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

Bob and Jan

I recently had the pleasure of meeting Bob and Jan. Bob has been using home oxygen now for some time due to a lung condition. At this particular meeting, Bob was using his EverGo Portable Oxygen concentrator which he has had for the last four months.

They are so pleased with it that they were happy to share their story – so read on and thank you BOB and Jan!

Quality of life is a huge issue for people with continuous oxygen requirements. Bob stated that his quality of life has improved simply because he can go out more. He is not reliant on his home oxygen supply anymore. And he now goes out without pushing a big cylinder around everywhere.

The biggest advantage in his view is to not have to constantly keep up his oxygen bottle supply (he needs 5 a day!). This alone made it difficult to travel away for any period of time. I can only imagine the challenge of packing the car with 5 bottles a day, for more than 3 days….space at a premium. What about luggage, grandchildren? It is much easier to pack the concentrator in the car, and of course there is plenty of room for Jan’s shopping now.

Bob and Jan have from the sound of things been taking full advantage of their new found freedom by doing some tripping around in their caravan. They can charge the batteries in the car (12 volt) and as they say – Bobs your Uncle! When he is out he uses it for up to 6 hours a day.

Speaking of Bob, thats him in the photo.

My research also found out that this particular concentrator is light weight, only 4.5 kilograms, has an easy to use touch screen interface ( which I can vouch for), appropriate alarms, Oxygen Percentage Indicator and extra long life batteries. It also comes all neatly packed in a carry bag.

I am aware that this sounds suspiciously like an advertisement for portable oxygen concentrators and I guess in a way it is but WHAT A GREAT AD THEY ARE. I hope that this inspires others or their families to explore this option to improve quality of life.

I wish this lovely couple all the best and many more travels.

Lisa

Teaching lung function to people who already know a bit

The following example of lung function from our lab illustrates an interesting physiological combination of abnormalities.




As anyone who has heard me teach on lung function testing will know, I think there are three steps to interpreting spirometry:

1. Is the forced expiratory ratio (FEV1/FVC) reduced (ie is the spirometry obstructive)? In this case it is not.


2. Is the FVC reduced (ie is there evidence of restriction)? In this case it is.


3. Is there a response to inhaled bronchodilator? A signficant response requires an improvement of 12% and 200ml from baseline in either FEV1 or FVC. In this case there is no such response.

Interpreting the spirometry alone, one could say that this is a restrictive pattern. However, one of the early signs of restriction on spirometry is an elevation of the forced expiratory ratio (FER). In this instance, the FER is tending down (62% at baseline). This raises the possibility that there is underlying obstruction with air trapping, leading to an appearance of restriction on spirometry.

Here is where lung volumes help. Since getting the 'body box' we are now able to do lung volume testing on every new patient. Lung volume measures here confirm that the apparent restriction is marginal - with a total lung capacity / TLC at 85% predicted around the lower limit of normal. Residual volume / RV is plumb average, and the ratio of RV/TLC tending up - suggesting a degree of air trapping.

Is this a true 'mixed defect'? That unusual combination of restriction and obstruction in the one patient? I think it is. Most commonly we see this appearance in older women with COPD and osteoporotic thoracic kyphosis. In this particular case the chest xray appearance is as follows:

Note the perfectly adequately expanded (in fact marginally hyperexpanded) right lung and the elevated hemidiaphragm on the left. This patient has airways disease with signficant obstruction, and in addition restriction due to a paralysed left hemidiaphragm.

A beautiful example!

Andrew

Lung Function Survey

A big thank you to all the medical practitioners that completed the recent survey on our Respiratory Lab. The response rate was a healthy 58%.

The aim of the survey was to rate the service we provided and use this information to implement quality improvement strategies.

The survey focused on rating various components of the service, seeking information on what barriers there are for referring patients and asking for constructive feedback on how we might improve the service.

The results were very encouraging. Seventy one percent of respondents had used the service previously. Of these the overall rating for the service was;

• very high 29%
• high 56%
• low 12%
• very low 1%
• na 2%

Of the 21% who had not referred a patient before the common reasons were lack of information about the service, spirometry on site and distance to travel to testing.

Eighteen comments were provided. A sample of these were;

'referral pad similar to limestone physicians group distributed to gp's'

'more education on GP use of service'

'appointment given at earliest are always good but at the same it I understand wait is bad'.

'

always very prompt and helpful'

'maybe need improved education with ‘others’

'Appt times!!'

'Not in Warrnambool'

'Lack of information about service-best indications for particular test'

'Pt info handouts on expected costs (often raised as a concern in early COPD)'

'make available for patients to see and have tests done locally in Horsham'

These comments highlighted a common thread that more information and education about lung function testing is warranted throughout the region.

During 2010 we intend to visit all practices in the catchment to meet with GP's and practice nurses. We will also continually make sure the medical community is kept up to date with what tests we are offering and dates we will be visiting various locations.

We are also able to offer practical demonstrations of our testing and in early 2010 plan to conduct a demonstration of cardiopulmonary exercise testing at or Hamilton rooms.

Referral forms are available via this link.

Once again thank you to all those who replied. This information is invaluable for the continued growth of this service.

Jessica

Symbicort catching up with Seretide in COPD.

An article published in the blue journal last month, accompanied by an editorial, draws to light two related phenomena. Firstly, the combination of an inhaled corticosteroid, long-acting beta-agonist and tiotropium is beneficial in chronic obstructive pulmonary disease. (This, at long last, gives respiratory physicians the opportunity to use 'triple therapy', a phrase which has an inexplicable allure for medicos). Secondly, for Astra-Zeneca and Symbicort (budesonide/eformoterol) it's all about catching up with Glaxo and Seretide (fluticasone/salmeterol). And they just might do it yet.

The study was a randomised, placebo controlled trial of Spiriva (Tiotropium) alone vs Spiriva and Symbicort (to use the local trade names) in combination. The Symbicort dose was 320/9mcg, which is not a dose marketted in Australia (where we have 100 or 200/6 or 400/12). Around 600 subjects were recruited, 300 or so in each arm. Subjects had to have pretty severe COPD, with an FEV1 of less than 50% predicted on their initial pre-bronchodilator spirometry, although 25% ended up categorised as moderate if the GOLD - compliant definition of post-bronchodilator FEV1 was used.

The goal of the study was to demonstrate improvement in lung function - which they did. There was a 6% improvement in pre-bronchodilator FEV1 at follow up in the 'triple therapy' (TT) group compared with the Spiriva-alone group. There were also more subjects in the TT group with a significantly improved quality of life. Most strikingly, there was a very significant (62%) reduction in exacerbations in the TT group (7.6% of patients vs 18.5% of patients) over the short 12 weeks of the trial. (It's worth noting that the definition of exacerbations here required a hospital attendance, not just an escalation of therapy with glucocorticoids directed by a doctor).

The benefits of this combination of inhaled medications in COPD now seems beyond dispute. There seems to be a class effect (ie Symbicort and Seretide are each beneficial) and we can expect Symbicort to get PBS listing in Australia at some point for patients with moderate COPD, although it does not yet currently have this.

The accompanying editorial in the blue journal does point out the following important points:

1. Although Seretide has not been demonstrated to reduce the frequency of exacerbations, the trials of Seretide in COPD had a more inclusive definition of exacerbation and the drugs can't be compared on this point on the data already to hand;
2. 40% of patients in this trial were already on 'triple therapy' before the trial, and the inhaled steroid and LABA had to be stopped. This may just be an example of trials catching up with clinical practice;
3. Not enough patients of moderate disease severity have been enrolled in the trials. Aparently a recent post-hoc analysis of the TORCH data (one of the Seretide trials) showed that patients categorised as moderate by GOLD criteria (post-bronchodilator FEV1 50-80%) had quite poor prognosis generally in terms of rate of loss of lung function, deterioration of quality of life and rate of exacerbations. If COPD is now being modelled as an inflammatory disorder and patients with relatively early disease do progress why are we not investigating the impact of antiinflammatory inhalers on earlier-stage disease?

So why do I think that Symbicort is working hard to catch up to Seretide, and that the unwritten primary-endpoint here was to win market share in patients with COPD? It strikes me that Astra-Zeneca learnt from the failure of Glaxo to demonstrate a survival-benefit for the Seretide/Spiriva combination in a big trial published in the New England Journal in 2007. Although a lot of useful secondary endpoints were hit in that trial, it is remembered as the trial that missed the jackpot. The current trial has notably not tried to aim so high. It is a short trial, with relatively few patients, and looks to me very much as if is has been put together to demonstrate that Symbicort is also 'good enough' to use in patients with COPD.

The trial authors list the following as goals of treatment in COPD:

• reducing symptoms
• improving health status and exercise tolerance
• reducing the risk of exacerbations.

These management goals are actually limited by the efficacy of the treatments we have available. They were designed for clinicians, not researchers. So having stuck to the established management goals, Astra-Zeneca have now proved that Symbicort helps to do all of what we are already doing better. It strikes me as circular thinking, and a little disappointing. Give me something new to offer my patients! Please.

Notably absent from the list of treatment goals is to 'reduce disease associated mortality'. It's not there as a goal because, apart from smoking cessation and oxygen in select patients, we don't know how to do it yet. Mortality reduction is the most meaningful of all possible treatment goals in established medical research traditions, but I suspect it is beyond the potential of our current medications in COPD.

Andrew

People we meet

Brona Manson (a previously mentioned Irish nurse) has been a practice nurse with the Mildura Aboriginal Health Service for about two and a half years. The service area extends to Robinvale, Swan Hill, Balranald and Dareton (NSW) all who have satellite clinics. Along with her many varied practice nurse duties (every one always seems to need Brona) her main role is supporting indigenous clients with chronic disease including respiratory patients.
Brona carries out “puffer”education with patients and conducts spirometry tests if needed but also utilizes the monthly visiting service offered by Regional Respiratory Medicine. Dr Bradbeer has been consulting at MAHS for the past 18 months along with a respiratory scientist and sometimes practice nurse (which is how I got to meet Brona).
Sleep medicine is a fairly recent service at the clinic. If indicated patients will undergo a home sleep study. Brona or another nurse will visit the patient in their home early in the evening to ‘wire’ them up, and then return to collect the equipment the following day. Downloaded information from the study is then sent to the sleep scientist in Hamilton to be analyzed and reported on. Patients also have access to CPAP (continuous positive airway pressure) machines if required. Brona will fit the patient with a mask, educate them on the use of the machine and offer follow up support as needed. A new area for her too she tells me, so is learning as she goes.
Brona says the biggest challenge to the Health Service is getting clients to attend the clinic even though a pick up and drop off service is provided to assist with access. According to Brona there are many indigenous clients in the community with respiratory or sleep problems who could benefit from the visiting specialist service offered by RRM. A somewhat disjointed referral system and non attendance at appointments means the service is probably not fully utilized. Patients who do attend seem very grateful for the expert care.

Irene Hill

Fit to Dive?

Recently on a trip to Mildura part of the regulator on the DLCO gas bottle was damaged. Thankfully it was still operational on the day. On return Vanessa went to visit some local dive experts to make sure it was fixed correctly.

They were very interested in our Respiratory Lab. In return, the visit generated some interest amongst our staff in what part Respiratory testing plays in Dive Medical Examinations.

Australia apparently has some of the strictest dive guidelines in the world and the Australian Standards 4005.1 need to be adhered to when assessing a diver for a medical examination.

A survey conducted in Queensland a few years ago attempted to assess the variability of opinion regarding fitness to dive among doctors doing dive medical examinations. There was a 64% response rate. Fifteen hypothetical cases were presented. They were asked to classify the cases as either fit to proceed with dive training, unfit to proceed, requiring a referral to specialist and fit after investigation.

Opinion varied greatly. There was a 70% consensus about unfitness in only 4 cases (one of which should have been referred according to AS guidelines) and fitness in only two cases (both should have been referred). For each case that the AS guidelines firmly state as unfit to dive at least one doctor passed as fit.

How does this relate to respiratory disease? Absolute contraindications for diving are Asthma, Lung cysts, obstructive lung disease, lungs that empty unevenly and previous thoracotomy. Relative contraindication are FEV1/FVC ratio of less than 75% and poor physical condition.

Jessica

Biases that make screening programs look good

Too often lung cancers are diagnosed at a late, untreatable stage, as was the cancer in the CT above. An effective lung cancer screening tool would be great!


Last week I described a recent trial that disappointed, failing to prove that lung cancer screening with low-dose CT (LDCT) saves lives. The designers of this trial are to be applauded for their trial design. They have understood, and tried to avoid, three forms of bias which can make a screening program looks like it is working - when it isn't. These biases have had an impact in the field of prostate and breast cancer screening also - where recent evidence suggests that benefits of screening in some populations (for example women aged 40-50) may have been overstated.

Imagine two people with very small, slow growing, early lung cancers attend different hospitals with indigestion, and are seen by different doctors who manage them independently. One doctor, on the barest provocation, arranges a CT chest for his patient and a small tumour is seen. The other patient does not undergo CT chest. After a run of investigations the first patient has his cancer removed and is followed up for 5 years before being declared free of disease. The second patient is discharged home, but 5 years later presents to his doctor coughing up blood - and a large lung cancer is found on chest xray. He too is treated surgically. Two years later, both patients present to their independent doctors with weight loss and abdominal pain. They are found to have distant spread of cancer and both die 6 months later. The first patient, it seems, survived 7.5 years from the time of diagnosis, the second only 2.5 years. Increasing survival from diagnosis for a lung cancer looks like a good thing, but in this instance survival may not really have been increased; both had cancer at time zero, but only one was diagnosed. This lead to an appearance of increased survival when the cancer was just diagnosed earlier. We call this lead time bias.

The second form of bias is like it. Suppose that a screening program only picks up slow-growing tumours. Suppose aggressive tumours generally make their presence felt clinically within about 6 months and are picked up clinically, and therefore not on screening CT. If a trial predominantly picks up slow-growing tumours then it is possible that a trial will seem to indicate increased survival time in patients undergoing screening only because they are the ones with all the slow-growing tumours. this is called 'length bias'.


Finally, lung cancer prevalence increases with age. It is likely that a number of older people die with lung cancer, rather than from it. This was certainly the finding in the recent Dante trial, the subject of the previous blog. A trial of LDCT screening may pick up, and 'cure', a number of indolent tumours that were never going to make their presence felt anyway. This is 'overdiagnosis bias'.

To overcome these biases it is very important that trials of screening programs are run in a randomised and controlled way. There must be a control group managed in 'usual' fashion. The results of a screening program cannot be compared to historical controls/cancer survival data. And they must be run over an adequate number of years to demonstrate if there really is an overall survival benefit. After all, a screening program that doesn't result in less people really dying from lung cancer, while it may serve to employ lots of people in medical jobs, is in essence a waste of time.

Andrew

Lung cancer screening

Why are we not screening for lung cancer?

So began an editorial in a recent edition of 'The Blue Journal'. In this particular edition, an Italian group was reporting on the DANTE trial, which investigated - in a randomised and controlled structure - the use of low dose CT scanning (LDCT) as a screening tool for lung cancer.

Now, although - as previously blogged - lung cancer is the leading cause of cancer death in our community, discussions about lung cancer screening don't rate a mention in the mainstream news. (Contrast this with prostate, breast, cervical and bowel cancer for example).

Efforts to determine whether our new, super-duper, multi-camera CT scanners can be utilised to screen for lung cancer have - to date - fallen over at the first hurdle. While they have demonstrated, repeatedly, that if you perform CT scans on lots of middle-aged smokers you identify lots of asymptomatic, early, curable tumours they have not yet proven that taking out these tumours saves lives.

The recent study has struggled at the same point.

What did they do? A total of 2,472 men aged 60 to 75 years, with at least a 20 pkt year smoking history (a packet a day for 20 years equivalent) were randomised to either a baseline LDCT scan and annual LDCT scans over 5 years, or else a baseline chest xray with annual clinical review. The current data cover follow up over a mean of 33 months (ie not a very long time yet).

What did they find? They found 60 patients (4.70%) with lung cancer in the LDCT group (63 cancers in total - some patients had more than one). Twenty-eight cancers were found in the initial scan ( ie over 2% of these people had cancers they didn't know about to begin with ), 25 were found on subsequent scans and ten were found because people developed symptoms between their annual scans. In the control group, they found 36 cancers in 34 patients; 8 at basline, 3 at routine review and the others because patients developed symptoms.

What did they do next? Lots of intervention! Thirty-nine of the 60 patients in the LDCT arm with cancer had resections, and of these 36 were complete resection. In the control group it was 18 of 34 resected, 17 completely. In the LDCT group there were 96 invasive procedures, vs 36 in the control group. As the investigators put it ''we performed three times as many invasive procedures and found twice as many lung cancer cases with LDCT than without it, ...(but) .. the absolute numbers of advanced and lethal lung cancer cases were unfortunately identical in the two arms.....moreover a significant proportion of major surgical procedures (13%) were performed for pulmonary lesions that ultimately turned out to be benign..."

What happened next after all that intervention? Mortality rates in the groups are identical to date. Put in plain English, the same number of people died in each arm of the study.

So, LDCT screening for lung cancer in asymptomatic patients with no history of cancer detects nearly twice as many cancers as a 'chest xray and annual specialist review' approach, leads to a raft of invasive and expensive interventions, and has not been proven to save any lives. Yet.

Andrew

Bronchial Provocation Testing

In recent years bronchial provocation tests have been developed in an attempt to enable clinicians to identify asthma more accurately. These tests have been limited in their use to pulmonary function laboratories because many require specialized equipment or specially trained staff. There are two broad categories of bronchial provocation test, “direct” and “indirect” challenge tests.
Direct challenge tests use pharmacological agents such as histamine or methacholine that act on specific receptors on the bronchial smooth muscle causing it to contract. Indirect challenge tests such as exercise, eucapnic hyperpnea (EVH), adenosine monophosphate (AMP), hypertonic saline or inhaled mannitol (which is what we use in our Lab) work by triggering the release of inflammatory mediators that in turn cause bronchial smooth muscle to contract in sensitive individuals.
We recently enjoyed a visit from Stuart Jack (pictured), the Territory Manager for CareFusion Australia & New Zealand who demonstrated the eucapnic hyperpnea (EVH) kit. EVH is regarded as the “gold standard” challenge to identify exercise-induced asthma particularly in elite athletes. It was developed because clinicians could not be certain that subjects undergoing standard exercise testing were exercising at a sufficiently high intensity to provoke exercise induced asthma. EVH involves the inhalation of dry air with added CO2 (5% CO2 21% O2 74% N2) for 6 minutes at a target ventilation rate based on the subjects FEV1.
Thanks Stuart for a very entertaining and informative visit.
Vanessa

Aspergillus - the prodigal picture

Several weeks ago I blogged about chronic invasive aspergillosis (chronic nectrotising aspergillosis as per the accompanying picture) in COPD / emphysema. The adjacent picture, which has just emerged from the archives of my previous talks and which was borrowed from a forgotten journal article, provides a very helpful schema for remembering how various aspergillus diseases relate to the host (patient) immune response. Thought it was worth posting all by itself.

Andrew

Internet addiction and sleepiness

Tomorrow marks the annual Regional Sleep Medicine day conference, this year being held at Portland District Health. While reading around a case I wish to present I came across some interesting, and sobering, new research on the impact of internet addiction and sleep.

It has been suggested that internet addiction may be an epidemic in the twentyfirst century. A recent study published in the 'Psychiatry and Clinical Neurosciences (2009; 63:455-462) surveyed 2336 high school students in a particular school district in South Korea - that number representing an 87% response rate. Using Young's internet addiction test (everyone should do it just once), 2.5% of boys were found to be internet-addicted, with 53.7% possibly addicted. For girls, the figures were 1.9% and 38.7% respectively.

Excessive daytime sleepiness (EDS) was defined as an Epworth Sleepiness Scale score of more than 10 - which is pretty bad for an adolescent. Using that criterion, and controlling for duration of internet use and sleep time, age, gender, smoking status, painkiller use, symptoms of insomnia, witnessed apnoeas and nightmares the odds ratio for EDS in internet addicts was 5.2(95% CI 2.7 to 10.2) when compared with non-addicts. That means that internet addicts were 5 times more likely to be excessively sleepy in the daytime than non addicts. There was a stepwise increase in prevalence of daytime sleepiness from non-addicts to possible addicts to addicts (7.9%, 13.5% and 28.6% when controlling for the above factors respectively). The attached table shows the increased incidence when controlled for the above associated factors (black) as opposed with the raw initial data.

What has me worried more is that there was a stastically significant increase in prevalence of every sleep problem on the questionnaire, following the same 'J-curve'. This included difficulties with initiation and maintenance of sleep, wakening early in the morning, 'insomnia symptoms', snoring, witnessed apnoeas ( a huge 11% of teen internet addicts), teeth grinding and nightmares.

I think that internet addiction will turn out to be a significant marker for other sleep problems and an independent cause of daytime sleepiness - perhaps by leading to hypervigilance during sleep. Sleep specialists and GPs should consider screening all of our adolescent patients for this - provied we can back this up wth strategies to assist in countering the addiction in those who are 'addicted' and 'possibly addicted'.

Watch this space!

Andrew

The AAPM Conference

The Australian Association of Practice Managers conference was held this month in Melbourne and I attended for one day. As we have a keen interest in being a paperless office the presentation relating to this showed me that we are very well structured and compliant to this stream of office procedure and found that there are several technology advances that we can adapt to improve even more. Life without paper is fantastic.

Our favourite office adaptation this month was the installation of the headsets for our reception staff, so easy to type and talk.

Maureen

Buying a CPAP machine

Part of my role as one of the Practice Nurses here at Regional Respiratory Medicine is to assist people who have been diagnosed as having Obstructive Sleep Apnoea (OSA) to get started on CPAP therapy.

CPAP stands for Continuous Positive Airway Pressure. Basically this is a pump that delivers air (not oxygen) at a fixed pressure through your nose via a mask to keep your upper airway open when sleeping. The idea is that this allows you to then have better quality sleep, which then has the flow on effect of more energy during the day. It does much more than this for your health in the long term, including decreasing your risk of having a heart attack in the future just to name one! But this is not what I want to focus on.

I find that when people are ready to buy their own machine, there is one common question that I get asked rather frequently –

“What sort of machine should I get?”

Well, my advice to people is always the same. I cannot favor or promote any particular CPAP company / machine over over another but generally; you can’t go wrong with the machines on offer out there today as they all will do the same thing. Advances in technology mean that machines of today have been designed for ease of use and comfort, combined with the latest software to record data.

There are a couple of things you might want to consider aside from cost (which is another commonly asked question).

Firstly, consider purchasing a machine that has an inbuilt humidification feature or the option of attaching one at a later date. Until you have tried out a machine it is hard to say for sure if this is a feature that you will or won’t use. However, as we all know, things can and do change - I believe it is better to have this option available.

Secondly, ask about the data which is able to be downloaded from each machine. Some machines provide basic compliance data, while other machines provide more detailed information. Again all information provided is useful to your Consultant during a review. More important than this will be how YOU are finding using your CPAP machine.

At the end of the day, all CPAP machines do the same job and it gets down to personal preference in ease of use, transportability, and cost.

All the best,

Lisa

The 'beta-agonist paradox'

"Clinicians need to be aware of how to identify and manage patients for whom beta-agonist treatment is a problem rather than a solution. They constitute a small but important sub-group of patients with difficult asthma".

As a consequence of recent conversations with hospital staff in Hamilton about our management of a patient with difficult asthma, I thought it would be appropriate to post a blog on this topic. Although beta agonists (such as salbutamol, terbutaline, eformoterol, salbutamol) are essential tools in the management of asthma - either as 'reliever' medications or as part of a 'preventer / maintenance' regime, their role in chronic persistent asthma may not be as simple as we would like to think.

The above quote is from Dr. D.Robin Taylor, at the University of Otago in Dunedin, New Zealand. Dr Taylor was at the coal-face of this issue in New Zealand in the early 1990s, when use of the beta-agonist fenoterol was associated with a spike in asthma related deaths which only ended when that medication was taken off the market. Although the Wikipedia entry on this drug suggests that the surge in deaths was all due to cardiac side effects from patients irresponsibly managing their asthma with massive doses of the medication out of hospital, the issue may not be quite that simple. The 'epidemic' of asthma deaths associated with that medication has helped to generate persistent research into the hypothesis that beta-agonists may paradoxically worsen asthma control in some situations.

I first heard Dr Taylor on this issue as a registrar back in 2002. I was struck by his description of a difficult asthmatic patient who was using bucket-loads of salbutamol as reliever, and who did not improve until - in a carefully managed hospital environment - that beta-agonist was withdrawn. The peak flow record was instructive and convincing.

In a recent issue of the American Journal of Respiratory and Critical Care Medicine (Vol 179, pp976-978) Dr Taylor's summary of evidence and opinion on the question of whether beta-agonists may sometimes be harmful has been published - as a 'clinical commentary'. (The material was initially presented at the 2008 American Thoracic Society conference).

The points I underlined in my copy are as follows:

• the FDA in the USA issued, in 2005, a 'black box' warning about the safety of long acting beta agonists eformoterol and salmeterol. The majority of the relevant committee felt that these medications should only be used in combination with an inhaled corticosteroid (ICS) in treatment of asthma, as the risk of treatment with the beta-agonist alone, without ICS, outweighed the benefit).
• beta-agonists are, if used consistently, pro-inflammatory in human airways (both in-vitro and in-vivo studies). ICS, which are anti-inflammatory, may therefore protect against adverse effects from beta-agonists. To my mind, however, this situation is far from ideal - i.e. that we would need to need to use a medication to treat a medication related side effect.
• although acute use of beta-agonists leads to airway smooth muscle relaxation, in a mouse model chronic beta-agonist stimulation leads to increased airway smooth muscle contractility - and potentially a heightened response to an asthma trigger (i.e. another mechanism - apart from the pro-inflammatory effects - by which the medication may make the disease worse!) "It would appear that acute and chronic B-agonist effects are not the same thing".

So there is evidence that persistent overuse of beta-agonists may cause, within the airways, a process that is difficult/impossible to distinguish from a worsening of the underlying disease process. Now that takes some mulling over!

Two quotes from Dr Taylor's article to summarize:

"...monotherapy with beta-agonists should clearly be avoided, and the use of combination inhalers to some extent guards against the possibility of LABA-related adverse effects. However, the concomitant use of ICS does not mean that adverse effects of beta-agonist are a non-issue: there is likely to be a threshold for adverse effects in relation to total beta-agonist exposure that may be crossed even when patients are taking ...ICS".

"Good asthma management should include appropriate diagnosis and treatment of beta-agonist toxicity......the characteristic features include unstable or intractable asthma with evidence of psychological and/or pharmacological beta-agonist inhaler dependence. The need for frequent "reliever" ... should cause alarm bells to ring, especially if the treatment yields progressively diminishing benefits in a patient with severe asthma (my emphasis)".

Now, I do not want any of my patients to simply stop using their reliever medication. However, we clearly must have a 'zero tolerance' approach to treating asthma with regular beta-agonist alone. Inhaled corticosteroids are essential. If asthma control is difficult then the first priority should be to review the delivery technique for any 'preventer' medication, as even the most competent patients often make a hash of it. But if, in spite of this, more and more salbutamol is required by a patient, with less and less response, then we should ask whether the beta-agonist might be part of the problem - and be ready to do something about that.

Andrew