Respiratory Distress in Newborn

Respiratory Distress in Newborn
by Marie-Josée Laflèche, MD July 21, 2015

Objectives Understand the fetal circulation and changes that occur at birth Review lung development in utero, the pathophysiology of respiratory distress syndrome and its management Explore the most common causes of distress in the newborn and its management Review basic principles of newborn care and neonatal resuscitation and discuss the use and significance of APGAR scores 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 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 Embryonic Period (0 – 6 weeks)
Trachea and Bronchi Pseudoglandular Period (6-16 weeks) Canalicular Period ( weeks) Saccular (Terminal Sac) Period (26 weeks – birth) Alveolar Period (late fetal period to childhood) laryngotracheal diverticulum

Trachea and Bronchi Pseudoglandular Period (6-16 weeks) Canalicular Period ( weeks) Saccular (Terminal Sac) Period (26 weeks – birth) Alveolar Period (late fetal period to childhood)

Pseudoglandular Period (6-16 weeks) Conducting airways up to terminal bronchioles Canalicular Period ( weeks) Saccular (Terminal Sac) Period (26 weeks – birth) Alveolar Period (late fetal period to childhood) No respiratory bronchioles

Lung Maturation Embryonic Period (0 – 6 weeks)
Pseudoglandular Period (6-16 weeks) Canalicular Period ( weeks) Respiratory bronchioles, alveolar duct and primitive alveoli Saccular (Terminal Sac) Period (26 – 36 weeks) Engarled airway surface, thinner alveolar walls Alveolar Period (late fetal period to childhood) 3. Changes to respiratory portion of respiratory tree. Lumen of bronchi and bronchioles become large relative to tissue ans tiisues become thinner. Dev of resp bronchioles and alveolar ducts. Formation of resp epithelium. Tissue becomes more vascular. Capillaries become closer to epithelium (type I alveolar). No possibility of gas exchanges yet 4. That process continues but at an increased rate (thinning of epithelium and increase proximity of newly forned capillary beds to resp epithelium. Type I alveolar cells are formed. Cappilaries bulge into alveoli – formation of capillary-epithelial boundary. GAS EXCHANGE CAN OCCUR AT THIS POINT – so possibility that the fœtus can survive if born prematurily

Lung Maturation Pseudoglandular Period (6-16 weeks)
Canalicular Period ( weeks) Saccular (Terminal Sac) Period (26 weeks – birth) 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 4. Squamous epithelium forms. During this period respiratory bronchioles end as terminal sacs. Terminal sacs become alveolar ducts. Alveoli form after birth. From 3rd to 8th year alveoli continue to develop 5. By 20 weeks, Type II alveolar cells begin producing surfactant which permits expansion of terminal sacs.Fœtus needs to weight 1000 grams and be between weeks before enough surfactant is produced to survive. So enough Surfactant and capillaries are necessary to survive. However, some fetus born before that with artificial surfactant have survived. SURFACTANT = Mixture of lipids and proteins produced by type II pneumocytes in the lung. Surfactant creates a thin layer within the alveoli that decreases surface tension, preventing collapse of alveoli. This increases the amount of available surface area for gas exchange.

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?
Umbilical vein and arteries Ductus Venosus Foramen Oval Ductus Arteriosus = khan academy Umbilical vein bring O2 blood to liver. 1) either enters the liver or 2) ductus venosus alors blood from umbilical vein to inferior vena cava R heart ----pulmonary arteries ( resistance in arterioles because of hypoxic pulmonary vasoconstriction because no O2 in alveoli) If  resistance =  pressure in pulmonary arteries---  pressure in R side of heart. (more than L heart) ---- blood flow across foramen ovale. Not much blood coming in from pulmonary veins. --- L ventricule --- aorta --- ductus arteriosus (from pulmonary arteries to aorta) ---- internal iliac arteries --- umbilical arteries (very low resistance in placenta

Changes right after birth
Placenta is removed Low to high resistance in umbilical veins and arteries Less flow in umbilical vein and ductus venosus 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  Wharton’s Jelly (contracts when temperature falls – squeeze on vessels inside) Placenta makes prostaglandins --- levels go down = constriction

Changes after birth Umbilical Vein (days) Ductus Venosus (days)
Ligamentum teres (round lig of liver) Ductus Venosus (days) Ligamentum venosus Closure of Foramen Ovale (minutes) Fossa ovale Ductus Arteriosus (constriction begins in first few hours of life) Ligamentum arteriosum Umbilical Arteries (constriction begins in first few hours of life Medial umbilical ligament  Umblical arteries close down and form a remnant that is called the medial umbilical ligament. Umbilical vein closes down and forms the ligamentum teres or round ligament of liver. Ductus venosus closes to form ligamentum venosus. The foramen ovale aslo closes to form the fossa ovale. The ductus arteriosus closes to form the ligamentum arteriosum.

Clinical presentation of respiratory Distress in the newborn?
Tachypnea Nasal flaring Chest wall retractions Grunting Cyanosis Apnea Lethargy Stridor Grunting (heard on expiration is working to keep alveoli open to increase oxygenation and or ventilation) Baby attempts to maintain alveolar volume by prolonging and increasing expiratory pressuresby breathing against partially closed glottis Nasal flaring = attempt to decrease airway resistance Suprasternal retractions / Tracheal tug = Upper Airway Obstruction Subcostal retractions = less specific sign Tachypnea without effort – Cardiac problem Tachypnea, apnea, lethargy and minimal retractions – Metabolic Acidosis of Sepsis

Video &list=PL7EA9354BC2DD8B67 mWpxVuU

Causes of respiratory distress
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 Truncus arteriosus Transposition of the great arteries * Tricuspid atresia Tetrology of Fallot Total anomalous pulmonary venous return (*) = ductal dependent lesions = require the ductus arteriosus for adequate pulmonary circulation. And coarctation of aorta, severe aotic stenosis Tetralogy of Fallot : R ventricular outlfow tract obstruction (pulmonary stenosis) Overriding aorta Ventricular septal defect R ventricular hypertrophy R to L shunt

Other Hypothermia Hypoglycemia Anemia, polycythemia/hyperviscosity syndrome Perinatal depression (asphyxiation / metabolic acidosis) Central apnea

History – what we need to know
Maternal Factors Newborn Factors Age and social situation Medical history (GDM) Medications Smoking/Alcohol/Drugs GBS status / infections Antenatal care Family History 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 Fam history (lung disordesr, congenital heart disease, early childhood deaths, consanguinity)

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 Tachypnea = more 60/min, Tachycardia (more 160min), decrease O2, Temp instability

Labs and Investigations
Blood work Investigations CBC with differential ABG Blood and CSF cultures if sepsis is suspected Blood glucose 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 Clear amniotic fluid. Half an hour later the baby’s breathing is laboured but no apparent cyanosis.

Case 2 - John Vital Signs Physical Examination HR 135/min RR 70/min
Rectal temp 36.5 C BP 66/42 mmHg (right arm) Rapid respiration, grunting and nasal flaring Rest of exam normal

Case 2 - John Chest X-Ray

Most probable condition?
Meconium Aspiration Syndrome (MAS) Respiratory Distress Syndrome (RDS) Transient Tachypnea of the Newborn (TTN) Persistent pulmonary hypertension of newborn (PPHN) Pneumonia / Sepsis 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 Most common cause of pulmonary hypertension.

Risk factors: C-section delivery Absence or interrupted labour Male infant Macrosomia Maternal diabetes

Most common presentation: Tachypnea bpm 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 No lab work Gaz, cbc radio (cœur généreux)

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 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 Physical Examination HR 135/min RR 70/min
Rectal temp 36.5 C BP 66/42 mmHg (right arm) Grunting, sub- and intercoastal retractions, nasal flaring, cyanosis. Diminished breath sounds PE otherwise normal.

Case 3 - James Chest X-Ray

Respiratory Distress Syndrome
Most common cause in preterm infants. Mostly affects infants born before 28 weeks but also 1/3 infants born at 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 Less surfactant (quantity AND quality)

Respiratory Distress Syndrome (RDS)
Risk factors: Prematurity Multifetal pregnancies Maternal diabetes Causes delayed pulmonary maturity Prenatal asphyxia DM = delayed pulmonary maturity despite macrosomia

Chest radiograph findings: 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 Decerase lung volumes also possible ABG, CBC + differential, electrolytes (K, Ca) glucose GROUND GLASS APPEARANCE

Treatment: Antenatal administration of corticosteroids in all pregnant women 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 Post natal corticosteroid administration for RDS decrease mortiality risk but it may increase the risk of cerebral palsy

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 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 Physical Examination HR 135/min RR 70/min
Rectal temp 36.5 C BP 66/42 mmHg (right arm) 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

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 Meconium is composed of desquamated cells, secretions, lanugo, water, bile pigments, pancreatic enzymes and amniotic fluid It is sterile although when aspirated is locally irritative, osbtructive and a medium for bacterial culture

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 Passage of meconium in amniotic fluid may respresent fetal hypoxemia Hypoxia = umbilical cord compression, placental insufficiency, infection

Chest radiograph findings: Patchy infiltrates or consolidation Hyperinflation Pleural Effusion Labs: ABG: acidosis, hypercapnia, hypoxemia (more than infants with TTN) Cultures of blood and tracheal aspirate Hyperinflation (secondary to small airway obstruction). Partial blockage leads to air trapping on expiration resulting in hyperexpansion of the lungs and possibly pulmonary air leak (pneumomediastinum or pneumothorax, PPHN is continuing hypoxia CXR can be confused with TTN or bacterial pneumonia

Treatment: Suction after delivery* Supportive Oxygen, Mechanical ventialtion Intubation if needed IV Antibiotics ? Ampiciliin and genta (broad spectrum) while awaiting the results of blood cultures because of the risk of infection and the difficulty of distinguishing between MAS and bacterial pneumonia

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) Severe cyanosis or desaturation unresponsive to supplemental O2. In infants with a R to L shunt via a patent ductus arteriosus, oxygenation is higher in the R brachial artery than in the descending aorta; thus cyanosis may be differential (O2 sat in lower extremities is more 5% lower thant the right upper extremity. TX: inhaled nitric oxide relaxes endothelial smooth muscle, dilating pulmonary arterioles, which increases pulmonary blood flow and repidly improves oxygenation.

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 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 “Accurate gestational age is critical because the variation of 1 week in the determined age of an extremely premature infant (25 weeks instead of 24 weeks, for example) produces a far different set of prognostic implications.

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 Keep in mind that a slightly low Apgar score (especially at 1 minute) is common for some newborns, especially those born after a high-risk pregnancy, cesarean section, or a complicated labor anddelivery. Lower Apgar scores are also seen in premature babies, who usually have less muscle tone than full-term newborns and who, in many cases, will need extra monitoring and breathing help because of their immature lungs. APGAR 0-3 at 5min may correlate with neonatal mortality but alone does not predictt later neurology dysfuntion The Apgar score is affected by gestational age, maternal medications, resuscitation, and cardiorespiratory and neurologic conditions. A number of factors may influence an Apgar score, including but not limited to drugs, trauma, congenital anomalies, infections, hypoxia, hypovolemia, and preterm birth (7)

Neonatal resuscitation
The 2010 AHA/AAP/ILCOR guidelines include a rapid assessment of the neonate’s clinical status base on the following questions: Is the infant full-term? Is the infant breathing or crying? 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 Warm and dry the infant and remove any wet linens immediately = infants have a large surface area relative to their body weight and can thus experience significant hypothermia from evaporation Stimulate the infant to elicit a vigorous cry (helps clear the lungs and mobilize secretions) Suction amniotic luid from the infant’s nose and mouth (clear the upper airway) Initiate further resuscitation if required (blow-by oxygen, positive pressure (bag-valve mask) ventilation with oxygen, chest compressions, medications CLEARING AIRWAY: There is evidence that suctioning of the nasopharynx can create bradycardia during resuscitation in the absence of obvious nasal or oral secretions, however, there is also evidence that suctionning in the presence of secretions can decrease respiratory resistance. Therefore it is recommended that suctioning immediately following birth should be reserved for babies who have obvious obstruction to spontaneous breathing or who require positive-pressure ventilation (PPV) IF MECONIUM: endotracheal suctioning of nonvigorous babies with meconium-stained amniotic fluid. Not stimulating baby decreases the risk of Meconium aspiration syndrome (MAS)???? Meconium aspiration in a newborn can lead to atelectasis, overdistention of the alveoli, pneumothorax, pneumonitis, surfactant deficiency, and persistent pulmonary hypertension

Airway / Stabilization (clear airway, provide warmth, dry, stimulate) Breathing (Ventilation)

Supplemental Oxygen: initiated with blended oxygen or room air if not available. O2 concentration should be adjusted to achieve targeted SpO2 levels, which are monitored by pulse oxymetry. If HR below 60bpm after 90 sec of resuscitation, oxygen concentration should be increased to 100% until recovery of normal heart rate. Positive pressure ventilation: if infant gasping or apneic. If HR less 100bpm. = administered to infant by bag-mask ventilation (BMV) HR should respond quickly, O2 sat should increase (this should improve in 5 – 10 breaths)

Ventilation corrective steps (MR SOPA) Mask readjustment (good seal) Repositioning of airway (sniffing position) Suction mouth before nose Open mouth slightly (ventilate with mouth open) Pressure increase Alternative airway (ETT) MRSOPA = ventilation corrective steps *** Mask, respositioning, suction, open mask, pressure increase, alternative airway Nose suction may induce gasp, drawing meconium from mouth into lungs

Airway / Stabilization (clear airway, provide warmth, dry, stimulate) Breathing (Ventilation) Chest compressions Drugs - Administration of epinephrine and/or volume expansion

HR BELOW 60 = CHEST COMPRESSION, increase O2 sat to 100%
HR BELOW 60 = CHEST COMPRESSION, increase O2 sat to 100%. Reassess every 45sec during chest compression 90 per min "one and two and three and breathe and..." 2 thumbs best method bottom 1/3 of sternum depth: 1/3 of chest Don't release contact Down slightly faster than up From foot or from head

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
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 utero
Maternal 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 = khan academy

Respiratory Distress in Newborn

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