COMPLICATIONS

OF DIABETES
Dr.Muhd Khairi Mohd Taibi
Pakar Perubatan Keluarga
Klinik Kesihatan Maran
 2 jenis komplikasi
DIABETES
ACUTE COMPLICATIONS

HYPOGLYCAEMIA

HYPERGLYCEMIA
• Diabetic ketoacidosis (DKA)
• Hyperosmolar non-ketotic syndrome
ACUTE EMERGENCIES OF
DIABETES MELLITUS

 1. Diabetes ketoacidosis (DKA)

 2. Hyperosmolar non-ketotic syndrome
 3. Hypoglycaemia

DEFINITION OF DKA
 Hyperglycaemia
 Hyperketonemia/ketonuria
 Acidosis
 Electrolyte imbalance
HYPERGLYCAEMIC EMERGENCIES

 DKA

3 - 8 episodes/1000 pts

20 - 30% new cases presenting in DKA.
 HONK

10% of DKA
 Mortality

DKA 5 - 10%

HONK 30 - 40%
Treatment Of DKA and NKH

- Fluid

- Electrolyte Abnormalities

- Hyperglycaemia

- Hypervolemia

- Metabolic acidosis

- Potassium and phosphate depletion.

Insulin


- Insulin lowers : PG 3.6-6.9 mmol/l/h

- Fluid repletion lower : PG 1.9-3.9 mmol/l/h

- Combination effect lower : PG 5.6-11.1 mmol/l/h

Insulin normalize ketone metabolism

Insulin Regimen

- Loading doss 15-20 unitS

- Continuous infusion
0.10 u/kg/h (DKA)
0.05u/kg/h (NKH)

Insulin infusion discontinued when PG<14 mmol/l

Fluid Replacement

- Fluid loss
3-6 l in DKA
8-10 L in NKH

- Fluid repletion is with isotonic Saline

- Rate of infusion dependant upon the clinical state

eg. : Shock- as fast as possible :-
not in Shock – 500ml/h for 1st hours
250 mls/hr for next 4 hours
CHRONIC COMPLICATIONS

1. MICROVASCULAR
 RETINOPATHY (EYE DISEASE)
 NEPHROPATHY (KIDNEY DISEASE)
 NEUROPATHY (NERVE DISEASE)

2. MACROVASCULAR
 CORONARY ARTERY DISEASE
 CEREBROVASCULAR
 PERIPHERAL VASCULAR DISEASE
 HOW DO YOU
MANAGE
THE COMPLICATIONS?
MANAGEMENT OF HYPOGLYCAEMIA
 Perform blood glucose strip immediately

Hypoglycemia JIKA RBS <

3.0mmol/L

Pesakit Tidak sedar

Pesakit sedar (mild) (Moderate to severe)

Beri refined karbohydrate secara oral Set IV ; infuse 10-

25mls of 50% Glucose
( Approx. 15gm glucose ) *
( Ulang 5 – 10 minutes jika tidak
berkesan)
Dikuti dengan complex carbohydrate
utuk mengelakkan berulang Ulang blood glucose
strip selepas 15 minute
dan beri 10% dextrose
Ulang blood glucose strip selepas 15 IV infusion*
minutes
Jika > 3.5 mmol ; observe 30 minutes
sebelum discharge
Nasihatkan pesakit tentang rawatan
sendiri hypoglycemia Admit /refer pesakit
(adjustment of dosage)

*Paramedics to manage with MO/FMS

 MANAGEMENT OF DKA

Confirmed Diagnosis dengan adanya

- hyperglycaemia
- ketonuria
*MA to refer MO

Set Ivuntuk mengantikan fluid yang secukupnya dengan IV 0.9% N/S

Pastikan :
- Nasogastric tube jika pesakit drowsy
- Bladder catheterization
- All vital signs including BP, PR, RR should be monitor every 15 minutes*

Arrange for urgent transportation for admission.*

Meanwhile may carry out as the” suggested DKA management “
 Suggested DKA management at Primary Care :*

Insulin :
IV 6 U stat then 6 U hourly by infusion.(0.1U/kg)

Fluid Replacement Regime (Total requirement 5-7 L)

IV 0.9% N/S : 1 litre over 30 minutes
1 litre next 1 hour
1 litre next 2 hours
1 litre next 4 hours
1 litre next 6 hours
Monitoring : If facility is available , biochemical monitoring ( BUSE,
RBS & ABG ) should be done hourly until patient’s blood glucose level
< 10mmol/l

* Paramedics to manage with MO/FMS

DIABETIC RETINOPATHY
Diabetic Retinopathy
 Major microvascular Complication of DM
 Strongly related with duration of DM
 Over 20% of patient by 5 yrs

By 20 yrs : all Type 1 DM and 80% of type 2
 Risk Factor
 Poor glycemic control
 Baseline retinopathy
 Proteinuria
 Hypertension
 Smoking
 Hyperlipidemia
PATHOGENESIS

 MICROVASCULAR OCCLUSION-causes retinal

ischaemia which causes retinal hypoxia
 NEOVASCULARISATION- caused by a
vasoformative substance occurs in an attempt to
revascularize the hypoxic retina-----on optic nerve
head, iris and retina.
 MICROVASCULAR LEAKAGE-increased
vascular permeability causes retinal oedema
Pathogenesis of diabetic retinopathy
Consequences of retinal ischaemia
Consequences of chronic leakage
 MANAGEMENT OF DIABETIC EYE
Diabetic Patient

Visual Acuity (VA)

Paramedic to do VA and refer
Funduscopy with Pupillary dilatation
A..Upon diagnosis for Type II and annually
B.After 5 years for Type I

Normal VA
Normal Fundus
Abnormal Fundus
Annual Check With or without affecting VA

Refer to CPG : Diabetic Please refer to Classification of Diabetic

Retinopathy 1996 ; Retinopathy for the characteristic
funduscopy findings
 Mild NPDR 9 monthly MO / FMS

Moderate NPDR 6 monthly FMS / MO

Severe NPDR / Refer

Proliferative / 2-4 monthly
Maculopathy Opthalmologist
 DIABETIC
NEPHROPATHY
Diabetic Nephropathy
 Commonest cause of End-Stage Renal Failure
 Microalbuminuria is earlierst evidence of
Nephropathy (30-300 mg/day)
 Risk Factor

Poor glycemic control

Duration of DM

Hypertension

Smoking

Male
 DM nephropathy almost always with retinopathy
RENAL REPLACEMENT PROGRAM-MALAYSIA
Primary Renal Disease 2000 – 2003

Year 2000 2001 2002 2003

New Dialysis Patient 1811 2036 2223 1992
% unknown cause 30 31 31 30
% diabetic nephropathy 45 46 50 51
% glomerulonephritis 9 7 6 5
% SLE 2 2 1 1
% polycystic kidney disease 1 2 1 1
% obstuctive nephropathy 3 4 3 3
% toxic nephropathy 0 1 0 0
% miscellaneous 9 8 7 8
 Course of Diabetic Nephropathy

Time (yrs) 0 5 20 30

Onset of Onset of End Stage

Diabetes Proteinuria Renal
PRECLINICAL Disease
INCIPIENT NEPHROPATHY OVERT NEPHROPATHY
NEPHROPATHY Hyperfiltration,
microalbuminuria, Rising S Cret,
rising blood pressure Decreasing GFR

Hypertension
STRUCTURAL CHANGES
(Increasing glomerular basement
membrane
thickening and mesangial expansion)

Adapted from Breyer JA et al. Am J Kid Dis 1992; 20(6): 535.

 CLASSIFICATION OF DIABETIC
NEPHROPATHY

Stage Glomerular filtration AlbuminExcretion Serum Creatinine

rate
Early Increased Normal Normal

Microalbuminuria Normal Increased Normal

Macroalbuminuria Decreased Increased Normal

Renal Impairment Decreased Increased Increased

End stage Renal Decreased Increased Greatly Increased

Failure
Protocol for microalbuminuria screening
 Type 1 : start at 5 yrs  Before screening ensure
after diagnosis then patient NOT:
heavy physical exercise
annually for those



UTI
above 12 yrs DM 
ketoacidosis
 Type 2: At diagnosis 
Febrile illness
then annually 
CCF
 If patient already 
uncontrolled DM (>15
mmol/l)
diagnosed as RF or 
uncontrolled HPT
obvious proteinuria (BP>180/110)
not need screening 
NSAIDS (3 days B4)
 MANAGEMENT OF PROTEINURIA AND
NEPHROPATHY
Urine Protein(Dipstick)

POSITIVE
Negative On 2 separate occassions (exclude
other causes e.g UTI, CCF
Test for microalbuminuria
POSITIVE
( 30-300mg/l )

Paramedics to refer
MO/FMS
NEGATIVE

Repeat urine
microalbumin yearly Refer FMS with a
Emphasize on *** 24-hr urine protein result.
Renal profile and BUSE.
 MANAGEMENT OF PROTEINURIA

Start ACE inhibitor. Monitor progress by serum creatinine

and BUSE after !/52

If Serum Creatinine
If renal function
> 300mg/L or
not
deteriorating

Continue treatment
Repeat Sr Creatinine and BUSE 6/12ly Refer Nephrologist to prepare patient for
Emphasize on *** further management .
Meticulous control of hypertension Treatment option includes dialysis ,
Meticulous blood glucose control transplantation
Early detection and treatment of UTIs
Avoidance of nephroptoxic agents
Moderate protein restriction 0.8g/kg body
weight )
DIABETIC
NEUROPATHY
Classification of diabetic
neuropathies
 Acute

Hyperglycemic neuropathy
 Persistent

Symmetrical
• Distal symmetrical neuropathies
• Acute painful neuropathy

Focal and Multifocal
• Pressure palsies-
• Mononeuropaties (Diabetic amyotrophy)
Symmetrical Distal symmetrical neuropathies
Acute painful neuropathy
Pressure palsies
Mononeuropaties (Diabetic amyotrophy)
Autonomic Diabetic neuropathies
 MANAGEMENT OF DIABETIC NEUROPATHY
Perform Neurological Assessment and
Examination

A. Upon diagnosis and annually

B. Once patient has symptoms

Special problem :
Assessment Procedures :
SEXUAL DYSFUNCTION
Very common problem but
Neurological assessment of lower limbs :
requires direct questioning ,
-Touch and pin prick sensation
as rarely spontaneously
-Vibration sense ( 128 Tuning fork ) discussed by patient
-Position sense
-Ankle jerk ( reduced or lost )
-Evidence of small muscle wasting and drop Screening / Confirmed
foot using International Index
-Others – warm skin, bounding pulse of Erectile Function-5
( IIEF – 5 )
(Refer App 2)

Cardiovascular Disease
Treatment options includes Screening
-Strict diabetic control Evaluate CV Fitness
-Symptomatic treatment for pain and
paresthesia
-Foot Care and Self inspection
-Neurotropic agents
Refer Urology for further ED
evaluation
 Screening:
International Index of
Erectile Function-5 (IIEF-5)

1. How do you rate your confidence that you could get and keep an
erection?
( 1 = very low; 2 = low; 3 = moderate; 4 = high; 5 = very high )
2. When you had erections with sexual stimulation, how often were your
erections hard enough for penetration?
( 0 = no sexual activity; 1 = almost never/never;
2 = a few times; 3 = sometimes; 4 = most times; 5 = almost always/always )
3. During sexual intercourse, how often were you able to maintain your
erection after you had penetrated your partner?
( 0 = did not attempt intercourse; 1 = almost never/never; 2 = a few times; 3 =
sometimes; 4 = most times; 5 = almost always/always )
4. During sexual intercourse, how difficult was it to maintain
your erection to completion of intercourse?
(0 = did not attempt intercourse; 1 = extremely difficult;
2 = very difficult; 3 = difficult; 4 = slightly difficult; 5 = not
difficult)
5. When you attempted sexual intercourse, how often was it
satisfactory for you?
(0 = did not attempt intercourse; 1 = almost never/never;
2 = a few times; 3 = sometimes; 4 = most times; 5 = almost
always/always)
Score of 21 or less suggest presence of ED
Mild ED = 13 - 21 score
Moderate ED = 9 - 12
Severe ED = 8 or less
 DIABETIC FOOT
CAUSES OF FOOT ULCER:
 PERIPHERAL NERVE PROBLEM
(NEUROPATHY) WITH LOSS OF PAIN
SENSATION
 PERIPHERAL VASCULAR DISEASE (PVD)

PVD also causes neuropathic ulceration by impairing

healing. Neuropathic ulcers occur at sites of increased
pressure, usually on plantar surface of the foot. Callus
develops as a result of the pressure.
The Diabetic foot
 Foot Ulcer
 Gangrene
 Charcot arthropathy
 Neuropathic oedema
MANAGEMENT OF DIABETIC FOOT
Screening
History – symptoms of peripheral neuropathy
injury or ulceration to feet

Examination of the foot 6/12 ly or at

least yearly ;

As in the “ Foot Care Module

Paramedics to refer MO/FMS

Treatment Options :
-Strict Control of Diabetes
-Treatment for neuropathy as in “ Step in managing
Neuropathy “
-Specific and intensive foot care depending on severity .

Self Care to be emphasized

MACROVASCULAR DISEASES
 TYPE II DIABETES :
AT LEAST A TWO-FOLD INCREASE IN THE
RISK OF DEVELOPING MACROVASCULAR
DISEASES
(WOMEN ARE NOT PROTECTED FROM THIS)

 MINOR DIFFERENCES EXISTED AMONGST

ETHNIC GROUPS AS TO WHICH OF THE
VASCULAR TERRITORY IS MORE AFFECTED.
 MANAGEMENT OF MACROVASCULAR
DISEASE IN PRIMARY CARE
Upon diagnosis and annually,perform
Cardiovascular Assessment
as below
History :
Determine the presence of angina, neurological
symptoms, claudication and past episodes of
vascular events.

Determine other risk factors for CVD involved

Examination :
Measure blood pressure
Listen for carotid bruits, palpate the peripheral
pulses.
Investigation:
Do Cardiovascular Disease Screening.
Do ECG and Chest X-Ray
Do Stress ECG , Echocardiograms and
Doppler Study when indicated
MANAGEMENT OF MACROVASCULAR

Treatment Options :
Strict Control of blood Sugar
Diet
Exercise Cdepending on cardiac status)
Control of modifying risk factors
-Stop smoking
-Blood Pressure ( refer CPG ; M’sia Hypertension
Consensus Guidelines 1998 )
-Dyslipidaemia ( refer CPG “ Consensus Statement
on Management of Hyperlipidaemia )

Aspirin and other antiplatelet agents upon diagnosis

The End