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Diabetic Ketoacidosis

Diabetic Ketoacidosis. Definition. 2009 ADA consensus statement on DKA Life-threatening condition characterized by hyperglycemia (glucose >250mg/dl) Ketonemia or ketonuria Arterial pH <7.3 Bicarb < 15mmol/L. Epidemiology/Statistics. Annual incidence 5-8 episodes/1000 person-years

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Diabetic Ketoacidosis

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  1. Diabetic Ketoacidosis

  2. Definition • 2009 ADA consensus statement on DKA • Life-threatening condition characterized by • hyperglycemia (glucose >250mg/dl) • Ketonemia or ketonuria • Arterial pH <7.3 • Bicarb < 15mmol/L

  3. Epidemiology/Statistics • Annual incidence 5-8 episodes/1000 person-years • Mortality ~5% in adult DKA • Underlying precipitating illness • Annual hospitalizations for DKA – 100,000 • Annual hospitalization cost exceeds $1 billion.

  4. Pathogenesis • Insulin deficiency and/or resistance • Excess of counter-regulatory hormones (glucagon, catecholamines, cortisol, GH) • Increased gluconeogenesis, glycogenolysis, proteolysis, lypolysis • Decreased glucose utilization in peripheral tissues

  5. Pathogenesis (cont’d)

  6. Precipitating Factors • Infections (30-50%) • Medication non-compliance or inadequate treatment (30%) • New onset diabetes (20%) • Others- CVA, MI, trauma, pancreatitis, alcohol and drug abuse, pregnancy, thyrotoxicosis, hypercortisolism, drugs

  7. Polyuria Polydipsia Polyphagia Weight loss Nausea, vomiting Abdominal pain Weakness Clouding sensorium History

  8. Evidence of dehydration dry mucus membrane decreased skin turgor orthostatic hypotension decreased UOP Fruity odor Tachycardia Hypotension Kussmaul’s respiration Altered mental status Shock Coma Physical Exam

  9. Diagnostic Studies • Blood work – • Chemistry panel, including Mg, PO4 • Serum ketones • UA with urine ketones • ABG/VBG • Serum Osmolality • Cbc with differential • Others: autoantibodies (anti-GAD, anti-islet cells), C-peptide, A1c, fasting lipid

  10. Diagnostic Studies (cont’d) • K+, Mg++, PO4-- depletion are usually found. • Initial serum K+ can be high due to extracellular shift of K+ secondary insulin deficiency and acidemia • Hyponatremia - osmotic pull of water into intravascular space, vomiting with fluid loss and free water replacement, or severe hyperlipidemia (pseudohyponatremia)

  11. Diagnostic Studies (cont’d) • Cr may be falsely elevated due to acetoacetate interference with measuring method • Leukocytosis is usually present, but usually wbc <25K and no left shift • Amylase, lipase, and LFT can be elevated • In rare cases, patients can have severe hyperlipidemia, requiring sample dilution, leading to factitiously pseudohypo- or normoglycemia

  12. Diagnostic Studies (cont’d) • Ketones in DKA are acetoacetate, acetone and B hydroxybutyrate (BHB is not detected by nitroprusside reaction) • During treatment for DKA, B hydroxybutyrate is converted to acetoacetate, so test for ketones may become more strongly positive despite improvement DKA

  13. EKG CXR if pneumodrome present Blood cx, urine cx, throat cx if indicated Diagnostic Studies (cont’d)

  14. Diagnosis • Diagnostic criteria • BG >250, HCO3 <15, pH <7.3 • Ketonemia or ketonuria • Differential diagnoses • Ketoacidosis – alcohol, starvation • AG metabolic acidosis - MUDPILES

  15. Diagnosis (cont’d)

  16. Treatment • 1. IV fluid • Initially administer 1-2 L 0.9%NS bolus • Switch to 0.45% NS infusion at rate 300-500 ml/hr if corrected Na+ is normal or high • When BG < or = 200 mg/dL, switch to 5% dextrose with 1/2NS at 150-250 ml/hr

  17. Treatment (cont’d) • 2. Insulin • Traditionally, IV regular insulin is used • Give loading dose at 0.1 units/kg as IV bolus then infuse at rate 0.1 units/kg/hr or • Start continuous infusion at 0.14 units/kg/hr • If BG does not fall by 50-70 mg/dl per hour, double infusion dose • Once BG reaches 200 mg/dl can reduce infusion rate (by 2-3units) to keep BG between 150-200 mg/dl until DKA resolves

  18. Treatment (cont’d) • 2. Insulin (cont’d) • Transition to SC insulin • Once AG < 12 meq/L [BG < 200 mg/dl, HCO3- >18 mEq/L, and pH > 7.3, AG < 12 meq/L] • if patient feels hungry and would like to eat, • not in NPO status

  19. Treatment (cont’d) • 2. Insulin (cont’d) • Start with both long- and rapid-acting insulin or around- the-clock regular insulin • Give 60 minutes before discontinuing IV insulin • Long-acting – NPH or glargine • Rapid-acting – aspart, or lispro • Newly diagnosed patients usually requires 0.5 – 0.8 units/kg/day • Half given as long acting and remaining half given before meals • Check FBG qac and hs and supplement with sliding scale insulin to keep BG 100-150 mg/dL

  20. Treatment (cont’d) • 2. Insulin (cont’d) • SC or IM route can also be used • Advantages • reduced nursing support, cost • Disadvantages • Pt’s discomfort • Uncertain absorption

  21. Treatment (cont’d) • 2. Insulin (cont’d) • Prospective, randomized open trial • Efficacy of subcutaneous lispro insulin (n = 20) compared to standard low dose intravenous regular insulin (n = 20) in uncomplicated DKA • No statistical differences in mean duration of treatment or amount of insulin administration, length of hospital stay, or mortality • Treatment of DKA in the ICU was associated with 39% higher hospitalization charges than was treatment with subcutaneous lispro in a non-intensive care setting ($14,429 +/- $5243 vs. $8801 +/- $5549, P <0.01). Am J Med 2004; 117: 291

  22. Treatment (cont’d) • 2. Insulin (cont’d) • Prospective, randomized, open trial • Efficacy of aspart insulin given at 1hr (SC-1h) or 2hr (SC-2h) compared to IV regular insulin in uncomplicated DKA • 45 patients – SC-1h, n =15, SC-2hr, n =15, IV-R, n = 15 • No statistical differences in mean duration of treatment or amount of insulin administration until correction of hyperglycemia or resolution of ketoacidosis • No difference in mortality or length of hospital stay Diabetes Care 2004; 27: 1873

  23. Treatment (cont’d) • 2. Insulin (cont’d) • SC rapid-acting insulin • Uncomplicated mild DKA • 0.3 U/kg, then 0.2 U/kg one hour later and then q2 hrs JCEM 2008; 93:1541.

  24. Treatment (cont’d) • 3. Electrolytes • Potassium • If initial serum K+ > 5.3 mEq/L, no supplement • If serum K+ between 3.3 and 5.3 mEq/L, give 20-30 mEq K+ in each liter of IV fluid to keep K at 4-5mEq/L • If serum K+ < 3.3 mEq/L, hold insulin and give 40 mEq K+ per hour until K+ > 3.3 mEq/L

  25. Treatment (cont’d) • 3. Electrolytes (cont’d) • Bicarbonate (100mmol in 400ml water with 20 mmol KCL over 2 hours until pH >7) • Give only if pH <6.9 • Phosphate • Replace if serum phosphate < 1.0 mg/dL • Magnesium • Replace with IV MgSO4 if serum Mg++ <1.5 mg/dL

  26. Treatment (cont’d) • 4. Monitoring frequency • Initially q1-2 hrs for first few hours, then q2-4 hrs until stable • Flow sheet

  27. Disposition • Discharge from ER • Mild DKA • Alert • Able to tolerate oral intake • Compliant • Good social support • Admission • All other cases, including those with comorbidities and poor social support

  28. Complications • Cardiac arrhythmias • From electrolyte abnormalities or acidosis • Hypoglycemia • From overzealous insulin dosage • Hypokalemia • Due to administration of insulin and bicarbonate • Hyperglycemia/DKA recurrence • Due to discontinuation of IV insulin prematurely or failure to cover with SC insulin

  29. Complications (cont’d) • Hyperchloremic metabolic acidosis • Excessive Cl- from IV fluid • Loss of HCO3- due to excretion of ketoanions as Na and K salts • Cerebral edema • Due to osmotically-driven movement of water into CNS • Occurs primarily in children • When plasma osmolality decreases too rapidly • Suspect when patient’s sensorium deteriorates or remains impaired despite resolution of DKA

  30. Complications (cont’d) • Pulmonary edema • Patients with widened A-a gradients, wet crackles on lung exam • Frequently monitor patients with cardiac disease or renal insufficiency • Venous and arterial thrombosis • DKA is a hypercoagulable state from endothelia injury, hypofibrogenolysis, and platelet hyperaggregation • DVT prophylaxis

  31. Prevention • Diabetic education • Sick day management • Frequent measurement of blood glucose • Home monitoring of ketones • Easily digestible liquid diet • Hold short acting insulin if not eating • Continue long acting insulin • Early access to professional advice • Case management for high-risk patients

  32. Management Errors • Not giving enough IV fluid • Overly rapid correction of hyperglycemia • Transitioning to SQ insulin too soon • Not allowing enough time for SQ insulin to start working before stopping IV insulin • Not repleting electrolytes

  33. References • 1. Kitabchi, AE et al. “Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association.” Diabetes Care 2006; 29: 2739. • 2. Kitabchi, AE et al. “Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state.” JCEM 2008; 93: 1541. • 3. American Diabetes Association. “Hospital Admission Guidelines for Diabetes.” Diabetes Care 2004; 27(Suppl 1): S103. • 4. Charfen, MA. “Diabetic Ketoacidosis.” Emerg Med Clin N Am 2005; 23:609.

  34. References (cont’d) • 5. Umpierrez, GE. “Treatment of Diabetic Ketoacidosis with Subcutaneous Insulin Aspart.” Diabetes Care 2004;27:1873. • 6. Umpierrez, GE. “Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis.” Am J Med 2004; 117 (5):291. • 7. Kitabchi, AE. “Management of Hyperglycemic Crises in Patients with Diabetes.” Diabetes Care 2001;24:131. • 8. American Diabetes Association. “Hyperglycemic Crises in Diabetes.” Diabetes Care 2004; 27 (Suppl 1): S94-102.

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