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 1 diabetes mellitus. A physical examination in the emergency department indicated postural hypotension, tachycardia, and Kussmaul respiration. The breath was noted to smell of “acetone.” Examination of the thorax suggested consolidation in the right lower lobe.
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|Laboratory Data ||Value ||Units |
|Sodium ||130 ||meq/L |
|Potassium ||5.0 ||meq/L |
|Chloride ||96 ||meq/L |
|CO2 ||14 ||meq/L |
|Blood urea nitrogen (BUN) ||20 ||mg/dL |
|Creatinine ||1.3 ||mg/dL |
|Glucose ||450 ||mg/dL |
|Arterial Blood Gases ||On Room Air || |
|pH ||7.39 || |
|Pco2 ||24 ||mmHg |
|Pao2 ||89 ||mmHg |
|[HCO3−] ||14 ||meq/L |
|Anion gap ||20 ||meq/L |
|Urinalysis || || |
|Urine ketones ||Positive 4+ || |
|Glucose ||Positive 4+ || |
|Serum Ketones ||Strongly positive 1:8 || |
|Chest X-Ray || || |
|Pneumonic infiltrate, right lower lobe || || |
The diagnosis of the acid-base disorder should proceed in a stepwise fashion:
The normal anion gap (AG) is 8–10 meq/L, but in this case, the AG is elevated (20 meq/L). Therefore, the change in AG (ΔAG) = ~10 meq/L.
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 AG is approximately equal to the decrement in bicarbonate.
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, indicating a superimposed respiratory alkalosis.
Therefore, this patient has a mixed acid-base disturbance with two components: (a) high AG acidosis secondary to ketoacidosis and (b) respiratory alkalosis (which was secondary to community-acquired pneumonia in this case). The latter resulted in an additional component of hyperventilation that exceeded the compensatory response driven by metabolic acidosis, explaining the normal pH. The finding of respiratory alkalosis in the setting of a high AG acidosis suggests another cause of the respiratory component. Respiratory alkalosis frequently accompanies 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 1 diabetes mellitus. Infections in DKA are common and may be a precipitating feature in the development of ketoacidosis.