9.Keto Asidosis Diabetik

7/29/2019 9.Keto Asidosis Diabetik

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Keto-Asidosis Diabetik

Pradana Soewondo

Division of Endocrinology and Metabolism,Department of Medicine, School of Medicine

University of Indonesia


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Diabetic Complications

Diabetic Ketoacidosis = DKA

Hyperosmolar Hyperglycemia

Nonketoric Coma = HHNC

RetinopathyNephropathy

Neuropathy

Macroangiopathy

Chronic :Acute :

Microangiopathy

CADPVD

Stroke

Hypoglycemia

Metabolic Decompensation


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Hyper-

glycemia Acidosis

Ketosis

DKA

Kitabchi and Wall

Hyperglycemia statesDM

HHNC

IGT

Stress

Metabolic Acidosis statesLactic acidosis

Hyperchloremic acidosis

Salicylism

Uremic acidosis

Drug-inducedacidosis

Ketotic statesKetotic hypoglycemia

Alkaholic ketotis

Starvation ketosis


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DKA Episode and Mortality Rate at Dr. CiptoMangunkusumo Hospital, Jakarta

Year Number of Cases Mortality rate %

1983-84 (9 months) 14 31,4

1984-88 (48 months) 55 40

1995 (12 months) 17 -

1997 (6 months) 23 18,7

1998-99 (12 months) 37 51

2002 (5 months) 39 15


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DKA HHNC

DKA HHNC


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PATOGENESISKAD


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LIPOLYSIS

A C E T O A C E T A T E

FATTY ACYL CoA

A C E T O N E3- H Y D R O X YB U T Y R A T E

MITOCHONDRION

K E T O N B O D I E S

HEPATOCYTE

CYTOSOL

FFA

Catecholamine

Growth Hormone

Insulin

SHUTTL

E

Insulin

FATTY ACYL CoA

Glucagon

FATTY ACYL CoA

CoA

KETOGEN

ESIS


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Triglyceride

Malonyl CoA

CPT 1Carnitine

Acyl Co A

Glycerol-3-P

Glucagon

Acetyl CoA

Insulin

Acetyl CoA

Acyl carnitine

Acyl carnitine

3 Hydroxybuyrate

3-HMG CoA

Acetoacetyl CoAAcyl Co A

Acetoacetate

CarnitineCPT 2

Acetone

b oxidat ion

+

--outer

inner

mitochondrial

membrane

Krebs

cycle

CYTOSOL

MITOCHON-DRION

Fatty acid


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DKA HHNC

Kadar Hormon dan FFA pada KAD


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Clinical Features of DKA

Abdominal pain

Leg cramps

Nausea and vomiting

Confusion and

drowsiness

Coma

Polyuria and nocturia

Weight loss

Weakness

Blurred vision

Kussmaul respiration


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Precipitating Factors of DKA & HHNC

Infection

Cerebro vascular

accident

Pancreatitis

Myocardial infarction

Trauma

Medication

Newly type 1

diabetes

Discontinuation of or

inadequate insulin

Substance abuse

Not found


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Average Water and Electrolyte Deficits in DKA

Water (liters) 5 - 7 liters

Sodium (mmol) 500

Chloride (mmol) 350

Potassium (mmol) 300 - 1000

Calcium (mmol) 50 - 100

Phosphate (mmol) 50 - 100

Magnesium (mmol) 25 - 50


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PrincipalManagement

of DKAand HHNC


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Hour Hydration Insulin K+Correction HCO3- correction

0 guyur 50 mEq per If pH

guyur six hour 7.1

guyur Start hour 2iv bolus iv,

Cont by infusion

dst dst dst

Management of DKAat Cipto Mangunkusumo Hospital, Jakarta

A B C D E

Lihat perincian pada slide berikut (per kolom)


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Jam 0 2 kolf 1/2 jam1 1 kolf 1/2 jam Guyur dengan NaCl 0,9%2 1 kolf 1 jam3 1 kolf 2 jam4 dst. bergantung kebutuhan

Sebaiknya dimonitor dengan CVP.

Jumlah cairan per 15 jam sekitar 5 liter.

Bila kadar Na+ > 155 mEq/L (osmolarity >350 mosm/L) gunakan1/2 n NaCl.

Bila kadar glukose darah < 200 mg/dl NaCl diganti dextrose 5%.

Rehidrasi B


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Pemberian Insulin C

Mulai jam ke 2 dengan bolus 180 mU/kg BB (7-10 U/jam) I.V

dilanjutkan dengan drip 90mU/kgBB/jam dalam NaCl 0,9%(3 4 U/jam)

Bila kadar gd < 200mg/dl kecepatan drip insulin dikurangisetengahnya menjadi 45mU/kg/jam (1,5 2 U/jam)

Bila kadar gd stabil 200-300mg/dl, drip 1 U/jam + slidingscale tiap 6 jam:

gd 350 mg/dl 20 unit

Bila pasien sudah bisa makan dan gd stabil dengan sliding

scale rutin 3 kali sehari dengan dosis tetap


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Koreksi K+ D

Pada jam 0 diberikan KCl 50 mEq per 6 jam dengan drip dalaminfusSetelah 6 jam di cek lagi kadar K+ Bila kadar K+ (mEq/L):

< 3 3-4,5 4,5-6 >6

75 50 25 0

mEq/ mEq/ mEq/6 jam 6 jam 6 jam

Bila sudah sadar, beri K+ per oral selama seminggu


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The Benefit of 3HB Measurement within 24hours management of DKA at RSCM Jakarta

Ika P, Soewondo P et al. RSCM, Jakarta 2001.

OBJECTIVE To observe the benefit of 3HB in 24 hour management of

DKA.

To describe the changing of parameter metabolic variable

during the first 24 hours in the management of DKA

METHOD

Hospital based, observational study, enrolliring DKA patients

19 from 39 DKA patients participated in this study

January-May 2002


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Enrollement

39 DKA patients

20 excluded 19 included

4 patients died

within 24 hours

15 patients

completely of study

Serial measurement of

Blood glucose, BGA,

AcAc, 3HB, Electrolyte

every 6 hours


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Measurements at presentation of DKA

N 19

Age (years) 48.16 12.51

Sex (M/F) 8/11

Blood Glucose 383 80.30

Arterial pH 7.24 0.21

Blood pCO2 18.87 7.19

Blood

bicarbonate

10.17 6.37

BUN 43.24 40.18

Serum Creatinine 2.48

Serum AcAc (+/-) +++ (Median)

Blood 3HB (mmol/L) 3.31 2.41

K + (mmol/L) 4.52 0.92

Na + (mmol/L) 127.1 9.92


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Changes of 3HB and AcAc in 24 hours

Hours

241812620

3,5

3,0

2,5

2,0

1,5

1,0

,5

0,0

3,0

2,0

1,0

0,0

3HB

AcAc


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7.3

7.2 art. blood pH

241812620

25

20

15

10

5

0

Blood 3HB

Serum AcAc

pCO2

HCO3

Anion Gap

BG (mmol/l)

Observ

asi24jam

pH darah

glucose

pCO2

HCO3

3HB


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0

2

6

12

18

24

Hour

Correlation 3HB and Blood pH

0.00 2.00 4.00 6.00

3HB

6.80

7.00

7.20

7.40

pH


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0

2

6

12

18

24

Hour

Correlation 3HB and Blood Bicarbonate

0.00 2.00 4.00 6.00

3HB

5.00

10.00

15.00

20.00

25.00

HCO3


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0

2

6

12

18

24

Hour

Correlation 3HB and Anion Gap

0.00 2.00 4.00 6.00

3HB

0.00

10.00

20.00

30.00

Anion

Gap


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Kesimpulan

KAD dan HHNK komplikasi akut DM dengan angka

kesakitan dan kematian yang tinggi.

Patogenesis KAD dan HHNK defisiensi insulin dan

peningkatan kadar hormon kontraregulator insulin.

Faktor pencetus utama Infeksi

Pemeriksaan benda keton - 3HB secara bedsite dapat

mempercepat diagnosis KAD bahkan dapat mencegah

KAD pada pasien DM saat sakit/demam.

Evaluasi 3HB serial membantu dalam pengelolaan

KAD - peralihan terapi titerasi insulin ke dosis tetap.


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9.Keto Asidosis Diabetik