MON-067 - Ischemic Pituitary Apoplexy After Cardiac Arrest: Secondary Adrenal Insufficiency Masking Arginine Vasopressin Deficiency

Introduction

Arginine vasopressin deficiency (AVP-D) is a rare consequence of pituitary apoplexy, occurring transiently in about 4% and persistently in 2% of cases, as destruction of 80-90% of hypothalamic vasopressin neurons is required for clinically significant AVP-D. The posterior pituitary's direct arterial supply from the superior hypophyseal arteries provides relative protection from vascular compromise compared to the anterior pituitary, which relies on the pressure-sensitive hypophyseal portal system. In contrast, central adrenal insufficiency (AI) is common, reported in up to 45-70% of cases. When present together, AI can mask partial AVP-D as increased AVP compensates for reduced AVP production. We present a rare case of partial AVP-D masked by central AI after suspected pituitary apoplexy.

Case

A 63-year-old male with heart failure underwent cardiac device implantation which was complicated by coronary sinus perforation leading to cardiac arrest, resulting in anoxic brain injury and cardiogenic shock. He was found to have new left oculomotor deficits and imaging demonstrated bilateral subdural hematomas with a left parasellar mass abutting the left cavernous sinus. Two months later, spontaneous improvement in the oculomotor deficits made cavernous sinus involvement unlikely. MRI evaluation was precluded by the patient’s MRI-incompatible cardiac device; however, CT sinus suggested pituitary involution without cavernous invasion. Laboratory workup revealed cortisol of < 1.0 mcg/dL, ACTH < 1.0 pg/mL, prolactin 1.0 ng/mL and LH 0.51 mlU/mL with preserved thyroid function, confirming central AI. Given spontaneous improvement in deficits coinciding with pituitary involution and hypopituitarism, presentation was consistent with pituitary apoplexy. Course was complicated by mild hypernatremia (151 mEq/L), low urine osmolality (248 mOsm/kg), and relatively preserved urine output (0.6-1.3 L/day), concerning for AVP-D partially masked by increased AVP secretion in AI. Desmopressin challenge and copeptin levels were limited due to heart failure. He was started on steroid replacement followed by AVP-D monitoring, remaining at sodium goal with free water intake and sodium restriction.

Discussion

This case highlights an atypical presentation of AVP-D in which central AI creates a counter effect on AVP. Cortisol deficiency removes osmotic suppression and upregulates AVP gene expression, promoting water reabsorption and attenuating the water loss typically seen in AVP-D. The dual processes created a milder AVP-D presentation without dramatic polyuria. This case further addresses diagnostic challenges due to MRI-incompatibility and highlights cardiac arrest and shock as clinical risk factors for pituitary apoplexy with characteristic CT imaging evolution.

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