Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes caused by relative or absolute insulin deficiency that results in hyperglycemia, ketosis, and acidosis. It occurs most often in patients with type 1 diabetes but can also affect those with type 2 diabetes. Treatment of DKA involves fluid resuscitation, intravenous insulin therapy, electrolyte replacement, and monitoring of glucose and acid-base levels until the condition is resolved. Complications can include hypokalemia, hypoglycemia, cerebral edema, and complications related to underlying illnesses. Strict diabetes management and patient education are needed to prevent DKA.

1. DIABETIC KETOACIDOSIS
IN ICU
PRESENTED BY:
DR. ZEENAT YASMEEN
ICU RESIDENT

2. Diabetic Ketoacidosis (DKA)
• 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.
• Can occur in both Type I Diabetes and Type II
Diabetes
In type II diabetics with insulin deficiency/dependence
• It is the presenting symptom for ~ 25% of Type I
Diabetics.

3. Hyperglycemia
Ketosis
Acidosis
*
Definition of Diabetic Ketoacidosis*
3

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

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 breakdown
Lipolysis
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. 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

11. 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.

12. 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

13. Initial Clinical Evaluation
• History and physical examination
Secure patient’s ABC
Mental status
Cardiovascular-renal status
Source of infection
• Evaluation of volume and hydration status
• Laboratory studies

14. • 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

15. 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

16. 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+

17. Anion Gap Formula
• Anion gap can be measured as
• AG=[(Na)-(Hco3+CL)]

18. Fluid Therapy in DKA
Normal saline, 1-2 L over 1-2 h
NS or ½ NS at 250-500 mL/h
Glucose < 250 mg/dl
D5%1/2NS saline

19. Caution during fluid management
• Fluid should be replace over 12-24hr
• patients are generally depleted 3-6lit in DKA.
• Monitor urine output,heart rate,blood
pressure and respiratory status.
• CARE must b taken in patient with CCF and
kidney disease.

20. 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.

21. 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

22. 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).

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

24. WHEN TO STOP IV INSULIN
• Give short acting insulin SC at twice the
hourly IV rate(if iv rate 5u/hr give 10u)
• Failure to give SC insulin may result in
rebound hyperglycemia and ketosis due to its
short acting effect.
• ENSURE pt has a meal and is eating and
awake.

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. pH > 7.0  no bicarbonate
pH < 7.0 and bicarbonate < 5 mEq/l  44.6 mEq
in 500 ml 0.45% saline over 1 h until pH > 7.0
Bicarbonate administration

27. Complications of DKA
1-Complications of associated illnesses e.g. sepsis
or MI.
2-Adult respiratory distress syndrome.
3-Thromboembolism (elderly).
4-Complications of treatment:
a-Hypokalemia: Which may lead to:
-Cardiac arrhythmias.
-Cardiac arrest.
-Respiratory muscle weakness.

28. b-Hypoglycemia.
c-Overhydration and acute pulmonary edema: particularly
in:
-Treating children with DKA.
-Adults with compromised renal or cardiac function.
-Elderly with incipient CHF.

29. d-Neurological complications: Cerebral Edema.
-It occurs mostly in children with DKA.
-Very dangerous and increases mortality.
-The risk is related to the severity, duration and rapid
correction of DKA.
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

31. THANK YOU