As with all medical conditions, there may be many causal factors. Further relevant information on causes of Kartagener syndrome may be found in:
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Because of the availability of antibiotics to treat acute respiratory tract infections, the incidence of bronchiectasis has dramatically decreased in the past 20 years. Incidence is highest among Eskimos and the Maoris of New Zealand. It affects people of both sexes and all ages.
The different forms of bronchiectasis may occur separately or simultaneously. In cylindrical bronchiectasis, the bronchi expand unevenly, with little change in diameter, and end suddenly in a squared-off fashion. In varicose bronchiectasis, abnormal, irregular dilation and narrowing of the bronchi give the appearance of varicose veins. In saccular bronchiectasis, many large dilations end in sacs. These sacs balloon into pus-filled cavities as they approach the periphery and are then called saccules. (See Forms of bronchial dilatation, page 560.)
This disease results from conditions associated with repeated damage to bronchial walls and abnormal mucociliary clearance, which cause a breakdown of supporting tissue adjacent to airways. Such conditions include:
❑ cystic fibrosis
❑ immunologic disorders (agammaglobulinemia, for example)
❑ recurrent, inadequately treated bacterial respiratory tract infections, such as tuberculosis, and complications of measles, pneumonia, pertussis, or influenza
❑ obstruction (by a foreign body — most common in children, tumor, or stenosis) in association with recurrent infection
❑ inhalation of corrosive gas or repeated aspiration of gastric juices into the lungs
❑ congenital anomalies (uncommon), such as bronchomalacia, congenital bronchiectasis, immotile cilia syndrome, and Kartagener’s syndrome, a variant of immotile cilia syndrome characterized by situs inversus, bronchiectasis, and either nasal polyps or sinusitis.
In bronchiectasis, hyperplastic squamous epithelium denuded of cilia replaces ulcerated columnar epithelium. Abscess formation involving all layers of the bronchial wall produces inflammatory cells and fibrous tissue, resulting in dilation and narrowing of the airways. Mucus plugs or fibrous tissue obliterates smaller bronchioles, whereas peribronchial lymphoid tissue becomes hyperplastic. Extensive vascular proliferation of bronchial circulation occurs and produces frequent hemoptysis.
Source: Professional Guide to Diseases (Eighth Edition), 2005
This disorder is characterized by unilateral, intermittent spasms of muscles of the face, eye, and mouth. The patient may have some voluntary control over the spasms. Typically, the spasms are aggravated by emotional upset and disappear during sleep. Spasms may interfere with swallowing and speech.
Rarely, these drugs cause orofacial dyskinesia.
These drugs may cause orofacial dyskinesia and other extrapyramidal effects. Movements are sustained, involving the eyes, mouth, face, and neck; they occur with prolonged treatment, especially after it has been reduced. Lip retraction and dysphagia are common.
Among the phenothiazines, the piperazine derivatives (perphenazine, prochlorperazine, fluphenazine, and trifluoperazine) most commonly cause this sign. Aliphatic phenothiazines (chlorpromazine) occasionally cause it. Piperidine phenothiazines (thioridazine and thiethylperazine) rarely cause orofacial dyskinesia. Other antipsychotic drugs (haloperidol, thiothixene, and loxapine) commonly cause this sign.
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
The different forms of bronchiectasis may occur separately or simultaneously. In cylindrical bronchiectasis, the bronchi expand unevenly, with little change in diameter, and end suddenly in a squared-off fashion. In varicose bronchiectasis, abnormal, irregular dilation and narrowing of the bronchi give the appearance of varicose veins. In saccular bronchiectasis, many large dilations end in sacs.
This disease results from conditions associated with repeated damage to bronchial walls and abnormal mucociliary clearance, which cause a breakdown of supporting tissue adjacent to airways. Such conditions include:
❑ mucoviscidosis (cystic fibrosis)
❑ immunologic disorders (agammaglobulinemia, for example)
❑ recurrent, inadequately treated bacterial respiratory tract infections, such as tuberculosis, and complications of measles, pneumonia, pertussis, or influenza
❑ obstruction (by a foreign body, tumor, or stenosis) in association with recurrent infection
❑ inhalation of corrosive gas or repeated aspiration of gastric juices into the lungs
❑ congenital anomalies (uncommon), such as bronchomalacia, congenital bronchiectasis, immotile cilia syndrome, and Kartagener’s syndrome, a variant of immotile cilia syndrome characterized by situs inversus viscerum, bronchiectasis, and either nasal polyps or sinusitis.
With bronchiectasis, hyperplastic squamous epithelium denuded of cilia replaces ulcerated columnar epithelium. Abscess formation involving all layers of the bronchial wall produces inflammatory cells and fibrous tissue, resulting in dilation and narrowing of the airways. Mucus or fibrous tissue obliterates smaller bronchioles, and peribronchial lymphoid tissue becomes hyperplastic. Extensive vascular proliferation of bronchial circulation occurs and produces frequent hemoptysis.
Source: Handbook of Diseases, 2003
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