We report a case of diabetic ketoacidosis (DKA) with normal anion-gap secondary to hyperchloremia at admission. Normal saline may not be the ideal fluid for resuscitation in this setting because saline rehydration can induce and/or sustain hyperchloremic acidosis.

A 7-year old child was admitted for evaluation of abdominal pain of 3-week duration. Two days after admission, he developed increasing abdominal pain and tachypnea with normal chest findings. Random blood glucose was ‘high’ on glucometer. Arterial pH (6.9) and urine ketone bodies (3+) suggested DKA. After 20 mL/kg normal saline (NS) bolus, standard DKA protocol (assuming 10% dehydration) was initiated. Serial measurements of acid-base and electrolyte status are shown in Table I. Normal anion-gap acidosis and persistent base deficit were noted during the stay. The possibility of underlying distal renal tubular acidosis [1] was ruled out based on renal bicarbonate excretion and urinary anion-gap.

TABLE I  Electrolyte and Acid–base Parameters Observed During the PICU Stay 

Hyperchloremic metabolic acidosis (HMA) in DKA, especially during recovery, have been reported [2] The mechanism of early HMA in our case could be gradual development of ketoacidosis and persistent urinary loss of ketoanions. A normal corrected sodium level in our patient suggested adequate oral water intake before admission to intensive care unit. HMA in children and adults during DKA management is associated with slow recovery from acidosis [3]. In a retrospective study [4], prolonged intensive care unit and hospital stay were observed in those with non-gap acidosis (secondary to hyperchloremia).

Use of normal saline as a rehydration fluid is known to cause dilutional-hyperchloremic acidosis. A recent trial [5] showed extended insulin requirement and hospital stay in those who received only NS as post-bolus rehydration fluid or those who received NS but were switched to during recovery when compared with children who received only N/2 saline. Earlier resolution of acidosis was observed when Plasmalyte (containing sodium 140 mEq/L, potassium 5 mEq/L, chloride 98 mEq/L, magnesium 3 mEq/L, acetate 27 mEq/L, gluconate 23 mEq/L; osmolality: 294 mOsm/L) was used [6] instead of NS in the initial 12-hours of management of DKA. An adult trial comparing NS with Ringer’s lactate (RL) failed to show significant difference in time-to-resolution of DKA [7]. The only randomized trial comparing NS with balanced electrolyte solution (BES) for fluid resuscitation in children with DKA revealed that BES consistently prevented HMA [8]. The benefit of BES is attributable to a serum-like pH (7.4) and lower (98mEq/L) chloride content when compared with NS and RL. However, theoretical risk of hyperkalemia exists with use of RL [9]. In India, the lack of universal availability of BES/Plasmalyte and N/2 saline limits their use.

Though saline rehydration is the current standard of care, the debate concerning the ideal resuscitation fluid in DKA continues [10]. Normal saline, being neither ‘normal’ nor physiological (pH 5.5 with a high chloride content) can sustain hyperchloremia as shown in this case. Randomized trials comparing balanced fluids (like RL) with NS for rehydration in DKA are needed to determine the choice of fluid in DKA. Pediatricians must be cognizant of hyperchloremic acidosis in DKA.

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