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By; Dr. Stacy Arvinna
 Baby of ‘X’
 Date Of Birth: 13/5/15, at 10 am
 Mother, 20 years, Para 1+1, Filipino
 Infectious screening; unknown. Blood group; B+.
 Antenatally:
1. Unbooked case.
2. History of early neonatal death.
 LMP Oct 2014
 Home delivered and cord cut under unsterile method.
 Mother claim child cried at birth. Noted child making
weird noise and rapid breathing at 15 minutes of life
so decided to bring to ETD. No cyanosis. No apnea.
 Referred at 6 hour of life from ETD for
presumed sepsis and admitted to NICU.
 Ballard score:32-34 weeks.
 Weight:1.99kg.
On examination;
 Baby appear active, crying, pink. Peripheries
slightly cool to touch, good pulse volume,
CRT<2s.
 Tachypnoiec, with grunting and nasal flaring.
 Presence deep subcostal recession.
 RR:72. SPO2: 85-89% on room air.
Temp:36.8. HR: 138. BP:90/50
 CNS- moving all four limbs, tone and reflexes
are normal.
 Respiratory system- no chest deformity.
Equal chest expansion and air entry. Equal
vesicular breath sound bilaterally.
 Cardiovascular system-apex beat not
displaced. S1S2 heard. No murmur.
 Abdomen –Soft, no liver or spleen palpable.
Umbilical with 2 arteries and 1 vein.
 VBG
pH: 7.250
pCO2: 60.6
pO2:37.2
hCO3 26.0
BE -3.1 mmol/L
SO2: 59.6%
 FBC
TW: 18.8
HB:19.6 g/dL
HCT: 61.4%
PLT: 314
 RENAL
PROFILE
Na:139
K: 5.8
Urea:2.4
Creatinine: 42
 Differential diagnosis
1. Respiratory distress syndrome
2. Transient tachypnoiec of newborn
3. Congenital Pneumonia
 Investigations
Started on BCPAP with FiO2 21%
Child still tachypnoiec with grunting and subcostal
recession.
SpO2: 88-90%
Changed to BCPAP with FiO2 28%
Child still tachypnoiec with grunting and subcostal
recession.
SpO2: 95-98%
 Decided for Survanta instillation. Given at 7th
hour of life.(5pm)
 Survanta 4ml/kg given. Procedure uneventful.
 Post survanta: Child less tachypnoiec. Less
subcostal recession and no grunting. SpO2; 98-
100% on BCPAP with FiO2 28%. PEEP 6cmH2O.
1. Prematurity at 32 weeks (according to
Ballard Scoring)
2. Presumed Sepsis (due to spontaneous
premature delivery and cover for GBS)
3. RDS Grade 1
 IVD D10% started with TF:60ml/kg/day
 Loaded with IV Aminophylline10mg/kg
 Start antibiotic
IV C-penicillin 100 000u/kg BD
IV Gentamycin 3.5mg/kg OD
 IM serotet
 Blood Culture taken.
 Repeat VBG post survanta.
 VBG (post
survanta)
pH: 7.259
pCO2: 48.0
pO2:39.2
hCO3 21.0
BE -6.3 mmol/L
SO2: 63.3%
 Trial of room air since 7.30am 14/5/15.
 1 episode of desaturation at 9.45am. SpO2
dropped to 68%. Stimulation done and SpO2
picked up back to 98-100% on room air.
 Started IV Aminophylline 2.5mg/kg
maintenance. Child was kept under room
air.
 Currently child stable on room air.
Aminophyline was off on 17/5/15.
 Baby was on BCPAP 28% for total of 15 hours.
 After survanta given at 7hour of life, baby
shows immediate improvement.
 No intubation required.
 Manage to wean off oxygen support. Baby
was on air since 14/5/15.
 Is this baby in respiratory distress?
 Tachypnea with RR>60
 Chest Recession(retractions in the intercostal,
subcostal, or supracostal spaces).
 Nasal Flaring
 Grunting
 Cyanosis
 apnea
 inspiratory stridor
 Respiratory distress occurs in approximately 7
percent of infants (according to American Family Physician)
 Most common cause
1. Transient tacypnea of newborn
2. Respiratory distress syndrome
3. Meconium aspiration syndrome
 Less common causes
1. Infection (pneumonia, sepsis)
2. Pneumothorax
3. Diagphragmatic hernia
4. Persistent pulmonary hypertension of newborn
Also known as wet lung.
It’s a benign disease
occur because of delay
resorption of fetal lung
fluid.
(according to Neonatology by
Lange)
Parenchymal
infiltrates
Wet silhoutte around
the heart
Intralobar fluid
accumulation
 Pneumonia, respiratory distress syndrome,
and sepsis may have similar manifestations,
so chest x-ray, and FBC usually are done. If
its indicated, blood cultures will be taken as
well.
 Recovery usually occurs within 2 to 3 days.
Treatment is supportive and involves giving
O2 support and monitoring ABGs or pulse
oximetry.
 Respiratory distress in infant born through meconium
stained amniotic fluid whose symptoms cannot be
otherwise explained. (by faranoff)
 First intestinal discharge composed of epithelial cells, fetal
hair, mucus, and bile.
• Prenatal
• Postnatal
 Sign of long exposure of meconium intrauterine- staining
of skin, nail and umbilicus of newborn.
 Incidence: 8-20% of all deliveries.
 Passage of meconium in infant of gestation <34 weeks is
unusual and may represent billious reflux secondary to
intestinal obstruction.
 Fetal distress cause Parasympathethic effect causes anal
sphicter relax.
Chest radiograph of
a full-term infant
with meconium
aspiration showing
coarse interstitial
infiltrates and left
pneumothorax.
 Suctioning at birth before the first breath
 Direct suction should be done before the first
cry and initial resuscitation steps.
 Endotracheal intubation as needed
 Mechanical ventilation as needed
 Supplemental O 2 as needed
 IV antibiotics ( ex: Ampicillin, Penicillin,
Gentamycin)
Also known as hyaline membrane disease.
Clinical diagnosis is warranted in preterm newborn with
respiratory distress that persist over 48-96 hours of life.
Incidence: 44% between birthweight 501g-1500g.
Survival has improved significantly after the introduction of
exogenous surfactant.
Classification
Mild
Moderate
Severe
Stage 1: slight reticular
(slight granular)
decrease in transparency
of the lung, no certain
difference to normal
finding.
Stage 2: Soft decrease in
transparency with an air
bronchogram, which
overlaps the heart. (its
always a sign of an alveolar
lung reaction)
Stage 3: like stage 2, but with
gradual stronger decrease in
transparency, as well as a blurry
diagphragm and heart.
Stage 4: White
lung. Practically
homogenic lung
opacity.
 Surfactant
• Specific treatment is intratracheal surfactant therapy.
 Supplementary O 2 as needed
 Mechanical ventilation as needed
 Prognosis with treatment is excellent; mortality is < 10%.
 Less premature infants (those> 1 kg) and those with lower
O 2 requirements (fraction of inspired O 2 [F io 2 ] < 40 to
50%) may respond well to supplemental O 2 alone or to
treatment with nasal continuous positive airway pressure
(CPAP).
 A treatment strategy of early (within 20 to 30 min after
birth) surfactant therapy is associated with significant
decrease in duration of mechanical ventilation, lesser
incidence of air leak syndromes and lower incidence of
bronchopulmonary dysplasia.
 Collection of air between the lung and the
chest wall that develops when air leaks out
of the lung.
 Features: Diminished sound of air entry and
leaving at affected side of lung.
 Positive transillumination test.
 X-ray is definitive diagnosis.
 characterized by a variable degree of
pulmonary hypoplasia associated with a
decrease in cross-sectional area of the
pulmonary vasculature and alterations of the
surfactant system.
 There are 3 basic types:
 the posterolateral Bochdalek hernia
(occurring at approximately 6 weeks'
gestation)
 the anterior Morgagni hernia
 the hiatus hernia.
 Scaphoid abdomen
 Barrel-shaped chest
 Respiratory distress (retractions, cyanosis,
grunting respirations)
 In left-sided posterolateral hernia,
auscultation of the lungs reveals poor air
entry on the left, with a shift of cardiac
sounds over the right chest.
 In patients with severe defects, signs of
pneumothorax (poor air entry, poor
perfusion) may also be found.
 Placement of a vented orogastric tube and
connecting it to continuous suction to prevent
bowel distention and further lung compression
 Avoiding mask ventilation and immediately
intubating the trachea
 Avoiding high peak inspiratory pressures with
mechanical ventilation; synchronizing ventilation
with the infant's respiratory effort
 Continuous monitoring of oxygenation, blood
pressure, and perfusion
 Maintaining glucose and ionized calcium
concentrations within reference range
Cause Patho-
physiology
Risk factors Clinical
features
Chest
radiograph
findings
Treatment prevention
TTN Mechanical
-Persistent
lung fluid
-Delayed
absorption/
clearance of
fetal lung
fluid
Biochemical
-stress
C-section
Macrosomia
Male
Maternal
asthma
Maternal
diabetes
Tachypnea
Nasal
Flaring
Often no
hypoxia or
cyanosis
Parenchymal
infiltrates
Wet silhoutte
around the
heart
Intralobar fluid
accumulation
Supportive.
Oxygen if
hypoxic.
MAS Lung
irritation
and
obstruction
Meconium
stained
amniotic
fluid
Post term
delivery
Preterm-
listeriosis
Tachypnea
Hypoxia
Poor tone
Meconium
stained
(skin, nail
and
umbilical)
Patchy
atelectasis
Consolidation
Find for
complication
pneumothorax,
pneumomediast
inum,
cardiomegaly,
Resuscitation
and Direct
suction,
oxygen,
Ventilation,
Surfactant
Antibiotic
Do not
impede
delivery for
suctioning,
amnioinfusion
of no benefitt
Cause Patho-
physiology
Risk factors Clinical
features
Chest
radiograph
findings
Treatment prevention
RDS Surfactant
deficiency
secreted by
pneumocyte
2
Lung under
development
Male
Maternal
diabetes 2’
hyperinsulin
emia
Preterm
delivery
Tachypnea
Hypoxia
Cyanosis
Nasal
flaring
Grunting
Intercostal
/subcostal
recessions
Homogenous
infiltrates
Air
bronchograms
Decreased
lung volumes
Grading 1-4(
severity)
Resuscitation,
oxygen,
Ventilation,
surfactant
Prenatal
corticosteroi
d if risk of
preterm
delivery
Pneu
motho
rax
Collection of
air between
the lung and
the chest wall
that develops
when air
leaks out of
the lung.
RDS
MAS
Continuous
use CPAP
Diminishe
d sound of
air entry
and
leaving at
affected
side
Radioluscency No treatment
if
asymptomatic
, chest tube.
-
Cause Patho-
physiology
Risk factors Clinical features Chest
radiograph
findings
Treatment
Pneumonia
or
Sepsis
Inflammation
of pulmonary
tissues
Associated
with
consolidation
of alveolar
spaces
In neonates:
must
consider
sepsis
-Prolonged
rupture of
membranes
-Maternal
fever
-Mother is a
GBS carrier
-Respiratory
distress
-Temp instability
-Lethargy
-Poor feeding
-Jaundice
-Apnea
CXR: Depends
on cause (GBS:
bilat. conso-
lidations, air
bronchograms)
Blood Culture:
may be positive
Elevated WBC’s
or neutropenia
Treat with
broad
spectrum
antibiotics
until cause of
pneumonia is
identified
and sepsis is
ruled out
Congenital
Diaphrag-
matic
hernia
Loops of
bowel in
chest area via
defect in
diaphragm
Hypoplastic
lungs
Often
associated
with other
anomalies
(CVS, CNS,
GI)
Respiratory
distress
-Cyanosis
-Scaphoid
abdomen
-Barrel chest
-Dullness to
percussion
-Absent breath
sounds
-Asymmetric
chest wall mvmt
CXR: portion of
GI tract in
thorax (usually
left), displaced
mediastinum
Treatment
and
prognosis
depends on
the degree of
lung
hypoplasia as
well as the
presence of
associated
anomalies
Cause Patho-
physiology
Risk factors Clinical
features
Chest
radiograph
findings
Treatment
PPHN
(Persistent
Pulmonary
Hyper-
tension of
the
Newborn)
-Persistence of
fetal circulation
-Right to left
shunt via PDA,
PFO,
intrapulmonary
channels
-↓ pulmonary
blood flow and
hypoxemia
cause
pulmonary
vasoconstriction
-Asphyxia
-MAS
-RDS
-Structural
abnormalities
(Diaphragmatic
hernia,
congenital
heart disease)
-Respiratory
distress
-Cyanosis
-May have CHF
(active
precordium,
gallop rhythm,
single S2, poor
capillary refill,
weak pulses,
hepatomegaly)
CXR:
abnormal
pulmonary
vascularity
Cardiomegaly
Echo:
increased
pulmonary
artery
pressure,
right to left
shunt
O2 given
early
May require
surgical
correction
of heart
defect
 Synthetic surfactant
◦ Has added spreading agents, hexadecanol (an alcohol) and
tyloxapol (a non-ionic surfactant)
◦ No protein
 Natural
◦ Made from animal extracts
 Adverse Effect
Transient bradycardia
Oxygen desaturation
Reflux
Pallor
Vasoconstriction
Hypotension
Apnea
◦ There is NO BENEFIT in administering surfactant after 18-24 hours
of age
 Dexamethasone dosage
◦ 4 doses of 6mg given 6 hours apart; or
◦ 2 doses of 12mg given 12 hours apart
(recommended to use Betamethasone instead as
dexamethasone causing cystic periventricular
leukomalacia)
 Eligible for:
◦ Usually given at all women between 24 to 36 weeks of
pregnancy at risk of preterm delivery.
◦ Patients administered with tocolytic agents
◦ Preterm PROM (in the absence of chorioamnionitis)
 Cautioned for:
◦ Poorly controlled GDM
◦ Chorioamnionitis
◦ Immunosuppressed mothers
 Nelson’s Textbook of Paediatrics
 Neonatology by Lange.
 Maternal, Fetal and Neonatal Physiology by
Susan Blackburn.
 http://www.aafp.org
 http://www.hopkinschildrens.org
 http://www.merckmanuals.com/professional
/pediatrics/perinatal-problems/
 http://emedicine.medscape.com
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Respiratory distress in neonates

  • 1. By; Dr. Stacy Arvinna
  • 2.  Baby of ‘X’  Date Of Birth: 13/5/15, at 10 am  Mother, 20 years, Para 1+1, Filipino  Infectious screening; unknown. Blood group; B+.  Antenatally: 1. Unbooked case. 2. History of early neonatal death.  LMP Oct 2014  Home delivered and cord cut under unsterile method.  Mother claim child cried at birth. Noted child making weird noise and rapid breathing at 15 minutes of life so decided to bring to ETD. No cyanosis. No apnea.
  • 3.  Referred at 6 hour of life from ETD for presumed sepsis and admitted to NICU.  Ballard score:32-34 weeks.  Weight:1.99kg. On examination;  Baby appear active, crying, pink. Peripheries slightly cool to touch, good pulse volume, CRT<2s.  Tachypnoiec, with grunting and nasal flaring.  Presence deep subcostal recession.  RR:72. SPO2: 85-89% on room air. Temp:36.8. HR: 138. BP:90/50
  • 4.  CNS- moving all four limbs, tone and reflexes are normal.  Respiratory system- no chest deformity. Equal chest expansion and air entry. Equal vesicular breath sound bilaterally.  Cardiovascular system-apex beat not displaced. S1S2 heard. No murmur.  Abdomen –Soft, no liver or spleen palpable. Umbilical with 2 arteries and 1 vein.
  • 5.  VBG pH: 7.250 pCO2: 60.6 pO2:37.2 hCO3 26.0 BE -3.1 mmol/L SO2: 59.6%  FBC TW: 18.8 HB:19.6 g/dL HCT: 61.4% PLT: 314  RENAL PROFILE Na:139 K: 5.8 Urea:2.4 Creatinine: 42  Differential diagnosis 1. Respiratory distress syndrome 2. Transient tachypnoiec of newborn 3. Congenital Pneumonia  Investigations
  • 6.
  • 7. Started on BCPAP with FiO2 21% Child still tachypnoiec with grunting and subcostal recession. SpO2: 88-90% Changed to BCPAP with FiO2 28% Child still tachypnoiec with grunting and subcostal recession. SpO2: 95-98%  Decided for Survanta instillation. Given at 7th hour of life.(5pm)  Survanta 4ml/kg given. Procedure uneventful.  Post survanta: Child less tachypnoiec. Less subcostal recession and no grunting. SpO2; 98- 100% on BCPAP with FiO2 28%. PEEP 6cmH2O.
  • 8. 1. Prematurity at 32 weeks (according to Ballard Scoring) 2. Presumed Sepsis (due to spontaneous premature delivery and cover for GBS) 3. RDS Grade 1
  • 9.  IVD D10% started with TF:60ml/kg/day  Loaded with IV Aminophylline10mg/kg  Start antibiotic IV C-penicillin 100 000u/kg BD IV Gentamycin 3.5mg/kg OD  IM serotet  Blood Culture taken.  Repeat VBG post survanta.  VBG (post survanta) pH: 7.259 pCO2: 48.0 pO2:39.2 hCO3 21.0 BE -6.3 mmol/L SO2: 63.3%
  • 10.  Trial of room air since 7.30am 14/5/15.  1 episode of desaturation at 9.45am. SpO2 dropped to 68%. Stimulation done and SpO2 picked up back to 98-100% on room air.  Started IV Aminophylline 2.5mg/kg maintenance. Child was kept under room air.  Currently child stable on room air. Aminophyline was off on 17/5/15.
  • 11.  Baby was on BCPAP 28% for total of 15 hours.  After survanta given at 7hour of life, baby shows immediate improvement.  No intubation required.  Manage to wean off oxygen support. Baby was on air since 14/5/15.
  • 12.  Is this baby in respiratory distress?
  • 13.  Tachypnea with RR>60  Chest Recession(retractions in the intercostal, subcostal, or supracostal spaces).  Nasal Flaring  Grunting  Cyanosis  apnea  inspiratory stridor  Respiratory distress occurs in approximately 7 percent of infants (according to American Family Physician)
  • 14.
  • 15.  Most common cause 1. Transient tacypnea of newborn 2. Respiratory distress syndrome 3. Meconium aspiration syndrome  Less common causes 1. Infection (pneumonia, sepsis) 2. Pneumothorax 3. Diagphragmatic hernia 4. Persistent pulmonary hypertension of newborn
  • 16. Also known as wet lung. It’s a benign disease occur because of delay resorption of fetal lung fluid. (according to Neonatology by Lange)
  • 17. Parenchymal infiltrates Wet silhoutte around the heart Intralobar fluid accumulation
  • 18.  Pneumonia, respiratory distress syndrome, and sepsis may have similar manifestations, so chest x-ray, and FBC usually are done. If its indicated, blood cultures will be taken as well.  Recovery usually occurs within 2 to 3 days. Treatment is supportive and involves giving O2 support and monitoring ABGs or pulse oximetry.
  • 19.  Respiratory distress in infant born through meconium stained amniotic fluid whose symptoms cannot be otherwise explained. (by faranoff)  First intestinal discharge composed of epithelial cells, fetal hair, mucus, and bile. • Prenatal • Postnatal  Sign of long exposure of meconium intrauterine- staining of skin, nail and umbilicus of newborn.  Incidence: 8-20% of all deliveries.  Passage of meconium in infant of gestation <34 weeks is unusual and may represent billious reflux secondary to intestinal obstruction.  Fetal distress cause Parasympathethic effect causes anal sphicter relax.
  • 20.
  • 21. Chest radiograph of a full-term infant with meconium aspiration showing coarse interstitial infiltrates and left pneumothorax.
  • 22.  Suctioning at birth before the first breath  Direct suction should be done before the first cry and initial resuscitation steps.  Endotracheal intubation as needed  Mechanical ventilation as needed  Supplemental O 2 as needed  IV antibiotics ( ex: Ampicillin, Penicillin, Gentamycin)
  • 23. Also known as hyaline membrane disease. Clinical diagnosis is warranted in preterm newborn with respiratory distress that persist over 48-96 hours of life. Incidence: 44% between birthweight 501g-1500g. Survival has improved significantly after the introduction of exogenous surfactant. Classification Mild Moderate Severe
  • 24.
  • 25. Stage 1: slight reticular (slight granular) decrease in transparency of the lung, no certain difference to normal finding. Stage 2: Soft decrease in transparency with an air bronchogram, which overlaps the heart. (its always a sign of an alveolar lung reaction)
  • 26. Stage 3: like stage 2, but with gradual stronger decrease in transparency, as well as a blurry diagphragm and heart. Stage 4: White lung. Practically homogenic lung opacity.
  • 27.  Surfactant • Specific treatment is intratracheal surfactant therapy.  Supplementary O 2 as needed  Mechanical ventilation as needed  Prognosis with treatment is excellent; mortality is < 10%.  Less premature infants (those> 1 kg) and those with lower O 2 requirements (fraction of inspired O 2 [F io 2 ] < 40 to 50%) may respond well to supplemental O 2 alone or to treatment with nasal continuous positive airway pressure (CPAP).  A treatment strategy of early (within 20 to 30 min after birth) surfactant therapy is associated with significant decrease in duration of mechanical ventilation, lesser incidence of air leak syndromes and lower incidence of bronchopulmonary dysplasia.
  • 28.  Collection of air between the lung and the chest wall that develops when air leaks out of the lung.  Features: Diminished sound of air entry and leaving at affected side of lung.  Positive transillumination test.  X-ray is definitive diagnosis.
  • 29.
  • 30.  characterized by a variable degree of pulmonary hypoplasia associated with a decrease in cross-sectional area of the pulmonary vasculature and alterations of the surfactant system.  There are 3 basic types:  the posterolateral Bochdalek hernia (occurring at approximately 6 weeks' gestation)  the anterior Morgagni hernia  the hiatus hernia.
  • 31.  Scaphoid abdomen  Barrel-shaped chest  Respiratory distress (retractions, cyanosis, grunting respirations)  In left-sided posterolateral hernia, auscultation of the lungs reveals poor air entry on the left, with a shift of cardiac sounds over the right chest.  In patients with severe defects, signs of pneumothorax (poor air entry, poor perfusion) may also be found.
  • 32.  Placement of a vented orogastric tube and connecting it to continuous suction to prevent bowel distention and further lung compression  Avoiding mask ventilation and immediately intubating the trachea  Avoiding high peak inspiratory pressures with mechanical ventilation; synchronizing ventilation with the infant's respiratory effort  Continuous monitoring of oxygenation, blood pressure, and perfusion  Maintaining glucose and ionized calcium concentrations within reference range
  • 33.
  • 34.
  • 35. Cause Patho- physiology Risk factors Clinical features Chest radiograph findings Treatment prevention TTN Mechanical -Persistent lung fluid -Delayed absorption/ clearance of fetal lung fluid Biochemical -stress C-section Macrosomia Male Maternal asthma Maternal diabetes Tachypnea Nasal Flaring Often no hypoxia or cyanosis Parenchymal infiltrates Wet silhoutte around the heart Intralobar fluid accumulation Supportive. Oxygen if hypoxic. MAS Lung irritation and obstruction Meconium stained amniotic fluid Post term delivery Preterm- listeriosis Tachypnea Hypoxia Poor tone Meconium stained (skin, nail and umbilical) Patchy atelectasis Consolidation Find for complication pneumothorax, pneumomediast inum, cardiomegaly, Resuscitation and Direct suction, oxygen, Ventilation, Surfactant Antibiotic Do not impede delivery for suctioning, amnioinfusion of no benefitt
  • 36. Cause Patho- physiology Risk factors Clinical features Chest radiograph findings Treatment prevention RDS Surfactant deficiency secreted by pneumocyte 2 Lung under development Male Maternal diabetes 2’ hyperinsulin emia Preterm delivery Tachypnea Hypoxia Cyanosis Nasal flaring Grunting Intercostal /subcostal recessions Homogenous infiltrates Air bronchograms Decreased lung volumes Grading 1-4( severity) Resuscitation, oxygen, Ventilation, surfactant Prenatal corticosteroi d if risk of preterm delivery Pneu motho rax Collection of air between the lung and the chest wall that develops when air leaks out of the lung. RDS MAS Continuous use CPAP Diminishe d sound of air entry and leaving at affected side Radioluscency No treatment if asymptomatic , chest tube. -
  • 37. Cause Patho- physiology Risk factors Clinical features Chest radiograph findings Treatment Pneumonia or Sepsis Inflammation of pulmonary tissues Associated with consolidation of alveolar spaces In neonates: must consider sepsis -Prolonged rupture of membranes -Maternal fever -Mother is a GBS carrier -Respiratory distress -Temp instability -Lethargy -Poor feeding -Jaundice -Apnea CXR: Depends on cause (GBS: bilat. conso- lidations, air bronchograms) Blood Culture: may be positive Elevated WBC’s or neutropenia Treat with broad spectrum antibiotics until cause of pneumonia is identified and sepsis is ruled out Congenital Diaphrag- matic hernia Loops of bowel in chest area via defect in diaphragm Hypoplastic lungs Often associated with other anomalies (CVS, CNS, GI) Respiratory distress -Cyanosis -Scaphoid abdomen -Barrel chest -Dullness to percussion -Absent breath sounds -Asymmetric chest wall mvmt CXR: portion of GI tract in thorax (usually left), displaced mediastinum Treatment and prognosis depends on the degree of lung hypoplasia as well as the presence of associated anomalies
  • 38. Cause Patho- physiology Risk factors Clinical features Chest radiograph findings Treatment PPHN (Persistent Pulmonary Hyper- tension of the Newborn) -Persistence of fetal circulation -Right to left shunt via PDA, PFO, intrapulmonary channels -↓ pulmonary blood flow and hypoxemia cause pulmonary vasoconstriction -Asphyxia -MAS -RDS -Structural abnormalities (Diaphragmatic hernia, congenital heart disease) -Respiratory distress -Cyanosis -May have CHF (active precordium, gallop rhythm, single S2, poor capillary refill, weak pulses, hepatomegaly) CXR: abnormal pulmonary vascularity Cardiomegaly Echo: increased pulmonary artery pressure, right to left shunt O2 given early May require surgical correction of heart defect
  • 39.  Synthetic surfactant ◦ Has added spreading agents, hexadecanol (an alcohol) and tyloxapol (a non-ionic surfactant) ◦ No protein  Natural ◦ Made from animal extracts  Adverse Effect Transient bradycardia Oxygen desaturation Reflux Pallor Vasoconstriction Hypotension Apnea ◦ There is NO BENEFIT in administering surfactant after 18-24 hours of age
  • 40.  Dexamethasone dosage ◦ 4 doses of 6mg given 6 hours apart; or ◦ 2 doses of 12mg given 12 hours apart (recommended to use Betamethasone instead as dexamethasone causing cystic periventricular leukomalacia)  Eligible for: ◦ Usually given at all women between 24 to 36 weeks of pregnancy at risk of preterm delivery. ◦ Patients administered with tocolytic agents ◦ Preterm PROM (in the absence of chorioamnionitis)  Cautioned for: ◦ Poorly controlled GDM ◦ Chorioamnionitis ◦ Immunosuppressed mothers
  • 41.  Nelson’s Textbook of Paediatrics  Neonatology by Lange.  Maternal, Fetal and Neonatal Physiology by Susan Blackburn.  http://www.aafp.org  http://www.hopkinschildrens.org  http://www.merckmanuals.com/professional /pediatrics/perinatal-problems/  http://emedicine.medscape.com

Notas del editor

  1. A surge in endogenous steroid and catecholamine accompanies term gestation and spontaneous vaginal delivery, and is responsible for some of maturational effects. Rapid clearance of fetal lung fluid clearance plays a key role in the transition of to air breathing. The bulk of this fluid clearance is mediaated by transepithelial sodium reabsorption therough amiloride-sensitive sodium channels in the alveolar epithelial cell with only limited contribution from mechanical factor or starling force.
  2. With adequate ventilatory support alone, surfactant production eventually begins, and once production begins, RDS resolves within 4 or 5 days. However, in the meantime, severe hypoxemia can result in multiple organ failure and death.
  3. Although both synthetic and natural surfactants are effective, natural surfactants tend to be more superior because of their surfactant associated protein content Also, natural surfactant have a more rapid onset and associated with a lower risk or pneumothorax Via two approaches Prophylactic strategy For high risk infants below a specified weight or gestational age given within 15 minutes after birth Allows surfactant to be administered before the hyaline membrane begins to develop and before the lungs are subjected to the traumatic effects of mechanical ventilation Treatment strategy aka rescue treatment Given to infants with established RDS