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.
|Blood urea nitrogen (BUN)||20||mg/dL|
|Arterial Blood Gases||On room air|
|Urine ketones||Positive 4+|
|Serum ketones||Strongly positive 1:8|
|Pneumonic infiltrate, right lower lobe|
The diagnosis of the acid-base disorder should proceed in a stepwise fashion:
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.
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.
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.
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.
The diagnosis of DKA is usually not challenging but should be considered in all patients with an elevated anion-gap and metabolic acidosis. Hyperglycemia and ketonemia (positive acetoacetate at a dilution of 1:8 or greater) are sufficient criteria for diagnosis in patients with Type 1 diabetes mellitus. The Δ[HCO3−] should approximate the increase in the plasma anion gap (ΔAG), but this equality can be modified by several factors. For example, the ΔAG often decreases with IV hydration, as glomerular filtration increases and ketones are excreted into the urine. The decrement in plasma sodium results from hyperglycemia, which induces the movement of water into the extracellular compartment from the intracellular compartment of cells that require insulin for the transport of glucose. Additionally, a natriuresis occurs in response to an osmotic diuresis associated with hyperglycemia. Moreover, in patients with DKA, thirst is very common and water ingestion often continues. The plasma potassium concentration is usually mildly elevated, but in the face of acidosis and as a result of the ongoing osmotic diuresis, a significant total-body deficit of potassium is almost always present. Recognition of this total-body deficit is critically important. The inclusion of potassium replacement in the therapeutic regimen at the appropriate time and with the appropriate indications (see below) is essential. Volume depletion is a very common finding in diabetic ketoacidosis and is a pivotal component in the pathogenesis of the disorder.
Patients with diabetic ketoacidosis often have a sustained and significant deficit of sodium, potassium, water, bicarbonate, and phosphate. The general approach to treatment requires attention to all those abnormalities. Successful treatment of DKA involves a stepwise approach, as follows:
Replace extracellular fluid (ECF) volume deficits. Since most patients present with actual or relative hypotension and, at times, impending shock, the initial fluid administered should be 0.9% NaCl infused rapidly until the systolic blood pressure is >100 mmHg or until 2–3 L cumulatively has been administered. During the initial 2–3 h of infusion of saline, the decline in blood glucose can be accounted for by dilution and increased renal excretion. Glucose should be added to the infusion as D5 NS or D5 0.45% NS once the plasma glucose declines to 230 mg/dL or less.
Abate the production of ketoacids. Regular insulin is required during diabetic ketoacidosis as an initial bolus of 0.1 U/kg body weight (BW) IV followed immediately by a continuous infusion of 0.1 U/kg BW per h in NS. The effectiveness of IV (not subcutaneous) insulin can be tracked by observing the decline in plasma ketones. Since the increment in the anion gap above the normal value of 10 meq/L represents accumulated ketoacids in DKA, the disappearance of ketoacid anions is reflected by the narrowing and eventual normalization of the anion gap. Typically, the plasma anion gap returns to normal within 8–12 h.
Replace potassium deficits. Although patients with DKA often have hyperkalemia due to insulin deficiency, they are ...
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