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Pituitary apoplexy (PA) is a clinical syndrome resulting from a hemorrhagic infarction of the pituitary gland. It is characterized by the sudden onset of visual disturbances, nausea, vomiting, headache and occasionally, signs of meningeal irritation and an altered mental status. The exact pathogenesis of PA remains to be elucidated, although tumor overgrowth of its blood supply remains the most popular theory. Main risk factors for the development of PA include systemic, iatrogenic, and external factors as well as the presence of an underlying pituitary tumor. The diagnostic approach of PA includes both neuroimaging and evaluation of pituitary secretory function. PA is a potentially life-threatening condition which should be managed with hemodynamic stabilization, correction of electrolyte abnormalities and replacement of hormonal deficiencies. PA treatment should be individualized based on the severity of the clinical picture which may vary widely. Treatment options include conservative management with periodic follow-up or neurosurgical intervention, which should be decided by a multidisciplinary team. We conducted a systematic review of the literature to unveil the frequency of PA predisposing factors, clinical and biochemical presentations, management strategies and outcomes.

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Not required for a Clinical Vignette.

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Pituitary apoplexy is a rare but potentially life-threatening complication of androgen deprivation therapy for prostate cancer. We present a case of a 70-year-old African American male with prostate cancer who developed symptoms of pituitary apoplexy, including hot flashes, nausea, vomiting, and cranial nerve III palsy, following the initiation of leuprolide therapy. Imaging revealed a pituitary adenoma with hemorrhage, and prompt multidisciplinary management was initiated. The patient was managed conservatively with improvement in symptoms. This case highlights the importance of recognizing the potential for pituitary apoplexy in patients receiving GnRH agonist therapy. We discuss the clinical presentation of GnRH agonist induced pituitary apoplexy, emphasizing that clinicians should maintain a high index of suspicion and promptly investigate any new neuro- ophthalmic symptoms in this group of patients. Ultimately, prompt diagnosis and treatment are crucial to mitigate the severity of this complication in patients with prostate cancer undergoing androgen deprivation therapy.

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PURPOSE: This is a case report of a patient experiencing hyponatremia who was ultimately diagnosed with pituitary apoplexy-associated cerebral salt wasting syndrome (CSWS). METHODS: Laboratory tests, clinical evaluations, and magnetic resonance imaging were performed by specialists. FINDINGS: The patient presented with severe headache, thirst, and polyuria. Results of laboratory tests indicated hyponatremia, decreased plasma osmolality, and elevated urine osmolality. Fluid restriction worsened the situation, and normal saline treatment helped return serum sodium and chloride levels to normal. Pituitary apoplexy-associated CSWS was finally considered. IMPLICATIONS: Pituitary apoplexy is a rare but reasonable etiology for CSWS with hyponatremia. Saline therapy is usually effective.

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BACKGROUND AND AIMS: Pituitary apoplexy (PA) is a rare neurosurgical emergency, associated with deficiency of one or more pituitary hormones. Few studies have explored the relative outcomes associated with conservative and neurosurgical intervention. METHODS: A retrospective evaluation of all patients with PA reviewed at Morriston Hospital was undertaken and diagnosis was obtained from Morriston database (Leicester Clinical Workstation database) between 1998 and 2019 from clinic letters and discharge summaries. RESULTS: Thirty-nine patients with PA were identified with a mean age of 74.5 years and 20 (51.3%) patients were women. Patients were followed up for a mean±SD 68.1±61.7 months. Twenty-three (59.0%) patients had a known pituitary adenoma. Commoner clinical presentations of PA were ophthalmoplegia or visual field loss. Following PA, 34 (87.2%) patients were noted to have a non-functioning pituitary adenoma (either pre-existing or new), while 5 (12.8%) patients had a pre-existing functional macroadenoma. Neurosurgical intervention was taken in 15 (38.5%) patients of which 3 (20.0%) patients also received radiotherapy, 2 (13.3%) patients had radiotherapy alone and the remainder managed conservatively. External ophthalmoplegia recovered in all cases. Visual loss remained in all cases. One (2.6%) patient with chromophobe adenoma had a significant second episode of PA requiring repeat surgery. CONCLUSION: PA often occurs in patients with undiagnosed adenoma. Hypopituitarism commonly occurred following conservative or surgical treatment. External ophthalmoplegia resolved in all cases, however, visual loss did not recover. Pituitary tumour recurrence and further PA episodes are rare.

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Pituitary apoplexy refers to a rare clinical syndrome consisting of signs and symptoms that occur due to rapid expansion of the contents of the sella turcica. It can occur spontaneously or associated with pituitary tumors. It can have a broad clinical spectrum, but usually presents with severe headache, visual impairment and hypopituitarism. Sudden onset of symptoms associated to imagiologic confirmation makes the diagnosis. Surgical treatment is advised when there is important compression of the optic tract. We present a case report and a review of the literature on pituitary apoplexy in pregnancy. The cases were reviewed to obtain information on maternal characteristics, clinical presentation, diagnostic studies, therapeutic modalities and maternal and fetal outcomes. Our review found 36 cases of pituitary apoplexy in pregnancy. Most of the cases occurred in the second trimester of pregnancy and headache was the most frequent symptom at presentation. Surgical therapy was required in more than half of the patients. In what respect maternal and fetal outcomes, there were 3 cases of preterm delivery and one case of maternal death. Our clinical case and literature review reinforces the importance of an early diagnosis to avoid potential adverse consequences.

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Pituitary apoplexy (PA) is a possible complication of pituitary adenoma but is rarely followed by cerebral infarction. The mechanism by which this occurs is not totally understood but is believed to have multiple aetiologies such as arterial compression due to mass effect, vasospasm induced by the presence of blood or by vasoactive agents. In this report, we present a man in his 80s with known pituitary adenoma with a sudden onset of left central facial palsy, left hemiparesis, paresis of the VI left pair and previously unrecognised atrial fibrillation in the ECG. At first, the signs of haemorrhage on imaging were unnoticed, which led to a diagnosis of ischaemic stroke that was submitted to thrombolysis. Due to complications during hospitalisation, the team suspected of PA with panhypopituitarism, confirmed by brain MRI and blood tests. The patient underwent conservative management with glucocorticoids with resolution of the acute adrenal insufficiency related symptoms.

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BACKGROUND: Pituitary apoplexy refers to hemorrhage or infarction within the pituitary gland resulting in acute neurological abnormalities. This condition is poorly described in dogs. OBJECTIVES: To document presenting complaints, examination findings, endocrinopathies, magnetic resonance imaging (MRI), treatments, and outcomes of dogs with pituitary apoplexy. ANIMALS: Twenty-six client-owned dogs with acute onset of neurological dysfunction. METHODS: Retrospective case series. Dogs were diagnosed with pituitary apoplexy if MRI or histopathology documented an intrasellar or suprasellar mass with evidence of hemorrhage or infarction in conjunction with acute neurological dysfunction. Clinical information was obtained from medical records and imaging reports. RESULTS: Common presenting complaints included altered mentation (16/26, 62%) and gastrointestinal dysfunction (14/26, 54%). Gait or posture changes (22/26, 85%), mentation changes (18/26, 69%), cranial neuropathies (17/26, 65%), cervical or head hyperpathia (12/26, 46%), and hyperthermia (8/26, 31%) were the most frequent exam findings. Ten dogs (38%) lacked evidence of an endocrinopathy before presentation. Common MRI findings included T1-weighted hypo- to isointensity of the hemorrhagic lesion (21/25, 84%), peripheral enhancement of the pituitary mass lesion (15/25, 60%), brain herniation (14/25, 56%), and obstructive hydrocephalus (13/25, 52%). Fifteen dogs (58%) survived to hospital discharge. Seven of these dogs received medical management alone (median survival 143 days; range, 7-641 days) and 8 received medications and radiation therapy (median survival 973 days; range, 41-1719 days). CONCLUSIONS AND CLINICAL IMPORTANCE: Dogs with pituitary apoplexy present with a variety of acute signs of neurological disease and inconsistent endocrine dysfunction. Dogs that survive to discharge can have a favorable outcome.

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BACKGROUND AND IMPORTANCE: Chordomas are centrally located, expansile soft tissue neoplasms that arise from the remnants of the embryological notochord. Hemorrhagic presentation is exceedingly rare and can resemble pituitary apoplexy. Moreover, a purely intrasellar location of a chordoma is extremely uncommon. We report a case of a hemorrhagic intrasellar chordoma in an adult male, which presented similarly to pituitary apoplexy and was resolved with surgical resection. CLINICAL PRESENTATION: A 69-year-old male presented with a 4 week history of acute onset headache and concurrent diplopia, with significantly reduced testosterone and slightly reduced cortisol. His left eye demonstrated a sixth cranial nerve palsy. Magnetic resonance imaging of the brain showed a large hemorrhagic mass in the pituitary region with significant compression of the left cavernous sinus and superior displacement of the pituitary gland. The patient underwent an endoscopic endonasal transsphenoidal approach for the resection of the lesion. Near total resection was achieved. Final pathology revealed chordoma with evidence of intratumoral hemorrhage, further confirmed by immunopositive stain for brachyury. Post-operatively, the patient had improved diplopia and was discharged home on low dose hydrocortisone. At 3-month follow-up, his diplopia was resolved and new MRI showed stable small residual disease. CONCLUSIONS: Apoplectic chordomas are uncommon given chordoma's characteristic lack of intralesional vascularity and represent a diagnostic challenge in the sellar region. Our unique case demonstrates that despite our initial impression of pituitary apoplexy, this was ultimately a case of apoplectic chordoma that responded well to endoscopic endonasal surgery.

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Pituitary apoplexy is an uncommon syndrome that often results in spontaneous hemorrhage or infarction of pituitary tumors or glands. We previously reported pituitary apoplexy occurred most frequently in nonfunctional pituitary adenomas among all types of pituitary incidentalomas. In the present study, we aimed to investigate the characteristics of pituitary apoplexy in patients with incidental nonfunctional pituitary adenomas. 65 patients with pituitary incidentaloma were enrolled. All patients underwent clinical/endocrinological/pathological investigations. As a result, 33 patients were diagnosed with nonfunctional pituitary adenomas. Of these, 12.1% of patients had pituitary apoplexy. There was no difference in tumor diameter, age, or sex between the apoplexy and the non-apoplexy groups. However, the liver enzymes aspartate transaminase and alanine aminotransferase were significantly higher, and plasma sodium and chloride levels were significantly lower in the apoplexy group than in the non-apoplexy group (each P < .05). In addition, low-density lipoprotein-cholesterol was significantly higher in the apoplexy group than in the non-apoplexy group (P < .05). Besides, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and prolactin deficiencies were significantly more frequent in the apoplexy group than in the non-apoplexy group (each P < .05), and growth hormone and adrenocorticotropic hormone deficiencies were more frequent in the apoplexy group than in the non-apoplexy group (P = .09 and.08, respectively). Furthermore, tumor diameter was not associated with pituitary apoplexy, whereas thyroid-stimulating hormone, luteinizing hormone, and follicle-stimulating hormone deficiencies were significantly associated with the apoplexy group (each P < .05). Hence, the present study indicated that pituitary apoplexy could not be related to tumor diameter. Moreover, hormonal deficiencies, hepatic dysfunction, hyponatremia or hypochloremia, and dyslipidemia might be indicators of pituitary apoplexy. There could be the possibility the treatment for dyslipidemia prevents pituitary apoplexy.

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Pituitary incidentaloma are being accidentally found during imaging procedures in approximately 10% of normal population. Facing pituitary incidentalomas endocrinologists have to decide about further management based on the assessment of hormonal activity, aetiology, size, and possible compressive symptoms. Treatment of choice for prolactinomas is medical therapy. Surgical treatment is a treatment of choice for other hormonally active tumours and in case of complications as defects of visual field, pituitary apoplexy with compressive symptoms, ophthalmoplegia respectively. Tumour not indicated for surgical treatment are followed-up by imaging techniques and in indicated cases also by endocrinological or visual field evaluation.

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Introduction: Pituitary apoplexy (PA) is a rare, and potentially life-threatening condition, caused by hemorrhage or infarction into the pituitary gland with a rapid expansion of the contents of the sella turcica, associated with sudden intense headache, neurological and endocrinological deterioration. The identification of risk factors is crucial for prevention and optimal management. Herein we report a case of PA occurring 1 month after the initiation of anabolic androgenic steroid abuse for bodybuilding. Case Report: A 40-year-old male patient presents with abrupt onset headache associated with left partial third cranial nerve palsy. The MRI shows a sellar lesion involving left cavernous sinus with a heterogenous anterior aspect of the lesion with hemorrhagic zones in favor of PA. Endocrine work-up shows high testosterone level in patient who was using exogenous testosterone without a medical prescription for a month. Conclusion: We report a case of PA of a pituitary neuroendocrine tumor occurring shortly after AAS. The association between PA and AAS should be considered as a potential risk.

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Pituitary apoplexy is a rare but potentially fatal endocrinological emergency which can be difficult to diagnose as presenting symptoms vary significantly. Optimal management requires early diagnosis and collaboration between ophthalmology, endocrinology and neurosurgical services. We present a case of pituitary apoplexy in a 52-year-old Caucasian female who was referred by her optometrist to Palmerston North Hospital Eye Clinic with a three-week history of sudden onset moderate bifrontal headaches, two weeks of non-specific peripheral visual changes and dense bitemporal inferior quadrantanopia on formal visual field testing. Ocular motility and slit lamp examination were unremarkable and retinal nerve fibre layer (RNFL) was relatively preserved on optical coherence tomography (OCT). MRI demonstrated a haemorrhagic pituitary macroadenoma elevating and compressing the optic chiasm without cavernous extension. Blood tests revealed mild hypothyroidism, hypocortisolism, hypogonadotropism and hyperprolactinaemia. The patient was commenced on hydrocortisone and levothyroxine replacement and proceeded for urgent transsphenoidal tumour resection at Wellington Regional Hospital. Histology revealed a non-functioning macroadenoma. The patient was asymptomatic and visual field tests had normalised three weeks post-operatively. Six weeks post-operatively, thyroid function and cortisol levels were normal and replacement therapies were ceased.

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