Malignant Hypernatremia Complicating a Hypothalamic Tumor: An Endocrine Emergency
https://doi.org/10.15605/jafes.041.S1
- Author:
Vijayrama Rao Sambamoorthy
1
;
Man Ee Chiew
1
;
Xe Hui Lee
1
Author Information
1. Endocrine Unit, Medical Department, Hospital Pulau Pinang
- Publication Type:Journal Article
- MeSH:
Hypernatremia;
Hypothalamic Neoplasms
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):94-
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Hypernatremia is a common yet high-mortality electrolyte
disorder. The hypothalamus maintains water homeostasis
via thirst sensation and arginine vasopressin (AVP)
secretion. Hypothalamic tumors, such as gliomas, can progressively destroy these osmoregulatory centres, leading to
“malignant” hypernatremia (>180 mmol/L). We report a
case of life-threatening hypernatremia in a patient with a
progressive hypothalamic glioma, exploring its complex
pathophysiology.
Case:A 41-year-old female with a progressive high-grade
hypothalamic glioma and persistent hydrocephalus
presented with generalized weakness, reduced oral intake,
and dehydration. Her initial Glasgow Coma Scale was
E4V3M6. Laboratory investigations revealed malignant
hypernatremia (serum sodium 209 mmol/L) and a serum
osmolarity of 441 mOsm/kg. Despite life-threatening
dehydration (urea 26.2 mmol/L, creatinine 343 umol/L),
she was still able to deceptively produce urine output of
400 mL/day with a concentrated urine osmolarity of 890
mOsm/kg. A 1 mcg IV desmopressin trial reduced urine
output to 60 mL/day and serum sodium by 10 mmol/L
within 14 hours, confirming relative AVP deficiency.
The patient’s malignant hypernatremia was gradually
corrected to 168 mmol/L over 1 week (8–12 mmol/L/day)
using controlled intravenous hydration. However, her
condition deteriorated due to hospital-acquired infection,
and she succumbed 10 days after admission.
Conclusion:This case underscores several critical learning points for
managing hypothalamic emergencies. First, hypothalamic
tumors can reset the osmostat or destroy osmoregulatory
centres, causing adipsic AVP deficiency. Second, clinicians
must be alert to “masked polyuria” where severe hypovolemia reduces the glomerular filtration rate, causing
urine output to appear “normal” despite underlying AVP
deficiency. This state of “relative polyuria” is a hallmark
of hypothalamic hypernatremia, thus indicating that a
normal urine output does not rule out AVP deficiency.
While desmopressin is indicated, its use in adipsic patients
demands strict fluid titration to prevent iatrogenic hyponatremia. Rapid hypotonic correction carries a proven risk of cerebral oedema, and sodium measurement accuracy varies
significantly across laboratory methods in extreme ranges.
- Full text:2026080415371166380EP_A134.pdf
