Neonatal Respiratory DistressNeonatal Respiratory Distress

Priscilla Joe, MDChildren’s Hospital and Research

Center at Oakland

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Neonatal Respiratory DiseaseNeonatal Respiratory Disease

Upper airway diseaseTrue parenchymal diseaseAirleak syndromesDisorders of developmentPrimary pulmonary vascular disease

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Upper Airway DiseaseUpper Airway Disease

Choanal atresiaPierre Robin sequenceVascular rings

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Choanal Atresia

Pierre Robin Syndrome

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Choanal Atresia/Upper Airway Choanal Atresia/Upper Airway ObstructionObstruction

Cyanotic when quiet or at rest, pink with crying

Inability to pass suction catheter through nares

Stridor

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Upper airway obstructionUpper airway obstruction

Insert an oral airwayProvide oxygenSuction secretionsMay require intubation

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Fetal Lung CharacteristicsFetal Lung Characteristics Decreased blood flow

– caused by compression of the pulmonary capillaries by fetal lung fluid

Pulmonary arteries– thick muscular layer present, very reactive to hypoxemia

Lung fluid secretion– fetal lungs secrete fluid, adequate lung volume is necessary for fetal

development

Fetal breathing– contributes to fetal lung development, moves fluid in and out of fetal lung

Surfactant– necessary amount to support breathing after birth, present after ~ 34

weeks gestation

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TransitionTransition

Clearance of fetal lung fluidIncreased complianceIncreased pulmonary blood flow

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Respiratory Distress Respiratory Distress SyndromeSyndrome

Disease of surfactant defiencySurfactant decreases surface tension

and improves lung complianceSurface tension: intrinsic tendency for

alveoli to collapse

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Compliance

Pressure

Volume

Opening pressures

Maximal volume

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RDS: Risk FactorsRDS: Risk Factors

Prematurity: Males Second born twins C-section Caucasian race

Secondary surfactant deficiency:

Maternal diabetes Asphyxia Pneumonia Pulmonary hemorrhage Meconium aspiration Oxygen toxicity

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RDS: Clinical FindingsRDS: Clinical Findings

Non-specific findings of respiratory distress– Grunting– Flaring– Retracting

O2 requirement

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RDS: RadiographyRDS: Radiography

Alveolar disease:• Diffuse reticular granular or “ground

glass”pattern• Air bronchograms• Underaeration

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RDS: TreatmentRDS: Treatment

Maintain FRC (CPAP vs. intubation)Surfactant replacementExogenous surfactants

– Survanta 4cc/kg– Infasurf 3cc/kg

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Surfactant Therapy for RDSSurfactant Therapy for RDS

Decreases mortality

Greatest benefit when used with antenatal steroids

Improvement in compliance, functional residual capacity, and oxygenation

Reduces incidence of air leaks

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Congenital PneumoniaCongenital Pneumonia

Common organisms:Group B streptococcusE.Coli, KlebsiellaChlamydia, Ureaplasma, mycoplasmaListeriaTORCHH. Influenza (nontypeable)

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Pneumonia: Risk FactorsPneumonia: Risk Factors

Maternal chorioamnionitisProlonged rupture of membanesPrematurityPostnatal exposures: Poor hand

washing, open skin lesions, contaminated blood products, infected breast milk

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PneumoniaPneumonia

Inflammation and edemaBronchial pluggingSurfactant inactivation

– Alveolar collapse– Ventilation/perfusion mismatch– Desaturation

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Pneumonia: Clinical FindingsPneumonia: Clinical Findings

Presents with non-specific findings of respiratory distress– Grunting – Flaring– Retracting

O2 requirement

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Pneumonia: RadiographyPneumonia: Radiography

There are no classic x-ray findings, in fact, the X-ray in pneumonia can look like anything– Fairly normal– Classic RDS– Classic for MAS

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Pneumonia: TreatmentPneumonia: Treatment

Respiratory support as indicated with either O2 or positive pressure

Treatment with appropriate antimicrobials– Initial ampicillin/gentamicin or

ampicillin/cefotaxime– Broader spectrum antibiotics for

nosocomial bacteria

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Meconium Aspiration Meconium Aspiration SyndromeSyndrome

Meconium contains epithelial cells and bile salts

Released with intrauterine stress or asphyxia

Present in 15% of all newborns. Only 5-10% develop MAS

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Meconium AspirationMeconium Aspiration

Airway plugging, with air trapping Inflammation, leading to inactivation of

surfactant Surfactant inactivation leads to decreased

compliance, and alveolar collapse Alveolar collapse = loss of FRC Loss of FRC = V/Q mismatch V/Q mismatch = desaturation

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Meconium aspiration: XrayMeconium aspiration: XrayAreas of hyperexpansion mixed with

patchy densities and atelectasis

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PneumothoraxPneumothorax

May occur spontaneously during delivery

Most common when receiving positive pressure

Space occupying lesion within the chest displacing lung, and if under tension, compromising venous return

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Pneumothorax: Clinical Pneumothorax: Clinical FindingsFindings

Presents with non-specific signs of respiratory distress– Grunting– Flaring– Retracting

O2 requirementUnequal, decreased breath sounds

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Pneumothorax: TreatmentPneumothorax: Treatment

O2 as needed– Nitrogen washout (pneumo contains 21%

O2, >75% nitrogen, if lung has 100% O2, nitrogen will diffuse out of pneumothorax)

Try to avoid positive pressure if ableEvacuate as needed by thoracentesis

or chest tube

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Developmental disturbancesDevelopmental disturbances

Pulmonary hypoplasiaCongenital diaphragmatic herniaSkeletal deformities

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Pulmonary hypoplasiaPulmonary hypoplasia

Cannot be assessed radiographically, pulmonary hypoplasia is a pathologic diagnosis

Suspect pulmonary hypoplasia if:– Rupture of membranes with anhydramnios– Renal anomalies– Restriction of the chest wall– Congenital diaphragmatic hernia

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Diaphragmatic HerniaDiaphragmatic Hernia

Scaphoid abdomenBowel sounds in the chestOther associated anomaliesDecreased breath soundsSevere hypoxemia

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Diaphragmatic HerniaDiaphragmatic Hernia

Wide range in clinical presentationHerniation of bowel leads to altered

development of the lungs bilaterally

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Persistent Pulmonary Persistent Pulmonary Hypertension of the NewbornHypertension of the Newborn

Primary pulmonary hypertension is a pure vascular disease

More often present in a mixed picture as in the setting of meconium aspiration syndrome or asphyxia

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PPHNPPHN

In response to an asphyxia event in utero, the fetus diverts all blood flow possible to vital organs (brain/heart/adrenals)

This leads to vasoconstriction of non-vital vascular beds, including the pulmonary bed

Remodeling of smooth muscle can occur

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PPHNPPHN

IncreasedPVR

RV outflow

AortaPA

PDA

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PPHN: Clinical FindingsPPHN: Clinical Findings

Respiratory distress with hypotensionHypoxemia out of proportion to degree

of distressDifference in pre and post ductal sats

– Right hand– Lower extremities– Hyperoxia test

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PPHNPPHN

Decreases R L shunt:

Decrease PVR

Increase pulmonary blood flow– Hyperoxia– Hypocarbia– Lack of acidosis

Increases R L shunt:

Increase PVR

Decrease pulmonary blood flow– Hypoxia– Hypercarbia– Acidosis

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PPHN: TreatmentPPHN: TreatmentImprove pulmonary blood flow:

– Keep well saturated– Normocarbia

Avoid:– Hypoxia– Hypercarbia– Acidosis

Supportive care: temperature regulation, fluids and lytes, antibiotics

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PPHN: TreatmentPPHN: Treatment

Conventional ventilation or HFOVNitric oxideSurfactant replacementECMO