DKA Dan HHS (DR Wisma) [PDF]

Citation preview

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



4



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)



8



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).



Terima kasih atas perhatiannya