Ketoacidosis Diabetic

Fauzia Noor Liani

Department of Internal Medicine

Ulin General Hospital – Lambung Mangkurat University School of Medicine
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Surabaya
 Introduction

Prevalence of diabetes in Indonesia  4.8% (2012),

DKA  the most common and serious acute
complication of DM,
•Patients with type 2 DM  develop DKA under stressful
conditions, such as trauma, surgery, or infections, ing or
reducing insulin dose
• 20% KAD patients has no trigger factor.

( Barski, 2012; Soewondo,2013 )

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 DEFINISI
• KAD adalah suatu keadaan di mana terdapat defisiensi
insulin absolut atau relatif dan peningkatan hormon kontra
regulator (glukagon, katekolamin, kortisol dan hormon
pertumbuhan) ; keadaan tersebut menyebabkan produksi
glukosa hati meningkat dan utilisasi glukosa oleh sel tubuh
menurun, dengan hasil akhir hiperglikemia.

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 Introduction...

The incidence DKA : USA  4.6 – 8 / 1000

patients DM.

(Savage,2011)

Insidence KAD in indonesia  no data,

limited from the hospital & particularly in
patients with type 2 DM.
(Gotera, 2010)

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DKA : insulin deficiency & ↑ counter-regulatory hormone
 disturbance metabolism: carbohydrate, protein & lipid
 ↑ catabolism with glucose production by the liver
(glycogenolysis & glyconeogenesis) & ↓ peripheral glucose
uptake  progressive hyperglycemia.

Triggers for DKA :

1. extreme stress : infection, myocardial ischemia,
surgical  40%,
2.  inadequate insulin treatment,
3. medications, such as corticosteroids.
(Savoldelli, 2010; Maletkovic, 2013)

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 Pathophysiology

Pathophysiology of diabetic ketoacidosis (DKA)

(Savoldelli, 2010)6
DIAGNOSIS KAD

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PATOFISIOLOGI

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 hyperglycemia, ketonemia, and
Triad of DKA
metabolic acidosis

Laboratory diagnostic criteria for DKA according to ADA

DKA

Mild Moderate Severe

Blood glucose (mg/dl) > 250 > 250 > 250

Serum pH < Serum 7.25 < 7.3 7.00 < 7.24 < 7.0

bicarbonate (mEq/L) 15 - 18 10 - <15 < 10

Ketonura + + +

Ketonemia + + +

Serum osmolality(mOsm/kg) variable variable variable

Anion gap >10 >12 >12

Mental status Alert Stupor/ drowsy coma

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(Gotera, 2010; Savoldelli, 2010; Smiley, 2011)
 Trauma and neuroendocrine stress response
surgery

↓insulin secretion ↑ counterregulatory hormones:

 ↑ catabolism, lipolysis
 ↓ glucose uptake
 stimulating glycogenolysis & gluconeogenesis

ketogenesis hyperglycemia

( Rhodes et al, 2005) diabetic ketoacidosis

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 management

There are many guidelines for the management

of DKA  should not be strictly
Therapy aims to correct the underlying
pathophysiological abnormalities fluid and
electrolyte balance, blood glucose levels, acid-
base disorders.
(Gotera, 2010; Perkeni, 2011)

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 DISCUSSION....

Fluid resuscitation  0.9 % NaCl 100 ml/kg or 5-8 L,

15-20 ml /kg/hour or more during the first hour ( ± 1 - 1,5
liters )  1 L in the next 2 hours  1 L / 4 hours,
Other authors  formula 2:2 , 4:80 , 18:30, 24:20
< 48 hours
CVP  fluid resuscitation  =//= fluid overload.
( Gotera , 2010; Savoldelli , 2010;Tjokroprawiro, 2012)

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Insulin  immediately: Dx & adequate rehydration (+)
Hypokalemia (-)  regular insulin 0.15 U/kg iv  0.1
U/kg/h (5 to 7 U/h).
Serum glucose ↓ ≤ 200 mg/dL  ↓ 0.02 - 0.05 U/kg/h.
RBG <80 m /dL  stop insulin 1 hour  continue
5% D 0.5 NS started when BG < 250 mg/dL.
(Gotera, 2010; PERKENI, 2011, Maletkovic, 2013)

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 DISCUSSION...
resolution hyperglycemic crisis & ability to eat : insulin
pump sc insulin (overlap 1 - 2 hours)
calculated  80% total dose iv insulin 50% Basal
insulin + 50 % bolus insulin,
prevent hypokalemia  Adding 20-30 mEq potassium to
each liter of infused fluid  additional doses may be
necessary. (Chaithongdi, 2011; PERKENI, 2011)

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In most DKA, metabolic acidosis  control : fluid
replacement & insulin therapy;
severe cases: pH <6.9 alkali therapy may be indicated
Bicarbonate 1-2 mEq/kg over 1- 2 hours.
(Savoldelli, 2010)

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Complications & resolution of DKA

Complications >>  pulmonal edema, hypertrigliserida,

iatrogenic complication >> Hypoglycemia and
hypokalemia  insulin & bicarbonat tx  monitoring

blood glucose <200 mg/dL and two

Criteria for the of the following:
resolution of  serum bicarbonate > 15 mEq/L,
 venous pH > 7.3,
DKA:  anion gap <12 mEq/L

(Savoldelli, 2010; Gotera, 2010; Chaithongdi, 2011)

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 PROGNOSIS
Outcomes  underlying precipitating illness, the initial
biochemical data, & systemic manifestations.
mortality  4.1%
predictor of mortality  age>>, coma, hypotension,
serious illness, & altered mental status
(Barski, 2012)

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