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Congenital Pneumonia Treatment & Management

  • Author: Muhammad Aslam, MD; Chief Editor: Ted Rosenkrantz, MD  more...
Updated: Mar 02, 2016

Approach Considerations

Therapy in infants with neonatal pneumonia is multifaceted. The goals of therapy are to eradicate infection and provide adequate support of gas exchange to ensure the survival and eventual well being of the infant.

Evidence-supported options for targeted treatment of inflammation independent of antimicrobial therapy are severely limited.[37] There is considerable speculation that current antimicrobial agents, directed at killing invasive organisms, may transiently worsen inflammatory cascades and associated host injury because dying organisms release proinflammatory structural and metabolic constituents into the surrounding microenvironment. This is not to imply that eradication of invasive microbes should not be a goal; however, other methods of eradicating pathogens or methods of directly dealing with the pathologic inflammatory cascades await further definition.

Drainage of a restrictive or infected effusion or empyema may enhance clearance of the infection and will improve lung mechanics.

Even if the infection is eradicated, many hosts develop long-lasting or permanent pulmonary changes that adversely affect lung function, quality of life, and susceptibility to later infections.

In pneumonia resulting from noninfectious causes, the quest for targeted, effective, and safe anti-inflammatory therapy may be of even greater importance.

Go to Pneumonia, Pediatric and Afebrile Pneumonia Syndrome for more complete information on these topics. Additionally, see Surgical Treatment of Infections of the Lung, Pleura, and Mediastinum for more complete information on this topic.


Antimicrobial Therapy

Initial empiric antibiotics are selected according to the susceptibility pattern of the likely pathogens, experience at the institution, and knowledge of delivery of drugs to the suspected infected sites within the lung. Empiric use of azithromycin or other macrolides for presumed Ureaplasma infection is not currently evidence based and should be reserved for infants who have that organism recovered from a normally sterile site or who are critically ill and do not have a more likely cause of infection.[38, 39]

Because bacteremia is common as both a cause and a consequence of congenital pneumonia, attaining an adequate plasma concentration of the antimicrobial agent via a parenteral route is essential. Alveolar delivery of antibiotics typically occurs via diffusion of non–protein-bound drug and is usually satisfactory if plasma concentrations and alveolar perfusion are adequate.

At most institutions, initial empiric therapy consists of ampicillin and either gentamicin or cefotaxime. Dosage regimens vary according to gestational and postnatal age, as well as renal function. Observational studies have suggested increased adverse outcomes, including an increased risk of death, in neonates who receive cefotaxime rather than gentamicin as a routine component of initial empiric neonatal treatment.[40, 41]

Whether the adverse outcomes with cefotaxime are causal, coincidental, or secondary to some other associated factor is unclear. Nevertheless, in some circumstances (eg, renal dysfunction, hearing or ear abnormalities, gram-negative central nervous system infection, maternal myasthenia gravis, high local incidence of gentamicin-resistant but cefotaxime-sensitive organisms), cefotaxime may be preferable to gentamicin.

Isolation of a specific pathogen from a normally sterile site in the infant allows revision of therapy to the drug that is least toxic, has the narrowest antimicrobial spectrum, and is most effective. Dosing intervals for ampicillin, cefotaxime, gentamicin, and other antimicrobial agents typically require readjustment in the face of renal dysfunction or once the infant is older than 7 days (if the infant still requires antimicrobial therapy).

If gram-negative pneumonia is suspected and beta-lactam antibiotics are administered, some data suggest that continuous exposure to an antimicrobial concentration greater than the mean inhibitory concentration for the organism may be more important than the amplitude of the peak concentration. Intramuscular or intravenous therapy with the same total daily dose but more frequent dosing may be advantageous if the infant fails to respond to conventional dosing. Comparative data to confirm the superiority of this approach are lacking. Whether this approach offers any advantage with use of agents other than beta-lactams is unclear.

Studies in human adults have demonstrated that aminoglycosides reach the bronchial lumen marginally when administered parenterally, although alveolar delivery is satisfactory.[42, 43] Endotracheal treatment with aerosolized aminoglycosides has been reportedly effective for marginally susceptible organisms in bronchi, whereas cefotaxime appears to attain adequate bronchial concentrations via the parenteral route. Limited in vitro and animal data suggest that cefotaxime may retain more activity than aminoglycosides in sequestered foci, such as abscesses, although such foci are rare in congenital pneumonia, and adequate drainage may be more important than antimicrobial selection.

Recovery of a specific pathogen from a normally sterile site (eg, blood, urine, cerebrospinal fluid) permits narrowing the spectrum of antimicrobial therapy and may thus reduce the selection of resistant organisms and costs of treatment. Repeated culture of the site after 24-48 hours is usually warranted to ensure sterilization and to assess the efficacy of therapy.

Endotracheal aspirates are not considered to represent a normally sterile site, although they may yield an organism that is a true invasive pathogen. Reculture of an endotracheal aspirate that identified the presumptive pathogen in a particular case may not be helpful because colonization may persist even if tissue invasion has been terminated.

Decreasing respiratory support requirements, clinical improvement, and resolution revealed on radiographs also support the efficacy of therapy.

When appropriate, assess plasma antibiotic concentrations to ensure adequacy and reduce the potential for toxicity. Failure to recover an organism does not exclude an infectious etiology; continuation of empiric therapy may be advisable unless the clinical course or other data strongly suggests that a noninfectious cause is responsible for the presenting signs.

Although meconium is usually sterile, most clinicians opt for adjunctive antimicrobial therapy when meconium was present in the amniotic fluid because concurrent aspiration of pathogens or antecedent bacteremia as a cause of intrauterine meconium passage and subsequent aspiration usually cannot be excluded.

Continue to perform careful serial examinations for evidence of complications that may warrant a change in therapy or dosing regimen, surgical drainage, or other intervention.

The duration of antimicrobial therapy for neonatal pneumonia has not been rigorously assessed in comparative trials. Most clinicians treat infants for 7-10 days if clinical signs resolve rapidly. If positive results on culture were found at a normally sterile site, continuing treatment for 7-10 days following sterilization is prudent. Longer periods of therapy may be warranted if a sequestered focus, such as empyema or abscess, is seen or if metastatic infection develops. Herpes simplex infection with central nervous system involvement may require 21 or more days of antiviral treatment.


Respiratory Support

Adequate gas exchange depends not only on alveolar ventilation, but also on perfusion and gas transport capacity of the alveolar perfusate (ie, blood). Preservation of pulmonary and systemic perfusion is essential, using volume expanders, inotropes, afterload reduction, blood products, and other interventions (eg, inhaled nitric oxide) as needed. Excellent lung mechanics do little good if perfusion is not simultaneously adequate.

Criteria for institution of and weaning from supplemental oxygen and mechanical support are similar to those for other neonatal respiratory diseases. Be aware that lung disease in these patients is often structurally heterogeneous, with subpopulations of normally inflated, hyperinflated, atelectatic, obstructed, fluid-filled, and variably perfused alveoli that may require multiple adjustments of ventilatory pressures, flows, rates, times, and modalities.

A number of respiratory management issues require special consideration in newborn infants in whom pneumonia is suspected. These include airway patency, ventilatory support, and pulmonary hypertension.

Airway patency

Assurance of airway patency may be more challenging in neonates with pneumonia because of the often profuse, potentially obstructive secretions and mucopurulent exudates of variable viscosity. Judicious suctioning is warranted. Deep suctioning should be avoided because it can cause airway trauma and swelling, which, in turn, may cause large airway obstruction.

Gentle vibration and percussion is used in some centers to mobilize the secretions, although appropriately designed studies do not support routine use of this technique. At least one report cautions that long-term routine percussion may be associated with brain injury in premature infants with a birth weight less than 1500 g.[44] Potential benefit may exceed potential risks with targeted use in specific infants with secretion problems.

Use of mucolytic agents, such as acetylcysteine or recombinant DNase, may be required to mobilize dense inspissated secretions but also may induce bronchospasm and be poorly tolerated.

Any endotracheal tube requires careful positioning and may require periodic replacement to ensure patency. Endotracheal perfluorocarbon and exogenous surfactant lavage have both been suggested as possible means of safely mobilizing thick potentially obstructive material, including meconium, even from distal airways. Bronchoscopic removal may be plausible if the airway is sufficiently large.

Prevention or reduction of atelectasis may reduce bacterial growth and/or bacterial translocation.[45]

Comparative trials of sufficient size to document the safety and efficacy of these approaches are sparse.

Ventilatory support

Ventilatory support may be rendered unusually challenging by alveoli with variable degrees of inflation from the unpredictable distribution of surfactant inactivation, partial airway obstruction, and fluid exudation.

Take care to ensure that the airway pressures required to attain alveolar stability interfere as little as possible with myocardial function, venous return, and alveolar perfusion. A survey of neonatal intensive care units in the United Kingdom reported volume-targeted ventilation as the most commonly used modality for neonatal pneumonia.[46]

The use of high-frequency or patient-triggered ventilatory techniques may offer better recruitment of alveolar lung volume, but data are sparse.

Neonatal pneumonia is associated with surfactant inactivation and/or increased catabolism.[47] Exogenous surfactant may be beneficial in selected infants.[48] Although randomized controlled trials in human infants for this indication are lacking, animal studies and an increasing number of clinical reports have suggested the adjunctive utility of exogenous surfactant.[49, 50] Many clinicians elect to administer surfactant when mechanical ventilation is required with greater than 60% oxygen concentration. Time to clinical response and requirement for multiple doses are both reported to be greater than in infants with respiratory distress syndrome.

Bolus administration of surfactant may be considered for neonates with meconium aspiration syndrome and progressive respiratory failure; surfactant adminstration should also be considered in neonates with group B streptococcal pneumonia.[48]

A guideline from the American Academy of Pediatrics (AAP) advises that rescue treatment with surfactant may be considered for infants with hypoxic respiratory failure attributable to secondary surfactant deficiency (eg, meconium aspiration syndrome or pneumonia).[51] However, the AAP notes that is important for medical personnel to have the requisite technical and clinical expertise to administer surfactant safely and to deal with multisystem illness.

Pulmonary hypertension

Pulmonary hypertension with significant intrapulmonary and extrapulmonary shunting is not uncommon with pneumonia, especially in postterm, term, and near-term infants with sufficient pulmonary vascular smooth muscle to develop systemic or suprasystemic pulmonary vascular resistance.

The optimal therapeutic strategy for pulmonary hypertension remains unresolved. Increased systemic vascular resistance, paralysis, inhaled nitric oxide[52] and/or infused epoprostenol are vigorously used by many clinicians, whereas others advocate less aggressive approaches.

A randomized collaborative trial in the United Kingdom demonstrated that extracorporeal membrane oxygenation (ECMO) was significantly better than conventional therapy in preventing death; however, infants with pneumonia comprised only a fraction of the total study population.[53] Among all newborn infants who are sick enough to require ECMO, those with an underlying diagnosis of pneumonia have a higher mortality rate than those with all noninfectious diseases, except congenital diaphragmatic hernia.[54]


Other Supportive Measures

Red blood cells should be administered to achieve a hemoglobin concentration of 13-16 g/dL in the acutely ill infant, to ensure optimal oxygen delivery to the tissues.

Delivery of adequate amounts of glucose and maintenance of thermoregulation, electrolyte balance, and other elements of neonatal supportive care are also essential.



Attempts at enteral feeding often are withheld in favor of parenteral nutritional support until respiratory and hemodynamic status is sufficiently stable.



If appropriate respiratory, hemodynamic, or nutritional support cannot be safely and effectively administered at the hospital of birth, stabilize the neonate and transfer to a tertiary care neonatal intensive care unit.



Consider intrapartum antibiotic chemoprophylaxis with penicillin or another appropriate antimicrobial agent in mothers at risk for early-onset group B streptococcal disease. Risk factors are as follows:

  • Known colonization of birth canal by group B Streptococcus
  • Premature delivery
  • Membrane rupture more than 18 hours before delivery
  • Intrapartum fever
  • Group B streptococcal bacteriuria
  • History of previous infant with early-onset neonatal group B streptococcal infection

Consult the Red Book for the most current recommendations for infants at risk for group B streptococcal sepsis/pneumonia.[55]

Prevention strategies may include antepartum and intrapartum broad-spectrum antibiotic treatment in mothers with preterm rupture of membranes or in whom chorioamnionitis is suspected.

In the presence of particulate amniotic fluid meconium, suction the trachea immediately after birth if the infant is not vigorous.[56]

Currently, there is little evidence demonstrating the potential efficacy of the following interventions in neonates:

  • Elevating the head
  • Use of antireflux medications
  • Differential policies for oral care and changes of suction and ventilator tubing
  • Other potential interventions
Contributor Information and Disclosures

Muhammad Aslam, MD Associate Professor of Pediatrics, University of California, Irvine, School of Medicine; Neonatologist, Division of Newborn Medicine, Department of Pediatrics, UC Irvine Medical Center

Muhammad Aslam, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.


Mariam L Abdul-Latif, MD Neonatal-Perinatal Medicine Fellow, Department of Pediatrics, University of California, Irvine, School of Medicine

Mariam L Abdul-Latif, MD is a member of the following medical societies: American Academy of Pediatrics, Texas Medical Association, Texas Pediatric Society

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.

Brian S Carter, MD, FAAP Professor of Pediatrics, University of Missouri-Kansas City School of Medicine; Attending Physician, Division of Neonatology, Children's Mercy Hospital and Clinics; Faculty, Children's Mercy Bioethics Center

Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Pediatric Society, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, Society for Pediatric Research, National Hospice and Palliative Care Organization

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Eastern Society for Pediatric Research, American Medical Association, Connecticut State Medical Society, Society for Pediatric Research

Disclosure: Nothing to disclose.


Roger G Faix, MD Professor, Department of Pediatrics (Neonatology), University of Utah School of Medicine

Roger G Faix, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, American Society for Microbiology, National Perinatal Association, Society for Pediatric Research, and Utah Medical Association

Disclosure: Nothing to disclose.

  1. Barton L, Hodgman JE, Pavlova Z. Causes of death in the extremely low birth weight infant. Pediatrics. 1999 Feb. 103(2):446-51. [Medline].

  2. Duke T. Neonatal pneumonia in developing countries. Arch Dis Child Fetal Neonatal Ed. 2005 May. 90(3):F211-9. [Medline].

  3. Heron MP, Smith BL. Deaths: leading causes for 2003. Natl Vital Stat Rep. 2007 Mar 15. 55(10):1-92. [Medline].

  4. Nissen MD. Congenital and neonatal pneumonia. Paediatr Respir Rev. 2007 Sep. 8(3):195-203. [Medline].

  5. Feria-Kaiser C, Furuya ME, Vargas MH, Rodriguez A, Cantu MA,. Main diagnosis and cause of death in a neonatal intensive care unit: do clinicians and pathologists agree?. Acta Paediatr. 2002. 91(4):453-8. [Medline].

  6. Barnett ED, Klein JO. Bacterial infections of the respiratory tract. Remington JS, Klein JO, eds. Infectious Diseases of the Fetus and Newborn Infant. 6th ed. Philadelphia, Pa: Elsevier Saunders Co; 2006. 297-317.

  7. Bone RC, Grodzin CJ, Balk RA. Sepsis: a new hypothesis for pathogenesis of the disease process. Chest. 1997 Jul. 112(1):235-43. [Medline].

  8. Stoll BJ, Hansen NI, Higgins RD, et al. Very low birth weight preterm infants with early onset neonatal sepsis: the predominance of gram-negative infections continues in the National Institute of Child Health and Human Development Neonatal Research Network, 2002-2003. Pediatr Infect Dis J. 2005 Jul. 24(7):635-9. [Medline].

  9. Srinivasjois RM, Kohan R, Keil AD, Smith NM. Congenital Mycoplasma pneumoniae pneumonia in a neonate. Pediatr Infect Dis J. 2008 May. 27(5):474-5. [Medline].

  10. Kotecha S, Hodge R, Schaber JA, et al. Pulmonary Ureaplasma urealyticum is associated with the development of acute lung inflammation and chronic lung disease in preterm infants. Pediatr Res. 2004 Jan. 55(1):61-8. [Medline].

  11. Katz B, Patel P, Duffy L, Schelonka RL, Dimmitt RA, Waites KB. Characterization of ureaplasmas isolated from preterm infants with and without bronchopulmonary dysplasia. J Clin Microbiol. 2005 Sep. 43(9):4852-4. [Medline].

  12. Heggie AD, Bar-Shain D, Boxerbaum B, Fanaroff AA, O'Riordan MA, Robertson JA. Identification and quantification of ureaplasmas colonizing the respiratory tract and assessment of their role in the development of chronic lung disease in preterm infants. Pediatr Infect Dis J. 2001 Sep. 20(9):854-9. [Medline].

  13. Ballard HO, Bernard P, Whitehead V, et al. Determining the incidence of Ureaplasma spp. and its role in development of bronchopulmonary dysplasia. [Abstract 3858.111]. Pediatric Academic Societies Meeting 2009. Baltimore, MD. May 3, 2009. Available at Accessed: June 11, 2009.

  14. Morioka I, Fujibayashi H, Enoki E, Yokoyama N, Yokozaki H, Matsuo M. Congenital pneumonia with sepsis caused by intrauterine infection of Ureaplasma parvum in a term newborn: a first case report. J Perinatol. 2010 May. 30(5):359-62. [Medline].

  15. Fischer C, Meylan P, Bickle Graz M, et al. Severe postnatally acquired cytomegalovirus infection presenting with colitis, pneumonitis and sepsis-like syndrome in an extremely low birthweight infant. Neonatology. 2010 Jun. 97(4):339-45. [Medline].

  16. Sanchez MO, Chang AB. Congenital rubella pneumonitis complicated by Pneumocystis jiroveci infection with positive long term respiratory outcome: a case report and literature review. Pediatr Pulmonol. 2009 Dec. 44(12):1235-9. [Medline].

  17. Chang JH, Huang YL, Chen CC, Li SY. Vertical transmission of Neisseria gonorrhoeae to a female premature neonate with congenital pneumonia. J Formos Med Assoc. 2013 Oct. 112(10):648-9. [Medline].

  18. Hermoso Torregrosa C, Carrasco Zalvide M, Ferrer Castillo MT. Streptococcus pneumoniae: an unusual pathogen in neonatal sepsis of vertical transmission. Arch Bronconeumol. 2012 Nov. 48(11):425-6. [Medline].

  19. Patel S, DeSantis ER. Treatment of congenital tuberculosis. Am J Health Syst Pharm. 2008 Nov 1. 65(21):2027-31. [Medline].

  20. Varik RS, Shubha AM, Lewin M, Alexander B, Kini U, Das K. Infantile pulmonary tuberculosis: the great mimic. Pediatr Surg Int. 2012 Jun. 28(6):627-33. [Medline].

  21. Wang SM, Hsu CH, Chang JH. Congenital candidiasis. Pediatr Neonatol. 2008 Jun. 49(3):94-6. [Medline].

  22. Iqbal Q, Younus MM, Ahmed A, et al. Neonatal mechanical ventilation: Indications and outcome. Indian J Crit Care Med. 2015 Sep. 19 (9):523-7. [Medline].

  23. Chen CH, Wen HJ, Chen PC, Lin SJ, Chiang TL, Hsieh IC. Prenatal and postnatal risk factors for infantile pneumonia in a representative birth cohort. Epidemiol Infect. 2012 Jul. 140(7):1277-85. [Medline].

  24. Boo NY, Cheah IG. Risk factors associated with necrotising enterocolitis in very low birth weight infants in Malaysian neonatal intensive care units. Singapore Med J. 2012 Dec. 53(12):826-31. [Medline].

  25. Puri A, Yadav PS, Saha U, Singh R, Chadha R, Choudhary SR. A case series study of therapeutic implications of Type IIIb4: A rare variant of esophageal atresia and distal tracheoesophageal fistula. J Pediatr Surg. 2013 Jul. 48(7):1463-9. [Medline].

  26. Haney PJ, Bohlman M, Sun CC. Radiographic findings in neonatal pneumonia. AJR Am J Roentgenol. 1984 Jul. 143(1):23-6. [Medline].

  27. Wiswell TE, Baumgart S, Gannon CM, Spitzer AR. No lumbar puncture in the evaluation for early neonatal sepsis: will meningitis be missed?. Pediatrics. 1995 Jun. 95(6):803-6. [Medline].

  28. Sherman MP, Goetzman BW, Ahlfors CE, Wennberg RP. Tracheal aspiration and its clinical correlates in the diagnosis of congenital pneumonia. Pediatrics. 1980 Feb. 65(2):258-63. [Medline].

  29. Giacoia GP, Neter E, Ogra P. Respiratory infections in infants on mechanical ventilation: the immune response as a diagnostic aid. J Pediatr. 1981 May. 98(5):691-5. [Medline].

  30. Chaaban H, Singh K, Huang J, Siryaporn E, Lim YP, Padbury JF. The role of inter-alpha inhibitor proteins in the diagnosis of neonatal sepsis. J Pediatr. 2009 Apr. 154(4):620-622.e1. [Medline].

  31. Gokdemir Y, Cakir E, Kut A, Erdem E, Karadag B, Ersu R, et al. Bronchoscopic evaluation of unexplained recurrent and persistent pneumonia in children. J Paediatr Child Health. 2013 Mar. 49(3):E204-7. [Medline].

  32. Gauvin F, Dassa C, Chaibou M, et al. Ventilator-associated pneumonia in intubated children: comparison of different diagnostic methods. Pediatr Crit Care Med. 2003 Oct. 4(4):437-43. [Medline].

  33. Gauvin F, Lacroix J, Guertin MC, et al. Reproducibility of blind protected bronchoalveolar lavage in mechanically ventilated children. Am J Respir Crit Care Med. 2002 Jun 15. 165(12):1618-23. [Medline].

  34. Labenne M, Poyart C, Rambaud C, et al. Blind protected specimen brush and bronchoalveolar lavage in ventilated children. Crit Care Med. 1999 Nov. 27(11):2537-43. [Medline].

  35. Klein JO. Diagnostic lung puncture in the pneumonias of infants and children. Pediatrics. 1969 Oct. 44(4):486-92. [Medline].

  36. Wigglesworth JS. Perinatal Pathology. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1996. 131-57, 184-7.

  37. Wynn JL, Neu J, Moldawer LL, Levy O. Potential of immunomodulatory agents for prevention and treatment of neonatal sepsis. J Perinatol. 2009 Feb. 29(2):79-88. [Medline].

  38. Ballard HO, Bernard P, Hayes D, et al. Use of azithromycin for the prevention of bronchopulmonary dysplasia: a randomized, double-blind, placebo controlled trial. [Abstract 4515.2]. Pediatric Academic Societies Meeting 2009. Baltimore, MD. May 4, 2009. Available at Accessed: June 11, 2009.

  39. Ballard HO, Bernard P, Whitehead V, et al. Use of azithromycin for the early treatment of Ureaplasma spp. in preterm infants: a randomized, double-blind, placebo controlled trial. [Abstract 4515.3]. Pediatric Academic Societies Meeting 2009. Baltimore, MD. May 4, 2009. Available at Accessed: June 11, 2009.

  40. Clark RH, Bloom BT, Spitzer AR, Gerstmann DR. Empiric use of ampicillin and cefotaxime, compared with ampicillin and gentamicin, for neonates at risk for sepsis is associated with an increased risk of neonatal death. Pediatrics. 2006 Jan. 117(1):67-74. [Medline].

  41. de Man P, Verhoeven BA, Verbrugh HA, Vos MC, van den Anker JN. An antibiotic policy to prevent emergence of resistant bacilli. Lancet. 2000 Mar 18. 355(9208):973-8. [Medline].

  42. Braude AC, Hornstein A, Klein M, Vas S, Rebuck AS. Pulmonary disposition of tobramycin. Am Rev Respir Dis. 1983 May. 127(5):563-5. [Medline].

  43. Pennington JE. Penetration of antibiotics into respiratory secretions. Rev Infect Dis. 1981 Jan-Feb. 3(1):67-73. [Medline].

  44. Harding JE, Miles FK, Becroft DM, et al. Chest physiotherapy may be associated with brain damage in extremely premature infants. J Pediatr. 1998 Mar. 132(3 Pt 1):440-4. [Medline].

  45. van Kaam AH, Lachmann RA, Herting E, et al. Reducing atelectasis attenuates bacterial growth and translocation in experimental pneumonia. Am J Respir Crit Care Med. 2004 May 1. 169(9):1046-53. [Medline].

  46. Chowdhury O, Wedderburn CJ, Lee S, Hannam S, Greenough A. Respiratory support practices in infants born at term in the United Kingdom. Eur J Pediatr. 2012 Nov. 171(11):1633-8. [Medline].

  47. Carnielli VP, Zimmermann LJ, Hamvas A, Cogo PE. Pulmonary surfactant kinetics of the newborn infant: novel insights from studies with stable isotopes. J Perinatol. 2009 May. 29 Suppl 2:S29-37. [Medline].

  48. Keiser A, Bhandari V. The role of surfactant therapy in nonrespiratory distress syndrome conditions in neonates. Am J Perinatol. 2016 Jan. 33 (1):1-8. [Medline].

  49. Herting E, Gefeller O, Land M, et al. Surfactant treatment of neonates with respiratory failure and group B streptococcal infection. Members of the Collaborative European Multicenter Study Group. Pediatrics. 2000 Nov. 106(5):957-64; discussion 1135. [Medline].

  50. Herting E, Sun B, Jarstrand C, et al. Surfactant improves lung function and mitigates bacterial growth in immature ventilated rabbits with experimentally induced neonatal group B streptococcal pneumonia. Arch Dis Child Fetal Neonatal Ed. 1997 Jan. 76(1):F3-8. [Medline].

  51. [Guideline] Engle WA. Surfactant-replacement therapy for respiratory distress in the preterm and term neonate. Pediatrics. 2008 Feb. 121(2):419-32. [Medline]. [Full Text].

  52. NINOSG. Inhaled nitric oxide in full-term and nearly full-term infants with hypoxic respiratory failure. The Neonatal Inhaled Nitric Oxide Study Group. N Engl J Med. 1997 Feb 27. 336(9):597-604. [Medline].

  53. ECMO. UK collaborative randomised trial of neonatal extracorporeal membrane oxygenation. UK Collaborative ECMO Trail Group. Lancet. 1996 Jul 13. 348(9020):75-82. [Medline].

  54. IELSO. 1999 Summary Report of the Registry for International Extracorporeal Life Support Organization. 1999. 1-10.

  55. AAP. Red Book. Available at Accessed: November 18, 2010.

  56. Wiswell TE, Gannon CM, Jacob J, Goldsmith L, Szyld E, Weiss K, et al. Delivery room management of the apparently vigorous meconium-stained neonate: results of the multicenter, international collaborative trial. Pediatrics. 2000 Jan. 105(1 Pt 1):1-7. [Medline].

  57. Guzoglu N, Demirkol FN, Aliefendioglu D. Haemorrhagic pneumonia caused by Stenotrophomonas maltophilia in two newborns. J Infect Dev Ctries. 2015 May 18. 9(5):533-5. [Medline].

  58. Hermansen CL, Mahajan A. Newborn respiratory distress. Am Fam Physician. 2015 Dec 1. 92 (11):994-1002. [Medline].

Anteroposterior chest radiograph in an infant born at 28 weeks' gestation was performed following apnea and profound birth depression. Subtle reticulogranularity and prominent distal air bronchograms were consistent with respiratory distress syndrome, prompting exogenous surfactant and antimicrobial therapy. Initial smear of endotracheal aspirate revealed few neutrophils but numerous, small, gram-negative coccobacilli. Culture of blood and tracheal aspirate yielded florid growth of nontypeable Haemophilus influenzae.
Full-term infant (note ossified proximal humeral epiphyses, consistent with full term) with progressive respiratory distress from birth following delivery to a febrile mother through thick, particulate, meconium-containing fluid and recovery of copious meconium from the trachea. Right clavicle is fractured without displacement. Note the coarse dense infiltrates obscuring the cardiothymic silhouette bilaterally with superimposed prominent air bronchograms. Listeria monocytogeneswas recovered from the initial blood culture.
Patchy infiltrates most prominent along left cardiothymic margin in a full-term infant (note proximal humeral ossific nuclei) born to an afebrile woman 18 hours after membranes ruptured. The infant was initially vigorous but developed gradual onset of progressive respiratory distress beginning at 2 hours and prompting endotracheal intubation and transfer to a tertiary center at age 10 hours. Note blunting of the right costophrenic angle, a thin radiodense rim along the lateral right hemithorax, and a fluid line in the right major fissure, all consistent with pleural effusion. Gram staining of pleural fluid recovered at thoracentesis indicated occasional gram-negative bacilli. Tracheal aspirate, pleural fluid, and blood all yielded Escherichia coliupon culture. The dense right upper lobe may appear to suggest lobar infiltrate, but upward bowing of the fissure is more suggestive of volume loss, as in atelectasis, than the bulging picture expected with dense pneumonic change. This lobe appeared normal and appropriately inflated on a subsequent film 2 hours later, also suggestive of atelectasis. Umbilical venous catheter and endotracheal tube were positioned properly on the follow-up film.
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