2 DIABETES KETOACIDOSIS (DKA) presentation
- 1. DIABETES DIABETES KETOACIDOSIS (DKA) KETOACIDOSIS (DKA) Lt Col G Sandala Lt Col G Sandala Ref: Dr. I. A. Lyaruu MD, Msc, Mmed Ref: Dr. I. A. Lyaruu MD, Msc, Mmed
- 2. Introduction Introduction • Is an acute complication of diabetes mellitus (DM) and most frequently occurs in Type 1 DM. It is rare in Type 2 DM, but can occur • Mortality increases with age and is usually due to an associated catastrophic illness (MI, CVA, sepsis etc) or acute complications.
- 3. Introduction Introduction • Precipitating factors for DKA (in a diabetic pt) – Infections – Reduction in insulin dosage – Missed injections – Failure to ↑ insulin dose during illness
- 4. PATHOLOGY PATHOLOGY • Hyperglyceamia • Hyperketoneamia – The above are usually secondary to severe insulin deficiency and ↑ secretion of the counerregulatory hormones
- 5. PATHOLOGY PATHOLOGY Resulting effects of the above • ↑ mobilization and delivery of substrates from muscles (aa, lactate, pyruvate) and adipose tissue (FFA, glycerol) to the liver • ↑ gluconeogenesis resulting into increased glucose production and hence hyperglycemia ( usually > 300 mg/dl)
- 6. Resulting effects; Resulting effects; • Increased ketogenesis leading to increased production of ketone bodies (β- hydroxybutyrate and acetoacetate) → Hyperketonemia. → acidosis (pH < 7.35) • Both hyperglycemia and Hyperketonemia contributes to increase the osmolarity of blood resulting to osmotic diuresis ultimately leading to dehydration.
- 7. Mechanisms of Acidosis Mechanisms of Acidosis • Hyperketoneamia • Loss of Na+ with ketones and its replacement with H+ • Kussmaul breathing → loss of CO2 → decrease in HCO3 → increase in pH of blood.
- 8. CLINICAL FEATURES OF DKA CLINICAL FEATURES OF DKA • Polyuria and polydypsia • Dehydration (dry skin and mucous membranes) • Abdominal pain (usually periumbilical mimicking an acute abdomen), anorexia, nausea and vomiting. • Paralytic ileus in severe cases
- 9. CLINICAL FEATURES OF DKA CLINICAL FEATURES OF DKA • Tachycardia • Orthostatic hypotension • Depressed mental function • Deep and rapid respiration (Kussmaul). • Sweet sickly smell on the patient’s breath (acetone breath)
- 10. DIAGNOSIS OF DKA DIAGNOSIS OF DKA • Clinical features above • ↑ serum glucose levels (250 – 1000 mg/dl) • ↑ Serum ketone levels (qualitative assessment using ketostix (strips) or acetest (tablets). These tests are based on the reaction between nitroprusside and acetoacetate. • Presence of ketonuria.
- 11. Other laboratory tests Other laboratory tests • Serum pH • Na+ or K+ anions • Serum HCO3 → decreased
- 12. Other laboratory tests Other laboratory tests • Serum Na+ → decreased 2o to hyperosmolarity → shift of water from extra vascular space into the intravascular space. • ↑ serum creatinine • Serum potassium, phosphate and magnesium may be low normal or high
- 13. – In elderly death is associated with presence of infection in many cases – In children death is associated with cerebral edema as a complication of DKA
- 14. MANAGEMENT OF DKA MANAGEMENT OF DKA (GOALS) (GOALS) • Correction of fluid and electrolyte imbalance • Reversal of metabolic abnormalities (insulin treatment) • Detection and treatment of precipitating illnesses (infection)
- 15. TREATMENT TREATMENT 1. Restoration of vascular volume; • Fluid deficit is approx. 5 – 12 L • Sodium deficit
- 16. TREATMENT TREATMENT • Regime for fluid administration – 1 L in 30 mins – 1 L in the following 1 hr. – 1 L every 2 hrs (to be adjusted in 6 hrs depending on the response to fluid therapy) • When glycemia falls to levels ≤ 11.1 mmol/L dextrose solutions are introduced to avoid hypoglycemia and minimize the risk of cerebral edema.
- 17. TREATMENT TREATMENT 2. Insulin Therapy • Short acting insulin is used – 0.1 U/kg of insulin given as a bolus i.v. – 0.1 U/kg of ins. actrapid sc. every 1 – 2 hrs till glycemia is approx. 11 mmol/L, then adjust the dose and frequency for the insulin injections
- 18. TREATMENT TREATMENT 3. Electrolyte (K+ ) Replacement Therapy • how ever serum K+ levels may be low, normal or high at presentation • insulin + fluid replacement → ins-mediated shift of K+ into the intracellular space + extracellular dilution of K+ → hypokalemia
- 19. TREATMENT TREATMENT 4. Correction of acidosis • In most patients acidosis disappears with standard therapeutic measures (Fluids and insulin). • Correction with alkali (bicarbonate) is unnecessary.
- 20. TREATMENT TREATMENT Note: – Insulin reduces lipolysis → ↓ FFA flux to the liver → decrease ketogenesis and hence lowers the acidosis. – Keto acids are oxidized leading to regeneration of HCO3 → decrease acidosis • Correction with bicarbonate is indicated in severe cases of acidosis (pH < 7.0) • Therapy should be discontinued when pH rises to above 7.1
- 21. TREATMENT TREATMENT 5. Treat any associated infection (s) with appropriate antibiotics.