Acute Exacerbation of Asthma in Childhood

Acute Exacerbation of Asthma in Childhood

AcuteExacerbation of Asthma in Childhood


AcuteExacerbation of Asthma in Childhood


Asthmais a chronic inflammatory disease that affects the airways. It causesairway hyper-responsiveness, mucosal edema, bronchial constriction,and excess mucus secretion. An acute exacerbation of asthma refers toan episode of progressive worsening of symptoms of asthma such asdyspnea, wheezing, coughing, tightness of chest. An acuteexacerbation is characterized by reduced expiratory airflow causingwheezing on expiration (Brunner et. al., 2008). Children frequentlypresent with acute asthmatic exacerbations that are life threatening.The airway obstruction is reversible on its own or with treatment.Effective treatment depends on accurate assessment and quickintervention. The purpose of this paper is to explain the assessment,pathogenesis and management of an acute exacerbation of asthma inchildhood.

Manycells and mediators such as eosinophils, mast cells, andT-lymphocytes play a role in the pathogenesis of an acuteexacerbation of asthma. Common triggers for such exacerbationsinclude cold, strong odors, smoke, exercise, airway infections,gastroesophageal reflux, and pollen. These irritants bind toimmunoglobulin E which activates mast cells to release chemicalmediators of inflammation (Holgate &amp Douglass, 2010). Thesemediators are histamine, bradykinin, prostaglandins, andleukotrienes. The mediators initiate the inflammatory response bypromoting increased blood flow to the airways. Fluid, therefore, leakfrom the vasculature causing bronchial edema narrowing the airwaysand increasing the work of breathing.

Prostaglandinscause direct bronchial smooth muscle contraction. The stimulation ofalpha-adrenergic receptors of the sympathetic system lead to furtherbronchoconstriction. Airway remodeling may occur in the case ofchronic inflammation causing further narrowing. The narrowing causesairway resistance, making expiration active (Brunner et. al., 2008).The turbulent flow of air in the constricted airways causes wheezingpredominantly during expiration.

Whiteblood cells are also attracted to the area promoting furtherinflammation and swelling. Histamine causes excess mucus productionand secretion. Formation of mucus plugs in the airways leads toairway obstruction causing breathlessness (Jin, 2015). Viralinfections lead to cellular cytokines release, which induceeosinophils and neutrophils infiltration to cause inflammation andswelling of the airways leading to dyspnea.


Achild with an acute exacerbation of asthma has impaired lung functionand reduced oxygen intake leading to a ventilation-perfusionmismatch. In addition to this, the use of accessory muscles tobreath, and coughing increases the oxygen demand of the child.Therefore, the priority nursing intervention is to relieve thesymptoms and promote normal ventilation (Brunner et. al., 2008).

Theadministration of a quick-relief bronchodilator is the firstintervention for immediate treatment of symptoms and exacerbations.Rapid-acting bronchodilators are used for emergency treatment. Beta2agonists stimulate the beta 2 receptors and cause airway dilation,therefore, reducing the work of breathing and promoting gaseousexchange (Kovesi et al., 2009). The most common drug used to relievebronchoconstriction quickly is Salbutamol given through nebulizationeither intermittently or continuously.

Thesecond step in the nursing management of an acute exacerbation ofasthma is the administration of supplemental oxygen. Supplementaloxygen treats hypoxia by increasing the oxygen concentration reachingthe lungs. Therefore, it reduces the ventilation-perfusion mismatchby attaining oxygen saturation levels of above 90% quickly. Oxygenadministration also enhances bronchodilation promoting breathing andrelieving hypoxemia that arising from an acute exacerbation ofasthma. It also promotes normal lung function (Kovesi et al., 2009).However, the nurse should oxygen monitor the child closely and theamount administered to prevent oxygen toxicity.


Salbutamolis used to manage a severe acute exacerbation of asthma in a child.The drug is administered continuously by nebulization. Three doses ofipratropium are added to the nebulizer at 20-minute intervals.Salbutamol is a rapid acting beta 2 adrenergic receptor stimulatingdrug. The drug stimulates Beta 2 adrenergic receptors found in thebronchial smooth muscles. Alpha- and beta2-adrenergic receptorsbalance is maintained by cyclic 3, 5-adenosine monophosphate (cAMP).Stimulation of alpha-adrenergic receptors of the sympathetic systemlead to bronchoconstriction while, the stimulation ofbeta2-adrenergic receptors cause bronchodilation (Kovesi et al.,2009).

Beta2-adrenergicstimulation activates the enzyme adenylyl cyclase that catalyzes theproduction of cyclic AMP from ATP. Consequently, the levels of cAMPincrease to prevent release chemical mediators responsible forinflammation. The cAMP also relaxes bronchial muscles, reducing theairway resistance and promoting breathing.

Ipratropium,on the other hand, is an anticholinergic drug. It blocks muscarinicreceptors in the bronchial smooth muscles, reducing the formation ofcyclic guanosine monophosphate, which promotes intracellular calciumremoval decreasing the contractility of smooth muscles. Therefore,ipratropium reduces the contraction of bronchial muscles leading toairway dilation. Ipratropium is also shown to reduce mucus secretionand blood flow to the airways reducing airway obstruction.

Thenurse should use the correct dosage and formulation duringnebulization. The return of normal breathing pattern and respiratoryrate with no adventitious breath sounds is indicative of effectivemanagement of an exacerbation. The nurse should also monitor for sideeffects closely which include tremors, palpitations, and tachycardia(Wark, 2006). Both Salbutamol and ipratropium are known to causetachycardia. Therefore, vitals should be checked half-hourly. Pulserate above 100beats/minute indicates tachycardia. ECG monitoring andauscultation of heart sounds should also be done to rule outpalpitations and arrhythmias. The blood pressure should also bechecked and serum potassium monitoring since Salbutamol can causehypokalemia. In conclusion, acute exacerbations of asthma in childrenare life threatening. The key to effective management is properassessment and interventions. It is important to educate the parentson how to avoid triggers and how to use the rapid acting Salbutamolinhaler at home.


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Holgate,S., &amp Douglass, J. (2010). Asthma.Abingdon: HEALTH Press.

Jin,L. (2015). NursingJournals | Nursing 31 August 2015, from

Kovesi,T., Schuh, S., Spier, S., Berube, D., Carr, S., Watson, W., &ampMcIvor, R. (2009). Achieving control of asthma in preschoolers.CanadianMedical Association Journal,182(4),E172-E183.

Wark,P. (2006). Asthma exacerbations middle dot 3: Pathogenesis. Thorax,61(10),909-915.