Respiratory distress syndrome is common breathing disorder and is a leading cause of death among the premature newborn (Kitano et al., 2018). It is a major health issue in newborns and a common reason for most of the infants admitted for neonatal intensive care. Around ten percent of the premature babies and twenty-seven percent of the late preterm infants develop respiratory distress syndrome. Infants born before thirty-four weeks of gestation are at higher risk of developing respiratory syndrome because they have difficulty in breathing because their lungs do not fully open.
They have not yet produce enough surfactant, a coating on the alveoli in the lungs that well-functioning of air exchanging sacs in the lungs (Gehlot et ak., 2020). Neonatal respiratory disease risk factors include caesarian section delivery, prenatal ultra-sonographic issues like struggling lung abnormalities, prematurity, gestational diabetes and meconium-stained amniotic fluid. Babies born at full term of gestation period rarely developed respiratory distress syndrome.
Preterm birth is a common risk factor for respiratory distress syndrome. This factor is due to various maternal risk factors such as low maternal body mass, periodontal diseases, previous preterm birth, poverty and poor parental care. Respiratory distress syndrome is caused by structural immaturity of the lungs and under development of surfactant (Suprenant &Coghlan, 2016).
The risk of premature babies developing respiratory distress syndrome increases with factors such as caesarean delivery, male sex and older sibling with respiratory distress syndrome. So, if the symptoms of respiratory distress in newborn are not recognized early enough it can lead to health issues, either short or long term such as respiratory failure, chronic lung diseases or even death (Katar & Degirmenci, 2019).
Health care practitioners in charge of the newborns should be able to readily recognize respiratory distress syndrome symptoms and signs from other similar health issues and therefore provide management approach so as to prevent short and long term complications or even death. Respiratory distress syndrome is a major cause of neonatal morbidity and mortality (Wickremasignhe & Neonatologist, 2017).
Healthy infants respiratory rate is thirty to sixty breaths per minute. However, when an infant’s respiratory rate is more than sixty breaths per minute might be due to respiratory distress signs. Increase in breathing rates in newborns could be as a result of nasal flaring, tachypnea and chest retractions (Katar & Degirmenci, 2019). The syndrome is more frequent in diabetic mothers and in male infants.
Pathophysiology of respiratory distress syndrome can be clearly understood through analysis of fetal surfactant metabolism and lung growth as well as risk factors. This report also analyzes preventive approaches of RDS.
Lung growth and development analysis is significant in understanding why and how respiratory distress syndrome occur. Lung development undergoes five main stages including embryonic stage, pseudo-granular stage, canalicular stage, saccular and alveolar stage in that order. During embryonic stage of lung development, trachea and both left and right main bronchi are formed while at pseudo granular stage, terminal bronchioles and conduction airwave are formed. At canicular stage, the alveolar ducts, respiratory bronchioles and separation of type I and type II pneumocytes take place. Finally, at saccular and alveolar stage, there is increment in gas exchange areas as well as septation and multiplication of alveoli. In this report it analyses the development of type II pneumocystis which are at the Centre of surfactant production and function. Type II pneumocytes are significant in maintaining structural development of alveoli and pulmonary (Saidha et al., 2020).
Surfactant overlies he alveolar surface and helps it in reducing the surface tension and therefore prevents alveolar from collapsing especially when end expiration causes low alveolar volumes. Surfactant reduces the pressure and maintains a satisfactory operation capacity during subsequent alveolar inflation. Therefore, lack of sufficient amount of surfactant in the pulmonary increases the risk of respiratory distress syndrome in infants and causes development of abnormalities of lung function as well atelectasis.
Low residual capacity in alveoli is experienced and may cause it to collapse at end-expiration. The pressure will be high in the lungs during inflation and therefore the work of breathing increases due to decrease in the lung compliance. Infants with respiratory distress syndrome mostly experience increased respiratory rate as the breathing system struggles to sustain ventilation in the alveolar (Wang et al., 2019). However, alveolar ventilation is inadequate because their alveolar have large physiological dead space and low tidal volume.
Coexistence of over inflation and atelectasis when an infant with RDS is receiving mechanical ventilation is likely to cause right –to-left shunting of inner walls of pulmonary as well as mismatching. This causes oxygen saturation and limits carbon dioxide excretion in pulmonary venous blood hence causing respiratory hypoxemia and acidosis. When hypoxemia persists for a long period it may cause reduced cardiac output, hypotension and metabolic acidosis. Metabolic acidosis increases resistance by the pulmonary vascular and reduces production of surfactant. When respiratory distress syndrome becomes severe, the arterial blood gases have mixed respiratory and metabolic acidosis (Bruschettini et al., 2020).
For an infant to maintain alveolar ventilation it generates higher negative pleural pressure and thus causing high rates of subcostal and intercostal recessions which leads to increased work of breathing. Many preterm babies are born with insufficient reserve of surfactant and therefore in early phase of respiratory distress syndrome the neonate has increased breathing works has it struggles to maintain sufficient ventilation. This is caused by fatigue and small quantities of the surfactant in the alveoli.
During early stages of lung injury due to respiratory distress syndrome, it causes leaking of proteins into the alveolar spaces and will further inhibit the small amount of surfactant present. In addition to acute lung injury, academia and hypoxemia affects the synthesis and functioning of the surfactant in the newborns with respiratory distress syndrome.
If respiratory distress syndrome is not detected early enough so that its treated and managed, at the age of 2-3 days’ production of endogenous surfactant commences and limits the clinical recovery from respiratory distress syndrome. Surfactant helps in reducing surface tension and therefore ensures achievement of optimum gas exchange through perfusion and ventilation matching. It improves lung compliance and decreases airwave resistance thus reducing work of breathing and improving functional residual capacity (Durmaz et al., 2016).
Prematurity is the greatest risk factor of respiratory distress syndrome due to low gestational age and thus impaired development of surfactant. Respiratory distress syndrome increases with decrease in the gestational age because RDS is due to immaturity of the lungs structure and surfactant deficiency.
Male infants are more likely to develop respiratory distress syndrome as compared to female.
The incidence of respiratory syndrome is greater in infants born through caesarean section delivery than for those born through vaginal delivery. Caesarean delivery and prematurity increases the risk (Durmaz et al., 2016).
When an infant is diagnosed with respiratory distress syndrome the newborn is usually admitted to a neonatal intensive care unit. Treatment involves either surfactant replacement therapy, oxygen therapy or use of a ventilator or nasal continuous positive airwave pressure machine.
The major risk factor of RDS is prematurity and thus poor development of the surfactant. Replacement of the surfactant in neonatal is done by use of a breathing tube. The breathing tube goes to the lungs and when the infant receives the surfactant, the infant is then connected to the ventilator to provide extra breathing support.
Oxygen therapy in neonatal involves delivering oxygen to the infant’s organs through the lungs so that the organs can function properly. Oxygen is delivered by use of ventilator or by nasal continuous positive airwave pressure.
Treatment of respiratory distress syndrome using a ventilator involves placing a tube down into the windpipe. It ensures the infant work breathing decreases since the ventilator breathes for the infant. a ventilator is used in a severe case of respiratory distress syndrome else a less invasive approach of using a nasal continuous positive airwave pressure machine is used.
From the Jack’s assessment data, it’s clear that he has respiratory health issues due to respiratory distress syndrome. Jack was delivered via vaginal delivery and his health was stable but a few hours of his life he starts to deteriorate. Infants with respiratory distress syndrome, usually present within the first few hours of life after delivery. Jack has respiratory distress with nasal flaring, subcostal or intercostal retractions and grunting. Grunting is due to struggle by the infant to sustain stable breathing while the lungs are not compliant.
Family centered care involves equal collaboration and participation by both the healthcare and family member teams. This will ensure information is unbiased and hence improve the quality of care. Jack’s mother and grandmother are involved in the care of jack at the neonatal unit. Parents can understand their babies well provide care with endless attention and affection. Jack’s mum when involved in decision making in health care provision will ensure that qualified care is provided in line with all considerations and preferences (Bruschettini et al., 2020).
Ability to readily recognize respiratory distress syndrome in the infants and comprehensive understanding of all the physiologic abnormalities will ensure optimal health care provision and management. However, Preventive measures are ideal for management of RDS when recognized early.
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Kitano, T., Takagi, K., Arai, I., Yasuhara, H., Ebisu, R., Ohgitani, A., & Minowa, H. (2018). Prenatal predictors of neonatal intensive care unit admission due to respiratory distress. Pediatrics International, 60(6), 560-564.
Saidha, S., Schneider, G., & Faria, J. (2020). A Newborn with Stridor and Respiratory Distress. JAMA Otolaryngology–Head & Neck Surgery, 146(2), 192-193.
Suprenant, S., & Coghlan, M. A. (2016). Respiratory distress in the newborn: An approach for the emergency care provider. Clinical Pediatric Emergency Medicine, 17(2), 113-121.
Wang, K. L., Suchomski, S. J., Goldstein, J. D., & Andreoli, S. M. (2019). Massive infantile myofibromatosis of the upper lip causing airway distress in a newborn. Auris Nasus Larynx.
Wickremasinghe, A. C., & Neonatologist, K. S. C. (2017). Respiratory Distress in the Newborn.
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