eMedicine Specialties > Pulmonology > Obstructive Airways Diseases

Status Asthmaticus: Differential Diagnoses & Workup

Author: Constantine Saadeh, MD, Chief, Department of Internal Medicine, Northwest Texas Hospital; President, Allergy ARTS, LLP; Clinical Professor, Departments of Internal Medicine, Pediatrics, Microbiology, and Immunology, Texas Tech Health Science Center
Contributor Information and Disclosures

Updated: Jun 4, 2009

Differential Diagnoses

Pulmonary Hypertension, Primary

Other Problems to Be Considered

Congestive heart failure
Croup
Stridor
Upper airway obstruction
Orthopnea

Workup

Laboratory Studies

  • Obtain a CBC count and differential to evaluate for infectious causes (eg, pneumonia, viral infections such as croup), allergic bronchopulmonary aspergillosis, and Churg-Strauss vasculitis. As noted earlier, when elevated, serum lactate levels (when obtained early at the onset of status asthmaticus) can correlate with improved lung function.
  • Obtain an arterial blood gas (ABG) value to assess the severity of the asthma attack and to substantiate the need for more intensive care. ABG determinations are indicated when the peak expiratory flow (PEF) rate or forced expiratory volume in one second (FEV1) is less than or equal to 30% of the predicted value or when the patient shows evidence of fatigue or progressive airway obstruction despite treatment. ABG values are important to help determine the severity of the asthma attack. The 4 stages of blood gas progression in persons with status asthmaticus are as follows:
    • The first stage is characterized by hyperventilation with a normal partial pressure of oxygen (PO2).
    • The second stage is characterized by hyperventilation accompanied by hypoxemia (ie, a low partial pressure of carbon dioxide [PCO2] and low PO2).
    • The third stage is characterized by the presence of a false-normal PCO2; ventilation has decreased from the hyperventilation present in the second stage. This is an extremely serious sign of respiratory muscle fatigue that signals the need for more intensive medical care, such as admission to the ICU and, probably, intubation with mechanical ventilation.
    • The last stage is characterized by a low PO2 and a high PCO2, which occurs with respiratory muscle insufficiency. This is an even more serious sign that mandates intubation and ventilatory support.

Imaging Studies

  • Obtain a chest radiograph to evaluate for pneumonia, pneumothorax, congestive heart failure, and signs of chronic obstructive pulmonary disease, which would complicate the patient's response to treatment or reduce the patient's baseline spirometry values.

Other Tests

  • The most important and readily available test to evaluate the severity of an asthma attack is the measurement of PEF. PEF monitors are commonly available to patients for use at home, and they provide patients with asthma with a guideline for changes in lung function as they relate to changes in symptoms. In most patients with asthma, a decrease in peak flow as a percent of predicted value correlates with changes in spirometry values.
  • According to the guidelines of the National Heart, Lung, and Blood Institute/National Asthma Education and Prevention Program,4 severe asthma exacerbation is usually associated with a PEF rate or FEV1 of less than 50% of the predicted value. Also, hospitalization is generally indicated when the PEF or FEV1 after treatment is greater than 50% of the predicted value but less than 70% of the predicted value. Hospitalization in the ICU is indicated when the PEF value or FEV1 is less than 50% of predicted.
  • A drop in the FEV1 to less than 25% of the predicted value indicates a severe airway obstruction.
  • A patient with an FEV1 of greater than 60% of the predicted value may be treated in an outpatient setting, depending on the clinical situation. However, if the patient's FEV1 or PEF rate drops to less than 50% of predicted, admission to the hospital is recommended.
  • Pulse oximetry and spirometry values should be used to monitor the progression of asthma. As the results indicate improvement, treatment may be adjusted accordingly.
    • If a portable spirometry unit is not available, a PEF rate of 20% or less of the predicted value (ie, usually <100 L/min) suggests severe airflow obstruction and impending respiratory failure.
    • Spahn et al5 demonstrate that the majority of children with asthma have normal spirometry results. According to Goldman et al6 and Marotta et al,7 the assessment of children with asthma is enhanced by the use of forced oscillation to measure respiratory resistance and reactance. As reported by Ducharme and Davis8,9 in 1997 and 1998, forced oscillation can be performed in the emergency department, and the results are reproducible.
    • According to various articles, impulse oscillometry resistance and reactance magnitudes have been shown to be more sensitive than FEV1 to the daily variability in adolescents with asthma (Goldman et al6 ), to the response to acute bronchodilation (Marotta et al7 and Skloot et al10 ), and to the response to exposure to toxic inhalants in persons with reactive airways (Skloot et al10 ). In patients with reactive airways, Saadeh et al11 report that impulse oscillometry detects false-negative spirometry values and provides a sensitive index of asthma control over the spectrum of mild-to-severe persistent asthma.

Procedures

  • With forced oscillation testing using the impulse oscillometry system (IOS), patients are tested for 30-40 seconds during quiet breathing, without forced respiratory efforts. A small loudspeaker pushes "burps" of air into patients and pulls them back from the mouthpiece 5 times each second.
    • The measurement of airflow resistance during normal breathing requires no maximal forced expiratory efforts and does not subject patients to bronchoprovocation from forced expiration. Resistance is distributed between large airways and smaller more peripheral airways, with distinct patterns attributable to each.
    • Bronchospasms and increased large airway resistance appear as increases in resistance at higher (25-35 cycles/s) components of oscillation frequency. Additionally, a pattern of increased resistance with increasing airflow is typical of a large airway bronchospasm. In such patients, resistance at the beginning and end of both inspiration and expiration is at its minimum, with increased levels during mid inspiration and mid expiration. In such patients, a deep inspiration is often followed by reflex bronchoconstriction and increased resistance for 30 seconds or more, signaling increased airway reactivity.
    • Peripheral airway inflammation and obstruction are signaled by increased resistance at low (5 cycles/s) oscillation frequencies that are decreased at higher oscillation frequencies (15 or 20 cycles/s). In association with the fall in resistance from 5 to 15 cycles per second, the magnitude of respiratory reactance in peripheral airway inflammation and obstruction increases.
    • Careful attention must be paid to whether patients have their lips fully closed around the mouthpiece. Patients with acute dyspnea may feel constrained breathing through a mouthpiece and may reflexively open their mouths to increase airflow during late inspiration. This is analogous to flaring alae nasi with dyspnea and results in characteristic airflow leak patterns. This causes underestimation of true airflow resistance. IOS tests with such airflow leak patterns must be repeated after reassuring the patient and ensuring closure of the lips around the mouthpiece.

Histologic Findings

Autopsy results from patients who died from status asthmaticus of brief duration (ie, developed within hours) show neutrophilic infiltration of the airways. In contrast, results from patients who developed status asthmaticus over days show eosinophilic infiltration. Autopsy results also show extensive mucus production and severe bronchial smooth muscle hypertrophy. However, the predominant response, based on results from bronchoalveolar lavage studies, is eosinophilic in nature. The eosinophil itself can lead to epithelial destruction through its own degrading products (eg, cationic proteins). This destruction can result in inflammation and, later, a neutrophilic response.

Staging

The 4 stages of status asthmaticus are based on ABG progressions in status asthma.

Patients in stage 1 or 2 may be admitted to the hospital, depending on the severity of their dyspnea, their ability to use accessory muscles, and their PEF values or FEV1 after treatment (>50% but <70% of predicted values).

Patients with ABG determinations characteristic of stages 3 and 4 require admission to the ICU. The PEF value or FEV1 is less than 50% of the predicted value after treatment.

  • Stage 1
    • Patients are not hypoxemic, but they are hyperventilating and have a normal PO2.
    • Data suggest that to possibly facilitate hospital discharge, these patients may benefit from ipratropium treatment via a handheld nebulizer in the emergency setting as an adjunct to beta-agonists.
  • Stage 2
    • This stage is similar to stage 1, but patients are hyperventilating and hypoxemic.
    • Such patients may still be discharged from the emergency department, depending on their response to bronchodilator treatment, but will require systemic corticosteroids.
  • Stage 3
    • These patients are generally ill and have a normal PCO2 due to respiratory muscle fatigue. Their PCO2 is considered a false-normal value and is a very serious sign of fatigue that signals a need for expanded care. This is generally an indication for elective intubation and mechanical ventilation, and these patients require admission to the ICU.
    • Parenteral corticosteroids are indicated, as is continued aggressive use of an inhaled beta2-adrenergic bronchodilator.
    • These patients may benefit from theophylline.
  • Stage 4
    • This is a very serious stage in which the PO2 is low and the PCO2 is high, signifying respiratory failure.
    • These patients have less than 20% lung function or FEV1 and require intubation and mechanical ventilation.
    • Patients in stage 4 should be admitted to the ICU. Switching from inhaled beta-2 agonists and anticholinergics to metered-dose inhalers (MDIs) via mechanical ventilator tubing is indicated.
    • Parenteral steroids are essential, and theophylline may be added, as with patients in stage 3.

More on Status Asthmaticus

Overview: Status Asthmaticus
Differential Diagnoses & Workup: Status Asthmaticus
Treatment & Medication: Status Asthmaticus
Follow-up: Status Asthmaticus
References
Further Reading

References

  1. Han P, Cole RP. Evolving differences in the presentation of severe asthma requiring intensive care unit admission. Respiration. Sep-Oct 2004;71(5):458-62. [Medline].

  2. Hanania NA, David-Wang A, Kesten S, Chapman KR. Factors associated with emergency department dependence of patients with asthma. Chest. Feb 1997;111(2):290-5. [Medline].

  3. Rodrigo GJ, Rodrigo C. Elevated plasma lactate level associated with high dose inhaled albuterol therapy in acute severe asthma. Emerg Med J. Jun 2005;22(6):404-8. [Medline].

  4. {Guideline} National Heart, Lung, and Blood Institute. Managing exacerbations of asthma. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma. National Guideline Clearinghouse. Available at http://www.guideline.gov/summary/summary.aspx?doc_id=11678&nbr=006027&string=asthma. Accessed August 2008.

  5. Spahn JD, Cherniack R, Paull K, Gelfand EW. Is forced expiratory volume in one second the best measure of severity in childhood asthma?. Am J Respir Crit Care Med. Apr 1 2004;169(7):784-6. [Medline].

  6. Goldman MD, Carter R, Klein R, Fritz G, Carter B, Pachucki P. Within- and between-day variability of respiratory impedance, using impulse oscillometry in adolescent asthmatics. Pediatr Pulmonol. Oct 2002;34(4):312-9. [Medline].

  7. Marotta A, Klinnert MD, Price MR, Larsen GL, Liu AH. Impulse oscillometry provides an effective measure of lung dysfunction in 4-year-old children at risk for persistent asthma. J Allergy Clin Immunol. Aug 2003;112(2):317-22. [Medline].

  8. Ducharme FM, Davis GM. Measurement of respiratory resistance in the emergency department: feasibility in young children with acute asthma. Chest. Jun 1997;111(6):1519-25. [Medline].

  9. Ducharme FM, Davis GM. Respiratory resistance in the emergency department: a reproducible and responsive measure of asthma severity. Chest. Jun 1998;113(6):1566-72. [Medline].

  10. Skloot G, Goldman M, Fischler D, Goldman C, Schechter C, Levin S, et al. Respiratory symptoms and physiologic assessment of ironworkers at the World Trade Center disaster site. Chest. Apr 2004;125(4):1248-55. [Medline].

  11. Saadeh CK, Goldman MD, Gaylor PB. Forced oscillation using impulse oscillometry (IOS) detects false negative spirometry in symptomatic patients with reactive airways. J Allergy Clin Immunol. 2003;111:S136.

  12. Newman LJ, Richards W, Church JA. Isoetharine-isoproterenol: a comparison of effects in childhood status asthmaticus. Ann Allergy. Apr 1982;48(4):230-2. [Medline].

  13. Haskell RJ, Wong BM, Hansen JE. A double-blind, randomized clinical trial of methylprednisolone in status asthmaticus. Arch Intern Med. Jul 1983;143(7):1324-7. [Medline].

  14. Press S, Lipkind RS. A treatment protocol of the acute asthma patient in a pediatric emergency department. Clin Pediatr (Phila). Oct 1991;30(10):573-7. [Medline].

  15. Heshmati F, Zeinali MB, Noroozinia H, Abbacivash R, Mahoori A. Use of ketamine in severe status asthmaticus in intensive care unit. Iran J Allergy Asthma Immunol. Dec 2003;2(4):175-80. [Medline].

  16. Elliot S, Berridge JC, Mallick A. Use of the AnaConDa anaesthetic delivery system in ICU. Anaesthesia. Jul 2007;62(7):752-3. [Medline].

  17. Burburan SM, Xisto DG, Rocco PR. Anaesthetic management in asthma. Minerva Anestesiol. Jun 2007;73(6):357-65. [Medline].

  18. Rishani R, El-Khatib M, Mroueh S. Treatment of severe status asthmaticus with nitric oxide. Pediatr Pulmonol. Dec 1999;28(6):451-3. [Medline].

  19. Mroueh S. Inhaled nitric oxide for acute asthma. J Pediatr. Jul 2006;149(1):145; author reply 145. [Medline].

  20. Mikkelsen ME, Pugh ME, Hansen-Flaschen JH, Woo YJ, Sager JS. Emergency extracorporeal life support for asphyxic status asthmaticus. Respir Care. Nov 2007;52(11):1525-9. [Medline].

  21. [Guideline] Dombrowski MP, Schatz M; ACOG Committee on Practice Bulletins-Obstetrics. ACOG practice bulletin: clinical management guidelines for obstetrician-gynecologists number 90, February 2008: asthma in pregnancy. Obstet Gynecol. Feb 2008;111(2 Pt 1):457-64. [Medline].

  22. Schultz TE. Sevoflurane administration in status asthmaticus: a case report. AANA J. Feb 2005;73(1):35-6. [Medline].

  23. Glover ML, Machado C, Totapally BR. Magnesium sulfate administered via continuous intravenous infusion in pediatric patients with refractory wheezing. J Crit Care. Dec 2002;17(4):255-8. [Medline].

  24. Scarfone RJ, Loiselle JM, Joffe MD, Mull CC, Stiller S, Thompson K, et al. A randomized trial of magnesium in the emergency department treatment of children with asthma. Ann Emerg Med. Dec 2000;36(6):572-8. [Medline].

  25. Bessmertny O, DiGregorio RV, Cohen H, Becker E, Looney D, Golden J, et al. A randomized clinical trial of nebulized magnesium sulfate in addition to albuterol in the treatment of acute mild-to-moderate asthma exacerbations in adults. Ann Emerg Med. Jun 2002;39(6):585-91. [Medline].

  26. [Best Evidence] Blitz M, Blitz S, Beasely R, Diner BM, Hughes R, Knopp JA, et al. Inhaled magnesium sulfate in the treatment of acute asthma. Cochrane Database Syst Rev. Oct 19 2005;CD003898. [Medline].

  27. Ram FS, Wellington S, Rowe BH, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev. Jan 25 2005;CD004360. [Medline].

  28. Ueda T, Tabuena R, Matsumoto H, Takemura M, Niimi A, Chin K, et al. Successful weaning using noninvasive positive pressure ventilation in a patient with status asthmaticus. Intern Med. Nov 2004;43(11):1060-2. [Medline].

  29. Leatherman JW, McArthur C, Shapiro RS. Effect of prolongation of expiratory time on dynamic hyperinflation in mechanically ventilated patients with severe asthma. Crit Care Med. Jul 2004;32(7):1542-5. [Medline].

  30. Shiue ST, Gluck EH. The use of helium-oxygen mixtures in the support of patients with status asthmaticus and respiratory acidosis. J Asthma. 1989;26(3):177-80. [Medline].

  31. Fuller CG, Schoettler JJ, Gilsanz V, Nelson MD Jr, Church JA, Richards W. Sinusitis in status asthmaticus. Clin Pediatr (Phila). Dec 1994;33(12):712-9. [Medline].

  32. Sacha RF, Tremblay NF, Jacobs RL. Chronic cough, sinusitis, and hyperreactive airways in children: an often overlooked association. Ann Allergy. Mar 1985;54(3):195-8. [Medline].

  33. Oguzulgen IK, Turktas H, Mullaoglu S, Ozkan S. What can predict the exacerbation severity in asthma?. Allergy Asthma Proc. May-Jun 2007;28(3):344-7. [Medline].

  34. Ciccolella DE, Brennan K, Kelsen SG, Criner GJ. Dose-response characteristics of nebulized albuterol in the treatment of acutely ill, hospitalized asthmatics. J Asthma. Sep 1999;36(6):539-46. [Medline].

  35. Mathison DA. Asthma in Adults, Evaluation and Management. In: Middleton E Jr, Reed CE, Ellis EF, Adkinson NF Jr, Yunginger JW, Busse WW, eds. Allergy Principles & Practice. 5th ed. St. Louis, Mo: Mosby-Year Book; 1998:901-20.

  36. Patterson R, Grammar LC, Greenberger P, eds. Status Asthmaticus. In: Allergic Diseases: Diagnosis and Management. 5th ed. Philadelphia, Pa: Lippincott-Raven; 1997:529-42.

  37. Richards W. Hospitalization of children with status asthmaticus: a review. Pediatrics. Jul 1989;84(1):111-8. [Medline].

  38. Schwartz HJ, Thompson JS, Sher TH, Ross RJ. Occult sinus abnormalities in the asthmatic patient. Arch Intern Med. Dec 1987;147(12):2194-6. [Medline].

  39. Sthoeger ZM, Eliraz A, Asher I, Berkman N, Elbirt D. The beneficial effects of Xolair (omalizumab) as add-on therapy in patients with severe persistent asthma who are inadequately controlled despite best available treatment (GINA 2002 step IV)--the Israeli arm of the INNOVATE study. Isr Med Assoc J. Jun 2007;9(6):472-5. [Medline].

Further Reading

Asthma Resources from Medscape and eMedicine

Asthma News and Articles

Asthma Clinical Reference

Asthma CME

Keywords

status asthmaticus, asthma, asthma treatment, asthma children, acute asthma, hyperactive airway disease, asthma, asthma emergency, allergen exposure, respiratory tract infection, pollen, mold, animal dander, house dust mites, wheezing, chest tightness, progressive shortness of breath, dry cough, viral respiratory illness, underuse of anti-inflammatory therapy, allergic bronchopulmonary aspergillosis, Churg-Strauss vasculitis, beta-agonists, theophylline, bronchoconstrictive response, broncho-constrictive response, peripheral airway inflammation, bronchodilator therapy

Contributor Information and Disclosures

Author

Constantine Saadeh, MD, Chief, Department of Internal Medicine, Northwest Texas Hospital; President, Allergy ARTS, LLP; Clinical Professor, Departments of Internal Medicine, Pediatrics, Microbiology, and Immunology, Texas Tech Health Science Center
Constantine Saadeh, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Rheumatology, American Medical Association, Southern Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Helen M Hollingsworth, MD, Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center
Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.