Clinical characteristics and risk factors for plastic bronchitis in children with severe Mycoplasma pneumoniae pneumonia: a retrospective observational study

doi:10.21203/rs.3.rs-3560651/v1

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Clinical characteristics and risk factors for plastic bronchitis in children with severe Mycoplasma pneumoniae pneumonia: a retrospective observational study

https://doi.org/10.21203/rs.3.rs-3560651/v1

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Background: Plastic bronchitis (PB) is a rare, underdiagnosed and potentially fatal condition that should not be overlooked in children, particularly in children with severe Mycoplasma pneumoniae pneumonia (SMPP). Therefore, we explored the risk factors for PB in children with SMPP and the diagnostic value for PB.

Methods: We retrospectively evaluated children with a clinical diagnosis of SMMP who were treated with bronchoscopy at Tianjin Children's Hospital from January 1, 2017, to December 31, 2021. According to the bronchoscopy and pathological examination results, the patients were divided into the PB group and the non-PB group. The clinical manifestations, laboratory data, imaging findings and treatments were analysed.

Results: Data from a total of 306 children with SMMP, including 109 children in the PB group and 197 children in the non-PB group, were reviewed. Procalcitonin (PCT), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), interleukin-6 (IL-6) and bronchial lavage fluid MP-DNA copy number levels were higher (P<0.05) while platelet (PLT) levels were lower (P<0.05) in the PB group. In addition, the incidence of pleural effusion, atelectasis, wheezing symptoms and hypoxemia in the PB group was significantly higher than that in the non-PB group (P<0.05). Multivariate logistic regression analysis showed that pleural effusion (odds ratio [OR], 3.148; 95% confidence interval [CI], 1.795-5.521; P<0.001), PLT (OR, 0.584; 95% CI, 0.439-0.776; P<0.001), and LDH (OR, 5.265; 95% CI, 1.488-18.630; P=0.011) were independent predictors of PB in children with SMPP. Receiver operating characteristic (ROC) curve analysis showed that the cut-off values for PLT and LDH in the diagnosis of PB were 242*10⁹/L [sensitivity 57.80%; specificity 69.04%; area under the curve (AUC) 0.648; P<0.001] and 542 U/L (sensitivity 58.72%; specificity 64.97%; AUC 0.646, P<0.001), respectively. Children in the PB group had longer hospital stays and corticosteroid use durations than those in the non-PB group (P<0.05).

Conclusions: The PLT level (≤242*109/L), LDH level (>542 U/L) and pleural effusion were risk factors for PB in children with SMPP. This provides a basis for the early identification of PB in children with SMPP.

Health sciences/Medical research

Health sciences/Risk factors

Severe Mycoplasma pneumoniae pneumonia (SMPP)

plastic bronchitis (PB)

children

risk factors

Plastic bronchitis (PB) is a rare disease that affects patients of all ages and is characterized by the formation of casts in the tracheobronchial tree, which can cause bronchial blockage and lead to ventilation dysfunction in the lungs. If the obstruction is not identified and eliminated in a timely manner, the disease can aggravate progressively and can even be life-threatening in severe cases. Owing to the lack of specific clinical and imaging features, false judgement and leakage judgement can easily occur. Mycoplasma pneumoniae is common pathogens in Community-acquired pneumonia (CAP). Mycoplasma pneumoniae is responsible for 7-20% of pediatric CAP ^[¹^], and can cause severe pneumonia ^[²^].Many cases of pneumonia in children infected with Mycoplasma pneumoniae are associated with varying degrees of intratracheobronchial mucus plug formation, particularly in patients with severe Mycoplasma pneumoniae pneumonia (SMPP)^[³^]. Therefore, we aimed to add to the few existing studies and improve the understanding of PB among paediatricians in order to improve the early diagnosis and timely treatment of this condition; thus, in this study, we analysed the clinical, laboratory, and radiological characteristics and treatments of PB in children with SMPP. Furthermore, we explored the disease-related risk factors for PB in children with SMPP and the diagnostic value for PB.

Study design

This was a single-centre retrospective observational study. The clinical data of 306 children with a clinical diagnosis of SMMP who were treated at Tianjin Children's Hospital (Tianjin, China) between January 2017 and December 2021 were analysed. For children with repeated hospitalizations, each hospitalization was recorded as an event. The patients were divided into the PB group (mucous plug group) and the non-PB group (control group) according to whether there was a plastic shape observed under the bronchoscope. The inclusion criteria were as follows: age ranging from 2 months to 16 years and underwent bronchoscopy examination. Evidence of M. pneumoniae infection was as follows: serum M. pneumoniae-IgM≥1:160, or seroconversion (increased antibody titers (≥4 folds), or M. pneumoniae-DNA positive on real-time polymerase chain reaction using a sputum sample or the bronchoalveolar lavage fluid(BALF) sample. Severe pneumonia that is defined as pneumonia with one of the followings: poor general condition, increased respiratory rate(infant>70/min, older children>50/min), dyspnea, cyanosis, multilobe involvement or > 2/3 lung involvement, extrapulmonary complication, pleural effusion, transcutaneous oxygen saturation in room air <92% ^[⁴^]. The diagnostic criteria of PB were as follows: plastic foreign body removed by bronchoscopy and diagnosis confirmed by pathology. Patients with chronic lung disease, previous recurrent respiratory tract infections, bronchopulmonary dysplasia, severe blood system disease, immune deficiency or other immune-associated diseases and patients with incomplete case information were excluded.

Demographic, clinical, laboratory, and radiological characteristics as well as treatments were collected and recorded. Laboratory tests were completed within 24 hours after the children were admitted to the hospital. The clinical data of patients in the PB group and the non-PB group were collected and mainly included the following: (1) demographic information: name, sex, and age; (2) clinical characteristics: hot peak, heat duration, wheezing, and hypoxemia; (3) laboratory tests: routine blood tests, inflammatory markers, blood biochemistry, immune indices, cytokines and so on; (4) radiological examination: atelectasis and pleural effusion; and (5) treatment: corticosteroid time and length of hospitalization.

Statistical analysis

SPSS 22.0 statistical software was used for the descriptive analysis of the data. The classification data are presented as percentages (%), and continuous data with a normal distribution are presented as the means ± standard deviations; otherwise, they are presented as median (minimum, maximum). The chi-square test was used for categorical data, and the t test and Mann‒Whitney U test were used for continuous data. The factors with significant differences were included in multivariate logistic regression analysis to examine the risk factors for PB in children with SMPP. The ROC curve was used to calculate the diagnostic value of each risk factor. P<0.05 was considered statistically significant.

Ethical statement

The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013) and was approved by the Ethical Committee of Tianjin Children's Hospital. The requirement for individual consent was waived due to the retrospective nature of this study.

Demographic and clinical characteristics

Data from a total of 306 children with SMMP, including 109 children (male 54 and female 55) with PB (PB group) and 197 children (male 94 and female 103) without PB (non-PB group), were reviewed in this study. The median age was 6 (5, 8) years in the PB group and 6 (5, 8) years in the non-PB group. There were no significant differences in the two indices between the two groups (all P>0.05). (Table 1)

The prevalence of wheezing and hypoxemia in the PB group and the non-PB group was 9.2% (10 of 109) vs. 5.6% (11 of 197) and 8.3% (9 of 109) vs. 5.1% (10 of 197), respectively. The differences were statistically significant (P <0.05). However, the hot peak and heat duration of the PB group and the non-PB group patients were 40.0 (39.6, 40.3) °C vs. 40.0 (39.4, 40.2) °C and 10.5 (9, 12) days vs. 10 (8, 13) days, respectively, with no significant difference (P >0.05). (Table 1)

Table 1 Demographic and clinical characteristics of patients with the PB group and the non-PB group (N=306)

Laboratory characteristics

The children in the PB group showed significantly higher PCT, LDH, AST, IL-6 and bronchial lavage fluid MP-DNA copy number levels than those in the non-PB group [PCT: 0.24 (0.13, 0.51)×10⁹/L vs. 0.160 (0.09, 0.33)×10⁹/L, P=0.001; LDH: 581.00 (433.50, 822.00) U/L vs. 469.00 (369.50, 623.50) U/L, P=0.00; AST: 40.00 (29.00, 60.00) U/L vs. 35.00 (25.00, 47.50) U/L, P=0.017; IL-6:47.87 (27.73, 94.08) pg/mL vs. 35.52 (21.87, 66.74) pg/mL, P=0.009; MP-DNA: 83.00 (21.00, 210.00) ×10⁵/mL vs. 25.00 (4.40, 98.50) ×10⁵/mL, P=0.00], while the PLT level was lower [235.00 (184.00, 293.50)×10⁹/L vs 274.00 (219.50, 367.00)×10⁹/L] (Table 2).

In addition, there were no significant differences in WBC count, NEUT, CRP, ALT, CK, CK-MB, FER, ESR, D-D, IgA and PA levels between the two groups (all P>0.05). (Table 2)

Table 2 Laboratory characteristics of patients with the PB group and the non-PB group (N=306)

Radiological characteristics

The prevalence of atelectasis and pleural effusion in the PB group and the non-PB group was 45.9% (50 of 109) vs. 39.6% (78 of 197) and 71.6% (78 of 109) vs. 42.1% (83 of 197), respectively, and the difference was statistically significant (P <0.05). (Table 3)

Table 3 Radiological characteristics and treatments of patients with the PB group and the non-PB group (N=306)

Treatments and prognosis

The children in the PB group had a longer duration of corticosteroid use than those in the non-PB group ([8 (6, 10) days vs. 6 (5, 7) days, P <0.05]. After the treatment, all the patients were cured and discharged. There were no severe complications or deaths in either group. However, the children in the PB group were hospitalized for a median of 10 (8,12) days, while children in the non-PB group were hospitalized for a median of 8 (7,10) days. Longer hospital stays were observed in the PB group (P<0.01). (Table 3)

Risk factors and diagnostic value analysis

As shown in Figure 1, by multivariate logistic regression analysis, the following factors were identified as potential risk factors for PB in children with severe Mycoplasma pneumoniae pneumonia: pleural effusion with an OR (95% CI) of 3.148 (1.795, 5.521), P<0.001; PLT with an OR (95% CI) of 0.584 (0.439, 0.776), P <0.001; and LDH with an OR (95% CI) of 5.265 (1.488, 18.630), P =0.014.

Figure 1. Logistic regression analysis of risk factors related to PB in children with SMPP

The diagnostic value to predict PB was further analysed by ROC curve analysis. Of the evaluated parameters, the sensitivity and specificity of PLT and LDH for the prognostic evaluation of PB were stronger. Specifically, the sensitivity of PLT for the diagnosis of PB was 57.80%, its specificity was 69.04%, its AUC was 0.648 (P<0.001), and the cut-off value was 242*10⁹/L. Similarly, the sensitivity of LDH was 58.72%, its specificity was 64.97%, its AUC was 0.646 (P<0.001), and the cut-off value was 542 U/L. The results showed that PLT ≤242*10⁹/L, LDH >542 U/L and pleural effusion were independent risk factors for PB in children with SMPP (Figure 2 and Table 4).

Figure 2. ROC curve analysis of PLT and LDH, which predicts the sensitivity and specificity of PB in children with SMPP. Vertical axis: sensitivity; horizontal axis: specificity.

Table 4. Diagnostic efficacy indicators of each index in the PB group and non-PB group

In this study, we evaluated the differences in clinical resentation, radiographic features, and biomarkers between PB group and the non-PB group. Then, a logistic regression model was used to select variables for prediction. It is especially suitable for areas where bronchoscopy is difficult to carry out, such as primary care hospitals and resource-limited countries. PB has different clinical symptoms and a potential risk of death. Its onset is lacks clear symptoms, and its diagnosis is mainly based on bronchoscopy and pathological examination of plastic foreign bodies. However, based on the limitation of bronchoscopy and the lack of a specific index for early diagnosis, it is necessary to explore indicators that are easier to detect and more sensitive. Many studies have focused on children with PB caused by MPP. However, for patients with severe cases, there are still fewer related studies. This research used SMPP as the study object and explored the risk factors for tracheobronchial mucus plug formation in children with SMPP and the diagnostic value for PB.

Our study showed that there were no significant differences between the two groups in terms of gender, age, hot peak, hot duration, WBC, NEUT, CRP, ALT, CK, CK-MB, FER, ESR, D-D, IgA and PA. This indicates that it is difficult to distinguish the presence of PB. Therefore, further research is needed.

The common diseases of childhood PB are lower respiratory tract infection, bronchial asthma, respiratory allergic diseases and cyanotic congenital heart disease ^[⁵^,⁶^]. Cai et al ^[⁷^] found that MP is the first pathogenic bacterium detected in children with PB after pneumonia, suggesting that MP infection is the primary pathogenic bacterium that causes PB. The mechanisms underlying PB caused by Mycoplasma pneumoniae (MP) infection may be related to the following factors: pseudostratified columnar ciliated epithelia, resulting in ciliary destruction and reduced wobble^[⁸^] ; inflammatory damage to the respiratory tract mucosa^[⁹^] and increased bronchi secretions^[¹⁰^]. In recent years, as the number of patients with SMPP has significantly increased, an increasing number of clinical reports of secondary PB have been published. Inflammatory stimulation caused tracheal mucosa injury, necrosis, increased mucus secretion, and accelerated the formation of plastic objects. The research results showed that the bronchial lavage fluid MP-DNA copy number levels were higher in the PB group than in the non-PB group. This indicates that MP infection is related to PB in children with SMPP.

In this study, biomarkers such as CRP and WBC were not useful for judging the PB group and the non-PB group. Inflammatory markers are often considered as parameters of predictive models of lung infection and sepsis ^[¹¹^]. Multiple cytokines stimulated by SMPP can be used as indicators to predict the disease of children ^[¹²^]. During the period of MP infection in children, the host immune system also activates many inflammatory cytokines. In this study, a large number of cytokines were elevated in both the PB group and the non-PB group. Our findings suggested that the PB group had higher PCT, IL-6, AST and LDH levels than the non-PB group. The high expression of biomarkers indicated that PB group produced a stronger inflammatory response which might affect the lungs and liver and cause complications such as lung injury and hepatic injury. LDH is a cytoplasmic enzyme in many organs. Increased LDH is related to inflammation and cellular hypoxia.An increased LDH level can reflect the degree of tissue damage or inflammation, and can be used as a biomarker to predict refractory MPP^[¹³^]. Zhong et al.^[¹⁴^]showed that LDH >482 U/L was an independent risk factor for PB in children with MPP. This is similar to the results of our research. Through this study, we found that LDH >542 U/L was a risk factor for PB in children with SMPP. In treating SMPP, the use of glucocorticoids can significantly reduce the concentration of LDH in plasma, suggesting that LDH can be used as an indicator for glucocorticoid therapy initiation in SMPP. Selected indicators can also be used to measure the effectiveness of treatment^[¹⁵^].

The changing levels of PLT after infection with MP are still under debate. Yang et al.^[¹⁶^]noted that PLT in patients with SMPP in the acute stage was lower than that in the control group. Jia et al.^[¹⁷^] conducted a meta-analysis of 57 studies and found that patients with severe COVID-19 are more likely to experience thrombocytopenia. Therefore, PLT can be used as a monitoring indicator for clinical practice. Our study showed that the PLT was lower in the PB group than in the non-PB group. Our study found that the decrease in PLT levels may be related to PB and that PLT≤242*10⁹/L was a risk factor for tracheobronchial mucus plug formation in children with SMPP. The lung is a major site of platelet production, and large numbers of megakaryocytes circulate through the lungs, where they dynamically release platelets. The present study showed that the contribution of the lungs to platelet biogenesis is substantial, accounting for approximately 50% of total platelet production^[1⁸^]. Therefore, we hypothesize that the reason for thrombocytopenia in the PB group was decreased platelet production.

Lobar pneumonia and even consolidation could be found in SMPP. In addition, more than half of children had multilobar infiltration, bilateral pneumonia, consolidation, pleural effusion, and atelectasis in SMPP. Consolidation could be caused by non-cellular infiltrate, such as edema or hemorrhage. They can also be caused by exudate and neutrophil infiltration wihin bronchiolar and alveolar lumens ^[¹⁹^].For the incidence of pleural effusion, atelectasis, wheezing symptoms and hypoxemia, there were significant differences between the PB group and the non-PB group. In this study, SMPP with BP had higher proportion of pleural effusion than SMPP. Further analysis indicated that pleural effusion was an independent predictor for PB in children with SMPP. Therefore, for children with SMPP, when pleural effusion occurs, we need to note whether PB is complicated.

Systemic glucocorticoid treatment is often used in MPP with acute onset, rapid progression, or severe disease, especially SMPP^[²⁰^]. Glucocorticoids are the most widely used immunosuppressive and adjunctive anti-inflammatory drugs and are the most extensively used adjunctive therapy in SMPP^[^21,22^]. Corticosteroid treatment is an important method for treatment of SMPP, and it has been reported to be well tolerated and efficacious in diminishing cell-mediated immune responses and therefore reducing immune-mediated pulmonary injury^[²³^].The initiation, dose, and duration of glucocorticoid treatment have been widely discussed among experts around the world. However, appropriate methods and optimal dosage of glucocorticoids have not been fully clarified^[²⁴^]. Miyashita et al. found that IL-18 and LDH may be important reference indicators for determining the use of glucocorticoids in SMPP, as the serum levels of IL-18 and LDH are positively correlated with the severity of SMPP ^[²⁵^].Ruochen Zhu et al. found that the expressions of IL-18 and IFN-γ in the early stage of SMPP might suggest their predictive effect of early application of glucocorticoid for effective treatment of SMPP in young children ^[²⁶^]. Regular doses are defined as methylprednisolone 1-2 mg/kg/day, and short courses are defined as 3-5 days. Methylprednisolone pulse therapy can be used when regular doses and courses of treatment are ineffective ^[^27,28^]. In the present study, children in the PB group had a longer duration of corticosteroid use than those in the non-PB group. Through the use of adjunctive corticosteroids, anti-infection drugs and symptomatic treatments, all patients were cured and discharged, and there were no severe complications or deaths. This indicates that an optimistic prognosis is expected after the prompt and positive treatment of PB caused by SMPP.

On the other hand, it should be noted that bronchoscopy plays a significant role in the diagnosis and treatment of PB. Timely bronchoscopy and alveolar lavage treatment can achieve good therapeutic effects(Figure 3). However, this research is focused on studying the diagnosis of PB in SMPP; research about its treatment is only in the initial stages, and additional elucidation is needed.

Figure 3. Airway Bronchoscopy. The images were captured via flexible bronchoscopy.(A) Complete obstruction of the airway by mucus plugs. (B) Patient airway after complete extraction of the mucus plugs. (C) Cast removed from the airway of a patient.

In summary, PLT level (≤242*10⁹/L), LDH level (>542 U/L) and pleural effusion were risk factors for PB in children with SMPP. Our predictive model used a combination of biomarkers and radiographic features. It may help pediatricians in differentiating BP from SMPP in the early stage. All of these factors need to be considered in clinical diagnosis due to their high sensitivity and ease of detection. This study provides a basis for the early identification of PB in children with SMPP. However, given the broad range of PB aetiologies, there is a dire need for further research to provide references for the diagnosis of PB caused by SMPP and promote their use in clinical practice.

PB: plastic bronchitis; SMPP: severe mycoplasma pneumoniae pneumonia.

Authors’contributions

Conception and design: S Mu, Y Zou; Administrative support: Y Zou; Provision of study materials or patients: Y Guo, J Zhai, B Huang; Collection and assembly of data: Y Guo, J Zhai; Data analysis and interpretation: S Mu; Manuscript writing: all authors; Final approval of manuscript: all authors.

Acknowledgements

Not applicable.

Competing interests

The authors declare they have no actual or potential competing financial interests.

Availability of data and materials

All the data generated or analysed during this study are included in this published article.

Consent for publication

Not Applicable.

Ethics approval and consent to participate

All the procedures in this study involving human participants were performed in accordance with the Declaration of Helsinki (as revised in 2013). This study was approved by the Ethics Committee of Tianjin Children's Hospital. The ethics committee waived the need for written informed consent provided by participants due to the retrospective nature of the study, because all patient data were analyzed anonymously,and no additional informed consent was required.

Funding

This work was supported by the Project of Health and Technology of Tianjin (NO. TJWJ2022QN081).

This work was funded by Tianjin Key Medical Discipline(Specialty) Construction Project(NO. TJYXZDXK-040A).References

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No competing interests reported.

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Clinical characteristics and risk factors for plastic bronchitis in children with severe Mycoplasma pneumoniae pneumonia: a retrospective observational study

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