alphabet soup of preemie problems - bch outreach

Alphabet Soup of Preemie Problems: RDS & BPD

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Objectives

▪Review aspects of fetal lung development, pulmonary function and vulnerabilities of the premature infant▪Discuss indications and updated management strategies for respiratory support of the premature infant with RDS▪Review causes of preterm lung injury

We’ve Come a Long Way…

NICU Respiratory History

▪1940’s and 50’s Oxygen and more oxygen▪1963 Patrick Bouvier Kennedy died of RDS at 34 weeks/2100 gms ▪1971 George Gregory uses CPAP for RDS▪1980’s Jet ventilators used for neonates▪1990 FDA approval for surfactant use▪1990’s -2000’s the more pressure the better▪Today back to CPAP and gentle ventilation

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Old School…

▪Intubation based on size, gestational age▪High pressures, high O2▪Chest physiotherapy ATC▪Suction whether you need it or not▪“Babies do not feel pain.”

Changes in Respiratory Management of the Preterm Neonate

▪Antenatal steroids▪Surfactant replacement therapy▪Permissive hypercapnia▪Gentler ventilatory modes (HFOV, PC, PS)▪Inhaled nitric oxide▪Non-invasive ventilation: NCPAP/SiPAP, HFNC, RAM▪Judicious use of oxygen▪Improved survival of preterm babies

Lung Development

▪8-10wks: guts into abdomen, diaphragm closes▪13-25wks: gas exchange sites forming, Type II endothelial cells appear (surfactant)▪24-34wks: thinning interstitium, capillary networks, surfactant produced/excreted▪36wks-10 yrs: alveoli increase #, size, shape

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Lung Development

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Impact of Preterm Birth on Lung Development▪Preterm infants, especially ELBW, in middle of canalicular stage, just beginning saccular stage▪Interruption of lung development due to

•Preterm birth•Air-breathing when lung should be fluid-filled•Mechanical ventilation and oxygen therapy

▪Diminished elasticity reduces pulmonary compliance due to•Altered collagen composition•Decreased elastin concentration

Impact of Preterm Birth on Lung Development

▪Immature antioxidant system -> more vulnerable to damage from O2 metabolites ▪Potential for remodeling and growth

•Surface area increases from 0.5m2 at 24 wks gestation to 4.5m2 at term

Respiratory Vulnerabilities

▪Newborn susceptible to respiratory distress due to limits on respiratory system:•Ribcage not well ossified•Respiratory muscles have low endurance and strength

•Floppy chest wall offers little resistance to collapse

•Obligate nose breathers•Tongue large, trachea and glottis small


▪Close proximity of trachea to bronchi -> rapid transmission of infection▪Immature mucosal lining -> less protection against infection▪Large dead space -> need to breathe twice as fast as adult to oxygenate


▪Higher metabolic rate at rest: increased O2 consumption compared to adult▪Operate close to maximum capacity normally▪Little compensatory reserve for increased demands

Respiratory Distress Syndrome

▪Most common cause of respiratory distress in premature infants•Incidence: inversely proportional to GA•Most babes <29 wks have RDS

▪Small proportion of term infants develop RDS•Damage to Type II cells and/or enzyme pathways

•IDM’s, C-sections, asphyxia

Risk Factors for Developing Respiratory Distress Syndrome

Increased risk▪Premature Birth

▪Sex▪Infant of a Diabetic Mother▪Asphyxia

▪C-section without labor▪Caucasian race▪Chorioamnioitis

▪Hydrops

Decreased risk▪Chronic intrauterine stress

▪PPROM▪Maternal HTN▪IUGR/SGA

▪Antenatal steroids▪Mat. drug use▪Tocolytic agents

RDS Pathophysiology

▪Insufficient volume of surfactant•Unstable alveoli collapse•Normal Functional Residual Capacity not established

•Each breath requires increased energy output

RDS Pathophysiology

▪Constriction of pulmonary vasculature•Decreased pulmonary blood flow•Damage to endothelial membranes•Decreased surfactant production

Surface Tension and Surfactant▪Surface tension

•The force that arises from the interaction of molecules of a liquid

•Opposes lung inflation, supports lung deflation

•Smaller diameter of alveolus requires higher pressures for inflation

•Surfactant coats alveolus reducing effort to inflate lungs from low volume

Respiratory-Functional Residual Capacity (FRC)

Hooper, S., te Pas, A., Lewis, R., & Morley, C. (2010). Establishing Functional Residual Capacity at Birth. Neoreviews, 11(9), e474-e483. http://dx.doi.org/10.1542/neo.11-9-e47420

Movie 1 - Time-lapsed phase contrast X-ray image sequence, showing the effect intermittent positive pressure ventilation (PPV) without a positive end-expiratory pressure (PEEP), on lung aeration at birth.

http://neoreviews.aappublications.org/highwire/filestream/18026/field_highwire_adjunct_files/0/Movie1_PPV_no_PEEP.mov

Movie 2 - Time-lapsed phase contrast X-ray image sequence, showing the effect intermittent positive pressure ventilation (PPV) with 5 cmH2O of positive end-expiratory pressure (PEEP), on lung aeration at birth.

http://neoreviews.aappublications.org/highwire/filestream/18026/field_highwire_adjunct_files/1/Movie2_PPV_with_PEEP.mov

Surfactant

▪Composed of surfactant proteins and phospholipids- oily liquid▪Synthesis controlled by enzymes, regulated by hormones: glucocorticoids▪Spreads easily, rapidly over lung surface

Surfactant

▪Reduces surface tension, aids lung expansion with lower pressures▪Stabilizes alveoli, maintains Functional Residual Capacity (FRC), prevents atelectasis▪Reduces damage to epithelium▪Aids fluid clearance from alveolar surface into interstitium▪Works as antimicrobial agent

RDS Pathophysiology

▪Death of alveolar epithelial cells/airway cells•Sloughing of cells, exudation of serum•Fibrin clots: hyaline membranes•Decreased surface area for gas exchange

RDS Clinical Findings

▪Physical Exam•Tachypnea, grunting, flaring, retracting within minutes or hours of life

•Pallor, cyanosis, hypotension•Decreased breath sounds, rales


▪CXR•Reduced lung volumes•“Ground glass” appearance: areas of atelectasis and hyperexpansion

26CXR: Air bronchograms


▪Blood gas: hypoxemia, acidosis (respiratory, metabolic, mixed)

RDS Prevention ▪Antenatal steroids (Betamethasone 48 hrs PTD)• Accelerate lung maturation• Single course for women between 24 and 34 wks

gestation at risk for preterm delivery• Reduces incidence of RDS by 50% in infants < 31

wks• Decreases neonatal mortality by 30%• Decreases incidence of IVH and NEC• No adverse consequences identified at this dose• Ongoing trials evaluating use of repeated doses in

undelivered moms at continued high risk

Unique Needs of the ELBW Baby: It’s All About Protection

▪What we do during those first minutes, to hours can affect outcomes▪All systems immature and vulnerable

6/27/201729

The Golden Hour

▪Definition •Taken from shock trauma medicine indicating the critical first hour as the most important for improving survival

•For the extremely preterm neonate, initial steps undertaken to optimize coordination and execution of care with the goal of minimizing injury and improving outcomes

GOAL: resuscitation without injury!

6/27/201730

We Are Better, Together!California Perinatal Quality Care Collaborative (CPQCC): Delivery Room Management

▪Collaborative aims:•Best practice “Bundle” to improve care at high risk deliveries addressing: ‒Teamwork with use of pre-resuscitation checklists and simulation based learning‒Optimization of respiratory care for the preterm baby‒Maintenance of normothermia, avoidance of hypo and hyperthermia

www.cpqcc.org6/27/201731

CPQCC Delivery Room Management Collaborative Outcomes

6/27/201732

Measure Collaborative Before/After n 20

Individual Before /After n 31

Non ParticipantBefore/After n 44

Rate of Hypothermia

39% to 21% 38% to 33% 42% to 34%

Rate of Intubation in DR

53% to 40% 44% to 36% 43% to 40%

Rate of Surfactant Administration in Delivery Room

37% to 20% 19% to 12% 18% to 16%

RDS Treatment Strategies▪Initial DR stabilization -California Perinatal Quality Care Collaborative (CPQCC) guidelines▪Surfactant replacement▪Support ventilation (lung protection is goal)

‒Non-invasive ventilation

‒Gentler mechanical ventilation

▪Fluids, electrolytes, glucose, calories, normothermia▪Prevent complications

•Infection

•BPD/CLD▪Inhaled nitric oxide

Delivery Room Stabilization: CPQCC

▪Maintain normal body temperature: 36.5-37.5•Warmer ( or isolette) on servo, chemical mattress

•Room temp 26oC (79oF) (6th ed. NRP)•ELBW <1000gm/<28wk GA‒Wrap without drying in polyethylene wrap/bag

‒Dry head, place cap•Monitor/record infant’s temp q 5mins•Studies: higher risk of mortality if admitted with low core body temp (<36.40C)


▪Pulse oximetry•Monitor O2 saturations and HR, response to interventions

•Place preductally (right hand or wrist)•Functional after 60-90 secs: place immediately•Normal O2 sats in first 5 mins of life‒Fetal: 50%‒2 mins: 65% to 70%‒5 mins: 80% to 85%

Targeted O2 Sats

1 min 60-65%

2 min 65-70%

3 min 70-75%

4 min 75-80%

5 min 80-85%


▪Optimize O2 administration•Blended air/oxygen•Preterm (<32wks): start at FiO2 21% to 40%‒Target sat 80-85% by 5 mins of age‒Adjust to condition/sat goals of unit

•Meta-analysis of completed trials‒All infants, including preterm had decreased mortality overall with use of RA compared with supplemental O2


▪Optimize respiratory support•Establish/maintain resp efforts/FRC without injury to lung from excessive PPV•Consider CPAP before intubation •PPV: use lowest pressure that gives response (sats, HR)‒Initial pressures 20-30cm▪Poor response: use prolonged inflation 3-5secs▪May need higher initial pressure

‒Good seal, patent airway (CO2 detector)


▪Optimize airway management•Stabilize with PPV via bag/mask beforeintubation

•4 large trials compared early surfactant administration (within 1hr) vs early CPAP‒Use of early CPAP to stabilize very preterm will result in decreased need for intubation/surfactant without increasing morbidity

Surfactant Replacement

▪Minimize acute lung injury and sequelae‒Improves oxygenation‒Decreases mean airway pressure (sometimes need to be prepared to do quickly!)‒No significant effect on BPD, IVH, ROP, NEC, length of stay‒Studies of long-term effects: neurodevelopment outcome similar to controls

Surfactant Replacement ▪Prophylaxis vs Rescue Treatment• Prophylaxis: give within 15 minutes of

birth• Rescue: give when babe has established

RDS• Moved from a prophylactic approach to

early rescue dosing ‒Indicated for intubated patients needing >30% FiO2

• No consistent criteria for when to use

Surfactant Replacement

▪Rescue decreases severity of BPD but not incidence▪Adverse effects

•Transient hypoxia, bradycardia•Acute airway obstruction•Transient falls in BP, CBF (cerebral blood flow)•Pulmonary hemorrhage

Surfactant Replacement▪To intubate or not to intubate?

•Stable at birth: should the patient be intubated for surfactant? Can destabilize patient & cause deterioration

Surfactant Replacement▪Dose: how many?

•Most respond well to one dose•Additional dosing depends on response to first•Criteria for repeating dose unclear‒Accepted: q 12hrs, FiO2 >40%‒Very little data re: optimal dose, timing

▪Administration•Bolus better than slow infusion: better distribution•Use ETT with side port, HV dose into lungs•Turning side to side not used at UCSF

Oxygen therapy

▪Most commonly used drug in neonatal care▪No concentration is “safe”▪Use blender, analyzers▪Continuous monitoring (HR, sats)▪Humidify, warm▪Maintain stable delivery, concentration▪Wean slowly with continuous monitoring▪O2 saturation: target ranges

•Under 1000gms: 85%-92% (PaO2 45-60 torr)***

•Beyond 36wks: 90-95%

Non-invasive Ventilation

▪High-Flow Nasal Cannula (HFNC)•Delivers higher flows (up to 8L/min) thru NC with high humidity (•95%)

•Used by many centers (64%) as primary support for preterms with RDS, apnea of prematurity, post-extub care

•Minimal research to establish safety/efficacy•No direct measure of pressure to airway, no pop-off

•May result in inadvertent PEEP, excessive in VLBW

Non-Invasive Ventilation▪Nasal CPAP• Standard of care for preterm infants weaning

off mechanical ventilation• Primary means of respiratory support in VLBW• Early use of NCPAP in VLBW assoc with

decreased rates of BPD/CLD, ROP (VON study)

• Even better: early NCPAP after early surfactant

• Good evidence that even VLBW/ELBW can be successfully treated with NCPAP without surfactant

Noninvasive Ventilation

▪Nasal CPAP• Indications‒ Spontaneous breathing, mild to

moderate RDS‒ Cannot maintain PaO2 of 60 torr in 60%

FiO2

‒ Support during weaning from mechanical ventilation

Noninvasive Ventilation

▪Nasal CPAP: Advantages‒ Establishes and maintains FRC‒ Conserves surfactant‒ Decreases resistance, increases

compliance‒ Reduces apnea, lung injury, inflammation‒ Conserves energy‒ Reduce need for mechanical ventilation

Non-invasive ventilation▪NCPAP: Disadvantages

‒Gaseous distension of bowel‒Increased rate of pneumos‒Difficulty keeping prongs in nose/mask on face, maintaining patency‒Infant agitation‒Labor intensive for neonatal nurse‒Risk for device related pressure ulcers, scarring, disfigurement

Mechanical Ventilation

▪Indications• Apnea unresponsive to stimulation or hand

ventilation• High and rising PaCO2 : >60mmHg =

respiratory failure• Increasing FiO2 needs: > 60% despite

NCPAP‒ Sign of low lung volumes‒ Indicator of severe RDS

CPQCC DR Guidelines for Intubation

▪Continued need for PPV▪Rising FiO2 requirements▪Obstructed breaths▪No response to CPAP▪Apnea

UCSF Conventional Ventilation Practice

▪Principles

‒Keep tidal volumes normal (4 to 5 ml/kg)‒Sats 88 to 92‒PaCO2 about 45 to 60 (permissive hypercapnea)‒ pH >7.25‒Extubate ASAP

Inhaled Nitric Oxide:Therapeutic effects

•Improves oxygenation: optimizes ventilation/perfusion matching•Reduces lung inflammation and edema•Antioxidant effect on lung injury•Protective effects on surfactant function•Beneficial effects on pulmonary vascular/alveolar development

Inhaled Nitric Oxide▪Early use in neonates to treat PPHN in term and late preterm infants•Early RCT’s in preterms‒Improved oxygenation‒Decreased need for mechanical ventilation‒Improved survival without increase in IVH (>1000gms)‒Trend toward decrease in CLD/BPD‒Improvement in neurodevelopmental outcomes at 2 yrs of age

Desaturation Episodes: Critical Points▪Fewer desaturations with proper positioning• Abdomen• Developmental positioning, nesting▪Minimal handling during desaturation episode• Assess need for sedation▪Be patient, most will recover with no intervention▪O2 titrations used as last resort for desaturation episodes▪Set tight sat alarms on monitor▪Document episodes, interventions, infant’s response

Bronchopulmonary Dysplasia (BPD)

Implications of Preterm Birth and RDS/Bronchopulmonary Dysplasia (BPD)

▪Preterm birth greatest cause of neonatal morbidity and death in US and globally▪Immature lungs require respiratory assistance▪Ventilation injures lungs: lung tissue inflammation leads to BPD▪80% of infants with BPD born before 30 wks gestation▪BPD: increases mortality, long-term implications for lung health and brain development

Bronchopulmonary Dysplasia (BPD)

▪A chronic pulmonary disorder characterized by •Pulmonary fibrosis•Brochiolar metaplasia•Emphysema•Interstitial edema

BPD: Definition/Description▪NICHD definition mild BPD

•Requiring O2 for a total of at least 28 days•Acute lung injury minimized by antenatal steroids and surfactant treatment

•Disrupted alveolar and vascular development: fewer, larger alveoli, pulmonary hypertension

•Less inflammation and fibrosis▪New description: significant BPD

•O2 at 36wks postmenstrual age and for more than 28 days

•Inability to maintain O2 sats of 90% or more in RA

Bronchopulmonary Dysplasia (BPD)▪Definition has evolved since it was first described in 1967 by Northway:

•Presence of persistent respiratory signs and symptoms along with the need for supplemental oxygen, and an abnormal CXR at 28 days of life

•Does not take into account extreme prematurity and level of required respiratory support

▪Current NICHD criteria:

‒Patients who are <32 weeks GA are assessed at 36 weeks PMA or when discharged home, whichever comes first

‒Patients who are >32 weeks GA are assessed between 29 to 55 days of age or when discharged home, whichever comes first

Current Definition of BPD:

(UpToDate 2017)

Gestational age

<32 week ≥32 week

Time point of assessment 36 weeks PMA or discharge to home, whichever comes first

>28 days but <56 days postnatal age or discharge to home, whichever comes first

Treatment with oxygen >21 percent for at least 28 days plus

Mild BPDBreathing room air at 36 weeks PMA or discharge, whichever comes first

Breathing room air by 56 days postnatal age or discharge, whichever comes first

Moderate BPDNeed* for <30 percent oxygen at 36 weeks PMA or discharge, whichever comes first

Need* for <30 percent oxygen at 56 days postnatal age or discharge, whichever comes first

Severe BPD

Need* for ≥30 percent oxygen and/or positive pressure (PPV or NCPAP) at 36 weeks PMA or discharge, whichever comes first

Need* for ≥30 percent oxygen and/or positive pressure (PPV or NCPAP) at 56 days postnatal age or discharge, whichever comes first

BPD Incidence

▪Inversely proportional to gestational age▪Of survivors corrected to 36 weeks

•85% of babies born at 22 weeks had an O2 requirement

•22% of babies born at 28 weeks had an O2 requirement

(Stoll et al., 2010)

BPD

▪Chronic lung disease▪Inversely proportional to gestational age▪Develops after acute pulmonary disease▪Chronic, constant recurrent lung injury⦿Lung injury and repair occur simultaneously

with organ growth and development▪Prolongs need for O2 , mechanical ventilation

Factors that Contribute to BPD

BPD

Hyperoxic Injury

Inflammation

Nutritional Problems Genetics

Sex-specific Differences

Alterations in Microbiome

Increased Pulmonary Arterial Muscularization

Barotrauma

Fetal Programing

Other

BPD: Multifactoral

•Lung immaturity: prematurity•Lung injury/inflammation‒ Barotrauma/volutrauma▪O2 toxicity: high or low levels, short or long term▪Occurs in ventilated infants without O2

•Infection‒Chorioamnionitis ▪Inflammatory cytokines present in high levels in amniotic fluid of babes who develop BPD

BPD Treatment▪Lung protection

•Extubate to nasal CPAP or SiPAP with low FiO2 to minimize toxicity to lung

•No air leak (PIE or pneumo)•Best ventilation strategy yet to be determined•Sats of 88% to 92% will provide adequate tissue oxygenation, help avoid complications of BPD

•Better weight gain •Prevent development of pulmonary hypertension, right-sided heart failure

•Avoid hyperoxia: ROP

BPD → Pulmonary HTN

(Mourani et al. Clinic Perinatol 2015)

Diagnosis of Pulmonary Hypertension

▪Cardiac catheterization – gold standard•Invasive

▪ECHO•Non-invasive•Right ventricular systolic pressure derived from tricuspid regurgitant jet velocity, or from estimated pulmonary pressures >50% of the systemic pressures

•Limitations such as interobserver reliability

Risk Factors for Development of Pulmonary Hypertension in Infants with Bronchopulmonary Dysplasia: Systemic Review and Meta-Analysis

▪Inclusion Criteria:•Studies involving preterm infants with BPD and pulmonary hypertension that reported an assessment of risk factors for pulmonary hypertension

▪Exclusion Criteria:•Animal models, adult population•Further cardiovascular or lung anomalies

Naguib, et al. 2016


Naguib, et al. 2016


▪Conclusions:

•Identified 9 risk factors consistently associated with development of pulmonary hypertension in infants with BPD

•In order of decreasing risk (same as table 3):

‒Prolonged duration of mechanical ventilation

‒Length of stay in hospital

‒Oligohydramnios

‒Lower birth weight

‒Use of HFOV

‒SGA

‒Sepsis

‒Lower GA at birth

‒Severity of BPD

Naguib, et al. 2016

Treatment of Pulmonary Hypertension in Bronchopulmonary Dysplasia

▪No controlled trial of pulmonary hypertension treatment in BPD has been conducted

▪Aggressively treat factors contributing to lung disease:

•Episodes of hypoxia

•Ventilatory insufficiency

•Bronchoconstriction

•Chronic reflux and aspiration

•Upper and lower airway obstruction

▪Immunoprophylaxis against respiratory infections

(Mourani & Abman, 2015)

Treatment of Pulmonary Hypertension in Bronchopulmonary Dysplasia▪Inhaled iNO

•local vasodilator

•Approved for the treatment of pulmonary hypertension of the newborn

•Has most safety data for preterm infants

▪Sildenafil (selective type 5 phosphodiesterase inhibitor)

•Systemic vasodilator

• Approved in adults, extensively used off-label for infants

(Mourani & Abman, 2015)

Treatment of Pulmonary Hypertension in Bronchopulmonary Dysplasia▪Trepostinil (Remodulin)

•Vasodilator

•Continuous IV or subcutaneous infusion

•Can create V/Q mismatch and intrapulmonary shunts → Desaturations

▪Bosentan

•Competitive antagonist of endothelin-1 (therefor blocks vasoconstriction)

▪PDA stent

•RV failure

Treatment of Pulmonary Hypertension in Bronchopulmonary Dysplasia▪Supplemental oxygen

•Target oxygen saturations >93% premature infants, >95% term infants

▪Diuretics

•Volume overload

•Spironolactone – additional benefit due to mineralcorticoid blockade in RV hypertrophy/PH, and can improve lung mechanics in BPD

In Summary:Simple Lung Protection Philosophy▪Lung protection from delivery to discharge▪Normal lung volume is good

•Over distension is bad•Atelectasis is bad

▪Stability is good

▪Working hard is bad▪Ventilator strategy is more important than ventilator type▪It is best to be off the ventilator

References

▪Cifuentes J. et al: Respiratory System Management and Complications. In Kenner C. and Lott J: Comprehensive Neonatal Nursing (3rd ed. pp 211-217). Saunders 2003

▪CPQCC: Delivery Room Management Quality Improvement Toolkit, revised 7/6/11

▪Durand, D.: Ventilator Strategies in the NICU: What’s New in 2010. Presentation at 7th National Advanced Practice Neonatal Nurses Conference. Contemporary Forums, San Francisco, March 2010

▪Farrow K., Steinhorn R.: Neonatal Respiratory Failure: Pathophysiology and Management. In Muers K. et al: ECMO Extracorporeal Cardiopulmonary Support in Critical Care (3rd ed. pp 253-265) ELSO 2005

▪Gardes J.: Bronchopulmonary Dysplasia. In Polin R., Yoder M. eds: Workbook in Practical Neonatology (4th ed. Pp 167-184) Saunders Elsevier 2007

References▪ Finer, N. N., Rich, W., Halamek, L. P., & Leone, T. A. (2012). The delivery room of the

future: The fetal and neonatal resuscitation and transition suite. Clinics in Perinatology, 39(4), 931-939.

▪ Kandraju, H., Murki, S., Subramanian, S., Gaddam, P., Deorari, A., & Kumar, P. (2013). Early routine versus late selective surfactant in preterm neonates with respiratory distress syndrome on nasal continuous positive airway pressure: A randomized controlled trial. Neonatology, 103(2), 148-154.

▪ Kumar, P., Denson, S. E., Mancuso, T. J., & Committee on Fetus and Newborn, Section on Anesthesiology and Pain Medicine. (2010). Premedication for nonemergency endotracheal intubation in the neonate. Pediatrics, 125(3), 608-615.

▪ Leone, T. A., Finer, N. N., & Rich, W. (2012). Delivery room respiratory management of the term and preterm infant. Clinics in Perinatology, 39(3), 431-440.

▪ Vaucher, Y. E., Peralta-Carcelen, M., Finer, N. N., Carlo, W. A., Gantz, M. G., Walsh, M. C., et al. (2012). Neurodevelopmental outcomes in the early CPAP and pulse oximetry trial. The New England Journal of Medicine, 367(26), 2495-2504.

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References⦿ Gardner S., Goldson E.: The Neonate and the Environment: Impact on

Development. In Merenstein and Gardner: Handbook of Neonatal Intensive Care (7th ed pp 285-296) Mosby Elsevier 2011

⦿ Gardner S. et al: Respiratory Diseases. In Merenstein & Gardner: Handbook of Neonatal Intensive Care (7th ed pp 581-641) Mosby Elsevier 2011

⦿ Gardner, S. et al: Pain and Pain Relief: . In Merenstein & Gardner: Handbook of Neonatal Intensive Care (7th ed pp 581-641) Mosby Elsevier 2011

⦿ Inselman S. et al: Growth and Development of the Lung. Journal of Pediatrics Vol 98 #1. January 1981, pp 1-6

⦿ Kenner C: Resuscitation and Stabilization of the Newborn. In Kenner C. and Lott J: Comprehensive Neonatal Nursing (3rd ed pp 211-217) Saunders 2003

⦿ Miller, N.: Techniques of Early Respiratory Management of Very Low Extremely Low Birth Weigh Infants. Neonatal Network, Vol. 29, No 3, May/June 2010, pp 153-160

References⦿ Peterson, S.: Understanding the Sequence of Pulmonary Injury in the

Extremely Low Birth Weight, Surfactant-Deficient Infant. Neonatal Network, Vol. 28, No. 4, July/Aug 2009, pp 221-229

⦿ Sosento I, Bancalari E: New Developments in the Presentation, Pathogenesis, Epidemiology and Prevention of Bronchopulmonary Dysplasia. In Bancalari E., Polin R.: The Newborn Lung: Neonatology Questions and Controversies (pp 187 -207) Saunders 2008

⦿ Stokowski, L. A. (2005). A primer on apnea of prematurity. Advances in neonatal care, 5(3), 155-170.

⦿UCSF Intensive Care Nursery VAP Task Force: Ventilator Associated Pneumonia Prevention Bundle. June 2007

⦿UCSF Intensive Care Nursery: SOP: Trial of Late Surfactant to Prevent BPD: A Study in Preterm Infants Receiving Inhaled Nitric Oxide (TOLSURF study)

⦿UCSF Medical Center Department of Nursing: Respiratory Care of the Neonate-Intensive Care (Neonatal). Nursing Procedures Manual. Revised 8/07

Questions?

Tanya Hatfield, RNC-NIC, [email protected]

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alphabet soup of preemie problems - bch outreach

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