One explanation of a better survival in former smokers is partly attributable to the prevention of smoking damage over time lower functional decay of the lung [ 19 ] and increased risk of cancer and cardiovascular diseases in smoker [ 18 ] and partly to the greater pharmacological efficacy of compounds containing ICS [ 20 ]. Interestingly, in a recent Delphi consensus project run in Italy, the most effective step to reduce lung functional decline were considered by the specialists interviewed to be smoking cessation [ 21 ].
Therefore, smoking cessation support programs should always be provided in the patient with COPD. Furthermore, GOLD also states potential consideration should be given to step down from triple therapy to a non-ICS treatment in case of ascertained pneumonia risk e. Bronchodilators, including dual bronchodilators, figure prominently into the treatment guidelines. The main results of this study were obtained on: reduction of exacerbation rate, lung function improvement in terms of trough FEV 1 improvement , mortality data and incidence of pneumonia.
Taken together, these characteristics should be obviously ascribed to COPD population rather than to an asthma population. For over a decade the respiratory community has debated the potential mortality benefits of ICS-containing treatments in COPD, but until now this benefit has not been prospectively shown [ 33 , 34 , 35 ].
As indicated previously pneumonia and exacerbations are key events during COPD disease, with different implications for individual patients. Macrolides have demonstrated a measurable efficacy in preventing exacerbations. In fact, a post-hoc pooled analysis by Rennard et al. However only two studies have shown in the early s that the use of long term oxygen therapy LTOT can lower mortality in patient with COPD associated to chronic hypoxemia.
As recently shown in an interesting review by Minervini et al. However, to date, there are no data comparing the two techniques and other studies should be conducted in order to clarify long term outcomes, side effect and costs linked to these different approaches.
A non-pharmacological treatment for COPD patients is represented by the pulmonary rehabilitation. The topic is still debated and controversial especially in COPD patients after a recent exacerbation due to conflicting evidences emerged from more recent trials: these last showed no benefit of rehabilitation on hospital readmissions and mortality versus older studies [ 44 ]. Nevertheless, the BTS guidelines suggest the use of respiratory rehabilitation in COPD patients having a view to improving: exercise capacity, dyspnea, health status and psychological wellbeing [ 45 ].
To date, the advantages of respiratory rehabilitation do not seem to be associated with the prevalent bronchitis or emphysematous status. For example, an approach to COPD pharmacotherapy used by Spanish investigators utilizes an easy table of four major phenotypes Non exacerbators, ACO, exacerbators with emphysema, exacerbators without emphysema with five treatments options bronchodilators, ICS, mucolytics, PDE4 inhibitors, macrolides , linking each of the four phenotypes with the appropriate treatment s [ 46 ].
Based on these considerations we propose a treatment algorithm easily summarized in Fig. This pathway will need to be confirmed through additional clinical trials and evidence, that will also consider a validated set of phenotyping criteria. The latest scientific evidence is helping to identify and possibly clarify these different patient phenotypes which could be crucial in determining the right treatment for the right patient.
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A Delphi consensus project. Patients with emphysema have symptoms such as a barrel chest, enlarged lungs, shortness of breath, and weight loss. It does not provide medical advice, diagnosis or treatment.
This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. With an accout for my. It is often caused by exposure to toxic chemicals or long-term exposure to tobacco smoke.
Emphysema is caused by loss of elasticity increased compliance of the lung tissue, from destruction of structures supporting the alveoli, and destruction of capillaries feeding the alveoli. The result is that the small airways collapse during exhalation although alveolar collapsibility has increased , leading to an obstructive form of lung disease airflow is impeded and air is generally "trapped" in the lungs in obstructive lung diseases.
Symptoms include shortness of breath on exertion typically when climbing stairs or inclines, and later at rest , hyperventilation, and an expanded chest. Emphysema patients are sometimes referred to as "pink puffers". This is because emphysema sufferers may hyperventilate to maintain adequate blood oxygen levels. Hyperventilation explains why mild emphysema patients do not appear cyanotic as chronic bronchitis another COPD disorder sufferers often do; hence they are "pink puffers" able to maintain almost normal blood gases through hyperventilation and not "blue bloaters" cyanosis; inadequate oxygen in the blood.
However, any severely chronically obstructed COPD respiratory disease will result in hypoxia decreased blood partial pressure of oxygen and hypercapnia increased blood partial pressure of Carbon Dioxide , called Blue Bloaters.
Clinical signs at the fingers include cigarette stains although actually tar and asterixis metabolic flap at the wrist if they are carbon dioxide retainers NOTE: finger clubbing is NOT a general feature of emphysema. Examination of the face reveals a plethoric complexion if there is a secondary polycythemia , pursed-lipped breathing, and central cyanosis. Examination of the chest reveals increased percussion notes particularly over the liver and a difficult to palpate apex beat all due to hyperinflation , decreased breath sounds, audible expiratory wheeze, as well as signs of fluid overload seen in advanced disease such as pitting peripheral edema.
Classically,clinical examination of an emphysematic patient reveals no overt crackles, however, in some patients the fine opening of airway 'popping' dissimilar to the fine crackles of pulmonary fibrosis or coarse crackles of mucinous or oedematous fluid can be auscultated. Diagnosis is by spirometry lung function testing , including diffusion testing. Diffusion tests such as DLCO will show a decreased diffusion capacity.
Other investigations might include X-rays, high resolution spiral chest CT-scan, bronchoscopy when other lung disease is suspected, including malignancy , blood tests, pulse. A way to help AAT is to put more into the blood flow and eat more protein. In normal breathing, air is drawn in through the bronchial passages and down into the increasingly fine network of tubing in the lungs called the alveoli , which are many millions of tiny sacs surrounded by capillaries.
These absorb the oxygen and transfer it into the blood. When toxins such as smoke are breathed into the lungs, the particles are trapped and cause a localized inflammatory response.
Chemicals released during the inflammatory response e. This leads to significant modifications of lung architecture[1], characterized mainly by intrapulmonary air collections and confining parenchyma collapse [1] ; as far as the process proceeds expiratory bronchial obstruction and thoracic cage expansion also occur, with the clinical picture of COPD. Mainly decreased is the ability to exude carbon dioxide due to ventilation deficit and, in the more serious cases, oxygen uptake is also impaired.
The activity of another molecule called alpha 1-antitrypsin normally neutralizes the destructive action of one of these damaging molecules.
After a prolonged period, hyperventilation becomes inadequate to maintain high enough oxygen levels in the blood. The body compensates by vasoconstricting appropriate vessels.
This leads to pulmonary hypertension, which places increased strain on the right side of the heart, the one that pumps deoxygenated blood to the lungs, and it often fails. The failure causes the heart muscle to thicken to pump more blood.
Eventually, as the heart continues to fail, it becomes larger and blood backs up in the liver. Emphysema occurs in a higher proportion in patients with decreased alpha 1-antitrypsin A1AT levels alpha 1-antitrypsin deficiency , A1AD.
In A1AD, inflammatory enzymes such as elastase are able to destroy the alveolar tissue the elastin fibre, for example. The pattern of emphysema in A1AD is described as panacinar involving the entire acinus as opposed to the centrilobular pattern seen with smoking; the former typically affects the lower lungs, and the former affects the upper lungs.
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