Suga T, Kagawa S, Goto H, Yoshioka K, Hosoya T
Department of Neurosurgery, Kamaishi Municipal Hospital, Iwate, Japan.
No Shinkei Geka. 1996 May;24(5):475-9.
A case of pituitary adenoma which had progressed from subclinical pituitary apoplexy to subacute pituitary apoplexy on the occasion of cerebral angiography is reported. A 29-year-old man, complaining of bitemporal hemianopsia, was admitted to our department. Plain skull X-p revealed enlargement and double floor of the sella turcica. No abnormal calcification was revealed. CT demonstrated an isodensity mass with a diameter of 4 x 4 cm, and with ring enhancement in the suprasellar region. The mass extended from the intrasellar region to the suprasellar region and had a signal of high intensity on T1-weighted images. Endocrinological examination revealed hyperprolactinemia with a serum level of 422 ng/ml and normal reaction of anterior pituitary hormones. On 3rd March, digital subtraction angiography with 5F catheter was performed with the patient under sedation. The contrast medium was ioxaglic acid (Hexabrix 320). A volume of 6 ml with a speed of 4 ml per second was injected for the internal carotid angiogram. A total volume of 60 ml was used. Serum saline with 10 unit per ml of heparin sodium was also used for flushing. During angiography, the patient's blood pressure was 125/60-115/60mm Hg. DSA revealed upward displacement of the proximal portion of the anterior cerebral artery, pocket formation, and staining of the tumor capsule. Six hours later, he complained of retroorbital headache. Next morning, he noticed complete lack of left visual acuity. On 7th March, right visual acuity degenerated to blindness. CT revealed that the mass had increased its density. With bifrontal osteoplastic craniotomy, the tumor with marked intratumoral hemorrhage was resected. Its histology was chromophobe adenoma. The patient's right visual acuity improved rapidly. On the occasion of cerebral angiography, we could observe that subclinical pituitary apoplexy deteriorated to subacute pituitary apoplexy. Rosenbaum postulated that injection of contrast media increased intravascular pressure leading to pituitary apoplexy. At present, we cannot postulate increased intravascular pressure with 5F catheter and DSA. We cannot rule out that, with underlying subclinical pituitary apoplexy, hemorrhagic infarction due to contrast media and the anti-coagulate effect of heparin sodium accelerated the intratumoral bleeding. Subclinical pituitary apoplexy is a vulnerable state because of its aggravation to symptomatic apoplexy under mild stress. We emphasize that an operation should be performed as early as possible in the case of subclinical pituitary apoplexy.
报告了一例垂体腺瘤病例,该病例在脑血管造影时从亚临床垂体卒中进展为亚急性垂体卒中。一名29岁男性,因双颞侧偏盲入院。头颅X线平片显示蝶鞍增大及蝶鞍底双重影。未发现异常钙化。CT显示鞍上区有一4×4cm大小的等密度肿块,呈环形强化。肿块从鞍内延伸至鞍上区,在T1加权像上呈高信号。内分泌检查显示高催乳素血症,血清水平为422ng/ml,垂体前叶激素反应正常。3月3日,在镇静状态下对患者进行了5F导管数字减影血管造影。造影剂为碘克沙酸(Hexabrix 320)。颈内动脉造影注入6ml,速度为每秒4ml。共使用60ml。每毫升含10单位肝素钠的生理盐水也用于冲洗。血管造影期间,患者血压为125/60 - 115/60mmHg。DSA显示大脑前动脉近端向上移位、袋状形成及肿瘤包膜染色。6小时后,患者诉眶后头痛。次日早晨,他发现左眼完全失明。3月7日,右眼视力恶化为失明。CT显示肿块密度增加。通过双额骨成形开颅术,切除了伴有明显瘤内出血的肿瘤。其组织学为嫌色性腺瘤。患者右眼视力迅速改善。在脑血管造影时,我们观察到亚临床垂体卒中恶化为亚急性垂体卒中。罗森鲍姆推测造影剂注射会增加血管内压力导致垂体卒中。目前,我们不能用5F导管和DSA推测血管内压力增加。我们不能排除在潜在的亚临床垂体卒中情况下,造影剂导致的出血性梗死以及肝素钠的抗凝作用加速了瘤内出血。亚临床垂体卒中因其在轻度应激下易加重为有症状的卒中而处于脆弱状态。我们强调,对于亚临床垂体卒中病例应尽早进行手术。