Respiratory Distress in New born

Presented by Dr. Ankit AgarwalGuided by: Dr. J.P. Jain

Dept. of PediatricsNIMS, Jaipur

Overview• General Considerations

– Epidemiology– Definition and Clinical Features– Assessment of severity– Causes– Approach to a New born with

resp. distress

• Meconium Aspiration Syndrome– Epidemiology– Etiopathogenesis– Clinical Features– Diagnosis – Management

• Respiratory Distress Syndrome– Epidemiology– Etiopathogenesis– Clinical Features– Diagnosis – Management– Surfactant Therapy– Complication

• Transient Tachypnea of Newborn– Epidemiology– Etiopathogenesis– Clinical Features– Diagnosis – Management

Epidemiology

• Commonest problem encountered within the first few hours of life.

• It occurs in approximately 1%-6% of live births

• Responsible for about 20% of neonatal mortality

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Definition and Clinical Features

Tachypnea

AND

Expiratory Grunt OR Inspiratory Retraction

Only Tachypnea is NOT Respiratory Distress

• Cyanosis• Nasal Flaring• Desaturation• Lethargy/Poor feeding

• Pallor• Decreased Breath Sounds

+\- Rales or Ronchi

Other Features

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Assessment of SeverityDowne’s Scoring System

Score 0 1 2

Respiratory Rate (rate/min)

<60 60-80 >80

Cyanosis None in room air No cyanosis in 40% oxygen

Requiring more than 40% ambient oxygen

Retractions None Mild Moderate to Severe

Grunting None Audible with Stethoscope

Audible without Stethoscope

Air Entry Good Decreased Barely Audible

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Modified Downe’s Scoring System

No cyanosis with oxygen support

Cyanosis in spite oxygen support

Interpretation:

<4: No Respiratory Distress

4-7: Clinical Distress

>7: Impeding Respiratory Failure

Downe’s Score should be noted every 30mins-1 hour to monitor progression of respiratory

distress.

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Silverman-Andersen Retraction Scoring

InterpretationScore 0-3 = Mild respiratory distress Score 4-6 = Moderate respiratory distress Score > 6 = Impending respiratory failure Score 10 = Severe Respiratory distress

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A progressively increasing O2 requirement to maintain saturation is also a sensitive indicator of the severity and progress of distress

>95% Term baby, pulmonary hypertension (PPHN) 88-94% 28-34 weeks preterm85-92% Below 28 weeks gestational age

Guidelines for monitoring oxygen saturation levels by pulse oximetry

MJAFI, Vol. 63, No. 3, 2007

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Causes

• Pulmonary• Extra-pulmonary

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Pulmonary Causes

1) Airway obstruction A) Nasal – choanal atresia, nasal edemaB) Oral cavity – macroglossia, micrognathia, GlosoptosisC) Laryngeal obstruction – laryngeal web, Subglottic

stenosis of larynx, Laryngomalacia, cord paralysis

D) Neck obstruction – cystic hygroma, cong goitreE) Tracheal obsruction – Tracheomalacia, TEF, Tracheal

stenosis

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2) Lung parenchymaA. Aspiration syndrome (MAS)B. Respiratory distress syndrome (HMD)C. Transient Tachypnea of new bornD. Pneumonia E. Pleural effusionF. Pulmonary hemorrhageG. Air leak – Pneumothorax, Pneumomediastinum

3) Developmental defects H. Agenesis of lungI. Hypoplasia of lungJ. Diaphragmatic herniaK. Tracheal agenesisL. TEF M. Asphyxiating Thoracic dystrophy (Jeune Syndrome)

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Extrapulmonary Causes

• CNS Trauma or Birth Asphyxia• Cardiac Failure• Metabolic acidosis• Persistent pulmonary hypertension• Diaphragmatic Hernia• Intercostal muscle Paralysis• Others: Hypothermia/Hyperthermia,

Hypoglycemia, Anemia/Polycythemia,

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Common CausesMedical• Transient Tachypnea

of new born• RDS(HMD)• Aspiration

syndromes• Pneumonia/sepsis• PPHN• CCF• Acidosis

Surgical• Pneumothorax• Diaphragmatic

hernia• TEF• Lobar emphysema• Phrenic nerve

paralysis

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New Born with Respiratory DistressWhat to do???

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HistoryWhat we need to know Why we need to knowWere there any risk factors in the antepartum period or evidence of fetal distress prior to delivery?

Birth asphyxia or PPHN

Did the mother receive antenatal steroids if it was a preterm delivery?

Antenatal steroids decrease the incidence of HMD by 50%

Was there a history of premature rupture of membranes and fever?

Congenital pneumonia orsepsis

Was there meconium stained amniotic fluid?

MAS is a possibility

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What we need to know. Why we need to knowWas resuscitation required at birth?

Resuscitation trauma/ PPHN/ acidosis

Did the distress appear immediately or a few hours after birth?

HMD appears earlier than pneumonia

Was it related to feeding or frothing at the mouth?

Tracheo-esophageal fistula or aspiration

Does the distress decrease with crying

Choanal atresia

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Signs-Will depend on causeWhat we need to look for Why we need to look forA preterm baby weighing <1500 gms with retractionsand grunt

Likely to have HMD.

Meconium stainedamniotic fluid with an increase in the anterio-posterior diameter of the chest (full chest)

Likely to be suffering from MAS

A depressed baby with poor circulation

Neonatal sepsis with or without congenitalpneumonia.

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What we need to look for Why we need to look forA near term baby with no risk factors and mild distress.

May have TTNB

An asphyxiated baby May have PPHN/acidosisA growth retarded baby with a plethoric look

May have polycythaemia.

Check for an air leak by placing a light source overthe chest wall in a darkened room.

Air leak syndrome

Inability to pass an 5F catheter through the nostrilof a term baby

Suggestive of choanal atresia.

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Investigation

Complete Blood Count with a Peripheral blood smear

Sepsis screen including C-reactive protein and μ ESR

Arterial blood gas (ABG) analysis

Blood glucose, Serum calcium

Cultures: Blood , Surface swab (where indicated), maternal vaginal swab

Chest radiograph with an oro-gastric tube in situ

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Management• Clear the airway, ensuring adequate breathing and circulation. • Continuous pulse oximeter monitoring.• Warm, humidified oxygen is given with a head box.• Maintenance of correct temperature is essential. • Fluid and electrolyte management: Electrolyte balance, fluids,

calcium and glucose homeostasis are all equally important.• Maintenance of adequate hemoglobin: Any neonate with

respiratory distress should have a packed cell volume (PCV) above 40% (but less than 75%).

• All preterm babies with respiratory distress should be started on broad spectrum antibiotics. In term babies, decision to start antibiotics would depend on the clinical situation, but the threshold should be low.

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Respiratory SupportRespiratory support is given in the form of continuous positive airway pressure (CPAP) or intermittent mandatory ventilation (IMV). Depends upon condition and severity of distress.

0 1 2 3PaO2

mmHg>60 50-60 <50 <50

PaCO2

mmHg<50 50-60 61-70 >70

pH >7.3 7.20-7.29 7.1-7.19 <7.1

ABG Scoring System

A score of >3 suggests ventilator/respiratory requirement Gen

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Indications for starting CPAP are • Downes’ or Silvermann score of >6 at birth • FiO2 requirement of >0.4 to maintain an acceptable

saturation on pulse oximeter. • ABG score of more than 3.

CPAP is said to have failed when the FiO2 requirement is >0.6 or the pressure required to maintain oxygenation exceeds 7-8 cm of H2O.

Mechanical Ventilation: Time cycled pressure limited ventilation is the modality of choice for ventilation. If patient triggered ventilation is used it is given as synchronized intermittent mandatory ventilation (SIMV).

Best outcome are seen in babies with impending respiratory failure or failed CPAP rather than in complete respiratory failure.

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Specific Management depends on the CAUSE of distress

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Meconium Aspiration Syndrome

Definition

MAS is defined as respiratory distress in an infant born through meconium-stained amniotic fluid (MSAF) whose symptoms

cannot be otherwise explained

J Perinatol. 2008 Dec

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Epidemiology

• Most common cause of respiratory distress in term and post-term infants.

• MSAF observed in 5-25% of all births out of which 10% develop MAS.

• One third require ventilator support• 10% develop air leaks • 5-10% of them have a fatal outcome

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What is meconium?

• The term was coined by Aristotle from the Greek word “meconium arion” meaning “opium like”

• Consists of gastrointestinal, hepatic and pancreatic secretions, cellular debris, swallowed amniotic fluid, lanugo, vernix caseosa and blood

• Appear in the fetal intestines by the 10th week of life gradually increasing in amount to reach 200gms at birth

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Cause of MSAF• The passage of meconium from the fetus into

amnion is prevented by lack of peristalsis(low motilin level) , tonic contraction of the anal sphincter, terminal cap of viscous meconium.

• Vagal Stimulation due to in utero hypoxia, acidosis, cord or head compression cause increased peristalsis and a relaxed anal sphincter.

• Fetal maturation (post term) causes high motilin level increased peristalsis

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Risk factors for MAS

• Post term pregnancy• Primigravida• Maternal Anemia• Chorioamnionitis• Prolonged Labour• Fetal Distress• IUGR• Maternal Age >30yrs• Maternal DM

• Maternal heavy cigarette smoking

• Pre-eclampsia / eclampsia

• Oligohydramnios• Antepartum

Hemorrhage

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Pathophysiology

1. Mechanical obstruction of airways 2. Chemical Pneumonitis3. Surfactant Inactivation

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Mechanical obstruction of airways

• With onset of respiration – meconium migrates from central to peripheral airways.

• Thick particulate and viscous meconium lead to complete or partial airway obstruction.

• Complete obstruction Atelectasis Ventilation-Perfusion (V-Q) mismatch

• Partial obstruction Ball-valve – air trapping Obstructive Emphysema Risk of pneumothorax (15 – 33%)

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Chemical pneumonitis

• Meconium in the airways initiates an inflammatory reaction

• Meconium inhibits oxidative burst and phagocytosis by neutrophil increased risk of infection

• Meconium induces production of inflammatory cytokines Injury of parenchyma and vascular leakage injury similar to ARDS

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Surfactant inactivation

• Bilirubin, fatty acid, triglycerides, cholesterol and proteins present in meconium alter phospholipid structure of surfactant reduced surfactant function

• Bile has cytotoxic effect on Type II Pneumocytes Reduced surfactant production.

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Clinical Features

History

• Maternal risk factors present• Term or Post term Infants• Meconium Stained Amniotic fluid (Thick pea

soup/Thin)• IUGR. • Many babies are depressed at birth.(in utero

aspiration)

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Physical examination

• Evidence of postmaturity: peeling skin, long fingernails, and decreased vernix.

• The vernix, umbilical cord, and nails may be meconium-stained, depending upon how long the infant has been exposed in utero.

• In general, nails will become stained after 6 hours and vernix after 12 to 14 hours of exposure .

• umbilical cord staining (thick-15min, thin-1hour)

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Meconium stained umbilical cord

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Meconium stained nails

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• Features of respiratory distress within first few hours of birth

• The chest typically appears barrel-shaped, with an increased anterior-posterior diameter caused by over inflation.

• Auscultation reveals rales and rhonchi -immediately after birth.

• Some patients are asymptomatic at birth and develop worsening signs of respiratory distress as the meconium moves from the large airways into the lower tracheobronchial tree.

• In case of massive meconium aspiration, meconium pigments may be absorbed from lungs excreted in urine. Urine may appear dark brown in colour.

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Diagnosis

MAS must be considered in any infant born through MSAF who develops

symptoms of Respiratory Distress with typical chest x ray findings

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Diagnosis

• A chest radiographs is characterized by hyperinflation of the lung field and coarse nodular opacities due to areas of atelectasis and consolidation.

• There are coarse irregular patchy infiltrates • A pneumothorax and pneumomediastinum

may be present .

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Diagnosis

• Arterial blood gas measurements typically show hypoxemia and hypercarbia.

• Infants with pulmonary hypertension and right-to-left shunting may have a gradient in oxygenation between preductal and postductal samples.

• Echocardiogram for evaluation of Persistent Pulmonary Hypertension.

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Management

• Prenatal management: Key management lies in prevention during prenatal period.

• Identification of high risk pregnancies and close monitoring. Pregnancy that continue past due date, induction as early as 41 weeks may help prevent meconium aspiration.

• If there is sign of fetal distress corrective measure should be undertaken or infant should be delivered in timely manner.

• Amnioinfusion has no role.

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Delivery Room Management

Baby delivered through MSAF

Intrapartum Suctioning

Assess the baby after 10-15 sec

Vigorous

• HR > 100/min• Spontaneous Respiration• Crying• Reasonable tone

No intervention

Non Vigorous

• Intubate• Tracheal Suction

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• When the infant is not vigorous:1. Place under radiant warmer but delay

stimulation.2. Clear airways as quickly as possible. 3. Intubation and then suction directly to the ET

tube. repeat until either ‘‘little meconium is recovered, or until the baby’s heart rate indicates that resuscitation must proceed without delay’’.

4. May also require saline lavage to remove thick particles.

5. After all meconium is sucked out, ventilate the baby with bag and mask.

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Postnatal Management

• Shift to NICU setup with respiratory support facilities available

• Gastric wash with normal saline to reduce gastritis and aspiration of meconium stained products.

• Close monitoring for Respiratory distress. • Most infants who develop symptoms will do

so in the first 12 hours of life.

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Postnatal Management Approach to the ill newborns:1. Maintain temperature2. O2 support by hood

3. 2/3rd restricted IV fluids4. Look for and manage hypoglycemia/ hypocalcemia/

hypotension 5. ??? Antibiotics6. Initiate CPAP/ventilation if indicated7. ??? Surfactant therapy (Bolus/Trachebroncial Lavage) - should

be used in setups where ECMO facility is unavailable8. iNO(Inhaled Nitric Oxide) – when PPHN complicates MAS9. ECMO (Extra Corporeal Membrane Oxygenation)10. Keep high suspicion for Air Leaks and PPHN

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Respiratory Distress Syndrome (RDS)

• Also known as Hyaline Membrane Disease (HMD)• Commonest cause of preterm neonatal mortality• RDS occurs primarily in premature infants; its

incidence is inversely related to gestational age and birth weight

Nelson Textbook of Pediatrics, 18th Ed.

Gestational age Percentages

Less than 28 wks 60-80%

32-36 wks 15-30%

37-39 wk 5%

Term Rare

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Risk Factors

Increased Risk Decreased Risk• Maternal diabetes• multiple births• cesarean section

delivery• perinatal asphyxia• cold stress• history of previously

affected infants

• Chronic or pregnancy-associated hypertension

• maternal heroin use• prolonged rupture of

membranes• antenatal

corticosteroid prophylaxis

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Etiology & Pathophysiology• Lack of surfactant due to immaturity of lungs

is the basic abnormality.• Surface-Active-Agent (Surfactant) which is

produced by type II alveolar cells, reduces surface tension and maintains alveolar stability at low pressure so that end-expiratory alveolar atelectasis does not occur.

• Surfactant production is also compromised in birth asphyxia, acidosis, hypothermia, Rh incompatibility, antepartum hemorrhage and shock

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Surfactant deficiency

End-Expiratory Alveolar Atelectasis

Hypoventilation

Hypo-perfusion of lungs

Epithelial Necrosis

Transudation of Plasma

Formation of Hyaline Membrane

V/Q mismatch

Reduced Compliance

↓p02↑pCO2

↓ pHPPHN

Surfactant deficiency

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Clinical Features• Maternal Risk factors present in history• Preterm Infant• Features of respiratory distress usually appear within

few minutes of birth to upto 6 hours of birth• Breath sounds may be normal or diminished with a

harsh tubular quality• Fine rales may be heard, especially posteriorly over

the lung bases• Apnea and irregular respirations occur as infants

tire and are ominous signs requiring immediate intervention

• Respiratory failure may occur in patients with rapid progression of the condition

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• Patient may have a mixed respiratory-metabolic acidosis, edema, ileus and oliguria.

• In most cases, the symptoms and signs reach a peak within 3 days, after which improvement is gradual

• Death is rare on the 1st day of illness, usually occurs between days 2 and 7– associated with alveolar air leaks (interstitial

emphysema, pneumothorax), pulmonary hemorrhage, or IVH.

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Diagnosis

• Amniotic Fluid Lecithin/Sphingomyelin Ratio– ≥2 suggests lung maturity. – ≤1.5 associated with HMD

• Phosphatidyl Glycerol estimation– More specific than L/S ratio– Absence is invariably associated with HMD

• Gastric Aspirate Shake Test– Unreliable if gastric aspirate is contaminated with blood

or meconium– Serial tests can be done to assess maturity of lungs during

course of disease

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• ABG initially shows hypoxemia and later worsening of hypoxemia, hypercapnia and metabolic acidosis

• On X-Ray Chest– Initial X-ray may be normal– Typical pattern develop at 6-12 hours

– Grade 1 (mild cases): symmetrical reticulogranular pattern due to scattered atelectasis

– Grade 2: widespread air bronchogram become visible– Grade 3: reticulogranular pattern becomes

increasingly confluent leading to formation of ground glass opacity due to marked underaeration

– Grade 4: complete white lung fields with obscuring of the cardiac shadow due to global atelectasis Re

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Prevention

• Suppress Premature labor to gain gestational maturity

• Delay induction of labour till pulmonary maturity is assured by L/S ratio

• Antenatal Steroids to mother– Betamethasone (12mg IM every 24 hr for 2 doses)– Dexamethasone(6mg IM every 12 hr for 4 doses)

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Management1. Shift to NICU setup with respiratory support facilities

available

2. Close monitoring for Respiratory distress.

3. Maintain temperature

4. O2 support by hood

5. 2/3rd restricted IV fluids

6. Look for and manage hypoglycemia/ hypocalcemia/ hypotension

7. ???Antibiotics

8. Initiate CPAP/ventilation if indicated

9. Surfactant therapy if indicated

10.Vitamin E

11. ???Post natal steroids Resp

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Surfactant• Surfactant reduces surface tension, improves lung compliance, and

stabilizes lung volumes at a lower transpulmonary pressure

• Surfactant’s secondary function is to enhance macrophage activity and mucociliary clearance, and to reduce inflammation.

• Types of Surfactant– Natural or Synthetic

• Indications– Prophylactic

• Premature infants at high risk of developing RDS secondary to surfactant deficiency (eg 32 weeks or low birth weight 1, 300 g)

• Infants in whom there is laboratory evidence of surfactant deficiency such as lecithin/sphingomyelin ratio 2:1 or the absence of phosphatidylglycerol

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• Indication– Rescue or therapeutic administration is indicated in

preterm or full-term infants who are suspected of having surfactant deficiency by inactivation and• who require endotracheal intubation and mechanical

ventilation secondary to respiratory failure

OR

• who require an FiO2 ≥ 40% or a PEEP of ≥7 to maintain adequate PaO2 and SpO2 and have Clinical and radiographic evidence of neonatal RDS or MAS.

– Surfactants may be used as a vehicle to deliver other drugs such as antibiotics, anti-inflammatory agents, and bronchodilators.

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• Indication– Postoperative development of ARDS following cardiac

surgery. Reduces time on ventilation and ICU and hospital stay.

– Porcine surfactant in RSV induced respiratory failure may improve gas exchange and respiratory mechanics and shorten the duration of ventilation and hospital stay.

• Contraindication– Presence of congenital anomalies incompatible with life

beyond the neonatal period– Respiratory distress in infants with laboratory evidence of

lung maturity– Diagnosis of congenital diaphragmatic hernia. Studies have

shown that early use of surfactant increases mortality.– Patient hemodynamically unstable– Active pulmonary hemorrhage Re

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• Frequency– Multiple doses of surfactant to infants with ongoing respiratory

insufficiency appears to be the most effective treatment regimen– It has resulted in greater improvements in oxygenation and

ventilatory requirements, a decreased risk of necrotizing enterocolitis, and decreased mortality.

– Additional doses of surfactant, given at 6–24-hour intervals, may be indicated in infants who experience increasing ventilator requirements or whose conditions fail to improve after the initial dose

Name Type Dose

Calfactant Bovine 105 mg/kg/dose (3 mL/kg)

Beractant Bovine 100 mg/kg/dose (4 mL/kg)

Poractant alfa Porcine 100–200 mg/kg/dose (1.25–2.5 mL/kg)

Lucinactant Synthetic 5.8 mL/kg

• Availability

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• DELIVERY TECHNIQUES– INSURE (Intubation, Surfactant, Extubation)• This technique features early surfactant replacement therapy

with prompt extubation to nasal CPAP. The technique is associated with less need for mechanical ventilation, lower incidence of BPD, and fewer air leak syndromes.

– Selective surfactant replacement therapy with mechanical ventilation followed by extubation from lower ventilator settings• This technique is initiated upon clinical evidence of RDS,

such as radiological findings, increased FIO2 requirement, and/or increased work of breathing.

– Pharyngeal instillation before first breath• There have been no randomized controlled trials in humans

to validate this technique. Animal studies have confirmed improvement of lung expansion and better survival rates.

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– Laryngeal mask airway (LMA) administration• In an animal studies on surfactant delivery, it was reported

that surfactant delivery could be accomplished sooner in the LMA group than ETT with equivalent efficacy. While far from conclusive, this method holds hope for areas in which ETT intubation skills are lacking.

– Bronchoalveolar lavage• Bronchoalveolar lavage has shown promise in the treatment of

MAS. Studies have demonstrated that surfactant lavage is a safe and effective alternative treatment for MAS.

• In animal studies, it is shown that distribution of intratracheally instilled surfactant has been largely determined by gravity, and unaffected by the position of the chest. Therefore, leaving the chest in a horizontal position may result in the most even distribution of surfactant to the lungs.

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Complication of Surfactant TherapyProcedural complications Physiologic complications

• Plugging of endotracheal tube (ETT) by

• surfactant• Hemoglobin desaturation and

increased need for supplemental O2

• Bradycardia due to hypoxia• Tachycardia due to agitation, with

reflux of surfactant into the ETT• Pharyngeal deposition of

surfactant• Administration of surfactant to

only one lung (ie, right mainstem intubation)

• Administration of suboptimal dose

• Apnea• Pulmonary hemorrhage from right

to left shunting• Increased necessity for treatment

for patent ductus arteriosus• Marginal increase in retinopathy of

prematurity• Volutrauma resulting from increase

in lung compliance failure to change ventilator settings accordingly

• Hyperventilation or hypoventilation, both of which can alter blood flow to the brain, leading to further complications

Complication can be prevented by slow administration of surfactant and by decreasing Fio2 and mean airway pressure after administration

Complication of RDS

• Intraventricular Hemorrhage• Air Leaks• Pulmonary Infection• Pulmonary Hemorrage• Hypoglycemia• DIC• Cardiac Failure• Metabolic alterations

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Transient Tachypnea of Newborn

• Also called Wet Lung Syndrome or Type II Respiratory Distress Syndrome

• The most common cause of neonatal respiratory distress constituting more than 40 percent of cases

• 11 per 1,000 live births..

• Represents a milder form of HMD or due to failure of drainage of alveolar fluids resulting in pulmonary edema decreased compliance and increased airway resistance Respiratory Distress

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Risk Factors

• Term or Near Term Babies• Male Child• Cesarean Section• Delayed cord clamping or cord milking• Macrosomia• Maternal Sedation• Large amount of IV Fluids to mother during

labor• Maternal Asthma• Maternal Diabetes Tr

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Clinical Features

• Tachypnea immediately after birth or within 6hrs after delivery with mild to moderate respiratory distress.

• These manifestations usually persist for 12-24hrs, but can last up to 72hrs

• Auscultation usually reveals good air entry with or without crackles

• Usually maintain good color and are alert.

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• X-Ray Chest– Hyperinflation of the lungs– Linear streaking at hila due to dilated lymphatics– Interlobar Fluid–Mild Cardiomegaly

• Chest x-ray usually shows evidence of clearing by 12-18 hrs with complete resolution by 48-72 hrs

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Fluid in the inter lobar fissure

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TTN is a clinical diagnosis of exclusion

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Management

• Continuous Monitoring of distress.• Supportive Management

• O2 by hood if required

• Provide adequate nutrition• ???Furosemide• ???Antibiotics

Usually a self limited condition and no active management is required

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12. Mechanical Ventilation in Neonatal Medicine zuhair aldajani

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