Approach to Respiratory Distress-HMD in
Newborn
• A 32 weeks preterm baby born to a GDM mother by LSCS, developed
distress, grunting, cyanosis soon after birth. His SPO2 was 90%,
hyperoxia test was positive. Downe’s score was 7, silverman-anderson
score 8. Urgent CXR was done which showed :
RDS
4
Now what next ???
• Baby shifted to NICU and put on warmer. RBS was normal, other
blood samples taken. IV fluids were started, ABG was done which
showed acidosis.
• Baby was put on nasal CPAP, meanwhile survanta was arranged.
• Baby then put on venti, surfactant given at 4 hours of life.
• Now clinically better.
SIGNS AND SYMPTOMS
• Tachypnea (RR > 60/min)
• Nasal flaring
• Retraction
• Grunting
• +/- Cyanosis
• +/- Desaturation
• Decreased air entry
General
Considerations
RD IN NB- Causes
• Pulmonary
- Parenchymal
- Extraparenchymal
• Non Pulmonary
- Heart
- Metabolic
- Brain
- Blood
- Abdominal
RD in Newborn – Causes
Pulmonary
Parenchymal Extraparenchymal
* RDS (HMD) * Upper airway obstruction
* TTN (RDS II) (Cloanal atresia, stenosis)
* Aspiration (Blood * Pneumothorax
meconium) * Pleural effusion
* PPHN * Cong. Diaph. hernia
* Pneumonia * Diaphragmatic paralysis
* Pulm. hemorrhage
* Pulm. hypoplasia
RD in Newborn – Causes
Extrapulmonary
Heart Metabolic Brain Blood
Abdominal
- CCF - Met. Acidosis - Haemorrhage - Hypovolemia - NEC
- PDA - Hypoglycemia - Edema - Hyperviscosity - Pneumo
- CCHD - Hypothermia - Drugs - Acute blood
peritonium
- Vascular - Sepsis - Pain loss - Large
mass
Surgical causes of respiratory distress
• Tracheo-esophageal fistula
• Diaphragmatic hernia
• Lobar emphysema
• Pierre -Robin syndrome
• Choanal atresia
Suspect surgical cause
• Obvious malformation
• Scaphoid abdomen
• Frothing
• History of aspiration
A progressively increasing O2 requirement to
maintain saturation is also a sensitive indicator
of the severity and progress of distress
>95% Term baby, pulmonary hypertension (PPHN)
88-94% 28-34 weeks preterm
85-92% Below 28 weeks gestational age
Guidelines for monitoring oxygen saturation levels
by pulse oximetry
MJAFI, Vol. 63, No. 3, 2007
General
Considerations
Hyperoxia test
test Method result diagnosis
Hyperoxia 100 % fio2 5-10
min
Pao2 increases to
> 100 torr
Pao2 increases by
< 20 torr
Parenchymal
lung disease
PPHN / CCHD
Hyperoxia-
hypervetilation
MV 100 % fio2 &
VR 100-150 /
min
Pao2 increases to
> 100 torr
w HV
Pao2 increases
at critical Pco2
No increase in
Pao2 with HV
Parenchymal
lung disease
PPHN
CCHD
Downe’s score
Silverman-Andersen Retraction Scoring
Interpretation
Score 0-3 = Mild respiratory distress
Score 4-6 = Moderate respiratory distress
Score > 6 = Impending respiratory failure
Score 10 = Severe Respiratory distress
General
Considerations
Investigation
Complete Blood Count with a Peripheral blood smear
Sepsis screen including C-reactive protein and μ ESR
Arterial blood gas (ABG) analysis
Blood glucose, Serum calcium
Cultures: Blood , Surface swab (where indicated),
maternal vaginal swab
Chest radiograph with an oro-gastric tube in situ
General
Considerations
Mathai ss et al ,MJAFI 2007; 63 : 269-272
RR
(bpm
Aspiration cong. Pneumonia, sev. HMD CDH
cardiac malformation
Approx. 6 Hours of age
Normal
60
Course of Neonatal Tachypnoea : Etiologic possibilities
Source : Baurn DJ, Birth Risks, Nastle Nutrition Workshop, 1993
TTNB
HMD
Evaluation of RD in NB – Clinical History
Antenatal History Most likely association
* Prematurity, IDMs * HMD
* PROM, maternal fever, * Pneumonia
Unclean vaginal exams,
UTI, diarrhoea
* Asphyxia/MSAF * Aspiration
* Caesarean delivery * TTN
* Polyhydramnios * Pulm. Hypoplasia
* Oligohydramnios * TE fistula, CDH
* H/o receiving steroids * RDS less
* Traumatic/breech delivery * ICH / Phrenic nerve paralysis
HMD/RDS
Respiratory Distress Syndrome (RDS)
• Also known as Hyaline Membrane Disease (HMD)
• Commonest cause of preterm neonatal mortality
• RDS occurs primarily in premature infants; its incidence
is inversely related to gestational age and birth weight
Nelson Textbook of Pediatrics, 18th
Ed.
Gestational age Percentages
Less than 28 wks 60-80%
32-36 wks 15-30%
37-39 wk 5%
Term Rare
Resp.
Dis.
Syn.
ETIOLOGY AND PATHOPHYSIOLOGY.
• Surfactant deficiency is the 1O
cause of RDS.
• Low levels of surfactant cause high surface tension
• High surface tension makes it hard to expand the alveoli.
• Tendency of affected lungs to become atelectatic at end-
expiration when alveolar pressures are too low to
maintain alveoli in expansion
• Leads to failure to attain an adequate lung inflation and
therefore reduced gaseous exchange
• With advancing gestational age, increasing amounts
of phospholipids are synthesized and stored in type II
alveolar cells .
• Wk 20: start of surfactant production and storage.
Does not reach lung surface until later
• Wk 28-32: maximal production of surfactant and
appears in amniotic fluid
• Wk 34-35; mature levels of surfactant in lungs
• Quality : The amounts produced or released may be
insufficient to meet postnatal demands because of
immaturity.
• Surfactant inactivating states eg maternal DM may
lead to surfactant of lower quality/ immature
• Rare genetic disorders may cause fatal respiratory
distress syndrome eg.
• Abnormalities in surfactant protein B and C genes
• gene responsible for transporting surfactant across
membranes (ABC transporter 3 [ABCA3]) are associated
with severe and often lethal familial respiratory disease
26
Clinical manifestation
• Tachypnea
• Nasal flaring
• Intercostal, sternal recession
• Grunting; closure of glottis during expiration
• Cyanosis

Approach to Respiratory Distress-HMD in Newborn.pptx

  • 1.
    Approach to RespiratoryDistress-HMD in Newborn
  • 3.
    • A 32weeks preterm baby born to a GDM mother by LSCS, developed distress, grunting, cyanosis soon after birth. His SPO2 was 90%, hyperoxia test was positive. Downe’s score was 7, silverman-anderson score 8. Urgent CXR was done which showed :
  • 4.
  • 5.
    Now what next??? • Baby shifted to NICU and put on warmer. RBS was normal, other blood samples taken. IV fluids were started, ABG was done which showed acidosis. • Baby was put on nasal CPAP, meanwhile survanta was arranged. • Baby then put on venti, surfactant given at 4 hours of life. • Now clinically better.
  • 6.
    SIGNS AND SYMPTOMS •Tachypnea (RR > 60/min) • Nasal flaring • Retraction • Grunting • +/- Cyanosis • +/- Desaturation • Decreased air entry
  • 7.
  • 8.
    RD IN NB-Causes • Pulmonary - Parenchymal - Extraparenchymal • Non Pulmonary - Heart - Metabolic - Brain - Blood - Abdominal
  • 9.
    RD in Newborn– Causes Pulmonary Parenchymal Extraparenchymal * RDS (HMD) * Upper airway obstruction * TTN (RDS II) (Cloanal atresia, stenosis) * Aspiration (Blood * Pneumothorax meconium) * Pleural effusion * PPHN * Cong. Diaph. hernia * Pneumonia * Diaphragmatic paralysis * Pulm. hemorrhage * Pulm. hypoplasia
  • 10.
    RD in Newborn– Causes Extrapulmonary Heart Metabolic Brain Blood Abdominal - CCF - Met. Acidosis - Haemorrhage - Hypovolemia - NEC - PDA - Hypoglycemia - Edema - Hyperviscosity - Pneumo - CCHD - Hypothermia - Drugs - Acute blood peritonium - Vascular - Sepsis - Pain loss - Large mass
  • 11.
    Surgical causes ofrespiratory distress • Tracheo-esophageal fistula • Diaphragmatic hernia • Lobar emphysema • Pierre -Robin syndrome • Choanal atresia
  • 12.
    Suspect surgical cause •Obvious malformation • Scaphoid abdomen • Frothing • History of aspiration
  • 13.
    A progressively increasingO2 requirement to maintain saturation is also a sensitive indicator of the severity and progress of distress >95% Term baby, pulmonary hypertension (PPHN) 88-94% 28-34 weeks preterm 85-92% Below 28 weeks gestational age Guidelines for monitoring oxygen saturation levels by pulse oximetry MJAFI, Vol. 63, No. 3, 2007 General Considerations
  • 14.
    Hyperoxia test test Methodresult diagnosis Hyperoxia 100 % fio2 5-10 min Pao2 increases to > 100 torr Pao2 increases by < 20 torr Parenchymal lung disease PPHN / CCHD Hyperoxia- hypervetilation MV 100 % fio2 & VR 100-150 / min Pao2 increases to > 100 torr w HV Pao2 increases at critical Pco2 No increase in Pao2 with HV Parenchymal lung disease PPHN CCHD
  • 15.
  • 16.
    Silverman-Andersen Retraction Scoring Interpretation Score0-3 = Mild respiratory distress Score 4-6 = Moderate respiratory distress Score > 6 = Impending respiratory failure Score 10 = Severe Respiratory distress General Considerations
  • 17.
    Investigation Complete Blood Countwith a Peripheral blood smear Sepsis screen including C-reactive protein and μ ESR Arterial blood gas (ABG) analysis Blood glucose, Serum calcium Cultures: Blood , Surface swab (where indicated), maternal vaginal swab Chest radiograph with an oro-gastric tube in situ General Considerations
  • 18.
    Mathai ss etal ,MJAFI 2007; 63 : 269-272
  • 19.
    RR (bpm Aspiration cong. Pneumonia,sev. HMD CDH cardiac malformation Approx. 6 Hours of age Normal 60 Course of Neonatal Tachypnoea : Etiologic possibilities Source : Baurn DJ, Birth Risks, Nastle Nutrition Workshop, 1993 TTNB HMD
  • 20.
    Evaluation of RDin NB – Clinical History Antenatal History Most likely association * Prematurity, IDMs * HMD * PROM, maternal fever, * Pneumonia Unclean vaginal exams, UTI, diarrhoea * Asphyxia/MSAF * Aspiration * Caesarean delivery * TTN * Polyhydramnios * Pulm. Hypoplasia * Oligohydramnios * TE fistula, CDH * H/o receiving steroids * RDS less * Traumatic/breech delivery * ICH / Phrenic nerve paralysis
  • 21.
  • 22.
    Respiratory Distress Syndrome(RDS) • Also known as Hyaline Membrane Disease (HMD) • Commonest cause of preterm neonatal mortality • RDS occurs primarily in premature infants; its incidence is inversely related to gestational age and birth weight Nelson Textbook of Pediatrics, 18th Ed. Gestational age Percentages Less than 28 wks 60-80% 32-36 wks 15-30% 37-39 wk 5% Term Rare Resp. Dis. Syn.
  • 23.
    ETIOLOGY AND PATHOPHYSIOLOGY. •Surfactant deficiency is the 1O cause of RDS. • Low levels of surfactant cause high surface tension • High surface tension makes it hard to expand the alveoli. • Tendency of affected lungs to become atelectatic at end- expiration when alveolar pressures are too low to maintain alveoli in expansion • Leads to failure to attain an adequate lung inflation and therefore reduced gaseous exchange
  • 24.
    • With advancinggestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells . • Wk 20: start of surfactant production and storage. Does not reach lung surface until later • Wk 28-32: maximal production of surfactant and appears in amniotic fluid • Wk 34-35; mature levels of surfactant in lungs • Quality : The amounts produced or released may be insufficient to meet postnatal demands because of immaturity. • Surfactant inactivating states eg maternal DM may lead to surfactant of lower quality/ immature
  • 25.
    • Rare geneticdisorders may cause fatal respiratory distress syndrome eg. • Abnormalities in surfactant protein B and C genes • gene responsible for transporting surfactant across membranes (ABC transporter 3 [ABCA3]) are associated with severe and often lethal familial respiratory disease
  • 26.
    26 Clinical manifestation • Tachypnea •Nasal flaring • Intercostal, sternal recession • Grunting; closure of glottis during expiration • Cyanosis

Editor's Notes

  • #4 White out , no heart borders
  • #16 While the Silverman Anderson Retraction Score is more suited for preterms with HMD, the Downes’ Score is more comprehensive and can be applied to any gestational age and condition.