Signs and symptoms of asthma

Asthma signs and symptoms range from minor to severe, and vary from person to person. You may have mild symptoms such as infrequent wheezing, with occasional asthma attacks. Between episodes you may feel normal and have no trouble breathing. Or, you may have signs and symptoms such as coughing and wheezing all the time or have symptoms primarily at night or only during exercise.

Asthma signs and symptoms include:

• Dypsnoea
• Chest tightness or pain
• Trouble sleeping caused by shortness of breath, coughing or wheezing
• An audible whistling or wheezing sound when exhaling
• Bouts of coughing or wheezing that are worsened by a respiratory virus such as a cold or the flu

Signs of worsening asthma:

• An increase in the severity and frequency of asthma signs and symptoms
• A fall in peak flow rates as measured by a peak flow meter, a simple device used to check how well your lungs are working
• An increased need to use bronchodilators — medications that open up airways by relaxing the surrounding muscles

Differential Diagnosis for Asthma

1.Cystic fibrosis

Differential symptoms/signs:

Chronic, sometimes productive cough with a possible family history of CF. Nasal polyposis at or before age 12 and symptoms related to other organ involvement, such as diarrhoea, malabsorption or failure to thrive.

Test:

Sweat chloride testing: level of sweat chloride >67.

Consider repeat testing.

2.Tracheomalacia

Differential signs/symptoms:

Symptoms are usually positionally dependent and occur within the first weeks or months of life.

Expiratory stridor and a barking brassy cough, wheezing respiratory distress with additional breath sound at the end of expiration (the bagpipe sign) are accompanied by the occasional extension of the neck with breathing, inspiratory stridor, episodes of holding of breath, anoxia, recurrent respiratory infections, retraction of intercostal and subcostal muscles, failure to thrive and respiratory and cardiac arrest.

Test:

The sensitivity of plain radiographs is 62%, using microlaryngoscopy and bronchoscopy as the reference standards.

In addition to CXR, barium oesophagography is useful for evaluating associated disease processes, such as tracheo-oesophageal fistula and reflux disease.

3.Vascular ring

Differential signs/symptoms:

Wheezing, shortness of breath, occasional stridor.

Test:

CT chest with contrast: double aortic arch, abnormal take-off of the innominate artery, anomaly of left pulmonary artery, right aortic arch, aberrant right subclavian, enlarged pulmonary veins.

4.Foreign body aspiration

Differential signs/symptoms:

Wheezing, shortness of breath, occasional stridor are common.

If the foreign body is in the peripheral airway, localised one-sided wheezing or collapse of the distal lung tissue is found.

Test:

CXR, CT chest or bronchoscopy shows the foreign body.

5.Vocal cord dysfunction

Differential Signs/symptoms:

Inspiratory and expiratory wheezing is often difficult to differentiate. Should be considered in steroid-resistant asthma patients.

Test:
Direct visualisation of the vocal cords with rhinolaryngoscopy during a spell. Inspiratory flow volume loop is helpful when abnormal (flattened).

6.Alpha-1 antitrypsin deficiency

Differential signs/symptoms:

Wheezing, resistant to management. May have family history of parents or grandparents dying of lung disease.

Test:
Testing for the alpha-1 antitrypsin phenotype.

7.COPD

Differential signs/symptoms:

Dyspnoea occurs with or without wheezing and coughing.

Examination may show barrel chest, hyper-resonance to percussion and distant breath sounds.

Test:
PFTs with residual volume (RV), total lung capacity (TLC) and a flow volume loop with bronchodilator showing an obstructive pattern with an increase in TLC and RV and a reduction in forced expiratory flow at one second (FEV1), FEV1/forced vital capacity (FVC) ratio with no response to bronchodilator.

CXR showing hyper-inflation of the lungs.

8.Bronchiectasis

Differential signs/symptoms:

Dyspnoea, cough and wheezing and, if severe, recurrent pulmonary infections.

Test:
High resolution CT chest: dilated airways, bronchial wall thickening.

Can occasionally be seen on CXR.

9.Pulmonary embolism

Differential signs/symptoms:

Patients have a wide variety of presentations but most common is shortness of breath and pleuritic pain.

Test:
Pulmonary angiogram is the preferred test, but carries risks. An acceptable alternate test is CT angiogram of the lung, which, if not available, can be replaced with the less sensitive V/Q scan.

10.Congestive heart failure

Differential signs/symptoms:

History of CAD or uncontrolled HTN; examination showing dependent oedema, elevated jugular venous pressure, and basal pulmonary crepitations.

Test:
CXR may show increased alveolar markings, fluid in fissures and pleural effusions.

Echocardiogram: reduced left ventricular ejection fraction.

11.Common variable immunodeficiency

Differential sign/symptoms:

History of recurrent, usually sinopulmonary, infections.

Test:
Serum IgG level below 5g/L (500 mg/dL).

Pathophysiology of Asthma

Pathophysiology

The pathophysiology of asthma is complex and involves the following components:

• Airway inflammation
• Intermittent airflow obstruction(Airway remodelling)
• Bronchial hyperresponsiveness

Asthma, allergic rhinitis, and atopic dermatitis are almost invariably accompanied by elevated levels of IgE.

Airway inflammation

Many asthmatics are atopic (an inherited a predisposition towards allergy) where your immune system develops an exaggerated response to certain foreign substances or allergens. Your body's immune system senses these allergens, perceives them as foreign, and begins to prepare to fight off them off as a foreign intruder. The process that takes place is often referred to as the allergic cascade, which generally occurs in 3 steps:

1. Sensitization
2. Early phase response
3. Late Phase response

1. Sensitization

Immunologically, your body senses the allergen as foreign and sets off a cascade of events stimulating several different types of immune cells (see diagram):

• T cells rapidly stimulate B cells
• B cells transform into plasma cells
• Plasma cells produce IgE antibodies specific to the allergen
• IgE antibodies bind to mast cells, lymphocytes, basophils

2. Early phase response

With re-exposure to the allergen your immune system senses the allergen as foreign leading to:

• The mast cell/ IgE complexes produced in the sensitization phase, binding to the allergen thinking that it is a foreign invader
• Mast cells then release inflammatory cells called mediators (e.g. histamine) that quickly travel throughout your body with the purpose of fighting off the foreign invaders such as bacteria and viruses.
• You begin to experience symptoms of your body’s overreaction to the allergen.

Cross-linking of IgE bound to mast cells triggers the release of preformed vasoactive mediators, synthesis of prostaglandins and leukotrienes, and the transcription of cytokines.

In the bronchial mucosa, these mediators of immediate-hypersensitivity reactions rapidly induce mucosal edema, mucous production, and smooth muscle constriction, and eventually elicit an inflammatory infiltrate.

You may begin wheezing, coughing or feeling short of breath as the immunologic response causes swelling and narrowing of the airways in your lung. You may only experience runny nose or watery, itchy eyes. The immunologic response begins nearly immediately with symptoms occurring very shortly after re-exposure lasting 3-4 hours.

3. Late Phase Response

Beginning at the same time as the early phase response, but not causing symptoms for several hours, is the late phase response. Mediators released by the re-exposure to an allergen also stimulate other kinds of immune cells called eosinophils. Eosinophils contain substances that when released normally fight off infections, but in asthma, the cells damage the lung causing more inflammation and worsening symptoms.

In the late phase, symptoms will not develop for at least 4 hours, but may last as long as 24 hours. Increased inflammation and obstruction of airflow may be more severe than what is seen during the early phase.

Airway remodelling

Airway remodeling in asthma is what happens in response to long-term, unresolved airway inflammation. When airway inflammation is not adequately treated, it can result in permanent structural changes in the airways.

In these cases, a certain degree of airway inflammation is always present. Over time, the body tries to fix this inflammation by triggering changes in the repair function of the lining of the airways.

• Increased airway wall thickness that involves both smooth muscle and collagen tissue
• Increased mucous glands and mucus production
• Increased vascularity, or blood supply, in the airways

Bronchial hyperresponsiveness(BHR)

Airway hyperresponsiveness is a characteristic feature of asthma and consists of an increased sensitivity of the airways to an inhaled constrictor agonist. Certain inhaled stimuli, such as environmental allergens, increase airway inflammation and enhance airway hyperresponsiveness. They are, however, similar to changes occurring in asthmatic patients that are associated with worsening asthma control.

The pathogenesis of exercise-induced bronchospasm is controversial. The disease may be mediated by water loss from the airway, heat loss from the airway, or a combination of both. The upper airway is designed to keep inspired air at 100% humidity and body temperature at 37°C (98.6°F). The nose is unable to condition the increased amount of air required for exercise, particularly in athletes who breathe through their mouths. The abnormal heat and water fluxes in the bronchial tree result in bronchoconstriction, occurring within minutes of completing exercise. Results from bronchoalveolar lavage studies have not demonstrated an increase in inflammatory mediators. These patients generally develop a refractory period, during which a second exercise challenge does not cause a significant degree of bronchoconstriction.

AV nicking (the Gunn sign): Impeded circulation results in a dilated or swollen vein peripheral to the crossing, causing hourglass constrictions on both sides of the crossing and aneurysmal-like swellings.

Investigation of Asthma

CLINICAL FEATURES AND DIAGNOSIS
The characteristic symptoms of asthma are wheezing, dyspnea, and coughing which are variable, both spontaneously and with therapy. Symptoms may be worse at night, and patients typically awake in the early morning hours. Patients may report difficulty in filling their lungs with air. There is increased mucus production in some patients, with typically tenacious mucus that is difficult to expectorate. There may be increased ventilation and use of accessory muscles of ventilation. Prodromal symptoms may precede an attack, with itching under the chin, discomfort between the scapulae, or inexplicable fear (impending doom).

Typical physical signs are inspiratory, and to a great extent expiratory, rhonchi throughout the chest, and there may be hyperinflation. Some patients, particularly children, may present with a predominant nonproductive cough (cough-variant asthma). There may be no abnormal physical findings when asthma is under control.

Diagnosis
The diagnosis of asthma is usually apparent from the symptoms of variable and intermittent airways obstruction, but is usually confirmed by objective measurements of lung function.

LUNG FUNCTION TESTS
Simple spirometry confirms airflow limitation with a reduced FEV1, FEV1/FVC ratio, and PEF. Reversibility is demonstrated by a >12% and 200 mL increase in FEV1 15 min after an inhaled short-acting 2-agonist or, in some patients, by a 2- to 4-week trial of oral glucocorticoids (prednisone or prednisolone 30–40 mg daily). Measurements of PEF twice daily may confirm the diurnal variations in airflow obstruction. Flow-volume loops show reduced peak flow and reduced maximum expiratory flow. Further lung function tests are rarely necessary, but whole body plethysmography shows increased airway resistance and may show increased total lung capacity and residual volume. Gas diffusion is usually normal but there may be a small increase in gas transfer in some patients.

AIRWAY RESPONSIVENESS
The increased AHR is normally measured by methacholine or histamine challenge with calculation of the provocative concentration that reduces FEV1 by 20% (PC20). This is rarely useful in clinical practice, but can be used in the differential diagnosis of chronic cough and when the diagnosis is in doubt in the setting of normal pulmonary function tests. Occasionally exercise testing is done to demonstrate the post-exercise bronchoconstriction if there is a predominant history of EIA. Allergen challenge is rarely necessary, and should only be undertaken by a specialist if specific occupational agents are to be identified.

The patient performs the peak flow meter test twice a day for about 2 weeks and records the results for review in a follow up appointment. The first test should be performed after waking in the morning, before taking bronchodilator medications. The patient should perform the peak expiratory flow maneuver 3 times and record the highest measurement. The second test should be done in the afternoon or early evening after taking a bronchodilator. Peak flows vary during the day and the early morning peak is lower than the evening peak. A variability greater than 20% indicates a reversible airway obstruction.

HEMATOLOGIC TESTS
Blood tests are not usually helpful. Total serum IgE and specific IgE to inhaled allergens (RAST) may be measured in some patients.

IMAGING
Chest roentgenography is usually normal but may show hyperinflated lungs in more severe patients. In exacerbations, there may be evidence of a pneumothorax. Lung shadowing usually indicates pneumonia or eosinophilic infiltrates in patients with bronchopulmonary aspergillosis. High-resolution CT may show areas of bronchiectasis in patients with severe asthma, and there may be thickening of the bronchial walls, but these changes are not diagnostic of asthma.

SKIN TESTS
Skin prick tests to common inhalant allergens are positive in allergic asthma and negative in intrinsic asthma, but are not helpful in diagnosis. Positive skin responses may be useful in persuading patients to undertake allergen avoidance measures.

Normal results for spirometry

The results of spirometry tests are compared to predicted values based on the patient's age, gender, and height. For example, a young adult in good health is expected to have the following FEV values:

FEV-0.5—50-60% of FVC
FEV-1—75-85% of FVC
FEV-2—95% of FVC
FEV-3—97% of FVC
In general, a normal result is 80–100% of the predicted value. Abnormal values are:

mild lung dysfunction—60–79%
moderate lung dysfunction—40–59%
severe lung dysfunction—below 40%


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Asthma: Definition and Incidence

According to the WHO:

Asthma attacks all age groups but often starts in childhood. It is a disease characterized by recurrent attacks of breathlessness and wheezing, which vary in severity and frequency from person to person. In an individual, they may occur from hour to hour and day to day.
This condition is due to inflammation of the air passages in the lungs and affects the sensitivity of the nerve endings in the airways so they become easily irritated. In an attack, the lining of the passages swell causing the airways to narrow and reducing the flow of air in and out of the lungs.

Other Definitions

Asthma is a medical condition that causes narrowing of the small airways in the lungs. Typically, asthma patients develop wheezing and have increased mucous production in their lungs. Asthma patients can have episodes of increased shortness of breath, often triggered by allergic reactions. Asthma sufferers often have the disease for many years, and the episodes of shortness of breath can be life-threatening.

Asthma is a chronic (long-lasting) inflammatory disease of the airways. In those susceptible to asthma, this inflammation causes the airways to narrow periodically. This, in turn, produces wheezing and breathlessness, sometimes to the point where the patient gasps for air. Obstruction to air flow either stops spontaneously or responds to a wide range of treatments, but continuing inflammation makes the airways hyper-responsive to stimuli such as cold air, exercise, dust mites, pollutants in the air and even stress and anxiety.

Incidence (Most common chronic respiratory illness in young children)

In the US: 6.4% USA; 17 million Americans (National Institute of Allergy and Infectious Diseases) including 5 million children; 8.1 million children, 51 per 1000; 14.5 million; 5% of population; 14.9 million in 1995 (National Heart, Lung and Blood Institute)

In Australia: Asthma affects 10-12% of adults in Australia. Asthma affects 14-16% of children in Australia (Australian Institute of Health and Welfare)

According to WHO estimates, 300 million people suffer from asthma and 255 000 people died of asthma in 2005.

Incidence in Malaysia:

Chan (1994) reported that 5 % of all outpatients in Ipoh General Hospital were
treated for asthma.

The Second National Health and Morbidity Survey (NHMS II) conducted in 1997
has shown that the estimated prevalence rate of asthma (self-reported) in
Malaysia was between 3.9 % to 4.4 % (mean 4.2 %). The age distribution based
on the Second National Health and Morbidity Survey shown that 4.5 % were
among age 0 1- 4 years and 4.1 % among adult.

Across all ages, the prevalence of asthma is between 8 - 10 %.
It is estimated that there are about 1.6 - 2.0 million of asthmatic cases in
Malaysia.

Treatment & Prognosis of Asthma

Treatment :

Asthma is a long-term disease that can't be cured. Every asthmatic child must have an asthma action plan.

Basically, there are two types of medications:

• Controller Asthma Medicines - prophylaxis
  
• Quick Relief Asthma Medicines - during asthma attack

Controller Asthma Medicines

Examples of controller or preventative asthma medicines include:

• Inhaled corticosteroids such as Aerobid, Asmanex, Azmacort, Flovent HFA, Pulmicort (available as a Turbuhaler an Respules for use with nebulizers for younger kids), and Qvar
• Advair, a combination corticosteroid and long-acting beta₂ agonist
• Leukotriene receptor antagonists, such as Singulair, Accolate, and Zyflo
• Long-acting beta₂ agonists, such as Serevent Diskus and Foradil
• Theophylline
• Other non-steroidal anti-inflammatory controller asthma medications include Intal and Tilade.
• Xolair injections for children with allergic asthma.

It is important to remember that a controller asthma medicine won't treat or stop an asthma attack.

Quick Relief Asthma Medicines

These types of asthma treatment actually provide relief when your child has asthma symptoms. They are usually given with a NEBULIZER OR A METERED DOSE INHALER. Younger children can often use an inhaler with a spacer or a spacer and mask.

Examples of quick relief asthma medicines include:

• Albuterol - Accuneb, Albuterol, Proventil, Ventolin (inhalation solution, nebules, HFA inhaler, inhaler, syrup, rotacaps)
• Levaluterol - Xopenex Soln, Xopenex HFA
• Pirbuterol - Maxair Autohaler (a breath-actuated metered dose inhaler)
• Terbutaline
• Atrovent

Oral steroids are also often used as an asthma treatment when a child has an asthma attack. Forms of oral steroids include prednisone and prednisolone (Prelone and Orapred). In general, prednisone is prescribed for older kids who can swallow pills and prednisolone, a syrup, is used for younger children who can't swallow pills yet.

Prognosis of Asthma

Although it is a chronic disease, the prognosis is usually GOOD =)

This is especially in children who only had mild attacks of asthma.

54% of cases in children will no longer carry the symptoms after a decade (10 years).

Overall, studies shown that 94% of the asthmatic adults survived the follow up period of eight years.

Aetiology of Asthma

Causes

In most cases of asthma in children, multiple triggers or precipitants are recognized, and the patterns of reactivity may change with age. Treatment can also change the pattern. Certain viral infections, such as respiratory syncytial virus (RSV) bronchiolitis in infancy, predispose the child to asthma.

• Respiratory infections: Most commonly, these are viral infections. In some patients, fungi (eg, allergic bronchopulmonary aspergillosis), bacteria (eg, mycoplasmata, pertussis), or parasites may be responsible. Most infants and young children who continue to have a persistent wheeze and asthma have high immunoglobulin E (IgE) production and eosinophilic immune responses (in the airways and in circulation) at the time of the first viral URTI. They also have early IgE-mediated responses to local aeroallergens.
• Allergens: In patients with asthma, 2 types of bronchoconstrictor responses to allergens are recognized.
  • Early asthmatic responses occur via IgE-induced mediator release from mast cells within minutes of exposure and last for 20-30 minutes.
  • Late asthmatic responses occur 4-12 hours after antigen exposure and result in more severe symptoms that can last for hours and contribute to the duration and severity of the disease. Inflammatory cell infiltration and inflammatory mediators play a role in the late asthmatic response. Allergens can be foods, household inhalants (eg, animal allergens, molds, fungi, roach allergens, dust mites), or seasonal outdoor allergens (eg, mold spores, pollens, grass, trees).
• Irritants: Tobacco smoke, cold air, chemicals, perfumes, paint odors, hair sprays, air pollutants, and ozone can initiate bronchial hyperresponsiveness (BHR) by inducing inflammation.
• Weather changes: Asthma attacks can be related to changes in atmospheric temperature, barometric pressure, and the quality of air (eg, humidity, allergen and irritant content).
• Exercise: Exercise can trigger an early asthmatic response. Mechanisms underlying exercise-induced asthmatic response remain somewhat uncertain. Heat and water loss from the airways can increase the osmolarity of the fluid lining the airways and result in mediator release. Cooling of the airways results in congestion and dilatation of bronchial vessels. During the rewarming phase after exercise, the changes are magnified because the ambient air breathed during recovery is warm rather than cool.
• Emotional factors: In some individuals, emotional upsets clearly aggravate asthma.
• Gastroesophageal reflux (GER): The presence of acid in the distal esophagus, mediated via vagal or other neural reflexes, can significantly increase airway resistance and airway reactivity.
• Allergic rhinitis, sinusitis, and chronic URTI: Inflammatory conditions of the upper airways (eg, allergic rhinitis, sinusitis, or chronic and persistent infections) must be treated before asthmatic symptoms can be completely controlled.
• Nocturnal asthma: Multiple factors have been proposed to explain nocturnal asthma. Circadian variation in lung function and inflammatory mediator release in the circulation and airways (including parenchyma) have been demonstrated. Other factors, such as allergen exposure and posture-related irritation of airways (eg, GER, sinusitis), can also play a role. In some patients, abnormalities in CNS control of the respiratory drive may be present, particularly in patients with a defective hypoxic drive and obstructive sleep apnea.