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ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
Upper respiratory infection prodrome (fever, coryza, cough, hoarseness).
Wheezing or rales.
Myalgia, malaise, headache (older children).
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Viral infection is a common cause of CAP in children. Viral pneumonia is most common in children younger than 2 years. Respiratory syncytial virus (RSV), human rhinovirus, adenovirus, parainfluenza (types 1–3), influenza (A and B) viruses, coronavirus, and human metapneumovirus are responsible for the large majority of cases. Severity of disease, severity of fever, radiographic findings, and the characteristics of cough or lung sounds do not reliably differentiate viral from bacterial pneumonias. Furthermore, viral infections may predispose to bacterial pneumonia. However, substantial pleural effusions, pneumatoceles, abscesses, lobar consolidation with lobar volume expansion, and “round” pneumonias are generally inconsistent with viral disease.
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A. Symptoms and Signs
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An upper respiratory infection frequently precedes the onset of lower respiratory disease due to viruses. Although wheezing or stridor may be prominent in viral disease, other findings, such as cough, signs of respiratory distress (tachypnea, retractions, grunting, and nasal flaring), and physical findings (rales and decreased breath sounds), are similar to those in bacterial pneumonia.
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B. Laboratory Findings
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Rapid viral diagnostic methods such as fluorescent antibody tests, enzyme-linked immunosorbent assay, and/or PCR should only be performed on nasopharyngeal secretions if the result will change management, is necessary a viral etiology in high-risk patients, or is required for epidemiology or infection control. The peripheral white blood cell count is not useful in distinguishing viral from bacterial disease.
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Chest radiographs frequently show perihilar streaking, increased interstitial markings, peribronchial cuffing, or patchy bronchopneumonia. Lobar consolidation or atelectasis may occur, however. Hyperinflation of the lungs may occur when involvement of the small airways is prominent.
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Differential Diagnosis
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The differential diagnosis of viral pneumonia is the same as for bacterial pneumonia. Patients with prominent wheezing may have asthma, airway obstruction caused by foreign-body aspiration, and acute bacterial or viral tracheitis.
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Viral pneumonia or laryngotracheobronchitis may predispose the patient to subsequent bacterial tracheitis or pneumonia as immediate sequelae. Bronchiolitis obliterans or severe chronic respiratory failure may follow adenovirus pneumonia. The results of studies evaluating the development of asthma after a viral pneumonia are variable. Bronchiectasis, chronic hypersensitivity pneumonia and unilateral hyperlucent lung (Sawyer-James syndrome) may follow measles, adenovirus, and influenza pneumonias.
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General supportive care for viral pneumonia does not differ from that for bacterial pneumonia. Patients can be quite ill and should be hospitalized according to the level of their illness. Because bacterial disease often cannot be definitively excluded, antibiotics may be indicated.
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Patients at risk for life-threatening RSV infections (eg, those with BPD or other severe pulmonary conditions, congenital heart disease, or significant immunocompromise) should be hospitalized and ribavirin should be considered. Rapid viral diagnostic tests may be a useful guide for such therapy.
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All children with influenza should be treated with the appropriate therapy for the specific type of influenza (A, B, H1N1). When available epidemiologic data indicate an active influenza infection in the community, antiviral therapy should be considered early for high-risk infants and children who appear to be infected. For dosing recommendations, refer to the American Academy of Pediatrics (AAP) 2018 Redbook. Children with suspected viral pneumonia should be placed in respiratory isolation.
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Although most children with viral pneumonia recover uneventfully, worsening asthma, abnormal pulmonary function or chest radiographs, persistent respiratory insufficiency, and even death may occur in high-risk patients such as newborns or those with underlying lung, cardiac, or immunodeficiency disease. Patients with coinfections, virus-virus coinfections, or virus-bacterium co-infections have worse outcomes.
+
Nolan
VG
et al: Etiology and impact of coinfections in children hospitalized with community-acquired pneumonia. J Infect Dis 2018; 218(2):179–188
[PubMed: 29228381]
.
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ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
Clinical syndrome characterized by one or more of the following findings: coughing, tachypnea, labored breathing, and hypoxia.
Irritability, poor feeding, vomiting.
Wheezing and crackles on chest auscultation.
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Bronchiolitis is the most common serious acute respiratory illness in infants and young children. The diagnosis of bronchiolitis is based on clinical findings including an upper respiratory infection that has progressed to cough, tachypnea, respiratory distress, and crackles or wheeze by physical examination. In most literature from the United States, this definition of bronchiolitis specifically applies to children younger than 2 years. One to 3% of infants with bronchiolitis will require hospitalization, especially during the winter months. Respiratory syncytial virus (RSV) is by far the most common viral cause of acute bronchiolitis. Parainfluenza, human metapneumovirus, influenza, and adenovirus are less common causes of bronchiolitis during early infancy.
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The most effective preventions against RSV infection are proper handwashing techniques and reducing exposure to potential environmental risk factors. Prophylaxis with a monoclonal antibody (palivizumab) is effective at reducing the rate of hospitalization and associated morbidity in high-risk premature infants and those with chronic cardiopulmonary conditions. Dosing recommendations in the United States are available in the AAP 2018 Redbook.
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A. Symptoms and Signs
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The usual course of RSV bronchiolitis is 1–2 days of fever, rhinorrhea, and cough, followed by wheezing, tachypnea, and respiratory distress. Typically, the breathing pattern is shallow, with rapid respirations. Nasal flaring, cyanosis, retractions, and rales may be present, along with prolongation of the expiratory phase and wheezing, depending on the severity of illness. Some young infants present with apnea and few findings on auscultation but may subsequently develop rales, rhonchi, and expiratory wheezing.
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B. Laboratory Findings and Imaging Studies
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A nasal wash can be used to identify the causative pathogen but is not necessary to make the diagnosis of bronchiolitis. The peripheral white blood cell count may be normal or show a mild lymphocytosis. Chest radiographs are not indicated in children who have bilateral, symmetrical findings on examination, who are not in significant respiratory distress, and who do not have elevated temperature. Chest radiograph findings are generally nonspecific and typically include hyperinflation, peribronchial cuffing, increased interstitial markings, and subsegmental atelectasis.
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Bacterial superinfection is a rare complication of viral pneumonia. The results of studies investigating the risk for the subsequent development of chronic airway hyperreactivity (asthma) are variable. Bronchiolitis due to RSV infection contributes substantially to morbidity and mortality in children with underlying medical disorders, including chronic lung disease of prematurity, CF, congenital heart disease, and immunodeficiency.
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Although most children with RSV bronchiolitis are readily treated as outpatients, hospitalization is required in infected children with hypoxemia on room air, a history of apnea, moderate tachypnea with feeding difficulties, and marked respiratory distress with retractions. Children at high risk for hospitalization include infants (aged < 6 months), especially with any history of prematurity, and those with underlying chronic cardiopulmonary disorders. While in the hospital, treatment should include supportive strategies such as frequent suctioning and providing adequate fluids to maintain hydration. If hypoxemia is present, supplemental oxygen should be administered. There is no evidence to support the use of antibiotics in children with bronchiolitis unless there is evidence of an associated bacterial pneumonia. Bronchodilators and corticosteroids have not been shown to change the severity or the length of the illness in bronchiolitis and therefore are not recommended. Studies evaluating the effectiveness of hypertonic saline and heated high-flow oxygen therapy are ongoing.
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Patients at risk for life-threatening RSV infections (eg, children born at < 35 weeks, children with other severe pulmonary conditions, congenital heart disease, neuromuscular disease, or significant immunocompromise) should be considered for RSV prophylaxis therapy. For more detail, refer to the AAP 2018 Redbook. High-risk patients with RSV bronchiolitis may need to be hospitalized and treated with ribavirin.
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The prognosis for most infants with acute bronchiolitis is very good. With improved supportive care and prophylaxis with palivizumab, the mortality rate among high-risk infants has decreased substantially.
+
Meissner
HC: Viral bronchiolitis in children. New Engl J Med 2016;374(1):62–72
[PubMed: 26735994]
.
+
Ralston
SL
et al: Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics 2014;134(5):e1474–e1502
[PubMed: 25349312]
.
++
ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
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M pneumoniae is a common cause of symptomatic pneumonia in older children although it may be seen in children younger than 5 years. Endemic and epidemic infection can occur. The incubation period is long (2–3 weeks), and the onset of symptoms is slow. Although the lung is the primary infection site, extrapulmonary complications sometimes occur. Extrapulmonary complications in CAP suggest the diagnosis of M. pneumoniae.
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A. Symptoms and Signs
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Fever, cough, headache, and malaise are common symptoms as the illness evolves. Although cough is usually dry at the onset, sputum production may develop as the illness progresses. Sore throat, otitis media, otitis externa, and bullous myringitis may occur. Rales and chest pain are frequently present on chest examination; decreased breath sounds or dullness to percussion over the involved area may be present.
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B. Laboratory Findings and Imaging Studies
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PCR is the gold standard for diagnosis. However, like other respiratory pathogens, Mycoplasma can be carried in the upper respiratory tract after resolution of active infection. Enzyme immunoassay (EIA) and complement fixation are sensitive and specific for M pneumoniae but may also be positive in asymptomatic children. Serologic (IgG) testing collected over 2 weeks showing a fourfold or greater rise in specific antibodies confirms the diagnosis of active respiratory disease due to M pneumoniae. The total and differential white blood cell counts are usually normal.
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Chest radiographs usually demonstrate interstitial or bronchopneumonic infiltrates, frequently in the middle or lower lobes. Pleural effusions are extremely uncommon.
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Extrapulmonary involvement of the blood, central nervous system, skin, heart, or joints can occur. Direct Coombs–positive autoimmune hemolytic anemia, occasionally a life-threatening disorder, is the most common hematologic abnormality that can accompany M pneumoniae infection. Coagulation defects and thrombocytopenia can also occur. Cerebral infarction, meningoencephalitis, Guillain-Barré syndrome, cranial nerve involvement, and psychosis all have been described. A wide variety of skin rashes, including erythema multiforme and Stevens-Johnson syndrome, can occur. Bronchiolitis obliterans due to Stephens-Johnson syndrome associated with M pneumoniae also has been reported.
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Antibiotic therapy with a macrolide for 7–10 days may shorten the course of illness. Ciprofloxacin is a possible alternative. Supportive measures, including hydration, antipyretics, and bed rest, are helpful.
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In the absence of the less common extrapulmonary complications, the outlook for recovery is excellent.
+
Atkinson
TP, Waites
KB:
Mycoplasma pneumoniae infections in childhood. Pediatr Infect Dis 2014;33(1):92–94
[PubMed: 24346598]
.
+
Meyer Sauteur
PM, Unger
WWJ, van Rossum
AMC, Berger
C: The art and science of diagnosing
Mycoplasma infection. Pediatr Infect Dis J 2018;37(11):1192–1195
[PubMed: 30169485]
.
++
ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
History of recurrent aspiration or an aspiration event.
New-onset respiratory distress, oxygen requirement, or fever, after the aspiration.
Any new-onset respiratory distress or increase in oxygen requirement in a child with known aspiration.
Focal findings on physical examination.
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Patients whose anatomic defense mechanisms are impaired are at risk of aspiration pneumonia (Table 19–6). Aspiration pneumonia may be acute or chronic but is more common in children with other underlying medical conditions (see Table 19–6). An acute aspiration event may lead to a typical pneumonia syndrome with fever, asymmetrical auscultation findings, and asymmetric imaging findings. Chronic aspiration pneumonitis is more indolent and can cause chronic respiratory symptoms of “rattling,” cough or wheezing, chronic chest infiltrates, bronchiectasis, or failure to thrive. Pneumonitis is worsened by gram-negative anaerobes and other bacteria present in the mouth.
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A. Symptoms and Signs
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Acute onset of fever, cough, respiratory distress, or hypoxemia in a patient at risk suggests acute aspiration pneumonia. Chest physical findings, such as rales, rhonchi, or decreased breath sounds, may initially be limited to the lung region into which aspiration occurred. Although any region may be affected, the right side—especially the right upper lobe in the supine patient—is commonly affected. In patients with chronic aspiration “chest rattling” is often described by parents. Generalized rales and wheezing may also be present.
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B. Laboratory Findings and Imaging Studies
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Chest radiograph abnormalities can vary widely. They may reveal lobar consolidation or atelectasis and focal or generalized alveolar or interstitial infiltrates. Complications such as empyema or lung abscess may complicate acute aspiration pneumonia. In some patients with chronic aspiration, perihilar infiltrates with or without bronchiectasis may be seen. If there is clinical concern, chest CT can better delineate these complications.
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In patients with chronic aspiration pneumonitis, attempts should be made to evaluate dysphagia. VFSS is typically performed to evaluate the swallow. Fiberoptic endoscopic examination of swallowing (FEES) is done at specialty centers to directly visualize the larynx during swallowing via laryngoscope. Radionuclide studies have low sensitivity to diagnosis aspiration. Although biomarkers such as lipid-laden macrophages obtained from BAL samples have low sensitivity and specificity, BAL may be considered to diagnose bacterial infection (see section Diagnosis of Respiratory Tract Infections). Anatomic abnormalities such as laryngeal cleft can be evaluated by rigid laryngoscopy/bronchoscopy. Tracheoesophageal fistula is rare and can be difficult to diagnose: UGI fluoroscopy series, rigid or flexible bronchoscopy, or esophageal endoscopy may aid in diagnosis. The role of esophageal disease, gastroesophageal reflux, and impaired esophageal motility in chronic aspiration may warrant evaluation by a gastroenterologist or multidisciplinary aerodigestive team.
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Differential Diagnosis
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In the acutely ill patient, bacterial and viral pneumonias should be considered. In the chronically ill patient, the differential diagnosis may include disorders causing recurrent pneumonia (eg, immunodeficiencies, ciliary dysfunction, or foreign body), chronic wheezing, or interstitial lung disorders (see the next section), depending on the presentation.
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Aspiration pneumonia leads to a chemical pneumonitis, and supportive treatment is recommended. Antimicrobial therapy for patients who are acutely ill from aspiration pneumonia includes coverage for anaerobic organisms. In general, clindamycin is appropriate initial coverage.
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Treatment of chronic aspiration pneumonitis may include the following: surgical correction of anatomic abnormalities; paced swallowing systems/bottles, thickening of liquids taken by mouth, swallowing therapy, improved oral hygiene, inhaled corticosteroids, and chest physiotherapy. In patients with compromise of the central nervous system, exclusive feeding by gastrostomy may be required. Because of the widespread causes and consequences of chronic aspiration, multidisciplinary aerodigestive management is often recommended.
+
Durvasula
VS, O’Neill
AC, Richter
GT: Oropharyngeal dysphagia in children: mechanism, source, and management. Otolaryngol Clin North Am 2014;47(5):691
[PubMed: 25213278]
.
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PNEUMONIA IN THE IMMUNOCOMPROMISED HOST
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ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
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Compromised immune function occurs following solid organ or hematopoietic stem cell transplantation, in patients with congenital immune deficits, and in patients receiving cancer chemotherapy or other immunosuppressant therapy, including chronic corticosteroids.
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Pulmonary infection, which is the most common infection in these patients, can present as focal pneumonia, pulmonary nodules, disseminated disease, or diffuse ILD. The underlying cause of the immunocompromised state often determines the spectrum of infectious agents responsible for disease (see also Chapter 33). Pneumonia in an immunocompromised host may be due to any common community-acquired bacteria or less common pathogens such as opportunistic fungi, Toxoplasma gondii, P jiroveci, anaerobic bacteria, Nocardia species, Legionella pneumophila, mycobacteria, and viruses. Multiple organisms are commonly isolated in culture.
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A. Symptoms and Signs
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Patients often present with subtle signs such as mild cough, tachypnea, or low-grade fever that can rapidly progress to high fever, respiratory distress, and hypoxemia or Children’s Interstitial and diffuse Lung Disease (chILD) syndrome. An obvious portal of infection, such as an intravascular catheter, may predispose to bacterial or fungal infection via hematogenous spread.
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B. Laboratory Findings and Imaging Studies
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Fungal, parasitic, or bacterial infection, especially with antibiotic-resistant bacteria, should be suspected in the neutropenic child. Cultures of peripheral blood and through intravascular catheters, sputum, tracheobronchial secretions, nasopharynx or sinuses, pleural fluid, biopsied lymph nodes, bone marrow, or skin lesions should be considered and obtained as soon as infection is suspected. Serum (1, 3)-β-d-glucan assays and serum and BAL galactomannan assays for invasive pulmonary fungal disease are being used in some centers. Urine can be tested for typical pathogens and Legionella urinary antigens.
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Invasive methods are commonly required to make a diagnosis. Appropriate samples should be obtained soon after a patient with pneumonia fails to respond to initial treatment. The results of these procedures usually lead to important changes in empiric therapy. Sputum is often unavailable in the young child. BAL frequently detects one or more organisms and should be done early in evaluation. The combined use of a wash, brushing, endobronchial biopsy, and lavage has a high yield. In patients with rapidly advancing, or more peripheral disease, lung biopsy becomes more urgent. The morbidity and mortality of this procedure can be reduced by VATS techniques.
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Because of the multiplicity of organisms that may cause disease, a comprehensive set of studies should be done on lavage and biopsy material. These consist of rapid diagnostic studies including culture, PCR, and antigen detection for viruses and rapid fluorescent antibody studies for P jiroveci and Legionella; Gram, acid-fast, and fungal stains; cytologic examination for viral inclusions; and cultures for anaerobic and aerobic bacteria, fungi, mycobacteria, and Legionella.
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Chest radiographs and volumetric CT scans may be useful in identifying the pattern and extent of disease. In early P jiroveci pneumonia, dyspnea and hypoxemia may be marked despite minimal radiographic abnormalities. Distinctive radiographic findings such as the halo sign can be seen in aspergillosis.
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Differential Diagnosis
++
The organisms causing disease vary with the type of immunocompromise present. For example, the splenectomized or sickle cell disease patient may be overwhelmed by infection with encapsulated bacteria. The child with HIV/AIDS or receiving immunosuppressant therapy or chemotherapy is more likely to have P jiroveci infection. The febrile neutropenic child who has been receiving adequate doses of intravenous broad-spectrum antibiotics or systemic steroid therapy may have fungal disease. The key to diagnosis is to consider all possibilities of infection.
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Depending on the form of immunocompromise, perhaps only one-half to two-thirds of new pulmonary infiltrates in such patients represent infection. The remaining infiltrates are caused by pulmonary toxicity of radiation, chemotherapy, or other drugs; pulmonary disorders, including hemorrhage, embolism, atelectasis, or aspiration; idiopathic pneumonia syndrome or acute respiratory distress syndrome in bone marrow transplant patients; recurrence or extension of primary malignant growths or immunologic disorders; transfusion reactions, leukostasis, or tumor cell lysis; or ILD, such as lymphocytic interstitial pneumonitis with HIV infection.
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Necrotizing pneumonia, lung abscess, and parapneumonic effusions can develop. Progressive respiratory failure, shock, multiple organ damage, disseminated infection, and death commonly occur in the infected immunocompromised host.
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Early use of broad-spectrum intravenous antibiotics is indicated in febrile, neutropenic, or immunocompromised children. Trimethoprim-sulfamethoxazole (for P jiroveci), macrolides (for Legionella) are/or antifungals may also be indicated early in the treatment of immunocompromised children before an organism is identified. Targeted therapy should be based on studies of specimens obtained from BAL or lung biopsy. Recent data suggest that use of noninvasive ventilation strategies early in the course of pulmonary insufficiency or respiratory failure may decrease mortality.
++
Prognosis is based on the severity of the underlying immunocompromise, appropriate early diagnosis and treatment, and the infecting organisms. Intubation and mechanical ventilation have been associated with high mortality, especially in hematopoietic stem cell transplant patients.
+
Collaco
JM, Gower
WA, Mogayzel
PJ
Jr: Pulmonary dysfunction in pediatric hematopoietic stem cell transplant patients: overview, diagnostic considerations, and infectious complications. Pediatr Blood Cancer 2007;49(2):117
[PubMed: 17029246]
.
+
Nouér Simone
A
et al: Earlier response assessment in invasive aspergillosis based on the kinetics of serum Aspergillus galactomannan: proposal for a new definition. Clin Infect Dis 2011;53(7):671
[PubMed: 21846834]
.
++
ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
High fever, malaise, and weight loss in the setting of pneumonia.
Chest radiographs and CT scans usually reveal lung cavities, often with air-fluid levels.
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Lung abscesses are thick-walled cavities that form from inflammation and central necrosis following an initial pulmonary infection. A lung abscess can occur in a previously well child, a child prone to aspiration, or in children with immunosuppression or underlying lung or systemic disease. Lung abscesses may also occur via embolic spread. Organisms such as staphylococci and streptococci more commonly affect the healthy host, while anaerobic and gram-negative organisms as well as Nocardia, mycobacteria, Legionella species, fungi (Candida and Aspergillus), and drug-resistant pathogens should be considered in the immunocompromised host or in patients not responding to typical antibiotic treatment.
+++
A. Symptoms and Signs
++
Symptoms and signs referable to the chest may or may not be present. High fever, malaise, and weight loss are often present. In infants, evidence of respiratory distress can be present.
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B. Laboratory Findings and Imaging Studies
++
Elevated peripheral white blood cell count with a neutrophil predominance or an elevated erythrocyte sedimentation rate or CRP may be present. Blood cultures are rarely positive except in the immunocompromised patient.
++
Chest radiographs usually reveal single or multiple thick-walled lung cavities, often with air-fluid levels. Local compressive atelectasis, pleural thickening, or adenopathy may also occur. Chest CT scan may provide better localization and understanding of the lesions.
++
In patients producing sputum, stains, and cultures may provide the diagnosis. Direct percutaneous aspiration of material for stains and cultures should be considered although complications can occur.
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Differential Diagnosis
++
Loculated pyopneumothorax, neoplasms, plasma cell granuloma, and infected congenital cysts and sequestrations should be considered. Pneumatoceles, non–fluid-filled cysts, are common in children with empyema and usually resolve over time.
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Although complications due to abscesses are now rare, mediastinal shift, tension pneumothorax, and spontaneous rupture can occur. Diagnostic maneuvers such as radiology-guided lung puncture to drain and culture the abscess may also cause pneumothorax or a bronchopulmonary fistula.
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Because of the risks of lung puncture, uncomplicated abscesses are frequently conservatively treated in the immune competent host with appropriate broad-spectrum intravenous antibiotics. Additional coverage for anaerobic gram-negative organisms and fungi should be provided for others. Prolonged therapy with 2–3 weeks of intravenous antibiotics followed by oral therapy may be required. Attempts to drain abscesses via bronchoscopy have caused life-threatening airway compromise. Surgical drainage or lobectomy is occasionally required, primarily in immunocompromised patients. However, such procedures may themselves cause life-threatening complications.
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Although radiographic resolution may be very slow (6 weeks–5 years), resolution occurs in most patients without risk factors for lower respiratory tract infections or loss of pulmonary function. In the immunocompromised or medically complex host, the outlook depends on the underlying disorder.
+
Chan
PC
et al: Clinical management and outcome of childhood lung abscess: a 16-year experience. J Microbiol Immunol Infect 2005;38:183
[PubMed: 15986068]
.
+
Patradoon-HoP
et al: Lung abscess in children. Paediatr Respir Rev 2007;8(1):77–84
[PubMed: 17419981]
.