Neuroscience · Year 2 · from Neuroscience
Case 2: Central Diabetes Insipidus
Patient Presentation
Demographics: 34-year-old male
Chief Complaint: Excessive thirst and urination for 3 weeks following head injury
History of Present Illness: The patient was involved in a motor vehicle collision 4 weeks ago, sustaining traumatic brain injury with brief loss of consciousness. CT at that time showed a small frontal contusion that was managed conservatively. He was discharged after 3 days. One week after discharge, he noticed he was drinking much more water than usual and urinating frequently, often waking 4-5 times per night to void. He estimates he is drinking 6-8 liters of water daily and producing large volumes of dilute urine. Despite the large fluid intake, he feels persistently thirsty. He has not had any fevers, dysuria, or other symptoms. He has no history of diabetes mellitus or psychiatric illness.
Physical Examination:
- Vital signs: BP 118/72, HR 78, Temp 37.0C
- General: Well-appearing, no distress
- HEENT: Mucous membranes slightly dry
- Neurological: Alert, oriented, no focal deficits; cranial nerves intact including visual fields
- Cardiovascular: Regular rate and rhythm
- Skin: Decreased turgor
Workup:
- Serum sodium: 148 mEq/L (elevated)
- Serum osmolality: 302 mOsm/kg (elevated, normal 275-295)
- Urine osmolality: 85 mOsm/kg (inappropriately dilute)
- Urine specific gravity: 1.002
- Random glucose: 95 mg/dL
- Serum creatinine: 1.1 mg/dL
- 24-hour urine volume: 9.2 liters
- Water deprivation test:
- After water deprivation: Urine osmolality remained 95 mOsm/kg despite serum osmolality rising to 298 mOsm/kg (failed to concentrate)
- After desmopressin 2 mcg IV: Urine osmolality increased to 580 mOsm/kg (appropriate response to exogenous ADH)
- MRI brain with pituitary protocol: Loss of posterior pituitary bright spot on T1; small residual frontal contusion; pituitary stalk appears normal
Diagnosis: Central diabetes insipidus secondary to traumatic brain injury
Treatment:
- Desmopressin (DDAVP) 0.1 mg orally twice daily, with instructions to hold one dose if excessive water retention occurs
- Serum sodium monitoring weekly initially, then monthly
- Free access to water with instruction to drink to thirst
- Endocrinology follow-up for anterior pituitary function assessment
- Education regarding the need for lifelong therapy and medical alert identification
Clinical Pearl: Central diabetes insipidus results from deficient ADH secretion from the hypothalamic-neurohypophyseal system. The water deprivation test differentiates central DI (responds to exogenous desmopressin) from nephrogenic DI (kidneys resistant to ADH). Loss of the posterior pituitary "bright spot" on T1 MRI reflects absence of stored ADH in the posterior pituitary. Post-traumatic DI may occur immediately after injury or develop over days to weeks, and some cases resolve spontaneously. The hypothalamus contains the supraoptic and paraventricular nuclei that produce ADH, which is transported to and released from the posterior pituitary.
Clinical Image
Image Description: Brain MRI demonstrating thalamic infarct. The thalamus serves as the relay station for sensory information traveling to the cerebral cortex. Damage to the ventroposterior nucleus causes contralateral hemisensory loss initially, followed by development of central neuropathic pain (Dejerine-Roussy syndrome) in many patients.
Attribution: Image from Radiopaedia (https://radiopaedia.org/), Creative Commons Attribution-NonCommercial-ShareAlike 3.0 license.