DIABETIC KETOACIDOSIS

IN ICU
PRESENTED BY:
DR. ZEENAT YASMEEN
ICU RESIDENT

Diabetic Ketoacidosis (DKA)

A state of absolute or relative insulin deficiency
aggravated and followed by
hyperglycemia, dehydration, and acidosisproducing 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.

Definition of Diabetic
Ketoacidosis*
Acidosis

*
Ketosis
Hyperglycemia
3

Pathogenesis of DKA

Beta-cell
failure
D/C
Insulin

Insulin
Deficiency

Glucotoxicity

Pathogenesis of DKA

Insulin
deficiency

Increased
glucagon
GH
cortisol
catecholamines

Carbohydrate Metabolism in DKA

Relative or absolute insulin deficiency

liver

glucose output
glycogenolysis

muscle

glucose uptake

Increased Glucose Production in DKA

Gluconeogenesis

Glucose

Activity of gluconeogenic
enzymes
(PEPCK, PC, PFK)

Glycerol

Amino acids
Lactate

TG
Lipolysis

Protein breakdown

Increased Production of Ketones in DKA

Ketogenesis
B-OH-B
Acetoacetate

FFA Glycerol
TG

Lipolysis

Pathogenesis of DKA
Live
r

Peripheral
tissue

Adipos
e
tissue

Liver

Increased
glucose
production

Decreased
glucose
uptake

Increased
release
FFA

Increased
ketogenesis

HYPERGLYCEMIA

KETOACIDOSIS

Osmotic diuresis

Decreased alkali reserve

Volume depletion

Metabolic acidosis

Diagnostic Criteria for DKA

DKA
Mild
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

Moderate

Severe

>250
7.25-7.3
>10
15-18
positive
positive
variable

>250
7.0-<7.24
>12
10- <15
positive
positive
variable

>250
<7.0
>12
<10
positive
positive
variable

alert

alert/
drowsy

stupor/
coma

Clinical Presentation of DKA

Symptoms
Polydipsia
Polyuria
Weakness
Weight loss
Nausea
Vomiting
Abdominal pain

Sign
Hypothermia
Tachycardia
Tachypnea
Kussmaul
breathing
Ileus
Acetone breath
Altered sensorium

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)

Alcohol
Stroke
Myocardial Infarction
Pancreatitis
Trauma
Medications (steroids)
Non-compliance with insulin

Initial Clinical Evaluation

History and physical examination

Secure patients ABC

Mental status
Cardiovascular-renal status
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 urinary ketones.
Laboratory studies:

ABGs
CBC with differential
CMP (glucose, electrolytes, bicarbonate, BUN, creatinine)
Serum ketones
Urinalysis
Bacterial cultures*
Cardiac enzymes*

* If clinically indicated

Serum Sodium
Hyponatremia is common in patients with DKA
Serum glucose
H 2O
H 2O

H 2O
H 2O

Na+
Correction of Serum sodium:
Corrected Na+ = [Na+] 1.6 x glucose (mg/dl) 100
100

Serum Potassium
Admission serum potassium is frequently elevated (due to a
shift of K- from the intracellular to the extracellular space)
Osmolality
Acidosis
K
+
K

K
+
K

K+

Insulin
Na+ regulates
Activity
of
KNa+/K+
pump

Anion Gap Formula

Anion gap can be measured as

AG=[(Na)-(Hco3+CL)]

Fluid Therapy in DKA

Normal saline, 1-2 L over 1-2 h

NS or NS at 250-500 mL/h
Glucose < 250 mg/dl

D5%1/2NS saline

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.

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.

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

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).

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
awake.

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

Bicarbonate administration

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 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.

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.

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

Summary
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

THANK YOU