A3 - Pediatric Glaucoma Flashcards
Primary vs secondary glaucoma
P: congenital abnormalities of AH outflow
- primary congenital
- juvenile open-angle
S: other abnormalities
- ocular anomalies
- systemic disease/syndrome acquired condns
- following cataract surgery
Primary glaucoma
-juvenile open-angle (JOAG)
AD
Present after 4 yo
Only thing wrong = high IOP
- no megalocornea
- no Haab
- AC appears normal
Manage similar to adult POAG
-surgery may be required
Primary glaucoma -primary congenital (PCG) or infantile glaucoma —inheritance —who —vision —laterality
AR or sporadic
-more frequently males
Higher prevalence in pop’s where consanguinity is common (2nd/3rd cousins marrying)
VA worse than 20/50 in many cases
Bilateral in 2/3 (genetics)
Primary glaucoma -primary congenital (PCG) or infantile glaucoma —blindness —dx —prognosis —pathophysiology
2-15% of cases
At birth 25%
Within first year 80%
Guarded
Incr resistence to AH outflow due to abnormal development of AC angle tissue
Primary glaucoma
-primary congenital (PCG) or infantile glaucoma
—classic triad*
—other signs/symptoms
Epiphora
Photophobia
Blepharospasm
Redness, clouding, megalocornea
Primary glaucoma
-primary congenital (PCG) or infantile glaucoma
—IOP
30-40mmHg
>20mmHg under anesthesia
-normal IOP in children is lower than adults (10-12mmHg newborns, 14mmHg in 7-8 yo)
Elevation can be gradual or sudden
Primary glaucoma
-primary congenital (PCG) or infantile glaucoma
—cornea
Enlargement/gradual swelling due to incr in IOP
Normal diameter of newborns = 9.5-10.5mm
By age 1, normal diameter = 10-11.5mm
Edema often presenting sign in children <3 mo
- swelling into stroma with breaks in Descemet’s = horizontal Haab striae
- edema resolves after IOP reduction, breaks in Descemet’s persist
- scarring and opacification may result
Primary congenital (PCG) or infantile glaucoma
-differentials by signs
—epiphora and/or red eye (4)
Conj-itis = pus
NLDO = eye not involved, just tearing
Keratitis/other K = superficial damage (glaucomatous damage is deep in cornea)
Ocular inflamm = cells/flare, cloudy view, history (juvenile RA, FB, etc)
Primary congenital (PCG) or infantile glaucoma
-differentials by signs
—corneal edema and/or opacification (6)
Corneal dystrophies = vessicles/specks
Sclerocornea/Peters anomaly
Keratitis
Birth trauma = forceps cause vertical breaks in Descemet’s
Sking disorders
Storage disease (mucopolysaccharidoses) = history will be positive/provide context
Primary congenital (PCG) or infantile glaucoma
-differentials by signs
—corneal enlargement (1)
Megalocornea
Primary congenital (PCG) or infantile glaucoma
-differentials by signs
—optic nerve cupping (5)
Physiological
Coloboma
Optic atrophy
ON hypoplasia
ON anomalies
Primary congenital (PCG) or infantile glaucoma -evaluation —exam —vision —EOMs —refr error —cornea
Full exam in office and under anesthesia
Poorer vision in affected eye
+/- nystagmus
Myopia and astigmatism possible
-corneal enlargement
Check for corneal: size, clarity, Haab (retroillumination)
Primary congenital (PCG) or infantile glaucoma -evaluation —measuring IOP —CCT —AC
Tonopen, Icare, Perkins
- do while being bottle fed
- asymmetry is suspicious
CCT higher in children with PCG (edematous stroma)
AC could be abnormally deep/distended
Primary congenital (PCG) or infantile glaucoma
-evaluation
—gonio
Under anesthesia
Iris insertion more anterior, TM and SS indistinct
Primary congenital (PCG) or infantile glaucoma
-evaluation
—ONH
Cupping
CD exceeds normal (0.30) for most infants
Asymmetry >0.20 between eyes is suspicious
Can be reversed in young children if caught early
Primary congenital (PCG) or infantile glaucoma -if left untreated
Can lead to blindness
Cornea can opacify and vascularize
-enlargement can continue until ~2-3 years with diameter >15mm
Other: buphthalmos, scleral thinning, myopic fundus changes, spontaneous lens dislocation
Secondary childhood glaucoma
- findings/associations
- causes
Anterior seg abnormalities (aniridia, Axenfeld-R, Peters, sclerocornea, microcornea, iris ectropion, ROP, iris/CB tumor)
Systemic diseases (Sturge-W, NF, lens-related (Marfan, Ehler-Danlos))
Steroid use, uveitis, infection, ocular trauma, after cataract surgery
Aphakic glaucoma
- when
- higher risk*
Following cataract surgery (15-50%)
Long-term risk can develop weeks-years after
Cataract surgery in infancy
Aphakic glaucoma
- mechanism
- angles
- outflow compromise
- treatment
Unclear
Appear open
Due to:
- abnormal development
- susceptability to sx-induced inflamm
- loss of lens support
Anterior vitrectomy - releive iris block
Surgical iridectomy
Treatment for childhood glaucomas
-surgery
Tx for most childhood glaucomas
PCG effectively tx with angle sx
- goniotomy (incision across TM)
- trabeculotomy (otomy = hole, opens TM
- if detected early, 80% have IOP control in 1-2 sx’s
Not as effective for secondary glaucomas
Treatment for childhood glaucomas
-secondary glaucomas
Similar to POAG or secondary adult glaucomas
-tx underlying problem, not necess sx
Treatment for childhood glaucomas
-medical therapy
Lower success rates and greater risk in children*
-serves vital role in pre/post/long-term care
Prognosis
-PCG
Poor prognosis:
-present at birth
—high proportion legally blind
-K diameter >14mm
Better with later onset (3-12mo)
-angle surgery and meds can be effective
Vision loss due to
Any combo of:
- K scarring/opacification
- ON damage
- myopic astigmatism
Need to tx RE and amblyopia
