AUTHOR AND EDITOR INFORMATION

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• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
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INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Pneumonia is an inflammatory pulmonary process that may originate in the lung or be a focal complication of a systemic process. Abnormalities of airway patency as well as alveolar ventilation and perfusion frequently ensue due to various mechanisms. These derangements may significantly alter gas exchange and dependent cellular metabolism in the many tissues and organs that determine survival and contribute to quality of life. Such pathologic problems, superimposed on the underlying difficulties associated with the transition from intrauterine to extrauterine life, pose critical challenges to the immature human organism. Recognition, prevention, and treatment of these problems are major factors in the care of high-risk newborn infants.

This article focuses on pneumonia that presents within the first 24 hours after birth. Although pneumonia is an important cause of morbidity and mortality among newborn infants, it remains a difficult disease to prospectively identify and treat. Clinical manifestations are often nonspecific, sharing respiratory and hemodynamic signs with a host of noninflammatory processes. Radiographic and laboratory findings also have limited predictive value. Attempts to identify specific microbes responsible for pneumonia are often unsuccessful for multiple reasons; for example, the organisms may be difficult to recover from intrapulmonary sites without contamination by airway commensals, the organisms may be uncultivable primarily or because of ongoing antimicrobial treatment, or inflammation may result from noninfectious causes, such as aspiration of meconium, amniotic contents, food, blood, and other agents.

Pathophysiology

The lungs assume sole responsibility for neonatal gas exchange following separation of the fetus from the placenta; such exchange includes both uptake of oxygen and release of carbon dioxide and other excretory gases. The exchange occurs by conduction of humidified atmospheric gas and mixed venous blood to the alveolar interface where rapid diffusion across the single cell layers of the alveolar epithelium and capillary endothelium attains near equilibrium under ideal circumstances.

Host defenses in the lung

To prevent and minimize injury and invasion by microorganisms and foreign substances, various defense mechanisms have evolved, both systemically and within the respiratory tract. Some mechanisms are nonspecific and are directed against any invasive agent, whereas others are targeted against only microbes or substances with specific antigenic determinants. Many of the defenses are compromised in the fetus and newborn infant, resulting in more frequent breaches and consequent disruption of normal lung structure and function.

Nonspecific defenses include the glottis and vocal cords, ciliary escalator, airway secretions, migratory and fixed phagocytes, nonspecific antimicrobial proteins and opsonins, and the normal relatively nonpathogenic airway flora. Anatomic structures of the upper airway and associated reflexes discourage particulate material from entering, while coordinated movement of the microscopic cilia on the tracheal and bronchial epithelia tends to sweep particles and mucous up the airway and away from the alveoli and distal respiratory structures.

Mucoid airway secretions provide a physical barrier that minimizes epithelial adhesion and subsequent invasion by microorganisms. These secretions typically contain complement components, fibronectin, and other proteins that bind to microbes and render them more susceptible to ingestion by phagocytes. Alveolar and distal airway secretions also include whole surfactant, which facilitates opsonization and phagocytosis of pathogens, as well as surfactant-associated proteins A and D (Sp-A and Sp-D), both of which modulate phagocytosis, phagocyte production of oxyradicals, and cytokine elaboration. 

The secretions also contain directly inhibitory and microbicidal agents, such as iron-binding proteins, lysozymes, and defensins. Typical benign airway commensals, such as alpha-hemolytic streptococci and coagulase-negative staphylococci, occupy mucosal sites and elaborate bacteriocins and other substances that prevent more pathogenic organisms from adhesion, replication, and possible opportunistic invasion.

Immunologic defense mechanisms targeted against particular pathogens typically emanate from specifically primed lymphocytes following presentation of processed antigen by macrophages. These mechanisms include cytotoxic, killer, suppressor, and memory functions; systemic and secretory antibodies; and consequent cascades of cytokines, complement, vasomotor regulatory molecules, hemostatic factors, and other agents. Secretory antibodies are typically multimeric and contain secretory component and J chains that render them more opsonic and more resistant to microbial proteases. Many of the biochemical cascades triggered by specific immune responses serve to localize microbial invasion, amplify and focus recruitment of phagocytes to the affected sites, and directly disrupt the structural and metabolic integrity of the microbes.

Newborn infants typically have sterile respiratory mucosa at birth, with subsequent uncontested colonization by microorganisms from the mother or environment. Accelerated access to distal respiratory structures and bypass of much of the ciliary escalator occur in infants who require endotracheal intubation. In these infants, increased physical disruption of epithelial and mucous barriers also occurs. In addition, interventional exposure to high oxygen concentrations, excessive airway pressures, and large intrapulmonary gas volumes may interfere with ciliary function and mucosal integrity.

Secretory antibodies and mucosal lymphoid tissue are absent or minimally functional for the first month of life postnatally. Systemic antibodies may enter pulmonary tissues but usually consist primarily of passively transmitted maternal antibodies, with reduced transplacental transport of maternal antibodies before 32 weeks' gestation. Specific systemic antibodies can be generated, but the many components of the necessary immunologic machinery are relatively sluggish.

Circulating complement components are present at approximately 50% of the concentration found in older children, although components of the alternative pathway are present in sufficient quantities to serve as effective opsonins.

The neonatal granulocyte number frequently decreases in response to early infection, whereas the phagocytes that are present often move much more sluggishly to the inflammatory focus, whether it is a microorganism or inanimate debris. Once at the targeted sites, phagocytes often ingest the invaders less efficiently, although intracellular microbicidal activities appear normal. Intercellular communication via cytokines and other mediators is blunted.

The net result of these and other developmental aberrations is that the fetal and neonatal inflammatory response is slower, less efficient, and much less focused than in older children. Infection is less likely to be localized and effectively inhibited by host defenses alone. Inflammation from particulate debris and other foreign substances is isolated less effectively and the injurious effector portions of the inflammatory cascade are targeted much less finely.

Pathogenesis

In neonatal pneumonia, pulmonary and extrapulmonary injuries are caused directly and indirectly by invading microorganisms or foreign material and by poorly targeted or inappropriate responses by the host defense system that may damage healthy host tissues as badly or worse than the invading agent. Direct injury by the invading agent usually results from synthesis and secretion of microbial enzymes, proteins, toxic lipids, and toxins that disrupt host cell membranes, metabolic machinery, and the extracellular matrix that usually inhibits microbial migration.

Indirect injury is mediated by structural or secreted molecules, such as endotoxin, leukocidin, and toxic shock syndrome toxin-1, which may alter local vasomotor tone and integrity, change the characteristics of the tissue perfusate, and generally interfere with the delivery of oxygen and nutrients and removal of waste products from local tissues.

The activated inflammatory response often results in targeted migration of phagocytes, with the release of toxic substances from granules and other microbicidal packages and the initiation of poorly regulated cascades (eg, complement, coagulation, cytokines). These cascades may directly injure host tissues and adversely alter endothelial and epithelial integrity, vasomotor tone, intravascular hemostasis, and the activation state of fixed and migratory phagocytes at the inflammatory focus. The role of apoptosis (noninflammatory programmed cell death) in pneumonia is poorly understood.

On a macroscopic level, the invading agents and the host defenses both tend to increase airway smooth muscle tone and resistance, mucous secretion, and the presence of inflammatory cells and debris in these secretions. These materials may further increase airway resistance and obstruct the airways, partially or totally, causing airtrapping, atelectasis, and ventilatory dead space. In addition, disruption of endothelial and alveolar epithelial integrity may allow surfactant to be inactivated by proteinaceous exudate, a process that may be exacerbated further by the direct effects of meconium or pathogenic microorganisms.

In the end, conducting airways offer much more resistance and may become obstructed, alveoli may be atelectatic or hyperexpanded, alveolar perfusion may be markedly altered, and multiple tissues and cell populations in the lung and elsewhere sustain injury that increases the basal requirements for oxygen uptake and excretory gas removal at a time when the lungs are less able to accomplish these tasks.

Alveolar diffusion barriers may increase, intrapulmonary shunts may worsen, and ventilation-perfusion mismatch may further impair gas exchange despite endogenous homeostatic attempts to improve matching by regional vasoconstriction or bronchoconstriction. Because the myocardium has to work harder to overcome the alterations in pulmonary vascular resistance that accompany the above changes of pneumonia, the lungs may be less able to add oxygen and remove carbon dioxide from mixed venous blood for delivery to end organs. The spread of infection or inflammatory response, either systemically or to other focal sites, further exacerbates the situation.

Frequency

International

Congenital pneumonia frequently occurs in newborn infants, although reported rates vary considerably depending on the diagnostic criteria used and the characteristics of the population under study. Most reports cite frequencies in the range of 5-50 per 1000 live births, with higher rates in the settings of maternal chorioamnionitis, prematurity, and meconium in the amniotic fluid.

Mortality/Morbidity

• Determination of mortality rates among infants with congenital pneumonia is complicated by variations in diagnostic criteria. Among infants with congenital pneumonia associated with proven blood-borne infection, mortality is in the range of 5-10%, with rates as high as 30% in infants with very low birth weight.
• Pneumonia is a contributing factor in 10-25% of all deaths that occur in neonates younger than 30 days.

Race

No increased risk associated with race or ethnic group has been well documented.

Sex

No increased risk associated with sex has been well documented.

Age

Congenital pneumonia can occur at any gestational age associated with potential extrauterine survival.

CLINICAL

Section 3 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
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• Follow-up
• Miscellaneous
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History

Diagnostic criteria remain controversial in the absence of histopathologic specimens. Criteria range from very liberal (to minimize the probability of missing a case) to very stringent (to minimize the possibility of labeling some other condition inappropriately). An example of the former includes only respiratory difficulties and persistent radiographic evidence of infiltrates. More stringent standards often mandate the additional presence of laboratory markers of systemic inflammation and inflammatory respiratory secretions (using quantitative or semiquantitative threshold criteria). Diagnosis in the clinical setting is usually based on a combination of historical, physical, radiographic, microbiologic, and laboratory findings.

• Prenatal features that suggest an increased risk for congenital pneumonia include the following:
• • Unexplained preterm labor
  • Rupture of membranes before the onset of labor
  • Membrane rupture more than 18 hours before delivery
  • Maternal fever (>38°C/100.4°F)
  • Uterine tenderness
  • Foul-smelling amniotic fluid
  • Infection of the maternal genitourinary tract
  • Previous infant with neonatal infection
  • Nonreassuring fetal well-being test results
  • Fetal tachycardia
  • Meconium in the amniotic fluid
  • Recurrent maternal urinary tract infection
  • Gestational history of illness consistent with an organism known to have transplacental pathogenic potential
• Review antenatal screening tests for infection, such as serologic tests for syphilis and birth canal tests for Neisseria gonorrhoeae, Chlamydia species, or group B Streptococcus, as well as any treatment courses and testing for cure.
• Intrapartum antibiotic therapy reduces the risk of postpartum maternal infection and infection of the infant in the presence of some of these risk factors but does not eliminate the risk. The potential for selection of pathogens resistant to antibiotics used for intrapartum therapy remains controversial.
• Absence of these risk factors does not exclude pneumonia.

Physical

Physical findings may be pulmonary, systemic, or localized. Many extrapulmonary findings are nonspecific and may be seen in many other common neonatal conditions. Some signs of respiratory distress cannot be manifested if the infant is affected by other processes that result in apnea, such as poor tolerance of labor, exposure to transplacental respiratory depressants, or CNS anomaly or injury.

• Pulmonary findings - All findings not necessarily present in all affected infants
• • Tachypnea (respiratory rate >60/min) may be present.
  • Expiratory grunting may occur.
  • Accessory respiratory muscle recruitment, such as nasal flaring and retractions at subcostal, intercostal, or suprasternal sites, may occur.
  • Airway secretions may vary substantially in quality and quantity but are most often profuse and progress from serosanguineous to a more purulent appearance. White, yellow, green, or hemorrhagic colors and creamy or chunky textures are not infrequent.
  • If aspiration of meconium, blood, or other proinflammatory fluid is suspected, other colors and textures reflective of the aspirated material may be seen.
  • Rales, rhonchi, and cough are all observed much less frequently in infants with pneumonia than in older individuals. If present, they may be caused by noninflammatory processes, such as congestive heart failure, condensation from humidified gas administered during mechanical ventilation, or endotracheal tube displacement. Although alternative explanations are possible, these findings should prompt careful consideration of pneumonia in the differential diagnosis.
  • Cyanosis of central tissues, such as the trunk, implies a deoxyhemoglobin concentration of approximately 5 g/dL or more and is consistent with severe derangement of gas exchange from severe pulmonary dysfunction as in pneumonia, although congenital structural heart disease, hemoglobinopathy, polycythemia, and pulmonary hypertension (with or without other associated parenchymal lung disease) must be considered.
  • Infants may have external staining or discoloration of skin, hair, and nails with meconium, blood, or other materials when they are present in the amniotic fluid. The oral, nasal, and, especially, tracheal presence of such substances is particularly suggestive of aspiration.
  • Increased respiratory support requirements such as increased inhaled oxygen concentration, positive pressure ventilation, or continuous positive airway pressure are commonly required before recovery begins.
  • Infants with pneumonia may manifest asymmetry of breath sounds and chest excursions, which suggest air leak or emphysematous changes secondary to partial airway obstruction.
• Systemic findings - Similar to signs and symptoms seen in sepsis or other severe infections
• • Temperature instability
  • Skin rash
  • Jaundice at birth
  • Tachycardia
  • Glucose intolerance
  • Abdominal distention
  • Hypoperfusion
  • Oliguria
• Localized findings
• • Conjunctivitis
  • Vesicles or other focal skin lesions
  • Unusual nasal secretions
  • Erythema, swelling, growth, unusual drainage, or asymmetry of other structures suggestive of inflammation
• Other findings
• • Adenopathy suggests long-standing infection and should suggest a more chronic causative agent.
  • Hepatomegaly from infection may result from the presence of some chronic causative agents, cardiac impairment, or increased intravascular volume. Apparent hepatomegaly may result if therapeutic airway pressures result in generous lung inflation and downward displacement of a normal liver.

Causes

Pneumonia that becomes clinically evident within 24 hours of birth may originate at 3 different times. The 3 types often overlap, and assigning a particular pneumonic episode to one of these categories may be difficult. The 3 categories of congenital pneumonia are: (1) true congenital pneumonia, (2) intrapartum pneumonia, and (3) postnatal pneumonia. Not all pneumonia diagnosed in the first 24 hours of life is infectious; nonetheless, many cases are infectious and benefit from targeted antimicrobial therapy.

True congenital pneumonia

• True congenital pneumonia is already established at birth. True congenital pneumonia may be established long before birth or relatively shortly before birth.
• The infant has clinical signs of pneumonia almost immediately after birth. Further deterioration is frequent as the process progresses and the infant is confronted with the exigencies of adapting to extrauterine existence.
• If the infant tolerated labor poorly or has been exposed to agents that depress respiratory effort, the infant may initially be apneic, with no ability to manifest signs of respiratory distress.
• Transmission of congenital pneumonia usually occurs via 1 of 3 routes:
• • Hematogenous transmission
  • • If the mother has a bloodstream infection, the microorganism can readily cross the few cell layers that separate the maternal from the fetal circulation at the villous pools of the placenta.
  • • The mother may be febrile or have other signs of infection, depending on the integrity of her host defenses, the responsible organism, and other considerations.
    • Transient bacteremia following daily activities, such as brushing teeth, defecating, and other potential disruptions of colonized mucoepithelial surfaces, is well known and may result in transmission without significant maternal illness.
    • The likelihood of hematogenous transmission is increased if the mother has continuous bloodstream infection with a relatively large quantity of microorganisms. In this case, the mother is more likely to have suggestive signs and symptoms.
    • Because host defenses are limited in fetuses, dissemination and illness may result. The fetus is likely to have systemic disease.
  • Ascending transmission: Ascending infection from the birth canal and aspiration of infected or inflamed amniotic fluid have significant common features. Infected amniotic fluid often involves ascending pathogens from the birth canal but may result from hematogenous seeding or direct introduction during pelvic examination, amniocentesis, placement of intrauterine catheters, or other invasive procedures. Ascension may occur with or without ruptured amniotic membranes.
  • Transmission via aspiration: Most bacterial infections produce clinical signs of infection in the mother, but infections may not be evident if the membranes rupture shortly after inoculation, similar to drainage of an abscess. Some nonbacterial organisms, such as Ureaplasma urealyticum, may be present in the amniotic cavity for long periods and cause minimal symptoms in the mother. If the fetus aspirates infected fluid prior to delivery, organisms that reach the distal airways or alveoli may need to cross only 2 cell layers (alveolar epithelium, capillary endothelium) to enter the bloodstream. Typically, these infants present with more pulmonary than systemic signs, but this is not always the case.

Intrapartum pneumonia

• Intrapartum pneumonia is acquired during passage through the birth canal.
• Intrapartum pneumonia may be acquired via hematogenous or ascending transmission, or it may result from aspiration of infected or contaminated maternal fluids or from mechanical or ischemic disruption of a mucosal surface that has been freshly colonized with a maternal organism of appropriate invasive potential and virulence.
• Infants who aspirate proinflammatory foreign material, such as meconium or blood, may manifest pulmonary signs immediately after or very shortly after birth.
• Infectious processes often have a honeymoon period of a few hours before sufficient invasion, replication, and inflammatory response have occurred to cause clinical signs.

Postnatal pneumonia

• Postnatal pneumonia in the first 24 hours of life originates after the infant has left the birth canal.
• Postnatal pneumonia may result from some of the same processes described above, but infection occurs after the birth process.
• Colonization of a mucoepithelial surface with an appropriate pathogen from a maternal or environmental source and subsequent disruption allows the organism to enter the bloodstream, lymphatics, or deep parenchymal structures.
• The frequent use of broad-spectrum antibiotics encountered in many obstetrical services and neonatal intensive care units (NICUs) often results in predisposition of an infant to colonization by resistant organisms of unusual pathogenicity. Invasive therapies typically required in these infants often allow microbes accelerated entry into deep structures that ordinarily are not easily accessible.
• Enteral feedings may result in aspiration events of significant inflammatory potential. Indwelling feeding tubes may further predispose infants to gastroesophageal reflux and other aspiration events. These infants are often relatively asymptomatic at birth or manifest noninflammatory pulmonary disease consistent with gestational age, but develop signs that progress well after 24 hours.

Other types of pneumonia

• Noninfectious pneumonia: This may occur in the first 24 hours of life.
• Infectious pneumonia
• • Organisms responsible for infectious pneumonia typically mirror those responsible for early onset neonatal sepsis. This is not surprising in view of the role that maternal genitourinary and gastrointestinal tract flora play in both processes. Group B Streptococcus was the most common bacterial isolate in most locales from the late 1960s to the late 1990s, when the impact of intrapartum chemoprophylaxis in reducing neonatal and maternal infection by this organism became evident. Escherichia coli has become the most common bacterial isolate among very low birth weight infants (£1500 g) since that time. Other prominent bacterial organisms include the following:
  • • Nontypeable Haemophilus influenzae
    • Other gram-negative bacilli
    • Listeria monocytogenes
    • Enterococci
    • Occasionally, Staphylococcus aureus
  • Among nonbacterial potential pathogens, U urealyticum has been recovered quite frequently from endotracheal aspirates shortly after birth in infants with very low birth weight and has been associated with various adverse pulmonary outcomes, including bronchopulmonary dysplasia. However, whether this organism is causal or simply a marker of increased risk is unclear.
  • Agents of chronic congenital infection, such as cytomegalovirus, Treponema pallidum, Toxoplasma gondii, and others, may cause pneumonia in the first 24 hours of life. Clinical presentation usually involves other organ systems as well.
  • Chlamydia organisms presumably are transmitted at birth during passage through an infected birth canal, although most infants are asymptomatic during the first 24 hours and develop pneumonia only after the first 2 weeks of life.
  • Respiratory pathogens, such as respiratory syncytial virus, influenza, adenovirus, and others, may be transmitted by contact with infected family members or caregivers shortly after birth, but infection by these organisms rarely is becomes apparent during the first 24 hours.

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Alveolar-capillary dysplasia
Arrhythmia
Asphyxia
Bronchial duplication
Chest wall injury or anomaly
Choanal atresia
Chylothorax
Diaphragmatic eventration
Heart block
Intracranial hemorrhage
Laryngeal cleft
Laryngeal nerve injury
Neuromuscular disorders
Phrenic nerve injury
Pulmonary hemorrhage
Pulmonary hypoplasia
Pulmonary lymphangiectasia
Spinal injury
Surfactant-related protein B deficiency
Tachycardia syndromes
Tracheoesophageal fistula
Transplacental medications
Vascular catheter accident
Other causes of airway obstruction
Other congenital heart diseases
Other inborn errors of metabolism
Other neuromuscular diseases

Consider any other diseases that may present with respiratory dysfunction in the first 24 hours of life.

Consider that any of the conditions listed above may have superimposed pneumonia as well.

WORKUP

Section 5 of 11  

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• Differentials
• Workup
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

The most useful laboratory tests for congenital pneumonia facilitate the identification of an infecting microorganism. Results can be used for therapeutic decisions as well as prognostic and infection control considerations.

• Culture
• • Conventional bacteriologic culture is used most widely and is currently most helpful.
  • Aerobic processing is sufficient for recovery of most responsible pathogens.
  • Although the foul smell of amniotic fluid in the setting of maternal chorioamnionitis is often attributable to anaerobes, these organisms are seldom shown to be causative.
  • Culture of fungi, viruses, U urealyticum, and other nonbacterial organisms often requires different microbiologic processing but may be warranted in suggestive clinical settings.
• Blood culture
• • Blood culture with at least 1 mL of blood from an appropriately cleaned and prepared peripheral venous or arterial site is essential because many neonatal pneumonias are hematogenous in origin and others serve as a focus for secondary seeding of the bloodstream.
  • Blood culture samples drawn through freshly placed indwelling vascular catheters may be helpful, but the possibility of contamination rises the longer the catheter is in place.
  • Multiple cultures of blood from different sites and/or those drawn at different times may increase culture yield, but limited circulating blood volume precludes this as the standard of care in neonates.
• Culture of specimens from lumbar puncture
• • Routine culture and analysis of spinal fluid in infants in whom congenital pneumonia is suspected is controversial because the yield is low and many infants with respiratory support requirements do not tolerate lumbar puncture well.
  • Spinal fluid may yield a pathogen when blood does not, especially following maternal antibiotic pretreatment.
  • Presence of a pathogen in the spinal fluid may indicate the need for alteration in the selection, dosage, and duration of antibiotic therapy even if cultures from other sites yield the same organism.
• Urine culture: During the first 3 days of life, urine culture is unlikely to be helpful because most urinary tract infections at this age are hematogenous.
• Culture of specimens from endotracheal aspiration
• • Culture and Gram stain of an endotracheal aspirate obtained by aseptic technique as soon as possible after intubation may be useful.
  • Under typical circumstances, airway commensals take as long as 8 hours to migrate down the trachea. At least one study demonstrated that culture of endotracheal aspirates obtained within 8 hours of birth correlates very well with blood culture results and probably reflects aspirated infected fluid. The longer the tube has been in place, the greater the likelihood that recovered organisms represent colonizing organisms rather than invasive pathogens; nonetheless, recovery of a single recognized pathogen in large quantities may be helpful in the selection of antibiotic therapy, especially if culture results from normally sterile sites are negative.
  • The absence of significant inflammatory cells in an endotracheal aspirate or other respiratory specimen suggests that organisms recovered from that site are unlikely to be truly invasive (unless the infant is markedly leukopenic). Thus, the organism represents colonization of the respiratory tract and not infection.
• Culture from extrapulmonary sites
• • Detection of microorganisms at inflamed extrapulmonary sites may be helpful because concurrent involvement of the lungs is not rare.
  • Studies of abscesses, conjunctivitis, skin lesions, and vesicles may be fruitful.
  • Take care to ensure that the specimen submitted is as free of contamination as possible. Tests such as organism-specific DNA probe or polymerase chain reaction (PCR)–based assay are less likely to be affected by such factors.
• Culture from other respiratory sites
• • Pleural fluid: In the presence of radiographically visible fluid, careful positioning of the infant and thoracentesis after sterile preparation of the sampling site may yield diagnostic findings on Gram stain, direct microscopy, and/or culture. Ultrasonography may reveal smaller fluid pockets and facilitate safer sampling under direct visualization. Although data from neonates are insufficient to draw conclusions, studies in older populations suggest a very high correlation with culture of lung tissue and/or blood.
  • Bronchoscopic alveolar lavage: Quantitative culture techniques have been assessed in non-neonatal populations and reported to offer a specificity of >80% depending on the threshold selected (values from >100 to 100,000 cfu/mL have been used). Data from studies of neonates with suspected congenital pneumonia are lacking.
  • Nonbronchoscopic protected specimen brush: Nondirected specimens have been obtained through endotracheal tubes 3 mm or greater internal diameter and intuitively appear to offer decreased probability of contamination. Data from neonates are sparse at present. Unlike bronchoscopically obtained specimens, ensuring sampling from a particular involved site is more difficult.
  • Lung puncture: Although used much less frequently than in previous decades, this technique may still be useful in circumstances in which pleural and subpleural lung surfaces are visibly involved and can be well-localized. Risk-benefit ratio merits careful consideration given the risk of such complications as pneumothorax, broncho-pleural fistula, hemothorax, and sampling a nondiagnostic site. This is a high-risk procedure and should not be considered a routine procedure in the diagnosis or treatment of pneumonia in the neonate.
• Limitations of cultures
• • A number of factors may interfere with the ability to grow a likely pathogen from the sites noted, including (but not limited to) the following: (1) pretreatment with antibiotics that limit in vitro but not in vivo growth, (2) contaminants that overgrow the pathogen, (3) pathogens that do not replicate in currently available culture systems,  and (4 ) patients in whom the process is inflammatory but not infectious, such as meconium aspiration.
  • Techniques that may help overcome some of these limitations include antigen detection, nucleic acid probes, PCR-based assays, or serologic tests.
  • Although once widely used, tests such as latex agglutination for detection of group B streptococcal antigen in urine, serum, or other fluids have fallen into disfavor because of poor predictive value; however, new generations of non–culture-based technologies continue to undergo development and may be more accurate and widely available in the future.
• Serologic tests
• • Serologic tests have limited use but may offer some insights in congenital pneumonia secondary to cytomegalovirus or toxoplasmosis.
  • Serologic tests for syphilis may suggest or confirm the presence of pneumonia alba, particularly in high-risk populations.
  • Giacoia and colleagues espoused the value of assessing antibody responses in acute and convalescent sera from infants using flora recovered from endotracheal aspirates.¹ This usually permits diagnosis only retrospectively, but may be useful in infants who fail to adequately respond to empiric therapy or for epidemiologic purposes.
  • Concerns persist regarding the specificity of such tests in distinguishing invasion from colonization.
• Markers of inflammation
• • The use of markers of inflammation to support a diagnosis of suspected infection, including pneumonia, remains controversial.
  • Various indices derived from differential leukocyte counts have been used most widely for this purpose, although noninfectious causes of such abnormal results are numerous. Many reports have been published regarding infants with proven infection who initially had neutrophil indices within reference ranges.
  • Quantitative measurements of C-reactive protein, procalcitonin, cytokines (eg, interleukin-6), and batteries of acute-phase reactants have been touted to be more specific but are plagued by concerns regarding limited positive predictive value.
  • • Lag from infection to abnormalities
    • Use of serial measurements, especially high negative predictive value
  • These tests may be useful in assessing the resolution of an inflammatory process, including infection, but they are not sufficiently precise to establish a diagnosis without additional supporting information. Decisions about antimicrobial therapy should not be based on inflammatory markers alone.

Imaging Studies

• Radiography
• • Numerous radiographic patterns are consistent with neonatal pneumonia and a multitude of other pathologic processes. A synthesis of all available information and careful consideration of the differential diagnosis is essential to establishing the diagnosis, although empiric antimicrobial treatment usually cannot be deferred because of inability to prospectively exclude the diagnosis.
• • A well-centered, appropriately penetrated, anteroposterior chest radiography is essential, although other views may be warranted to clarify anatomic relationships and air-fluid levels.
  • Be aware that any image reflects conditions only at the instant when the study was performed. Because neonatal lung diseases, including pneumonia, are dynamic, initially suggestive images may require reassessment based on subsequent clinical course and findings in later studies.
  • When considering pneumonia, devote particular attention to the following:
  • • Costophrenic angles
    • Pleural spaces and surfaces
    • Diaphragmatic margins
    • Cardiothymic silhouette
    • Pulmonary vasculature
    • Right major fissure
    • Air bronchograms overlying the cardiac shadow
    • Lung expansion
    • Patterns of aeration
  • Diffuse relatively homogeneous infiltrates that resemble the ground-glass pattern of respiratory distress syndrome are suggestive of a hematogenous process, although aspiration of infected fluid with subsequent seeding of the bloodstream cannot be excluded.
  • Patchy irregular densities that obscure normal margins are suggestive of antepartum or intrapartum aspiration, especially if such opacities are distant from the hilus.
  • Patchy irregular densities in dependent areas that are more prominent on the right side are more consistent with postnatal aspiration.
  • Generalized hyperinflation with patchy infiltrates suggests partial airway obstruction from particulate or inflammatory debris, although the contribution of positive airway pressure from respiratory support must be considered.
  • Pneumatoceles (especially with air-fluid interfaces) and prominent pleural fluid collections also support the presence of infectious processes.
  • Single or multiple prominent air bronchograms 2 or more generations beyond the mainstem bronchi reflect dense pulmonary parenchyma (possibly an infiltrate) highlighting the air-filled conducting airways.
  • A well-defined dense lobar infiltrate with bulging margins is unusual.
  • Lateral or oblique projections may help to better define structures whose location and significance are unclear.
• Ultrasonography: Ultrasonography may be helpful in selected circumstances. Ultrasonography is particularly useful for identifying and localizing fluid in the pleural and pericardial spaces. However, the presence of air within the lungs limits the use of ultrasonography.
• CT scanning or MRI: These imaging modalities may be helpful in selected circumstances. CT or MRI may be helpful for evaluating suspected tumors, aberrant vessels, sequestered lobes, or other primary pulmonary anomalies and for establishing the presence of infiltrate, atelectasis or other acquired processes.

Procedures

• Thoracentesis
• • If significant pleural fluid is detected radiographically or sonographically, consider thoracentesis for Gram stain, culture, and biochemical tests.
  • The risk of pneumothorax or laceration of intercostal vessels is real but can be minimized by the use of proper technique, including use of the Z-technique (stretching the skin down over the entry site, so that release after the procedure will permit the return of tissues to their usual location with occlusion of the path of the needle), entry over the superior rib margin at a dependent site where fluid is most likely to collect, continuous aspiration once the skin is penetrated, and no further advancement once fluid is obtained.
  • This procedure may be therapeutic as well as diagnostic if the pleural fluid is impinging on lung or cardiac function.
• Bronchoscopy: Transbronchial biopsy and guided aspiration or brush specimens obtained via direct bronchoscopy may be advantageous in some circumstances. The technique of direct rigid bronchoscopy may be used in larger infants; fiberoptic technique is occasionally possible in smaller infants or infants in whom the site is not easily reached using the rigid technique. Both this technique and protected brush tracheal aspirate sampling may not be well tolerated in infants with significant lung disease and poor gas exchange who are very dependent on continuous positive pressure ventilation.
• Protected brush tracheal aspirate sampling
• • Sites distant from the larger bronchi often cannot be sampled.
  • Specimens may have an increased risk of contamination with oral or airway commensals compared with bronchoscopic sampling but are thought to be more accurate than a conventional endotracheal aspirate.
• Lung aspiration
• • If a prominent infiltrate can be adequately localized in multiple planes, direct aspiration of the infected lung may be performed for culture or biopsy.
  • Lung aspiration is associated with a greater risk of postprocedural air leak and usually requires a larger-bore needle than is used to obtain pleural fluid.
  • Because the risk associated with this procedure is high, this technique is usually reserved for circumstances in which empiric therapy is failing, less invasive cultures and detection tests are unrewarding, and/or the infant continues to deteriorate.
  • With advances in surgical techniques and increased experience, many clinicians prefer to seek open surgical biopsy or thoracoscopic sampling in such circumstances, especially because success and specimen size are greater and the ability to deal directly with any complication is enhanced.

Histologic Findings

Tissue samples of lung tissue in human infants have typically been obtained from an unrepresentative population. The sample population usually includes only infants with severe pulmonary disease that results in death or threatens to do so or infants who die of other causes and have coincidental sampling of the lung. Consequently, direct observations regarding histologic changes in mild or moderate pneumonia are sparse and are often supplemented by extrapolation from animal disease models, human adults with similar diseases, or more severe cases in human infants that resulted in death or biopsy. Despite these limitations, certain observations in congenital pneumonia recur, whether or not a specific pathogen is implicated.

Macroscopically, the lung may have diffuse, multifocal, or very localized involvement with visibly increased density and decreased aeration. Frankly hemorrhagic areas and petechiae on pleural and intraparenchymal surfaces are common. Airway and intraparenchymal secretions may range from thin and watery to serosanguineous to frankly purulent and frequently are accompanied by small-to-moderate pleural effusions that display variable concentrations of inflammatory cells, protein, and glucose.

Frank empyema and abscesses are unusual in newborn infants. Particulate meconium or vernix may be visible, especially in the more proximal airways, following aspiration episodes. Superimposed changes, such as air leak, emphysema, and sloughed airway mucosa, may be seen as a consequence of volutrauma, pressure-related injury, oxygen toxicity, and other processes that reflect the vigorous respiratory support often provided to these infants in an attempt to manage derangements of gas exchange caused by the underlying illness.

With conventional microscopy, inflammatory cells are particularly prominent in alveoli and airways. Mononuclear cells (macrophages, natural killer cells, small lymphocytes) are usually noted early, and granulocytes (eosinophils, neutrophils) typically become more prominent later. Microorganisms of variable viability or particulate debris may be observed within these cells. If systemic neutropenia is present, the number of inflammatory cells may be reduced. Alveoli may be atelectatic from surfactant destruction or dysfunction, partially expanded with proteinaceous debris (often resembling hyaline membranes), or hyperexpanded secondary to partial airway obstruction from inflammatory debris or meconium.

Microscopic examination of tissue following polyclonal immunohistochemistry staining can identify the herpes virus.

Hemorrhage in the alveoli and in distal airways is frequent. Vascular congestion is common; vasculitis and perivascular hemorrhage are seen less frequently. Inflammatory changes in interstitial tissues are less common in newborns than in older individuals.

Examination of the placenta may be useful. An unusually large placenta with a thick umbilical cord or necrotizing funisitis is suggestive of congenital syphilis, with an increased risk of congenital pneumonia alba. Although results of early maternal serologic screening may have been negative, later infection or unappreciated false-negative results from the prozone phenomenon may occur. Careful microscopic examination for trophozoites may establish a diagnosis of congenital toxoplasmosis long before other confirmatory tests become available. Other evidence of inflammation or infection derived from gross inspection, microscopy, or specific microbiologic testing also may be useful.

TREATMENT

Section 6 of 11  

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Medical Care

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.

Options for targeted treatment of inflammation independent of antimicrobial therapy are severely limited. Considerable speculation suggests 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 eradicating invasive microbes should not be a goal; however, other methods of eradication or methods of directly dealing with the pathologic inflammatory cascades await further definition.

Even if the infection is eradicated, many hosts develop long-lasting or permanent pulmonary changes that affect lung function, the 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.

• Antimicrobial therapy
• • Initial empiric antibiotics are selected according to the susceptibility pattern of the likely pathogens, experience at the institution and tempered by knowledge of delivery of drugs to the suspected infected sites within the lung.
  • Drainage of a restrictive or infected effusion or empyema may enhance clearance of the infection and improves lung mechanics.
  • Because congenital pneumonia frequently results from bloodstream infection or frequently seeds the circulation secondarily, attaining an adequate plasma concentration of the antimicrobial agent via a parenteral route is essential. Alveolar delivery of antibiotics typically occurs via diffusion of a free 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. A large observational study by Clark et al has suggested an increased risk of death in neonates who receive cefotaxime rather than gentamicin.²
  • Recovery of a specific pathogen from a normally sterile site (eg, blood, urine, cerebrospinal fluid) permits narrowing the spectrum of antimicrobial therapies and may thus reduce the selection of resistant organisms and costs of therapy. Repeated culture of the site after 24-48 hours is usually warranted to ensure sterilization and to assess the efficacy of therapy.
  • 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 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, 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.
• Respiratory support
• • Adequate gas exchange depends not only on alveolar ventilation, but also on perfusion and gas transport capacity of the alveolar perfusate. 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 and weaning of supplemental oxygen and mechanical support are similar to those for other neonatal respiratory diseases.
  • Beware of remarkable heterogeneity of lung disease, with multiple 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.
• Hemodynamic support
• • RBCs should be administered to ensure 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 aspects of clinical care.
• Nutritional support: 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 and transfer the neonate to a tertiary care NICU.
• A number of respiratory management issues require special consideration in newborn infants in whom pneumonia is suspected.
• • Airway patency
  • • Assurance of airway patency may be more challenging 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 its use. 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.
    • 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.
    • 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.
    • Exogenous surfactant may be beneficial in selected infants. 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. 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.
    • 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.
    • The use of high-frequency or patient-triggered ventilatory techniques may offer better recruitment of alveolar lung volume, but data are sparse.
  • 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 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.³ 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.

MEDICATION

Section 7 of 11  

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The frequency of bacterial infection as the primary cause or as a superimposed complication of pulmonary inflammation in general, and congenital pneumonia in particular, usually mandates antibiotic administration as the cornerstone of therapy.

Agents typically used initially include a combination of ampicillin and either gentamicin or cefotaxime. The selection of cefotaxime or gentamicin must be based on experience and considerations at each center and in each patient. This combination therapy provides reasonable antimicrobial efficacy against the pathogens that typically cause serious infection in the first days of life. Other agents or combinations may be appropriate for initial empiric therapy if justified by the range of pathogens and susceptibilities encountered in a particular clinical setting.

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 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 (IM) treatment or intravenous (IV) therapy with the same total daily dose but a more frequent dosing interval 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. 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.

Drug Category: Antibiotics

The frequency of bacterial infection as the cause or a major complication of congenital pneumonia usually mandates antibiotics as the cornerstone of therapy. Below are the most commonly used antibiotics in congenital pneumonia. Consult appropriate neonatal references such as Neofax. Similarly, an appropriate reference should be used when using adjunctive therapy such as bronchodilators, mucolytics, or inhaled steroids.

FOLLOW-UP

Section 8 of 11  

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Transfer

If appropriate respiratory, hemodynamic, or nutritional support cannot be safely and effectively administered at the hospital of birth, stabilize and transfer the infant to an NICU.

Deterrence/Prevention

• Consider intrapartum antibiotic chemoprophylaxis with penicillin or another appropriate antimicrobial agent in mothers with the following risk factors for early-onset group B streptococcal disease:
• • 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 Red Book for the most current recommendations for infants at risk for group B streptococcal sepsis/pneumonia.⁴
• 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.
• Data regarding potential efficacy of elevating the head; use of antireflux medications; differential policies for oral care and changes of suction and ventilator tubing; and other potential interventions are lacking in neonates.

Complications

• Restrictive pleural effusion
• Infected pleural effusion
• Empyema
• Systemic infection with metastatic foci
• Pulmonary Hypertension, Persistent-newborn
• Air leak syndrome, including pneumothorax, pneumomediastinum, pneumopericardium, and pulmonary interstitial emphysema
• Airway injury
• Obstructive airway secretions
• Hypoperfusion
• Chronic lung disease
• Hypoxic-ischemic and cytokine-mediated end-organ injury

Prognosis

• Although quantitation of risk is difficult and strongly influenced by gestational age, congenital anomalies, and coexisting cardiovascular disease, there is a consensus that congenital pneumonia increases the following:
• • Chronic lung disease
  • Prolonged need for respiratory support
  • Childhood otitis media
  • Reactive airway disease
  • Complications attendant to these conditions
• Continued growth and development of pulmonary and other tissues offers good prospects for long-term survival and progressive improvement in infants who survive.

Patient Education

• Counsel parents regarding the need to prevent exposure of infants to tobacco smoke.
• Educate parents regarding the benefit infants may receive from pneumococcal immunization and annual influenza immunization. Discuss potential benefits and costs of respiratory syncytial virus immune globulin.
• As part of anticipatory primary care, educate parents regarding later infectious exposures in daycare centers, schools, and similar settings and the importance of hand washing.
• Emphasize careful longitudinal surveillance for long-term problems with growth, development, otitis, reactive airway disease, and others complications.
• For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article Bronchoscopy.

MISCELLANEOUS

Section 9 of 11  

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• Introduction
• Clinical
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to consider the diagnosis in the absence of maternal risk factors for infection
• Failure of obstetric care providers to initiate intrapartum chemoprophylaxis in mother with identified risk factors
• Failure to initiate neonatal antibiotics in a timely manner
• Failure to suction the neonatal airway when particulate meconium is in amniotic fluid and the infant is not vigorous at birth

MULTIMEDIA

Section 10 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  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.
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Media type:  Radiograph

Media file 2:  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 monocytogenes was recovered from the initial blood culture.