Asthma

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----- Original Message ----- From: Kathi

Sent: Saturday, September 14, 2002 11:40 PM

Subject: Asthma

Asthma Last Updated: July 17, 2002 AUTHOR INFORMATION Author: Barry Brenner, MD, PhD, Chairman, Department of Emergency of Medicine, Professor, Departments of Emergency Medicine and Internal Medicine, University of Arkansas for Medical Sciences Barry Brenner, MD, PhD, is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, and American College of Physicians Editor(s): Bessman, MD, Chairman, Department of Emergency Medicine, Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, s Hopkins University; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Blackburn, DO, Program Director, Department of Emergency Medicine, Maricopa Medical Center; Assistant Professor, Department of Surgery, University of Arizona; Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistan Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Adler, MD, Instructor, Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School INTRODUCTION Background: Asthma is a common disorder that accounts for 1.5-2 million ED visits each year in the United States. In urban centers, cases of acute asthma may comprise 2.5-10% of all ED visits. Pathophysiology: Acute asthma is a condition characterized by paroxysmal spasmodic narrowing of the bronchial airways due to inflammation of the bronchi and contraction of the bronchial smooth muscle. The inflammatory component is central to the pathogenesis of symptoms: bronchoconstriction and airway hyperresponsiveness lead to dyspnea and wheezing. An additional important mechanism underlying acute asthma involves antigen-antibody interactions, which activate membrane phospholipase and result in production of arachidonic acid. Arachidonic acid is metabolized by cyclooxygenase to vasoactive prostaglandins (eg, thromboxanes, prostacyclins) or leukotrienes and their precursors. All are potent smooth muscle contractors that produce airway hyperresponsiveness and inflammation. The pharmacologic inhibition of leukotriene synthesis and/or action has a beneficial effect on induced and spontaneous asthma, demonstrating that leukotrienes can be important mediators of acute asthma and reactive airway disease (RAD). Aspirin, a cyclooxygenase inhibitor, produces severe bronchospasm in sensitive individuals. Leukotriene inhibitors reverse this sensitivity, providing further evidence that leukotrienes are important mediators of asthma. A balance between the adrenergic and cholinergic systems controls bronchomotor tone. Beta-agonist stimulation induces bronchodilation, and beta-blockers cause bronchoconstriction. More specific beta2-agonists have been developed to avoid the tachycardia associated with nonspecific beta-agonist agents. Cholinergic stimulation may cause bronchoconstriction. Anticholinergic agents (eg, ipratropium, atropine) produce bronchodilation. The airway narrowing in acute asthma manifests itself most commonly as wheezing. The initial component is generally rapidly reversible bronchospasm of the smooth muscles that develops into more refractory inflammation of the airways characterized by bronchial edema, tenacious viscid secretions, mucous plugging, and atelectasis. Common causes of acute asthma include smoking, respiratory infections, exposure to allergens (eg, mold), animal dander (especially that of cats), and cold, dry weather. A strong association had been thought to exist in women between the perimenstrual phase of their cycle and asthma symptoms, but the latest data indicate that this is not true. A familial association is present in RAD. Frequency: In the US: Incidence of acute asthma, defined as the number of persons who develop asthma within a specific time period, is approximately 0.2-0.4% annually. Childhood asthma persists into adulthood in 30% of cases. Those with symptoms persisting into the second decade of life usually have asthma throughout adulthood. Asthma prevalence is 4-8% (ie, 10-20 million persons); one half of these cases are children (ie, 7-19% of all children). Internationally: Asthma prevalence varies from 1-30% across nations; the prevalence increases with increased urbanization and affluence. Increases in asthma mortality in recent years have been noted in Australia, Canada, United Kingdom, Germany, and Switzerland. Mortality/Morbidity: Overall, the death rate from acute asthma has increased from 13 deaths per million in 1982 to 19 deaths per million in 1991. This is a remarkable 40% increase in just 10 years. Race: Prevalence of acute asthma in African American and Puerto Rican Hispanic populations is 11% and 6%, respectively, while that in Caucasians is 3%. The lower socioeconomic conditions of these groups may serve to explain the increased prevalence; however, in other countries, acute asthma is associated with affluence. Sex: In children younger than 10 years, the male-to-female ratio is 2:1. Between the ages of 18 and 54 years, the ratio is reversed, with women being affected twice as often as men. Women visit the ED and are hospitalized for acute asthma twice as often as men. Previous data suggested that 40% of these hospitalizations occur during the premenstrual phase of the cycle; more current data from larger studies has not borne out these initial findings. The menstrual cycle may be a trigger for asthma in few women or a cofactor, inciting asthma along with other well-described triggers. Age: Children younger than 10 years of age constitute 50% of cases. CLINICAL History: Specific historical factors are key in the assessment of acute asthma. Duration and precipitating factors are related to the following: Weather Animal exposure Current medications and compliance (eg, need for medication, dose of steroids) Last use of medications Date of medication Severity and risk of admission and mortality are assessed as follows: Number of ED visits per year, length of time since most recent ED evaluation Duration of time since last hospitalized Hospitalizations per year, excluding ICU Length of time since last ICU admission Number of ICU admissions per year Previous endotracheal intubation Duration of present symptoms: Duration of more than 2 days is associated with a higher admission rate than duration of less than 2 days. Degree of dyspnea The clinician should address whether the condition is truly asthma. Implicated causes of RAD and dyspnea include the following: Smoking more than 20 packs of cigarettes a year Chronic obstructive pulmonary disease (COPD), bronchopulmonary dysplasia, or other pulmonary disease history History of heart disease (cardiac asthma) Sarcoid, human immunodeficiency virus (HIV), cystic fibrosis Chest pain or pleuritis Physical: Accessory muscle use Ability to lie flat: Patients with mild acute asthma are able to lie flat. In more severe cases, the patient assumes a sitting position. As the severity increases, the patient increasingly assumes a hunched-over sitting position with the hands supporting the torso, termed the tripod position. If symptomatology becomes more severe, profuse diaphoresis occurs. The diaphoresis presents concomitantly with a rise in PCO2 and hypoventilation. In the most severe form of acute asthma, the patient may struggle for air and/or be bradypneic and be profusely diaphoretic; almost no breath sounds may be heard, and the patient is willing to lie recumbent. Ability to speak/staccato speech Central cyanosis Level of alertness Presence or absence of peripheral edema Stridor Subcutaneous emphysema Bilateral breath sounds Wheezing: Inspiration-expiration ratio reveals prolongation of the expiratory phase (eg, 1:1 mild, 1:3 severe). Air entry: In children, assess supraclavicular and intercostal retractions, accessory muscle use, and nasal flaring. Causes: Respiratory infections Allergens, particularly cats Exercise Weather, including cold and dry air, weather changes, significant increases in humidity Air pollution Aspirin ingestion Yellow dyes, particularly tartrazine, found in yellow gelatins: This is related to decrease in estrogens and downregulation of progesterone receptors. Organic particle exposure, including the following: Cotton (byssinosis) Detergent manufacture (Bacillus subtilis) Red cedar Grains Chemical irritants (ie, toluene diisocyanate) may be related to nocturnal asthma. Low serum epinephrine levels High serum histamine levels The worst bronchospasm is usually about 4 am, and the best airflow is at approximately 4 pm; therefore, asthma control is labile. ED visits are decreased and mortality increased at night, possibly because of acid reflux, sinusitis, or postnasal dripping during sleep. DIFFERENTIALS Panic Disorders Pediatrics, Croup or Laryngotracheobronchitis Sarcoidosis Other Problems to be Considered: Anaphylaxis (adult, pediatric) Bronchiolitis (pediatric) Foreign body ingestion (pediatric, adult incompetent, neurologically impaired) Polyarteritis nodosa WORKUP Lab Studies: The white blood cell (WBC) count may be elevated if the patient is taking prednisone, has received catecholamines (ie, epinephrine), or has been under significant stress. Eosinophilia may be helpful in diagnosing acute asthma in a patient with new-onset wheezing and bronchospasm reversible with beta2-agonists. Although potassium may be diminished with beta2-agonist treatment, this hypokalemia rarely produces any clinically significant effects. Serum theophylline levels are helpful in monitoring patient compliance and excluding inadvertent theophylline toxicity. Arterial blood gas Arterial blood gas (ABG) measurement provides important information in acute asthma. This test may reveal dangerous levels of hypoxemia or hypercarbia secondary to hypoventilation; typically, results are consistent with respiratory alkalosis. Because of the accuracy and utility of pulse oximetry, only patients whose oxygenation is not restored to over 90% with oxygen therapy require an ABG. The clinical picture usually obviates the need for ABG. Hypercarbia is of concern in that it reflects inadequate ventilation and may indicate the need for mechanical ventilation if the PCO2 is elevated severely; however, the decision to proceed with endotracheal intubation and mechanical ventilation is a clinical assessment. Imaging Studies: Chest x-ray Chest x-ray (CXR) of patients with acute asthma rarely reveals clinically significant findings, although it may show streaky infiltrates or hyperinflation of the lung fields. Patients with pleuritic chest pain require a chest film to exclude pneumothorax or pneumomediastinum, particularly if subcutaneous emphysema is present. CXR is indicated in those with fever to rule out pneumonia. Acute sinusitis may exacerbate asthma, and sinus x-ray results are frequently positive in patients who have acute asthma and a fever. With new-onset asthma and eosinophilia, a CXR may be useful in identifying prominent streaky infiltrates persisting less than 1 month, indicating Loeffler pneumonia. The infiltrates of Loeffler pneumonia are peripheral with central sparing of the lung fields. These findings have been described as the radiographic negative of pulmonary edema. Other Tests: Electrocardiogram and ECG monitoring Patients with asthma who are severely symptomatic should have ECG monitoring, as with any significantly ill patient. Sinus tachycardia and ECG evidence of right heart strain are common in patients with acute asthma. Improvement is shown with beta2-agonist therapy. Supraventricular tachycardia raises the consideration of theophylline toxicity. Arrhythmias, other than supraventricular tachycardia, are rare. Pulse oximetry Pulse oximetry measurement is desirable in all patients with acute asthma to exclude hypoxemia. The hypoxemia of uncomplicated acute asthma is readily reversible by oxygen administration. Oxygenation decreases 4-10 mm Hg with beta-agonist inhalant therapy due to increases in V/Q mismatch. Therefore, all patients with acute asthma should have oxygen saturation measured by pulse oximetry, or they simply should be placed on oxygen therapy. In children, pulse oximetry is used to grade severity of acute asthma. Oxygen saturation of 97% or above constitutes mild asthma, 92-97% constitutes moderate asthma, and less than 92% signifies severe asthma. Spirometry provides a physiologic assessment of airflow and degree of bronchospasm. It gives a more objective assessment of the level of bronchospasm than subjective findings of dyspnea and degree of wheezing. Peak expiratory flow rate (PEFR) measurement is common in the ED because it is inexpensive and portable. Serial measurements document response to therapy and, along with other parameters, are helpful in determining whether to admit the patient to the hospital or discharge from the ED. A limitation of PEFR is that it is quite dependent on effort by the patient. PEFR in the ED can be compared to asymptomatic PEFR, if known. Unfortunately, patients often do not know their asymptomatic PEFR, and the reference group for the ideal PEFR percent predicted (based on age, sex, height of the asthmatic) may not be accurate for the population of acute asthmatics seen in that ED (eg, inner-city asthma). TREATMENT Prehospital Care: Therapy for acute asthmatic episodes can be initiated in the prehospital setting. The primary treatment approach is administration of beta-adrenergic agents by a metered-dose inhaler (MDI), hand-held nebulizer, and/or subcutaneous injection. Emergency Department Care: The mainstay of therapy for acute asthma in the ED is inhaled beta2-agonists. The most effective particle sizes are 1-5 microns. Larger particles are ineffective because they are deposited in the mouth and central airways. Particles smaller than 1 micron are too small to be effective since they move in the airways by Brownian motion and do not reach the lower airways. Standard delivery systems and routes are as follows: Albuterol 7.5 mg inhaled over 60-90 minutes divided tid. Dilution of 2.5 mg in 3 mL of saline or use of premixed nebules is standard. Oxygen or compressed air delivery of the inhaled beta-agonists should be at a rate of 6-8 L/min. For children, use 0.15 mg/kg every 20 minutes for 3 doses. An equivalent method of beta-agonist delivery is the MDI, which has a standard 90 mcg of drug per inhalation and is used in conjunction with a spacer or holding chamber. The dose is 6-8 puffs into the spacer, which is then inhaled by the patient. For most patients who respond to the first treatment, hourly treatments at the same dose are effective. If the patient has a poor response to the MDI/holding chamber, an increase in treatment frequency to every 30 minutes is warranted. The advantage of the MDI/holding chamber is that it requires little or no assistance from the respiratory therapist; the patient can be discharged from the ED with a spacer and albuterol canister. Continuous nebulization may be superior to the MDI/holding chamber method in a patient with PEFR less than 200 L/min. The dose of albuterol is 5-15 mg in 70 mL of isotonic saline. For children, this method is reserved for severe asthma at an albuterol dose of 0.3-5 mg/kg/h. Based on meta-analyses, there is no advantage of intravenous albuterol over inhaled albuterol, even in severe asthma. Metabolic effects include a slight tendency toward tachycardia. Many patients who present with tachycardia and acute asthma actually decrease their heart rate with inhaled beta-agonist therapy. Also, inhaled beta-agonists decrease potassium by an average of 0.4 mEq/L. Patients who respond poorly or not at all to an inhaled beta-agonist regimen usually respond to parenteral beta 2-agonists, such as 0.25 mg terbutaline or 0.3 mg of 1:1000 concentration of epinephrine administered subcutaneously. This is the best treatment choice if bronchospasm does not improve after 2-3 treatments with inhaled beta-2 agonists. Ipratropium 0.5 mg has had variable benefit in controlled trials demonstrating most consistent efficacy in children and smokers. The NAEPP guidelines of 1997 recommend its use in acute asthma exacerbations. For severe asthma, magnesium has been shown to be beneficial (see Cochrane review) with 2 g over 30 min often recommended. However, higher and faster doses have been effective in asthma and demonstrated safety has been shown for almost 50 years in the obstetrics literature with rates as high as 1 g/min for 3g. Intravenous leukotrienes can be recommended at this time (montelukast) 7 mg (not available currently), or 10 mg oral producing a prompt dramatic increase in FEV1 in severe ED asthmatics. In general, 3-4 hours in the ED is adequate time to determine if patients with acute asthma can improve symptomatically and demonstrate flow rates sufficiently improved for safe discharge from the ED. To allow time for glucocorticoids to take effect, extended treatment in a clinical holding area has been demonstrated to be effective. Such units have avoided 60% of admissions to the hospital for acute asthma by treating and observing the patient for as long as 12 hours. These units are appropriate if nursing care and monitoring are adequate. In one holding unit, asthma study patients were discharged within 12 hours at 50% of predicted PEFR if they had no high-risk relapse factors (see list above) or at 60% of predicted PEFR if they had one or more high-risk relapse factors. At time of discharge, patients were given albuterol inhalers and prednisone tablets, avoiding delay and inconvenience of filling the prescriptions and possible noncompliance. At 2 weeks following the ED visit, a 9% relapse rate was noted, considerably less than the 20% for most EDs. Inability to obtain medications due to socioeconomic factors should lower the threshold for hospital admission for patients who have asthma and PEFR of 50-70% of predicted or personal best rate. MEDICATION The goals of therapy are to maintain SaO2 greater than 92% and treat dehydration if it is clinically apparent. Antibiotics should be administered only if bacterial sinusitis, bronchitis, or pneumonia is suspected clinically. Asthma exacerbation severity and therapeutic choices instituted should be evaluated according to the percent of predicted FEV1 or PEFR. Drug Category: Glucocorticoids -- These anti-inflammatory agents restore the beta2-agonist receptors in the bronchial smooth muscles and, therefore, restore the response to beta2-agonists. Glucocorticoids are indicated if response to the first or second beta2-agonist inhaler treatment is incomplete. Additional high-risk patients for whom steroids may be recommended are those who require frequent ED visits, have been admitted with asthma exacerbations, have been intubated, are already on outpatient steroids, or have been experiencing an episode for longer than 3 days. The onset of action of steroids is approximately 4 hours in children and 6 hours in adults. Bioavailability of orally and parenterally administered steroids is no different. Drug Name Methylprednisolone (Solu-Medrol, Depo-Medrol) -- For treatment of inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation. Adult Dose 80-125 mg IV Pediatric Dose Loading dose: 2 mg/kg IV Maintenance dose: 0.5-1 mg/kg/dose IV q6h for up to 5 d Contraindications Documented hypersensitivity; viral, fungal, or tubercular skin infections Interactions Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia if taking concurrent diuretics Pregnancy C - Safety for use during pregnancy has not been established. Precautions Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications Drug Name Prednisone (Deltasone) -- Useful in treatment of inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation. Adult Dose 40-60 mg PO Pediatric Dose 4-5 mg/m2/d PO; alternatively, 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve Contraindications Documented hypersensitivity, viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, fungal or tubercular skin infection, GI disease Interactions Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Abrupt discontinuation may cause adrenal crisis; adverse effects include hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections Drug Name Triamcinolone (Aristocort) -- Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Adult Dose 60 mg IM, followed by additional doses of 20-100 mg IM; doses given when signs and symptoms recur Pediatric Dose <6 years: Not recommended 6-12 years: 0.03-0.2 mg/kg IM at 1- to 7-d intervals 12 years: Administer as in adults Contraindications Documented hypersensitivity; fungal, viral, and bacterial skin infections Interactions Coadministration with barbiturates, phenytoin, or rifampin decreases effects Pregnancy C - Safety for use during pregnancy has not been established. Precautions Multiple complications (eg, severe infections, hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, cushing's syndrome, moon face, unhealthy weight gain, loss of clotting factor, increase in pain levels, als, disruption of hormone levels and ability to sleep, sluggishness, irritability, tooth loss, narrow-angle glaucoma, decrease serum potassium levels, cardiovascular disease) may occur; abrupt discontinuation may cause adrenal crisis Drug Category: Bronchodilators -- Their primary action is to decrease muscle tone in both the small and large airways in the lungs, thus increasing airflow and ventilation. This category includes beta-adrenergic, methylxanthine, and anticholinergic medications. Drug Name Albuterol (Proventil, Ventolin) -- Bronchodilator in reversible airway obstruction due to asthma. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on heart rate. Adult Dose 7.5 mg INH over 60-90 min divided tid; dilute 2.5 mg in 3 mL of saline or use premixed nebules Pediatric Dose 0.15 mg/kg INH q20min for 3 doses Contraindications Documented hypersensitivity Interactions Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, or sympathomimetic agents Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in hyperthyroidism, diabetes mellitus, sensitivity to sympathomimetic amines, coronary insufficiency, hypertension Excessive use may result in tolerance Adverse reactions may occur more frequently in children aged 2-5 y Drug Name Epinephrine (EpiPen, Adrenaline, Bronitin) -- Alpha-agonist effects increase peripheral vascular resistance and reverse peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist activity of epinephrine produces bronchodilatation. Adult Dose 0.01 mL/kg SC; not to exceed 0.3-0.5 mL (0.3-0.5 mg) of 1:1000 solution Pediatric Dose Not established Contraindications Documented hypersensitivity, cardiac arrhythmias, angle-closure glaucoma, use as local anesthetic in areas such as fingers or toes (vasoconstriction may produce sloughing of tissue); use during labor (may delay second stage) Interactions Increases toxicity of beta- and alpha-blocking agents and of halogenated inhalational anesthetics Pregnancy C - Safety for use during pregnancy has not been established. Precautions Rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias Caution in elderly, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency Drug Name Terbutaline (Brethaire, Bricanyl) -- Selective beta2-agonist acts directly on beta2-receptors, relaxing bronchial smooth muscle, relieving bronchospasm, and reducing airway resistance. Adult Dose 0.25 mg SC; repeat q15-30 min prn 2 puffs MDI q4-6h 5 mg PO tid; not to exceed 15 mg/d Pediatric Dose <12 years: 0.25 mg SC; repeat q15-30min prn; 2 puffs MDI q4-6h; 0.05 mg/kg/dose PO tid, not to exceed 5 mg/d 12 years: Administer as in adults Contraindications Documented hypersensitivity, tachycardia resulting from cardiac arrhythmias Interactions Concomitant beta-blockers may inhibit bronchodilating, cardiac, and vasodilating effects of beta-agonists; concomitant MAOIs may result in hypertensive crisis; concurrent oxytocic drugs such as ergonovine may result in severe hypotension Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Through intracellular shunting, terbutaline may decrease serum potassium levels, which can produce adverse cardiovascular effects; decrease is usually transient and may not require supplementation Drug Name Ipratropium (Atrovent) -- Chemically related to atropine, has antisecretory properties. When applied locally, inhibits secretions from serous and seromucous glands lining nasal mucosa. Adult Dose Nebulizer: 1 unit dose vial (500 mcg) INH tid/qid, with doses 6-8 hours apart MDI: 2 inhalations qid; not to exceed 12/d Pediatric Dose 0.25-0.50 mg INH after first dose of beta2-agonist inhaler 1997 NAEPP guidelines recommend 0.25 mg INH q20min for 3 doses, then q2-4h prn, or by MDI 4-8 puffs Contraindications Documented hypersensitivity Interactions Drugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol increases effects Pregnancy B - Usually safe but benefits must outweigh the risks. Precautions Not indicated for acute episodes of bronchospasm; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction Drug Name Ipratropium and albuterol (Combivent) -- Ipratropium is chemically related to atropine. It has anti-secretory properties and, when applied locally, inhibits secretions from serous and seromucous glands lining the nasal mucosa. Albuterol is a beta-agonist for bronchospasm refractory to epinephrine. It relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility. Recommended to "test spray" 3 times before using the first time and in cases where the aerosol has not be used for >24 h. Adult Dose 2 inhalations qid; may take additional inhalations prn; not to exceed 12 inhalations/24 h Pediatric Dose Not established Contraindications Documented hypersensitivity Interactions Drugs with anticholinergic properties (eg, dronabinol) may increase toxicity; albuterol increases effects of ipratropium Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction Drug Name Theophylline (Theo-Dur, Theo-24, Aminophylline) -- Purported efficacy thought to be due to its potentiation of exogenous catecholamines, stimulation of endogenous catecholamine release, and diaphragmatic muscular stimulation. Its effects as bronchodilator are mild, and toxicity (levels >20 mg/dL) is common. Adult Dose Loading dose: 6 mg/kg lean body weight IV over 20-30 min Drip (1 g in 250 mL D5W): 0.5-0.7 mg/kg/h Pediatric Dose 1 mg/kg/h IV Contraindications Documented hypersensitivity, uncontrolled arrhythmias, peptic ulcers, hyperthyroidism, uncontrolled seizure disorders Interactions Aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects; effects may increase with allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon Pregnancy C - Safety for use during pregnancy has not been established. Precautions Caution in peptic ulcer, hypertension, tachyarrhythmias, hyperthyroidism, and compromised cardiac function; do not inject IV solution faster than 25 mg/min; patients with pulmonary edema or liver dysfunction at greater risk of toxicity because of reduced drug clearance Drug Name Ketamine (Ketalar) -- Acts on cortex and limbic system, decreasing bronchospasm. A dissociative anesthetic agent. Adult Dose Initial dose: 1-4.5 mg/kg IV Maintenance dose: One third to one half initial dose IV Pediatric Dose Initial dose: 0.5-2 mg/kg IV Maintenance dose: One third to one half initial dose Contraindications Documented hypersensitivity, angina, thyrotoxicosis, aneurysms, hypertension, congestive heart failure Interactions Increases CNS effects of narcotics, barbiturates, and hydroxyzine; thyroid hormones and muscle relaxants increase toxicity Pregnancy D - Unsafe in pregnancy Precautions Caution in patients with intracranial hypertension or systemic hypertension; may increase bronchial secretions, prompting some practitioners to administer concomitant antisecretory agent (ie, glycopyrrolate) routinely as preventive measure Resuscitative equipment should be immediately available when administering this medication Drug Category: Inhaled volatile anesthetics -- These agents may aid in smooth muscle relaxation. Drug Name Halothane (1-2%) -- Leads to moderate effects on bronchial muscular relaxation and causes bronchodilation. Adult Dose 24 years: 0.84 MAC 42 years: 0.76 MAC 81 years: 0.64 MAC Pediatric Dose Infants: 1.08 MAC 3 years: 0.91 MAC 10 years: 0.87 MAC 15 years: 0.92 MAC Contraindications Documented hypersensitivity Interactions Caution when administering epinephrine or norepinephrine Pregnancy C - Safety for use during pregnancy has not been established. Precautions Hepatic dysfunction may occur FOLLOW-UP Further Outpatient Care: In general, the patient may be discharged from the hospital if the PEFR or the patient's personal best expiratory flow rate is 70% or more of predicted rate and if symptoms are minimal or absent. Patients who have mild symptoms but have PEFR of 50-70% of predicted or personal best could be considered for discharge if high-risk factors for relapse are not present. However, patients with PEFT of 50-70% of predicted or personal best rate who may be unable to obtain medications for socioeconomic reasons have a lower admission threshold. Consider referral to an asthma specialist, as consultation and guidance have been shown to reduce the risk of future ED visits. Education about triggers from asthma, the significant of nocturnal exacerbations (10-fold more asthmatics are intubated at night), use of PEFR, especially at night, written action plan telling the patient what to do in response to certain symptoms or certain PEFR values, and emphasizing the importance of not running out of medications or even running low on medications (note MDI only reliable for number of actuations listed on the canister; almost no patient counts the number of actuations, and floating techniques for canister are unreliable and no longer recommended). Tell the patient to keep an extra canister, especially of beta-agonists. At least 25% of ED visits are for patients who have run out of their beta-agonists, and many take chances all night long waiting for the pharmacy to open or to see their PMP in the morning. In general, discharging a patient on effective inhaled corticosteroids (eg, budesonide) is beneficial. In the immediate post-ED period (2-3 wk), there were some gender differences (with one study actually finding worsening of asthma with inhaled flunisolide in women). However, overall, the benefit of having an inhaled corticosteroid instituted in ED patients outweighs the risks, since many of these patients will never follow up with a PMP and would never have inhaled corticosteroids instituted. Complications: Complications of prolonged steroid use include the following: Respiratory distress/arrest Death Prognosis: Excellent if compliant with proper therapies Risk factors for death from asthma include labile asthma, history of more than 3 ED visits or more than 2 hospitalizations, either ICU admission or endotracheal intubation within the past year, recent withdrawal from corticosteroids, current use of systemic corticosteroids, comorbid conditions (eg, heart disease, HIV), and psychiatric disease. BIBLIOGRAPHY Appel D, Karpel JP, Sherman M: Epinephrine improves expiratory flow rates in patients with asthma who do not respond to inhaled metaproterenol sulfate. J Allergy Clin Immunol 1989 Jul; 84(1): 90-8[Medline]. Bloch H, Silverman R, Mancherje N, et al: Intravenous magnesium sulfate as an adjunct in the treatment of acute asthma. Chest 1995 Jun; 107(6): 1576-81[Medline]. Brenner BE: Bronchial asthma in adults: presentation to the emergency department. Part I: Pathogenesis, clinical manifestations, diagnostic evaluation, and differential diagnosis. Am J Emerg Med 1983 Jul; 1(1): 50-70[Medline]. Brenner BE: Bronchial asthma in adults: presentation to the emergency department. Part II: Sympathomimetics, respiratory failure, recommendations for initial treatment, indications for admission, and summary. Am J Emerg Med 1983 Nov; 1(3): 306-33[Medline]. Chapman KR, Verbeek PR, White JG, et al: Effect of a short course of prednisone in the prevention of early relapse after the emergency room treatment of acute asthma. N Engl J Med 1991 Mar 21; 324(12): 788-94[Medline]. Fiel SB, Swartz MA, Glanz K: Efficacy of short-term corticosteroid therapy in outpatient treatment of acute bronchial asthma. Am J Med 1983 Aug; 75(2): 259-62[Medline]. Kelsen SG, Kelsen DP, Fleeger BF, et al: Emergency room assessment and treatment of patients with acute asthma. Adequacy of the conventional approach. Am J Med 1978 Apr; 64(4): 622-8[Medline]. TG, Elenbaas RM, Pingleton SH: Use of peak expiratory flow rates to eliminate unnecessary arterial blood gases in acute asthma. Ann Emerg Med 1982 Feb; 11(2): 70-3[Medline]. McDermott MF, DG, Zalenski RJ, et al: A comparison between emergency diagnostic and treatment unit and inpatient care in the management of acute asthma. Arch Intern Med 1997 Oct 13; 157(18): 2055-62[Medline]. McFadden ER, Kiser R, DeGroot WJ: Acute bronchial asthma: Relations between clinical and physiologic manifestations. New Engl J Med 1973; 288: 221-225[Medline]. McFadden ER Jr: Dosages of corticosteroids in asthma. Am Rev Respir Dis 1993 May; 147(5): 1306-10[Medline]. McFadden ER Jr, Warren EL: Observations on asthma mortality. Ann Intern Med 1997 Jul 15; 127(2): 142-7[Medline]. National Asthma Education and Prevention Program: Guidelines for the diagnosis and management of asthma. Bethesda: NIH Publication No. 97-4051 1997. Available at: http://www.nhlbi.nih.gov/nhlbi/othcomp/opec/naepp/naeppage.htm. Nowak RM, Pensler MI, Sarkar DD, et al: Comparison of peak expiratory flow and FEV1 admission criteria for acute bronchial asthma. Ann Emerg Med 1982 Feb; 11(2): 64-9[Medline]. Scarfone RJ, Fuchs SM, Nager AL, et al: Controlled trial of oral prednisone in the emergency department treatment of children with acute asthma. Pediatrics 1993 Oct; 92(4): 513-8[Medline]. Tuxen DV: Permissive hypercapnic ventilation. Am J Respir Crit Care Med 1994 Sep; 150(3): 870-4[Medline].

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Hi everyone, Hope you all enjoyed your holiday. I have been on meds

Enbrel, Plaquinel and Arava for about a year now. Lately I have been

having trouble breathing. We think it may be Asthma. Do anyone else

have trouble breathing? It is worse when I am lying down.

Thanks, Jenn

HAPPY NEW YEAR