Clinical Pathway Neonatal Pneumonia

Pathophysiology
Pneumonia that becomes clinically evident within 24 hours of birth may

originate at three different times. The three categories of congenital
pneumonia are as follows:
 True congenital pneumonia
 Intrapartum pneumonia
 Postnatal pneumonia
True congenital pneumonia

True congenital pneumonia is already established at birth. It may become
established long before birth or relatively shortly before birth. Transmission of
congenital pneumonia usually occurs via one of three routes:
 Hematogenous
 Ascending
 Aspiration
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 a well-known phenomenon and may result in hematogenous
transmission without significant maternal illness. However, 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 infection from the birth canal and aspiration of infected or inflamed
amniotic fluid have significant common features. Infection of 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.
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 species (U urealyticum or U parvum), may be present in the
amniotic cavity for long periods yet 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 two cell layers (alveolar
epithelium and 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. It
may be acquired via hematogenous or ascending transmission, 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.
Postnatal pneumonia
Postnatal pneumonia in the first 24 hours of life originates after the infant has
left the birth canal. It 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 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.
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. [6, 7]
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 air trapping, 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 airway
and vascular constriction or dilatation. 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.
https://emedicine.medscape.com/article/978865-overview#a3
Inappropriate
Invading Poorly targeted by Invading foreign
responses by own’s
microorganisms own’s immune system bacteria
immune system
Direct Injury Indirect Injury
Synthesis & secretion of microbial Mediated by structural or secreted

enzymes, proteins, toxic lipids, & toxins molecules
Alter local vasomotor tone & integrity, change

Disrupt host cell membranes, metabolic
characteristics of tissue perfusate, & interfere with
machinery, & the extracellular matrix
oxygen & nutrients delivery & removal of waste.
Activated inflammatory response. The invading agents and the host defenses
Results to targeted migration of phagocytes, release increase airway smooth muscle tone and
of toxic substances; initiation of poorly regulated resistance, mucous secretion, and the presence
cascades of inflammatory cells and debris in these
secretions.
Injure host tissues; adversely alter endothelial &

epithelial integrity, vasomotor tone, intravascular
increase airway resistance and obstruct the
hemostasis, and activation state of fixed & migratory
airways, partially or totally
phagocytes at the inflammatory focus.
 conducting airways offer much more resistance and may become obstructed
 alveoli may be atelectatic or hyperexpanded
 alveolar perfusion may be markedly altered
 multiple tissues and cell populations in the lung and elsewhere sustain injury
increases the basal requirements for oxygen uptake and excretory gas removal at a time
Alveolar diffusion barriers may increase, intrapulmonary shunts may worsen, and ventilation-
perfusion mismatch may further impair gas exchange despite endogenous homeostatic attempts
The myocardium has to work harder to overcome the alterations
lungs may be less able to add oxygen and spread of infection or inflammatory response,
remove carbon dioxide from mixed venous either systemically or to other focal sites,
blood for delivery to end organs further exacerbates the situation.

Clinical Pathway Neonatal Pneumonia

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Clinical Pathway Neonatal Pneumonia

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Pathophysiology

Pneumonia that becomes clinically evident within 24 hours of birth may

True congenital pneumonia

If the mother has a bloodstream infection, the microorganism can readily

Direct Injury Indirect Injury

Synthesis & secretion of microbial Mediated by structural or secreted

Alter local vasomotor tone & integrity, change

Injure host tissues; adversely alter endothelial &

The myocardium has to work harder to overcome the alterations

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