DIABETES MELITUS DAN

KOMPLIKASI NYA
 PENDAHULUAN

Dampak pembangunan kesehatan Indonesia 

pergeseran pola penyakit  penyakit menahun/
degeneratif ↑  penyakit jantung koroner, hipertensi,
diabetes melitus (DM), hiperlipidemia
 Berkaitan dengan perubahan pola hidup
Di Indonesia  epidemi DM tipe II
50% terdiagnosis  2/3 dalam terapi  1/3 terkendali
DM  penyakit seumur hidup  peran penting tim
medis, pasien & keluarga pasien
 DEFINISI

Diabetes Melitus
 penyakit metabolik yang biasanya herediter, dengan tanda2
hiperglikemia dan glukosuria, disertai dengan atau tidak
adanya gejala klinik akut ataupun kronik, sebagai akibat
kurangnya insulin efektif di dalam tubuh
 Gangguan primer terletak pada metabolisme karbohidrat,
yang disertai juga dengan gangguan metabolisme lemak dan
protein
 KLASIFIKASI & PATOFISIOLOGI

Diabetes Melitus Tipe I

 Destruksi sel β pankreas
 Defisiensi insulin absolut
Diabetes Melitus Tipe II
 Resistensi insulin di perifer
 Jumlah reseptor ↓
 Kualitas reseptor ↓
 Kelainan pasca reseptor
 Campuran keempat faktor di atas
Diabetes Melitus Tipe Lain
Diabetes Kehamilan
 GEJALA KLINIS

Gejala klasik  poliuria, polidipsia, polifagia, BB ↓

Gejala lain  lemah, kesemutan, mata kabur, disfungsi

ereksi (pria), pruritus vulvae (wanita)
 DIAGNOSIS

Gejala Klasik DM + Glukosa Darah Sewaktu > 200 mg/dL

Gejala Klasik DM + Glukosa Darah Puasa > 126 mg/dL

Glukosa Darah 2 Jam pada Tes Toleransi Glukosa Oral

(TTGO) > 200 mg/dL
 normal atau
kriteria DM digolongkan ke dalam kelompok
prediabetes

 Glukosa Darah Puasa Terganggu (GDPT):

 Hasil pemeriksaan glukosa plasma puasa antara 100 – 125 mg/dL
dan
 pemeriksaan TTGO glukosa plasma 2-jam < 140 mg/Dl

 Toleransi Glukosa Terganggu (TGT):

 Hasil pemeriksaan glukosa plasma 2 -jam setelah TTGO antara 140 – 199 mg/dL
dan
 Glukosa plasma puasa < 100 mg/dL

 Bersama-sama didapatkan GDPT dan TGT

 Diagnosis prediabetes dapat juga ditegakkan berdasarkan hasil

pemeriksaan HbA1c yang menunjukkan angka 5,7 – 6,4%.
 PENATALAKSANAAN

Edukasi
Terapi Gizi Medis
Latihan Jasmani
Intervensi Farmakologis
 OHO
 Insulin
 Profil Obat
Antihiperglikemi
a Oral yang
Tersedia di
Indonesia
 KOMPLIKASI

Penyulit Akut
 Ketoasidosis diabetik
 Hiperosmolar non ketotik
 Hipoglikemi

Penyulit Menahun
 Makroangiopati  pembuluh darah jantung, otak, tepi
 Mikroangiopati  retinopati & nefropati diabetik
 Neuropati
2 Na (mEq/l) + glukosa (mg/dl)/18 + SC/2,8).
Hyperglycemic Crises in Adult Patients With Diabetes
: Abbas E. Kitabchi, akitabchi@utmem.edu.
Diabetes Care 2009 Jul; 32(7): 1335-1343.
EFFECTIVE SERUM
OSMOLARITY: 326
 DKA – cause or trigger
Incidence
New-onset diabetes 5-40%
Acute illness 10-20%
Insulin omission/non-adherence 33%

Infection 20-38%
Heart attack, stroke, pancreatitis <10%
Diabetic ketoacidosis
Insulin deficiency

Glucose uptake Lipolysis

Glycerol Free fatty

acids

Hyperglycaemia Gluconeogenesis
Ketogenesis
Glucosuria Ketonemia

Osmotic diuresis Electrolyte Ketonuria

depletion

Urinary water losses Dehydration

Acidosis
 Ketones

Used as fuel when calories are restricted

Physiological ketosis when fasting or

with prolonged exercise
Insulin deficiency  lypolysis and
ketone production  acidosis
 beta-hydroxybutyrate
 acetoacetate
 acetone
 Ketones

Beta-hydroxybutyrate predominant –
not detected by test strips or acetone
tablets
Ketoacidosis may be present without
detectable urinary ketones
Blood ketone testing may enable early
identification of DKA
Earlier clinical symptoms and
signs of DKA

• Polyuria
• Polydipsia

• Polyphagia

• Tiredness

• Muscle cramps

• Flushed facial appearance

Later clinical symptoms and signs
of DKA
• Weight loss
• Nausea and vomiting
• Abdominal pain
• Dehydration
• Acidotic breath
• Hypotension
• Shock
• Altered consciousness
• Coma
 DKA – laboratory findings
Blood glucose >14mmol/L (252mg/dL)
Ketones Urine: moderate to large
Blood: >3mmol/L
Osmolality Increased – high blood glucose and
urea/creatinine, dehydration
Electrolytes Low/normal Na+ and Cl-
Low/normal/high K+ (often misleading)
Low HCO3 (normal 23-31)
Anion gap >10 mild
>12 moderate to severe
Blood gases pH <7.30, HCO3 <15 (mild)

pH <7.00, HCO3 <10 (severe)

 DKA – treatment
Rehydration 1. Correct shock with bolus saline
2. Rehydration rate depends on clinical
status, age and kidney function
Normal saline (0.9%) for resuscitation
and rehydration initially
Glucose/saline solution when glucose
around 14 mmol/L (252mg/dL)
Rehydrate steadily over 48 hours
3. Consider NG tube

Potassium Essential after resuscitation and when

urine output confirmed
 DKA – treatment
Insulin Infusion: 0.1 units/kg/hour after
resuscitation, saline established and BG
falling
Rate should be increased by 10-20% if
glucose not fallen by 2-3 mmol/L (45-
54mg/dL) over first hour

Monitoring BG, BP, urine output and hourly

neurological status
Blood gases and electrolytes 2-hourly
initially
 What is HHS?

Ketosis may be present

Coma not always present

Primarily in older people

with/without history of type 2
diabetes
Always associated with severe
dehydration and hyperosmolar state
Develops over weeks