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 Table of Contents  
EDITORIAL
Year : 2020  |  Volume : 7  |  Issue : 5  |  Page : 233-234

Necrotizing pneumonia in children: Is it rare anymore?


Department of Pediatric Intensive Care, NMC Royal Hospital, Abu Dhabi, UAE

Date of Submission18-Aug-2020
Date of Acceptance25-Aug-2020
Date of Web Publication14-Sep-2020

Correspondence Address:
Dr. Govind Benakatti
NMC Royal Hospital, Abu Dhabi
UAE
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JPCC.JPCC_134_20

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How to cite this article:
Benakatti G. Necrotizing pneumonia in children: Is it rare anymore?. J Pediatr Crit Care 2020;7:233-4

How to cite this URL:
Benakatti G. Necrotizing pneumonia in children: Is it rare anymore?. J Pediatr Crit Care [serial online] 2020 [cited 2020 Nov 25];7:233-4. Available from: http://www.jpcc.org.in/text.asp?2020/7/5/233/295019



Necrotizing pneumonia (NP), as term denotes, is characterized by the destruction and liquidation of lung parenchyma, resulting in cavity formation, air leaks, and/or intense suppuration. Therefore, it has protracted and severe clinical course unlike community-acquired pneumonia (CAP). Infection triggered vasculitis of intrapulmonary vessels and thrombotic occlusion, resulting in coagulative and liquefactive necrosis of the lung parenchyma.[1] Parapneumonic pleural effusions (PPEs) and empyema are the common results of this pathogenesis, and if necrotic regions extend to the pleura, bronchopleural fistula (BPF) may form. Rarely, thromboses of the multiple intrapulmonary vessels can result in pulmonary gangrene of an entire lobe.[1]

Although NP, described as relatively uncommon, is being increasingly recognized over the past decades[2] and nowadays, it is not uncommon to be seen in day-to-day practice of pediatricians and intensivists. This may be due to the evolution of antibiotic prescriptions, increased awareness, use of advanced diagnostic methods, and evolution of bacteria and host–pathogen interactions. Periodic evolution of bacteria and their virulence are well known. These may occur due to selection pressures in-response to antibiotic prescriptions, use of vaccines, and changing ecological factors. Incidence of NP in the present study is estimated to be 3.3% of children with pneumonia.[3] However, authors have excluded empyema and other complicated pneumonias, despite them being part of spectrum of NP. Authors have stated that lung abscess, NP, and empyema/PPE constituted 25.2% (352/1393) of total pneumonias, indicating higher true prevalence. Staphylococcus is emerging as the most common pathogen in the past two decades followed by pneumococcus. In developed nations, while there are reports of expanding nonvaccine serotype-induced pneumococcal NP (PNP) also, staphylococcal empyemas.[4-6] However, in general, PNP has been diminished there because of wide spread utilization of pneumococcal vaccine. [7,8]

Pathogenesis of NP is incompletely understood. Some of the bacterial virulence factors have been studied in this process. Staphylococcal α-toxin (pore-forming toxins) is shown to cause the activation of NLRP3 inflammasome and platelet–neutrophil aggregation-induced vasculitis/vessel clogging, leading to severe alveolar necrosis.[9] Panton–Valentine leukocidin (PVL) (pore-forming exotoxin linked to severe invasive infections) and methicillin-resistant Staphylococcus aureus have also been looked for association. However, findings are inconsistent unlike skin and soft tissue infections.[10],[11],[12] However, the role of PVL in causing rapidly progressive, hemorrhagic, NP has been well reported in CAP as well as hospital-acquired pneumonia.[13],[14] Of pneumococci, serotype 3 (has thick capsule, evades opsonophagocytic, and is known to induce intense inflammation) and serotype 19A (has greater invasive potential, has a growth advantage over other serotypes, and is often resistant to antibiotics) have been seen closely associated with NP.[15],[16]

Other bacteria including Gram-negatives (Pseudomonas, Klebsiella, Legionella, Acinetobacter sp., etc.) are also known to cause NP but are seen in small numbers or sporadic case reports. They are often seen in patients with comorbidities and hospital-acquired settings. Although studies are limited, viruses are known to attract secondary bacterial pneumonia and their interactions are well implicated in NP. With regard to the role of anaerobes (as routinely no efforts are made to culture or isolate them), adult studies have shown that they play a minor role in causing NP.[1]

Clinical features of NP are like CAP except being severe in nature. NP occurs in healthy individuals with no known risk factors or comorbidities. It manifests as prolonged and severe pneumonia; patients are often disproportionately sick and can have features of intense suppuration (empyema), pneumothorax/BPF, etc., that progress despite initial appropriate antibiotic therapy. It is often described as a complication of bacterial pneumonia. However, it may be possible that necrotic process could be the primary pathology from the beginning itself depending on host–pathogen interactions and pathogen virulence. Despite its serious nature, death is uncommon in NP. Apart from prolonged antibiotics, draining pleural fluid/pus, pneumothorax, and respiratory support, cardiovascular resuscitation and attention to hemodynamics, electrolyte imbalances, fluids, and nutrition are crucial for good outcome. Additional therapies such as lung or lobar resection, intravenous immunoglobulin, and extracorporeal membrane oxygenation are rarely needed in unresponsive cases, and evidence is limited to individual reports.

Thus, in recent decades, NP is increasingly recognized disease in children and not anymore uncommon. Additional molecular diagnostic tests apart from cultures may help increase the pathogen identification. Identification of serotypes is important to further understand the epidemiology, pathogenesis, prevention, etc. Further research on microbiology, host–pathogen interaction, and immunogenomic studies to identify the patients at risk of developing NP will help better understanding, treatment, and outcome.



 
  References Top

1.
Chatha N, Fortin D, Bosma KJ. Management of necrotizing pneumonia and pulmonary gangrene: A case series and review of the literature. Can Respir J 2014;21:239-45.  Back to cited text no. 1
    
2.
Masters IB, Isles AF, Grimwood K. Necrotizing pneumonia: An emerging problem in children? Pneumonia (Nathan) 2017;9:11.  Back to cited text no. 2
    
3.
Ahmed M, Sanjay KS, Keshavamurthy ML, Basavaraja GV. Retrospective study of etiology, clinical features, management and outcomes in children with necrotizing pneumonia. J Pediatr Crit Care 2020;7:255-59.  Back to cited text no. 3
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4.
Grijalva CG, Nuorti JP, Zhu Y, Griffin MR. Increasing incidence of empyema complicating childhood community-acquired pneumonia in the United States. Clin Infect Dis 2010;50:805-13.  Back to cited text no. 4
    
5.
Byington CL, Hulten KG, Ampofo K, Sheng X, Pavia AT, Blaschke AJ, et al. Molecular epidemiology of pediatric pneumococcal empyema from 2001 to 2007 in Utah. J Clin Microbiol 2010;48:520-5.  Back to cited text no. 5
    
6.
Spencer DA, Iqbal SM, Hasan A, Hamilton L. Empyema thoracis is still increasing in UK children. BMJ 2006;332:1333.  Back to cited text no. 6
    
7.
Griffin MR, Zhu Y, Moore MR, Whitney CG, Grijalva CG. U.S. hospitalizations for pneumonia after a decade of pneumococcal vaccination. N Engl J Med 2013;369:155-63.  Back to cited text no. 7
    
8.
Fletcher MA, Schmitt HJ, Syrochkina M, Sylvester G. Pneumococcal empyema and complicated pneumonias: Global trends in incidence, prevalence, and serotype epidemiology. Eur J Clin Microbiol Infect Dis 2014;33:879-910.  Back to cited text no. 8
    
9.
Tong SY, Davis JS, Eichenberger E, Holland TL, Fowler VG Jr. Staphylococcus aureus infections: Epidemiology, pathophysiology, clinical manifestations, and management. Clin Microbiol Rev 2015;28:603-61.  Back to cited text no. 9
    
10.
Shallcross LJ, Fragaszy E, Johnson AM, Hayward AC. The role of the Panton-Valentine leucocidin toxin in staphylococcal disease: A systematic review and meta-analysis. Lancet Infect Dis 2013;13:43-54.  Back to cited text no. 10
    
11.
Sicot N, Khanafer N, Meyssonnier V, Dumitrescu O, Tristan A, Bes M, et al. Methicillin resistance is not a predictor of severity in community-acquired Staphylococcus aureus necrotizing pneumonia – Results of a prospective observational study. Clin Microbiol Infect 2013;19:E142-8.  Back to cited text no. 11
    
12.
Vardakas KZ, Matthaiou DK, Falagas ME. Comparison of community-acquired pneumonia due to methicillin-resistant and methicillin-susceptible Staphylococcus aureus producing the Panton-Valentine leukocidin. Int J Tuberc Lung Dis 2009;13:1476-85.  Back to cited text no. 12
    
13.
Gillet Y, Issartel B, Vanhems P, Fournet JC, Lina G, Bes M, et al. Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Lancet 2002;359:753-9.  Back to cited text no. 13
    
14.
van der Flier M, van Dijk NB, Fluit AC, Fleer A, Wolfs TF, van Gestel JP. Fatal pneumonia in an adolescent due to community-acquired methicillin-resistant Staphylococcus aureus positive for Panton-Valentine-leukocidin. Ned Tijdschr Geneeskd 2003;147:1076-9.  Back to cited text no. 14
    
15.
Tsai YF, Ku YH. Necrotizing pneumonia: A rare complication of pneumonia requiring special consideration. Curr Opin Pulm Med 2012;18:246-52.  Back to cited text no. 15
    
16.
Reinert R, Jacobs MR, Kaplan SL. Pneumococcal disease caused by serotype 19A: Review of the literature and implications for future vaccine development. Vaccine 2010;28:4249-59.  Back to cited text no. 16
    




 

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