DIABETIC EMERGENCIES

2. • Include
• 1] Diabetic Ketoacidosis
• 2]Hyperosmolar non ketotic diabetic coma [Hyperosmolar Hyperglycemic
state]
• 3] hypoglycemia

4. DIABETIC KETOACIDOSIS
• Diabetic Ketoacidosis ia a acute, major, life threatening complication of
diabetes.
• DKA is a complication of DM type 1
• Its less likely to occur in type 2 DM.

5. DEFINITION
DKA is a extreme metabolic state in which there is absolute or relative
deficiency of insulin,
Resulting in hyperglycemia and accumulation of ketocids in blood with
subsequent metabolic acidosis.

7. CLINICAL FEATURES
Dka begins with anorexia, nausea , vomiting and abdominal pain.
Altered consciousness, drowsiness and confusion.
Kussmaul;’s breathing ie rapid ,deep and swallow breathing
Fruity odour to breath due to acetone
Polyuria and polydipsia , increased thirst .
If fever is present , its suggestive of infection

8. INVESTIGATIONS
Urine examination shows glucose and ketones.
Plasma glucose levels and ketone values are raised.
Plasma potassium levels maybe normal or raised in the
initial stages
Plasma sodium level are usually low plasma bicarbonate
level is low
Ph is low and hydrogen ion concentration is high

9. DIAGNOSTIC CRITERIA
Blood glucose level more than 250mg/dL
Arterial pH less than 7.3
Serum bicarbonate less than 15mEq/L
Anion gap is more than 12mEq/L
Moderated ketonaemia and ketouria

10. MANAGEMENT
• Treat the patient in ER Or ICU with full monitoring
Rapid assessment of ABCD
Aim:Replacement of Fluid deficit
Insulin treatment
Monitoring and maintaining electrolyte and potassium balance
Look for precipitating infections cause .

12. HYPERGLYCAEMIC HYPEROSMOLAR STATE
Its usually a complication of Dm type 2
This is a syndrome characterized by extreme dehydration resulting from a
sustained hyperglycaemic diuresis under circumstances in which the patient is
unable to drink sufficient water.
Biochemical hallmark of he syndrome is extreme hyperglycaemia in absence
of significant ketoacidosis.

13. CLINICAL FEATURES
Cns manifestations altered consiousness ranging altered
sensorium to coma , convulsions.

14. LAB FINDINGS
Plasma glucose is markedly elevated usually around 1000mg/dL.
Serum osmolarity is markedly raised
Prerenal azotemia with elevation of BUN and creatinine.
Marginal decrease in bicarbonate level about 20mmol/l
Ph more than 7.3
Increased anion gap seen in 40% of hhs patients

15. MANAGEMENT
Fluid replacement: The average fluid deficit is 10L that should be corrected intravenously.
Initially 2-3L of isotonic saline should be given over 1-2 hours subsequently 0.45% saline
should be used if serum sodium is more than 150mmol/L. Once the plasma glucose
approaches 300mg/dL 5% dextrose –saline solution is given.
Insulin: Regular insulin should be given as a low dose IV infusion. It should be started after
initial bolus of saline has been given. The goal is to keep plasma glucose around 200mg/dL.
Rapid reduction in glucose levels is undesirable.
Potassium supplementation is required.

16. • Lactic acidosis should be treated with Intravenous sodium bicarbonate
• Infection must be treated with antibiotics.

17. MANAGEMENT
1. Oral carbohydrate: if hypoglycemia is recognized early.
2. Intravenous dextrose is indicated is severe hypoglycemia when mental
function is impaired and prolonged hypoglycemia is anticipated.50ml of 50%
dextrose should be given initially followed by infusion of 5-10% dextrose. Oral
carbohydrate should be administered as soon as the patient is able to eat.
3. Glucagon: severe hypoglycemia maybe treated with glucagon 1 mg SC or IM