الفهرس 
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Abstract
The present study is a descriptive cross-sectional case control study aimed to evaluate cardiac changes in pediatric patients with diabetic ketoacidosis through electrocardiogram and echocardiography. The study included 120 participants (90 pediatric patients with diabetic ketoacidosis and 30 controls). Results of the present study showed that the mean age of pediatric patients with DKA was 11.75 ± 4.27 years and ranged from 2.5 up to 17 years, which was comparable to the previous study done by Aygün D et al at Istanbul University Faculty of Medicine Department of Pediat¬rics, Pediatric Emergency and Intensive Care Unit between May 2008 and May 2009 and found that the mean age of the studied participants was 9.21±4.72 years and ranged between 1 and 16 years (Aygün D et al., 2017). Our studied participants consist of 36 (40%) were male and 54 (60%) were female, which was comparable to the previous study done by Aygün D et al who found that 24 (60%) of the patients were male and 16 (40%) were fe¬male (Aygün D et al., 2017). Our studied participants consist of 36 (40⁒) were from urban and 54 (60⁒) were from rural. Our results show that the heart rate was found to be increased at the time of DKA and then returned to its normal limits after treatment, the mean heart rate of the cases at the time of diagnosis was 110.5 ± 16.89 beats/min and ranged from 85 – 140 beats/min, after correction the mean heart rate was decreased to 97 ± 17.15 beats/min and ranged from 70 – 120 beats/min, with highly statistically significant difference between before and after correction of DKA condition (p<0.001), this results was comparable to the previous study done by Aygün D et al who found that the mean heart rate was 112.00 ± 29.22 beats/min at the time of diagnosis (min-max: 68-187 beats/min) and 97.10 ± 25.86 beats/min after treat¬ment (min-max: 58-167 beats/min). The change in the heart rate was found to be statistically significant (p<0.0001) (Aygün D et al., 2017). This tachycardia can potentially be associated with dangerous hyperkalemia. This acidosis-associated hyperkalemia can speed cardiac repolarization or decrease the conduction speed through the myocardium. However, multiple additional factors can also cause tachycardia, including re-entry circuits, abnormal automaticity, or after-depolarizations occurring within the myocardium. A common cause of re-entry circuits within the myocardium is electrolyte abnormality involving calcium and potassium. (Cubbon RM, Kearney MT, 2007) Our results show that the mean of both systolic and diastolic BP was found to be decreased in 33.3⁒ of cases (n=30) at the time of DKA and then returned to their normal limits after treatment. The mean systolic BP at the time of DKA was 91 ± 9.49 mmhg and ranged from 80 – 110 mmhg, after correction the mean it was increased to 108 ± 4.02 mmhg and ranged from 100 – 110 mmhg, also the mean diastolic BP at the time of DKA was 61 ± 9.49 mmhg and ranged from 50 – 80 mmhg, after correction it was increased to 72 ± 7.53 mmhg and ranged from 60 – 80 mmhg, with highly statistically significant difference between before and after correction of DKA condition for both systolic and diastolic BP (p<0.001). Dehydration from fluid loss secondary to glucosuria is a central feature of DKA, and this dehydration can lead to hypovolemia and systemic hypotension. (Wolfsdrof J, et al,2007) As regard the mean random blood glucose we found that it was 472.2 ± 102.29 mg/dL and ranged from 274 – 580 mg/dL, after correction of DKA condition it was decreased to 175.5 ± 12.2 mg/dL and ranged from 150 – 190 mg/dL, with highly statistically significant difference between before and after correction of DKA (p<0.001), this results was comparable to the previous study done by Aygün D et al who found that the mean blood glucose value at the time of diagnosis was 422±103.66 mg/dL (Aygün D et al., 2017). In the blood gas test, at the time of diagnosis the mean venous Ph level was found as 7.25 ±0.06 and ranged from 7.1 – 7.3, the mean sodium bicarbonate level was 9.96±3.2 mmol/L and ranged from 4.8 – 16.7 mmol/L, and the mean BE.ecf was 17.31 ± 4.38 and ranged from -24.7 – -10. After correction of DKA the mean venous Ph was increased to 7.36 ± 0.02 and ranged from 7.35 – 7.4, the mean sodium bicarbonate level was increased to 21.2 ± 1.84 and ranged from 18 – 24, and the mean BE.ecf was increased to -1.8 ± 2.05 and ranged from -5 – 2, with highly statistically significant difference between before and after correction of DKA for all the previous mentioned variables (p<0.001). These results were comparable to the previous study done by Aygün D et al who found that, at the time of diagnosis the mean venous pH level was found as 7.23±0.16 and the mean sodium bicarbonate level was 14.64±6.49 mmol/L (Aygün D et al., 2017). DKA is so named due to high levels of water-soluble ketone bodies, leading to this acidosis. (Abulebda K, et al ,2019) (Agarwal HS, 2019) Our results shows that almost all cases have Ketone in their urine, after correction of DKA no Ketone was found in the urine of the studied cases, with highly statistically significant difference between before and after correction (p<0.001). As regard the electrolyte disturbance at the time DKA diagnosis, our results showed that, the mean potassium level before correction was 5.0769 ± 0.67 mmol/L and ranged from 4 – 6 mmol/L, and declines to 4.02 ± 0.51 mmol/L and ranged from 3.3 – 4.8 mmol/L after correction. With highly statistically significant difference between before and after correction of DKA for k+.The study done by Adrogue HJ,etal at 1986 revelead that the mean k+ level at time of DKA was 5.7±1.1.( Adrogue HJ,etal at 1986)Also, the study done by Fulon M in 1990 reveled that the mean k+ level was 7±0.4 at time of diagnosis of DKA. (Fulon M, 1990) Insulin promotes potassium entry into cells. When circulating insulin is lacking, as in DKA, potassium moves out of cells, thus raising plasma potassium levels even in the presence of total body potassium deficiency. (Rose BD and Post TW, 2001) Most of urinary potassium is derived from potassium secretion in the distal nephron, particularly by the principal cells in the cortical collecting tubule. This process is mainly influenced by two factors: aldosterone and the distal delivery of sodium and water (Rose BD and Post TW, 2001). In cases of severe volume depletion, the ability to handle a potassium load is impaired due to decreased distal fluid delivery, which can diminish potassium secretion despite the hypovolemia‐induced secondary hyperaldosteronism. (Rose BD and Post TW, 2001) In Our study hyperkalemia was reported in 40 of 90 patients (44.4⁒) and become normal in all after treatment. The mean sodium was 136.4 ± 3.25 mmol/L and ranged from 133 – 143 mmol/L before correction, and become, 138.1 ± 2.18 mmol/L and ranged from 134 – 143 mmol/L after correction with highly statistically significant difference between before and after correction of DKA for Na+. These results were comparable to the previous study done by Aygün D et al who found that the mean for sodium was 133.72±4.51 mmol/L before correction, and become 138.88±4.40 mmol/L after correction. In our study 20⁒of cases (n=18) were having mild hyponatremia, improved after correction. Hyponatremia may result as following, When the renal threshold for glucose is exceeded (w170–200 mg/dL [w9.4–11.1 mmol/L]), glucosuria and hyperketonemia cause osmotic diuresis, dehydration, and electrolyte wasting (including sodium, potassium, magnesium, calcium, and phosphate loss. (Cashen k, et al, 2019) The mean calcium was 9.39 ± 0.46 mg/dL and ranged from 8.5 – 9.9 mg/dL before correction, and rises to 9.28 ± 0.47 mg/dL and ranged from 8.2 – 9.8 mg/dL after correction, with highly statistically significant difference between before and after correction of DKA for ca+ (p<0.001). DKA as a cause of severe hypercalcemia has not previously been described. Hypercalcemia in DKA is likely secondary to severe metabolic acidosis and insulin deficiency. (Topaloglu AK, etal, 2005). Other DKA-related factors are IGF-1 deficiency. (Bereket A, etal, 1996) and hyperglycemia. (Balint E, etal, 2001) Our results show that the mean urea was 27.5 ± 7.58 and ranged from 16 – 40, 27.4 ± 7.35 and ranged from 15 – 40 after correction of DKA, with no statistically significant difference between before and after correction (p=506). While the mean creatinine was 0.66 ± 0.23 and ranged from 0.3 – 1.1 after correction it was decreased to 0.51 ± 0.11 and ranged from 0.4 – 0.7, with highly statistically significant difference between before and after correction (p<0.001). The creatinine level may increase in DKA due to 3 causes. First, diabetic patients may have diabetic nephropathy. Second, dehydration may develop in the course of DKA because of osmotic diuresis of glucose and ketoacids. (Marshall SM, et al, 1992). Finally, interference of ketoacids with the plasma creatinine assay can result in falsely high plasma creatinine concentration (Molitch ME, et al, 1980) Arrhythmia, acute myocardial infarction, and sudden death may be observed during diabetic ketoacidosis. Acute cardiac complications observed in diabetic keto ke¬toacidosis have generally been attributed to electro¬lyte imbalance. Hypokalemia, hyperkalemia, hypo¬calcemia, hypophosphatemia, and hypomagnesemia may develop in diabetic ketoacidosis. (Savage MW, et al, 2011) As regard the electrocardiographic findings our results show that, the mean QT interval period was found as 0.21±0.07ms at the time of diagno¬sis and 0.18 ± 0.06ms of DKA after treatment. Although the QT interval period was within the normal limits in both periods, the change in the QT interval was not found to be statistically significant. The mean QTc interval period was found as 0.45±0.05sec (Min-Max: 0.35 - 0.5) at the time of diagno¬sis and decreases to 0.42±0.03ms (Min-Max: 0.38 - 0.47) after treatment. The QTc interval period was prolonged in 27 of 90 patients at time of DKA and after correction it was return to normal range in 18 of 27 patients and still prolonged in 9 patients., the change in the QTc interval was found to be statistically significant (p>0.001). This result was comparable to the previous study done by Aygün D et al who found that the mean QTc time was found as 447±45ms (min-max: 380-560ms) at the time of diagnosis and was decreased to 418±32ms (min-max: 350-500ms) after treatment. The initial QTc time was found to be at the upper limit of normal and the follow-up values were found to be within the normal limits. The change in the QTc time (30ms) was found to be statistically signif¬icant (p<0.0001). The result of QTc time was also comparable to the previous study done by Kuppermann N, etal who found that the mean (SD) QTc during DKA was 450 (38) milliseconds (range, 378-539 milliseconds). After recovery from DKA, the mean (SD) QTc decreased to 407 (36) milliseconds (range, 302-485 milliseconds; difference, 43milliseconds; 95% confidence interval, 23-63 milliseconds) (P.001). Fourteen of the 30 children (47%) had prolonged QTc during DKA (range, 450-539 milliseconds). After recovery from DKA, only 4 children (13%) had persistent QTc prolongation (range, 451-485 milliseconds). (Kuppermann N, et al, 2008) The mean PR interval period was found as 0.101±0.019sec (Min -Max:0.06-0.16) at the time of diagno¬sis and was increased to 0.114±0.027sec (Min -Max:0.06-0.12) after treatment. Although the PR interval period was within the normal limits in both periods, the change in the PR interval was found to be statistically significant (p>0.001). This result was compared with the previous study done by Aygün D et al who found that the mean PR interval period was found as 0.148±0.23 sec (min-max:0. 120-0.200 sec) at the time of diagno¬sis and 0.135±0.19 sec after treatment (min-max: 0.120-0.200 sec). Although the PR interval period was within the normal limits in both periods, the change in the PR interval was found to be statistically significant (p<0.0001). (Aygün D, et al, 2017) ST segment change is an important finding during di¬abetic ketoacidosis. ST segment change has even been reported on fetal ECGs in pregnant women with diabet¬ic ketoacidosis. (Yli BM, et al, 2011) In our study the ST segment was found to be isoelectric in all patients before correction and after correction. No elevation or depression was detected before and after correction of DKA. This result was compared with the previous study done by Aygün D et al who found that Slight ST segment depression devel¬oped during DKA in only four of forty patients and there was no significant correlation between ST segment de¬pression and heart rate. The mean T wave amplitude was found as 1.45±0.57 mm (Min -Max: 1- 2.5) at the time of diagno¬sis and was decreased to 1.28±0.5 mm (Min -Max: 1 - 2.5) after treatment. Although the T wave amplitude was within the normal limits in both periods, the change in the T wave amplitude was found to be statistically significant (p<0.001). As regard the echocardiographic findings: experimental studies suggest that metabolic acidosis impairs the contractile function of the heart, but whether this occurs in humans is uncertain. (Adrogué HJ and Madias NE, 1998) The clinical literature regarding cardiac function during ketoacidosis is revealing. Maury and colleagues reported echocardiographic information from 10 patients who presented with ketoacidosis over a 6-month period. Seven had DKA, three had alcoholic ketoacidosis. For all patients, the left ventricular fractional shortening was normal at the time of presentation and once the acidosis had resolved, after 24–36 h of treatment. Three of the patients had pH values of 6.9, 6.76, and 6.75. (Maury E, etal,1999) A comparison of patients presenting with hyperglycaemia, with and without ketoacidosis found that in the ketotic group, myocardial performance was enhanced during the acute phase and later returned to normal. In the non-ketotic group, it remained normal throughout. Both groups had normal lactate, creatinine phosphokinase, and cardiac enzyme levels throughout the study period. (George AK, etal,1996) Our results show that, the mean LA was found as 20.66±2.21 at the time of diagno¬sis and 21.21±2.41 after treatment. Although the mean LA was within the normal limits in both periods, the change in the LA was found to be statistically significant (p=0.024). The mean AAO was found as 20.1±2.15 at the time of diagno¬sis and 20.35±2.25 after treatment. Although the mean AAO was within the normal limits in both periods, the change in the mean AAO was found to be not statistically significant (p=0.743). The mean RVAW was found as 4.46±0.53 at the time of diagno¬sis and 4.53±0.76 after treatment. The change in the RVAW was found to be not statistically significant (p=0.095). The mean RV was found as 13.11±2.53 mm at the time of diagno¬sis and 12.7±1.7 after treatment. The change in the mean RV was found to be not statistically significant (p=0.216). The mean LVS was found as 4.99±1.06 at the time of diagno¬sis and was decreased to 4.33±0.79 after treatment. The mean LVS was decreased after correction of DKA, the change in the mean of LVS was found to be statistically significant (p<0.001). The mean LVEDD was found as 36.05±2.3mm at the time of diagno¬sis and 37.93±3.07 after treatment. The mean LVEDD before correction was smaller than its mean after correction of DKA, the change in the mean of LVEDD was found to be statistically significant (p<0.001). This result was comparable to the study done by Goerge et al who found that the mean LVEDD before correction was larger than its mean after correction but both were within normal limits and the change in the mean was not to be statistically significant. The mean LVESD was found as 19.83±1.68 at the time of diagno¬sis and 22.26±3.83 after treatment. The mean LVESD before correction was smaller than its mean after correction of DKA, the change in the mean of LVESD was found to be statistically significant (p<0.001). This result was compared to the study done by George AK, etal,1996 that found the mean LVESD before correction was smaller than its mean after correction but both were within normal limits and the change in the mean was not to be statistically significant. The mean LVPW was found as 5.19±0.88 at the time of diagno¬sis and 4.71±0.67 after treatment. The mean LVPW before correction was higher than its mean after correction of DKA, but both within its normal limits and the change in the mean of LVPW was found to be statistically significant (p<0.001). The mean FS% was found as 43.9±3.16 at the time of diagno¬sis and 41.5±5.92 after treatment. The mean FS% before correction was higher than its mean after correction, but both were within its normal limits and the change in the mean of FS% was found to be not statistically significant (p=0.108). Our result was comparable to Maury study on 10 patient who find that the mean FS% was found as 37.8±3.9 at time of diagnosis and 36.6±2.6 after treatment. The mean FS% before correction was higher than its mean after correction but both were within its normal limit at both time of period, and the change in the mean of FS% was found to be not statistically significant (p=2.6). Diabetic ketoacidosis (DKA) is an acute complication of type 1 diabetes and it is characterized by hyperglycemia, metabolic acidosis, and ketonemia. Diabetic ketoacidosis develops as a result of insulin deficiency and increased epinephrine, glucagon, cortisol, and growth hormone. DKA is usually accompanied by dehydration, catecholamine release and alterations in the potassium homeostasis. The most frequent causes of DKA are infections and poor adherence to treatment. (Cubbon RM and Kearney MT, 2007). The cardiovascular problems in DKA include arrhythmias due to electrolyte imbalance, adverse effects of acidosis, acute myocardial infarction and pulmonary oedema. Our study is descriptive cross-sectional case-control study aiming to evaluate the cardiac change in DKA through ECG and Echocardiography. 90 patients were included in the study who were admitted in AUCH presented with DKA within one year versus 30 children as a control group. complete history taking, physical examination, laboratory investigation (especially electrolytes), ECG and ECHO were done for all patients presented by DKA during the acidosis and after the correction, and also for the control group. comparison was done between ECG and ECHO parameters for the cases and control group, also between the cases during acidosis and after correction to evaluate the cardiac changes during DKA. We found that 60⁒ of our patients presented with tachycardia that improved with correction of acidosis in 40⁒ of patients while continued in the resting 20⁒.30⁒ of cases was presented with systemic hypotension that was resolved completely with correction of acidosis. 40⁒ of patient was presented with sever acidosis and hyperkalemia that was improved with correction. Mild hyponatremia was observed in 33.3⁒ of cases during acidosis that was improved after correction. As regard ECG changes in DKA we found in our study QTc interval prolongation in 60⁒ of our cases during acidosis, after correction it was returned to normal limit in 50⁒ of cases and was still prolonged in 10⁒ of cases. Other ECG parameters were normal. As regard ECHO changes in DKA, our study revealed that the left ventricular contractility was enhanced during acidosis. Patients with DKA should be closely monitoring for serum electrolyte specially k+. ECG monitoring is essential in those patients for early detection of hyper or hypokalemia or any ECG changes secondary to acidosis and k+ changes, also ECHO monitoring for detection of any change in myocardial contractility to provide early treatment of this changes.