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KETOASIDOSIS DIABETIKUM DAN STATUS HIPERGLIKEMIK HIPEROSMOLAR Dr. Wismandari Wisnu SpPD-KEMD Divisi Metabolik Endokrin Departemen Ilmu Penyakit Dalam FKUI / RSCM 2018
Data Pribadi § Nama lengkap : dr. Wismandari Wisnu, SpPD, KEMD, FINASIM § Tempat/tgl lahir : Jakarta, 12 Februari 1972 § Alamat : Jl. Karyawan no 14B, Jakarta 12310 Riwayat Pendidikan § S1, Sp-1 dan Sp-2 di Fakultas Kedokteran Universitas Kedokteran Riwayat Pekerjaan § Humas Divisi Metabolik Endokrin, Departemen Ilmu Penyakit Dalam FKUI/RSCM (2009-sekarang) § Koordinator Kelas Internasional Mahasiswa S1 FKUI (2018-sekarang) § Koordinator Kelas Reguler Mahasiswa S1 FKUI (2017) § Koordinator tingkat 5 mahasiswa S1 FKUI (2012-2017) § Wakil Koordinator mahasiswa Departemen IPD (2010-sekarang) § Dokter PTT di Puskesmas Kecamatan Cilandak, Jakarta Selatan (2000-2003) Organisasi/Kepanitiaan Anggota IDI cabang Jakarta Selatan Bidang Humas PB PAPDI Bidang Organisasi PB Perkeni
Bendahara Perkeni Jaya Bendahara PAPDI Jaya Anggota Internasional : AOTA, ISE, AFES
TOPIK • Definisi KAD dan HHS • Patogenesis KAD dan HHS • Tatalaksana KAD dan HHS • Pencegahan
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Komplikasi Akut DM
• Hipoglikemia • Hiperglikemia - KAD (Keto Asidosis Diabetikum) - HHS (Hyperosmolar hyperglycemic state)
Slide 5
WHAT IS DIABETIC KETOACIDOSIS ? Ê Acute decompensated metabolic state due to § severe insulin deficiency § over-activity of glucagon & other counter-regulatory
hormone Ê Common in Type 1; Rare in Type 2 Ê Potentially life-threatening Ê High mortality Ê Incidence : 5-8 /1000 diabetic persons/yr Ê Mortality rates 9-14 % - Has improved with insulin useà 2% Watkins et al. In: Diabetes and its Management 2003
FAKTOR PRESIPITASI / PREDISPOSISI KETOASIDOSIS DIABETIKUM • Riwayat pemberian insulin inadekuat • Diabetes onset baru (20 – 25%) • Penyakit akut • • • •
Infeksi (30 – 40%) Penyakit serebrovaskular Infark miokar Pankreatitis akut
Kitabchi et al, Diab Care 2001;24(1):131–53.
• Obat • • • • •
Klozapin / olanzapine Kokain Lithium Penghambat SGLT-2 Terbutaline
• Tidak diketahui
FAKTOR PRESIPITASI / PREDISPOSISI STATUS HIPEROSMOTIK HIPERGLIKEMIA • Riwayat pemberian insulin inadekuat (21 – 41%) • Diabetes kasus baru • Penyakit akut • Infeksi (32 – 60%) • Pneumonia • Infeksi saluran kemih • Sepsis • Penyakit serebrovaskular • Infark miokard • Pankreatitis akut • Emboli paru akut • Obstruksi gastrointestinal • Dialisis, peritoneal • Thrombosis mesenteric
Kitabchi et al, Diab Care 2001;24(1):131–53.
• Gagal ginjal • Heat stroke • Hipothermi • Hematom subdural • Luka bakar berat • Endokrin • Akromegali • Tirotoksikosis • Sindrom Cushing • Obat (Beta-adrenergic blockers, calcium-channel blockers, klorpromazine, klortalidon, cimetidine, klozepin, diazoxid, asam ethakrinik, obat imunosupresif, L-asparaginase, loksapin, olanzapine, fenitoin, propranolol, steroid, diuretic tiazid, total parenteral nutrition)
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PATHOGENESIS OF DKA AND HHS Absolute Insulin Deficiency
↓Protein Synthesis
↑ Lipolysis
↓ Alkali Reserve
↑ Proteolysis
Absent or Minimal Ketoacidosis
↑ Gluconeogenic Subrates
↑FFA to Liver ↑ Ketogenesis
Relative Insulin Deficiency
↑ Counterregulatory Hormones
↑Glucose Utilization
↑Gluconeogenesis
↑Glucogenolysis
Hyperglycemia
↑ Ketoacidosis
Glyucosuria ( Osmotic diuresis) Loss of water and electrolytes
Triacylglycerol
Dehydration
Hyperlipidemia
Decreased fluid intake
Impaired renal function
HHS DKA
Hyperosmolarity
Ketoasidosis Diabetikum
Characterized by the triad of • uncontrolled hyperglycemia, • Metabolic acidosis • increased total body ketone concentration
DIABETES CARE, VOLUME 32, NUMBER 7, JULY 2009
Metabolic Acidosis states •Lactic acidosis •Hyperchloremic acidosis •Salicylism •Uremic acidosis •Drug-induced acidosis
Hyperglycemia states •DM •NKHC •IGT •Stress Hyper-
Acidosis
glycemia
DKA
Ketotic states •Ketotic hypoglycemia •Alkaholic ketotis •Starvation ketosis
Ketosis
Kitabchi and Wall
Mekanisme ketoasidosis diabetes Absolute insulin deficiency
Lipolisis
↑ Counter regulatory hormones ↓ Protein synthesis ↑ Gluconeogenic substances
↑ FFA to liver ↑ Ketogenesis
↑ Proteolysis
↓ Glucose utilization
↑ Gluconeogenesis
↓ Alkali reserve
Hyperglycemia
↑ Ketoacidosis
Glycosuria (osmotic diuresis)
↑ Triglyserides
Loss of water and electrolytes
↑ Hyperlipidemia
Kitabchi et al, Diab Care 2001;24(1):131–53.
Dehydration Impaired renal function
↑ Glycogenolysis
Hyperosmolar Hyperglycemic Syndrome (HHS) Characterized by: • • • •
severe hyperglycemia Hyperosmolality dehydration In the absence of significant ketoacidosis
These metabolic derangements result from the combination of absolute or relative insulin deficiency and an increase in counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). DIABETES CARE, VOLUME 32, NUMBER 7, JULY 2009
Mekanisme HHS ↑ Counter regulatory hormones ↓ Protein synthesis
Relative insulin deficiency
↑ Proteolysis
Absent to minimal ketogenesis
↑ Gluconeogenic substances ↓ Glucose utilization
↑ Gluconeogenesis
↑ Glycogenolysis
Hyperglycemia Glycosuria (osmotic diuresis) Loss of water and electrolytes Dehydration
Kitabchi et al, Diab Care 2001;24(1):131–53.
Impaired renal function
Decreased fluid intake
Hyperosmolarity
Slide 14
Diagnosis Ketoasidosis Diabetes Tanda
Gejala
Ê Penurunan nafsu makan
Ê Takiardia
Ê Mual
Ê Hipotensi
Ê Muntah
Ê Hipotermia
Ê Rasa haus Ê Poliuria Ê Lemas Ê Nyeri perut Ê Berat badan turun
Ê Penuruanan kesadaran Ê Kulit kering dan hangat Ê Napas Kussmaul Ê Bau napas aseton
ANAMNESIS KETOASIDOSIS DIABETIKUM
STATUS HIPERGLIKEMIA HIPEROSMOLAR (SHH)
• Mual/ muntah
• Riwayat polyuria
• Haus/polyuria
• Berat badan turun
• Nyeri perut
• Berkurangnya asupan oral yang terjadi dalam beberapa minggu
• Sesak nafas • Gejala berkembang dalam waktu 250 mg/dL) >250 mg/dL)
SHH Berat (Kadar GD >250 mg/dL)
Kadar GD >600 mg/Dl)
pH arteri
7. 25 – 7.30
7.00 – 7.24
7.30
Bikarbonat serum
15 - 18
10 - 15
18
Keton urin
Positif
Positif
Positif
Kecil
Keton serum
Positif
Positif
Positif
Kecil
Osmolalitas serum efektif
Bervariasi
Bervariasi
Bervariasi
> 320 mOsm/kg
Anion gap
> 10
> 12
> 12
Bervariasi
Status mental Sadar Sadar/ mengantuk Stupor/ Koma Stupor / Koma GD: Glukosa darah, Osmolalitas serum efektif = 2x [Na+ ukur (mEq/L)] + glukosa (mg/dL)/18. Anion gap = (Na+)-[(Cl- + HCO3- (mEq/L)] Kitabchi et al, Diab Care 2001;24(1):131–53.
TATALAKSANA Pemberikan cairan
Terapi insulin
Koreksi Kalium
Koreksi asidosis
H + PIN PAPDI. Panduan Praktik Klinis Ilmu Penyakit Dalam. 2015
Monitor
PRIMARY MANAGEMENT OF DKA/HHS 20
Bicarbonate
IV Fluids
pH ˂ 6,9 Determine hydration status Severe Hypovelemia
Mild dehydration
No HCO3-
Cardiogenic shock
Hemodynamic Administer 0,9% Monitoring/ NaCL ( 1.0 L/hr Pressor Evaluated corrected Serum Na+
Serum Na + High 0,45% NaCL (250-500 ml/Hr) depending on hydration state
Serum Na+ Normal
Serum Na+ Low 0,9% NaCL (250-500 ml/Hr) depending on hydration state
When serum glucose reaches 200 mg/dl (DKA) or 300 mg/dl (HHS), change to 5% dextrose With 0.45% NaCL at 150-250 ml/hr
Potassium
Insulin: Reguler
pH ˂ 6,9 100mmol in 400ml H20 +20mEq KCL, infuse for 2 hours Repeat every 2 hours Until pH ≥ 7 Monitor Serum K+ every 2 hrs
IV Route (DKA and HHS)
0.1 U/kg/B.Wt as IV bolus
0.1 U/kg/hr IV Continous Insulin infusion
IV Route (DKA and HHS)
0.1 U/kg Bwt/hr As IV Continous Insulin infusion
If serum glucose does not fall by at Leatst 10% in first hour , give 0.14 U/kg as IV bolus , then continue Previous Rx
When serum glucose Reaches 200 mg/dl, reduce Reguler insulin infusion to 0.02 – 0.05 U/kg/hr IV, or give Rapid-acting insulin at 0.1 U/kg SC every 2 hrs. Keep Serum glucose between 150 And 200 mg/dl until resolution of DKA
Establish adequate Renal function (urine Output – 50 ml/hr)
K+ 5.2 mEq/L
Hold insulin and give 20 – 30 mEq/hr Until K+> 3.3 mEg/L
When serum glucose reaches 300 mg/dl, reduce reguler insulin infusion to 0.02 – 0.05 U/kg/hr . Keep serum glucose between 200 and 300 mg/dl until patient Is mentally alert
Do not give K+, But check serum K+ Every 2hrs
K+ = 3.3 – 5.2 mEq/L
Give 20-30 mEq K+ in each Liter of IV fluid to keep serum K+ between 4 - 5 mEg/L
Check electrolytes, BUN, venous pH, creatinine and glucose every 2-4 hr until stable. After resolution of DKA or HHS and when patient is able to eat , initiate SC multidose Insulin regimen . To transfer from IV to SC , continue IV insulin infusion for 1- 2 hrs After SC insulin begun to ensure adequate plasma insulin levels . In Insulin native Patiients, start at 0.5 U/kg to 0.8 U/kg body weight per day and adjust insulin as needed. Look for precipitating cause (s)
Diabetes Care 2001 Jan; 24(1): 131-153
PRIMARY MANAGEMENT OF DKA/HHS– REFERRAL PREPARATION 21
IV Fluids Determine hydration status Severe Hypovelemia
Cardiogenic shock
Mild dehydration
Hemodynamic Monitoring/Pressor
Administer 0,9% NaCl (10 L/hr)
Evaluated corrected Serum Na+ Serum Na + High
Serum Na + Normal
0,45% NaCL (250-500 ml/Hr) depending on hydration state
0,9% NaCl (250-500 ml/Hr) depending on hydration state Serum Na + Low When serum glucose reaches 200 mg/dl (DKA) or 300 mg/dl (HHS), change to 5% dextrose With 0.45% NaCL at 150-250 ml/hr
Diabetes Care 2001 Jan; 24(1): 131-1
PRIMARY MANAGEMENT OF DKA/HHS– REFERRAL PREPARATION 22
Bicarbonate pH ≥ 6,9
No HCO3-
pH ˂ 6,9
100mmol in 400ml H20 +20mEq KCL, infuse for 2 hours
Repeat every 2 hours Until pH ≥ 7 Monitor Serum K+ every 2 hrs
Diabetes Care 2001 Jan; 24(1): 131-1
PRIMARY MANAGEMENT OF DKA/HHS– REFERRAL PREPARATION 23
Insulin : Reguler IV Route (DKA and HHS) 0.1 U/kg/B.Wt as IV bolus
IV Route (DKA and HHS) 0.1 U/kg Bwt/hr As IV Continous Insulin infusion
0.1 U/kg/hr IV Continous Insulin infusion
If serum glucose does not fall by at Least 10% in first hour , give 0.14 U/kg as IV bolus , then continue Previous Rx
Diabetes Care 2001 Jan; 24(1): 131-1
EVALUASI TERAPI INSULIN • Periksa elektrolit, pH vena, kreatinin • GD tiap 2 – 4 jam sampai pasien stabil • Setelah resolusi KAD atau SHH dan mampu makan berikan regimen insulin subkutan • Mengganti insulin IV ke subkutan: lanjutkan infus insulin IV selama 1 – 2 jam setelah insulin subkutan dimulai untuk mencapai kadar insulin plasma yang adekuat • Pada pasien insulin-naïve, mulai dengan 0.5 U//hari – 0.8 U/KgBB /hari dan sesuaikan sesuai kebutuhan
PIN PAPDI. Panduan Praktik Klinis Ilmu Penyakit Dalam.
PRIMARY MANAGEMENT OF DKA/HHS– REFERRAL PREPARATION 25
Potassium Establish adequate Renal function (urine Output – 50 ml/hr)
K+ 5.2 mEq/L
Hold insulin and give 20 – 30 mEq/hr Until K+> 3.3 mEg/L
Do not give K+, But check serum K+ Every 2hrs
K+ = 3.3 – 5.2 mEq/L Give 20-30 mEq K+ in each Liter of IV fluid to keep serum K+ between 4 - 5 mEg/L
Diabetes Care 2001 Jan; 24(1): 131-1
PEMANTAUAN Pantau tekanan darah, nadi, napas, status mental, asupan cairan dan urin tiap 1 – 4 jam
PIN PAPDI. Panduan Praktik Klinis Ilmu Penyakit Dalam.
KOMPLIKASI • Renjatan hipovolemik
Komplikasi pengobatan
• Trombosis vena
• Hipoglikemia
• Pendarahan saluran cerna atas
• Hipokalemia
• Sindrom distres pernapasan akut
• Overload edema serebral
PROGNOSIS • Mortalitas KAD : 2% untuk usia 65 tahun. • Mortalitas SHH 20 – 30%
PREVENTION (1) • Better access to medical care • Intensive patients education • Effective communication à 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 • Hand held meter with BG and 3HB strips can be helpful for avert DKA episode
KESIMPULAN • KAD dan HHS adalah kondisi kompikasi akut diabetes yang mengancam nyawa • Terdapat faktor predisposisi yang harus dihindari pada pasien diabetes • Tatalaksana KAD adalah rehidrasi, insulin, koreksi kalum, koreksi asidosis dan monitor ketat • Lakukan pencegahan terjadinya KAD dan HHS dengan cara mentatalaksana kondisi akut dengan baik, tingkatkan monitor gula darah dan jangan stop obat diabetes jika mengalami kondisi akut
REFERENSI 1.
Krisis hiperglikemia Dalam: Alwi I, Salim S, Hidayat R, Kurniawan J, Tahapary D. Penyunting. Penatalaksanaan bidang ilmu penyakit dalam: panduan Praktik Klinis. Jakarta: Interna Publishing; 2015. Hal 109 -14.
2.
Soewondo Pradana. Ketoasidosis Diabetik. Dalam: Sudowo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiati S. Penyunting. Buku ajar ilmu penyakit dalam. Edisi V. Jakarta: Interna Publishing; 2009. Hal 1906 – 1911.
3.
Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335 – 43.
4.
Misra S, Oliver NS. Diabetic ketoacidosis in adults. BMJ. 2015; 351: 5660-7.
5.
Lupsa BC, Inzucchi SE. Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome Dalam: Loriaux L. Endocrine Emergencies: Recognition and treatment. Springers; 2014. Hal 15 – 31.
6.
Taylor SI, Blau JE, Rother KI. SGLT2 Inhibitors May Predispose to Ketoacidosis. J Clin Endocrinol Metab 2015; 100:2849.
7.
Kitabchi AE, Razavi L.Hyperglycemic Crises: Diabetic Ketoacidosis (DKA), And Hyperglycemic Hyperosmolar State (HHS). In: http://www.endotext.org/diabetes/diabetes24/diabetesframe24.htm (Accessed on January 30, 2013).
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