ophthalmology

Lectures: Dr. Giyath aldeen

Lens
Anatomy of the lens
The crystalline lens is a biconvex, avascular transparent structure enclosed
by a capsule.
The lens consists of:
1- Nucleus: the central compacted core, which represents the older lens fibers
formed during intrauterine life and early years of life.
2- Cortex: represents the newly formed epithelial cells, which elongate to
form new lens fibers (which are softer than that of nucleus) surrounding the
old fibers (nucleus). These new lens fibers are continuously laid down
subcapsularly throughout life, resulting in that the older layers acquire
progressively deeper localizations within the lens.
3- The capsule: which is the thickest basement membrane in the body and
responsible for moulding the lens substance during accommodation.

Cross
section
through
the lens
- A ring of zonular fibers, which insert in the equatorial region, suspends the
lens from the ciliary body. As the zonule keeps the lens attached to the ciliary
body, it can mould and change the shape of the lens during accommodation.
Contraction of the ciliary muscles causing decrease in the tension of zonule on
the lens capsule which is change the lens shape to more sphere by its elasticity
and increasing the power of lens. "Accommodation"
- The lens grows in both anteroposterior and equatorial dimensions throughout
life. It is the only organ in the body which is continuously grow to the end of
life.

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Symptoms and signs of diseases of lens:
1- Cataract: lead to painless gradual impairment visual acuity.
2- Presbyopia: decrease in accommodation (due to decreased elasticity)
leading impairment of near vision.
3- Nuclear sclerosis: lead to increase the difference between the refractive
indices of the nucleus and cortex causes "index (lenticular) myopia".
4- Monocular diplopia: due to opacification or tilting of lens producing two
images in the same eye due to diffraction of light.

Cataract
The normal lens is transparent, any congenital or acquired opacity in the lens
or its capsule, irrespective to the effect on vision, is a cataract.
Types of cataract:

1- According to its site within the lens:

a- Posterior subcapsular: just anterior to the posterior capsule.
b- Anterior subcapsular: just posterior to the anterior capsule.
c- Cortical: cataract involving the cortex.
d- Nuclear: cataract involving the nucleus.
Cataract can be detected by slit-lamp, direct ophthalmoscope (as black dots
in the red reflex or total loss of red reflex if it is mature), B-scan and even by
naked eye as leukocoria (white pupil) when it is mature.

2- According to maturation:
a- Immature: if there is involvement of part of lens (any part), and other
parts are still transparent.
b- Mature: complete opacification of the entire lens.
c- Hypermature Cataract: is a mature cataract in which there is partial
liquefaction of the cortex, leakage of resultant fluids from the lens towards
aqueous humor, shrinkage of lens and folding of capsule. So, the size of the
lens become smaller than when it is mature.
d- A morgagnian cataract is a hypermature cataract in which the total
liquefaction of the cortex has allowed the nucleus to sink inferiorly.
e- Intumescent Cataract (phacomorphic cataract): In case of immature or
mature cataract, if there is influx of fluids from aqueous humor towards lens
lead to swelling of the lens. Some time, this swelling will progress to a level
sufficient to occlude the angle of AC results in "Intumescent Glaucoma".

3- According to its onset: into either acquired or congenital.

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 Acquired cataract
Causes:
1- Age-related cataract: due to biochemical changes that occur with
advancing age in the proteinaceous matter of the lens converting soluble into
insoluble protein causing opacification, usually develops after the age of 60.

2- Pre-senile cataract: develops before the age of 60 in the following

conditions:
a- Diabetes Mellitus: high level of glucose in the lens is metabolized into
sorbitol by aldose reductase, then accumulation of sorbitol causes secondary
osmotic overhydration, refractive changes (Myopia), and then cataract.
b- Myotonic dystrophy: 90% of patients develop cataract in the third decade.
c- Atopic dermatitis: 10% of patients with severe atopic dermatitis develop
cataract in the second to fourth decades of life.
d- Neurofibromatosis type 2.

3- Traumatic cataract: trauma is the most common cause of unilateral

cataract in young individuals:
a- Direct penetrating injury to the lens.
b- Concussion by blunt.
c- Electrical shock is a rare cause.
d- Ionizing radiation.
e- Infrared radiation; as in glassblowers.

4- Drug-induced cataract:
a- Steroids: both systemic and topical steroids are cataractogenic.
b- Chlorpromazine: both corneal and lenticular deposits are dose related and
usually irreversible, high dose (>2400 mg daily) may cause retinotoxicity.
c- Amiodarone (anti-arrhythmic): lens deposits occur in 50% of patients.
d- Gold: lens deposits occur in 50% of patients on treatment for longer than 3
years.
e- Allopurinol: used in hyperuricaemia and chronic gout.

5- Secondary cataract: is a complicated (secondary) cataract develops as a

result of some other primary ocular disease:
a- Chronic anterior uveitis: it is the most common cause of secondary
cataract.
b- Acute congestive angle-closure glaucoma.
c- High (pathological) myopia.
d- Hereditary fundus dystrophies, such as retinitis pigmentosa.

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Treatment of catract: SURGERY
There is NO effective medical treatment
.
Indications of surgery:
1- Visual improvement: is the most common indication, whether it is mature
or immature. If the patient feels that his vision is not enough to perform daily
requirements, surgery is indicated.
2- Medical indications: e.g., Intumescent Cataract (phacomorphic cataract)
which might lead to intumescent glaucoma. Other example is dense cataract
impaired visualization of retina or its laser treatment in diabetic patients.
3- Cosmetic indication: is rare, as mature cataract causing white pupil
(Leukocoria).

Anesthesia used is general, local, and topical. Choices one of them is according
to method of surgery, general health of the patient and surgeon preference.
Biometry
Biometry facilitates calculation of the lens power likely to result in the
desired postoperative refractive outcome; in its basic form this involves the
measurement of two ocular parameters, keratometry and axial (anteroposterior)
length.
Anaesthesia
The majority of cataract surgery is performed under local anaesthesia (LA),
sometimes in conjunction with intravenous or oral sedation. General
anaesthesia is required in some circumstances such as children and many young
adults, very anxious patients,some patients with learning difficulties, epilepsy,
dementia and those with a head tremor.
•Sub-Tenon block involves insertion of a blunt-tipped cannula through an
incision in the conjunctiva and Tenon capsule 5 mm from the limbus
inferonasally and passing it around the curve of the globe through the
sub-Tenon space.
•Peribulbar block is given through the skin or conjunctiva with 25-mm
needle. It generally provides effective anaesthesia and akinesia. Penetration of
the globe is a rare but severe complication, and for this reason peribulbar is
avoided, or approached with great caution in longer eyes .
•Topical anaesthesia involves drops or gel which can be augmented with
intracameral preservative-free lidocaine.

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Types of cataract surgery:
1- Intracapsular cataract extraction (ICCE) ± AC IOL (anterior chamber,
intraocular lens): →
Need large circumferential, 10-12mm,
about 160° limbal or corneal incision.
Removal of catractous opacified lens
totally by insertion a cryoprobe (its
temperature is -80°) and freeze the lens
capsule and moving it to destruct all
zonules and taken the lens out. Finally,
implantion of artificial intraocular lens
(IOL) in the anterior chamber in front of
iris and suturing the incision. This
operation has disadvantages of prolonged
period of rehabilitation; the stitches may
stretch the cornea causing Astigmatism
and high incidence of vitreous loss.

2- Extracapsular cataract extraction (ECCE) + PC IOL (posterior

chamber intraocular lens): →
Here a smaller incision 8-10 mm, about 120°-140° of the circumference of
cornea or limbus. The anterior capsule only is cut near to its periphery and
removes it (Capsulotomy). Then, the nucleus is extracted out, and the retained
lens material (cortex) is taken out by fluid irrigation and aspiration. Therefore,
the posterior capsule and the peripheral part of anterior capsule is still attached
in its position to the Zonules. Finally, PC IOL is implanted in the bag between
the posterior capsule and the peripheral part of anterior capsule (in the position
of previous cataractous lens). This operation is characterized by having less
length incision, rapid rehabilitation, less astigmatism and less incidence of
vitreous loss because the posterior capsule is still intact.

3- Phacoemulsification + PC IOL: most recent method, 3.2 mm incision +

foldable or injectable IOL, sutureless because the incision is so small.
Like ECCE, anterior capsule is removed but the nucleus is not delivered as a
one piece but it emulsified and fragmented into small pieces by high frequency
mechanical partitioned machine (its frequency is nearly equal to the frequency
of ultrasound). So, there is no need to do a large incision like in ICCE or
ECCE. The remnant of cortex also removed by irrigating and aspirating fluid.
Finally, implantation of a foldable or injectable lens manufactured of soft

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material can be inserted into the PC through this small wound. This operation
does not need suture and patient can leave hospital at the day of surgery and
resume his life after few days. Astigmatism is either minor degree or nil
because the incision is so small.
Positioning
IOL consists of an optic and haptics. The optic is the central refracting
element, and the haptics the arms or loops that sit in contact with peripheral
ocular structures to centralize the optic. Modern cataract surgery, with
preservation of the lens capsule, affords positioning of the IOL in the ideal
location – ‘in the bag’. Complicated surgery, with rupture of the posterior
capsule, may necessitate alternative positioning in the posterior chamber with
the haptics in the ciliary sulcus, or in the anterior chamber (AC) with the
haptics supported in the angle or iris claw Artisan – AC positioning requires a
specific lens type.
An update procedures like trans- scleral fixation and Glued IOL implantation
also used in complicated surgeries.

Operative complications
• Rupture of the posterior lens capsule
• Posterior loss of lens fragments
• Posterior dislocation of IOL
• Suprachoroidal haemorrhage
Postoperative complications
• Acute postoperative endophthalmitis
• Delayed-onset postoperative endophthalmitis
• Posterior capsular opacification
• Anterior capsular fibrosis and contraction
• Cystoid macular oedema
• Corneal decompensation
• Malposition of the IOL
• Retinal detachment
Aphakia
Congenital or acquired absence of the lens from the eye, or its absence from
the pupillary area (luxated). An aphakic eye is usually strongly hypermetropic
where parallel rays of light are brought to a focus behind the retina.
All accommodation is abolished (why?)

Treatment:
1- High powered convex lenses in spectacles: High power spectacles lens
causing magnification of the images on the retina (about 30% magnification),
which will produce anisoconia (different sizes of image on the retina coming
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 from the 2 eyes). Normal eye sending normal size image while aphakic eye
with high power spectacle producing large image (30%). The cerebral cortex
cannot fuse those 2 images with such high difference in their sizes. Other
disadvantages of high power spectacles are including, limitation of visual field
and heavy weight.
* Cerebral cortex cannot fuse images difference in more than 5%. Therefore
any difference which is more than 5% causing diplopia.
2- Contact lens (1% magnification). This is can be used without diplopia in
aphakic eye if the other eye is phakic or pseudophakic.
3- IOL (intraocular lens): is the best way of correction as there is no
magnification at all.

Congenital cataract
Occurs in about 3:10.000 live birth, 2/3rd of cases are bilateral.
Causes:
1- Isolated hereditary cataracts:
Account for about 25% of cases, mode of inheritance is most frequently AD
(Autosomal dominant), yet AR (Autosomal Recessive) and X-linked
inheritance can occur.
2- Metabolic cataract:
a- galactosaemia (Galactose -1-phosphate uridyl transferase "GPUT").
b- Lowe's (oculocerebral) syndrome: rare inborn error of amino acid
metabolism which predominantly affects boys (X-linked).
3- Prenatal infections:
a- Congenital Rubella: cataract presents in 15% of cases.
b- Others: Cytomegalovirus, Herpes simplex and Varicella.
4- Chromosomal abnormalities:
a- Down syndrome (Triosomy 21).
b- Other: Patau syndrome (Triosomy 13), Edward syndrome

Ocular assessment
Determination in the neonate of the visual significance of lens opacity is
based principally on the appearance of the red reflex and the quality of the
fundus view.
•A very dense cataract occluding the pupil; the decision to operate is
straightforward.

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 •A less dense but still visually significant cataract will permit visualization of
the retinal vasculature with the indirect but not with the direct ophthalmoscope.
•A visually insignificant opacity will allow clear visualization of the retinal
vasculature with both the indirect and direct ophthalmoscope.
•Other indicators of severe visual impairment include absence of central
fixation, nystagmus and strabismus.
•Morphology
○Blue dot opacities.
○Nuclear opacities .
○Lamellar opacities.
○Coronary (supranuclear) cataract.
○Central ‘oil droplet’ opacities characteristic of galactosaemia.
○Posterior polar cataract.
○Sutural.
○Anterior polar cataract .
•Assessment of family members.
•Ultrasonography for eye .
•Special tests such as forced-choice preferential looking and visual evoked
potentials may provide useful supporting information.

Treatment: SURGERY .
We assess the density of cataract through visualization of retina by direct and
indirect ophthalmoscope. If the cataract is so dense, visualization of retina is
difficult or impossible then surgery is indicated.
Surgery is by lensectomy (removal of the entire cataractous lens) + limited
anterior vitrectomy (removal of anterior surface of the vitreous just posterior to
the lens) should be done with it as opacification of anterior vitreous face occur
in 100% of childs after surgery. Lensectomy and anterior vitrectomy done by
special machine called vitrectomy machine.

Correction of aphakia in congenital cataract:

1- Unilateral aphakia: either IOL or contact lens (NO role for glasses).why?
2- Bilateral aphakia: in addition to IOL and contact lens, it can be corrected
by spectacles.

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 Ectopia lentis

Is refers to a displacement of the lens from its normal position. The lens may
be completely dislocated "Luxated" (complete destruction or cut of zonules) or
partially dislocated "Subluxated".

Causes:
1- Acquired:
- Trauma.
- Large eye {high myopia, buphthalmus (congenital glaucoma)} , due to
stretching of zonules that causes their destruction.
- Anterior uveal tumour, as it pushes the lens away from the ciliary body
leading to destruction of zonules.
- Hypermature cataract because of redundant capsule.
2- Congenital:
a- Without systemic association: AD, AR or associated with aniridia
(congenital absence of iris).
b-With systemic association: e.g., Marfan's syndrome, Weill-Marchesani
syndrome, homocystinuria, Ehlers-Danlos syndrome.

Complications of ectopia lentis:

1- Refractive errors: myopia (as the lens moves forward) and astigmatism (as
the lens is tilted).
2- Glaucoma: due to pupillary block that raises the pressure inside the
posterior chamber that pushes and bows the iris anteriorly "Iris bombé" and
causes obstruction of the angle of the anterior chamber ending with glaucoma.
3- Endothelial touch: damage to the endothelium of cornea.
4- Lens induced uveitis: rare, occurs due leakage of lens matter to the
intraocular cavities where it is regarded as foreign body, so there will be
inflammatory reaction causing uveitis.

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Treatment of ectopia lentis:

Indications for treatment:

1- Refractive error: treated by spectacles and surgery if not corrected by
spectacles.
2- Glaucoma: - If the lens is clear, so we do YAG PI (Yttrium-Aluminum-
Garnet Peripheral Iridotomy, where we create a fistula
between anterior and posterior chamber through a hole at the
periphery of iris).
- If there is cataract, we do lens extraction.
3- Endothelial touch → removal of lens.
4- Lens induced uveitis (which is chronic) → removal of lens.

The end

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 5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

Dr. Mohammed Qasim

Lecture
Optic nerve
Applied anatomy:
The optic nerve carries about 1.2 million afferent nerve fibers, which are
representing the axons of retinal ganglion cells. Most of these (90%) synapse in
the lateral geniculate body "LGB" (carrying visual stimulation), and the rest
(10%) reach other centers, notably the pre-tectal nuclei in the mid brain
carrying light pupillary reflex (afferent: optic nerve, efferent: oculomotor nerve
for light pupillary reflex).
The optic nerve is approximately 5 cm long from globe to optic chiasm, where
decussation occurs, the temporal fibers for each nerve pass to ipsilateral optic
tract, while nasal fiber cross to contralateral optic tract (crossing fibers).
Any injury to the axons of ganglion cells before LGB causes optic disc atrophy
seen by fundoscopy (ipsilateral if pre-chiasmal and bilateral if post-chiasmal),
while the injury that occurs after LGB (optic radiation and occipital cortex), will
not cause optic disc atrophy.
Visual centre lies mainly on the medial surface of the occipital cortex.
Optic nerve can be subdivided into four segments:
1- Intra-ocular segment (optic disc, nerve head): about 1mm depth & 1.5mm
in diameter.
2- Intra-orbital segment: 30mm, this part has S shape allowing the eye for
movement without nerve stretching (i.e. the distance from the apex of orbit
to the posterior part of eyeball is less than 3.0 cm).
3- Intra-canalicular segment: 6 mm.
4- Intra-cranial segment 10 mm, joins the chiasm.
* The optic nerve is surrounded by Pia, Arachnoid and Duramater, so the CSF
reaches up to the posterior sclera around the optic nerve.

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Axoplasmic transport:
It is the movement of cytoplasmic organelles within a neuron between the cell
body and the terminal synapse of Ganglion cells.
Retinal cotton-wool spots are the result of accumulation of cytoplasmic
organelles due to interruption of axoplasmic flow between the retinal ganglion
cells and their terminal synapses.
Papilloedema is similarly caused by hold-up of axoplasmic flow at the lamina
cribrosa (600 small pores present at posterior sclera for exit of optic nerve
fibers).

Signs of optic nerve dysfunction:

1- Decreased visual acuity.
2- Diminish light pupillary reflex.
3- Dyschromatopsia (impairment of color vision): affected eye sees the colors
less bright.
4- Diminished light brightness sensitivity.
5- Visual field defect: depends on the type of the pathology, e.g. central
scotomas, centrocaecal scotomas and altitudinal.

Special investigations for optic nerve:

1- Manual kinetic Perimetry (Goldmann).
2- Automated Perimetry.
3- Neuroimaging
a- MRI: detect tumors or degenerative diseases like multiple sclerosis.
b- CT SCAN: mainly in cases of trauma and acute cerebral hemorrhage.
c- Angiography: for detection of intracranial vascular disorders ex, stenosis
dissection, occlusion, arterio-venous malformations and aneurysms .
4- Visual Evoked Potential (VEP): is a recording of the electrical activity of
the visual cortex by stimulation of the retina (diagnose any damage from
ganglion cell to occipital cortex)
5- ERG (Electro-Retinography) : is recording of the electrical activity for
retinal receptors (rod and cones).
6- Fluorescein angiography: to differentiate between optic nerve diseases like
the drusen (deposition of hyaline like substance in the optic disc) and
papilloedema, as drusen do not leak dye while papilloedema leak the dye.

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 5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

Classification of optic neuropathy

 Inflammatory. Optic neuritis, including demyelinating,

 parainfectious, infectious and non-infectious, and neuroretinitis.
 Glaucomatous.
 Ischaemic. non-arteritic, and arteritic,
 Hereditary. Leber hereditary optic neuropathy,.
 Nutritional and toxic. Ex excessive smoker with alchol or use of
Ethambutol(anti TB).
 Papilloedematous. Secondary to raised intracranial pressure.
 Traumatic..
 Compressive. Including secondary to an orbital lesion.
 Infiltrative. Inflammatory conditions (e.g. sarcoidosis), tumours and
infective agents.

Optic neuritis
It is an inflammatory or demyelinating process affecting the optic nerve.
1- Ophthalmoscopic classification:
a- Retrobulbar neuritis: in which the optic disc appearance is normal, at least
initially (as in longstanding cases may end with optic disc atrophy), because
the optic nerve head is not involved. It is the most frequent type in adult and
is frequently associated with multiple sclerosis.
b- Papillitis: in which the pathological process affects the optic nerve head. It
is characterized by variable hyperaemia and oedema of the optic disc, which
may be associated with parapapillary flame-shaped haemorrhages. Papillitis
is the most common type of optic neuritis in children, although can also
affect adults.
2- Etiological classification:
a- Demyelinating: which is by far most common cause usually young females
with Multiple Sclerosis (MS).
b- Para-infectious: it is follow a viral infection or immunization.
c- Infectious: which may be sinus-related or associated with syphilis, cat-
scratch fever and cryptococcal meningitis (patients with AIDS or Herpes
zoster).
d- Autoimmune: may be associated with systemic autoimmune disease ex
Sarcoidosis .

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 5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

Treatment is according to the etiology, if the cause is demyelination in MS, the

patient need urgent IV Methylprednisolone, then oral Prednisolone because the
vision is severely affected.

Optic atrophy
It is an important sign of advanced optic nerve disease. It is of two types:
1- Primary optic atrophy:
It is occurs without antecedent swelling of the optic nerve head. It may be
caused by lesions affecting the visual pathways from the retro-laminar portion
of the optic nerve to the lateral geniculate body. Lesions anterior to the optic
chiasm result in unilateral optic disc atrophy, whereas those involving the
chiasm and optic tract will cause bilateral optic disc atrophy.

Causes:
- Retro-bulbar neuritis (not papillitis, as it is preceded by disc swelling).
- Compressive lesions, such as tumors and aneurysms.
- Hereditary optic neuropathies.
- Toxic and nutritional optic neuropathies.
Signs:
- Pale, flat disc with clearly delineated margin.
- Reduction in number of small blood vessels on the disc surface.
2- Secondary optic atrophy:
It is preceded by swelling of the optic nerve head.
Causes:
- Papillitis.
- Chronic papilloedema.
- Anterior Ischaemic Optic Neuropathy(AION): usually occurs in old age
patients, it is of two types; non arteritic [in diabetes, hypertension] and arteritic
.e.g. Giant cell arteritis.

Signs:
- White or dirty grey, slightly raised disc with poorly delineated margins due to
gliosis.
- Reduction in number of small blood vessels on the disc surface.

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 5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

Papilloedema
It is swelling of the optic nerve head secondary to raised intracranial pressure.
It is nearly always bilateral, although it may be asymmetrical.
All other causes of disc oedema in the absence of raised ICP are referred to as
"disc swelling" and usually produce visual impairment.
All patients with papilloedema should be suspected of having an intracranial
mass until proved otherwise. However, not all patients with raised ICP have
necessarily developed papilloedema.

1- Early features of papilloedema:

- Visual symptoms are absent and visual acuity is normal.
- Optic disc shows hyperaemia and mild elevation.

2- Established papilloedema:
- Transient visual obscurations lasting a few seconds.
- Visual acuity is normal or reduced.
- Optic disc shows severe hyperaemia, moderate elevation and indistinct margin.
3-Chronic
1. VA is variable and the visual fields begin to constrict-
2. Disc elevation; cotton wool spots and haemorrhages are characteristically
no longer present
3- Atrophic papilloedema:
- Visual acuity is severely impaired.
- Optic discs are dirty grey color, slightly elevated and indistinct margin.

Differential diagnosis of papilloedema:

1- Malignant hypertension.
2- Bilateral papillitis.
3- Bilateral compressive thyroid ophthalmopathy.
4- Bilateral simultaneous AION.
5- Bilateral compromised venous drainage in central retinal vein occlusion or
carotid-cavernous fistula.

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 5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

DIFFERENTIAL DIAGONOSIS OF DISC SWELLING

Pupillary reaction
Anatomy

LIGHT REFLEX

The pupillary light reflex consists of four neurons.

1. The first connects the retina with the pre-tectal nucleus in the mid-brain at
the level of the superior colliculus. The reflex is mediated by the retinal
photoreceptors. Impulses originating from the nasal retina are conducted by
fibres which decussate in the chiasm and pass up the optic tract to terminate
in the contralateral pre tectal nucleus. Impulses originating in the temporal
retina are conducted by uncrossed fibres which terminate in the ipsilateral
pre tectal nucleus.
2. The second connects the pre tectal nucleus to both Edinger-Westphal
nuclei by internuncial fibers. This is why a unilateral light stimulus evokes
a bilateral and symmetrical pupillary constriction. Damage to these
internuncial neurons is responsible for light-near dissociation in
neurosyphilis and pinealomas.
3. The third connects the Edinger-Westphal nucleus to the ciliary ganglion
inside the orbit. In the orbit, these parasympathetic fibers pass in the

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 5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

inferior division of the third nerve and reach the ciliary ganglion via the
nerve to the inferior oblique muscle.

4. The fourth leaves the ciliary ganglion and passes with the short ciliary
nerves to innervate the sphincter pupillae. The ciliary ganglion is located
within the muscle cone, just behind the globe. It should be noted that,
although the ciliary ganglion contains other nerve fibers (sensory and
sympathetic), only the parasympathetic fibers synapse there.

NEAR REFLEX

The near reflex triad consists of: (1) increased accommodation, (2) convergence
of the visual axes and (3) constriction of the pupils. The term 'light-near
dissociation' refers to a condition in which the light reflex is absent or abnormal,
although the near response is intact. Vision is not a prerequisite for the near
reflex, and there is no clinical condition in which the light reflex is present but
the near response absent. Although the final pathways for the near and light
reflexes are the same (i.e. third nerve, ciliary ganglion, short ciliary nerves), the
centre for the near reflex is ill-defined. There are probably two supranuclear
influences: the frontal and occipital lobes. The mid-brain centre for the near
reflex is probably located in a more ventral location than the light reflex (in pre-
tectal nucleus) and this may be one of the reasons why compressive lesions such
as pinealomas preferentially involve the dorsal pupillomotor fibers, sparing the
ventral fibers until late.

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 5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

SYMPATHETIC SUPPLY

The sympathetic supply consists of three neurons:

1. The first starts in the posterior hypothalamus and descends, uncrossed,

down the brain stem to terminate in the ciliospinal centre of Budge located
between C8 and T2.
2. The second passes from the ciliospinal centre of Budge to the superior
cervical ganglion in the neck. During its long course, it is closely related to
the apical pleura where it may be damaged by bronchial carcinoma
(Pancoast's tumor) or during surgery on the neck.
3. The third ascends along the internal carotid artery to enter the skull, where
it joins the ophthalmic division of the trigeminal nerve. The sympathetic
fibres are also passing through ciliary ganglia but without relay and it are
reaching the ciliary body and the dilator pupillae muscle via the nasociliary
nerve and the long ciliary nerves.

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 5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

Afferent pupillary conduction defects

A total afferent defect (TAPD, amaurotic pupil) is caused by a complete optic

nerve lesion and is characterized by the following:

1. The involved eye is completely blind (i.e. no light perception).

2. Both pupils are equal.
3. When the affected eye is stimulated neither pupil reacts but when the
normal eye is stimulated both pupils react normally.
4. The near reflex is normal in both eyes.

A relative afferent defect (RAPD, Marcus Gunn pupil) is caused by an

incomplete optic nerve lesion or severe retinal disease, but not by a dense
cataract. The clinical features are those of an amaurotic pupil but more subtle.
The difference between the pupillary reactions is enhanced by the 'swinging-
flashlight test' in which each pupil is stimulated in rapid succession. When the
abnormal pupil is stimulated it dilates instead of constricting. This paradoxical
reaction of the pupil to light occurs because the dilatation of the pupil, by
withdrawing the light from the normal eye, outweighs the constriction produced
by stimulating the abnormal eye.

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5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

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5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

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5TH YEAR/JMU MEDICAL COLLEGE/ NEUROPHTHALOLOGY ASSIT. PROF DR MOHAMMED QASIM

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Dr. Farooq Al Saad

FRCS oph Glasgow,MRCS oph Ed lecture 7

FABMS oph, Advaced FICO London

TRAUMA IN OPHTHALMOLOGY

EYELID TRAUMA

1- Haematoma (Black eyes) (Panda eyes):

It is the most common result of blunt injury to the eyelid or forehead (due to
continuous space below the tense aponeurosis of scalp that extends to the loose
space around the eye) and it is generally innocuous. It is important to exclude the
following serious associated conditions:

a- Trauma to the globe.

b- Orbital walls fracture.

c- Basal skull fracture.

2- Laceration:
Two types of eyelid laceration:

a- Superficial lacerations: they are parallel to the lid margin without gaping.

Treatment: suturing with 6-0 black silk or nylon; the sutures are removed after 5–6
days.

b- Lid margin lacerations: which are invariably gape and must therefore be
carefully sutured with perfect alignment to prevent notching.

* Improper suturing may end with notching or fibrosis (scars) that causes foreign
body sensation and then corneal abrasion.

NOTE :Initial approximation of the tarsal plate with an absorbable suture and lid
margin with a silk suture.

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 3- Canalicular laceration:
Suspected in case of injury to lid medial to punctum ,it can involve
superior or inferior canalicula or both ,repair should done with in 24
hour and silicone tubing Leave in situ for about 3 to 6 months.

ORBITAL FRACTURES

- Blow-out floor fracture:

It is typically caused by sudden increase in the orbital pressure by a striking

object such as a fist or tennis ball. Since the bones of the lateral wall and roof are
usually able to withstand such trauma, the fracture most frequently involves the
floor and occasionally, the medial orbital wall may also be fractured by such type of
trauma.

Signs:
1- Periocular signs: include ecchymosis, oedema and subcutaneous emphysema.

2- Infra- orbital nerve anesthesia: involving the lower lid, cheek, side of the
nose, upper lip, upper teeth and gums.

3- Vertical diplopia: happens due to:

a-Haemorrhages and oedema of the orbit restricting the movements of the

globe.

b- Mechanical entrapment of the inferior rectus or inferior oblique muscle or

both within the fracture.

c- Direct extraocular muscle injury.

4- Enophthalmos may be present if the fracture is large.

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 5- Ocular damage, e.g. hyphaema, angle recession and retinal dialysis.

6-proptosis: due to orbital hematoma.

7-Visual function, especially acuity, should be recorded and monitored as necessary,

particularly in the acute situation

NOTE

* Angle recession: recession of the angle between the periphery of the iris and
anterior face of ciliary body, which seen by gonioscope. Angle recession per se is an
innocuous thing, but may indicate severe trauma and associated with damage to
the trabecular meshwork that may cause "Angle recession glaucoma", which can
occur after a long time (years).

* Retinal dialysis: it is retinal detachment but with large tear at ora serrata
(junction between retina and cilliary body )

Treatment of Blow out floor fracture:

A-Initially : systemic antibiotics; the patient should be instructed not to blow the
nose to avoid transmission of bacteria from maxillary sinus to the orbit.

B-Urgent intervention needed in :

1-White-eyed’ fracture is a subgroup for which urgent repair is required to

avoid permanent neuromuscular damage. The scenario is generally seen in
patients less than 18 years of age, typically with little visible external soft tissue
injury, and usually affects the orbital floor. It involves the acute incarceration of
herniated tissue in a trap-door effect occurring due to the greater elasticity of
bone in younger people. Patients may experience acute nausea, vomiting, and
headache; persistent activation of the oculocardiac reflex can occur. CT
features may be subtle.
2-Early marked enophthalmos may also be an indication for urgent repair. it is
aimed at prevention of permanent vertical diplopia and/or cosmetically
unacceptable enophthalmos.

C-If no indication for urgent intervention:

1- Wait for 2 weeks (not more as fibrosis make the surgery difficult or
impossible) until oedema and inflammation settles, then check for diplopia in
primary position and down gaze, if the diplopia still exists after 2 weeks then
the surgery is indicated to release the muscles and put a bone graft or synthetic
material to close bone gapping in orbital floor.

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 2- Enophthalmos more than 2 mm which causing cosmetic blemish.usualy occur if
one half or more of orbital wall is affected this is an indication for surgery.

Orbital haemorrhage
Orbital (retrobulbar) haemorrhage is important chiefly due to the associated risk of acute
orbital compartment syndrome with compressive optic neuropathy, and can lead to
irreversible blindness of the affected eye in severe cases.

Diagnosis
Proptosis, eyelid oedema and ecchymosis, haemorrhagic chemosis, ocular motility
dysfunction, decreased visual acuity, elevated intraocular pressure, optic disc
swelling,imaging like CT orbit to confirm diagnosis but not always needed.

Treatment

1-Canthotomy.

2-Cantholysis. Following canthotomy, the lower lid is retracted downwards and the
inferior crus of the lateral canthal tendon transected.

TRAUMA TO THE GLOBE

• Closed injury is commonly due to blunt trauma. The corneoscleral wall of the globe is
intact.
• Open injury involves a full-thickness wound of the corneoscleral envelope.
• Contusion is a closed injury resulting from blunt trauma. Damage may occur at or
distant to the site of impact.
• Rupture is a full-thickness wound caused by blunt trauma. The globe gives way at its
weakest point, which may not be at the site of impact.
• Laceration is a full-thickness defect in the eye wall produced by a tearing injury,
usually as the result of a direct impact.

• Lamellar laceration is a partial-thickness laceration.

• Incised injury is caused by a sharp object such as glass or a knife.
• Penetrating injury refers to a single full-thickness wound, usually caused by a sharp
object, without an exit wound. A penetrating injury may be associated with intraocular
retention of a foreign body.
• Perforation consists of two full-thickness wounds, one entry and one exit, usually
caused by a missile

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General principles of management of ocular trauma:

1- Initial assessment:

a- Determination of any associated life-threatening problems, and general

condition should be stabilized.

b- History: circumstances, timing and likely object.

c- Thorough examination of both eyes and orbits.

2- Special investigations:

a- Plain radiographs: when a foreign body is suspected, to localize it and plan

for the surgery.

b- CT: superior to (a) in detection and localization of intraorbital foreign body. It

is also used in determining the integrity of intracranial, facial and intraocular
structures.

* NB: MRI should never be performed if a metallic foreign body is suspected as this
may induce more traumas and damage by its movement again.

c- Ultrasound: detection of intraorbital foreign body, globe rupture (as the

rupture may be posteriorly hidden), retinal detachment.

d- Electrophysiological tests (VEP, EOG, ERG) in assessing the integrity of the

optic nerve and retina.

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Dr. Farooq Al Saad

FRCS oph Glasgow,MRCS oph Ed lecture 8

FABMS oph,,Advaced FICO London

BLUNT TRAUMA

Causes: squash balls, luggage straps and champagne corks.

Complications:

1- Anterior segment complications:

a- Corneal abrasion: epithelial loss, which stains with fluorescein, treated by

pressure bandage.

b- Hyphaema: haemorhage in the anterior chamber usually occurs in children

and young persons. The source of bleeding is the iris or ciliary body.
Secondary bleeding can occur during the first week and is more serious
than initial bleeding.

Complications of hyphaema

* Hyphaema may cause secondary glaucoma by three ways: EITHER through

occluding of the trabecular meshwork by blood cells and proteins, OR by
pupillary block OR by the associated iritis and its complications e.g. Anterior
and posterior synechia.

Corneal staining (haemosiderosis) can occur due to persistent Hyphaema

specially if associated with rising IOP. It is due to deposition of iron on corneal
endothelium which leads to sever affection of VA where penetrating
keratoplasty indicated.

Treatment of hyphaema

* If hyphaema fills more than half of the anterior chamber, the patient should be
admitted to hospital with complete bed rest, and if it is mild hyphaema and fills
less than half of the anterior chamber, the patient is discharged but with

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 complete bed rest in home. Bed rest is important step in treatment of
hyphaema to avoid secondary bleeding.

* Surgery ("Paracentesis") is indicated when there is persistent total hyphema,

sever and persistent rising IOP or corneal staining. In paracentesis, washing of
AC is usually done with replacement of blood by a visco-elasitc substance or
fluid e.g. normal saline, ringer solution .

c- Traumatic mydriasis: it is often permanent due to damage to the iris

sphincter muscles.

d- Iridodialysis: is a dehiscence of the iris from the ciliary body at its root,
usually has a D shape, it is innocuous and asymptomatic or occasionally can
cause monocular diplopia (2 pupils).

e- Ciliary body: - Ciliary shock (ocular hypotonia).

- Angle recession initially may present with decrease IOP but

later on lead to glaucoma.

f- Lens: 1-cataract.

2-sublaxated lens (partial damage to zonule)

3-dislocation (360 degree damage to to zonule)

g- Rupture of the globe: usually anterior with prolapse of intraocular tissues,

but occasionally posterior (occult).

2- Posterior segment complications:

a- PVD (posterior vitreous detachment): it may be associated with vitreous
haemorrhage, retinal tear and pigment cells similar to tobacco dust, which are
seen floating in the anterior vitreous.

b- Commotio retinae: concussion of the sensory retina resulting in cloudy

swelling area of retina due. If the oedema is persists and involving the macula,
permanent diminish in VA.

c- Choroidal rupture.

d- Retinal break: retinal dialysis, tears and holes.

e- Optic neuropathy: is an uncommon but often devastating cause of

permanent visual loss (occur due to damage to small vessel supply it).

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 f- Optic nerve avulsion: is rare and typically occurs when an object intrudes
between the globe and the orbital wall, displacing the eye.

PENETRATING TRAUMA
Causes:

Penetrating trauma is three times more common in males than in females, and
in younger age group than in old age group. The most frequent causes are assault,
domestic accidents and sort. The extent of the injury is determined by the size of
the object, its speed at the time of impact and its composition.

Complications:

1- Anterior segment complications:

a- Small corneal lacerations: with formed anterior chamber, it does not require
suturing as it heals spontaneously.

b- Medium-sized corneal lacerations: usually require suturing to reform the

anterior chamber, especially if the anterior chamber is shallow or flat.

c- Corneal lacerations with iris prolapse:

In the 1st 24h, reposition of the iris and suturing of lacerations.

After the 1st 24h, the iris should be abscised and then suture the lacerations.

d- Corneal lacerations with lenticular (lens) damage:

Suturing of the laceration and removing of the damaged lens.

e- Anterior scleral laceration ± Iridociliary prolapse and vitreous

incarceration:

If anterior scleral laceration only, then suturing only,

If associated with Iridociliary prolapse and vitreous incarceration , then

reposition of exposed viable uveal tissue and cut prolapsed vitreous flush
within the wound otherwise subsequent vitreoretinal traction occur and lead
to retinal detachment.

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 2- Posterior segment complications:
- Posterior scleral lacerations: usually associated with retinal breaks unless
very superficial. The sclera should be sutured (if possible ) with treatment of
retinal break prophylactically by cryotherapy/laser to avoid rhegmatogenous
R.D.

INTRAOCULAR FOREIGN BODIES

An Intraocular foreign body may traumatize the eye by the following

mechanisms:

1- Mechanically (laceration).

2- Introduce infection.

3- Toxic effects on the intraocular structures.

Stones and organic foreign bodies are prone to result in infections.

Glass, plastics, gold and silver are inert, so we can leave the object if it has no effect.

Iron and copper foreign bodies undergo dissociation and result in siderosis and
chalcosis respectively, and we have to remove the object immediately or within
few days.

Siderosis:
Intraocular ferrous foreign body undergoes dissociation resulting in the
deposition of Iron in the intraocular epithelial cells (especially in lens and retina)
that leads to toxic effect on cellular enzymes that leads to cell death

So may lead to cataract, glaucoma and uveitis.

Treatment: iron foreign body should be removed.

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Chalcosis:
The ocular reaction to an intraocular foreign body with a high copper content
involves a violent endophthalmitis-like picture which often progress to phthisis
bulbi.

Treatment: Copper foreign body should be removed.

ENUCLEATION (EXCISION OF THE EYEBALL)

Primary enucleation: should be performed only for sever injuries, with no

prospect of retention of vision when it is impossible to repair the sclera.

Secondary enucleation: may be considered following primary repair if the eye is

severely and irreversibly damaged, particularly if it is also unsightly and
uncomfortable.

It has been recommended that enucleation should be performed within 10 days

of the original injury in order to prevent the very remote possibility of sympathetic
ophthalmitis.

SYMPATHETIC OPHTHALMITIS

It is a very rare, bilateral, granulomatous panuveitis which occurs after open

ocular injuries usually associated with uveal prolapse or less frequently
following intraocular surgery, when the uveal tissue came in contact with
conjunctiva. It occurs due to antibody formation against the uveal tract lead to
severe immunological inflammation of the injured eye and the fellow eye.

The traumatized eye is referred to as the "exciting eye", and the fellow eye,
which also develop uveitis, is called "Sympathizing eye".

Presentation:

65% of cases present between 2 weeks to 3 months after initial injury, 90% of
all cases occur within the first year but it can occurs later on after many years e.g.
20 years.

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Signs:

- The exciting eye shows evidence of the initial trauma and is frequently very red
and irritable.

- The sympathizing eye becomes photophobic and irritable.

- Both eyes then develop a chronic granulomatous anterior uveitis with iris
nodules and large keratic precipitates.

- Bilateral disc swelling and multifocal choroiditis.

Course:

Rarely, the uveitis is mild and self-limiting, but usually, intraocular

inflammation becomes chronic and if not treated appropriately, it may lead to
cataract, glaucoma and phthisis bulbi in both eyes. Generally prognosis poor

Treatment:

1- Systemic steroid.

2- Topical steroid.

3- Short acting mydriatics.

4- Systemic Immunosuppressive agents in resistant cases.

CHEMICAL INJURIES

Chemical injuries range in severity from trivial to potentially blinding.

The majority are accidental, but a few are due to assault.. Alkali burns are twice as common as

acid burns, since alkalis are more widely used both at home and in industry.

Alkalis tend to penetrate more deeply than acids, as the latter coagulate surface proteins,

forming a protective barrier; the most commonly involved alkalis are ammonia, sodium

hydroxide and lime so that lead to more severe damage as deep peneteration.

, Sulphuric acid may be complicated by thermal effects and high velocity impacts associated

with car battery explosion

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Emergency treatment
A chemical burn is the only eye injury that requires emergency treatment without formal
clinical assessment. Immediate treatment is as follows:
• Copious irrigation is crucial to minimize duration of contact with the chemical and
normalize the pH in the conjunctival sac as soon as possible, and the speed and
efficacy of irrigation is the most important prognostic factor following chemical
injury
• Double-eversion of the upper eyelid should be performed so that any retained
particulate matter trapped in the fornices is identified and removed.
• Debridement of necrotic areas of corneal epithelium should be performed at the slit
lamp to promote re-epithelialization and remove associated chemical residue.
• Admission to hospital will usually be required for severe injuries .

SPECIFIC

• Steroids reduce inflammation and neutrophil infiltration, and address

anterior uveitis.
• Cycloplegia may improve comfort.
• Topical antibiotic drops are used for prophylaxis of bacterial infection
• Ascorbic acid reverses a localized tissue scorbutic state and improves wound
healing, promoting the synthesis of mature collagen by corneal fibroblasts.
• Citric acid is a powerful inhibitor of neutrophil activity and reduces the
intensity of the inflammatory response.
• Tetracyclines are effective collagenase inhibitors and also inhibit neutrophil
activity and reduce ulceration.

Surgery
 Early surgery may be necessary to promote revascularization of
the limbus, restore the limbal cell population and re-establish the
fornices.
 Late surgery for treating corneal scar by keratoplasty.

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