respiratory distress syndrome in newborn

8/2/2019 Respiratory Distress Syndrome in Newborn

1/24

Respiratory Distress Syndromein Newborn

N. Kononenko


2/24

Definition. RDS is an acute pulmonarydisorder of premature infants, first describedby pathologists who noted widespreadatelectasis and eosinophilic material liningthe overdistended terminal bronchioles

The condition is a surfactant deficiency

syndrome resulting from immaturity. Theincidence of this disorder depends ofgestational age and increases from 1% infull-term newborn to 5% at 35-36 weeks,20% at 30-32weeks, to 65% at 29-30 weeksof gestation.


3/24

Aetiology of RDS is deficiency of surfactantsynthesis, release, destroying, inhibition and

immaturity of lung tissue and chest.

The main perinatal risk factors for RDS ar1)factors that affect state of lung development atbirth include prematurity, maternal diabetes andgenetics factors;

2)factors that may acutely impair surfactantproduction, release, or function include perynatalhypoxia and asphyxia (hypoxemia, acidosis),

congenital infection, cesarean section, multiplypregnancy, hypovolemia, cold stress in newborn.


4/24

The source of surfactant

Surfactant is produced by Type II

alveolar cells since 20-24 weeks ofgestation, but completely present after35 weeks of gestation.


5/24

Components of surfactant

Surfactant.

Lipids Proteins90% 10%

Phospholipids Neutral lipids80% 20%

Phosphatidyl- Phosphatidyl- Otherglycerol choline (Lecithin) lipids5% 70% 5%

Saturated DesaturatedPhosphatidylcholine Phosphatidylcholine

45% (dipalmitoyl lecithin).

25%

Surfactant is a surface-active material comprised of a mixture rich inphospholipids, and lesser amounts of proteins and other lipids.

Surfactant proteins have big role in the function of surfactant (A, B, D). Themost important B.


6/24

Surfactant acts as an anti-atelectasis factor in the alveolarlining by lowering surface tensionat diminished lung volumes.

This allows for maintenance offunctional residual capacity,which acts as a reservoir to

prevent wide fluctuation inarterial PO2 and PC02 duringrespiration.

Function of surfactant


7/24

Function of surfactant

Prevent collapse of alveoli during expiration

Protect alveolar epithelium from damage and

promote mucociliar clearance Provide antibacterial activity against Gram

positive microorganisms

Stimulate macrofages

Participate in regulation of microcirculationand permeability of alveolar wall, that allowsto prevent lung edema


8/24

Pathogenesis of RDSPrematurity > decreased surfactant synthesisand release >deficiency in pulmonarysurfactant >increased alveolar surfase

tension > atelectasis >pulmonaryhypoventilation > hypoxemia, hypercarbia >acidosis > increased pulmonary vascularresistance and vasoconstriction > pulmonaryhypoperfusion > increased vascularpermeability and pulmonary capillary leak >deposition of serum protein, fibrin > hyaline

membranes formation>diffusion block.


9/24

Symptoms of RDS

Tachypnoe >60 per min Chest retractions Expiratory grunting Cyanosis


10/24

Silverman Retraction Score

Results of Silverman Retraction Score assessment:


11/24

The chest x-ray film reticulogranular

patternof lung at the

beginning of RDS, air bronchogramsat

the progressing RDS

"ground-glass"appearancedue todiffuse bilateralatelectasis.


12/24

Tests for estimatingsurfactant maturity

Foam stability or shake test.

These tests depend on the ability of surfactant-rich fluid to formstable bubbles when mixed and shaken with ethanol.

Stable bubbles all the way around the test tube are suggestiveof mature lungs. No bubbles or single, vary small bubbles inmeniscus - high risk of RDS.


13/24

Tests for estimatingsurfactant maturity

Lecithin/sphingomyelin ratio:Since lecithin is a majorcomponent of surfactant, and sphingomyelin concentration isrelatively constant during gestation, the L/S ratio can be used asa measure of lung maturity.

An L/S of > 2.0 carries a low risk of RDS and is generallyattained at 34-35 weeks' gestation.Ratios of1.5-2.0 carry a 40% risk of RDS,values of 35 weeks' gestation. Thus, its presence isindicative of lung maturity, but its absence offers no definitivehelp in management. The measurement can be performed onblood- or meconium-contaminated fluid.


14/24

Laboratory studies. Monitoring of heart rate, respiratory rate,

blood pressure, pulsoxymetria.

Complete blood count - diagnose anemia,polycythemia, infection.

Arterial blood gas measure PaO2 , PaCO2, acid-base status.

Blood glucose, blood culture,

coagulation test.


15/24

Causes of respiratory distress

in the newborn. There are many pulmonary and non-

pulmonary causes of RD in the neonatalperiod.

Pulmonary: RDS, meconium aspirationsyndrome, neonatal pneumonia, persistentpulmonary hypertension, transient tachypneaof the newborn, congenital pulmonary

malformation; non-pulmonary: congenital heart disease,

anemia, CNS injury, asphyxia, hypoglycemia,metabolic disease


16/24

To distinguish neonatal cardiac diseasefrom pulmonary disease

to place the infant in 100% oxygen (less than 5minutes), so called hyperoxia test.

In general, the child with cyanotic congenital heart

disease will not be able to generate a PaO2 greaterthan 100 mm Hg because of fixed intracardiacshunting that bypasses the pulmonary circulation.

The child with severe lung disease, however, will be

able to improve oxygenation substantially greaterthan 100 mm Hg, especially if given positive pressureventilation (PPV).


17/24

Management of RDS.

The keys to management of infants with RDS: to prevent hypoxia and acidosis (this allows normal tissue metabolism,

optimises surfactant production, and prevents right-to-left shunting), to optimise fluid management (avoiding hypovolemia and shock on the

one hand and edema, particularly pulmonary edema, on the other), to reduce metabolic demands, to prevent worsening atelectasis, to minimise barotrauma and hyperoxic lung damage.

General supportive care includes:

optimal thermal environment to keep the skin temperature of infant at36.50C, fluids, electrolytes and nutritional support, protection from infection.


18/24

Respiratory therapy.

The goal is the provision of adequate supplementaloxygen to maintain arterial oxygen tension (PaO2)

of 60-80 mm Hg and an arterial saturation of 92-95%.

PaO2 levels less than 50 mm Hg are associated withpulmonary vascular vasoconstriction, and thosegreater than 100 mm Hg may increase the risk of

retinopathy of prematurity and pulmonary oxygentoxicity. Warmed (32- 340C), humidified oxygen may be

delivered via a clear, plastic hood or via nasal prongs,or a respirator.


19/24

Surfactant Replacement Therapy

In patients with RDS, surfactants have been shown to decrease theneed for supplemental oxygen therapy, lower mortality rates, anddecrease the incidence of air-leak syndromes. The incidence of BPDhas also been reduced in some studies.

Two general classes of surfactant are available for replacementtherapy:natural surfactants prepared from mammalian lungs Survanta,Curosurf, Alveofactsynthetic surfactants Exosurf, Pneumactant

Although natural surfactant extracts seem to have a better immediateeffect (less supplemental oxygen required, fewer pneumothoraces),

long-term clinical outcomes (e.g., chronic lung disease, death) withsynthetic surfactants are comparable.

Surfactant therapy: prophylaxis for infants at high risk forRDS (infants less than 30 weeks' gestation, less than 1250 g)

"rescue" treatment


20/24

Continuous Positive Airway Pressure(CPAP)

is applied when FiO2 greater than 0.40-0.60is required to maintain PaO2 at 5080 mmHg, or when there is significant clinicalworsening during the first day of life.

Method using CPAP (4-8 cm H2O) - a facemask, nasal prongs, nasopharyngeal tube, orendotracheal tube.

The application of CPAP opens atelectaticalveoli, conserves the functional properties ofsurfactant.


21/24

Incication for mechanicalventilation in RDS

Mechanical ventilation is initiated when the diagnosis ofrespiratory failure is made.

Laboratory criteria for respiratory failure Respiratory acidosis with pH < 7.20 and PCO2 > 60 mm Hg

Severe hypoxemia with PaO2 < 50-60 mm Hg despite anFiO2of 0.7-1.0 and an adequate trial of continuous positiveairway pressure

Clinical criteria for respiratory failure 1. Severe retractions 2. Cyanosis 3. Intractable apnea


22/24

Complications of RDS

acute air leak syndrome (pneumothorax,

pneumopericardium, pneumomediastinum,pulmonary interstitial emphysema), patentductus arteriosus, intracranial hemorrhage,infections (pneumonia, sepsis), pulmonary

hemorrhage;

chronic bronchopulmonary dysplasia,retinopathy of prematurity, neurologic sequel.


23/24

Preventive Strategies The prenatal and perinatal management of women to prevent

premature labor is still the most critical issue. The use of maternal glucocorticoid therapy to pharmacologically

induce surfactant maturation, production, and secretion in thefetus.

Antenatal steroids (ANS) strongly recommended in all preg-nancies between 24 and 34 weeks' gestation at risk for pretermdelivery. ANS should not be used in infants greater than 34weeks' gestation unless there is evidence of pulmonaryimmaturity.

In addition, mothers less than 30 to 32 weeks' gestation with

premature rupture of membranes in the absence of amnionitisalso should be treated.

ANS preparations used are either dexamethasone 6 mgintramuscularly every 12 hours for four doses or betamethasone12 mg intramuscularly every 24 hours for two doses. Theoptimal effect for ANS is 24 hours to 7 days after treatment.


24/24

Thank your for attention!

respiratory distress syndrome in newborn

Documents