As I am sure we are all well aware the burden of disease for respiratory illness is high. COPD is the 4th leading cause of death in the world (behind heart disease, cancer and stroke)and researchers estimate by 2020 its will be the 3rd leading cause of death world wide.
It is also estimated that by 2020 it will be the 5th leading cause of morbidity (DALY).
From these figures it is no surprise that the demand for respiratory consulting is high, hence to meet this demand we are very fortunate to have some Melbourne based physicians providing consulting services for Regional Respiratory Medicine.
Over the next month Dr. Daniel Steinfort will be consulting in Horsham. Daniel has been consulting in Horsham for 18 months. In Melbourne he is based at the Royal Melbourne Hospital and is currently undertaking his PHD.
Dr. Camelia Borta will begin consulting with us during May and has undertaken to visit the practice for fortnightly periods approximately every six weeks. Camelia is currently working at Casey Hospital, Berwick. This will enable us to provide extra consulting to Mount Gambier.
Jessica
Friday, April 30, 2010
Friday, April 23, 2010
Hamilton Sleep Disorders Centre
The Hamilton Sleep Disorders Centre opened its doors in May 2005, hence is approaching it 5th birthday. Happy Birthday!
In that time the centre has conducted over 2000 sleep studies ranging from diagnostic, cpap implementation, cpap reviews, MSLT, and MWT.
The centre draws patients to Hamilton from the Wimmera, Limestone Coast and Greater Green Triangle area. In the last year Portland District Health has also opened the doors to a in-laboratory sleep services, which is helping to service the demand in the region.
The vast majority of diagnosis that come through the sleep centre doors are Obstructive Sleep Apnoea and although the centre has seen a great deal of patients there is still a significant amount that have OSA and don't realize.
A common comment I hear at the sleep centre is 'I think I've actually had this for years'. What sparks them to be investigated is varied from doctors referral, bed partner nagging (due to snoring or witnessed apnoeas), friend being diagnosed and realising their story sounds similar to their own, job requirements or their own motivation.
So, I thought this was a good opportunity to refresh everyone minds about some OSA Stats.
The Quick Facts
1. OSA is said to be prevalent in 5% of the population but some studies have predicted it may be present in up to 10% of middle aged men.
2. Patients on 3 or more Blood Pressure medications are 70% more likely to have OSA.
3. Around 23% of patients with Type II Diabetes have OSA
4. OSA suffers are seven times more likely to have an accident
5. Depression is strongly linked to OSA and insomnia
6. 50% of snorers have OSA
When OSA is diagnosed and successfully managed it can have a positive impact on hypertension, type II diabetes, snoring, accidents, depression and the risk associated with cardiovascular disease.
It is very important to keep Obstructive Sleep Apnoea on the agenda.
Jessica
In that time the centre has conducted over 2000 sleep studies ranging from diagnostic, cpap implementation, cpap reviews, MSLT, and MWT.
The centre draws patients to Hamilton from the Wimmera, Limestone Coast and Greater Green Triangle area. In the last year Portland District Health has also opened the doors to a in-laboratory sleep services, which is helping to service the demand in the region.
The vast majority of diagnosis that come through the sleep centre doors are Obstructive Sleep Apnoea and although the centre has seen a great deal of patients there is still a significant amount that have OSA and don't realize.
A common comment I hear at the sleep centre is 'I think I've actually had this for years'. What sparks them to be investigated is varied from doctors referral, bed partner nagging (due to snoring or witnessed apnoeas), friend being diagnosed and realising their story sounds similar to their own, job requirements or their own motivation.
So, I thought this was a good opportunity to refresh everyone minds about some OSA Stats.
The Quick Facts
1. OSA is said to be prevalent in 5% of the population but some studies have predicted it may be present in up to 10% of middle aged men.
2. Patients on 3 or more Blood Pressure medications are 70% more likely to have OSA.
3. Around 23% of patients with Type II Diabetes have OSA
4. OSA suffers are seven times more likely to have an accident
5. Depression is strongly linked to OSA and insomnia
6. 50% of snorers have OSA
When OSA is diagnosed and successfully managed it can have a positive impact on hypertension, type II diabetes, snoring, accidents, depression and the risk associated with cardiovascular disease.
It is very important to keep Obstructive Sleep Apnoea on the agenda.
Jessica
Thursday, April 22, 2010
Restless Legs Syndrome
Frustration. Exhaustion. Inability to rest or sleep without twitchy or uncomfortable legs. An overwhelming urge to move affected limb.
Many people would not realize that these distinctive symptoms actually have a name and therefore go undiagnosed and untreated resulting in restlessness, difficulty in sleeping and daytime sleepiness.
Restless legs syndrome (RLS) is a central nervous disorder possibly with some genetic predisposition or related to an imbalance of dopamine in the brain. Dopamine is a brain chemical that affects movement and as levels normally drop at night this may explain why RSL is worse at this time. Iron is a significant factor in the production of dopamine which may account for the link between low iron levels and RLS symptoms.
RSL may be acerbated, but not caused by stress or psychiatric conditions.
As indicated RLS usually affects the legs particularly the calves but some people may experience symptoms in the upper legs, feet, hands or arms.
Primary RSL seems to have no cause. Those affected may have developed the condition during childhood and this may have been attributed to growing pains (or even ADHD). There is a tendency for the condition to increase with age with significant increase in severity often seen after age 50.
With secondary RLS there is usually a link to another condition. These include anaemia, kidney disease, Parkinson’s disease, pregnancy, thyroid problems, neurologic lesions, sleep apnoea or narcolepsy, and alcoholism.
There are certain medications that when taken may trigger or increase RSL symptoms, as may the withdrawal of some drugs.
Diagnosis is usually made on the basis of reported symptoms and medical history. The four established criteria are:
• Irresistable urge to move your legs along with uncomfortable sensations (may be described as creeping, crawling, pulling, tingling, itching, pain, burning)
• Symptoms commence or get worse at rest (sitting, lying down)
• Symptoms are partially relieved by activity (stretching, walking)
• Symptoms are worse at night
Blood tests or other investigations may be done to exclude other possible causes.
RSL doesn’t lead to other serious conditions but symptoms can become incapacitating for some sufferers especially excessive tiredness from sleep deprivation.
There is no cure for RLS but there are treatments available that can manage the condition and relieve discomfort. This may involve treatment of underlying conditions, lifestyle techniques which may require changes in daily behavior or habits, use of support groups and in severe cases transcutaneous electric nerve stimulation (TENS) for a short time at night may be of help. Medications are commonly prescribed but there is no one drug that works for everyone and they should always be used with caution as may have side effects or increase the symptoms of RSL. Usually the drugs prescribed are ones used for other conditions but have been found to be beneficial with symptoms of RLS. They may include dopaminergic agents, Benzodiazepines, non benzodiazepine sedatives, opiates and narcotics and hypertensive medications.
RSL may necessitate referral to a sleep specialist for further evaluation. This may require observation overnight at a sleep clinic where sleep can be monitored for periodic limb movements during sleep. However a diagnosis can usually be made without a sleep study.
Irene
Many people would not realize that these distinctive symptoms actually have a name and therefore go undiagnosed and untreated resulting in restlessness, difficulty in sleeping and daytime sleepiness.
Restless legs syndrome (RLS) is a central nervous disorder possibly with some genetic predisposition or related to an imbalance of dopamine in the brain. Dopamine is a brain chemical that affects movement and as levels normally drop at night this may explain why RSL is worse at this time. Iron is a significant factor in the production of dopamine which may account for the link between low iron levels and RLS symptoms.
RSL may be acerbated, but not caused by stress or psychiatric conditions.
As indicated RLS usually affects the legs particularly the calves but some people may experience symptoms in the upper legs, feet, hands or arms.
Primary RSL seems to have no cause. Those affected may have developed the condition during childhood and this may have been attributed to growing pains (or even ADHD). There is a tendency for the condition to increase with age with significant increase in severity often seen after age 50.
With secondary RLS there is usually a link to another condition. These include anaemia, kidney disease, Parkinson’s disease, pregnancy, thyroid problems, neurologic lesions, sleep apnoea or narcolepsy, and alcoholism.
There are certain medications that when taken may trigger or increase RSL symptoms, as may the withdrawal of some drugs.
Diagnosis is usually made on the basis of reported symptoms and medical history. The four established criteria are:
• Irresistable urge to move your legs along with uncomfortable sensations (may be described as creeping, crawling, pulling, tingling, itching, pain, burning)
• Symptoms commence or get worse at rest (sitting, lying down)
• Symptoms are partially relieved by activity (stretching, walking)
• Symptoms are worse at night
Blood tests or other investigations may be done to exclude other possible causes.
RSL doesn’t lead to other serious conditions but symptoms can become incapacitating for some sufferers especially excessive tiredness from sleep deprivation.
There is no cure for RLS but there are treatments available that can manage the condition and relieve discomfort. This may involve treatment of underlying conditions, lifestyle techniques which may require changes in daily behavior or habits, use of support groups and in severe cases transcutaneous electric nerve stimulation (TENS) for a short time at night may be of help. Medications are commonly prescribed but there is no one drug that works for everyone and they should always be used with caution as may have side effects or increase the symptoms of RSL. Usually the drugs prescribed are ones used for other conditions but have been found to be beneficial with symptoms of RLS. They may include dopaminergic agents, Benzodiazepines, non benzodiazepine sedatives, opiates and narcotics and hypertensive medications.
RSL may necessitate referral to a sleep specialist for further evaluation. This may require observation overnight at a sleep clinic where sleep can be monitored for periodic limb movements during sleep. However a diagnosis can usually be made without a sleep study.
Irene
Tuesday, April 20, 2010
Adult 'whooping cough'
I’m waiting for the health department to issue another ‘Pertussis Alert’, like they did last year.
Whooping cough is not something that I learnt a great deal about, or saw a lot of, while studying to be a respiratory specialist. Perhaps it was not deemed serious enough a condition. As a result, I have had to slowly shed a skepticism towards this organism, Bordetella pertussis, and the role it plays in respiratory disease in adults. In clinical practice I have occasionally been embarrassed by failure to detect the diagnosis in patients referred with troublesome cough – being pipped to the post by diligent general practitioners. It seems, however, that I am not alone. A review of the literature on PubMed in search of a decent review of management of infection with Bordetella pertussis, cause of whooping cough in children, was disappointing.
Why does this matter? We just diagnosed another patient with pertussis infection last week – the diagnosis being based on the clinical presentation and the presence of specific IgA on serological testing. My impression of that woman’s illness was that it seemed very much like the illness doing the rounds of my family in recent weeks, which brought it close to home. Full sympathy to her husband who valiantly tried to remain in the marriage bed through distressing bouts of coughing at night time.
General practitioners around the region are making the diagnosis more often than me. The impression is of a significant outbreak. It is certainly not a rare disease.
Amongst the papers I have found and read in my renewed enthusiasm for this bug, the most interesting was a paper in the Brazilian infectious disease journal This paper, freely available online, beautifully describes the sort of clinical presentation I have seen a couple of times with this infection. In the case they present, the symptoms were ‘ cough and a fear of sleep’.
They make the points well that:
- the cough of pertussis is not just paroxysmal. The paroxysms are violent and uncontrolled and
- as a consequence are associated with an inability to breathe during coughing bouts (‘I just get short of breath with the coughing’) and
- in adults, who are able to clear away laryngeal secretions during the day, the paroxysms are predominantly a nocturnal problem (secretions build up and occlude the airway at night time, resulting in fragmentation of sleep). That means that we doctors, who see them in the light of day, seldom witness the worst of it.
The authors of that paper also suggest that rather than serology, PCR of upper airway secretions should be utilized early.
I tend to have referred to me patients with chronic cough only; the wait for an appointment cures many ills. Bordetella pertussis, we doctors have been taught, may be an important cause of chronic cough in adults. Of course, it must, by definition, also be cause of ‘acute’ cough (every chronic cough begins sometime) - mostly an acute and distressing coughing illness. I think it’s worth reflecting on whether we should apply ourselves more often to making the diagnosis early. By the time the patient has had the cough for more than 5 days, it is unlikely that antibiotics (generally macrolides are most useful - the best evidence being for clarithromycin and azithromycin) do anything more than shorten the period of infectivity. Certainly a recent Cochrane review suggested as much; there is no evidence that any treatments have an impact on symptoms.
It may be that if we listen carefully to the symptoms our patients relay to us early in the history of a coughing illness (how would a child with whooping cough describe their symptoms if they could talk?) and target investigations appropriately, early use of antibiotics – which is otherwise discouraged in upper respiratory infections – for adult patients with ‘whooping cough’ could save our patients a lot of inconvenience and demoralizing ill health.
Andrew
Whooping cough is not something that I learnt a great deal about, or saw a lot of, while studying to be a respiratory specialist. Perhaps it was not deemed serious enough a condition. As a result, I have had to slowly shed a skepticism towards this organism, Bordetella pertussis, and the role it plays in respiratory disease in adults. In clinical practice I have occasionally been embarrassed by failure to detect the diagnosis in patients referred with troublesome cough – being pipped to the post by diligent general practitioners. It seems, however, that I am not alone. A review of the literature on PubMed in search of a decent review of management of infection with Bordetella pertussis, cause of whooping cough in children, was disappointing.
Why does this matter? We just diagnosed another patient with pertussis infection last week – the diagnosis being based on the clinical presentation and the presence of specific IgA on serological testing. My impression of that woman’s illness was that it seemed very much like the illness doing the rounds of my family in recent weeks, which brought it close to home. Full sympathy to her husband who valiantly tried to remain in the marriage bed through distressing bouts of coughing at night time.
General practitioners around the region are making the diagnosis more often than me. The impression is of a significant outbreak. It is certainly not a rare disease.
Amongst the papers I have found and read in my renewed enthusiasm for this bug, the most interesting was a paper in the Brazilian infectious disease journal This paper, freely available online, beautifully describes the sort of clinical presentation I have seen a couple of times with this infection. In the case they present, the symptoms were ‘ cough and a fear of sleep’.
They make the points well that:
- the cough of pertussis is not just paroxysmal. The paroxysms are violent and uncontrolled and
- as a consequence are associated with an inability to breathe during coughing bouts (‘I just get short of breath with the coughing’) and
- in adults, who are able to clear away laryngeal secretions during the day, the paroxysms are predominantly a nocturnal problem (secretions build up and occlude the airway at night time, resulting in fragmentation of sleep). That means that we doctors, who see them in the light of day, seldom witness the worst of it.
The authors of that paper also suggest that rather than serology, PCR of upper airway secretions should be utilized early.
I tend to have referred to me patients with chronic cough only; the wait for an appointment cures many ills. Bordetella pertussis, we doctors have been taught, may be an important cause of chronic cough in adults. Of course, it must, by definition, also be cause of ‘acute’ cough (every chronic cough begins sometime) - mostly an acute and distressing coughing illness. I think it’s worth reflecting on whether we should apply ourselves more often to making the diagnosis early. By the time the patient has had the cough for more than 5 days, it is unlikely that antibiotics (generally macrolides are most useful - the best evidence being for clarithromycin and azithromycin) do anything more than shorten the period of infectivity. Certainly a recent Cochrane review suggested as much; there is no evidence that any treatments have an impact on symptoms.
It may be that if we listen carefully to the symptoms our patients relay to us early in the history of a coughing illness (how would a child with whooping cough describe their symptoms if they could talk?) and target investigations appropriately, early use of antibiotics – which is otherwise discouraged in upper respiratory infections – for adult patients with ‘whooping cough’ could save our patients a lot of inconvenience and demoralizing ill health.
Andrew
Thursday, April 15, 2010
$20 a pack
In the news this week has been Kevin Rudd's proposal to increase the cost of cigarettes by up to $6.60 per pack, to raise the needed revenue for his health reforms. If this recommendation is successful cigarettes will cost around $20 per pack, so a pack a day smoker will be out of pocket $140 per week and about $7280 per year!
What does research indicate about price hikes in cigarettes? It shows that prices increases do lead to cessation in smoking. There is a price elasticity effect. This economic term can be used to justify this proposal. Price elasticity refers to the amount a product rises or falls in relation to a price increase or decrease.
In 1999, a World Bank review concluded that, all else being equal, price rises of about 10% would on average reduce tobacco consumption by about 4% in developed countries and about 8% in developing countries.
It has also been demonstrated that price increases are particularly effective for younger people, while have less of an impact on older smokers.
I was listening to Professor Rob Moodie speak about this issue last night. He said 80% of people backed a price increase and this recommendation had been on the table for a long time. Interestingly, when asked if cigarette should become illegal he did not think so and talked about ideally cigarettes becoming a 'boutique habit'. An interesting term, which refers to a minimal number of people smoking (those who can afford it I guess) and also smoking less.
The term boutique sounds a little too sophisticated for my liking and as all the research shows there is no safe level of smoking. Conversely, harm minimization strategies have a lot of merit so any policy or preventative strategy that reduces the prevalence of smoking is a good thing.
If this increase in tax takes effect it will be the first tax increase in 10 years (on cigarettes) in Australia and will put us back on par with the rest of the world. Not only does the tax hike have the capacity to raise billions of dollars for the health reforms, it also has the capacity to save the government some of the 31 billion dollars in health care for smokers. There are other hidden costs society carries due to smoking such as cleaning up after smokers (butts, cigarette packets), loss in productivity due to smoking related issues and absenteeism from the work force. Not to mention the human cost of the morbidity and mortality and the families this directly effects.
This tax is long over due, so hopefully all forms of government will work together to have this legislation passed.
Jessica
Tuesday, April 13, 2010
Fixing the ugly asthma blog post
A couple of weeks ago I posted a blog about asthma phenotypes which was lacking in graphics. To try to make up for this, today's blog is all about the missing graphics.
That post discussed a paper from the blue journal from the USA, which surveyed hundreds of asthmatics and found that they clustered in five quite distinctive clinical groups. Details are in the previous blog, or indeed the original paper.
Although a wide range of variables were used in the analysis to assign people to clusters (initially 34, whittled down to 11 ultimately). However, using three variables only (basline FEV1, maximum FEV1 after maximal bronchodilator, and age of onset of asthma) as follows...
Just FYI, the colours correspond to clinical state as follows:
Blue = mild atopic asthma
Green = mild to moderate atopic asthma
Yellow = late onset non-atopic asthma
Orange = severe atopic asthma
Red = severe asthma with fixed airflow obstruction.
I think that the possibility of differentiating between clinical phenotypes of asthma based on three simple clinical parameters is very attractive, and could have significant implications for both research and clinical practice.
Andrew
That post discussed a paper from the blue journal from the USA, which surveyed hundreds of asthmatics and found that they clustered in five quite distinctive clinical groups. Details are in the previous blog, or indeed the original paper.
Although a wide range of variables were used in the analysis to assign people to clusters (initially 34, whittled down to 11 ultimately). However, using three variables only (basline FEV1, maximum FEV1 after maximal bronchodilator, and age of onset of asthma) as follows...
...patients could be assigned to clusters with 80% accuracy. In this diagram, the blobs represent assignment of cluster based on the three-variable approach as opposed to the 11 variable approach. (ie for cluster 4, 72% of patients assigned to cluster 4 based on 11 variables were also assigned to cluster 4 based on the three variables only).
Just FYI, the colours correspond to clinical state as follows:
Blue = mild atopic asthma
Green = mild to moderate atopic asthma
Yellow = late onset non-atopic asthma
Orange = severe atopic asthma
Red = severe asthma with fixed airflow obstruction.
I think that the possibility of differentiating between clinical phenotypes of asthma based on three simple clinical parameters is very attractive, and could have significant implications for both research and clinical practice.
Andrew
Monday, April 12, 2010
Antibiotics in COPD exacerbations? Show me the sputum!
Are antibiotics needed in treatment of acute exacerbations of COPD (AECOPD)?
I have been reading a paper in the Blue journal from mid January which tries to address this question. As it was deemed editorial – worthy, it caught my eye.
To date, we administer antibiotics to patients with exacerbations of chronic obstructive airways disease based on the Anthonisen criteria. These were defined for a paper published in 1987 – now some years ago – and take into account increasing breathlessness, sputum volume and sputum purulence. There were limitations to that trial, not least among which was the absence of corticosteroids, such as prednisolone, from treatment regimes. We know that corticosteroids hasten clinical and physiological recovery and shorten hospital stays in patients with COPD. We don’t know that about antibiotics.
This recent, Dutch, study randomized 223 patients who between them suffered 265 episodes of exacerbation to receive either doxycycline 200mg daily for 7 days or placebo, in addition to a standardized treatment regime which included intraveinous and then oral prednisolone. Patients likely to have pneumonia (xray signs, fever) were excluded reasonably well. The primary endpoint was clinical response on Day 30, meaning that their symptoms and signs had either completely resolved or improved without getting worse again.
They found the following:
• At day 30 there was no significant difference between the groups
• At day 10, however (before which time you would generally hope to be sending someone home from hospital – the norm being around 7 to 9 days in our sort of institution), there was a slight difference in favour of the treatment group in terms of clinical response (80 vs 69% clinically responded. P=0.03). 67% of the doxy group were ‘cured’ at day 10, vs 51% of the placebo group (P=0.01). The difference was not statistically significant at day 30.
• More patients were changed from placebo to open-label antibiotic because of lack of efficacy than from doxy to open-label antibiotic for the same reason, at day 10 (15vs28%, P=0.01) and day 30 (33vs45%, P=0.13)
• Symptom scores were more improved at day 10 for the doxy group than for the placebo group, but not at day 30
• Microbiological outcomes varied at day 10. Common bugs were H.influenzae (41%), Pneumococcus (24%), Moraxella catarrhalis (22%). 52 of 78 patients in the doxy group who grew bacteria were cleared (67% ) vs 25 of 73 patients (34%) in the placebo group.
• 46 of the doxy group and 62 of the placebo group (37 vs 46%) had treatment failure.
• Withdrawal from the trial was similar in both groups, but 23 (17% ) of the placebo group withdrew for lack of efficacy, as opposed to only 8 (6%) of the doxy group withdrawing for that reason
The doxy seemed, in sub-group analysis, particularly beneficial in patients with increased sputum volume and purulence and a C-reactive protein of over 50.
The question raised by the article, and also by the editorial, is whether antibiotics really need to be added in to treatment regimes for patients with acute exacerbations of COPD. I suppose there are two ways of looking at this.
From my perspective, as doctor and holder of the keys to the pharmacy, it may well be correct to say that absence of benefit at 30 days is reason to withhold antibiotics from patients with acute exacerbations of COPD. It should be pointed out, however, that we all use corticosteroids in AECOPD in the absence of precisely the same benefit.
Why do we do this? Well, perhaps here we consider the patients perspective. We use corticosteroids because patients feel better faster, and because they stay in hospital for less time. We like it when our patients feel better faster, because psychologically any improvement is linked to our intervention, which in turn encourages future adherence to suggested treatment regimes.
If my doctor tells me that they are withholding a treatment with a narrow-spectrum antibiotic that will probably make me feel better quicker because it won’t still be having that effect in a month, I would probably be a little annoyed.
I would like to see a study setting out to prove whether what we already know about steroids. applies to antibiotics too: Do some patients feel better quicker, and get out of hospital sooner, if they take antibiotics –regardless of the effect at 30 days? Perhaps the study has been done. Time to get on PubMed.
Of course the argument is more complex than this. Antibiotic resistance is a major public health problem. However, the very real clinical issue of how we maintain our patients’ confidence by introducing treatments that work to help them achieve tangible health improvements, didn’t make it into the discussion about this paper in the AJRCCM.
Andrew
I have been reading a paper in the Blue journal from mid January which tries to address this question. As it was deemed editorial – worthy, it caught my eye.
To date, we administer antibiotics to patients with exacerbations of chronic obstructive airways disease based on the Anthonisen criteria. These were defined for a paper published in 1987 – now some years ago – and take into account increasing breathlessness, sputum volume and sputum purulence. There were limitations to that trial, not least among which was the absence of corticosteroids, such as prednisolone, from treatment regimes. We know that corticosteroids hasten clinical and physiological recovery and shorten hospital stays in patients with COPD. We don’t know that about antibiotics.
This recent, Dutch, study randomized 223 patients who between them suffered 265 episodes of exacerbation to receive either doxycycline 200mg daily for 7 days or placebo, in addition to a standardized treatment regime which included intraveinous and then oral prednisolone. Patients likely to have pneumonia (xray signs, fever) were excluded reasonably well. The primary endpoint was clinical response on Day 30, meaning that their symptoms and signs had either completely resolved or improved without getting worse again.
They found the following:
• At day 30 there was no significant difference between the groups
• At day 10, however (before which time you would generally hope to be sending someone home from hospital – the norm being around 7 to 9 days in our sort of institution), there was a slight difference in favour of the treatment group in terms of clinical response (80 vs 69% clinically responded. P=0.03). 67% of the doxy group were ‘cured’ at day 10, vs 51% of the placebo group (P=0.01). The difference was not statistically significant at day 30.
• More patients were changed from placebo to open-label antibiotic because of lack of efficacy than from doxy to open-label antibiotic for the same reason, at day 10 (15vs28%, P=0.01) and day 30 (33vs45%, P=0.13)
• Symptom scores were more improved at day 10 for the doxy group than for the placebo group, but not at day 30
• Microbiological outcomes varied at day 10. Common bugs were H.influenzae (41%), Pneumococcus (24%), Moraxella catarrhalis (22%). 52 of 78 patients in the doxy group who grew bacteria were cleared (67% ) vs 25 of 73 patients (34%) in the placebo group.
• 46 of the doxy group and 62 of the placebo group (37 vs 46%) had treatment failure.
• Withdrawal from the trial was similar in both groups, but 23 (17% ) of the placebo group withdrew for lack of efficacy, as opposed to only 8 (6%) of the doxy group withdrawing for that reason
The doxy seemed, in sub-group analysis, particularly beneficial in patients with increased sputum volume and purulence and a C-reactive protein of over 50.
The question raised by the article, and also by the editorial, is whether antibiotics really need to be added in to treatment regimes for patients with acute exacerbations of COPD. I suppose there are two ways of looking at this.
From my perspective, as doctor and holder of the keys to the pharmacy, it may well be correct to say that absence of benefit at 30 days is reason to withhold antibiotics from patients with acute exacerbations of COPD. It should be pointed out, however, that we all use corticosteroids in AECOPD in the absence of precisely the same benefit.
Why do we do this? Well, perhaps here we consider the patients perspective. We use corticosteroids because patients feel better faster, and because they stay in hospital for less time. We like it when our patients feel better faster, because psychologically any improvement is linked to our intervention, which in turn encourages future adherence to suggested treatment regimes.
If my doctor tells me that they are withholding a treatment with a narrow-spectrum antibiotic that will probably make me feel better quicker because it won’t still be having that effect in a month, I would probably be a little annoyed.
I would like to see a study setting out to prove whether what we already know about steroids. applies to antibiotics too: Do some patients feel better quicker, and get out of hospital sooner, if they take antibiotics –regardless of the effect at 30 days? Perhaps the study has been done. Time to get on PubMed.
Of course the argument is more complex than this. Antibiotic resistance is a major public health problem. However, the very real clinical issue of how we maintain our patients’ confidence by introducing treatments that work to help them achieve tangible health improvements, didn’t make it into the discussion about this paper in the AJRCCM.
Andrew
Predicted Reference Values
Predicted reference values assist in the interpretation of lung function results and are derived from equations determined by testing large populations of normal healthy individuals who are never smokers and working out the contribution (weighting) of different factors on lung function. They are usually determined by gender, age, height, ethnicity and sometimes weight.
Defining Normality
Many labs define the range of normality for spirometry as values higher than the 80% of the mean predicted value (MPV) for FEV1 and FVC. A more scientific approach is to define the normal range as the range in which we are confident that 95% of the population lies. The 95% confidence interval is defined by the mean and the standard deviation.
Lower Limit of Normal (LLN)
Establishing the LLN should be done by analyzing some measure i.e. FVC or FEV1 in healthy subjects and then determining the variability of that measurement. In clinical medicine the fifth percentile is often defined as the LLN because it represents the segment of healthy subjects farthest below the average even though subjects in the fifth percentile are healthy they are arbitrarily defined as “abnormal” for clinical purposes.
Some clinicians use a fixed percentage (measured value divided by the reference value x 100) of the reference value to determine the degree of abnormality and eighty percent (80%) is often used as the limit of normal. Unfortunately this method leads to errors because the variability around the predicted value is relatively constant in adults. In other words the scatter of normal values does not vary with the size of the predicted value.
The inserted figure illustrates why using fixed percentages such as 80% of the predicted can lead to misclassification and introduces both age and height biases. The shaded areas represent the “normal” range from 100% of the predicted value down to the fifth percentile. The dashed line shows a fixed percentage of the predicted in this case 80% as is sometimes used to represent the LLN.
In tall young subjects 80% of the predicted is often less than the fifth percentile; using 80% as the limit can allow a patient who really does have decreased lung function (in the fifth percentile or lower) to be misclassified as normal. This situation is a false negative result; the patient has disease but the test does not indicate abnormality.
Similarly an elderly patient who is short may have a lung function parameter than is less than 80% of the predicted but well within the statistically normal range (above the fifth percentile). This short elderly subject would be misclassified as having lung disease when in fact she is within the “normal” range (i.e. a false positive result).
A more statistically sound approach for classifying abnormality is to compute the z-score or standard deviation score (SDS). If lung function varies in a normal fashion the mean ± 1.96 standard deviations (SDs) defines the 95% confidence interval. Statistically, 95% of the healthy population falls within approximately 2 SDs of the mean. The remaining subjects fall into either the highest or lowest 2.5% of the distribution. For many pulmonary function variables, only the LLN (i.e. below the mean) is significant. The z-score or SDS can be calculated easily if the variability (residual standard deviation) of the reference population is known.
Normal predicted values for ventilatory function generally vary as follows
1. Sex - for a given height and age males have a larger FEV1 & FVC but a slightly lower FEV1/FVC
2. Age – After age 25 all indices gradually fall and the fall in FEV1/FVC is due to the greater decline in FEV1 than FVC although the precise rate of decline is probably masked due to the complex interrelationship between age and height.
3. Height – All indices other then FEV1/FVC increase with standing height
4. Ethnic Origin – Caucasians have the largest FEV1 & FVC of the various ethnic groups. Whilst Polynesians are among the lowest.
The purpose of reference values is to remove the variability in spirometry due to gender; age etc. and the reference source should be carefully considered and not left to equipment manufacturers but there are no universally accepted reference values. The major problem with many portable spirometers is that they report results as a percentage of predicted and do not include LLN.
We know that clinical decisions should be based on well-defined lower limits of normal rather than fixed percents of predicted (in adults) and to assist in the interpretation of our reports in our lab we have just introduced the LLN values to our suite of reports.
Vanessa
Friday, April 9, 2010
Rural health outcomes
Living in a rural environment has many advantages and is the only way of life for some but what impact does it have on residents health status?
The location you live and its impact on your health has been topical during the week. Listening to triple J Wednesday they had a forum on how you postcode may affect your health. Many of the listeners lived in the city and stated places with access to parks, beaches, good public transport all impacted positively on their health status. Places where people where reliant on using the car and the environment was not seen as being conducive to an outdoors lifestyle where seen as being adverse for health.
So how does living rurally impact our health. The callers to triple J had subjective analysis of their health and again subjectively many rural residents would feel the country environment enhanced their health rather than hindered.
Unfortunately the health statistics tell a very different story. Rural residents report lower levels of health in areas such as injury, depression and suicide, cardiovascular disease, cancer compared to those residing in non rural locations (Fagar et al 2000).
Why is this. The social determinants of health have an impact on these figures.The World Health Organisation (WHO, 2008) commission on the social determinants of heath states “avoidable health inequities arise because of circumstances in which people grow, live, work and age and the systems put in place to deal with illness”. These circumstances can be influenced by government policy, economic and social conditions (WHO, 2008). Social determinants of health relevant to a rural lifestyle are geographical and social isolation, aging population, culture of rural communities, lower socio economic status and environmental conditions.
The location you live and its impact on your health has been topical during the week. Listening to triple J Wednesday they had a forum on how you postcode may affect your health. Many of the listeners lived in the city and stated places with access to parks, beaches, good public transport all impacted positively on their health status. Places where people where reliant on using the car and the environment was not seen as being conducive to an outdoors lifestyle where seen as being adverse for health.
So how does living rurally impact our health. The callers to triple J had subjective analysis of their health and again subjectively many rural residents would feel the country environment enhanced their health rather than hindered.
Unfortunately the health statistics tell a very different story. Rural residents report lower levels of health in areas such as injury, depression and suicide, cardiovascular disease, cancer compared to those residing in non rural locations (Fagar et al 2000).
Why is this. The social determinants of health have an impact on these figures.The World Health Organisation (WHO, 2008) commission on the social determinants of heath states “avoidable health inequities arise because of circumstances in which people grow, live, work and age and the systems put in place to deal with illness”. These circumstances can be influenced by government policy, economic and social conditions (WHO, 2008). Social determinants of health relevant to a rural lifestyle are geographical and social isolation, aging population, culture of rural communities, lower socio economic status and environmental conditions.
In addressing health inequity we need to address these issues. We know access to services to being a strong influence on rural people health. Ways we are seeking to address this is providing services in rural communities (Hamilton, Horsham, Mount Gambier, Portland, Mildura) to decrease patients travel time and to also provide greater access to services through additional physicians.
The latter is a relevant point and we are very close to having another full time physician employed here. The benefits of this will be significant.
It is important to be aware of the social determinants of health in a rural context and to look at ways of addressing these issues.
Jessica
Thursday, April 1, 2010
Shift work and sleep
Shift work is a way of life for much of the population, increasingly so, as our society becomes much more 24/7.
What are the implications on our health related to shift work? A variety of studies have been conducted and have demonstrated that night shift workers have disturbed sleep and excessive sleepiness related to day time shift workers. These symptoms have been attributed to the fact that workers behavioral sleep-wake schedules are out of phase and often in direct opposition to their endogenous circadian rhythms.
Results from a usa study suggested that the prevalence of insomnia or excessive sleepiness is 32% and 26% in night and rotating shift workers, respectively.
The researchers also concluded (as other studies have) that circadian rhythm and other
sleep disorders are more prevalent in night-shift workers compared with day workers and that insomnia, excessive sleepiness, and circadian rhythm disorders are associated with significant
morbidity (accidents and absenteeism) in shift-work samples.
The researchers also looked at the risk for heart disease. The findings indicate a risk related to shift work although it is not specific to insomnia or excessive sleepiness symptoms.
This effect remained significant after controlling for additional risk factors (body mass index, smoking status, hypertension, alcohol intake and diabetes, P < .05). This finding is consistent
with previous research that has shown an increased risk for cardiovascular
disease in shift workers compared with day workers.
For many of us that work in the sleep disorders field the irony is that shift work is part and parcel of the job.
Jessica
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