P1.030: A rare case of Syndrome of inappropriate antidiuretic hormone( SIADH) in a 9-month-old male developed after ventriculoatrialsunt revision

Introduction: Syndrome of inappropriate antidiuretic hormone secretion is one of the rare complication after ventriculoatrial (VA) shunt revision. SIADH can lead to significant morbidity if unrecognized, particularly in patients with altered neuroanatomy or cerebrospinal fluid (CSF) dynamics. We report a rare case of SIADH in a 9-month-old male who underwent a VA revision.

Case Description: A 9-month-old male with chromosome 13q microdeletion and a history of a large occipital meningoencephalocele, born at term, presented with progressive swelling over the site of a ventriculoatrial (VA) shunt. The patient had previously undergone ventriculoperitoneal (VP) shunt placement shortly after birth, which was later converted to a VA shunt due to recurrent hydrocephalus and multiple shunt revisions.

At the time of presentation, the patient was alert with no signs of lethargy, vomiting, or fever. A shunt series revealed no mechanical obstruction or disconnection. However, a CT scan of the brain showed a slight increase in ventricular size and hyperdense cerebrospinal fluid (CSF), raising concern for evolving hydrocephalus. A shunt tap was performed, with drainage of 10 mL of CSF, and the patient was admitted to the Pediatric Intensive Care Unit.

The patient underwent VA shunt revision. Within 24 hours postoperatively, he developed altered mental status and generalized seizure activity. Emergent neuroimaging demonstrated no hydrocephalus but showed dysmorphic, slit-like lateral ventricles, consistent with post-shunt overdrainage. Laboratory evaluation revealed hyponatremia (serum sodium 125–127 mmol/L), elevated urine sodium (241 mmol/L), low serum osmolality (258 mOsm/kg), and high urine osmolality (614 mOsm/kg), consistent with Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH).

Management included hypertonic saline boluses, continuous 3% NaCl infusion, and enteral sodium supplementation at 1 mEq/kg every 6 hours. Seizures resolved with normalization of serum sodium levels, which were closely monitored during the hospital course. The patient’s neurological status improved, and he was subsequently discharged in stable condition.

Discussion: This case highlights a rare occurrence of SIADH following VA shunt revision, leading to hyponatremia-induced seizures. This case underscores the importance of monitoring serum sodium and fluid status postoperatively in patients undergoing shunt revisions.

Conclusion: Patient in this case developed SIADH following ventriculoatrial (VA) shunt revision. This case underscores the potential complications associated with shunt surgeries, particularly the development of electrolyte imbalances like SIADH. The pathophysiology of SIADH in this context may be related to various factors such as intracranial pressure changes or direct effect of the shunt procedure on the hypothalamic-pituitary axis. Early recognition and management of SIADH are crucial, as untreated, it can lead to serious complications, including hyponatremia and neurological impairment. This report highlights the importance of monitoring for this rare but significant complication in patients undergoing VA shunt revision and encourages a multidisciplinary approach to diagnosis and treatment.