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Central diabetes insipidus in children with acute brain insult
Yun-Hsuan Yang1, Jainn-Jim Lin, Shao-Hsuan Hsia
1Division of Pediatric Neurology, Chang Gung Children's Hospital and Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Insights
Central diabetes insipidus in children following brain injury is rare but associated with high mortality. Early diagnosis within 2 days and high serum sodium levels are key indicators of poor outcomes.
Area of Science:
- Pediatric critical care medicine
- Pediatric endocrinology
- Pediatric neurology
Background:
- Central diabetes insipidus (CDI) is a rare complication of severe central nervous system (CNS) injuries.
- The clinical presentation and outcomes of acquired CDI in children after acute brain insult are not well-documented.
Purpose of the Study:
- To describe the clinical characteristics, management, and outcomes of pediatric patients with acquired CDI following acute CNS injury.
- To identify predictors of mortality in this patient population.
Main Methods:
- Retrospective review of 54 pediatric patients (3 months–18 years) admitted to a tertiary pediatric intensive care unit between January 2000 and February 2008.
- Analysis of etiologies, timing of CDI diagnosis, serum sodium levels, co-occurring syndromes, and mortality.
Main Results:
- Common etiologies included CNS infection (35.2%), hypoxic-ischemic events (31.5%), head injury (18.5%), and vascular lesions (14.8%).
- CDI was diagnosed within 2 days of injury in 72.2% of patients; 74.0% developed maximum serum sodium >160 mEq/L.
- Overall 2-month mortality was 77.8%. Early CDI diagnosis and hypernatremia were significant predictors of outcomes.
Conclusions:
- Acquired central diabetes insipidus in children after acute CNS injury is associated with a high mortality rate.
- Early detection of CDI within 48 hours and a maximum serum sodium concentration exceeding 160 mEq/L are critical indicators for predicting patient outcomes.
Abstract:
Central diabetes insipidus occurs in patients with overwhelming central nervous system injuries, and may be associated with brain death. The clinical picture of children with acquired central diabetes insipidus after acute brain insult is seldom reported. We retrospectively reviewed cases dating from January 2000-February 2008 at a tertiary pediatric intensive care unit. Fifty-four patients (28 girls, 26 boys), aged 3 months to 18 years, were enrolled. Etiologies included severe central nervous system infection (35.2%), hypoxic-ischemic events (31.5%), head injury (18.5%), and vascular lesions (14.8%). In 39 (72.2%) patients, diabetes insipidus was diagnosed during the first 2 days after acute central nervous system injury, and 40 (74.0%) developed maximum serum sodium concentrations of >160 mEq/L. In 16, sequential cerebral salt wasting syndrome developed after their initial diabetes insipidus presentation. Overall mortality at 2 months after admission was 77.8%. Our results demonstrate that patients who develop central diabetes insipidus after acute central nervous system injury manifest high mortality. Development of central diabetes insipidus within the first 2 days and a maximum plasma sodium >160 mEq/L were significant predictors of outcomes.
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