Respiratory distress syndrome is a breathing disorder that is associated with breathing difficulties in the neonates and is thus also known as neonatal respiratory distress, infant respiratory syndrome, and hyaline membrane disease. The condition has been identified as one of the primary causes of infant morbidity and mortality (Sardesai et al., 2017). The syndrome is more common in children that are born in pre term and affect all the newborns that take birth before 28 weeks of pregnancy. In rare cases, it can also be observed in children who do not undergo a pre term birth. The condition occurs as the lungs of the children are not able to deal with the surfactants that keep the lungs expanded to ensure that the child is able to breathe the air once they are out of the womb (Delara et al., 2019).
The disease is prognosed within 24 hours of birth in most cases and is managed to prevent further complications in the child. The lack of oxygen and breathing difficulties in the child with respiratory distress syndrome are visible within a few hours of birth and are managed immediately (Dani et al., 2018). This paper will explore the critical aspects that are associated with the disease. Further, the molecular and biochemical manifestations of the disease will also be discussed in detail through assessment of pathophysiology of the health condition. This paper will also discuss the prevention strategies that can limit the incidences of respiratory distress syndrome in the neonates. Finally, the treatment procedures and the management of the health condition will also be discussed in this paper through an evidence based approach by the synthesis of information from published articles and books.
The etiology of the respiratory distress syndrome is associated with developmental immaturity of the lungs in particular conjunction with the surfactant synthesis. Surfactants are produced by the type II pneumocytes and are detectable in the child from 24 weeks of gestation (Sardesai et al., 2017). The nature of these molecules is heterozygous with the presence of lipids and proteins. The surfactant molecules coat the alveolar surface to minimize the surface tension and prevent alveolar collapse once the infant is out of the womb to inhale the air. Therefore, the cause of respiratory distress syndrome is attributed only to two primary causes. These are reduced surfactant production of surfactant deficiency and immature lung structure (Delara et al., 2019). The surfactant molecules function by spreading a thin layer between the air and liquid interface in the alveolar tissue and thereby minimizing the surface tension preventing alveolar collapse. This becomes even more critical in cases where the low alveolar volumes are reached at the end expiration (Spinelli et al., 2020). The surfactants also reduce the pressure that is needed or alveolar inflation in the body and thus maintain the functional residual capacity of the lings.
In absence of the required amount of surfactants the infants with respiratory distress syndrome progress to atelectasis and several other anomalies associated with lung function. In cases of poor surfactant availability in the lungs, the alveoli collapse at the end expiration giving rise to breathing difficulties and the inducing onset of the respiratory distress syndrome in the infants (Banerjee et al., 2019). In this case, the pressure required to inflate the lungs is high and the compliance of the lungs is significantly decreased. Further, the tidal volume of the lungs is reduced and a large physiological dead space is created. The respiratory rate of the infant goes up to mitigate the poo3r ventilation and respiratory distress but the alveolar ventilation is restricted due to collapse. Intra pulmonary shunting is also observed in certain cases where artificial ventilation is provided to combat the effects of respiratory distress syndrome (Sweet et al., 2017). This shunting further causes limitation on the excretion of carbon di oxide from the system and affects the oxygen saturation of the venous blood.
As a consequence, hypoxemia and respiratory acidosis may be observed in the patient. This further accelerates the deterioration of the heath and leads to metabolic acidosis and respiratory acidosis in the patient. Reduced cardiac output and hypotension are also observed in these cases in the patients that suffer from respiratory distress syndrome. A higher negative pleural pressure is generated in the body and increased breathing mechanism is adopted by the body to compensate the oxygen demands and the alveolar ventilation (Papazian et al., 2019). This deterioration is characteristic in the children that are born with poor surfactant production and availability in the lungs. At pathological level, poor ventilation and alveolar collapse result in the alveolar epithelial cell necrosis. The epithelial cells become detached from the basement membrane and result in small patches of hyaline membrane on the denuded area and thus affects the gaseous exchange. At the initial stages, there is patchy visibility of the symptoms. However, within the 24 hour span, a generalized hyaline membrane is formed.
If the condition is left untreated, the respiratory distress syndrome in the infants can result in chronic lung disease of prematurity. Respiratory distress syndrome is also critically associated with premature births. In the sacular stage of lung development that occurs in week 28-36 of child development, the gas exchange surface area increases and the airways wall thin out (Sweet et al., 2017). Finally, the alveolar stage is achieved in week 36 and is characterized by alveolar formation and maturation. This enhances the gas exchange in the body and promotes the achievement of effective pulmonary function. Presence of adequate amount of fetal lung fluid volume and fetal breathing movements is also critical for lung maturation. In premature births, these stages are not completed with complete efficiency and thus results in the development of respiratory distress syndrome (Blondonnet et al., 2016).
The poorly developed alveoli collapse due to lack of maturation in such cases and thus result in limited pulmonary function and gaseous exchange. The poor development of type II cells in premature births is also associated with the development of respiratory distress syndrome (Sweet et al., 2019). The type II cells are important as they play a crucial role in the maintenance of the structural integrity of the pulmonary alveoli and gas exchange facilitation. These cells are also liable to damage due to oxidative stress and therefore, triggering of respiratory distress syndrome in infants has a severe impact on these cells further resulting in cascade causing severe alveolar damage and limiting air ventilation in the body (Delara et al., 2019).
Respiratory distress syndrome is associated with multiple risk factors that can be classified into maternal and infant factors. Maternal factors that are associated with the disease include multiple pregnancies, elective caesarean section, gestational diabetes, and intrahepatic cholestasis of pregnancy. The infant factors that are associated with the respiratory distress syndrome include premature births, male gender, familial disposition, hypothermia, ethnicity, pulmonary infections, pulmonary hemorrhage, meconium aspiration syndrome, pulmonary hypoplasia, and congenital diaphragmatic hernia (Blondonnet et al., 2016). However, the greatest risk associated with the development of respiratory distress syndrome is premature birth or low gestational age. The development of disease in these cases is associated with poor surfactant production. About 50% of the infants that are born before 30 weeks of gestation are at risk of development of respiratory distress syndrome. About 60-80% of infants born at 26-28 weeks develop the syndrome, further, infants that are born between 32-36 weeks possess only a 15% chance of developing the respiratory distress syndrome providing a clear link between gestation period and disease incidence.
It has also been deduced that boys are more likely to develop the syndrome with a male to female ratio of 1.3:1 (Spinelli et al., 2020). This difference in the disease incidence has been associated with the androgenic action of the pneumocytes type II that delays the maturation of the surfactants. Ethnicity has also been associated with disease incidence in children. The disease incidence is higher in Caucasian children compared to infants of other races. Respiratory distress syndrome incidence in an infant has also been associated with multiple pregnancies in the mother. The second twin in multiple pregnancies is at higher risk of developing respiratory distress syndrome. The risk is more significant after a gestation of 29 weeks (Derwall et al., 2018). For infant born through caesarean section, the risk of development of respiratory distress syndrome is high and remains unaffected by the time of gestation period. This is associated with the delayed removal of the lung fluid and the lack of cortisol response that is associated with spontaneous labour (Spinelli et al., 2020).
Moreover, the health of the mother, in particular, maternal diabetes also plays an important role in the incidence of respiratory distress syndrome in infants. When the mother is diabetic the child possesses an abnormal pattern of surfactant synthesis. Insulin supplementation in the mothers for sugar control delays the development of type II pneumocytes. Familial incidence of respiratory distress syndrome has also been reported in certain cases where the genetic disposition of the health condition is under exploration. Partial or complete deficiency of gene SP-B has been found to be associated with the development of the disease that affects the surfactant production and disease development in the infants (Amigoni et al., 2017). Maternal health in terms of cholestasis is also important for the determination of the incidence of respiratory distress syndrome in the infants. It has been deduced that maternal intrahepatic cholestasis of pregnancy is significantly associated with the occurrence of the respiratory distress syndrome in the child. This has been associated as the bile acids have been known to deteriorate the surfactants in the alveoli triggering the syndrome. In certain cases, the disease can also be triggered by a secondary deficiency of surfactant due to intrapartum asphyxia and pulmonary infections (Monica et al., 2017).
The primary method of prevention of occurrence of the respiratory distress syndrome is to prevent premature births and provide complete gestational growth to the child. It is also crucial to prevent untimely cesarean births. Prevention of necrotic addiction in the mothers, and a healthy lifestyle during pregnancy and gestation period can also be helpful in limiting the innate causes of the respiratory distress syndrome in the infants (Amigoni et al., 2017). In certain cases, prophylactic surfactant administration is also done for the management of respiratory distress syndrome. This is a preventive measure where the endotracheal incubation and surfactant administration is done to the infants that possess a high risk of respiratory distress syndrome development. The surfactant replacement therapy is preferable for the infants that possess a great risk of the development of the syndrome. In certain cases where the fetus must be delivered between 24-34 weeks, the mother must be provided with a dose of Betamethasone 12mg intramuscular at the gap of 24 hours or in fractions of four doses at least 48 hours before the time of delivery. Administration of this drug promotes the surfactant production in the infant and thus prevents the severity of respiratory distress syndrome in the child (Monica et al., 2017). The neonates that are born before 30 weeks of gestation are also provided with the prophylactic intratracheal surfactant therapy to reduce the risk of deaths and pulmonary morbidity.
The treatment of the respiratory distress syndrome involves administration of intratracheal surfactant, oxygen supplementation, and mechanical ventilation. The intratracheal therapy with surfactant availability is done for the infants that develop the respiratory distress syndrome. The therapy requires endotracheal intubation and is necessary to achieve the required ventilation and oxygenation in the infants. However, less invasive ventilation techniques are also used in the treatment of the syndrome these therapies include nasal continuous positive airway pressure therapy (CPAP) and is commonly used with the premature infants (McPherson & Wambach, 2018). The infants with the respiratory distress syndrome that are receiving CPAP may still require an increasing fraction of the inspired oxygen are also known to benefit from incubation in conjunction with surfactant administration to enhance ventilation and limit the respiratory distress. The intratracheal surfactant in the infants has also been popularly administered with the use of a thin catheter to limit the cases of extensive respiratory problem and exacerbation.
This treatment procedure is found to be suitable as direct application of the surfactant is known to immediately help compensate the alveolar expansion and reduce the risks of development of interstitial emphysema, bronchopulmonary dysplasia, intraventricular hemorrhage, and pneumothorax emphysema (McPherson & Wambach, 2018). The common surfactants that are used for the treatment include Beractant, Poractant alfa, Calfactant, and Lucinatant. Beractant is a lipid bovine extract that is used in supplementation with the protein B and protein C and palmitic acid and the colfosceril palmitate. A dosage of mg/Kg is often prescribed for every six hours with about four doses needed on average. The Calfactant is a calf lung extract that is used as a surfactant and contains phospholipids, neutral lipids, fatty acids as well as protein B and protein C. The dosage required for its administration is 105mg/Kg in every 12 hours with the requirement of upto 3 doses in total. Another common surfactant used is the Lunicactant that is a synthetic surfactant and possesses the pulmonary surfactant protein B analog, known as the Sinapultide peptide (Kl4), fatty acids, and phospholipids. This surfactant is administered at dosage 175mg/Kg and is administered in ever six hours for 4 doses (Monica et al., 2017).
Effective management of the health condition of these children ensures that there is reduced mortality, reduced pulmonary air leaks and reduced need for invasive ventilation. In conjunction with these immediate benefits, long term benefits that include improved long-term neuro development of the infant reduced health care costs and reduced chances of development of bronchopulmonary dysplasia care also included (Chang et al., 2016). Therefore, the goal for the adequate management of the health condition of neonates that are suffering from the respiratory distress syndrome includes promotion of the survival without further complications of the risk and minimizing of the existing risks and adverse effects that may include pulmonary gas leaks and bronchopulmonary dysplasia. There are multiple therapies that exist for the management of the respiratory distress syndrome. For the management of the condition in children where the syndrome has manifested includes two major strategies. These are the administration of the antenatal glucocorticoids and thyroptin releasing hormone. The efficacy of the antenatal glucocorticoids has been assessed in multiple clinical trials for the respiratory distress syndrome in the infants (Chang et al., 2016).
The administration of antenatal glucocorticoids limits the incidences of neonatal deaths. It has been studied that, “intraventricular haemorrhage, necrotizing enterocolitis, infectious morbidity, need for respiratory support and neonatal intensive care unit admission” are all reduced by the administration of antenatal glucocorticoids (Jasani et al., 2016). The mechanism of action behind this management strategy is that the administration of the antenatal glucocorticoids accelerates the growth of the lungs with a multimodal action (Monica et al., 2017). Administration of antenatal glucocorticoids results in promotion of growth of type II pneumocytes and this, in turn, promotes surfactant production in the lungs. Another mode of management of the respiratory distress syndrome in the infants is done through the administration of thyroptin releasing hormone. The thyroptin releasing hormone contains thyroxine that enhances the surfactant production in the lungs. Unlike the thyroxine hormones T3 and T4, thyroptin releasing hormone readily crosses the placenta and enhances the production of surfactant phospholipids (Amigoni et al., 2017).
Oxygen therapy or oxygen supplementation is also done in the patients with the respiratory distress syndrome development through ventilation support to prevent hypoxia and further deterioration of the health. Mechanical ventilation is used and oxygen is often given through a nasal cannula or Hudson mask. Sedation of the patient is done to minimize the pain. Regular breathing tests are performed to ensure the efficacy of the treatment and management of the condition (Chang et al., 2016). Blood thinners are also provided to prevent clot formation and fluid build-up in the lungs is restricted through these management strategies. The stress ulcers of the stomach are also kept under management for the health condition in severe cases. To maintain the temperature of the child, the infant is placed in an incubator or a radiant heater bed.
It is also assured that a skin probe is placed at the mid epigastrium if the child with a reflecting tape. In the child shows signs of metallic acidosis due to the respiratory distress, slow infusions of sodium bicarbonate are used though peripheral IV administration (Jasani et al., 2016). Normal saline may also be administered in conjunction with high frequency ventilation to minimize the risk of barotrauma. It is critical that the fluid therapy of the infant is readjusted in every eight to twelve hours based on the intake and the output and serum electrolyte concentrations for complete recovery and respiratory distress management in the child. A chest film must be obtained immediately after the initiation of therapy and every 24 hours until complete stabilization of the infant (Amigoni et al., 2017).
This paper provides a complete description of the respiratory distress syndrome that occurs in the neonates and is one of the major causes of the child mortality and morbidity, The disease is caused when the alveoli collapse and fail to function properly resulting in the development of a hyaline matrix causing respiratory distress and hypoxia in the infants. This paper identifies the pathophysiology the respiratory distress syndrome and identifies that there are two primary causes of this syndrome. The etiology of the condition is either caused by the poor surfactant production or premature births where the pulmonary growth is compromised. The surfactant molecules cover the alveoli at the air and fluid junction and prevent their collapse. However, lack of adequate surfactant availability results in breathing complexity in the infants. This paper also identifies maternal as well infantal risk factors that are associated with the development of the health condition. The genetic and environmental risks are also included in this paper. Moreover, the prevention and treatment strategies that are associated with clinical practice for respiratory distress syndrome have also been highlighted with a coherent discussion on the management of the health condition in the neonates with both short term and long term benefits of successful management.
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