Apoplejía hipofisaria

Servicio de Neurocirugía. Hospital Clinico Universitario. Zaragoza
Neurocirugia (Asturias, Spain) (Impact Factor: 0.29). 12/2003; 14(6). DOI: 10.1016/S1130-1473(03)70508-9
Source: OAI


Pituitary apoplexy is an infrequent complication of pituitary adenomas, caused by hemorrhagic or ischemic infarction in the tumor, with typical clinical presentation: severe headache of sudden onset, visual disturbances, sleep tendency or comma.
Along the last ten years we have treated eight patients with pituitary apoplexy. The diagnostic was clinically established in all of them. Seven cases com-plained of severe headache and vomiting. Eight patients reported visual disturbances. In one case low level of consciousness and meningeal irritation were the only findings. In six cases the apoplexy was the first pituitary adenoma manifestation. MRI and CT studies demons-trated the pituitary stroke in seven patients.
Surgical trans-sphenoidal decompression was performed in seven patients, requiring urgent management in only one case.
All patients experienced a marked visual improvement, but there was no amelioration of endocrine preoperative disturbances in any case. We conclude that quick diagnosis, early onset of hormonal therapy and urgent or delayed trans-sphenoidal surgery, depending on clinical manifestations, constitute the principies of the appropriate treatment of pituitary apoplexy.

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Available from: Rajab Al-Ghanem, Feb 20, 2014
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    ABSTRACT: The authors report a case of pituitary apoplexy that developed in a patient shortly after bromocriptine therapy was started for a growth hormone-secreting pituitary adenoma. The tumor was associated with visual impairment and ocular palsies, and was treated by transsphenoidal decompression. Although spontaneous tumor necrosis cannot be excluded, a causal role of bromocriptine treatment is suggested.
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    ABSTRACT: Hypopituitarism is a major manifestation of pituitary adenoma apoplexy. We postulated that the acute deterioration in pituitary function may be caused by compression of portal vessels and the pituitary stalk, secondary to a sudden increase in intrasellar contents. If this were the case, one would predict improvement in pituitary function to occur after surgical decompression. We studied pituitary function in eight patients presenting with the clinical syndrome of pituitary adenoma apoplexy before and on multiple occasions after urgent surgical decompression. Partial or complete hypopituitarism was seen in all subjects at the time of presentation. Serum cortisol levels were inappropriately low (5.9 +/- 1.4 micrograms/dL; 162.8 +/- 38 nmol/L) for the degree of stress in seven patients and appropriately elevated in only one subject (55.3 micrograms/dL; 1525.7 nmol/L). High normal increments in cortisol levels were noted in three subjects given test doses of cosyntropin. Patients were given glucocorticoids before, during, and for 2 days after surgery. Serum cortisol concentrations measured on or after the third day when glucocorticoids had already been stopped were normal in seven subjects and consistently low in one. These seven subjects were discharged on no replacement and were subsequently documented by dynamic testing to have normal pituitary-adrenal function. Gonadal function improved in two of four men and in one of two women who had hypogonadism on presentation. Improvement in thyroid function was documented in two of three subjects with preoperative hypothyroidism. Gradual improvement and almost complete resolution of the neuroophthalmological abnormalities occurred days to weeks after decompression. These observations demonstrate that urgent surgical decompression after pituitary tumor apoplexy was associated with improvement not only in neurological defects but also in pituitary function. The rapid improvement in pituitary function indicates not only that the hypopituitarism was reversible, but also that it might be caused by compression of the portal circulation and pituitary stalk by the sudden increase in intrasellar contents.
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    ABSTRACT: Thirty-seven patients with pituitary apoplexy were analyzed with an emphasis on clinical presentation and visual outcome. Their mean age was 56.6 years, with a male to female ratio of 2:1. Presenting symptoms included headache (95%), vomiting (69%), ocular paresis (78%), and reduction in visual fields (64%) or acuities (52%). Computed tomographic scanning correctly identified pituitary hemorrhage in only 46% of those scanned. Thirty-six patients underwent transsphenoidal decompression. By immunostaining criteria, null-cell adenomas were the most frequent tumor type (50%). Long-term steroid or thyroid hormone replacement therapy was necessary in 82% and 89% of patients, respectively. Long-term desmopressin therapy was required in 11%, and 64% of the male patients required testosterone replacement therapy. Surgery resulted in improvement in visual acuity deficits in 88%, visual field deficits in 95%, and ocular paresis in 100%. Analysis of the degree of improvement in preoperative visual deficits with the timing of the surgery demonstrated that those who underwent surgery within a week of apoplexy had significant recovery in their visual acuities. In the stable, conscious patient with residual vision in each eye, surgical decompression should be performed as soon as possible, because delays beyond 1 week may retard the return of visual function.
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