Diabetic Ketoacidosis

Diabetic Ketoacidosis • Accumulation of acetoacetate and β -hydroxybutyrate • ketone bodies are organic acids →metabolic acidosis with an ↑unmeasured AG. • Provoked by intercurrent illness, trauma, or cessation of insulin therapy. • the degree of hyperglycemia does not correlate with the severity of the acidosis. • Blood sugar levels are often in the 300–500 mg·dl–1 range. • leukocytosis, abdominal pain, GI ileus, and mildly ↑ amylase levels are all common in DKA, Pt may Dx as acute abdomen. Treatment • Regular insulin 10 units iv bolus followed by an insulin infusion nominally at (blood glucose/150) units·h–1 • Isotonic iv fluids as guided by V/S and urine OP; anticipate 4–10 l deficit • When urine >0.5 ml·kg–1·h–1, give KCl 10–40 mEq·h–1 (with continuous ECG) • When glucose ↓ to 250 mg·dl–1, add dextrose 5% at 100 ml·h–1 • Consider sodium bicarbonate to correct pH <7.1 • When glucose levels ↓ below 250 mg·dl–1, glucose should be added to the iv fluid while insulin therapy continues.

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K replacement is a key concern in patients with DKA, Because of the diuresis, the total body potassium stores are reduced. • acidosis by itself causes a shift of potassium ions out of the cell. • the serum potassium concentration may be normal or even slightly elevated while the patient is acidotic. • as the M. acidosis is corrected, K shift back into the cells → serum K ↓acutely. • early and vigorous K replacement is required in these Pt, except RF Pt • Hypophosphatemia occurs with the correction of the acidosis and, if severe, may cause impairment of ventilation resulting from skeletal muscle weakness in the vulnerable patient. • Diabetic may have lactic acidosis without DKA, absence ketone bodies A→ ↓ LOC B→ hypoventilation, hypoxia, muscle weakness with ↓ Phos C→ hypovolemia, M→ lytes abnormalities R→ ARF from severe dehydration In addition to all the consideration of diabetic Pt (see card)