Neonatal Respiratory System

Neonatal Respiratory System 2

Contents

Embryology and System Development 3

Transition from Intrauterine to Extrauterine Life 4

Resuscitation of the Infant with Respiratory Distress 6• ResuscitationEquipment 6

• ResuscitationProcedure 7

Differential Diagnosis 7

History and Respiratory System Assessment 8

Common Neonatal Respiratory Disorders 9• RespiratoryDistressSyndrome 9

• TransientTachypneaoftheNewborn 12

• MeconiumAspirationSyndrome 13

• Pneumonia 15

• PersistentPulmonaryHypertensionof theNewborn 16

• Air-LeakSyndrome 18

• CongenitalDiaphragmaticHernia 21

• ApneaofPrematurity 22

• ChronicLungDisease/BronchopulmonaryDysplasia 24

Special Respiratory Concerns with the Premature Infant 28

Related Nursing Care 29

References 32

Additional Readings 33

ObjectivesUponcompletionofthiscourse,theparticipantwillbeableto:

• Describethetransitionfromintrauterinetoextrauterinelife.

• Identifytheequipmentthatshouldbereadilyavailableforaneonatalresuscitation.

• ListthemedicationsrecommendedintheAAP/AHANeonatalResuscitationProgram.

• Describeassessmentanddiagnosticstrategiesofcommonneonatalrespiratorydisorders.

• Definenursinginterventionsformanagingtheinfantwithrespiratorydistress.

Sandra L. Gardner, RN, MS, CNS, PNPDirector of Professional Outreach ConsultationAurora, Colorado

Vicky L. Armstrong, RNC, MSNVP Neonatal Nursing ServicesNationwide Children’s HospitalColumbus, Ohio


forcesactonair-liquidinterfaces,causingawaterdroplettobeadup.Asurface-activecompoundcalledsurfactantreducesthesurfacetensionandallowsthedroplettospreadoutintoathinlayer.Inthelungs,thesurface-tensionforcestendtocausethealveolitocollapse.Surfactantisneededtolowerthesurfacetensionwithinthesealveolitopreventtheircollapseattheendofexpiration.Surfactantisasurface-activeagentcomposedofphospholipids(includinglecithinandsphingomyelin),cholesterol,lipids,andproteinsandissynthesizedintypeIIalveolarepithelialcells.Thesecellsbegintoappearinthelungbetween 20and24weeksofgestation.

Embryology and System DevelopmentTherearefivestagesintheembryonicdevelopmentofnormallunggrowth:embryonic,pseudoglandular,canalicular,terminalsac,andalveolar.AsshowninFigure1,theembryonicstageoccursfromconceptiontoweek5,withthemajoreventbeingtheformationoftheproximalairways.Thelungbudappearsandbeginstodivide,thepulmonaryveindevelopsandextendstojointhelungbud,andthetracheadevelops.Instage2,thepseudoglandularstage,formationoftheconductingairwaysoccurs(weeks6–16).Cartilageappearsandthemainbronchiform.Formationofnewbronchiiscompleteandthecapillarybedisformed.Duringthecanalicularstage(weeks17–24),themajorfeatureisformationofacini(gas-exchangingsites).Thereisanappearanceofcuboidalcells,thecapillariesinvadetheterminalairsacwalls,typeIIalveolarcellsappear,andtheairwaychangesfromglandulartotubularandincreasesinlengthanddiameter.Thealveolarsacsareformedandthereisdevelopmentofgas-exchangesitesintheterminalsacstage(weeks25–37).Inthealveolar,orfinal,stage(week37–postnatal),expansionofthesurfaceareaoccurs.Thisstagecontinuesupto8yearsafterbirth.

Thesurfaceofthelungislinedbyalayeroffluidthatcreatesanair-liquidinterface.Surface-tension

Figure 1. The five phases of the process of tracheobronchial airway development.

n = number of branches.

Reproduced, with permission, from Leuthner SR: Anatomy and development of the lung. In Weisman LE, Hansen TN, eds: Contemporary Diagnosis and Management of Neonatal Respiratory Diseases, 3rd ed. © 2003, Handbooks in Health Care Co, p 2.

K e y L e a r n i n g s

»Therearefivestagesintheembryonicdevelopmentofnormallunggrowth.

»Thefinalstagecontinuesupto8yearsafterbirth.

»Thesurfaceofthelungislinedbyalayeroffluidthatcreatesanair-liquidinterface.

» Surfactantisneededtolowerthesurfacetensionwithinthealveolitopreventtheircollapse.


subclavian,andcoronaryarteriesbeforemixingwithbloodshuntedacrosstheductusarteriosus.Theremainderofthebloodenteringtherightatriummixeswithbloodfromthesuperiorvenacavaandcontinuesintotherightventricleandpulmonaryarteries.Mostofthisbloodshuntsacrosstheductusarteriosusintothedescendingaorta.

Oncetheinfantisdeliveredandthetransitiontoextrauterinelifebegins,respiratoryandcardiovascularchangesoccurindependentlybutsimultaneously.Fetallungfluidisreplacedbyair,sotheliquid-liquidinterfaceofalveolibecomesanair-liquidinterfaceandsurfacetensionforcesbegin.Surfactantdecreasesthesurfacetensionwiththefirstbreathandarterialoxygentensionrises,resultinginreversalofhypoxemia-inducedpulmonaryvasoconstriction.Thepulmonaryvascularresistancebeginstodeclineasaresultofincreasingoxygensaturationsanddecreasingcarbondioxidelevels,resultinginanincreasein

Transition from Intrauterine to Extrauterine LifeThetransitionfromintrauterinetoextrauterineenvironmentandfromfetaltopostnatallifebeginswiththeclampingoftheumbilicalcordandtheinfant’sfirstbreath.

Inutero,fetalcirculation(Figure2)dependsontheplacentaandthreefetalducts:theductusvenosus,theforamenovale,andtheductusarteriosus.Theplacentaallowsfortheexchangeofgases,nutrients,andmetabolicwasteproducts.Itisalow-resistancecircuitthatmaintainsalowfetalsystemicvascularresistance,whilethepulmonaryfetalcircuitmaintainsahighpulmonaryvascularresistance.Subsequently,theincreasedpulmonaryvascularresistanceandlowsystemicvascularresistancepromoteright-to-leftshuntingthroughthefetalducts.Theductusvenosusallowspartoftheoxygenatedbloodcarriedbytheumbilicalveintobypasstheliver.Oxygenatedbloodenteringtheheartflowsthroughtheforamenovaleintotheleftatrium,thenperfusesthebrainandtheheartviathecarotid,subclavian,andcoronaryarteries.Theductusarteriosusdirectsbloodfromthemainpulmonaryarterytothedescendingaorta.Fetaladmixtureattheforamenovaleandductusarteriosuslowersfetalarterialoxygentensionto~25–35mmHg.Thelowfetaloxygentensionhelpstomaintainpulmonaryarteryvasoconstriction,allowingbloodtobypassthelungandflowinsteadthroughtheforamenovaleandductusarteriosus.

Insummary,fetalbloodflowsfromtheplacentaviatheumbilicalvein,bypassestheliverviatheductusvenosus,andenterstheinferiorvenacava.Fromtheinferiorvenacava,bloodenterstherightatrium,wherethemajorityofitisshuntedthroughtheforamenovaleintotheleftatrium.Bloodcontinuesintotheleftventricle,whereitmixeswithbloodreturningfromthepulmonaryveins,andistheninjectedintotheascendingaorta.Fromtheascendingaorta,itsuppliesthecarotid,

Figure 2. Fetal circulation.

Tohead

Toarm

Ductusarteriosus

Leftatrium

Left lung

LeftventricleDuctusvenosus

Inferiorvenacava

Renal arteries & veins

Aorta

ArterialbloodVenousbloodMixedarterial-venousblood

Toleftleg

Hypogastricarteries

Bladder

Placenta

Umbilicalcord

Umbilicus Umbilicalarteries

Portal vein

Umbilical vein

Liver

Superior venacava

Pulmonaryartery

Foramenovale

Rightatrium

Rightventricle

Right

Hepaticvein

Aorta

Toarm

Once the infant is delivered and the transition to extrauterine life begins, respiratory and cardiovascular changes occur independently but simultaneously.


ductusarteriosusclosesfunctionallyat15–24hoursofagebutdoesnotcloseanatomicallyfor3–4weeks(Tables1and2).

pulmonarybloodflow.Decreasingprostaglandinlevelsalsowillfacilitatethereversalofthepulmonaryvasoconstriction.Removaloftheplacentalcircuitbytheclampingoftheumbilicalcordresultsinincreasingsystemicvascularresistance.Simultaneouscardiovascularchangesincludetheclosingoffetalshunts.Theductusvenosusfunctionallyclosesastheumbilicalcordisclamped.Functionalclosureoftheforamenovaleoccursatbirthfromthechangingatrialpressuresandincreasingsystemicvascularresistance.Theleftatrialpressureisnowgreaterthantherightatrialpressure.WithincreasingarterialoxygentensionanddecreasinglevelsofprostaglandinE,the

Table 1. Summary of Main Transitional Events from Fetal to Neonatal CirculationLoss of fetal lung fluid

Secretion of surfactant

Establishment of functional residual capacity

Fall in pulmonary vascular resistance

Rise in systemic vascular resistance

Closing of fetal shunts

Increasing pulmonary blood flow

Table 2. Transition from Fetal to Neonatal Circulation

First Period of Reactivity(early reactivity)

Period of Relative Inactivity(deep sleep)

Second Period of Reactivity(secondary reactivity)

Time Course Birth to 30–45 minutes 45 minutes to 2–4 hours 3–4 hours thereafter

CNS Alert, eyes open; vigorous, active crying; increased tone and highly responsive to stimuli

Somnolent, eyes closed; difficult to arouse or interest; decreased tone and general responsiveness; can be awakened only briefly

Hungry; progresses normally through wake, feed, quiet alert, drowsy, and deep sleep in cyclic fashion

Color Ruddy with acrocyanosis Pale, no cyanosis Pink, no cyanosis

Heart Rate High (140–160 BPM) and very reactive

Low (90–120 BPM) and briefly reactive

Varies with wake/sleep cycle

Respiratory Rate High (40–60 BPM), mild retractions, moist rales

Low (20–40 BPM), no retractions, no rales; occasional periodic breathing

Varies with wake/sleep cycle

Blood Pressure Should rise slowly but steadily through all stages

Bowel Sounds Active bowel sounds; belly distended; may pass meconium and urine

Inactive bowel sounds; less distention; belly easily palpated

Active bowel sounds; air swallowing and distention with crying

Adapted from Molteni RA: Neonatal Respiratory Distress Clinical Education Aid. © 1992 Abbott Nutrition, p 3.


»Inutero,fetalcirculationdependsontheplacentaandfetalducts.

»Lowfetaloxygentensionallowsbloodtobypassthelung.

»Atdelivery,respiratoryandcardiovascularchangesoccurindependentlybutsimultaneously.


• Suctioncatheters(5For6F,8F,10F,12For14F)• Laryngealairwaymask• Resuscitationbagwithmanometerorpressure-releasevalve(capableofdelivering90%–100%oxygen)

• Laryngoscopewithextrabatteries• Straightblades:sizes0and1withextrabulbs• Endotrachealtubes(2.5,3.0,3.5,4.0mminternaldiameter)

• Stylet• CO2detectororcapnograph• Alcoholsponges• Scissors• Tapeorsecuringdeviceforendotrachealtube• 8Ffeedingtube;20-mLsyringe• Facemasks(newborn,prematuresizes)• Oxygensourcewithflowmeterandtubing;oxygenblenderfordeliveryofoxygenfrom 21%to100%)

• Compressedairsource• Pulseoximeter;oximeterprobe• Thermoregulationsupplies:plasticbagorplasticwrap;chemicallyactivatedwarmingpad;transportincubator(prewarmed)

Resuscitation of the Infant with Respiratory DistressAnticipationisakeycomponentofthesuccessfulresuscitationofadistressednewborn.Maternalorfetalconditionsthatplaceanewbornatriskforrespiratorydepression/distressatbirthmustberecognized.AccordingtotheAmericanAcademyofPediatrics(AAP)andtheAmericanHeartAssociation(AHA),“Everynewbornhasarighttoaresuscitationperformedatahighlevelofcompetence.Theproperequipmentmustbeimmediatelyavailableatdelivery,andhealthcareprofessionalsmustbeskilledinresuscitatinganewbornandcapableofworkingsmoothlyasateam” (Kattwinkel2011)

Resuscitation Equipment

Resuscitationequipmentshouldbeavailable,readytouse,andfunctionalatalltimes,andshouldinclude: • Radiantwarmer,towels,andblankets(prewarmed)• Stethoscope• Bulbsyringe• Mechanicalsuctionandtubing• Meconiumaspirator

Table 3. Medications for Neonatal Resuscitation

Medication*Concentration to Administer

Preparation Dosage/Route† Total Dose/Infant: Weight/Total mg/Total mL

Rate/Precautions

Epinephrine 1:10,000 3-mL or 10-mL ampules

0.1–0.3 mL/kg

IV or ET

Weight Total mL 1 kg 0.1–0.3 mL2 kg 0.2–0.6 mL3 kg 0.3–0.9 mL4 kg 0.4–1.2 mL

Give rapidly

May dilute with normal saline to 1–2 mL if giving ET

Use two different-sized syringes—one size for IV dosage and one size for ETT dosage (NiermeyerandClarke2011)

Volume Expanders

Lactated Ringer’s solution or normal saline

100–250 mL 10 mL/kg

IV per umbilical vein

Weight Total mL1 kg 10 mL2 kg 20 mL3 kg 30 mL4 kg 40 mL

Give over 5–10 minutes

* Sodium bicarbonate is not a recommended therapy in neonatal resuscitation guidelines. Use only after adequate ventilation is established and there is no response to other therapies (NeoFax 2011) † IV = intravenous, ET = endotracheal Adapted from Kattwinkel J, ed. Neonatal Resuscitation Textbook. © 2011 American Academy of Pediatrics and American Heart Association.


Differential DiagnosisThedifferentialdiagnosisforneonatalrespiratorydistressisverybroad(seeTables5and6).Thepractitionermustcarefullyreviewthematernalhistory,observetheinfant’sdiseasecourse,andassesstheresultsofthephysicalexamination.Laboratorytestsandradiologicfindingsareadjunctstothedifferentialdiagnosis.

MedicationsrecommendedintheAAP/AHANeonatalResuscitationProgram(NRP)(Kattwinkel2011)shouldalsobereadilyavailable,includingintravenousfluids(dextrose10%;normalsalineforflush)andumbilicalvesselcannulationmaterials(Table3).

Resuscitation Procedure

Masteryofneonatalresuscitationskillsisnecessaryforperformingsuccessfulresuscitation.TheAAP/AHANRPisanationalprogramthatprovideshealthcareprofessionalswiththeknowledgeandskillstoresuscitatenewborninfantsbyusingastandardizedapproach(Kattwinkel2011)

Becausetheclinicalassessmentofcyanosisisnotreliable,andnewbornsduringtransitionmaytakeseveralminutestoincreasetheirbloodoxygensaturations,usingapulseoximeterassistsindeterminingtheneedforsupplementaloxygen.Placethepulseoximeterprobepreductally(ontherightarm),and,afterthepulseoximeterisreadingreliably,adjustthepercentageofsupplementaloxygenconcentrationtoachievetargetsaturationsinTable4.

Table 5. Pulmonary Disorders

Common Less Common

Respiratory distress syndrome Pulmonary hypoplasia

Transient tachypnea Upper airway obstruction

Meconium aspiration syndrome Rib cage abnormalities

Pneumonia Space-occupying lesions

Air-leak syndrome Pulmonary hemorrhage

Table 4: Targeted Preductal Pulse Oximetry Ranges in the First 10 Minutes of Life in Normal, Term Newborns

Time SpO2 Values

1 minute 60% – 65%

2 minutes 65% – 70%

3 minutes 70% – 75%

4 minutes 75% – 80%

5 minutes 80% – 85%

10 minutes 85% – 95%


»Thedifferentialdiagnosisforneonatalrespiratorydistressisverybroad,andmayincludepulmonary,vascular,metabolic,orneuromusculardisorders.

Table 6. Extrapulmonary DisordersVascular Metabolic Neuromuscular

Persistent pulmonary hypertension Congenital heart disease Hypovolemia, anemia Polycythemia

Acidosis Hypoglycemia Hypothermia

Cerebral edema or hemorrhage Drugs Muscle disorders Spinal cord problems Phrenic nerve damage

Adapted from: Kattwinkel et al. 2010.


»Anticipationisakeycomponentofthesuccessfulresuscitationofadistressednewborn.

»Resuscitationequipmentandmedicationsshouldbeavailable,readytouse,andfunctionalatalltimes.


Table 7. History

Mother Prenatal history and careFamily illnessesAgePregnancy-related complicationsMedications Substance abuseGravida, para, abortions, living children Blood type, antibody screening

Intrapartum Intrapartal complicationsTime of rupture of membranes

(spontaneous or artificial)Description of amniotic fluid (clear,

foul-smelling, meconium-stained)Onset and duration of labor

(spontaneous or induced)MedicationsEvidence of fetal distressMethod of delivery

Vaginal (especially forceps, vacuum extraction)Cesarean

Infant Apgar scoresResuscitative interventionsGestational-age examinationGeneral physical examination

Table 8. Respiratory System Assessment

Color

Pink Reddish-pink hue of skin, nailbeds, and mucous membranes

Cyanosis Blue discoloration of skin, nailbeds, and mucous membranes

Acrocyanosis Peripheral cyanosis of hands and feet

Plethora Ruddy color

Pallor Pale, white skin

Type of Breathing

Apnea Cessation of breathing for >20 seconds, usually with color changes and bradycardia

Periodic respirations

Intermittent cessation of respiration; usually pauses between breaths <15 seconds

Dyspnea Labored or difficult breathing

Bradypnea Abnormally slow respiratory pattern; 20–30 BPM of slower, deeper respirations

Tachypnea Respiratory rate >60 BPM

Respiratory Effort

Chest movement

Depth of respiration, symmetry, synchrony

Paradoxical respiratory effort

Inward pull of lower thorax and bulging of abdomen with each breath

Retractions Inward pull of chest wall on inspiration

Other Respiratory Findings

Expiratory grunt Audible, forced expiration through a partially closed glottis

Delays expiration and increases gas exchange by increasing end-expiratory pressure

Nasal flaring Increased size of nares with respiration to decrease airway resistance

Stridor High-pitched crowing sound caused by narrowing of glottis or trachea

table continued on next page

Figure 3. The normal lung.

History and Respiratory System Assessment


Common Neonatal Respiratory Disorders

Respiratory Distress Syndrome

Respiratorydistresssyndrome(RDS)iscausedbyaprimaryabsenceordeficiencyofsurfactant.Endogenoussurfactantpreventsincreasedsurfacetension,whichcanleadtoalveolarcollapse.

Incidence (MoïseandHansen2003;Cifuentsetal.2002)

• 40,000infantsperyearintheUS

• 14%oflow-birth-weightinfants

• 60%–80%ofinfants<28weeks’ gestationalage

• Inverselyproportionaltogestationalage

Infants at Risk/Predisposing Factors

• Prematureinfants

• Maleinfants

• Infantsofdiabeticmothers—surfactantproductioncanbeinhibitedduetotheinfant’shyperinsulinemicstate

• Perinatalasphyxia—surfactantproductioncanbedecreasedduetotransientfetaldistress

Pathophysiology

Theabsenceordeficiencyofsurfactantresultsinincreasedalveolarsurfacetension,leadingtoalveolarcollapseanddecreasedlungcompliance(stifflungs).Withdecreasedlungcompliance,greaterandgreaternegativepressuremustbegeneratedtoinflatethelungwitheachsucceedingbreath.Widespreadalveolarcollapse,oratelectasis,resultsinmismatchesofventilationandperfusion(V/Qratio)andhypoventilation.Collapsedareasofthelungmaycontinuetoreceivecapillarybloodflow,butgasexchangedoesnotoccur.Intrapulmonaryshuntingcausesfurtherhypoxemia.Hypercarbiaalsodevelops,whichleadstorespiratoryacidosis.Hypoxiaatthecellularlevelresultsinanaerobicmetabolismand,subsequently,metabolicacidosis.Withthehypoxemiaandresultingacidosis,thereisincreasedpulmonaryvascularresistanceandvasoconstriction,leadingtopulmonaryhypoperfusionandadditionalhypoxemia.

Table 8. Respiratory System Assessment

Wheeze High-pitched, continuous lung sounds similar to dry whistling sound produced by air passing through a narrowed lumen

Chest Shape/Symmetry

Barrel-shaped chest

Suggests increased chest volume, eg, transient tachypnea of the newborn, meconium aspiration syndrome, persistent pulmonary hypertension

Bell-shaped chest

Suggests decreased chest volume, eg, respiratory distress syndrome, pulmonary hypoplasia

Chest wall asymmetry

Results from volume differences between two sides of thoracic cavity, eg, atelectasis, pneumothorax, unilateral pulmonary emphysema, cystic lung disease

Auscultation of Breath Sounds

Assess air movement and quality of breath sounds:Normal breath soundsAdventitious breath soundsBronchovesicular (expiration equals inspiration)RalesRhonchiWheezePleural friction rub

table continued from previous page


»Assessmentshouldincludeahistoryofthemother,infant,andintrapartumissues.

»Arespiratorysystemassessmentshouldincludetheinfant’scolor,typeofbreathing,respiratoryeffort,chestshape/symmetry,andauscultationofbreathsounds.


TheclinicalcourseofRDSisvariablebutself-limiting.Thereisprogressiveworseningoverthefirst2–3days,asevidencedbyincreasingoxygenrequirementsandpoorlungperformance.Postnatalsurfactantproductionbeginsat~48–72hoursofageandresultsinimprovedlungcomplianceanddecreasingrespiratorydistress.Thisrecoveryphaseisusuallyprecededbyaperiodofspontaneousdiuresis.

Management

Managementbeginswithpreventivemeasures.Administrationofantenatalsteroidsresultsinacceleratedmaturityofthefetallungs.TheincidenceandseverityofRDSaredecreasedininfantswhosemothersreceivedcorticosteroids24–48hoursbeforedelivery.Corticosteroidsaremosteffectivewheninfantsarelessthan34weeksgestationalageandthedrugisadministeredforatleast24hoursbutnolongerthan7daysbeforedelivery.Thereappearstobeanadditiveeffectintheimprovementoflungfunctionwiththecombineduseofantenatalsteroidsandpostnatalsurfactant.

ThegoalsoftreatingRDSaretopreventalveolarcollapse,optimizetissueoxygenationandcarbondioxideelimination,minimizeoxygenconsumption,andprovidesupportivecare.Administrationofoxygen,continuouspositiveairwaypressure,andpositive-pressureventilationmaybeneededtoprovideadequatetissueoxygenation,relievehypoxicvasoconstriction,andreduceright-to-leftshunting.Arterialbloodgases,pulseoximetry,andtranscutaneousoxygenmonitorsprovideinformationneededtomaintainthearterialoxygentensionwithinanacceptablerange.Positiveendexpiratorypressure,providedbyeithernasalprongsortrachealintubation,canbeusedtopreventatelectasisbymaintainingalveolardistentionthroughouttherespiratorycycle.Sedativesandanalgesicsmaybegiveniftheinfant’srespiratoryeffortsinterferewitheffectivepositive-pressureventilation(Table9).Supportivecareincludesmaintaininganeutralthermalenvironment,hydration,andcirculatorysupport;antibiotics;andstandardneonatalcare.

Clinical Presentation

Theusualclinicalpresentationisseenwithin6hoursafterbirthandincludesthefollowing:

Nasalflaring Anattempttodecreaseairwayresistanceandtakeinmoreoxygen

Grunting Anattempttomaintainfunctionalresidualcapacity

Retractions Areflectionofnoncompliantorstifflungsandcompliantchestwall

Tachypnea Anattempttomaintainminuteventilationandpreventlungcollapse

Hypoventilation Aresultofmusclefatigue

Diminishedbreathsounds

Areflectionofdecreasedairentry

Edematousextremities

Aresultofalteredvascularpermeability

Cyanosis Aresultofincreasinghypoxemia

Arterialbloodgasesdemonstratehypoxemiainroomair,hypercarbia,andmixedacidemia.WithmildRDS,thechestradiographshowsaground-glass,reticulogranularappearance(diffusealveolaratelectasissurroundingopenbronchi),airbronchograms(aeratedbronchioles),anddecreasedlungvolumes(diffuseatelectasis).WithsevereRDS,a“whiteout”patternisseenonthechestfilm,withlittleaerationandtheheartborderobscuredorfuzzy.

Management of RDS begins with preventive measures.

Used with permission from Gardner SL, et al. Merenstein and Gardner’s Handbook of Neonatal Intensive Care, 7th ed. © 2011 Mosby.

Figure 4. Lungs with mild RDS.

Figure 5. Lungs with severe RDS.


Table 9. Sedatives, Analgesics, and Muscle Relaxants for Neonates (NeoFax 2011)

Dose Side Effects

Sedatives

Lorazepam 0.05–0.1 mg/kg/dose IV slow pushUsual dosing interval: Q 4–8 hr

Respiratory depressionHypotension

Midazolam* 0.05–0.15 mg/kg/dose over at least 5 minutes IV, IM

Q 2–4 hr

Respiratory depression and respiratory arrestHypotensionSeizure, seizure-like activity following rapid

bolus administrationDue to side effects and insufficient evidence,

IV midazolam is not recommended as a sedative for neonates

Chloral hydrate 25–75 mg/kg/dose PO or PRUsual dosing interval: Q 6 hrDilute oral preparation or give after a feeding

CNS, respiratory, myocardial depressionIleus and bladder atonyIndirect hyperbilirubinemiaCardiac arrhythmiasDo not use in patients with significant liver or

kidney disease

Analgesics

Morphine 0.05–0.2 mg/kg/dose over at least 5 minutes IV, IM, SQ

Usual dosing interval: Q 4 hrContinuous IV infusion: Loading dose first— 100–150 mcg/kg over 1 hour followed by

10–20 mcg/kg/hr

Respiratory depression HypotensionBradycardia Urine retentionDecreased gut motility Tolerance and withdrawal with prolonged

administration (weaning regimen needed)Reversed with naloxone

Fentanyl 0.5–4 mcg/kg/dose IVUsual dosing interval: Q 2–4 hrContinuous IV infusion: 1–5 mcg/kg/hr

Fewer respiratory and cardiovascular effects than with morphine

With large, rapid boluses:Muscle rigidity HypotensionSeizure activity Bradycardia

Tolerance and significant withdrawal with continuous infusion >5 days (weaning regimen needed)

Reversed with naloxone

Muscle Relaxants

Pancuronium bromide* 0.1 mg/kg/dose IV(0.04–0.15 mg/kg/dose), as needed for

paralysisUsual dosing interval: 1–2 hoursContinuous IV infusion: 0.05–0.2 mg/kg/hr

TachycardiaHypotension/HypertensionHypoxemiaPeripheral edema Increased salivationReversed with atropine or glycopyrrolate

followed by neostigmine

Vecuronium bromide* 0.1 mg/kg/dose IV(0.03–0.15 mg/kg/hr), as needed for paralysisUsual dosing interval: 1–2 hours

Minimal cardiovascular effects when used alone

Bradycardia, hypotension when used concurrently with narcotics

Hypoxemia IV = intravenous, IM = intramuscular, PO = oral, PR = rectal, SQ = subcutaneous.* Should be administered by adequately trained individuals familiar with its actions, characteristics, and hazards.


developmentofcomplicationssuchasairleaks,patentductusarteriosus,orthebeginningsofchroniclungdisease/bronchopulmonarydysplasia(CLD/BPD)maydelayrecoveryfordays,weeks,orevenmonths.Mortalityisinverselyproportionaltogestationalage.Theincidenceofchroniclungdiseaseis<10%ininfantswithabirthweight>1000gto~50%ininfantswithabirthweight<1000g.

Transient Tachypnea of the Newborn

Themostcommonlycitedcauseoftransienttachypneaofthenewborn(TTN)isdelayedabsorptionoffetallungfluid.


• Termandlate-preterm(“near-term”)infants

• Precipitousdelivery

• Cesareandelivery,especiallyintheabsenceof labor

• Maleinfants

• Prenatalexposuretomethamphetamine

Pathophysiology

Inutero,thefetallungsarefilledwithfluid.Duringnormalvaginaldelivery,thefluidisusuallyforcedoutbythethoracicsqueeze.Theremainderofthefluidinthelungsisclearedbythepulmonaryveinsandlymphaticsystem.Withaprecipitousorcesareandelivery,absenceofthegradualchestcompressionthatoccursduringnormalvaginalbirthcausesfluidtoberetained.Accumulationofthisinterstitialfluidinterfereswithforcesthattendtokeepthebronchiolesopenandeventuallycausesthebronchiolestocollapse(airtrapping).Airtrappingandhyperinflationcanincreasepulmonaryvascularresistanceandleadtopotentialpersistentpulmonaryhypertension.


Theclinicalpresentationcanbedifficulttodistinguishfromthatofotherneonataldisorderssuchasbacterialpneumonia,sepsis,andRDS.Theonsetofsymptomsisusually0.5–6hoursafterbirth;respiratoryratesupto120–140BPMarethemostcommonsymptom.Grunting,nasalflaring,andretractionsmayoccurwithvaryingseverity.

OthertreatmentsforRDSincludesurfactantreplacementtherapy,high-frequencyventilation,continuouspositiveairwaypressure(CPAP),andpatient-triggeredventilation.

Surfactantreplacementtherapyhasbecomeastandardtreatment.ItimprovesoxygenationandstabilizesalveoliwitharesultantreductionintheseverityofRDS.Commercialpreparationsusedinsurfactantreplacementtherapyareusuallygivenasaliquidbolusintotheendotrachealtube,withthedosedividedintoaliquotsandadministeredwiththeinfantindifferentpositions.

High-frequencyventilation(HFV),includinghigh-frequencyoscillationandhigh-frequencyjetventilation,appearstoproduceadequategasexchangeatlowerpeakairwaypressureswhilepotentiallyreducingbarotraumaandthedevelopmentofchroniclungdisease.Itusessmalltidalvolumesatnearorlessthananatomicdeadspaceatrapidrates.

BubbleCPAPisachievedbysubmergingtubingunderwateratapredetermineddepth,whichallowstheairflowtobubbleout.BubbleCPAPhaschestwallvibrationssimilartoHFVand,comparedwithconventionalventilation,reducedminutevolumeandrespiratoryrate.

Synchronizedintermittentmandatoryventilationandassist/controlmodeventilationarereferredtoaspatient-triggeredventilation.Synchronizedintermittentmandatoryventilationusesairwayflow,airwaypressure,changesinchestwallimpedance,orabdominalmovementstodetecttheonsetofinspiratoryefforts.Spontaneousbreathstriggertheventilatortomaintaintherate.Duringepisodesofapnea,controlledbreathsoccuratthepresetrate.Intheassist/controlmode,aspontaneousbreathtriggersamechanicalbreath.Thismodealsodeliverscontrolledbreathsatthepresetrateduringapnea.Patient-triggeredventilationhasbeenshowntoimprovegasexchangeandreduceasynchronybetweeninfant-generatedandventilator-generatedbreaths.

Prognosis (MoïseandHansen2003;Bhutani1996)

MostinfantswithRDSrecoverwithoutfurtherproblems,usuallywithin3–5days.WithsevereRDS,therequirementforassistedventilation,the


Incidence (ClarkandClark2012;Yoderetal.2002)

• 8%–25%ofallUSbirths>34weeksgestationhavemeconiuminamnioticfluid

• ~10%ofthoseinfantsdevelopMAS• changesinobstetricalpracticeappeartobedecreasingtheincidence


• Termorpostterminfants• Termorpostterm,small-for-gestational-ageinfants

• Anyeventcausingfetaldistress,suchas: – Reducedplacentaloruterinebloodflow – Maternalhypoxiaand/oranemia – Placentalorumbilicalcordaccidents• African-Americanrace• Chorioamnionitis/infection

Pathophysiology

Meconiumisnormallyretainedinthefetalgutuntilpostnatallife,butpassageofmeconiumoccursinresponsetofetaldistress(hypoxicbowelstimulation).Therectalsphinctertoneormusclemayrelaxaftervagalreflexstimulationandreleasemeconiumintotheamnioticfluid.Thefetusbeginsgaspinginresponsetoasphyxiaandmayinhalemeconiumintotheairway.Withtheinfant’sfirstbreath,meconiumcanbeaspiratedintothelungs.Thisaspiratedthickmeconiumcanresultin:

• Partialairwayobstruction(aball-valveobstruction),leadingtoairtrappingandoverdistentionoftheairways,withalveolarruptureandairleaks

• Completeairwayobstruction,leadingtosmallairwayatelectasis

• Inflammatoryresponseofthetracheobronchialepitheliumtomeconium,leadingtochemicalpneumonitis

• Possiblesurfactantdisplacementorinactivationofendogenoussurfactant

Unevenpulmonaryventilationwithhyperinflationofsomeareasandatelectasisofothersleadstoventilation-perfusionmismatchesand,subsequently,hypercarbiaandhypoxemia.Hypoxemiamayworsenpulmonaryvasoconstriction,resultinginfurtherhypoxemia andacidemia,andsetupaviciouscycle.

Arterialbloodgasesrevealhypoxemiainroomair,mildhypercarbia,andmildtomoderateacidosis.Chestradiographsshowhyperinflation(fromairtrapping)andstreakyinfiltrates(interstitialfluidalongthebronchovascularspace)fromthehilum.

Management

TreatmentofTTNconsistsofsupplementaloxygen(usually<40%fractionalinspiratoryoxygen[FiO2]),pulseoximetryand/ortranscutaneousmonitoring,antibiotics(ifinfectionissuspected),aneutralthermalenvironment,andgeneralsupportiveneonatalcare.Oralfeedingsshouldbedelayedtopreventaspirationfromhighrespiratoryrates.

Prognosis

AlthoughTTNisself-limitingandusuallyclearswithin1–3days,itisadiagnosisofexclusionmadeaftertheinfanthasrecovered.Infantsgenerallyrecovercompletelywithoutanyresidualrespiratoryproblems.

Meconium Aspiration Syndrome

Meconiumaspirationsyndrome(MAS)isthemostcommonaspirationsyndromecausingrepiratorydistressinnewborns.

Meconium aspiration syndrome is the most common aspiration syndrome causing respiratory distress in newborns.

Figure 6. Transient tachypnea of the newborn.


Priortorecentresearch,nasopharyngealandoropharyngealsuctionwereadvocatedasapreventivestrategyforMAS.Resultsofa12-centerrandomizedcontrolledstudyfoundnosignificantdifferenceintheneedformechanicalventilation,mortality,durationofoxygenuse,numberofventilatordays,andlengthofstaybetweensuctionedandnonsuctionedgroupsofterminfantsbornthroughmeconium-stainedamnioticfluid(Gardneretal.2011;Vainetal.2004).SinceroutinesuctioningdoesnotpreventMAS,suctionisonlyrecommendedfordepressedinfants(nonvigorousneonateswithdepressedtoneandrespirationsand/oraheartrate<100BPMandneonateswithrespiratory symptoms (VelaphiandVidyasagar2006).

AdditionaltreatmentisrequiredforinfantswhodevelopMAS.BecausemeconiuminthealveolicaninjuretypeIIalveolarepithelialcellsandinterferewithendogenoussurfactantproduction,surfactantreplacementtherapymayimproveoxygenation.Respiratorystatusshouldbeconstantlymonitoredwithpulseoximetryortranscutaneousmonitoring,frequentbloodgases,andclinicalassessmenttodeterminetheneedforoxygenandpositive-pressureventilation.Supportivecareincludes,butisnotlimitedto,broad-spectrumantibioticsforsuspectedinfection,correctionofmetabolicabnormalities,maintenanceoffluidbalance,aneutralthermalenvironment,andminimalstimulation.Sedativesandanalgesicsmaybe giveniftheinfant’srespiratoryeffortsinterfere witheffectivepositive-pressureventilation (Table9).PotentialcomplicationsassociatedwithMASincludeair-leaksyndrome,chemicalpneumonitis,persistentpulmonaryhypertension,andend-organdamage.

OthertreatmentinterventionsforMASdependonthediseaseprogressionandmayincludehigh-frequencyventilation(discussedintheRDSsection),nitricoxide,andextracorporealmembraneoxygenation(ECMO).

Inhalednitricoxide(iNO),apotentandselectivepulmonaryvasodilator,iseffectivetherapyforpersistentpulmonaryhypertensionandreducestheneedforECMO.Inhalednitricoxideselectivelylowerspulmonaryarterypressureandimprovesoxygenationwithoutcausingadverseeffectsoncardiacperformanceorsystemicbloodpressure.


UsuallyinfantswithMAShaveahistoryoffetaldistressandmeconium-stainedfluid.Respiratorydistresscanrangefrommildtosevere,withvaryingdegreesofcyanosis,tachypnea,retractions,grunting,nasalflaring,andcoarseralesandrhonchi.Thechestappearsbarrel-shaped(increasedanteroposteriordiameter)fromgastrapping.Arterialbloodgasesmayreflectvaryingdegreesofhypoxemia,hypercarbia,andacidosis.Thechestradiographshowscoarse,patchyareasofdecreasedaeration(atelectasis)andareasofhyperaeration(airtrapping).Later,chemicalpneumonitiscanbecomeapparentonthe chestfilm.

Management

Priortobirth,earlyrecognitionofthecompromisedfetus,appropriateintervention,andpreventionofcesareandeliveryarepreventivestrategiesformeconiumaspiration(Meydanlietal.2001;Sheineretal.2002;Yoderetal.2002).Infusionofasterileisotonicsolutionintotheamnioticsac(amnioinfusion)isusedtodilutemeconium,correctoligohydramniosoftenassociatedwithmeconium-stainedamnioticfluid,anddecreasecordcompressionandacidemia.However,amnioinfusiondoesnotreducetheriskformoderatetosevereMASorperinataldeathandisnotrecommendedforthepreventionofMAS

(Fraseretal.2005).

Figure 7. Meconium aspiration syndrome.


• Excessiveintrapartummanipulation

• Maternalfever

• Maternalviral,bacterial,orotherinfection

• Prolongedlabor

• Maternalurinarytractinfection

• Amnionitis

• Immatureimmunesystem• Invasiveproceduressuchasintubationandassistedventilation

• NosocomialinfectionsacquiredintheNICU

Pathophysiology

Transmissionoccurstransplacentally,intrapartally,orpostnatally.Pathologicorganismsinclude,butarenotlimitedto,thoselistedinTable10.Transplacentalpneumoniacandevelopfromaspirationoringestionofinfectedamnioticfluidorfromtransmissionoforganismsfromaninfectedmotheracrosstheplacentatothefetus.Intrapartumpneumoniaresultsfromcolonizationoftheneonatebyascensionoforganismsafterruptureofmembranes,passagethroughaninfectedbirthcanal,oraspirationofinfectedamnioticfluidatbirthorwithresuscitativeefforts.Postnatalpneumoniausuallydevelopsfromhospital-acquiredornosocomialsourcessuchasunwashedhandsandopenskinlesions,aswellascontaminatedequipment,nutritionalproducts,orbloodproducts.

Itenhancesgaseousexchangebyimprovingventilation-perfusionmismatchinganddecreasingintrapulmonaryshunting.However,progressiveatelectasisanddecreasedcardiacperformancelimittheeffectivenessofiNO.Potentialtoxicitiesincludebothmethemoglobinemiaanddirectlunginjuryfromnitricdioxide.

ECMOisaprocessofprolongedcardiopulmonarybypassthatprovidescardiorespiratorysupportuntilthelungsrecover.Itisusedwithinfantswhohavereversiblelungdiseaseandwhohavenotrespondedtomaximalmedicaltherapy.ECMOisoftenusedtotreatinfantswithpredictablyfatalpulmonaryfailurefromdiseasessuchasMAS,andinfantswithabirthweight>2kgwithRDS,pneumoniaandsepsis,andpersistentpulmonaryhypertension.ECMOisperformedbyeithervenoarterialorvenovenoustechniques.SignificantcomplicationsaccompanyECMOusesothatspecificselectioncriteriahavebeenestablishedtodeterminecandidatesforthishighlyinvasivetherapy.

Prognosis (Orlando1997) Meconiumaspirationsyndromeisusuallyresolvedby1weekoflifeforinfantswhodonotrequireassistedventilation,butmaypersistininfantsrequiringprolongedassistedventilation.Theoutcomedependsontheseverityoftheasphyxialinsultandtheextentoflungdamagecausedbythediseaseanditspotentialcomplications.

Pneumonia

Neonatalpneumoniacanbecausedbybacterial,viral,protozoan,fungal,orotherpathogenssuchas Treponema pallidum or Chlamydia trachomatis Itcanoccurasaprimaryinfectionoraspartofageneralizedinfection.

Incidence (CareyandTrotter1997)

• 1%oftermneonates

• 10%ofpretermneonates


• Prematureinfants

• Prolongedruptureofmembranes>24hours

Table 10. Pneumonia: Pathologic Organisms

Transplacental Intrapartum Postnatal Nosocomial

Cytomegalovirus

Rubella

T pallidum

Toxoplasma gondii

Varicella

Enterovirus

Listeria monocytogenes

Herpes simplex virus

C trachomatis

Group B streptococci

Escherichia coli

Klebsiella sp

Staphylococcus aureus

Staph. epidermidis

Herpes simplex virus

Candida sp

Cytomegalovirus

Group B streptococci

Enteroviruses

Respiratory syncytial virus


hasbeenidentified.Someviralpneumoniascanbetreatedwithpharmacologicagentssuchasacyclovirorvidarabineforherpessimplexvirus,andribavirinforrespiratorysyncytialvirus(RSV).Supportivetreatmentisneededforrespiratoryproblems,hematologicinstability,andacid-baseimbalance.Oxygenandpositive-pressureventilationmayberequiredinadditiontovolumeexpanders,bloodproducts,andvasopressorsiftheinfantisinshock.Withcontinueddeterioration,theinfantmayrequirenewertreatmentoptions,includinggranulocytetransfusion,intravenousimmunoglobulins,colony-stimulatingfactors, high-frequencyventilation,inhalednitricoxide, andextracorporealmembraneoxygenation.

Prognosis (SpeerandWeisman2003)

Overallmortalityfromsepsis,bothrelatedandunrelatedtopneumonia,rangesfrom5%to10%interminfantsandisashighas67%ininfantswithabirthweight<1500g.

Persistent Pulmonary Hypertension of the Newborn

Persistentpulmonaryhypertensionofthenewborn(PPHN)hasbeendescribedasthepersistenceofthecardiopulmonarypathwayseeninthefetus,butwithoutthepassageofbloodthroughtheplacenta.Itischaracterizedbyhighresistanceinthepulmonaryarteries,whichproducesanobstructionofbloodflowthroughthelungsandright-to-leftshuntingthroughtheductusarteriosusand/orforamenovale.PPHNmaybeidiopathicorsecondarytoanotherdisordersuchasMASorsepsis

Incidence (WeardenandHansen2003)

• 1.9:1000livebirths


• Late-preterm(“near-term”),term,orpostterm neonates

• Underdevelopmentofthepulmonaryvascularbed—decreasedcross-sectionalareaofpulmonaryvascularbedsecondarytohypoplasia(eg,Potter’ssyndrome,diaphragmatichernia)

Clinical Presentation and Diagnostic Workup

Ahighindexofsuspicionofpneumoniaisthekeytoearlydiagnosis.Theclinicalpresentationisoftennonspecificandincludestemperatureinstability,apnea,tachycardia,tachypnea,grunting,nasalflaring,retractions,lethargy,poorperipheralperfusion,andpoorfeeding.Skinlesionsmaybefoundininfantswithcongenitalpneumoniacausedbyherpessimplexvirus,Candidasp,orT pallidum Ashocklikesyndromeisoftenseeninthefirst7daysoflifewithearly-onsetgroupBß-hemolyticstreptococcus(GBS)sepsis.

Bacterialandviralcultures,rapidviralscreeningtests,andantigentests(latexagglutination,counterimmunoelectrophoresis)shouldbeperformedoninfantswithsuspectedpneumonia.AGramstainoftrachealaspiratemaybeusefulifdoneduringthefirst8hoursoflife,butitmaynotdifferentiateovertpulmonaryinfectionfromearlycolonization.AcompletebloodcountwithdifferentialandplateletsaswellasaC-reactiveprotein(CRP)areusefuldiagnostictests.Thechestradiographmayshowpatchyopacifications,unilateralorbilateralalveolarinfiltrates,pleuraleffusions,and/orchangesinlungvolume.GBSpneumoniaisdifficulttodifferentiatefromRDS onachestradiograph.

Management

Foraninfantwithsuspectedbacterialpneumonia,broad-spectrumantibiotics,suchasampicillinandanaminoglycoside,shouldbestartedimmediatelyandadjusted,ifnecessary,oncetheorganism

Figure 8. Pneumonia.


acidosis.ThereisnoclassicchestradiographfindingforPPHN;rather,thex-rayreflectstheunderlyinglungdisease.Itmayshowaprominentmainpulmonaryarterysegment,mildtomoderatecardiomegaly,andvariableprominenceofthepulmonaryvasculature(normalordecreasedvascularmarkings).

Thediagnosticwork-upforPPHNmayincludeahyperoxia/hyperventilationtestand/orpreductalandpostductalPaO

2tests.Withthehyperoxia/hyperventilationtest,theinfantisplacedin100%FiO2andhyperventilatedatrates>100BPM.AnincreaseinPaO2from<50mmHgbeforethetestto>100mmHgafterthetestisindicativeofPPHN.Preductalandpostductalbloodissampledtodemonstratearight-to-leftshuntthroughtheductusarteriosus.Bloodisdrawnsimultaneouslyfromapreductalsite(rightradialoreithertemporalartery)andapostductalsite(umbilical,femoral,orposteriortibialartery).Inthehypoxemicinfant,ductalshuntingisdemonstratedwithaPaO2difference>15–20mmHgbetweenthepreductalandpostductalsites.Pulseoximetryalsodemonstratesanarterialoxygenpercentsaturation(SaO2)differencebetweentherightarmandtherestofthebodyandsupportsthediagnosisofPPHN.

Management

Thegoaloftreatmentistocorrecthypoxemiaandacidosisandpromotepulmonaryvasculardilation.Treatmentconsistsofpositive-pressureventilation,pharmacologicsupport,supportivecare,andperhapstheuseofhigh-frequencyventilation,nitricoxide,andECMO.Useofmechanicalventilationtoproducealkalosisresultsinpulmonaryvasodilation,whichdecreasespulmonaryvenousreturnandimprovespulmonaryperfusionandoxygenation.Thisapproachisnotwithoutrisks,asmechanicalhyperventilationcanimpedevenousbloodreturnandreducecardiacoutput,whichfurtherreduces

• Maldevelopmentofthepulmonaryvascularbed—abnormalpulmonaryvascularstructureresultinginexcessivemuscularization(eg,fetalductalclosure,congenitalheartdisease)

• Maladaptationofthepulmonaryvascularbed—functionalpulmonaryvasoconstrictionwithnormalstructuraldevelopmentandanatomy(eg,MAS,coldstress,asphyxia,sepsis)

• Maternalfactors(tobaccouse,obesity,diabetes, asthma,useofpublicinsurance/lackofprivate insurance,blackorAsianrace,premature ruptureofmembranes)

• Cesareandelivery

• Large-for-gestational-age(LGA)infant

Pathophysiology

Theneonatalpulmonaryvasculatureissensitivetochangesinarterialoxygentension(PaO2)andpH.Withhypoxemiaandacidemia,thepulmonaryvasculatureconstricts,resultinginincreasedpulmonaryvascularresistanceandaventilation/perfusion(V/Q)ratiomismatch.Thisleadstoanimpairedreleaseofendogenousnitricoxide.Highpulmonaryvascularresistancepromotesbloodflowawayfromthelungsthroughtheductusarteriosusintothesystemicsystemandresultsinright-to-leftshunting.Italsomaintainshigherright-sidedpressuresintheheart.Whenrightatrialpressureisgreaterthanleftatrialpressureandpulmonaryarterypressureisgreaterthansystemicpressure,bloodflowfollowsthepathofleastresistancethroughtheforamenovaleandductusarteriosus,againbypassingthelungs.Thispromotionofright-to-leftshuntingresultsinhypoxemiaduetovenousadmixture.Thecyclerepeatsashypoxemiaincreasespulmonaryvascularresistance,resultinginfurtherintrapulmonaryshunting,hypoxemia,andpulmonaryvasoconstriction.


ClinicalpresentationisvariableduetothedifferentetiologiesofPPHN.Respiratorydistressandcyanosisworsendespitehighconcentrationsofinspiredoxygen.Arterialbloodgasesdemonstrateseverehypoxemia,normalormildlyelevatedarterialcarbondioxidetension(PaCO2),andmetabolic

There is no classic chest radiograph finding for PPHN; rather, the x-ray reflects the underlying lung disease.


Prognosis (Hoskoteetal.2008;Gardneretal.2011)

Theprognosisvariesaccordingtodiseaseetiology,severity,andmodeoftreatment.TreatmentwithiNOresultsinnoincreaseinadversepulmonaryoutcomesorneurodevelopmental/behavioralabnormality.Outcomesat1yearinchildrentreatedwithiNOshowalowerincidenceofrespiratorymorbiditythanthosetreatedwithconventionalmechanicalventilationorECMO.RegardlessofconventionaltherapyortreatmentwithECMO,survivorsofPPHNmayhavesignificantpulmonaryandneurodevelopmentalimpairment.

Air-Leak Syndrome

Airleaksdevelopfromalveolarruptureandtheescapeofairintotissueinwhichairisnotnormallypresent(pleura,mediastinum,pericardium,orextrathoracicareas).

Incidence (Gardneretal.2011)

Thegenerationofincreasedlungpressurenecessaryforthefirstbreathofliferesultsinspontaneousairleaksin2%–10%ofhealthytermneonates.Theincidenceofair-leaksyndromeinthesickorpretermnewbornvarieswiththeunderlyinglungdiseaseaswellaswithresuscitationandventilationmethods:

•16%–36%ofneonatesresuscitatedwithbag/maskorbag/ETTorwhoareventilatedwith CPAPorIMV

•15%–33%incidenceinterminfantswithMAS

UseofsurfactantforRDSenableslowerlevelsofventilatorysupport,especiallypressure,toadequatelyventilatetheimmaturelungandthusresultsinalowerincidenceofairleaks.

oxygenation.Inducedhypocarbiacanalsodiminishcerebralbloodflow.

AmoreconservativeapproachattemptstominimizebarotraumawhilemaintainingPaO

2 between50and70mmHgandPaCO2between 40and60mmHg.Theappropriatepeakinspiratorypressureforeitherventilatoryapproachisthendeterminedbytheinfant’schestexcursion.

InhalednitricoxideorECMOmaybeneededifaninfantdoesnotrespondtomaximalmedicaltreatment(seeMASManagementsectiondescribingECMOandnitricoxide).

Pharmacologicmanagementincludesavarietyofagents.Vasopressors,whichincreasesystemicvascularresistance,andvolumeexpanderscanbeusedtokeepthesystemicpressurenormalorabovenormalinanattempttoreducethepulmonaryandsystemicpressuregradient,therebydecreasingright-to-leftshunting.Systemicvasodilators(suchastolazolineandsodiumnitroprusside)havebeenusedinthepasttotreatPPHNwithvariableandunpredictableresultsandareassociatedwithsystemichypotensionandotherserioussideeffects.Becauseoftheiradverseeffects,useofsystemicvasodilatorsisnolongerrecommended,especiallywiththeadventofselectivepulmonaryvasodilationobtainedwithiNOtherapy.Useofphosphodiesteraseinhibitors(suchasmilironeandsildenafil)improvesvasodilationandincreasescardiacoutputbuthasnotbeenstudiedinlarge,randomizedtrialsandisconsideredexperimental (Gardneretal.2011).Sedatives,analgesics,andmusclerelaxantsareusedwhentheinfant’srespiratoryeffortsinterferewithpositive-pressureventilation(Table9).Supportivecareincludescontinuousmonitoringofarterialbloodpressure,pulseoximetry,maintenanceoffluidandelectrolytebalance,andprovisionofaneutralthermalenvironment,hematologicsupport,andminimalstimulation.



Theclinicalpresentationofair-leaksyndromeisoutlinedinTable11.

Transilluminationprovidesapreliminarydiagnosisforpneumothorax.Itworksbyplacingahigh-intensity,fiberopticlightsourceoverthechestwallandcomparingtheringofthelightbilaterally.Normallungandpleuraaredense,solightisabsorbed.Thepresenceofairpocketsproduceslightaroundthefiberopticlight.However,negativetransilluminationdoesnotruleoutpneumothorax.Thedefinitivediagnosisforairleaksisachestradiograph,eitherananteroposterior(A-P)vieworanA-Pandalateralview.Thechestradiographwillidentifythelocationandextentofairoutsidethetracheobronchialtree.

Management

Anitrogenwashoutcanbeusedtotreatpneumo-mediastinumornontensionpneumothorax.Theinfantisplacedin100%oxygenfor6–12hourstoestablishadiffusiongradientbetweenthepleuralairandthepleuralcapillariessothatairismorerapidlyabsorbedbythecapillaries.Nitrogenwashoutisnotrecommendedforpreterminfantsbecauseoftherelationshipbetweenhighoxygenconcentrationsinthebloodandretinopathyofprematurity.Evenuseof100%oxygenfor“nitrogenwashout”interminfantsshouldbeusedwithcautionduetonewunderstandingaboutthetoxiceffectsofoxygen(oxidativestress)(Gardneretal.2011).Tensionpneumothoracesrequireemergencytreatment.Needleaspirationcanbeusedtoremoveairquicklyandthecathetercanbeleftinplaceuntilachesttubeisinserted.Achest(thoracostomy)tubeandchestdrainagesystemwillrestorenegativepressureandexpandthelung.Localanesthesiawith1%xylocaineandananalgesicshouldbegivenforpainrelief.

Infants at Risk/Predisposing FactorsThesefactorsincludehypoplasticlungs,RDS,MAS,orcongenitalmalformations;theuseofventilatoryassitanceorvigorousresuscitativeefforts;andpost-thoracicsurgery.

Pathophysiology

Airleaksdevelopfromabnormaldistributionofgasandsubsequentalveolaroverdistentionandrupture.Airrupturesoutofthealveoliandmovesalongthepulmonarybloodvesselsorperibronchialtissues.Theescapingairflowstowardthepointofleastresistance.Thelocationoftheairleakdetermineswhichair-leaksyndromedevelops:

Pulmonaryinterstitial emphysema(PIE)

Airthatistrappedininterstitialspace

Pneumo- mediastinum

Airthathastraveledalongthepulmonarybloodvesselsandenteredthemediastinum

Pneumothorax Airthathasescapeddirectlyintothepleuralspace

Tensionpneumothorax

Freepleuralairthatcompressesthelung

Pneumo- pericardium

Airthathasenteredthespacebetweentheheartandthepericardialsac

Pneumo- peritoneum

Airthathastraveleddownwardintotheabdominalcavityandenteredtheperitonealspaceviathepostmediastinalopeningsinthediaphragm

Airembolism Thoughttoarisewhenairrupturesoutofalveoliintosmallpulmonaryveins

The definitive diagnosis for air leaks is a chest radiograph.


Table 11. Air-Leak Syndrome: Types, Symptoms, Diagnoses, ManagementAir Leak Clinical Presentation Chest Radiograph Findings General Management

Pulmonary interstitial emphysema (PIE)

Increased oxygen requirementsCO

2 retentionIncreased noncompliant lung

Small dark bubbles of air outside the tracheobronchial tree but trapped within the lung tissue

Positive-pressure ventilationHigh-frequency ventilationOptional: selective main stem

bronchus intubation

Pneumomediastinum Generally asymptomaticTachypneaBulging sternum

“Spinnaker sail sign”: thymus gland lifted by the mediastinal air

“Angel wing sign”: both lobes of thymus lifted

Mediastinal tube placement

Pneumothorax If symptomatic, see: Tachypnea Grunting Retractions Cyanosis

May not show any changes, or may show air in pleural space outlining the visceral pleura

Usually no specific management if air leak is small

Needle aspiration and/or chest tube if air leak is large and neonate is compromised

Optional: nitrogen washout

Tension pneumothorax TachypneaGrunting/retractionsCyanosisHypotensionDecreased breath soundsChest asymmetryShift in point of maximal impulseDistended abdomen

Pocket of air impinging on the lung

Mediastinal shift may/may not be evident

Needle aspirationChest tube placement

Pneumopericardium Distant/absent heart soundsBradycardiaDiminished/absent pulsesMarked hypotensionCyanosis and/or pallorReduced EKG voltage

Dark circle surrounding the heart

Decreased heart size

Needle aspirationPericardial tube placement

Pneumoperitoneum Distended abdomenPulmonary function may be

compromised

Dark layer over the abdomenBlurring or obscuring of

normal bowel pattern

Usually none requiredOptional: insertion of

soft catheter into the peritoneum

Air embolism CatastrophicSudden cyanosisCirculatory collapseAir-blood mixture crackles and pops with each heartbeatAir-blood mixture aspirated from the umbilical artery catheter

Bizarre picture of intracardiac and intravascular air

No effective treatment


Management

Immediaterecognitionofthedefectinthedeliveryroomisakeycomponentinmanagementofaninfantwithacongenitaldiaphragmatichernia.Bag-and-maskventilationshouldbeavoidedtopreventtheaccumulationofairinthestomachandbowel,whichwillcompromiserespiratoryexpansionandworsenrespiratoryfunction.Instead,immediateintubationandventilation,usingthelowestpossiblepressure,shouldbeinstituted.Alargedouble-lumenorogastrictubeplacedtolow,intermittentsuctionpreventsstomachandboweldistention.Otherinterventionsincludeestablishingintravenousaccessandprovidinganeutralthermalenvironment.Elevatingtheheadofthebedandpositioningtheinfantsothattheaffectedsideisdownallowsformaximalexpansionoftheunaffectedlung.Sedatives,analgesics,and musclerelaxantsareusedforpainreliefandasynchronyofinfant-andventilator-generatedbreaths(Table9).Thedefinitivetreatmentissurgicalcorrectionofthehernia.Thedevelopmentofpulmonaryhypertensionisfrequentlyseenpostoperatively(seePersistentPulmonaryHypertensionoftheNewborn).

Congenital Diaphragmatic Hernia

Acongenitaldiaphragmatichernia(CDH)istheherniationoftheabdominalcontentsintothechestthroughadefectinthediaphragm.Ninetypercentoftheseherniasoccurontheleftsideandintheposterolateralportionofthediaphragm.

Incidence (Lovvornetal.2011)

• 1:4000livebirths

• Morecommoninmalethanfemaleinfants


• None

Pathophysiology

Closureofthediaphragmoccursat8–10weeks’gestationalage.Ifclosureisdelayed,thebowelcanmoveintothethoraciccavityandresultinadiaphragmatichernia.Thestomachaswellasthesmallandlargebowel,spleen,andlivercanalsoherniateintothechest.Thepresenceoftheabdominalcontentsinthethoraxdoesmorethanjustcauselunghypoplasiabycompression.Decreasednumbersofbronchialgenerationsandalveoliareseen,andthepulmonaryarteryissmall.Increasedmuscularizationofthepulmonaryarteriesisalsopresent.Boththebronchialandvascularchangesrestrictpulmonarybloodflow,whichcanresultinpersistentpulmonaryhypertension.


AhistoryofpolyhydramniosisfrequentlyassociatedwithCDH,becausethethoraciclocationoftheintestineinterfereswiththeintrauterineflowofamnioticfluid.Severityofsignsandsymptomsandageatonsetdependontheextentoflunghypoplasiaandthedegreeofinterferencewithventilation.Clinicalpresentationincludesascaphoidabdomen,barrel-shapedchest,cyanosis,dyspnea,retractions,shiftedheartsounds,anddecreasedorabsentbreathsoundsontheaffectedside.Chestandabdominalradiographsshowloopsofbowelinthechest(althoughthesemaynotbeevidentuntiltheinfanthasswallowedadequateair),sparseorabsentabdominalbowelgas,amediastinalshift,andamarkedlyelevatedorindistinctdiaphragm.

The definitive treatment is surgical correction of the hernia.

Figure 9. Congenital diaphragmatic hernia.


brainstemfunction,whichcontrolsrespirations.Inaddition,thecentralresponsivenesstocarbondioxideisbluntedinpreterminfants.Adiminishedresponsetoperipheralchemoreceptorslocatedinboththeaorticarchandthecarotidarterieshas

Prognosis (Lovvornetal.2011;Milleretal.2005)

NeonateswithCDHwhodonotpresentwithrespiratorydistressinthefirst24hoursoflifehaveasurvivalrateapproaching100%.FornewbornswithCDHwhorequiremechanicalventilationinthefirst18–24hoursoflife,thesurvivalrateisabout64%.Pulmonaryhypoperfusionontheaffectedsidemaypersistforyearsasthenumberofbronchiandalveoliremainsreducedandincreasedmuscularizationofthepulmonarybloodvesselscontinues.Forsurvivors,gastroesophagealrefluxcanbealong-termproblemaftersurgicalrepair.

Apnea of Prematurity

Apneaisacessationofrespirationlasting>20secondsandassociatedwithphysiologicalterationssuchasbradycardiaand/orcolorchange.Itcanbeobstructive,central,ormixed.Withobstructiveapnea,respiratoryeffortsareobserved,butthereisblockedairflowfromcollapseoftheupperairway.Centralapneainvolvesthecessationofbothrespiratoryeffortsandairflow,withnoairwayobstruction.Themostcommonclassificationinpreterminfantsismixedapnea,whichinvolvesapauseinrespiratoryeffortprecededorfollowedbyairwayobstructionattheupperairwaylevel.

Incidence (Schmidtetal.2007;Gardneretal.2011)

Incidenceofapneaisrelatedtogestationalage,sothattheyoungerthepreterminfantthegreatertheincidenceofapnea:85%ofpreterms<34weeksgestationhaveapneaofprematurity.


Primaryapneaisadevelopmentalphenomenonofpreterminfantsthatmustbedistinguishedfromsecondaryapnea,whichisapneacausedfromanother,treatablecause.FactorscontributingtoapneainthepretermarelistedinTable12.

Pathophysiology

Apneaofprematurityisadiagnosisofexclusionwhenotherunderlyingcausesofapneahavebeenruledoutforinfantsof<37weeksgestationalage.Ithasbeenrelatedtoneuronalimmaturityof

Table 12. Factors Contributing to Apnea

Infection Septicemia, meningitis, pneumonia

Respiratory distress

Airway obstruction, CPAP application, congenital anomalies of the upper airway (eg, choanal atresia, laryngotracheal malacia), RDS, air leaks

Cardiovascular disordersCongestive heart failure,

patent ductus arteriosus, prostaglandin E infusion

Gastrointestinal disorders

Vomiting, necrotizing enterocolitis

Gastroesophageal reflux as a factor contributing to apnea is not supported by research

Central Nervous System disorders

Analgesics/anesthetics (either intrapartal/postnatal), intraventicular hemorrhage, seizure, infection, bilirubin encephalopathy, tumors/ischemia

Metabolic disorders

Electrolyte imbalance (hypo/hypernatremia, hypocalcemia), hypoglycemia, inborn errors of metabolism

Hematopoietic Anemia, polycythemia

Environmental

Hypothermia, rapid increase in environmental temperature, feeding, vigorous suctioning, stooling, stretching/movement, fatigue/stress, positioning, sleep state (increased apnea in active vs quiet sleep)

Modified from Gardner SL, Hines ME, Dickey LA: Respiratory diseases. In Gardner SL, Carter BS, Hines ME, Hernandez JA, eds: Merenstein and Gardner’s Handbook of Neonatal Intensive Care, 7th ed. St Louis, Mosby; 2011.


Thestandardlong-termtreatmentforapneaofprematurityistheuseofmethylxanthines,specificallycaffeine,theophylline,andaminophylline,whichactonthebrainstemrespiratoryneuronstoexertacentralstimulatoryeffect.Othereffectsincludeimprovedsensitivitytocarbondioxideresponse,increaseddiaphragmaticcontractions,increasedcatecholamineactivity,enhancedrestingpharyngealmuscletone,anddecreaseddiaphragmfatigue.Doxapram,aperipheralchemoreceptorstimulator,hasalsobeenusedforinfantswithapnea;itincreasesbothminuteventilationandtidalvolume.However,doxapramcontainsbenzylalcoholandrequirescontinuousinfusion,soitisnotrecommendedfornewborns.

alsobeennoted.ThesereceptorssensechangesinPaO

2,pH,andPaCO2thataffecttheregulationofrespirationsandrelaythemtotherespiratorycenterinthebrain.Upperairwayobstructioncontributestoapneabecausethenegativepressuregeneratedduringinspirationmayresultinpharyngealandlaryngealcollapse.


Cessationofrespiratoryeffortwithcyanosis,pallor,hypotonia,orbradycardiaisnoted.Frequentswallowing-likemovementsinthepharynxduringapneacanbeaproblem,becauseswallowingdirectlyinhibitstherespiratorydrive.

Management

Treatmentoftheinfantwithapneaofprematuritybeginswithassessmentandmonitoring(Table13).Tactilestimulation,oxygenadministration,and/orbag-and-maskventilationcanbeusedtostimulateaninfantwhoisexperiencinganapneicepisode.

The standard long-term treatment for apnea of prematurity is the use of methylxanthines.

Table 13. Apnea MonitoringType of Monitor Characteristics/Capabilities Problems

Impedance monitoring with EKG electrodes

Detects changes in electrical impedance as size of thorax increases and decreases during respiration

Unable to detect obstructive apneaObstruction may not trigger a respiratory alarmHeart rate may not decrease with episode of

apneaSensitivity level usually set so monitor will

sound in presence of shallow respirations (false alarm)

Pulse oximetry Continuous measurement of hemoglobin saturation with oxygen

Decreased accuracy during hypoperfusion, hypothermia, and active movement

Three-channel pneumocardiogram

Assesses respiratory effort, heart rate, pulse oximetry

Overnight or 24-hour recording

Motion and cardiogenic artifacts can interfere with respiratory signals

Two-channel pneumocardiogram

Assesses respiratory effort, heart rateContinuous recording on memory chip x 2–

3 weeksAllows analysis of apnea, bradycardia, or both

Motion and cardiogenic artifacts can interfere with respiratory signals

Polysomnography Expanded sleep studyEEG, ECG, EMG, chest wall, and abdominal

movement analysis, end-tidal CO2, oxygen

saturation, continuous esophageal pH determination, nasal air flow

Involves use of transducers and electrodes

Inductance plethysmography

Uses chest and abdominal belts to monitor respirations

Detects obstructive apnea and decreases false alarms

Belt slippage Changes in body position



LunginjuryisiatrogenicwithmultifactorialpredisposingfactorsinteractingtoresultinCLD/BPD(Gardneretal.2011)

• Preterminfants:inverselyproportionaltoearlygestationandlowbirthweight

• Malegender

• Respiratorysupport:

– Oxygentoxicityfromsupplementaloxygen

– Barotrauma/volutraumafrommechanical ventilation

• Patentductusarteriosus

• Nurtitionaldeficiency:small-for-gestational-age(SGA)infants;poorpostnatalnutrition;antioxidantdeficiencyofpreterminfants

• Fluidoverload

• Familyhistoryofasthma

• Infectionand/orinflammation

Pathophysiology

Oxygentoxicity,excessivetidalvolume,andothercontributoryfactorscauselunginjury,whichinturnproducesaninflammatoryreaction,capillaryleak,abnormallungmechanics/surfactantfunction,andairwayobstruction.Apatternofconstantandrecurringlunginjury,repair,andscarringoccurs.Thisproducescellular,airway,andinterstitialchanges,includinginflammation,atelectasis,emphysema,inactivationofsurfactant,pulmonaryedema,decreasedlungcompliance,increasedairwayresistance,ventilation/perfusionmismatch,overdistention,airtrapping,andincreasedproductionofmucus.Thesepulmonaryfunctiondisturbancesleadtohypoxemia,hypercarbia,andsomedegreeofbronchialhyperactivity.Bronchialhyperactivityandairwaysmooth-musclehypertrophy(whichdecreaseslumensize)causebronchospasmsorconstrictions.Thehypoxemiaorongoingmarginaloxygenationinducespulmonaryarteryvasoconstriction,vascularmuscularhypertrophy,andhypertension,resultinginpulmonaryhypertensionandsubsequentlyincreasingstressoftheright-sidedcardiacfunction.

Infantswhofailtorespondtomethylxanthinesorwhocontinuetohaveapneawhileonthesemedicationsmayrespondtocontinuouspositiveairwaypressure(CPAP),whichincreasesfunctionalresidualcapacityandstabilizesthechestwall.CPAPisbeneficialtoinfantswithmixedandobstructiveapnea,butnotcentralapnea.InfantswhofailtorespondtomedicationsandCPAPrequirepositive-pressureventilation.Supportivecareincludesprovisionofaneutralthermalenvironment,useofpulseoximetryand/ortranscutaneousmonitoring,andpositioningtopreventflexingoftheneck.

Prognosis (Pillekampetal.2007;Gardneretal.2011)

Apneaofprematurityusuallybeginsinthefirstweekoflifeandspontaneouslyresolvesat 36weeks’postmenstrualage(PMA).Someinfantsmayrequirehomemonitoringafterdischargefromthehospital.

Chronic Lung Disease (CLD)/Bronchopulmonary Dysplasia (BPD)

Infantsrequiringsupplementaloxygenat28– 30daysoflifeorat36weeks’PMAhaveCLD/BPD(Walshetal.2004).The“newBPD/CLD”oftoday’smorepreterm,lower-birth-weightinfantsmaynothavethecharacteristicx-raychangesofcysticlungdisease.Arrestedlungdevelopmentresultingininterferencewithalveolarizationandvascularizationischaracteristicofthe“newBPD/CLD”(Clarketal.2001)

Incidence (Gardneretal.2011)

CLD,asignificantclinicalproblem,hasanincidenceof23%–85%inverylow-birth-weightpreterminfants.Thiswidevariationinincidenceisduetovariationsinrespiratorycarepracticesthatexposetheimmaturelungtooxygentoxicityandbarotraumasandvolutrauma.Therefore,theincidenceofCLDvariesamongNICUs;increaseduseofintubation,mechanicalventilation,andhigherpressuresisassociatedwithmoreCLD/BPD,whileuseofnoninvasiverespiratorystrategies,suchasnasalcontinuouspositiveairwaypressure(NCPAP),isassociatedwithlowerrates.


appearbubbly(aircystscontinuetoenlarge) andareextensivelyhyperinflated,emphysemahasprogressedconsiderably,andcardiomegaly(indicatingright-sidedheartfailure)ispresent.

Management

ThetreatmentgoalsforCLD/BPDaretopromotegrowthandtohealtheinfant’slungs.Oxygenadministrationandpositive-pressureventilationareboththecauseofandthetreatmentforBPD.Adequateoxygenationisrequiredtopreventrecurrenthypoxemiaandreducepulmonaryhypertension.Thisapplieswhethertheinfantisawakeorasleep,cryingorfeeding.Thelowestoxygenconcentrationandventilatorsettingstoproduceacceptableventilationandoxygenationshouldbeused.InfantswithCLD/BPDareoftenabletoventilatethemselvesbeforetheyareabletooxygenate,sothatweaningtheventilatoroccursbeforeweaningfromsupplementaloxygen.Weaningfromrespiratorysupportshouldbedoneslowlytoavoidtheeffectsofhypoxemia(suchaspulmonaryhypertension)andhyperoxia(increasinglunginjuryandincidenceandseverityofretinopathyofprematurity[ROP]).Maintainingadequatehemoglobinconcentrationisnecessarytomaximizeoxygendeliverytothetissues.

PharmacologicmanagementiscriticalforinfantswithBPD.Excessiveinterstitialfluidaccumulatesinthelungandcanresultindeteriorationofpulmonaryfunction,addingtotheexistinghypoxemiaandhypercarbia.Pharmacologicmanagementincludesdiuretics,bronchodilators,andsteroids(Table15).

Table 14. Overall Signs and Symptoms of CLD/BPDRapid and shallow

respirations Crackles

Increased work of breathing Decreased air entry

Hyperinflated chest Atelectasis

Hypoxemia Hypercarbia

Pulmonary hypertension with right-sided cardiac failure

Intercostal/substernal retractions


ThemostcommonalterationofpulmonaryfunctionininfantswithCLD/BPDisincreasedairwayresistance.Inadditiontolowpulmonarycompliance,thisresistanceresultsinincreasedworkofbreathing,hypoventilation,andretentionofcarbondioxide.IninfantswithmildCLD,thereisaninitialneedforpositive-pressureventilation,whichmustbemaintainedlongerthanwasanticipated,followedbydaysorweeksofoxygensupplementation.Retractions,crepitantrales,and

diminishedbreathsoundsoccur.IntheearlyphaseofmoderatetosevereBPD,oxygenandventilatorypressurerequirementsincreaserelentlessly.Chestradiographsshowprogressiveoverdistentionofthelungs.Clinically,abarrel-shapedchestisnoted,andtheinfantdemonstrateslabilitywithhandlingandacuteepisodesofbronchospasms.Generally,ifrespiratorysupportcanbedecreasedduringthefirstmonthoflife,thesubsequentcourseofBPDisrelativelybenign.Butifincreasedsupportisneededatthistime,asevere,protractedcourseisusual.BPDoftenbecomesaprogressivediseaseifitpersistsbeyond1monthofage.Growthfailureisprominentandosteopeniaiscommon.Right-sidedcardiacfailure,bronchospasms,inspiratorystridor,overproductionofairwaysecretions,andsystemichypertensionarecommonininfantswithprogressiveCLD/BPD(Table14).

WithmildBPD,chestradiographfindingsareidenticaltothoseforRDS.AsBPDprogresses,coarse,irregular-shapeddensitiesandaircystsstarttodevelop.WithadvancedBPD,thelungs

Pharmacologic management is critical for infants with BPD.

Figure 10. Chronic lung disease.


Table 15. Pharmacologic Management of Infants with CLD/BPD

Medication Action Side Effects

Diuretics Decreases interstitial fluid and pulmonary edema

Furosemide Decreases interstitial pulmonary edemaLowers pulmonary vascular resistance and improves

ventilation-perfusion ratiosImproves lung compliance and lung mechanics Improves oxygenationRoutine/sustained use in infants with or developing

CLD cannot be recommended based on current evidence (BrionandPrimhak2002)

Electrolyte imbalance (hypokalemia, hypocalcemia, hypochloremia, hyponatremia)

Metabolic acidosisRenal and gallstone formationDehydration OtotoxicityRequires KCL supplementation

Thiazide Diuretics:Chlorothiazide HydrochlorothiazideUsed in combination

with spironolactone, a potassium-sparing drug

Decreases interstitial pulmonary edemaImproves pulmonary functionDecreases airway resistanceIncreases pulmonary complianceImproves pulmonary function and lung mechanicsFurther study required to assess whether

thiazides reduce mortality, decrease duration of supplemental oxygen, ventilator use, and length of stay and improve long-term outcomes (Brionetal.2002)

Electrolyte imbalance (hypercalcemia, hypomagnesemia, hyponatremia, hypokalemia, hypophosphatemia)

Hyperglycemia/glycosuriaMetabolic alkalosisGI upset/vomiting, diarrheaIrritability/lethargyRash

Do not use in patients with significant impairment of renal or hepatic function

Bronchodilators Improves pulmonary mechanics

Inhaled:AlbuterolTerbutaline sulfateIsoproterenol Ipratropium bromide

Increases surfactant productionDecreases pulmonary edemaEnhances mucociliary transportIncreases lung compliance and decreases airway resistance

TachycardiaTremorsHypertensionIrritabilityGastrointestinal disturbances (nausea,

vomiting)Paradoxical bronchoconstriction

Systemic:Methylxanthines Caffeine citrate

Aminophylline Theophylline

Decreases pulmonary resistanceStimulates central nervous system Increases inspiratory driveImproves skeletal muscle and diaphragm contractility and increases lung compliance

Actions as noted for caffeine citrateIncreases surfactant production

Mild Tachycardia, diuresis, dysrhythmias,

hyperglycemia/glucosuria, ketonuria, vomiting/hemorrhagic gastritis, irritability, seizures

Vomiting, tachycardia, tremors, gastroesophageal reflux, electrolyte abnormalities, agitation, GI irritation, hyperglycemia, CNS irritability, sleeplessness

AlbuterolTerbutaline sulfate

Decreases pulmonary resistance/adjunct to methylxanthine

Tachycardia, tremors, hypertension, irritability, gastrointestinal disturbances, hypokalemia (albuterol)

table continued on next page


Diuretictherapydecreasesexcessivelungfluid.Bronchodilatorandsystemicmethylxanthineshavebeenusedforbothreactiveairwaydiseaseandairwayhyperreactivity.Corticosteroidspromoteweaningfromtheventilatoranddecreasetheinflammatoryresponse,therebyimprovingpulmonaryfunction.

Optimalnutritionisrequiredforgrowthanddevelopment.Meetingthenutrientneedsofapreterminfantmaybelimitedbyfluidrestrictionandfeedingintolerance,thereforeahigh-calorie,nutrient-densefeedingwouldbeadvisable.AdequatevitaminAiscriticalfornormalgrowthand

differentiationofepithelialcells,andappropriateintakeofmineralsandvitaminDisnecessarytopreventthedevelopmentofosteopeniaofprematurity.

TheenvironmentsurroundingtheinfantisimportantforrecoveryfromCLD/BPD.Minimizingagitationtopreventthehypoxemiaandbronchospasmsthatoftenaccompanyagitationisessential.Sedationmaybeneededinadditiontoevaluationofnoise,light,andtouchtoavoidoverstimulation,whichhasanegativeeffectonweightgain,respiratoryfunction,anddevelopment.

table continued from previous page

Table 15. Pharmacologic Management of Infants with CLD/BPD

Medication Action Side Effects

Corticosteroids Promotes weaning from ventilator and decreases inflammatory response

Dexamethasone Use of postnatal steroids is associated with both short and long-term adverse effects

Routine use of postnatal steroids to prevent/treat CLD is not recommended and should be limited to exceptional clinical circumstances, under carefully designed study protocols, and with written informed parental consent (American Academy of Pediatrics 2006)

Improves pulmonary status, probably by decreasing tracheobronchial and alveolar inflammation and decreasing pulmonary edemaFacilitates gas exchange Increases lung complianceDiminishes airway resistance

Short-term adverse effects (Gardneretal.2011)

HyperglycemiaHypothalamic-pituitary-adrenal axis

suppressionRenal calcificationProtein depletion/tissue catabolism

(failure to gain weight/increase BUN)

Gastric irritation/perforation/bleedingRestlessness/irritabilityMyocardial hypertrophyHypertensionIncreased risk for infection

Long-term adverse effects (Gardneretal.2011)

Slower growth (somatic, head growth)

Arrested lung development (alveolarization, vascularization)

Neurotoxic: reduced brain size/ growth; cerebral palsy; cognitive deficits

Increased severity of retinopathy of prematurity

Contributes to long-term conditions/diseases: renal, cardiovascular, immune system, neurologic, behavioral deficits


»Persistentpulmonaryhypertensionofthenewbornischaracterizedbyhighresistanceinthepulmonaryarteries,whichproducesanobstructionofbloodflow.

»Airleaksdevelopfromalveolarruptureandtheescapeofairintotissue.

»Acongenitaldiaphragmatichernia(CDH)istheherniationoftheabdominalcontentsintothechestthroughadefectinthediaphragm.

»RecognitionofCDHinthedeliveryroomisakeycomponentinmanagement.

»Apneaisacessationofrespirationlasting>20secondsandassociatedwithphysiologicalterationssuchasbradycardiaand/orcolorchange.

»Themostcommonalterationofpulmonaryfunctionininfantswithchroniclungdisease(CLD)/bronchopulmonarydysplasia(BPD)isincreasedairwayresistance.

»BPDoftenbecomesaprogressivediseaseifitpersistsbeyond1monthofage.

»TreatmentgoalsforCLD/BPDaretopromotegrowthandhealthelungs,pharmacologicmanagement,optimalnutrition,andaproperenvironment


»Respiratorydistresssyndrome(RDS)iscausedbyaprimaryabsenceordeficiencyofsurfactant.

»ThegoalsoftreatingRDSaretopreventalveolarcollapse,optimizetissueoxygenationandCO2elimination,minimizeO2consumption,andprovidesupportivecare.

»Themostcommonlycitedcauseoftransienttachypneaofthenewbornisdelayedabsorptionoffetallungfluid.

»Meconiumaspirationsyndrome(MAS)isthemostcommonaspirationsyndromecausingrespiratorydistressinnewborns.

»Priortobirth,earlyrecognitionofthecompromisedfetus,appropriateintervention,andpreventionofcesareandeliveryarepreventivestrategiesforMAS.

»Neonatalpneumoniacanbecausedbybacterial,viral,protozoan,fungal,orotherpathogens.

Prognosis (Adams2003;BarringtonandFiner1998)

Survivaltodischargeisinverselyrelatedtodurationofventilation.Improvementinpulmonaryfunctionoccursslowlyover1–3years.Morbiditiesaremostcommoninthesmallest,sickestpretermsandinclude:chronicrespiratorydifficulties,rehospitalizationsinthefirst2yearsoflifeforrespiratoryinfections,right-sidedheartfailureandcorpulmonale,growthrestriction,osteopenia/fractures,cognitiveimpairment,cerebralpalsy,behaviorandattentionproblems,hearingloss,retinopathyofprematurity,anddeath.Overallmortalityrangesfrom25%to40%,withmostdeathsrelatedtoinfectionorcardiopulmonaryfailureassociatedwithpulmonaryhypertensionorcorpulmonale.

Special Respiratory Concerns with the Premature InfantTheclinicianorbedsidecaregivershouldbealerttospecialrespiratoryconcernswiththeprematureinfant,asoutlinedinTable16(Gardneretal.2011)


Table 16. Premature Infants: Special Respiratory Considerations

Concern/Condition Impact/Result

Brain respiratory control center

May lack sufficient maturity to consistently regulate respirations; therefore, may experience periodic breathing and apnea

Compliant (immature) chest wall

Insufficient breathing and retractions

Noncompliant lungs Increased work for respiratory muscles, leading to increased work of breathing and retractions

Surfactant deficiency Collapsed alveoli plus intrapulmonary shunting, resulting in hypoxemia

Pulmonary vascular smooth muscle

Not as well developed as in term infants, so fall in pulmonary vascular resistance occurs more rapidly

Immaturity of terminal air sacs and associated vasculature

Poor gas exchange

Immaturity of diaphragm and other muscles of respiration

Inspiratory difficulty

Peripheral chemoreceptors (in aortic arch and carotid arteries)

Blunted response; therefore, can experience apnea

Muscle fiber type distribution

Muscles may be more susceptible to fatigue

Ductus arteriosus Ductal smooth muscle does not have a fully developed constrictor response to oxygen

Ductal tissue exhibits increased dilatory response to prostaglandins

Persistently high circulating levels of prostaglandins

May remain patent, shunting blood away from systemic organs

Lower hemoglobin Limited oxygen-carrying capacity

Related Nursing Care

Nursing Diagnosis: Impaired Gas Exchange

Patient Outcome• Infantwillmaintainadequategasexchangeandeffectivebreathingpattern,asevidencedby:

—Respiratoryrate40–60BPM —Heartrate110–160BPM —Clearandequalbreathsounds —Mildtonoretractions —Lackofnasalflaringandgrunting —Pinkcolor —Pulseoximetryvalues92%–94%oras

prescribedforgestationalandchronologicalageanddiseaseprocess

—Bloodgaseswithinnormallimits

Interventions• Assessforsignsofimpairedgasexchange/respiratorydistresseveryhourandasnecessary(PRN)

—Nasalflaring —Expiratorygrunt —Tachypnea —Cyanosis —Retractions—notetypeanddegree ■Type: suprasternal,substernal, intercostal,subcostal ■Degree: mild,moderate,severe • Auscultatebreathsoundsandnoteadventitioussoundsevery1–2hoursandPRN

—Airmovement —Equality—compareandcontrasteachsideof

chest —Clarity—clear,rales,rhonchi

• Maintainapatentairway:

—Smallrollundershoulders(ifneeded) —Withendotrachealtube(ETT): ■SuctionPRN ■AssessanddocumentETTsizeand

position—noteinsertiondepth(marklocatedatinfant’slips)


» Bealertforspecialrespiratoryconcernswith theprematureinfant.


■UseETTadaptororclosedsuctionsystemtoallowsuctioningwithoutremovinginfantfromventilator

—Withnasalcontinuouspositiveairwaypressure(NCPAP)orbubbleCPAP:

■Keepinfantcalm;swaddleifnecessary(cryingreleasespressurethroughmouth)

■Maintainpatencyofnaresandnasal prongs

■Guardagainstpressurenecrosis

• Administeroxygenincorrectamountandbycorrectrouteofdelivery

—Analyzeanddocumentinspiredoxygenpercentageeveryhourandwithchanges

—Documentoxygenadministrationtemperature

—Assessanddocumentpulseoximetryeveryhour,changesinpulseoximetryvalues,interventions,andresponsetointerventions

• Assessanddocumentalarmlimitseveryshift;assessanddocumentventilatorsettingseveryhourandwithchanges

• Assess,document,andnotifyphysician/practitionerofbloodgasresults

• Maintainpulseoximetry(oxygensaturation)ortranscutaneousmonitor(transcutaneousandpartialpressureofoxygen[TcPO2]andcarbondioxidepressure[TcPCO2])

—Pulseoximetry:

■ NoteprobesiteandchangePRN ■ Placeprobesolightsourceand

photodetectorareoppositeoneanother ■ Shieldprobefromambientlight,especially

ifphototherapyisinuse ■ Setmonitoralarmsaccordingtounitpolicy ■ DocumentreadingseveryhourandPRN

—Transcutaneousmonitor: ■Positionprobeonaflat,well-perfusedarea ■Changeprobepositionevery4hours

andPRN ■Preferredtemperaturerange:43ºCfor

preterminfants,44ºCforterminfants

■Setmonitoralarmsaccordingto unitpolicy

■DocumentreadingseveryhourandPRN

• Maintainend-tidalCO2monitoringifordered

• Ifchesttuberequired:

—Assistwithtransilluminationprocess

—Assistwithneedleaspirationofchest —Assistwithchesttubeplacement: ■Administeranalgesic ■Monitorvitalsignsduringprocedure ■Placechesttubetochestdrainagesystem

at15–20cmH2Opressure ■Notebubblingactivity —Documenttolerancetoprocedure

• Ifchesttubeinplace:

—Maintaintubestability: ■Tapeallconnectionssecurely ■Securetubingfrominfanttobedtorelieve

tension at insertion site ■Assessforkinksintubing —Donotstrip/milkchesttube;thisgenerates

extremelyhighpressures —Bubblingactivityslowsseveralhoursafter

chesttubeplacementandusuallystopsafter72hours

—Ifnobubblingnotedfor24hours,placechesttubetounderwaterseal(providesanoutletforanyreaccumulatedairaftersuctionisdiscontinued);donotclamptube

—Afterdiscontinuingchesttube,useanocclusivedressing(suchaspetrolatumgauze)for48hours

—Keepocclusivedressingatbedsideforapplicationatinsertionsiteifchesttubebecomesdislodged

—Assessanddocumentamountofchesttubedrainageeveryhouroreveryshift

—AssessanddocumentbubblingactivityeveryhourandPRN

—Repositioninfantevery2–4hourstofacilitateremovalofair

—Elevateheadofbed


• Repositioninfantevery2–4hours

• Provideclustercarewithminimalhandling

• Assessinfant’sresponsetoandtoleranceofhandlingandprocedurestodetermineappropriatenursingcare

• Administersedatives,analgesics,andmusclerelaxantsasordered

—Assessresponsetomedications

• Maintainneutralthermalenvironment

• Providesupporttofamily

Nursing Diagnosis:Ineffective Airway Clearance

Patient Outcome

• Infantwillhaveanadequatelyclearairway,asevidencedby:

—Clearandequalbreathsounds

—Respiratoryrate40–60BPM

—Pinkcolor

—Unlaboredrespirations

Interventions

• Assessrespiratorystatuswithcontinuouscardiorespiratorymonitoring,withvitalsigns(every2–4hours)andPRN

• Administeraerosolmedications

• Assessneedforsuctioningonthebasisof:

—Qualityofbreathsounds

—Currentcondition

—Bloodgasresults

—Oxygensaturationreadings

—Generalclinicalappearance:

■ Chestmovement

■ Color

• SuctionPRN

—Useclosedsuctioningsystemwithappropriate-sizedsuctioncatheters

—Assesspatienttoleranceofsuctioningprocedure

—Documentamount,characteristics,andcolorofsecretions

—Assessanddocumentauscultatoryfindingsofbreathsoundsbeforeandaftersuctioning

• Initiateappropriateinterventionstominimizehypoxia(bagventilationpresuctioningorpostsuctioning)

—Determinedegreeofhypoxiabypulseoximeterortranscutaneousmonitorreadingsandtimetoreturntobaseline

—Notedegreeofbradycardia,ifany,andtimetoreturntobaseline

—Noteanyotherphysiologicchanges

• Allowinfanttorestaftersuctioningprocedureandbeforeothermajorstressactivities

• Repositioninfantevery2–4hoursandPRN

• Maintainadequatehydration

Additional Nursing Diagnoses:

Theseinclude,butarenotlimitedto,thefollowing:

High risk for injury:intraventricularhemorrhage,airleaks,orotherrelatedtotreatmentforrespiratorydisorders

Alteration in comfort:pain,relatedtochesttubeplacementandotherprocedures

High risk for fluid volume deficit:relatedtodiseaseprocess,fluidloss,andIVadministration

High risk for fluid volume excess:relatedtorenalinabilitytoexcreteanyvolumeoverloadandtoiatrogenicfluidvolumeexcess

Inadequate nutrition:lessthanbodyrequirements,relatedtoincreasedcaloricexpendituresanddecreasednutritionalintake

Knowledge deficit:relatedtolackofparentalunderstandingofthediseaseprocess


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