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Subsections
Diabetic Ketoacidosis Treatment

Endocrinology

Diabetic Ketoacidosis Treatment

Initial/Prep/Goals

  1. ABCs, IV access, O2, monitor frequently
  2. Goals of acute treatment

Medical/Pharmaceutical Algorithms

  1. Correct Fluid Loss
    • Helps decrease acidosis and hyperglycemia
    • If cardiac compromised (i.e. hypotensive)
      • Rapid infusion with normal/isotonic saline (NS) or Lactated Ringer's (LR) until SBP > 80 mmHg
      • Give 1-2 L NS bolus over 45-60 minutes and repeat until shock corrected
    • If no cardiac compromise
      • NS (0.9% NaCl) infusion at 15-20 mL/kg/hr (or 1-1.5 L during first hour)
      • Subsequent choice for fluid replacement dependent on patient status; corrected deficits should be seen in first 24 hours
      • Serum Na+ should be corrected for hyperglycemia
        • For each 100 mg/dL glucose increase above 100 mg/dL, add 1.6 mEq to Na+ value
        • If Na+ normal/elevated: change to 1/2 NS (0.45% NaCl) at 250-500 mL/hr (general rate)
        • If Na+ low: continue with NS (0.9% NaCl) at 250-500 mL/hr (switch to 1/2 NS when sodium normalizes)
      • Keep urine output 1-2 mL/kg/hr
    • When BG reaches 200 mg/dL [11.1 mmol/L] and sodium normalizes
      • Add 5% Dextrose in 1/2 NS (0.45% NaCl) at 150-250 mL/hr until DKA resolves
      • *Note*: Hyperglycemia is corrected (6 hrs) before ketoacidosis (12 hrs)
      • Adding 5% Dextrose prevents hypoglycemia as insulin administration continues
    • Avoid too rapid fluid administration
      • Can cause cerebral edema
      • Rarely seen if > 20 years old
      • Occurs in first 24 hrs
      • Unpredictable
      • Headache is first symptom, then neurological deterioration
        • Should prompt head CT or MRI
      • > 50% die or have permanent neurological sequelae
      • If cerebral edema does occur, treatment usually with mannitol infusion and mechanical ventilation
  2. Correct Electrolyte abnormalities
    • Potassium (K+) Correction
      • Establish adequate renal function (i.e. urine output ~50 mL/hr)
      • Hypokalemia must be corrected BEFORE insulin therapy
      • If K+ < 3.3 mEq/L
        • Hold insulin
        • Give KCl at 20-40 mEq/hr until K+ > 3.3 mEq/L
          • *Note*: KCl at 40 mEq/hr IV is max rate
          • Oral potassium may be given if required (physician discretion)
          • Requires hourly checks, cardiac monitoring
      • If K+ is 3.3-5.3 mEq/L
        • Give 20-30 mEq K+ in each liter of IV fluid
          • Maintain serum K+ 4-5 mEq/L
          • Check q2h
      • If K+ > 5.3 mEq/L
        • DO NOT give K+
        • Requires monitoring q2h or until serum K+ < 5.0 mEq/L
    • Sodium Bicarbonate (NaHCO3)
      • Indicated only in life-threatening acidosis
      • If pH ≥ 6.9
        • Use NOT RECOMMENDED
      • If pH is < 6.9
        • Add 100 mEq [100 mmol] bicarbonate + 20 mEq KCl [20 mmol] in 400 mL H2O
          • Infuse at 200 mL/hr over 2 hrs
        • Check bicarbonate and potassium q2h
        • Repeat if necessary until pH ≥ 7.0
    • Sodium
    • Phosphate
      • Not usually needed except in severe deficiency with comorbid conditions (physician discretion)
        • Indicated only to prevent muscle weakness if cardiac dysfunction, anemia, or respiratory depression present
      • If phosphate < 1.0
        • Add 20-30 mEq/L potassium phosphate (K2PO4) at 1.5 mL/hr (4.5 mmol/hr of K2PO4)
      • *Note*: Replace fraction of potassium with K2PO4
        • K2PO4: replace 1/3 potassium
        • KCl: replace 2/3 potassium
    • Magnesium
      • If Mg2+ < 1.2 mg/dL and symptomatic
        • Add 1-2 g of MgSO4 IM or IV over 1 hr
  3. Insulin Therapy
    • Make sure K+ is > 3.3 mEq/L [3.3 mmol/L]
    • ADA preferred route of administration is continuous IV infusion of low-dose regular insulin
      • Short half-life, ease of titration
      • Low-dose therapy without bolus preferred
        • Initial bolus controversial
        • May saturate insulin receptors
        • Greater glucose drop in first hr
        • However, in the absence of initial bolus, doses < 0.1 units/kg/hr ineffective
    • Preferred regimen
      • Low-dose, continuous IV infusion: 0.14 units/kg/hr (no bolus)
        • Anticipate BG drop by 10% in first hour
        • Expect BG decrease rate 50-70 mg/dL/hr
      • If BG drop inadequate (< 10% in first hour or < 50 mg/dL/hr)
        • Give 0.14 units/kg IV bolus
          • Then continue with prior infusion rate or increase infusion rate 50-100% (physician discretion)
          • Continue at increased rate until adequate
    • Alternative regimen
      • Low-dose with bolus
        • Higher risk for hypoglycemia
      • Initial bolus: 0.1 units/kg IV
        • Then continuous IV infusion with 0.1 units/kg/hr
      • If BG drop inadequate (< 10% in first hour or < 50 mg/dL/hr)
        • Give 0.14 units/kg IV bolus
          • Then continue with prior infusion rate or increase infusion rate 50-100% (physician discretion)
          • Continue at increased rate until adequate
    • When BG reaches ≤ 200 mg/dL [11.1 mmol/L] (and pH > 7.3, serum bicarbonate > 18 mEq/L [18 mmol/L])
      • Add 5% Dextrose to IV fluids as required
      • Reduce IV infusion rate to 0.02-0.05 units/kg/hr or give rapid-acting insulin at 0.1 units/kg SC q2h
        • To transfer from IV to SC insulin: continue IV infusion for 1-2 hrs after initiating SC insulin
        • Ensures adequate plasma insulin levels
      • Maintain BG 150-200 mg/dL [8.3-11.1 mmol/L] until resolution of DKA
    • Start standard insulin therapy when DKA is resolved
  4. Monitoring
    • Morbidity in DKA is often iatrogenic
      • Hypokalemia from not replacing K+
      • CHF from over-aggressive fluid resuscitation
        • Rarely, cerebral edema
      • Hypoglycemia from not monitoring glucose levels
      • Alkalosis from too much HCO3-
    • Meticulous flow sheets for
      • VS, I&O, Insulin given
      • Electrolytes
        • K+ (hourly)
        • Cl-
        • HCO3-, pH, CO2
    • Indicators of recovery in most institutions are
      • pH > 7.3 and urine ketone-free
      • Evidence is accumulating to utilize point-of-care ß-OHB determinations < 1 mmol/L (2 occasions) as indicator of recovery
        • Occurs significantly earlier than urine ketone clearance
    • DKA is considered resolved when
      1. Blood glucose is < 11.1 mmol/L
      2. Serum bicarbonate > 18 mmol/L OR venous pH > 7.3
      3. Note that clearance of serum or urine ketones takes longer to resolve than blood glucose and pH

Disposition

  1. Admission criteria
    • ICU generally if severely acidotic
    • All pregnant patients with DKA
  2. Consults
    • Endocrinologist
  3. Discharge/Follow-up instructions
    • Some sources suggest that specific patients may be discharged
      • Mild DKA
      • Reliable pt
      • Underlying cause does not require treatment
      • Close follow-up

Related Topics

References

  1. American Diabetes Association (ADA). Standards of Medical Care in Diabetes- 2023. Diabetes Care. Jan 2023;46(S1): s1-291. Available at: https://diabetesjournals.org/care/issue/46/Supplement_1 [Accessed March 2024]
  2. In: Tintinalli JE, Ma OJ, Yealy DM, et al; (eds). Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th ed., McGraw-Hill, 2020; Chapter 225
  3. Lizzo JM, Goyal A, Gupta V. Adult Diabetic Ketoacidosis. StatPearls [Internet]. Available at: https://www.ncbi.nlm.nih.gov/books/NBK560723/. [Accessed March 2024]
  4. American Diabetes A. Standards of Medical Care in Diabetes-2019. Diabetes Care. Jan 2019; 42(1)
  5. Standards of medical care in diabetes--2015: summary of revisions. Diabetes Care. 2015;38 Suppl:S4.
  6. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. ADA Consensus Statement: Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care, Jul 2009;32(7):pp.1335-1343
  7. American Diabetes Association (ADA). Standards of Medical Care in Diabetes- 2014. Diabetes Care, Jan 2014;37(S1):S14-S80
  8. Goyal N, Miller JB, Sankey SS, Mossallam U. Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med. May 2010;38(4):pp.422-427
  9. Chiasson JL, Aris-Jilwan N, Bélanger R, et al. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ 2003;168(7):859-66
  10. Laffel L. Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev Nov-Dec 1999;15(6):412-26
  11. Kannan CR. Bicarbonate therapy in the management of severe diabetic ketoacidosis. Crit Care Med Dec 1999;27(12):2833-2834
  12. Wagner A, Risse A, Brill HL. Therapy of severe diabetic ketoacidosis. Zero-mortality under very-low- dose insulin application. Diabetes Care May 1999;22(5):674-677
  13. Paton RC, Sathiavageeswaran M. Severe diabetic ketoacidosis. Diabet Med Oct 1999;16(10):884
  14. Noyes KJ, Crofton P, Bath LE, et al. Hydrxybuterate near-patients testing to evaluate a new endpoint for intravenous insulin therapy in the treatment of diabetic ketoacidosis in children. Pediatric Diabetes 2007;8(3):150-6

Contributor(s)

  1. Ho, Nghia, MD
  2. Singh, Ajaydeep, MD
  3. Shaw, Iissha, PharmD Candidate

Updated/Reviewed: March 2024