GINA2009
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ASSESSMENT OF SEVERITY |
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MANAGEMENT–COMMUNITY SETTINGS |
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The severity of the exacerbationFigure (4.4-1 ) determines |
Most patients with severe asthma exacerbations shoul |
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the treatment administered. Indices of severity,bepartreatedicularlyin an acute care facility (such as a hospital
PEF 187 |
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(in patients older than 5 years), pulse rate, |
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emergency department) where monitoring, including |
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objective measurement of airflow obstruction, oxyge |
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respiratory rate, and pulse oximetry, should be |
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monitored during treatment. |
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saturation, and cardiac function, is possible. Milder |
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exacerbations, defined by a reduction in peak flow of |
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than 20%, nocturnal awakening, and increased use of |
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Figure 4.4-1. Severity of Asthma Exacerbations* |
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Mild |
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Moderate |
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Severe |
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Respiratory arrest |
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imminent |
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Breathless |
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Walking |
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Talking |
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At rest |
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Infant—softer |
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Infant stops feeding |
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shorter cry; |
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OR |
REPRODUCE! |
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difficulty feeding |
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Can lie down |
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Prefers sitting |
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Hunched forward |
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Talks in |
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Sentences |
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Phrases |
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Words |
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Alertness |
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May be agitated |
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Usually agitated |
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Usually agitated |
Drowsy or confused |
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Respiratory rate |
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Increased |
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Increased |
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Often > 30/min |
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Normal rates of breathing in awake children: |
ALTER |
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Age |
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Normal rate |
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< 2 months |
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< 60/min |
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2-12 months |
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< 50/min |
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1-5 years |
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< 40/min |
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6-8 years |
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< 30/min |
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NOT |
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Accessory muscles |
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Usually not |
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Usually |
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Paradoxical thoraco- |
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and suprasternal |
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abdominal movement |
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retractions |
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Wheeze |
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Moderate, often only |
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Usually loud |
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Absence of wheeze |
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oud |
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end expiratory |
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Pulse/min. |
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< 100 |
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100-120 |
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>120 |
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Bradycardia |
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Guide to limits of normal pulse rate in children: |
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Infants |
2-12 months–Normal Rate |
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< 160/min |
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Preschool |
1-2 years |
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< 120/min |
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School age |
2-8 years |
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< 110/min |
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Pulsus paradoxus |
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Absent |
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May be present |
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Often present |
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Absence suggests |
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< 10 mm Hg |
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10-25 mm Hg |
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> 25 mm Hg (adult) |
respiratory muscle |
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MATERIAL |
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20-40 mm Hg (child) |
fatigue |
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PEF |
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Over 80% |
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Approx. 60-80% |
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< 60% predicted or |
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after initial |
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personal best |
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bronchodilator |
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(< 100 L/min adults) |
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% predicted or |
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or |
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% personal best |
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response lasts < 2 hrs |
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PaO |
2 (on air)† |
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Normal |
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> 60 mm Hg |
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< 60 mm Hg |
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Test not usually |
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and/or |
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necessary |
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Possible cyanosis |
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Pa |
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< 45 mm Hg |
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< 45 mm Hg |
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> 45 mm Hg; |
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2 |
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Possible respiratory |
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failure (see text) |
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SaO |
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% (on air) † |
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> 95% |
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91-95% |
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< 90% |
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COPYRIGHTED |
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Hypercapnea (hypoventilation) develops more readily in young children than in |
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adults and adolescents. |
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*Note: The presence of several parameters, but not necessarily all, indicates the general classification of the exac †Note: Kilopascals are also used internationally; conversion would be appropriate in this regard.
ASTHMA MANAGEMENT AND PREVENTION |
65 |
short acting-agonists can usually be treated in a Assessment 2
community setting. If the patient responds to the increase
in inhaled bronchodilator treatment after the firstAbrieffew history and physical examination pertinent t doses, referral to an acute care facility is not required,exacerbationut should be conducted concurrently with t further management under the direction of a primarypromptcare initiation of therapy. The history should inc
physician may include the use of systemic glucocorticoseverity- |
and duration of symptoms, including exerc |
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of -agonist required will depend on the severity of the |
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REPRODUCE! |
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steroids. Patient education and review of maintenancelimitation and sleep disturbance; all current medica |
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therapy should also be undertaken. |
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including dose (and device) prescribed, dose usually |
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taken, dose taken in response to the deterioration, and |
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Treatment |
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patientis response (or lack thereof) to this therapy; ti |
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onset and cause of the present exacerbation; and risk |
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Bronchodilators. For mild to moderate exacerbations, |
factors for asthma-related death. |
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repeated administration of rapid-acting -inhaledagonists |
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The physical examination should assess exacerbation |
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(2 to 4 puffs every 20 minutes for the first hour) is usually |
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severity by evaluating the patientis ability to compl |
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the best and most cost-effective method of achieving rapid |
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sentence, pulse rate, respiratory rate, use of accessor |
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reversal of airflow limitation. After the first hour, the dose |
OR |
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muscles, and other signs detailedFigurein4.4-2. Any |
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complicating factors should be identified (e.g., pneu |
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exacerbation. Mild exacerbations respond to 2 to 4 puffs |
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atelectasis, pneumothorax, or pneumomediastinum). |
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every 3 to 4 hours; moderate exacerbations will require 6 |
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to 10 puffs every 1 or 2 hours. Treatment should also be |
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Functional assessments such as PEF1 orandFEVarterial |
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titrated depending upon the individual patientis response, |
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oxygen saturation measurements are strongly recommend |
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and if there is a lack of response or other concern about |
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as physical examination alone may not fully indicate t |
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how the patient is responding, the patient should be |
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referred to an acute care facility. |
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severity of the exacerbation, particularly the degree |
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hypoxemiaALTER. Without unduly delaying treatment, a |
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213,214 |
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baseline PEF or FEV1 measurement should be made |
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Many patients will be able to monitor their PEF after the |
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initiation of increased bronchodilator therapy. |
before treatment is initiated. Subsequent measure |
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should be made at intervals until a clear response to |
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Bronchodilator therapy delivered via a metered-dose NOT |
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treatment has occurred. |
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inhaler (MDI), ideally with a spacer, produces at least an |
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equivalent improvement in lung function as the same dose |
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164,211 |
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Oxygen saturation should be closely monitored, prefera |
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delivered via nebulizer. At the clinic level,-this route of |
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mg of prednisolone/kg or equivalentMATERIALduring a 24-hour |
In adults a chest X-ray is not routinely required, but |
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delivery is the most cost212effective,provided patients are |
by pulse oximetry. This is especially useful in ch |
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because objective measurements of lung function m |
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able to use an MDI. No additional medication is necessary |
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if the rapid-acting inhaled-agonist produces a complete |
difficult. Oxygen saturation in children should no |
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greater than 95%, and oxygen saturation less than 92% is |
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response (PEF returns to greater than 80% of predicted or |
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a good predictor of the need for hospitalization |
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personal best) and the response lasts for 3 to 4 hours.(Evidence C |
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Glucocorticosteroids. Oral glucocorticosteroids (0.5 to 1 |
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COPYRIGHTED |
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be carried out if a complicating cardiopulmonary proces |
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period) should be used to treat exacerbations, especially if |
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suspected, in patients requiring hospitalization, a |
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they develop after instituting the other short-term treatment |
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those not responding to treatment where a pneumothorax |
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options recommended for loss of control (see “Stepping up |
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may be difficult to diagnose clinically.Similarly, in children |
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treatment in response to loss of control” in Component 3). |
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routine chest X-rays are not recommended unless ther |
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If patients fail to respond to bronchodilator therapy, as |
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are physical signs suggestive of parenchymal. disea |
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indicated by persistent airflow obstruction, prompt transfer |
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to an acute care setting is recommended, especially if they |
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are in a high risk group. |
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Although arterial blood gas measurements are not |
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routinely required, they should be completed in patients |
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with a PEF of 30 to 50% predicted, those who do not |
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MANAGEMENT–ACUTE CARE SETTINGS |
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respond to initial treatment, or when there is concern |
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regarding deterioration. The patient should continue |
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Severe exacerbations of asthma are life-threatening medical |
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supplemental oxygen while the measurement is made. |
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emergencies, treatment of which is often most safely undertaken |
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in an emergency departmentFigure. 4.4-2 |
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A PaO |
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< 60 mm Hg (8 kPa) and a normal or increased |
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illustrates the |
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(especially > 45 mm Hg, 6 kPa) indicates the |
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PaCO |
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approach to acute care-based management of exacerbations. presence of respiratory failure.
66 ASTHMA MANAGEMENT AND PREVENTION
Figure 4.4-2: Management of Asthma Exacerbations in Acute Care Setting
Initial Assessment (see Figure 4.4-1)
•History, physical examination (auscultation, use of accessory muscles, heart rate, respiratory1 , oxygenrate, PEF or FEV saturation, arterial blood gas if patient in extremis)
Initial Treatment
• Oxygen to achieve 2O saturation ≥ 90% (95% in children)
• Inhaled rapid-acting-agonist continuously for one hour. 2
• Systemic glucocorticosteroids if no immediate response, or if patient recently took oral glucocorticosteroid, or
• Sedation is contraindicated in the treatment of▼an exacerbation.
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Reassess after 1 Hour |
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Physical Examination, PEF,2O saturation and other tests as |
needed |
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▼ |
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Criteria for Moderate Episode: |
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Criteria for Severe Episode: |
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REPRODUCE! |
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PEF 60-80% predicted/personal best |
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History of risk factors for near fatal asthma |
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PEF < 60% predicted/personal best |
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Physical exam: moderate symptoms, accessory muscle |
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Physical exam: severe symptoms at rest, chest retraction |
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Treatment: |
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OR |
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• Oxygen |
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No improvement after initial treatment |
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Treatment: |
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Inhaled -agonist and inhaled anticholinergic every |
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60 min |
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Oxygen |
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• Oral glucocorticosteroids |
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• Inhaled -agonist and inhaled anticholinergic |
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• Continue treatment for 1-3 hours, provided there is |
improvement |
2 |
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• Systemic glucocorticosteroids |
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• Intravenous magnesium |
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Reassess after 1-2 Hours |
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NOT |
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▼ |
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Good Response within 1-2 Hours: |
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Incomplete Response within 1-2 |
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Poor Response within 1-2 Hours: |
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Hours: |
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DO |
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• Risk factors for near fatal asthma |
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• |
Response sustained 60 min after |
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last |
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• Physical exam: symptoms severe, |
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treatment |
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• |
Risk factors for near fatal asthma |
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• |
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• |
Physical exam: mild to moderate signs |
drowsiness, confusion |
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Physical exam normal: No distress |
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PEF < 60% |
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PEF < 30% |
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PEF > 70% |
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O 2 saturation not improving |
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• PCO |
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> 45 mm Hg |
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O 2 saturation > 90% (95% children) |
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• |
P O |
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< 60mm Hg |
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Admit to Acute Care Setting |
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Admit to Intensive Care |
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• Oxygen |
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• Oxygen |
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• Inhaled 2 -agonist + anticholinergic |
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• Inhaled -agonist ± anticholinergic |
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• Intravenous glucocorticosteroids |
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MATERIAL |
2 |
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• Consider intravenous-agonist |
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• Systemic glucocorticosteroid |
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• Intravenous magnesium |
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2 |
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• Consider intravenous theophylline |
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• Monitor PEF, O 2 saturation, pulse |
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• Possible intubation and mechanical |
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ventilation |
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Reassess at intervals |
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Improved: Criteria for Discharge Home |
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Poor Response (see above): |
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• PEF > 60% predicted/personal best |
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• |
Admit to Intensive Care |
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• Sustained on oral/inhaled medication |
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Incomplete response in 6-12 hours |
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Home Treatment: |
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• |
COPYRIGHTED |
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(see above) |
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Continue inhaled-agonist |
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2 |
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• Consider admission to Intensive |
Care |
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• Consider, in most cases, oral glucocorticosteroids |
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• Consider adding a combination inhaler |
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if no improvement within 6-12 hours |
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• Patient education: Take medicine correctly |
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Review action plan |
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Improved (see opposite) |
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Close medical follow-up |
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|
ASTHMA MANAGEMENT AND PREVENTION |
67 |
Treatment Additional bronchodilators.
The following treatments are usually administeredIpratropium bromideAcombination. of nebulized- 2
concurrently to achieve the most rapid resolution ofagonistthe with an anticholinergic (ipratropium bromide)
exacerbation: |
may produce better bronchodilation than either drug |
217 |
|
2 |
alone231 (Evidence B ) and should be administered before |
REPRODUCE! |
|
Oxygen. To achieve arterial oxygen saturation of ≥ 90% |
methylxanthines are considered. Combination- |
|
2 |
(≥ 95% in children), oxygen should be administered byagonist/anticholinergic therapy is associated with l
nasal cannulae, by mask, or rarely by head box in some |
|
hospitalization rates(Evidence A ) and greater |
|||||||||
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212,232,233 |
|
||
infants. PaCO2 may worsen in some patients on 100 |
|
improvement in PEF and FEV1 233 |
(Evidence B ). Similar |
||||||||
percent oxygen, especially those with more severe airflow |
|
212 |
|||||||||
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data have been reported in the pediatric literature |
|||||
obstruction. Oxygen therapy should be titrated against |
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|||||||
218 |
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(Evidence A ). However, once children with asthma are |
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||||||
pulse oximetry to maintain a satisfactory oxygen. saturat |
on |
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219 |
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hospitalized following intensive emergency departm |
|||||
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||||||
Rapid-acting inhaled ß2–agonists. |
Rapid-acting inhaled |
|
treatment, the addition of nebulized ipratropium brom |
||||||||
|
nebulized-agonist and systemic glucocorticosteroids |
||||||||||
-agonists should be administered at regular220-222 intervals |
2 |
|
234 |
||||||||
2 |
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|
|
appears to confer no extra benefit. |
|||||
(Evidence A |
). Although most rapid-acting- onists |
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OR |
235 |
||||
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||||||
have a short duration of effect, the long-acting broncho- |
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||||||||
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TheophyllinIn.e view of the effectiveness and relati |
|||||
dilator formoterol, which has both a rapid onset of action |
|
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||||||||
|
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|
|
safety of rapid-acting-agonists, theophylline has a |
|||||
and a long duration of effect, has been shown to be |
|
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|
|
2 |
|
|||||
|
minimal role in the management of acute asthma.Its |
||||||||||
equally effective without increasing side effects, though |
|
|
|||||||||
it is considerably more expensive. The importance of |
|
use is associated with severe and potentially fatal s |
|||||||||
|
effects, particularly in those on long-term therapy w |
||||||||||
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|
148 |
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this feature of formoterol is that it provides support and |
|
|
|||||||||
reassurance regarding the use of a combination of |
|
sustained-release theophylline, and their bronchodila |
|||||||||
|
effect is less than-thatagonistsof . The benefit as |
||||||||||
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|
NOT |
ALTER |
2 |
|
|||
formoterol and budesonide early in asthma exacerbations. |
|
||||||||||
|
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|
|
add-on treatment in adults with severe asthma exacer- |
|||||
|
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|
|
bations has not been demonstrated. However, in one |
|||||
A modestly greater bronchodilator effect has been shown |
|
|
|
||||||||
|
|
|
|
|
|
study of children with near-fatal asthma, intravenou |
|||||
with levabuterol compared to racemic albuterol in both |
|
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|
|||||||
adults and children with an asthma exacerbation. In |
|
theophylline provided additional benefit to patients |
|||||||||
|
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|
|
223-226 |
|
receiving an aggressive regimen of inhaled and |
|||||
large study of acute asthma in children,and in adults not |
|||||||||||
intravenous-agonists, inhaled ipatropium bromide, and |
|||||||||||
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|
227 |
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previously treated with glucocorticosteroids, levabuterolDO |
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2 |
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|||||
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226 |
- |
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||
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intravenous systemic glucocorticosteroids. |
||||||
|
|
MATERIAL |
|
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|
236 |
|||
treatment resulted in lower hospitalization rates compared |
|
|
|||||||||
to racemic albuterol treatment, but in children the length of |
|
Systemic |
|||||||||
|
227 |
|
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|
|
Systemic glucocorticosteroids. |
|||||
hospital stay was no different. |
|
|
|
glucocorticosteroids speed resolution of exacerbation |
|||||||
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||||||
|
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|
should be utilized in the all but the mildest |
|||||
Studies of intermittent versus continuous nebulized short237,238- |
|
|
|||||||||
|
|
|
|
|
|
exacerbations (Evidence A ), especially if: |
|||||
acting -agonists in acute asthma provide conflicting |
|
|
|
||||||||
results. In a systematic review of,sixtherestudieswere |
|
• The initial rapid-acting inhaled-agonist therapy fails |
|||||||||
2 |
|
|
|
228 |
|
|
|
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|
|
|
no significant differences in bronchodilator effect or |
|
2 |
|||||||||
COPYRIGHTED |
|
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|
|
to achieve lasting improvement |
|||||
hospital admissions between the two treatments. In |
• The exacerbation develops even though the patient |
||||||||||
|
|
|
|
229 |
|
|
|||||
patients who require hospitalization, onefoundstudy |
|
|
was already taking oral glucocorticosteroids |
||||||||
that intermittent on-demand therapy led to a significantly |
|
|
|||||||||
|
|
|
|
|
|
|
• Previous exacerbations required oral |
||||
shorter hospital stay, fewer nebulizations, and fewerglucocorticosteroids. |
|
||||||||||
palpitations when compared with intermittent therapy given |
|
|
|||||||||
every 4 hours. A reasonable approach to inhaled therapy |
|
Oral glucocorticosteroids are usually as effective as |
|||||||||
in exacerbations, therefore, would be the initial use of |
|
|
|
||||||||
|
|
|
|
|
|
administered intravenously and are preferred because |
|||||
continuous therapy, followed by intermittent on-demand |
|
|
239,240 |
||||||||
|
|
|
|
|
|
route of delivery is less invasive and less. expensi |
|||||
therapy for hospitalized patients. There is no evidence to |
|
|
|||||||||
support the routine use of intrave-agonousits in |
|
If vomiting has occurred shortly after administrati |
|||||||||
|
glucocorticosteroids, then an equivalent dose should |
||||||||||
|
|
2 |
230 |
|
|
||||||
patients with severe asthma exacerbations. |
|
re-administered intravenously. In patients dischar |
|||||||||
|
|
|
|
|
|
||||||
Epinephrine. |
|
|
|
|
|
the emergency department, intramuscular administrat |
|||||
A subcutaneous or intramuscular injection |
241 |
|
|
||||||||
|
|
|
|
|
|
may be helpful, especially if there are concerns about |
|||||
of epinephrine (adrenaline) may be indicated for acute |
|
|
|
|
|||||||
treatment of anaphylaxis and angioedema, but is not |
compliance with oral therapy. Oral glucocorticosteroids |
||||||||||
require at least 4 hours to produce clinical improvemen |
|||||||||||
routinely indicated during asthma exacerbations. |
|
Daily doses of systemic glucocorticosteroids equival |
|||||||||
68 ASTHMA MANAGEMENT AND PREVENTION
60-80 mg methylprednisolone as a single dose, or 300-400 |
Leukotriene modifiers. There is little data to suggest a |
mg hydrocortisone in divided doses, are adequate for role for leukotriene modifiers in acute. asthma |
|
|
258 |
hospitalized patients, and 40 mg methylprednisolone or |
|
200 mg hydrocortisone is probably adequate in most |
Sedatives. Sedation should be strictly avoided during |
cases238,242 (Evidence B ). An oral glucocorticosteroid dose exacerbations of asthma because of the respiratory
of 1 mg/kg daily is adequate for treatment of exacerbationsdepresant effect of anxiolytic and hypnotic drugs.
in children with mild persistent. A 7-dasthmaycourse |
|
|
REPRODUCE! |
||
association between the use of these drugs and avoida |
|||||
|
|
243 |
|
has been demonstrated. |
|
in adults has been found to be as effective as a 14-dayasthma deaths |
|||||
|
|
|
209,259 |
|
|
course , and a 3- to 5-day course in children is usually |
|
|
|||
244 |
|
|
|
|
|
considered appropriateEvidence( |
B ). Current evidence |
Criteria for Discharge from the Emergency Department |
|||
suggests that there is no benefit to tapering thevsdose. Hospitalizationof |
|
||||
oral glucocorticosteroids, either in the shortover-term |
|
|
|
||
several weeks(Evidence B |
). |
245 |
Criteria for determining whether a patient should be |
||
246 |
|
|
|
|
|
|
|
|
discharged from the emergency department or admitted |
||
Inhaled glucocorticosteroids. |
Inhaled glucocortico- |
the hospital have been succinctly reviewed and strat |
|||
steroids are effective as part of therapy for asthmabased on consensus260 . Patients with a pre-treatment exacerbations. In one study, the combination of highFEV-doseor PEF < 25% percent predicted or personal best, or inhaled glucocorticosteroids and salbutamol in acutethose1 with a post-ORtreatment1 orFEVPEF < 40% percent
asthma provided greater bronchodilation than salbutamolpredicted or personal best, usually require hospitali alone247 (Evidence B ), and conferred greater benefit thanPatients with post-treatment lung function of 40-60% the addition of systemic glucocorticosteroids acrosspredictedall may be discharged, provided that adequate parameters, including hospitalizations, especiallyfollowfor -up is available in the community and compliance
patients with more severe attacks. |
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assured. Patients with post-treatment lung functi |
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248 |
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≥ 60% predicted can be discharged. |
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NOT |
ALTER |
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Inhaled glucocorticosteroids can be as effective as oral |
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glucocorticosteroids at preventing relapses.Patients |
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Management of acute asthma in the intensive care uni |
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249,250 |
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beyond the scope of this document and readers are |
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discharged from the emergency department on prednisone |
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referred to recent comprehensive261reviews. |
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and inhaled budesonide have a lower rate of relapse than |
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those on prednisone alone(Evidence B ). A high-dose |
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237 |
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For patients discharged from the emergency departmen |
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of inhaled glucocorticosteroid (2.4 mg budesonide daily in |
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- |
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to 40 |
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four divided doses) achieves a relapse rate similarDO |
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MATERIAL |
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• Ipratropium bromide is unlikely to provide addition |
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mg oral prednisone daily(Evidence ). Cost is a |
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• At a minimum, a 7-day course of oral glucoco- |
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251 |
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rticosteroids for adults and a shorter course |
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significant factor in the use of such high-doses of inhaled |
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(3-5 days) for children should be prescribed, along wi |
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glucocorticosteroids, and further studies are required to |
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document their potential benefits, especially cost |
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continuation of bronchodilator therapy. |
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252 |
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• The bronchodilator can be used on an as-needed |
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effectiveness, in acute. asthma |
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basis, based on both symptomatic and objective |
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Magnesium. |
Intravenous magnesium sulphate (usually improvement, until the patient returns to his or |
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given as a single 2 g infusion over 20 minutes) is not |
exacerbation use of rapid-acting inhaled-agonists. |
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2 |
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COPYRIGHTED |
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recommended for routine use in asthma exacerbations, |
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benefit beyond the acute phase and may be quickly |
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but can help reduce hospital admission rates in certain |
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patients, including adults1 25with-30% predictedFEV |
at |
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discontinued. |
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• Patients should initiate or continue inhaled gluc |
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presentation, adults and children who fail to respond to |
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initial treatment, and children whose1 failsFEVto improve |
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corticosteroids. |
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above 60% predicted after 1 hour of care (Evidence A ). |
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• The patientis inhaler technique and use of peak flo |
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253,254 |
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meter to monitor therapy at home should be reviewed. |
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Nebulized salbutamol administered in isotonic magnesium |
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Patients discharged from the emergency departmen |
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sulfate provides greater benefit than if it is delivered in |
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255,256 |
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with a peak flow meter and action plan have a better |
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normal saline (Evidence A ). Intravenous magnesium |
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response than patients discharged without these |
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sulphate has not been studied in young children. |
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8 |
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resources. |
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• The factors that precipitated the exacerbation shou |
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Helium oxygen therapy. A systematic survey of studiesbe identified and strategies for their future a |
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that have evaluated the effect of a combination of helium |
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implemented. |
and oxygen, compared to helium alone, suggests there is |
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• The patientis response to the exacerbation should be |
no routine role for this intervention. It might be considered |
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for patients who do not respond to standard therapy. |
evaluated. The action plan should be reviewed and |
written guidance provided. |
|
257 |
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ASTHMA MANAGEMENT AND PREVENTION |
69 |
•Use of controller therapy during the exacerbation shouldPregnancy be reviewed: whether this therapy was increased
promptly, by how much, and, if appropriate, why oral During pregnancy the severity of asthma often change
glucocorticosteroids were not added. Consider |
and patients may require close follow-up and adjustme |
||
providing a short course of oral glucocorticosteroidsofmedicationsto |
. In approximately one-third of women |
||
be on hand for subsequent exacerbations. |
asthma becomes worse; in one-third asthma becomes |
||
the emergency department for follow-up with specialistwomen without asthma. ForREPRODUCE!this reason, using |
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|
less severe; and in the remaining one-third it remain |
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• The patient or family should be instructed to contaunchangedt during pregnancy. |
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265-267 |
the primary health care professional or asthma |
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specialist within 24 hours of discharge. A followAlthough-up |
there is a general concern about the use of any |
||
appointment with the patient's usual primary caremedication in pregnancy, poorly controlled asthma can professional or asthma specialist should be madehave an adverse effect on the fetus, resulting in i within a few days of discharge to assure that treatmentperinatal mortality, increased prematurity, and low bir is continued until baseline control parameters,weight266,267 . The overall perinatal prognosis for children
including personal best lung function, are reachedborn. to women with asthma that is well-managed during |
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Prospective data indicate that patients dischargedpregnancyfrom is comparable to that for children born to |
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OR |
care do better than patients returned to routine. |
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268 |
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caremedications to obtain optimal control of asthma is jus |
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262 |
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ALTER |
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even when their safety in pregnancy has not been |
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An exacerbation severe enough to require hospitalization |
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unequivocally proven. For most medications used to tr |
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may reflect a failure of the patientis self-management plan. |
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asthma there is little evidence to suggest an increa |
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Hospitalized patients may be particularly receptive to |
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to the fetus. Appropriately monitored use of theophyll |
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information and advice about their illness. Health care |
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351 |
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inhaled glucocorticosteroids, -agonists, and |
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providers should take the opportunity to review patient |
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2 |
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NOT |
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leukotriene modifiers (specifically montelukast) i |
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understanding of the causes of asthma exacerbation , |
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avoidance of factors that may cause exacerbations |
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associated with an increased incidence of fetal |
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abnormalities. Inhaled glucocorticosteroids have been |
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369 |
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(including, where relevant smoking cessation), theshown to prevent exacerbations of asthma during |
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purposes and correct uses of treatment, and the actions |
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269,270 |
(Evidence B ). As in other situations, the |
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to be taken to respond to worsening symptoms or peak |
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pregnancy |
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focus of asthma treatment must remain on control of |
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flow values(Evidence A ). |
- |
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271 |
263 |
DO |
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symptoms and maintenance of normal lung function. |
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MATERIAL |
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Acute exacerbations should be treated aggressively in |
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Referral to an asthma specialist should be considered for |
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hospitalized patients. Following discharge from |
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order to avoid fetal hypoxia. Treatment should include |
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nebulized rapid-acting-agonists and |
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continuous supervision, the patient should be reviewed by |
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2 |
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oxygen and systemic glucocorticosteroids should be |
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the family health care professional or asthma specialist |
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instituted when necessary. |
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regularly over the subsequent weeks until personal best |
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lung function is reached. Use of incentives improves |
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While all patients should have adequate opportunity to |
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primary care follow up but has shown no effect on long |
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COPYRIGHTED |
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discuss the safety of their medications, pregnant p |
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term outcomes. Patients who come to the emergency |
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264 |
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with asthma should be advised that the greater risk t |
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department with an acute exacerbation should be |
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baby lies with poorly controlled asthma, and the safety |
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especially targeted for an asthma education program, if |
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one is available. |
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most modern asthma treatments should be stressed. Ev |
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with a good patient/health care professional relationsh |
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independent printed material, such as a statement fr |
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COMPONENT 5: SPECIAL |
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the US National Asthma Education and Prevention |
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Program on the treatment of asthma during pregnancy, |
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CONSIDERATIONS |
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272 |
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265,273 |
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will provide important additional reassurance. |
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Special considerations are required in managing asthma
Surgery in relation to pregnancy; surgery; rhinitis, sinusitis, and
nasal polyps; occupational asthma; respiratory infections;
Airway hyperresponsiveness, airflow limitation, and gastroesophageal reflux; aspirin-induced asthma; and
anaphylaxis.
mucus hypersecretion predispose patients with asth
intraoperative and postoperative respiratory complicati
70 ASTHMA MANAGEMENT AND PREVENTION
The likelihood of these complications depends on the
severity of asthma at the time of surgery, the typeTreatmentof of rhinitis may improve asthma286,287symptoms surgery (thoracic and upper abdominal surgeries pose(theEvidence A ). Anti-inflammatory agents including greatest risks), and type of anesthesia (general anesthesiaglucocorticosteroids and cromones as well as leukotrie with endotracheal intubation carries the greatest risk)modifiers. and anticholinergics can be effective in
These variables need to be assessed prior to surgeryconditionsand |
. However, some medications are selectivel |
||
be rapidly reduced 24 hours following surgery, as |
Rhinitis and its ImpactREPRODUCE!on Asthma (ARIA) initiative can |
||
pulmonary function should be measured. If possible,effectivethis |
against rhinitis1 -antagonists)(e. ., H and others |
||
evaluation should be undertaken several days before against asthma (e.g.2,-agonists)288 (Evidence A ). Use of surgery to allow time for additional treatment. In particular,intra-nasal glucocorticosteroids for concurrent rhin if the patientis1 isFEVless than 80% of personal best, a been found to have a limited benefit in improving as brief course of oral glucocorticosteroids should be and reducing asthma morbidity in some but not all
|
274,275 |
). |
|
289-291 |
|
|
125,292 |
considered to reduce airflow limitation(Evide ce C |
studies. Leukotriene modifiers, allergen-specific |
||||||
Furthermore, patients who have received systemic |
|
|
284,293 |
|
294,295 |
||
immunotherapy , and anti-IgE therapy are effective |
|||||||
|
|
|
in both conditionsEvidence( |
A ). |
|||
glucocorticosteroids within the past 6 months should have |
|
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|
||||
systemic coverage during the surgical period (100 mg |
|
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|
|||
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|
|
Additional information on this topic from the Allergi |
||||
hydrocortisone every 8 hours intravenously). This should |
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|||
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|
284 |
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|
|
found at http://www.whiar..org |
||||
prolonged systemic glucocorticosteroid therapy may inhibit |
|
OR |
|
||||
276 |
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|
|
wound healing(Evidence C ). |
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|
Sinusitis. Sinusitis is a complication of upper respir |
||||
Rhinitis, Sinusitis, and Nasal Polyps |
|
infections, allergic rhinitis, nasal polyps, and othe |
|||||
|
|
|
nasal obstruction. Both acute and chronic sinusitis c |
||||
|
|
|
worsen asthma. Clinical features of sinusitis lack |
||||
Upper airway diseases can influence lower airway function |
296 |
|
|
||||
|
|
|
diagnostic precision, and CT Scan confirmation is |
||||
in some patients with asthma. Although the mechanisms |
ALTER |
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|
||||
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|
|
recommended when available. In children with suspec |
||||
behind this relationship have not been established, |
|
|
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|
|||
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|
|
rhinosinusitis, antibiotic therapy for 10 days is |
||||
inflammation likely plays a similarly critical role in the |
(Evidence B |
|
|||||
|
|
|
recommended297 |
). Treatment should also |
|||
pathogenesis of rhinitis, sinusitis, and nasal polyps as |
|
|
|
||||
in asthma. |
|
NOT |
|
|
|
|
|
|
|
include medications to reduce nasal congestion, such |
|||||
|
|
|
topical nasal decongestants or topical nasal or even |
||||
Rhinitis. The majority of patients with asthmaDOhave a systemic glucocorticosteroids. These agents remain |
|||||||
|
- |
|
|
|
|
279,288 |
|
|
|
|
secondary to primary asthma therapies. |
||||
history or evidence of rhinitis and up to 30% of patients |
|
|
|
|
|||
|
277,278 |
|
|
|
|
|
|
with persistent rhinitis have or develop. asthma |
Nasal polyps. Nasal polyps associated with asthma and |
||||||
|
|
|
|||||
Rhinitis frequently precedes asthma, and is both a risk |
|
|
|
298 |
|||
factor for the development of279asthmaandis associated |
|
|
|
|
|||
rhinitis, and sometimes with aspirin hypersensit, are |
|||||||
|
|
|
seen primarily in patients over 40 years old. Between 36% |
||||
with increased severity and health resource use in |
|
|
|
|
|||
280 |
|
|
and 96% of aspirin-intolerant patients have polyps, and |
||||
asthma . Rhinitis and asthma share several risk factors: |
|
|
|
|
|||
|
|
|
29% to 70% of patients with nasal polyps may have |
||||
common indoor and outdoor allergens such as house dust |
298,299 |
|
|
|
|||
|
|
|
asthma . Children with nasal polyps should be |
||||
mites, animal dander, and, less commonly, pollen affecting |
|
|
|
||||
281,282 |
MATERIAL |
283 |
assessed for cystic fibrosis and immotile cilia sy |
||||
both the nose and bronchi, occupational sensitizers, |
|
|
|
|
|
||
and non-specific factors like aspirin. For these reasons, |
|
|
|
||||
the Allergic Rhinitis and its Impact on Asthma (ARIA) |
Nasal polyps are quite responsive to topical |
||||||
|
|
288 |
|
|
|||
|
|
|
glucocorticosteroids. A limited number of patients with |
||||
initiative recommends that the presence of asthma must |
|
|
|
||||
|
|
|
glucocorticosteroid-refractory polyps may benefit from |
||||
be considered in all patients with rhinitis, and that in |
|
|
|
||||
|
|
284 |
|
|
|
|
|
planning treatment, both should be considered.together |
|
|
|
|
|||
|
|
|
Occupational Asthma |
|
|||
Both asthma and rhinitis are considered to be |
|
Once a diagnosis of occupational asthma is established |
|||||
|
|
|
|||||
inflammatory disorders of the airway, but there are some |
|
|
|
|
|||
|
|
|
complete avoidance of the relevant exposure is ideally |
||||
differences between the two conditions in mechanisms, |
|
|
300-302 |
||||
|
|
|
important component of management. Occupational |
||||
clinicalCOPYRIGHTEDfeatures, and treatment approach. Although the |
|
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|
|||
|
|
|
asthma may persist even several years after removal f |
||||
inflammation of the nasal and bronchial mucosa may be |
|
|
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|
|||
|
|
|
exposure to the causative agent, especially when the |
||||
similar, nasal obstruction is largely due to hyperemia in |
|
|
|
||||
|
|
|
patient has had symptoms for a long time before cessat |
||||
rhinitis, while airway smooth muscle contraction plays a |
303,304 |
|
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|
|||
285 |
|
|
of exposure . Continued exposure may lead to increasingly |
||||
dominant role in asthma. |
|
|
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|
|
|
ASTHMA MANAGEMENT AND PREVENTION |
71 |
can often persist for weeks after the infection isphysicalcleared,examination often reveals nasal polyps. Asth anti-inflammatory treatment should be continued forandthishypersensitivity to aspirin often develop subs
|
|
305 |
|
Gastroesophageal Reflux |
|
|
|||||||
severe and potentially fatal asthma exacerbations, |
|
|
|||||||||||
lower probability of subsequent remission, and, ultimately, |
|
|
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|
|||||||
|
|
306 |
|
The relationship of increased asthma symptoms, |
|||||||||
permanently impaired lung function. Pharmacologic |
|
||||||||||||
therapy for occupational asthma is identical to theraparticularlyfor |
at night, to gastroesophageal reflux remai |
||||||||||||
other forms of asthma, but it is not a substitute uncertain,for |
although this condition is nearly three t |
||||||||||||
|
|
|
|
prevalent in patients with asthma compared to the gene |
|||||||||
adequate avoidance. Consultation with a specialist in |
|
|
. Some of these patients also have a hiatal |
||||||||||
|
|
|
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|
|
318,319 |
|||||||
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|
|
population |
|||||||||
asthma management or occupational medicine is advisable. |
|
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|
|||||
|
|
|
|
hernia; furthermore, theophylline 2and-agonistsoral |
may |
||||||||
The British Occupational Health Research Foundation |
increase the likelihood of symptoms by relaxing the l |
||||||||||||
|
|
|
|
esophageal ring. |
|
|
|
|
|||||
Guidelines for the prevention, identification, and |
|
|
|
|
|
|
|
|
|||||
management of occupational asthma are available at |
A diagnosis of gastroesophageal reflux in patients wi |
||||||||||||
http://www.bohrf.org.uk/downloads/asthevre.pdf. |
|||||||||||||
|
|
|
|
asthma can best be made by simultaneously monitoring |
|||||||||
Respiratory Infections |
|
|
|
esophageal pH and lung function. Medical management |
|||||||||
|
|
|
|
should be given for the relief of reflux symptoms a |
|||||||||
|
|
|
|
often effective. Patients may be advised to eat smal |
|||||||||
Respiratory infections have an important relationship to |
|
|
|
|
|
|
|
|
|||||
asthma as they provoke wheezing and increased |
|
more frequent meals; avoid food or drink between meals |
|||||||||||
|
|
|
|
|
|
|
REPRODUCE! |
|
|||||
307 |
|
|
|
and especially at bedtime; avoid fatty meals, alcohol, |
|||||||||
symptoms in many patients. Epidemiological studies |
theophylline, and oral-agonists; use proton pump |
|
|||||||||||
|
|
|
|
|
|||||||||
have found that infectious microorganisms associated |
|
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|
|
2 |
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|
|||||
|
|
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|
|
|
OR |
|
and elevate the head of the |
||
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|
|
|
inhibitors -orantagonists;H |
|||||||||
with increased asthma symptoms are often respiratory |
|
|
2 |
|
|
|
|
|
|||||
308 |
309 |
|
|
bed. However, the role of anti-reflux treatment in as |
|||||||||
viruses, but seldom bacteria. Respiratory syncytial |
control is unclear, as it does not consistently improv |
||||||||||||
|
|
45 |
|
||||||||||
virus is the most common cause of wheezing ,in infancy |
|
|
|
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|
|||||
|
|
|
|
function, asthma symptoms, nocturnal asthma, or the u |
|||||||||
while rhinoviruses (which cause the common cold), are the |
|
|
|
|
|
|
|
|
|||||
|
|
|
|
of asthma medications in subjects with asthma but |
|||||||||
principal triggers of wheezing and worsening of asthma in |
|
|
|
|
|
|
|||||||
310 |
|
|
|
|
ALTER |
|
|
|
|
||||
|
|
|
clear reflux-associated respiratory symptoms. Subgro |
||||||||||
older children and adults. Other respiratory viruses, |
of patients may benefit, but it appears difficult t |
||||||||||||
such as parainfluenza, influenza, adenovirus, and |
|||||||||||||
|
|
|
|
|
|
|
320 |
|
|||||
|
|
|
|
which patients will respond to this. therapy |
|
||||||||
coronavirus, are also associated with increased wheezing |
|
|
|
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|
|||||
311 |
|
|
|
NOT |
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|
|
|
|
|
|
and asthma symptoms. Adults with asthma may be at |
Surgery for gastroesophageal reflux is reserved for t |
||||||||||||
|
|
370 |
|
||||||||||
increased risk of serious pneumococcal disease. |
severely symptomatic patient with well-documented |
||||||||||||
|
|
|
DO |
||||||||||
|
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esophagitis and failure of medical management. In pat |
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A number of mechanisms have been identified that explain |
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with asthma, it should be demonstrated that the refl |
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why respiratory infections trigger wheezing and increased |
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321,322 |
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airway responsiveness, including damage to airway |
causes asthma symptoms before surgery is advised. |
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epithelium, stimulation of virus-specific IgE antibody, |
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enhanced mediator release, and the appearance of a late |
Aspirin-Induced Asthma (AIA) |
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312 |
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asthmatic response to inhaled antigen. hus, there is |
Up to 28% of adults with asthma, but rarely children wit |
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evidence that viral infections are an “adjuvant” to the |
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asthma, suffer from asthma exacerbations in respons |
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inflammatory response and promote the development of |
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MATERIAL |
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aspirin and other nonsteroidal anti-inflammatory drug |
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airway injury by enhancing airway inflammation. |
(NSAIDs). This syndrome is more common in severe |
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323 |
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asthma . |
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Treatment of an infectious exacerbation follows the same |
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principles as treatment of other asthma exacerbations— |
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that is, rapid-acting inhaled-agonists and early |
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The clinical picture and course of aspirin-induced as |
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324 |
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2 |
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(AIA) are characteristic. The majority of patients first |
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introduction of oral glucocorticosteroids or increases in |
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experience symptoms, which may include vasomotor |
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inhaled glucocorticosteroids by at least four-fold a e |
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recommended. Because increased asthma symptoms |
rhinitis and profuse rhinorrhea, during the third to |
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decade of life. Chronic nasal congestion evolves, and |
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COPYRIGHTED |
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full period to ensure adequate control. |
The hypersensitivity to aspirin presents a unique |
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within minutes to one or two hours following ingest |
The role of chronic infectionChlamydiawithpneumoniae |
aspirin, an acute, often severe, asthma attack develops, |
and Mycoplasma pneumoniae in the pathogenesis or |
and is usually accompanied by rhinorrhea, nasal |
314 |
obstruction, conjunctival irritation, and scarlet fl |
worsening of asthma is currently unc.Thertainbenefit |
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315-317 |
head and neck. This may be provoked by a single aspirin |
from macrolide antibiotics remains unclear. |
72 ASTHMA MANAGEMENT AND PREVENTION
or other cyclooxygnease-1 (COX-1) inhibitor and include Generally, asthma patients, especially those with adu violent bronchospasm, shock, loss of consciousness,onsetand asthma and associated upper airway disease (nasal
even respiratory arrest. |
polyposis), should be counseled to avoid NSAIDs, taking |
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325,326 |
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acetominophen/paracetemol instead. |
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Persistent marked eosinophilic inflammation, epithelial |
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disruption, cytokine production, and upregulation of |
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Anaphylaxis and Asthma |
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insect stings and bites,REPRODUCE!latex hypersensitivity,- |
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adhesion molecules are found in the airways of patients |
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with AIA . Airway expression of interleukin-5 (IL-5),Anaphylaxis is a potentially life-threatening condit |
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327,328 |
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which is involved in recruitment and survival of eosinophils, |
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is also increased. AIA is further characterized by |
can both mimic and complicate severe asthma. Effectiv |
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treatment of anaphylaxis demands early recognition of |
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328 |
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increased activation of cysteinyl leukotriene pathways, |
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event. The possibility of anaphylaxis should be cons |
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which may be partly explained by a genetic polymorphism |
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in any setting where medication or biological substan |
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of the LTC4 synthase gene found in about 70% percent of |
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patients. However, the exact mechanism by which |
are given, especially by injection. Examples of documen |
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329 |
causes of anaphylaxis include the administration of |
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aspirin triggers bronchoconstriction remains. unknown |
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330 |
allergenic extracts in immunotherapy, food intoleranc |
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(nuts, fish, shellfish, eggs, milk), avian-based vacc |
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The ability of a cyclooxygenase inhibitor to trigger reactions |
OR |
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depends on the drug's cyclooxygenase inhibitory potency, |
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329 |
lactam antibiotics, aspirin and NSAIDs, and angiotensin |
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as well as on the individual sensitivity. of the patient |
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converting enzyme (ACE) inhibitors), and exercise. |
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A characteristic history of reaction is considered adequate |
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Symptoms of anaphylaxis include flushing, pruriti |
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for initiating avoidance strategies. However, the diagnosis |
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urticaria, and angioedema; upper and lower airway |
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can only be confirmed by aspirin challenge, as there are |
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involvement such as stridor, dyspnea, wheezing, or apn |
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no suitablein vitrotests for diagnosis. The aspirin challenge |
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dizziness or syncope with or without hypotension; and |
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test is not recommended for routine practice as it is associatedALTER |
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gastrointestinal symptoms such as nausea, vomiting |
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with a high risk of potentially fatal consequences and must |
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cramping, and diarrhea. Exercise-induced anaphylaxis, |
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only be conducted in a facility with cardiopulmonary |
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often associated with medication or food allergy, is a |
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resuscitation capabilities. Further safeguards are thatNOTunique physical allergy and should be differentiate |
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331 |
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patients should only be challenged when their asthma is in |
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remission and their1 isFEVgreater than 70% of predicted exercise-induced bronchoconstriction. |
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or personal best. Bronchial (inhalational) and nasalDO |
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338 |
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Airway anaphylaxis could account for the sudden onset o |
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- |
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challenges with lysine aspirin are safer than oral challenges |
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332,333 |
asthma attacks in severe asthma and the relative |
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and may be performed in specialized centers. |
resistance of these attacks to increased -doses of |
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Once aspirin or NSAID hypersensitivity develops, it is |
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2 |
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agonists. If there is a possibility that anaphylaxis |
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180 |
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present for life. Patients with AIA should avoid aspirin, |
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involved in an asthma attack, epinephrine should be th |
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products containing it, other analgesics that inhibit COX-1, |
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334 |
bronchodilator of choice. Prompt treatment for |
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and often also hydrocortisone hemisuccinate. Avoid- |
anaphylaxis is crucial and includes oxygen, intramus |
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ance does not prevent progression of the inflammatory |
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disease of the respiratory tract. Where an NSAID is |
epinephrine, injectable antihistamine, intravenous |
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COPYRIGHTED |
MATERIAL |
hydrocortisone, oropharyngeal airway, and intravenous |
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indicated, a cyclooxygenase-2 (COX-2) inhibitor may be |
fluid. Preventing a recurrence of anaphylaxis depend |
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352 |
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consideredwith appropriate physician supervision and |
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335 |
identifying the cause and instructing the patient |
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observation for at least one hour after administration |
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(Evidence B |
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avoidance measures and self-administered emergency |
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). Glucocorticosteroids continue to be the |
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treatment with pre-loaded epinephrine339syringes. |
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mainstay of asthma therapy, but leukotriene modifiers may |
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also be useful for additional control of the underlying |
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disease |
(Evidence B ). For NSAID-sensitive patients |
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332,336 |
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with asthma who require NSAIDs for other medical |
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74 ASTHMA MANAGEMENT AND PREVENTION
