OR11-5 Early Prevalence of Neuroendocrine Dysfunction after Spontaneous Aneurysmal Subarachnoid Haemorrhage: Interim Findings from a Prospective Cohort Study

The prevalence of neuroendocrine dysfunction after aneurysmal subarachnoid haemorrhage (SAH) is highly varied between 0-55%, with little known of time of onset and recovery. We aimed to examine prevalence, time of onset, progression and predictors of neuroendocrine dysfunction in patients with aneurysmal SAH. All patients admitted with spontaneous aneurysmal SAH, without known prior pituitary dysfunction or recent exposure to glucocorticoids, were prospectively recruited. Serum cortisol at 8AM was measured on days 1, 3, 5, 7 and 10 of admission while serum free T4, TSH, LH/FSH, estradiol/testosterone, and prolactin were evaluated on day 7 post intervention (surgical or endovascular) or day 10 of admission if there was no intervention. Complete pituitary function including IGF-1, were re-evaluated at 3 months. 32 patients (mean age: 56.4 ±13.3 years, 66% female) were recruited. 19 were categorized as World Federation of Neurological Societies (WFNS) low-grade (1-3) on arrival and 13 were high-grade (4-5). 25 and 5 subjects had endovascular and surgical interventions respectively, while 2 had none. 30-day mortality rate was 9.4% (3/32), with death occurring within a week in all 3 patients. Of the 29 who survived beyond a week, none developed early corticotroph deficiency. Mean cortisol levels were 876.9 (±406.9), 770.4 (±329.7), 674.1 (±278.7), 668.1 (±269.0) and 643.0 (±350.1) nmol/L on days 1,3,5,7, and 10 respectively. A homogenous control group of critically ill post coronary bypass patients were recruited to compare values of cortisol during the acute phase. There were no significant differences in mean serum cortisol between SAH patients and controls apart from day 1 levels, with controls having a higher mean cortisol level, 1109.1 ±410.1 nmol/L (p=0.03). 9.4% (3/29) and 41.4% (12/29) had early thyrotroph and gonadotroph deficiency respectively. Prolactin was normal in all patients. There was no significant association between WFNS grade and type of intervention on development of pituitary dysfunction. The mortality rate at 3 months was 18.8% (6/32), and there was no significant association between early cortisol levels, thyrotroph or gonadotroph deficiency and mortality status at this point. At 3 months, repeat testing revealed normal pituitary function (including IGF-1) in all patients except one with persistent gonadotroph deficiency. Pituitary dysfunction after aneurysmal SAH is uncommon. Early gonadotroph and thyrotroph deficiencies that occur are likely due to acute illness that recovers on follow up. However acute Day 1 basal cortisol post SAH while not deficient, is significantly lower than that in non-neurological critical illness. References: (1) Kreitschmann-Andermahr et al., J Clin Endocrinol Metab. 2004;89(10):4986-92. (2) Hannon MJ et al., J Clin Endocrinol Metab. 2013;98(8):3229-37. (3) Klose M et al., Clin Endocrinol. 2010;73(1):95-101. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.