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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
Retinopathy Nephropathy Neuropathy CAD PVD Stroke

Diabetic Ketoacidosis = DKA

Hyperosmolar Hyperglycemia Nonketoric Coma = HHNC

Metabolic Decompensation

Sebab Kesadaran Menurun pada Diabetes Melitus

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

Diagnosis Banding Koma


Glukosa mg/d L
DKA HONK >300 >500

Keton
+s/d4+ 0 s/d+

Hipervent. Dehid.
++ 0 ++ +++

TD
N/ N/

Kulit
hngt N

Hipoglik
Asidosis Laktat Non Metab

< 50

lmb

20-200 N/

trc s/d + 0 s/d trc

+++ 0 s/d +

Rnd

hngt

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

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

A1C (%)*

Blood Glucose Monitoring (FPG, PPG, Bed time)

<6.5

6.5-7

7-8

8-10

>10

Continue

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

Target Achieved

Target not Achieved

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

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

Continue Treatment

Intensification Therapy OR

Target Achieved

Target not Achieved

Target Achieved

Target not Achieeved

Target Achieved

Target not Achieved

Continue Treatment

Intensification Therapy OR

*surrogate average blood glucose might be used

Continue Treatment

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
DM HHNC IGT Stress

Metabolic Acidosis states


Lactic acidosis Hyperchloremic acidosis Salicylism Uremic acidosis Drug-induced acidosis

Hyperglycemia

Acidosis

DKA

Ketotic states
Ketotic hypoglycemia Alkaholic ketosis Starvation ketosis

Ketosis

Kitabchi and Wall

DKA Episode and Mortality Rate at Dr. Cipto Mangunkusumo Hospital, Jakarta

Year

Number of Cases Mortality rate %


14 55 17 23 37 39 31,4 40 18,7 51 15

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

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 Hydration Insulin K+Correction HCO3- correction

A
0

B
guyur guyur guyur

D
50 mEq per six hour

E
If pH <7 7-7.1 >7.1

Start hour 2 iv bolus iv, Cont by infusion dst

dst

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

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