Predictive factors and outcomes of children with necrotising pneumonia

Necrotizing pneumonia (NP) is rare (3.2%) complication of community acquired pneumonia (CAP) in children. It is defined as the development of necrosis and liquefaction of the consolidated lung parenchyma due to infectious pathogens, resulting in the formation of multiple thin-walled cysts or cavities. It was first reported in an adult in 1940 and only reported in children 54 years later (1994). The underlying mechanisms are poorly understood, with postulated interactions of host susceptibility, virulence of bacterial pathogens and viral-bacterial co-infection. The lung necrosis is caused by direct effect of the pathogen or toxins causing an exaggerated cytokine-mediated inflammatory response and secondary vascular changes (vasculitis and intravascular thrombosis). Streptococcus pneumoniae and Staphylococcus aureus are the main pathogens causing NP, though a proportion of NP caused by Mycoplasma Pneumoniae is rising in recent years. 
NP can present with highly variable clinical course, the majority of children demonstrate severe disease with high, prolonged fever, dyspnoea, and clinical and radiological signs of extensive consolidation of lung parenchyma. The clinical diagnosis is mainly based on imaging examinations and Chest CT is considered as the gold standard for diagnosing NP. However, waiting time for CT may be long. It has been reported that the average time for finding NP via CT is 17 days, which may lead to delayed diagnosis and missed optimal treatment time. However, a typical appearance of NP seen in the chest radiograph, initial chest CT scan is not always necessary.

 

The predictive factors for necrotizing pneumonia include duration of fever, hospital stay, CRP, PCT, and D-dimer. The ROC curves for fever duration, CRP, PCT, and D-dimer were plotted and found to have diagnostic value for predicting the occurrence of NP when fever duration >11.5 d, CRP >48.35 mg/L, and D-dimer > 4.25 mg/L [area under ROC curve (AUC)=0.909, 0.836, and 0.747, all P < 0.001] (J Qian et al, 2022). Honghan et al (2023) found that bacterial co-infection, chest pain, LDH, CRP, duration of fever, and D-dimer were the influencing factors for NP. Persistent fever is related to excessive inflammatory reaction, the higher the CRP, the more serious the condition. LDH is a biomarker of tissue injury. The level of D-dimer > 1367.5ng/mL is an independent risk factor for NP and D-dimer is a marker of inflammation and a specific marker of the fibrinolytic system, and its high level implies a hypercoagulable state. In this hypercoagulable state, the lungs are prone to thrombus and vascular occlusion, which affect the blood supply and further develop into NP. Hacimustafaoglu et al. 2004). Li et al. (2011) have reviewed the factors associated with increased risk of fatal outcome in patients with community-acquired NP caused by Staphylococcus aureus and found that influenza-like symptoms, hemoptysis, and leucopenia are the predictors of unfavorable prognosis.

 

NP has high local complications during acute phase of illness. NP is complicated by parapneumonic effusion (PPE)/empyema in high proportion of children (63-97%). Some developed bronchopleural fistula (BPF), pneumothorax, septicaemia, and respiratory failure. In patients with necrotizing pneumonia, 46.6% required chest tubes, 6.1% underwent video-assisted thoracoscopic surgery, and 27.6% were mechanically ventilated. Pneumothorax was identified in 16.7% and pyothorax in 27.4%. The overall mortality rate was 4.1%. Despite prolonged hospitalisation (median 13–27 days) and fever (median 9–16 days), most patients recover completely with low mortality rate. By 6 months of follow-up, almost all chest Xrays become normalized. The long-term outcomes of paediatric NP are good. Long-term impairment of pulmonary function is rare, even in children with severe complications (air leak or empyema).