Lens Anatomy & Cataracts PDF

Equator: 12 & 6 Poles: Anterior pole: front surface of the lens Posterior pole: faces the vitreous and retina The lens capsule: a very elastic transparent non-elastic membrane which completely surrounds the lens Its thickness is not uniform First layer of the lens Very perme...

Equator: 12 & 6 Poles: Anterior pole: front surface of the lens Posterior pole: faces the vitreous and retina The lens capsule: a very elastic transparent non-elastic membrane which completely surrounds the lens Its thickness is not uniform First layer of the lens Very permeable and elastic Elasticity provides the bending of the lens = accommodation to see at near The lens epithelium: consists of a single layer of cubical cells covering the anterior surface of the lens substance and lying between the latter and the capsule Anterior: Only anterior epithelium Posterior: No posterior epithelium Role: Important metabolic activity of the lens occurs here and provides proteins and amino acids for the lens The lens fibers and lens substance: the bulk of the lens is composed of successive lamina of fibers B/w them, the lens substance comprises a cortex and a nucleus The lens cortex: consists of a long hexagonal transparent fibers which are arranged in structure of an onion The nucleus: consists of the compressed central portions of lens cortex which gradually undergoes a process of sclerosis The suspensory ligament of the lens (the zonule): the zonule is a band-shaped gel-structure stretching from the ciliary body to the periphery of the lens. Zonule is inserted into the zonular lamellar in a belt The strength of the ligament varies with time and age ○ Young: zonules are tight ○ Age: weaker and flaccid Lens chemistry: Metabolic needs of the lens (TED) ○ Transparent (if it's not transparent = cataract) > Elasticity (provided by the capsule) > Development of new fibers Metabolism is being done by active pump ○ Happens in the epithelium ○ Keeps the transparency & dehydration of the lens ○ Sodium ions go OUT and potassium ions go IN (boards ?) maintains the transparency of the lens; if is the other way around… lens will be filled with water and swell and loses its transparency = cataract The adult lens contains ~65% water and 34% proteins. The remaining 1% is made up of inorganic compounds Lens dehydration is maintained by an active sodium pump in the epithelium Substance for lens energy require water soluble proteins Water soluble proteins: Crystallins (common) ○ 3 types of crystallins, alpha, beta, gamma ○ Young: proteins are soluble and important to maintain dehydration of the (responsible to keep water out and to not form cataracts) ○ As we get older, there is alteration in chemistry and more water insoluble proteins fill up the lens and keep water in so that is why we have cataracts in older age The exact cause of cataractogenesis is obscure, the loss of transparency is due to a disturbance of the structure of the lens. The disturbance may be of the following: Hydration process (lens is full of water because of reverse active pump) ○ Biochemical ○ Electrolytic and permeability factors produce abnormal osmotic gradient leading to swelling (active pump reverses as Na moves in and K out = lens hydrated and swells = cataract) Coagulative process ○ An irreversible chemical change whereby the proteins become coagulated. Denaturation of the lens proteins may initiate or potentiate formation of insoluble proteins ○ More insoluble proteins that do not help with the dehydration of the lens Degeneration and sclerosis of nuclear fibers ○ With age, fibers become sclerosis = formation of cataract All 3 together are responsible for the formation of cataract Cataract Epidemiology Cataracts remain the leading cause of blindness Age-related cataract is responsible for 48% of world blindness, which represents ~18 million people Cataracts are also an important cause of low vision in both developed and developing countries ○ Hypermature: becomes super liquified ○ A “liquified” lens: structures are all still connected versus Morganian, the structures are not connected ○ Mature vs. Hypermature Cataract Classification of cataract Congenital/Developmental ○ Congenital if you were born with or been formed within 1st year of life Congenital cataract due to systemic disease Metabolic: ○ Galactosemia (Galactose accumulates in blood due to enzyme deficiency and its inability to metabolize; is autosomal recessive) ○ Lowe Syndrome (x-linked disease; chubby cheeks, deep embedded sunken eyes, cataracts, and glaucoma, and Vit D deficiency) ○ Fabry’s disease (x-linked lysosomal disorder = excess lipid deposition in tissues; vortex epitheliopathy cataract develops ○ Hypoparathyroidism (decreased parathyroid hormone) Prenatal infection: ○ Congenital rubella (~25% of cases), other intrauterine infection (TORCH- toxoplasmosis, rubella, cytomegalovirus, herpes) Common infection that causes congenital infection? (Boards ?) Rubella**** Chromosomal abnormalities: ○ Down Syndrome ~5% Trisomy 21 ○ Patau (Trisomy 13) ○ Edward (Trisomy 18) syndrome Types of congenital cataracts morphology Polar type (anterior or posterior) ○ Happens either in anterior or posterior pole ○ Etiology (embryonic or acquired w/ perforation) Embryonic lens development is abnormal Or perforation in the eye ○ Depending on the density of opacity, VA varies (dense = VA severely affected) ○ Posterior polar cataract ○ White opacity in the anterior or posterior capsule: Looks like either a big, medium, or large white snowball in the posterior arc ○ Bilateral and does not progress ○ No systemic involvement but eye has other findings Anterior pole: associated w/ persistent pupillary membrane Remnant of the hyaloid artery; floats and connects to cataract in ant. Lens ○ Anterior PPM and sutural stellate ^ Posterior pole: Mittendorf dot Hyaloid remnant behind posterior pole ○ Management varies Depends on the density Snowball huge = operate Small snowball = does not operate ○ Anterior polar ^  ○ Posterior polar and Mittendorf dot ^ Sutural stellate ○ Variable form opacities at the sutures Most common congenital opacity you can find in anyone!!!! (~60% of the world has it) White dot in Y-suture ○ VA: does not affect VA ○ Etiology >> embryonic ○ Usually bilateral but not always and does NOT progress; very frequent and common congenital cataract ○ Management: do nothing about it ○ Whole Y suture involved; sutural opacity Nuclear: ○ Etiology: embryonic development of the nucleus ○ First congenital cataract that affects the VA ○ Not progressive (does not become dense) ○ Round w/ fine pulverulent opacities variable in density (2) Mild form: in nucleus, small, only partially affects VA Severe form: big, wide, disc in nucleus; significantly affects VA ○ Bilateral and does not progress ○ Systemic involvement: Cataract that you get in Rubella***** ○ Associated eye findings: Microphthalmia (small eye) Pigmentated retinopathy (salt and pepper retinopathy)  Systemic finding: Deafness ○ Frequency: It is a frequent cataract One of the most common congenital cataracts that affects VA ○ Management: 99% you need to operate for patient to see well ○ Mild nuclear cataract ○ Severe form of nuclear cataract; patient has Rubella as well Blue dot: ○ Etiology: fetal embryonic development (ant. cortex, ant. nucleus) ○ Bilateral, does not affect VA nor progress ○ Dot bluish hue opacities: Found in the anterior cortex and nucleus ○ Association w/ other cataracts: Usually seen w/ sutural stellate ○ Frequency: pretty frequent ○ Management: none ○ Zonular or lamellar **** KNOW THIS  ○ Etiology (3 reasons) Genetic (gene mutation) Toxicity Systemic disease Lowe’s Syndrome ○ Vitamin D deficiency that leads to the cataract and they have sunken eyes ○ Cataract that affects the lamellar zones Like a V ○ Frequency: pretty frequent ○ VA variable but can be a cataract that really affect the VA in the most dramatic way and VA can be highly affected #1 decreased VA ○ Granular, linear spoke opacities at a specific location “Rider’s” ○ Eye involvement and progression: Bilateral and progresses slightly ○ Management: Always surgery because VA is highly affected ○ Classical lamellar cataract ○ Central oil droplet ○ Etiology (Which of the following systemic diseases causes this type of cataract? ***Boards ?) Galactosemia ○ Time development:  When does it develop? First few weeks of life; assuming the baby has Galactosemia ○ VA and progression: Affects the vision because it is very central and not progressive ○ Difficult to see w/ direct illumination in SLE but seen in retro as a round droplet ○ Management is important to alter the progression of the cataract Need to remove the kid from any milk products! If oil drop is very dense = operate but if not just leave it ○ Management in congenital cataract Bilateral congenital cataract requires urgent surgery (take the whole lens out (lensectomy and vitrectomy) and the fitting of spectacle &/or contact lenses to correct the aphakia (usually high hyperopia) ○ In babies, cannot do IOL because the capsule is not strong enough so take the whole thing out = lensectomy ○ 2 years; NO IOL in cataract surgery unless the kid is 2 years old**************** boards and test question ○ How old can you do a lensectomy cataract surgery? (Boards ?) Wait at least 4-6 weeks old; the earliest that you can do it Unilateral congenital cataract treatment ○ Treat w/ contact lens (cannot give +20 specs) ○ Early IOL and hopefully IOL stays in eye F/U for children w/ congenital cataract should continue because of the risk for developing certain conditions like strabismus or nystagmus Consider therapy to avoid amblyopia ○ Patching ○ Developmental can start early but after 1st year of life, could also be considered juvenile May involve nucleus, deeper layers of cortex or the capsule  Coronary Developmental** NOT congenital Ring type of opacity surrounding the nucleus VA and progression ○ VA not affected but is more of distortion of vision ○ Not progressive Opacities surrounding nucleus forming a ring Eye involvement and progression: ○ Bilateral and does not progress Management: ○ No need for operation ○ Occur in ~3-6:10,000 births ○ Common to see opacities that either affect VA OR do affect VA ○ Unilateral: big problem and will develop amblyopia if not fixed quickly ○ Bilateral: 2/3rd of congenital cataracts ○ Can cause amblyopia in infants ○ 10% of child blindness ○ Associated w/ other eye signs Strabismus and nystagmus ○ It is divided to: Systemic diseases association Non-systemic association Hereditary by gene mutation ○ The common cause is genetic mutation usually autosomal DOMINANT 3 causes that is passed from mother to child ○ Birth trauma ○ Poor oxygenation ○ Maternal malnutrition Mothers w/ heavy alcohol and drug abuse Senile (primary acquired) ○ Classification of SENILE cataract according to an atomic location******* ○ Subcapsular (beneath the capsule)- anterior or posterior, nuclear, cortical- anterior or posterior, mixed (more than one layer being affected, most common) ○ Progressive opacification of the lens affecting elderly people not suffering from local or systemic disease  This is due to a process of aging and degeneration Not hereditary; everyone is going to get cataracts in some way or form and the severity varies too Yes genetically determined Environmentally influenced? Yes, cataracts can develop earlier due to environmental conditions Ex: heavy exposure to UV ○ Cataracts are usually bilateral but are always asymmetric (most of the times) ○ Gender: Males and females are equally going to get it ○ Risk factors: (speeds up the formation of cataract) #1: UV-light Smoking Nutrition Undernutrition in developing countries Alcohol Illnesses w/ severe dehydration Crohn's disease; any GI disease ○ Variable decreased VA (can vary due to cataract progression) Immature cataracts VA Early: mild changes ○ Even 20/20 up to 20/30 Moderate: ○ 20/40 to 20/60 Severe ○ 20/70 or worse Mature cataracts VA: is a lot worse CF, LP ○ Could experience glare due to cataract progressing ○ Monocular diplopia if one cataract in one eye is worse than the other the eye is so blurred that they see double ○ Decreased color clues (what happens to a patient’s color vision with cataracts? Boards question- colors go to the invisible spectrum = become yellowish or reddish) ○ Seeing black scotoma in the center ○ Decreased contrast sensitivity The quality of vision (20/50 is quantity) ○ Cortical cataract**** comes from the periphery Since opacity is peripheral, the vision is good in the day because pupil constricts = good central vision and bad at night because pupil dilates Causes refractive error causes hyperopic shifts Appear as grayish/white opacities  White dusts, white vacuoles, more advanced is a stalk (like a lines/ tooth coming out of cortex) Progress is slow but faster than nuclear cataracts Starts with vacuoles and/or dot formation leading to spoking In mature stage, looks completely white Cortex is from top to bottom = evaluate carefully when dilated because it is coming from the periphery and is grading by percentage because the cataract is white/gray Slightly worse VA than nuclear cataract Grade 1 30% of cortex is opacified VA: 20/20 Grade 2 30-60% of cortex is opacified VA: 20/20 to 20/25 Grade 3 60-80% of cortex is opacified VA: 20/30 to 20/40 Grade 4 Whole cortex from top to bottom is opacified VA: 20/30 , 20/40 , 20/60 Early cortical cataract  Grade 2 Cortical Cataract Grade 3 Cortical Cataract Grade 4 Cortical Cataract ○ Nuclear cataract****- starts from posterior to anterior nucleus Since the opacity is central, vision is good at night because pupil dilates and they can use periphery to see, and poor in the day because pupil constricts and cannot use periphery to see Causes refractive error May get myopic shift Changes in color of the nucleus from light yellow, dark yellow, orange, to dark brown (4 color variations)**** Progress is slow and takes time to develop Before Grade 1: we call it a trace cataract The color is barely yellow, starting off basically Cataracts between 1 & 2 (Grade 1+ means as if it getting to the next stage 2)  Grades 1, 2, 3, 4 (Lens Opacification Classification System III) Grade 1: light yellow color ○ VA: 20/20; barely does a thing Grade 2: dark yellow color ○ VA: 20/20; if a patient has 20/40 VA with a grade 2 cataract = something else is going on Grade 3: orange color; causes some kind of decrease in VA ○ VA: 20/25 Grade 4: brown color ○ VA: 20/30 to 20/40 Important to know approximate VA loss for each grade because for a patient that has expected visual loss, we know if the visual loss is only related to the lens. If it is not, we use the information that something else is going on. VA related to grading Grade 1 NC (light yellow) Grade 2 NC  Grade 2 & 3 NC Really yellow (anterior portion) is a grade 2 Orange (posterior portion) is a grade 3 Grade 3 Grade 4 NC ○ ○ Subcapsular senile cataract posterior and anterior  Occur just under the capsule of the lens Starts as a small, opaque, granular dirty area at one part of the capsule in the back or front of the lens and progresses Cataract located at the nodal point of the eye (decreased distance and near) Anterior SC (if just yellow involved) Will only see white dots Don’t see this a lot (10%) Posterior SC (the “leopard” subcapsular cataract, if black and yellow is involved) 90% will see this Worst cataract you can get It interferes w/ distance and reading vision Reduces vision under daytime conditions because central Causes a lot of glare or halos around lights at night Grading (how much of the black is covering the capsule) ASC/PSC Grade 1 ○ Up to 5-10% ○ VA: 20/25 to 20/30 ASC/PSC Grade 2 ○ Up to 30% of the capsule ○ VA: 20/30 to 20/40, sometimes to 20/50 ASC/PSC Grade 3 ○ Up to 50% of the capsule ○ VA: 20/40 to 20/60 ASC/PSC Grade 4 ○ Above 50% ○ VA: 20/70 up to 20/100 sometimes or worse Fastest progression of the 3 categories of cataracts ○ Treatment for cataracts: Glasses: Cataract alters the refractive power of the natural lens so glasses may allow good vision to be maintained Surgical removal: when VA can’t be improved w/ glasses When is it recommended? What VA is required? ○ When VA is worse than 20/40 and above (driving vision) Do we need to wait for the cataract to mature before extraction? ○ No, we need to operate on the immature stage because mature stage can cause some complications as it is difficult and hard Surgical techniques Phacoemulsification method (current method) Extracapsular method- similar to phaco. but leave post. capsule in Intracapsular method (whole lens being taken out, done on mature cataracts and kids)  Grade 2 PSC Grade 3 PSC Grade 4 PSC Advanced Grade 4 PSC  Grade 4 ASC White opacities in capsule and this is anterior SC Grading is the same as PSC ○ Posterior Subcapsular Cataract: note the central location, which gives rise to severe glare disability Acquired ○ Traumatic Causes: Mechanical Concussion or blunt injury: ○ Injury of lens fibers ○ Capsule injury or tear ○ Loss of permeability Perforating injury (perforates/penetrates the eye) Other causes ○ By radiation (two types of radiation that causes cataract: ionizing— gamma rays, X-rays, UV-C and infrared  light— people who work w/ glass blowers (glass blowers cataract) Forms of traumatic cataract Mild: Punctate opacities (White and pigmented) in the capsule/cortex/iris pigment ○ Has different sizes and with trauma, will see the iris pigment is released and pigment is stuck in anterior capsule in the lens that is called the Vossius ring Pigment ring from imprinting of iris pigment Moderate: Rosette- flower-shaped cataract: it may progress to total traumatic cataract ○ Looks like a flower in the anterior part of the lens; affects VA; etiology: blunt trauma Forms between anterior capsule and cortex** ○ Total cataract: it develops when the lens capsule is severely damaged; penetrating injury  ○ The whole lens is destroyed, nucleus is floating and coming towards the pupil ○ Requires reconstruction of the eye ○ Penetration T/F: Traumatic cataracts 2ry to radiation may not have VA loss. True, only VA loss if on visual axis and dense - unlike Rosette and total which have severe VA loss. Other causes: ionizing radiation/IR, electric shock, lightning ○ Posterior subcapsular cataract caused by ionizing radiation^ ○ anterior capsule exfoliation ("glass blower" cataract), IR (non-ionizing) radiation VA in Rosette cataract and management Anterior Rosette cataract is more common but can also get posterior Surgery  VA and management in total cataract Surgery and reconstruction of eye VA and management in radiation cataract Subjective for cataract surgery; variable Always look for other complications of trauma in the presence of a traumatic cataract ○ Complicated secondary (cataracts is the complication of another ocular disease)** Definition: Cataracts associated with other ocular disease Etiology: Congenital ○ Aniridia (No iris; just pupil) ○ Primary hyperplastic vitreous Channels of the hyaloid vascular path that normally disappears but in this, it stays Acquired ○ Uveitis (iridocyclitis) ○ High myopia (16, 17 D) ○ Glaucoma (Glaucomflecken) Angle-closure glaucoma In acute angle-closure, you have synechiae the connection of pupillary margin that is known pupil block and causes ischemia and necrosis of the anterior capsule of the lens Necrosis of the capsule cortex secondary to the pupillary block and clogs the angle (Glaucomflecken) ○ Retinal detachment ○ Retinitis pigmentosa ○ GAOTC Geographic atrophy of the choroid (hereditary choroid disease also known as GYRAT) ○ Neoplasia Tumors Types of cataracts (varies)  ○ Anterior capsular and anterior cortical opacities which under an anterior chamber inflammation can Secondary complication cataracts always associated to anterior chamber inflammation at the same time Treat anterior chamber inflammation first before the cataract surgery**** (boards ?) ○ PSC centrally located, irregular borders, opacity that extends to the equator and progress ○ VA is usually affected but not always severely affected Management ○ Underlying cause ○ Surgery/when to do it Ectopia lentis ○ Dislocation implies zonules are broken and lens is out of place; can move anywhere and completely loose Anterior chamber ○ Patient has Weill-Marchisani Syndrome Posterior Superior Inferior ○ Subluxation that moved to the side; inferior nasal ○ Lens moved to the side ○ Subluxation implies at least one zonules are still intact, lens is going to move to the side, left, right, or in different directions ○ Congenital w/o systemic disease and the lens somehow is being displaced or moved in some direction Familial ectopia lentis Autosomal dominant inheritance Eye involvement and symmetry ○ Involves both eyes and symmetrical Direction of displacement ○ Subluxation: superior temporal Ectopia lentis et pupillae (ectopic lens w/ pupillary movement at the same time) Autosomal recessive Eye involvement and symmetry ○ Bilateral and symmetrical Characteristic pattern involving pupil ○ Pupil goes opposite peaks ○ Subluxated in one direction and the pupil is going to be peaked in the other direction** Associated ocular findings in cornea, iris, lens, ONH, retina ○ Cornea: megalocornea ○ Iris transillumination ○ Small lens ○ Lens cataracts ○ Retinal detachment ○ ONH glaucoma ○ Congenital aniridia (sometimes)  ○ Pupil is going one direction; lens is going to another ○ Congenital w/ systemic disease Marfan syndrome (tendency to have subluxated lens) Inheritance mode: AD Musculoskeletal abnormalities: Long hands, long fingers, long face, long arms/legs Cardiovascular disease: Severe Direction of lens displacement: superior temporal subluxation of the lens Associated findings in iris, ONH, and retina ○ ONH glaucoma ○ Retinal detachment ○ Iris transillumination Homocystinuria Metabolism error affecting liver Inheritance error: Autosomal recessive Hair and skin complexity: light skin and fragile, very blonde Mental development: decreased mental development; not retarded but decreased Direction of lens displacement: ectopia lentis with subluxation inferior nasal Associated findings in iris, ONH, and retina ○ Iris atrophy ○ ONH atrophy ○ Retinal detachment Weill-Marchesani Syndrome (opposite of Marfan’s) Inheritance mode: both ○ AR: more severe ○ AD Musculoskeletal abnormalities: short, chubby, everything in Marfan's but short Mental development:  Direction of lens displacement: not subluxated but dislocated into the anterior chamber***** ○ Sometimes get stucks in pupil and causes pupillary block which leads to secondary angle closure glaucoma Associated findings in angle, pupil, and lens ○ Narrow-angle ○ Pupil is blocked by lens ○ Lens is small ○ General symptoms presented Decreased VA due to refractive error Lens is subluxated, you’re not looking through lens so you loose RE Distortion If lens is moved through the side, you're going to get distortion and a lot of glare Glare Double vision ○ General signs and complications seen Iris Atrophy Phaco/lens Cataracts formed earlier Small lens Shallow AC ONH Glaucoma Retina Retinal detachment ○ Management (will ask this on test and boards) For subluxated lens: remember it is moved from its place Correction: ○ Pupilloplasty (distort the pupil to get full view of IOL and moves it to its place) ○ Relocation Removal w/ correction ○ If it cannot be done, removal with new lens For anterior dislocated lens Immediate removal w/ correction  For posterior dislocated lens Removal ***************** Vitrectomy Correction ○ Secondary to systemic disease (systemic diseases causing cataracts) Cutaneous disorders (involving the skin) Atopic dermatitis: Anterior subcapsular plaque type w/ posterior involvement as well ○ Typical anterior subcapsular plaque ○ Very regular borders ○ May have some posterior involvement with some spoke type opacities (star-like) ○ ○ Associated w/ other ocular disorders (cornea and TF) Keratoconus KCS ○ Time of presentation: 4th decade of life ○ 10% in the young age of pt’s w/ the disease (earlier than 30) ○ VA: Central and dense so VA is highly affected and will need surgery ○ anterior subcapsular (irregular shape), atopic dermatitis  ○ anterior subcapsular (dense), atopic dermatitis Muscular disorders Myotonic dystrophy (destroying the muscles, people have long faces because loose and weak muscles): Christmas tree cataract ○ Most common board question*** What systemic disease causes christmas tree cataract? Myotonic dystrophy- they appear as colorful lights in the cortex and nucleus in the lens ○ Posterior subcapsular stellate opacities later in life ○ Time of presentation: Late 30s or 40s ○ Lid and pupil involvement: Lid ptosis Light-near dissociation = light reflex is very slow and near reflex is stronger ○ Retinal involvement: Retinitis pigmentosa ○ VA: Colorful opacities cause extreme glare and distortion but VA is not significantly decreased ○  ○ face is long and droopy ○ stellate PSC, (late stage) Myotonic dystrophy, will have VA loss (affects nodal point) Metabolic disease Diabetes mellitus: bilateral white snowflake cataract in young age that- may progress rapidly ○ A juvenile cataract; happens in young ages ○ Progresses rapidly ○ Diabetics get sooner senile cataracts and progress a lot faster ○ Juvenile Diabetic Cataract White punctate or snowflake anterior opacities May mature within few days  ○ Adult Diabetic Cataract Cortical and subcapsular opacities May progress more quickly than non-diabetics ○ Also accelerated senile cataract ○ sutural stellate (aka Y suture - congenital), snowflake (cortical), juvenile diabetic cataract Wilson’s disease: hepatolenticular degeneration- green sunflower cataract ○ Fleischer-ring (copper accumulated in eye) ○ Also causes corneal involvement ^^ ○ VA: anterior subcapsular cortex so affects VA significantly ○ Wilson's ("sunflower"), remove (ASAP - dense, on visual axis) Galactosemia > oil droplet cataract ○ Secondary to medications/drug/radiation  Categories of drugs Phenothiazines (antipsychotics/antidepressants)- Fluoxetine, Sertraline, Citalopram, Duloxetine, Chlorpromazine ○ Can cause anterior polar/capsular opacities (tiny white dots in anterior capsule ○ Chlorpromazine (Central, anterior capsular granules) HBP medication (Amiodarone) ○ Can cause anterior pigmented opacities ○ Can also cause vortex epitheliopathy also ○ Steroids (Prednisone, Hydrocortisone, Methylprednisolone) ○ Can cause dense, central PSC** ○  ○ PSC: Systemic or topical steroids ^ Miotics (long-acting anti-cholinesterases)- Physostigmine or Neostigmine ○ Can cause dense nuclear &/or cortical cataract 2ry complicated cataracts in the anterior capsular (or subcapsular) and anterior cortical regions of the lens are more common and progress rapidly with inflammatory conditions such as uveitis GAOTC (geographic atrophy of the choroid) GAOTC (geographic atrophy of the choroid) is a condition that can cause a complicated 2ry cataract, especially spoke wheel pattern PSC -pt will also have hereditary RPE changes  PSC caused by high myopia (-20 D) PSC caused by RP Retinitis pigmentosa is HIGHLY associated w/ complicated 2ry cataract - usually spoke wheel pattern PSC -called Ausher's Syndrome when associated with deafness Management of Senile Cataract (learn well please because if boards asks about lens, will ask a lot about post-op care) Cataract Surgery IOL implantation Post-op care Complications of cataract surgery Cataract sx/ preoperative evaluation General Health Investigations: general body/health check-up ○ Hemoglobin ○ Blood sugar Uncontrolled diabetes  If operated, induce an acute diabetic retinopathy and 50x more than increase of infection probability Controlled diabetes Day of surgery, do NOT take diabetic medication because if so, under anesthesia, can induce a hypoglycemic attack and is lethal! Day before is fine but never day of ○ Urine examination ○ ECG and X-ray chest ○ BP Uncontrolled HTN If they’re operated, can form an malignant HTN and severe which leads to (boards ?) hemorrhage between scleral and choriod and that hemorrhage will push structures to the front and complications are severe Absolutely cannot do on uncontrolled HTN Need to take their medication on the same day to avoid spikes of BP during surgery; surgeons have recommended to take two Ocular evaluation ○ VA/BCVA: Check VAs always ○ Pupils: Always check pupillary response in every eval ○ IOPs: Important because cat.sx. will have a spike in IOP so must know before surgery and compare ○ DFE/Careful macular evaluation: Surgery can induce macular edema so you have to know the macula status before surgery ○ VF’s/Amsler Grid ○ Ultrasonography/B-scan If they cannot see behind the eye with a very dense cataract, B-scan is done ○ Laser interferometry/PAM (Potential Acuity Measurement) Eval that predicts the VA after cataract surgery Will the VA improve or not or is something else affecting the cataract? ○ Keratometry Need to know before because for proper IOL that will be placed ○ A-scan ultrasonography (Biometry) Measure axial length that is used to calculate IOL power ○ EXTRA- sometimes done depending on surgeons: Contrast sensitivity test (quality of vision, not snellen number) IOP Power Calculation (SRK formula) ○ IOL Power = A - 2.5 L - 0.9 K ○ A: Standard value that can change ○ L: Axial length depending on the eye ○ K: Most flat K in keratometry ○ A constant can be adjusted based on the eye ○ 3rd generation formula Improved accuracy Better result and simple Take into of axial length and K-reading to predict the effective lens position Optimization of formula; position of the lens will change the value whether if its anterior or posterior ○ ELP (Effective Lens Position) Not precise because IOL is not the same thickness as actual lens (thinner) and anterior chamber depth/size increases after surgery Must take into consideration of AC depth, not just the position of IOL ELP = distance from cornea to lens Explains the position of the IOL post-op Assumptions in ELP Shallow ELP: Short eye, Flat K’s Deeper ELP: Longer eye, steeper K’s Errors in predicting the ELP: refractive surprise Shallow AC = sitting more anterior = lower IOL power  ○ 4th generation Holladay 2: IOL calculation formula 7 parameters: axial length, K-reading but white to white (corneal diameter), pre-op rx, anterior chamber depth (changes after cat. sx), lens thickness, and patient’s age All these 7 factors are inputted into this formula Considered one of the most accurate IOL formulas today Informed consent is taken The eyelashes of the eye to be trimmed Povidone-Iodine 5% solution ○ Eye is disinfected with this Antibiotic drops are instilled/dosage ○ 2 days before surgery q 6 hrs ○ Some have done 24 hrs before surgery Pupil is dilated (avoid certain drops in hypertensives) ○ Use Phenylephrine 10%- has a tendency to raise BP ○ If HTN, avoid the 10% and 2.5% is used w/ multiple drops Flurbiprofen (Ocufen) 0.3%: a non-steroidal anti-inflammatory drug these drops are instilled q 15 min ○ NSAIDs stop prostaglandin synthesis so will decrease inflammation and is vital* in order to avoid the pupil closing during surgery (pupillary miosis during surgery) Other medications may be given as required e.g., antiglaucoma drugs, antihypertensives, anti-asthmatics etc ○ Boards ?: can continue taking glaucoma drugs! only restriction in medications are for diabetics to take their meds on the same day to avoid severe hypoglycemic Anesthesia: most cases of cataracts are operated under local anesthesia except in young children ○ Retrobulbar anesthesia: back of the eye Always blocks facial nerve ○ Peribulbar anesthesia: around the eye Types of anesthetics: ○ Lignocaine or Xylocaine 2% which are the main anesthetic agent Drops or gel forms ○ Bupivacaine 0.75% Other substances used ○ Adrenaline 1 in 200,000: adrenaline avoids vasoconstriction of vessels; we want the anesthetic to be absorbed from the eye and adrenaline decreases systemic absorption so the whole anesthetic can be taken from ocular tissue Not used when ? ○ Hyaluronidase 7-15 IU per mL Diffuse equally of anesthetic in the whole eye Cataract sx/surgical procedures  Intracapsular cataract extraction (ICCE) ○ Types of cataracts: Two main categories of lens being taken out of capsule is hypermature cataracts or congenital cataract in kids ○ 12 mm corneal incision, at the same time of taking lens out making a iridectomy (iris incision) and in that opening, lens will come out ○ Lens position: anterior chamber IOL ○ Type of IOL implanted: anterior chamber IOL ○ Disadvantages: lots of them If not placed correctly, it may move and one of the haptic legs can grab the corneal/iridectomy opening and rips it off Cornea >> complications and RE Incision is big with distorted cornea and causes huge RE residual post-op and astigmatism Uvea Lots of anterior chamber inflammation; uveitis Glaucoma Very common to get glaucoma UGH syndrome Uveitis Glaucoma Hyphema: blood in anterior chamber Vitreous Prolapse; can move to the front because there is no barrier and no IOL to stop it As vitreous moves to the front, the retina may become detached Macula Macular edema Retina Retinal detachment Serious infection Higher because it is very invasive  ○ Advantages: Only one to consider is when there is a posterior chamber IOL placed posteriorly, posterior opacification can occur and that wouldn't happen here ○ Extracapsular cataract extraction (ECCE) everything is taken out except the capsule ○ ○ Conventional (limbal incision) Old surgery ○ Advantages: Support Prevents vitreous from bulging forwards and acts as a barrier to anterior/posterior segment Barrier b/w anterior and posterior segment >> less rare ○ Disadvantages Capsular remnants Capsule reopacification and needs can happen anytime after surgery, even years Large incision/sutures >> RE Causes high RE and astigmatism All complications from ICCE is being taken away ○ Steps: Partial thickness limbal incision (10-2 o’clock)  Exactly at the limbus 10 mm in size Anterior chamber entry Lose aqueous because of incision so in order to avoid, they inject VES Inject VES (1% Sodium Hyaluronate) Prevents anterior chamber from closing and protects the cornea from being damaged Anterior capsulotomy: Canopener technique Canopener technique (opening is not nice and smooth like a can opener) Extension of incision ○ 3-4 mm cortex Hydrodissection ○ Hole in anterior cortex so they Inject saline solution and try to separate the capsule from the cortex ○ Blue represents the separation of capsule from cortex Removal of nucleus Cortex aspiration VES injected into capsular bag IOL implantation Aspiration of excess VES Suture wound ○ Big incision so sutures has to be placed Subconjunctival injection of antibiotic/steroid Small incision cataract surgery (SICS) (scleral tunnel incision) ○ ○ 5-7 mm incision size at sclera (smaller)  ECCE/SICS:Incision size, where the incision was made, and type of capsulotomy (3 differences between ECCE and SICS) ○ Sutureless cataract surgery ○ Scleral tunnel incision/size ○ Inject VES ○ Anterior Capsulotomy CCC (Continuous Curvilinear Capsulorhexis- breaking the capsule) - make a C opening the capsule Hydrodissection Removal of nucleus Cortex aspiration VES injected into the capsular bag IOL Implantation Aspiration of excess VES Subconjunctival injection of antibiotic/steroid Advantages No suture required ○ Any incision < 8 mm can heal by itself, no suture required and lower chances of RE Phacoemulsification (scleral tunnel/clear corneal incision) ○ Scleral tunnel/ clear corneal incision Like a vacuum cleaner; being sucked out and then breaks down Less invasive ○ Small incision/size lot smaller, 2-3 mm incision ○ Don’t lose aqueous as much because the incision is small and VES may not be required based on ability of surgeon ○ CCC Additionally, Hydrodelineation only done here  ○ Hydrodissection/ Hydrodelineation (KNOW these terms*** as they will appear on boards) Inject nucleus (has 2 layers, center = harder & epi nucleus they separate the layers- Hydrodelineation) ○ Nucleus emulsification and aspiration using phacoemulsification needle (1 mm titanium needle vibrated at ultrasonic speed 40,000/sec) ○ Cortex aspiration ○ Foldable IOL lens Since incision is small, IOL has to be foldable. SILICONE MATERIAL. ○ ○ Advantages: No suture No RE Faster healing time ○ Disadvantages: Cornea: if viscoelastic material is not used, surgeon has to be careful to not damage corneal endothelium Greater risk of nucleus drop: be really careful to not drop the nucleus out of site when emulsifying May destroy capsule if dropped Expensive technique Greater expertise required to master the technique (obvi) Laser-Assisted Cataract Surgery Type of laser- Femtosecond laser: Nd-YAG laser (IR-A) Same laser as in Nd-YAG capsulotomy  Functions/Uses (substitutes blades/needles, breaks down the lens) ASKS THIS ALL THE TIME IN BOARDS ○ Corneal incisions Instead of using blades/needles, use laser ○ Capsulotomy / CCC Instead of needles to make CCC, use laser ○ Phacolysis: fragment nucleus ○ RE correction: correct if used IOL Types Posterior chamber lens (PCL) - 90% of the time? Anterior chamber lens (ACL) By material ○ PMMA (Polymethyl Methacrylate) ○ Silicone ○ Acrylic (foldable) - latest material that has been introduced Phacoemulsification procedure, the foldable lens that Less probability in developing PCO Effect of material of IOL for PCO (secondary cataract) ○ The material does have something to do with PCO ○ PMMA has the most probability of PCO, second most common is silicone IOL types by function Monofocal ○ Principle: Only focus on one focal point and designed to correct leftover refractive error and distance vision ○ Astigmatism correction: Also corrects astigmatism ○ Monofocal lens and near vision: Blur near vision and are going to have to wear specs for near Monofocal w/ toric: correct sphere and cyl that is left over Toric ○ Astigmatic correction: ○ Toric lens and near vision Presbyopia correcting IOLs/Two types ○ Multifocal (ex: AcrySof IQ ReSTOR - ReZoom-Tecnis) Has concentric zones that focus in different focal points This creates a problem, doesn’t work because the patient is going to be confused in looking in different zones and will have a lot of glare and distortion Latest brand is IQ Vivity ○ Accommodative (ex: Crystalens and Trulian) Lens naturally bends to create accommodation so they made a lens that has the same movement as the natural lens for accommodation Accommodative effect of the lens as bending of the real lens  Near VA is bad and cannot create nature with plastic lens; will need glasses for near New EDOF IOLs: Extended Depth of Focus IOLs are like multifocals and focus more for far and intermediate-range of vision. Intermediate being computer working distance. Advantage over multifocals ( Ex Tecnis Symfony IOL , Tecnis Symfony toric, Tecnis Synergy, Vivity EDOF) ○ Aspheric ** and will have one focal point that increases in the periphery and provides vision for distance and intermediate zones only. Near zone is gone. ○ Limit aberration zones, good for vision; less glare and distortion IOL New Technology Light Adjustable lenses The Light Adjustable Lens is made of a special photosensitive material that changes the shape and power of your implanted lens in response to ultraviolet (UV) light to optimize your vision ○ Silicone, bending material that when using UVC, (365 nm) light, they bend and change the size of the IOL and corrects the refractive error that is residual or left over. It is precise in changing the lens. The Light Delivery Device (LDD) non-invasively delivers this UV light to precisely reshape your lens based on the visual correction that is needed to target your custom prescription. The FDA-approved LAL is Rx SIGHT New upcoming: the Perfect lens Are they successful?? The theory behind is successful. You change the shape of the lens and correct the residual RE. Are they popular?? No. We do not have enough information/data about it yet but it sounds great. But they do believe this is the future of IOL lenses. LIGHT TREATMENT SCHEDULE Initial Light Treatment is few weeks after sx ○ Why? They need to know how much residual RE. wait at least 2-4 weeks after surgery. Do the UV treatment and change the shape of the lens in diopters for the compensation. Additional Light Treatments ( amount varies)(as desired) ○ Need to compensate for it and will vary on the case. Few days after each prior light treatment ○ Has to be separated in 3 days (Do monday, and come back thursday to do it) Lock-In Treatments ○ After it is finished, you have finished the treatment and treat the whole thing and lock in the shape. 2 treatments required and few days apart. Remember the patient has to be protected by external UV so they must be wearing UV PROTECTION GLASSES the entire time when they are out. Light Adjustable IOL’s Contraindications ○ This IOL has a filter that does not allow UV in faster so you shouldn’t do this on IOL w/ UV adjustment with patients on medications that attract UV light Ex: Antidepressants (Phenothiazines), Amiodarone, Tetracyclines, Sulfas ○ Should not do on patients w/ macular disease ○ Taking cancer treatment: chemoxiphen - toxic to the retina and do not want to mix UV w/ it Advantages ○ Future of IOL surgery Disadvantages ○ Danger to the eye will damage the back of the eye because there is always some escape ○ The pupil must be VERY dilated to see the whole IOL (disastrous results) ○ Very very expensive $$$ Complications Post-Op Management (please know this) F/U visits: ○ 4 MAIN visits; can have more but 4 are required ○ 1st visit: 1 day ○ 2nd visit: 1 week ○ 3rd visit: 3-4 weeks ○ 4th visit: 6-8 weeks What is verified in each visit ○ VA ○ SLE Done in each visit Expect some inflammation; but the alarming ones (PDES rule) ○ IOP Done in each visit ○ DFE (not in all) Dilated pupil in 2nd and 3rd visit can be done unless really needed but it is dangerous so wait Dilate patient in 3rd or 4th visit to check retinal health ○ Ref (@ specific visit refraction has a value) Check Ref 3rd visit if there is RE left over after surgery Final rx is given 6-8 weeks (4th visit) to give the eye time to stabilize Things to be monitored: the 4-letter rule ○ Ptosis ○ Double (diplopia) ○ Erythema (red eye) ○ Swelling Cataract sc for the other eye/time lapse  ○ Yes but wait to operate at least 1 month or 2 months before other eye Post-Op Management Instructions/Topical meds Painkillers (take Advil or Aspirin) Eyeshield (wear at least for 1 week after surgery especially when they sleep) Antibiotic drops (never taper antibiotics) ○ Vigamox (Moxifloxacin), Moxeza (similar to Vigamox), Zymar (Gatifloxacin), Besivance (Besifloxacin), Ciprofloxacin, Tobramycin, Polytrim ○ ***used for 1 week then discontinued Steroid drops (for inflammation) (must taper steroids) ○ PredForte, Durezol ○ 1st week is used for QID for both steroids and NSAIDS ○ 2nd-3rd week: decrease to TID ○ 4th to 6th week: BID ○ 7th week -> QD and then stop NSAIDs (for inflammation) ○ Acular PF, Voltaren, Nevanac, Llevro (Nepafenac) IOP meds if needed? ○ ***(Boards ? and test questions) no prostaglandins glaucoma drops can be used after cataract surgery!!! Because prostaglandins can induce cystoid macular edema Latanoprost (Xalatan), Bimatoprost (Lumigan), Travoprost, Taflupros cannot be used Water/shower/swimming ○ Shower: always with a shield ○ Avoid forceful water in eye ○ No swimming for a month Strenuous activity/Exercise ○ Avoid for a month after cataract surgery Stress use of sunglasses Early (first 2 weeks after surgery) less emergent complications of cataract surgery Mild ptosis can occur and will go away Mild Diplopia and goes away in a few days Ocular HTN ○ IOP will go high! Don’t be alarmed Corneal edema (early acute) ○ Natural so you can use hypertonic solutions and present in the first 2 days Wound leak at corneal incision/Seidel test ○ Aqueous escaping and Seidel will ○ Apply fluorescein and ask patient to blink forcefully and see a fountain ○ Always check anterior chamber intact if seidel test (+) If the aqueous is leaking, the anterior chamber will shrink in size and this is alarming  Anterior uveitis >>> consequence UGH Hyphema >>> consequence UGH IOL decentration/pupillary capture (consequences) ○ Always check decentration in the first 2 weeks More worrisome in early complications: ○ Persistent IOP increase Dangerous because it can lead to glaucoma afterwards ○ Wound leak w/ flat AC Flat AC due to escape of this is an emergent Treat w/ cycloplegics, patch the eye and have to close the leakage area The danger of flat AC is that it can lead to *****(board? and test) choroidal detachment Choroid gets separated from the sclera ○ Capsular rupture w/ vitreous prolapse >> Vitreous wick syndrome (other consequences) Vitreous prolapse -> vitreous escape -> Vitreous goes through pupil & AC, and touches the endothelium of the cornea Corneal endothelium damage from the vitreous is vitreous wick syndrome** ○ Causes raise in IOP, macular edema, RD ○ Complete IOL dislocation ○ Malignant glaucoma 2ndary angle closure glaucoma!! Aqueous escapes after surgery, goes to the back of the eye with vitreous, lots of liquid in posterior vitreous chamber and causes damage Aqueous misdirection ○ Retinal breaks/Retinal detachment/Choroidal detachment ○ Endophthalmitis even in the first 2 days and even 2 weeks (most serious infection after cataract surgery) Intermediate to Late (after a month, 3-4 weeks) Complications of Cataract Surgery Chronic anterior uveitis ○ Uveitis can be treated w/ steroids but will be on medications for along time and ends up harming the patient Severe ocular HTN leading to glaucoma ○ IOP that cannot be controlled, very IOP! More IOP = more probability of developing glaucoma and damaging the ON Chronic corneal edema >>> CD ○ Edems that is going to be there the first day but after 48 hrs should disappear ○ If it does not disappear, the edema will decompensate due to chronic corneal edema Epithelial down growth (Dr. B’s favorite) ○ Incomplete wound closure  ○ Epithelial cells from the conj will grow over and form a membrane on the corneal endothelium ○ Has serious complications Corneal damage Increase IOP (pupillary block glaucoma) Clog the angle (cells go and clog the Schlemm’s canal angle) Use cycloplegics and treat cornea with freezing protectant ○ Late hyphema (eight-ball hyphema) ○ Red anterior chamber (blood will cause damage) Will damage corneal endothelium IOP increased (2ndary open-angle glaucoma) ○ ○ Not great to have; little hyphema is fine ○ (board ? and test ?): how to treat NO ASPIRIN AND NSAIDS Head inclination Steroids to help the inflammation and decrease the amount of bleeding Control the IOP Irrigate the anterior chamber to take out the blood Medication: used in hospital and treated in hospital: also to decrease bleeding: aminocaproic acid (antifibrinolytic agent to prevent further bleeding and this is done in advanced treatment for hyphema) Post capsule opacification Cystoid macular edema Serious complications of cataract surgery Infectious endophthalmitis ○ Rare but can cause permanent severe reduction of vision Can happen w/in few days (3-4 days or 1st two weeks) but it can happen later too but it is harder In the early: first 2 weeks  Delayed: same infection after 6 weeks of cataract surgery What does this tell us? Gives us the info. that the infection is fungal, not bacterial because fungal takes time Severe delayed infections take time, we’re facing fungal. Not bacterial ○ Most cases w/in 2 weeks of surgery but later ○ Typically, patients present w/ a short hx of a reduction in their vision and a red painful eye ○ ALL structures of the eye are affected ○ This is an ophthalmic EMERGENCY***** ○ 1st: take a sample from vitreous and anterior chamber Send it to treat whatever organism is involved with the infection AC paracentesis ○ Vitreous TAP and TX Go with nurses and suck the vitreous out ○ Don’t wait for lab results so treat immediately Not topical or oral; has to go IV ○ Tx: Intravitreal injections of antibiotics or Vitrectomy Fortified topical antibiotics/oral antibiotics Vancomycin** and Amikacin *** (boards?) When VA is LP or worse is when to perform vitrectomy! (boards ?) Topical steroids for inflammation Oral steroids for inflammation Tx in delayed endophthalmitis Fungal: Amphotericin B** MECINOZAL. TETRACONZAOLE F/U check-ups : every 24 hours Critical period to see improvement: 48 hours after treatment ○ If no improvement or eye has gotten worse: eye is gone ○ Posterior capsular opacification (can happen early as few days, weeks, months, 2-3 years) ○ PMMA causes a lot of posterior capsular opacification ○ The difference between is where they come from ○ 1) Fibrous type Opacification comes from residual epithelium cells that stay there in the capsule (anterior epithelial cells) Fibrous metaplasia ○ 2) Pearl type (Elschnig pearls) Comes from residual equatorial cells ○ Treatment is by YAG capsulotomy Cleaning the capsule w/ a cross-pattern (12-6, 3-9, 1-7) Capsular opening size and complication if incorrect size Has to do correct size of laser If too small, patient will be looking though opacification and will have a lot glare distortion If it too big, IOL may be dislocated Choosing the best time for YAG capsulotomy (very important) Early YAG: creates a lot of complications ○ Will dislocate the IOL ○ Will create vitreous prolapse (causes macular edema, RD, Vitreous wick) ○ Cannot be done even 3 months after cataract surgery, must wait 6 months! Pupil before procedure Should not dilate pupil to avoid lens dislocation! Complications of YAG capsulotomy- must have enough training Like any procedure, YAG laser is being used and may have complications (life is not perfect :( Increased IOP  Cleaning capsule and doctor’s error: break the IOL and dislocate the IOL May burn the cornea because we are working with a laser (epithelial burns or endothelial damage, decrease endothelial cells in the cornea) Anterior chamber inflammation: uveitis Too much laser or excessive treatment: will create vitreous prolapse*** CME and retinal detachment ○ Secondary cataract PCO ○ Fibrous membrane on top of IOL that was placed Soemmering’ ring posterior capsular opacification (can laser and open up post cataract surgery) ○ Capsule that is open and being cleaned ○ Was this done correctly? No because patient is looking through a clear zone and through opacification zones in which this causes glare distortion. This shows that the opening was too small.  ○ Vitreous prolapse into anterior chamber ^ , vitreous is coming through the pupil and damages ○ Vitreous prolapse w/ Vitreous wick syndrome ○ Connection with the cornea and pulling the vitreous, Vitreous wick syndrome