CLINICAL INERTIA

IN TYPE 2 DIABETES MELLITUS

Patient’s Perspective
Djoko Wahono Soeatmadji
 Illness ?
Subjective feeling and objective
findings…
Cardinal manifestation of disease

Disease ?
Is an abstraction… in reality there is
no disease… albeit it’s a useful one
Dengue hemorrhagic fever ?
Malignancy ? Hypertension ?
Diabetes Mellitus ?

The Illness ?
The Disease ?
 Patient’s valuation
Quality of life

Patient’ perspective of life

Life expectancy
Doctor’s valuation
• The failure of medical education…

• The failure of scientific medicine…

 Background
• Type 2 DM is a chronic, progressive, devastating,
and costly disease.

• Often asymptomatic.

• Defect of insulin secretion has been happened

since prediabetes.

• Related to micro and macrovascular

complications.
 Type 2 DM progresses
before diagnosis
 Classic signs or symptoms of diabetes might only appear
after several years of even sustained hyperglycemia.
 disease is present 9 to 12 years before diagnosis
 by the time diabetes diagnosis, up to 50% of beta cell function may
have already been lost.

Predicted and observed decline in β-cell function

from the time of diagnosis (based on UKPDS 16)

Holman RR. Diab Res Clin Pract 1998;40(Suppl.):S21–5. Harris MI et al. Diabetes Care. 1992; 15:815-819; Bagust A et al. QJM.
2003;96:281-288; DeFronzo RA. Diabetes. 2009;58:773-795; Colagiuri S et al. Diabetes Care. 2002;25:1410-1417.
Type 2 Diabetes is A Progressive Disease

Lifestyle
Oral; Oral + Insulin; Insulin

Type 2 Diabetes is a Progressive Disease requiring timely treatment

escalation
 Type 2 DM is a progressive disease with
early onset of foundation for complications
Glucose mmol/l 20 Postprandial glucose

15

10 Fasting glucose

NGT
Prediabetes
(IFG / IGT)
Diabetes
Proportional amount of
nsulinin in relation to

200
Insulin resistance
normal (%)

100
Risk of
diabetes Impaired islet cell function Insulin
0
–10 –5 0 5 10 15 20 25 30
years
Complications

International Diabetes Center. Type 2 Diabetes BASICS. Minneapolis, Minn: International Diabetes Center; 2000.
 Clinical Inertia and
“Bad Glycaemic Legacy”

Prato SD. Megatrials in type 2 diabetes. From excitement to frustration? Diabetologia. 2009; 52: 1219-26.
 Clinical Inertia
• Inertia = tendency to remain unchanged.

• Inertia in medical context = “resistance to

change in a timely manner in people whose
health is likely to improve with
intensification.”

• One cause of glycaemic control failure in type

2 DM.
Reach G. Clinical inertia: a critique of medical reason. Springer International Publishing: Switzerland; 2015.
Definition of Clinical Inertia
Healthcare
Clear and available providers know,
guideline. understand, and
apply the guideline.

Adequate facilities.

Reach G. Clinical inertia: a critique of medical reason. Springer International Publishing: Switzerland; 2015.
Clinical Inertia in Type 2 DM

Strain WD, et al. Diabetes Research and Clinical Practice. 2014; 105: 302-12.
 Risk Factor of Clinical Inertia

No subjective feelings Ualitity of life

No decrease quality of life

*Thematic vagabonding: goals continually shift over time, so that decisions are never consistent and final goal states are
never achieved.
Connor PJ, Hillen JM, Johnson PE, Rush WA, Blitz G. Clinical inertia and outpatient medical errors. Advances in Patient Safety: Vol 2.p.293-308.
Risk Factors for Clinical Inertia in Type 2 DM Patients:
Patient’s Reaction

Only about a third of the people with diabetes were accepting of their
diagnosis, and the majority had different reactions.

Strain WD, et al. Diabetes Research and Clinical Practice. 2014; 105: 302-12.
Quality of Life vs Life Expectancy

Wikman A, Marklund S, Alexanderson K. J Epidemiol Community Health 2005; 59: 450-4. Reach G. Patients’ nonadherence and
doctors’ clinical inertia: two faces of medical irrationality. Diabetes Manag. 2015; 5(3): 167-81.
THANK YOU
 The impact of a 12 month
clinical inertia on outcomes
– a T2DM cohort of 110,543 UK patients, treated
between May 1990 and January 2010

Patients with HbA1c ≥ 7.0% At 5.3 years, significantly increased risk

not receiving therapy
intensification within 1 year
26% of all patients
of:
 MI 67% (CI 39–101%)
 Stroke 51% (CI 25–83%)
 HF 64% (CI 40–91%)
 Composite CVE 62% (CI 46–80%)

Paul et al. Cardiovasc Diabetol 2015;14:100 doi:10.1186/s12933-015-0260-x

IDF Diabetes Atlas; 7th Edition, 2015.
 Insulin secretion defect has been
happened since prediabetes (IGT)
NGT IGT T2DM
2500
ISR (from C-peptide)

2000

1500

1000

500

0
0 30 60 90 120 0 30 60 90 120 0 30 60 90 120

12
Glucose (mmol/L)

10
8
6
4
2

0 30 60 90 120 0 30 60 90 120 0 30 60 90 120

Adapted from Fritsche et al. Horm. Metab. Res. 2000 Jun;32(6):230-2

Conservative vs Proactive Management
OAD OAD OAD + multiple
Diet
monotherapy OAD combination daily insulin
10 monotherapy OAD + injections
uptitration basal insulin
Conservative
9

HbA1c (%)
management
(traditional stepwise
approach) 8

6 Diet
10 OAD monotherapy
OAD +
9 multiple
HbA1c (%)

Proactive OAD OADs OAD + basal daily insulin

combinations uptitration insulin injections
management 8
(early combination
approach)
7

6
Duration of diabetes
HbA1c, glycated haemoglobin; OAD, oral anti-diabetic agent.

1. Del Prato S, et al. Int J Clin Pract. 2005;59;1345–55. 2. Campbell IW, et al. Br J Cardiol. 2000;7:625–31.
 UKPDS: Micro and macrovascular complications
increase as a function of HbA1C in T2DM

Estimated 37%
Microvascular decrease in
60 endpoints microvascular risk
Adjusted incidence per 1000

for each 1%
50 reduction in HbA1c (P
person years (%)

< 0.0001)
40
Estimated 14%
30 MI decrease in myocardial
infarction risk for each
20 1% reduction in HbA1c
(P < 0.0001)
10

0
5.5 6.5 7.5 8.5 9.5 10.5
Updated mean HbA1c concentration (%)

HbA1c, glycated haemoglobin; MI, myocardial infarction; T2DM, type 2 diabetes mellitus;
UKPDS, United Kingdom Prospective Diabetes Study.

Stratton IM, et al. BMJ. 2000;321:405–12.

 UKPDS ‘legacy effect’: reductions in relative
risk at 10-year post-study follow-up
0.91
Any diabetes-related endpoint 0.83 0.99 P = 0.04

0.83
Diabetes-related death 0.73 0.96 P = 0.01

Death from any cause 0.87

0.79 0.96 P = 0.007

0.85
Myocardial infarction 0.97 P = 0.01
0.74

Stroke 0.91
0.73 1.13 P = 0.39

0.82
Peripheral vascular disease 0.56 1.19 P = 0.29
0.76
Microvascular disease 0.64 0.89 P = 0.001

-
-

-
Data represent point estimate and 95% CI 0.1 0.5 1 5 10
Intensive better Conventional better
Intensive = Sulfonylurea or insulin in 5-year UKPDS.
Median HbA1c at end of UKPDS 7.9%
With glucose control, it matters both how well a patient
Conventional = diet only in 5-year UKPDS.
Median HbA1c at end of UKPDS 8.5%
is treated now and how well the patient was treated in the past
Holman RR, et al. N Engl J Med. 2008;359:1577–89.
 UKPDS ‘legacy effect’: reductions in relative
risk at 10-year post-study follow-up
0.91
Any diabetes-related endpoint 0.83 0.99 P = 0.04

0.83
Diabetes-related death 0.73 0.96 P = 0.01

Death from any cause 0.87

0.79 0.96 P = 0.007

0.85
Myocardial infarction 0.97 P = 0.01
0.74

Stroke 0.91
0.73 1.13 P = 0.39

0.82
Peripheral vascular disease 0.56 1.19 P = 0.29
0.76
Microvascular disease 0.64 0.89 P = 0.001

-
-

-
Data represent point estimate and 95% CI 0.1 0.5 1 5 10
Intensive better Conventional better
Intensive = Sulfonylurea or insulin in 5-year UKPDS.
Median HbA1c at end of UKPDS 7.9%
With glucose control, it matters both how well a patient
Conventional = diet only in 5-year UKPDS.
Median HbA1c at end of UKPDS 8.5%
is treated now and how well the patient was treated in the past
Holman RR, et al. N Engl J Med. 2008;359:1577–89.
 In newly diagnosed patients, risk reductions are
observed for efery 1% reduction in HbA1C

Relative risk reduction† 95% CI

Microvascular complications  37% 33 – 41
Any diabetes-related endpoint  21% 17 – 24
Diabetes-related death  21% 15 – 27
All-cause mortality  14% 9 – 19
Fatal and non-fatal MI  14% 8 – 21

†All P < 0.0001

Newly diagnosed T2DM at baseline; 7.5 – 12.5 years’ follow-up (median = 10.0 years)

CI, confidence interval; HbA1c, glycated haemoglobin;

MI, myocardial infarction; T2DM, type 2 diabetes mellitus

1. Stratton IM, et al. Brit Medicine J. 2000; 321:405–12. 2. Colagiuri, et al. National evidence based guideline for blood glucose cont
rol in type 2 diabetes. Diabetes Australia and the NHMRC,Canberra 2009.
 Illness vs Disease

Wikman A, Marklund S, Alexanderson K. J Epidemiol Community Health 2005; 59: 450-4. Reach G. Patients’ nonadherence and doctors’ clinical
inertia: two faces of medical irrationality. Diabetes Manag. 2015; 5(3): 167-81.
 Risk Factor of Clinical Inertia

*Thematic vagabonding: goals continually shift over time, so that decisions are never consistent and final goal states are
never achieved.
Connor PJ, Hillen JM, Johnson PE, Rush WA, Blitz G. Clinical inertia and outpatient medical errors. Advances in Patient Safety: Vol 2.p.293-308.
Risk Factors for Clinical Inertia in Healthcare Providers:
Adherence to Guideline

Reach G. Clinical inertia: a critique of medical reason. Springer International Publishing: Switzerland; 2015.
Risk Factors for Clinical Inertia in Healthcare Providers:
Phillips et al

Healthcare providers overrate the quality of care

given.

“Soft excuses” to avoid intensifying care.

Lack the relevant knowledge, tools, training,

office systems.

Reach G. Clinical inertia: a critique of medical reason. Springer International Publishing: Switzerland; 2015.
 Risk Factors for Clinical Inertia
in Healthcare Providers

• Competing demands.
• Insufficient / limited time.
• Lack of experience or confidence.
• Fear of initiating insulin.
• Variety of guidelines.

Khunti K, Wolden ML, Thorsted BL, Andersen M, Davies MJ. Diabetes Care. 2013; 36: 3411-7.
Khunti S, Davies MJ, Khunti K. Learning from Practice. 2015; 15(2): 65-9.
O’Connor PJ. Health Research and Educational Trust. 1854-61. DOI:10.1111/j.1475-6773.2005.00437.x.
Risk Factors for Clinical Inertia in Type 2 DM Patients:
Concerns about the Risks

Strain WD, et al. Diabetes Research and Clinical Practice. 2014; 105: 302-12.
Risk Factors for Clinical Inertia in Type 2 DM Patients:
Knowledge about Hypoglycaemia

Strain WD, et al. Diabetes Research and Clinical Practice. 2014; 105: 302-12.
Clinical Inertia in Initiation of Insulin

“Psychological”
Insulin Resistance

Chen KW, Huang YY, Chuang YJ. J Diabetes Metab 2012; 3: 5; Reach G. Diabetes Manag. 2015; 5(3): 167-81.
 Management of Clinical Inertia for
Healthcare Providers
• Continuing education.
• Consistent follow up procedure and proactive
reminder.
• Implementation of positive emotions.
• Self-performance evaluation.
• Use of guidelines.

Reach G. Clinical inertia: a critique of medical reason. Springer International Publishing: Switzerland; 2015.
Khunti S, Davies MJ, Khunti K. Learning from Practice. 2015; 15(2): 65-9.
O’Connor PJ. Health Research and Educational Trust. 1854-61. DOI:10.1111/j.1475-6773.2005.00437.x.
Connor PJ, Hillen JM, Johnson PE, Rush WA, Blitz G. Clinical inertia and outpatient medical errors. Advances in Patient Safety: Vol 2.p.293-308.
Reach G. Patients’ nonadherence and doctors’ clinical inertia: two faces of medical irrationality. Diabetes Manag. 2015; 5(3): 167-81.
A simple 4-step pathway

Strain WD, et al. Diabetes Research and Clinical Practice. 2014; 105: 302-12.
Key principles

Strain WD, et al. Diabetes Research and Clinical Practice. 2014; 105: 302-12.
 Practice points

Reach G. Patients’ nonadherence and doctors’ clinical inertia: two faces of medical irrationality. Diabetes Manag. 2015; 5(3): 167-81.
 Management of Clinical Inertia for
Office Systems
• Frequent office visit.
• Information clinical systems.
• Financial incentives.

Reach G. Patients’ nonadherence and doctors’ clinical inertia: two faces of medical irrationality. Diabetes Manag. 2015; 5(3): 167-81.