**3. Transition from foetal to extra-uterine life**

The transition from foetal to extra-uterine life is a process of rapid physiologic changes in the neonate that begin in utero as the foetus prepares for transition from intrauterine placental support to extra-uterine self-maintenance. The process can last for up to 12 h after birth and depends on the gestational age, placenta, maternal health and congenital anomalies of the neonate. The foetus is preparing to the transition by foetal breathing, producing surfactant storing glycogen in the liver, producing catecholamines and depositing brown fat. After the umbilical cord is cut, placenta no longer does the work of lungs as they begin to exchange gasses. The first breath inflates the lungs and causes circulatory changes: the resistance to blood flow through lungs falls and more blood flows through pulmonary arteries to the lungs. Three foetal shunts close and this results in neonatal circulation. The three processes of the transition—(1) the replacement of amniotic fluid in the alveoli with air, (2) the onset of regular breathing and (3) the increase in pulmonary blood flow—may all be deranged soon after birth and RD ensues [7]. The failure of alveoli fluid clearance results in transient tachypnoea of the newborn (TTN) and causes in turn decreased lung compliance. The deficiency of surfactant mainly in preterm neonates or in term infants of diabetic mothers causes collapse of the alveoli and diffuse and progressive atelectasis that result in decreased lung compliance and small functional residual capacity (FRC) and cause HMD. The abnormal persistence of elevated pulmonary vascular resistance either due to underdevelopment, maldevelopment or maladaptation of pulmonary vessels results in persistent pulmonary hypertension of a newborn (PPHN). PPHN is often associated with congenital anomalies (i.e. congenital diaphragmatic hernia) or chronic intrauterine stress (meconium aspiration syndrome (MAS)).

At the time of birth, the umbilical cord is still pulsating. For term and preterm neonates, delayed cord clamping is recommended. The preterm neonates born before 32 weeks of gestation with delayed cord clamping had better neuro-developmental outcomes at the age of 18 months [8, 9]. Too early umbilical vein clamping, even before the first breath of the neonate, may lead to a prolonged period of low cardiac output, which along with the undeveloped self-regulation system leads to a reduction of brain blood flow. Delayed cord clamping allows blood to enter the neonate's circulation and by that enhances the performance of the left ventricle, which is the most important for the normal cardiac output and stable haemodynamics especially in foetal distress with compromised haemodynamics at birth [10].

**Pulmonary disease Gestational age, risk factors**

• Preterm

• Neonates of diabetic mothers

• Late preterm • Elective caesarean section

• Term > preterm • Perinatal depression

• Term • Perinatal depression

mother

Pneumothorax Preterm > term Air entrance

Pneumonia Infection of the

Lack of surfactant

Failure of adequate alveoli fluid clearance at birth

Persistence of elevated pulmonary vascular resistance

Meconiumstained amniotic

Bacterial or viral infection

into the pleural space

Term>preterm Diagnostic

Term > preterm Normal

surfactant proteins

Term, preterm lack of

**Table 2.** The etiologic and radiologic assessment of respiratory state of a neonate.

fluid

Hyaline membrane

disease

Transitional tachypnoea of the newborn

Persistent pulmonary hypertension

Meconium aspiration

Congenital heart

defect

Congenital malformation of organs

Metabolic, neuromuscular diseases

Genetic defect of surfactant proteins

syndrome

**Aetiology Roentgenogram Ultrasound**

Bilateral perihilar linear streaking, patchy

Clear lung fields with decreased pulmonary

Non-symmetric bilateral patchy infiltrates

Diffuse reticulogranular ground glass pattern with air bronchograms and small lung volume; grading from mild (grade 1) to most severe

Chronic lung disease of different patterns

(grade 4)

Patchy infiltrates Pulmonary

Edge of collapsed lung Absence of pleura

infiltrates

vascularity

Term > preterm May be diagnostic Echocardiography

Diffuse reticulogranular ground glass pattern with air bronchograms and small-lung volume; grading from mild (grade 1) to the most severe pattern (grade 4)

Coalescent B-lines- 'white lung', thickened and irregular pleural

Respiratory Care of the Neonate

49

Compact B-lines in the inferior and less compact in the superior fields (double lung point) or bilateral numerous noncompact B-lines and normal pleural line and pleural

Echocardiography

consolidation with air bronchograms, pleural line anomalies, pleural effusion, B-lines in nonconsolidation area

Subpleural consolidation

diagnostic

sliding and B-lines, subpleural consolidation

line

http://dx.doi.org/10.5772/intechopen.69674

sliding
