Asthma and COPD exacerbation - Emergency

Editor's Notes

• #4: General An episode can progress over several days or hours (usual scenario) or progresses rapidly over 1 to 2 hours.
• #5: The goals of initial home management are to relieve symptoms and prevent deterioration to a severe and potentially life-threatening attack.
• #6: Patients with a history of recurrent, severe asthma exacerbations may have been prescribed oral glucocorticoids to have available at home and may be advised by their clinician to take an initial dose (eg, prednisone 40 mg) and notify their clinician. UPTODATE page 4+5
• #8: It is important that therapy not be delayed, so the history and physical examination should be obtained while initial therapy is being provided
• #11: Oxygen saturation: preferably by pulse oximetry and is a key parameter in young children who may not be able to perform lung function Patients with signs of impending respiratory failure should not be asked to perform peak flow. Current guidelines recommend the use of transcutaneous pulse oximetry monitoring particularly among patients who are in severe distress, have a forced expiratory volume in one second (FEV1) or peak expiratory flow less than 50 percent of baseline, or are unable to perform lung function measurements [2]. There is no contraindication to the use of continuous transcutaneous oximetry during all asthmatic attacks. Arterial blood gases are typically reserved for patients who are poorly responsive to initial treatment or deteriorating. A chest X-ray is rarely indicated unless there are physical signs of other or additional complicating features such as foreign body aspiration. A complete blood count may be appropriate for patients with fever or purulent sputum, but modest leukocytosis is common in asthma exacerbations due to viral infection or secondary to corticosteroid administration. Leukocytosis associated with corticosteroid administration does not cause a shift to the left as is seen in bacterial infections. Serum electrolytes should be monitored in patients who take diuretics regularly and in patients with coexistent cardiovascular disease as short-acting inhaled β2-agonists can produce transient decreases in potassium, magnesium, and phosphate.2 The combination of high-dose β2-agonists and systemic corticosteroids occasionally may result in excessive elevations of glucose and lactic acid
• #12: Patients with persistent dyspnea whose PEF is below 25 percent of normal despite initial bronchodilator therapy (meaning that if the PEF is this low initially, give bronchodilator and see if there is improvement rather than doing an immediate ABG)
• #17: — Supplemental oxygen should be administered to most patients with a moderate or severe asthma exacerbation, particularly those who are hypoxemic (SpO2 <90 percent) or for whom continuous oxygen saturation monitoring is not available. Usually, oxygenation is easily maintained with nasal cannula, but occasionally face mask delivery is needed. ----- three treatments are administered within the first hour. The delivery method varies with the setting and severity of the attack (table 3) [2]: High-dose inhaled SABA therapy can be associated with hypokalemia and lactic acidosis. ●Standard nebulization – Albuterol 2.5 to 5 mg by jet (also called "hand-held" or "updraft") nebulization every 20 minutes for three doses, then 2.5 mg to 5 mg every one to four hours as needed. Of note, the higher doses are associated with more frequent and severe sympathomimetic side effects and are generally reserved for very severe, refractory attacks *(MDI) – Albuterol by MDI with a spacer or valved-holding chamber device (eg, Aerochamber, Optichamber, Vortex, and others), four to eight puffs every 20 minutes, for the first hour. Most patients can then transition to dosing every one to four hours, and rarely require dosing at more frequent intervals. ●Continuous nebulization – * Four to six carefully administered inhalations from an MDI with chamber/spacer have generally been found to equal one nebulizer treatment, Many emergency departments (including our own) continue to rely on nebulized administration of beta agonists for acutely ill asthmatic patients, taking advantage of the simplicity of delivery during the patient's tidal breathing. As patients recover in the hospital from acute, severe attacks, the transition can be made from nebulized beta agonists to beta agonists by MDI with a valved holding chamber (“spacer”) without loss of efficacy and with the opportunity for patient education in proper inhaler technique ---- We typically stop inhaled short-acting anticholinergic therapy once the patient is admitted to the hospital, except in patients with refractory asthma who require treatment in the intensive care unit, are on monoamine oxidase inhibitor therapy (who may have increased toxicity from sympathomimetic therapy due to impaired drug metabolism), have chronic obstructive pulmonary disease with an asthmatic component, and those whose asthma has been triggered by beta-blocker therapy.
• #18: The primary therapy of acute exacerbations is pharmacologic, which includes short-acting inhaled β2-agonists and, depending on the severity, systemic corticosteroids, inhaled ipratropium, and O2. Treatments are typically administered concurrently to facilitate rapid improvement
• #19: New evidence supports the use of heliox versus oxygen for nebulized β2-agonist administration in patients with moderate to severe exacerbations who do not respond to standard therapy.3,30 Heliox is a combination of helium and oxygen (often 70:30) that has a lower density than air which reduces resistance to flow and increases ventilation by converting turbulent flow to more efficient laminar flow.31 Limited data suggest that the benefits with heliox therapy are apparent in those with severe exacerbations by improving PEF and reducing the risk of hospitalizations in both children and adults
• #20: onset of action of systemic glucocorticoids is not clinically apparent until as long as six hours after administration. Thus, the beneficial effect is not likely to be observed during the few hours that the patient spends in the medical office or emergency department [42]. Early administration helps to minimize the delay in improvement anticipated with systemic glucocorticoids
• #21: in the absence of vomiting or respiratory failure, oral administration can be used instead of intravenous administration. Oral prednisone and methylprednisolone are rapidly absorbed (peak serum levels achieved at one hour after ingestion) with virtually complete bioavailability, and their efficacy is comparable to intravenous methylprednisolone. Thus, 40 to 60 mg of prednisone administered in a medical office may provide the maximal benefit to be derived from systemic glucocorticoids in acute asthma. Intravenous glucocorticoids should be given to patients who present with impending or actual respiratory arrest, or are intolerant of oral glucocorticoids [2]. The exact dose of glucocorticoids to use for patients with life-threatening asthma is largely based on expert opinion Transition from parenteral to oral administration of glucocorticoids can occur when the patient can tolerate and absorb oral medication. Duration: As a rough guide, most severe attacks that require hospitalization will resolve (with return of lung function to baseline) in 10 to 14 days. The duration of glucocorticoid therapy can be tailored to individual responses. Patients can stop their oral glucocorticoids upon resolution of their symptoms together with recovery of their self-monitored peak flow values (eg, when peak expiratory flow is greater than 70 percent of baseline) as long as they begin or maintain use of inhaled glucocorticoids following discontinuation of oral glucocorticoids. Tapering oral glucocorticoids is not necessary if the duration of glucocorticoid treatment is less than three weeks (a duration too brief to cause adrenal atrophy) and if inhaled glucocorticoids are concomitantly prescribed for ongoing therapy (to prevent relapse
• #22: patients should receive close monitoring, including serial measurements of vital signs, pulse oximetry, and lung function (eg, peak expiratory flow), to assess the response to treatment.
• #24: Discharge planning after an ED visit or hospitalization includes arrangement for follow-up care within one week
• #29: myocardial depression and increased ventricular irritability have been observed with halothane, particularly when used in the presence of acidosis, beta-agonists, and theophylline. full-time anesthesiologist at the bedside Sedatives should not be given because anxiety may be a sign of hypoxemia, which could be worsened by central nervous system depressants.
• #33: Leukotriene receptor antagonists are an established therapy for chronic asthma, but the role of these medications in the management of acute exacerbations is unclear [80-84].
• #34: -MethylxanthinesThese agents are not as potent as the beta agonists when used alone for the treatment of asthma and provide no further bronchodilation beyond that achieved with inhaled beta agonists alone when used in combination (figure 3) [86,87]. In addition, methylxanthines appear to increase the incidence of adverse effects when combined with beta-agonist bronchodilators. For patients who are taking oral theophylline at presentation, we typically continue maintenance oral therapy (and check a theophylline blood level) during hospitalization; but if continued oral intake is not possible, we would very rarely use intravenous therapy with aminophylline or theophylline. 2. because most respiratory infections that trigger an exacerbation of asthma are viral rather than bacterial [3]. In general, we reserve antibiotics for treatment of suspected bacterial sinusitis or pneumonia complicating an asthmatic attack. It is possible that measurement of serum procalcitonin levels will allow identification of a bacterial etiology among patients whose asthma exacerbations are triggered or complicated by a respiratory tract infection 3. increased fluid therapy is not indicated in acute asthma management because the capillary leak from cytokines and increased negative intrathoracic pressures may promote edema in the airways
• #35: In the absence of anticipated intubation difficulty, rapid sequence intubation is preferred. Nasal intubation is not recommended.
• #41: TRIGGERS — Respiratory infections are estimated to trigger approximately 70 percent of chronic obstructive pulmonary disease (COPD) exacerbations. Viral and bacterial infections cause most exacerbations, whereas atypical bacteria are a relatively uncommon cause. The remaining 30 percent are due to environmental pollution, pulmonary embolism, or have an unknown etiology
• #43: complication of severe exacerbation is acute respiratory failure. ABG usually is obtained to assess the severity of an exacerbation. The diagnosis of acute respiratory failure in COPD is made based on an acute drop in PaO2 of 10 to 15 mm Hg or any acute increase in PaCO2 that decreases the serum pH to 7.3 or less. Additional acute clinical manifestations of respiratory failure include restlessness, confusion, tachycardia, diaphoresis, cyanosis, hypotension, irregular breathing, miosis, and unconsciousness.
• #45: the severity of symptoms (based on instruments such as the COPD Assessment Test [CAT] and the modified Medical Research Council Dyspnea Scale), the degree of airflow limitation (based on the FEV1)
• #55: 10 to 14 days can be effective for most patients Therapy with antibiotics generally should be continued for at least 7 to 10 days.