Respiratory Distress Syndrome

Developed by - Lisa Fikac, MSN, RNC-NIC

Expiration Date - 10/1/17

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.

1.1 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 and Creative Memories are the sources for all graphics unless otherwise noted.

The author would like to thank Stacey Cashwell for her work as original author.

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

RDS.

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 -

Table from - Midtrimester preterm premature rupture of membranes. (2014). In UpToDate 2014. Retrieved July 17, 2014. Used with permission under CFVHS licensure for use of UpToDate.

The embryonic phase occurs between 4 to 5 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 6 to 17 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. 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 24 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 24-26 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 terminal phase occurs between 25 to 37 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. • At approximately 26-28 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 38 weeks gestation and continues through postnatal life until approximately 3 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.

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) • 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 20-24 weeks gestation. Surfactant is first detectable at about 25-30 seeks gestation. The neonate is able to maintain alveolar stability at about 33-36 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 26-30 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 28-30 weeks

gestation. • Phosphatidylglycerol (PG) appears at about 35-36 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.

• A ratio of >2:1 is considered a mature ratio. o At 28-30 weeks gestation, sphingomyelin is slightly higher than lecithin. o At 30-32 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 ~ 27-34 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. • 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 -

• 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 O2 and CO2. • Approximation of the capillaries and terminal air sacs for effective gas exchange. • Adequate surfactant production to stabilize the alveoli.

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 the 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.

• 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.

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 40,000 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 o An increase in energy expenditure for the infant to breathe

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

o This may be due to a greater risk of asphyxia.

• Siblings of a former low birthweight infant with a history of RDS

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 pauses in breathing that may last 5-10

seconds with ventilation lasting 10-15 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 pressure 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 • Intercostal

o Nasal flaring - an attempt to increase oxygen intake by decreasing airway resistance

o See-saw respirations - may be a sign of respiratory failure • Oxygen requirement - increasing

o 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 PaO2. 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 > 150-160 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 • Changes in peripheral pulses

o 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 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 - o Small lung volumes o Hazy lung fields o Fine, reticulogranular pattern of density with air bronchograms -

"ground-glass" appearance This is caused by areas of atelectasis adjacent to areas of

hyperexpanded alveoli.

Photograph from - Pathophysiology and clinical manifestations of respiratory distress syndrome in the newborn. (2014). In UpToDate 2014. Retrieved July 17, 2014. Used with permission under CFVHS licensure for use of UpToDate.

• Arterial blood gases (ABGs) demonstrate - o Hypoxemia - PaO2 < 50 mmHg in room air o Hypercapnea or hypercarbia - increased PaCO2 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 help to rule out hypo/hypernatremia, hypocalcemia, hypoglycemia as possible causes of respiratory distress.

RDS is a disease that is self-limited until the infant can produce adequate amounts of surfactant at about 48-72 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 - 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 and Respiratory Support

The benefits of surfactant replacement therapy include -

• Reduced in mortality and morbidity • Improved lung compliance and decreased resistance which reduces the pressure

required to inflate the lungs and decreases the infant's work of breathing • Improved ventilation which increases PaO2, 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

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.

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).

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 to 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

Algorithm from - Prevention and treatment of respiratory distress syndrome in preterm nfants. (2014). In UpToDate 2014. Retrieved August 19, 2014. Used with permission under CFVHS licensure for use of UpToDate.

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 - 85-93%* • > 1500 grams - 90-95%*

*This practice may vary depending on institution

ABGs or capillary blood gases (CBGs) are monitored with the following targets -

ABG CBG

pH 7.30-7.45 7.35-7.45

PaCO2 35-45 mmHg 35-50 mmHg

PaO2 50-80 mmHg

35-45 mmHg - not useful for assessing

oxygenation

From Karlsen, K. (2012). The S.T.A.B.L.E. Program: Post-Resuscitation/Pre-Transport Stabilization Care of Sick Infants – Guidelines for Neonatal Healthcare Providers, 6th Edition. Park City, UT: The S.T.A.B.L.E. Program.

Pulmonary status may also be monitored with chest x-rays as needed. X-rays help -

• Document 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

• 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 15-30 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. • 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.

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

Some facilities may use oral sucrose as a pain relief measure. However, additional research is needed in its use in the preterm infant.

The infant with RDS can develop both acute and chronic complications that can occur from -

• 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

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?

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.

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