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Published on: November 8, 2018
The temporal relationship between glucose-corrected serum sodium and neurological status in severe diabetic
Andrew Durward1, Lee P Ferguson, Dan Taylor
1Evelina Children's Hospital, Guy's and St Thomas' NHS Foundation Trust, London, UK.
Insights
Diabetic ketoacidosis (DKA) can cause cerebral edema. Monitoring glucose-corrected serum sodium levels may provide an early warning for developing cerebral edema in children with DKA.
Area of Science:
- Pediatric Endocrinology
- Neurology
- Metabolic Disorders
Background:
- Cerebral edema is a serious complication of diabetic ketoacidosis (DKA).
- The exact relationship between fluid/electrolyte shifts and cerebral edema during DKA treatment remains unclear.
- Understanding these dynamics is crucial for preventing severe neurological outcomes in children with DKA.
Purpose of the Study:
- To investigate the temporal relationship between osmolar and acid-base changes and the development of cerebral edema in children undergoing DKA treatment.
- To identify potential early warning markers for cerebral edema in pediatric DKA patients.
Main Methods:
- Retrospective cohort study of 53 children with severe DKA.
- Cerebral edema diagnosis based on neurological status, response to osmotherapy, and neuroimaging.
- Analysis of temporal profiles of osmolar and acid-base parameters using a mixed-effects model, adjusted for risk factors.
Main Results:
- No significant differences in initial demographic, osmolar, or acid-base variables among groups.
- Distinct temporal trajectories for effective osmolality and glucose-corrected serum sodium in children who developed late-onset cerebral edema.
- Glucose-corrected serum sodium showed a decrease in the late-onset edema group and an increase in controls, correlating with edema onset.
Conclusions:
- Glucose-corrected serum sodium levels may serve as a valuable early indicator for predicting cerebral edema in DKA.
- Temporal monitoring of glucose-corrected sodium is recommended for children with severe DKA.
- Further research is warranted to validate these findings and optimize DKA management protocols.
Objective:
Cerebral oedema is a potentially devastating complication of diabetic ketoacidosis (DKA). The relationship between osmolar changes, acid-base changes and development of cerebral oedema during therapy is unclear.
Design:
Retrospective cohort study on 53 children with severe DKA (mean pH at presentation 6.92±0.08). Cerebral oedema was diagnosed using neurological status, response to osmotherapy, and neuroimaging, and classified as: early (occurring ≤1 h after presentation, n=15), late (1-48 h, n=17) or absent (controls, n=21). The temporal profiles for various osmolar and acid-base profiles were examined using a random coefficients fractional polynomial mixed model, adjusted for known risk factors.
Results:
The three groups could not be differentiated by demographic, osmolar or acid-base variables at presentation. All osmolar and acid-base variables showed non-linear temporal trajectories. Children who developed late onset oedema showed dramatically different temporal profiles for effective osmolality and glucose-corrected serum sodium (both p<0.001). Glucose-corrected sodium provided better qualitative discrimination, in that it typically fell in children who developed late oedema and rose in controls. The maximum between-group difference for both variables approximated the median time of clinical cerebral oedema onset. Blood glucose and acid-base temporal profiles did not differ between the groups. Late onset oedema patients received more fluid in the first 4 h, but this did not influence the osmolar or glucose-corrected sodium trajectories in a predictable fashion.
Conclusions:
Glucose-corrected serum sodium may prove a useful early warning for the development of cerebral oedema in DKA.
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