外伤性“TERSON综合征+”:气性脑膨出伴视神经萎缩

S. Chowdhury, M. Srivastava, N. Chowdhury
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摘要

介绍。Terson综合征是一种蛛网膜下腔出血(SAH)伴视网膜下腔出血。这种新病例的视力下降是由于出血本身,长期阻塞黄斑/其他光感受器,导致严重的视力丧失。SAH引起神经系统问题,这可能成为玻璃体出血的危险因素。高血压是导致Terson综合征的最常见原因,但创伤也是毁灭性的原因,因为它可能导致不可逆转的视觉后果,如完全失去对光的感知或失明。的目标。我们在此报告一例Terson综合征合并疾病特征的额叶SAH。案件描述。当有外伤性气脑膨出时,使血液有空间向骨视神经管吸收,在神经鞘周围形成血肿,造成神经鞘周围的压迫,导致视神经萎缩。在道路交通事故(RTA)中,直接创伤性剥离可以损伤视神经,但即使没有这种损伤,血液也可能在视神经周围积聚,从而导致血肿的形成,随后压力引起视神经萎缩。此外,血液可以缓慢地流动到玻璃体下空间/视网膜下空间(在内限制膜或ILM下),如本例所示,可能有胶质细胞增生覆盖典型的船型血液。通过在眶底(OFTA)近顶点处注射三次曲安奈德,可解决视膜下出血或神经胶质瘤,但视神经萎缩夺取视力。该方案被用于治疗外伤性压迫性(视神经周围血肿)视神经病变和外伤性视网膜病变伴玻璃体下出血。结论。Terson综合征合并疾病的诊断是通过处理计算机断层扫描(CT)和磁共振成像(MRI)的所有特征来建立的。此外,还表现为脑气、视神经鞘血肿、视神经萎缩和玻璃体下胶质增生出血,典型的船型。光学相干地形图显示出血部分仍存在,但因视神经萎缩而丧失视力。OCT显示玻璃体下腔有血块。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Traumatic “TERSON SYNDROME PLUS”: Pneumocephalocele with optic atrophy
Introduction. Terson Syndrome is subarachnoid hemorrhage (SAH) with sub retinal hemorrhage flowing through channel. Reduced vision in such fresh case is due to hemorrhage itself, blocking macula/other photo receptors in the long run macular cellophane retinopathy which causes profound visual loss. SAH causes neurological problems which can become a risk factor for evacuating blood from vitreous. Hypertension is commonest cause to cause Terson Syndrome, but trauma is also devastating cause as it can lead to irreversible visual consequences like total loss of perception of light or blindness. Aim. Here we describe a case of Terson Syndrome plus disease features SAH in frontal lobe. Description of the case. When there is traumatic pneumocephalocele, it gives space to blood to imbibe towards bony optic canal and form hematoma around nerve sheath which causes compression around the same and leads to optic atrophy. Optic nerve can be injured by direct traumatic dissection during road traffic accidents (RTA), but even without that blood may accumulate around optic nerve and in turn leads to formation of hematoma and subsequently pressure induced optic atrophy. Moreover, blood can slowly travel to sub hyaloid space/sub retinal space (beneath internal limiting membrane or sub ILM) with probable gliosis covering typical boat shaped blood as seen in this case. This sub ILM hemorrhage or gliosis may have resolved through three injections of Triamcinolone in the orbital floor (OFTA) near apex, but optic atrophy snatches vision. This protocol was followed to treat traumatic compressive (peri optic hematoma) optic neuropathy and traumatic retinopathy associated with sub hyaloid hemorrhage. Conclusion. Diagnosis of Terson syndrome plus disease was established by addressing all features on computed tomography (CT) scan and magnetic resonance imaging (MRI). Plus, features include pneumocephalus, optic nerve sheath hematoma, optic atrophy and gliosis over sub-hyaloid hemorrhage, typical boat shaped. The part of hemorrhage still endured as seen on optical coherence topography, but vision was lost by virtue of optic atrophy. OCT shows clot in sub hyaloid space.
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