Diabetes Care Improvement Packages. Role of Primary Care · UKPDS: Improving HbA 1c Control Reduced...
Transcript of Diabetes Care Improvement Packages. Role of Primary Care · UKPDS: Improving HbA 1c Control Reduced...
Diabetes Care Improvement Packages.
Role of Primary Care
Dr Jeremy Krebs Clinical Leader and Endocrinologist
Wellington Hospital
Diabetes Mellitus
How big is the problem?
Diabetes Care Improvement Packages
Does hyperglycaemia matter?
Management Goals
Insulin
New Zealand Virtual Diabetes Register end-2005 to end-2012 – latest data
0
50000
100000
150000
200000
250000
2005 2006 2007 2008 2009 2010 2011 2012
Increase is in both genders,
also across all ethnicities
0.00%
5.00%
10.00%
15.00%
20.00%
25.00%
30.00%
35.00%
40.00%
45.00%
50.00%
00-04 05-09 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85+
Rate
(B
ase=
Pra
cti
ce e
nro
lled
po
pu
lati
on
)
Age group
New Zealand Diabetes Prevalance Rate as of 31 Dec 2006
European/Other Mäori Pacific people Indian
0.00%
5.00%
10.00%
15.00%
20.00%
25.00%
30.00%
35.00%
40.00%
45.00%
50.00%
00-04 05-09 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85+
Rate
(B
ase=
Pra
cti
ce e
nro
lled
po
pu
lati
on
)
Age group
New Zealand Diabetes Prevalance Rate as of 31 Dec 2007
European/Other Mäori Pacific people Indian
0.00%
5.00%
10.00%
15.00%
20.00%
25.00%
30.00%
35.00%
40.00%
45.00%
50.00%
00-04 05-09 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85+
Rate
(B
ase=
Pra
cti
ce e
nro
lled
po
pu
lati
on
)
Age group
New Zealand Diabetes Prevalance Rate as of 31 Dec 2008
European/Other Mäori Pacific people Indian
0.00%
5.00%
10.00%
15.00%
20.00%
25.00%
30.00%
35.00%
40.00%
45.00%
50.00%
00-04 05-09 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85+
Rate
(B
ase=
Pra
cti
ce e
nro
lled
po
pu
lati
on
)
Age group
New Zealand Diabetes Prevalance Rate as of 31 Dec 2009
European/Other Mäori Pacific people Indian
0.00%
5.00%
10.00%
15.00%
20.00%
25.00%
30.00%
35.00%
40.00%
45.00%
50.00%
00-04 05-09 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85+
Rate
(B
ase=
Pra
cti
ce e
nro
lled
po
pu
lati
on
)
Age group
New Zealand Diabetes Prevalance Rate as of 31 Dec 2010
European/Other Mäori Pacific people Indian
0.00%
5.00%
10.00%
15.00%
20.00%
25.00%
30.00%
35.00%
40.00%
45.00%
50.00%
00-04 05-09 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85+
Rate
(B
ase=
Pra
cti
ce e
nro
lled
po
pu
lati
on
)
Age group
New Zealand Diabetes Prevalance Rate as of 31 Dec 2011
European/Other Mäori Pacific people Indian
Direct same-scale comparison of prevalence curves 2005 and 2011
VDR 2012: major points
Diagnosed diabetes prevalence at December 2012 is 225,731, an increase of 8.5% above December 2011 (17,600, ≈ 50 per day) .
All DHBs showed increases – from 3 - 13%.
Peak prevalence in Pacific and Asian groups is now at 45% in older adults. In Maori is now at 35% in older adults.
The majority of diabetes (69%) is still within the European/Other community.
Diabetes Mellitus
How big is the problem?
Diabetes Care Improvement Packages
Does hyperglycaemia matter?
Management Goals
Insulin
Traditional Model of Diabetes Care
Secondary Care
Primary Care
Gestational DM
Type 1 Paediatrics
• Access to specialist advice / services
• Limited input to overall population
• Disparities in Access / Care
• Information sharing
Type 2
How can we improve diabetes care?
What? (Primary and Secondary Care)
– Improved Communication
– Improved Sharing of Data
– Improved Two-way Flow of Patients
How
– Shared Care
– Combined Community Clinics
– More Multi-Disciplinary Approach
– Acceleration of therapy in primary care
Diabetes Care Improvement Plan
– Prevent and slow progression of diabetic complications, especially heart disease, renal failure, impaired vision and lower limb amputations
– Reduce disparities between different population groups
– Reduced frequency of diabetes-related presentations to hospital emergency departments
– Reduce rates of hospital admission for diabetes and related complications
– Prevent or delay the onset of diabetes
The CCDHB model’s key components
Combined Primary and Secondary Diabetes Clinical Network
Practice population management
Performance measures
Collaborative case service in priority practices
Workforce development
Nurse practice partnership
Self Management Groups
Hospital specialist service focused on complex, Type 1, paediatric, gestational and renal diabetes
Key Goals
Get quality services to the population that need it
Foster patient self management
Maximise the skills and confidence of the workforce
Traditional Model of Diabetes Care
Secondary Care
Primary Care
Gestational DM
Type 1 Paediatrics
• Access to specialist advice / services
• Limited input to overall population
• Disparities in Access / Care
• Information sharing
Type 2
Primary Care
Secondary Care
Paediatrics
Practice
Practice
Gestational DM
Type 1
Practice
Practice
Practice
Practice
Practice
Practice
Practice
Practice
New Model for Diabetes Management in the Wellington Region
Clinical Network
Outreach
Self Management
Groups
Diabetes Mellitus
How big is the problem?
Diabetes Care Improvement Packages
Does hyperglycaemia matter?
Management Goals
Insulin
Skyler JS. Endocrinol Metab Clin 1996;25:243–254.
HbA1c and Risk of Diabetes Related
Complications
Target
HbA1c <7%
17
15
13
11
9
7
5
3
1
6 7 8 9 10 11 12 HbA1c (%)
Rela
tive r
isk
Retinopathy
Nephropathy
Neuropathy
Microalbuminuria
Incidence rates of MI and microvascular endpoints by mean HbA1c (UKPDS)
20
40
60
80
Incid
en
ce p
er
1,0
00 p
ati
en
t-years
Study population: white, Asian Indian, and Afro-Caribbean UKPDS patients (n = 4,585)
Adjusted for age, sex, and ethnic group
5 6 7 8 9 1 0 1 1
Myocardial
infarction
Microvascular
disease
Updated mean HbA1c (%)
Error bars = 95% CI
Adapted from Stratton IM, et al. Br Med J 2000; 321:405–412.
0 0
UKPDS: Improving HbA1c Control Reduced Diabetes-Related Complications
UKPDF=United Kingdom Prospective Diabetes Study.
Data adjusted for age, sex, and ethnic group, expressed for white men aged 50–54 years at diagnosis and with mean duration of diabetes of 10 years.
Stratton IM et al. UKPDS 35. BMJ 2000;321:405–412.
EVERY 1%
reduction in HbA1c
REDUCED RISK
(P<0.0001)
1%
Diabetes-
related
deaths
Myocardial
infarctions
Microvascular
complications
Amputations or deaths
from peripheral
vascular disorders
Relative Risk N=3642
14
After median 8.5 years post-trial follow-up
Aggregate Endpoint 1997 2007
Any diabetes related endpoint RRR: 12% 9%
P: 0.029 0.040
Microvascular disease RRR: 25% 24%
P: 0.0099 0.001
Myocardial infarction RRR: 16% 15%
P: 0.052 0.014
All-cause mortality RRR: 6% 13%
P: 0.44 0.007
RRR = Relative Risk Reduction, P = Log Rank
Figure 4:Legacy Effect of Earlier Glucose Control
0
10
20
30
40
50
60
70
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14
Numbers at risk
Conventional
Intensive
Steno-2 Post Trial: Mortality of any cause
80
80
80
78
77
75 69
72
63
65
51
62
43
57
Log-rank P=0.015
30
39
Years of follow-up
Cu
mu
lati
ve
in
cid
en
ce
of
de
ath
(%
)
Gaede et al. NEJM 2008
Steno-2 Post Trial: Any CVD events
0
10
20
30
40
50
60
70
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14
Numbers at risk
Conventional
Intensive 80
80
70
72
60
65
46
61
38
56
29
50
25
47
14
31
Years of follow-up
Cumulative incidence of patients with a major CVD event during follow-up
Log-rank P=0.0002
Cu
mu
lati
ve
in
cid
en
ce
of
CV
D e
ve
nts
(%
)
Gaede et al. NEJM 2008
7 patients Laser treatment
16 patients Dialysis
5 patients Progression to nephropathy
3 patients Major cardiovascular event
8 patients Cardiovascular death
5 patients Death
Number of patients with type 2 diabetes and
microalbuminuria needed to treat for 13 years to
prevent one...
(from Gaede et al 2008 Steno 2, 13 year study)
Recent Trials of Glycaemic Control
Advance, Accord
10 year post diagnosis, middle age
Despite intensive HBA1c management have failed to show CVD benefit
Accord The Action to Control Cardiovascular Risk in Diabetes Study Group
N=10,000
– 1/3 already on insulin
– 1/3 prevalent CVD events
– Age 62
– Diabetes for 10 years
– HbA1c 8.3
Strategy of (ultra) intensive glycaemic control aiming for HbA1c 6 (achieved 6.3)
The mean difference during the trial was 1.1%
Accord
Accord June 2008 Primary Outcome: First occurrence of nonfatal MI, stroke or death from
Cardiovascular cause
352 vs 371
events
HR 0.9 (0.78-
1.04, p=0.16)
Intensive N (%)
Standard N (%) HR (95% CI) P
Primary 352 (6.86) 371 (7.23) 0.90 (0.78-1.04) 0.16
Secondary
Mortality 257 (5.01) 203 (3.96) 1.22 (1.01-1.46) 0.04
Nonfatal MI 186 (3.63) 235 (4.59) 0.76 (0.62-0.92) 0.004
Nonfatal Stroke 67 (1.31) 61 (1.19) 1.06 (0.75-1.50) 0.74
CVD Death 135 (2.63) 94 (1.83) 1.35 (1.04-1.76) 0.02
CHF 152 (2.96) 124 (2.42) 1.18 (0.93-1.49) 0.17
Year Post-
randomization
% o
f P
art
icip
ants
0.0
0.5
1.0
1.5
2.0
2.5
3.0
3.5
4.0
4.5
5.0
1st 2nd 3rd 4th 5th 6th
Intensive
Standard
Diabetes Mellitus
How big is the problem?
Diabetes Care Improvement Packages
Does hyperglycaemia matter?
Management Goals
Insulin
Treatment Targets NZ Primary Care Handbook 2012
Less than 50% of Adults With Type 2 Diabetes Have Achieved HbA1cGoals
NHANES=National Health and Nutrition Examination Survey of a US population.
Adapted from Saydah SH et al. JAMA. 2004;291:335–342.
HbA1c level
<7%
Blood pressure
<130/80 mmHg
Total cholesterol
<200 mg/dl
Achieved all 3
treatment goals
CV Risk Factors
44.3
29.0 33.9
5.2
37.0 35.8
48.2
7.3
0
10
20
30
40
50
60
Ad
ults, %
NHANES III (1988–1994) (n=1204)
NHANES 1999–2000 (n=370)
US Population
13
Glycaemic Control Target HbA1c 48-58 mmol/mol
(6.5 - 7.5%)
Diet and Lifestyle
Oral Hypoglycaemics
Monotherapy
Combination therapy
Insulin
Management Strategy
Natural History of Type 2 Diabetes
cross-sectional, median values
06
7
8
9
0 3 6 9 12 15
HbA
1c (
%)
Years from randomisation
Conventional
Intensive
6.2% upper limit of normal range
Clinical Inertia
aUS Physicians; 1994–2002 bMean number of months that elapsed until a new or additional treatment was started. cMonotherapy switched to another agent or additional agent added.
Brown JB et al. Diabetes Care. 2004;27:1535–1540; American Diabetes Association. Diabetes
Care. 2007;30(suppl 1):S4–S41; Nathan DM et al. Diabetologia. 2006 Aug;49(8):1711–21.
First HbA1c on
Treatment
Best HbA1c on
Treatment
Last HbA1c before
Switch or Additionc
ADA goal
EASD goal
27b
months
35b
months
8.2
7.7
8.8
7.6
7.1
9.1
6
7
8
9
10
Metformin monotherapy (n=513 episodes)
Sulfonylurea monotherapy (n=3394 episodes)
0
Hb
A1c,
%
ADA=American Diabetes Association. EASD=European Association for the Study of Diabetes.
11
Traditional Type 2 Diabetes Management: A “Treat-to-Fail Approach”
OAD=oral anti-hyperglycaemic drug.
Adapted from Campbell IW. Need for intensive, early glycaemic control in patients with type 2 diabetes. Br J Cardiol. 2000;7(10):625–631.
Del Prato S et al. Int J Clin Pract. 2005;59:1345–1355.
7
8
6
9
10
OAD
monotherapy
Diet and
exercise
OAD
combination
OAD
up-titration
OAD plus
multiple daily
insulin
injections
OAD plus
basal insulin
Hb
A1c,
%
Mean HbA1c
of patients
Duration of Diabetes
Published Conceptual Approach
Time
12
The Therapeutic Challenge in Managing Type 2 Diabetes
We need treatments that:
– Additive to traditional treatments
– Can be used in presence of complications (eg kidney failure, heart disease)
– Acceptable to patients
– Minimise rather than worsen complications of diabetes
– (preferably) not increase weight
– (ideally) not cause hypos
Type 2 Diabetes
De Fronzo J. Diabetes 1998; 37:667–687.
Insulin Resistance
hepatic
glucose
production glucose uptake
-cell Dysfunction
impaired
insulin secretion
Genetic Susceptibility
Obesity, Sedentary Lifestyle
Pathogenesis of Type 2 Diabetes: Insulin Resistance and -cell dysfunction
Major Targeted Sites of Oral Drug Classes
Buse JB et al. In: Williams Textbook of Endocrinology. 10th ed. Philadelphia: WB Saunders; 2003:1427–1483; DeFronzo RA. Ann Intern Med.
1999;131:281–303; Inzucchi SE. JAMA 2002;287:360-372; Porte D et al. Clin Invest Med. 1995;18:247–254.
DPP-4=dipeptidyl peptidase 4; TZDs=thiazolidinediones.
Glucose
absorption
Hepatic glucose
overproduction
Impaired insulin
secretion
Insulin
resistance
Pancreas
↓Glucose level
Muscle
and fat Liver
Biguanides
TZDs Biguanides
Sulfonylureas
GLP-1 mimetics
TZDs
α-Glucosidase
inhibitors
Gut
DPP-4 inhibitors
DPP-4 inhibitors
Biguanides
15
GLP-1 mimetics
Type 2 Diabetes Algorithm
Diet and Lifestyle
Metformin
GLP-1 Agon DPPIV Ant Glitazone SU Acarbose
Insulin
Weight loss
No hypos
But Injectable
Weight neutral
Oral agent
No hypos
Oral agent
No hypos
But GI side effects
No hypos
But weight gain, heart
failure, fractures,
bladder cancer. ?IHD
risk
Oral agent
Good evidence
But weight gain,
hypos
Diabetes Mellitus
How big is the problem?
Diabetes Care Improvement Packages
Does hyperglycaemia matter?
Management Goals
Insulin
Insulin Therapy
Feel Better
– More energy
– Less infections
Better HbA1c
• Microvascular
• ? Macrovascular
Flexibility
Injections
Weight gain
More hypo’s
Driving issues
Needle phobias
Pro’s Con’s
DCCT Research Group.
N Engl J Med 1993;329:977–986
Trade off of Intensifying Insulin therapy
0
10
20
30
40
50
60
70
80
90
100
5.5 6.0 6.5 7.0 7.5 8.0 8.5 9.0 9.5 10.0 10.5
Hypoglycaemia
Complications
HbA1C
Ris
k o
f d
evelo
pin
g
hyp
og
lycaem
ia/c
om
pli
cati
on
s (
%)
Insulin and Type 2 Diabetes: The Who?
Anyone!
– Poor glycaemic control (HbA1c >60 mmol/mol)
– Symptoms of hyperglycaemia
But consider:
– Is it realistic
• Self inject?
• Risk of hypoglycaemia
• Age and Co-morbidities
Glucose
(mg/dl)
50 –
100 –
150 –
200 –
250 –
300 –
350 –
0 –
50 –
100 –
150 –
200 –
250 –
-10 -5 0 5 10 15 20 25 30 Years of diabetes
Adapted from Burger HG, et al. 2001. Diabetes Mellitus, Carbohydrate Metabolism, and Lipid Disorders. In Endocrinology.
4th ed. Edited by LJ DeGroot and JL Jameson. Philadelphia: W.B. Saunders Co., 2001.
Originally published in Type 2 Diabetes BASICS. International Diabetes Center, Minneapolis, 2000.
Relative
function
(%)
Fasting
glucose
Obesity IFG Diabetes Uncontrolled
hyperglycemia
Insulin resistance
Progressive Decline in Insulin Secretion
Postprandial
glucose
Insulin secretion Clinical
diagnosis
Insulin Therapy: The What?
? Once daily intermediate acting insulin
? Twice daily intermediate acting insulin
? Mixed insulins
? Basal bolus regimen
? Regular or analogue
Little evidence to support one over another
in Type 2.
How to Decide on What?
Pattern of hyperglycaemia
• Fasting vs Post-prandial
• Morning vs Evening
What will the patient do?
• Inject once or several times per day?
• Willing to test glucose levels?
• Able to interpret result and modify insulin?
53
Role of Self Monitoring of Blood Glucose
Type 2 DM on lifestyle alone/Metformin
– Useful intermittently to establish effect of food/exercise on glycaemia
– Useful to examine pattern of glucose elevation to aid commencement of further treatment
Type 2 DM on oral hypoglycaemic agents
– As above, plus
– Monitoring for hypoglycaemia
Type 1 DM and Type 2 on insulin
– Needed to rationally adjust insulin doses, plus
– Factors above
54
Glucose Focused Testing Examples
Actionable information for informed decision-making
Paired Testing … Testing to explore cause and effect BG
variance related to life events or
activities, such as food, lifestyle, and
current medication. Supports patient
self-learning and engagement.
Adjustment Testing …
BG testing to support activities to determine dose adjustment.
Pattern Testing …
Multi-point BG profiles for a specific
duration to use
pattern analysis to identify problem areas for
remediation.
83 159 134 203 103 178 102 93 201 136 123 156 237 142 90 147 93 138 132 201 173
xx
xx
xx
x
xx x x
xx
x xx x
xx
x
0 0 0 0 0 0 0 00 0 0 00 0 0 0 0 0 0 0 0
4/4/07 4/5/07 4/6/07
0 0 0 0 0 0 0 0 0
7:10 9:20 12:00 2:10 6:45 8:35 11:00 7:00 9:15 12:30 2:20 7:15 9:20 11:41 6:45 9:00 12:00 2:10 7:30 9:45 11:40
x
83 159 134 203 103 178 102 93 201 136 123 156 237 142 90 147 93 138 132 201 173
xx
xx
xx
x
xx x x
xx
x xx x
xx
x
0 0 0 0 0 0 0 00 0 0 00 0 0 0 0 0 0 0 0
4/4/07 4/5/07 4/6/07
0 0 0 0 0 0 0 0 0
7:10 9:20 12:00 2:10 6:45 8:35 11:00 7:00 9:15 12:30 2:20 7:15 9:20 11:41 6:45 9:00 12:00 2:10 7:30 9:45 11:40
x
Types of Insulin
Basal Insulins
• Isophane (Protophane, Humulin N)
• Analogs (Glargine, Detimir)
Bolus Insulins
• Actrapid, Humulin R
• Analogs (Novorapid, Humalog, Apidra)
Mixed Insulins
• Penmix 30/70,
• Humalog Mix 25 and 50
Insulin comparisons
Adapted from Monnier L et al. Diabetes Care 2003;26:881–5
PPG
FPG
50% 55% 60% 70%
50% 45% 40% 30%
30%
70%
<7.3 7.3–8.4 8.5–9.2 9.3–10.2 >10.2
0
20
40
60
80
100
HbA1c range (%)
% c
on
trib
utio
n to
Hb
A1c
Most insulin is initiated when HbA1c >8.5%
To normalise blood glucose both FPG and PPG must be reduced
Success Comes From Using the Most Appropriate Tools
What about the oral agents? Continue or Stop?
Metformin
– Good evidence to continue
Glitazones
– Some evidence but increased risk of heart failure
Sulphonylureas
– Often continue in short-term
– No real benefit to continue in the long-term?
Most Commonly
Add in once daily intermediate or long acting insulin (NPH insulin or Glargine).
Evening if FPG>6mmol/L
Morning if hyperglycaemia mostly later in day
May need to look at twice daily insulin
• Wean off sulphonylurea
Insulin Therapy: The When?
Poor Glycaemic control:
– HbA1c > 53mmol/mol (7.0%) despite maximal tolerated oral therapy ?
Symptomatic
Insulin Therapy: The When?
Prepare patient in advance.
• Progressive disease. Likely to be needed at some stage.
Don’t use insulin as a threat!
• If you don’t exercise you will need insulin….
When the patient is ready!
• Optimised diet and lifestyle
• Optimised oral hypoglycaemics
• Compliance
• Home glucose monitoring
Insulin Therapy: Summary Why?
• DCCT and UKPDS. Reduced complications
Who?
• All with Type 1 diabetes
• Anyone with Type 2 diabetes, but…
What?
• Anything goes. Start with once daily NPH insulin (protophane/humulin N) or Glargine. Continue Metformin.
When?
• Consider when HbA1c > 53 mmol/mol (7.0%) despite optimal other care
• When the patient is ready