**4. Assessment of the respiratory distress of the neonate**

The evaluation of a neonate with RD is based on clinical, laboratory and radiologic investigations. In clinical evaluation, the respiratory effort, breathing efficacy and the breathing effect on other organs are assessed (**Table 1**). Signs of respiratory effort may be less pronounced or not visible in three cases: (1) the neonate, who has had RD for a long time, eventually becomes tired and signs of respiratory effort are reduced. Tiredness is a pre-terminal sign of respiratory failure. (2) A neonate with central nervous depression because of either intoxication, or encephalopathy, brain malformation, or increased intracranial pressure, breathes insufficiently without increased respiratory effort. These neonates breathe insufficiently due to reduced breathing impulse. (3) A neonate with neuromuscular disease may have respiratory failure without a significantly seen respiratory effort.

Classic laboratory signs of respiratory failure include acidosis (pH < 7.25), hypoxia (PaO<sup>2</sup> < 50–60 mm Hg (6.7–8 kPa), FiO<sup>2</sup> 0.6–0.8) and hypercapnia (PaCO<sup>2</sup> > 60 mm Hg (8 kPa)) which are late signs of RD. Radiologically, neonatal chest may be scanned by X-rays [11, 12] or, lately more in use, by ultrasound (US) waves [13–17]. In utero, routine foetal US scan following development and screening for malformations may reveal intra- or extra-thoracic malformations, better differentiated by magnetic resonance imaging (MRI). Combining the risk and etiologic factors for neonatal RD, gestational age and radiologic investigations, the pulmonary disease causing the RD may be diagnosed (**Table 2**), since the clinical picture and laboratory signs are almost not of any help in defining the aetiology of neonatal RD.


**Table 1.** The clinical assessment of airway and breathing in a neonate.


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

The evaluation of a neonate with RD is based on clinical, laboratory and radiologic investigations. In clinical evaluation, the respiratory effort, breathing efficacy and the breathing effect on other organs are assessed (**Table 1**). Signs of respiratory effort may be less pronounced or not visible in three cases: (1) the neonate, who has had RD for a long time, eventually becomes tired and signs of respiratory effort are reduced. Tiredness is a pre-terminal sign of respiratory failure. (2) A neonate with central nervous depression because of either intoxication, or encephalopathy, brain malformation, or increased intracranial pressure, breathes insufficiently without increased respiratory effort. These neonates breathe insufficiently due to reduced breathing impulse. (3) A neonate with neuromuscular disease may have respiratory

Classic laboratory signs of respiratory failure include acidosis (pH < 7.25), hypoxia (PaO<sup>2</sup>

signs are almost not of any help in defining the aetiology of neonatal RD.

3. Auscultatory phenomena Arterial blood oxygen

**Table 1.** The clinical assessment of airway and breathing in a neonate.

1. Breathing rate Chest movement Heart rate

0.6–0.8) and hypercapnia (PaCO<sup>2</sup>

**Respiratory effort Breathing efficacy Effect on other organs**

saturation

are late signs of RD. Radiologically, neonatal chest may be scanned by X-rays [11, 12] or, lately more in use, by ultrasound (US) waves [13–17]. In utero, routine foetal US scan following development and screening for malformations may reveal intra- or extra-thoracic malformations, better differentiated by magnetic resonance imaging (MRI). Combining the risk and etiologic factors for neonatal RD, gestational age and radiologic investigations, the pulmonary disease causing the RD may be diagnosed (**Table 2**), since the clinical picture and laboratory

<

> 60 mm Hg (8 kPa)) which

paleness, mottled skin

Disturbance of consciousness

Chest auscultation Skin colour: cyanosis,

especially in foetal distress with compromised haemodynamics at birth [10].

**4. Assessment of the respiratory distress of the neonate**

failure without a significantly seen respiratory effort.

50–60 mm Hg (6.7–8 kPa), FiO<sup>2</sup>

48 Selected Topics in Neonatal Care

2. Intercostal, jugular, supraclavicular or subcostal retractions

6. Use of auxiliary respiratory muscles

7. Nasal flaring, head nodding

4. Feeding difficulties 5. Expiratory grunting

8. Gasping

#### **5. Respiratory support in delivery room**

Routine care in delivery room depends on whether we expect and take care of extreme premature neonates or near term or term neonates with breathing difficulties. In case of near term or term neonates, care starts with providing warmth, clearing airway if necessary, drying and stimulating the neonate. Care of preterm infants is different because we immediately place him/her into a heated polyethylene bag with small opening for the nose and mouth and further stabilize him/her under the heater to assure normal body temperature, prevent hypothermia and desiccation [18]. The stabilization of the neonate with RD in the delivery room comprises proper head positioning with wiping of the mouth, and rarely, in the case of more secretion, not removed by wiping, we may perform gentle suction of the neonate's mouth, then nose. We have to avoid the deep insertion of the catheter and vigorous suctioning of mouth which may cause reflex bradycardia. In the case of meconium staining and aspiration, suction of trachea under visual inspection with laryngoscopy guidance is needed first and then intubation and further washing out meconium from the trachea. In case of apnoea, gasping or bradycardia of <100 beats/minute, it is necessary to ventilate neonate's lungs with positive pressure ventilation considering the use of lowest effective inspiratory pressures and volumes to prevent damage to the lungs (barotrauma and volutrauma). Ventilation should fill neonatal lung with a gas mixture of air and oxygen. To prevent and reduce the oxidative stress, caused by excessive use of oxygen in the inspired air, it is necessary to be careful with the use of oxygen. For measuring the arterial oxygen saturation (SpO<sup>2</sup> ) in the peripheral blood, the pulse oximeter should be attached to the right wrist [19]. Latest guidelines recommend starting ventilation of term neonates with FiO<sup>2</sup> 0.21 and later increasing the FiO<sup>2</sup> according to the value of the measured SpO<sup>2</sup> . Ventilation of preterm neonates should be started with FiO<sup>2</sup> of 0.21, gradually rising the FiO<sup>2</sup> in accordance with the measured value of SpO<sup>2</sup> . Ventilation of the extremely premature infants (born before 28 weeks gestation) should be started with FiO<sup>2</sup> 0.30, while of very premature infants (28–31 weeks of gestation) with the FiO<sup>2</sup> from 0.21 to 0.30. If neonate is spontaneously breathing, the constant positive pressure is applied for the stabilization of respiration (continuous positive airway pressure) of 6 cm of H<sup>2</sup> O through a mask, nasal tubes or endotracheal tube using neonatal respirator (neonatal resuscitator; T-piece device), intended for stabilization of the neonate in the delivery room. The maximum positive inspiratory pressure should not exceed 20–25 cm H<sup>2</sup> O, which is used only in the case of apnoea or bradycardia [6]. No differences in mortality and morbidity of premature neonates have been demonstrated in comparing resuscitation starting with low (FiO<sup>2</sup> ≤0.30) or high levels of oxygen (FiO<sup>2</sup> ≥0.6) [20]. Currently, there is insufficient evidence of sustained lung inflation efficacy and safety in the cardiopulmonary resuscitation and stabilization of the neonate in the delivery room [21, 22].

duration of artificial ventilation and oxygen demand and decrease risk for bronchopulmonary dysplasia (BPD) and the need for patent ductus arteriosus (PDA) ligation [23, 24]. At the age of 2 years, positive effects on cognitive development were observed, but in the same group of children at the age of 5 years they were no longer detected [25]. In a premature neonate with RD, the less invasive artificial ventilation and surfactant therapy are usually combined with early prophylactic intravenous administration of caffeine to achieve the highest level of respiratory support in the least invasive form [26, 27]. Since methylxanthines affect the diaphragmatic activity and increase the tidal volume, we may use them to increase the

Oxygen is necessary for aerobic metabolic processes in the body. The excess of oxygen is detrimental to neonates, particularly the premature infants with immature antioxidant, antiinflammatory mechanisms and a greater amount of free iron. Hyperoxia affects not only the lung but also other organs, with the greatest effects to central nervous system (convulsions) and eyes (retinopathy of prematurity (ROP)). In comparison with a 'higher' level of SpO<sup>2</sup> (91–95%), the 'lower' level (85–89%) has been shown to diminish the risk of ROP and BPD, but unfortunately at the same time increase mortality, the incidence of necrotizing enterocolitis and poor neuro-developmental outcome [29]. Based on research, current recommendations

Hypercapnia is associated with acidosis and compromised cardiovascular function, while hypocapnia decreases cerebral blood flow. There is some conflicting evidence on higher PaCO<sup>2</sup> levels and the impact on mortality, severe intraventricular haemorrhage (IVH), BPD, ROP and neurodevelopmental outcome [30, 31]. Therefore, the optimal target carbon dioxide levels are not established; based on available data, it should be between 46 in 60 mm Hg (6.1–8 kPa) for

Blood gas is monitored in arterial samples, so an indwelling arterial line is necessary in taking care of a neonate with moderate or severe RD. Venous and capillary samples are not appropri-

Pulmonary surfactant, a macromolecular lipoprotein complex, secreted by the alveolar epithelial cells type II, reduces the surface tension in the pulmonary alveoli at the end of exhalation. Sufficient amount of surfactant in the mature lungs prevents complete collapse of the lungs at the end of exhalation. A part of the inhaled air remains to be 'trapped' in the pulmonary alveoli, what is called the FRC. In each subsequent breath, it is not necessary to re-open

measurements. They may be of use for PaCO<sup>2</sup>

overestimate it, and pH monitoring, although they slightly underestimate it.

of preterm infants who require oxygen therapy to be between 90 and 94%,

of term neonates who require oxygen therapy

Respiratory Care of the Neonate

51

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

monitoring, although they slightly

muscle strength in floppy neonates [28].

setting alarm limits to 89 and 95% [6]. The SpO<sup>2</sup>

**7. Treatment with oxygen**

propose the SpO<sup>2</sup>

should be above 92%.

ventilated neonates.

ate for PaO<sup>2</sup>

**8. Surfactant**

#### **6. Methylxanthines**

Methylxanthines stimulate the respiratory centre to increase its responsiveness to the partial pressure of carbon dioxide in the blood and reduce respiratory depression by hypoxia. They also improve respiratory muscle strength. Therapy with caffeine has proven to reduce the duration of artificial ventilation and oxygen demand and decrease risk for bronchopulmonary dysplasia (BPD) and the need for patent ductus arteriosus (PDA) ligation [23, 24]. At the age of 2 years, positive effects on cognitive development were observed, but in the same group of children at the age of 5 years they were no longer detected [25]. In a premature neonate with RD, the less invasive artificial ventilation and surfactant therapy are usually combined with early prophylactic intravenous administration of caffeine to achieve the highest level of respiratory support in the least invasive form [26, 27]. Since methylxanthines affect the diaphragmatic activity and increase the tidal volume, we may use them to increase the muscle strength in floppy neonates [28].
