Respiratory Distress Syndrome (rds)

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Intensive Care Nursery House Staff Manual




Copyright © 2004 The Regents of the University of California



Respiratory Distress Syndrome (RDS) 


INTRODUCTION: RDS, also known as hyaline membrane disease, is the commonest 

respiratory disorder in preterm infants.  The clinical diagnosis is made in preterm infants 

with respiratory difficulty that includes tachypnea, retractions, grunting respirations, 

nasal flaring and need for ↑ F




.  In the last three decades, introduction of antenatal 

steroids and exogenous surfactant has greatly improved outcomes in RDS; however, it 

remains a principal clinical problem. 


EPIDEMIOLOGY: RDS affects 40,000 infants each year in the US and accounts for 

approximately 20% of neonatal deaths.  RDS typically affects infants <35 weeks 

gestational age (GA) but may affect older infants who have delayed lung maturation.  

Low GA is the greatest risk factor for RDS, and its incidence varies inversely with birth 

weight among AGA infants (Table 1).  Other factors may also influence the risk of RDS 

among preterm infants (Table 2). 


Table 1.  Incidence of RDS by Birth Weight. 

Birth Weight (g)   

Incidence of RDS 









1,001-1,250   48% 

1,251-1,500   27% 


Table 2. Other risk factors for RDS. 

Increased Risk 



Prematurity    Chronic 



Male gender 




Prolonged rupture of membranes 

Familial predisposition   


Maternal hypertension or toxemia 

Cesarean section without labor   








   Maternal use of narcotics/cocaine 

Infant of diabetic mother   


Tocolytic agents 




Hemolytic disease of the newborn 

Non-Immune hydrops fetalis 




PATHOPHYSIOLOGY: The primary cause of RDS is inadequate pulmonary 

surfactant.  The structurally immature and surfactant-deficient lung has ↓ compliance and 

a tendency to atelectasis; other factors in preterm infants that ↑ the risk of atelectasis are 

decreased alveolar radius and weak chest wall.  With atelectasis, well perfused but poorly 

ventilated areas of lung lead to V/Q mismatch (with intra-pulmonary shunting) and 

alveolar hypoventilation with resultant hypoxemia and hypercarbia.  Severe hypoxemia 

and systemic hypoperfusion result in decreased O


 delivery, anaerobic metabolism and 

Respiratory Distress Syndrome 



Copyright © 2004 The Regents of the University of California


subsequent lactic acidosis.  Hypoxemia and acidosis may further impair oxygenation by 

causing pulmonary vasoconstriction, resulting in right-to-left shunting at the levels of the 

foramen ovale and ductus arteriosus.  

Other factors, such as 

baro/volutrauma and high F




, may 

initiate release of inflammatory 

cytokines and chemokines causing 

more endothelial and epithelial cell 

injury.  The injury results in reduced 

surfactant synthesis and function as 

well as increased endothelial 

permeability leading to pulmonary 

edema.  Leakage of proteins into the 

alveolar space further exacerbates 

surfactant deficiency by causing 

surfactant inactivation.  

Macroscopically, the lungs appear 

congested, atelectatic and solid.  

Microscopically, diffuse alveolar 

atelectasis and pulmonary edema are 

seen.  An eosinophilic membrane 

composed of a fibrinous matrix of 

materials from the blood and cellular 

debris (the hyaline membrane) lines the visible airspaces that usually constitute dilated 

terminal bronchioles and alveolar ducts. 


CLINICAL FEATURES: Signs of RDS appear immediately after birth or within 4 h.  

RDS is characterized by tachypnea (>60 breaths/min), intercostal and subcostal 

retractions, nasal flaring, grunting, and cyanosis in room air.  Tachypnea is due to an 

attempt to increase minute ventilation to compensate for a decreased tidal volume and 

increased dead space.  Retractions occur as the infant is forced to generate a high 

intrathoracic pressure to expand the poorly compliant lungs.  Grunting results from the 

partial closure of the glottis during forced expiration in an effort to maintain FRC.   After 

an initial improvement with resuscitation and stabilization, an uncomplicated course is 

often characterized by a progressive worsening for 48 to 72 h.  Recovery usually 

coincides with a diuresis after an initial period of oliguria.  Other clinical features may 

include hypotension, acidosis and hyperkalemia.  The typical chest radiograph shows low 

lung volumes and a bilateral, reticular granular pattern (ground glass appearance) with 

superimposed air bronchograms.  In more severe cases, there is complete “white out” of 

the lung fields.  Application of positive airway pressure may minimize or even eliminate 

these radiographic findings.  Acute complications include air leaks and intracranial 

hemorrhage.  Long-term, RDS has been associated with an increased incidence of chronic 

lung disease, ROP, and neurologic impairment. 


MANAGEMENT: The goals of management of an infant with RDS are to: 

•Avoid hypoxemia and acidosis 




Immature Lung


V/Q Mismatch 


Hypoxemia & Hypercarbia 

Respiratory & 

Metabolic Acidosis

High Fi0


 & Baro or Volutrauma 

Pulmonary Vasoconstriction


Cell Influx 



Impaired endothelial and 

epithelial integrity 

Proteinaceous exudate 





Lung Injury 

Chronic Lung Disease / BPD





Respiratory Distress Syndrome 



Copyright © 2004 The Regents of the University of California


•Optimize fluid management: avoid fluid overload and resultant body and pulmonary 

edema while averting  hypovolemia and hypotension 

•Reduce metabolic demands and maximize nutrition 

•Minimize lung injury secondary due to volutrauma and oxygen toxicity 

The three most important advances in prevention and treatment of RDS have been: (a) 

antenatal glucocorticoids, (b) continuous positive airway pressure (CPAP) and positive 

end-expiratory pressure (PEEP), and (c) surfactant replacement therapy.  These have 

dramatically decreased morbidity and mortality from RDS.   


1. Antenatal glucocorticoids accelerate fetal lung maturity by increasing formation and 

release of surfactant and maturing the lung morphologically.  Physiologic stress levels of 

corticosteroids administered to the mother initiate a receptor-mediated induction of 

specific developmentally regulated proteins in the fetus.  Administration of 

glucocorticoids at least 24 to 48 h (and no more than 7 d) before preterm delivery 

decreases both incidence and severity of RDS.  They are most effective before 34 weeks.   

However, antenatal steroids should still be considered when therapy is less than 24 h 

before anticipated delivery because a reduction in neonatal mortality and RDS can still 

occur in this time frame.  Repeated (>3) courses of corticosteroids have been associated 

with decreased fetal growth and poorer neurological outcomes.  Antenatal steroids also 

reduce the incidence of intraventricular hemorrhage, an effect that is independent of 

lessened pulmonary morbidity and that may be secondary to stabilization of cerebral 

blood flow or maturation of cerebral vasculature.  The effects of antenatal steroids and 

surfactant have been demonstrated to be additive in improving lung function. 


2. Exogenous surfactant: It has been shown in multiple randomized controlled trials that 

the use of exogenous surfactant in preterm infants improves oxygenation, decreases air 

leaks, reduces mortality due to RDS, and decreases overall mortality.   

A. Timing of surfactant administration: Two approaches have been used for 

surfactant delivery: prophylactic and rescue treatment.  Prophylactic administration 

involves giving surfactant soon after birth, as soon as the infant has been stabilized.  

The theoretical benefit of this approach is that replacement of surfactant before RDS 

develops will avoid or ameliorate lung injury.  Animal studies have shown that the 

lung epithelium of very premature subjects can be damaged within minutes of onset 

of ventilation.  The damage can result in protein leak which subsequently interferes 

with surfactant function.   Rescue administration involves giving surfactant to 

infants who have established RDS and require mechanical ventilation and 

supplemental O


.  The advantage of this approach is that patients are not treated 

unnecessarily.  Because surfactant currently can only be given via an endotracheal 

tube, this would prevent intubation and mechanical ventilation of infants who would 

do well without surfactant and avoid unnecessary baro/volutrauma, adverse 

physiological effects of laryngoscopy, and possible inadvertent hyperventilation.  Past 

studies have shown greater reduction in neonatal mortality with prophylactic 

administration versus rescue, especially in infants greatest at risk for RDS (i.e., <27 

weeks GA).  However, with the use of nasal CPAP in VLBW infants and higher rates 

of antenatal steroid administration, there exists controversy on the optimal timing of 

surfactant administration, balancing the benefits of early surfactant administration 

Respiratory Distress Syndrome 



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with the advantages of avoiding mechanical ventilation and volutrauma.  The current 

approach to the timing of surfactant therapy at UCSF is summarized in Table 3. 




Table 3. Guidelines for intubation and timing of surfactant administration in 

preterm infants. 

  Gest. Age 




  Timing of 

   (Weeks) Steroids*  





















(a) If intubation

 & mech. 

  Prophylactic, unless  




  vent. needed at birth  

    in room air by age 20 min 




(b) Early CPAP, if not stable    Rescue 





 & mech. vent. 




(c) Early CPAP, if stable 

  Do not give surfactant 



Yes or No 

Manage as for ≤27 weeks and (+) steroids 









*Steroid therapy indicates mother received 2 doses at least 24 h before and not more than 

7 d before birth. 

For indications for intubation, see Table 4. 



B. Administration and dose of surfactant: For prophylactic administration, the 

position of the endotracheal (ET) tube should be verified by two people before 

surfactant is given.  Attach the surfactant syringe to the side port of the ET tube, 

occlude end of ET tube, and administer surfactant as a single aliquot over ≈ 5 sec.  

For rescue therapy, obtain chest radiograph to confirm tube position.  Administer 

surfactant through a feeding tube inserted to (but not past) the end of the ET tube.  

Administer in same manner as with prophylactic treatment.  Slower administration 

may interfere with its efficacy.  After administration, the infant should be hand 

ventilated and may transiently require higher ventilatory support.  Several studies 

have shown that two doses, 12 h apart, may be more effective than single dose 

therapy.  More than 2 doses is rarely required and is rarely effective.  The dose of 

surfactant is: 

   Infasurf™  3mL/kg 

   Survanta™  4 mL/kg 


C. Criteria for rescue treatment:  Rescue treatment with surfactant should be given to 

preterm infants who have: 

•Respiratory distress, necessitating intubation and assisted ventilation, 

•No radiological evidence of another disease process,  

Respiratory Distress Syndrome 



Copyright © 2004 The Regents of the University of California


and require either 





 > 0.3 or a mean airway pressure ≥7 cmH




D. Complications:  Although surfactant administration is relatively safe, complications 

include obstruction of the endotracheal tube, transient increases in O



and ventilatory settings, and pulmonary hemorrhage, an infrequent adverse effect 

reported in 2-6% of infants given surfactant. 


3. Oxygen should be administered to preterm infants in concentrations sufficient  to 

maintain PaO


 between 50-70 mmHg or saturation (by pulse oximetry) between 85-92%.  

Higher O


 concentrations may exacerbate lung injury and will increase the risk of 

retinopathy of prematurity.  


4. Respiratory Management: Please see the section on Respiratory Support (P. 10) for a 

more complete discussion of ventilation strategies.  The initial decision in respiratory 

management of an infant with RDS is whether the infant can be adequately managed with 

nasal CPAP (i.e., no treatment with surfactant) or should receive endotracheal intubation, 

surfactant therapy and mechanical ventilation.  Endotraheal intubation should be 

performed in infants that require prophylactic surfactant administration or who meet the 

criteria listed in Table 4. 


Table 4. Indications for intubation of preterm infant during resuscitation. 


•GA ≤27 weeks and no maternal steroids 

•For other infants, any of the following: 








-Requires F






- ↑ work of breathing (grunting, retractions, flaring) 


<7.25   -PaCO


 >60 mmHg 



The goals of ventilatory management in the intubated infant are to maintain adequate 

oxygenation and ventilation while minimizing ventilator induced lung injury.  To achieve 

these aims, utilize a strategy of permissive hypercarbia, maintaining PaCO


 between 45-

55 mmHg, theoretically reducing volutrauma and preventing deleterious effects of 

hypocarbia.  To reduce further the risk of volutrauma, adjust ventilatory pressures to 

maintain tidal volume between 4-5 mL/kg.  Administration of surfactant improves lung 

mechanics (↑ lung compliance) and increases oxygenation by reducing atelectasis and 

increasing FRC.  It is extremely important to recognize the time frame of these changes.  

After surfactant administration, there may be very rapid improvements in 

pulmonary function that necessitate rapid weaning of ventilator settings.  Close 

attention must be paid to tidal volume, blood gas tensions, transcutaneous CO


 and pulse 

oximetry values in order to avoid inadvertent hyperventilation, hyperoxia and over-

distension of the lung, all of which can result in lung injury.  Although it may be 

necessary to wean F




, inspiratory pressure and ventilator rate, one should decrease 

PEEP with extreme caution.  Infants in the early phases of RDS will rarely maintain 

Respiratory Distress Syndrome 



Copyright © 2004 The Regents of the University of California


adequate lung inflation if PEEP is <5 cmH


O, even after administration of 


Recently, much effort has been directed towards other, less invasive modalities of 

respiratory support to prevent lung injury, specifically nasal CPAP.  CPAP, as treatment 

for RDS, was first described in 1971 by George Gregory at UCSF.  Modifications in the 

nasal CPAP delivery system have generated renewed interest in nasal CPAP for the 

ventilatory management of RDS.  Randomized controlled trials have shown a decreased 

need for mechanical ventilation in VLBW infants treated with nasal CPAP, although the 

impact on mortality and chronic lung disease have not been defined.  Furthermore, recent 

reports indicate that approximately 70% of infants with birth weight <1,000 g will not 

be adequately managed with nasal CPAP and will require intubation and mechanical 

ventilation.  Nevertheless, in order to minimize ventilator-induced lung injury, early 

extubation to nasal CPAP is a reasonable strategy.  Criteria for extubation to nasal 

CPAP in the first week of life are: 

Adequate respiratory drive, and 

Mean airway pressure ≤7 cmH


O, and 

• F






Nasal CPAP is delivered via a specialized nasal mask or prongs, utilizing a patient-

demand flow system.  CPAP is administered between 4 and 6 cmH


O.  Lower pressures 

do not maintain lung inflation and higher pressures often cause gastric distension.  

Limitations to the use of nasal CPAP include hypercarbia, frequent episodes of apnea, 

gastric distension and breakdown of nasal skin and mucosa from the mask/prongs. 

The method and timing of further weaning, from nasal CPAP to supplemental O



nasal cannula, varies with gestational age, post-natal age, weight and stability of the 

individual patient.  Some infants require a gradual transition to nasal cannula through 

“sprinting,” a process in which infants are trialed on nasal cannula for a portion of the 

day and then returned to nasal CPAP.  As the infant demonstrates increased tolerance of 

these trials, the length of these trials is slowly extended..  The time of these trials often 

coincides with feeds, in order to minimize handling of VLBW infants (e.g., if feedings 

are q3 hours, trials of nasal cannula are usually increased in 3 hour intervals). 


5. Antibiotic therapy: The clinical and radiographic features of pneumonia may be 

indistinguishable from RDS at birth.  As a result, all infants with RDS should have blood 

cultures and CBC drawn, and should receive empiric antibiotic therapy (Ampicillin and 

Gentamicin).  Generally, antibiotics may be discontinued if the blood culture has no 

growth after 48 hours, unless prenatal history or clinical scenario warrants extended 



6. Thermoregulation: Careful temperature control is imperative in all VLBW infants 

and is especially important in infants with RDS to minimize metabolic demands and 

oxygen consumption.  RDS can limit oxygen uptake leading to hypoxia which limits the 

ability of an infant to increase their metabolic rate when cold stressed, resulting in a fall 

in body temperature.  An incubator or radiant warmer must be utilized to maintain a 

neutral thermal environment for the infant. For further discussion, see the sections on 

VLBW Infants (P. 65) and Health Care Maintenance (P. 48). 

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