Diabetes Mellitus

The Disease and Its Management

Dr. PANDJI MOELJONO, Sp.PD,KEMD,FINASIM

SUBDEP PENYAKIT DALAM
RUMKITAL Dr. RAMELAN
DIABETES: A GROWING EPIDEMIC
Definisi
Diabetes mellitus is a group of metabolic
diseases characterized by hyperglycemia
resulting from defects in insulin secretion,
insulin action, or both
(Expert Committee on the Diagnosis and Classification of Diabetes mellitus 2002)

Long-term damage, dysfunction, and failure

of various organs especially the eyes, kidneys,
nerves, heart, and blood vessels
 The Pathophysiology of Type 2 Diabetes
Includes Three Main Defects
Islet
Insulin deficiency

Pancreas Alpha cell

produces Beta cell
excess produces
glucagon less insulin
Excess Diminished
glucagon insulin

Diminished
insulin
Hyperglycemia Muscle and fat
Liver

Excess glucose output Insulin resistance

(decreased glucose uptake)
Adapted from Buse JB et al. In Williams Textbook of Endocrinology. 10th ed. Philadelphia, Saunders, 2003:14271483; Buchanan TA Clin
Ther 2003;25(suppl B):B32B46; Powers AC. In: Harrisons Principles of Internal Medicine. 16th ed. New York: McGraw-Hill, 2005:21522180;
Rhodes CJ Science 2005;307:380384.
5
 Kelainan Fungsi /
Jumlah Sel Genetik

Tipe I (Autoimun)
Faktor Lingkungan
Virus
Sistim imun INSUFISIENSI Diet
(Ab anti pankreas) INSULIN Obesitas
Hamil

Marker :
Insulin auto Ab Kelainan Aktifitas Insulin
Islet cell auto Ab o.k. Reseptor
Glutamic acid
dicarbosaflase
Au Ab (GAD. Abs)

Ideopatik
Symptoms :
Polyuria
Polydipsia
Weight loss
Sometimes polyphagia
Blurred vision
Diagnosis
Symptoms of diabetes plus glucose > 200 mg/dl

or

Fasting plasma glucose > 126 mg/dl

or

2-h plasma glucose > 200 mg/dl during an OGTT

 Current criteria for the diagnosis of diabetes (2010)
A1C 6.5%: The test should be performed in a laboratory using a
method that is National Glycohemoglobin Standardization Program
(NGSP) certified and standardized to the Diabetes Control and
Complications Trial (DCCT) assay.
FPG 126 mg/dl (7.0 mmol/l): Fasting is defined as no caloric intake for
at least 8 h.
2-h plasma glucose 200 mg/dl (11.1 mmol/l) during an oral glucose
tolerance test (OGTT): The test should be performed as described by
the World Health Organization using a glucose load containing the
equivalent of 75 g anhydrous glucose dissolved in water.
In a patient with classic symptoms of hyperglycemia or hyperglycemic
crisis: a random plasma glucose 200 mg/dl (11.1 mmol/l)
The glycemic targets for GDM should be at the
following levels :
1. Fasting Plasma Glucose (FPG) 105 mg/dl.
2. 1-h Postprandial Plasma Glucose (1-h PP) < 155
mg/dl.
3. 2-h Postprandial Plasma Glucose (2-h PP) < 130
mg/dl.
 DIABETES vs PRE-DIABETES

Fasting 2 hours post

Blood prandial (mg/dl)
Glucose
Normal < 100 * < 140
Pre-Diabetes 100 * 125 140 199
Diabetes 126 200

If FBG is > 100, have a 10-15% chance of

developing DM in next 7 years.
UKPDS :
Progressive Deterioration of -Cell Function
100

75 Th/Expectation
Beta Cell Function (%)

Post-
50 prandial
Hypergly- Facts
cemia
IFG T2 DM T2DM phase III
25 IGT phase I T2DM
phase II

0
-12 10 -6 -2 0 2 6 10 14
Years from Diagnosis
Modified from Lebovitz H. Diabetes Review 1999;7:139-53
Fig. 1. Proposed sequence of the key pathological features of type 2 diabetes as
discussed in this review.

Mark N. Feinglos, md, cm

M. Angelyn Bethel, md
 Natural History of Type 2 Diabetes
Years from -10 -5 0 5 10 15
diagnosis
Onset Diagnosis

Insulin resistance
Insulin secretion

Impaired Fasting Metabolic Syndrome

Glucose

Post-Meal glucose
Microvascular complications
Fasting glucose
Cardiovascular Complications
Pre-diabetes Type 2 diabetes

Ramlo-Halsted BA, Edelman SV. Prim Care. 1999;26:771-789 14

Nathan DM. N Engl J Med. 2002;347:1342-1349
 Penyakit Akibat Pola Hidup Tidak Sehat : Sindroma Metabolik = SIMET 5
(Pengalaman Klinik : Tjokroprawiro 2005-2007)

STAGE 0 STAGE 1 STAGE 2 STAGE 3 STAGE 4

Pola Hidup Tidak Sehat Obesitas Preklinikal Klinikal
Pola Hidup Sehat (Pola Makan dan Aktifitas) (Obesitas Abdominal) SIMET, Pre-DM, Obesitas Anak PJK, DMT2, DM-Anak,Stroke

Prevalensi Sindroma Metabolik di Surabaya 2005

(Penelitian Pendahuluan) Waist Circumference = WC
Non DM : 32.0% DM Sesudah Terapi : 43.3% > 90 cm > 80 cm
DM Nave : 59.0% DM Obesitas : 81.7%
Prevalensi Pria : 4 5 x lebih sering daripada Wanita

10 Komponen Kumpulan Penyakit 4 Gula Darah Puasa 1 Trigliserida

Pada Sindroma-Metabolik
1 Obesitas Abdominal > 100 mg/dl > 150 mg/dl
2 Resistensi Insulin, Pre-Diabetes, Diabetes
3 Dislipidemia - Aterogenik : Kelainan salah satu atau lebih
dari Kol, Kol-HDL, Kol-LDL, TG
4 Kenaikan Tekanan Darah 2 Kolesterol-HDL
5 Kecenderungan Trombosis (Sumbatan) 3 Tekanan Darah < 40 mg/dl
6 Fungsi Antitrombosis Menurun
7 Gangguan Fungsi Endotel > 130/85 mmHg < 50 mg/dl
Petanda : Mikroalbuminuria, yaitu adanya Protein dalam
Urine > 30 mg/24 jam atau ACR > 30 mg/g kreatinin
8 Kenaikan kadar Kortisol Sindroma Metabolic LP (INA) : > 90 cm ( ) dan > 80 cm ( )
9 Perlemakan Hati
10 Penyakit Kardiovaskuler (PJK, IMA, Stroke, dll)
(Menurut IDF 2005) :
Plus 2 dari 4 Faktor tersebut diatas
ACR = Albumin Creatinine Ratio, IDF = International Diabetes Federation, IMA = Infark Miokard Akut, PJK = Penyakit Jantung Koroner
III. Klasifikasi Etiologis DM
FASTING GLUKOSA BERBEDA SECARA
METABOLIK & HORMONAL DENGAN
PRANDIAL

Insulin Insulin prandial

puasa (glukosa uptake/utilzation

Glukagon Makanan
Glukosa Glukosa
puasa prandial
Glukosa darah puasa Glukosa darah prandial
SEKRESI INSULIN NORMAL
Sekresi Insulin Pada DM Tipe II
Gambar. Variabilitas
responsi insulin
terhadap OGTT
pada NIDDM

Untuk mengatasi resistensi insulin, sel harus mampu

sekresi insulin lebih banyak dan sepanjang mampu DM,
GTG (-) maka DM tipe II sekresi insulin bervariasi
Pola Sekresi Insulin DM Tipe I

Sekresi insulin tergantung sisa masa sel

Glycemic Control
 Management
A. Aim

Short term : Longer term :

Eliminate symptoms Prevent complications
Maintain general well being Reduce morbidity
and mortality

Strategy :
Normalizing glucose,
lipid, and insulin levels

Activities :
Management with holistic
approach and self care
principles
 Treatment Modalities

Diet/Medical nutrition therapy

Exercise
Anti hyperglycemic agents
Education
Pancreas transplantation
Cloning treatment (experiment)
 Update on PERKENI
Guidelines
The Indonesian Society of
Endocrinologist's
Diabetes Mellitus National Clinical
Practice Guidelines
Konsensus PERKENI 2011
Tujuan :
Perubahan perilaku pasien dan keluarganya
Cara :
Berikan dukungan dan nasehat positif
Berikan informasi secara bertahap
Mulai dengan hal hal yang sederhana
Gunakan alat bantu
Lakukan pendekatan dan simulasi
Berikan pengobatan sesederhana mungkin
Jangan terlalu memaksakan kehendak kita
Berikan motivasi, penghargaan dan diskusikan hasil
pengelolaan
 Diet/Nutrition Therapy/Meal planning
Nutrient Composition of Diabetic Diet

PERKENI A D A and B D A
(Indonesian Soc.of Endoc.)
10-15% 10-15%
20-25% 30%

60-70%
55%

Carbohydrate Fat Protein Carbohydrate Fat Protein

 PERENCANAAN MAKAN
KOMPOSISI :
Karbohidrat : 60 70 %
Protein : 10 15 %
Lemak : 20 25 %
JUMLAH KALORI :
Hitung BMI ( IMT ) = BB ( kg ) / TB ( m )2
IMT wanita ( normal ) = 18,5 23,5 kg/ m2
IMT laki ( normal ) = 22,5 25 kg / m2
Status gizi : BB Idaman = ( TB 100 ) 10%
BB kurang : < 90% BBI
BB Normal : 90 120% BBI
BB lebih : 110 120 % BBI
Gemuk : > 120% BBI
Exercise

30 minutes: 3 - 4 times / week

Continuous
Rhytmical
Interval
Progressive
Endurance training
 Anti Diabetic Agents

Hypoglycemic Agents

Anti Hyperglycemic Agents

 Pharmacologic Targets of Current Drugs Used in the Treatment of T2DM

GLP-1 analog (exenatide

liraglitide (R/ VICTOSA) DPP-4 inhibitors
Prolong GLP-1 action, stimulate insulin secretion,
injectable) suppress glucagon release
Improves glucose-dependent insulin secretion,
suppresses glucagon secretion, slows gastric emptying
Thiazolidinedio
nes
Increase glucose uptake in
skeletal muscle and decrease
lipolysis in adipose tissue
Sulfonylureas
Increase insulin secretion from
pancreatic -cells -glucosidase
Meglitinides inhibitors ( R/
Increase insulin secretion from GLUCOBAY )
pancreatic -cells Delay intestinal carbohydrate absorption
DDP-4=dipeptidyl peptidase-4; GLP-1=glucagon-like peptide-1; T2DM=type 2 diabetes mellitus
Adapted from Cheng AY, Fantus IG. CMAJ. 2005; 172: 213226.
 GLP-1 Secretion and Inactivation
Meal

Intestinal
GLP-1 GLP-1 t = 1 to 2 min
release

Active
GLP-1

DPP-4

GLP-1
inactive
(>80% of pool)

GLP-1 = glucagon-like peptide1; DPP-4 = dipeptidyl-peptidase4

 Blocking DPP-4 can Improve Incretin Activity and
Correct the Insulin/Glucagon Ratio in T2DM
Insulin
T2DM
Incretin
Further impaired
Response HYPERGLYCEMIA
islet function
Diminished

Glucagon

DPP-4 Inhibitor
Insulin

Incretin
Improved islet IMPROVED
Activity
function GLYCEMIC CONTROL
Prolonged

Glucagon
HGO= Hepatic Glucose Output
Adapted from Unger RH. Metabolism. 1974;23:581.
Insulin actions include :
Ability of insulin to lower circulating glucose
concentrations
Suppress glucose production : liver
Stimulate glucose utilization : muscle plus fat

Additional metabolic, vascular & mitogenic actions

 PRINCIPLES OF INSULIN
TREATMENT

Insulin regiment mimicking normal

(endogenous) physiologic insulin
secretion
 The Physiological Requirement for
Insulin
Basal

Pancreatic output :
basal prandial

Basal insulin : the amount of insulin necessary to prevent fasting

gluconeogenesis (fasting hyperglycemia) and ketogenesis
Prandial insulin : the amaount of insulin necessary to cover meals without
development of posprandial hyperglycemia
Insulin Preparation

Basal Insulin
Prandial Insulin
(Pre)mixed Insulin
 Berdasar lama kerja, insulin terbagi menjadi empat
jenis, yakni:

insulin kerja cepat (rapid acting insulin)

insulin kerja pendek (short acting insulin)
insulin kerja menengah (intermediate acting
insulin)
insulin kerja panjang (long acting insulin)
Insulin campuran
 Profil farmakokinetik insulin manusia dan insulin analog

Tampak awal dan lama kerja relatif berbagai jenis insulin. Lama kerjanya bervariasi antar dan intraindividu.
Hirsh IB. N Engl J Med 2005; 352: 17483
 Novel Biological Action of Insulin
Vasodilatation Cardio-protective
NO release Animals, human
eNOS expression

Anti-apoptotic
Platelet inhibition Heart, other tissues
NO release in platelets
cAMP

Anti-oxidant Anti-atheroscelrotic
Vascular (other) actions ApoE null mouse
ROS generation
IRS-1 null mouse
IRS-2 null mouse

Anti-inflammatory Profibrinolytic
NFkB, IkB Anti-thrombotic PAI-1
TF
MCP
ICAM-1
CRP

Dandona et al. Circulation 2005; 111: 1448-1454

Combination Therapy in T2DM:
Insulin Plus Oral Hypoglycemic Agents
Insulin Plus Sulphonylurea - BIDS
Some insulin is endogenous, with natural
secretory pattern
Biguanide Plus Insulin
Reduces hepatic insulin resistance
May achieve better control with less insulin
Can reduce weight gain
Alpha Glucosidase Inhibitor Plus Insulin
Reduces posotprandial glucose level
Thiazolidinedione Plus Insulin
Reduces peripheral insulin resistance
Reduces insulin requirement
Must balance TZD and insulin carefully to minimize
weight gain
Benefits of Insulin and Oral Agents Combination

Improves glycemic control

Treats multiple physiologic abnormalities
Less insulin is needed to achieve good glycemic
control
Reduces potensial for weight gain
Patients:
more practical and less frightening
improved psychological acceptance, patients
continue the oral drugs
less / minimal education is needed
treatment can be started in an
outpatients-setting
better compliance, and cost may be less
Glycemia Normal Goal Further Action
Required*
Average Preprandial <110 80 to 120 <80
Fasting Glucose (mg/dL) >140

Average Postprandial <140 <160 >180

Glucose (mg/dL)

HbA1C (%) <6 <7 >8

Further Action Required = Get off your rear and DO something

Adapted from the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus
Diabetes Care 1999;22:S32-S41
 Good Fair Poor
Fasting blood glucose (mg/dl) 80-109 110-125 126
2hpp blood glucose (mg/dl 80-144 145-179 180
A1C (%) <6.5 6.5-8 >8
Total- cholesterol (mg/dl) <200 200-239 240
LDL-cholesterol (mg/dl) <100 100-129 >130
HDL-cholesterol (mg/dl) >45
Triglyceride (mg/dl) <150 150-199 200
Body mass index (kg/m2) 18.5-22.9 23-25 >25
Blood pressure (mmHg) <130/80 130-140/80-90 >140/90

Perkeni, 2006,2011
LESSONS FROM UKPDS:
BETTER CONTROL MEANS FEWER COMPLICATIONS
EVERY 1% REDUCED
reduction in A1C RISK*

Deaths from diabetes

Heart attacks

Microvascular complications
1%
Peripheral vascular disorders

UKPDS 35. BMJ 2000; 321: 405-12.

*p<0.0001
 Complications :
Infeksi
Acute : Chronic
Neuropathy

Microangiopathy Macroangiopathy

Ketoacidosis
Retinopathy CAD
Nonketotic Hyperosmolar
Nephropathy PVD
syndrome
Neuropathy Stroke
Lactic asidosis
Hypoglikemi/koma.
 Diabetes: A malignant vascular disorder
Most common cause Stroke
of blindness in
younger people 2-4 x risk for stroke
and coronary heart
disease *)
Diabetic
Retinopathy

Cardiovascular
disease

Diabetic
Myocardiac infarct
Nephropathy
*) Most common
Most common cause of cause of death in
renal failure Dialysis
Diabetic diabetics
Neuropathy

Most common cause of

lower limb amputation

National Diabetes Information Clearinghouse. Diabetes StatisticsComplications of Diabetes.

http://www.niddk.nih.gov/health/diabetes/pubs/dmstats/dmstats.htm#comp.
Penyulit Menahun KOMPLIKASI DM

51
Blood Flow Decrease by Smoking
Before smoking After smoking

(Photograph from Dr. Matsuo)

 Genetic determinants of
individual susceptibility

Repeted changes
in cellular metabolism

hyperglicemia Diabetic tissue

Cummulative long term damage
changes in stable
macromolecules

Independent accelerating
factors (e.g hypertension,
hyperlipidemia

FIG. 1. General features of hyperglycemia-induced tissue damage.

Pathobiology of Diabetic Vacsular Complication
The Role of Oxidative Stress
(Michael Brownlee, Banting Lecture 2004)

1. Polyol Pathway (1966)

2. AGE Pathway (1980)
3. PKC Pathway (early 1990)
4. Hexosamine Pathway (late 1990)
 FIG. 2. Hyperglycemia increases flux through the polyol pathway. From Brownlee M: Biochemistry and
molecular cell biology of diabetic complications.
Nature 414:813820, 2001.
 FIG. 3. Increased production of AGE precursors and its pathologic consequences. From Brownlee M:
Biochemistry and molecular cell biology of diabetic complications.
Nature 414:813820, 2001.
 Hyperglicemia Consequences of hyperglycemia-
induced activation of PKC.

DAG

PKC
and isoform

+eNOS ET -1 TGF - PAI -1 NF -B NAD(P)H

VEGF

Collagen Fibrinolysis ROS

Fibronectin
Pro inflammatory
Gene expression
Vascular
Blood flow Vascular
Permeability
abnormalities Capillary occlusion
angiogenesis
occlusion Multiple effect
 FIG. 5. Hyperglycemia increases flux through the hexosamine pathway.
From Brownlee M: Biochemistry and molecular cell biology of diabetic complications.
Nature 414:813820, 2001.
Power AC (2006) : Diabetes Mellitus.
Harrisons Endocrinology
Hyperglycemia

Intracellular Glucose
Aldose
reductase

AGEs Sorbitol
DAG Fruc-6-P

Abnormal Circulating Alterations in ? PKC Flux in

hexosamine
protein redox activation
AGEs pathway
Function potential ,
ROS

Altered Altered gene Growth

Renal ,Vascular, Altered PAI-1,
Enzyme expression Factors
Altered Cell Connective Cell function growth
Function tissue effect function factors
Cytokines, (Cpla2),
Growth Factor eNOS

Complication
of Diabetes
Oxidative Damage
 Klasifikasi Lain
Jenis Serabut Saraf

Neuropati Sensorik
Neuropati Otonom
Neuropati Motorik
Respons terhadap Terapi
Fenomena Reversibel Cepat
Manifestasi yang telah Menetap

Thomas PK. International Textbook of Diabetes Mellitus, 2004

 SIGNS AND SYMPTOMS OF
NEUROPATHY (Apfel 1999)

Small-fiber sensory Large-fiber sensory Autonomic

------------------------------------------------------------------------------------------------------------
Burning pain Loss of vibration sense Heart rate abnormalities
Hyperesthesia Loss of proprioception Postural hypotension
Paresthesias Loss of reflexes Abnormal sweating
Lancinating pain Slowed NCVs Gastroparesis
Loss of pain & temp. Neuropathic diarrhea
Foot ulceration Impotence
Loss of visceral pain Retrograde ejaculation
 Dr PANDJI MULYONO, SpPd KEMD
SUBDEP PENY DALAM RUMKITAL Dr RAMELAN
FK WIJAYA KUSUMA
SURABAYA
HIPOGLIKEMI
HIPOGLIKEMI
Kadar gula darah < 60 mg/dl
Koma gula darah < 30 mg/dl

Penyebab Hipoglikemi pada DM

:
OHA induce
Insulin induce
 CEREBRAL CORTEX

Neuroglycopenic
symptoms
Hypoglycaemia

Hypothalamus

Parasympathetic
Sympathetic
nervous system nerves

Adrenal
medulla

Adrenaline
Tremor Heart Sudomotor
eccrine
sweat glands
Pounding heart
Autonomic Sweating
symptoms
Perception
interpretation
and action

Mekanisme terjadinya hipoglikemi

(Dikutip dari : Service, 1995)
Gejala dan Tanda Hipoglikemi :

1. Neuroglikopeni :
Daya berpikir menurun

Sulit berbicara

Nyeri kepala

Mata kabur

Kesadaran menurun sampai koma

Kejang
Gejala dan Tanda Hipoglikemi :
2. Adanya Rangsangan Adrenergik :
Takhikardi
Palpitasi
Gemetar
Berkeringat dan pucat
Rasa lapar
Mual
Cemas
Hipoglikemi dibagi 3 derajat :

I. Ringan

II. Sedang

III. Berat
 TERAPI HIPOGLIKEMI

1. Pisang / roti / KH lain

2. gula , tetesi gula kembali atau madu dibawah lidah

3. Injeksi D 40% i.v 25 cc dilanjutkan infus D 10% atau

Martos 10% dapat diulang tiap 1/2 jam sampai sadar

4. Injeksi efedrin 25 - 50 mg atau glukagon 1 mg i.m.

Bila kadar gula darah diketahui

Kadar gula darah D 40%

<30 mg/dl 3 fl

30 - 60 mg/dl 2 fl

60 - 100 mg/dl 1 fl

(Askandar Tj., 1996)

KETO ASIDOSIS
METABOLIK
PENCETUS KAD :

Infeksi
Penghentian insulin atau terapi insulin
yang tidak adekuat
Penderita baru
IMA
Obat steroid
20% tidak diketahui
 Decreased Insulin & Increased Counterregulatory Hormones
(Glucagon, Catecholamines, & Cortisol)

INCREASED LIPOLYSIS INCREASED GLUCOSE PRODUCTION INCREASED

AND TG BREAKDOWN & PROTEOLYSIS
DECREASED GLUCOSE UPTAKE
Increased Plasma
Increased FFA Amino Acids
in Plasma

Stimulate Precursors for Increased

Increased FFA HYPERGLYCEMIA Amino Acids
to Liver Gluconeogenesis Gluconeogenesis to Liver
Glucosuria
Increased
Ketogenesis Osmotic Diuresis

Loss of Electrolytes
Ketonemia & ketonuria

Cellular Dehydration
Decreased Alkali
Reserve
Volume Depletion

Acidosis Impaired Renal Function

Patofisiologi KAD (Dikutip dari : Kitaochi, 1994)

KRITERIA DIAGNOSIS KAD

1. Klinik : Poliuria, polidipsia, mual / muntah,

pernafasan kussmaul (dalam dan frekuen),
lemah, dehidrasi, hipotensi sampai syok,
kesadaran terganggu sampai koma.
2. Darah : hiperglikemi lebih dari 300 mg/dl
(biasanya melebihi 500 mg/dl), bikarbonat
kurang dari 20 mEg/l (dan pH<7.35), ketonemia
3. Urin : glukosuria dan ketonuria
KLASIFIKASI KAD
TERAPI KAD
Protokol terapi KAD terdiri dari 2 fase yaitu : Fase I (fase gawat)
Fase II (fase rehabilitasi)
Dengan batas kadar glukosa darah antara kedua fase tersebut sekitar 250
mg/dl.

FASE I :
1. Rehidrasi : Na cl 0.9% atau RL 2 liter/2 jam pertama, lalu 80 tetes/menit
selama 4 jam, lalu 30-50 tetes/menit selama 18 jam (4-6 liter/24 jam),
diteruskan sampai 24 jam berikutnya.
2. Insulin dosis rendah intravena : 4-8 unit/jam I.v sampai fase II.
3. Infus K : 75 mEq (bila K <2.5 mEq/l), 50 mEq (K = 2.5 -3.0 mEq/l) dan 25
mEq (K = 3.0 - 3.5 mEq/l) per 24 jam
4. Infus bikarbonat : bila pH <7.20 atau bikarbonat <12 mEq/l : 50-100 mEq
langsung drip dalam 2 jam, bolus 50-100 mEq diberikan bila pH kurang
dari 7.0
5. Antibiotika up to date dan dosis adekuat.
TERAPI KAD
FASE II :

1. Maintenance : Nacl 0.9%, atau potakol R (IR 4-8 U),

maltosa 10% (IR 8-12 U) bergantian 20 tetes/menit

2. Kalium : p.e (bila K < 4 mEq/l) atau per os (air tomat

atau kaldu 1-2 gelas)

3. Insulin reguler : 3 x 8-12 U s.c

4. Makanan lunak Karbohidrat kompleks peroral

HIPER OSMOLAR NON
KETOTIK
KOMA HIPEROSOMOLER NON KETOTIK (KHONK)

Hiperglikemi
Dehidrasi berat
Tanpa asidosis metabolik dan ketosis
Privalensi lebih jarang 1/5 - 1/6 KAD
DM tipe-2 usia tua
Mortalitas 30.4% kasus KHONK
Faktor Pencetus :

Faktor pencetus KHONK yang paling penting adalah

infeksi dan penyakit kardiovaskuler.
Namun dapat juga disebabkan o.k. iatrogenik
seperti hiperalimentasi parenteral, peritoneal
dialysis hipertonik, pembedahan dan pemberian
obat-obat kortikosteroid dan diuretic.

(Kuzuya T, 1999)
 KRITERIA DIAGNOSIS KHONK

Diagnosis klinik KHONK bila didapatkan :

1. Glukosa darah >800 mg/dl

2. Anamnesis DM tidak ada atau meragukan
3. Pernafasan Kussmaul tidak ada
4. Ketonuri dan ketonemia negatif atau
positif ringan.
KRITERIA DIAGNOSIS KHONK

Faktor penunjang diagnosis klinik HONK

1. pH darah >7.3
2. Adanya prerenal azotemia
3. Hipernatremi (>150 mEq/l)
4. Gangguan kesadaran
5. Gejala neurologik (konvulsi)

Diagnosis Pasti KHONK : Diagnosis klinik +

Osmolaritas > 325.

Osm/l = 2X (Na + K) + Glukosa (mg/dl) + BUN

18 2.8
TERAPI

= KAD
Bila Na <150 mEq/l cairan Nacl 0.9%
Na > 150 mEq/l cairan hipotonik
Tanpa Nabic.
LACTIC ACIDOSIS
ESS DX :
Severe acidosis with hyperventilation
pH darah < 7.30
Serum bicarbonat < 15 meq/l
Anion gap > 15 meq/l
Absent serum keton
Serum lactat > 5 mmol/l

ANION GAP N = (Na+ + K+) (Cl + HCO3) = 16 7

(unnaeasua red anion)

pH rumus Henderson Hasselbach :

CO2 content meq/L

pH = 6.10 + Log
pCO2 mmHg x 0,03
Normal sumber asam lactat :
Erithrosit
Otot
Kulit
Otak
Hati
Asam Lactat Glukose
Ginjal

Symtom and Sign :

Terutama hiperventilasi, bila penyebab
hipoksia/kolap vaskuler, klinis variabel ~ penyulit
dasar.
Tensi normal, sirkulasi perifer baik, sianosis (-).
Pencegahan Diabetes Mellitus

1. Primer, untuk orang yang resiko tinggi.

2. Sekunder, mencegah/menghambat
komplikasi.
3. Tertier, mencegah kecacatan
1. Age 45 years
2. Over weight (BMI 25 kg/m2)
3. First = degree relative with diabetes
4. Habitual physical inactivity
5. Member of a high-risk ethnic population (e.g., African-American,
Latino, Native American, Asian-American, Pacific Islander)
6. Previously identified pre-diabetes (IFG or IGT)
7. History of GDM or delivery of a baby weighing > 9 lbs
8. Hypertensive ( 140/90 mmHg)
9. HDL cholesterol level 35 mg/dl (0.90 mmol/l) and/or a
Triglyceride level 3 250 mg/dl (2.82 mmol/l).
10. PCOS
11. History of vascular disease.
 Monitor Pengelolaan Diabetes Terbaik

1. HbA1c (A1C)
2. Fructosamine
Correlation Between AIC level and
Mean Plasma Glucose
AIC (%) Mean Plasma Glucose
mg% mmol/L
6 133 7.5
7 170 9.9
8 205 11.5
9 240 13.5
10 275 15.5
11 310 17.5
12 345 19.5
Rohlfing CL et al. Diabetes Care 25; 275:, 2002