Physical Examination It is important to assess for signs of respiratory distress, including tachypnea Use of accessory respiratory muscles, and cyanosis. On lung examination, there may be wheezing and rhonchi throughout the chest, typically more prominent in expiration than inspiration. Localized wheezing may indicate an endobronchial lesion. Evidence of allergic nasal, sinus, or skin disease should be assessed. When asthma is adequately controlled, the physical examination may be normal.
Pulmonary Function Tests Spirometry often shows airflow obstruction, with a reduction in forced expiratory volume in 1 s (FEV 1 ) and FEV forced vital capacity (FVC) ratio. However, spirometry may be normal, especially if asthma symptoms are adequately treated. Bronchodilator reversibility is demonstrated by an increase in FEV 1 by >200 mL and >12% from baseline (FEV 1 )15 min after a short-acting p agonist. Airway hyper responsiveness is characteristic of asthma; it can be assessed by exposure to direct bronchoconstrictors such as methacholine or histamine. Greater airway responsiveness is associated with increased asthmatic symptoms. The peak expiratory flow rate (PEFR) can be used by the pt to track asthma control objectively at home. Measurement of lung volumes is not typically performed, but increases in total lung capacity and residual volume may be observed. The diffusing capacity for carbon monoxide is usually normal.
Other Laboratory Tests Blood tests are usually not helpful. CBC may demonstrate eosinophilia . Specific IgE measurements for inhaled allergens ( radioallergosorbent test [RAST]) or allergy skin testing may assist in determining allergic triggers. Total serum IgE is markedly elevated in bronchopulmonary aspergillosis (BPA). Exhaled nitric oxide levels can provide an assessment of eosinophilic airway inflammation.
Radiographic Findings Chest x-ray is usually normal. In acute exacerbations, pneumothorax may be identified. In BPA, eosinophilic pulmonary infiltrates may be observed. Chest CT scan is not typically performed in routine asthma but may show central bronchiectasis in BPA.
Differential Diagnosis The differential diagnosis of asthma includes other disorders that can cause wheezing and dyspnea . Upper airway obstruction by tumor or laryngeal edema can mimic asthma, but stridor in the large airways is typically noted on physical examination. Localized wheezing in the chest may indicate an endobronchial tumor or foreign body. Congestive heart failure can cause wheezing but is typically accompanied by bibasilar crackles. Eosinophilic pneumonias and Churg -Strauss syndrome may present with wheezing. Vocal cord dysfunction can mimic severe asthma and may require direct laryngoscopy to assess. When asthma involves chronic airflow obstruction, distinguishing it from chronic obstructive pulmonary disease (COPD) can be very difficult.
TREATMENT OF ASTHMA & STATUS ASTHMATICS By Ananya S HSC20MB0011
TREATMENT OF ASTHMA Setting goals - Asthma is a chronic condition but may be controlled with appropriate treatment in the majority of patients. The goal of treatment should be to obtain and maintain complete control but aims may be modified according to the circumstances. Avoidance of aggravating factors - Reducing exposure to pet. House dust mite exposure may be minimised by replacing carpets with floorboards and using mite impermeable bedding. Measures to reduce fungal exposure and medications known to precipitate or aggravate asthma should be avoided. Smoking cessation is particularly important, as smoking not only encourages sensitisation but also induces relative glucocorticoid resistance in the airway .
STEPWISE APPROACH Step 1: Occasional use of inhaled short-acting β2-adrenoreceptor agonist bronchodilators For patients with mild intermittent asthma (symptoms less than once a week for 3 months and fewer than two nocturnal episodes per month), it is usually sufficient to prescribe an inhaled short-acting β2-agonist, such as salbutamol or terbutaline , to be used as required Step 2: Introduction of regular preventer therapy Regular anti-inflammatory therapy (preferably inhaled glucocorticoids (ICS), such as beclometasone , budesonide (BUD), fluticasone , mometasone or ciclesonide ) should be started in addition to inhaled β2-agonists taken on an as-required basis for any patient who : Has experienced an exacerbation of asthma in the last 2 years Uses inhaled β2-agonists three times a week or more Reports symptoms three times a week or more Is awakened by asthma one night per week. For adults, a reasonable starting dose is 400 μg beclometasone dipropionate (BDP) or equivalent per day in adults, although higher doses may be required in smokers. Alternative but much less effective preventive agents include chromones , leukotriene receptor antagonists and theophyllines .
Step 3: Add-on therapy Add-on therapy should be considered in adults taking 800 μg /day BDP (or equivalent).The addition of a long-acting β2-agonist (LABA) to an inhaled glucocorticoid provides more effective asthma control compared with increasing the dose of inhaled glucocorticoid alone. Fixed combination inhalers of glucocorticoids and LABAs have been developed; these are more convenient, increase adherence and prevent patients using a LABA as monotherapy – the latter may be accompanied by an increased risk of life-threatening attacks. Step 4: Poor control on moderate dose of inhaled glucocorticoid and add-on therapy : In adults, the dose of inhaled glucocorticoid may be increased to 2000 μg BDP/BUD (or equivalent) daily. A nasal glucocorticoid preparation should be used in patients with prominent upper airway symptoms. Leukotriene receptor antagonists, long-acting antimuscarinic agents, theophyllines or a slow-release β2-agonist may be considered.
Step 5: Continuous or frequent use of oral glucocorticoids At this stage, prednisolone therapy (usually administered as a single daily dose in the morning) should be prescribed in the lowest amount necessary to control symptoms. Patients who are on long-term glucocorticoid tablets (> 3 months) or are receiving more than three or four courses per year will be at risk of systemic side-effects. The risk of osteoporosis in this group can be reduced by giving bisphosphonates . In patients who continue to experience symptoms and asthma exacerbation and demonstrate impaired lung function despite step 5 treatment, omalizumab , a monoclonal antibody directed against IgE , should be considered for those with a prominent atopic phenotype, and mepolizumab , a monoclonal antibody that blocks the binding of IL-5 to its receptor on eosinophils , should be considered in those with eosinophilic -mediated disease. Step 6: Step-down therapy Once asthma control is established, the dose of inhaled (or oral) glucocorticoid should be titrated to the lowest dose at which effective control of asthma is maintained.
STATUS ASTHMATICS The course of asthma may be punctuated by exacerbations with increased symptoms, deterioration in lung function, and an increase in airway inflammation. Exacerbations are most commonly precipitated by viral infections but moulds ( Alternaria and Cladosporium ), pollens (particularly following thunderstorms) and air pollution are also implicated. Most attacks are characterised by a gradual deterioration over several hours to days but some appear to occur with little or no warning: so-called brittle asthma.
Management - Mild To Moderate Short courses of ‘ rescue ’ glucocorticoids ( prednisolone 30–60 mg daily) are therefore often required to regain control. Indications for ‘rescue’ courses include : symptoms and PEF progressively worsening day by day, with a fall of PEF below 60% of the patient’s personal best recording onset or worsening of sleep disturbance by asthma persistence of morning symptoms until midday progressively diminishing response to an inhaled bronchodilator symptoms that are sufficiently severe to require treatment with nebulised or injected bronchodilators .
Acute Severe Asthma
Management of Acute Severe Asthma High doses of i Oxygen - High concentrations (humidified if possible) should be administered to maintain the oxygen saturation above 92% in adult nhaled bronchodilators - Short-acting β2-agonists are the agent of choice. Ipratropium bromide provides further bronchodilator therapy and should be added to salbutamol in acute severe or life-threatening attacks. Systemic glucocorticoids - These reduce the inflammatory response and hasten the resolution of an exacerbation. If above steps fail, Intravenous magnesium may provide additional bronchodilatation in patients whose presenting PEF is below 30% predicted. Indications for endotracheal intubation and intermittent positive pressure ventilation (IPPV)