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- How to define diabetic ketoacidosis?
The diagnostic criteria for diabetic ketoacidosis (DKA) include blood glucose
>250 mg/dl, ketonemia/ketonuria [plasma β-(OH) butyrate >3 mmol/L, plasma
acetone/acetoacetate positive in >1:2 dilution and/or urine ketones ≥3+], and
blood pH <7.3 with serum bicarbonate <15 mEq/L. The presence of ketoacidosis
in a diabetic patient with blood glucose <250 mg/dl is termed as euglycemic
diabetic ketoacidosis. The common causes of euglycemic DKA include preg-
nancy, starvation, alcohol intake, and suboptimal treatment with insulin.
Recently, the use of SGLT2 inhibitors has been shown to be associated with
euglycemic DKA in both patients with T1 and T2DM.- What are the biochemical parameters to be monitored in a patient with DKA?
The biochemical parameters to be monitored in a patient with DKA include
blood glucose, arterial pH, serum anion gap, and potassium. Hourly monitoring
of blood glucose is recommended for initial 24h to titrate the rate of insulin
infusion. When blood glucose level is reduced to <200 mg/dl, 5 % dextrose
infusion should be added to prevent hypoglycemia, and the dose of insulin infu-
sion is to be reduced. Arterial pH and serum anion gap should be monitored
every four to six hours, and with effective treatment, arterial pH increases and
serum anion gap progressively decreases. Serum K+ should be monitored at
baseline and every four to six hours. The presence of hypokalemia at presenta-
tion suggests severe depletion of body stores of potassium, and hypokalemia
may worsen after insulin infusion therapy. Monitoring of plasma β-(OH) butyr-
ate may be useful, but estimation of urine ketones by Rothera’s test or Ketostix
may not be rewarding. Failure to respond to therapy suggests inadequate fluid
replacement, suboptimal insulin therapy, occult infection, or other causes of
metabolic acidosis (lactic acidosis or uremia).- A patient with T1DM who presented with DKA was optimally managed with
insulin infusion and fluids with normalization of arterial pH and anion gap;
however, ketonuria is persisting. How to interpret?
Ketone bodies (acetone, acetoacetate, and β-hydroxybutyrate), being lipophilic,
accumulate in adipose tissue. The slow release of ketone bodies into circulation
from adipose tissue explains the persistence of ketonuria even after recovery
from DKA. Further, in patients of DKA who present with severe dehydration or
shock, acetoacetate is converted to β-hydroxybutyrate, and after recovery from
DKA, β-hydroxybutyrate is rapidly converted to acetoacetate and acetone and
excreted in urine. Therefore, during recovery phase of DKA, serum
β-hydroxybutyrate level progressively declines, whereas urinary ketones (ace-
tone, acetoacetate) persist or may even increase.12 Diabetes in the Young