Mycoplasma pneumoniae (MP) is a major pathogen causing community-acquired pneumonia in children, especially in school-age children, with an incidence rate of 28%–50% (1–4). Refractory Mycoplasma pneumoniae pneumonia (RMPP) is defined as persistent fever and radiographic progression despite adequate macrolide treatment. This condition has received increasing attention and poses significant clinical challenges (3–5). RMPP is associated with several severe complications, including pleural effusion, pulmonary embolism, pulmonary necrosis, and particularly plastic bronchitis(PB) (5–7). PB, a rare and severe pulmonary disease in children, is primarily diagnosed through bronchoscopy. It involves the formation of obstructive mucous casts within the airways, leading to symptoms such as atelectasis and dyspnea, and may cause severe complications such as respiratory failure or death (1–3). The emergence of RMPP has further complicated treatment and is increasingly linked to the development of PB (7–9). The pathogenesis of PB is thought to involve intense inflammation, airway injury, impaired mucociliary clearance, and viscous secretions (10, 11). With the increasing application of bronchoscopy in severe pneumonia, more and more cases of RMPP complicated with PB have been identified (7, 9).

Early identification of PB in children with RMPP is crucial for timely bronchoscopic intervention to remove the casts, thereby improving outcomes and reducing adverse prognoses (6, 7). However, predicting the occurrence of PB in RMPP patients remains challenging. This study aimed to identify the risk factors for PB in RMPP and develop a practical predictive nomogram based on clinical characteristics to facilitate early diagnosis and intervention.

RMPP is typically characterized by a long course of disease, poor treatment outcomes, and numerous complications, which can be life-threatening in severe patients. Recently, the incidence of RMPP has increased by as much as 40%, highlighting the growing importance of early detection and management of complications (4). PB, recognized as one of the serious complications of RMPP, presents with a gradual onset and a significantly high mortality rate. Therefore, our study aims to develop a nomogram prediction model for the occurrence of PB in RMPP based on clinical data, facilitating early intervention and providing clinical guidance.

Common clinical manifestations of RMPP include cough, persistent fever, and chest pain, which are consistent with the symptoms observed in children with RMPP complicated with PB in this study. Our further analysis indicates that both the peak temperature and duration of fever in the PB group are higher than those in the non-PB group, suggesting a more severe inflammatory response in the PB group (4, 8), Additionally, both local immune responses and systemic immune-inflammatory reactions in the PB group are stronger than those in the non-PB group (3). Furthermore, ZHANG et al. have identified that in children with RMPP experiencing high fever, the accelerated evaporation of bodily fluids can lead to moisture loss in the respiratory tract, resulting in thickened mucus secretions in the trachea and fostering the development of PB (4). Moreover, we found that the average age of children in the PB group is higher than that in the non-PB group [(7.88 ± 2.61) vs. (6.89 ± 2.48) years], mainly occurring in preschool children. The research conducted by Wang Z et al. aligns closely with our findings, suggesting that age is a critical factor influencing the prognosis of RMPP (3). The reason may be potentially linked to the underdeveloped immune responses in preschoolers. A robust cellular immune response may lead to necrosis of airway epithelial cells and significant ciliary dysfunction in children with RMPP, thereby impairing airway immune function and mucociliary clearance, which increases the likelihood of mucus plug formation (6, 8).

Our study suggested that levels of CRP, LDH, and ESR in the PB group are significantly higher than those in the non-PB group (P < 0.05). Multivariate regression analysis identifies CRP > 20 mg/L, pleural effusion, and elevated LDH as independent risk factors for PB in children with RMPP. CRP levels serve as effective markers for monitoring disease progression, assessing prognosis, and reflecting the severity of the inflammatory response linked to MP infection. Gong et al. identified CRP > 40 mg/L as a risk factor for RMPP (7, 9), while Zhang et al. indicated that CRP ≥ 16.5 mg/L is a risk factor (10). These cut-off values are different from the results of our study. This difference may be related to factors such as bacterial infection in the research subjects, early intervention to inhibit the inflammatory response, and detection timing. In the early phases of RMPP infection, CRP levels may not peak. Therefore, dynamic monitoring of CRP is crucial for the early identification of PB. An ongoing rise in CRP necessitates alert regarding the potential onset of PB and prompt intervention with FB. Additionally, LDH, an enzyme that facilitates the conversion of pyruvate to lactic acid, is released into the serum following cellular damage and is frequently utilized as a key indicator for inflammatory diseases in clinical practice (10). For PB in children with RMPP, an excessive pulmonary inflammatory response increases cell membrane permeability, leading to augmented release of intracellular LDH into the bloodstream (15). Some recent study found elevated LDH levels as critical predictors of RMPP occurrence (11–13), and our study further found that increased LDH is also an independent risk factor for PB in children with RMPP. In addition, the increase in LDH activity is related to the severity of pulmonary inflammation, and LDH can be used as a marker for glucocorticoid therapy in RMPP (8), and high LDH levels often indicate poor response to glucocorticoid therapy in RMPP children (16).

Imaging features provide an important basis for clinical judgment of pulmonary conditions and complications in RMPP children. Chest imaging findings in RMPP children often show inflammatory infiltration, atelectasis, pleural effusion, and may progress to bronchiolitis obliterans (17). Our findings showed that pleural effusion is an independent risk factor for PB in RMPP children, aligning with results from various studies (18, 19). The reasons why RMPP complicated with PB is prone to pleural effusion may be as follows: RMPP children have severe systemic inflammatory responses, and cytokine storms promote neutrophil infiltration, aggravating the pleural reaction and leading to significant exudation and pleural effusion. In children in the PB group, airway obstruction due to mucus plugging results in more intense pleural responses, increasing the likelihood of pleural effusion (20).

We established a nomogram prediction model based on three indicators, namely CRP > 20 mg/L, pleural effusion, and elevated LDH. This model demonstrated an AUC ROC of 0.783 (95% CI 0.71–0.86), indicating strong reliability. Zhang et al. constructed a nomogram model based on 5 risk factors (persistent fever before FB, extra-pulmonary complications, pleural effusion, duration of cough, and LDH level) for early identification of PB in RMPP children (21). Shen et al.'s study showed that the RMPP nomogram prediction model constructed by fever duration exceeding 10.5 days, pleural effusion, white blood cells > 10.13 × 10⁹/L, neutrophil count > 6.43 × 10⁹/L, CRP > 29.45 mg/L, LDH > 370.50 U/L, neutrophil-to-lymphocyte ratio > 3.47, and serum uric acid < 170.5 μmol/mL has good predictive performance (16). The above studies all indicate that inflammatory factors (CRP, LDH) combined with imaging examinations (pleural effusion) can effectively predict early identification of PB caused by RMPP.

This study did not investigate the optimal timing of bronchoscopic intervention. Previous studies have indicated that bronchoscopy in children with PB should be performed earlier than in those without PB, particularly within 4–10 days of disease onset, to achieve satisfactory clinical outcomes (22). Furthermore, evidence suggests that even earlier intervention (e.g., within 12 h of admission) may reduce the risk of dyspnea in children with PB caused by Mycoplasma pneumoniae infection (23). In our study, the PB group exhibited elevated inflammatory markers—CRP >20 mg/L, pleural effusion, and increased LDH levels—indicating a pronounced systemic inflammatory response. Although no significant difference was observed in the incidence of secondary fiberoptic bronchoscopy (FB) between the PB and non-PB groups, previous studies have demonstrated that cast removal via bronchoscopy rapidly alleviates respiratory obstruction and inflammation, potentially reducing the need for repeat FB (24). The lack of a significant difference in our study may be attributable to the limited sample size. Notably, substantial heterogeneity exists across studies regarding the indications and timing of bronchoscopic intervention, which may be influenced not only by variations in disease progression and clinical characteristics but also by clinicians’ awareness and experience with PB.The optimal clinical threshold for recommending bronchoscopy warrants further investigation.

This study has several limitations: (1) it is a retrospective analysis conducted at two centers, and (2) the sample size is limited, lacking prospective cohorts to validate the nomogram model. And the reliability of the predictive indicators warrants further validation through larger, multi-center, prospective studies.

The incidence of PB in children with RMPP is 25.4%. We established a nomogram prediction model based on three indicators, namely CRP > 20 mg/L, pleural effusion, and elevated LDH. This nomogram may facilitate early screening of high-risk children in clinical practice, potentially reducing adverse outcomes.