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Status Asthmaticus Workup

  • Author: Constantine K Saadeh, MD; Chief Editor: Ryland P Byrd, Jr, MD  more...
 
Updated: Dec 17, 2014
 

Approach Considerations

The selection of laboratory studies depends on historical data and patient condition. Tests that should be performed in patients with status asthmaticus include the following:

  • Complete blood count (CBC)
  • Arterial blood gas (ABG)
  • Serum electrolyte levels
  • Serum glucose levels
  • Peak expiratory flow measurement
  • Chest radiographs
  • Electrocardiogram (in older patients)
  • Blood theophylline levels (if indicated)
  • IgE level in selected patients
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Chest Radiography

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

Chest radiography is indicated in patients who have an atypical presentation or in those who do not respond to therapy.

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Complete Blood Count

Obtain a CBC and differential to evaluate for infectious causes (eg, pneumonia, viral infections such as croup), allergic bronchopulmonary aspergillosis, and Churg-Strauss vasculitis. When elevated, serum lactate levels (when obtained early at the onset of status asthmaticus) can correlate with improved lung function.

A CBC and differential may demonstrate an elevated white blood cell count, with or without a shift to the left. The CBC count may also indicate a bacterial infection. However, beta-agonists and corticosteroids may result in demargination of white cells with an increase in the peripheral white cell count.

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Arterial Blood Gas

An ABG value can be obtained to assess the severity of the asthma attack and to substantiate the need for more intensive care. However, the use of blood gas determination is controversial. The information generated by this measurement may be helpful in determining whether or not to intubate a patient with asthma. However, such decisions are usually made on the basis of clinical grounds in a patient who is either in respiratory arrest or impending respiratory arrest.

If a patient with acute asthma has adequate peripheral oxygen saturation, is receiving further therapy, and does not warrant immediate intubation, then the usefulness of blood gas data should be weighed against the potential pain and agitation that running this test may cause in a child. Improvement or deterioration in acute asthma can generally be followed clinically. Indwelling arterial catheters reduce the pain issue and generate highly reliable and reproducible information.

ABG determinations are indicated when the peak expiratory flow (PEF) rate or the forced expiratory volume in 1 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.

The 4 stages of blood gas progression in persons with status asthmaticus are as follows:

  • Stage 1 - Characterized by hyperventilation with a normal partial pressure of oxygen (PO 2)
  • Stage 2 - Characterized by hyperventilation accompanied by hypoxemia (ie, a low partial pressure of carbon dioxide [PCO 2] and low PO 2)
  • Stage 3 - Characterized by the presence of a false-normal PCO 2; 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 an ICU and, probably, intubation with mechanical ventilation.
  • Stage 4 - Characterized by a low PO 2 and a high PCO 2, which occurs with respiratory muscle insufficiency; this is an even more serious sign that mandates intubation and ventilatory support.
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Serum Electrolyte and Serum Glucose Levels

Serum electrolyte measurement, particularly of serum potassium levels, is important. Medications used to treat status asthmaticus may cause hypokalemia. A low pH may result in a transient elevation of potassium.

Serum glucose levels may become elevated from stress, the use of beta-agonist agents, such as epinephrine, and the use of corticosteroids. Because of poor stores, however, hypoglycemia may develop in younger children in response to stress.

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Blood Theophylline Levels

Blood theophylline levels provide an important monitoring component in patients taking this medication (either at home or while hospitalized) and especially in patients who have received a bolus infusion of theophylline followed by continuous intravenous (IV) infusion. The volume of distribution of theophylline is 0.56 mg/L in children and adults. A dose of 1 mg/kg of theophylline raises the serum level by approximately 2 mg/dL.

If the patient has been receiving theophylline at home, obtain a serum theophylline level before therapy. Following a loading dose (if needed), obtain a serum level 30 minutes after the end of the infusion. For serum theophylline steady-state levels, obtain a serum sample at 24-36 hours in children younger than 6 months, at 12-24 hours for those aged 6 months to 12 years, and at 24 hours for children aged 12 years and older.

Factors that decrease theophylline clearance (increase levels) include cimetidine, erythromycin and other macrolide antibiotics, viral infections, cirrhosis, fever, propranolol, and ciprofloxacin.

Factors that increase theophylline clearance (decrease levels) are IV isoproterenol, phenobarbital, smoking, phenytoin, and rifampin.

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Pulmonary Function Testing

PEF, FEV1, and spirometry

The most important and readily available test to evaluate the severity of an asthma attack is the measurement of peak expiratory flow (PEF). PEF monitors are commonly available to patients for use at home and they provide asthmatic patients 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 percentage of predicted value correlates with changes in spirometry values.

Although the forced expiratory volume in one second (FEV1) is also used to monitor the degree of airway obstruction, in patients who are acutely ill, PEF monitoring is more commonly performed.

According to the guidelines of the National Heart, Lung, and Blood Institute/National Asthma Education and Prevention Program,[5] hospitalization is generally indicated when the PEF or FEV1 after treatment is greater than 50%, but less than 70%, of the predicted value. Hospitalization in an ICU is dependent on the severity of symptoms, use of accessory muscles, and ABG results, as well as an FEV1 less than 50%.

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.

Spirometry can be employed 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.

Pulse oximetry

Pulse oximetry provides a continuous evaluation of oxygen saturation, which is vitally important because the primary cause of death in status asthmaticus is hypoxia.

The advantages of pulse oximetry are that pulse oximetry is readily available, it is noninvasive, it provides continuous monitoring, and it is a good indicator of hypoxemia resulting from a ventilation/perfusion mismatch.

The disadvantages of pulse oximetry are that movement artifact can be significant and the modality may provide an erroneous reading when pulsatile flow is inadequate (ie, shock with poor perfusion) or in the presence of anemia.

Other

Findings may be diminished in other pulmonary function tests (eg, maximum expiratory flow rate, mid-maximum expiratory flow rate, forced vital capacity). Functional residual capacity and residual volume increase because of air trapping, However, these tests require the child being in a body plethysmograph, which is impractical in the severely ill child.

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Impulse Oscillometry Testing

In patients with reactive airways, Saadeh et al reported 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.[6]

Patients can be shown the results of forced oscillation testing that occur with peripheral airway inflammation and obstruction. Review the test results with patients and show them the improvement with inhaled corticosteroids and the deterioration when they are not compliant with anti-inflammatory medications. This information may materially enhance patients' awareness of the need for continuing treatment, despite an absence of wheezing.

Technique

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 inspiration and expiration is at its minimum, with increased levels during midinspiration and midexpiration. 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 5-15 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 when 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.

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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.

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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 an 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 an ICU. Parenteral corticosteroids are indicated, as is the 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% of predicted lung function or FEV1 and require intubation and mechanical ventilation.

Patients in stage 4 should be admitted to an ICU. Switching from inhaled beta2-agonists and anticholinergics to metered-dose inhalers (MDIs) via mechanical ventilator tubing is indicated. Parenteral corticosteroids are essential, and theophylline may be added, as with patients in stage 3.

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Contributor Information and Disclosures
Author

Constantine K Saadeh, MD President, Allergy ARTS, LLP; Principal Investigator, Amarillo Center for Clinical Research, Ltd

Constantine K 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, Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Michael R Bye, MD Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Michael Goldman Professor of Internal Medicine, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

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.

Jan Malacara, PA-C Consulting Staff, Allergy ARTS, LLP

Disclosure: Nothing to disclose.

Adam J Schwarz, MD Consulting Staff, Critical Care Division, Pediatric Subspecialty Faculty, Children's Hospital of Orange County

Adam J Schwarz, MD is a member of the following medical societies: American Academy of Pediatrics and Phi Beta Kappa

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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

  2. Vaschetto R, Bellotti E, Turucz E, Gregoretti C, Corte FD, Navalesi P. Inhalational anesthetics in acute severe asthma. Curr Drug Targets. 2009 Sep. 10(9):826-32. [Medline].

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

  4. Vital Signs: Asthma Prevalence, Disease Characteristics, and Self-Management Education --- United States, 2001—2009. CDC MMWR. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6017a4.htm?s_cid=mm6017a4_w. Accessed: August 20, 2014.

  5. [Guideline] National Heart, Lung, and Blood Institute. Managing exacerbations of asthma. National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma. National Guideline Clearinghouse; [Full Text].

  6. 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.

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

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

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

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

  11. Andrews T, McGintee E, Mittal MK, et al. High-dose continuous nebulized levalbuterol for pediatric status asthmaticus: a randomized trial. J Pediatr. 2009 Aug. 155(2):205-10.e1. [Medline].

  12. Best evidence topic reports. Bet 3. Endotracheal adrenaline in intubated patients with asthma. Emerg Med J. 2009 May. 26(5):359. [Medline].

  13. Stephanopoulos DE, Monge R, Schell KH, Wyckoff P, Peterson BM. Continuous intravenous terbutaline for pediatric status asthmaticus. Crit Care Med. 1998 Oct. 26(10):1744-8. [Medline].

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

  15. Chiang VW, Burns JP, Rifai N, Lipshultz SE, Adams MJ, Weiner DL. Cardiac toxicity of intravenous terbutaline for the treatment of severe asthma in children: a prospective assessment. J Pediatr. 2000 Jul. 137(1):73-7. [Medline].

  16. Kalyanaraman M, Bhalala U, Leoncio M. Serial cardiac troponin concentrations as marker of cardiac toxicity in children with status asthmaticus treated with intravenous terbutaline. Pediatr Emerg Care. 2011 Oct. 27(10):933-6. [Medline].

  17. Castro-Rodriguez JA, Rodrigo GJ. Efficacy of inhaled corticosteroids in infants and preschoolers with recurrent wheezing and asthma: a systematic review with meta-analysis. Pediatrics. 2009 Mar. 123(3):e519-25. [Medline].

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

  19. Ream RS, Loftis LL, Albers GM, Becker BA, Lynch RE, Mink RB. Efficacy of IV theophylline in children with severe status asthmaticus. Chest. 2001 May. 119(5):1480-8. [Medline]. [Full Text].

  20. Wheeler DS, Jacobs BR, Kenreigh CA, Bean JA, Hutson TK, Brilli RJ. Theophylline versus terbutaline in treating critically ill children with status asthmaticus: a prospective, randomized, controlled trial. Pediatr Crit Care Med. 2005 Mar. 6(2):142-7. [Medline].

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

  22. Ciarallo L, Brousseau D, Reinert S. Higher-dose intravenous magnesium therapy for children with moderate to severe acute asthma. Arch Pediatr Adolesc Med. 2000 Oct. 154(10):979-83. [Medline].

  23. Glover ML, Machado C, Totapally BR. Magnesium sulfate administered via continuous intravenous infusion in pediatric patients with refractory wheezing. J Crit Care. 2002 Dec. 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. 2000 Dec. 36(6):572-8. [Medline].

  25. Bessmertny O, DiGregorio RV, Cohen H, 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. 2002 Jun. 39(6):585-91. [Medline].

  26. 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. 2005 Oct 19. CD003898. [Medline].

  27. 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. 2003 Dec. 2(4):175-80. [Medline].

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

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

  30. Tobias JD. Inhalational anesthesia: basic pharmacology, end organ effects, and applications in the treatment of status asthmaticus. J Intensive Care Med. 2009 Nov-Dec. 24(6):361-71. [Medline].

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

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

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

  34. Coleman NE, Dalton HJ. Extracorporeal life support for status asthmaticus: the breath of life that's often forgotten. Crit Care. 2009. 13(2):136. [Medline]. [Full Text].

  35. Hebbar KB, Petrillo-Albarano T, Coto-Puckett W, Heard M, Rycus PT, Fortenberry JD. Experience with use of extracorporeal life support for severe refractory status asthmaticus in children. Crit Care. 2009. 13(2):R29. [Medline]. [Full Text].

  36. Noizet-Yverneau O, Leclerc F, Bednarek N, et al. [Noninvasive mechanical ventilation in paediatric intensive care units: which indications in 2010?]. Ann Fr Anesth Reanim. 2010 Mar. 29(3):227-32. [Medline].

  37. 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. 2005 Jan 25. CD004360. [Medline].

  38. 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. 2004 Nov. 43(11):1060-2. [Medline].

  39. 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. 2004 Jul. 32(7):1542-5. [Medline].

  40. 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].

  41. Kim IK, Phrampus E, Venkataraman S, Pitetti R, et al. Helium/oxygen-driven albuterol nebulization in the treatment of children with moderate to severe asthma exacerbations: a randomized, controlled trial. Pediatrics. 2005 Nov. 116(5):1127-33. [Medline].

  42. Kudukis TM, Manthous CA, Schmidt GA, Hall JB, Wylam ME. Inhaled helium-oxygen revisited: effect of inhaled helium-oxygen during the treatment of status asthmaticus in children. J Pediatr. 1997 Feb. 130(2):217-24. [Medline].

  43. Anderson M, Svartengren M, Bylin G, Philipson K, Camner P. Deposition in asthmatics of particles inhaled in air or in helium-oxygen. Am Rev Respir Dis. 1993 Mar. 147(3):524-8. [Medline].

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

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

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

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

  48. 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. 2002 Oct. 34(4):312-9. [Medline].

  49. Gorelick M, Scribano PV, Stevens MW, Schultz T, Shults J. Predicting need for hospitalization in acute pediatric asthma. Pediatr Emerg Care. 2008 Nov. 24(11):735-44. [Medline].

  50. 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. 2003 Aug. 112(2):317-22. [Medline].

  51. Moore PE, Ryckman KK, Williams SM, Patel N, Summar ML, Sheller JR. Genetic variants of GSNOR and ADRB2 influence response to albuterol in African-American children with severe asthma. Pediatr Pulmonol. 2009 Jul. 44(7):649-54. [Medline].

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

  53. 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. 2004 Apr 1. 169(7):784-6. [Medline].

 
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Figure depicting antigen presentation by the dendritic cell, with the lymphocyte and cytokine response leading to airway inflammation and asthma symptoms.
 
 
 
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