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(Chest. 2001;120:1058-1061.)
© 2001 American College of Chest Physicians

Emergency Department Visits in Asthma

Should All Be Prevented?

Valentin Popa, MD, FCCP (Sacramento, CA ).

Dr. Popa is from the Department of Medicine, University of California at Davis.

Correspondence to: Valentin Popa, MD, FCCP, Department of Medicine, University of California at Davis, 8100 Timberlake Way, Sacramento, CA 95823

Each year, despite a wide and efficient array of asthma treatments, patients with asthma make approximately 1.8 million visits to emergency departments (EDs),1 with African Americans accounting for five times more visits than whites.2 Compared to other countries, the mortality rate from asthma in the United States is smaller and has increased very little in the past 25 years.3 Although the rate is approximately 100 times less than the mortality rate due to COPD,4 it remains substantial, close to 2 deaths per 100,000 population.3 Obviously, we should try to prevent any death from asthma. Should we also try to prevent all ED visits for severe asthma?

Identifying the risk factors for an ED visit may help prevent this costly and inconvenient form of health care. In this issue (see page 1129), Ford et al report that low-income African Americans in Harlem make repeated visits to ED because their asthma is very severe. In a population with different racial and economic characteristics, Dales et al5 have shown that the predictors of frequent visits to EDs are, indeed, those indicative of severe asthma. Repeated ED visits suggests undertreatment rather than poor health-care access, as had been postulated before,6 since the patients making these repeat ED visits see their primary-care physician more often than those with single ED visits. The undertreatment is perceived as insufficient physician involvement, because 69% of patients visiting the ED of Harlem Hospital Center, despite having a primary-care physician, viewed the ED as their preferred source of care. The lack of steroid medication defines undertreatment. This lack can be absolute5 or relative, insufficient for the degree of asthma severity.7 8

To prevent most ED visits, we should apply a more aggressive treatment in patients with severe asthma than indicated in the Guidelines for Diagnosis and Treatment for Asthma.9 Also, we should improve self-care and bring together patients, physicians and nonphysicians involved in education.

Unsatisfactory self-care includes a lack of proper self-administration of drugs, panic in case of asthma attacks,10 inability to act according to the asthma knowledge, lack of a written asthma action plan, and various psychosocial attitudes interfering with avoidance coping measures.8

The comprehensive Guidelines for the Diagnosis and Treatment of Asthma, which were published by an expert panel,9 are essential reading for physicians involved in asthma care. Some have objected to their complexity10 or to the fact that the classification of asthma severity is not evidence-based.11 12 Because of their complexity, the primary-care physician may need to discuss with an allergist or pulmonologist some of the recommendations, in particular those pertaining to severe asthma.

At times, the classification of asthma severity in four steps9 seems disconcerting. At each step, there are characteristic clinical and physiological features that are assumed to occur simultaneously, but a footnote indicates that they may also overlap. I just saw a patient with continuous symptoms (severe persistent asthma) requiring daily use of a short-acting inhaled ß2-agonist and limitation of his activity (moderate persistent asthma), but with a peak expiratory flow of 80% of predicted (mild persistent asthma). According to the guidelines, the highest step defines the severity, in this case, the severe persistent step. However, the step would remain the same if all, not only part, of the manifestations would fit the criteria of severe persistent asthma. Most importantly for patients with severe asthma, the response to treatment is not used to stage severity of the disease. In the patient mentioned above, inhaled steroids could be started or doubled if already prescribed, but if the patient was already taking these drugs, he should probably go directly to the ED and be hospitalized. Not surprisingly, two studies, one carried out in a selected asthmatic population (Ford et al) and the other in a general asthmatic population,13 could not validate the parallelism between symptoms or between symptoms and FEV1 changes.13 Thus, the same step may be associated with a different constellation and intensity of symptoms, as well as different response to treatment (from none to some); it may require different new recommendations. Equivalent changes in peak expiratory flow and FEV1, which are tests of different physiologic sensitivity, could indicate different levels of severity. Also, the presence of wheezing and dyspnea at rest, symptoms with the highest positive predictive value for asthma,14 may have a different connotation in different patients. For instance, the attacks may appear spontaneously, without an obvious removable trigger, or may follow exposure to an avoidable allergic or nonallergic trigger. Their treatments should be different, not the standard treatment of any severe, persistent asthma.

The compact presentation of the guidelines did not allow the panel to point out the three key goals in the prevention and treatment of severe asthma exacerbations: the improvement should be substantial, rapid, and monitored. This means therapy with more short-acting ß2-agonists than had been inhaled before and, unless the exacerbation is mild, administration of systemic steroids. The mode of administration of the former should be by jet nebulization because equipotent doses delivered via metered-dose inhaler are inconvenient for the patient during moderate and severe exacerbations. Jet nebulization is recommended on page 38 of the guidelines, in the section on "home management of asthma exacerbations" on page 60, but not on page 62. The dose and dosing interval are not addressed. The recommended dose of systemic steroids needs some tailoring since it depends on many factors (eg, past exacerbations or baseline treatment). In moderate-to-severe exacerbations, the 2 mg/kg dose may work faster and more efficiently than the commonly recommended dose of 60 mg/day. At these steps, starting with high doses of inhaled steroids and then stepping down works faster than the step-up strategy. This approach is recommended by the guidelines (page 44), but the doses listed are half the equivalent of the 1,600 µg budesonide dose recently found to be effective15 in patients with poorly controlled asthma. It is also surprising that in patients with severe asthma, the guidelines recommend therapy with high-dose inhaled steroids (> 600 µg budesonide) but not systemic steroids.

We may prevent numerous ED visits, but many asthma specialists,16 17 including myself, feel that even the best treatment may leave some patients with poorly controlled asthma. Different asthma phenotypes with different types of inflammation18 19 might respond differently to steroids. This poorly controlled subset and two additional subsets, one presenting with severe exacerbations and fragile general health and the other with a history of near-fatal asthma attacks (ie, high CO2 and/or intubation), should be directed to the ED.

Fatal and near-fatal exacerbations of asthma are frequently, but not invariably, associated with recent severe asthma, poor medical compliance, previous hospital admissions, and eventual intubation.20 21 Importantly, fatal or near-fatal asthma may have a rapid or a slow onset.20 21 These risk factors need to be promptly recognized. For the following reasons, the treatment needs to start immediately (particularly in rapid-onset exacerbations), aggressively, and in the ED: (1) death in asthma is due to asphyxia, and O2 treatment, closely monitored, may be life-saving; (2) the administration of ß2-adrenergic drugs by continuous jet nebulization requires ECG monitoring in many hospitals; (3) the blood concentration of steroids peaks earlier if given IV rather than orally; and (4) the patients with severe asthma are not only unstable from a respiratory standpoint but also tend to have many comorbid conditions.

These examples show that even detailed guidelines cannot cover all situations and need clarification by a specialist. The current trend is to exclude the primary-care physician from the hospital and to replace him/her with a hospitalist, brought in primarily to discharge patients as fast as possible. This will leave the primary-care physician with mostly noninteractive sources of information (eg, books, articles, and guidelines).

In addressing asthma education, the guidelines advance an idealized proposal based on team effort with the principal clinician introducing the key educational message. However, today, at least in some parts of this country, patient education is assigned to registered nurses and respiratory therapists. They may not share with the treating physician the content of their message and inadvertently may contradict the physician’s recommendations. I will always remember Max Samter, the renowned allergist and editor of clinical immunology textbooks, who in the early 1970s periodically organized educational sessions at his home in Evanston, IL. I am sure that his patients, many of them from Chicago’s west side, where the University of Illinois Hospital is located, would have never considered the ED as their main source of care.

Identifying areas that can be improved reflects an optimistic attitude. Today, we have the means to treat severe asthma, safely, quickly, and selectively, and we also can enjoy what we are doing. To instill a perennial value in this attitude, I will borrow two Latin precepts and paraphrase another: primum nil nocere (first do not harm), qui celer dat bis dat (who gives fast gives twice), and qui amat artem amat asthmam (who loves the [medical] art loves asthma).

References

  1. Weiss, KB, Gergen, PJ, Hodgson, TA (1992) An economic evaluation of asthma in the United States. N Engl J Med 326,863-866
  2. Burt, CW, Knapp, DE (1996) Ambulatory care visits for asthma: United States, 1993–1994. Adv Data 277,1
  3. Beasley, CRW, Pearce, NE, Crane, J (1998) Worldwide trends in asthma mortality during the twentieth century. Sheffer, AL eds. Fatal asthma ,31-41 Marcel Dekker (New York, NY).
  4. Higgins, MW, Thom, T (1989) Incidence, prevalence and mortality: intra- and intercountry differences. Hensley, MJ Saunders, NA eds. Clinical epidemiology of chronic obstructive pulmonary disease ,23-39 Marcel Dekker (New York, NY).
  5. Dales, RE, Schweitzer, I, Kerr, P, et al (1995) Risk factors for recurrent emergency visits for asthma. Thorax 50,520-524[Abstract]
  6. Targonski, PV, Persky, VW, Orris, P, et al (1994) Trends in asthma mortality among African Americans and Whites in Chicago, 1968 through 1991. Am J Public Health 84,1830-1833[Abstract/Free Full Text]
  7. Turner, MO, Noertjojo, K, Vedal, S, et al (1998) Risk factors for near-fatal asthma: a case control study in hospitalized patients with asthma. Am J Respir Crit Care Med 157,1804-1809[Abstract/Free Full Text]
  8. Adams RJ, Smith BJ, Ruffin RE. Factors associated with hospital admissions and repeat emergency department visits for adults with asthma. Thorax 200; 55:566–573
  9. National Heart, Lung, and Blood Institute. Expert panel report 2: guidelines for the management of asthma. Bethesda, MD: National Institutes of Health, April 1997; Publication No. 97-4051
  10. Sibbald, B (1988) Patient self care in asthma. Thorax 44,97-101[Abstract]
  11. Kemp, JP (2000) Guidelines update: where do the new therapies fit in the management of asthma? Drugs 59(suppl),23-28
  12. Bousquet, J (2000) Global initiative for asthma (GINA) and its objectives. Clin Exp Allergy 30(suppl),2-5
  13. Liard, R, Laeynaert, B, Zureik, M, et al (2000) Using global initiative for asthma guidelines to assess asthma severity in populations. Eur Respir J 16,615-620[Abstract]
  14. Sistek, D, Tschopp, J-M, Schindler, C, et al (2001) Clinical diagnosis of current asthma: predictive value of respiratory symptoms in the SAPALDIA study. Eur Respir J 17,214-219[Abstract/Free Full Text]
  15. Reddel, HK, Jenkins, CR, Marks, GB, et al (2000) Optimal asthma control, starting with high doses of inhaled budesonide. Eur Respir J 15,226-235
  16. Bousqet, J (2000) Discussion. Clin Exp Allergy 30(suppl),9
  17. Holgate, S (2000) Discussion. Clin Exp Allergy 30(suppl),9
  18. Wenzel, S, Schwatz, L, Langmack, E, et al (1999) Evidence that severe asthma can be divided pathologically into two inflammatory subtypes with distinct physiologic and clinical characteristics. Am J Respir Crit Care Med 160,1001-1008[Abstract/Free Full Text]
  19. Payne, DNR, Wilson, NM, James, A, et al (2001) Evidence for different subgroups of difficult asthma in children. Thorax 56,345-350[Abstract/Free Full Text]
  20. Fraser, PM, Speizer, FE, Waters, SDM, et al (1971) The circumstances preceding death from asthma in young people in 1968 to 1969. Br J Dis Chest 65,71-84[Medline]
  21. Woolcock, AJ (1998) Natural history of fatal asthma. Sheffer, AL eds. Fatal asthma ,31-41 Marcel Dekker (New York, NY).



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