Respiratory · Year 1 · from Respiratory
Case 1: Diabetic Ketoacidosis
Clinical Image
Source: Wikimedia Commons - Davenport Diagram - Public Domain
Case Presentation
A 22-year-old woman with type 1 diabetes presents to the emergency department with nausea, vomiting, abdominal pain, and confusion for 1 day. She ran out of insulin 3 days ago. On examination, she is lethargic but arousable, with dry mucous membranes, poor skin turgor, and fruity breath odor. Vital signs show heart rate 118 bpm, blood pressure 95/60 mmHg, respiratory rate 32/min with deep labored breaths (Kussmaul respiration), and temperature 37.2C.
Laboratory results show serum glucose 520 mg/dL, serum sodium 128 mEq/L, potassium 5.8 mEq/L, chloride 92 mEq/L, bicarbonate 8 mEq/L, BUN 32 mg/dL, and creatinine 1.8 mg/dL. Arterial blood gas shows pH 7.12, PaCO2 22 mmHg, PaO2 98 mmHg.
Systematic ABG interpretation:
- pH: 7.12 indicates severe acidemia
- Primary disorder: HCO3 of 8 is markedly low, indicating metabolic acidosis as the primary disorder
- Anion gap: Na - (Cl + HCO3) = 128 - (92 + 8) = 28 mEq/L (elevated, normal 8-12)
- Expected compensation: Winter's formula: expected PaCO2 = (1.5 x 8) + 8 = 20 mmHg, range 18-22. Measured PaCO2 is 22 mmHg, indicating appropriate respiratory compensation
- Delta-delta ratio: (28-12)/(24-8) = 16/16 = 1.0, indicating pure anion gap metabolic acidosis
The elevated anion gap is due to accumulation of beta-hydroxybutyrate and acetoacetate (ketoacids). Kussmaul respiration represents maximal respiratory compensation - deep, rapid breathing to eliminate CO2 and partially correct acidemia. Despite PaCO2 of 22 mmHg (dramatic hyperventilation), pH remains severely low because the metabolic acidosis is so profound.
Treatment includes IV insulin, aggressive fluid resuscitation with normal saline, and potassium replacement (serum K will fall precipitously with insulin therapy). Serial monitoring of pH, anion gap, and electrolytes guides therapy. The patient's pH normalizes over 12 hours with resolution of ketoacidosis.
Key Learning Points
- DKA causes anion gap metabolic acidosis from ketoacid accumulation
- Kussmaul respiration is the respiratory compensation (deep, rapid breathing)
- Winter's formula calculates expected PaCO2 for metabolic acidosis compensation
- Delta-delta ratio near 1 indicates pure anion gap acidosis; less than 1 suggests concurrent non-gap acidosis
- Serum potassium may be elevated despite total body depletion due to acidosis-induced cellular shifts