{"id":6574,"date":"2026-05-08T20:19:48","date_gmt":"2026-05-08T20:19:48","guid":{"rendered":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/?p=6574"},"modified":"2026-05-11T16:11:17","modified_gmt":"2026-05-11T16:11:17","slug":"a-case-of-pituitary-apoplexy-with-cavernous-sinus-involvement","status":"publish","type":"post","link":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/volume-4-issue-2\/a-case-of-pituitary-apoplexy-with-cavernous-sinus-involvement\/","title":{"rendered":"A Case Of Pituitary Apoplexy With Cavernous Sinus Involvement"},"content":{"rendered":"

ABSTRACT<\/strong><\/h2>\n

INTRODUCTION<\/strong><\/h3>\n

Pituitary apoplexy is a rare condition often characterized by sudden onset headache, visual symptoms, hormonal disturbances and alterations in mental status. Clinical manifestations may be variable, ranging from sudden onset headache in isolation, headache associated with ophthalmoparesis or bitemporal visual field deficits and even total blindness. Pituitary apoplexy involving ophthalmoparesis is often suggestive of cavernous sinus involvement with concurrent disruption of cranial nerve III, IV and VI function.<\/p>\n

CASE REPORT<\/strong><\/h3>\n

The routine hip replacement surgery for an 81 year old female was aborted because it was noted that she had ventricular tachycardia during surgery. Following recovery from anesthesia, a neurological evaluation revealed a complete ptosis and fixed globe of the left eye. Emergent imaging showed a pituitary macroadenoma with apoplexy affecting cranial nerves III, IV and VI due to cavernous sinus infiltration. She was started on IV cortisol to correct the corticosteroid deficiency, stabilize blood pressure and circulation and reduce swelling of the pituitary gland to improve her acute symptoms.The patient\u2019s electrolytes and hormonal levels were closely monitored, and she was followed regularly with visual acuity and visual field testing, and pupillary and extraocular muscle movement evaluations.<\/p>\n

After resolution of the acute event, the patient still showed a complete left upper lid ptosis and reduced visual acuity in the left eye.\u00a0 Ocular motility in the left eye still demonstrated poor supraduction and infraduction as well as poor abduction and adduction, resulting in diplopia. The patient continues to be closely monitored by neurosurgery, neurology, endocrinology, and ophthalmology.<\/p>\n

CONCLUSION<\/strong><\/h3>\n

Patients with confirmed pituitary apoplexy require prompt medical attention, including hemodynamic stabilization, control of renal function and electrolytes, monitoring of pituitary hormonal function, and high dose corticosteroids. Visual acuity, visual fields, ocular motility, and level of consciousness should also be followed closely.<\/p>\n

Keywords:\u00a0 <\/strong>pituitary apoplexy, pituitary adenoma, cavernous sinus, cranial nerves, visual fields, ophthalmoparesis, ptosis<\/em><\/p>\n

INTRODUCTION<\/strong><\/h2>\n

Pituitary adenomas can result in hormonal imbalances, visual field loss, and headaches. When complicated by pituitary apoplexy, although rare, these tumors can become life threatening. The subsequent hemorrhaging of the tumor can lead to detrimental hypotension and vision loss. A dangerous cycle of hemodynamic dysregulation ensues when a pituitary apoplexy develops. Concurrent surgery, comorbidities, hormone therapy, and several other factors can exacerbate this condition.<\/p>\n

This case presents a patient with sudden onset diplopia, sudden and almost complete ptosis and poor vision after an episode of ventricular tachycardia following an emergently aborted, routine hip replacement surgery. Post-operatively, the patient also experienced an inability to move the left eye in any direction causing diplopia (mostly horizontal), poor vision, an afferent pupillary defect and almost complete left lid ptosis.<\/p>\n

CASE REPORT<\/strong><\/h2>\n

An 81-year-old Caucasian female was taken into surgery for a routine hip replacement. Her medical history was significant for hypertension controlled with Lisinopril 10 mg daily PO. She had no history of diabetes, cardiac or pulmonary disease, or other conditions. Her ocular history was negative except for unremarkable bilateral cataract extractions approximately ten years prior. She denied any allergies to medications.<\/p>\n

On the morning of surgery, the patient\u2019s blood pressure, resting pulse, respiration rate and oxygen saturation were all normal. The anesthesiologist sedated the patient without complications. Approximately five minutes into sedation and prior to the beginning of the surgery, the patient went into ventricular tachycardia. The hip surgery was aborted, and the patient was revived and fully awake after approximately thirty minutes.<\/p>\n

Once awake, the patient showed an almost complete ptosis of the left upper lid and a fixed left globe (Figure 1). <\/em>Emergent neurological and ophthalmological consultations agreed that urgent magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) were necessary to establish the diagnosis. Cavernous sinus involvement was suspected based on the likely involvement of cranial nerves III, IV and VI resulting in almost complete left ptosis (approximately 90%)\u00a0 and the inability of the left eye to move in any direction of gaze (approximately 5% ability for supraduction and infraduction and the same for abduction and adduction).<\/p>\n

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Figure 1<\/strong>. EOM testing demonstrated inability of the left eye to move in any direction of gaze.<\/p>\n

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An MRI of the brain with contrast showed a 2.3 x 2.0 x 2.0 cm sellar and suprasellar space-occupying mass replacing most of the pituitary gland with suspicion for intralesional bleeding consistent with a diagnosis of a macroadenoma with pituitary apoplexy (Figure 2). The mass was causing sagging of the sellar floor along the lateral side, encroaching on the sphenoid sinus and obscuring the infundibular stalk. It invaded the left cavernous sinus and left internal carotid artery. The optic chiasm was deviated along its superior border. An MRV with contrast was normal.<\/p>\n

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Figure 2<\/strong>. MRI of the brain with contrast demonstrating a 2.3 x 2.0 x 2.0 cm mass in the sellar and suprasellar spaces with suspicion of intralesional bleeding consistent with a diagnosis of macroadenoma with pituitary apoplexy.<\/p>\n

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Blood work was ordered, including a CBC with differentials, urea and electrolyte levels, liver function tests, PT\/PTT, IGF1, GH, PRL, TSH, T4, LH, FSH, cortisol and estradiol. Labs showed dangerously low levels of cortisol, causing a significant drop in blood pressure and subsequently, the patient was diagnosed with pituitary apoplexy. She was started on IV cortisol to correct the corticosteroid deficiency, stabilize blood pressure and circulation and reduce swelling of the pituitary gland to improve her acute symptoms.<\/p>\n

During this immediate post-op period the patient was seen in the eye clinic. Ocular motility in the right eye was full in all directions of gaze. The left eye showed a fixed globe with an inability of the eye to move in any direction.\u00a0 The right upper lid position was normal but there was a significant ptosis (approximately 95%) in the left upper lid. Pupils were equal, round and reactive to direct light but a Grade 3 afferent pupillary defect was present in the left eye. The patient\u2019s visual acuity was OD 20\/40 (pinhole to 20\/25+) and OS 20\/200 (no improvement with pinhole). Her visual acuity prior to surgery was unknown, as she was new to the clinic. Dilated fundus exam showed a normal fundus, vasculature and macula OD. There was evidence of optic nerve pallor OS.<\/p>\n

Humphrey visual fields were obtained one week after the initial visit as the patient had been too weak to sit up at prior evaluations. Figure 3 shows a bitemporal hemianopia suggestive of pituitary involvement.<\/p>\n

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Figure 3<\/strong>.\u00a0 24-2 Humphrey visual field testing of left eye (Figure 3A) and right eye (Figure 3B) showing bitemporal hemianopia suggestive of pituitary involvement.<\/p>\n

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It was the opinion of the specialties involved in the patient\u2019s care that the patient\u2019s pituitary apoplexy was triggered primarily by a drop in blood pressure. However, the etiology is multifactorial. The pituitary adenoma resulted in malfunction of blood pressure regulation due to the inability to produce hormones such as vasopressin. In addition, increased pressure in the sella turcica most likely compressed the hypothalamus, impairing blood pressure control. General anesthesia is also known to drop blood pressure. These factors combined caused a dangerous cycle of hypotension. She is currently under the care of endocrinology, neurosurgery, neurology and ophthalmology. She is followed in ophthalmology every three months.<\/p>\n

DISCUSSION<\/strong><\/h2>\n

The pituitary gland is located in a depression in the skull base known as the sella turcica. It is attached to the hypothalamus by a stalk containing the blood vessels that supply the pituitary gland. The pituitary gland consists of two parts, an anterior part (front) and a posterior part (back). Both the anterior and posterior pituitary release hormones that control numerous other organs. The anterior pituitary releases hormones responsible for regulating metabolism, blood pressure, blood sugar, secondary sex characteristics, muscle and bone density, ovulation, and energy levels. The posterior pituitary regulates water and sodium levels, as well as functions in childbirth and breastmilk production.3 <\/sup>\u00a0A disruption of any of these processes can result in a cascade of adverse effects.<\/p>\n

Pituitary adenomas are slow-growing and typically benign tumors. The prevalence of pituitary adenoma is approximately 17%, but the incidence of clinically relevant pituitary adenomas is about 1 case per 1000 people.4\u00a0 <\/sup>Clinically relevant pituitary adenomas are those that cause hormonal imbalances, visual field defects, or oculomotor palsies. A pituitary macroadenoma (>10mm) is also typically considered clinically relevant. It is important to distinguish between functional and non-functional adenomas. Functional adenomas secrete excess hormones, while non-functional adenomas secrete normal hormone levels or inactive hormones. However, non-functional adenomas can still result in hormone abnormalities due to compression of pituitary tissue and surrounding structures or ocular complications due to optic chiasm and cranial nerve compression.<\/p>\n

Pituitary apoplexy is caused by a spontaneous hemorrhage or an infarction of the pituitary adenoma. It is a medical emergency, requiring prompt attention as well as possible surgical intervention. It\u2019s a rare condition, with 2\u201312% of adenomas potentially complicated by pituitary apoplexy. In pituitary apoplexy, the initial problem is typically a lack of secretion of adrenocorticotropic hormone (ACTH), which functions in the secretion of cortisol by the adrenal glands. A sudden decrease in cortisol can lead to a constellation of symptoms called an \u201cadrenal crisis.\u201d 3, 4, 5\u00a0 <\/sup>This cortisol deficiency can cause low blood pressure, hypoglycemia (which can lead to coma) and abdominal pain. The low blood pressure can often be life-threatening, as in our patient, and requires immediate medical attention.<\/p>\n

Patients with acromegaly or Cushing syndrome may be more at risk for pituitary apoplexy, complicating 3-10% of patients with pituitary corticotrophic macroadenomas. This increased prevalence may be due to excess hormones fueling the growth of the pituitary adenoma.3, 4, 5<\/sup><\/p>\n

The clinical presentation of pituitary apoplexy is typically marked by severe, sudden-onset headache in 95% of cases. The headache results from stretching of the dura mater along the walls of the sella that are supplied by the meningeal branches of the trigeminal nerve, as well as irritation of the trigeminal nerve itself caused by the expanding pituitary mass.4, 5<\/sup><\/p>\n

Ocular paresis from pituitary apoplexy results from involvement of the cavernous sinus that leads to compression of cranial nerves III, IV and\/or VI. \u00a0<\/sup>Cases of pituitary apoplexy with oculomotor involvement have an incidence of 37-60%.2, 3, 4<\/sup> Compression of the inferior optic chiasm classically results in a bitemporal superior quadrantanopia. Hemianopsia may occur with greater chiasmal damage. The clinical manifestation of pituitary apoplexy may vary, however, ranging from sudden headache in isolation, to headache associated with ophthalmoparesis or bitemporal visual field defects.5 <\/sup><\/p>\n

Diagnosis of pituitary apoplexy is typically achieved with MRI and blood work. Treatments include timely correction of hormonal deficiencies as well as surgical intervention. Many patients diagnosed with pituitary apoplexy eventually develop hormonal deficiencies that require long-term hormone supplementation.6 <\/sup><\/p>\n

The clinical presentation of pituitary apoplexy depends on the speed of onset of infarction or hemorrhage and the volume of hemorrhage. These factors influence the degree of compression of the pituitary gland and adjacent neuro-ophthalmologic structures. Acute, severe pituitary apoplexy can cause serious neurological deficits, coma and even death. Alternatively, subclinical apoplexy may present with mild symptoms that develop over days or weeks.7, 8, 9<\/sup><\/p>\n

Pituitary apoplexy can be a potentially life-threatening condition in high-risk patients with pituitary adenomas. Contributing factors for apoplexy include head trauma, sudden changes in arterial blood pressure, hormone therapy, somatostatin analog therapy, dopamine agonists, diabetes, cardiac surgery, laparoscopic surgery, history of radiation therapy, anticoagulation, pregnancy, increased intracranial pressure and mechanical ventilation at high altitudes.8, 9\u00a0\u00a0 <\/sup>Many of these factors result in blood flow fluctuation, stimulation of the pituitary gland and\/or an anticoagulated state. Other contributing factors can include a history of major surgery, anticoagulation\/clotting disorders, myocardial infarction, estrogen therapy, history of head trauma\/injury with shock, radiotherapy and pregnancy. Table 1 below summarizes possible contributing factors for pituitary apoplexy. 8, 9<\/sup><\/p>\n

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\u00a0<\/strong><\/p>\n

Possible Contributing Factors for Pituitary Apoplexy<\/strong><\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Blood pressure variations<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Major surgery<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Diabetes<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Anticoagulation<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Clotting disorders<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Myocardial infarction<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Estrogen therapy<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Dopamine agonist therapy<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Head trauma \/ Traumatic Injury with shock<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Radiotherapy<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0 Pregnancy<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Increased Intracranial Pressure<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

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Table 1.<\/strong> Summary of contributing factors for pituitary apoplexy<\/p>\n

\u00a0<\/em><\/strong><\/p>\n

Pituitary adenomas are vulnerable to hemorrhage and ischemia due to several factors. Pituitary adenomas may outgrow their blood supply, resulting in ischemia. Tumor expansion may also cause ischemia by compressing the superior pituitary vessels against the sellar diaphragm. 8, 9 <\/sup>\u00a0\u00a0Internal features of the adenoma may also lead to hemorrhage and ischemia. The high metabolism of the pituitary adenoma, coupled with limited angiogenesis and reduced vessel density compared to normal pituitary tissue, may result in acute ischemia and infarction with abrupt disruption of tissue metabolism.12 <\/sup>Pituitary tumors are five times more likely to bleed than other brain tumors.\u00a0 <\/sup>The blood supply of tumors comes from the nearby inferior hypophyseal artery creating a higher blood pressure, increasing the risk of bleeding. Tumors may also be more sensitive to blood pressure fluctuations and those blood vessels may contain abnormalities that make them vulnerable to damage and subsequent hemorrhage.13<\/sup><\/p>\n

A therapeutic approach for this condition should begin with immediate supportive measures to ensure hemodynamic stability, including the assessment and management of fluid and electrolyte balance. An urgent biochemical and endocrine assessment should be initiated including CBC with differentials, urea and electrolyte levels, liver function tests and blood clotting screening. Imaging (preferably MRI, if not contraindicated) should be performed urgently after systemic workup. Intravenous hydrocortisone therapy should be initiated if the patient is considered to be hemodynamically unstable, shows signs of altered consciousness, or has visual deficits.14<\/sup><\/p>\n

Approximately 70% of patients require surgery, while an estimated 30% of patients can be treated conservatively with IV glucocorticoids and careful fluid and electrolyte monitoring.18<\/sup><\/p>\n

The necessity of surgical intervention in the treatment of pituitary apoplexy is somewhat controversial. Rajasekaran et al created guidelines for identifying the best therapeutic approach for the treatment and management of pituitary apoplexy. Table 2 summarizes these guidelines based on the progression of clinical signs and symptoms to determine the appropriate timing and need for surgical intervention.8, 9, 11<\/sup> Early surgical management is recommended in cases of significant neuro-ophthalmic signs, including deteriorating visual acuity, visual field defects or reduced level of consciousness. Surgical intervention within eight days of symptom onset yields the most favorable visual outcomes.4, 8, 11 <\/sup>Of note, ocular paresis of cranial nerves III, IV and VI in the absence of other neuro-ophthalmic signs is not an indication for surgical intervention. 8, 12\u00a0 <\/sup>Surgery is typically performed via the transsphenoidal route with decompression.12<\/sup><\/p>\n

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Suspected Pituitary Apoplexy Treatment Guidelines<\/strong><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n\n\n\n
\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Supportive measures to ensure hemodynamic stability<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Assessment and management of fluid\/electrolyte balance<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Consider hydrocortisone replacement<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u2193<\/p>\n\n\n\n
Urgent biochemical and endocrine assessment (full blood count, urea and electrolytes, liver function tests, clotting factors, IGF 1, GH, PRL, TSH, T4, LH, FSH, cortisol, testosterone (if male) and estradiol (if female)<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u2193<\/p>\n\n\n\n
Urgent MRI to confirm diagnosis or pituitary CT scan if MRI is contraindicated<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u2193<\/p>\n\n\n\n
Consult with endocrinology and neurosurgery teams once diagnosis is confirmed<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u2193<\/p>\n\n\n\n
Visual Acuity Evaluation:<\/strong>\u00a0 Does the patient have severe and persistent or deteriorating visual defects and\/or deteriorating level of consciousness?<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0 YES:<\/strong>\u00a0 consider surgical management<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0 NO:<\/strong>\u00a0 conservative management is acceptable: close monitoring by neurology\/ neurosurgery, ophthalmology and endocrinology<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u2193<\/p>\n\n\n\n
Is the patient stable or improving?<\/strong><\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0 YES:\u00a0 <\/strong>continue conservative management<\/p>\n

\u25cf\u00a0\u00a0\u00a0\u00a0\u00a0 NO:\u00a0 <\/strong>consider surgical management<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Table 2. <\/strong>A summary of guidelines based on the progression of clinical signs and symptoms to determine the appropriate timing and\/or surgical intervention in pituitary apoplexy. 8,9,11<\/sup><\/p>\n

If a conservative, non-surgical plan is initiated, the patient needs close monitoring. In cases of reducing visual acuity, deteriorating or expanding visual defects, or deteriorating levels of consciousness, surgical management should be reconsidered.12 <\/sup>There are no current studies that indicate how soon surgery should be performed in the setting of worsening symptoms.<\/p>\n

CONCLUSION<\/strong><\/h2>\n

Pituitary apoplexy is a rare, potentially serious condition that can be difficult to diagnose due to its variable and often non-specific clinical presentation. MRI is the diagnostic imaging of choice to show hemorrhagic or necrotizing pituitary tumors leading to the pituitary apoplexy.<\/p>\n

Patients with confirmed pituitary apoplexy require prompt medical attention, including hemodynamic stabilization, control of renal function and electrolytes, monitoring of pituitary hormonal function, and high-dose corticosteroids. Visual acuity, visual fields, ocular motility, and level of consciousness should also be followed regularly.<\/p>\n

In the case of severe loss of visual acuity, sudden amaurosis, worsening visual fields, worsening neurological symptoms, hypothalamic involvement or decreased levels of consciousness, urgent decompressive surgery is advised. If none of these symptoms are present, a more conservative medical approach, including regular assessments of visual acuity, visual fields, and extraocular motility, is recommended. Fluid and electrolyte balances must be monitored closely as well. In the case of obvious clinical deterioration, surgical decompression must once again be considered.<\/p>\n

A multidisciplinary approach involving neurosurgery, endocrinology, and eye care is important to provide comprehensive care and the best chance of a positive outcome to patients with pituitary apoplexy.<\/p>\n

\u00a0<\/strong><\/p>\n

REFERENCES<\/strong><\/h3>\n
    \n
  1. Murad-Kejbou S, Eggenberger E (nov 2009). \u201cPituitary apoplexy:\u00a0 evaluation, management and prognosis.\u201d\u00a0 Current opinion in Ophthalmology. 20 (6): 456-61.<\/li>\n
  2. Briet C, Salenave S, Bonneville JF, et al. Pituitary apoplexy. Endocr Rev 2015; 36:622\u201345.<\/li>\n
  3. Semple, P.L.; De Villiers, J.C.; Bowen, R.M.; Lopes, M.B.S.; Laws, E.R. Pituitary Apoplexy: Do Histological Features Influence the Clinical Presentation and Outcome? J. Neurosurg. 2006, 104, 931\u2013937.<\/li>\n
  4. Randeva, H.S.; Schoebel, J.; Byrne, J.; Esiri, M.; Adams, C.B.; Wass, J.A. Classical Pituitary Apoplexy: Clinical Features, Management and Outcome. Clin. Endocrinol. 1999, 51, 181\u2013188.<\/li>\n
  5. Rovit RL, Fein JM. Pituitary Apoplexy: a Review and Reappraisal. J Neurosurg. 1972; 37:280-288.<\/li>\n
  6. Briet C, Salenave S, Chansom P. Pituitary apoplexy. Endocrinol Metab Clin North Am 2015; 44:\u00a0 199-209.<\/li>\n
  7. C. Briet, S. Salenave, J. F. Bonneville, E. R. Laws, and P. Chanson, \u201cPituitary Apoplexy,\u201d Endocrine Reviews 36, no. 6 (2015): 622\u2013645.<\/li>\n
  8. Rovit RL, Fein JM. Pituitary Apoplexy: a Review and Reappraisal. J Neurosurg. 1972; 37:280-288.<\/li>\n
  9. Reid RL, Quigley ME, Yen SS. Pituitary apoplexy, a review. Arch Neurol. 1985;42:712-719.<\/li>\n
  10. Biousse V, Newman NJ, Oyesiku NM. Precipitating factors in pituitary apoplexy. J Neurol Neurosurg Psychiatry. 2001; 71:542-545.<\/li>\n
  11. Randeva, H.S.; Schoebel, J.; Byrne, J.; Esiri, M.; Adams, C.B.; Wass, J.A. Classical Pituitary Apoplexy: Clinical Features, Management and Outcome. Clin. Endocrinol. 1999, 51, 181\u2013188.<\/li>\n
  12. Melmed, S, and Auchus, R.J.. Williams Textbook of Endocrinology<\/em>. Elsevier, 2024.<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    Pituitary apoplexy case in an 81\u2011year\u2011old woman presenting with ptosis, fixed globe, visual field loss and adrenal crisis, stressing rapid MRI, steroids…<\/p>\n","protected":false},"author":165,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_seopress_robots_primary_cat":"107","_seopress_titles_title":"","_seopress_titles_desc":"Pituitary apoplexy case in an 81\u2011year\u2011old woman presenting with ptosis, fixed globe, visual field loss and adrenal crisis, stressing rapid MRI, steroids...","_seopress_robots_index":"","_et_pb_use_builder":"","_et_pb_old_content":"","_et_gb_content_width":"","footnotes":""},"categories":[61,107],"tags":[],"class_list":["post-6574","post","type-post","status-publish","format-standard","hentry","category-neuro","category-volume-4-issue-2","et-doesnt-have-format-content","et_post_format-et-post-format-standard"],"_links":{"self":[{"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/posts\/6574","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/users\/165"}],"replies":[{"embeddable":true,"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/comments?post=6574"}],"version-history":[{"count":3,"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/posts\/6574\/revisions"}],"predecessor-version":[{"id":6591,"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/posts\/6574\/revisions\/6591"}],"wp:attachment":[{"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/media?parent=6574"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/categories?post=6574"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/wp-json\/wp\/v2\/tags?post=6574"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}