Respiratory distress

Respiratory distress

Respiratory distress is the leading cause for admission to the neonatal nursery. Causes of respiratory distress are diverse and the range of treatments available is broad. Following is a brief overview of some of the more common causes of respiratory distress in the newborn cared for by nurses and midwives in the special care nursery.

There are 5 cardinal signs (clinical manifestations/signs & symptoms) which we look for in an infant that are associated with respiratory distress. In the image below, click on the symbols to explore the cardinal signs or read the text version below the image. Respiratory distress is assumed in the presence of two or more of these cardinal signs. (Sinha et al 2017)

Respiratory disorders cared for in the SCN

The following conditions are respiratory disorders that are cared for in the SCN.

Respiratory Distress Syndrome (RDS)

Respiratory Distress Syndrome (RDS) previously referred to as Hyaline Membrane Disease (HMD), is a developmental disorder of the premature lung in which the underlying factor is pulmonary surfactant deficiency (Kain and Mannix 2023). The deficiency of surfactant leads to high alveolar surface tension, atelectasis and overall decreased functional residual capacity within the lungs (Gardner et al 2021). Increased risk is directly proportionate with decreasing gestational age (Sinha 2014). However, this condition can also affect the term infant due to either pulmonary surfactant dysfunction, caused by meconium aspiration syndrome, perinatal asphyxia, or impaired surfactant synthesis, such as infants of diabetic mothers that have been poorly controlled (Atar, et al 2012).

Transient Tachypnoea of the Infant (TTN)

Transient Tachypnoea of the Infant (TTN) also referred to as Wet Lung, is a common cause of respiratory distress in infants, due to a delayed clearance of fetal lung fluid (Gupta et al 2021). This delay in clearance interferes with gas exchange (Gupta et al 2021) due to a decreased lung compliance and decreased tidal volume and capillary and pulmonary congestion. Studies have shown that prior to birth approximately 35% of fetal lung fluid clears due to a catecholamine surge with approximately a further 30% cleared during labour (Subramanian 2024). Therefore, infants that are born via an elective caesarean section with no labour are at increased risk of this condition (Subramanian 2024). In infants with TTN the remaining fluid in the lungs compress the airway, causing airway obstruction with gas trapping and ventilation/perfusion (V/Q) mismatch, hypoxemia, increased work of breathing and respiratory distress (Reuter et al 2014).

Pneumonia

Pneumonia is an infection of the fetal lung due to either transplacental, or aspiration of infection amniotic fluid, or infection of the neonatal lung acquired during hospital admission referred to as a nosocomial infection. Usual pathogens are bacteria e.g. Group B streptococcus (GBS), streptococcus pneumoniae, staphylococcus aureus, listeria and Escherichia coli; and viruses such as herpes simplex virus, respiratory syncytial virus, influenza A and B (Gardener et al 2021). Infection of lung may be Intrauterine (Transplacental or aspiration of infected amniotic fluid) or Neonatal (Acquired).

Bronchopulmonary Dysplasia (BPD)

Bronchopulmonary Dysplasia (BPD), also referred to as Chronic Lung Disease (CLD), is one of the most common causes of morbidity and mortality in preterm infants (Sahni and Mowes 2023). BPD is diagnosed based on gestational age (GA), postmature age (PMA), oxygen (O2) exposure and O2 requirements at 36 weeks PMA. The current definition includes either a continuous O2 requirement for the first 28 days and/or O2 requirement at 36 weeks PMA for infants born less than 32 weeks’ gestation (Nuthakki et al 2023). The exact pathophysiology is unclear; however, it is generally a complication of the premature lung and trauma of early respiratory support and oxygen (Kain and Mannix 2023).

Apnoea

Apnoea is described as the cessation of air flow and respiration for a period of 20 seconds, or shorter if associated with bradycardia, cyanosis, or pallor. More common in premature infants usually peaks day five to seven post-natal age, however, can occur in term infants with associated identifiable conditions (Gardner et al 2021 Kain and Mannix 2023, Sinha et al 2017).

Apnoea in infants falls into four categories:

1. Central usually lack of diaphragmatic activity caused by lack of signal from the central nervous system.
2. Obstructive, caused by an obstruction of airflow in the upper airways, can be associated with poor neck flexion/positioning, or mucosa.
3. Mixed a combination of central and obstructive.
4. Lastly Apnoea of Prematurity (APO)- (will be discussed further below).

(Gardner et al 2021 Kain and Mannix 2023, Sinha et al 2017)

Apnoea of Prematurity (AOP).

The preterm infants less than 34 weeks’ gestation have an immature cerebral cortex and brainstem which are less responsive to changes in carbon dioxide. This combined with poorly integrated central nervous system drive and upper airway patency and respiratory muscle fatigue make them more susceptible to apnoea. This is known as AOP which is diagnosed based on exclusion of all other causes (Gardner et al 2021 Kain and Mannix 2023, Sinha et al 2017).

Treatment for AOP in infants less than 34 weeks, includes the daily administration methylxanthines such as Caffeine Citrate, which is central nervous system stimulant, respiratory stimulant, which increases the respiratory centre output, smooth muscle relaxation and cardiac output. Thus, overall improvement in the contractility of the diaphragm and hence increasing the force of contraction and decreasing muscular fatigue (Kain and Mannix 2023).

The pathophysiology of Meconium aspiration syndrome (MAS) is complex. Meconium is present in the fetal intestine early in gestation. It is comprised of gastrointestinal, hepatic and pancreatic secretion, cellular debris, swallowed amniotic fluid, lanugo, and vernix (Argyridis and Arulkumaran 2016, Mota-Rojas et al 2022). However, due to lack of strong peristalsis, and low levels of motilin, the passage in-utero is uncommon until term.

A vagal response secondary to a hypoxic event in utero can cause increased peristalsis and a relaxed anal sphincter resulting in meconium passage (Argyridis and Arulkumaran 2016). Further fetal distress and hypoxia may initiate gasping in this may result in meconium-stained amniotic fluid (MSAF) being inhaled into the airways in utero or on taking the first breath after birth. If meconium particles are aspirated into the lungs (MAS), they cause a physical obstruction of the airways, creating a ball-valve effect in the airways, resulting in partial or complete obstruction that causes atelectasis (lung collapse) or areas of overexpansion due to gas trapping and air leaks (Mota-Rojas et al 2022, Kain and Mannix 2023). Meconium is a potent trigger for inflammatory mediators. It activates key innate immune pathways, leading not only to lung inflammation (chemical pneumonitis) and surfactant dysfunction (Mota-Rojas et al 2022, Gardner et al 2021). This can result in further lung tissue damage, progressing to disease of the parenchymal, atelectasis, hypoventilation, and acidosis.  This can contribute to the development of persistent pulmonary hypertension (PPHN). Acidosis can further worsen PPHN by promoting right-to-left shunting of blood away from the lungs, which causes severe hypoxemia. This hypoxemia, in turn, impairs ventricular function and further complicates PPHN. Left ventricular dysfunction raises left atrial pressure, leading to pulmonary venous hypertension, which exacerbates hypoxemia and in severe cases even death (Gardner et al 2021 Kain and Mannix 2023, Sinha et al 2017). 

Persistent Pulmonary Hypertension of the Newborn (PPHN)

Persistent Pulmonary Hypertension of the Newborn (PPHN) is the failure of pulmonary circulation to adapt to normal extrauterine life and is characterized by the inability to achieve a typical postnatal decrease in pulmonary vascular resistance (PVR). This results in elevated pulmonary artery pressure, reduced pulmonary blood flow, and right-to-left shunting through the patent foramen ovale (PFO) and/or patent ductus arteriosus (PDA) (Gardner et al 2021 Kain and Mannix 2023, Sinha et al 2017).

After birth, systemic vascular resistance (SVR) increases due to the loss of the placenta, while PVR remains equal to or greater than SVR. This high PVR imposes significant strain on the heart, potentially leading to right heart failure, particularly in the presence of hypoxemia (Gardner et al 2021 Kain and Mannix 2023, Sinha et al 2017). The combination of pulmonary hypertension and left-to-right shunting through the PDA and/or PFO diverts blood away from the pulmonary vascular bed while the heart remains structurally normal. The abnormally elevated PVR causes deoxygenated blood to flow through the ductus arteriosus and foramen ovale into systemic circulation, resulting in systemic arterial hypoxemia (Gardner et al 2021 Kain and Mannix 2023, Sinha et al 2017).  Consequently, hypoxia can trigger metabolic acidosis, pulmonary vasoconstriction, and decreased lung compliance (Gardner et al 2021 Kain and Mannix 2023, Sinha et al 2017).