Diabetic ketoacidosis and hyperglycemic hyperosmolar state


















Sepsis
Urinary tract infection
Pneumonia
Myocardial infarction
Stroke
Gastrointestinal bleeding
Medication noncompliance
Newly diagnosed diabetes



Presentation

Classic presentation


  • Classic symptoms of hyperglycemia including polyuria, polydipsia, polyphagia, dizziness, and weakness.
  • Abdominal pain, nausea, and vomiting.
  • Altered mental status.
  • Deep breathing (Kussmaul respiration) with fruity odor.
  • Table 59.2 lists the differential diagnoses of patients in DKA.


Table 59.2. Differential diagnosis of DKA











Ketoacidosis
• Alcoholic ketoacidosis
Anion-gap acidosis
• Salicylate toxicity
• Toxic alcohols (methanol, ethylene glycol, propylene glycol)
• Uremia
• Lactic acidosis (sepsis, shock)
Hypoglycemia
Trauma




Critical presentation


  • Profound hypotension due to severe dehydration.
  • Coma, requiring airway protection.

Diagnosis and evaluation


  • Signs of dehydration

    • Dry mucous membranes
    • Altered mental status
    • Orthostatic hypotension
    • Tachycardia.

  • Signs of hyperglycemia

    • Kussmaul respirations
    • Fruity odor of ketones (some people cannot smell this).

  • Diagnostic tests

    • Glucometry – point of care glucose level is typically greater than 250mg/dL (13.89 mmol/L) (may read “high”).
    • Treatment of presumed DKA should begin with rehydration and evaluation for precipitating cause in the setting of a “high” glucometer reading. Further treatment often awaits laboratory results.
    • Chemistry is critical for obtaining glucose and electrolyte levels and calculating anion gap (anion gap = sodium – [chloride + bicarbonate]).

      • Serum potassium is often elevated and will correct with insulin therapy, fluid replacement, and correction of acidosis. Remember: DKA patients are often depleted in total body potassium.
      • Other electrolytes such as magnesium, phosphate, and calcium may also be depleted during DKA and monitoring them is important.
      • Consider checking serum lipase to exclude pancreatitis as a precipitating factor for the hyperglycemia. But keep in mind that hyperglycemia can cause pancreatitis as well.
      • Serial chemistry monitoring every 1–2 hours is recommended during treatment because of rapid fluid and electrolyte shifting.
      • Sodium should be adjusted for elevated glucose. Na+ artificially decreases approximately 1.6 mEq/L for every 5.55 mmol/L (100 mg/dL) the glucose is above normal. For example, if the sodium is measured at 120 mEq/L, blood glucose is 400 mg/dL, the glucose is 300 units above normal (3 × 1.6 = 4.8). Therefore the corrected sodium is 120 + 4.8 >124.8 mEq/L. Above glucose levels of 400 mg/dL, the correction is less reliable and a correction factor of 2.4 mEq/L appears to be more accurate.

    • Serum acetone measurement indicates presence of ketonemia and may correlate with the degree of dehydration and breakdown of fatty acids that occur in DKA.
    • Blood gas measurement is important for determining the degree of acidosis. Venous blood gas has been demonstrated to be as reliable as arterial blood gas for pH monitoring.
    • Chest radiography to exclude pneumonia as a precipitating cause of DKA.
    • Urinalysis evaluates the presence of ketonuria (commonly acetoacetate) and/or presence of urinary tract infection.
    • Critical pitfall: Negative urine ketone testing does not exclude the presence of DKA.
    • ECG evaluates the presence of ischemia or STEMI (ST-segment elevation myocardial infarction) and provides important morphological features of electrolyte abnormalities before starting insulin and potassium therapy.

Critical management


















ABCs
Aggressive fluid replacement
Insulin therapy (0.1 units/kg/hour IV drip)
Potassium repletion
Other electrolyte repletion
Treat underlying cause (e.g., infection, AMI, stroke)
Consider sodium bicarbonate for pH <7.0



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Feb 17, 2017 | Posted by in CRITICAL CARE | Comments Off on Diabetic ketoacidosis and hyperglycemic hyperosmolar state

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