Developed by - Lisa Fikac, MSN, RNC-NIC. Original Author - Stacey Cashwell, MSN, RN. Expiration Date - 10/2/14

Transcription

1 Developed by - Lisa Fikac, MSN, RNC-NIC Original Author - Stacey Cashwell, MSN, RN Expiration Date - 10/2/14

2 This continuing education activity is provided by Cape Fear Valley Health System, Training and Development Department, which is an Approved Provider of Continuing Nursing Education by the North Carolina Nurses Association, an accredited approver by the American Nurses Credentialing Center s Commission on Accreditation. 1.3 Contact hours will be awarded upon completion of the following criteria: Completion of the entire activity Submission of a completed evaluation form Completion of post-test with a grade of at least 85%. The planning committee members and content experts have declared no financial relationships which would influence the planning of this activity. Microsoft Office Clip Art is the source for all graphics unless otherwise noted.

3 Describe the etiology of Respiratory Distress Syndrome (RDS) Discuss the clinical presentation, management, complications, and outcomes of RDS

4 As with most disease processes, it is helpful to understand the background of the particular disease. Since Respiratory Distress Syndrome (RDS) and each baby's individual course depend on his particular point of lung development, let's look at the course of pulmonary development from fetal through postnatal life... The development of the lungs is sequential and occurs in five phases - Embryonic phase Pseudoglandular phase Canalicular phase Saccular phase Alveolar phase The embryonic phase occurs between 4 to 6 weeks gestation The main event of this phase is formation of the proximal airway Lung buds appear and begin to divide The pulmonary vein appears during this phase and elongates to join the lung buds The trachea develops, and by the end of this period there are - o Three divisions of primitive lobes and bronchi on the right o Two divisions of primitive lobes and bronchi on the left The pseudoglandular phase occurs between 7 to 16 weeks gestation The main event of this phase is the formation of conducting airways At this time cartilage appears, and the main bronchi develop The tracheobronchial tree branches into the trachea and terminal bronchioles o After this occurrence, the tree only increases in size and length without additional formation of branches The major lobes of the lungs are identified, and the capillary bed is formed

5 o This connects the bronchial blood supply but does not connect with the terminal air sacs The connective tissue, muscle, and lymphatics are identifiable The canalicular phase occurs between 17 to 28 weeks gestation The main event of this phase is the formation of the acini During this phase, Type II alveolar epithelial cells that eventually become the alveolar lining begin to appear Capillaries begin to proliferate and invade the walls of the terminal airways The airway structure changes from glandular to tubular and increases in size and length Lung fluid production begins during this period o Using extrapolated data derived from studies of lambs, it is believed that the term infant secretes about 250 ml/day of lung fluid o A reduction in amount or loss of lung fluid may result in lung hypoplasia o Lung fluid aids in the - Development and maturation of lung cells Formation, size, and shape of the air space Alveolar sacs appear between weeks gestation Keep in mind that during this phase of development - o There is insufficient air-blood surface area for gas exchange o Type II alveolar epithelial cells are incapable of releasing sufficient surfactant to sustain adequate respirations The saccular phase occurs between 29 to 35 weeks gestation The main event of this phase is the development of gas-exchange sites Terminal air sacs appear as an out-pouching of the alveolar ducts, or terminal bronchioles o The air sacs look like a "bunch of grapes" o The alveolar ducts increase in number and maturity Mature type II alveolar epithelial cells begin to cluster at the alveolar ducts Capillaries and vascularization increase with the eventual fusion of the endothelium and epithelium o This creates the blood-gas barrier needed to sustain extrauterine life The overall size of the lungs increases quickly

6 At approximately weeks, there is sufficient differentiation in the lung structures and cells to allow oxygen exchange to occur o In other words, extrauterine life can be sustained The alveolar phase occurs between 36 weeks gestation and continues through postnatal life until approximately 8 years of age This phase is marked by the expansion of gas-exchange surface area and continued proliferation of the alveoli The alveolar wall and interstitial spaces become very thin, and the single capillary network comes into close proximity to alveolar membrane

7 The lungs are elastic organs that contract like a balloon and expel air through the upper airway structures (e.g., bronchi, trachea) This natural physiologic tendency of the lungs to contract is known as recoil tendency Two factors that contribute to recoil tendency are - The presence of elastic fibers throughout the lung tissue which are stretched by inspiration or chest expansion and attempt to contract back to their original shape o Approximately one-third of the lungs' tendency to contract can be attributed to this factor Surface tension of the fluid lining the alveoli o Approximately two-thirds of the lungs' tendency to contract can be attributed to this factor o The forces of surface tension act on air-fluid interfaces causing water to "bead up". A surface-active compound, like soap or surfactant, reduces the surface tension and lets the droplet spread out in a thin film o Surface tension forces in the lung tend to cause alveoli to collapse. A compound, such as surfactant, reduces surface tension and allows the alveoli to remain open Surfactant is the primary surface-active agent present in the lungs, and it greatly reduces the surface tension of water Fetal lungs excrete surfactant into the amniotic fluid and can be detected during pregnancy It is composed of the following phospholipids - Lecithin Sphingomyelin Cholesterol Phosphatidylinositol (PI) Phosphatidylcholine (PC)

8 Phosphatidylglycerol (PG) The role of surface-active phospholipids, such as surfactant, is to - Line the terminal air sacs which are composed mainly of Type I and Type II pneumocytes o Type I pneumocytes cover ~ 95% of the alveolar surface which is where gas exchange occurs o Type II pneumocytes are greater in number but cover < 5% of the alveolar surface It is believed that surfactant is produced and secreted by these cells They first appear around weeks gestation Surfactant is first detectable at about seeks gestation The neonate is able to maintain alveolar stability at about weeks gestation Maintain alveolar stability by reducing surface tension at the air-fluid interface o Surface tension pressures in the lungs generally cause the alveoli to collapse o Surface-active agents reduce the surface tension allowing the droplet to smooth to a thin film that allows the alveoli to remain open and gas exchange to occur Surfactant is essential to normal lung function because it - Decreases surface tension at the end of expiration AND Increases surface tension during inspiration, or lung expansion Surfactant prevents atelectasis at the end of expiration and facilitates elastic recoil on inspiration, stabilizing the lungs to maintain acceptable blood gas pressures and decrease the work of breathing. Changing levels of surfactant components can aid in determining fetal lung maturity Lecithin and phosphatidylinositol (PI) levels remain low until about weeks' gestation o These levels increase rapidly after this and peak at 36 weeks gestation Sphingomyelin levels remain stable, with a small peak occurring between weeks gestation Phosphatidylglycerol (PG) appears at about weeks gestation and increases until term o Some health care providers question if this is more indicative of lung maturity than the lecithin/sphingomyelin (L/S) ratio The L/S ratio may be used to assess lung maturity

9 A ratio of >2:1 is considered a mature ratio o At weeks gestation, sphingomyelin is slightly higher than lecithin o At weeks gestation, there are equal amounts of both o At >32 weeks gestation, there are increasing amounts of lecithin and decreasing amounts of sphingomyelin Infants of diabetic mothers (IDM) may develop RDS despite a mature L/S ratio due to deficient or delayed surfactant production o Fetal hyperinsulinism may adversely affect lung maturation by antagonizing the action of cortisol Chronic fetal stress accelerates surfactant production allowing for a mature L/S ratio in premature infants Other Factors Affecting Fetal Lung Development Glucocorticoids affect surfactant synthesis and enhance elastin and collagen production which improves lung compliance Glucocorticoids have demonstrated a positive effect on lung maturation and may be useful in minimizing or preventing RDS The administration of antenatal steroids is most effective in the fetus ~ weeks gestation when given at least 48 hours prior to but no longer than 7 days prior to delivery The primary steroids used are betamethasone or dexamethasone and are given as a multidose series, not a single dose o Betamethasone is usually considered the first steroid choice because of improved safety and effectiveness o Dosage and dosing interval may vary with the specific drug selected Antenatal steroids may be given along with tocolytic agents used to stop premature labor Contraindications of antenatal steroids include - o The presence of prolonged rupture of the membranes since this may obscure an infectious processes o Systemic fungal infection o Diabetic ketoacidosis o Long-term, high dose therapy since it may result in renal suppression o Large doses since it may cause hypokalemia, especially if the mother is receiving diuretic therapy Catecholamines stimulate the secretion of surfactant into the alveolar space This results in an increase in surfactant and saturated phosphatidylcholine (PC) in the lung fluid and improved lung stability o This is supported by an increased L/S ratio

10 Catecholamines inhibit fetal lung fluid secretion and promote reabsorption of the fluid within the alveoli at the time of delivery o These processes work together to prepare the fetus for the transition to pulmonary-based respirations Hyperinsulinemia inhibits surfactant development in the infant of the poorly controlled diabetic mother Fetal hyperinsulinism adversely affects fetal lung maturation by antagonizing the action of cortisol So, what is the actual cause...is it hyperinsulinemia???...is it hyperglycemia???...or is it both??? o Insufficient data is available to definitively support either conclusion. Therefore, further research is needed! Although the mechanism of action is uncertain, it is thought that insulin interferes with the glucocorticoids necessary for the production of surfactant Pulmonary maturation may be accelerated by any condition that places chronic stress on the fetus, such as - Hypertensive disorders o Pregnancy induced hypertension (PIH) o HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome o Cardiovascular-related disorders o Renal-related disorders Maternal drug use during pregnancy Smoking during pregnancy Maternal health issues such as - o Hemoglobinopathies o Sickle cell disease o Diabetes mellitus (Class F-T) o Hyperthyroidism o Maternal steroid administration Chorioamnionitis Placental insufficiency or infarction Prolonged rupture of the amniotic membranes Placental bleeding Pulmonary maturation may be delayed by -

11 Maternal factors o Poorly controlled diabetes mellitus - Class A, some Class B and C o Non-hypertensive chronic glomerulonephritis Fetal factors o Acidosis o Hypovolemia o Erythroblastosis fetalis o Intrapartum asphyxia Postnatal factors o Hypothermia o Acidosis o Hypovolemia The following prerequisites must be met for gas exchange to occur - Ample terminal air sac development to provide adequate surface area for gas exchange Thinning of the alveolar walls to support effective gas exchange of O 2 and CO 2 Approximation of the capillaries and terminal air sacs for effective gas exchange Adequate surfactant production to stabilize the alveoli

12 In theory, the fetus does not have respirations because there is no air to breathe in the amniotic fluid, but respiratory movements do occur and begin around the end of the first trimester In utero, tactile stimuli, like brushing against uterine wall or movement of cord, and fetal asphyxia trigger these movements For unknown reasons, these respiratory movements usually disappear during the third trimester During the third trimester, the lungs remain collapsed This minimizes filling of the lungs with fluid and/or debris found in the amniotic fluid, but the alveolar epithelium does secrete small amounts of fluid into the alveoli up to the time of delivery o This helps to maintain only clean fluid in the lungs At birth, the infant begins to breathe within seconds after delivery and establishes normal respiratory effort during the first minute of life Effective respirations with sufficient inspiratory pressures open the alveoli o Newborns are usually able to generate sufficient inspiratory pressures to accomplish this feat Once the alveoli are opened, the respiratory effort needed to maintain open alveoli is minimal o This means the second and subsequent breaths are much easier for the infant Certain "at risk" infants are unable to accomplish this transition and develop respiratory distress syndrome (RDS) during the early hours of life

13 Since type II pneumocytes do not secrete surfactant until the last 1-3 months of gestation, premature and even a few term infants are "at risk" for developing RDS

14 Respiratory distress syndrome (RDS) is a disorder of the lungs that appears at or shortly after birth RDS is primarily a disease of immaturity of the anatomy and physiology of the lungs The alveolar epithelium fails to secrete an adequate amount of surfactant to decrease the surface tension of the alveolar fluid and allow easy alveolar opening during inspiration RDS is the most common cause of respiratory failure in the newborn Approximately 20,000 to 30,000 infants per year are affected by RDS Other historical names for RDS include hyaline membrane disease (HMD) and Mikity- Wilson Disease So, what exactly is going on? Anatomically, the premature infant's pulmonary structures and alveoli are not sufficiently developed There is a diminished pulmonary capillary bed and surface area for gas exchange The interstitial distance is increased between the alveolar and endothelial cell membranes, making gas exchange more difficult The lungs have an inability to maintain expansion Therefore, the lung tissue is unable to support oxygenation and ventilation Physiologically, surfactant production and excretion is insufficient to maintain alveolar stability and prevent alveolar collapse This reduces lung compliance which prevents the establishment of a normal functional residual after each breath This can lead to - o Diffuse areas of atelectasis in the lungs o Compromise of oxygenation and ventilation

15 o An increase in energy expenditure for the infant to breathe

16 The incidence of RDS is inversely related to gestational age So, the lower the gestational age of the infant, the higher the incidence of RDS RDS affects ~ 10% of all premature infants The majority of infants who develop RDS are born at <28 weeks gestation RDS occurs more frequently in males with a ratio of 2:1 (male:female) Risk Factors There are multiple risk factors that predispose an infant to develop RDS. Those risk factors include - Premature birth is the single most common cause of RDS o Surfactant store are quickly consumed after birth o The pulmonary system is anatomically immature Chronic intrauterine stress, which may include the following etiologies - o Prolonged rupture of membranes o Maternal hypertension o Maternal narcotic/cocaine use o Intrauterine growth restricted (IUGR) or small for gestational age (SGA) infants Maternal diabetes can result in decreased or inadequate surfactant production o Especially if the infant is <37-38 weeks gestation o Fetal hyperinsulinism may adversely affect lung maturation by antagonizing the action of cortisol Elective Cesarean birth, especially without labor o There is a decrease in production of prostaglandin o There is increased pulmonary vascular resistance Pulmonary hypoperfusion due to an acute antepartum hemorrhage Asphyxia at birth and/or in the early hours of life Second born twin

17 o This may be due to a greater risk of asphyxia Siblings of a former low birthweight infant with a history of RDS

18 Frequently, the infant who presents with RDS is the preterm infant who appears to be of an appropriate for gestational age (AGA) size, with good Apgar scores, and otherwise looks healthy Respiratory distress begins shortly after birth with worsening pulmonary insufficiency during the first 24 to 48 hours of life The infant presents with increasing respiratory difficulty with results in hypoxia and hypoventilation There are several differential diagnoses to consider when assessing respiratory distress. Potential diagnoses include - Pneumonia Transient tachypnea of the newborn (TTN) Pneumothorax Anomalies of the respiratory system Physical assessment findings include - Respiratory rate may exhibit the following variations - o Tachypnea - RR >60 breaths per minute o Periodic breathing - cyclic periods of apnea that may last 5-10 seconds with ventilation lasting seconds o Apnea - periods of not breathing that lasts longer than 20 seconds and may be accompanied by bradycardia, cyanosis, hypotonia, or pallor Work of breathing may exhibit the following variations - o Retractions - the premature infant's chest wall has weak structural support Considerable negative pressures is required to open the alveoli and maintain a residual capacity Collapsed airways cause retractions and deformity of the chest wall instead of expansion of the poorly compliant lungs Retractions may include supraclavicular, sternal, substernal, and intercostal

19 o Nasal flaring - an attempt to increase oxygen intake by decreasing airway resistance o See- saw respirations - may be seen as a sign of respiratory failure Oxygen requirement - increasing Color may exhibit the following variations - o Pink - initially o Acrocyanosis - normal for the first 24 hours of life o Central cyanosis - a late and serious sign Cyanosis requires a large change in PaO 2. So, the lack of cyanosis does not necessarily mean that the infant is not experiencing problems Breath sounds may exhibit the following variations - o Expiratory grunting - an inborn CPAP mechanism where the infant tries to exhale against the partially closed glottis in order to maintain alveolar distention o Decreased breath sounds o Râles Cardiovascular findings may include - o Tachycardia - HR > bpm o Murmur - A patent ductus arteriosus (PDA) murmur may be heard after the first 24 hours of life PDA with a right-to-left shunt diminishes blood flow to the pulmonary artery and pulmonary system resulting in hypoxia, hypoxemia, acidosis, and cardiomegaly Blood flow to the aorta and systemic circulation is increased, potentially causing cardiomegaly, edema, and changes in peripheral pulses PDA with a left-to-right shunt diminishes blood flow to the aorta and systemic circulation, potentially compromising perfusion to the brain, gastrointestinal (GI) tract, kidneys and myocardium Blood flow increases to the pulmonary artery and pulmonary system, leading to pneumonia and/or congestive heart failure (CHF) o Delayed capillary refill time - > 3 seconds o Hypotension is not routinely seen, but may occur Oliguria is common in the first 48 hours of life o This is most likely due to hypoxia, hypotension, and/or shock Diagnostic studies used include - X-ray findings may include -

20 o Small lung volumes o Hazy lung fields o Fine, reticulogranular pattern of density with air bronchograms - "groundglass" appearance This is caused by areas of atelectasis adjacent to areas of hyperexpanded alveoli Arterial blood gases (ABGs) demonstrate - o Hypoxemia - PaO 2 < 50 mmhg in room air o Hypercapnea or hypercarbia - increased PaCO 2 level o Acidosis - may have respiratory, metabolic, or mixed causes An echocardiogram may be done to evaluate for the presence of a PDA Laboratory tests o Hemoglobin (Hgb) helps to rule out anemia and polycythemia as the cause of respiratory distress o CBC with differential and C- reactive protein (CRP) may be used to rule out sepsis o Electrolytes helps to rule out hypo/hypernatremia, hypocalcemia, hypoglycemia as possible causes of respiratory distress

21 RDS is a disease that is self-limited until the infant can produce adequate amounts of surfactant at about hours of age Of course, the best course of action is to prevent or lessen the course of RDS. This may be accomplished by - Administration of antenatal steroids Use of L/S ratio, fetal lung maturity, and PG determination to assist in timing for labor induction or elective Cesarean birth No elective deliveries prior to 39 weeks gestation Perinatal management to avoid pulmonary circulation compromise in the infant o Prenatal management of - Maternal hypotension Avoidance of over sedation Maternal hypoxia Fetal distress o Postnatal management of - Resuscitation without delay Correction of hypoxia and/or acidosis Treatment of hypovolemia Monitoring of temperature and blood glucose to avoid hypothermia and hypoglycemia RDS treatment goals are to - Provide sufficient support to prevent atelectasis of alveoli, hypoxia, hypoxemia, and hypercapnea Prevent additional lung injury Surfactant Replacement Therapy The benefits of surfactant replacement therapy include - Reduction in mortality and morbidity

22 Improvement in lung compliance and decreased resistance which reduces the pressure require to inflate the lungs and decreases the infant's work of breathing Improves ventilation which increases PaO 2, decreases right-to-left intrapulmonary shunting, and improves overall oxygenation Available FDA approved surfactant products include - Beractant (Survanta ) - bovine lung extract Poractant alfa (Curosurf ) - porcine lung extract Calfactant (Infasurf ) - calf lung extract There are two treatment methods which are related to timing - Prophylactic treatment for infants < 27 weeks gestation o Endotracheal tube administration of surfactant is done soon after birth Rescue treatment may be given to infants who experience an increasing oxygen requirement during the first day of life, usually > 40% FiO 2 o Multiple doses may be given o Infants who received prophylactic surfactant replacement may also receive rescue treatment o The goal is to avoid progressive alveolar atelectasis Surfactant replacement requires endotracheal intubation for administration However, there is an alternative surfactant administration where the infant is intubated, surfactant is given, and the infant is extubated. This is known as the INSURE technique Respiratory Support The previous standard of treatment for RDS was mechanical ventilation This treatment is invasive and damages the lungs further and may lead to bronchopulmonary dysplasia (BPD)

23 The immaturity and vulnerability of preterm infant lungs in combination with mechanical ventilation contribute to barotrauma, volutrauma, and oxygen toxicity This creates injury that can lead to pulmonary edema, inflammation, and fibrosis which increases the risk of infection and the need for long-term oxygen therapy Currently, the goal of respiratory support is promote early extubation and transition the infant to continuous positive airway pressure (CPAP) as soon as possible to minimize the length of time on mechanical ventilation. CPAP can help to - Establish and maintain an adequate functional residual capacity which supports the release of endogenous surfactant AND Prevent additional damage created by the use of mechanical ventilation CPAP is most often given through the nasal route and may be used in conjunction with caffeine citrate. Caffeine is used for its respiratory stimulation properties The degree of respiratory support required varies for each infant. Some infants may require mechanical ventilation, while others require CPAP or high-flow nasal cannula Mechanical ventilation may be used for infants with profound hypoxemia and/or hypercapnea Oxygenation is monitored through pulse oximetry, and oxygen should be titrated based upon target saturations for the infant - < 1500 grams % * > 1500 grams % * * This practice may vary depending on institution ABGs or capillary blood gases (CBGs) are monitored with the following targets -

24 ABG CBG ph PaCO mmhg mmhg PaO mmhg mmhg - not useful for assessing oxygenation Pulmonary status may also be monitored with chest x-rays as needed. X-rays help - Document changes and improvement or deterioration of disease Validate endotracheal tube and umbilical line placement Document complications - o Pneumonia o Pneumothorax o Necrotizing enterocolitis (NEC) Implications for future practice include the consideration of - Initial management of spontaneously breathing infants with nasal CPAP Using the INSURE method for administration of surfactant Extubation as soon as possible in conjunction with each individual infant's needs Cardiac Support In caring for the infant with RDS, it is important to monitor the infant for signs of shock and/or hypotension such as - Weak peripheral pulses Decreased perfusion o Mottling skin o Coolness to touch o Prolonged capillary refill time > 3 seconds Changes in color o Pallor o Cyanosis

25 Heart rate o Bradycardia (HR < 100 bpm) With evidence of poor perfusion may be a sign of imminent cardiac arrest o Tachycardia (HR > 180 bpm) This can be an indication of poor cardiac output and/or congestive heart failure Blood pressure - hypotension is a late sign of cardiac decompensation When treating shock and/or hypotension, it is important to treat the underlying cause. Therefore, treat - Cardiogenic shock potential causes - o Hypoxia o Hypoglycemia o Hypothermia o Acidosis o Infection o Electrolyte imbalance Hypovolemic shock potential causes - o Intrapartal blood loss (e.g. placental abruption, twin-to-twin transfusion, etc.) o Postnatal hemorrhage (e.g. brain, lung, scalp) Septic shock The infant with RDS who is in shock and/or who has hypotension may need - Volume replacement o Normal saline, lactated ringers, or blood products o 10 ml/kg over minutes Inotropic support o Dopamine - first choice Lower doses are associated with improved renal perfusion and increased urine output Higher does cause vasoconstriction and increased BP o Dobutamine - second choice Has more effect on cardiac output than dopamine but less effect on BP Keep these basic principles in mind when administering inotropes - If the infant is hypovolemic, provide volume first

26 Administration through a central venous line is preferred, but inotropes may be given through a large vein IV o Monitor the peripheral IV site frequently for signs of extravasation The infusion is given continuously on an IV pump Begin the infusion at lower doses and titrate to the infant's response Monitor the infant's HR and BP closely Fluid and Nutrition Adequate treatment of RDS includes provision of appropriate fluids and electrolytes. This includes the following - Accurate measurement of intake and output Monitoring for signs of dehydration or fluid overload by assessment of - o Vital signs - BP, HR, capillary refill o Skin turgor o Mucous membranes o Presence of edema o Fontanels Provision of appropriate fluid intake, including replacement of any drainage Adequate calories for growth must be balanced without increasing the fluid load. This may done by using - o Total parenteral nutrition (TPN) o Lipids Initiation of early feedings has been shown to decrease the days to full feeds, lower the percentage of weight loss and return to birthweight o Initial feedings may be gut priming or trophic feeds Monitoring daily weights Evaluation of the following laboratory values - o Electrolytes o BUN, creatinine o Carbon dioxide o Glucose o Hematocrit Use of a humidified isolette is beneficial because it helps to prevent heat and insensible water loss through conduction, convection, evaporation, and radiation A relative humidity of > 85% can reduce transepidermal water loss during the first week of life of the preterm infant to levels that approximate those of a more mature infant

27 Pain Management Intubation, mechanical ventilation, and endotracheal suctioning are considered painful procedures. Therefore, comfort measures and analgesia should be incorporated into care of the infant Frequently used medications include fentanyl and morphine. However, the effectiveness of analgesia for preterm infants is unclear and may also have long-term consequences of which we are not currently aware Non-pharmacologic interventions that can be used alone or in combination with analgesics include - Facilitated tucking such as swaddling Non-nutritive sucking Non-noxious sensory stimulation to alleviate pain Skin-to-skin care with parents as the baby's condition allows

28 The infant with RDS can develop both acute and chronic complications that can occur from the disease process, treatment, or both To decrease the risk of complications, it is important to begin treatment with the least invasive therapy first and progress to more complicated treatment as the course of the infant's condition dictates Potential acute complications of RDS include - Sudden deterioration of the infant's condition may be caused by - o Accidental extubation or disconnection of the airway circuit o Airway obstruction due to secretions o Intraventricular hemorrhage (IVH) Air leaks o Pneumothorax o Pulmonary interstitial emphysema (PIE) o Pneumomediastinum o Pneumopericardium Central nervous system complications o Hypoxic-ischemic injury o Increased intracranial pressure (ICP) o Intraventricular hemorrhage Cardiac complications o Patent ductus arteriosus (PDA) o Decreased cardiac output Renal effects o Oliguria may follow episodes of hypoxia, hypotension, or shock o Hypo or hypernatremia Infection due to - o Use of endotracheal tubes, central lines, and other invasive procedures Pulmonary hemorrhage

29 Potential chronic complications of RDS include - Bronchopulmonary dysplasia o Increased risk for developing asthma later Retinopathy of prematurity* Developmental delay* Tracheal stenosis *Thought - Are these complications related to the disease process of RDS or more as the result of being born prematurely?

30 The potential morbidities experienced by infants who have RDS are generally more likely to be related to preterm birth and include - Mild to severe cognitive disabilities Cerebral palsy Developmental issues such as motor delays and perceptual problems ROP Sequelae of IVH Chronic lung disease like BPD may occur with slow resolution over time The child may require frequent admissions to the hospital for respiratory problems during the early years Simple infections may escalate more quickly and require hospitalization

31 American Psychological Association. (2010). Publication Manual of the American Psychological Association, 6th Edition. Washington, DC: Author. Bonner, K.M. & Mainous, R.O. (2008). The nursing care of the infant receiving bubble CPAP therapy. Advances in Neonatal Care, 8(2), Chow, J.M. & Douglas, D. (2008). Fluid and electrolyte management in the premature infant. Neonatal Network, 27(6), F.A. Davis Company. (2009). Taber s Cyclopedic Medical Dictionary, 21st Edition Online. (Retrieved February 28, 2012). Gardner, S.L., Carter, B.S., Enzman-Hines, M., & Hernandez, J.A. (2011). Merenstein & Gardner's Handbook of Neonatal Intensive Care, 7th Edition. St. Louis: Mosby-Elsevier. Karlsen, K. (2006). the S.T.A.B.L.E. Program: Post-Resuscitation/Pre-Transport Stabilization Care of Sick Infants Guidelines for Neonatal Healthcare Providers, 5th Edition. Park City, UT: The S.T.A.B.L.E. Program. Miller, N.E. (2010). Techniques of early respiratory management of very low and extremely low birth weight infants. Neonatal Network, 29(3), Kaneyasu, M. (2012). Pain management, morphine administration, and outcomes in preterm infants: A review of the literature. Neonatal Network, 31(1), Peterson, S.W. (2009). Understanding the sequence of pulmonary injury in the extremely low birth weight, surfactant-deficient infant. Neonatal Network, 28(4), Snyder, T., Walker, W., & Clark, R.H. ( 2010). Establishing gas exchange and improving oxygenation in the delivery room management of the lung. Advances in Neonatal Care, 10(5), Verklan, M.T. & Walden, M. (2010). Core Curriculum for Neonatal Intensive Care Nursing, 4th Edition. St. Louis: Saunders-Elsevier.

32 The authors would like to thank Creative Memories for their kind permission for our use of their graphics in Mother-Baby University learning activities.