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

A number of factors conspired yesterday to create our best and most productive day in Mildura to date.

Ms Mills was happy with the ride. Which was just as well, as she was bringing the mobile lung function lab with her. Our gas cylinder was too big for the plane, so had been sent on ahead, by road.

The bigger plane halved the duration of the flight by comparison with the last trip. That, and the longer daylight hours (although the Chief told us he could fly this plane with his eyes closed in the dark) meant we could fit in a full working day in Mildura.

Which was just as well. Ms Mills had the lung function lab operational in no time (she really is very good at her job). The cylinder had arrived, with attached regulator only slightly mangled but useable. After a trio of quick tests the gear was hurriedly, but in expert fashion, dismantled and we hastened to present at lunch-time meeting of the Tristar - 'nice place you've got here. Sure it's big enough?' - Medical Group clinical staff. Sadly this meant that our lunch venue was predetermined and not up to its usual standard.

Every patient turned up, thanks to the efforts of the local Irish nurse. We saw some patients from outside the aboriginal health service. The tests all worked and were all useful. The local Tristar GPs were very interested that we have helped the aboriginal health service establish a home sleep study service, which the health service is happy to open up to outside referrals. I am looking forward to continuing to offer the lung function testing service from the same base.

All-in-all it was a very satisfactory day, capped off by a picturesque flight home over a wet agrarian landscape.

Andrew

Invasive aspergillosis in COPD

Patients with COPD can, as previously blogged, suffer a range of illnesses caused by the ubiquitous fungus, Aspergillus fumigatus. Of all of these, chronic invasive aspergillosis is the entity I have seen least. Until the last few days.

When I first began to get a handle on aspergillus disease, I thought that invasive aspergillosis was the domain of bone-marrow transplant recipients. It turns out that patients with COPD (particularly emphysema) develop a more indolent form of the disease which looks radiologically pretty similar. However, the prevalence of this condition amongst patients with COPD is unknown. Mortality rates are quoted as between 72 and 95%. And they are not falling, in contrast with mortality rates amongst bone-marrow transplant recipients with invasive aspergillosis..

We should consider this diagnosis in all patients with COPD who have progressive lung infiltrates, or pneumonia which fails to resolve as it should after standard antibiotics.

I have just read a helpful review article in a COPD journal on this topic, and have been reminded that aspergillus spores are tiny - about 2-3microns. When inhaled they end up in the furthest reaches of the respiratory tree - the alveoli. There they can germinate into hyphae which - unless they are mopped up by polymorphonuclear cells - can become invasive.

People with COPD are prone to invasive aspergillosis becuause:
- they are often malnourished;
- they have impaired airway ciliary function;
- consumption of broad spectrum antibiotics may have altered the airway microflora to benefit the fungus;
- aspergillus may be able to grow in a biofilm in these patients, like pseudomonas and haemophilus;
- use of corticosteroids has impaired neutrophil function and altered the distribution of neutrophils.

Diagnosis of invasive aspergillosis can be regarded as either proven, probable or possible. To prove the diagnosis requires demonstration of hyphae in tissue - ie a biopsy, which might carry with it considerable morbidity in these patients. A probable diagnosis can be based on a coalescence of appropriate host, clinical and mycological factors (eg the patient is in an at risk group with the right presentation, the CT scan looks right and the fungus is there - in repeated culture or in a bronchoscopy specimen). It is reasonable to embark on treatment based on a probable - rather than proven - diagnosis (sounding very similar here to the 'clinical conference consensus' vs 'pathology gold standard' diagnostic conversation in fibrosing lung disease).

Voriconazole should probably be the first line treatment of this condition. In Australia, however, Voriconazole is available on the PBS only for patients with invasive aspergillosis who have not tolerated Amphotericin B. These criteria were not drawn up for the COPD patients with this diagnosis who are generally ambulatory, slowly losing weight, progressively breathless but at home. Rather they were established with the sick bone-marrow transplant patient in mind. It makes far more sense to initiate the ambulatory COPD patients on oral Voriconazole than to admit them to hospital for a protracted course of amphotericin B. We are, however, going to have to do a lot more research with these patients even to demonstrate that they are a significant population before that realisation trickles through to the PBS.

Andrew

COPD and stiff arteries

COPD is increasingly prevalent, and an increasingly common cause of death. It is currently the fourth leading cause of death in the USA. Patients with COPD often die of other diseases, such as cardiac disease - which is currently the leading cause of death in that country and ours. In the last 10 years there has been increasing recognition that COPD is a disease with systemic effects, beyond the lungs. Death from ischaemic heart disease has been associated with lowered FEV1 (a fivefold in death from AMI as FEV1 fell from 109 to 88% of predicted in a US population). However, establishing how COPD may be a discrete risk factor in cardiovascular disease, distinct from the common risk factor of cigarette smoking, is proving difficult.

A paper in the September 15th edition of the AJRCCM (180 pp513-520) has shed some light on this subject, and scored an accompanying editorial. In this study 18 men with COPD were matched (smoking history and age) with 17 controls who did not have COPD. Pulse wave velocity and pulse wave analysis at carotid, radial and femoral arteries indicate significantly increased arterial stiffness in the subjects with COPD. A complicated array of tests of endothelial function did not indicate any difference between the groups.

Central arterial stiffness is, according to the article and the editorial, a predictor of cardiovascular mortality. It is usually due to either smooth muscle or endothelial dysfunction or elastin loss - or a combination of all three. Given the equivalent endothelial function between the groups in this study, the authors surmised that COPD may lead to elastin degradation in arterial walls. This may be a means by which COPD leads to increased cardiovascular risk independent of other risk factors.

Other studies have suggested that there is endothelial dysfunction in COPD, and that it is worse in patients with lower FEV1 or more extensive emphysema - evidence which is not in agreement with that presented in the recent study. Obviously more work - much more work -needs to be done (I hate hearing that line at conferences, but there it is!)

Anyway, the most tantalising part of the picture is the question of clinical relevance. All of this cardiovascular science is news to me, but it turns out that simvastatin has been shown to reduce arterial stiffness in patients with rheumatoid arthritis. There is also some evidence that statins reduce lung parenchymal destruction and pulmonary vascular remodelling in smoking-related lung disease. So although this is far from being evidence based medicine, we might have some reason to anticipate statins becoming part of routine respiratory medicine in the future.

Andrew

Australasian Sleep Association conference

I've just enjoyed a day at the Sofitel on Collins - not a bad location for the Australasian Sleep Association conference. A good opportunity to catch up with the latest directions in research, as well as to reconnect with colleagues from around the country. I'm tweeting my responses to the presentations as I go - so if anyone is interested, feel free to check out my take on the ASA conference this year @DrBradbeer on Twitter.
Andrew

Lab news

With the advent of day light saving and spring in the air I was looking forward to a walk up to the Frances Hewett Community Health Centre where I had been invited to speak at the monthly meeting of the Respiratory Support Group.
Alas in the freezing cold and blistering rain I drove the short distance not expecting a large turnout. To my surprise a dedicated group had braved the conditions to enjoy the support of a group of individuals including their families and carers who suffer from a lung condition.
My objectives with my power point presentation were to review basic pulmonary anatomy and physiology, give an understanding of the reasons lung function tests are performed, describe the technique and basic interpretation of spirometry and know how lung function tests are clinically applied.
A number of the group had undergone a lung function test at some stage in their lives including the visiting nursing student from Latrobe who during her training had undergone a lung function test and all commented on the effort required to perform an acceptable test.
The presentation provoked some lively discussion. The most interesting and challenging question of the session was ‘how long do you think you would have to train to be a freediver in a competitive apnea sport?’ I am hoping this is not a reflection of how those in the group have felt whilst undergoing a lung function test in our lab?
To quote a comment in the latest ANZSRS newsletter ‘letting the mind wander like this is healthy as long as the piece of string remains attached so that it can find its way back’
Vanessa

Practice Nurses

This week an additional practice nurse began working at RRM. This will enable full time nurse support. The role of the practice nurse has evolved over the past eighteen months to the point where its difficult to imagine how we ever managed without one! Having full time nurse support increases the quality of care for patients and provides essential support in patient education for respiratory and sleep conditions.

One of our consulting rooms now is totally dedicated to the nurses. The practice continues to grow and there is a need to employ new staff which is fantastic, only one issue where are we going to put everybody!

Jessica

High resolution CT scanning and IPF

With the recent arrival of a new CT scanner in Hamilton, I've been reading an article in this month's Respirology journal by a group from the University of Michigan. This review recaps evidence and their clinical practice when it comes to diagnosis of idiopathic pulmonary fibrosis.

An editorial in the same journal reiterates that there are, as yet, no proven treatments for this condition - although colleagues at the Royal Melbourne Hospital and The Alfred Hospital in Melbourne are currently participating in a trial of two novel endothelin receptor antagonists (like Bosentan, currently used to trat pulmonary hypertension) in IPF. (These trials are currently enrolling patients with IPF, with minimal honeycomb change and with a forced vital capacity on spirometry of over 50% predicted).

Idiopathic pulmonary fibrosis is a diagnosis now often made without lung biopsy. A multidisciplinary evaluation must exclude known causes of pulmonary fibrosis which can result in the same radiological appearance - such as pulmonary fibrosis associated with connective tissue disease (eg rheumatoid arthritis or scleroderma); chronic hypersensitivity pneumonitis; or asbestosis - and must include a high resolution CT scan of the chest. If the CT appearance is agreed to demonstrate features of usual interstitial pneumonia - which is the pathological/radiological appearance in idiopathic pulmonary fibrosis - in the absence of an underlying cause then IPF is diagnosed.

As simple as that! The major centres / city hospitals tell us, however, that there is a lot of operator variability outside of the major centres. Which means that it is important for people with this condition to be evaluated in an environment where people really know their stuff. Or perhaps, according to the major centres, all patients with IPF should be evaluated in the major centres.

The following table was offered as, in my opinion, a quite useful summary of the important radiological features of usual interstitial pneumonia:

Definite usual interstitial pneumonia

• subpleural basal distribution
• predominant honeycomb
• interlobular septal thickening
• traction bronchiectasis
• no predominant ground glass attenuation

Consistent with usual interstitial pneumonia

• subpleural, basal distribution
• minimal or equivocal honeycomb
• interlobular septal thickening
• traction bronchiectasis
• no predominant ground glass attenuation

Suggestive of alternate diagnosis

• No honeycomb, with one or more of the following as the predominant HRCT finding;
• upper or mid lung distribution
• peribronchovascular distribution
• ground glass attenuation
• micronodules
• discrete cysts
• air trapping
• consolidation

This seems to be the poster they hang on the wall of the registrars' reporting room at Ann Arbor. I'll have to run it past my local radiology colleagues and see what they think - but it looks pretty good to me.

Supports for patients with a diagnosis of pulmonary fibrosis are lacking in the Australian community. The Pulmonary Fibrosis Foundation in the USA runs a pretty informative website and supports good research. I am not aware of a comparable group in Australia.

Andrew