A 9-Year-Old Boy with Fever, Cough, and Respiratory Distress

Posted by • March 22nd, 2013

In the newest Case Record of the Massachusetts General Hospital, a 9-year-old boy was admitted to the hospital because of fever, cough, respiratory distress, and chest pain. Imaging revealed ill-defined nodular opacities throughout all lung lobes, areas of consolidation, and mediastinal and hilar lymphadenopathy.

The diagnosis of pediatric pneumonias is best approached by multifactorial evaluation of the characteristics of the host (e.g., age and immune status), potential exposures that include epidemiologic considerations, and the radiographic appearance of the pulmonary process.

Clinical Pearls

How does the age of a pediatric patient relate to the microbiology of community-acquired pneumonia?

The array of microbes associated with community-acquired pediatric pneumonias is closely related to the age of the patient, which is not the case in adults. Viruses are most common in infants and young children. The differential diagnosis of pneumonia in a newborn must also include infections with group B streptococcus, Listeria monocytogenes, or gram-negative organisms. Among older children and adolescents, atypical bacteria predominate. Pneumococcal pneumonia is a possibility despite prior immunization; one study showed the incidence of uncomplicated infection to be essentially unaffected by vaccination in the group 5 to 17 years of age.

What is the differential diagnosis from an infectious standpoint of nodular infiltrates on a chest film in a child?

Nodular infiltrates indicate endobronchial and bronchiolar spread of infection, which is commonly seen in bacterial pneumonias, aspiration-associated respiratory viruses, tuberculous and nontuberculous mycobacteria, endemic mycoses, Pneumocystis jiroveci pneumonia, aspergillosis, and nocardiosis. Pneumocystis and angioinvasive aspergillosis are seen exclusively in immunocompromised hosts. The endemic mycoses (histoplasmosis, coccidioidomycosis, and blastomycosis), which may have a nodular appearance on radiographs and can affect persons regardless of their immune status. Although nocardiosis is uncommon in children, it can occur in persons with a competent immune system, manifesting as a subacute respiratory illness. It requires no specific exposures and may cause nodular infiltrates on imaging. Septic emboli may also be nodular in appearance.

Morning Report Questions

Q: What is hypersensitivity pneumonitis and how is it diagnosed? 

A: Hypersensitivity pneumonitis (also known as extrinsic allergic alveolitis) is a noninfectious, immune, inflammatory interstitial lung disease with a broad clinical spectrum that must be in the differential diagnosis. Schuyler and Cormier developed criteria that integrate the various aspects of the disease; the presence of any four major criteria and at least two minor criteria establishes a definitive diagnosis of hypersensitivity pneumonitis. Major criteria include a history of symptoms compatible with hypersensitivity pneumonitis (e.g., weight loss, cough, shortness of breath, febrile episodes, and fatigue); evidence of exposure to the offending antigen through patient history or detection of precipitins (IgG and IgM antibodies) in serum or bronchoalveloar-lavage (BAL) fluid; radiographic changes consistent with the diagnosis (fleeting, micronodular, and interstitial, in middle and lower lung zones); lymphocytosis on BAL (CD4:CD8 T-cell ratio, <1.0); histologic changes consistent with hypersensitivity pneumonitis on lung biopsy; and a positive natural challenge or controlled inhalational challenge that produces symptoms or objective abnormalities on reexposure to the offending environment. Minor criteria include bibasilar rales, decreased carbon monoxide diffusing capacity, and arterial hypoxemia at rest or with exertion.

Table 2. Diagnostic Criteria for Hypersensitivity Pneumonitis.

Q: What is the appropriate management of hypersensitivity pneumonitis?

A: The first line therapy for hypersensitivity pneumonitis is removal or minimization of antigen exposure. Pharmacologic management of hypersensitivity pneumonitis with glucocorticoid therapy is directed at the inflammatory component of the disease. Acute hypersensitivity pneumonitis can be treated with a 2-to-4-week regimen of glucocorticoids, whereas subacute to chronic cases can require weeks or months of treatment with variable doses and responses. The use of steroid-sparing therapies (e.g., azathioprine and macrolide antibiotics) has also been described.

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