hiperglikemic crisis in diabetes
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Hyperglycemic Crises in Diabetes
Case Discussion
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LEARNING ISSUES
• PATHOGENESIS• PRECIPITATING FACTORS• CASE REPORT
– DIAGNOSIS• History and physical examination• Laboratory findings
– TREATMENT
• COMPLICATIONS• PREVENTION
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KRISIS HIPERGLIKEMIA
• Komplikasi akut• Penyebab Krisis Hiperglikemia
tersering:
• KAD (Keto Asidosis Diabetikum)• HONK (Hiper Osmoler Non Ketotik)
(ADA, 2004)
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KRISIS HIPERGLIKEMIA
• KAD– Penyebab tersering
krisis hiperglikemia– Dapat mengenai DMT1
atau DMT2– 25% kasus baru DMT1– 2 / 10 kasus
DMT2/tahun– Mortalitas < 5% pada
senter yang maju– Prognosis jelek pada
manula, hipotensi
• HONK – 30% dari keadaan
darurat hiperglikemia– mortalitas tinggi 33%– Prognosis jelek pada
manula atau adanya hipotensi
(Krentz et al., 1997; Marshall et al., 1997;ADA,2004)
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PATOGENESIS KAD
• Hormon Insulin rendah
• Disertai Hormon Kontra Insulin – Glukagon
– Katekolamin
– Kortisol
– Growth hormon
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INSULIN KONTRA INSULIN
PATOGENESIS KAD
LIPOLISIS
OKSIDASI ASAM LEMAK
ASETO ASETAT & - OH BUTIRAT
KETONEMIA ASIDOSIS
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FAKTOR PENCETUS KAD INSULIN
HIPERGLIKEMIA PEMECAHAN JARINGAN LEMAK
HYPEROSMOLARITY ASAM LEMAK BEBAS
DIUREUSIS OSMOTIK OKSIDASI
EKSKRESI GLUKOSA URINE PEMBENTUKANKETON
PENURUNAN VOLUME
ASIDOSIS KETOSIS
KAD
KEASAMAN DARAH
PENINGKATAN URINE
K+
AcetoacetateBeta-Hydroxybutyrate
acetone
glucagon
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PATOFISIOLOGI HONK
DEFISIENSI INSULIN
Glycogenolysis Gluconeogenesis
PRODUKSI GLUKOSA HEPAR
PENGGUNAAN GLUKOSA TERGANGGU
Hyperglycemia
DIURESIS OSMOTIK
PENGGANTIAN CAIRANTIDAK ADEKUAT
PENURUNAN VOLUME CAIRAN INTRAVASKULER DALAM JUMLAH BESAR
PENGGANTIAN CAIRANTIDAK ADEKUAT
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TIDAK ADANYA KETOSIS PADA HONK ADA 3 SEBAB YANG DAPAT MENEKAN LIPOLISIS:
1. Insulin masih cukup menekan lipolisis
2. Hiperosmolaritas yang berat
3. Respons yang kurang dari Hormon Katabolik (Katekolamin, Kortisol)
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KONSEKUENSI KAD & HONK
–GLUKOSURIA
–DIURESIS OSMOTIK
–CAIRAN TUBUH
–KALIUM
–NATRIUM
–ELEKTROLIT LAINNYA
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DIAGNOSIS BANDING
• Starvation Ketosis• Alcoholic Ketosis (AKA)• high–anion gap metabolic acidosis,
(lactic acidosis) • Efek obat-obatan
– salicylate, methanol, ethylene glycol, and paraldehyde, and
• Gagal ginjal kronik
ADA, 2004
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LEARNING ISSUES
• PATHOGENESIS• PRECIPITATING FACTORS• CASE REPORT
– DIAGNOSIS• History and physical examination• Laboratory findings
– TREATMENT
• COMPLICATIONS• PREVENTION
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CASE 1
Ny R / 44 tahun
Keluhan Utama: Tidak
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KRITERIA Dx KAD & HONK
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OSMOLALITAS
Calculated Osmolality = 2 (Na) + Glucose + BUN 18 2,8
(Na dalam meq/I; Glucose & BUN dalam mg/dl)
• Measured Serum Osmolality (Osmometer)(normal ± 290 mOsm/I)
• Calculated Serum Osmolality dengan rumus:
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OSMOLAR GAP & ANION GAP
Osmolar Gap = Measured – Calculated Osmolality
Anion Gap = (Na + K) – (CI – CO2)(Normal 8-12 meq/I)
Dx klinik Lakto Asidosis (KLA) apabila:Glukosa Darah 250 mg/dlAnion Gap > 15-20 meq/I
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DEFISIT PADA KAD & HONK
KAD HONK
Total air (L)
Air (ml/kg)
Na+ (mEq/kg)
Cl- (mEq/kg)
K+ (mEq/kg)
PO4 (mmol/kg)
Mg++(mEq/kg)
Ca++ (mEq/kg)
6
100
7-10
3-5
3-5
5-7
1-2
1-2
9
100-200
5-13
5-15
4-6
3-7
1-2
1-2
Dikutip: ADA, 2004
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PENGELOLAAN KAD (ADA, 2004)
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PENGELOLAAN KAD (ADA, 2004)
KALIUMK < 3,3 mEq/L, Stop Insulin
•Koreksi K 40 mEq per jam s/d K > 3,3 mEq/L
(2/3 KCl dan 1/3 KPO4)
K > 5 mEq/L
•Stop K
•Check K tiap 2 jam
K > 3,3 – < 5 mEq/L
•Koreksi 20 – 30 mEq/L per liter cairan
•Pertahankan K 4 – 5 mEq/L
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PENGELOLAAN KAD (ADA, 2004)Natrium Bikarbonat
pH < 6,9 pH < 6,9 – 7,0 pH > 7
NaHCO3 (100 mmol) diencerkan pada 400 ml H2O, per infus 200 ml / jam
NaHCO3 (50 mmol) diencerkan pada 200 ml H2O, per infus 200 ml / jam
Tanpa NaHCO3
Ulangi HCO3 tiap 2 jam sampai pH > 7
Pantau serum K
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PENGELOLAAN KAD (ADA, 2004)
JIKA GLUKOSA SUDAH 250 MG/DL
• Dextrose 5% ganti dengan NaCL 0,45% (150/200 ml/jam)• Insulin 0,05-0,1 U/kg/jam per infus atau 5 - 10 U SC/2jam•Pertahankan glukosa 150 – 200 mg/dl
•Pemantauan tiap 2 jam: elektrolit, serum kreatinin, BUN dan glukosa
•Jika pasien NPO, teruskan Insulin IV, dan Insulin suplemen
•Jika pasien mulai makan dapat diberikan insulin dosis multipel
•Insulin infus baru dihentikan jika insulin SC telah 1 – 2 jam
•Eksplorasi faktor pencetus
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HONK (ADA, 2005)
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LEMBAR MONITORING
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LEMBAR MONITORING
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Kelainan EKG Hipokalemia
prolongation of QT intervalST segment depression
Flat or diphasic T wavesProminent U waves
Prolongation of PR intervalSinoatrial block
Konsekuensi Hipokalemia:
•Aritmia•Cardiac arrest•Otot pernafasan lemah
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TERIMA KASIH