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Updated: Dec 24 2021

Diabetic Ketoacidosis (DKA)

Images
https://upload.medbullets.com/topic/109032/images/slide49.jpg
  • Snapshot
    • A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg.
  • Introduction
    • Complication of type I diabetes
      • result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine
    • Precipitated by
      • infections
      • MI
      • drugs (steroids, thiazide diuretics)
      • noncompliance
      • pancreatitis
      • undiagnosed DM
  • Presentation
    • Symptoms
      • abdominal pain
      • vomiting
    • Physical exam
      • Kussmaul respiration
        • increased tidal volume and rate as a result of metabolic acidosis
      • fruity, acetone odor
      • severe hypovolemia
      • coma
  • Evaluation
    • Serology
      • blood glucose levels > 250 mg/dL
        • due to ↑ gluconeogenesis and glycogenolysis
        • tissues unable to use the high glucose as it is unable to enter cells
      • arterial pH < 7.3
        • ↑ anion gap due to ketoacidosis, lactic acidosis
      • ↓ HCO3-
        • consumed in an attempt to buffer the increased acid
      • hyponatremia
        • dilutional hyponatremia
          • glucose acts as an osmotic agent and draws water from ICF to ECF
      • hyperkalemia
        • acidosis results in ICF/ECF exchange of H+ for K+
        • depletion of total body potassium due to cellular shift and losses through urine
      • moderate ketonuria and ketonemia
        • due to ↑ lipolysis
        • β-hydroxybutyrate > acetoacetate
          • β-hydroxybutyrate not detected with normal ketone body tests
      • hypertriglyceridemia
        • due to ↓ in capillary lipoprotein lipase activity
          • activated by insulin
      • leukocytosis
        • due to stress-induced cortisol release
      • H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted
  • Treatment
    • Fluids
    • Insulin with glucose
      • must prevent resultant hypokalemia and hypophosphatemia
      • labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin
        • due to transcellular shift of potassium out of the cells to balance the H+ being transfered into the cells
        • Upon administration of insulin, potassium will shift intracellularly, possibly resulting in dangerous hypokalemia
    • Long lasting insulin
      • after the anion gap has closed during initial treatment
  • Prognosis, Prevention, and Complications
    • 5-10% mortality
    • Life-threatening mucormycosis
      • thrive in ketoacidotic state
    • Rhizopus infection
    • Cerebral edema
    • Cardiac arrhythmias
      • due to electrolyte imbalances
    • Heart failure
      • due to hypovolemia
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