Updated: Jun 30, 2009
Not all children who wheeze have asthma. Most children younger than 3 years who wheeze are not predisposed to asthma. Only 30% of infants who wheeze go on to develop asthma. Reactive airway disease has a large differential diagnosis and must not be confused with asthma.
Clinical factors suggestive of childhood asthma include recurrent wheezing, symptomatic improvement with a bronchodilator, recurrent cough, exclusion of alternative diagnoses, and suggestive peak flow findings.
Asthma Resources from Medscape and eMedicineNumerous environmental stimuli induce an allergen-antibody interaction, causing a release of mediators that create airway inflammation. Airway inflammation is the primary factor responsible for smooth muscle hyperresponsiveness, edema, and increased mucous production, resulting in increased work of breathing. A complex interaction occurs between inflammatory cells and airway epithelium. Mediators released from mast cells induce edema, mucous secretion, and bronchospasm. These mediators include histamine, tryptase, heparin, leukotrienes, platelet-activating factor, cytokines, interleukins, and tumor necrosis factor. The other inflammatory cells (ie, eosinophils, lymphocytes) also release mediators and create a toxic environment to respiratory epithelial cells.
In infants and children younger than 3 years, the intrapulmonary airways are so small that any lower airway infection results in diminished airway function. Other anatomical factors, such as poor collateral ventilation, decreased elastic recoil pressure, and a partially developed diaphragm, may predispose the very young child to respiratory compromise.
Speculation exists that all infants are born with highly responsive airways. Increased immunoglobulin E (IgE) levels have been found in those younger than 2 years. A decrease in airway responsiveness may be associated with environmental allergens, viral respiratory diseases, and hereditary factors.
Rhinovirus infections are an important contributor to asthma exacerbations in children. Hence, therapies against rhinovirus might reduce the risk of severe exacerbations.2
Breastfeeding might protect children younger than 24 months of age against recurrent wheezing. The cytokine, TGF-B1, in human milk may have both suppression and enhancement functions in the immune reaction.
Exposure to maternal environmental tobacco smoke during pregnancy or the first year appears to predispose children to reactive airway disease.
Current research on the genetic basis for the pathogenesis of asthma may lead to new diagnostic and preventive treatments. The ADAM33 gene on the short arm of chromosome 20 is hypothesized as being important in the development and pathogenesis of asthma.
Risk of developing asthma is 7% if neither parent has asthma, 20% if one parent has asthma, and 64% if both parents have asthma. In the United States, approximately one half of all ED and clinic visits for asthma are children younger than 18 years. Pediatric asthma is a chronic, multifactorial, lower airway disease that affects 5-15% of children (2.7 million children in the United States alone). ED visits peak in the fall. School holidays disrupt the spread of infections with a subsequent decrease in hospitalization. Asthma prevalence appears to be increasing worldwide. Air pollutants may play a role in the prevalence increase. Higher prevalence occurs in poverty stricken urban areas where children are less likely to have routine doctor visits and access to the availability of medications.
A correlation may exist between high levels of exposure to cockroach allergen and the frequency of asthma-related health problems in inner-city children.3 Homes in poverty areas were more likely to have high cockroach allergen levels. Asthma may develop in children from early exposure to cockroach allergen.4
Status asthmaticus appears to be on the rise; several retrospective studies reflect an increase in hospital admissions, particularly in those younger than 4 years. Fewer hospital and ED visits occur in children using inhaled corticosteroid therapy.
An algorithm has been developed to determine the risk factors for developing persistent asthma symptoms among children younger than 3 years of age who had 4 or more episodes of wheezing during the previous year.5 The Asthma Predictive Index included either (1) one of the following: parental history of asthma, a physician diagnosis of atopic dermatitis, or evidence of sensitization to aeroallergens; or (2) two of the following: evidence of sensitization to foods, ≥4% peripheral blood eosinophilia, or wheezing apart from colds.
An association may exist between obesity and childhood asthma. Increased resistin, an adipokine produced by adipose tissue, may play a negative predictive role in asthma.6
Worldwide, the prevalence of asthma is increasing. Asthma is found to be more common in Western countries than in developing countries. Asthma is more prevalent in English-speaking countries. Prevalence increases as a developing country becomes more Westernized and urbanized.
Reactive airway disease is more common in black and Hispanic children; hospitalization rates in African Americans are 4 times greater than in the white population.
No correlation exists with income or education level from a retrospective review.
The male-to-female ratio is 1.5:1
The peak prevalence of asthma is in those aged 6-11 years.
| Anaphylaxis | Pediatrics, Respiratory Distress
Syndrome |
| Pediatrics, Anaphylaxis | Pneumonia, Aspiration |
| Pediatrics, Croup or
Laryngotracheobronchitis | |
| Pediatrics, Foreign Body Ingestion | |
| Pediatrics, Pneumonia |
Cystic fibrosis
Enlarged mediastinal mass
Gastroesophageal reflux (GER)
Laryngeal webs
Roundworms
Tracheoesophageal fistula
Vascular rings
Ventricular septal defect (VSD)
| Height in Inches | Average Rate | Range* | Height in Inches | Average Rate | Range* |
|---|---|---|---|---|---|
| 40 | 150 | 110-190 | 56 | 330 | 240-420 |
| 41 | 160 | 115-205 | 57 | 340 | 240-420 |
| 42 | 170 | 120-220 | 58 | 360 | 260-460 |
| 43 | 180 | 130-220 | 59 | 375 | 270-480 |
| 44 | 190 | 135-245 | 60 | 390 | 280-500 |
| 45 | 200 | 145-255 | 61 | 400 | 290-510 |
| 46 | 210 | 150-270 | 62 | 415 | 300-530 |
| 47 | 220 | 160-280 | 63 | 430 | 310-550 |
| 48 | 230 | 165-295 | 64 | 445 | 320-570 |
| 49 | 240 | 175-305 | 65 | 460 | 330-590 |
| 50 | 250 | 180-320 | 66 | 480 | 345-615 |
| 51 | 260 | 190-330 | 67 | 500 | 360-640 |
| 52 | 270 | 195-345 | 68 | 515 | 370-660 |
| 53 | 280 | 200-360 | 69 | 530 | 380-680 |
| 54 | 300 | 215-385 | 70 | 550 | 395-705 |
| 55 | 315 | 225-405 | 71 | 570 | 410-730 |
Provide oxygen during transport, cardiorespiratory monitoring and pulse oximetry, beta-agonist nebulization, and intravenous access if the patient is in moderate-to-severe respiratory distress. Subcutaneous terbutaline or epinephrine may be considered if severe distress and very poor air movement are present.
Mild-to-moderate exacerbations (PEF >50% and/or oxygen saturation >92% on room air)
Albuterol is recommended for the initial treatment of mild-to-moderate acute exacerbations of asthma, administered either by a metered-dose inhaler with spacer (with or without mask) or by a hand-held nebulizer.
Two to six puffs of albuterol via metered-dose inhaler with spacer or 0.15 mg/kg (2.5 mg minimum dose, 5 mg maximum dose) via hand-held nebulizer every 20 minutes for up to 3 doses is recommended.
Oral dexamethasone 0.6 mg/kg/dose (first-line treatment) or oral prednisolone 2 mg/kg/dose (second-line treatment).
Severe exacerbations (PEF <50% and/or oxygen saturation <92% on room air) or exacerbations refractory to first-line treatment
Nebulized ipratropium bromide and short-acting beta-agonists, every 20 minutes for up to 3 treatments, are recommended for the treatment of children (250 mcg/dose) and adolescents (500 mcg/dose) with severe exacerbations.
Supplemental oxygen (by nasal cannula or mask, whichever is better tolerated) to maintain an oxygen saturation >92% is recommended during the delivery of short-acting beta-agonists and anticholinergics in patients with severe exacerbations.
Oral dexamethasone 0.6 mg/kg/dose (first-line treatment) or oral prednisolone 2 mg/kg/dose (second-line treatment) may be administered if early response to bronchodilators, otherwise parenteral steroids (dexamethasone or methylprednisolone) should be given.
Management of status asthmaticus
Management of status asthmaticus includes continuous inhaled beta-agonist of 0.5 mg/kg/h, nebulized ipratropium, IV dexamethasone 0.6 mg/kg, and intravenous magnesium 25-40 mg/kg (given over 20 min as a single dose up to a maximum of 2 g) concurrently for the child in severe respiratory distress. Consideration for IM or SC epinephrine or terbutaline. IV hydration is recommended in severe asthmatic requiring admission. Patient should be kept NPO in case of respiratory failure and need for intubation.
Frequent evaluation of the patient's cardiorespiratory status is imperative. Pulse oximetry and noninvasive end-tidal CO 2 monitoring are ideal. Serial blood gas measurements may be necessary if the patient remains critically ill. If a child fails to improve with these interventions, admission to an ED observation area, inpatient unit, or pediatric critical care unit should be initiated. Continued failure to respond with mental status changes is an ominous finding and suggests rising pCO2. Consider noninvasive positive pressure ventilation (PPV) (eg, continuous positive airway pressure [CPAP] 3-5 cm H2 O, intermittent positive airway pressure [IPAP] 10-18 cm H2 O) prior to rapid sequence intubation. Consider the increased risk of pneumothorax if intubated. Optimize ventilator settings.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
These agents relieve reversible bronchospasm by relaxing smooth muscles of the bronchi. Systemic beta-agonists allow systemic delivery of medication to the pulmonary system in medical conditions where bronchoconstriction may inhibit delivery of medication to desired site because of little to no air movement. Oral administration is less effective than inhaled beta-adrenergic agonists, and has therefore fallen into disfavor. Does not appear to alter admission.
Salmeterol is a highly selective, long-acting beta2-adrenergic agonist with bronchodilatory activity. Salmeterol's benzene moiety resembles the structure of catecholamines, and occupies the active site of beta2-adrenergic receptor, while the long, lipophilic side chain of salmeterol, binds to the so-called exosite near the beta2-receptors. The binding at the exosite allows the active portion of the molecule to remain at the receptor site and continually engage and disengage with the receptor, therefore providing a long duration of action. This agent stimulates intracellular adenyl cyclase to catalyze the conversion of adenosine triphosphate to cyclic-3',5'-adenosine monophosphate (cAMP). Increased cAMP levels result in relaxation of bronchiolar smooth muscle, bronchodilation, and increased bronchial airflow.
Long-acting beta2-agonist. Not for emergent use since onset is 30 min or more. By relaxing the smooth muscles of the bronchioles in conditions associated with bronchitis, emphysema, asthma, or bronchiectasis, can relieve bronchospasms. Effect may also facilitate expectoration.
Adverse effects are more likely to occur when administered at high or more frequent doses than recommended. Available as a dry powder for inhalation in 50 mcg blister packs.
Prevention: 50 mcg inhaled bid approximately 12 h apart
Prevention:
<4 years: Not established
>4 years: Administer as in adults
Concomitant use of beta-blockers may decrease bronchodilating, and vasodilating effects of beta agonists such as salmeterol; concurrent administration with methyldopa may increase pressor response; coadministration with oxytocic drugs may result in severe hypotension; ECG changes and hypokalemia resulting from diuretics may worsen when coadministered with salmeterol
Documented hypersensitivity; angina, tachycardia, and cardiac arrhythmias associated with tachycardia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Not indicated to treat acute asthmatic symptoms; black box FDA warning describes that chronic use may result in increased asthma morbidity and mortality, use only as additional therapy for patients not adequately controlled on other asthma-controller medications (eg, low- to medium-dose inhaled corticosteroids) or patients whose disease severity clearly warrants initiation of treatment with 2 maintenance therapies, including salmeterol
Beta-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility. May decrease mediator release from mast cells and basophils and inhibit airway microvascular leakage. MDI delivers 90 mcg/actuation.
Continuous therapy may reduce need for mechanical ventilation.
Quick relief:
MDI: 2-4 actuations (180-360 mcg) q4h prn
Asthma exacerbation:
MDI:
>20 kg: 6 actuations (540 mcg) inhaled PO q20min initially
Nebulizer: 0.15 mg/kg/dose in 2 mL in 0.9% NaCl administered q20min; not to exceed 5 mg/dose; alternatively, 0.5 mg/kg/h continuous nebulization; not to exceed 15 mg/h
Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, TCAs, and sympathomimetic agents
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hyperthyroidism, diabetes mellitus, hypokalemia, muscle tremors, and cardiovascular disorders
Used for treatment or prevention of bronchospasm. A selective beta2-agonist agent. Albuterol is a racemic mixture, while levalbuterol contains only the active R-enantiomer of albuterol. The S-enantiomer does not bind to beta2-receptors but may be responsible for some adverse effects of racemic albuterol, including bronchial hyperreactivity and reduced pulmonary function during prolonged use.
Asthma exacerbation: 1.25-2.5 mg via nebulizer q20min for 3 doses, then 1.25-5 mg q1-4h prn
Asthma exacerbation: 0.075 mg/kg (minimum dose 1.25 mg) inhaled via nebulizer q20 min for 3 doses, then 0.075-0.15 mg/kg (not to exceed 5 mg/dose) q1-4h prn
Decreased efficacy with beta-blockers; digoxin levels may be decreased; may potentiate the kaliuretic effects of drugs such as loop or thiazide diuretics
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Doses higher than 0.63 mg tid may cause tachycardia; immediate hypersensitivity reactions reported; caution in patients with hypokalemia; may cause paradoxical bronchospasm and increased pulse rate or blood pressure
These agents decrease muscle tone in the small and large pulmonary airways.
A quaternary ammonium anticholinergic bronchodilator acting at muscarinic receptors of the parasympathetic nervous system. Chemically related to atropine. Has antisecretory properties and, when applied locally, inhibits secretions from serous and seromucous glands lining the nasal mucosa.
Synergistic with beta2-agonists. Each actuation delivers 17 mcg. Solution for nebulization available as 0.02% (500 mcg/vial).
Asthma exacerbation:
Nebulizer: 500 mcg q20min for 3 doses, then as needed
MDI: 8 actuations inhaled PO q20min prn up to 3 h
Asthma exacerbation:
Nebulizer: 500 mcg q20min for 3 doses, then q2-4h prn
MDI: 4-8 actuations inhaled PO q20min prn up to 3 h
Drugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol increases effects of ipratropium
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Not indicated for acute episodes of bronchospasm; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction
These agents act to decrease the muscle tone in the small and large pulmonary airways.
Elicits alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
Asthma exacerbation: 1:1000 solution (1 mg/mL) 0.1-0.5 mg SC q20min for 3 doses
Asthma exacerbation: 1:1000 solution (1 mg/mL) 0.01 mg/kg up to 0.3 mg/dose SC q20min for 3 doses
<30 kg: EpiPen Jr (1:2000) SC delivers 0.15 mg/dose
>30 kg: EpiPen (1:1000) SC delivers 0.3 mg/dose
Increases toxicity of beta- and alpha-blocking agents and of halogenated inhalational anesthetics
Documented hypersensitivity; cardiac arrhythmias or angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; not to use during labor (may delay second stage of labor)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in elderly patients, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias
Acts directly on beta2-receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance.
Asthma exacerbation: 0.25 mg/dose SC repeated q20min once; not to exceed total dose of 0.5 mg in a 4-h period
Asthma exacerbation: 0.01 mg/kg SC up to 0.3 mg q20min up to 3 doses; alternatively, 2-10 mcg/kg IV loading dose over 10 min, then continuous IV infusion of 0.08-0.4 mcg/kg/min
Concomitant use with beta-blockers may inhibit bronchodilating, cardiac, and vasodilating effects of beta-agonists; concomitant administration of MAOIs may result in hypertensive crisis; concurrent administration of oxytocic drugs such as ergonovine with terbutaline may result in severe hypotension
Documented hypersensitivity; tachycardia resulting from cardiac arrhythmias
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Paradoxical bronchoconstriction may occur with excessive use; through intracellular shunting, terbutaline may decrease serum potassium levels, which can produce adverse cardiovascular effects; decrease is usually transient and may not require supplementation
These agents provide bronchodilation at the cellular level. The exact mechanism is unknown (eg, alteration of intracellular calcium, inhibition of phosphodiesterase, and/or antagonism of prostaglandins). Routine addition to beta-agonist provides benefit in ED management. May be of benefit in impending respiratory failure.
Potentiates exogenous catecholamines, stimulates endogenous catecholamine release and diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation.
For bronchodilation, near toxic (>20 mg/dL) levels are usually required.
No role in acute asthma exacerbation.
Considered in children who are responding poorly on maximal therapy.
Loading dose: 6 mg/kg IV
Maintenance dose: 0.7 mg/kg/h IV infusion
Loading dose: 6 mg/kg IV infused over 20-30 min
Maintenance dose:
6 weeks to 6 months: 0.5 mg/kg/h IV infusion
6 months to 1 year: 0.6-0.7 mg/kg/h IV infusion
1-9 years: 1-1.2 mg/kg/h IV infusion
9-12 years: 0.9 mg/kg/h IV infusion
>12 years: Administer as in adults
Aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects of theophylline; theophylline effects may increase with allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon
Documented hypersensitivity; uncontrolled arrhythmias; peptic ulcers; hyperthyroidism; uncontrolled seizure disorders
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in peptic ulcer, hypertension, tachyarrhythmias, hyperthyroidism, and compromised cardiac function; do not inject IV solution >25 mg/min; patients with pulmonary edema or liver dysfunction are at greater risk of toxicity because of reduced drug clearance
These agents decrease acetylcholine release at the neuromuscular junction and may decrease resting tone of smooth muscle.
Thought to produce bronchodilation through counteraction of calcium-mediated smooth muscle constriction.
2 g IV infused over 20-30 min
25-40 mg/kg IV not to exceed 2 g/dose, infuse over 20-30 min
Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine
Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
A - Fetal risk not revealed in controlled studies in humans
Magnesium may alter cardiac conduction leading to heart block in digitalized patients; respiratory rate, deep tendon reflex, and renal function should be monitored when electrolyte is administered parenterally; caution when administering magnesium dose because it may produce significant hypertension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia
This agent is a blend of oxygen and helium that is less dense than air.
Reduces airway resistance in bronchi with turbulent flow because of low density. Decreases the work of breathing, hence, delaying the onset of respiratory muscle fatigue, allowing other therapies to work.
Available in mixtures of 80:20 (helium:oxygen), 70:30, and 60:40.
80:20 mixture at 10 L/min by nonrebreather mask; may increase to 15 L/min
80:20 mixture at 10 L/min by nonrebreather mask
None reported
None reported
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
None reported
Nonbarbiturate anesthetic/analgesic agent. An induction agent for airway management in patients with status asthmaticus and has a brief bronchodilatory effect.
Acts on the cortex and limbic system, decreasing bronchospasm.
Intubation: 0.1 mg/kg IV followed by 0.5 mg/kg/h IV infusion for 3 h
Administer as in adults
Increases CNS effects of narcotics, barbiturates, and hydroxyzine; thyroid hormones and muscle relaxants increase toxicity of ketamine
Documented hypersensitivity; angina; thyrotoxicosis; aneurysms; hypertension; congestive heart failure
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Resuscitative equipment should be immediately available during administration of medication
These agents inhibit degranulation of sensitized mast cells following exposure to specific antigens.
Inhibits histamine release and slow-reacting substance of anaphylaxis from mast cell. MDI delivers 800 mcg/actuation. Solution for nebulization available as 20 mg/2 mL
Prevention:
MDI: 2-4 actuations inhaled qid
Prevention:
MDI: 2 actuations tid/qid
Nebulizer: 20 mg (2 mL) inhaled via nebulization bid/qid
None reported
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in severe renal or hepatic impairment; symptoms may reoccur when withdrawing drug
These agents inhibit the synthesis of leukotriene.
Effective in aspirin-induced, cold air, and exercise-induced asthma. Not for use in acute episodes of asthma. Prophylactic use only.
Hepatic transaminase levels should be evaluated before initiation. Contraindicated in patients with active liver disease.
Prevention: 600 mg PO qid
Prevention:
<12 years: Not recommended
>12 years: Administer as in adults
Theophylline should be reduced by 50% for those taking both agents; coadministration with propranolol results in increased beta-blocker activity; coadministration with warfarin results in increased PT (monitor closely)
Documented hypersensitivity; active liver disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hepatic impairment, may increase LFTs; neuropsychiatric events have been reported, and following further FDA evaluation, the prescribing information has been updated to include case reports during postmarketing surveillance that include agitation, aggression, anxiousness, dream abnormalities, hallucinations, depression, insomnia, irritability, restlessness, suicidal thinking and behavior (including suicide), and tremor
Cysteinyl leukotriene-receptor antagonist. Inhibits aspirin-induced, cold air, and exercise-induced asthma.
Not for use in acute episodes of asthma.
Prevention: 20 mg PO bid between meals
Prevention:
<5 years: Not established
5-11 years: 10 mg PO bid
>12 years: Administer as in adults
Erythromycin and theophylline reduce plasma concentrations; coadministration with warfarin results in increase in PT (monitor closely); coadministration with aspirin increases zafirlukast effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Not a bronchodilator; have appropriate rescue medication available; caution in hepatic impairment; neuropsychiatric events have been reported, and following further FDA evaluation, the prescribing information has been updated to include case reports during postmarketing surveillance that include agitation, aggression, anxiousness, dream abnormalities, hallucinations, depression, insomnia, irritability, restlessness, suicidal thinking and behavior (including suicide), and tremor
Cysteinyl leukotriene-receptor antagonist. Inhibits aspirin-induced, cold air, and exercise-induced asthma. Not for use in acute episodes of asthma.
Prevention: 10 mg PO every evening
Prevention:
<1 year: Not established
12-23 months: 1 packet of 4 mg oral granules PO every evening
2-5 years: 4 mg-chew tab or granules every evening
6-14 years: 5 mg PO every evening
>14 years: Administer as in adults
None reported
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Not a bronchodilator; have appropriate rescue medication available; neuropsychiatric events have been reported, and following further FDA evaluation, the prescribing information has been updated to include case reports during postmarketing surveillance that include agitation, aggression, anxiousness, dream abnormalities, hallucinations, depression, insomnia, irritability, restlessness, suicidal thinking and behavior (including suicide), and tremor
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli. Oral prednisone should never be substituted for an inhaled corticosteroid in children with a severe acute asthma exacerbation.
Frequent use of inhaled corticosteroid therapy is associated with less ED visits and less hospitalizations. Current research has not proven any long-term adverse effects with children receiving long-term inhaled corticosteroid.
Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, and IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates, and improves pulmonary microcirculation. Has multiple glucocorticoid and mineralocorticoid effects.
Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.
Patients can be switched from an IV to PO regimen in a 1:1 ratio.
Asthma exacerbation: 16 mg PO/IM/IV for 2 d
Asthma exacerbation: 0.6 mg/kg PO/IM/IV; not to exceed 16 mg to be given in 2 separate doses (ie, initial dose, then 2nd dose administered 24-48 h afterward)
Effects decrease with coadministration of barbiturates, phenytoin and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use
Glucocorticosteroid that occurs naturally and synthetically. Used for both acute and chronic asthma. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Loading or initial dose should be taken all at once in the am; may suppress natural cortisone production; hence, requires tapering the dose upon discontinuation.
As soon as the dose for relief is found, a maintenance dose may be established until the nonsteroidal drugs are effective; must always use a decreasing dose to avoid serious renal suppression.
In seasonal allergy a "booster" of prednisone may speed resolution of symptoms. Quite effective in "exhaustion" stage of seasonal allergy.
Tapered dose for asthma exacerbation: 30 mg PO on day 1, 25 mg PO in am on day 2, continue decreasing dose by 5 mg/d each day until 5 mg is administered on day 6, then discontinue
Other regimens: Up to 60 mg PO qd, or every other day to control symptoms, or 40-60 mg/d for 3-10 d
Asthma exacerbation: 0.25-2 mg/kg PO qd or q2d
Decreases effects of salicylates and toxoids (for immunizations); phenytoin, carbamazepine, barbiturates, and rifampin decrease effects of corticosteroids
Documented hypersensitivity; viral, fungal, or tubercular skin lesions
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hyperthyroidism, osteoporosis, cirrhosis, nonspecific ulcerative colitis, peptic ulcer, diabetes, and myasthenia gravis
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Asthma exacerbation: 5-60 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve
Alternatively, administer 5-60 mg/d for 7 d without taper
Asthma exacerbation: 1-2 mg/kg PO qd or divided bid/qid; taper over 2 wk as symptoms resolve
Alternatively, administer above dose 7 d without taper
Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI bleeding or ulceration
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
For treatment of inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation. Allows reduction of ongoing airway inflammation. May increase responsiveness to beta2-agonists by increasing the number of beta2-adrenergic receptors. Prophylactic inhaled steroids in those diagnosed with asthma may impede airway remodeling, bronchial hyperreactivity, and future airway damage.
Systemic adverse effects rarely occur with inhaled corticosteroids. Systemic response time is the same in IV and PO.
Steroid use is recommended if minimal improvement occurs after first beta2-agonist treatment, the patient was recently discontinued from steroids, the patient reports a history of asthma symptoms for a few days before presentation, or URI-associated symptoms are present.
Asthma exacerbation: 125 mg IV qid
Asthma exacerbation: 1-2 mg/kg/d PO qd or divided bid; alternatively, 0.5-2 mg/kg/dose IV q6h
Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics
Documented hypersensitivity; viral, fungal, or tubercular skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Inhibits bronchoconstriction mechanisms, produces direct smooth muscle relaxation, may decrease number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Has extremely potent vasoconstrictive and anti-inflammatory activity. Alters level of inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Available as powder for inhalation in 90 mcg/actuation (actuation delivers ~80 mcg) or 180 mcg/actuation (actuation delivers ~160 mcg). Also available as suspension for nebulized inhalation in 0.25-mg/2 mL, 0.5-mg/2 mL, and 1-mg/2 mL. Indicated for maintenance treatment of asthma and prophylactic therapy.
Dry powder oral inhalant (Flexhaler): 180-360 mcg inhaled PO bid initially; may increase if needed, not to exceed 720 mcg bid
Dry powder oral inhalant (Flexhaler):
<6 years: Not established
≥6 years: 180 mcg inhaled PO bid initially; for some patients a starting dose of 360 mcg bid may be required; not to exceed 360 mcg bid
Nebulization (Respules):
<1 year: Not established
1-8 years: 0.5-1 mg inhaled via nebulization qd or divided bid; not to exceed 1 mg/d
None reported
Documented hypersensitivity; viral, fungal, and bacterial infections
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Prolonged use may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria; adverse effects include oral thrush, hoarseness, adrenal suppression, glaucoma, skin bruising, and alteration in bone metabolism; not for acute asthma
The combination of H1 and H2 antagonists may be useful in anaphylaxis not responding to H1 antagonists alone.
If no response to H1 antagonist alone, coadministration with this H2 antagonist treats itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis.
300-800 mg PO q6-8h; not to exceed 2400 mg/d
300 mg q6-8h IV/IM; not to exceed 2400 mg/d
20-40 mg/kg/d (300 mg/5 mL syr) PO divided bid/qid
Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Elderly persons may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur
May be considered in patients with severe asthma caused by allergens and unresponsive to other treatments.
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. Indicated for moderate-to-severe persistent asthma in patients who react to perennial allergens in whom symptoms are not controlled by inhaled corticosteroids.
Prevention: 150-375 mg SC q2-4wk; inject slowly over 5-10 sec due to viscosity; not to exceed 150 mg/injection site
Precise dose and frequency established by serum total IgE level (IU/mL)
<12 years: Not established
>12 years: Administer as in adults
None reported
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Not effective to treat acute asthma; do not abruptly discontinue inhaled corticosteroids when initiating omalizumab; anaphylaxis may occur following any dose, even if no reaction occurred to the first dose (observe patient for at least 2 h after administration in setting able to manage life-threatening anaphylaxis); patients should carry an epinephrine syringe (EpiPen) and know how to initiate emergency self-treatment; malignancy incidence among omalizumab-treated patients (0.5%) was numerically higher than among patients in control groups (0.2%); malignancies were of various types, and further long-term observation is needed to fully assess risk; may cause injection-site reaction
Monitoring
Follow-up of pediatric asthma patients may be conducted by phone or in person; may include physical examination and/or spirometry; and may be performed by a case manager, registered nurse, nurse practitioner, or physician. Follow-up is recommended:
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reactive airway disease in children, asthma, pediatric asthma, exercise induced asthma, exercise-induced asthma, asthma treatment, asthma assessment, asthma symptoms, asthma triggers, asthma causes, bronchospasm, obstructive airway disease, childhood asthma, hypersensitivity reaction, wheeze, wheezing, RAD, airway inflammation, upper respiratory infection, tachypnea, dyspnea, cyanosis, intercostal retractions, nasalpolyps, nasal secretions, diaphoresis, hyperresonance, pulsus paradoxus, decreased peak expiratory flow rate, pectus carinatum, clubbing, subcutaneous emphysema, respiratory syncytial virus infection, RSV infection, Mycoplasma pneumoniae, pet dander, cockroach allergen, dust mite allergen, molds, pollen, weather changes, bronchiolitis, gastroesophageal fistula, cystic fibrosis
Eric S Chin, MD, Consulting Staff, Department of Emergency Medicine, Kaiser Permanente Hospital, South San Francisco
Disclosure: Nothing to disclose.
Debra Slapper, MD, Consulting Staff, Department of Emergency Medicine, St Anthony's Hospital
Debra Slapper, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner
Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center
Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.
Clinical guidelines
Managing asthma long term in children 0-4 years of age and 5-11 years of age. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma. Bethesda (MD): National Heart, Lung, and Blood Institute; 2007 Aug. p. 281-325.
Global Initiative for Asthma (GINA), National Heart, Lung and Blood Institute (NHLBI). Global strategy for asthma management and prevention. Bethesda (MD): Global Initiative for Asthma (GINA), National Heart, Lung and Blood Institute (NHLBI); 2007. 92 p.
Managing exacerbations of asthma. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma. Bethesda (MD): National Heart, Lung, and Blood Institute; 2007 Aug. p. 373-417.
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