A simplified approach to the DKA patient

1. MANAGEMENT OF DIABETIC
KETOACIDOSIS (DKA)
Dr./ Sahar H. Mostafa
Consultant of Internal Medicine
El-Mataria Teaching hospital-Cairo

3. Hyperglycemia
Ketonemia
Acidosis
DKA

4. Mechanism in DKA
Counter-Regulatory
Hormones
 GH
 Cortisol
 Catecholamines
 Glucagon
Insulin deficiency
 ↑HGP(+gluconeogenesis &
glycogenolysis)
 HYPERGLYCEMIA
 ↓Perpheral Glucose utilization
 HYPERGLYCEMIA
 ↓FFAs(+lipolysis & ketogenesis)
 KETONEMIA

5. HYPERGLYCEMIA 
Glucosuria
Osmotic diuresis ACIDOSIS
Dehydration
Mechanism in DKA

6. a. Blood glucose level > 250 mg/dl
b. Arterial pH < 7.3
c. Serum HCO3 level < 15 mEq/l
d. Moderate Ketonuria & Ketonemia
Diagnostic Criteria for DKA

7. The clinical severity of DKA
depends on the magnitude
of acidosis > the degree of
hyperglycemia
Pearl

8. Initial Evaluation-
Perform Immediately
 Good history and clinical examination,
including vital signs, chest, heart, abdomen,
neurological examination
 A flow sheet is essential: fluid intake and
output, state of hydration are noted
 If coma or shock ---> urinary catheter,
nasogastric tube
It should be noted that management of DKA is
individualized in every case

9. Initial Evaluation-
Perform Immediately
 Obtain baseline blood glucose and acetone
 ABG
 Urine glucose and acetone
 Serum Electrolytes
 Blood urea and serum creatinine
 CBC, with differential
 Complete urine examination
 CXR
 ECG
 Cultures(as needed)

10. Remember that:
 There may be more than one cause of
coma in the same patient:
 Diabetic coma and uremic coma, or
 Diabetic coma and Cerebrovascular
accident

11. Remember that:
 Vascular thrombosis occurs more with
hyperosmolar coma (HNKC)
 Abd pain (Periumbilical) may mimic
pancreatitis
(S. amylase is increased but not of pancreatic
origin]

12. Remember that:
 A precipitating cause of coma may be more
serious than DKA itself if neglected:
 Infection as UTI or chest infection,
 Myocardial infarction; so ECG is mandatory
 Mesenteric vascular occlusion/ intestinal
obstruction
 Cerebrovascular insult; so neurological
examination is essential

13. 1. Fluid replacement
Management

14. Fluid replacement
 Start with normal saline infusion as
follows:
1000 -2000 ml in the 1st 1-2 Hrs, for a 70
kg man
(15 – 20 ml/Kg/Hr)
(until BP stabilized and urine flow
established by 50-100 ml/hour)

15. Fluid replacement
 The patient can generally be viewed as being
10% dehydrated (TBW=60-63% body weight
in male & 52-55% in female)
 ½ of total calculated deficit should be
corrected over 1st 8 hours plus the urine and
any GIT loss. The second ½ over 16 hours

16. Fluid replacement
 Add 5% dextrose or dextrose in 0.45%
saline to IV fluids when Bl. glucose reach
 250 mg/dl at rate of 100-200ml/hour
 Fluid therapy depends upon degree of
dehydration, age, weight, presence of
cardiovascular diseases or other
associated conditions

17. 2. INSULIN
Management

18. We are using only regular insulin
The dose should be given by an insulin
syringe matching the insulin bottle
concentration

19. INSULIN
 An initial IV bolus 10-15 U may be given
(0.15 U/Kg as bolus)
 ICU dose = 0.1 U / kg / Hr of R insulin
 Syringe pump: 50 ml saline + 7 Units /h =
10-15 Drops / min

20. INSULIN
Another method, if ICU is not yet available:
 Bolus dose of R insulin= 0.3 U / Kg (½ of it IV & ½
IM)
{for a 70 kg man: 10 U IV and 10 U IM}
 Then  0.1 U/Kg/Hr
{for a 70 kg man: 7 U/Hr OR 15 U / 2 Hs) IM
Until disappearance of acetone from urine

21. INSULIN
Then, after resolution of DKA :
   Obtain blood Glucose every 4
hours and get the sliding scale of R
Insulin SC in 5 in 5 units increments for
every 50 mg blood glucose above 150 mg;
to a max. of 20 U
Overlap of IV and SC routes of R insulin may be
done for 1-2 hours to avoid return of ketosis

22. INSULIN
 Rate of fall of Bl glucose should  50 - 80
mg/dl/1st Hr
If this doesn’t occurs, you can double infusion
rate(if in ICU), OR you can give 10 U/Hr IV(In
case ICU not available)
 The serum glucose level is better not to be
allowed to fall to < 220 mg % during the first 4-
5 Hs of ttt

23. 3. POTASSIUM
Management

24. POTASSIUM
 Initially, best to wait for results of admission of
S. K+ levels
 Generally if anuria is present, hold off K+ until
urine flow is established
 Check for signs of Hypokalemia:
 Ileus
 Hyporeflexia
 Muscle weakness, cramps
 Abnormal ECG: low T, or appearance of U wave

25. POTASSIUM
 If Serum K+ = 3.3 – 5.5 mEq/l
 Add 20 - 30 mEq K Cl / 6 Hs {or roughly for
every one liter of IV Fluids}
 Usually 80-160 mEq is given in 1st 12 hours in adults
 If Serum K+ <3.3 mEq/L
 Hold Insulin
 Give 40 mEq K Cl / Hr; until K+ level reach  3.3

26. POTASSIUM
 If Serum K+  5.5 mEq/L
 Don’t give K+ supplementation
 Only Check level / 2 Hrs
 Oral K+ supplementation is continued later on;
because total body losses may reach up to 500 mEq / l
{ average urinary K+ loss of 3 - 7 mEq / kg occurs for Ds – Wks}

27. 4. BICARBONATE
Management

28. BICARBONATE
 HCO3 infusion is NOT needed in every case;
because it can provoke ↓K+ and shift of O2-Hb
dissociation curve to LEFT, impairing O2 delivery to
Ts
 HCO3 infusion is given Only if:
 Arterial ph < 7.0, or
 S. HCO3 < 8 mEq/l, or
 There is hyperventilation

29. BICARBONATE
Why it is unnecessary to correct pH if  7 with
HCO3 infusion ?
 It’s known that insulin will suppress lipolysis-->
↓FFAs delivered to the liver, thus --> blocking
ketogenesis
 The remaining ketoacids are cleared &/or oxidized,
thus --> regeneration of S. HCO3

30. BICARBONATE
 50-100 mEq of HCO3 are infused over 2 Hs
 pH 6.9 --> give 44 mEq (1 amp) over 1 H
 ph < 6.9 --> give 88 mEq (2 amp) over 2 Hs
 Until ph  7.0
Both: S. HCO3 and S. K+ should be checked
ever 4 hours until stability

31. 5. PHOSPHATE /
MAGNESIUM / CALCIUM
Management

32. PHOSPHATE / MAGNESIUM / CALCIUM
 N= 2.5-4.5 mg/dl
 Initially PO4 levels are high(shift from ICF),
then it drops during ttt to < 1 mg/dl with
potential life threatening risk
 Manifestations of critical hypophosphatemia:
 Respiratory and skeletal muscle weakness
 Hemolytic Anemia
 Shift of O2-Hb dissociation curve to LEFT
 TTT: Give 1/3 of K+ supplements as K PO4
 The remaining 2/3 as K Cl

33. PHOSPHATE / MAGNESIUM / CALCIUM
 N Ca+ = 4.4 - 5.2 mg/dl
 N Mg+ = 1.7 – 2.2 mg/dl
 Hypomagnesemia usually occurs due to
intracellular shift (with K+ & Ph) following
insulin ttt
 Hypercalcemia may be found in DKA (due to
increase Ca + efflux from bone as a result of
metabolic acidosis)
 Give calcium (if low) and magnesium
supplementation to compensate for their loss

34. Electrolyte disturbance
Heart failure due to:
 fluid overload
 acidosis (causing myocardiac depression)
 Shock due to:
a. Volume depletion
b. Acidosis
c. MI
d. Septicemia
KEEP AN EYE ON:

35.  Acute gastric dilatation or erosive gastritis
 Paralytic Ileus
 Cerebral edema (suspect if initial
improvement occurs then patient
deteriorates); Causes:
a. Rapid fall of glucose (decrease of blood glucose
should be by no more than 50-80 mg/dl/hour)
b. Rapid infusion of IV fluid
c. Too much HCO3
d. Hyponatremia
KEEP AN EYE ON:

36. ARDS with hypoxemia in the absence of
pneumonia or chronic pulmonary or heart
disease, due to rapid ↓↓colloid osmotic pressure
 ↑lung water with ↓of its compliance
Disequilibrium (13%), esp. in children,
due to correction with Hypotonic Solutions
KEEP AN EYE ON:

37. DIC
Hypoglycemia
Acute renal failure
Insulin resistance (try to increase insulin
dose)
KEEP AN EYE ON:

38. Associated lactic acidosis (due to
hypoperfusion)
Increased anion gap, due to the
metabolic acidosis (N= 8-12 mEq/l)
Anion Gap = Na – { Cl + HCO3} =
134 - { 108 +16 } = 10
KEEP AN EYE ON: