Combined central diabetes insipidus and cerebral salt wasting after craniotomy

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Introduction

Sodium disturbances and polyuria in children after craniotomy for intracranial lesions are not uncommon. Diabetes insipidus (DI) of central origin is often cited as a cause of high serum sodium [1] while cerebral salt wasting (CSW) is a recognised cause of hyponatraemia in these patients [2]. DI and CSW can both result in polyuria; patients with central DI suffer from free water loss while patients with CSW have severe salt loss. Both syndromes may occur at various times in the postoperative period. A combination of the above mentioned diseases could occur in the clinical setting and this can lead to difficulty in diagnosis and cause problems in maintaining normal fluid and sodium status. Proper differentiation is essential, as the treatment for each entity is different. CSW and DI in the same clinical setting have not been previously described in the paediatric age group. We report two cases of combined DI and CSW in the immediate postoperative period.

Case reports

Case 1. CXH is a 10 year old girl who presented with 1 month's history of visual and gait disturbances.MRI of the brain showed a large suprasellar tumour with hydrocephalus. A ventriculo-peritoneal shunt was inserted immediately. She needed two operations to completely excise the tumour. Histology showed pilocytic astrocytoma. Postoperatively, she developed evidence of central diabetes insipidus and required intravenous pitressin before urine output was successfully controlled. She remained stable till the fifth postoperative day (POD) when she developed hyponatraemia that was very resistant to treatment despite hypertonic saline replacements. She was also clinically dehydrated. Urine sodium was 296 mEql/l/l and FeNa was 10.8. With aggressive saline replacements, hyponatraemia was corrected and kept within normal limits on a regimen of enteral feeds and intravenous saline replacements according to urine output and sodium measurements. Fludrocortisone was started. After tenth POD, urinary sodium began to decline consistently below 150 mEql/l by the fifteenth POD and less than 70 mEql/l by a month POD.

Case 2. NWS presented at 1.5 months of age with rhinorrhea and nasal mass. MRI showed a nasal mass with intracranial extension. Consent for surgery was not given until a year and a half later. By that time, a repeat MRI showed the tumour had extended into the left orbit and ethmoid sinus. A lateral rhinotomy, craniotomy with tumour excision and craniofacial reconstruction was performed. Histology revealed a low-grade nasal glioma. Postoperatively, he developed central diabetes insipidus requiring intravenous pitressin before urine output was controlled. However, serum sodium continued to drop even though urine output did not change significantly. On the second POD, the child developed a generalised tonic clonic seizure that was aborted with intravenous Valium and dilantin. Computer tomography scan of the head showed residual tumour in the left orbit and suprasellar region, evidence of CSF leak but no haemorrhage or cerebral oedema. Central venous pressure had dropped to +3 cmH₂O. Serum and urine sodium was 117 mEql/l and 176 mEql/l. FeNa was 9.6. Hyponatraemia was corrected gradually with normal saline and hypertonic saline replacements. However, urinary sodium levels continued to rise over the ensuing days, reaching a peak of 295 mEql/l on the sixth POD and there was massive solute diuresis. He required aggressive replacements with hypertonic saline to keep serum sodium within limits. However, urinary sodium persisted between 120–135 mEql/l thereafter and on the tenth POD, fludrocortisone was started at 10 μg/kg/day. Subsequently, urinary sodium dropped to 56 mEql/l two weeks after surgery and remained below 30 mEql/l after three weeks post surgery. Intravenous pitressin was successfully weaned off and the patient started on intranasal DDAVP.

Discussion

CSW syndrome is characterised by hyponatraemia (<130 mEq/l), dehydration, and inappropriate urinary sodium loss that responds to fluid and saline replacements. Osmotic diuresis often accompanies this syndrome. The main feature of central DI is massive diuresis of dilute urine with low sodium content thus resulting in hypernatraemia and dehydration. Both clinical states are characterised by diuresis but in CSW, hyponatraemia is present while in DI, the patient experience hypernatraemia. In the neurosurgical intensive care setting, ensuring sodium homeostasis is important to maintain an environment without major flux in osmolality. CSW may develop in patients with an established diagnosis of DI. Early recognition can be achieved by measuring osmolality and sodium in the plasma and urine as well as plasma ANP levels. The cornerstone of CSW management remains replacing sodium and water loss with normal or hypertonic saline. In our experience, mineralcorticoid therapy appears to be an effective adjunct [3].