Neonate Module Pedia Notes
Neonate Module Pedia Notes
Neonate Module Pedia Notes
Appears ill
Extremely PT
Gelatinous
Bleeds and bruises
easily
postmature
Paler
Thicker skin
Cavernous hemangioma
o
Deep blue masses
o
Trap platelets and produce DIC
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
Cranial synostosis
o
Premature fusion of sutures
o
Identified by a
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
suggests
irregular calcification
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
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
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
retention cyst
seen on gums
disappear spontaneously
dont cut
NECK
short
Congenital torticollis
o
Head to turn toward & face to turn away from affected
side
o
Plagiocephaly, facial asymm, hemihypoplasia develops if
unttt
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
PT may breath w/
o
Cheyne-Stokes/periodic respiration or
o
Complete irregularity
breathing is diaphragmatic
o
during inspiration
abdomen protrudes
ABDOMEN
abdominal wall
o
normally weak
umbilical cord
o
omphalitis acute local inflamm of the periumbilical
tissue
2 arteries
1 vein (AVA)
GENITALS
N scrotum is large
o
Size inc by trauma of breech or by a transitory hydrocele
imperforate anus
o
assess by
do gentle suction
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
heat of newborn
o
4x that of an adult
EXTREMITIES
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
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
hearing impairment
o
universal screening is recommended
NURSERY CARE
infants temp
o
taken via axillary
normal: 36.4- 37 C
monitoring
thereafter
- every 8 hrs
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)
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
by history alone
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
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
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.
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
develop in infants
DM mother
asphyxia
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
16-18 wk
18-20 wk
THE CRANIUM
Forceps or vacuum-assisted deliveries d/t:
o Erythema
o Abrasions
o Ecchymoses
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
-
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
4
-
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
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
-
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
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
cordocentesis
o
demonstrating
fetal hypoxia
lactic acidosis
PATHOPHYSIOLOGY AND PATHOLOGY
hypoxia alone
o
not cause lethal brain injury
o
should be combined with ischemia
CLINICAL MANIFESTATIONS
cerebral edema
o
may develop in the next 24 hours
o
anticipate seizure
give Phenobarbital
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
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
scaphoid abdomen
o
suggests diaphragmatic hernia
aka eventration
given through
o
IV
o
SQ
o
intratracheal
o
IM
c/I
o
if mother has opiate addiction
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
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
sodium bicarbonate
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
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
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
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 femur
o
traction-suspension of both lower extremities
Fracture of forearm
o
Splints
pe
o
o
flattened nose
asymmetric nares
pattern
Abd mass
Erythema of abd wall
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
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
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
Genetic defect
Prematurity
-
AOG 35-36wk
Exclusive BF
AOG 37-38wk
Jaundice b4 discharge
Male gender
o Decreased risk
AOG >41wk
Black race
5.
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
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
Pallor
Heart failure
Shock
o d/t
Hemolysis
Underproduction of erythrocytes
o Cause
Hemolytic dse of NB
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:
Pallor
Poor wt gain
Dec act
Tacypnea
Tachycardia
Feeding probs
o Contributing factors:
Brochopulmonary dysplasia
Cyanotic CHD
NEC
Prematurity
BPD
1.
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.
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.
-
Hemolytic or hyporegenerative
Rh (+) infant
Ectopic preg
Amniocentesis
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
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.
-
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
2.
3.
4.
5.
6.
7.
8.
9.
-
Adult
Adult hgb
Promptly
changed to
alkaline hematin
Yellow-brown rxn
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
-
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
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