ASSOCIATION OF PHYSICIAN OF INDIA

During the 1970s and early 1980s a series of papers reporting into asthma deaths in the United Kingdom were published. The consensus was that the majority (80%) of these deaths were associated with potentially preventable factors and that many deaths occurred in young people. Most deaths occurred outwith hospital but even in hospital management was often sub-optimal. To many patients, General Practitioners and General Physicians asthma was a common disorder which they could handle competently both in its long term management and acute exacerbations. The reports challenged these beliefs.(1, 2, 3, 4,5) This led to the development of the first British Guidelines on Asthma Management in 1990 which were subsequently reviewed in 1995 and again in 1997 (6, 7, 8). They were an attempt to define the parameters required for proper assessment, underlined the role of corticosteroids, inhaled bronchodilators and oxygen in the management of acute asthma and highlighted the need for appropriate patient education. Guidelines themselves cannot alter management. They have to be taken by individual healthcare workers and applied locally. At about this time the importance of evidence based medicine was being recognised, not only by the profession, but by managers in the National Health Service and Government. This led to the development of SIGN (Scottish Intercollegiate Guidelines Network) based on the concept of taking common medical problems and developing evidence based guidelines of management for local implementation supported and backed by the Government in Scotland:- as outlined by Professor Petrie in his lecture (9). One of the weaknesses of the British Guidelines on Asthma Management was the lack of recording of the evidence on which statements were made:- the background papers were not published. SIGN has now produced three guidelines covering different aspects of asthma management:- hospital in-patient management of asthma, primary care management of asthma and emergency management of acute asthma. The latest being published within the last 2 months (10, 11, 12). All have been extensively researched but the recommendations are designed to be taken and applied locally with the encouragement of local Trust Managers. What has happened since the introduction of the first Asthma Guidelines? Success has been patchy but where enthusiastic doctors have applied them locally there is evidence of significant improvement in day to day care with fewer hospital admissions (13). Audit of care has helped to focus on the problems encountered by each practice and where appropriate adjustments have been made then improvements in management have occurred. (14). A key issue in reducing hospital admissions and the severity of attacks lies within improving care within the community with better assessments, more appropriate long term management and improved patient education raising the awareness of the signs of failing control and what action to take. Asthma deaths in England rose steadily in the 1980s possibly reflecting better diagnoses and increased incidence but have subsequently fallen through 1990s. Some of the asthma deaths now reported in the over 65s may in fact due to COPD as many such patients currently attend Practice Asthma Clinics, if so the improvement in asthma deaths may be more marked (14). However, in the 10-19 year-old range there has been little or no change in death rates with figures of 130 deaths in 2 years between 1991 and 1992 (15). In the United Kingdom adolescent years give rise to problems of compliance with treatment and denial of disease effecting patients with diabetes as well as asthma and present a challenge to our healthcare workers. In an acute severe asthma attack the development of intense inflammation within the bronchial walls leads to progressive decrease in the calibre of bronchi and bronchioles many of which become blocked with intraluminal mucous consisting to shed epithelium and inflammatory cells (16). Bronchodilators will not resolve the inflammation, nor will inhaled or nebulied steroids penetrate the areas of most intense inflammation thus the cornerstone of treatment is systemic (oral or intravenous) corticosteroids in the appropriate dose. Bronchodilators may help to relieve some of the bronchospasm and reduce mucosal oedema giving some respite to the patient but by acting on the pulmonary vascular bed they may increase hypoxia in severely ill patients. Progressive narrowing of the airway increases the ventilation perfusion imbalance while blocking of bronchi by mucous plugs increases the physiological arterial venous shut with airways being perfused but not ventilated. Both factors lead to increasing hypoxia which may persist for several days after lung function has apparently returned towards normal (17). Initially hypoxia leads to hyperventilation and the PaCO2 falls. However, as the FEV1 and peak flow decrease the PaCO2 tends to rise, firstly into the normal range, then above, due to alveolar hypoventilation resulting from extensive ventilation perfusion mismatching, arterial venous shunting and tachypnoea. When this occurs it is indicative of severe or life-threatening asthma attack which may require mechanical ventilation. The hypoxia is the most serious and dangerous effect of severe asthma leading to cardiac and cerebral hypoxia and death and should be treated aggressively with high flow oxygen (60% or above). Controlled oxygen is not required and may be dangerous. These patients have normal hypoxic drive and returning the PaO2 to normal will not lead to a further rise in PaC02 (18, 19). As the bronchial narrowing worsens, the lungs become progressively hyperinflated as inspired air is not fully expelled during expiration leading to air trapping such that the patients FRC may be increased towards their pre attack total lung capacity. The hyperinflation often recovers before there is much change in the FEV1 or peak flow readings. In the presence of tachypnoea on the basis of hyperinflation and increasing hypoxia many patients become anxious and agitated. Such patients do not require sedation, indeed early studies showed sedation to be a significant factor in between 40 and 80% of asthma deaths. With increasing hyperinflation the force required to inflate the lungs increases dramatically leading to increased negative inter-thoracic pressure on inspiration. The large swings of intra-pleural pressure are reflected in similar swings in systolic and diastolic blood pressure:- pulsus paradoxus, which can be detected using sphygmomanometry. It was originally thought that pulsus paradoxus was a useful prognostic indicator but recent studies show poor correlation with outcome and it is no longer recommended as a measurement in severe asthma. 50% of asthma deaths occur 24 hours after, 25% from 1-24 hours and only 25% within one hour of the onset of the final acute episode leaving adequate time for appropriate action to be taken (22). It is unusual for deaths to occur once the patient has reached hospital. Patients often delay seeking help at night or at weekends. Education pointing out the symptoms and peak flow indicators of uncontrolled asthma need to be constantly re-inforced. In up to 66% there was a history of poorly controlled asthma for several weeks before the final acute episode. Wide swings in diurnal peak flows are often noted indicating increased bronchial reactivity. Appropriate action early by patients and doctors could have prevented many of these fatalities. Many patients dying have had a recent acute severe attack, (10-20% treated in hospital), usually treated with oral steroid which have been abruptly stopped without the introduction or increase in inhaled corticosteroids. Such patients are particularly vulnerable to a further severe attack. A recent national audit of management of acute attacks in General Practice revealed that such failures remain common but feedback to the GPs led to significant improvement in subsequent years (23). Any assessment of an acute asthma attack must take into account the investigation of potential trigger factors. Acute episodes may follow the ingestion of certain seafoods (shellfish), ingestion of preservatives, or the prescription of Aspirin or non-steroidal anti-inflammatory drugs. Avoidance of such foods and more care with prescribing can prevent such attacks. Recent studies have underlined the importance of psychosocial factors in patients currently dying of acute asthma attacks (24). It is recommended that hospitals and primary care physicians keep "At Risk" Registers for patients with brittle asthma who tend to deteriorate rapidly, those who have previously been admitted to Intensive Care, those with frequent admissions and those with poor social backgrounds. Increasing nocturnal, morning or exercise symptoms with falling peak flow and increased use of bronchodilators are indicators of worsening control and require early contact with the healthcare services. The symptoms in an acute attack include worsening breathlessness, cough or wheeze, difficulty in speaking, distress, agitation, altered conscious level. The patient gets little or no help from their bronchodilator and may need to use it every 2 hours or less. The peak flow may fall precipitously. Any of these features requires urgent medical attention often with referral to hospital. The patient should use their bronchodilator by inhaler with spacer or nebuliser and start oral steroids (if available) while awaiting for attention or travelling to hospital. Simple clinical assessments give invaluable information both as to the state at presentation and response to treatment. A pulse rate of > 110 in adults and 120 in children, a respiratory rate of > 25 in adults and 40 in children, inability to complete a sentence in one breath or difficulty in feeding are all indicators of severe attacks. The presence of cyanosis, poor respiratory effort, bradycardia, hypotension, confusion, coma and a silent chest are features of life-threatening asthma. The initial pulse rate and its changes with treatment are good prognostic indicators. When available baseline peak flow readings should be taken and repeated to monitor response. Ideally they should be related to the patient’s best achievable results but this is not often available. The results should be expressed as a percentage of predicted for age, sex and height. A peak flow of between 50 and 33% of best/predicted is an indicator of a severe asthma attack, while one below 33% is found in life-threatening situations. However, in acute severe or life-threatening situations treatment should not be delayed while a peak flow is undertaken:- treat first and record peak flow later (25). If available pulse oximetry may provide useful additional information to the clinical findings. An arterial oxygen saturation (Sa02) of less than 92% breathing air is usually found in acute severe asthma and very low levels may be recorded in life-threatening episodes. An initial SaO2 of less than 80% is associated with an increased risk of admission to Intensive Care Units. Knowledge of the inspired oxygen concentration is essential when reporting Sa02. Continuous monitoring of Sa02 using oximetry is recommended in patient’s hospitalised with severe attacks (26, 27). Arterial blood gases are essential in the assessment of acute severe and life-threatening asthma or if the patient deteriorates while on effective treatment. The PaO2, PaCO2 and PH should all be recorded (28). Chest X-ray is only necessary if complications such as pneumothorax, pneumonia or pulmonary emboli are suspected, if there is doubt about the diagnosis or if the patient deteriorates on treatment. A method of triage for patients presenting in an Accident and Emergency Unit or Receiving Ward improves outcome. Patients with features of life-threatening asthma should be seen immediately and those with evidence of an acute severe asthma attack within 10 minutes (29). The core therapies for the treatment of acute severe or life-threatening asthma are inhaled beta 2 agonists, oxygen and systemic corticosteroids. Inhaled beta 2 agonists given in high dose by nebuliser or repeated activations of an MDI by a spacer device act quickly to relieve symptoms with few side effects. The dose may be repeated within 15 minutes and again at 30 minutes and thereafter according to the severity and response to treatment (30, 31). Anti cholinergic agents should not be used as first line treatment but may be added in severe and life threatening episodes (32). Parenteral beta 2 agonists and adrenaline may be added in severe cases. Intravenous Aminophylline alone has no advantages over beta 2 agonists and is more toxic. Meta analysis of 13 controlled trials suggest that IV Aminophylline adds little to routine management of acute asthma but it is still recommended in life threatening situations (33). High flow oxygen, 60% or above, should be given by facemasks (with reservoir bag) to all patients with acute severe or life-threatening asthma. When an air compressor driven nebuliser is used oxygen should be given by nasal cannulae (34). Systemic corticosteroids in adequate doses should be given to all patients with acute severe or life-threatening asthma. Several studies have shown that non or inadequate use of corticosteroids were a major factor in asthma fatalities. In the majority of cases oral corticosteroids are as effective as intravenous but if the patient is vomiting, cannot swallow tablets or if their conscious level is altered intravenous Hydrocortisone should be given, As it takes several hours for corticosteroids to be fully effective, they should be introduced as early as possible (35, 36). Patients with life-threatening asthma or those with acute severe asthma not responding to treatment and showing deteriorating in peak flow, persistence or worsening of hypoxia, hypercapnoea, falling PH, or rising H+ ion concentration, exhaustion, feeble respiration, drowsiness, confusion and coma or respiratory arrest should be considered for mechanical ventilation. Intubation for ventilation should be undertaken by a suitable qualified anaesthetist using rapid sequence induction. With appropriate treatment most patients reaching hospital with acute severe or life-threatening asthma should survive and return home. After recovery patients must be started on appropriate dose of inhaled steroid and educated about the features leading to the attack including indicators of failing control and appropriate trigger factors.