Cases reported "Pituitary Apoplexy"

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1/145. pituitary apoplexy after cardiac surgery presenting as deep coma with dilated pupils.

    Acute clinical deterioration due to infarction or haemorrhage of an existing, often previously unrecognized, pituitary tumour is a rare but well-described complication. It can occur spontaneously or may be caused e.g. by mechanical ventilation, infection or surgical procedures. We report on a case of pituitary apoplexy occurring in a 64-year-old patient 3 weeks after cardiac surgery. The patient presented with deep coma and dilated pupils. magnetic resonance imaging revealed a haemorrhagic pituitary tumour. After prompt endocrinologic replacement therapy with levothyroxine and hydrocortisone the patient regained consciousness. Neurological examination revealed right oculomotor nerve palsy and bilateral cranial nerve VI palsy. Subsequent trans-sphenoidal removal of a nonfunctional macroadenoma with large necrotic areas was performed. The patient recovered completely. To our knowledge, pituitary tumours presenting with a combination of deep coma and dilated pupils must be considered exceedingly rare. Possible pathophysiologic mechanisms are discussed. As our case illustrates, even in severe cases complete recovery is possible if the diagnosis is suspected, and diagnostic and therapeutic measures are initiated in time.
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2/145. 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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3/145. 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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4/145. Acute painful oculomotor nerve paresis caused by pituitary apoplexy--a case report.

    In a typical case of pituitary apoplexy, a patient, who may or may not be known to harbor a pituitary adenoma, suddenly develops a severe headache. The headache may be retro-orbital, frontal, frontotemporal, or diffuse and may be associated with neck stiffness, neck pain, or both. ophthalmoplegia may develop within a few hours after the onset of headache. Here we report a rare case of one middle-aged female with pituitary apoplexy initially presenting with acute onset of pupil-involved third cranial nerve palsy, headache and peri-ocular pain. Emergent neuroimaging revealed pituitary apoplexy and immediate intravenous corticosteroid was given and third nerve paresis was improved thereafter. Definite tumor removal was done smoothly after steroid treatment and complete recovery of ophthalmoplegia was noted 2 weeks after operation.
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5/145. 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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6/145. A rare fatal course of disease in a patient with spontaneous pituitary apoplexy. Case report and literature review.

    A rare fatal course of a spontaneous pituitary apoplexy is described and its histological and pathophysiological causes are discussed. A review of the literature gives an overview of the historical and epidemiological data.
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7/145. pituitary apoplexy probably due to TRH and GnRH stimulation tests in a patient with acromegaly.

    pituitary apoplexy is the most serious and life-threatening complication of pituitary adenomas. Most of the cases occur spontaneously but it may occur also after a number of events such as the pituitary stimulation tests. We report a case of acromegaly due to a giant pituitary adenoma in which pituitary apoplexy developed 88 hours after TRH/GnRH stimulation test. The patient had severe headaches, nausea, vomiting, visual disturbance and mental alteration and the computed tomography (CT) scans revealed intratumoral and intraventricular bleeding. The pituitary mass was removed by transsphenoidal approach. The patient developed pneumonia and died on the 9th postoperative day. pituitary apoplexy was confirmed at surgery and on histological examination. Immunohistochemical staining was positive for GH and PRL. This case indicates that pituitary apoplexy may develop several days after TRH/GnRH stimulation test.
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ranking = 1.5
keywords = pituitary
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8/145. Rathke's cleft cyst with pituitary apoplexy: case report.

    We report a Rathke's cleft cyst which presented as pituitary apoplexy, a rare presentation. A 46-year-old woman suffered sudden headache and visual loss. T1-weighted MRI 3 weeks after this apoplectic episode demonstrated a cystic lesion between the anterior and posterior lobes of the pituitary, with some high-signal material layering in it. The mass showed spontaneous regression on an image 3 weeks later. Trans-sphenoidal surgery confirmed the diagnosis of a Rathke's cleft cyst with a haematoma within it.
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9/145. 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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10/145. Spontaneous resolution of pituitary adenoma after apoplexy.

    A patient with typical pituitary apoplexy with documented intralesional hemorrhage and spontaneous resolution is presented. There was no evidence of a tumor at a 3-month follow-up.
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ranking = 1.25
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