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Necrotizing pneumonia: an emerging problem in children?
I Brent Masters1, Alan F Isles1, Keith Grimwood2,3
1Department of Respiratory and Sleep Medicine, Lady Cilento Children's Hospital, South Brisbane, QLD Australia.
Background:
In children, necrotizing pneumonia (NP) is an uncommon, severe complication of pneumonia. It is characterized by destruction of the underlying lung parenchyma resulting in multiple small, thin-walled cavities and is often accompanied by empyema and bronchopleural fistulae.
Review:
NP in children was first reported in children in 1994, and since then there has been a gradual increase in cases, which is partially explained by greater physician awareness and use of contrast computed tomography (CT) scans, and by temporal changes in circulating respiratory pathogens and antibiotic prescribing. The most common pathogens detected in children with NP are pneumococci and Staphylococcus aureus. The underlying disease mechanisms are poorly understood, but likely relate to multiple host susceptibility and bacterial virulence factors, with viral-bacterial interactions also possibly having a role. Most cases are in previously healthy young children who, despite adequate antibiotic therapy for bacterial pneumonia, remain febrile and unwell. Many also have evidence of pleural effusion, empyema, or pyopneumothorax, which has undergone drainage or surgical intervention without clinical improvement. The diagnosis is generally made by chest imaging, with CT scans being the most sensitive, showing loss of normal pulmonary architecture, decreased parenchymal enhancement and multiple thin-walled cavities. Blood culture and culture and molecular testing of pleural fluid provide a microbiologic diagnosis in as many as 50% of cases. Prolonged antibiotics, draining pleural fluid and gas that causes mass effects, and maintaining ventilation, circulation, nutrition, fluid, and electrolyte balance are critical components of therapy. Despite its serious nature, death is uncommon, with good clinical, radiographic and functional recovery achieved in the 5-6 months following diagnosis. Increased knowledge of NP's pathogenesis will assist more rapid diagnosis and improve treatment and, ultimately, prevention.
Conclusion:
It is important to consider that our understanding of NP is limited to individual case reports or small case series, and treatment data from randomized-controlled trials are lacking. Furthermore, case series are retrospective and usually confined to single centers. Consequently, these studies may not be representative of patients in other locations, especially when allowing for temporal changes in pathogen behaviour and differences in immunization schedules and antibiotic prescribing practices.
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