Diabetes

Mellitus

Dr T P Yeow
 You should be able to discuss..
Epidemiology, Pathophysiology & classica5on
Overview of normal glucose metabolism and what goes wrong in diabetes
Screening and diagnosis- who, how, cut o
Approach to management
Non- phamacologial & Pharmacological anBglycaemic agents
non diabetes medicaBons -eg Aspirin, ACE inh, staBn
Monitoring and treatment target for Glycemic control, lipid level and blood
pressure
Management of complica5ons
Diabe5c emergencies:
Hypoglycemia, Diabetes ketoacidosis (DKA) and hyperosmolar Hyperglycemic
state (HHS)
For DKA and HHS-Principles of acute management in relaBon to Fluids,
Electrolytes and Insulin
Care of diabetes paBents having surgery
GestaBonal Diabets Mellitus (O&G)
 Ministry of Health
Malaysia

Diabetes Epidemic in
Malaysia
Feisul Idzwan Mustapha MBBS, MPH, AM(M)
Public Health Specialist
Disease Control Division, MOH

MYSIR 2013
Prince Hotel, Kuala Lumpur
27 September 2013

dr.feisul@moh.gov.my

 Prevalence of Diabetes, 18 years (2006 &
16
2011)
15.2
14

11.6
12

10
Total diabetes
Prevalence (%)

8.0
8 Known
Undiagnosed
6 7.0 7.2
4.5 IFG

4 4.9
4.2
2

NHMS III (2006) NHMS 2011

4
 Prevalence of Diabetes, 30 years (1996,
2006 & 2011)
25

20.8
20

14.9
15
Total diabetes
Prevalence (%)

Known
10.7
9.5 Undiagnosed
10
8.3 10.1
IFG
6.5
5.4 5.3
5
4.3

1.8 4.7

NHMS II (1996) NHMS III (2006) NHMS 2011

5
 Prevalence of Diabetes, 18 years,
by age groups (1996, 2006 & 2011)
40.0
36.2 36.6

35.0
31.6
30.3
30.0
26.7 26.1
24.4 24.5
25.0 22.8
Prevalence (%)

20.6 20.8

20.0 17.6 18.2 NHMS II (1996)

16.1
15.0 15.3
15.0 13.1
NHMS III (2006)

9.4
10.9 10.3 9.8
10.7 NHMS 2011
10.0
6.4 6.4
4.9 5.3 4.9
4.1
5.0 2.1 3.1 2.9
2.0

0.0 2.0

Age groups
6
 Prevalence of Diabetes, 18 years,
by States (2011)
30.0
Total
24.8
25.0
22.5
Known
22.0
19.7 Undiagnosed
20.0
17.1 16.7 IFG
Prevalence (%)

16.2 16.5
15.0
15.0 13.4
12.3
11.6 11.3

10.0 9.0 8.8

5.0

0.0

7
 Usual Place of Treatment (2011)
60
56.0

50

40
Percentage

30
24.6

20
15.0

10

2.5 1.6 0.2

0

8
High blood sugars in adults, ASEAN
region, 2010

9
Obesity in adults, ASEAN region, 2010
18.0

16.0

14.0

12.0
Prevalence %

10.0

8.0 Male
6.0 Female

4.0

2.0

0.0

10
DIABETES MELLITUS-THE DISEASE

New CPG for 2015 being
developed do look out
for new version!
 Pathophysiology of Type 2 Diabetes
3. Increase Glucagon
From Pancrease

CHO
Glucagon 2. Defec5ve -cell
Secre5on
Insulin
Glucose
Glucose
Pancreas
Excessive Glucose
Liver ProducBon

1. Decreased
Glucose Uptake
FFA (Insulin Resistance)
Adipocytes
Muscle
(Fat)

FFA competes
with glucose FFA Excessive
uptake TNF Lipolysis

Adapted: Diarmurd Smith, RCSI

 Pathophysiology of T2DM
Glucose inux > glucose oudlow from plasma
compartment
Increase hepaBc gluconeogenesis (HG) at fasBng
Impaired suppression of HG post prandial
Impaired peripheral glucose disposal post prandial
Progressive impairment of insulin kineBcs
PancreaBc alpha cell hypersecreBon of glucogon
Abnormality in increBn system ( GLP-1 & GIP)
Increased delivery of faey acids to the liver favours their
oxidaBonincreased gluconeogenesis
Hyperlipidaemia promotes hepatosteatosis
1 2
 Clinical dien5a5on of DM
T1DM T2DM
DKA DKA NO DKA
(Can also present DKA)
Family In view of high background Strong family history of T2DM
history of T2 prevalence of T2DM- many
DM T1DM (many malaysian) has
family hx of T2DM)

Overweight/ Lean Obese

Obese (T1DM can also be obese - (Can be lean)
high naBonal prevalence of
obesity)
C-PepBde/ low Measurable/ high (if Insulin resistance)
Insulin (In acute glucotoxicity C pepBde/insulin
can be low therefore best to measure only
ager resoluBon of glucose toxicity)
AnBbodies GAD anBbody + NegaBve

 Type 1 DM
Type 2 DM
GestaBonal DM
GeneBc
Beta cell dysfuncBon-MODY
Insulin resistance- lipoatrophic DM
PancreaBc Exocrine dysfuncBon
Secondary Diabetes
Acromegaly/ Cushing s
Drug induced
Steroid
Rare immune mediated- eg sB man syndrome
Syndrome assoc with DM

SCREENING AND DIAGNOSIS
 Who should be screened?
Symtoma5c: asymptoma5c individuals
Any individual all adults who are overweight or obese and have one or
more addiBonal risk factors for diabetes:
who has First-degree relaBve with diabetes
symptoms History of cardiovascular disease Hypertension
suggesBve of glucose
Impaired glucose tolerance (IGT) or impaired fasBng
(IFG) on previous tesBng
diabetes High density lipoprotein (HDL) cholesterol <0.9 mmol/L or
triglycerides (TG) >2.8 mmol/L
Physical inacBvity
Other clinical condiBons associated with insulin resistance
(e.g. severe obesity and acanthosis nigricans
Women who delivered a baby weighing >4 kg or
were diagnosed with gestaBonal diabetes mellitus (GDM)
Women with polycysBc ovarian syndrome

 Screening tests & Diagnositc tests
Screening can be done by measuring either
venous or capillary blood using glucometer
Diagnos5c tests that can be performed are
A1c
oral glucose tolerance test (OGTT)
fasBng blood glucose
random blood glucose
 DiagnosBc Value for OGTT- IDF 2005
Category 0 min Glucose (mmol/L) 120min Glucose (mmol/L)
Normal < 6.1 ( < 5.6 ADA) <7.8
Impaired FasBng Glucose 6.1-6.9 -
Impaired Glucose - 7.8-11.1
Tolerance
Diabetes Mellitus 7.0 11.1

Asymptoma5c pa5ent- 2 abnormal readings

Symptoma5c pa5ent- 1 abnormal reading
Screening for T2DM in Symptomatic Individual
Screening for T2DM in Asymptomatic Individual
Recent new development in the use of
HbA1c

A1c is no longer reported as %

A1c can be used to screen and diagnose
diabetes
 NEW: global A1c reference system
In 1994, the InternaBonal FederaBon of Clinical
Chemistry and Laboratory Medicine (IFCC) Working
Group on StandardisaBon of A1c developed a global
A1c reference system with an improved intra- assay
and inter-assay coecients of variaBon

A1c are NO LONGER reported in % alone- it is now
reported in
IFCC-A1c values in SI units (mmol A1c/mol Hb) &
NaBonal Glycohaemoglobin StandardizaBon
Program (NGSP-A1c) units (%)
 Using A1c as a Screening Tool to Diagnose Diabetes
Pros (compared to OGTT): Cons:
1. more convenient Rarer haemoglobinopathies
2. Result more reproducible (e.g. homozygous sickle cell)
Stable during transportaBon and complex thalassaemia
(cf glucose sample handling may interfere with A1c
inuences glycolysis) Cost- net cost of A1c is ~13x
Low day-to-day variability higher than glucose
3. therapeuBc decisions are Cut o dier between
based on A1c value ethniciBes selecBon of
anyway, regardless of the threshold and adjustment
ndings on the OGTT by countries maybe
required
 What A1c is level is diagnosBc of DM?
ADA advocate A1c of >6.5% as diagnosBc for DMin
Malaysian populaBon, based on the MSSM data
1. A1c of 6.3% (45mmol/mol) has a specicity of 97%
in diagnosing diabetes (based on Malaysian MSSM
data)
2. A1c has low sensiBvity above 5.6% (38 mmol/mol)
therefore individuals with A1c between 5.6%
and 6.2% are recommended to undergo an OGTT

Ref :Prevalence of diabetes in Malaysia W. M. Wan Nazaimoon

et al. Diabet. Med 30, 825 (2013)
APPROACH TO MANAGEMENT
 History in a new case of Diabetes

Specic Polyuria, polydipsia, polyphagia, weight loss, nocturia, malaise,

symptoms faBgue, altered vision and frequent infecBons.

Risk factors that Age over 30 years, family history, ethnic group, overweight,
pre-dispose to physical inacBvity, hypertension, obstetric history of large
diabetes babies or gestaBonal diabetes, medicaBons causing
hyperglycaemia

Risk factors for Personal or family history of CVD, smoking, hypertension,

complicaBons dyslipidaemia and ESRD.
Already Cardiovascular symptoms, neurological symptoms, foot and toe
developed problems, recurrent infecBons (especially urinary and skin),
complicaBons bladder and sexual dysfuncBon
Lifestyle Smoking, alcohol, occupaBon, dietary habits and physical
acBvity

Treatment target for T2DM
 A1c Target should be individualized

A1c should be near to normal especially in young /newly
diagnosed paBents, and those who have yet to develop
diabetes complicaBons
PrevenBon (from complicaBons) is beeer than cure
Harm of severe hypoglycaemia may outweigh benets of
strict control in some paBents> less stringent A1c target
should be applied to this high risk groups. For example
PaBents with co-morbidiBes may be more at risk from hypoglyaemia
PaBents with short life expectancy
ANTI-HYPERGLYCAEMIC AGENTS-
ORAL/ INEJECTABLES/INSULIN
 Pharmacologic IntervenBon in T2DM
Decreased
CHO AbsorpBon

Increase Insulin SecreBon

Acarbose CHO
Sulfonylureas/ Meglitinides

Glucose Insulin

Suppress HepaBc Pancreas

Metformin Glucose ProducBon

Adipocytes
Muscle (Fat)
Enhanced Glucose
Uptake

Thiazolidinediones

Reduce Lypolysis Weight Loss

(FFA, TNF)
Agents
 Pharmacologic IntervenBon with increBn hormone
Suppress appe5te

Slows down Increase Insulin Secre5on

CHO
absorp5on

Glucose Insulin

Suppress Liver Pancreas

Decreased Glucose ProducBon
Glucagon

Adipocytes
Muscle (Fat)
increase Glucose
Uptake into cells

Weight Loss
(with GLP-1)
 Commonly used in Klink Kesihatan
(must know)
Class Mechanism Advantages Disadvantages Cost
Biguanides AcBvates AMP- Extensive GastrointesBnal Low
kinase experience LacBc acidosis
HepaBc No hypoglycemia B-12 deciency
glucose Weight neutral contraindicated in
producBon ? CVD renal and heart failure
SUs / Closes KATP Extensive experience Hypoglycemia Low
Megli5nides channels Microvasc. risk Weight gain
Insulin Low durability
secreBon ? Ischemic
precondiBoning
Insulin AcBvates insulin Universally eecBve Hypoglycemia Varia
receptor Unlimited ecacy Weight gain ble
peripheral Microvascular risk ? Mitogenicity
glucose uptake Injectable
Training requirements
SBgma
 More commonly used as second line/ rarely available in KK-1
(nice to know)
Class Mechanism Advantages Disadvantages Cost
TZDs PPAR- acBvator No hypoglycemia Weight gain High
insulin sensiBvity Durability Edema / heart
TGs, HDL-C failure
? CVD (pio) Bone fractures
? Possible
heightened risk of MI
associated with
rosiglitazone
? Possible risk of
Bladder cancer assoc
with pioglitazone

-GIs Inhibits - No hypoglycemia GastrointesBnal Mod.
glucosidase Nonsystemic Dosing frequency
Slows carbohydrate Post-prandial Modest A1c
absorpBon glucose
? CVD events
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of
print]

 More commonly used as second/ rarely available in KK-2
(nice to know)
Class Mechanism Advantages Disadvantages Cost
DPP-4 Inhibits DPP-4 No hypoglycemia Modest A1c High
inhibitors Increases GLP-1, GIP Well tolerated ? PancreaBBs
UrBcaria
GLP-1 AcBvates GLP-1 R Weight loss GI High
receptor Insulin, glucagon No hypoglycemia ? PancreaBBs
agonists gastric emptying ? Beta cell mass Medullary ca
saBety ? CV protecBon Injectable
SGLT2 selecBvely inhibits weight and Side eects include high
SGLT2, a transporter modest blood signicant increased of
in the proximal tubule, pressure reducBon genitalia and urinary
thus reducing glucose low risk of tract infecBon
reabsorpBon hypoglycaemia Contraindicated in
concomitant treatment
with loop diureBc
Contraindicated in renal
impairment eGFR <60
mL/min/1.73 m2
 Rarely used (nice to know)

Class Mechanism Advantages Disadvantages Cost

Amylin AcBvates amylin Weight loss GI High
mime5cs receptor PPG Modest A1c
glucagon Injectable
gastric emptying Hypo w/ insulin
saBety Dosing frequency
Bile acid Bind bile acids No hypoglycemia GI High
sequestrants HepaBc glucose Nonsystemic Modest A1c
producBon Post-prandial Dosing frequency
glucose
CVD events
Dopamine-2 AcBvates DA receptor No hypoglyemia Modest A1c High
agonists Modulates ? CVD events Dizziness/syncope
hypothalamic control Nausea
of metabolism FaBgue
insulin sensiBvity
General Guidelines for Use of Oral An5-diabe5c
Agents (OAD)
or in combinaBon with
OAD can be used as monotherapy
other OAD(s), and/or injectable agents (e.g insulin, GLP-1
receptor agonist)
As rst line therapy, medormin is the preferred choice. Other
OAD agents are acceptable alternaBves.
If glycaemic targets are not achieved, intensicaBon of
treatment should be made
If monotherapy fails, combinaBon of other agents is
recommended.
When indicated, start with a minimal dose of OAD agent,
while re-emphasising diet and physical acBvity.
Standard Approach to the Management of T2DM:
Treatment Intensification

g es
a n Insulin
C h
t yle
ifes Oral + Insulin + +
L

Oral Combination +

Diet, Exercise, Oral Monotherapy

Adapted from Riddle MC. Endocrinol Metab Clin North Am. 2005; 34: 7798.
34
 Physiological Paeern of Insulin requirement

MealBme insulin excursions.

50 Rapid rise; short duraBon

40
Serum insulin (mU/l)

30

20
Flat basal insulin prole

10

0
0800 1200 1600 2000 2400 0400 0800
Breakfast Lunch Dinner

Y Kruszynska, et al. Diabetologia 1987;30:16.

 Insulin

Short acBng Long acBng

Human Analogue Human Analogue

Novorapid/ Insulatard/
Actrapid/ Lantus/
Humalog Humilin N
Humilin R Levemir

Insulin type Onset of ac5on Time to peak Dura5on of
eect ac5on

short ac5ng
Regular About 30 min 2 to 4 h 5 to 8 h
Lispro, aspart 5 to 15 min 45 to 75 min 2 to 4 h

long ac5ng
NPH About 2 h 6 to 10 h 18 to 28 h
Insulin glargine About 2 h No peak 20 to >24 h
Insulin detemir About 2 h No peak 6 to 24 h
INSULIN Add Basal Insulin
REGIMES
(progressive beta cells dysfunction in T2DM)

Break Lunch dinner

OHA
INSULIN
REGIMES Add Mixtures of
short and intermediate-
ac5ng insulin- bd

break lunch dinner bedBme

INSULIN
REGIMES 4 InjecBon a day Basal Bolus
-more suited for T1DM

b/f lunch dinner bedBme (BASAL)

Bolus bolus bolus
Lipoatrophy
Lipohypertrophy
ConBneous Glucose Monitoring System
MANAGEMENT OF CO-
MORBIDITIES AND
COMPLICATIONS
 Diabetes and
Co-morbidiBes complicaBons
Co-morbidiBes- e,g, Hypertension,
Hyperlipidaemia
ComplicaBons Micro and Macro-vascular
(Dont forget sexual dysfuncBon)
How and when to screen?
primary and secondary prevenBon?
when to refer
 Hypertension and Diabetes
Common
Start phamacotherapy if BP persistently
>140/90 mmHg opBmal treatment reduces
cardiovascular and nephropathy risk
ACE-inhibitor is rst choice (based on
extensive evidence)
ACEi and ARB are contraindicated in pregnancy
MulBple drugs ogen needed
 Hyperlipidaemia and Diabetes
Screening should be done annually (minimum)
All paBents above age of 40 should be treated
with a staBn regardless of cholesterol (level 1
evidence) target LDL <2.6mmol/L
All paBents with overt CVD should be treated
with a staBn-target LDL <1.8 mmol/L
StaBn is contraindicated in pregnancy
 ComplicaBon 1- ReBnopathy
IniBal assessment should be conducted at rst
review and annually thereager
How:
Visual acuity with Snellen chart (refracBve error corrected
with pinhole, and if paBent wear glasses for bifocal or
presbyopia this must be worn during test)
Fundus camera (increasingly available in all KKs)
Opthalmoscope (if no fundus camera)
Treatment- risk factor modicaBons
Referral- know indicaBon for urgent referral (opth)
 ComplicaBon 2- Nephropathy
Normal creaBnine DOES NOT RULE OUT nephropathy
Standard urine dipsBck for proteinuria should be done in all
paBents annually
NegaBve protein on dipsBck DOES NOT RULE OUT
nephropathy
If dipsBck negaBve for protein check for urine microalbumin
If microalbuminuria is posiBve conrm with repeat test in 3-6
months
If microalbuminuria is negaBverepeat test annually
Proteinuria predicts nephropathy. NormalizaBon of
microalbuminuria retard deterioraBon of GFR
ACE I or ARBs should be iniBated in paBents with
microalbumin or proteinuria as it has been shown to reduce
proteinuria and reverse microalbuminuria
 ComplicaBon 3- neuropathy
Know how to examine for neuropathy
Tight glycamic slows progression
No pharmacological therapy has been shown
to completely eecBve in treaBng painful
peripheral neuropathy
Tricyclic anBdepressant (Amitriptyline),
AnBconvulsant (eg gabapenBve), pregabaline,
duloxeBne, opiods etc have been used with
variable eect
 ComplicaBon 4- coronary artery
disease
Massive topic in itself- management similar to
coronary artery disease in general
Aspirin
Strong evidence that aspirin is eecBve for
secondary prevenBon of CVD
Unclear if aspirin is eecBve for primary
prevenBon generally aspirin NOT advised for
primary prevenBon (unless for paBents >65 year
old where background risk for CVD rises)
 ComplicaBon 5- diabeBc foot
Foot care- by paBents/carer
Annual feet examinaBon by HCPs
What is involved in feet examinaBon?
Ogen result from a combinaBon of ischemia
(Peripheral vascular disease), painless
neuropathy and poor wound healing
 ComplicaBon 6- others
Sexual dysfuncBon
Diabetes and mental health
DIABETES EMERGENCIES
Hypoglycaemia-dierent severity warrants
dierent management

Neuroglycopaenic
symptoms usually
starts from glucose
3 mmol/L


Hypoglycaemia
unawareness is
DANGEROUS

*Adapted from Kedia N. 2011;4:337-346.

Acute Hypoglycaemia-mild to moderate

15 grams of
simple
carbohydrate=
=1 table spoon
of honey
=34 cup of juice
=3 tea spoon of
table sugar
 Severe Hypoglycaemia (unconscious pa5ent)
Glucagon IM (NOT available in Malaysia)
25-50ml 50% Dextrose iv over 1-3 minutes

Diagnosis of hypoglycaemia is INCOMPLETE without
establishing a cause
Why? So that measures can be put in place to avoid
repeat incident
Missed meal/exercise? reeducate
In appropriate OHA/ Insulin change treatment regime
Liver/renal failure?
Sepsis?
 Diabetes Ketoacidosis (DKA)
A consequence of absolute or relaBve insulin deciency,
usually accompanied by an increase in counter-regulatory
hormones such as glucagon, corBsol and epinephrine. This
hormonal imbalance leads to hepaBc gluconeogenesis and
glycogenolysis, resulBng in severe hyperglycaemia. Enhanced
lipolysis increases serum free faey acids with producBon of
large quanBBes of ketone bodies (acetone, acetoacetate and
3-beta-hydroxybutyrate) and consequent metabolic acidosis.
The osmoBc diuresis induced by hyperglycaemia combined
with ketone-induced nausea and vomiBng leads to severe
uid depleBon and life-threatening electrolyte imbalance.

Reference: hep://www.diabetologists-abcd.org.uk/
JBDS_DKA_Management.pdf
 DiagnoBc criteria for Diabetes
Ketoacidosis
All three must be met:
1. Capillary blood glucose >11 mmol/L (or
known DM)
2. Capillary ketones >3 mmol/L or urine ketones
2+
3. Venous pH <7.3 and/or bicarbonate < 15
mmol/L
 Management of DKA
FLUIDS
INSULIN
POTASSIUM
MONITOR
Principle of DKA management
FLUIDSThe main aims for uid replacement are to restore
circulatory volume and clear ketones

How much uids and how fast?
Give rst pint 0.9% NaCl over 15minsif SBP
<90mmhgrepeat 1 more pint
Subsequent uids over 1-2-4 hourly
> 6L / 24 hour may be needed
monitor use CVP line if in doubt
Replace ongoing urinary loss
Prevent over hydraBon especially in elderly or renal and
cardiac impaired
Isnt it counter-intui5ve to give Dextrose infusion in DKA?
5% dextrose when glucose< 14mmol/L to allow introducBon
of more insulin to suppress lipolysis and ketogenesis
Insulin infusion

0.1U/kg/hour infusion

Monitor:
ReducBon of blood ketones concentraBon
Rise of venous bicarbonate (by 3mmol/L per hour)
Fall of blood glucose (by 3mmol/L per hour)

If these targets are not achieved, the rate of the
insulin infusion should be increased
 Potassium
ECF
ICF

INSULIN
Beta Agonist

Rapid reduc5on of K with insulin treatment (withold insulin infusion

temporarily if baseline K is <3.5 mmol/L)

Replacement usually required with 2nd litre of uid
with 40mmol KCL if K <3 mmol/L
With 30mmol KCL over 2 hours if K 3-4 mmol/L
With 20mmol KCL over 1 hour if K 4-5 mmol/L
Withhold replacement if K >5 mmol/L
Bicarbonate

Usually unnecessary
Insulin promotes ketoanion metabolismBicarbonate
generated acidosis corrected
There is limited evidence that Bicarbonate is beneBal
in DKA
there is no study on paBents with PH <6.9

POTENTIAL HARM
HCO3+ H+carbonic acid H2O+ CO2
CO2 enters cellsgenerate H+ intracellularly
Worsened intracellular acidosis
Paradoxical CNS acidosis
Volume expansion
Hypernatraemia
Overshoot alkalemia

 Consider Sodium Bicarbonate if
pH remain <6.9 despite insulin and
hydraBon
Renal impairment
Cardiovascular disease suscepBble to
arrhythmia secondary to acidosis
Precipita5ng factors- NO diagnosis of DKA is
complete without determining the precipita5ng
factor (same logic as Hypoglycaemia)

Western series
Infection Commonest-30-50%
(MSU/ Blood culture/ CXR)
Newly diagnosed >10%

Poor compliance Social Deprivation

Younger
Eating disorders
Unknown 30-40%
Monitoring

Fluid balance
uid chart
Beware of uid overload in elderly
Urinary catheter not always needed
Beware of Hypokalaemia- maintain K >3.5
Blood pressure- CVP if
Poor LV funcBon
Renal impairment
OxygenaBon
Increasing hypoxia ?ARDS
Mental state
Increasing confusion despite treatment ?cerebral
oedema
NG tube if impaired consciousness

 Hyperglycemic Hyperosmolar State(HHS)
Similar to DKA but progresses on over many days.
the dehydraBon and metabolic disturbances are more extreme
PaBent may be ketoBc, but lesser degree than DKA because
the residual insulin minimizes ketosis but does not control
hyperglycemia
vascular complicaBons such as myocardial infarcBon, stroke
or peripheral arterial thrombosis are common
It has a higher mortality (50%) than DKA
ICU admission and careful monitoring needed

Diagnos5c criteria
Hypovolaemia
Glucose >30 mmol/L
Serum Osmolarity > 320mmol/L
Serum osmolarity= 2x (Na and K) + glucose +Urea

 Management of DM pa5ent in hospital

A1c- Inaccurate in paBents who had recent bleeding/

haemolyzing/ transfusion
Change of diabetes medicaBon in hospitalized
paBents
Sulphonylurea- risk of hypos if fasBng
Medormin-hold for 24 hours if due surgery/ contrast
C/I- sepsis/ CCF/ RF- risk of lacBc acidosis
TZD- Contraindicated in CCF or liver failure
DPP4 inh- dose reduce in renal failure