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Tracheobronchial obstruction

The focus of this chapter is primarily on metallic stents. For a detailed overview of the results of placement of plastic tube stents for tracheobronchial obstructions due to malignant tumors, the interested reader is referred to one of the review articles on stenting of the tracheobronchial system written by experienced interventional bronchoscopists (thoracic endoscopist) (Colt and Dumon 1995 Mehta and Dasgupta 1999 Rafanan and Mehta 2000 Wood 2001). [Pg.261]

A small series of four patients with malignant tracheobronchial obstruction was presented by Col-REAVY et al. (2000). Stenting was successful in all four patients and led to dramatic relief of stridor. Mean survival was 6 months. One patient died some hours after stent insertion due to bleeding from a site where laser recanalization was carried out, but did not bleed from the stent insertion site. One patient required laser treatment 3 months after stent placement for tumor regrowth. [Pg.263]

A larger patient population was reported by Beer et al. (1999). A total of 27 Palmaz stents were placed in 21 patients with malignant obstructive tracheobronchial obstructions (trachea, n=2 left main stem bronchus, n=8 intermediate bronchus, n=7 right main stem bronchus, n=l lobar bronchi, n=4). Following stent insertion, six patients had no further respiratory distress, and the remaining 15 patients reported relief of dyspnea. In seven patients, postobstructive pneumonia was successfully treated by stent placement. Mean survival time was 12 months. Restenosis occurred in four patients and was treated with redilation in three, and laser ablation in one patient. [Pg.263]

Treatment of tracheobronchial obstructions in cancer patients can be difficult, if previous palliative measures had been already undertaken. We believe that complicated interventions are best carried out by an experienced team of interventional radiologist and tracheobronchial endoscopists... [Pg.267]

Beer M, Wittenberg G, Sandstede J, Beissert M, Schmidt M, Ender J, Krahe T, Hahn D (1999) Treatment of inoperable tracheobronchial obstructive lesions with the Palmaz stent. Cardiovasc Intervent Radiol 22 109-113 Bjarnason H, Cahill B, Klow NE et al. (1999) Tracheobronchial... [Pg.267]

Colreavy MP, Keogh 1, Hone S, Lacy PD, Gaffney RJ, Walsh MA (2000) Nitinol stents their value in tracheobronchial obstruction. Clin Otolarynology 25 233-239 Colt HG, Dumon JF (1995) Airway stents. Present and future. [Pg.268]

George PJM, Irving JD, Khagani A, Dick R (1992) Role of Gianturco expandable metal stent in the management of tracheobronchial obstruction. Cardiovasc Intervent Radiol 15 375-381... [Pg.268]

Sawadi S, Tanigawa N, Kobayashi M, Furui S, Ohta Y (1993) Malignant tracheobronchial obstructive lesions treatment with Gianturco expandable metallic stents. Radiology 188 205-208... [Pg.268]

Strecker EP, Liermann D, Barth KH et al. (1990) Expandable tubular stents for treatment of arterial occlusive diseases experimental and clinical results. Radiology 175 87-102 Tan BS, Watkinson AF, Dussek JE, Adam AN (1996) Metallic endoprostheses for malignant tracheobronchial obstruction initial experience. Cardiovasc Intervent Radiol 19 91-96... [Pg.270]

Westaby S, Jackson JW, Pearson FG (1982) A bifurcated silicone rubber stent for relief of tracheobronchial obstruction. J Thorac Cardio Surg 38 200-205... [Pg.270]

Zwischenberger JB, Wittich GR, van Sonnenberg E, Johnson RF, Alpard SK, Anand SK, Morrison RJ (1997) Airway simifiation to guide stent placement for tracheobronchial obstruction in lung cancer. Ann Thorac Surg 64 1619-1625... [Pg.270]

Cahill BC, Harmon KR, Shumway SJ, Mickman JK, Hertz MI (1992) Tracheobronchial obstruction due to silicosis. Am Rev Respir Dis 145 719-721... [Pg.27]

An understanding of common mechanisms of death due to poisoning can help prepare the care-giver to treat patients effectively. Many toxins depress the central nervous system (CNS), resulting in obtundation or coma. Comatose patients frequently lose their airway protective reflexes and their respiratory drive. Thus, they may die as a result of airway obstruction by the flaccid tongue, aspiration of gastric contents into the tracheobronchial tree, or respiratory arrest. These are the most common causes of death due to overdoses of narcotics and sedative-hypnotic drugs (eg, barbiturates and alcohol). [Pg.1248]

Asthma is a chronic inflammatory condition characterized by bronchial hyper-responsiveness and reversible airway obstruction. Cytokine release from a variety of cell types such as eosinophils, lymphocytes and other inflammatory cells produces epithelial sloughing, plasma protein extravasation from the tracheobronchial microcirculation and airway remodeling. Bronchial mucosal inflammation is present in all patients. The primary goal of asthma management is to maintain control of the disease process by reducing symptoms and improving lung function. [Pg.201]

The parasympathetic division is the dominant portion of the pulmonary autonomic nervous system in all mammals. Airway smooth muscle is richly supplied with muscarinic receptors and stimulation of M3 receptors results in smooth muscle contraction and bronchoconstriction. Cholinergic stimulation is the primary mechanism of bronchospasm in horses with recurrent airway obstruction (Robinson et al 1996). Parasympathetic innervation can be demonstrated throughout the tracheobronchial tree of the horse but smooth muscle contraction evoked by stimulation of cholinergic nerves is more pronounced in the trachea than in the smaller bronchi. It is expected that parasympathetic blockade with a muscarinic antagonist will have the greatest effect in large, central airways. [Pg.316]

Mast cell stabilizers are indicated for the treatment of inflammatory airway disease in some horses. Inflammatory airway disease is observed in yoimg horses the clinical syndrome is characterized by poor exercise performance, chronic cough and the presence of exudate in the tracheobronchial tree. A subset of horses with inflammatory airway disease will have metachromatic inflammation in bronchoalveolar lavage, with mast cells constituting 2-5% of the total cell count. This form of chronic lower airway inflammation probably represents a local pulmonary hypersensitivity reaction. There is controversy as to whether this form of inflammatory airway disease represents an early form of recurrent airway obstruction. Nebulization of sodium cromoglicate (200 mg) will improve the clinical signs of respiratory disease and will stabilize mast cell histamine release (Hare et al 1994). [Pg.322]

The effect of plasma leakage on airway resistance depends on the amount of mechanical obstruction caused by the increase in mucosal thickness, accumulation of intraluminal fluid and possible reflex bronchocon-striction. In addition, the impact on airway conductance depends on where in the tracheobronchial tree the fluid accumulates. Theoretical models predict that increased mucosal wall thickness itself may have little effect on airflow, but it could exa erate the luminal narrowing caused by bronchoconstriction (James etal., 1989 Wiggs et al., 1990 Yager et ai., 1991). Although this effect probably would be negligible in the trachea and large bronchi, it could be important in peripheral airways. [Pg.150]

Lower respiratory disorders are conditions that obstruct or restrict tracheobronchial tubes, preventing exchange of gases. These conditions are called chronic obstructive pulmonary disease (COPD), and include bronchitis, chronic bronchitis, bronchiectasis, emphysema, asthma, and chronic asthma. [Pg.174]

Z Maintenance of an adequate airway and breathing is necessary if there is obstruction resulting from bronchial secretions and bronclio.spasm. This may require the use of an oral airway (or insertion of an endotracheal tube if medical assistance is available) and assisted ventilation (e.g., mask with manual inflator). Oxygen is valuable because of the potential for hypoxia resulting from airway obstruction secondary to increa.sed tracheobronchial secretions and bronchospasm (Munidasa et al.. 2004). When hospitalized, endotracheal intubation and assisted ventilation may be required (Proudfooi and Vale, 1996),... [Pg.584]

Some conditions obstmct or restrict tracheobronchial tubes and prevent the exchange of gas within the lungs. These conditions are referred to as chronic obstructive pulmonary disease. These include bronchitis, bronchiectasis, emphysema and asthma. [Pg.290]

With high-level exposure, laryngeal edema, tracheobronchitis, and abmpt airway obstruction may occur. Irritation of the lower respiratory tract and lung parenchyma causes tracheobronchial mucosal sloughing, chemical pneumonitis, and nonoardiogenic pulmonary edema. [Pg.214]

Patients should be able to cooperate during the procedure. Some patients with severely symptomatic SVCOS may have difficulties in lying flat on the examination table. In these circumstances, the procedure should be undertaken under general anesthesia. A minority of patients will present with simultaneous tracheobronchial narrowing, due to malignant mediastinal compression. Stenting of the airways should precede management of the caval obstruction in such patients. [Pg.118]

Song and co-workers (1999) placed their self-developed potentially retrievable covered metallic stent in eight patients with tracheobronchial malignant obstructions (esophageal cancer, n=4 lung cancer, n=2 tracheal cancer, n=l gastric cancer, n=l). Stents were successfully placed in all patients but one. In this case a hinged stent (combined tracheal and bronchial stent) was placed too caudal so... [Pg.264]


See other pages where Tracheobronchial obstruction is mentioned: [Pg.251]    [Pg.264]    [Pg.265]    [Pg.267]    [Pg.251]    [Pg.264]    [Pg.265]    [Pg.267]    [Pg.242]    [Pg.95]    [Pg.2523]    [Pg.182]    [Pg.91]    [Pg.187]    [Pg.228]    [Pg.59]    [Pg.259]    [Pg.171]    [Pg.50]    [Pg.247]    [Pg.247]    [Pg.248]    [Pg.249]    [Pg.251]    [Pg.251]    [Pg.254]    [Pg.260]    [Pg.264]   
See also in sourсe #XX -- [ Pg.263 , Pg.264 ]




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