CASE VIGNETTE ANALYSIS (PEDIATRIC CASE)

I. Questions:
As stated in the scenario, a 10-year-old boy is possibly diagnosed with asthma due to the
symptoms reported during the physical assessment. The patient is seen having difficulty
breathing, coughing, and making a “funny sound”, which is also known as asthma wheezing. All
of these symptoms eventually lead to a chronic disease that causes the airways of the lungs to
swell and narrow, which is asthma. Though the patient has no prior history of this, asthma could
be developing even with no known family history of the condition. Moreover, having an
abnormal level of respiratory rate, increased use of accessory muscles to breathe to push air
through the bronchus, presence of inspiratory and expiratory wheezing, and a low level of pulse
oximetry also could indicate that the patient is truly suffering from asthma.
In my opinion, the most important nursing measure that should be performed is assessing
the patient’s level of anxiety. The patient was said to be a 10-year-old boy with no genetic
history. And with this, the patient may feel overwhelmed by the situation. Moreover, due to his
difficulty breathing, anxiety may result from that struggle. Other nursing measures are
monitoring his vital signs, providing a calm, quite environment for the patient to rest, elevate the
HOB, as ordered, teach the patient to use pursed-lip breathing for exhalation to improve the
breathing, and give oxygen and medication as prescribed.
The underlying pathophysiology of asthma includes three components: airway
inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness. According to
Morris (2022) the mechanism of inflammation in asthma may be acute, subacute, or chronic, and
the presence of airway edema and mucus secretion also contributes to airflow obstruction and
bronchial reactivity.  There are varying degrees of eosinophil and mononuclear cell infiltration,
mucus hypersecretion, epithelium desquamation, smooth muscle hyperplasia, and airway
remodeling. A breakdown of the natural equilibrium between two "opposing" populations of Th
cells may cause asthmatic airway inflammation. Th1 and Th2 lymphocytes are the two distinct
subtypes that have been identified. Interleukin (IL)-2 and IFN-, which are crucial for cellular
defense mechanisms in response to infection, are produced by Th1 cells. IL-4, IL-5, IL-6, IL-9,
and IL-13 are a family of cytokines produced by Th2 that can mediate allergic inflammation.
Morris (2022) also added that numerous alterations, such as acute bronchoconstriction,
airway edema, persistent mucous plug development, and airway remodeling, might impede
airflow obstruction. Acute bronchoconstriction, which is the main element of the early asthmatic
response, is the result of immunoglobulin E-dependent mediator release following exposure to
aeroallergens. Airway edema, often known as the late asthmatic reaction, happens 6–24 hours
after an allergen exposure. An exudate of serum proteins and cell debris makes up chronic
mucous plug development, which might take weeks to clear out. Airway remodeling is linked to
structural alterations brought on by chronic inflammation and may significantly impact how
reversible a blockage of the airway is. And lastly, with bronchial hyperresponsiveness, results
when the tidal volume is close to the volume of the pulmonary dead space, which limits
hyperinflation's ability to compensate for the airflow blockage. Ventilation-perfusion mismatch
is caused by unequal changes in airflow resistance, the ensuing uneven distribution of air, and
modifications in circulation brought on by elevated intra-alveolar pressure as a result of
hyperinflation. Alveolar hypoxia-induced vasoconstriction also adds to this discrepancy.
Vasoconstriction is seen as another coping mechanism for ventilation/perfusion imbalance.