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Asthma Mountainside Pediatrics

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					  Asthma

BY DR MAHMOOD
           INTRODUCTION
• Background: Asthma is a common disorder that
  primarily involves the airways. Traditionally,
  asthma has been considered a disorder of
  airway smooth muscle mediators and anatomic
  elements of the airway mucosa. Although the
  causes of asthma are separated into allergic and
  nonallergic ones, considerable crossover is
  observed in the features of both types of
  asthma, and treatment varies little between them
             INTRODUCTION
• Airway inflammation is associated with airway
  hyperreactivity or bronchial hyperresponsiveness (BHR),
  which is defined as the inherent tendency of the airways
  to narrow in response to a variety of stimuli (eg,
  environmental allergens and irritants).
• Approximately 500,000 annual hospitalizations (34.6% in
  persons <18 y) are because of asthma. The cost of
  illness related to asthma is around $6.2 billion. Each
  year, an estimated 1.81 million people (47.8% £18 y)
  require treatment in the emergency department. Among
  children and adolescents aged 5-17 years, asthma
  accounts for a loss of 10 million school days and costs
  caretakers $726.1 million because of work absence.
             Pathophysiology
• Interactions between environmental and genetic factors
  result in airway inflammation, which limits airflow and
  leads to functional and structural changes in the airways
  in the form of bronchospasm, mucosal edema, and
  mucus plugs.
• Airway obstruction causes increased resistance to
  airflow and decreased expiratory flow rates. These
  changes lead to a decreased ability to expel air and may
  result in hyperinflation. The resulting overdistention helps
  maintain airway patency, thereby improving expiratory
  flow; however, it also alters pulmonary mechanics and
  increases the work of breathing.
           Pathophysiology
• Hyperinflation compensates for the airflow
  obstruction, but this compensation is limited
  when the tidal volume approaches the volume of
  the pulmonary dead space; the result is alveolar
  hypoventilation. Uneven changes in airflow
  resistance, the resulting uneven distribution of
  air, and alterations in circulation from increased
  intraalveolar pressure due to hyperinflation all
  lead to ventilation-perfusion mismatch. Hypoxic
  vasoconstriction also contributes to this
  mismatch.
                Pathophysiology
• In the early stages, when ventilation-perfusion mismatch results in
  hypoxia, hypercarbia is prevented by the ready diffusion of carbon
  dioxide across alveolar capillary membranes. Thus, asthmatic
  patients who are in the early stages of an acute episode have
  hypoxemia in the absence of carbon dioxide retention.
  Hyperventilation triggered by the hypoxic drive also causes a
  decrease in PaCO2.
• An increase in alveolar ventilation in the early stages of an acute
  exacerbation prevents hypercarbia. With worsening obstruction and
  increasing ventilation-perfusion mismatch, carbon dioxide retention
  occurs.
• In the early stages of an acute episode, respiratory alkalosis results
  from hyperventilation. Later, the increased work of breathing,
  increased oxygen consumption, and increased cardiac output result
  in metabolic acidosis. Respiratory failure leads to respiratory
  acidosis.
           Pathophysiology
• New insights in the pathogenesis of asthma
  suggest the role of lymphocytes. Airway
  inflammation in asthma may represent a loss of
  normal balance between two "opposing"
  populations of Th lymphocytes. Two types of Th
  lymphocytes have been characterized: Th1 and
  Th2. Th1 cells produce IL-2 and IFN-a, which
  are critical in cellular defense mechanisms in
  response to infection. Th2, in contrast,
  generates a family of cytokines (IL-4, -5, -6, -9,
  and -13) that can mediate allergic inflammation.
          Pathophysiology
• Evidence exists that the prevalence of
  asthma is reduced in association with
  certain infections (Mycobacterium
  tuberculosis, measles, or hepatitis A);
  exposure to other children (eg, presence
  of older siblings and early enrollment in
  childcare); and less frequent use of
  antibiotics. Furthermore, the absence of
  these lifestyle events is associated with
  the persistence of a Th2 cytokine pattern.
                Pathophysiology
• Under these conditions, the genetic background of the child, with a
  cytokine imbalance toward Th2, will set the stage to promote the
  production of IgE antibody to key environmental antigens (eg, dust
  mites, cockroaches, Alternaria, and possibly cats).
• Therefore, a gene-by-environment interaction occurs in which the
  susceptible host is exposed to environmental factors that are
  capable of generating IgE, and sensitization occurs.
• A reciprocal interaction seems to exist between the two
  subpopulations in which Th1 cytokines can inhibit Th2 generation
  and vice versa.
• Allergic inflammation may be the result of an excessive expression
  of Th2 cytokines. Alternately, the possibility that the loss of normal
  immune balance arises from a cytokine dysregulation in which Th1
  activity in asthma is diminished has been suggested in recent
  studies.
                       Frequency

• In the US: Approximately 17.3 million Americans have asthma. The
  prevalence of asthma in the general population is 5%, and it has
  increased 40% in the past decade. Asthma accounts for more
  school absences and more hospitalizations than any other chronic
  illness. In most children's hospitals in the United States, it is the
  most common diagnosis at admission.
• Internationally: Worldwide, 130 million people have asthma. The
  prevalence is 8-10 times higher in developed countries (eg, United
  States, Great Britain, Australia, New Zealand) than in the developing
  countries. In developed countries, the prevalence is higher in low
  income groups in urban areas and inner cities than in other groups.
             Mortality/Morbidity
•  Morbidity and mortality associated with asthma have increased over
  the last 2 decades. This increase is attributed to increasing
  urbanization. Despite advancements in our understanding of asthma
  and the development of new therapeutic strategies, the morbidity
  and mortality rates due to asthma definitely increased between 1980
  and 1995.
• In the United States, the mortality rate due to asthma has increased
  in all age, race, and sex strata.
• In the United States, the mortality rate due to asthma is more than
  17 deaths per 1 million people (ie, 5000 deaths per y). From 1975-
  1993, the number of deaths nearly doubled in people aged 5-14
  years. In the northeastern and midwestern United States, the
  highest mortality rate has been among persons aged 5-34 years.
                        Race
The prevalence of asthma is higher in minority groups (eg,
  blacks, Hispanics) than in other groups; however,
  findings from one study suggest that much of the recent
  increase in the prevalence is attributed to asthma in
  white children.
About 5-8% of all black children have asthma at some
  time.
The prevalence in Hispanic children is reported to be as
  high as 15%.
In blacks, the death rate is consistently higher than in
  whites.
                   Sex
• Before puberty, the prevalence is 3 times
  higher in boys than in girls.
• During adolescence, the prevalence is
  equal among males and females.
• Adult-onset asthma is more common in
  women than in men.
                  Age
• In most children, asthma develops before
  they are aged 5 years, and, in more than
  half, asthma develops before they are
  aged 3 years.
                  CLINICAL
History: The National Asthma Education and
  Prevention Program Expert Panel Report II
  (EPR-2), "Guidelines for the Diagnosis and
  Management of Asthma," highlights the
  importance of correctly diagnosing asthma.
To establish the diagnosis of asthma, the clinician
  must establish the following: (a) episodic
  symptoms of airflow obstruction are present, (b)
  airflow obstruction or symptoms are at least
  partially reversible, and (c) alternative diagnoses
  are excluded.
                  CLINICAL
• The severity of asthma is classified as mild
  intermittent, mild persistent, moderate persistent,
  or severe persistent.
• These categories do not always work well in
  children. First, lung function is difficult to assess
  in younger children. Second, asthma that is
  triggered solely by viral infections does not fit
  into any category. While the symptoms may be
  intermittent, they may be severe enough to
  warrant hospitalization.
                          CLINICAL

• Patients with mild intermittent disease have symptoms
  fewer than 2 times a week, and pulmonary function is normal
  between exacerbations. Exacerbations are brief, lasting from a few
  hours to a few days. Nighttime symptoms occur less than twice a
  month. The variation in peak expiratory flow (PEF) is less than 20%.
• Patients with mild persistent asthma have
  symptoms more than 2 times a week but less than once a day.
  Exacerbations may affect activity. Nighttime symptoms occur more
  than twice a month. Pulmonary function test results (in age-
  appropriate patients) demonstrate that the forced expiratory volume
  in 1 second (FEV1) or PEF is less than 80% of the predicted value,
  and the variation in PEF is 20-30%.
                   CLINICAL
• Patients with moderate persistent asthma have
  daily symptoms and use inhaled short-acting beta2-
  agonists every day. Acute exacerbations in patients with
  moderate persistent asthma may occur more than 2
  times a week and last for days. The exacerbations affect
  activity. Nocturnal symptoms occur more than once a
  week. FEV1 and PEF values are 60-80% of the
  predicted values, and PEF varies by more than 30%.
• Patients with severe persistent asthma have
  continuous or frequent symptoms, limited physical
  activity, and frequent nocturnal symptoms. FEV1 and
  PEF values are less than 60% of the predicted values,
  and PEF varies by more than 30%.
                    CLINICAL
• Symptoms of asthma may include wheezing,
  coughing, and chest tightness.
  – Wheezing
     • A musical, high-pitched, whistling sound produced by airflow
       turbulence is one of the most common symptoms.
     • In the mildest form, wheezing is only end expiratory. As
       severity increases, the wheeze lasts throughout expiration.
     • In a more severe asthmatic episode, wheezing is also
       present during inspiration. During a most severe episode,
       wheezing may be absent because of the severe limitation of
       airflow associated with airway narrowing and respiratory
       muscle fatigue.
                CLINICAL
– Coughing: Cough may be the only symptom of
  asthma, especially in cases of exercise-induced or
  nocturnal asthma. Usually, the cough is
  nonproductive and nonparoxysmal. Also, coughing
  may be present with wheezing.
– Children with nocturnal asthma tend to cough after
  midnight, during the early hours of morning.
– Chest tightness: A history of tightness or pain in the
  chest may be present with or without other symptoms
  of asthma, especially in exercise-induced or nocturnal
  asthma.
                 CLINICAL
• Other nonspecific symptoms: Infants or young
  children may have history of recurrent bronchitis,
  bronchiolitis, or pneumonia; a persistent cough
  with colds; and/or recurrent croup or chest
  rattling.
• Most children with chronic or recurrent
  bronchitis have asthma. Asthma is the most
  common underlying diagnosis in children with
  recurrent pneumonia.
• Older children may have a history of chest
  tightness and/or recurrent chest congestion.
                        CLINICAL
• During an acute episode, symptoms vary according to
  the severity.
   – Symptoms during a mild episode: Patients may be breathless
     after physical activity such as walking. They can talk in
     sentences and lie down, and they may be agitated.
   – Symptoms during a moderate severe episode: Patients are
     breathless while talking. Infants have feeding difficulties and a
     softer, shorter cry.
   – Symptoms during a severe episode: Patients are breathless
     during rest, are not interested in feeding, sit upright, talk in words
     (not sentences), and are usually agitated.
   – Symptoms with imminent respiratory arrest : The child is drowsy
     and confused. However, adolescents may not have these
     symptoms until they are in frank respiratory failure.
                         CLINICAL
• Physical: Physical examination in the absence of an acute episode
  (eg, during an outpatient visit between acute episodes)
   – During an outpatient visit, it is not uncommon for a patient with mild
     asthma to have normal findings at physical examination. Patients with
     more severe asthma are likely to have signs of chronic respiratory
     distress and chronic hyperinflation.
   – Signs of atopy or allergic rhinitis, such as conjunctival congestion and
     inflammation, ocular shiners, a transverse crease on the nose due to
     constant rubbing associated with allergic rhinitis, and pale violaceous
     nasal mucosa due to allergic rhinitis, may be present.
   – The anteroposterior diameter of the chest may be increased because of
     hyperinflation. Hyperinflation may also cause an abdominal breathing
     pattern.
   – Lung examination may reveal prolongation of the expiratory phase,
     expiratory wheezing, coarse crackles, or unequal breath sounds.
                      CLINICAL
• Physical: Physical examination during an acute episode
  may reveal different findings in mild, moderately severe,
  and severe episodes and in status asthmaticus with
  imminent respiratory arrest.
   – Mild episode: The respiratory rate is increased. Accessory
     muscles of respiration are not used. The heart rate is less than
     100 beats per minute. Pulsus paradoxus is not present.
     Auscultation of chest reveals moderate wheezing, which is often
     end expiratory. Oxyhemoglobin saturation with room air is
     greater than 95%.
   – Moderately severe episode: The respiratory rate is increased.
     Typically, accessory muscles of respiration are used, and
     suprasternal retractions are present. The heart rate is 100-120
     beats per minute. Loud expiratory wheezing can be heard.
     Pulsus paradoxus may be present (10-20 mm Hg).
     Oxyhemoglobin saturation with room air is 91-95%.
                      CLINICAL
• Physical: Severe episode: The respiratory rate is often
  greater than 30 breaths per minute. Accessory muscles
  of respiration are usually used, and suprasternal
  retractions are commonly present. The heart rate is more
  than 120 beats per minute. Loud biphasic (expiratory
  and inspiratory) wheezing can be heard. Pulsus
  paradoxus is often present (20-40 mm Hg).
  Oxyhemoglobin saturation with room air is less than
  91%.
   – Status asthmaticus with imminent respiratory arrest: Paradoxical
     thoracoabdominal movement occurs. Wheezing may be absent
     (associated with most severe airway obstruction). Severe
     hypoxemia may manifest as bradycardia. Pulsus paradoxus
     noted earlier may be absent; this finding suggests respiratory
     muscle fatigue.
                 Causes
In most cases of asthma in children,
  multiple triggers or precipitants exist, and
  the patterns of reactivity may change with
  age.
Treatment can also change the pattern.
Certain viral infections, such as respiratory
  syncytial virus (RSV) bronchiolitis in
  infancy, predispose the child to asthma.
                   Causes
• Respiratory infections: Most commonly, these
  are viral infections.
• In some patients, fungi (eg, allergic
  bronchopulmonary aspergillosis), bacteria (eg,
  mycoplasmata, pertussis), or parasites may be
  responsible.
• Most infants and young children who continue to
  have a persistent wheeze and asthma have high
  immunoglobulin E (IgE) production and
  eosinophilic immune responses (in the airways
  and in circulation) at the time of the first viral
  URTI.
                     Causes
• Allergens: In patients with asthma, 2 types of
  bronchoconstrictor responses to allergens exist.
  – Early asthmatic responses occur via IgE-induced
    mediator release from mast cells within minutes of
    exposure and last for 20-30 minutes.
  – Late asthmatic responses occur 4-12 hours after
    antigen exposure and result in more severe
    symptoms that can last for hours and contribute to the
    duration and severity of the disease.
  – Allergens can be foods, household inhalants (eg,
    animal allergens, molds, fungi, roach allergens, dust
    mites), or seasonal outdoor allergens (eg, mold
    spores, pollens, grass, trees).
                Causes
• Irritants: Tobacco smoke, cold air,
  chemicals, perfumes, paint odors, hair
  sprays, air pollutants, and ozone can
  initiate BHR by inducing inflammation.
• Weather changes: Asthma attacks can be
  related to changes in atmospheric
  temperature, barometric pressure, and the
  quality of air (eg, humidity, allergen and
  irritant content).
                  Causes
• Exercise: Exercise can trigger an early
  asthmatic response. Heat and water loss from
  the airways can increase the osmolarity of the
  fluid lining the airways and result in mediator
  release. Cooling of the airways results in
  congestion and dilatation of bronchial vessels.
• During the rewarming phase after exercise, the
  changes are magnified because the ambient air
  breathed during recovery is warm rather than
  cool.
                   Causes
• Gastroesophageal reflux (GER): The
  presence of acid in the distal esophagus,
  mediated via vagal or other neural reflexes, can
  significantly increase airway resistance and
  airway reactivity.
• Allergic rhinitis, sinusitis, and chronic URTI:
  Inflammatory conditions of the upper airways
  (eg, allergic rhinitis, sinusitis, or chronic and
  persistent infections) must be treated before
  asthmatic symptoms can be completely
  controlled.
               DIFFERENTIALS
Airway Foreign Body
Allergic Rhinitis
Aspergillosis
Aspiration Syndromes
Bronchiectasis
Bronchiolitis
Bronchopulmonary Dysplasia
Cystic Fibrosis,
Gastroesophageal Reflux
Laryngomalacia,
Primary Ciliary Dyskinesia
Subglottic Stenosis,
Vascular Ring Right Aortic Arch
                    WORKUP
• Lab Studies:

• Pulmonary function test (PFT) results are not reliable in
  patients younger than 5 years. In young children (3-6 y)
  and older children who can't perform the conventional
  spirometry maneuver, newer techniques, such as
  measurement of airway resistance using impulse
  oscillometry system, are being tried. Measurement of
  airway resistance before and after a dose of inhaled
  bronchodilator may help to diagnose bronchodilator
  responsive airway obstruction.
                    WORKUP
• Spirometry: In a typical case, an obstructive defect is
  present in the form of normal forced vital capacity (FVC),
  reduced FEV1, and reduced forced expiratory flow over
  25-75% of the FVC (FEF 25-75). The flow-volume loop
  can be concave. Documentation of reversibility of airway
  obstruction after bronchodilator therapy is central to the
  definition of asthma. FEF 25-75 is a sensitive indicator of
  obstruction and may be the only abnormality in a child
  with mild disease. In an outpatient or office setting,
  measurement of the peak flow rate by using a peak flow
  meter can provide useful information about obstruction in
  the large airways. Take care to ensure maximum patient
  effort. However, a normal peak flow rate does not
  necessarily mean a lack of airway obstruction.
               WORKUP
• Plethysmography: Patients with chronic
  persistent asthma may have
  hyperinflation, as evidenced by an
  increased total lung capacity (TLC) at
  plethysmography. Increased residual
  volume (RV) and functional residual
  capacity (FRC) with normal TLC suggests
  air trapping. Airway resistance is
  increased when significant obstruction is
  present.
              WORKUP
• Bronchial provocation tests: Bronchial
  provocation tests may be performed to
  diagnose BHR. These tests are performed
  in specialized laboratories by specially
  trained personnel to document airway
  hyperresponsiveness to substances (eg,
  methacholine, histamine). Increasing
  doses of provocation agents are given,
  and FEV1 is measured. The endpoint is a
  20% decrease in FEV1 (PD20).
                        WORKUP
• Exercise challenge: In a patient with a history of exercise-induced
  symptoms (eg, cough, wheeze, chest tightness or pain), the
  diagnosis of asthma can be confirmed with the exercise challenge.
  In a patient of appropriate age (usually >6 y), the procedure involves
  baseline spirometry followed by exercise on a treadmill or bicycle to
  a heart rate greater than 60% of the predicted maximum, with
  monitoring of the electrocardiogram and oxyhemoglobin saturation.
  The patient should be breathing cold, dry air during the exercise to
  increase the yield of the study. Spirographic findings and the PEF
  rate (PEFR) are determined immediately after the exercise period
  and at 3, 5, 10, 15, and 20 minutes after the first measurement. The
  maximal decrease in lung function is calculated by using the lowest
  postexercise and highest preexercise values. The reversibility of
  airway obstruction can be assessed by administering aerosolized
  bronchodilators.
                 WORKUP
• Blood testing: Eosinophil counts and IgE levels
  may help when allergic factors are suspected.
• Recent evidence suggests the usefulness of
  measuring the fraction of exhaled nitric oxide
  (FeNO) as a noninvasive marker of airway
  inflammation, in order to adjust the dose of
  inhaled corticosteroids treatment. Currently
  FeNO measurement, due to high cost of
  equipment, is used primarily as a research tool.
             Imaging Studies
• Chest radiography: Include chest radiography in the
  initial workup if the asthma does not respond to therapy
  as expected. In addition to typical findings of
  hyperinflation and increased bronchial markings, a chest
  radiograph may reveal evidence of parenchymal
  disease, atelectasis, pneumonia, congenital anomaly, or
  a foreign body. In a patient with an acute asthmatic
  episode that responds poorly to therapy, a chest
  radiograph helps in the diagnosis of complications such
  as pneumothorax or pneumomediastinum.
• Paranasal sinus radiography or CT scanning:
  Consider using these to rule out sinusitis.
           Histologic Findings
• Asthma is an inflammatory disease characterized by the
  recruitment of inflammatory cells, vascular congestion,
  increased vascular permeability, increased tissue
  volume, and the presence of an exudate. Eosinophilic
  infiltration, a universal finding, is considered a major
  marker of the inflammatory activity of the disease.
  Histologic evaluations of the airways in a typical patient
  reveal infiltration with inflammatory cells, narrowing of
  airway lumina, bronchial and bronchiolar epithelial
  denudation, and mucus plugs. Additionally, a patient with
  severe asthma may have a markedly thickened
  basement membrane and airway remodeling in the form
  of subepithelial fibrosis and smooth muscle hypertrophy
  or hyperplasia.
               TREATMENT
• Medical Care: The goals of asthma therapy are
  to prevent chronic and troublesome symptoms,
  maintain normal or near-normal pulmonary
  function, maintain normal physical activity levels
  (including exercise), prevent recurrent
  exacerbations of asthma, and minimize the need
  for emergency department visits or
  hospitalizations, provide optimal
  pharmacotherapy with minimal or no adverse
  effects, and meet the family's expectations for
  asthma care.
              TREATMENT
• Mild intermittent asthma
• Long-term control: Usually, no daily medication
  is needed.
• Quick relief: Short-acting bronchodilators in the
  form of inhaled beta2-agonists should be used
  as needed for symptom control. The use of
  short-acting inhaled beta2-agonists more than 2
  times a week may indicate the need to initiate
  long-term control therapy.
                 TREATMENT
• Mild persistent asthma
• Long-term control: Anti-inflammatory treatment in the
  form of low-dose inhaled corticosteroids or nonsteroidal
  agents (eg, cromolyn, nedocromil) is preferred. Some
  evidence suggests that leukotriene antagonists may be
  useful as first-line therapy in children. Recently, the use
  of montelukast was approved for children aged 2 years
  and older.
• Quick relief: Short-acting bronchodilators in the form of
  inhaled beta2-agonists should be used as needed for
  symptom control. Use of short-acting inhaled beta2-
  agonists on a daily basis or increasing use indicates the
  need for additional long-term therapy.
               TREATMENT
• Moderate persistent asthma
  – Long-term control: Daily anti-inflammatory treatment
    in the form of inhaled corticosteroids (medium dose)
    is preferred. Otherwise, low- or medium-dose inhaled
    corticosteroids combined with a long-acting
    bronchodilator or leukotriene antagonist can be used,
    especially for the control of nocturnal or exercise-
    induced asthmatic symptoms.
  – Quick relief: Short-acting bronchodilators in the form
    of inhaled beta2-agonists should be used as needed
    for symptom control. The use of short-acting inhaled
    beta2-agonists on a daily basis or increasing use
    indicates the need for additional long-term therapy.
                TREATMENT
• Severe persistent asthma
• Long-term control
  – Daily anti-inflammatory treatment in the form of
    inhaled corticosteroids (high dose) is preferred. Other
    medications, such as a long-acting bronchodilator
    leukotriene antagonist or theophylline, can be added.
  – Quick relief: Short-acting bronchodilators in the form
    of inhaled beta2-agonists should be used as needed
    for symptom control. The use of short-acting inhaled
    beta2-agonists on a daily basis or increasing use
    indicates the need for additional long-term therapy.
                   TREATMENT
• Acute severe asthmatic episode (status asthmaticus)
• Treatment goals are the following:
   – Correction of significant hypoxemia with supplemental oxygen: In
     severe cases, alveolar hypoventilation requires mechanically
     assisted ventilation.
   – Rapid reversal of airflow obstruction by using repeated or
     continuous administration of an inhaled beta2-agonist: Early
     administration of systemic corticosteroids (eg, oral prednisone or
     intravenous methylprednisolone) is suggested in children with
     asthma that fails to respond promptly and completely to inhaled
     beta2-agonists.
   – Reduction in the likelihood of recurrence of severe airflow
     obstruction by intensifying therapy: Often, a short course of
     systemic corticosteroids is helpful.
                   Diet
• When a patient has major allergies to
  dietary products, avoidance of particular
  foods may help. In the absence of specific
  food allergies, dietary changes are not
  necessary. Unless compelling evidence for
  a specific allergy exists, milk products do
  not have to be avoided.
                MEDICATION
• Albuterol sulfate (Proventil, Ventolin) -- This beta2-
  agonist is the most commonly used bronchodilator.
  Albuterol is used as needed, and prolonged use may be
  associated with tachyphylaxis due to beta2-receptor
  downregulation and receptor hyposensitivity.
• Oral inhaler: 90 mcg per inhalation, 2 inhalations q4-6h;
  more inhalations may be used in severe, acute episodes;
  more frequent dosing can be used to treat acute
  symptoms.
• Nebulizer: 2.5 mg via nebulization of 0.5% solution in 2-
  3 mL of sodium chloride solution q4-6h
            MEDICATION
• Pirbuterol acetate (Maxair) -- Available
  as a breath-actuated or ordinary inhaler.
  The ease of administration with the breath-
  actuated device makes it an attractive
  choice in the treatment of acute symptoms
  in younger children who otherwise cannot
  use an MDI. Strength is 200 mcg per
  inhalation.
               MEDICATION
• Levalbuterol (Xopenex) -- Nonracemic form of
  albuterol, levalbuterol (R isomer) is effective in
  smaller doses and is reported to have fewer
  adverse effects (eg, tachycardia, hyperglycemia,
  hypokalemia). The dose may be doubled in
  acute severe episodes when even a slight
  increase in the bronchodilator response may
  make a big difference in the management
  strategy (eg, in avoiding patient ventilation). 0.63
  mg by nebulizer q8h
                MEDICATION
• Drug Category: Long-acting beta2-agonist -- Long-
  acting bronchodilators are not used for the treatment of
  acute bronchospasm. They are used for the preventive
  treatment of nocturnal asthma or exercise-induced
  asthmatic symptoms.
• Currently, 2 long-acting beta2-agonists are available in
  the United States: salmeterol (Serevent) and
  formoterol (Foradil). Salmeterol is discussed below.
  Salmeterol is available as a combination of salmeterol
  and fluticasone (Advair).
• Pediatric Dose<12 years: Not established
  >12 years: 1 inhalation of inhalation powder (50 mcg)
  q12h; data in children are limited .
             MEDICATION
• Drug Category: Methylxanthines --
  These agents are Theophylline (Theo-24,
  Theolair, Theo-Dur, Slo-bid) -- Available in
  short- and long-acting formulations.
  Because of the need to monitor the drug
  levels , this agent is used infrequently.
            MEDICATION
• Initial dose: 10 mg/kg PO sustained-
  release tablets and capsules; not to
  exceed 300 mg/d
  First dose adjustment: 13 mg/kg PO; not
  to exceed 450 mg/d
  Second dose adjustment: 16 mg/kg PO;
  not to exceed 600 mg/d
             MEDICATION
• Drug Category: Mast cell stabilizers -- These
  agents are Cromolyn sodium (Intal) and
  nedocromil sodium (Tilade) .
• ,These nonsteroidal anti-inflammatory agents
  are used primarily in preventive therapy.
• Adult DoseCromolyn: 20 mg in 2 mL nebulizer
  solution q6-8h
  Nedocromil: 2-4 inhalations bid/tid; 1.75
  mg/actuation .
• Pediatric DoseCromolyn: Administer as in
  adults
  Nedocromil: Administer as in adults
           MEDICATION
Drug Category: Corticosteroids --
 Steroids are the most potent anti-
 inflammatory agents. Inhaled steroids
 include beclomethasone, triamcinolone,
 flunisolide, fluticasone, and
 budesonide.
             MEDICATION
• Beclomethasone (Beclovent, Vanceril, QVAR)
  -- Inhibits bronchoconstriction mechanisms;
  causes direct smooth muscle relaxation; and
  may decrease the number and activity of
  inflammatory cells, which, in turn, decreases
  airway hyperresponsiveness.
• Pediatric Dose,Low dose: 84-336 mcg/d (42
  mcg/oral inhalation, 2-8 inhalations q24h)
  Medium dose: 336-672 mcg/d (42 mcg/oral
  inhalations, 8-16 inhalations q24h)
  High dose: >672 mcg/d (42 mcg/oral inhalation,
  >16 inhalations q24h)
                MEDICATION
• Fluticasone (Flovent) -- Has extremely potent
  vasoconstrictive and anti-inflammatory activity.
• Pediatric Dose;
• Low dose: 88-176 mcg/d (44 mcg/oral inhalation, 2-4
  inhalations q24h)

• Medium dose: 176-440 mcg/d (110 mcg/oral inhalation,
  2-4 inhalations q24h)

• High dose: >440 mcg/d (110 mcg/oral inhalation, >4
  inhalations q24h or 220 mcg/oral inhalation, 2 inhalations
  q24h)
              MEDICATION
• Budesonide (Pulmicort Turbuhaler or
  Respules) -- Has extremely potent
  vasoconstrictive and anti-inflammatory activity.
• Pediatric Dose:
  Low dose: 100-200 mcg/d (1 inhalation q24h)
  Medium dose: 200-400 mcg/d (1-2 inhalation
  q24h)
  High dose: >400 mcg/d (>2 inhalations q24h)
  Nebulizer (inhalation susp): 0.25-0.5 mg bid; not
  to exceed 1 mg/d
                   MEDICATION
• Drug Category: Systemic corticosteroids -- These agents are
  used for short courses (3-10 d) to gain prompt control of
  inadequately controlled acute asthmatic episodes. They are also
  used for long-term prevention of symptoms in severe persistent
  asthma as well as for suppression, control, and reversal of
  inflammation. Frequent and repetitive use of beta2-agonists has
  been associated with beta2-receptor subsensitivity and
  downregulation; these processes are reversed with corticosteroids.
• Higher-dose corticosteroids have no advantage in severe asthma
  exacerbations, and intravenous administration has no advantage
  over oral therapy. The usual regimen is to continue frequent multiple
  daily dosing until the FEV1 or PEF is 50% of the predicted or
  personal best values; then, the dose is changed to twice daily. This
  usually occurs within 48 hours.
           MEDICATION
• Drug Category: Systemic
  corticosteroids --      Prednisone
  (Deltasone, Orasone) and prednisolone
  (Pediapred, Prelone, Orapred) --
  Immunosuppressants for the treatment of
  autoimmune disorders; may decrease
  inflammation by reversing increased
  capillary permeability and suppressing
  PMN activity. 1-2 mg/kg/d PO for 3-10 d;
  not to exceed 60-80 mg/d
           MEDICATION
Drug Category: Systemic corticosteroids
 -- Methylprednisolone (Solu-Medrol) --
 May decrease inflammation by reversing
 increased capillary permeability and
 suppressing PMN activity. 1 mg/kg IV q6h
            MEDICATION
• Drug Category: Leukotriene modifier --
  Knowledge that leukotrienes cause
  bronchospasm, increased vascular
  permeability, mucosal edema, and
  inflammatory cell infiltration leads to the
  concept of modifying their action by using
  pharmacologic agents. These are either 5-
  lipoxygenase inhibitors or leukotriene-
  receptor antagonists.
           MEDICATION
• Drug Category: Leukotriene modifier :
• Zafirlukast (Accolate) -- Selective
  competitive inhibitor of LTD4, LTE4
  receptors.
• Pediatric Dose
• 5-11 years: 10 mg PO bid
• >12 years: Administer as in adults
              MEDICATION
• Montelukast (Singulair) –
• The advantages are that it is chewable, it has a
  once-a-day dosing, and it has no significant
  adverse effects.
• Pediatric Dose
• 12-23 months: 1 packet of 4 mg oral granules
  PO hs
• 2-6 years: 4 mg PO hs
• 6-14 years: 5 mg PO hs
• >14 years: Administer as in adults
              MEDICATION
• Drug Category: Monoclonal antibody -- These
  agents bind selectively to human IgE on the
  surface of mast cells and basophils.
  Omalizumab (Xolair) -- Recombinant, DNA-
  derived, humanized IgG monoclonal antibody
  that binds selectively to human IgE on surface of
  mast cells and basophils. Reduces mediator
  release, which promotes allergic response.
  Pediatric Dose<12 years: Not established
  >12 years: Administer as in adults
              FOLLOW-UP
• Further Inpatient Care:

• Admit patients for treatment of acute severe
  episodes if they are unresponsive to outpatient
  care (eg, they have worsening bronchospasm,
  hypoxia, evidence of respiratory failure).
• Once the patient is admitted, further
  investigations (eg, PFTs, allergy testing, and
  investigations to rule out other associated
  conditions and complications) can be performed.
                   FOLLOW-UP
• Regular follow-up visits (1-6-mo intervals) are essential
  to ensure control and appropriate therapeutic
  adjustments.
• Outpatient visits should include the following:
   – Interval history of asthmatic complaints, including history of
     acute episodes (eg, severity, measures and treatment taken,
     response to therapy)
   – History of nocturnal symptoms
   – History of symptoms with exercise and exercise tolerance
   – Review of medications, including use of rescue medications
   – Review of home-monitoring data (eg, symptom diary, peak flow
     meter readings, daily treatments)
               FOLLOW-UP
• Patient evaluation should include the following:
  – Assessment for signs of bronchospasm and
    complications
  – Evaluation of associated conditions (eg, allergic
    rhinitis)
  – Pulmonary function testing (in appropriate age group)
• Address issues of treatment adherence and
  avoidance of environmental triggers and
  irritants.
                   FOLLOW-UP
• Any patient with a high risk of asthma should be referred
  to a specialist. The following may suggest a high risk:
   – History of sudden severe exacerbations
   – History of prior intubation for asthma
   – Admission to an ICU because of asthma
   – Two or more hospitalizations for asthma in the past year
   – Three or more emergency department visits for asthma in the
     past year
   – Hospitalization or an emergency department visit for asthma
     within the past month
   – Use of 2 or more canisters of inhaled short-acting beta2-agonists
     per month
             FOLLOW-UP
• Deterrence/Prevention:

• The goal of long-term therapy is to prevent
  acute exacerbations.
• The patient should avoid exposure to
  environmental allergens and irritants that
  are identified during the evaluation.
           Complications

• Pneumothorax status asthmaticus with
  respiratory failure
• Fixed (nonreversible) airway obstruction
• Death
                       Prognosis
• Of infants who wheeze with URTIs, 60% are asymptomatic by age 6
  years; however, children who have asthma (recurrent symptoms
  continuing at age 6 y) have airway reactivity later in childhood.
• Some findings suggest a poor prognosis if asthma develops in
  children younger than 3 years, unless it occurs solely in association
  with viral infections.
• Individuals who have asthma during childhood have significantly
  lower FEV1 and airway reactivity and more persistent
  bronchospastic symptoms than those with infection-associated
  wheezing.
• Children with mild asthma who are asymptomatic between attacks
  are likely to improve and be symptom-free later in life.
• Children with asthma appear to have less severe symptoms as they
  enter adolescence, but half of these children continue to have
  asthma.
                Patient Education

•   Patient and parent education should include instructions on how to use
    medications and devices (eg, spacers, nebulizers, MDIs). The patient's MDI
    technique should be assessed on every visit.
•   Discuss the management plan, which includes instructions about the use of
    medications, precautions with drug and/or device usage, monitoring
    symptoms and their severity (peak flow meter reading), and identifying
    potential adverse effects and necessary actions.
•   Write and discuss in detail a rescue plan for an acute episode. This plan
    should include instructions for identifying signs of an acute attack, using
    rescue medications, monitoring, and contacting the asthma care team.
•   Parents should understand that asthma is a chronic disorder with acute
    exacerbations; hence, continuity of management with active participation by
    the patient and/or parents and interaction with asthma care medical
    personnel is important.
•   Emphasize the importance of compliance with and adherence to treatment.
            Patient Education
• Incorporate the concept of expecting full control of
  symptoms, including nocturnal and exercise-induced
  symptoms, in the management plans and goals (for all
  but the most severely affected patients).
• Avoid unnecessary restrictions in the lifestyle of the child
  or family. Expect the child to participate in recreational
  activities and sports and to attend school as usual.
• For excellent patient education resources, see
  eMedicine's Asthma Center. Also, visit eMedicine's
  patient education articles Asthma, Asthma FAQs,
  Understanding Asthma Medications, Asthma in Children,
  and Asthma in School Children: Educational Slides.
          MISCELLANEOUS
• Medical/Legal Pitfalls:

• Failure to recognize the severity of an acute
  severe episode (ie, status asthmaticus) and to
  initiate aggressive management (eg, intubation
  and ventilation) can lead to fatal complications
  such as respiratory failure and even death.
• Failure to diagnose pneumothorax can lead to
  serious consequences.
• Identification of associated or complicating
  conditions (eg, allergic rhinitis or sinusitis) is
  important for comprehensive management.
          MISCELLANEOUS
• Special Concerns:

• In children, long-term use of high-dose steroids
  (systemic or inhaled) may lead to adverse
  effects, including growth failure. Recent data
  from the Childhood Asthma Management
  Program (CAMP) study and results of the long-
  term use of inhaled steroids (budesonide)
  suggest that the long-term use of inhaled
  steroids has no sustained adverse effect on
  growth in children.

				
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