Home » Health » Surfactant Replacement in Neonates with Respiratory distress syndrome type

Surfactant Replacement in Neonates with Respiratory distress syndrome type

The innovation of surfactant replacement therapy in the treatment of respiratory distress syndrome has proven to increase the survival and minimize the complications of the premature neonate. Replacing surfactant has lessened time on ventilators, and allowing the neonate and parents an opportunity to grow together earlier outside of intensive care. This paper will discuss the etiology of respiratory distress syndrome type I, the treatment options and nursing care of the neonate during surfactant replacement.

Respiratory distress syndrome type I is a decrease production of surfactant, a noncelluar chemical produced in the type II alveolar in the lungs that’s primary function is to decrease the surface tensions and attraction between the type I alveolar walls. Respiration requires the alveolar walls to inflate and deflate continuously, while ventilating the alveoli are exposed to moisture causing an attraction between the alveolar walls. (Kenner, Lott, & Flandermeyer, 271) Surfactant primary function is to neutralize the attraction to prevent alveolar collapse during deflation.

The fetus begins to develop the type II alveoli at 22nd to 24th week of gestation, however these immature alveoli are incapable of supplying enough surfactant to meet the infant’s respiratory needs. The fetus surfactant production begins to become adequate at the middle terminal stage of alveoli development and production becomes optimal at the 34th-to-36th week. (Porth, 1306) There are four types of surfactant produced by the type 2 alveoli known as primary surfactant proteins SP-A, SP-B, SP-C, and SP-D. SP-A and SP-D roles are inhibiting production of surfactant influencing cleansing and phagocytosis in the alveoli.

SP-B and SP-C surfactants are the hydrophobic molecules that relieve the alveolar surface tension (Hartshorn, 963) Risk factors for developing RDS prenatally are conditions that compromise fetal development and gestation time. These include maternal hypertension, gestational diabetes excluding classes D, F, and R, intrauterine growth restriction, preterm labor, and drug abuse. The neonate high risk factors are birth prior to 32 weeks, weighing less then 1300 grams and laboratory data suggesting poor lung maturity discussed later.

The highest risk factor for RDS type I is an insulin dependent diabetic mother, because boluses of insulin injections severely decrease the fetus production of surfactant. (Porth, 1306)) Chronic hypoxic events during pregnancy associated with mild to moderate maternal hypertension have shown however to sometime accelerate fetal lung maturity and surfactant production leading to a decrease in neonatal respiratory complications.

This due to cortical steroid secretion that stimulate an increased production of surfactant in response to the stresses of hypoxic events. (Porth, 1306) The symptoms of oncoming RDS may at first not be present in a fetus greater then 28 weeks since they have produced enough surfactant to thrive outside of uterine life for a short time. However the high initial pressure to breathe the first breath remains constant with each subsequent breath causing extreme effort for ventilation due to the non-expanding alveolus.

The surfactant deficient alveoli also form an attraction to protein and fibrin fluids leading to a hyaline membrane that forms a barrier to gas exchange further depleting oxygenation status. (Graus, Evans, Kohen, Kristensen, & Pharm, 40) Once onset of symptoms occurs the neonate will display tackypnea with retractions from accessory muscle use due to the poor lung compliance and the excess amount of strength needed to breathe. In an effort to self regulate intrathroacic pressure and alveolar expansions the neonate will grunt in order to prevent alveolar collapse and maintain thoracic pressure.

Nursing assessment of an infant with RDS type I will reveal at first severe tachypnea with a symmetrical possibly barrel shaped chest. The neonate in an effort to maintain thoracic pressure and gas exchange will display nasal flaring, grunting, and suprasternel chest retractions. (Uebel, 68) The neonate may display circumoral and acrocyanosis; complete peripheral and central cyanosis becomes evident in advanced disease.

Auscultation is difficult in neonates because the sounds tend to be hyperresonant and transmitted throughout the chest, careful comparison of sounds of both lungs is important to reveal airleaks and pnemothroacs. Cardiac changes may present with tachycardia or bradycardia, hypotension and prolong distress may lead into pulmonary hypertension resulting in patent ductus arteriosis causing a systolic murmur. (Porth, 592) The nurse also needs to assess the neonate’s serum glucose and calcium because decreases in the values will further cause respiratory cardiac and neurological compromise.

Prenatal diagnosis of RDS can be attained through laboratory values of the Lecithin/sphingomyelin ratio (L: S), and the testing for phosphatidylglycerol or PG test. If the L: S ratio is less then 2:1or the PG is absent then RDS is evident. . (Bower, Barnhart, betiti, Hendon, Masi-lynch, & Wilson, 824) Post birth test includes a bedside click test for surfactant presence in tracheal aspirates has been proven to be effective. (Osborn, Jeffery, Bredemeyer, Polverino, Reid, 8) A Chests x-ray will reveal diffuse microatectelectasis, widespread air bronchograms, with reticulogranularity indicating alveolar collapsing.

Comparing the initial cord blood gas levels with the current blood gas levels will indicate respiratory insufficiency. (Uebel, 68) The treatment of RDS has many facets in order to maintain gas exchange. These options include controlled mechanical ventilation, extracorpeal membrane oxidation, and high frequency ventilation. These treatment options are effective but put the neonates at risk for bronchopulmonary dysplasia, throat damage, machine failure, necrotizing enterocolitis, and intraventricular hemorrhage with long term therapy.

These treatment options also delayed and prevented parental and neonatal bonding as well as altering the family’s growth and development. Neonates with surfactant defiency were treated with some success and with fewer complications with continuos positive airway pressure that prevents alveolar collapse and lessen the effort to ventilate. This treatment is less intimidating to the parents and makes bonding and holding the neonate more accessible (Lott, Kenner & Flandermeyer, 260)

A relatively new treatment developed for RDS has been surfactant replacement therapy, which include the administration of surfactant preparation into the neonate’s lungs to promote alveolar compliance. This form of treatment has been shown to decrease the amount of time of ventilator support decreasing complications associated with them. (Rodriquez & Martin, 595) Surfactant is also part of the treatment of meconium aspiration and neonatal pneumonia and recently has been used successfully to treat transfusion related lung injuries for neonates being treated for hyperbillirubinaemia.

Exogenous surfactant has been available in the United States since the early nineties and can be made artificially like Exosurf, or derived from bovine like survanta and infasurf. (Kenner, Lott, & Flandermeyer, 272) Studies have demonstrated that there is not a dramatic difference between artificial and natural surfactants, however natural surfactant is preferred because of earlier improvements and decreases in pnemothoracs. (Cochrane review) Surfactant replacement therapy is only effective if the lungs are deficient in surfactant.

Contradictions for use are evidence of lung maturity on radiographs, neonates greater 48 hours of age. (Grauaus, Evans, Kohan, Kristenson & Pharm,40) If the neonate is severely compromised with conditions incompatible with beyond the neonatal time period then rescue surfactant may not be appropriate. Rescue treatments should be performed to any neonate less then 800 grams and less then 32 weeks old. Non-rescue treatment should be performed when the neonate has obvious evidence of surfactant deficiency and requires greater then 30% oxygen to maintain oxygen saturation of 90% and an oxygen partial pressure greater then 50%. (Woodrum, NICU-web)

Critical nursing diagnosis and expected prior to and during surfactant administration are primarily; Risk for ineffective airway clearance related to administration of fluid surfactant into bronchus. (Carpenito, 509) The goal of this diagnosis is to ensure a slow safe administration of surfactant without forming a block in the endo-tracheal tube or bronchus. Risk for injury related rapid fluctuations in ventilation capabilities by the neonate secondary to surfactant introduction is a crucial diagnosis with an expected outcome that the neonates ventilation status will be continuously assessed and adjusted to maintain safe oxygen parameters.

Nursing care interventions prior to administration involves many crucial assessments of the neonate. Since surfactant dosing is based on weight, the infant should be accurately weighed to ensure appropriate dosing. Assessment of chest radiograms is essential prior to administration to verify proper endo-tracheal tube placement. Assessment of endo-treacheal tubes and lungs for mucous plugs also needs to be monitored and treated.

The neonate’s oxygen status is assessed and needs to be adequate to prevent further desaturation during administration, if the neonate is not ventilating well then ventilator settings need to be adjusted prior to administration. The endo-treacheal tube needs to suctioned to clear bronchus at least 15 minutes prior to dosing administration is not contradicted if the secretions are blood tinged. The neonate also needs to be on an oximeter, cardiorespiratory monitor, transcutaneos carbon dioxide monitor, and a blood pressure monitor to allow frequent assessment.

The equipment needed for administration will include a 5 French sterile feeding tube, catheter, or endo-tracheal tube delivery port. (Bower, Barnhart, betiti, Hendon, Masi-lynch, & Wilson, 827) Positioning of the neonate for administration varies with the type of surfactant used Exosurf requires the infant head to be turned from left to right with administration, while survanta requires 4 positions for each aliquots. These involve the neonate head down and turned left to right, and head up left to right.

The neonate will remain in each position for 30 seconds while dosing. With survanta the dose is given in 4 increments with each position change. The dosing increment should be given over 2-3 seconds, in the endo-tracheal tube just beyond the end in the trachea. (Kenner, Lott, & Flandermeyer, 275) Exosurf is given similarly as survanta through the endo-tracheal tube, however Exosurf dose not require four increments of dosing. (GlaxxoWelcome) While administrating the nurse needs to assess the neonates condition and response to therapy.

If dosing is too rapid for the neonate bradycardia and a drop in oxygen saturation will indicate the need to slow down. During administration variables to monitor are chest wall movements, oxygen saturation, ventilator settings skin color respirations and heart rate. (Bower, Barnhart, betiti, Hendon, Masi-lynch, & Wilson, 827) These assessments are crucial because surfactant replacement may be complicated with oxygen toxicity, which leads to bronchopulmonary dysplasia, pulmonary hemorrhage retinal damage and intraventicular hemorrhage due to a rapid response to treatment.

The ventilator settings may need to be adjusted frequently during administration to prevent these complications monitoring oxygen saturation and transcutaneous carbon dioxide levels will aide in prevention. (Mallano, 43) The nurse needs to also watch for the displacement of endo-tracheal tubing, reflux of surfactant, and the neonate’s behavior and toleration of position changes during treatment. (Kenner, Lott, Flandermeyer, 275) Nursing assessments afterward are similar to ones needed during administration.

Frequent ventilator adjustments in response to increasing oxygenation with possible rapid weaning and decreasing the fraction injected oxygen from the ventilator. (Mallano, 43) Assessments of decrease heart rate, rhythm, increased oxygen saturation, decreased respiration’s, quality, shallow chest movements, decreased blood pressure, pale skin color and vigor need to be assessed frequently to avoid hyperoxemia. Endo-tracheal suctioning should not be performed 1 to 2 hours to prevent removal of surfactant. . (Kenner, Lott, Flandermeyer, 275)

If the neonate does not respond to first dose then a repeat dose may be given no less then 6 hours later for survanta and 12 hours later for Exosurf. Transient effects of surfactant are also possible in which the neonate may seem to respond and gradually begin to deteriorate again, and ventilator settings would need to increase. Generally the treatment should be repeated no more then 3 times. (Woodrum, NICU-WEB) A Crucial aspect of caring for the neonate with RDS type I is educating and comforting the parents.

The crisis of a distressed newborn is very psychologically damaging that parents become scared and confused. Evaluating and consoling the parent’s psychological needs as soon as possible is necessary to aid the delicate task of bonding in an intensive care environment. Educating parents on the disease and treatment course, while allowing them to voice concerns fears and feelings. The parents may have a spectrum of feelings of guilt, fear, and denial; the nurse needs help parents grasp reality, help correct misconceptions in order to support the family with honesty and sincerity.

Successful long term and short-term outcomes for the distressed neonate are dependent on parental bonding, love and touch. (Old, London, & Ladewig, 874-875) Surfactant therapy has proven effective in treating respiratory distress type 1 by lessening the time on ventilators, increasing effectiveness of safer respiratory care techniques. The therapy has also allowed parental bonding without the intimidation and restrictions of mechanical ventilation, and decrease chronic hospitalizations after the neonatal period due to damage caused by ventilators.

Cite This Work

To export a reference to this essay please select a referencing style below:

Reference Copied to Clipboard.
Reference Copied to Clipboard.
Reference Copied to Clipboard.
Reference Copied to Clipboard.