Neonatal Respiratory Distress (I)

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Review Focus

• Lung development• Predisposing risk factors• Respiratory Disorders

– Respiratory Distress Syndrome– Pneumonia– Transient Tachypnea of the Newborn– Persistent Pulmonary Hypertension of the Newborn– Meconium Aspiration Syndrome

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Anatomy & Physiology

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ANATOMY &PHYSIOLOGY

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Predisposing Risk Factors

• Prematurity• Infants of diabetic mothers• Birth asphyxia• Cesarean section• Congenital anomalies• Maternal drugs• Acid-Base imbalance

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Respiratory Disorders

• Respiratory Distress Syndrome• Transient tachypnea of the New Born• Pneumonia• Air Leak• Chronic lung disease (CLD) (separate lecture)• Meconium aspiration syndrome• Persistent Pulmonary Hypertension of the

newborn (PPHN)• Pulmonary Hemorrhage

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Respiratory Distress Syndrome(RDS or HMD)

• Developmental disorder starting at or soon after birth and occurring most frequently in infants with immature lungs

• 20,000-30,000 infants per year affected in the US

• Incidence related to gestational age

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Neonatal respiratory distress syndrome is a condition of pulmonary insufficiency.

NRDS is due to a lack of alveolar surfactant along with structural immaturity of the lungs.

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It is directly related to prematurity60–80% of infants less than 28 wk 15–30% of those between 32 and 36 wkin about 5% beyond 37 wkThe incidence is highest in preterm male or white infants

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RDS Cont’d• Pathophysiology

– Surfactant deficiency– Uncomplicated course characterized by peak severity

at 1-3 days– Onset of recovery at ~72 hrs (usually coinciding with

diuresis)• Risk factors

– Low gestatinal age– Male predominance– Maternal diabetes– Prenatal depression

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RDS Cont’d• Clinical

– Respiratory distress (grunting, flaring, retractions, tachypnea)

– Cyanosis– Definitive diagnosis is made with CXR

• Pulmonary function– Decreased lung compliance– Decreased FRC– Shunting of blood through atelectatic areas leading to

hypoxia– Unstable alveoli (Smaller alveoli will collapse during

exhalation– Laplace’s Law)

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RDS Cont’d

• Pathophysiology– Decreased surfactant production– Presence of hyaline membranes located at junction

of dilated respiratory bronchioles and dilated alveolar ducts

– Hyaline membranes contain cellular debris from injured epithelium and fibrinous matrix components

– Minimally aerated lungs, diffuse alveolar atelectasis

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RDS Cont’d• Prevention

– Antenatal corticosteroid administration ( at least 24-48 hours prior to delivery) **per ACOG guide line only one course of bethamethasone recommended

– Administration of betamethasone two 12mg IM dose 24hrs apart to women 48hr before the delivery of fetuses between 24 and 34 wk of gestation significantly reduces the incidence and the mortality and morbidity of HMD

– Tocolytic agents to arrest premature labor13

Administration of a first dose of surfactant 200mg/kg into the trachea of all babies under 27wks immediately after birth (prophylactic within 15 min) or symptomatic premature babies during the first few hours of life (early rescue) reduces air leak and mortality from HMD but does not alter the incidence of BPD

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•Management–Artificial surfactant replacement–Respiratory support and monitoring–Oxygen supplementation–Fluid and metabolic management

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Treatment – Mechanical ventilation

Persistent apnea Arterial blood pH less than 7.20Arterial blood pCO2 of 60mm Hg or higherArterial blood pO2 of 50mm Hg or less at oxygen concentrations of 70–100% and

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Mechanical ventilation

The aim is to stabilize the lung after recruitment to optimal lung volume with adequate positive end-expiratory pressure (PEEP) or continuing distending pressure on HFOV [high-frequency oscillatory ventilators] to keep the lung open during the whole respiratory cycle

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Treatment of NRDS can be divided into 4 phases

Recruitment Stabilization Recovery weaning

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Treatment - NO

Inhaled nitric oxide (iNO) has acutely improved oxygenation, but it may not improve the overall outcome of infants with HMD/RDS

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RDS is characterized by atelectasis and decreased lung volumes resulting from surfactant deficiency.

The physiologic basis for iNO use in the preterm infant who has RDS depends on 3 mechanisms:

- Reversal of pulmonary hypertension - Improved ventilation-perfusion

matching - Decreased inflammatory response

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RDS Cont’d

• CXR

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Respiratory distress syndrome

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RDS Test Your knowledge

• At what gestational age is the fetal lung first capable of supporting extra uterine life with out medical intervention?– A. 19-23 weeks– B. 24-25 weeks– C. 26-28 weeks– D. 29-33 weeks

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RDS Test Your knowledge

• *****Surfactant improves lung function by:– A___. Reducing surface tension at the air-liquid

interface in the alveolus– B. Promoting structural maturation of the lung– C. Inhibiting alveolar fluid clearance– D. Increasing opening pressure

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RDS Test Your knowledge

• Respiratory grunting represents the infant’s attempt to– A. Prevents alveolar collapse at the end of

expiration– B. Decrease upper airway resistance– C. Decrease functional residual capacity– D. Overcome large airway obstruction

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RDS Test Your knowledge

• Medical management of the infant with RDS complicated by patent ductus arteriosus would include all of the following except– A. Indomethacin– B. Prostaglandin E– C. Fluid restriction– D. Diuretics

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Transient Tachypnea of the New born (TTN)

• Pathophysiology– Delayed clearance of fetal lung fluid– Usually resolves by 48 to 72 hours– Starts at birth– Occurs in 1-2% of all live births in the US

• Risk Factors– Delivery by C/S– Maternal diabetes– Perinatal depression– Maternal sedation– Precipitous delivery

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TTN Cont’d

• Clinical presentation– Tachypnea 60-140 BPM– Grunting– Nasal flaring– Barrel shaped chest– Mild intercostals retraction– Possible mild cyanosis

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TTN Cont’d

• Management– Respiratory support and monitoring– Oxygen supplementation– Some may require CPAP

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TTN Cont’d, Diagnosis confirmed by CXR

Hyper expansion and lung fluid

Neonate at age 6 hours30

TTN Cont’d

Same patient at age 2 days 31

Pneumonia

• Pathophysiology– Transplacental (intrauterine infection)– Aspiration of contaminated amniotic fluid (and/or

meconium– Hematogenous– Inhalation– Occurs in 1% of term infants and 10% in preterm

infants in the US

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Pneumonia Cont’d

• Pathogens – Early: Group B streptococci (GBS), E. Coli,

Klebsiella, Listeria– Late: above plus Staphylococcus aureus,

Pseudomonas, fungal, Chlamydia,– Other: Ureaplasma, viral (cytomegalovirus,

herpes, respiratory syscytial virus, enterovirus, rubella), syphilis

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Pneumonia Cont’d

• Risk factors– Prolonged rupture of membranes >24 hrs– Maternal fever/chorioamnionitis– Foul smelling amniotic fluid– Gasping due to fetal asphyxia leading to increased risk

of aspiration• Clinical presentation

– Respiratory distress, cyanosis, hypercapnia, tachycardia, lethargy, poor feeding

– Fever especially if herpes or enterovirus

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Pneumonia Cont’d

• Diagnosis– by CXR (typically abnormal at 24-72 hours after

symptom)– CXR finding can appear very similar to RDS (especially

if GBS***)• Management

– Respiratory support and monitoring– Gram stain and culture of blood and tracheal

secretions– Antibiotics

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X-ray - patchy infiltrate in perihilar area.

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May lead to diffuse involvement of entire lungs

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Air LeakPneumothrax

• Divided into two categories– Spontaneous -occurring in an otherwise healthy,

full term infants shortly after birth and usually spontaneously resolve

– Iatrogenic -occurring in infants with underlying lung pathology regardless of gestational age or following invasive procedures ( intubation, central catheter placement)

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Air LeakPneumothrax

• Physiology– Air between parietal pleura lining the chest wall and the

visceral pleura covering the lung• Risk factors

– Aspiration of blood, meconium, amniotic fluid– Lung diseases including RDS, pulmonary hypoplasia,

congenital diaphragmatic hernia, pneumonia– Intubated infant with improving compliance– Ventilated infant with expiratory efforts opposing

ventilated breaths– Spontaneous pneumothorax can occur in 1-2% of health

full term infants, often asymptomatic

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Air LeakPneumothrax

• Clinical presentation– Respiratory distress, cyanosis, apnea, and bradycardia– Affected side with decreased breath sounds and increased

anterior posterior (AP) diameter– Displaced point of maximal impulse– If under tension, acute decrease in BP, heart rate and

respiratory rate– Increased risk of intraventricular hemorrhage due to

decreased venous return if tension pneumothorax or sudden improvement in cerebral perfusion following chest tube placement

– Increased risk of syndrome of inappropriate anti-diuretic hormone

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Air LeakPneumothrax

• Diagnosis– Trans illuminate: Place probe bilateral axilla region

and below diaphragm– Tran illumination may be falsely negative in large

infants or small leaks and falsely positive if subcutaneous edema, lobar emphysema, or pneumomediastinum

– CXR

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Air LeakPneumothrax

• Management– Ventilator: decrease PEEP, decrease PIP, decrease I time, increase rate

– Consider 100% oxygen to obtain nitrogen washout if smaller leaks

– Needle aspiration– Chest tube placement

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Air LeakPneumomediatinum

• Higher incidence for infant with MAS• CXR shows sail sign of the thymus being lifter

by air• Majority asymptomatic since air is seldom

under tension• If symptomatic, may have tachypnea, muffled

heart sounds, and cyanosis• It resolves spontaneously

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Air LeakPneumopericardium

• Air leakage into the pericardial sac• Symptoms dependent upon level of tension and

include cyanosis, muffled heart sounds, hypotension (due to inferior vena cava compression and decreased cardiac venous return leading to decreased stroke volume)

• The only treatment is pericardial needle aspiration if severe symptoms

• High mortality rate47

Air LeakPulmonary interstitial

emphysema(PIE)• Air leak into the interstitial space• Majority of infant are premature and

ventilated with severe RDS• Interstitial air leads to decreased lung

compliance, ventilation/perfusion mismatch, increased dead space

• Manage by decreased MAP, consider HFV, if unilateral involvement, can position infant on side of affected lung, consider selective bronchial intubation.

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Pulmonary interstitial emphysema

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Meconium Aspiration Syndrome (MAS)

• Pathophysiology– Mechanical obstruction– Chemical inflammation– Surfactant inactivation– Associated with air leaks

• Risk factors– Full term or post mature– Fetal distress– In utero hypoxia– Mechonium stained amniotic fluid

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MAS Cont’d

• Clinical– Severe respiratory distress beginning shortly after

birth

• Pulmonary function– Decreased lung compliance– Decreased alveolar ventilation and perfusion or

poorly ventilated areas leading to hypoxemia– Increased pulmonary vascular resistance (due to

local pulmonary vasoconstriction

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MAS Cont’d• Prevention

– If meconium stained amniotic fluid, suction nasopharynx at the perineum and direct tracheal suctioning if new born is not vigorous

• Management– Respiratory ventilator support and monitoring-ideal to maintain

adequate expiratory time to prevent air trapping– Manage pulmonary hypertension, monitor for signs of pneumothorax– Surfactant administration due to surfactant inactivation by

meconium and decreased surfactant production following alveolar injury

– Antibiotics since 1. meconium increases bacterial growth 2. often cannot distinguish from pneumonia, and 3. sepsis may be precipitant for aspiration

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Persistent pulmonary Hypertension (PPHN)

• Incidence: 1-2 per 1000 birth• Etiology

– Maladaptation: normal structure of pulmonary vascular bed but PVR remains elevated. e.g. hypoxia, asphyxia, hypothermia, hyperviscosity (polycythemia), pneumonia, sepsis

– Maldevelopment: abnormal structure of pulmonary vascular beds leading to vascular smooth muscle hypertrophy e.g. intrauterine hypoxia, perinatal asphyxia, meconium aspiration, fetal ductus arteriosus closure, pulmonary hypoplasia, diaphragmatic hernia, alveolar capillary dysplasia

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PPHN Cont’d• Pathophysiology

– Increased PVR leads to right-to-left shunting at the atrial or ductal level

– The resultant decrease in pulmonary blood flow leads to hypoxia• Clinical:

– Usually full term or post term– Infant typically presents within the first 24 hrs of life with severe

cyanosis, respiratory distress, severe hypoxemia (less effect on CO2 retention), labile oxygenation

– Single or narrowly split, loud S2– Preductal oxygen sats > postductal oxygen sats

• CXR:– Decreased pulmonary vascular markings, normal, or increased heart

size

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PPHN Cont’d

• Management– Obtain ECHO to rule out congenital heart disease– ECHO findings C/W PHTN include pulmonary

pressures similar to systemic pressure, tricuspid regurgitation, bowing of ventricular septum in LV, right-to –left shunting across PDA

– Treat with antibiotics since may be associated with sepsis

– Treat any underlying lung disease– Administer 100% oxygen to increase pulmonary

vasodilatation

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PPHN Cont’d• Management

– Sedation, maximize oxygen carrying capacity with PRBC, maintain cardiac output (inotropic support if needed) to keep SBP slightly elevated to increase left to right shunting, ventilator support (PEEP-need to monitor closely as it may decrease cardiac output, hyperventilation with alkalization, consider HFV)

– Inhaled nitric oxide: a specific pulmonary vasodilator– In the past nitroprusside and tolazoline were used as

vasodilators– need to monitor cyanide levels with nitroprusside– Need to monitor systolic BP as both these drugs may cause

systemic vasodilatation– ECMO if above therapies fail

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Pulmonary Hemorrhage

• Pathophysiology– Due to acute increase in capillary hydrostatic

pressure (secondary to a left-to-right shunt from PDA or vasoconstriction following perinatal depression)

– This increased pressure leads to capillary vessel breakage and large amount of fluid leakage

• Risk factors– PDA, sepsis, left ventricular failure, ?? Surfactant

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Pulmonary Hemorrhage Cont’d• Clinical presentation

– Bloody tracheal secretions– Respiratory distress, cyanosis– Cardiovascular instability

• Pulmonary function– Acute decrease in lung compliance– Severe hypoxemia

• Management – Increase PEEP to enhance alveolar distention and impede

pulmonary blood flow– Assess clotting factors and administer blood products as needed– Treat PDA– Consider echocardiogram to assess left ventricular function

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