Congenital Pneumonia Clinical Presentation

  • Author: Roger G Faix, MD; Chief Editor: Ted Rosenkrantz, MD   more...
 
Updated: Mar 29, 2011
 

History

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.

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Physical Examination

Physical findings may be pulmonary, systemic, or localized. All pulmonary findings are not necessarily present in all affected infants. 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

Respiratory manifestations may include persistent tachypnea (respiratory rate >60/min), expiratory grunting, and accessory respiratory muscle recruitment (eg, nasal flaring and subcostal, intercostal, or suprasternal retraction).

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. Aspiration of meconium, blood, or other inflammatory fluid may produce other colors and textures reflective of the aspirated material.

Rales, rhonchi, and cough should prompt careful consideration of pneumonia in the differential diagnosis, although all these signs are observed much less frequently in infants with pneumonia than in older individuals. Alternative causes include noninflammatory processes, such as heart failure, condensation from humidified gas administered during mechanical ventilation, or endotracheal tube displacement. .

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. This may result from pneumonia, but congenital structural heart disease, hemoglobinopathy, polycythemia, and pulmonary hypertension (with or without other associated parenchymal lung disease) must also be considered.

Infants may have external staining or discoloration of skin, hair, and nails with meconium, blood, or other materials that were 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 common.

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

In the neonate, the systemic findings seen in pneumonia are similar to the signs and symptoms seen in sepsis or other severe infections. Systemic findings include the following:

  • Temperature instability
  • Rash
  • Jaundice at birth
  • Tachycardia
  • Glucose intolerance
  • Abdominal distention
  • Hypoperfusion
  • Oliguria

Other systemic findings include adenopathy and hepatomegaly. Adenopathy suggests long-standing infection. Hepatomegaly from infection may result from certain 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.

Localized findings

Localized findings may include the following:

  • Conjunctivitis
  • Vesicles or other focal skin lesions
  • Unusual nasal secretions
  • Erythema, swelling, growth, unusual drainage, or asymmetry of other structures suggestive of inflammation

True congenital pneumonia

Infants whose pneumonia is already established at birth have 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.

Intrapartum pneumonia

Infants who aspirate proinflammatory foreign material (eg, meconium or blood) during passage through the birth canal may manifest pulmonary signs immediately after or very shortly after birth. In contrast, infants with 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

Infants who become infected after leaving the birth canal are often relatively asymptomatic at birth or manifest noninflammatory pulmonary disease consistent with gestational age, but develop signs that progress well after 24 hours.

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Complications of Congenital Pneumonia

Congenital pneumonia is associated with a number of potential complications, including the following:

  • Restrictive pleural effusion
  • Infected pleural effusion
  • Empyema
  • Systemic infection with metastatic foci
  • Persistent pulmonary hypertension of the 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
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Contributor Information and Disclosures
Author

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

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

Disclosure: Ikaria Consulting fee Consulting; Biosynexus Consulting fee Review panel membership

Specialty Editor Board

Steven M Donn, MD  Professor of Pediatrics, University of Michigan Medical School; Director, Division of Neonatal-Perinatal Medicine, Department of Pediatrics, CS Mott Children's Hospital, University of Michigan Health System

Steven M Donn, MD is a member of the following medical societies: American Pediatric Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Brian S Carter, MD, FAAP  Professor of Pediatrics (Neonatology), Vanderbilt University School of Medicine; Director, Neonatal Follow-up Program, Monroe Carell Jr Children's Hospital at Vanderbilt

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

Disclosure: Nothing to disclose.

Chief Editor

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

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

Disclosure: Nothing to disclose.

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