پاتو فیزیو لوژی گلوکوم اطفال دکتر علی صالحی

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پاتو فیزیو لوژی گلوکوم اطفال دکتر علی صالحی. Types of Glaucoma. Open-Angle Glaucoma Angle-Closure Glaucoma Normal-Tension Glaucoma (NTG) Congenital Glaucoma Secondary Glaucoma Pigmentary Glaucoma Pseudoexfoliative Glaucoma Traumatic Glaucoma Neovascular Glaucoma - PowerPoint PPT Presentation

Transcript of پاتو فیزیو لوژی گلوکوم اطفال دکتر علی صالحی

اطفال گلوکوم لوژی فیزیو پاتو

علیصالحی دکتر

Types of Glaucoma

• Open-Angle Glaucoma• Angle-Closure Glaucoma• Normal-Tension Glaucoma (NTG)• Congenital Glaucoma• Secondary Glaucoma• Pigmentary Glaucoma• Pseudoexfoliative Glaucoma• Traumatic Glaucoma• Neovascular Glaucoma• Irido Corneal Endothelial Syndrome (ICE)

Congenital Or Infantile Glaucoma

• Primary congenital, or infantile, glaucoma is elevated

intraocular pressure with onset in the first year of

life.

• It 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.

• approximately 70% of cases are bilateral.

• Although diagnosis is made in only 25% of

affected infants at birth, disease onset occurs

within the first year of life in more than 80% of

cases.

Pediatric glaucomas• Constitute a heterogeneous group of diseases that may

result from an intrinsic disease or structural

abnormality of the aqueous outflow pathways

(primary glaucoma)

• Or from abnormalities affecting other regions of the eye

(secondary glaucoma).

• A variety of systemic abnormalities are also associated

with pediatric glaucoma.

Systemic diseases with Glaucoma

• Aniridia

• Marfan's syndrome

• Sturge-Weber syndrome

• Neurofibromatosis

• Down's syndrome

• Steroid therapy, including inhaled steroids for

asthma and nasal steroids for allergies .

causes• Genetic (e.g. congenital glaucoma, infantile

glaucoma, juvenile glaucoma) • Following cataract surgery (aphakic glaucoma) • Due to ocular inflammation (iritis) • Trauma • Malformations of the eye (Axenfeld-Rieger,

aniridia , Peters anomaly) • Diseases which affect the rest of the body

(Sturge-Weber Syndrome, Lowe Syndrome, congenital rubella)

Aniridia

Axenfeld anomaly

Peters anomaly

• Primary congenital glaucoma typically presents in

the neonatal or infantile period with the classic

triad of epiphora, photophobia, and

blepharospasm.

• Corneal clouding from microcystic edema can occur,

accompanied by gradual enlargement of the

corneal diameter. As the edema extends through

the corneal stroma, breaks called Haab striae can

occur in Descemet’s membrane.

Congenital Glaucoma (Primary Congenital Glaucoma)

Clinical Findings

• Progressive corneal edema with breaks in

Descemet’s membrane (Haab striae)

• Elevated IOP, typically non-sedated between 30

and 40 mmHg

• Corneal enlargement

• The normal intraocular pressure is lower in

infants and young children than adults.

• A newborn has an average intraocular pressure

of 10-12 mm Hg, increasing to 14 mm Hg by age

7 or 8 years of age.

• An asymmetric measurement or an elevated

measurement in the presence of other clinical

signs helps make the diagnosis of glaucoma.

General Pathology

• Primary congenital glaucoma may represent an

arrest of the normal development of the anterior

chamber.

• The iris and ciliary body have an anterior insertion

with an open angle.

• The trabecular meshwork is present and appears

patent, but the trabecular beams are thickened and

the deeper tissues appear compressed.

• The disease is more common in males, typically is

bilateral, and does not have a racial or geographic

preference.

• Most cases are sporadic, but there is an autosomal

recessive(AR) inheritance pattern either autosomal

dominant (AD) for some cases.

• (GLC3A locus on chromosome 2p21).

Risk Factors

• The only known risk factors are genetic

consanguinity and affected siblings.

• The risk of congenital glaucoma in the second

child is approximately 5%, and the risk increases

to 25% with two affected siblings.

Diagnosis

• The diagnosis of primary congenital glaucoma

can often be made clinically, even without an

accurate measurement of intraocular pressure.

The hallmark of the disease, however, is an

elevated intraocular pressure in the absence of

other conditions that can cause glaucoma,

such as Axenfeld-Reiger syndrome or aphakia.

• . A newborn’s cornea is typically 9.5-10.5 mm in

diameter and increases to 10.0-11.5 mm by age

1.

• Any diameter above 12.5 mm suggests an

abnormality, especially if there is asymmetry

between the two eyes.

Differential diagnosis

• The differential diagnosis depends on the major

presenting symptom.

• For the classic triad of epiphora, photophobia, and

blepharospasm, the differential diagnosis includes:

nasolacrimal duct obstruction

• conjunctivitis

• corneal abrasion

• and uveitis.

• For corneal clouding and edema, the differential diagnosis

includes :

• congenital corneal dystrophies

• birth trauma with tears in Descemet’s membrane keratitis

• congenital ocular anomalies like sclerocornea or Peters

anomaly or

• storage disesases like mucopolysaccharidoses or cystinosis

• For corneal enlargement, the differential diagnosis includes :

• high axial myopia and megalocornea.

• For optic nerve cupping the differential diagnosis includes:

• physiologic cupping

• optic nerve coloboma

• optic nerve atrophy

• optic nerve hypoplasia

• an optic nerve malformation

Prognosis

• Glaucoma that presents from 3-12 months of age has a

favorable prognosis, with 80-90% of cases achieving

good control of intraocular pressure with angle surgery.

• The vision loss in children is multifactorial and does not

depend exclusively on the health of the optic nerve.

• Affected children can develop significant myopia

from axial elongation of the globe,

• astigmatism from unequal enlargement of the

cornea, corneal scarring

• Even dislocation of the lens from excessive anterior

segment enlargement.

• Correction of the refractive error and aggressive

treatment of associated amblyopia and/or

strabismus is required to maximize visual outcome.

• Visual acuity is worse than 20/50 in at least 50%

of cases.

• This condition is bilateral in about two-thirds of

patients

• occurs more frequently in males (65%) than in

females (35%).

Pathophysiology

• The basic pathologic defect in PCG remains

controversial.

• Barkan originally proposed a Thin, imperforate

membrane that covered the anterior chamber

angle and blocked aqueous outflow.

• By age 1 year, normal corneal diameter is

10-11.5 mm

• a diameter greater than 12.5 mm suggests

abnormality.

• Glaucoma should be suspected in any child

with a corneal diameter greater than 13 mm.

Medical therapy

• Medical therapy for primary congenital glaucoma

is typically used as an adjunct to surgery.

• Oral carbonic anhydrase inhibitors include

acetazolamide (Diamox 10-20 mg/kg/day divided

into 3 or 4 doses) and methazolamide (Neptazane

5-10 mg/kg QID).

• Side affects include weight loss, lethargy, and

metabolic acidosis.

• Topical carbonic anhydrase inhibitors include

dorzolamide 2% (Trusopt) and brinzolamde 1% (Azopt)

drops TID.

• These medications may produce less reduction in

intraocular pressure than oral carbonic anhydrase

inhibitors, but also appear to have fewer systemic side

affects.

• Beta-blockers (timolol or equivalent) can also be

given topically, usually using a lower starting

concentration of 0.25% drops BID. Side affects

include:

• respiratory distress, caused by apnea or

bronchospasm, and bradycardia.

• A combined beta-blocker/carbonic anhydrase

inhibitor (Cosopt) drop BID has been shown to

be effective in reducing intraocular pressure in

children requiring more than one topical

medication.

• Prostaglandin analogs latanoprost 0.005%

(Xalatan), travoprost 0.004% (Travatan), and

bimatoprost 0.03% (Lumigan) have been

effective in reducing intraocular pressure,

although use is discouraged in the presence

of inflammatory condition

• Miotic agents (pilocarpine, echothiophate) and

adrenergic agents (epinephrine, dipivefrin) are

not usually effective.

• The alpha2-adrenergic agonist brimonidine

(Alphagan) is contraindicated in children under

age 2 because of potentially serious lethargy,

hypotonia, hypothermia, and CNS depression.

Medical follow up

• Primary congenital glaucoma requires lifelong

serial measurements of intraocular pressure,

corneal diameter, refractive error, and optic

nerve cupping.

• Any change in medical regimen should be

followed in 1-2 weeks to assess the efficacy of

the new treatment regimen.

Surgical follow up

• In the short term, these patients require frequent follow

up to monitor for infection or excessive inflammation.

Long term, just like patients on medical therapy, these

patients require serial measurements of intraocular

pressure, corneal diameter, refractive error, and optic

nerve cupping. If an adequate assessment of the clinical

response is not possible in the outpatient clinic, an

examination under anesthesia can be performed.

Complications

• The most common complication after surgery is

poor control of intraocular pressure.

• The success rate for angle surgery is approximately

80% after 1 or 2 procedures, while the other

procedures report a success rate of 33-80%.

پزشکان چشم خیریه انجمناصفهان

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خیام از زیبا :رباعی

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. خوردگی  چین حتی مغز پایین و مغز باالی قسمتو های

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رسان پیام . گسترشمیدهد  را مغز به

• بد غذای یک شما اگر

باشید خورده را طعم

غذای یک طعم میتوانید

کنید درک را خوب

زندگی تلخیهای از پس،

بتوانید تا درسبگیرید

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قلبهستشو شبیه خوشه روی انگور های حبهاون دونه هر

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داره نقشبسزایی

نوع این و است استخوان به کرفسشبیه ساقهسبزیجات از

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کرقسهم ٪۲۳از  و داره . ٪۲۳سدیم سدیمچنانچه

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افزایش باعث هستشکه دونه از پر انجیرو تعداد

از جلوگیری همچنین و مرد اسپرم حرکتمیشود . شدن عقیم

تخمدان عملکرد و سالمت به زیتونمیکند .کمک

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و داراست را

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. میگردد چشم