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Juvenile Asthma and Viral Bronchiolitis

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Stacey Gregory

on 5 November 2013

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Transcript of Juvenile Asthma and Viral Bronchiolitis

Juvenile Asthma and Viral Bronchiolitis
Differential Diagnosis
While both diseases lead to dyspnea, air-trapping, and
edematous airways with bronchoconstriction, the underlying
causes and etiologies are different. RSV occurs seasonally in the
United States, with the majority of infections occuring in winter, from December through March, with a spike in mid February. There are some regional differences, so practitioners should be aware of these to aid in the diagnosis of RSV and other childhood lower respiratory infections that cause bronchiolitis (human metapneumovirus and parainfluenza virus) (Fauci et al, 2008, p 1123-1126). Asthma in some individuals can also occur seasonally, with peaks during spring and fall allergy seasons, as well as in winter, when children spend more time indoors and are exposed to greater concentration of dust mites and pet dander. Winter also coincides with exposure to cold air outdoors. Viral respiratory illness, exercise, food allergies, and stress can also trigger asthma attacks, causing some individuals to have asthmatic exacerbations without regard to seasonal cycles. Additionally, GERD, hormonal fluctuations associated with menstruation, and occupational exposures can all predispose
individuals to asthma
(Fauci et al, 2008, p. 1600-1601.
Bronchiolitis, on the other hand, stems from infection,
usually RSV in small children, and is necrotizing to lung epithelium. An infiltrate of lymphocytes and mononuclear cells forms in the bronchioles and alveolar thickening with fluid build up in the alveoli occurs. The submucosa becomes edematous with the infiltrations of eosinophils, neutrophils, and monocytes, and a build-up of inflammatory and immune cell debris that includes fibrin and products of immune cell activation combine with the viscous mucous, forming plugs in the airways. Uneven ventilation, atelectasis and narrowing and occlusion of peripheral airways leads to perfusion mismatch and hypoxemia.
Airflow is obstructed, especially with expiration. Air-trapping and hyperinflation occur, decreasing lung compliance, increasing the work of breathing, decreasing alveolar ventilation and leading to hypercapnia (Fauci et al., 2008, p 1123-1124; McCance et al., 2010, p 1326-1327).
Asthma is a chronic, episodic inflammatory
disease of the lower airways. Hyperreactive eosinophils
and T lymphocytes, as well as activated mucosal mast cells are often found infiltrating the airway mucosa of those with asthma. The subjective disease severity and the degree of inflammation are poorly correlated and significant asthma inflammation may be found in atopic patients without any asthmatic symptoms. That being said, however, the usual course of the disease starts with inflammation of the airways, with thickening of the basement membrane related to collagen deposition in response to eosinophilia. Eosinophils release fibrinogenic factors in response to epithelial injury and shedding of cells. This shedding also leads to mucosal membrane edema and proliferation, as well as leaking of of plasma proteins from bronchial vessels., contributing to the viscosity of mucous formation, leading to the presence of mucous plugs in the smaller airways (Fauci et al, 2008, p 1597).
Asthma exacerbations or attacks are treated with inhaled bronchodilators, usually beta-adrenergic agonists, that relieve bronchoconstriction quickly. Anticholinergic medication, such as inhaled ipratropium bromide can be a good addition to rescue therapy if beta-adrenergic agonists are not fully effective, or can be used alone if the patient cannot tolerate beta-adrenergic agonists. Additionally, removal of the offending trigger during acute episodes of asthma is advised to better control symptoms (McCance et al., 2010, p. 1333-1334; Fauci et al., 2008, p. 1602-1603).
Asthma treatment consists of a two pronged
approach. Controller therapy is aimed at preventing episodic or chronic exacerbations of asthma, using
inhaled and oral corticosteroids as well as antileukotrienes, cromolyns and sometimes immunomodulatory treatments such as methotrexate or cyclosporine. In addition, those who have atopic allergies find that immunotherapy (also called "allergy shots") is helpful as prophylaxis to asthma exacerbations. The use of peak flow meters can help patients and practitioners determine how successful asthma controller therapy is during asymptomatic
times. (Fauci et al., 2008, p. 1603-1604;
McCance et al., 2010, p. 1333-1334).
The treatment of the symptoms of bronchiolitis is largely supportive. If the disease is severe, the child may require assisted ventilation, supplemental oxygen, suctioning of secretions, and hydration therapy. Nasal CPAP and heliox have shown promise in decreasing hospitalization time, along with systemic steroids. Although there is no scientific evidence that inhaled bronchodilators help relieve symptoms or speed recovery, they are commonly used on an empiric basis (Fauci et al., 2008, p. 1124; McCance et al., 2010, 1326-1327)
When a child has bronchiolitis and requires hospitalization, treatment of the symptoms as well as the underlying cause of the disorder is best practice. Viral illness is usually self limiting, but some success has been seen with aerosolized antiviral medications such as ribavirin. Treatment with this modality has shown a modest beneficial effect in alleviating lower respiratory tract illness and blood-gas abnormalities. The American Academy of Pediatrics recommends its use in infants who are severely ill and at high risk for complications of RSV or hMPV infection
(Fauci et al., 2008, p 1124).
Seeing the forest, in spite of the trees -
Differential diagnosis in acute presentation.

Pathophysiology: Differences and similarities of Asthma and Bronchiolitis

Additionally, diagnostic tests may show similar results, especially decreased FEV1 and other pulmonary function tests. X-rays may show atelectasis and hyperinflation in the lungs, either unilaterally, or bilaterally, as well as hyperluminosity on film (DiagnosisPro, 2013; McCance et al, 2010, pp 1326-1334; Porth, 2004, pp. 372-374, 380-385; Fauci et al, 2008, pp. 1589, 1596-1607).
According to DiagnosisPro (2013), bronchiolitis and childhood asthma share several clinical manifestations:

Cyanosis, tachycardia, acute dry barking cough, decreased or distant breath sounds, bronchospasm, dyspnea at rest and on exertion, often with syncope or lightneadedness, sudden onset of dyspnea, low diaphragm with percussion, prolonged expiratory phase, pursed lip breathing, rales, and wheezing. Additional signs may include barrel chest or increased anterior-posterior diameter, and expiratory wheezing.
Clinical tests used to determine the diagnosis of acute asthma or bronchiolitis include radiographic studies, nasal swabs, and lung function testing. Physical examination and history are key to making a positive diagnosis. The modified asthma predictive index (API) can assist in establishing the diagnosis, as well as severity and appropriate treatment modality (McCance et al, 2010, p. 1333).

Additional testing used to establish asthma may include a methacholine challenge, allergic atopy testing, and positive response to inhaled bronchodilators (McCance et al, 2010, p.1327, 1333; Fauci et al, 2008, p 1602; Porth, 2004, p 383).

Emergency room testing may also include blood draw labs for blood gases, pH, and indicators of inflammation such as ESR or CRP, as well as a CBC with differential to establish eosinophilia or high white cell counts to indicate inflammatory or infectious states (DiagnosisPro, 2013).
Case Study
H. N a 3 year-old normally healthy, immunized girl with a runny nose and mild cough
for the last 3-4 days woke up in the middle of the night with severe shortness of breath.
She had expiratory wheezing. She was taken to the emergency department with HR 130,
RR 44, Sat 93% and temp 37C. On physical exam, she had tight end-expiratory
wheezing, intercostal and supraclavicular accessory muscles of respiration to help her
breathe. A chest X-ray revealed hyperluscent and over-inflated lungs. Blood testing revealed an arterial blood pH of 7.25.

Because H. N. has a recent history of rhinorrhea and cough, it is important for the practitioner to rule out RSV or other viral cause of bronchiolitis. Wheezing, mild tachycardia, and tachypnea as well as air-trapping and overinflation of the lungs are common to both bronchiolitis and acute episodes of asthma. The arterial pH of 7.25 is indicative of respiratory acidosis, which occurs with hypoventilation. Tight end-respiratory wheezing with intercostal and supraclavicular accessory muscles are a common mechanism to increase chest expansion in young children with higher chest compliance due to increased cartilage and flexibility of the rib cage.

All the signs are extremely non-specific for either disease, with the exception of the child's afebrile status. With RSV or other infectious respiratory virus, the child would normally exhibit a low grade fever, and may have a recent history of other signs and symptoms of infection, such as diarrhea, nausea and vomiting, and perhaps several days of anorexia or feeding difficulties (DiagnosisPro, 2013).

Because of this one aspect of the child's presentation, I am leaning toward the diagnosis of an acute asthmatic episode and treat accordingly, with respiratory therapy consisting of nebulized albuterol and possibly a short-acting systemic corticosteroid administration in the ED with a follow up of the pediatrician to manage the disease with controller medication, education, and trigger management.
DiagnosisPro. (2013). Disease comparison results for asthma and bronchiolitis. Available at
Fauci, A. S., Braunwald, E., Kasper, D. L., Hauser, S. L., Longo, D. L., Jameson, J. L., and
Loscalzo, J. (2008). Harrison's Principles of Internal Medicine (17th ed.). New York, NY: McGraw Hill Medical.
McCance, K. L., Huether, S. E., Brashers, V. L., and Rote, N. S. (2010). Pathophysiology:
The Biologic Basis for Disease in Adults and Children (6th ed.). Maryland Heights, MO: Mosby Elsevier.
Porth, C. M. (2004). Essentials of Pathophysiology: Concepts of Altered Health States.
Philadelphia, PA: Lippincott Williams & Wilkins.
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