respiratory distress in newborn by marie-josée laflèche, md2016 - july 21, 2015

Respiratory Distress in Newborn

by Marie-Josée Laflèche, MD2016 - July 21, 2015

Objectives

1. Understand the fetal circulation and changes that occur at birth

2. Review lung development in utero, the pathophysiology of respiratory distress syndrome and its management

3. Explore the most common causes of distress in the newborn and its management

4. Review basic principles of newborn care and neonatal resuscitation and discuss the use and significance of APGAR scores

5. Describe the 3 commonly measured growth parameters and understand the concepts of low birth weight, prematurity, psychosocial issues and their implications/significance.

Case 1 - Jane

A female infant is born to a community hospital by spontaneous vaginal delivery at 34 weeks to a sixteen-year-old single primigravida. She does not remember when her membranes ruptured. There had been no antenatal care. Her birth weight is 1.8kg, APGAR 51 95. No alcohol, no drugs, occasional smoking (1-2 cig/week)

Half an hour later the baby’s breathing is laboured, baby is grunting and there is apparent cyanosis.

Vital Signs: HR 140, RR 90, T 100.3F.

Lung Development

1. Embryonic Period (0 – 6 weeks)

• Trachea and Bronchi

2. Pseudoglandular Period (6-16 weeks)

3. Canalicular Period (16-26 weeks)

4. Saccular (Terminal Sac) Period (26 weeks – birth)

5. Alveolar Period (late fetal period to childhood)

Lung Development

1. Embryonic Period (0 – 6 weeks)


• Conducting airways up to terminal bronchioles




Lung Maturation1. Embryonic Period (0 – 6

weeks)



• Respiratory bronchioles, alveolar duct and primitive alveoli

4. Saccular (Terminal Sac) Period (26 – 36 weeks)

• Engarled airway surface, thinner alveolar walls


Lung Maturation1. Pseudoglandular Period (6-16

weeks)



4. Alveolar Period (36 weeks to childhood)

• Mature alveoli

Surfactant production

• Type II alveolar cells begin production by 20 weeks

• Prevents collapse of terminal sacs

• 26-28 weeks and weight 1kg to have enough surfactant to survive

Lung at Birth• At birth lungs are filled with

fluid

• Fluid is cleared through:

• Mouth and nose

• Pulmonary Capillaries

• Lymphatics

• Lungs fill with air

Adaptations of fetal circulation?

1. Umbilical vein and arteries

2. Ductus Venosus

3. Foramen Oval

4. Ductus Arteriosus

Changes right after birth

1. Placenta is removed

• Low to high resistance in umbilical veins and arteries

• Less flow in umbilical vein and ductus venosus

2. Lungs take air in

• O2 -- Dilatation of arteriole – decrease resistance in pulmonary arteries

• pressure in R side of heart + blood flow in L atrium = closing of Foramen ovale

• prostaglandin levels + O2 = constriction of ductus arteriosus

Changes after birth

1. Umbilical Vein (days)

• Ligamentum teres (round lig of liver)

2. Ductus Venosus (days)

• Ligamentum venosus

3. Closure of Foramen Ovale (minutes)

• Fossa ovale

4. Ductus Arteriosus (constriction begins in first few hours of life)

• Ligamentum arteriosum

5. Umbilical Arteries (constriction begins in first few hours of life

• Medial umbilical ligament

Clinical presentation of respiratory Distress in the newborn?• Tachypnea

• Nasal flaring

• Chest wall retractions

• Grunting

• Cyanosis

• Apnea

• Lethargy

• Stridor

Video

https://www.youtube.com/watch?v=NBA9iigiDgk&list=PL7EA9354BC2DD8B67

https://www.youtube.com/watch?v=t7T-mWpxVuU






Causes of respiratory distress

Respiratory

• Transient Tachypnea of the Newborn (TTN)

• Respiratory Distress syndrome (RDS)

• Meconium Aspiration Syndrome (MAS)

• Persistent pulmonary hypertension of newborn (PPHN)

• Pneumonia / Sepsis

• Pneumothorax


Cardiac - Cyanotic congenital heart defects

1. Truncus arteriosus

2. Transposition of the great arteries *

3. Tricuspid atresia

4. Tetrology of Fallot

5. Total anomalous pulmonary venous return


Other

• Hypothermia

• Hypoglycemia

• Anemia, polycythemia/hyperviscosity syndrome

• Perinatal depression (asphyxiation / metabolic acidosis)

• Central apnea

History – what we need to know

Maternal Factors

Age and social situation

Medical history (GDM)

Medications

Smoking/Alcohol/Drugs

GBS status / infections

Antenatal care

Family History

Newborn Factors

Gestational age of infant

Type of delivery (C/S), time of ROM (more 18 hours), maternal fever, complications

Birth weight

Meconium in amniotic fluid

Clinical presentation

APGAR scores, need for resuscitation

Physical Examination– what we need to know

Vitals signs

Inspection :

Work of breathing, cyanosis, pallor, scaphoid abdomen, meconium staining, asymmetric chest wall mvt, tone

Palpation:

Tracheal deviation, displaced apical beat, thrill may be palpable in precodium

Auscultation

Air entry, bronchial/vesicular air sounds, adventitious sounds, bowel sounds

Heart sounds, murmurs

Transillumination of chest wall for pneumothorax

Any deformities

Labs and Investigations

Blood work

• CBC with differential

• ABG

• Blood and CSF cultures if sepsis is suspected

• Blood glucose

Investigations

• Chest radiograph

• Echocardiogram

• Pulse oximetry

• Oxygen challenge test

Case 2 - John

A male infant is born to a community hospital by planned C-section for breech positioning at 39 weeks to a 26-year-old single primigravida with no significant medical history. His birth weight is 3.8kg, APGAR 51 95. Clear amniotic fluid.

Half an hour later the baby’s breathing is laboured but no apparent cyanosis.

Case 2 - John

Vital Signs

HR 135/min

RR 70/min

Rectal temp 36.5 C

BP 66/42 mmHg (right arm)

Physical Examination

Rapid respiration, grunting and nasal flaring

Rest of exam normal

Case 2 - John

Chest X-Ray

Most probable condition?

1. Meconium Aspiration Syndrome (MAS)

2. Respiratory Distress Syndrome (RDS)

3. Transient Tachypnea of the Newborn (TTN)

4. Persistent pulmonary hypertension of newborn (PPHN)

5. Pneumonia / Sepsis

6. Hypoglycemia

Transient Tachypnea of the Newborn (TTN)

Most common cause in term babies

Caused by ineffective clearance of amniotic fluid from lungs with delivery (persistent postnatal pulmonary edema)

More commonly seen with C/S delivery as no mechanical force of labour to help expel fluid from lungs

Usually symptomatic within 2 hours of delivery and resolves within 72 hrs


Risk factors:

C-section delivery

Absence or interrupted labour

Male infant

Macrosomia

Maternal diabetes


Most common presentation:

Tachypnea 60-150bpm

Nasal flaring

Grunting

Retracting

**Almost immediately after birth


Chest radiograph findings:

Perihilar streaking (engorgement of lymphatic system with retained fluid) – vascular redistribution

Fluid in fissure

Interstitial edema

« Wet silhouette » around heart

Transient Tachypnea of the Newborn (TTN)Treatment

Supportive

Responds well to O2

CPAP if distress worsens

IV fluids or gavage feedings if cannot tolerate oral feeding

Evolution

Usually recovers in first 72hrs

Case 3 - James

A male infant is born to a community hospital by spontaneous vaginal delivery at 28 weeks to a 24-year-old single primigravida with gestational diabetes. His birth weight is 1.8kg, APGAR 51 85. Clear amniotic fluid.

Half an hour later the baby’s breathing is laboured, he is lethargic and there is apparent cyanosis.

Case 3 - James

Vital Signs

HR 135/min

RR 70/min

Rectal temp 36.5 C



Grunting, sub- and intercoastal retractions, nasal flaring, cyanosis.

Diminished breath sounds

PE otherwise normal.

Case 3 - James

Chest X-Ray







6. Hypoglycemia

Respiratory Distress Syndrome

Most common cause in preterm infants. Mostly affects infants born before 28 weeks but also 1/3 infants born at 28-34 weeks and 5% after 34 weeks.

Less surfactant is produced by type II alveolar cells in immature lungs causing increase in alveolar surface tension and decrease compliance = atelectasis, pulmonary vascular constriction, hypoperfusion and lung tissue ischemia.

Usually immediately after birth or in first few hours

Respiratory Distress Syndrome (RDS)

Risk factors:

Prematurity

Multifetal pregnancies

Maternal diabetes

Causes delayed pulmonary maturity

Prenatal asphyxia



Homogenous opaque infiltrates / ground glass

Air bronchograms

Loss of heart borders / atelectasis

Decrease air volumes

Labs:

ABG: hypoxia, hypercarbia, acidosis

Blood, CSF and tracheal aspirate cultures


Treatment:

Antenatal administration of corticosteroids in all pregnant women 23-34 weeks who are at increased risk of preterm delivery within the next 7d to prevent or decrease severity of RDS

Promotes lung maturity by increasing synthesis and release of surfactant.

Oxygen

Mechanical ventilation / CPAP

Surfactant replacement

Reduces mortality and morbidity in preterm infants born less 30 weeks GA

Case 4 - Jamie

A female infant is born to a community hospital by spontaneous vaginal delivery at 41+1 weeks to a healthy 24-year-old single primigravida. Her birth weight is 3.2kg, APGAR 51 95. Meconium was present in amniotic fluid.

Half an hour later the baby’s breathing is laboured, she is lethargic and there is apparent cyanosis.

Case 4 - Jamie

Vital Signs

HR 135/min

RR 70/min

Rectal temp 36.5 C



Tachypnea, grunting, intercoastal retractions, nasal flaring, cyanotic

Diminished breath sounds, rales, rhonchi

Meconium stains of skin and nail beds

PE otherwise normal.

Case 4 - Jamie

Chest X-Ray







6. Hypoglycemia

Meconium Aspiration Syndrome (MAS)

10-15% of infants are meconium stained – of these, 5% develop MAS

Aspiration can occur before, during or after delivery

Meconium causes airway obstruction, chemical pneumonitis and surfactant inactivation


Symptoms similar to TTN but presentation suggest more severe condition

Risk factors:

Term or post-term

Fetal distress in utero / Hypoxia

Maternal diabetes / hypertension

Pre-eclampsia



Patchy infiltrates or consolidation

Hyperinflation

Pleural Effusion

Labs:

ABG: acidosis, hypercapnia, hypoxemia (more than infants with TTN)

Cultures of blood and tracheal aspirate


Treatment:

Suction after delivery*

Supportive

Oxygen, Mechanical ventialtion

Intubation if needed

IV Antibiotics ?

Persistent Pulmonary Hypertension

of the Newborn (PPHN)Caused by the abnormal persistence of elevated PVR (failure of relaxation of pulmonary vasculature) that leads to R to L shunting of deoxygenated blood through the foramen ovale and the ductus arteriosus, resulting in systemic hypoxemia

Most common causes involves perinatal asphyxia or hypoxia

Presentation:

Usually occurs in term infants in first 24hrs

Tachypnea, retractions, grunting and cyanosis. Difference in pre- and postductal saturation is a common finding

Can be accompanied by a systolic murmur of tricupsid insufficiency.

Can contribute to significant morbidity and mortality in both term and preterm infants (death, neurologic injuries)

Persistent Pulmonary Hypertension

of the Newborn (PPHN)Associated with PPHN:

Meconium Aspiration Syndrome

Respiratory Distress Syndrome (term and preterm)

Congenital diaphragmatic hernia

Pneumonia/Sepsis

Transient Tachypnea of the newborn

Abnormalities of lung development

Structural cardiac disease

Diagnosis: echocardiogram, cyanosis unresponsive to O2

Treatment: supportive care (O2, mechanical ventilation, fluid therapy and ionotropic agents for circulatory support, correction of acidosis)

Case 1 - Jane

A female infant is born to a community hospital by spontaneous vaginal delivery at 34 weeks to a sixteen-year-old single primigravida. She does not remember when her membranes ruptured. There had been no antenatal care. Her birth weight is 1.8kg, APGAR 51 95. No alcohol, no drugs, occasional smoking (1-2 cig/week)

Half an hour later the baby’s breathing is laboured and there is apparent cyanosis.

Vital Signs: HR 140, RR 90, T 100.3F.

Case 1 – problem list

Preterm (under 37 weeks) – accurate dates?

Low birth weight

Adolescent mother – increased risk of STIs

Single – no support from father? Family?

PPROM – increase risk of infections

No antenatal care – unknown GBS status

Tobacco use– at risk of low birth weight

Case 1 - Jane

Infants born to adolescent mothers are at greater risk of :

Lower birth weight

Vertically acquired STIs (due to higher incidence of STIs in the adolescent population

Poorer developmental outcomes

Increased risk of fetal death

APGAR criterias?

Activity (Muscle tone)

Pulse (Heart Rate)

Grimace (Reflex irritability)

Appearance (Color)

Respiration (Crying)

Why use APGAR?

Developed in 1952 by an anesthesiologist named Virginia Apgar

Reflects fetal to neonatal transition

Used to determine quickly wether a newborn needs immediate medical care

Very subjective

Five-minute APGAR scores less 3 are predictives for neonatal and infantile death and increase risk of CP

Neonatal resuscitation

The 2010 AHA/AAP/ILCOR guidelines include a rapid assessment of the neonate’s clinical status base on the following questions:

1. Is the infant full-term?

2. Is the infant breathing or crying?

3. Does the infant have good muscle tone?

If the answer to all 3 questions is yes = no need for resuscitation. Newborn is managed by routine neonatal care


Routine care: term infants with clear amniotic fluid, adequate respiratory effort and good muscle tone

Warm and dry the infant

Stimulate the infant to elicit a vigorous cry (dry, suction,flick foot, rub back)

Clearing of airway (if needed)

Skin-to-skin with mother


Resuscitation :

A. Airway / Stabilization (clear airway, provide warmth, dry, stimulate)

B. Breathing (Ventilation)


Ventilation corrective steps (MR SOPA)

1. Mask readjustment (good seal)

2. Repositioning of airway (sniffing position)

3. Suction mouth before nose

4. Open mouth slightly (ventilate with mouth open)

5. Pressure increase

6. Alternative airway (ETT)


Resuscitation :

A. Airway / Stabilization (clear airway, provide warmth, dry, stimulate)

B. Breathing (Ventilation)

C. Chest compressions

D. Drugs - Administration of epinephrine and/or volume expansion

Case 1 - Jane

Describe the 3 commonly measured growth parameters and understand the concepts of low birth weight, prematurity, psychosocial issues and their implications/significance.

Growth Parameters and Gestational age

3 Growth Parameters:

Length, Weight and Head Circumference

Growth charts: plotted vs gestational age

CDC vs WHO

Birth to 24 months

Preterms from 22 weeks to 50 weeks GA

Term – 37 to 42 weeks gestation

Preterm – less 37 weeks

Post-term – more than 42 weeks

Consequences of prematurity

12% of all babies are born premature

Most premature infants are characterized by low birth weight (less 2500g)

May be unable to feed by mouth, breathe without apneas or thermo-regulate

Immaturity of major organs

At increased risk of: IVH, RDS, CHD, NEC, Hypoglycemia, Hypothermia, Anemia etc.


IUGR : deviation in expectal fetal growth pattern, caused by multiple adverse conditions. Less 3rd percentile for GA at birth. Not all IUGR infants are SGA. Can be symmetric or asymmetric.

SGA = less 10th percentile

AGA = between 10th – 90th percentiles

LGA = more 90th percentile

LBW = less 2.5kg, VLBW = less 1.5kg, ELBW = less 10kg

Factors limiting fetal growth in uteroMaternal Factors

• Poor weight gain in 3rd trimester

• Preeclampsia

• Prescriptions or drug use

• Maternal infections

• Uterine abnormalities

Placental Factors

• Placenta previa

• Placental abruptions

• Abnormal umbilical vessel insertions

Fetal Factors

• Fetal malformations

• Metabolic diseases

• Chromosomal abnormalities

• Congenital infections

Thank you!

Resources

Uptodate

app.med-u.org

Merck Manual

Learnpediatrics.com – respiratory distress in newborn

respiratory distress in newborn by marie-josée laflèche, md2016 - july 21, 2015

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