MEKELLE UNIVERSITY

COLLEGE OF HEALTH SCIENCE

SCHOOL OF MEDICINE

DEPATRTMENT OF PEDIATRICS AND CHILD HEALTH

Seminar on newborn assessment and common
neonatal problems
07/06/ 2016 e.c.
Prepared by
Dejen Takele
Fremariam G/medhin
Frey Gebre
Moderator Dr. Kiros W. (pediatrician)
 Outlines
• Introduction
• newborn assessment
• Neonatal jaundice
• Neonatal sepsis
• prematurity and its complications
• Perinatal Asphyxia
 Introduction
• A neonate is a newborn of 28 days old or less.
• Represents a time of transition from the intrauterine
environment.
• There are several classifications of neonates based on
different criteria

 Based on the neonatal period

– Very Early (birth – 24 hrs)
– Early(1 day – 7 days)
– Late (7 days – 28 days)
 Continued…
 Based on Gestation age
– Preterm (<37 weeks)
– Term (37 – 42 weeks)
– Post-term (>42 weeks)

 Based on Birth Weight

– Large birth weight(>4000 gm)
– Normal birth weight (2500 – 4000 gm)
– Low birth weight (1500 – 2500 gm)
– Very low birth weight (<1500gm)
– Extremely low birth weight(<1000gm)
 Continued…
Based on weight to Gestational age

• AGA- if the birth weight lies between 10 to 90 centile

for the specified GA.

• LGA – if the weight lies above 90 centile for the

specified GA

• SGA –if the weight lies below 10 centile for the

specified GA.
Weight for GA chart
 Assessment of the newborn
• Assessment of the newborn should begin with a review
of the maternal and family history, the pregnancy, and
the delivery.
• Details of this history should include the following
information,
– Demographic and social data
– Maternal medical conditions
– Past medical illnesses in the mother and family,
– Previous maternal reproductive problems
– Events occurring in the present pregnancy
– Description of the labor
 Physical Examination
• The initial examination of a newborn infant should be
performed as soon aspossible after delivery.
• Temperature, pulse, respiratory rate, color, signs of
respiratory distress, tone, activity, and level of
consciousness of infants should be monitored frequently
until stabilization.
• For high-risk deliveries, this examination should take
place in the delivery room and should focus on
congenital anomalies, maturation and growth, and
problems of cardiopulmonary and metabolic adaptation
to extrauterine life.
• After a stable delivery room course, a second
andmore detailed examination should be
performed within 24 hr of birth.
• If an infant remains in the hospital longer than
48 hr, repeat assessments should be
performed throughout the hospital stay
including a discharge examination within 24 hr
of discharge.
• Infants should not be discharged from the
hospital without a final examination because
certain abnormalities, particularly cyanosis
and heart murmurs, often appear or disappear
in the immediate neonatal period;
• in addition, evidence of disease that has just
been acquired may be noted
• G/A , twitching, activity, edema
• skin- cyanosis, lanugo,
• skull- caput, cphalhematoma, subgaleal hematoma,
micro/macrocephaly, delichocephaly, fontanel, craniotabes
• face-dysmorphic
• eyes- leucokorria, pupillary reflex
• ear-pinna
• nose-patency
• mouth-precocious dentition, clefts, ankyloglossia
• neck-torticollis
• Chest-Breast or nipple abnormalities
-lung-grunting, RD
• Heart-dextrocardia, CHD
• Abdomen-abdominal masses, Abdominal distention,
omphalocele,
• Genitals- hydrometrocolpos, hydrocele, hypospadias or
epispadias
• Anus-passage of meconium, imperforate anus
• Extremities- polydactyly, syndactyly, clubfoot, simian
crease.
• Neurologic- neonatal reflexes
• A variety of conditions that affect the newborn originate in
utero, during birth or in the immediate postnatal period.
• Some commonly encountered neonatal morbidities include
 Prematurity
 Congenital malformations
 Respiratory distress
 Neonatal infections
 Perinatal asphyxia
 Neonatal jaundice
 Birth injuries
 Neonatal hematologic problems/ bleeding disorders
Neonatal Jaundice
 Outline of presentation
1. Introduction
2. Metabolism of Bilirubin
3. Etiology of Hyperbilirubinemia in neonates
4. Approach to Jaundiced neonates
5. Therapy of Neonatal Hyperbilirubinemia
6. Kernicterus
 introduction
Jaundice
 The most common condition that requires medical
attention in new born
 It is a yellow coloration of the skin and sclera in new born
 It is a benign problem
 Observed during in the 1st week of life in Approximately
60% in term and 80% of preterm infants
 Usually results from the accumulation of unconjugated,
non polar, lipid soluble bilirubin in the skin.
 It may excessively rise
leads Neurotoxic, Death, lifelong neurologic Sequale..
 Metabolism of biluribinCont…

5 neonatal jaundice
 NADPH
O2
Heme Oxygenase

FE
NADP
H2O

NADPH CO

Biliverdin
Reductase NADP

BILIRUBIN ALBUMIN

neonatal jaundice
LIVER
 Non – heme source
Hb → globin + haem
1 mg / kg
1g Hb = 34mg bilirubin

Bilirubin ALB

Ligandin(Y - acceptor)
Intestine

Bilirubin glucuronidase
Bil glucuronide
Bil glucuronide

β glucuronidase bacteria
Bilirubin

Stercobilin

Bilirubin metabolism
neonatal jaundice
 Risk factors for severe Hyperbilirubinemia
A. Major Risk factor
 Jaundice observed in 1st 24hr
 Pre discharge TsB/TcB level in the high risk zone
 Blood incompatibility with positive direct anti-
globlin test ( haemolytic disease, G6PD)
 Gestational age 35-36wks
 Previous sibling received phototherapy
 Cephalo hematoma
 EBF(Wt loss, not nursing well…)
 East asian race
22
 B. Minor risk factors
 Predisecharge TsB orTCB in high intermidiate risk zone
 Gestational age 37-38 weeks
 Jaundice occur before discharge
 Previous sibling with jaundice
 Macrosomic infant of a diabetic mother.
 Maternal age >25year, male in gender
C. Decreased risk of Jaundice
TsB/TcB level in the low risk zone
Gestational age >41 weeks
Exclusive bottle feeding
Black race
Discharge from hospital after 72hr

23
,

24
 causes of IB

1-Increased the load of bilirubin to be

metabolized by the liver (hemolytic aneamia,
polycythemia, shortened RBC life, Increased
enterohepatic circulation, infection).
2-Damage or reduces the activity of the
transferase enzyme or other related enzymes
(genetic defficency hypoxia, infection).
3. Blocks the transferase enzyme (drug and
other substances requiring glucoronic acid
conjugation).

4. An absence or decreased amounts of the

enzyme or reduction bilirubin uptake by liver
cell (genetic defects, prematurity)
Jaundice appearing in the 1 24 hr st

• Hemolytic diseases
• RH/ABO Incompatibility
• Mild Bd group incompatibility (Kelly, Duffy Ags)
• Enzyme deficiency of RBC: G6PD,pyruvate kinase
• RBC membrane defect
• Maternal drugs like diazepam , sulphonamides etc.
• Criggler-najjar/Gilbert syndrome
• Congenital infections-TORCH
• Erthroblastosis fetalis
• Hemorrhage
 Jaundice b/n 24hr to 2weeks of age

Physiologic Jaundice
Breast milk /feeding Jaundice
Infection-(sepsis ,UTI, )
Heamolysis
Bruising, blood extravasation
Polycythemia
Crigller Najjar Syndrome(cong. nonheamolytic
jaundice…)
 Jaundice at >2weeks of age

Un conjugated
Physiologic or Breast milk Jaundice
Infection (sepsis, congenital)
Hypothyroidism
Hemolytic aneamia eg . G6 PD deficiency
High gastro intestinal obstruction
Conjugated
Bile duct Obstruction
Neonatal hepatitis
……bilirubin………

30
 classsification

A.Physiologic jaundice
B.Pathologic jaundice
C.Jaundice associated with breast milk/
feeding
Signs Physiologic Jx Pathologic Jx

Clinical Jx Visible in 2-3day With in 24hrs

TSB rise <5mg/dl/day >5mg/dl/day
TSB Term<12mg/dl Term>12mg/dl
Preterm<15 mg/dl Preterm>15 mg/dl
Conj BBn <1.5mg/dl >1.5mg/dl
Jaundice Term <1 week Term >1week
persists for Preterm <2weeks Preterm >2weeks
• Physiologic jaundice in newborns occurs because of the
following factors
1. Shorter life span of RBC
2. Immature liver
3. Absence of bacteria in the gut &
counteract of beta glucuronidase
 Exaggerated when aggravated by:
• Prematurity .PNA
• Hypothermia .Hypoglycemia
• Acidosis .cephalohematoma
Factors which increase risk of hyperbillirubinemia
• Hypoproteinemia
• competitive binding
– drugs such as sulfisoxazole and moxalactam,
– acidosis, and
– increased free fatty acid concentration secondary to hypoglycemia,
starvation, or hypothermia
• Increased susceptability of neurons
• asphyxia,
• prematurity,
• hyperosmolality, and
• infection
 Pathophysiology
ABO incompatibility
• Although it is not as common (especially in a
first pregnancy), a similar problem of
incompatibility may happen between the
blood types (A, B, O, AB) of the mother and
baby in the following situations:

35
Rh incompatibility

36
 Breast milk jaundice

• Occurs in about 2% of breast fed term infants

• Usually after the 7th day of life.
• Maximum concentration can reach as high as 10
to 30 mg/dl during the 2nd to 3rd week of life
• Gradually decreases even if the baby is
continued on breast feeding
• May persist for 3 to10 weeks at lower levels

37
 Etiology

• The milk, containing non esterified long

chain fatyacid which inhibits the action of
glucoronyl trasferase
• The other reason is the milk contains beta
glucoronidase that causes enhanced
absorption of bilirubin from the gut.

38
Breast feeding jaundice
• Occurs within the first week of life in breast fed
neonates.
• Breast fed infants have higher bilirubin level than
formula fed neonates
• More than 13% of breast fed infants develop
Hyperbilirubinemia of >12mg/dl

This may be due to :

1. decreased milk intake and dehydration
2. Reduced caloric intake
 Clinical evaluation
• It may be present at birth or at any neonatal period depending on
the etiology
• It occur in cephalocuadal progression and disappear in the opposite
direction
• Dermal pressure may reveal the anatomic progression of Jaundice
Eg. - face= 5-7 mg/dl
-Mid abd. = 15mg/dl
-Sole/palm= 20mg/dl
• Jaundice from deposition of indirect bilirubin in the skin tends to
appear bright yellow or orange
but if obstructive type (direct bilirubin) has greenish
/ mudy yellow.

40
 Family hx
 previous sibling with jaundice
 Other family members with jaundice
 Aneamia, splenectomy or any known hereditary for hemolytic
disease
Hx of pregnancy and delivery
– Maternal illness (viral or other infection)
– Maternal drug use
– Delivery history e.g. PROM ,sepsis, prolonged labor..
– Delayed cord clumping
– Birth trauma
Post Natal hx
 Loss of stool color
 Breast feeding
 Wt loss more than average
 Sx/sn of hypothyroidism
 Exposure to parental Nutrition
05/12/07 E.C Dr. Dawit S. neonatal jaundice 41
 P/E

• Proper classification of the newborn according to

gestational age,weight and both.
• Pallor, petechea ,HSM
• Bruises and cephalhematoma
• Micro /macrocephaly
• Dark urine and clay colored stool
• Examination targeted to specific cause
• Sx/sn of kernictures
• Cataract
• Omphalitis
 Investigations
 TSB with conjugated fraction
 CBC
 Blood group & Rh of the baby with direct
coomb’s test
 Blood group & Rh of the mother with indirect
coomb’s test.
 Specific investigations for suspected specific
problems
– LFT, TFT, U/S liver and Bile ducts
 Principle of management
 Treatment of the Underlying cause or decreasing
risk factor
Photo Therapy
Exchange Transfusion
Complication Treatment
Other supportive Mgt
Correction Thermoregulation
Feeding (ongoing) lactation
Follow up and Prevention

44
 Phototherapy
 There are two types:
1. Conventional
2. Intensive types of phototherapy
 The mechanisms by which phototherapy works are:-
A. Photoisomerization
It will convert the toxic bilirubin to non toxic molecule.
B. Structural isomerization (Intermolecular cyclization)
Convert bilirubin to lumirubin.
C. Photoxidation:- Converts bilirubin to polar, colorless
product
• Bilirubin absorbs light maximally in the blue range
(420-470 nm). 45
• While baby is under phototherapy:
– Babies eyes & genitalia should be securely covered
– Take baby off phothotherapy every 2 to 3 hours
– Monitor fluid and electrolyte status b/c they have
insensible water loss
– Increase fluid intake by 20 ml/kg to compensate the
insensible water loss
– Monitor temperature regularly
• The distance b/n the neonate & the light should be
around 10-45 cm.
• Blue lights with a wavelength of 420−470nm most
efficient for phototherapy.
• Currently blue jackets are available with minimal
thermal energy & fluid loss. 46
• Two types
» Prophylactic
» Therapeutic

• Prophylactic phototherapy should be

started soon after birth before clinical
jaundice is available like
– Rh isoimmunization
– BW<1000gm
– Severely bruised baby
47
 Suggested MaximaI ldirect Serum Bilirubin Concentrations
(mg/dL) in Preterm Infants usually phototherapy is
initiated.

UNCOMPLICATED( COMPLICATED
BIRTHWEIGHT (g) Tsb mg/dl) (TSB Mg/dl)
<1,000 12–13 10–12

1,000–1,250 12–14 10–12

1,251–1,499 14–16 12–14

1,500–1,999 16–20 15–17

2,000–2,500 20–22 18–20

02/13/2024 48
 Complications associated with
phototherapy
 Overheating, dehydration (increased insensible
water loss, diarrhea)
 Retinopathy
 Skin rash (erythematous macular rash, purpuric
rash associated with transient Porphyrinemia)
 Bronze baby syndrome (which occurs in the
presence of direct hyperbilirubinemia)
 Which may be due to photo induced porphyrines,
often common in cholestatic jandice.
49
 Exchange transfusion
•Most effective way of treating Jaundice and anemia
•Indications
1. Hydrops fetalis
2. History of previous sibiling requiring an exchange
transfusion because of Rh isoimmunization in a baby born
with palor ,HSM and +ve direct coombs test
 Cord Hgb < 11gm
 Cord TSB >5 mg
 Rate of rise of TSB > 1mg/dl/hr Despite phototherapy
 Despite phototherapy if Hgb is between 11 to 13 gm
3. Any TSB > 12.5 mg/dl in the 1st 24 hrs
4. Any TSB >20 mg/dl In the neonatal period
5. Symptoms suggestive of kernicterus
50
• There are 3 types
– Double
– Partial
– Volume to volume
• For double exchange transfusion we double
the total blood volume of the baby

51
• Partial used in neonates with anemia or
polycythemia
• After we prepare the blood the FF materials
should be available
 Disposable syringes
 Umbilical cannula of 6 & 9 number
 Normal saline
 Resuscitation tray

52
 Technique and Precaution to be taken
• Under strict aseptic conditions
– umbilical vain is canulated with polyvinyl catheter to
distance of maximum 7cm in full term
– When free flow blood obtained the catheter is usualy in
large hepatic vein or inferior venacava. Then the exchange
may performed through peripheral arterial (drawn out)
and venous (infused in) line /uvc.
– Exchange transfusion should carried out over 45-60 minute
period with Aspiration of 20ml of infant blood alternating
with infusion of 20ml of blood.
– Smaller Aliqoutes (5-10ml) may indicated for sick and
premature infants
05/12/07 E.C Dr. Dawit S. neonatal jaundice 53
 Precaution to be taken
• Explain the procedure and its risk to parents and take their
consent
• Ensure the stomach is empty prior to procedure
• Check the date of donation of blood ,look for clot, Blood
group,
• The aliquat volume should not exceed 3-5% of the blood
volume of baby
• During the procedure, keep the blood well mixed (avoid
sedmentation )
• Never leave the umbilical catheter end open to avoid air
embelism
• Timing ,volume to be exchange.
05/12/07 E.C Dr. Dawit S. neonatal jaundice 54
 Post exchange instruction
• Give vit. k’ im stat (1mg)
• Continue medication which the baby was taking
• Monitor v/s every 30 minute
• Watch for bleeding
• Continue phototherapy
• Check for blood sugar, TsB, hct after 2hr then 6-
12hrs.
• Oral feed may start after 1-2hr of the procedure
(if the baby is well/stable).
05/12/07 E.C Dr. Dawit S. neonatal jaundice 55
 Pharmacologic agents

Intravenous immunoglobilin
– inhibit hemolysis by blocking antibody recepter on RBCs

– decreased exchange Transfusion needs

Phenobarbital
– increases the conjugations and excretions
– decreases postnatal TSB level but affects the cognitive
Ursodeoxycholic acid –increase bile flow
metalloporphrene (synthetic )
– inhibit the formation of bilirubin by compititive inhibtion of heme
oxygenase.
– decreases TSB level, need of phototherapy..
05/12/07 E.C Dr. Dawit S. neonatal jaundice 56
 COMPLICATIONS
1. Catheter related
– Infection
– Haemorrhage
– NEC
– Portal and splenic vein thrombosis
– Air embolism
2. Hemodynamic problems
– Overload cardiac failure
– Hypovolaemic shock
– Arrhythmia (Catheter tip near sinus node in Rt Atria)
57
3. Electrolyte imbalance
– Hyperkalemia (old blood)
– Hypocalcaemia
– Increase or decrease Blood glucose
– Acidosis (sometimes late alkalosis due to
breakdown of citrate)
– Tissue hypoxia (old blood )

58
 KERNICTERS (Billirubin encephalopathy
• is neurologic syndrome resulting from the
deposition of unconjugated billirubin in brain cells
.
• Sites of billirubin staining and necrosis include
-Basal ganglia - Hippocampal cortex
-Sub thalamic nucleus - cerebellum
• Cerebral cortex is spared
• Half of the neonates with kernicters at autopsy
have extra neuronal lesions like ATN, necrosis of
GI mucosa and pancreas
 Disruption of blood brain barrier by:- risk
facters
 Multifactorial and involves an interaction
between
• Unconjugated bilirubin level
• Albumin binding and
• Unbound bilirubin level
• Passage across the blood brain barrier &
• Neuronal susceptibility to injury
• can occur at any Neonatal period (usually 2-5
day after birth in term) and as late as 7th day in
premature
• early signs may be indistingueshable from
sepsis,asphyxia,Hypoglycemia and other Acut
systemic illness
 Acute bilirubin encephalopathy
Phase 1 D1-2 Phase 3 >7D
• Poor motor reflex • Hypertonia decreases
• Hypotonic • Hearing and visual abnormality
• Lethargic • Seziure
• Poor feeding • Poor feeding
• lehargic

Phase 2 D3-4
• Fever
• Seizure and depressed sensorium
• Hypertonic
• Opistothonus posturing
• Paralysis of upward gaze

62
 Chronic form
• 1st year
• Hypotonia
• Active DTR
• Obligatory tonic neck reflexes
• Delayed motor skills

• After 1st year

• Movement disorde(choreoathetosis,ballismus and tremor), upward gaze,
sensory neural hearing loss
 Prognosis
• Kernicterus will develop in 30-35% of infants
with untreated hemolytic disease and bilirubin
levels
>25-30mg/dl.
• Overt neurologic sign have a grave prognosis: >
75% of such infants die and 80% of affected
survivors have bilateral Choreo-athetosis with
involuntary muscle spasm.
• MR, Deafness, Spastic quadriplegia, Cerebral
palsy are common.
05/12/07 E.C Dr. Dawit S. neonatal jaundice 64
 Neonatal sepsis
A serious blood bacterial infection in an infant less than 4 weeks of age.
Babies with sepsis may be overly sleepy, floppy, weak, and very pale.
Infections in the newborn are often classified by their timing relative to birth
and include
– congenital,
– perinatal,
– early-onset, and
– late-onset disease.
• These are clinically useful designations because the mechanisms of
infection, etiologies, and outcomes are distinct at each stage.
• Congenital infection denotes infection acquired in utero.
– usually it is chronic perinatal infection, can chronic or acute, via vertical
transmission
– Such infections are generally caused by viral or other non bacterial organisms and
are often associated with injury to developing organs
Perinatal infection= infection occur between
28th weeks of GA and 7th day of life after
delivery.
• Perinatal acquired organisms include both
bacteria and viruses, some of which are the
same as those causing congenital infection but
often manifest with different features.
 Neonatal infections are unique:
 Transmission from the mother occurs via diverse modes
 Maternal infections are often not diagnosed during pregnancy
( Asymptomatic, non-specific)
 Etiologies are different (bacteria, fungi, virus, protozoa)
 Immature immunity (mechanism of defending against infection is poor)
 Features are variable (subclinical, mild to severe, focal/systemic,
malformations) depending on :
 Timing of exposure
 Inoculum size
 Immune status
 Virulence of organisms
 Bacterial Sepsis
• Neonates with bacterial sepsis may have either
nonspecific manifestations or focal signs of
infection
• The initial manifestation may involve only limited
symptomatology and only one system, such as
apnea alone or tachypnea with retractions, or
tachycardia, or the infant may present with an
acute catastrophic manifestation with multiorgan
dysfunction and shock.
• Despite advances in maternal and neonatal care,
infections remain a frequent and important cause
of neonatal and infant morbidity and mortality.
• Up to 10% of infants have infections in the 1st mo
of life.
• Newborn infection is more common in areas with
limited access to healthcare than in areas with
well-established healthcare infrastructure
• The overall incidence of neonatal sepsis
ranges from 1 to 5 cases per 1,000 live births.
• Globally, neonatal sepsis and other severe
• infections were responsible for an estimated
430,000 neonatal deaths in 2013,
• accounting for approximately 15% of all
neonatal deaths.
• A number of bacterial and nonbacterial agents may
infect newborns in the intrapartum or postpartum
period
• Although HSV, HIV, HBV, HCV, and TB can each result
in trans placental infection, the most common mode
of transmission for these agents is intrapartum ,
during labor and delivery with passage through an
infected birth canal (HIV, HSV, HBV), or postpartum ,
from contact with an infected mother or caretaker
(TB) or with infected breast milk (HIV)
• Any microorganism inhabiting the
genitourinary or lower gastrointestinal tract
may cause intrapartum and postpartum
infection.
• The most common bacteria are group B
streptococcus (GBS), Escherichia coli, and
Klebsiella spp.
• Salmonella spp. are common causes of gram-
negative sepsis in developing countries
• The more common viruses are
cytomegalovirus (CMV), HSV, enteroviruses,
and HIV
• The most common bacterial causes of neonatal
meningitis are GBS, E. coli, and L. monocytogenes.
S. pneumoniae, other streptococci, nontypable H.
influenzae, both coagulase-positive and
coagulase-negative staphylococci, Klebsiella,
Enterobacter, Pseudomonas, Treponema pallidum,
and
• Mycobacterium tuberculosis infection involving
the central nervous system (CNS) may also result
in meningitis.
 Early-onset sepsis
• Early-onset sepsis is defined as the onset of
symptoms before 7 days of age, although some
experts limit the definition to infections occurring
within the 1st 72 hr of life.
• Early-onset infections are acquired before or during
delivery (vertical mother-to-child transmission).
Etiology
− Group B Streptococcus
− E.coli ,
_L.monocythogen
EONS
• Chorioamnionitis results from microbial invasion
of amniotic fluid, often as a result of prolonged
rupture of the chorioamniotic membrane.
• The term chorioamnionitis refers to the clinical
syndrome of intrauterine infection, which includes
maternal fever, with or without local or systemic
signs of chorioamnionitis (uterine tenderness, foul
smelling vaginal discharge /amniotic fluid,
maternal leukocytosis, maternal and/or fetal
tachycardia).
• Chorioamnionitis may also be asymptomatic,
diagnosed only by amniotic fluid analysis or
pathologic examination of the placenta.
• The rate of histologic chorioamnionitis is
inversely related to gestational age at birth
and directly related to duration of membrane
rupture.
• Chorioamnionitis was thought to result from infection of
the amniotic fluid but is now better defined by the term
intrauterine inflammation or infection at birth (Triple I) .
• This is defined by
– fetal tachycardia,
– maternal leukocytosis (>15,000 cells in the absence of
corticosteroids),
– purulent fluid from the cervical os,
– biochemical or microbiologic amniotic fluid changes consistent
with infection, and
– fever (≥39.0°C/10.2°F)
• Rupture of membranes for >24 hr was once
considered prolonged because microscopic
evidence of inflammation of the membranes is
uniformly present when the duration of rupture
exceeds 24 hr.
• At 18 hr of membrane rupture, however, the
incidence of early-onset disease with group B
streptococcus (GBS) increases significantly; 18 hr is
the appropriate cutoff for increased risk of
neonatal infection
 Late-onset sepsis
• Late-onset sepsis is generally defined as the onset of symptoms
at ≥7 days of age.
• Similar to early onset sepsis, there is variability in the definition,
ranging from an onset at >72 hr of life to ≥7 days of age
• it develop after delivery from organisms acquired in the hospital
or the community.
• These are generally nosocomial infections.
• This is usually a different group of pathogens.
− Coagulase negative staphylococcus
− Staphylococcus aureus
− Gram negative rods
− Fungi, i.e Candida Albicans
 LONS
• After birth, neonates are exposed to infectious agents in
the neonatal intensive care unit (NICU), the nursery, or in
the community (including family).
• Postnatal infections may be transmitted by direct contact
with hospital personnel, the mother, or other family
members; from breast milk (HIV, CMV); or from inanimate
sources such as contaminated equipment.
• The most common source of postnatal infections in
hospitalized newborns is hand contamination of
healthcare personnel, underscoring the importance of
hand washing.
 Very-late-onset infections
• Very-late-onset infections (onset after age 1
mo) may also occur, particularly in very-low-
birthweight (VLBW) preterm infants or term
infants requiring prolonged neonatal intensive
care.
• The incidence of neonatal bacterial sepsis
varies from 1-4 per 1,000 live births, with
geographic variation and changes over time.
• Studies suggest that term male infants have a
higher incidence of sepsis than term females.
• This sex difference is less clear in preterm low-
birthweight (LBW) infants.
• Attack rates of neonatal sepsis increase
significantly in LBW infants in the presence of
maternal chorioamnionitis, congenital
immune defects, mutations of genes involved
in the innate immune system, asplenia,
galactosemia (E. coli), and malformations
leading to high inocula of bacteria (e.g.,
obstructive uropathy).
 pneumonia in the newborn

 Is more common in early onset neonatal sepsis

 Some peculiarities of pneumonia in the NB
• Minimal clinical signs
• Generalized signs of sepsis predominate esp. in premature NBs
• Some Neonates can have Apnea rather than Tachypnea.
• Clinical signs of pneumonic consolidation may not be evident in the neonatal
period

87
Dr. Dawit S.Neonatal infections
02/13/2024
 Bacterial meningitis

 About one third of babies with neonatal sepsis can have coexisting meningitis
 It is more common with late onset neonatal sepsis
 Clinical evidence of meningial irritation are usually absent in the new born
period
 So to diagnose meningitis in New born we should see other Clinical clues

88
Dr. Dawit S.Neonatal infections
02/13/2024
MENINGITIS CONT.…

In a baby with sepsis the findings of

-convulsion/twitching
-staring look/fixed eye
-Bulged anterior fontanel
-abnormal excessive high pitched cry
Should arouse the suspicion of meningitis and
proceed with lumbar puncture.
 meningitis
• The incidence of meningitis is 0.2-0.4 per 1,000 live births
in newborn infants and is higher in preterm infants.
• Bacterial meningitis may be associated with sepsis or may
occur as a local meningeal infection.
• Up to one third of VLBW infants with late-onset meningitis
have negative blood culture results .
• The discordance between results of blood and CSF cultures
suggests that meningitis may be underdiagnosed among
VLBW infants and emphasizes the need for culture of CSF
in VLBW infants when late-onset sepsis is suspected and in
all infants who have positive blood culture results.
• Most cases of meningitis result from hematogenous
dissemination.
• Less often, meningitis results from contiguous spread as
a result of contamination of open neural tube defects,
congenital sinus tracts, or penetrating wounds from fetal
scalp sampling or internal fetal electrocardiographic
monitors.
• Cerebral abscess formation, ventriculitis, septic infarcts,
hydrocephalus, and subdural effusions are complications
of meningitis that occur more often in newborn infants
than in older children.
• Metabolic factors, including hypoxia, acidosis,
hypothermia, and inherited metabolic
disorders (e.g., galactosemia), are likely to
contribute to risk for and severity of neonatal
sepsis
 Infection in Premature Infants

• The most important neonatal factor predisposing to infection is prematurity

or LBW.
• Preterm LBW infants have a 3- to 10-fold higher incidence of infection than
full-term normal-birth weight infants.
• Possible explanations include
(1) maternal genital tract infection is considered to be an important cause of
preterm labor, with an increased risk of vertical transmission to the newborn;
(2) the frequency of intra amniotic infection is inversely related to gestational
age
(3) premature infants have documented immune dysfunction; and
(4) premature infants often require prolonged intravenous access, endotracheal
intubation, or other invasive procedures that provide a portal of entry or impair
barrier and clearance mechanisms, putting them at continued risk for hospital-
acquired infections.
 BACTERIAL SYSTEMIC INFECTIONS IN THE NEONATE

Neonatal infections by age of onset

Characteristics early onset late onset late, late onset
Age at onset -birth-7days - 7-30days ->30days
Obst. complications -common -uncommon - variable
Source of pathogens - maternal genitalia -genitalia / community/ environment environment

C/ms -multisystem -multisystem/focal -multisystem/focal

Site nursery,NICU,community NICU,community NICU,community
Meningitis - 1/3rd - 2/3rd - more than 2/3rd
 Clinical Manifestations

Perinatal Infection may result in:

Spontaneous abortion
Congenital malformations
IUGR
Preterm delivery
Still birth
Acute neonatal diseases
Asymptomatic persistent infection with late sequale
No apparent infection in neonatal period later may
overt.
 Clinical Manifestations

• The maternal history provides important information about

maternal exposures to infectious diseases, bacterial
colonization, immunity (natural and acquired),and obstetric risk
factors (prematurity, prolonged ruptured membranes, maternal
chorioamnionitis).
• Signs and symptoms in the neonate are often subtle and
nonspecific.
• Temperature instability,
• tachypnea,
• lethargy, and
• poor feeding are common initial signs and should raise
suspicion for systemic or focal infection
 SIRS
• the systemic inflammatory response to a variety of clinical insults,
manifested by 2 or more of the following conditions:
– Temperature instability <35°C (95°F) or >38.5°C (101.3°F)
– Respiratory dysfunction:
– Tachypnea >2 SD above the mean for age
– Hypoxemia (PaO 2 <70 mm Hg on room air)
– Cardiac dysfunction:
– Tachycardia >2 SD above the mean for age
– Delayed capillary refill >3 sec
– Hypotension >2 SD below the mean for age
– Perfusion abnormalities:
– Oliguria (urine output <0.5 mL/kg/hr)
– Lactic acidosis (elevated plasma lactate and/or arterial pH <7.25)
– Altered mental status
• Sepsis: the systemic inflammatory response to an infectious process
 IMCI and who criteria for severe infections in children

• Neurologic: convulsions, drowsy or unconscious, decreased

activity, bulging fontanel
• Respiratory: respiratory rate >60 breaths/min, grunting, severe
chest indrawing, central cyanosis
• Cardiac: poor perfusion, rapid and weak pulse
• Gastrointestinal: jaundice, poor feeding, abdominal distention
• Dermatologic: skin pustules, periumbilical erythema or
purulence
• Musculoskeletal: edema or erythema overlying bones or joints
• Other: temperature >37.7°C (99.9°F; or feels hot) or <35.5°C
(95.9°F; or feels cold)
• A variety of noninfectious conditions can
occur together with neonatal infection or can
make the diagnosis of infection more difficult
• Because bacterial sepsis can be rapidly
progressive, the physician must be alert to the
signs and symptoms of possible infection and
must initiate diagnostic evaluation and
empirical therapy in a timely manner.
 Investigations

– CBC with D/C

– Immature:mature ratio (> 0.2)
– Gastric aspirate for plymorphs with in 1hr of age (>
5PMNs/HPF)
– CRP
– Micro-ESR
– U/A
– Culture (blood, CSF, urine)
– CXR
– Antigen detection (GBS, Pneumococcus)
 Con’d
• Various serum biomarkers have been
investigated for their ability to identify infants
with serious bacterial infection (SBI).
• An immature-to-total phagocyte count (I/T
ratio) (≥0.2) has the best sensitivity of the
neutrophil indices for predicting neonatal
sepsis.
• After the newborn period, serum C-reactive protein
(CRP) and procalcitonin have demonstrated
reasonable sensitivity and specificity for SBI.
• CRP may be monitored in newborn infants to assess
response therapy.
• Their value in the initial diagnosis of sepsis in the
newborn period has yet to be clarified, as does the
value of these biomarkers in determining optimal
length of empirical therapy in infants with negative
cultures.
 culture based

• Blood Culture >1 mL of whole blood, from 2

sites Gold standard for bacteremia
• CSF Culture When clinically feasible Optimize
antimicrobial therapy
• Urine Culture >72 hr of life Not useful for EOS;
potential benefits for LOS
• Tracheal aspirate Culture Neonates with
endotracheal tube in place and signs of
progressive respiratory distress
General Approach to Management
 Breast feeding encourage
 Supportive treatment (fever controlling)
 Hypotension management
 Respiratory Support
 Empiric Antimicrobial Therapy
 Coagulation factors—fresh frozen plasma .
 Vaccinations
 Growth and development assesment
General Approach to Management
• In the absence of specific signs of focal infection,
therapy for presumed infection in the neonate is often
empirical and initiated on the basis of fever or
hypothermia, listlessness, irritability, or apneic episodes.
• Antibiotics are chosen to cover the organisms typically
causing neonatal sepsis, including GBS, gram negative
organisms, Listeria , and Enterococcus .
• Since the latter 2 organisms are intrinsically resistant to
cephalosporins, ampicillin is generally included in the
empirical treatment of infants with presumed neonatal
infection
 Early-onset sepsis
• Ampicillin + aminoglycoside
– 10 days for bacteremia;
– 14 days for GBS
– and uncomplicated meningitis; extend to 21-28 days for
complicated infections
• Consider a third-generation cephalosporin
(cefotaxime preferred) or carbapenem for meningitis.
• Tailor therapy to pathogen.
• Consider discontinuation of therapy if pathogen not
isolated.
 Late-onset sepsis

• Vancomycin + aminoglycoside
– Duration dependent on pathogen and site
• Alternatives to vancomycin may be considered based on local
epidemiology and clinical presentation.
• Aminoglycoside-based regimen preferred to cephalosporin given
reduced risk of resistance.
• Consider cephalosporin if meningitis suspected.
• Consider a carbapenem if third generation cephalosporin recently
received.
• Consider amphotericin for fungal etiologies.
• Tailor therapy to pathogen.
• Consider discontinuation of therapy if pathogen not isolated.
 PREVENTION STRATEGIES

• Intrapartum antibiotics (IAP)

– Administration of penicillin or ampicillin 4 hr before
parturition
– Successfully reduces rates of EOS caused by GBS
– No effect on LOS GBS
• Fluconazole prophylaxis
– Administration of weight-based dosing to neonates
<1,500 g
– Most beneficial in NICUs with high baseline rates of
invasive candidiasis
• BLF supplementation
– with a probiotic, Lactobacillus rhamnosus (GG)
– BLF is a human milk glycoprotein with a role
– in innate immune response.
– LGG enhances the activity of lactoferrin.
– BLF supplementation with and without LGG
reduced the incidence of 1st LOS in 472 VLBW
neonates inlarge randomized, double-blind RCT.
• Screening and treatment of all pregnant
women for HIV, syphilis, HBsAg, HCV, GBS,
gonorrhea
 Complications
•Neonatal seizure
•Hypotension ,shock/dehydration
•DIC /bleeding,
•hyperbilirubinemia/ kerniectures
•Organ failure
• Later complications of sepsis include
– respiratory failure,
– pulmonary hypertension,
– cardiac failure,
– shock,
– renal failure,
– liver dysfunction,
– cerebral edema or thrombosis,
– adrenal hemorrhage and/or insufficiency,
– bone marrow dysfunction (neutropenia, thrombocytopenia,
– anemia), and
– disseminated intravascular coagulopathy (DIC).
Prematurity and its complications
• Different degrees of prematurity are defined by
G.A or birth weight .

• Based on G.A – late preterm –(34-37wk)

- very preterm(28-320)
- extremely preterm (below 28)
Based on birth wt – LBW-( below 2500gm)
- VLBW(below 1500gm)
ELBW ( below 1000gm)
• Causes
-Fetal – fetal distres , MG, erythroblastosis ,
-Uterine – bicornuate uterus , incompetent
cervix
-Placental – placental dysfunction , PP,AP
-Maternal – infection , preeclampsia, chronic
medical illnes .
-Other - prom, polyhydroaminos, polytruama.
 Clinical feature
• Low birth wt ( below 2.5 kg low birth length9
below 47 cm), HC9 below 33, chest
circumference ( below 30 cm ), fine and wolly
scalp hair , pimk and shiny skin covered by
lanugo hair. ,nails that don’t reach finger tips
ears shapless and soft , less than 3 mm in
diameter breast nodles , external genitalia in
females ( prominent labia minora )and in
males ( undesended testes )
• Respiration- weak shallow with attacks of
apnia due immature respiratory center
• GIT – weak suckling , swallowing , digestion
and absorbtion
• Activity – weak crying and activity .
• Physiological juandice.
 Complications
• Res – RDS ,apnia of prematurity, prone to
congenital pneumonia , prone to broncho
plumenary dysplasia
• CVS – PDA, hypotention ( due hyovolumia ,
cardiac dysfunction)
• CNS – kernicterus , HEI , IVH
• GIT- NEC
• Renal – immature kidney , decreased capacity
to concentrate urine , acidosis, DHN
• Hematology – prone to iron and follic acid
deficiency anemia , prone to bleeding ( vit k
deficiency )
• Immunology – prone to infection and sepsis due
deficient humoral and cellular response and
decreased trens placental ab .
• Nutritional – prone to rickets , hypoglycemia and
hypocalcemia due weak suckling ,
swallowing ,digesttion and absorbtion , high
growth rate
• Hypothermia – due large surface area relative
to wt , excess heat loss , poor sub cutaneous
fat , immature heat regulating center.
• Retinopathy of prematurity
 managment
• Proper ante natal care
• Immediate post natal care
• Incubator care
• Feeding
PERINATAL ASPHYXIA
 Definition of terms
• Hypoxia - refers to decreased arterial concentration of oxygen.
• Anoxia - is a term used to indicate the consequences of complete
lack of oxygen
• Ischemia - refers to blood flow to cells or organs that is insufficient
to maintain their normal function.
• Perinatal period - defined as the period from the 28th wks of
gestation through the 7th day after birth.
• Perinatal asphyxia – is a perinatal insult to the fetus or newborn
due to hypoxia and/or ischemia of various organs leading to
physiologic and/or biochemical organ changes.
 DEFINITION of PERINATAL ASPHYXIA
 WHO defines as
* failure to initiate and sustain breathing at birth or it is 5th minute Apgar.

score of 0-3.
* It can also be defined as placental or pulmonary gas exchange
impairment leading to hypoxemia and hypercarbia.
• AAP and ACOG Criteria for diagnosis of perinatal asphyxia
. An arterial cord pH < 7.0 and base deficit more than 12
. Apgar score of less than 7 at 5 minutes.
. Evidence of altered neurological status (altered level of consciousness,
seizures, hypotonia, obtundation).
 Continued
 This definition using APGAR score is not
applicable in
. Preterm babies
. Babies birth trauma and
. congenital neurologic abnormality
APGAR score assesses physiologic response to birth
process
Signs 0 1 2
HR -None - <100 ->100

Respiration -None -Slow (irregular) -Good, crying

Muscle tone -Floppy -Some flexion -Active

motion

Grimace -None -Irritability -Cough or

sneeze
 Epidemiology
 Perinatal asphyxia is the second commonest cause of neonatal mortality only
preceded by infection and the commonest cause of disability in surviving
newborn
 mortality rate(%)
. Preterm birth complication =37%
. Intrapartum related complication = 28%
. Severe infection = 24%
. congenital =6%
continued
 ETIOLOGY AND RISK FACTOR
1.Antepartum = 20%
 Inadequate oxygenation of maternal blood.: exam
- cardiopulmonary failure, hypoventilation during
anesthesia
 Low maternal BP.; exam-acute blood loss,…
 Maternal chronic vascular disease; exa-chr.HTN.,…
 Premature separation of placenta,…
2.Intrapartum = 70%
 CPD ;exam -persistent occipital posterior position…
 Drugs; exam - oxytocin
 Cord compression
 ETIOLOGY
 Meconium aspiration.  Breech delivery
 Prolonged labor  Uterine rupture
3.Postpartum = 10%
 Severe anemia
 Shock
 Severe form of cyanotic CHD.
 Sever pulmonary disease
 Prematurity
 Neurologic abnormalities
 Severe infections
 PATHOPHYSIOLOGY

 during the normal course of labor cause most babies to be

born with little O2 reserve. These include the following:
1. Decreased blood flow to placenta due to uterine
contractions,
some degree of cord compression, maternal dehydration,
and maternal alkalosis due to hyperventilation
2. Decreased O2 delivery to the fetus from reduced placental
blood flow.
3. Increased O2 consumption in both mother and fetus
 PATHOPHYSIOLOGY
 Hypoxia-ischemia causes a number of physiologic and
biochemical alterations:
 With brief asphyxia, there is a transient increase,
followed by a decrease in heart rate (HR), mild elevation
in blood pressure (BP), an increase in central venous
pressure (CVP), and essentially no change in cardiac
output (CO).
 This is accompanied by a redistribution of CO with an
increased proportion going to the brain, heart, and
adrenal glands
 PATHOPHYSIOLOGY
 this diversion of blood flow to vital deep nuclear
structures of the brain does not occur. hence
results in the typical pattern of injury to the
subcortical and brainstem nuclei.
 With prolonged asphyxia, there can be a loss of
pressure autoregulation and/or CO2 vasoreactivity.
This, in turn, may lead to further disturbances in
cerebral perfusion, particularly when there is
cardiovascular involvement with hypotension
and/or decreased CO.
 PATHOPHYSIOLOGY
 organ injury typically correlates with areas of decreased blood
flow and areas of relatively higher metabolic demand,
especially brain tissue decrease
in cerebral blood
flow (CBF) results in anaerobic metabolism and
eventual cellular energy failure due to
increased glucose utilization in the brain and a
fall in the concentration of glycogen,
phosphocreatine, and adenosine triphosphate
(ATP).
 PATHOPHYSIOLOGY
 Prolonged asphyxia typically results in diffuse injury to
both cortical and subcortical structures. Due to increased
amounts of lactate and inorganic phosphates. Excitatory
and toxic amino acids, particularly glutamate, accumulate
in the damaged tissue. prompting overactivation of N -
methyl-D -aspartate (NMDA) and kainite
receptors. This receptor overactivation increases cellular
permeability to sodium and calcium ions.
 intracellular accumulation of these ions results in
cytotoxic edema and neuronal death
 PATHOPHYSIOLOGY

 Death can be either immediate or delayed and either necrotic or

apoptotic.
1. Immediate neuronal death (necrosis) - can occur due to
intracellular osmotic overload of Na+ and Ca2+ from ion pump failure
2.Delayed neuronal death (apoptosis) - occurs secondary to
uncontrolled activation of enzymes (e.g., Ca2+-dependent lipases) ,
generation of free radicals , generation of nitric oxide (NO) , and depletion
of energy stores.
 PATHOPHYSIOLOGY

3. Reperfusion - of previously ischemic tissue may

cause further injury because it can promote the
formation of excess reactive oxygen species causing
damage to cellular lipids, proteins, and
nucleic acids as well as to the blood-brain barrier.
This may result in an influx of neutrophils that, along
with activated microglia, release injurious cytokines
(e.g., interleukin 1-β and tumor necrosis factor α).
 PATHOPHYSIOLOGY…

Fig.6-summary of the pathway for brain injury due to hypoxic ischemic insult.
Fig-3.Bilateral acute infarctions of the frontal lobe are shown. The infarctions depicted in the figure (arrows) are
consistent with watershed infarctions secondary to global hypoperfusion in term baby. The lesions depicted in the
image are consistent with an acute ischemic event, occurring within 24 hours of death. The regions most
susceptible to hypoperfusion include the end-artery zones between the anterior, middle, and posterior cerebral
arteries

139
 CLINICAL PRESENTATIONS
 CLINICAL FEATUTRES
• Depends on duration & severity of asphyxia
 A. In the fetus: Fetal monitoring shows:
– Slow, weak, irregular heartbeats
– Scalp pH less than 7.2
– Action: Intrapartum resuscitation
- give mother high oxygen concentration and
- Position change
- prepare for immediate delivery.
 B. After delivery:
• Meconium staining of the newborn, amniotic fluid and vernix
caseosa

. Decreased consciousness with failure of spontaneous breathing.

• Low Apgar score with cyanosis and flaccidity.
 CLINICAL PRESENTATIONS…
C .early neonatal manifestations of perinatal asphyxia :
• ORGAN INVOLVEMENT o The commonly affected organ in PNA
is:
• kidney (50%) ▪ CVS (25%) ▪ GIT
• CNS (28%) ▪ Pulmonary (23%)
1 .BRAIN = Hypoxic-ischemic encephalopathy (HIE)
 Pathology:
 In severe , prolonged asphyxia ; consequences may include:
• Brain edema : both cytotoxic and vasogenic
• Intracranial hemorrhage
 CLINICAL PRESENTATIONS…
 B . With reperfusion(resuscitation ) = secondary neuronal death may
occur due to:
• Release of excitatory amino acids e.g. aspartate and glutamate
• Increased calcium & sodium entry into cells = brain edema
• Release of neurotoxin mediators e.g. nitric oxide , free radicals and
lactate
TABLE 1- Sarnat Clinical staging of hypoxic ischemic encephalopathy
signs Stage-1 Stage-2 Stage-3

Level of Hyperalert lethargy Stuperous,coma

Consciousness
Muscle tone normal hypotonic flaccid

posture normal flexion decerebration

Tendon hyperactive hyperactive absent

reflex/clonus
myoclonus present present absent

Moro reflex strong weak absent

143
Table-2.Sarnat staging of …
pupils mydriasis miosis Unequal, poor light
reflexes
seizures none common decerebration
EEG-finding normal Low voltage Burst, suggesting to
changing to seizure isoelectronic
activity pattern
duration <24hrs.if 2-14days Days to weeks
progress,may
be normal
10/06/2007

outcome good variable Death,sev.def.

 CLINICAL PRESENTATIONS…
 2 . Cardiac : - Heart failure, hypotension
 3. Respiratory : - Meconium aspiration, persistent
pulmonary hypertension of newborn, respiratory distress.
 4 . Renal : - Acute tubular necrosis, hematuria, oliguria (<
0.5ml/kg/hour)
 5. GIT :-Necrotizing enterocolitis and intestinal perforation
 6. Metabolic: -Hypoglycemia, hypocalcemia,
hypomagnesemia, hyponatremia lactic acidosis and
syndrome of inappropriate secretion of ADH
 DIAGNOSIS
• According to the ACOG/P. ,Essential criteria for Dx.
 Profound metabolic acidosis (cord PH.<7 )
 Early onset of encephalopathy.
 Multiple organ dysfunction.
 Exclusion of other causes of neonatal encephalopathy.
APGAR score < 7 at 5 min
 DIAGNOSIS…
• Laboratory investigations:-
 CBC,
 CSF-analysis.
 RBG.
 Serum electrolytes; calcium, sodium
 DIAGNOSIS…
• Imaging modalities :-
1. Cranial sonography:-high specificity & sensitivity for locating
hemorrhages & defining ventricular sizes.
2. Head CT.:-most useful for diagnosing intracranial hemorrhage &
brain calcification, brain edema.
3. Head MRI. :-most sensitive for detecting periventricular white matter
injury, deep gray matter injury , arterial infarction , hemorrhage...
4. EEG.:-distinguish neonatal seizures from others & also identify
subclinical seizure, also used to both to detect and monitor seizure
activity.
 TREATMENT
• Major goals of treatment of HIE include , The maintenance of
physiologic homeostasis & Treatment of the outward manifestation of
brain injury.
• Central aspects of supportive care include:-
1.Maintenance of adequate ventilation:-
 Give oxygen if the neonate is hypoxic.
 Give artificial ventilation if breathing is compromised.
2.Maintenance of sufficient brain & organ perfusion.
 Give 2/3rd of maintenance fluid.
 Keeping systemic arterial pressure at 45-50mmHg.
 TREATMENT…

3.Maintenance of normal metabolic status.

 Correcting acid-base balance.
 Maintain blood glucose level at about 75-100mg/dl.
 Calcium level should be kept in the normal level.
4.Control of seizure:-
 Benzodiazepam are important for transient control of seizure attack.
(diazepam(.25mg/kg or lorazepam(.05)
 Phenobarbitone is used with a loading dose of 20mg/kg. ,IV or PO. If
seizure persists , give 10mg/kg. of Phenobarbitone up to 40mg/kg.,
then maintenance dose of 3-4mg/kg. divided in to two doses.
 TREATMENT…
 If seizure not controlled, add phenytoin with loading dose of
20mg/kg. ,&maintenance of 3-4mg/kg. divided into two doses PO. Or
IV.
 For unresponsive seizure , give pyridoxine(vitamin B6)100mg. IV. Or
pyridoxine phosphate 10mg/kg. IV. Should be given.
 TREATMENT…
Therapeutic hypothermia
 Three Criteria mainly :-
 Infants >/=36weeks GA with birth weight>2000gm.
 Younger than 6hours at admission.
 Evidence of moderate to severe encephalopathy.
 Evidence of neonatal distress ,Infant must have 2 or more of
the following-APGAR score of 5 or less at 10 minutes, cord or
arterial PH<7,ventilation or resuscitation at 10minutes.
 Core temperature goal of 33-34ºC .for 72hours.
 TREATMENT…
Mechanism of action:-
 Reduces cerebral metabolism , prevents edema.
 Decreases energy utilization.
 Reduces cytotoxic amino acid accumulation & NO.
 Suppresses free radical activity.
 Attenuates secondary neuronal damage.
 Inhibits cell death/apoptosis.
 Reduces extent of cell damage.
 TREATMENT…
• Two types:-
1.Whole body (Systemic cooling)&
2.Head-cooling(selective cooling)
 TREATMENT…
 management of other organ system dysfunctions
Congestive heart failure – diuretics , dopamine
dobutamine
Acute renal failure – dopamine
Gastrointestinal – delay PO. feeding
Hematologic failure – blood component
replacement
 PROGNOSIS
 The outcome of HIE. ,correlates with the timing & severity of
the insult , ranging ,complete recovery-death
 Stage 1 or mild HIE: <1% mortality, 98% to 100% of newborns
will have a normal neurologic outcome.
 Stage 2 or moderate HIE: 20% to 37% die or have abnormal
neurodevelopmental outcome.
 Stage 3 or severe HIE: 76%-82% Death from effects of severe
systemic asphyxia is more likely with severe HIE or from
elective withdrawal of medical technology when there is
severe brain injury that will result in severe neurologic
disability .
 PROGNOSIS
 Predictors of death or severe cognitive &motor deficit includes:-
 A low APGAR score at 20 minutes.
 Absence of spontaneous respirations at 20 minutes.
 Persistence of abnormal neurologic signs at 2weeks.
 Stage-3(sever) encephalopathy.
 Combined severe MRI.& EEG. Abnormalities.
 Microcephaly & poor head growth during the 1st. Year.
 Follow up
 All survivors of moderate-severe encephalopathy requires high-risk
medical & neurodevelopmental f/up :-
 For early identification of neurodevelopmental complications
 Prompt referral for developmental & neurologic care intervention
services.
References

• Nelson text book 21th edition.

• Manual of Neonatal care 8th edition.
 Thank You for Being Patient Till
the ENd

10/06/2007 PNA/HIE 161