Respiratory distress in newborn for postgraduate students

1. Dr Kyi San Thi

2. Outline
 Introduction
 Features of Respiratory Distress
 Causes of RD in NB
 Diagnostic approach
 General Mx of RD
 TTN
 RDS
 MAS
 Pneumonia/Neonatal Sepsis
 Congenital Anomalies
 Non Respiratory causes of RD

3. Respiratory Distress in Newborn
 common emergency admitted to NICU
 a working Dx should be made in the first few minutes
of seeing the baby
 immediate life saving measures should be done

4. Features of RD in newborn
 Tachypnoea – more than 60 breaths /minute
 Expiratory grunt
 chest wall retraction (
subcostal,intercostal,sternal,suprasternal)
 Nasal flaring
 Cyanosis/oxygen need

5. Neonatal Respiratory Distress
Etiological classification
Pulmonary
causes
Systemic
causes
Anatomical
causes
- RDS
- Pneumonia
- TTN
- MAS
- Other aspiration
syndrome
- Air leak syndrome
- Lung hemorrhage
- Lung hypoplasia
- Congenital
malformations
- Infections
- Metabolic causes
- Temperature
- Anemia or
Polycythemia
- Congenital heart
disease
- Pulmonary
hypertension
- Neuromuscular
disorder
- Upper airway
obstruction
- Airway malformation
- Space occupying
lesion
- Rib cage anomalies
- Phrenic nerve injury

7. RR
(bpm
MAS ,cong. Pneumonia, sev. HMD
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

8. Approach to respiratory distress
History
• Gestation
• Onset of distress
• Antenatal history
• Maternal Medical condition – DM , CHD , PE , APH
• steroids
• Predisposing factors- PROM, fever, multiple VE
• Meconium stained amniotic fluid , foul smell liquor
• Antenatal USG scan- AFI , fetal anomalies
• Birth history – Mode of delivery ,Difficult delivery, Birth
Asphyxia

9. Approach to respiratory distress
Examination
• Severity of respiratory distress
• Neurological status
• Blood pressure, CR T
• Hepatomegaly
• Cyanosis
• Features of sepsis
• Look for malformations

10. Evaluation of RD in NB – Chest Exam.
 Increased A-P diameter of chest
- Pneumothorax, emphysema or CDH
 Asymmetric chest movement
- Tension pneumothorax, pleural effusion, CDH,
Diaphragmatic paralysis, PIE.
 Auscultation
- Breath sounds ,
- crackles – Pneumonia & HMD
 Transillumination of the chest

11. Grading of Distress Severity
 Silvlerman- Anderson Score ( more suitable for
preterms with HMD )
 Downes’ Score (more comprehensive and applied for
any gestation and condition )
 a proressively increasing FiO2 requirement is also a
sensitive indicator of the severity.

12. Downes’ score
score 0 1 2
Respiratory Rate
(breaths/min)
60 60 – 80 >80 or apnea
episode
cyanosis None In room air In40%oxygen
Retraction None Mild Moderate to
severe
Grunting None Audible with a
stethoscope
Audible without a
stethoscope
Air entry clear Mild ? Marked?

13.  Score 0-3 ( Mild RD )
 Score 4-6 ( Moderate RD)
 Score 7 – 10 ( Severe RD )
 Score > 6 impending respiratory failure
 scoring should be assessed at half hourly intervel.

16. Investigations
• CBC , PCV
• RBS
• Sepsis screen
• Chest X-ray
• Blood gas analysis

19. RadiographicFeatures Possible Diagnosis
Ground Glass apearance •RDS
•Pneumonia
Diffuseparenchymal infiltrates •MAS
•Pneumonia
•Pulmonary lymphangiectasia
Lobarconsolidation •Pneumonia
•Lobar sequestration
•CCAM
Patchyareas alternating with
emphysema
•MAS
Pleural effusion •Pneumonia
•Pulmonarylymphangiectasia
Reticular granular pattern •RDS
•Pneumonia

20. RadiographicFeatures Possible Diagnosis
Lossof lung volume •RDS
•MAS
Fluid accumulations in interlobarspaces •TTN
•Pulmonary lymphangiectasia
Hyperinflation •MAS
•Pulmonarylymphangiectasia
Atelectasis •MAS
•RDS
Pneumothorax/pneumomediastinum •Spontaneous
•MAS
•RDS
•Pneumonia
"Cystic" mass •CCAM
•CDH
•Pulmonary sequestration

21. Treatment
 Specific Treatment : according to the cause
 Supportive therapy
(1) Checking the Baselines : T , PR , Glucose , RR , O2 saturation
(2) Fluids and electrolytes , Temperature , glucose
(3) Antibiotics if infective cause cannot be excluded
(4) Respiratory support
 Supplemental O2
 CPAP
 Mechanical ventilation

22. Mornitoring
 vital signs : RR, PR , CRT
 Severity
 continuous pulse oximeter mornitoring to decide
intubation and ventilation
 ABG

23. Oxygen therapy
Indications
• All babies with distress
• Cyanosis
• Pulse oximetry SaO2 < 90%
 * Cautious administration in pre-term
 currently recommended range of oxygen saturation
targets is 91-95% in preterm.

24. Oxygen
 nasal prongs
 nasal catheter
 head box
 face mask
 incubator

27. CPAP
continuous postive airway pressure
 can be delivered by means of a ventilator or machine
 alternatively by a simplified system providing blended
oxygen flowing past the infants’s airway with the end
of tubing submerged in sterile water to the desired
depth to generate pressure ( bubble CPAP )
 To go on CPAP an infant needs to be breathing
spontaneously

29. CPAP : General characteristics
 a continuous flow of humidified gas is circulated past
the infant’s airway typically at a set pressure
maintaining an elevated end-expiratory lung volume
while the infant breaths spontaneously
 air-oxygen mixture and airway pressure can be
adjusted

30. CPAP
 Advantages
- less invasive and less barotrauma than MV
- used early in RDS , prevent alveolar and airway
collapse and so reduce the need for MV
- decrease the frequency of obstructive and mixed
apneic spells in some infants

31. CPAP
 Disadvantages
- does not improve ventilation
- inadequate respiratory support in severe changes in
pulmonary compliance and resistance
- swallow air can elevate the diaphragm
- barotrauma

32. CPAP : Indications
 early treatment of premature infants with minimal RD
and minimal need for supplemental oxygen to prevent
ateleatasis
 moderately frequent apneic spells
 after recent extubation
 weaning chronically ventilator dependent infants

33. Mechanical Ventilation :
Indications
Any acute or chronic cardiopulmonary insufficiency
 May be due to problem with lung, cardiovascular
system, CNS, or various metabolic disorders
 Absolute indications for mechanical ventilation
1. prolonged apnea
2. Pa O2 < 50 mmHg
3. PaCO2 > 60 mmHg with persistent acdemia
4. General anesthesia

34. Mechanical Ventilation : Modes
Noninvasive Neonatal Ventilation
 Continuous Positive Airway Pressure
Invasive Neonatal Ventilation
 Conventional Mechanical Ventilation
 Intermittent Mandatory Ventilation
 Synchronized Intermittent Mandatory Ventilation
 Assist/Control Ventilation
 Pressure-Support Ventilation
 Patient-Triggered Ventilation
 High-Frequency Ventilation
High-Frequency Jet Ventilation
High-Frequency Oscillatory Ventilation
 Extracorporeal Membrane Oxygenation

36. Transient Tachypnea of Newborn
 Most common cause of respiratory distress
 Residual fluid in fetal lung tissues
 Risk factors- maternal asthma, c- section, male sex,
macrosomia, maternal diabetes
 especially seen in near term and term babies

37. TTN
 Tachypnea immediately after birth or
within two hours, with other predictable
signs of respiratory distress.
 Symptoms can last few hours to two days.
 CXR shows diffuse parenchymal
infiltrates, a “ wet silhouette” around
heart, or intralobar fluid accumulation

38.  delayed reabsorption of fetal lung fluid which
eventually will clear over several hours to days
 Treatment: Supportive : may need O2, probably too
tachypneic to PO feed so start IV fluids

39. X-ray
Fluid in the
fissure

42. RDS
 Formerly known as hyaline membrane disease
 Deficiency of pulmonary surfactant in an immature
lung
 Disease of prematurity

43. Epidemiology
 Major cause of morbidity and mortality in preterm infants
 20,000-30,000 newborn infants each year
 Incidence and severity of RDS are related inversely to
gestational age and birthweight of newborn infant
 26-28 weeks' gestation : 50%
 30-31 weeks' gestation : <30%
 Overall incidence in 501-1500 grams: 42%
 501-750 grams: 71%
 751-1000 grams: 54%
 1001-1250 grams: 36%
 1251-1500 grams: 22%
 occurs in 60-80% of infants < 28 wk of gestational age, in
15-30% of those between 32 and 36 wk, and rarely in those
> 37 wk.

44. Risk of RDS
 The risk of RDS increases with
maternal diabetes, multiple births, cesarean delivery,
precipitous delivery, asphyxia, cold stress, and a
maternal history of previously affected infants
 The risk of RDS is reduced in pregnancies with
chronic or pregnancy-associated hypertension,
maternal heroin use, prolonged rupture of
membranes, and antenatal corticosteroid prophylaxis,
IUGR

45. Surfactant
 Complex lipoprotein
 Composed of 6
phospholipids and 4
apoproteins
 70-80% phospholipids, 8-
10% protein, and 10%
neutral lipids

46. Surfactant
 Surfactant lowers surface tension and increases
compliance in alveoli leading to alveolar collapse. It is
a phospholipid composed of lecithin and
sphingomyelin, made by type II pneumocytes.
 The lecithin:sphingomyelin (LS) ratio is altered in RDS
(less lecithin, LS ratio low, < 2)

48. clinical course of RDS
 increasing severity during the first 24–48 h, followed
by a period of stability lasting another 48 hr before
improvement occurs.
 Severity of the disease may be expressed in terms of
oxygen requirements and need for assisted ventilation.
 In the 24 h prior to recovery a diuresis usually occurs.

49. Diagnosis
 Clinical course : Onset of progressive respiratory
failure shortly after birth
 Characteristic chest radiograph
 ABG
 Hypoxia
 Hypercarbia
 acidosis

50. CXR

52. Treatment
 Surfactant Therapy
 Assisted Ventilation Techniques
 Supportive Care
 Thermoregulation
 Fluid Management
 Nutrition

53. Prophylactic therapy
Extremely preterm <28 wks
<1000 gm
Rescue therapy
Any neonate diagnosed to have RDS
Surfactant therapy - Issues
Dose 100mg/kg phospholipid Intra tracheal

55. Epidemiology
 Meconium-stained amniotic fluid is found in 10-15% of
births and usually occurs in term or post-term infants.
 Meconium aspiration syndrome (MAS) develops in 5%
of such infants; 30% require mechanical ventilation,
and 3-5% die.

56. Pathophysiology

58.  Partial airway obstruction
 complete airway obstruction
 Surfactant destruction
 Chemical pneumonitis & Bacterial pneumonia
 Asphyxia
 PPHN
Complication of MAS

59. Alarm of MAS
1- Thick meconium
2-Fetal tachycardia
3- lack of increase heart rate during intra partum
monitoring
4-Low cord PH

60. Clinical sign
 Classic sign :Post maturity- nail, skin , umblical cord
are heavily stained with a yellowish pigment
 Early sign (resp . Distress) : grunting & cyanosis &
nasal flaring & retraction & marked tachypnea
 Characteristic sign : chest overinflation and
rhochi

61. Radiography of M.A.S
 Coarse , nodular , irregular pulmonary densities
with areas of diminished aeration or consolidation.
 Hyperinflation of the chest .
 Atelectasis
 Flattening of diaphragm
 Cardiomegally
(manifestation of the underlying prenatal hypoxia)

62. Chest.X.Ray

64. Treatment
 supportive care and standard management for
respiratory distress
 exogenous surfactant and/ or iNO to infants with
MAS and hypoxemic respiratory failure or
pulmonary hypertension requiring mechanical
ventilation
 Mechanical ventilation : HFV , ECMO

66. Pneumonia
Congenital
Onset is usually within 6
hrs of birth:
Intrapartum
Onset is usually within
48 hrs
Nosocomial
Onset is after 48 hours
• Bacterial: Streptococci
(group B streptococci)
• Coliforms (E. coli,
Klebsiella, Serratia, Shigella,
Pseudomonas spp., etc.)
• Pneumococci
• Listeria sp.
• Viral
• CMV
• Rubella virus
• Herpes simplex virus
• Coxsackievirus
• Other
• Toxoplasmosis
• Chlamydia sp.
• Ureaplasma urealyticum
• Candida
• Bacterial:
• Group B streptococci
• Coliforms
• Haemophilus sp.
• Staphylococci
• Pneumococci
• Listeria sp.
• Viral:
• Herpes simplex virus
• Varicella-zoster virus
• Bacterial:
• Staphylococci
• Streptococci
• Pseudomonas sp.
• Klebsiella sp.
• Pertussis
• Viral:
• RSV
• Adenovirus
• Influenza viruses
• Parainfluenza viruses
• Common cold viruses
• Other:
• Pneumocystis jiroveci

67. Pneumonia
 Pneumonia & Sepsis have various manifestations
including typical signs of distress as well as
temperature instability.

68. Pneumonia
 Risk factors- prolonged rupture of membranes,
prematurity, maternal fever,foul smelling liquor ,
attempted home delivery , multiple VE
 Risk factors – spread from caregivers , staffs , IV
canulation , intervention , too many visitors in
nursery
 Clinical features : features of respiratory distress +
temperature instability + jaundice ,
heaptosplenomegaly , other features of sepsis

71. Pneumonia/ Sepsis
71

72. X-Ray
 Patchy infiltrates (aspiration)
 Bilateral diffuse granular pattern
 Streaky
 Loss of volume
 Densities
72

73. Pneumonia
 Investigation
- full septic screening
- CXR
- ABG
 Treatment
- supportive
- antibiotics
- CPAP , Mechanical ventilation

74. Pneumonia : Treatment
Appropriate Antibiotics
 Current Unit Protocol (must be based on routine bacterial
surveillance)
 Updated information on local predominant aetiological
pathogens & their antibiotic susceptability
 or resistance pattern in one's own hospital (or) one's own
baby unit

75. Initial antibiotic treatment of unknown origin in EOS
 (1) – IV Ampicillin + IV Gentamicin (Situations where resistant strains are unlikely)
 (2) – IV Ampicillin + IV Cefotaxime(especially in places where aminoglycoside - resistance is high)
 *Add metronidazole if suspicion of anaerobic infection (e.g. NEC)
For severely ill term/ preterm newborn, or preterm infants with a prenatal
history indicating bacterial infection
 (1) – IV Ampicillin + IV Cefotaxime + IV Aminoglycoside
 (2) – IV 3rd gen Cephalosporin (Cefotaxime/Ceftazidime )+ IV
Aminoglycoside
 *Note-check maternal HVS result if available
Antibiotic treatment in cases of initial treatment failure and pathogens are
still unknown
 (1) – IV 3rd Cephalosporin + IV Amikacin
 (2) – IV Sulperazone monotherapy (Cefoperazone + Beta lactamase
inhibitor-Sulbactam)
 (3) – IV Sulperazone combination therapy with other A/B if such combintions
are indicated

76. for initial treatment of Late onset sepsis
 (1) – IV Ampicillin or Cloxacillin+ IV Gentamicin (Situations where
resistant strains are unlikely)
 (2) – IV Flumox + IV Gentamycin
 (3) – IV Ampicillin + IV Cefotaxime (Especially in places where
aminoglycoside - resistance is high and Staph infection is very unlikely)
 (4) – IV 3rd gen Cephalosporin + IV Amikacin/Gentamycin
in cases of initial treatment failure and pathogens are still unknown
 (1) – IV 3rd gen Cephalosporin + IV Amikacin
 (2) – IV Sulperazone monotherapy (Cefoperazone + Beta lactamase
inhibitor-Sulbactam)
 (3) – IV Sulperazone combination therapy with other A/B if such
combintions are indicated
 (4) – IV Expanded-spectrum Penicillin (Piperacillin/Mezlocillin ) + IV
Cefotaxime + IV Aminoglycoside

79. Pneumothorax
Etiology
Spontaneous, MAS, Positive pressure
ventilation (PPV)
Clinical features
features of respiratory distress, indistinct heart sounds ,
Breath Sound absent or decreased
Bed side test
Transillumination test
Management
Needle aspiration, intercostal tube drainage

80. Pneumothorax
80

81. Pneumothorax
 Right lateral decubitus view of pneumothorax
81

82. Pneumopericardium
82

84. Congenital Abnormalities of the Lung and
Thorax
 Congenital Heart Disease (CHD)
 Congenital Diaphragmatic Hernia (CDH)
 Congenital Cystic Adenomatiod Malformation
 Tracheal Abnormalities
 Esophageal Atresia
 Pulmonary Hypoplasia
84

85. Congenital Heart Disease
 Defect present at birth- often picked up on early
ultrasound
 Increased risks:
 family history of CHD
 Maternal diabetes
 maternal TORCH infecton
 maternal alcohol , drug abuse, anti epileptics
85

86. CHD
 Two types of CHD
 Acyanotic-blood returning to Right side of heart passes
thru lungs—usually defect in heart wall, or obstructed
valve or artery
 Pink baby
 Sats within normal limits
 Cyanotic-have a mixing of oxygenated blood with
venous blood—shunting ductus, PFO, ASD, VSD
 Blue baby
 Low sats
86

87. Congenital Heart disease
Cyanotic Heart Disease-
 Tetralogy of fallot- ( VSD, Pulmonary stenosis,
overriding aorta, RVH)
 Tricuspid atresia
 Transposition of great vessel
 Total anomalous pul. venous return
 Truncus arteriosus.

88. Hyperoxia Test
 Obtain ABG–> Then place the patient on 100%
O2 for 10 minutes then repeat ABG , If the
cyanosis is pulmonary , the PaO2 should be
increased by 30 mm of Hg. If the cause is cardiac ,
there will be minimal improvement in PaO2.

89. CHD
 Clinical Features
 features of Respiratory distress
 Heart rate
 Slow, fast, variable
 murmur
 BP and Pulses in all extremities
 CRT
 Saturations depend upon defect.
 Acyanotic lesions sats are more normal
 Cyanotic lesions acceptable sats are low
 ~ 70% is acceptable; ideally on 21% FiO2
89

90. CHD : Investigation
 Labs and Tests
 ABGs—dependent upon defect
 Chest X-Ray
 Heart shape and size
 Pulmonary blood flow
 Echocardiogram
 Best test to aid in diagnosis
 Cardiac Cath for possible intervention
90

91. Congenital Diaphragmatic
Hernia
 The defect may be at the esophageal hiatus (hiatal),
paraesophageal (adjacent to the hiatus), retrosternal
(Morgagni), or at the posterolateral (Bochdalek) portion of
the diaphragm.
 The term congenital diaphragmatic hernia typically refers
to the Bochdalek form.
 The Bochdalek hernia - up to 90% of the hernias
 80-90% occurring on the left side.
 The Morgagni hernia - 2-6%
 The overall survival from the CDH Study Group is 67%.

92. Congenital Diaphragmatic
Hernia
92

93. Congenital diaphragmatic hernia
 Respiratory distress is a cardinal sign
 occur immediately after birth or after a “honeymoon”
period
 of up to 48 hr
 Early respiratory distress, within 6 hr after birth, is thought
to be a poor prognostic sign.
 scaphoid abdomen and increased chest wall diameter.
 Bowel sounds may also be heard in the chest with
decreased breath sounds bilaterally.
 The point of maximal cardiac impulse may be displaced
away from the side of the hernia if mediastinal shift has
occurred.

94. CDH
94

95. Left Congenital Diaphragmatic
Hernia
 X Ray – best diagnostic
tool
95

96. CDH : Management
 Aggressive respiratory support
 rapid endotracheal intubation, sedation, and possibly
paralysis.
 Conventional mechanical ventilation, HFOV, and
ECMO are the 3 main strategies to support respiratory
The ideal time to surgical repair the diaphragmatic
defect is under debate.
 Most experts wait at least 48 hr after stabilization and
resolution of the pulmonary hypertension

97. Congenital Cystic Adenomatoid
Malformation
 Ideally diagnosed in utero
 Develops during pseudoglandular stage, but CCAM
can form up to 35 weeks
 Normally compromised at delivery requiring
immediate intubation
97

98. CCAM
98

99. Clincal Features
 Features of respiratory distrss , recurrent respiratory
infection, and pneumothorax.
 Breath sounds may be diminished, with mediastinal
shift away from the lesion on physical examination
 DDx : a diaphragmatic hernia

100.  large multicystic mass in
the left hemithorax with
mediastinal shift

101. Management
 Antenatal intervention in severely affected infants
 In the postnatal period, surgery is indicated for
symptomatic patients.
 Sarcomatous and carcinomatous degeneration have
been described in patients with CCAM, so surgical
resection by 1 year of age is recommended to limit
malignant potential. The mortality rate is <10%.

102. Persistent Pulmonary
Hypertension (PPHN)
 Pulmonary hypertension resulting in severe
hypoxemia secondary to R>L shunt through PFO
and/or PDA
 Usually affecting term or near-term infants
 May be extremely difficult to manage
102

103. Persistent pulmonary hypertension
(PPHN)
Causes
• Primary
• Secondary: MAS, asphyxia, sepsis
Management
• Severe respiratory distress needing
ventilatory support, pulmonary vasodilators
• Poor prognosis

104. Fetal Circulation
104

105. PPHN
 Clinical features
 Features of respiratory distress
 Pre and Post-ductal saturations to monitor shunting-
best indicator if ECHO not available
 X-Ray
 Depends on cause
 Usually with decreased blood flow, minimal lung markings
 ABG
 Respiratory and metabolic acidosis
105

106. Management
• Severe respiratory distress needing ventilatory
support
• pulmonary vasodilators
• Poor prognosis

107. Non Respiratory causes of Distress
S & S Diagnosis Management
 Hypothermia/ - check temperature - heat or cool as
Hyperthermia necessary
 Hypovolemia - obtain prenatal history - gingerly give volume
 Hypoptension - measure blood pressure - give volume and/or
vasopressor
 Hypoglycemia - blood glucose measurement - give glucose
 Anemia - measure hematocrit - transfuse with PRBC
 Polycythemia - measure hematocrit - partial exchange transfus
(lower Hct)
107

108. Respiratory distress in a neonate with asphyxia
• Myocardial dysfunction
• Cerebral edema
• Asphyxial lung injury
• Metabolic acidosis
• Persistent pulmonary hypertension