DR. ZEENAT YASMEEN
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
In type II diabetics with insulin deficiency/dependence
• It is the presenting symptom for ~ 25% of Type I
Definition of Diabetic Ketoacidosis*
Diagnostic Criteria for DKA
Plasma glucose (mg/dl)
Effective serum Osmol
Alteration in sensoria
or mental obtundation
Clinical Presentation of DKA
The onset of DKA is usually relative short, ranging from hours
to a day or two.
Causes of DKA
• Stressful precipitating event that results in
increased catecholamines, cortisol, glucagon.
Infection (pneumonia, UTI)
Non-compliance with insulin
Initial Clinical Evaluation
• History and physical examination
Secure patient’s ABC
Source of infection
• Evaluation of volume and hydration status
• Laboratory studies
Initial Laboratory Studies
• Immediate determination of blood glucose by finger
stick, and serum ketones (3-BH) by finger stick or
• Laboratory studies:
CBC with differential
CMP (glucose, electrolytes, bicarbonate, BUN, creatinine)
* If clinically indicated
Hyponatremia is common in patients with DKA
Correction of Serum sodium:
Corrected Na+ = [Na+] 1.6 x glucose (mg/dl) – 100
Admission serum potassium is frequently elevated (due to a
shift of K- from the intracellular to the extracellular space)
Anion Gap Formula
• Anion gap can be measured as
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
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
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
• Add dextrose5% to IV fluid when blood
• For DKA goal blood glucose 150-200mg/dl
until anion gap close.
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
CHANGING THE INSULIN
• 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(150200mg/dl).
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
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
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
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
Complications of DKA
1-Complications of associated illnesses e.g. sepsis
2-Adult respiratory distress syndrome.
4-Complications of treatment:
a-Hypokalemia: Which may lead to:
-Respiratory muscle weakness.
c-Overhydration and acute pulmonary edema: particularly
-Treating children with DKA.
-Adults with compromised renal or cardiac function.
-Elderly with incipient CHF.
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
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