DKA by Dr. A. Mandour.pptx
- 3. UNDERSTANDING DIABETES Diabetes mellitus, often referred to simply as DIABETES. Diabetes is a condition in which the body: • Does not produce enough insulin, and/or • Does not properly respond to insulin Insulin is a hormone produced in the pancreas. Insulin enables cells to absorb glucose in order to turn it into energy. 3
- 4. Type 1 vs. Type 2 Type 1 diabetes Type 2 diabetes Diagnosed in children and young adults Typically diagnosed in adulthood Previously known as Juvenile Diabetes Also found in overweight children Insulin-dependent Non-insulin-dependent Body does not produce insulin Body fails to produce and properly use insulin
- 6. Blood Glucose Alterations Complications of blood glucose alterations • Hypoglycemia • Hyperglycemia • Ketosis • Acidosis • DKA (Hyperglycemia + Ketosis + Acidosis) Normal fasting blood glucose level 4-6 mmol/L
- 8. DIABETIC KETOACIDOSIS (DKA) Hyperosmolar Hyperglycemic State (HHS)
- 9. DIABETIC KETOACIDOSIS (DKA) • A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. • Can occur in both Type I Diabetes and Type II Diabetes – In type II diabetics with insulin deficiency/dependence • The presenting symptom for ~ 25% of Type I Diabetics.
- 11. Diabetic KetoAcidosis (DKA) 1. 160,000 Admissions to private hospitals/year 2. Cost = over 1 billion $ annually 3. 65% = <19 years old 4. Main cause of death in children with diabetes (approximately 85%) 5. Cerebral edema in 69%
- 12. Hyperosmolar Hyperglycemic State (HHS) • An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. • Occurs predominately in Type II Diabetics – A few reports of cases in type I diabetics. • The presenting symptom for 30-40% of Type II diabetics. • Not commonly associated with ketonaemia and acidosis
- 14. The biochemical criteria for the diagnosis of DKA3,4 • Hyperglycemia - blood glucose greater than 11.1 mmol/L • Ketosis - ketones present in blood and/or urine • Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L Classic Triad of DKA
- 15. DKA is generally categorized by the severity of the acidosis. • MILD – Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L • MODERATE – Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L • SEVERE – Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L CLASSIFICATION OF DKA
- 17. Risk factors for DKA at onset • Age <12 yrs • No first degree diabetic relative • Lower socioeconomic status • High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs • Poor access to medical care • Uninsured • Usage of SGLT-2 inhibitor – euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism
- 19. Why do ketones develop? No carbohydrate intake • fasting • gastroenteritis • Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity • onset of diabetes (insufficient secretion) • interruption of insulin delivery in established pt Increase in insulin resistance • infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors
- 20. Causes of DKA/HHS • Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. – Infection (pneumonia, UTI) – Alcohol, drugs – Stroke – Myocardial Infarction – Pancreatitis – Trauma – Medications (steroids, thiazide diuretics) – Non-compliance with insulin
- 22. PATHOPHYSIOLOGY OF DKA Wolfsdorf J, Glaser N, Sperling MA; American Diabetes Association. Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(5):1150-1159.Reprinted with permission from The American DiabetesAssociation.
- 26. DKA is a complex metabolic state of: hyperglycemia, ketosis, and acidosis Symptoms include: – Deep, rapid breathing – Fruity breath odor – Very dry mouth – Nausea and vomiting – Lethargy/drowsiness DKA is life-threatening and needs immediate treatment
- 27. Symptoms of DKA/HHS • Polyuria • Polydypsia • Blurred vision • Nausea/Vomiting • Abdominal Pain • Fatigue • Confusion • Obtundation
- 28. Physical Examination in DKA/HHS • Hypotension, tachycardia • Kussmaul breathing (deep, labored breaths) • Fruity odor to breath (due to acetone) • Dry mucus membranes • Confusion • Abdominal tenderness
- 30. Diagnostic Criteria for DKA and HHS Mild DKA Moderate DKA Severe DKA HHS Plasma glucose mmol/L > 14 > 14 > 14 > 33.3 Arterial pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30 Sodium Bicarbonate (mEq/L) 15 – 18 10 - <15 < 10 > 15 Urine Ketones Positive Positive Positive Small Serum Ketones Positive Positive Positive Small Serum Osmolality (mOsm/kg) Variable Variable Variable > 320 Anion Gap > 10 > 12 > 12 variable Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma Serum ketones positive if > 1mg/dl or < 0.1 mmol/L Anion gap Na + K – Cl – Hco3 target < 10
- 33. Identify and Treat the Precipitating Factor • Insulin omission – MOST COMMON CAUSE of DKA • New diagnosis of diabetes • Infection / Sepsis • Myocardial infarction – Small rise in troponin may occur without overt ischemia – ECG changes may reflect hyperkalemia • Thyrotoxicosis • Drugs
- 34. Treatment of DKA • Once resolved – Convert to home insulin regimen – Prevent recurrence • Initial hospital management – Replace fluid and electrolytes – IV Insulin therapy – Glucose administration – Watch for complications – Disconnect insulin pump
- 35. Treatment of DKA Fluids and Electrolytes • Fluid replacement –Restores perfusion of the tissues •Lowers counterregulatory hormones •Increase insulin sensitivity –Average fluid deficit 3-5 liters
- 36. Initial fluid resuscitation • 15 to 20 mL/kg lean body weight per hour • (approximately 1000 mL/hour in an average-sized person) for the first couple of hours • Maximum of <50 mL/kg in the first four hours • 1-2 liters of normal saline over the first 2 hours • Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours-When fluid overload is a concern • If hypernatremia develops ½ NS can be used
- 37. Treatment of DKA Fluids and Electrolytes • Hyperkalemia initially present – Resolves quickly with insulin drip – Once urine output is present and K<5.0, add 20-40 meq KCL per liter. • Phosphate deficit – May want to use Kphos • Bicarbonate not given unless pH <7 or bicarbonate <5 mmol/L
- 38. Treatment of DKA Insulin Therapy • IV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulin • Follow with hourly regular insulin infusion • Glucose levels – Decrease 4 to 5.5 mmol/L per hour – Minimize rapid fluid shifts
- 39. Treatment of DKA Glucose Administration • Supplemental glucose – Hypoglycemia occurs • Insulin has restored glucose uptake • Suppressed glucagon – Prevents rapid decline in plasma osmolality • Rapid decrease in insulin could lead to cerebral edema • Glucose decreases before ketone levels decrease • Start glucose when plasma glucose < 16.6 mmol/L
- 40. Insulin-Glucose Infusion for DKA Blood glucose Insulin Infusion D5W Infusion <70 0.5 units/hr 150 cc/hr 70-100 1.0 125 101-150 2.0 100 151-200 3.0 100 201-250 4.0 75 251-300 6.0 50 301-350 8.0 0 351-400 10.0 0 401-450 12.0 0 451-500 15.0 0 >500 20.0 0
- 41. Treatment of HHS • Hydration!!! – Even more important than in DKA • Find underlying cause and treat! • Insulin drip – Should be started only once aggressive hydration has taken place. – Switch to subcutaneous regimen once glucose < 11mmol/L and patient eating. • Serial Electrolytes – Potassium replacement.
- 42. Pottasium Replacement • If the initial K is below 3.3 mmol/L, IV potassium chloride (KCl; 20 to 40 mmol/hour, before insulin therapy till raise the serum potassium concentration into the normal range of 4 to 5 mmol/L • 3.3 to 5.3 given iv K with insulin infusion • If above 5.3 not to given iv K till level less than than
- 43. Resolution of ketoacidosis in DKA • ●Normalization of the serum anion gap (less than 12 mEq/L) and blood beta- hydroxybutyrate levels • ●Patients with HHS are mentally alert and the effective plasma osmolality has fallen below 315 mOsmol/kg • ●The patient is able to eat
- 44. Caveat • Urinary ketones by the nitroprusside method can be used for the initial diagnosis of ketoacidosis • It should not be used for monitoring resolution of DKA. • Nitroprusside reacts mainly with acetoacetate, to a much lesser degree with acetone (which is not an acid), and not with beta-hydroxybutyrate. • A positive nitroprusside test may persist for up to 36 hours after resolution of the ketoacidosis due to a positive reaction with acetone, which is slowly eliminated,
- 45. Once DKA Resolved Treatment • Most patients require 0.5-0.6 units/kg/day • Pubertal or highly insulin resistant patients – 0.8-1.0 units/kg/day • Long acting insulin – 1/2-2/3 daily requirement – NPH, Lente, Ultralente or Lantus • Short acting insulin – 1/3-1/2 given at meals – Regular, Humalog, Novolog • Give insulin at least 2 hours prior to weaning insulin infusion.
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- 48. Complications of DKA • Infection – Precipitates DKA – Fever – Leukocytosis can be secondary to acidosis • Shock – If not improving with fluids r/o MI • Vascular thrombosis – Severe dehydration – Cerebral vessels – Occurs hours to days after DKA • Pulmonary Edema – Result of aggressive fluid resuscitation • Cerebral Edema – First 24 hours – Mental status changes – Tx: Mannitol – May require intubation with hyperventilation
- 50. Prevention of DKA / HHS • Type 1 diabetes – Education around sick day management – Continuation of insulin even when not eating – Frequent monitoring when ill • Type 2 diabetes – Education around sick day management – Frequent monitoring when ill
- 51. Prevention of DKA Sick Day Rules • Never omit insulin – Cut long acting in half • Prevent dehydration and hypoglycemia • Monitor blood sugars frequently • Monitor for ketosis • Provide supplemental fast acting insulin • Treat underlying triggers • Maintain contact with medical team
- 54. Conclusion • Successful management requires – Judicious use of fluids • Establish good perfusion – Insulin drip • Steady decline • Complete resolution of ketosis – Electrolyte replacement – Frequent neurological evaluations – High suspicion for complications • Determine etiology to avoid recurrent episodes