Bronquiectasia: definición, causas y tratamiento
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Bronquiectasia: definición, causas y tratamiento
- 1. BRONQUIECTASIS R1MI Jorge Antonio Mirón Velázquez
- 2. DEFINICIÓN «Dilatación anormal irreversible y el engrosamiento de las paredes de los bronquios» Fase final de procesos patológicos Destrucción de la pared bronquial Tejidos de soporte Tos Crónica - meses a años Expectoración mucopurulenta copiosa Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 3. PREVALENCIA 52/100 000 – US > Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 4. FISIPATOLOGÍA • Bronquios • Tamaño mediano Inicial • Bronquios distales • Bronquiolos Llenos de moco Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 5. Inflamación transmural Edema de la mucosa Erosión y ulceración del epitelio neo vascularización Infección Bacteriana Crónica + Obstrucción de la vía aérea Impedimento del drenaje Respuesta inmunitaria inapropiada Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 6. Granulomas submucosos Hipertrofia del músculo liso Perdida del epitelio Arteriolas tortuosas – Anastomosis broncopulmonares Perdida de ciliios Metaplasia escamosa Hipertrofia de las glándulas bronquiales Intenso infiltrado: neutrófilos, linfocitos, monocitos Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 7. INFECCIONES Infecciones en la infancia: • Neumonía severa • Pertusis • Sarampión • tuberculosis Infecciones: • Adenovirus, herpesvirus • S. Aureus • K. pneumoniae • P. aeruginosa Infección por Mycobacterium • Bronquitis • Estenosis de la pared bronquial Mycobacterium avium complejo • Caucásicos • Mujeres 50 a 70 años • Inmunocompromiso Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 8. OBSTRUCCIÓN BRONQUIAL Obstrucción Colapso Inflamación Bronquiectasia local Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008 Obstrucciones internas • Adenomas, Fibromas, Condromas, Papilomatosis Obstrucciones externa Estenosis bronquial
- 9. ASPIRACIÓN Y LESIÓN POR INHALANTES Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 10. FIBROSIS QUÍSTICA Una de las causas más comunes Autosómico recesivo >200 mutaciones 1-3 % Diagnóstico tardío Lobo superior + Cultivo para Pseudomonas aeruginosa Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 11. OTRAS CAUSAS • Azoospermia obstructiva + infecciones sinopulmonares crónicas (sin anormalidades ciliares) Síndrome de Young • Autosómico recesivo • Genes: DHA1, 5 y 11- dineinas • Defectos del movimiento de cilios Dicinesia ciliar primaria • Aspergillus fumigatus • Pacientes con asma y fibrosis quística – millieu • Eosinofilia sistemica y local, Ig G y E especificos • Criterios de Rosemberg Patterson (sin F.Q.) Alergia broncopulmonar al Aspergillus • Inmunodeficiencias primarias • Colagenopatias Desordenes inflamatorios Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 12. ¿A QUIENES DEBERÍA INVESTIGASE UNA BRONQUIECTASIA? Tos productiva persistente con al menos uno de los siguientes factores proclives Inicio de presentación a edad joven Historia de síntomas relacionados muchos años Ausencia de historial de tabaquismo Expectoración diaria en gran cantidad de características purulenta Hemoptisis Colonización de esputo por P. aeruginosa. Pasteur M. C. «British Thoracic Society guideline for non-CF bronchiectasis” BTS.
- 13. CUADRO CLÍNICO Tos podría ser el único síntoma durante años Expectoración: Empeora por la mañana, Intermitente Infecciones frecuentes, Taponamiento bronquial Terapia antimicrobiana Bronquiectasia «seca» Tos mínimamente productiva Hemoptisis Historia de infecciones recurrentes o secundario a Infección por pertusis, neumonía severa y tuberculosis Tos Crónica Expectoración mucopurulenta Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 14. EXACERBACIÓN Aumento en la frecuencia e intensidad de la tos Disnea Producción de esputo fiebre, Hemoptisis Dolor de pecho Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 15. EXPLORACIÓN FÍSICA Estertores crepitantes inspiratorios tempranos y mesoinspiratorios Roncus difusos Expiración prolongada Paquioniquia Osteoartropatía hipertrófica pulmonar Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 17. ESTUDIOS PLASMATICOS [Ig G, M y A] IgE Aspergillus RAST /CAP Precipitinas antti aspergilLus
- 18. Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008 ESTUDIOS RADIOLÓGICOS RADIOGRAFÍA DE TÓRAX Signo del anillo Líneas en «rieles» Radiopacidad en « dedo en guante» Datos de atelectasia
- 19. TOMOGRAFÍA DE ALTA RESOLUCIÓN Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 20. CLASIFICACIÓN RADIOLÓGICA Reid 1950 – Tomografía computada Cilíndrica: Contorno regular, diámetro aumentado, Paredes lisas Varicosa Dilataciones irregulares, saculaciones o trayectos tortuosos que asemejan una vena Quisticas o saculares Distorsión quística en las vías aéreas distales, podría ser focal o diseminado. Resultando en sáculos que aparecen como racimos de uvas. Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 21. Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 22. MANEJO Identificar la causa primaria Control de infecciones Higiene Bronquial Aclaramiento de moco Mejorar la función pulmonar Reducir las exacerbaciones Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 23. CONTROL DE INFECCIONES Resolver la perpetuación del a bronquiectasia Antibioticoterapia - exacerbaciones H. Influenzae Pseudomonas aeruginosa Nocardia asteroides Mycobacterium spp. (vida libre) Antimicoticos Aspergillus Fumigatus Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 24. EXACERBACIÓN Exacerbación que requiere antibioticorerapia Incremento de la tos + sibilancias+ disnea + síntomas sistémicos Incremento del esputo purulento Incremento del volumen o la viscosidad Pasteur M. C. «British Thoracic Society guideline for non-CF bronchiectasis” BTS.
- 25. Toma de cultivo de expectoración • Amoxicilina 500mg bid o claritromicina 500mg bid x 14 días Prima línea sin cultivo • Ciprofloxacino 500 750 mg bid x 14 días Colonización por Pseudomonas Pasteur M. C. «British Thoracic Society guideline for non-CF bronchiectasis” BTS.
- 26. HIGIENE BRONQUIAL Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008 Mal apego Hipoxemia potencial Incomodidad torácica
- 27. Dispositivo de vibración mecánica de presión espiratoria positiva Dispositivo de vibración mecánica con válvula Flutter Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 28. ACLARAMIENTO DE MOCO Estado inflamatorio crónico Hipersecreción de moco Prevenir la retención de expectoraciones Mantener un estado de hidratación adecuado Humidificación del oxigeno inhalado Nebulizacion Solución salina 0.9% Solución Salina 3%, Acetilcisteina Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008
- 29. BIBLIOGRAFÍA Fishman A. et Al. «Fishman’s pulmonary deseases and disorders». 4th edition . McGraw Hill; 2008 Adam A. Et Al. «grrainger and allison’s diagnnóstic radiology». 6th Edition. Churchil-Livingsone-Elsevier. 2015 Pasteur M. C. «British Thoracic Society guideline for non-CF bronchiectasis” BTS. Thorax.2010
Notas del editor
- The abnormal bronchial dilatation in bronchiectasis principally affects the medium-sized bronchi, but often extends to the more distal bronchi and bronchioles. The affected bronchi show transmural inflammation, mucosal edema, cratering, ulceration, and neovascularization
- t has been suggested that following bronchial obstruction, airways proximal to the collapse are exposed to strong dilating forces caused by the difference in the atmospheric pressure in the bronchi and the negative pressure in the pleural space. Over time, these forces acting on weakened, inflamed airways may result in permanent and pathological airway dilatation.
- Aspiration or inhalation of foreign matter, such as noxious fumes or particulates into the airways, may result in bronchiectasis. This may involve aspiration of oropharyngeal secretions containing microaerophilic and anaerobic bacteria, which may result in a necrotizing pneumonia. Refluxed material from the esophagus or stomach containing food particles, gastric, biliary, and pancreatic secretions, and gut microbes may enter and damage airways, especially if the aspiration events are large and repeated. Depressed sensorium (stroke, alcohol and drug use, seizure, postanesthetic), brain stem dysfunction (amyotrophic lateral sclerosis, multiple sclerosis, syringomyelia), defective laryngeal function (postsurgery, postirradiation), esophageal disorders (dysmotility, gastroesophageal reflux disease [GERD], achalasia, tracheoesophageal fistula), and gastric disorders (gastric outlet obstruction) influence the likelihood and frequency of aspiration. Bronchiectasis may present years after foreign body aspiration (aspiration is often unrecognized), though bronchiectasis has been seen to occur in animals as soon as 2 to 8 weeks after experimental foreign body introduction into the bronchial tree. GERD is the most common condition in this category contributing to the risk of bronchiectasis, and several studies are available documenting increased frequency of reflux in patients with bronchiectasis, asthma, and pulmonary fibrosis, all chronic pulmonary inflammatory conditions. The cause-effect conundrum of GERD in these conditions is still being debated. However, given the high rate of association of GERD with bronchiectasis and the fact that it is often treatable, GERD evaluation should be part of the bronchiectasis work-up
- cysticfibrosistransmembrane conductance regulator (CFTR)
- ABPA manifests as recurring episodes of asthma, pulmonary infiltrates, and central bronchiectasis that may progress to fibrosis Rosenberg-Patterson 1977 criteria for diagnosis of ABPA. Primary criteria (1–6 suggestive, +7 definite) : 1. Episodic bronchial obstruction 2. Peripheral eosinophilia 3. Positive immediate skin test to Aspergillus 4. Positive preciptin test to Aspergillus 5. Increased total serum IgE 6. History of transient or fixed lung infiltrates 7. Proximal bronchiectasis Secondary (supportive) criteria: . Brown plugs/flecks in sputum 2. Positive late (6–12 h/Arthus) skin test to Aspergillus
- Cough is invariably present and often may be the only symptom for years. Purulent, tenacious sputum production, frequently worse in the morning (having accumulated during recumbency in sleep) is present in most patients. Sputum production may be intermittent, being affected by recurrent infections, bronchial plugging, and antibiotic therapy. “Dry bronchiectasis” presenting as cough, minimal sputum expectoration, and/or hemoptysis is occasionally described. Hemoptysis may be seen in 40 to 70 percent of patients and may vary from blood streaks to large clots.
- Increasing cough, dyspnea, and volume of sputum production, fever, hemoptysis, and chest pain are hallmarks of acute exacerbations. Often patients give a history of recurrent chest infections, although single episodes of severe pneumonia, tuberculosis, or pertussis with secondary pneumonia may also result in bronchiectasis.
- Chest auscultation usually reveals findings of early and mid-inspiratory crackles as well as diffuse rhonchi and prolonged expiration. Bronchial breath sounds may be heard in severe cases or patients with a complicating pneumonia. Digital clubbing and hypertrophic pulmonary osteoarthropathy, although common in the pre-antibiotic era, are rarely seen now. In severe advanced cases, there may be evidence of respiratory insufficiency and cor pulmonale.
- The chest x-ray may be abnormal and show the presence of increased pulmonary markings, ringlike structures, atelectasis, dilated and thickened airways (tram lines), and mucus plugging (finger-in-glove) appearance; however, the chest radiograph may be normal even in the presence of bronchiectasis
- The HRCT has been proved to be a reliable and noninvasive method for assessment of bronchiectasis. HRCT can accurately (sensitivity of 97 percent) diagnose bronchiectasis, localize and describe areas of parenchymal abnormality, and identify bronchiolar abnormalities and mucus plugging to the level of fifth- and sixth-order bronchi. It also can identify focal areas of air trapping as an indicator of small airway disease. It is indicated in the evaluation of bronchiectasis when surgical resection is contemplated, bronchiectasis is strongly suspected clinically and routine chest radiographs are normal, and other parenchymal abnormalities have to be better defined. Airway dilatation can be detected by finding tram lines or end-on-ring appearance. A luminal diameter more than 1.5 times the adjacent vessel is indicative of bronchiectasis (Fig. 125-1). Bronchial wall thickening may also be seen. Evidence of small airway plugging with debris (tree-in-bud) may also be seen (Fig. 125-3). Reports are available suggesting that the distribution and pattern of bronchiectasis may be sufficient to implicate a specific cause. Cartier et al. found that bilateral predominantly upper lobe bronchiectasis is seen most commonly in CF and allergic bronchopulmonary aspergillosis, a unilateral upper lobe predominance in tuberculosis and a lower lobe predominance in childhood viral infections