Diabetic Ketoacidosis (DKA)

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