Kartagener’s syndrome, or visceral inversion-sinusitis-bronchodilatation syndrome, also known as familial bronchodilatation, is a congenital autosomal recessive disorder that accounts for 6% to 9% of all visceral translocations (1/8000) and 0.5% of bronchodilatation (0.3% to 0.5%). In 1904, Siewart first reported a case of bronchiectasis with visceral transposition, and in 1933, Kartagener’s reported four cases with the triad of total visceral transposition, bronchiectasis, and paranasal sinusitis, hence the name. 1976 In 1981, Sleigh et al. found that the cilia were not completely immobile, but had abnormal movements, resulting in ineffective discharge of secretions causing bronchial dilation, so they called this congenital disorder primary cilia motility disorder or cilia motility random syndrome. Kartagener’s syndrome is a subtype of PCD, and when PCD is accompanied by visceral ectasia, it is called Kartagener’s syndrome. Kartagener’s syndrome has a familial tendency and can occur in the same or alternate generations, with a history of consanguineous marriage between the parents. However, no familial manifestations were found in this case. Due to the impaired activity of the ciliated epithelium of the respiratory tract, mucus cilia transport function is reduced and secretions cannot be discharged, causing recurrent long-term chronic infections, which form the pathological basis of bronchiectasis and paranasal sinusitis. Cilia are widely present in the respiratory tract, middle ear, fallopian tubes, sperm flagella, and in tissues and organs such as the brain and spinal ventricles. Kartagener syndrome can be accompanied by pneumonia, conductive deafness, ectopic pregnancy, infertility, and hydrocephalus. The disease often has its first onset in childhood, but is easily misdiagnosed. The main clinical manifestations are: recurrent cough, sputum, hemoptysis, nasal congestion, runny nose, dizziness, headache, etc. A few patients are seen for infertility. Kartagener’s syndrome with rheumatoid arthritis has been reported. Kartagener syndrome is now used in patients with PCD presenting with concomitant organ transposition. the diagnosis of PCD relies on typical clinical presentation and mucosal biopsy for cilia, radioaerosol inhalation lung scan, saccharin test, and cilia oscillation frequency measurement. Bush A et al. suggested that patients with the following clinical conditions need to be evaluated for PCD: (1) newborns with chronic rhinitis or full-term newborns with unexplained respiratory distress; (2) children with persistent cough and sputum, especially with a history of rhinitis and nasal congestion; (3) visceral transposition; (4) placement of middle ear drainage tubes without relief of ear leakage; (5) children with unexplained bronchiectasis; (6) children with diagnosed (6) children with unknown lung disease that is poorly treated with asthma medication; (7) children who have received multiple courses of medication for lung infections. The diagnosis can be confirmed by taking a nasal mucosal biopsy or bronchoscopy to remove the bronchial mucosal epithelium to observe the number of cilia and structural abnormalities under electron microscopy. Since exhaled NO values are much lower in patients with PCD than in normal or asthmatic subjects, the NO exhalation test can be used as a screening tool for PCD. The possibility of PCD should be considered in patients with early recurrent respiratory diseases of unknown origin, such as bronchiectasis and otitis media, and the possibility of Kartagener syndrome should be considered in patients with bronchiectasis with visceral translocation. In addition bronchiectasis is congenitally rare and is due to congenital bronchial dysplasia, the presence of congenital defects or genetic disorders that prevent further development of the periphery of the lung, resulting in dilated developed bronchi, such as bronchial chondrodysplasia (Williams-Camplen syndrome). bronchiectasis in Kartagener syndrome occurs after birth, but congenital anomalies also The presence of a congenital anomaly. Bronchiectasis is also seen in Young syndrome, which is characterized by obstructive sperm deficiency, normal but inactive sperm production, chronic sinusitis, recurrent pulmonary infections and bronchiectasis. The diagnosis of Kartagener syndrome is further supported by the presence of visceral transposition in addition to paranasal sinusitis and bronchiectasis in this patient. Imaging examination: It is an important basis for clinical diagnosis of Kartagener syndrome. Chest X-ray, CT scan, and ultrasound examination all reveal visceral transposition. Treatment: Similar to other causes of bronchiectasis, H. influenzae, Pneumococcus, and Staphylococcus aureus are the common infectious flora and can be treated with sensitive antibiotics and other symptomatic management. For recurrent infections of the upper and lower respiratory tracts resulting in bronchiectasis, although successful surgical treatment has been reported, the choice of whether to perform surgery should be made carefully. During periods of non-acute respiratory tract infection, acute exacerbations should be prevented. Immunomodulators and vaccination with influenza and/or pneumococcal vaccines may be used to boost resistance and help reduce respiratory infections. Principles of treatment of sinusitis in Kartagener’s syndrome: conservative treatment includes the selection of sensitive antibiotics for treatment during acute exacerbation of sinus and lung disease, based on the results of secretion culture to identify the causative organism; intranasal glucocorticoids are available for those with nasal polyps; antihistamines can be used for those with allergic rhinitis; local saline, antibiotics (aminoglycosides) or antiseptics can be used for intranasal irrigation. When conventional conservative treatment is ineffective, especially when the culture of nasal secretions indicates the presence of drug-resistant bacteria or characteristic pathological changes, or when nasal polyps are present, surgical treatment is required. Surgical principles: Based on the removal of irreversible lesions, the morphology and physiological functions of the nasal and sinus mucosa are improved by reconstructing the nasal cavity and sinus ventilation and drainage pathways. At present, with the further understanding of the disease and the continuous development of nasal endoscopic surgery, more aggressive surgical treatment is advocated for the nasal-sinus disease of Kartagener syndrome. Effective treatment of it may mitigate the progression of bronchial and pulmonary disease.