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NT ป 5
THERMOREGULATION
ลกษณะการหายใจของทารกแรกเกด
3-4 วนแรกหลงคลอด การหายใจไมสม าเสมอ
เมอหลบสนทการหายใจจะสม าเสมอ ไมเกน 60 คร งตอ
นาท
อาจม periodic breathing
THERMOREGULATION
1. Heat production
2. Heat loss
Heat production
1. Physical thermogenesis
– voluntory muscle activity
– involuntory muscle activity
shivering method
2. Nonshivering thermogenesis or chemical thermogenesis
– Brown fat (เรมมเมออายครรภ 26-30 wks
จนกระทงเตมทหลงเกด 3-5 wks)
– Brown fat พบทระหวางกระดกสะบก รอบคอ รกแร
– รอบๆไตและตอมหมวกไต
Chemical thermogenesis
Cold Thermal receptor Hypothalamus
Sympathetic nerve
Norepinephrine release
กระตน brown fat metabolism
Triglyceride NEFA + Glycerol
+ พลงงานความรอนhydrolysis
กระตนการท างานของ lipase
Heat loss
1. พนทผวกายเทยบกบน าหนนกววกาก
2. Subcutaneous fat นอย
3. Vasomotor activity ยงไกด
Heat loss
1. Convection
2. Conduction
3. Radiation
4. Evaporation
1. Convection 2. Conduction
Heat loss
3. Radiation
Heat loss
4. Evaporation
Cooling
Norepinephrine
Pulmonary vasoconstriction
Increased pulmonary
artery pressure
Increased right to leftshunting
Peripheral vasoconstriction
Accumulation of lactic acidosis
Anaerobic metabolism
Hypoxia
การเปลยนแปลงทเกดขนเมอทารกมอณหภมกายต า
ทารกแรกเกดเสยงวอการเกดภาวะอณหนภกกายว า
(hypothermia )
: BT < 36.5o C
ควรใหนทารกอยใน neutral thermal environment
Thermal neutral zone
ชวงอณหภมของสภาพแวดลอมทท าให
ทารกสามารถรกษาอณหภมรางกายให
ปกตอยได โดยมการใชพลงงานนอยทสด
ขนกบ อายครรภ อายหลงคลอด และ ขนาดของรางกาย
Neutral thermal environmental temperatures
Temperature
Age and weight At start (oC) 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
Apgar score
• A practical method for assessing a neonate
• Assess at 1 and 5 minute after birth
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)
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
Hany Aly. Respiratory Disorders in the Newborn: Identification and Diagnosis Pediatr. Rev. 2004;25;201-208
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
Investigation ?
Complete blood count
Chest X-Ray
± Arterial blood gas (severity of
baby)
Electrolyte
(as indicated)
Glucometer
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)
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
Lokesh Guglani, Satyan Lakshminrusimha and Rita M. Ryan. Transient tachypnea of the newborn. Pediatr. Rev. 2008;29;e59-e65.
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
Meconium aspiration syndrome: MAS
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
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
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
Ball-valve effect
Meconium aspiration
Proximal airway obstruction
AcidosisHypoxiaHypercapnea
Peripheral airwayobstruction
Completes
Atelectasis
V/Q mismatch
Partial
Ball-valve effect
Air-trapping
Air leaks
Inflammatory and chemical pneumonitis
Surfactant dysfunction
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
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
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
Respiratory distress syndrome:
RDS
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
Clinical signs
• Begin at or immediate after birth
• Rapid breathing, cyanosis in room air
• Grunting and chest retractions
Respiratory distress syndrome
Chest radiography
• Homogenous opaque infiltrates and air bronchograms
“Ground glass appearance”
• Diffuse, fine granular infiltration
• Usually hypoaeration
Respiratory distress syndrome
After surfactant replacementRDS
After surfactant replacementRDS
Infection : Pneumonia
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
GROUP “B” STREPTOCCAL PNEUMONIA
Take home message
TTNB MAS RDS Pneumonia
Risk factor C/S MeconiumstainPost-term
Preterm, DM PROM, PretermMaternal fever
Natural history Onset earlyResolve within 48-72 hrs
Onset shortly after birthMild-severe
Immediate after birth
VarySigns of sepsis
CXR Normo-hyperaerationMinor fissureProminent vascular marking
HyperaerationConsolidationAtelectasisPneumothorax
HypoaerationGround-glass appearanceBilateral
NormalaerationInfiltration uni/bilateral
Cyanosis in newborn
Clinical conditions that may cause cyanosis in newborn
Respiratory Cardiac
Pulmonary vascular :
PPHN
Central nervous system
สาเหตจากทางปอดและทางเดนหายใจ
การตรวจพบ
หายใจเรว หายใจล าบาก
Chest retraction, expiratory grunting
เสยงปอดผดปกต
Chest x-ray ผดปกต
ใหออกซเจน อาการเขยว
จะดขนหรอหายไป
สาเหตจากโรคหวใจ
การตรวจพบ
หายใจเรว มกไมม chest retraction
ฟงปอดปกต ยกเวน congestive heart failure
Heart murmur +
Chest x-ray : หวใจโต หรอ pulmonary vascular
markings ลดลง
ใหออกซเจน PaO2 เพมขนนอยมากหรอไม
เปลยนแปลง
สาเหตจาก PPHN
การตรวจพบ
Severe hypoxemia
Severe acidosis
Tachypnea
No anatomical cardiac lesions
May have hypovascularity on the chest
radiograph, relatively clear lung fields
สาเหตทางระบบประสาทสวนกลาง
การตรวจพบ
หายใจตน ไมสม าเสมอ
แขนขาออนแรง
อาการเขยวหายไปเมอกระตนหรอให ออกซเจน
แนวทางการวนจฉย
1. ประวต
Preterm, post-term
น าเดนกอนคลอดนาน
Perinatal distress, meconium
อาการเขยวเกดขนเมอไร*
เขยวคงทหรอมากขน
Mode of delivery
2. การตรวจรางกาย
ควรใหทารกสงบ หายใจ
room air (ถาไม distress มาก)
Central หรอ peripheral
cyanosis, different cyanosis
Heart murmur, ลกษณะการ
หายใจ
แนวทางการวนจฉย
3. การตรวจทางหองปฏบตการ
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
แนวทางการวนจฉย
Hyperoxia test
ให O2 100% ทาง oxygen hood อยางนอย 5-10 min
PaO2 < 100 mmHg
PaO2 > 150 mmHg ไมใชโรคหวใจชนดเขยวแนนอน
cyanotic congenital heart disease
PPHN
PaO2 100-150 mmHg อาจเปนโรคหวใจชนด complete
intracardiac mixing และ PBP มาก
การดแลรกษา
การดแลรกษาโดยทวไป
รกษาอณหภมกายใหปกต
IV fluid,glucose
Adequate tissue
oxygenation
การรกษาจ าเพาะ
แกไขตามสาเหตRespiratory failure
PPHN
CHD ตองอาศย PDA
Congenital cyanotic heart disease ท PBF ขนกบ flowทผาน ductus arteriosus ให Prostaglandin E1 เรม 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
การดแลรกษา
Definition
Apnea : Cessation of breathing for longer than 20 seconds or
shorter duration + Pallor
Cyanosis
Bradycardia
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
Etiology factors contribute to apnea in preterm infant
NeoReviews,
2002
Bacteria
Virus: RSV
Magnesium
Prostaglandin
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
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
Pathophysiologic mechanism predisposing to apnea of prematurity
NeoReviews,
2002
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,
2002
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
Treatment
First : Exclude other medical causes
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
Aminophyline & Cafeine
Hyperbilirubinemia
Hyperbilirubinemia TSB > 2 mg/dl
Neonates appear jaundiced TSB > 5 to 7 mg/dL
Hyperbilirubinemia
Neonatal bilirubin
metabolism
Uptake
Conjugation
Excretion
Production
กลไกทางสรรวทยาของภาวะตวเหลองในทารกแรกเกด
1. มการสราง bilirubin กอนเขาสตบมากขน
• ปรมาณเมดเลอดแดงมาก
• อายของเมดเลอดแดงสน (70-90 วน) เมอเปรยบเทยบกบของ
ผใหญซงเทากบ 120 วน
• Bilirubin ทมาจากแหลงอนทไมใชจากเมดเลอดแดงมาก
• การดดซมกลบของ unconjugated bilirubin ในล าไส
(enterohepatic circulation of bilirubin) มาก
2. กระบวนการก าจด bilirubin ในเลอดท าไดนอย
• Hepatic uptake นอยเนองจากเซลลตบขาด bilirubin-binding
protein (ligandin)
• Conjugation นอยเนองจากเอนซยม UDP-glucuronyl
transferase มเพยงรอยละ 0.1-1 ของระดบในผใหญ
• การขบถายของ bilirubin ยงท าไดไมเตมท
กลไกทางสรรวทยาของภาวะตวเหลองในทารกแรกเกด
Physiologic jaundice
1 สปดาห 2 สปดาห3-5 วน
TSB 5-6 mg/dL
TSB 10-12 mg/dL
อาย
TSB mg/dL
Preterm
Fullterm
Pathologic jaundice
ทควรหาสาเหต มดงน
• อาการตวเหลองภายใน 24-36 ชวโมงหลงเกด
• TSB เพมขนในอตราทมากกวา 5 มก./ดล./24 ชม.
• TSB มากกวา 12 มก./ดล.ในทารกเกดครบก าหนด
หรอ 10-14 มก./ดล. ในทารกเกดกอนก าหนด
• อาการตวเหลองทนานเกน 10-14 วนหลงเกด
• Direct serum bilirubin > 20 %ของ total bilirubin
การประเมนอาการตวเหลอง
ประเมนภาวะตวเหลองรวมดวยทกครงเมอวด vital signs
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
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
2. Undersecretion
• Metabolic and endocrine condition
• Hypothyroidism
• Infants of diabetic mother
• Prematurity
• Obstructive disorders
• Biliary atresia
Causes of neonatal hyperbilirubinemia
3. Mixed
• Sepsis
• Intrauterine infections
• Hepatitis
• Asphyxia
4. Uncertain mechanism
• Race - Thai - Chinese
• Breast milk jaundice
Causes of neonatal hyperbilirubinemia
Causes of neonatal hyperbilirubinemia
ประวตส าคญ
• การตงครรภ การคลอด
• การกนนม
• ประวตครอบครว บตรคนกอน ประวตภาวะเมดเลอด
แดงแตกงาย (G-6PD def, thalassemia เปนตน )
การตรวจรางกายทส าคญ
• อาการและอาการแสดงของโรคตดเชอตงแต
ในครรภหรอหลงเกด
• ภาวะเลอดออกทผวหนงหรอ soft tissue
• คล าไดตบมามโต
การตรวจทางหองปฏบตการทส าคญ
• ระดบ bilirubin, Hct
• Blood type, Rh, Direct Coombs’ test ในทารก
• Peripheral smear for RBC morphology
• Reticulocyte count
• G-6PD level
Laboratory investigation in prolonged jaundice
• Liver function test
• Congenital infection
• Sepsis
• Metabolic defect eg. hypothyroidism
แนวทางการประเมนอาการตวเหลองกอนจ าหนาย
กอน D/C ทารกแรกเกดทกคนควรไดรบการประเมนถง
ความเสยงทจะม severe hyperbilrubinemia
โดยเฉพาะ D/C กอนอายครบ 72 ชม.
1. กลม Low risk : ทารกแรกเกด GA ≥38 สปดาห ทปกตด
ไมมปจจยเสยง
2. กลม Medium risk : ทารกแรกเกด GA≥38 สปดาหทมปจจย
เสยงหรอ GA 35-37+6 สปดาหทปกต
3. กลม High risk : ทารกแรกเกด GA 35-37+6 สปดาห
ทมปจจยเสยง
แนวทางการดแลรกษาภาวะตวเหลอง
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.
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.
Management of hyperbilirubinemia :
Healthy term newborn
< 24 ---- ----
25-48 > 12 > 15
49-72 > 15 > 18
> 72 > 17 > 20
> 96 > 20
Age(hours)
Considerphoto
phototherapy
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.
Phototherapy
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
Complication from phototherapy
1. insensible water loss
2. Loose stool
3. Retinal damage
4. Bronze baby syndrome
• 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
Management of hyperbilirubinemia :
Healthy term newborn
< 24 ---- ----
25-48 > 20 > 25
49-72 > 25 > 30
> 72 > 25 > 30
Age(hours)
ExchangeTransfusionIf photo fails
Exchangetransfusion
And intensivephoto
Exchange transfusion
Blood for exchange transfusion1. 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
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
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
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
แนวทางการรกษาภาวะตวเหลองจากนมแม
• ประเมนวาทารกไดรบนมแมเพยงพอหรอไม หากไมเพยงพอ
ใหทารกดดนมแมบอยขนทก 2-3 ชม
• หากระดบบลรบนมากกวา 18-20 มก./ดล.
- Phototherapy ไมตองงดนมแม
- ตดตามดอาการและตรวจระดบบลรบน
• หากระดบบลรบนสง > 25 มก./ดล.
- Phototherapy + งดนมแมรวมดวย 24-48 ชม.
- ควรอธบายใหแมเขาใจเพอไมใหเกดทศนคตทไมด
เกยวกบนมแม
Neonatal resuscitation
1-112
การเตรยมตวส าหรบการชวยกชพ
ทารกแรกเกดทกรายควรไดรบการประเมนวา
ตองการการดแลชวยเหลอเบองตนหรอไม
Copyright ©2010 American Academy of Pediatrics
ขนตอนการชวยกชพ
2-114
Evaluating the Newborn
ทนทททารกเกด , ถามค าถามเหลาน:
Meconium stained amniotic fluid
1. Vigorous infant- ทารกหายใจด และ- Good muscle tone- Heart rate >100 ครง /นาท
2. Not vigorous
Meconium stained amniotic fluid
Not vigorous infants
(ไมหายใจ หายใจชา
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) ดดในปาก และจมก
( No tracheal suction : not improve
outcome and may cause complications)
( หายใจด
good muscle tone
HR >100)
2-117
Meconium Present and Newborn Not Vigorous
Tracheal Suction
ให oxygen, monitor heart rate
ใส laryngoscope, use 12F or 14F suction
catheter ดดในปาก
ใส endotracheal tube ใน trachea
ตอ endotracheal tube กบ suction source
5-118
Suctioning Meconium via Endotracheal Tube
• ตอทอชวยหายใจกบ
meconium aspirator ซง
ตอกบเครองดดเสมหะ
• ใชนวมออดรเปดของ
meconium aspirator
เพอใหเกดแรงดด
• ท าการดดพรอมๆกบดงทอ
ชวยหายใจออก ท าซ าตามความจ าเปน
Click on the image to play video
2-119
Evaluating the Newborn
ทนทททารกเกด , ถามค าถามเหลาน:
2-120
Initial Steps
ใหความอบอนแกทารก วางทารกใต radiant warmer,
จดทาศรษะ open the airway
เชดตวใหแหง กระตนใหหายใจ
เอาผาเปยกออก จดทาศรษะ
2-121
Opening the Airway
Sniffing” position
2-122
Dry, Stimulate to Breathe, Reposition
Click on the image to play video
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
1-124
การประเมน
ภายหลงการดแลชวยเหลอเบองตน การชวยเหลอขนตอไป ขนกบผลการประเมนดงตอไปน
2-125
Central Cyanosis and Acrocyanosis
1-126
Neonatal hypoglycemia
Definition hypoglycemia
• ภาวะน าตาลในเลอดต าในทารกทกคนไมวาอายเทาไร คอ
พลาสมากลโคส < 47 มก/ดล.
• น าตาลกลโคสในเลอดจะต ากวากลโคสในพลาสมา 10-15 %
• ในทางปฏบตระดบน าตาลกลโคสทถอวาต าและตองการการดแล
รกษาคอ พลาสมากลโคส < 40 มก/ดล.
หรอน าตาลกลโคสในเลอด< 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.
• 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
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
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
Macrosomia : fetal weight >90th percentile for gestational ageA plethoric appearance and excessive fat accumulation
Cause of hypoglycemia
1. Utilization of glucose(Hyperinsulinism)
2. Production/store
3. Utilization of glucose and/or Production
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
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
• 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
• 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
BG < 35 มก/ดล BG <25 มก/ดล BG 25-40 มก/ดล
า ก LPT, LGA/IDM และ Term SGA
ม ม ากา แ ด ดปก
า ก าย 4-24 ม
ให ก นนม ก 2-3 ม จ BG ก นก นนมแ ละม
า กแ ก ก ด - 4 ม
มก นนม ายใน 1 ม หล ก ด
จ BG หล ก นนม 30 นา
ให ก นนม า า ม มป หา
และ จ BG หล ก น 1 ม
ให ก นนม า า ม มป หา
และ จ BG หล ก น 1 ม
IV glucose ให ก นนม ห
IV glucose าจ า ป น
ให ก นนม ห
IV glucose าจ า ป น
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
แ น ม แน า กา ดแล ก า า ก Late preterm (LPT), LGA/IDM และ า ก ก ด ก าหนด ป น SGA
ม ม ากา แ ด า ะน า าลใน ล ด า
Necrotizing enterocolitis
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 pregavageresiduals, emesis, mild abdominal distension, occult blood possiblepresent 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 orgross gastrointestinal bleeding, marked abdominal distension
b. Abdominal radiographs demonstrate significant intestinaldistension with ileus, small bowel separation (edema in bowel wallor peritoneal fluid), unchanging or persistent “rigid” loops,pneumatosis intestinalis, portal vein gas.
Bowel rest
Parenteral antibiotics
Parenteral nutrition
Repeat abdominalexam.
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 ofvital signs, evidence of septic shock or marked gastrointestinalhemorrhage.
c. Abdominal radiograph may demonstrate pneumoperitoneum inaddition 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
Congenital infection
Intrauterine infection
ToRCHS infection
To = Toxoplasmosis
R = Rubella infection
C = Cytomegalo virus infection CMV
H = Herpes simplex infection
S = Syphilis
3 forms of toxoplasma
Cyst
Tachyzoite
Oocyst
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
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
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
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
Skin Ears Endocrine
Rash PetechiaeEcchynosisJaundice Cyanosis Edema
Sensorineural hearing loss
MyxedemaDiabetes insipidusHypopituitarism
Clinical manifestations
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
Investigations
Postnatal investigations
• CBC : anemia and thrombocytopenia
• Liver function tests
• CSF
• Cranial ultrasonography ± CT brain for hydrocephalus
and calcification
• Ophthalmologic examinations
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.
Treatments
Active chrorioretinitis
CNS involvement, eg. CSF protein >1 gm/dL
Treatments
Prednisolone 1 MKD PO bid
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
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
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 %
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
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
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
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
Treatment of mother and CRS
• No specific therapy
• Terminate pregnancy if infected before 5 month
• Follow up newborn
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
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
Clinical Manifestations
Hepatosplenomegaly, conjugated hyperbilirubinemia
Thrombocytopenia with petechiae/purpura
(“blueberry muffin” spots)
Small size for gestational age, microcephaly
Intracranial calcifications
Chorioretinitis
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
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
• 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
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%
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 mouthIf left untreated, more than 70% of cases progress to disseminated disease
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) and70% (HSV-1)
• Poor prognosis : hemorrhagic pneumonitis, severecoagulopathy, liver failure, and meningoencephalitis
• >40% of patients who have disseminated disease do notdevelop skin lesions
Clinical manifestations
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
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
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
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
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
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
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
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
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
• 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
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
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
Mother : no Tx or Tx < 4 wk before deliveryInfant : normal physical examinationSingle 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 daysProcaine penicillin G 50,000 U/kg IM OD x 10 days
Single dose of Benzathine penicillin 50,000 U/kg IM
Varicella-Zoster Virus (VZV)
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
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
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)
• Perinatally acquired varicella : serious complications
pneumonia
bacterial superinfections
(toxic shock syndrome and necrotizing fasciitis)
Cerebellar ataxia, encephalitis, meningitis
Clinical Manifestations of CVS
• 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
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
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)
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
Care of exposed people
Varicella vaccine adminstered by 3-5 days after exposure
All exposed susceptible patient should be dischaged as
soon as possible
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
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
Hypospadia
• Urethral opening that is on the ventral surface of penile shaft
• >> penoscrotal hypospadia : consider VCUG
10% dilate prostatic utricle
>> 10% boy with hypospadia : undescendedtestis, inguinal hernia
Recommended