Severe Asthma in a Paediatric Patient - Essay Example

Severe Asthma in a Paediatric Patient ID Number Word Count Module Severe paediatric asthma brings increases morbidity and mortality in children. Asthma is a condition that results from the hypersensitivity of the airways and inflammation of the airways. Exacerbations in severe paediatric asthma result from the chemotactic response of the immune system of the sensitized child to an allergic insult or a viral infection that results in enhanced inflammation of the airways, bronchospasms and increased mucus secretions. As a consequence the airways get blocked reducing the availability of oxygen in the lungs and upsetting normal homeostasis. Unless severe asthma is adequately treated it can become life threatening. Treatment regimen in the case of severe paediatric asthma is giving high concentrations of oxygen to the patient, nebulized salbutamol and systemic corticosteroids. Key Words – Severe paediatric asthma, hypersensitivity of the airways, inflammation of the airways, immune system, bronchospasms, mucus secretions, salbutamol and corticosteroids. Table of Contents 1. Introduction and Background : 4 2. Pathophysiology of Asthma : 6 3. Clinical Manifestations and Clinical Investigations : 10 4. Psychological Factors : 11 5. Drugs Used in Severe Paediatric Asthma : 12 6. Conclusion : 15 : Introduction and Background One of the most frequent causes of children being presented in hospitals is asthma. The important concern with paediatric asthma is that a significant percentage of children hospitalized with a severe attack of asthma are likely to die. This makes understanding paediatric asthma and maintaining guidelines for managing severe paediatric asthma important to the reduction of paediatric mortality in hospitality (Paediatric Guidelines, 2006). Weinberger 2008 p.633, defines asthma as a disease characterized by hyper-responsiveness of the airways to various stimuli, resulting in airway obstruction that is reversible to a substantial degree either spontaneously or as a result of treatment”. The airway obstruction observed in asthma arises from the different levels of severity of broncho-spasm and inflammation. Inflammation in asthma is the result of mucosal oedema and the secretion of mucous (Weinberger, 2008). Guill, 2004, points out that asthma does not occur as a set of episodic events spread over periods of time, but is rather present as a state of inflammation and hyper-responsiveness of the airway that presents in a varying manner in an individual suffering from asthma and also among the different individuals having asthma. Such an observation suggests the severity of an asthmatic event in a child varies from time and time and the severity of an asthmatic event is not necessarily the same between different individuals (Guill, 2004). Figure – 1 Normal and Blocked Airways (Weinberger, 2008) The varying severity of asthma in children gives rise to asthmatic events that may be present with minimal symptoms that have hardly any impact on the health of the child to asthmatic events with life threatening potential. The available indicators of the severity levels of asthma in children are the prevalence of asthma symptoms, hospital admissions and the mortality rates. These indicators show a variance in different parts of the world. In the United Kingdom, within the age group of five to fourteen, the present ration of prevalence of wheeze symptoms over yearly risk of admission to hospital due to asthma is 56 to 1 and in the case of mortality from a severe asthmatic attack is 66,400 to 1. These figures indicate the hierarchical mode of the severity of asthma in children. In practice, however, such a hierarchical mode in the severity of asthmatic events may be difficult to discern due to differences in the availability and quality of care provided; differences present in the care provided at primary and secondary level and differences in the care provided to overnight admissions, day stay and emergency room presentations within secondary care and differences in the diagnosis or definition of asthma at the various levels of care provided (Anderson et al, 2008). Pathophysiology of Asthma The dearth of studies into asthma in children had led to the lack of proper clarity on the pathophysiology of asthma in children. However, the spurt in the incidence of asthma in young children and adolescents led to more investigations into the nature of asthma in children, causing an improvement of the understanding of the same (Larsen, 1999). The important characteristics of asthma consist of persistent inflammation of the airways with varying frequency and intensity episodes of airway obstruction and airway hyper responsiveness. In individuals prone to asthma, this can be taken as the ease with which the airways constrict to stimuli, which include normal exposures like exercise and hyperventilation of cold air. The severity of the episode of asthma in both adults and children is related to the level of airway responsiveness to nonallergic and nonsensitizing stimuli and allergic and sensitizing stimuli like allergen exposure and viral infections. Stimuli like allergens and viral infections aggravate the hyper responsiveness of the airways by producing inflammation within the airways. Frequent airway insults in childhood can cause changes in neuronal control of these airways, resulting in chronic alterations to both the anatomy and physiology of the lungs, thereby affecting its normal function (Larsen, 1999). Figure – 2 Photomicrograph of an airway from an asthmatic patient. Note focus of epithelial cell sloughing (large arrow), which may allow exposure of nerve endings to airway lumen. If epithelial cells (short arrow) are infected by respiratory viruses, local release of inflammatory mediators can contribute to increased vascular congestion and oedema (*), and infiltrates by a mixed population of inflammatory cells (arrowheads). (Larsen, 1999). Inflammation of airways contributes by a large measure to the pathology of asthma, which is true even when the episode of asthma is mild. The inflammation of the airways can occur from several causes, which include the entry into the airways by eosinophils, through the activation of T cells inside the airways, enhancement in the number of mast cells present, and desquamation of the epithelium of the airways. In older children the inflammatory response is similar to that of adults, but there is less clarity on the similarity between the inflammatory response of in young children and infants with that of adults (Larsen, 1999). The role of allergens in the pathophysiology of severe asthma is significant with their ability to enhance the hypersensitivity of the airways. Antibodies of the IgE class are an essential component of the immunity protection in the human body. However, IgE can also cause spontaneous hypersensitivity reactions in sensitized individuals, like individuals prone to asthma, on exposure to antigens that include allergens (Nester et al, 2004). Figure – 3 Mechanism of Immediate IgE-Mediated Hypersensitivity in Asthma Cross-linking of cell-bound IgE antibody causes the mast cell to degranulate : V Histamine and other mediators are released : V Mediators cause capillary dilation, increased capillary permeability, airway constriction mucus secretion and pain : V Airway blockage leading to severe asthma (Nester et al, 2004). Into the inflamed airways in asthma, the antigen (allergen) induces the release of chemical mediators from the IgE sensitized mast cells and also from eosonophils that are attracted to the area of inflammation. The result of this is increased mucus secretion and spasms in the bronchi that have a profound effect on breathing, due to the restricted airways. In addition to this, mediators with the exception of histamine, essentially the lipids, like leukotrines and prostaglandins and the protein cytokines also contribute to the increased mucus production and induce spasms of the bronchi. The net result on the inflamed airways is blockage due to mucus and reduction in the airway due to spasms of the bronchi. Passage of air through the bronchi is negatively impacted, resulting in reduced oxygen availability in the lungs, upsetting normal homeostasis. This causes the child to wheeze and gasp during breathing trying to force air through the blocked and reduced airways in an attempt to increase the oxygen availability in the lungs for normal homeostasis (Nester et al, 2004). Viral infections cause a similar action in the inflamed airways. Viral infections cause an immediate response that has a powerful chemotactic effect on the neutrophils, monocytes and lymphocytes, leading to enhanced inflammation of the airways in an individual with asthma. Secondary to this cytokines are released, which prolong inflammation and cause the activation of eosinophils, basophils, lymphocytes and mast cells. The consequences include smooth muscle hyperplasia and bronchial hyper-responsiveness. In addition there is increased collagen deposition underneath the basement membrane, resulting in further narrowing of the bronchi and bronchospasms. The net result is reduced air intake into the lungs, limiting the availability of oxygen in the lungs for normal homeostasis (Cantani, 2008). Occlusion of the airways that result from smooth muscle broncho-constriction, oedema of the airways and the development of mucus plugs in essence make up the pathophysiological basis for the gas exchange or homeostasis abnormalities seen in severe asthma. The resultant gas exchange abnormalities result in the development of extensive pulmonary shunting, though shunt may be absent in children with effective hypoxic vasoconstriction and good collateral ventilation. The administration of relatively low concentrations of supplemental oxygen is sufficient to correct mild hypoxia that may occur with severe asthma, but severe hypoxemia that commonly results from atelectasis and excessive of mucus secretion require higher supplementary oxygen. Increase of obstruction in the airways due to broncho spasms and mucus plugs cause the initial hypocapnia to change to hypocapnia and finally on to hypercapnia, as a result of alveolar hypoventilation or exhaustion of the child. In the case of severe respiratory acidosis, resulting from hypercapnia, a metabolic lactic acidosis may be coexistent. There is still lack of clarity on the pathogenesis of lactic acidosis in acute severe asthma, though there is belief that it may be related to fatigue of the diaphragm or the excessive use of beta-agonists in the interventions in the management of severe asthma (Restepro & Peters, 2008). The respiratory system in younger children is not fully developed, as it is only by the age of eight that the respiratory system attains full development. This character of the anatomic development, places an extra burden in dealing with infants and younger children with severe asthma. Key factors that have to be noted in the under developed respiratory system in infants and young children are immature lungs with a smaller surface area, relatively smaller upper and lower airways, which are easily blocked and have a significant impact on the entry of air during severe asthma and the more horizontal ribs reduce air expansion (Hoskins & Chandler, 2007). Clinical Manifestations and Clinical Investigations Bronchospasms and blockage of the airways due to mucous secretions is an essential feature of severe asthma, which leads to hypoxemia and imbalance in the ventilation and perfusion in the lungs. Acute respiratory discomfort is demonstrated by the child along with the use of accessory muscles to breathe. The child is too breathless to talk and the lips may have turned blue. The heart rate in children between two and five years is enhanced to more than 130 beats per minute, while in the case of children between five and eighteen years 120 beats per minute. Respiratory rate in children below five years increases to more than fifty breaths per minute, while in children above five years to eighteen years the respiratory rate is more than thirty breaths per minute. Oxygen saturations (SpO2) demonstrated is less than ninety-two percent in air and peak flow between 33% and 50% predicted in some children. Should the sever asthma condition be life threatening then the presentation of the child changes to silent chest, poor effort, lack of consciousness or altered consciousness, cyanosis, SpO2 less than 85% in air and peak flow less than 33% predicted (Paediatric Guidelines, 2006). Pulse oximetry and peak expiratory flow rate (PEFR) are two primary diagnostic aids for severe asthma in children. PEFR is not always used in the diagnosis of severe asthma in children. Use of PEFR is to be enhanced as a diagnostic aid for the diagnosis of severe asthma in children, particularly in children six years and below in age (Ly, 2007). Psychological Factors There is increased understanding that inadequate symptom perception increases the emotional factors involved during breathlessness in severe asthma among adults, contributing to greater morbidity and mortality. This leads to psychological factors compounding the distress during severe asthma attacks in adults. There is limited understanding on how this translates for children. Nevertheless indications from adult experiences and early studies indicate that psychological factors like emotions have a role to play in the perception of dyspnea in children during severe asthmatic attacks and easing of these emotions through positive actions reduce the distress in severe asthma in children (Von Leupoldt, Riedel & Dahme, 2006). Drugs Used in Paediatric Severe Asthma Care has to be shown in the choice of drugs, formulations, doses, routes and methods of administration for children. This is because children cannot be considered as small adults, whereby all drugs used for adults in severe asthma may be given to children in smaller doses. This reason for this is the pharmacokinetics and pharmocodynamics of a drug may be markedly different in children in comparison to adults (Royal Pharmaceutical Society of Great Britain, 2004). The best way in which patients receive their drugs is through the steps taken by a qualified health care professional to assess the medication needs of the patient and prescribe the necessary medication, which is then dispensed by a chemist or given by in a hospital. This traditional means for drug dispensing hardly suits an emergency case of paediatric asthma. A legal alternative has been put in place since 2000 in the form of the Patient Group Directions (PGD) that enable certain health care professionals to administer medicines to a group of patients according to laid out conditions in the PGD. The PGD enables the administration of medications in the case of paediatric asthma without the requirement for a prescription (National Prescribing Center, 2004). Table – 1 Health Care Professionals involved in PGD (Section 3.2) Health Care Professionals Midwife, Nurse, Pharmacist, Optometrist, Podiatrist/Chiropodist, Radiographer, Orthoptist, Physiotherapist and Ambulance Paramedic (National Prescribing Center, 2004). The criterion for use of drugs in severe asthma is to correct changes in airways, breathing and circulation. This is due to the airway blockage due to inflammation, broncho-spasms and mucus secretion arising from the hypersensitiveness of the airways, which alters the gas exchange or homeostasis in paediatric asthma. To alleviate the hypoxia being experienced the first step in medications is to administer a high concentration of oxygen. Oxygen may be administered via non-re-breathing mask, stoma in laryngectomee and other neck breathing patients. Oxygen is administered in high concentrations irrespective of the saturation levels of oxygen (Paediatric Guidelines, 2006). The next step in the drug administration during severe paediatric asthma is the providing an inhaled beta-agonist, like the most commonly used salbutamol through either a metered dose inhaler (MDI) or through a nebulizer. The use of a beta-agonist is to ease the constriction in the bronchi as a result of the broncho-spasms and thereby increase the size of the airways and reducing the blockage of the airways. In case of failure in response to the use of salbutamol, then Ipratropium aerosol is recommended (Weinberger, 2008). Table – 2 Intervention Medication: Dosage and Decisions for Usual Treatment of Acute Symptoms of Asthma Medication Dosage When to use Albuterol (salbutamol), levalbuterol terbutaline, or pirbuterol by metered dose inhaler (see Figure 4 for administration issues). Two to four inhalations is usual, but up to six inhalations can be used (one at a time) and is equivalent to the most common dosage by nebulizer. As needed for cough, wheezing and labored breathing. Scheduled use has no advantage over use as needed and may be deleterious for some patients. Repeated requirements for bronchodilator use during an exacerbation generally warrant a short course of an oral corticosteroid. Prednisone, prednisolone, methylprednisolone and dexamethasone as tablets. Liquid formulations and oral disintegrating tablets of prednisolone for young children (parenteral forms indicated only when concerned about oral retention). Dosage as prednisone or prednisolone: see Table 1. If bronchodilator subresponsiveness is identified by incomplete resolution of symptoms and signs from even repeat use of the bronchodilator, continue till asymptomatic; re-evaluate if not improving within 5 days or asymptomatic within 10 days. Dont taper.[63-65] Ipratropium aerosol 0.5 mg with 2.5-5 mg albuterol by nebulizer. Indicated for severe acute asthma in the emergency room or hospital when response to a ß2 agonist is inadequate for relief of respiratory distress. (Weinberger, 2008) Exacerbations in severe paediatric asthma is essentially brought on by the chemotactic response of the immune system to an allergic insult in the airways or due to a viral infection, which leads to increased inflammation, broncho-spasms and mucus secretion in sensitised children. Reduction in the immune system response is the next step in the drugs regimen in severe asthma is through the use of inhaled corticosteroids. Systemic corticosteroids are extremely useful in reducing the airway inflammation (Rodrigo, 2008). Key components in the drugs used in the treatment of severe paediatric asthma are the requirement for high concentrations of oxygen, assessment of severity, mainstay of treatment is nebulized salbutamol, ipratorium to be used in severe cases and lack of response to salbutamol, and parenteral ephedrine should never be used in the treatment of paediatric asthma (Paediatric Guidelines, 2006). Conclusion Severe paediatric asthma is a cause for concern due to the morbidity and mortality that results from it. Severe paediatric asthma is in essence due to the inflammation and hypersensitivity of the airways that lead to blockage of the airways. Allergic insults and viral infections bring about a response from the immune system that aggravate the inflammation of the airways and cause bronchospasms and increased mucus secretion, causing blockage of the airways and upsetting normal homeostasis. Sever paediatric asthma should be treated aggressively using high concentrations of oxygen, nebulized salbutamol and systemic corticosteroids. . Literary References Anderson, H. R., Gupta, R., Kapetanakis, V., Asher, M. I., Clayton, T., Robertson, C. F., Strachan, D. P. & The ISAAC Steering Committee. 2008, ‘International Correlations Between Indicators of Prevalence, Hospital Admissions and Mortality for Asthma in Children’, International Journal of Epidemiology, vol.37, no.3, pp.573-582. 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