Luthfan Budi Purnomo
PERKENI Cabang Jogjakarta
Seminar “AtoZ Tindakan Pencabutan Gigi
pada Pasien Medik Compromis (2014)


Diabetes is associated with increased
requirement for surgical procedures and
increased post-operative morbidity and
mortality
The stress response to surgery and resultant
hyperglycemia, osmotic diuresis, and
hypoinsulinemia can lead to peri-operative
ketoacidosis or hyperosmolar syndrome


Hyperglycemia impairs leukocyte function and
wound healing
The management goal is to optimize metabolic
control through close monitoring, adequate
fluid and caloric repletion, and judicious use
of insulin
DIABETES IS NOT MILD DISEASE
Microvascular complication
Macrovascular complication
Stroke
Diabetic
Retinopathy
Leading cause
of blindness
in working age
adults1
2 to 4 fold increase in
cardiovascular
mortality and stroke3
Cardiovascular
Disease
8/10 diabetic patients
die from CV events4
Diabetic
Nephropathy
Leading cause of
end-stage renal disease2
1 Fong
Diabetic
Neuropathy
Leading cause of nontraumatic lower
extremity amputations5
DS, et al. Diabetes Care 2003; 26 (Suppl. 1):S99–S102. 2Molitch ME, et al. Diabetes Care 2003; 26 (Suppl.
1):S94–S98.
3 Kannel WB, et al. Am Heart J 1990; 120:672–676. 4Gray RP & Yudkin JS. In Textbook of Diabetes 1997.
5Mayfield JA, et al. Diabetes Care 2003; 26 (Suppl. 1):S78–S79.
NATIONAL
5.7%
1.7%
1985
WHO, Study Group 1985
RISKESDAS, 2007
2007
11.1%
Maluku Utara
6.2%
Lampung
5.7%
National
1.7%
Papua
RISKESDAS, 2007
KADAR GLUKOSA DARAH
DIATUR DAN DIKENDALIKAN
DALAM RENTANG YANG SEMPIT
Puasa: 80 - <100 mg/dl
2jPP/sesaat: 80 - <140 mg/dl


Insulin
Counter-insulin hormone
-glucagon
-cathecolamine
-growth hormone
-glucocorticoids
INSULIN
GLUCAGON
CATECHOLAMINE
GLUCOCORTICOID
GROWTH HORMONE
BLOOD GLUCOSE
Fasting hyperglycemia
Post prandial hyperglycemia
A round the clock hyperglycemia
Breakfast
Day time
Lunch
Dinner
Fasting
Bed time
Fasting blood glucose
Blood glucose at bed time
+
Gluconeogenesis
-Cells
hypertrophy
Fewer
-Cells
Insufficient
insulin
+
↓ Glucose
uptake
–
↑ Glucose
Excessive
glucagon
+
↑ HGO
HGO=hepatic glucose output
Adapted from Ohneda A, et al. J Clin Endocrinol Metab. 1978; 46: 504–510; Gomis R, et al. Diabetes Res Clin Pract. 1989;
6: 191–198.
1.
2.
3.
4.
A1c ≥6,5% atau
Glukosa plasma puasa ≥126 mg/dl atau
2-jam setelah TTGO ≥200 mg/dl
Ada tanda khas DM, glukosa plasma sesaat
≥200 mg/dl
Tipe 1
Destruksi sel beta , umumnya menjurus
defisiensi insulin absolut
•Automun
•Idiopatik
Tipe 2
Bervariasi, dominan resistensi insulin
disertai defisiensi insulin relatif sampai
dominan defek sekresi insulin disertai
resistensi insulin
Tipe lain
Defek genetik fungsi sel beta; defek
genetik kerja insulin; penyakit eksokrin
pankreas; endokrinopati; infeksi
Diabetes
mellitus
gestasional
DIABETIC COMPLICATIONS
Acute
Hypoglycemia
Diabetic Ketoacidosis (DKA)
Hyperglycemic Hyperosmolar State
(HHS)
Chronic
Macrovascular
CAD
Stroke
PAD
Microvascular
Retinopathy
Nephropathy
Neuropathy
Cardiomyopathy
Diabetic foot
Slide 17
Diabetes
STEP 1
Healthy life style
Healthy life style
STEP 2
STEP 3
+
Mono therapy
Healthy life style
Note:
1.
2.
Therapy failed if
target of HbA1c < 7%
is not achieved within
2-3 months for each
step
In case of no HbA1c
test, the use of blood
glucose level is also
permitted. Average
blood glucose level
for a few BG test in
one day can be
converted to HbA1c
(ref: ADA 2010)
+
Healthy life style
2 OAD Combination
+
Combination 2 OAD
Alternative option, if :
+
• No insulin is available
Basal insulin
• The patient is objecting insulin
• Blood glucose is still not optimally
controlled
Healthy life style
+
3 OAD Combination
*Intensive Insulin: use of basal insulin together with insulin prandial
Insulin
Intensification*
Incretins :GLP-1 analogue(exenatide)/DPP-4 inhibitors Improves
glucose-dependent insulin secretion
from pancreatic β-cells, suppresses
glucagon secretion from -cells,
slows gastric emptying
Thiazolidinediones
Increase glucose
uptake in skeletal
muscle and decrease
lipolysis in adipose
tissue
Meglitinides
Increase insulin secretion from
pancreatic -cells
Sulfonylureas
Increase insulin secretion
from pancreatic -cells
-Glucosidase inhibitors
Delay intestinal
carbohydrate absorption
GLP = glucagon-like peptide.
Adapted from Cheng and Fantus. CMAJ. 2005;172:213–226.
Slide 18
Class
Generic
Glibinclamide
Mg/tab
Duration
of action
(hr)
Freq/
day
1-2
5-10
5-20
12-16
1
30,60,80
30320
24
1-2
30
30120
6-8
2-3
1,2,3,4
0.5-6
24
1
Repaglinid
1
1.5-6
3
1-1.5
Nateglinid
120
360
3
0.5-0.8
PPG
15-30
15-45
50-100
100300
Glikuidon
Glimepiride
Pioglitazone
18-24
PERKENI Guidelines 2012
FBG
Both
1
Indep of
meals
0.5-1.4
FBG
3
With 1st
food
0.5-0.8
PPG
TZD
Acarbose
1.5
FBG vs.
PPG
12-24
Sulfonylureas
Before
meals
A1C
reduction
2.5-15
Gliklazid
α-glucosidase
inhibitor
Time
2.5-5
Glipizid
Glinid
Daily
dose
(mg)
Class
Biguanides
DPP-IV
inhibitors
Fixed dose
combination
drug
Generic
Mg/tab
Daily dose
(mg)
Duration
of action
(hr)
Freq
/day
Metformin
500-850
500-3000
6-8
1-3
Metformin XR
500-750
500-2000
24
1
Vildagliptin
50
50-100
12-24
1-2
Sitagliptin
25,50,10
0
25-100
24
1
Saxagliptin
5
5
24
1
Metformin+
Glibenclamide
25-500/
1.25-5
Glib max
20 mg/day
12-24
1-2
Glimepiride +
metformin
1-2/
250-500
2-4/
500-1000
Pioglitazone+
metformin
15-30/
500-850
Piog max
45 mg/day
Sitagliptin +
metformin
50/
5001000
Sita max
100
mg/day
Vildagliptin +
metformin
50/
5001000
Vilda max
100
mg/day
PERKENI Guidelines 2012
2
18-24
1
1
12-24
2
Time
A1C
reduction
FBG vs.
PPG
With or
after
meals
1.5
FBG
Indep of
meals
0.6-0.8
Both
With or
after
meals
Onset of
Action
Peak of
Action
Duration of
Action
Presentation
30-60 min
120-180 min
5-8 hour
Vial,
Pen/Cartridge
Insulin Lispro (Humalog®)
5-15 min
30-90 min
3-5 hour
Pen/Cartridge
Insulin Glulisine (Apidra®)
5-15 min
30-90 min
3-5 hour
Pen
Insulin Aspart (Novorapid®)
5-15 min
30-90 min
3-5 hour
Pen, Vial
Type of Insulin
Insulin Prandial (Meal-Related)
Insulin Short-Acting
Regular (Actrapid®, Humulin® R)
Insulin Analog Rapid-Acting
PERKENI Consensus Guidelines, 2011.
Onset of
Action
Peak of
Action
Duration of
Action
Presentation
2-4 hour
4-10 hour
10-16 hour
Vial,
Pen/Cartridge
Insulin Glargine (Lantus®)
2-4 hour
No Peak
20-24 hour
Pen
Insulin Detemir (Levemir®)
2-4 hour
No Peak
16-24 hour
Pen
70% NPH 30% Regular
(Mixtard®, Humulin® 30/70)
30-60 min
Dual
10-16 hour
Pen/Cartridge
70% Insulin Aspart Protamin
30% Insulin Aspart (Novomix® 30)
10-20 min
Dual
15-18 hour
Pen
75% Insulin Lispro Protamin
25% Insulin Lispro (HumalogMix® 25)
5-15 min
Dual
16-18 hour
Pen/Cartridge
Type of Insulin
Insulin Intermediate-Acting
NPH (Insulatard®, Humulin® N)
Insulin Long-Acting
Insulin Campuran
PERKENI Consensus Guidelines, 2011.


The responses include
 Release of catabolic hormones
 Inhibition of insulin secretion and action
Anti-insulin effects of surgical stress
 Insulin resistance induced by circulating
stress hormones
 Effect of surgical stress on pancreatic
β cell function
The Peri-operative Milieu Hypercatabolism
(Dagogo-Jack & Alberti, 2002;;Marks, 2003; Dhatariya et al., 2011)


Poor peri-operative glycaemic control
Complications of diabetes:
► Cardiovascular disease
► Microvascular disease
Dhatariya et al., 2011
Blood pressure test
 Blood pressure response to standing up (fall
in systolic blood pressure): 10 mmHg
(normal), 11-29 mmHg (borderline), ≥30 mmHg
(abnormal)
 Blood pressure response to sustained
handgrip (increase in diastolic blood
pressure): ≥16 mmHg (normal), 11-15 mmHg
(borderline), 10 mmHg (abnormal)
Primary care
referral
Preoperative
assessment
Surgical
outpatient
Theatre and
recovery
Hospital
admission
Discharge
Post-operative
care
(Dhatariya et al., 2011)
Primary care
referral
Surgical
outpatient
Preoperative
assessment
Theatre and
recovery
Hospital
admission
Discharge
Post-operative
care
Ensure that potential effects of diabetes and associated
co-morbidities on the outcome of surgery are
considered
Ensure that diabetes and co-morbidities are optimally
managed
(Dhatariya et al., 2011)


A1c <8.5%
Blood glucose levels 108-180 mg/dl
(Dhatariya et al., 2011)
Primary care
referral
Preoperative
assessment
Surgical
outpatient
Theatre and
recovery
Hospital
admission
Discharge
Post-operative
care
Arrange pre-operative assessment
Avoid overnight pre-operative admission to
hospital whenever possible
(Dhatariya et al., 2011)
Primary care
referral
Preoperative
assessment
Surgical
outpatient
Theatre and
recovery
Hospital
admission
Discharge
Post-operative
care
Ensure that glycaemic control optimized prior to
surgery
Ensure that co-morbidities are recognized and
optimized prior to admission
(Dhatariya et al., 2011)
Preoperative
assessment
Primary care
referral
Surgical
outpatient
Theatre and
recovery
Hospital
admission
Discharge
Post-operative
care
Minimize the metabolic consequences of
starvation and surgical stress
Maintain optimal blood glucose control throughout
the admission
Prevent hospital acquired foot pathology
(Dhatariya et al., 2011)
Primary care
referral
Theatre and
recovery
Preoperative
assessment
Surgical
outpatient
Hospital
admission
Discharge
Post-operative
care
Avoid unnecessary use of VRIII (insulin infusion)
Check the blood glucose prior to induction of
anesthesia
Monitor the blood glucose regularly
Maintain the blood glucose in the range 108-180
mg/dl
(Dhatariya et al., 2011)
Primary care
referral
Preoperative
assessment
Surgical
outpatient
Theatre and
recovery
Hospital
admission
Discharge
Post-operative
care
Ensure glycaemic control, fluid and electrolyte balance
are maintained
Optimize pain control
Encourage an early return to normal eating and drinking,
facilitating return to the usual diabetes regimen
(Dhatariya et al., 2011)
Primary care
referral
Preoperative
assessment
Surgical
outpatient
Theatre and
recovery
Hospital
admission
Discharge
Post-operative
care
Ensure early discharge
Ensure that factors likely to delay discharge are
identified at the pre-operative assessment
(Dhatariya et al., 2011)