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* Less than half of patients with critical [[Congenital heart disease|congenital heart defects]] were routinely identified. [10,42-44].  
* Less than half of patients with critical [[Congenital heart disease|congenital heart defects]] were routinely identified. [10,42-44].  


== Antenatal corticosteroid therapy ==
=== Antenatal corticosteroid therapy ===
* Antenatal [[Corticosteroid|corticosteroid therapy]] should be administered to all pregnant women at 23 to 34 weeks who are at increased risk of [[Premature birth|preterm delivery]] within the next seven days to prevent or decrease the severity of [[RDS|neonatal RDS]].  
* Antenatal [[Corticosteroid|corticosteroid therapy]] should be administered to all pregnant women at 23 to 34 weeks who are at increased risk of [[Premature birth|preterm delivery]] within the next seven days to prevent or decrease the severity of [[RDS|neonatal RDS]].  
* [[Corticosteroid|Coericosteroids]] enhances maturational changes in fetal lung architecture and biochemistry with increased synthesis and release of [[surfactant]], resulting in improved neonatal lung function.  
* [[Corticosteroid|Coericosteroids]] enhances maturational changes in fetal lung architecture and biochemistry with increased synthesis and release of [[surfactant]], resulting in improved neonatal lung function.  
* Assisted ventilation techniques
 
=== Assisted ventilation techniques ===
* Respiratory support that prevents and reduces [[atelectasis]] should be administered to all preterm infants who are at risk for [[RDS]].  
* Respiratory support that prevents and reduces [[atelectasis]] should be administered to all preterm infants who are at risk for [[RDS]].  
* In our center, nasal continuous positive airway pressure (nCPAP) is the preferred modality to provide positive end-expiratory pressure (PEEP). Limited data suggest that nasal intermittent positive pressure ventilation (NIPPV) may be a reasonable alternative to nCPAP.
* The less invasive modalities have replaced intubation and mechanical ventilation as the initial intervention that provides positive pressure to reduce the risk of atelectasis. Nasal continuous positive airway pressure (nCPAP) is the preferred modality to provide positive end-expiratory pressure.
* These less invasive modalities (nCPAP and NIPPV) have replaced intubation and mechanical ventilation as the initial intervention that provides positive pressure to reduce the risk of atelectasis. However, for some patients who do not adequately respond to nCPAP or NIPPV, intubation and mechanical ventilation with PEEP may be needed (algorithm 1).
* Intubation and mechanical ventilation with PEEP may be needed in case of failed previous maneuvers.
* Nasal continuous positive airway pressure — In preterm infants at-risk for or with established RDS without respiratory failure, nCPAP is the initial preferred intervention versus the combined regimen of endotracheal intubation, surfactant therapy, and mechanical ventilation [1,3-7]. This approach is consistent with our own practice (algorithm 1) and the recommendations from the American Academy of Pediatrics (AAP), American Heart Association (AHA), International Liaison Committee on Resuscitation (ILOR) guidelines, and the European Consensus Guidelines [1,2,8,9]. (See 'Management approach' below.)
* Prophylactic caffeine therapy is recommended in extremely low birth weight infants (BW <1000 g) as these patients universally will have apnea of prematurity and are at greatest risk for developing BPD. 17.  
* Prophylactic caffeine therapy is recommended in extremely low birth weight infants (BW <1000 g) as these patients universally will have apnea of prematurity and are at greatest risk for developing BPD.17].  
* Other indications for mechanical ventilation include:
* Failure of CPAP
* Respiratory acidosis, documented by an arterial pH <7.2 and partial pressure of arterial carbon dioxide (PaCO2) >60 to 65 mmHg  
* Patients with neonatal RDS who fail continuous positive airway pressure (CPAP) (defined as pH below 7.25 or who require oxygen supplementation of an FiO2 ≥0.40) require intubation and administration of surfactant. CPAP failure increases with decreasing gestational age and is associated with increased mortality and morbidity. This was illustrated in a large cohort of preterm infants that reported failure rates of CPAP of 43 percent for infants born between 25 and 28 weeks gestation, and 21 percent for those born between 28 and 32 weeks gestation [19]. After adjusting for confounding factors, the incidence of death or BPD was increased for infants regardless of gestational age who failed CPAP compared with those in whom CPAP was successful.
* Hypoxemia documented by an arterial partial pressure of oxygen (PaO2) <50 mmHg despite oxygen supplementation, or when the fraction of inspired concentration (FiO2) exceeds 0.40 on nCPAP  
* Long-term outcome
* Severe apnea  
* However, the use of CPAP is still associated with long-term morbidity. This was illustrated in an observational Australian study that correlated pulmonary function for extremely preterm survivors (gestational age <28 weeks) at eight years of age with neonatal respiratory care over three time periods (1991 to 1992, 1997, and 2005) [20]. Although the use of nasal CPAP increased over the three time periods, there was no improvement in pulmonary function at eight years of age (eg, risk of airflow obstruction). In fact, contrary to expected results, the 2005 cohort with the longest duration of CPAP use had the highest degree of airflow obstruction at eight years of age and greatest risk of BPD. However, interpretation of these results must take in to consideration other temporal factors including the marked decrease in the use of postnatal steroids (which reduces the risk of BPD) in 2005 compared with the other time periods and the higher mortality rate in the earliest time period of 1991 to 1992, which may have reduced the number of survivors at risk for BPD. Other limitations in comparing results across the three time periods included the potential increased duration of CPAP usage in 2005 for other conditions including apnea of prematurity and recurrent episodes of deoxyhemoglobin.
* These findings are consistent with those reported in a neonatal rodent model that demonstrated adverse long-term effects of CPAP and oxygen exposure used to treat recurrent intermittent hypoxia and hyperoxia on airway reactivity [21].
Endotracheal intubation and mechanical ventilation
 
Indications
 
Endotracheal intubation and mechanical ventilation are indicated for patients who fail to respond to less invasive forms of ventilation. In our practice, intubation and ventilation are initiated when one or more of the following criteria are verified (algorithm 1):
 
●Respiratory acidosis, documented by an arterial pH <7.2 and partial pressure of arterial carbon dioxide (PaCO2) >60 to 65 mmHg.
 
●Hypoxemia documented by an arterial partial pressure of oxygen (PaO2) <50 mmHg despite oxygen supplementation, or when the fraction of inspired concentration (FiO2) exceeds 0.40 on nCPAP.
 
●Severe apnea.
 
Choice of ventilatory mode — Mechanical ventilation due to volutrauma, barotrauma, and oxygen toxicity is a risk factor for BPD for preterm infants with RDS. Although there are several different mechanical ventilation modalities, including pressure control ventilation, volume control, and high-frequency positive pressure ventilation, the optimal mode of ventilation to reduce mortality and BPD remains unclear in patients with RDS who require mechanical ventilation. Based on the available literature, the initial ventilatory mode for preterm infants with RDS used in our center is synchronized volume-targeted ventilation. Target tidal volumes for volume guarantee are set at 4 to 6 mL/kg with permissive hypercarbia (PaCO2 50 to 55 mmHg with pH ≥7.2). Endotracheal tube leaks are minimized by optimizing tube position and size. We do not routinely use high-frequency ventilators in treating neonates who require respiratory support, because this mode of ventilation does not add any significant benefit over the less costly and easier to operate conventional ventilators. (See "Pathogenesis and clinical features of bronchopulmonary dysplasia", section on 'Mechanical ventilation' and "Mechanical ventilation in neonates".)
 
Regardless of the choice of ventilator, the goal is to use settings that minimize volutrauma, barotrauma, and oxygen toxicity, thereby reducing the risk of BPD, but still reach the target oxygen saturation and PaCO2 levels, discussed in the next section.
 
Target oxygen saturation — The goal of target oxygen saturation is to set a range so that both hypoxia and the excess use of oxygen can be avoided. In our center, we target oxygen saturation levels based upon pulse oximetry (SpO2) between 90 and 95 percent.
 
Data comparing high and low target oxygen saturation levels demonstrate that values above 95 percent and below 89 percent are associated with poorer outcome in very preterm infants. This evidence is discussed in detail separately. (See "Neonatal target oxygen levels for preterm infants", section on 'Oxygen target levels'.)
 
Target carbon dioxide levels — In our practice, the target PaCO2 levels for ventilated preterm infants are between 45 and 60 mmHg.
 
●When PaCO2 exceeds 60 mmHg, pH usually falls below 7.25, which may compromise cardiovascular function in the initial stages of RDS. In infants managed via an nCPAP-based strategy, PaCO2 exceeding 60 mmHg and pH <7.2 are indications of respiratory failure requiring intubation and mechanical ventilation. Sudden unexplained hypercapnia (in the absence of apnea) may be a sign of airway obstruction, air leak, or patent ductus arteriosus, and should be managed accordingly.
 
●Hypocapnia (PaCO2 <40 mmHg) is most likely to occur in intubated, ventilated patients and is an indication for decreasing ventilator support. Apart from the risk of excessive ventilator support causing lung damage, hypocapnia also decreases cerebral blood flow.
 
However, the optimal target for PaCO2 is not established as illustrated by the following:
 
●Supportive data for our approach are provided by secondary analysis of data from the SUPPORT study showing that higher PaCO2 levels were associated with increased risk of mortality, severe intraventricular hemorrhage, BPD, or neurodevelopmental impairment [24].
 
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Revision as of 05:59, 23 March 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Prenatal diagnosis

  • Most congenital heart defects can be identified by fetal echocardiography.
  • Guidelines of the International Society for Ultrasound in Obstetrics and Gynecology recommends Ultra Sound assessment of the outflow tracts. [41].
  • Less than half of patients with critical congenital heart defects were routinely identified. [10,42-44].

Antenatal corticosteroid therapy

  • Antenatal corticosteroid therapy should be administered to all pregnant women at 23 to 34 weeks who are at increased risk of preterm delivery within the next seven days to prevent or decrease the severity of neonatal RDS.
  • Coericosteroids enhances maturational changes in fetal lung architecture and biochemistry with increased synthesis and release of surfactant, resulting in improved neonatal lung function.

Assisted ventilation techniques

  • Respiratory support that prevents and reduces atelectasis should be administered to all preterm infants who are at risk for RDS.
  • The less invasive modalities have replaced intubation and mechanical ventilation as the initial intervention that provides positive pressure to reduce the risk of atelectasis. Nasal continuous positive airway pressure (nCPAP) is the preferred modality to provide positive end-expiratory pressure.
  • Intubation and mechanical ventilation with PEEP may be needed in case of failed previous maneuvers.
  • Prophylactic caffeine therapy is recommended in extremely low birth weight infants (BW <1000 g) as these patients universally will have apnea of prematurity and are at greatest risk for developing BPD. 17.
  • Other indications for mechanical ventilation include:
  • Respiratory acidosis, documented by an arterial pH <7.2 and partial pressure of arterial carbon dioxide (PaCO2) >60 to 65 mmHg
  • Hypoxemia documented by an arterial partial pressure of oxygen (PaO2) <50 mmHg despite oxygen supplementation, or when the fraction of inspired concentration (FiO2) exceeds 0.40 on nCPAP
  • Severe apnea

References

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