Penatalaksanaan Terkini

Kegawatdaruratan pada Diabetes

Sarwono Waspadji
Pusat Diabetes dan Lipid,
Divisi Metabolik-Endokrin, Departemen Ilmu Penyakit Dalam,
FKUI / RSUPN Cipto Mangunkusumo,
Jakarta

Diabetic Complications

Acute

Chronic :

Microangiopathy

Macroangiopathy

Hypoglycemia

Diabetic Ketoacidosis = DKA

Hyperosmolar Hyperglycemia
Nonketoric Coma = HHNC

Retinopathy
Nephropathy
Neuropathy

Metabolic Decompensation

CAD
PVD
Stroke

Sebab
Sebab Kesadaran
Kesadaran Menurun
Menurun pada
pada Diabetes
Diabetes Melitus
Melitus

Ketoasidosis
Ketoasidosis Diabetik
Diabetik
Hiperosmolar
Hiperosmolar non
non Ketotik
Ketotik
Asidosis
Asidosis Laktat
Laktat
Hipoglikemia
Hipoglikemia
Sebab
Sebab Lain
Lain -- Trauma
Trauma
-- Obat
Obat
-- Penyakit
Penyakit Lain
Lain ::
Stroke
Stroke
Koma
Koma hepatik
hepatik
Uremik
Uremik

Diagnosis Banding Koma

Glukosa
mg/d L

Keton

DKA

>300

+s/d4+

++

HONK

>500

0 s/d+

Hipoglik

< 50

Asidosis
Laktat
20-200
Non
Metab

N/

trc s/d +
0 s/d trc

Hipervent. Dehid.

TD

Kulit

++

N/

hngt

+++

N/

lmb

+++

Rnd

hngt

0 s/d +

0 s/d + Variasi N

Hipoglikemia
Simtom:
Efek adrenergik alfa:
sekresi insulin menurun,
cerebral blood flow meningkat
peripheral vasoconstriction
Efek adrenergik beta:
glycogenolisis otot dan hati
stimulasi release glukagon
lipolisis
uptake glukosa otot menurun
increase c.o.p, cerebral flow
Efek adrenomedullary discharge of Catecholamine
augmentasi efek adrenergik
alfa dan beta

Gejala neuroglikopenik, gejala adrenergik

Hipoglikemia kronik berkepanjangan - demensia

Kadar Glukosa Darah dan Gejala Hipoglikemik Akut

g 72
l
................................................................. Neuroglikopenia
u
Disfungsi Kognitif
ringan
k 54
o
................................................................ Aktivasi gejala
s
Keringat
autonomik
a 36
Gemetar
.....................................

Berdebar ...... Neuroglikopenia

berat
d
Kejang
a 18
............................................................... Koma
r

a
h

Waktu

Respons Perubahan Hormonal pada Hipoglikemia:

Penurunan sekresi insulin
Peningkatan katekolamin dan epinefrin
Peningkatan sekresi glukagon
Peningkatan sekresi kortisol
Peningkatan hormon pertumbuhan

Diagnosis Relatif mudah: pemeriksaan GD

Trias Whipple:
Keluhan dan gejala hipoglikemia s/d kesadaran menurun,
Kadar Glukosa < 45 mg/dL (pada wanita dapat < 30 mg/dL),
Bangun kembali setelah diberikan glukosa

Perlu pemantauan yang lama jika pasien memakai obat long

acting
Jika hipoglikemia berkelanjutan dapat menyebabkan
kerusakan otak permanen, demensia

Penatalaksanaan Hipoglikemia
Ringan: Berikan gula murni (bukan pemanis) yang
cukup sampai keluhan hilang
Pastikan pemberian makanan / kalori cukup
untuk selanjutnya, terutama jika OAD long acting

Berat: Berikan glukosa 40 % IV sampai pasien sadar

Berikan infus rumatan D10 6-8 jam perkolf
cek glukosa darah setiap jam
jika < 100 mg/dL berikan kembali bolus D40
Jika sudah 2 kali berturut-turut >100 mg/dL, setiap 2 jam
Jika sudah 2 kali berturut-turut > 100 md/dL, setiap 4 jam,
dst sampai yakin bahwa kadar glukosa darah stabil aman
Perhatikan obat hipoglikemik yang dipakai:
Obat kerja panjang, pemantauan dapat lama, berhari
Perhatikan pula fungsi ginjal dan hati dan usia pasien

In
se su
cr lin
et
ag
og
ue
M
et
s
fo
rm
in
in glu
hi c
bi os
to id
r
TZ s ase
D
s

Oral Antidiabetic Agents: side

effects

Risk of hypoglycaemia

Weight gain

Gastrointestinal
side-effects

Lactic acidosis

Oedema

Anaemia

*Observed in patients with renal impairment

Adapted from DeFronzo RA. Ann Int Med. 1999; 131: 281303.

Principles in Selecting
Antihyperglycemic Interventions
Effectiveness in lowering blood glucose

Extraglycemic effect that may reduce

longterm complications
Safety profile
Tolerability
Ease of use
Cost
Nathan DM et al. Clinical Diabetes. 2009; 27 (1): 4-16

Algorithm for Management of Type 2 DM without Metabolic Decompensation

Indonesian Society of Endocrinology 2007
Diagnosis Type 2 DM
Lifestyle changes

Blood Glucose Monitoring

(FPG, PPG, Bed time)

A1C (%)*

6.5-7

<6.
5

Continue

Monotherapy* :
Metformin
AGI
TZD
Specific Condition:
SU
Meglitinides
Short/Rapid-acting
Insulin analog

Target
Achieved

Continue
Treatment

Target
not
Achieved

7-8

8-10

Oral Combination
Oral## :
SU
Metformin
AGI
TZD
Meglitinides
Specific condition:
Short/Rapid-acting
Insulin analog
Pre-mixed
Insulin analog

Combination
Oral+Insulin :
Metformin
TZD
SU
Long-acting
Insulin
Short/Rapid-acting
Insulin analog
Pre-mixed
Insulin analog
NPH
Other Combination

Target
Achieved

Intensification
Therapy OR

Continue
Treatment

*surrogate average blood glucose

might be used

Target
not
Achieved

Intensification
Therapy OR

Target
Achieved

Continue
Treatment

>10

Target
not
Achieeved

Insulin Therapy:
Short/Rapid-acting
Insulin analog
NPH or
Long-acting
Insulin
Pre-mixed
Insulin analog
In selected Patients
with A1C> 10%
OHO Combination
might be effective

Target
not
Achieved

Target
Achieved
Continue
Treatment

Intensification
Therapy OR

Intensification of
Insulin Treatment
Basal+bolus

Management of Hyperglycemia
In Patients
General Principles:
Maximal blood glucose control, avoiding
hypoglycemia
Meticulous, Prudent, Individualized
Management of T2DM synchronized with other
disease management

In critically ill patients, more over in

metabolic decompensation, the blood
glucose target should be more
aggressive and achieved quicker

Sasaran Glukosa darah yang dianjurkan

Pasien Tidak Kritis : Senormal mungkin
(110 180 mg/dL)
Insulin mungkin diperlukan
Sedekat mungkin dengan 130 mg/dL
Pasien Kritis: Senormal mungkin
(110 180 mg/dL)
Umumnya memerlukan insulin
Sedekat mungkin dengan 110 mg/dL
* Beberapa Institusi mungkin menganggap nilai ini
terlalu over agresif karena kepedulian akan risiko hipoglikemia
A D A Clinical Practice Recommendation
Diabetes Care. 2007;3(suppl 1): S 32-33

The Nice-Sugar Study

ICU setting 3 or more consecutive days
Intensive (81-108 mg/dL)
Conventional (<180 mg/dL)
Outcome mortality at 90 days
3054 intensive control vs. 3050 conventional
Similar characteristic baseline
Primary outcome available for 3010 and 3012 respectively
829 (27.5 %) mortality in intensive control, OR 1.14
751 (24.9%) mortality in conventional group
Severe hypoglycemia (< 40 mg/dL)
206 (6.8%) in intensive control
15 (0.5 %) in conventional group
The NICE Sugar study investigators.
Intensive vs. conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283-97

Blood Glucose Target

Critically ill surgical patients: as normal as possible
(110 140 mg/dL)*
Insulin is needed, IV protocol
Close to 110 mg/dL (A)
Critically ill non surgical pts: as normal as possible
(110 140 mg/dL)*
Insulin is needed, IV protocol
Keep BG < 140 mg/dL (C)
Non critically ill: as normal as possible, no specific goals
Insulin is preferred
FBG <126 mg/dL, Random BG<180-200 mg/dL (E)
* Some institutions might considered this blood glucose target as
over aggressive due to their cautious attitude toward hypoglycemia

Pemantauan kadar glukosa darah harus cermat

A D A Clinical Practice Recommendation
Diabetes Care. 2009;32(suppl 1): S 32-33

Hyperglycemia states

Metabolic Acidosis states

DM
HHNC
IGT
Stress

Lactic acidosis
Hyperchloremic acidosis
Salicylism
Uremic acidosis
Drug-induced
acidosis

Hyperglycemia

Acidosis

DKA

Ketosis
Ketotic states
Ketotic hypoglycemia
Alkaholic ketosis
Starvation ketosis

Kitabchi and Wall

DKA Episode and Mortality Rate at Dr.

Cipto Mangunkusumo Hospital, Jakarta
Year

Number of Cases Mortality rate %

1983-84 (9 months)
1984-88 (48 months)
1995
(12 months)
1997
(6 months)
1998-99 (12 months)
2002
(5 months)

14
55
17
23
37
39

31,4
40
18,7
51
15

Pathogenesis of DKA and HHNC

HHNC
DKA

Precipitating Factors of DKA & HHNC

Infection
Cerebro vascular accident
Pancreatitis
Myocardial infarction
Trauma
Medication
Newly diagnosed type 1 diabetes
Discontinuation of or inadequate insulin
Substance abuse
Not found

Clinical Features of
DKA

Polyuria and nocturia

Weight loss
Weakness
Blurred vision
Kussmaul respiration

Abdominal pain
Leg cramps
Nausea and vomiting
Confusion and
drowsiness
Coma

DKA

HHNC

HHNC

HHNC

Principal Management of DKA and HHNC

Management of DKA
at Cipto Mangunkusumo Hospital, Jakarta
Hour

A
0

Hydration

B
guyur
guyur
guyur

Insulin

K+Correction

D
50 mEq per
six hour

Start hour 2
iv bolus iv,
Cont by infusion
dst

dst

HCO3- correction

E
If pH
<7 7-7.1 >7.1

dst

Penatalaksanaan Ketoasidosis Diabetik

1. Rehidrasi Cepat
* 1 jam 2 kolf, 1 jam 1 kolf, dst
* Na Cl Fisiologis
* 1/2 N, 2A - Kalau Na > 150 mek/l
2. Insulin
Bolus 10 U IV. G.D setiap jam
Drip 5 U/jam sampai g.d. < 200 mg/dl - D5 %
Drip 2,5 U/jam sampai g.d. stabil 200 - 300 mg/dl
Drip 1 U/jam + sliding scale g.d. tiap 4 jam
Dosis terbagi 3-4 kali sehari
***Dosis Kecil 5 U IM *** Pemantauan dengan Urin
3.Kalium < 3,5 mek/L -- 50 mek/L 4. Na HCO3
3,5 - 5 mek/L -- 25 mek/L
pH < 7 - 7,1
>5 mek/L
-- 0
5. Faktor Presipitasi

Suhendro 2008
Pengukuran asam laktat perlu pada pengelolaan KAD
Serum laktat > 4 mmol/L petanda prognostik buruk
Jika disertai kesadaran menurun prognostik buruk
Perlu pengelolaan yang ketat sejak awal
Pasang CVP segera
Hidrasi dicapai dengan lebih cepat

Prevention (1)
Better access to medical care
Intensive patients education
Effective communication acute illness

Review sick-day management

Insulin treatment
Blood glucose goal
Treat fever and infection
Start easy digestible liquid diet

Do not stop insulin or oral anti diabetes

Prevention

(2)

Increase BG monitoring during acute

illness
Check ketone bodies (either urine or
blood) when BG > 300 mg/dL

Peran Dokter Umum

Pencegahan terjadinya Hiperglikemia
dengan mengelola DM sebaik-baiknya
mencegah komplikasi kronik
mencegah komplikasi akut DKA
menghindari komplikasi hipoglikemia

Jika menjumpai pasien tersangka

komplikasi akut:
Pastikan bukan hipoglikemia, kalau ragu,
jangan takut memberikan D40
Jika bukan hipoglikemia, tetapi KAD:
Infus NaCl dan segera kirim ke RS
Jikalau ada (misal di RS primer)
dapat diberikan insulin, kemudian rujuk
Memerlukan perawatan yang cermat, segera
di RS dengan peralatan yang memadai

Hatur Nuhun

Hibiscus rosasinensis