Pathogenesis of DKA

Metabolic actions of insulin

Increase Glycogenesis Glycolysis Glucose transport to muscle and adipose tissue Triglyceride and fatty acid synthesis Protein synthesis Decrease Gluconeogenesis Glycogenolysis Lipolysis Ketogenesis Fatty acid oxidation Protein degradation

In the absence of Insulin

Hepatic Gluconeogenesis increases. Peripheral uptake of glucose by muscle and adipose tissue decreases. Rising glucose levels leads to hyperglycaemic state. Resulting osmotic diuresis leads to fluid and electrolyte loss causing dehydration. Increase in osmolality and renal hypoperfusion leads to accumulation of ketones and H ions.

In the absence of insulin cont..

In parallel rapid lipolysis occurs. This leads to elevated circulating free fatty acid levels. Free fatty acids are broken into fatty acyl-coA with in the liver. And this in turn converted to ketone bodies within the mitochondria. Accumulation of ketones produces a metabolic acidosis. Vomiting leads to loss of fluid and electrolyte depletion which causes renal hypoperfusion. which in turn leads to impaired excretion of ketones and H ions.

final out come of the pathological processes

Hyperglycaemia. Dehydration . Metabolic acidosis. Electrolyte imbalance.

Why DKA
DKA precipitated by concomitant infection. (Respiratory tract infection, urinary tract infection etc) Poor glycaemic control.

Diabetic Ketoacidosis Management

DKA
Blood sugar 200mg/dl Ketone ++ in urine. Bicarbonate less than 16. PH less than 7.35.

Clinical features
Hyperventilation with ketotic breath. Dehydration with tachycardia. Hypotension. Decreased skin turgour. Dry tongue. Drowsiness / Shock (in severe cases)

Investigations
Plasma glucose. Serum urea and electrolytes. Arterial blood gases. Urinary ketone bodies. Full blood count. Chest x ray. ECG. Blood cultures

Management principles
Rehydration. Insulin therapy. Observation of vital signs.

Rehydration
IV fluids. 1 litre of sodium chloride 0.9% over 1 hour. 1 litre of sodium chloride 0.9% over 2 hours. 1 litre of sodium chloride 0.9% over 2 hours. 1 litre of sodium chloride 0.9% over 4 hours. 1 litre of sodium chloride 0.9% over 4 hours. 1 litre of sodium chloride 0.9% over 4 hours. 1 litre of sodium chloride 0.9% over 8 hours.

Insulin therapy
Soluble insulin (Actrapid or Humulin S) infusion is prepared in a concentration of 1 unit of insulin per ml of sodium chloride 0.9%. prepared soluble insulin is given in a rate of 6 units per hour iv, until blood glucose level falls to <14mmol/L . Aim for blood glucose drop of 3-5 mmol/l per hour.

Potassium treatment
Start potassium when starting insulin infusion. 20 mmol Kcl with each liter of IV saline. Discontinue potassium if over 5.5 mmol/l. Monitoring blood glucose hourly Electrolytes 2 hrly.

Observations
Regular Plasma glucose levels. Regular blood urea and Serum electrolytes. Venous bicarbonate. Hourly fluid input and output , blood pressure and heart rate. ECG for T wave changes. Fluid input output charts. Regular assessment of neurological status.

When blood sugar is <14 mmol/l

Iv therapy. Reduce insulin infusion to 3 units per hour. And administer 500ml glucose 10% with potassium chloride. Continue sodium chloride 0.9% at 250 ml/hour till acidosis resolves.

 If blood glucose level falls below 10 mmol/l on 3units per hour, reduce insulin infusion to 2 units /hour. Do not reduce the insulin infusion below this. Alternatively administer 500 ml glucose 10% with potassium chloride and insulin at 100ml/hour and adjust infusion to maintain blood glucose within 6-12 mmol/l

Subsequent management 4 hours onwards

Allow oral intake if swallowing is safe normal bowel sounds and no vomiting. Measure blood urea, electrolytes and bicarbonate twice daily until bicarbonate within normal reference range.

 Maintain sodium chloride 0.9% at 250 ml/hour until bicarbonate in reference range and patient eating normally. Once dehydration/ acidosis corrected and patient is eating then transfer on to normal insulin regime.