Diabetic

Ketoacidosis (DKA)

Introduction
Diabetic ketoacidosis (DKA) is an acute, major,
life-threatening complication of diabetes.
DKA is defined:
o Clinically as an acute state of severe uncontrolled
diabetes that requires emergency treatment with
insulin and intravenous fluids.
o Biochemically as an increase in the serum
concentration of ketones greater than 5 mEq/L, a
blood glucose level of greater than 250 mg/dL
(although it is usually much higher),blood pH of less
than 7.2, and a bicarbonate level of 18 mEq/L or
less.

Pathophysiology
DKA is characterized by hyperglycemia, acidosis, and
ketonuria.
DKA is consequence of absolute or relative insulin
deficiency with increase in counter-regulatory
hormones .

Insulin and counter-regulatory hormone

Gluconeogenesis and glycogenolysis Hyperglycemia .

Lipolysis

Free Fatty Acids Ketogenesis

Ketonemia and ketonuria pH and bicarbonate serum

levels Metabolic acidosis Ketoacidosis.

Pathophysiology cont.
Hyperglycemia Glycosuria Osmotic diuresis
dehydration and tissue hypoperfusion.
Hyperglycemia, osmotic diuresis, serum
hyperosmolarity, and metabolic acidosis
concentration disturbance.
Osmotic diuresis Potassium Sodium loss in the urine.

Causes and Precipitating

Factors
The most common precipitants
1.Infections (3050%): pneumonia, urinary tract
infections, sepsis, gastroenteritis
2.Inadequate insulin treatment (2040%):
includes noncompliance, insulin pump failure

Other precipitants

Clinical Features
Signs:
Symptoms:
1.Dehydration:
1.Polydypsia.
o Dry skin and mucous .
2.Polyuria.
o Orthostatic
3.Hyperglycemia.
hypotension.
4.Nausea, lethargy,
o Tachycardia.
anorexia, weakness.
o Reduced JVP.
5.Abdominal pain.
o Reduced mental
6.Reduced motility of GI.
function
7.Vomiting.
2.Ketosis:

Investigations
Glucose level.
Serum Ketones.
Acid-base status: pH, Serum bicarbonate.
Electrolytes: Na +K+ Mg +2
ECG
CBC, WBC.
Urinalysis.
Cardiac markers, Liver enzymes and Amylase.
Chest X-Ray.
Blood and urine culture.

Management
Assess:
o Serum electrolytes, Acid-base status and
Renal function.

Replace fluids:
o 23 L of 0.9% saline over first 13 h (1015
mL/kg per hour)
o subsequently, 0.45% saline at 150300 mL/h
o change to 5% glucose and 0.45% saline at
100200 mL/h when plasma glucose reaches
250 mg/dL (14 mmol/L).

Management cont.
Administer short acting insulin: IV (0.1
units/kg) or IM (0.3 units/kg), then 0.1
units/kg/hour by continuous IV infusion; increase 2to 3-fold if no response by 24 h. If initial serum
K+ is < 3.3 mmol/L ,do not administer insulin until
the potassium is corrected to > 3.3 mmol/L.
Assess patient: What precipitated the episode
(noncompliance, infection, trauma, infarction,
cocaine)? Initiate appropriate workup for
precipitating event (cultures, CXR, ECG).
Measure capillary glucose every 12 h; measure
electrolytes (especially K+, bicarbonate,
phosphate) and anion gap every 4 h for first 24 h.

Management cont.
Monitor vital signs, mental status, fluid intake
and output every 14 h.
Replace K+: 10 mEq/h when plasma K+ < 5.5
mEq/L, ECG normal, urine flow and normal
creatinine documented; administer 4080
mEq/h when plasma K+ < 3.5 mEq/L or if
bicarbonate is given.
Continue above until patient is stable,
glucose goal is 150250 mg/dL, and
acidosis is resolved. Insulin infusion may be
decreased to 0.050.1 units/kg per hour.

Complications
Cerebral edema
Cardiac dysrhythmia
Pulmonary edema
Nonspecific myocardial injury may occur in
severe DKA
Microvascular changes consistent with diabetic
retinopathy