Newborn nt ปี 5

1. NT ปี 5

2. THERMOREGULATION

3. ลักษณะการหายใจของทารกแรก
เกิด
 3-4 วันแรกหลังคลอด การหายใจไม่สม่าเสมอ
 เมื่อหลับสนิทการหายใจจะสม่าเสมอ ไม่เกิน 60 ครั้งต่อ
นาที
 อาจมี periodic breathing

4. THERMOREGULATION
1. Heat production
2. Heat loss

5. Heat production
1. Physical thermogenesis
– voluntory muscle activity
– involuntory muscle activity
shivering method
2. Nonshivering thermogenesis or chemical
thermogenesis
– Brown fat (เริ่มมีเมื่ออายุครรภ์ 26-30 wks
จนกระทั่งเต็มที่หลังเกิด 3-5 wks)
– Brown fat พบที่ระหว่างกระดูกสะบัก รอบคอ รักแร ้
– รอบๆไตและต่อมหมวกไต

6. Chemical thermogenesis
Cold Thermal receptor Hypothalamus
Sympathetic nerve
Norepinephrine release
กระตุ้น brown fat metabolism
Triglyceride NEFA + Glycerol
+ พลังงานความร้อน
hydrolysis
กระตุ้นการทางานของ
lipase

7. Heat loss
1. พื้นที่ผิวกายเทียบกับน้าหนันักวัวกาก
2. Subcutaneous fat น้อย
3. Vasomotor activity ยังไก่ดี

8. Heat loss
1. Convection
2. Conduction
3. Radiation
4. Evaporation

9. 1. Convection 2. Conduction
Heat loss

10. 3. Radiation
Heat loss
4. Evaporation

12. Cooling
Norepinephrine
Pulmonary vasoconstriction
Increased pulmonary
artery pressure
Increased right to left
shunting
Peripheral vasoconstriction
Accumulation of lactic acidosis
Anaerobic metabolism
Hypoxia
การเปลี่ยนแปลงที่เกิดขึ้ นเมื่อทารกมีอุณหภูมิกายต่า

13. ทารกแรกเกิดเสี่ยงว่อการเกิดภาวะอุณหนัภูกิกายว่า
(hypothermia )
: BT < 36.5o C
ควรใหนั้ทารกอยู่ใน neutral thermal environment

14. Thermal neutral zone
 ช่วงอุณหภูมิของสภาพแวดล้อมที่ทาให้
ทารกสามารถรักษาอุณหภูมิร่างกายให้
ปกติอยู่ได้ โดยมีการใช้พลังงานน้อยที่สุด
 ขึ้นกับ อายุครรภ์ อายุหลังคลอด และ
ขนาดของร่างกาย

15. Neutral thermal environmental temperatures
Temperature
Age and weight At start (o
C) Range
0-6 hours
< 1,200 g 35.0 34.0-35.4
1,200-1,500 g 34.1 33.9-34.4
1,501-2,500 g 33.4 32.8-33.8
> 2,500 g 32.9 32.0-33.8

16. Apgar score
• A practical method for assessing a neonate
• Assess at 1 and 5 minute after birth

17. Respiratory distress
• Clinical presentation of respiratory distress in
newborn :
apnea, cyanosis, grunting, tachypnea (>60/min)
inspiratory stridor, nasal flaring, poor feeding
chest retractions
(intercostal, subcostal, supracostal spaces)

18. Differential diagnosis of respiratory distress in newborn
Transient tachypnea of the newborn
Meconium aspiration syndrome
Respiratory distress syndrome
Pneumonia
Pneumothorax
Persistent pulmonary hypertension
of the newborn (PPHN)
Congenital malformation of lung
Diaphragmatic hernia
Pulmonary causes Nonpulmonary causes
Neuro : Meningitis, IVH
CVS : Congenital heart disease
Metabolic : Hypoglycemia
Hypo/Hypernatremia
Hemato : Anemia, Polycythemia
Others : Sepsis
Subtemperature
Maternal medications
Welty S, Hansen TN, Corbet A. Respiratory distress in the preterm infant. In: Taeusch HW, Ballard RA, Gleason CA, editors.
Avery’s diseases of the newborn. 8th ed. Philadelphia: Saunders, 2005: 688-703
Hany Aly. Respiratory Disorders in the Newborn: Identification and Diagnosis Pediatr. Rev. 2004;25;201-208

19. Hany Aly. Respiratory Disorders in the Newborn: Identification and Diagnosis Pediatr. Rev. 2004;25;201-208

20. Chest examination
• MAS : Hyperinflated of chest
• RDS : Decreased in air entry
• Pneumothorax : Decreased breath sound or
distant heart sound
• Diaphragmatic hernia : hyperinflated of chest and
flatted abdomen

21. Investigation ?
Complete blood
count
Chest X-Ray
± Arterial blood
gas (severity of
baby)
Electrolyte
(as indicated)
Glucometer

22. Complete blood count
Consider sepsis
• Neutropenia (WBC < 5,000 cells/uL)
• Absolute neutrophil count < 1,750 cells/uL
• Absolute band count > 2,000 cells/uL
• Immature neutrophil/total neutrophil ratio
(I/T ratio) > 0.2
• Thrombocytopenia (platelet < 150,000 /uL)

23. Transient tachypnea of the newborn
Clinical signs:
• Term & Preterm
• Tachypnea (RR 60-120/min), chest wall retraction
• Self-limited disease
• Need O2 supplementation at the onset of disease and
then progressively decrease
• Symptoms usually resolve within 48-72 hours

24. Lokesh Guglani, Satyan Lakshminrusimha and Rita M. Ryan. Transient tachypnea of the newborn. Pediatr. Rev. 2008;29;e59-e65.

25. Transient tachypnea of the newborn
Radiographic abnormalities
• Hyperaeration
• Prominent perihilar streaking
• Prominent vascular marking, minor fissure
• Small pleural effusions may be seen
• Radiographic abnormalities resolve over the first
2-3 days after birth

27. Meconium aspiration syndrome:
MAS

28. Meconium aspiration syndrome
Meconium
• Viscous green liquid, odorless
• First evidence in fetal intestine 10th – 16th week of
gestation
• Composition: GI secretion, cellular debris, mucus,
bile, blood, lanugo

29. Meconium aspiration syndrome
Clinical signs
• Mature, post mature, SGA
• Long finger nails, dry and peeling skin
• Meconium stain on nails, hair, skin and umbilical cord

31. Respiratory symptoms
• Begin at birth, shortly thereafter
• Tachypnea, retraction, nasal flaring, cyanosis
• Chest : barrel shaped
• Coarse crepitation, inspiratory and expiratory rhonchi
with prolonged exhalation
Meconium aspiration syndrome

33. Ball-valve effect

34. Meconium aspiration
Proximal airway
obstruction
Acidosis
Hypoxia
Hypercapnea
Peripheral
airway
obstruction
Completes
Atelectasis
V/Q mismatch
Partial
Ball-valve effect
Air-trapping
Air leaks
Inflammatory and
chemical pneumonitis
Surfactant dysfunction

35. Diagnosis of MAS
Meconium-stained amniotic fluid or infant or both
Respiratory distress at birth or shortly after birth
Positive radiographic features
“Presence of meconium in endotracheal suctioning
automatically established the diagnosis”
Tsu F. Yeh. Core concepts: meconiuma aspiration syndrome: pathogenesis and current management. NeoReviews 2010;11;e503-e512

36. Radiographic finding
• Variable
• Coarse linear peribronchial infiltrations
• Areas of atelectasis
• Pleural effusion 20-30%
• Severe cases :
- progress to diffuse and homogeneous opacification
- gradually resolve over weeks
• Pneumothorax, pneumomediastinum 25%
Meconium aspiration syndrome

40. 1. Antibiotic
 Meconium is a good media for gram negative
bacilli
 Indication
• History of perinatal infection
• Undergone vigorous resuscitation
• Required mechanical ventilator
2. O2 supplement
Management MAS
Tsu F. Yeh. Core concepts: meconiuma aspiration syndrome: pathogenesis and current management. NeoReviews 2010;11;e503-e512

41. Respiratory distress syndrome:
RDS

42. Respiratory distress syndrome
• “Hyaline membrane disease”
• Most common cause of respiratory distress in
premature infants born at < 28 weeks’ gestation
• 1/3 infants born at 28 to 34 weeks’ gestation
• < 5% infants born after 34 weeks’ gestation
• Etiology : surfactant deficiency

43. Clinical signs
• Begin at or immediate after birth
• Rapid breathing, cyanosis in room air
• Grunting and chest retractions
Respiratory distress syndrome

44. Chest radiography
• Homogenous opaque infiltrates and air bronchograms
“Ground glass appearance”
• Diffuse, fine granular infiltration
• Usually hypoaeration
Respiratory distress syndrome

45. After surfactant replacementRDS

46. After surfactant replacementRDS

47. Infection : Pneumonia

48. Infection : Pneumonia
• Common pathogens : group B streptococci (GBS),
Staphylococcus aureus, Streptococcus pneumoniae,
and gram-negative enteric rods
• Risk factors for pneumonia include
prolonged rupture of membranes (PROM),
prematurity and maternal chorioamnionitis
• Signs and symptoms : temperature instability,
tachypnea, drowsiness

49. GROUP “B” STREPTOCCAL PNEUMONIA

50. Take home message
TTNB MAS RDS Pneumonia
Risk factor C/S Meconium
stain
Post-term
Preterm, DM PROM,
Preterm
Maternal fever
Natural history Onset early
Resolve within
48-72 hrs
Onset shortly
after birth
Mild-severe
Immediate
after birth
Vary
Signs of sepsis
CXR Normo-
hyperaeration
Minor fissure
Prominent
vascular
marking
Hyperaeration
Consolidation
Atelectasis
Pneumothorax
Hypoaeration
Ground-glass
appearance
Bilateral
Normal
aeration
Infiltration
uni/bilateral

51. Cyanosis in newborn

52. Clinical conditions that may cause
cyanosis in newborn
Respiratory Cardiac
Pulmonary
vascular :
PPHN
Central
nervous
system

53. สาเหตุจากทางปอดและทางเดินหายใจ
การตรวจพบ
 หายใจเร็ว หายใจลาบาก
 Chest retraction,
expiratory grunting
 เสียงปอดผิดปกติ
 Chest x-ray ผิดปกติ
 ให ้ออกซิเจน อาการเขียว
จะดีขึ้นหรือหายไป

54. สาเหตุจากโรคหัวใจ
การตรวจพบ
 หายใจเร็ว มักไม่มี chest retraction
 ฟังปอดปกติ ยกเว ้น congestive heart failure
 Heart murmur +
 Chest x-ray : หัวใจโต หรือ pulmonary vascular
markings ลดลง
 ให ้ออกซิเจน PaO2 เพิ่มขึ้นน้อยมากหรือไม่
เปลี่ยนแปลง

55. สาเหตุจาก PPHN
การตรวจพบ
 Severe hypoxemia
 Severe acidosis
 Tachypnea
 No anatomical cardiac lesions
 May have hypovascularity on the chest
radiograph, relatively clear lung fields

56. สาเหตุทางระบบประสาทส่วนกลาง
การตรวจพบ
 หายใจตื้น ไม่สม่าเสมอ
 แขนขาอ่อนแรง
 อาการเขียวหายไปเมื่อกระตุ้นหรือให ้
ออกซิเจน

57. แนวทางการวินิจฉัย
1. ประวัติ
 Preterm, post-term
 น้าเดินก่อนคลอดนาน
 Perinatal distress, meconium
 อาการเขียวเกิดขึ้นเมื่อไร*
เขียวคงที่หรือมากขึ้น
 Mode of delivery

58. 2. การตรวจร่างกาย
 ควรให ้ทารกสงบ หายใจ
room air (ถ ้าไม่ distress มาก)
 Central หรือ peripheral
cyanosis, different cyanosis
 Heart murmur, ลักษณะการ
หายใจ
แนวทางการวินิจฉัย

59. 3. การตรวจทางห ้องปฏิบัติการ
1) Hct, dextrostix, calcium, drop of blood
2) ABG (pH, PaO2, PaCO2)
3) Chest x-ray
4) Hyperoxia test
5) Preductal & post ductal blood gas
6) EKG, echocardiography
แนวทางการวินิจฉัย

60. Hyperoxia test
ให ้O2 100% ทาง oxygen
hood อย่างน้อย 5-10 min
PaO2 < 100 mmHg
PaO2 > 150 mmHg ไม่ใช ้โรคหัวใจชนิดเขียวแน่นอน
cyanotic congenital heart disease
PPHN
PaO2 100-150 mmHg อาจเป็นโรคหัวใจชนิด complete
intracardiac mixing และ PBP มาก

61. การดูแลรักษา
การดูแลรักษาโดยทั่วไป
 รักษาอุณหภูมิกายให ้ปกติ
 IV fluid,glucose
 Adequate tissue
oxygenation
การรักษาจาเพาะ
 แก ้ไขตามสาเหตุ
Respiratory failure
PPHN
CHD ต ้องอาศัย PDA

62. Congenital cyanotic heart disease ที่ PBF ขึ้นกับ flow
ที่ผ่าน ductus arteriosus
 ให ้Prostaglandin E1
 เริ่ม infusion 0.05-0.1 g/kg/min when desired effects
 dose 0.05, 0.025 & 0.01 g/kg/min
 If unresponsive, dose may be increased to 0.4
g/kg/min
Side effects : fever, seizure, cutaneous flushing tachycardia,
bradycardia, apnea, BP  cardiac arrest
การดูแลรักษา

63. Definition
Apnea :
Cessation of breathing for longer than 20 seconds or
shorter duration + Pallor
Cyanosis
Bradycardia

64. Definition
Periodic breathing
• Recurring cycles of breathing of 10 to 15 seconds
duration, interrupted by pauses of at least 3 seconds
in duration
• Without change in heart rate or skin color
• Immaturity of respiratory control
• REM sleep, not occur in first 2 days of life
• Prevalence : 100% in preterm BW < 1,000 gm
• No treatment
Definition

65. Etiology factors contribute to apnea in
preterm infant
NeoReviews,
Bacteria
Virus: RSV
Magnesium
Prostaglandin

66. Apnea of prematurity
• Common disorder in preterm infants who require
neonatal intensive care
• Immaturity of the respiratory control system
• Requires therapeutic intervention to avoid potential
morbidity
• Incidence inversely related to gestational age

67. Pathogenesis
• Poorly myelinated of central neurons generator
• Reduced number of dendrites and synaptic connection
-> impaired capability for sustained ventilatory drive
• Neurotransmitter deficiency
• Highly chest wall compliant
• Excessive neck flexion

68. Pathophysiologic mechanism predisposing to
apnea of prematurity
NeoReviews,

69. Type of apnea of prematurity
• 3 types based on the presence or absence of upper
airway obstruction
1. Central apnea : Total cessation of inspiratory efforts
with no evidence of obstruction
2. Obstructive apnea : Chest wall motion without air flow
through out the entire apneic episode
3. Mixed apneas : Consists of obstructed respiratory
efforts usually following central pauses
NeoReviews,

70. Diagnostic procedures
• Physical examination
• Blood tests : checking for blood counts, electrolyte
levels and infection
• Measurement of the levels of oxygen in the baby's
blood
• X-ray : check for problems in the lungs, heart, or
gastrointestinal system
• Apnea study : monitoring breathing effort,
heart rate, and oxygenation

71. Treatment
First : Exclude other medical causes

72. Xanthine therapy:
Aminophylline
• Major mechanism of action : competitive antagonism
of adenosine receptors
• Increases minute ventilation
• Improves CO2 sensitivity
• Decreases hypoxic depression of breathing
• Enhances diaphragmatic activity
• Decreases periodic breathing

73. Aminophyline & Cafeine

74. Hyperbilirubinemia

75. Hyperbilirubinemia TSB > 2 mg/dl
Neonates appear jaundiced TSB > 5 to 7 mg/dL
Hyperbilirubinemia

76. Neonatal
bilirubin
metabolism
Uptake
Conjugation
Excretion
Production

77. กลไกทางสรีรวิทยาของภาวะตัวเหลืองในทารกแรกเกิด
1. มีการสร ้าง bilirubin ก่อนเข ้าสู่ตับมากขึ้น
• ปริมาณเม็ดเลือดแดงมาก
• อายุของเม็ดเลือดแดงสั้น (70-90 วัน) เมื่อเปรียบเทียบกับของ
ผู้ใหญ่ซึ่งเท่ากับ 120 วัน
• Bilirubin ที่มาจากแหล่งอื่นที่ไม่ใช่จากเม็ดเลือดแดงมาก
• การดูดซึมกลับของ unconjugated bilirubin ในลาไส ้
(enterohepatic circulation of bilirubin) มาก

78. 2. กระบวนการกาจัด bilirubin ในเลือดทาได ้น้อย
• Hepatic uptake น้อยเนื่องจากเซลล์ตับขาด bilirubin-binding
protein (ligandin)
• Conjugation น้อยเนื่องจากเอ็นซัยม์ UDP-glucuronyl
transferase มีเพียงร ้อยละ 0.1-1 ของระดับในผู้ใหญ่
• การขับถ่ายของ bilirubin ยังทาได ้ไม่เต็มที่
กลไกทางสรีรวิทยาของภาวะตัวเหลืองในทารกแรกเกิด

79. Physiologic jaundice
1 สัปดาห์ 2 สัปดาห์3-5 วัน
TSB 5-6 mg/dL
TSB 10-12 mg/dL
อายุ
TSB mg/dL
Preterm
Fullterm

80. Pathologic jaundice
ที่ควรหาสาเหตุ มีดังนี้
• อาการตัวเหลืองภายใน 24-36 ชั่วโมงหลังเกิด
• TSB เพิ่มขึ้นในอัตราที่มากกว่า 5 มก./ดล./24 ชม.
• TSB มากกว่า 12 มก./ดล.ในทารกเกิดครบกาหนด
หรือ 10-14 มก./ดล. ในทารกเกิดก่อนกาหนด
• อาการตัวเหลืองที่นานเกิน 10-14 วันหลังเกิด
• Direct serum bilirubin > 20 %ของ total bilirubin

81. การประเมินอาการตัวเหลือง
ประเมินภาวะตัวเหลืองร่วมด ้วยทุกครั้งเมื่อวัด vital signs

82. Dermal zone of jaundice
Dermal Bilirubin (mg/dl)
zone Mean + SD range
1 5.9 + 0.3 4.3 - 7.9
2 8.9 + 1.7 5.4 - 12.2
3 11.8 + 1.8 8.1 - 16.5
4 15.0 + 1.7 11.1 - 18.3
5 > 15
K ramer Li 1969
5 5
3
2
1
4
5 5
 
◦
4

83. 1. Over production
• Fetomaternal blood group incompathibility
• Congenital spherocytosis, eliptocytosis SAO
• G-6-PD deficiency
• Thalassemia
• Extravascular blood
• Hematomas
• Enclosed hemorrhage
• Polycythemia
• Increased enterohepatic circulation
• Gut obstruction
Causes of neonatal hyperbilirubinemia

84. 2. Undersecretion
• Metabolic and endocrine condition
• Hypothyroidism
• Infants of diabetic mother
• Prematurity
• Obstructive disorders
• Biliary atresia
Causes of neonatal hyperbilirubinemia

85. 3. Mixed
• Sepsis
• Intrauterine infections
• Hepatitis
• Asphyxia
4. Uncertain mechanism
• Race - Thai - Chinese
• Breast milk jaundice
Causes of neonatal hyperbilirubinemia
Causes of neonatal hyperbilirubinemia

86. ประวัติสาคัญ
• การตั้งครรภ์ การคลอด
• การกินนม
• ประวัติครอบครัว บุตรคนก่อน ประวัติภาวะเม็ดเลือด
แดงแตกง่าย (G-6PD def, thalassemia เป็นต ้น )

87. การตรวจร่างกายที่สาคัญ
• อาการและอาการแสดงของโรคติดเชื้อตั้งแต่
ในครรภ์หรือหลังเกิด
• ภาวะเลือดออกที่ผิวหนังหรือ soft tissue
• คลาได ้ตับม ้ามโต

88. การตรวจทางห ้องปฏิบัติการที่สาคัญ
• ระดับ bilirubin, Hct
• Blood type, Rh, Direct Coombs’ test ในทารก
• Peripheral smear for RBC morphology
• Reticulocyte count
• G-6PD level

89. Laboratory investigation in prolonged jaundice
• Liver function test
• Congenital infection
• Sepsis
• Metabolic defect eg. hypothyroidism

90. แนวทางการประเมินอาการตัวเหลืองก่อนจาหน่าย
ก่อน D/C ทารกแรกเกิดทุกคนควรได ้รับการประเมินถึง
ความเสี่ยงที่จะมี severe hyperbilrubinemia
โดยเฉพาะ D/C ก่อนอายุครบ 72 ชม.

91. 1. กลุ่ม Low risk : ทารกแรกเกิด GA ≥38 สัปดาห์ ที่ปกติดี
ไม่มีปัจจัยเสี่ยง
2. กลุ่ม Medium risk : ทารกแรกเกิด GA≥38 สัปดาห์ที่มีปัจจัย
เสี่ยงหรือ GA 35-37+6 สัปดาห์ที่ปกติ
3. กลุ่ม High risk : ทารกแรกเกิด GA 35-37+6 สัปดาห์
ที่มีปัจจัยเสี่ยง
แนวทางการดูแลรักษาภาวะตัวเหลือง

92. AAP. Pediatrics 2004;114 : 297-316

93. Guidelines for phototherapy in hospitalized
infants of 35 or more weeks’ gestation.
• Use total bilirubin. Do not subtract direct
reacting or conjugated bilirubin.
• Risk factors = isoimmune hemolytic disease,
G6PD deficiency, asphyxia, significant lethargy,
temperature instability, sepsis, acidosis, or
albumin <3.0 g/dL.

94. Guidelines for phototherapy in hospitalized
infants of 35 or more weeks’ gestation.
• It is an option to provide conventional phototherapy
in hospital or at home at TSB levels 2-3 mg/dL
below those shown but home phototherapy should
not be used in any infant with risk factors.

95. Management of hyperbilirubinemia :
Healthy term newborn
< 24 ---- ----
25-48 > 12 > 15
49-72 > 15 > 18
> 72 > 17 > 20
> 96 > 20
Age
(hours)
Consider
photo
phototherapy

96. Guideline for Initial Phototherapy in
Preterm Neonates
Total serum bilirubin (mg/dL)
BW (g) Healthy Sick
2,001 - 2,500 12 - 15 10 - 12
1,500 - 2,000 10 - 12 8 - 10
1,001 - 1,500 7 - 10 6 - 8
< 1,000 5 - 7 4
Fanaroff & Martin’s neonatal-perinatal medicine: diseases of the fetus
and infant. 9thed. St. Louis: Elsevier Mosby, 2011:1443-96.

98. Phototherapy

99. Response to phototherapy
MB Age Action
< 18 - Wean to conventional
phototherapy
< 12 - Discharge home
< 14 49-72 Discontinue photo, D/C home
< 15 >72 h Discontinue photo, D/C home
Check rebound MB 24 hours after discontinue

100. Complication from phototherapy
1.  insensible water loss
2. Loose stool
3. Retinal damage
4. Bronze baby syndrome

101. AAP. Pediatrics 2004;114 : 297-316

102. • Immediate exchange transfusion is recommended if infant
shows signs of acute bilirubin encephalopathy or if TSB is
≥ 5 mg/dL above these lines.
• Measure serum albumin and calculate B/A ratio.
• Use total bilirubin. Do not subtract direct reacting or
conjugated bilirubin.
Guidelines for exchange transfusion in
Infants 35 or more weeks’ gestation

103. Management of hyperbilirubinemia :
Healthy term newborn
< 24 ---- ----
25-48 > 20 > 25
49-72 > 25 > 30
> 72 > 25 > 30
Age
(hours)
Exchange
Transfusion
If photo fails
Exchange
transfusion
And intensive
photo

104. Exchange transfusion
Blood for exchange transfusion
1. Fresh blood <7 days old (Hct 45-50%)
ratio PRbC + FFP = 2 : 1
2. In Rh hemolytic disease
blood gr O Rh negative
Cross match against mother and infant
3. In ABO incompatibility
PRC gr. O + FFP gr. AB
cross match against mother and infant

105. 4. In nonimmune hyperbilirubinemia cross
matched against plasma and Rbc of infant
5. Volume of exchange transfusion
double volume of infant blood
= 2 x 80 ml/kg
Exchange transfusion

106. Technique of exchange transfusion
1. Place on radiant warmer
2. Monitor BP, cardiac monitor
3. Assistants : record volumes of blood & US.
4. Check and warm blood to 37oC
5. Put on umbilical vein
6. Exchange by push-pull technique
BW <1,500 gm = 5 ml/time
BW 1,500 - 2,500 gm = 10 ml/time
BW 2,500 - 3,500 gm = 15 ml/time
BW >3,500 gm = 20 ml/time
Recommend time for exchange = 1 hour
7. After exchange transfusion continue phototherapy

107. Complication of exchange transfusion
1. Hypocalcemia and hypomagnesemia
2. Hypoglycemia
3. Acid-base balance
4. Hyperkalemia
5. Cardiovascular complication
6. Bleeding
7. Infection
8. Graft-versus-host disease

108. แนวทางการรักษาภาวะตัวเหลืองจากนมแม่
• ประเมินว่าทารกได ้รับนมแม่เพียงพอหรือไม่ หากไม่เพียงพอ
ให ้ทารกดูดนมแม่บ่อยขึ้นทุก 2-3 ชม
• หากระดับบิลิรูบินมากกว่า 18-20 มก./ดล.
- Phototherapy ไม่ต ้องงดนมแม่
- ติดตามดูอาการและตรวจระดับบิลิรูบิน
• หากระดับบิลิรูบินสูง > 25 มก./ดล.
- Phototherapy + งดนมแม่ร่วมด ้วย 24-48 ชม.
- ควรอธิบายให ้แม่เข ้าใจเพื่อไม่ให ้เกิดทัศนคติที่ไม่ดี
เกี่ยวกับนมแม่

109. Neonatal resuscitation

110. 1-112
การเตรียมตัวสาหรับการช่วยกู้ชีพ
ทารกแรกเกิดทุกรายควรได ้รับการประเมินว่า
ต ้องการการดูแลช่วยเหลือเบื้องต ้นหรือไม่

111. Copyright ©2010 American Academy of Pediatrics
ขั้นตอนการช่วยกู้ชีพ

112. 2-114
Evaluating the Newborn
ทันทีที่ทารกเกิด , ถามคาถามเหล่านี้:

113. Meconium stained amniotic fluid
1. Vigorous infant
- ทารกหายใจดี และ
- Good muscle tone
- Heart rate >100 ครั้ง /นาที
2. Not vigorous

114. Meconium stained amniotic fluid
Not vigorous infants
(ไม่หายใจ หายใจช ้า
poor muscle tone
HR < 100)
tracheal suction immediately
after birth and before
stimulation
Vigorous infant Bulb syringe or large-bore
suction catheter (12-14 F)
ดูดในปาก และจมูก
( No tracheal suction : not improve
outcome and may cause complications)
( หายใจดี
good muscle tone
HR >100)

115. 2-117
Meconium Present and Newborn Not Vigorous
Tracheal Suction
ให ้oxygen, monitor heart rate
ใส่ laryngoscope, use 12F or 14F suction
catheter ดูดในปาก
ใส่ endotracheal tube ใน trachea
ต่อ endotracheal tube กับ suction source

116. 5-118
Suctioning Meconium via Endotracheal Tube
• ต่อท่อช่วยหายใจกับ
meconium aspirator ซึ่ง
ต่อกับเครื่องดูดเสมหะ
• ใช ้นิ้วมืออุดรูเปิดของ
meconium aspirator
เพื่อให ้เกิดแรงดูด
• ทาการดูดพร ้อมๆกับดึงท่อ
ช่วยหายใจออก ทาซ้าตามความ
จาเป็น
Click on the image to play video

117. 2-119
Evaluating the Newborn
ทันทีที่ทารกเกิด , ถามคาถามเหล่านี้:

118. 2-120
Initial Steps
 ให ้ความอบอุ่นแก่ทารก วางทารกใต ้
radiant warmer,
 จัดท่าศีรษะ open the airway
 เช็ดตัวให ้แห ้ง กระตุ้นให ้หายใจ
 เอาผ ้าเปียกออก จัดท่าศีรษะ

119. 2-121
Opening the Airway
Sniffing” position

120. 2-122
Dry, Stimulate to Breathe, Reposition
Click on the image to play video

121. 2-123
Evaluation: Respirations, Heart Rate
Decisions and actions
during newborn
resuscitation are based
on Respirations
Heart Rate
Click on the image to play video

122. 1-124
การประเมิน
ภายหลังการดูแลช่วยเหลือเบื้องต ้น
การช่วยเหลือขั้นต่อไป ขึ้นกับผลการประเมินดังต่อไปนี้

123. 2-125
Central Cyanosis and Acrocyanosis

124. 1-126

125. Neonatal hypoglycemia

126. Definition hypoglycemia
• ภาวะน้าตาลในเลือดต่าในทารกทุกคนไม่ว่าอายุเท่าไร คือ
พลาสมากลูโคส < 47 มก/ดล.
• น้าตาลกลูโคสในเลือดจะต่ากว่ากลูโคสในพลาสมา 10-15 %
• ในทางปฏิบัติระดับน้าตาลกลูโคสที่ถือว่าต่าและต ้องการการดูแล
รักษาคือ พลาสมากลูโคส < 40 มก/ดล.
หรือน้าตาลกลูโคสในเลือด< 35 มก/ดล
David H. Adamkin, Ccmmittee on Fetus and Newborn. Postnatal Glucose Homeostasis in Late-Preterm and Term Infants.
Pediatrics 2011;127:575-9.

127. • Infants of diabetic mothers
Developed asymptomatic hypoglycemia early as 1 hour
after birth and usually by 12 hour of age
• Large for gestational age or small for gestational age
infant : hypoglycemia early as 3 hours of age

128. Risk factors
Antenatal : maternal diabetes mellitus, maternal obesity,
rapid infusion of glucose immediately before delivery,
ß-adrenergic agonist or antagonist therapy
Neonatal : SGA, LGA, prematurity, perinatal stress
(asphyxia), hypothermia, polycythemia
illed-infant (sepsis, respiratory distress)
suspected inborn errors of metabolism or endocrine
disorder, microphallus or midline defect
Hypoglycemia

129. Clinical manifestation
Irritability, tremors, jitteriness
Exaggerated Moro reflex
High-pitched cry
Seizure or myoclonic jerks
Lethargy, limpness, hypotonia
Coma, cyanosis
Apnea or irregular breathing or tachypnea
Temperature stability, vasomotor instability
Poor suck or refusal to feed
Hypoglycemia

130. Macrosomia : fetal weight >90th percentile for gestational age
A plethoric appearance and excessive fat accumulation

131. Cause of hypoglycemia
1. Utilization of glucose
(Hyperinsulinism)
2. Production/store
3. Utilization of glucose and/or
Production

132. Maternal hyperglycemia
Fetal hyperglycemia
Fetal hyperinsulinemia
Fetal substrate uptake
Increase metabolic rate
and O2 consumption
Hypoxia
Increase synthesis
erythropoietin and RBC mass
Polycythemia
Suppress production
of surfactant
Respiratory distress
syndrome
Macrosomia
Infant of diabetic mother

133. Treatment of hypoglycemia
• Asymptomatic + DTX 25-40 mg%
Enteral feeding : 10%D/W & infant formula ??
Infant formula : Carbohydrate, protein and fat
- Provide sustained supply substrate
- Stimulate gluconeogenesis
Increase blood glucose approximate 30 mg/dL after
feeding 30-60 mL of infant formula

134. • Asymptomatic + DTX < 20-25 mg/dL
IV therapy :
- Initial bolus 200 mg/kg of 10% D/W
(2 mL/kg of 10%D/W)
- Continuous infusion of dextrose GMR 6-8 mg/kg/min
- Check blood glucose 30 minutes after bolus, then
every 1-2 hours until stable
Avoid induction iatrogenic hyperglycemia
stimulate excess insulin secretion
induce rebound hypoglycemia
Treatment of hypoglycemia

135. • Symptomatic infant + DTX < 40 mg/dL
IV therapy
Maintain blood glucose > 50-60 mg/dL
Should be permitted to continue feeding (as tolerate)
Wean iv therapy if blood glucose stable for 12-24 hours
Decrease infusion rate by 10-20%
Failure to tolerate weaning from iv glucose
indicate of the pervasive disorder :
metabolic defect or idiopathic hyperinsulinism

136. BG < 35 มก/ดล
BG <25 มก/ดล
BG 25-40 มก/ดล
า ก LPT, LGA/IDM และ Term SGA
ี มมี ากา แ ด ดปก
า ก าย 4-24 ม
ใหกนนม ก 2-3 ม จ BG ก นกนนมแ ละม
า กแ ก กด - 4 ม
มกนนม ายใน 1 ม หล กด
จ BG หล กนนม 30 นา ี
ใหกนนม า า มมีป หา
และ จ BG หล กน 1 ม
ใหกนนม า า มมีป หา
และ จ BG หล กน 1 ม
IV glucose ใหกนนม ห
IV glucose าจา ปน
ใหกนนม ห
IV glucose าจา ปน
IV glucose
BG <25 มก/ดล
BG <35 มก/ดล
BG 35-40 มก/ดล
LPT = Late preterm
LGA = Large for gestational age
IDM = Infant of diabetic mother
BG = Blood glucose
IV glucose = 10%D/W 2 มล./กก ด ย glucose 5-8 มก/กก/นา ี

137. Necrotizing enterocolitis

138. Stage I Suspected
a. Any or more historical factors producing perinatal stress
b. Systemic manifestation: temperature instability, lethargy, apnea,
bradycardia
c. Gastrointestinal manifestation: poor feeding, increasing pregavage
residuals, emesis, mild abdominal distension, occult blood possible
present in stool
d. Abdominal radiographs demonstrate mild ileus.
Bowel rest
Repeat physical exams
Repeat abdominal films
Stage II Definite
a. Signs and symptoms listed in Stage I plus persistent occult or
gross gastrointestinal bleeding, marked abdominal distension
b. Abdominal radiographs demonstrate significant intestinal
distension with ileus, small bowel separation (edema in bowel wall
or peritoneal fluid), unchanging or persistent “rigid” loops,
pneumatosis intestinalis, portal vein gas.
Bowel rest
Parenteral antibiotics
Parenteral nutrition
Repeat abdominal
exam.
Repeat abd. Films, lab,
U/S, paracentesis
Stage III Advanced
a. Any one or more historical factors
b. Signs and symptoms listed in stage I and II plus deterioration of
vital signs, evidence of septic shock or marked gastrointestinal
hemorrhage.
c. Abdominal radiograph may demonstrate pneumoperitoneum in
addition to other findings listed in stage II c.
Surgical treatment
a. resection and stomas
(most patients)
b. Primary anastomosis
(selected patients)
c. VLBW with perforation
– consider peritoneal
drainage alone, initially

144. Congenital infection

145. Intrauterine infection
ToRCHS infection
To = Toxoplasmosis
R = Rubella infection
C = Cytomegalo virus infection CMV
H = Herpes simplex infection
S = Syphilis

146. 3 forms of toxoplasma
Cyst
Tachyzoite
Oocyst

147. Congenital Toxoplasmosis
• Incidence of 0.1 to 1 in 1,000 live births
• Infection during pregnancy : by
- ingesting oocysts-infected cat feces
- ingestion of pseudocysts present in undercooked meat
• Most infected women :
- no symptoms
- 15% acute flu-like illness with lymphadenopathy
NeoReview. August 2010

148. Congenital Toxoplasmosis
• Risk of vertical transmission:
increase with GA at the time of infection
- 1st trimester : 10-20%
- 2nd trimester : 30%
- 3rd trimester : 65%
• Overall risk of transmission in pregnancy : 20-50%
• Severity of fetal disease inverse related to GA at the
time of infection
(50% in 1st trimester, 25% in 2nd trimester and <3% in
3rd trimester)
Fanaroff & Martin’s Neonatal-Perinatal Medicine. Disease of the
fetus and infant. 9th edition, 2011

149. Clinical manifestations
• 70-90% of infected infant are asymptomatic at birth
• 10% to 30% symptomatic newborns present with
a systemic form of the disease
• Classic triad:
– Chorioretinitis: focal necrotizing retinitis, yellow-white
cotton like patches, retinal edema
– Hydrocephalus: periaqueductal obstruction
– Intracranial calcifications: scatter in white matter,
basal ganglia

151. Clinical manifestations
Systemic sign CNS Eyes
IUGR
Prematurity
Low APGAR score
Temperature instability
Lymphadenopathy
Hepatosplenomegaly
Myocarditis
Pneumonitis
Feeding problem
Band of metaphyseal
plate
Hydrocephalus
Seizure
Muscular twitching
Opisthotonus
Hypsarrthmia
Paralysis
Difficult swallowing
Respiratory distress
Microcephaly
Visual impairment
Chorioretinitis
Retinal detachment
Iris nodule
Glaucoma
Strabismus
Nystagmus
Micropthalmia

152. Skin Ears Endocrine
Rash
Petechiae
Ecchynosis
Jaundice
Cyanosis
Edema
Sensorineural
hearing loss
Myxedema
Diabetes insipidus
Hypopituitarism
Clinical manifestations

153. Diagnosis
• Antenatal diagnosis :
- PCR for parasite DNA detection in amniotic fluid or
fetal blood
- Isolating the organism from the placenta or fetal blood
• Postnatal diagnosis : IgM +ve and high titer of IgG
- IgG can detect for 1-2 months postinfection
- IgM can persist for 6-24 months

154. Investigations
Postnatal investigations
• CBC : anemia and thrombocytopenia
• Liver function tests
• CSF
• Cranial ultrasonography ± CT brain for hydrocephalus
and calcification
• Ophthalmologic examinations

155. Treatments
Pyrimethamine
• 2 MKD for 2 days followed by 1 MKD x 4 weeks
and then Mondays, Wednesdays, and Fridays to
complete 12 months of therapy
Sulfadiazine
• 100 MKD in 2 divided doses x 1 yr
Folic acid
• 10 mg 3 time/week
Infectious Diseases of the Fetus and Newborn Infant. 6th ed.

156. Treatments
Active chrorioretinitis
CNS involvement,
eg. CSF protein >1 gm/dL
Treatments
Prednisolone 1 MKD PO bid

157. Pregnant women :
- Avoid foods/products that may be contaminated
with T gondii oocytes by cooking food at safe
temperatures; peeling or thoroughly washing fruits and
vegetables
- Washing kitchen utensils and hands with hot soapy
water
- Wearing gloves when touching soil, sand or cat litter
Prevention

158. Congenital rubella syndrome
Rubella infection :
• 30% subclinical
• Symptomatic pt. : mild, occur 14-21 days after infection
• Pregnant woman : low-grade fever, malaise, rash
(macular, begin face and neck, proceed downward,
disappear over 3-4 days)
• Postauricular, suboccipital and post. cervical
lymphadenopathies
• Dx: serology confirm of 4-fold increase in IgG,
positive IgM

159. Risk factor developing CRS
Maternal infection
gestational age Incidence CRS
first 12 weeks 81 %
13-16 weeks 54 %
17-22 weeks 36 %
23-30 weeks 30 %
31-36 weeks 60 %
> 36 weeks 100 %

160. The malformation depend on gestational age
• Multiple defects occur after very early exposure
• Almost every fetus expose during first month of
pregnancy develops abnormal
• Cardiac defect : before GA 10 wk
• Deafness : before GA 16 wk
• GA > 20 wk : rare

161. Antenatal diagnosis
• Cord blood rubella-specific IgM and PCR of amniotic fluid
• Ultrasound anomalies
Postnatal diagnosis
• Isolation of rubella virus from many body sites
(pharyngeal secretions, eye, throat, CSF, stool, and urine)
• Detect rubella specific IgM
Congenital rubella syndrome

162. Manifestations
• Sensorineural hearing loss
• Cardiac defect : PDA, pulmonary artery stenosis, TOF
• Eye : Congenital cataract, retinopathy, microphthalmia
Salt and-pepper chorioretinitis
• Radiolucencies of long bones
• Neuro : mental retardation, meningoencephalitis,
behavioral disorder
• Thrombocytopenia and dermal erythropoiesis
• Delayed manifestation : DM, thyroid disease
Congenital rubella syndrome

164. Investigations:
• CBC : anemia and thrombocytopenia
• liver function tests
• Echocardiography
• Lumbar puncture
• Chest and long bone radiographs
• Serial hearing and ophthalmologic assessments
• Screening for endocrine complications (DM and
hypothyroidism) indicated for long-term management
Congenital rubella syndrome

165. Treatment of mother and CRS
• No specific therapy
• Terminate pregnancy if infected before 5
month
• Follow up newborn

166. Prevention for CRS infant
Immunization : rubella vaccine
Avoid within 1 month of conception or
during pregnancy
Contact isolation of CRS infant
at least 1 year

167. Human Cytomegalovirus
 Transmission
prenatal (congenital, placental)
natal (50% of exposed infants become infected)
postnatal (human milk in preterm infants, blood
transfusion, transplant)
 Primary maternal infection results in fetal infection in
30% to 40% of cases
 The risk of fetal infection correlates with viral load
in the fetal amniotic fluid or in the newborn’s plasma

168. Clinical Manifestations
 Hepatosplenomegaly, conjugated hyperbilirubinemia
 Thrombocytopenia with petechiae/purpura
(“blueberry muffin” spots)
 Small size for gestational age, microcephaly
 Intracranial calcifications
 Chorioretinitis

170. CMV pneumonitis
 Occur in infant < 4 months
 Symptomatic and radiography
similar to afebrile pneumonia
 CXR : Hyperinfaltion
Diffuse increase pulmonary
marking
Focal atelectasis
Thickening bronchial wall
 3% of patient : death

171. Diagnosis
 Prenatal Dx
- Viral culture of the amniotic fluid 100% specificity
- PCR of amniotic fluid (after 21 weeks’ gestation)
 Postnatal Dx
- Isolation of CMV from urine, stool, respiratory tract
secretion or CSF obtained within 3 weeks of birth
- CMV IgG, IgM
IgG titer no detetced in 4-9 mo of age -> exclude CMV

172. • Antiviral agents indication
serious, life-threatening
Symptomatic CMV (pneumonitis, hepatitis,
thrombocytopenia) : Red book 2009
Ganciclovir : acts as a chain terminator during elongation of
newly synthesized viral DNA
Treatment of CMV
Remington, Klein et al Infectious diseases of the fetus and
newborn infant. 7th ed 2011

173. Herpes Simplex Virus
Epidemiology
• Neonatal herpes is usually the result of HSV-2 infection
• Most cases of neonatal infection, mothers do not give a history of
active genital herpes at the time of delivery
• In USA, prevalence of neonatal herpes = 0.05-0.3: 1,000 live births
• The transmission rate
intrapartum infection : 88% to 93%
postpartum infection 5-10%
intrauterine infection < 2%

174. Clinical manifestations
• Neonatal HSV infection typically presents within 1-3
weeks
• 3 types : Localized disease, CNS disease
Disseminated disease
 Localized disease : presents as vesicles or zoster-like
eruptions on skin, eyes, or mouth
If left untreated, more than 70% of cases progress to
disseminated disease

175.  Disseminated disease
- Nonspecific presentations : poor feeding, fever, lethargy,
apnea, convulsion, respiratory distress, hepatomegaly,
jaundice and disseminated intravascular coagulation
• Associated with mortality rates between 50% (HSV-2) and
70% (HSV-1)
• Poor prognosis : hemorrhagic pneumonitis, severe
coagulopathy, liver failure, and meningoencephalitis
• >40% of patients who have disseminated disease do not
develop skin lesions
Clinical manifestations

176.  CNS disease : 30% and 1/3 of cases without skin findings
- Clinical signs include seizures, lethargy, irritability, tremors,
poor feeding, temperature instability, and a bulging
fontanelle
- At least 50% of patients suffer long-term sequelae, despite
high-dose acyclovir treatment
- Seizures at or before initiation of antiviral therapy are
associated with an increased risk for morbidity
Clinical manifestations

177. Diagnosis
• All infants should be examined for vesicles
• Viral cultures after 48 hours of age are collected from various
sites, including mouth, nasopharynx, conjunctiva, rectum,
skin vesicles, urine, stool, blood, and CSF
• HSV-PCR testing from CSF: HSV encephalitis
• Electroencephalography and brain imaging : useful adjuncts
to diagnosis if negative HSV-PCR
• Liver function and coagulation tests : to evaluate
disseminated disease

178. Treatment
• For skin-eye-mouth disease :
Acyclovir iv 20 mg/kg/dose q 8 hr for 14 days
• For disseminated disease and encephalitis, treatment for at
least 21 days
• For HSV encephalitis, acyclovir should be continued until CSF
PCR test results become negative
• Topical ophthalmic drugs are helpful for eye lesions

179. Congenital syphilis
 Spirochete “Treponema pallidum”
 Occurs after infection of the placenta in pregnant
women with secondary syphilis
 Transmission can occur at any stage of pregnancy
 40%of pregnancies with syphilis result in spontaneous
abortion, stillbirth and perinatal death

180.  Congenital syphilis : early & late disease
 Early disease : first 2 postnatal years
 30-40% stillborn, 75% asymptomatic at birth
 Most affected children develop symptoms between the
3rd -4th weeks after birth
 Early disease : nonimmune hydrops fetalis, IUGR,
hepatosplenomegaly, jaundice (syphilitic hepatitis),
condyloma lata, pseudoparalysis, lymphadenopathy
snuffles (syphilitic rhinitis, followed by a maculopapular rash)
Clinical Manifestations

181.  Dermatology : pink and oval macules-> coppery brown
and desquamate (40%)
 vesiculobullous eruptions involving the palms and soles
 Hematology : Coombs-negative hemolytic anemia
leukocytosis, thrombocytopenia or leukopenia
 Renal : Nephrotic syndrome : 2 to 3 months
 CNS : meningitis, choroiditis, hydrocephalus, seizures
optic nerve atrophy, or cranial nerve palsies
 Bone: Osteochondritis, long bones and ribs (8 months)
Wimberger sign : bilateral destruction of the upper
medial tibial metaphyses (75-100%)
Clinical Manifestations

183.  Saber shins
Higoumenakia sign (unilateral enlargement of the
sternoclavicular portion of the clavicle)
Clutton joints (bilateral knee effusions)
 Late disease:
Interstitial keratitis: 5-20 yrs
8th nerve deafness : 10-40 yrs
Hutchinson teeth : peg- shaped, notched central incisors
Saddle nose, frontal bossing
Clinical Manifestations

185. Diagnosis
 Presumptive diagnosis: treponemal, nontreponemal test
• Treponemal tests :
Fluorescent treponemal antibody absorption (FTA-ABS)
The particle agglutination (TP-PA) tests
• Nontreponemal tests :
Venereal Disease Research Laboratory (VDRL) slide test
Rapid plasma reagin (RPR) test

186. Diagnosis
 VDRL or RPR titer of infant > mother at least four-fold
indicating fetal antibody synthesis->Congenital syphilis
sensitivity 4–13%, specificity 99%
 Excluded congenital syphilis if
- VDRL/RPR tests : non-reactive before age of 6 months
in an infant who has not received treatment
- TPPA/TPHA and FTA-ABS : non-reactive before
1 year of age in an infant who has not received treatment
Eur J Clin Microbiol Infect Dis (2010) 29:495–501

187. • Infant should be evaluate if the mother
- Syphilis untreat or inadequately treated or treatment if
not document
- Syphilis during pregnancy treated with nonpenicillin
regimen (erythromicin)
- Syphilis treated less than 1 month before delivery
- Syphilis treated before pregnancy but with insufficient
serologic follow up
Investigation
Red book 27th edition, 2008

188.  Nontreponemal test
 Complete blood and platelet counts
 Cerebrospinal fluid examination
(high wbc count, high protein)
 Long bone radiographs
 Ophthalmologic examination, neuroimaging, auditory
brainstem response, and liver function testing are added
if infection is strongly suspected
Investigation
Red book 27th edition, 2009

189. Guide for interpretation of syphilis
Red book 27th edition, 2009
VDRL/RPR TPPA, FTA-ABS Interpretation
Mother Infant Mother Infant
- - - - No syphilis, incubation syphilis
+ + - - No syphilis in mother and infant
(false positive)
+ +/- + + Maternal syphilis with possible infant
infection
+ + + + Recent or previous syphilis in mother
and possible infant infection
- - + + Mother successfully treated for syphilis
before or early pregnancy, or mother
with Lyme disease (false positive)
Infant syphilis unlikely

190. Mother : no Tx or Tx < 4 wk before delivery
Infant : normal physical examination
Single dose of Benzathine penicillin 50,000 U/kg IM
PGS 50,000 U/kg iv q 12 hr (or q 8 hr if age > 1 wk) x 10 days
Procaine penicillin G 50,000 U/kg IM OD x 10 days
Single dose of Benzathine penicillin 50,000 U/kg IM

191. Varicella-Zoster Virus (VZV)

192. Varicella-Zoster Virus (VZV)
 Herpesviridae family
 VZV : transferred transplacentally from the mother
to the fetus
 Perinatally acquired varicella in the newborn classically
occurs in the first 10 days after birth if the mother
is infected from 5 days before to 2 days after delivery

193.  Fetal infection in the first 20 weeks of GA ->
varicella embryopathy or congenital varicella syndrome
 The incidence CVS among infant born to mother with
varicella 1-2%
 The usual interval from onset of rash in mother to onset
in neonate is 9-15 days
Varicella-Zoster Virus (VZV)
Red book 27th edition, 2008

194. Clinical Manifestations of CVS
• Skin lesions with dermatomal distribution (72%)
• Neurologic defects (62%)
• Eye diseases (52%)
• Skeletal anomalies (44%)
• 30% of symptomatic infants die in the first postnatal
months
• The most characteristic findings of CVS :
limb hypoplasia with cicatricial skin scarring
chorioretinitis, cataracts, and brain abnormalities
(cortical atrophy, intellectual disability and seizures)

196. • Perinatally acquired varicella : serious complications
pneumonia
bacterial superinfections
(toxic shock syndrome and necrotizing fasciitis)
Cerebellar ataxia, encephalitis, meningitis
Clinical Manifestations of CVS

197. • PCR or by immunofluorescence techniques in skin
scrapings or from vesicle fluid
• Acute recent infection : IgM +ve and IgG +ve
• Persistence of VZV antibodies in the infant beyond
8 months of age is highly suggestive of intrauterine
acquisition of varicella
Diagnosis

198. Treatment
 Infants who have clinical signs of active varicella
infection -> IV acyclovir until no new lesions develop
 Antibiotics should be administered for bacterial
superinfections
 Pregnant woman with varicella infection -> oral acyclovir
 Pregnant with serious complication of varicella infection
-> Tx with IV acyclovir

199. Isolation of the hospitalized patient
 Patient with varicella :
standard precaution, airborne and contact precaution
(until all lesions are crusted)
 Exposes susceptible patients :
airborne and contact precautions from Day 10-21
after exposure (Day 10-28 for infant who received
VZIG or IVIG)

200. Candidate for VZIG/IVIG
-Susceptible pregnant woman (within 72-96 hr)
- Newborn infant whose mother had onset of chickenpox within
5 days before delivery or within 48 hours after delivery
- Hospitalized preterm infant (GA ≥28 wk) whose mother lacks a
reliable history of chickenpox or serologic evidence of protection
against varicella
- Hospitalized preterm infant (GA <28 wk or ≤1,000 gm birth
weight) regardless of maternal history of varicella or varicella-
zoster virus serostatus

201. Care of exposed people
 Varicella vaccine adminstered by 3-5 days after exposure
 All exposed susceptible patient should be dischaged as
soon as possible

202. Toxoplasmosis CMV
Maternal Asymptomatic
Lymphadeno-pathy, fever
fatique, headche
Asymptomatic
Neonatal Classic triad:
-Hydrocephalus
-Chorioretinitis (14%)
-Intracranial calcification (9%)
Other:
-Seizure
-Microcephaly (1-5%)
-Hepatosplenomegaly
-Jaundice
-Encephalitis
-Anemia
-Thrombocytopenia
-Microcephaly (37%)
-Chorioretinitis (20%)
-Intracranial calcification
(periventricular)
-Hearing loss (58%)
-Seizure (23%)
-IUGR
-Petechiae
-Hepatosplenomegaly
-Jaundice
-Mental retardation
-Prematurity

203. Herpes Rubella Syphilis
Maternal Oral or genital lesion Fever, coryza,
conjunctivitis, MP
rash
Lymphadenopathy
No ANC, VDRL result
Fever, rash, chancre
Neonatal 3 categoreis:
1. Localized lesion:
skin, eye, mouth,
lesion within 6-9 days
2. Encephalitis:
siezure, hypotonia
within 10-14 days
3. Dissiminated with
multiorgan
involvement: sepsis
Classic triad:
-Sensorineural
hearing loss
-Ocular: cataract,
-CHD: PDA,
pulmonic valve
stenosis
Other:
-Blueberry muffin
Hepatosplenome
galy
-Microcephaly
-Hydrop fetalis
-Persistent rhinitis
-Snuffles
-Rash
-Hepatosplenomegaly
-Anemia
-Jaundice
-Osteochonditis
-Failure to thrive

205. Hypospadia
• Urethral opening that is on the ventral surface
of penile shaft
• >> penoscrotal hypospadia : consider VCUG
10% dilate prostatic utricle
>> 10% boy with hypospadia : undescended
testis, inguinal hernia