A previously healthy 4 year old boy is brought to an urgent care center by his mother for difficulty breathing for one day. Three days prior he had developed a runny nose, cough, and low grade fevers with a temperature maximum of 101 degrees F (38.3 degrees C). He continued to take liquids well, but his solid intake has decreased. His temperature this morning was 103 degrees F (39.4 degrees C) and he was breathing fast and working hard to breathe. He does not have any ill contacts. He has never been hospitalized or had any surgeries. He was born at term without any complications. He is not taking medications other than acetaminophen. His immunizations are up to date for his age (except he had not received the pneumococcal conjugate vaccine). His parents and 10 year old sister are healthy and the remainder of his family history is non-contributory. There are no smokers in the household, and he has not traveled recently. He does not have a history of choking or vomiting. He has not had frequent ear or skin infections. He does not have a history of foul-smelling stools.
Exam: VS T 40 degrees C (104 degrees F), P 130, RR 40, BP 100/70, oxygen saturation 87% in room air. His height and weight are in the 50th percentile for his age. He is awake and alert, in moderate distress. His conjunctiva and TMs are normal. His nasal mucosa is erythematous with yellowish discharge. His lips and mucous membranes are dry. His neck is supple, with several small anterior cervical lymph nodes. Lungs: Moderate subcostal, intercostal, and supraclavicular retractions, symmetric expansion, dullness to percussion at the right base, increased vocal fremitus over the right base, decreased air entry over right lower lobe with crackles, no wheezes. Heart: Tachycardia, regular rhythm without murmur. Pulses are 2+, and capillary refill time is 3 seconds. His abdomen, skin, and neurological examinations are unremarkable.
CBC WBC 20,000, 70% segs, 11% bands, 15% lymphs, 3% monos, 1% eos. Hemoglobin 12.4, platelet count 280,000. Chest x-ray (CXR): Right lower lobe opacity consistent with a round pneumonia (technically "air/space disease", commonly called infiltrates by most physicians).
Because of the hypoxia, he is given supplemental oxygen (with subsequent improvement in oxygen saturation), as hospitalization arrangements are made. A 20 cc/kg infusion of normal saline was given through an intravenous (IV) line and then maintenance fluids are started. A blood culture is obtained and he is started on IV cefuroxime. He improves over the next day. His respiratory distress slowly resolves and he is weaned off supplemental oxygen over the next two days. His blood culture shows no growth. He is discharged home on high dose amoxicillin for a total of 10 days of therapy. His discharge diagnosis is probably pneumococcal pneumonia.
Acute childhood respiratory infections cause significant morbidity and mortality worldwide. Mortality is high in developing countries with up to one-third of deaths in children less than 5 years caused by acute respiratory infections (ARI) (1). The disparity in mortality is due to the severity of infection (perhaps due to differences in nutrition, overall health, immunization practices, and medical care availability) since the incidence of acute respiratory infections is similar between developed and developing countries with infants experiencing about 4-8 episodes per year (1). In the US, mortality from ARIs has declined since 1968 (1,2).
There are 2 basic classification systems used for acute respiratory tract infections: the case-management classification system used by the World Health Organization (WHO) and the "traditional" clinical classification system (1). The case management system divides ARIs by symptoms (i.e., stridor, wheezing, and no wheezing) and their severity (i.e., mild, moderate, severe, and very severe). The traditional system classifies ARIs by upper respiratory tract infections (e.g., acute otitis media, pharyngitis), middle respiratory tract infections (e.g., croup and epiglottitis), and lower respiratory tract infections (e.g., bronchiolitis, bronchitis, pneumonia). Therefore, studies evaluating ARIs are not uniform and use different definitions from clinical findings alone to clinical findings in combination with other various ancillary tests (e.g., chest radiography).
Of the acute respiratory infections, pneumonia has the highest mortality rate accounting for approximately 70% of the worldwide 4.5 million deaths from acute respiratory infections (4). Although mortality from pneumonia in children in the United States has declined by 97% between 1939 and 1996 (5), pneumonia continues to be a leading cause of morbidity in children. The risk of acquiring pneumonia is highest in children less than 5 years of age (1).
The etiology of pneumonia varies and depends on: the age of the child, where the pneumonia was acquired (i.e., community vs. nosocomial), local epidemiology (e.g., influenza epidemics), host factors (e.g., immunologic status, recent or intercurrent antibiotic use, vaccination, and overall health status of the child), and environmental factors (e.g., travel, season of the year, daycare, or crowded living conditions) (4,6-9). Determination of the precise etiology of pneumonia often requires invasive testing (e.g., lung biopsy), and therefore, this is done infrequently. Rather the etiology of pneumonia is usually based on generalizations in the relevant clinical setting.
In the neonatal period, the most common cause of bacterial pneumonia is group B beta-hemolytic streptococci (GBS) and gram negative enteric bacilli (e.g., E.coli), the same organisms associated with neonatal sepsis (4). In infants and children outside of the neonatal period, viruses are the most common cause of pneumonia (4,6,10-11) and respiratory syncytial virus (RSV) is one of the most common causes in infancy, especially in premature infants (9,12). Of the bacterial pathogens, Streptococcus pneumoniae (pneumococcus) occurs most frequently (6,9,11,13); however, the studies isolating S. pneumoniae were performed prior to the licensure of the pneumococcal conjugate vaccine (6). Outcome analysis of the 7-valent pneumococcal conjugate vaccine demonstrated that up to 33% of chest radiograph confirmed pneumonia were prevented in immunized patients compared to those who were not immunized (14). Therefore, a different bacterial pathogen may supersede S. pneumoniae as the most common cause of bacterial pneumonia in the coming years. Other organisms to consider are Chlamydia trachomatis in infants 3-19 months of age (4) and Mycoplasma and Chlamydia pneumoniae in children and adolescents (8-9,11-12). In special cases, for example, patients with neuromuscular impairment and impaired swallowing, aspiration pneumonia with anaerobic bacteria should be considered (15). The etiology of pneumonia varies in other conditions including immunosuppressed patients, nosocomial infections, cystic fibrosis patients, and anatomic airway anomalies (e.g., tracheostomies). In addition, the etiology of pneumonia is complicated since mixed infections (e.g., viral-bacterial) can occur in 16-34% of patients (7,11,13).
The lower respiratory tract in healthy persons is sterile (16). Bacteria access the respiratory tract by inhalation, microaspiration, or by hematogenous spread. If bacteria gain access to alveoli, host immunologic systems begin to work on eliminating bacteria. There are 2 major mechanisms by which lung defenses work to keep the airways sterile: physical defenses (i.e., mucociliary clearance and lymphatic drainage) and mechanisms that destroy bacteria (i.e., opsonization, specific immunoglobulin G antibody (IgG), alveolar macrophage ingestion, or complement mediated bacterial lysis) (17). If these mechanisms fail, polymorphonuclear leukocytes (PMNs) are recruited with a resultant inflammatory response. Perpetuation of this inflammatory response leads to pneumonia. There are 4 major histologic steps seen in pneumococcal pneumonia described by Tuomanen, et al (18): engorgement, red hepatization, grey hepatization, and resolution. Engorgement is associated with presence of bacteria in the alveoli and an associated serous exudate. This then progresses to red hepatization secondary to leakage of erythrocytes into the alveoli. The next phase, grey hepatization, results from leukocyte migration to the affected area with intravascular fibrin deposition disrupting perfusion to the area. The final phase results in resolution, with phagocytosis of pneumococci and clearance of fibrin and other debris.
Outside of the neonatal period, pneumonia is suspected in patients with clinical signs and symptoms suggestive of impairment of the lower respiratory tract. Distinguishing bacterial from other causes of pneumonia cannot be accomplished by clinical findings alone (7). Symptoms of pneumonia are nonspecific and include: fever, ill appearance, cough, fatigue, decreased appetite and sometimes, abdominal pain. Signs of lower respiratory tract involvement include: tachypnea (greater than 50 breaths/minute in children less than 12 months, and greater than 40 breaths/minute for older children) (4), cyanosis, increased work of breathing (i.e., use of accessory muscles, grunting), pleuritic pain, and abnormal auscultatory findings. These signs do not differentiate a viral from bacterial process. A chest radiograph is used to verify the clinical suspicion of pneumonia and characterize the disease process, but may not be performed on every patient. Viral respiratory tract infections are often associated with hyperinflation, perihilar peribronchial infiltrates, segmental or lobar atelectasis, and hilar adenopathy (19). Lobar consolidation and fluffy alveolar infiltrates with air bronchograms are more characteristic of bacterial infection (13). However, there is overlap between these two groups (13). Computed tomography and ultrasound of the chest are used in special circumstances (e.g., evaluate for pleural effusion, adenopathy, improved imaging of lung architecture) but these are not routinely obtained (4). Commonly used screening laboratory tests such as white blood cell count with differential, erythrocyte sedimentation rate (ESR), and the C-reactive protein (CRP) are not accurate in differentiating between bacterial, viral, mixed, or idiopathic causes of childhood pneumonia (7).
Determination of precise etiology of pneumonia is difficult due to the lack of sensitive and specific tests. Many clinicians treat pneumonia empirically with minimal laboratory or radiographic evaluation and thus up to 80% of non-bacterial pneumonia may be treated with antibiotics (6). This approach is satisfactory when clinical risk is deemed to be low. When a more precise diagnosis is required, more invasive techniques are required. Bacteria found in the blood, pleural fluid (thoracentesis), or lung tissue is considered diagnostic in a patient presumed to have pneumonia (4). Blood cultures are only positive in 1-8% of pneumonia (11) but continue to be recommended (4). Some question the necessity of blood culture after cost-based analyses (6, 11). Transthoracic needle aspirates, transtracheal aspirates, and open lung biopsy (the gold standard for diagnosis) are rarely performed due to the risk involved for these procedures (11,20), except in severe cases or in immunocompromised hosts (4). Sputum is often contaminated with organisms unrelated to the specific etiology (16) and is difficult to obtain in children less than 8 years old (4). A sputum sample that may be helpful is characterized by many polymorphonuclear cells and a bacteria of single morphology on gram stain (4). Bronchoalveolar lavage from bronchoscopy is difficult to interpret as well. The results are non-specific (i.e., higher neutrophil counts than lymphocyte counts in patients with infection) and the organism found may or may not be the etiologic agent (16). Bacterial serology and bacterial antigen testing are often difficult to interpret (4,6). Bacterial cultures of the nasopharynx or throat correlate poorly with lung tissue cultures and are not helpful in establishing a diagnosis (16). Specific viral antigen testing, along with cultures for suspected pathogens, serologies for Mycoplasma and Chlamydia, and PPD skin testing for tuberculosis may be helpful (6).
Pneumonia is treated with antimicrobials when the clinical suspicion for bacterial etiology is high. Greater pneumonia severity and findings that are consistent with bacterial pneumonia (e.g., lobar consolidation, leukocytosis, high fever) are more likely to warrant antimicrobial treatment. Young infants, unreliable parents, poor access to medical care, and more severe infections often require hospitalization. Treatment of pneumonia is often empirically based and thus, information on antibiotic resistance patterns and mechanisms of resistance is important to determine the most appropriate treatment. For S. pneumoniae, the most common mechanism of resistance to penicillins is alteration of penicillin-binding sites that can be overcome with higher doses of the drug (6). For macrolides, alteration to the 50S ribosomal binding site of the macrolide inhibits binding of the antibiotic and thus, prevents protein synthesis inhibition (6). In addition, there is also an increase in efflux pumps for macrolides and this property can be overcome by using macrolides that achieve high tissue concentrations at the site of infection (e.g. azithromycin) (6). Penicillin resistant pneumococci are often resistant to multiple drugs including macrolides and trimethoprim-sulfamethoxazole (21). Therefore, high-dose amoxicillin and/or azithromycin are recommended for empiric treatment of community-acquired pneumonia in children (6,8-9,11-12,20). Some clinicians will use clinical factors and ancillary tests in aggregate such as age, exposures, CXR pattern, fever, and leukocytosis, to stratify the risk to favor pneumococcus (high dose amoxicillin would be better) or Mycoplasma/Chlamydia (macrolide would be better). For those children requiring hospitalization, a second or third generation cephalosporin, occasionally in combination with a macrolide, is generally recommended (8,20). Most treatment regimens are continued for a total of 7-14 days although this is based on little evidence (4).
Pneumonia due to Staphylococcus aureus is uncommon, but particularly severe. S. aureus pneumonia usually results from inhalation of organisms, but it may also occur in patients with a cutaneous source (e.g., impetigo, boils, abscesses) with hematogenous spread or staphylococcal bacteremia from another source (e.g. osteomyelitis, central line infection). If S. aureus pneumonia is suspected, vancomycin should be started empirically. Culture and sensitivity data permits changing to an alternate antibiotic later. Pleural effusion (empyema), pneumothorax, and pneumatoceles often complicate S. aureus pneumonia.
Pleural effusions can be classified in several ways. They can be a transudate or an exudate based on their protein content. A subpulmonic effusion versus an empyema is more clinically relevant. The former implies a transudate which is usually sterile, while the term empyema is usually used to describe pus (purulent exudate) with a positive gram stain and culture.
The overall outcome in children with pneumonia is excellent. The majority of children will recover without complications (11). Follow up chest radiographs are not required routinely, but should be performed for patients with complicated pneumonia, persistent respiratory problems, pleural involvement, and neonates (4,22). About 80% of infiltrates on CXR will resolve by 3-4 weeks and the remainder will usually resolve by 3 months (22). Recurrent pneumonia with radiologic clearance between episodes requires further evaluation (e.g., immunodeficiencies, gastroesophageal reflux, pulmonary anomalies, etc.) (4).
Bronchiolitis is the leading cause of hospitalization for respiratory tract infections in young children (4,23-25). Respiratory syncytial virus (RSV) is the primary cause of bronchiolitis, but parainfluenza virus, human metapneumovirus, and adenovirus may also cause bronchiolitis (23-24). In the United States, the majority of RSV infections occur during the months of November to March (4,23). RSV infections account for a significant amount of morbidity and health care expense in the young age group (24).
RSV is transmitted by direct contact with large droplets or fomites. Transmission can be limited by good handwashing (23). RSV bronchiolitis results from the spread of RSV to the lower respiratory tract after an incubation period 2-8 days where the virus undergoes replication in the nasopharynx (23). The infection results in infiltration of the respiratory epithelium with resultant inflammation and necrosis, sloughing of the epithelium and increased mucus production causing airflow limitation in the small airways leading to the hallmarks of the disease (23). Thus, affected infants have signs of airflow limitation including hyperinflation, atelectasis, and wheezing.
The diagnosis is often made on clinical grounds during the RSV season. Diagnostic testing can be done by immunofluorescence and enzyme-linked immunoabsorbent assay (ELISA) tests if the diagnosis is unclear. Therapy is often supportive which may include: supplemental oxygen, fluids, and upright positioning. Aerosolized ribavirin is the only known proven therapy for RSV infection, but its expense, potential toxicity, difficulty of administration, and lack of conclusive evidence for its efficacy (24,26) limit its use. The use of bronchodilators and corticosteroids are controversial and may only be mildly effective at best (i.e., not been proven to be highly efficacious) (24-26). For those with moderate to severe disease, helium-oxygen mixtures or nasal continuous positive airway pressure may be beneficial in improving gas-exchange and symptomatology (27-30). Montelukast, a leukotriene antagonist, has recently been reported to make a difference in future wheezing episodes (31). Prophylaxis with palivizumab (RSV monoclonal antibody) or RSV-IVIG is given to select pediatric populations recommended by the American Academy of Pediatrics during RSV season to reduce RSV infection risk (32). Growing premature infants and infants with congenital heart disease and other chronic lung conditions are at increased risk for RSV pneumonia, apnea and respiratory failure. Healthy term infants with RSV usually develop mild bronchiolitis. Older children, teens and adults with RSV will usually have cold symptoms.
Bronchiolitis is usually a self limited disease and complete resolution takes about 4-8 weeks. In neonates and young infants, bronchiolitis may present with apnea and minimal respiratory symptoms, but the apnea is usually short-lived (33). Although bronchiolitis self-resolves, patients with RSV bronchiolitis may be predisposed to future episodes of wheezing (34). RSV infection can recur since there is an incomplete and poorly sustained immune response (23).
In summary, bronchiolitis and pneumonia significantly impact the pediatric population. Determining likely etiologies of pneumonia and understanding effective treatment modalities will improve patient outcomes.
Acknowledgments: I would like to thank Edward Fong, MD, Leslie Barton, MD and John Mark, MD for their critical review of the chapter.
1. Which of the following is the most common cause of pneumonia outside of the neonatal period?
. . . . . a. S. pneumoniae
. . . . . b. Mycoplasma
. . . . . c. Viruses
. . . . . d. Chlamydia
2. S. pneumonia resistance to penicillins is due to:
. . . . . a. Production of beta-lactamase
. . . . . b. Alteration of penicillin binding proteins
. . . . . c. Increased efflux pumps
. . . . . d. Low tissue bioavailability
3. True/False: Nasopharyngeal and throat cultures are useful in determining etiology of bacterial pneumonia.
4. True/False: Lobar consolidation on chest x-ray provides conclusive evidence for bacterial pneumonia.
5. Which factor does not appear to affect the etiology of pneumonia?
. . . . . a. Age
. . . . . b. Vaccination status
. . . . . c. Current antibiotic use
. . . . . d. Birth rank
6. The most common cause of bronchiolitis is:
. . . . . a. Respiratory syncytial virus
. . . . . b. Human Metapneumovirus
. . . . . c. Parainfluenza
. . . . . d. Adenovirus
7. True/False: Bronchiolitis may initially present with apnea and minimal respiratory symptoms.
8. Treatment of bronchiolitis should include all of the following except: a. Supplemental oxygen for infants with hypoxia. b. Intravenous fluids and close monitoring of nutritional status. c. Good handwashing. d. Antibiotics.
9. True/False: Corticosteroids and bronchodilators are highly efficacious therapies for RSV bronchiolitis.
Pneumonia case presenting with abdominal pain: Yamamoto LG. Abdominal Pain with a Negative Abdominal Examination. In: Yamamoto LG, Inaba AS, DiMauro R (eds). Radiology Cases In Pediatric Emergency Medicine, 1994, volume 1, case 3. Available online at: www.hawaii.edu/medicine/pediatrics/pemxray/v1c03.html
Staph pneumonia case: Yamamoto LG, Young LL. Tachypnea and Abdominal Pain. In: Yamamoto LG, Inaba AS, DiMauro R (eds). Radiology Cases In Pediatric Emergency Medicine, 1995, volume 2, case 5. Available online at: www.hawaii.edu/medicine/pediatrics/pemxray/v2c05.html
Series of pediatric chest radiographs: Yamamoto LG. Test Your Skill In Reading Pediatric Chest Radiographs. In: Yamamoto LG, Inaba AS, DiMauro R (eds). Radiology Cases In Pediatric Emergency Medicine, 1995, volume 3, case 20. Available online at: www.hawaii.edu/medicine/pediatrics/pemxray/v3c20.html
Another series of pediatric chest radiographs: Yamamoto LG. Test Your Skill In Reading Pediatric Chest Radiographs. In: Yamamoto LG, Inaba AS, DiMauro R (eds). Radiology Cases In Pediatric Emergency Medicine, 1996, volume 4, case 5. Available online at: www.hawaii.edu/medicine/pediatrics/pemxray/v4c05.html
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Answers to questions
1.c. Overall, viruses cause the majority of pneumonias in children; however, the incidence of viral pneumonia decreases with age, becoming less common in older children and adolescents.
4.False. Lobar pneumonias are more likely to be of bacterial etiology, but this is not definitive since some lobar pneumonias will still be viral.