Bronchiectasis

Bronchiectasis is defined as expansion and destruction of larger bronchi as a result of chronic infections and inflammatory processes. Some common causes include cystic fibrosis, immune defects and recurrent infections. However, idiopathic etiology is suspected Chance. Chronic cough and sputum are typical symptoms of putrid; there are occasionally additionally fever and dyspnea. Diagnosis is based on history and imaging techniques. this is groundbreaking usually a high-resolution CT, however, may already allow diagnosis chest radiograph. Therapy and prophylaxis of acute exacerbations done with antibiotics, secretion drainage and treatment of possible complications such as infections and Super hemoptysis. Treatment of underlying disease is important and should always be performed whenever possible.

Bronchiectasis is defined as expansion and destruction of larger bronchi as a result of chronic infections and inflammatory processes. Some common causes include cystic fibrosis, immune defects and recurrent infections. However, idiopathic etiology is suspected Chance. Chronic cough and sputum are typical symptoms of putrid; there are occasionally additionally fever and dyspnea. Diagnosis is based on history and imaging techniques. this is groundbreaking usually a high-resolution CT, however, may already allow diagnosis chest radiograph. Therapy and prophylaxis of acute exacerbations done with antibiotics, secretion drainage and treatment of possible complications such as infections and Super hemoptysis. Treatment of underlying disease is important and should always be performed whenever possible. A bronchiectasis etiology is best known as the common endpoint of various diseases which cause chronic inflammation of the airways, berachtet. Bronchiectasis may be many areas of the lungs affecting (diffuse bronchiectasis) or only occur in one or two areas (focal bronchiectasis). Diffuse bronchiectasis can develop in patients with hereditary diseases, immunological or anatomical disorders of the airways most often. In developed countries, many cases initially appear to be idiopathic, probably because the onset is so slow that the initiating problem can not be determined at the time at which the bronchiectasis is recognized. With newer, improved genetic and immunological assays, an increasing number of reports describing the discovery of an etiology in these idiopathic cases after careful, systematic assessment. Cystic fibrosis (CF Cystic fibrosis) is the most common identified cause, and not previously diagnosed CF may be responsible for up to 20% of idiopathic cases. And heterozygous patients who have no clinical manifestations of CF usually have an increased risk of bronchiectasis. Also, immunodeficiencies as the “common variable immune deficiency” (CVID) can cause diffuse bronchiectasis, as well as rare abnormalities of the airways. Malnutrition and HIV infection also appear to increase the risk. Congenital defects in mucociliary clearance, such as primary ciliary dyskinesia (PCD) syndromes can also be a cause, and explain where appropriate, some idiopathic cases. Diffuse bronchiectasis sometimes complicates general autoimmune disorders such as RA or Sjögren’s syndrome. Allergic bronchopulmonary aspergillosis, a hypersensitivity reaction to Aspergillus spp (allergic bronchopulmonary aspergillosis (ABPA)) which is very common in people with asthma, but sometimes in patients with cystic fibrosis can lead to bronchiectasis. In developing countries, most cases are probably caused by TB, especially in patients with compromised immune function due to malnutrition and HIV infection. Focal bronchiectasis typically develops as a result of untreated pneumonia or obstruction (eg. As by foreign bodies, tumors, postoperative changes, lymphadenopathy). Mycobacteria (tuberculosis or non-tuberculous) can cause both focal bronchiectasis and settle in the lungs of patients who are already affected by bronchiectasis due to other disorders (see Fig. Predisposing factors for bronchiectasis). Predisposing factors for bronchiectasis Category examples and comments infections by bacteria Bordetella pertussis Haemophilus influenzae Klebsiella sp. Moraxella catarrhalis Mycoplasma pneumoniae, Pseudomonas aeruginosa Staphylococcus aureus Fungal Aspergillus sp. Histoplasma capsulatum mycobacterial Mycobacterium tuberculosis non-tuberculous mycobacteria Viral Adenovirus Herpes simplex virus influenza measles respiratory syncytial virus Congenital disorders ?1-antitrypsin deficiency in severe cases can lead to bronchiectasis Ziliendefekte Can bronchiectasis, sinusitis, otitis media and male Unfruchtbarkei t cause 50% of patients with primary ciliary dyskinesia have situs inversus primary ciliary dyskinesia (clinical triad of Dextrocardia, sinus disease, Situs inversus) Cystic fibrosis caused viscous secretions by malfunction in the transport of Na and Cl often colonized by P. aeruginosa or S. aureus complicates primary immunodeficiencies Chronic granulomatosis defects of the complement system hypogammaglobulinemia, common variable immunodeficiency secondary particularly HIV-In fection immunosuppressants airway obstruction, endobronchial tumor cancer Extrinsic compression due to tumor mass or lymphadenopathy Aspirated foreign body or intrinsic (eg. B. Bronchialstein) Mucoid impaction allergic bronchopulmonary aspergillosis postoperatively lobar resection due to kinking or twisting of the remaining lobes connective tissue diseases and systemic RA often causes bronchiectasis (often subclinical); frequently may experience Inflammatory Bowel Disease Bronchopulmonary complications in men and in patients with long-standing RA Sjogren’s syndrome bronchiectasis due to the increased viscosity of bronchial secretions, leading to blockages, poor clearance and chronic infection SLE bronchiectasis at up to 20% of patients due to unknown mechanisms up to 85% after the onset of chronic inflammatory bowel disease, and 10-15% before bronchiectasis is more common in ulcerative colitis, but may also occur in Crohn’s disease Recurrent polychondritis – congenital structural defects Lymphatic yellow nail syndrome Tracheobronchial Williams-Campbell syndrome (cartilage deficiency) Tracheobronchomegaly (eg. B. Meunier-Kuhn syndrome) Vascular Lung (a congenital malformation in which a non-functioning mass of lung tissue precludes normal communication with the tracheobronchial tree and its arterial blood supply from the systemic circulation receives) Inhalation Toxic ammonia chlorine nitrogen direct airway injury, the structure and function changes Other transplants Can also be secondary to recurrent infections because of immunosuppression be Adapted from Barker, AF: bronchiectasis. The New England Journal of Medicine 346: 1383-1393, 2002. Pathophysiology The pathophysiology of bronchiectasis is not fully understood, probably in part because it is the common end point of a heterogeneous group of disorders that predispose chronic inflammation of the airways. Diffuse bronchiectasis seems to begin when a causative disease causing inflammation of small and medium airways releasing inflammatory mediators from intraluminal neutrophils. The inflammatory mediators destroy elastin, cartilage and muscles in larger airways, leading to irreversible bronchodilation. At the same macrophages and lymphocytes form in the inflamed small and medium sized airways infiltrates, which thicken the mucous walls. This thickening causes the airway obstruction that is often detected during lung function tests. With progression of the disease, the inflammation spreads to the respiratory tract and causes fibrosis of the surrounding lung parenchyma. What the small airways inflamed, depends on the etiology of bronchiectasis. Some common causes include impaired airway clearance (by the production of thick, viscous mucus in CF, lack Zilienmotilität in PCD, or damage to the cilia and / or airways secondary to infection or injury), and impaired immune defenses; these factors predispose patients to chronic infection and inflammation. In the case of immunodeficiency (CVID in particular), an autoimmune inflammation also help. Focal bronchiectasis occurs usually when a large airway is blocked. The resulting inability to cough secretions, leading to a cycle of infection, inflammation and damage to the airway wall. The right middle lobe is mostly involved because his bronchus is small and angled and lymph nodes in the immediate vicinity. Lymphadenopathy due to non-tuberculous mycobacterial infection sometimes causes bronchial obstruction and focal bronchiectasis. During ongoing inflammation alters the anatomy of the respiratory tract, colonizing pathogenic bacteria (including mycobacteria sometimes) the respiratory tract. Among the most common organisms include Haemophilus influenzae (35%), Pseudomonas aeruginosa (31%), Moraxella catarrhalis (20%), Staphylococcus aureus (14%) and Streptococcus pneumoniae (13%). S. aureus colonization is strongly associated with CF; a finding of S. aureus cultures over should the suspected undiagnosed CF. increase. A colonization by P. aeruginosa tends to indicate a severe disease and is a rapid decline in lung function. The settlement of several organisms is widespread, and antibiotic resistance is a concern in patients who require frequent doses of antibiotics to treat exacerbations. Complications As the disease progresses, chronic inflammation and hypoxemia cause neovascularization of bronchial (not pulmonary) artery. Bronchial rupture easily, resulting in massive hemoptysis. Other vascular complications are pulmonary hypertension due to vasoconstriction, arteritis and sometimes shunt of the bronchial to the pulmonary vessels. Colonization with multidrug-resistant organisms may lead to chronic, low-grade inflammation of the airways. This inflammation can progress to recurrent exacerbations and impaired airway obstruction in pulmonary function tests. Symptoms and signs The symptoms typically begins slowly and worsens over the years, accompanied by episodes of acute exacerbation. The most common symptom of bronchiectasis produced a chronic cough, thick, tough, often purulent sputum. Dyspnea and wheezing occur frequently, and it can develop pleuritic chest pain. In advanced cases, hypoxemia, and right heart failure can improve dyspnea due to pulmonary hypertension. Coughing up blood, which may be solid, occurs due to neovascularization of the airways. Acute exacerbations are common and often result from new or worsening infection. Acute exacerbations are characterized by a worsening cough and dyspnea, and enlargement of the volume and purulence of sputum. Mild fever and constitutional symptoms (eg. As fatigue, malaise) may also be present. Typical test results are halitosis and pathological respiratory sounds such as wheezes, pipes and hum. Also clubbed fingers may be present. In advanced cases, symptoms of hypoxemia, pulmonary arterial hypertension (eg. As shortness of breath, dizziness) and right heart failure often. Chronic rhinosinusitis and nasal polyps may be present, especially in patients with cystic fibrosis or PCD. reduce fat-free body mass in general, which may be due to inflammation and cytokine excess, and in patients with CF, malabsorption. Diagnosis history and physical examination chest X-ray High-resolution chest CT lung function tests for the original investigation and recording the progression of Erkan Kung Specific tests for suspected causes Diagnosis is based on history, physical examination and x-rays. Usually, a chest x-ray recording is first made. Clinically bronchiectasis can be confused with chronic bronchitis. Important differential diagnostic criteria are the much larger occurring, pus penetrated daily Sputummengen in bronchiectasis and advanced airways that are recognized by imaging methods. Imaging techniques chest x-ray is abnormal in general and can be diagnostic. Radiographic findings that indicate bronchiectasis, include thickening of the airway walls and / or Atemwegsdilatation; ill-defined, typical findings, linear perihilar densities with obscurity of the central pulmonary arteries, indistinct rings due thickened airway in cross section (parallel to the x-ray), and “tram lines” (or tramway track mark) caused by thickened, dilated airways perpendicular to the X-ray beam. Dilated airways filled with mucus, can also cause occasional elongated tubular opacities. The radiological image may vary depending on the underlying disease. In derCF bronchiectasis is predominantly localized in the upper lobes, while it increases in focal Anomlitäten shows X-ray examinations due to endobronchial obstruction. Method of choice to detect the extent of bronchiectasis exactly, is a high resolution CT, and has a sensitivity and specificity of almost 100%. Typical CT findings are Atemwegsdilatation (wherein the inner lumen of two or more air paths, the diameter of the adjacent artery exceeds) and the sign of a sealing ring (a thickened, dilated in the respiratory appears next to a smaller artery in transaxial view). A lack of normal bronchial tapering off can lead to visible bronchi of medium size that extend almost to the pleura. “The tram lines” are plainly visible in the CT. While the airway damage increases over time, the bronchiectasis of cylindrical proceeds to varicose and then cystic findings continued in imaging. Nonspecific findings are atelectasis, mucus and consolidated lung parenchyma and rarefied vessels. In a Traktionsbronchiektase, draws or distorting the pulmonary fibrosis airways in a way that simulates the bronchiectasis in imaging. Bronchiectasis with permission of the publisher. From Coakley R., R. Boucher, Fell S., et al. In Bone’s Atlas of Pulmonary and Critical Care Medicine. Edited by J. Crapo. Philadelphia, Current Medicine, 2005. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/bronchiectasis_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/ – / media / manual / professional / ? images / bronchiectasis_high_de.jpg lang = en & thn = 0 ‘, title:’ bronchiectasis ‘description:’ u003Ca id = “v37893105 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eDieses contrast-enhanced CT of the chest of a patient with cystic fibrosis is severe bronchiectasis in the central regions of the lung with advanced airways and cystic changes. u003c / p u003e u003c / div u003e ‘

Health Life Media Team

Leave a Reply