A female infant is born at 38 weeks gestation to a G2P1 mother with known gestational diabetes via scheduled, repeat C-section. Initial Apgar scores are 8 and 9 at 1 and 5 minutes, respectively. About an hour later, the child begins to develop tachypnea (RR 70), nasal flaring, and grunting, which improves with supplemental oxygen via nasal cannula. A chest X-ray is obtained, which showed findings consistent with the diagnosis of Transient Tachypnea of the Newborn. What findings would be expected on chest X-ray for this patient?

A. Diffuse parenchymal infiltrates with fluid in the interlobar fissure

B. Diffuse parenchymal infiltrates with air bronchograms or lobar consolidation

C. Diffuse, bilateral ground-glass opacities with air bronchograms

D. Diffuse, patchy infiltrates with areas of hyperinflation

E. Left-sided intrathoracic stomach bubble with shift of the mediastinum and cardiac silhouette to the right

The correct answer is A, Diffuse parenchymal infiltrates with fluid in the interlobar fissure. There is a great Pediatrics in Review article from 2014 titled Respiratory Distress in the Newborn that discusses the majority of these disease processes, linked below in the references.


Answer Choice A: Diffuse parenchymal infiltrates with fluid in the interlobar fissure

This is the correct answer! Transient Tachypnea of the Newborn (TTN) is a common newborn cause of respiratory distress due to retained fetal lung fluid in term and late pre-term infants. During fetal development, the lung alveoli are fluid-filled, and towards the end of pregnancy, the fetus starts removing this alveolar fluid to allow for effective gas exchange. This process is enhanced by labor, so naturally, TTN tends to occur more often in neonates who do not undergo labor (i.e. precipitous labor and scheduled C-sections). Other risk factors include gestational age <39 weeks, fetal distress, maternal sedation, and maternal diabetes. This disease process is usually self-limited and normally does not require use of mechanical ventilation. However, use of antenatal corticosteroids (such as 2 doses of Betamethasone) given at least 48 hours prior to C-section can help decrease respiratory morbidity in these infants.


Answer Choice B: Diffuse parenchymal infiltrates with air bronchograms or lobar consolidation

Neonatal Pneumonia can be acquired at birth or during pregnancy (perinatal vs congenital pneumonia). Perinatal pneumonia is the most common cause of neonatal pneumonia, with the common causative organism being Group B Streptococcus (GBS). Congenital pneumonia, however, can be passed transplacentally from the mother and can be caused by a myriad of organisms, such as Rubella, Cytomegalovirus, Adenovirus, Enteroviruses, Mumps, Toxoplasma gondii, Treponema pallidum, Mycobacterium tuberculosis, Listeria monocytogenes, Varicella Zoster virus, and HIV. Risk factors for developing this infection include prolonged rupture of membranes (PROM), maternal infection, and prematurity.

This infectious process often presents as part of a generalized septic illness, requiring blood and CSF cultures and empiric antibiotics (see our previous episode on Management of the Febrile Neonate for further discussion). There is also a great neonatal early-onset sepsis calculator published by Kaiser Permanente if you need further guidance on obtaining a blood culture and starting empiric antibiotics in infants at least 34 weeks gestation. It calculates your patient’s septic risk based on gestational age, maternal temperature, ROM duration, maternal GBS status, and use of intrapartum antibiotics. The higher the maternal temperature and longer the ROM, the more likely it will recommend considering a blood culture and starting empiric antibiotics.


Answer Choice C: Diffuse, bilateral ground-glass opacities with air bronchograms

Respiratory Distress Syndrome (RDS) is incredibly common in premature infants due to alveolar surfactant deficiency. But before we can talk about how infants get surfactant, we should take a step back and talk globally about the 5 embryonal stages of lung development.

  1. The first stage, Embryonic, is the first 6 weeks of development where the trachea and bronchi are formed. If this stage has defective growth, infants can develop tracheoesophageal fistulas (TEF) or pulmonary sequestration.
  2. The second stage, Pseudoglandular, lasts from weeks 7-16, and this is where the bronchioles, terminal bronchioles, and lung circulation develop. This is also where infants can develop defects such as bronchogenic cysts, congenital diaphragmatic hernias (talked about in detail in a minute), and congenital cystic adenomatoid malformations.
  3. The third stage, Canalicular, is from weeks 17-24, and now the respiratory bronchioles and primitive alveoli develop. If these grow incorrectly, infants can develop pulmonary hypoplasia, RDS, BPD, and alveolar capillary dysplasia.
  4. The fourth stage, Terminal Sac, lasts from weeks 25-36 weeks gestation. This is when the fetus develops alveolar ducts, thin-walled alveolar sacs, and throughout this stage, they increasingly gain function in Type 2 pneumocytes. These Type 2 pneumocytes are the surfactant-producing cells in the lungs. If children are born during this stage, they are at risk for developing RDS and Bronchopulmonary Dysplasia (BPD).
  5. The fifth and final stage is the Alveolar stage and goes from week 37 until the infant is born. This is when the lungs develop definitive alveoli and mature Type 2 pneumocytes. Infants born during this stage are at risk for developing TTN, MAS, neonatal pneumonia, and Persistent Pulmonary Hypertension (PPHN).

So back to RDS, these kids are typically born before 36 weeks and have not yet developed enough surfactant. Surfactant decreases the surface tension in the alveoli and prevents microatelectasis and low lung volumes and instead allows the alveoli to remain open and allow for gas exchange.

Risk factors for RDS include prematurity, gestational diabetes, multiple gestation, and male infants. Infants of a diabetic mother are at increased risk because hyperinsulinemia has been shown to delay fetal lung development. However, administration of corticosteroids 48 hours prior to delivery (2 doses of Betamethasone) has been shown to stimulate surfactant production and decrease the rate of RDS in premature infants.  


Answer Choice D: Diffuse, patchy infiltrates with areas of hyperinflation

Meconium Aspiration Syndrome (MAS) is due to neonates aspirating meconium, which causes a chemical pneumonitis and partial obstruction, leading to air trapping and hyperaeration. Additionally, meconium has many components, one of which is bile acids. These bile acids locally inactivate pulmonary surfactant, causing atelectasis.

Meconium is present in the fetal GI tract as early as 16 weeks, but it does not move into the descending colon until about 34 weeks gestation. Therefore, it is uncommon to see MAS prior to 37 weeks gestation.

Risk factors include meconium stained amniotic fluids, post-term gestation (>40 weeks gestation), fetal stress, and African American ethnicity.


Answer Choice E: Left-sided intrathoracic stomach bubble with shift of the mediastinum and cardiac silhouette to the right

These findings would be suggestive of Congenital Diaphragmatic Hernia (CDH). Due to a defect in the diaphragm, abdominal organs are able to migrate into the chest during embryonic development, leading to pulmonary hypoplasia on the affected side(s). Per a Pediatrics in Review article from 1999, about 85% of the diaphragmatic defects are left-sided, 13% right-sided, and 2% bilateral. CDH can be a solitary defect, combined with multiple other defects, or due to chromosomal abnormalities (i.e. Trisomies 18 and 21). This defect might be noted prenatally with low maternal serum alpha-fetoprotein (MS-AFP) and ultrasonographic findings of polyhydramnios and an intrathoracic gastric bubble. If you’re interested in reading more about management of CDH, there’s a great NeoReviews article from the AAP in 2016 listed in the references.



  1. Reuter S, Moser C, Baack M. Respiratory distress in the newborn. Pediatr Rev. 2014 Oct;35(10):417-28; quiz 429. doi: 10.1542/pir.35-10-417. PMID: 25274969; PMCID: PMC4533247.
  2. Hermansen CL, Mahajan A. Newborn Respiratory Distress. Am Fam Physician. 2015 Dec 1;92(11):994-1002. PMID: 26760414.
  3. Kuzniewicz MW, Puopolo KM, Fischer A, Walsh EM, Li S, Newman TB, Kipnis P, Escobar GJ. A Quantitative, Risk-Based Approach to the Management of Neonatal Early-Onset Sepsis. JAMA Pediatr. 2017 Apr 1;171(4):365-371. doi: 10.1001/jamapediatrics.2016.4678. PMID: 28241253 
  4. Escobar GJ, Puopolo KM, Wi S, Turk BJ, Kuzniewicz MW, Walsh EM, Newman TB, Zupancic J, Lieberman E, Draper D. Stratification of risk of early-onset sepsis in newborns > 34 weeks’ gestation. Pediatrics. 2014 Jan;133(1):30-6. doi: 10.1542/peds.2013-1689. Epub 2013 Dec 23. PMID: 24366992
  5. Kuzniewicz MW, Walsh EM, Li S, Fischer A, Escobar GJ. Development and Implementation of an Early-Onset Sepsis Calculator to Guide Antibiotic Management in Late Preterm and Term Neonates. Jt Comm J Qual Patient Saf. 2016 May;42(5):232-9. doi: 10.1016/s1553-7250(16)42030-1. PMID: 27066927.
  6. Van Meurs K, Lou Short B. Congenital diaphragmatic hernia: the neonatologist’s perspective. Pediatr Rev. 1999 Oct;20(10):e79-87. doi: 10.1542/pir.20-10-e79. PMID: 10512896.

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