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 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.
Highlights
Pleural effusions that complicate pneumonia in children are usually described as one entity-“parapneumonic” pleurisy [1,2,3]
Of 281 positive exudates S. pneumoniae was identified in 88%, H. influenzae type b – in 5%, S. pyogenes – in 8% and S. aureus – in 4%
Pleural effusions are more likely to complicate necrotizing pneumonia – X-ray evidence of lung destruction we found in 23% of children with Sinpneumonic Effusions (SPE) and up to 80% of Metapneumonic Effusion (MPE), the rest being with massive lobar or bilateral infiltrates
Summary
Pleural effusions that complicate pneumonia in children are usually described as one entity-“parapneumonic” pleurisy [1,2,3] Their development is classically described as going through “exudative, fibrinopurulent and organizing phases” [4]. Simple parapneumonic effusions have pH > 7.2 and glucose > 2.2 mmol/l, no organisms in culture or gram stain and no need for pleural fluid drainage [5]. In our experience these effusions develop after antibiotic treatment had been started and they differ in origin from “complicated effusions”. For patients with “complicated effusions” the difference to recovery was only 14 hours (0.5 days)
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