Cases reported "Pituitary Apoplexy"

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1/51. Post-traumatic pituitary apoplexy--two case reports.

    A 60-year-old female and a 66-year-old male presented with post-traumatic pituitary apoplexy associated with clinically asymptomatic pituitary macroadenoma manifesting as severe visual disturbance that had not developed immediately after the head injury. skull radiography showed a unilateral linear occipital fracture. magnetic resonance imaging revealed pituitary tumor with dumbbell-shaped suprasellar extension and fresh intratumoral hemorrhage. Transsphenoidal surgery was performed in the first patient, and the visual disturbance subsided. decompressive craniectomy was performed in the second patient to treat brain contusion and part of the tumor was removed to decompress the optic nerves. The mechanism of post-traumatic pituitary apoplexy may occur as follows. The intrasellar part of the tumor is fixed by the bony structure forming the sella, and the suprasellar part is free to move, so a rotational force acting on the occipital region on one side will create a shearing strain between the intra- and suprasellar part of the tumor, resulting in pituitary apoplexy. Recovery of visual function, no matter how severely impaired, can be expected if an emergency operation is performed to decompress the optic nerves. Transsphenoidal surgery is the most advantageous procedure, as even partial removal of the tumor may be adequate to decompress the optic nerves in the acute stage. Staged transsphenoidal surgery is indicated to achieve total removal later.
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2/51. Pituitary metastasis from carcinoma of the urinary bladder mimicking pituitary apoplexy--case report.

    A 70-year-old male presented with pituitary metastasis from transitional cell carcinoma of the urinary bladder manifesting as sudden headache, transient unconsciousness, and visual disturbance mimicking apoplexy of pituitary adenoma. Computed tomography showed a suprasellar tumor with intratumoral and intraventricular hemorrhage. magnetic resonance imaging demonstrated an intra- and suprasellar mass lesion mimicking pituitary adenoma. diabetes insipidus developed soon after. The tumor was subtotally removed. Histological examination revealed transitional cell carcinoma. An intratumoral hemorrhage may be associated with a pituitary metastasis if the patient presents with symptoms such as pituitary apoplexy.
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3/51. pituitary apoplexy following metastasis of bronchogenic adenocarcinoma to a prolactinoma.

    A 42-year-old house wife presented with worsening headaches over 6 months in the absence of visual symptoms or symptoms suggestive of focal neurology. She was a life-long smoker. Systems review was unremarkable apart from secondary amenorrhoea and galactorrhoea of 6 months duration. Her serum prolactin was found to be 620 mU/l (60-400), FT4 12.6 nmol/l (9.8-23.1), TSH 1.38 mU/l (0.35-5.5), oestradiol < 73 pmol/l, LH and FSH of 4.4 and 12.6 mIU/l, respectively. She was on bromocriptine. A presumptive diagnosis of pneumonia, based on pyrexia and CXR findings, was made and she was started on IV antibiotics. Two days later she developed meningism and deterioration of conscious level. (Lumbar puncture results: no organisms, 312 neutrophils and 164 lymphocytes). CT scan revealed a 2.5-cm pituitary adenoma, with suprasellar extension. A repeat hormonal profile revealed FSH 1.4, LH < 0.3 mU/l, oestradiol < 73 pmol/l, prolactin 488 mU/l (60-400), and low random cortisol at 29 nmol/l. T1-weighted MRI revealed a large pituitary mass with evidence of haemorrhage. The patient subsequently underwent a transsphenoidal exploration with resection of the pituitary lesion. Whilst awaiting the histopathology results, CT of chest revealed a 1. 5-cm diameter rounded well defined density in the right lower lobe associated with hilar, pre- and right para-tracheal lymphadenopathy. The histopathology of the pituitary lesion, obtained piecemeal, revealed fragments of fibrous tissue infiltrated by sheets of acidophilic prolactin-positive cells, in keeping with a prolactinoma. In addition, other fragments with blood clot included highly atypical epithelial cells with mitotic figures. These were negative for prolactin but showed HMFG-and CEA-positivity, excluding them from a pituitary lineage. Transbronchial biopsy revealed moderately differentiated adenocarcinoma, with evidence of lymphatic spread. The overall conclusion was of bronchogenic adenocarcinoma, metastasizing to a prolactinoma and complicated by apoplexy.
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4/51. Transient diabetes insipidus and hypopituitarism after pituitary apoplexy: a rare association with pericardial effusion and painless thyroiditis.

    pituitary apoplexy in a 38-year-old male patient with acromegaly who presented with pericardial effusion, anterior pituitary dysfunction, and diabetes insipidus is described. With corticosteroid therapy, there was good initial recovery of pituitary function and regression of pericardial effusion. On withdrawal of corticosteroids, he developed painless thyroiditis, with transient thyrotoxicosis. Subsequently, the pituitary function tests remained normal for a year, but later he gradually developed hypogonadotropic hypogonadism, hypocortisolism, growth hormone deficiency, and progressive pituitary atrophy, resulting in empty sella syndrome.
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5/51. gonadotropin-releasing hormone-induced partial empty sella clinically mimicking pituitary apoplexy in a woman with a suspected non-secreting macroadenoma.

    pituitary apoplexy has been reported as a rare complication of dynamic testing used for the study of pituitary functional reserve. In 1993, a diagnosis of non-secreting macroadenoma with moderate functional hyperprolactinaemia was made in a 43-year-old woman. Soon after the start of therapy with bromocriptine up to 5 mg/die, the patient complained of nausea and postural hypotension. As the symptoms persisted even when the dose was reduced to 2.5 mg/die, the patient was transferred to therapy with quinagolide at the dosage of 37.5 microg/die. PRL levels quickly normalized (range 1.4-5.7 ng/ml) as well as menstrual cycles, and no side-effect was reported. In 1995 a sellar magnetic resonance imaging (MRI) showed no shrinkage of the known macroadenoma. In 1996, few hours after a gonadotropin-releasing-hormone (GnRH) test, which showed normal LH and FSH response and with baseline PRL levels in the normal range, the patient started complaining of severe frontal headache, nausea and vomiting. No gross visual defects were present. An emergency computed tomography (CT) showed no evident hemorrhagic infarction in the macroadenoma. The symptoms completely resolved in few days with steroidal and antiemetic therapy. A new MRI performed in 1998 showed a partial empty sella and PRL levels were in the normal range under dopaminergic treatment. The pituitary functional reserve proved normal on dynamic testing. The temporal association between the onset of symptoms and the GnRH test strongly suggests an association between the two events. No evident signs of pituitary apoplexy (either on emergency CT or hormonal evaluation) were detected. The authors suggest that GnRH can cause severe side-effects that mimic pituitary apoplexy without related morphological evidence and that, in our particular case, it can have caused the gradual disappearance of the non-secreting macroadenoma. Moreover, a causal role of the chronic dopaminergic treatment cannot be completely ruled out.
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6/51. Emergency department presentation of pituitary apoplexy.

    pituitary apoplexy is an acute infarction of pituitary gland, and potentially life-threatening condition that may be highly variable in its clinical presentation. We report a 54-year-old man presenting to the emergency department with an isolated oculomotor nerve palsy. Computed tomography (CT) scan revealed an isodense mass within sellar region and subsequently, magnetic resonance imaging (MRI) revealed a pituitary apoplexy causing a compression of right oculomotor nerve. The patient received hydrocortisone immediately, and did well with medical management. An isolated oculomotor nerve palsy is very rarely the presenting sign of pituitary apoplexy. When correctly diagnosed and treated, the third nerve palsy appears to be reversible. A pathophysiology, differential diagnosis, and treatment is described.
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7/51. Chiasmal apoplexy due to hemorrhage from a pituitary adenoma into the optic chiasm: case report.

    OBJECTIVE AND IMPORTANCE: Chiasmal apoplexy, defined as hemorrhage into the optic chiasm, generally is caused by an intrachiasmal vascular malformation. We report the first case of chiasmal apoplexy due to hemorrhage from a pituitary macroadenoma into the optic chiasm. CLINICAL PRESENTATION: A 52-year-old man presented with headache, sudden and severe deterioration of visual acuity in the left eye, and a bitemporal visual field deficit. magnetic resonance imaging revealed a large intra- and suprasellar homogeneously enhancing mass, which elevated a markedly thickened optic chiasm. After emergent transsphenoidal resection of the pituitary adenoma, vision did not improve. INTERVENTION: A pterional craniotomy was subsequently performed, during which a hematoma was found and evacuated from within the substance of the left optic nerve and chiasm. The hematoma cavity was found to communicate with the sella through a defect in the diaphragm. Vision improved dramatically after the operation. CONCLUSION: Chiasmal apoplexy resulting from pituitary adenoma should be distinguished from pituitary apoplexy, particularly because it requires a different surgical treatment. Clinical and radiographic features that may help distinguish the two are discussed.
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8/51. Spontaneous haemorrhage into an empty sella turcica mimicking pituitary apoplexy.

    We present a case of spontaneous haemorrhage into an empty sella turcica with the features of subclinical pituitary apoplexy. A 66-year-old woman with a previously resected pituitary adenoma presented four months later with progressive headache and visual deterioration. Cranial MRI demonstrated hyperacute blood products in a recurrent pituitary adenoma. Operative findings were of subacute blood in an empty sella turcica. There was no operative or subsequent histological evidence of tumour recurrence. The intrasellar haemorrhage was evacuated via a trans-sphenoidal approach, resulting in a rapid improvement in visual function. Endocrine deficits required thyroxine, corticosteroid and desmopressin supplementation. Haemorrhage into an empty sella turcica has not been previously described and needs to be suspected as a clinical entity in patients presenting with the features of pituitary apoplexy. awareness of this clinical condition will prevent preoperative misdiagnosis.
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keywords = sella turcica, turcica, sella
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9/51. Apoplexy of pituitary macroadenoma after combined test of anterior pituitary function.

    pituitary apoplexy has been reported as a very rare complication of combined tests of anterior pituitary function and of TRH or gonadotropin-releasing hormone (GnRH) administration in pituitary tumor. A 34-year-old man with a GH-secreting pituitary macroadenoma and diabetes mellitus received an injection of 400 microg TRH, 100 microg GnRH, and 0.15 U/Kg regular insulin. Twenty minutes later, he complained of a severe headache and vomited. visual acuity and visual field did not change and his headache was persistent during the next 24 hours of conservative management. magnetic resonance imaging (MRI) of the sella turcica done the day after the event showed definitive elevation of the optic chiasm and slight enlargement of tumor and focal areas of mixed high signal and low signal intensities in the macroadenoma on noncontrast T1-weighted images. headache subsided markedly within a day of octreotide therapy. Transsphenoidal removal of the pituitary tumor was performed 9 days after the hormone study. Ischemic necrosis and hemorrhage were confirmed in the acidophilic adenoma with positive immunostaining for GH. Postoperative course was uneventful and his serum insulin-like growth factor-1 (IGF-1) level and blood glucose levels were normalized. Three months after the surgery the dynamic test was repeated without adverse effects. To our knowledge, this is a very rare case of apoplexy of GH-secreting pituitary adenoma after a combined stimulation test of anterior pituitary function.
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keywords = sella turcica, turcica, sella
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10/51. Laparoscopic anterior lumbar interbody fusion precipitating pituitary apoplexy.

    OBJECTIVE: pituitary apoplexy may be the first presentation of a previously undiagnosed pituitary adenoma. Although many mechanisms of pituitary apoplexy have been proposed in the literature, the exact pathogenesis remains unclear. Many predisposing events have been implicated in the pathogenesis, however, the role of laparoscopy precipitating pituitary apoplexy has not been previously described. The authors present a case of pituitary apoplexy in a previously undiagnosed pituitary adenoma, which presented in the immediate post-operative period after a laparoscopic anterior lumbar interbody fusion. CLINICAL PRESENTATION: A 45-year-old man presented with a sudden onset of headache, photophobia, diplopia, visual field deficits, and decreased visual acuity in the immediate post-operative period after an uneventful laparoscopic anterior lumbar interbody fusion. Results of computed tomography of the brain revealed a hyperdense suprasellar mass without any signs of subarachnoid blood. The patient underwent magnetic resonance imaging, which revealed a hemorrhagic pituitary tumor with lateral and suprasellar extension, with compression of the cavernous sinus and optic chiasm, respectively. An urgent transsphenoidal decompression of the hemorrhagic pituitary adenoma was performed. Post-operatively, the patient demonstrated marked neurological improvement with recovery of visual acuity and extraocular movements. CONCLUSION: To the authors' knowledge, this is the first case reported in the literature of a laparoscopic procedure precipitating pituitary apoplexy. Recognition of this rare complication of laparoscopic surgery, and the importance of rapid diagnosis and urgent surgical treatment are emphasized.
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