Community-acquired Pneumonia in Pediatric Populations
Community-acquired Pneumonia in Pediatric Populations
Authors:
Christopher J. Haines, DO, FAAP, FACEP, Assistant Professor of Pediatrics and Emergency Medicine, Drexel University College of Medicine; Director, Department of Emergency Medicine; Medical Director, Critical Care Transport Team, St. Christopher's Hospital for Children, Philadelphia, PA.
Aun Woon Soon, MD, Pediatric Resident, St. Christopher's Hospital for Children, Philadelphia, PA.
Danielle Mercurio, DO, Pediatric Resident, St. Christopher's Hospital for Children, Philadelphia, PA.
Peer Reviewer:
Dennis A. Hernandez, MD, FAAP, FACEP, FAAEM, Medical Director, Pediatric Emergency Services, Florida Hospital for Children, Walt Disney Pavilion, Florida Hospital, Orlando.
Classically, pneumonia is defined as an infection of the lung parenchyma. However, worldwide, a variety of definitions exist, including fever, hypoxia, a constellation of other clinical symptoms, and radiologic findings. In pediatric and adolescent populations, early diagnosis will assist emergency department (ED) physicians with correctly managing and subsequently avoiding potential morbidity and mortality of this common infectious disease. This article will focus on community-acquired pneumonia (CAP), which will be defined as an acute lower respiratory tract infection causing changes in the clinical exam of a previously healthy patient.
Ann M. Dietrich, MD, Editor
Epidemiology
Secondary to various definitions, difficulty in obtaining sputum samples from children and infants, and variation in seasonality, the global incidence of community-acquired pneumonia is difficult to determine. According to the World Health Organization (WHO), pneumonia is the leading cause of death in children worldwide, with an estimated mortality of 1.4 million children per year younger than the age of 5 years.1 This is more than AIDS, malaria, and tuberculosis combined. In addition, there are an estimated 150 million cases of pneumonia in children younger than 5 years of age, with up to 20 million requiring hospitalization for severe illness. Importantly, only 30% of the children diagnosed with pneumonia receive antibiotic treatment.2 In the United States, the incidence of disease in this same age group is estimated at 35-40 cases per 1000, and 7 cases per 1000 in adolescents aged 12 to 15 years.3 Prior to the regular use of pneumococcal conjugate vaccine PCV7, disease estimates were significantly higher.
Pneumonia is more common during the winter months, likely due to indoor crowding in cold weather. It spreads via respiratory droplets from person to person, or via fomite transmission. In general, hosts with compromised mucociliary clearance are more susceptible to pneumonia, and it is presumed that dry heat used during the winter season can impede mucociliary clearance in healthy individuals. Children from families with smokers, wood-burning stoves, and lower socioeconomic status are at an increased risk, as well as adolescents who smoke or consume alcohol. Overall, boys are affected more commonly than girls.4
Etiology
Pneumonia is caused by bacteria, viruses, atypical organisms, and fungus, with etiology varying by age group. Because invasive testing is not indicated in most cases encountered in the ED, etiology is often inferred by history, clinical exam, or detection of microorganisms in the upper respiratory tract by polymerase chain reactions (PCR) or serologic assay. Even in those exhaustively sampled, up to 50% of patients with pneumonia show no specific microbial cause. Further, simultaneous infection with multiple agents (viral and bacterial) is common. Table 1 provides a summary of common causes of pneumonia by age group with key clinical features.5
Table 1: Microbial Causes of Community-Acquired Pneumonia in Children
|
Age |
Etiologic Agents |
Clinical Features |
|
Modified from: Principles and Practice of Pediatric Infectious Disease, 3rd ed. 2008. |
||
|
Birth to 3 weeks |
Group B streptococcus |
Part of early-onset septicemia and/or meningitis |
|
Gram (-) enteric bacteria |
Nosocomial, occurs within 1 week of birth |
|
|
Listeria monocytogenes |
Part of early-onset septicemia |
|
|
Mycoplasma or Ureaplasma |
Maternal infection, afebrile |
|
|
Treponema pallidum |
Part of congenital syndrome |
|
|
Cytomegalovirus |
Part of systemic infection |
|
|
Herpes simplex virus |
Part of disseminated infection |
|
|
3 weeks to 3 months |
Group B streptococcus |
Part of late-onset septicemia and/or meningitis |
|
Chlamydia trachomatis |
Maternal infection, afebrile, subacute, interstitial infiltrates on CXR |
|
|
Bordetella pertussis |
Risk of secondary pneumonia from cough and aspiration |
|
|
Streptococcus pneumoniae |
Acute onset, high fever, focal findings |
|
|
Respiratory syncytial virus |
Peaks at 2-7 months, wheezing and crackles predominate |
|
|
Parainfluenza virus |
Similar to RSV, common in fall to spring season |
|
|
3 months to 5 years |
RSV, parainfluenza, influenza, hMPV, adenovirus, rhinovirus |
Most common cause, low-grade fever, diffuse findings, insidious onset |
|
Streptococcus pneumonia |
Most likely cause of lobar pneumonia, acute onset, high fever, focal findings |
|
|
Haemophilus influenzae |
Non-typeable strains in immune-compromised hosts, type b in non-vaccinated |
|
|
Staphylococcus aureus |
CA-MRSA becoming more common |
|
|
Mycoplasma pneumoniae |
Usually in children > 4 years, similar to viral syndrome |
|
|
Mycoplasma tuberculosis |
HIV and endemic areas |
|
|
5 to 15 years |
Streptococcus pneumoniae |
Most likely cause of lobar pneumonia, acute onset, high fever, focal findings, complications |
|
Mycoplasma pneumoniae |
Very common cause, clinically similar to viral syndrome |
|
|
Chlamydia pneumoniae |
Unsure incidence, probably common in older children |
|
Neonates
Most cases of pneumonia seen within the first seven days of life are a result of vertical transmission from the maternal genital tract, either by aspiration or contact with infected secretions or amniotic fluid. This is considered early-onset disease, and the most common cause is group B streptococcus. Risk factors for neonatal pneumonia include prolonged rupture of membranes, maternal chorioamnionitis, and premature birth. Although much less common, hematogenous spread from an infected mother may also occur. Severe disease, including acute respiratory distress syndrome (ARDS) and/or systemic infection, can be caused by group B streptococcus, Listeria monocytogenes, Escherichia coli, Haemophilus influenzae, group D streptococcus, Ureaplasma urealyticum, and gram-negative bacilli (anaerobes).
Late-onset disease includes any pneumonia that presents after day 7 of life to 3 months of age. The most common causes include late-onset group B streptococcus, Chlamydia trachomatis, Bordetella pertussis, and several organisms associated with congenital syndromes. Ten percent of all infants born to mothers colonized with C. trachomatis during birth will become symptomatic in the first two to three weeks of life. In addition, B. pertussis should be considered in any neonate greater than 7 days old presenting with pulmonary hypertension and pneumonia symptoms. Most cases of pneumonia that occur in association with B. pertussis are secondary and related to aspiration after prolonged coughing episodes. Other congenital infections or perinatal infections such as cytomegalovirus (CMV), herpes simplex virus (HSV), and Treponema pallidum can cause severe pneumonia. Infants with these organisms present with a combination of respiratory distress and systemic toxicity.
Viruses
Viral etiologies are the most common cause of CAP in children younger than 1 year of age. Viruses cause 80% of community-acquired pneumonia in children younger than 2 years of age, and 49% in those 2-5 years old.6 Respiratory syncytial virus (RSV) is the most common causative agent, although human metapneumovirus (hMPV), parainfluenza virus types, influenza viruses A and B, adenovirus, rhinovirus, enteroviruses, and coronavirus have also been identified in the lower respiratory tracts of young children. Recently, bocaviruses and human parechovirus 1 have been associated with lower respiratory tract illness. RSV is most common during the first 6 months of life, and illness varies in presentation from bronchiolitis-like symptoms to focal findings without wheezing. While adenovirus infections occur throughout the year, RSV, hMPV, and influenza viruses occur most commonly during the late fall and winter. Parainfluenza and rhinoviruses are more common during the spring and early fall seasons.
Bacteria
The single most common cause of bacterial pneumonia in the United States in individuals older than 30 days of life is Streptococcus pneumoniae. School-aged children are less likely to suffer from viral etiologies in comparison to younger children and infants, making bacterial agents more probable. Other common causes of CAP include Moraxella catarrhalis and Staphylococcus aureus. Once a common cause of pneumonia, Haemophilus influenzae type b pneumonias have markedly decreased with the use of Hib vaccine. Uncommon causes of CAP in the United States include non-typeable H. influenzae, gram-negative organisms, methicillin-resistant Staphylococcus aureus (MRSA), and Streptococcus pyogenes. Both MRSA and S. pyogenes can cause necrotizing pneumonia with rapidly progressive hypoxemia and formation of pleural effusion within hours of symptom onset.
Atypical Organisms
Mycoplasma pneumoniae is more common in children older than 5 years of age, with a slower transmission rate compared to viral etiologies. The median interval between family member transmission is generally about three weeks. Additionally, Chlamydophila pneumoniae (formerly Chlamydia pneumoniae) accounts for up to 20% of CAP cases in all children.6 Co-infections of M. pneumoniae with C. pneumoniae or S. pneumoniae are also quite common. Both M. pneumoniae and C. pneumoniae are common causes of CAP in adolescents. The incidence of atypical pneumonia is increasing in the preschool population.
Special Populations
In general, children with sickle cell disease, chronic lung disease, gastroesophageal reflux disease (GERD), asthma, cystic fibrosis, congenital heart disease, and immunodeficiencies are at higher risk for CAP. Non-typeable H. influenzae cases are not uncommon in patients with chronic lung disease, immunodeficiency, or aspiration syndromes. In particular, Pneumocystis jirovecii (formerly Pneumocystis carinii) and Legionella pneumophila should be considered as part of the differential diagnosis in all immune-compromised patients. In the United States, most cases of primary Mycobacterium tuberculosis occur in children born to recent immigrants from TB-endemic countries or HIV-infected individuals. In addition, children with white blood cell defects have an increased risk of gram-negative bacilli, Legionella pneumophila, S. aureus, Aspergillosis species, Fusarium species, Pneumocystis jirovecii, and potentially serious viral pathogens such as rubeola, VZV, CMV, and EBV.
Geography should also be considered when evaluating and treating any patient with respiratory symptoms. Coccidioides immitis, Blastomyces dermatitidis, and Histoplasma capsulatum are three common fungi in the environment that can be aspirated, causing pneumonia in previously healthy patients. Coccidioides immitis is a frequent cause of CAP in several southwestern states and is endemic to many South American vacation spots. Risk factors for coccidioidomycosis include activities resulting in exposure to ground dust, such as construction, landscaping, mining, agriculture, archaeological excavation, military maneuvers, dirt biking, and natural events such as earthquakes or windstorms. In the southeastern and central states, as well as those bordering the Great Lakes, Blastomyces dermatitidis is found in moist soil and wood and causes distinct lung and skin pathology. Finally, Histoplasma capsulatum is endemic in the Mississippi and Ohio River valleys and is commonly found in poultry house litter, caves, areas harboring bats, and in bird roosts. Bacterial pathogens such as Brucella abortus, Chlamydophila psittaci, Coxiella burnetii, and Francisella tularensis are transmitted from infected birds, animals, or humans. A brief travel and exposure history can assist ED physicians in identifying these risk factors. (See Table 2.)
Table 2: Diagnostic Clues: Community-acquired Pneumonia in Children
|
Diagnostic Clue |
Description |
|
Adapted from Pediatrics in Review 2008;29:151.3 |
|
|
Age |
< 30 days, toddler, school-age |
|
Season |
Late fall, winter, early spring |
|
Fever |
Height, duration, onset |
|
Associated symptoms |
Headache, congestion, rash, myalgia, malaise, diarrhea, vomiting, sore throat |
|
Associated pain |
Abdominal, stomach, chest, ear |
|
Nature of cough |
Productive, dry, staccato, worsening |
|
Risk for foreign body |
Developmental age |
|
Underlying disorders |
Reactive airway disease, immunodeficiency, malignancy, sickle cell disease, cystic fibrosis, seizure disorder, substance abuse |
|
Exposure risk |
Sick contacts, recent immigration from endemic areas |
|
Travel history |
Asia, Africa, Middle East, Latin America, geographic regions of the United States |
|
Immunization status |
Pneumococcal conjugate, Haemophilus influenzae type b, DTaP, TDaP, annual influenza |
|
Animal exposure/insect bites |
Birds, cattle, sheep, bats, chickens, soil-dwelling animals |
Pathogenesis
Pneumonia can occur in healthy individuals if their host defenses are impaired. The small hairs in the anterior nares filter large particles from the respiratory mucosa, which is comprised of ciliated, mucus-producing cells. These cells can beat the cilia synchronously to push foreign invaders and cellular debris out of the body. When a patient's airway has been overwhelmed by viral pathogens or environmental factors, such as smoke, these cilia may slow down, causing decreased mucociliary clearance. Also, any compromise to the cough reflex by medications, alcohol, or neuromuscular disease can introduce pathogens into the lung parenchyma. The mucous produced in the cells throughout the respiratory tract contain secretory IgA, which primarily functions in the humoral immune system by marking bacteria and invaders for opsonization by phagocytic cells. While this aids in the body's natural ability to fight infection, it also activates an inflammatory cascade within the lower respiratory tract and lung parenchyma. As a result, alveoli fill with white blood cells, cellular debris, and fluid, causing a reduction in lung compliance and obstruction of air flow to the distal airways.
After approximately 24 hours, fibrin is deposited and contracts over several days, causing further leakage of red blood cells and debris into surrounding alveolar tissue. The resolution stage begins as macrophages engulf and digest this fibrous material. Atelectasis and localized tissue destruction can lead to further compromise in air exchange. While various presentations are seen in different patient populations, the pattern of parenchymal damage is generally dictated by the invading organism. The following are five patterns of pneumonia:
Lobar: involvement of a single lobe or segment of a lobe (classic S. pneumoniae) (see Figure 1);
Figure 1: Right Middle Lobe Pneumonia
PA and lateral views of the chest, which show evidence of a right middle lobe pneumonia.
Images courtesy of P. Kochan, MD, of St. Christopher's Hospital for Children Radiology Department, Philadelphia, PA.
Bronchopneumonia: involvement of airways and surrounding interstitium (S. pyogenes, S. aureus);
Necrotizing: vast involvement (aspiration, S. pneumoniae, S. pyogenes, S. aureus);
Caseating granuloma: primary tuberculosis;
Interstitial and peribronchial disease with secondary parenchymal infiltration: diffuse involvement (many viruses, secondary bacterial infection).
Clinical Manifestations
Due to its many causative agents, CAP presents differently among the varied patient populations. Classic symptoms include abrupt onset fever, cough, and tachypnea. However, these symptoms are not pathognomonic. Nonspecific signs of lower respiratory tract infections include tachypnea, nasal flaring, decreased breath sounds, grunting, and crackles or rales. (See Table 3.) Further, it is well described in the literature that 5-10% of children will have radiographic evidence of pneumonia without any respiratory symptomatology.7 In an effort to better serve developing countries without readily available imaging modalities, the WHO established guidelines for the diagnosis of lower respiratory tract infections in children. According to the WHO guidelines, the best indicators of pneumonia are tachypnea and retractions, with tachypnea as defined in Table 3.8 Regardless of definition, emergency practitioners should be cognizant that tachypnea is not specific to respiratory pathology, but can also be a sign of metabolic acidosis or cardiac disease. In regard to physical exam findings, crackles have been reported to have a sensitivity of 75% and specificity of 57% for pneumonia, while wheezing and a prolonged expiratory phase were more commonly associated with bronchiolitis or a viral etiology.9 In a large, prospective cohort study in an urban pediatric ED, it was shown that hypoxia, lack of wheeze, and focal lung findings placed children at an increased risk of radiologic pneumonia.10 Table 3 summarizes the clinical manifestations of children with CAP.
Table 3: Clinical Manifestations of Community-acquired Pneumonia in Children
|
Pediatric Signs of Respiratory Distress |
|
|
SBI = serious bacterial infection a Bilavsky E, Shouval DS, Yarden-Bilavsky H, et al. Are grunting respirations a sign of serious bacterial infection in children? Acta Paediatr 2008;97:1086-1089. Adapted from: World Health Organization's Criteria for Community-acquired Pneumonia in Children. |
|
|
Tachypnea |
Breaths/minute, consider cardiac or metabolic causes |
|
0-2 months |
> 60 |
|
2-12 months |
> 50 |
|
1-5 years |
> 40 |
|
> 5 years |
> 20 |
|
Dyspnea |
|
|
Accessory muscle use |
Sign of inspiration requiring extra effort |
|
Retractions |
Sign of partially blocked airflow |
|
Suprasternal |
May be seen alone with mild disease |
|
Subcostal |
May be seen in mild, moderate, or severe disease |
|
Intercostal |
Generally seen in moderate to severe disease |
|
Nasal flaring |
|
|
Grunting |
Indicates SBI in previously healthy children > 3 monthsa |
|
Apnea |
|
|
Crackles |
Indicates distal airway narrowing by fluid, mucus, or pus |
|
Altered mental status |
|
|
Pulse oximetry |
< 90% on room air |
Neonates
In general, infants younger than 2 months of age with pneumonia will present with respiratory distress, increased work of breathing, and systemic toxicity. When present during the first days of life, neonatal pneumonia can resemble acute respiratory distress syndrome (ARDS) or transient tachypnea of the newborn. However, young infants with Chlamydia trachomatis, Bordetella pertussis, and Ureaplasma are often afebrile (afebrile pneumonia of infancy). Premature infants who have been discharged from the neonatal intensive care unit (NICU) may not mount fever, but instead display episodes of apnea or cyanosis as their only clinical indicator of pneumonia. Any afebrile infant aged 3 weeks to 3 months who presents with tachypnea, short, sudden bursts of cough (staccato), and crackles should be evaluated for C. trachomatis infection. Indicators of an acute infection include eosinophilia on a complete blood count, as well as elevated serum IgM levels. In an infant, signs of potential severe lung disease and respiratory compromise/failure include cyanosis, nasal flaring, and grunting.
Viral Pneumonia
Viral pneumonia is more gradual in onset than bacterial pneumonia and is usually preceded by an upper respiratory tract infection with low-grade fever and rhinorrhea. Any significant increase in congestion, fever, fussiness, cough, post-tussive emesis, or irritability can indicate a descending infection into the lower respiratory tract. Some viruses, such as adenovirus and influenza, can cause an associated viral syndrome with malaise, abdominal pain, and diarrhea. Auscultatory findings typically include diffuse wheezing, rhonchi, and crackles. Hypoxia is variable but can be severe in young infants, immune-compromised patients, or those with underlying lung disease.
Bacterial Pneumonia
Although the clinical presentation is variable, specific findings or patterns may assist the ED physician with the diagnosis. A classic pattern of pneumonia presentation includes a previously healthy child with an abrupt onset of fever, with or without a preceding upper respiratory tract infection. Associated with this pattern are variable degrees of hypoxemia and respiratory distress, which are dependent upon the presence of pyogenic bacteria, pleural effusion, and/or systemic disease. In addition, children with pyogenic infections will appear toxic, with high fevers, rigors, and tachypnea. The presence of cough is variable and may not manifest until day 3-4 of illness, as debris from the lungs is swept into the upper airways causing a cough reflex. Older children may complain of chest or abdominal pain and have a productive cough with rust-colored or bloody sputum. Physical exam findings include decreased air movement, decreased tactile fremitus, dullness to percussion, and rales/rhonchi in affected lung regions. Classically, the absence of wheezing is a positive predictor of pneumonia.
Prolonged Course of Illness
When fever and cough persist for longer than 7 to 10 days, M. pneumoniae, C. pneumoniae, and Coxiella burnetii (Q fever) should be considered. The typical presentation of Mycoplasma pneumoniae infection includes malaise, headache with photophobia, myalgias, fever, sore throat, gastrointestinal symptoms, and a nonproductive progressive cough that worsens as other symptoms improve. Rhinorrhea is not usually seen. Physical findings are usually restricted to fine crackles at the bilateral bases of the lungs. Chest radiography (CXR) (see Figure 2) may show bilateral patchy infiltrates. M. pneumoniae infection may be associated with bullous myringitis, urticaria, arthritis, hemolytic anemia, or Stevens-Johnson syndrome. Q fever may present with a prolonged illness course and is generally associated with fever, cough, and intractable headache. Additionally, round parenchymal opacities may be seen on CXR.
Figure 2: Mycoplasma Pneumonia
PA film showing multifocal patchy opacities likely secondary to mycoplasma pneumonia.
Images courtesy of P. Kochan, MD, of St. Christopher's Hospital for Children Radiology Department, Philadelphia, PA.
History of Reactive Airway Disease
Children with wheezing and signs of pneumonia present a particularly difficult diagnostic dilemma for ED physicians. A large, prospective study showed that the strongest predictors of radiographic pneumonia in children with wheeze were the presence and degree of fever. Children with fever of 39.0°C or greater in the ED were five times more likely to have radiographic pneumonia, while those with hypoxia (pO2 < 92%) were three times more likely to have radiographic pneumonia.11 Overall in this study, 20% of children with both fever and hypoxia had radiographic pneumonia, while the overall rate of pneumonia in this entire population was only 4.9%. A similar study conducted in children younger than 18 months of age with wheezing found that while grunting and oxygen saturation less than or equal to 93% were associated with focal infiltrates on CXR, first-time wheezing, fever, and tachypnea were not. This study also reported that the combination of grunting and oxygen saturation less than or equal to 93% was highly specific for pneumonia.12
Aspiration Pneumonia
Aspiration pneumonia can occur in children of all ages. In general, aspiration of gastric contents or oral secretions causes severe irritation of the alveolar surfaces and reactive inflammation with or without secondary bacterial infection. While this presentation is most common in children and adolescents with musculoskeletal disorders, it must also be considered in any patient with anatomic abnormalities of the proximal airway or digestive tract, history of substance abuse, intoxicated patients, history of seizure disorder, foreign body aspiration, and any patient who has recently undergone procedural sedation. Secondary infections may occur in up to 50% of patients with acute aspiration syndrome and may include a variety of mixed flora (S. aureus, Klebsiella, Proteus, Pseudomonas, E. coli, and anaerobes such as Bacteroides, Fusobacterium, Peptostreptococcus, and Prevotella melaninogenica).13 Table 4 summarizes the most common constellation of clinical pneumonia syndromes in children in the United States.
Table 4: Common Clinical Pneumonia Syndromes of Childhood
|
Syndrome |
Typical Cause |
Age Group |
Clinical Features |
Radiographic Findings |
|
* MC = Most common Adapted from: Pediatrics in Review 2008;29:152.3 |
||||
|
Bacterial |
Streptococcus pneumoniae |
All ages, MC* 1 mo to 6 yrs |
Abrupt onset, high fever, focal findings, chest and/or abdominal pain |
Focal infiltrate |
|
Atypical infancy |
Chlamydia trachomatis |
3 wks to 3 mos |
Tachypnea, no fever, staccato cough, crackles |
Interstitial infiltrate |
|
Atypical |
Mycoplasma pneumoniae |
> 5 yrs |
Insidious onset, low-grade fever, systemic symptoms (headache, malaise, etc.) |
Diffuse, bilateral infiltrates, often "patchy" |
|
Viral |
Multiple viruses |
All ages, MC* 3 mos to 5 yrs |
URI symptoms, wheezing, +/- low-grade fever, diffuse exam findings |
Variable, diffuse interstitial infiltrates common |
Differential Diagnosis
The ED physician should construct a broad differential when children present with signs and symptoms consistent with pneumonia. Alternative diagnoses, especially in the setting of a child without fever or with chronic symptoms, should include foreign body aspiration, asthma, gastroesophageal reflux disease (GERD), cystic fibrosis, and congestive cardiac failure. It is also important to consider etiologies that may result in recurrent pneumonias. These etiologies include anatomic lesions, such as vascular rings, cysts, pulmonary sequestration, and immunologic disorders such as human immunodeficiency virus (HIV) infection, chronic granulomatous disease, and hypogammaglobulinemia.
Evaluation
Routine imaging and/or measurement of laboratory values is unnecessary in mildly ill patients who may be managed as outpatients. However, patients who are moderately ill or fail to show improvement in symptoms on empiric treatment, who are immunocompromised or have an underlying chronic disease, or who require hospitalization for pneumonia warrant further testing and workup.
Laboratory Studies
Blood Tests. Complete blood count with differential and acute phase reactants (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP] concentration, serum procalcitonin concentration) may aid in the diagnosis of CAP, but should not be used to distinguish either the presence or cause of CAP. However, in patients requiring admission, acute phase reactants can be used to assess response to therapy. The typical pattern of labs consistent with a bacterial pneumonia include increased WBC count, left shift/bandemia on differential, and increased acute phase reactants.
Cultures. Blood culture is a specific but insensitive test for pneumonia. It is found to be positive in, at most, 10-12% of children with pneumonia and 30-40% in patients with a parapneumonic effusion and empyema. Moderate-quality evidence suggests obtaining blood cultures when children fail to respond to traditional therapy, have prolonged or progressive symptoms, or have clinical deterioration.14 Nasopharyngeal culture is usually unreliable because many bacterial pathogens are also common commensals. Sputum cultures can be obtained from older children who are able to produce sputum. An appropriate sputum specimen has less than 10 squamous epithelial cells and greater than 25 neutrophils per low-power field, and a predominant organism. Pleural fluid culture is typically done in patients with more than minimal pleural effusion via diagnostic and/or therapeutic thoracocentesis.
Rapid Diagnostic Tests. Molecular testing using polymerase chain reaction (PCR) techniques and immunofluorescence on nasopharyngeal secretions may be helpful in guiding the clinical decision process in patients suspected of having CAP. However, the presence of a viral agent in the upper respiratory tract does not exclude the presence of secondary bacterial pneumonia. Common rapid diagnostic tests that are available include tests for RSV, influenza, adenovirus, parainfluenza, and M. pneumoniae. Tracheal aspirates are only required for patients with severe or life-threatening pneumonia.
Invasive Studies. Invasive procedures are usually done to obtain lower respiratory tract specimens for culture and in patients who are seriously ill, who show minimal improvement on empiric treatment, are immunocompromised, or who have developed severe complications. These studies include a diagnostic/therapeutic thoracocentesis, bronchoalveolar lavage, percutaneous needle aspiration of affected lung tissue, and lung biopsy. A surgical or pulmonary consultation should be obtained when such complications are suspected.
Imaging
Indications for chest radiography in children with clinical evidence of pneumonia are included in Table 5.14 When radiographs are indicated, posteroanterior (PA) and lateral views should be obtained. It is important to note that radiologic findings may lag behind clinical findings, and that patients who are dehydrated may have a normal-appearing chest radiograph prior to volume repletion. A decubitus view can help in determining whether the fluid is free-flowing or loculated.
Table 5: Indications for Radiographs by Setting
|
Emergency Department |
Inpatient |
|
Suspected or documented hypoxemia with or without significant respiratory distress |
All patients admitted, to document presence, size, and character of parenchymal infiltrations and to identify complications |
|
Failure of initial antibiotic therapy (to identify complications of pneumonia) |
Follow-up CXR if no clinical improvement or deterioration within 48-72 hours of antibiotic initiation |
|
Suspected foreign body aspiration or cardiac disease |
Follow-up CXR in 4-6 weeks in patients with recurrent pneumonia involving same lobe or lobar collapse at initial CXR to identify anatomic abnormality |
Other imaging modalities that may be used in the setting of pneumonia include ultrasonography and computed tomography (CT) scan of the chest. Ultrasonography often can determine the location, quantity, and quality of fluid (e.g., thickness, fibrinous streaking, and presence of loculations). Chest CT is used to better visualize the extent of parenchymal involvement.
Management
Inpatient vs. Outpatient. The majority of CAP may be treated by clinical suspicion, limited diagnostic tests, and with outpatient management. Current evidence shows that children admitted for CAP may be treated with oral medication and supportive care, as intravenous line placement and invasive testing show no cost or outcome benefit. Therefore, a child may be discharged from the ED in the absence of clinical signs and symptoms of systemic illness, complication of CAP, inability to tolerate oral medication, or hypoxia.
Indications for hospitalization of pediatric patients with CAP are reviewed in Table 6.
Table 6: Inpatient vs. Outpatient Management of Children with CAP
|
Indication |
Outpatient |
Inpatient |
Intensive Care |
|
Respiratory distress/oxygen saturation |
SpO2 > 92% |
SpO2 < 92% |
Endotracheal intubation, CPAP, BiPAP |
|
Tachycardia |
Resolved with fever defervescence |
Sustained tachycardia |
|
|
Blood pressure |
Stable |
Unstable on presentation, positive response to resuscitation |
Pharmacological support required |
|
Mental status |
Altered mental status, sleepiness in infant, etc. |
||
|
Oral tolerance |
Stable |
Variable; IV antibiotics required |
Variable; IV antibiotics required |
|
Age |
< 3-6 months, unless C. trachomatis proven and relatively nonsymptomatic |
If symptoms present within day of life 0-3, NICU admission likely |
|
|
Complicating factors |
CA-MRSA, virulence Parapneumonic effusion Empyema Lung abscess |
||
|
Social concerns |
Reliable family |
Concerns for compliance with medication, judgment of illness, and follow-up |
Supportive Therapy. Supple-mental oxygen therapy is indicated in any patient whose oxygen saturation is persistently 92% or less. In dehydrated patients or those at risk for aspiration due to severe respiratory distress, intravenous hydration may be necessary. Chest physiotherapy is not recommended for routine treatment of CAP in any population despite its consistent use in 15% of cases.14 Finally, pain and fever should be adequately controlled with age-appropriate antipyretics or analgesics.
Antimicrobial Therapy. Medical management for community-acquired pneumonia frequently depends on the patient's age, epidemiologic and clinical information, causative organism, and/or diagnostic laboratory and imaging studies. At this time, there is no reliable technique to distinguish viral and bacterial causes of CAP, and, therefore, all children with an apparent diagnosis should receive antibiotic therapy. Typical antimicrobial regimens are reviewed in Table 7.
Table 7: Empiric Therapy for Pediatric Community-acquired Pneumonia (CAP)
|
Site of Care |
Patient |
Causative Agent |
Therapeutic Agent |
Length of Therapy (days) |
|
The above recommendations represent general guidelines for the treatment of pneumonia. Practitioners should tailor the selection of antimicrobials in children with pneumonia based on the individual patient circumstances, geography, and community drug sensitivities. |
||||
|
Outpatient |
< 5 years old |
Bacteria |
Oral amoxicillin Alternative: amoxicillin-clavulanate |
10 |
|
Atypical |
Oral azithromycin Alternatives: clarithromycin, erythromycin |
5 |
||
|
≥ 5 years old |
Bacteria |
Oral amoxicillin Alternative: amoxicillin-clavulanate |
10 |
|
|
Atypical |
Oral azithromycin Alternatives: clarithromycin, erythromycin, doxycycline, levofloxacin |
5 |
||
|
Inpatient |
Fully immunized with conjugate vaccines for H. influenzae type b and S. pneumoniae Local penicillin resistance in invasive strains of pneumococcus is minimal. |
Bacteria |
IV ampicillin IV penicillin G Alternatives: IV ceftriaxone |
10 |
|
Atypical |
IV azithromycin, then transition to oral therapy if possible on days 2 or 3 Alternatives: IV erythromycin, levofloxacin, clarithromycin, doxycycline |
5 |
||
|
CA-MRSA |
Vancomycin Clindamycin |
Possibly > 10 |
||
|
Not fully immunized for H. influenzae type b and S. pneumoniae Local penicillin resistance in invasive strains of pneumococcus is significant. |
Bacteria |
IV ceftriaxone IV cefotaxime Alternative: levofloxacin |
10 |
|
|
CA-MRSA |
Vancomycin Clindamycin |
Possibly > 10 |
||
Viruses. Infants and young children who are mildly ill with diffuse findings on chest examination will generally not require antimicrobials. Effective antivirals are not available for most viral pneumonias except for influenza. In children with moderate to severe CAP consistent with influenza virus infection (high fever, malaise, myalgia, diarrhea), as well as during widespread local circulation of influenza viruses, treatment with oseltamivir (Tamiflu) or zanamivir (Relenza) should be started immediately. As early antiviral treatment has been shown to provide significant benefit, treatment should not be delayed until confirmation of a positive influenza test.
Monitoring Response
Children with pneumonia who are treated as outpatients (including those who were not initially treated with antibiotics) should be followed up within 24 to 48 hours. Appropriately treated children generally show signs of improvement within 48 to 72 hours. In children with a worsening condition, it is important to consider initial or repeat chest radiography to evaluate for the development of complications and the need for hospitalization. Patients with suspected atypical pneumonia who were initially treated with macrolides may require pneumococcal coverage if they fail to improve clinically.
Complications
Bacterial pneumonias are more likely to be associated with complications compared to atypical and viral etiologies. Major pulmonary complications associated with bacterial pneumonias include parapneumonic effusion, empyema, necrotizing pneumonia, lung abscess, and pneumatoceles. See Table 8 for a complete list of complications associated with CAP.
Table 8: Complications Associated with Community-acquired Pneumonia
Pulmonary
- Pleural effusion or empyema
- Pneumothorax
- Lung abscess
- Bronchopleural fistula
- Necrotizing pneumonia
- Acute respiratory failure
Metastatic
- Meningitis
- Central nervous system abscess
- Pericarditis
- Endocarditis
- Osteomyelitis
- Septic arthritis
Systemic
- Systemic inflammatory response syndrome or sepsis
- Hemolytic uremic syndrome
Adapted from: Clinical Practice Guidelines by the Pediatric Infectious Diseases Society and the IDSA, 2011.
Parapneumonic Effusions. Parapneumonic effusions (PPE) are inflammatory fluid collections adjacent to a pneumonic process seen in about 40% of cases of bacterial pneumonia. Effusions are typically caused by a sympathetic response to a bacterial infection, extension of infection, or an immune-complex phenomenon. Due to lack of opsonins and complements, the pleural fluid is readily infected, causing it to be purulent (empyema). Affected children are usually ill-appearing and typically present with respiratory distress, persistent fever, tachypnea, chest pain, and splinting. On physical exam, there will be decreased breath sounds and dullness to percussion on the affected side. Plain radiographs can establish the diagnosis of an effusion, while a decubitus view will assist with the differentiation of free-flowing vs. loculated fluid. (See Figure 3.) Ultrasonography may be used to localize and estimate the size of an effusion, in addition to identifying an optimal position for chest tube placement. CT may be used to better visualize the extent of parenchymal involvement, although it is usually not necessary in planning the management of complicated pneumonias.18 Surgical consultation should be considered if drainage is required.
Figure 3: Parapneumonic Effusion
Right and left decubitus films showing evidence of complex, loculated right parapneumonic effusion that is not free-flowing. There is also a right lower lobe airspace consolidation.
Images courtesy of P. Kochan, MD, of St. Christopher's Hospital for Children Radiology Department, Philadelphia, PA.
Small free-flowing effusions may be treated with antibiotics alone, while moderate to large effusions will need to be drained, typically by thoracentesis, chest tube drainage, video-assisted thorascopic surgery (VATS) with chest tube drainage, intrapleural fibrinolytic therapy, and/or thoracotomy. In the setting of moderate to large pleural effusions, broad-spectrum antimicrobial agents should be considered.
Necrotizing Pneumonia. Necrotizing pneumonia usually occurs as a result of localized lung infection by highly virulent, pyogenic bacteria. As a result, the affected lung tissue undergoes liquefaction and necrosis. Complications such as formation of a lung abscess, pneumatocele (thin-walled, air-containing cysts in the lung parenchyma, see Figure 4), or a bronchopleural fistula may be associated with necrotizing pneumonia. The most common causative pathogen is S. pneumoniae, or, less commonly, S. aureus (especially CA-MRSA) or S. pyogenes. Clinical manifestations are similar but usually more severe than non-necrotizing pneumonia. The presentation with necrotizing pneumonia may be variable and include hemoptysis, prolonged fever, toxic appearance, and persistent hypoxia despite appropriate antimicrobial therapy. Chest radiography will reveal a radiolucent lesion. A CT scan may be used to further delineate the extent of parenchymal involvement. A decreased parenchymal contrast enhancement on the CT scan correlates with impending necrosis and cavitation. (See Figure 5.) Initial broad-spectrum antimicrobial coverage is indicated with signs or radiographic evidence of a necrotizing pneumonia.
Figure 4: Pneumatocele
Note pneumatocele in the right upper lobe, commonly seen as a complication of necrotizing pneumonia.
Image courtesy of P. Kochan, MD, of St. Christopher's Hospital for Children Radiology Department, Philadelphia, PA.
Figure 5: Necrotizing Pneumonia
Chest CT showing a complex and mottled appearance of the right upper lobe consistent with necrotizing pneumonia.
Image courtesy of P. Kochan, MD, of St. Christopher's Hospital for Children Radiology Department, Philadelphia, PA.
Lung Abscess and Empyema. Lung abscess is a collection of fluid within the lung parenchyma. The etiology may include a variety of pathologic processes, including necrotizing pneumonia, aspiration, bacteremia, and septic emboli. Further, lung abscesses may develop as a consequence of subacute or chronic airway infection (cystic fibrosis, prolonged intubation). Clinical manifestations include fever, cough, dyspnea, sputum production, chest pain, hemoptysis, and putrid breath. On chest radiograph, the diagnosis can be made based on the finding of an air-fluid level in a cavity at least 2 cm in diameter, with a well-defined wall. Anaerobic bacteria are the typical causative organisms, with Peptostreptococcus spp., Bacteroides spp., Prevotella spp., and Veillonella spp. being most common. S. aureus and gram-negative rods may also be involved. Tuberculosis should be considered as part of the differential diagnosis in a child with a lung abscess. Clindamycin is commonly used empirically to treat lung abscesses. However, culture specimens obtained via bronchoscopy or direct aspiration of the abscess may be necessary in complex cases or when there is a lack of response to initial empiric therapy.
Figure 6: Lung Abscess
Chest CT showing evidence of a left lung abscess.
Image courtesy of P. Kochan, MD, of St. Christopher's Hospital for Children Radiology Department, Philadelphia, PA.
Figure 7: Empyema
Ultrasound image showing complex collection in the left pleural space (note the septations), likely representing a nonmobile empyema.
Image courtesy of P. Kochan, MD, of St. Christopher's Hospital for Children Radiology Department, Philadelphia, PA.
Figure 8: Empyema
Chest CT showing evidence of empyema in the left lung.
Image courtesy of P. Kochan, MD, of St. Christopher's Hospital for Children Radiology Department, Philadelphia, PA.
In contrast, empyema is a collection of pus in the pleural space. The fluid accumulation causes pressure on lung tissue and associated pleural space, with resultant respiratory compromise and pleuritic pain. Additional symptoms consistent with empyema include dry cough, night sweats, fever and chills, shortness of breath, malaise, and unintentional weight loss. Risk factors for the development of empyema include bacterial pneumonia, lung abscess, recent chest surgery, and trauma or injury to the chest wall. Ultrasound and chest CT are typically utilized to characterize the collection. (See Figures 7 and 8.) Surgical intervention is frequently required for thoracocentesis, chest tube placement, and decortication in severe cases.
Prognosis
Mortality due to CAP is uncommon beyond infancy in the United States, secondary to access to healthcare, availability of antimicrobial therapy, and enhanced immunization rates. Few studies have examined the long-term outcome of children with pneumonia. However, there is evidence of decreased lung function in adults with a history of pneumonia before the age of 7 years.19 In regard to children, there is sparse information about the long-term outcome after pneumonia.
Summary
CAP is a commonly encountered disease process in the emergency department. Early recognition and appropriate management can minimize morbidity and mortality. In addition, the early recognition of complications may facilitate timely intervention.
References
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Classically, pneumonia is defined as an infection of the lung parenchyma. However, worldwide, a variety of definitions exist, including fever, hypoxia, a constellation of other clinical symptoms, and radiologic findings. In pediatric and adolescent populations, early diagnosis will assist emergency department (ED) physicians with correctly managing and subsequently avoiding potential morbidity and mortality of this common infectious disease.Subscribe Now for Access
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