Diabetic ketoacidosis, Causes, Sign & Symptoms, Diagnostic evaluation, Treatment, Complications, Pathogenesis

1. Diabetic ketoacidosis (DKA) is a life-threatening condition, characterized by hyperglycemia,
ketoacidosis, and ketonuria. develops when cells in the body are unable to get the sugar
(glucose) they need for energy because there is not enough insulin.
When your cells don't get the glucose they need for energy, your body begins to burn fat for
energy, which produces ketones. Ketones are chemicals that the body creates when it breaks
down fat to use for energy. The body does this when it doesn’t have enough insulin to
use glucose. When ketones build up in the blood, they make it more acidic. causing the
chemical imbalance (metabolic acidosis) called diabetic ketoacidosis.
The key role of glucose in the body is fuel for energy, and the brain depends completely on
glucose to operate normally. Brain functions such as thinking, learning and memory are closely
tied to glucose levels.
People with type 1 diabetes are at risk for ketoacidosis, since their bodies don't make
any insulin.
DKA can happen to people with type 2 diabetes, but it's rare. If you have type 2, especially when
you're older, you're more likely to have a condition with some similar symptoms called HHNS
(hyperosmolar hyperglycemic nonketotic syndrome). It can lead to severe dehydration.
Causes
 Stress
 4I: Infection ,Infarction, Insulin Insufficiency,Illness
Infection as : urinary tract infection (UTI), gastroenteritis, flu or pneumonia
Illness as : myocardial infarction, pneumonia, prostatitis, UTI
Sign & Symptoms
 Excessive thirst
 Frequent urination
 Nausea and vomiting
 Abdominal pain
 Weakness or fatigue
 Shortness of breath
 Fruity breath
 Confusion
 High blood sugar level (hyperglycemia)
 High ketone levels in your urine

2. Diagnostic evaluation:
1. Serum blood glucose level (more than 250mg/dl)
2. Serum and urine ketone bodies are present.
3. in severe DKA , Serum bicarbonate Hco3 (<10 mEq/L), and PH are decreased (< 7.00)
4. Serum Na, K levels may be deceased, normal, or high due to fluids shift and dehydration.
5. BUN, creatinine, hemoglobin, and hemotocrit are elevated due to dehydration.
Ketones? :
- Ketone is a chemical produced when there is a shortage of insulin in the blood and the
body breaks down body fat for energy.
- Ketones in the urine is a sign that your body is using fat for energy instead of using
glucose because not enough insulin is available to use glucose for energy.
- Ketones in the urine is more common in type 1 diabetes.
Treatment:
Initiation of treatment:
• Give oxygen if arterial pO2 < 80mmHg or sats < 100 mmHg
• IV line.
-Urinary Foley's catheter (if in shock).
Start fluids, K+ and insulin
• Monitor BP and ECG
 Fluid replacement
Give sodium chloride 0.9% intravenously as follows:
1L NaCl 0.9% : Over 30 minutes
1L NaCl 0.9% : Over 1 hour
1L NaCl 0.9% : Over 2 hour
1L NaCl 0.9% : Over 4 hour
1L NaCl 0.9% : Over 6 hour
1L NaCl 0.9% : Over 8 hour
 Insulin
Only short-acting insulin is used for correction of hyperglycemia in DKA.
• Administer stat dose of 6 units Human Actrapid IV (15 units IM if IV access delayed)
• Dilute 50 units of human Actrapid insulin to 50mL with sodium chloride 0.9%
• Commence at a rate of 6 units per hour.
• Aim for a 36-72mg/dl decrease in glucose per hour.
• Never stop insulin infusion. If glucose falls to <72mg/dl, commence glucose 10%.
 After recovery
When the patient is able to eat and the urine is free of ketones, commence previous SC insulin
therapy and stop insulin by IV infusion 30 minutes after first SC dose (15mins if the SC insulin is
Novorapid®, Novomix® 30 or one of the Humalog® preparations).

3. Complications of DKA
The three major complications of diabetic ketoacidosis are:
1. Hypoglycemia: Hypoglycemia indicates blood sugar level that is below the normal
lows. With insulin treatment, cells become active and picks up the sugar fast that
causes the blood sugar level to drop rapidly. Any quick drop of blood sugar results
into hypoglycemia.
2. Hypokalemia: Hypokalemia indicates a very low level of the electrolyte potassium in
the blood. Insulin treatment infuses sufficient insulin in the blood at one stroke,
insulin and fluids help in the entry of potassium into the cells, which decreases and
depletes the level of potassium in the blood. Continuously low level of potassium in
blood can impair muscle, activities of nerve, and can also impair heart.
3. Cerebral edema: It is a rare complication of diabetic ketoacidosis. it may be related to
rapid fluid replacement. Cerebral edema most frequently occurs in children.
The nurse’s role
 Ongoing clinical assessment of the patient: this involves regular (at least hourly) monitoring of
vital signs and level of consciousness during the acute phase.
 Accurate monitoring of fluid balance: this includes accurate intake and output charts.
Prescribed fluids should be administered and patients monitored for signs of complications
related to fluid overload, dehydration and electrolyte imbalance;
 Insulin therapy.
 Regular monitoring of capillary blood glucose and ketones.
 Monitoring of metabolic acidosis and electrolytes.
 Provide psychological support for patients: this includes keeping the patient and relatives fully
informed about the patient’s clinical condition and the care given.
Pathogenesis of DKA
A-The basic underlying mechanisms are:
-Absolute def iciency of circulating insulin.
-secretion of insulin counterregulatory hormones; glucagon, adrenaline, cortisol and growth hormone.
B-This leads to disturbances in the following physiological processes:
-glucose utilization (hyperglycemia).
- proteolysis ( amino acids, glutamine and alanine).
- lipolysis ( glycerol and FreeFattyAcids).
- glycogenolysis (breakdown of muscle glycogen  lactate).
- gluconeogensis (glutamine & alanine & glycerol & lactate).

4. C-This results in the following metabolic abnormalities:
1-Hyperglycemia.
2-Hyperketonemia: 2 main mechanisms:
a- Production of ketone bodies (ketogenesis):
-Increase FFAs  hepatic uptake  FFAs enter the mitochondria  oxidation to form acetoacetic acid.
-Large part of acetoacetic acid  reduced to  -hydroxy butyric acid ( -HBA).
-Small part of acetoacetic acid is decarboxylated to acetone.
The 3 ketone bodies are released to the blood in a ratio between acetoacetic acid to -HBA of 8 : 1 .
b- Utilization of ketone bodies.
D-The consequences of these metabolic abnormalities are:
a-Hyperglycemia:
-Osmotic diuresis.
-Excessive urinary losses of H2O & Na, K.
-Dehydration and hypotension.
b-Hyperketonemia:
-Ketonuria.
-  Blood acidity
-Obligate losses of sodium and potassium due to  urinary excretion of ketone bodies (salt)  alkaline reserve.
E-Electrolytes and acid base disturbances during DKA:
a-Serum K: Usually high (hyperkalemia) secondary to:
1-Shift of K from intracellular to extracellular compartment due to:
-Insulin deficiency and hyperglycemia.
-Extracellular hyperosmolarity.
-Acidosis.
- Catabolism and breakdown of cellular protein.
2-Impaired cellular uptake of K.
b-Serum sodium: Usually low secondary to:
-Hyperglycemia leads to  osmotic flux of H2O from intracellular to extracellular space.
-Obligate sodium loss with ketonuria.
c-Metabolic acidosis: Secondary to:
- Production and  utilization of strong acids; acetoacetic acid and -HBA.
- Alkaline reserve (sodium and K losses).