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IRDS and BPD
Transcript of IRDS and BPD
Incidence of IRDS is directly related to lung immaturity and gestational age.
The more premature the infant, the less the surfactant production and higher the probability of IRDS
What is Surfactant?
A substance that helps prevent the alveoli from collapsing during breathing by reducing surface tension
Improves lung compliance and stabilizes lung volumes at a lower transpulmonary pressure
A complex system of lipids, proteins and glycoproteins, produced by Type II Pneumocytes (specialized lung cells).
Prevention & Diagnosis
Hyaline Membrane Disease...
The name above came from the characteristic histopathology seen in the lungs of babies who have died from IRDS.
Hyaline membranes appear as waxy layers lining collapsed alveoli
Appear Glassy when stained
...is a syndrome of the premature infant caused by developmental insufficiency of surfactant and structural immaturity of the lungs.
The lack of surfactant production can be a genetic mutation, rather than a consequence of prematurity.
Hyaline Membrane Disease?
IRDS and BPD
Prevention of IRDS is possible with administration of glycocorticoids (a group of hormones) to mothers preparing to give birth prematurely.
These hormones speed up the process of surfactant production
If the birth is due to occur prior to 27 weeks gestation, glycocorticoids are given without testing lung maturity.
Commonly known as
RDS type I
Infant Respiratory Distress Syndrom (IRDS)
RDS of Newborn
Surfactant Difficiency Disorder
These membranes typically consist of fibrin, cellular debris, RBCs, neutrophils, and macrophages.
Allong with Hyaline membranes, the lungs typically present with bleeding, over distention of airways, and damage to lining cells
The incomplete development of the lungs resulting in the unusually low number or size of Bronchopulmonary segments or alveoli.
IRDS is not to be confused with Pulmonary Hypoplasia...
The surfactant is then extruded through
lamellar bodies into the alveoli
The lamellar bodies then unfold into a complex
layer of the air spaces.
This is the layer of surfactant reponsible
for reducing surface tension and allowing majority
of elastic recoil
Currently Available Surfactants, by...
Natural, from pig lungs (porcine), extracted from material derived from minced pig lung
100-200 mg/kg/dose (1.25-2.5 ml/kg
Natural, from cow lungs (Bovine), extracted from calf lung lavage fluid
105 mg/kg/dose (3ml/kg)
Natural, from cow lungs (bovine), extracted from minced cow lung with added DPPC
100 mg/kg/dose (4 ml/kg)
As of March 6, 2012, Lucinactant is the first synthetic
surfactant cleared by the FDA for use to treat neonatal RDS.
> 50% occurrence in babies born at 26-28 weeks
25% occurrence in babies born at 28-31 weeks
< 5% in babies born at or after 35 weeks
IRDS occurs shortly after birth with noticeable signs of distress, including:
Tachypnea (rapid breathing)
retractions (accessory muscle use)
As the condition of the disease progresses, and
more alveoli collapse, the patient becomes more
acidotic and experiences respiratory failure with
increased periods of apnea.
The clinical course and outcome of mortality for these infants depends on size and maturity of the infant and his/her lung function.
The lower the birth weight and more premature, the worse the condition
--- babies less than 1000 grams and born before 25 weeks gestation
Other complications in IRDS patients may include:
Patent Ductus Arteriosus (PDA) due to PPHN
low blood pressures
chronic lung changes
According to the American College of Ostetricians and Gynocologists (ACOG), glycocorticoids should be administered to mothers giving birth prior to 34 weeks gestation.
In pregnancies greater than 30 weeks, the fetal lung maturity can be tested by way of amniocentesis.
Lecithen/Sphingomyelin ratio is a test of fetal amniotic fluid to assess for fetal lung maturity
Lecithen and Sphingomyelin are two glycoproteins found in Surfactant
Lecithen makes the surfactant mixture more effective
The outward flow of pulmonary secretions from the fetal lungs into the amniotic fluid maintains the level of lecithin and sphingomyelin equally until 32–33 weeks gestation, when the lecithin concentration begins to increase significantly while sphingomyelin remains nearly the same
Therefore, a higher ratio suggests that there is more surfactant present in the lungs and the baby will have less difficulty breathing at birth.
L/S of 2:1 or higher suggests lung maturity and decreased likelihood of RDS
L/S of less than 1.5:1 suggests lung immaturity and greater risk for RDS
Phosphatidylglycerol is a glycerophospholipid found in pulmonary surfactant
Once surfactant is secreted by the type II cells, it must be spread over the remaining type I cellular surface area.
Phosphatidylglycerol is thought to be important in spreading of surfactant over the Type I cellular surface area
The presence of PG suggests lung maturity
A ratio of less that 33 indicates lung immaturity,
33-55 is intermediate, and greater than 55 indicates maturity of the lungs
When correlated with a L/S ratio of 2.2 or higher
Post-delivery treatment of the IRDS infant begins with Oxygen therapy, usually accompanied with Non-Invasive (NIV) Continuous Positive Airway Pressure (CPAP) assistance.
The CPAP provides a small amount of continuous pressure to the airways and alveoli, stenting them open
improving surface area and gas exchange.
Flow begins from source (either ventilator or air blender)
Passes through heated humidifier and water column
vibrations create pressure (bubbles)
Pressure is enough to open baby's lungs and assist breathing
Does not force lungs open
If the condition of the newborn worsens, endotracheal intubation will be initiated.
If respiratory distress is severe at birth, the baby will be intubated prior to the CPAP (it is a preferred route of surfactant instillation)
Pressures must be monitored very closely in newborns due to there sensitive lungs. Pressures to high can cause air leaks and pneumothorax, leading to Bronchopulmonary Dysplasia.
This is especially true after instilling surfactant due to rapid increase in compliance
Known as BPD
is a lung disorder of the premature infant that is usually associated with the treatment of IRDS
Increased use of PPV &
As stated earlier:
Lung damage can occur with psitive pressure ventilation PPV.
Increases pressures into the sensitive lungs of premature infants can cause them to over-expand (Barotrauma).
This leads to air leaking and conditions such as pneumothorax.
this also causes the damaged tissue to scar, leaving it impaired, resulting in a mismatch of ventiltion
BPD can also be caused from high oxygen levels used to oxygenate the patient
The high oxygen concentration causes O2 free radicals to be produced
these free radicals attack lung tissue causing tissue destruction and scaring
Stiffening of the lungs
Other situations such as trauma, pneumonia or any other type of lung infection causing damage and scaring to the newborn can cause BPD.
Most children with BPD survive and are able to live normal lives, although recovery is sure to be a slow process.
Children recovering may still need continued medication, breathing treatments, or even supplemental oxygen at home
Some even need continued mechanical ventilation at home
In rare cases, for the rest of their lives
About 5,000 to 10,000 babies in the U.S. each year aqcuire BPD
An all time high
due to more premature infants surviving because of advanced therapies and ventilator treatments.
Chest X-Rays of BPD show lungs that appear to be spongy, with enlarged areas of air. These are over distended alveoli.
Colfosceril palmitate (Exosurf) - a mixture of DPPC with hexadecanol and tyloxapol added as spreading agents
A synthetic form of Surfactant
Classic respiratory distress syndrome (RDS). Bell-shaped thorax is due to generalized underaeration. Lung volume is reduced, the lung parenchyma has a fine granular pattern, and peripherally extending air bronchograms are present.
Moderately severe respiratory distress syndrome (RDS). The reticulogranular pattern is more prominent and uniformly distributed than usual. The lungs are hypoaerated. Increased air bronchograms are observed.
Severe respiratory distress syndrome (RDS). Reticulogranular opacities are present throughout both lungs, with prominent air bronchograms and total obscuration of the cardiac silhouette. Cystic areas in the right lung may represent dilated alveoli or early pulmonary interstitial emphysema (PIE).
The following diagnostic criteria is of use only if the baby has been on > 21% oxygen for at least 28 days.
Breathing room air at 36 weeks post-menstrual age or discharge (whichever comes first) for babies born before 32 weeks,
breathing room air by 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks gestation.
Need for <30% oxygen at 36 weeks postmenstrual age, or discharge (whichever comes first) for babies born before 32 weeks,
need for <30% oxygen to 56 days postnatal age, or discharge (whichever comes first).
Need for >30% oxygen, with or without positive pressure ventilation or continuous positive pressure at 36 weeks postmenstrual age, or discharge (whichever comes first) for babies born before 32 weeks,
need for >30% oxygen with or without positive pressure ventilation or continuous positive pressure at 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks' gestation.
No available medical treatment can immediately resovle BPD.
The goals are to support breathing and oxygentation
Jet ventilation may be used
Bronchodilators to support lung function
Diuretic therapy is important to reduce fluid build up.
These patients may also need tube feedings and reduced liquids, depending on the severity of the condition
Hyaline Membrane Disease
In the late 1920s, a man named von Neergaard idedentified the function of pulmonary surfactant. the significance however, was not yet understood by the medical community. It wasnt until the middle of the 1950s that the importance of surfactant and low surface tension in the lungs was truely understood by Pattle and Clements, essentially rediscovering its importance.
In 1963, Patrick Bouvier Kennedy, son of President John F. Kennedy and First Lady Jacqueline Kennedy, died of RDS two days after his premature birth at 34 weeks gestation.
Hyaline Membrane Disease