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Pituitary function in paediatric survivors of severe traumatic brain injury
P Poomthavorn1, W Maixner, M Zacharin
1Department of Endocrinology and Diabetes, The Royal Children's Hospital, Melbourne, Australia.
Insights
Children surviving severe traumatic brain injury (TBI) are at risk for pituitary dysfunction. Regular monitoring of pituitary function is recommended for these pediatric patients to ensure proper growth and development.
Area of Science:
- Pediatric Endocrinology
- Neurotrauma
- Hormone Physiology
Background:
- Traumatic brain injury (TBI) can lead to hypopituitarism, a condition affecting hormone production.
- Pediatric TBI survivors are particularly vulnerable to pituitary deficits impacting growth and development.
- Limited research exists on pituitary dysfunction following childhood TBI.
Purpose of the Study:
- To investigate the prevalence of pituitary dysfunction in pediatric survivors of severe TBI.
- To identify potential endocrine deficits in this patient population.
Main Methods:
- Retrospective identification of 117 severe TBI survivors from 1020 pediatric admissions over 10 years.
- Enrollment of 54 patients for quality of life questionnaires and assessment of endocrine dysfunction.
- Hormone testing performed as clinically indicated.
Main Results:
- Nine out of 54 (16.7%) pediatric TBI survivors exhibited pituitary dysfunction.
- Four of these nine patients presented with multiple pituitary hormone deficiencies.
- The study included patients with TBI onset from 0.25 to 16.80 years, with follow-up ranging from 0.9 to 8.5 years.
Conclusions:
- Pediatric survivors of severe TBI are at risk for developing pituitary dysfunction.
- Assessment of pituitary function is crucial in the long-term management of these children.
- Early detection and intervention can mitigate the effects of hormone deficiencies.
Background:
Traumatic brain injury (TBI)-mediated hypopituitarism is an increasingly recognised problem. Paediatric survivors of TBI may be vulnerable to the possible effects of pituitary deficits as pituitary hormones control normal growth and development. Research concerning pituitary dysfunction following childhood TBI is limited.
Aim:
To identify pituitary dysfunction in paediatric survivors of severe TBI.
Methods:
Of 1020 children who sustained a TBI and were admitted to the Royal Children's Hospital, Melbourne, Australia over 10 years, 117 were identified as survivors of severe TBI. 54 patients (31 males) were enrolled and administered questionnaires regarding quality of life and possible endocrine dysfunction. Where indicated, hormone testing was performed.
Results:
29 of the 54 patients underwent hormonal investigations, while 21 who had satisfactory questionnaires did not (four patients had already been diagnosed with pituitary deficiencies). In those 29 patients, TBI occurred at ages ranging from 0.25 to 16.80 years (median 9.7 years). Time from TBI to study ranged from 0.9 to 8.5 years (median 4.5 years). Of the 54 patients, nine had pituitary dysfunction, of whom four had multiple pituitary hormone deficiencies.
Conclusions:
Our study that confirms that paediatric survivors of severe TBI may develop pituitary dysfunction. Pituitary function should therefore be determined in these patients.
