Asthma

Asthma is a disease of the respiratory system characterized by chronic inflammation of the airways, whose clinical manifestations are heterogeneous and variable over time and consist of wheezing (wheezing), respiratory distress, oppression chest and cough.

The origin of the disease is complex and involves inflammation, intermittent obstruction, and hyperreactivity (increased bronchoconstrictor response) of the airways. The presence of edema and mucus secretion contribute to both obstruction and increased reactivity. The disease can have an acute, subacute, or chronic course, depending on the frequency, duration, and intensity of its clinical manifestations.

The manifestations of asthma occur in response to numerous triggering stimuli, both endogenous (internal to the person) and exogenous (from the environment). The underlying mechanisms include direct stimulation of the smooth muscles of the bronchial tree and indirect stimulation for their own cells to secrete active substances that produce the inflammatory reaction and bronchoconstriction. Among these triggering stimuli are exposure to an inappropriate environment (cold, wet or with allergens), exercise or effort and reactions to food or other substances as a consequence of increased intestinal permeability. Viral and bacterial illnesses of the upper respiratory tract and emotional stress can worsen symptoms.

Symptoms of asthma are wheezing, shortness of breath, chest tightness, and unproductive coughing at night or early in the morning. These symptoms occur with varying frequency and intensity, interspersed with asymptomatic periods where most patients feel fine. Conversely, when asthma symptoms flare up, an asthma attack occurs. It can be a short-term respiratory crisis, or prolonged with daily asthmatic attacks that can persist for several weeks. In a severe crisis, the airways can close, preventing the lungs from performing their gas exchange function (taking in oxygen and expelling carbon dioxide) to the point that vital organs cannot function either. In these cases, the asthmatic attack can cause death.

There are multiple therapeutic alternatives to avoid symptoms, control and alleviate them, as well as to recover from asthma attacks, with inhalers being the most frequent use.^{[citation required ]}

Classification

The asthma attack.

• Asthma produced by effort. Between 40 and 80% of the children's asthmatic population has broncoconstriction during the exercise, of short duration.
• Night asthma. It is another presentation, more frequent in poorly controlled patients, whose mortality (70 %) reaches the maximum in the early morning.
• Occupational asthma.
• Allergy asthma.
• Seasonal asthma.
• Unstable or chaotic asthma.

Based on the patterns of bronchial obstruction measured through flowmetry or spirometry-type recording devices:

• Intermittent asthma: the symptom appears less than once a week with night symptoms less than twice a month. The exacerbations tend to be brief and between a crisis and the next the patient is asymptomatic. In lung breathing tests, PEF or FEV1 are greater than 80%.
• Persistent asthma: has three varieties, mild persistent with symptoms more than once a week and PEF or FEV₁ 80 %, moderate persistent with daily symptoms and PEF or LVEF₁ between 50% and 80% and persistent severe with continuous symptoms.

As a basis for the control levels of patients already diagnosed with asthma:

• Controlled: without daily or night symptoms, you do not need rescue medications, no exacerbations and a normal PEF.
• Partially controlled: daytime symptoms or more than twice a week, some nocturnal symptom, often merits the use of rescue drugs more than twice a week, with one or more crisis per year.
• Not controlled: three or more asthma features, with weekly exacerbations.

Epidemiology

Asthma is a common disease that varies widely from country to country. It affects around 3 to 7% of the adult population, being more frequent in children. It is one of the most important chronic diseases, that is, of prolonged duration, in children. It is more frequent in males in a 2:1 ratio, but upon reaching puberty, this ratio tends to equalize. In the last twenty years there has been an increase in its incidence due in part to environmental contamination and its consequences, and in part to the increase in the world population. For example, the World Health Organization reported that 8% of the Swiss population suffered from asthma, compared to only 2% 25-30 years ago.

The disease has a strong hereditary component, expressed as a family history of rhinitis, urticaria and eczema, for example. However, many asthmatics do not have a family history indicating an atopic association. Up to now, none of the infectious hypotheses proposed as the origin of the picture have been proven.

The highest levels of global asthma, according to the Global Initiative for Asthma (GINA) in February 2004, occurred in approximately 30% of children in the United Kingdom, New Zealand, and Australia or 20% of children in Peru, New Zealand and Australia (varies depending on the research method used for calculations) and approximately 25% of adults in Great Britain, Australia and Canada.

There is a higher percentage of smokers and allergic concomitant diseases such as rhinitis, conjunctivitis and dermatitis among patients diagnosed with allergic asthma than in other patients.

Causes

Bronchial asthma is common in young people with a history of recurrent colds, or with a family history of asthma. Asthma attacks are related to the consumption of certain foods or the presence of certain allergens.

The causes that cause bronchial asthma and motivate the response of mainly immunological mechanisms are classified as:

• Extrinsic: Initiated in childhood with positive family history for allergies and is associated with type 1 hypersensitivity and other allergic manifestations (IgE), induced by allergen agents such as pollen, wool, dust, etc., or atmospheric pollution, irritating matter, weather variations, aspergilosis and others. In about 50% of children with asthma and a smaller percentage of adults, allergen exposure is partially or substantially responsible for asmatic inflammation through hypersensitivity reactions. The crises are sudden, self-limited and short in duration. They cure with good prognosis, respond to immunotherapy and long-term steroids by inhaled with tiny systemic absorption, so the effects on the rest of the body are virtually nonexistent.
• Intrinsic or idiopathic: It usually begins over 35 years and without personal or family history. It starts with non-immunological stimuli, without elevating IgE, represented by microbes, fungi, cough, psychic disorders, stress, etc.
• Mixtures: Frequency of bacterial nature of intrinsic and extrinsic factors.

Environmental

There are several environmental risk factors that are associated with asthma:

• Air of poor quality, produced by automotive pollution or high levels of ozone, tends to be repeatedly associated with increased asmatic morbidity and has been suggested an association with the first occurrence of asthma in an individual.
• Environmental smoke, especially for maternal smokers, is associated with increased risk of prevalence and asmatic morbidity including respiratory infections.
• Viral infections at an early age, together with exposure to other children in childcare may be protective against asthma, although the results are controversial and this protection may appear in the context of genetic predisposition.
• The use of early antibiotics in life can cause the appearance of asthma by modifying the normal microbial flora of an individual, predisposing it to a modification of the immune system.
• Celiac disease and non-Celiac gluten sensitivity without acknowledging or treating, as they usually have no digestive symptoms or are mild, are often associated with recurrent processes of high respiratory pathways of an immuno-allergic nature, such as asthma, rhinitis and pharynoamigdalitis, among others. Approximately 20% of people with non-cellic gluten sensitivity without treatment present, associated with gluten intolerance, IgE allergies mediated to one or more inhalers, food or metals, among which the most common are dust mites, grams, hair of dogs or cats, fish or nickel.
• caesareans tend to associate with asthma more often than vaginal delivery, apparently for reasons similar to antibiotics, i.e. a modification of the microbial and immune component of the individual born by a caesarean.
• Psychological stress.
• Viral infections. Several viral infections such as HSV, VSV, CSV, have been correlated with various types of asthma

Increased intestinal permeability

Illness of the wall of the intestine with increased permeability. The two most potent factors that cause it are certain intestinal bacteria and gluten, regardless of genetic predisposition, i.e., both in celiacs and in non-Celiacs. This allows the unchecked passage of substances to the bloodstream, with the consequent possible development of autoimmune diseases, inflammatory, infections, allergies, asthma or cancers, both intestinal and other organs.

In addition to inhalation, asthma can be caused by reactions to food or substances that enter through the intestine. For this reason, the increase in intestinal permeability seems to play a key role. Approximately 40% of people with asthma have been shown to have increased intestinal permeability.

The intestine has a layer of cells inside that form a barrier. Its mission is, in addition to digesting nutrients, to act by defending the body from the external enemy of the environment (substances that we ingest and microorganisms present in the intestine). It does this by keeping the tight junctions between cells (the "pores" of the intestine) closed, to prevent the uncontrolled access of substances, toxins, chemicals, microorganisms and macromolecules, which could otherwise enter the bloodstream. When these intercellular tight junctions do not function well and instead of being closed or practically closed, as they should be, they are open without control, an increase in intestinal permeability occurs ("pores" too open). This opening causes substances to enter the body and, depending on the person's genetic predisposition, autoimmune and inflammatory diseases, infections, allergies, asthma or cancers, both intestinal and in other organs, may develop.

The two most potent factors that cause increased intestinal permeability are certain intestinal bacteria and gliadin (main toxic fraction of gluten), regardless of genetic predisposition, that is, both in celiac and non-celiac patients. Other possible causes are prematurity and exposure to radiation, chemotherapy, or certain toxins.

Genetics

More than 100 genes have been associated with asthma in at least one genetic study. Although a gene replication component still needs to be added to the study, by 2005, some 25 genes had been associated with asthma. asthma in six or more different populations, including GSTM1, IL-10, IL-4, IL-13, CTLA-4, CD14, TNF, and β-2 adrenergic receptor (ADRB2).

Many of these genes are related to the immune system or modulate inflammation processes. However, despite this list of genes and their possible association with asthma, the results are not entirely consistent between different populations, that is, these genes are not associated with asthma under all conditions, but rather cause Asthma genetics is a complex interplay of various additional factors.

Pathogenesis

Inflamed airways and broncoconstriction in asthma.

The pathogenesis of asthma is complex, but it includes three fundamental components:

• Airway inflation.
• Intermittent obstruction to airflow.
• Bronchial hyperreactivity.

Airway inflammation

Although asthma is known to be a condition caused by acute, subacute, or chronic inflammation (from the Latin inflammatio, to ignite, make fire) of the airways, the presence of edema or secretions it contributes to both obstruction and hyperresponsiveness. Many inflammatory cells are involved in this inflammation: mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes. The activation of these cells and the subsequent production of inflammatory mediators may be of greater relevance than the mere presence of these cells in the airways.

This chronic inflammatory process may lead to structural changes, such as fibrosis, thickening or hypertrophy of bronchial smooth muscle, hypertrophy of glands, and angiogenesis, which may lead to irreversible airway obstruction.

Cellular immunity

Initial studies in patients dying of status asthmaticus revealed marked inflammation of the bronchial tree with histological studies of the affected airways confirming the presence of longstanding inflammatory cells.

The use of bronchoalveolar lavage has shown that mast cells play an important role as mediators of the immediate response to allergen, airway inflammation, and food-related and exertion-induced hyperresponsiveness. Other cells responsible for chronic inflammation causing bronchial hyperresponsiveness are macrophages, eosinophils and T lymphocytes, all of which are activated in asthma, even in asymptomatic patients. A line of T lymphocytes, T_H2 cells, are programmed to produce certain cytokines that lead to the characteristic eosinophilic inflammation. This programming involves antigen-presenting cells, such as dendritic cells in the epithelium of the airways. Other inflammatory mediators produce reactions such as vascular congestion, edema, increased mucus production, etc.

On the bronchial epithelium, an increased expression of the major histocompatibility complex type II and other infiltrating cells such as monocytes are demonstrated. The clinical severity of asthma is closely correlated with the severity of the inflammatory response, suggesting a complicated interplay between these cells and the mediators they generate, such as IL-3, IL-5, and GM-CSF. For example, alveolar macrophages from asthmatic patients produce twice as much GM-CSF as non-asthmatic subjects. IL-4 and Interferon gamma are elemental in the biosynthesis of IgE.

Intermittent airflow obstruction

Airflow obstruction is caused by several factors: acute bronchoconstriction, airway edema, chronic mucus plug formation, and airway remodeling. Bronchoconstriction is caused by the release of immunoglobulin E-dependent mediators upon exposure to an airborne allergen and is the first component of the early asthmatic response. The edema occurs between 6 and 24 hours after contact with the allergen, and its appearance corresponds to the late asthmatic response. The formation of mucous plugs occurs due to the accumulation of exudate rich in proteins and cellular debris, and takes weeks to develop. Airway remodeling is associated with structural changes of the bronchial tree due to inflammation maintained over time and affects the way The reversibility of the obstruction is very important.

Pathology

The morphological changes seen in asthma have been described mainly from samples of patients who died from status asthmaticus, that is, an acute asthma syndrome, however, it seems that the histopathology in cases non-fatal is very similar. Grossly, the lungs appear distended due to overinflation and areas of atelectasis may appear. The most conspicuous finding is the occlusion of the bronchi and bronchioles by thick plugs of mucus.

Under the microscope, mucous plugs contain coils of epithelial cells forming so-called Curschmann coils, which can often be seen in the sputum of asthmatic patients. In addition, the mucus contains Charcot-Leyden crystals and eosinophils. Other histologic features of asthma include thickening of the bronchial epithelial basement membrane, edema, and an infiltrate over the bronchial walls with prominence of eosinophils and hypertrophy of the bronchial wall muscle as well as submucosal glands, reflecting prolonged bronchoconstriction.

In bronchial lavage of asthmatic patients, increased numbers of inflammatory cells, including eosinophils, macrophages, and lymphocytes, are observed compared with non-asthmatic patients, even in asymptomatic asthmatic patients with normal lung functions—including patients with allergic asthma such as with non-allergic asthma.

Clinical picture

	Sibilances The sound of the sibilances heard through a stethoscope.
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The most characteristic symptoms of bronchial asthma are dyspnea or respiratory distress of variable intensity and duration and with the presence of bronchial spasms, usually accompanied by coughing, mucus secretions and wheezing. It is also characterized by chest rigidity in the patient and his wheezing. In some patients these symptoms persist at a low level, while in others, the symptoms can be severe and last several days or weeks. Under more severe conditions, lung ventilatory functions can be impaired, leading to cyanosis and even death.

Evolution

The evolution of the asthmatic reaction constitutes a process whose main phases are:

• Early phase. It takes place as a reaction of immunological or non-immunological mechanisms against allergenic agents, microbials, etc. and is characterized by constriction of light (aberture in the duct) of bronchioles.
• Late phase. It comes from the persistence of the state of crisis and is an accentuation of the same characterized by edema and bronchial hyperreactivity, that is, an easy predisposition to broncoconstriction.
• Chronic phase. It takes place when the previous state does not decrease after the usual treatment and, often, cough, accentuates bronchial irritation. This involves damage to the epithelial lining of the bronchial, persistence of bronchial hyperreactivity and blocking moco of the airways.

When asthma or its symptoms, such as a cough, do not improve, it may be due to:

• Some trigger in the patient's environment, such as at home, school or work: dust, animals, cockroaches, mold and pollen, cold air, tobacco smoke, among others.
• Some occupational trigger, in which it is characteristic that the patient improves during the weekends or when on vacation.
• The patient is not taking any medication, including the inhaler, in the right way. In some cases it will be necessary to change medication for some more effective for long-term control.
• Asthma may be more serious than it is thought, so recurring asthma cases should be consulted with asthma specialists.
• It may not be asthma, but another disease that affects the patient.

Diagnosis

The diagnosis of asthma begins with an evaluation of the clinical picture, family history and history of risk or previous attacks taking into account the time of evolution of the picture and attacks. Most cases of asthma are associated with allergic conditions, so diagnosing conditions such as rhinitis and eczema lead to suspicion of asthma in patients with the correct symptoms: coughing, choking, and chest tightness. Physical examination usually usually reveals the wheezing that characterizes asthma. It is important to assess whether the patient already received any treatment before the medical consultation, as well as the triggering events of the crisis.

The physical examination is vital, sometimes there is not enough time to examine it in detail, however, the characteristic wheezing is perceived on auscultation. In some severe cases, the bronchoobstruction is such that auscultatory silence occurs, however, the rest of the clinic is so florid due to respiratory incapacity that the diagnosis does not warrant the perception of wheezing for the treatment of these severe asthma attacks. Such distress and thirst for air may indicate a serious attack that requires immediate rescue treatment to reverse the bronchospasm before continuing with a detailed physical examination. Inspection of the chest may show subcostal or intercostal indrawing or retraction. The dimensions of the thorax in chronic asthmatic patients vary in comparison with non-asthmatic children, characteristic of rib flattening. The inspection can reveal details to the diagnosis, such as the discovery of allergic dermatitis, conjunctivitis, etc.

There are several tests that help diagnose asthma, including lung function tests, allergy tests, blood tests, chest and sinus x-rays.

Lung Function

Lung function tests include:

• Spirometry: measures respiratory capacity and expiration speed and is used to determine the amount of lung obstruction. Spirometry can be measured after treatment begins to evaluate the effectiveness of this.
• Spiratory flow: It is the maximum spiration speed measured with a special device for it.^{[chuckles]required]} It can be important in the diagnosis and monitoring of asthma. Ideally, the results should be compared to the best previous measurements of the patient using their own peak flow meter.
  

  Spiral flow peak meters.
• Metacoline test: used mostly in adults, metacoline is inhaled, which causes the airways to become narrow in the presence of asthma, causing lung function values to fall. The effects of metacoline are reversed with a bronchodilator at the end of the test.
• Saturation of oxygen and gasometry in more severe cases.

X-ray

The chest X-ray allows us to identify some characteristics in the thoracic organs that are related to bronchial asthma, as well as to confirm or rule out other associated diseases. In this way, the exam is indicated when the patient debuts; any known asthmatic child who has sudden symptoms to rule out the possibility of a foreign body, laryngotracheobronchitis, pneumonia, or other pathologies; when the response to treatment is poor; when added sounds are heard in addition to wheezing and when the patient has a change in the behavior of their asthma attacks.^{[citation required]}

Air entrapment images tend towards the intercostal spaces which horizontalizes the ribs on the radiograph. As there is edema, an infiltrate can be seen surrounding the bilateral pulmonary hila, which is nothing more than peribronchial edema with such mucous content that it is visualized on the radiograph as an increase in the bronchovascular network.^{[citation required]}

Treatment

The conventional treatment of bronchial asthma can be:

• Symptom: It is intended to interrupt the crisis by means of quick-acting medicines such as adrenaline, corticosteroids, oxygen therapy, etc.
• Preventive: Indicates the regular use of bronchodilators, antihistamines, corticosteroids, respiratory therapy, specific immunotherapy, etc.

Treatment should include identifying triggers such as pollen, mites, dust, tobacco smoke, pet hair, or aspirin and limiting or, if possible, eliminating exposure to those triggers. If avoiding stimulating factors proves insufficient, then medical treatment can be resorted to. Desensitization (gradual process whereby the response to a stimulus is eliminated by repeating the stimulus until no more response is produced) is, for the moment, the only cure available for this disease. Other forms of treatment include pharmacological relief, preventive medications, long-acting β2-receptor agonists, and emergency treatment.

Medical treatment

The specific pharmacological treatment recommended for patients with asthma depends on the severity of their disease and the frequency of onset of symptoms. Specific asthma treatments are classified roughly under preventive medicines and emergency. The EPR-2 report (Expert Panel Report 2), a protocol for the diagnosis and management of asthma, as well as reports from other international societies are used and supported by many clinicians.

KTR respiratory kinesiology is indicated as a central pillar in the treatment.

Bronchodilators are recommended for short-term relief in virtually all patients with asthma. For those who have only occasional attacks, no other type of medication is needed. For those with moderately persistent symptoms, i.e., more than two attacks per week, low-concentration inhaled glucocorticoids are suggested or, alternatively, an oral leukotriene modifier, a mast cell membrane stabilizer, may be given. or theophylline. For individuals presenting with daily seizures, a higher dose of glucocorticoid is suggested in conjunction with inhaled long-acting β-2 agonists or a leukotriene modifier or theophylline may substitute for the β-agonist -2. In severe asthmatic attacks, oral glucocorticoids can be added to these treatments during severe attacks.

The discovery in 2006 that asthma can be caused by the overgrowth of a special type of NK cell may ultimately lead to the development of a better and more targeted group of drugs. NK T cells appear to be resistant to corticosteroids, one of the current main lines of treatment. Other promising investigational options include the use of statins, which are drugs that lower the level of cholesterol in the blood plasma. and the use of fish oil supplements, to reduce inflammation in the airways.

Corticosteroid treatment has been identified as having better efficacy than treatment with leukotriene receptor antagonist drugs.

Nebulizers

Classic salmeterol inhaler, a bronchodilator.

Nebulizers provide a more continuous, long-lasting dose by vaporizing medicine diluted in saline, which the patient inhales until the full dose is delivered. There is no evidence that they are more effective than a spacer. Flare-up relief includes medications:

• Agonists of adrenergic receptors β₂ short duration, such as salbutamol, levalbuterol, terbutalin and bitolterol. The side effects that included the appearance of tremors have been greatly reduced with inhaled treatments, which allows the medication to target specifically in the lungs. Medicines that are administered by mouth or injected tend to be distributed by the rest of the body, increasing the possibility of the occurrence of adverse effects, including heart effects by agonist activity of β receptors₁ causing arterial hypertension and heart rate disorders. With the outlet of more selective drugs, these side effects have become less frequent. Agonists of β adrenergic receptors₂ They usually produce desensitation in the patient, so its effectiveness can decrease with its chronic use, resulting in the appearance of refractory asthma and sudden death.
• Less selective adrenergic agonists such as inhaled adrenaline and ephedrine tablets have also been used. These drugs have heart-adverse effects at similar or lower frequencies than albuterol. Being used as a symptomatic relief medicine and not for prolonged use, inhaled adrenaline has proven to be an effective agent in the culmination of a asthmatic crisis. In emergency situations, these drugs can be administered in an injected manner, although this practice has decreased due to side effects.
• Anticolinergic drugs, such as ipratropio bromide may be used and do not have the heart effects, so they can be administered in patients with heart disease, however, take about an hour to have effect and are not as powerful as agonists of β adrenergic receptors.₂.
• Inhaled glucocorticoids are usually considered preventive medications, however, the benefit of 250 μg of beclomethasone has been shown when taken in a combination with 100 μg of albuterol.

Long-Acting Agonists

Long-acting bronchodilators have a very similar molecular structure to short-acting β₂ agonists, but have longer side chains, resulting in a 12-hour duration of effect, so which are used for symptomatic relief at night. Despite the fact that individuals who use these medications report an improvement in symptom control, they are not medications that replace the requirement for routine preventives, and because they take a long time to take effect, the use of short-acting dilators may be necessary. In 2005, the US Food and Drug Administration wrote a report alerting the public that the use of long-acting β₂ agonists has been noted to lead to worsening asthma symptoms and some cases of death. sudden.

Some of the commercially available long-acting β₂ agonists include salmeterol, formoterol, babmuterol, and an oral preparation of albuterol. Combinations of these long-acting β₂ agonists along with inhaled steroids have become more common, the most common being the combination of salmeterol and fluticasone.

Vaccines

Inmunotherapy with specific allergens (vaccines) has demonstrated its usefulness in the management of bronchial asthma in primary health care (PHC) as it is the only treatment capable of changing the natural course of the disease. Its greatest effectiveness is in the mild and moderate intermittent and persistent forms.

Sublingual immunotherapy has proven to be an effective treatment in children with rhinitis and asthma caused by sensitization to seasonal allergens (such as allergy to pollen) and its use in several European countries currently exceeds that of classical subcutaneous immunotherapy. In the case of sensitizations caused by perennial allergens (which manifest throughout the year, such as allergy to dust mites, animal hair, etc.), the evidence is not conclusive and more studies are needed to demonstrate the efficacy of sublingual immunotherapy.

Allergen immunotherapy, administered both subcutaneously and sublingually, is absolutely contraindicated in children under two years of age, people with uncontrolled or poorly controlled asthma, patients with active autoimmune diseases, and AIDS patients. Its initiation during pregnancy is absolutely contraindicated, but a well-tolerated pre-existing treatment could be continued, with caution and under medical supervision. In children between the ages of two and five, allergen immunotherapy is only indicated in specific cases.

Pharmaceutical

Symptom control during asthma attacks includes reducing wheezing and shortness of breath, which usually occurs effectively with the use of short-acting bronchodilators. It is customary to provide these medications in the form of portable metered dose inhalers. In younger patients, for whom coordination of inhalers is difficult, or who find it difficult to hold their breath for 10 seconds after inhalation, such as the elderly, the use of a spacer, which is a cylinder, may be recommended. plastic that mixes medication with air in a single tube, making it easier for the patient to receive a full dose of medication and allowing the active agent to be dispersed in smaller, inhalable portions.

Stage I

These are relatively mild and intermittent cases with symptoms or seizures occurring less than 1 time per week or with nocturnal symptoms about 2 times per month, CO2 partial pressure of 35 to 45 mmHg, O2 partial pressure of 80 mmHg and an FEV of 800 ml and with a peak flow >50% of the stipulated value. These are cases in which, during a crisis, it is recommended to nebulize with 3-5 ml of physiological solution with one of the following bronchodilators, with a frequency of every 4 to 6 hours:

• Ipratropio bromide plus fenoterol.
• Salbutamol or terbutalin.
• Clembuterol or metaproterenol.

If it does not improve, subcutaneous terbutaline can be administered every hour for 2 doses or by intravenous infusion.

Stage II

These are relatively mild but persistent cases with symptoms or seizures occurring more than 1 time per week but less than 1 time per day or with nocturnal symptoms more than 2 times per month, a partial pressure of CO₂ of 35 mmHg, a partial pressure of O₂ between 60 and 80 mmHg and an FEV between 300-800 ml and with a peak flow <50% of the stipulated value. These are cases that, during a crisis, it is recommended to nebulize the same as stage I and if it does not improve, use:

• Aminophylline diluted in physiological solution by IV every 4 to 6 hours or by continuous infusion, in the opinion of the treating health professional.
• Cases of aminophylline poisoning are common in patients receiving extrahospital oral theophylline, in patients with COPD, heart disease, elderly people and patients with chronic liver disease. You can use 3 or 4 doses of adrenaline.

Stage III

These are moderate cases requiring the use of beta-mimetics on a daily basis or with altered physical activity on a daily basis and nocturnal symptoms more than 1 time per week, a partial pressure of CO₂ of 40-45 mmHg, an O₂ partial pressure less than 60 mmHg and with a peak flow <30% of the stipulated value. These are cases in which, during a crisis, nebulization and aminophylline are recommended as in stage II and if no improvement is used:

• Parental steroids, such as hydrocortisone or methylprednisolone.
• Inhaled steroids such as beclometasone dipropionate or budesonide.
• Oral steroids, like prednisone.

Stage IV

These are patients with frank respiratory failure, cyanosis, a silent chest on auscultation, and a weak inspiratory effort. Treatment is usually similar to stage III with endotracheal intubation and mechanical ventilation.

Forecast

In most cases of asthma, the disease produces intervals of respiratory distress and suffocation, which can be discouraging or even disabling for the patient and not fatal. With proper treatment and adherence to therapeutic recommendations, patients with asthma can maintain a productive life. Occasionally, the disease resolves on its own. In its most severe forms, pulmonary hyperinflation can progress over time to eventually cause emphysema. Bacterial infections superimposed on asthma can lead to chronic bronchitis, bronchiectasis, or pneumonia. In some less common cases, especially in adult patients, uncontrolled asthma can lead to cor pulmonale and heart failure.

Therapeutic advice

Act on the cause of the asthma if it is of allergic origin, carrying out the eviction (separation) of the allergen, either by trying to desensitize it. The results are good with mites, pollens and less effective with animals. In order to prevent seizures, asthmatics can use devices (peak-flow) to measure their expiratory peak-flow velocity, control bronchial obstruction and therefore adapt their treatment with the result obtained (bronchodilator action decision for example, fasting or modification of the background treatment in collaboration with the doctor). Therefore, it is very important to develop a therapeutic education of the patient.

According to several clinical trials, an increase in the consumption of fruits, vegetables and grains helps stop the progression of asthma. In the case of switching to a vegetarian diet, 71% of subjects reported a significant reduction in symptoms after 4 months and 92% after one year. Antioxidant supplements (vitamin A, C, E), vitamin B8 or polyunsaturated fatty acids (omega 3 and 6), however, do not have a proven effect.

What should not be done in the therapeutic management of asthma.