1. Caring for patients with cataract, glaucoma.
Lecturer: Lilya Ostrovska

2. Cataract Causes Age Congenital (genetic, metabolic) Trauma Infection
Inflammation
Surgical
Drugs (eg steroids)

3. Cataract
May be induced by surgical procedure: lens touch; gas; oil

4. Cataract types Nuclear sclerosis Posterior subscapsular
Congenital (rubella)
Trauma

5. CONGENITAL CATARACT 1. Important facts 2. Classification 3. Causes
In healthy neonates
In unwell neonates

6. Important facts 33% - idiopathic - may be unilateral or bilateral
33% - inherited - usually bilateral
33% - associated with systemic disease - usually bilateral
Other ocular anomalies present in 50%

7. Classification of congenital cataract
Anterior polar
Posterior polar
Coronary
Cortical spoke-like
Lamellar
Central pulverulent
Sutural
Focal dots

8. Anterior polar cataract
May be dominant inheritance
Capsular
Pyramid
With persistent pupillary
membrane
With Peters anomaly

9. Posterior polar cataract
Ocular associations
Persistent hyaloid remnants
Posterior lenticonus
Persistent hyperplastic primary vitreous

10. Coronary (supranuclear) cataract
Usually sporadic
Round opacities in deep cortex
Surround nucleus like a crown

11. Cortical spoke-like cataract
Systemic associations
Fabry disease
Mannosidosis

12. Lamellar cataract Systemic associations
Usually dominant inheritance
Round central shell-like opacity
surrounding clear nucleus
May have riders
Systemic associations
Galactosaemia
Hypoglycaemia
Hypocalcaemia

13. Central pulverulent cataract
Dominant inheritance
Spheroidal opacity within nucleus
Relatively clear centre
Non-progressive

14. Sutural cataract Opacity follows shape of Y suture
Usually X-linked inheritance
Opacity follows shape of Y suture

15. Focal dot opacities Blue dot cortical opacities Common and innocuous
May co-exist with other opacities

16. Causes of cataract in healthy neonate
Hereditary
(usually dominant)
Idiopathic
With ocular anomalies
. PHPV
Aniridia
Coloboma
Microphthalmos
Buphthalmos

17. Causes of cataract in unwell neonate
Intrauterine infections
Rubella
Toxoplasmosis
Cytomegalovirus
Varicella
Metabolic disorders
Galactosaemia
Hypoglycaemia
Hypocalcaemia
Lowe syndrome

18. Management of Cataract
ECCE (Extracapsular cataract extraction)
But longer wound healing time

19. Cataract Surgery
Small incisional Phacoemulsification surgery (Developed by Kelman, USA)

20. Before IOL implantation was developed
Aphakic spectacles
Contact lenses

21. : First IOL implants

22. Choice of IOL Insertion through small incision High biomcompatilbility
Allows good retinal view
Stable centration
Low PCO (posterior capsular opacification) rate

23. IOL choice Why foldable/injectable
IOL choice Why foldable/injectable? Minimise incision size to reduce healing time and astigmatism
PMMA(rigid) : Non-foldable+large incision
Acrylic: Injectable through mm currently.

24. Preparation for cataract surgery
Biometry: The calculation of required IOL power
Keratometry (K) (corneal curvature)
Axial length (AL) of eye (ultrasound)
IOL power= A constant-2.5xAL-0.9K
Eg: x x45= dioptres IOL power

25. Phacoemulsification with IOL implantation

26. Phacoemulsification: surgical sequence
Corneal tunnel
CCC (continuous curvilinear capsulorrhexis
Hydrodissection
Phacoemulsification
Aspiration of cortical lens matter
IOL insertion

27. Phaco parameters

28. Phaco+IOL surgery Hydrodissection

29. Phaco+IOL surgery Phacoemulsification

30. Phaco+IOL surgery Aspiration of cortex

31. Phaco+IOL surgery Foldable IOL insertion

32. Typical injectable IOL
Superflex lens: 6.25mm x 12.50mm
C-Flex lens 5.75mm x mm

33. Cflex/Superflex injector

34. Loading the Superflex IOL

35. Superflex insertion

36. Superflex insertion

37. Superflex insertion

38. Endoscope view of Superflex

39. Cataract surgery Postoperative management Eye pad overnight
Antibiotic+steroid drops for up to one month
Change glasses at one month

40. Complications of cataract surgery (many!)
Posterior capsular rupture and vitreous loss
Dropped nucleus
IOL dislocation
Endophthalmitis
Retinal detachment

41. Cataract surgery complications

42. Cataract surgery: complications

43. GLAUCOMA

44. 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.
And you thought glaucoma was a disease in which there was too much pressure in the eye! So did most ophthalmologists until several years ago.

45. 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.”

46. GLAUCOMA
What causes it?
There is a dose-response relationship between intraocular pressure and the risk of damage to the visual field.
But pressure certainly plays a role. Glaucoma is just too complicated to fit a nice simple definition.

47. ADVANCED GLAUCOMA INTERVENTION STUDY
The Advanced Glaucoma Intervention Study documented that pressure does play a crucial role in the visual field damage of many patients. Note that the greater the percentage of visits in which the pressure was below 28, the less visual field defects developed.

48. GLAUCOMA How do we diagnose it?
IOP is not helpful diagnostically until it reaches
approximately 40 mm Hg at which level the
likelihood of damage is significant.
Visual fields are also not helpful in the early stages
of diagnosis because a considerable number of neurons must be lost before VF changes can be
detected.
Optic nerve damage in the early stages is difficult
or impossible to recognize.
50% of people with glaucoma do not know it!
The three mainstays of glaucoma diagnosis are inadequate. The actual intra-ocular pressure is too imprecise, and the changes in the visual field and the optic nerve occur too late to prevent most of the damage.

49. Intraocular pressure is not the only factor
GLAUCOMA
Intraocular pressure is not the only factor
responsible for glaucoma!
95% of people with elevated IOP will never have the damage associated with glaucoma.
One-third of patients with glaucoma do not have
elevated IOP.
Most of the ocular findings that occur in people
with glaucoma also occur in people without glaucoma.
Sobering facts!

50. CHARACTERISTICS OF IOP
Normal range: mm Hg
Follows non-Gaussian curve with right
skewed tail
30-50% of open angle glaucoma patients
have IOP <22 mmHg
Diurnal flucuation normally < 6 mmHg
Women have slightly higher pressures

51. GLAUCOMA Anatomy of anterior chamber angle
The aqueous humor is manufactured by the non-pigmented ciliary epithelium in the posterior chamber.

52. GLAUCOMA
Iris bombé
Iris Bombe with secluded pupil

53. GLAUCOMA Population distribution of IOP
Two standard deviations above the mean occurs at about mmHg.

54. GLAUCOMA IOP Variables Gender influences: Normal vs glaucoma:
Large intra-day fluctuations as seen on the right are a risk factor for glaucoma

55. GLAUCOMA Angle Anatomy
Normal anatomy. The aqueous humor is made in the posterior chamber and escapes through the trabecular meshwork of the anterior chamber.

56. GLAUCOMA How do we measure IOP? Applanation Tonopen Schiotz Air
Non-contact

57. GLAUCOMA Schiotz Applanation Tonometry
These techniques illustrate the two most common means of measuring intra-ocular pressures. Applanation is probably the most accurate method but requires a slit lamp to use it.

58. Goldmann applanation tonometer
GLAUCOMA
Goldmann applanation tonometer

59. GLAUCOMA
Tonopen

60. GLAUCOMA
Goldmann perimeter
Glaucoma visual fields

61. GLAUCOMA
The normal visual field: an island of vision in a sea of darkness:
Is this island of vision seen from a right eye or a left eye?

62. THE VISUAL FIELD
Humphrey automated perimetry

63. Visual fields in glaucoma
Early
Late

64. GLAUCOMA Cup-to-disk ratio
No two disks are alike. Signs suggesting glaucoma as seen in the right photo include a large cup, nasalization of vessels, and pallor of the cup. Note the peripapilary depigmentation on the right which can make the true cup:disk ratio difficult to estimate.

65. GLAUCOMA DISK CUPPING Normal Glaucoma
In glaucoma of all types, if not controlled. There is progressive enlargement of the cup, increased pallor of the base of the cup, and nasalization of the disk vessels.

66. GLAUCOMA Glaucomatous cupping
Whie there is lots of variation in glaucomatous disks, three common characteristics stand out: large cups, pale color and nasalization of the vessels.

67. GLAUCOMA The histology of glaucomatous optic nerve cupping:
Normal:
Note how vessels can hide under the lip of the disk which helps explain the apparent loss of continuity of vessels clinically.

68. GLAUCOMA Development of disk pallor
Optic nerve signs of glaucoma progression
Increasing C:D ratio
Development of disk pallor
Disc hemorrhage (60% will show progression of
visual field damage)
Vessel displacement
Increased visibility of lamina cribosa

69. Ocular hypertension treatment study (OHTS study)
GLAUCOMA
Ocular hypertension treatment study (OHTS study)
GOALS: To evaluate the effectiveness of topical ocular hypotensive
medications in preventing or delaying visual field loss
and/or optic nerve damage in subjects with ocular hyper-
tension at moderate risk for developing open-angle
glaucoma (POAG).
POPULATION: 1636 participants aged years with IOP 24-32
mm HG in one eye, and in the other, randomly
assigned to observation and treatment groups.

70. GLAUCOMA
OHTS parameters
TREATMENT GOALS: Reduce pressure to less than or equal to 24 mm Hg with a minimum pressure reduction of 20% from the baseline.
OUTCOME MEASURES: Development of reproducible visual field abnormality or development of optic disc deterioration.
MEDICATIONS USED: beta-adrenergic antagonists,
prostaglandin analogues, topical carbonic anhydrase inhibitors, alpha-2 agonists, parasympathomimetic agents, and epinephrine.

71. GLAUCOMA OHTS Conclusions
At 60 months, the probability of developing glaucoma was:
9.5% in observation group
4.4% in treatment group

72. GLAUCOMA OHTS parameters that influence the risk of developing POAG
IOP
Age
Cup-disk ratio
Central corneal thickness

73. GLAUCOMA
Percentage of OHTS participants in observation group who developed POAG (mean follow-up = 72 mo)
IOP vs central corneal thickness
Note that eyes with the thinnest corneas and highest pressures are at the greatest risk for developing open angle glaucoma.

74. GLAUCOMA
Normal central corneal thickness: 545 – 550 u Add or subtract 2.5 mmHg for each 50 u change in central corneal thickness

75. GLAUCOMA Types of glaucoma I. Primary: A. Congenital B. Hereditary
C. Adult (common types)
1. Narrow angle
2. Open angle
(Normal tension glaucoma)
II. Secondary
A. Inflammatory
B. Traumatic
C. Rubeotic
D. Phacolytic
etc.
This lecture covers only congenital and adult varieties of glaucoma but it is important to realize there are many other causes.

76. Congenital Glaucoma Onset: antenatally to 2 years old Signs
Elevated IOP
Buphthalmos
Haab’s striae
Corneal clouding
Glaucomatous cupping
Field loss
Symptoms
Irritability
Photophobia
Epiphora
Poor vision
Haab’s striae are found only in congenital glaucoma.

77. Buphthalmos and cloudy corneas
Congenital Glaucoma
Buphthalmos and cloudy corneas
The right eye in each patient has congenital glaucoma.

78. Congenital Glaucoma Haab’s striae Buphthalmos, glaucomatous
cupping, and
cloudy cornea OD
Normal OS
Haab’s striae

79. Narrow Angle Glaucoma Onset: 50+ years of age Symptoms
Severe eye/headache
pain
Blurred vision
Red eye
Nausea and vomiting
Halos around lights
Intermittent eye ache
at night
Signs
Red, teary eye
Corneal edema
Closed angle
Shallow AC
Mid-dilated, fixed
pupil
“Glaucomflecken”
Iris atrophy
AC inflammation
The classical signs and symptoms of narrow angle glaucoma.

80. GLAUCOMA Angle anatomy Grade I Grade 0 Grade III Grade II
Anterior chamber angles vary widely. Only Grade I angles are occludable and might lead to an angle closure attack, similar to what a Grade 0 looks like.

81. GLAUCOMA Anatomy of Angle Closure Glaucoma
When the trabecular meshwork is obstructed, outflow is impaired and pressure rises. This can occur due to congenitally narrowed angles, the development of synechiae (top right), or rubeosis with a flat chamber (bottom right).

82. Narrow Angle Glaucoma Mid-dilated, fixed pupil
Mid-dilated, fixed pupils and cloudy corneas during an angle closure attack.

83. Narrow Angle Glaucoma Treatment: Peripheral Iridotomy
The permanent surgical cure for narrow angle glaucoma.

84. Open Angle Glaucoma Aka: chronic simple glaucoma (CSG) and primary open angle glaucoma (POAG)
Risk Factors IOP Diabetes Age Myopia Race Gender Family history Cardiovascular Central corneal disease thickness Hormones

85. Open Angle Glaucoma Signs Elevated IOP Visual field loss Symptoms
Onset: 50+ years of age
Signs
Elevated IOP
Visual field loss
Glaucomatous disk changes
Symptoms
Usually none
May have loss of central
and peripheral vision
late
Remember: most patients with open angle glaucoma have no symptoms. This is the best reason to have periodic eye examinations with pressure checks and optic nerve evaluations.

86. Normal Tension Glaucoma (NPG, LTG, LPB, NTG)
Similar to OAG but IOP always < 21 mmHg
Higher prevalence of vasospastic disorders,
blood dyscrasias, autoimmune diseases
May be related to episodic hypotension,
hyopthyroidism
A diagnosis of exclusion!!!

87. Open Angle Glaucoma Risk factors HISTORY: Positive family history
EXAMINATION:
C/D 0.6 or greater
Vertical
elongation of disc
Inf. rim thinner
than sup.
C/D asymmetry >
0.2
HISTORY:
Positive family history
African American and Hispanic background
History of trauma
History of steroid use

88. GLAUCOMA Medical Surgical Beta-blockers Carbonic anhydrase inhibitors
Treatment
Medical
Surgical
Miotics
Beta-blockers
Carbonic anhydrase
inhibitors
Prostaglandin
analogues
Alpha-2 agonists
Argon laser trabeculoplasty
Trabeculectomy
Filtering procedure
Cyclocryotherapy
Cyclolaser ablation
Iridotomy
No treatment works all the time!

89. GLAUCOMA
Treatment
Mechanisms of drug action vary and many people require multiple medications.

90. GLAUCOMA Surgical treatment of glaucoma Argon laser trabeculoplasty
Filtration
procedures
These are the two most common surgical procedures for open angle glaucoma with success rates of 80+%.

91. GLAUCOMA Filtration blebs
Creating a path for the aqueous to escape into the sub-conjunctival space is the aim of filtration surgery.

92. THANKS FOR YOUR ATTENTION !