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Diabetic Ketoacidosis

An 18-year-old man with insulin-dependent diabetes mellitus (type I) is seen in the emergency room. He did
not take his insulin during the previous 24 hours because he did not feel well and was not eating. He now
complains of weakness, nausea, thirst, and frequent urination. On physical examination he is found to have
deep and rapid respirations. At 2 AM the following laboratory data are obtained:

The diagnosis of diabetic ketoacidosis is made, and the man is admitted to the hospital. Intravenous saline is
administered, and insulin therapy is begun. At 3 AM, [HCO 3-] is administered with more insulin. The results
of therapy are illustrated below.

1. What type of acid-base disorder does this man have?

2. Why did this man develop hyperkalemia?

3. Why did the serum [K+] fall during the first hour of insulin infusion?

4. What effect will intravenous administration of [HCO3-] have on the serum [K+]?

5. What is the mechanism for the polyuria in this man? What effect, if any, does the increased urine output
have on his K+ homeostasis?

6. This man's serum [Na+] was 135 mEq/L before the initiation of therapy. By 7:00 AM it had risen to 152
mEq/L. What is the mechanism for the development of hypernatremia (i.e., increased serum [Na+])?

1. The acid-base disorder of this man is a metabolic acidosis. In the absence of insulin the metabolism of fats
and carbohydrates is altered such that nonvolatile acids (ketoacids) are produced. The nonvolatile acids are
rapidly buffered by cellular and extracellular buffers. Buffering in the extracellular fluid decreases the plasma
[HCO3-]. The deep rapid breathing reflects the respiratory compensation (PCO2 is lowered).

2. Hyperkalemia in this patient is a result of a shift of K+ out of cells (e.g., skeletal muscle) into the extracellular
fluid. This shift occurs because of the lack of insulin and the hypertonicity of the ECF secondary to the
elevated [glucose]. The acidosis is probably not a major contributing factor to the development of
hyperkalemia in this situation. When acidosis is induced by mineral acids (e.g., HCl), movement of H + into
cells during the process of intracellular buffering results in a shift of K + out of the cell and into the ECF.
However, with organic acidosis, as occurs in this situation, the cellular buffering of the organic acids does not
shift a significant amount of K+ out of the cell.

3. Insulin causes K+ to move into cells. The mechanism responsible for this effect of insulin appears to be
related to stimulation of the Na+, K+-ATPase. With increased activity of the Na+, K+-ATPase, K+ uptake into
the cell is enhanced. In addition, insulin's effect on glucose metabolism will lower the serum [glucose]. As a
consequence, the osmolality of the ECF will decrease and cause additional K+ to move into cells.

4. The administration of HCO3- would increase the blood pH and shift some K + into cells. The HCO3- containing
intravenous fluid would also increase the volume of the ECF and dilute the K + in this compartment. Studies
in experimental animals have shown that the dilution of K+ by expansion of the ECF is the primary
mechanism by which the infusion of an [HCO3-]-containing solution decreases the serum [K+].

5. The polyuria is a result of an osmotic diuresis induced by glucose. When the filtered load of glucose is below
the Tm for glucose reabsorption in the proximal tubule, all of the filtered glucose is reabsorbed. However, in
this man the filtered load of glucose will exceed the glucose T m. Consequently, the nonreabsorbed glucose
(filtered load - Tm) will remain in the lumen of the proximal tubule where it will act as an osmotically active
particle. As NaCl and water are reabsorbed by the proximal tubule, the concentration of the nonreabsorbed
glucose will increase. With this increase in concentration, an osmotic gradient opposite to that generated by
the NaCl reabsorptive process is developed. Because proximal tubule reabsorption is isosmotic, the presence
of this glucose osmotic gradient will inhibit a portion of proximal tubule NaCl and water reabsorption.
Because of the glucose-induced osmotic diuresis, delivery of NaCl and water will be increased to the distal
tubule and collecting duct, which will stimulate K + secretion at these sites. As a result, K + excretion from the
body will be increased. Increased K+ excretion together with the shift of K+ from the ICF to the ECF
secondary to the insulin deficiency and hyperosmolality will lead to progressive depletion of whole body K+.
Accordingly, an increase in serum [K+] is not always indicative of positive K+ balance. This man is in negative
K+ balance, and is at risk of the development of hypokalemia when insulin is administered and the metabolic
abnormalities are corrected.

6. The glucose-induced osmotic diuresis causes a loss of water from the body in excess of solute. This may lead
to the development of hypernatremia. However, the hyperglycemia causes a shift of water from the ICF to
the ECF, which dilutes the ECF Na+. As therapy is initiated and the hyperglycemia is corrected, water will
move back into the ICF and thereby lead to the development of hypernatremia.