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
Thursday, June 17, 2010
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
Tuesday, June 15, 2010
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
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
Tuesday, June 8, 2010
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.
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
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
Monday, June 7, 2010
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
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
Tuesday, June 1, 2010
Swine flu and invasive aspergillosis.
Medscape sent round some articles at the start of the week. One in particular, which consisted of two case reports and a discussion, caught my interest. The case report was from respiratory specialists at Columbia University and the University of California.
Two patients, both men, contracted H1N1 influenza (swine flu) last year and ultimately succumbed to respiratory and systemic complications of that disease. In each case:
- acute respiratory distress syndrome (ARDS) developed rapidly;
- influenza was not diagnosed immediately;
- high doses of corticosteroids were given as methylprednisolone to treat the ARDS;
- the influenza virus was complicated by invasive aspergillosis.
In each case, bronchoscopy was performed within the first few hours of intubation, and evidence of aspergillus, a fungus, was detected. In one this was clearly invasive infection, evident on biopsy samples from the airway.
Now aspergillus in the lungs is becoming a bit of an interest of mine. The article I read today confirms that there is increasing recent evidence that patients with COPD are at risk of invasive aspergillosis. Prevalence of this problem, however, in the massive population of patients with COPD is probably very low. There is understood to be a very high mortality rate in such patients (upwards of 95%). For a number of reasons, documentation of the extent of the problem is limited. A good review of this issue from 3 years ago is given here.
In the cases discussed, it was suggested that the impact of influenza virus on airway and systemic defence mechanisms (reduced white blood cells, reduced movement of ‘cilia’ – fine hairs on the airway walls) combined with the steroids, which are a disaster for airway immune defence, created a great environment for aspergillus to get a toehold.
New information for me was the availability of some blood tests to assist in the diagnosis of invasive aspergillosis. A serum galactomannan assay has been available since around 2006 in the USA and for longer in Europe. It has moderate diagnostic accuracy for invasive aspergillosis. Bronchoalveolar lavage galactomannan has been demonstrated to be quite sensitive and specific for invasive aspergillosis in the lungs.
I am not sure that this assay is available in Australia, and will need to find out. As (swine) flu season is upon us we should probably have a reasonable index of suspicion that the aspergillus isolates we grow in cultures – particularly of our hospitalized patients- may not simply be contaminants. Perhaps invasive aspergillosis, which many of us have considered to be unlikely to occur outside of the profoundly immunosuppressed, is on the rise. Further evaluation with CT chest and bronchoscopy should be considered, and considered early in patients who are unwell.
Andrew
Two patients, both men, contracted H1N1 influenza (swine flu) last year and ultimately succumbed to respiratory and systemic complications of that disease. In each case:
- acute respiratory distress syndrome (ARDS) developed rapidly;
- influenza was not diagnosed immediately;
- high doses of corticosteroids were given as methylprednisolone to treat the ARDS;
- the influenza virus was complicated by invasive aspergillosis.
In each case, bronchoscopy was performed within the first few hours of intubation, and evidence of aspergillus, a fungus, was detected. In one this was clearly invasive infection, evident on biopsy samples from the airway.
Now aspergillus in the lungs is becoming a bit of an interest of mine. The article I read today confirms that there is increasing recent evidence that patients with COPD are at risk of invasive aspergillosis. Prevalence of this problem, however, in the massive population of patients with COPD is probably very low. There is understood to be a very high mortality rate in such patients (upwards of 95%). For a number of reasons, documentation of the extent of the problem is limited. A good review of this issue from 3 years ago is given here.
In the cases discussed, it was suggested that the impact of influenza virus on airway and systemic defence mechanisms (reduced white blood cells, reduced movement of ‘cilia’ – fine hairs on the airway walls) combined with the steroids, which are a disaster for airway immune defence, created a great environment for aspergillus to get a toehold.
New information for me was the availability of some blood tests to assist in the diagnosis of invasive aspergillosis. A serum galactomannan assay has been available since around 2006 in the USA and for longer in Europe. It has moderate diagnostic accuracy for invasive aspergillosis. Bronchoalveolar lavage galactomannan has been demonstrated to be quite sensitive and specific for invasive aspergillosis in the lungs.
I am not sure that this assay is available in Australia, and will need to find out. As (swine) flu season is upon us we should probably have a reasonable index of suspicion that the aspergillus isolates we grow in cultures – particularly of our hospitalized patients- may not simply be contaminants. Perhaps invasive aspergillosis, which many of us have considered to be unlikely to occur outside of the profoundly immunosuppressed, is on the rise. Further evaluation with CT chest and bronchoscopy should be considered, and considered early in patients who are unwell.
Andrew
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