Is It Baby That's Born Premature and Trying to Breathe Have Chest Retractions
Pediatr Rev. 2014 Oct; 35(ten): 417–429.
Respiratory Distress in the Newborn
Suzanne Reuter
*Department of Neonatal-Perinatal Medicine, Sanford School of Medicine–Academy of South Dakota, Sanford Children'southward Specialty Clinic, Sioux Falls, SD.
Chuanpit Moser
†Department of Pediatric Pulmonology, Sanford School of Medicine–University of South Dakota, Sanford Children'southward Specialty Clinic, Sioux Falls, SD.
Michelle Baack
*Department of Neonatal-Perinatal Medicine, Sanford School of Medicine–University of Southward Dakota, Sanford Children'southward Specialty Clinic, Sioux Falls, SD.
‡Sanford Children's Health Research Center, Sioux Falls, SD.
Educational Gap
Respiratory distress is mutual, affecting upwards to 7% of all term newborns, (1) and is increasingly common in even modest prematurity. Preventive and therapeutic measures for some of the most mutual underlying causes are well studied and when implemented can reduce the burden of affliction. (ii)(3)(4)(5)(half-dozen)(vii)(8) Failure to readily recognize symptoms and treat the underlying crusade of respiratory distress in the newborn tin can lead to short- and long-term complications, including chronic lung disease, respiratory failure, and even death.
Objectives
Subsequently completing this commodity, the reader should be able to:
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Use a physiologic approach to understand and differentially diagnose the most common causes of respiratory distress in the newborn babe.
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Distinguish pulmonary illness from airway, cardiovascular, and other systemic causes of respiratory distress in the newborn.
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Appreciate the risks associated with tardily preterm (34–36 weeks' gestation) and early term (37–38 weeks' gestation) deliveries, especially by caesarean section.
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Recognize clinical symptoms and radiographic patterns that reverberate transient tachypnea of the newborn (TTN), neonatal pneumonia, respiratory distress syndrome (RDS), and meconium aspiration syndrome (MAS).
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Identify the short- and long-term complications associated with common neonatal respiratory disorders, including pneumothorax, persistent pulmonary hypertension of the newborn, and chronic lung affliction.
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Empathise management strategies for TTN, pneumonia, RDS, and MAS.
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Implement up-to-date recommendations for the prevention of neonatal pneumonia, RDS, and MAS.
Introduction
Respiratory distress is ane of the most common reasons an infant is admitted to the neonatal intensive care unit of measurement. (1) 15 pct of term infants and 29% of tardily preterm infants admitted to the neonatal intensive intendance unit of measurement develop significant respiratory morbidity; this is even higher for infants built-in before 34 weeks' gestation. (2) Sure risk factors increment the likelihood of neonatal respiratory disease. These factors include prematurity, meconium-stained amniotic fluid (MSAF), caesarian section delivery, gestational diabetes, maternal chorioamnionitis, or prenatal ultrasonographic findings, such as oligohydramnios or structural lung abnormalities. (2)(9)(x)(11)(12)(13)(xiv) However, predicting which infants will get symptomatic is not e'er possible before birth. Regardless of the cause, if not recognized and managed quickly, respiratory distress can escalate to respiratory failure and cardiopulmonary arrest. Therefore, information technology is imperative that whatsoever health intendance practitioner caring for newborn infants tin can readily recognize the signs and symptoms of respiratory distress, differentiate various causes, and initiate management strategies to prevent significant complications or decease.
Definition, Signs, Symptoms
Respiratory distress in the newborn is recognized as i or more signs of increased work of animate, such as tachypnea, nasal flaring, chest retractions, or grunting. (ane)(fifteen) Normally, the newborn's respiratory rate is 30 to 60 breaths per minute. Tachypnea is defined as a respiratory rate greater than 60 breaths per infinitesimal. (15) Tachypnea is a compensatory mechanism for hypercarbia, hypoxemia, or acidosis (both metabolic and respiratory), (16) making it a mutual merely nonspecific finding in a large variety of respiratory, cardiovascular, metabolic, or systemic diseases. Pulmonary disease may incite tachypnea, especially in neonates. The natural rubberband property of the lungs is to deflate. When balanced past the outward recoil of the chest wall, functional balance chapters (FRC) occurs at the stop of expiration to prevent alveoli from collapsing. The newborn chest wall, composed primarily of cartilage, is more than pliable, predisposing neonatal lungs to pulmonary atelectasis and decreased FRC. (16)(17)(eighteen) Pulmonary compliance refers to a given change in volume (ΔVolume) for every given change in pressure (ΔPressure), substantially the ability of the alveoli to fill with air nether a set pressure. If lung compliance is decreased, such as with transient tachypnea of the newborn (TTN), respiratory distress syndrome (RDS), pneumonia, or pulmonary edema, there is a subtract in tidal book. To accomplish sufficient minute ventilation, the respiratory rate must increase. Hypoxemia further increases tachypnea. (16)(18) Therefore, afflicted newborns present with marked tachypnea. Because tachypnea is a nonspecific symptom, boosted clinical findings assistance in narrowing the cause to a respiratory disorder.
Increased work of breathing results from mismatched pulmonary mechanics from increased airway resistance (ΔPressure/Volumetric Flow), decreased lung compliance (ΔVolume/ ΔPressure), or both. Airway resistance increases when there is obstacle of air flow. The critical importance of airway radius is indicated in the equation R = V(8lη/πr(four)), where R is resistance, V is flow, l is length, η is viscosity, and r is radius. (19) If the airway radius is halved, resistance increases 16-fold. Nasal flaring is a compensatory symptom that increases upper airway diameter and reduces resistance and piece of work of breathing. Retractions, evident by the use of accessory muscles in the neck, rib cage, sternum, or belly, occur when lung compliance is poor or airway resistance is high. Noisy breathing may point increased airway resistance, and the blazon of noise auscultated may help localize airway obstruction (Table 1). Stertor is a sonorous snoring audio heard over extrathoracic airways that indicates nasopharyngeal obstruction. Stridor is a high-pitched, monophonic breath sound that indicates obstacle at the larynx, glottis, or subglottic area. Wheezing may also be loftier pitched just is typically polyphonic, is heard on expiration, and indicates tracheobronchial obstruction. Grunting is an expiratory sound acquired by sudden closure of the glottis during expiration in an attempt to maintain FRC and prevent alveolar atelectasis. Because lung compliance is worse at very low or very high FRC, achieving and maintaining physiologic FRC is essential in the management of respiratory disorders with poor compliance, such every bit RDS or TTN. On the other stop of the spectrum, meconium aspiration syndrome (MAS) is an example of lower airway obstruction with air trapping. These newborns oftentimes have loftier lung volumes, which adversely affects their lung compliance. Regardless of the cause, it is vital to recognize symptoms and act quickly. If the newborn cannot sustain the extra piece of work of breathing to meet its respiratory needs, respiratory failure follows. This failure may manifest as impaired oxygenation (cyanosis) or ventilation (respiratory acidosis). Without prompt intervention, respiratory arrest is imminent.
Table ane.
Noisy Breathing Characteristics in Term Infants
| Type | Definition | Causes |
| Stertor | Sonorous snoring sound, mid-pitched, monophonic, may transmit throughout airways, heard loudest with stethoscope well-nigh mouth and nose | Nasopharyngeal obstruction—nasal or airway secretions, congestion, choanal stenosis, enlarged or redundant upper airway tissue or tongue |
| Stridor | Musical, monophonic, aural breath sound. Typically high-pitched. Types: Inspiratory (above the song cords), biphasic (at the glottis or subglottis), or expiratory (lower trachea) | Laryngeal obstacle—laryngomalacia, vocal string paralysis, subglottic stenosis, vascular ring, papillomatosis, strange torso |
| Wheezing | High-pitched, whistling audio, typically expiratory, polyphonic, loudest in chest | Lower airway obstruction—MAS, bronchiolitis, pneumonia |
| Grunting | Low- or mid-pitched, expiratory sound caused by sudden closure of the glottis during expiration in an endeavor to maintain FRC | Compensatory symptom for poor pulmonary compliance—TTN, RDS, pneumonia, atelectasis, congenital lung malformation or hypoplasia, pleural effusion, pneumothorax |
Pathogenesis
The causes of respiratory distress in a newborn are diverse and multisystemic. Pulmonary causes may be related to alterations during normal lung development or transition to extrauterine life. Normal lung evolution occurs in 5 phases (20) (Table two). Respiratory illness may result from developmental abnormalities that occur before or after birth. Early on developmental malformations include tracheoesophageal fistula, bronchopulmonary sequestration (abnormal mass of pulmonary tissue non connected to the tracheobronchial tree), and bronchogenic cysts (abnormal branching of the tracheobronchial tree). Afterwards in gestation, parenchymal lung malformations, including congenital cystic adenomatoid malformation or pulmonary hypoplasia from congenital diaphragmatic hernia or severe oligohydramnios, may develop. More mutual respiratory diseases, such every bit TTN, RDS, neonatal pneumonia, MAS, and persistent pulmonary hypertension of the newborn (PPHN), issue from complications during the prenatal to postnatal transition menses. Although mature alveoli are nowadays at 36 weeks' gestation, a keen deal of alveolar septation and microvascular maturation occur postnatally. The lungs are not fully developed until ages 2 to v years. (20)(21) Therefore, developmental lung disease can also occur afterwards nativity. Bronchopulmonary dysplasia (BPD), for example, is a meaning lung affliction that complicates prematurity due to arrested alveolarization in developing lungs exposed to mechanical ventilation, oxygen, and other inflammatory mediators earlier normal development is complete. Every bit defined by an ongoing oxygen requirement at 36 weeks' adjusted gestational historic period, BPD affects up to 32% of premature infants and 50% of very depression-birth-weight infants. (22)
Table 2.
Developmental Stages of Lung Development and Respiratory Disease Pathogenesis
| Developmental Stage | Embryonic | Pseudoglandular | Canalicular | Last Sac | Alveolar |
| Gestation | 0–six weeks | 7–sixteen weeks | 17–24 weeks | 25–36 weeks | >37 weeks |
| Structural morphogenesis | Trachea, bronchi | Bronchioles, terminal bronchioles, lung circulation | Respiratory bronchioles, primitive alveoli | Alveolar ducts, thin-walled alveolar sacs, increasing functional type 2 cellsa | Definitive alveoli and mature type 2 cellsa |
| Disease manifestation | Tracheoesophageal fistula, pulmonary sequestration | Bronchogenic cyst, built diaphragmatic hernia, congenital cystic adenomatoid malformation | Pulmonary hypoplasia, RDS, BPD, alveolar capillary dysplasia | RDS, BPD | TTN, MAS, neonatal pneumonia, PPHN |
Differential Diagnosis
The underlying cause of respiratory distress in a newborn varies and does non always lie within the lungs (15) (Table 3). Thus, afterward initial resuscitation and stabilization, information technology is important to utilize a detailed history, physical examination, and radiographic and laboratory findings to make up one's mind a more specific diagnosis and accordingly tailor management. A thorough history may guide in identifying gamble factors associated with common causes of neonatal respiratory distress (Table 4). A detailed physical test should focus beyond the lungs to identify nonpulmonary causes, such as airway obstruction, abnormalities of the breast wall, cardiovascular disease, or neuromuscular affliction, that may initially present as respiratory distress in a newborn. Radiographic findings can identify diaphragmatic paralysis, congenital pulmonary malformations, and intrathoracic infinite–occupying lesions, such as pneumothorax, mediastinal mass, and built diaphragmatic hernia, that tin compromise lung expansion. Pregnant tachypnea without increased work of animate should prompt additional laboratory investigation to identify metabolic acidosis or sepsis. Hypoglycemia, hypomagnesemia, and hematologic abnormalities may result in a depressed ventilatory drive or impaired oxygen ship to the peripheral tissues, and so laboratory evaluation should too be considered with these clinical findings. Hypermagnesemia may contribute to respiratory distress and affect a newborn'southward capacity to respond to resuscitation due to hypotonia and a depressed respiratory drive or even apnea.
Table 3.
Differential Diagnosis of Respiratory Distress in the Newborn
| Airway |
| Nasal obstruction, choanal atresia, micrognathia, Pierre Robin sequence, macroglossia, congenital loftier airway obstacle syndrome, including laryngeal or tracheal atresia, subglottic stenosis, laryngeal cyst or laryngeal web, vocal cord paralysis, subglottic stenosis, airway hemangiomas or papillomas, laryngomalacia, tracheobronchomalacia, tracheoesophageal fistula vascular rings, and external compression from a neck mass |
| Pulmonary |
| RDS,a TTN,a MAS,a neonatal pneumonia,a pneumothorax,a PPHN,a pleural effusion (congenital chylothorax), pulmonary hemorrhage, bronchopulmonary sequestration, bronchogenic cyst, built cystic adenomatoid malformation or congenital pulmonary airway malformation, pulmonary hypoplasia, congenital lobar emphysema, pulmonary alveolar proteinosis, alveolar capillary dysplasia, congenital pulmonary lymphangiectasis, and surfactant protein deficiency |
| Cardiovascular |
| Cyanotic and select acyanotic congenital center defects,a neonatal cardiomyopathy, pericardial effusion or cardiac tamponade, fetal arrhythmia with compromised cardiac part, and high-output cardiac failure |
| Thoracic |
| Pneumomediastinum, chest wall deformities, mass, skeletal dysplasia, and diaphragmatic hernia or paralysis |
| Neuromuscular |
| Central nervous organisation injury (birth trauma or hemorrhage),a hypoxic-ischemic encephalopathy,a cerebral malformations, chromosomal abnormalities, medication (neonatal or maternal sedation, antidepressants, or magnesium), congenital TORCH infections, meningitis, seizure disorder, obstructed hydrocephalus, arthrogryposis, congenital myotonic dystrophy, neonatal myasthenia gravis, spinal muscular atrophy, congenital myopathies, and spinal cord injury |
| Other |
| Sepsis,a hypoglycemia,a metabolic acidosis,a hypothermia or hyperthermia, hydrops fetalis, inborn mistake of metabolism, hypermagnesemia, hyponatremia or hypernatremia, severe hemolytic disease, anemia, and polycythemia |
Table 4.
Perinatal History Associated With Common Respiratory Diseases in the Newborn Infant
| Respiratory Disease | Risk Factors |
| TTN | Caesarian section, precipitous delivery, late preterm or early on term, maternal sedation or medication, fetal distress, gestational diabetes |
| Neonatal pneumonia | Maternal group B streptococcus carrier, chorioamnionitis, maternal fever, PROM, prematurity, perinatal depression |
| RDS | Prematurity, gestational diabetes, male person babe, multiple gestation |
| MAS | MSAF, postterm gestation, fetal distress or perinatal depression, African American ethnicity |
| Pulmonary hypoplasia | Oligohydramnios, renal dysplasia or agenesis, urinary outlet obstruction, premature PROM, diaphragmatic hernia, neuromuscular disorder (loss of fetal respirations/bell-shaped chest) |
Cardiovascular illness may be difficult to distinguish from pulmonary causes of respiratory distress (Tabular array 5). Most congenital heart defects present with cyanosis, tachypnea, or respiratory distress from cardiac failure. Timing may be an important clue to differentiation because very few congenital heart defects nowadays immediately afterwards birth; more than ofttimes they present several hours to days later delivery as the ductus arteriosus closes. (2) Table 5 aids in this differentiation.
Table 5.
Differentiation of Cyanotic Heart Affliction From Pulmonary Affliction Among Infants in Respiratory Distressa
| Variable | Cyanotic Heart Disease | Pulmonary Disease |
| History | Previous sibling with congenital eye affliction | Maternal fever |
| Diagnosis of congenital eye disease by prenatal ultrasonography | MSAF | |
| Preterm delivery | ||
| Physical test | Cyanosis | Cyanosis |
| Gallop rhythm or murmur | Astringent retractions | |
| Single second centre sound | Split second heart sound | |
| Big liver | Temperature instability | |
| Mild respiratory distress | ||
| Breast radiograph | Increased heart size | Normal center size |
| Decreased pulmonary vascularity (except in transposition of the great vessels or total dissonant pulmonary venous return) | Abnormal pulmonary parenchyma, such as total whiteout or patches of consolidation in pneumonia, fluid in the fissures in TTN or ground glass appearance in RDS | |
| Arterial claret gas | Normal or decreased Paco 2 | Increased Paco 2 |
| Decreased Pao 2 | Decreased Pao 2 | |
| Hyperoxia test | Pao ii <150 mm Hg | Pao 2 >150 mm Hg (except in astringent PPHN) |
| Echocardiography | Abnormal heart or vessels | Normal heart and vessels |
Pulmonary hypertension should be considered in whatever baby with respiratory distress and cyanosis. This condition results when there is a failure to transition from in utero to postnatal pulmonary circulation afterward delivery. Pulmonary vascular resistance remains high, resulting in cyanosis from dumb pulmonary blood flow and right-to-left shunting of blood across the foramen ovale and ductus arteriosus. Shunting further contributes to systemic hypoxemia and metabolic acidemia—both of which contribute to ongoing increased pulmonary vascular resistance. PPHN may be primary or secondary to respiratory disease, particularly congenital diaphragmatic hernia, MAS, or RDS. When PPHN occurs without concurrent pulmonary illness, differentiating from cyanotic heart affliction is difficult. The response to ventilation with 100% oxygen (hyperoxia exam) can help distinguish the two atmospheric condition. In some neonates with PPHN, the Pao 2 volition increase to to a higher place 100 mm Hg, whereas it volition non increase above 45 mm Hg in infants with cyanotic center defects that have circulatory mixing. (5)(23)
Common Case Scenarios
Four case scenarios are highlighted to assistance in identifying the most common causes of respiratory distress in the newborn followed by give-and-take most the pathophysiology, hazard factors, prevention, and management strategies for each disorder.
Case 1
A 3.2-kg female infant is delivered by caesarean section at 38 weeks' gestational age without a trial of labor. Her Apgar scores are 9 and nine at 1 and 5 minutes, respectively. She develops tachypnea and subcostal retractions with nasal flaring at one hour of life. Temperature is 97.9°F (36.half dozen°C), pulse is 165 beats per minute, and respiratory rate is 74 breaths per minute. Aside from increased work of breathing, her concrete examination findings are normal. The breast radiograph is shown in Figure 1. She requires supplemental oxygen via nasal cannula with a fraction of inspired oxygen (Fio 2) of 0.3 for 36 hours. She and so weans to room air. Her respiratory rate is 35 breaths per infinitesimal, and she has no increased work of breathing.
Case ane: Transient tachypnea of the newborn is characterized past streaky, pulmonary interstitial markings and fluid in the fissure apparent on chest radiograph. Case two: Neonatal pneumonia with bilateral opacities, air bronchograms, and pleural effusions is apparent. Case 3: Respiratory distress syndrome is characterized by diffuse, bilateral, ground glass fields with air bronchograms secondary to lengthened atelectasis. Case 4: Meconium aspiration syndrome causes a chemical pneumonitis, fractional airway obstruction, and a localized surfactant inactivation that leads to areas of hyperinflation mixed with lengthened, patchy infiltrates radiographically.
Transient Tachypnea of the Newborn
TTN, besides known as retained fetal lung fluid syndrome, presents with early on respiratory distress in term and late-preterm infants. TTN is a frequent cause of respiratory distress in newborns and is caused by impaired fetal lung fluid clearance. Ordinarily in utero, the fetal airspaces and air sacs are fluid filled. For effective gas commutation to occur subsequently nascency, this fluid must be cleared from the alveolar airspaces. Late in gestation and before birth, the chloride and fluid-secreting channels in the lung epithelium are reversed so that fluid absorption predominates and fluid is removed from the lungs. This procedure is enhanced by labor, so that commitment earlier labor onset increases the risk of retained fetal lung fluid. (xx) Factors that increase the clearance of lung fluid include antenatal corticosteroids, fetal thorax compression with uterine contractions, and a release of fetal adrenaline in labor, which enhances uptake of lung fluids. (24)
Infants with TTN usually present with tachypnea and increased work of breathing, which persists for 24 to 72 hours. Breast radiographs reveal excess diffuse parenchymal infiltrates due to fluid in the interstitium, fluid in the interlobar fissure, and occasionally pleural effusions (Effigy 1). Management is supportive. Infants may require supplemental oxygen, and frequently the distending forces of continuous positive airway pressure (CPAP) are necessary to assist in maintaining alveolar integrity and driving fluid into apportionment. Claret gases oftentimes reveal a mild respiratory acidosis and hypoxemia. The course of TTN is self-limited and does not usually crave mechanical ventilation.
Preventive measures may include avoiding elective caesarean section earlier the onset of labor in infants younger than 39 weeks' gestation. This is because the most common risk factors for TTN include delivery before 39 weeks' gestation, (1)(2)(three)(9)(25)(26) precipitous commitment, fetal distress, maternal sedation, and maternal diabetes. Although it is well known that premature infants have a higher gamble of respiratory problems, the consequences of early-term delivery (37–38 weeks' gestation) are underrecognized. Early-term infants have an increased take a chance of requiring respiratory support, mechanical ventilation, and neonatal service; delivery past caesarean section in this population is mutual and further increases risk. (25) In addition, a single course of antenatal glucocorticoids (2 doses of betamethasone) at least 48 hours earlier an elective term caesarean delivery decreases respiratory morbidity among infants. (27) On the basis of multiple cohort studies and expert stance, we recommend a careful consideration almost elective delivery before spontaneous onset of labor at less than 39 weeks' gestation and encourage pediatricians to exist aware of the increased risk of respiratory morbidity in belatedly preterm and early-term newborns. (1)(2)(3)(ix)(25)(26)
Case 2
A 2.9-kg male infant is born by vaginal commitment at 39 weeks' gestational age later on rupture of membranes for 22 hours. Apgar scores are 8 and 8 at 1 and 5 minutes, respectively. He requires an Fio 2 of 0.4 in the delivery room. He is tachypneic and has acrocyanosis. There are coarse rales noted bilaterally. Temperature is 98.6°F (37°C), pulse is 144 beats per minute, and respiratory rate is 65 breaths per minute. Despite being given CPAP, his grunting and tachypnea worsen, and he requires intubation and ventilation for progressive increased piece of work of breathing, respiratory acidosis, and oxygen requirement during the side by side half dozen hours. The chest radiograph is shown in Effigy 1.
Neonatal Pneumonia
Respiratory infections in the newborn may exist bacterial, viral, fungal, spirochetal, or protozoan in origin. Infants may larn pneumonia transplacentally, through infected amniotic fluid, via colonization at the fourth dimension of birth, or nosocomially. (20) Perinatal pneumonia is the most mutual form of neonatal pneumonia and is acquired at birth. Grouping B streptococcus (GBS) is the most common organism that affects term infants. (28)(29) Built pneumonia occurs when the causative organism is passed transplacentally to the fetus. The nigh common pathogens are rubella, cytomegalovirus, adenovirus, enteroviruses, mumps, Toxoplasma gondii, Treponema pallidum, Mycobacterium tuberculosis, Listeria monocytogenes, varicella zoster, and human being immunodeficiency virus. (30) Immaturity of the baby'due south immune system and the pulmonary anatomical and physiologic features make the newborn at higher take chances of infection. The underdeveloped respiratory cilia and the decreased number of pulmonary macrophages result in decreased clearance of pathogens from the respiratory system. Newborns besides have macerated cellular and humoral immune function, which is even more pronounced in the premature baby. (28)
Risk factors for perinatal pneumonia include prolonged rupture of membranes (PROM), maternal infection, and prematurity. (1) Infants present with increased piece of work of breathing and oxygen requirement. Chest radiography often reveals diffuse parenchymal infiltrates with air bronchograms or lobar consolidation. Pleural effusions may likewise be seen. In dissimilarity to older infants and children, neonatal pneumonia is role of a generalized sepsis illness; thus, obtaining blood and cerebrospinal fluid cultures and initiating broad-spectrum antibiotic therapy is recommended for whatever symptomatic baby. (31)(32)
In the newborn with early on-onset pneumonia or sepsis, a combination of penicillin and an aminoglycoside are the preferred initial treatment. (31) For infants who have been hospitalized in a neonatal intensive care unit for more than than four days, organisms such as methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis require vancomycin therapy. Infants who develop pneumonia in the plant nursery or at home are likely to have infections caused by respiratory viruses (adenovirus, respiratory syncytial virus, and flu virus), gram-positive bacteria (streptococcal species and S aureus), and gram-negative enteric leaner (Klebsiella, Proteus, Pseudomonas aeruginosa, Serratia marcescens, and Escherichia coli). (xxx) Infants with pneumonia caused by Chlamydia trachomatis present later in the newborn period (iv–12 weeks of age) with a staccato cough but no wheezing or fever. (33) Chlamydial conjunctivitis may also be present (5 to 14 days after birth). Chest radiography reveals diffuse bilateral infiltrates, and a complete claret jail cell count with a differential reveals eosinophilia. Treatment of chlamydial pneumonia or conjunctivitis (fifty-fifty without pneumonia) requires systemic macrolide antibody therapy and ophthalmologic follow-up. Regardless of the causal organism, newborns with pneumonia crave supportive care in addition to antibiotics. Many infants volition require not only supplemental oxygen but likewise CPAP and mechanical ventilation. Other supportive measures include intravenous nutrition and vasopressors for cardiovascular support. PPHN is a common complexity of neonatal pneumonia.
On the basis of strong evidence, prevention of neonatal pneumonia and its complications focuses on maternal GBS screening, intrapartum antibiotic prophylaxis, and advisable follow-up of newborns at high gamble later delivery. (iv)(31)(32)(34) Anyone caring for newborns should be able to recognize at-run a risk infants and whether appropriate intrapartum antibody prophylaxis has been administered. They must as well know which infants crave boosted screening, observation, and antibiotic initiation after nascence. Guidelines have been established by the Centers for Disease Control and Prevention and endorsed past the American Academy of Pediatrics and the American College of Obstetrics and Gynecology for best do management of at-risk infants. (iv) Infants who require boosted attention include those born to mothers who are GBS carriers (civilisation or polymerase chain reaction positive), those with a history of GBS bacteruria, those affected past GBS or with an unknown GBS status only who were delivered at less than 37 weeks' gestation, those with PROM of 18 hours or long, or those with intrapartum fever (≥100.4°F [38°C]). (iv)(31) The preferred intrapartum antibiotic for these situations is intravenous penicillin (5 million units followed past 2.5 million to 3.0 million units every 4 hours) administered at least four hours before delivery; cefazolin may be used for penicillin-allergic women who are at depression take a chance for anaphylaxis. (iv)(31) For severely penicillin-allergic women, clindamycin culture sensitivity should be performed, and if female parent'south strain is sensitive (75% of cases), clindamycin should be used. Vancomycin is reserved for severely allergic women with resistant strains. (4)(31) In addition to intrapartum antibody prophylaxis, promising GBS vaccines are in clinical trials (35) and may be widely accustomed by patients (36) but are not withal set for general use.
Since widespread implementation of maternal GBS screening and intrapartum antibiotic prophylaxis administration, the incidence of early on-onset GBS infection has decreased from 1.8 cases per ane,000 to 0.3 case per 1,000 live births. (31)(32) All the same, cases and deaths continue to occur with GBS as the leading offender. (31)(34)(35) Well-nigh of the term infants affected are born to mothers without or with an unknown GBS status but who had PROM or fever and did not receive antibiotic administration during labor. (34) Others are built-in to women who received inadequate prophylaxis (<4 hours before commitment or macrolide antibiotic employ). (31) Many missed opportunities for prevention increase the burden of disease. (29)
Thus, it is imperative to appropriately manage any newborn with the same risk factors cautiously after nascence. According to updated 2010 guidelines, any infant who develops signs or symptoms of illness requires a total diagnostic evaluation (including blood and spinal fluid cultures) and antibiotic initiation. (4)(31)(32) If maternal chorioamnionitis is suspected simply the babe has no signs or symptoms of disease, a limited evaluation (blood culture and complete blood prison cell count), along with antibiotic therapy initiation for at to the lowest degree 48 hours, is recommended. (4)(31)(32) Asymptomatic, at-hazard infants, who did not receive acceptable antibiotic prophylaxis, require a limited evaluation and observation for 48 hours, simply antibody initiation is not necessary unless clinical suspicion arises. (4)(31)(32) Asymptomatic, at-chance infants who received adequate intrapartum antibiotic prophylaxis should be observed for 48 hours. Adherence to these guidelines will decrease the incidence of neonatal pneumonia and let for early on detection and treatment that may foreclose life-threatening complications, such every bit PPHN or death.
Case 3
A 1.5-kg male is delivered via vaginal delivery considering of preterm labor at 33 weeks' gestation. Apgar scores are vii and 8 at 1 and v minutes, respectively. The infant is cyanotic and requires CPAP immediately after commitment. He has subcostal retractions, grunting, and nasal flaring. Auscultation reveals decreased air entry in the lung fields throughout. Temperature is 98.2°F (36.8°C), pulse is 175 beats per minute, and respiratory charge per unit is 70 breaths per infinitesimal. He requires an Fio 2 of 0.4. His chest radiograph is shown in Figure 1.
Respiratory Distress Syndrome
RDS, also known as hyaline membrane disease, is a mutual cause of respiratory disease in the premature infant. RDS is too seen in infants whose mothers take diabetes in pregnancy. RDS is caused by a deficiency of alveolar surfactant, which increases surface tension in alveoli, resulting in microatelectasis and depression lung volumes. Surfactant deficiency appears every bit diffuse fine granular infiltrates on radiograph (Figure 1). Pulmonary edema plays a primal function in the pathogenesis of RDS and contributes to the development of air bronchograms. Excess lung fluid is attributed to epithelial injury in the airways, decreased concentration of sodium-absorbing channels in the lung epithelium, and a relative oliguria in the first 2 days after nascency in premature infants. (37) Infants typically ameliorate on onset of diuresis past the fourth 24-hour interval afterward birth.
Infants with RDS typically present within the get-go several hours of life, often immediately subsequently delivery. Clinically, infants have marked respiratory distress with tachypnea, nasal flaring, grunting, and subcostal, intercostal, and/or suprasternal retractions. Grunting occurs when an infant attempts to maintain an acceptable FRC in the face up of poorly compliant lungs past partial glottic closure. Every bit the infant prolongs the expiratory phase against this partially airtight glottis, there is a prolonged and increased residuum volume that maintains the airway opening and also an aural expiratory sound. Infants with RDS accept cyanosis and crave supplemental oxygen. Mild cases of RDS may reply to the distending pressures of CPAP, but more severe cases require endotracheal intubation and administration of exogenous surfactant into the lungs. Currently, in that location are no universal guidelines that dictate if and when to administer exogenous surfactant. Some institutions abet administration of prophylactic surfactant in the kickoff 2 hours of life for all premature infants younger than xxx weeks' gestation. Others begin with noninvasive ventilation (CPAP) and reserve intubation and surfactant administration only for infants who crave more than than 35% to 45% oxygen concentration to maintain an arterial PaO2 greater than fifty mm Hg. In determining a management strategy, it is important to consider the administration of antenatal corticosteroids, the clinical presentation, radiographic findings, and the infant's oxygen requirements. (38)
The class of RDS is self-limited and typically improves by age 3 to 4 days in correlation with the same diuresis phase and equally the infant begins to produce endogenous surfactant. (20) Use of mechanical ventilation before this is supportive and should continue with circumspection to avoid ventilator-induced lung injury. Infants who do not improve with surfactant administration should be evaluated for the presence of a patent ductus arteriosus or other congenital center affliction. The baby who initially improves with assistants of surfactant and after deteriorates should as well exist evaluated for nosocomial pneumonia. (20) On admission, information technology is appropriate to initiate antibiotic therapy in the newborn with RDS considering pneumonia may present clinically in the same mode and findings on chest radiographs can be indistinguishable from RDS.
Preventing premature nascence will lower the incidence of RDS. However, attempts to prevent premature births have been largely unsuccessful, with the rate of premature births still 11.5% of all births in 2012. To benefit those infants who will deliver prematurely, multiple randomized clinical trials strongly back up the use of maternal antenatal corticosteroids. Ii doses of betamethasone significantly reduce the incidence of RDS, intraventricular hemorrhage, and mortality in infants age 23 to 29 weeks' gestation. (5)(39)(twoscore)
Case 4
A four.four-kg female infant is delivered via caesarean section at 41 weeks' gestational age because of presumed large for gestational age status. The amniotic fluid is stained with thick meconium. She is limp and cyanotic at birth with minimal respiratory effort. Apgar scores are 2 and 7 at 1 and v minutes, respectively. Temperature is 99°F (37.two°C), pulse is 177 beats per minute, and respiratory rate is 80 breaths per minute. Physical examination findings are meaning for marked increased piece of work of breathing with nasal flaring, subcostal and suprasternal retractions, a butt-shaped chest, and coarse rhonchi in bilateral lung fields. Her breast radiograph is shown in Figure one.
Meconium Aspiration Syndrome
MSAF occurs when the fetus passes meconium before birth. Infants built-in through MSAF are at risk for aspiration of meconium in utero or immediately after nativity. Any infant who is born through MSAF and develops respiratory distress afterward commitment, which cannot be attributed to some other cause, is diagnosed as having MAS.
Meconium is composed of lanugo, bile, vernix, pancreatic enzymes, desquamated epithelia, amniotic fluid, and mucus. Meconium is present in the gastrointestinal tract as early on as 16 weeks' gestation but is not present in the lower descending colon until 34 weeks' gestation; therefore, MSAF is seldom seen in infants younger than 37 weeks' gestation. (41) In the compromised fetus, hypoxia or acidosis may issue in a peristaltic wave and relaxation of the anal sphincter, resulting in meconium passage in utero. Aspiration may occur in utero or immediately after nascency as the compromised fetus gasps.
Meconium is toxic to the newborn lung, causing inflammation and epithelial injury as information technology migrates distally. The pH of meconium is 7.1 to vii.2. The acidity causes airway inflammation and a chemical pneumonitis with release of cytokines. (41) Equally meconium reaches the pocket-size airways, partial obstruction occurs, which results in air trapping and hyperaeration. The typical chest radiograph initially appears streaky with lengthened parenchymal infiltrates. In time, lungs become hyperinflated with patchy areas of atelectasis and infiltrate among alveolar amplification (Effigy 1). Surfactant is inactivated past the bile acids in meconium, resulting in localized atelectasis, and so alternatively, radiographs may resemble those of RDS with low lung volumes. Although air leak syndromes may occur with other respiratory diseases of the newborn, pneumomediastinum, pneumothorax, and PPHN are common in MAS (Figure 2).
Common complications of meconium aspiration syndrome include pneumothorax (left upper) and persistent pulmonary hypertension of the newborn (right upper) characterized past cyanosis with normal lung fields and decreased pulmonary vascular markings.
Management is directed at strategies to back up the infant. Supplemental oxygen is required, and CPAP and mechanical ventilation may also be considered in astringent cases. Replacement with exogenous surfactant is common do and reduces the need for extracorporal membrane oxygenation (ECMO) and the take chances of pneumothorax. (42) Because MAS results in a ventilation-perfusion mismatch whereby ventilated alveolar units are not perfused by pulmonary blood vessels, astringent hypoxemia may event and further increases pulmonary vascular resistance. Echocardiography helps confirm PPHN by revealing ventricular septal wall flattening, tricuspid regurgitation, and right-to-left shunting at the patent ductus arteriosus. Inhaled nitric oxide is a selective pulmonary vasodilator without systemic effects. It is often used with loftier-frequency ventilation in severe cases of MAS to maintain adequate oxygenation and ventilation and reduce the need for ECMO. Initiation of broad-spectrum antibiotic therapy is appropriate because meconium is a growth medium for gram-negative organisms. Balance pulmonary compromise is mutual later on MAS. As many as l% of afflicted infants are diagnosed every bit having reactive airway disease during their first half-dozen months of life, and persistent pulmonary insufficiency is seen in children equally old as 8 years. (43)
Because of the meaning morbidity associated with MAS, preventive measures are important. Historically, oropharyngeal and nasopharyngeal suctioning was performed on the meconium-stained infant after delivery of the head but before delivery of the shoulders and was initially thought to be an effective preventive measure. (44) However, a big, multicenter randomized controlled trial in 2004 plant that this exercise does not prevent MAS or decrease the need for mechanical ventilation or hospital length of stay. (45) Consequently, routine suctioning on the perineum is no longer indicated. Endotracheal suctioning immediately after nascence was also a routine practice for all meconium-stained infants until a large randomized controlled trial found that intubating and suctioning vigorous infants built-in through MSAF had no benefit and increased the charge per unit of complications. (46) This finding has been confirmed by additional, well-designed studies, (47) prompting a change in practice guidelines in 2000. Current evidence still supports immediate endotracheal suctioning of the depressed baby as divers past a low heart rate (<100 beats per minute), poor muscle tone, and no spontaneous respiratory attempt. (8) Intubation and suctioning the vigorous, spontaneously breathing baby is non recommended. (eight)(47)(48)
Approximately 13% of all live births are through MSAF. Although the number of cases has decreased during the past decade, 4% to v% of these will develop MAS. (thirty)(41) Previously, many postterm infants (≥42 weeks' gestation) developed MAS. However, a recent meta-assay provides evidence that consecration of labor at 41 weeks' gestation reduces the risk of MAS and perinatal death without increasing the gamble of caesarean section. (7) Therefore, many obstetricians do not allow pregnancies to advance beyond 41 weeks' gestation. In improver, advances in fetal heart rate monitoring have identified compromised fetuses, allowing for timely obstetric intervention that may help forbid in utero aspiration of meconium. Amnioinfusion or transcervical infusion of saline into the amniotic cavity has been proposed as a do to subtract the incidence of MAS. Although amnioinfusion is benign for the distressed fetus with oligohydramnios, best evidence does not signal a reduced risk of moderate to severe MAS or perinatal death. (49)
Determination
Learning to readily recognize respiratory distress in the newborn and understanding physiologic abnormalities associated with each of the various causes will guide optimal management. Although decreasing the incidence through preventive measures is ideal, early recognition and handling of the common neonatal respiratory diseases will decrease both short- and long-term complications and related bloodshed of at-risk infants.
Glossary
| BPD | bronchopulmonary dysplasia |
| CPAP | continuous positive airway pressure |
| ECMO | extracorporal membrane oxygenation |
| Fio2 | fraction of inspired oxygen |
| FRC | functional residual capacity |
| GBS | grouping B streptococcus |
| MAS | meconium aspiration syndrome |
| MSAF | meconium-stained amniotic fluid |
| PPHN | persistent pulmonary hypertension of the newborn |
| PROM | prolonged rupture of membranes |
| RDS | respiratory distress syndrome |
| TTN | transient tachypnea of the newborn |
Footnotes
Author DISCLOSURES
Drs Reuter, Moser, and Baack take disclosed no financial relationships relevant to this article. This commentary does not incorporate data virtually unapproved/investigative commercial products or devices.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4533247/
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