什么是光?光是一种电磁波。什么是电磁波?电磁波是能量的一种,凡是高于绝对零度的物体,都会释放电磁波。什么是绝对零度?绝对零度(absolute zero)是热力学的最低温度,是粒子动能低到量子力学最低点时物质的温度。绝对零度是仅存于理论的下限值,其热力学温标写成K,等于摄氏温标零下273.15度(-273.15℃)。绝对零度只存在于理论中,无法真正达到。也就是说,在我们的世界中,所有的物体都会发射电磁波。但是我们并不能感知(看到)所有的电磁波。电磁波具有波粒二象性。电磁波的电场(或磁场)随时间变化,具有周期性。在一个振荡周期中传播的距离叫波长。按照波长将电磁波进行分类,对应我们平时接触的各种光的概念。图中”Visible“那部分就是我们所能看到的电磁波,也就是通常意义上的光。 可以看出,人眼能感知的电磁波范围很小(380nm-740nm)。超出人眼感知范围的光,叫做不可见光。也可以换一种说法叫”不可见电磁波“。这些电磁波虽然不可见,但是依然可以被我们获取和利用,例如收音机。总结一句:光是人眼能感知的(波长380nm-740nm)电磁波。我们如何看到颜色?为什么人类(准确来说是人眼)只能感知那么小范围的电磁波?这主要受光感受器的影响。所谓光感受器也就是电磁波的接收装置。电磁波无处不在,但是只有被人眼捕捉到,我们才能感知到。换句话说:我们看到电磁波,需要一个捕捉装置和一个接收装置。人眼的电磁波捕捉装置包括角膜、瞳孔、晶状体和视网膜。最后负责接收的是光感受器,具体来说是视杆细胞和视锥细胞(Rods and cones)。人眼视杆细胞和视锥细胞的数量、分布和功能不同。一只眼睛大约有1亿2千万个视杆细胞,主要分布在黄斑以外的广泛视网膜,负责感知光的明暗。人眼视锥细胞数量约是视感细胞的1/20(约6百万),集中在黄斑区域,负责感知色彩。人类有三种视锥细胞,分别感知红色、绿色、蓝色。(这也是三原色的由来)。 三种视锥细胞的数量不同。感知红色的视锥细胞数量最多,绿色居中,蓝色最少。日常生活中,我们使用红色来起警示作用,正是因为红色更容易被感知。将颜色分为暖色调(红色为主)和冷色调(蓝色为主),也是基于此。红、率、蓝三原色的按照不同比例组合,就构成了我们所能看到的所有色彩。如果视锥细胞的种类或者数量减少,那么就会产生不同类型的色盲或者色弱。能看到颜色的不止人类。狗狗也能看到颜色,但是狗狗的视锥细胞只有两种,只能感知绿色和蓝色。(“人不如狗”的强力反击)猫也有三种视锥细胞,但是数量远不及人类。因此猫对颜色的敏感程度不如人类。蝴蝶有四种视锥细胞,能看到紫外光。目前已知视锥细胞种类最多的是螳螂虾(Mantis shrimp)。螳螂虾是皮皮虾的远方亲戚。螳螂虾拥有12种视锥细胞。它看到的世界应该更加绚丽多彩吧?
双行睫患者青年男性,自幼双眼反复异物感,曾行拔倒睫治疗。查体如图。双眼下睑内侧1/2见异常睫毛生长。异常睫毛排列整齐,较纤细、柔软,均从睑板腺开口长出,刷刮角膜、球结膜。部分睑板腺见两根睫毛生长。患者的姐姐、妹妹、儿子均有类似体征。诊断:先天性双行睫双行睫(Distichiasis, Double eyelashes),是一种相对罕见的遗传性疾病,呈现家族聚集性。常见的基因突变位于16号染色体的FOXC2基因。男女患病率无明显差异。异常睫毛可同时累积双眼上下眼睑,也可只发生在上睑或下睑(本例患者)。异常睫毛虽然自睑板腺长出,但是一般不影响睑板腺的正常功能。临床表现因异常睫毛的数量和位置而不同。多表现为反复异物感、眼红、眼痒。由于FOXC2基因主要影响胚胎时期淋巴和血管的形成,部分患者会合并淋巴循环障碍和心血管方面的疾病。以双行睫合并下肢水肿较为多见。此病称为Lymphedema-distichiasis syndrome (LDS)(具体可参考我转载的一篇文章)。因此鉴别诊断方面,要注意询问和检查患者是否有下肢和心脏方面的表现。淋巴循环障碍和心血管方面的疾病可能在患者年级大时才表现出来,需要告知患者并注意随访。治疗方法主要是破坏异常的毛囊。可以采用电解、冷冻和切开直视下破坏毛囊。电解和冷冻虽然创伤较小,但是效果不确切,现已多不采用。本例患者采用的方法是:沿灰线切开,分离睑板和皮肤,直视下破坏毛囊。术后第一天效果见下图。双行睫的发病例目前未见报道。笔者在pubmed查询时,看到的相关文章更多是动物方面的,尤其是狗狗。双行睫在狗狗算是一个比较多见的疾病,尤其是以下三个犬种。狗狗的双行睫多采用电解治疗。有相关方面疾病,欢迎咨询和就诊。
学会了以下操作,您就可以在离开医院后仍然保持和我的联系。如果您有对病情仍然不明白的地方,或是任何关于本次就诊疾病相关的问题都可以随时通过这个方式联系上我。 第一步:进入“网上诊室”公众号,如下图。 (如果找不到,在微信上方放大镜图标搜索“网上诊室”即可) 第二步:点击页面下方“咨询医生”,如下图。 第三步:选择您想要得到的帮助,如下图
NORD gratefully acknowledges David A. Stevenson, MD, Professor, Stanford University, and Amy Calhoun, MD, Assistant Professor, University of Iowa, for assistance in the preparation of this report.Synonyms of Lymphedema-Distichiasis Syndromelymphedema with distichiasisGeneral DiscussionLymphedema-distichiasis syndrome is a rare genetic multisystem disorder characterized by swelling of the legs because of fluid accumulation and the development of extra eyelashes (distichiasis). Distichiasis may range from a few extra lashes to a full set of extra eyelashes. Swelling most often affects both legs (bilateral) and usually occurs around puberty. Additional anomalies sometimes associated with this disorder include early onset varicose veins, droopy eyelids (ptosis), heart defects, cleft palate, abnormal heart rhythm, and abnormal curvature of the spine (scoliosis). Lymphedema-distichiasis syndrome is caused by mutations of theFOXC2gene and is inherited in an autosomal dominant pattern.Signs & SymptomsThe symptoms of lymphedema-distichiasis vary greatly from case to case even among members of the same family. The most common finding is the extra row of eyelashes (distichiasis). Most patients also develop swelling (edema) or puffiness of the legs because of the accumulation of protein-rich fluid (lymph) in the soft layers of tissue under the skin.The severity of lymphedema (swelling due to the accumulation of lymph fluid) varies, but usually involves only the legs. In most cases, both legs are affected (bilateral). In some cases, swelling may cause tightness, discomfort and unusual tingling sensations (paresthesias) in the affected areas. Typically, lymphedema develops around puberty, although it can develop as early as before the person is born or in adulthood.Males develop lymphedema at an earlier age than females and are more likely to develop cellulitis. Cellulitis is a bacterial infection that is often associated with lymphedema. Cellulitis is characterized by swollen, reddened skin that may feel warm and tender.Distichiasis may range from a few extra lashes to a full set of extra eyelashes. This can be very hard to see and is often missed by routine examination. Associated eye abnormalities may occur including an abnormal sensitivity to light (photophobia), inflammation of the delicate membrane that lines the inside of the eyelids (conjunctivitis), irritation of the curved transparent outer layer of fibrous tissue covering the eyeball (cornea), and the development of a small tender bump on the eyelid (stye). Drooping or sagging of the eyelids (ptosis) may also occur.Many individuals with lymphedema-distichiasis syndrome develop varicose veins, a condition marked by twisted, widened and enlarged veins just below the surface of the skin. In some cases, varicose veins may precede the development of lymphedema. In individuals with lymphedema-distichiasis, varicose veins develop at a much younger age and with greater frequency than in the general population.Congenital heart disease has been reported in some individuals with lymphedema-distichiasis syndrome, especially a condition known as tetralogy of Fallot. Tetralogy of Fallot consists of a combination of four different heart defects: a ventricular septal defect; obstructed outflow of blood from the right ventricle to the lungs (pulmonary stenosis); a displaced aorta, which causes blood to flow into the aorta from both the right and left ventricles; and the abnormal enlargement of the right ventricle. This combination of abnormalities typically leads to poor blood flow to the lungs and poor blood oxygenation. The symptoms tend to worsen with time if this remains untreated and can be life-threatening.In some patients, irregular heartbeats (arrhythmias) may develop.Rarely, additional abnormalities have been reported to occur in association with lymphedema-distichiasis syndrome including crossed eyes (strabismus), incomplete closure of the roof of the mouth (cleft palate), side-to-side curvature of the spine (scoliosis), webbing of the neck, and cysts on the outermost layer of the membranes (meninges) that cover the spinal cord (spinal extradural cysts). Very rarely, patients may have total body swelling prior to birth (hydrops fetalis). Also very rarely, patients may have breathing problems due to abnormal lymph flow in their lungs.CausesLymphedema-distichiasis syndrome occurs due to changers or disruptions (mutations) in the forkhead family transcription factor (FOXC2) gene. It is currently unknown exactly how mutations in this gene lead to the symptoms of lymphedema-distichiasis syndrome.Lymphedema is caused by the accumulation of protein-rich fluid (lymph) in areas of the body, typically due to dysfunction or abnormality of the lymphatic system. The lymphatic system is a circulatory network of vessels, ducts, and nodes that filter and distribute lymph and blood cells throughout the body. In lymphedema-distichiasis syndrome it is possible that the lymphedema develops due to obstruction, malformation, underdevelopment (hypoplasia), or improper function of various lymphatic vessels. One group of researchers, Mellor et al., showed that the venous valves failed in both the superficial and deep veins in the lower limbs of individuals withFOXC2mutations suggesting that theFOXC2gene is important for the normal development and maintenance of venous and lymphatic valves. Their group also showed that lymph vessel function in people with lymphedema distichiasis syndrome was negatively affected by gravity, possibly explaining why the legs are primarily affected when the mutation is present in every cell in the body.Lymphedema-distichiasis syndrome is an autosomal dominant genetic disorder. Dominant genetic disorders occur when only a single copy of an abnormal gene is necessary to cause a particular disease. The abnormal gene can be inherited from either parent or can be the result of a mutated gene in the affected individual. The risk of passing the abnormal gene from an affected parent to an offspring is 50% for each pregnancy. The risk is the same for males and females.Affected PopulationsLymphedema-distichiasis affects males and females in equal numbers. Lymphedema develops in males at an earlier age than females. The prevalence of this disorder in the general population is unknown. Lymphedema-distichiasis syndrome may go undiagnosed making it difficult to determine its true frequency in the general population.Related DisordersSymptoms of the following disorders can be similar to those of lymphedema-distichiasis. Comparisons may be useful for a differential diagnosis.The hereditary lymphedemas are the disorders most commonly confused with lymphedema-distichiasis syndrome. The disorder which is most similar is hereditary lymphedema type II or Meige syndrome. Persons with Meige syndrome have pubertal onset of lymphedema (swelling due to accumulation of tissue fluid) this is not typically associated with other symptoms or malformations. This disorder is autosomal dominant, but the gene is not known.Hereditary lymphedema type IA, also known as Milroy disease, typically presents much earlier than lymphedema-distichiasis or Meige. Most patients have lower limb lymphedema at birth or in the first year of life. This disorder is also autosomal dominant and is caused by mutations in theFLT4orVEGFR3gene.Hypotrichosis-lymphedema-telangiectasia syndrome is another disorder associated with lower limb lymphedema. The lymphedema typically occurs in childhood. This is associated with loss of hair and telangiectasias which are most commonly seen on the palms of the hands. It is caused by mutations inSOX18and can be either autosomal dominant or autosomal recessive.Yellow nail syndrome typically presents much later in life than lymphedema-distichiasis, Milroy, Meige, or hypotrichosis-lymphedema-telangiectasia. It is a rare disorder characterized by yellow, thickened, and curved nails with almost complete stoppage of nail growth. Loss of the strip of hardened skin at the base and sides of a fingernail (cuticles) may also occur. Separation of the nails from the nail bed (onycholysis) may cause the nails to fall out. Yellow nail syndrome is usually associated with the presence of fluid in the lungs (plural effusion) and swelling of the arms and legs (lymphedema). Other respiratory problems may occur such as chronic inflammation of the bronchi and bronchioles (bronchiectasis), chronic bronchitis, and/or ongoing inflammation of the membranes that line the sinus cavities (sinusitis). Lymphedema usually occurs around puberty. The genetic etiology of yellow nail syndrome is unknown although it has been associated in some patients with mutations to theFOXC2gene and is inherited in an autosomal dominant pattern. (For more information on this disorder, choose “Yellow Nail” as your search term in the Rare Disease Database.)None of the above disorders have distichiasis.DiagnosisA diagnosis of lymphedema-distichiasis syndrome is primarily made based upon a thorough clinical evaluation, a detailed patient history, and the identification of characteristic findings (i.e., primary lymphedema, distichiasis).FOXC2molecular testing is available clinically to help confirm a diagnosis. A variety of specialized tests may be performed to determine the extent of the disorder. Such tests include lymphoscintigraphy or an echocardiogram. During lymphoscintigraphy, a substance known as a contrast medium is injected into a lymphatic vessel (usually in a hand or foot). A series of x-rays are taken that show the medium as it moves through the lymphatic vessels giving physicians a picture of the health and structure of the lymphatic vessels. During an echocardiogram, reflected sounds waves are used to create an image of the heart, which can reveal congenital heart defects potentially associated with lymphedema-distichiasis syndrome.Standard TherapiesTreatmentThe treatment of lymphedema-distichiasis syndrome is directed toward the specific symptoms that are apparent in each individual. Treatment is aimed at reducing swelling and preventing infection. Complete decongestive therapy (CDT) is a form of treatment in which specialized massage techniques are coupled with therapeutic bandaging, meticulous skin care, exercise, and the use of well-fitted compression garments such as fitted stockings. Antibiotics may be used to treat recurrent infections such as cellulitis or as a preventive (prophylactic) measure in individuals with recurrent infections.Distichiasis may be managed with lubrication or plucking (epilation). More definitive treatments for distichiasis include cryotherapy, electrolysis, or lid splitting. Cryotherapy is the application of extreme cold to destroy diseased tissue. Electrolysis uses a short-wave radio frequency to destroy the extra eyelashes. Lip splitting is a surgical procedure in which the eyelid is split open to expose the root (follicle) of the eyelashes. Each extra eyelash is then removed (excised). In some cases, cryotherapy or electrolysis is used in conjunction with lid splitting.In some patients, surgery may be performed to treat other abnormalities such as ptosis or cleft palate. Individuals with heart abnormalities may be monitored regularly.Genetic counseling is recommended for affected individuals and their families. Other treatment is symptomatic and supportive.ReferencesJOURNAL ARTICLESde Bruyn G, Casaer A, Devolder K, et al. Hydrops fetalis and pulmonary lymphangiectasia due to FOXC2 mutation: an autosomal dominant hereditary lymphedema syndrome with variable expression. Eur J Pediatr. 2012;171(3):447-50.Mellor RH, Tate N, Stanton AWB, Hubert C, Maekinen T, Smith A, Burnand K, Jeffery S, Levick JR, Mortimer PS; Mutations in FOXC2 in humans (lymphedema distichiasis syndrome) cause lymphatic dysfunction on dependency. J Vasc Res. 2011; 44:381-4.Shimoda H, Bernas MJ, Witte MH. Dysmorphogenesis of lymph nodes in foxc2 haploinsufficient mice. Histochem Cell Biol. 2011;135(6):603-13.Sanches-Carpintero R, Dominguez P, Nunez MT, Patino-Garcia A, Spinal extradural arachnoid cysts in lymphedema-distichiasis syndrome. Genet Med. 2010; 12: 532-5.Connell F, Brice G, Jeffery S, Keely V, Mortimper P, Mansur S. A new classification system for primary lymphatic dysplasias based on phenotype. Clin Genet. 2010; 77:438-452.Connell F, Brice G, Mortimer P. Phenotypic characterization of primary lymphedema. Ann NY Acad Sci. 2008;1131:140-6.Mellor RH, Brice G, Stanton AW, French J, Smith A, Jeffery S, Levick JR, Burnand KG, Mortimer PS; Lymphoedema Research Consortium. Mutations in FOXC2 are strongly associated with primary valve failure in veins of the lower limb. Circulation. 2007;115:1912-20.Berry FB, Tamimi Y, Carle MV, Lehmann OJ, Walter MA. The establishment of a predictive mutational model of the forkhead domain through the analyses of FOXC2 missense mutations identified in patients with hereditary lymphedema with distichiasis. Hum Mol Genet. 2005;14:2619-27.Kriederman BM, Myloyde TL, Witte MH, et al., FOXC2 haploinsufficient mice are a model for human autosomal dominant lymphedema-distichiasis syndrome. Hum Mol Genet. 2003;12:1179-85.Brice GW, Mansour S, Bell R, et al., Analysis of phenotypic abnormalities in lymphoedema-distichiasis syndrome in 74 patients with FOXC2 mutations or linkage to 16q24. J Med Genet. 2002;39:478-83.Erickson RP, Dagenais SL, Caulder MS, et al., Clinical heterogeneity in lymphoedema-distichiasis syndrome with FOXC2 truncating mutations. J Med Genet. 2001;38:761-6.Fang J, Dagenais SL, Erickson RP, et al., Mutations in FOXC2 (MFH-1), a forkhead family transcription factor, are responsible for the hereditary lymphedema-distichiasis syndrome. Am J Med Genet. 2000;67:1382-8.Mangion J, Rahman N, Mansour S, et al., A gene for lymphedema-distichiasis maps to 16q24.3. Am J Hum Genet. 1999;65:427-32.INTERNETBrice GW, Mansour S, Ostergaard P, et al. Milroy Disease. 2006 Apr 27 [Updated 2014 Sep 25]. In: Adam MP, Ardinger HH, Pagon RA, et al., editors. GeneReviews [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2018. Available from:https://www.ncbi.nlm.nih.gov/books/NBK1239/Accessed July 26, 2018.Online Mendelian Inheritance in Man (OMIM). The Johns Hopkins University. Lymphedema, Hereditary, II. Entry No: 153200. Last Edited 03/25/2015. Available at:http://omim.org/entry/153200Accessed July 26, 2018.Online Mendelian Inheritance in Man (OMIM). The Johns Hopkins University. Lymphedema, Hereditary, IA. Entry No: 153100. Last Edited 03/30/2018. Available at:http://omim.org/entry/153100Accessed July 26, 2018.Online Mendelian Inheritance in Man (OMIM). The Johns Hopkins University. Lymphedema-Distichiasis Syndrome. Entry No: 153400. Last Edited 08/17/2016. Available at:http://omim.org/entry/153400Accessed July 26, 2018.Years Published2008, 2012, 2015, 2018The information in NORD’s Rare Disease Database is for educational purposes only and is not intended to replace the advice of a physician or other qualified medical professional.The content of the website and databases of the National Organization for Rare Disorders (NORD) is copyrighted and may not be reproduced, copied, downloaded or disseminated, in any way, for any commercial or public purpose, without prior written authorization and approval from NORD. Individuals may print one hard copy of an individual disease for personal use, provided that content is unmodified and includes NORD’s copyright.National Organization for Rare Disorders (NORD)
顾名思义,所谓瞳孔就是眼睛(瞳)上的洞(孔)。英语有个短语叫“the apple of one's eye”,代指珍贵之物,这里的apple其实指的是瞳孔(pupil)。解剖上讲,瞳孔是由虹膜“围”成的结构。它是光线进入眼内的唯一途径。关于“瞳孔”,有不少有趣的东西,我们来漫谈一二。瞳孔的形状在大众的印象里,瞳孔是圆的。但是,养过猫的朋友们会有不同的理解。的确,人类的瞳孔是圆形的,而且是正圆形。然而其他动物却不完全是。比如猫、蛇、牛、马、羊……为什么会有这样的不同?这要从动物的习性来讲。一般来说,夜间行动为主的动物,瞳孔是竖椭圆形的,比如猫和蛇。相较与圆形,竖椭圆形的瞳孔在变化的程度和效率上都要更高一些。在夜间,这样的瞳孔可以提供更大的进光量,增加夜间眼睛对环境的感知能力。而在白天,竖椭圆形的瞳孔可以变得极小,再加上眼睑的遮光作用,可以将进光量控制在最小程度。谈到这里,有两句歌词一直在脑海中萦绕:“眼睛瞪得像铜铃,射出闪电般的精明”以及“眼眯成一条线,轻轻踮着脚尖”。牛、马、羊这些处在食物链下层食草动物,时刻得提防着捕食者的行踪。包括吃草的时候。这些食草动物动物为了保证高效率进食的同时“盯”着捕食者,将瞳孔进化成横椭圆形。而且它们在低头吃草的同时,眼睛会上转一定程度。食草动物的眼睛长在头的两侧,配合横形瞳孔可以进一步扩大水平视野。真是聪明至极又懒的出奇。“天苍苍,野茫茫,风吹草低见牛羊”,你看到牛羊的同时,他们也在看你,而且还在低头吃草。狮子和猎豹虽然都是猫科动物,但是它们的瞳孔都是圆的。狗和狼的瞳孔是圆的。狐狸是犬科动物,但是它的瞳孔是竖椭圆形。还有一些很奇特的瞳孔形状,比如乌贼的“W”形。总之,瞳孔的形状是为了适应生存环境。瞳孔的颜色正常瞳孔有两种颜色:红与黑。大多数情况下是黑色的,由于巩膜和色素膜给眼睛营造了一个“暗箱”。照相的时候,瞳孔可能是橘红色的。橘红色是视网膜的反光。现在的相机一般自带去红眼功能,所以红眼也很少见。 不正常的瞳孔可以是白色、黄色,或者其他颜色。医学上有“白瞳症”:先天性白内障、视网膜母细胞瘤、Coats病、PHPV等。白内障发展到一定程度,瞳孔可以呈现黄色或者暗红色。铜、铁等金属残留在晶状体上,可以使瞳孔看起来像有铜锈、铁锈的颜色。“看不穿 是你失落的魂魄,猜不透 是你瞳孔的颜色”。很多女孩子为了漂亮,佩戴各种颜色的美瞳。这里两处的瞳孔其实指的是“虹膜”。如果真的给瞳孔上色,那看不清的是自己,不是别人。瞳孔与大小瞳孔的大小随着环境不断改变。光线强时瞳孔小,光线弱时瞳孔大。瞳孔大小随着年龄增长逐渐变小。老人家的瞳孔比较小,小孩子瞳孔比较大。说到这里要提一下“萌”这个字。看起来萌不萌,其实基本取决于瞳孔大小。小孩子瞳孔偏大,看起来萌;猫在晚上瞳孔特别大,看起来萌;美瞳的瞳孔直径一般在5mm左右,假装很萌;熬夜以后,瞳孔也会偏大,貌似很萌。但是瞳孔大,不一定都很萌,也可能是呆。两眼放空、双目无神的瞳孔应该也是偏大的。最后,说两个成语。双瞳剪水:形容眼睛清澈明亮。唐·李贺《唐儿歌》:“一双瞳人剪秋水。”双瞳如豆:形容目光短浅。清·蒲松龄《聊斋志异·王桂庵》:“笑君双瞳如豆,屡以金资动人。”图片来自网络,如有侵权请联系本文作者。
蠕形螨导致睑缘炎蠕形螨在眼睑睫毛附近定植蠕形螨的生存周期蠕形螨在睫毛附近生存显微镜中的蠕形螨 蓝色:蛹 黄色:幼虫 红色:成虫显微镜中的蠕形螨蠕形螨蠕形螨在睫毛附近生长蠕形螨
这周接诊一个打美容针失明的患者。来诊前一天晚上19时许在某机构注射自体脂肪填充太阳穴。打液体黄金的过程中即出现疼痛不适,遂中止手术。凌晨3时许发现右眼看不见东西。到我门诊时已经是上午10点左右。看一眼患者,问了两句病情,心中已经默默叹了一口气(又是一个美容针打瞎眼睛的)。再看一眼眼底,确定OAO(眼动脉阻塞),随即进行“抢救”,然后收入院治疗。结局很不好。虽然我们尽了全力,但是从注射到我接诊已经过了15个小时左右,早已错过了治疗时机。叹息过后,我们来分析一下。1.什么是液体黄金?“液体黄金”其实就是自体脂肪,也就是自己身上的脂肪。某些人为了宣传效果,想出这样一个自以为高大上名称。就是说把自己身上某个部位的脂肪抽出来,经过一定的处理,再给你打到另外一个部位,瞬间脂肪变黄金。2.为什么打美容针会失明?上面这张图解释了打美容针失明的原理。由于注射时的压力远远超过末梢动脉的压力,注射物(包括玻尿酸、自体脂肪、填充物等)通过面部动脉(鼻外侧动脉、鼻背动脉、内眦动脉、滑车上动脉、眶上动脉等)逆流而上,回到眼动脉或者更上游的颈内动脉。在注射停止后,逆流而上的物质再顺流而下,进入眼部血管,造成栓塞。栓塞的部位不同,结局也不同。本例患者注射的位置时太阳穴,与上面提到的情况不太一样。太阳穴的位置时颞浅动脉供应的。颞前动脉属于劲外动脉的分支。本例患者逆流而上的自体脂肪回到静脉动脉,再进入颈内动脉分支-眼动脉,引起失明。总而言之,压力导致逆流,逆流导致阻塞,阻塞变成悲伤。悲伤逆流成河。3.颈内动脉的分支那么多,为什么其他分支供血的地方没事?人体很多部位的供给动脉不是一条,很多是网状结构;而且即便真的堵了,也可以通过侧支循环的建立,重新获得营养,实现功能的恢复。然而,一个眼球的眼动脉只有一条,其分支——视网膜中央动脉也只有一条,而且没有侧支循环。所以,堵了就堵了。4.这样的病例多吗?我没有做过统计分析,也没有找到类似的数据,所以不能说具体比例是多少。但是,类似的病例不在少数。从我入行到现在,每年总会遇到几例。而且近些年似乎有增多的趋势。这类患者全部是女性,年龄基本在20-40岁。她们无一例外都是在私立的“美容机构”接受面部注射。这些“美容机构”有大型连锁机构,也有小诊所。面部注射的部位包括:脸颊、鼻唇沟、眉弓、额头、太阳穴。注射材料包括玻尿酸和自体脂肪,也有联合假体植入的。5.这个病好治吗?不好!我接诊的此类病例,有当天就诊的,有等了两三天的,也有在当地治疗一段时间的。治疗的效果都不好,最差的一例半边脸坏死。治疗效果不好,我很无奈。为了寻找更好的治疗方案,特地拜访(google)整形美容界的领军者韩国。然而,韩国的眼科医生也很无奈。Seoul National University College of Medicine的SUNG WOOK PARK总结了2003-2012年他们接诊的12例此类患者,见TABLE 1。(OAO:眼动脉阻塞;CRAO:视网膜中央动脉阻塞;BRVO:视网膜分支动脉阻塞;Autologous fat:自体脂肪;Hyaluronic acid:透明质酸;Collagen:胶原;NLP:无光感)这12例患者全是女性,年龄多在30岁左右(26岁4个,占33%,难道26岁是人生的什么坎儿?)发生OAO和CRAO的共9例(75%)。这9例患者中7例(7/9,77.8%)最后无光感,另外2例分别是光感和0.3,也是很差很差的结局。发生BRVO的患者占25%,结局也好不到哪里去。虽然有两个视力1.0,但是都有视野缺损。SUNG WOOK PARK还总结了其他部分学者的报告(TABLE 2)。一眼望过去最后结局是大片的NLP(无光感)。6.怎么预防?不做这类手术自然就不会有这样的风险。最后说一下自己的感想。颜值在任何时代都重要,尤其是当下。然而,一个人的吸引力包含很多方面的特征,比如:人格、智慧、知识。与其冒着风险去提高颜值来迎合这个浮躁的社会,不如静下心来读几本好书。有句话叫作:腹有诗书气自华。
白内障手术可能是全世界范围内开展最广泛的眼科手术。合理的用药对术后恢复非常重要。笔者根据国内外指南,结合所在单位的具体情况,推荐术后用药如下:左氧氟沙星滴眼液;妥布霉素地塞米松滴眼液;玻璃酸钠滴眼液;妥布霉素地塞米松眼膏;具体用法:术后第1周:三种滴眼液 每日各4次(不分先后次序,两种药水间隔10分钟),眼膏 每晚1次。术后第2周:滴眼液每日3次,眼膏 每晚1次术后第3周:滴眼液每日2次,眼膏 每晚1次术后第4周:滴眼液每日1次,眼膏 每晚1次。特别说明:1.术后按照医嘱,按时复查;2.以上用药方法供参考,实际用药需要手术医生的具体指导。
XtraFocus (Morcher) 小孔+add on设计IC-8 (AcuFocus) 通过小孔成像增加景深多焦点IOL 这一类已经得到广泛应用Scharioth Macular Lens (Medicontour) 中央“增视”+add on设计 用于AMD患者Femtis IOL (Oculentis) 专为飞秒辅助白内障手术设计 大小襻设计-夹在囊袋上Harmoni Modular IOL System (ClarVista Medical) 分体设计 中央度数可更换人类历史上第一个IOL植入术 致敬Sir Harold RidleyFluidVision (PowerVision) 注“水”的IOL 通过变形实现可调节一个兔子实验 在已经植入的IOL上打激光 改变其屈光状态——真正的未来