Inhaler use-Are we getting it right?

A large proportion of our patients at Regional Respiratory Medicine present with chronic obstructive pulmonary disease (COPD) and/or asthma.

Part of the treatment plan often includes the use of one or more inhaled medications which if taken regularly, as prescribed, using the correct technique, allow people to play an active part in symptom control and maintaining their health.

Unfortunately, optimal control may not be achieved due to incorrect technique when these devices are used.

Research summarized by the The National Asthma Council of Australia (NACA) 2008 suggests that up to 90% of patients in clinical studies demonstrated incorrect technique using a standard metered dose inhaler (MDI) or dry-powder inhalers (DPI).

Also –
Error rates increase with age and severity of airflow obstruction / disease
Most often people are not aware of technique errors
Incorrect technique is more likely when an MDI is used without a spacer
There is an increase in associated side -effects

This has the flow on effect of further exacerbations and potential side – effects.

A spacer device used with inhalers for those with asthma and COPD can help reduce some user error problems such as difficulty co-coordinating breath and actuation, as well as being unable to reach a high enough inspiratory flow rate. Other common difficulties include poor cognitive abilities, osteoarthritis (limited dexterity), inability to achieve a good seal around mouth piece and inability to understand instructions due to poor English language skills.

We know that spacers used with an MDI -
Is equal to or better than a nebulizer
Should be used with Inhaled Cortico Steroids
Increases bronchodilation
Need less drug to get same effect
Cheaper to buy and maintain
Associated with less side-effects

HOWEVER, we still be must be aware of the potential problems with this mode of delivery.

Common mistakes made include –
Inadequate lip seal around mouthpiece
Time delay between delivering dose and inhalation (the dose stays suspended for only a short time in the spacer device and a portion of the medication ends up on the inside walls of the device if not taken straight away)
Failure to shake medication for initial/subsequent doses
Failure to wait one minute between doses
Poor spacer care and hygiene (build up of static on inner surface of spacer walls)

There is good news is from the NACA which has gathered evidence and developed guidelines to help improve asthma control. They recommend a checklist based assessment of technique followed by step by step inhaler technique. Nothing new here – the key is for this to be repeated regularly! Being shown once is not enough, as is written instructions alone.

So, expect to be asked to show us how you use your inhaler medication, even if you have been using it for years, and don’t forget to clean those spacers.

A Safe and Happy New Year to all!


Lisa

In summary, we need to be sure that each prescribed inhaler is appropriate to the individual and that they are able to use it effectively. Healthcare professionals need to be aware of the common mistakes made with each type of device and ensure their own technique is correct.

Lung volume testing in the elderly

Our population is ageing. As the proportion of elderly increases, it is increasingly important for health- care professionals to be aware of the limitations of some of our most trusted investigations in evaluating the health of our elderly patients.

A paper in the Blue Journal from the start of the month outlines this issue with clarity with regard to lung volume testing. We perform lung volume testing regularly on new patients referred to our service since we obtained equipment 18 months ago to allow us to do this accurately by plethysmography. When a patient performs this maneuver their results are compared against an expected normal range. This ‘normal range’ is calculated using equations which take into account age, height, weight and some derivative measures (such as body surface area and body mass index). These complex equations are pre-loaded in the software we use.

Until now, however, no-one has ever created reference equations for populations of patients aged over sixty-five.

This recent study, from Madrid, took a population of white patients aged between 65 and 85 years who were free of pulmonary or cardiac disease and who had never smoked. Around 320 of these participants peformed lung volume testing, using two different techniques (plethysmography, and helium dilution). Their results were compared against a ‘normal range’ based on equations from a middle aged population. The results from the different techniques were also compared.

Firstly, significant variability between the two modes of testing was found within individuals. Although this was not a surprising finding to anyone who does lung function testing, it is a reminder of the importance of comparing apples with apples. We should not compare lung volume results obtained with dilution techniques to results obtained with plethysmography in any one individual. (As an aside, dilution measures of lung volumes are more difficult to peform in any case and seem to only become more difficult if pathology is present – ie when they are really important. Plethysmography is quicker and more accurate).

The second finding was that the ‘extrapolated’ equations from middle-aged adults overestimated normal and therefore suggested many participants, who had been screened and found to be free of disease, to be below the normal range. For total lung capacity, for example, (TLC is one of the results obtained from lung volume testing) middle-aged reference equations found that between 11.8% and 55.5% of the women and between 14.1% and 25.9% of the men in the group were below the lower limit of normal – when really no more than 2.5% of the healthy population should be in that position.

We need to think about putting these reference equations into our equipment for use in patients in this age range. Meanwhile we need to be cautious about inferring to much from unexpectedly ‘abnormal’ results in older patients.

How safe is Spirometry?

A recent publication by CG Araujo and LC Vianna in the Primary Care Respiratory Journal (2009); 18(3): p185-188 is headed: How often does spirometry testing induce cardiac arrhythmias?

This is something every Respiratory Scientist might want to know! How likely is it for spirometry to induce cardiovascular complications in our patients?

This study was carried out in Rio de Janeiro, Brazil, and used as its subjects 735 persons (548 men), who were referred to their centre for clinical diagnosis and/or exercise testing. They were aged from 10 to 98 years (mean age 54 years SD +/- 15). Each subject was submitted to a conventional medical examination and spirometry testing prior to a maximal cardiopulmonary exercise test (CPET). A continuous digital electrocardiogram (ECG) was recorded during spirometry and CPET, and later reviewed by the same physician who supervised the procedures.

The results: 64% of subjects did have cardiac arrhythmias during one or both procedures (33% during spirometry) and the arrhythmias occurred more often in those with pre-existing disease. In 59 % of the 64% of subjects, the arrhythmias caused were supraventricular (half of them one or more isolated beats), and only 5% presented with more complex arrhythmias including frequent premature ventricular beats or non-sustained ventricular tachycardia. No episodes of ventricular tachycardia occurred during spirometry.

The researchers conclude that spirometry is a safe procedure in terms of its induction of cardiac arrhythmias. Any spirometry-induced arrhythmias tended to be both simple and clinically irrelevant and were always short-lasting even in patients with mild or moderate obstructive pulmonary disease. Interestingly the researchers found that the large majority of the arrhythmias occurred during the “take a full breath” phase of the flow-volume loop manoeuvre.

The limitations of the study as described by the authors is that they selected a convenient sample of primarily Caucasian and upper socioeconomic strata subjects, a substantial number of whom had long-term chronic diseases, which might have affected the frequency and type of cardiac arrhythmias. The strengths of the study were that the study comprised a large number of consecutively enrolled subjects who were evaluated by a single physician who supervised all procedures.

The researchers also suggested that if easily available, it might be informative (particularly with men with a history of palpitations) to add ECG recording during spirometry, because in 70% of the 21% of patients who had reported a history of palpitations at the medical interview, spirometry and/or CPET induced a cardiac arrhythmia.

So, spirometry is a safe procedure (Phew!) with some interesting effects on the heart which could be further investigated.

Heather

The big kill

New years resolutions are a topic of conversation around this time of year. I normally have a couple (exercise more and learn to play the guitar this coming year) and invariably if there is not enough motivation behind these resolutions they will fail (get fitter for the former and spend time with son who is also learning guitar for the latter).

Many peoples new years resolution will be to to quit smoking. To be successful in this endeavour there needs to be a motivating reason. This is the most powerful tool you have when quitting smoking and focusing on this will get you through some tough times. Common reasons for quitting may be smoking kills, smoking causes diseases, improved physical appearance, saving money and setting a better example for your children.

I will focus on the former. The leading cause of preventable death in Victoria is smoking. Smoking-caused deaths (11.9%) in every area of the state outstrip other major avoidable deaths caused by alcohol (2.4%), other drugs (.3%)and road deaths (1.2%), even when combined.

The annual deaths caused by smoking can be broken down into to diseases. Lung cancer leads the ways with 1480 deaths, mouth and throat cancer 59, other cancers 416, heart disease 700, stroke 218 and chronic bronchitis and emphysema 1011.

Data recorded in 2008 breaks these statistics down into local regions. For the Southern Grampians region the number of deaths attributed to smoking is 13.2% which is slightly higher than the state average.

The quit website details ways to quit. Remember the first step to successfully quitting is exploring the reasons why you want to quit.

Jessica

The year it was

Once again we are nearing the end of the year, Christmas a mere 3 days away! While its seems the year has flashed by, once I reflect on the changes that have occured at RRM this year January 09 seems a distance memory.

Staff wise the practice grew this year with additional administration, nursing and respiratory scientist support. We had regular visits from Melbourne Respiratory Physicians Dr. Garun Hamilton (Hamilton), Dr. Daniel Steinfort (Horsham) and Dr. Dinesha de Silva (Portland). We are very happy that these physicians will continue to consult at RRM in 2010.

Approximately 1200 lung function test were performed this year, making it our busiest year to date. Also more sleep studies were able to be conducted with the opening of the Portland sleep centre in February 2009.

While its nice to reflect, 2010 presents many opportunities and challenges. Top of the priority list is employing an additional full time Respiratory and Sleep Physician (they are very elusive).

During the Christmas period our office will be open on all normal workdays except for the public holidays. Both the Hamilton and Portland Sleep Laboratory will be closed over January, reopening 27/1/10 and 1/2/10, respectively.

Have a wonderful, safe and happy Christmas and New year period.

Jessica

An evening and a day at the sleep centre:MSLT

A typical night at the sleep centre involves two diagnostic studies and one cpap implementation study. This week my shift was slightly different with two cpap studies and a MSLT.

One of the cpap patients was an implementation.They had been diagnosed with severe OSA (AHI>30). They had never tried cpap previously, hence after a recap of what OSA is and how cpap manages this condition, we spent so time fitting masks to find the most appropriate one. The other cpap study was a review. They had been using an autoset machine for a month, had a mask they were happy with thus needed to have a titration study to confirm what pressure their cpap machine should be set to.

The third patient was having a MSLT the following day. They had previously had a diagnostic study which showed no significant OSA but they reported high levels of daytime sleepiness. The night prior to a MSLT a diagnostic study is required.

So what is a MSLT and why might it be required? It stands for multiple sleep latency tests and basically it measures how long it takes for a patient to fall asleep.

The following morning (after the diagnostic study) after breakfast and a period of recreation a series of 4 or 5 naps are scheduled. Each nap is around 20 minutes and during this time patients are asked to lie in bed and try to fall asleep. The sleep technologist will watch each nap via the computer screen and check if sleep has been achieved and if so has REM (rapid eye movement) occurred. At the end of 20 minutes if the patient is asleep they will be woken by the sleep technologist

Patients must have a drug screened urine sample on the day of the test and are asked to not have any products with caffeine on the day of the test or prior.

It is used as a way to assess excessive levels of sleepiness and as a diagnostic tool for narcolepsy.

Jessica

Does streptococcal infection cause narcolepsy?

Narcolepsy is a lifelong neurological disorder which manifests as a problem with sleep; too much sleep. The hallmark symptom of this condition is 'cataplexy', which describes a sudden loss of muscle tone triggered by strong emotions. Narcolepsy affects around one in two-thousand people in our community. Most GPs will have one patient in their patient population with bona-fide narcolepsy.

As with many disorders, as the genetic and cellular basis of narcolepsy has become better understood, the tools upon which we rely for diagnosis have begun to look increasingly clumsy. The standard diagnostic test is a multiple sleep latency test; performed in the sleep lab, we essentially invite our patient to prove how sleepy they are by taking multiple naps during the course of the day. In the last decade, however, it has become apparent that:

1. There is a very tight genetic association with narcolepsy, with almost all patients demonstrating a particular HLA profile (HLA-DQB1*0602).
2. Narcolepsy is caused by the loss of hypocretin secreting neurons in the hypothalamus

To date, only five patients with narcolepsy worldwide have not demonstrated these associations. These findings have led to the hypothesis that narcolepsy is an autoimmune disorder. A recent study has tested the hypothesis that perhaps narcolepsy is a condition in which an infective organism triggers a destructive immune response.

Why should we consider that possibility? We already know, and have known for a long time, that the immune response associated with - for example -streptococcal infection can cause secondary damage in organs not related to the initial infection. Streptoccal antigens can mimic cardiac tissue, leading to rheumatic fever and valvular heart disease. A similar process affecting the brain may cause Sydenhams chorea, and post-strep glomerulonephritis is well described. Could narcolepsy be a manifestation of post-streptococcal neurological damage in the hypothalamus?

What evidence is there for this in narcolepsy? Well, til recently not much. However, with the publication of the study mentioned above - in Sleep Journal in August - the landscape has changed a little.

What did they do? The study involved multiple centres in North America, Europe and Asia. All patients had the HLA type mentioned above and were hypocretin deficient, or had the HLA type and clear cataplexy. Patients were divided into four groups according to the duration of their disease (less than one year, one to three years, three to ten years or more than10 years). They also studied age matched, healthy controls. Amongst other things, serological evidence of streptococcal infection was sought, with anti-streptolysin O and anti DNAseB antibody assays measured.

What did they find? They found that the more recent the onset of the narcolepsy the more likely a patient was to have serological evidence of streptococcal infection as follows (patients vs controls):

• 43% vs 4.5% of the 'less than one year group' had evidence of both ASO and antiDNAseB. 65% vs 26% had one or the other;
• 33% vs 9.5% of the 1-3 yr group had both, 57% vs 30% had one or the other

These differences were statistically significant. There was no significant difference in the other groups. This level of serological evidence of infection is comparable to what is seen in rheumatic fever and Sydenham's chorea.

What does this mean? This is very interesting evidence. If repeated in other populations of well selected narcolepsy it could have significant implications. There may turn out to be a place for immunotherapy or antibiotics in the management of narcolepsy - if the diagnosis is made early. (At present, the only treatments available are medications that help people stay awake, such as modafinil or dexamphetamine)

Andrew

More than 100 years ago....

When studying up on autoset technology I found mentioned the
Hering -Breuer Reflex (not something I can remember from my distant anatomy and physiology lectures). This is the reflex that limits excessive expansion and contraction of the chest during respiration prior to sending impulses to the brain via the vagus nerve.

Joseph Breuer (15 Jan 1842-20 June 1925) was an Austrian Physicist whose achievements included being a father of five children and showing how the sense of balance functions. He also undertook psychoanalytic work with friend Sigmund Freud and documented a study supporting “the talking cure” where patient’s symptoms were reduced or disappeared just by describing them to him. He was also responsible for changing the way scientists viewed the relationship between the lungs and nervous system.

In 1868, Breuer and Hering reported that a maintained distention of the lungs of anesthetized animals decreased the frequency of the inspiratory effort or caused a transient apnoea. The stimulus for this reflex is pulmonary inflation.
There are both inflation and deflation reflexes that help regulate the rhythmic ventilation of the lungs, thereby preventing over distension and extreme deflation. These reflexes arise outside the respiratory centre in the brain; that is, the receptor sites are located in the respiratory tract, mainly in the bronchi and bronchioles. They are activated by either a stretching or a nonstretching and compression of the lung; the impulses are transmitted from the receptor sites through the vagus nerve to the brainstem and thence to the respiratory centre.The inflation reflex acts to inhibit inspiration and thereby prevents further inflation. When the lung tissue is stretched by inflation, the stretch receptors respond by sending impulses to the respiratory centre, which in turn slows down inspiration. As the expiratory phase begins, the receptors are no longer stretched, impulses are no longer sent, and inspiration can begin again. This is called the Hering–Breuer deflation reflex. It is also believed that in addition to the cessation of impulses from the stretch receptors, there may be an activation of compression receptors which transmit impulses that inhibit expiration, thus allowing inspiration to begin.
The relevance of this and APAP therapy is that some autosets are programmed to not respond to apnoeas above 10cm H2O since these episodes are more likely to be central in nature. The rationale used is that higher pressures will cause the Hering-Breuer reflex and if the pulmonary stretch receptors get overstretched they send a signal to the brain to stop breathing, leading to more central events.
Users should understand though that pressure does still increase in response to obstructive hypopnoeas, snoring and flow limitation.

Irene

Borderline pulmonary hypertension in Scleroderma

The lost table from my previous post on this topic, showing difference in 6 minute walk test distance covered in a group of 29 patients with systemic sclerosis but no heart or lung disease, who develop pulmonary hypertension on exertion, divided into two halves - above and below median pulmonary artery pressure. From recent paper in AJRCCM.



Figure 1. Six-minute-walk distance (mean ± SD) in patients with mean pulmonary arterial pressure values above (white) and below (black) the median as measured at rest (P < 0.005), at 25W (P < 0.005), at 50W (P < 0.0005), and at maximal exercise (not significant). *P < 0.005; **P < 0.0005.

Andrew

OSA and traffic accidents

Many studies have demonstrated that patients with OSA have a higher rate of road accidents.

A study earlier this year OSA as a cause of road traffic accidents took 163 patients with OSA (AHI>10) who were diagnosed by a PSG. Of these participants 18.4% drove for a living. Patients were asked to self report about any accidents they have had or near misses in the last three 3 years.

From this information participants were then divided into two groups, accidents and near misses and those who had had none. Both groups were compared by age, BMI, ESS, daytime PaO2 and PaCO2, functional outcome of sleep questionnaire (FOSQ) and PSG data.

The researchers demonstrated patients who have had road traffic accidents and near misses had more severe OSA, higher AHI's, excessive daytime sleepiness and lower quality of life.

It is estimated that over 50% of Australian truck drivers have mild OSA or worse. Access economics has estimated that the cost of sleep disorders in the Australian community is over $7 billion and much of this can be attributed to OSA.

In Victoria alone it is estimated fatigue results in more than 70 deaths and 500 serious injuries per year. Again it is estimated that a significant percentage of this fatigue is due to sleep disorders.

Being awake for more than 17 hours then driving has the same effect on someone as a blood alcohol level of being .05. Extend that to 24 hours without sleep and there is a similar effect on driving performance as having a blood alcohol concentration of .10. At this level there is a seven time greater risk of having an accident.

The TAC has an interesting case study on various advertising campaigns they have used to educate the community about the consequences of fatigue on our roads.

Jessica

Spirometry

Bronchial provocation testing was our topic for last month and this month lets talk about spirometry
Spirometry is a measure of airflow and lung volumes during a forced expiratory manoeuvre from full inspiration. The measurements made during spirometry are sometimes referred to as ‘dynamic lung volumes’. Although the simplest of all respiratory function tests correct interpretation requires that it be performed correctly

Spirogram
A diagrammatic representation of lung volumes and capacities based on a simple spirogram which we see every day. Relationships between the subdivisions and relative sizes as compared with TLC are shown. Resting expiratory level is used as a starting point for FRC determinations because it remains more stable than other identifiable points during repeated measurements

Volume-Time Curve
Spirometry measures airflow obstruction, airflow reactivity, lung restriction and normal lung function and these can be graphed in a volume-time or flow-volume format.
The volume-time curve produces FVC & FEV1. We can then calculate the ratio of these to obtain FEV1/FVC or FER. Accurate measurement of FEV1 requires an acceptable spirometer, preferably one that allows inspection of the volume-time curve and back-extrapolation. Additionally we can measure mid expiratory flow which gives an indication of small airway function & PEF which tells us how much force the patient is able (or willing) to generate

Mathematically these can be converted on some equipment to flow-volume curves and many conditions have typical curves. A flow-volume curve usually records flow in liters per second and the volume is recorded in liters, BTPS

Flow-Volume Loop
Expiratory and inspiratory flow-volume curves constitute a flow-volume loop and most modern spirometers can produce flow-volume loops. Visual pattern recognition from repeatable maximal flow volume loops, if available will help decide whether the measurement was performed correctly, as well as confirming the presence of abnormality

Of all the pulmonary function tests performed, spirometry remains the most widely used test. Although the simplest pulmonary function test, special emphasis must be placed on the performance of each test and the technician must have a sound understanding of the criteria for judging the acceptability and repeatability of test data based on the most recent guidelines published by the American Thoracic Society/European Respiratory Society (ATS/ERS) Task Force on Standardization of Lung Function Testing

Vanessa

Mild pulmonary hypertension in scleroderma

Scleroderma / systemic sclerosis is a rare connective-tissue disease. In this condition, hardening of ‘elastic’ tissue throughout the body results in a range of end-organ problems. Scleroderma affects the skin, gastro-intestinal tract, lungs, kidneys. It affects the blood vessels.

Blood vessel problems in the fingers and toes cause ‘Raynaud’s phenomenon’. Problems in the kidneys can cause dramatic renal failure. Problems in the lungs cause a condition called ‘pulmonary hypertension’.

In the last 15 years there has been a progressive increase in the number of medical treatments available for treatment of pulmonary hypertension. With this has come an increased amount of research into what had previously been something of an ‘orphan’ condition. Treatment (with prostacyclin analogues; with endothelin receptor antagonists (Bosentan); with the phosphodiesteraseE5 inhibitor Sildenafil, sometimes known as Viagra™) remains expensive and tightly controlled. Often treatment is not accessed until people have severe, or end stage, pulmonary hypertension. I have a handful of patients with scleroderma, and looked after many such patients when working in London. In London the bar for access to treatment for pulmonary hypertension seemed significantly lower than it is in Australia.

So I read, with much interest, a recent report from Austria/Germany/California about the impact of even high-normal pulmonary artery pressures (PAP) on the exercise tolerance of people with scleroderma. Twenty-nine patients with systemic sclerosis but no evidence of lung or heart disease participated in this trial. They all had normal resting pulmonary artery pressures on echocardiogram, but demonstrated an increase in systolic pulmonary artery pressure with exercise ( to over 40mmHg) or a deceased exercise capacity (peak VO2 <75% predicted). They all proceeded to have a more accurate measure of pulmonary artery pressure obtained via catheterization of the right side of the heart ( an invasive procedure, something like an angiogram). A cardiopulmonary exercise test was performed while the right heart catheter was in place to measure changes in PAP with exercise. Subsequently – right heart catheter now removed, but within 48 hours - they went on to perform a 6 minute walk test (6MWT). This test is as simple as it sounds. The supervisors of the 6MWT were not aware of the right-heart-catheter results.

The median resting PAP of the group was 17mmHg. A resting PAP greater than that level was associated with a reduced distance walked on 6MWT, reduced peak V02 and reduced maximal work rate. An early increase in PAP at low work levels showed essentially the same correlations, but PAP at peak exercise did not show an association with distance walked on 6MWT or peak V02 and maximal work rate.

These results are very interesting, and could be quite important. They suggest that people with scleroderma who have high-normal pulmonary artery pressures, and particularly those who show an early rise in PAP during exercise, have a lowered exercise capacity. The possibility that these people may have a worse prognosis needs to be considered and investigated. (There is evidence that patients with scleroderma, pulmonary fibrosis (which is often associated with scleroderma) and a resting PAP > 17mmHg have decreased survival when compared with patients whose PAP was <17mmhg (5- year survival 16.7% vs 62.2%)). Ultimately it may well turn out to be important to treat such patients with even high-normal PAP early with the available medications.

The wheels of evidence-based medicine turn slowly for ‘orphan’ conditions such as pulmonary hypertension. Translation of this sort of research, fascinating though I may find it, into meaningful therapeutic changes will take many years.

I have had no end of trouble with hyperlinks and pics on this post - will post table from the paper seperately.

If the mask fits, wear it!

Today I traveled to Portland, where the weather was very pleasant to visit the PDH sleep centre. During the morning we spent some time refreshing or for some newer staff members learning how to fit a cpap mask.

I was one of the ‘refreshers’ and thought I was quite experienced when it came to fitting masks but there were a few useful pieces of information that challenged my way of thinking.

Different people, places and companies all have their own ideas, routines or procedures when fitting cpap masks but the main two points are find a mask the minimizes leak and maximizes patient comfort.

I veered toward being a nasal mask advocate, always letting the patient try a full face as a comparison but was of the belief that nasal if they fitted well, the patient was able to tolerate it and there were no leaks it was a good choice. My reasoning being full faces having more surface area seemed to provide more opportunities to leak.

Nasal pillows were on my last resort list, although on many occasions I have seen them be very effective in managing OSA. If a patient arrived armed with some research and wanted to try them of course I would oblige but other than that I did not always offer patients the choice to try these on. My reasoning this time was nasal pillows can be very fiddly, difficult to fit and less tolerant of higher pressures.

The advice given today was always allow the patient to try on the three different sorts of masks. Unless they try them on we cannot make a judgment as to what fits them, what the patient finds the most comfortable and ultimately it is the patient who chooses the mask.

For the record I had on a nasal mask for a while today at 10cmH20. It was more comfortable than I remember and I think it is important to periodically wear different mask to give an insight into what the patients are experiencing. Kath tried on nasal pillows at 20cmH20. The mask tolerated this pressure and so did Kath! Raelene fitted her first mask on Gerri and also experienced cpap for the first time.

Pictured above are the three different types of masks mentioned. Our trainer today suggested we try to use cpap for a week to gain an even greater understanding of what our patient’s experience. Maybe I will blog about this at a later date.


Jessica

Spirometry Course

As the newest recruit to our Lung Function Testing Lab, I attended the Spirometry Course held at the Alfred Hospital in Melbourne on the 5th and 6th of November. This I enjoyed.

The Course was very well presented. The presenters were interesting and had a wealth of experience. They interspersed the Theory sessions with great hands-on Prac sessions to keep us all awake, and some quite complicated information was clearly presented with time to absorb it.

Thorough information was presented on how to achieve the proper standards of Quality Assurance, incorporating equipment and personnel, so that all tests done can be reliable, and provide an accurate clinical picture of each patient’s lung function. I realized at this point just how well our Lab measures up in this area.

I returned with an enthusiasm to 1) learn more in the areas of the documentation and analysis of Quality Control data, 2) look at research done on FEV6 ( the Forced Expiratory Volume at 6 seconds) which might be introduced as a measure of patient performance, and 3) to perfect my instructions to patients performing the test.

This was a thoroughly thought-provoking, challenging and enjoyable experience. Thank you to the presenters.

Heather.

Non-adherence to treatment regimes in difficult asthma

The accompanying picture of a Seretide ™ combined corticosteroid/ long- acting beta-agonist inhaler device hopefully evens the score a little in the war of the combination puffers on this blog (see comment on the post about use of eformoterol/budesonide in COPD) Each of Seretide ™ and Symbicort™ are excellent medications in airways disease (can I say it often enough?)– particularly asthma…… if our patients take them!

Which brings me to the topic of this post: non-adherence with prescribed medications in difficult asthma. A recent study from Northern Ireland, published in the American Journal of Respiratory and Critical Care Medicine (The Blue Journal) at the start of November, looked at this issue in a population of asthmatics referred to a tertiary – hospital ‘difficult asthma’ program. These were patients with persistent asthma symptoms in spite of regular combination inhaler use (one of the two above), with some on maintenance oral prednisolone. Around forty percent were referrals from other respiratory specialists to the hospital program.

I see many patients with ‘difficult asthma’, although they make up only about 5% of the adult asthmatic population. In general the first question I ask myself is always ‘does this person really have asthma?’ Frequently they do not, and the failure of asthma therapy reflects an initial misdiagnosis. The second question is ‘Is this person really using their medications?’ This recent study is the first that looks rigorously at adherence to prescribed medications amongst adults with ‘difficult asthma’.

The findings were startling. Although everyone claimed to use all of their medication as prescribed when asked at the commencement of the study, of 182 consecutive patients seen in the service 78% used less than their prescribed amount of combination inhaler medication, with at least 35% using less than half of what they were prescribed. Twenty-one percent used more of their combination inhaler (preventer) than had been prescribed, leaving 1% of patients using medication as prescribed!

The study then looked further at patients prescribed maintenance oral prednisolone, and found that 45% were non-adherent with that medication.

There were three variables that were associated with poor adherence to treatment. These were female gender (nearly 2/3 of the group on the whole was female. 42% of them were in the least-adherent group, where only 23% of the men were); low quality of life; and frequent hospitalizations in the previous year.

How was data collected? In Northern Ireland all medications that a patient is taking are prescribed by one GP only. Review of the number of prescriptions issued by that GP, compared against the dose of medication which the person is supposed to be using, allowed a reasonable measure of compliance to be obtained in this study. In the case of oral prednisolone dosing, regular use of prednisolone should lead to suppression of adrenal cortisol secretion. Blood test measures of prednisolone and cortisol levels were used in that patient group to evaluate compliance.

The findings of this study require reflection. Doctors of patients with ‘difficult asthma’ will be considering a range of alternative treatment approaches, including use of maintenance prednisolone orally, use of theophylline or montelukast (Singulair ™) or else a more expensive biological therapy (for example, Xolair™(omalizumab), with others on the horizon). It’s important that we don’t proceed to the more complicated, dangerous or expensive medications without clarifying whether the standard medications are, in fact, being used.

The authors of this study state that they believe ‘the key message off this study – that non-adherence is a significant issue in an unselected population with difficult-to-control asthma and significant asthma-related morbidity….is valid and needs to be proactively identified and addressed’. I agree. I suspect, however, that a systemic change in the way we distribute medication and monitor compliance may be required to effectively achieve this.

Andrew