兔眼球爆裂伤合并无菌海水浸泡后角膜超微结构改变

目的 观察实验兔眼眼球爆裂伤后暴露于海水所引起的角膜超微结构改变,探讨爆裂伤合并海水浸泡眼球的抢救最佳时间.方法 24只健康成年新西兰白兔,用鞭炮爆炸方法造成眼球爆裂伤,各兔右眼浸泡于无菌海水中,左眼暴露空气中作对照,经10 min、0.5h、1h、2h、4h、8h后取出裂伤伤口处角膜,每时间组4只眼球用透射电子显微镜观察其超微形态学变化,以判断角膜各层组织的活性.结果 海水浸泡0.5h,角膜上皮细胞发生脱水、坏死、脱落,角膜内皮细胞脱落;海水浸泡1h,角膜基质细胞出现胞质内空泡、细胞脱水、皱缩,角膜后弹力层脱失;而空气对照组在伤后2～4h、甚至更长时间发生上述超微结构改变.结论 兔眼眼球爆裂伤后暴露于海水中的角膜组织超微结构损伤较单纯暴露于空气中者发生早且组织损伤亦重,海水浸泡1h后角膜的病理改变即为不可逆转.发生海战时,对海水浸泡眼球裂伤,最好在0.5h之内进行角膜裂伤的清创缝合,超过1h,则意义不大.     

眼外伤异常电生理临床分析（附100例报告）

具有异常电生理改变的100例单眼外伤中,14眼仅VEP PT延长,显示黄斑、黄斑旁或视神经的钝伤,由FFA及视野加以证实.10眼VEP PT延长,PA下降或消失者显示黄班或视神经挫伤严重,可合并颅脑伤,视力严重下降或无光感.38例同时伴有FERGb波下降,显示损伤广泛而严重,可有眼球破裂、视网膜玻璃体及前房的出血,晶体混浊等.10眼VEP ERG波形全消失,则为眼球严重挫伤及伤后感染、眼球萎缩.28眼仅有FERGb波异常,则显示损伤不在中心区.     

兔眼球爆炸伤后视网膜节细胞凋亡及其与谷氨酸的关系

目的：了解兔眼球爆炸伤后视网膜节细胞的病理改变及其与玻璃体谷氨酸浓度变化的关系。方法：对10只成年灰兔用同一种爆炸物、用电子传感器进行检测制作近乎相同的实验眼眼球爆炸伤模型，于伤后不同时限点按序处死，分别取实验眼和对照眼进行视网膜DNA片段末端标记(TUNEL)光镜观察，并分别取实验眼和对照眼的玻璃体测定其谷氨酸含量，对实验资料进行统计学分析。前瞻性、自身对照、实验研究。结果：眼球爆炸伤后20～40天视网膜DNA片段末端标记(TUNEL)光镜观察发现实验眼视网膜节细胞呈不同程度阳性着色。提示眼球爆炸伤后视网膜存在节细胞凋亡；同时眼球爆炸伤后实验眼玻璃体内谷氨酸含量明显增加，与对照眼间存在显著差异。结论：我们推测眼球爆炸伤后出现显著的非屈光性视力障碍可能与视网膜节细胞凋亡有关。而伤后玻璃体谷氨酸浓度增加可能是诱发细胞凋亡的因素之一。     

高原环境下兔眼球挫伤后视网膜脑红蛋白的表达调控研究

目的研究高原环境下兔眼球挫伤后视网膜脑红蛋白（NGB）的表达水平调控,探讨高原环境下眼球挫伤的损伤修复机制及救治。方法在高原环境用重击法造成2月龄健康北京青紫蓝兔眼球挫伤,随机分为吸氧组和非吸氧组,吸氧组动物模型在自制氧箱中以35％氧浓度每天持续给氧10h,于伤后12h、1d．3d,7d、14d分别摘取眼球,40g/L多聚甲醛固定．石蜡包埋切片,免疫组化检测NGB,比较吸氧组和非吸氧组NGB表达水平的不同。结果高原环境下兔眼球钝挫伤后吸氧组较非吸氧组NGB表达低,在3d和7d时差异有统计学意义（P〈0．05）。结论高原环境下兔眼球挫伤后通过吸氧可调控视网膜NGB的表达水平,伤后1d内视网膜处于应激期,吸氧等措施可减轻应激损伤,1～14d吸氧可大大促进视网膜损伤修复。     

爆炸伤眼科救治中的教训

某次房屋中爆炸,伤31人,亡5人。受伤人中眼伤28人(43眼),占伤亡总人数77%,占受伤人数90%。伤眼中其附属器均有不同程度的损伤。角、巩膜穿通伤19眼(10人),为伤眼的44%;眼球挫伤、视网膜震荡等24眼(15人),为眼伤的56%。由于非专业眼科人员,不熟悉眼科基本知识,     

兔眼钝挫伤后视网膜 Müller细胞GFAP表达的变化

目的:探讨眼球钝挫伤后视网膜Müller细胞表达GFAP的变化规律。方法:20只兔子40眼随机分为正常对照组、挫伤组,以 3J 能量自由落体的方式制作兔眼挫伤性视网膜病变模型,于不同时段将动物麻醉致死,摘除眼球,制成病理切片用于GFAP免疫组织化学染色。图像分析系统测量视网膜GFAP表达阳性率与灰度值,并应用SPSS 12.0软件包进行统计学分析。结果:挫伤组和正常对照组视网膜内界膜下可见少许棕色阳性GFAP着色。挫伤组伤后1d,GFAP的阳性表达开始加强,随伤后时间的推移,GFAP的免疫染色已从内界膜向神经纤维层、节细胞层、内丛状层、外核层,直至神经上皮层下发展,并呈现着色加深的强阳性表达。GFAP表达的平均灰度值的统计学分析结果也显示:挫伤组和正常对照组存在统计学差异（P＜0.05）。结论:眼球钝挫伤后视网膜Müller细胞GFAP的表达持续增强,早期Müller细胞反应性胶质化对视网膜损伤有修复作用。     

眼挫伤的血—房水屏障改变

目的 探讨外伤性葡萄膜炎与血－房水屏障破坏的关系。方法 新西兰兔１８只，以自由落体打击力制备双眼重型闭合性眼球挫伤模型；以＾１３１Ｉ为示踪剂进行房水免疫学测定。并与正常兔眼作对照。结论 兔眼钝伤后可致较严重的血－房水屏障破坏。伤后１周为快速修复期，４周时完全修复。     

眼球钝挫伤ERG与病理改变的关系

检查轻，重度兔眼挫伤后ＥＲＧａ，ｂ波及ＯＰｓ波的改变，用镧示踪法观察血视外屏障及其它组织结构改变。轻型挫伤ＥＲＧｂ波暂时降低，无示踪剂渗漏，光感受器外节轻度破坏。重型挫伤ＥＲＧａ，ｂ波及ＯＰｓ波明显降低，视风膜色素上皮细胞及外层视网膜细胞严得损害，伴有血视网膜外屏障破坏。结果提示眼球挫伤后视力的预后和组织损伤的程度有直接关系。     

眼挫伤实验模型及其影响因素评估

目的探讨眼挫伤动物模型的实用性。方法分别用铜球自由落体、高压水柱或气柱致伤兔眼,观察91只兔眼致伤情况及病理改变。结果只要达到一定致伤强度,不同性状致伤物均可使兔眼产生类似损伤,其致伤程度主要与致伤物质量（m）、致伤时即时速度（Vt）以及致伤物和眼球接触面积有关。致伤物质量越大、致伤时即时速度越快、接触面积越小,则致伤程度越严重,且易向眼后段延伸。在几种实验条件下,固态致伤物致伤以自由落体致伤方式较好,其所涉变量少,可控范围大,重复性好,易于操作和定量计算。在一定范围内液态或气态致伤物对眼前段影响大,而固态致伤物则对眼后段影响更明显。结论对眼后段致伤情况评估以自由落体模型为优,对眼前段致伤观察则可选择液态或气态致伤物。     

眼挫伤后房角后退青光眼的临床分析

眼球挫伤的发病率占眼外伤的34％，甚者可造成眼球的复合伤致解剖结构变形而引发各种并发症，而前房角结构的改变和前房角后退是眼球挫伤的严重并发症。临床上对外伤后继发性青光眼病因分析往往倾向于房角后退的结构改变。本文回顾1990～2003年我院治疗的眼球钝挫伤房角后退患者153眼的临床资料，探讨眼球挫伤后继发高眼压的原因。     

挫伤性脉络膜破裂的眼底荧光血管造影探讨

目的　探讨眼钝挫伤后脉络膜破裂视力损害的原因。方法　通过眼底荧光血管造影观察伤后眼底改变。结果　18 例眼球钝挫伤后脉络膜破裂中,16 例黄斑部直接损害,同时10 例有脉络膜视网膜充盈倒置,14 例有黄斑拱环模糊。结论　FFA 有助于鉴别不同层次的脉络膜损伤。伤后黄斑部直接损伤是视力损害的主要原因,脉络膜视网膜充盈倒置、黄斑拱环模糊,证明伤后视盘血供及黄斑血液循环障碍,是视力损害的重要因素     

5. Traumatic Intrastromal Corneal Cyst

This case report describes the clinical and pathological characteristics of an intrastromal epithelial corneal cyst. This lesion tends to occur after relatively minor trauma, in younger patients, and is a slowly progressive disorder that develops over many years. The eye shows no signs of inflammation. The cyst typically appears opalescent but may be characterized by a fluid level. Pathologically, the cyst cavity is lined by cells with features similar to those of limbal corneal epithelium. Treatment consists of removal or destruction of the epithelial cells lining the cavity.     

Characteristics of the blood filling of the eye in the early stages following alkali burns

In experiments on 60 rabbits a correlative connection between the intensity and character of changes in hemodynamics, the level of intraocular pressure and severity of eye lesion has been established as well as the direct dependence between expressiveness and duration of reduction in blood circulation on severity of burn lesion. Burn disease of a mild and moderate degree was accompanied by expressed, but transitory reduction in the blood supply of the vascular tract within first hours after trauma. Signs of restoration of blood circulation intensity appeared already 24 hours after burn. In severe and extremely severe burns, hemodynamic disturbances were more expressed and longer. Inverse connection is established between changes in intraocular pressure and hemodynamics in the vascular tract of the eye in its burn trauma.     

角膜外伤后眼前段组织的临床病理变化

目的 观察角膜外伤后眼前段组织的组织病理学改变。方法 对因角膜外伤后摘除眼球标本117例进行光镜观察,其中因眼挫伤致角膜裂伤18例,角膜穿孔伤99例。结果 角膜伤口闭合好者眼前段组织呈急性、亚急性和慢性炎症改变,虹膜粘连和纤维膜形成;晚期因继发性青光眼、视网膜脱离、眼内炎和眼球萎缩致视功能丧失。角膜伤口闭合不良者易形成角膜瘘,常见原因为角膜上皮细胞内卷,虹膜和玻璃体嵌顿,角膜伤口处组织缺损较大且位于角膜中央。眼内炎发生率极高,眼前段组织炎症反应剧烈,较短时间内由于眼内毒素作用致眼球毁灭。结论 角膜外伤后依伤口的位置、形状、大小和闭合情况不同致眼前段组织的病理表现不同。     

外伤性低眼压视网膜结构的改变

目的：观察外伤性低眼压后视网膜结构变化，探讨可能的损伤机制。方法：制作外伤性前部PVR导致低眼压的兔眼模型，伤后分别于2周、4周、8周、16周测量眼压后取眼球，视网膜做普通病理切片，HE染色观察，16周的视网膜部分做电镜观察。结果：伤后2周、4周、8周光学显微镜下，实验组视网膜显微结构没有明显的变化；伤后16周，光学显微镜下，实验组视网膜变薄，外核层、内核层以及节细胞细胞数减少；伤后16周扫描电镜下见光感受器外节排列紊乱。肿胀。结论：长期低眼压视网膜结构会出现严重的损害，可能与低眼压造成视网膜血液循环淤滞有关。     

A case of corneal keloid: clinical, surgical, pathological, and ultrastructural characteristics.

A 69-year-old patient developed a localised, whitish, elevated, corneal lesion with a smooth and glistening surface following trauma, without evidence of corneal perforation. Twelve months later, the lesion showed evidence of slow growth. An excisional biopsy was then performed. Histopathologically, the lesion was covered by non-keratinised squamous epithelium and was comprised of randomly oriented collagen fibres containing active fibroblasts. Blood vessels were noted deep in the lesion. Ultrastructurally, the cell population was formed by fibroblasts and myofibroblasts, similar to keloids of the skin. The clinical, pathological, and ultrastructural features of the corneal lesion are compatible with a corneal keloid.     

Axonal Injury in the Lateral Geniculate Body: Radiological Diagnosis

Damage to the lateral geniculate body by diffuse axonal injury in brain trauma is uncommon. The authors present the clinical case and in vivo fibre tractography using diffusion tensor magnetic resonance imaging of this lesion in a patient presenting with homonymous sectoranopia after a traumatic head injury.     

Principles of intraocular ossification exemplified by secondary choroid ossification

Intraocular ossification seems to follow general pathogenic principles. Ossification requires besides local changes in carbon dioxide tension and local increase of phosphate ions first a rich vascular supply--therefore the peripapillary region is always involved, alone or in conjunction with other sites--and second probably a direct or indirect influence of the Retinal Pigment Epithelium (RPE). The growth of the bone occurs slowly and leads to a relative uniform morphology. Osteogenesis is triggered by chronic intraocular changes (of the RPE), and ossification is almost always combined with a longstanding retinal detachment. The primary lesion (e.g. trauma, inflammation or tumor) plays a minor or no role. Differences between secondary intraocular bone formation (following a well known lesion) and primary choroidal osteomas could be explained by a different strength of the osteogenic (RPE-)stimulus. In the light of our investigations (29 phthitic or chronically hypotonic eyes, 12 of them with intraocular bone formation) and the literature primary osteomas of the choroid have to be interpreted more likely as secondary processes, possibly following a (birth-)trauma, than as congenital choristomas.     

Replacement of the liquid vitreus with sodium hyaluronate in monkeys: II. Long-term evaluation

Highly purified, large molecular weight fractions of Na-hyaluronate (Healon) dissolved in physiological buffer solution in 1% concentration form viscous pastes. When 1 ml of this paste was implanted into the vitreous space of 82 owl monkey (Aotus trivirgatus) eyes, no pathological changes could be observed months or years (up to 9 years) after implantation. Implantations were made as many as seven times into the same eye without observable pathological changes in the eye. Subcortical lenticular opacities occurred in 4% of all implantations and pigmented chorioretinal lesions occurred in 8% of all implantations. The chorioretinal lesions developed in some cases after injection of balanced salt solution (BSS). This pathology was studied with electronmicroscopy. No correlation could be found between the Na-hyaluronate implantation and the development of these lesions. This pathology is believed to be caused by the surgical trauma during the exchange of half of the total volume of the liquid vitreus with balanced salt solution. During this process a mechanical dislocation between the retinal pigment epithelium and the neuroretina can occur which triggers pigment cell proliferation and subsequent pathological changes. No evidence was found of any immunogenic reaction caused by the implantation of Na-hyaluronate. The increase in vitreous protein resulting from implantation of Na-HA was three times that found after implantation of either BSS or Healon. Neither Healon nor Na-HA caused significant changes in IOP.