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http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
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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
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.
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
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.
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
28.
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
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
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)
47.
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.
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
54.
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.
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)
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
65.
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
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
77.
78.
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
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%.
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.
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
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
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
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