Penatalaksanaan Terkini Kegawatdaruratan pada DiabetesSarwono Waspadji

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

Diabetic Complications Diabetic Ketoacidosis = DKA Hyperosmolar Hyperglycemia Nonketoric Coma = HHNCRetinopathy NephropathyNeuropathyMacroangiopathyChronic :Acute MicroangiopathyCADPVDStroke Hypoglycemia Metabolic Decompensation

Sebab Kesadaran Menurun pada Diabetes Melitus Ketoasidosis DiabetikHiperosmolar non KetotikAsidosis Laktat

HipoglikemiaSebab 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 NMetab

HipoglikemiaSimtom:Efek adrenergik alfa: sekresi insulin menurun, cerebral blood flow meningkatperipheral vasoconstriction Efek adrenergik beta: glycogenolisis otot dan hatistimulasi release glukagonlipolisisuptake glukosa otot menurunincrease c.o.p, cerebral flowEfek adrenomedullary discharge of Catecholamineaugmentasi efek adrenergik alfa dan beta

Gejala neuroglikopenik, gejala adrenergikHipoglikemia kronik berkepanjangan - demensia

Kadar Glukosa Darah dan Gejala Hipoglikemik Akut

g 72luk 54o sa 36

d a 18rah

................................................................. Neuroglikopenia Disfungsi Kognitif ringan

................................................................ Aktivasi gejala Keringat autonomik Gemetar ..................................... Berdebar ...... Neuroglikopenia berat Kejang ............................................................... Koma Waktu

Diagnosis Relatif mudah: pemeriksaan GDTrias Whipple: Keluhan dan gejala hipoglikemia s/d kesadaran menurun, Kadar Glukosa < 45 mg/dL (pada wanita dapat < 30 mg/dL), Bangun kembali setelah diberikan glukosaPerlu pemantauan yang lama jika pasien memakai obat long actingJika hipoglikemia berkelanjutan dapat menyebabkan kerusakan otak permanen, demensia Respons Perubahan Hormonal pada Hipoglikemia:Penurunan sekresi insulinPeningkatan katekolamin dan epinefrinPeningkatan sekresi glukagonPeningkatan sekresi kortisolPeningkatan hormon pertumbuhan

Penatalaksanaan HipoglikemiaRingan: Berikan gula murni (bukan pemanis) yang cukup sampai keluhan hilang Pastikan pemberian makanan / kalori cukup untuk selanjutnya, terutama jika OAD long actingBerat: Berikan glukosa 40 % IV sampai pasien sadar Berikan infus rumatan D10 6-8 jam perkolf cek glukosa darah setiap jamjika < 100 mg/dL berikan kembali bolus D40Jika sudah 2 kali berturut-turut >100 mg/dL, setiap 2 jamJika 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, berhariPerhatikan pula fungsi ginjal dan hati dan usia pasien

Oral Antidiabetic Agents: side effectsTZDsMetforminInsulin secretagoguesRisk of hypoglycaemiaWeight gainGastrointestinal side-effectsAdapted from DeFronzo RA. Ann Int Med. 1999; 131: 281303. a-glucosidase inhibitors*Observed in patients with renal impairmentOedemaLactic 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 CostNathan DM et al. Clinical Diabetes. 2009; 27 (1): 4-16

Diagnosis Type 2 DMLifestyle changes A1C (%)*6.5-77-88-10Oral CombinationOral# :SUMetforminAGITZDMeglitinidesSpecific condition:Short/Rapid-acting Insulin analogPre-mixed Insulin analog Monotherapy* :MetforminAGITZDSpecific Condition:SU MeglitinidesShort/Rapid-actingInsulin analogCombination Oral+Insulin :MetforminTZDSULong-acting InsulinShort/Rapid-acting Insulin analogPre-mixed Insulin analogNPHOther Combination>10Insulin Therapy:Short/Rapid-acting Insulin analogNPH or Long-acting InsulinPre-mixed Insulin analogIn selected Patients with A1C> 10% OHO Combination might be effectiveTargetAchievedTargetnot AchievedTargetAchievedTargetAchievedTargetAchievedTargetnot AchievedTargetnot AchieevedTargetnot AchievedIntensificationTherapy OR ContinueTreatmentContinueTreatmentIntensificationTherapy OR

ContinueTreatmentIntensificationTherapy ORContinueTreatmentIntensification of Insulin TreatmentBasal+bolus

Algorithm for Management of Type 2 DM without Metabolic Decompensation Indonesian Society of Endocrinology 2007

Continue

Management of HyperglycemiaIn PatientsGeneral Principles:Maximal blood glucose control, avoiding hypoglycemia Meticulous, Prudent, IndividualizedManagement of T2DM synchronized with other disease managementIn 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 diperlukanSedekat mungkin dengan 130 mg/dLPasien Kritis: Senormal mungkin (110 180 mg/dL)Umumnya memerlukan insulinSedekat mungkin dengan 110 mg/dL

* Beberapa Institusi mungkin menganggap nilai ini terlalu over agresif karena kepedulian akan risiko hipoglikemia A D A Clinical Practice RecommendationDiabetes Care. 2007;3(suppl 1): S 32-33

The Nice-Sugar StudyICU setting 3 or more consecutive daysIntensive (81-108 mg/dL)Conventional (

Blood Glucose TargetCritically ill surgical patients: as normal as possible (110 140 mg/dL)*Insulin is needed, IV protocolClose to 110 mg/dL (A)Critically ill non surgical pts: as normal as possible (110 140 mg/dL)*Insulin is needed, IV protocolKeep BG < 140 mg/dL (C)Non critically ill: as normal as possible, no specific goalsInsulin is preferredFBG

Hyper-glycemiaAcidosisKetosisDKAKitabchi and WallHyperglycemia statesDMHHNC IGTStressMetabolic Acidosis statesLactic acidosisHyperchloremic acidosisSalicylism Uremic acidosisDrug-induced acidosis Ketotic statesKetotic hypoglycemiaAlkaholic ketosisStarvation ketosis

DKA Episode and Mortality Rate at Dr. Cipto Mangunkusumo Hospital, Jakarta Year Number of Cases Mortality rate %

1983-84 (9 months)1431,41984-88 (48 months)5540 (12 months)17- (6 months)2318,71998-99 (12 months)37512002 (5 months)3915

Pathogenesis of DKA and HHNCHHNCDKA

Precipitating Factors of DKA & HHNC Infection Cerebro vascular accident Pancreatitis Myocardial infarction TraumaMedicationNewly diagnosed type 1 diabetesDiscontinuation of or inadequate insulinSubstance abuse Not found

Clinical Features of DKAAbdominal painLeg crampsNausea and vomitingConfusion and drowsinessComa Polyuria and nocturiaWeight lossWeaknessBlurred visionKussmaul respiration

DKAHHNCHHNC

HHNC

Principal Management of DKA and HHNC

Hour Hydration Insulin K+Correction HCO3- correction

0guyur 50 mEq per If pH guyur six hour 7.1 guyur Start hour 2 iv bolus iv, Cont by infusion dst dst dstManagement of DKA at Cipto Mangunkusumo Hospital, JakartaA B CD 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 Cepat2. InsulinBolus 10 U IV. G.D setiap jamDrip 5 U/jam sampai g.d. < 200 mg/dl - D5 %Drip 2,5 U/jam sampai g.d. stabil 200 - 300 mg/dlDrip 1 U/jam + sliding scale g.d. tiap 4 jam Dosis terbagi 3-4 kali sehari3.Kalium< 3,5 mek/L -- 50 mek/L3,5 - 5 mek/L -- 25 mek/L>5 mek/L -- 04. Na HCO3 pH < 7 - 7,15. Faktor Presipitasi***Dosis Kecil 5 U IM *** Pemantauan dengan Urin

Suhendro 2008Pengukuran asam laktat perlu pada pengelolaan KADSerum laktat > 4 mmol/L petanda prognostik burukJika disertai kesadaran menurun prognostik burukPerlu pengelolaan yang ketat sejak awalPasang CVP segeraHidrasi dicapai dengan lebih cepat

Prevention (1)Better access to medical careIntensive patients educationEffective communication acute illnessReview sick-day managementInsulin treatmentBlood glucose goalTreat fever and infectionStart 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 UmumPencegahan terjadinya Hiperglikemiadengan mengelola DM sebaik-baiknyamencegah komplikasi kronik mencegah komplikasi akut DKAmenghindari 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 RSJikalau ada (misal di RS primer)dapat diberikan insulin, kemudian rujukMemerlukan perawatan yang cermat, segeradi RS dengan peralatan yang memadai

Hibiscus rosasinensisHatur Nuhun

*Every year many of patients with diabetes die from diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemia nonketotic coma (HHNC). DKA is mostly occur in type 1 diabetic patients, but may also occur in type 2 diabetics, while HHNC usually happen in adult type 2 diabetic. Both DKA and HHNC are emergencies diabetic complications that refer to metabolic decompensation derangement.1 * ****Diabetic ketoacidosis may be defined as the triad of hyperglycemia, acidosis and ketosis, mainly caused by insulin deficiency, either relative or absolute. *There are no epidemiological data regarding to DKA and HHNC in Indonesia. Hospital-based data showed that DKA still remained as a life threatening illness with high mortality rate. Additionally, its prevalence in type-2 diabetes was still increasing. In Cipto Mangunkusumo Hospital during a five months period (January-May 2002) there were 39 DKA episodes with a mortality rate of 15 %.5**In the meantime HHNC characterize by hyperglycemia, hyperosmolarity and without significant of ketosis. In many cases the clinical features of DKA and HHNC are overlap and may be observed simultaneously in the same individual; therefore we propose these conditions of metabolic decompensation in diabetes were different only in magnitude of dehydration and the severity of acidosis.2,3*There is a somewhat different in the management of DKA and HHNC, but we can divided the whole of treatment of these metabolic derangement into six categories. The first four of which should be carried out simultaneously: 2,6Replacement of fluid lossesCorrection of hyperglycemia and metabolic acidosis (in DKA patient) Replacement of electrolyte lossesDetection and treatment of precipitating factors and complicationsConversion to a durable diabetes management regimen after the correction of DKA and HHNCPrevention of recurrence conditions

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