LECTURE

INFANT RESPIRATORY
DISTRESS SYNDROME
(IRDS)

Lecturer: associate professor Volosin A.N.

Definition
Symptom complex of severe respiratory failure, which
arises as a rule during the first hours of baby’s life.
Most often this syndrome is determined by neonatal
pneumopathy.

Neonatal pneumopathies are the group of perinatal lungs

diseases, which aren’t associated with any infection.

IRDS also called neonatal respiratory distress

syndrome or respiratory distress syndrome of
newborn is first of all a syndrome caused in premature
infants by the insufficiency of surfactant production
and structural immaturity in the lungs
 CLASSIFICATION
OF NEONATAL PNEUMOPATHIES
• Hyaline membrane disease (HMD);
• Edematic-hemorrhagic syndrome;
• Atelectasis of newborn.
IRDS and HMD are the synonyms in English language sources
Short description of pneumopathies

HM are dense protein mass, which is formed from blood proteins

and is mainly composed of fibrin.
These membranes cover the inner surface of pulmonary alveoli.

Edematic-hemorrhagic syndrome is characterized by diffuse

edema of lungs with multiple haemorrhages in pulmonary tissue.

Atelectasis is condition of alveoli, when their cavities deflate and

have slit-like form. Primary and secondary atelectasises are
marked out. We also distinguish disseminated and segmental atelectases.
 PATHOGENESIS OF IRDS
Surfactant is substance, which ensures elasticity of pulmonary
tissue. In case of its deficiency pulmonary tissue deflates and
respiratory failure develops.
Surfactant deficit leads to:
• severe hypoxemia and hypoxia, hypercapnia, acidosis,
hypoglycemia, hypocalcemia and other metabolic derangements;
• pulmonary hypertension and systemic hypotension, hypovolemia,
microcirculation disturbance, peripheric edemas;
• muscular hypotonia;
• neurologic disorders;
• heart failure;
• inclination to hypothermia;
• functional intestinal obstruction.
 EPIDEMIOLOGY
IRDS
affects about 1% of newborn infants and is the
leading cause of death in preterm infants. The
incidence decreases with advancing gestational age,
from about 50% in babies born at 26–28 weeks, to
about 25% at 30–31 weeks. The syndrome is more
frequent in the second born of premature twins.
 RISK FACTORS OF IRDS
• Premature delivery
• Infants delivered via Caesarean section (without maternal labor)
• Perinatal hipoxia
• Delivery complications that lead to acidosis in the newborn
at birth (e.g. acute hemorrhage)
• Maternal diabetes
• Fetal [prenatal] infections
• Multiple pregnancy (twins or more)
• Rapid labor
• Male infants
• Hypothermia
• Family history of IRDS
The incidence of IRDS decreases with:
– The usage of antenatal steroids;
– Pregnancy-induced or chronic maternal
hypertension;
– Prolonged rupture of membranes;
– Maternal narcotic addiction.
 CLINICAL SYMPTOMS OF IRDS
The symptoms usually appear within first minutes of birth.
In case of HMD clinical symptoms of respiratory failure are
revealed in 1-4 hours after birth.
• Bluish color of the skin and mucus membranes (cyanosis)
• Brief stop in breathing (apnea)
• Decreased urine output
• Grunting
• Nasal flaring
• Puffy or swollen arms or legs
• Rapid breathing (dyspnea - more than 60 breaths/min)
• Shallow breathing
• Blowing of cheeks
• Spumous saliva around patient’s mouth
• Unusual breathing movement – drawing back of the chest during
inspiration
Clinical features of neonatal respiratory distress

The photo depicts a preterm newborn with RDS exhibiting

substernal and intercostal retractions, nasal flaring,
and circumoral cyanosis.
 EDEMATIC-HEMORRHAGIC
SYNDROME
• Diagnostic sign is bloody discharge from
patient’s nose, mouth or endotracheal tube,
spumous fluid of pink color, which runs
from baby’s mouth.
• Apart from pulmonary edema and
pneumorrhagias, skin hemorrhagic
syndrome and intestinal bleedings can be
detected.
 SILVERMAN SCORE

Feature Score Score Score

observed «0» «1» «2»
Chest Synchronized Lag on Seesaw
Movement Respiration Respirations Respirations
Intercostal
None Just Visible Marked
Retractions
Xiphoid Just Visible
None Marked
Retractions

Nares Dilation None Marked

Minimal

Expiratory None Audible With Audible With

Grunt Stethoscope Unaided Ear
 EVALUATION OF RESPIRATORY STATUS
(Silverman score)

Total Score of 0 indicates no respiratory

distress.

Total Score of 1-3 indicates feebly apparent

respiratory distress.

Total Score of 4-6 indicates moderated distress.

Total Score of 7-10 indicates severe distress.

 DIFFERENTIAL DIAGNOSIS
• Pulmonary air leaks (e.g., pneumothorax, interstitial emphysema,
pneumomediastinum, pneumopericardium);
• Any infection may cause respiratory distress and may co-exist with IRDS;
Pneumonia is often caused by beta-haemolytic streptococcus and often co-
exists with IRDS.
• Aspiration of amniotic fluid, blood, or meconium may occur.
• Intracranial birth injury.
• Transient tachypnoea of the newborn usually occurs in term or near-term
infants and usually after caesarean delivery.
• Congenital anomalies of upper airways (e.g., choanal atresia)
• Congenital anomalies of the lungs (e.g., diaphragmatic hernia, lobar
emphysema, pulmonary sequestration).
• Congenital heart anomalies.
• Primary persistent pulmonary hypertension of the newborn (persistent fetal
circulation).
• Metabolic problems (e.g. hypothermia, hypoglycaemia).
• Haematological problems (e.g. anemia, polycytaemia).
 BRONCHOPULMONARY DYSPLASIA
(BPD)
Wilson-Mikity’s syndrome develops in babies at gestational age less than 32
weeks and body weight less than 1500 g. Usually BPD becomes apparent on
15-35-th day of life.
Reason: immaturity of elastic elements of pulmonary tissue
• Dyspnea – up to 60 breaths/min;
• Cyanosis;
• Fits of apnea;
• Dry cough;
• Drawing back of the chest during inspiration;
• Intoxication syndrome isn’t typical;
• Duration of clinical presentations of BPD is from 1 month to 1
year and more.
 BPD in a 33-day-old preterm infant
Frontal chest X-ray demonstrates uniform distribution of reticular opacities
and small clearings
 EXAMINATION
• Blood gases: respiratory and metabolic acidosis along with
hypoxia. Metabolic acidosis results from poor tissue
perfusion.
• Pulse oximetry is used as a non-invasive tool to monitor
oxygen saturation, which should be maintained at 90-95%.
• Chest X-ray.
• Monitor full blood count, electrolytes, glucose, renal and
liver function.
• Echocardiogram to rule out structural heart diseases.
• Bacteriological examinations to rule out sepsis.
 COMPLICATIONS OF IRDS
– Complications related to procedures, e.g. trauma to vocal
cords because of tracheal intubation; infection, embolism or
thrombosis from venous or arterial catheterisation.
– Alveolar rupture: pneumothorax, pneumomediastinum etc.
– Intracranial haemorrhage: the risk is increased in those who
require mechanical ventilation.
– Persistent pulmonary hypertension.
– Occurrence of pulmonary haemorrhage increases in very
premature infants, especially following surfactant therapy.
– Hospital acquired infection.
– Necrotising enterocolitis and/or gastrointestinal perforation.
– Apnoea of prematurity is common in immature infants, and
its incidence increases with surfactant therapy, possibly due
to early extubation.
 TREATMENT OF IRDS
(etiotropic)
Nowadays such preparations of natural surfactant as Curosurf,
Survanta, Alveofact, Biosurf and synthetic surfactant as Exosurf
neonatal are used most often.

• Exogenous surfactants are introduced into trachea. The earlier

it is introduced the better results we can get. The term for its
effective introduction is the first 6-8 hours after birth. In case
of necessity introduction of surfactant may be repeated.
• For example, initial dose for Curosurf is 200 mg/kg
(2,5 ml/kg). Repeat dose is 50 % of initial dose.
It may be introduced twice every 12 hours.
Chest X-ray in a premature infant with RDS
Left, initial X-ray shows poor lung expansion, air bronchogram, and
appearance of reticular nodose granular net.
Right, repeat chest X-ray made 3 hours later after surfactant therapy
demonstrates marked improvement.
Symmetric surfactant effect in a 36-week-gestationalage infant of a diabetic
mother.
(a) Pretreatment radiograph shows diminished lung expansion, diffuse bilateral
reticulogranular opacities, and air bronchograms.
(b) Repeat radiograph, made 6 hours later after endotracheal introduction of one dose of
surfactant, reveals marked improvement in lung aeration
Asymmetric surfactant effect in a 2-day-old, 32-week-gestational age newborn
with RDS
Frontal chest radiograph demonstrates multifocal residual consolidations similar to
pneumonia or meconium aspiration syndrome
 TREATMENT OF IRDS
(continuation 1)
Temperature protection
• It is necessary for the prevention of hypothermia of newborn child,
as far as on the background of hypothermia surfactant synthesis
either decreases or stops at all. Temperature in infant incubator must
be 34-35° C.
Ensuring of patency of airways
• At first aspiration contents from airways is prescribed. Some time
later vibratory massage, physiotherapy and aerosol therapy are used
for that.
Feeding and infusion therapy
• During the first 2-3 days enteral feeding isn’t used because the risk of
arising of cardiopulmonary decompensation is very high at that time
• Correction of metabolic acidosis (blood pH less than 7,25) with the
help of 4 % sodium hydrogen carbonate solution.
 TREATMENT OF IRDS
(continuation 2)
Control of gas composition of blood
• Oxygenotherapy in infant incubator or artificial lung ventilation.
Control of PaO2 and PaCO2 (carbon dioxide).
Control of hematocrit (packed cell volume (PCV))
• If PCV drops lower than 0,4 then whole blood or packed red cell
transfusion is prescribed.
Treatment of hypovolemia
• Intravenous transfusions of 5-10 % albumin solution, fresh frozen
plasma (FFP), 0,9 % sodium chloride and 5 % glucose solutions.
Control of arterial pressure (AP)
• If systolic pressure is lower than 45 millimeter of mercury then
cardiotonic agents are prescribed (e.g. dopamine).
 TREATMENT OF IRDS
(termination)
Antibiotic therapy
• Combination of one of semisynthetic penicillins or
cephalosporins with one of aminoglycosides is used most
often.
Vitamin therapy
• Vitamins E and A are prescribed obligatory. Vitamin E
decreases frequency of the development of retinopathy and
vitamin A - necrotizing enterocolitis in newborn children.
Other drugs
• Diuretics. Furosemide is used only in case of pulmonary
edema.
• Glucocorticoids are used on the background of signs of
adrenal failure.
 PROGNOSIS

• The outcome has improved in recent years with

the increased use of antenatal steroids to improve
pulmonary maturity, early postnatal surfactant
therapy to replace surfactant deficiency and
gentler techniques of ventilation to minimise
damage to the immature lungs.
• The prognosis is much better for babies weighing
over 1500g.
 PREVENTION OF IRDS

• Antenatal corticosteroids (dexamethasone)

accelerate fetal surfactant production and lung
maturation. They reduce IRDS, intraventricular
haemorrhage and mortality by 40%.
• Tocolytics, e.g. atosiban, nifedipine or ritodrine,
may delay premature delivery by 48 hours and
therefore enable time for antenatal corticosteroids
to be given.
• Good control of maternal diabetes.
• Avoid hypothermia in the neonate.
THANK YOU FOR YOUR ATTENTION