Dr Ifraim Sajid house officer allama iqbal medical college lahore/jinnah hospital lahore presentation on DKA comprehensive and easy to digest. presentation was prepared on 16 dec 2015. one thing must be remembered that DKA is life threatening but reversible complication of more un controled diabetes,,,,,early and aggressive management can save lives ......... always assume that a child is 10% dehydrated ,blood sugar should be monitored hourly and ABGs and serum eletrolytes should be monitored 2-4 hourly.......... prevention should be done regarding development of cerebral edema,because in that case survival rate is 15%. treating under lying infection is very important part of management ..... thanks in anticipation Dr ifraim sajid house officer ,jinnah hospital lahore

2.  A state of absolute or relative insulin deficiency
aggravated and followed by
 hyperglycemia, dehydration, and acidosis-
producing derangements in metabolism, including
production of serum acetone.
 It is the presenting symptom for ~ 25% of Type I
Diabetics.

3. Hyperglycemia
Ketosis
Acidosis
*
3

4. Diagnostic Criteria for DKA
DKA
Mild Moderate Severe
Plasma glucose (mg/dl)
pH
Anion gap
Bicarbonate (mEq/l)
Urine ketones*
Serum ketones*
Effective serum Osmol
(mOsm/kg)†
Alteration in sensoria
or mental obtundation
>250
7.25-7.3
>10
15-18
positive
positive
variable
alert
>250
7.0-<7.24
>12
10- <15
positive
positive
variable
alert/
drowsy
>250
<7.0
>12
<10
positive
positive
variable
stupor/
coma

5. Insulin
deficiency
Increased
glucagon
GH
cortisol
catecholamines
Pathogenesis of DKA

6. Carbohydrate Metabolism in DKA
Relative or absolute insulin deficiency
glucose output
glycogenolysis
liver
glucose uptake
muscle

7. Increased Glucose Production in DKA
Gluconeogenesis Glucose
Protein breakdownLipolysis
Glycerol Amino acids
Lactate
TG
Activity of gluconeogenic
enzymes
(PEPCK, PC, PFK)

8. Increased Production of Ketones in DKA
Lipolysis
FFA Glycerol
Ketogenesis
B-OH-B
Acetoacetate
TG

9. Pathogenesis of DKA
Liver
Increased
glucose
production
Decreased
glucose
uptake
Peripheral
tissue
HYPERGLYCEMIA
Increased
release
FFA
Increased
ketogenesis
Adipose
tissue
Liver
KETOACIDOSIS
Osmotic diuresis
Volume depletion Metabolic acidosis
Decreased alkali reserve

10. Sign
Hypothermia
Tachycardia
Tachypnea
Kussmaul breathing
Ileus
Acetone breath
Altered sensorium
Symptoms
Polydipsia
Polyuria
Weakness
Weight loss
Nausea
Vomiting
Abdominal pain
The onset of DKA is usually relative short, ranging from hours
to a day or two.

11.  Infection (pneumonia, UTI)
 Non-compliance with insulin
 Trauma
 Medications (steroids)
 Pancreatitis

12.  History and physical examination
 Secure patient’s ABC
 Mental status
 Cardiovascular-renal status
 Source of infection
 Evaluation of volume and hydration status
 Laboratory studies

13. Blood glucose
ABGs
Serum ketones
Urinary ketones
Urine complete
S osmolality &anion gap
Blood culture
CBC
Chest Xray

14. Serum Sodium
 Hyponatremia is common in patients with DKA
H2O
H2O
H2O
Serum glucose
Na+
H2O
Correction of Serum sodium:
Corrected Na+
= [Na+
] 1.6 x glucose (mg/dl) – 100
100

15. Serum Potassium
 Admission serum potassium is frequently elevated (due to
a shift of K-
from the intracellular to the extracellular space)
K+
Osmolality
Acidosis
K+
Insulin
regulates
Activity of
Na+
/K+
pump
Na+
K-
K+
K+
K+

16.  Anion gap can be measured as
 AG=[(Na)-(Hco3+CL)]

17. Most of the patient are 5-10%
dehydrated(polyurea,vomiting,hyperventilation
and diarrhea)
Normal saline and R/L are given
ALWAYS ASSUME THAT A CHILD IS 10%
DEHYDRATED

18.  Fluid replacement =fluid deficit +maintenace
fluid
 Fluid deficit=100ml/kg
 Mantenance fluid;
 100ml/kg upto10yrz
 1000+50ml/kg over 10 kg
 1500+20ml/kg >20kg

19.  Should be given as continuous IV infusion
 Dose is 0.1U/kg
 Insuline infusion is given separately from the
replacement fluids so the rates can be
calculated separately
 If blood glucose decreases to 250mg/dl glucose
is given as 5% dextrose

20. time therapy
1st
hour fluid 10-20ml/kg IV bolus
NS or RL
Insuliin drip at 0.05-
0.1U/kg/hr
From 2nd
hour untill
DKA resolution
IV
rate=85ml/kg+mainten
ane –bolus infusion/
23hr
0.45 NS + cont insuline
drip
20meq/L KCL
5%dextrose if BSR<250

21. Monitor urine output,heart rate,blood pressure
and respiratory status.
CARE must b taken in patient with CCF and
kidney disease.

22. Blood glucose ………1H*
S/E 2-4 hrly
ABGs 2-4 hrly( first 24 hrs)

23. Intravenous Insulin Therapy in DKA
I.V. Bolus: 0.1 U/kg
I.V. drip: 0.1 U/kg/h
Glucose < 250 mg/dl and
HCO3 > 15 mmol/l, then,
I.V. drip: 0.05 – 0.1 U/kg/h
Until c0rrection of anion gap

24. Is replaced when there is severe acidosis (ph <7.0-
7.1
Biarbonate is given in adose of 1-2
meq/kg over 2 hrs

25. Potassium replacement
K+
= > 5.5 mEq/l; no supplemental is required
K+
= 4 - 5 mEq/l; 20 mEq/L of replacement fluid
K+
= 3 - 4 mEq/l; 40 mEq/L of replacement fluid
If admission K+
= <3 mEq/l give 10-20 mEq/h until
K+
>3 mEq/l, then add 40 mEq/L to replacement fluid

26.  Appropriate antiobiotics are given to control
any infection

27.  Patients with DKA should be treated with IV insulin until
ketoacidosis is resolved.
 Criteria for resolution of DKACriteria for resolution of DKA::
 BSRBSR 180-240mg/dl180-240mg/dl
 Serum bicarbonate level ≥ 18 mEq/LSerum bicarbonate level ≥ 18 mEq/L
 pH ≥ 7.3pH ≥ 7.3
 Pt is conscious and taking oralyPt is conscious and taking oraly
 Any identified precipitating fators (e.g infection)Any identified precipitating fators (e.g infection)
have been traeatedhave been traeated

28. 1- shock
2-thromboembolism
3-pulmonary edema
4-cerebral edema

29. Cerebral edema;
Mechanism: The brain adapts by producing intracellular
osmoles (idiogenic osmoles) which stabilize the brain
cells from shrinking while the DKA was developing.
When the hyperosmolarity is rapidly corrected, the
brain becomes hypertonic towards the extracellular
fluids → water flows into the cells → cerebral edema

30.  Diabetic Ketoacidosis is a common, serious
and expensive complication in patients with
type 1 and type 2 diabetes
 Prevention of metabolic decompensation
through patient education, strict surveillance of
glucose homeostasis and aggressive diabetes
management might reduce the high morbidity
and mortality associated with diabetic
ketoacidosis
Summary