eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Pulmonary Hypoplasia: Treatment & Medication

Author: Terry Chin, MD, PhD, Associate Professor of Pediatrics, Pediatric Allergy/Immunology/Pulmonology, Department of Pediatrics, University of California Irvine School of Medicine; Associate Director, Miller Children's Hospital at Long Beach Memorial Medical Center
Coauthor(s): Girija Natarajan, MD, Assistant Professor, Division of Neonatology, Children's Hospital of Michigan & Wayne State University; Ibrahim Abdulhamid, MD, Assistant Professor of Pediatrics, Wayne State University; Director of Pediatric Pulmonary Medicine, Clinical Director of Pediatric Sleep Laboratory, Children's Hospital of Michigan
Contributor Information and Disclosures

Updated: Mar 5, 2009

Treatment

Medical Care

  • In fetuses with pulmonary hypoplasia, before delivery and depending on the underlying lesion, a few interventions can be performed to increase the fetal lung volume and improve lung development.
    • Preterm rupture of membranes without signs of fetal distress or intrauterine infection is treated conservatively with or without tocolytics, antibiotics, and steroids in various combinations. Attempts have been made to seal the defect in the membranes by transcervically using "fibrin glue." However, this technique requires a preliminary cerclage, increases the risk of infection, and has limited efficacy.
    • Serial amnioinfusions are increasingly used in cases of preterm rupture of membranes at less than 32 weeks' gestation. This procedure, if successful, has been shown to decrease the risk of pulmonary hypoplasia and significantly improve perinatal outcome.
  • After delivery, the infant needs respiratory support, which can range from supplying supplemental oxygen to mechanical ventilation, including high-frequency ventilation and extracorporeal membrane oxygenation (ECMO). Ventilatory strategies have veered toward the use of permissive hypercapnia, especially in cases of congenital diaphragmatic hernia (CDH), with an increased survival rate in several reports. Partial liquid ventilation has also been used, without definite advantages.
    • ECMO is particularly indicated in infants with diaphragmatic hernia associated with pulmonary hypoplasia and when mild hypoplasia is complicated by persistent pulmonary hypertension. A decreased response to nitric oxide is believed to occur with pulmonary hypertension associated with hypoplasia.
    • Surfactant administration of 4 mL/kg in pulmonary hypoplasia secondary to CDH has been shown to be efficacious in improving oxygenation, decreasing the need for ECMO, and improving the survival rate if prophylactically administered at birth. Animal studies have shown that surfactant significantly improved lung mechanics and gas exchange and that lung tissue stores of surfactant protein B and phosphatidylcholine were low in diaphragmatic hernia.
    • Dialysis for support of renal function is provided in some cases, but it should be started only after careful consideration. Patients with severe chronic renal impairment with pulmonary hypoplasia have a poor prognosis; the ultimate outcome is difficult to improve, even with optimal renal and respiratory support.
    • Some studies suggest that strict infection control may improve the outcome of neonates with CDH without the need for ECMO.20
  • CDH has been associated with chronic pulmonary damage as well as cardiovascular disease, GI disease, failure to thrive, neurocognitive defects and musculoskeletal abnormalities.21
  • Management of any of the congenital cystic lung abnormalities such as cystic adenomatoid malformation (CAM) needs to consider the spontaneous improvement and possible resolution that occurs over months to years in many of these lesions.22
    • Their management must be individualized with very large lesions resulting in lung hypoplasia or fetal hydrops with possible fetal surgery required.23
    • In most cases of fetal lung lesions, continued observation with postnatal therapy occurs.24

Surgical Care

  • In patients with severe CAM who have an extremely poor prognosis, fetal surgery is possible in certain centers. A multidisciplinary team with expertise in fetal surgery should evaluate both the fetus and the pregnant mother. A major indication for fetal surgery is the presence of hydrops and a gestation of less than 32 weeks. Thoracocentesis can allow for drainage of fluid from the CAM, but the fluid usually rapidly reaccumulates.
  • Intrauterine vesicoamniotic shunts and endoscopic ablation of posterior urethral valves are other techniques that are currently used in fetuses with urinary tract obstruction and pulmonary hypoplasia. With careful case selection, pulmonary hypoplasia is prevented, and postnatal renal and respiratory function is improved.
  • Percutaneous fetal endoluminal tracheal occlusion (FETO) with a balloon, inserted at 26-28 weeks' gestation, can be considered for infants with isolated CDH with poor prognosis.25 This procedure was found to be minimally invasive, may reverse pulmonary hypoplasia changes, and may improve survival rate in these highly selected cases. In addition, the airways can be restored before birth.
    • In experimental animals, fetal tracheal occlusion (TO) induces lung growth and morphologic maturation. Fetoscopic TO with a clip may lead to accelerated lung growth and prevent pulmonary hypoplasia. However, one study showed that fetal TO used to treat severe CDH resulted in modest improvements in neonatal pulmonary function that are of questionable clinical significance
    • After delivery, surgery to correct diaphragmatic hernia, to correct CAM, and to decompress pleural effusions may be life-saving and curative in some cases.
  • The optimal time of surgery and the duration of ventilatory support used before surgery are controversial. The decision is made based on the lesion and the center's preferences.
  • Management of any of the congenital cystic lung abnormalities such as CAM needs to consider the spontaneous improvement and possible resolution that occurs over months to years in many of these lesions.22 The risks of subsequent cancer are poorly understood and "probably overstated," and the degree of compensatory lung growth are also not well defined.

Consultations

  • These patients should be followed by a pediatric pulmonologist after birth. Appropriate diagnostic tests can be performed. If early surgery is not performed during infancy, close follow-up of these patients are needed. As indicated above, some cystic lung abnormalities can spontaneously resolve over months to years. Newborns who have been referred for a cystic lesion observed by fetal ultrasonography may have complete resolution on chest CT scanning. Also, the occurrence of pneumonia or repeated respiratory infections may suggest surgical intervention is needed in a patient who has been conservatively managed.
  • Consult a pediatric surgeon for CDH, CAM, or any other lesion that requires surgery. Also, consult a pediatric surgeon in cases that involve pulmonary hypertension or respiratory failure that requires ECMO.
  • Consult a nephrologist and a urologist if a renal obstructive, cystic, or agenetic lesion is the cause of the pulmonary hypoplasia.
  • Consult a cardiologist and cardiothoracic surgeon if the patient has a causative or coexisting cardiac lesion, such as anomalous pulmonary venous connection.
  • Consult a neurologist in cases of congenital neuromuscular diseases.

Medication

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.

Glucocorticoids

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)

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

Adult

6 mg IM q12h for 4 doses is the maternal prenatal dose

Pediatric

Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization; may antagonize neuromuscular blocking agents

Documented hypersensitivity; systemic fungal infection

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use; caution in CHF, seizure disorder, diabetes mellitus, hypertension, tuberculosis, and osteoporosis


Betamethasone (Celestone Soluspan)

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

Adult

12 mg IM qd for 2 doses is the maternal prenatal dose

Pediatric

Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization; may antagonize neuromuscular blocking agents

Documented hypersensitivity; systemic fungal infection

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use

Surfactants

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)

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

Adult

Not indicated

Pediatric

100 mg (ie, 4 mL)/kg divided in 4 aliquots intratracheally administered at least 6 h apart

Pregnancy
Precautions

Must be warmed to room temperature; administer only under carefully supervised conditions because of risk of acute airway obstruction; transient bradycardia, oxygen desaturation, pallor, vasoconstriction, hypotension, endotracheal tube blockage, apnea, and hypercapnia may occur during administration; other adverse effects include pulmonary interstitial emphysema, air leaks, and nosocomial sepsis; monitor heart rate and oxygen saturation during administration; monitor arterial blood gas after administration


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).

Adult

Not indicated

Pediatric

3 mL/kg intratracheally; may repeat q6-12h; not to exceed 3-4 doses

Pregnancy
Precautions

Administer only under carefully supervised conditions because of risk of acute airway obstruction; transient bradycardia, oxygen desaturation, pallor, vasoconstriction, hypotension, endotracheal tube blockage, apnea, and hypercapnia may occur during administration; other adverse effects include pulmonary interstitial emphysema, air leaks, and nosocomial sepsis; monitor heart rate and oxygen saturation during administration; monitor arterial blood gas after administration

More on Pulmonary Hypoplasia

Overview: Pulmonary Hypoplasia
Differential Diagnoses & Workup: Pulmonary Hypoplasia
Treatment & Medication: Pulmonary Hypoplasia
Follow-up: Pulmonary Hypoplasia
Multimedia: Pulmonary Hypoplasia
References
[ CLOSE WINDOW ]

References

  1. Gallot D, Marceau G, Coste K, et al. Congenital diaphragmatic hernia: a retinoid-signaling pathway disruption during lung development?. Birth Defects Res A Clin Mol Teratol. Aug 2005;73(8):523-31. [Medline].

  2. Montedonico S, Sugimoto K, Felle P, Bannigan J, Puri P. Prenatal treatment with retinoic acid promotes pulmonary alveologenesis in the nitrofen model of congenital diaphragmatic hernia. J Pediatr Surg. Mar 2008;43(3):500-7. [Medline].

  3. Sugimoto K, Takayasu H, Nakazawa N, Montedonico S, Puri P. Prenatal treatment with retinoic acid accelerates type 1 alveolar cell proliferation of the hypoplastic lung in the nitrofen model of congenital diaphragmatic hernia. J Pediatr Surg. Feb 2008;43(2):367-72. [Medline].

  4. Nogueira-Silva C, Moura RS, Esteves N, Gonzaga S, Correia-Pinto J. Intrinsic catch-up growth of hypoplastic fetal lungs is mediated by interleukin-6. Pediatr Pulmonol. Jul 2008;43(7):680-9. [Medline].

  5. Gonzaga S, Henriques-Coelho T, Davey M, et al. Cystic adenomatoid malformations are induced by localized FGF10 overexpression in fetal rat lung. Am J Respir Cell Mol Biol. Sep 2008;39(3):346-55. [Medline].

  6. Logan JW, Rice HE, Goldberg RN, Cotten CM. Congenital diaphragmatic hernia: a systematic review and summary of best-evidence practice strategies. J Perinatol. Sep 2007;27(9):535-49. [Medline].

  7. Bush A, Hogg J, Chitty LS. Cystic lung lesions - prenatal diagnosis and management. Prenat Diagn. Jul 2008;28(7):604-11. [Medline].

  8. Baguma-Nibasheka M, Kablar B. Pulmonary hypoplasia in the connective tissue growth factor (Ctgf) null mouse. Dev Dyn. Feb 2008;237(2):485-93. [Medline].

  9. Deprest J, Jani J, Van Schoubroeck D, et al. Current consequences of prenatal diagnosis of congenital diaphragmatic hernia. J Pediatr Surg. Feb 2006;41(2):423-30. [Medline].

  10. Zaupa P, Kleinlein B, Hollwarth ME. Bilateral congenital diaphragmatic hernia and gastroschisis in a newborn: can low intrathoracic pressure prevent the pulmonary hypoplasia?. Pediatr Surg Int. Jul 2007;23(7):711-3. [Medline].

  11. Deprest JA, Flemmer AW, Gratacos E, Nicolaides K. Antenatal prediction of lung volume and in-utero treatment by fetal endoscopic tracheal occlusion in severe isolated congenital diaphragmatic hernia. Semin Fetal Neonatal Med. Feb 2009;14(1):8-13. [Medline].

  12. Gerards FA, Twisk JW, Fetter WP, Wijnaendts LC, van Vugt JM. Predicting pulmonary hypoplasia with 2- or 3-dimensional ultrasonography in complicated pregnancies. Am J Obstet Gynecol. Jan 2008;198(1):140.e1-6. [Medline].

  13. Tsukimori K, Masumoto K, Morokuma S, et al. The lung-to-thorax transverse area ratio at term and near term correlates with survival in isolated congenital diaphragmatic hernia. J Ultrasound Med. May 2008;27(5):707-13. [Medline].

  14. Obenauer S, Maestre LA. Fetal MRI of lung hypoplasia: imaging findings. Clin Imaging. Jan-Feb 2008;32(1):48-50. [Medline].

  15. Taylor GA, Atalabi OM, Estroff JA. Imaging of congenital diaphragmatic hernias. Pediatr Radiol. Jan 2009;39(1):1-16. [Medline].

  16. Matsushita M, Ishii K, Tamura M, et al. Perinatal magnetic resonance fetal lung volumetry and fetal lung-to-liver signal intensity ratio for predicting short outcome in isolated congenital diaphragmatic hernia and cystic adenomatoid malformation of the lung. J Obstet Gynaecol Res. Apr 2008;34(2):162-7. [Medline].

  17. Okuyama H, Kubota A, Kawahara H, Oue T, Kitayama Y, Yagi M. Correlation between lung scintigraphy and long-term outcome in survivors of congenital diaphragmatic hernia. Pediatr Pulmonol. Sep 2006;41(9):882-6. [Medline].

  18. Lin AE, Pober BR, Adatia I. Congenital diaphragmatic hernia and associated cardiovascular malformations: type, frequency, and impact on management. Am J Med Genet C Semin Med Genet. May 15 2007;145C(2):201-16. [Medline].

  19. Koumbourlis AC, Wung JT, Stolar CJ. Lung function in infants after repair of congenital diaphragmatic hernia. J Pediatr Surg. Oct 2006;41(10):1716-21. [Medline].

  20. Morikawa N, Kuroda T, Honna T, et al. The impact of strict infection control on survival rate of prenatally diagnosed isolated congenital diaphragmatic hernia. Pediatr Surg Int. Oct 2008;24(10):1105-9. [Medline].

  21. Peetsold MG, Heij HA, Kneepkens CM, Nagelkerke AF, Huisman J, Gemke RJ. The long-term follow-up of patients with a congenital diaphragmatic hernia: a broad spectrum of morbidity. Pediatr Surg Int. Jan 2009;25(1):1-17. [Medline].

  22. Fitzgerald DA. Congenital cyst adenomatoid malformations: resect some and observe all?. Paediatr Respir Rev. Mar 2007;8(1):67-76. [Medline].

  23. Nicolai T. Management of the upper airway and congenital cystic lung diseases in neonates. Semin Fetal Neonatal Med. Feb 2009;14(1):56-60. [Medline].

  24. Wilson RD. In utero therapy for fetal thoracic abnormalities. Prenat Diagn. Jul 2008;28(7):619-25. [Medline].

  25. Gucciardo L, Deprest J, Done' E, et al. Prediction of outcome in isolated congenital diaphragmatic hernia and its consequences for fetal therapy. Best Pract Res Clin Obstet Gynaecol. Feb 2008;22(1):123-38. [Medline].

  26. Askenazi SS, Perlman M. Pulmonary hypoplasia: lung weight and radial alveolar count as criteria of diagnosis. Arch Dis Child. Aug 1979;54(8):614-8. [Medline].

  27. Cock ML, Albuquerque CA, Joyce BJ, Hooper SB, Harding R. Effects of intrauterine growth restriction on lung liquid dynamics and lung development in fetal sheep. Am J Obstet Gynecol. Jan 2001;184(2):209-16. [Medline].

  28. Kasprian G, Balassy C, Brugger PC, Prayer D. MRI of normal and pathological fetal lung development. Eur J Radiol. Feb 2006;57(2):261-70. [Medline].

  29. Keller RL, Hawgood S, Neuhaus JM, et al. Infant pulmonary function in a randomized trial of fetal tracheal occlusion for severe congenital diaphragmatic hernia. Pediatr Res. Nov 2004;56(5):818-25. [Medline]. [Full Text].

  30. Szabo I, Vizer M, Halvax L. Amnioinfusion to prevent pulmonary hypoplasia after premature rupture of membranes. Am J Obstet Gynecol. Jun 2001;184(7):1583-4. [Medline].

  31. Taylor GA, Atalabi OM, Estroff JA. Imaging of congenital diaphragmatic hernias. Pediatr Radiol. Jan 2009;39(1):1-16. [Medline].

  32. Thibeault DW, Haney B. Lung volume, pulmonary vasculature, and factors affecting survival in congenital diaphragmatic hernia. Pediatrics. Feb 1998;101(2):289-95. [Medline]. [Full Text].

  33. Warburton D, Olver BE. Coordination of genetic, epigenetic, and environmental factors in lung development, injury, and repair. Chest. Jun 1997;111(6 Suppl):119S-122S. [Medline].

  34. Wedegärtner U, Schroder HJ, Adam G. Fetal MRI in experimental tracheal occlusion. Eur J Radiol. Feb 2006;57(2):271-7. [Medline].

  35. Winn HN, Chen M, Amon E, Leet TL, Shumway JB, Mostello D. Neonatal pulmonary hypoplasia and perinatal mortality in patients with midtrimester rupture of amniotic membranes--a critical analysis. Am J Obstet Gynecol. Jun 2000;182(6):1638-44. [Medline].

  36. Yoshimura S, Masuzaki H, Gotoh H, Fukuda H, Ishimaru T. Ultrasonographic prediction of lethal pulmonary hypoplasia: comparison of eight different ultrasonographic parameters. Am J Obstet Gynecol. Aug 1996;175(2):477-83. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

pulmonary hypoplasia, pulmonary aplasia, bronchopulmonary dysplasia, BPD, treatment, diagnosis, underdevelopment of the lung, hypoplastic lung, carina, congenital diaphragmatic hernia, cystic adenomatoid malformation, CAM, prolonged rupture of membranes, fetal renal dysplasias, lung hypoplasia, oligohydramnios, hydrops fetalis, respiratory distress, apnea, ventilatory support, pneumothorax, arthrogryposis, Potter facies, hypertelorism, epicanthus, retrognathia, depressed nasal bridge, abdominal masses, tracheoesophageal fistula, imperforate anus, communicating bronchopulmonary foregut malformation, pleural effusion, asphyxiating thoracic dystrophy, achondroplasia, thanatophoric dwarfism, osteogenesis imperfecta, thoracic neuroblastoma, hydrothorax, urinary tract obstruction, renal dysplasia, tetralogy of Fallot

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Terry Chin, MD, PhD, Associate Professor of Pediatrics, Pediatric Allergy/Immunology/Pulmonology, Department of Pediatrics, University of California Irvine School of Medicine; Associate Director, Miller Children's Hospital at Long Beach Memorial Medical Center
Terry 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 Thoracic Society, California Thoracic Society, Clinical Immunology Society, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

Coauthor(s)

Girija Natarajan, MD, Assistant Professor, Division of Neonatology, Children's Hospital of Michigan & Wayne State University
Girija Natarajan, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Ibrahim Abdulhamid, MD, Assistant Professor of Pediatrics, Wayne State University; Director of Pediatric Pulmonary Medicine, Clinical Director of Pediatric Sleep Laboratory, Children's Hospital of Michigan
Ibrahim Abdulhamid, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Sleep Medicine, and American Thoracic Society
Disclosure: Nothing to disclose.

Medical Editor

Susanna A McColley, MD, Director of Cystic Fibrosis Center; Head, Division of Pulmonary Medicine; Associate Professor, Department of Pediatrics, Children's Memorial Medical Center of Chicago, Northwestern University
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, and American Thoracic Society
Disclosure: Genentech Honoraria Speaking and teaching; Genentech Consulting fee Consulting; Novartis Consulting fee Consulting; Altus Consulting fee Consulting; Axcan Scandi Consulting fee Consulting; Boston Scientific Consulting fee Consulting

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Heidi Connolly, MD, Associate Professor of Pediatrics and Psychiatry, University of Rochester; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center
Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Michael R Bye, MD, Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society
Disclosure: Merck Honoraria Speaking and teaching

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.