PAL – Distressed Newborn

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Presentation transcript:

PAL – Distressed Newborn Brittany Greene

Case Stem A female infant is born in a community hospital by assisted breech delivery at 34 weeks to a 16 year old single primigravida. There had been no antenatal care. Her birth weight is 1.8 kg, and Apgar scores 51 95. 30 mins later, the baby’s breathing is laboured and there is apparent cyanosis.

Objectives Review the basic principles of newborn care and neonatal resuscitation and discuss use and significance of Apgar scores Understand the fetal circulation and the 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 Describe 3 commonly measured growth parameters and understand the concepts of low birth weight, prematurity, psychosocial issues, and their implications/significance

Fetal Circulation Ductus arteriosus Foramen ovale Ductus venosus

Changes at Birth Alveolar fluid clearance Lung expansion Circulatory changes Increased O2 tension at birth enhances epithelial resorption of sodium and fluids Initial breaths generate high transpulmonary pressure which drives fluid from air spaces to interstitium Thoracic squeeze during delivery Increasing inspiratory pressure expands alveolar air spaces and establishes FRC + stimulates surfactant release Clamping of cord removes the low resistance placenta causing a rise in neonatal systemic BP, and lung expansion reduces pulmonary vascular resistance and pulmonary artery pressure Decreased right-to-left shunt at DA and increased left-to-right shunt Increased lung perfusion  increased O2 saturation  closure of DA LA pressure rises and RA pressure falls, until LA pressure exceeds RA  FO closes

Lung Development in Utero Early Embryonic Phase(3-7 weeks) Pseudoglandular Phase (5-17 weeks) Canalicular Phase (16-26 weeks) Saccular Phase (24-36 weeks) Alveolar Phase (36 weeks to 8 years) 1. Lung buds form 2. Bronchial tree and acinar tubes develop, few terminal buds 3. Completion of branching, terminal airways developing into alveoli, differentiation of Type I and II pneumocytes. May be possible to have limited gas exchange towards end of stage 4. Development of true alveoli, production of surfactant 5. True alveolar ducts and alveoli form

Surfactant LaPlace’s Law: P = 2T/R T is surface tension P is pressure necessary to keep the sphere open T is surface tension R is radius of the sphere With surfactant reducing the surface tension, even at low volumes, less pressure is needed to maintain open alveoli  maintains alveolar volume and stability Pressure is proportional to surface tension and inversely proportional to radius Lipoprotein complex Hydrophilic groups at the air-water interface of alveoli Hydrophobic tails (DPPC) face the air, reducing surface tension

APGAR Score Quick evaluation of newborn at 1 and 5 mins 10 point score with > 7 being normal, 4-6 requiring assistance, and < 4 requiring resuscitation Apgar Sign 2 1 Appearance (skin colour) Normal colour all over (hands & feet pink) Normal colour but hands & feet are bluish Bluish-gray or pale Pulse (HR) Normal (>100 bpm) < 100 bpm Absent pulse Grimace (“reflex irritability”) Pulls away, sneezes, coughs, or cries with stimulation Facial movement only (grimaces with stimulation) Absent (no response to stimulation) Activity (muscle tone) Active, spontaneous movement Arms and legs flexed with little movement No movement, floppy tone Respiration (RR and effort) Normal rate and effort, good cry Slow or irregular breathing, weak cry Absent (no breathing)

Basic Principles of Newborn Care Rapid assessment: if “yes” to all 3 questions  dry the baby, place skin-to-skin with mother, covered with dry linen to maintain T Term gestation? Crying or breathing? Good muscle tone? If “no” to any  baby should receive one or more of the 4 categories of action (in sequence) Initial stabilization – provide warmth, clear airway if necessary, dry, stimulate Ventilation Chest compressions Administration of epi and/or volume expansion

Newborn Resuscitation Algorithm

Case 1 Male newborn baby weighing 2.62 kg born to 35 yo mother by c-section at 35+4 weeks GA because of oligohydramnios. APGAR scores at 51 and 95. The baby develops tachypnea soon after birth.

Transient Tachypnea of the Newborn Presentation Tachypnea within 2 hrs of birth, other signs of respiratory distress. Often no hypoxia or cyanosis Pathophys Residual pulmonary fluid in lung after delivery Risk Factors Maternal asthma, male, macrosomia, maternal DM, c-section CXR Findings “Wet silhouette” around heart, intralobar fluid accumulation, diffuse paranchymal infiltrates Management Self-limited, symptoms last up to 2 days, provide supp O2 via hood or nasal cannula to maintain SpO2 > 90%, tube feeding, IV fluids if needed Prognosis Excellent If doesn’t improve after 4-6 hrs or initial CBC abnormal, obtain blood culture, begin antibiotics (amp + gent)

Case 2 A baby is born by spontaneous vaginal delivery at 30 weeks to a 25 yo primigravida. Her birth weight is 2.05 kg, and Apgar score is 81. RR 40 and poor air entry bilaterally, no adv. sounds. Within a few mins, she becomes cyanosed and cry is feeble. With suction and supp O2, RR becomes irregular and grunting is heard.

Respiratory Distress Syndrome (Hyaline Membrane Disease) Presentation Immediately after birth, tachypnea, grunting, retractions, hypoxia, cyanosis Pathophys Immature type II alveolar cells  less surfactant, increased alveolar surface tension, decreased compliance  pulmonary vascular constriction, hypoperfusion, lung tissue ischemia  formation of hyaline membranes  bronchopulmonary dysplasia Risk Factors Prematurity (1/3 of infants born at 28-34 wks), male, maternal DM CXR Findings Homogenous opaque infiltrates, diffuse atelectasis, air bronchograms Management Prevention – give antenatal corticosteroids to pregnant women at <34 wks if high risk of preterm delivery within 7 days. Nasal CPAP. If respiratory failure, intubate. Indicated if persistent resp. acidosis on CPAP, hypoxemia on CPAP, severe apnea. Surfactant therapy via ETT– exogenous surfactant replacement most effective if given within first 30-60 mins of life. Supportive care – prophylactic abx, maintain temperature, tube feeds Prognosis Acute complications – alveolar rupture, infection, IVH, PDA, pulmonary hemorrhage, NEC, GI perforation, apnea of prematurity Chronic – BPD, retinopathy of prematurity, neurologic impairment Hyaline membranes = combination of sloughed epithelium, protein, edema ACS enhances maturational changes in fetal lung architecture and biochem, with increased synthesis and release of surfactant. Mechanical ventilation is a risk factor for BPD – try to avoid it with CPAP. Bronchopulmonary dysplasia – chronic lung disease, requiring O2 at corrected GA of 36 weeks. it’s directly related to high volume/pressure from mechanical ventilation. Highest risk at youngest GAs.

Case 3 A female baby is delivered at 42+6 wks GA by emergency c-section because of fetal distress and thick MSAF. Birth weight is 3 kg. Apgar is 3 at 1 min. The baby is grunting with moderate retractions.

Meconium Aspiration Syndrome Presentation Respiratory distress immediately after delivery, with hypoxia. Baby born through meconium stained amniotic fluid, or evidence of meconium staining on exam. Pathophys Fetal passage of meconium in utero  aspiration of mec  irritation, obstruction, medium for bacterial culture Risk Factors Post-term neonates, small for GA, fetal hypoxia CXR Findings Patchy atelectasis or consolidation, hyperinflation Management if MSAF – use minimal stimulation and keep baby head down to prevent breathing in meconioum No evidence for routine amnioinfusion or suctioning (if HR>100, spont. respitation, reasonable tone). Supportive care, supp. O2. Prophylactic abx until cultures neg. Prognosis Pulmonary sequelae – reactive airway disease common Neurodevelopmental impairment – possibly due to underlying intrauterine hypoxia and chronic infection Mec composed of desquamated cells, secretions, lanugo, water, bile pigments, pancreatic enzymes, amniotic fluid Normal – passage of mec occurs early in first trimester, then slows after 16 wks and becomes infrequent by 20 wks, as anal sphincter is innervated. Passage may be caused by increased peristalsis and relaxation of anal sphincter due to increased vagal outflow with cord compression or increased sympathetic inflow during hypoxia.

Less Common Causes Infection Pneumothorax Presents as respiratory distress, temperature instability hours to days after birth RFs: prolonged rupture of membranes, prematurity, maternal fever Bilateral infiltrates on CXR ± pleural effusions, serial blood cultures Pneumothorax Can occur spontaneously, or secondary to infection, MAS, lung deformity Persistent pulmonary hypertension of the newborn Pulmonary vascular resistance fails to decrease after birth Can occur spontaneously, or secondary to MAS, infection, TTN

Differential Diagnosis of Respiratory Distress in the Newborn Most common (in order of incidence) Transient tachypnea of the newborn (TTN) Respiratory distress syndrome (RDS), aka hyaline membrane disease Meconium aspiration syndrome Less common, but significant Delayed transition Infection (pneumonia, sepsis) Persistent pulmonary hypertension of the newborn (PPHN) Pneumothorax Non-pulmonary causes, e.g. anemia, congenital heart disease, congenital malformation, medications, neurologic or metabolic abnormalities, polycythemia, upper airway obstruction

Additional Information

Growth Parameters Growth is a reflection of overall health and nutritional status Pattern of growth, not just absolute number Height Weight Normal birth weight is 2.5 – 4.5 kg (5.5 to 10 lbs) Head circumference

Prematurity Definitions: any birth occurring before 27 weeks GA Late preterm = GA 34-37 weeks Very preterm = GA < 32 weeks Extremely preterm = GA < 28 weeks Associated with 1/3 of all infant deaths, 50% mortality rate if born at or before 25 weeks Short term complications – respiratory distress, retinopathy, PDA, bronchopulmonary dysplasia, late-onset sepsis, necrotizing enterocolitis, IVH Long term complications – neurodevelopmental disabilities, e.g. CP, respiratory disorders, gastrointestinal problems, vision and hearing impairment

Low Birth Weight Premature infants can be classified by birth weight Low BW if < 2500 g Very Low BW if < 1500 g Extremely BW if < 1000 g Assess birth weight by percentile for GA Both low birth weight premature infants and small for gestation age (at term) infants have increased mortality and morbidity