Summer 2015 Diagnostics Section Bulletin

Spring 2015 Diagnostics Section Bulletin

Editor
Jeffrey M. Haynes, RRT, RPFT

Pulmonary Function Laboratory
St. Joseph Hospital
Nashua, NH
Work Email: jhaynes@sjhnh.org
Home Email: jhaynes3@comcast.net

Chair:
Katrina Hynes, BAS, RRT, CPFT
Assistant Supervisor
Special Pulmonary Evaluation Laboratory
Mayo Clinic
Rochester, MN 55905
(507) 284-4545
Hynes.Katrina@mayo.edu

Former Chair
Matthew J O’Brien, RRT, RPFT
Pulmonary Diagnostic Lab
University of Wisconsin Hospital and Clinics
600 Highland Ave Room E5/520
Madison, WI 53792-5772
(608) 263-7001
Fax: (608) 263-7002
mobrien@uwhealth.org


Technologist’s Notes
Spirometer Calibration: It’s Not Just for Breakfast Anymore

Jeffrey M. Haynes, RRT, RPFT

Every morning in PFT labs across the world, the day begins with a calibration check of the spirometer. A 3-liter syringe creates bidirectional flow at varying speeds with an expected reading of 3L +/- 3.5%.

Once achieved, the calibration syringe is typically put away for the rest of the day. This practice assumes that technical gremlins only occur during the overnight hours. It is more probable, however, that spirometry accuracy may be affected during patient testing (e.g. debris blown onto the screen of a pressure differential pneumotachometer).

I inspect the metal screen on my pressure differential pneumotach before every test and repeat the 3L calibration check whenever something looks out-of-place (e.g. values >120% of predicted). Clinicians who perform testing with a pneumotach element that is changed between patients (e.g. Pitot tube) should repeat the calibration check before each test because it cannot be assumed that the new element will perform as well as the one used for the morning calibration check. This is especially true if the pneumotach element is cleaned and recycled back into patient testing.

As shown in the exaggerated photo below, the cleaning and/or reassembly process has the potential to affect pneumotach structure and functionality.

Haynes Figure 1

Race Corrections for Pulmonary Function Data

Ralph Stumbo, RRT, CPFT, Group Health Cooperative, Pulmonary, Critical Care and Sleep Medicine, Tacoma, WA

We are all aware of the importance of doing daily, weekly, and monthly quality control (QC) on our equipment. It’s our way of documenting that the equipment we are using is measuring accurately.

However, documenting that the equipment is measuring correctly does not mean you can guarantee that the patient results are accurate. That is quality assurance (QA). Just as a good QC program has many facets and is impacted by many interconnected parts and systems, a good QA program also has many individual parts, of which a QC program is one.

Reference values

A QA program is what allows us to say, “these results are accurate.” One part of a QA program that is often overlooked is our choice of reference values to separate normal from abnormal. This gives us the ability to take it one step further and say, “this patient is normal” or “this patient is abnormal.”

This is very important; after all, when everything else is stripped away, isn’t that why we are testing the patient? Do any of us just test the patient and then send the results to the physician without any reference values? Just the raw data?

No, not if we plan to continue working in this field for very long. Why? Because without a comparison to normal the results are of no value to the physician or the patient and the patient might as well have had no testing at all.

Which predicted is the right predicted?

More important than using a predicted value is using the right predicted for the patient. The 2005 American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines give us some guidance for determining which reference values should be used: “specific recommendations for selecting reference values to be used in any lung function laboratory have also been discussed. These include the following: matching age-range, anthropometric, race/ethnic, socio-economic and environmental characteristics between subjects investigated by the laboratory and the reference population from which the prediction equations have been drawn.”

The guidelines go on to say, “subjects being tested should be asked to identify their own race/ethnic group, and race/ethnic-specific reference equations should be used whenever possible.” According to a study by Tang et al. in the February 2005 edition of the American Journal of Human Genetics, we are correct 99.86% of the time at identifying our genetically verifiable race.

Of course, race is a touchy, emotionally charged subject. It’s all over the news lately and can be the cause of fear and strife. While we should be above all that, it does not mean that we have to stick our heads in the sand and deny that race differences even exist. This approach is not helping anyone, especially the patient. No one thinks twice about separating male from female, and technologists would readily tell you there are huge differences in lung function values between the sexes. The same has been documented for lung function values between the races, and this has given rise to more accurate race specific reference values.

The Global Lung Function Initiative

So, how big of a deal is it? Are we making a “mountain out of a mole hill?” Few of us (hopefully none of us) would even consider using a calibration syringe that was off by 5%. The ATS/ERS guidelines give us an allowance of 0.5% for syringe accuracy. Our equipment has tolerances of less than 3%, but according to the MESA, NHANES III, and CARDIA studies, blacks have lung values that are between 14-19% less than Caucasians. For U.S. Asians the MESA study determined their lung values to be 12% less than Caucasians. NHANES III, MESA, and other studies have found that no correction is needed for Hispanics or Native Americans. Samoan and Pacific Islanders are about 9-15% less than Caucasians. If someone in any of these races is near his respective lower limit of normal (LLN) he would be classified as abnormal if using Caucasian reference values.

Fortunately, the Global Lung Function Initiative (GLI) has released robust reference equations for spirometry that include racial values for Caucasians, Blacks, Southern Asians, Northern Asians, and “other,” a category to be used when a person is of mixed races. Most manufactures have now incorporated the GLI predicteds into their newer software. For a lot of us, we will need to continue to use the NHANES III racial predicteds until our software is upgraded.

“First, do no harm . . .”

If we do not correct for race, many of our patients would be incorrectly labeled as having disease when in fact they do not. This will harm our patients’ health and create social and economic burdens for them and the health care system. The solution is simple: first, follow the ATS/ERS guidelines and produce high quality results. Second, make sure you have a good QA program that includes using the appropriate GLI or NHANES III racially correct predicted sets.

Editor’s Note: Ralph’s remarks highlight the importance of considering race when classifying pulmonary function data. Some clinicians using older reference equations (including NHANES III) believe that selecting “Asian” in the demographic section of their PFT software applies a correction; it does not. In a study by Kim et al., in the May edition of the Annals of Occupational and Environmental Medicine, applying NHANES III to normal Southeast Asian subjects misclassified 30% as abnormal. Every pulmonary function laboratory should use the GLI reference equations for spirometry. For more information, visit lungfunciton.org.


Eosinophilic Bronchitis: An Important Asthma Masquerader

Jeffrey M. Haynes, RRT, RPFT

Cough, wheezing, and dyspnea are symptoms not limited to asthma. There are a variety of ailments, such as congestive heart failure, vocal cord dysfunction, tracheal stenosis, and chronic bronchitis that can mimic asthma. Indeed, the large number of asthma masqueraders makes the diagnosis of asthma challenging in many cases. A less recognized asthma masquerader is eosinophilic bronchitis.

The chief complaint of patients with eosinophilic bronchitis is chronic cough. The airways have a very high eosinophil count and very high exhaled nitric oxide, just like asthma. However, patients with eosinophilic bronchitis do not exhibit the airway hyper-responsiveness that would be seen in asthmatics.

What makes eosinophilic bronchitis particularly deceptive is its marked responsiveness to corticosteroids. Consequently, a trial of inhaled corticosteroids to diagnose asthma will yield a positive result, even though the patient does not have asthma! A prescription for a combined long-acting bronchodilator and corticosteroid will be very effective in eosinophilic bronchitis; however, the long-acting bronchodilator will be completely unnecessary.

Eosinophilic bronchitis is not an uncommon problem. Brightling et al. found that eosinophilic bronchitis accounted for 13% of chronic cough.1 In a study conducted at my facility, we found that 17% of patients presenting for methacholine challenge had already been prescribed inhaled corticosteroids, making eosinophilic bronchitis ripe for misdiagnosis.2

References

  1. Brightling CE, et al. Eosinophilic bronchitis is an important cause of chronic cough. Am J Respir Crit Care Med 1999;160(2):406-410.
  2. Haynes JM et al. Frequency of anti-inflammatory therapy use at the time of methacholine challenge testing. Respir Care 2003;48(11):1105.

DLCO: It Takes Two, Baby

Jeffrey M. Haynes, RRT, RPFT

The 2005 American Thoracic Society/European Respiratory Society guidelines for diffusion capacity testing recommend that a minimum of two tests be obtained and note that testing is considered repeatable if the values agree within 10% or 3 units of measure (ml/min/mm Hg).

Technologists may be tempted, in the interest of time, to only record one effort; however, as shown below, effort #1 had a significantly higher DLCO and alveolar volume (VA) than efforts #2 and #3 (suspicious for an air leak). Had only one test been performed the patient’s DLCO would have been overestimated.

This scenario has the potential to lead to the misinterpretation of the response to pulmonary hypertension therapy, mistaken suitability for lung volume reduction surgery, or the continuance of lung-toxic chemotherapy or amiodarone therapy. Life-impacting decisions may be based on the pulmonary function data you produce, so forget the shortcuts and get with the guidelines!

Haynes Figure 2

Quarterly Care Report: Conflicting Methacholine Challenge Tests

Jeffrey M. Haynes, RRT, RPFT

Editor’s Note: This is an overview of a previously published case report: Haynes JM. Conflicting methacholine challenge tests. Respir Care 2006;51(1):62-66.

An 11-year-old boy experienced almost daily wheezing, dyspnea on exertion, and sleep perturbation because of cough. In addition, nadir peak expiratory flow (PEF) was below 100 L/min, which was ~30% of predicted (328 L/min), compatible with severe persistent asthma.

After the initiation of therapy with 180 mcg of albuterol three times per day, the patient’s domiciliary PEF rose to >200 L/min and his symptoms improved. The patient was subsequently prescribed fluticasone 220 mcg twice daily. After weeks of combined albuterol and fluticasone therapy, the patient’s PEF was >300 L/min and his symptoms had regressed to a mild intermittent status.

Three weeks after the initiation of fluticasone therapy the patient presented to the hospital for a methacholine challenge test. The patient did not take his albuterol or fluticasone on the day of testing, but had been using his fluticasone daily up until the day of testing. The baseline spirometry was normal. (See table 1)

Haynes Table 1

The methacholine challenge test revealed a PC20 (the provocational concentration of methacholine that resulted in a 20% decrease in FEV1) of >20 mg/mL. (See table 2)

Haynes Table 2

In response to this “negative” methacholine challenge, the patient was declared “non-asthmatic” by his pediatrician, and the albuterol and fluticasone therapy were discontinued. Shortly after the discontinuance of therapy, the patient’s symptoms and variable PEF returned. Two weeks following the discontinuance of therapy, the patient returned for a repeat methacholine challenge test. The baseline spirometry was again normal. (See table 3)

Haynes Table 3

However, on this occasion the patient demonstrated significant bronchoconstriction in response to methacholine inhalation, with a PC20 of 8.85 mg/mL. (See table 4)

Haynes Table 4

Given the change in PC20, accompanying changes in symptoms, and PEF variability, the second methacholine challenge was interpreted as a “positive test,” markedly increasing the post-test probability of asthma.

Discussion

Methacholine challenge tests are administered to assess bronchial reactivity when some possibility of asthma exists. In other words, there is a clinical suspicion of asthma or there is a possibility of asthma that needs to be ruled out.

By definition, suspicion includes some element of doubt. When one reviews this case, it is difficult to understand why there was much doubt about an asthma diagnosis. The patient’s classic asthma symptoms and variable PEF values, both of which improved in a stepwise fashion with beta agonist, then corticosteroid therapy, made the pre-test probability of asthma very high.

Based on these findings it could be easily argued that a methacholine challenge wasn’t necessary. In addition, there was clearly a lack of appreciation for the effect of corticosteroid therapy on PC20 , which led to the false conclusion that the patient did not have asthma and the ill-advised decision to discontinue clearly beneficial therapy.

It is therefore important for the interpreting physician to be aware of any pertinent medications the patient is taking at the time of methacholine challenge testing. Although there is no official recommendation in the current American Thoracic Society guidelines for methacholine challenge testing regarding the withholding of corticosteroids, we recommend patients withhold corticosteroids for at least one week (preferably several weeks) prior to methacholine challenge testing to allow adequate “washout” of the effects of corticosteroids on airway smooth muscle responsiveness.


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