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A 23-year-old woman was admitted with a 3-day history of fever, cough productive of blood-tinged sputum, confusion, and orthostasis. Past medical history included Type I diabetes mellitus. A physical examination in the emergency department indicated postural hypotension, tachycardia, and Kussmaul respiration, and the breath was noted to smell of "acetone." Examination of the thorax suggested consolidation in the right lower lobe.

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Laboratory DataUnits
Blood urea nitrogen (BUN)20mg/dL
Creatinine (Creat)1.3mg/dL
Arterial Blood GasesOn room air
Anion gap20meq/L
Urine ketonesPositive 4+
GlucosePositive 4+
Serum ketonesStrongly positive 1:8
Chest x-ray
Pneumonic infiltrate, right lower lobe

Approach to Diagnosis

The diagnosis of the acid-base disorder should proceed in a stepwise fashion:

  1. The normal anion gap (AG) is 10 meq/L, but in this case the anion gap is elevated (20 meq/L). Therefore, the change in AG (ΔAG) = 10 meq/L.

  2. Compare the ΔAG and the Δ[HCO3]. In this case, the ΔAG, as noted above, is 10 and the Δ[HCO3] (25 − 14) is 11. Therefore, the increment in the anion gap is approximately equal to the decrement in bicarbonate.

  3. The next step is to estimate the respiratory compensatory response. In this case, the predicted Paco2 for an [HCO3] of 14 should be approximately 29 mmHg. This value is obtained by adding 15 to the measured [HCO3] (15 + 14 = 29) or by calculating the predicted Paco2 from the Winter equation: 1.5 × [HCO3] + 8. In either case, the predicted value for Paco2 of 29 is significantly higher than the measured value of 24. Therefore, the prevailing Paco2 exceeds the range for compensation alone and is too low.

  4. Therefore, this patient has a mixed acid-base disturbance with two components: (a) high anion-gap acidosis secondary to ketoacidosis and (b) respiratory alkalosis secondary to community-acquired pneumonia. The respiratory alkalosis resulted in an additional component of hyperventilation that exceeded the compensatory response driven by metabolic acidosis, explaining the normal pH in this case. The finding of respiratory alkalosis in the setting of a high-gap acidosis suggests another cause of the respiratory component, which in this case may be attributed to the community-acquired pneumonia.

The clinical features in this case include hyperglycemia, hypovolemia, ketoacidosis, central nervous system (CNS) signs of confusion, and superimposed pneumonia. This clinical scenario is consistent with diabetic ketoacidosis (DKA) developing in a patient with known Type I diabetes mellitus. Infections in DKA are common and may be a precipitating feature in the development of ketoacidosis.


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