American Journal of Pediatrics

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Parapneumonic Pleural Effusions Consist of Two Distinct Entities

Received: 27 October 2019    Accepted: 22 November 2019    Published: 04 December 2019
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Abstract

Pleural effusions (PE) complicating pneumonia are usually considered as one entity. But some effusions collect from the start of pneumonia (“sinpneumonic”-SPE), others appear after antibiotics have been started started (“metapneumonic” – MPE). Material, methods. It is a retrospective clinical study (1980-1990s); with new therapies tested over next 20 years. Included are 2561 children with pneumonia (1 month – 14 years); 424 of them had PE, classified as SPE (173) or MPE (251 – 59%). Usual labs and immune complexes levels in blood and PE were studied. Results. Of 281 positive PE S. pneumoniae was identified in 88%, H. influenzae type b – 5%, S. pyogenes – 8%, S. aureus – 4%. MPE was mostly seen in necrotizing pneumonia in under-5 children, particularly with antibiotics started late-after 4th day. MPE starts with initial short drop of temperature that recurs to 39,5-40,5°C and lasts 5-20 days, refractory to antibiotic changes. PE are always serous or serous-fibrinous with WBC <1000/mm3, pH>7.3, glucose >3.0 mmol/l; X-ray show costal pleura fibrin deposition. Initial blood WBC, CRP, procalcitonin levels are elevated, normalizing with necrotic pneumonia resolution. From this point ESR rapidly rises to 40-80 mm/h – a landmark of MPE. We found a much higher levels jf pneumococcal antigens containing immune complexes with complement consumption in MPE, compared to SPE – in both blood and PE. This suggested an immune mechanism of MPE and justified the administration of steroids (prednisolone 1 mg/kg/d for 2-4 days) that stops fever within 1-2 days (100% cases). Full fibrin resorption occurs in 1-2 months, rarely more, making unnecessary fibrinolysis, drainage or thoracoscopy. Conclusions. MPE is an immunopathologic complication of pneumonias’ antibiotic treatment that results from microbial cells destruction by antibiotics liberating an antigen excess favoring immune complexes formation, pleura being the shock organ. Recognition of MPE is paramount for the therapy choice, particularly – steroids, and for reducing invasive procedures.

DOI 10.11648/j.ajp.20190504.28
Published in American Journal of Pediatrics (Volume 5, Issue 4, December 2019)
Page(s) 270-275
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This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Pneumonia, Pleural Effusion, Immune-mediated Mechanism, New Treatment, Reducing Invasive Procedures

References
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[2] Balfour-Lynn IM, Abrahamson E, Cohen G, et al. and on behalf of the Paediatric Pleural Diseases Subcommittee of the BTS Standards of Care Committee. BTS guidelines for the management of pleural infection in children. Thorax. 2005; 60: i1–i21.
[3] Segerer FJ, Seeger K, Maier A et al. Therapy of 645 children with parapneumonic effusion and empyema. A German nationwide surveillance study. Pediatr. Pulmonol. 2016 Sep 20. doi: 10.1002/ppul.23562.
[4] Andrews NC, Parker EF, Shaw RP, et al. Management of non-tuberculous empyema. Am Rev Respir Dis. 1962; 85: 935–6.
[5] Heffner JE, Brown LK, Barbieri C, Barbieri C, Deleo JM. Pleural fluid chemical analysis in parapneumonic effusions. A meta-analysis. Am J Respir Crit Care Med. 1995; 151: 1700–8.
[6] Tagarro A, Otheo E, Baquero-Artigao F et al. Dexamethasone for parapneumonic pleural effusion: A Randomized, double-blind, clinical trial. J Pediatr. 2017; 185: 117-123.
[7] Tatochenko V. K, Panasiuk NL, Katosova LK [Circulating immune complexes in children with synpneumonic and metapneumonic pleurisy]. Probl Tuberk. 1985; (7): 52-5. Article in Russian.
[8] Botvinjeva V., Panasyuk N., Shamsiev F, [Immunnologic characteristics of sin- and methapneumonic pleurisy in children]. Pediatria (Moscow) 1987; # 10: 30-33.
[9] Manerov F. k., Pauli B. A., Chernov O. M. et al. [Clinical variants of pneumococcal pneumonia and characteristics of their course and outcome]. Pediatria (Moscow) 1990; #3: 22—28.
[10] Buckingham SC, King MD, Miller ML. Incidence and etiologies of complicated parapneumonic effusions in children, 1996 to 2001. Pediatr Infect Dis J. 2003 Jun. 22 (6): 499-504.
[11] Cruz Hernandez M,, Cabrerizo Portero D. [The use of hyaluronidase in the treatment of metapneumonic pleural empyema] Rev Esp Pediatr. 1953; 9 (53): 897-902.
[12] Aguado MT, Celada A. [Activation of the alternative complement pathway in pleural fluid of patients with pneumonia]. Allergol. Immunopathol. (Madr). 1982; 10 (3): 215-20. PMID: 6924537.
[13] Blanc P., Dubus J.-C., Bosdure E., Minodier P. Pleurésies purulentes communautaires de l’enfant. Où en sommes-nous? Arch Pediatr. 2007; 14: 64–72.
[14] Cameron RJ, Davies HR. Intra-pleural fibrinolytic therapy versus conservative management in the treatment of adult parapneumonic effusions and empyema. Cochrane Database Systematic Reviews. 2008; 2: CD002312.
[15] Long AM, Smith-Williams J, Mayell S et al. 'Less may be best'-Pediatric parapneumonic effusion and empyema management: Lessons from a UK center. J Pediatr Surg. 2016; 51 (4): 588-91.
[16] Butler T. "The Jarisch-Herxheimer reaction after antibiotic treatment of spirochetal infecions: A review of recent cases and our understanding of pathogenesis". American. Tropic, Med, and Hygiene. 2017; 96 (1): 46–52.
[17] Tatochenko V., Bacradze M., Agaronjan A. [The Jarisch-Herxheimer reaction in a child with community-acquired pneumonia: a clinical case]. Pediatr. Pharmacol. 2018; 15 (3): 255-9.
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  • National Medical Research Center of Child Health, Moscow, Russia

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    Vladimir Tatochenko. (2019). Parapneumonic Pleural Effusions Consist of Two Distinct Entities. American Journal of Pediatrics, 5(4), 270-275. https://doi.org/10.11648/j.ajp.20190504.28

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    Vladimir Tatochenko. Parapneumonic Pleural Effusions Consist of Two Distinct Entities. Am. J. Pediatr. 2019, 5(4), 270-275. doi: 10.11648/j.ajp.20190504.28

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    AMA Style

    Vladimir Tatochenko. Parapneumonic Pleural Effusions Consist of Two Distinct Entities. Am J Pediatr. 2019;5(4):270-275. doi: 10.11648/j.ajp.20190504.28

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  • @article{10.11648/j.ajp.20190504.28,
      author = {Vladimir Tatochenko},
      title = {Parapneumonic Pleural Effusions Consist of Two Distinct Entities},
      journal = {American Journal of Pediatrics},
      volume = {5},
      number = {4},
      pages = {270-275},
      doi = {10.11648/j.ajp.20190504.28},
      url = {https://doi.org/10.11648/j.ajp.20190504.28},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.ajp.20190504.28},
      abstract = {Pleural effusions (PE) complicating pneumonia are usually considered as one entity. But some effusions collect from the start of pneumonia (“sinpneumonic”-SPE), others appear after antibiotics have been started started (“metapneumonic” – MPE). Material, methods. It is a retrospective clinical study (1980-1990s); with new therapies tested over next 20 years. Included are 2561 children with pneumonia (1 month – 14 years); 424 of them had PE, classified as SPE (173) or MPE (251 – 59%). Usual labs and immune complexes levels in blood and PE were studied. Results. Of 281 positive PE S. pneumoniae was identified in 88%, H. influenzae type b – 5%, S. pyogenes – 8%, S. aureus – 4%. MPE was mostly seen in necrotizing pneumonia in under-5 children, particularly with antibiotics started late-after 4th day. MPE starts with initial short drop of temperature that recurs to 39,5-40,5°C and lasts 5-20 days, refractory to antibiotic changes. PE are always serous or serous-fibrinous with WBC 3, pH>7.3, glucose >3.0 mmol/l; X-ray show costal pleura fibrin deposition. Initial blood WBC, CRP, procalcitonin levels are elevated, normalizing with necrotic pneumonia resolution. From this point ESR rapidly rises to 40-80 mm/h – a landmark of MPE. We found a much higher levels jf pneumococcal antigens containing immune complexes with complement consumption in MPE, compared to SPE – in both blood and PE. This suggested an immune mechanism of MPE and justified the administration of steroids (prednisolone 1 mg/kg/d for 2-4 days) that stops fever within 1-2 days (100% cases). Full fibrin resorption occurs in 1-2 months, rarely more, making unnecessary fibrinolysis, drainage or thoracoscopy. Conclusions. MPE is an immunopathologic complication of pneumonias’ antibiotic treatment that results from microbial cells destruction by antibiotics liberating an antigen excess favoring immune complexes formation, pleura being the shock organ. Recognition of MPE is paramount for the therapy choice, particularly – steroids, and for reducing invasive procedures.},
     year = {2019}
    }
    

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  • TY  - JOUR
    T1  - Parapneumonic Pleural Effusions Consist of Two Distinct Entities
    AU  - Vladimir Tatochenko
    Y1  - 2019/12/04
    PY  - 2019
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    DO  - 10.11648/j.ajp.20190504.28
    T2  - American Journal of Pediatrics
    JF  - American Journal of Pediatrics
    JO  - American Journal of Pediatrics
    SP  - 270
    EP  - 275
    PB  - Science Publishing Group
    SN  - 2472-0909
    UR  - https://doi.org/10.11648/j.ajp.20190504.28
    AB  - Pleural effusions (PE) complicating pneumonia are usually considered as one entity. But some effusions collect from the start of pneumonia (“sinpneumonic”-SPE), others appear after antibiotics have been started started (“metapneumonic” – MPE). Material, methods. It is a retrospective clinical study (1980-1990s); with new therapies tested over next 20 years. Included are 2561 children with pneumonia (1 month – 14 years); 424 of them had PE, classified as SPE (173) or MPE (251 – 59%). Usual labs and immune complexes levels in blood and PE were studied. Results. Of 281 positive PE S. pneumoniae was identified in 88%, H. influenzae type b – 5%, S. pyogenes – 8%, S. aureus – 4%. MPE was mostly seen in necrotizing pneumonia in under-5 children, particularly with antibiotics started late-after 4th day. MPE starts with initial short drop of temperature that recurs to 39,5-40,5°C and lasts 5-20 days, refractory to antibiotic changes. PE are always serous or serous-fibrinous with WBC 3, pH>7.3, glucose >3.0 mmol/l; X-ray show costal pleura fibrin deposition. Initial blood WBC, CRP, procalcitonin levels are elevated, normalizing with necrotic pneumonia resolution. From this point ESR rapidly rises to 40-80 mm/h – a landmark of MPE. We found a much higher levels jf pneumococcal antigens containing immune complexes with complement consumption in MPE, compared to SPE – in both blood and PE. This suggested an immune mechanism of MPE and justified the administration of steroids (prednisolone 1 mg/kg/d for 2-4 days) that stops fever within 1-2 days (100% cases). Full fibrin resorption occurs in 1-2 months, rarely more, making unnecessary fibrinolysis, drainage or thoracoscopy. Conclusions. MPE is an immunopathologic complication of pneumonias’ antibiotic treatment that results from microbial cells destruction by antibiotics liberating an antigen excess favoring immune complexes formation, pleura being the shock organ. Recognition of MPE is paramount for the therapy choice, particularly – steroids, and for reducing invasive procedures.
    VL  - 5
    IS  - 4
    ER  - 

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