Diabetic ketoacidosis managment

1. DIABETIC KETOACIDOSIS
PRESENTED BY:
DR. Eyad Hamad Miskawi
supervised by : Dr. Eyas Saleh

2. Hyperglycemia
Ketosis
Acidosis
*
Definition of Diabetic Ketoacidosis*
2

3. Pathogenesis of DKA
Insulin
Deficiency
Beta-cell
failure
D/C
Insulin
Glucotoxicity

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

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

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

7. 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

8. 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

9. Clinical Presentation of DKA
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.

10. Causes of DKA
• Stressful precipitating event that results in
increased catecholamines, cortisol, glucagon.
 Infection (pneumonia, UTI)
 Alcohol
 Stroke
 Myocardial Infarction
 Pancreatitis
 Trauma
 Medications (steroids)
 Non-compliance with insulin

11. • Immediate determination of blood glucose by finger
stick, and serum ketones (3-BH) by finger stick or
urinary ketones.
• Laboratory studies:
 ABG’s
 CBC with differential
 CMP (glucose, electrolytes, bicarbonate, BUN, creatinine)
 Serum ketones
 Urinalysis
 Bacterial cultures*
 Cardiac enzymes*
Initial Laboratory Studies
* If clinically indicated

12. Replacement of fluids losses
Correction of hyperglycemia/metabolic
acidosis
Replacement of electrolytes losses
Detection and treatment of precipitating
causes
Conversion to a maintenance diabetes
regimen (prevention of recurrence)
Management of DKA

13. Fluid Therapy
• Assume 10-15% dehydration
• Begin with a 10-20 ml/kg bolus of NS
• Replace calculated deficit evenly over 36 hours -
generally 1.5 x maintenance for the next several
hours is appropriate
• Do not exceed 40ml /kg in the initial 4 hours
• Double bag system
 NS at 1.5 x M until glucose below 300 mg/dl
 D10 NS to be mixed with NS to achieve desired
glucose concentration

14. Insulin bolus ??
•Insulin bolus or not?
• Insulin should be started about an hour after IV fluid
replacement is started to allow for checking
potassium levels and because insulin may be more
dangerous and less effective before some fluid
replacement has been obtained.
• Although the incidence of life-threatening
hypokalemia due to aggressive insulin administration
is very low, there is little to no advantage in starting
insulin prior to rehydration and evaluation of serum
potassium levels. Initial bolus of insulin does not
change overall management of DKA

15. Insulin Therapy
• IV infusion with basal rate 0.1 U/kg/hr
• Ideal glucose decline is about 50-100 mg/hr
• Continue insulin until urinary (blood) ketones are cleared
and anion gap is closed

16. Blood Glucose monitoring in DKA
• Check initial blood glucose q1h.Goal
decrease in blood glucose is 50-75mg/dl/hr
• Once stable(3consecutie values decrease in
target range)change blood glucose
monitoringq2h.Resume q1h blood glucose
monitoring for each change in the insulin
infusion rate.
• Add dextrose5% to IV fluid when blood
glucose <250mg/dl.
• For DKA goal blood glucose 150-200mg/dl
until anion gap close.

17. CHANGING THE INSULIN
INFUSION RATE
• Decrease IV insulin by 50%if blood glucose
decrease by >100mg/dl/hr in any 1hr period
• Increase insulin drip by 50%/hr if change in
blood glucose is <50mg/dl/hr
• When blood glucose decrease to 250mg/dl
insulin infusion may need to be decrease
50% to maintain glucose at target levels(150-
200mg/dl).

18. Transition to Subcutaneous Insulin
Patients with DKA should be treated with IV insulin until
ketoacidosis is resolved.
 Criteria for resolution of DKACriteria for resolution of DKA::
 BGBG ≤≤ 200 mg/dL200 mg/dL
 Serum bicarbonate level ≥ 18 mEq/LSerum bicarbonate level ≥ 18 mEq/L
 Venous pH ≥ 7.3 and anion gap closedVenous pH ≥ 7.3 and anion gap closed

19. WHEN TO STOP IV INSULIN
• When the condition is stable, pH exceeds 7.3,
and bicarbonate is greater than 18 mEq/L,
the patient is allowed to eat a meal preceded
by the usual subcutaneous (SC) dose of
regular insulin.

20. 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

21. Sodium
Pseudohyponatremia, add 1.6 mEq of Na to every
100mg/dL of glucose above normal
Expect that the Na+
level will rise during treatment
If Na+
does not rise, true hyponatremia may be present (risk
of cerebral edema) and should be treated

22. Bicarbonate
• Bicarbonate should be used only when there is severe
depression of the circulatory system or cellular metabolism
• Not recommended unless pH <7.0 and bicarbonate < 5
mEq/l, not even then, unless above true
∀ → 44.6 mEq in 500 ml 0.45% saline over 1 h until pH > 7.0
• Bicarbonate administration leads to increased cerebral
acidosis
• HCO3
-
+ H+
= CO2 + H2O.
 Bicarbonate passes the BBB slowly
 CO2 diffuses freely
 exacerbating cerebral acidosis and cerebral depression

23. Bicarbonate
• Bicarbonate should be used only when there is severe
depression of the circulatory system or cellular metabolism
• Not recommended unless pH <7.0, not even then, unless
above true
• Bicarbonate administration leads to increased cerebral
acidosis
• HCO3
-
+ H+
= CO2 + H2O.
 Bicarbonate passes the BBB slowly
 CO2 diffuses freely
 exacerbating cerebral acidosis and cerebral depression

24. • A 10 y/o male (~30 kg) presents to the ED with a
one-day history of emesis and lethargy.
• Vitals show T 37C, HR 110, RR 25, BP 99/65.
Patient is lethargic, but oriented. Exam reveals the
odor of acetone on the breath, dry lips, but otherwise
unremarkable
• Labs: pH 7.05, PaCO2 20, HCO3 9 , PaO2 100, BE
-20, Na+
133, K +
5.2, Cl 96, CO2 8, BS 600. Urine
shows 4+ glucose and large ketones
Case Scenario #1

25. • How much fluid would you administer as a bolus?
• What is the value of anion gap ?
• Would you administer bicarbonate?
• What is the “true” serum sodium?
• How much insulin would you administer?
• What IVF would you start? At what rate?
Case Scenario #1

26. Answers
• 600 cc over 20 min
• 28 high
• No cardiovascular collapse and therefore
there is no justification for the administration
of bicarbonate.
• 133 +(600-100)= 142
• 0.1*30= 3u/hr
• 1.5*(10*100+10*50+10*20)= 2550cc q 24 hrs

27. Pearls on DKA
• Diagnosis : pH < 7.3 , RBS > 300, Hco3 < 15
• Correct dehydration over 48 hours
• Bolus fluid only with hemodynamic
compromise
• Sodium bicarbonate when pH <7.0 and Hco3
< 5 and circulatory compromised .
• No rule of insulin bolus .
• Monitor K level while you are treating .
• Remember to find the cause and treat it.

28. THANK YOU