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Hello, I'm Norman Swan.
Welcome to this program in our series on guidelines and type 2 diabetes.
Every year there are about 3.8 million deaths globally
attributable to diabetes.
In Australia, type 2 diabetes is the fastest-growing chronic disease,
with the total number of Australians with diabetes and pre-diabetes
estimated at a whopping 3.2 million,
and it's the sixth-leading cause of death.
This program looks at two NHMRC evidence-based guidelines that are new
and address complications and comorbidity in type 2 diabetes.
They are the evidence-based guidelines for diagnosis and management
of kidney disease in type 2 diabetes,
and the guidelines for the management of diabetic retinopathy.
For those of you watching on your computers,
you can type your questions directly in to the studio.
Just click on the LiveTalk tab at the top of the web page you're looking at.
That also means, of course, that we can ask questions of you.
Here's one to get you going:
Click away on that one, and we'll give you results of that in a moment.
As usual, there are a number of useful resources available
on the Rural Health Education Foundation's website:
Now let me introduce our panel to you.
Stephen Twigg is an endocrinologist at the University of Sydney
and President of the Australian Diabetes Society.
- Welcome, Stephen. - Good evening.
Alan Cass is the senior director
of the George Institute for International Health,
and director of the Poche Indigenous Health Centre
at the University of Sydney.
- Welcome, Alan. - Good evening, Norman.
Paul Mitchell is Professor of Ophthalmology
at the University of Sydney, and runs the Blue Mountains Eye Study.
- Welcome, Paul. - Thanks, Norman. Good to be here.
And David Guest is a rural general practitioner in Goonellabah in NSW.
- Welcome. - Thanks, Norman.
David, challenging,
dealing with comorbidities in general practice, I assume.
It's a growing area.
It's a bigger and bigger problem.
It's something that's taking more and more of GPs' time.
If you get systems in place, you can probably cope with the challenge.
Talk to me about the trends that are going on, Stephen.
As you've mentioned already, diabetes is on the rise.
We believe that approximately 100,000 people per year in Australia
are developing diabetes.
It's very similar to the worldwide trend.
There are a number of factors that are probably critical in the process
in terms of the development of diabetes.
The prevalence changes in different groups in Australia?
Yes, there are certainly higher-risk groups,
particularly an ageing population.
There are certain ethnic groups that
are at higher risk than others.
There are also issues
to do with lifestyle change.
As we can see on this slide - this data
is from the turn of the millennium -
approaching a million people, or 7.4%
of adults aged over 25 had diabetes
in Australia at that time, well over 90%
of it being type 2 diabetes.
The other conditions, impaired fasting
glucose and impaired glucose tolerance,
or as you referred to them,
the pre-diabetes conditions,
also extremely common.
So approaching one in four
Australian adults have some form
of glucose abnormality.
NORMAN: Extraordinary.
It's a remarkable figure.
NORMAN: It's also age-dependent?
Yes, very much so.
If we dissect this out further,
the same study, the AusDiab study,
demonstrated a strong age-dependence
for diabetes, indicating that
the ability of the pancreas to produce
insulin tends to deteriorate with time.
Approaching one in four Australian
adults in their 70s will have diabetes
in comparison to a much lower percentage
of people earlier in their life.
We're trending upwards faster than we thought?
Very much so.
World Health Organisation data, recent trends have suggested,
rather than seven million people per year developing diabetes,
it's more like ten million people.
We're going to hear about that in the more recent estimates,
in the next year 2010 data from the International
Diabetes Federation and WHO.
NORMAN: This graph shows we're
tracking faster than we thought.
And the Australian data, very similar.
In the AusDiab study,
whilst 'e' on the far right is an estimate
based on previous decades,
in the last decade, the late '90s,
then into the 2000s,
the figures are well above what
the estimates were on the trend line.
A study from the Australian Institute
of Health and Welfare 2006 indicated
it's more like 1.5 million people
who have diabetes,
then increasingly, 100,000 a year.
So really, even off that scale,
if we look at more recent estimates
of diabetes in the Australian community.
We're talking here about absolute risk, global risk,
just as much as we're talking about glucose?
Definitely.
Glucose, if you like, is the marker.
People with diabetes have two- to fourfold
the rate of cardiovascular disease as the general community.
As you've pointed out, it does emphasise global cardiovascular risk
and the importance of tight blood pressure and cholesterol control.
David, on the day of broadcast, yesterday's Medical Journal of Australia
described the fact that general practitioners are not measuring
absolute risk to the rate they should be.
What are the barriers to measuring absolute risk?
It's a GP-education problem to start with.
There are tools available now that make it much easier.
I have a preference for a computerised electronic health record.
Getting data out of the computer makes these sort of assessments much easier.
A website which I think is the one recommended by various colleges
to assess absolute cardiovascular- disease risk is available on the web
and available on the desktop. That's a very useful tool for GPs.
You've got an example of this risk tool that's in the guideline?
That's right, Norman.
If we look at the next slide, this is an example.
This is for people with diabetes.
The charts are divided into those with and without diabetes.
People with diabetes are a high-risk group.
They can be stratified on the basis of their cardiovascular risk
in terms of looking at their systolic blood pressure,
their cholesterol, HDL total cholesterol, HDL ratio,
gender status and smoking status.
It's possible then to identify
whether a person would be deemed at a high cardiovascular risk,
in which case the intensity of the management of their surrogate markers -
their blood pressure, their cholesterol, their glucose
and also antiplatelet therapy can be modified appropriately.
NORMAN: You're arguably more likely to save their life
by managing those other factors than their sugar?
It's not one or the other, but it's both.
All of them are important.
For example, diabetic retinopathy glucose is the major factor
that will contribute to that complication.
In terms of cardiovascular disease in people with diabetes,
the risk is probably approaching 15% to 20% of the variation
in risk will be glucose, depending upon the degree of glycaemic control.
And cholesterol and blood-pressure control, very important in that setting.
How important, Paul, are these other risk factors than glucose?
We know that glucose control can help diabetic retinopathy,
but those other risk factors?
- There's growing evidence, isn't there? - That's right.
The effect of good diabetes glucose control
on preventing the development and progression of diabetic retinopathy
has been shown both in type 1 and in type 2 in the UKPDS.
That latter study, UKPDS,
actually demonstrated almost an equivalent effect in type 2 diabetes
of blood-pressure management.
Indeed, recent studies,
the ACCORD studies and the RASS study, just recently published,
have shown that in fact really tight blood-pressure control,
perhaps with modern blood-pressure agents, ARBs,
can actually reduce the incidence of diabetic retinopathy
and may result in regression of existing retinopathy lesions.
And in kidney disease, Alan Cass?
Again, the key factors to control are blood pressure.
Also, how well you control glycaemia is a key factor
in terms of progression of kidney disease.
NORMAN: What's the management challenge, Stephen?
Diabetes, as we know, is extremely challenging.
There's the combination of lifestyle management and pharmacotherapy.
There's the importance of vigilance with respect to diabetes management,
because, as we know, targets can be difficult to maintain over time.
When we look at the optimisation of care, in terms of patient care,
we have tight blood pressure, blood glucose and cholesterol targets
monitoring for complications.
This slide indicates that in general, we will achieve a lot
if we have a generic, crowd-based approach.
If we go on to the one which shows the management challenge to optimise care,
once we can assess cardiovascular risk for the individual
and we can target more appropriately lipids and blood pressure and glycaemia
for the particular person - the career stage of their diabetes -
then we can expect to achieve even better outcomes
when we customise or individualise the care.
Whilst the world is obsessed with obesity, it's not the whole story?
Definitely not.
We have these other major risk factors, we have to target those.
We try and bring our waists in and reduce body weight
if not stop it going higher,
but there's a lot we can do to prevent end-organ damage from diabetes.
Alan, you've got a lot of experience working with Indigenous communities.
Indigenous rates of type 2 diabetes and complication rates are enormous.
Is it a different disease or just worse?
I think the evidence is that it's not a different disease,
that the issues of poverty, poor access to care,
a whole series of factors come together
that make the same common problems of diabetes
and related chronic illnesses worse
rather than an entirely different approach being needed.
What are the targets we should be aiming for?
The RACGP has generic targets, as shown here -
glycaemia, total cholesterol and blood pressure.
In general, these will work well for patients and for health professionals.
So, the A1C target, less than or equal to 7%.
Total cholesterol, less than 4.
These days, we focus on LDL cholesterol, less than 2.5, if not down to 2.
Then blood pressure, less than or equal to 130/80.
However, if we do customise or individualise it
for the person who has significant proteinuria,
we want a tighter blood-pressure target than that.
People with known ischemic heart disease,
we want a tighter LDL cholesterol level - less than 1.8.
And depending upon the stage of the person's diabetes,
early on we know that tight glycaemic control can
reap rewards decades down the track.
There's even quite a push for HbA1c levels 6% to 6.5%
early on after the diagnosis.
That's controversial.
If you look at the most recent type 2 diabetes guidelines
for glycaemic control, which you might address in subsequent weeks -
I know we're not addressing those today -
the generic targets, A1C, less than 7.0%,
and we know we can achieve that for a lot, if not all, of our patients.
We can achieve it for a lot.
There's increasing data, again from ACCORD and ADVANCE
and VADT, a number of studies over the last 18 months, 2 years,
that early on in the diagnosis - and also from the UKPDS follow-up -
early on, we need to aim for very tight glycaemic control, get in early.
We know that in general,
type 2 diabetes is a delaying diagnosis of four to five years
between when it develops and when it's diagnosed.
We're missing years there when we can help achieve tight control
of these surrogate markers for our patients.
Paul, you've been following this group of people in the Blue Mountains
for many years, many of whom have diabetes.
Getting them early makes a difference?
Absolutely. In fact, one of the messages that has come out in the last year
is this issue of metabolic memory.
So, good control of diabetes in the first period of diabetes
is really important.
It's been shown in the UKPDS in type 2 diabetes
that good diabetic control over the period of the study persisted,
despite the fact that the haemoglobin A1C levels
in intensive versus routine control...
We've got a graph to that effect to show.
That metabolic memory effect was shown initially in the DCCT
and is now being shown in UKPDS for retinopathy
and for other complications.
That probably tells us where the challenge is.
We know that on average, we're picking people up with diabetes
several years after the diabetes is established.
For primary care and the health system generally,
what can we do to opportunistically pick up people?
For example, coming each year,
most Australians do attend a general practitioner's at least once.
There is strong evidence in the Australian context
that if we opportunistically screen 50- to 69-year-olds for diabetes,
we can pick it up earlier and intervene
and prevent heart attacks, strokes and premature mortality.
Are you doing that, David? Putting you on the spot.
Yes, probably indirectly.
A lot of patients have lots of blood tests.
You'll flip through and see that
the sugars are in the 6s or occasionally higher,
and it behoves us to concentrate on that and get a fasting glucose,
get a two-hour glucose-tolerance test done and see where we're up to.
Just take us through quickly the algorithm
to remind us of the basic management of the glycaemic side of things
before we move on to the complications.
The algorithm involves intensive lifestyle management.
That is both the diet
and regular physical activity.
We do find in most people
as time goes on
they do require pharmacological agents
in addition to focusing on lifestyle.
In terms of the HbA1c targets
that will help determine what type
of additional medications are needed
and when, following the initial
lifestyle intervention,
metformin is our first-line agent.
It certainly is effective
at lowering blood-glucose levels,
has a relatively low
side-effect profile, well tolerated,
and on top of that,
in the UKPDS we've referred to,
had good outcomes in terms of
cardiovascular
and microvascular outcomes.
Subsequent to that though,
as time goes on,
HbA1cs often deteriorate and people need
more than metformin alone.
Sulphonylureas in Australia for decades
have been our second port of call.
Then, multiple third-line options.
Each of the third-line options will
sit on that line
because they are newer agents
which might be less well studied
than sulphonylureas,
or they have challenges
associated with them, for example,
injections, as in the case of insulin.
NORMAN: We've got the results
of your first poll question.
We asked where you were located:
Here are the findings.
16% evenly split between metropolitan, regional and remote.
And that big one, the blue one, is rural.
Welcome to you all.
It's good to see such an even split and an appropriate split
in terms of your location.
I'm going to ask the second question now, which is:
So, we'll get your answers to that while I ask David Guest,
what is the general practice annual cycle of care
when you've got somebody with diabetes?
With patients with established diabetes,
it's a protocol with which to manage them.
It involves clinical measures that we probably should do
every time we see the patient, but certainly six-monthly,
you need to check the blood pressure,
the weight and hopefully the feet,
but that's sometimes something
we don't get around to.
Annual tests needed,
HbA1c certainly annually,
more frequently
depending on the level of control.
We want to know
what the lipids are doing,
and HDL in particular in relation to
some new risk-factor calculators.
With diabetic nephropathy,
we want to keep an eye on
the albumin in the urine.
There's also the necessity for
second-yearly eye examination,
either yourself or more commonly
where I come from,
with optometrists and ophthalmologists.
Keep on eye on the social factors -
smoking, alcohol, exercise, diet areas.
If you get yourself into
a regular pattern with that,
either on your own
or with the help of your team,
you can keep your diabetic patient
under control.
Take us through the issues
in terms of chronic kidney disease.
Chronic kidney disease is common in diabetes.
Chronic kidney disease is manifest evidence of kidney damage.
The way that this is picked up is either through a simple blood test,
then estimation of the glomerular filtration rate,
where the GFR is less than 60ml per minute,
evidence of significant kidney damage.
The other way is through
picking up protein leakage into the urine - microalbuminuria -
through to more overt nephropathy.
When we think about how we measure these things
in terms of the serum creatinine on one hand,
how much protein in the urine on the other hand
and the estimation of GFR, it's sometimes complex.
Some of the keys to be cognisant of is that often
leakage of albumin into the urine, microalbuminuria,
is one of the earliest markers.
This usually occurs when someone has normal renal function.
NORMAN: How best to measure that?
There are different ways in which that's measured.
Ways that are felt to be equally valid
would be a spot, particularly morning urine
for albumin-creatinine ratio or a timed urine collection,
again, looking for albumin.
We were originally trained in terms of 24-hour urines,
but in terms of common use in primary care,
both of those methods are commonly used.
NORMAN: That should be part
- of the annual cycle of care? - Yes.
Today's patients expect fasting blood tests,
so during the urine test at the same time has become part of the protocol,
part of the routine.
So that's...
You've knocked off a lot of your kidneys before your creatinine rises.
Absolutely right. That's the way to pick it up early, focusing on the albumin.
A key thing with the creatinine, a common measure -
we do it on many patients -
is that you might have lost half of your kidney function
before you get an abnormally elevated creatinine measure.
That's where the simple calculation of the estimated GFR,
which is done routinely by labs throughout Australia now,
will provide a more ready measure
of the amount of renal dysfunctional damage.
Why are we interested in that?
Both of those are important.
Both the level of albumin in the urine and the level of kidney dysfunction
are known predictors of events for people with diabetes.
In other words, chronic kidney disease predicts heart attacks and strokes.
Correct. Why are we interested? It's very common.
From AusDiab, perhaps a quarter of people with diabetes
have evidence of chronic kidney disease.
And of all people with chronic kidney disease,
what's the diabetes in relation to the cause for end-stage kidney disease?
Diabetes is now the leading cause of end-stage kidney disease in Australia
and in similar countries throughout the world,
and interestingly also in developing countries.
That relentless drive of diabetes contributing to end-stage kidney disease
is quite clear in the Australian context.
The ADVANCE study related cardiovascular disease risk
with albuminuria and renal disease.
Absolutely correct.
The ADVANCE study was a large, randomised-control trial
with over 11,000 type 2 diabetics
looking at blood-pressure control and glycaemic control.
There is quite clear evidence there
that both of these markers are
predictors of heart attacks and strokes
and progression of kidney disease
to renal death or dialysis.
Both independently and together,
they add one to the other,
so people at highest risk are people
with reduced kidney function and
significant albumin leakage in urine.
NORMAN: Do they go hand in hand?
They do go hand in hand.
The figure that one in four people with diabetes
probably has some early kidney disease is about the figure for retinopathy.
It used to be thought that retinopathy occurred before kidney disease.
That's before we measured kidney disease properly.
They do go hand in hand.
We know that once kidney disease really starts to accelerate,
retinopathy really gets a hold on particularly macular oedema.
People, as their creatinine starts to rise,
that's when we see retinopathy, if it hadn't already needed treatment,
really become aggressive.
Because they're parallel processes according to severity?
Probably a parallel process,
but certainly people who have got significant proteinuria
have a major increased risk for macular oedema.
What are the other risk factors for diabetic retinopathy?
The principal risk factor is glycaemic control,
but in type 2 diabetes, it looks like blood pressure control
is probably almost or as important.
Lastly, blood lipid control might also be important.
Data from field studies suggests that
an aggressive approach to blood lipids might also be helpful,
although that's not so solid.
We certainly know that
elevated lipids are associated with macular oedema specifically.
The nice thing about that is, it's blood pressure
and glycaemic control
that are also related to progression of kidney disease.
So similar approaches to management of these factors that complicate diabetes
can reap the rewards
in terms of keeping people's vision and keeping their kidney function.
How reversible is diabetic retinopathy?
It's quite reversible in the early stages.
The recent data on this came from the...
Got a blank on the study? It'll come to you later.
One of the most recent study of ARBs
showed that if you had retinopathy at the first two stages,
microaneurysms only or a few microaneurysms and retinal haemorrhages,
those stages were reversible with really tight blood-pressure control.
But once the retinopathy became slightly more advanced than that,
then it was not reversible.
These are the direct study findings.
We'll come back to do more on diabetic retinopathy in a moment.
I've got the answer to the poll question, which is:
The red is six-monthly, and it's 27%.
18% said it depends on the patient.
54.5% said annually.
What's the right answer, Professor Twigg?
STEPHEN: I would say annually, but it depends on the patient.
You're happy with both?
You've got a thinking physician there. I'd prefer a thinking physician any day.
Annually is the cycle of care.
NORMAN: So most people have got it right.
As is recommended in the NHMRC guidelines,
which Stephen co-wrote.
Just testing, just testing.
We've talked about screening, just to go back to kidney disease.
We've talked about the test that you do.
What about albumin-excretion rates?
What validity does that have?
People use both albumin-creatinine ratios and albumin-excretion rates
in screening for damage to the kidney causing albumin leakage into the urine.
Both are tests that are valid and have good sensitivity
and specificity in terms of their role in screening
and measuring response to therapy for diabetics.
What are confounders when you're doing urine tests?
It's critical that there are a number of key confounders.
Urine infection, *** in women,
people who might have exercised significantly in the preceding 24 hours.
Many Australians who eat high-protein diets,
these people will have artificially elevated readings, for example,
and some medications, for example nonsteroidals
and others that are commonly taken.
When you're talking about blood pressure control,
are we talking about angiotensin receptor blockers and ACE inhibitors
or others work as well?
The answer is both.
Yes, there is accumulating evidence from a number of trials
that for people who have,
in terms of prevention of early chronic kidney disease in diabetes
and people with early stages that ACE inhibitors and ARBs
might have a particular protective role.
As well as that, it's the overall level of blood pressure control.
Indeed, there now seems to be added evidence
that even for people who are normotensive with diabetes
that there is the same benefit
as people with any level of blood pressure
in lowering their blood pressure in terms of kidney disease, for example.
As you implied earlier, Paul,
similar findings now for diabetic retinopathy?
Certainly the UKPDS didn't differentiate between different blood pressure agents,
and there's never really been fantastic data suggesting
that one class of blood pressure lowering medication would be better.
Recent studies of ACE inhibitors and ARBs
seem to show the best effects,
but there hasn't been a head-to-head comparison.
Stephen?
I agree. You look at all the national and international guidelines
and first-line for hypertension for people with diabetes
is an ACE inhibitor or ARBs.
As Paul and Alan mentioned though,
the critical issue is tight blood pressure control.
Lipid control is not as strong but still worth doing?
Lipid control is important,
because people with diabetes have high cardiovascular risk.
There is not strong evidence that
lipid control prevents progression of kidney disease.
But they are at high risk of heart attack and stroke,
therefore require good lipid control in that context.
David, were you going to say something?
Just agreeing that at the macrovascular level, that's what you're looking for.
The place of aspirin in patients?
Does aspirin help with kidney or eye disease?
Here we go. Put on your seatbelts. We're in for a rough trip now.
Perhaps I can address the issue of lipids.
No, let's have the aspirin question. Professor Twigg?
For secondary prevention, there's no question antiplatelet therapy
is critically important,
and that gets back to the cardiovascular link.
You've got to have an event before you start the aspirin
- for it to be of benefit? - Yes.
For primary prevention,
this is where cardiovascular risk tables can be extremely helpful.
If a person is deemed to be at high risk,
you'd be prone to use antiplatelet therapy. I would under those conditions.
NORMAN: But there's no evidence for it. - That's for cardiovascular protection.
There is, but you have to extrapolate.
There was the Hypertension Optimal Treatment study,
which had 1,700 with type 2 diabetes in it,
but they're only 10% of that population.
Aspirin worked very well there.
There was also the Physicians' Health Study for primary prevention.
From a cardiovascular point of view, there's a basis for using aspirin
under those conditions.
It is complex in people with diabetes.
There's some evidence that maybe aspirin resistance occurs -
resistance to the action of aspirin.
And what is the correct dosage?
From the point of view of kidneys and eyes,
we'll move on to my esteemed colleagues.
But from the cardiovascular point of view,
tables can be helpful for antiplatelet therapy.
I'll come back to Paul 'cause I so rudely interrupted him.
To go on the aspirin point,
one of the original diabetic retinopathy studies, the ETDRS,
looked at whether aspirin was beneficial for people with diabetic retinopathy.
It really showed no benefit over no aspirin.
Of course, in people who needed aspirin for cardiovascular reasons,
there was no contraindication to giving aspirin
because there was no increase in haemorrhages,
even in people with severe retinopathy.
There was no increase in vitreous haemorrhage.
So it's safe, but there are no protective effects on its own.
Can I add to that?
Stephen talked about the HOT trial.
There was a recent analysis,
presented this year at the World Congress of Nephrology,
showing that people in that trial who had chronic kidney disease -
people we're talking about here
with chronic kidney disease in the context of diabetes -
had the greatest absolute benefit from aspirin therapy of the entire group.
Because they're at much higher cardiovascular risk.
Even though they had some increase in some risks,
the added benefit in terms of the prevention of, in that case,
heart attack and vascular events outweighed that.
So people with CKD had particular benefit from aspirin therapy.
And smoking cessation affects the kidneys and eyes?
Smoking has been looked at a lot in terms of retinopathy,
but no good data suggests that cessation of smoking benefits retinopathy.
NORMAN: So smoke doesn't get in your eyes?
I'm sure it does, and it's great to stop if you've got diabetes.
It gets in your eyes from macular degeneration rather than anything else.
- What about kidneys? - There is evidence people who smoke
are at greater risk of progression of chronic kidney disease.
What about protein restriction with grade 3 renal disease?
I wouldn't advocate that now.
That was something...
So generations of people with impaired kidneys
have been eating that horrible stuff all that time?
Correct. The evidence of benefit is
that it might at best delay the onset of dialysis by one or two months.
And you feel every month of that.
The clinical care guidelines are very helpful here
in terms of the points that Paul has raised
about aspirin not being a risk in terms of intercurrent retinopathy.
They are nicely covered in the guidelines,
and as Alan points out, the smoking issue too.
Even the executive summary,
I'd encourage people to go online and have a look at it.
Excellent marketing, Professor Twigg. We're most impressed.
What about salt reduction in kidney disease? Does that have any benefit?
Salt reduction is becoming increasingly an issue of focus in Australia.
In general we eat a high-salt diet.
A lot of that is about not salt that we add but that salt is in...
..takeaway foods and foods that we buy at the supermarket.
It's quite clear that the high-salt diet has implications for hypertension.
Therefore, I think it will be an area of increasing focus -
how can we reduce that
in terms of interaction with the food industry, for example,
so we can lower blood pressure?
That will be very relevant for management of diabetes.
A question from New South Wales -
'What is the incidence of chronic kidney disease with gestational diabetes?'
Maybe I can answer the gestational diabetes part,
then pass on to the colleagues for chronic kidney disease.
Gestational diabetes by definition is diabetes that develops in pregnancy,
then usually resolves shortly afterwards.
You wouldn't expect kidney disease with it?
Yes. It does affect about 5% of the pregnant population.
After saying that, pregnancy-induced hypertension and pre-eclampsia
and eclampsia, they do cosegregate with gestational diabetes,
probably through body weight and equivalent risks.
In terms of renal disease per se,
in some of the renal disease-related conditions, there is some link.
I'll stop there and pass on to others.
The actual risk of significant renal disease
at the time of gestational diabetes or pre-eclampsia, for example, is low.
People who might already have overt diabetic nephropathy
at the time of becoming pregnant
and high blood pressure and things are at more risk
in that condition of worsening of renal function
and of having greater difficulty in managing those comorbid conditions.
There are a lot of people interested in following people
after having the pregnancy, having a baby,
in terms of their then ongoing risk of developing type 2 diabetes
and related chronic kidney disease,
where it does appear that there is, in long-term, some increased risk.
Another question is, 'How does steroid abuse
influence the incidence of chronic kidney disease
in existing type 2 diabetes?'
I assume we're talking anabolic steroid abuse here.
That's not something I have any particular knowledge about.
You haven't got many muscled-up...
What about steroids as in corticosteroids?
There's obviously concerns about obesity and its interaction with diabetes
as to whether that's a risk factor for development and progression
of chronic kidney disease in diabetes.
But again, it's not something that features steroid use,
in terms of development of chronic kidney disease.
Let's have a look at our first case study.
Back a while, back about 10, 11 years,
I was working in the coal fields then.
I went to the doctor because the diabetes had sort of caught up with us,
the high blood pressure and that.
The doctor had taken blood tests and that and said, oh, yeah,
there's something wrong with your kidneys.
So I had to go to Townsville.
They took a biopsy on the kidney. They thought it was a diseased kidney.
They took a biopsy, and the result of that was, neither kidney was diseased.
We had to go and see a dietitian in Mackay when he came back.
They said, don't eat this and don't eat that. Eat this and eat that.
So he did it, but nobody ever said, you've got to follow it up.
It wasn't until about five years ago that he started feeling down.
He said he was feeling a bit tired a lot.
I said, you need a good sleep. Stop eating so much.
He got the flu. He was away working in a mine.
He used to fly in and out. And then he got sick.
He flew back in, and I couldn't believe he was a person when I opened the gate.
I thought, what's wrong with you? He said, I'm really sick.
Jeez, it nearly killed me. It was just something unbelievable.
That's when he asked his doctor if he could get his kidneys checked,
and lucky he did do that.
Next I know, I'm at the renal area of the doctor's.
It just went from there.
I knew something was wrong when he didn't come out.
I kept seeing people going out, and I thought, something's wrong.
Then I thought, oh, no.
When I walked in and saw the faces, I knew then.
It just hits you like a brick.
It all happened so quick.
It obviously was over a long period of time.
Probably the good life caught up.
Personally, it gets back to the way you're brought up, I guess.
The foods that you eat when you're in your younger days,
grog, everyone does it.
A lot of people overindulge.
It just depends.
It gets back to your diet and the way you look after your body.
I didn't show him, I'd just go out and cry.
I couldn't handle it.
Not only my father died, his father died of it.
I've got aunties on my mother's side that have died of it
down in South Australia.
So you think, he's got it, so I must have it.
It knocked the whole lot of us. Really knocked the family.
The grandkids just couldn't believe Poppy could get sick,
not their poppy.
Not a good story there, David.
No, no. Like he said, it happened so quick,
but it really is something over a decade or more, isn't it?
I think it's probably a good idea when we have patients with diabetes early on
that we have our registers set up so we can keep track of them.
It would be even better if we could negotiate some plan
on how we're going to manage it according to the cycle of care
so they don't get away from us.
And using a team.
And using a team to ease the burden, particularly on rural GPs
who don't have much time.
He looked as if he was trucking along with a haemoglobin of about 9.
I think that's right.
They talk about the devastating impact of diabetes and kidney disease
on the family.
The key issue is multiple missed opportunities for engagement
in the management of the diabetes.
He talked about all the factors we know are crucial -
his blood pressure, diet,
all of the approaches to management that could have made a difference
and prevented his severe kidney failure.
This problem is writ large again and again across the country.
I'm going to ask you another question.
How would you rate your understanding of correlation between serum lipid levels,
good blood glucose control and blood pressure control
and eye complications?
It's probably a bit better since we've been speaking about it for a while.
Let's see how you rate it now.
While you're answering those questions, we've got another case study to watch.
Let's look at Darren's story.
My name's Darren Dorey.
In September, I'll be 43.
I live in Warrnambool, in the south-west corner of Victoria.
It's approximately 300km or three hours from Melbourne,
a little seaside town that is a nice, little friendly community.
I was diagnosed with type 2 diabetes when I was 27.
I was told to change diet,
and I was put on some tablets.
But as time went by and I didn't feel any different,
I got more and more slack with it.
Probably for the next ten years, I lost focus on control of the diabetes.
At the time I was told, you have to have your eyes checked.
OK, well, that's pretty serious.
I drive a truck for a living, so I've got to keep on top of the eyes.
After a couple of years of going, yep, your eyes are fine,
you stop worrying about it.
Around about 2001
I was starting to struggle a little bit with seeing some road signs.
I went in to the optometrist's to get some glasses.
She had a look in my eyes and said, you've got a massive bleed in the eye.
She said, you need laser surgery and you need it now.
I walked out of the ophthalmologist's rooms
after having something like 300, 400 shots of laser in the eye.
I ended up having a vitrectomy.
Probably 18 months later, I developed a cataract,
which I had out in about 2006, in the left eye.
That brought back vision beautifully.
It was like, wow, a whole new world. This is all good.
In 2007 I'd actually gone back to truck driving.
I guess going back into trucks was,
for the diabetes, one of the worst things I did.
I did a lot of travel where you'd take off for a few days' trip
and forget to take your medications with you.
I noticed it was getting harder to read the paperwork,
and the headlights of cars started to become more glarey -
the lights would flare.
I thought, I'd better go back to the ophthalmologist.
He looked at my eyes and said, 'Are you still in sales?'
I said, 'No, I'm a truck driver.'
He just said, 'Not anymore you're not. Hand in your licence tomorrow.'
I then had to go home to my wife and four kids and say,
'I don't have a job, and it looks like I might be going blind.'
The same day, our landlord called over to mention that
he'd put the house on the market and we'd have to move.
Yeah, life just crumbled.
Paul Mitchell, entirely preventable?
I think that blindness from diabetic retinopathy should be preventable.
There really should not be any cases
of people who go blind from this disease anymore.
There are still people going blind from it,
and there will still be some people.
But if you look at every one of those cases,
you can really detect what went wrong.
Clearly, in the early stages of his diabetes, he was poorly managed.
He put his head in the sand.
Maybe his doctors didn't impress on him
the absolute importance of having regular checks,
but it should have been prevented.
After he had that first lot of therapy, it looks like he again lost contact.
He should have had pretty intense follow-up after that first therapy.
But he didn't go, and he went back to driving again.
If you look at Darren's story, there are many circumstances where really,
the wrong path was taken, and his blindness, or severe vision loss,
could have been prevented.
How do you screen your patients for retinopathy, David?
Do you send them to the optometrist?
I send them off to the optometrist or ophthalmologist,
probably a 50/50 split, or a bit more to the ophthalmologist where we are.
Question from Michael Stuckey in Queensland -
'Why not annual retinopathy screening?' Paul?
It's been looked at.
Around the world, most diabetes associations recommend annually,
but in fact, the development of retinopathy occurs relatively slowly.
It's been shown that two-yearly is actually sufficient.
If someone has difficult-to-control diabetes,
if they've already got other complications,
of course they need to be seen more frequently,
even if they have no retinopathy.
How good are the screening tests?
This is ophthalmoscopy?
Yeah, this is ophthalmoscopy.
The eye doctor, or optometrist, wouldn't use a handheld ophthalmoscope.
He would use a slit lamp with a much wider area,
being able to screen the retina much more effectively
than the handheld ophthalmoscope.
We also have the potential availability
for clinics of non-mydriatic photography.
This is what they're using in some Aboriginal communities?
That's right. That's very effective.
You see a blown-up picture, you can immediately see
if there are any retinopathy lesions.
The standard though, at the moment, would be pupil dilation?
Yeah. The standard is pupil dilatation, then examination of the retina
by someone who can do it properly -
an ophthalmologist, an optometrist or a well-trained GP or physician.
What are the criteria for referral to an ophthalmologist?
Certainly non-ophthalmologists can manage people with diabetes
in terms of retinal screening
until the point at which any significant retinopathy is present -
anything more than the occasional haemorrhage or microaneurysm.
From that point people should see an ophthalmologist.
Marisa Pilla from North Queensland asks,
'Is there any ACE inhibitor that's superior to the others
in helping to prevent retinopathy or the worsening of the condition?'
We don't know.
There are two recent studies looking at two different ARBs
and they both showed beneficial effects,
but there's been no head-to-head comparison.
She also asks about antioxidants.
The AREDS study suggested
that a certain cocktail might help macular degeneration.
Does it help in diabetic retinopathy?
There's no evidence that it helps diabetic retinopathy.
Talk us through laser photocoagulation here.
There are some new therapies coming on
when you've got microaneurysms and bleeds.
Once ophthalmologists take over follow-up and management
of people with diabetes,
what they're really critically interested in doing is
evaluating the patient at an interval
so that they would detect vision-threatening retinopathy
and could apply laser treatment at the optimal time.
The indications for laser treatment are the presence of either new vessels,
and this is an advanced stage of the background type of retinopathy.
New vessels are fragile, they bleed, they don't really help,
they don't bring new blood to the area.
The second is macular oedema.
This is the more frequent and more important complication to detect.
That is harder to detect with ophthalmoscopy.
That's why you really need an ophthalmologist or optometrist
to examine the patient.
And the treatment of macular oedema?
The treatment of macular oedema is currently laser treatment
using the guidelines that have been around for 25 years.
It's reasonably effective but not brilliantly effective.
Certainly many people will still lose vision.
We now have some other adjunctive therapies that can help.
The main one is anti-VEGF therapy.
This is vascular endothelial growth factor.
- This is like Avastin or Lucentis. - That's right.
These agents are an adjunct to therapy.
They don't do away with the need for laser,
but they can help to dry out the macula
until laser treatment can be a bit more effective.
Laser treatment is probably more effective if it's applied
when the macular oedema is resolved.
And the role of fluorescein angiography?
Becoming less and less.
Fluorescein is not a particularly pleasant test to have done.
We actually do it very rarely.
We might do it at the onset,
before we start laser treatment for macular oedema, once,
but we rarely repeat it these days.
We don't do it at all for screening
or for the follow-up of people with diabetic retinopathy.
Unlike retinal detachment, vitrectomy has a different reason.
You're trying to get rid of the haemorrhage from the vitreous?
There are two circumstances.
The first is to get rid of the haemorrhage and scar tissue,
because new vessels that bled will then develop scarring,
and that scarring will cause traction on the retina.
Because retinal detachment is increased in diabetes?
Correct, and it's a tractional type of retinal detachment.
The other type of need for vitrectomy surgery
is for traction on the macula itself,
which can cause macular oedema to persist and be chronic.
But we are doing less and less vitrectomies now
because physicians are managing people with diabetes much better.
We're seeing less people presented at Act V, Scene IV,
and we're needing to do a lot less vitrectomy surgery.
Just to explain, the vitrectomy involves microdissection to remove scar tissue.
Correct. It involves usually two ports on the side of the eye
with instrumentation which can dissect and peel off membranes
and coagulate blood vessels.
People have said that doing cataract surgery can also damage the retina.
What risks are there in cataract surgery and diabetes?
This is an important issue, and it's still important.
We know that people with diabetes develop cataract much earlier
than people without diabetes.
There's a direct effect of glucose on the lens in the eye.
The type of cataract they get is a cortical cataract -
the spokes when you dilate the pupil -
you can see them quite easily with an ophthalmoscope -
or an opacity on the back of the lens.
The problem is that when people with diabetes develop cataract,
they may also be developing retinopathy.
If there is any early macular oedema or moderate retinopathy,
then you can develop macular oedema after cataract surgery,
perhaps as a response to the inflammation of the surgery itself.
One of the issues that all ophthalmologists know
is that we must stabilise the retinopathy before cataract surgery
as much as we possibly can.
What about access to good ophthalmological care
when you're living in a small country town?
This is always difficult.
Ophthalmologists like to live in the nicer suburbs,
and don't necessarily go to the country so often.
But in all country areas in Australia, there is some degree of access.
It always needs to be better, but there is reasonable access.
And if there isn't, you need to let us know
so the College of Ophthalmologists can look at this.
Local ophthalmologists in some of the larger rural areas
will be prepared to travel to smaller areas
if they think there's a reasonable need.
This non-mydriatic screening can be transmitted for people to look at.
Correct. Right now there's another application to the Medicare group
to consider funding non-mydriatic photography.
This would produce a fantastic way of screening people.
It means they wouldn't have to travel a long way
to see an optometrist or eye doctor.
GPs themselves could read the photographs quite well
with relatively minor training.
That has not yet been approved, but we're hoping it will be.
Let's have a look at Darren's story again, and what his life is like now.
My left eye has been left with 25% vision.
The right eye, about 10%.
The hardest thing with the eyes is that they see totally differently.
I describe it as being like the old fun mirrors at Luna Park,
where everything is distorted,
or fog up your windscreen, jump in your car of a cold morning,
going for a drive without a clean windscreen.
Then put a few little lines and black dots into your line of vision
then go cross-eyed so you've got double vision on top of that.
I was never actually told
about the correlation between diabetes and depression.
If my sugar levels were high, my moods would swing.
But once I lost the sight, the depression came in like a tidal wave.
It became all-encompassing to the fact where I attempted suicide.
I lost all self-esteem, I lost all self-worth.
It cost me my marriage. I haven't seen my children for two years.
October '07, my life fell into a hole - a very, very deep black hole.
It took me another six months to crawl my way out of it and restart my life.
One of the biggest things that helped me get my life back on track,
or helped me out of the hole that I was in,
I made an appointment to see my GP and couldn't get in,
so they said, we've got another doctor here with an appointment open.
Do you mind seeing someone else?
I said, I just need a script, so that would be great.
I sat down with this new female doctor. Very young, she was.
She had a look at my file and said,
you haven't had this test done for a while. You haven't had this test.
What's going on here? What's going on there?
We'd better take control of this.
It was almost a light-bulb moment for me,
like, someone is listening, someone is taking note.
The GP I was seeing, we had a good rapport,
but it just became the usual,
yep, I've run out of tablets. Can you help me here?
It was in and out, script in hand, thanks very much, see you later.
She also linked me in with the local psychiatric services
through the local hospital, and I was given a case manager,
who, once again, showed a lot of compassion and care
and was listening to me.
Also Vision Australia really came on board
and helped me with a lot of adaptive stuff.
They sent out a person to help me learn how to walk again.
It sounds silly, but you learn to feel the ground rather than see the ground.
I couldn't see the normal, everyday things anymore,
simple things like how to put something in the microwave, push the button to go.
I couldn't see that button.
I couldn't feel that button 'cause they're flat-panel.
Vision Australia said,
we've got these dots, put them on the go and stop buttons.
I can't read how many minutes I've got up,
so I count how many times it beeps.
It's just one of the little things you take for granted
that suddenly become an issue.
It was the supports behind me that helped me.
I'm now employed by South West Healthcare,
Psychiatric Services Department.
Vision have come down from Melbourne and put in a program
which helps with email, it enlarges the font automatically.
I can't read normal-size font.
Also, enlarged keys or enlarged stickers on the keyboard.
Without them, I've got no hope.
The main thing for someone who's new to diabetes,
or even a doctor that's treating a new diabetic,
is to emphasise what it is and how it works.
Doctors need to emphasise, you won't feel it coming.
As I said earlier, I expected to have signs.
If there's any damage, I expected to have the signs of it coming.
You don't feel it coming.
It creeps up very, very slowly until suddenly it's out of control.
A lot of the things I did was, if it's serious, they'll tell me about it.
Of course they think you've understood it, so they let it go.
Suddenly it becomes a huge issue down the track.
I honestly feel, if it had been more of a team effort
between my GP and myself, maybe I wouldn't have lost the sight.
Tragic, David.
DAVID: Yes.
You feel bad as a GP when you see a story like that.
There's a place for having a register of your diabetic patients
and reviewing that regularly
and getting your team to help you in the management of these patients
and make sure they're not lost to follow-up and you can keep on them.
I joke with our diabetes educator who visits our surgery
that we play good cop, bad cop.
She tells them all the things they have to do, then I come in and say,
Sharon says this, so you'd better do the right thing for next time.
Let me get the results of the poll question:
6% of you said you had no understanding. Hopefully we've improved that tonight.
62% said you've got moderate, and 31%, comprehensive.
So over 90% of you have got a reasonable understanding,
at least on a self-assessment basis.
We won't be administering any multichoice questionnaires tonight.
Paul, not a good story there, but you're saying it's becoming rarer.
It's becoming rarer. One of the points we could say about Darren
is that he's been through the gamut of therapy.
Usually their vision is stable from that point.
Usually there's no further progression,
because the disease becomes relatively quiescent
after it's done all that damage.
He probably will hold his vision from now on.
We should be looking at his case and say, this should have been prevented.
We really need to work hard to prevent all these cases, and I think we can.
We mustn't forget the psychosocial issues.
Depression goes along with it.
It makes diabetes worse.
Absolutely. It's an important part of the package.
We know people with diabetes
have a two- to threefold higher prevalence rate of depression.
It's a vicious cycle.
What are your takeaway messages for the audience, David?
Know who your diabetic patients are,
and keep them under careful, close review.
Don't try and do it all yourself.
Your diabetes educators, dietitians, podiatrists,
they're all there to help, and make sure the necessary gets done.
- And get the targets right. - Get the numbers right.
Paul?
At least two-yearly, I review by competent examiner.
Make sure that you really work hard
at the control of diabetes blood pressure and blood lipids.
- Alan? - Chronic kidney disease is common.
It can be readily detected and followed with simple blood and urine tests.
And again, blood pressure and glycaemic control
are crucial to preventing progression.
For me, those two case histories show
that too many people fall through the cracks.
Both as individuals in our own clinical practice
and the health system generally,
we need to do something better to prevent those disastrous outcomes.
- Stephen? - Vigilance is key.
Diabetes does tend to be a progressive condition,
and the complications.
We need to get to know our patients well.
Work with them as one of the key members of the team.
Recognise that we can prevent at many different levels.
Hopefully we can prevent many people from developing diabetes,
many others from diabetes complications developing
once they've been diagnosed with diabetes.
Even those who develop more severe later-stage complications,
there's a lot that we can do.
Never give up, prevent at multiple different levels
and get to know your patient.
Thank you all very much. Very interesting and very important.
I hope you got a lot from the program too.
The series of four programs we're making on type 2 diabetes guidelines
will be available in December free on DVD.
To order, visit the Foundation's website.
Copies of the guidelines can be downloaded from Diabetes Australia:
www.diabetes.com.au.
If you're obtaining even more information
about issues raised in tonight's program,
there are a number of resources available
on the Rural Health Education Foundation's website:
Don't forget to complete and send in your evaluation forms
and register for CPD points by completing the attendance sheet.
I'm Norman Swan.
From all of us, see you next time.
Funded by the Australian Government Department of Families, Housing,
Community Services and Indigenous Affairs.
Captions by Captioning & Subtitling Internationa�