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osmotic diuresis vomiting increased insensible fluid losses lactic acidosis

DEHYDRATION renal Na+ loss poor tissue perfusion

Fig. 3. Pathophysiology of diabetic ketoacidosis. (From Glaser NS, Styne DM. Endocrine disorders. In: Behrman R, Kliegman R, editors. Nelson essentials of pediatrics. 3rd edition. Philadelphia: WB Saunders; 1997; with permission.)

present with DKA is generally preserved within the normal range because of the impermeability of the blood-brain barrier to hydrogen ions [53,54].

Laboratory abnormalities in diabetic ketoacidosis


A diagnosis of DKA can be made when the serum glucose concentration is more than 200 mg/dL and venous pH is less than 7.30 (or the serum bicarbonate concentration is less than 15 mmol/L) in the presence of elevated urine or serum ketone concentrations. DKA with near-normal glucose concentrations also has been described but occurs infrequently [55-57]. This euglycemic DKA may occur in pregnancy and in patients who have known diabetes who have administered insulin before coming to the emergency department. Children who have DKA who have prolonged vomiting and minimal oral intake before presentation also may present with lower initial glucose concentrations. Much of the variability in serum glucose concentrations at presentation may be explained by differences in hydration and nutritional status [35]. Prolonged fasting or poor nutrient intake before the development of DKA decreases substrate availability and results in lower serum glucose concentrations at presentation, whereas more severe dehydration favors higher glucose concentrations. In the absence of pre existing renal disease or unusually high carbohydrate intake, blood glucose concentrations of 500 to 600 mg/dL imply that dehydration is of sufficient severity to diminish the glomerular filtration rate by approximately 30% to 40%. Blood glucose concentrations more than 800 mg/dL suggest that the glomerular filtration rate is decreased by 50% or more [58].


Concentrations of ketone bodies (beta-hydroxybutyrate [[3OHB] and AcAc) are elevated in DKA. The serum bicarbonate concentration is low because bicarbonate is used as a buffer against metabolic acidosis, which results in increased anion gap acidosis. Some degree of hyperchloremic acidosis frequently coexists with increased anion gap acidosis in DKA [47], and the anion gap reflects the combination of these processes. Although concentrations of 3OHB and AcAc are elevated in patients who have DKA, the ratio of 3OHB:AcAc is increased during DKA as a result of changes in the redox potential (NADH/NAD+ ratio) in hepatic mitochondria [59]. Although the ratio of 3OHB:AcAc is typically 1:1 in anormal individual, this ratio rises to as high as 10:1 in persons who have DKA. These changes are important mainly because the nitroprusside reaction used to test urine ketone concentrations detects only AcAc and not 3OHB. Although urine testing can be relied on to help diagnose DKA, the urine ketone concentration should not be relied on as an indication of DKA severity or treatment response, particularly because the ratio of 3OHB:AcAc decreases during DKA treatment. Bedside blood ketone meters recently were developed and provide a rapid means for accurately measuring 3OHB rather than AcAc in children who have DKA [60]. How these measurements might best be used to enhance diagnosis and treatment of DKA, however, remains to be determined.

Metabolic acidosis stimulates chemoreceptors in the CNS, which results in partial correction of the metabolic acidosis via hyperventilation and a decrease in the partial pressure of CO2. There is a linear relationship between serum bicarbonate concentration and pCO2, and this relationship suggests that end-tidal CO2 measurements may be used as a rapid screen for acidosis in children who have suspected DKA or to follow the course of acidosis in children who have DKA (Fig. 4) [61].

Electrolyte abnormalities

Hyperglycemia results in fluid movement from the extravascular to the intra-vascular space and a decrease in the serum sodium concentration. This decrease can be calculated as a 1.6 mEq/L decrease in sodium concentration for every 100 mg/dL increase in serum glucose more than 100 mg/dL [62]. Hyperlipidemia caused by lipolysis also may affect serum sodium measurements and result in a decrease in measured serum sodium concentrations [63].

Typically, serum potassium concentrations at presentation are in the highnormal range or even above the normal range. Redistribution of potassium ions

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