22. Clinical and laboratory characteristics of central diabetes insipidus following intracranial surgery at Vietnam National Children’s Hospital
Main Article Content
Abstract
An observational study was conducted to describe the clinical laboratory characteristics of central diabetes insipidus in 43 children who underwent intracranial surgery at the Surgical Intensive Care Unit of Vietnam National Children’s Hospital from 3/2021 to 3/2024. The preoperative diagnoses were brain tumors (55.8%), followed by traumatic or non-traumatic cerebral hemorrhage (30.2%), and other conditions (14.0%). Within the first 24 hours after surgery, 58.1% of patients developed diabetes insipidus, 93.0% experienced onset within 48 hours. The maximum urine output at onset was 8.1 ml/kg/h (IQR 5,6 – 10,0 ml/kg/h), while the maximum urine output during follow-up was 10.2 ml/kg/h (IQR 6.6 – 11.4 ml/kg/h). Hypernatremia was present in 100% of patients. There was a moderate positive correlation between the maximum urine output and the maximum serum sodium concentration. Monitoring urine output and serum sodium concentration were essential in postoperative intensive care period for early detection of pediatric central diabetes insipidus.
Article Details
Keywords
Central diabetes insipidus, intracranial surgery
References
2. Alharfi IM, Stewart TC, Foster J, Morrison GC, Fraser DD. Central diabetes insipidus in pediatric severe traumatic brain injury. Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies. 2013; 14:203-9.
3. Joshi RS, Pereira MP, Osorio RC, Oh T, Haddad AF, Pereira KM, et al. Identifying risk factors for postoperative diabetes insipidus in more than 2500 patients undergoing transsphenoidal surgery: a single-institution experience. Journal of neurosurgery. 2022; 137: 647-57.
4. Boughey JC, Yost MJ, Bynoe RP. Diabetes insipidus in the head-injured patient. The American surgeon. 2004; 70:500-3.
5. Hannon MJ, Crowley RK, Behan LA, O’Sullivan EP, O’Brien MM, Sherlock M, et al. Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality. The Journal of clinical endocrinology and metabolism. 2013; 98: 3229-37.
6. Lobatto DJ, de Vries F, Zamanipoor Najafabadi AH, Pereira AM, Peul WC, Vliet Vlieland TPM, et al. Preoperative risk factors for postoperative complications in endoscopic pituitary surgery: a systematic review. Pituitary. 2018; 21:84-97.
7. Capatina C, Paluzzi A, Mitchell R, Karavitaki N. Diabetes Insipidus after Traumatic Brain Injury. Journal of clinical medicine. 2015; 4:1448-62.
8. Saldarriaga C, Lyssikatos C, Belyavskaya E, Keil M, Chittiboina P, Sinaii N, et al. Postoperative Diabetes Insipidus and Hyponatremia in Children after Transsphenoidal Surgery for Adrenocorticotropin Hormone and Growth Hormone Secreting Adenomas. The Journal of pediatrics. 2018; 195:169-74.e1.
9. Yang Y-H, Lin J-J, Hsia S-H, Wu C-T, Wang H-S, Hung P-C, et al. Central Diabetes Insipidus in Children With Acute Brain Insult. Pediatric Neurology. 2011; 45:377-80.
10. Lobatto DJ, Vliet Vlieland TPM, van den Hout WB, de Vries F, de Vries AF, Schutte PJ, et al. Feasibility, safety, and outcomes of a stratified fast-track care trajectory in pituitary surgery. Endocrine. 2020; 69:175-87.
11. Pratheesh R, Swallow DMA, Rajaratnam S, Jacob KS, Chacko G, Joseph M, et al. Incidence, predictors and early post-operative course of diabetes insipidus in paediatric craniopharygioma: a comparison with adults. Child’s Nervous System. 2013; 29:941-9.
12. Agha A, Rogers B, Mylotte D, Taleb F, Tormey W, Phillips J, et al. Neuroendocrine dysfunction in the acute phase of traumatic brain injury. Clinical endocrinology. 2004; 60:584-91.