The year of the Lung

2010 has been declared The year of the Lung, by the Forum of International Respiratory Societies (FIRS). This declaration was made 40th Union World Conference on Lung Health in Cancún, Mexico on 6 December 2009.



Why did the forum feel the need to make this declaration? The underlying reason is to rise awareness of respiratory disease. The forum feels this is still an under resourced and recognised area globally. Some of the facts stated on their website are:

• Hundreds of millions of people struggle each year for life and breath due to lung diseases, including tuberculosis, asthma, pneumonia, influenza, lung cancer and chronic obstructive pulmonary disorder, and more than 10 million die.


• Chronic respiratory diseases cause approximately 7% of all deaths worldwide and represent 4% of the global burden of disease;


• Lung diseases afflict people in every country and every socioeconomic group, but take the heaviest toll on the poor, the old, the young and the weak;


• Deadly synergies exist between diseases such as tuberculosis and HIV/AIDS, influenza and asthma, COPD and lung cancer;


• Diseases once primarily found in industrialized countries, such as asthma, COPD and lung cancer, are now major problems in low- and middle-income countries and threaten to overwhelm public health services;


• The cost of lung disease runs to billions of dollars each year in lost productivity and increased health care expenses – to say nothing of diminished and ruined lives;


• Yet public demand and political commitment remain inadequate to effect significant change.

Globally the forum recognises;

• The connection between breath and life is fundamental, yet the evidence shows that lung health is not high on the public health agenda:


• Tobacco use remains legal, although it kills more than 5 million people each year, including 1.3 million who die of lung cancer, and it affects the health of hundreds of thousands of others who are exposed to its effects secondhand;


• No new drugs have been developed for tuberculosis in more than 5 decades and the only vaccine is nearly a century old, yet there were more than 9 million new cases in 2007, and this curable disease kills 1.7 million each year;


• Pneumonia kills more than 2 million children under 5 each year – one child every 15 seconds -- despite the fact that it can be treated effectively and inexpensively;


• Most of the 250,000 deaths from asthma each year can be attributed to lack of proper treatment.


• Although it will be the 3rd leading cause of death worldwide by 2020, COPD is frequently not diagnosed;


• Nearly half of the world’s population lives in or near areas with poor air quality.

There are many aims that the forum and its partners aims to achieve during this 12 month period. One of these aims is to 'to ensure that every health worker, parent, child, teacher, employer, religious leader, community leader, media representative and government official understands the risks and symptoms of lung diseases and how to keep lungs healthy, because lung health is essential to breath and life'.

We all have a role to play in this no matter how big or how small. Strategies and interventions on how we can affect change should always be on the agenda. Whether it is being an advocate for tobacco control measures, speaking to a community group about lung disease or providing a patient with resources so they may learn more about a particular lung disease.

Jessica

The chicken or the egg...

It seems I can’t read an article about depression without insomnia being mentioned or an article about insomnia without depression being mentioned.

It is generally recognized that people suffering from depression may as a result suffer from insomnia. Also that people suffering from ongoing insomnia often suffer from depression.
So I set out to try and discover if the two conditions are coexisting how do we know if it is the depression causing insomnia or the insomnia causing depression and will treating one successfully treat the other.

Of course I found a myriad of articles written on the subject.

A study by clinical Psychologist Dr David Morawetz was conducted with a group of patients who suffered from chronic insomnia, of which two thirds also suffered from depression. These patients were subjected to a 6-8 week self help program (Sleep Better Without Drugs) to help improve their sleep. Using strict evaluation criteria 87 % of subjects were sleeping significantly better at follow up and 70% of those who were depressed before treatment were no longer, or significantly less, depressed. Of those who did not learn to sleep better none experienced a significant reduction in depression.

His conclusion was that for patients that suffered from both chronic insomnia and depression successfully treating the insomnia (in this case without medication) can eliminate or significantly reduce the depression.

“Sleep disturbances are a hallmark of depression, but insomnia can actually unleash the mood disorder. Treating sleep disturbances might help prevent depressive episodes”. (Hara Estroff Marano, July 01,2003)

In the past most experts agreed that depression caused insomnia but new (drug) treatments to improve depression did not seem to alleviate insomnia, supporting the idea that insomnia could be a contributor or predictor of depression (interestingly the elderly being most at risk).
A longitudinal study by Michael Perlis PhD (University of Rochester Sleep Research Laboratory) showed that insomnia appears to precede episodes of depression by about 5 weeks suggesting it may be more than just a symptom of depression but may actually unleash the mood disorder.
His studies showed that people most at risk of depression are those patients with severe “middle insomnia” described as waking up frequently during the night but eventually falling back to sleep each time…really quite a common occurrence amongst the population. He says the findings are especially significant because they suggest that targeted treatment for insomnia will increase the likelihood and speed of recovery from depression.

Given the connection has been made between insomnia and depression, trials and studies into improving sleep patterns are continually being conducted.

Often people are unaware of the consequences of disturbed sleep patterns, including insomnia, and their possible relationships to other conditions, hence may not seek treatment.

Just to confuse the issue evidence from other research also suggests that in a certain proportion of depression sufferers insomnia has an antidepressant effect (apparently all to do with the serotonin and dopamine neurotransmitter systems).

Irene

Measuring severity of COPD.

Chronic obstructive pulmonary disease is increasingly recognised as a systemic disorder. Muscle wasting and deconditioning and vascular dyfunction are present in this condition (the latter the subject of a previous blog). How should we measure and discuss disease severity in such a systemic condition?

I chewed over this question a little when giving a talk to GPs in Warrnambool last year, and again on the ward round with the registrar this morning (prompted by the sort of patient represented by the attached CXR - how's the hyperexpansion!?). I also tried to skewer our radiologist yesterday because I am irritated by radiological comments on 'severity' ('there is evidence of severe emphysema', for example, on interpretation of a CT) when I think that 'extent' is what is meant ('There is evidence of extensive generalised emphysema').

I'd hate to be guilty of the same crime myself. In particular, I need to ask myself the following question; 'Is severe obstruction on spirometry equivalent to severe COPD?"

Our guidelines (for example, the global initiative in obstructive lung disease - 'GOLD' ) do provide neat summary tables of how spirometry correlates with severity in COPD. These are easier to remember than the wordier paragraphs that outline how a range of other factors should also be taken into consideration when we wish to evaluate the real disease 'severity'. As a consequence we may tend to become over-reliant on spirometry alone. It is certainly not the only, nor perhaps even the most, meaningful measure of severity of disease.

As befits a systemic condition, there are multi-component indices which provide measures of disease severity. In 2004 the BODE (Body mass index (B), degree of airflow Obstruction (O), dyspnoea (D) and exercise capacity (E)) index was validated as a measure of severity which proved predictive of mortality. The initial paper was printed in the New England Journal of Medicine. In this scale, dyspnoea was measured with a modified Medical Research Council dyspnoea scale, and exercise capacity with a 6 minute walk test. The latter of these is difficult to employ extensively in clinical practice, and partly for this reason further efforts to define a clinically useful scale have been ongoing.

In December a paper promoting a new, and simple scale, was published in the blue journal. The DOSE (dyspnoea (MRC dyspnoea scale), obstruction (FEV1 % predicted), smoking status, exacerbation frequency) index was derived froma dataset of patients with COPD in Devon, and then validated in Devon, London, Tokyo and Holland datasets. The four components were selected from a range of proposed markers as being most consitently associated with health status measured using the Clinical COPD Questionnaire. (Interestingly, current smoking status was predictive of poor health status, where overall tobacco consumption measured by packet years was not).

A numerical score between zero and four was assigned for each of the four indices, and the four scores were added together to give the 'DOSE' Index score.

The score derived from this approach was found reproducibly to correlate significantly with health status meaures obtained by the more complicated COPD clinical questionnaire. A DOSE index score of more than four was also found to correlate with hospital admissions, respiratory failure and exercise capacity (negative correlation) when 6MWT was measured (in the Japanese cohort only). DOSE index results were found to increase over time throught the 8 years of the study, suggesting disease progression. Although MRC dyspnoea scale score and FEV1% measures on their own also correlated with hospital admissions, the correlation was weaker than the composite index.

How is this relevant to our practice? An index such as this, which is easy to administer, and which identifies patients with more severe disease - specifically those most likely to need hospitalisation - will help us target the more intensive of our interventions in clinical practice. It may even provide a useful way for us to monitor the effectiveness of our interventions. Sometimes the stuff we should all be doing regularly with our patients with COPD (quantifying breathlessness, reviewing smoking history, checking spirometry) happens best if it is proceduralised and done by practice staff (rather than the consultant physician - did I really just say that?). This DOSE index could be a very useful tool to facilitate just such a procedure in this practice....

The Paperless Office

This can be you.

We are living in a paperless zone at our office and wondering how we could have ever worked any other way. No-one enjoys working in a maze of paper and all the associated problems that come from this.

If you are considering becoming paperless and have some trepidation towards the change, don’t, you will not regret it. All you require is: the willingness, planning, education and the ability to just get on with it.

Simple changes in the use of existing software and implementing technology [inexpensive] all make efficient changes to how information arrives and leaves the office – no more filing or looking for room to store all those files.

Think about the amount of space used at your office, or off-site, to accommodate the storing, the cost of this and then you start to understand the real cost of not making your office paperless.

What we enjoy most about our paperless office is this, we do not mislay or loose important information, with a couple of clicks on the keyboard we are able to retrieve documents; no time spent pouring through dusty old files. The best thing of all is that we have been given TIME, everyone’s favourite, and can spend our working hours carrying out tasks that are more proactive and productive.

If you would like to discuss how we planned and implemented our paperless office please email me [maureenwestern@regionalmedicine.com.au] and I would be very happy to discuss this with you.

Maureen

Portland sleep centre equipment upgrade

Both the Portland and Hamilton Sleep Disorders Centres reopen this coming week, after being closed during the Christmas and January period.

During this period Portland's diagnostic equipment has been upgraded to the E-series making it identical to the Hamilton equipment. This allows for greater clarity in signals, aiding in sleep staging and reporting. With staff at both locations now using the same equipment the ability to train staff will be enhanced and as will trouble shooting when necessary.

The Somte PSG's, that where previously used in Portland will now have the capacity to be used in ambulatory settings. During the last 12 months one unit was utilized for this purpose. It was based at Mount Gambier and sent to Horsham on a needs bases.

Referral forms for both in-laboratory and home sleep studies can be downloaded here.

The referrals forms also provide some guidance as to which patients are appropriate for a home based sleep study and which patients require an in-laboratory based study. It is important to note that in -laboratory studies are still the gold standard for the diagnosis of obstructive sleep apnoea and is an essential adjunct to the diagnosis of many other sleep disorders.

Jessica

Can you change your VO2 max?

For the last two weeks I have been in South Australia on holidays. While over there the state was a buzz because Lance Armstrong was in Adeliade for the tour down under. Everywhere we looked elite and recreational cyclists seemed to have taken over the streets and this was highlighted when the public where invited to join Lance on a community ride around Glenelg (he sent the invitation out through twitter). A staggering 7000 people joined him!

This got me thinking about information I had previously heard about Lance being super human producing extermly low lacate levels (hence not fatiguing as quickly) and having a high VO2 max.

It is reported that his VO2 max is 85 milliliters of oxygen per kilogram of body weight per minute. An average untrained person has a VO2 max of 45 and with training can get it to 60. Exercise physiologists have estimated that an untrained Lance Armstrong would have a VO2 max of 60, hence an average person trained level is his untrained.

So how do you change your Vo2 max? Training volume and training intensity are the key factors. Research has shown the biggest increases can be found in sedendary individuals as they have the most room to improve. Such cases have demonstrated an increase as high as 20%.

Factors other than genetics that influnce VO2 max are age (decrease 30% by the age of 60), gender (female valuse are normally 20% lower than males) and altitude. Altitude is interesting. As there is less oxygen at higher altitudes an athlete will generally have a 5% decrease in VO2 max with a 5000 feet gain in altitude. This is why many athletes undertake altitude training prior to competition.

Vo2 max alone will not predict the winner of an endurance event but most elite althletes will have a VO2 max over 60.

We offer cardiopulmonary testing to community members who are interested in having these results to help inform their training program. Who knows what your potential might be?

Jessica

VO2 max as an indicator for insulin resistance

The measure of VO2 max through cardiopulmonary exercise testing has many uses for both medical and exercise professionals. A quick search of recent studies involving VO2 max (maximal oxygen uptake) revealed many and varied studies. They ranged from the effect of habitual smoking on measured and predicted VO2 max, the relationship between velocity reached at VO2 max and time trial performance in elite Australian rules footballers, determinants of VO2 max decline with age and does respiratory muscle training increase physical performance?

The study that caught my eye was low cardiorespiratory fitness in people at risk for type 2 diabetes: early marker for insulin resistance. Researchers took a group with significant risk factors for type 2 diabetes but were yet to show signs of insulin resistance syndrome (IRS) and compared their cardiorespiratory fitness to a control group from the same area who were deemed to have less association with risk factors for type 2 diabetes. Both groups were matched for sedentary nature, age, gender and BMI. The study showed individuals at risk for IRS and T2DM had a VO2max (22 +/- 6 ml/kg/min) 15% lower than the control group VO2max (26 +/- 9 ml/kg/min) (p <>

An interesting study since the study matched groups for sedentary nature, age, gender and BMI. Gender excluded these are all shown to be some of the highest risk factors for T2DM along with family history, diet, hypertension, gestational diabetes, race and as previously blogged obstructive sleep apnoea.

Jessica

MIP and MEP

Recently a patient was referred to the lab for the above test who presented with a cluster of disabling signs and symptoms who had previously contracted poliomyelitis. Post Polio Syndrome although rarely life threatening can result in under ventilation if the patient has untreated respiratory muscle weakness and aspiration pneumonia from a weakness in the muscles controlling swallowing.
Maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) are measurements that may aid in evaluating respiratory muscle weakness. Measurement of MIPS/MEPS are the most widely used test to assess muscle pressure as it has no adverse effects and is non invasive.
Healthy adults can generate a MIP of greater than -60cmH2O and MEP of greater than 80cmH2O (both pressures tend to be higher in males and decline with age). Pressures lower than these may indicate neuromuscular disease affecting the muscles of respiration. However, other disorders may reduce the pressures by placing the respiratory muscles at a mechanical disadvantage. For example, the pressures may be reduced if there is chest wall deformity. MIP may be reduced by hyperinflation/gas trapping which flattens the diaphragm and places the intercostal muscles at a disadvantage. MEP may also be reduced in severe lung diseases. A MEP of less than 40cmH2O leads to an ineffective cough.
Several studies have demonstrated that MIP and MEP may be very useful in the diagnosis and follow-up of pulmonary and cardiac disease. A reduction in MIP has been shown to be associated with a progressive clinical worsening in patients affected by myasthenia gravis or Guillain-Barré syndrome. In addition it has been suggested that an imbalance between the pressure generated by the inspiratory muscles and the MIP may lead to the development of hypercapnia in patients with COPD. Indeed both MIP and MEP have been shown to be useful in detecting the presence of iatrogenic myopathy, such as steroid-induced myopathy or in predicting post-operative pulmonary complications following coronary artery by-pass surgery.
MIP and MEP are useful in the assessment of respiratory failure. They are sometimes used to predict whether a patient can be weaned from a ventilator. They are occasionally helpful in the diagnosis of unexplained breathlessness in association with a low vital capacity.
However, their usefulness is limited by the wide range of normal values and the fact that the tests are very effort-dependent. MIP and MEP are hard to perform and require a highly motivated subject.

Vanessa

Non-invasive ventilation in acute respiratory failure

I was asked an excellent question on the ward-round recently by one of our clever interns. Confronted by a patient with severe chronic lung disease who has become critically unwell, and having decided that intubation and mechanical ventilation via endo-tracheal tube would not be pursued, I was asked whether we would use non-invasive ventilation (NIV). Non-invasive ventilation involves the application of mechanical breathing support without the use of an endotracheal tube or tracheostomy, usually via an occlusive mask applied over the nose and mouth.

For the benefit of my interns, then, I thought it would be worth reviewing the recent literature on the use of non-invasive ventilation in the acute hospital setting. Unfortunately, there isn’t a hell of a lot of new information by the way of guidelines. However, there is some….

Firstly, in patients with COPD the following guidelines are based on recommendations from the global initiative in obstructive lung disease (GOLD):

• Selection criteria for NIV:
  o Moderate to severe dyspnoea with use of accessory muscles and paradoxical abdominal motion
  o Moderate to severe acidosis (pH <= 7.35) and/or hypercapnoea (PaCO2>45mmHg)
  o Respiratory frequency > 25bpm
  

Now it’s seldom quite so cut-and dried, but for those who like lists then you can learn that one.

There are contraindications to NIV which should be remembered:

Exclusion Criteria:

• respiratory arrest
• cardiovascular instability
• change in mental status / uncooperative patient
• high aspiration risk
• viscous or copious secretions
• recent facial or gastroesophageal surgery
• craniofacial surgery
• fixed nasopharyngeal abnormalities
• burns
• extreme obesity
  

A recent German review of over 2900 publications, weighted according to level of evidence, has come up with the following recommendations for use of NIV in acute respiratory failure – following the motherhood statement that ‘NIV should be preferred to invasive ventilation wherever possible to avoid the risk of ventilator-tube associated complications such as ventilator associated pneumonia’, (a level A recommendation);

• in hypercapnoeic acute respiratory failure (ARF) NIV reduces rate of hospital acquired pneumonia, length of hospital stay and mortality – both in hospital and in ICU (Level A)
• patients with cardiopulmonary oedema should be treated with CPAP or NIV (CPAP is fine. Level A recommendation. Very important – don’t just give them lasix. CPAP treats the heart failure by increasing intrathoracic pressure and reducing venous return – reducing preload on the failing ventricle and allowing it to contract more effectively.... all to do with the Starling curve. Complicated, but CPAP doesn’t just support their breathing, it treats the heart failure. Everyone with APO should get CPAP – says the respiratory physician - but remember that CPAP can drop blood pressure, so be wary in patients with hypotentsion)
• in immunocompromised patients with ARF, for reasons unclear, NIV reduces mortality (Level A)
• to prevent post-extubation failure and to facilitate weaning of intubated patients with hypercapnoeic respiratory failure (Level A)
• in patients who decline invasive intervention, NIV may be an acceptable alternative (Level B)
• to lessen dyspnoea in palliative care (level C)
  

In patients with simply acute hypoxic respiratory failure, the failure rate of NIV is 30 to 50 % and NIV is not generally recommended (except in those immunocompromised patients).

Hope that helps.

Andrew

How much sleep is enough?

What qualifies as a goods night sleep? This is different for everyone but researchers have found that the average number of hours an adult should sleep per night is around 8. That being said some people need as little as six hours while others feel they need nine. The best indicator of if you are getting enough sleep is how you function the next day. If after six hours sleep you wake feeling unrefreshed and experience high levels of daytime tiredness then there is a fair chance that you could do with an extra hour or so per night.

In our society it has become somewhat of a badge of honour to apparently be able to get by on little sleep. Many influentual figures in society have stated they get by on very little sleep. Margaret Thatcher reportedly survived on 4 hours per night and our current PM Kevin Rudd is said to have as little as 3 hours per night. Perhaps we need to take these reported levels of sleep with a grain of salt as they may be used to promote the idea they are hard working and motivated or perhaps it is simply that work interferes with getting an adequate amount of sleep. Not getting enough sleep is a reality for many people not just politicians.

When people have ample opportunity to sleep but have difficulty initiating sleep or maintaining sleep it is described as insomnia. Approximately one third of the population will experience insomnia at some stage during their life. Mostly it is caused by an acute phase in their life such as stress, jet lag, or medical condition and resolves quickly. For others the problem can be ongoing and is thus described as chronic insomnia.

This sleep deprivation can cause impaired judgement, accidents, and mood swings. It is important to establish if there is a reason why enough sleep is not being achieved. It may be due to lifestyle, work, illness, sleeping environment or sleep hygiene.

Sleep hygiene refers to the habits that are established around sleep. Sometimes these habits are reinforced over years and have a disruptive effect on sleep. Recently the partner of a poor sleeper told me they have the TV on all night and her husband wakes several times a night not being able to get back to sleep so has the laptop close to the bed and can spend hour on the Internet. This is not uncommon and is an example of bad habits that have built up over the years having a negative impact not only on the individual but also the bed partner.

Take a look at the sleep hygiene download from our website to see if there is anything you can do to improve your sleep.

Jessica

Can Spiriva® save lives?

Tiotropium (Spiriva®) is almost universally prescribed for treatment of chronic obstructive pulmonary disease. It has been demonstrated to improve lung function (better spirometry, less air trapping) and health-related quality of life, and to reduce the frequency of exacerbations and hospitalizations in studies that compared use of tiotropium to placebo.

But can it save lives?

To date, several interventions in particular clinical settings in patients with COPD have been demonstrated to improve survival. These include; smoking cessation; use of supplemental oxygen in patients with persistent and profound hypoxaemia (low blood levels of oxygen); use of non-invasive ventilation in patients with ventilatory failure (high levels of carbon-dioxide in the blood; and even lung volume reduction in a very select group of patients. An analysis of data collected in the previously-published UPLIFT trial was released in the Blue Journal in mid-November, and suggests that tiotropium used regularly may be added to this list.

This was an interesting study. Two groups of patients (totaling 5993 patients) with COPD were randomized to receive either tiotropium or placebo. They were allowed to take any other inhalers except anticholinergics, and were even allowed to smoke (30% of them were smokers). Many patients discontinued the drug (44.6% in the placebo arm and 36.2% in the treatment arm) but continued in the study over its four year duration, and then a 30 day follow up period, during which tiotropium was stopped and ipratroprium (Atrovent ®) administered. .

During the 1440 days of the treatment period, 411 patients died while receiving placebo and 381 while receiving tiotropium (Hazards ratio (95% CI) 0.84 (0.73-0.97) p-0.016). If those in the two groups who discontinued treatment were included there was still a significant difference ( 491 vs 430, HR 0.87 (0.76-0.99), p-0.034). However, the follow-up period was a particularly bad one for those in the tiotropium group. During that period, 16 patients from the tiotropium group died, as opposed to only four from the placebo group. Six of those ‘tiotropium group’ deaths were patients who had remained on the medication right up until the end of the study – raising the question of whether withdrawal of the medication may have been harmful. By the end of the follow-up period, the survival difference was not statistically significant.

In a sub-group analysis it seemed as if smoking status at baseline might be a significant differentiator. Not too much was made of this in the discussion, but certainly for those patients still smoking there was no difference in risk of death between the two groups (medication vs placebo).

I think that the study design was a bit messy, including smokers and non-smokers and with a real hotch-potch of other inhalers in play. In this regard, however, it can certainly claim to be like real life. This recently-published new analysis of old data from the UPLIFT study gives us even more reason to prescribe tiotropium, and encourage our patients to remain on it.

Andrew