Patient Management: Spirometric Evaluation of Asthmatic Patients in the Oral Surgery Office: A Pilot Study

by Brian J. Freund, BSc., DDS, MD, FRCDC and Marvin Schwartz, BSc., DDS, MSc.


Clinical evaluation of the patient with asthma is of limited usefulness. The addition of simple spirometry can aid in the rapid and accurate assessment of airway impairment that may not be clinically evident. In this pilot study, spirometric testing revealed that 4.5 percent of all patients presenting for wisdom tooth removal under office general anesthetic had moderate airway obstruction that was minimally responsive to salbutamol and yet displayed no clinical symptoms. No correlation was found between reduced responsiveness to salbutamol and smoking, age or sex. A weak inverse relationship was found between reduced salbutamol responsiveness and having a current prescription for a steroid asthma medication.

Asthma is a condition that is recognized in approximately 10 percent of children and adults in our society with up to another 5 percent remaining undiagnosed.1,2 The disease spans the spectrum of severity from mild and easily controlled to severe and potentially life threatening. Some studies suggest that both the rate of asthma associated hospitalization and asthma associated mortality is on the rise despite improvements in monitoring and treatment.3-5 For this reason, the diagnosis and control of the asthmatic patient is of concern within the medical and dental communities.

For the oral surgeon or dental anesthetist who administers deep intravenous sedation or general anesthetic in an office setting, appropriate assessment of the condition is critical in determining the ideal anesthetic approach. Intra-operative bronchospasm is more likely in a poorly controlled asthmatic and is associated with significant adverse outcomes in general anesthesia and deep sedation.6-12 Since bronchospasm is by nature transient, a true pre-anesthetic assessment of asthmatic patients is very difficult. Furthermore, it is clear from the respiratory literature that history and clinical assessment by auscultation are notoriously inaccurate in establishing the potential severity of ventilatory compromise.13,14

Practitioners who perform office anesthesia must establish adequate criteria for pre-anesthetic assessment of all asthmatic patients that will help determine their state of control and therefore their suitability for office general anesthesia or deep sedation. Currently most practitioners will assess asthmatics with a combination of careful history taking and chest auscultation. These techniques however, may not give an adequate indication of ventilatory function or response to therapy.

The purpose of this study was to determine whether simple spirometry would be a useful adjunct in the pre-anesthetic assessment of asthmatic patients in the office setting.


Patient selection was based on the following inclusion criteria:

— patients referred to the office for extraction of wisdom teeth during 2001

— male and female patients between the ages of 14 and 45 (to reduce the likelihood of concomitant COPD or ‘cardiac asthma’)

— a pre-existing physician-diagnosed condition of asthma (including exercise induced)

— a regularly used prescription medication for asthma (bronchodilator and/or inhaled steroid)

— smokers and non-smokers

Exclusion criteria

— upper respiratory tract infection within the past 4 weeks

— diagnosis of COPD or congestive heart failure

— emergency room visit or hospital admission for respiratory problems within the past 4 weeks

Those asthmatics meeting the specified criteria were assessed clinically and subjected to simple spirometry. Spirometric tests included forced vital capacity (FVC) which is a subject’s ability to exhale as hard and fast as possible after fully inflating the lungs, forced expiratory volume (FEV1) which is measured by the spirometer as the volume expired in the first second of FVC and peak expiratory flow (PEF) which is the peak flow rate. Subjective assessments such as wheezing, shortness of breath and cough, as noted by the patient, were recorded. Medications currently prescribed, history of hospital admission for asthma, smoking history and history of upper respiratory tract infections were documented.

Physical examination of the chest by auscultation was carried out for wheezing or other adventitial sounds.

Spirometric testing was done with a Monaghan spirometer in the office at the time of consultation. Measurements of FEV1, FVC and peak flow were taken three times each and the best of each category accepted.14 The results where reported quantitatively as well as a percentage of normal using prediction equations for spirometric tests.15 Patients with FEV1 of less than 80 percent of normal or FEV1/FVC of less than 80 percent were given two puffs of the beta-agonist salbutamol via an aerochamber16 and after 5 minutes, re-tested.

Patients were then grouped as ‘normal’ if their original or post beta-agonist test results were more than 80 percent of predicted values or ‘reduced function’ if their post beta-agonist test results were less than 80 percent of predicted values. Those with normal spirometry on the day of consultation were again tested on the day of surgery to ensure consistency. Those with reduced function after treatment with salbutamol were referred to their physicians for optimization or admitted to hospital for their procedure.


The sample pool consisted of 722 patients who underwent surgery for removal of wisdom teeth under intravenous general anesthetic. Based on the inclusion and exclusion criteria, a cohort of 96 asthmatic subjects was tested by spirometry. None of the asthmatic subjects admitted to any subjective symptoms or had any significant objective findings on chest auscultation during the initial assessment. Of the original 96 asthmatics tested by spirometry, 41 fell below 80 percent of ‘normal’ based on the calculated normal range for each subject. These subjects were treated with salbutamol and re-tested. Thirty-three of these subjects did not respond sufficiently to the beta-agonist to bring their test values into the predicted normal range (> 80 percent). These patients were considered to be poorly responsive and potentially at risk in the event of a bronchospasm. This reduced function (‘at risk’) group represented 4.5 percent of the total pool of surgeries performed (considerably less than the 13 percent of patients with a diagnosis of asthma) but were not identified on history or clinical exam. A summary of the results is presented in Fig. 1 and Table 1.


Asthma is a disorder of the airways characterized by variable airflow limitation and increased airway hyper-responsiveness to a variety of stimuli with paroxysmal or persistent symptoms.13 Clinically, it can be manifested as wheezing, coughing, a feeling of tightness of the chest or shortness of breath.

The stimuli that can cause this reaction can be grouped as triggers and inducers.17 Triggers are stimuli that provoke transient bronchoconstriction. Some of these include cold air, strong smells, exercise, smoke and anxiety. Inducers are stimuli that cause airway inflammation and increase sensitivity to bronchospastic triggers. This latter group includes allergens, viral respiratory infections and some chemicals or drugs.

At least three types of asthmatic responses have been identified. An isolated early response, an early followed by late response and an isolated late response.18 The early response begins within 10 minutes and peaks within 30 minutes, while the late response begins within 3 to 4 hours and peaks several hours thereafter.

The asthmatic responses are a reaction initiated by the above-mentioned triggers and inducers but facilitated by inflammatory mediators. These mediators are released by mast cells and include: histamine, bradykinin, leukotrienes and prostaglandins. The initial response is sudden and manifests as smooth muscle constriction of the airways. It can be effectively and rapidly reversed with adrenergic agents or methylxanthines.19

The late and more chronic response is a cellular mediated sub-mucosal inflammation of the bronchial lining.18 This results in loca
l edema and an increase in mucous secretion. The late response is most effectively overcome with glucocorticoids; but they require time to be efficacious.5 Similarly, the new group of leukotriene receptor antagonists such as montelukast (Singulair Merck Frosst) appears to be effective in moderating the late response.20 It is critical to know whether the asthmatic patient who is symptomatic is suffering from an easily reversible bronchospastic attack or whether there are underlying inflammatory changes.

Two additional, significant factors must be considered by the practitioner administering the general anesthetic. First, the choice of drugs administered is important. Barbiturates are potent histamine releasing agents and can cause significant bronchoconstriction.20 Also, many narcotics induce or aggravate asthma through a variety of mechanisms. Narcotics cause the release of histamine peripherally as well as suppressing respiratory drive and depressing the cough reflex via their central action.21 In the face of an asthmatic attack, this combination of drugs can be lethal. Second, the anxiety that the surgical procedure evokes can potentially trigger an asthmatic reaction.

The prevalence of asthma in the North America is approximately 10 percent for adults and children. At the age of 30 the male to female ratio is approximately equal, while in the childhood years boys are three times as likely to have asthma.22,23 In our study group, the prevalence of asthma was 13 percent. The patients comprising the study group were nearly equal when considering gender (56 percent female and 44 percent male). The mean age of patients in the study group was 19 years with a range of 14 to 45 years.

The difference between the prevalence of asthmatics expected and that found in our study may be due to a bias in the patient population presenting to our clinic. The availability of parenteral anesthesia as well as greater expertise in dealing with compromised patients may lead to more selective referrals to an Oral Surgeon. It is likely that a general practitioner’s patient population would have a lower proportion of asthmatics, more closely approximating the prevalence in the general population. In our experience, general practitioners will sometimes remove third molars for patients who do not require general anesthesia and/or who are not medically compromised.

None of the 96 patients reporting a history of asthma and having a current prescription for asthma medication had objective clinical findings such as wheezing on examination. Despite this, 41 patients showed impairment on spirometric testing in the mild to moderate range.

The tests performed included ‘forced expiratory volume in the first second’ (FEV1), ‘forced vital capacity’ (FVC) as well as ‘peak expiratory flow (PEF). In an obstructive disorder such as asthma or COPD, FEV1 is usually decreased and FVC is decreased or unchanged as compared with the predicted values. The ratio of FEV1 over FVC is also decreased. This is the inverse of restrictive conditions.14,24,25 The measured values are considered indicative of mild impairment when they are in the range of 65 percent to 80 percent of the predicted norm. The impairment is moderate if values are between 50 percent and 65 percent while less than 50 percent of normal is considered severe.26 An FEV1, less than 40 percent of predicted normal, correlates strongly with rapidly worsening gas exchange.27

The group of 41 with spirometric impairment showed comparative values reflecting a reduction in FEV1 of 50 percent to 80 percent of normal. These patients were then treated with salbutamol via an MDI aerosol delivery device prior to re-testing. Of these 41 subjects, 33 (or 4.5 percent of the total surgical pool) showed minimal response to the adrenergic agent. Their spirometric values did not climb into the normal range as would be expected.

The results of this study agree with others that lack of subjective complaints from an asthmatic patient and lack of findings on physical examination do not correlate well with compromised ventilatory function.13,14 Furthermore, nearly one third of the asthmatic group was minimally responsive to salbutamol implying an underlying inflammatory airway condition. This is significant since a bronchospastic event during an anesthetic would be much more difficult to manage effectively for this group.

No correlation was found between reduced responsiveness to salbutamol and smoking, age or sex. A weak inverse relationship was found between reduced salbutamol responsiveness and having a current prescription for a steroid asthma medication. This suggested that subjects in possession of steroid asthma medication were less likely to have inflammatory changes in their airways.

This pilot study does show that spirometry can be performed effectively in an office setting (requiring an average of 3 minutes) and provide information not readily available through history and examination. However, it does not address any potential relationship between spirometrically detected ventilatory impairment and increased risk of anesthesia related adverse outcomes. Such a follow-up study would be useful prior to advocating spirometry as part of the regular pre-anesthetic evaluation of the asthmatic patient.

The spirometer used in this study was an inexpensive Monaghan 403 (Monaghan Medical Corporation, Plattsburgh, NY), which was purchased from a local medical supply company. Many different types of portable machine are available with more sophisticated computerized spirometers costing several thousand dollars and testing upwards of 10 different ventilatory parameters. However, even a rudimentary mechanical peak flow meter can have excellent utility in the dental office.

Dr. Freund is a part-time clinical instructor at the U. of T. He maintains a private practice in Oral & Maxillofacial surgery.

Dr. Schwartz is President of the Great Lakes Society of Oral & Maxillofacial Surgeons. He is on staff at Scarborough Grace Hospital.

Oral Health welcomes this original article.


1.Joseph CL, Foxman B, Leickly FE, Peterson E, Ownby D. Prevalence of possible undiagnosed asthma and associated morbidity among urban schoolchildren. J. Pediatr. 1996; 129(5):735-42.

2.Taylor MR, Holland CV, O’Lorcain P. Asthma and wheeze in schoolchildren. Ir. Med. J. 1996; 89(1):34-5.

3.Mormile F, Chiappini F, Feola G, Ciappi G. Deaths from asthma in Italy (1974-1988): is there a relationship with changing pharmacological approaches? J. Clin. Epidemiol. 1996; 49(12):1459-66.

4.Harju T, Keistinen T, Tuuponen T, Kivela SL. Hospital admissions of asthmatics by age and sex. Allergy 1996; 51(10):693-6.

5.Bain DJ, Munt PW. Optimal use of inhaled steroids in adult asthmatics. Can. J. of CME. 1992; Oct:29-46.

6.Bishop MJ. Cheney FW. Anesthesia for patients with asthma. Low risk but not no risk. Anesthesiology. 85(3):455-6, 1996 Sep.

7.Sheffer AL: NIH Expert panel on the management of asthma. J Allergy Clin Immunol 1991; 88:425-534.

8.Posner KL, Kendall-Gallagher D, Wright IH, Glosten B, Gild WM, Cheney FW Jr: Linking process and outcome of care in a continuous quality improvement program for anesthesia services. Am J Med Qual 1994; 9:129-37.

9.Schnider SM, Papper EM: Anesthesia for the asthmatic patient. Anesthesiology. 1961; 21:886-92.

10.Olsson GL: Bronchospasm during anaesthesia. A computer-aided incidence study of 136,929 patients. Acta Anaesthesiol Scand 1987;31:244-52.

11.Kumeta Y, Hattori A, Mimura M, Kishikawa K, Namiki A: A survey of perioperative bronchospasm in 105 patients with reactive airway disease. Masui J 1995; 44:396-401.

12.Pizov R, Brown RH, Weiss YS, Baranov D, Hennes H, Baker S, Hirshman CA: Wheezing during induction of general anesthesia in patients with and without asthma. Anesthesiology. 1995; 82:1111-6

13.Ernst P, Fitzgerald JM, Spier S. Canadian Asthma Consensus Conference Summary of recommendations. Can. Resp. J. 1996; 3(2):89-100.

14.Levy RD. Pulmonary Function Testing in Clinical Practice. Can. J. of Diag. 1995; May:53-69.

15.Braunwald E, Isselbacher KJ, Pertersdorf RG, Wilson JD, Ma
rtin JB, Fauci AS. Eds Harrison’s Principles Of Internal Medicine 11th edition, McGraw Hill, New York, N.Y., 1987 Appendix 10.

16.Dolovich M, Ruffin R, Corr D, Newhouse MT. Clinical Evaluation of a Simple Demand Inhalation MDI Aerosol Delivery Device. Chest 1983; 84(1):36-41.

17.Dales RE. Asthma Management- Unlocking the Stranglehold. Allergy 1997; 10(3):10-15.

18.Hargreave FE. Late-phase asthmatic responses and airway inflammation. J. of Allergy and Clin. Immun. 1989; 83(2):525-27.

19.Rivington RN, Boulet LP, Cote J, Kreisman H, Small DI, Alexander M, Day A, Harsanyi Z, Darke AC. Efficacy of Uniphyl, Salbutamol, and Their Combination in Asthmatic Patients on High-dose Inhaled Steroids. Am. J. Respir. Crit. Med. 1995; 151(2):325-32.

20.Pizzichini E. Leff JA. Reiss TF. Hendeles L. Boulet LP. Wei LX. Efthimiadis AE. Zhang J. Hargreave FE. Montelukast reduces airway eosinophilic inflammation in asthma: a randomized, controlled trial. European Respiratory Journal. 1999;14(1):12-18.

21.Miller RD. Ed. Anesthesia, Churchill Livingston, New York, N.Y., 1981 pp 451-69.

22.Braunwald E, Isselbacher KJ, Pertersdorf RG, Wilson JD, Martin JB, Fauci AS. Eds Harrison’s Principles Of Internal Medicine 11th edition, McGraw Hill, New York, N.Y., 1987 pp 1060-65.

23.Nelson DA, Johnson CC, Divine GW, Strauchman C, Joseph CL, Ownby DR. Ethnic differences in the prevalence of asthma in middle class children. Ann. Allergy Asthma Immunol. 1997; 78(1):21-6.

24.Pino JM, Garcia-Rio F, Prados C, Alvarez-Sala R, Diaz S, Villasante C, Villamor J. Value of peak expiratory flow in bronchodynamic tests. Allergol. Immunopathol. Madr. 1996; 24(2):54-7.

25.Quadrelli SA, Roncoroni AJ, Porcel G. Analysis of variability in interpretation of spirometric tests. Respiration 1996; 63(3):131-6.

26.American Thoracic Society — Official Statement. Lung Function Testing: Selection of Reference Values And Interpretive Strategies. Am. Rev. Resp. Dis. 1991; 144:1202-18.

27.Wagner PD, Hedenstierna G, Rodriguez-Roisin R. Gas exchange, expiratory flow obstruction and clinical spectrum of asthma. Eur. Respir. J. 1996; 9(6):1278-82.