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Diabetic Ketoacidosis (DKA) Algorithm

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Presentation

  • 3Ps – Polyuria, Polydipsia, Polyphagia
  • Non-specific symptoms:
    • Weakness, vomiting, abdominal pain, blurry vision
  • Physical Exam:
    • Acetone smell
    • Dehydration / tachycardia / hypotension / shock
    • Kussmaul’s respiration (deep/labored breathing secondary to acidosis)
Pathophysiology of Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar Syndrome (HHS)
Pathophysiology of Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar Syndrome (HHS)

Pathogenesis and Pathophysiology of Diabetic Ketoacidosis
Pathogenesis and Pathophysiology of Diabetic Ketoacidosis

Diagnosis

  • DKA diagnostic criteria:
    • Hyperglycemia: serum glucose > 250 mg/d
    • Acidosis: arterial pH < 7.3, anion gap > 10, serum bicarbonate <18 mEq/l
    • Ketosis: ketonuria or ketonemia
      • Serum beta-OH-butyrate is the preferred method for measuring ketonemia

DKA Diagnosis

□ D-Diabetes, Blood Sugar > 250
□ K-Ketones in urine/serum
□ A-Acidosis-pH<7.3, HCO3<18
Diabetic Ketoacidosis (DKA) - Summary (Diagnosis and Treatment)
Diabetic Ketoacidosis (DKA) – Summary (Diagnosis and Treatment)

Causes

  • Infection (UTI, pneumonia, gastroenteritis, pancreatitis) in 40-50%
  • Infarction (ACS, MI)
  • Infraction (patient noncompliance with therapy)
  • Infant (pregnancy)
  • Ischemic (CVA)
  • Illegal (alcohol, drug abuse/cocaine abuse)
  • Iatrogenic (prescription drug interactions, e.g. steroids)
  • Idiopathic (new onset type 1 diabetes or other cause)

Treatment

Initial Resuscitation

  • Altered sensorium based on level of combination of hyperosmolarity and acidosis (Diabetes Care 2010;33:1837–1839)
  • Start with 2L IV Normal Saline empiric before labs

IV Fluids

  • Start with 2L IV Normal Saline bolus
  • Fluid deficit about 100ml/kg (7-8L deficit) secondary to glucose osmotic diuresis
  • Can decrease glucose to 300 with IV fluids

Sodium

  • Falsely lowered level (hyponatremia) secondary to hyperglycemia
  • Correction: Add 1.6 to Na for every 100 over 100 in glucose level
  • Corrects with IV Fluids
  • 1/2 Normal Saline: Switch to 1/2 NS when Na normalizes

Insulin

  • Mechanism of Action: Stops ketogenesis and breakdown of fatty acids
  • Caution: Hypokalemia
    • Prevalence 5.6% (3 out of 54 patients with hypokalemia) (Am J Emerg Med. 2012;30(3): 481)
    • Do not start insulin until you check potassium → if patient hypokalemic, can drop K even more → arrhythmia
    • Hold insulin until K>3.3
  • Dose: Start 0.1 U/kg/h gtt
  • Monitor
    • If glucose not decrease by 50mg/dl in first hour → double rate or SQ insulin bolus
    • If Glucose >1000 mg/dl, rapid correction puts patient at risk for cerebral edema
    • Glucose reaches 200mg/dl:
      • i. Reduce Insulin gtt to 0.02-0.05 U/kg/hr or
      • ii. Rapid acting insulin 0.1 U/kg SC every 2 hours
    • Anion gap closed
      • i. Goal: Resolution of acidosis/ketosis (not euglycemia) → do not stop insulin until anion gap closed
      • ii. Transition dose SQ insulin (5 Units per 50 over 150-max 20)
      • iii. D/C insulin gtt one hour after SQ dose
  • Dextrose: When glucose is < 200 mg/dl, add D5 to replacement fluids
    • Allows continued insulin administration until ketonemia is controlled while at the same time avoiding hypoglycemia
Diabetic Ketoacidosis Algorithm
Diabetic Ketoacidosis Algorithm

Guidelines for the diagnosis and management of diabetic ketoacidosis
Guidelines for the diagnosis and management of diabetic ketoacidosis

Potassium

  • Total body potassium deficit (average deficit 3-5 meq/kg)
  • May see relative hyperkalemia because of acidosis
  • Repletion: PO (if able to tolerate) and IV
  • Do not start insulin until potassium is > 3.3

HCO3 (Bicarbonate)

Other Electrolytes

  • Magnesium → depleted secondary to osmotic diuresis, ok to replete
  • Phosphorus → may precipitously drop with treatment of DKA, must replete

Monitoring

Complications

  • Hypoglycemia – overzealous DKA treatment
  • Hyperglycemia – undertreatment
  • Hypokalemia
    • Caused by insulin tx, correction of acidosis and volume expansion
  • Return of DKA (Must bridge with SQ insulin dose)
  • Hyperchloremia
  • Cerebral Edema
    • Prognosis: mortality (20-50%), 1/3 survivors in vegetative state
    • Risk factors: age < 5, new onset DM
    • Symptoms: Depressed LOC/AMS (Altered Mental Status), pupillary changes, seizures
    • Treatment
      • Mannitol 1-2 gm/kg
      • Consider: Intubation, Dexamethasone, hypertonic saline (5-10ml/kg)

Read Also : Pitfalls in the Management of Diabetic Ketoacidosis (DKA)

References

  • Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009 Jul;32(7):1335-43. doi: 10.2337/dc09-9032. PMID: 19564476; PMCID: PMC2699725. (https://pubmed.ncbi.nlm.nih.gov/19564476/)
  • Nyenwe EA, Razavi LN, Kitabchi AE, Khan AN, Wan JY. Acidosis: the prime determinant of depressed sensorium in diabetic ketoacidosis. Diabetes Care. 2010 Aug;33(8):1837-9. doi: 10.2337/dc10-0102. Epub 2010 May 18. PMID: 20484127; PMCID: PMC2909073. https://pubmed.ncbi.nlm.nih.gov/20484127/
  • Arora S, Cheng D, Wyler B, Menchine M. Prevalence of hypokalemia in ED patients with diabetic ketoacidosis. Am J Emerg Med. 2012 Mar;30(3):481-4. doi: 10.1016/j.ajem.2011.01.002. Epub 2011 Feb 11. PMID: 21316179. https://pubmed.ncbi.nlm.nih.gov/21316179/
  • Goyal N, Miller JB, Sankey SS, Mossallam U. Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med. 2010 May;38(4):422-7. doi: 10.1016/j.jemermed.2007.11.033. Epub 2008 Jun 2. PMID: 18514472. https://pubmed.ncbi.nlm.nih.gov/18514472/
  • Kitabchi AE, Murphy MB, Spencer J, Matteri R, Karas J. Is a priming dose of insulin necessary in a low-dose insulin protocol for the treatment of diabetic ketoacidosis? Diabetes Care. 2008 Nov;31(11):2081-5. doi: 10.2337/dc08-0509. Epub 2008 Aug 11. PMID: 18694978; PMCID: PMC2571050. https://pubmed.ncbi.nlm.nih.gov/18694978/
  • Viallon A, Zeni F, Lafond P, Venet C, Tardy B, Page Y, Bertrand JC. Does bicarbonate therapy improve the management of severe diabetic ketoacidosis? Crit Care Med. 1999 Dec;27(12):2690-3. doi: 10.1097/00003246-199912000-00014. PMID: 10628611. https://pubmed.ncbi.nlm.nih.gov/10628611/
  • Latif KA, Freire AX, Kitabchi AE, Umpierrez GE, Qureshi N. The use of alkali therapy in severe diabetic ketoacidosis. Diabetes Care. 2002 Nov;25(11):2113-4. doi: 10.2337/diacare.25.11.2113. PMID: 12401775. https://pubmed.ncbi.nlm.nih.gov/12401775/
  • Middleton P, Kelly AM, Brown J, Robertson M. Agreement between arterial and central venous values for pH, bicarbonate, base excess, and lactate. Emerg Med J. 2006 Aug;23(8):622-4. doi: 10.1136/emj.2006.035915. PMID: 16858095; PMCID: PMC2564165. https://pubmed.ncbi.nlm.nih.gov/16858095/
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