Cataract Notes

7/31/2019 Cataract Notes

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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 theposterior 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


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An altered refractive state gives poor vision, low contrast, glare sensitivity, diplopia/polyopia. This

problem is greatest in posterior sub cap cataract as it is closest to the nodal point.

Objective-signs

Signs include a red flex such as from a camera, ripples in indirect illumination. The red reflex is formed

by light reflected form the RPE/choroid. Opacities block light to form shadows. If it is behind the nodal

point in the vitreous, there is a with movement. If it is in front of the nodal point, it is an against

movement. In direct illumination, there is no depth in a diffuse setting.

There is absorption by lens protein, but reflection at the back of the lens makes posterior lens coloured.

They can be graded by comparative photos, or by Wisconsin. This is where the lens is divided into pie

sectors, 8 inner and 8 outer zones. Recording eg (5/8 pheriph. 1/8 cen)

12.2

Nucleus sclerosis is caused from light damaging

proteins. The lens appears like a yellow haze in the

nucleus and post cortex. There is often a myopic shift.

Though not a treatment, mydriasis may improve

vision as light bypasses cataract.

Cortical cataracts have a wedge and spoke

appearance. There is water accumulation between

the fibres. Patients have a hyperopic shift in this case as well as increased glare.

Posterior sub-capsular cataract is the least common form. It is a cataract in the posterior portion of the

lens. The location makes it visually most debilitating. It is caused by medications, migration of bow cells,

and thinning of posterior capsule.

Assessment- how do you detect them

Often it is advised to wait and watch. Sometimes you should intervene especially with neonates

preventing amblyopia onset or surgery with aphakia.

Surgery: as cataract has few ocular complications, surgery can be delayed. It should be taken if there are

eye complications or if it impedes life-style. Only 1% of surgeries have unsuccessful outcomes.

In some cases of cataract, the reported disability appears inconsistent with the relatively good VA. It can

be due to low contrast VA. Usually there is a 2 line VA loss between high contrast and low contrast. It

can also be due to glare sensitivity. With glare, there should only be a 2 line loss.

Glare testing is conducted via a brightness acuity tester (BAT). It is an illuminated spherical bowl. The

patient looks out through a hole and VA is measured with and without background light. Mydriasis in

this test gives a worst case outcome. The most common glare test is using a pen torch.


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Plan- optometric & medical management

There should be a guarded but positive prognosis for surgery. With refractive outcomes, often myopes

prefer to remain myopic and hyperopes prefer either plano or +0.25D. Also the option of monovision

can be considered if the patient has had past experience. Also, the state of the macula and optic nerve

needs to be considered.

Testing of macula function can be by colour discrimination, low CS VA, low luminance VA, hyperacuity,

laser interferometer or an MfERG.

Tests of optic nerve function include APD, visually evoked response, LC/HC, low luminance. If there is

poor prognosis, surgery may still be of benefit but you should have lower expectations. In addition,

diabetics have a high rate of complications.

12.3

Historical surgical procedures: couching. This is outdated and may be used in 3rd

world countries. It

involves pushing the lens backwards (surgical subluxation). Needling involves the rupture of a capsulewith a fine needle.

Currently, there are 2 types of lens extractions. There is the Intra capsular cataract extraction (ICCE),

which takes the lot, and the extra capsular cataract extraction (ECCE). This extraction leaves the

bag/capsule intact. There are 2 types of ECCE: Conventional expression where we take the nucleus out

and, phakoemulsification, which is now the treatment of choice.

Lens extraction by ICCE, is a large cut made superiorly. There is injection of a chromotrypsin to break the

zonules. Subsequently, lens is removed. However, this requires a large surgical cut of up to 20mm, and

there is no bag to carry IOL. The IOL can be placed in the anterior chamber or facilitates vitreous

prolapse, hence increasing the chance of ret detachment.

ECCE: This method requires a smaller cut (3-5mm). It retains a normal vitreous, and decreasing the

chance of retinal detachment. The anterior capsule is torn and there is mechanical removal of the lens.

This is done by softening the cortex and squeezing the nucleus out. It also uses a phacoemulsification

which involves a high speed agitator that disrupts the lens. It progressively divides and conquers. It

carriers a suction that removes broken up tissue. It in essence is a jack hammer with a vacuum cleaner.

It also retains a bag to carry the IOL.

Ocular anesthetics:

General (rare)Local: ICCE and ECCE. Needle injected between the EOM in the retrobulbar. This gets to the ganglia.

Topical (phaco): drops

Topical and intra ocular mydriatic.

Wound closure:

Some ECCE and ICCE will be closed with sutures. Sutures at times can pull on the cornea, increasing

curvature. It can also contribute to astigmatism. By cutting loose a corneal suture, it can lead to ATR


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astig, and tightening suture can lead to WTR astig.

No stitch surgery is performed in ECCE. Here there is no control of astigmatism. Incisions are usually in a

step method.

Sutures that rub and irritate will need removal. In cases with high astig- greater than 2.5D- sutures along

180 can be removed to reduce pull.

Aphakia produces 10-12D of hypermetropia. Correction can be via spectacles, CL, or an IOL. The IOL can

be placed in the anterior chamber where it is fixed on the iris, and the AC angle is also fixed, or can be

placed in the posterior chamber in the bag, sutured in the sulcus. This form is the best location and has

the best optics. An IOL also has UV block protecting the retina, and can be single vision/astig, multifocal

or simultaneous focus or movable IOL.

Other forms of surgical methods involve a pars plana lensectomy, which is an approach behind the iris. It

is a complicated procedure for secondary, traumatic, congenital and diabetic patients. It may also

involve a vitrectomy.

A fento-second LASER can be used. It can make an incision, dividing the nucleus into 1/4s and

conquering the nucleus. It gives a better control and a better outcome. Surgery is more expensive for

the patient and for the surgeon.

Monovision can be performed by unequal refractive states. It is OK for low ADDs (up to 1.5D), but in

high adds, it can induce suppression.

Post surgical follow up is at 1 day, 1 week, 3 weeks, 6 weeks, 12 weeks, 1 year.

Though rare, complications usually occur early. There can be ptosis, papillary block, wound leak causing

endophthalmitis, perceived glare or halos (dysphotpsia), and AC debris and corneal striae in the anterior

eye, and IOL displacement can also occur.

Late post surgical complications include suture exposure, sutural astigmatism, dysphotopsia and CME.

This needs a conservative management with NSAID 2 week pre surgery, and 6 weeks post surgery.

Capsular opacification can occur 1-2 years post surgery. Management is with a YAG laser of tissue and

capsule.

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