OBJECTIVE: We report a case of adipsic diabetes insipidus (ADI) post-astrocytoma resection. METHODS: Clinical and laboratory data are presented. RESULTS: A 16-year-old female with a history of incompletely resected hypothalamic astrocytoma was admitted with a headache. Head magnetic resonance imaging showed an interval increase in a suprasellar lesion with extension to the third ventricle. Following a second stage resection, she developed an increased urine output with diluted urine resulting in a negative fluid balance; however, she was unable to sense thirst. Blood tests showed a serum sodium of 155 mEq/dL (normal, 136 to 145 mEq/dL), serum osmolality at 321 mOs/kg (normal, 285 to 295 mOs/kg) and a urine osmolality of 128 mOsm/kg (normal, 300 to 1,600 mOsm/kg). Serum creatinine and potassium were normal. Pituitary hormone profiles were found to be normal: growth hormone 0.171 ng/mL (normal, 0.123 to 8.05 ng/mL), luteinizing hormone 3.44 mIU/mL (normal, 7.59 to 89.08 mIU/mL), follicle-stimulating hormone 5.60 mIU/mL (normal, 2.55 to 16.69 mIU/mL), thyroid-stimulating hormone 2.9 mIU/mL (normal, 0.35 to 4.94 mIU/mL), free thyroxine 0.92 ng/dL (normal, 0.7 to 1.48 ng/dL), adrenocorticotropic hormone 19.56 pg/mL (normal, 7.2 to 63.3 pg/mL), and prolactin 7.25 ng/mL (normal, 5.18 to 26.53 ng/mL). The patient was treated with desmopressin acetate 120 μg tablets twice daily with a fixed fluid intake of 1.5 to 2.0 L/day with close monitoring of fluid intake, output, and body weight. The response was good with a gradual reduction of serum sodium level of around 7 to 9 mEq/L/day. CONCLUSION: ADI is a rare entity of central diabetes insipidus, where the absence of polydipsia can be challenging in diagnosing and managing the condition. Cases of ADI are likely under reported and clinicians need to be aware of this condition.
OBJECTIVE: We report a case of adipsic diabetes insipidus (ADI) post-astrocytoma resection. METHODS: Clinical and laboratory data are presented. RESULTS: A 16-year-old female with a history of incompletely resected hypothalamic astrocytoma was admitted with a headache. Head magnetic resonance imaging showed an interval increase in a suprasellar lesion with extension to the third ventricle. Following a second stage resection, she developed an increased urine output with diluted urine resulting in a negative fluid balance; however, she was unable to sense thirst. Blood tests showed a serum sodium of 155 mEq/dL (normal, 136 to 145 mEq/dL), serum osmolality at 321 mOs/kg (normal, 285 to 295 mOs/kg) and a urine osmolality of 128 mOsm/kg (normal, 300 to 1,600 mOsm/kg). Serum creatinine and potassium were normal. Pituitary hormone profiles were found to be normal: growth hormone 0.171 ng/mL (normal, 0.123 to 8.05 ng/mL), luteinizing hormone 3.44 mIU/mL (normal, 7.59 to 89.08 mIU/mL), follicle-stimulating hormone 5.60 mIU/mL (normal, 2.55 to 16.69 mIU/mL), thyroid-stimulating hormone 2.9 mIU/mL (normal, 0.35 to 4.94 mIU/mL), free thyroxine 0.92 ng/dL (normal, 0.7 to 1.48 ng/dL), adrenocorticotropic hormone 19.56 pg/mL (normal, 7.2 to 63.3 pg/mL), and prolactin 7.25 ng/mL (normal, 5.18 to 26.53 ng/mL). The patient was treated with desmopressin acetate 120 μg tablets twice daily with a fixed fluid intake of 1.5 to 2.0 L/day with close monitoring of fluid intake, output, and body weight. The response was good with a gradual reduction of serum sodium level of around 7 to 9 mEq/L/day. CONCLUSION: ADI is a rare entity of central diabetes insipidus, where the absence of polydipsia can be challenging in diagnosing and managing the condition. Cases of ADI are likely under reported and clinicians need to be aware of this condition.