Cardiac arrest has been described in children with diabetic ketoacidosis (DKA). Aim. To evaluate QTc and QTd in type 1 diabetic children with DKA. Methods. Twelve-lead ECG was done to 30 type 1 diabetic children with DKA at presentation and recovery. Corrected QT interval and QT dispersion (QTd) were assessed. Results. QTc and QTd mean values were significantly decreased in patients after than before DKA recovery ( ). Procedure. Sixteen patients (53, 3%) had prolonged QTc during DKA (range 451–538？ms) that dropped to one patient after recovery, his QTc (453？ms) returned to normal 5 days after hospital discharge. Nineteen patients (63.3%) had prolonged QTd (>50？ms) that dropped to three after recovery. The fact that three patients had normal QTc but prolonged QTd increases the privilege of QTd over QTc as a better marker for cardiac risk in those patients. Anion gap was significantly associated with QTc and QTd prolongation ( ). Patients had no electrolyte abnormalities or hypoglycemia to account for QTc or QTd prolongation. Conclusion. Prolonged QTc and QTd frequently occur in DKA positively correlated to ketosis. Cardiac monitoring for patients with DKA is mandatory. 1. Introduction Cardiac arrhythmias and arrest have been described in children with diabetic ketoacidosis and generally have been presumed to be caused by electrolyte abnormalities [1]. A previous study has reported a prolongation of QTc in children receiving ketogenic diets [2] and in other conditions associated with ketosis in absence of electrolyte [3]. The association between ketotic conditions and prolonged QTc and/or sudden death raises the suggestion of whether ketosis may directly affect cardiac repolarization and be a cause of arrhythmia and/or SCD in DKA patients. QT dispersion (QTd) is defined as the interlead variability in the duration of the QT interval in the 12-lead electrocardiogram [4]. It is a significant parameter that can be used to assess the homogeneity of cardiac repolarization and autonomic function. Prolonged QTd was previously suggested as the best predictor of cardiac death in patients with type 2 DM [5]. This study aimed to evaluate QTc and QTd in children with type 1DM during DKA. 2. Patients and Methods This study included 30 children with type 1 DM who were presented with DKA 15 were newly diagnosed and 15 were following up in the diabetes clinic. They were 15 males and 15 females, their age ranged from 5 to 13 years with a mean age years (Table 1). DKA was defined according to ISPAD criteria [6]. Patients with congenital or rheumatic heart diseases,
References
[1]
N. Glaser, P. Barnett, I. Mc Caslin, et al., “Risk factors for cerebral edema in children with diabetic ketoacidosis,” The New England Journal of Medicine, vol. 344, no. 4, pp. 264–269, 2001.
[2]
T. H. Best, D. N. Franz, D. L. Gilbert, D. P. Nelson, and M. R. Epstein, “Cardiac complications in pediatric patients on the ketogenic diet,” Neurology, vol. 54, no. 12, pp. 2328–2330, 2000.
[3]
J. M. Freeman, E. H. Kossoff, and A. L. Hartman, “The ketogenic diet: one decade later,” Pediatrics, vol. 119, no. 3, pp. 535–543, 2007.
[4]
J. Kautzner and M. Malik, “QT interval dispersion and its clinical utility,” Pacing and Clinical Electrophysiology, vol. 20, no. 10, pp. 2625–2640, 1997.
[5]
P. M. Okin, R. B. Devereux, B. V. Howard, R. R. Fabsitz, E. T. Lee, and T. K. Welty, “Assessment of QT interval and QT dispersion for prediction of all-cause and cardiovascular mortality in American Indians: the strong heart study,” Circulation, vol. 101, no. 1, pp. 61–66, 2000.
[6]
J. Wolfsdorf, M. E. Craig, D. Daneman et al., “Diabetic ketoacidosis in children and adolescents with diabetes,” Pediatric Diabetes, vol. 10, supplement 12, pp. 118–133, 2009.
[7]
H. Bazett, “An analysis of the time relationships of electrocardiograms,” Heart, vol. 7, pp. 353–370, 1920.
[8]
M. Viitasalo, L. Oikarinen, H. Swan et al., “Ratio of late to early T-wave peak amplitude in 24-h electrocardiographic recordings as indicator of symptom history in patients with long-QT syndrome types 1 and 2,” Journal of the American College of Cardiology, vol. 47, no. 1, pp. 112–120, 2006.
[9]
N. Kuppermann, J. Park, K. Glatter, J. P. Marcin, and N. S. Glaser, “Prolonged QT interval corrected for heart rate during diabetic ketoacidosis in children,” Archives of Pediatrics and Adolescent Medicine, vol. 162, no. 6, pp. 544–549, 2008.
[10]
M. Malik and A. J. Camm, “Mystery of QT(c) interval dispersion,” American Journal of Cardiology, vol. 79, no. 6, pp. 785–787, 1997.
[11]
D. M. Roden, “Drug-Induced Prolongation of the QT Interval,” The New England Journal of Medicine, vol. 350, no. 10, pp. 1013–1022, 2004.
[12]
A. Stevens, D. P. Robinson, J. Turpin, T. Groshong, and J. D. Tobias, “Sudden cardiac death of an adolescent during dieting,” Southern Medical Journal, vol. 95, no. 9, pp. 1047–1049, 2002.
[13]
B. S. Rana, M. M. Band, S. Ogston, A. D. Morris, S. D. Pringle, and A. D. Struthers, “Relation of QT interval dispersion to the number of different cardiac abnormalities in diabetes mellitus,” American Journal of Cardiology, vol. 90, no. 5, pp. 483–487, 2002.
[14]
M. Psallas, N. Tentolouris, A. Cokkinos, D. Papadogiannis, D. V. Cokkinos, and N. Katsilambros, “QT dispersion: comparison between diabetic and non-diabetic individuals and correlation with cardiac autonomic neuropathy,” Hellenic Journal of Cardiology, vol. 47, no. 5, pp. 255–262, 2006.
[15]
M. M. Massin, B. Derkenne, M. Tallsund et al., “Cardiac autonomic dysfunction in diabetic children,” Diabetes Care, vol. 22, no. 11, pp. 1845–1850, 1999.
