| ID | 89 |
|---|---|
| Name | BRONCHIAL ASTHMA |
| Cause | |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | Investigations: 1. X-Ray chest: Hyperinflated lungs in acute attack with pegion chest deformity in lateral view. Lobar collapse may be seen if mucus occludes a large bronchus. 2. Pulmonary function test: i. Demonstration of airflow obstruction by using spirometry. Or, ii. Peak expiratory flow (PEF)- sharp overnight fall (morning dipping) & subsequent rise during the day in patients with asthma, i.e a diurnal variation in PEF more than 20% is considered diagnostic, which doesn’t occur in patients with COPD. 3. Tests for allergic status: i. Skin prick tests- presence of atopy may be demonstrated. ii. Determination of total and allergen-specific IgE. iii. Complete blood count or picture (CBC/CBP)- may show peripheral blood eosinophilia. 4. Therapeutic test- these patients respond quickly with bronchodilators, & there is complete or partial reversibility of obstruction following bronchodilator therapy. |
| Management | Management of chronic persistent asthma:12 Management of asthma is now considered as step wise fashion. Initial treatment is chosen for an individual according to the severity of disease. It is better to start with a treatment regimen which is likely to control the symptoms then step-down the drugs used rather than step-up. Step 1: Occasional symptoms less frequently than daily (Mild intermittent): Occasional use of inhaled short-acting b2-adrenoceptor agonist bronchodilators (SABA, e.g salbutamol or terbutaline) as required. If the patient requires more than occasional use, i.e more than once daily or 3 times each week, and/or nocturnal episode once in a week, indicates the need for long-term control therapy, and move to step.2 Step 2: Daily symptoms (Mild persistent): Regular (daily) inhaled short-acting 2-adrenoceptor agonist bronchodilator (SABA) + a low-dose anti-inflammatory inhaled corticosteroid (ICS) e.g beclomethasone diproprionate, starting dose of 200mcg or fluticasone propionate 125mcg or budesonide 200mcg twice daily; higher dosage may be required in smokers. Alternative drug may be given instead of an inhaled steroid, but is less effective, such as sodium cromoglicate or nedocromil sodium or a leukotriene receptor antagonist or theophylline (these are effective in childhood, rather than in adult). If not controlled with this medication, move to step.3 Step 3: Severe symptoms, poorly controlled despite regular use of low-dose ICS (Moderate persistent): Regular inhaled short-acting b2-adrenoceptor agonist bronchodilator (SABA) as required + a medium dose ICS (e.g beclomethasone diproprionate up to 500mcg daily); or a low-dose ICS (as above), plus a long-acting b2-agonist (LABA, e.g salmeterol 25mcg/puff, 2 puffs twice daily); or a low-dose ICS (as above), plus an oral leukotriene modifier (e.g montelukast 10mg daily, but it is less effective than LABA as add-on therapy). Step 4: Severe symptoms, poorly controlled despite step 3 with moderate dose ICS management (Severe persistent): Regular inhaled short-acting b2-adrenoceptor agonist bronchodilator (SABA) as required + a medium to high dose ICS (e.g beclomethasone diproprionate 500mcg up to 2000mcg daily), plus an inhaled long-acting b2-adrenoceptor agonist (LABA, e.g salmeterol 25mcg/puff, 2 puffs twice daily), plus addition of a fourth drug, such as an oral leukotriene modifier (e.g montelukast 10mg daily), or sustained-release theophylline (initially 200mg orally 12 hourly then 200-600mg orally 8-12 hourly), or lipoxygenase inhibitor e.g zileuton (600mg orally 6 hourly) may be given. Step 5: Severe symptoms with deterioration despite step 4 management: With above treatment (step 4), add regular oral steroid therapy e.g prednisolone lowest single dose (usually 40mg/day) necessary to control symptoms. If the patient is still deteriorating inspite of prednisolone, transfer the patient to the hospital for further management. Using this type of ‘step’ approach to asthma management patient compliance is likely to be better when control of symptoms is achieved rapidly. Regular review is important and if there has been good symptomatic control for 3-6 months a step-down of treatment should be made. Other management: 1. Complete bed rest in propped up position. 2. O2 inhalation (35-60% or 4-6 litres/m) if required 3. Antibiotics- one course of appropriate antibiotic should be given to prevent secondary infection (if any). 4. Allergens and other precipitating factors should be avoided or treated accordingly. 5. Breathing exercise may be helpful. 6. Exercise induced asthma: This is usually common in atopic children with episodic asthma. Regular inhalation of sodium chromoglycate to be continued for 4 weeks. Assessment of severity of acute asthma: Features, of severity: o Pulse rate > 120/min o Pulsus paradoxus (>10mm Hg) o Unable to speak in sentences o Peak flow <50% of expected N.B: Apparent distress & respiratory rate may be misleading. Management of asthma exacerbations at home: A. Assessment of severity of asthma exacerbations: See above. B. Initial management: 1. Inhaled SABA- up to two treatments 20 minutes apart of 2-6 puffs by MDI or nebulizer treatments. If good response (no wheezing or dyspnea), contact doctor for follow-up instructions and further management. If incomplete response (persistent wheezing and dyspnea), or poor response (marked wheezing and dyspnea)- i. add oral systemic corticosteroid, ii. continue or repeat inhaled SABA immediately. If distress is severe and nonresponsive to initial treatment, specialist advice is essential and patients should be transferred to the hospital emergency department immediately. Management of acute severe asthma in hospital: 1. Full assessment including PEF or FEVl & 2. Arterial blood gas analysis Initial management- 1. Oxygen: High concentradton and high flow rate (usually 60%). There is no contraindication of using higher concentration of oxygen in acute severe asthma. If arterial blood gas analysis is possible, a PaO2 of > 8.5-9 kPa should be maintained. 2. I.V access for rapid intravenous medication. 3. Corticosteroids: One dose of hydrocortisone 200mg i.v followed by prednisolone 40mg/day orally. If asthma is very severe and patient is unable to swallow or vomiting occurs i.v hydrocortisone should be maintained. 4. Nebulized b2-adrenoceptor agonists e.g salbutamol 2.5mg-5mg or terbutaline 5-10mg 4-hourly initially but if necessary repeat within 30 min. Intravenous aminophylline is not recommended in acute severe asthma. To evaluate the condition, PEF & arterial blood gases should be estimated at appropriate intervals. If satisfactory improvement- Reduce nebulised b2-adrenoceptor agonists to 6 hourly then- Change from giving (b2-adrenoceptor agonist by nebuliser to metered dose inhaler (MDI) or other type of inhaler then- Make sure that the patient is stable (including PEF) on the drugs & doses, he will be taking outside hospital then- On discharge, ensure that the patient fully understands: - how and when treatment should be taken; - which drugs he should adjust himself and how; - what to do if his asthma deteriorates. If response is not satisfactory- Add nebulised ipratropium bromide 500mgm and/or i.v aminophylline (check if on oral theophylline) 5mg/kg (dissolve in 20ml of dextrose in aqua then give slow i.v in 20 min. then continue the drug in 0.5-lmg/kg/hour) or try i.v b2-adrenoreceptor agonist e.g salbutamol 2.5-5mg initially then- Monitor PaCO2 carefully then- Assisted ventilation if patient fails to respond. Indications for assisted ventilation- - Coma - Respiratory arrest - Exhaustion, confusion, drowsiness - Deterioration of arterial blood gas tensions despite optimal therapy, such as- Pa02 < 8kPa and falling PaCO2> 6kPa and rising pH <7.3 and falling |
| Introduction | Bronchial asthma is a chronic inflammatory disorder of the airways, characterised by paroxysms of breathlessness, chest tightness, wheezing and cough resulting from narrowing of the airways by a combination of- i. muscle spasm, ii. mucosal swelling or oedema due to inflammation and iii. viscid bronchial secretion. |
| History | |
| Etiology | Etiology: A. Atopic or extrinsic asthma- (tends to develop episodic asthma) 1. Family history usually present. 2. It begins in the childhood. 3. Allergic history- type I hypersensitivity reaction. 4. Those who readily form IgE antibodies against allergens. Allergens enter within bronchi & react with antibody & mast cell stimulated and produces histamin, kinins, SRS-A & broncho-constriction occurs. B. Non-atopic or intrinsic asthma (tends to develop chronic asthma) 1. Unknown etiology 2. May be due to depletion of prostaglandins. C. Precipitating factors- 1. Occupational hazards or sensitizers- may lead to occupational asthma. 2. Bronchial irritation by smokes, dusts & air-pollution. 3. Cold air and exercise. 4. Bacterial infection of respiratory tract. 5. Dietary allergens. 6. Drugs 7. During menstruation. 8. Emotional factors |
| Clinical Features | Clinical feature: Symptoms: 1. Sudden onset of severe respiratory distress & wheezing with restlessness & feeling of tightness in the chest. 2. Cough- may be unproductive or coughing up of tough viscid sputum 3. Patient may give history of previous asthmatic attack. Signs: 1. Respiratory muscles and accessory respiratory muscles are prominent. Prominent supraclavicular fossa; widening and deepening of inter-costal spaces may be present. 2. Movement of the chest wall diminished symetrically; chest may be silent. 3. Hyper-resonant on percussion; breath sound is vesicular with prolong expiration; bilateral extensive high pitched polyphonic expiratory & inspiratory rhonchi and some crepitations. Life-threatening features: o Can’t speak o Central cyanosis o Exhaustion, confusion, 0 concious level o Bradycardia o Silent chest o Unrecordable peak flow Arterial blood gases in life-threatening asthma- o A normal (5-6 kPa) or high CO2 tension o Severe hypoxaemia (<8kPa) specially if being treated with oxygen o Low pH or high [H+] |
| Preventions | Prevention: Asthma is often preventable if the ‘trigger factors’ known to provoke asthma attacks can be identified and eliminated. Early treatment of chest infection, discontinuence of cigarette smoking and the drugs like cromolyn sodium (inhaler) and ketotifen are essential aspects of preventive care |
| Treatment | |
| Complications | |
| Prognosis | |
| Types | Clinical types: Episodic Asthma: Sudden attack of dyspnoea (chiefly expiratory) accompanied by wheezing cough, which is initially unproductive but productive later on. Inbetween attack patient is well (no rhonchi). Chronic Asthma: Like episodic asthma, but some degree of dyspnoea persist inbetween attacks. Cough, mucoid sputum and recurrent attack of respiratory track infection is common. In between attacks a few rhonchi still present. Severe acute asthma (Status asthmaticus): This term has replaced ‘status asthmaticus’ as the description of life-threatening attacks of ashma, characterised by respiratory distress and arterial hypoxaemia which does not response to usual bronchodilators. |
| Classification | Clasification of asthma severity 1. Intermittent asthma: Episodic asthma with sudden attack of dyspnoea accompanied by wheezing cough; asthmatic attacks 2 days or less in a week; not interfere with normal life activities; fewer than two nocturnal episodes in a month. Patients with mild intermittent asthma usually remain asymptomatic and normal FEVI (> 80%) in between exacerbations. 2. Persistent asthma: a. Mild asthma: Asthmatic attack > 2 days in a week (but not daily); dyspnoea only with activity; minor interference with normal activities; 3 to 4 nocturnal episodes in a month. FEVI is normal and is > 80%. b. Moderate asthma: Asthmatic attack all days in a week; dyspnoea interferes with limits of usual activities; more than one nocturnal episodes in a week, but not every night. FEVt is reduced and is > 60% but < 80%. c. Severe asthma: Continuous asthmatic suffering throughout the day; dyspnoea at rest, extreme interference with normal activities, even conversation; nocturnal episodes often every night in a week. FEV, is reduced and is < 60%. |
| Observation | |
| Pathology | Pathological changes in asthma i. Desquamatiom of epithelium. ii. Thickening of basement membrane. iii. Submucosal oedema with infiltration of granulocytes. iv. Smooth muscle hypertrophy & hyperplasia. v. Hyperplasia of mucous glands. vi. Vasodilatation. vii.Mucous plug formation. On aetiological basis asthma can be divided into- 1. Early-onset or extrinsic or atopic childhood asthma. 2. Late-onset or intrinsic or non-atopic adult asthma. |
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