cardiac arrhythmias and arrest have been described in children with diabetic ketoacidosis and generally have been presumed to be caused by electrolyte abnormalities .
a previous study has reported a prolongation of qtc in children receiving ketogenic diets   and in other conditions associated with ketosis in absence of electrolyte .
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 .
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 .
this study aimed to evaluate qtc and qtd in children with type 1 dm during dka .
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 9.59  2.21 years ( table 1 ) .
patients with congenital or rheumatic heart diseases , systolic left ventricular dysfunction , and unreliable identification of the end of the t wave in the ecg as well as patients taking medications that could affect qtc were excluded from the study .
patients were enrolled in the study after taken a written informed consent from parents or guardians .
patients were treated according to standard dka protocol at presentation and abgs , serum electrolytes ( na , k , ca , mg , creatinine ) were withdrawn , and the anion gap [ na (cl+ hco3 ) ] was assessed .
twelve - lead ecg were done by a single pediatric cardiologist who was masked to patients ' clinical and laboratory data .
qtc was estimated according to bazett 's formula , where rr interval was measured in relation to the previous qrs complex qtc = qt / r - r  interval ( bazett , 1920 ) .
the standard 12-lead ecg was recorded at 25  mm / s along with a lead ii rhythm strip recorded at 50  mm / s ; qt and rr intervals were measured .
qt interval was measured from the onset of the qrs complex to the end of t wave .
the end of qt interval was defined as the intersection of a tangent to the steepest downslope of the dominant repolarization wave with the isoelectric line .
three separate measurements were obtained from each ecg , and the mean of these measurements was used as the value for the qtc .
prolonged qtc was defined as a qtc of at least 0.45  s ( 450  ms ) .
qt - interval dispersion was defined as the difference between maximum and minimum non - rate - corrected qt - interval duration .
follow - up ecgs was recorded at time of hospital discharge or at patient 's first outpatient visit ( median 22 days after initial ecg with a range from 5 to 30 days ) .
collected data were analyzed using spss program version 16 to obtain the quantitative variables as mean  sd and range and qualitative variables as number and percentage .
p values less than 0.05 were considered statistically significant and p values less than 0.01 were considered statistically highly significant .
  qtc was found to be prolonged ( more than 450  ms ) in 16 patients : 9 patients with new onset diabetes and 7 patients with known diabetes during dka ( range 451539  ms ) .
the mean qtc values of patients during dka were 450  89  ms , which were significantly decreased after recovery from dka ( 428  2  5  ms , p < 0.001 ) .
only one child had persistent prolonged qtc ( 453  ms ) even after recovery from dka which returned to normal 5 days after hospital discharge ( table 2 ) .
nineteen patients ( 63.3% ) had prolonged qtd ( > 50  ms ) : 10 were newly diagnosed patients with type 1 dm and 9 patients were known diabetics .
three children had persistent prolongation of qtd after recovery from dka and were returned to normal within one week after hospital discharge .
three patients were found to have normal qtc ( 444  ms , 447  ms , and 445  ms , resp . ) although they have increased qtd ( 51  ms , 52  ms , and 51 , resp . ) .
none of the children enrolled in the study experienced cardiac arrhythmias during dka treatment .   during dka , patients with prolonged qtc and those with prolonged qtd had a significant higher anion gap and lower ph at presentation compared to those with normal qtc and qtd values , while no significant difference was found between both groups of patients in other biochemical or clinical data ( tables 3 and 4 ) .
the initial anion gap was positively correlated with qtc values ( r = 0.67 , p < 0.0001 ) ( figure 1 ) and qtd value ( r = 0.69 , p < 0.001 ) during dka .   
none of children experienced hypoxia or hypoglycemia ( blood glucose level < 70  mg / dl ) , 5 patients had mild hypokalemia at the time of ecg recording ( range from 3.1 to 3.3 
meq / l ) , while s. mg and s. ca were within reference range in all patients with no significant correlation between s. ca , k , and mg with qtc or qtd was found .
arrhythmias and cardiac arrest have been reported as complications of dka and generally have been presumed to be caused by electrolyte abnormalities . 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 .
previous studies supported the association of other ketotic conditions with qtc prolongation and deaths in patients receiving ketogenic diets [ 2 , 9 , 12 ] .  
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 .
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 .
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 . 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 .  
the only limitation of the present study is the use of anion gap as an indicator of ketosis without measuring serum ketonesconcentration .   in conclusion
 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 ( p < 0.01 ) . 
 procedure . 
 sixteen patients ( 53 , 3% ) had prolonged qtc during dka ( range 451538  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 ( p < 0.0001 ) . 
 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 
2. Patients and Methods
3. Results
4. Discussion