Oral vs Inhaled Corticosteroids Following Emergency Department Discharge of Patients With Acute Asthma

Oral vs Inhaled Corticosteroids Following Emergency Department Discharge of Patients With Acute Asthma

3 Targeted tuberculin testing and treatment of latent tuberculosis infection. Am J Respir Crit Care Med 2000; 161:S221– S247 4 Tulsky JP, White MC, Da...

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3 Targeted tuberculin testing and treatment of latent tuberculosis infection. Am J Respir Crit Care Med 2000; 161:S221– S247 4 Tulsky JP, White MC, Dawson C, et al. Screening for tuberculosis in jail and clinic follow-up after release. Am J Public Health 1998; 88:223–226 5 Nolan CM, Roll L, Goldberg SV, et al. Directly observed isoniazid preventive therapy for released jail inmates. Am J Respir Crit Care Med 1997; 155:583–586 6 Bock NN, Metzger BS, Tapia JR, et al. A tuberculin screening and isoniazid preventive therapy program in an inner-city population. Am J Respir Crit Care Med 1999; 159:295–300 7 Schluger NW, Huberman R, Holzman R, et al. Screening for infection and disease as a tuberculosis control measure among indigents in New York City, 1994 –1997. Int J Tuberc Lung Dis 1999; 3:281–286 8 Malotte CK, Hollingshead JR, Larro M. Incentives vs outreach workers for latent tuberculosis treatment in drug users. Am J Prev Med 2001; 20:103–107 9 Lorvick J, Thompson S, Edlin BR, et al. Incentives and accessibility: a pilot study to promote adherence to TB prophylaxis in a high-risk community. J Urban Health 1999; 76:461– 467 10 Matteelli A, Casalini C, Raviglione MC, et al. Supervised preventive therapy for latent tuberculosis infection in illegal immigrants in Italy. Am J Respir Crit Care Med 2000; 162:1653–1655 11 Halsey NA, Coberly JS, Desormeaux J, et al. Randomised trial of isoniazid versus rifampicin and pyrazinamide for prevention of tuberculosis in HIV-1 infection. Lancet 1998; 351:786 –792 12 Gordin F, Chaisson RE, Matts JP, et al. Rifampin and pyrazinamide vs isoniazid for prevention of tuberculosis in HIV-infected persons: an international randomized trial. JAMA 2000; 283:1445–1450 13 Whalen CC, Johnson JL, Okwera A, et al. A trial of three regimens to prevent tuberculosis in Ugandan adults infected with the human immunodeficiency virus; Uganda-Case Western Reserve University Research Collaboration. N Engl J Med 1997; 337:801– 808 14 Update: fatal and severe liver injuries associated with rifampin and pyrazinamide for latent tuberculosis infection, and revisions in American Thoracic Society/CDC Recommendations–United States, 2001. Am J Respir Crit Care Med 2001; 164:1319 –1320 15 Global Tuberculosis Report 2000. Geneva, Switzerland: World Health Organization, 2000

Oral vs Inhaled Corticosteroids Following Emergency Department Discharge of Patients With Acute Asthma is a lung disease that is characterized by A sthma the presence of increased responsiveness of the airways to various stimuli, reversible expiratory airflow obstruction, and inflammatory changes in the submucosa of the airways. Over the past decade, it has become increasingly recognized that airways inflammation is a major component of asthma.1,2


Due to their potent anti-inflammatory effects, therapy with systemic corticosteroids (oral, IM, or IV) is recommended in all patients presenting to the emergency department with an acute exacerbation of asthma.3,4 Furthermore, a short course of oral corticosteroids following emergency department discharge significantly reduces the number of relapses and the amount of ␤-agonist use without an increase in side effects.5 Despite ⬎ 40 years of experience with the use of corticosteroids in asthma patients, many issues remain unresolved. The optimal dosing schedule of corticosteroids in patients with acute asthma is an issue of much debate, and a precise doseresponse relationship has not been determined.6 –10 While the benefit of therapy with both systemic and inhaled corticosteroids for reducing the number of relapses in patients following an acute attack and in patients with chronic asthma is indisputable, the benefit of corticosteroid therapy in patients with acute asthma is less clear. A meta-analysis preformed by Rodrigo and Rodrigo11 has suggested that the administration of parenteral corticosteroids in addition to inhaled ␤2-agonists in patients with acute asthma on their arrival at the emergency department neither improved airflow obstruction nor reduced the need for hospitalization. These authors suggested that the failure of steroids to influence the early course of patients with acute asthma is due to the fact that it may take up to 24 h for the effects of corticosteroids to become evident. However, in a randomized placebo-controlled study,12 these same authors have demonstrated that extremely high doses of inhaled glucocorticoids together with salbutamol in patients with acute asthma who were treated in the emergency department significantly improved pulmonary function when compared to the use of salbutamol alone, with this difference being evident by 90 min. It has been suggested that locally acting (inhaled) corticosteroids may cause local vasoconstriction and thereby decrease edema formation and plasma exudation.13 In this issue of CHEST, Edmonds and coinvestigators (see page 1798) present a meta-analysis that indicates that there is some evidence that therapy with high-dose inhaled corticosteroids (beclomethasone dipropionate, ⱖ 2,000 ␮g or equivalent per day) may replace therapy with oral corticosteroids following the emergency department discharge of patients who have been treated for an acute asthma exacerbation. However, the confidence intervals for the primary end points were wide, and the authors caution that equivalence cannot be claimed. Is there any reason to abandon the standard CHEST / 121 / 6 / JUNE, 2002


practice of administering a short course of oral corticosteroids after discharge from the emergency department to patients who have experienced an acute exacerbation of asthma? The metaanalysis by Edmonds and coworkers provides no compelling evidence to change this practice. Oral corticosteroids in a dose equivalent of 40 mg prednisone per day are effective, cheap, and safe. This dose does not cause significant hypothalamicpituitary-adrenal suppression when used for ⬍ 7 to 10 days. What role then do inhaled corticosteroids have in the management of patients with acute asthma? Rowe and colleagues14 have demonstrated that the addition of an inhaled corticosteroid (budesonide, 1,600 ␮g/d) to therapy with oral corticosteroids reduced the number of relapses of patients with acute asthma who had been discharged from the emergency department. These data, together with the study by Rodrigo and Rodrigo,12 suggest that patients with an acute asthma exacerbation may benefit from therapy with both systemic and inhaled corticosteroids in the emergency department and after discharge. Paul E. Marik, MD, FCCP Pittsburgh, PA Joseph Varon, MD, FCCP Houston, TX Dr. Marik is Professor of Medicine, University of Pittsburgh Medical Center, and Dr. Varon is Associate Professor of Medicine, Baylor College of Medicine. Correspondence to: Joseph Varon, MD, FCCP, 2219 Dorrington, Houston, TX 77030; e-mail: [email protected]

References 1 Djukanovic R, Roche WR, Wilson JW, et al. Mucosal inflammation in asthma. Am Rev Respir Dis 1990; 142:434 – 457 2 McFadden ER, Hejal RB. The pathobiology of acute asthma. Clin Chest Med 2000; 21:213–224 3 National Institutes of Health. Guidelines for the diagnosis and management of asthma: expert panel 2. Bethesda, MD: National Institutes of Health, National Heart and Lung, and Blood Institute, April 1997 4 Beveridge RC, Grunfeld AF, Hodder RV, et al. Guidelines for the emergency management of asthma in adults: CAEP/ CTS Asthma Advisory Committee; Canadian Association of Emergency Physicians and the Canadian Thoracic Society. Can Med Assoc J 1996; 155:25–37 5 Rowe BH, Spooner CH, Ducharme FM, et al. Corticosteroids for preventing relapse following acute exacerbations of asthma. Cochrane Database Syst Rev 2000; CD000195 6 Emerman CL, Cydulka RK. A randomized comparison of 100-mg vs 500-mg dose of methylprednisolone in the treatment of acute asthma. Chest 1995; 107:1559 –1563 7 McFadden ER. Dosages of corticosteroids in asthma. Am Rev Respir Dis 1993; 147:1306 –1310 8 Manser R, Reid D, Abramson M. Corticosteroids for acute severe asthma in hospitalized patients. Cochrane Database Syst Rev 2001; CD00075320-10000000-00943 1736

9 Bowler SD, Mitchell CA, Armstrong JG. Corticosteroids in acute severe asthma: effectiveness of low doses. Thorax 1992; 47:584 –587 10 Haskell RJ, Wang BM, Hansen JE. A double-blind randomized trial of methylprednisolone in status asthmaticus. Arch Intern Med 1983; 143:1324 –1327 11 Rodrigo G, Rodrigo C. Corticosteroids in the emergency department therapy of acute adult asthma: an evidence-based evaluation. Chest 1999; 116:285–295 12 Rodrigo C, Rodrigo G. Inhaled flunisolide for acute severe asthma. Am J Respir Crit Care Med 1998; 157:698 –703 13 McFadden ER. Inhaled glucocorticoids and acute asthma: therapeutic breakthrough or nonspecific effect? Am J Respir Crit Care Med 1998; 157:677– 678 14 Rowe BH, Bota GW, Fabris L, et al. Inhaled budesonide in addition to oral corticosteroids to prevent asthma relapse following discharge from the emergency department: a randomized controlled trial. JAMA 1999; 281:2119 –2126

Predicting Outcome in Primary Graft Failure effective allograft function is essential I mmediate for successful lung transplantation. Yet, despite

progress in lung preservation and improvements in surgical techniques and perioperative care, primary graft failure (PGF) continues to be a significant cause of early morbidity and mortality.1 The incidence of PGF has been reported to occur in 13 to 35% of lung transplant recipients.2 The clinical spectrum of early graft dysfunction ranges from mild hypoxemia with associated radiographic infiltrates to full-blown ARDS with hemodynamic instability manifesting within 24 h following the transplant procedure. In addition, histopathologic specimens of lung tissue from patients experiencing severe graft dysfunction reveal nonspecific diffuse alveolar damage. Thus, PGF represents a syndrome consisting of elevated pulmonary vascular resistance, pulmonary edema, and hypoxemia. Although a number of expressions have been used to describe this syndrome, the term primary graft failure has evolved to describe post-transplantation ischemia-reperfusion injury.3 Some of the identified risk factors include prolonged graft ischemia time, increasing donor age, recipient diagnosis of pulmonary hypertension, and use of cardiopulmonary bypass.4 – 6 However, another group reported no increase in mortality for patients with prolonged graft ischemia time or recipient diagnosis.7 Thus, the unpredictable nature and increased mortality of PGF have created a need to better understand the mechanism of ischemia-reperfusion lung injury. Ischemia-reperfusion is the major etiologic factor associated with the development of PGF. This phenomenon involves a complex cascade of interactions Editorials