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Sudeshna Banerjee M.SC (N) 2 Year Hfcon

Neonatal acute respiratory distress syndrome (RDS) is caused by surfactant deficiency in newborns. Surfactant production increases after 24 weeks gestation and is essential for lung function. RDS causes respiratory distress within hours of birth due to surfactant's role in reducing surface tension. Treatment focuses on supportive care like CPAP, ventilation if needed, and surfactant replacement therapy which reduces mortality and chronic lung disease. Complications include air leaks, low cardiac output, and gastric issues.

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Sanjay Kumar Sanju
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117 views30 pages

Sudeshna Banerjee M.SC (N) 2 Year Hfcon

Neonatal acute respiratory distress syndrome (RDS) is caused by surfactant deficiency in newborns. Surfactant production increases after 24 weeks gestation and is essential for lung function. RDS causes respiratory distress within hours of birth due to surfactant's role in reducing surface tension. Treatment focuses on supportive care like CPAP, ventilation if needed, and surfactant replacement therapy which reduces mortality and chronic lung disease. Complications include air leaks, low cardiac output, and gastric issues.

Uploaded by

Sanjay Kumar Sanju
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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NEONATAL ACUTE

RESPIRATORY
DISTRESS
SYNDROME

SUDESHNA BANERJEE
M.SC (N) 2ND YEAR
HFCON
Definition
Acute lung disease of the newborn caused by
surfactant deficiency. RDS is the clinical expression of
surfactant deficiency and its histologic counterpart,
Hyaline Membrane Disease (HMD).
Development of Lungs
Surfactant
Surfactant is identifiable in fetal lung as early as 16 weeks,
though its proper secretion begins after 24 weeks gestation
and is synthesized most abundantly after the 35th week of
gestation.

Pulmonary Surfactants are phospholipids synthesized in the


type II cells lining the alveoli surfactant.
Phospholipid produced by alveolar type II cells.
Lowers surface tension.
As alveoli radius decreases, surfactant’s ability to lower
surface tension increases.
The half-life of surfactant is 30 hours
Function of the Causes of surfactant
Surfactant deficiency
Decrease the surface Pulmonary infections e.g. group B Strep
tension
Pulmonary hemorrhage
To promote lung
expansion during Meconium aspiration pneumonia
inspiration.
O2 toxicity; barotrauma or volutrauma
to the lungs.
To prevent alveolar
collapse and loss of
lung volume at the Congenital diaphragmatic hernia and
end of expiration. pulmonary hypoplasia
Pathophysiology
Risk factors
Prematurity
Multiple births
Maternal diabetes, C-section without labor
Perinatal asphyxia
Cold stress
White race, male sex
Hypothermia, hypothyroidism
2nd twin
Clinical Manifestations
Appear within minutes of birth may not be recognized for several hours in
larger preterm.
Tachypnea (>60 breaths/min), nasal flaring, subcostal and intercostal
retractions, cyanosis & expiratory grunting.
Breath sounds may be normal or diminished and fine rales may be heard.
Progressive worsening of cyanosis & dyspnea.
Cyanosis and pallor increase & grunting decreases.
Apnea and irregular respirations are ominous signs.

In most cases, symptoms and signs reach a peak within 3 days, after which
improvement occurs gradually.
Diagnosis
Chest x-ray:
Grade 1 (mild cases): The lungs show fine homogenous ground
glass shadowing.
Grade 2: Widespread air bronchogram become
visible.
Grade 3: Confluent alveolar shadowing.
Grade 4: Complete white lung fields with obscuring of
the cardiac shadow.
Investigations cont…
• Blood gas analysis:
Shows low oxygen and excess acid in the body fluids.

• Laboratory findings are initially characterized


by hypoxemia and later by progressive hypoxemia,
hypercapnia, and variable metabolic acidosis.
Progression of the disease
Acute phase
 First 48-72 hr. after birth, newborn begins to have tachypnea,
chest tightness.
 The sign and symptoms are peak on day 1-2.
 Patients may die if they did not receive adequate treatment.

Recovery phase
 Start on day 3-5
 Type II Pneumocytes are regenerated
 Decrease oxygen requirement
Management
Antenatal corticosteroid therapy:
Betamethasone 12 mg IM for 2 doses, 24 hrs apart, or Dexamethasone 6 mg IM
for 4 doses, 12 hrs apart.
 They induce surfactant production and accelerate fetal lung maturation.
 Are indicated in pregnant women 24-34 weeks' gestation
 Optimal benefit begins 24 hrs after initiation of therapy and lasts seven days.

 Early surfactant therapy: prophylactic use of surfactant in preterm newborn


<27 weeks' gestation.

 Early CPAP administration in the delivery room.


Treatment
Supportive treatment:
 Body temperature -
 Scheduled “touch times” to avoid hypothermia and
minimize oxygen consumption.

 Placed in an isolette or radiant warmer to maintain core


temperature between 37 ± 0.5 °C.
Nutritional support -
For the 1st 24 hour, 10%DW should be infused through a
peripheral vein at a rate of 65–75 mL/kg/day.

For VLBW and ELBW, TPN should be added Day 2-3, Na 3-4
mEq/kg/day and K 2-3 mEq/kg/day should be added

Give a blood transfer when Hct is less than 40%


Oxygen therapy
 Warm humidified oxygen should be provided at a concentration
initially sufficient to keep PaO2 50-80 mmHg, pH 7.25-7.45,
PaCO2 40-50 mmHg and SpO2 90–95%.

 To maintain normal tissue oxygenation while minimizing the risk


of oxygen toxicity.

 O2 box is not recommended for newborn with VLBW and ELBW


because of high concentration of O2 may increase risk of ROP
(Retinopathy of prematurity).
Cont…
 If the PaO2 cannot be maintained above 50 mmHg at inspired
oxygen concentrations of 60% or greater, applying CPAP at a
pressure of 5–10 cm H2O by nasal prongs (CPAP prevents
collapse of surfactant-deficient alveoli, improves ventilation-
perfusion matching).

 The amount of CPAP required usually decreases abruptly at


about 72 hour of age, and infants can be weaned from CPAP
shortly thereafter.
Complications of CPAP
 Pulmonary air leaks - over distension of the lungs caused by
inappropriately high pressures
 Decreased cardiac output due to reduction in the venous
return, decreased right ventricular stroke volume
 Gastric distension and ‘CPAP belly syndrome’
 Nasal irritation, damage to the septal mucosa, or skin damage
and necrosis from the fixing devices.
Mechanical ventilation
Continue positive airway pressure (CPAP) is being use with 4-8 cm. H2O.
 To make Functional residual capacity (FRC) for the lung to prevent
atelectasis.
 Usually started with 5 cm·H2O and increased by 1 cm·H2O in
subsequent with increase oxygen by 10%.

Initial settings:
• Continuous flow, pressure-limited, ventilator conventional.
• PEEP 4-5 cm H2O
• Frequency 40-60/min
• FiO2 50-60%
Cont…
Routes of administration:
 Nasal prongs
 Nasopharyngeal tube

Indication for ventilator-


 Apnea with no improvement
 Cyanosis or PaO2 ≤ 40 mmHg (when using CPAP and high
oxygen concentration)
 Signs of Respiratory failure
 PaCO2 > 60 mmHg
 Metabolic acidosis
Surfactant replacement therapy
Surfactant replacement therapy can reduce mortality and
incidence of Chronic pulmonary disease.
There are 2 types of surfactant :
1. Natural surfactant extract
 Bovine(Survanta), Porcine(Curosurf)

 Natural surfactants appear to be superior, perhaps of their


surfactant-associated protein content.

 Natural surfactants have a more rapid onset and are


associated with a lower risk of pneumothorax and improved
survival.
Cont…
2. Synthetic surfactant
 Exosurf and ALEC (Artificial Lung Expanding
Compound)

3. Newer surfactant
• Synthetic surfactants with synthetic peptides modelled
on surfactant proteins, Aerosolized surfactants.

Dose:
• Survanta 100mg/kg for the first and subsequent doses.
• Curosurf 200mg/kg for the first dose and 100mg/kg for
the subsequent doses or 100mg/kg for all the doses.
Cont…
The main indications :
Prophylactic treatment:
 Being use for infant delivered during 23-29 wk of
gestation and birth weight 600-1250 g
 Neonates with gestation < 30 weeks of gestation.
 Surfactant given within 15 minutes of birth before a diagnosis
of RDS is made.

 Results :
Improve dyspnea in first 48-72 hr of life (Decrease O2
requirement, ventilation improved)
Decreased incidence of pneumothorax
Decrease mortality
Complications of surfactants:
• Transient hypoxia, bradycardia and fluctuating BP

• Rapid changes in lung compliance leading to

barotrauma if not monitored.

• Pulmonary hemorrhage - more with natural(5-6%) as


compared to synthetic (1 -3%).
Pharmacotherapy – beyond
surfactant:

Nitric oxide
• Inhaled nitric oxide (iNO)– a selective pulmonary
vasodilator improves oxygenation inpreterm
infants with severe RDS.

• Nitric oxide may be a signaling molecule in


parenchymal lung growth & may reduce lung
injury and chronic lung disease.
Nursing diagnosis
Impaired Gas Exchange related to decreased volumes and
lung compliance, pulmonary perfusion and alveolar
ventilation.
Ineffective breathing pattern r/t inadequte pulmonary
development secondary to prematurity.
Ineffective thermoregulation r/t lack of subcutaneous fat
secondary to prematurity and low birth weight and lack of
subcutaneous fat stores.
Imbalanced nutrition, less than body requirements r/t absent
sucking reflex secondary to preterm birth and type of feeding.
Risk for infection r/t immature body systems secondary to
prematurity.
Risk for impaired parent, infant attachment r/t premature birth
& separation, lack of privacy

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