Neonatal Nursing: Respiratory Distress Syndrome - Essay Example

Neonatal Nursing: Respiratory Distress Syndrome Introduction One of the common problems encountered in preterm babies is respiratory distress syndrome (RDS), which is also known as hyaline membrane disease (Cloherty, 2004). RDS is a respiratory condition that occurs mostly in premature infants (Pramanik and Rosenkranz, 2009). The incidence and severity of this condition is inversely related to the gestational age of the newborn infant. The condition contributes to significant morbidity and mortality among preterm population because of which it has been extensively studied, leading to several advances in the treatment like administration of antenatal steroids, placental transfusion, continuous positive airway pressure or CPAP administration, bubble nasal CPAP, surfactant therapy and supportive therapy (Pramanik and Rosenkranz, 2009). All these have contributed to improvements in the morbidity and mortality of preterm babies with RDS. Important supportive therapies which have evolved are diagnosis and management of patent ductus arteriosus, management of fluids and electrolytes, usage of prophylactic flucanazole and trophic feeding and nutrition therapy (Pramanik and Rosenkranz, 2009). It is important for nurses working in neonatal intensive care units to monitor patients with RDS closely. In this essay, a premature neonate with RDS will be discussed. Appropriate, anatomy, physiology, pathyphysiology and management related to RDS will be discussed along with critical analysis and review of the treatment provided in the hospital. Neonatal patient Baby X, a male infant, was born on 21/4/2011 to a primigravida mother at 35 weeks of gestation through spontaneous normal vaginal delivery. The birth weight was 2832 grams. The mother conceived after in vitro fertilization. The baby was born in a good condition. APGAR Score at 1 minute was 9/10 and at 5 and 10 minutes was 10/10. Heart rate was more than 100 per minute. At 12 minutes of life, baby X was noticed to have sternal recession, nasal flaring and grunting because of which he was transferred to the neonatal unit. A diagnosis of respiratory distress, prematurity and ?sepsis was made. The baby was kept in an incubator for warmth. Intravenous cannula was inserted and blood samples sent for routine investigations and blood culture. The bay was started on 10 % dextrose solution intravenously at 60ml/kg/day. Chest X-ray was taken after 4 hours of life. CPAP was initiated. The chest X-ray was suggestive of respiratory distress syndrome. The CPAP requirement on the first day of life was CPAP 6 cm/h2o and 21 percent oxygen (air). The aim of saturations was atleast 94 percent. The baby was kept nil by mouth and broad spectrum intravenous antibiotics were started. On the second day, the baby was weaned from CPAP to nasal cannula oxygen. The intravenous fluids were increased to 90ml/kg/day with 10 percent dextrose. Intravenous antibiotics were continues while awaiting blood culture reports. The baby was continued to be Nil by Mouth and in incubator. Cranial ultrasound done of the third day of life was normal. The fluids were increased to 120 ml per kg per day. Gradually, naso- gastric feeds with formula milk were initiated and gradually increased. Intravenous fluids were proportionately decreased. Mild sternal recessions were noticed clinically. On the fourth day, the fluids were increased to 150 ml per kg per day and by fifth day, the baby was on full nasogastric tube feeds and off oxygen supplementation. Mother was encouraged to give breast feeds. Baby was transferred to the crib on the 6th day. On the 7th day, baby was on full breast feeds, feeding normally and tolerating well room air. He was then transferred to mothers side. The diagnosis on baby X was prematurity with respiratory distress syndrome. Diagnosis and clinical history RDS is frequent in white male preterm infants, gestational diabetes mothers, in preterm infants born through Caesarean section, second born twins and in those infants with family history of respiratory distress syndrome (Pramanik and Rosenkranz, 2009). RDS can also occur in those who suffered from intrapartum asphyxia, pulmonary hemorrhage, oxygen toxicity, meconium aspiration pneumonia, pulmonary hypoplasia and congenital diaphragmatic hernia (Pramanik and Rosenkranz, 2009). RDS incidence decreases with prolonged rupture of membranes, chronic maternal hypertension, use of antenatal steroids and maternal narcotic addiction (Pramanik and Rosenkranz, 2009). Physical examination findings are basically consistent with maturity assessment. Signs of RDS are progressive and include expiratory grunting, tachypnea, cyanosis, subcostal and intercostal retractions and nasal flaring (Cloherty, 2004). In neonates who are extremely immature, apnea and hypothermia may also be present. More often than not, several other conditions coexist with RDS and complicate its course. Some such conditions include metabolic problems, pneumonia, hematologic problems, transient tachypnea of newborn, aspiration syndrome, pulmonary air leak syndrome and congenital anomalies of the lung. Differential diagnosis of RDS include acute anemia, gastroesophageal reflux, aspiration syndrome, hypoglycemia, cardiopulmonary bypass, pneumomediastinum, pneumothorax, pneumonia, polycythemia, transient tachypnea of newborn and sudden infant death syndrome (Pramanik and Rosenkranz, 2009). A diagnosis of RDS is made based on clinical picture and some tests including chest X-ray. Chest X-ray reveals diffuse and bilateral reticular granular appearances, also known as ground-glass appearances, along with air bronchograms and poor lung expansion. Arterial blood gas analysis is very important to ascertain the degree of RDS and also response to treatment. The blood gas analysis reveals a mixture of metabolic and respiratory acidosis along with hypoxia. metabolic acidosis mainly occurs because of lactic acidosis secondary to anerobic metabolism and poor perfusion of the tissues. Respiratory acidosis occurs because of overdistension of the terminal airways and alveola atelectasis. Hypoxia occurs because of right-to-left shunts, patent ductus arterosus and patent foramen ovale (Pramanik and Rosenkranz, 2009). Oxygen saturation can be monitored non-invasively through pulse oximetry. The aim of treatment should be to maintain saturation above 90-95 percent with as much minimum oxygen supply as possible (Cloherty, 2004). In selected patients with murmur, echocrdiogram is performed to ascertain the degree of patent ductus arteriossus and also to evaluate the function and structure of the heart (Pramanik and Rosenkranz, 2009). Other tests are performed to assist the neonatologist to provide supportive treatment. Management of RDS begins from antenatal period. Mothers at risk for preterm delivery must receive antenatal steroids (Murphy et al, 2008). There is however controversy as to whether single or two doses of steroids must be administered. in institutions where two doses are given the duration between the doses is 12 hours. Multiple doses, weekly, in anticipated preterm deliveries also is a much debated issue with some studies pointing to the risk of cerebral palsy and intrauterine growth retardation in those who have received multiple doses and some studies refuting these findings (Wapner et al, 2007). Other strategies to prevent RDS include those to prevent preterm delivery like tocolytics, bed rest and antibiotics. Fetal lung maturity can be tested by estimating the lecithin-to-sphingomyelin ratio in the amniotic fluid obtained by amniocentesis. Another test is to ascertain the presence of phosphatidylglycerol in the amniotic fluid. In those with siblings affected with RDS, antenatal testing for SP-B must be done to rule out genetic causes of surfactant deficiency (Pramanik and Rosenkranz, 2009). Sequelae of RDS include bronchopulmonary dysplasia, septicemia, patent ductus arteriosus, apnea and bradycardia, pulmonary hemorrhage, retinopathy of prematurity, necrotizing enterocolitis, periventricular leukomalacia and intraventricular hemorrhage. Periventricular leukomalacia is associated with audiovisual and neurodevelopmental problems. Strategic goals of treatment of RDS include minimizing these sequelae (Pramanik and Rosenkranz, 2009). Chronological anatomy and physiology of lung Lungs begins to develop as a tracheal outgrowth from the foregut and completes in early childhood. There are 5 distinct stages of the organogenesis of the lung and they are the embryonic stage between 26-52 days, the pseudoglandular stage between 52 days to 16 weeks of gestation, canalicular phase between 17- 26 weeks of gestation, saccular stage between 24- 36 weeks of gestation and the alveolar atge between 36 weeks of gestation to 36 months postnatal. The infant under discussion is in the saccular or the terminal sac phase of lung development. In this phase, the pulmonary parenchyma grows and the connective tissue thins out between the air spaces. maturation of the surfactant system occurs during this phase. It is important to note that at birth, the lung is functional but structurally immature because of missing of the alveoli which are the main gas exchanging units. The airspaces that are present are the transitory ducts and saccules that are smooth walled with thick primitive septa and a double capillary network. Formation of alveoli occurs from 336 weeks onwards through a process of septation and because of this the surface area for gas exchange increases (Post and Copland, 2002). Morphogenesis of lung is a complex procedure and is influenced by several controlling factors like growth factors, transcription factors, integrins, extracellular matrix molecules and intercellular adhesion molecules. These factors, along with local gene networks influence the morphogenesis of the lung branching, the patterning of the endoderm, vascularization and response to mechanical stress (Post and Copland, 2002). Thus, the lungs of the 35 weeker is immature with no recruitment of alveoli and decreased production of surfactant. Added to these aspects, there are other aspects which makes it difficult for the neonatologist to intubate the baby. The head is large and needs to be stabilized during intubation. The neck is short and the tongue is large making the airway prone for obstruction. The nostril are small and become obstructed easily. The laynx is located more anteriorly and situated between C3-C4 vertebrae unlike in adults where it is situated at C6 (Pescod, 2005). The trachea is short and the right main bronchus is more angled than the left and hence right main bronchus intubations are more common. The narrowest part of the upper airways is the cricoid ring (Pescod, 2005). Pathophysiology The main cause of RDS is surfactant deficiency. Relative deficiency of surfactant leads to decreased lung compliance and functional residual capacity leading to increased dead space. This contributes to large ventilation-perfusion mismatch and also right-to-left shunt. The shunt may involve upto 80 percent of cardiac output (Pramanik and Rosenkranz, 2009). Macrosopically, the lungs in babies with RDS appear rudy and airless like liver (Pramanik and Rosenkranz, 2009). Thus, babies with RDS need more critical opening pressure to inflate the lungs. Microscopically, the lungs display diffuse atelectasis of distal air spaces along with distension of perilymphatic areas and also distal airways. the atelaectasis is progressive and this along with barotrauma and oxygen toxicity causes damage to the epithelial and endothelial cells that line the distal airways leading to exudation of the fibrinous matrix from the blood. The matrix forms the hyaline membrane that lines the alveoli. Hyaline membrane can form within half an hour after birth. In premature babies who are larger, endogenous surfactant synthesis begins within 36-76 hours after birth and this contributes to healing. In the recovery phase, the alveolar cells regenerate and thus increased production of surfactant is evident. In babies who are extremely premature, critically ill or born to mothers with chorioamnionitis, bronchopulmonary dysplasia, a chronic lung condition can occur (Pramanik and Rosenkranz, 2009). Surfactant is a complex lipoprotein that is made up of 4 apoproteins and 6 phospholipids. The the principle phospholipid is dipalmitoyl phosphatidyl choline, also known as lecithin. However, the marker for lung function is phosphatidyl glycerol which is actually not essential for normal lung function. The four apoproteins are SP-A, SP-B, SP-C and SP-D. SP-B and SP-C are apoproteins which comprise of 2-4 percent of the total surfactant and are present in commercially available surfactant preparations. Both of them work in concert and facilitate adsorption and spread of lecithin (Hawgood and Clements, 1994). Lecithin, when spread across the alveoli decrease the surface tension at the alveolar air-fluid interface during expiration, preventing atelectasis. SP-B and SP-C enhance the spreading, stability and adsorption of surfactant lipids that are essential to decrease the surface tension of the alveolus. Deficiency of SP-B manifests are respiratory distress syndrome with pulmonary hypertension or even congenital alveolar proteinosis. Deficiency of this apoprotein can occur in near-term and term babies also and cn contribute to RDS and death in them. SP-A regulates inflammation of the lung. It binds to various microorganisms and facilitates phagocytosis and their clearance from lungs. SP-D also has similar functions. Components of pulmonary surfactant are mainly synthesized in the Golgi apparatus of the type-2 alveolar cells. These components are packaged in multilamellar vesicles and secreted through exocytosis (Hawgood and Clements, 1994) . Impairment of surfactant synthesis in premature infants leads to atelectasis, ventilation-perfusion inequality and hypoventilation. All these amount to hypoxemia and hypercarbia. The patients develop metabolic and respiratory acidosis too, because of which pulmonary vasoconstriction occurs. This leads to impairment in the epithelial and endothelial integrity with protein exudate. The exudate forms the membrane and this is known as the hyaline membrane. Surfactant production may be further imapired by acidosis, hypoxia, hypothermia and hypotension. The premature and atelectatic lungs are easily vulnerable to oxygen toxicity, volutrauma and barotrauma, which easily cause influx of inflammatory cells, thus exacerbating vascular injury that eventually leads to bronchopulmonary dysplasia. The injury is worsened in the presence of free-radical injury and antioxidant deficiency (Pramanik and Rosenkranz, 2009). Observation series Delivery of a preterm baby must be attended by an experienced neonatologist. This is more so in case of preterm babies who are less than 28 weeks of gestation. These neonates are at increased risk of maladaptation leading to further inhibition of the production of surfactant. The patient under study is a 35 weeker. He was initiated on CPAP soon after RDS was diagnosed. One potential alternative for immediate intubation is continuous nasal positive airway pressure in those premature infants who are breathing spontaneously (Murray et al, 2008). Such an intervention decreases the risk of development of severe bronchopulmonary dysplasia. Nasal bubble CPAP is an useful strategy in this regard. There are reports than application of CPAP soon after birth in the delivery room itself, decreases the need for intubation and mechanical ventilation (Pramanik and Rosenkranz, 2009). The advent of artificial surfactant therapy has decreased the mortality rate associated with RDS by atleast 50 percent. Several trials have proved that it is useful to administer surfactant early, followed by rapid extubation to nasal CPAP. Such a strategy has proven to extubate the neonates rapidly, thus preventing other mechanical ventilation problems (Pramanik and Rosenkranz, 2009). Intratracheal surfactant must be administered in babies with RDS whose oxygen requiremnt is more than 0.4. The best time for administering surfactant is within 2 hours after birth. According to a metanalysis by Stevens et al (cited in (Pramanik and Rosenkranz, 2009)), early surfactant with extubation to nasal CPAP decreases the need for mechanical ventilation, bronchopulmonary dysplasia and air leak syndrome when compared to administration of surfactant in later phase along with mechanical ventilation. It has been indicated that administration of surfactant in the delivery room may have better outcomes especially in those who are extremely premature. Infact, it is recommended to administer surfactant routinely as a prophylaxis in all neonates born less than 27 weeks of gestation (Cloherty, 2004). Baby X improved with just CPAP support and did not require surfactant therapy. Baby X was initiated on CPAP on Day-1 and weaned to nasal cannula oxygen on Day-2. CPAP keeps the alveoli of the lungs open during the end of expiration, thus decreasing right-to-left shunt. It is administered using nasal prongs. There are several types of prongs for CPAP and the most useful of them are short binasal prongs because these reduced the chances of reintubation. CPAP may be used as an adjunct to surfactant therapy or as a respiratory support after extubation (Pramanik and Rosenkranz, 2009). The goal of therapy in respiratory distress syndrome is to maintain pH between 7.25- 7.4, paO2 of 50-70 mmHg and pCO2 of 40-65mmHg (Pramanik and Rosenkranz, 2009). Supportive therapy 1. Regulation of temperature It is very important to regulate the temperature in preterm infant with RDS because hypothermia increases the consumption of oxygen and thus further compromises the clinical condition in the patients. Thus, it is very important to prevent hypothermia in the delivery room, during resuscitation and also during transport. Neutral thermal environment can be provided using double walled incubator or a radiant warmer. Hence baby X was kept in incubator. 2. Fluids, electrolytes and nutrition Baby X was started on 10 percent dextrose at 60ml per kg per day and then gradually increased. In babies with RDS, the initial intravenous fluid that must be initiated is 5-10 percent dextrose at a rate of 60-80 ml per kg per day. The blood sugar levels must be monitored closely along with serum electrolytes, serum calcium and phosphorus and also renal function and input-output balance. Body weight and urine output must be recorded to gauge any fluid imbalances. It is important to add calcium to the initial intravenous fluids. However, intravenous sodium bicarbonate does not have much role. Electrolytes must be added after the baby starts passing urine and also based on serum electrolyte values. The fluid intake must be gradually increased o 120-140 ml per kg per day. In extremely premature babies with large body surfaces, since the insensible losses can be very high, the fluid intake can be increased to 200- 300 ml per kg or even more. Once the neonate is stable, intravenous nutrition inclusing amino acids and lipids, known as total parenteral nutrition must be initiated within 24- 48 hours after birth. Oral feeds must be initiated as soon as possible and trophic feeds with breast milk must be provided. the feeds are given with orogastric tubes to stimulate the development of the gut. the feeds are increased as tolerated and intravenous fluids are decreased proportionately. It is very important to provide adequate micronutrients, macronutrients, antioxidants and vitamins for optimal brain, lung, eye and somatic development (Pramanik and Rosenkranz, 2009). Cardiovascular and circulation The condition of the baby must be monitored using parameters like blood pressure, peripheral perfusion and heart rate. Suitable volume expanders and vasopressers must be given to maintain adequate perfusion and blood pressure. packed cell transfusion must be administered if needed. Blood loss and anemia can be prevented by placental transfusion at the time of delivery and also by limiting the quantity of blood drawn for blood tests. In extremely premature neonates, erythropoietin may be useful (Pramanik and Rosenkranz, 2009). Antibiotics Antibiotics must be initiated routinely in all babies with RDS after taking blood samples for culture. The antibiotics must be discontinued if the cultures are negative and no maternal risk factors are present (Pramanik and Rosenkranz, 2009). Baby Xs antibiotics were discontinued once the cultures were negative. Conclusion Respiratory distress syndrome almost exclusively occurs in preterm infants and must be suspected in any preterm baby with respiratory distress. It occurs mainly due to relative surfactant deficiency. The main crux of treatment is CPAP and surfactant therapy along with supportive therapy. Surfactant many not be necessary in bigger babies like baby X. Supportive therapy includes fluid and electrolytes management, nutrition, warmth, and control and prevention of infection. It is very important to manage RDS appropriately because of the devastating sequelae associated with it. References Cloherty, J.P., Eichenwald, E.C., and Stark, A.R. (2004). Manual of Neonatal Care. London: Lippincott. Hansen, B.M., Hoff, B., Greisen, G., et al. (2004). Early nasal continuous positive airway pressure in a cohort of the smallest infants in Denmark: neurodevelopmental outcome at five years of age. Acta Paediatr., 93, 190-195. Hawgood, S., Clements, J.A. (1990). Pulmonary surfactant and its apoproteins. J Clin Invest., 86(1), 1-6. Murray, P.G., Stewart, M.J. (2008). Use of Nasal Continuous Positive Airway Pressure During Retrieval of Neonates With Acute Respiratory Distress. Pediatrics.,121, e754-e758. Pramanik, A.K., Rosenkranz, T. (2009). Respiratory Distress Syndrome. Medscape Reference. Retrieved from http://emedicine.medscape.com/article/976034-treatment#showall Pescod, D. (2005). Pediatric Anatomy and Physiology. Retrieved from http://www.developinganaesthesia.org/index2.php?option=com_content&do_pdf=1&id=48 Post, M., and Copland, I. (2002). Overview of lung development. Acta Pharmacol Sinica, 23, 4-7. Murphy, K.E., Hannah, M.E., Willan, A.R., et al. (2008). Multiple courses of antenatal corticosteroids for preterm birth (MACS): a randomised controlled trial. Lancet, 372, 2143-2151. Wapner, R.J., Sorokin, Y., Mele, L., et al. Long-term outcomes after repeat doses of antenatal corticosteroids. New England Journal of Medicine, 357, 1190-1198. Read More