1. Cataract
Tahir Masoud
17th March 2010

2. Definition
A cataract is an opacity in the natural lens that can cause visual problems.

3. Why is it important?
Age-related cataract is responsible for 48% of world blindness, which represents about 18 million people, according to the World Health Organization (WHO).
At least 5-10 million new visually disabling cataracts occur yearly, with modern surgical techniques resulting in 100, ,000 irreversibly blind eyes.

4. 1.2% of the entire population of Africa is blind, with cataract causing 36% of this blindness.
In a survey conducted in 3 districts in the Punjab plains, the overall rates of occurrence of senile cataract was 15.3% among 1269 persons examined who were aged 30 years and older and 4.3% for all ages. This increased markedly to 67% for ages 70 years and older.

5. In the UK 30% of persons of 65 years and over have visually impairing cataract in one or both eyes.
It is estimated that 2.4 million people aged 65 and older in England and Wales have visually impairing cataract in one or both eyes

6. An analysis of blind registration forms in the west of Scotland showed senile cataract as one of the 4 leading causes of blindness.

7. Anatomy
The lens is surrounded by a thick lens capsule which is the basement membrane of the lens epithelial cells.
Epithelial cells at the lens equator continue to be produced throughout life
Older lens fibres are compressed into a central nucleus
Younger fibres around the nucleus make up the cortex.

10. Causes
Aging
Long-term ultraviolet (UV) light, especially from sunlight
Systemic disease
Diabetes
Myotonic dystrophy
Atopic dermatitis
Neurofibromatosis type 2

11. Past eye infections, injuries or surgery Smoking Drugs
Steroids
Chlorpromazine
Busulphan
Amiodarone
Gold
Hereditary

12. Classification Morphological Maturity Cortical Nuclear Subcapsular
Christmas tree
Maturity
Immature
Mature
Hypermature
Morgagnian

13. Age
Congenital
Presenile
Senile
Cause
Primary
Secondary

23. Congenital cataract Present at birth or appear shortly thereafter
These cataracts may show many different patterns.
The opacity may be confined to the area of the embryonic or fetal nucleus with clear cortex surrounding this.

24. Prenatal infections: Rubella, CMV, HSV, Varicella
Maternal ingestion of thalidomide, steroids
Systemic disease
Metabolic: Galactosemia, Galactokinase deficiency
Hereditary
Autosomal dominant
Recessive
X-linked

25. Chromosomal abnormalities
Down syndrome (trisomy 21)
Patau syn (trisomy 13)
Edward syn (trisomy 18)

27. Secondary Cataract Develop as a direct effect of eye diseases
glaucoma,
iritis
eye tumors ,
retinitis pigmentosa
retinal detachment.

28. Symptoms
Blurred vision
Distortion
Glare
Diplopia
Myopic shift

29. Assessment Vision acuity test Slit lamp Ophthalmoscopy
In most cases, eye drops are used to dilate pupils before the exam.
Tonometry

30. Treatment
If symptoms from a cataract are mild, a change of glasses may be all that is needed for you to function more comfortably.
Surgery is the only way to remove the cataract.
Cataract surgery should be considered when cataracts cause enough loss of vision to interfere with daily activities.

31. Types of cataract surgery
Intracapsular
Extracapsular
Phacoemulsification
ECCE

32. Extracapsular cataract extraction is the preferred method of cataract surgery
It preserves the posterior portion of the lens capsule
Posterior chamber IOL can be implanted in the capsular sac
An IOL is a tiny, transparent, convex lens made of different materials which is inserted in the eye during surgery.

33. Glaucoma
Tahir Masoud th March 2010

34. Glaucoma
A group of disorders in which there is eventual development of an optic neuropathy with characteristic changes at the optic nerve head.
Depression of visual function and eventual loss of visual field.
Raised intra-ocular pressure often appears to be a significant factor in its development.

35. Why is glaucoma important
Glaucoma causes significant visual disability in the UK, accounting for 15% of registrable blindness
In a white population, POAG occurs in approximately 1-2% of the population over 40, increasing with age to 4% or more of the over 80-year olds.

36. Anatomy and physiology
Schwalbe line
Trabeculum
Schlemm canal
Scleral spur
Iris processes

37. Aqueous is actively secreted by the non-pigmented epithelium of the pars plicata (anterior) of the ciliary body
Approximately 90% of aqueous leaves through the trabeculum into the Schlemm canal and drains into episcleral veins (trabecular or conventional route)

38. 10% of aqueous passes across the face of the ciliary body into suprachoroidal space and then drains into the venous system (uveoscleral or unconventional route)

39. IOP can be reduced by Reducing the aqueous production
Increasing the aqueous outflow

40. Optic nerve head 2% of population have cup-disc ratio > 0.7
Small physiological cup
Large physiological cup
Normal vertical cup-disc ratio is 0.3 or less
2% of population have cup-disc ratio > 0.7
Total glaucomatous cupping

41. Classification Primary congenital forms
Primary open-angle glaucomas (POAG)
Primary juvenile glaucoma
POAG/high pressure glaucoma
POAG/normal pressure glaucoma
Primary open-angle suspect
Ocular hypertension
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.

42. Primary angle-closure glaucoma(PACG)
Secondary open-angle glaucomas
Secondary open-angle glaucomas caused by ocular disease
Iatrogenic secondary open-angle glaucomas
Primary angle-closure glaucoma(PACG)
Pupillary block
Plateau iris syndrome

43. Primary open-angle glaucomas (POAG)
Glaucomatous optic atrophy
Normal pressure glaucoma
Online Journal of Ophthalmology
Primary open-angle glaucoma (POAG) is one of the leading causes of visual impairment and blindness in the UK.1
POAG can encompass a range of disorders, which can be characterised as generally bilateral, but often asymmetric, progressive optic neuropathies and an open anterior chamber angle.2,3
POAG may be categorised as normal pressure when IOP is normal without treatment, although other typical characteristics exist.1
References
Kroese M, Burton H. J Epidemiol Community Health 2003;57:752–754.
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
American Academy of Ophthalmology. Preferred Practice Pattern – Primary Open-Angle Glaucoma, 2005. 43

44. Primary angle-closure
Acute angle-closure
Acute/intermediate angle-closure
Online Journal of Ophthalmology
Primary angle-closure glaucoma is defined by the presence of iridotrabecular contact and a number of mechanisms may be responsible for appositional or synechial closure of the anterior chamber.1
Three forms of the condition may manifest2,3:
Acute, symptomatic form, uncommon in Europe, which may or may not lead to significant glaucomatous optic nerve damage
Intermediate mildly symptomatic form
Chronic, asymptomatic form
Primary angle-closure can be staged into the following three groups1,2:
Primary angle-closure suspect
Primary angle-closure
Primary angle-closure glaucoma
References
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Foster PJ et al. Br J Ophthalmol 2002;86:238–242. 44

45. Lens-induced secondary open-angle glaucoma
Glaucoma classification Secondary open-angle glaucomas caused by ocular disease
Exfoliative glaucoma
Pigmentary glaucoma
Lens-induced secondary open-angle glaucoma
Glaucoma associated with intraocular haemorrhage
Uveitis glaucoma
Glaucoma due to intraocular tumours
Glaucoma associated with retinal detachment
Open-angle glaucoma due to ocular trauma
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008. 45

46. Secondary open-angle glaucomas
Heterochromic iridocyclitis fuchs (uveitis), secondary open-angle glaucoma
Pigment dispersion syndrome
Uveitis glaucoma
This classification may be given when uveitis is associated with elevated IOP, optic nerve and/or visual field defects.1
Pigment dispersion syndrome
This condition is typically characterised by dense trabecular pigmentation4 caused by the accumulation of melanin granules in the trabecular meshwork, resulting in open anterior angle chambers.2,3
Exfoliative glaucoma
This condition occurs as a result of exfoliative syndrome, an age-related disorder of the extracellular matrix. It predisposes to both open-angle and angle-closure glaucoma.4
References
Moorthy RS et al. Surv Ophthalmol 1997;41:361–394.
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Ritch R. Am J Ophthalmol 1998;126:442–445.
Ritch R. Curr Opin Ophthalmol 2001;12:124–130.
Exfoliative glaucoma
Online Journal of Ophthalmology: 46

47. Lens-induced (phacolytic) glaucoma
Phacomorphic malignant glaucoma
Lens-induced secondary open-angle glaucoma is caused when lens protein obstructs the trabecular meshwork.1
Lens proteins may be associated with a cataract, cataract surgery, or other trauma/surgery to the lens.1
Phacolytic glaucoma is the term given specifically to obstruction by lens protein from a mature or hypermature cataract with intact capsule.1
Reference
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Phacolytic glaucoma, histology
Phacolytic acute open-angle glaucoma
Online Journal of Ophthalmology: 47

48. Secondary open-angle glaucomas Neovascular secondary glaucoma
Neovascular secondary angle-closure glaucoma
Neovascular glaucoma is an uncommon type of glaucoma that is difficult to treat and often results in blindness.1
The condition is most commonly caused by diabetic retinopathy, ischaemic central retinal vein occlusion and ocular ischaemic syndrome.1
Other uncommon causes include ocular radiation, ocular tumours, uveitis and other retinal diseases.1
Ischaemia of the optic nerve head and/or retina is the main reason for visual loss with high IOP.1
Reference
Hayreh SS. Prog Retin Eye Res 2007;26:470–485.
Florid iris neovascularisation
Online Journal of Ophthalmology: 48

49. Secondary open-angle glaucomas Trauma and secondary glaucoma
Lens luxation with acute pupillary block glaucoma
Several mechanisms can lead to glaucoma following ocular trauma.1
Secondary traumatic glaucomas can be caused by both open-angle and angle-closure pathomechanisms.1
Examination may reveal the following:
Chemical burns
Hyphema
Traumatic cataract
Swollen lens
Uveitis
Angle recession
Ruptured iris sphincter
Reference
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Hyphema, total, secondary open-angle glaucoma
Online Journal of Ophthalmology: 49

50. Risk factors for angle-closure
Shallow anterior chamber depth, associated with1:
Female gender
Increasing age
Asian (particularly Chinese) origin
Shorter globe axial length1
Environmental factors1:
Seasonal variation
Extreme temperatures
Prolonged periods indoors in a dark environment
An association has been found between a shorter axial length and a higher incidence of primary angle-closure.1
The demographic risk factors of female gender, Asian origin and elderly age all contribute to a shallow anterior chamber, which is associated with the highest risk of angle-closure glaucoma.1
Reference
Foster PJ. Semin Ophthalmol 2002;17:50–58.
1. Foster PJ. Semin Ophthalmol 2002;17:50–58. 50

51. Patient history POAG is often asymptomatic Angle-closure glaucoma
Eye pain and redness
Halos
Headaches
The first step in the diagnosis of glaucoma is assessment of presenting complaint. Most glaucomas are asymptomatic until well advanced, therefore identification may have to be reliant on assessment of risk factors and assessment of glaucomatous changes.
Glaucoma symptoms that may be noted are visual blurring and discomfort, haloes around lights and/or glare, poor light to dark adaptation, and difficulty in tracking fast-moving objects.1
Taking a comprehensive medication history is also essential as there are certain medications that may lead to glaucoma or glaucoma-like conditions. These include:
Steroids – associated with ocular hypertension and open-angle glaucoma
Anticholinergics/tricyclic antidepressants – associated with angle-closure glaucoma
Anticonvulsants – associated with nasal peripheral loss without disc changes
Family history must also be noted due the hereditary nature of primary open-angle glaucoma.2
References
South East Asia Glaucoma Interest Group (SEAGIG). Asia Pacific Glaucoma Guidelines, 2003.
Tielsch JM et al. Arch Ophthalmol 1994;112:69–73.
South East Asia Glaucoma Interest Group (SEAGIG). Asia Pacific Glaucoma Guidelines, 2003. 51

52. Ophthalmic history
Trauma, previous eye surgery or laser, previous ophthalmic medications
Medication history
Social history
Family history
Risk factors in family
Blindness or eye disease in the family

53. Examinations & investigations
Visual acuity
Slit-lamp examination
Applanation tonometry
Gonioscopy
Optic nerve head and retinal nerve fibre layer evaluation
Visual field examination (perimetry)
Pachymetry
All patients should undergo a comprehensive physical eye examination.
An ophthalmologist should ensure that they have the necessary equipment and training to provide1:
Complete examination of the pupil, anterior segment, optic nerve head and retinal nerve fibre layer, and fundus
Measurement of IOP, central corneal thickness, visual field and visual acuity
Reference
American Academy of Ophthalmology. Preferred Practice Pattern – Primary Open-Angle Glaucoma, 2005. 53

54. Examinations & investigations Slit-lamp examination
Online Journal of Ophthalmology
During the glaucoma assessment, slit-lamp examination should be used to assess:
The pupils for reactivity and an afferent pupillary defect1
The anterior segment, prior to and after dilation, for evidence of physical findings associated with narrow angles, corneal pathology, or a secondary mechanism for elevated IOP such as pseudoexfoliation, pigment dispersion, iris and angle neovascularisation, or inflammation1,2
The fundus, through a dilated pupil whenever feasible, in order to search for other abnormalities that might account for visual field defects (e.g. optic nerve pallor, tilted disc, disc drusen, optic nerve pits, optic nerve hypoplasia, neurological disease, macular degeneration, and other retinal disease)1
Optimal examination of the peripheral retina requires the use of the indirect ophthalmoscope or slit-lamp fundus biomicroscopy. Optimal examination of the macula and optic nerve requires the use of the slit-lamp biomicroscope and accessory diagnostic lenses1
Slit-lamp biomicroscopic examination should also include the eyelid margins and lashes, tear film, conjunctiva, sclera, cornea, anterior chamber, and assessment of peripheral anterior chamber depth, iris, lens, and anterior vitreous.2
References
American Academy of Ophthalmology. Preferred Practice Pattern – Primary Open-Angle Glaucoma, 2005.
American Academy of Ophthalmology. Preferred Practice Pattern – Comprehensive Adult Medical Eye Evaluation, 2005.
Acute angle-closure glaucoma 54

55. Examinations & investigations Slit-lamp examination – applanation tonometry
National Eye Institute, National Institutes of Health
The Goldmann applanation tonometry (GAT) mounted at the slit lamp is the gold standard for assessment of IOP.1
Before use, it is important to ensure that the tonometer is calibrated to the desired threshold tension levels.2
Topical anaesthesia must be applied as the prism tip must touch the cornea.
If GAT is unavailable or unsuitable for the patient, other tonometry methods that may be employed are1:
Air puff tonometry
Pneumatonometry
Tono-Pen XL
Ocuton self-tonometry
Pascal dynamic contour tonometry (DCT)
Ocular Response Analyser (ORA)
Rebound (Icare) tonometry
References
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
South East Asia Glaucoma Interest Group (SEAGIG). Asia Pacific Glaucoma Guidelines, 2003.
European Glaucoma Society, 2008 55

56. Examinations & investigations Direct gonioscopy
European Glaucoma Society, 2008
Direct gonioscopy allows the use of contact goniolens to permit the light from the anterior chamber to pass through the cornea so that the angle may be viewed.1
The most commonly used lenses for direct gonioscopy are:
Koeppe (contact fluid required)
Layden (sized for infants; contact fluid required)
Worst
For this procedure, the patient must be lain on their back. A direct view of the anterior chamber angle is possible and both eyes can be compared simultaneously.1
Reference
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Rich R, courtesy of South East Asia Glaucoma Interest Group (SEAGIG). 56

57. Assessment of the optic disc
Observe the scleral ring to size the optic disc
Identify the size of the rim
Examine the RNFL
Optic nerve head (ONH) and retinal nerve fibre layer (RNFL) evaluation can be divided into two parts1:
Qualitative
Contour of the neuroretinal rim
Optic disc haemorrhages
Peripapillary atrophy
Bared circumlinear vessels
Appearance of the RNFL
Quantitative
Optic disc size (vertical disc diameter)
Cup/disc ratio (vertical)
Rim/disc ratio
RNFL height
Careful study of the optic disc neural rim for small haemorrhages is important as these may precede visual field loss and further optic nerve damage.2
References
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Drance S et al. Am J Ophthalmol 2001;131:699–708.
Examine the region of the peripapillary atrophy
Look for retinal and optic haemorrhages
Photographs by Ki Ho Park, courtesy of South East Asia Glaucoma Interest Group (SEAGIG). 57

58. Optical coherence tonometry
Examinations & investigations Optic nerve head/retinal nerve fibre layer imaging
Red-free photography
Optical coherence tonometry
The preferred technique for optic nerve head and retinal nerve fibre layer evaluation involves magnified stereoscopic visualisation, preferably through a dilated pupil. Red-free illumination may aid in evaluating the retinal nerve fibre layer.1
Colour stereophotography or computer-based image analysis of the optic nerve head and retinal nerve fibre layer are the best currently available methods to document optic disc morphology and should be performed.1
Newer imaging techniques are now available for documentation of the optic disc. These include2,3:
The Heidelberg retinal tomogram (HRT)
Scanning laser polarimetry (GDx)
Optical coherence tomography (OCT)
Retinal nerve fibre layer imaging by OCT is reliable, despite the fact that age, ethnicity, axial length and optic disc size can affect the machine’s normative range. Also, scan quality can be affected by movement, media opacities, myopia and severity of disease.4
The HRT is considered a promising tool, although the relationship between progressive structural and visual field change has yet to be fully elucidated.5
References
American Academy of Ophthalmology. Preferred Practice Pattern – Primary Open-Angle Glaucoma, 2005.
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Thomas R, Parikh RS. Community Eye Health 2006;19:36–37.
Chang R, Budenz DL. Curr Opin Ophthalmol 2008;19:127–135.
Strouthidis NG, Garway-Heath DF. Curr Opin Ophthalmol 2008;19:141–148.
Ki Ho Park, courtesy of South East Asia Glaucoma Interest Group (SEAGIG). 58

59. Examinations & investigations Visual field examination – perimetry
Testing of visual field is mandatory in glaucoma assessment and management1 in order to define the state of optic nerve function and visual impairment.
All patients with glaucoma or suspected glaucoma should undergo frequent visual field examinations.2
Standard automated perimetry (SAP) is the preferred technique for evaluating the visual field.1,3
Kinetic testing is an acceptable alternative when patients cannot perform SAP or if it is not available.3 However, the method is not considered suitable for detection of early glaucomatous field loss and small defects may be lost between isopters.1
It is important to use a consistent examination strategy when visual field testing is repeated.3
Characteristics of glaucomatous visual field defects include4:
Asymmetrical across horizontal midline in early/moderate cases
Located in mid-periphery, 5–25 degrees from fixation, in early/moderate cases
Reproducible
Not attributable to other pathology
Clustered in neighbouring test points (localised)
Defect should correlate with the appearance of the optic disc and neighbourhood.
References
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Chauhan BC et al. Br J Ophthalmol 2008;92:569–573.
American Academy of Ophthalmology. Preferred Practice Pattern – Primary Open-Angle Glaucoma, 2005.
South East Asia Glaucoma Interest Group (SEAGIG). Asia Pacific Glaucoma Guidelines, 2003.
Mild loss of visual field
Severe loss of visual field 59

60. Treating the mechanisms of glaucoma1,2
Medical Rx
IOP reduction
Laser trabeculoplasty
Abnormal anatomy
Work with multidisciplinary team to treat systemic problems
Contributing diseases
Laser iridoplasty Iridotomy
Lens extraction Vitreous surgery
Reduction of IOP
Choose the appropriate medication1,2:
Most likely to reach target IOP
Best safety profile
Minimal inconvenience
Start with monotherapy wherever possible.1,2
Laser trabeculoplasty is also an effective treatment option.2
Treatment of angle-closure
Treatment may involve1:
Deepening of peripheral angle-closure
Iridotomy – to reduce pupil block
Argon laser peripheral iridoplasty – to flatten peripheral iris
Lens extraction – to reduce pupil block and displace iris posteriorly
Vitreous surgery
References
South East Asia Glaucoma Interest Group (SEAGIG). Asia Pacific Glaucoma Guidelines, 2003.
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
Filtration surgery trabeculotomy
1. South East Asia Glaucoma Interest Group (SEAGIG). Asia Pacific Glaucoma Guidelines, 2003.
2. European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008. 60

61. Glaucoma treatment Pharmacological medication Laser treatment Surgery
Objective: to review the different options for treatment of underlying disease mechanisms and abnormal eye anatomy
Pharmacological medication
Laser treatment
Surgery 61 61

62. Alpha-2 agonists Beta-blockers Betaxolol Timolol Brimonidine
Apraclonidine
Prostaglandin analogues
Bimatoprost
Latanoprost
Travoprost

63. Miotics Pilocarpine Carbonic anhydrase inhibitors
Systemic: Acetazolamide
Topical: Dorzolamide, Brinzolamide

64. Laser treatment Primary open-angle glaucoma
Laser trabeculoplasty – outflow enhancement
Cyclophotocoagulation – inflow reduction in end-stage 64

65. Laser treatment Angle closure and angle-closure glaucoma
Laser iridotomy – pupillary block relief
Laser iridoplasty (gonioplasty) – modification of iris contour
Cyclophotocoagulation – inflow reduction for end-stage glaucoma 65

66. Surgery Incisional surgery options for glaucoma
Characteristics required
Type of surgery
Open-angle glaucoma
Outflow enhancement
Glaucoma draining
Filtering surgery*
Drainage device
Chronic angle-closure glaucoma
Pupillary block relief
Widening of anterior chamber angle inlet
Iridectomy
Trabeculectomy
Lens extraction
Acute angle closure (± glaucoma)
Angle surgery
Goniosynechialysis
Childhood glaucoma
Angle Surgery
Glaucoma drainage
Goniotomy/trabeculotomy
Trabeculectomy†
There are various incisional surgery techniques, whose indications depend on the type of glaucoma being treated. The decision to use a particular type of surgery should depend on1:
The target IOP for that individual patient
Previous ophthalmic history
Risk profile
The preferences and experiences of the surgeon
The patient’s opinions and expectations
Pre-operative assessment should identify any risk factors for failure of surgery, which include2:
Asian or African ethnicity
Previous surgery
Young age
Aphakia
Pseudophakia
Active ocular inflammation
Prolonged use of topical glaucoma medications
Tendency to form keloids
Neovascular glaucoma
References
European Glaucoma Society. Terminology and Guidelines for Glaucoma (3rd ed), 2008.
South East Asia Glaucoma Interest Group (SEAGIG). Asia Pacific Glaucoma Guidelines, 2003. 66