2. DKA IDI

Emergency in Diabetes Management :

“From Bedside to Clinical Practice

Sony Wibisono MDiabetes and Nutrition Centre - dr. Sutomo

Hospital Faculty of Medicine Airlangga University

Surabaya,11 April 2012

Topic of Presentation1. Why should we decrease blood

sugar in hospital hyperglycemia

2. Emergency in diabetes3. Treatment Emergency in

diabetes4. Insulin treatment in hospital

What evidence exists that in-hospital hyperglycemia is associated with adverse

outcomes?BG > 110 mg/dL with or without DM pts AMI : ↑mortality and CHF.FBG >126 mg/dL , RBG >200 mg/dL : 18 x in-hospital mortality, ↑ LOS (9 vs. 4.5 days).

Cardiac surgery suffer ↑ mortality, Deep-wound infections, > overall infection Critical illness conventional tx , > mortality, sepsis, ARF, and neuropathy

Poor outcome in patients with CVA: BG 110 - 126 mg/dl < 121 - 144 mg/dL < 140 mg/dLPregnancy complicated

ACE Position Statement on Inpatient Diabetes and Metabolic Control, Endocr Pract. 2004;10(No. 1)

Does reduction of hyperglycemia improve outcomes?

Reduces morbidity and mortality in acutely ill patients

• Intensive iv insulin inf (>110 mg/dL): mortality ↓ 34% (prospective trial)• Cardiac surgery pts : first 3 postop days : ↓ mortality of 57% and 50%• Long term survival rates AMI improved by 28% at 3.4 years. If normoglycemia • Deep sternal wound infection in cardiac surgery pts directly - ↑ BG postoperation

• ↓ 66%—to a rate equal to that seen in the non diabetic population• ↓ sepsis (46%), ARF (41%), transfusions (50%), and polyneuropathy (44%)• LOS ↓ 1 day each 50 mg/dL, ↓ average 3-day post op• Savings of more than $680/patientACE Position Statement on Inpatient Diabetes and Metabolic Control, Endocr Pract. 2004;10(No. 1)

To what extent does the impact of metabolic regulation extend beyond merely glycemic

regulation?

• Beneficial effects insulin– Inhibits lipolysis; ↑ FFA → poor outcomes, cardiac arrhythmias.

– Inhibits inflammatory GF (activator protein 1 and early growth response gene-1)

– Stimulates e-NOs, ↑ nitric oxide, → arterial vasodilation, other beneficial effects on oxidation and inflammation.

– Euglycemia/ near euglycemia, inhibit proinflammatory cytokines, adhesion molecules, and chemokines

What methods for such regulation should be used?

• Insulin, intravenous as a continuous or subcutaneous

• Indications for iv insulin therapy, but are not limited to:• Critical illness• Prolonged NPO (nothing by mouth) status in patients who are insulin deficient

• Peri operative period• After organ transplantation• Total par enteral nutrition therapy• Elevated glucose exacerbated by high-dose glucocorticoid therapy• Stroke• Labor and delivery• As a ose-finding strategy prior to conversion to subcutaneous (SQ) insulin therapy

• Other illnesses requiring prompt glucose control

Emergency in Diabetes1. Hypoglycemia2. Lacto acidosis3. Diabetic Keto Acidosis4. Hyperglycemia Hyperosmolar

State

*******

I IATROGENIC : 1 Insulin (Iatrogenic, Accidental)2 Sulphonylureas (Iatrogenic, Accidental)

II SPONTANEOUS :1 Pancreatic Causes,2 Extra Pancreatic Neoplasms

1 Pancreatic Causes :Insulinoma (Benign, Malignant, Multiple, Microadenomatosis)

Insular Hyperplasia ( Nesidioblastosis , Functional Hyperinsulinism )Pluriglandular Syndrome, MEN-Type IPancreatitis

2 Extra Pancreatic Neoplasms :IGF-2 secreting Sarcomas (Fibrosarcoma etc)

Primary IGF-2 secreting Carcinomas (Hepatic, Adrenal, Gastric)Small Cell Insulin-secreting Tumors

Various Causes of Hypoglycemia(Summarized : 2002)

Classification, Pathogenesis, and Treatment(Clinical Experience : Tjokroprawiro 2000,2002)

Hypoglycemia in Clinical Pratice

Non-DiabetogenicDiabetogenic

OHA-Induced

Honey Moon Period

- Very High C-peptide- Diabetic Diet- No Refined Cbh.- D-5% infusion

Insulin Induced

D-10% Infusion

Non-Honey Moon

- Normal C-peptide- Refined Cbh is allowed- D-10% infusion

DNA Mutation

- High C-peptide- D-5% infusion- Diabetic Diet

Hypertrophic

Insulinoma

- Very High C-Peptide- D-5% infusion- Diabetic Diet- CT-Scan etc.

Non-Pancreatic

(Hepatogenic-Nephrogenic)- D-10% infusion

- Refined Cbh is allowed

Pancreatic

R/ MedicalR/ Surgical

IGF-2 secretingTumors

or

R/ Surgical

PETUNJUK PRAKTIS TERAPI HIPOGLIKEMIA DENGAN RUMUS 3-2-1

PETUNJUK PRAKTIS TERAPI HIPOGLIKEMIA DENGAN RUMUS 3-2-1

Kadar GlukosaTerapi Hipoglikemia Dengan Rumus 3-2-1Glukosa mg/dl (Askandar Tjokroprawiro, 1996)1 Flakon = 25 ml

40% (10 gram)

30 mg/dl :Injeksi Intravena Dekstrosa 40%, bolus 3 FlakonRumus - 3

30-60 mg/dl :Injeksi Intravena Dekstrosa 40%, bolus 2 FlakonRumus - 2

60-100*) mg/dl :Injeksi Intravena Dekstrosa 40%, bolus 1 FlakonRumus - 1


State

Tx : Kausal

Dx : Hiperglikemia plus Anion Gap > 20 mEq(K + Na) - (Cl + CO2) > 20 mEq atau

(Na) - (Cl + CO2) > 15 mEq

KOMA ASIDOSIS ASAM LAKTAT (KAAL)(Tipe A dan Tipe B)

(Summarized : Tjokroprawiro 1991-1998)

ASAM LAKTAT + H2O + O2 B i k a r b o n a t

Terganggu

Infeksi, Shock, Peny. Kardiovaskuler/AngiopatiLFT-RFT , DM + Biguanide, Gg. Oksigenasi : PPOM, dll

KAAL - Tipe A

(Primer : Hipoksia)1. Semua jenis shock2. Decomp. Cordis3. Asfiksia4. Intoksikasi CO

KAAL - Tipe B

Kelainan Sistemik1. DM

2. Neoplasia3. RFT/LFT terganggu4. Konvulsi

Obat1. Biguanide2. Salisilat

3. Alkohol (Metanol, Etanol)4. Glukosa-Alkohol (Sorbitol, dll)


State

↑Growth Hormone↑Glucagon↑Cortisol

↑Catecholamine

Absolute def Insulin

Relative Insulin def

↑ Lipolisis

↑ FFA LIVER

↑ KETOGENESIS

KETOACIDOSIS

Glucose unitilization ↓

↑ proteolysis

Triacylglycerol

↓ protein sintesis

↑ gluconeogenic substrate

↑ gluconeogenesis

Abscent or minimalketogenesis

Hyperlipidemia

Hyperglycemia

Glucosuria(osmotic diuresis)Loss water and electrolytes

Dehidration

Impaired renal function

Hyperosmolarity HHS

DKA

Stress, infection and/or insuf insulin intake

↓ fluid intake

↑ glycogenolisis

(Krentz et al 1997, Marshall et al 1997, Tjokroprawiro 1991-1998)

HYPERGLYCEMIA HYPEROSMOLAR STATE (HHS)

(Krentz et al 1997, Marshall et al 1997, Tjokroprawiro 1991-1998)

Pathogenesis Diagnosis Therapy

Precipitating Factors :

1Thiazide2Glucose Drinks3Infection4Corticosteroid5Beta Blocker6Phenytoin7Cimetidine8Chlorpromazine

Pathophysiology

Grossly Elevated GlucagonRelative Insulin Deficiency

Sufficient Insulin to inhibit lipolysis

TETRALOGY HHS : 1H + 3 NO

Tetralogy + 5 = PENTALOGY HHS (Definite Dx)

Glucose (mg/dl) Ureum (mg/dl)

18 6Osm/l = 2x (Na + K) + +5

Supporting Findings :1(pH > 7.30)2Neurological Sign 3Prerenal uremia4Mental Impairment 5Severe Dehydration6More than 60 years old

+

+

Clinical Dx (Suspect):

1IH: Glycemia > 800 mg/dl 2NO: DM History or 3NO: Kussmaul , 4NO: Ketonuria or

(Tetralogy HHS)

+ +

1 Tx DKAPlasma Na <150 mEq/l

Normal Saline

Hypotonic Saline

b Plasma Na >150 mEq/l

2 a

Comparison of DKA to HHS

Am Fam Physician 2005;71:1723-30.

TREATMENT DKA & HHS

Complete initial evaluation, start IV fluids (1.0 L of 0.9 % NaCl per hour initialy) or 15 -20 ml/Kg

IV fluid

Insulin

Bicarbonate

potasium

Determine hydration status

Hypovolemic shock

Mild hypotensio

n

Cardiogenic shock

0.9 %NaCl (1 L/hr) or plasma expander

or both

Evaluate corrected Na+

Hemodynamic monitor

Serum Na+

lowSerum Na+ normal

Serum Na+

High

0.9 %NaCl (4-14ml/Kg/hr) depending hyration status

0.45 %NaCl (4-14 ml/Kg/hr) depending hydration status

When BG 150 – 250 mg/L. D5% with 0.45% NaCl and ↓ Insulin 0.05-0.1U/Kg/hr until keton – or Osm ≤320 mmol/kg

IV insulin infus

(0.1U/Kg/hr)

Check BG /hr, if does not fall ≤ 50 mg/l in 1st hr,

double dose hourly until BG fall 50-

70 mg/l

check BG / 4hr and start SC

insulin

If K+ < 3.3mmol/L,hold isnulin and give 40 mmol/L until K+≥3.3mmol/L

If K+≥5 mmol/,don’t give K, check K/2 hr

If K+≥ 3.3 - < 5 mmol/L, give 20-30 mmol K+/IV fluid

to maintain at 4-5 mmol/L

Check chemistry/2-4 hr until stable.

Look for precipatating

factor

Dilute NaBic 44.6

mmol) in 200 ml H2O.

Infuse at rate of

200ml/hour

After 1 hr hydrationpH < 7 pH ≥7

Repeat NaBic /

2hr until pH>7.

Monitor K

No NaBic

DKA TREATMENT


IV fluid

Insulin

potasium

Determine hydration status

Hypovolemic shock

Mild hypotensio

n

Cardiogenic shock

0.9 %NaCl (1 L/hr) or plasma expander

or both

Evaluate corrected Na+

Hemodynamic monitor

Serum Na+

lowSerum Na+ normal

Serum Na+

High

0.9 %NaCl (4-14ml/Kg/hr)

depending hyration status

0.45 %NaCl (4-14 ml/Kg/hr) depending

hydration status

When BG 150 – 250 mg/L change to D5% with 0.45% NaCl and decrease Insulin

0.05-0.1U/Kg/hr until keton – or Osm ≤320 mmol/kg

IV insulin infus

(0.1U/Kg/hr)



70 mg/l

After resolution of DKA or HHS,

check BG / 4hr and start SC insulin







factor

HHS TREATMENT

Am Fam Physician 2005;71:1723-30.

Strength of Recommendations*

(Askandar Tjokroprawiro, 1991-1998)Terapi KAD - Revisi 1998Terapi KAD - Revisi 1998

1 Rehidrasi :NaCl 0.9% atau RL, 2 L / 2 jam pertama, lalu 80 tt/mselama 4 jam, lalu 30 tt/m selama 18 jam (4-6 L/24 jam),

diteruskan sampai 24 jam berikutnya ( 20 tt/m) : Rumus 2,4,18-242 IDRIV :4-8 unit/jam i.v (Rumus Minus Satu)

FASE-I 3 Infus K+ :25 mEq (bila K+ = 3.0-3.5 mEq/l), 50 mEq (K+ = 2.5 - 3.0),per 24 jam 75 mEq (bila K+ = 2.0-2.5), dan 100 mEq (bila K+ < 2.0 mEq)

4 Infus BIK :bila pH < 7.2 - 7.3 atau BIK <12 mEq/l : 50-100 mEq dripdalam 2 jam (bolus BIK 50-100 mEq diberikan bila pH < 7.0)

5Antibiotika :up to date dan dosis adekuat

Glukosa Darah + 250 mg/dl atau reduksi +

1 Maintenance : NaCl 0.9% atau Pot. R (IR 4-8u) , Maltosa 10% (IR 6-12u) bergantian : 20 tt/m (Start Slow, Go Slow, Stop Slow)

FASE-II 2 Kalium : p.e (bila K+< 4 mEq/l) atau per os (air tomat/kaldu)3 IR : 3 x 8-12 U sc (ingat : Rumus Kali Dua)4 Makanan lunak Kbh kompleks per oral

Rumus : 2,80,30,20 ; Rumus 2,4,18,24 ; Minus Satu; Kali Dua; Rumus 5-1 ; Rumus 2,5-1 ;

(Askandar Tjokroprawiro, 1991-1998)Terapi HHS - Revisi 1998

1 Rehidrasi :NaCl 0.9% atau RL, 2 L / 2 jam pertama, lalu 80 tt/mselama 4 jam, lalu 30 tt/m selama 18 jam (4-6 L/24 jam),

diteruskan sampai 24 jam berikutnya ( 20 tt/m) : Rumus 2,4,18-242 IDRIV :4-8 unit/jam i.v (Rumus Minus Satu)

FASE-I 3 Infus K+ :25 mEq (bila K+ = 3.0-3.5 mEq/l), 50 mEq (K+ = 2.5 - 3.0),per 24 jam 75 mEq (bila K+ = 2.0-2.5), dan 100 mEq (bila K+ < 2.0 mEq)

4 :Antibiotikaup to date dan dosis adekuat

Glukosa Darah + 250 mg/dl atau reduksi +

1 Maintenance : NaCl 0.9% atau Pot. R (IR 4-8u) , Maltosa 10% (IR 6-12u) bergantian : 20 tt/m (Start Slow, Go Slow, Stop Slow)

FASE-II 2 Kalium : p.e (bila K+< 4 mEq/l) atau per os (air tomat/kaldu)3 IR : 3 x 8-12 U sc (ingat : Rumus Kali Dua)4 Makanan lunak Kbh kompleks per oral

Rumus : 2,80,30,20 ; Rumus 2,4,18,24 ; Minus Satu; Kali Dua; Rumus 5-1 ; Rumus 2,5-1 ;


Insulin

potasium

IV insulin bolus

(0.1U/Kg/hr)



70 mg/l

After resolution of DKA or HHS,

check BG / 4hr and start SC insulin







factor

IV insulin infus

(0.1U/Kg/hr)

REGULASI CEPAT DENGAN INSULIN

(Pengalaman Klinik : Askandar Tjokroprawiro, 1993, 1994, 1996)

Dapat dibagi menjadi :1. R.C. Intravena

2. R.C. Subkutan

Perlu diketahui, bahwa pada pelaksanaan RC (Regulasi Cepat), perlu diingat beberapa rumus antara lain :

1. Rumus Minus-Satu

2. Rumus Kali-Dua

2 00 - 300 1x 3 x 43 00 - 400 2x 3 x 64 00 - 500 3x 3 x 85 00 - 600 4x 3 x 106 00 - 700 5x 3 x 12

Rumus Minus Satu Rumus Kali Dua

6 Minus 1 = 5 6 Kali 2 = 12

Glukosa Awal Dosis Insulin Dosis RumatanSebelum R-C (mg/dl) Intravena a 4 U/jam Insulin Subkutan (unit)

Regulasi Cepat Intravena (RCI)(Tjokroprawiro 1987, 1993, 1994, 1995, 1996, 1997, 1998)

(Contoh : Kasus Glukosa Darah 650 mg/dl)Hiperglikemia >200 mg/dl

THANK YOU FOR YOUR ATTENTION

2. DKA IDI

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