Predictors of cardiac troponin release after a marathon

Objectives: Exercise leads to an increase in cardiac troponin I in healthy, asymptomatic athletes after a marathon. Previous studies revealed single factors to relate to post-race cardiac troponin I levels. Integrating these factors into our study, we aimed to identify independent predictors for the exercise-induced cardiac troponin I release. Design: Observational study. Methods: Ninety-two participants participated in a marathon at a self-selected speed. Demographic data, health status, physical activity levels and marathon experience were obtained. Before and immediately after the marathon fluid intake was recorded, body mass changes were measured to determine fluid balance and venous blood was drawn for analysis of high-sensitive cardiac troponin I. Exercise intensity was examined by recording heart rate. We included age, participation in previous marathons, exercise duration, exercise intensity and hydration status (relative weight change) in our model as potential determinants to predict post-exercise cardiac troponin I level. Results: Cardiac troponin I increased significantly from 14. ±. 12. ng/L at baseline to 94. ±. 102. ng/L post-race, with 69% of the participants demonstrating cardiac troponin I levels above the clinical cut-off value (40. ng/L) for an acute myocardial infarction. Linear backward regression analysis identified younger age (β=. -0.27) and longer exercise duration (β=. 0.23) as significant predictors of higher post-race cardiac troponin I levels (total r=. 0.31, p<. 0.05), but not participation in previous marathons, relative weight change and exercise intensity. Conclusions: We found that cardiac troponin I levels significantly increased in a large heterogeneous group of athletes after completing a marathon. The magnitude of this response could only be partially explained, with a lower age and longer exercise duration being related to higher post-race cardiac troponin I levels

The management of diabetic ketoacidosis in children

The object of this review is to provide the definitions, frequency, risk factors, pathophysiology, diagnostic considerations, and management recommendations for diabetic ketoacidosis (DKA) in children and adolescents, and to convey current knowledge of the causes of permanent disability or mortality from complications of DKA or its management, particularly the most common complication, cerebral edema (CE). DKA frequency at the time of diagnosis of pediatric diabetes is 10%–70%, varying with the availability of healthcare and the incidence of type 1 diabetes (T1D) in the community. Recurrent DKA rates are also dependent on medical services and socioeconomic circumstances. Management should be in centers with experience and where vital signs, neurologic status, and biochemistry can be monitored with sufficient frequency to prevent complications or, in the case of CE, to intervene rapidly with mannitol or hypertonic saline infusion. Fluid infusion should precede insulin administration (0.1 U/kg/h) by 1–2 hours; an initial bolus of 10–20 mL/kg 0.9% saline is followed by 0.45% saline calculated to supply maintenance and replace 5%–10% dehydration. Potassium (K) must be replaced early and sufficiently. Bicarbonate administration is contraindicated. The prevention of DKA at onset of diabetes requires an informed community and high index of suspicion; prevention of recurrent DKA, which is almost always due to insulin omission, necessitates a committed team effort