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Asthma In The Pediatric Patient by Karen Fields, M.S.P.A.S., PA-C
Bipolar Affective Disorder by Karen Fields, M.S.P.A.S., PA-C

Continuing Medical Educaton: Type 2

Gamekeeper's Thumb, Mallet Finger, and Jersey Finger-PowerPoint Presentation by Dawn Mueller, M.S.P.A.S., PA-C
Adhesive Capsulitis-Orthopaedics and Sports Medicine Symposium-PowerPointPresentation by Karen Fields, M.S.P.A.S., PA-C
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Asthma in the Pediatric Patient

Karen E. Fields, M.S.P.A.S., PA-C
Independent Case Study & Research
Orthopaedics and Sports Medicine
The materials on are intended for Medical professionals only
and should not be used without proper consultation with your medical providers.
Medicine is an evolving process and this material is a contribution of the developing information available
© Copyrighted 2001 All rights Reserved


Asthma is the most common chronic disease of childhood, affecting over five million children under the age of 18 in the United States alone. Historically, it has been described as reversible airflow obstruction due to airway hyper-responsiveness, edema, and inflammation.   Symptoms include wheezing, coughing, chest tightness, and shortness of breath.   Acute exacerbations may occur during which the patient may experience respiratory fatigue or even failure requiring hospitalization. Asthma is diagnosed by its chronicity and recurrences. Pulmonary function tests (PFTs) are the most useful indicator of severity of asthma, but may only show abnormalities during an acute exacerbation. In between exacerbations, patients may be asymptomatic and PFTs may be normal. However, recent evidence has been showing that airway remodeling is not completely reversible and that patients with persistent asthma may suffer decline in pulmonary function over time, particularly if appropriate treatment is not initiated in a timely fashion. The treatment of asthma is based on a four step tier that categorizes patient based on frequency and severity of symptoms as well as pulmonary function. Medications utilized include short and long acting beta-agonists, inhaled and oral corticosteroids, leukotriene modifiers, mast cell inhibitors, and theophylline. The prognosis for children with mild disease is generally good with most outgrowing their symptoms by adulthood. Those with moderate to severe disease usually have symptoms persisting into adulthood with varying degrees of loss of pulmonary function. While asthma is not a significant cause of pediatric death, mortality rates from asthma have been increasing, and prognosis appears to be dependent on appropriate treatment, monitoring, and patient and caregiver education.


The following case introduces a three year old African American male who presented to the office for a sick visit. The history was gathered primarily through his mother. She reported that the child had been coughing, wheezing and had clearrhinorrhea for the past two months. The patient’s mother stated that he had a productive cough with exercise. After runninga short distance he would start coughing, wheezing, and bringing up phlegm. Occasionally after coughing a while, he would vomit. The cough was worse at night and had been increasing in intensity, waking him up nightly. His mother denied fever, chills, anorexia, change in bowel or bladder habits, or a history of asthma, bronchiolitis, bronchitis, pneumonia, tuberculosis, emphysema, or hemoptysis.

A focused physical was performed and was largely unremarkable. Examination of the ears showed intact, pearly tympanic membranes with good light reflection and no retraction, bulge, erythema, or fluid seen. The ear canals were clear without erythema, bleeding, or discharge. The nasal turbinates were pink but swollen with a moderate amount of green mucous seen in the anterior nares. There was no septal deviation, perforation, nasal polyps, or bleeding. Examination of the mouth showed no lesions, exudate or bleeding, and the throat was pink without lesions, exudate or swelling. The patient’s neck was supple with full range of motion and the trachea was midline. There was no cervical or supraclavicular lymphadenopathy. Examination of the chest showed good respiratory excursion with no increase in anteroposteral diameter. There was no rib or sternal tenderness to palpation. The lung fields were resonant to percussion and auscultation throughout. There were no rales, rhonchi, or wheezes present. The patient did not cooperate to perform tactile fremitus or egophony, bronchophony, or whispered pectoriloquey. Cardiac examination revealed a regular rhythm of 102 bpm with normal S1, S2; no S3 or S4, gallops, or murmurs. There were no abnormal pulsations, heaves, or thrills. The abdominal examination was unremarkable with normoactive bowel sounds, tympanitic percussion throughout, and no tenderness to palpation. There were neither masses nor hepatosplenomegaly, guarding, rebound, or rigidity.

The patient was diagnosed with allergic rhinitis and asthma. He was treated with Zyrtec syrup and told to take one half teaspoon every night at bedtime. Secondly, he was prescribed an albuterol metered dose inhaler with an aerochamber and mask and was to take two puffs every four hours when needed for coughing. He was to follow-up in two weeks for reevaluation, but did not return before the end of the rotation.

Asthma is a complex clinical syndrome that is characterized by reversible airflow obstruction, airway hyper-responsiveness, airway edema, and eosinophilic and lymphocytic inflammation.1 It is the most common chronic disease of childhood and is responsible for a significant proportion of missed school days, childhood emergency department visits and hospitalizations.2,3 Asthma often begins in early childhood, though it may have its onset at any age. Thirty percent of those ultimately diagnosed with asthma have their first symptoms by age one.3 The airways in patients with asthma are hyper-reactive to a variety of stimuli, and after exposure to a stimulus, airway resistance increases due to smooth muscle contraction, increased bronchial secretions, and inflammation of the bronchial wall.4 Triggers include allergens such as animal dander and pollens, respiratory infections, exercise, cold air, and airborne irritants such as cigarette smoke.1,5 Clinical exacerbation may be acute or insidious, but includes a nonproductive cough, wheezing, tachypnea, dyspnea, use of accessory muscles in breathing, prolonged expiration, cyanosis, and tachycardia.3 Pulmonary function tests (PFTs) are the mainstays of assessing severity of asthma. During acute exacerbations, forced expiratory volume in one second (FEV1) and vital capacity are diminished while the residual volume, functional residual capacity, and total lung capacity are usually increased.5 Forced expiratory flow between 25% and 75% of vital capacity (FEF25-75%) and peak expiratory flow rate (PEFR) may also be decreased but these will return to normal after administration of a bronchodilator.3 Arterial blood gases (ABGs) may show mild hypoxia and hypocapnia in mild or moderate disease, but may show respiratory acidosis if the patient’s condition worsens.4 Chest radiographs will show bilateral hyperinflation with flattening of the diaphragms.5 PFTs, ABGs, and radiographs may be within normal limits in between acute exacerbations.

Long-term treatment for asthma is based on a four step categorization of patients. Mild intermittent asthmatics are treated with short-acting beta-agonist bronchodilators when needed with no daily medication. Mild persistent asthmatics are given a short-acting beta-agonist for quick relief of flare-ups, but also need daily medication of either a low dose inhaled corticosteroid or cromolyn or nedocromil, which are mast cell stabilizers.5 Moderate persistent asthma requires daily medication of either a medium dose of inhaled corticosteroids or a long-acting beta-agonist bronchodilator in addition to a short-acting beta-agonist for acute symptoms. Lastly, severe persistent asthmatics need inhaled corticosteroids in high doses and a long-acting beta-agonist. In addition, they may need systemic corticosteroids either daily or every other day.5

Treatment for acute exacerbations of asthma may be handled in the emergency department or in the pediatrician’s office, but often include oxygen to maintain saturation above 90-95%, systemic glucocorticoids, and bronchodilators administered through nebulizer treatments. Severely ill patients may require intubation with mechanical ventilation and epinephrine or terbutaline given either by mouth, intravenously, or subcutaneously.2

Morbidity and mortality rates for asthma have increased since the 1970s, and statistics have shown that most deaths occur from under-recognition and under-treatment of asthma. Most patient with mild symptoms generally do well as they get older, but those with more severe symptoms in childhood tend to have persistent disease. Early intervention may alter the natural course of childhood asthma and gives the primary care provider an opportunity to positively impact the course of disease for many children.5


Asthma is characterized by airway hyper-responsiveness to a non-specific stimuli. Stimuli may include inhaled allergens such as dust mites, pollens, molds, cockroaches, cold air,exercise, and cigarette smoke.3,5 Both large and small airways may be involved and pathologic features include shedding of airway epithelium, edema, mucus plug formation, mass cell activation, and collagen deposition beneath the basement membrane.3,5 Heightened airway sensitivity is present to a minor degree though the patient may by asymptomatic, and persons may have increased hyper-responsiveness during viral respiratory illnesses or exposures to air pollutants, allergens, or chemicals.3 The primary immune mechanism involved is the association of the antigen with immunoglobulin E (IgE). This binds to cell surfaces and triggers the release of histamine, leukotrienes C4, D4, and E4, and platelet activating factor that lead to bronchospasm, local inflammation, and immune response.3,4 Histamine increases permeability of venules and allows protein and fluid to leak out of them. It also increases airway secretions and can stimulate irritant receptors in the airway walls.4 This leads to a reflex vagal release of acetylcholine near smooth muscles which potentiates further bronchoconstriction.4 Mast cells in the lungs are also activated and play a role in the early events of the asthmatic attack. Eosinophils are prolific, and both eosinophilic and neutrophilic infiltration are potentiated during the late phase of airway hyper-responsiveness.3,4 This infiltration is accentuated in fatal asthma exacerbations.5

This inflammatory cascade results in bronchoconstriction and mucosal edema that cause airway obstruction that is most severe during expiration. Atelectasis may occur in segments or subsegments of the lungs which aggravates the already present ventilation perfusion mismatch. Hyperinflation of the lung leads to decreased compliance which increases the work of breathing. Intrathoracic transpulmonary pressure is increased which is necessary for expiration through obstructed airways. This may lead to further narrowing or complete closure of some airways as well as increasing the risk of pneumothorax. Also, increased intrathoracic pressure may interfere with venous return leading to pulsus paradoxus.3 Over the course of the disease, persistent airway inflammation can lead to remodeling of the airways and to irreversible changes.5

   Epidemiology and Risk Factors

Asthma affects ten million people in the United States, or four percent of the total U.S. population.4 It is the most common chronic disorder in children and adolescents, affecting about five million children under the age of 18 and 1.3 million under the age of five.1 As many as 10-15% of boys and 7-10% of girls have asthma at some time during childhood. In the prepubescent population, twice as many boys are affected as girls, but after puberty, the incidence is equal.3 African American children have a higher incidence of asthma than do children of other races.4 In children under fifteen, asthma is responsible for ten million lost school days, 3,028 doctor visits, 570,000 emergency visits, and 164,000 hospitalizations.1 In 1990, The estimated economic cost of asthma in the U.S. was 6.2 billion dollars. Mortality is uncommon in the U.S., but still reaches 3000 deaths per year.4

Risk factors for the occurrence of asthma are poverty, African American race, maternal age of less than twenty years at time of birth, birth weight of less than 2500 grams, maternal smoking, small home size, large family, and intense allergenic exposure in infancy.3 Half of the children with asthma have a family history of asthma, rhinitis, eczematous dermatitis, or urticaria. Both active and passive smoking may predispose a child or adolescent to the development of asthma, and air pollutants may also contribute to disease onset.4 Other risk factors include frequent respiratory infections in early childhood, obesity in African American or Hispanic children, and poor parenting skills.3

Clinical Presentation and Physical Exam

A proper history in the patient with asthma will answer some basic questions. First is the type of symptoms that occur in an attack, such as chest tightness, coughing, tachypnea, or dyspnea. Second is to ascertain as to when symptoms occur and what causes them or alleviates them. Also, the clinician must determine the frequency and severity of the symptoms and what effect they have daily life and activities. One must ask what medications are used and the frequency of use. Also, the practitioner should get a detailed understanding of the patient’s environment and understand where the child spends most of his or her time (daycare, school, home), what the environmental exposures are at these places (pets, fireplaces, carpeting, molds, cigarette smoke, etc), and if the child’s bedroom and major living areas at home have irritants that may cause exacerbations (carpeting, pets, bedding, etc).1

The history typically given is one of dyspnea with recurrences and remissions. The child in the midst of an acute attack may give have a recent history of a viral respiratory infection or exposure to an irritant. In a majority of children, dyspnea worsens at night. The patient or his or her caregiver may report wheezing, but cough may be the only sign of an attack.4

Early in an exacerbation, signs and symptoms include a tight, non-productive cough, wheezing, tachypnea, and dyspnea. Wheezing may be prominent, but also may be absent if air flow is extremely poor.3 Tachypnea is a common finding but it is important to remember that respiratory rate varies in children according to age.2 The child may display shortness of breath leading to difficulty walking or talking, and prolonged and difficult expiration.3 The patient may be using accessory muscles to aid in breathing, and the clinician may see intercostal retractions and contracting abdominal or sternocleidomastoid muscles. The patient may show slow expiration against pursed lips. If intrathoracic pressures are markedly different during between inspiration and expiration, pulsus paradoxus will ensue with a difference of more than 15 mmHg during inspiration.4 In a severe attack, the patient may appear cyanotic, will have difficulty speaking, or may have a decreased level of consciousness. Respiratory distress may ensue which is suggested by accessory muscle use and an increased respiratory rate. A normal or decreased respiratory rate may signal fatigue, and when airway obstruction is worsening, wheezing will progress from expiratory wheezing to both inspiratory and expiratory wheezing and from audible to none. A patient in severe respiratory distress will usually assume a hunched-over position, called the tripod position, which makes breathing easier.3 Nasal flaring may also be noted. Crackles may be heard due to mucus plugging or atelectasis.2 The child may also sweat profusely and have a low-grade fever due to the enormous work of breathing. Abdominal pain and vomiting are common, particularly in younger children.3

   Laboratory Tests and Imaging

Laboratory testing and imaging modalities used may include any of the following: pulmonary function tests (PFTs), peak expiratory flow rate (PEFR), chest radiograph, allergy testing, bronchoprovocation challenge with methacholine or exercise, imaging of paranasal sinuses if sinusitis is suspected, reflux studies if gastroesophogeal reflux are suspected, and microscopic examination of sputum.1,3 Sputum will be tenacious, rubbery, and whitish and will show numerous eosinophils and granules from disrupted cells. Blood work will also show eosinophilia with elevated IgE levels, but normal serum protein levels.3 The degree of eosinophilia tends to reflect the severity of asthma and indicate whether steroid therapy is appropriate.4

PFTs are useful in assessing the degree of airway obstruction and the efficacy of gas exchange. They aid in measuring the response of airways to inhaled allergens, chemicals, or following exercise. Bronchoprovocation challenges combine asthma stimulants with PFTs to determine the triggers and allergens specific to a patient. PFTs can be most valuable when performed before and after the administration of a bronchodilator, a test which measures the degree of airway reversibility.3 Significant reversibility is indicated by a increase of at least 12% of FEV1.1

In mild asthmatics in the midst of a remission, no abnormalities may be detected in PFTs. During an acute exacerbation, PFTs generally show a decrease in FEV1 and vital capacity, and an increase in total lung capacity, residual volume, and functional residual capacity.5 PEFR and FEF25- 75% will be decreased as well.3 It is also important to assess the FEV1/FVC ratio since a reduction of this ratio from expected values is specific for an obstructive disease process rather than a restrictive process.4

PEFR can be done at home by patients or with assistance from their parents and can be used to measure expiratory flow two or three times a day. This can provide an objective measurement as to the degree of airway obstruction.3 Since it is primarily a measurement of large airway function and lacks sensitivity as a diagnostic indicator, it is not as helpful in diagnosis of asthma as it is in monitoring of an asthmatic patient. However, it can be used in between office visits to monitor the degree of variability and assess ongoing disease severity to help guide medication needs.1,3 A decreased PEFR indicates increased airway resistance and indicates the onset of an exacerbation even when symptoms are not evident. A diurnal variation of greater than 15-20% is a defining feature of asthma, and a variation of greater than 30% indicates increased bronchial responsiveness and worsening asthma with increased susceptibility to airway obstruction.3,5 When this fall occurs, early intervention and additional medication therapy can be initiated.3

Arterial blood gases (ABGs) are useful only during an acute attack and are important in evaluating the asthmatic patient during an attack requiring hospitalization.3,5 During remission, ABGs will be normal, and Po2 will be low when the patient is symptomatic.3 Early in a true exacerbation, they will show a normal to low Pco2 level and respiratory alkalosis. Blood pH will be normal or even slightly alkalotic due to hyperventilation, but will develop into acidosis when the buffering capacity of blood is exhausted.3 Respiratory acidosis and increasing CO2 tension indicates further airflow obstruction and may signal impending respiratory failure.5

A chest radiograph may be ordered in a child with asthma, but is not a routine study. It is usefulto rule out other causes of respiratory disease or asthma complications such as pneumonia, pneumothorax, pneumomediastinum, or foreign body.2 In asthma, the lungs will appear hyperinflated with flattening of the diaphragms. Lung markings are commonly increased.3 Atelectasis may be seen in as many as six percent of children during acute exacerbations.3 Atelectasis may be difficult to differentiated from pneumonia even with a chest radiograph, but can be determined if the film shows a local infiltrate in addition to the clinical presentation in which the patient will demonstrate a high fever.2

   Differential Diagnosis

Most children with recurrent episode of coughing and wheezing have asthma.3 The differential diagnosis for a child with asthma is related to the patient’s age. Congenital abnormalities are usually seen in infants and young children and include laryngotracheomalacia, vascular rings, airway stenosis or web, and enlarged lymph nodes. Asthma can be confused with croup, acute bronchiolitis, pneumonia, and pertussis.5 Other causes include cystic fibrosis, immunologic deficiency disease, and hypersensitivity pneumonitis.3 In a child in respiratory distress who presents to the emergency department, vocal cord dysfunction, foreign body aspiration, and heart disease must be considered. Vocal cord dysfunction can present with wheezing, chest tightness, shortness of breath, and cough and can be easily confused with asthma. It can be differentiated based on a normal oxygen saturation.2 A child suffering from foreign body aspiration may not present with the text book case of stridor, drooling, cough or unilateral wheezing. The chest radiograph may be normal or may show unilateral hyperinflation. This differential should be considered with high suspicion in a child with no previous history of asthma or poor response to therapy.2

   Diagnosis and Treatment

Treatment of asthma is based on the National Heart, Lung, and Blood Institute Guidelines which established six goals of therapy and four components of successful management. These include preventing chronic and troublesome symptoms, preventing exacerbations of symptoms leading to office or emergency department visits, maintaining normal levels of activity and normal pulmonary function, providing optimal therapy with minimal adverse affects, and ensuring patient and family satisfaction with care. Components of management should include: regular assessment and monitoring, control of precipitating and aggravating factors, pharmacologic therapy, and education the child and family about daily management of the condition as well as the emergency plan for acute episodes.1

General measures for treatment are based on avoiding allergens, improving bronchodilation, and reducing mediator induced inflammation.3 The hyperreactivity of the airway can be dealt with by minimizing exposure to irritants and maintaining relative humidity in the home to less than 50% as humidity greater than this provides an environment in which dust mites to thrive.3 The most effective strategy in managing asthma exacerbations involves recognizing early warning signs and treating an exacerbation early. The caregiver must be able to properly assess asthma severity and understand how to respond when the PEFR drops to less than 50-80% of personal best. Prompt communication with the clinician is imperative, and the child must be removed from exposure to irritants or allergens.5 A plan for home management may be instituted using a flow chart that clearly outlines what medications in specific dosages can be administered based on the child’s symptoms. This plan may be individualized for the child, but must be simple enough so that the patient and family can understand and follow it.6

Treatment for asthma is based on a four step approach which categorizes patients based on the frequency and severity of their symptoms.

Step one classification for mild intermittent asthma includes symptoms less than or equal to two times a week and nighttime symptoms less than or equal to twice per month with FEV1 or PEFR greater than or equal to 80% of the predicted value with less than 20% variability. The patient must be asymptomatic with normal PEFR between exacerbations and exacerbations should be brief.5

Step two, or mild persistent has symptoms more than twice a week, but not more than once a day with night symptoms more than two times a month. FEV1 or PEFR is greater than or equal to 80% of predicted with 20-30% variability.5 Children with mild asthma have good school attendance, good exercise tolerance, and little or no interruption of sleep. Chest radiograph shows no hyperinflation of the chest, and PFTs may show mild, reversible airway obstruction with little or no increase in lung volume.3

Step three, or moderate persistent asthmatics have daily symptoms. Exacerbations of asthma affect activities and occur more than twice a week. Nocturnal symptoms occur more than once a week, FEV1 or PEFR is between 60-80% of predicted value, and PEFR variability is greater than 30%.5 Children with moderate asthma may have impaired school attendance with decreased exercise tolerance. The child may lose sleep at night, and hyperinflation may be evident clinically as well as on chest radiograph.3

Lastly, step four, or severe persistent asthmatics have continual symptoms with frequent exacerbations that limit physical activity. They have frequent nighttime symptoms, and FEV1 or PEFR is less than or equal to 60% of the predicted value with PEFR variability of greater than 30%.5 They may miss significant amounts of school and have their sleep interrupted often. They have poor exercise tolerance, and may require recurrent hospitalizations. They may have increased anteroposterior diameter of the chest as a result of chronic hyperinflation and PFTs will show less reversibility in response to inhaled bronchodilators.3

The medications used for asthma are classified by action and duration of action. These include quick-relief medications and long-term control medications.5 Long-term control medications include anti-inflammatory agents such as inhaled corticosteroids (ICS) or oral corticosteroids, long-acting bronchodilators such as salmeterol, leukotriene modifiers such as montelukast, zafirlukast, and zileuton, and mast cell stabilizers such as cromolyn and nedocromil. Quick relief medications include inhaled beta-2-agonists such as albuterol, pirbuterol, or terbutaline. Also, a less frequently used class of drugs are the anticholinergics.5

Pharmacologic therapy for step one, or mild intermittent asthma consists of a short-acting beta-2-agonist as needed for wheezing. No long term control medications are needed.3 Treatment for step two, mild persistent asthma, includes the same quick relief treatment as in step one, but adds one daily anti-inflammatory medication. This can be a low dose ICS, cromolyn or nedocromil, a leukotriene modifier, or sustained-release theophylline, which is the least preferred modality.1,4 Quick relief medications for moderate persistent asthma and severe persistent asthma is as in step one and two, but may also require a nebulizer to deliver albuterol during acute flare-ups.1 In addition, a low to medium dose ICS with a long-acting beta-2-agonist or simply a medium dose ICS should be employed. Theophylline, again, can be used, but is not the preferred therapy.1 Lastly is treatment for step four, or severe persistent asthma. For long term relief, anti-inflammatory medications are required continuously. Regimens should include regular high dose ICS and may include systemic corticosteroids, preferably on an alternate day dosing schedule.1,3 Repeated attempts should be made to reduce systemic oral corticosteroid use and maintain control with ICS. In addition, the patient may still require a long acting bronchodilator.1

Short-acting beta-2-agonists are a mainstay of treatment because of their ability to give quick symptom relief within five to ten minutes. They act by relaxing bronchial smooth muscle.1 Overuse of these drugs may be the first signal to the clinician of increasing asthma severity.7 Anti-inflammatory treatment should be instituted when the use of albuterol or pirbuterol exceeds twice per week or the patient is refilling their metered dose inhaler (MDI) more than once a month. Corticosteroids play a large role the treatment of more severe asthma and are the mainstays of anti-inflammatory treatment. They can increase responsiveness to beta-agonists, inhibit cytokines and release of inflammatory mediators, reduce edema, and improve lung function.7 ICS are more effective than systemic preparations in long-term treatment and have fewer side effects than systemic treatment. However, systemic corticosteroids may be necessary if ICS do no control the symptoms adequately (most often in patients suffering from severe persistent asthma) or may be necessary for a severe acute exacerbation.7

Additive therapy of long-acting beta-2-agonists, leukotriene modifiers, cromolyn and nedocromil, or theophylline may be used in difficult to control asthma or when attempting to lower the dosages of ICS or oral steroids.7 Cromolyn and nedocromil can be used in children over 12 with persistent asthma and offer alternatives to ICS in mild persistent disease.1,3 There seems to be little benefit of continuing treatment with cromolyn in patients who require ICS therapy, but continued treatment with nedocromil may reduce the dosage requirements of ICS.3

Salmeterol, a long acting beta-agonist, provides 12 hour efficacy whose onset of action is thirty minutes. This inhaled drug offers improved control of nocturnal symptoms and produces more effective symptom control when added to ICS than if ICS dosage alone is increased.1 Because of its slow onset of action, it cannot be used as a rescue medication for an acute exacerbation, and patients and family should be counseled to not use the inhaler this way.1,7

Theophylline is not used nearly as often as it was in the past, but can still provide an added benefit in severe asthma and may have a steroid sparing effect.7 It works to inhibit adenosine receptors, increase cyclic AMP, block prostaglandins, and stimulate the diaphragm to aid in respiration. Blood levels must be followed periodically to avoid toxic levels and other medications or medical conditions may contribute decreased clearance which will increase serum levels.7

Leukotriene modifiers improve symptoms and pulmonary function and decrease the need for quick-relief medications. They are useful to lower the doses of ICS for mild persistent asthma and may be effective when added to ICS therapy in moderate persistent asthma or for exercise induced asthma when dosed the night before exercise.1 They do not yet have a clear role in severe persistent asthma but their role may expand to include treatment for moderate and severe asthma as suggested by recent clinical evidence.1,7


Although asthma has classically been described as reversible airway obstruction, and may remit in the child with mild disease, asthma may become moderately to fully irreversible and severe irreversible airflow obstruction may develop irregardless of appropriate therapy. It has been shown that subjects with persisting asthma show an greater decline in pulmonary function when compared with normal subject, and abnormal physiology is reflected in both reduced airflow rates and increased airway responsiveness. Factors that may adversely impact the outcome of a patient into adulthood are: female gender, environmental tobacco smoke exposure in childhood, personal tobacco smoking in adolescence, age at onset, severity and duration of childhood asthma,severity of lung function abnormality in childhood, degree of bronchodilator reversibility, degree of airway hyper-responsiveness, and delay in initiating anti-inflammatory medications. Timing of introduction of ICS has shown to be an important determinant of irreversible airway remodeling, and to achieve highest benefit, should be initiated within one year of diagnosis of asthma.8 Also, the type of treatment initiated is relevant to the natural history of the disease. Children who were treated with a long-acting beta-agonist had deterioration of lung function over one year as compared to those given ICS who improved over a year’s time. Other studies have shown a faster decline in FEV1 in patients treated solely with bronchodilator therapy than those treated with ICS. Lastly,investigations have shown that ICS improved clinical status, airway caliber and responsiveness in childhood asthmatic patients, but the effect was incomplete in most patients and the majority of children did not achieve a long-lasting remission.8

Long-term outcome studies have suggested that children with mild symptoms generally outgrown their asthma, while patients with more severe symptoms tend to have disease persistent into adulthood.5 While death from childhood asthma is rare,mortality rates have been increasing. Reasons for this increase is unknown, but may be due to increased prevalence, lack of access or utilization of medical care, or an over-reliance on bronchodilators with delay of proper treatment with steroids or other therapy.3 Increasing mortality may also be due to under-recognition of asthma severity or under-treatment of asthma, particularly in labile patients.5 Education of patients and caregivers can help to decrease adverse outcomes by increasing patient knowledge of asthma and its treatment, improving communication with the clinicians, and improving compliance with treatments.3


While mortality from asthma is relatively rare, asthma is a significant cause of pediatric morbidity, reflecting in emergency department visits, hospitalizations, and days of missed school. With studies showing an irreversible component to airway remodeling and pulmonary function, timely and appropriate treatment becomes necessary to prevent further morbidity into adulthood. Treatment with inhaled corticosteroids appears to affect the outcome of patients with persistent asthma, and are the anti-inflammatory medication of choice. Other medications enable the dose of corticosteroids to be reduced and may prevent the use of systemic steroids. Education also plays a critical role in appropriate treatment and in the reduction of morbidity from asthma. By educating patients and caregivers in the appropriate use of medications and measures to reduce irritant exposure, the hope is to reduce exacerbations and maximize both pulmonary function and quality of life by minimizing hospital visits and increasing school attendance and activity tolerance.


1. Fishcer, T.J. “Asthma In Children.”Conn’s Current Therapy.53rd ed.Rakel (ed) W.B. Saunders, 2001.

2.Smith, S.R & Strunk, R.C.“Emergency Medicine: Acute Asthma in the Pediatric Emergency Department.”Pediatric Clinics of North America.1999 Dec; 46(6).
3.Behrman (ed.).“Asthma.”Nelson Textbook of Pediatrics.W.B. Saunders, 2000.
4. Effros, R.M, & Kaufman, J.“Asthma and Other Allergic Disorders.”Textbook of Primary Care Medicine.3rd ed.Nobel (ed.).Mosby, 2001.
5.Boguniewicz, M. & Leung, D.Y.M.“Allergic Disorders.”Current Pediatric Diagnosis and Treatment.15th ed.Hay (ed.). New York: Lange, 2001.
6.Ponte, C.M.“Comprehensive Care In the Allergy/Asthma Office: Education of the Patient with Asthma.”Immunology and Allergy Clinics of North America.1999 Feb;19(1).
7.Tan, R.A.“The Difficult Asthmatic: General Pharmacologic Approach to Asthma.”Immunology and Allergy Clinics of North America.2001 Aug; 21(3).
8.Sears, M.R.“The Pathobiology of Asthma: Implications for Treatment.”Clinics in Chest Medicine.2000 Jun; 21(2).

History and Physical

Identifying Data: J.H. is a three year old African American male who resides in Philadelphia with his mother and siblings.
Source: Mother 
Reliability: Appears reliable
Chief Complaint: Per Mom:"He has been coughing a lot at night for two months."
HPI: This is a 3 y/o AA male who presents to the office today for a sick visit c/o cough, wheezing, and rhinorrhea for the past two months.Mom states that he has had a productive cough with exercise.He will run a short distance then start coughing, wheezing, and bringing up phlegm.After coughing a while, he sometimes vomits. He also has had a cough at night increasing in intensity, waking him up nightly.Mom denies fever, chills, anorexia, change in bowel or bladder habits, h/o asthma, allergies, bronchiolitis, bronchitis, pneumonia, TB, hemoptysis, murmurs, palpitations, or heart trouble. 
Past Medical History: 
General State of Health:  Well child who is behind on immunizations and has not been seen for two years. 
Childhood Illnesses:  H/O URI at age 9 months; Conjunctivitis and Preseptal cellulitis age 23 months. 
Adult Illnesses:  N/A 
Psychiatric Illnesses:  No h/o of behavioral or psychiatric issues. 
Accidents and Injuries:  None reported 
Operations: None 
Hospitalizations: June 14, 2000 at Temple Children’s for Conjunctivitis andPreseptal Cellulitis.Discharged later that same day. 
Current Health Status: 
Current Medications: None 
Allergies: NKDA 
Diet: Pt is eating all table foods, drinks approx 24 oz whole milk per day, with fruits, vegetables, meats. Has 2 cups of juice per day. 
Screening Tests: Last PPD was Aug ‘99.Last lead was April ‘99 and 16 mcg/dl.Last CBC was April 1999 and was normal. 
Immunizations: DtaP: #1, #2, #3; IPV: #1, #2, #3; MMR #1; Varivax #1; Hep B #1, #2, #3; HIB #1, #2, #3.Needs: Prevnar #1, DtaP #4, HIB #4. 
Alcohol/Tobacco/Drugs: Mother denies smoke exposure in the home and intrauterine exposure to ETOH, tobacco, or drug/medication use. 
Sleep Patterns: Pt sleeps from 8P-7A, takes one nap from 1-2hr/day.
Exercise/Leisure Activities: Pt is a normally active 3 year old.
Safety Measures: Home safety measure of smoke detectors, child gates, locked cabinets. Car safety with car seats and seat belts. 
Family History:  Diabetes, HTN (relation to pt is unknown). 
Psychosocial History:  Pt lives at home in Philadelphia with mother and siblings. He is in daycare during the weekdays.  Mother denies smoke exposure in the home. 
 Review of Systems: (focused) 
 General:  Wt: 43 3/4#.Energy level is normal. Mother denies fatigue, fever. 
 Skin: Mother denies changes in appearance of skin, hair or nails, any h/o of rashes, lumps, sores, pruritis, color changes, or treatment for any skin conditions.
 Eyes: Mother denies recent changes in vision, diplopia, blurriness, redness, pain, or h/o cataracts. 
 Ears: Mother reports no change in hearing. Mother denies tinnitus, vertigo with or without change in head position, discharge or earaches. 
 Nose/Sinuses:  Mother reports clear nasal drainage x2mo.She denies h/o hay fever, or sinus infections. 
 Mouth/Throat:  Mother denies sore throat, hoarseness of voice. 
 Neck:  Mother denies stiffness, injury, new lumps, swelling, or goiter. 
 Endocrine: Mother denies diarrhea, constipation, weight loss, hair skin or nail changes, heat or cold intolerance, palpitations, polydipsia, polyphagia, polyuria. 
 Hematologic: Mother denies bruising easily, anemia, blood transfusions or reactions to blood products, difficulty clotting or controlling bleeding, or clots. 
 Respiratory: See HPI. 
 Cardiac:  See HPI.
 GI: Mother denies changes in appetite, dysphagia, diarrhea, constipation, nausea, abdominal pain, hematochezia, melena, h/o jaundice, liver disease, or any food intolerances. 
 Genito-Urinary:  Pt is toilet-trained. Mother denies changes in toilet habits, incontinence, dysuria, nocturia, frequency, change in volume, stream, hesitancy, urgency, hematuria, or h/o urinary infection or stones. 
 Musculo-skeletal: Mother denies muscle weakness, pain, tenderness, stiffness, pain or swelling in joints, h/o broken bones, sprains, arthritis.
 Neurologic: Mother denies h/o of hydrocephalus, intraventricular or intracranial hemorrhage, seizures, headaches, syncope. 
 Physical Exam: (focused)......
 Vitals: Wt: 43 3/4 lbs; Ht: not measure; P: 102/min and regular; R:29/min and regular;BP: 90/56 R arm sitting; T: 98.0. 
 General: Pt. is an alert male, age 3years, who is alert, active, in no acute distress.He has no gross physical or neurological abnormalities. 
 Skin: Good color and turgor, warm to touch, with no excoriations. Capillary refill is normal with no clubbing present. 
 Head: Atraumatic, symmetrical, normocephalic, normal hair distribution, no dryness or dandruff noted. 
 Eyes: Visual acuity not tested. Position of eyes is normal and equal bilaterally, eyebrows have no scaliness. No edema or legions to eyelids. Conjunctiva normal color, no corneal defects or iris markings. PERRLA, EOMI, no lid lag, nystagmus, or strabismus. Funduscopic: + red reflex bilaterally, disc round without Papilledema or cupping, disc is pale orange, no hemorrhages, exudates, or AV nicking noted bilaterally. 
 Ears: No tragal or pinna tenderness. Auricles have no deformities, lesions. Auditory acuity is intact grossly. Canals clear bilaterally, without erythema, swelling, exudate, or foreign bodies. TMs intact bilaterally, pearly, without erythema, bulging, or retraction. 
 Nose/Sinuses: Nares patent bilaterally, nasal mucosa and turbinates pink and moderately swollen, green mucous noted anteriorly.No polyps; no septal deviation, perforation, or bleeding. No frontal or maxillary sinus tenderness to palpation. Sinuses clear to transillumination. 
 Throat/Mouth: Lips of normal pink color and moisture, no lumps, cracking, ulcers, or scaliness. Teeth in good repair; mucous membranes moist without ulcerations or lesions. Symmetrical rise of uvula, tonsils present and normal appearing. Soft palate, anterior and posterior pillars, uvula, tonsils and pharynx all pink without lesions, exudate or nodules. 
 Neck: Supple with FROM; trachea midline, no obvious lesions, scars, masses; thyroid movement with swallowing is symmetrical, no thyromegaly 
 Nodes: No cervical, supraclavicular, axillary, epitrochlear, or inguinal lymphadenopathy. 
 Chest: Good symmetrical respiratory excursion, no retractions. AP diameter not increased, no sternal/rib tenderness to palpation; tactile fremitus equal bilaterally (pt would not cooperate); perucssion note resonant bilaterally in all lung fields. Lung felds clear to auscultation and resonant throughout. Breath sounds bronchial at midline and vesicular in periphery. No rales, rhonchi, rubs, or wheezes. No egophony, bronchophony, or whispered pectriloquey (pt would not cooperate). 
 Heart: Apical impulse palpated just medial to LMCL in 5th ICS. No abnormal pulsations, heaves, or thrills. Regular rhythm of 102 bpm with normal S1, S2; no S3 or S4, gallops, or murmurs. 
 Abdomen: Flat, no visible pulsations, peristalsis, or distention. Normoactive bowel sounds in all four quadrants. No epigastric, renal, iliac or femoral bruits. Tympanitic percussion throughout. Liver span 6 cm by percussion in right MCL, percussion to R. 10th ICS dull on inspiration and expiration. No tenderness, masses, or hepatosplenomegaly with palpation, no guarding, rebound, or rigidity. Aorta pulsations normal, no CVA tenderness. 
 Musculoskeletal: TMJ: FROM, no click, upon opening or closing of jaw.  Spine: C-spine FROM, no tenderness, warmth, erythema, crepitations, enlargements, or nodules. Thoracic and lumbar curvatures normal, no tenderness to palpation, FROM.  BUE and BLE. FROM, 5/5 strength bilaterally in all major muscle groups. Normal tone, no fasiculations, atrophy, tenderness, warmth, erythema, crepitations, enlargements, or nodules. 
 Neurological: Mental Status: Pt is alert and oriented, with appropriate behavior, speech, and affect. 
I–not tested
II-not tested
III, IV, VI– PERRLA, EOMI without nystagmus or strabismus, visual fields grossly intact bilaterally by confrontation.
V– facial sensation to light touch and sharp/dull intact bilaterally. Corneal reflex intact bilaterally. Jaw closure normal. 
II–facial muscle strength intact bilaterally, no weakness. 
III– hearing grossly intact; Weber is equal bilaterally, Rinne: AC>BC. 
X, X– Gag reflex intact, no uvula deviation or fasiculations, articulation clear.  XI– Trapezius and SCM muscles strong and symmetrical. 
XII– No asymmetry, fasiculations, or deviations of the tongue. 


Light touch, sharp/dull intact to all extremities equally bilaterally, position and vibratory sense, stereognosis, graphesthesia, and 2-point discrimination intact equally bilaterally. 
Body position and posture is normal appearing, no involuntary movement, muscle tone is normal in all extremities without fasiculations. No atrophy noted. Strength is 5/5 BUE, BLE in all major muscle groups. Grip strength 5/5 bilaterally. DTRs: Biceps, triceps, brachioradialis, patellar, Achilles present and +2/4 bilaterally. Plantar reflex is normal (Babinski not present), ankle clonus not present. 
Rapid alternating and point to point movements normal with no resting or intention tremor present. Posture and gait normal. Tandem, toe and heal walking performed without abnormality. Rhomberg negative, no pronator drift present. 
 Genitalia Tanner stage 1, circumcised without penile lesions or urethral discharge. Testes present and descended bilaterally without masses or tenderness. No inguinal hernia.
 Rectal: No anal or perianal lesions, fissures, erythema, excoriations; sphincter tone good, no prolapse. Rectal walls smooth, no masses or tenderness. Prostate not palpable (due to age). Stool brown, guaiac-negative. 
 Labs/Radiologic: None performed 
 Impression: 1) Allergic Rhinitis 
2) Asthma 
 Plan: 1) Zyrtec syrup 1mg/mL: ½ tsp po qHS. 
2) Albuterol MDI: two puffs q4 hours prn cough 
3) Aerochamber with mask 
4) Recheck in two weeks for efficacy of therapy. 
5) Schedule Health Maintenance Visit ASAP. 
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