eMedicine Specialties > Emergency Medicine > Pediatric

Pediatrics, Pneumonia

Mark I Neuman, MD, MPH, Assistant Professor of Pediatrics, Harvard Medical School; Attending Physician, Division of Emergency Medicine, Children's Hospital Boston

Updated: Jul 24, 2009

Introduction

Background

Pneumonia and other lower respiratory tract infections are the leading cause of death worldwide. Other respiratory tract diseases such as croup (laryngotracheobronchitis), bronchiolitis, and bronchitis are beyond the scope of this article and are not discussed further. Approximately 150 million new cases of pneumonia occur annually among children younger than 5 years worldwide, accounting for approximately 10-20 million hospitalizations.1 Although the diagnosis is usually made on the basis of radiographic findings in developed countries, the World Health Organization (WHO) has defined pneumonia solely on the basis of clinical findings obtained by visual inspection and timing of the respiratory rate.2,3,4,5  

It is important for the physician to understand that the typical causes and presentations of pneumonia in infants and children are variable, depending upon the child's age and underlying medical condition.

Pathophysiology

Pneumonia results from inflammation of the alveolar space and may compromise air exchange. While often complicating other lower respiratory infections such as bronchiolitis or laryngotracheobronchitis, pneumonia may also occur via hematogenous spread or aspiration. Most commonly, this inflammation is the result of invasion by bacteria, viruses, or fungi, but it can occur as a result of chemical injury or may follow direct lung injury (eg, near drowning).

Four stages of lobar pneumonia have been described. In the first stage, occurring within 24 hours of infection, the lung is characterized microscopically by vascular congestion and alveolar edema. Many bacteria and few neutrophils are present. The stage of red hepatization (2-3 d), so called because of its similarity to the consistency of liver, is characterized by the presence of many erythrocytes, neutrophils, desquamated epithelial cells, and fibrin within the alveoli. In the stage of gray hepatization (2-3 d), the lung is gray-brown to yellow because of fibrinopurulent exudate, disintegration of red cells, and hemosiderin. The final stage of resolution is characterized by resorption and restoration of the pulmonary architecture. Fibrinous inflammation may extend into the pleural space, causing a rub heard by auscultation, and it may lead to resolution or to organization and pleural adhesions.

Bronchopneumonia, a patchy consolidation involving one or more lobes, usually involves the dependent lung zones, a pattern attributable to aspiration of oropharyngeal contents. The neutrophilic exudate is centered in bronchi and bronchioles, with centrifugal spread to the adjacent alveoli.

In interstitial pneumonia, patchy or diffuse inflammation involving the interstitium is characterized by infiltration of lymphocytes and macrophages. The alveoli do not contain a significant exudate, but protein-rich hyaline membranes similar to those found in adult respiratory distress syndrome (ARDS) may line the alveolar spaces. Bacterial superinfection of viral pneumonia can also produce a mixed pattern of interstitial and alveolar airspace inflammation.

Miliary pneumonia is a term applied to multiple, discrete lesions resulting from the spread of the pathogen to the lungs via the bloodstream. The varying degrees of immunocompromise in miliary tuberculosis, histoplasmosis, and coccidioidomycosis may manifest as granulomas with caseous necrosis to foci of necrosis. Miliary herpesvirus, cytomegalovirus, or varicella-zoster virus infection in severely immunocompromised patients results in numerous acute necrotizing hemorrhagic lesions.

Factors that bypass or inactivate local defenses (eg, tracheostomy tubes, immotile cilia syndrome) predispose the child to pneumonia. The result is loss of surfactant activity with local collapse and consolidation.

Pneumonia may be classified by the causative organism, the anatomic location, or the tissue response.

Frequency

United States

A WHO Child Health Epidemiology Reference Group publication cited the incidence of community-acquired pneumonia among children younger than 5 years in developed countries as approximately 0.026 episodes per child-year.1

In a prospective multicenter study of 154 hospitalized children with acute community-acquired pneumonia in whom a comprehensive search for etiology was sought, a pathogen was identified in 79% of children. Bacteria accounted for 60%, of which 73% were due to Streptococcus pneumoniae; Mycoplasma pneumoniae and Chlamydia pneumoniae were detected in 14% and 9%, respectively. Viruses were documented in 45% of children. Notably, 23% of the children had concurrent acute viral and bacterial disease.6 In the study, preschool-aged children had as many episodes of atypical bacterial lower respiratory infections as older children. Multivariable analyses revealed that high temperature (38.4°C) within 72 hours after admission and the presence of pleural effusion were significantly associated with bacterial pneumonia.

Thompson et al reported annual influenza-associated hospitalizations in the United States by hospital discharge category, discharge type, and age group.7 After elderly persons, the second highest rates of influenza-associated hospitalizations were in children younger than 5 years.

In a randomized double blind trial, the heptavalent pneumococcal vaccine reduced the incidence of clinically diagnosed and radiographically diagnosed pneumonia among children younger than 5 years by 4% and 20%, respectively.8

International

The WHO Child Health Epidemiology Reference Group estimated the median global incidence of clinical pneumonia to be 0.28 episodes per child-year.1 This equates to an annual incidence of 150.7 million new cases, of which 11-20 million (7-13%) are severe enough to require hospital admission. Ninety-five percent of all episodes of clinical pneumonia in young children worldwide occur in developing countries.

Mortality/Morbidity

According to the WHOs Global Burden of Disease 2000 Project, lower respiratory infections were the second leading cause of death in children younger than 5 years (about 2.1 million [19.6%]).

  • Most children are treated as outpatients and fully recover. However, in young infants and immunocompromised individuals, mortality is much higher.
  • In studies of adults with pneumonia, a higher mortality rate is associated with abnormal vital signs, immunodeficiency, and certain pathogens.

Race

Pneumonia affects children of all races; however, certain conditions that may predispose to pneumonia have racial predilections. For example, cystic fibrosis is far more common in white children. Children with sickle cell anemia are at increased risk for pneumonia as a result of sickling within the pulmonary vasculature and functional asplenia.

Age

Pneumonia in the pediatric population is most common in infants and toddlers and least common in adolescents and young adults.

Clinical

History

In children, etiologic agent, age of the patient, and underlying illnesses all affect the historical features of the illness.

  • Neonates  
    • The infant may present with tachypnea; signs of respiratory distress, such as grunting, flaring, and retractions; lethargy; poor feeding; or irritability. Fever may not be present in newborns; however, hypothermia and temperature instability may be observed.
    • Cyanosis may be present in severe cases.
    • Nonspecific complaints, such as irritability or poor feeding, may be the presenting symptoms.
    • Cough may be absent in the newborn period.
    • Early-onset group B streptococci infection usually presents via ascending perinatal infection as sepsis or pneumonia within the first 24 hours of life. Chlamydia trachomatis pneumonia should be considered in infants aged 2-4 weeks and is often associated with conjunctivitis.
  • Infants  
    • After the first month of life, cough is the most common presenting symptom.
    • Infants may have a history of antecedent upper respiratory symptoms.
    • Depending upon the degree of illness, tachypnea, grunting, and retractions may be noted. Vomiting, poor feeding, and irritability are also common.
    • Infants with bacterial pneumonia often are febrile, but those with viral pneumonia or pneumonia caused by atypical organisms may have a low-grade fever or may be afebrile. The child's caretakers may complain that the child is wheezing or has noisy breathing.
  • Toddlers and preschool children    
    • A history of antecedent upper respiratory illness is common.
    • Cough is the most common presenting symptom.
    • Vomiting, particularly post-tussive emesis, may be present. Chest pain may be observed with inflammation of or near the pleura. Abdominal pain or tenderness is often seen in children with lower lobe pneumonia. 
    • The presence and degree of fever is dependent upon the organism involved.
  • Older children and adolescents    
    • Atypical organisms, such as Mycoplasma, are more common in this age group.
    • In addition to the symptoms observed in younger children, adolescents may have other constitutional symptoms, such as headache, pleuritic chest pain, and vague abdominal pain. Vomiting, diarrhea, pharyngitis, and otalgia/otitis are other common symptoms.

Physical

  • Early in the physical examination, identifying and treating respiratory distress, hypoxemia, and hypercarbia is important. Signs such as grunting, flaring, severe tachypnea, and retractions should prompt the clinician to provide immediate respiratory support. An assessment of oxygen saturation by pulse oximetry should be performed early in the evaluation of all children with respiratory symptoms. When appropriate and available, capnography may be useful in the evaluation of children with potential respiratory compromise.
  • Visual inspection of the degree of respiratory effort and accessory muscle use should be performed to assess for the presence and severity of respiratory distress. The examiner should simply observe the patient's respiratory effort and count the respirations for a full minute. In infants, observation should include an attempt at feeding, unless the baby has extreme tachypnea.
  • Auscultation is perhaps the most important portion of the examination of the child with respiratory symptoms. The examination often is very difficult in infants and young children for several reasons.  
    • Babies and young children often cry during the physical examination making auscultation difficult. The best chance of success lies in prewarming hands and instruments and in using a pacifier to quiet the infant. The opportunity to listen to a sleeping infant should never be lost.
    • Older infants and toddlers may cry because they are ill or uncomfortable, but, most often, they have stranger anxiety. For these children, it is best to spend a few minutes with the parents in the child's presence. If the child sees that the parent trusts the examining physician then he or she may be more willing to let the examiner approach. A small toy may help to gain the child's trust. Any part of the examination using instruments should be deferred as long as possible, because the child may find the medical equipment frightening. Occasionally, if the child is allowed to hold the stethoscope for a few minutes, it becomes less frightening. Even under the best of circumstances, examining a toddler is difficult. If the child is asleep when the physician begins the evaluation, auscultation should be performed early.
    • It is not unusual for children with respiratory symptoms to have a concomitant upper respiratory infection with copious upper airway secretions. This creates another potential problem, transmission of upper airway sounds. In many cases, the sounds created by upper airway secretions can almost obscure true breath sounds and lead to erroneous diagnoses. If doubt exists as to the etiology of sounds heard through the stethoscope, the examiner should listen to the lung fields and then hold the stethoscope near the child's nose. If the sounds from both locations are approximately the same, the likely source of the abnormal breath sounds is the upper airway.
    • Even when the infant or young child is quiet and has a clear upper airway, the child's normal physiology may make the examination difficult. The minute ventilation is the product of the respiratory rate and tidal volume. In young children, respiratory rate makes a very large contribution to the overall minute ventilation. In other words, babies take many shallow breaths as opposed to a few deep ones. Therefore, a subtle finding, particularly one at the pulmonary bases, can be missed.
    • The sine qua non for this disease has always been the presence of crackles or rales. Although often present, focal crackles as a stand-alone physical examination finding is neither sensitive nor specific for the diagnosis of pneumonia.9,10,11  Additionally, not all children with pneumonia have crackles.
    • Other examination findings suggestive of pneumonia include focal wheezing or decreased breath sounds in one lung field.
    • Similarly, certain more diffuse lung infections may result in generalized crackles or wheezing.
  • Percussion may reveal important information. Occasionally, a child presents with a high fever and cough but without ausculatory findings suggestive of pneumonia. In such cases, percussion may help to identify an area of consolidation.
  • Pneumonia may occur as a part of another generalized process. Therefore, signs and symptoms suggestive of other disease processes, such as rashes and pharyngitis, should be sought during the examination.

Causes

Pathogens implicated in pneumonia vary with the age of the child, the underlying patient-specific risk factors, immunization status, and seasonality.

  • Newborns and infants
    • In the neonate, pathogens that may infect the infant via the maternal genital tract include group B streptococci, Escherichia coli and other fecal coliforms, and C trachomatis. Group B streptococci most often is transmitted to the fetus in utero, usually as a result of colonization of the mother's vagina and cervix by the organism.
      • Affected infants commonly present within the first few hours after birth, but if infection is acquired during the delivery, the presentation may be delayed.
      • The usual presenting symptoms include tachypnea, hypoxemia, and signs of respiratory distress.
      • Physical examination may reveal diffuse fine crackles, and the chest radiograph may demonstrate a ground-glass appearance and air bronchograms.
    • Newborns may be affected by the bacteria and viruses that cause infections in older infants and children. Risk factors for infection include older siblings, group daycare, and lack of immunization, particularly against pertussis.
    • In the young infant, aged 1-3 months, continued concern about perinatally acquired pathogens mentioned above as well as the unusual Listeria monocytogenes remains. However, most pneumonia in this age group is community acquired and involves Streptococcus pneumoniae, Staphylococcus aureus, and non-typeable Haemophilus influenzae. 
      • Although the young unimmunized or incompletely immunized infant remains at theoretical risk for H influenzae and pneumococcal disease, herd immunity gained from widespread immunization of the population has been generally protective.
      • Most lower respiratory disease in the young infant occurs during the respiratory virus season and is viral in origin, particularly in the patient with clinical bronchiolitis. The most common agents include parainfluenza viruses, influenza virus, adenovirus, metapneumovirus, and respiratory syncytial virus (RSV). Morbidity and mortality from RSV and other viral infections is higher among premature infants and infants with underlying lung disease.
    • Atypical organisms may also cause infection in infants. Of these, C trachomatis, Ureaplasma urealyticum, cytomegalovirus, and Pneumocystis carinii (PCP) are the most common. Pneumocystis pneumonia is generally limited to immunocompromised infants.
    • Bordetella pertussis may affect infants. Only 80% of fully immunized children are protected against pertussis and immunity to this disease wanes in late adolescence. Since infants have not completed the vaccination series and because adults are a potential reservoir for infection, both groups are at risk.
    • Streptococcus pneumoniae is by far the most common bacterial pathogen in this age group.
    • Infection with Staphylococcus aureus may be complicated by lung abscess, parapneumonic effusions, and empyema.12
  • Young children
    • Viruses are a common cause of pneumonia among toddlers and preschoolers. The usual culprits are those previously discussed. Tsolia et al identified a viral infection among 65% of hospitalized children with community-acquired pneumonia.13
    • Streptococcus pneumoniae is by far the most common bacterial cause of pneumonia. Among hospitalized children, Streptococcus pneumoniae accounts for 21-44% of disease.6,14,15 In a recent study to evaluate the effectiveness of heptavalent pneumococcal conjugate vaccine in prevention of pneumonia in children younger than 5 years, Black et al showed a 32.2% reduction in the first year of life and a 23.4% reduction between 1-2 years, but only a 9.1% reduction in children older than 2 years.16,8
  • Children in this age group are also at risk for infection by M pneumoniae.
  • Older children and adolescents
    • M pneumoniae is a frequent cause of pneumonia among older children and adolescents. Mycoplasma accounts for 14-35% of pneumonia hospitalizations in this age group.6,13,17
    • C pneumoniae can cause pneumonia in this age group.
    • Older adolescents may have lost their immunity to pertussis and may become infected by this organism. Unlike the whooping cough in infants, pertussis in older patients usually causes a paroxysmal cough, which persists for more than 3 weeks and may last up to 3 months.
    • Bacterial pneumonia in this age group most often is caused by Streptococcus pneumoniae.
  • Other rare organisms
    • Histoplasma capsulatum, which is found in nitrate-rich soil, usually is acquired as a result of inhalation of spores. Chicken coops and other bird roosts and decaying wood are oft-cited sources. The infection is usually asymptomatic; however, infants and young children are at risk for symptomatic infection, which may cause respiratory distress and hypoxemia.
    • Blastomyces dermatitides is a dimorphic yeast, which is found in certain geographic locations, most notably the Ohio and Mississippi River valleys. As with histoplasmosis, blastomycosis is acquired by inhalation of spores. Although 3 distinct forms of infection exist, the most common is acute pneumonia, which most often resolves without treatment.
    • Cryptococcus neoformans is a common infection among pigeon breeders, but it is unusual in other immunocompetent individuals. Cryptococcosis may occur in as many as 5-10% of patients with AIDS. In immunocompetent patients, this organism causes no symptoms or a mild pneumonia and requires no treatment.
    • Mycobacterial pneumonia has recently been noted with increasing frequency in some inner-city areas. Children in homeless shelters and group homes and those with household contacts are at particular risk. Similarly, the diagnosis must be considered in immunocompromised children.
  • RSV is a common cause of lower respiratory tract infection in children. Serious infections with this organism usually occur in infants with underlying lung disease. Bacterial superinfection may also complicate RSV pneumonia.
  • The herpesviruses rarely may cause pneumonia. In infants, the usual agent is herpes simplex, and, in older children, pneumonia may complicate common varicella infections.
  • Influenza A is a less common pathogen.
  • Legionella species may cause pneumonia in immunocompromised children.
  • Children with cystic fibrosis may be infected with various organisms such as Staphylococcus aureus, Pseudomonas aeruginosa , Burkholderia cepacia , and other multidrug-resistant organisms.
Not all pneumonia is caused by infectious agents. Children who have severe gastroesophageal reflux may develop chemical pneumonitis secondary to recurrent aspiration. Inhalation of certain chemicals or smoke may cause pulmonary inflammation. Additionally, children with impaired swallowing, gastrointestinal motility, or a gastrostomy tube may be prone to aspiration pneumonia.

Differential Diagnoses

Acute Respiratory Distress Syndrome
Pneumonia, Aspiration
Asthma
Pneumonia, Bacterial
Bronchiolitis
Pneumonia, Empyema and Abscess
Bronchitis
Pneumonia, Immunocompromised
Foreign Body Aspiration
Pneumonia, Mycoplasma
Pediatrics, Respiratory Distress Syndrome
Smoke Inhalation
Pertussis

Workup

Laboratory Studies

Very few laboratory studies are particularly useful in the evaluation of the child with pneumonia.

  • Although it is true that many of the etiologic organisms may be identified by culture or immunofluorescent antibody techniques, in practice, these are too costly and time consuming for routine use. Furthermore, the results of such tests are rarely available in less than several hours, thus making them even less useful to the emergency clinician.
  • Complete blood count
    • In cases of pneumococcal pneumonia, the WBC count is often elevated. 
    • Prior to widespread pneumococcal immunization, Bachur et al observed that approximately 25% of febrile children with a WBC count >20,000/mm3, but without lower respiratory tract findings on examination, had radiographic pneumonia (termed occult pneumonia).18
    • Although blood testing was obtained less frequently in the post-Prevnar era, recent studies by the same group demonstrated that leukocytosis was still associated with occult pneumonia.19,20
  • Cultures
    • Bacteremia is rarely associated with pneumonia in children, and blood culture is not routinely required in immunocompetent children.21
    • Blood cultures should be obtained when the patient is critically ill, immunocompromised, or has persistent symptoms. Additionally, blood cultures are useful in patients with high fever and large areas of consolidation—mostly to make a microbiologic diagnosis.
    • Sputum cultures should be reserved for unusual cases or very ill patients.
  • Sputum Gram stain 
    • In the cooperative older child with a productive cough, a sputum Gram stain may be obtained.
    • In order to be useful, the specimen must contain less than 10 epithelial cells and more than 25 WBC per high-powered field. Very few children are able to cooperate with such a test.
  • Consideration should be given for rapid viral testing in young infants with simple infiltrates.

Imaging Studies

  • The criterion standard test for the diagnosis of pneumonia is a 2-view plain chest radiograph. However, when chest radiographs are subjected to blinded readings, they may not differentiate between viral disease and bacterial disease.

    A, Anteroposterior radiograph of a child with a l...

    A, Anteroposterior radiograph of a child with a left lower lobe infiltrate. B, Lateral radiograph of the same child with a left lower lobe infiltrate.



    Anteroposterior radiograph of a child with a roun...

    Anteroposterior radiograph of a child with a round pneumonia.



    A, Anteroposterior radiograph of a child with pre...

    A, Anteroposterior radiograph of a child with presumptive viral pneumonia. B, Lateral radiograph of the same child with presumptive viral pneumonia.


    • Although unilateral and/or lobar infiltrates are often seen in bacterial pneumonia, several studies have found that the pattern of radiologic features could not accurately distinguish a bacterial etiology from a viral etiology.22,23
    • In contrast, a large Finnish series concluded that an alveolar (equivalent to a lobar) infiltrate is an insensitive but reasonably specific indication of bacterial infection.24
    • At either extreme (from typical bronchiolitis with scattered infiltrates to dense lobar pneumonia with a large pleural effusion), the level of diagnostic certainty provided by radiologic findings increases.
  • For M pneumoniae, 3 radiographic patterns may be observed: (1) peribronchial and perivascular interstitial infiltrates, (2) patchy consolidations, and (3) homogeneous acinar consolidations like ground-glass.25 The lower fields of the lungs are most often affected, and enlargement of the hilar glands is common.
  • In viral pneumonias, 4 common radiographic findings were detected: parahilar peribronchial infiltrates, hyperexpansion, segmental or lobar atelectasis, and hilar adenopathy.26
  • Although no radiographic findings are specific for C pneumoniae, a combination of the clinical and radiographic findings strongly suggests the diagnosis before laboratory diagnosis is available. In a study of 125 cases of Chlamydia pneumonia, Radkowski et al demonstrated that most chest films showed bilateral hyperexpansion and diffuse infiltrates with a variety of radiographic patterns including interstitial, reticular nodular, atelectasis, coalescence, and bronchopneumonia. Pleural effusion and lobar consolidation were not seen.27
  • Round pneumonia on chest radiographs should raise suspicion for a bacterial etiology, particularly Streptococcus pneumoniae and Staphylococcus aureus.

Other Tests

  • On occasion, it may be prudent to perform skin testing for tuberculosis, particularly if high risk for exposure.
  • Cold agglutinins 
    • In the young child or school-aged child with pneumonia, particularly the patient with a gradual onset of symptoms and a prodrome consisting of headache and abdominal symptoms, a bedside cold agglutinins test may help confirm the clinical suspicion of mycoplasmal infection.
    • This test is easily performed by placing a small amount of blood in a specimen tube containing anticoagulant and inserting this into a cup filled with ice water. After a few minutes in the cold water, the tube is held up to the light, tilted slightly, and slowly rotated. Small clumps of red blood cells coating the tube are indicative of a positive test result.
    • Unfortunately, this test is positive in only half the cases of mycoplasmal infection and is not very specific.
  • Urine latex agglutination test: Although antigen detection assays for S pneumoniae lack a high specificity in children, Neuman and Harper observed that 76% of febrile children with a lobar infiltrate on chest radiograph had a positive rapid urine antigen assay.28

Procedures

  • When a child has a significant pleural effusion identified on chest radiograph, a thoracentesis should be performed. A lateral decubitus radiograph may be obtained to determine whether the thoracic fluid is free-flowing. Ultrasonography or fluoroscopy may be useful to aid in placement of a traditional or pigtail thoracostomy tube for small-to-moderate–sized effusions.
    • Fluid recovered from the pleural space should be sent for Gram stain and culture, along with pH, glucose, protein, and lactate dehydrogenase (LDH).
    • If the thoracentesis reveals an empyema, a thoracostomy tube may be required.

Treatment

Prehospital Care

  • Pulse oximetry should be performed during the prehospital evaluation of such children, and supplemental oxygen should be administered.
  • Children who are in severe respiratory distress should undergo tracheal intubation if unable to maintain oxygenation or decreasing levels of consciousness.
  • Continuous positive airway pressure (CPAP) and bi-level positive airway pressure (BiPAP) may be used to help support respiratory effort as a stand-alone intervention or as a bridge to intubation.

Emergency Department Care

  • Initial priorities in children with pneumonia include the identification and treatment of respiratory distress, hypoxemia, and hypercarbia. Grunting, flaring, severe tachypnea, and retractions should prompt immediate respiratory support.
  • [#pneumoniapeds]The vast majority of children diagnosed with pneumonia in the ED may be treated on an outpatient basis with oral antibiotics.
    • High-dose amoxicillin may be used as a first-line agent for children with uncomplicated community-acquired pneumonia, which provides coverage for Streptococcus pneumoniae. Cephalosporins and macrolide antibiotics such as azithromycin are also acceptable alternatives. (Treatment guidelines are available from the Cincinnati Children's Hospital Medical Center.29 )
    • Macrolide antibiotics, such as azithromycin, may be used if Mycoplasma is suspected.
    • A recent study suggests that penicillin and macrolide resistance among Streptococcus pneumoniae isolates have been increasing.30
  • Viral pneumonia
    • RSV: Most infants with RSV pneumonia do not require antimicrobials. Hospitalization should be considered for infants who are younger than 2 months of age or premature, due to risk of apnea in this age group.31 Serious infections with this organism usually occur in infants with underlying lung disease.
    • Influenza A pneumonia that is particularly severe or when it occurs in a high-risk patient may be treated with zanamivir or oseltamivir. Check for resistance patterns for other antiviral agents indicated for treatment or chemoprophylaxis of influenza.
    • Oseltamivir (Tamiflu) resistance has emerged in the United States during the 2008-2009 influenza season.
      • The US Centers for Disease Control and Prevention (CDC) has issued revised interim recommendations for antiviral treatment and prophylaxis of influenza. Preliminary data from a limited number of states indicate a high prevalence of influenza A (H1N1) virus strains resistant to oseltamivir (Tamiflu). Because of this, zanamivir (Relenza) is recommended as the initial choice for antiviral prophylaxis or treatment when influenza A infection or exposure is suspected. A second-line alternative is a combination of oseltamivir plus rimantadine rather than oseltamivir alone. Local influenza surveillance data and laboratory testing can assist the physician regarding antiviral agent choice.
      • Influenza A viruses, including 2 subtypes (H1N1) and (H3N2), and influenza B viruses currently circulate worldwide, but the prevalence of each can vary among communities and within a single community over the course of an influenza season. In the United States, 4 prescription antiviral medications (oseltamivir, zanamivir, amantadine, rimantadine) are approved for treatment and chemoprophylaxis of influenza. Since January 2006, the neuraminidase inhibitors (oseltamivir, zanamivir) have been the only recommended influenza antiviral drugs because of widespread resistance to the adamantanes (amantadine, rimantadine) among influenza A (H3N2) virus strains. The neuraminidase inhibitors have activity against influenza A and B viruses, whereas the adamantanes have activity against only influenza A viruses.
      • In 2007-2008, a significant increase in the prevalence of oseltamivir resistance was reported among influenza A (H1N1) viruses worldwide. During the 2007-2008 influenza season, 10.9% of H1N1 viruses tested in the United States were resistant to oseltamivir. Complete recommendations are available from the CDC.
  • Children who are toxic appearing may require resuscitation and respiratory support.
    • Chest radiography should be performed to identify the presence of an effusion/empyema.
    • Antibiotic therapy should include vancomycin (particularly in areas where penicillin-resistant streptococci have been identified) and a second- or third-generation cephalosporin.

Consultations

  • Consultation is not needed in the care of most children with pneumonia.
    • Children who have underlying diseases may benefit from consultation with the specialist involved in their long-term care. For example, most children with cystic fibrosis are monitored by a pulmonologist.
    • Consultation with a pediatric infectious disease specialist may be appropriate in the treatment of a child with persistent or recurrent pneumonia.
    • Children with pleural effusions or empyema should be referred to a tertiary medical center, where thoracentesis can be performed. This procedure may be performed in an emergency department setting and may require subspecialty consultation.

Medication

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.


Amoxicillin (Amoxil, Trimox)

Interferes with synthesis of cell wall mucopeptides during active multiplication resulting in bactericidal activity against susceptible bacteria. Appropriate first-line agent in children in whom pneumococcal disease is strongly suspected. It offers the advantages of being relatively palatable and having a tid-dosing schedule. It has limited activity against gram-negative bacteria due to resistance.

Dosing

Adult

250-500 mg PO tid; not to exceed 1500 mg/d

Pediatric

40 mg/kg/d PO divided tid
5 kg: 62.5 mg PO tid
5-10 kg: 125 mg PO tid
>10 kg: 250 mg PO tid

Interactions

Reduces the efficacy of oral contraceptives; probenecid increases serum concentrations

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; caution in patients who are allergic to cephalosporin antibiotics; appearance of a rash should be carefully evaluated to differentiate a nonallergic ampicillin rash from a hypersensitivity reaction; rash and GI upset are adverse effects


Penicillin VK (Beepen-VK, Pen Vee K)

Inhibits the biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached and most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects. May be used as an alternative to amoxicillin in treatment of outpatients with pneumonia in whom pneumococcal disease is strongly suspected. Penicillin has limited activity against gram-negative bacteria.

Dosing

Adult

250-500 mg PO qid; not to exceed 2000 mg/d

Pediatric

40 mg/kg/d PO divided qid

Interactions

Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, causing a decrease in the effectiveness of penicillins when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal impairment and in patients who are allergic to cephalosporin antibiotics; rash and GI upset are adverse effects


Cefuroxime (Zinacef)

Second-generation cephalosporin maintains gram-positive activity that first-generation cephalosporins have; adds activity against Proteus mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and Moraxella catarrhalis. Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.

Dosing

Adult

250-500 mg PO q12h; 750-1500 mg IV/IM q8h

Pediatric

Suspension: 30 mg/kg/d PO bid
Tablets: 250 mg PO q12h
IV: 150-200 mg/kg/d IV divided q8h

Interactions

Disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patients receiving potent diuretics such as loop diuretics; coadministration with aminoglycosides increase nephrotoxic potential; probenecid increases levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Administer half dose if CrCl is 10-30 mL/min and one-quarter dose if <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy; caution in patients allergic to penicillin; skin rashes and GI upset are adverse effects


Cefpodoxime (Vantin)

Inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins. The tablet should be administered with food.

Dosing

Adult

200 mg/dose PO q12h

Pediatric

10 mg/kg/d PO divided bid

Interactions

Probenecid increases the serum concentrations of cefpodoxime.

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in penicillin allergy, renal impairment; adverse effects include nausea, vomiting, and diarrhea


Cefprozil (Cefzil)

Binds to one or more of the penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.

Dosing

Adult

250-500 mg/dose PO q12h or 500 mg PO qd

Pediatric

30 mg/kg/d PO divided bid

Interactions

Probenecid increases effect of cefprozil; coadministration with furosemide and aminoglycosides increases nephrotoxic effects of cefprozil

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in penicillin allergy, renal impairment; adverse effects include nausea, vomiting, and diarrhea


Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.

Dosing

Adult

1-2 g IV/IM qd

Pediatric

50-75 mg/kg/d IV/IM qd; not to exceed 1 g

Interactions

Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity; not to be used in hyperbilirubinemic neonates

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; caution in breastfeeding women and in those allergic to penicillin; adverse effects include nausea, vomiting, and diarrhea; not to be used in newborns, as it causes hyperbilirubinemia


Cefotaxime (Claforan)

Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.

Dosing

Adult

1-2 g IV/IM q6-8h; not to exceed 12 g/d

Pediatric

<50 kg: 100-200 mg/kg/d IV/IM divided q6-8h
>50 kg: Administer as in adults

Interactions

Probenecid may increase cefotaxime levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal impairment; caution in breastfeeding women and in those allergic to penicillin; adverse effects include nausea, vomiting, and diarrhea; associated with severe colitis


Erythromycin (EES, Eryc, E-Mycin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections. DOC for adults and children >4 y, unless suspect pneumococcal disease. These agents are effective against many of the atypical organisms. Erythromycin is available in 4 forms: base, stearate, estolate, and ethylsuccinate. Erythromycin estolate causes the least GI distress.

Dosing

Adult

Base: 500 mg PO qid for 7 d
Ethylsuccinate (EES): 800 mg PO qid for 7 d or 400-800 mg PO qid
Base, stearate, or estolate: 250-500 mg PO qid

Pediatric

Newborns: 50 mg/kg/d (base) PO divided qid for 14 d or 30-50 mg/kg/d (base and ethylsuccinate) PO divided q6-8h

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; may increase the toxicity of ergotamine

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur


Erythromycin and sulfisoxazole (Pediazole)

Erythromycin is a macrolide antibiotic with a large spectrum of activity. Binds to the 50S ribosomal subunit of the bacteria, which inhibits protein synthesis. Sulfisoxazole expands erythromycin's coverage to include gram-negative bacteria. Sulfisoxazole inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid. Dose is based on the erythromycin component.

Dosing

Adult

250 mg PO qid (unlikely to be prescribed to adults)

Pediatric

<2 months: Not recommended
>2 months: 50 mg/kg/d divided tid/qid

Interactions

May enhance warfarin's anticoagulation action effects and hemorrhage could occur; thiopental anesthetic effects may be enhanced; risk of nephrotoxicity may increase when administered concurrently with cyclosporine; serum hydantoin levels may increase when administered concurrently with sulfisoxazole; methotrexate-induced bone marrow suppression may be enhanced when administered concurrently with sulfisoxazole; may increase sulfonylurea concentrations and cause hypoglycemia in diabetic patients; tolbutamide bioavailability may be prolonged when administered with sulfamethizole Coadministration with diuretics may increase incidence of thrombocytopenia with purpura; sulfonamides free-drug concentration may be increased when administered concurrently with indomethacin; sulfonamides when used concomitantly with methenamine mandelate may form a precipitate in acidic urine; probenecid and salicylates may displace sulfonamides from plasma albumin resulting in increased free-drug concentrations potentiating its
toxicity; coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment; megaloblastic anemia due to folate deficiency; G-6-PD deficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in liver impairment; GI adverse effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur; caution in patients with renal dysfunction and HIV; maintain adequate fluid intake to prevent crystalluria and stone formation


Clarithromycin (Biaxin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

250-500 mg PO bid

Pediatric

15 mg/kg/d PO divided q12h

Interactions

Toxicity increases with coadministration of fluconazole and pimozide; clarithromycin effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, HMG CoA-reductase inhibitors; cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents

Contraindications

Documented hypersensitivity; coadministration of pimozide or cisapride

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; give half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies; abnormal metallic taste, nausea, diarrhea, and abdominal pain are adverse effects; do not refrigerate suspension


Azithromycin (Zithromax)

Azithromycin inhibits RNA synthesis by binding to 50S ribosomal subunit.

Dosing

Adult

Day 1: 500 mg PO
Days 2-5: 250 mg PO qd

Pediatric

Day 1: 10 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg PO qd; not to exceed 250 mg/d

Interactions

May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Contraindications

Documented hypersensitivity; hepatic impairment; do not administer with pimozide

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients; adverse effects include nausea, vomiting, and diarrhea

Antiviral

Inhibits DNA synthesis and viral replication.


Acyclovir (Zovirax)

Inhibits activity of both HSV-1 and HSV-2. DOC for treatment of pneumonia in children with herpes viruses (eg, herpes simplex, varicella).
Patients experience less pain and faster resolution of cutaneous lesions when used within 48 h from rash onset.

Dosing

Adult

10 mg/kg/dose IV q8h; infuse over 1 h

Pediatric

Administer as in adults

Interactions

Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity of acyclovir

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in renal failure or when using nephrotoxic drugs (rapid IV infusion can cause renal injury)


Ribavirin (Virazole)

For treatment of severe lower respiratory tract RSV infections in infants and children with an underlying compromising condition. Inhibits replication of RNA and DNA viruses.

Dosing

Adult

Reconstitute 6 g into 300 mL of sterile water to make a concentration of 20 mg/mL; administer as aerosol q12-18h/d for 3 d up to 7 d for RSV pneumonia

Pediatric

2 g aerosolized over 2 h tid for 3 d using a Viratek small particle aerosol generator (SPAG-2)

Interactions

Concomitant use of ribavirin and nucleoside analogues may increase risk of developing lactic acidosis; concurrent use with didanosine has been noted to increase the risk of pancreatitis and/or peripheral neuropathy in addition to lactic acidosis

Contraindications

Documented hypersensitivity to ribavirin or any component of the formulation; women of childbearing age who will not use contraception reliably; pregnancy, ClCr <50 mL/min; hemoglobinopathies (eg, thalassemia major, sickle cell anemia); patients with autoimmune hepatitis, anemia, or severe heart disease

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Use with caution in patients requiring assisted ventilation because precipitation of the drug in the respiratory equipment may interfere with safe and effective patient ventilation; carefully monitor patients with COPD and asthma for deterioration of respiratory function

Follow-up

Further Inpatient Care

  • Hospitalization and treatment with parenteral antibiotics should be considered for certain groups of children:
    • Infants younger than 6 months of age
    • Children with immunocompromise
    • Children who appear toxic, have respiratory distress, or require supplemental oxygen
    • Children in whom outpatient treatment has failed
  • Additionally, many patients without distress are admitted for hydration.
  • In some admitted patients, further testing to identify the etiologic agent is warranted.

Further Outpatient Care

  • Most children with uncomplicated pneumonia recover without sequelae.
  • In children who remain well appearing but have recurrent or chronic symptoms, further testing is warranted. Further testing may include skin testing to identify fungal pathogens and tuberculosis, sweat testing to identify cystic fibrosis, titers against rare organisms, and bronchoscopy.

Inpatient & Outpatient Medications

  • The initial outpatient treatment of children with pneumonia depends upon the clinical findings and the patient's age.
  • Children in whom pneumococcal disease is suspected initially should be treated with amoxicillin or penicillin.
  • A macrolide antibiotic alone, or in combination with sulfisoxazole or an oral cephalosporin is an alternative.
  • For most other children, particularly school-aged children, azithromycin alone or in combination with sulfisoxazole may be given. Other macrolide agents are acceptable alternatives to erythromycin.
  • Children who are being admitted should be treated with cefuroxime or another broad-spectrum cephalosporin.
  • Vancomycin may be added to the treatment of toxic-appearing children in areas where there is a high rate of penicillin resistance among pneumococcal isolates.
  • Acyclovir is indicated for the treatment of pneumonia caused by herpesviruses.

Transfer

  • Infants and children being admitted for pneumonia may require transfer because they need admission to a critical care unit.
  • Transfer should be considered when pneumonia complicates chronic illness. In such patients, the purpose of the transfer is continuity of care with the child's subspecialist.
  • Since the great risk faced by children with pneumonia is respiratory compromise, the unit performing the transfer should feel comfortable with the full spectrum of respiratory support that may be required.

Deterrence/Prevention

  • Several vaccines exist that may prevent certain types of pneumonia.
    • Heptavalent pneumococcal vaccine is recommended for all children in the United States.
    • Influenza vaccines are recommended for young children and those with chronic pulmonary disease including asthma.
    • H influenzae type b vaccine is given to all children and has reduced the incidence of infections caused by this organism.
    • Varicella vaccine has a dramatic impact upon the incidence of varicella.
    • An injection of RSV-specific immunoglobulins holds some promise for the prevention of severe RSV infections in certain infants. Likely candidates for this treatment are former premature infants and those with chronic heart and lung diseases.

Complications

  • Fortunately, most children with pneumonia recover without complications.
  • Persistent effusions and empyemas are the most common serious complications of bacterial pneumonia.
  • Pulmonary abscess
  • Respiratory distress
  • Sepsis

Prognosis

  • Patients who were placed on a protocol-driven pneumonia clinical pathway are more likely to have favorable outcomes.
  • The prognosis for most forms of pneumonia is excellent. Most cases of viral pneumonia resolve without treatment; common bacterial pathogens and atypical organisms respond to antimicrobial therapy.
  • The prognosis for varicella pneumonia is somewhat more guarded.
  • Staphylococcal pneumonia, although rare, can be very serious despite treatment.
  • Immunocompromised children, those with underlying lung disease, and neonates are at high risk for severe sequelae.
  • Some forms of viral pneumonia, particularly adenoviral disease, may cause necrotizing bronchiolitis or bronchiolitis obliterans.

Patient Education

  • Parents should be cautioned to look for the signs of increasing respiratory distress and to seek medical attention immediately should any of these signs appear.
  • Most children treated with outpatient antibiotics will be much improved within 48 hours after the initiation of treatment. If such improvement does not occur, medical attention should be sought.
  • For excellent patient education resources, visit eMedicine's Pneumonia Center. Also, see eMedicine's patient education articles Bacterial Pneumonia and Viral Pneumonia.

Miscellaneous

Medicolegal Pitfalls

  • Attempting to treat neonates and very young infants on an outpatient basis
  • Failure to recognize and treat signs of respiratory compromise and sepsis
  • Failure to give parents clear discharge instructions

Multimedia

A, Anteroposterior radiograph of a child with a l...

Media file 1: A, Anteroposterior radiograph of a child with a left lower lobe infiltrate. B, Lateral radiograph of the same child with a left lower lobe infiltrate.

Anteroposterior radiograph of a child with a roun...

Media file 2: Anteroposterior radiograph of a child with a round pneumonia.

A, Anteroposterior radiograph of a child with pre...

Media file 3: A, Anteroposterior radiograph of a child with presumptive viral pneumonia. B, Lateral radiograph of the same child with presumptive viral pneumonia.

References

  1. Rudan I, Tomaskovic L, Boschi-Pinto C, Campbell H. Global estimate of the incidence of clinical pneumonia among children under five years of age. Bull World Health Organ. Dec 2004;82(12):895-903. [Medline].

  2. Addo-Yobo E, Chisaka N, Hassan M, et al. Oral amoxicillin versus injectable penicillin for severe pneumonia in children aged 3 to 59 months: a randomised multicentre equivalency study. Lancet. Sep 25-Oct 1 2004;364(9440):1141-8. [Medline].

  3. Hansen J, Black S, Shinefield H, et al. Effectiveness of heptavalent pneumococcal conjugate vaccine in children younger than 5 years of age for prevention of pneumonia: updated analysis using World Health Organization standardized interpretation of chest radiographs. Pediatr Infect Dis J. Sep 2006;25(9):779-81. [Medline].

  4. Puumalainen T, Quiambao B, Abucejo-Ladesma E, et al. Clinical case review: a method to improve identification of true clinical and radiographic pneumonia in children meeting the World Health Organization definition for pneumonia. BMC Infect Dis. Jul 21 2008;8:95. [Medline].

  5. Cevey-Macherel M, Galetto-Lacour A, Gervaix A, et al. Etiology of community-acquired pneumonia in hospitalized children based on WHO clinical guidelines. Eur J Pediatr. Feb 24 2009;[Medline].

  6. Michelow IC, Olsen K, Lozano J, et al. Epidemiology and clinical characteristics of community-acquired pneumonia in hospitalized children. Pediatrics. Apr 2004;113(4):701-7. [Medline].

  7. Thompson WW, Shay DK, Weintraub E, et al. Influenza-associated hospitalizations in the United States. JAMA. Sep 15 2004;292(11):1333-40. [Medline].

  8. Black SB, Shinefield HR, Ling S, et al. Effectiveness of heptavalent pneumococcal conjugate vaccine in children younger than five years of age for prevention of pneumonia. Pediatr Infect Dis J. Sep 2002;21(9):810-5. [Medline].

  9. Lynch T, Platt R, Gouin S, Larson C, Patenaude Y. Can we predict which children with clinically suspected pneumonia will have the presence of focal infiltrates on chest radiographs?. Pediatrics. Mar 2004;113(3 Pt 1):e186-9. [Medline].

  10. Mahabee-Gittens EM, Grupp-Phelan J, Brody AS, et al. Identifying children with pneumonia in the emergency department. Clin Pediatr (Phila). Jun 2005;44(5):427-35. [Medline].

  11. Rothrock SG, Green SM, Fanelli JM, Cruzen E, Costanzo KA, Pagane J. Do published guidelines predict pneumonia in children presenting to an urban ED?. Pediatr Emerg Care. Aug 2001;17(4):240-3. [Medline].

  12. Mishaan AM, Mason EO Jr, Martinez-Aguilar G, et al. Emergence of a predominant clone of community-acquired Staphylococcus aureus among children in Houston, Texas. Pediatr Infect Dis J. Mar 2005;24(3):201-6. [Medline].

  13. Tsolia MN, Psarras S, Bossios A, et al. Etiology of community-acquired pneumonia in hospitalized school-age children: evidence for high prevalence of viral infections. Clin Infect Dis. Sep 1 2004;39(5):681-6. [Medline].

  14. Nascimento-Carvalho CM, Ribeiro CT, Cardoso MR, et al. The role of respiratory viral infections among children hospitalized for community-acquired pneumonia in a developing country. Pediatr Infect Dis J. Oct 2008;27(10):939-41. [Medline].

  15. Juven T, Mertsola J, Waris M, et al. Etiology of community-acquired pneumonia in 254 hospitalized children. Pediatr Infect Dis J. Apr 2000;19(4):293-8. [Medline].

  16. Black S, Shinefield H, Fireman B, et al. Efficacy, safety and immunogenicity of heptavalent pneumococcal conjugate vaccine in children. Northern California Kaiser Permanente Vaccine Study Center Group. Pediatr Infect Dis J. Mar 2000;19(3):187-95. [Medline].

  17. Tajima T, Nakayama E, Kondo Y, et al. Etiology and clinical study of community-acquired pneumonia in 157 hospitalized children. J Infect Chemother. Dec 2006;12(6):372-9. [Medline].

  18. Bachur R, Perry H, Harper MB. Occult pneumonias: empiric chest radiographs in febrile children with leukocytosis. Ann Emerg Med. Feb 1999;33(2):166-73. [Medline].

  19. Murphy CG, van de Pol AC, Harper MB, Bachur RG. Clinical predictors of occult pneumonia in the febrile child. Acad Emerg Med. Mar 2007;14(3):243-9. [Medline].

  20. Rutman MS, Bachur R, Harper MB. Radiographic pneumonia in young, highly febrile children with leukocytosis before and after universal conjugate pneumococcal vaccination. Pediatr Emerg Care. Jan 2009;25(1):1-7. [Medline].

  21. Shah SS, Alpern ER, Zwerling L, McGowan KL, Bell LM. Risk of bacteremia in young children with pneumonia treated as outpatients. Arch Pediatr Adolesc Med. Apr 2003;157(4):389-92. [Medline].

  22. Courtoy I, Lande AE, Turner RB. Accuracy of radiographic differentiation of bacterial from nonbacterial pneumonia. Clin Pediatr (Phila). Jun 1989;28(6):261-4. [Medline].

  23. Wahlgren H, Mortensson W, Eriksson M, Finkel Y, Forsgren M, Leinonen M. Radiological findings in children with acute pneumonia: age more important than infectious agent. Acta Radiol. Jul 2005;46(4):431-6. [Medline].

  24. Korppi M, Kiekara O, Heiskanen-Kosma T, Soimakallio S. Comparison of radiological findings and microbial aetiology of childhood pneumonia. Acta Paediatr. Apr 1993;82(4):360-3. [Medline].

  25. Guckel C, Benz-Bohm G, Widemann B. Mycoplasmal pneumonias in childhood. Roentgen features, differential diagnosis and review of literature. Pediatr Radiol. 1989;19(8):499-503. [Medline].

  26. Wildin SR, Chonmaitree T, Swischuk LE. Roentgenographic features of common pediatric viral respiratory tract infections. Am J Dis Child. Jan 1988;142(1):43-6. [Medline].

  27. Radkowski MA, Kranzler JK, Beem MO, Tipple MA. Chlamydia pneumonia in infants: radiography in 125 cases. AJR Am J Roentgenol. Oct 1981;137(4):703-6. [Medline].

  28. Neuman MI, Harper MB. Evaluation of a rapid urine antigen assay for the detection of invasive pneumococcal disease in children. Pediatrics. Dec 2003;112(6 Pt 1):1279-82. [Medline].

  29. [Guideline] Cincinnati Children's Hospital Medical Center. Evidence based care guideline for community acquired pneumonia in children 60 days through 17 years of age. Cincinnati (OH): Cincinnati Children's Hospital Medical Center. Jul. 2006;[Full Text].

  30. Neuman MI, Kelley M, Harper MB, File TM Jr, Camargo CA Jr. Factors associated with antimicrobial resistance and mortality in pneumococcal bacteremia. J Emerg Med. May 2007;32(4):349-57. [Medline].

  31. Willwerth BM, Harper MB, Greenes DS. Identifying hospitalized infants who have bronchiolitis and are at high risk for apnea. Ann Emerg Med. Oct 2006;48(4):441-7. [Medline].

  32. Murray CJ, Lopez AD. Progress and directions in refining the global burden of disease approach: a response to Williams. Health Econ. Jan 2000;9(1):69-82. [Medline].

Keywords

pneumonia in children, symptoms of pneumonia in children, treatment of pneumonia in children, bacterial pneumonia, respiratory syncytial virus, RSV, lower respiratory tract infection, empiric antibiotics, interstitial pneumonia, miliary pneumonia, lobar pneumonia, bronchopneumonia, dyspnea, hypoxemia

Contributor Information and Disclosures

Author

Mark I Neuman, MD, MPH, Assistant Professor of Pediatrics, Harvard Medical School; Attending Physician, Division of Emergency Medicine, Children's Hospital Boston
Mark I Neuman, MD, MPH is a member of the following medical societies: Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Garry Wilkes, MBBS, FACEM, Director of Emergency Medicine, Bunbury Hospital, Western Australia; Medical Director, St John Ambulance, WA Ambulance Service; Adjunct Associate Professor, Edith Cowan University; Clinical Associate Professor, Rural Clinical School, University of Western Australia, Australia.
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center
Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Laura E Ferguson, MD, Brent R King, MD, and Lakshmi V Atkuri, MD, to the development and writing of this article.

Further Reading

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)