Pneumonia is an infection of the lung and lower respiratory tract, below the level of the larynx. Globally, pneumonia is a leading cause of morbidity and mortality, with an estimated 120 million cases annually resulting in nearly 1.3 million deaths.¹ The greatest burden of disease and mortality occurs in the developing world, and young children under the age of 2 account for 81% of pediatric deaths from pneumonia. Although survival in industrialized countries is better than in the developing world, the burden of disease remains high, with an estimated 2 to 2.6 million cases annually, resulting in nearly a million hospitalizations.² This chapter addresses the clinical and radiographic diagnosis of pneumonia, common viral and bacterial causes, evidence-based treatments, and appropriate disposition and follow-up for children seen in the ED. Wherever possible, you will see special mention of unusual microbes, changing patterns of immunization and resistance, and special considerations for children with underlying medical conditions. If you have limited pediatric experience, you may find the section on the use and interpretation of chest radiographs in children helpful.

Pneumonia occurs through invasion of the lower respiratory tract by pathogens. Anatomic and mechanical barriers to infection include the nasal hairs and turbinates, cilia, epiglottis, and cough reflex. Humoral immunity is largely mediated by secretory immunoglobulin A, whereas cellular immunity and phagocytic cells (e.g., alveolar macrophages) further protect against infection. Infectious agents may be inhaled or aspirated directly into the lungs, invade respiratory epithelium and spread contiguously, or, less commonly, reach the lungs hematogenously. Viral inoculation is typically by droplet or fomite (e.g., influenza, respiratory syncytial virus), whereas bacterial pneumonia often follows colonization of the nasopharynx. Infection can result in injury or death of the respiratory epithelium, interstitial inflammation, or alveolar injury. The air space fills with exudate and WBCs, which disrupt oxygenation and cause air space collapse, with eventual ventilation-perfusion mismatch.

In most cases, the causative agent is never known. Definitive microbiologic diagnosis requires invasive procedures such as bronchial lavage or sampling of pleural effusion for culture, which are unavailable or impractical in the ED.

Overall, viruses predominate in younger children, although bacterial, atypical, fungal, parasitic, and opportunistic organisms can also cause disease. Infection with Mycobacterium tuberculosis can occur in areas where it is endemic and among children with immunodeficiency, so one should take into account local and regional epidemiology, individual immunization status, and underlying health problems that may influence which pathogens are likely. The types and causes of pneumonia vary considerably according to the age of the child; a few general rules and specific exceptions are described below.^3,4

The cardinal symptoms of lower respiratory tract infection include cough, fever, tachypnea, and respiratory distress. However, signs and symptoms vary by age and specific causative agents. Both age-based etiology and pathogen-specific clinical patterns of disease are described below.

AGE-SPECIFIC CAUSES OF PNEUMONIA

Neonates

Neonates (0 to 30 days of age) require special consideration because they are at risk from bacterial pathogens acquired from the birth canal at or around the time of delivery. Specific organisms of concern include group B streptococci, gram-negative enteric bacteria such as Klebsiella and Escherichia coli, and Listeria monocytogenes. Late-onset neonatal pneumonia may be caused by Staphylococcus aureus, Streptococcus pneumoniae, or Streptococcus pyogenes. Pneumonia due to maternal genital Chlamydia trachomatis has been largely eliminated in developed countries through the systematic screening and treatment of pregnant women⁵ but is still a consideration if the mother has had little or no prenatal care. Any neonate with pneumonia is also at risk of sepsis, and between birth and 3 months, infants with pneumonia should be evaluated for sepsis.

Infants and Children between 30 Days and 2 Years of Age

Pneumonia in older infants and toddlers is usually viral rather than bacterial.⁶ Common causes include respiratory syncytial virus, influenza virus, parainfluenza virus, human metapneumovirus, and adenovirus. In this age group, the most common bacterial cause of community-acquired pneumonia remains S. pneumoniae. Other agents include Haemophilus influenzae type b in nonimmunized children and nontypeable H. influenzae in all children. Less common but important pathogens include S. aureus and Bordetella pertussis.

Children 2 to 5 Years Old

As children get older and attend day care or school, they come into contact with many pathogens, particularly respiratory viruses.

In children between 2 and 5 years of age, most community-acquired pneumonia is caused by respiratory viruses, followed by S. pneumoniae, H. influenzae type b, or nontypeable H. influenzae.^4,7 Mycoplasma and Chlamydophila pneumoniae are thought to be less common in children <5 years old.^4,7,8 Pneumonias due to varicella-zoster virus, measles, H. influenzae type b, B. pertussis, and some strains of Pneumococcus are increasingly rare in areas of widespread vaccination and herd immunity.

Children 5 to 13 Years Old

In children from age 5 to adolescence, Mycoplasma pneumoniae is thought to be a chief cause of community-acquired pneumonia, with C. pneumoniae and S. pneumoniae still important considerations.^7,9 Less common bacterial causes include S. aureus and Legionella.⁶ M. tuberculosis is a rare but important agent to consider. Pertussis immunity from the newer acellular vaccine appears to wane (in the 5 years after vaccination), so consider Bordetella even in the immunized child if clinical symptoms are strongly suggestive.¹⁰

Adolescents

By adolescence, most patients are assumed to have the same infectious risks as healthy adults. The prevalence of specific pathogens may vary according to region, season, and cyclical epidemics in the population. In North America, the role of atypical agents, especially mycoplasma and C. pneumoniae, is estimated to be significant, but data and guidelines from other parts of the industrialized world (e.g., Europe) suggest regional differences.¹¹

UNIQUE AND HIGH-RISK GROUPS

Tuberculosis remains a consideration for children with known exposures and those from endemic areas such as Native reserves, Alaska, northern Canada, and some inner-city settings. Consider tuberculosis in immigrants from high-prevalence areas of the world, including Africa, Asia, and parts of Eastern Europe.

Children with underlying disease are at risk for specific infections. For example, younger children with cystic fibrosis are often infected with S. aureus in the first years of life, and later with Pseudomonas. Children with sickle cell disease are particularly susceptible to infection with encapsulated bacteria (e.g., pneumococcus, Salmonella, Klebsiella), which can cause acute chest syndrome and sepsis. Children with congenital or acquired immune deficiencies such as human immunodeficiency virus infection, malignancy, and congenital immunodeficiencies are at risk for opportunistic infections with agents such as Pneumocystis jirovecii, cytomegalovirus, and fungi.¹

Unvaccinated children and those with incomplete immunization are at risk of serious morbidity and mortality from a variety of vaccine-preventable pathogens. They should be managed accordingly.

PATHOGEN-SPECIFIC PATTERNS OF DISEASE

“Typical pneumonias” classically present with high fever, chills, pleuritic chest pain, and productive cough and suggest a bacterial cause, especially S. pneumoniae. In contrast, “atypical pneumonias” are characterized by gradual onset over days to weeks, low-grade fever, nonproductive cough, and malaise, and suggest infection with agents like mycoplasma or C. pneumoniae. Unfortunately, there is significant overlap in the agents causing these symptoms, and it is not possible to pinpoint specific causative organisms by clinical findings alone.^4,12 If definitive identification of the pathogen is important, perform laboratory testing.

Despite these limitations, some patterns of disease do suggest certain etiologies (Table 125-1). Staphylococcal pneumonia, which may follow influenza, is notorious for rapidly progressing symptoms, high fever, toxicity, and presence of pulmonary abscesses. C. trachomatis infection in infants (which is rare where there is prenatal screening and treatment) often presents with a staccato cough, diffuse rales, and lack of fever, so-called afebrile pneumonitis. Scattered rales, rare wheezes, and bilateral interstitial infiltrates are all possible findings. Older children may complain of sore throat and dysphagia. B. pertussis and respiratory viruses are also implicated as possible causes.¹³ Mycoplasma infection typically produces a hacking, dry cough and may be associated with extrapulmonary manifestations including arthralgias, rash, and even CNS symptoms.¹⁴ An upper respiratory tract prodrome followed by paroxysmal cough, gasping respirations, and color change is characteristic of B. pertussis infection (whooping cough); the postinfection cough may persist for months. Consider tuberculosis with prolonged cough in the setting of identified risk factors and characteristic radiographic findings. Note that classic signs and symptoms of tuberculosis such as hemoptysis or tuberculosis-positive sputum may be absent in children, especially those with immune deficiencies.¹⁵ Tuberculosis in infants and young children tends to progress more rapidly from infection to clinical disease than it does in older children and adults, and hematogenous spread to extrapulmonary sites is also possible.^16,17

Wheezing in a young infant with respiratory infection typically points to bronchiolitis of viral origin. In older, school-age children, wheezing may suggest viral infection or Mycoplasma pneumonia.⁵ Distinguishing between viral and bacterial causes of pneumonia is often difficult, and radiographs may not provide a specific diagnostic pattern.

SEVERE DISEASE

The British Thoracic Society Guidelines for community-acquired pneumonia in children defines severe disease in infants as a fever >38.5°C, respiratory rate >70 breaths/min, nasal flaring, grunting, cyanosis, apnea, and poor feeding. Severe disease in older children is similarly defined by fever >38.5°C, signs of respiratory distress (respiratory rate >50 breaths/min, cyanosis, grunting), and signs of dehydration.³

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of pneumonia includes both infectious and noninfectious conditions as well as extrapulmonary disorders that may mimic or complicate lower respiratory tract infection (Table 125-2). Formulating a differential diagnosis is especially important for infants and very young children, who may have undiagnosed congenital anomalies.

For children with respiratory distress but no fever, look for causes other than pneumonia. Congenital heart disease may present with cyanosis, quiet tachypnea, or respiratory distress related to congestive heart failure (see chapter 126, “Congenital and Acquired Pediatric Heart Disease”). Kussmaul breathing suggests diabetic ketoacidosis or other metabolic disease. Toddlers are particularly at risk for foreign body aspiration and ingestion of toxins. Adolescents may intentionally or unintentionally take drug overdoses that speed or slow breathing.

HISTORY

Relevant history depends on age of the patient and the underlying health of the child. Many complaints are nonspecific (e.g., cough and fever) and are common to both upper and lower respiratory tract disease. The predictive value of specific signs and symptoms is discussed below (see “Physical Examination” section).

Ask about the presence, timing, and duration of cough, fever, rapid breathing, and difficult breathing. Ask about specific exposures, sick contacts, travel, and pets, when relevant.

Choking or persistent or recurrent lower respiratory tract symptoms suggest foreign body aspiration. Recurrent pneumonias may signify underlying disease such as cystic fibrosis, immune disorders, or anatomic abnormalities.

In young children, abdominal pain may be a clue to lower lobe pneumonia or effusion.

Fever is a common but nonspecific sign of both upper and lower respiratory tract infections.

Birth History

Because neonates may acquire infections perinatally, be sure to ask questions about the mother’s prenatal and perinatal health, including maternal infections (e.g., chlamydia, gonorrhea, group B streptococci, genital herpes, and human immunodeficiency virus status), intrapartum or postpartum fever, and any specific antibiotic or antiviral therapy received during labor and delivery. Other perinatal risk factors include prolonged rupture of membranes, prematurity, and immediate peripartum complications. Meconium aspiration may cause chemical or bacterial pneumonia in the first 24 to 72 hours of life. Neonatal stays in hospital suggest an underlying health problem and also increase the risk of nosocomial infection.

Medical History

Ask about the child’s hospitalizations since birth and major illnesses, especially chronic respiratory problems (e.g., asthma, recurrent wheezing). In the young child, consider an undiagnosed respiratory, cardiac, renal, or immune dysfunction. Children with congenital respiratory problems (e.g., cystic fibrosis, neuromuscular disorders, immune compromise) are at increased risk of infection with common and rare agents, respiratory failure, and treatment failure. Adjust treatment and disposition accordingly (see Table 125-4).

Social History

Take a brief, focused social history, because it may influence both diagnosis and treatment. For example, children from the far north, Native reserves, or countries with high rates of tuberculosis may be exposed to this uncommon but serious infection. A travel history may also be relevant. Children born to human immunodeficiency virus–positive mothers are at risk of vertical transmission and immunocompromise. Social history may also influence treatment decisions. For outpatient management, make sure that caregivers understand instructions, can afford medication, and can provide the required care (see “Disposition and Follow-Up” section below).

Immunization History

Always inquire about childhood immunizations, and review records for confirmation when possible. Table 106-4 in chapter titled Emergency Care of Children provides a typical childhood immunization schedule. Ensure that enough time has elapsed to develop protective antibodies—typically 4 to 6 weeks for primary vaccination and 1 week for a booster. An unvaccinated child is at risk of serious morbidity, and even death, from vaccine-preventable illness.

Annual immunization against influenza is recommended for children ≥6 months of age and for those at high risk due to underlying health conditions. Influenza vaccine must be given annually to account for seasonal antigenic changes (see “Special Considerations” section below). Priority is given to children with asthma, cystic fibrosis, and other pulmonary diseases; those with significant cardiac, renal, and immune disorders; and those with diabetes. Caregivers and healthcare providers should also be immunized to avoid transmission to these at-risk children.¹⁸

Around the globe, immunization against polio, pertussis, measles, and H. influenzae type b infection has significantly lowered the risk of pneumonias and respiratory failure associated with these diseases. In some cases, simple herd immunity has decreased the chances that a child will come into contact with these once-feared diseases, but sporadic outbreaks exist in nonimmunized populations.

Immunization against varicella (chickenpox) should protect against the secondary pneumonias associated with this virus, although use of the vaccine is not yet universal. Similarly, the administration of the bacillus Calmette-Guérin vaccine to provide partial protection against certain forms of tuberculosis varies by state, province, and country.

The introduction of a seven-strain pneumococcal conjugate vaccine (Prevnar^®, PCV-7) in 2000 to 2001 led to dramatic decreases in invasive disease and modest but promising trends in the reduction of pneumococcal pneumonias, especially in children <2 years old.^19,20 Early reports suggested a somewhat diminished impact in human immunodeficiency virus–positive children.²¹ Vaccine-specific serotypes are being replaced globally by nonvaccine strains, although newer PCV-10 and PCV-13 vaccines are expected to counteract some of this serotype substitution. Children who received the initial PCV-7 series should receive a booster with PCV-13 to gain additional immunity.¹⁹ Vaccine coverage is universal in Canada but varies by state and private insurance provider in the United States.

The older 23-valent polysaccharide vaccine (Pneumovax^®) is effective in children ≥2 years of age, and it should be confirmed that the vaccine has been given to children with sickle cell disease, those who have undergone splenectomy, and others at high risk for pneumococcal disease. A booster may be required.

PHYSICAL EXAMINATION

In the developing world where imaging equipment and laboratory tests are limited, the World Health Organization has proposed a diagnostic algorithm based entirely on the presence or absence of tachypnea, respiratory distress, and lower chest retractions or indrawing. Although physicians in industrialized nations have many tools at their disposal, the diagnosis of pneumonia can still be made clinically.

Rapid respiratory rate is a simple, standardized screening tool for pneumonia⁴ (Table 125-3).

Children at very high altitudes may have a resting respiratory rate higher than children at sea level do, so oxygen saturation may be a more useful measure. Note that children who are severely malnourished or dehydrated or have impending respiratory failure may not be capable of generating rapid respiratory rates.

Markers of respiratory distress include nasal flaring, tracheal tug, and intercostal indrawing. Lower chest or “abdominal” indrawing or retractions and grunting suggest more severe pneumonia.²⁵ In infants, intermittent apnea, grunting, and an inability to feed are surrogate markers of dyspnea. Cough is less common in neonates or very young children, and productive cough is rarely seen before late childhood.

Document oxygen saturation, because hypoxia on room air (arterial oxygen saturation <93% at sea level) increases the risk of oral amoxicillin treatment failure in severe pneumonia,²⁶ and oxygen saturation <93% is a strong independent predictor of radiographic pneumonia.²⁷

Auscultate the chest using an appropriately sized stethoscope with the chest fully exposed, assessing all lung zones. Localized fine crackles (rales), coarse breath sounds (rhonchi), or diminished breath sounds suggest pneumonia, but sound recognition may not be consistent across observers²³; a toxic appearance and overall impression of illness as judged by the clinician show better diagnostic sensitivity than focal auscultatory findings.⁴

CLINICAL DIAGNOSIS