TREATMENT Severe Acute Asthma, ALTERNATIVE THERAPIES

TREATMENT Severe Acute Asthma

The primary goal is prevention of life-threatening asthma by early recognition of signs of deterioration and early intervention. As such, the principal goals of treatment include

1. Correction of significant hypoxemia
2.  Rapid reversal of airflow obstruction
3. Reduction of the likelihood of recurrence of severe airflow obstruction
4. Development of a written action plan in case of a further exacerbation

These goals are best achieved by early initiation of treatment and close monitoring of objective measures of oxygenation and lung function. Early response to treatment as measured by the improvement in FEV1 at 30 minutes following inhaled β2-agonists is the best predictor of outcome.  Providing adequate oxygen supplementation to maintain oxygen (O2) saturations above 90% (or above 95% in pregnant women) is essential. In children younger than 6 years of age, in whom lung function measures are difficult to obtain, a combination of objective (e.g., oxygen saturation, capillaryCO2, respiratory rate, and heart rate) and subjective measures may be used to assess
severity. The primary therapy of acute exacerbations is pharmacologic, which includes inhaled short-acting β2-agonists and, depending on the severity, systemic corticosteroids and O2 (Figs. 26–6 and 26–7). It is important that therapy not be delayed, so the initial history and physical examination should be obtained while initial therapy is being provided. Patients at risk for life-threatening exacerbations require special attention. Risk factors include a history of previous severe asthma exacerbations (e.g., hospitalizations, intubations, or hypoxic seizures), complicating illnesses (e.g., cardiac disease, diabetes, illicit  drug use, or psychosis), use of more than two canisters per month of
short-acting inhaled β2-agonists, and current intake of oral corticosteroids or recent withdrawal from oral corticosteroids.  A complete blood count may be appropriate for patients with fever or purulent sputum, but many patients will have a leukocytosis

from a viral infection or secondary to corticosteroid administration. Routine chest radiographs have not been shown to be of value unless physical findings suggestive of consolidations or pneumothoraces are present.  Serum electrolytes should be monitored if highdose continuous inhaled or systemic β2-agonists are to be used because they can produce transient decreases in potassium, magnesium, and phosphate.  The combination of high-dose β2-agonists and systemic corticosteroids occasionally may result in excessive elevations of glucose. Initial response should be achieved within minutes, and most patients experience significant improvement within the first 30 to 60 minutes of therapy, with most patients doubling their FEV1 or PEF.28 In patients ultimately admitted to the hospital, only a 10% to 20% predicted improvement is seen within the first 2 hours.Hypoxemia, primarily a result of ventilation-perfusion mismatch, is immediately correctable by low-flow oxygen.  While reversal of lung function into the normal range may take 12 to 24 hours, complete restoration takes much longer—up to 3 to 7 days. A strategy to   prevent recurrence such as systemic corticosteroids and PEF monitoring should be used.  It is essential to provide the patient with a
self-management plan that includes a written action plan for dealing with exacerbations. Patients at risk for severe exacerbations should be taught how to use a peak-flow meter and monitor morning peak flows at home.  In young children, an increased respiratory rate, increased heart rate, and inability to speak more than one or two words between breaths are signs of severe obstruction.  Oxygen saturations by pulse oximetry and peak flows should be measured in all patients not
completely responding to initial intensive inhaled β2-agonist therapy.Initially, on admission, the peak flows or clinical symptoms should be monitored every 2 to 4 hours. Prior to discharge from the emergency department or hospital, the patient should be given a sufficient supply of prednisone, taught the purpose of the medications and proper inhaler technique, and given an appointment for a follow-up visit.   Early recognition of deterioration and aggressive treatment are the keys to successful treatment of acute asthma exacerbations. Thus patient and/or parent education teaching self-management skills and written action plans for early institution of therapy for acute exacerbations

improve outcomes.7 For more moderate to severe patients, this therapeutic plan also may include the availability of oral prednisone to begin at home.  Easy access by telephone to health care providers is also needed. Because of the rapid progression to severe asthma that can occur, patients and parents should be encouraged to communicate promptly with their asthma care provider during an exacerbation. Systemic corticosteroids and aggressive use of inhaled β2-agonists continue to be the cornerstones of therapy for acute severe asthma exacerbations. Figures 26–6 and 26–7 illustrate the recommended therapies for the treatment of acute asthma exacerbations in home and emergency department/hospital settings, respectively.  The dosages of the drugs for acute severe asthma are provided in Table 26–6. Institutions should strongly consider developing critical-pathways/treatment algorithms for their emergency departments because their implementation
has been shown to improve outcomes and decrease the cost of care.

NONPHARMACOLOGIC THERAPY
Infants and young children may be mildly dehydrated owing to increased insensible loss, vomiting, and decreased intake. Unless dehydration has occurred, increased fluid therapy is not indicated in acute asthma management because the capillary leak from cytokines and increased negative intrathoracic pressures may promote edema in the airways.  Correction of significant dehydration is always indicated, and the urine specific gravity may help to guide therapy in young children, in whom the state of hydration may be difficult to determine.  Chest physical therapy and mucolytics are not indicated in the

therapy of acute asthma. Sedatives should not be given because anxiety may be a sign of hypoxemia, which could be worsened by central nervous system depressants. Antibiotics also are not indicated routinely because viral respiratory tract infections are the primary cause of asthma exacerbations. Antibiotics should be reserved for patients who have signs and symptoms of pneumonia (e.g., fever, pulmonary consolidation, and purulent sputum from polymorphonuclear leukocytes). Mycoplasma and Chlamydia are infrequent causes of severe asthma exacerbations but should be considered in patients with high oxygen requirements.espiratory failure or impending respiratory failure as measured
by rising PaCO2 (>45 mm Hg) or failure to correct hypoxemia with supplemental oxygen therapy is treated with intubation and mechanical ventilation. In order to prevent barotrauma and pneumothoraces from excess positive pressure, it is recommended that controlled hypoventilation or permissive hypercapnia be used (correcting the hypoxemia, PaO2 > 60 mm Hg, but allowing the PaCO2 to rise to the high 60 mm Hg range).

PHARMACOTHERAPY

β2-AGONISTS 

The short-acting inhaled β2-agonists are the most effective bronchodilators and the treatment of first choice for the management of severe acute asthma.  Up to 66% of adults presenting to an emergency department require only three doses of 2.5 mg nebulized albuterol to be discharged.  Most well-controlled clinical trials have demonstrated equal to greater efficacy and greater safety of aerosolized β2-agonists over systemic administration regardless of the severity of obstruction. Systemic adverse effects, hypokalemia, hyperglycemia, tachycardia, and cardiac dysrhythmias are more pronounced in patients receiving systemic β2- agonist therapy. Children younger than 2 years of age achieve clinically significant responses from nebulized albuterol.  Effective doses of aerosolized β2-agonists can be delivered successfully through mechanical ventilator circuits to infants, children,

and adults in respiratory failure secondary to severe airways obstruction.  Frequent administration of inhaled β2-agonists (every 20 minutes or continuous nebulization) has been found to be superior to the same dosage administered at 1-hour intervals.  In the subset of more severely obstructed patients, continuous nebulization decreases the hospital admission rate, provides greater improvement in the FEV1 and PEF, and reduces duration of hospitalization when compared with intermittent (hourly) nebulized albuterol in the same total dose. Thus continuous nebulization is recommended for patients having an unsatisfactory response (achieving less than 50% of normal FEV1 or PEF) following the initial three doses (every 20 minutes) of aerosolized β2-agonists and potentially for patients presenting initially with PEF or FEV1 values of less than 30% of predicted normal.  The doses of inhaled β2-agonists for severe acute asthma (see Table 26–6) have been derived empirically. The β2-agonists follow a log-linear dose-response curve. In addition, the dose-response curve is shifted to the right by more severe bronchospasm or by increased concentrations of bronchospastic mediators, which is characteristic of functional antagonists.  The ability to increase the dose of the short-acting aerosolized β2-agonists by as much as five- to tenfold over doses producing adequate bronchodilation in chronic stable asthmatics is what contributes to their efficacy in reversing the bronchospasm of acute severe asthma.  The nebulizer dose of inhaled β2-agonists for children often is listed on a weight basis (milligrams per kilogram). However, a fixed minimal dose (2.5 mg albuterol or equivalent), as opposed to a weight-adjusted dose, is more appropriate in younger children because children younger than 5 years of age receive a lower lung dose.  Adults dosed on a weight basis demonstrate excessive cardiac stimulation, so they have fixed maximal doses27 (see Table 26–6). Initial doses of inhaled β2-agonists can produce vasodilation, worsening ventilation-perfusion mismatch, slightly lowering oxygen saturation or Pao2. High-doses of inhaled β2-agonists can produce a decrease in serum potassium concentration, an increase in heart rate, and an increase in serum glucose concentration.
However, both children and adults receiving continuously nebulized β2-agonists have demonstrated decreased heart rates as their lung function improves.  Thus an elevated heart rate is not an indication
to use lower doses or to avoid using inhaled β2-agonists. Some controversy exists concerning the most cost-effective delivery system (MDI plus holding chamber versus nebulization) to be used in treating severe acute asthma in the emergency department and hospital (see below).  The DPIs are currently not indicated for the treatment of severe acute asthma exacerbations. Patients with more severe obstruction may not be able to generate sufficient peak inspiratory flows for adequate delivery.

CORTICOSTEROIDS
Systemic corticosteroids are indicated in all patients with acute severe asthma not responding completely to initial inhaled β2-agonist administration (every 20 minutes for three to four doses). Intravenous therapy offers no therapeutic advantage over oral administration.2This therapy usually is continued until hospital discharge. Tapering the dose in acute asthma following discharge from the hospital appears unnecessary, provided that patients are prescribed inhaled corticosteroids for outpatient therapy. Most patients achieve 70% of predicted normal FEV1 within 48 hours and 80% of predicted by 6 days after plateauing by day 3. Thus, maintaining systemic corticosteroid courses for 10 to 14 days may be unnecessarily long in some patients. Indeed, many patients not admitted to the hospital respond to 3- to 5-day courses of systemic corticosteroids. Short courses of oral prednisone (3 to 10 days) have been effective in preventing hospitalizations in infants and young children.2 It is recommended that a full dose of the corticosteroid be continued until the patient’s peak flow reaches 80% of predicted normal or personal best. Multiple daily dosing of systemic corticosteroids for the initial therapy of acute asthma exacerbations appears warranted because
receptor-binding affinities of lung corticosteroid receptors are decreased in the face of airway inflammation. However, patients with less severe exacerbations may be treated adequately with oncedaily administration. High-dose and very-high-pulse-dose corticosteroid regimens have not been shown to enhance the outcomes in severe acute asthma but are associated with a higher likelihood of
side effects. A recommended practice is to increase or double the dose of inhaled corticosteroids in patients who are experiencing a deterioration of their asthma control to prevent an exacerbation that requires emergency care. Studies of inhaled corticosteroids (ICSs) in acute exacerbations of asthma have provided conflicting results. Currently, there is insufficient evidence supporting efficacy in the emergency department setting.  However, there is some evidence that prescribing ICSs on discharge from the emergency department reduces the risk of relapse. This policy seems like a reasonable recommendation because inflammation is the underlying cause of deterioration in most cases.

ANTICHOLINERGICS
Inhaled ipratropium bromide generally produces a further improvement in lung function of 10% to 15% over inhaled β2-agonists alone. In children and adults, multiple-dose ipratropium bromide added to initial therapy also produced a reduced hospitalization rate in the subset of patients with an FEV1 of less than 30% of predicted at baseline. Ipratropium bromide, a quaternary amine, is poorly absorbed and produces minimal or no systemic effects. Care should be used when administering ipratropium bromide by nebulizer. If a tight mask or mouthpiece is not used, the ipratropium bromide that deposits in the eyes may produce pupillary dilatation and difficulty in accommodation. Ipratropium bromide is not a vasodilator, so unlike β2-agonists it will not worsen ventilation-perfusion mismatc.

ALTERNATIVE THERAPIES
The emergency department use of aminophylline, a moderate bronchodilator,for acute asthma has not been recommended for a number of years. Clinical trials of aminophylline in adults and children hospitalized with acute asthma have not reported sufficient evidence of efficacy (improvement in lung function and reduced hospital stay) but have reported an increased risk of adverse effects.   However, two studies of aminophylline in children with severe disease suggested a possible small benefit in reducing intensive care unit admissions. Adverse effects of theophylline include nausea and vomiting and potentiation of the cardiac effects of the inhaled β2-agonists. Magnesium sulfate is a moderately potent bronchodilator that is similar to aminophylline, producing relaxation of smooth muscle and central nervous system depression. The use of intravenous magnesium sulfate in patients presenting to the emergency department is controversial (see below). The adverse effects of magnesium sulfate include hypotension, facial flushing, sweating, nausea, loss of deep tendon reflexes, and respiratory depression. Patients have required dopamine to treat the hypotension.
Helium is an inert gas of low density with no pharmacologic properties that can lower resistance to gas flowand increase ventilation because the low density decreases the pressure gradient needed to achieve a given level of turbulent flow, converting turbulent flow to aminar flow. Helium is given as a mixture of helium and oxygen (heliox), usually 60% to 70% helium with 30% to 40% oxygen. As
with a number of experimental approaches, heliox was reported to be  efficacious in initial nonrandomized clinical trials. However, the small number of randomized, controlled trials completed to date have failed to document efficacy. Although heliox is free of adverse effects, its use is limited to patients with a low inspired oxygen requirement because the decrease in density generally is insignificant clinically with less than 60% helium. The inhalational anesthetics halothane, isoflurane, and enflurane all have been reported to have a positive effect in children and adults with severe asthma that is unresponsive to standard medical therapy. The proposed mechanisms for inhalational anesthetics include direct action on bronchial smooth muscle, inhibition of airway reflexes, attenuation of histamine-induced bronchospasm, and interaction with β2-adrenergic receptors. well -controlled trials with these agents have not been completed. Potential adverse effects include myocardial depression, vasodilation, arrhythmias, and depression of mucociliary function. In addition, the practical problem of delivery and scavenging these agents in the intensive care environment as opposed to the operating room is a concern. The use of volatile anesthetics cannot be recommended based on insufficient evidence of efficacy.
Ketamine has been recommended for rapid induction of anesthesia in patients with asthma who require intubation and mechanical ventilation.  Ketamine is thought to produce bronchodilation from
a combination of an increase in circulating catecholamines, direct smooth muscle relaxation, and inhibition of vagal flow.  Anecdotal reports have suggested that ketamine is useful as a short-term adjunct in severe acute asthma; controlled trials have not provided sufficient evidence of efficacy, however. Ketamine has several significant adverse effects, including the anesthesia emergence reaction, which can alter mood and cause delirium. These emergence phenomena occur in at least 25% of patients over 16 years of age; the incidence seems to be much lower in younger patients.  Other risks include an increase in heart rate, arterial blood pressure, and cerebral blood flow because
of its sympathetic effects.

SPECIAL POPULATIONS
6 Infants and children younger than 4 years of age may be at greater risk of respiratory failure than older children and adults. Although treated with the same drugs, these younger children require the use of a facemask as opposed to a mouthpiece for delivery of aerosolized medication. Use of the facemask reduces delivery of drug to the lung by one-half so that a minimal dose is recommended as
opposed to a weight-adjusted dose. The facemask should be sized appropriately and should fit snugly over the nose and mouth. Use of the “blow by” method, where the therapist or parent places the mask or extension tubing near the child’s nose and mouth, should be discouraged because holding the mask as few as 2 cm from the patient’s face reduces lung delivery of the aerosol by 80%.

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TREATMENT Asthma

 AEROSOL THERAPY FOR ASTHMA

Aerosol delivery of drugs for asthma has the advantage of being site-specific and thus enhancing the therapeutic ratio.  Inhalation of short-acting β2-agonists provides more rapid bronchodilation than either parenteral or oral administration, as well as the greatest degree of protection against EIB and other challenges. Inhaled corticosteroids produce a greater reduction of BHR than corticosteroids administered systemically. Specific agents (e.g., cromolyn, nedocromil, formoterol, salmeterol, and ipratropium) are only effective by inhalation.  Given the international ban on the production and use of chlorofluorocarbons (CFCs), the manufacturers of CFC-propelled metered-dose inhalers (MDIs) are developing new devices for delivering topically active medication.  Therefore, an understanding of aerosol drug delivery is essential to optimal asthma therapy. Table 26-4 lists the factors determining lung deposition of therapeutic aerosols.

DEVICE DETERMINANTS OF DELIVERY
Devices used to generate therapeutic aerosols include jet nebulizers, ultrasonic nebulizers, MDIs, and dry-powder inhalers (DPIs).

 

The single most important device factor determining the site of aerosol deposition is particle size.  Devices for delivering therapeutic aerosols generate particles with aerodynamic diameters from 0.5 to 35 microns.  Particles larger than 10 microns deposit in the oropharynx, particles between 5 and 10 microns deposit in the trachea and large bronchi, particles 1 to 5 microns in size reach the lower
airways, and particles smaller than 0.5 microns act as a gas and are exhaled. In asthma, the airways, not the alveoli, are the target for delivery. Respirable particles are deposited in the airways by three mechanisms:
(1) inertial impaction,
(2) gravitational sedimentation, and
(3) Brownian diffusion. 
The first two mechanisms are the most important for therapeutic aerosols and probably are the only factors that can be manipulated by patients. Each delivery device within a classification generates specific aerosol characteristics, so extrapolation of delivery data from one device cannot be done for the other devices in the class. For instance, MDIs can deliver 5% to 50% of the actuated dose; DPIs, 10% to 30% of the labeled dose; and nebulizers, 2% to 15% of the starting dose.  MDIs and DPIs are portable and convenient, unlike nebulizers. MDIs consist of a pressurized canister with a metering valve; the canister contains active drug, low-vapor-pressure propellants such as chlorofluorocarbon (CFC) or hydrofluoroalkane (HFA), cosolvents, and/or surfactants.  With any change in these components, the Food and Drug Administration (FDA) considers it to be a new drug that requires stability, safety, and efficacy studies prior to approval. The drug is either in solution or a suspended micronized powder. In order to disperse the suspension for accurate delivery, the canister must
be shaken. The metering chamber measures a liquid volume, and therefore, the device must be held with the valve stem downward so that the chamber is covered with liquid  (Fig. 26-4). When the
canister is actuated, the device releases the propellant and drug in a forceful spray whose particles are large (mass median aerodynamic diameter [MMAD] = 45 microns)  (see Fig. 26–4). As evaporation
occurs, the particle size is reduced to a final MMAD of 0.5 to 5.5 microns depending on the MDI. The aerosol cloud of a CFCpropelled MDI extends at least 10 in beyond the MDI at the lowest
MMAD, and that of an HFA-propelled MDI extends about 6 in. The breath-actuated MDI Autohaler, is cocked with a lever to “load” the dose of medication, a baffle is opened by inspiratory pressure,
and the dose is expelled from the canister metering chamber. While the need for hand-lung coordination for proper actuation is reduced significantly with breath-actuated MDIs, these devices do not allow the use of a spacer device.

Spacer devices are used frequently with an MDI to decrease oropharyngeal deposition and enhance lung delivery. However, not all spacer devices produce similar effects. The design of spacers varies from simple open-ended tubes that separate the MDI from the mouth to holding chambers with one-way valves that open during inhalation (the preferred system). The purpose of a spacer is to allow evaporation of the propellant prior to inhalation. Use of a spacer allows inhalation after actuation of the device, obviating the need for good hand-lung coordination, and permits a greater number of drug particles to achieve a respirable droplet size.  Additionally, the largeparticles that normally would deposit in the oropharynx “rain out” in the spacer. All the available spacers significantly reduce oropharyngeal deposition from MDIs, with the holding-chamber devices being
superior to the open-ended tubes.  This reduction in oropharyngeal deposition is an important factor in reducing local adverse effects (i.e.,hoarseness and thrush) from inhaled corticosteroids.   The change in lung delivery depends on both the MDI and the drug, where one spacer device may enhance delivery with one MDI preparation and decrease delivery with others.  Finally, over time, holding chambers can build up static electricity that attracts small particles to the sides of the chamber, significantly reducing aerosol availability. It is recommended that spacers be washed weekly with household detergent, with a single rinse, and allowed to drip dry. Dry micronized powders can be inhaled directly into the lung. Four DPIs for asthma are available for use in the United States (i.e., Diskus, Rotahaler, Turbuhaler, and Aerolizer), with others under development.  Each has unique characteristics with advantages and disadvantages (Table 26–5). The primary advantage of DPIs is that they are breath-actuated and require minimal hand-lung coordination.  Some DPIs are more flow-dependent than others. Thus, similar to MDIs and spacers, delivery data from one DPI cannot
be extrapolated to another. Nebulizers come in two basic types, the jet nebulizer and the ultrasonic nebulizer. Jet nebulizers produce an aerosol from a liquid solution or suspension placed in a cup. A tube connected to a stream of compressed air or oxygen flows up through the bottom and draws the liquid up an adjacent open-ended tube. The air and liquid strike a baffle, creating a droplet cloud that is then inhaled.  Ultrasonic nebulizers produce an aerosol by vibrating liquid lying above a transducer
at speeds of about 1 mHz.  Both produce similar degrees of lung deposition, with the exception that ultrasonic nebulizers are ineffective for nebulizing micronized suspensions.  The aerosol output and
lung delivery vary significantly among the commercially available jet nebulizers even when operated in the same manner.  Increasing fill volume will increase the total amount of drug delivered; however, it
also will take longer for the patient to nebulize the dose. TheMMAD of the droplets is related directly to the gas flow, with flows of 5 to 12L/ min providing an aerosol cloud with an MMAD of 4 to 8 microns for most jet nebulizers.

PATIENT DETERMINANTS OF DELIVERY (See Table 26–4)

The most important patient factor determining aerosol deposition is inspiratory flow.  High inspiratory flows increase the degree of deposition owing to impaction of particles of any size, thereby increasing deposition centrally (i.e., throat and large airways) and decreasing peripheral deposition. Holding chambers enhance the clinical efficacy in patients with poor hand-lung coordination but may offer no advantage in patients who can use an MDI optimally alone. Optimal inspiratory flow for most MDIs is
slow and deep (approximately 30 L/min).  In general, DPIs require

higher inspiratory flows (≥60 L/min) and a change in inhalation technique (i.e., deep, forceful inspiration) for optimal actuation, which, in turn, increases the amount of drug delivered to the larger central airways.  However, this difference in delivery may not produce clinically significant differences.  Patients should be cautioned not to exhale into DPIs because this causes loss of dose and moistens the dry powder, causing aggregation into larger particles. Patient factors that cannot be controlled include interpatient variability in airway geometry (particularly the differences between children and adults)  and the effects of bronchospasm, edema, and mucus hypersecretion. Mild
obstruction increases aerosol deposition; however, severe obstruction probably leads to increased central deposition from impaction.  The absolute delivery to the lung is not as important as consistency of delivery, assuming that a sufficient dose to produce the desired therapeutic
effect is achieved. No single inhalation device is the best for all patients. Table 26–5 lists the differing characteristics of inhalation devices. Appropriate inhalation technique is essential to achieve optimal
drug delivery and therapeutic effect. The components are illustrated in Figure 26–5. Approximately 50% to 80% of a dose from MDIs and DPIs impacts on the oropharynx and is then swallowed;
the rest is either left in the device or exhaled.  It is important that actuation occurs during inhalation, although the time during inspiration is unimportant.  Although radiolabeled studies indicate improved
delivery by holding the actuator 2 to 3 cm in front of an open mouth to allow more evaporation and less impaction, physiologic studies with bronchodilators have failed to document an advantage for this
method.  Many patients do not use their MDIs optimally, and patient instruction with demonstration is the most effective means of improving inhaler technique. Even with instruction, up to 30% of
patients, particularly young children and the elderly, cannot master the use of an MDI. For these patients, attachment of a holding-chamber device to the MDI or use of a breath-actuated MDI can improve effi- cacy significantly.  Mouth rinsing following treatment with MDIand DPI-inhaled corticosteroids is important to minimize local effects and oral absorption. Delivery from high-resistance DPIs is more flow-dependent than from low-resistance DPIs. The Turbuhaler device has a greater flow dependency than the Aerolizer and the Diskus. Children 6 to 12 years of age received approximately one-half the dose of radiolabeled budesonide via Turbuhaler than those older than 12 years of age, whereas children younger than 6 years of age received

one-quarter of the dose. The Aerolizer and the Diskus deliver about 15% of the dose to the airways, and this appears to be similar at both 30 and 60 L/min inspiratory flows; both have been approved for children aged 5 and 4 years, respectively.

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MENSTRUATION RELATED ASTHMA

MENSTRUATION RELATED ASTHMA
Premenstrual worsening of asthma has been reported in as many as 30% to 40% of women in some studies, whereas worsening of pulmonary functions has been reported even in women not aware of worsening symptoms.The pathophysiology is uncertain because estrogen replacement in postmenopausal women has been shown to worsen asthma, whereas estradiol and progesterone administration have been variably reported to improve or have no effect on asthma in women with premenstrual asthma.Studies would indicate that, in general, bronchial responsiveness and symptoms improve in asthmatics during pregnancy.The clinical significance of menstruationrelated asthma is still unclear because some studies have reported that up to 50% of emergency department visits by women were premenstrual, whereas others have reported no association with menstrual

FOODS, DRUGS, AND ADDITIVES
Documentation in the literature of food allergens as triggers for asthma is not available.  However, additives, specifically sulfites used as preservatives, can trigger life-threatening asthma exacerbations. Beer, wine, dried fruit, and open salad bars in particular have high concentrations of metabisulfites.  Severe oral corticosteroid-dependent patients should be warned about ingesting foods processed with sulfites. Another additive producing bronchospasm is benzalkonium chloride, which is found as a preservative in some nebulizer solutions of antiasthmatic drugs. Aspirin and other nonsteroidal anti-inflammatory drugs can precipitate an attack in up to20%of adults with asthma.  The mechanism
is related to cyclooxygenase inhibition, and 5-lipoxygenase inhibition can prevent the symptoms.  The prevalence increases with age. The greatest frequency occurs in severe corticosteroid-dependent asthmatics in their fourth and fifth decades who also have perennial rhinitis and nasal polyposis (presence of several polyps).  Other drugs that do not precipitate bronchospasm but which prevent its reversal are the β-blocking agents 

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FACTORS CONTRIBUTING TO ASTHMA SEVERITY

FACTORS CONTRIBUTING TO ASTHMA SEVERITY

VIRAL INFECTIONS
Viral infections are primarily responsible for exacerbations of
asthma.  Viral upper respiratory tract infections are a major precipitant of acute asthma in children, being involved in up to 20% to 40% of acute episodes.Infants are particularly susceptible to airways obstruction and wheezing with viral infections because of their small airways. The most common cause of exacerbations in both children and adults is the common rhinovirus.Other viruses isolated include respiratory syncytial virus (RSV), parainfluenza virus, coronavirus, and influenza viruses.
The inflammatory response to viral infection is thought to be associated directly with the increasing BHR. Certain viruses (RSV and parainfluenza virus) are capable of inducing specific IgE antibodies, and rhinovirus can activate eosinophils directly in asthmatics. The increase in asthma symptoms and BHR that occurs may last for days or weeks following resolution of the symptoms of the viral infection. The NAEPP recommends annual influenza vaccinations for patients with asthma.
 

ENVIRONMENTAL AND OCCUPATIONAL FACTORS
Agents and events and the mechanisms that are known to trigger asthma are listed in Table  The general mechanisms are unknown but presumably are the result of epithelial damage and inflammation
in the airway mucosa. Ozone and sulfur dioxide, common components of air pollution, have been used to induceBHRin animals. Exposure to 0.2 ppm ozone for 2 to 3 hours can induce bronchoconstriction and increase BHR in asthmatics. Sulfur dioxide in the ambient atmosphere is highly irritating. It presumably induces bronchoconstriction through mast cell or irritant-receptor involvement. Asthma produced by repeated prolonged exposure to industrial inhalants is a significant health problem. It has been estimated that occupational asthma accounts for 2% of all asthmatic persons. Persons with occupational asthma have the typical symptoms of asthma with cough, dyspnea, and wheeze. Typically, the symptoms are related to work and improve on weekends and during vacations.In some instances, symptoms may persist even after termination of exposure.
 

PSYCHOLOGICAL FACTORS
Emotions and stress rarely can precipitate attacks of asthma but more commonly worsen an attack in progress.2 Bronchoconstriction from psychological factors appears to be mediated primarily through excess parasympathetic input. Atropine has been shown to block experimental psychogenic bronchoconstriction. It is most important to emphasize to patients and to parents of asthmatic children that asthma is not an emotional disease; however, calming influences and relaxation techniques may benefit the patient who becomes severely emotionally distraught during an asthma attack.
 

SINUSITIS AND RHINITIS
Disorders of the upper respiratory tract, particularly sinusitis and rhinitis, have been linked with asthma formany years. Asmany as40% to 50% of asthmatics have abnormal sinus radiographs. However, chronic sinusitis may just represent a nonbacterial coexisting condition  with allergic asthmatics because the histologic changes in the paranasal sinuses are similar to those seen in the lung and nose. Some studies have shown that asthma symptoms improve with treatment of sinusitis. The mechanism by which sinusitis aggravates asthma is unknown. The treatment of allergic rhinitis with inhaled corticosteroids and cromolyn but not antihistamines will reduce BHR in asthmatic patients. It has been postulated that transport of mucus chemotactic factors and inflammatory mediators from nasal passages duringallergic rhinitis into the lung may accentuate BHR.
 

GASTROESOPHAGEAL REFLUX
Gastroesophageal reflux has been associated with asthma for many years. Nocturnal asthma may be associated with nighttime reflux. Reflux of acidic gastric contents into the esophagus is thought to initiate a vagally mediated reflex bronchoconstriction. Also of concern is that most medications that decrease airways smooth muscle tone have a relaxant effect on gastroesophageal sphincter tone as well. The therapeutic approach most commonly taken for patients with gastroesophageal reflux and asthma is to initiate standard antireflux therapy and observe the asthma symptoms.

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picture asthma

 

Representative illustration of the pathology found in the asthmatic
bronchus compared with a normal bronchus (upper right). Each section
demonstrates how the lumen is narrowed. Hypertrophy of the basement membrane,
mucus plugging, smooth muscle hypertrophy, and constriction contribute
(lower section). Inflammatory cells infiltrate, producing submucosal edema, and
epithelial desquamation fills the airway lumen with cellular debris and exposes
the airway smooth muscle to other mediators (upper left).

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asthma

Asthma has been known since antiquity, yet it is a disease that still defies precise definition. The word asthma is of Greek origin and means “panting.” More than 2000 years ago, Hippocrates used the word asthma to describe episodic shortness of breath; however, the first detailed  clinical description of the asthmatic patient was made by Aretaeus in the second century.1 An expert panel of the National Institutes of Health, the National Asthma Education and Prevention Program (NAEPP), has provided the following working definition of asthma2:
Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T-lymphocytes, macrophages, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning.
These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli.This definition encompasses the important heterogeneity of the clinical presentation of asthma by describing the scientific and clinically accepted characteristics of asthma.

EPIDEMIOLOGY

An estimated 14 to 15 million persons in the United States have asthma (about 5% of the population).Asthma is the most common chronic disease among children in the United States, with approximately 5 million children affected. Over the past two decades in the United States, the prevalence of asthma has increased by 75%, whereas the rate in children younger than age 5 has increased 160%.In the United States, as in other Western industrialized countries,the prevalence of asthma has reached epidemic proportions. Asthma accounts for 1.6% of all ambulatory care visits (13.7 million) and results in more than 470,000 hospitalizations and 2 million emergency department visits per year.3 Asthma is the third leading cause of preventable hospitalization in the United States, and hospitalizations for asthma among children 0 to 17 years of age have increased 4.5% per year, whereas total hospitalizations for all causes in children actually decreased. Children have the highest prevalence of asthma, at 68.6 per 1000 population younger than 18 years of age.
Asthma accounts for more than 10 million missed school days per year. The prevalence of disabling asthma in children has increased 232% over the past 20 years compared with a 113% increase from all other chronic conditions in childhood. In young children (0 to 10 years of age), the risk of asthma is greater in boys than in girls, becomes about equal during puberty, and then is greater in women than in men.3Ethnic minorities continue to share the burden of asthma disproportionately.
African-Americans and Hispanics have a higher prevalence than whites, but this appears to be a result of urbanization and not race or socioeconomic status. African-Americans are three times as likely to be hospitalized and approximately 2.5 times more likely to die from asthma.3 In addition, African-Americans and Puerto Ricans living in inner cities are four times more likely to experience emergency department visits than whites. These patterns are likely a result of poor access to care.
The estimated cost of asthma in the United States in 1998 was $12.6 billion.The average societal burden of asthma (including both direct and indirect medical expenditures) in the United States averages $640 per patient per year, with direct medical expenditures accounting for 40% to 50% of total costs.  Emergency care of acute asthma exacerbations makes up the largest portion of direct medical costs. In 1997, an estimated cost of $1 billion dollars per year in lost productivity accrued from parents staying home to care for their children.
The natural history of asthma is still not well defined. Although asthma can occur at any time, it is principally a pediatric disease, with most patients being diagnosed by 5 years of age and up to 50% of children having symptoms by 2 years of age. Between 30% and 70% of children with asthma will improve markedly or become symptom-free by early adulthood; chronic disease persists in about 30% to 40% of patients, and generally 20% or less develop severe chronic disease. Atopic status is the strongest indicator of a poor prognosis, although initial severity also predicts severity as an adult.Diminished lung growth may occur in children with uncontrolled severeasthma. Lowlung function and increased bronchial hyperresponsiveness
are independent risk factors for low lung function in early
adulthood.In adults, most longitudinal studies have suggested a more rapid
rate of decline in lung function in asthmatics than in normal volunteers,
primarily reflected in forced expiratory volume in 1 second  (FEV1). However, the annual decline in FEV1 is less than in smokers or in patients with a diagnosis of emphysema. In general, asthmatics with less frequent attacks and normal lung function on initial assessment have higher remission rates, whereas smokers have the lowest remission and highest relapse rates.  The level of bronchial hyperresponsiveness (BHR) tends to predict the rate of decline in FEV1, with a greater decline with high levels of BHR. Thus airways obstruction in asthma not only may become irreversible but also may worsen over time owing to airway remodeling (see below).Although both the prevalence and the morbidity from asthma are increasing, the death rate from asthma in the United States appears to have reached a plateau of about 5000 deaths per year and may be on the decline.3 Despite the relatively low number of asthma deaths,80% to 90% are preventable.2 Most deaths from asthma occur outside the hospital, and death is rare after hospitalization. The most common cause of death from asthma is inadequate assessment of the severity of airways obstruction by the patient or physician and inadequate therapy. the most common cause of death in hospitalized patients is also inadequate or inappropriate therapy. Thus the key to preventio of death from asthma, as advocated by the NAEPP, is education.

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Traditional Cough Medicine

If you want to mix their own traditional cough medicine, combine the ingredients needed to become a useful medicinal herb as a cough suppressant, reduction of bronchial secretions, or respiratory stimulants and driving out phlegm. no different from herb-counter cough medicines in pharmacies or drug stores.
The following types of herbs that can be tried.
Remedy 1:
8 grams kencur, 2 pieces of betel leaf, 2 grams of the fruit of fennel, sage leaves 2 grams, 0.05 grams of fruit cubeb, 0.05 grams of cardamom. All material is boiled with 135 ml of water and taken twice a day for two weeks.
Remedy 2:
1 clove garlic, 1 tablespoon ginger juice, water, turmeric, lemon juice, honey and 3 tablespoons of boiled water. Potions steamed, then drunk three or four times a day or two teaspoons.
Remedy 3:
3 pieces of cardamom, 15 points cubeb, 1 teaspoon cumin, 1 teaspoon fennel, pulosari 1 finger, 2 finger rhizome kencur, washed, finely ground, crushed with 1 tablespoon of coconut oil and eucalyptus oil 1 teaspoon, to grease chest and neck.
Remedy 4:
4 pieces cubeb, 1 finger cinnamon bark, washed and cut if necessary, boil with 4 cups of clean water to eat so that only a half; after cold filtered and drunk with pure honey as needed (three times a day).



For dry coughs:
Lemon
Take 1 piece of orange juice a lot of water, wring it out and add 2 tablespoons of honey. Stir and drink twice a day (morning and evening).
Brimbing wuluh
Take 10 Blimbing wuluh fruit, wash and then finely ground. Add 1 cup cooking water and a little salt a little. Having squeezed and filtered, drink twice a day (morning and evening).
Kencur
Take 1 finger rhizome kencur (do not removed the skin). Rinse and finely chewed directly with a little salt. Swallow and gelontor by drinking warm water. Do twice a day.
Sage leaves
Take 1 handful sage leaves along the stems and leaves 1 handful acid. Boil 3 cups water to be 2 cups. Let stand until cool, strain and drink twice daily.
As an expectorant:
Cardamom
Pour boiling 5 grams of fruit powder with a cup of boiling water fennel. After chilling filtered, add 1 teaspoon of honey. Toss well, drink well. Taken twice a day until healed.
Aloe vera
Take 1 stick prickly aloe vera leaves removed. Rinse and grated, squeezed, and then mixed with 6 tablespoons of honey. Drink several times.
As a laxative sputum:
Ginger
Take 1 / 2 segment ginger and mash until smooth. Add 2 cups water and boil until half an hour. Drink decoction 2-3 times daily.
For shortness of breath:
Make sure water buffalo
Take a handful of herbs patikan buffalo. Add water and pulverized. Squeeze into 1 / 2 cup and drink.
Fennel
Take 10 drops of fennel oil. Pour boiling water with 1 tablespoon hot water. Drink while warm. Do it three times a day until healed.
To cough more than 100 days and dry:
Lote upas
Take 30 grams of tuber lote upas still fresh, washed and shredded. Add 2 tablespoons of cooking water. Strain and add 1 tablespoon of honey. Stir and then drink three times a day.

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treatments for asthma

Asthma is a disease that is sometimes annoying for the sufferer. I have to deal with recommendations for asthma sufferers it is a traditional medicine that munkin you can try for yourself:

1. Prepare as much as 2 pieces of radish juice and then boiled with water is mixed to taste, wait until boiling and then drain into a glass waiting for it to cool and then mixed with native honey mix well. drink 3 times a day.
2. Prepare 2 segment of white ginger and eggplant cooked (can fry / boil) to use as side dishes for food.
3. Prepare ginger 3 sections and then clean it in the juice runs out and then mixed with boiled water until boiling and then input into the glass let sit for 18 hours and then mixed with honey drink every morning.

good luck...

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Asthma

Asthma is one of the respiratory disease that is often experienced by all people both men and women.Originally the word asthma comes from the greek is "asthma" means difficult to breathe.Many cases of asthma in people who have not received good treatment due to medical expenses. Routine treatment should not be interrupted, social disruption.Asthma is a disease that is caused due to allergies or heredity.The cause of asthma is most often due to factors such as allergies allergy: house dust, animal dander, cigarette smoke, smoke, mosquito coils, cold weather, too tired, too many thoughts, stress and others.This disease has the potential to disrupt the growth and development. This disease if not handled properly, can attack every organ and function of growth without exception. for it is recommended to asthma sufferers to eat a lot and contains protein, vitamin is needed by our bodies.Symptoms commonly experienced by people with asthma are coughing up phlegm and wheezing and shortness of breath caused by narrowing of the respiratory tract.Treatment of asthma. actual asthma can not be cured but it can relieve asthma symptoms, like shortness of breath when people with asthma are shortness of breath immediately give relief medication in the form of shortness of breath or swallow inhaler. prevent yourself from allergies that can cause allergic asthma disease relapses, mild exercise to provide endurance, swim because it can expand pernapasa channel. eat foods that are nutritious and good for the body.

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