Influenza A virus is among the important viral pathogens that cause respiratory tract infections among children. Moreover, atelectasis caused by influenza A is clinically common. Influenza A is highly prevalent during winter and spring with children being at high risk. Atelectasis caused by influenza A has similar epidemiological characteristics to those of influenza A. We observed a 68.35% (54/79) incidence rate of atelectasis caused by influenza during winter (December to February) in our hospital between 2017 and 2019; moreover, 88.61% (70/79) of the confirmed cases were aged < 6 years. This is consistent with previous epidemiological studies on pediatric influenza in China and other countries [2, 3]. Young children are at a high risk of influenza A and subsequent atelectasis, which could be attributed to the immature immune function, decreased anti-infection ability, and insufficient ability of the body to inhibit post-infection virus replication. Our findings indicated that the incidence of atelectasis caused by influenza A was higher in males than in females (with a male-to-female ratio of 1.94:1). However, this study has a relatively small sample size; moreover, related previous studies in China and other countries lacked a large sample size. Therefore, the exact gender characteristics of atelectasis caused by influenza A remain unclear.
Atelectasis is characterized by absent or reduced lung gas volume resulting from various causes, which is accompanied by collapsed lung tissue and reduced lung volume. Infections are an important cause of pediatric atelectasis. After a child is infected with influenza A virus, a strong inflammatory response could cause accumulation and release of many inflammatory cells, sputum congestion, reduced airway mucociliary clearance ability, and other pathophysiological changes, leading to atelectasis. The clinical atelectasis symptoms caused by influenza A range in severity. They are mostly characterized by acute onset with similar typical symptoms as to those of atelectasis caused by infections with other pathogens [4, 5]. Fever and cough with expectoration of different degrees are the main manifestations with fever being the initial symptom in most cases. Children with persistent hyperpyrexia could present with complicated febrile convulsion. Laboratory examinations may present with increased D-dimer, FDP, creatine kinase isoenzyme, and transaminase levels, as well as electrolyte disturbance. Notably, the proportion of patients with maximum temperature > 40℃ was high (65.82%) with the longest duration being 12 days. Therefore, persistent hyperpyrexia could be an important indicator of pediatric influenza A progressing to atelectasis. Prolonged hyperpyrexia indicates ineffectively controlled inflammation, which causes congestion, edema, necrosis, and shedding of the bronchial mucosa, as well as lumen blocking and compression, which results in atelectasis.
We found that 42 (53.16%) cases with atelectasis caused by influenza A that presented with mixed infections. The main pathogens include Mycoplasma pneumoniae, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, etc. A prospective observational study on influenza virus by Casalino et al.  reported that only 5.6% and 28.6% of influenza-negative and influenza-positive patients, respectively, had complicated bacterial infections. This indicates a similar incidence as that observed in this study. Influenza A virus can destroy host epithelial cells, which reduces the host’s resistance to external pathogens and contributes toward secondary mixed infections. Influenza virus has been shown to remove sialic acid residues of glycoproteins on the surface of the host cell membrane through neuraminidase. This exposes receptors that bind bacteria bind to cells, which facilitates bacterial colonization and subsequent infections . Wu et al.  reported that influenza A virus significantly reduced the response-ability of host macrophages and neutrophils to Streptococcus pneumoniae, as well as the levels of influenza virus-specific antibody. This results in an increased probability of mixed infections among patients with influenza A. There is currently no definite conclusion regarding the pathogen most likely to cause concurrent infection with influenza. Although we observed a high mixed infection rate in atelectasis caused by influenza A, there were different proportions of patients infected with Mycoplasma pneumoniae and different bacteria (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis). Therefore, we could not determine the pathogen most likely to cause complicated infections. Moreover, we employed a limited sample size; therefore, there is a need for future studies with larger studies to perform more detailed assessments.
Regarding influenza A treatment, various guidelines in China and other countries have indicated that antiviral treatment application at the early disease stage (within 48 hours of onset) could reduce influenza complications, minimize mortality, and shorten hospital stay [1, 9]. It remains difficult to clinically diagnose influenza within 48 hours. We found that most pediatric patients with atelectasis caused by influenza A did not have an early-stage diagnosis. However, a majority of the patients showed relatively good responses to treatment with neuraminidase inhibitors oseltamivir or peramivir at 48 hours after disease onset. For those who did not, glucocorticoid and/or gamma globulin treatment had a good response. During the follow-up period, two pediatric patients presented recurrent respiratory tract infections and post-activity shortness of breath; further, mosaic perfusion images were observed on lung CT. Occlusive bronchiolitis should be carefully considered and doctors should pay attention to the long-term complications of influenza virus infection.
The effect and status of bronchoscopic lavage in the treatment of infectious atelectasis remain unclear in China and other countries. Previous studies have suggested that infection-induced atelectasis could subside spontaneously after anti-infective treatment and that bronchoscopic treatment could be excessive . We believe that the advantages of bronchoscopy outweigh its disadvantages. Bronchoscopic alveolar lavage removes pathogens adhered to the airway surface by inflammatory media, effectively reduces direct and indirect pathogen-induced damages to bronchial mucosa, improves lung expansion ability, facilitates lung inflation and pulmonary circulation restructuring, effectively improves clinical pediatric atelectasis symptoms, shortens the disease course, and reduces complications. Among our included patients, 57 were treated with bronchoscopy, which showed sufficient efficacy in all of them. Bronchoscopic examination can also be used for differential diagnosis and identifying other complications. In our study, bronchoscopy revealed significant mucus plug blockage in 6 pediatric patients; among them, 2 underwent bronchial cast removal through the bronchoscope. This blockage could be attributed to increased airway mucus secretion and decreased clearance ability after cilia damage caused by post-infection continuous inflammatory stimulation. Pulmonary atelectasis complicated by mucus plugs or bronchial casts is a serious complication of influenza A virus infection. In these cases, tracheoscopy is indicated and bronchial cast removal via bronchoscopy is the most direct and effective diagnosis and treatment method [11, 12].