First ever world spirometry day

On Thursday October 14^th, free spirometry will be offered world wide. This event will be one of the top opportunities to raise awareness about lung health through the public and the media. The European Respiratory Society and the European Lung Foundation will coordinate the organizing of the event.

Spirometry is the most common method for testing lung function. It is simple, quick and non invasive. The test specifically measures the amount (volume) and/or speed (flow) of air that can be inhaled and exhaled by the lungs. Spirometry is an important tool and is helpful in assessing conditions such as asthma and pulmonary fibrosis and perhaps most importantly chronic obstructive pulmonary disease.

These spirometry events have a dual purpose. On the one hand they have a public health impact enabling many people who have not been tested previously to have their lung function measured. In Berlin approximately 20% of people tested were advised to visit their doctor for further examination. On the other hand, these events provide a focus on lung health and lung disease, facilitating increased public awareness.

The results of six of these events in summary found that in over 12,500 people tested, nearly 20% has some degree of airway obstruction, nearly 50% were smokers and 5% had asthma.

The organizers of these events conclude that spirometry testing is a useful way to detect airway obstruction at an early stage in life, in a large proportion of residents.

On World Spirometry Day, Manse Medical will organize and run an event to offering free spirometry. CareFusion and Bird Heath Care have generously offered support in the way of filters and noseclips for the event.

More details will be posted nearer to the date.

Vanessa

WHAT ARE YOU EATING FOR A GOOD NIGHTS SLEEP?

I recently read a magazine article which focused on sleep and what factors affect our ability to get a good nights rest. We all know that there are many things in our daily life which will have an impact on this area – stress, anxiety, work hours, illness, drugs, exercise, social habits, babies, pain, body temperature, diet, and the list goes on….

I am going to focus in part on food. Research tells us that there are certain foods that can help you get to sleep. This list includes foods such as bananas, nuts and peanut butter, milk, apples, fish, yogurt, cheese (particularly cheddar, Swiss, gruyere), soy products, lettuce (think The Tale of Peter Rabbit and the Flopsy Bunnies – soporific effect) and there are certainly others that I have missed. Why are these foods recommended over others?

The thing that these foods have in common is that they are high in something called tryptophan. Tryptophan is an amino acid which the body cannot make itself but is needed by our nerve cells to make serotonin. Serotonin is a brain neurotransmitter that helps promote feelings of relaxation, calmness and sleepiness. We need enough of this hormone serotonin in our system to get to sleep and this in turn is dependent on our tryptophan levels. Tryptophan is also in competition with other amino acids to reach the brain.

Interestingly, it is NOT recommended that we load ourselves up with these magic sleep inducing foods.

It is important to understand that studies have shown that tryptophan helps with only one phase of our sleep cycle – that of getting to sleep. It won’t necessarily keep you asleep.

Our typical sleep cycle is divided into REM and non- REM sleep. REM (or rapid eye movement) is the stage of sleep when we dream. Non-REM sleep is divided into four stages of sleep – stage 1 being lighter sleep through to progressively deeper stage 4 sleep, followed by REM. This cycle usually takes about 90 - 120 minutes, and we have about 4 or 5 of these cycles a night, with the amount of REM increasing in length with each cycle.

Excess tryptophan has in fact been shown to increase the amount non-REM sleep and actually decrease REM sleep time. Deep sleep is an important time for the body to renew itself and REM sleep an important time for the brain to process and sort information. It is linked to both memory and production of certain neurotransmitters like serotonin and dopamine which directly affect our day time mood.

From my research, there seems to be a general consensus about meals for sleep.
It is recommended that you eat a lighter rather than heavier evening meal about 4 hours prior to your usual bed time so that you body is not working overtime at active digestion.

Evidence shows that eating a small carbohydrate rich snack with tryptophan containing foods (a protein) 1 -2 hours prior to bed to be beneficial. Carbohydrate consumption stimulates the release of insulin which assists in transporting those competing amino acids from the bloodstream, making tryptophan more readily available.
Select your proteins (and portions) wisely as many animal foods high in tryptophan are also high in other amino acids (like tyrosine) which potentially stimulate the brain with the release of adrenalin for example and can have the opposite desired effect.

So that warm glass of milk as a snack before bedtime is a good idea to help you get to sleep but only if you are taking a considered approach to your overall dietary habits (not just focusing on specific foods) and addressing any other potential sleep stressors.
For more information on setting yourself up for a good nights sleep and creating healthy sleep habits, you can download our sleep hygiene recommendations available on our website.

Lisa

A chest x-ray for sore ankles?

A young male patient presents with painful, inflamed ankles and is ordered a chest x-ray. He thinks maybe the doc didn’t quite hear him right.

But possibly his doctor is right on to what is happening and suspects Lofgren’s syndrome (named after Swedish Researcher Sven Lofgren 1910-1978).

This is a type of sub acute sarcoidosis which may present with erythema nodosum (tender red nodules), bilateral hilar adenopathy (enlarged lymph nodes on the border of the lungs), arthritis and fever.

The cause is unknown but environmental triggers have been implicated, combined with a genetic susceptibility. There is variable instances of this disease around the world but you may be more vulnerable if you are Irish, Scandinavian, African or Puerto Rican and less prone if Japanese. There has also been some association with those working in specific professions including health care workers, school teachers, agricultural workers exposed to agricultural dust, insecticides, pesticides and moulds, suppliers of building materials, hardware or gardening materials and firefighters.

Other risk factors are being female (85%), being young to middle age (mean age of disease is 35) and seasonal considerations, with the disease being more common in the spring in the Northern Hemisphere.

The patient may present with arthralgia, cough or shortness of breath, fever or malaise along with erythema nodosum (more likely if female) and bilateral ankle inflammation (more likely if male).

The diagnosis can be made with the assistance of a chest x-ray which will show mediastinal lymphadenopathy or pulmonary infiltration, lung function tests which may indicate decreased forced vital capacity, as well as elevated serum calcium and ACE levels. A lymph node biopsy may also confirm the diagnosis.

Generally the disease has a good prognosis and is usually benign and self limiting over a 6 month to 2 year period. Normal serum ACE levels at diagnosis and a particular HLA type (DRB1*03 positive as opposed to negative which points to a non resolving disease) are good prognostic markers

Management is supportive, with use of non steroidal anti inflammatories and short term bed rest. Occasionally corticosteroids will be given for severe symptoms such as severe arthritis.

Differential diagnoses may include infection, cellulitis, osteomyelitis, gout, polyarthritis, lymphoma, fungal infections, tuberculosis and bronchiogenic carcinoma to name a few.

But just remember that chest x-ray for anyone presenting with inflammatory ankle symptoms.

Irene

Lung cancer chemotherapy - Iressa is back.

Iressa / Gefitinib was the great white hope on the lung cancer scene about 6 years ago, then faded into obscurity for a while. The problem was that the ISEL study did not demonstrate that this oral chemotherapeutic agent ( a tyrosine kinase inhibitor) was better than placebo in terms of survival benefit. There was, however, evidence of tumour response. That is, tumours seemed to get smaller, but people didn't live longer.

Further studies have demonstrated benefit in more select patient groups - much to the relief, I am sure, of AztraZeneca. The drug has recently been licensed in Australia for use in patients with locally advanced or metastatic non-small cell lung cancer if their tumours express activating mutations of the epidermal growth factor (EGFR) tyrosine kinase.

The IPASS trial, conducted in Asia, demonstrated that, in patients with a previous light smoking or non-smoking history, who had mutations of the EGFR tyrosine kinase and who had not received previous chemotherapy, Iressa was superior to a combination of carboplatin/paclitaxel in terms of disease free survival (9.5 vs 6.3 months). The INTEREST trial demonstrated equivalency of Iressa when compared with docetaxal in patients with locally advanced or metastatic NSCLC who had previously received platinum-based chemotherapy.

It's noteworthy that Iressa is now indicated as a first line chemotherapy in appropriately selected patients (ie those meeting the above criteria). Tarceva/Erlotinib, another EGFR tyrosine kinase inhibitor, is still only licensed for patients whose NSCLC has progressed in spite of first-line platinum based chemotherapy (ie second line). As far as I am aware.

It is bound to become more clear, over the next few months / years, exactly which patients do benefit from these medications - and others like them. Perhaps this will even give us a clearer indication of prognosis in patients with lung cancer.

Andrew

To nap or not to nap?

The concept of sleep inertia has presented it's self to me a couple of times in the past few weeks. Once when I mentioned to a sleep scientist that I am like 'a bear with a sore head' if I have a day time nap (the cause most likely sleep inertia). Another time was when I was talking to an emergency services worker, discussing the pro's and con's of napping during night shift. I also saw a promo for a morning show that was airing a segment on 'Napping the key to health and happiness' but I missed watching this.

So what are the pro's and con's of napping?
One of the cons can be sleep inertia. This is especially relevant to emergency services workers who may take naps during night shift. Sleep inertia is bascially a temporary state of lowered arousal occurring immediately after awakening from sleep and producing a temporary decrease in cognitive performance. Sleep inertia can be influenced by factors such as the duration of prior sleep, and the sleep stage prior to awakening. Abrupt awakening during a slow wave sleep (stage 3 and 4) episode produces more sleep inertia than awakening in stage 1 or 2, REM sleep being intermediate. Studies have demonstrated that sleep inertia can last from 1 min to 4 h but usually last around 15 to 30min. The practical implications for those working in our emergency service is that being woken to respond to an immediate emergency gives them no time to recover from the effects of sleep inertia. Being awaken for deep NREM sleep has been shown to decrease reaction time which is highly dangerous for those driving (fire and ambulance crews) and health professionals responding to an emergency.

Conversely, the benefits of a power nap (15 to 30 minutes) have been well document as a way to ward off fatigue and improve cognitive function. There is still a level of sleep inertia but this can be minimised by a short nap (stage 1&2) and having adequate time to 'wake up' after this nap before preforming any important tasks.

Health and Safety recommendations such as these from the Queensland Government reinforce this with recommendations sleep inertia can be minimised for workers who are on-call for emergencies by the following steps;

• Minimising naps taken at work that exceed 40 minutes; and
• Planning for recovery times of up to 30 minutes for workers who may be subject to sleep inertia, before they are to perform hazardous tasks.

Jessica

Home sleep study update

A couple of years ago, in 2008, there was a moment of angst in the sleep-medicine specialist field, when Medicare decreed that they were no longer going to pay for home sleep studies.

At that time, there was no ‘item number’ to cover a home sleep study. The place of home sleep studies in the diagnosis and management of obstructive sleep apnoea, let alone other sleep disorders, had been examined in only a few studies in the literature and there was not a consensus from the community of specialist sleep physicians as to how and when these studies should be done.

Nevertheless, home sleep studies could be done and were being done. Aggressive expansion of home sleep study business models, some industry-driven (ie CPAP companies) and some physician-owned, was occurring. And it was occurring in the country.

From where I sit (that is, in Hamilton) the reason given for this expansion didn’t really hold water. City based specialists and companies were saying that home sleep studies needed to be done because patients such as mine needed access to services. Reading between the lines, that meant that it was easier to stay in the big cities and to negotiate with a chain of pharmacies to put 200 home sleep study devices in towns around the state than to negotiate with hospital administrators to set up state-of-the-art sleep labs, and to back them up with specialist consulting services. The resulting service was limited. The development of skills in regional centres was scant (pharmacy staff trained to put on leads). Medicare fees were drained from the country back to Melbourne, rather than reinvested locally (for example, in a local medical practice or sleep lab). When things got tricky, country people still had to travel to the city to see a sleep specialist. And the impression was given that sleep studies are easy. Like getting your blood pressure checked.

In spite of the above uncertainty, a review of the evidence did suggest that home sleep studies were useful in people with a very high clinical probability of having severe obstructive sleep apnoea. After careful consideration, we decided that it was a service that we should carefully offer, and so we established a handful of home sleep study outlets in our region. We considered the distinctives of our service to be; a sleep specialist reviewed every referral to ensure that a home sleep study is appropriate, prior to authorising performance of the home sleep study; analysis and reporting of the sleep study occur locally (it can’t be assumed that sleep study analysis for home sleep studies in Australia even occurs in Australia any more, with at least one of the major providers of home sleep studies outsourcing analysis of data to sleep scientists in India); the reporting sleep specialist always analyses the raw data (not just the analysis summary provided by the scientist); sleep specialist clinical review is available locally if required.

When Medicare declared a moratorium of sorts on home sleep studies I thought that sounded reasonable. Of course, with substantial business under threat the big providers of home sleep studies negotiated hard for an allowance to continue to provide home sleep studies as they already were. And that permission was granted, in October 2008, although with a much lower fee from medicare for the service, while the whole area was carefully reevaluated.

The Medical Services Advisory Committee has just reported to the Minister for Health after an evaluation of all the literature related to ‘unattended’, or home based, sleep studies. Eighty studies were identified, evaluating home sleep studies performed in ‘non-specialist’ (for example a GP clinic or pharmacy) setting, a ‘referral setting’ (ie referred to a specialist for the study) and a paediatric setting. (14, 60 and 6 studies applicable to each setting respectively).

The document reads:

The Committee recommended funding of Type 2 (unattended) studies in patients >18 years of age once within a 12 month period with the following conditions.
(a) the patient is referred for the investigation by a medical practitioner who has formed a reasonable clinical view that the patient has a high probability of having OSA
*[(b) the necessity for the investigation is determined by a qualified sleep medicine practitioner (as defined in the explanatory notes to the MBS) prior to the investigation;] [*referred study]
(c) a qualified sleep medicine practitioner has:
(i) established quality assurance procedures for the data acquisition; and
(ii) personally analysed the data and written the report;
(d) during a period of sleep, the investigation is a recording of a minimum of seven channels which must include continuous EEG, continuous ECG, airflow, thoraco‐abdominal movement , oxygen saturation; and two or more of EOG, chin EMG and body position.
(e) interpretation and report of the investigation (with analysis of sleep stage, arousals, respiratory events and assessment of clinically significant alterations in heart rate) are provided by a qualified sleep medicine practitioner based on reviewing the parameters recorded under (d) above.


The home sleep study service which we provide, and the business behind it (for example, who reports the sleep study, and how carefully is the data analysed by the sleep specialist, all of which is invisible to the ‘consumer”) meets all of the above requirements. We will continue to provide this service.

A home sleep study service in country towns does not, however, live up to our goal of providing a regional sleep medicine service which is equal to anything available in the major cities. Excellent inpatient sleep laboratories and availability of clinical expertise in sleep medicine (doctors, nurses, psychologists), along with access to therapeutic devices such as CPAP at reasonable prices, are all required. We’ve achieved a lot in this regard over the last 4 to 5 years, but there’s more on the agenda.

Andrew

Chill out and sleep

The title of this blog could refer to a couple of areas of sleep hygiene. One being body temperature and sleep, while the other relaxation and sleep. The former will be discussed.

Body temperature is an important factor in sleep onset. A drop in body temperature normally happens 1 to 1.5 hours prior to falling asleep. As the core body temperature drops (only a matter of .5 to 1 degree) people begin to feel sleepy signaling its time for bed.

One hypothesis is that in some insomniac subjects their core body temperature remains higher than is necessary to initiate and maintain sleep. Studies have been conducted looking at sleep and core body temperature throughout the night. It has been demonstrated that the trough in temperature occurs prior to the longest sleep period and studies with insomniacs show they may may be a limited ability to cool the core body temperature sufficiently for optimal sleep.

What does this means in a particle sense.

• taking a hot bath 90 minutes prior to bed may help reduce core body temperature, as once out of the bath temperature will drop quickly. Make sure this in not immediately prior to bed as there needs to be sufficient time for the bodies temperature to drop.
  
• Avoid strenuous exercise immediately prior to bed
• take notice of when you feel sleepy in the evening and heed these cues

Jessica

Tablets for OSA?

Are there any new treatments on the horizon for obstructive sleep apnoea?

Well, yes … and no. One reason we follow up our patients who have significant obstructive sleep apnoea is so that we can offer them the benefit of alternative therapy if they are unhappy with CPAP therapy. While there are no particularly exciting new options available at present, occasionally a paradigm-changing treatment possibility comes along. If there were a simple treatment available in tablet form for obstructive sleep apnoea, a treatment that caused no side effects, wouldn’t that be terrific?

Now, there’s no reason to get particularly excited – but I think some cause to be interested – in the results of a trial of two tablets, Ondansetron and Fluoxetine – which was published in Sleep journal at the start of this month.

Each of these medications works on serotonin receptors. Serotonin is a neurotransmitter – a chemical messenger between nerves. It is found in many places in the body. The authors of this study commented particularly on two of these sites, and their associated effects.

Firstly, serotonin in the brainstem can promote muscle tone in the muscles that dilate the upper airway when we are awake via 5-HT2 receptors. Secondly, other serotonin receptors (5-HT3) in the ‘nodose’ ganglion (great name) promote REM-related apnoea (cessation of breathing in REM sleep). The hypothesis was that if they could stimulate the former and block the latter receptor then they might be able to effectively treat OSA.

So they randomized 44 patients to treatment with either placebo, placebo plus ondansetron (which is an anti-nausea tablet and blocks 5-HT3 receptors) or fluoxetine (5-HT2 receptor agonist/stimulator and antidepressant) and ondansetron, in two doses – lower and higher.

Interestingly they found that the treatment was very well tolerated, and that treatment with the highest dose of medications in combination led to a reduction in apnoea-hypopnoea index of 13 respiratory events per hour, or 40.5% from baseline, by day 28 of treatment. There was no change on the placebo or ondansetron alone, and a tend towards change on the low dose combination.

I think these results represent a very interesting direction in investigation, which needs to be developed much more fully. Characteristics of patients in whom such a treatment may be beneficial will need to be clearly defined, and it certainly is too early to be recommending this treatment to anyone.

Serotonin agonists are commonly used in treatment of depression, and those of us who report sleep studies consider the possibility that they might have an impact on the severity of sleep-disordered breathing we observe while reporting (as well as on sleep quality in general). I suspect, however, that within a few years we will be treating some OSA patients with tablets that have minimal side effects.

Andrew

Sitting verus supine vital capacity

Whilst working in Mt Gambier recently one of our Respiratory Physicians, Dr Borta asked me to measure a patient’s supine vital capacity which is one of our less common noninvasive respiratory function test measures.

Evaluation of diaphragm strength can be accomplished by measuring the vital capacity in an upright or sitting position followed by a measurement made in the supine position.

Here Lisa, one of our Respiratory Nurses demonstrates the supine and sitting positions.

It is well established in healthy volunteers that lung volume and vital capacity decrease after moving from the upright to supine position. This phenomenon is thought to be due to the shifting of blood to the pulmonary vasculature, changes in the position of the diaphragm, and the weight of the abdominal viscera pressing against the diaphragm. In healthy adults, the FVC falls by approximately 7.5 ± 5.7%.This change is exaggerated in many patients with severe diaphragmatic weakness, though it has not been well evaluated in Amyotrophic Lateral Sclerosis (ALS) patients, the assessment of ΔFVC has been suggested as a screening test for diaphragmatic weakness.
Interpreting an increased reduction in vital capacity in the supine position as diaphragm dysfunction should be made cautiously if the patient’s body mass index is greater than 45 kg/m² as a reduction may not indicate diaphragm dysfunction, but rather an increase in the resistance to diaphragm descent.

Lechtzin et al. studied 25 patients with ALS and demonstrated that supine FVC is an excellent measure of diaphragmatic strength in patients with ALS. It is apparent that the diaphragm becomes weak well before the upright FVC is reduced but using the supine FVC < 75% predicted as a cutoff is a highly sensitive and specific measure of diaphragmatic weakness. Longitudinal studies need to be performed to determine whether supine FVC is a better predictor of future outcomes than measures currently in use. It is not known whether early detection of respiratory muscle weakness and intervention leads to improved outcomes in ALS but it will allow interventions to be developed that target mild respiratory impairment.

Vanessa

An evening @ Portland Sleep Lab

On Monday night I had the opportunity to spend a few hours at the Portland Sleep Lab working with Gerri. I have been there many times but never when the lab has been operating.

For those who have never been to the Portland District Hospital, where the sleep lab is based, the picture provided shows the wonderful view that can be seen from some rooms in the hospital. Not a bad place to spend a night!

Apart from the great views, the Portland Sleep lab is equipped with sophisticated technology. Operating the latest version of profusion (sleep study software package). Since January this year when the E-series from compumedics was installed the communication process between Hamilton and Portland sleep labs has been streamlined.

It's fantastic for Western Victoria to boast two high quality sleep laboratories operating within this region. Next on the agenda is a sleep laboratory in Dimboola to service our patients that come from the Wimmera.

More information about this in the coming weeks.....

Jessica

Health Promotion and Education

Sometimes I give an instruction to a patient during a lung function test and am amazed when the patient does almost the opposite of what I requested. This has lead me down an interesting path of looking at the teaching-learning process in relation to adult learners.

The aim of the information and education we provide is to reducing levels of psychological distress, aid compliance and ultimately patient satisfaction (Poroch, 1995). The more informed the person is, the more likely they will have favorable health outcomes and experience less psychological stress) Joanna Briggs Institute, 2000).

Teaching is more then just imparting knowledge, as learning is more than simply listening to instructions; we want our patients to understand the information. According to O’Brien (2004), the skills required for effective health education include knowledge of the subject matter, communication skills and empathy. Barriers are time constraints, lack of resources and knowledge, disagreement with the patient regarding their expectations, powerlessness, frustration and cultural differences. These barriers of course can be overcome by a planned approach where realistic goals have been agreed upon.
We need to be able to think critically and make clinical judgments in order to meet our patients’ needs. This can be achieved by asking the patient if words are understood and welcoming questions whilst observing non-verbal cues as well as assessing a patient’s learning needs and preferred learning style whether it be visual, auditory or physical. Patient information needs are highly diverse and shaped by gender, age, socio-economic status as well as beliefs, preferences and styles of coping which are all difficult to identify and define.

According to the 1992 National Adult Literacy Survey, one out of every five adults in the United States cannot understand written materials that require only basic proficiency in reading. The average adult in the United States cannot read above eight grade level. Therefore health care providers must prepare materials at the lowest possible reading level preferably the sixth grade level (age nine). People with good reading skills are not offended by simple reading material and most prefer easy-to-read material (Davis et al 1998). Lowering the reading level does not significantly alter the meaning of the text. Studies have shown that regardless of the reading ability and socio-economic status, patients are able to read a simpler brochure quicker and with better comprehension.
Seventy percent of newspapers sold in the UK have been found to be written at a reading age of 12 (Nicklin, 2002).
It is widely recognized that patients often forget things they are told during their consultation therefore written information can be used as a useful adjunct to verbal communication. Two popular formulas are used to determine the readability of written materials; the greater the number of polysyllabic words, the greater the reading difficulty; and the longer the sentences, the greater the reading difficulty.
The following data has inspired me to evaluate the information we provide to our patients. The following approaches have been found to ease patients’ reading. Using short, familiar words of one or two syllables, avoiding medical terminology whenever possible, using short sentences under ten words, using the second-person pronoun (“you”), using active rather then passive voice and using numerals rather than spelled numbers (Nicklin,2002). Information should be non-alarmist, non-patronizing and include a publication date indicating it is up to date.
Pictures apparently enhance memory, lists are easier to read than paragraphs, and in order to facilitate reading, ensure there is adequate white space on the page, set margins left-justified and ragged-right and use 12-point font (Heath, 1999). Health information is apparently accessed by 60-80% of internet users and studies show that 72% of these folk believe online information is credible. Due to the unregulated nature of the Internet we are in a fortunate position of being able to direct our patients to credible sites.
Every interaction we have with our patients and their families is an ideal opportunity to focus on risk management, health promotion and to provide teaching that can influence and affect their lives.

Vanessa

Vmax Logic Tree

Logic Tree software enables clients using Vmax software (which is what we use in our Lab) to custom design interpretation modules to run for each patient at the completion of their lung function test. It is comprised of two components; a software platform, and a development tool to design and edit modules.

Having participated in the ‘Inter-rater reliability in the interpretation of lung function tests’ study conducted by The Institute for Breathing and Sleep, Austin Health, Melbourne last year which was presented as a poster at the recent ANZSRS meeting in Brisbane it is clearly evident there is significant variation in interpretation of lung function tests across different labs.

In an effort to ensure our Lab is interpreting data according to ATS guidelines we have recently installed the Logic Tree module. We have now incorporated this quick and easy step into our post lung function test routine for each patient.
The flow chart attached gives an example of how the logic is used to report spirometry.

Not only has it been educational for me to be involved in the installation but now having had the time to look at the module in detail I can appreciate how it will be easy to custom design the interpretation if required.

This tool assists our physicians in reporting their patient’s pulmonary function tests which is not only useful from a resources point of view but also from a consistency perspective. Thus it standardises interpretative protocols and reporting phrases which leads to consistency in reporting especially helpful for referring doctors.

The Logic Tree ensures our Lab is interpreting data according to ATS guidelines and the Logic Tree will be an important aid in preparing our Lab for accreditation in the future.

Vanessa

Manse Medical

As of July 1 2010 our practice has changed names to Manse Medical. The name change is to reflect the provision of more than consultant respiratory services and reflect the enhanced commitment to providing patient services and education pertaining to sleep medicine.

The name change also represents the commitment to providing consulting services at our practice by three Melbourne based physicians Drs Camelia Borta, David Cunnington and Daniel Steinfort.

In the coming weeks you will notice the change of logo for our practice. New referral forms for lung function testing and sleep studies will be distributed shortly.

Our website address and blog will remain at the same but will also undergo a face lift to reflect the changes to the practices name.

The regular visits by the three Melbourne based physician has enabled Dr. Andrew Bradbeer the opportunity to expand his sleep consulting services. Longer consultations are now available for patients with complex sleep disorders.

It is estimated that almost 90% of Australians suffer from a sleep disturbance at some time in their life, with 30% suffering a sleep disorder. Outcomes range from medical comorbidities such as hypertension and myocardial infarction from OSA to increased risk of work place and traffic accidents. This demonstrates not only a personal cost but a significant large social and economic cost. This cost is estimated to be $3-$7 billion per year.

This is a major public health issue but is still under represented on the National Health Agenda. Statistics on the Government NHMRC funding in 2002 show that sleep research received 1.1% of the pool of funding, compared with CVD 16.6%, Mental Health 23.3%, Cancer 19.2% and diabetes 6.8%.

Over the coming 6 months we aim to provide further professional and community education on sleep medicine to raise awareness of these disorders and their impact.

Jessica

What is the CAT?

The one that rules at our house is Wiggam and he’s pretty cute.
With acronyms being so common, if you go looking for CAT it may also be the Centre for Appropriate Technology or Computed Axial Tomography.

The CAT I’m going to talk about is the COPD Assessment Test.

The COPD Assessment Test is a relatively new patient -completed instrument that has been designed to provide a simple and reliable measure of health status in patients with Chronic Obstructive Pulmonary Disease (COPD). It was developed by a multidisciplinary group of international experts including Professor Paul Jones (PhD, FRCP, Professor of Respiratory Medicine, St George's Hospital Medical School, London, England) who is a world leader in the science of health status measurement in lung disease and Professor Christine Jenkins ( Clinical Professor of Medicine at the University of Sydney, thoracic physician at Concord Hospital, and head of the Airways Group at the Woolcock Institute of Medical Research in Sydney).

COPD is a progressive and largely irreversible disease characterized by emphysema and chronic bronchitis which may result in breathlessness, cough and sputum. Patients with COPD often experience an increasing deterioration of their health related quality of life (HRQL).
“Health-related quality of life, utility and productivity outcome instruments have an important role to play in the general well being of subjects with COPD. The ease with which these questionnaires can be understood and completed is pertinent to issues of compliance and therefore of accuracy in assessing the impact of this progressive, chronic disease”. (Health-related quality of life, utility, and productivity outcomes instruments: ease of completion by subjects with COPD – Stahl et al 2003.)
This 2003 study identified how subjects experienced difficulty in completing a number of well used and new questionnaires. It appeared that age, disease severity, gender and socio economic status all impacted on the ability of the COPD subjects to complete the questionnaires. This article also suggests that the indirect assessment of subject’s HRQL, via relatives, care providers or other health professionals, tends to underestimate the level of HRQL impairment.

Over the past decade, more and more research on the development and validation of questionnaires has been undertaken to quantify the impact of disease on daily life and well being from the subject’s point of view. One reason is recognising that individual patients are most concerned about their symptoms (e.g. dyspnoea) and their function (e.g. ability to perform physical tasks), rather than objective measures such as expiratory airflow (B.Gupta& S.Kant: Health Related quality of Life in COPD: The Internet Journal of Pulmonary Medicine, 2009 V11, No.1)
I found many disease specific and generic questionnaires deemed appropriate to respiratory health. Among them are the SF-12, EQ-5D, HS-COPD, EQ-5D, WPAI-COPD, SOLDQ, QLRIQ (see what I mean by acronyms). There is also the Sickness Impact Profile (SIP), Nottingham Health Profile (NHP), Quality Well Being (QWB), and the St George Respiratory Questionnaire (SGRQ) which is more complex but has a strong correlation to the CAT. Some of these have been used in research studies and looking at these assessment tools I can see why the subjects may have struggled to complete them. A number appear quite complex and time consuming. For example the SIP is a 136 item questionnaire that takes 20-30 minutes to complete.

This brings us back to the CAT. According to the user guide (GlaxoSmithKline 2009) it is a validated, short and simple patient-completed questionnaire which has been developed for use in routine clinical practice. Its development involved literature reviews and consultation with physicians and patients. It is not a diagnostic tool (unlike FEV) but rather a tool to measure health status which may give a better understanding to the patient and clinician as to the impact and progression of their COPD. The CAT consists of 8 questions that are easy to understand and that patients should be able to complete independently. Each response attracts a score between 0-5 which is then added to produce a total score. Further research is currently being conducted to define ranges of CAT score severity and to better understand the clinical relevance in a CAT score from one visit to the next. The Cat Development Steering Group has proposed some potential management considerations according to a patient’s score, correlated to impact level and a broad clinical picture (based on appropriate items from the previously mentioned SGRQ). But the scenarios given are for illustrative purposes only as individual patients will vary in the way COPD affects them. For example a score over 30 rates a very high impact level, over 20 is high, 10-20 medium and less than 10 rates a low impact level.
The CAT score needs to be considered in relation to an individuals disease though there is not always a strong relationship between disease stage and health status score (Jones PW. Health status measurement in chronic obstructive pulmonary disease Thorax 2001; 56 880-7).
Its usefulness may be in initial assessment of and monitoring the progression of COPD in patients (perhaps even identifying specific areas of impairment), or possibly to assess the degree of recovery following an acute exacerbation. Its use in assessing whether an individual patient has had a worthwhile response to specific therapy is limited (but it is more reliable for assessing response to therapy in groups of patients). Recommended use of the CAT is every 3-6 months.

Why might we use the CAT?
It is simple and quick to complete (a few minutes).
It provides a framework for discussion with the patient.
It may help identify where COPD has the greatest effect on a patients life.
It may assist in better informed management decisions of the disease.

Used in conjunction with other COPD clinical assessment tools (e.g. spirometry) it can help to ensure a patient is optimally managed. It is recognized that how the CAT is used will vary according to a particular healthcare setting (and country) and we will need to consider if and how we can incorporate it into our practice to ensure it is useful and relevant.

The use of generic questionnaires versus disease specific questionnaires is a discussion in itself.

Irene

Pulmonary Rehabilitation

Recently I have performed lung function tests for patients who have attended a Pulmonary Rehabilitation (PR) program since their previous testing, which has prompted me to look further into the effectiveness of Pulmonary Rehabilitation on persons with COPD.
Whilst the research has found that Pulmonary Rehabilitation improves health status and quality of life by improving exercise tolerance and shortness of breath, a study by Carone et al (2007) looked into its effectiveness in the most severe category of COPD, i.e. patients with chronic respiratory failure (CRF). They found that PR is equally effective in the most severe category of COPD, i.e. patients with chronic respiratory failure (CRF), and supports the prescription of PR also in these patients.
In another study Riario-Sforza et al (2009)looked at a group of patients with COPD undergoing PR, and evaluated the number needed to treat (NNT) to achieve an increase in physical capacity, as defined by a significant improvement in the six-minute walk test (6MWT). The NNT in the overall study group was 2 and the same NNT was obtained in GOLD stages of COPD 2, 3, and 4, but was 8 in stage 1. They found therefore that PR is highly effective in improving the exercise capacity of patients with COPD, as demonstrated by a valuable NNT, with better results in patients with a more severe disease.
The objective of a third study by Di Meo et al (2008) was to identify predictors of improvement in the 6-minute walked distance (6MWD) in elderly COPD patients after PR. Although they could not develop a model accurately predicting the response to rehabilitation, they concluded from their study that "among elderly patients with COPD, a comprehensive PR programme can significantly improve the 6MWD even in the presence of chronic hypoxemia, and that the most physically impaired patients achieve the greatest benefit from rehabilitation."
This is great news for people with COPD, and especially for those whose condition is worse. Participating in the course will provide improvement in breathlessness, ability to exercise, and quality of life, and the worse the condition is the greater improvement that can be achieved.

Heather

Nicotine and Nicotine Replacement Therapy- Fact or Fiction?

The World Health organization describes smoking as an “EPIDEMIC” that will cause 1/3 of all adult deaths world wide by 2020(WHO 1999) and that tobacco kills 5.4million people a year from cancer, heart disease, and other illnesses (WHO 2008).

Indeed Quit (2009) estimate that 17.4% of people in Australia are daily smokers and tobacco use is the largest cause of death and disease in Australia with >15,000 people dying annually.

We also know that many people who smoke would like to quit and that these people are likely to have one or more quit attempts under their belt. Unfortunately, there are still some misconceptions out there about nicotine and nicotine replacement therapy (NRT) which may be preventing people from attempting to quit or correctly using therapy to increase their chances of a successful quit attempt.

A review article in Pharmacist (Vol 25, No12, Dec 2006,pg 969-973) highlights some of these commonly held misconceptions.

Here are some quick myths dispelled –

1. Nicotine is the most harmful ingredient in cigarettes.

Not so, nicotine helps maintain addiction (helps keep people smoking) and is not responsible for tobacco related diseases. It is all the other toxins and chemicals which cause disease. It is not carcinogenic.

2. Nicotine causes cancer.

Again, nicotine is not carcinogenic. There is no clinical evidence associating NRT with a higher chance of developing cancer.

3. Smoking while using NRT is unsafe and increases the risk of heart attack.

Not true. Those smoking while using NRT are advised (when able) to stop smoking to help minimize potential side – effects of high nicotine levels such as nausea/ vomiting and help them achieve their quit goal, not due to increased cardiovascular risk factors.

4. Using more than one form of NRT is unsafe.

More than one form of NRT can safely be used together. In fact using NRT together with behavioral interventions can significantly increase the likelihood of a successful quit attempt. It’s all about finding what is right for you.

5. NRT is as addictive as cigarettes.

Nicotine in cigarettes is highly addictive and has a fast delivery system via smoke. On the other hand, all forms of NRT are delivered at a much slower rate to the body and have almost no (or very low) addiction potential.

6. NRT is just as harmful as smoking during pregnancy.

NRT use is safer than ongoing smoking throughout pregnancy which can lead to lower birth weights, premature birth and increased risk of miscarriage. Once again it is the smoke from a cigarette that has known toxins that are harmful to a foetus. NRT use should be carefully considered for those who are unable to quit using other non- pharmalogical interventions.

7. NRT is just as harmful as smoking while breastfeeding.

There is well documented evidence of the risks to babies exposed to cigarette smoke with the most common one being sudden infant death syndrome. NRT use decreases the exposure to smoke. Nicotine is excreted in the breast milk but the levels of nicotine produced from NRT are low (estimated to be 50 times less than the mothers exposure) and therefore not likely to be hazardous to the breastfed baby.

The article summarizes all the evidence quite nicely in the following statement –

“Using nicotine replacement therapy to quit is always safer than continuing to smoke”.

As they say it is never too late to QUIT.

Lisa

Very old, Chinese and sleeping well

For my money, the paper of the week through my mailbox last week was a report about sleep habits in very old Chinese patients, which was published in Sleep journal at the start of May.

The report was an analysis of data collected in 2005 in the 'Chinese Longitudinal Healthy Longevity Survey' (CLHLS). The survey participants included over 15000 individuals over the age of 65. Most remarkably, there were over 2700 participants over 100 years old, making this an entirely unique dataset.

Unfortunately, only two question were asked about sleep in that survey - which didn't leave the researchers a hell of a lot to work with. ("How do you rate your sleep quality recently" and "How many hours on average do you sleep every day including napping?"). They did manage to look at the data every which way, and were able to evaluate the impact of other health problems and age itself on these two parameters.

Why is this interesting? Well, it used to be common wisdom that people sleep less as we get older. However, there have been studies demonstrating that once health problems are taken into account, there is no reduction in sleep time associated with increasing age in adults.

In this Chinese study, very old (over 100 years) Chinese tended more often to sleep 'too little or too much (my words; more sleeping less than 6 hours, and more sleeping more than 10 hours) when compared with younger old Chinese. Most of this was due to poorer health, which was significantly associated with poorer sleep quality and sleep hours outside of the 7-9 hour 'healthy sleep' window throughout all age groups. There was no significant variability in sleep duration between the age groups below 100 years. Between the ages of 65 and 100+ in this study there was no reduction in good sleep quality over the years. In fact, older participants (over 100 years) were more likely to have good sleep quality then younger participants when socioeconomic status, social support and health practice were controlled for.

These results seem to suggest that bad sleep is not necessarily a part of healthy ageing. The associated editorial in the journal suggest that the study demonstrates that, amongst the oldest old (over 80), age was a very strong predictor of good sleep quality. (I found it difficult to extract that much from the data - but surely the editorial couldn't be wrong). Could it be that 'good health predicts longer and better sleep, and longer and better sleep predicts good health'? Watch this space.

One statistic which you won't be hearing much about from doctors is that current smokers and alcohol users were, in contrast to other studies, more likely to have good sleep quality....

Andrew

Commitment to Quality Improvement

Commitment to continuous quality improvement or simply being proud of what we do?

I have spent quite a bit of time fussing over the appearance and content of our reports recently and have wondered if this has been the best use of my time.

Coincidently, the recent Australian & New Zealand Society of Respiratory Science monthly report touched on a similar topic where they were discussing what makes a professional. They were referring to a video interview of a group of professional woodworkers. There was unanimous agreement on two things. The first was knowing how to recognize and, more importantly, correct mistakes. The other was accepting that you will spend a lot of time fussing over joints and details knowing you will never be paid for the effort – you do it for the pride in your work.

In our industry there is a difference between quality work and pushbutton work so I think the above points are very valid and could apply to our team.

In order to present quality data we need to be able to recognise errors and know how to deal with them. The article I am referring to asked the questions if VA is greater than TLC is it the VA that is wrong or the TLC? Are the data behind the TLC calculation OK? Do you know how the TLC is derived?

Our reports are clear and easy to understand. Data is reported in both a tabular and graphical format and we understand how the software gathers the data.

So I believe this attention to detail and the time spent on the appearance and content of our reports is important as it is the end result of our training and expertise and reflects our team’s professionalism.


Vanessa

CPAP Adherence

There have been several blogs on this site about Obstructive Sleep Apnoea (OSA) which have touched on cause, diagnosis, risks and treatment options. The most successful treatment is Continuous Positive Airway Pressure (CPAP) which is the delivery of a prescribed air pressure via a machine and mask (face, nose, nasal) to help splint open a person’s airway open whilst they are asleep. But CPAP is only effective if the equipment is functioning optimally and there is adherence to therapy. This sounds simple enough but many people struggle with treatment for various reasons.

A good summary of adherence was given in a presentation by Sharon Takaoka M.D in 2007 which described adherence as the degree to which an individual follow a prescribed regime. A process of balancing cost versus benefits occurs. Obviously if the benefits outweigh the costs the individual is more likely to adhere to treatment. In the case of CPAP if the person feels there is a significant improvement in their quality of life (either because they have reduction in symptoms or because they understand the medical implications of not using CPAP) they are more likely to continue with therapy despite the “costs” involved.

The following are some of the factors related to CPAP adherence or more accurately non adherence as outlined by Takaoka.

There are patient related factors such as lesser severity of symptoms, little or no perceived benefit from therapy, failure to understand the importance of therapy, use of prescription medications/non prescription drugs or alcohol, lack of social support, other medical illnesses and physical limitations.

There are therapy related factors such as the complexity of device use, adverse reactions, lack of efficacy, expense and the chronic nature of the illness.

And thirdly clinician related factors such as a poor relationship between client and clinician, lack of follow up, unrealistic expectations, unwillingness or inability to educate patients and a lack of knowledge of a patient’s medical history.

Lisa has previously mentioned the vast range of machines and masks available which have developed over time in response to the varying needs of clients.

The appropriate choice of equipment is one very important factor which impacts on a clients ability to adhere to treatment. The most suitable type of delivery (set pressure versus variable pressure, use of flexible pressure), the type of mask that fits best and is comfortable and the use of accessories such as humidification, ramp and altitude compensation all contribute to compliance.

Accurate CPAP titration is also very important. This can be determined in a sleep lab where a technician can observe the clients response to CPAP in all positions. Auto trials where the client uses CPAP with variable pressure over a period of weeks at home can also be used to determine appropriate pressure. Either way it is important that an optimal pressure is determined which will eliminate snoring and arousals, ensure the client has normal oxygen levels and allows them to have a good amount of continuous sleep.

How well a person is able to adhere to treatment often depends on how well adverse effects are dealt with.

Knowing and recognizing the common adverse effects related to CPAP are important as patients who complain of side effects tend to use CPAP less than patients without side effects (Engleman et al. Chest 1996; 109: 1470)

Most of the side effects are related to pressure or airflow or mask-nose interface.

According to data available (Strollo PJ et al) the most common adverse effects from CPAP therapy are: mask marks on the face (48%), nasal bridge discomfort/breakdown (33%), nasal congestion (26%), dry nose or dry and red eyes (21-22%), machine noise( 17%) , ear pain (8%), prolific rhinitis (7%), facial acne under mask (6%), difficulty inhaling(6%).

Other known adverse effects are nose bleeds, air swallowing, tube condensation, claustrophobia/anxiety, inconvenience, poor portability and relationship problems. There are various strategies that can be used to reduce or eliminate these side effects but trouble shooting is a worthy subject on its own and will be addressed at another time.

Patient education is a huge factor in CPAP compliance. It is beneficial if a client has a good understanding of what OSA is, its implications and how CPAP is going to help. The client needs to have positive but realistic expectations and allow time for adjustment and optimization.

So with CPAP what is an actual measure of adherence or compliance? There appears to be little evidence which actually specifies this.

Clinicians generally recommend 4-5 hours use a night for at least 70 percent of the time to obtain clinical benefit. Obviously the longer the better. But there has been evidence of improvement in daytime sleepiness with less than 4 hours use a night. Another point of interest is that OSA is typically worse in REM sleep and REM sleep usually occurs more often in the second half of the night. For this reason CPAP may be more beneficial in the second half of the night. My experience is that patients are more likely to use CPAP earlier in the night rather than later if using it for only part of the night.

It appears that early patterns of use are a good predictor of long term adherence. The first month of use (and sometimes first four days) is often indicative of continued use over one month. If usage is not established by 3 months then alternative treatment should be considered. (Weaver et al Sleep 1997; 20:278. Kribbs et al Am Rev Respir Dis 1993, 147:887)

In summary adherence can be improved using a three way approach: by using appropriate technological interventions, by using proven behavioural interventions and by reducing known side effects.

Irene

Dr. Camelia Borta

We are very fortunate to have Dr. Camelia Borta commit to continue to consulting at our practice for an ongoing period. Dr. Borta will consult here when her commitments at Melbourne allow her. Visits will usually be for a duration of a fortnight with a frequency of between 4-8 weeks. This will allow for Dr. Borta to follow up her own patients providing a great continuity of service.

Dr. Borta will mainly see Respiratory referrals. Urgent Respiratory referrals will still be seen by Dr.Bradbeer. Dr. Borta's commitment to the practice will allow Dr. Bradbeer the opportunity to concentrate on additional sleep medicine consulting.

Sleep medicine is an evolving discipline and encompasses much more than obstructive sleep apnoea. Referrals of patients with more complicated sleep problems are increasingly common. Such patients often require more time with the consultant - particularly in the initial consultation. Our scheduling of appointments has recently been reorganised to allow for this to happen for such patients.

We are still in the process of securing the services of an additional full time Respiratory physician. We hope to have some good news pertaining to this within the coming months.

Please do not hesitate to contact us if you would like some further information about the referring process.

Jessica

Sniff Nasal Inspiratory Pressure

Adding to the repertoire of tests we offer we are hoping to be able to perform the Sniff Nasal Inspiratory Pressure (SNIP) test as soon as the nasal adaptors arrive.
SNIP has been shown useful in assessing inspiratory muscle strength, and is thought to more closely reflect changes in oesophageal pressure during inspiratory efforts.
The SNIP measurement appears to be better than MIP (Maximal inspiratory pressure) in monitoring the evolution of neuromuscular disease and may prove to be a better predictor of hypercarbia and subsequent intervention.
Indications:
To assess and quantify the degree of respiratory muscular weakness that may occur with neuromuscular disease, obstructive lung disease causing hyperinflation, chest deformities, and unexplained dyspnoea
To obtain clinical information about the potential for effective cough and ability for secretion clearance
As Maureen is demonstrating (whilst smiling I might add) in the photo, SNIP is the measurement of pressure through a plug occluding one nostril during a maximal sniff performed through the contralateral nostril. It is an accurate and non invasive approximation of oesophageal pressure swing during sniff manoeuvres but has been found to underestimate oesophageal pressure swing in subjects with nasal obstruction, patients with chronic obstructive pulmonary disease and severe neuromuscular patients.

Heritier et al[1] found that SNIP provides a reliable and noninvasive estimation of oesophageal pressure swing during sniff manoeuvres (sniffPes) in normal subjects and in patients with neuromuscular or skeletal disorders by simultaneously measuring the oesophageal pressure using an oesophageal balloon and the validity of this method may be impaired by severe nasal congestion.
In this study 10 normal subjects performed 338 sniffs of variable intensity and 12 patients with neuromuscular or skeletal disorders performed 181 maximal sniffs. Nasal mucosal congestion was induced by nebulization of increasing doses of histamine in four normal subjects.

In conclusion the SNIP manoeuvre has predicted normal values, is noninvasive and is easier to perform than MIP. It could be considered as the first simple test to use in order to assess inspiratory muscle weakness. In addition, because it is as reproducible as MIP, it can be suitable to follow inspiratory muscle function in chronic neuromuscular patients. Because, of the important limit of agreement between SNIP and MIP, these two methods are not interchangeable but complimentary.

Vanessa
[1] Heritier F, Rahm F, Pashe P & Fitting JW. 1994. Am. J. Respir. Crit Care Med., Vol 150, No 6, 12, 1678-1683.

Asthma and obesity

I am enjoying having opportunity this week to catch up on some of the talks from the American Thoracic Society conference, which was held in New Orleans just over two weeks ago. I’m impressed that they are available online already.

One symposium looked at the interaction between obesity and respiratory / critical care medicine. I’ll probably blog more about this as I work through the talks.

Dr Stephanie Shore, PhD, from the Harvard School of Public Health, gave an excellent lecture on obesity and asthma at that session. The following is a summary of what I got out of that talk.

Firstly, we do know that asthma and obesity interact in the following ways:
- there is an increased prevalence of asthma amongst obese individuals;
- as people become more obese, the likelihood of new asthma developing increases;
- obesity leads to reduced control of asthma;
- obesity leads to increased severity of asthma;
- weight loss helps improve asthma control;
- and obese mice…..

What have mice got to do with it? Well, many data relevant to human health were initially derived from mice, so it turns out that obese mice have something to teach us. And obese mice have a tendency to develop asthma. But more of that later.

Why is there more asthma amongst people who are obese? Is this a new sort of asthma? Does obesity give some people asthma? Or is it the same old sort of asthma, with obese individuals simply predisposed.

It looks more like the former suggestion – ie obese individuals with asthma have a particular sort of asthma. Obese individuals with asthma have less eosinophils in bronchoalveolar lavage fluid (fluid that is washed through the smallest airways at bronchoscopy). They also are less sensitive to the impact of corticosteroid. All of this suggests that they do not have ‘allergic asthma’ of the sort that occurs almost universally in children with asthma, but less frequently in older asthmatics.

What’s going on there? There is ‘more thought than data’ when it comes to how obesity may contribute to asthma development. The ideas include the suggestions that there may be:
1. Common aetiologies. The same processes that contribute to the development of obesity may contribute to the development of asthma. These may be congenital / in-utero issues; dietary factors; genetic abnormalities or acquired exposures
2. Co-morbid problems. People with obesity suffer from more lipid abnormalities, gastro-oesophargeal reflux, obstructive sleep apnoea, diabetes and hypertension. Do these associated problems contribute to the development of asthma. GORD and OSA have been shown to. The others, maybe.
3. Obesity impacts on lung mechanics, leading to reduced functional residual capacity and reduced tidal volume. Either of these mechanisms may lead to airway hyperresponsiveness – and asthma.
4. Systemic inflammation or other systemic consequences of obesity may contribute to development of asthma.

With regards to this last issue, in particular, Dr Shore embarked on a little tutorial on adiponectin. I didn’t know too much about this hormone, so was helped by the tute. Like leptin, adiponectin is produced in fat cells (adipocytes) and circulates in several different forms in the blood stream. Its levels are reduced in obesity. It sensitizes to the effect of insulin (so low levels contribute to insulin resistance) and it has anti-inflammatory properties (so low levels in obesity can lead to more inflammation). Dr Shore’s lab had researched the impact of this compound in the lungs of mice. In mice given adiponectin, allergen –induced airway hyperresponsiveness (AHR) and inflammation is reduced. In adiponectin deficient mice there is increased allergen induced AHR and inflammation. Transgenic mice that overexpress adiponectin demonstrate reduced airway inflammation. The suggestion (idea rather than data) is that adiponectin may be a mediator of airway inflammation in people who are obese – not just in mice – contributing to the development of asthma.

The important clinical information for now is that weight loss helps. There have been, in the last 10 years, 10 studies looking at patients with bariatric-surgery – induced weight loss and 4 looking at patients with dietary weight loss, with regards to the impact of weight loss on asthma control. They have demonstrated:
- improved lung function parameters;
- reduced medication use;
- reduced symptoms;
- improved asthma control;
- improved asthma-related quality of life;
- reduced severity of asthma and reduced frequency of hopitalisation ….

….as a consequence of weight loss in people with asthma.

So, there is evidence that obese patients with poorly controlled asthma should be encouraged to lose weight. It will help bring their asthma under control.

Andrew

Obstructive sleep apnoea year in review

I've just been watching an online presentation from the ATS conference last month. Doug Bradley, from Canada, extracted from the literature what he considered to be the most significant papers from the last year with regards to obstructive sleep apnoea.

The first, as customarily seems to be the case, was from his own lab. This study, published in circulation journal, was looking at whether fluid shift from the legs to the neck, in men with heart failure, during sleep overnight, was associated with obstructive and central sleep apnoea (two different groups of patients). It was demonstrated that this does, in fact, seem to happen. People with heart failure and leg swelling do tend to shift fluid overnight. Their legs get thinner, their necks get fatter and they develop sleep disordered breathing. Worse leg swelling is associated with worse sleep disordered breathing. Patients with more leg swelling are more likely to develop central rather than obstructive sleep apnoea. CPAP therapy makes no difference to the leg oedema but does reduce the neck swelling.

Children with obstructive sleep apnoea often find it difficult to do a sleep study. Access to specialist sleep labs for kids is difficult. For this reason, most ENT specialists in America still perform adenotonsillectomies without sleep studies prior (only 10% of kids having that surgery in the USA have had a sleep study - and I'm sure it's the same here). For that reason, a study published in the blue journal which looked at urinary protein biomarkers of OSA also got a guernsey. This was pretty interesting. There were 9 urinary proteins that are increased in kids with OSA as opposed to snorers and non-snoring controls, and 3 that were reduced. The ability to diagnose OSA in kids with a urine dipstick test may be around the corner - although the point was made that these kids were highly selected, and in particular had no evidence of upper respiratory infection.

Two further studies looked at the impact of exercise on sleep apnoea. The first, also published in the blue journal, put patients through a three month program of exercise of oropharyngeal muscles. The AHI fell by 40% over three months, and the Epworth sleepiness scale score also fell. The second study second study, by the same South American group, looked at patients aged between 42 and 70 years who had both heart failure and sleep apnoea. After a 4 month observation period, 4 months of exercise training ensued. AT the end of that four months the AHI dropped by 40% in the OSA group (but not in patients with CSA) and the nadir oxygen saturation overnight inthe OSA group rose by 5% . All good.

A 5 year follow up study of stroke survivors in Spain evaluated mortality in patients who had moderate to severe OSA and complied with CPAP therapy, as opposed to those who did not. Of 223 patients initially evaluated, 189 were ready to go into the study 2 months after their stroke. Of these, 166 were evaluated and 96 found to have an apnoea-hypopnoea index of more than 20 (an incidence of significant OSA of close to 60% in this population). 28 (29%) of those patients were unable to comply with CPAP - and 68% of those patients died within 5 years. 68 (71%) of the patients complied with CPAP, and only 50% of those patients died within 5 years. Of patients with only mild to moderate OSA (AHI less than 20) the 5 year mortality was 35-40%, which was not significantly higher than patients with no OSA.

CPAP compliance is not great in patients post-stroke OSA. Dr Bradley suggested that part of the reason may be, as shown by researchers in his lab, patients with OSA post stroke are often not sleepy.

Andrew