Dka pathphysiology & management 2014 - copy


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Lecture By Dr. Zeenat Yassmin
ICU Doctor, Meeqat Hospital, Madina, KSA

Published in: Education, Health & Medicine
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Dka pathphysiology & management 2014 - copy

  2. 2. Diabetic Ketoacidosis (DKA) • A state of absolute or relative insulin deficiency aggravated and followed by • hyperglycemia, dehydration, and acidosis-producing derangements in 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 • It is the presenting symptom for ~ 25% of Type I Diabetics.
  3. 3. Definition of Diabetic Ketoacidosis* Acidosis * Ketosis Hyperglycemia 3
  4. 4. Pathogenesis of DKA Beta-cell failure D/C Insulin Insulin Deficiency Glucotoxicity
  5. 5. Pathogenesis of DKA Insulin deficiency Increased glucagon GH cortisol catecholamines
  6. 6. Carbohydrate Metabolism in DKA Relative or absolute insulin deficiency liver glucose output glycogenolysis muscle glucose uptake
  7. 7. Increased Glucose Production in DKA Gluconeogenesis Glucose Activity of gluconeogenic enzymes (PEPCK, PC, PFK) Glycerol Amino acids Lactate TG Lipolysis Protein breakdown
  8. 8. Increased Production of Ketones in DKA Ketogenesis B-OH-B Acetoacetate FFA Glycerol TG Lipolysis
  9. 9. Pathogenesis of DKA Liver Increased glucose production Peripheral tissue Adipose Decreased glucose uptake Increased release FFA Liver tissue Increased ketogenesis HYPERGLYCEMIA KETOACIDOSIS Osmotic diuresis Decreased alkali reserve Volume depletion Metabolic acidosis
  10. 10. Diagnostic Criteria for DKA DKA Mild Plasma glucose (mg/dl) pH Anion gap Bicarbonate (mEq/l) Urine ketones* Serum ketones* Effective serum Osmol (mOsm/kg)† Alteration in sensoria or mental obtundation Moderate Severe >250 7.25-7.3 >10 15-18 positive positive variable >250 7.0-<7.24 >12 10- <15 positive positive variable >250 <7.0 >12 <10 positive positive variable alert alert/ drowsy stupor/ coma
  11. 11. Clinical Presentation of DKA Symptoms Polydipsia Polyuria Weakness Weight loss Nausea Vomiting Abdominal pain Sign Hypothermia Tachycardia Tachypnea Kussmaul breathing Ileus Acetone breath Altered sensorium The onset of DKA is usually relative short, ranging from hours to a day or two.
  12. 12. Causes of DKA • Stressful precipitating event that results in increased catecholamines, cortisol, glucagon.         Infection (pneumonia, UTI) Alcohol Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids) Non-compliance with insulin
  13. 13. Initial Clinical Evaluation • History and physical examination     Secure patient’s ABC Mental status Cardiovascular-renal status Source of infection • Evaluation of volume and hydration status • Laboratory studies
  14. 14. Initial Laboratory Studies • Immediate determination of blood glucose by finger stick, and serum ketones (3-BH) by finger stick or urinary ketones. • Laboratory studies:        ABG’s CBC with differential CMP (glucose, electrolytes, bicarbonate, BUN, creatinine) Serum ketones Urinalysis Bacterial cultures* Cardiac enzymes* * If clinically indicated
  15. 15. Serum Sodium  Hyponatremia is common in patients with DKA Serum glucose H2O H 2O H2O H 2O Na+ Correction of Serum sodium: Corrected Na+ = [Na+] 1.6 x glucose (mg/dl) – 100 100
  16. 16. Serum Potassium  Admission serum potassium is frequently elevated (due to a shift of K- from the intracellular to the extracellular space) Osmolality Acidosis K+ K+ K+ K+ K+ Na+ K- Insulin regulates Activity of Na+/K+ pump
  17. 17. Anion Gap Formula • Anion gap can be measured as • AG=[(Na)-(Hco3+CL)]
  18. 18. Fluid Therapy in DKA Normal saline, 1-2 L over 1-2 h NS or ½ NS at 250-500 mL/h Glucose < 250 mg/dl D5%1/2NS saline
  19. 19. Caution during fluid management • Fluid should be replace over 12-24hr • patients are generally depleted 3-6lit in DKA. • Monitor urine output,heart rate,blood pressure and respiratory status. • CARE must b taken in patient with CCF and kidney disease.
  20. 20. Blood Glucose monitoring in DKA • Check initial blood glucose q1h.Goal decrease in blood glucose is 50-75mg/dl/hr • Once stable(3consecutie values decrease in target range)change blood glucose monitoringq2h.Resume q1h blood glucose monitoring for each change in the insulin infusion rate. • Add dextrose5% to IV fluid when blood glucose <250mg/dl. • For DKA goal blood glucose 150-200mg/dl until anion gap close.
  21. 21. Intravenous Insulin Therapy in DKA I.V. Bolus: 0.1 U/kg I.V. drip: 0.1 U/kg/h Glucose < 250 mg/dl and HCO3 > 15 mmol/l, then, I.V. drip: 0.05 – 0.1 U/kg/h Until c0rrection of anion gap
  22. 22. CHANGING THE INSULIN INFUSION RATE • Decrease IV insulin by 50%if blood glucose decrease by >100mg/dl/hr in any 1hr period • Increase insulin drip by 50%/hr if change in blood glucose is <50mg/dl/hr • When blood glucose decrease to 250mg/dl insulin infusion may need to be decrease 50% to maintain glucose at target levels(150200mg/dl).
  23. 23. Transition to Subcutaneous Insulin  Patients with DKA should be treated with IV insulin until ketoacidosis is resolved.  Criteria for resolution of DKA:  BG ≤ 200 mg/dL  Serum bicarbonate level ≥ 18 mEq/L  Venous pH ≥ 7.3 and anion gap closed
  24. 24. WHEN TO STOP IV INSULIN • Give short acting insulin SC at twice the hourly IV rate(if iv rate 5u/hr give 10u) • Failure to give SC insulin may result in rebound hyperglycemia and ketosis due to its short acting effect. • ENSURE pt has a meal and is eating and awake.
  25. 25. Potassium replacement K+ = > 5.5 mEq/l; no supplemental is required K+ = 4 - 5 mEq/l; 20 mEq/L of replacement fluid K+ = 3 - 4 mEq/l; 40 mEq/L of replacement fluid If admission K+ = <3 mEq/l give 10-20 mEq/h until K+ >3 mEq/l, then add 40 mEq/L to replacement fluid
  26. 26. Bicarbonate administration pH > 7.0 → no bicarbonate pH < 7.0 and bicarbonate < 5 mEq/l → 44.6 mEq in 500 ml 0.45% saline over 1 h until pH > 7.0
  27. 27. Complications of DKA 1-Complications of associated illnesses e.g. sepsis or MI. 2-Adult respiratory distress syndrome. 3-Thromboembolism (elderly). 4-Complications of treatment: a-Hypokalemia: Which may lead to: -Cardiac arrhythmias. -Cardiac arrest. -Respiratory muscle weakness.
  28. 28. b-Hypoglycemia. c-Overhydration and acute pulmonary edema: particularly in: -Treating children with DKA. -Adults with compromised renal or cardiac function. -Elderly with incipient CHF.
  29. 29. d-Neurological complications: Cerebral Edema. -It occurs mostly in children with DKA. -Very dangerous and increases mortality. -The risk is related to the severity, duration and rapid correction of DKA.   Mechanism: The brain adapts by producing intracellular osmoles (idiogenic osmoles) which stabilize the brain cells from shrinking while the DKA was developing. When the hyperosmolarity is rapidly corrected, the brain becomes hypertonic towards the extracellular fluids → water flows into the cells → cerebral edema
  30. 30. Summary  Diabetic Ketoacidosis is a common, serious and expensive complication in patients with type 1 and type 2 diabetes  Prevention of metabolic decompensation through patient education, strict surveillance of glucose homeostasis and aggressive diabetes management might reduce the high morbidity and mortality associated with diabetic ketoacidosis
  31. 31. THANK YOU