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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
Neonatal Respiratory System 3
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.
Neonatal Respiratory System 4
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.
Neonatal Respiratory System 5
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.
K e y L e a r n i n g s
»Inutero,fetalcirculationdependsontheplacentaandfetalducts.
»Lowfetaloxygentensionallowsbloodtobypassthelung.
»Atdelivery,respiratoryandcardiovascularchangesoccurindependentlybutsimultaneously.
Neonatal Respiratory System 6
• 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.
Neonatal Respiratory System 7
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%
K e y L e a r n i n g s
»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.
K e y L e a r n i n g s
»Anticipationisakeycomponentofthesuccessfulresuscitationofadistressednewborn.
»Resuscitationequipmentandmedicationsshouldbeavailable,readytouse,andfunctionalatalltimes.
Neonatal Respiratory System 8
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
Neonatal Respiratory System 9
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
K e y L e a r n i n g s
»Assessmentshouldincludeahistoryofthemother,infant,andintrapartumissues.
»Arespiratorysystemassessmentshouldincludetheinfant’scolor,typeofbreathing,respiratoryeffort,chestshape/symmetry,andauscultationofbreathsounds.
Neonatal Respiratory System 10
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.
Neonatal Respiratory System 11
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.
Neonatal Respiratory System 12
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.
Infants at Risk/Predisposing Factors
• Termandlate-preterm(“near-term”)infants
• Precipitousdelivery
• Cesareandelivery,especiallyintheabsenceof labor
• Maleinfants
• Prenatalexposuretomethamphetamine
Pathophysiology
Inutero,thefetallungsarefilledwithfluid.Duringnormalvaginaldelivery,thefluidisusuallyforcedoutbythethoracicsqueeze.Theremainderofthefluidinthelungsisclearedbythepulmonaryveinsandlymphaticsystem.Withaprecipitousorcesareandelivery,absenceofthegradualchestcompressionthatoccursduringnormalvaginalbirthcausesfluidtoberetained.Accumulationofthisinterstitialfluidinterfereswithforcesthattendtokeepthebronchiolesopenandeventuallycausesthebronchiolestocollapse(airtrapping).Airtrappingandhyperinflationcanincreasepulmonaryvascularresistanceandleadtopotentialpersistentpulmonaryhypertension.
Clinical Presentation
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
Neonatal Respiratory System 13
Incidence (ClarkandClark2012;Yoderetal.2002)
• 8%–25%ofallUSbirths>34weeksgestationhavemeconiuminamnioticfluid
• ~10%ofthoseinfantsdevelopMAS• changesinobstetricalpracticeappeartobedecreasingtheincidence
Infants at Risk/Predisposing Factors
• 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.
Neonatal Respiratory System 14
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.
Clinical Presentation
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.
Neonatal Respiratory System 15
• 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
Infants at Risk/Predisposing Factors
• 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
Neonatal Respiratory System 16
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
Infants at Risk/Predisposing Factors
• 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.
Neonatal Respiratory System 17
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.
Clinical Presentation
ClinicalpresentationisvariableduetothedifferentetiologiesofPPHN.Respiratorydistressandcyanosisworsendespitehighconcentrationsofinspiredoxygen.Arterialbloodgasesdemonstrateseverehypoxemia,normalormildlyelevatedarterialcarbondioxidetension(PaCO2),andmetabolic
There is no classic chest radiograph finding for PPHN; rather, the x-ray reflects the underlying lung disease.
Neonatal Respiratory System 18
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.
Neonatal Respiratory System 19
Clinical Presentation
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.
Neonatal Respiratory System 20
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
Neonatal Respiratory System 21
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
Infants at Risk/Predisposing Factors
• None
Pathophysiology
Closureofthediaphragmoccursat8–10weeks’gestationalage.Ifclosureisdelayed,thebowelcanmoveintothethoraciccavityandresultinadiaphragmatichernia.Thestomachaswellasthesmallandlargebowel,spleen,andlivercanalsoherniateintothechest.Thepresenceoftheabdominalcontentsinthethoraxdoesmorethanjustcauselunghypoplasiabycompression.Decreasednumbersofbronchialgenerationsandalveoliareseen,andthepulmonaryarteryissmall.Increasedmuscularizationofthepulmonaryarteriesisalsopresent.Boththebronchialandvascularchangesrestrictpulmonarybloodflow,whichcanresultinpersistentpulmonaryhypertension.
Clinical Presentation
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.
Neonatal Respiratory System 22
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.
Infants at Risk/Predisposing Factors
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.
Neonatal Respiratory System 23
Thestandardlong-termtreatmentforapneaofprematurityistheuseofmethylxanthines,specificallycaffeine,theophylline,andaminophylline,whichactonthebrainstemrespiratoryneuronstoexertacentralstimulatoryeffect.Othereffectsincludeimprovedsensitivitytocarbondioxideresponse,increaseddiaphragmaticcontractions,increasedcatecholamineactivity,enhancedrestingpharyngealmuscletone,anddecreaseddiaphragmfatigue.Doxapram,aperipheralchemoreceptorstimulator,hasalsobeenusedforinfantswithapnea;itincreasesbothminuteventilationandtidalvolume.However,doxapramcontainsbenzylalcoholandrequirescontinuousinfusion,soitisnotrecommendedfornewborns.
alsobeennoted.ThesereceptorssensechangesinPaO
2,pH,andPaCO2thataffecttheregulationofrespirationsandrelaythemtotherespiratorycenterinthebrain.Upperairwayobstructioncontributestoapneabecausethenegativepressuregeneratedduringinspirationmayresultinpharyngealandlaryngealcollapse.
Clinical Presentation
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
Neonatal Respiratory System 24
Infants at Risk/Predisposing Factors
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.
Neonatal Respiratory System 25
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
Clinical Presentation
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.
Neonatal Respiratory System 26
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
Neonatal Respiratory System 27
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
Neonatal Respiratory System 28
»Persistentpulmonaryhypertensionofthenewbornischaracterizedbyhighresistanceinthepulmonaryarteries,whichproducesanobstructionofbloodflow.
»Airleaksdevelopfromalveolarruptureandtheescapeofairintotissue.
»Acongenitaldiaphragmatichernia(CDH)istheherniationoftheabdominalcontentsintothechestthroughadefectinthediaphragm.
»RecognitionofCDHinthedeliveryroomisakeycomponentinmanagement.
»Apneaisacessationofrespirationlasting>20secondsandassociatedwithphysiologicalterationssuchasbradycardiaand/orcolorchange.
»Themostcommonalterationofpulmonaryfunctionininfantswithchroniclungdisease(CLD)/bronchopulmonarydysplasia(BPD)isincreasedairwayresistance.
»BPDoftenbecomesaprogressivediseaseifitpersistsbeyond1monthofage.
»TreatmentgoalsforCLD/BPDaretopromotegrowthandhealthelungs,pharmacologicmanagement,optimalnutrition,andaproperenvironment
K e y L e a r n i n g s
»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)
Neonatal Respiratory System 29
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)
K e y L e a r n i n g s
» Bealertforspecialrespiratoryconcernswith theprematureinfant.
Neonatal Respiratory System 30
■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
Neonatal Respiratory System 31
• 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
Neonatal Respiratory System 32
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