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Introduction • The role of vision in our lives is difficult to define, because it is so deeply personal and
intimate • Whenever there is a failure in the vision, its not only the eyes, that are said to be in
darkness but the whole life is in darkness. • Loss of vision means loss of independence. Among the
various causes of blindness ,retinal detachment is one which is an ocular emergency.
Definition Retinal detachment is a disorder of the eye in which the retina peels away from its
underlying layer of support tissue. A detached retina is a serious and sight-threatening event. And
unless the retina is reattached soon, permanent vision loss may result.
Retina The retina is the inner most layer of the eye. It is composed of nerve tissue. The optical
system of the eye focuses light on the retina much like light is focused on the film in a camera.
Layers of retina The retina is composed of 10 layers Pigmented epithelium Photoreceptors;

bacillary layer (outer and inner segments photoreceptors) External (outer) limiting membrane
Outer nuclear. Outer plexiform Inner nuclear Internal limiting membrane Inner plexiform layer
Ganglion cell layer Nerve fiber layer
How does retina forms images ? Vitreous Humour Comprises a large portion of the eyeball It is a
clear gel that occupies the space behind the lens and the retina
Epidemiology The incidence of retinal detachment in otherwise normal eyes is around 5 new cases
in 100,000 persons per year Detachment is more frequent in middleaged or elderly populations,
with rates of around 20 in 100,000 per year The lifetime risk in normal individuals is about 1 in 300
Retinal detachment is more common in people with severe myopia (above 5–6 diopters), in whom
the retina is more thinly stretched. In such patients, life time risk rises to 1 in About two thirds of
cases of retinal detachment occur in myopics. Myopic retinal detachment patients tend to be younger
than nonmyopic ones.
Type • There are three types of retinal detachment: • rhegmatogenous • tractional • exudative
Rhegmatogenous retinal detachment –It occurs due to a break in the retina (called a retinal tear)
Retinal breaks are divided into three types – holes, tears and dialyses.
Exudative, serous, or secondary retinal detachment –It occurs due to inflammation, injury or
vascular abnormalities Fluid accumulating underneath the retina without the presence of a hole,
tear, or break. Rare
Tractional retinal detachment –It occurs when fibrous or fibrovascular tissue, pulls the sensory
retina from the retinal pigment epithelium.
Risk factors • Severe myopia • Retinal tear • Family history •Other eye diseases or disorders, such as
retinoschisis, uveitis, degenerative myopia, or lattice degeneration• Eye injury • Tumors • Systemic
diseases such as diabetes & sickle cell disease • Complications from cataract surgery
Sign and symptims Warning signs Flashes of light (photopsia) A sudden increase in the number
of floaters Blurred vision Seeing a shadow or a curtain descending from the top of the eye or
across
Diagnosis Elicit history for any of the following: • History of trauma • Previous ophthalmologic
surgery • Previous eye conditions (eg, uveitis and vitreous hemorrhage) • Duration of visual
symptoms and visual loss. Physical examination should include the following: • Checking of visual
acuity • External examination for signs of trauma and checking of the visual field • Assessment of
pupil reaction • Measurement of intraocular pressure in both eyes • Slit-lamp examination •
Examination of the vitreous for signs of pigment or tobacco dust• Fundus photography or
ophthalmoscopy. Fundus photography : larger instrument than the ophthalmoscope • Ultrasound
Significance of timely treatment • Visual improvement is much greater when the retina is repaired
before the macula is detached. • Once the retina is reattached, vision usually improves and then
stabilizes.
Treatment General principles of treatment: 1. Find all retinal breaks 2. Seal all retinal breaks 3.
Relieve present (and future) vitreo retinal traction
Surgical Methods Cryopexy and laser photocoagulation Scleral buckle surgery Pneumatic
retinopexy Vitrectomy
Cryopexy Cryotherapy (freezing) is used to wall off a small area of retinal detachment Uses nitrous
oxide to freeze the tissue behind the retinal tear This prevents fluid passing through the hole.
Laser Photocoagulation • If the retina is torn or the detachment is slight • Laser burn the edges of
the tear and halt progression. • Stimulates the scar tissue formation to seal the edges of the tear
Scleral buckle surgery Surgeon sews silicone bands to the sclera (the white outer coat ofthe eyeball)
The bands push the wall of the eye inward against the retinal hole Cryotherapy (freezing) is
applied around retinal breaks prior to placing the buckle. Subretinal fluid is drained as part of the
buckling procedure The buckle remains in situ The most common side effect of a scleral operation
is myopic shift. Myopic shift: the operated eye will be more short sighted after the operation.ypes of
scleral buckling: Radial scleral buckle Circumferential scleral buckle Encircling buckles
Pneumatic retinopexy Generally under local anesthesia Gas bubble (SF6 or C3F8 gas) is injected
into the eye after which laser or freezing treatment The patient's head is then positioned Have to
keep their heads tilted for several days.Pneumatic retinopexy The surface tension of the gas/water
interface seals the hole in the retina Combined with cryopexy or laser photocoagulation
Vitrectomy Tiny incision in the sclera Remove vitreous Gas is often injected to into the eye
During the healing process, the eye makes fluid that gradually replaces the gas and fills the eye.
Vitrectomy Using gas in this operation : no myopic shift after the operation Silicon oil (PDMS), if
filled needs to be removed after a period of 2–8 months
COMPLICATIONS AFTER SURGERY • Discomfort • Watering • Redness • Swelling • Itching • Blurred

vision
Prognosis 85 percent of cases will be successfully treated with one operation 15 percent requiring
2 or more operations After treatment patients gradually regain their vision over a period of a few
weeks, although the visual acuity may not be as good as it was prior to the detachment, particularly if
the macula was involved in the area of the detachment. Currently, about 95 percent of cases of
retinal detachment can be repaired successfully
Pre operative management • Assess the visual acuity of the client’s non-operative eye prior to
surgery • Assess the client’s support systems and the possible effect of impaired vision on lifestyle
and ability to perform ADLs in the postoperative period • Safety measures such as installing hand
rails,especially if the client has limited vision in the unaffected eye • Remove all eye makeup and
contact lenses or glasses prior to surgery • Mydriatic (pupil-dilating) or cycloplegic (ciliary- paralytic)
drops and drops to lower intraocular pressure may be prescribed preoperatively.
POST – OPERATIVE MANAGEMENT • Monitor status of the eye dressing following surgery. • Assess
dressings for the presence of bleeding or drainage • Maintain the eye patch or eye shield in place. The
eye patch or shield helps prevent inadvertent injury to the operative site • Place the client in a
semi-Fowler’s or Fowler’s position , having the client lie on the unaffected side.These positions reduce
intraocular pressure in the affected eye. • Assess the client and medicate or assist to avoid vomiting
coughing , sneezing or straining as needed. These activities increase intraocular pressure• After
surgery for a detached retina,the client is positioned so that the detachment is dependent or inferior.
For example , if the outer portion of the left retina is detached , the client is positioned on the left
side . Positioning so that the detachment is inferior maintains pressure on that area of the retina,
improving its contact with the choroid. • Assess comfort and medicate as necessary for complaints of
an aching or scratchy sensation in affected eye . Immediately report any complaint of sudden, sharp
eye pain to the physician.• Assess for potential surgical complications: a. Pain in or drainage from the
affected eye b. Hemorrhage with blood in the anterior chamber eye c. Flashes of light, floaters, or the
sensation of a curtain being drawn over the eye (indicators of retinal detachment) d. Cloudy
appearance to the cornea (corneal edema) • Evidence of any of the above manifestations or unusual
complaints by the client should be reported to the physician at once • Approach the client on the
unaffected side.This approach facilitates eye contact and communication.• Place all personal articles
and the call bell within easy reach . These measures prevent stretching and straining by the client •
Assist with ambulation and personal care activities as needed. Assistance may be necessary to
maintain safety • Antibiotic ,anti-inflammatory and other systemic and eye medications as prescribed .
Medications are prescribed post operatively to prevent infection or inflammation of the operative site,
maintain pupil constriction , and control intraocular pressure • Administer antiemetic medication as
needed. It is important to prevent vomiting to maintain normal intraocular pressures
Home care • Adequate lighting • Promote unrestricted ambulation • Removal of hazards like rugs,
clutters, unnecessary furnitures • Provision of hand rails in hallways, bathrooms • Access to radio and
television • Voice activated switches • Pill organizers • Large print newspapers, magazines• Double
vision • Glaucoma • Bleeding into the vitreous, within the retina, or behind the retina • Cataract •
Drooping of the eyelid • Infection around the scleral buckle • Endophthalmitis
Prognosis Treatment failures usually involve either the failure to recognize all sites of detachment,
the formation of new retinal breaks,or proliferative vitreo retinopathy Involvement of the macula
portends a worse prognosis Damage to vision may occur during reattachment Surgery 10 percent
of patients with normal vision experience some vision loss after a successful reattachment surgery.
Conclusion Visual impairment is more than a physiologic deficit. It is a loss that has physical and
emotional effects on the person afflicted. So as far as possible prevent those causes of blindness.
Reseach input • Problem statement- Outcome of surgery after macula-off retinal detachment –
results from MUSTARD, one of the largest databases on buckling surgery in Europe • ABSTRACT.
Purpose: To evaluate the anatomical success rate of scleral buckling surgery in the treatment of
rhegmatogenous retinal detachment and to evaluate the differences in outcome between patients
suffering macula-off retinal detachment and those without a macular involvement. • Methods: As a
retrospective interventional case series, Munster Study on Therapy Achievements in Retinal
Detachment (MUSTARD) is one of the largest ever established of retinal detachment patients and
their outcome after buckling surgery, with 4325 patients who underwent surgery between 1980 and
2001. In 53.94% (n = 2134) of 3956 patients with nontraumatic retinal detachment, the macula was
involved. The main outcome measure was the achievement of dry anatomical attachment of the
retina. • Results: The success rate in patients with macula-off retinal detachment is 80.46% and thus
7.78% lower (p < 0.01) than that in those patients with their macula intact whose success rate
amounted to 88.24%. The overall success rate of all 4325 MUSTARD patients was 83.98%. •
Conclusions: Scleral buckling is an established and mostly successful method for the treatment of
retinal detachment. As our case series has demonstrated, even eyes with macula-off can be treated
successfully by this procedure, thereby avoiding the complications of primary vitrectomy.
onjunctivitis ANATOMY: It is the mucous membrane covering the under surface of the lids and anterior
part of the eyeball up to the cornea. Palpebral ; covering the lids—firmly adherent. Forniceal ; covering
the fornices—loose—thrown into folds. Bulbar ; covering the eyeball—loosely attached except at limbus.
Also marginal and limbal parts and plica semilunaris. Nerve supply – Sensory: Ophthalmic division of
trigeminal Blood supply: Posterior conjunctival arteries derived from arterial arcade of lids which is
formed by palpebral branches of nasal and lacrimal arteries of the lids. Anterior conjunctival arteries
derived from the anterior ciliary arteries – muscular br. of ophthalmic artery to rectus muscles. Venous
drainage; Palpebral and Ophthalmic veins.
Physiology physiology : : : Smooth surface. Secretes mucin and aqueous component of tear film.
Highly vascular: supplies nutrition to the peripheral cornea. Aqueous veins drains from anterior chamber
maintenance of IOP. Lymphoid tissue helps in combating infections. Basic secretion—reflex secretion.
CONJUNCTIVITIS (PINK EYE):MECHANISM * inflammation of the conjunctiva. ETIOLOGY * Viral /

bacterial * irritants (allergies, chemicals, UV light)
Acute Bacterial Conjunctivitis:Acute Bacterial Conjunctivitis Mucopurulant conjunctivitis Caused by:

Staph epidermidis and Staph aureus –usually. Strep pneumonae, H influensae and Morexella lucanatae
occasionally
Symptoms: *Acute onset of redness, grittiness, burning and discharge. *Photophobia may be present
(corneal involvement) *Stickiness of the eyelids *Usually bilateral disease Signs: *Conjunctival
hyperaema *Mild papillary reaction *Mucopurulant discharge *Lid crusting *No lymphadenopathy.
*Normal VA
Purulant cojunctivitis (Adult gonococcal ) Symptoms: *Hyperacute condition *Extremely profuse, thick,
creamy puss from the eye or eyes
Signs: *Severe conjunctival chemosis *May be membrane formation *Periocular edema *Ocular
tenderness *Gaze restriction *Lamphadenopathy *Corneal involvement Treatment Systemic and topical
antiboitics
VIRAL CONJUNCTIVITIS:
The leading cause of a red, inflamed eye is viral infection A number of different viruses can be
responsible
Signs & symptoms: Vary from moderate to severe. Eye redness (hyperemia) is a common Swollen, red
eyelids More tear production in the eyes than usual Make you feel as though there is something in the
eye Creamy white or thick yellow drainage. Sensitivity to light (photophobia) 60
Allergic Conjunctivitides:Allergy is an altered or exaggerated susceptibility to various foreign

substances or physical agents which are harmless to the great majority of individuals. It is due to an
antigen antibody reaction. Allergens is an agent capable of producing a state or manifestation of allergy.
Symptoms: Itching, lacrimation, photophobia, FB sensation, burning. Signs: Giant papilla, ptosis,
hyperemia, mucus, trantas dots, punctate keratopathy, corneal ulcer.
DIAGNOSIS : Ophthalmic examination Culture discharge Slit lamp examination TREATMENT Warm
compress 3-4 times daily (10-15 min.) If bacterial (antibiotics) If viral- self limiting
Prevention:: Highly contagious Spread by direct contact with infected people Proper washing and
disinfecting can help prevent the spread Wash your hands frequently, particularly after applying
medications to the area Avoid touching the eye area Never share towels or hankies Change bed linen
and towels daily if possible Disinfect all surfaces, including worktops, sinks and doorknobs To reduce
pain from conjunctivitis use a cold or warm compress on the eyes
Applying Eye Drop Medicine:STEP ONE: Tilt your head back. Using your middle finger, gently press the
corner of the eye by the side of the nose. STEP TWO: Use your index finger to pull down the lower lid.
Then apply the eye drop medicine. STEP THREE: After applying the eye drop, let go of your lower lid.
Close the eye and keep the middle finger in place for at least two minutes. If you’re applying more than
one type of drop, wait at least 15 minutes for the next application. Use a facial tissue to wipe away excess
drops on eyelids .
RETINA : light-sensitive layer of tissue sends visual messages through the optic nerve
Retinal detachment :Retinal detachment Definition: The separation of neurosensory retina (NSR) from
the retinal pigment epithelium (RPE) by subretinal fluid (SRF). pulled away from the underlying choroid
small areas of the retina torn => retinal tears or retinal breaks retinal cells deprived of oxygen if not
promptly treated => permanent vision loss
Types of RD:Rhegmatogenous RD (RRD) Tractional RD Exudative RD Combined
tractional-rhegmatogenous RD
Rhegmatogenous RD (RRD) :Rhegmatogenous RD (RRD) Affect about 1 in 10,000 of the population each
year. Both eyes may eventually involved in about % of cases. Acute PVD (Posterior Vitreous
Detachment): A separation of the cortical vitreous from the internal limiting membrane (ILM) of the
sensory retina posterior to the vitreous base. Myopia: Over 40% of all RDs occur in myopic eyes. Trauma:
Responsible for about 10% of all cases of RD and is most common cause in children.
Tractional Retinal detachment :1. PDR ( proliferative diabetic retinopathy ) 2. ROP ( retinopathy of
prematurity ) 3. Penetrating posterior segment trauma
Exudative Retinal detachment :1. Choroidal tumor: Melanomas, metastases 2. Inflammation: Posterior
scleritis
SYMPTOMS floaters - bits of debris in field of vision that look like spots, hairs or strings floaters light
flashes shadow or curtain over a portion of visual field blur in vision
C an occur as a result of: t rauma a dvanced diabetes a n inflammatory disorder, such as sarcoidosis s
hrinkage of the jelly-like vitreous that fills the inside of the eye
vitreous liquid leaks through retinal tear and accumulates underneath retina retina can peel away from
underlying layer of blood vesselsFactors that may increase risk of retinal detachment: aging - more
common in people older than 40 previous retinal detachment in one eye family history of retinal
detachment extreme nearsightedness previous eye surgery previous severe eye injury or trauma
TREATMENTS Retinal tears: laser surgery (photocoagulation) freezing (cryopexy) Retinal detachment:
pneumatic retinopexy scleral buckling vitrectomy
PHOTOCOAGULATIONCRYOPEXYPNEUMATIC RETINOPEXYPNEUMATIC RETINOPEXY
SCLERAL BUCKLING
VITRECTOMY
Nursing care: Asses visual status and functional vision in the unaffected eye to determine self care needs.
Prepare the client for surgery by explaining possible surgical interventions and technique to alleviate
some of the client's anxiety. Discourage straining during defecation, bending down and hard coughing,
sneezing or vomiting to avoid activities that increase intraocular pressure. Assist with ambulation, as
needed, to help the client remain independent. Approach the clients from the unaffected side to avoid
startling him. Provide assistance with activities of daily living to minimize frustation adn strain. Orient the
client to his environment to reduce the risk of injury. Posoperatively instruct the client to lie on his back or
on his unoperated side to reduce intraocular pressure in the affected area. 135
Corneal foreign body is foreign material on or in the cornea, usually metal, glass, or organic material.
Symptoms: Foreign body sensation, Tearing, History of trauma ,photophobia , pain , red eye Signs:
Corneal foreign body with or without rust ring, edema of the lids, conjunctiva, and cornea, foreign body
can cause infection and/or tissue necrosis.
Workup 1.History and document visual acuity. One or two drops of topical anesthetic may be necessary
to control pain. 3.Slit-lamp Examination: If there is no evidence of perforation, evert the eyelids and
inspect for foreign bodies. 4.Dilate the eye and examine the vitreous and retina 5.Consider a B-scan US,
CT of the orbit. Treatment 1.Apply topical anesthetic, remove the foreign body with a spud or forceps at a
slit lamp. If multiple superficial foreign bodies, its easier to remove with irrigation. 2.Measure the size of
the resultant corneal epithelial defect. 3.Treat as for corneal abrasion.
onjunctivitis :
CPtregium :
Ptregium Definition Of Pterygium: A pterygium is a fleshy growth that invades the cornea. It is an
abnormal process in which the conjunctiva grows into the cornea. Definition Of Pterygium It is a fibro
vascular, triangular and degenerative condition of conjunctiva. 68
PowerPoint Presentation:
Types of Pterygium : There are two types: Progressive Pterygium : These types of pterygium are those
which progress day by day. Non Progressive Pterygium : Those which after limited growth has been
occur than stop their generation. 69
Etiology: The exact cause is not known. The probable causes are: i. Commonly occurs in people living in
hot & dry climate. ii. Dusty atmosphere. iii. Common in outdoor workers. iv. Common in males. v. It may
occur nasal than temporal side. 70
Symptoms: Redness Irritation Dryness Tearing May cause decreased vision ( when it reaches the visual
axis of cornea) Sign : Visible triangular fold of conjunctiva. Triangular shape with the apex, or head,
extending onto the cornea. 71
Treatment 1. Local: i. Lubricant eye drops. ii. Topical steroids for inflammation. 2. Surgical: i. Surgical
excision when the pterygium progressive towards the cornea . 72
Precautions: Use sun glasses. Protect from sunlight Use eye goggles when working. (laborers, welders)
Wash eye with water after work in sunlight. 73
Trachoma::
Trachoma: Trachoma is the world’s leading cause of preventable blindness Trachoma is a contagious
bacterial infection in the eye which causes blindness after multiple reinfections. 74
Trachoma is caused by the bacterium Chlamydia trachomatis Chlamydia trachomatis is spread through
direct contact with an infected person. Flies also play a major role in the spread of the disease. Poor
sanitation, dirty water, and lack of hygiene are causes of trachoma. 75
Intervention::
Intervention: S urgery for trichiasis. A ntibiotics . F acial cleanliness to prevent transmission. E
nvironmental change to prevent transmission. 76
DISORDERS OF THE GLOBE OF THE EYE:

77 DISORDERS OF THE GLOBE OF THE EYE KERATITIS CORNEAL ABRASION OR ULCER
SCLERITIS CATARACT GLAUCOMA MACULAR DEGENERATION DIABETIC RETINOPATHY
RETINAL DETACHMENT UVEITIS
Anatomy of cornea::
Anatomy of cornea: 78
79
KERATITIS:
80 KERATITIS MECHANISM * inflammation and ulceration of the cornea ETIOLOGY * herpes simplex
virus (cold sores) * other bacteria & fungi * trauma * dry air or intense light (welding)
Bacterial keratitis. Viral keratitis Fungal keratitis 81
82 SYMPTOMS AND SIGNS * pain or numbness of the cornea * decreased visual acuity * irritation *
tearing * photophobia * mild conjunctivitis
83 DIAGNOSIS * examination of cornea using slit lamp * medical history * previous upper respiratory
tract infection TREATMENT * eye patch to protect from photophobia
CORNEAL ABRASION OR ULCER:

84 CORNEAL ABRASION OR ULCER ETIOLOGY * foreign bodies * trauma (fingernail, contact lenses)
SYMPTOMS AND SIGNS * pain / redness & tearing * something constantly in eye * vision impairment
85 DIAGNOSIS * visual examination * fluorescien (stain) TREATMENT * remove foreign bodies * eye
wear for protection. * eye dressing to reduce movement
SCLERITIS:
86 SCLERITIS MECHANISM * Inflammation of sclera ETIOLOGY * rheumatoid arthritis * digestive
disorders (Crohn’s) SYMPTOMS AND SIGNS * Dull pain * Intense redness * loss of vision (posterior
sclera inflammation) * if untreated can lead to perforation or loss of eye
87 DIAGNOSIS * ophthalmic examination * Blood work to uncover underlying cause TREATMENT *
MILD : eye drops (antibiotics) * SEVERE : immunosupressive drugs * PERFORATION : surgery
The lens: :
The lens: The crystalline lens is the only structure continuously growing throughout the life. Changeable
refractive media. Capsule, epithelium and lens fibers. Congenital anomalies and effect of systemic
diseases. Cataract. 88
Anatomy of lenses::
Anatomy of lenses: Location posterior to iris anterior to vitreous Shape biconvex Structure lens capsule
lens cortex lens nucleus 89
90
Equator Anterior capsule Posterior capsule Diameter:9-10mm Thickness:4-5mm Lens zonule 91
Physiology of lens::
Physiology of lens: No vessel, nerve and transparent. Derive nutrients from the aqueous humor
Significant refractive medium Accommodative function No immediate relation with adjacent tissues
Complex metabolism Simple disorders: transparency and location change 92
CATARACT:
93 CATARACT Definition: * Gradual deterioration of lens. Opacification of the lens ETIOLOGY Any
factors that change the intraocular environment to affect lens metabolism. Such as: ageing, mechanical,
chemical, operation, inflammation, metabolic Malformation Congenital factors
Risk factors::
Risk factors: UV Diarrhea Malnutrition Diabetes Smoking Drinking alcohol 94
Mechanism: many factors lens capsular damage osmosis increase, loss of protective screen,metabolic
disorders protein degeneration, cell apoptosis lens opacify cataract 95
CLASSIFICATION : by cause : congenital, senile(age-related), complicated, metabolitic, drug-induced,
toxic, traumatic, secondary by age : congenital, acquired by location : cortical, nuclear, subcapsular by
shape : dot-like, coronary, lamellar by degree : immature, intumescent, mature, hypermature 96
97 SYMPTOMS AND SIGNS * Cloudy / white opaque area of the lens * reduce visual acuity * Blurring of
vision * photosensitivity DIAGNOSIS * Visual examination * pen light of slit lamp confers the presence of
a cataract TREATMENT * Intra-capsular phacoemulsification (involves breakage of cataract then
aspiration) * Extra-capsular phacoemulsification: (artificial lens replacement)
98
GLAUCOMA:
GLAUCOMA What is it? A disease of progressive optic neuropathy with loss of retinal neurons and their
axons (nerve fiber layer) resulting in blindness if left untreated.
GLAUCOMA:
GLAUCOMA “Glaucoma describes a group of diseases that kill retinal ganglion cells.” “High IOP is the
strongest known risk factor for glaucoma but it is neither necessary nor sufficient to induce the
neuropathy.”
GLAUCOMA:
GLAUCOMA Angle Anatomy
GLAUCOMA:
GLAUCOMA How do we measure IOP? Applanation Tonopen Schiotz Air Non-contact
GLAUCOMA:
GLAUCOMA Tonometry Applanation Schiotz
Glaucoma: what is happening:

Glaucoma: what is happening Either: the drain blocks here Or poor blood supply here Damages the optic
nerve..looks ‘caved in’, called ‘cupped’
Characteristic pattern to loss of visual field Rim of optic nerve becomes thinner as disc caves in and
becomes more cupped
Types of glaucoma:
Types of glaucoma Congenital Secondary Juvenile Chronic open angle Acute closed angle Many
different types
GLAUCOMA:
107 GLAUCOMA Chronic Open-Angle Glaucoma MECHANISM * Increased intraocular pressure due to
a malfunction in eyes aqueous humor drainage system - can lead to optic nerve damage ETIOLOGY *
trauma * overuse of steriods
108 SYMPTOMS AND SIGNS * Gradual loss of peripheral vision. * If untreated - eventually complete
vision loss DIAGNOSIS * ophthalmic examination * tonometry (pressure measure) TREATMENT *
Medication that helps decrease aqueous humor production or opens drainage system * laser to open
drainage * surgery (bypass)
109 Acute Angle-Closure Glaucoma MECHANISM * complete blockage of aqueous humor drainage
system ETIOLOGY * trauma
110 SYMPTOMS AND SIGNS * Blurred vision * severe eye pain * redness of the eye * nausea &
vomiting * photophobia (sees “halo” around light) * hazy cornea (elevated pressure) * if untreated -->
blindness DIAGNOSIS * goniolens (special lens to view the opening) TREATMENT * LASER
IRIDOTOMY (creation of a hole in the iris between the anterior and posterior chamber) * medications to
reduce pressure
Acute glaucoma:
Acute glaucoma Emergency Can be more gradual Red eye Achy, abdominal pain Misty vision Go from
light into dark Small eye, shallow anterior chamber, pupil mid dilated, Iris lens contact Push the iris
forward Eye feels hard
Chronic glaucoma:
Chronic glaucoma Painless, common in elderly Don’t notice anything wrong detected by optometrist
Screening vital field, pressure, disc
Blindness::
Blindness: DEFINITIONS: blindness : visual acuity of less than 3/60 or its equivalent. low vision : visual
acuity of less than 6/ 18 but ≥ 3/60 or corresponding to visual field loss to less than 20° in the better eye
with best possible correction. avoidable blindness : blindness which could be either treated or prevented
by known cost-effective means. 141
CAUSES OF BLINDNESS::
CAUSES OF BLINDNESS: In Developed Countries : accidents, glaucoma, diabetes, vascular
diseases(hypertension),cataract and degeneration of ocular tissues esp. of the retina and hereditary
conditions. In Developing Countries : cataract-62.6% refractive errors-19.7% glaucoma-5.8% post.
segment disorder-4.7% surgical complication-1.2% 142
Causes Of Childhood Blindness : refractive errors, trachoma, conjunctivitis, xerophthalmia , congenital
cataract , retinopathy of prematurity. Causes Of Avoidable Blindness : cataract, trachoma, childhood
blindness, refractive errors, glaucoma, diabetic retinopathy 143
Reheblitation ::
Reheblitation : Skills person with blindness or low vision may need Compensatory skills Visual efficiency
skills Literacy and Braille skills Listening skills Orientation and mobility skills Social interaction skills
Independent living skills Recreation and leisure skills Career and transition skills 144
In general, students with blindness and low vision should learn the same information as general
education students although more time and accommodations might be needed. Counseling to deal with
reactions from others Possible teaching of care for prosthetic eye Adaptations for color or visual
discrimination problems Responding to traffic signals, etc. Provide a copy of teacher’s notes Read aloud
Supply audio tapes/CDs of print materials Use hands-on models and manipulatives 145
Assist through touch and sound, more than sight, for those with little or no functional vision. Use
specialized equipment. Provide equal access to the core curriculum. Do not re-arrange the furniture or
leave items in the path. Determine the LRE based on student needs and strengths, preferences, and
related services needs. In general, provide appropriate lighting, tactile materials, necessary print size,
and decrease visual clutter. 146
Use programs to magnify computer screens. Scan materials for access. Provide Braille if the student
uses it. Use of a guide dog may be needed. May scan in materials and use a synthesizer that reads the
text to the student Voice recognition software applications 147
Request large print materials in advance. Get training on the use of optical devices and software.
Encourage student relationships and interaction. Support emotional and learning needs. Provide daily
cues. Consult with vision specialist regularly. Use tactile materials. Reduce glare on materials. Speak in
normal tones. Tell the student when you are leaving the room. Maintain high expectations and give
regular feedback. 148
BASIC REHABILITATION:
BASIC REHABILITATION The activities on the basic rehabilitation are directed at rehabilitating the
person’s social functions with the purpose of optimum accomplishing a self-dependent life . The following
basic rehabilitation activities take place at the NRCB : 149
Training in orientation and mobility this training helps students to move in new conditions - :
Training in orientation and mobility this training helps students to move in new conditions - 150
Visual rehabilitation the better usage of poor sight:

Visual rehabilitation the better usage of poor sight 151
Cooking :
Cooking 152
Useful skills rehabilitates the previous everyday skills and assists the acquisition of new ones
under the conditions of bad damaged or missing sight:
Useful skills rehabilitates the previous everyday skills and assists the acquisition of new ones under the
conditions of bad damaged or missing sight 153
Braille training assists the overcoming of the informational deficit :

Braille training assists the overcoming of the informational deficit 154
Physical education :
Physical education 155
Computer training for blind people, operating a computer with synthetic speech or a Braille
display Computer training for visually impaired people, operating a computer with a visual
monitor:
Computer training for blind people, operating a computer with synthetic speech or a Braille display
Computer training for visually impaired people, operating a computer with a visual monitor 156
ntroduction • Retinal detachment is a disorder of the eye in which the retina separates from the layer
underneath. Symptoms include an increase in the number of floaters, flashes of light, and worsening
of the outer part of the visual field. This may be described as a curtain over part of the field of vision.
Without treatment permanent loss of vision may occur.
3. • The mechanism most commonly involves a break in the retina that then allows the fluid in the
eye to get behind the retina. A break in the retina can occur from a posterior vitreous detachment,
injury to the eye, or inflammation of the eye. Other risk factors include being short sighted and
previous cataract surgery. Retinal detachments also rarely occur due to achoroidal tumor. Diagnosis is
by either looking at the back of the eye with an ophthalmoscope or by ultrasound
4. Epidemiology • The incidence of retinal detachment in otherwise normal eyes is around 5 new
cases in 100,000 persons per year. Detachment is more frequent in middle-aged or elderly
populations, with rates of around 20 in 100,000 per year. The lifetime risk in normal individuals is
about 1 in 300. Asymptomatic retinal breaks are present in about 6% of eyes in both clinical and
autopsy studies. • Retinal detachment is more common in people with severe myopia, in whom the
retina is more thinly stretched. In such patients, lifetime risk rises to 1 in 20. • Retinal detachment is
more frequent after surgery for cataracts.
5. Contd… • Although retinal detachment usually occurs in just one eye, there is a 15% chance of it
developing in the other eye, and this risk increases to 25–30% in patients who have had a retinal
detachment and cataracts extracted from both eyes.
6. Risk factors • Severe myopia, • Retinal tears, • Trauma, • Family history, • Complications from
cataract surgery. • Injury • Advanced diabetes
7. • Activities that increase intra ocular pressure can cause retinal detachment: • High-impact sports
or in high speed sports. • Diving and skydiving • As bungee jumping or roller coaster rides. • Valsalva
maneuver • Weightlifting
8. • Aging — retinal detachment is more common in people over age 50 • Previous retinal
detachment in one eye • A family history of retinal detachment • Extreme nearsightedness (myopia)
• Previous eye surgery, such as cataract removal • Previous severe eye injury • Previous other eye
disease or inflammation
9. Genetic factors promoting local inflammation and photoreceptor degeneration may also be
involved in the development of the disease. Glaucoma AIDS Cataract surgery Diabetic
retinopathy Eclampsia Family history of retinal detachment Homocysteinuria Malignant
hypertension Metastatic cancer, which spreads to the eye (eye cancer) Retinoblastoma Severe
myopia Smoking and passive smoking Stickler syndrome Von Hippel-Lindau disease
10. Signs and symptoms • A rhegmatogenous retinal detachment is commonly preceded by a

posterior vitreous detachment which gives rise to these symptoms: flashes of light (photopsia) –
very brief in the extreme peripheral (outside of center) part of vision a sudden dramatic increase in
the number of floaters a ring of floaters or hairs just to the temporal (skull) side of the central vision
11. • Bright flashes of light, especially in peripheral vision • Blurred vision • Floaters in the eye •
Shadow or blindness in a part of the visual field of one eye
12. Diagnosis • Retinal detachment can be examined by: Ultrasound. Fluorescein Angiography
Tonometry Ophthalmoscopy Refraction Test Color Vision Test Visual Acuity Slit-lamp
Examination
13. Types RHEGMATOGENOUS RETINAL DETACHMENT – • A rhegmatogenous retinal detachment

occurs due to a break in the retina (called a retinal tear) that allows fluid to pass from the vitreous
space into the subretinal space between the sensory retina and the retinal pigment epithelium.
Retinal breaks are divided into three types – holes, tears and dialyses. Holes form due to retinal
atrophy especially within an area of lattice degeneration. Tears are due to vitreoretinal traction.
Dialyses are very peripheral and circumferential, and may be either tractional or atrophic. The
atrophic form most often occurs as idiopathic dialysis of the young.
14. Exudative, serous, or secondary retinal detachment – • An exudative retinal detachment occurs
due to inflammation, injury or vascular abnormalities that results in fluid accumulating underneath
the retina without the presence of a hole, tear, or break. • Although rare, exudative detachment can
be caused by the growth of a tumor on the layers of tissue beneath the retina, namely the choroid.
This cancer is called a choroidal melanoma.
15. Tractional Retinal Detachment – • A tractional retinal detachment occurs when fibrous or
fibrovascular tissue, caused by an injury, inflammation or neovascularization, pulls the sensory retina
from the retinal pigment epithelium
16. Treatment • There are several methods of treating a detached retina, each of which depends on
finding and closing the breaks that have formed in the retina.
17. Cryopexy and Laser Photocoagulation • Cryotherapy (freezing) or laser photocoagulation are
occasionally used alone to wall off a small area of retinal detachment so that the detachment does
not spread.
18. Scleral Buckle Surgery • Scleral buckle surgery is an established treatment in which the eye
surgeon sews one or more silicone bands to the sclera. The bands push the wall of the eye inward
against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of
vitreous traction thereby allowing the retina to reattach. • Cryotherapy (freezing) is applied around
retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling
procedure. The buckle remains in situ.
19. Pneumatic Retinopexy • This operation is generally performed in the doctor's office under local
anesthesia. It is another method of repairing a retinal detachment in which a gas bubble is injected
into the eye after which laser or freezing treatment is applied to the retinal hole. The patient's head is
then positioned so that the bubble rests against the retinal hole. Patients may have to keep their
heads tilted for several days to keep the gas bubble in contact with the retinal hole.
20. Vitrectomy • Vitrectomy is an increasingly used treatment for retinal detachment. It involves the
removal of the vitreous gel and is usually combined with filling the eye with either a gas bubble or
silicone oil (PDMS). An advantage of using gas in this operation is that there is no myopic shift after
the operation and gas is absorbed within a few weeks. PDMS, if used, needs to be removed after a
period of 2–8 months depending on surgeon's preference. A disadvantage is that a vitrectomy always
leads to more rapid progression of a cataract in the operated eye.
21. Prognosis • 85 percent of cases will be successfully treated with one operation with the remaining
15 percent requiring 2 or more operations. • After treatment patients gradually regain their vision
over a period of a few weeks, although the visual acuity may not be as good as it was prior to the
detachment, particularly if the macula was involved in the area of the detachment.
22. • Currently, about 95 percent of cases of retinal detachment can be repaired successfully.
Treatment failures usually involve either the failure to recognize all sites of detachment, the
formation of new retinal breaks, or proliferative vitreoretinopathy. Prognosis
23. Prevention • Use protective eye wear to prevent eye trauma. • Control of blood sugar in diabetic
patients. • Frequent visits to eye specialist.
24. Summary • Introduction • Epidemiology • Risk factors • Signs and symptoms • Diagnosis • Types •
Treatment • Prognosis • Prevention
NTRODUCTION
The retina is a multilayer of exquisitely organized neurons that line the back of the eye (picture 1 and
picture 2). It is designed to convert photons into neural impulses that travel along the visual pathways
to the visual cortex. The retinal photoreceptors are some of the most metabolically active cells in the
body. They line the outer portion of the neurosensory retina and their outer segments are in contact
with the retinal pigment epithelia and underlying choroid. The choroidal circulation has the highest
blood flow rate per cubic centimeter of tissue in the human body and provides a critical supply of
oxygen to the outer third of the neurosensory retina and, in particular, to the retinal photoreceptors.
Retinal detachment occurs when the multilayer neurosensory retina separates from the underlying
retinal pigment epithelium and choroid. This separation can occur passively due to accumulation of
fluid between these two layers, or it may occur actively due to vitreous traction on the retina, such as
with diabetic traction retinal detachment.
Separation between the neurosensory retina and the underlying choroidal circulation results in
ischemia and rapid and progressive photoreceptor degeneration [1]. The amount of photoreceptor
degeneration and loss of vision can be minimized by rapid diagnosis and treatment [2-4]. Without
treatment, most symptomatic retinal detachments progress to involve the entire retina and lead to
loss of vision.
Understanding the basic pathophysiology involved in the process of retinal tear formation and retinal
detachment and understanding the symptoms and signs of the early stages of this process are
important in identifying high-risk patients, preventing the development of retinal detachments, and
preventing loss of vision.
PATHOPHYSIOLOGY
Retinal detachments can be rhegmatogenous (caused by a break in the retina; “rhegma” is Greek for
tear) or nonrhegmatogenous (caused by leakage or exudation from beneath the retina [exudative
retinal detachment] or vitreous traction pulling on the retina [traction retinal detachment]). On
occasion the retina appears to be detached but is actually not; this is termed pseudo retinal
detachment.
A full-thickness retinal break may exist as a round retinal hole, as a linear break, or as a
horseshoe-shaped retinal tear. In all of these cases, there is a discontinuity in the retina that allows
vitreous fluid to pass through the retinal break into the subretinal space, resulting in retinal
detachment.
Rhegmatogenous retinal detachment — Rhegmatogenous retinal detachments are the most common
type of retinal detachment. By definition, they are caused by a full-thickness retinal hole or retinal
tear. Although distinct from traction retinal detachments (see 'Traction retinal detachment' below),
these full-thickness holes or tears are also usually caused by vitreous traction on the retina. Unlike a
traction retinal detachment, however, the traction does not directly pull the retina off the underlying
tissue; instead, fluid that leaks through the hole or tear results in retinal detachment.
Holes and tears can be asymptomatic or symptomatic; asymptomatic breaks in the retina are much
more common than symptomatic breaks but much less likely to lead to retinal detachment. Thus,
most retinal holes or tears found in an asymptomatic patient do not result in retinal detachment,
whereas symptomatic retinal breaks often result in retinal detachment.
Posterior vitreous detachment — Posterior vitreous detachment (PVD) is the most common cause of
retinal holes and tears, which may lead to rhegmatogenous retinal detachment (picture 3) [5,6]. The
vitreous is a clear gel-like structure in the back of the eye composed of collagen fibrils and hyaluronic
acid that slowly liquefies throughout life. These pockets of liquid can break through the posterior
vitreous face and cause PVD from the retina. This event, which occurs typically in patients between
the ages of 50 and 75 years, results in a new onset of cobweb-like floaters and/or increased floaters
(see below).
Vitreous detachment usually occurs over one week but may take up to three months to completely
develop. Any areas in which there might be an abnormally strong vitreoretinal adhesion are areas
that, due to vitreous traction, may develop a full-thickness horseshoe retinal tear or operculated
retinal tear. The aforementioned lattice degeneration is an example of an area that has an abnormally
strong vitreoretinal connection. Anything that tugs on the retina will cause photopsias or flashes of
light that last seconds and may be associated with eye movement. In addition, patients who develop a
full-thickness retinal tear may also tear a small retinal blood vessel, resulting in a vitreous hemorrhage
and an increasing number of floaters or blurred vision.
Thus, nontraumatic rhegmatogenous retinal detachments begin with the normal and acute
development of PVD. If the patient also has areas of abnormally strong vitreoretinal adhesion, as in
areas of lattice degeneration, a full-thickness retinal tear or hole can develop. Liquid vitreous within
the eye can percolate through the retinal break creating retinal detachment.
Traumatic retinal detachment — Patients who sustain an ocular injury also can develop a
full-thickness retinal break or retinal dialysis. These may lead to subretinal migration of liquid vitreous
and the development of a retinal detachment (picture 4). This is much less common than
spontaneous rhegmatogenous detachment [7].
Nonrhegmatogenous retinal detachment
Traction retinal detachment — Traction retinal detachments occur when the vitreous has an
abnormally strong attachment to the retina and contracts, thus pulling the retina off the back of the
eye. This is typically seen in patients who have proliferative diabetic retinopathy, vitreomacular
traction syndrome, retinopathy of prematurity, or sickle cell retinopathy and who subsequently
develop retinal neovascularization. The areas of neovascularization and fibrosis between the retina
and the vitreous create a strong adhesion between these two tissues. With vitreous contraction, the
retina is pulled away from the back of the eye and a traction retinal detachment is created. (See
"Diabetic retinopathy: Prevention and treatment", section on 'Vitrectomy'.)
Traction retinal detachment can also occur in patients who have had perforating trauma and have
developed a fibrotic transvitreal retinal band that contracts. In addition, there are rare cases of
patients who have an abnormally strong adhesion between the vitreous and the macula (the central
part of the retina). Vitreous contraction in these cases can lead to a localized macular traction
detachment called vitreomacular traction syndrome [8].
Exudative retinal detachment — Exudative retinal detachment occurs in patients who do not have a
full-thickness retinal break but rather have an accumulation of fluid beneath the retina. These types
of retinal detachments are often associated with inflammatory conditions [9], may occur
spontaneously as with central serous chorioretinopathy, or can occur in association with choroidal
neoplasms/metastases. Traditional retinal reattachment surgeries are not effective since exudative
retinal detachments are not associated with a full-thickness retinal break. Diagnosing and treating the
underlying etiology of the exudative retinal detachment is critical in curing the problem and restoring
vision [10].
Lattice degeneration — Lattice degeneration is a relatively common condition found in about 6 to 8

percent of eyes and characterized by focal retinal thinning in the periphery of the retina, associated
with overlying vitreous liquefaction, sclerotic lattice-like vessels, and abnormally strong areas of
vitreoretinal adhesion. An atrophic retinal hole may occur within a patch of lattice degeneration,
which can cause a slowly developing and often asymptomatic peripheral retinal detachment in young
patients with myopia.
Thus, lattice degeneration can be viewed as an asymptomatic precursor to retinal tears and potential
detachment. Significant new tears or detachment occur in only 1 percent of patients with lattice
degeneration [11]. While prophylactic therapy for these lesions to prevent retinal detachment has
been considered, most studies do not support this approach since tears are just as likely to occur in
areas of the retina that appear normal. However, prophylactic laser barrier photocoagulation around
focal areas of lattice degeneration in very high-risk eyes (such as history of giant retinal tear in the
fellow eye) may be reasonable. (See 'Prevention' below.)
Pseudo retinal detachment — There are a number of cases in which the retina appears to be
detached but it is not:
●Peripheral senile retinoschisis is a splitting of the peripheral retina with an elevated retinal layer; this
generally has a very good prognosis
●White without pressure is a white reflex at the vitreoretinal interface that is normally seen in some
patients
●Choroidal lesion or swelling or infolding due to choroidal neoplasms, swelling, or hypotonia
These causes of a pseudo retinal detachment need to be diagnosed by a retina specialist or

ophthalmologist [12].
EPIDEMIOLOGY/RISK FACTORS
Nontraumatic rhegmatogenous retinal detachment occurs in approximately 1 in 10,000 people per

year [13,14]. Myopia is a major risk factor. In a case-control study of 253 patients with idiopathic
retinal detachment and 1138 controls, an eye with a spherical equivalent refractive error of -1 to -3
diopters had a fourfold increased risk of retinal detachment compared with a non-myopic eye; the
risk was increased 10-fold if the refractive error was greater than -3 diopters [15]. These data suggest
that almost 55 percent of nontraumatic detachments in eyes without previous surgery are
attributable to myopia.
Retinal detachment is also a complication of cataract surgery and an association with current use of
fluoroquinolones has been reported [16,17]. (See "Cataract in adults", section on 'Outcomes'.)
Posterior vitreous detachment (PVD) typically occurs in patients between the ages of 50 and 75 years.
However, it can occur earlier in patients who are myopic, have had a history of ocular trauma, or have
had ocular inflammation, all of which lead to a more rapid vitreous liquefaction. Patients with a
unilateral PVD are very likely to develop PVD in the other eye; in one series of 51 patients, 90 percent
developed PVD in the contralateral eye within three years [18]. Patients diagnosed with an
uncomplicated PVD have a 3.4 percent chance of developing a retinal tear within six weeks [19].
Lattice degeneration is present in 6 to 8 percent of the general population and in approximately 30

percent of patients with nontraumatic rhegmatogenous retinal detachment [20]. Nevertheless, most
patients with lattice degeneration do not develop a retinal detachment. In a prospective study of 276
untreated patients with lattice degeneration (423 eyes) followed for 1 to 25 years (mean 10.8 years),
symptomatic retinal detachments occurred in only 3 of 276 patients (1 percent) and 0.7 percent of
eyes [21]. Tractional retinal tears were slightly more common, occurring in eight patients (2.9 percent)
and 1.9 percent of eyes; one of these led to a clinical retinal detachment. Clinical or progressive
subclinical retinal detachment occurred in three eyes (2 percent) with atrophic holes. Asymptomatic
retinal detachment was seen in 10 of 150 eyes with atrophic holes (6.7 percent) and had a much less
serious prognosis than symptomatic detachment. The risk of retinal detachment in patients with
lattice degeneration is much higher if the patient has already had one retinal detachment [22].
Asymptomatic retinal breaks have been reported in approximately 6 percent of eyes in clinical and
autopsy studies [23]. The natural history of such breaks was investigated in a cohort study of 196
patients (235 involved eyes) who were followed from 1 to 33 years (mean 11 years) [24]. Nineteen
eyes (8 percent) originally had or developed 22 areas of subclinical detachment. Ten eyes had acute
PVD, which caused symptomatic retinal tears in three eyes, one of which also had a clinical retinal
detachment. The chance of retinal detachment due to an asymptomatic retinal break in people in
which a retinal detachment had not occurred in either eye was only approximately 0.5 percent. These
findings suggest that asymptomatic retinal breaks do not show any significant tendency toward
retinal detachment, with the exception of a few cases that progress to subclinical retinal detachment.
Other risk factors for retinal detachment include a family history of retinal detachment [25] or
vitreous abnormalities.
CLINICAL PRESENTATION
Patients with the most common cause of retinal detachment, rhegmatogenous detachment following
spontaneous posterior vitreous detachment (PVD), usually complain of an increasing number of
floaters in one eye. The floaters may look like a cobweb or like one particularly large floater that
appears to move in and out of central vision. The large floater represents the fibrous ring around the
optic nerve and may have the appearance of "a large housefly."
These symptoms are usually associated with acute PVD and result from the sudden separation of the
vitreous gel from the surface of the retina. This sometimes dramatic presentation of vitreous floaters
or debris can range from being an inconvenience or a nuisance to being visually disabling. The floaters
usually resolve with time, settle down outside the visual axis, and/or become less noticeable.
As the posterior vitreous face separates from the underlying retinal surface, it may encounter areas of
abnormally strong vitreoretinal adhesions. At these sites, the separating vitreous will tug on the
surface of the retina and create a mechanical depolarization of the axons running through the nerve
fiber layer of the retina. This is usually interpreted by the patient as a flash of light or photopsia that
lasts less than one second and is sometimes associated with eye movement. These photopsias may be
more easily seen in the dark or at night and are usually pinpointed to the affected eye. This
appearance contrasts with the fortification spectra often described in patients with ocular migraines;
this zigzagging light typically lasts 10 to 20 minutes, is seen in the peripheral visual field of both eyes,
and is sometimes associated with blurry central vision. (See "Approach to the patient with visual
hallucinations", section on 'Retinal pathology' and "Approach to the patient with visual hallucinations",
section on 'Migraine aura'.)
Small retinal vessels may avulse or a small horseshoe retinal tear can be created if sufficient
vitreoretinal traction is applied to the retina. In this circumstance, patients complain of a shower of
black spots consistent with vitreous hemorrhage. Sometimes this shower of spots progresses, leaving
the patient with a large vitreous hemorrhage and significantly impaired vision. For patients who
present with floaters or flashes, decrease in vision is the most important symptom suggesting a
retinal tear [19]. Patients who are found to have a dense vitreous hemorrhage on slitlamp
biomicroscopy associated with an acute PVD have a 10-fold increased risk of also having a retinal tear
and developing a retinal detachment.
Approximately 30 to 50 percent of patients who develop a full-thickness horseshoe retinal tear in the
setting of a symptomatic vitreous detachment will go on to develop a rhegmatogenous retinal
detachment [7]. Liquefied vitreous fluid has a tendency to percolate through retinal breaks under
residual traction causing a neurosensory retinal detachment. Patients who reach this stage often
complain of a slowly progressive peripheral visual field defect in the affected eye. Interestingly, they
frequently describe a photo stress response in the area of the detached retina. In other words, when
they are exposed to a bright light, the retinal photopigments in the area of the detached retina are
bleached; the inability of the detached retina to quickly regenerate the retinal photopigments results
in darkening of the visual field defect.
The rate of progression of retinal detachment varies depending upon the size of the retinal break,
location of the break, and movements of the eye. Large horseshoe retinal tears or giant retinal tears
that have persistent vitreoretinal traction will usually allow a retinal detachment to progress over the
period of hours to days. By contrast, small horseshoe retinal tears or operculated holes often result in
more slowly progressive retinal detachment that can take one to four weeks to develop [7].
As the retinal detachment progresses from the full-thickness retinal breaks posteriorly towards the
macula, the size of the visual field defect will enlarge in a corresponding fashion. Patients will lose the
ability to read once the retinal detachment involves the macula or the central area of the retina
responsible for reading vision. Vision in patients with macula-off rhegmatogenous retinal detachment
usually ranges between 20/40 and count fingers.
Differential diagnosis — Idiopathic vitreous floaters are the most common cause of floaters. In
addition to PVD and full-thickness retinal tear, other causes of floaters include:
●Vitreous hemorrhage
●Vitreous inflammation (eg, toxoplasmic chorioretinitis)
●Ocular lymphoma
●Intraocular foreign body
DIAGNOSIS
Patients presenting to primary care with sudden onset of floaters, or photopsias should be initially
evaluated by a test of visual acuity and confrontational evaluation of visual fields. Patients with visual
loss or who are found to have monocular decreased visual field should be seen urgently by an
ophthalmologist or retinal surgeon [19]. When possible, all patients should also be evaluated with
slitlamp biomicroscopy and a dilated retinal examination. Patients without high-risk features (visual
field loss, subjective or objective decreased vision, vitreous hemorrhage, or vitreous pigment on
slit-lamp examination) may be referred to an ophthalmologist more electively.
Patients who are referred to an ophthalmologist or retina specialist undergo a careful history and
ophthalmic examination. Anterior segment examination is performed looking for pigmented vitreous
cells behind the lens of the eye. These cells are known as "tobacco dust" and represent liberated
retinal pigment epithelial cells that have floated into the vitreous from under the retina. Patients who
have pigmented cells behind the lens have a very high probability of having a full-thickness retinal
break. Funduscopic examination of these patients will usually reveal vitreous debris and often a white
fibrous ring, called a Weiss ring, which corresponds to the area of contact between the posterior
vitreous face and the round optic nerve.
A careful 360 degree peripheral retinal examination using an indirect ophthalmoscope also should be
performed. Peripheral retina examination allows identification of vitreoretinal abnormalities,
vitreoretinal areas of abnormal traction, round atrophic holes, operculated retinal breaks, or
full-thickness horseshoe retinal tears. Scleral depression during ophthalmoscopy is a very helpful
technique for improving the view of the peripheral retina.
Patients should also undergo examination of the fellow eye as there is a relatively high rate of
bilateral retinal tears or detachments and an asymptomatic tear or detachment could otherwise be
missed.
In patients with dense vitreous hemorrhage, a good ophthalmoscopic view of the retina may not be
possible. No view of the posterior pole or peripheral retina will be obtained in cases where the
vitreous cavity is filled with blood. In such cases, use of an ophthalmic B-scan ultrasound is needed to
help identify large retinal breaks and/or retinal detachment (image 1). Ultrasound usually reveals the
dense vitreous hemorrhage floating in the vitreous cavity as well as the presence of any retinal
elevation. Since the resolution of ultrasonography is not as good as visual examination, patients with
dense vitreous hemorrhages are often followed carefully with sequential B-scan ultrasounds or earlier
surgical intervention with small-gauge vitrectomy and careful examination of the retinal periphery
[26]. (See 'Vitrectomy' below.)
TREATMENT
Posterior vitreous detachment management — Most patients who present with posterior vitreous
detachment (PVD) and do not have any retinal breaks or retinal tears on a 360 degree peripheral
retina examination require only reassurance and education. In a meta-analysis of retrospective
studies that included 1600 patients with symptomatic PVD, delayed retinal tears (not seen on initial
examination) were found in 1.8 percent; 83 percent of the patients with late tears had vitreous or
retinal hemorrhage at initial examination or developed new symptoms [27]. While studies have tried
to identify subsets of patients who may not require additional evaluation after the initial examination
[28], we suggest that most patients should be seen in follow-up at about three months. Patients who
describe photopsias or have evidence of retinal bleeding, but no full-thickness or retinal detachment,
may require an earlier follow-up in approximately one to two months.
The floaters often resolve over a period of 3 to 12 months; they settle down outside the visual axis
and/or become less noticeable or bothersome. In some cases, however, floaters may be a permanent
symptom and, if disabling, may require vitrectomy to treat.
In general, patients with a PVD do not require any specific activity limitations. Patients who develop
worsening symptoms of flashes, significantly more floaters, and/or loss of peripheral or central vision
should be reevaluated with a careful peripheral retinal examination.
Retinal hole or tear — Patients who have a full-thickness symptomatic operculated retinal hole or
horseshoe retinal tear, but no retinal detachment, clearly benefit from laser retinopexy or
cryoretinopexy. These patients are advised that their risk of developing a retinal detachment is
around 30 percent and that treatment reduces this risk to less than 1 percent. Since the risks of laser
treatments or cryoretinopexy are minimal, the risk/benefit ratio strongly favors treating symptomatic
retinal breaks prophylactically.
Patients who undergo laser photocoagulation may be seated in front of a slit lamp after numbing the
affected eye with topical drops. A contact lens is then placed on the surface of the eye in order to
visualize the retinal break using the slit-lamp biomicroscope. Once identified, the retinal break is
surrounded by two to three rows of confluent 200 to 300 micron size laser burns. The laser intensity
necessary for these treatments can vary between 100 and 500 milliwatts depending upon the amount
of cataract present and fundus pigmentation.
Patients may also be treated with a laser indirect ophthalmoscope that allows the clinician to examine,
depress, and laser the retina at the same time. This delivery system allows for more peripheral
treatment of the retina.
Patients who are treated with cryoretinopexy usually have a subconjunctival injection of lidocaine
over the area of the full-thickness retinal break. Using the indirect ophthalmoscope, the
cryoretinopexy probe is placed on the surface of the conjunctiva underneath the retinal break. A
freezing ball is created at the tip of this probe that freezes through the sclera, choroid, and retina. A
number of cryoretinopexy spots are created in order to contiguously surround the retinal break
(figure 1).
Once either treatment is completed, it takes approximately one to two weeks for the body to form its
maximal amount of chorioretinal adhesion. Patients are usually advised to minimize eye movement
(such as with reading) during this period. Sitting on a couch and watching TV is actually quite effective
in minimizing head and eye movement.
Rhegmatogenous retinal detachment — Without treatment, most symptomatic retinal detachments

progress to involve the entire retina and lead to loss of all vision. Thus, treatment is indicated for
nearly all patients with symptomatic detachments.
Patients who present with a full-thickness retinal break and a small retinal detachment can be treated
with delimiting laser photocoagulation or cryoretinopexy barrier. The chorioretinal scar created with
these procedures may hold the retinal detachment in place and prevent it from spreading and
threatening the macula. These treatments are most appropriate for small peripheral retinal
detachments and for asymptomatic retinal detachments. The process is similar to that discussed for
the treatment of a retinal tear. (See 'Retinal hole or tear' above.)
Patients who present with a frank rhegmatogenous retinal detachment will require other techniques
in order to reattach the retina. These techniques include a pneumatic retinopexy, a temporary
peribulbar balloon, scleral buckle placement, and/or pars plana vitrectomy.
Asymptomatic retinal detachments appear to have a better prognosis. A case series of 16 patients
with 18 eyes with asymptomatic rhegmatogenous retinal detachments found that none became
symptomatic over a mean follow-up of 46 months [29]. The patients in this cohort were relatively
young (mean age 56), none had a superior detachment, all had at least a partial demarcation line on
presentation, and only 3 of the 18 detachments had retinal tears (many had atrophic holes). As such,
it is uncertain whether these results are generalizable to all patients with asymptomatic retinal
detachments.
While awaiting further data, we suggest that patients with small asymptomatic inferior
rhegmatogenous detachments due to atrophic holes be followed with close monitoring or offered
laser photocoagulation. For now, we would continue to treat other patients with asymptomatic
detachments.
Patients with significant rhegmatogenous retinal detachment will require one of three procedures for
reattachment: pneumatic retinopexy, scleral buckling, or vitrectomy. Few randomized trials are
available to determine the optimal selection of one procedure over another, and the decision is often
subjective [11]. Pneumatic retinopexy is an office procedure with lower costs and fewer complications
and is appropriate as a first-line procedure for non-complex cases. When not successful, the more
invasive procedures can be performed.
Pneumatic retinopexy — Pneumatic retinopexy is a procedure performed in the office and includes
cryoretinopexy of the retinal break followed by injection of an intravitreal gas bubble (picture 5). With
strict head positioning, retinal breaks that are in the superior part of the retina can be tamponaded by
the intravitreal gas bubble, closed, and sealed by the chorioretinal adhesion induced by
cryoretinopexy. Once the retinal break is closed, the retinal epithelial cells quickly reabsorb the
subretinal fluid, thereby reattaching the retina. This process of reabsorption usually takes about 24 to
48 hours [30,31].
It may also be possible to use pneumatic retinopexy in patients with retinal breaks that are in the
inferior portion of the retina, using an inverted technique that requires patients to maintain a
head-down position for six to eight hours [32].
Pneumatic retinopexy leads to successful retinal attachment about 70 to 80 percent of the time after
one procedure. In cases of failure, most patients are treated with scleral buckle placement and/or
vitrectomy.
Scleral buckle — Scleral buckle is performed in the operating room. After a retrobulbar injection or
infusion of lidocaine and bupivacaine, cryoretinopexy to the retinal breaks is performed, followed first
by suturing of an exoplant to the outside of the sclera that indents the wall of the eye and closes the
retinal breaks, and then by drainage of subretinal fluid, if needed (figure 2). The scleral indentation
created by the sutured exoplant not only helps close the retinal break and allow the chorioretinal
retinal adhesion to form, but also helps reduce the vitreoretinal traction present.
A modification of the technique involves placing a small balloon catheter underneath a retinal break
to temporarily close it and allow sealing of the hole over a period of 12 to 24 hours. Once the retinal
hole is sealed and closed and the subretinal fluid is reabsorbed, the balloon catheter can be safely
removed.
A randomized, controlled trial of 198 patients with primary, uncomplicated retinal detachment found
no significant differences in outcome in patients assigned to pneumatic retinopexy compared with
scleral buckling [31].
Scleral buckle placement leads to successful retinal reattachment approximately 80 to 90 percent of

the time after one surgery. In cases of failure, most patients are treated with vitrectomy.
Vitrectomy — Patients with more complicated retinal detachments may require a vitrectomy (figure
3). With this procedure, three sclerotomies are made on the outside of the eye: one that allows fluid
to infuse into the eye, and two others that are used to introduce instruments into the back part of the
eye. Using a light pipe and a vitreous cutter, all of the central and peripheral vitreous is removed and
all of the vitreoretinal traction on any of the breaks excised. The patient's retina can be flattened
intraoperatively using an air bubble or heavier than water perfluorocarbon liquid. These patients are
usually left with intravitreal air, a long-acting gas bubble (SF6 or C3F8), or silicone oil [33].
Vitrectomy leads to successful retinal reattachment approximately 80 to 90 percent of the time after
one surgery. In cases of failures, patients often require more extensive vitreoretinal procedures such
as combined cataract extraction and intraocular lens placement, lensectomy, extensive epiretinal
membrane peeling, subretinal fibrous band removal, relaxing retinotomies, and silicone oil
tamponade. Virtually all patients over age 50 treated with vitrectomy will develop a visually
significant cataract within 6 to 18 months.
Other causes of retinal detachments — Patients who present with traction retinal detachments
(severe diabetic retinopathy, penetrating ocular injury, or vitreomacular syndrome) may also benefit
from surgical retinal reattachment; all of these cases require surgical intervention with a pars plana
vitrectomy. During this surgery, extensive peeling is often required, utilizing end-grabbing forceps and
intravitreal scissors. Once the vitreoretinal traction is relieved the retina can be reattached as
previously described and left with an intravitreal tamponade.
Patients who present with an exudative retinal detachment must have the etiology of this
detachment identified and treated. Surgical repair of this type of retinal detachment is not
recommended in most cases.
PREVENTION
There is no evidence that posterior vitreous detachment (PVD) can be prevented. On the other hand,
since vitreoretinal abnormalities such as lattice degeneration with atrophic holes, vitreoretinal tags,
or small round retinal holes can lead to retinal detachment, it has been suggested that such patients
may benefit from prophylactic laser or cryoretinopexy. However, a major limitation of prophylactic
therapy is that most retinal detachments are due to retinal tears that develop in areas of the retina
that appear normal prior to vitreous detachment [20]. Thus treatment of visible lesions associated
with retinal detachment may prevent a tear at those sites but not a tear in normal-appearing retina. A
systematic review of studies involving patients with asymptomatic vitreoretinal abnormalities found
no trials that met inclusion criteria, and thus no conclusions could be made about prophylactic
therapy [34].
In the absence of definitive data, the most important aspect of prevention is education of the patient
about the symptoms of retinal tear or retinal detachment. Early identification of retinal tears and
rapid treatment of this problem usually results in the prevention of a retinal detachment and
significant loss of vision. Also, there are some very high-risk patients, such as patients who have
developed a giant retinal tear in the fellow eye, in whom prophylactic treatment may be reasonable.
Photoreceptor neuroprotection — The visual prognosis after retinal detachment repair is often
limited. Various animal models of retinal detachment have been developed to better understand the
cellular and molecular mechanisms underlying this vision loss.
Animal models have demonstrated that photoreceptor apoptosis typically occurs in a stereotypic
manner in response to retinal detachment [1,35-38]. Separation of the neurosensory retina from the
underlying choroidal circulation results in ischemia and retinal degeneration as soon as 12 hours after
detachment. Studies of human patients with retinal detachment have also shown a similar pattern of
photoreceptor cell loss [39-41].
A number of potential neuroprotective agents are being tested clinically, which may prevent some of
this retinal degeneration and improve final visional outcome in patients with macula off retinal
detachments [42].
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The
Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level,
and they answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read
materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more
detailed. These articles are written at the 10th to 12th grade reading level and are best for patients
who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Detached retina (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Without treatment, most symptomatic retinal detachments progress to involve the entire retina and
lead to loss of vision. (See 'Introduction' above.)
●Retinal detachments are classified as "rhegmatogenous" if they are the result of a full-thickness
retinal hole or retinal tear and as "nonrhegmatogenous" otherwise. (See 'Pathophysiology' above.)
●Rhegmatogenous detachments are most common, and they are often a consequence of posterior
vitreous detachment (PVD), a normal event in people between the ages of 50 and 75. In some
patients, areas of adhesion during PVD can pull on the retina and cause a tear. Rhegmatogenous
detachments can also occur after ocular trauma, though this is a rare occurrence. (See
'Rhegmatogenous retinal detachment' above.)
●Nonrhegmatogenous detachments can occur in patients with proliferative diabetic retinopathy,

retinal neovascularization, or inflammatory conditions and in other settings. (See
'Nonrhegmatogenous retinal detachment' above.)
●Risk factors for rhegmatogenous detachments include myopia, focal thinning of the periphery of the
retinal called lattice degeneration, and a family history of retina tears or detachments. Asymptomatic
retinal breaks do not typically progress to retinal detachment. (See 'Epidemiology/risk factors' above.)
●Patients with a symptomatic PVD who develop a full-thickness retinal tear are at high risk for retinal
detachment. The most common symptom of PVD is an increasing number of floaters in one eye.
Flashes of light (photopsias) are also common during PVD, and if a small retinal vessel is torn the
patient may note a shower of black spots (red blood cells) and/or a marked decrease in vision. (See
'Clinical presentation' above.)
●Patients with retinal detachment (due to PVD or other etiologies) will typically note a peripheral
visual field defect. (See 'Clinical presentation' above.)
●Patients with symptoms of a PVD should be quickly examined by an ophthalmologist to exclude a
retinal tear or detachment. Patients with a new and progressive visual field defect suggestive of a
retinal detachment require urgent evaluation. (See 'Diagnosis' above.)
●In the absence of retinal breaks or tears or vitreous pigmented cells, most patients with PVD require
no specific treatment but should be re-examined by an ophthalmologist in one to three months. (See
'Posterior vitreous detachment management' above.)
●Patients with a retinal hole or tear in the presence of a symptomatic PVD should generally be
treated by an ophthalmologist with laser photocoagulation or cryoretinopexy to prevent retinal
detachment. (See 'Retinal hole or tear' above.)
●Patients with a retinal detachment will generally be treated with one or more of the following
procedures: laser or cryoretinopexy, pneumatic retinopexy, scleral buckle, or vitrectomy. Patients
with small peripheral retinal detachments may be treated with barrier procedures, such as
cryoretinopexy or laser photocoagulation. Some patients with asymptomatic rhegmatogenous retinal
detachments may be closely monitored without therapy or treated with barrier procedures. (See
'Rhegmatogenous retinal detachment' above.)
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REFERENCES
Yang L, Bula D, Arroyo JG, Chen DF. Preventing retinal detachment-associated photoreceptor cell loss
in Bax-deficient mice. Invest Ophthalmol Vis Sci 2004; 45:648.
Wilson CA, Khawly JA, Hatchell DL, Machemer R. Experimental traction retinal detachment in the cat.
Graefes Arch Clin Exp Ophthalmol 1991; 229:568.
Matthews GP, Das A, Brown S. Visual outcome and ocular survival in patients with retinal
detachments secondary to open- or closed-globe injuries. Ophthalmic Surg Lasers 1998; 29:48.
Sarrafizadeh R, Hassan TS, Ruby AJ, et al. Incidence of retinal detachment and visual outcome in eyes
presenting with posterior vitreous separation and dense fundus-obscuring vitreous hemorrhage.
Ophthalmology 2001; 108:2273.
Rumpf J. Jules Gonin. Inventor of the surgical treatment for retinal detachment. Surv Ophthalmol
1976; 21:276.
Hikichi T, Trempe CL, Schepens CL. Posterior vitreous detachment as a risk factor for retinal
detachment. Ophthalmology 1995; 102:527.
Byer NE. Natural history of posterior vitreous detachment with early management as the premier line
of defense against retinal detachment. Ophthalmology 1994; 101:1503.
Margherio RR, Trese MT, Margherio AR, Cartright K. Surgical management of vitreomacular traction
syndromes. Ophthalmology 1989; 96:1437.
Wolfensberger TJ, Tufail A. Systemic disorders associated with detachment of the neurosensory retina
and retinal pigment epithelium. Curr Opin Ophthalmol 2000; 11:455.
Eagle RC Jr. Mechanisms of maculopathy. Ophthalmology 1984; 91:613.

D'Amico DJ. Clinical practice. Primary retinal detachment. N Engl J Med 2008; 359:2346.
Char DH. Coats' syndrome: long term follow up. Br J Ophthalmol 2000; 84:37.
Wilkes SR, Beard CM, Kurland LT, et al. The incidence of retinal detachment in Rochester, Minnesota,
1970-1978. Am J Ophthalmol 1982; 94:670.
Haimann MH, Burton TC, Brown CK. Epidemiology of retinal detachment. Arch Ophthalmol 1982;
100:289.
Risk factors for idiopathic rhegmatogenous retinal detachment. The Eye Disease Case-Control Study
Group. Am J Epidemiol 1993; 137:749.
Etminan M, Forooghian F, Brophy JM, et al. Oral fluoroquinolones and the risk of retinal detachment.
JAMA 2012; 307:1414.
Pasternak B, Svanström H, Melbye M, Hviid A. Association between oral fluoroquinolone use and
retinal detachment. JAMA 2013; 310:2184.
Hikichi T, Yoshida A. Time course of development of posterior vitreous detachment in the fellow eye
after development in the first eye. Ophthalmology 2004; 111:1705.
Hollands H, Johnson D, Brox AC, et al. Acute-onset floaters and flashes: is this patient at risk for retinal
detachment? JAMA 2009; 302:2243.
Byer NE. Rethinking prophylactic therapy of retinal detachment. In: Advances in Vitreoretinal Surgery,
Stirpe M (Ed), Ophthalmic Communications Society, New York 1992. p.399.
Byer NE. Long-term natural history of lattice degeneration of the retina. Ophthalmology 1989;
96:1396.
Folk JC, Arrindell EL, Klugman MR. The fellow eye of patients with phakic lattice retinal detachment.
Wilkinson CP, Rice TA. Michels Retinal Detachment, Mosby-Year Book, St. Louis 1997.
Byer NE. What happens to untreated asymptomatic retinal breaks, and are they affected by posterior
vitreous detachment? Ophthalmology 1998; 105:1045.
Go SL, Hoyng CB, Klaver CC. Genetic risk of rhegmatogenous retinal detachment: a familial
aggregation study. Arch Ophthalmol 2005; 123:1237.
Kelley LM, Walker JP, Wing GL, et al. Ultrasound-guided cryotherapy for retinal tears in patients with
vitreous hemorrhage. Ophthalmic Surg Lasers 1997; 28:565.
Coffee RE, Westfall AC, Davis GH, et al. Symptomatic posterior vitreous detachment and the incidence
of delayed retinal breaks: case series and meta-analysis. Am J Ophthalmol 2007; 144:409.
van Overdam KA, Bettink-Remeijer MW, Klaver CC, et al. Symptoms and findings predictive for the
development of new retinal breaks. Arch Ophthalmol 2005; 123:479.
Cohen SM. Natural history of asymptomatic clinical retinal detachments. Am J Ophthalmol 2005;
139:777.
Hilton GF, Tornambe PE. Pneumatic retinopexy. An analysis of intraoperative and postoperative
complications. The Retinal Detachment Study Group. Retina 1991; 11:285.
Tornambe PE, Hilton GF. Pneumatic retinopexy. A multicenter randomized controlled clinical trial
comparing pneumatic retinopexy with scleral buckling. The Retinal Detachment Study Group.
Chang TS, Pelzek CD, Nguyen RL, et al. Inverted pneumatic retinopexy: a method of treating retinal
detachments associated with inferior retinal breaks. Ophthalmology 2003; 110:589.
Machemer R. [Development of pars plana vitrectomy. My personal contribution]. Klin Monbl

Augenheilkd 1995; 207:147.
Wilkinson C. Interventions for asymptomatic retinal breaks and lattice degeneration for preventing
retinal detachment. Cochrane Database Syst Rev 2001; :CD003170.
Lewis GP, Charteris DG, Sethi CS, et al. The ability of rapid retinal reattachment to stop or reverse the
cellular and molecular events initiated by detachment. Invest Ophthalmol Vis Sci 2002; 43:2412.
Hisatomi T, Sakamoto T, Goto Y, et al. Critical role of photoreceptor apoptosis in functional damage
after retinal detachment. Curr Eye Res 2002; 24:161.
Cook B, Lewis GP, Fisher SK, Adler R. Apoptotic photoreceptor degeneration in experimental retinal
detachment. Invest Ophthalmol Vis Sci 1995; 36:990.
Berglin L, Algvere PV, Seregard S. Photoreceptor decay over time and apoptosis in experimental
retinal detachment. Graefes Arch Clin Exp Ophthalmol 1997; 235:306.
Arroyo JG, Yang L, Bula D, Chen DF. Photoreceptor apoptosis in human retinal detachment. Am J
Ophthalmol 2005; 139:605.
Chang CJ, Lai WW, Edward DP, Tso MO. Apoptotic photoreceptor cell death after traumatic retinal
detachment in humans. Arch Ophthalmol 1995; 113:880.
Sebag J, Sadun AA. Apoptotic photoreceptor cell death after traumatic retinal detachment in humans.
Arch Ophthalmol 1996; 114:1158.
Lewis GP, Talaga KC, Linberg KA, et al. The efficacy of delayed oxygen therapy in the treatment of
experimental retinal detachment. Am J Ophthalmol 2004; 137:1085.
Topic 6910 Version 33.0
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Types of retinal detachment
Rhegmatogenous
Caused by breaks in the retina
Associated with:
Age
Myopia
Cataract surgery
Trauma
Degenerative retinal lesions
Stickler’s syndrome
Juvenile X-linked retinoschisis
Marfan’s syndrome
Tractional
Caused by chronic traction from scars on the retinal surface and across the vitreous cavity
Associated with:
Proliferative diabetic retinopathy
Proliferative vitreoretinopathy
Retinopathy of prematurity
Penetrating eye injury
Sickle cell retinopathy
Retinal vein occlusion
Exudative
Caused by leakage of fluid into the subretinal space
Associated conditions:
Inflammatory (uveitis, scleritis)
Hydrostatic (malignant hypertension, toxaemia of pregnancy)
Neoplastic (choroidal melanoma, haemangioma, metastasis)
Vascular (Coat’s disease, retinal macroaneurysm)
Maculopathy (neovascular macular degeneration, central serous choroidoretinopathy)
Congenital disorders (nanophthalmos, optic disc pit)
Most retinal breaks form when the vitreous separates from the retina as part of the normal ageing
process. This event, posterior vitreous detachment, is the result of a lifetime process of degenerative
liquefaction and shrinkage of the vitreous (fig 22).8 Although posterior vitreous detachment is benign
in most people and may go unnoticed, those with symptoms carry a 10-15% risk of developing retinal
breaks.9 10 Posterior vitreous detachment is rare before the age of 40, but the prevalence increases
steadily thereafter, to around 40% in the seventh decade. By the ninth decade, up to 86% of the
population develop a partial or complete posterior vitreous detachment.11
Go to:
What symptoms should alert me to a threatened retinal detachment?
Flashes and floaters
Photopsia and floaters can occur in conditions other than posterior vitreous detachment (box 2).
Photopsia associated with posterior vitreous detachment results from traction on the retina as the
vitreous pulls away. It is usually described as recurrent, brief flashes in the temporal peripheral field,
but can occur anywhere. Floaters are caused by vitreous opacities casting shadows on the retina.
Posterior vitreous detachment makes them more mobile and thus more noticeable. Vitreous
condensation around the optic nerve often manifests as an irregular ring or crescent shaped opacity
(“Weiss ring”) after posterior vitreous detachment (fig 22).). Some patients recall a dramatic event of
bright flashes accompanied by showers of black dots that later coalesced into “strands,” “cobwebs,”
or “cloudy haze.” Such descriptions suggest vitreous haemorrhage from avulsed blood vessels (fig 22))
or the liberation of retinal pigment epithelial cells through retinal breaks.
Box 2 Causes of photopsia and floaters

Photopsia (perception of light not attributable to an incident light)
Posterior vitreous detachment
Flick phosphene
Migraine
Postural hypotension
Choroidal tumours
Optic nerve pathology
Transient ischaemic attacks
Floaters (perception of mobile spots, lines, or haze due to vitreous opacities)
Age related macular degeneration
Posterior vitreous detachment
Vitreous haemorrhage (diabetic retinopathy, trauma)
Asteroides hyalosis
Uveitis
Retinitis pigmentosa
Symptomatic posterior vitreous detachment carries a considerable risk of breaks that are likely to
progress to retinal detachment. Autopsy studies have shown that 4-9% of the population will develop
asymptomatic retinal breaks in their lifetime, most of which do not progress to detachment.8 12 In
contrast, a retrospective case series of 295 patients presenting with photopsia or floaters found
retinal detachment in 61% of 80 eyes that had developed retinal breaks.13
Visual field defects, blurring, and distortion
When the retina is separated from the retinal pigment epithelium, the visual field defect is opposite
the site of the detachment because of the optical inversion of images. It is commonly described as a
dark curtain or shadow, appearing first in the periphery and moving to the centre over hours, days, or
even weeks as the detachment extends. Visual acuity decreases when the macula becomes detached,
and the patient may notice distortion of images. Without prompt treatment, total retinal detachment
and blindness are almost inevitable.
Go to:
Who is at risk of developing retinal detachment?
Retinal detachment occurs more commonly with age as posterior vitreous detachment becomes more
prevalent. Cataract surgery is thought to accelerate vitreous liquefaction and posterior vitreous
detachment.14 A retrospective, population based study found that the eight year cumulative risk of
retinal detachment approached 1% after cataract surgery, almost nine times higher than expected.15
The risk increases further if vitreous is lost during surgery.16
Myopic patients (with increased axial length) are more likely to develop posterior vitreous
detachment at a younger age.11 The peripheral retina in these eyes is less robust and commonly
habours degenerative lesions, such as lattice, where the retina is thinned and firmly adherent to the
vitreous.17 Retinal detachment from atrophic holes, without posterior vitreous detachment, is
relatively common in highly myopic people.18 Cataract surgery in very myopic patients carries a
particularly high risk of detachment.19
Many retrospective studies have shown that trauma is an important cause of retinal detachment in
young patients.20 21 A direct blow to the eye induces breaks in the retina, usually in the form of
retinal dialysis (lifting of the retinal edge at the periphery), and tears and atrophic holes from retinal
contusion can also develop. Ocular trauma induces premature posterior vitreous detachment,
possibly through liquefaction of the vitreous from leakage of blood and protein.22
Prospective and retrospective case series report retinal detachment in up to 23% of second eyes as
the features that played a role in the previous detachment are replicated.23 24 Family history is also a
risk factor because features such as increased axial length and degenerative retinal lesions are
heritable traits.25
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How to assess a patient with suspected retinal detachment
If the presenting symptoms and risk factor profile suggest retinal breaks or detachment, further
ophthalmic assessment is indicated. The completeness of the assessment will depend on the
availability of equipment and the skills of the examiner (fig 3)3).
etinal breaks. A slit lamp is needed to assess the anterior vitreous for pigment granules (“tobacco
dust”), which correlate with a 90% risk of retinal breaks.26 The anterior vitreous is best visualised
with an oblique slit beam through a dilated pupil.
Macroscopic vitreous haemorrhage is associated with a 70% risk of retinal breaks.27 When dense
vitreous haemorrhage precludes examining the fundus, ultrasonography can identify the detachment.
Because ultrasound does not image the retinal periphery well, retinal breaks there cannot be
diagnosed with certainty by this method.
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Decisions to refer: when, to whom, and how urgently?
All patients with a recent onset of retinal detachment should be referred immediately. Time can be
saved by referring the patient directly to the ophthalmologist who will perform the surgery. In some
countries, retinal detachments are mostly repaired by specialist vitreoretinal surgeons. If immediate
referral is not possible, the patient should be instructed to lie down with the face on the side of the
detachment to the pillow (opposite the field defect) to minimise the detachment extending towards
the macula.
There is no general consensus on how soon patients presenting with a symptomatic posterior vitreous
detachment and no other visual symptoms should be referred for a definitive examination. The
referral should be made as soon as possible, certainly within days, in view of the considerable risk of
retinal breaks associated with the presentation. The patient should be instructed to return earlier if
symptoms worsen or a visual field defect develops.
Go to:
Treatment of retinal break and detachment
Retinal breaks caused by posterior vitreous detachment are treated using laser therapy or
cryotherapy to create a scar adhesion between the retina and retinal pigment epithelium. This
treatment is almost 100% successful, but new breaks can develop elsewhere.28 Prophylactic
treatment of asymptomatic breaks or degenerative retinal lesions has not been shown to reduce the
risk of retinal detachment.29
Once the retina is detached, additional surgical procedures are required to reattach it and seal the
breaks. Most retinal detachments not involving the macula are repaired on the same day or the
following day. For patients presenting with the macula already detached, the macula should be
reattached within five days, but the urgency of the surgery is influenced by individual factors such as
the duration of symptoms, the height of macular detachment, and visual acuity.6
Scleral buckling and vitrectomy with gas tamponade are the most common surgical approaches to
repairing retinal detachment (fig 5)5).. Pneumatic retinopexy can be performed in some cases, but
enthusiasm for this technique outside North America has been minimal. In 95% of cases the retina will
be reattached, sometimes after more than one operation.30 Successful reattachment of the retina
does not always correlate with a good visual outcome, and patients presenting with poorer vision are
less likely to achieve good final visual acuity.6 Macular detachment has a poorer visual outcome, and
the chance of regaining good vision diminishes with the duration of detachment.6 Results are best
when the detachment is repaired before the macula becomes involved, and this can be achieved only
through early diagnosis and urgent referral.
An external file that holds a picture, illustration, etc.
Object name is kanh465690.f5.jpg
Fig 5 Surgery for retinal detachment. A—in scleral buckle surgery, the retinal break is treated with
cryotherapy or laser therapy, and an explant (usually a silicone band or strip) is sutured on the outer
surface of the sclera to indent the wall of the globe. This interrupts the flow of fluid through the break,
allowing it to close. Subretinal fluid is drained through a small sclerotomy or left to be absorbed into
the choroid. B—the vitrectomy approach involves removing the vitreous through sclerotomies made
in the pars plana. Subretinal fluid is drained internally, and laser therapy or cryotherapy is applied
around the flattened retinal break. The vitreous cavity is filled with a tamponade (usually gas but
occasionally silicone oil) to hold the retina in place while scarring develops around the break. In some
cases, pneumatic retinopexy may be less invasive: a bubble of gas is injected into the vitreous cavity,
and the patient’s head is positioned to place the bubble on the retinal break; once the retina is
flattened, the break can be treated with laser therapy or cryotherapy
Go to:
Postoperative care
After the operation, topical antibiotics and corticosteroids are routinely prescribed, and cycloplegics
and ocular hypotensive agents may be prescribed in some patients. If intraocular gas has been
instilled, vision will be poor. As the gas is resorbed over weeks to months, the gas-fluid interface will
become apparent to the patient as an undulating line that moves downward. Worsening vision is not
expected and should be reported to the surgeon immediately. Severe pain is also unusual and should
be reported. Headache and nausea suggest an acute rise in intraocular pressure. Patients with
intraocular gas are usually asked to maintain a certain head posture, typically for one week. Air travel
must be avoided while the gas remains, and intraocular gas is a contraindication for volatile gas
anaesthesia.
Ongoing research
The scleral buckling versus primary vitrectomy in rhegmatogenous retinal detachment study (SPR
study) aims to determine the best approach for managing more complex retinal detachments
Sutureless vitrectomy systems promise less invasive surgery and reduced discomfort
Pharmacological vitreolysis may simplify repairs of difficult tractional detachment
Tissue adhesives designed to seal retinal breaks may obviate the need for intraocular tamponade
Research continues in ways to prevent proliferative vitreoretinopathy, which remains the leading
cause of failed surgery
Additional educational resources
Review articles
Brucker AJ, Hopkins TB. Retinal detachment surgery: the latest in current management. Retina
2006;26(suppl 6):S28-33.
Gariano RF, Kim CH. Evaluation and management of suspected retinal detachment. Am Fam Physician
2004;69:1691-8.
Ghazi NG, Green WR. Pathology and pathogenesis of retinal detachment. Eye 2002;16:411-21.
Scott JD. Future perspectives in primary retinal detachment repair. Eye 2002;16:349-52.
Internet resources
Emedicine—www.emedicine.com/emerg/topic504.htm (Larkin GL. Retinal detachment. April 2008.)
Handbook of Ocular Disease Management—www.revoptom.com/handbook/sect5r.htm (Sowka JW,

Gurwood AS, Kabat AG. Retinal detachment. 2001.)
Information resources for patients
All About Vision—www.allaboutvision.com/conditions/retinadetach.htm
Health Encyclopedia—www.healthscout.com/ency/68/207/main.html
Macula Center—www.maculacenter.com/EyeConditions/RetinalDetachment.htm
Medicine Net—www.medicinenet.com/retinal_detachment/article.htm
Medline Plus—www.nlm.nih.gov/medlineplus/ency/article/001027.htm
Summary points
Retinal detachment affects 1 in 10 000 people each year, but the incidence is much higher in
association with myopia, cataract surgery, trauma, previous retinal detachment, and family history
Most retinal detachments can be repaired successfully, but the key to optimum visual recovery is
prompt diagnosis and treatment
Photopsia and new floaters are symptoms of posterior vitreous detachment, which precedes retinal
detachment
Retinal detachment should be considered in any patient presenting with an acute onset of visual
symptoms, and these patients should be referred urgently
If symptoms are accompanied by decreased vision or visual field loss, referral should be immediate
Go to:
Notes
HKK and AJL were involved in all stages of the manuscript preparation. HKK is guarantor.
Competing interests: None declared.
Provenance and peer review: Commissioned; externally peer reviewed.
Go to:
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Introduction • The role of vision in our lives is difficult to define, because it is so deeply personal and

Layers of retina The retina is composed of 10 layers Pigmented epithelium Photoreceptors;

COMPLICATIONS AFTER SURGERY • Discomfort • Watering • Redness • Swelling • Itching • Blurred

CONJUNCTIVITIS (PINK EYE):MECHANISM * inflammation of the conjunctiva. ETIOLOGY * Viral /

Acute Bacterial Conjunctivitis:Acute Bacterial Conjunctivitis Mucopurulant conjunctivitis Caused by:

Allergic Conjunctivitides:Allergy is an altered or exaggerated susceptibility to various foreign

DISORDERS OF THE GLOBE OF THE EYE:

CORNEAL ABRASION OR ULCER:

Glaucoma: what is happening:

Visual rehabilitation the better usage of poor sight:

Braille training assists the overcoming of the informational deficit :

10. Signs and symptoms • A rhegmatogenous retinal detachment is commonly preceded by a

13. Types RHEGMATOGENOUS RETINAL DETACHMENT – • A rhegmatogenous retinal detachment

Lattice degeneration — Lattice degeneration is a relatively common condition found in about 6 to 8

●Choroidal lesion or swelling or infolding due to choroidal neoplasms, swelling, or hypotonia

These causes of a pseudo retinal detachment need to be diagnosed by a retina specialist or

Nontraumatic rhegmatogenous retinal detachment occurs in approximately 1 in 10,000 people per

Lattice degeneration is present in 6 to 8 percent of the general population and in approximately 30

●Vitreous inflammation (eg, toxoplasmic chorioretinitis)

●Intraocular foreign body

Rhegmatogenous retinal detachment — Without treatment, most symptomatic retinal detachments

Scleral buckle placement leads to successful retinal reattachment approximately 80 to 90 percent of

INFORMATION FOR PATIENTS

●Basics topic (see "Patient education: Detached retina (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Nonrhegmatogenous detachments can occur in patients with proliferative diabetic retinopathy,

Use of UpToDate is subject to the Subscription and License Agreement.

Eagle RC Jr. Mechanisms of maculopathy. Ophthalmology 1984; 91:613.

Machemer R. [Development of pars plana vitrectomy. My personal contribution]. Klin Monbl

Topic 6910 Version 33.0

The use of UpToDate is subject to the Subscription and License Agreement.

Types of retinal detachment

Caused by breaks in the retina

Degenerative retinal lesions

Juvenile X-linked retinoschisis

Proliferative diabetic retinopathy

Penetrating eye injury

Sickle cell retinopathy

Retinal vein occlusion

Inflammatory (uveitis, scleritis)

Hydrostatic (malignant hypertension, toxaemia of pregnancy)

Neoplastic (choroidal melanoma, haemangioma, metastasis)

Vascular (Coat’s disease, retinal macroaneurysm)

Maculopathy (neovascular macular degeneration, central serous choroidoretinopathy)

Congenital disorders (nanophthalmos, optic disc pit)

What symptoms should alert me to a threatened retinal detachment?

Flashes and floaters

Box 2 Causes of photopsia and floaters

Posterior vitreous detachment

Optic nerve pathology

Transient ischaemic attacks

Floaters (perception of mobile spots, lines, or haze due to vitreous opacities)

Age related macular degeneration

Posterior vitreous detachment

Vitreous haemorrhage (diabetic retinopathy, trauma)

Who is at risk of developing retinal detachment?

How to assess a patient with suspected retinal detachment

Decisions to refer: when, to whom, and how urgently?

Treatment of retinal break and detachment

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Pharmacological vitreolysis may simplify repairs of difficult tractional detachment

Emedicine—www.emedicine.com/emerg/topic504.htm (Larkin GL. Retinal detachment. April 2008.)