Secondary congenital glaucoma history, anatomy, histology, treatment, signs and symptoms, medication and prevalence.

1. Congenital
Glaucoma

2. History
The discovery of the disease called glaucoma dates back to the 17th century. And it is the main cause of blindness
has been known since the 19th century world wide. In the Hippocratic Aphorisms the term "glaykoseis“ was used
to describe blindness that comes along with aging and a glazed appearance of the pupil.
Al- Tabari
10th Century
Hippocratic treatment
Dr. Richard Bannister
Oculist-1622

3. Definition &
Anatomy
 aqueous humor out flow in the anterior segment.
 In people with glaucoma, the drainage canal is partially
or completely blocked. Fluid builds up in the chambers
and this increases pressure within the eye. High IOP can
damage the optic nerve and visual field.
Glaucoma is a pathogenic condition. And it is a group of eye diseases
in which the optic nerve is damaged leading to irreversible loss of
vision. In most cases, this damage is due to an increased pressure
within the eye.

4. Sequence Of
Glaucoma High pressure is not always dangerous, however in susceptible individuals high pressure can damage the optic
nerve, the nerve that transmit messages from the eyes to the brain. As the nerve fibers are damaged, the vision
begins to fail, starting with peripheral side vision. And if left untreated, may lead to total blindness.

5. Types of Glaucoma
There are several types of glaucoma. The two main types are open-angle
and angle-closure. These two types involve in increase of intraocular
pressure (IOP), or pressure inside the eye.
1- Open-angle glaucoma:
It caused by partial blockage of the drainage canal. The angle between the
cornea and the iris is "open", meaning the entrance to the drain is clear, but
the flow of aqueous humor is somewhat slow.

6. Types of Glaucoma
2- Close -angle glaucoma:
Caused by a sudden and complete blockage of aqueous humor
drainage. The IOP rises rapidly and may lead to total vision loss
quickly.
 Demands immediate medical attention
Narrow Angle

7. Primary Congenital Glaucoma
(PCG)
 PCG refers to glaucoma resulting from maldevelopment of the aqueous outflow system. which has an isolated
poor development of the trabecular meshwork that is called : ISOLATED TRABECULODYSGENESIS
 Barkan’s membrane theory - A thin, imperforate membrane covering the anterior chamber angle of the eyes
prevents aqueous humor outflow, and leads to increased IOP.
1- Flat anterior iris insertion 2- Concave iris insertion

8. Primary Congenital Glaucoma (PCG)
Signs and symptoms:
1. Epiphoria
2. Photophobia
3. Blepharospasm
4. Buphthalmos
5. Haab striae
6. Corneal opacification
 The optic nerve cupping may occur rapidly and early in infants
Also, it may be reversible with normalization of IOP.
Buphthalmos Corneal opacification
Haab striae

9. PCG Risk
FactorsAlthough it is generally agreed that the IOP elevation in PCG is due to an abnormal development of the anterior chamber
angle, there is no universal agreement on the subject. Below are some PCG abnormal theories:
Mann (1928)
Burian, and Braley (1955)
Maumenee (1958)
PCG result
from a developmental abnormality of anterior chamber angle
tissue derived from neural crest cells, leading to aqueous
outflow obstruction by one or more of several mechanisms.

10. PCG Treatments
1- Goniotomy:
is a surgical procedure in which the doctor uses a lens called a
goniolens to see the structures of the front part of the eye (A/C).
An opening is made in the trabecular meshwork, the new opening
provides a way for fluid to flow out of the eye.

11. PCG
Treatments
2- Trabeculotomy:
A piece of tissue in the eye's drainage angle is removed to create an
opening. This new opening allows fluid (aqueous humor) to drain
out of the eye.
 Trabeculotomy performed when cornea is cloudy.

12. Medicatio
nsProstaglandin-related drugs
Xalatan® (latanoprost) 0.005% (qd)
Beta-blockers
Timolol solution 0.25% (qd, bid)
Carbonic anhydrase inhibitors
Dorzolamide 2% (bid, tid)
 Medical therapy for pediatric glaucoma patients is often administered to reduce the IOP temporarily, to clear the
cornea, and to facilitate surgical intervention.

13. Medication
the most serious systemic
concerns associated with topical
glaucoma medication use in
children.
Central nervous system (CNS)
toxicity with alpha-2 agonists,
Alphagan.

14. Post-treatment
 Some children with congenital glaucoma and elevated IOP respond to medical therapy. Which depend on
Structural defects ,Age, Systemic syndromes, Corneal clarity, Severity of glaucoma, and Corneal
diameter.
 Between 3 and 6 weeks after surgery the postoperative control of the photophobia, tearing, and
Blepharospasm usually reflect the effectiveness of surgery.
 Follow up visitation exams include, vision testing, external examination, refraction, ophthalmoscopy,
corneal assessment, and tonometry.
 Visual rehabilitation is as important of in the management of disease as controlling IOP. Anisometropia
and Amblyopia must be manage to give the child best chance for good vision.

15. PCG Prevalence
 60 % of pediatric glaucoma cases are diagnosed by the age of 6 months and 80% within the
first year of life. And 65% of patients are male.
 PCG with elevated IOP occurs in about 1 out of 10,000 births and results in blindness in
approximately 10% of cases . And reduced vision (worse than 20/50) in about half of all
cases.
 PCG is typically bilateral, although a significant IOP elevation may occur in only one eye in
25 to 30% of the cases.
 In patient with clear cornea both procedure goniotomy & trabeculotomy yields a 70-80%
success rate.

16. Conclusion
 Glaucoma is one of the leading causes of blindness in the United States. It can occur at any age
but is more common in older adults.
 Surgical therapy is the most effective and definitive form of treatment for the developmental
glaucoma.
 The most common form of glaucoma has no warning signs in adult. In the other hand, the triad
signs in PCG should be considered seriously.
 Elevated IOP – causes stretching and rupture of the zonules can cause lens subluxation. Blunt
trauma can cause hyphemas, retinal detachment, and rupture of the globe.