DIABETIC KETOACIDOSIS.pptx

dka

1. DIABETIC KETOACIDOSIS CURRENT MANAGEMENT APPROACHES DR. EMMANUEL TWENEBOAH ST. FRANCIS XAVIER HOSPITAL SENIOR MEDICAL OFFICER

2. Diabetes Mellitus is a clinical syndrome characterised by chronic hyperglycaemia as a result of ABSOLUTE or RELATIVE LACK of Insulin and/or Insulin resistance.

3. CLASSIFICATION TYPE 1 DIABETES MELLITUS- absolute lack of Insulin due to autoimmune destruction of the B cells of the pancreas. Patient would require Insulin therapy. TYPE 2 DIABETES MELLITUS- relative lack of insulin and/or insulin resistance. May progress to Type 1 eventually requiring Insulin for survival GESTATIONAL DIABETES- carbohydrate intolerance of variable severity with onset in Pregnancy. If patient meets diagnostic targets, likely disease existed before pregnancy

4. THE BURDEN OF DIABETES The number of people with diabetes rose from 108 million in 1980 to 422 million in 2014. B y 2045 this will rise to  700 million Prevalence has been rising more rapidly in low- and middle-income countries than in high-income countries. Between 2000 and 2016, there was a 5% increase in premature mortality from diabetes. In 2019, an estimated 1.5 million deaths were directly caused by diabetes. Another 2.2 million deaths were attributable to high blood glucose in 2012. More than 1.1 million children   and adolescents  are living with type 1 diabetes

5. CLINICAL INERTIA Failure to establish appropriate targets and escalate treatment to achieve treatment goals. Reluctance of Clinicians to initiate insulin therapy

6. ACUTE COMPLICATIONS OF DM Diabetic Ketoacidosis Hyperosmolar Hyperglycaemic State (initially HONK) Hypoglycaemia

7. DIABETIC KETOACIDOSIS Acute, major, life-threatening complication of Diabetes characterised by hyperglycaemia, ketone body formation and metabolic acidosis.

8. PATHOPHYSIOLOGY

9. Criteria and classification of (DKA) DKA Mild Moderate Severe Plasma glucose (mg/dl) mmol/l >250 mg/dl > 13.9mmol/L >250mg/dl > 13.9mmol/L 250mg/dl > 13.9mmol/L Arterial pH 7.25-7.30 7.00-7.24 <7.00 Serum bicarbonate (mEq/L) 15-18 10- 15 <10 Urine ketone* + + + Serum ketone* + + + Effective Serum Osmolality** Variable Variable Variable Anion Gap*** >10 >12 >12 Mental Status Alert Alert/drowsy Stupor/coma

10. CAUSES The “five I’s” that cause diabetic ketoacidosis and hyperosmolar hyperglycemic state Infection Urinary, respiratory, skin Infarction Myocardial infarction, stroke, bowel, bone, skin Infant on board Pregnancy Indiscretion with diet Non-compliance with diabetic diet (e.g., sugar, carbohydrates or alcohol) Insulin lack Pump failure, skipping insulin doses

11. MANAGEMENT IDEALLY in the ICU/HDU setting Close monitoring is essential Patients should be examined at least hourly Cornerstones of management are: fluid and potassium replacement; weight-based fixed rate intravenous insulin infusion (FRIII); and close biochemical monitoring of capillary ketones, serum electrolytes, venous pH and capillary glucose.

12. Metabolic treatment targets Reduction of the blood ketone concentration by 0.5 mmol/L/hour. Increase the venous bicarbonate by 3.0 mmol/L/hour. Reduce capillary blood glucose by 3.0 mmol/L/hour. Maintain potassium between 4.0 and 5.5 mmol/L.

13. Venous access is essential. Two wide bore cannulae (so IV fluids and Insulin can given simultaneously) Take samples for FBC, BUE and Cr, Urine R/E Chest X ray ECG, Cardiac Enzymes Cultures- urine and blood ABGs Ketone levels Bicarbonate levels

14. FLUID THERAPY Fluid resuscitation is very critical. Fluid of choice is Ringers Lactate Normal Saline * Administer 1-3 L during the first hour. Administer 1 L during the second hour. Administer 1 L during the following 2 hours Administer 1 L every 4 hours, depending on the degree of dehydration and central venous pressure readings Essential to start hydration at least an hour before insulin therapy Watch out for fluid overload- auscultate the lung bases regularly For children, 10-20mls/kg in the first 1-2 hours. Total fluid therapy should not exceed 40-50mls/kg for the first 4 hours

15. INSULIN THERAPY Extensive evidence indicates that “low-dose” intravenous insulin administration should be the standard of care. Start insulin infusion after the patient has received initial volume expansion; i.e., ∼1–2 h after starting fluid replacement therapy. The dose is 0.1 unit · kg −1  · h −1  . It may be necessary to estimate the patient’s weight; treatment should not be delayed waiting for an accurate weight. An intravenous insulin bolus (0.1 unit/kg) is unnecessary , may increase the risk of cerebral oedema, and should not be used at the start of therapy. The dose of insulin should remain at 0.1 unit · kg −1  · h −1  at least until resolution of DKA (pH >7.30, bicarbonate >15 mmol/l, and/or closure of the anion gap), which invariably takes longer than normalization of blood glucose concentrations

16. When RBS falls below 13mmol/L, switch to a dextrose containing fluid (5% D) It may be necessary to use 10% or even 12.5% dextrose to prevent hypoglycaemia while continuing to infuse insulin to correct the metabolic acidosis. If the patient demonstrates marked sensitivity to insulin (e.g., some young children with DKA and patients with hyperosmolar hyperglycemic state), the dose may be decreased to 0.05 units · kg −1  · h −1 , or less, provided that metabolic acidosis continues to resolve.

17. Where continuous infusion is not possible, insulin can be given subcutaneously or intramuscularly 1 -2 hourly Sliding scale- ??

18. ELECTROLYTE THERAPY DKA is associated with a significant total body deficit of serum electrolytes No supplement is required when K+ > 5.2mmol/L K < or = 5.2mmol/l , start potassium replacement to maintain levels at 4-5mmol/L K lower than 3.3mmol/L , Insulin should not be started Sodium bicarbonate use has not shown to have any impact on clinical outcomes

19. Proper management of DKA involves prompt initiation of IV fluids, insulin therapy, electrolyte replacement and recognition and treatment of precipitating factors Close monitoring of patients condition by regular clinical and laboratory data and the use of management protocols ensure better outcomes. Prevention of DKA through structured educational programs and identification of risk factors for recurrence should be part of patients care plan

20. THANK YOU