Asthma is a chronic inflammatory disorder of the lower airways. Asthma may be diagnosed any time after one year of age and is usually detected by a persistent dry cough, particularly at night, in the early morning or with exercise. It is usually accompanied with chest tightness, shortness of breath and a wheeze. Narrowing of the airways is caused by inflammation, extra mucous and bronchoconstriction (Ambulances for Asthma, 2007). Asthma can be triggered by environmental exposures, infections, human induced factors such as stress or exercise, and for some individuals the trigger might still be unknown.
It has three main components that can be characterised as follows:
The airway can become obstructed due to this response, however early management can reverse these elements. Alveolar hypoventilation occurs leading to VQ mismatch, CO2 retention and air trapping.
Australia has one of the highest asthma prevalence rates in the world with 10% of Australians reporting asthma as a current condition in the 2007-2008 National Health Survey, (Australian Bureau of Statistics, 2009). 447 Australians died from asthma in 2008, the greatest since 2000 and a 16% rise on the previous year. 77% of deaths occurred in adults aged 60 years or older and one in ten deaths were under 40 (Australian Bureau of Statistics, 2010). Populations at increased risk of morbidity and mortality associated with asthma include older adults, asthmatics in rural/remote areas and Aboriginals and Torres Strait Islanders (Marks, Correll, & Williamson, 2005). Asthma is a major cause for hospitalisation particularly in children and is one of the top five most common reasons for seeing a general practitioner (Department of Health, WA, 2009). It is estimated that 60% of asthma deaths are associated with avoidable factors such as over-reliance on medications, delay in seeking help, a failure to recognise the severity of asthma and lack of regular medical review (Ambulances for Asthma, 2007).
Asthma is characterised by hyper-reactive airways and inflammation leading to episodic, reversible bronchoconstriction in response to a variety of stimuli (Cameron, et al, 2004).
Extrinsic asthma is a type 1 hypersensitivity reaction induced by an extrinsic allergen. IgE-mediated activation of mucosal mast cells results in the release of primary mediators (histamine, eosinophilic and neutrophillic chemotactic factors) and secondary mediators including leukotrienes, prostaglandin D2, platelet-activating factor and cytokines.
The result is: bronchoconstriction by direct and cholinergic reflex actions, increased vascular permeability and increased mucous secretions (Cameron et al, 2004).
Intrinsic asthma is initiated by diverse non-immune mechanisms including respiratory infections, drugs such as aspirin and beta-blockers, pollutants and occupational exposure, emotion and exercise (Cameron et al, 2004).Types of Asthma:
|Extrinsic (outside cause):||Intrinsic (inherent cause):|
Classic allergic asthma resulting in bronchospasm, increased mucous secretions, and increased vascular permeability.
Non-immune mechanisms such as respiratory infections, drugs such as aspirin and beta-blockers, pollutants, emotions and exercise.
The principle goals for treating asthma exacerbations are:
The severity of the exacerbation determines the treatment required. Peak Expiratory Flow (PEF), pulse rate, respiratory rate, and pulse oximetry should be monitored during treatment (Global Strategy for Asthma Management and Prevention [GSAMP] 2008).
PEF is a useful tool for short and longer term reversibility testing in subjects with pre-existing airflow obstruction. The change in PEF is more meaningful than the absolute value found in normative tables; a value greater than 20% decline is abnormal and greater than 50% decline indicates a severe exacerbation (Horan, 2010). Greater than 60l/min in PEF is suggested as the best criterion for defining reversibility (British Thoracic Society/ Scottish Intercollegiate Guidelines Network [BTS], 2008). However in severe acute asthma only 65% of people can complete the manoeuvre (Horan, 2010).
Many patients with acute severe asthma are hypoxaemic, so supplementary oxygen should be administered urgently to maintain a SpO2 of 94-98% (BTS, 2008). There is now emerging evidence that hyperoxia may be harmful to a more widespread group by releasing pulmonary hypoxic vasoconstriction, worsening V/Q matching and increasing hypercapnia (Rodrigo, et al, 2003) . A randomised control trial showed a decrease in PaCO2 in a group receiving 28% O2 and an increased PaCO2 in a group receiving 100% O2 (Chien, et al, 2000). Oxygen saturation in children should normally be greater than 95% and an oxygen saturation of less than 92% is a good predictor of the need for hospitalisation (GSAMP, 2008).
Most cases of acute asthma will respond to bolus nebulisation of B2 agonists; prehospital administration of Short-Acting Beta Agonists (SABAs) reduces airflow obstruction and relieves symptoms (BTS, 2008; Markenson, et al, 2004; Richmond et al, 2005). Paramedics should have available a nebuliser and/or an inhaler plus spacer/holding chamber for SABA administration (National Heart Lung & Blood Institute [NHLBI], 2007). Continuous nebulisation of B2 agonists with an appropriate nebuliser may be more effective than bolus nebulisation in acute asthma for patients with a poor response to initial therapy (BTS, 2008). Metered dose inhalers with spacers can be used for patients with exacerbations of asthma other than those that are life-threatening (Cates, Crilly, & Rowe, 2006).
Inhaled B2 agonists are as efficacious and preferable to intravenous B2 agonists in adult acute asthma. Intravenous B2 agonists should be reserved for those patients in whom inhaled therapy cannot be used reliably (BTS, 2008).
Adrenaline has some theoretical advantages over pure B2-agonists in that its additional alpha-agonist actions of vasoconstriction and mucosal shrinkage may improve airway calibre (Berston & Soni, 2009); it should be given for severe exacerbations and only if other treatments such as Beta2 agonist and ipratropium bromide are unavailable. Paramedics should not delay transport of the patient to the appropriate medical facility. The treatment may be repeated while transporting the patient (NHLBI, 2007)..
Steroids reduce mortality, relapses, subsequent hospital admission and requirement for B2 agonist therapy. The earlier treatment is given in the acute attack the better the outcome. (Rowe, Spooner, Ducharme, Bretzlaff, & Bota, 2001; Rowe, Spooner,
Ducharme, Bretzlaff, & Bota, 2007).
Knapp & Wood (2003) and Stead & Whiteside (1999) undertook studies comparing hospital admission rates for patients with moderate to severe asthma who received intravenous methylprednisolone in the prehospital setting versus in the emergency department. Both found significant benefit in that earlier administration of corticosteroids in the prehospital setting resulted in less hospital admissions for those suffering acute asthma. These studies however were only small and consequently lacked statistical power. Steroids remain recommended for all episodes of acute asthma; steroid tablet medication has been found to be as effective as intravenous administration of steroid medications provided that the tablet can be swallowed and retained (Rowe, et al, 2001).
Ipratropium Bromide (Trade name: Atrovent) is an anticholinergic agent. Combining nebulised ipratropium bromide with a nebulised B2 agonist produces significantly greater bronchodilation than a B2 agonist alone, leading to a faster recovery and shorter duration of admission but may not be beneficial in milder exacerbations or after stabilisation. (Rodrigo, Rodrigo, & Burschtin, 1999; Stoodley, Aaron & Dales, 1999). Therefore, it is recommended to add nebulised ipratropium bromide to B2 agonist treatment for patients with acute severe or life threatening asthma or those with a poor initial response to B2 agonist therapy.
St John WA