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  • DKA is defined by a lack of insulin or an excess of hyperglycemic hormones leading to an inability by the tissues to use glucose. This leads to lipolysis and the synthesis of ketoacids that will be used as fuel. Ketoacids will trigger metabolic acidosis and polyuria leading to severe dehydration
  • Triggering factors:
    • Inaugural in DM1 (common, revealing about 10% of DM1) or DM2 (rare)
    • Noncompliance or iatrogenic (inadequate insulin coverage, steroids, beta-agonists)
    • Infection or inflammation (e.g., pneumonia, UTI, foot ulcer, abdominal [appendicitis, cholecystitis, pancreatitis, etc.])
    • MI
    • Pregnancy
    • Trauma
  • Mortality in DKA is primarily due to the underlying precipitating illness and only rarely due to the metabolic complications of hyperglycemia or ketoacidosis. The prognosis of DKA is substantially worse at the extremes of age and in the presence of coma and hypotension
  • DKA can present as severe, pseudosurgical abdominal pain. Accurate diagnosis will prevent unnecessary surgery

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Figure 210-1. Pathophysiology and Clinical Features of DKA
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Management of DKA:

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Management of Diabetic Keto-Acidosis
  • Fluids
    • Average fluid deficit in DKA is 6 L
    • If clinically hypovolemic (hypotension, tachycardia), start with 500–1,500 mL of colloid bolus
    • Initial fluid should be NS bolus 10–15 mL/kg
    • After that, change to 1/2 NS with 20 mEq/L potassium
    • Ongoing intraoperative blood and fluid losses should be replaced as usually
    • Once blood sugar dropped to 250 mg/dL and anion gap is still present, fluid can be changed to D5W with 1/2 NS. This will allow insulin administration to reduce ketone without causing hypoglycemia
  • Insulin
    • Regular insulin 10 U IV bolus followed with an infusion at (blood glucose/150) U/h
    • If glucose <90, do not stop insulin but rather increase IV glucose administration
    • When patient resumes PO alimentation, consider changing to SQ insulin
  • Electrolytes
    • Follow electrolytes closely every 4–6 h (every 2 h at very beginning) until anion gap closed
    • Potassium; need usually 10–15 mEq/h for at least first 4 h, irrespective of initial potassium level, for a goal 4–5 mEq/L, as potassium will shift back to intracellular compartment because of insulin, and lead to hypokalemia if uncorrected
    • Phosphate goal should be 1–2 mg/dL
    • Magnesium goal should be 2 mEq/L
  • Acidosis
    • Typically will correct itself with insulin treatment
    • Administer bicarbonate only if pH <7.0 or hemodynamic instability (rare)
  • Triggering factor
    • Diagnose and treat
  • Other
    • Consider thromboprophylaxis depending on risk
    • Education to prevent recurrence
1. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care. 2001 Jan;24(1):131–153.   [PubMed: 11194218]
2. Kreisberg RA. Diabetic ketoacidosis: an update. Crit Care Clin. 1987 Oct;3(4):817–834.   [PubMed: 3139263]
3. Kitabchi AE, Umpierrez GE, Fisher JN, Murphy MB, Stentz FB. Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. J Clin Endocrinol Metab. 2008 May;93(5):1541–1552.   [PubMed: 18270259]
4. De Beer K, Michael S, ...

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