AVERY.

Casi todas las neumonías adquiridas por vía materna producen signos clínicos en los
primeros 3 días de vida. Se calcula que la incidencia de la neumonía precoz es del 0,5% de todos
los recién nacidos vivos. Son dos los tipos de neumonía que pueden tener su origen en la madre;

1. La neumonía congénita o intrauterina

2. La neumonía transnatal

En la neumonía postamnionitis la invasión de las bacterias u otros microorganismos infecciosos

como virus, micoplasma u hongos. S e cree que es una infección ascendente ´provocada por la
flora vaginal y que se inicia en el amnios a nivel del orificio cervical, desde donde se propaga a la
placa amniótica a través de las membranas.

Factores que predisponen a la amnionitis y a la neumonía:

1. Parto prematuro: La asociación entre amnionitis y parto prematuro se podría explicar por
una deficencia del desarrollo de factores bacteriostáticos en el líquido amniótico.

2. Rotura prematura de membranas antes de que comience el parto

3. Rotura prolongada de las membranas (más de 14 horas)
4. Parto activo prolongado con dilatación cervical.
5. Exploraciones digitales obstétricas frecuentes.

El cultivo y la tinción de gran del aspirado traqueal recogido en las 8 horas siguientes al parto
también también resulta útil (Sherman y cols 1984) ya que la traquea es normalmente esteril y es
de esperar que la intubación no haya producido colonización. La presencia de bacterias en la
tinción de gran tiene una exactitud predictiva positiva del 47% (Sherman 1980) y una exactitud
predictiva negativa del 79%. En vista del alto numero de resultados positivos falsos se estudio la
presencia de leucocitos, demostrando que las muestras iniciales de aspirado traqueal que
contienen tanto leucocitos como bacterias tienen alota posibilidad de sufrir neumonía.

En todos los casos donde se sospecha de neumonía deben hacerse tanto hemocultivo como un
análisis de líquido cefalorraquídeo, ya que puede existir meningitir.

Remington & Klein

PNEUMONIA
Pneumonia, inflammation of the lungs, in the fetus and newborn can be classified into four categories
according to the time and mode of acquisition of inflammation:
1. Congenital pneumonia acquired by the transplacental route: Pneumonia is one component of generalized
congenital disease.
2. Intrauterine pneumonia: This is an inflammatory disease of the lungs found at autopsy in stillborn or live-
born infants who die within the first few days of life, usually associated with fetal asphyxia or intrauterine
infection, and includes infectious and noninfectious causes.
3. Pneumonia acquired during birth: Signs of pneumonia occur within the first few days of life, and infection
is due to microorganisms that colonize the maternal birth canal.
4. Pneumonia acquired after birth: The illness manifests during the first month of life, either in the nursery or
at home; sources of infection include human
contacts and contaminated equipment.

Although helpful as a general framework for understanding neonatal pneumonia, these four categories have
clinical features and pathologic characteristics that overlap. Management of pneumonia is essentially the same
for all four categories, requiring aggressive supportive measures for the respiratory and circulatory systems
along with treatment for the specific underlying infectious disorder. Pneumonia in the neonate may be caused
by viruses, bacteria, or parasitic organisms. Detailed information about causative organisms mentioned in this
chapter other than bacteria is found in the appropriate chapters in this book; bacterial disease is covered in
detail here. Pneumonia acquired by the transplacental route may be caused by rubella, cytomegalovirus,
herpes simplex virus, adenoviruses [147], mumps virus [148], Toxoplasma gondii, L. monocytogenes, or T.
pallidum. Some of these organisms and enteroviruses, genital mycoplasmas, M. pneumoniae [148a], C.
trachomatis, and Mycobacterium tuberculosis are also responsible for intrauterine pneumonia resulting from
aspiration of infected amniotic fluid. Fatal pneumonitis caused by echovirus has also been reported in
newborns (see Chapter 24) [149]. Isolation of Trichomonas vaginalis from the tracheal aspirates of infants
with pneumonia suggests a possible association of this organism with respiratory tract disease in the neonate
[150,151]. GBS is the most frequent cause of bacterial pneumonia acquired at delivery. Pneumonia caused by
GBS and other bacteria such as E. coli or L. monocytogenes may resemble hyaline membrane disease.

Pneumonias acquired after birth, either in the nursery or at home, include those caused by respiratory viruses
such as respiratory syncytial virus, influenzavirus, or adenoviruses; gram-positive bacteria such as
pneumococci and S. aureus; gram-negative enteric bacilli; Legionella pneumophila [151a] C. trachomatis;
Mycoplasma; and Pneumocystis carinii [152]. A fatal case of adenovirus serotype 14 with pathologic features
consistent with bronchiolitis and acute respiratory distress syndrome occurred in a 12-day-old infant in 2006
[153]. Pneumonia caused by nonbacterial microorganisms is discussed in the appropriate chapters. Bacterial
pneumonia and neonatal sepsis acquired during or soon after birth share many features of pathogenesis,
epidemiology, and management, and these aspects are discussed in Chapter 6. Discussion of pneumonia in the
fetus and newborn not presented elsewhere in the text follows.

PATHOGENESIS AND PATHOLOGY

Congenital or Intrauterine Pneumonia
Histologic features of congenital or intrauterine pneumonia have been described from autopsy findings in
infants who are stillborn or who die shortly after birth (usually within 24 hours). An inflammatory reaction is
found in histologic sections of lung. Polymorphonuclear leukocytes are present in the alveoli and often are
mixed with vernix and squamous cells. Infiltrates of round cells may be present in interstitial tissue of small
bronchioles and interalveolar septa [154–159]. Alveolar macrophages may be present and have been
associated with duration of postnatal life and inflammatory pulmonary lesions [160]. The inflammation is
diffuse and usually is uniform throughout the lung. Bacteria are seen infrequently, and cultures for bacteria
are often negative. Davies and Aherne [157] noted that the usual characteristics of bacterial pneumonia are
missing in congenital pneumonia; among these characteristics are pleural reaction, infiltration or destruction
of bronchopulmonary tissue, and fibrinous exudate in the alveoli.

The pathogenesis of congenital pneumonia is not well understood [161]. Asphyxia and intrauterine infection,
acting alone or together, seem to be the most important factors [157]. It is thought that microorganisms of the
birth canal contaminate the amniotic fluid by ascending infection after early rupture of maternal membranes
or through minimal and often unrecognized defects in the membranes. Evidence of aspiration of amniotic
fluid is frequent [157]. Naeye and colleagues [162–164] proposed that microbial invasion of the fetal
membranes and aspiration of infected amniotic fluid constitute a frequent cause of chorioamnionitis and
congenital pneumonia. Bacteriologic studies have produced equivocal results, however.

Many infants with congenital pneumonia do not have bacteria in their lungs, yet cultures of the lung of some
infants without pneumonia do yield bacteria [165]. Fetal asphyxia or hypoxia seems to be a factor in most
cases of congenital pneumonia. The asphyxia may cause death directly or by eliciting a pulmonary response
consisting of hemorrhage, edema, and inflammatory cells. From his studies of congenital pneumonia, Barter
[166] concluded that hypoxia or infection may produce similar inflammationin the lungs. In addition,
Bernstein and Wang [167] found that evidence of fetal asphyxia was frequently present at autopsy in infants
with congenital pneumonia who also had generalized petechial hemorrhage, subarachnoid and intracerebral
hemorrhage, liver cell necrosis, or ulceration of the gastrointestinal mucosa.

Although it is likely that asphyxia and infection can produce similar inflammatory patterns in lungs of the
fetus, available information is insufficient to determine which is more important or more frequent. In a review
of fetal an perinatal pneumonia, Finland [168] concluded that “pulmonary lesions certainly play a major role
in the deaths of the stillborn and of infants in the early neonatal period. Infection, on the other hand, appears
to play only a minor role in what has been called ‘congenital pneumonia,’ that is, the inflammatory lesion
seen in the stillborn or in those dying within the first few hours, or possibly the first day or two; it assumes
greater importance in pneumonias that cause death later in the neonatal period.” Davies [169] noted that the
histologic presentation of congenital pneumonia seems to represent aspiration of materials in amniotic fluid,
including maternal leukocytes and amniotic debris, rather than infection originating in the pulmonary air
spaces. Evidence of infiltration of alveoli or destruction of bronchopulmonary tissue is rarely present.

MICROBIOLOGY
Most information about the bacteriology of fetal and neonatal pneumonia has been derived from studies done
at autopsy of stillborn infants and of infants who die during the first month of life. A study reviewing causes
of death of infants with very low birth weight concluded, on the basis of histologic studies done at autopsy,
that pneumonia was an underrecognized cause of death in these infants [178]. Barter and Hudson [165]
reported bacteriologic studies at autopsy of infants with and without pneumonia. The incidence of bacteria in
the lungs increased with age in infants dying with and without pneumonia. Among the infants with
pneumonia, bacteria were cultured from the lungs of 55% of stillborn infants and infants who died during the
first day of life, 70% of infants who died between 24 hours and 7 days of age, and 100% of infants who died
between 7 and 28 days of age. Among the infants without pneumonia, bacteria were cultured from the lungs
of 36% of stillborn infants and infants who died within the first 24 hours, 53% of infants who died between 24
hours and 7 days of age, and 75% of infants who died between 7 and 28 days of age. The bacterial species
were similar in the infants with and without pneumonia, with the exception of GBS, which was found only in
infants with pneumonia.

These results were corroborated by Penner and McInnis [159]. Bacteria were cultured from 92% of the lungs
of fetuses and neonates with pneumonia and from 40% of the lungs of fetuses and neonates without
pneumonia. Davies [179] did lung punctures in stillborn and live-born infants immediately after death, and
bacteria were cultured from the lungs of 74% of 93 infants, although pneumonia was diagnosed in only 9
cases. Barson [180] identified bacteria in lung cultures at autopsy of 252 infants dying with
bronchopneumonia; positive cultures were obtained in 60% of infants dying on the first day of life and in 78%
of infants dying between 8 and 28 days of age. Bacteria were cultured at autopsy from the lungs of many
infants with and without pneumonia. Information about bacterial etiology of pneumonia also can be obtained
by culturing blood, tracheal aspirates, and pleural fluid and by needle aspiration of the lungs of living children
with pneumonia.

EPIDEMIOLOGY
Incidence
Table 7–2 presents the incidence of pneumonia at autopsy of stillborn and live-born infants. Pneumonia is a
significant cause of death in the neonatal period [202], and infection of amniotic fluid leading to pneumonia
may be the most common cause of death in extremely premature infants [203]. The definition of pneumonia
in the autopsy studies usually was based on the presence of polymorphonuclear leukocytes in the pulmonary
alveoli or interstitium or both. The presence or absence of bacteria was not important in the definition of
pneumonia. The incidence rates for congenital and neonatal pneumonia at autopsy are similar despite the
different periods of study (1922- 1999) and different locations [154–156,158,167,178,201– 205] (with the
single exception of a report from Helsinki [170]): 15% to 38% of stillborn infants and 20% to 32% of live-
born infants had evidence of pneumonia. The incidence rates for pneumonia were similar in premature and in
terminfants. Rates of pneumonia derived from epidemiologic studies are scarce. Sinha and colleagues [206]
reported an attack rate of 0.4 per 100 infants diagnosed during a nursery stay, and 0.03 and 0.01 per 100
infants diagnosed at pediatric office visits and in hospital or emergency department visits. They
acknowledged a paucity of data with which to compare their rates, which they derived from retrospective
review of data from a large health maintenance organization.

DIAGNOSIS
Clinical Diagnosis
A history of premature delivery, prolonged interval between rupture of maternal membranes and delivery,
prolonged labor, excessive obstetric manipulation, and presence of foul-smelling amniotic fluid frequently are
associated with neonatal infection, including sepsis and pneumonia. The clinical manifestations of pneumonia
may be subtle and nonspecific at the onset, and specific signs of respiratory infection may not be evident until
late in the course of illness. Most commonly, pneumonia is associated with evidence of respiratory distress,
including tachypnea, retractions, flaring of nasal alae, and increasing requirement for oxygen.

Radiologic Diagnosis
A chest radiograph is the most helpful tool for making the diagnosis of pneumonia. The radiograph of an
infant with intrauterine pneumonia may contribute no information, however, or show only the coarse mottling
of aspiration. If the radiologic examination is done early in the course of meconium or other aspiration
pneumonias, typical radiologic features may not yet have developed. The radiograph of an infant with
pneumonia acquired during or after birth may show streaky densities or confluent opacities. Peribronchial
thickening, indicating bronchopneumonia, may be present. Pleural effusion, abscess cavities, and
pneumatoceles are frequent in infants with staphylococcal infections, but also may occur in pneumonia caused
by group A streptococci, E. coli [173], or K. pneumoniae [172]. Diffuse pulmonary granularity or air
bronchograms similar to that seen in respiratory distress syndrome have been observed in infants with
pneumonia related to GBS [215]. Computed tomography (CT) with contrast médium enhancement is
beneficial in localizing pulmonary lesions such as lung abscess and distinguishing abscess from empyema,
pneumatoceles, or bronchopleural fistulas [192]. Ultrasound examination was used to diagnose hydrothorax in
utero at 32 weeks of gestation [216]. Although it is impossible to distinguish bacterial from viral pneumonia
on the basis of a chest radiograph alone, several features may help distinguish between the two. Findings that
are more characteristic of viral pneumonias include hyperexpansion, atelectasis, parahilar peribronchial
infiltrates, and hilar adenopathy, which is associated almost exclusively with adenovirus infection. Alveolar
disease, consolidation, air bronchograms, pleural effusions, pneumatoceles, and necrotizing pneumonias are
more characteristic of bacterial processes [217

Microbiologic Diagnosis
Because of the difficulty in accessing material from a suppurative focus in the lower respiratory tree,
microbiologic diagnosis of pneumonia is problematic. Although cultures of material obtained from lung
aspiration have been shown to yield bacterial pathogens in about one third of a group of seriously ill infants
with lung lesions accesible to needle aspiration [218], this rate of positive results is unlikely to be obtained in
an unselected group of infants with pneumonia. Diagnosis may be based on isolating pathogens from other
sites. When generalized systemic infection is present, cultures of blood, urine, or cerebrospinal fluid may
yield a pathogen. Bacteremia may be identified in about 10% of febrile children with pneumonia [219]. If a
pleural effusion is present and the bacterial diagnosis is not yet evident, pleural fluid biopsy or cultura or both
may be helpful. Bacterial cultures of the throat and nasopharynx are unrevealing or misleading because of the
high numbers of respiratory pathogens present.

Tracheal aspiration through a catheter is frequently valuable when performed by direct laryngoscopy, but the
aspirate may be contaminated when the catheter is passed through the nose or mouth. Sherman and colleagues
[220] performed a careful study of the use of tracheal aspiration in diagnosis of pneumonia in the first 8 hours
of life. Tracheal aspirates were obtained from 320 infants with signs of cardiorespiratory disease and
abnormalities on the chest radiograph; 25 infants had bacteria present in the smear of the aspirate, and the
same organisms were isolated from cultures of 14 of 25 aspirates. Thureen and colleagues [221] found that
tracheal aspirate cultures failed to define an infectious cause of deterioration in ventilated infants. Positive
tracheal aspirates were found with equal frequency among infants with clinically suspected lower respiratory
tract infection and in “well” controls. Tracheal aspirate cultures may provide useful information about
potential pathogens in pneumonia or bacteremia, but rarely indicate the risk or timing of such complications
[222]. Often, surveillance cultures of tracheal aspirate material are used to guide empirical therapy when a
new illness develops in an infant with a prolonged course on a ventilator.

Bronchoscopy can provide visual, cytologic, and microbiologic evidence of bacterial pneumonia [223].
Aspiration of pulmonary exudate (lung puncture or “lung tap”) can be used to provide direct, immediate, and
unequivocal information about the causative agent of pneumonia [218]. This procedure is now performed
rarely; most reports of its use in infants and young children precede the introduction of antimicrobial agents
[224,225]. Open lung biopsy has been used to identify the etiology of lung disease in critically ill infants and
seems to have been most helpful at a time when corticosteroids for bronchopulmonary dysplasia were
withheld if there was concern about pulmonary infection. Cheu and colleagues [226] identified three
infections in 17 infants who had open lung biopsies: respiratory syncytial virus in 1 infant and Ureaplasma
urealyticum in 2 infants. Although the optimal indications for use of corticosteroids in bronchopulmonary
dysplasia are controversial [227,228], generally corticosteroids are not withheld if indicated because of low
likelihood of an infectious process [229].

KLAUS M., Fanaroff A., Cuidados del recién nacido de alto riesgo. Quinta edición. Editorial Mw Graw Hill.
2003. Pag. 100,

La neumonía en el recién nacido tiene una amplia gama de aspectos clínicos y radiológicos que muchas veces
simulan enfermedad por membrana hialina o síndrome de aspiración. Por esta razón todos los recién nacidos
con cualquier grado intenso de insuficiencia respiratoria, sea por deficiencia de agente tensoactivo, síndrome
de aspiración o una causa idiopática, deben considerarse potencialmente sépticos.

Management of Neonates With Suspected or Proven Early-Onset Bacterial Sepsis

Richard A. Polin and the COMMITTEE ON FETUS AND NEWBORN

Pediatrics 2012;129;1006; originally published online April 30, 2012; DOI:
10.1542/peds.2012-0541

Tracheal Aspirates
Cultures and Gram stains of tracheal aspirate specimens may be of value if obtained immediately after
endotracheal tube placement.36 Once an infant has been intubated for several days, tracheal aspirates are
of no value in the evaluation of sepsis.37
36. Sherman MP, Goetzman BW, Ahlfors CE,
Wennberg RP. Tracheal asiration and its
clinical correlates in the diagnosis of
congenital pneumonia. Pediatrics. 1980;65 (2):258–263

37. Srinivasan HB, Vidyasagar D. Endotracheal

aspirate cultures in predicting sepsis in
ventilated neonates. Indian J Pediatr. 1998;
65(1):79–84