{"id":4423296,"date":"2026-07-30T16:58:36","date_gmt":"2026-07-30T21:58:36","guid":{"rendered":"https:\/\/myendoconsult.com\/learn\/?p=4423296"},"modified":"2026-07-30T16:58:37","modified_gmt":"2026-07-30T21:58:37","slug":"empty-sella-syndrome-all-you-need-to-know","status":"publish","type":"post","link":"https:\/\/myendoconsult.com\/learn\/empty-sella-syndrome-all-you-need-to-know\/","title":{"rendered":"Empty Sella Syndrome &#8211; all you need to know"},"content":{"rendered":"\n<h1 class=\"wp-block-heading\">Empty Sella \u2014 High-Yield Notes<\/h1>\n\n\n\n<p class=\"wp-block-paragraph\"><em>Source: The MyEndoConsult Team<\/em><\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">1. Definition &amp; Classification<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>Empty sella (arachnoidocele)<\/strong> = herniation of the subarachnoid space (CSF) into the sella turcica \u2192 pituitary flattened against the sellar floor, stalk elongated.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\">Radiologic grading<\/h3>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Grade<\/th><th>Criteria<\/th><\/tr><\/thead><tbody><tr><td><strong>Partial<\/strong><\/td><td>&lt;50% of sellar space filled with CSF<\/td><\/tr><tr><td><strong>Complete<\/strong><\/td><td>&gt;50% CSF; <strong>gland thickness &lt;2 mm<\/strong><\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<blockquote class=\"wp-block-quote is-layout-flow wp-block-quote-is-layout-flow\">\n<p class=\"wp-block-paragraph\">&#8220;Empty sella&#8221; is <strong>always a radiologic finding<\/strong>, not a clinical diagnosis. <strong>&#8220;Empty sella syndrome&#8221;<\/strong> = empty sella + symptoms (headache, visual changes, hormonal dysfunction).<\/p>\n<\/blockquote>\n\n\n\n<h3 class=\"wp-block-heading\">Etiology \u2014 Primary vs Secondary<\/h3>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Primary Empty Sella (PES)<\/th><th>Secondary Empty Sella (SES)<\/th><\/tr><\/thead><tbody><tr><td><strong>No prior sellar pathology<\/strong><\/td><td>Identifiable preceding sellar insult<\/td><\/tr><tr><td>Diaphragm sellae insufficiency + \u2191CSF pressure + pituitary volume changes<\/td><td>Pituitary destruction or shrinkage<\/td><\/tr><tr><td><strong>Multiple pregnancies (58%)<\/strong><\/td><td><strong>Pituitary surgery<\/strong><\/td><\/tr><tr><td><strong>Obesity (~50%)<\/strong><\/td><td><strong>Radiotherapy<\/strong><\/td><\/tr><tr><td><strong>Arterial hypertension (~27%)<\/strong><\/td><td><strong>Pituitary apoplexy<\/strong><\/td><\/tr><tr><td><strong>Idiopathic intracranial hypertension<\/strong><\/td><td><strong>Sheehan&#8217;s syndrome<\/strong> (postpartum necrosis)<\/td><\/tr><tr><td>Sleep apnea<\/td><td><strong>Hypophysitis<\/strong> (lymphocytic, IgG4, ICI-induced)<\/td><\/tr><tr><td>Menopause-related pituitary involution<\/td><td><strong>Traumatic brain injury<\/strong><\/td><\/tr><tr><td><\/td><td>Pituitary infection (TB, fungal)<\/td><\/tr><tr><td><\/td><td><strong>Medical shrinkage of adenoma<\/strong> (DA on prolactinoma, SSA on somatotroph)<\/td><\/tr><tr><td><\/td><td><strong>Congenital hypopituitarism<\/strong> (ectopic posterior pituitary, stalk dysgenesis)<\/td><\/tr><tr><td><\/td><td>Suprasellar mass causing chronic \u2191ICP (meningioma)<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\">Epidemiology<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>F:M = 5:1<\/strong>; peak middle age.<\/li>\n\n\n\n<li>Autopsy prevalence <strong>5.5\u201312%<\/strong>.<\/li>\n\n\n\n<li>Imaging prevalence <strong>~12%<\/strong> of general population (rising with MRI ubiquity).<\/li>\n\n\n\n<li><strong>In idiopathic intracranial hypertension (IIH): 70\u201394%<\/strong> have empty sella.<\/li>\n\n\n\n<li>IIH itself: ~1\/100,000 general; much higher in obese women of reproductive age.<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">2. Pathogenesis of Primary Empty Sella<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\">Three converging factors:<\/p>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Suprasellar \/ CSF factor<\/strong> \u2014 chronically or intermittently raised ICP (idiopathic, obesity, OSA, pregnancy\/labor, HTN). Impaired CSF dynamics in <strong>77%<\/strong> and impaired CSF absorption in <strong>84%<\/strong> of PES patients.<\/li>\n\n\n\n<li><strong>Diaphragm sellae insufficiency<\/strong> \u2014 partial or complete absence of the dural diaphragm allows pulsatile CSF transmission into the sella.<\/li>\n\n\n\n<li><strong>Pituitary volume changes<\/strong> \u2014 physiological hyperplasia during pregnancy\/lactation, then involution after menopause (explains the <strong>5:1 female predominance<\/strong>).<\/li>\n<\/ol>\n\n\n\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"1200\" height=\"600\" src=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/pathophysiology-of-ESS.jpg\" alt=\"\" class=\"wp-image-4423298\" srcset=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/pathophysiology-of-ESS.jpg 1200w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/pathophysiology-of-ESS-300x150.jpg 300w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/pathophysiology-of-ESS-768x384.jpg 768w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/pathophysiology-of-ESS-480x240.jpg 480w\" sizes=\"auto, (max-width: 1200px) 100vw, 1200px\" \/><figcaption class=\"wp-element-caption\">Pathophysiology of Empty Sella.  Created with<a href=\"https:\/\/www.biosketch.art\"> Biosketch.art<\/a> medical illustrator<\/figcaption><\/figure>\n\n\n\n<blockquote class=\"wp-block-quote is-layout-flow wp-block-quote-is-layout-flow\">\n<p class=\"wp-block-paragraph\">In extreme cases: bone erosion of sellar floor \u2192 <strong>CSF rhinorrhea<\/strong> \u2192 \u2191risk of meningitis.<\/p>\n<\/blockquote>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">3. Radiologic Approach<\/h2>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>MRI is the modality of choice.<\/strong> Required sequences:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Sagittal and coronal T1W pre- and post-gadolinium<\/strong><\/li>\n\n\n\n<li><strong>Coronal T2W<\/strong> (confirms CSF intensity)<\/li>\n\n\n\n<li>FLAIR \u2014 intrasellar fluid completely suppresses (true CSF)<\/li>\n\n\n\n<li>DWI \u2014 no restriction (excludes cystic neoplasms)<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Typical findings<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>CSF in continuity with overlying subarachnoid space.<\/li>\n\n\n\n<li>Flattened residual gland at sellar floor; <strong>pituitary volume often &lt;611 mm\u00b3<\/strong>.<\/li>\n\n\n\n<li>Stalk thinned but <strong>midline<\/strong> (asymmetry suggests SES or other pathology).<\/li>\n\n\n\n<li>Sellar bony remodeling\/enlargement if chronic \u2191ICP.<\/li>\n\n\n\n<li>Optic chiasm may herniate into sella (both PES and SES).<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Indirect signs of intracranial hypertension (to look for)<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Flattening of the <strong>posterior sclera<\/strong><\/li>\n\n\n\n<li><strong>Prominent perineural subarachnoid spaces<\/strong> along optic nerves<\/li>\n\n\n\n<li><strong>Vertical tortuosity<\/strong> of optic nerve sheath<\/li>\n\n\n\n<li><strong>Widened optic nerve sheath diameter<\/strong><\/li>\n\n\n\n<li>Transverse sinus stenosis<\/li>\n\n\n\n<li>Tonsillar descent<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Differential pitfalls<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Rathke cleft cyst<\/strong> \u2014 homogeneous, no CSF continuity, may have proteinaceous T1 hyperintensity.<\/li>\n\n\n\n<li><strong>Arachnoid cyst<\/strong> \u2014 distinguishing requires demonstrating CSF communication (sometimes cisternogram).<\/li>\n\n\n\n<li><strong>Cystic adenoma \/ craniopharyngioma<\/strong> \u2014 solid components, enhancement.<\/li>\n\n\n\n<li><strong>Ectopic posterior pituitary<\/strong> (congenital) \u2014 bright spot at median eminence, hypoplastic gland.<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">4. Endocrine Dysfunction<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Prevalence \u2014 PES<\/h3>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Finding<\/th><th>Frequency<\/th><\/tr><\/thead><tbody><tr><td><strong>Any pituitary hormone dysfunction<\/strong><\/td><td><strong>~29\u201352%<\/strong><\/td><\/tr><tr><td><strong>Panhypopituitarism<\/strong> (of those with hypopit)<\/td><td>~30\u201340%<\/td><\/tr><tr><td>Partial \/ isolated deficiency<\/td><td>60%<\/td><\/tr><tr><td><strong>Hyperprolactinemia<\/strong> (usually mild, &lt;50 ng\/mL)<\/td><td>~10%<\/td><\/tr><tr><td>Hormonal deterioration over follow-up<\/td><td>~3%<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\">Hormones most often affected (in order)<\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Growth hormone (GHD)<\/strong> \u2014 most common isolated deficiency in PES. IGF-1 correlates with pituitary volume.<\/li>\n\n\n\n<li><strong>Gonadotropins (LH\/FSH)<\/strong> \u2014 secondary hypogonadism.<\/li>\n\n\n\n<li>ACTH, TSH \u2014 less common in PES, more common in SES.<\/li>\n\n\n\n<li><strong>AVP (ADH) deficiency<\/strong> \u2014 uncommon in PES (think SES, hypophysitis, surgery).<\/li>\n<\/ol>\n\n\n\n<h3 class=\"wp-block-heading\">Hyperprolactinemia in PES<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Mechanism: <strong>stalk effect<\/strong> \u2014 CSF column compresses\/displaces stalk \u2192 \u2193dopamine delivery.<\/li>\n\n\n\n<li>Typically &lt;50 ng\/mL.<\/li>\n\n\n\n<li>Responds to dopamine agonists; gonadal status and ICP affect dynamics.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Hormonal hypersecretion (&#8220;invisible microadenoma&#8221; in an empty sella)<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Rare but recognized: <strong>Cushing&#8217;s disease, acromegaly, prolactinoma<\/strong>.<\/li>\n\n\n\n<li>An empty sella appearance increases the rate of <strong>MRI-negative Cushing&#8217;s disease<\/strong> \u2014 pituitary compression reduces visible adenoma volume.<\/li>\n\n\n\n<li>In acromegaly, PES coexistence is associated with lower preoperative PRL and lower nadir GH on OGTT.<\/li>\n\n\n\n<li><strong>Functional imaging<\/strong> (11C-methionine PET, 68Ga-DOTATATE if SSTR-expressing) can localize occult adenomas when MRI is unhelpful.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Predictors of pituitary dysfunction in PES<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Male sex<\/strong> (paradoxically higher hypopit rate when men have PES)<\/li>\n\n\n\n<li><strong>Complete<\/strong> (vs partial) empty sella on imaging<\/li>\n\n\n\n<li>Reduced residual pituitary volume \/ thickness<\/li>\n<\/ul>\n\n\n\n<blockquote class=\"wp-block-quote is-layout-flow wp-block-quote-is-layout-flow\">\n<p class=\"wp-block-paragraph\"><strong>Hormonal evaluation indicated in ALL patients<\/strong> with empty sella \u2014 even when incidental. Most deficits are stable, but baseline assessment matters. Repeat testing later if new symptoms.<\/p>\n<\/blockquote>\n\n\n\n<h3 class=\"wp-block-heading\">Suggested baseline workup<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Morning cortisol \u00b1 ACTH stimulation test<\/li>\n\n\n\n<li>Free T4, TSH<\/li>\n\n\n\n<li>LH, FSH, testosterone (men) \/ estradiol + menstrual history (women)<\/li>\n\n\n\n<li>IGF-1 (consider GH stimulation test if low or clinical concern)<\/li>\n\n\n\n<li><strong>Prolactin<\/strong> (assess for stalk effect)<\/li>\n\n\n\n<li>Serum\/urine osmolality + Na+ if symptoms suggest AVP deficiency<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">5. Clinical Features<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Symptom prevalence in PES<\/h3>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Symptom<\/th><th>Frequency<\/th><\/tr><\/thead><tbody><tr><td><strong>Headache<\/strong><\/td><td><strong>~80%<\/strong><\/td><\/tr><tr><td>Visual disturbances<\/td><td>~20%<\/td><\/tr><tr><td>Papilledema (if IIH)<\/td><td>Variable<\/td><\/tr><tr><td>Neurological (dizziness, syncope, seizures, depression)<\/td><td>~40%<\/td><\/tr><tr><td>Endocrine (galactorrhea, menstrual irregularity, infertility, ED, gynecomastia)<\/td><td>Variable<\/td><\/tr><tr><td><strong>CSF rhinorrhea<\/strong><\/td><td>Rare but serious \u2014 \u2191meningitis risk<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\">Profile of the typical PES patient<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Middle-aged, <strong>obese<\/strong>, <strong>multiparous<\/strong> woman with <strong>chronic headache<\/strong> and <strong>arterial hypertension<\/strong>.<\/li>\n\n\n\n<li>May overlap with <strong>IIH<\/strong> \u2014 papilledema, transient visual obscurations, pulsatile tinnitus, sixth-nerve palsy.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Eye findings to look for<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Worsening visual acuity, blurred vision, diplopia<\/li>\n\n\n\n<li><strong>Optic neuritis-like presentations<\/strong><\/li>\n\n\n\n<li><strong>Reduced retinal nerve fiber layer (RNFL) on OCT<\/strong> \u2014 even in asymptomatic PES \u2014 useful for monitoring<\/li>\n\n\n\n<li>Papilledema \u2192 mandates IIH workup (LP for opening pressure, MRV)<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Vascular association<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>PES is associated with <strong>cerebral small-vessel disease<\/strong> \u2014 periventricular white-matter hyperintensities, enlarged perivascular spaces (common pathway with chronic HTN\/obesity).<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">6. Differential Diagnosis Considerations<\/h2>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Setting<\/th><th>Think<\/th><\/tr><\/thead><tbody><tr><td>Woman with postpartum hemorrhage, failure to lactate, amenorrhea, fatigue<\/td><td><strong>Sheehan&#8217;s syndrome<\/strong> \u2192 progressive panhypopit, often years later \u2014 empty sella develops over time<\/td><\/tr><tr><td>Postpartum or peripartum woman with thickened stalk, then atrophy<\/td><td><strong>Lymphocytic hypophysitis<\/strong> (may resolve to empty sella)<\/td><\/tr><tr><td>Patient on ICI (ipilimumab, nivolumab) developing hypopit<\/td><td><strong>ICI-induced hypophysitis<\/strong><\/td><\/tr><tr><td>Recent macroprolactinoma on cabergoline, now with worsening vision<\/td><td><strong>Chiasm herniation into empty sella<\/strong> \u2014 reduce\/stop DA, consider chiasmapexy<\/td><\/tr><tr><td>Child\/young adult with short stature, ectopic posterior pituitary<\/td><td><strong>Congenital hypopituitarism<\/strong> (PROP1, POU1F1, LHX3\/4, HESX1 mutations)<\/td><\/tr><tr><td>Persistent ACTH-dependent Cushing&#8217;s, normal MRI, sella appears empty<\/td><td><strong>MRI-occult corticotroph adenoma<\/strong> \u2014 pursue BIPSS; consider functional imaging<\/td><\/tr><tr><td>TBI months\/years ago, new fatigue, libido loss<\/td><td><strong>Post-traumatic hypopituitarism<\/strong> (up to 25% post-moderate-severe TBI)<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">7. Treatment<\/h2>\n\n\n\n<h3 class=\"wp-block-heading\">Address the underlying mechanism<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Idiopathic intracranial hypertension:<\/strong> weight loss (target 5\u201310%), <strong>acetazolamide<\/strong> (250 mg\u20134 g\/day); topiramate as adjunct; LP-drainage \/ VP shunt or <strong>dural venous sinus stenting<\/strong> for refractory cases.<\/li>\n\n\n\n<li><strong>Obesity \/ OSA:<\/strong> CPAP, weight management.<\/li>\n\n\n\n<li><strong>Hypertension:<\/strong> standard BP control.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Endocrine management<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Replace deficits<\/strong> per the Endocrine Society 2016 hypopituitarism guideline:\n<ul class=\"wp-block-list\">\n<li><strong>Glucocorticoid first<\/strong> (hydrocortisone 15\u201320 mg\/day in divided doses; stress dosing education).<\/li>\n\n\n\n<li>Levothyroxine (only after cortisol replaced \u2014 risk of precipitating adrenal crisis).<\/li>\n\n\n\n<li>Sex steroid replacement (testosterone, or estrogen \u00b1 progestin).<\/li>\n\n\n\n<li>Growth hormone (in symptomatic adult GHD or pediatric GHD).<\/li>\n\n\n\n<li>Desmopressin for AVP deficiency.<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Hyperprolactinemia:<\/strong> dopamine agonist (cabergoline first-line).<\/li>\n\n\n\n<li><strong>Hypersecretion (rare):<\/strong> treat the underlying tumor \u2014 TSS, DA, SSA, etc.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\">Surgical \/ interventional indications<\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>CSF rhinorrhea<\/strong> \u2014 endoscopic skull base repair \u00b1 sellar reconstruction.<\/li>\n\n\n\n<li><strong>Chiasm herniation with progressive visual loss<\/strong> \u2014 transsphenoidal <strong>chiasmapexy<\/strong> (sellar packing to elevate the chiasm). Most often seen after over-treated macroprolactinoma.<\/li>\n\n\n\n<li><strong>Sellar floor erosion<\/strong> with risk of meningitis \u2014 osseous remodeling.<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">8. Pearls &amp; Pitfalls<\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li>An incidental empty sella is <strong>not<\/strong> by itself a diagnosis \u2014 but it always warrants <strong>a baseline pituitary hormone panel<\/strong>.<\/li>\n\n\n\n<li><strong>Middle-aged, obese, multiparous, hypertensive woman with chronic headache and empty sella<\/strong> \u2192 think IIH; check fundi and order MRV.<\/li>\n\n\n\n<li><strong>Empty sella + papilledema + obesity + female<\/strong> \u2192 reaches for the LP and opening pressure.<\/li>\n\n\n\n<li><strong>Galactorrhea + mild \u2191PRL (&lt;50 ng\/mL) + empty sella<\/strong> \u2192 stalk effect, not a prolactinoma. Cabergoline if symptomatic.<\/li>\n\n\n\n<li><strong>CSF rhinorrhea in a patient with empty sella<\/strong> is an emergency \u2014 meningitis risk; refer to skull-base surgery.<\/li>\n\n\n\n<li><strong>Patient with macroprolactinoma on long-term cabergoline who develops new vision changes<\/strong> \u2192 think <strong>chiasm herniation into empty sella<\/strong>; reduce dose, image, consider chiasmapexy. Do not assume tumor regrowth.<\/li>\n\n\n\n<li><strong>MRI-negative Cushing&#8217;s disease<\/strong> with apparent empty sella \u2192 don&#8217;t stop at MRI; pursue BIPSS, and consider 11C-methionine PET.<\/li>\n\n\n\n<li><strong>Acromegaly with an &#8220;empty&#8221; sella<\/strong> \u2192 still investigate; somatotroph adenomas can occur within an empty sella (reported in up to 14% of newly-diagnosed acromegalics in some series).<\/li>\n\n\n\n<li><strong>Sheehan&#8217;s syndrome<\/strong> is often diagnosed years to decades after the precipitating delivery \u2014 failure to lactate, persistent amenorrhea, and fatigue are early clues. Empty sella develops over years.<\/li>\n\n\n\n<li><strong>Male sex with PES<\/strong> is associated with higher hypopituitarism rates than female sex \u2014 counter-intuitive but consistent across cohorts.<\/li>\n\n\n\n<li><strong>A &#8220;complete&#8221; empty sella<\/strong> carries a higher rate of hypopituitarism than partial \u2014 radiologic gradation matters.<\/li>\n\n\n\n<li>Replacing <strong>levothyroxine before glucocorticoids<\/strong> in a patient with multiple deficiencies can precipitate adrenal crisis \u2014 <strong>cortisol first, always<\/strong>.<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">9. Quick-Recall Numbers<\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li>F:M ratio: <strong>5:1<\/strong><\/li>\n\n\n\n<li>Autopsy prevalence: <strong>5.5\u201312%<\/strong>; imaging prevalence: <strong>~12%<\/strong><\/li>\n\n\n\n<li>PES in IIH patients: <strong>70\u201394%<\/strong><\/li>\n\n\n\n<li>Hypopituitarism in PES: <strong>~29\u201352%<\/strong> (meta-analysis 52%)<\/li>\n\n\n\n<li>Panhypopit (within hypopit group): ~30\u201340%<\/li>\n\n\n\n<li>Most common deficits: <strong>GH &gt; gonadotropins<\/strong><\/li>\n\n\n\n<li>Hyperprolactinemia (stalk effect): ~10%; <strong>typically &lt;50 ng\/mL<\/strong><\/li>\n\n\n\n<li>Headache in PES: <strong>~80%<\/strong>; visual symptoms ~20%<\/li>\n\n\n\n<li>Multiple pregnancies in PES cohorts: <strong>~58%<\/strong><\/li>\n\n\n\n<li>Obesity in PES: ~50%; HTN ~27%<\/li>\n\n\n\n<li>&#8220;Complete&#8221; empty sella threshold: <strong>gland &lt;2 mm thick or &gt;50% CSF<\/strong><\/li>\n\n\n\n<li>Hormonal deterioration on follow-up: <strong>~3%<\/strong><\/li>\n\n\n\n<li>IIH prevalence: <strong>~1\/100,000<\/strong> general; ~20\/100,000 in obese reproductive-age women<\/li>\n<\/ul>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h2 class=\"wp-block-heading\">10. Must-Read References<\/h2>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>Chiloiro S, Giampietro A, Bianchi A, Tartaglione T, Capobianco A, Anile C, De Marinis L.<\/strong> Primary empty sella: a comprehensive review. <em>Eur J Endocrinol.<\/em> 2017;177(6):R275\u2013R285. doi:10.1530\/EJE-17-0505 <em>The single most useful review article on PES \u2014 pathogenesis, classification, endocrine evaluation, management framework. Essential.<\/em><\/li>\n\n\n\n<li><strong>Auer MK, Stieg MR, Crispin A, Sievers C, Stalla GK, Kopczak A.<\/strong> Primary empty sella syndrome and the prevalence of hormonal dysregulation: a systematic review and meta-analysis. <em>Dtsch Arztebl Int.<\/em> 2018;115(7):99\u2013105. doi:10.3238\/arztebl.2018.0099 <em>The meta-analysis source for the 52% hypopituitarism prevalence figure and pattern of deficits.<\/em><\/li>\n\n\n\n<li><strong>Guitelman M, Basavilbaso NG, Vitale M, Chervin A, Katz D, Miragaya K, et al.<\/strong> Primary empty sella (PES): a review of 175 cases. <em>Pituitary.<\/em> 2013;16(2):270\u2013274. doi:10.1007\/s11102-012-0416-6 <em>Largest single-cohort PES study; source of the obesity\/HTN\/multiparity epidemiology figures.<\/em><\/li>\n\n\n\n<li><strong>Carosi G, Brunetti A, Mangone A, Baldelli R, Tresoldi A, Del Sindaco G, et al.<\/strong> A Multicenter Cohort Study in Patients With Primary Empty Sella: Hormonal and Neuroradiological Features Over a Long Follow-Up. <em>Front Endocrinol (Lausanne).<\/em> 2022;13:925378. doi:10.3389\/fendo.2022.925378 <em>The most current long-term natural-history data \u2014 informs the &#8220;29% hormonal alteration at baseline, 3% deterioration over time&#8221; management strategy.<\/em><\/li>\n\n\n\n<li><strong>De Marinis L, Bonadonna S, Bianchi A, Maira G, Giustina A.<\/strong> Primary empty sella. <em>J Clin Endocrinol Metab.<\/em> 2005;90(9):5471\u20135477. doi:10.1210\/jc.2005-0288 <em>The foundational clinical review by the De Marinis \/ Giustina group; still the most-cited classical reference.<\/em><\/li>\n\n\n\n<li><strong>Fleseriu M, Hashim IA, Karavitaki N, Melmed S, Murad MH, Salvatori R, Samuels MH.<\/strong> Hormonal Replacement in Hypopituitarism in Adults: An Endocrine Society Clinical Practice Guideline. <em>J Clin Endocrinol Metab.<\/em> 2016;101(11):3888\u20133921. doi:10.1210\/jc.2016-2118 <em>The treatment standard for the hypopituitarism that follows empty sella diagnoses.<\/em><\/li>\n\n\n\n<li><strong>Friedman DI, Liu GT, Digre KB.<\/strong> Revised diagnostic criteria for the pseudotumor cerebri syndrome in adults and children. <em>Neurology.<\/em> 2013;81(13):1159\u20131165. doi:10.1212\/WNL.0b013e3182a55f17 <em>The modified Dandy criteria for IIH \u2014 essential for differentiating the IIH-driven empty sella cases.<\/em><\/li>\n\n\n\n<li><strong>Himes BT, Bhargav AG, Brown DA, Kaufmann TJ, Bancos I, Van Gompel JJ.<\/strong> Does pituitary compression\/empty sella syndrome contribute to MRI-negative Cushing&#8217;s disease? A single-institution experience. <em>Neurosurg Focus.<\/em> 2020;48(6):E3. doi:10.3171\/2020.3.FOCUS2084 <em>Important link between empty sella and MRI-occult Cushing&#8217;s disease \u2014 relevant when a hypercortisolemic patient has a normal-looking MRI.<\/em><\/li>\n\n\n\n<li><strong>Barzaghi LR, Donofrio CA, Panni P, Losa M, Mortini P.<\/strong> Treatment of empty sella associated with visual impairment: a systematic review of chiasmapexy techniques. <em>Pituitary.<\/em> 2018;21(1):98\u2013106. doi:10.1007\/s11102-017-0842-6 <em>The reference for chiasmapexy indications and techniques \u2014 useful when a treated macroprolactinoma causes secondary chiasm herniation.<\/em><\/li>\n\n\n\n<li><strong>Maira G, Anile C, Mangiola A.<\/strong> Primary empty sella syndrome in a series of 142 patients. <em>J Neurosurg.<\/em> 2005;103(5):831\u2013836. doi:10.3171\/jns.2005.103.5.0831 <em>Classic surgical neurology series describing the CSF-dynamics rationale for PES and the spectrum of presentations.<\/em><\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"<p>Empty Sella \u2014 High-Yield Notes Source: The MyEndoConsult Team 1. Definition &amp; Classification Empty sella (arachnoidocele) = herniation of the subarachnoid space (CSF) into&hellip;<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[568],"tags":[],"class_list":["post-4423296","post","type-post","status-publish","format-standard","hentry","category-board-review"],"_links":{"self":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/4423296","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/comments?post=4423296"}],"version-history":[{"count":3,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/4423296\/revisions"}],"predecessor-version":[{"id":4423300,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/4423296\/revisions\/4423300"}],"wp:attachment":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/media?parent=4423296"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/categories?post=4423296"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/tags?post=4423296"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}