Chronic obstructive pulmonary disease

from Wikipedia, the free encyclopedia
Classification according to ICD-10
J44.0 Chronic obstructive pulmonary disease with acute lower respiratory infection
J44.1 Chronic obstructive pulmonary disease with acute exacerbation, unspecified
J44.8 Other specified chronic obstructive pulmonary disease
Chronic bronchitis: asthmatic (obstructive) - emphysematous - obstructive
J44.9 Chronic obstructive pulmonary disease, unspecified
ICD-10 online (WHO version 2019)

The Chronic obstructive pulmonary disease ( English c hronic o bstructive p ulmonary d isease , abbreviation: COPD , rarely c hronic o bstructive l ung d isease , COLD , c hronic o bstructive a irway d isease , COAD ; translated "permanently atemwegsverengende pulmonary disease," German also called chronic obstructive airways disease ) is a disease of the lungs with a permanent narrowing of the airways, which makes it difficult to breathe out (airway obstruction ). The narrowing is caused by an inflammation of the small airways (obstructive bronchiolitis), which leads to the production of mucus and destruction of the lung tissue ( pulmonary emphysema ), which causes the airways to collapse when you exhale. The cause is the long-term inhalation of harmful particles, for example when smoking. Patients often suffer from symptoms of chronic bronchitis with coughing and increased sputum and shortness of breath when exerted. Since the obstruction hinders exhalation, it often leads to overinflation of the lungs up to the barrel chest . The progression of the disease can only be prevented by eliminating the cause (e.g. stopping smoking).

Epidemiology

Estimates assume that three to five million people in Germany , around 16 million in the USA and around 600 million worldwide have COPD. We have to speak of a global phenomenon. In the United States, COPD is the fourth most common cause of death : it is a widespread disease . Of the ten most common fatal diseases , it is the only one that is increasing in frequency.

Since 2001, the GOLD initiative launched by the World Health Organization (WHO) and the National Institutes of Health (NIH) has been trying to implement an optimized approach in the diagnosis and treatment of COPD worldwide and to combat ignorance among the population.

A study published in Salzburg in January 2007 found that a quarter of the people examined over the age of 40 suffered from COPD.

Pathophysiology

Three related complexes contribute to the pathophysiology of COPD. This is

Recent findings on pathophysiology

More recent findings suggest that there are differences in the composition of the products of cytokine gene expression in the inflammatory infiltrate , especially in contrast to bronchial asthma . At the cellular level, COPD mainly shows an increase in T lymphocytes , neutrophils and macrophages . In particular, the number of CD8-positive lymphocytes is increased, which has been directly linked to the deterioration in lung function. The above and other circulating pro-inflammatory (pro-inflammatory) messenger substances and neurohumoral activation cause damage outside the lungs. COPD can be called a systemic disease . The heart, muscles, blood vessels and bones are affected. The activation of the sympathetic nervous system is viewed as neurohumoral activation in particular . COPD patients have an increased risk of an iron deficiency caused by inflammatory processes, which in turn can increasingly lead to acute exacerbations of chronic obstructive bronchitis or COPD (AECOPD).

causes

Smoke

The majority of all COPD patients are smokers , former smokers or people exposed to passive smoking , which is why COPD is sometimes also referred to as the smoker's lung . Smoking (90% of those suffering from chronic bronchitis are smokers or ex-smokers) leads to a high concentration of free oxygen radicals ( superoxides , hydrogen peroxide , hypochlorous acid ) in the respiratory tract - see cigarette smoke . In addition, the body's own protective mechanisms against "self-digesting" the lungs are negatively affected by the numerous ingredients in tobacco smoke.

However, on the basis of regular examinations of the respiratory function, only 15–20% of all smokers show a decrease in respiratory performance over the years to such an extent that the development of COPD can be predicted with great probability. Once the diagnosis has been made, it is usually too late for a cure and only mitigating measures can be taken.

environmental pollution

Smoking is no longer considered the number 1 risk factor for COPD by all experts; Another unfavorable influence in developing countries is the pollution of breathing air through the combustion of biogenic material. Various substances present in the air are not to be underestimated as triggering factors, between 25 and 45% of all COPD sufferers worldwide have never smoked, although the problem of passive smoking was excluded. Other examples of an increased risk of COPD are various dust particles at workplaces (e.g. farmers in the cattle shed or construction workers who come into contact with mineral dusts). The literature shows COPD rates of 9 to 31% for these workers. Such influences may play a rather subordinate role in Europe and the USA. On the other hand, here as well as in large cities and metropolitan areas around the world, dust pollution from automobile mass transport is a problematic factor.

Workload

Chronic bronchitis, possibly with an asthmatic ("asthmoid") component, occurs more frequently in people who are exposed to organic or inorganic dust . It is more frequently diagnosed in workers in cotton mills, weaving mills, and rope mills.

Infections

Epidemiological studies indicate a connection between acute respiratory infections and the development of COPD. For example, viral pneumonia in childhood is said to favor the later development of COPD. Apart from rhinoviruses , however, no viral pathogens have been recognized as causing exacerbations . The main bacterial pathogens in exacerbations are Streptococcus pneumoniae , Haemophilus influenzae and Moraxella catarrhalis - in the late stages of the disease also gram-negative rod- shaped bacteria such as Pseudomonas aeruginosa . Tuberculosis can also be the cause of the development of COPD.

Inheritance

The results of twin research suggest that genetic aspects also play a role in this disease development. Alpha-1 antitrypsin deficiency is an important factor in up to 3% of cases .

Recent research shows that a variant of alpha-1 antitrypsin helps against worm disease , but increases the risk of COPD .

This mutation appears to originate in Scandinavia , where Viking populations suffered from severe worm infestation.

nutrition

A frequent diet with foods that contain nitrite ( e.g. as nitrite curing salt ), such as ham or sausage, increases the risk of COPD according to a study. The cause seems to be the formation of reactive nitrogen compounds , which can lead to emphysema-like structural changes in the lungs.

Symptoms

The main symptoms of COPD are A temnot, H Usten and A uswurf - often referred to as "AHA" symptoms.

The cough in patients with COPD has been chronic for months or years. It is usually most pronounced in the morning after waking up. In the course of the season, the cough is often stronger in autumn and winter than in spring and summer. A sudden onset, a location-dependent cough (for example at work) or the absence of sputum are atypical for COPD and more likely to indicate other diseases.

In addition to coughing, sputum is another major symptom of COPD. Analysis of the quality of the sputum allows conclusions to be drawn about the underlying disease. In COPD, the sputum is usually a little brownish and is coughed up relatively easily in the morning. Blood can also be found in the sputum of a COPD patient ( hemoptysis ). If there is haemoptysis, other diseases must be ruled out (for example, bronchial carcinoma , heart failure or tuberculosis ). In the case of emphysema, however, there is little or no sputum. In COPD, around 60 ml of sputum is coughed up every day. After giving up smoking, the amount of coughed up sputum decreases until there is no expectoration.

As stress dyspnea occurring under exertional dyspnea is called. Their extent increases in the course of the disease and can lead to a complete restriction of movement (immobility) of the patient. To assess the course of the disease, it is important to determine the respective extent of the restriction. For example, you will be asked about the number of steps at which you are short of breath. While exertional dyspnea in COPD usually occurs very soon after the start of exercise, in patients with bronchial asthma it occurs more likely after a few minutes of exertion ( exertional asthma ).

Diagnosis and classification of stages or severity

The diagnosis is based on the patient's symptoms, but primarily on the results of the lung function tests . The following classification was published by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) in 2007 and corresponds to the current guidelines of the German Respiratory League from 2007.

Severity criteria
I (easy) FEV1> 79% target, FEV 1 / FVC <70% with / without symptoms (cough, sputum)
II (medium) 49% target <FEV1 <80% target, FEV1 / FVC <70%, with / without chronic symptoms (cough, sputum, dyspnoea)
III (difficult) 30% target <FEV1 <50% target, FEV1 / FVC <70% with / without chronic symptoms (cough, sputum, dyspnoea)
IV (very difficult) FEV1 <31% target, FEV1 / FVC <70% or FEV1 <50% target plus chronic respiratory failure

FEV 1 = forced expiratory volume in the first second of exhalation = one-second capacity , here after using a bronchodilating drug ( bronchodilator ), FVC = forced vital capacity (see lung function )

The GOLD guideline of 2011 changes this classification of the severity and takes into account not only quantified symptoms but also the risk of exacerbations (disease flare-ups), while the guidelines of the Respiratory League have not yet been updated accordingly. Instead of defining the severity grades 1 to 4, there is now an assignment to groups A, B, C and D, which are decisive for the therapy decisions (see section “Therapy”).

Severity FEV 1 Symptoms Risk of exacerbation
A. ≥ 50% few symptoms (CAT <10 or mMRC grade ≤ 1) low
B. ≥ 50% increased symptoms (CAT ≥ 10 or mMRC grade> 1) low
C. <50% few symptoms (CAT <10 or mMRC grade ≤ 1) high
D. <50% increased symptoms (CAT ≥ 10 or mMRC grade> 1) high

A low risk of exacerbation exists if at most one exacerbation has occurred in the last 12 months. If there is more than one exacerbation or an exacerbation with associated hospitalization, the risk of exacerbation is increased. Symptoms are considered relatively mild if the mMRC values ​​are 0 or 1 and the CAT value is less than 10; higher values ​​are referred to as increased symptoms.

The highest risk parameter is always decisive for determining the severity. For example, if a patient still has a relatively good FEV 1 value, but has a high risk of exacerbation and a CAT value above 10, then the severity is D (not B).

Another, multidimensional severity classification is the BODE index, which takes body mass index, obstruction, dyspnea and exercise capacity into account .

Late-stage clinical categories

In the past, severe forms of late-stage COPD with obstructive pulmonary emphysema were often clinically divided into two types:

  • Pink Puffer ("pink puffers"): This is a type with a gaunt to cachectic appearance ("pulmonary cachexia"), severe dyspnoea and a rather dry cough. These patients rarely have mild cyanosis , as the compensatory work of breathing reduces hypoxia and hypercapnia . The hematocrit is in the normal range.
  • Blue Bloater : These patients are often overweight and have coughs with more sputum. Despite pronounced cyanosis with considerable hypoxia and hypercapnia , the dyspnoea is less pronounced. The "blue bloater" tolerates its lack of oxygen better than the "pink buffer" and also reacts by increasing the formation of red blood cells ( polyglobules ). With a lower oxygen supply, more oxygen can still be transported because more hemoglobin is available. In this case, the percentage of hemoglobin is less loaded with oxygen - hence the cyanosis (blue discoloration of the blood, which carries less oxygen).

A clear division of patients into one of these two categories is no longer common, however, because in most cases there is a mixed picture. Likewise, the general association of the “blue bloater” with chronic obstructive bronchitis and the “pink buffer” with emphysema is no longer valid.

therapy

The goal of treatment is to reduce or stop the progression of the disease and improve the patient's quality of life. A prerequisite for any meaningful treatment is to first eliminate harmful influences. Smokers must give up smoking, and passive smoking must also be avoided. If the disease was triggered by other influences, exposure to the pollutants must be stopped immediately. Ending exposure to pollutants is the only way to demonstrably improve the prognosis of the disease. In addition to the lung function test and spiroergometry , the 6-minute walk test can also be used to check the success . With the help of a CAT questionnaire, the patient can regularly check his or her health status and, if the test results deteriorate, seek medical help in good time or adjust therapeutic measures. COPD patients are often at risk of osteoporosis, which is why a calcium-rich diet is recommended.

Medication

COPD is mainly treated with inhalable drugs that are administered as metered dose aerosols or powder with the help of inhalers or powder inhalers , less often than inhalation solutions that are nebulised with electrically operated inhalers. In view of the fact that 40–80% of patients make critical mistakes when inhaling, easy handling of the inhaler should be ensured with thorough instruction in its correct operation.

Bronchodilators

Bronchodilators are active ingredients that widen the airways and thus lead to a reduction in airway resistance. They reduce the tone of the airway muscles, which, through their contraction and relaxation, regulate the width of the airways. Bronchodilators thus reduce the shortage of breath and improve resilience. The bronchodilators used in the therapy of COPD can be divided into three groups: beta-2 agonists (synonymous: beta-2 sympathomimetics, beta-2 mimetics), anticholinergics ( synonymous : parasympatholytics) and methylxanthines ( theophylline ). The active ingredients differ in terms of the mechanism by which the airway muscles are influenced, as well as in terms of effectiveness and the undesirable effects that can occur.

In the group of beta-2 agonists and anticholinergics, a distinction is still made between short-acting and long-acting active ingredients. The duration of the short-acting drugs in both groups is about 4–6 hours. The long-acting beta-2 agonists work for about 12 hours, while the long-acting anticholinergics last for about 24 hours.

In the step-by-step therapy of COPD, patients from severity level I are recommended to use short-acting bronchodilators if necessary (acute and emergency therapy). Long-acting bronchodilators are also used from severity level II. Here beta-2 agonists and anticholinergics can be used alone as a monotherapy or together as part of a combination therapy (dual bronchodilation). In combination therapy, the effects of the individual preparations add up.

The choice of medication depends on the patient's individual response and the extent of the adverse effects.

The rate and extent of undesirable effects are low with the correct dosage due to the fact that the active ingredients are preferably used by inhalation. The most common undesirable effect of anticholinergics is dry mouth (about 16% of patients). The more common side effects of beta-2 agonists are tremors and headache. With very high doses and overdoses of beta-2 agonists, there is an increase in mortality in patients with previous diseases of the cardiovascular system . Therefore, careful indication and regular therapy monitoring are recommended for the respective patients.

Compared to beta-2 agonists and anticholinergics, theophylline's bronchodilator effect is weak. It is the third choice and can be used from severity level II. With regard to the use of theophylline, it is important to have a narrow therapeutic range with the risk of serious side effects in the event of an overdose. The most common undesirable effects are headache and nervousness, serious side effects from overdose are drop in blood pressure, seizures and bleeding in the gastrointestinal tract. Drug monitoring may be indicated to determine the optimal dosage .

Frequently used active ingredients are, for example, ipratropium bromide and tiotropium bromide (short-acting and long-acting anticholinergics) as well as fenoterol or salbutamol (short-acting beta-2 agonists) and salmeterol or formoterol (long-acting beta-2 agonists).

According to a 2011 meta-analysis in the British Medical Journal that included around 6,500 patients, the use of soft mist inhalers (Respimat®) for tiotropium was associated with a 52% increased risk of death compared to traditional inhalers. A subsequent study with around 17,100 patients, which examined the safety and effectiveness of the Soft Mist Inhaler in comparison to the conventional inhaler, and which was published in 2013, did not reveal any increased risk of using the device. However, it was not possible to prove any effectiveness superior to that of the conventional inhaler.

Glucocorticoids

Glucocorticoids can be administered inhalatively as well as orally and intravenously.

  • inhaled glucocorticoids
    Inhaled glucocorticoids are used together with long-acting beta-2 agonists in the form of combination preparations in the long-term therapy of COPD from severity III.
    Monotherapy with inhaled glucocorticoids is not suitable. Combination preparations can lead to a reduction in the exacerbation rate in COPD patients in an advanced stage of the disease (severity III and IV), combined with a reduction in the annual fall in FEV1. Furthermore, there may be an improvement in symptoms and quality of life (recorded with the help of questionnaires). However, since only a certain proportion of COPD patients, especially those with frequent exacerbations, respond to the administration of inhaled glucocorticoids, regular evaluation of the success of the therapy is recommended. If the therapy does not improve, it is recommended to discontinue the therapy with inhaled glucocorticoids, as is the case if side effects predominate.

An indication of the response to this therapy is the number of eosinophils in the blood. A number greater than 4% or 400 / µL is an indication of this procedure. Inhaled glucocorticoids used are, for example, budesonide , beclometasone or fluticasone . The combined long-acting beta-2 agonists are, for example, formoterol and salmeterol .

  • oral glucocorticoids
    Oral glucocorticoids, such as prednisolone , are used briefly in the treatment of exacerbations in COPD. Long-term therapy with oral glucocorticoids is not indicated.
  • intravenous glucocorticoids
    As an alternative to oral administration, intravenous glucocorticoids can be administered in addition to bronchodilators in the event of an acute exacerbation with an FEV1 of less than 50% of the target value, for example in a dose of one prednisolone equivalent over about 1–2 weeks.

PDE-4 inhibitors

Roflumilast is a PDE-4 inhibitor that was developed by Nycomed and was approved by the EMA and the FDA in 2010 for the treatment of inflammation in COPD.

Therapy recommendations of the GOLD guidelines

According to the therapy recommendations of the GOLD guideline from 2011, the various active ingredients can be used in the following ways in the various patient groups (see above) in stable COPD:

Patient group First choice Second choice Alternative 1
A. short-acting anticholinergic (SAMA) if necessary or short-acting beta-2 agonist (SABA) if necessary long-acting anticholinergic (LAMA) or long-acting beta-2 agonist (LABA) or SAMA plus SABA Theophylline
B. LAMA or LABA LAMA plus LABA SABA and / or SAMA, theophylline
C. inhaled corticosteroid (ICS) plus LABA or LAMA LAMA plus LABA PDE-4 inhibitors, SABA and / or SAMA, theophylline
D. ICS plus LABA or LAMA ICS plus LAMA or ICS plus LABA plus LAMA or ICS plus LABA plus PDE-4 inhibitor or LAMA plus LABA or LAMA plus PDE-4 inhibitor Carbocysteine, SABA and / or SAMA, theophylline
ABBREVIATION Duration of action Drug group
SAMA (Short Acting) short (Muscarinergic Antagonist) Anticholinergic
LAMA (Long Acting) long (Muscarinergic Antagonist) Anticholinergic
SABA (Short Acting) short (Beta agonist) Beta-2 agonist
LABA (Long Acting) long (Beta agonist) Beta-2 agonist
ICS Inhaled corticosteroid

1 Medicinal products of the alternative choice can be used alone or in combination with active ingredients of the first and second choice.

Other supportive medications

In acute bacterial exacerbations of COPD (AECOPD), potent antibiotics should be administered, as the exacerbations have a negative impact on the course of the disease. The first choice is amoxicillin together with a β-lactamase inhibitor such as clavulanic acid . Second-choice agents are fluoroquinolones of groups 3 and 4. Long-term antibiotic administration , as practiced in cystic fibrosis , is currently being reviewed in clinical studies. Mucopharmaceuticals (such as acetylcysteine ) can provide relief in individual cases. Antitussives (such as codeine ), on the other hand, should only be used for dry coughs, as long as there is no additional risk of respiratory depression. If there is an iron deficiency that worsens the prognosis, the use of iron supplements should be considered. The effectiveness of the natural substance ectoin against chronic pneumonia was proven in an inhalation study carried out in the Ruhr area .

Indications for antibiotic therapy in acute exacerbations of chronic obstructive bronchitis or AECOPD:

  • With mild AECOPD: only with moderate to severe COPD after GOLD and purulent sputum, not with a procalcitonin value below 0.1 ng / mL
  • For moderate AECOPD: only with purulent sputum and a procalcitonin value from 0.1 ng / mL
  • With severe AECOPD: always.

Breathing aid

In the case of chronic respiratory failure caused by COPD, there are options for respiratory assistance: Long-term oxygen therapy and forms of ventilation . Regular training of the lung muscles with expiratory lung trainers can also make breathing easier in the long term. Special versions of these devices also make it easier to cough up the stuck mucus. This is achieved by the devices, due to their special construction, causing the airways to vibrate when you exhale. However, the use of an expiratory lung trainer is not recommended in the presence of a pneumothorax and should be discussed with a doctor. Even without aids, you can better ventilate the lungs and minimize symptoms through the "coachman's seat" (upper body upright, both arms supported on the knees and inhale and exhale deeply) and exhaling against resistance, for example lip brake (exhale in gusts against the pressure of the lips).

Oxygen administration

If the oxygen partial pressure (pO 2 ) values ​​are consistently below 60 mm Hg (severe hypoxemia ) in the blood gas analysis and the pCO 2 values ​​are not increased more, one speaks of oxygenatory or hypoxemic respiratory insufficiency (formerly respiratory partial insufficiency). Then a long-term supply of oxygen (long-term oxygen therapy) via a nasal cannula can significantly improve the condition and hold back complications such as pulmonary hypertension (pulmonary hypertension) and right heart failure and increasing deterioration in the fitness level. Life expectancy can improve if long-term oxygen therapy starts early enough in the course of the disease and is used for up to 24 hours a day. There are various systems for use at home ( liquid oxygen , oxygen concentrator ). Transportable devices are particularly suitable for patients who are mobile. By selecting an appropriate system, it must be prevented that the patient is immobilized .

Even if the resilience of patients with COPD is likely to increase through the administration of oxygen during exercise, the previous studies are insufficiently informative due to methodological deficiencies and low patient numbers to be able to make clear recommendations.

Ventilation

If the pCO 2 values ​​are permanently elevated ( hypercapnia , ventilation insufficiency, hypercapnic respiratory insufficiency, earlier global respiratory insufficiency), ventilation is possible. Here, too, the treatment can be carried out at home using suitable equipment. A ventilatory insufficiency means that the body can no longer provide the necessary work of breathing (work of the "breathing pump"). To protect yourself from complete exhaustion, the respiratory drive is reduced, which means a setpoint adjustment for the pCO 2 . In the acute situation ("exacerbated COPD" with pH values below 7.35 in the arterial blood) in the hospital, non-invasive ventilation methods are initially used to support the breathing pump , if possible . Innovative therapy methods such as pump-free extracorporeal lung support (iLA, interventional lung assist ) can also reduce the respiratory drive and work of breathing in this situation so that the patient can recover. The home ventilation therapy called, or "intermittent self-ventilation," pursued to relieve the respiratory pump by predominantly nocturnal ventilation so that the recovered respiratory pump in ventilator-free time is more powerful the purpose.

Lung volume reduction

Bronchoscopic lung volume reduction

Here, endobronchial one-way valves are bronchoscopically inserted into the corresponding lung lobes, which lead to atelectasis with subsequent volume reduction in the respective lung area. In this way, neighboring areas can be decompressed and better supplied with oxygen. Although the procedure is now beyond the trial trial stage, it has so far only been offered at larger centers.

This method can be used primarily in patients of the emphysema type of COPD who should also be non-smokers and of normal weight. The prerequisites are that the pulmonary emphysema is more pronounced in the corresponding lung lobe than in the rest of the lungs, there is little collateral ventilation and there is a sufficient degree of overinflation in the body plethysmography .

Surgical lung volume reduction

The reduction in lung volume is achieved surgically. Some patients benefit from it. The prerequisite for this procedure is that not the entire lung is diffusely emphysematous, but the pulmonary emphysema is locally circumscribed and limited. The procedure involves opening the rib cage and complications.

Lung transplant

A last option of therapy ( ultima ratio ) is lung transplantation (LTPL), in which either one or both lungs are transplanted. Due to the comorbidity of many COPD patients is found for this but only in individual cases indication .

Therapy of acute respiratory distress in COPD

Infection of the lungs or bronchi, in particular, can lead to a sudden deterioration in lung function in patients with the underlying disease COPD. This so-called exacerbation of infections is a common cause of severe shortness of breath that emergency services face outside of the hospital.

Basically, in an emergency, the same drug groups are used for treatment as for long-term therapy. Since sometimes patients with shortness of breath can no longer inhale the medication deeply enough through a spray, the medication is finely nebulized with oxygen or injected directly into the bloodstream via an infusion.

As standard therapy in an emergency, beta-2 sympathomimetics are finely nebulized for inhalation (e.g. salbutamol ) and parasympatholytic drugs (e.g. ipratropium bromide ) for inhalation. Furthermore, cortisone preparations (e.g. methylprednisolone ) are preferably injected directly into the bloodstream, the dose being 20-40 mg prednisolone equivalent. At higher initial doses of more than 100 mg as part of a cortisone blast, a study showed an increased mortality in ICU-dependent patients. If effective deep inhalation of the nebulized medication is not possible, beta2-sympathomimetics can also be injected into the bloodstream (e.g. terbutaline or reproterol ). The supply of additional oxygen is indicated when the oxygen saturation in the blood falls below 90%. Attention must be paid to any disturbed respiratory drive, which can be present in long-term COPD sufferers. Then the oxygen supply must be controlled and carefully dosed. If the standard measures do not stabilize and the patient is facing exhaustion of the lungs, artificial ventilation support through a tracheal tube or NIV procedure may be necessary. Passive CPAP therapy alone, without pressure support when breathing in, is not sufficient for exacerbated COPD.

In addition to standard therapy, various drugs can also be used, the effectiveness of which is questionable in exacerbated COPD: Theophylline was a standard drug for a long time, but is now only used as a reserve drug due to the side effects and limited therapeutic range. Magnesium , lidocaine and volatile anesthetic gases (e.g. sevoflurane ) as well as ketamine are attributed to bronchodilator properties, so that these are used in addition to standard therapy in individual cases.

Finally, the cause of the exacerbation should also be identified at an early stage. B. be treated with antibiotics.

Literature and evidence

General literature

  • Airmail - magazine for respiratory patients . Patient League Respiratory Diseases e. V., AG Lungensport in Deutschland e. V.
  • 1991: Hilmar Burchardi: Etiology and pathophysiology of acute respiratory failure (ARI). In: J. Kilian, H. Benzer, FW Ahnefeld (ed.): Basic principles of ventilation. Springer, Berlin a. a. 1991, ISBN 3-540-53078-9 , 2nd, unchanged edition, ibid. 1994, ISBN 3-540-57904-4 , pp. 47-91; here: pp. 81–87 ( obstructive respiratory diseases ).
  • 2006: Adrian Gillissen (Ed.): The chronic obstructive pulmonary disease. 3. Edition. UNI-MED Verlag, Bremen 2006, ISBN 3-89599-892-3 .
  • 2008: Herbert Renz-Polster, Steffen Krautzig, Jörg Braun: Basic textbook internal medicine with StudentConsult access: compact-tangible-understandable . 4th edition. Urban & Fischer Verlag, Elsevier, Munich 2008, ISBN 978-3-437-41053-6 .
  • 2009: Roland Kaiser : respite (= autobiographical experience with COPD). Edition Koch, Innsbruck 2009, ISBN 978-3-7081-0507-9 .
  • 2013: Thomas Linnemann: Quality of life, partnership and sexuality in COPD (electronic resource), supervisor: Jürg Hamacher. Saarland University and State Library, Saarbrücken 2013, DNB 1052909175 ( Dissertation University of Saarland , Saarbrücken 2012, online PDF, free of charge, 230 pages, 12.8 MB)
  • 2020: Gerd Herold and colleagues: Internal Medicine 2020. Self-published, Cologne 2020, ISBN 978-3-9814660-9-6 .

Review articles

  • Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , pp. 77-81 ( acute exacerbation of chronic obstructive bronchitis ).
  • GOLD: Update 2013
  • Marc Decramer, Wim Janssens, Marc Miravitlles: Chronic obstructive pulmonary disease. In: The Lancet . 379, 2012, pp. 1341-1351, doi: 10.1016 / S0140-6736 (11) 60968-9 .

Guidelines

Web links

Individual evidence

  1. ↑ National Association of Statutory Health Insurance Physicians for Permanent Airway Narrowing Lung Disease (COPD) .
  2. ↑ The top 10 causes of death
  3. ↑ copdcoalition.eu ( Memento of the original from July 13, 2015 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. @1@ 2Template: Webachiv / IABot / www.copdcoalition.eu
  4. ↑ L. Schirnhofer, B. Lamprecht u. a .: COPD prevalence in Salzburg, Austria: results from the Burden of Obstructive Lung Disease (BOLD) Study. In: Chest. Volume 131, Number 1, January 2007, pp. 29-36, ISSN  0012-3692 . doi: 10.1378 / chest.06-0365 . PMID 17218553 .
  5. ↑ Herbert Renz-Polster, Steffen Krautzig, Jörg Braun: Basic textbook internal medicine with StudentConsult access: compact-tangible-understandable . 4th edition. Urban & Fischer Verlag, Elsevier, 2008, ISBN 978-3-437-41053-6 , pp. 461 ff .
  6. ^ S. Andreas, SD Anker et al.: Neurohumoral activation as a link to systemic manifestations of chronic lung disease. In: Chest. Volume 128, Number 5, November 2005, pp. 3618-3624. doi: 10.1378 / chest.128.5.3618 . PMID 16304321 . (Review).
  7. ^ Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , pp. 77-81 ( acute exacerbation of chronic obstructive bronchitis ).
  8. ↑ Annabel H Nickol, Matthew C Frize et al. a .: A cross-sectional study of the prevalence and associations of iron deficiency in a cohort of patients with chronic obstructive pulmonary disease. In: BMJ Open. 5, 2015, p. E007911, doi: 10.1136 / bmjopen-2015-007911 .
  9. ↑ Susann Krieger: Pathology textbook for alternative practitioners. Reference work with therapy information. 6th edition. Haug, Stuttgart 2011, ISBN 978-3-8304-7426-5 , p. 142.
  10. ↑ abr: Biofuels and particulate matter more important than tobacco smoke? New risk factors for bronchi. ( Memento of May 11, 2012 in the Internet Archive ) (PDF; 2.7 MB) In: Medical Tribune. No. 42, October 16, 2009, Pneumology Special, p. 21 f.
  11. ↑ A. Biedermann, T. Köhnlein: Alpha-1-antitrypsin deficiency - a hidden cause of COPD: overview of pathogenesis, diagnosis, clinical features and therapy . In: Deutsches Ärzteblatt . Volume 103, Issue 26, dated June 30, 2006, pp. A-1828 / B-1569 / C-1518.
  12. ↑ Phyllis M. Quinn et al. : IgE-tailpiece associates with α-1-antitrypsin (A1AT) to protect IgE from proteolysis without compromising its ability to interact with FcεRI , nature , Scientific Reports (2016). 10.1038 / srep20509
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