS
<500ml
UTZ criteria: amniotic fluid index <5cm
Assoc w/:
a. Congenital anomalies
b. IUGR
c. Severe renal, bladder or urethral anomalies
d. Drugs that interfere w/ fetal urination
Most evident after 20 wk AOG
o
Dec urination of fetus
Rule out rupture of membranes if N sized bladder on UTZ
Causes fetal compression abn s/a:
a. Clubfoot
b. Spadelike hands
c. Flattened nasal bridge
PULMONARY HYPOPLASIA - Most serious complication of
chronic oligohydramnios
Risk of UC compression do saline amnio-infusion
In combination w/ inc AFP level, uterine bleeding or IUGR
inc risk of intrauterine fetal demise

Antenatal screening
Used to detect:
a. Down syndrome
b. Neural tube defects
c. Tay-Sachs dse
d. Hemoglobinopathies
e. Cystic fibrosis
Screening methods:
a. Maternal blood tests
b. Fetal UTZ
c. Dx tests on cells or fluids obtained by amniocentesis or
chorionic villus sampling & by fetal bld / tissue sampl.
Second-trimester Screening (15-18wk) of maternal serum AFP
Used to screen for
o
open neural tube defects
o
Gastrochisis
o
Omphalocele
o
Congenital nephrosis
o
twins
90% affected preg detected by inc MSAFP level
Low MSAFP assoc w/:
a. Incorrect gestational age estimates
b. Trisomy 18 or 21
c. IUGR

o
Effective screening strategies to detect down syndrome incl
combination of:
a. maternal age
b. Nuchal translucency on UTZ
c. Serum markers s/a AFP, unconjugated estriol, total HCG,
free B subunit of HCG, inhibin A, ang preg-assoc plasma
CHON A
The integrated test
o
Most effective strategy
o
Combines 1st and 2nd tri screening
o
Can ID 94% of affected preg w/ 5% false (+) or 85% w/
1% false (+)
Chromosomal analysis of cells obtained by amniocentesis or
chorionic villus biopsy makes dx
4.

UTERUS INAPPROPRIATELY LARGE OR SMALL

a. LGA
Multiple fetuses
Hydramnios
Excessively large infant
b. SGA
Oligohydramnios
Poor IUGR
5. PROM
PROM
Risks
Earlier than 24H
fetal infection & premature birth
b4 delivery
At term
- onset of labor w/in 48
- chorioamnionitis and UC compression
Before 37 wk
- Longer latency until labor starts - added
risks of cord prolapsed, oligohydramnios,
abruption placenta, fetal malposition,
pulmonary hypoplasia, uterine-induced
deformations and extremity contractures.
Factors
Risk for
Prolonged & difficult labor
Mechanical & hypoxic
damage
Tumultuous short labor w/ precipitous
Birth asphyxia & IC
delivery
hge
Placental separation before delivery &
Brain damage from
Abn implantation or compression of
fetal hypoxia
cord
Brown or muddy amniotic fluid
Meconium has been
passed
Vacuum extraction or forceps
IC hge
Trial of labor after previous CS
Uterine rupture &
hypoxic-ischemic
encephalopathy
Mild maternal hypoxemia 2 to
Severe fetal hypoxia
hypoventilation or hypotension from
and shock
epidural anesthesia
6.

7.

intracranial hemorrhage
o
greater in infants delivered via

vacuum extraction

forceps
c/s delivery

o
o
o

indicated for

breech presentation
predisposes infants for respiratory difficulty for 1-2 days
transient tachypnea

most frequently assoc problem

hyaline membrane dss (rds)

develop in infants

not born to women not in labor

uncertain pulmonary maturity

DM mother

asphyxia

CHAPTER 96 THE FETUS

o

ultrasonography
o
safe and accurate procedure to use in fetus
fetal growth
o
can be assessed at 6-8 wks
o
1st trimester - crown-rump length
o
2nd tri - biparietal diameter
o
Term - abdominal circumference, femoral length
fetal maturity
o
assessed through

gestational age

can also be done through dating last mens

period

surfactant content of amniotic fluid

extent of calcification by UTZ

placental maturity index

first audible fetal heart tone

16-18 wk

initial fetal movt

18-20 wk

CH99 Nervous System D/O

-

CNS damaged d/t:

o Hypoxia
o Asphyxia
o Hge
o Trauma
o Hypoglycemia
o Direct cytoxicity
Etiology of CNSS damage:
o Acute perinatal complications
o Postnatal hemodynamic instability
o Devtal abnormalities
Predisposing factors for brain injury:
o Chronic & acute maternal illness resulting in uteroplacental
dysfunction
o Intrauterine infection
o Macrosomia/dystocia
o Malpresentation
o Prematurity
o IUGR

THE CRANIUM
Forceps or vacuum-assisted deliveries d/t:
o Erythema
o Abrasions
o Ecchymoses

o SQ fat necrosis of facial or scalp soft tissues

Subconjunctival & retinal hge 2ndary to a sudden inc in
intrathoracic pressure during passage of the chest thru the
birth canal
o Hge are temporary
o Resolve w/in 1st 2 wk of life
Caput succedaneum diffuse, sometimes ecchymotic,
edematous swelling of the soft tissues of the scalp involving
the area presenting during vertex delivery
o Edema disappears w/in the 1st few days of life
o Molding of the head & overriding of the parietal bones
o Hemorrhagic caput shock
o Analogous swellin discoloration & distortion of the face in
face presentations
Cephalhematoma a subperiosteal hge
o Limited to the surface of one cranial bone
o 1-2% of live births
o Lesion becomes a firm tense mass w/ a palpable rim
localized over 1 area of the skull
o Resorbed w/in 2wk-3mo
o Begin to calcify by end of 2nd wk
o X-ray: widening of diploic space
Subgaleal hge collection of blood beneath the aponeurosis
that covers the scalp the entire length of the occipital-frontalis
mm
o 2ndary to a linear skull fracture, suture diastasis or
fragmentation of the superior margin of the parietal bone, &
rupture of the emissary vein
o Extensive subgaleal bleeding 2ndary to a hereditary
coagulopathy (hemophilia)
o Presents as a firm fluctuant mass, w/c inc in size after birth
o Monitor for hypotension & hyperbilirubinemia
o Resolve over 2-3wk period
Fractures of the skull result of pressure from forceps or
from maternal symphysis pubis, sacral promontory or ischial
spines
o Linear fractures most common

Cause no symp & require no ttt

o Depressed fractures complication of forceps delivery or
fetal compression

Elevate severe depressions to prevent cortical injury

from sustained pressure
o Fracture of the occipital bone w/ separation of the basal &
squamous portions

Disruption of underlying vascular sinuses

Breech deliveries from traction on the hyperxtended

spine of the infant

EPIDEMIOLOGY
30% of premature <1500g
Inversely r/t AOG and BW
o 5% infants 1250-1500g - severe IVH (Gr. 3 or 4)
o 11.4% infants <1000g
o 60-70% infants 500-700g IVH
Overall incidence for severe cranial UTZ abn among PT
<1000g is 22%
Incidence of PVL from 2% to 7% over a 15yr period

PATHOGENESIS
IVH in premature occurs in the gelatinous subependymal
germinal matrix
Periventricular area site of origin for embryonal neurons &
fetal glial cells
Immature BV in the periventricular area + poor tissue vascular
support hemorrhage
Germinal matrix involutes as infant approaches FT
Periventricular hemorrhagic infarction (Grade 4)
o d/t venous congestion
Predisposing factors for IVH
o Prematurity
o Respiratory distress syndrome
o Hypoxic-ischemic or hypotensive injury
o Reperfusion injury of damaged vessels
o Inc or dec cerebral blood flow
o Reduced vasc integrity
o Inc venous pressure
o Pneumothorax
o Hypervolemia
o HPN
-

INTRACRANIAL-INTRAVENTRICULAR HGE &

PERIVENTRICULAR LEUKOMALACIA
ETIOLOGY
result from:
o trauma or asphyxia
o primary hemorrhagic disturbance
o congenital vascular anomaly
IC bleeding assoc w/:
o DIC
o Isoimmun thrombocytopenia
o Neonatal vit K deficiency

involves the ventricles of premature delivered spont w/o

apparent trauma

Patho of PVL involve both intrauterine & postnatal

Complex interaction bet:
o Cerebral vasculature & regulation of cerebral blood flow
o Disturbances in the oligodendrocyte precursors required for
myelination
o Maternal/fetal infection & inflamm
hypoxia-ischemia, venous obstruction from IVH or undetected
fetal stress dec perfusion to brain periventricular hge &
necrosis
PVL is charac by focal necrotic lesions in the periventricular
white matter & diffuse white matter damage
Risk for PVL inc in infants w/severe IVH & ventriculomegaly
Possible promoters of White matter d/o
o Fetal growth restriction
o Hypothyroxinemia
o Hypocarbia/hypercarbia
o Fetal vasculitis
o Maternal/placental infection
o Other cytokine promoters
Possible protectors against WMD
o Antenatal corticosteroids
o PG inhibitors
o Toxaemia/magnesium

CLINICAL MANIFESTATION
Majority have no clinical symp
Severe IVH acute deterioration on the 2nd or 3rd d of life
1st clinical indications
o Periods of apnea, Pallor or cyanosis
o Poor suck
o Abn eye signs
o High-pitched, shrill cry
o Muscular twitching, convulsions, dec mm tone
o Met acidosis
o Shock
o Dec Hct or failure of Hct to inc after transfusion
IVH rarely present at birth
o 50% 1st day of life
o 75% w/in 1st 3d of life
o Small % will have late hge bet 14-30d
o Rare after 1st mo of life as a primary event
PVL usu clinically asymp until neurologic sequelae of white
matter damage become apparent as spastic motor deficits
o Usu occurs later as an early echodense phase (3-10d of
life) ffd by typical echolucent (cystic) phase (4-10d of life)
Severity of hge define by location & degree of ventricular
dilatation from CT scan
G
Bleeding isolated to the subependymal
r
area
a
d
e
1
G
r
a
d
e
2
G
r
a
d
e
3
G
r
a
d
e

1
G
r
a
d
e
2
G
r
a
d
e

Intraventricular & parenchymal hge

4
-

3 levels of inc severity of IVH detected by UTZ

G
Bleeding confined to germinal matrixr
subependymal region or to<10% of the
a
ventricle (35% of IVH cases)
d
e

> 50% involvement w/ dilated ventricles

Bleeding w/in the ventricle but w/o

evidence of ventricular dilatation

Intraventricular hge w/ ventricular

dilatation

Intraventricular bleeding w/ 10-50% filling

of the ventricle (40% of IVH cases)

Ventriculomegaly defined as
M
0.5
il
cmd
1c
m
M
1o
1.5
d
cm
S
>1.
e
5c
v
m
e
r
e
DIAGNOSIS
IC hge suspected on basis of:
o History
o Clinical manif
o Knowledge of BW-specific risks for intraventricular hge
Assoc clinical signs of IVH are nonspecific or absent
Recommended: premature <34wk AOG do routine realtime cranial UTZ thru ant fontanel to screen for IVH
<1000g are at highest risk do cranial UTZ w/in 3-5d of age
UTZ preferred imaging technique for screening
1,001-1500g examine w/in 1st 7-14d of life
All at risk ff-up UTZ at 36-40wk PMA to eval adeq for PVL,
coz cystic changes r/t perinatal injury may not be visible for at
least 2-4wk
UTZ detects
o Precystic & cystic symmetric lesions of PVL
o Asymm intraparenchymal echogenic lesions of cortical
hemorrhagic infarction
Serial UTZ determines:
o Delayed devt of cortical atrophy
o Porencephaly
o Severity, progression or regression of posthemorrhagic
hydrocephalus
3-5% of VLBW develop posthemorrhagic hydrocephalus
VP shunt insertion

o If initial scan Abn, add interval UTZ to monitor devt of

hydrocephalus
IVH represents only one facet of brain injury in term or PT
MRI more sensitive tool for evaluation of extensive
periventricular injury
CT or diffusion-weighted MRI for FT in whom brain injury is
suspected coz UTZ may not reveal edema or
intraparenchymal hge & infarction

PROGNOSIS
Majority w/ grade 1 or 2 IVH have N neurodevt
30% <1000g w/ N cranial UTZ have CP or low cognitive
performance at 18mos
Assoc w/ poor prognosis (cerebral palsy & abn psychomotor
or cognitive outcome)
o Severe IVH (Grade 3 or 4)
o Progressive hydrocephalus requiring VP shunt
o Intraparenchymal hge
o Extensive PVL
Highest risk group has incidence of 32% severe IVH & 9%
PVL:
o <24wk
o <750g
o 1 min APGAR <3
Parenchymal lesions or ventricular enlargement high risk of
mental retardation at 6yr ff up
-

Most infants w/ IVH & acute ventricular distention do not

develop posthemorrhagic hydrocephalus
10% LBW w/ IVH develop hydrocephalus
o Enlarging HC
o Apnea
o Bradycardia
o Lethargy
o Bulging fontanel
o Widely split sutures
Symptomatic hydrocephalus clinical signs delayed 2-4wk
despite progressive ventricular distention w/ compression &
thinning of the cerebral cortex
Majority hav spont regression

PREVENTION
Improve perinatal care
Judicious mgt of CPD & operative delivery
Fetal or neonatal hge caused by maternal idiopathic
thrombocytopenic purpura or alloimmune thrombocytopenia
steroids, IV Ig or fetal PLT transfusion & CS
Women receiving Phenobarbital or phenytoin during preg
IV Vit K b4 delivery
Impt factors that may impact risk for devt of IVH and PVL
o Resp status & F/E mgt incl acidosis
o Hypocarbia
o Hypoxia
o Hypotension
o Wide fluctuation in neonatal BP
o Pneumothorax
Single course of antenatal corticosteroids:
o 24-34wk AOG at risk for preterm delivery

o Dec the risk of death, grade 3 & 4 IVH (betamethasone &

dexamethasone) & PVL (betamethasone only)
Prophylactic low-dose indomethacin (0.3mg/kg/d for 3d) to
VLBW PT reduces the incidence of severe IVH
o Dec cerebral blood flow
o Higher risk for cerebral ischemia

TTT
No ttt is available for IVH
Seizure anticonvulsant
Anemia & coagulopathy transfusion w/ PRBC or FFP
Shock & acidosis slow admin of NaHCO3 & fluid
resuscitation
progressive & symp posthemorrhagic hydrocephalus VP
shunt insertion
serial lumbar punctures, V-tap, reservoirs, & externalized
ventricular drains assoc risk of infxn & of
punctureporencephaly
HYPOXIA-ISCHEMIA

Anoxia - complete lack of oxygen

Hypoxia - decreased oxygen

Ischemia - decreased blood flow

hypoxic-ischemic encephalopathy - impt cause of permanent

damage to CNS tissues

greatest risk of adverse outcome

o
fetal acidosis pH < 7
o
5- min APGAR score of 0-3
o
altered tone
o
depressed level of consciousness
o
seizure
ETIOLOGY

fetal hypoxia caused by the ff

o
inadequate oxygenation of maternal blood
o
low maternal blood pressure from maternal blood
loss
o
excessive oxytocin use resulting to inadequate
relaxation of uterine muscles , thus, inadequate
placental filling
o
premature separation of placenta
o
knotting of cord
o
placental insufficiency

Doppler umbilical waveform velocimetry

o
demonstrate increased fetal vascular resistance

cordocentesis
o
demonstrating

fetal hypoxia

lactic acidosis
PATHOPHYSIOLOGY AND PATHOLOGY

hypoxia alone
o
not cause lethal brain injury
o
should be combined with ischemia

hypoxia and ischemia anaerobic metabolism generation

of
lactate

glutamate in damaged tissue

inc intracellular sodium and calcium tissue swelling and

edema

prodn of free radicals and nitric oxide shunting of blood

with transient perfusion of the
o
brain
o
heart
o
adrenals

CLINICAL MANIFESTATIONS

intrauterine growth with increased vascular resistance

o
first indication of fetal hypoxia

presence of metabolic and respiratory acidosis

cerebral edema
o
may develop in the next 24 hours
o
anticipate seizure

give Phenobarbital

seizure may also be d/t

hypocalcemia

hypoglycemia

infection
o
cranial nerve fxns are spared
DIAGNOSIS

UTZ
o
limited use in term infant with hypoxia
o
preferred modality for preterm infant

MRI
o
preferred modality d/t sensitivity

amplitude integrated EEG (aEEG)

o
determines which infants are at highest risk for
significant brain injury
TREATMENT

cerebral hypothermia
o
decrease rate of apoptosis
o
suppresses prodn of mediators known to be
neurotoxic
o
most effective when done within 6 hours upon injury

CHAPTER 100 DELIVERY ROOM

-

Most common delivery room emergency failure to initiate &

maint effective respirations

RESPIRATORY DISTRESS AND FAILURE

Disorder of respiration in newborn infant categorized into

o
central nervous system failure

depression of respiratory center

o
peripheral respiratory difficulty

interference w/ O2 and CO2 exchange

bilateral choanal atresia

o
if resp movt are made w/ mouth closed but infants fail to
move air in and out of lungs

hypoplasia of the mandible w/ post displacement of tongue

o
temporarily relived by pulling tongue or mandible forward

scaphoid abdomen
o
suggests diaphragmatic hernia

aka eventration

shift of apical impulse of heart

o
compatible w/ tension pneumothorax

pneumothorax on first day suggests

o
pulmonary hypoplasia
o
renal malformation

FAILURE TO INITIATE OR SUSTAIN RESPIRATION

usu in CNS as a result of asphyxia or peripherally d/t

neuromusc d/o

Common in preterm infants weighing < 1000g

Poorly sustained ventilation

o
Pulmonary hypoplasia assoc w/ oligohydramnioas as in
Potter synd
o
Bilateral pleural effusions (hydrops fetalis)
o
Severe intrauterine pneumonia

narcosis (loss of consciousness) to mother d/t

morphine, meperidine, fentanyl, barbiturates, or

tranquilizers administration b4 delivery

from maternal anesthesia during 2nd stage of labor

o
give naloxone hydrochloride (Narcan) 0.1mg/kg

given through
o
IV
o
SQ
o
intratracheal
o
IM

c/I
o
if mother has opiate addiction

precipitates neoneatal withdrawal with

seizure

repeat administration may be necessary d/t short

half-life
NEONATAL RESUSCITATION

fig 100-1 , p 724

goal: prevent morbidity & mortality assoc w/ hypoxic ischemic

tissue injury & to reestab adeq spont respiration & CO

room air
o
prefered initial gas for neonatal resuscitation

100% oxygen
o
if normal oxygen saturation was not achieved with room
air after 90 sec
o
initial gas used if pulmonary hypertension is suspected

successful ventilation determined by

o
adequate chest rise
o
symmetric breath sounds
o
improved pink color
o
HR > 100/ min
o
spontaneous respiration
o
presence of end-tidal CO2
o
improved tone

Umbilical vein
o
cannulated and used for immediate administration of
drugs using neonatal resuscitation

Epinephrine
o
given at 0.1-0.3 ml/k IV or intratracheal, repeated every
3-5 min
o
indications

asystole

failure to respond to combined resuscitation

given if pt does not respond to dopamine or

dobutamine

emergency volume expansion

o
isotonic crystalloid solution
o
O-negative RBC

sodium bicarbonate

given only after effective ventilation

because therapy increases blood CO2 , producing

respiratory acidosis, complicating an existing
metabolic acidosis
Restoration of O2 and tissue perfusion main ttt of met
acidosis assoc w/ asphyxia
dobutamine or dopamine
o
given first before epinephrine
o
continuous infusion
o

MECONIUM.

meconium staining
o
suction infant immediately even if shoulder is not yet
delivered
o
If good resp effort & HR >100/min suction w/ bulb or
suction cath
o
If infant is depressed & HR <100 tracheal intubation
and suctioning
SHOCK
Result of severe asphyxia or he during gestation. Labor or
delivery
Causes of bleeding
o
Hemolysis
o
Placental abruption, previa or tear
o
Traumatic injury to the UC or internal organs
o
IC bleeding
Clinical manif
o
Signs of resp distress
o
Cyanosis
o
Pallor
o
Flaccidity
o
Cold mottled skin
o
Tachy/bradycardia
Edema & hepatosplenomegaly hydrops fetalis or heart
failure w/o shock
Supportive ttt
o
type O Rh (-) blood for hge
o
N saline for hypovolemia
NaHCO3 for met acidosis
PNEUMOTHORAX

Higher risk in infants requiring (+) pressure ventilation or

those w/ meconium stained amniotic fluid

Emergent evacuation of pneumothorax w/o xray confirmation

indicated
o
Unresponsive to resuscitation efforts
o
Asymm breath sounds
o
Bradycardia
o
cyanosis

Transillumination
o
confirms the diagnosis
AIRWAY OBSTRUCTION

EXIT procedure
o
ex utero intrapartum procedure
o
allows time to secure airway in infants known to have
airway obstruction before infants are separated from
placenta

ABDOMINAL WALL DEFECTS

gastrochisis
o
more common defect
o
not covered by membrane
o
gently place the exposed intestine in a sterile clear
plastic bag after delivery

omphalocele
o
membrane often covers
o
care taken to prevent rupture

INJURY DURING DELIVERY

VISCERA

liver
o
only internal organ other than the brain that is frequently
injured
o
results from pressure from breech presentation
o
hepatic rupture subcapsular hematoma
o
appear normal for 1st 1-3d
o
early suspicion, UTZ dx & prompt supportive therapy

adrenal glands
o
adrenal hemorrhage appears with breech delivery, LGA
or infants w/ DM moms
o
may be d/t trauma, anoxia, or severe stress
o
90% are unilateral, 75% are R-sided
FRACTURES
Clavicle

s/s
o
does not move arm freely on affected side
o
crepitus or bony irregularity palpated
o
discoloration over affected site
o
moro reflex absent on affected side
o
spasm of sternocleidomastoid

treatment
o
immobilization

callus formation
o
develops within a week after tx
o
signifies fracture

fracture of humerus or brachial palsy

o
resp for limitation of movt & absence of moro reflex on
affected side
Extremities

fracture with humerus

o
2-4wk of immobilization

fracture of femur
o
traction-suspension of both lower extremities

Fracture of forearm
o
Splints

Dislocation and epiphyseal separation

o
Rarely from birth trauma
o
Forcible manipulation
o
Swelling, sligh shortening, limit movt, painful passive
motion and external rotation
Nose

most prevalent injury is dislocation of cartilaginous portion of

septum from the vomerian groove & columella

pe

o
o

flattened nose
asymmetric nares

pattern
Abd mass
Erythema of abd wall

CH102 Digestive System D/O

NEONATAL NECROTIZING ENTEROCOLITIS
Most common life-threatening emergency of the GIT in the NB
Charac by mucosal or transmural necrosis of the int
Multifactorial
Incidence is 1-5% in NICU
Inversely related to BW and AOG
PATHOLOGY & PATHOGENESIS
Factors contributing to devt of a necrotic segment of the int:
o
Gas accumulation in the submucosa of the bowel wall
(Pneumatosis intestinalis)
o
Progression of the necrosis to perforation, peritonitis &
death
Distal part of ileum & proximal segment of colon are most
involved
Assoc w/ intestinal immaturity
Triad:
o Intestinal ischemia (injury)
o Enteral nutrition (metabolic substrate)
o Pathogenic organisms
PREMATURITY greates R/F for NEC
Results from an interaction bet loss of mucosal integrity d/t:
o Ischemia, infection and inflammation
o Hosts response to that injury (circulatory, immunologic,
inflammatory)
Coagulation necrosis characteristic histologic finding of
intestinal specimens
E. Coli, Klebsiella, Clostridiium perfringens, S epidermidis and
rotavirus
In most, no pathogen is identified
Rarely occurs before initiation of enteral feeding
Much less common in infants fed human milk
Aggressive enteral feeding may predispose it
CLINICAL MANIFESTATIONS
Insidious or sudden catastrophic onset
Onset: 1st 2wk of life but can be upto 3mos in VLBW
Age of onset is inversely r/t AOG
1st signs of impending dse:
o Lethargy
o Temp instability
o Abd distention and gastric retention
Obvious bloody stools in 25%
Unusual to progress from mild to severe after 72H
GIT
Abd distention
Abd tenderness
Feeding intolerance
Delayed gastric
emptying
Vomiting
Occult blood in stool
Change in stool

SYSTEMIC
Lethargy
Apnea
Temp instability
Not right
Acidosis
Glucose
instability
Poor

perfusion/shock
DIC
(+) blood culture

DIAGNOSIS
A very high index of suspicion in treating preterm at risk
Plain Abd xrays make a dx of NEC
PNEUMATOSIS INTESTINALIS (air in the bowel wall)
diagnostic of NEC
Portal venous gas sign of severe dse
o Hepatic UTZ
Pneumoperitoneum indicates perforation
Differential dx: infections, GI obstruction, volvulus, isolated
intestinal perforation
o Idiopathic focal intestinal perforation occur spont or after
early use of postnatal steroids & indomethacin
TTT
No definitive ttt
Preventing further injury w/:
o Cessation of feeding
o Nasogastric decompression
o IVF
o Careful attention to resp status, coag profile & A/B balance
Systemic Abx for gram +/- & anaerobic
Ventilation for apnea, hypoxia or hypercapnia
Stabilize infant by:
o Intravasc volume replacement w/ crystalloid or blood
products
o cardiovascular support w/ volume & inotropes
o correction of hematologic, metabolic & electrolyte abn
sequential anteroposterior & cross-table lateral or lateral
decubitus abd x-rays to detect int perforation
Indications for surgery:
o Perforation on abd roentgenograms (pneumoperitoneum)
o (+) abd paracentesis (stool or organism on gram stain from
peritoneal fluid)
Relative indications for explore lap:
o Failure of med mgt
o Single fixed bowel loop on roentgenograms
o Abd wall erythema
o Palpable mass
Ideally, do surgery after intestinal necrosis but b4 perforation
& peritonitis
Peritoneal drainage
o Helpful for pxs in extremis w/ peritonitis who are unstable to
undergo surg
PROGNOSIS
Med mgt fails in 20-40% w/ pneumatosis intestinalis
Early postop complications:
o Wound infection
o Dehiscence
o Stomal probs (prolapse, necrsosis)
Later complications:
o Intestinal strictures at the site of the necrotizing lesion

Resection of the obstructive stricture

Complications of postop NEC:

o Short-bowel syndrome (malabsorption, growth failure,

malnutrition)
o Complications r/t central venous catheters (sepsis,
thrombosis)
o Cholestatic jaundice
Premature w/NEC who had surgery or who have concomitant
bacteremia inc risk for adverse growth & neurodevtal
outcome

PREVENTION
Exclusively breast-fed
Gut stimulation protocol of minimal enteral feeds ffd by
judicious volume advancement
Probiotic preparations
JAUNDICE & HYPERBILIRUBINEMIA IN THE NB
Jaundice during the 1st wk of life in
o 60% FT
o 80% PT
Yellow d/t accum of unconjugated, nonpolar, lipid-soluble
bilirubinn pigment in the skin
Unconjugated bilirubin neurotoxic
Conjugated bilirubin serious hepatic d/o or systemic
illnesses
ETIOLOGY
Fetal Stage
Adult Stage
Route of
Placenta
Hepatobiliary & GIT
elimination
bilirubin
Lipid-soluble unconj
Water-soluble conj
Unconjug hyperbilirubinemia
o Inc load of bilirubin to be metabolized by the liver

Haemolytic anemia

Polycythemia

Shortened red cell life as a result of immaturity or

transfused cells

Inc enterophepatic circ

Infection
o Damages or reduces the act of the transferase enz or other
related enzymes

Genetic def

Hypoxia

Infection

Thyroid def
o Competes or blocks the transferase enz

Drugs requiring glucuronic acid conjugation

o Leads to an absence or dec amts of enz or to redxn of
bilirubin uptake by liver cells

Genetic defect

Prematurity
-

R/F of severe hyperbilirubinemia of 35 or >wk AOG

o Major R/F

Predischarge TSB in the high-risk zone

Jaundice in the 1st 24H

Blood group incompatibility w/ (+) DAT

AOG 35-36wk

Previous sibling received phototherapy

Cephalohematoma or significant bruising

Exclusive BF

East asian race

o Minor R/F

Predischarge TSB in the high intermed risk

AOG 37-38wk

Jaundice b4 discharge

Previous sibling w/ jaundice

Macrosomic infant of DM mom

Maternal age >25

Male gender
o Decreased risk

TSB in the low-risk

AOG >41wk

Exclusive bottle feeding

Black race

Discharge from hospital after 72H

CLINICAL MANIFESTATION
Cephalocaudal progression
o Face 5mg/dl
o Mid-abd 15mg/dl
o Soles 20mg/dl
Clinical exam cnt be depended on to estimate serum levels
Jaundice 5-8mg/dl
Jaundice from
Bright yellow or
deposition of indirect
orange
bilirubin
Obstructive Jaundice
Greenish or muddy
yellow
Present w/ lethargy & poor feeding w/ttt may progress to
acute bilirubin encephalopathy
DIFFERENTIAL DIAGNOSIS
1. Jaundice in 1st 24H of life
o
Erythroblastosis fetalis

Unusually high proportion of direct-reacting bilirubin

in infants who hav received intrauterine transfusions
for erythroblastosis fetalis
o
Concealed hge
o
Sepsis
o
Congenital infxn (syphilis, CMV, rubella, toxoplasmosis)
2. 2nd or 3rd day
o
Usu physiologic
o
Familial non-hemolytic icterus (Crigler Najjar synd)
o
Early-onset BF jaundice
3. 3rd day 1 wk
o
Bacterial sepsis
o
UTI
o
Infxns s/a syphilis, toxoplasmosis, CMV or enterovirus
4. After 1st wk
o
Breast-milk jaundice
o
Septicaemia
o
Congenital atresia
o
Paucity of the bile ducts
o
Hepatitis
o
Galactosemia
o
Hypothyroidism
o
CF

Congenital haemolytic anemia crisis r/t red cell

morphology & enz deficiencies
1st mo
o
Hyperalimentation-assoc cholestasis
o
Hepatitis
o
Cytomegalic inclusion dse
o
Syphilis
o
Toxoplasmosis
o
Familial non-hemolytic icterus
o
Congenital atresia of the bile ducts
o
Galactosemia
o
Inspissated bile syndrome ff haemolytic dse of NB
o

5.

FT, low risk, asymp monitor TSB

Significant hyperbilirubinemia complete dx eval:
o Direct & indirect bilirubin fractions
o Hgb
o Retic ct
o Blood type
o Coombs test
o Periph blood smear
Hemolysis
o Indirect hyperbilirubinemia
o Reticulocytosis
o Smear w/ evidence of RBC destruction
Differential for direct hyperbilirubinemia
o Hepatitis
o Congenital bile duct d/o (atresia, paucity, byler dse
o Inborn errors of metabolism
o CF
o Sepsis

PHYSIOLOGIC JAUNDICE (ICTERUS NEONATORUM)

N indirect- reacting bilirubin in UC = 1-3mg/dl
Rises at a rate of <5mg/dl/24H
Infa
Ons
Pea
nt
et
k

2nd3rd d

Res
oluti
on
4th5th d

2nd
&3rd
d
1012m
g/dl
PT
3rd6th7thth
th
4 d
8 d
9th d
15m
g/dl
Inc bilirubin prodxn from breakdown of fetal rbc w/ limitation in
conjugation of bilirubin by the immature liver
R/F for elevated indirect hyperbilirubinemia:
o Maternal age
o Race (Chinese, Japanese, Korean, Native Ame)
o Maternal DM
o Premature
o Drugs (vit K, novobiocin)
o Altitude
o Polycythemia
o Male
FT

o Trisomy 21
o Cutaneous bruising
o Blood extravasation (cephalhematoma)
o Oxytocin induction
o BF
o Wt loss
o Delayed bowel movt
o Fam fx who had physiologic jaundice
Prediction based on the 1st 24-72H
Indirect bilirubin dec to adult (1mg/dl) by 10-14d
Persistent indirect hyperbilirubinemia beyond 2 wk suggests:
o Hemolysis
o Hereditary glucuronyl transferase def
o Breast-milk jaundice
o Hypothyroidism
o Int obstruction
Jaundice assoc w/ pyloric stenosis
o Caloric deprivation
o Def of hepatic UDP-glucuronyl transferase
o Inc in enterohepatic circulation of bilirubin from ileus
Dx estab only by precluding known causes of jaundice on
basis of hx, clinical findings, and labs
Determine cause of jaundice:
o Appears 1st 24-36H of life
o Serum bilirubin rising at a rate faster than 5mg/dl/H
o Serum bilirubin >12mg/dl in FT or 10-14mg/dl in PT
o Jaundice persists after 10-14d of life
o Direct-reacting bilirubin is 2mg/dl
Other factors suggesting nonphysiologic cause of jaundice:
o Hemolytic dse
o Pallor
o Hepatomegaly
o Splenomegaly
o Failure of phototherapy
o Vomiting
o Lethargy
o Poor feeding
o Excessive wt loss
o Apnea
o Bradycardia
o Abn v/s (hypothermia)
o Light-colored stools
o Dark urine positive for bilirubin
o Signs of kernicterus

PATHOLOGIC HYPERBILIRUBINEMIA
Assoc r/f:
o Asian race
o Prematurity
o Breast-feeding
o Wt loss
Gilbert syndrome def or inactivity of bilirubin glucuronyl
transferase
G6PD def & mutation of promoter region of UDP-glucuronyl
transferase -1 indirect hyperbilirubinemia in the absence of
signs of hemolysis
Greatest risk: BILIRUBIN-INDUCED NEURO DYSFXN
o
Occurs w/ high indirect bilirubin
Kernicterus (bilirubin encephalopathy) depends on
o Level of indirect bilirubin

o Duration of exposure to elevated levels

o Cause of jaundice
o Infants well-being
Neurologic injury occurs at lower bilirubin in:
o Preterm
o Asphyxia
o IVH
o Hemolysis
o Drugs that displace bilirubin from albumin

JAUNDICE ASSOC W/ BREASTFEEDING

Breast-milk jaundice
o
In 2% of breast-fed FT after 7thd of life
o
d/t presence of glucuronidase in some milk
o
Max conc 10-30mg/dl during the 2nd-3rd wk
o
If BF cont., bilirubin may persist for 3-10wks at lower
levels
o
If discontinued, bilirubin falls rapidly
o
Resumption of BF, bilirubin return to prev high levels
o
Phototherapy beneficial
Breast-feeding jaundice
o
1st wk of life
o
Hyperbilirubinemia (>12mg/dl) in 13%
o
d/t dec milk intake w/ dehydration & dec caloric intake
o
d/t giving supplements of glucose water to breast-fed
infants
o
ttt:
1. Frequent BF (>10/24H)
2. Rooming-in w/ night feeding
3. Discouraging 5% dextrose or water supplementation
4. Ongoing lactation support
CONGENITAL ATRESIA OF THE BILE DUCTS
>2 wk or assoc w/ acholic stools & dark urine
Immed dx eval incl det of direct bilirubin
KERNICTERUS
Bilirubin encephalopathy
Deposition of unconj bilirubin in the basal ganglia & brainstem
nuclei
Multifactorial & involves interaction bet:
o Unconjug bilirubin levels
o Alb binding & unbound bilirubin levels
o Passage across the BBB
o Neuronal susceptibility
Kernicterus is rare
o in healthy FT
o in absence of hemolysis if serum is <25mg/dl
In BF infants, Kernicterus when bilirubin >30mg/dl
Onset: 1st wk of life
The more immature, the more susceptible
CLINICAL MANIFESTATIONS
o Acute form
o
Phase 1 (1st 1-2d): poor suck, stupor, hypotonia, seizures
o
Phase 2 (middle of 1st wk): hypertonia of extensor mm,
opisthotonus, retrollis, fever
o
Phase 3 (after 1st wk): hypertonia
o Chronic form

1st yr: hypotonia, active DTR, obligatory tonic neck reflex,

delayed motor skill
2nd yr: opisthotonus & seizures abate but irreg involuntary
movt, mm rigidity, hypotonia inc steadily
By 3 yr: movt d/o (choreoathetosis, ballismus, tremor),
upward gaze, sensorineural hearing loss, mental
deficiency, dysarthric speech, seizures, extrapyramidal
signs, squinting

PATHOLOGY
Stained yellow by unconj bilirubin:
o Corpus subthalamicum
o Hippocampus
o Adjacent olfactory areas
o Striate bodies
o Thalamus
o Globus pallidus
o Putamen
o Inferior clivus
o Cerebellar nuclei
o Cranial nerve nuclei
Nonpigment areas damaged, charac by:
o Neuronal loss
o Reactive gliosis
o Atrophy of involved fiber systems inn late dse
Bilirubin interferes w/ O2 utilization by cerebral tissue, by
injuring the cell membrane
INCIDENCE & PROGNOSIS
Kernicterus in 1/3 of infants w/ unttt hemolytic dse & bilirubin
>25-30mg/dl
Overt neurologic signs have a grave prognosis
75% die
80% affected survivors bilateral choreoathetosis w/
involuntary muscle spasm
PREVENTION
Some recommened universal screening for hyperbilirubinemia
in 1st 24-48H of life
Preventable causes of kernicterus (AAP):
o Early discharge <48H w/ no early ff-up, esp in 35-37wk AOG
o Failure to check bilirubin if jaundice in the 1st 24H
o Failure to recognize r/f for hyperbilirubinemia
o Underestimation of severity of jaundice by clinical assx
o Lack of concern regarding presence of jaundice
o Delay in meas bilirubin despite marked jaundice or delay in
phototherapy in elevated bilirubin
o Failure to respond to parental concern regarding jaundice,
poor feeding, lethargy
AAP Mgt guideline for infants at least 35wk:
o Jaundiced <24H requires meas of bilirubin, infant eval for
poss hemolytic dse
o Ff-up w/in 2-3d of discharge to all neonates discharged
<48H after birth, esp 38wk AOG
Advice to nurse infant q 2-3H
Avoid routine supplement w/ water or glucose H2O
TTT OF HYPERBILIRUBINEMIA
Prevent indirect-reacting bilirubin related neurotoxicity
Primary ttt:

o Phototherapy
o Exchange transfusion
Phototherapy require 6-12H to have a measurable effect

Phototherapy
Bilirubin absorbs light maximally in the blue rang (420-470nm)
Major product from phototherapy is a result of reversible
photo-isomerization reaction
Other major product from phototherapy is lumirubin
Therapeutic effect of phototherapy depends on:
o Light energy emitted in the effective range of wavelengths
o Distance between the lights & the infant
o Surface area of exposed skin
o Rate of hemolysis & in vivo metabolism
o Excretion of bilirubin
special blue fluorescent tubes, placing lamps w/in 15-20cm
of infant
Reduce the need for exchange transfusions
Bilirubin & Hct monitored q 4-8H
Bilirubin monitoring cont at least 24H after cessation of
phototherapy
Complications assoc w/ phototherapy:
o Loose stools
o Erythematous macular rash
o Purpuric rash assoc w/ transient porphyrinemia
o Overheating
o Dehydration
o Hypothermia from exposure
o Bronze baby syndrome dark, grayish-brown skin
discoloration in infants undergng phototherapy
C/I: porphyria
Infants eyes shud b closed to prevent light exposure &
corneal damage
Meas directly & details of exposure recorded (type & age of
bulbs, duration of exposure, distance from the light source to
infant)
Monitor for anemia

IV Ig
Adjunctive ttt for hyperbilirubinemia d/t isoimmune hemolytic
dse
Recommended when bilirubin is approaching exchange levels
despite maximal interventions including phototherapy
0.5-1g/kg/dose repeat in 12H

Metalloporphyrins
Alt therapy for hyperbilirubinemia
Competitive enzymatic inhib of the rate limiting conversion of
heme-protein to biliverdin by heme-oxygenase
Single IM dose on the 1st day of life may reduce need for
phototherapy
Beneficial for:
o ABO incomp
o G6PD def
o when blood products are discouraged as w/ jehovahs
witness
Complications: Transient erythema if receiving phototherapy
Exchange Transfusion

If intensive phototherapy has failed to reduce bilirubin to a

safe range
If risk of kernicterus exceeds the risk of procedure
Potential complication
o Met acidosis
o Electrolyte abn
o Hypoglycemia
o hypoCa
o thrombocytopenia
o volume overload
o arrhythmia
o NEC
o Infection
o Graft vs Host dse
o Death
>25mg/dl
Mgt of NB readmitted for Phototherapy or exchange
transfusion
If TSB >25mg/dl or >20mg/dl in a sick infant or infant <38 wk
AOG do blood type & crossmatch
If isoimmune hemolytic dse & TSB rising in spite of
phototherapy IV Ig 0.5-1g/kg over 2H & repeat in 12H if
needed
If wt loss >12% or evidence of dehydration formula or
expressed breast milk
For infants receiving intensive phototherapy
o Breastfeed or bottle feed q 2-3H
o If TSB >25mg/dl repeat TSB w/in 2-3H
o If TSB 20-25mg/dl repeat w/in 3-4H
o If TSB is not dec or is moving closer to level for exchange
transfusion exchange transfusion
o If TSB is <13-14mg/dl discont phototherapy

CH103 Blood D/O

ANEMIA IN THE NEWBORN
Hgb inc w/ advancing AOG
Cord blood Hgb
o At term - 16.8g/dl (14-20g/dl)
o VLBW 1-2g/dl below those at term
Anemia - < than normal range of hgb for BW & postnatal age
Physiologic dec in hgb content
o At 8-12wk in term (Hgb 11g/dl)
o At 6 wk in PT (7-10g/dl)
CS have lower hct
Anemia at birth
o manif as:

Pallor

Heart failure

Shock
o d/t

Acute or chronic fetal blood loss

Hemolysis

Underproduction of erythrocytes
o Cause

Hemolytic dse of NB

Tearing or cutting of UC during delivery

Abn cord insertion

Communicating placental vessels

Placenta previa or abruption

Nuchal cord
Incision into placenta
Internal hge (liver, spleen, intracranial)
@-thalassemia
Congenital parvovirus infection
Hypoplastic anemia
Twin-twin transfusion in monozygotic twins w/ AV
placental connections

Transplacental hemorrhage
o Bleeding from the fetal into the maternal ciruculation in 515% preg
o DX:

Kleihauer-Betke test demonstrate significant amts

of fetal hgb & RBCs in maternal blood on day of
delivery

Cytometry methods to detect fetal cells in blood

o If severe anemia w/ heart failure emerg exchange
transfusion

Acute blood loss results in severe distress at birth

o Initially w/ a N hgb, no hepatosplenomegaly & early onset of
shock

Chronic blood loss

o Marked pallor, less distress, low hgb w/ microcytic indices
o If severe, Heart failure
Anemia in first few days after birth
o Hemolytic dse of NB mos freq
o Hemorrhagic dse of NB
o Bleeding from improperly tied or clamped UC
o Large cephalohematoma
o IC hge
o Subcapsular bleeding from rupture of liver, spleen, adrenals
or kidneys
Delayed anemia result of hemolytic dse of NB w/ or w/o
exchange transfusion or phototherapy
1st mo of life
o Congenital hemolytic anemia (spherocytosis)
Neonatal pd 2ndary to G6PD def & pyruvate kinase
o Hereditary nonspherocytic hemolytic anemia
Bleeding
o Hemangiomas of the Upper GIT
o Ulcers caused by aberrant gastric mucosa in a meckel
diverticulum
common cause of anemia among hospitalized
o Repeated blood sampling
Causes anemia in infants maintained on TPN
o Def of minerals s/a copper
Anemia of prematurity
o In LBW 1-3mos after birth
o Assoc w/ hgb 7-10g/dl
o Manif as:

Pallor

Poor wt gain

Dec act

Tacypnea

Tachycardia

Feeding probs
o Contributing factors:

Repeated phlebotomy for blood tests

Shortened RBC survival
Rapid growth
Transition from fetal (low PaO2 & hgb sat) to
neonatal life (high PaO2 & hgb sat)

TTT of neonatal anemia by BT depends on:

o Severity
o Hgb level
o Co-morbid dse that interfere w/ O2 delivery

Brochopulmonary dysplasia

Cyanotic CHD

Resp distress syndrome

o Risk of transfusion

Hemolytic transfusion rxns

Exposure to blood product preservatives

Inc risk of ROP

NEC

Graft vs host rxn

Transfusion-acquired infection (CMV, Parvovirus,

Hep B & C)
o Risk of CMV eliminated by use of leukoreduced blood
o <1500g use CMV Abs-(-) leukoreduced blood
o HIV & hep B & C Abs screening of donated blood
o Asymp FT w/ Hgb 10g/dl monitored
o Warrant transfusion

Symptomatic born after abruption placenta

w/ severe hemolytic dse of NB

o RBC transfusion

PT w/ repeated episodes of apnea & bradycardia

Hgb 8g/dl or lower

Asymp neonates w/ Reticulocytopenia & hgb <7g/dl

o In need of hgb levels 12-14g/dl

Respiratory distress symd

Severe bronchopulmonary dysplasia

o No transfusion needed

Mild asymp anemia

o PRBC (10-20ml/kg ) at a rate of 2-3ml/kg/hr

2ml/kg raises hgb 0.5-1g/dl

o Hge shud be ttt w/ whole blood

Alt: fluid resuscitation ffd by PRBC

o Recombinant human erythropoietin to prevent or ttt
chronic anemia assoc w/:

Prematurity

BPD

Hyporegenerative anemia of erythroblastosis fetalis

o Therapy w/ r-HuEPO must be supplemented w/ iron & poss
vit E
o Routine use of erythropoietin not recommended in VLBW

HEMOLYTIC DISEASE OF THE NEWBORN

-a.k.a. Erythroblastosis fetalis
- caused by passage of maternal Ab against paternal RBC Ag
-characterized by inc. destruction of RBCs
-More than 60 different Ag are responsible but the MOST
COMMON are:
a. D Antigen of the Rh Group (90%)
b. ABO Incompatibility

1.

Hemolytic Disease of the Newborn due to Rh Incompatibility

90% of cases
10% are due to C or E antigen

Pathogenesis
3x more frequent among whites than blacks
Rh (+) blood enters the circulation of a Rh(-) woman OR
when >1mL of Rh(+) fetal blood enters a Rh (-) womans
circulation in the ff. cases:
a. Maternal-fetal circulation
b. Abortion
c. During delivery
FORMATION OF D-ANTIBODIES
IgM initially is formed first later IgG is formed. IgG
crosses the placenta and causes hemolysis
RARE in the first pregnancy because transfusion occurs
in the ff:
a. Near the time of delivery
b. Too late for the mother to form antibodies
Small chance of sensitization d/t:
a. 55% of Rh(+) fathers are heterozygous (D/d)
b. Fetal-maternal transfusion occurs in only 50% of
preg.
Inject anti-D gamma globulin (RhoGAM) into the mother
immed after delivery of each Rh(+) infant
Clinical Manifestations
Compensatory capacity of hematopoietic system is
exceeded Profound anemia pallor, signs of cardiac
decompensation, massive anasarca, & circulatory
collapse
Hydrops fetalis excessive abn fluid in 2/more fetal
compartments (skin, pleura, pericardium, placenta,
peritoneum, amniotic fluid)
Severity of hydrops r/t:
a. Level of anemia
b. Degree of reduction in serum alb d/t hepatic dysfxn
Heart failure inc R heart pressure edema & ascites
Pulmonary edema or bilateral pleural effusions birth
asphyxia
Dec PLT prodxn or (+) concurrent DIC Petechiae,
purpura & thrombocytopenia
In severe, bilirubin pigments stain the ff yellow:
a. Amniotic fluid
b. Cord
c. Vernix caseosa
Jaundice generally evident on 1st day of life coz bilirubinconjugating and excretory system are unable to cope w/
load massive hemolysis
Indirect-reacting bilirubin accum. risk of bilirubin
encephalopathy
Hypoglycemia r/t hyperinsulinism & hypertrophy of
pancreatic islet cells
High cord levels of bilirubin severe hemolysis
s/s of erythroblastosis may be superimposed resulting
from spont or induced premature delivery
Laboratory Data
(+) direct Coombs test and anemia
cord blood Hgb content proportional to severity of dse

o
hydrops fetalis 3-4g/dl
blood smear shows polychromasia & marked inc in
nucleated RBCs
inc reticulocyte ct
N or inc WBC
thrombocytopenia in severe
cord bilirubin 3-5mg/dl

Diagnosis
DDX: demo of blood group incompatibility and
corresponding Abs bound to the infants RBC
Antenatal Dx
Possibility of sensitization in Rh (-) women
o
Hx of previous transfusion
o
Prev Abortion
o
Prev pregnancy
Test for potential incompatibility
Maternal titer of IgG Abs to D antigen assayed at 12-16,
28-32, 36 wk
Hemolytic dse if:
a. Elevated Abs titer at beginning of preg
b. Rapid rise in titer of 1:64
Abs titer against D antigen at a titer of 1:16 during a
subseq preg Doppler UTZ of the middle cerebral
artery then PUBS
Real-time UTZ used to detect progression of dse
Early UTZ signs of hydrops:
a. Organomegaly
b. Double-bowel wall sign (bowel edema)
c. Placental thickening
Progression of hydrops to:
a. Polyhydramnios
b. Ascites
c. Pleural or pericardial effusions
d. Skin or scalp edema
Hydrops when fetal Hgb <5g/dl and frequent when
<7g/dl
Real-time UTZ predicts fetal well-being by the Biophys
profile
Doppler UTZ assesses fetal distress by demonstrating
inc vascular resistance in fetal art. (middle cerebral)
UTZ guided transabdominal aspiration of amniotic fluid
performed at 18-20 wks AOG
Spectrophotometry measures bilirubin that enters the
amniotic fluid
Risks of amniocentesis and cordocentesis:
a. Fetal death
b. Fetal bleeding
c. Fetal bradycardia
d. Worsening of alloimmunization
e. PROM
f.
Preterm labor
g. Chorioamnionitis
In fetus w/o hydrops anemia detected by inc in peak
velocity of systolic blood flow in the middle cerebral art by
Doppler UTZ
PUBS std approach to assess the fetus if Doppler &
real-time UTZ suggest an affected fetus
PUBS performed:

a.
b.

To determine fetal Hgb levels

To transfuse PRBCs in serious fetal anemia (Hct 2530%)

Postnatal Dx
Immed after birth of any infant to an Rh (-) woman
Blood from UC or infant examined for ABO, Rh type, Hct
and Hgb and Direct Coombs test
(+) Coombs meas baseline serum bilirubin & RBC
panel to ID RBC Abs present in mothers serum
Treatment
Main Goals:
a. Prevent intrauterine or extrauterine death from
severe anemia & hypoxia
b. Avoid neurotoxicity from hyperbilirubinemia
1. Treatment of an unborn Infant
Intravascular (umbilical v) transfusion of PRBC ttt of
choice for fetal anemia
Hydrops or fetal anemia (Hct <30%) indication for
umbilival vein transfusion in infants w/ pulmo immaturity
Intravascular fetal transfusion
o
Sedation w/ diazepam
o
Fetal paralysis w/ pancuronium
Transfusion should achieve a post-transfusion Hct of 4555% & repeated q 3-5wk
Indications for delivery:
o
Pulmonary maturity
o
Fetal distress
o
Complications of PUBS
o
35-37wk AOG
Survival rate for intrauterine transfusions 89%
Complication rate is 3%
o
Rupture of memb & preterm delivery
o
Infection
o
Fetal distress requiring CS
o
Perinatal death
2.
-

3.
-

TTT of a liveborn infant

Fresh. Low titer, group O, leukoreduced & irradiated Rh
(-) blood
signs of severe hemolytic anemia evident at :
o
birth
o
immed resuscitation & supportive therapy
o
temp stabilization
o
monitoring before proceeding w/ exchange
transfusion
correction of acidosis w/ 1-2meg/kg of NaHCO3
small transfusion of compatible PRBCs for anemia
volume expansion for hypotension
assisted ventilation for resp failure
Exchange Transfusion
Additional factors for deciding early exchange
transfusion:
o
Previous kernicterus or severe erythroblastosis in a
sibling
o
Retic ct >15%
Hgb, hct & serum bilirubin meas q 4-6H
FT w/ 20mg/dl or > inc risk of kernicterus

Rh (-), leukoreduced and irradiated RBCs to correct

anemia in dse up to 6-8wk of age
Dangerously high levels of serum bilirubin:
o
>6mg/dl in 1st 6H
o
10mg/dl in 2nd 6H
o
Rate of rise >0.5-1mg/dl/H
Meas of unbound bilirubin more sensitive predictor of
risk assoc w/ hyperbilirubinemia
Before delivery
o
Type O, Rh (-) donor w/ low titer of anti-A and anti-B
antibodies
o
Shud b compatible w/ moms serum by indirect
coombs test
After delivery
o
Rh (-) donor whose cells are compatible w/ both
infants & mothers serum
o
Type O generally used
o
If infant & mom has same blood type use same
blood type
Before 2nd & subsequent transfusions
o
Complete cross match
o
Indirect coombs test
Whole blood or packed leukoreduced and irradiated
RBCs reconstituted w/ FFP to an Hct of 40%
Exchange carried out over a 45-60minn period, w/
aspiration of 20ml of infant blood alt w/ infusion of 20ml
of donor blood
o
Smaller aliquots (5-10ml) for sick & PT
Goal: isovolumetric exchange of two blood volumes of
infant (2 x 85ml/kg)
Acidosis & hypoxia from resp distress, sepsis or shock
compromised by acute acid load in citrated blood do
Fresh heparinized blood
Blood pH & PaO2 monitored coz infant become acidotic
& hypoxic during exchange transfusion
Acute Complications:
o
5-10% infants
o
Transient bradycardia w/ or w/o Ca infusion
o
Cyanosis
o
Transient vasospasm
o
Thrombosis
o
Apnea w/ bradycardia requiring resusc
o
Death
o
NEC - rare
Infectious risks: CMV, HIV, hepatitis
After exchange transfusion, bilirubing level meas q 4-8H
bilirubin may rebound 40-50% w/in H
Late complications
o
Anemia

Hemolytic or hyporegenerative

Ttt: iron, erythropoietin, blood transfusion

Mild graft vs host rxn manif as diarrhea rash,

hepatitis or eosinophilia
o
cholestasis
Inspissated bile syndrome
o
Persistent icterus in assoc w/ elevations in direct
and indirect bilirubin in infants w/ hemolytic dse
o
Clears spont w/in wks or mos
Portal vein thrombosis & portal HPN
o
Children subjected to exchange transfusion as NB

Assoc w/ prolonged, traumatic, or septic umbilical

vein cath
Prevention of Rh Sensitization
o
300ug of Human anti-D globulin (1ml of RhoGAM)
IM w/in 72H of delivery of:

Rh (+) infant

Ectopic preg

Abd trauma in preg

Amniocentesis

Chorionic villus biopsy

Abortion
o
This qty is sufficient to eliminate 10ml of antigenic
fetal cells from maternal circ
o
RhoGAM admin at 28-32wk & again at birth (40wk)
more effective than single dose
o

HEMOLYTIC DSE OF THE NB CAUSED BY BLOOD GROUP A

& B INCOMPATIBILITY
Most common cause of hemolytic dse of NB
15% of live births at risk
0.3-2.2% manifests
Results in milder
Generally type A1 more antigenic
IgM do not cross the placenta
IgG - Cross placenta
o found in moms who have become immunized against A or B
factors from a previous incompatible preg
Immune Abs - primary mediators in ABO isoimmune dse
CLINICAL MANIFESTATIONS
Weakly to mod (+) Coombs test & spherocytes in blood smear
HS
Hgb is normal or as low as 10-12g/dl
Retic ct inc 10-15%
Extensive polychromasia & inc nus of NRBCs
DIAGNOSIS
Exchange transfusion w/ type O blood of the same Rh type as
the infant
Post-discharge monitoring of Hgb/Hct
OTHER FORMS OF HEMOLYTIC DSE
PUBS meas fetal Hct
Congenital infxn (cytomegalic inclusion dse, toxoplasmosis,
rubella & syphilis)
o Anemia
o Jaundice
o Hepatosplenomegaly
o Thrombocytopenia
o (-) direct coombs test
Homozygous @-thalassemia assoc w/ severe hemolytic
anemia
o (-) direct coombs test
HS & other red cell membrane defects
o Anemia & jaundice
o kernicterus
Congenital def s/a pyruvate kinase or G6PD
o Hemolytic anemia producing jaundice in 1st wk of life
PLETHORA IN THE NB (POLYCYTHEMIA)

ruddy, deep red-purple appearance assoc w/ a high hct d/t

polycythemia
Central Hct 65% or >
Incidence of neonatal polycythemia inc at:
o High altitudes
o Postmature (3%) vs term (1-2%)
o SGA (8%) vs LGA (3%) v save (1-2%)
o 1st day of life (peak 2-3H)
o Recipient infant of twin-twin transfusion
o Delayed clamping of UC
o Infants of DM moms
o Trisomy 13,18,21
o Adrenogenital syndrome
o Neonatal graves dse
o Hypothyroidism
o Infants of HPN moms or those on propanolol
o Beckwith-Wiedemann syndrome
o Growth restriction exposed to chronic fetal hypoxia

CLINICAL MANIFESTATIONS
Irritability
Lethargy
Tachypnea
Respiratory distress
Cyanosis
Feeding disturbances
Hyperbilirubinemia
Hypoglycemia
Thrombocytopenia
Severe complications:
o Seizure
o Stroke
o Pulmo HPN
o NEC
o Renal vein thrombosis
o Renal failure
Hyperviscosity present
o In central Hct values of 65% or >
o When whole blood viscosity is >18cycles/sec
o Coz neonatal RBCs have dec deformability & filterability
stasis in the microcirculation
TTT
Symptomatic polycythemic NB
o Partial exchange transfusion w/ N saline
Asymptomatic
o Partial exchange NOT considered if Hct is <70-75%
Volume to be exchanged = blood volume X (Observed
desired Hct/observed Hct)
Reported adverse outcomes:
o Speech deficits
o Abn fine motor control
o Reduced IQ
o School probs
o Other neuro abn
HEMORRHAGE IN THE NB
NORMAL: Mod dec in factors 2, 7, 9, 10 occurs by 48-72H
after birth w/ gradual return to birth levels by 7-10d of age
Transient def of Vit K- dependent d/t

1.
2.
3.
-

o lack of free vit K from mom

o absent bact intestinal flora for synth of vit K
prolongation of def bet 2nd-7thd spont & prolonged bleeding
prevented by vit K therapy

CNS or bleeding posing immed threat to life

o FFP, Vit K and Blood asap

Swallowed blood syndrome

o Blood or bloody stools are passed
o 2nd or 3rd d of life
o Confused w/ hge of GIT
o Swallowed during delivery or from fissure in moms nipple

Early-onset
Birth to 24H
Site of hge: cephalohematoma, subgaleal, intracranial, GIT,
umbilicus, intraabd
Etiology: Phenobarbital, phenytoid, warfarin, rifampin, INH,
inherited coagulopathy
Prevention: vit K at birth or to mom (20mg) b4 birth
Incidence: very rare
Classic dse
2-7d
Site: GIT, ear-nose-throat-mucosal, intracranial, circumcision,
cutaneous, injection sites
Etiology: Vit K def, BF
Prevetion: parenteral vit K at birth, oral vit K require repeated
dosing over time
Incidence: 2% if not given vit K
Late onset
1-6mos
SiteL intracranial, GIT, cutaneous, ear-nose-throat-mucosal,
injection sites, thoracic
Etiology: Cholestasis malabsorption of vit K ( biliary atresia,
CF, hepatitis), abetalipoCHON def, idiopathic in asian BF
infants, warfatin ingestion
Prevention: parenteral & high dose oral vit K during
malabsorption or cholestasis
Incidence: depend on primary dse
Resulting from severe transient def in vit K-dependent factors
is charac by:
o Bleeding that thends to be GIT, nasal, subgaleal, IC or
postcircumcision
PT, blood coag time & PTT prolonged
Factors 2, 7, 9, 10 decreased
1mg of vit K IM in FT infants
o Not uniformly effective in prophylaxis in PT
Slow IV infusion of 1-5mg of Vit K1 in hemorrhagic dse
Serious bleeding in PT or w/ liver dse transfuse FFP or
whole blood
Severe form of def of Vit K-dep coag factors in infants born to
moms receiving phenobarbital & phenytoin
o Severe bleeding in 1st 24H of life
o PT shud b obtained
o Give 1-2mg of vit K IV
o If PT is still prolonged 10ml/kg of FFP

Infants
Fetal hgb
Alkali-resistant

DIC
o Results in consumption of coagulation factors & bleeding
o Often PT
o Charac by asphyxia, hypoxia, acidosis, shock,
hemangiomas, infxn
o Correct primary clinical prob:

Infection

Interrupting consumption

Replacing clotting factors

Test gives a Pink

rxn
Widespread SQ ecchymoses
o in PT or immed after birth
o Result of fragile superficial BV
o Vit K1 to mom during labor has no effect
o venous obstruction by nuchal cord or sudden inc in
intrathoracic pressure during delivery gen bluish
suffusion to face, head & neck
o 2-3wk for suffusion to disappear

CH107 the Endocrine System

1.

2.

3.
4.
5.
6.
7.

8.

9.
-

Adult
Adult hgb
Promptly
changed to
alkaline hematin
Yellow-brown rxn

Pituitary dwarfism not apparent at birth

a. panhypopituitary male infants have neonatal
hypoglycemia, hyperbilirubinemia, micropenis
Primary hypothyroidism asymp at birth
a. cretinism - Constipation, prolonged jaundice, goiter,
lethargy, poor periph circulation (mottled skin or cold
extremities
b. Infants of moms receiving antithyroid meds
Transient hypothyroxinemia most common in ill VLBW
Transient hyperthyroidism infants of moms w/
hyperthyroidism or moms w/ thyroid meds
Transient hypoparathyroidism manif as tetany of NB
Acute adrenal hge after breech or other traumatic
deliveries or in assoc w/ overwhelming infxn
Congenital adrenal hyperplasia suggested by vomiting,
diarrhea, dehydration, hyperK, hypoNa, shock, ambiguous
genitals or clitoral enlargement
Gonadal dysgenesis webbing of neck, lymphangiectactic
edema, hypoplasia of the nipples, cutis laxa, low hairline at
nape of neck. Low-set ears, high-arched palate, deformities of
nails, cubitus valgus
Transient DM dehydration, loss of wt, acidosis in SGA

INFANTS OF DIABETIC MOTHERS

Diabetic moms have a high incidence of:
o Polydramnios, Preeclampsia, Pyelonephritis, Preterm labor,
Chronic HPN
High fetal mortality rate esp after 32wk
Fetal loss assoc w/ poorly controlled maternal DM
(ketoacidosis) & congenital anomalies

If complicated by vasc dse growth restriction esp after

37wk AOG
Neonatal mortality rate 5X than nonDM moms

PATHOPHYSIOLOGY
Maternal hyperglycemia fetal hyperglycemia FETAL
HYPERINSULINEMIA inc hepatic glucose uptake &
glycogen synth, accelerated lipogenesis, & augmented protein
synthesis
Related patho findings:
o Hypertrophy and hyperplasia of the pancreatic islet Bcells
o Inc weight of the placenta & infant organs except for the
brain
o Myocardial hypertrophy
o Inc amt of cytoplasm in liver cells
o Extramedullary hematopoiesis
Hyperinsulinism & hyperglycemia fetal acidosis inc rate
of stillbirth
Separation of placenta at birth interrupts glucose infusion into
neonate w/o a proportional effect on hyperinsulinism
hypoglycaemia & lipolysis during 1st hr after birth
Congenital anomalies d/t hyperglycemia-induced
teratogenesis
Chronic fetal hypoxia
o Elevated amniotic fluid erythropoietin levels
o Inc fetal neonatal morbidity
CLINICAL MANIFESTATION
Large & plump d/t inc body fat & enlarged viscera
Puffy, plethoric facies
May have normal or low BW if delivered before term or mom
has assoc vascular dse
Hypoglycemia in 25-50% of infants of diabetic mothers & 1525% of gestation DM moms
Nadir in infants blood glucose conc bet 1-3H; spont recovery
begin by 4-6H
Jumpy, tremulous & hyperexcitable in 1st 3d of life
Hypotonia, lethargy & poor sucking may occur
Early appearance of these signs hypoglycaemia
Late appearance hypoCa
-

Tachypnea 1st 2 days of life

o Manif of hypoglycaemia, hypothermia, polycythemia,
cardiac failure, transient tachypnea, cerebral edema from
birth trauma or asphyxia
o Higher incidence of resp distress syndrome r/t antagonistic
effect of insulin on stimulation of surfactant synth by cortisol
Cardiomegaly common (30%)
o Heart failure in 5-10%
o Asymmetric septal hypertrophy may occur
o Inotropic agents worsen obstruction C/I
o CHD
o Birth trauma d/t fetal macrosomia
Neuro devt & ossification centers are immature
o Correlate w/ brain size & AOG than body wt
Inc incidence of hyperbilirubinemia, polycythemia, & renal v
thrombosis
Suspect renal v thrombosis in infants w/ flank mass,
hematuria, & thrombocytopenia

Congenital anomalies inc 3x

1. Cardiac malformations (VSD, ASD, TGA, truncus
arteriosus, double-outlet R ventricle, tricuspid atresia,
coarctation of the aorta)
2. Lumbosacral agenesis
3. Other anomalies: Neural tube defects, hydronephrosis,
renal agenesis & dysplasia, duodenal or anorectal
atresia, situs inversus, double ureter, holoprosencephaly

PROGNOSIS
Physical devt is normal
Predisposed to childhood obesity & extend to adult
Symptomatic hypoglycemia inc risk of impaired intellectual
devt

TREATMENT
Frequent prenatal eval of all preg women w/ overt or
gestational DM
o Eval fetal maturity
o Biophysical profile
o Doppler velocimetry
o Plan delivery in hospitals
Periconceptional glucose control reduces the risk of
anomalies
Glucose control during labor reduces incidence of neonatal
hypoglycaemia
Type 1 DM w/ tight glucose ctrl deliver infants w/ BW similar to
nonDM moms
Glyburide dsnt cross placenta
Asymptomatic infants do blood glucose determination w/in
1H of birth then q H for next 6-8H
If normoglycemic oral or gavage feeding w/ breat milk or
formula at 3H intervals
If cant tolerate oral feeding discontinue feeding and give
glucose by peripheral IV infusionat 4-8mg/kg/min
Hypoglycaemia frequent feeding & IV infusion of glucose
Avoid Bolus injection of glucose further hyperinsulinemia &
rebound hypoglycemia
HYPOGLYCEMIA
Early feeding decreases incidence
Increases incidence: Prematurity, Hypothermia, Hypoxia,
Maternal DM, Maternal glucose infusion in labor, IUGR
Serum glucose decline after birth until 1-3H of age
In healthy FT, serum glucose values are rarely:
o <35mg/dl 1-3H of life
o <40mg/dl 3-24H
o <45mg/dl after 24H
CLINICAL MANIFESTATIONS
Incidence is highest in SGA
Affects 5-15% of growth-restricted infants
Onset of s/s: few hrs to a wk after birth
Order of freq:
o Jitteriness or tremors
o Apathy
o Episodes of cyanosis

Convulsions
Intermittent apneic spells or tachypnea
Weak or high-pitched cry
Limpness or lethargy
Difficulty feeding
Eye rolling
Episodes of swearting sudden pallor, hypothermia & cardiac
arrest
Determine whether s/s disappear w/ admin of sufficient
glucose to raise blood sugar to N levels

o
o
o
o
o
o
o
-

TTT
Symptoms other than seizures IV bolus of 200mg/kg
(2ml/kg) of 10% glucose
If IV of 20% glucose inadeq hyperinsulinemia is probably
present admin diazoxide
If diazoxide unsuccessful octreotide
If Severe persistent hyperinsulinemic hypoglycemia
subtotal pancreatectomy
Serum glucose meas q 2H after initiating therapy until above
40mg/dl
Subsequently, levels meas q 4-6H & ttt reduced &
discontinued when serum gluc is & when baby is asymp for
24-48H
At risk infants, Serum glucose meas
o w/in 1H of birth
o q 1-2H for 1st 6-8H
o q 4-6H until 24H

normoglycemic high-risk infants

o oral or gavage feeding w/ human milk or formula started at
1-3H of age and cont at 2-3H intervals for 24-48H
o IV infusion of glucose at 4mg/kg/min if poor oral feeding or if
asymp transient neonatal hypoglycemia develops

PROGNOSIS
Good in asymp w/hypoglycemia of short duration
Recurs in 10-15% after adeq ttt
Recurrence common if IVF are discontinued too rapidly
before oral feedings are well-tolerated
Prolonged, recurrent, severe symptomatic hypoglycemia
neurologic sequelae
Poorer prognosis
o Symptomatic infants w/ hypoglycemia, esp LBW
o Persistent hyperinsulinemic hypoglycemia
o Infants of DM mothers