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Children’s Hospital Paper On Asthma
Erica Anacleto
California State University, Stanislaus
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Children’s Hospital Paper On Asthma
During the clinical rotation on the Apollo floor at the Children’s Hospital Central
California (CHCC) in Madera, California, the author of this paper had the opportunity to care for
an asthmatic nine-year-old female patient (S.K.). This patient was born prematurely at 27 weeks
gestation and has had chronic lung problems her entire life, with asthma being her primary
problem. This patient has presented to CHCC emergency department several times for acute
respiratory distress related to her asthma and has been admitted for further treatment of her acute
asthmatic exacerbations. The author of this paper will look at the incidence of asthma in the
pediatric population as well as the increased incidence in premature infants, the genetic
implications, the pathophysiology, the clinical manifestations, analysis of laboratory and
diagnostic tests, treatments, and the potential long term effects of asthma in the pediatric
population.
Incidence
Hockenberry and Wilson (2013) stated that asthma is considered one of the most
common chronic diseases of children, contributing to the primary reason for school absences and
is classified as the third leading cause of hospitalizations in children younger than 15 years of
age. They also stated that the prevalence of asthma is increasing in the United States along with
morbidity and mortality (Hockenberry and Wilson, 2013). According to Akinbami, Moorman,
Bailey, Zahran, King, Johnson and Liu (2012) there was an estimated seven million children (age
0-17 years old) that were diagnosed with asthma since 2010. From 2008-2010 it was noted that
children had a higher incidence of asthma at 9.5% over adults over the age of 18 years of age at
7.7% (Akinbami et al., 2012).
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A study done in Sweden by Crump, Winkleby, Sundquist and Sundquist (2011)
statistically looked at the asthma risk in young adults born extremely premature, which they
defined as 23-27 weeks gestation. In this study they looked at all infants born from 1973 through
1979 that were the only child in the family and followed them to the ages of 25.5 to 35 years to
be able to identify whether asthma medications were prescribed to these individuals in 20052007 and what they found was that overall young adults that were born extremely premature
were found to be 2.4 times more likely to be prescribed asthma medications than those who were
born term (Crump et al. (2011).
The diagnosis of chronic asthma that patient S.K. has and the fact that she was born at 27
weeks gestation fits appropriately into the incidence that extremely premature infants born at 2327 weeks gestation have an increased risk for acquiring asthma as seen in the study by Crump et
al. (2011).
Genetic Implications
The National Heart, Lung, and Blood Institute (NHLBI) (2012) stated that the exact
cause of asthma is unknown at this time and that some think that early in life genetic and
environmental factors interact to cause asthma. The factors include: An inherited tendency to
develop allergies, called atopy; Parents who have asthma; Certain respiratory infections during
childhood; Contact with some airborne allergens or exposure to some viral infections in infancy
or in early childhood when the immune system is developing (NHLBI, 2012).
Although patient S.K.’s mother and father have no history of asthma, patient S.K. does
have four brothers two of which do not have asthma and two that do have asthma. Interestingly,
the two brothers that have asthma were also born premature, but as stated by patient S.K. she has
the most complications with her asthma when compared to her brothers.
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Pathophysiology
As described by Nievas and Anand (2013) asthma begins with airway inflammation, then
swelling and mucous production begin, followed by plugging of the airways and ultimately
airway narrowing. These factors cause increased airway resistance, which causes the patient to
work harder to breath. Air trapping and hyperinflation of the lungs occurs because the patient
begins inspiration before completing the previous expiration and this leads to hypoxemia (Nievas
and Anand, 2013).
Another explanation described by Online Physician (2011) of asthma is when interactions
between environmental and genetic factors result in airway inflammation. This leads to
bronchospasm, mucosal edema and mucus plugs, which then leads to airway obstruction and
increased resistance to airflow and decreased expiratory flow rates. This causes hyperinflation of
the lungs causing alveolar hypoventilation, which leads to ventilation-perfusion mismatch. The
ventilation-perfusion mismatch leads to hypoxemia and in early stage hypoxemia without carbon
dioxide retention occurs and with worsening obstruction carbon dioxide retention occurs which
ultimately leads to respiratory alkalosis in early stage and later results in metabolic and
respiratory acidosis (Online Physician, 2011).
Analysis of Clinical Manifestations
Nievas and Anand (2013) describe the clinical manifestations of children with severe
acute asthma as being tachypneic, increased respiratory effort, the use of accessory breathing
muscles, nasal flaring, diaphoresis, and anxiety. In more serious cases children may present
obtunded, or in respiratory failure, or in the most severe cases they can present in
cardiopulmonary arrest (Nievas and Anand, 2013).
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Hockenberry and Wilson (2013) include coughing (productive and nonproductive),
shortness of breath, audible wheeze, nail bed cyanosis, restlessness, on auscultation coarse and/or
loud breath sounds, crackles, inspiratory and expiratory wheezing, and patients with repeated
episodes of acute asthma exacerbations can have physical changes which include a barrel chest,
elevated shoulders, and use of accessory muscles (Hockenberry and Wilson, 2013).
As documented and noted in patient S.K.’s electronic medical record, she presented to the
emergency department in respiratory distress. Although this was the only clinical description
noted in her record, while the author walked with the patient on the apollo floor of the hospital,
the author did note that the patient was having some nasal flaring, intercostal retractions,
intermittent moist cough, and on auscultation the patient had coarse lung sounds with inspiratory
and expiratory sounds and some decreased lung sounds at the base of her lungs.
The clinical manifestations of asthma as described by the current literature can clearly
been seen in the patient’s clinical manifestations, both on presentation and while receiving
treatment in the hospital. Although the author cannot remember the patient’s current height and
weight, it is possible that the patient may have a lowered height and weight due to her being born
at 27 weeks gestation and possibly due to the inhaled corticosteroids she is taking for her asthma.
There has not been any research that has been done that proves that asthma has an affect of
children’s growth and development.
Analysis of Laboratory and Diagnostic Test/Values
Patient S.K. had a complete blood count (CBC), chemistry panel, c-reactive protein,
blood gas (venous), and a chest radiograph done when admitted to through the emergency
department. The CBC was mostly done to rule out infection, the chemistry panel was mostly
likely done to assess the patient’s electrolytes and kidney values prior to starting the patient on
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intravenous fluids, c-reactive protein was done to assess the patient’s level of systemic
inflammation and the blood gas was most likely done to evaluate how well the patient was
ventilating. A chest radiograph was mostly likely done to assess for any atelectasis or signs of
pneumonia. The patients CBC was within normal limits, with the exception of an elevated red
blood cell count and hematocrit, which is due to the patient hemoconcentrating because of
decreased blood oxygen levels, therefore creating more red blood cells to carry oxygen
throughout the body. The absolute eosinophil level was elevated as well but can be seen in
asthmatic patient’s due to their allergies. The lactic acid was elevated and most likely due to the
patient’s work of breathing or due to the inhaled albuterol. The c-reactive protein was elevated
indicating a an elevated systemic inflammation. The blood gas values revealed a hypoxia and
hypercapnia, with the patient hypoventilating and showing signs of respiratory acidosis. The
patient’s chest radiography revealed hyperinflation of the lungs and chronic changes seen with
chronic asthma patients.
According to Hockenberry and Wilson (2013) the recommended diagnostic tests used for
an acute asthma patient include clinical manifestations, history, physical exam, laboratory tests
(CBC), pulmonary function tests, which include the spirometer and the peak expiratory flow rate
and a chest radiograph. When comparing the literature to what the patient actually had done, the
only tests that the patient did not receive was the spirometer and the peak expiratory flow rate.
However, this does not go to say that the patient did not have them done at a later time, some
time after the author had completed the rotation. Then most likely reason why the patient did not
have these tests done on admit or shortly after is because she is a chronic asthmatic patient that is
seen regularly at this hospital for acute asthma exacerbations and her lung function is probably
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well known by the physician. It also could be that her exacerbation was very bad this time and
the focus was to get the patient better before assessing her lung function.
Treatments
According to CHCC hospital policy and procedures on asthma pathway (2012), it states
that the patient should be on a modified regular diet, which is age appropriate, no concentrated
sweets and encourage fluids. Saline lock intravenous (IV) catheter unless IV fluids have been
ordered or IV medications. If poor oral intake of food and water and/or vomiting then patient is
to be started on IV fluids at one time maintenance using D5 ½ NS add 20 mEq KCL/L. Inhaled
medications include Fluticasone MDI, Ipratropium MDI, and Albuterol per protocol, either
intermittent, low dose continuous or high dose continuous. Systemic steroids can include one of
the three with Prednisolone orally, Prednisone orally or methylprednisolone IV. Acetaminophen
is added for fever greater than 38 – 38.9 C or mild pain and Ibuprofen is added for a fever greater
than 38.9 C or moderate pain. Vital signs are checked every two hours times two, then every
four hours and as needed, no activity restrictions, oxygen as needed to maintain saturations
greater than 92%.
Nievas and Anand (2013) describe that the treatment for severe acute asthma
exacerbations should include monitoring in the pediatric intensive care unit, oxygen to maintain
saturation greater than 92%, IV fluids for dehydration since oral in take is generally poor with
sever asthma situations, start corticosteroids to control inflammation, especially airway
inflammation, Beta-agonists to promote bronchodilation, Albuterol treatment and it was noted
that continuous albuterol treatment works very well on severe asthma, intravenous Terbutaline
can be used in patients that are not responding to continuous Albuterol, Ipratropium can be used
as another bronchodilator, Magnesium Sulfate can be used to cause smooth muscle relaxation,
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Methylxanthines can also be used for bronchodilation, Helium-oxygen mixture (Heliox)which
can reduce airflow resistance, Ketamine can be used for its brochodilatory effects and bi-level
positive airway pressure can be helpful with gas exchange (Nievas and Anand, 2013).
A stepwise approach for escalating therapy in an asthmatic patient that Nievas and Anand
(2013) diagrammed in their article was as follows: First use Albuterol, Ipratropium, Steroids;
Second start Continuous Albuterol; Third start IV Magnesium; Fourth initiate Heliox treatment;
Fifth administer IV Terbutaline; Sixth give IV Theophylline; Seventh initiate Non-Invasive
Ventilation; Eighth administer IV Ketamine; Ninth initiate intubation of the patient; and tenth
start mechanical ventilation (Nievas and Anand, 2013).
While hospitalized patient S.K. was receiving oxygen via mask at 11 liters per minute,
continuous low dose albuterol for bronchodilation, Fluticasone propionate (Flonase nasal spray)
to help with inflammation, Ipratropium MDI for bronchodilation, Prednisone orally to reduce
inflammation, Acetaminophen as needed and Ibuprofen as needed for fever and Advair MDI
(Fluticasone propionate inhaler diskus) to reduce airway inflammation. All of these medications
prescribed for patient S.K. were to help the patient be able to breath easier and oxygenate better.
Potential Long Term Effects/Complications
Long-term management/teaching
The CHCC (2013) states that the patient should do a pulmonary function test, use a peak
flow meter, obtain an asthma action plan, and take medications as prescribed and know how to
use an MDI. It is also recommended that the patient receive a flu vaccine from their primary
care physician. Patients should be taught about some common triggers that can make asthma
worse, which include dust, cockroaches, mold, allergies, smoke, exercise and extreme weather
changes. Inform patient or parent that they should call the doctor if: the patient has difficulty
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breathing and the rescue medicine is not working, wheezing gets very bad, more coughing, nasal
flaring, retractions, increased respiratory rate, paleness around nose and mouth, shortness of
breath, not able to eat, started acting very sick, difficulty waking up, very irritable or anxious, or
a fever of 100.4 F (CHCC, 2013).
Outpatient follow-up or care needed
The follow-up care for asthmatic patients mostly involves compliance with medications
and compliance with the teachings mentioned above to avoid certain asthma triggers. CHCC
discharge sheet (2012) states that the patient should always use a spacer with inhaled
medications, monitor peak flow daily, contact primary doctor if changes occur in respiratory
pattern, and recheck with your primary doctor as indicated on discharge sheet within set number
of days.
Long-term medications
Long-term medications would include the same medications that patient S.K. is currently
taking, which is Albuterol inhaler, Advair inhaler, Flonase nasal spray, oral prednisone, and
Ipratropium Bromide inhaler. According to Hockenberry and Wilson (2013) drug therapy
includes long-term control medications, quick-relief medications, corticosteroids, betaadrenergic agonists, anticholinergics, and leukotrienes.
Dietary restrictions
According to CHCC (2012) it is recommended to have a no salt diet, limit concentrated
sweets, increase calcium and phosphorous, and reduce high fat foods.
Future Growth and development
The potential long-term effects of growth and development in the asthmatic patient
regarding the medications used are not well known and only some studies have shown a decrease
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in height in some children. In regards to the future and growth and development of the child as
whole from the diagnosis of asthma, that can depend on the severity of the patient’s asthma.
Some children live well into their adult years with minimal complications, others unfortunately
live a life that is very complicated by their asthma exacerbations and suffer greatly from physical
changes that occur, such as lung remodeling, severe damage to their lungs and barrel chest.
Conclusion
In conclusion, when looking at the provided literature for asthma and the care that patient
S.K. received at CHCC in Madera, it can be seen that the literature and the policy guidelines of
CHCC correlate well and all the standards were met during her time in the hospital.
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References
Akinbami, L., Moorman, J., Bailey, C., Zahran, H., King, M., Johnson, C., & Liu, X. (2012).
Trends in asthma prevalence, health care use, and mortality in the United States, 20012010. National Center for Health Statistics, (94) (pp. 1-8). Retrieved from:
http://www.cdc.gov/nchs/data/databriefs/db94.pdf
Children’s Hospital Central California (2012). Asthma pathway. Retrieved from Children’s
Hospital Central California, Madera, California.
Children’s Hospital Central California (2013). Asthma education information for patients and
families. Retrieved from Children’s Hospital Central California, Madera, California.
Crump, C., Winkleby, M., Sundquist, J., & Sundquist K. (2011). Risk of asthma in young adults
who were born preterm: A Swedish national cohort study. Journal of American Academy
of Pediatrics, 127, e913-921. doi: 10.1542/peds.2010-2603
Hockenberry, M. & Wilson, D. (2013). The child with respiratory dysfunction.
Wong’s essentials of pediatric nursing (pp. 736-746). St Louis, Missouri: Elsevier
National Heart, Lung & Blood Institute. (2012). What causes asthma? Retrieved from:
http://www.nhlbi.nih.gov/health/health-topics/topics/asthma/causes.html
Online Physician. (2011). Pathophysiology of bronchial asthma – what happens in asthma.
Retrieved from: http://health.wikinut.com/Pathophysiology-of-Bronchial-Asthma-Whathappens-in-asthma/13ko4xai/