Arrhythmias and cardiac arrest have been reported as complications of DKA and generally have been presumed to be caused by electrolyte abnormalities [1
]. In the present study, QTc and QTd prolongation were found in 16 and 19 patients, respectively, during DKA. After recovery, only one patient had persistent QTc prolongation and 3 had persistent QTd prolongation which returned to normal within one week following discharge. Since patients had no electrolyte disturbances (hypokalemia, hypomagnesemia and hypocalcemia) or hypoglycemia that could account for QTc prolongation, so the role of ketoacidosis in causing such prolongation and delayed cardiac repolarization was suggested.
Prolongation of QT interval is a serious condition that provides substrate for the development of potentially life-threatening arrhythmias torsade de pointes [11
]. Previous studies supported the association of other ketotic conditions with QTc prolongation and deaths in patients receiving ketogenic diets [2
The fact that three patients who had normal QTc were found to have increased QTd increases the privilege of QTd as a better marker of cardiac risk than QTc in those patients. This result agreed with that reported by Rana et al. who found prolonged QTd to be the best predictor for cardiac death in patients with DM [13
]. Moreover, Psallas et al. found that prolonged QTd interval may predict cardiac mortality in patients with diabetes and suggested that it may be a useful adjuvant index in the evaluation of cardiovascular risk in patients with type 2 diabetes and microalbuminuria [14
Children with long-standing diabetes but without DKA reported to have prolonged QTc and a greater frequency of other abnormalities in cardiac autonomic function compared with age-matched control subjects. Those abnormalities were thought to be manifestations of diabetic neuropathy [15
]. In the present study QTc prolongation could not be attributed to preexisting manifestations of diabetic neuropathy because QTc returned to normal after recovery from DKA in most of children. In addition, QTc prolongation was present in patients with new onset DM in addition to those with known diabetes.
The anion gap was significantly greater at presentation in children with a prolonged QTc and QTd. In addition, a significant positive correlation was found between QTc and QTd values and initial anion gap in patients during DKA reflecting the role of ketosis in causing QTc and/or QTd prolongation, which agreed with Best et al. who described QTc prolongation in children receiving ketogenic diets [2
The only limitation of the present study is the use of anion gap as an indicator of ketosis without measuring serum ketonesconcentration.
In conclusion, prolonged QTc occurs frequently during DKA and is correlated with ketosis. ECG and cardiac monitoring of children during DKA should be strictly followed.