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 Diabetic Complications
Diabetic Ketoacidosis = DKA
Hyperosmolar Hyperglycemia
Nonketoric Coma = HHNC
Diabetic Ketoacidosis = DKA
Hyperosmolar Hyperglycemia
Nonketoric Coma = HHNC
Retinopathy
Nephropathy
Neuropathy
Retinopathy
Nephropathy
Neuropathy
Macroangiopathy Macroangiopathy
Chronic : Chronic : Acute Acute
Microangiopathy Microangiopathy
CAD
PVD
Stroke
CAD
PVD
Stroke
Hypoglycemia
Metabolic Decompensation
Sebab Kesadaran Menurun pada Diabetes Melitus Sebab Kesadaran Menurun pada Diabetes Melitus
Ketoasidosis Diabetik
Hiperosmolar non Ketotik
Asidosis Laktat
Hipoglikemia
Sebab Lain - Trauma
- Obat
- Penyakit Lain :
Stroke
Koma hepatik
Uremik
Ketoasidosis Diabetik
Hiperosmolar non Ketotik
Asidosis Laktat
Hipoglikemia
Sebab Lain - Trauma
- Obat
- Penyakit Lain :
Stroke
Koma hepatik
Uremik
Diagnosis Banding Koma
Glukosa Keton Hipervent. Dehid. TD Kulit
mg/d L
DKA >300 +s/d4+ ++ ++ N/ hngt
HONK >500 0 s/d+ 0 +++ N/ N
Hipoglik < 50 0 0 0 N lmb
Asidosis
Laktat 20-200 trc s/d + +++ 0 Rnd hngt
Non N/ 0 s/d trc 0 s/d + 0 s/d + Variasi N
Metab
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
u
k 54
o
s
a 36
d
a 18
r
a
h
................................................................. Neuroglikopenia
Disfungsi Kognitif ringan
................................................................ Aktivasi gejala
Keringat autonomik
Gemetar
..................................... Berdebar ...... Neuroglikopenia
berat
Kejang
............................................................... Koma
Waktu
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
Respons Perubahan Hormonal pada Hipoglikemia:
Penurunan sekresi insulin
Peningkatan katekolamin dan epinefrin
Peningkatan sekresi glukagon
Peningkatan sekresi kortisol
Peningkatan hormon pertumbuhan
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
Oral Antidiabetic Agents: side
effects
Risk of hypoglycaemia
Weight gain

Gastrointestinal
side-effects

Adapted from DeFronzo RA. Ann Int Med. 1999; 131: 281303.
*Observed in patients with renal impairment
Oedema
Lactic acidosis

Anaemia
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
Diagnosis Type 2 DM Diagnosis Type 2 DM
Lifestyle changes Lifestyle changes
A1C (%)* A1C (%)*
6.5-7 6.5-7 7-8 7-8 8-10 8-10
Oral Combination
Oral
#
:
SU
Metformin
AGI
TZD
Meglitinides
Specific condition:
Short/Rapid-acting
Insulin analog
Pre-mixed
Insulin analog
Oral Combination
Oral
#
:
SU
Metformin
AGI
TZD
Meglitinides
Specific condition:
Short/Rapid-acting
Insulin analog
Pre-mixed
Insulin analog
Monotherapy* :
Metformin
AGI
TZD
Specific Condition:
SU
Meglitinides
Short/Rapid-acting
Insulin analog
Monotherapy* :
Metformin
AGI
TZD
Specific Condition:
SU
Meglitinides
Short/Rapid-acting
Insulin analog
Combination
Oral+Insulin :
Metformin
TZD
SU
Long-acting
Insulin
Short/Rapid-acting
Insulin analog
Pre-mixed
Insulin analog
NPH
Other Combination
Combination
Oral+Insulin :
Metformin
TZD
SU
Long-acting
Insulin
Short/Rapid-acting
Insulin analog
Pre-mixed
Insulin analog
NPH
Other Combination
>10 >10
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
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
Achieved
Target
Achieved
Target
not
Achieved
Target
not
Achieved
Target
Achieved
Target
Achieved
Target
Achieved
Target
Achieved
Target
Achieved
Target
Achieved
Target
not
Achieved
Target
not
Achieved
Target
not
Achieeved
Target
not
Achieeved
Target
not
Achieved
Target
not
Achieved
Intensification
Therapy OR
Intensification
Therapy OR
Continue
Treatment
Continue
Treatment
Continue
Treatment
Continue
Treatment
Intensification
Therapy OR
Intensification
Therapy OR
Continue
Treatment
Continue
Treatment Intensification
Therapy OR
Intensification
Therapy OR
Continue
Treatment
Continue
Treatment
Intensification of
Insulin Treatment
Basal+bolus
Intensification of
Insulin Treatment
Basal+bolus
Algorithm for Management of Type 2 DM without Metabolic Decompensation
Indonesian Society of Endocrinology 2007
Continue Continue
<6.5 <6.5
Blood Glucose Monitoring
(FPG, PPG, Bed time)
*surrogate average blood glucose
might be used
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
A D A Clinical Practice Recommendation
Diabetes Care. 2009;32(suppl 1): S 32-33
Pemantauan kadar glukosa darah harus cermat
Hyper-
glycemia
Acidosis
Ketosis
DKA
Kitabchi and Wall
Hyperglycemia states
DM
HHNC
IGT
Stress
Metabolic Acidosis states
Lactic acidosis
Hyperchloremic acidosis
Salicylism
Uremic acidosis
Drug-induced
acidosis
Ketotic states
Ketotic hypoglycemia
Alkaholic ketosis
Starvation ketosis
DKA Episode and Mortality Rate at Dr.
Cipto Mangunkusumo Hospital, Jakarta
Year Number of Cases Mortality rate %
1983-84 (9 months) 14 31,4
1984-88 (48 months) 55 40
1995 (12 months) 17 -
1997 (6 months) 23 18,7
1998-99 (12 months) 37 51
2002 (5 months) 39 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
Abdominal pain
Leg cramps
Nausea and vomiting
Confusion and
drowsiness
Coma
Polyuria and nocturia
Weight loss
Weakness
Blurred vision
Kussmaul respiration
DKA
HHNC
HHNC
HHNC
Principal Management of DKA and HHNC
Hour Hydration Insulin K
+
Correction HCO3
-
correction
0 guyur 50 mEq per If pH
guyur six hour <7 7-7.1 >7.1
guyur Start hour 2
iv bolus iv,
Cont by infusion
dst dst dst
Hour Hydration Insulin K
+
Correction HCO3
-
correction
0 guyur 50 mEq per If pH
guyur six hour <7 7-7.1 >7.1
guyur Start hour 2
iv bolus iv,
Cont by infusion
dst dst dst
Management of DKA
at Cipto Mangunkusumo Hospital, Jakarta
Management of DKA
at Cipto Mangunkusumo Hospital, Jakarta
A B C D E A B C D E
Penatalaksanaan Ketoasidosis Diabetik
* 1 jam 2 kolf, 1 jam 1 kolf, dst
* Na Cl Fisiologis
* 1/2 N, 2A - Kalau Na > 150 mek/l
1. Rehidrasi Cepat
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
3.Kalium < 3,5 mek/L -- 50 mek/L
3,5 - 5 mek/L -- 25 mek/L
>5 mek/L -- 0
4. Na HCO3
pH < 7 - 7,1
5. Faktor Presipitasi
***Dosis Kecil 5 U IM *** Pemantauan dengan Urin
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
Hibiscus rosasinensis
Hatur Nuhun