Pathogenesis and Treatment of Acute Severe Asthma

1
Asthma
Results inCause
Prognosis
The risk of death in asthmatic person is higher to
approximately twice that in other person.
13, 14
Asthma is a chronic inflammatory disease of the airways
that causes airway hyperresponsiveness, mucosal edema,
and mucus production. 1, 3, 14
Course of disease
 Atopic asthma-eczema
 Non atopic asthma
1, 3
Secondary prevention
 Allergen-specific
immunotherapy
 Control of environmental
allergens. 7,14
Evaluation
 Access the airway
 Assess and evaluate
changes in vital signs
obstruction
1, 3
Nursing Interventions
 Obtain a history of allergic reactions
to medication
 Assess the patient’s respiratory
status by monitoring the severity of
symptoms
1, 7,14, 15
Pharmacologic Therapy
 Short- acting beta 2-agonist-
salbutamol
 Long-acting beta 2 agonist-
satmeterol
 Inhaled corticosteroid-
beclomethasone 2,6,11,14
Tre
atm
ent
Primary prevention
 Avoidance of personal exposure to
common risk factors
 Avoidance of direct and indirect
exposure to tobacco smoke
12, 14
Diagnosis
 Complete family history
 Acute wheeze and tachypnoea
 Triad of cough and breathlessness
1, 14, 15,
Clinical features
 Coughing
 Dyspnea
 Wheezing
 Shortness of breath
Risk factors
 Family history
 Allergies
 Occupational exposure
 Obesity
 Smoking 12,14
Pathogenesis
Activation when the mast cells are activated, it releases several mediators
These mediators perpetuate the inflammatory response, causing 
increased blood flow, vasoconstriction, and fluid leak from the
vasculature, attraction of white blood cells to the area
Progression increased mucus production, decreases the ability to bring air
into the alveoli low oxygenation red blood cells are able to exchange.
Aetiology
Acute bronchoconstriction due to
allergens results from a release of
mediators from mast cells that
directly contract the airway. 1, 14,
Leads to
need for
immedia
Diagnoses
1, 4, 6, 13, 14
1, 3.12
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Answers to assignment 2
Based on both family history, clinical manifestation, and laboratory diagnosis in the cases study, Mr. Jackson Smith has been diagnosed with
acute severe asthma. The family confirmed that the patient has a history of asthma having been diagnosed when he was two years old. According
to Mr. Smith’s clinical signs, he presented with severe dysponoea, high respiratory rates, and the blood gas results indicated chances of
respiratory acidosis and hypoxia, having raised level of Partial pressure of carbon dioxide (paCO2) and Low levels of arterial oxygen pressure
values (PaO2). Acute severe asthma takes place when the airway diameter is reduced due to physiological contraction of the smooth muscles,
inflammation of the bronchial walls and mucus hypersecretion along the airway (Wawrzyniak et al., 2017). According to Gon and Hashimoto
(2018), repeated damage and regeneration of airway’s smooth muscles epithelial cells due to exposure to environmental allergens and
inflammation leads to physiological dysfunction and histological changes of mucosal epithelium. Furthermore, Whitsett and Alenghat (2015),
described the hallmark of asthma attack to an increased airway responsiveness (AHR) which is inflated airway narrowing as a response to
allergen with the degree of AHR being associated to asthma symptoms and prerequisite for treatment.
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