Clinical Manifestation of Necrotizing Pneumonia in Healthy Children.
- Author:
Seong Phil BAE
1
;
Do Hyun KIM
;
Sang Hoon CHAE
;
Ihl Sung PARK
;
Keong Bae PARK
;
Mi Yong SHIN
;
Joon Soo PARK
;
Young Tong KIM
Author Information
1. Department of Pediatrics, Soonchunhyang University Cheonan Hospital, Soonchunhyang University College of Medicine, Cheonan, Korea. pjstable@schmc.ac.kr
- Publication Type:Original Article
- Keywords:
Necrotizing pneumonia;
Pathogenesis;
Child;
Pneumatocele
- MeSH:
Bacterial Infections;
C-Reactive Protein;
Child*;
Chungcheongnam-do;
Female;
Fever;
Follow-Up Studies;
Gyeonggi-do;
Hospitalization;
Hospitals, University;
Humans;
Immunoglobulins;
Leukocytosis;
Lung;
Pediatrics;
Pleural Effusion;
Pneumonia*;
Pneumonia, Mycoplasma;
Radiography;
Retrospective Studies;
Streptococcus;
Thorax
- From:Soonchunhyang Medical Science
2013;19(2):87-92
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: Necrotizing pneumonia (NP) is a severe complication of lobar pneumonia caused by various pathogens. The immunopathogenesis and clinical characteristics of NP in children are not clearly understood. We wanted to evaluate the clinical characteristics and suggest in part the immunopathogenesis of NP. METHODS: We reviewed retrospectively the medical charts and radiographic materials of eight patients with NP, who were diagnosed by chest radiography and chest computed tomography at the Department of Pediatrics, Soonchunhyang University Hospitals at Cheonan and Bucheon from January 2002 to December 2011. RESULTS: They were previously healthy, 2.1 to 4.6 years of ages (mean, 2.8+/-1.0 years) and three boys and five girls. All of them had pleural effusion. Five patients had pneumonic consolidations in right upper lung field. Three patients had pneumatocele. They developed leukocytosis (mean, 19,400+/-6,400/mm3), higher C-reactive protein level (mean, 25.1+/-8.0 mg/dL). The etiologic agents were revealed in two patients; Streptococcus pneumonia (S. pneumonia) was revealed in one patient and S. pneumonia and Mycoplasma pneumonia in the other patient. Three patients were treated with additional intravenous immunoglobulin. Clinical improvement was prolonged: fever lasted 10 to 23 days, and length of hospitalization was 15 to 36 days. NP or pneumatocele were completely resolved on the follow-up radiographic studies in all of the patients. CONCLUSION: Although the previously healthy young children with NP had protracted clinical course, they recovered without any problematic sequelae. Our results suggest that the immunopathogenesis of NP in children may be associated with the exaggerated immune reaction of the host to insults from initial bacterial infections, rather than the pathogen-induced cytopathies.
