1. MEKELLE
UNIVERSITY
CHS
DEPARTMENT OF
PEDIATRICS &
CHILD HEALTH
SEMINAR ON MANAGEMENT OF COMMON NEONATAL PROBLEMS
By:
KIROS W/GERIMA
KIBRA SEBUH
KIFLOM SEYOUM
KESATEA G/WAHD
WORKU ASFAW
12/23/2013 1

2. Seminar outline
 Neonatal Sepsis
Hypothermia
Respiratory distress syndrome
Perinatal Asphyxia
Neonatal Seizure
Neonatal Jaundice
Rh and ABO incompatibility
New born Anemia
Hypoglycemia
References and Sources
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3. NEONATAL SEPSIS
by Kiros Weldegerima
12/23/2013 3

4. Sepsis Outline of presentation
• Classifications
• Risk factors
• Clinical Manifestations
• Meningitis and Pneumonia
• Diagnostic work up
• Management principles
• Prevention Strategies of Sepsis
• Hypothermia and its management
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5. Neonatal Sepsis
Infection or sepsis is a problem faced to all new
borns
But the risk and severity is high in small and
premature infants
It is the cause of 30-50 % of Neonatal mortality
in developing countries
Sepsis in the Neonate includes meningitis,
septicemias, pneumonia, Arthritis,
osteomyelitis, and UTI or combinations of
those.
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6. • Neonatal Sepsis can be divided as early and
late onset depending on the time of
occurrence
• Early-onset neonatal sepsis occurs with in the
first 72 hrs of life in 90% of cases
– Is caused by organisms prevalent in the
maternal genital tract
– Or in the labor room or operation theatre
where the neonate exposes initially to the
Environment
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7. Early onset Causative Agents
– Majority are caused by Group B
streprococcus, E-coli, klebsiela and
enterobacter
– Majority manifest with respiratory distress
due to an early intrauterine pneumonia
– The manifestation of illness is earlier than
the time limit of 1 week (24hr=85%, 24-
48hr=5%, 2-6 days=10)
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8. RISK FACTORS
Neonatal sepsis is associated with certain high
risk obstetric factors;
-Birth asphyxia
-Unclean vaginal examination
-foul smelling liquor
-prolonged labor(>24 hours)
-preterm and low birth weight Neonates
-prolonged rupture of membranes(>18 hours)
-maternal pyrexia
12/23/2013 8

9. Late onset causative Agents
• Late onset neonatal sepsis occurs after 7 days
most of which is after the first week of life up to
90 days.
• Most are caused by gram negative bacteria
– Klebsiela, enterobacter, E-coli, pseudomonas
and salmonella
– Gram positives like staphylococcus aureus
also contribute as causes of late onset sepsis.
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10. Infection Acquiring areas
Late onset infections are acquired as
nosocomial after delivery in:
-the normal newborn nursery
-Neonatal Intensive care Unit or
-the Community.
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11. Sources of infection in late onset
The usual sources of late onset neonatal sepsis:
-Incubators
-Resustation Equipment
-Feeding bottles
-Catheters
-Infusion sets and sites
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12. Clinical features
• It may be subtle especially in those who
are very small and premature
• This is mostly due to depressed immunity
of the premature neonates
• Early manifestations could be change in
behavior or feeding patterns
• But Gradually/sometimes suddenly they
develop signs and symptoms
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13. Clinical features of sepsis
Common clinical Features are
-Lethargic/Unconscious
-Inactive/Unresponsive
-failure to suck
-Hyperthermia/Hypothermia
-Respiratory Distress/Apnea
-failure to gain weight/weight loss
-Anemic/pale conjunctiva, palms
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14. Bacterial meningitis
• About a 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
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15. 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.
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16. Lumbar puncture result that Indicates
meningitis
> 30 cells/ml in Neonates , other than
Neonate >5 cells/ml of CSF
>60% polymorphs cells
–CSF glucose /blood glucose ratio <50%
–Protein>150 mg/dl in Terms and >175
in preterm
–Presence of microorganisms
–If the CSF not clear may also suggest
abnormality.
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17. 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
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18. Diagnostic work up of sepsis
• Clinical features + presence of high risk
obstetric factors
• Blood culture and sensitivity
• CSF analysis when indicated
• Chest X-ray
• Urine analysis and /or urine culture
• Head to Toe physical examination to identify
focus of infection (bone, joint, skin, GI)
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19. Management
• Depending on the etiologic agent but
Till etiologic agent is identified:-
– Good broad spectrum coverage i.e. for gram +ve
and gram –ve organisms is essential
• First line drugs
– Crystalline penicillin 100,000iu/kg /day in two
divided doses and
– Gentamicin 5 mg/kg/day in two divided doses
– Change crystalline penicillin with Ampicillin if
Listeria monocytogens is incriminated as the
causative agent
12/23/2013 19

20. Management
In meningitis the dose of Ampicillin and
Crystalline penciline are doubled.
 Second line drugs
–Ceftriaxone 50mg/kg/dose BID +
– Aminoglycoside dose which is also 50mg/kg
BID.
• Dose of ceftriaxone is doubled in cases of
meningitis
• Supportive therapy to correct metabolic
complications
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21. Management cont.
Duration of therapy
-suspected sepsis( blood culture –ve)= 7
days
-proven sepsis(blood culture +ve)=14 days
-Gram positive meningitis=14 days
-Gram negative meningitis=21 days
-Septic arthritis/osteomyelitis=4-6 weeks
12/23/2013 21

22. Prevention strategies of Neonatal
infections
Universal precautions
-Hand washing before entering labor ward and
before and after examining each infant
-wear Gowns and slippers when entering NICUs
-Health care providers with acute infections(
fever,ARI,skin lesions and Viral exanthemas)
should be restricted from providing care to the
Neonates
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23. Prevention Cotd…
-keep clean both the NICU and labor ward by
Cleaning and Fumigating at regular interval
-Proper skin and cord care
-Keep all Equipments used in NICU and labor
ward clean so there will be no infection source.
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24. Hypothermia
• Skin temperature of <36.5 and core
temperature of <35.5
• Neonates have high surface area to volume
ratio ,so heat loss is so much higher.
• After birth , the skin and core temperature of
the baby fall by 0.1 and 0.3/min respectively
.Which is equivalent to heat loss of 200kcal/kg
body weight/minute.

25. Mechanisms of heat loss/production
Mechanisms of heat loss:
1 Convection
2 Conduction
3 Radiation
4 Evaporation(common source of heat loss)
Mechanism of heat production
1 muscular activity
2 metabolic thermogenesis(most important
source of heat production in the new born)

26. Thermo Regulation
Thermo neutral environment :This is the ideal
temperature at which the baby can maintain
normal body temperature.
The optimal function of heat generating system
is dependent up on the integrity of
-CNS thermo regulation system
-adequacy of brown fat
-availability of glucose and oxygen
-NBW and term gestational age.

27. Stages of hypothermia
 36-36.4 c (96.8-97.5f)
-mild hypothermia (cold stress)
 32-35.9 c (89.6-96.6f)
-moderate hypothermia
 <32 c (89.6f)
-severe hypothermia (neonatal cold injury)

28. Warm chain system
• System of keeping the baby warm immediately after
birth,in delivery room,post partum ward
,transportation and while nursing the baby at home.
components:
-immediate drying
-warm resuscitation
-skin to skin contact with the mother
-immediate initiation of breast feeding
-bathing and weighing post pond
-appropriate clothing and bedding
-warm transportation.

29. Causes of hypothermia
External factors
cold environment,wet or naked baby ,blood
sampling,IV sampling
Poor ability to conserve heat
large surface area,poor insulation,paucity of fat,
Poor metabolic heat production
-deficiency of brown fat(preterm ,SFD)
-CNS problems
-hypoxia
-hypoglycemia

30. Sign and symptoms of hypothermia
1 peripheral vasoconstriction
Acrocyanosis
cold extrimity
decreased peripheral perfusion
2 CNS depression
Lethargy
Poor feeding
Apnea and bradycardia
3 Increased metabolism
hypoglycemia
hypoxia
metabolic acidosis
4 Increased pulmonary arterial pressure
tachypenia
respiratory distress

31. Management of hypothermia
There are 3 methods:
1.Kangaroo mother care
2.Warming in an open care using a radiant
heater
3.Warming in an incubator
Hazard’s of temperature control:
hyperthermia
undetected infection
volume depletion.

32. RESPIRATORY DISTRESS and APNEA
IN THE NEWBORN
PREPARED BY KIBRA.S
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33. RESPIRATORY DISTRESS
Definition
• The presence of any one of the following four
clinical features :
– RR > 60/min ( counted two times for full one
minute)
– Significant lower chest indrawing
– Grunting
– Central cyanosis
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34. ETIOLOGY
1.Pulmonary cause
Lung parenchyma disease Congenital airway
obstruction
Intrathoracic
malformation
Hyaline membrane disease Choanal atresia, nasal
edema
Pulmonary hypoplasia or
agenesis
Meconium aspiration
syndrome
Maroglossia, micrognathia,
retrognathia
Diaphragmatic hernia
Congenital pneumonia Congenital goiter, cystic
hygroma
Intra thoracic cyst
Transient tachypnea of the
newborn
Subglottic stenosis ,
laryngomalacia
Congenital lobar
emphysema
Bronchopulmonary
dysplasia
Tracheomalacia, congenital
tracheal stenosis
Pulmonary hemorrhage,
air leak
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35. 2.Extrapulmonary cause
Cardiac Metabolic Neurological Hematological
Congenital heart
Hypoglycemia Neonatal meningitis Anemia
disease
Congestive heart
failure
Hypocalcaemia Neonatal seizure Polycythemia
Cardiac arrhythmia Hypothermia Hypoxic ischemic
encephalopathy
Metabolic acidosis Extreme immaturity
Intracranial bieed
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36. APPROACH
 History
• Gestational age
• Previous preterm baby
• Antenatal steroid prophylaxis
• Maternal DM
• Ante partum hemorrhage
• PROM
• Prolonged duration of labor
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37. CONT’D
• Maternal fever
• Unclean vaginal examination
• Foul smelling, meconium stained liquor
• Hx of intrapartum or post partum suctioning
• Excessive salivation
• Difficulty of feeding
• Hx of traumatic delivery
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38. CONT’D
Physical Examination
Vital sign, capillary refill time and SO2
Meconium staining of the cord or nail
Hyperinflated chest or with bowel sound
Cyanosis, tachycardia, murmur
Scaphoid abdomen, hepatomegally
Evidences of intracranial bleed
Unable to pass nasal catheter
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39. CONT’D
Investigation
• Blood group of mother and baby
• CBC , CXR
• Septic screening & complete septic work up
• Serum electrolytes and blood sugar
• gastric aspirate (shake test, PMN cells)
• Cord pH, arterial blood gas
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40. MANAGMENT
General MX
– Give vit.k if not given
– Basic support care
• Keep in thermo neutral zone
• Breast feeding or assist feeding
• Maintain adequate oxygenation & circulation
Specific TX for specific problems
– Chest tube, decongestive measures, volume expanders,
antibiotics, surgical correction
12/23/2013 40

41. Hyaline Membrane Disease
 Incidence
– Primarily in premature infants; inversely
proportional to GA & birth weight
 Risk factor
– Prematurity
– Maternal DM
– Male sex
– 2nd born twins
– C/S delivery
– Perinatal asphyxia
Protective factor
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42. Pathogenesis
12/23/2013 42

43. CONT’D
Clinical Feature
-Signs occur with in minutes or hours of
birth, reach peak with in 3 days
-Characteristically
• Tachypnea
• Nasal flaring
• SC or IC retraction
• Cyanosis
• Expiratory grunting
12/23/2013 43

44. CONT’D
Diagnosis
─based on clinical picture in conjunction with
characteristic chest radiograph
─The CXR abnormalities:
Low lung volume
Diffuse reticulogranular ground glass appearance
with air bronchogram
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45. CXR findings in Classic RDS
* Bell-shaped thorax
* ↓lung volume
* Air bronchogram
extended beyond cardiac
border
* Absolutely opaque lung
(whiteout lung)
12/23/2013 45

46. CONT’D
Management
Basic supportive care
Specific measures
Prevent hypoxia & acidosis
Warm humified o2 administration
 CPAP(indication, procedure & complication)
 Assisted ventilation
Surfactant replacement therapy
(poractant,calfactant,beractant)
Prevention
Prenatal testing & appropriate prophylaxis
12/23/2013 46

47. Congenital pneumonia
• Is acquired transplacentally or perinatally
• Accounts for >50% of cases of RD in the new born
 Risk factor
–PROM
–Prolonged labour (> 24 hrs)
–Unclean vaginal examinations.
–Foul smelling liquor
–Maternal fever
12/23/2013 47

48. CONT’D
Causative organisms:
-Group B streptococcus
-Gram negative organisms : E.coli, klebsiela, pseudomonas
-Staph aureus and Listeria monocytogens
 Clinical manifestations
Respiratory distress soon after birth
Recurrent apneic attack
They are often asphyxiated and sick at birth
 Prolonged capillary filling time
 Hypothermia
Cough is rare
12/23/2013 48

49. Investigations
– CBC, esp. ANC
– Gastric aspirate for PMN
– Blood culture
– CXR(infiltrates, lobar consolidation, interstitial
reticular opacities)
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50. Management
– Basic supportive therapy
– Specific
• Emperical broad spectrum antibiotics
– Penicillin/Ampicillin 100mg/kg in 2 divided doses +
Gentamicin 4mg/kg q24hr or 2.5 mg/kg q12hr
12/23/2013 50

51. Meconium Aspiration Syndrome
Definition
• Respiratory distress in newborn infants
born through meconium stained
amniotic fluid whose symptom cannot
be otherwise explained
Incidence
─10-15% of births-meconium stained amniotic fluid
– 5% -meconium aspiration pneumonia
• 30% require mechanical ventilation
• 3-5% expire
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52. CONT’D
 Risk factors
• Placental dysfunction
• Fetal hypoxia
• Ante partum haemorrhage
• Post maturity or SGA
• Listeriosis
• Breech delivery
12/23/2013 52

53. CONT’D
Pathophysiology
─Fetal hypoxia
– Peristalsis & IU passage of meconium
– Meconium stained amniotic fluid
– Meconium aspiration
– Peripheral & proximal air way obstruction,
inflammatory &chemical pneumonitis
12/23/2013 53

54. CONT’D
Clinical feature
– Respiratory distress- onset soon after birth in a
baby born to mother with meconium stained
liquor .
– Hyper inflated chest
– Meconium stained skin and cord
– Urine may appear dark and brown
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55. CONT’D
Investigation
– CXR
• Hyperinflation
• Bilateral fluffy shadows
• Evidence of air leak
12/23/2013 55

56. 12/23/2013 56

57. CONT’D
Management
─Prevention of meconium aspiration
• Prevention of IU hypoxia
• Intrapartum suctioning
– Postnatal suctioning
• Thick meconium
– Direct laryngoscopy & tracheal suction
– Stabilize the baby
– Stomach wash
– Work up for sepsis
– Antibiotics can be started
• Thin meconium
– Depressed baby-do all like thick meconium
– Active baby-no tracheal suctioning and needs close observation
12/23/2013 57

58. APNEA
Definition
– Cessation of respiratory airflow
– Absence of respiratory movement
• Apnea vs periodic breathing
Incidence
– Increases with decreasing GA
12/23/2013 58

59. Classification
• Based on the cause
– Primary(apnea of
prematurity)
– Secondary
• Based on presence of
continued inspiratory
effort and upper airway
obstruction
– Central
– Obstructive
– Mixed
12/23/2013 59

60. CONT’D
Pathogenesis
unable to react to hypercapnia
• Impaired respiratory response(hypercapnia)
• Apnea
• ↓HR, Pao2
• Hypoperfusion and hypoxia
• Hypercapnia
• Recurrent apnea(≥3 attacks in one hour)
• Brain damage & multiorgan damage
12/23/2013 60

61. CONT’D
Management
General management
– ABC of resuscitation
– Avoid vigorous suctioning
– Keep NPO for 24 hrs put them on maintenance IVF
– Keep in thermoneutral environment
– Treat the underlying cause of apnea
Specific therapy
• Drug─theophylline
─aminophylline
─ caffeine
• Positive pressure ventilation
12/23/2013 61

62. prepared by kiflom seyoum
12/23/2013 62

63. Layout
• Definition
• epidemiology
• Pathophysiology
• Risk factors
• Clinical features
• Management
• Prevention
• Neonatal seizure
12/23/2013 63

64. Perinatal Asphyxia
Definition:
 PNA is an insult to the fetus or newborn due to lack of oxygen (
hypoxia ) and /or a lack of perfusion ( ischemia ) to various organs.
 Failure to establish efficient breathing at one minute of age(APGAR
score 0 - 6) with hypo/hypertonia and/or seizure.
 This definition using APGAR score is not applicable in
 Preterm babies
 Babies with birth trauma
 Congenital neurologic abnormalities
12/23/2013 64

65. Epidemology
• Ranges 1-1.5% in gneral
• 9% in babes born <36 weeks of gastion
• 0.3% in babies born >36 weeks of gastion
• Accounts 23% of perinatal death
• 23-30% of survivors have permanent damage
like CP
12/23/2013 65

66. Timing of ingury
• Asphyxia can occur in the,
 Antepartem
 Intrapartem
 Postnatal priod
12/23/2013 66

67. Risk factors
1 .Antepartem condition
 Abnormal maternal oxygenation ( sever
animia, cardiopulmonary disease)
Inadequate placental perfusion( sever HTN,
maternal vascular disease)
Congenital infection or anomalies
12/23/2013 67

68. Conti…
2. intrapartem events
Interruption of umblical circulation (true
knote, cord prolaps)
inadequate placental perfusion ( abrabtio
placenta, utrine rupture, abnormal utrin
contraction )
Abnormal maternal oxygenation
Vasa previa
12/23/2013 68

69. Conti…
• 3, post natal disorders
Persistent plumnary hypertention of the new
born
Sever circulatory insuficency ( acut blood loss,
septic shock )
12/23/2013 69

70. Eitology and pathphysiology
90% of insult occur due to placental
insufficiency
Decrease oxygen supply &
Decrease carbon dioxide and hydrogen
removal
<10% are post natal insult due to pulmonary,
CVS or neurologic insufficiency
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71. Cont…
• When the new born is depraved of O2 an
initial period of rapid breathing occur
• This is followed by primary apnea
• Which responds to O2 administration and
physical stimulation
12/23/2013 71

72. Cont…
If asphyxia contnues the new born devoleps
Gasping respiration
Decreased puls rate
Blood pressure fail
And the new born develops secondary apnea
which will respond only to advanced life
support including CPAP
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73. Con…
• If asphyxia is not reversed on time there will
be hypoxic damage that leads to ischemic
challenge
• A diving reflex will be initiated that causes
shunting of blood to vital organs
12/23/2013 73

74. Clinical feature
• Depends on the organ affected
• Target organs of prenatal asphyxia
 Kidney in 50% of cases
 CNS in 28% of cases
 CVS in 25% of cases
 Pulmonary 23% of cases
12/23/2013 74

75. Renal dysfunction
• Often accompanies prenatal asphyxia
• renal damage ranges from reversible cloudy swelling &
hydropic digeneration of tubles to infarction of the
entire nephron.
• Decrease in UO(<0.5ml/kg/hr which may last 2 day to 2
weeks
• Protein & cast may present in the urin
• Gross hematuria may present
• Elevation of BUN& creatinine may occur
• Poly urea may flow oliguric phase or they may develop
anuria
12/23/2013 75

76. CVS dysfunction
• May cause myocardial ischemia which usually
is transient
• Patients show tachypnea,tachycardea &
hepatomegally consistent with heart fealur
• Rarely causes cardiogenic shock and death
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77. Pulmonary dysfunction
1.Plumonary edema
Due to myocardial dysfunction
May have sign of respiratory distress
2.Acute respiratory distress syndrome
Increased plumnary capilary permebility to
plasma protien which leads to inactivation of
surfactant
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78. Hypoxic ischemic encephalopathy
• The most serous complication of perenatal asphyxia
• The neuralgic squale often persists
• Hypoxia impairs cerebral oxidative mechanism and
leads to myocardial depression this leads to fail in
cerebral blood flaw
• And then ischemia of the brain tissue occur
• Persistance of hypoxia increase anarobic glycolysis
which leads to lactic acidosis
• Worsening of lactic acidosis if not corrected on time
cuases loss of cerebral vascular auto regulation
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79. Conti…
• Most of the time prolonged partial episode of
aspheyxia is because of abruptio placenta
• And usually it causes diffuse cerebral necrosis
• Clinically this may be present in the form of seizure
and paresis.
• Acute total asphysia which is mainly due to cord
plolapse primerly affects brain stem,thalamus, &
basal ganglia.
• This may manifest in the form disturbance of
respiration,heart rate & blood pressure
12/23/2013 79

80. Investstigations
• EEG-to determine severity presence of seizure
• Cranial u/s- to determine presence ICH &
brain edeama
• CT scan –early (2-4 days) brain edema
-late(2-4weeks) for encephalomalesia
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81. Sarnat staging of hypoxic-ischemic encephalopathy.
Grade2 Grade 3 (severe)
(moderate)
Grade 1
(mild)
Level of Irritable/hyperalert Lethargy Coma
consciousness
Normal or Hypotonia Flaccid
hypertonia
Muscle tone
Tendon reflexes Increased Increased Depressed or absent
Seizures Absent Frequent Frequent
Complex reflexes Normal weak Absent
High mortality and
neurological disability
(50% Death 50%
major sequelae)
Variable
(80% ) Normal
Good
(100%) Normal
Prognosis
12/23/2013 81

82. Management of perinatal asphyxia
• Anticipate need for neonatal resuscitation
from maternal obstetric & labor history
• Avoid blood pressure fluctuation
• Intravenous fluid 2/3 of maintenance
• Appropriate ventilation support
• Correct metabolic abnormalities
• Prophylactic anti convulsant (phenobarbital)..?
12/23/2013 82

83. Therapeutic hypothermia
• It improves out come after perinatal asphyxia
• The only effective neuro protective therapy
currently available for Tx of neonatal
encephalopathy
• Safe and easy to administer
• Selective head cooling & whole body
cooling…?
12/23/2013 83

84. Prevention of prenatal asphyxia
The minimum preventive measure which is
provided during perinatal period is much better
than a sophisticated care provided to an
asphyxiated new born.
Prenatal assessment of changing fetal and
placental condition by clinical assessment and
altrasonography
Fetal BPP
Monitor progress of labor
Effective neonatal resuscitation
12/23/2013 84

85. Neonatal seizure
The most important & common indicator of
significant neurologic dysfunction in the
neonatal period
The immature brain is more likely to develop
seizure
Not similar to adult b/c of ariboraisation of
axons dendrites & myelin sheath
12/23/2013 85

86. Cont…
• They are five clinical types of NS
1.subtle
2.clonic
3.Tonic
4.spasem
5.Myoclonic
12/23/2013 86

87. Con…
• Based on EEG NZ classified into three
Electroclinical seizure
Electrical seizure
Clinical seizure
12/23/2013 87

88. causes
1.Age 1-4 days
HIE
IVH
Drug toxicity,(lidocain,pencilin)
Acute metabolic disorder
12/23/2013 88

89. Conti…
Age (4-14 days)
Infection
Metabolic disorder
Benign neonatal convelsion
kernicterus
12/23/2013 89

90. Cont…
Age (2-8wks)
Infection
Head injury
Inherited disorder of cortical development
12/23/2013 90

91. Diagnosis
Post natal & prenatal history
Blood should be obtaine
Lumbar puncture
EEG(show paroxysmal activity, sharp wave )
12/23/2013 91

92. Management of NS
Treatment of the underlying etiology
Complete control of clinical as well as
electrographic seizure vs clinical seizure
control…?
Neonates required assisted ventilation after
receiving IV or PO loading doses of AED
12/23/2013 92

93. CONT…
1.Phenobarbitol
 The drug of first choice in the neonatal seizure
 20mg/kg loading dose, if not effective an additional
dose of 5-10mg/kg until a maximam dose of 40mg/kg,
 the mentenance doses is 3-6mg/kg
2.Phenytoin
 If no response phenytoin loading dose of 15-40mg/kg
can be given
 Rate must note exced 0 .5-1mg/kg/min to pereven
cardiac toxicty
12/23/2013 93

94. Cont…
3.Lorazepam;
the initial drug used to control acute seizure
Can be used as first line or second line Tx in
the new born who didn’t respond to
phenobarbitol or phenytone
4.diazepam;
It is highly lipophilic so cleared very quickly
out carring the risk of recurrence of seizure
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95. When to discontinu…..?
• At the time of discharge
• two wks or three month after discharge if the
neonate had sever PNA
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96. prognosis
• Mortality from neonatal seizure has decreased
from 40% to 20%.
• The correlation b/n EEG & prognosis is very clear
• Prolonged electrographic seizure >10min/hr,
multifocal periodic electrographic discharge,&
spread of electrogrophic seizure to contralateral
hemospher has poor prognosis
• Seizure due to HIE 50% of them have normal out
come
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97. NEONATAL JAUNDICE
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97

98. JAUNDICE
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 Visible form of bilirubinemia
 Adult sclera >2mg / dl
 Newborn skin >5 mg / dl
 Occurs in 60% of term and 80% of preterm
neonates
 Is common problem and is mostly benign.
 However, significant jaundice occurs in 6 % of
term babies
98

99.  The conjugated bilirubin will go to bowel with bile.
 In adults E.coli and C.perfirngens present but absent in
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neonets.
 β-glucourinidase enzyme present in newborns.
Conjugation and enterohepatic resorption.
99

100. 12/23/2013
 Direct Vs Indirect?
 Van den Bergh reaction
 Indirect billirubin acts as an anti-oxidant
 It is only the indirect billirubin which crosses the
BBB and results in billirubin encephalopathy
100

101. Physiologic Jaundice
 Jaundice becomes evident as physiologic in
neonates B/c :
A. Short life span of RBCs(70-90days)
B. RBC mass is increased
C. Immature ligandine
D. Less UDPGT
E. High activity β-glucuronidase (gut)
F. Decreased flora in the gut
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101

102. Physiologic jaundice ( Icterus
neonatorum)
Preterm Term
Peak time 4th -7th days 2nd – 4th day
Peak level 8 – 12 mg/dl 5 -6 mg/dl
Resolution time Before 10th day 5th – 7th day
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102

103. Physiologic Vs pathologic
Signs PhysiologicJx Pathologic Jx
Clinical Jx Visible in2-3day With in 24hrs
TSB rise <5mg/dl/day >5mg/dl/day
TSB Term<12mg/dl
Preterm<15mg/dl
Term>12g/dl
Preterm>15mg/dl
Conj BBn <1.5mg/dl >1.5(2)mg/dl
Jaundice
persisting
Term <1 week
Preterm <2weeks
Term >1week Preterm
>2weeks
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103

104. Jaundice associated with breast feeding
Breast milk Breast feeding
Cause ?glucouronidase in
BM
↓ intake
Time of
onset
After 1st week In the 1st week
Max level 10 – 30 mg/dl Any
Treatment Discontinuation for
2 – 3 days
Continuing
breast feeding
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104

105. ETIOLOGY OF JAUNDICE
1. Jaundice appearing in the 1st 24 hr
 Rh incompatability(erythroblastosis fetalis)
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 ABO incompatibility
 Mild BG incompatibility (Kelly, Duffy Ags)
 Defect (G6PD def. and spherocytosis
 TORCHS
 Criggler Najar syndrome
 Transient familial neonatal jaundice
105

106. Cont…
2.Jaundice appearing with in 24-72hr of age
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 Physiological jaundice
 Conditions w/c aggravate physiologic Jx.
 Cephalhematoma
 Hypothermia
 Prematurity
 Hypoglycemia
 Multiple bruises
 hypoxia
106

107. Cont…
3. prolonged jaundice( after 72 hrs.)
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 TORCHS
 Sepsis
 Hypothyroidism
 Biliary Artesia
 Breast milk jaundice
 Drugs (vit. K, oxytocin,diazepam)
 Metabolic disease eg. galactosemia
107

108. Hemolytic disease of the
newborn
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 Rh incompatibility
 Less common but sever than ABO incompatibility
 90% due to D antigen
 Black vs white
 Severity from mild hemolysis to sever anemia
 Dx by blood group incompatiblity
 Reduce risk of sensitization with 300μg of human
anti- D globulin during ANC ff up
108

109. Cont…
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 ABO incompatibility
 Most common cause of HDN but mild
 0.3-2.2% only manifest the disease.
 Type O mother with type A or B infant.
 Jaundice the only clinical manifestation.
 Hemoglobin level usually normal.
 Dx by ABO incompatibility (weak to moderate
positive direct coombs test)
109

110. Clinical assessment of jaundice
 Jaundice in the newborn progresses in cephalocaudal
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direction
 Face =5-7mg/dl
 Chest =10mg/dl
 lower abdomen /thigh= 12mg/dl
 Sole/palms≥15mg/dl
110

111. Work up neonates with Jx
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History
 Age of onset
 Family history of Jaundice,pallor,splenectomy
 Previous sibling with Jaundice
 Maternal illness during pregnancy
 Maternal drug intake
 Delivery history e.g. PROM ,sepsis, prolonged
labor
111

112. Cont’d
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P/E
 Proper classification of the newborn according to
GA, & wgt.
 Pallor, petechea
 Bruises and cephalhematoma
 Dark urine and clay colored stool
 Examination geared to specific cause
112

113. Investigations
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 TSB with conjugated fraction
 Hct with RBC morphology and reticulocyte
count
 Bg of the baby with direct coomb’s test
 Bg of the mother with indirect coomb’s test.
 Specific investigations for suspected specific
problems
113

114. Management
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 Aim
 lower serum billirubin
 decrease neurtoxicity
 Principles of treatment
 Avoid drugs w/c interfere with BBn
metabolism
 Treat factors w/c↑ neurotoxicity
 Give adequate feeding
 Specific therapy
 Decrease serum billirubin
114

115. 12/23/2013
 Lower serum Billirubin
 Phototherapy
 Exchange transfusion
 Phototherapy
 Indicated when TSB rises more than normal
but not exchange transfusion level
 May be therapeutic or prophylactic
115

116. Prophylactic phototherapy
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INDICATIONS
 RH isoimmunization with sever hemolysis
 Birth weight<1000gm(EVLBW)
 Sever multiple bruises
SIDE EFFECTS
 Erythematous skin rash
 Retinal damage
 Increased insensible water loss
 Bronze baby syndrome
 Loose stool
 Low calcium
116

117. Exchange transfusion( ET)
 Most effective way of treating Jaundice and
anemia
 Could be partial or double exchange transfusion
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INDICATIONS
 Rh isoimmunization with hydrops fetalis
 History of previous sibling required ET with pallor
 Cord blood Billirubin >5mg/dl
 Rise in Billirubin >0.5mg/dl/hr despite
phototherapy
 Hemoglobin <11gm/dl
 TSB >20mg/dl
 VLBW, preterm, sepsis
117

118. Choice of blood for exchange BT
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 ABO incompatibility
 Use O blood of same Rh type
 Rh isoimmunization
 Emergency 0 -ve blood
 Ideal 0 -ve suspended in AB plasma
 or baby's blood group but Rh –ve
 Other situations
 Baby's blood group
118

119. Exchange transfusion
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COMPLICATIONS
 Portal vein thrombosis
 Umbilical vein perforation/bleeding
 Necrotizing enterocolitis
 Cardiac arrest/arrhythmia
 Hypoglycemia, hypocalcemia, hypomagnisemia,
hyperkalemia
 Increased risk of infection
 Respiratory and metabolic acidosis
119

120. KERNICTERS (Billirubin encephalopathy)
 Definition: neurologic syndrome resulting from
deposition of unconjugated billirubin in brain cells .
 Sites of billirubin staining and necrosis include
-Basal ganglia , Hippocampal cortex, Sub thalamic
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nucleus & cerebellum
 Cerebral cortex is spared
 Half of the neonates with kernicters at autopsy have
extra neuronal lesions
120

121. Pathophysiologic mechanism
 Unconjugated BBn is nonpolar ,lipid soluble and can
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traverse BBB.
 Factors that ↑ billirubin toxicity
 Hypoxia (asphyxia)
 Hypothermia & hypoglycemia
 sepsis
 Prematurity
 Acidosis
 Hypoalbuminemia
121

122. Clinical staging of KI
Stage-1 Poor Moro reflex, decreased tone, lethargy,
poor -
feeding, vomiting, high pitched cry
Stage-2 Opisthotonus, fever, seizure, rigidity,
oculogyric - crises,
paralysis of upward gaze
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Stage-3 Spasticity is decreased
Stage-4 Late sequale including spasticity,athetosis,
- deafness,MR,paralysis of the upward gaze
122

123. Clinical progression of encephalopathy
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123

124. Thank
you!