No abstract

We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine.

No abstract

The effect of crystalloid volume loading on serum colloid osmotic pressure, arterial oxygen (Po2), alveolar-arterial oxygen gradient (A-aDo2), and cerebral lateral ventricle dimensions was prospectively studied in 18 patients with diabetic ketoacidosis. Serial measurements showed concomitant decreases in colloid osmotic pressure, hematocrit, arterial Po2 (p less than 0.001), and significant increases in A-aDo2 (p less than 0.001) during treatment. Serial echoencephalograms were taken of 11 of the 18 patients; each patient served as his or her own control. Nine of these 11 patients showed significant decreases in lateral ventricle width during treatment; seven patients showed the echoencephalographic "hash" marks characteristic of cerebral edema. Follow up studies showed resolution of these abnormalities. Volume loading with large amounts of crystalloid solution seems to produce an acute hypooncotic state that may cause the development of both subclinical pulmonary and cerebral edema.