MON-001 - A Rare and Fatal Cause of Central AVP Deficiency: Hypoxic-Ischemic Brain Injury Secondary to Diabetic Spinal Infection

Introduction:
Central arginine vasopressin deficiency (AVP-D) occurs due to impaired antidiuretic hormone secretion and may lead to life-threatening hypernatremia and polyuria in critically ill patients. While the most common causes are tumors and trauma in the neurohypophyseal area, although rare, it may also result from hypoxic-ischemic brain injury. Prompt recognition is essential, as delayed diagnosis can worsen neurologic outcomes. We present a rare case of AVP-D following global hypoxic brain damage caused by spinal cord compression from an occult paravertebral abscess in a patient with poorly controlled type 2 diabetes (T2D).

Clinical

Case:
A middle-aged Hispanic male with poorly controlled T2D and hypertension initially presented with lower extremity weakness that rapidly progressed to paraplegia and airway compromise requiring endotracheal intubation. During his ICU stay, he developed profound polyuria and severe hypernatremia (serum sodium >180 mEq/L). Physical examination revealed mydriasis and flaccid paralysis with initially preserved reflexes, which progressively disappeared over the following days.
Laboratory evaluation revealed a serum osmolality of 366 mOsm/kg H₂O with inappropriately dilute urine (urine osmolality 179 mOsm/kg H₂O, urine sodium < 20 mEq/L, specific gravity 1.010), consistent with hypotonic polyuria. Glycated hemoglobin was 9.3%. Brain MRI showed subarachnoid exudates, diffuse hypoxic-ischemic changes, and evidence of tonsillar herniation into the foramen magnum. Thoracic MRI revealed a prevertebral phlegmon causing spinal cord compression. In view of severe hypernatremia, dextrose 5% and tap water were initiated. Intravenous desmopressin 2mcg every 8 hours was administered 5 times consecutively with marked clinical and biochemical response, confirming the diagnosis of central AVP-D. Despite correction of hypernatremia, he developed refractory shock and died.
Autopsy revealed a spontaneous bacterial paravertebral abscess attributed to diabetes-associated immune dysfunction and microvascular complications, resulting in spinal cord compression, global hypoxic-ischemic brain injury, and subsequent AVP-D.

Conclusion:
This case illustrates hypoxic-ischemic brain injury as a rare cause of AVP-D in critically ill patients. Severe hypernatremia and hypotonic polyuria should elicit early evaluation, even in the absence of direct pituitary lesions, neurosurgical procedures, or trauma. Furthermore, poorly controlled diabetes may trigger a cascade of infectious, neurologic, and endocrine complications which could lead to catastrophic neurologic and endocrine sequelae. This case emphasizes the importance of early infection recognition and glycemic control.

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