)Presentation based on diabetic ketoacidosis fresh pptx

It is a ppt on schizophrenia

1. Diabetes ketoacidosis

2. Introduction DKA is an acute metabolic complication of diabetes that us a consequence of absolute insulin deficiency. 2 Causes

3. Pathogenesis of dka : Clinical triad Blood glucose > 11.1 mmol /L or 200mg/dL known Diabetes Hyperglycaemia >3.0 mmol /L on fingerprick testing More than 2+ on urine dipstick testing Hyperketonaemia 3 Venous bicarbonate <15 mmol /L Venous pH < 7.3 Metabolic Acidosis

4. Insulin deficiency and counter regulatory hormones: DKA typically arises from an absolute or relative deficiency of insulin coupled with an increase in counter-regulatory hormones such as glucagon, cortisol, catecholamines, and growth hormone. This hormonal imbalance promotes gluconeogenesis and glycogenolysis , leading to hyperglycemia , and stimulates lipolysis, resulting in the release of free fatty acids. Ketogenesis: The free fatty acids released from adipose tissue are transported to the liver, where they undergo β- oxidation to form ketone bodies, primarily acetoacetate and β- hydroxybutyrate . These ketone bodies accumulate in the blood, leading to ketosis and subsequent metabolic acidosis due to their acidic nature. Hyperglycaemia and osmotic diuresis: The elevated blood glucose levels exceed the renal threshold, resulting in glucosuria . This osmotic diuresis leads to significant fluid and electrolyte losses, causing dehydration, hypovolemia , and electrolyte imbalances, particularly of sodium and potassium.

5. 6 Metabolic acidosis: The accumulation of ketone bodies lowers the blood pH, leading to metabolic acidosis. The body attempts to compensate through respiratory mechanisms, such as Kussmaul respiration, to expel carbon dioxide and mitigate acidosis. Electrolyte imbalances: Despite total body potassium depletion due to urinary losses, serum potassium levels may appear normal or elevated initially due to the shift of potassium from the intracellular to the extracellular compartment in response to acidosis and insulin deficiency. However, with insulin therapy and correction of acidosis, potassium shifts back into cells, potentially leading to hypokalemia if not properly managed.

6. Clinical assessment 8

7. Investigations

8. Management 10 Fluid replacement Insulin replacement Potassium replacement IV bicarbonate and phosphate Ongoing management Aims of DKA management are to correct circulating volume and electrolyte imbalance and halting Lipolysis and suppressing ketogenesis A referral to diabetes specialist team should be made as early as possible with review within 24 hours Regular clinical and biochemical review is essential Vital signs should be regularly assessed Supportive measures may include nasogastric tube insertion for vomiting or reduced level of consciousness and catheter insertion to assess urinary output

9. Fluid replacement - A rapid fluid Nokia over 10-15 minutes may be required if systolic blood pressure is <90 Mahfouz - The 0.9% saline infusion should be continued to correct circulating volume with 10% glucose recommended to prevent hypoglycaemia when blood sugar level is below 14 mmol /L - More cautious approach in pregnant, young adults and older patients with history of kidney or heart failure 11

10. Insulin replacement Blood glucose and blood ketone should be monitored hourly Response to treatment should be assessed by a blood ketone concentration falling by at least 0.5 mmol /L/hr If blood ketones are not falling by at least 0.5 mmol /L/hr then the insulin infusion should be increased according to Local protocols. Long acting insulin analogue in a dose equivalent to the individual’s usual regiment should continue to be administered subcutaneously during the initial management of DKA The fixed straight insulin infusion should be continued until DKA has resolved, defined as blood ketone less than 0.6 mmol /L, bicarbonate >15 mmol /L and venous pH >7.3

11. Potassium replacement - Potassium is not usually recommended with the initial 1 L of 0.9% sodium chloride as the primary focus at this stage is on restoring circulating volume adrenal failure may be present -Potassium should be measured urgently on a venous blood gas sample, and then reassessed after 1 hour,2 hour and then 2 hourly thereafter Serum Potassium Treatment 3.5-5.5 mmol /L 0.9% NaCl + 40 mmol /L KCl >5.5 mmol /L K not added to the fluid replacement <3.5 mmol /L Begin cardiac monitoring Involve the critical care team as additional K is required

12. The use of IV bicarbonate therapy is not generally recommended due to lack of evidence of benefit, but maybe considered in the context of PH of <6.9 Acidosis may reflect an adaptive response, improving oxygen delivery to the tissues and so excessive by corporate may induce a paradoxical fall in cerebral fluid pH Levels of <0.6 mmol /L are often corrected, particularly in the presence of respiratory muscle weakness Intravenous bicarbonate and phosphate

13. Ongoing management 15 Restoration of the usual insulin regimen by subcutaneous injection should not be instituted until the patient is barking, stable and able to eat and drink normally The fixed state insulin infusion should be continued for 30 minutes after short acting insulin is given at a mealtime Using an insulin pump, then the infusion should be started during the daytime at the usual basal rate, and the fixed insulin infusion should be continued until the next meal bonus is given

14. Thank you