2012 semdsa guideline for the management of type 2 diabetes mellitus aslam amod 1st fcpsa congress...

2012 SEMDSA Guideline for the Management of Type 2 Diabetes

Mellitus

Aslam Amod

1st FCPSA Congress

19 May 2012, Cape Town

Amod A et al. The 2012 SEMDSA guideline for the management of type 2 diabetes. JEMDSA. 2012;17(1):S1-S94.

Available at http://www.jemdsa.co.za

The Guideline & Steering Committee

Chairperson: Aslam Amod

Section 1 Definition, diagnosis and organisation

Ayesha A Motala Definition, classification, diagnosis and screening

Naomi S Levitt Organisation of Diabetes Care

Section 2 Lifestyle Modification

Jeannie Berg, Madelein Young, Natalie Grobler

Diabetes self management education, Medical nutrition therapy

Andrew Heilbrunn Physical activity and type 2 diabetes

The Guideline & Steering Committee (2)


Section 3 Glycaemic Control

Larry A Distiller Assessment of Glycaemic Control

Aslam Amod, Fraser Pirie, Joel Dave

Glycaemic control: Non-insulin therapiesInsulin-based therapies The SEMDSA 2012 algorithm

Ken Huddle Hypoglycaemia, Diabetes in pregnancy

Daksha Jivan Hyperglycaemic emergencies

Imran Paruk In-hospital management of type 2 diabetes



Section 4 Complications and co-morbidities

Wayne May Obesity in type 2 diabetes

Derick Raal, Dirk Blom Cardiovascular risk and dyslipidaemia

Brynne Ascott-Evans Aspirin therapy

Susan Brown Hypertension

Willie Mollenze Chronic kidney disease and Retinopathy

Paul Rheeder, Lynne Tudhope, Gerda van Rensburg

Neuropathy and foot problems in type 2 diabetes



Section 5 Diabetes in Special Circumstances

Yasmin Ganie, Michelle Carrihill

Type 2 diabetes in children and adolescents, management of sick days

Sophie Rauff Type 2 diabetes in older persons

Danie van Zyl Type 2 diabetes in high risk ethnic groups

Hoosen Randeree Type 2 diabetes during Ramadaan

Duma Khutsoane Type 2 diabetes in HIV infected individuals

Pankaj Joshi Prevention/Delay of Type 2 Diabetes

Peter Raubenheimer Diabetes and driving

The Advisory CommitteeSEMDSA / Association of Clinical Endocrinologists (ACE-SA) Members

Philip Erasmus, Gregory Arthur Hough, Stanley Landau, Puvanesveri Naiker, MAK Omar, Helena Oosthuizen, William Toet, Carsten Weinreich, Holger Wellmann

Department of Health (Chronic Diseases)

Anne Croasdale , Melvyn Freeman, Sandhya Singh

Society of General / Family Practitioners, Angelique Coetzee, Philip Erasmus

Diabetes Education Society of South Africa (DESSA)

Jeannie Berg, Gerda van Rensburg, Madelein Young

Diabetes South Africa (DSA) Leigh-Ann Bailie , Ranga Kuni

Medical Aids Margaret Campbell (Discovery)

Council of Medical Schemes (CMS) Selaelo Mametja

Introduction

• Target Audience– All healthcare professionals (medical & allied)

– Focus on primary care, but also general physician

– Funders of healthcare

– Undergraduates and postgraduates

• Not for “experts”

– Self-proclaimed or otherwise

• Disclaimer

International Diabetes Federation. IDF Diabetes Atlas [cited 2012 Mar 18]. Available from: http:// www.idf.org/diabetesatlas

Disclaimer

• This guideline is not intended to replace professional judgement, experience and appropriate referral.

• These guidelines are intended to inform general patterns of care, to enhance diabetes prevention efforts and to reduce the burden of diabetes complications in people living with this disease.

• They reflect the best available evidence at the time, and practitioners are encouraged to keep updated with the latest information in this rapidly changing field.

• While every care has been taken to ensure accuracy, reference to product information is recommended before prescribing.

• SEMDSA assumes no responsibility for personal or other injury, loss or damage that may result from the information in this publication.

• Unless otherwise specified, these guidelines pertain to the care of adults with type 2 diabetes at primary care level.

Epidemiology / Prevalence

• Type 2 > 90% – Local studies using 1985 WHO criteria

• Rural African: 3.5%

• Urban Coloured: 10.8%

• Urban Indian: 13%

• 30-85% undiagnosed

– >90% are obese

• IDF Atlas 5th edition• 6.5% of adults aged 20-79 years

International Diabetes Federation. IDF Diabetes Atlas [cited 2012 Mar 18]. Available from: http:// www.idf.org/diabetesatlas

Diagnosis and screening

Diagnosis (WHO criteria)

Diagnostic test IFG IGT Diabetes

Fasting plasma glucose (FPG) a

Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT)b

Glycated haemoglobin A1c (HbA1c) c

Random plasma glucose (RPG) d

World Health Organization. Definition and diagnosis of diabetes mellitus and intermediate hyperglycaemia [cited 2011 Sep 20]. Available from: http://whqlibdoc.who.int/publications/2006/9241594934_eng.pdf.


Diagnostic test IFG

Fasting plasma glucose (FPG) a 6.1 to 6.9 mmol/L


<7.8 mmol/L (if measured)

Glycated haemoglobin A1c (HbA1c) c -


-


Diagnostic test IGT

Fasting plasma glucose (FPG) a

<7.0mmol/L (if

measured)


7.8 to 11.0 mmol/L

Glycated haemoglobin A1c (HbA1c) c -


-


Diagnostic test Diabetes

Fasting plasma glucose (FPG) a > 7.0 mmol/l, or


> 11.1 mmol/l, or

Glycated haemoglobin A1c (HbA1c) c > 6.5%, or


≥ 11.1 mmol/l if classic symptoms or hyperglycaemic

crisis is present




<7.0mmol/L (if

measured)> 7.0 mmol/l, or



7.8 to 11.0 mmol/L > 11.1 mmol/l, or

Glycated haemoglobin A1c (HbA1c) c - - > 6.5%, or

Random plasma glucose (RPG) d - -


crisis is present




<7.0mmol/L (if




7.8 to 11.0 mmol/L > 11.1 mmol/l, or




crisis is present

For clinical purposes, the diagnosis of diabetes should always be confirmed by repeating the test on another day (preferably the same test), unless there is unequivocal hyperglycaemia with acute metabolic decompensation or obvious symptoms (polyuria, polydipsia and weight loss).




<7.0mmol/L (if




7.8 to 11.0 mmol/L > 11.1 mmol/l, or




crisis is presenta “Fasting” is defined as no caloric intake for at least eight hoursb The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in 250 ml water ingested over five minutes




<7.0mmol/L (if




7.8 to 11.0 mmol/L > 11.1 mmol/l, or




crisis is presentd The classic symptoms of hyperglycaemia include polyuria, polydipsia and weight loss. “Hyperglycaemic crisis” refers to diabetic ketoacidosis or hyperosmolar nonketotic hyperglycaemia.




<7.0mmol/L (if




7.8 to 11.0 mmol/L > 11.1 mmol/l, or




crisis is presentc Provided that: -The test method meets stringent quality assurance criteria -The assay is NGSP certified and standardised to the DCCT assay-There are no conditions present which preclude its accurate measurement

Use of HbA1c in the diagnosis of diabetes mellitus

For the diagnosis of diabetes

HbA1c > 6.5%

HbA1c < 6.5% does not exclude diagnosis by blood glucose

Glucose–based tests (FPG, OGTT) are still valid

Interpretation of HbA1c < 6.5%

No recommendation, because of insufficient evidence


Requirements to fulfill (provisos) for use of HbA1c for diagnosis

Stringent quality assurance tests in placea

Assays standardised to criteria aligned with international reference valuesb

Low cost and wide availability

No conditions present which preclude accurate measurement

a Appropriate conditions for assay method: Standardised assay, low coefficient of variability, and calibrated against International Federation of Clinical Chemists (IFCC) standards b DCCT aligned and NGSP certified


Choice between HbA1c and plasma glucose should be based on local considerations

Cost

Availability of equipment

National quality-assurance system

Population characteristics (e.g. prevalence of malaria or haemoglobinopathies)

Crucial to ensure that accurate blood glucose measurement be generally available at primary healthcare level before introducing HbA1c measurement as a diagnostic tool

Factors which influence HbA1c measurement

Erythropoiesis

Increased HbA1c: Iron deficiency, vitamin B12 deficiency, decreased erythropoiesisDecreased HbA1c: Administration of erythropoietin, iron or vitamin B12, reticulocytosis, chronic liver disease

Altered haemoglobin

Genetic or chemical alterations in haemoglobin may increase or decrease HbA1c: Haemoglobinopathies, HbF, methaemoglobin

GlycationIncreased HbA1c: Alcoholism, chronic renal failure

Decreased HbA1c: Aspirin, vitamins C and E, certain haemoglobinopathies, increased intra-erythrocyte pH

Erythrocyte destruction

Increased HbA1c with increased erythrocyte life span: SplenectomyDecreased HbA1c with decreased erythrocyte life span: Haemoglobinopathies, splenomegaly, rheumatoid arthritis, drugs (e.g. antiretrovirals, ribavirin, dapsone)

Assays

Increased HbA1c: Hyperbilirubinaemia, carbamylated haemoglobin, alcoholism, large doses of aspirin, chronic opiate useDecreased HbA1c: HypertriglyceridaemiaVariable HbA1c: Haemoglobinopathies

Note: Some of these factors cannot be detected by certain assays

Screening

• Diagnosis vs. screening

• Targeted screening advocated

– High rate of undiagnosed diabetes

– Age > 45 or any age with multiple risk factors

– Repeat every 3 yrs or more frequently

– Use FPG, OGTT or HbA1C

• Exclude diabetes

– FPG < 5.6 mmol/L; if not do OGTT

– RPG < 5.6 mmol/L; if not do FPG or OGTT

– HbA1C – do OGTT if 6.0 to 6.4%

Random PG

<5.6mmol/L

5.6 – 11.0mmol/L

≥ 11.1 mmol/L + Symptoms

Diabetes excluded

InconclusiveDo FPG or OGTT

Diabetes

Fasting PG

<5.6mmol/L

6.0 – 6.9mmol/L

5.6 – 5.9mmol/L

≥ 7.0mmol/L

Diabetes excluded

IFG(Repeat)

InconclusiveDo OGTT

Diabetes(Repeat)

HbA1C

Normal 6.0 – 6.4%

Normal – 5.9%

≥ 6.5%

Diabetes excluded

InconclusiveDo FPG/OGTT

Clinical judgement

Diabetes(Repeat)

2hr OGTT

< 7.8mmol/L

7.8 – 11.0mmol/L

≥ 11.1 mmol/L

Diabetes excluded

IGT(Repeat)

Diabetes(Repeat)

Glycaemic targets

Individualised glycaemic targets

Patient type Target HbA1c

Target FPG Target PPG

YoungNewly diagnosedNo cardiovascular diseaseLow CV risk

< 6.5%4.0 - 7.0mmol/l

4.4 - 7.8mmo/l

Majority of patients < 7%4.0 - 7.0mmol/l

5.0 -10.0mmol/l

ElderlyHypoglycaemic unawarePoor short-term prognosisEstablished CV diseaseHigh CV risk

< 7.5%(< 8.0%)

5.0 - 8.0 mmol/l

< 12.0mmol/l

Translating HbA1C into estimated average glucose (eAG)

HbA1c

(%)Estimated average glucose

(mmol/L)

6 7.0

7 8.6

8 10.2

9 11.8

10 13.4

11 14.9

12 16.5

Nathan DM et al for the A1c-Derived Average Glucose (ADAG) Study Group. Translating the A1C assay into estimated average glucose values. Diabetes

Care 2008; 31: 1473– 1478

Glycaemic control: Pharmacological therapy

General Considerations

• Type 2 diabetes is not a homogeneous disease– Try to understand the pathophysiology in each individual

patient

• Majority of patients treated at PHC level

– Poor access to / use of laboratory testing esp. HbA1C and renal function

– Increase number of agents that can be prescribed safely by PHC doctors and nurses without complex monitoring

• Accumulating data on dangers of hypoglycaemia as a risk marker for CV death

• Potential remission / cure in obese patients with substantial weight loss

Alternative therapies for special circumstancescPreferred therapies

SU = sulphonylurea. Not glibenclamide ; DPP-4i = Dipeptidyl peptidase inhibitor; eGFR = estimated glomerular filtration rateaSevere decompensation includes any of: FPG > 15mmol/L, HbA1C > 11%, marked polyuria & polydipsia, weight loss > 5% or ketoacidosis. Refer the patient for specialist care (Step 4).bRefer to Table I for expected HbA1C reductions.cRefer to textdIf at diagnosis, the patient’s HbA1C is >9% without features of severe decompensation, consider initiating therapy at STEP 2.

Use this algorithm only if the patient does NOT have features of severe decompensationa.Progress down this algorithm within 3 months if HbA1C remains above 7% (or individualised target).

Choose therapies that are likely to produce the HbA1c reduction required to achieve the targetb Do not proceed with drug therapy without annual serum eGFR measurement

Incretin AcarboseSTEP 2: COMBINE ANY 2 DRUGSd

STEP 3: COMBINE 3 DRUGS

Basal Insulin

Metformin + SU + Acarbose

Metformin + SU + Incretin

STEP 4: MORE ADVANCED THERAPIES

SU DPP-4i Acarbose

Metformin + Pre-mix insulin (if not used yet)

SU

Metformin + SU + Basal Insulin (or Metformin + Pre-

mix)

Metformin

Refer to specialist forBasal + mealtime insulin

± Metformin ± Acarbose ± Incretin

Metformin

Lifestyle measures plus

STEP 1: INITIATE AT LEAST ONE ORAL DRUG AT DIAGNOSIS

Glycaemic control: SEMDSA 2012 algorithm for type 2 diabetes

Glycaemic control: SEMDSA 2012 algorithm for type 2 diabetes

Use this algorithm only if the patient does NOT have features of severe decompensationa.

Progress down this algorithm within 3 months if HbA1C remains above 7% (or individualised target).

Choose therapies that are likely to produce the HbA1c reduction required to achieve the targetb

Do not proceed with drug therapy without annual serum creatinine / eGFR measurement

aSevere decompensation includes any of: FPG > 15mmol/L, HbA1C > 11%, marked polyuria & polydipsia, weight loss > 5% or ketoacidosis. Refer the patient for specialist care (Step 4).

bRefer to Table for expected HbA1C reductions.

Alternative therapies for special

circumstances

Preferred therapies

Glycaemic control: SEMDSA 2012 algorithm


SU DPP-4i AcarboseMetformin

Lifestyle measures

plus


circumstances

Preferred therapies




Lifestyle measures

plus


Basal Insulin

SUMetformin

dIf at diagnosis, the patient’s HbA1C is >9% (but without features of severe decompensation), consider initiating therapy at STEP 2


circumstances

Preferred therapies




Lifestyle measures

plus


Basal Insulin

SUMetformin





mix)


circumstances

Preferred therapies




Lifestyle measures

plus


Basal Insulin

SUMetformin





mix)

STEP 4: MORE ADVANCED THERAPIES

Metformin + Pre-mix insulin (if not used yet)

Refer to specialist for

Basal + mealtime insulin

± Metformin ± Acarbose ± Incretin

Non-insulin therapiesMetformin

A1c ↓ Therapeutic considerations Disadvantages

↓↓

Negligible hypoglycaemia risk as monotherapy

Weight neutral (promotes less weight gain when combined with other agents).

Proven reduction in CV events and mortality in obese subjects (primary endpoint in UKPDS).

Metformin-XR has better GI tolerability (is preferred to switching to another class).

Frequent GI side effects; 5-10% discontinuation.

Lactic acidosis (rare).

Vitamin B12 deficiency.

Renal impairment: reduce dose to 1000mg/d if eGFR <45 and discontinue if eGFR < 30ml/min/1.73m2

Contraindications: Cardiac failure, PAD, Liver disease, COPD, IV Contrast media

Metformin in the 2012 SEMDSA algorithm

• Step 1: Monotherapy– Initial therapy of choice

– Start at time of diagnosis in all patients (overweight and normal weight) unless specifically contra-indicated.

• Step 2: Dual therapy– Can be added as a second-line agent in patients where

treatment has been initiated with any other class of anti-diabetic drug.

• It is recommended that metformin therapy continue even when other classes of anti-diabetic agents (including insulin) are added subsequently.

Sulphonylureas

HbA1c Therapeutic

considerations Disadvantages

↓↓

Generally well tolerated.Proven reduction in microvascular endpoints.Relatively rapid glucose-lowering response.

Consider using another class in patients at high risk of hypoglycaemia. If SU must be used in such individuals, gliclazide-MR < glimepiride / glipizide < glibenclamide.

Can cause severe hypo, (especially glib. in renal impairment).

Weight gain; 2 to 5kg; worst with glibenclamide

May blunt myocardial ischemic preconditioning (especially glibenclamide).

Glibenclamide contra-indicated if eGFR<60ml/min/1.73m2; glimepiride and glipizide dose may need to be reduced.

SU in the 2012 SEMDSA algorithm

• Step 1: Monotherapy – at diagnosis in persons intolerant of metformin, or in normal

weight individuals or those with marked symptoms of hyperglycaemia.

• Step 2: Dual therapy– Add as 2nd drug to metformin, or any other drug used at

Step 1

• Step 3: Triple therapy – with metformin and basal insulin, or metformin and incretin.

• In gestational diabetes, glibenclamide is the sulphonylurea of choice (for specialist use only)

Non-insulin therapiesMeglitinides

HbA1c Therapeutic


↓ to ↓↓

Nateglinide is the least effective secretagogue.

Targets postprandial glycemia; use if fasting glucose is at target but HbA1c remains high.

Associated with less hypoglycemia compared to SU in the context of missed meals; useful for patients with unpredictable meals.

Causes hypoglycemia.

Causes weight gain.

May blunt myocardial ischemic preconditioning.

Frequent dosing (mealtime).

Meglitinides in the 2012 SEMDSA algorithm

• Instead of SU

– If FPG is at target but HbA1C and PPG levels are elevated

Non-insulin therapiesAcarbose

HbA1c ↓ Therapeutic


↓

Negligible hypoglycaemia risk as monotherapy.

Non-systemic effect.

Weight neutral.

Targets post-prandial hyperglycaemia

49% reduction in CV risk (pre-planned 2o analysis in STOP-NIDDM Trial)

GI effects (gas, flatulence, diarrhea).

Frequent dosing (mealtime).

Non-insulin therapiesDPP-4 Inhibitors

HbA1c Therapeutic


↓

Negligible hypoglycaemia risk as monotherapy

Weight neutral.

Improves post-prandial control.

Drug-specific recommendations for hepatic and renal disease.

Occasional reports of urticaria/angioedema

Cases of pancreatitis observed

Newer agent with unknown long-term safety.

DPP-4 inhibitors in the 2012 SEMDSA algorithm

Contraindications to DPP-4 inhibitors

There is a compelling indication for insulin therapy

History of a serious hypersensitivity reaction to DPP-4 inhibitors.

Patients with a history of acute pancreatitis, chronic or recurring pancreatitis and those with pancreatic cancer.

DPP-4i and Acarbose in the 2012 SEMDSA algorithm

At Step 3: Add-on therapy as part of an oral 3-drug regimen Inadequate glycemic control on combination therapy with

metformin and sulphonylurea, and

Patient is a poor candidate for insulin therapy, and

Required reduction in HbA1C is < 1%

Discontinue after 3-6 months if HbA1C reduction is < 0.5%


At Step 2: Add-on therapy as part of an oral 2 drug regimen Inadequate glycemic control on monotherapy with metformin or

sulphonylurea, and

Unable to tolerate or has contraindications to addition of the 2nd as yet unused agent from the above mentioned (metformin or sulphonylurea), and




At Step 1: Use as monotherapy Candidate for oral therapy and is intolerant of or has

contraindications to use of both metformin and sulphonylureas, and



GLP-1 Agonists

HbA1c Therapeutic


↓↓

Negligible hypoglycaemia risk as monotherapy.

Enhances satiety and causes weight loss.Possible potential for improved beta cell mass and function.

Avoid initiating therapy in individuals whom the potential for dehydration poses a considerable risk (e.g., frail elderly, multiple co-morbid conditions, etc.)

Injectable

Initial GI side effects (nausea, vomiting, diarrhea)

Cases of acute pancreatitis observed

Causes C-cell hyperplasia / medullary thyroid tumors in animals (liraglutide)

Newer agent with unknown long-term safety.

GLP-1 agonists in the 2012 SEMDSA algorithm

Contraindications to GLP-1 use

There is a compelling indication for insulin therapy

History of hypersensitivity to GLP-1 agonist

Renal failure (consult product label to assess suitability)

Personal or family history of medullary thyroid carcinoma or Multiple Endocrine Neoplasia syndrome type 2 (liraglutide).

Patient has severe gastrointestinal disease, including gastroparesis.

Patient has a history of pancreatitis

Relative exclusions to use include triglyceride level > 10mmol/L, gallstones with intact gallbladder, and alcohol abuse.

Planned treatment regimen includes a DPP-4 inhbitor, meglitinide or acarbose (unstudied)


At Step 3: Add on therapy as part of a 3 drug regimen:

Inadequate glycemic control on combination therapy with maximally tolerated doses of metformin and sulphonylurea, and

Patient is not a candidate for a 3rd oral agent from step 3, and

Patient is a poor candidate for insulin therapy, and

Required reduction in HbA1C is < 1.5% in order to reach patient

specific goalOnly continue therapy beyond 6 months if there has been a good clinical response to therapy:

• HbA1C reduction >0.5% AND weight loss >3%, OR

• HbA1C reduction >1%, OR

• Weight loss >5%


At Step 2: Add on therapy as part of a 2 drug regimen:

Patient has not achieved desired HbA1c and with optimum doses of one oral agent and is not a candidate for any other agent (oral or insulin) available at Step 2; and

Required reduction in HbA1C is < 1.5% in order to reach patient

specific goal

Only continue therapy beyond 6 months if there has been a good clinical response to therapy:

• HbA1C reduction >0.5% AND weight loss >3%, OR

• HbA1C reduction >1%, OR

• Weight loss >5%

Circumstances where insulin therapy may not be desirable

Insulin allergy

Failure or inability to master injections or self-titration

Frequent or severe hypoglycemia despite multiple dosage adjustments

Circumstances exist where the risk of severe hypoglycemia and/or its potential consequences are significant and/or catastrophic

• Workers with frequent rotating shifts• Occupations such as truck or bus drivers / heavy machine

operators)

Obesity related morbidity which has worsened or is likely to worsen significantly with weight gain from insulin therapy

Thiazolidenediones

• Rosiglitazone– Increased CV outcome events

– Voluntarily withdrawn in SA

• Other problems– Fluid retention, ppt heart failure

– Weight gain

– Long bone fractures

– Bladder cancer

• Not included in the algorithm

Lipids

Lipid targets

• Aligned with LASSA and SA HeartTotal cholesterol < 4.5mmol/L

LDL cholesterol < 1.8mmol/La

HDL cholesterol > 1.0 mmol/L (men)> 1.2 mmol/L (women)

Triglycerides < 1.7mmol/La The LDL-cholesterol goal is < 2.5 mmol/l in patients with type 2 diabetes who meet all of the following criteria:

1. No cardiovascular disease and no chronic kidney disease

2. Less than 40 years old OR duration of diabetes less than 10 years

3. No other cardiovascular risk factor

Lipids

• Measure 10-hr fasting lipid profile at diagnosis

• Subsequent monitoring targeted only at abnormalities (no need for full profile in every patient)

• Specialist referral: TG > 5 mmol/l in the controlled diabetic, or > 15 mmol/l before treatment.

Initiate statin therapy in all patients with:

• Existing cardiovascular disease (i.e. ischaemic heart disease, cerebrovascular disease or peripheral vascular disease).

• Chronic kidney disease (eGFR < 60 ml/minute/1.73m2).

• Age >40 years or diabetes duration >10 yrs with one or more additional cardiovascular risk factor– hypertension, cigarette smoker, low HDL-cholesterol level,

family history of early coronary heart disease, microalbuminuria

Statins

• Consider statin + ezetimibe if patient is unable to tolerate / achieve LDL cholesterol goals on the maximum dose of a highly potent statin

• Simvastatin should not be co-prescribed with most antiretroviral agents

• Use low doses of simvastatin with CCB’s.

• Never initiate therapy with Simvastatin 80 mg/day

Referrals

• Baseline TG >15mmol/L

• TG > 5mmol/l with low HDL, despite good glycaemic control

• Combination therapy (statin + fibrate) being considered.

Blood pressure

Highlights: Blood pressure targets

• Previous SBP target lacks clinical evidence base

• Definition of hypertension– SBP ≥ 140mmHg

– DBP ≥ 80mmHg

• Target BP– SBP 120-140mmHg

– DBP 70-80mmHg

Rhonda M, Cooper-DeHoff, Egelund EF, Pepine C. Blood pressure lowering in patients with diabetes—one level might not fit all. Nature Reviews Cardiology. 2011;8:42-49

In-hospital management: regular meal pattern maintained

• Well controlled– Continue usual therapy

• Poorly controlled: Basal bolus therapy– Estimate TDD (conservatively 0.2 to 0.5u/kg)

– Basal (50%) + prandial (50%) insulin

• Correction dose insulin– Correction factor (CF) = 100/TDD or 85/TDD

– Correction dose = (Measured BG – target BG) ÷ CF

Umpierrez G, Smiley D, Zisman A, et al. Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes (RABBIT 2 trial). Diabetes Care. 2007;30:2181-2186.

Example

• 45yr old weighing 100kg taking Actraphane 40u/20u BID prior to hospitalisation

– Estimated TDD = 60u

– Give 30u NPH/long acting analogue at night +

– 10u TDS rapid analogue or short acting regular

– Target preprandial glucose 7.8mmol/L; <10 at any other time

– CF = 100/60 = 1.7 (85/60 for regular human insulin)

• If post-meal BG is 20mmol/L, correction dose = 20 (current) - 10 (target) x 1.7 =17u

• Add 80% of daily correction dose to next days basal-bolus insulin

In-hospital management: regular meal pattern disrupted

• NPO– Use only correction dose insulin, or NPH twice daily or long

acting analogue once daily

• Bolus eneteral feeds– Basal bolus therapy + correction doses

• Continuous enteral feeds– NPH 12-hrly or long acting analogue ± scheduled regular

insulin, OR

– Premixed insulin 8-hourly

• TPN– IV insulin infusion (infusion protocol), or

– 50% TDD added to TPN as regular insulin, and 50% given as basal

– Calculate TDD : 1u/10g carbohydrate

Adapted from Gunderson Lutheran Medical Center protocol Am J Health –Syst Pharm 2007; 64: 392

In-hospital management: critically ill patients

• Insulin infusion preferred if facilities and staff training exist; if not use basal-bolus + correction doses

• Target BG is 7.8 – 10.0 mmol/L; not lower than 6.1mmol/L

• Mix 50u insulin in 100ml 5% dextrose water

• Detailed response protocol needed for staff

Glucose (mmol/l)

10.0-13.9 14.0-16.6 16.7-20.0 >20.0

Bolus injection

4 units 6 units 8 units 10 units

Infusion rate

2 u/hr 3 u/hr 4 u/hr 5 u/hr

ADA/EASD 2012 Algorithm

2012 semdsa guideline for the management of type 2 diabetes mellitus aslam amod 1st fcpsa congress...

Documents

diabetes slide

diabetes mellitus aslam

diabetes derick raal

idf diabetes atlas

aslam amod section

semdsa guideline

cape town slide

michelle carrihill type