Related Experiment Video
Updated: Aug 15, 2026

The Establishment of Calvarial Suture-Bony Composite Defects in Rats: A Standardized Model for Suture-Regenerative Therapy Investigation
Published on: May 10, 2024
Cerebral salt wasting syndrome after calvarial remodeling in craniosynostosis
1Department of Plastic Surgery, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Insights
Postoperative hyponatremia in pediatric craniosynostosis patients may indicate cerebral salt wasting syndrome (CSWS), not SIADH. Early recognition and normal saline treatment are crucial for preventing complications.
Area of Science:
- Neurosurgery
- Pediatric Endocrinology
- Nephrology
Background:
- Calvarial remodeling in pediatric craniosynostosis can lead to hyponatremia and increased urine output.
- Untreated hyponatremia can cause cerebral edema, increased intracranial pressure, and circulatory collapse.
Purpose of the Study:
- To investigate the cause of postoperative hyponatremia in pediatric craniosynostosis patients.
- To differentiate between Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion and Cerebral Salt Wasting Syndrome (CSWS).
Main Methods:
- Nine pediatric patients undergoing calvarial remodeling for craniosynostosis were studied.
- Postoperative levels of Atrial Natriuretic Peptide (ANP), Brain Natriuretic Peptide (BNP), Antidiuretic Hormone (ADH), serum/urine sodium, and osmolarity were monitored.
- Patients received appropriate sodium and fluid replacement.
Main Results:
- ANP and BNP levels significantly increased postoperatively, returning to normal by day 5.
- ADH levels remained within the normal range.
- Urinary sodium increased, while serum sodium and osmolarity were maintained with appropriate fluid and sodium replacement.
Conclusions:
- Postoperative hyponatremia after calvarial remodeling in pediatric craniosynostosis is likely due to CSWS, not SIADH.
- Distinguishing CSWS from SIADH is critical for appropriate management.
- CSWS patients require normal saline resuscitation and prophylactic normal saline administration.
Abstract:
Hyponatremia and increased urine output after calvarial remodeling have been noted in pediatric patients with craniosynostosis. If not treated properly, patients develop hypoosmotic conditions that can lead to cerebral edema, increased intracranial pressure, and collapsed circulation. Postoperative hyponatremia after central nervous system surgery is considered as the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Recently, however, cerebral salt wasting syndrome (CSWS) instead of SIADH has been reported frequently. CSWS is associated with a decreased serum sodium level, increased urinary sodium level, increased urine output, decreased ECF volume, increased atrial natriuretic peptide (ANP) level, and increased brain natriuretic peptide (BNP) level. We experienced nine patients with craniosynostosis who underwent calvarial remodeling. By postoperative day 1, the ANP and BNP levels increased by 3-6 folds compared with the preoperative levels. They returned to the normal levels by postoperative day 5. The ADH level was within the normal range even after operation. The urinary sodium level increased in all patients by postoperative day 1 and 3. But the serum sodium level, and serum and urine osmolarity were normal due to appropriate replacement of sodium and fluid. After calvarial remodeling, the potential development of CSWS should be considered and distinguished from SIADH. The patients with CSWS require normal saline resuscitation and should prophylactically receive normal saline.
More Related Videos
08:03Midface Hypoplasia and Cranial Base Morphology in Syndromic Craniosynostosis: A Comparative Analysis Study Using a Predictive Regression Model
Published on: November 4, 2025
11:31Repair of a Critical-sized Calvarial Defect Model Using Adipose-derived Stromal Cells Harvested from Lipoaspirate
Published on: October 31, 2012
Related Concept Videos
Cytotoxic Edema: Pathophysiology
Cerebral Edema l: Introduction
Increased Intracranial Pressure ll: Pathophysiology