Medication Summary

Preterm rupture of membranes and an imminent preterm delivery is managed with tocolytics to control contractions and to prevent delivery, as indicated. Maternal steroids to accelerate lung maturity of the fetus are indicated in preterm labor.

The most common tocolytic agents used for the treatment of preterm labor are magnesium sulphate (MgSO4), indomethacin, and nifedipine. In the past, beta-mimetic agents, such as terbutaline or ritodrine, were the agents of choice, but in recent years their use has been significantly curtailed due to maternal and fetal side effects, such as maternal tachycardia, hyperglycemia, and palpitations. The use of these agents can lead to pulmonary edema, myocardial ischemia, and cardiac arrhythmia. The tocolytic agents currently used to treat preterm labor appear to be equally efficacious in delaying delivery for at least 48 hours. Although MgSO4 is associated with more maternal toxicity, indomethacin is associated with more fetal and neonatal toxicity. For more information, see Preterm Labor.

Class Summary

These agents are used to induce or accelerate lung maturity in a preterm newborn at less than 32 weeks' gestation or when lung immaturity is known by amniotic fluid assay. Long-acting steroids (eg, dexamethasone, betamethasone) are recommended by a National Institutes of Health (NIH) Consensus Conference panel for all pregnancies at 24-34 weeks' gestation at risk of preterm delivery, in patients with preterm rupture of membranes at less than 30-32 weeks' gestation, and in complicated pregnancies with anticipated delivery before 34 weeks' gestation unless the corticosteroid will have an adverse effect on the mother.

Dexamethasone (Decadron)

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Decreases frequency of respiratory distress syndrome, surfactant therapy, and serious intraventricular hemorrhage. Optimal benefit occurs within 24 h and lasts for 7 d.

Betamethasone (Celestone Soluspan)

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Decreases frequency of respiratory distress syndrome, surfactant therapy, and serious intraventricular hemorrhage. Optimal benefit occurs within 24 h and lasts for 7 d.

Class Summary

These agents are administered at birth to newborns to improve lung mechanics and oxygenation when treating airspace disease. Following inhaled administration, surface tension is reduced, and alveoli are stabilized, thus decreasing the work of breathing and increasing lung compliance.

Beractant (Survanta)

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A semisynthetic bovine lung extract that contains phospholipids, fatty acids, and surfactant-associated proteins B (7 mcg/mL) and C (203 mcg/mL).

Calfactant (Infasurf)

A natural calf lung extract that contains phospholipids, fatty acids, and surfactant-associated proteins B (260 mcg/mL) and C (390 mcg/mL).

Follow-up

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Media Gallery

Chest radiograph of a newborn with primary pulmonary hypoplasia of the right lung showing shift of the mediastinum to the right hemithorax.
CT scan of the same patient (a newborn with primary pulmonary hypoplasia of the right lung) showing absence of the right lung. Note branching of the left lower lobe bronchus (horizontal arrow) and absence of airways in the right side (vertical arrow).
A posteroanterior radiograph of a 3-month-old infant with primary pulmonary hypoplasia of the right lung.
Lateral view of the same patient (a 3-month-old infant with primary pulmonary hypoplasia of the right lung) showing one dome of the diaphragm.
Bronchogram of the same patient (a 3-month-old infant with primary pulmonary hypoplasia of the right lung) showing absence of the airways in the right side and presence of the left main bronchus and its branches.
A chest radiograph of a 14-year-old child with primary pulmonary hypoplasia of the right side causing secondary scoliosis.
A chest radiograph of a newborn with achondroplasia and small chest causing hypoplasia of both lungs.
A chest radiograph of a newborn with diaphragmatic hernia in the right hemithorax shortly after birth.
CT scan of the same child (a newborn with diaphragmatic hernia in the right hemithorax shortly after birth) showing the presence of abdominal contents in the right hemithorax. Note the presence of the left lower bronchus and its main branches (horizontal arrow) and absence of the right lower lobe bronchus. The liver in the right hemithorax is indicated by the upper arrow.
A chest radiograph of a 10-month-old child after repair of a right diaphragmatic hernia showing loss of lung volume in the right hemithorax.
MRI of the same patient (a 10-month-old child after repair of a right diaphragmatic hernia) showing loss of right lung volume and smaller right pulmonary artery than the left pulmonary artery (arrow).

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Table 1. Factors and/or Their Receptors Possibly Involved with Abnormal Lung Growth

Transcription Factors	Growth Factors
Thyroid transcription factor-1 (TTF-1) ^[12]	Vascular endothelial growth factor receptors (VEGFR1 and VEGFR2) ^[15]
GATA-4^[20]	Insulinlike growth factors (IGF-1 and IGF-2) and their receptors (IGF-1R and IGF-2R)^[18]
FOG-2^[23]	Epidermal growth factors and its receptor family (eg, ErbB receptors)^[21]
Hepatocyte nuclear factor (HNF3ß10)	Mitogen-activated protein kinases
	Connective tissue growth factor^[25]

Table 2. Causes of Secondary Pulmonary Hypoplasia

Small Fetal Thoracic Volume	Prolonged Oligohydramnios	Decreased Fetal Breathing Movements	Congenital Heart Diseases With Poor Pulmonary Blood Flow
CDH	Fetal renal agenesis	Central nervous system (CNS) lesions	Tetralogy of Fallot
Cystic adenomatoid malformation (CAM)	Urinary tract obstruction	Lesions of the spinal cord, brain stem, and phrenic nerve	Hypoplastic right heart
Pulmonary sequestration	Bilateral renal dysplasia	Neuromuscular diseases (eg, myotonic dystrophy, spinal muscular atrophy)	Pulmonary artery hypoplasia
Pleural effusions with fetal hydrops, hydrothorax	Bilateral cystic kidneys	Arthrogryposis multiplex congenital secondary to fetal akinesia	Scimitar syndrome causing a unilateral right-sided pulmonary hypoplasia
Thoracic neuroblastomas	Prolonged rupture of membranes (PROM)	Maternal depressant drugs	Trisomies 18 and 21
Malformations of the thorax (eg, asphyxiating thoracic dystrophy)	Premature PROM
Diaphragmatic anomalies (eg, abdominal wall defects, eventration of the diaphragm)	Potter syndrome
Musculoskeletal disorders (eg, achondroplasia, thanatophoric dysplasia, osteogenesis imperfecta)
Abdominal masses causing compression

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Author

Terry W Chin, MD, PhD Associate Clinical Professor, Department of Pediatrics, University of California, Irvine, School of Medicine; Associate Director, Cystic Fibrosis Center, Attending Staff Physician, Department of Pediatric Pulmonology, Allergy, and Immunology, Memorial Miller Children's Hospital

Terry W Chin, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Allergy, Asthma and Immunology, American College of Chest Physicians, American Federation for Clinical Research, American Thoracic Society, California Society of Allergy, Asthma and Immunology, California Thoracic Society, Clinical Immunology Society, Los Angeles Pediatric Society, Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Nandini Kataria, MD Fellow in Pediatric Pulmonology, Miller Children’s and Women’s Hospital Long Beach, University of California, Irvine, School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Girish D Sharma, MD, FCCP, FAAP Professor of Pediatrics, Rush Medical College; Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush Children's Hospital, Rush University Medical Center

Girish D Sharma, MD, FCCP, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Additional Contributors

Susanna A McColley, MD Professor of Pediatrics, Northwestern University, The Feinberg School of Medicine; Director of Cystic Fibrosis Center, Head, Division of Pulmonary Medicine, Children's Memorial Medical Center of Chicago

Susanna A McColley, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Sleep Disorders Association, American Thoracic Society

Disclosure: Received honoraria from Genentech for speaking and teaching; Received honoraria from Genentech for consulting; Partner received consulting fee from Boston Scientific for consulting; Received honoraria from Gilead for speaking and teaching; Received consulting fee from Caremark for consulting; Received honoraria from Vertex Pharmaceuticals for speaking and teaching.

Khanh Van Lai, MD Fellow in Pediatric Pulmonology, Miller Children's Hospital, University of California, Irvine, School of Medicine

Khanh Van Lai, MD is a member of the following medical societies: American Thoracic Society

Disclosure: Nothing to disclose.

Bich-Trang Hoa, MD Fellow in Pediatric Pulmonology, Miller Children's Hospital, University of California, Irvine, School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The current authors would like to acknowledge the contributions of the following to this article:

Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center;

Girija Natarajan, MD, Assistant Professor, Division of Neonatology, Children's Hospital of Michigan, Wayne State University School of Medicine; and

Ibrahim Abdulhamid, MD, Associate Professor of Pediatrics, Wayne State University School of Medicine; Director of Pediatric Pulmonary Medicine, Clinical Director of Pediatric Sleep Laboratory, Children's Hospital of Michigan

Disclosure: Nothing to disclose.

Pediatric Pulmonary Hypoplasia Medication

Medication Summary

Glucocorticoids