Ophthalmology for Oxford course and Duke-Elder exams

Lens and cataracts

Cornea does majority of refracting (due to air-cornea interface differential densities). Lens only 1/3.

TERMINOLOGY
Phakic = natural lens; pseudophakic = artificial lens; aphakik eye = cataract removed but not replaced

ANATOMY
Recall that the lens has 3 layers – the outer capsule, the middle lens cortex, and the inner hard lens
nucleus. Cataracts can form at any of the different layers, and the location gives clues of the
causative insult and explain visual complaints. The lens layer become more relevant in surgery – with
cataract extraction, a round hole is tear through AC, cortex and nucleus is sucked out, and prosthetic
lens injected in the remaining outer capsule (acts like a sac).

The lens is suspended behind iris, by zonular fibres. These fibres attach at equator of lens and
connect lens to surrounding ciliary body. The ciliary body is a ring of muscle sitting behind iris.
Trauma and surgery can break zonules, causing lens to de-centre or fall to back of eye

ACCOMODATION
The ciliary body is a ring of muscle that sits directly underneath iris. It can only be seen O/E with
mirrors. The ciliary body is important because (1) it produces aqueous fluid that nourishes the eye
and (2) controls lens focusing. When the ciliary sphincter muscle contracts, the zonules relax, and
lens round up – allowing close-up reading.

CATARACTS
The lens begins as a clear magnifying glass, but can opacify with time. Most cataracts are of
idiopathic aetiology, though many associated conditions ca lead to congenital and environemtally-
induced lens opacities.

NUCLEAR SCLEROTIC CATARACTS

NSCs are MC type of cataract, and some consider them to be normal maturation of lens. Over time,
lens become larger and brunescent (yellow or brown), especially in the denser central nucleus. If this
goes on logn enough, the opacity eventually leads to visual obstruction and glare problems. The lens
can become so big that it pushes the iris forward, placing the patient at risk for angle closure
glaucoma. With far-advanced cataracts, the middle cortical layer liquefies and become milky white
while the nucleus gets hard and falls to the bottom of capsular bag. These end-stage Morgagnian
cataracts are rarely seen in DCs and are hard to surgically remove. End-stage glaucoma can leak
proteins into aqueous fluid and results in macrophage clogging up trabecular meshwork, also
contributing to glaucoma.

Some patients w NSCs develop “second sight” where it seems that the vision improves. This is
because the round cataracts lens is more powerful, so offsets co-existing presbyopia, allowing older
patients to read better. Their vision has not improved – it is just that their cataracts act as weak
bifocals.

POSTERIOR SUBCAPSULAR CATARACTS

PSCs form on the back of the lens – on the surface of posterior capsular bag. These cataracts tend to
occur with patients on steroids, DM, and Hx ocular inflammation. The opacity looks like
breadcrumbs or sand sprinkled on back of lens. This posterior location creates significant visual
difficulty despite its innocuous appearance on slit-lamp. This is due to optics of the eye. The eye has
overall refractive power of 60D (40D from cornea, 20D form lens) – the nodal point of the system is
near the back of the lens. As you can closer to this nodal point, a greater number of light rays will be
Ophthalmology for Oxford course and Duke-Elder exams

affected. Thus small posterior cataracts cause more significant vision problems than anterior ones. It
is quite common, and often occur in conjunction with some degree of NSC.
CONGENITAL CATARACTS
Lens opacities in children are of concern because they can mask deadly disease (DDx for leukocoria –
see “paediatrics”), and because they can have devastating effects on LT vision.

Can be idiopathic or inherited. If small or anteriorly located, they may be visual insignificant.
However, when approaching a leukocoric pupil – R/O potentially deadly disease. This includes
cataracts masqueraders like retinoblastoma, and deadly causes of cataracts like TORCH infection and
galactosaemia.

True cataracts needs to be removed quickly, usually within the 1 st 2 months of life, because they are
highly ambylogenic. Cataract surgery is challenging in this age-group as children have impressive
inflammatory responses and are not easy to examine pre-op and post-op. After taking cataract out,
you usually do not implant a prosthetic implant in newborns, but wait a few years because eyes are
still growing. The family must deal with powerful aphakic glasses or contact lens placement until
child is old enough for secondary lens implantation.

TRAUMATIC CATARACTS
Cataract can form after blunt or penetrating injuries to eye. These traumatic cataracts are more
common in young men. When the outer lens capsule breaks, the inner lens swells with water and
turns white. The lenses are very soft and easy to suck out, but removal and implant placement can be
complicated as blunt force often tears zonular support. If lens is barely hanging in position, consult a
retina specialist to remove the cataract from behind (pars plana approach) – to keep lens from falling
back in the eye.

POSTERIOR CAPSULAR OPACIFICATION

PCO is not true cataracts, but an after cataract that forms after cataract surgery. During this surgery,
the cortex and nucleus is sucked out and the new lens is injected into the remaining capsule. Residual
lens epithelial cells are left behind after surgery. These orphaned epithelial cells get confused and
migrate along the back surface of implant and opacify the posterior capsular bag.

This is a common occurrence and easily treated in clinic with a laser (YAG capsulotomy). A YAG laser
is used to blast a hole in the posterior capsule (not a large hole as you don’t want implant to fall into
back of eye, just big enough for visual access).

LENS SWELLING
The cells that make up adult lens have no innervation or blood supply. They derived entirely from
surrounding aqueous fluid. Because of this low O2 tension, these lens cells survive almost entirely on
glycolysis. Poorly controlled DM can have very high glucose – if high enough, lens metabolism can
shunt down a sorbital pathway – this build-up in lens creates an osmotic swelling of lens with
resulting refractive changes. If diabetic patient complains of episodic blurring, find out what their
HbA1C. If it is due to high BM – do not Rx glasses, as the visual changes may just be from lens
swelling.
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LENS DISLOCATION
Lens can dislocate from traumatic force e.g. punch to eye, but also dislocated due to inherited
diseases that affect zonular strength.

MARFAN’S
AD disease of firbillin. These patients have tall body habitus, arachnodactyly and can have lens
subluxation with lens dislocating upwards. This can create large astigmatism as patient is looking
through edge of lens. This may eventually require cataract extraction.
HOMOCYSTINUREA
AR disorder due to absence of cystathionine B-synthetase, which catalyse conversion of
homocysteine to cystathionine. These patients have Marfanoid habitus, arachnodactyly, and 50%
incidence of mental retardation. The lens zonules are largely composed of cysteine, and without
good cysteine, the zonules become brittle and may break. The majority of these patients develop
downwards lens dislocations. They also have poor peripheral circulation, prone to
thromboembolism under GA.

CATARACTS SURGERY
Pre-op (are they suitable?)
 Ophthalmoscope rough guide: if you can see in (through their lens)  the patient can see
out. More objectively – use 20/50 as guideline for surgery (minimal driving acuity).
 Anaesthetic risk?
 Patient preference or condition (if bedbound and happy with vision, no need).
 Acuity isn’t everything.
o One big problem is glare – in the dark, patient see fine. But drive into sun or into
headlights at night – they are blinded by scattering of light through their hazy
cataracts. So they stop driving at night.
o Test glare via shining a light into their eye (or more formally through brightness
acuity tester, BAT device – a light-bulb illuminated hemisphere with a view hole that
induces glare).
o Another indication is the presence of underlying retinal disease e.g. DR. If cataracts
interfere with careful fundus examination or laser Tx, lens must come out!
 Pre-op measurements – choosing the implant power
o The goal in cataract surgery is to put the ideal power IO lens into eye so patient
won’t need extra glasses for viewing distant objects. Formally, formulas are used,
but in simple terms this can be determined by:
 Corneal curvature. The cornea-air interface actually performs the majority
of refractive power of eye. It performs approximately 40D of refraction,
while lens makes up the last 20D. A person with powerful cornea will need
less powerful lens. The curvature is measured with a keratometer.
 Length of eye. The shorter the eye, the more powerful lens you will need to
focus onto retina. Measure this with A-scan mode of hand-held USS.
Operation
1. Anaesthesia
a. Dilate pupil, prep, and anaesthetise the eye (simple tetracaine eyedrops)
b. Rarely retrobulbar block by lido/bupiv injection into retrobulbar muscle cone to
knock out sensation through V1 as well as KO eye movements via CN3 and CN6. The
CN4 actually runs outside the muscle cone, so there is still some residual eye torsion
movement after block.
2. Enter the eye
a. Cutting through cornea (fastest), or spend more time tunnelling in from sclera (but
can extend easily if run into surgical complications).
Ophthalmology for Oxford course and Duke-Elder exams

3. Capsulorhexis
a. Tear a hole in anterior capsule of the lens (rhexis). Important step! If rhexis too
small, harder to get cortex and nucleus out; as well as risk incorrect tear (rip
extending radially outwards to equator).
b. If you lose your capsule, you lose pieces of lens into back of eye. Poor capsular
support also makes implant placement harder.
4. Phacoemulsify
a. Phaco handpiece to carve up lens nucleus. Machine oscillates at ultrasonic speeds to
allow grooving of ridges into lens.
b. After grooving, the lens can be broken into small pieces and sucked out one-by-one.
5. Cortical removal
a. Cortex is soft but wants to stick to capsular bag. You don’t want to leave too much of
it because it can cause inflammation and PCO.
b. Strip it off with suction and vacuum it out
c. Care with posterior capsule – because it is the support for the new lens, and also
maintain barrier between anterior and posterior chambers, keeping vitreous jelly
from entering AC.
6. Lens insertion
a. Use foldable lens that can be directly injected into capsule bag
b. If lost capsular support (e.g. break posterior capsule during phaco or cortex
removal), lens placed onto of the entire capsular bag, right behind iris (in the
sulcus).
i. Sulcus is the potential space between lens capsule and abck of iris.
c. If support for this sulcus placement is questionable (i.e. lots of complication), lens
can be placed in anterior chamber on top of iris, or sutured to back surface of iris
(tricky!)
7. Closure
a. Many small incision corneal wounds are self-healing. But some require closure with
10-0 nylon suture that eventually biodegrade.
Post-op
 Abx drop e.g. ciprofloxacin
 Shield over eye
 F/U next day. Continued usage of Abx drop but also steroid drop to reduce inflammation.

TINTED YELLOW SUNGLASSES

Makes image sharper because tinting limit spectrum of colour that hits retina. (All lens have
chromatic aberration as different wavelengths bend differently, so images don’t focus perfectly – the
blue component focuses slightly in front of retina, red slightly behind retina).