11.3 Cataracts Metabolism takes place via anaerobic glycolysis in the epithelium.

Energy is needed for ion pumps and protein synthesis. It also provides for antioxidants (glutathione) Fluid flux: water enters the lens via the thin posterior capsule. It is pumped out of the anterior epithelium. Lens growth. Bow cells elongate and loose nucleus form fibres. Lens fibres elongate and meet a suture lines. There is a continuous addition of fibres to outer coats with age, leading to increased protein density. Compression promotes cataract formation, and yellowing is from chromaphores accumulating. Also, expansion and ageing give posterior capsule thinning. Types of cataract include congenital, acquired and senile (most common) In the lens anterior, there can be epicapsular stars, persistent pupillary membrane (PPM), and lenticonus (bulgy cone lens cortex and thinning of capsule in the anterior) In posterior lens: can get mittendorf dot. This can affect vision dramatically if the dot is on the nodule point. There can also be nets or whorls resulting from vitreous condensations. Congenital: It is not usually sight debilitating. It can be associated with neural and underdevelopment and tropia. It is usually non-progressive. The cataract would be axial or sutural. There will be chalky white clusters or may be polychromatic. If it is cerulena it refers to blue dots in the deep cortex (near nucleus). If it is pulverulent it is a dense cataract located in embryonic nucleus. It if is zonular, its a "zone of cataracter"in the outer nucleus. If it is coronary, when zonular has riders (wedges/lines) into the cortex. If it is sight debilitating, it can be a remnant mesodermalvasuclar tissue (mitttendorf dot) in the posterior pole. It can be associated with a systemic disorder such as galactosemia or rubella. In this case a GP should perform a blood work up. Acquired cataracts in many cases are cataractogenic in a dose and time dependent manner. It is most common from cortico-steroids, antipsychotics, some cholesterol reducing drugs, miotics, pesticides, etc. Secondary/metabolic cataracts are most common from diabetes, galactosemia, myotic dystrophy, atopic dermatitis, various syndromes (down's, marfans, alport), and associated eye disease such as (retinitis pigmentosa, uveitis and glaucoma) Cataracts could also be from trauma such as blunt injury, explosive, penetrating or radiating heat or electrical shock. Early changes may reserve. If there is severe trauma, there may be subluxation of the lens. The cataract could be in a rosette or stellate form.

Subjective- symptoms

migration of bow cells.how do you detect them Often it is advised to wait and watch. Opacities block light to form shadows. diplopia/polyopia. 1/8 cen) 12. Surgery: as cataract has few ocular complications. If it is in front of the nodal point. There is absorption by lens protein. This problem is greatest in posterior sub cap cataract as it is closest to the nodal point. low contrast. surgery can be delayed. The patient looks out through a hole and VA is measured with and without background light. Posterior sub-capsular cataract is the least common form. This is where the lens is divided into pie sectors. In direct illumination. It should be taken if there are eye complications or if it impedes life-style.An altered refractive state gives poor vision. or by Wisconsin. The red reflex is formed by light reflected form the RPE/choroid. ripples in indirect illumination. It is an illuminated spherical bowl. Though not a treatment. 8 inner and 8 outer zones. Sometimes you should intervene especially with neonates preventing amblyopia onset or surgery with aphakia. and thinning of posterior capsule. The lens appears like a yellow haze in the nucleus and post cortex. It can also be due to glare sensitivity. there is no depth in a diffuse setting. there should only be a 2 line loss. Glare testing is conducted via a brightness acuity tester (BAT). Only 1% of surgeries have unsuccessful outcomes. Recording eg (5/8 pheriph. Patients have a hyperopic shift in this case as well as increased glare. It is caused by medications. . The location makes it visually most debilitating. If it is behind the nodal point in the vitreous. In some cases of cataract.2 Nucleus sclerosis is caused from light damaging proteins. Objective-signs Signs include a red flex such as from a camera. Mydriasis in this test gives a worst case outcome. Cortical cataracts have a wedge and spoke appearance. With glare. but reflection at the back of the lens makes posterior lens coloured. The most common glare test is using a pen torch. There is water accumulation between the fibres. it is an “against” movement. mydriasis may improve vision as light bypasses cataract. glare sensitivity. There is often a myopic shift. the reported disability appears inconsistent with the relatively good VA. Usually there is a 2 line VA loss between high contrast and low contrast. Assessment. there is a “with” movement. It is a cataract in the posterior portion of the lens. They can be graded by comparative photos. It can be due to low contrast VA.

3 Historical surgical procedures: couching.Plan. Subsequently. It progressively divides and conquers. There is the Intra capsular cataract extraction (ICCE). It retains a normal vitreous. Also the option of monovision can be considered if the patient has had past experience. which is now the treatment of choice. Topical (phaco): drops Topical and intra ocular mydriatic. It in essence is a jack hammer with a vacuum cleaner. low luminance. With refractive outcomes. visually evoked response. This gets to the ganglia. LC/HC. lens is removed. and the extra capsular cataract extraction (ECCE). It involves pushing the lens backwards (surgical subluxation). hyperacuity.25D. It also uses a phacoemulsification which involves a high speed agitator that disrupts the lens. and decreasing the chance of retinal detachment. diabetics have a high rate of complications. there are 2 types of lens extractions. There are 2 types of ECCE: Conventional expression where we take the nucleus out and. By cutting loose a corneal suture. It can also contribute to astigmatism. Needle injected between the EOM in the retrobulbar. It carriers a suction that removes broken up tissue. laser interferometer or an MfERG. ECCE: This method requires a smaller cut (3-5mm). low luminance VA. and there is no “bag” to carry IOL. Needling involves the rupture of a capsule with a fine needle. this requires a large surgical cut of up to 20mm. This is outdated and may be used in 3rd world countries. Sutures at times can pull on the cornea. Also. hence increasing the chance of ret detachment. which takes the lot. Lens extraction by ICCE. In addition. This extraction leaves the bag/capsule intact. Currently. low CS VA. phakoemulsification. It also retains a bag to carry the IOL. Tests of optic nerve function include APD. increasing curvature. The IOL can be placed in the anterior chamber or facilitates vitreous prolapse. surgery may still be of benefit but you should have lower expectations. it can lead to ATR . There is injection of a chromotrypsin to break the zonules. the state of the macula and optic nerve needs to be considered. often myopes prefer to remain myopic and hyperopes prefer either plano or +0. Ocular anesthetics: General (rare) Local: ICCE and ECCE. 12. Testing of macula function can be by colour discrimination. This is done by softening the cortex and squeezing the nucleus out. If there is poor prognosis. Wound closure: Some ECCE and ICCE will be closed with sutures.optometric & medical management There should be a guarded but positive prognosis for surgery. is a large cut made superiorly. The anterior capsule is torn and there is mechanical removal of the lens. However.

Here there is no control of astigmatism.greater than 2. It may also involve a vitrectomy. Sutures that rub and irritate will need removal. sutural astigmatism. sutured in the sulcus. Surgery is more expensive for the patient and for the surgeon.5D). and tightening suture can lead to WTR astig.5D. Correction can be via spectacles. traumatic. Other forms of surgical methods involve a pars plana lensectomy. Though rare. CL. which is an approach behind the iris. and AC debris and corneal striae in the anterior eye. No stitch surgery is performed in ECCE. dysphotopsia and CME. In cases with high astig. It is OK for low ADDs (up to 1. The IOL can be placed in the anterior chamber where it is fixed on the iris. Aphakia produces 10-12D of hypermetropia. complications usually occur early. dividing the nucleus into 1/4s and conquering the nucleus. or an IOL. A fento-second LASER can be used. and IOL displacement can also occur.astig. It gives a better control and a better outcome. and can be single vision/astig. and 6 weeks post surgery. Incisions are usually in a step method.sutures along 180 can be removed to reduce pull. . congenital and diabetic patients. Monovision can be performed by unequal refractive states. An IOL also has UV block protecting the retina. It is a complicated procedure for secondary. perceived glare or halos (dysphotpsia). Management is with a YAG laser of tissue and capsule. 3 weeks. 12 weeks. wound leak causing endophthalmitis. There can be ptosis. it can induce suppression. or can be placed in the posterior chamber in the bag. papillary block. Late post surgical complications include suture exposure. It can make an incision. 6 weeks. This form is the best location and has the best optics. This needs a conservative management with NSAID 2 week pre surgery. multifocal or simultaneous focus or movable IOL. Capsular opacification can occur 1-2 years post surgery. but in high adds. Post surgical follow up is at 1 day. 1 year. and the AC angle is also fixed. 1 week.

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