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Central diabetes insipidus in pediatric severe traumatic brain injury
Ibrahim M Alharfi1, Tanya Charyk Stewart, Jennifer Foster
1Department of Pediatrics, Western University, London, ON, Canada.
Insights
Central diabetes insipidus occurs in 18% of pediatric severe traumatic brain injury patients. Early onset and cerebral edema significantly increase mortality risk in these critical cases.
Area of Science:
- Pediatric critical care medicine
- Neurotrauma research
- Endocrinology
Background:
- Severe traumatic brain injury (TBI) in children presents significant mortality challenges.
- Central diabetes insipidus (CDI) is a potential complication of TBI, impacting fluid and electrolyte balance.
- Understanding CDI's incidence and associated factors in pediatric TBI is crucial for improving outcomes.
Purpose of the Study:
- To determine the occurrence rate of central diabetes insipidus (CDI) in pediatric patients with severe traumatic brain injury (TBI).
- To identify clinical, injury, biochemical, imaging, and intervention variables associated with mortality in these patients.
- To analyze factors differentiating survivors from non-survivors with CDI post-TBI.
Main Methods:
- Retrospective chart and imaging review of pediatric trauma patients.
- Inclusion criteria: Injury Severity Score ≥ 12, severe TBI (GCS ≤ 8, head AIS ≥ 4), and development of acute CDI.
- Data collected included demographics, injury characteristics, biochemical markers, imaging findings, and interventions.
Main Results:
- The incidence of acute CDI in pediatric severe TBI was 18% (32 of 180 patients).
- CDI patients had a high mortality rate (87.5%), with 71.4% declared brain dead post-CDI diagnosis.
- Early CDI onset (within 2 days), low Glasgow Coma Scale scores, fixed pupils, prolonged PTT, and cerebral edema on CT were associated with mortality.
Conclusions:
- Central diabetes insipidus (CDI) is a significant complication in pediatric severe traumatic brain injury (TBI), with an 18% incidence.
- Early CDI onset and cerebral edema on head CT are key predictors of mortality.
- Survivors were more likely to receive intracranial pressure monitoring, thiopental coma, and decompressive craniectomy.
Objectives:
To determine the occurrence rate of central diabetes insipidus in pediatric patients with severe traumatic brain injury and to describe the clinical, injury, biochemical, imaging, and intervention variables associated with mortality.
Design:
Retrospective chart and imaging review.
Setting:
Children's Hospital, level 1 trauma center.
Patients:
Severely injured (Injury Severity Score ≥ 12) pediatric trauma patients (>1 month and <18 yr) with severe traumatic brain injury (presedation Glasgow Coma Scale ≤ 8 and head Maximum Abbreviated Injury Scale ≥ 4) that developed acute central diabetes insipidus between January 2000 and December 2011.
Measurements And Main Results:
Of 818 severely injured trauma patients, 180 had severe traumatic brain injury with an overall mortality rate of 27.2%. Thirty-two of the severe traumatic brain injury patients developed acute central diabetes insipidus that responded to desamino-8-D-arginine vasopressin and/or vasopressin infusion, providing an occurrence rate of 18%. At the time of central diabetes insipidus diagnosis, median urine output and serum sodium were 6.8 ml/kg/hr (interquartile range = 5-11) and 154 mmol/L (interquartile range = 149-159), respectively. The mortality rate of central diabetes insipidus patients was 87.5%, with 71.4% declared brain dead after central diabetes insipidus diagnosis. Early central diabetes insipidus onset, within the first 2 days of severe traumatic brain injury, was strongly associated with mortality (p < 0.001), as were a lower presedation Glasgow Coma Scale (p = 0.03), a lower motor Glasgow Coma Scale (p = 0.01), an occurrence of fixed pupils (p = 0.04), and a prolonged partial thromboplastin time (p = 0.04). Cerebral edema on the initial computed tomography, obtained in the first 24 hrs after injury, was the only imaging finding associated with death (p = 0.002). Survivors of central diabetes insipidus were more likely to have intracranial pressure monitoring (p = 0.03), have thiopental administered to induce coma (p = 0.04) and have received a decompressive craniectomy for elevated intracranial pressure (p = 0.04).
Conclusions:
The incidence of central diabetes insipidus in pediatric patients with severe traumatic brain injury is 18%. Mortality was associated with early central diabetes insipidus onset and cerebral edema on head computed tomography. Central diabetes insipidus nonsurvivors were less likely to have received intracranial pressure monitoring, thiopental coma and decompressive craniectomy.
Related Concept Videos
Diabetes Insipidus I: Introduction
Diabetes Insipidus II: Pathophysiology
Traumatic Brain Injury l: Introduction
Increased Intracranial Pressure l: Introduction
Cerebral Edema ll: Pathophysiology
Increased Intracranial Pressure ll: Pathophysiology

