Pediatric Pneumonia Treatment & Management
- Author: Nicholas John Bennett, MBBCh, PhD, MA(Cantab), FAAP; Chief Editor: Russell W Steele, MD more...
Treatment decisions in children with pneumonia are dictated based on the likely etiology of the infectious organism and the age and clinical status of the patient. Antibiotic administration must be targeted to the likely organism, bearing in mind the age of the patient, the history of exposure, the possibility of resistance (which may vary, depending on local resistance patterns), and other pertinent history (see Etiology and Clinical Presentation).
After initiating therapy, the most important tasks are resolving the symptoms and clearing the infiltrate. With successful therapy, symptoms resolve much sooner that the infiltrate. In a study of adults with pneumococcal pneumonia, the infiltrate did not completely resolve in all patients until 8 weeks after therapy (although it was sooner in most patients). If therapy fails to elicit a response, the whole treatment approach must be reconsidered.
The Pediatric Infectious Diseases Society and the Infectious Diseases Society of America created evidence-based guidelines for the management of community-acquired pneumonia (CAP) in infants and children older than 3 months. These guidelines discuss site-of-care management, diagnosis, antimicrobial therapy, adjunctive surgical therapy, and prevention. While these guidelines do not represent the only approach to diagnosis and therapy, these recommendations may assist in decreasing morbidity and mortality rates in children with CAP.
Pulse oximetry should be performed during the prehospital evaluation of children with suspected pneumonia, and supplemental oxygen should be administered, if necessary; however, many school-aged children do not require hospitalization and respond well to oral antibiotics. Usually, these patients are not toxic or hypoxic enough to require supplemental oxygen. Unless they are vomiting, they do not require intravenous fluids or antibiotics. A parapneumonic effusion that requires drainage usually dictates a hospital admission.
Children younger than 5 years are hospitalized more often, but their clinical status, degree of hydration, degree of hypoxia, and need for intravenous therapy dictate this decision. Hospitalization should be considered for infants who are younger than 2 months or premature because of the risk of apnea in this age group.
Children who are toxic-appearing may require resuscitation and respiratory support. Treatment of critically ill children (those requiring ventilation) should include timely administration of appropriate antibiotics. Delays of only a few hours in one retrospective study were associated with significantly longer durations of ventilation, ICU stay, and total hospitalization. Chest radiography should be performed to identify the presence of an effusion/empyema (See Chest Radiography). Drainage of a restrictive or infected effusion or empyema may enhance clearance of the infection and improves lung mechanics. Antibiotic therapy should include vancomycin (particularly in areas where penicillin-resistant streptococci have been identified) and a second- or third-generation cephalosporin.
RBCs should be administered to ensure a hemoglobin concentration of 13-16 g/dL in the acutely ill infant to ensure optimal oxygen delivery to the tissues. Delivery of adequate amounts of glucose and maintenance of thermoregulation, electrolyte balance, and other elements of neonatal supportive care are also essential aspects of clinical 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. Children who are in severe respiratory distress should undergo tracheal intubation if they are unable to maintain oxygenation or have decreasing levels of consciousness. (See Pharmacologic Therapy)
Increased respiratory support requirements such as increased inhaled oxygen concentration, positive pressure ventilation, or CPAP are commonly required before recovery begins. Bi-level positive airway pressure (BiPAP) may also be used to help support respiratory effort as a stand-alone intervention or as a bridge to intubation. Criteria for institution and weaning of supplemental oxygen and mechanical support are similar to those for other neonatal respiratory diseases. Extra humidification of inspired air (eg, room humidifiers) is also not useful, although supplemental oxygen is frequently humidified for patient comfort.
Adequate gas exchange depends not only on alveolar ventilation, but also on the perfusion and gas transport capacity of the alveolar perfusate (ie, blood). Preservation of pulmonary and systemic perfusion is essential, using volume expanders, inotropes, afterload reduction, blood products, and other interventions (eg, inhaled nitric oxide) as needed. Excellent lung mechanics do little good if perfusion is not simultaneously adequate.
Be aware that lung disease is often structurally heterogeneous, with subpopulations of normally inflated, hyperinflated, atelectatic, obstructed, fluid-filled, and variably perfused alveoli that may require multiple adjustments of ventilatory pressures, flows, rates, times, and modalities.
Chest percussion is usually unnecessary in children with pneumonia. Studies in adults have not shown benefit; however, no definitive studies have been performed in children. Although most children do not expectorate sputum, they are able to clear it from their lungs and to swallow it. In young infants with bronchiolitis, chest percussion can be helpful in moving mucus and improving air entry (postpercussion auscultation often results in increased wheezes and crackles because of the better air entry) and oxygenation. However, the few studies that have involved children have not shown shortened hospital stays.
The choice of an initial, empiric agent is selected according to the susceptibility and resistance patterns of the likely pathogens and experience at the institution, and the selection is tempered by knowledge of delivery of drugs to the suspected infected sites within the lung.
The vast majority of children diagnosed with pneumonia in the outpatient setting are treated with oral antibiotics.
High-dose amoxicillin is used as a first-line agent for children with uncomplicated community-acquired pneumonia, which provides coverage for S pneumoniae. Second- or third-generation cephalosporins and macrolide antibiotics such as azithromycin are acceptable alternatives but should not be used as first-line agents because of lower systemic absorption of the cephalosporins and pneumococcal resistance to macrolides. Treatment guidelines are available from the Cincinnati Children's Hospital Medical Center and, more recently, from the Infectious Diseases Society of America (IDSA).
Macrolide antibiotics are useful in school-aged children, because they cover the most common bacteriologic and atypical agents (Mycoplasma, Chlamydophila, Legionella). However, increasing levels of resistance to macrolides among pneumococcal isolates should be considered (depending on local resistance rates). One study suggests that penicillin and macrolide resistance among S pneumoniae isolates has been increasing.
Hospitalized patients can be safely treated with narrow-spectrum agents such as ampicillin, and this is the mainstay of current guidelines for pediatric community-acquired pneumonia.[50, 51, 45] Children who are toxic appearing should receive antibiotic therapy that includes vancomycin (particularly in areas where penicillin-resistant pneumococci and methicillin-resistant S aureus [MRSA] are prevalent) along with a second- or third-generation cephalosporin.
If gram-negative pneumonia is suspected and beta-lactam antibiotics are administered, some data suggest that continuous exposure to an antimicrobial concentration greater than the mean inhibitory concentration (MIC) for the organism may be more important than the amplitude of the peak concentration. Intramuscular treatment or intravenous therapy with the same total daily dose but a more frequent dosing interval may be advantageous if the infant's condition fails to respond to conventional dosing. Comparative data to confirm the superiority of this approach are lacking. Whether this approach offers any advantage with use of agents other than beta-lactams is unclear.
Studies in human adults have demonstrated that aminoglycosides reach the bronchial lumen marginally when administered parenterally, although alveolar delivery is satisfactory.[52, 53] Endotracheal treatment with aerosolized aminoglycosides has been reportedly effective for marginally susceptible organisms in bronchi, whereas cefotaxime appears to attain adequate bronchial concentrations via the parenteral route. Limited in vitro and animal data suggest that cefotaxime may retain more activity than aminoglycosides in sequestered foci, such as abscesses, although such foci are rare in congenital pneumonia, and adequate drainage may be more important than antimicrobial selection.
Recovery of a specific pathogen from a normally sterile site (eg, blood, urine, CSF) permits narrowing the spectrum of antimicrobial therapies and may thus reduce the selection of resistant organisms and costs of therapy. Repeated culture of the site after 24-48 hours is usually warranted to ensure sterilization and to assess the efficacy of therapy. Endotracheal aspirates are not considered to represent a normally sterile site, although they may yield a pathogen that is a true invasive culprit. Reculture of an endotracheal aspirate that identified the presumptive pathogen in a particular case may not be helpful because colonization may persist even if tissue invasion has been terminated.
Decreasing respiratory support requirements, clinical improvement, and resolution revealed on radiographs also support the efficacy of therapy. When appropriate, assess plasma antibiotic concentrations to ensure adequacy and reduce the potential for toxicity. Failure to recover an organism does not exclude an infectious etiology; continuation of empiric therapy may be advisable unless the clinical course or other data strongly suggests that a noninfectious cause is responsible for the presenting signs.
Continue to perform careful serial examinations for evidence of complications that may warrant a change in therapy or dosing regimen, surgical drainage, or other intervention.
Evidence-supported options for targeted treatment of inflammation independent of antimicrobial therapy are severely limited. Considerable speculation suggests that current antimicrobial agents, directed at killing invasive organisms, may transiently worsen inflammatory cascades and associated host injury because dying organisms release proinflammatory structural and metabolic constituents into the surrounding microenvironment. This is not to imply that eradicating invasive microbes should not be a goal; however, other methods of eradication or methods of directly dealing with the pathologic inflammatory cascades await further definition. In pneumonia resulting from noninfectious causes, the quest for targeted, effective, and safe anti-inflammatory therapy may be of even greater importance.
A few small studies in adults suggest that glucocorticoid use might be beneficial in the treatment of serious (hospitalized) community-acquired pneumonia, although the study designs and sizes limit the ability to properly interpret this data. Until definitive studies are performed, steroids should not be routinely used for uncomplicated pneumonia.
Most infants with respiratory syncytial virus (RSV) pneumonia do not require antimicrobials. Serious infections with this organism usually occur in infants with underlying lung disease.
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 [Tamiflu], zanamivir, amantadine, rimantadine) are approved for treatment and chemoprophylaxis of influenza.
Influenza A pneumonia that is particularly severe or when it occurs in a high-risk patient may be treated with zanamivir or oseltamivir. The neuraminidase inhibitors have activity against influenza A and B viruses, whereas the adamantanes have activity against only influenza A viruses.
Check for resistance patterns for other antiviral agents indicated for treatment or 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.
In 2007-08, a significant increase in the prevalence of oseltamivir resistance was reported among influenza A (H1N1) viruses worldwide. During the 2007-08 influenza season, 10.9% of H1N1 viruses tested in the United States were resistant to oseltamivir.
These prompted the US Centers for Disease Control and Prevention (CDC) to issue revised interim recommendations for antiviral treatment and prophylaxis of influenza. 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.
Complete recommendations are available from the CDC.
Herpes simplex virus pneumonia is treated with parenteral acyclovir.
CMV pneumonitis should be treated with intravenous ganciclovir or foscarnet.
Invasive fungal infections, such as those caused by Aspergillus or Zygomycetes species, are treated with amphotericin B or voriconazole.
Bronchodilators should not be routinely used. Bacterial lower respiratory tract infections rarely trigger asthma attacks, and the wheezing that is sometimes heard in patients with pneumonia is usually caused by airway inflammation, mucus plugging, or both and does not respond to bronchodilator. However, infants or children with reactive airway disease or asthma may react to a viral infection with bronchospasm, which responds to bronchodilators.
Management of Pleural Effusions
A thin layer of fluid (approximately 10 mL) is usually found between the visceral and parietal pleura and helps prevent friction. This pleural fluid is produced at 100 mL/h. Ninety percent of the fluid is reabsorbed on the visceral surface, and 10% is reabsorbed by the lymphatics. Pleural fluid accumulates when the balance between production and reabsorption is disrupted. A transudate accumulates in the pleural cavity when changes in the hydrostatic or oncotic pressures are not accompanied by changes in the membranes. Increased membrane permeability and hydrostatic pressure often result from inflammation and result in a subsequent loss of protein from the capillaries and an accumulation of exudates in the pleural cavity.
When a child with pneumonia develops a pleural effusion, thoracentesis should be performed for diagnostic and therapeutic purposes (see Thoracentesis). The pleural fluid should be obtained to assess pH and glucose levels and a Gram stain and culture, CBC count with differential, and protein assessment should be performed. Amylase and lactase dehydrogenase (LDH) levels can also be measured but are less useful in a parapneumonic effusion than effusions of other etiologies. The results are helpful in determining if the effusion is a transudate or exudate and help to determine the best course of management for the effusion.
Drainage of parapneumonic effusions with or without intrapleural instillation of a fibrinolytic agent (eg, tissue plasminogen activator [TPA]) may be indicated. Chest tube placement for drainage of an effusion or empyema may be performed. Video-assisted thoracic surgery (VATS) procedure may be performed for decortication of organized empyema or loculated effusions.
For more information, see Infections of the Lung, Pleura, and Mediastinum.
Attempts at enteral feeding often are withheld in favor of parenteral nutritional support until respiratory and hemodynamic status is sufficiently stable.
Severe respiratory compromise may require intubation and transfer to a suitable intensive care unit (ICU) for more intensive monitoring and therapy. Indications for transfer include refractory hypoxia, decompensated respiratory distress (eg, lessening tachypnea due to fatigue, hypercapnia), and systemic complications such as sepsis.
Transfer may need to be initiated at a lower threshold for infants or young children, as decompensation may be rapid. Transfer of very sick infants or young children to a pediatric ICU is best done with a specialist pediatric transfer team, even if that entails a slightly longer wait, compared with conventional medical transport or even air transport.
Severe coughing, especially in the context of necrotizing pneumonias or bullae formation, may lead to spontaneous pneumothoraces. These may or may not require treatment depending on the size of the pneumothorax and whether it is under tension and compromising ventilation and cardiac output.
Other complications include the following:
Systemic infection with metastatic foci
Air leak syndrome, including pneumothorax, pneumomediastinum, pneumopericardium, and pulmonary interstitial emphysema
Obstructive airway secretions
Chronic lung disease
Hypoxic-ischemic and cytokine-mediated end-organ injury
Aside from avoiding infectious contacts (difficult for many families who use daycare facilities), vaccination is the primary mode of prevention. Since the introduction of the conjugated HIB vaccine, the rates of HIB pneumonia have significantly declined. However, the diagnosis should still be considered in unvaccinated persons, including those younger than 2 months, who have not received their first shot.
Conjugated and unconjugated polysaccharide vaccines for S pneumoniae have been developed for infants and children, respectively. The pneumococcal 7-valent conjugate vaccine (diphtheria CRM197 protein; Prevnar) that was introduced in 2000 contains epitopes to 7 different strains. Pneumococcal vaccine polyvalent (Pneumovax) covers 23 different strains. A new 13-valent conjugated vaccine (Prevnar 13) was approved in 2010 and replaces PCV7 for all doses. Children who have completed their vaccine schedule with PCV7 should get a booster dose with PCV13.
In a 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.[56, 21]
However, since the initiation of the heptavalent pneumococcal vaccine in 2000, researchers have found that nearly two thirds of invasive pneumococcal disease cases in young children have been caused by 6 serotypes not included in that vaccine. Those serotypes, along with the original 7, have been incorporated into pneumococcal vaccine valent-13 (Prevnar 13), which was approved in February 2010.
A paper at the 33rd Annual Meeting of the European Society for Paediatric Infectious Diseases reports on the impact of the 10-valent pneumococcal conjugate vaccine, PCV10, in unvaccinated children. The study assessed pneumonia rates from 2011 to 2013 in 116,672 children and found that for hospital-diagnosed pneumonia, there was a relative rate reduction of 12% in the 2012/13 season, compared with the 2005/06 and 2007/08 seasons. For hospital-treated primary pneumonia, there was a relative rate reduction of 28% in the 2012/13 season, compared with the 2005/06 and 2007/08 seasons.
The 23-valent polysaccharide vaccine (PPVSV) is recommended for children 24 months or older who are at high risk of pneumococcal disease.
Influenza vaccine is recommended for children aged 6 months and older. The vaccine exists in 2 forms: inactivated vaccine (various products), administered as an intramuscular injection, and a cold-adapted attenuated vaccine (FluMist; MedImmune), administered as a nasal spray, which is currently licensed only for persons aged 2-49 years.
Although the influenza vaccine is especially recommended for children at high risk, such as those with BPD, cystic fibrosis, or asthma, the use of FluMist is cautioned in persons with known asthma because of reports of transient increases in wheezing episodes in the weeks after administration. However, in years when vaccine strains have been mismatched with the circulating influenza strains, FluMist has provided good protection (approximately 70%), even when the inactivated vaccine was entirely useless.
Clinical trials are ongoing to lower the age of administration of Fluzone (made by Aventis Pasteur), one of the inactivated intramuscular vaccines, to 2 months (currently approved for children 6 mo or older) to help protect this high-risk, but unvaccinated, population. The safety and efficacy of this approach remains unknown.
PCP prophylaxis with trimethoprim-sulfamethoxazole 3 times a week is widely used in immunocompromised children and has all but eradicated this organism in patients receiving prophylaxis.
The use of pneumococcal and H influenzae type B vaccines and penicillin prophylaxis in patients with sickle cell disease have helped reduce the incidence of bacterial infections in these children.
RSV prophylaxis consists of monthly intramuscular injections of palivizumab at a dose of 15 mg/kg (maximum volume 1 mL per injection; multiple injections may be required per dose). This strategy is currently recommended for high-risk infants only (ie, premature infants and newborns with congenital heart disease). Monthly injections during the RSV season approximately halve the rate of serious RSV disease that leads to hospitalization. This expensive therapy is generally restricted to infants at high risk, such as children younger than 2 years with chronic lung disease of prematurity, premature infants younger than 6 months (or with other risk factors), and children with significant congenital heart disease.
Malnutrition is a known risk factor for infections, but zinc deficiency in particular has been shown to increase the risk for childhood pneumonia. In areas of the world where zinc deficiency is common, supplementation may significantly reduce the incidence of childhood pneumonia.
Consultation is not needed in the care of most children with pneumonia. However, 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, and 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.
Although some pneumonias are destructive (eg, adenovirus) and can cause permanent changes, most childhood pneumonias have complete radiologic clearing. If a significant abnormality persists, consideration of an anatomic abnormality is appropriate.
Careful longitudinal surveillance for long-term problems with growth, development, otitis, reactive airway disease, and other complications should be performed.
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|Category||Laboratory and Imaging Findings||Clinical Findings||Differential Diagnosis|
|1||Persistent or recurrent radiologic findings||Persistent or recurrent fever and symptoms||Cystic fibrosis, immunodeficiencies, obstruction (intrinsic [eg, foreign body] or extrinsic [eg, compressing nodes or tumor]), pulmonary sequestration, bronchial stenosis, or bronchiectasis|
|2||Persistent radiologic findings||No clinical findings||Anatomic abnormality (eg, sequestration, fibrosis, pleural lesion)|
|3||Recurrent pulmonary infiltrates with interval radiologic clearing||No clinical findings||Asthma and atelectasis that has been misdiagnosed as a bacterial pneumonia; aspiration syndrome, hypersensitivity pneumonitis, idiopathic pulmonary hemosiderosis, or a mild immunodeficiency disorder|