Differential diagnosis in eye

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DISCLAIMER--PLEASE READ

While every attempt has been made to have dosages, medications, and treatment recommendations as

accurate and up to date as possible, this manual is no substitute for clinical judgement and knowledge.

Tthe authors are not liable for any action taken on the basis of this manual.

Pediatric Ophthalmology

Edited and Revised by Balaji Gupta MD, Meagan Celmer MD

1. Congenital abnormalities

Eyelids

Ankyloblepharon
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fusion of lids

AD with incomplete penetrance

surgery

Blepharophimosis

AD with almost 100% penetrance

congenital tetrad syndrome with epicanthus inversus, telecanthus, blepharoptosis and phimosis

strabismus, nystagmus, microphthalmus, lacrimal drainage problems, short PF, brow hair crossing in

midline, flat brow, infertile females, hypoplastic tarsal plate with tight lower skin leading to ectropion

chromosomes are usually normal

Diff dx when no family history:

Waardenburgs syndrome

Williams syndrome

FAS

Trisomy 18

oculodigital syndrome

Crytophthalmos

Skin covers all ocular structures

Distichiasis

pull, electrolysis, cryo double freeze thaw

surgery split tarsus and pull our each hair

Ectropion

usually with Downs or blepharophimosis

variation with total bilateral eversion of upper lids in newborns with marked chemosis and prolapse of

conjunctiva

Entropion

rare, by defn is isolated


4/71

surgery based on corneal status

congenital horizontal tarsal kink

180 degree bend of the upper tarsus to appose globe

needs early surgery due to infection and corneal scarring

Epiblepharon

bilateral mild skin excess in lower lid with vertical cilia, most commonly asians

r/o frank entropion

observe and lubricate

surgery for corneal problems with simple excision of skin or Quickert sutures

Epicanthus

rare at birth but up to 20% by 2 yo

palpebralis (simple) equal, most common

inversus - below, often with other abnormalities

tarsalis - above, asians

supraciliaris - from eyebrow

Euryblepharon

horizontally widened PF with anterior and downward placed lateral canthus and ectropion laterally

observe since usually improves, consider tarsal strips procedure

Eyelid Coloboma

usually full thickness isolated defect in upper lid at inner 1/3 junction

20% are bilateral

lower lid at lateral 1/3 often with systemic syndromes, especially AD Treacher Collins

lower lid often partial thickness with adjacent margin deformities such as trichiasis

Cornea


5/71

Megalocornea

>13 mm (or > 12 mm in newborn)

nl endothelial density

r/o congenital glaucoma

simple

usually isolated, nonprogressive

anterior megophthalmos

bilateral, most commonly XLR

normal lens is too small for ciliary ring and leads to subluxation

F carriers may have slightly larger cornea

iris TI defects

ectopic pupil

increased IOP

cataracts

rarely associated with renal cell cancer

microcornea


6/71

Axenfeld- Rieger syndrome

ocular

Iris strands and hypoplasia with posterior embyrotoxin

Can look like ICE syndrome

Glaucoma in 50%

high iris insertion

cryptless iris

iris TI defects

corectopia

ectropion uvea

microcornea

megalocornea

systemic

craniofacial anomalies

mental retardation

maxillary hypoplasia

telecanthus

microdontia

skeletal and spine deformities

hypospadias

pituitary gland anomalies

redundant periumblical skin

Peters anomaly

Posterior corneal defect, stromal opacity, and iris strands

80% bilateral


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often the leukoma clears with time

associated with the PAX6 gene

Congenital opacities

facets, nebula, macula, leukoma

corneal keloid probably from intrauterine trauma

Corneal dermoid, congenital glaucoma

sclerocornea

bilateral or unilateral

central clearer than peripheral cornea

often with other ocular problems

Forceps injury

Localized unilateral opacity with tears of Descemets membrane

Astigmatism and amblyopia

Mucopolysaccharidosis, mucolipidosis

Bilateral diffuse clouding with smooth epithelium

MPS IS (Scheies syndrome)

Mucolipidosis IV

Conjunctival bx reveals abnormal cytoplasmic vacuoles

CHED

Bilateral diffuse opacity with corneal edema and increased corneal thickness

CHSD

AD flaky or feathery stromal clouding with normal thickness and smooth epithelium

Optic Nerve

hypoplasia

non genetic, non-progressive loss of axons before full maturity


8/71

small disc with yellow ring surrounding it with or without pigment borders

superior segment hypoplasia may be associated with maternal diabetes

variable amounts with variable vision

trial of patching in unilateral cases

associations

maternal DM

young maternal age

first child

intrauterine infections

LSD

ethanol

anticonvulsants

systemic

basal encephaloceles

cerebellar vemis hypoplasia

4th ventricle dilation

posterior fossa cysts

visual pathway tumors

septo-optic dysplasia

(De Morsiers syndrome)

short stature, nystagmus, bilateral ON hypoplasia

less than 10% have useful vision (>20/100)

midline defects of chiasm, septum pellucidum, corpus callosum, hypothalamus, 3rd ventricle, pituitary

gland

cerebral/cerebellar atrophy, hydrocephalus, porencephalic cysts

15-60% have pituitary hypofunction, especially growth hormone


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Coloboma

sporadic, but AD genetic forms have been identified

ocular

posterior embryotoxin, exudative RD, posterior lenticonus

Systemic

Dandy Walker cyst, absent corpus callosum, encephaloceles

CHARGE syndrome includes coloboma, heart defects, atresia of choanae, retarded growth, genitourinary

abnormalities, and ear problems

Aicardi syndrome with infantile spasms, no corpus callosum, double X chromosome, multiple punched

out lesions

genetic

Chromosomal abnormalities include trisomy 18, 22, 13-15

Mecek Gruber, Goltz, and Lenz Microphthalmia syndrome

Morning Glory

unilateral, nongenetic

usually isolated without other findings

enlarged, excavated ON with central core of glial tissue with a pigmented raised annulus of subretinal

tissue that may have a blue color

usually very poor vision

variety of other ocular signs may be found

up to 30% get serous RD

systemic

basal encephalocele, absent corpus callosum, cleft palate, renal abnormalities

Pupil

Miosis

Abnormal dilator muscle or persistent pupil membrane

Unilateral or bilateral, sporadic or hereditary


10/71

microcornea

megalocornea

iris atrophy

iris TI defects

myopia

abnormal angle

congenital rubella

Lowes syndrome

Mydriasis

Many are the form fruste of aniridia, esp if central iris structures are missing

Must consider neurologic, pharmocologic, and traumautic etiologies

Retinal

Situs inversus

bilateral in 80%, often in tilted discs

congenital tortuosity

usually arterial, may be AD, associated hyperopia

consider Tetralogy of Fallot, heart defects

prepapillary arterial loops

1:2000, bilateral in 10%, usually inferior artery, not a hyaloid remnant

associated artery obstruction, VH, hyphema

av malformation and Wyborn Mason syndrome

aka racemose angiomas, macrovessels

Wyborn Mason has CNS vasculopathy

Congenital hypertrophy of RPE (CHRPE)

>4 lesions, FH indicative of polyposis


11/71

lesions quandrant

present in 2/3 of all kindreds

grouped are called bear tracks

can have thin rim of hypopigmentation

hypopigmented spots inside which slowly enlarge

peripheral lesions may be elevated

combined harmartoma

90% present with decreased vision with tumors of posterior pole

+FA leakage from vessels

usually no growth, but contraction of glial tissue

variable pigment

in differential of melanoma and other tumors

persistant hyaloid artery

association with PHPV, prepapillary hemorrhage

2. Ectopia lentis

Ectopia lentis et pupillae

AR, similar to simple ectopia with oval slitlike pupils

often asymmetric and displaced in the opposite direction of the lens

atophic looking, may poorly dilate, iris transillumination defects

up to 30% with nuclear/cortical cataract that can rapidly progress

axial myopia with potential retinal detachment

Homocystinuria

AR, 1/200,000 newborns, five times higher in Irish

absence of cystathionine synthetase resulting in increased homocystine in urine and blood


12/71

ocular

subluxated lenses inferonasally not present at birth but progressive

90% have subluxation by the third decade

often spherophakic lens which can dislocate into anterior chamber

long axial length predisposes to retinal detachment, esp after surgery

peripheral chorioretinal degeneration

systemic

fair coarse hairfair skinmalar flushpoor peripheral circulationmental retardationmarfanoid

habitusdecreased platelet lifearterial/venous thrombiosteoporosispancreatitisgeneral anesthetia

increases risk of arterial and venous thrombi

dietary management (low methionine and high cystine) may help

Marfan syndrome

AD, most frequent heritable cause of lens dislocation, 4/100,000

15% have no family history

ocular

up to 60% of patients have superotemporal subluxated lenses

can be present at birth, progressive or stationary

iris hypoplasia

iridodonesis

iris transillumination defects

myopia

high astigmatism

keratoconus

miosis

fetal angle with glaucoma

increased axial length and dislocated lenses predispose to retinal detachment


13/71

systemic

skeletal and cardiovascular defects

antibiotics for SBE prophylaxis prior to surgery

echocardiogram, increased urine hydroxyproline

long extremities

long fingers

joint laxity

pectus excavatums

coliosis

aortic insufficiency

dilation of ascending aortaaortic aneurysm

Simple ectopia lentis

AD, often present at birth

bilateral, symmetric, superotemporal subluxation with iridodonesis

often small spherical lenses

no systemic problems

glaucoma more common with later onset

Weill Marchesani Syndrome

AR, 1:100,000

spherophakia, ectopic lens inferonasally with eventual dislocation

high myopia up to 20 diopters

episodic pupil block glaucoma are almost inevitable and is worsened with miotics

cycloplegics can induce pupil block

stubby broad hands and feet

joint stiffness


14/71

muscular appearance

thick skin

Misc

congenital glaucoma

Ehlers Danlos

hyperlysinemia

sulfite oxidase deficiency

Lowes syndromeaniridia

3. Glaucoma

1/2 of all childhood glaucoma is secondary and acquired

Congenital

M>>F, worse prognosis if at birth (10%), infantile much better

over 80% are diagnosed by 12 months of age

tearing

photophobia

blepharospasm

bilateral in 75%

IOP >20

peripheral iris vessels

iris processes

high iris insertion

corneal edema

corneal enlargement

Haabs striae


15/71

genetics

most cases are sporadic

affected parent has 5% chance of having affected child

no hereditary relationship to POAG or steroid response

measurements

normal eye at birth has


16/71

ectopia lentis

aniridia

congenital cataract

trauma

familial iris hypoplasia(AD)

aphakia

Metabolic

Lowes syndrome

mucopolysaccharidosis

Systemic

Neurofibromatosis type 1

Rubella

chronic uveitis

Down syndrome

Rubinstein-Taybi syndrome

Oculodentodigital syndrome

Aniridia

1:100,000

20/200 Visionnystagmusmacular hypoplasiaoptic nerve hypoplasia (75%)congenital

cataractssubluxationmicrophakiacorneal hazeprogressive pannus glaucoma

common cause of blindness in 30-50% of pts

due to angle closure as well as mesodermal tissue in angle

poor surgical results with vitreous loss and cataracts

AN1 (85%)

familial with isolated ocular manifestations in AD pattern with complete penetrance but variable

expressivity

2/3 of patients have affected parents

usually punctate cortical opacities needing surgery 30-40 yo

AN2 (13% )

del of short arm chrm 11p-


17/71

sporadic nonfamilial associated with Wilms tumor (nephroblastoma)

may get visually significant nuclear cataracts

1/4 with Wilms tumor which is often diagnosed before age 5

GU abnormalitiessevere mental retardationfacial dysmorphismhemihypertrophylong facieslow set ears

with poor lobesMillers syndrome

WAGR (Wilms tumor, aniridia, genitourinary abnormalities, mental retardation)

AN3 (3%)

Gillespiess syndrome, AR, with mental retardation and cerebellar ataxia

no Wilms tumor, CT shows abnormal structure of brain

normal macula and optic nerve

4. Infections

Ophthalmia Neonatorium

Conjunctivitis in the newborn period

Affects only 0.1% of neonates with prophylaxis

all prophylaxis effective against GC, not against TRIC

10% of cervix with GC or TRIC

W/U gram/giemsa (cytoplasmic inclusions), blood and chocolate conjunctival cultures, DFA or

chlamidiazyme

GC and TRIC infections may be associated with systemic disease

CLINICAL EXAM CANNOT DEFINE ETIOLOGY

GC

Hyperacute with purulent discharge

PCN IV 100,000 units/kg/day qid x 7days in isolated setting

note the emergence of some resistant strains to penicillin with an alternative regimen IV cefotaxime

irrigate with saline q4, AS 0.5% bid


18/71

RPR, FTA, and notify public health

TRIC

3-13 weeks of age

TC ungt 1% tid x 3 wks, Erythromycin 50mg/kg P.O. qid x 2 wks

if fails (10%) repeat/Bactrim 0.5 ml/kg/day bid x 2 wks

treat the parents

check for otitis media, pneumonitis

HSV

only in a systemic disease setting

chemical (toxic) conjunctivitis

Misc

many bacteria have been cultured, but ? pathogens

if w/u negative, use topical agents of choice

Preseptal/Orbital cellulitis

Staphylococcus, Streptococcus, and H. flu most common

sinusitis is a common cause of orbital cellulitis

other causes include URI, trauma, minor skin faruncle, dental disease

blood cultures positive only 5% in post septal cases

age may suggest a more benign course with


19/71

Limitation of movement

APD, color vision loss

demarcation of skin findings at end of orbital septum

TORCHS

Toxoplasmosis

3,000 children affected every year

70% pregnant women seronegative

although placental transfer common in infected mothers, many infants will be normal

IgM in infants is highly suggestive

systemic disease

hepatosplenomegaly

diarrhea

vomiting

anemia

convulsions

hydrocephalus

CT with intracranial calcifications

ocular

80% of patients with systemic disease have ocular involvement

up to 1/3 of children have bilateral visual loss

will have unilateral visual loss

isolated eye involvement is rare

bilateral retinochoroiditis involving the macula

microphthalmos


20/71

Cataract (10%)

Nystagmus (25%)

Strabismus (30%)

optic atrophy

Can even consider treating prior to birth in cases of known acquisition during pregnancy

Rubella

80% infected if mom gets it 1st trimester

of these 80% get defects, 50% have ocular problems

salt/pepper retinopathy

cataracts

glaucoma

iridocyclitis

corneal opacities

iris hypoplasia

microphthalmia

rare to have glaucoma and cataracts

all are over 20 yr old, uncommon congenital condition in U.S.

CMV

2% of all newborns get it (most common congenital infection) but 95% is subclinical

maternal viremia is most common method of transmission, but can occur during birth

consider lab studies in any newborn with congenital ocular defects not explained by other causes

systemic

fever

hepatosplenomegaly

jaundice


21/71

deafness

pneumonitis

seizures

periventricular calcifications

motor retardation

microcephaly

ocular

variable and nonspecific

necrotizing retinitis

hemorrhage

cataracts

iridocyclitis

optic nerve atrophy

Peter's

strabismus

nystagmus

up to 1/4 of severely affected infants have bilateral retinochoroiditis in multiple areas

Lab

IgM in a neonate is strong presumptive evidence

liver bx and studies of cells in the urine

CT calcifications

Congenital HSV is type 2

Acquired either transplacentally or retrograde through vagina

Up to 50% of infants can acquire it if mother has active lesions at birth

Some are asymptomatic with ocular symptoms later on


22/71

skin vesicles, conjunctivitis, keratitis, cataracts, retinitis

Syphilis

90% infected if mom has primary or secondary syphilis

systemic

bone

bone marrow

lungs

hepatosplenomegaly

CNS

failure to thrive

moist lesions of anus and mouth

rhinitis

saber shins

Hutchinson's triad: peg teeth, sensorineural hearing loss, interstitial keratitis

ocular

bilateral salt/pepper retinopathyglaucomairitiscataractsVaricella

rare clinically

CR scars, Horner's, optic nerve hypoplasia, microphthalmia

can have severe vitritis/retinitis, anterior uveitis

5. Leukocoria

Cataracts

1/3 genetic, 1/3 diseases, 1/3 idiopathic

monocular are not metabolic or genetic


23/71

capsule forms in 5th week and limits entry of organisms

opacities >3mm are visually significant

Anterior

polar

1/3 are bilateral

abnormal separation of lens from surface ectoderm

90% sporadic

pyramidal

2 mm projecting cone with surrounding cortical opacity

bilateral and sporadic

subcapsular

idiopathic, trauma, often acquired

lenticonus

Alports

X linked dominant

Difficult capsulorhexis

Chronic steroid use may present with PSC cataracts

hereditary nephritis

sensorineural deafness

PPMD

whitish dots in macular and mid periphery

Central

Nuclear

either the embryonic or fetal nucleus


24/71

usually non-progressive

bilateral are often AD inherited

Sutural

Lamellar

acquired usually after 6 months

progressive

hypoglycemia and galactosemia can cause lamellar pattern

Posterior

Posterior lenticonus

looks like PSC, bowl like central outpouching

unilateral, progressive

at surgery, post capsule often thin wispy and difficult to peel off opacity

PHPV

posterior capsular

associated with Downs syndrome

Oil Drop cataract

associated with galatosemia

Lowe's

XLR

Systemic

hypotonia

hyporeflexia

mental retardation

Aminoaciduria

metabolic acidosis


25/71

growth retardation

renal failure

often with early death

ocular

most commonly small thick opaque bilateral cataracts

pupils can be very miotic with lens adhesions

female carriers have white punctate opacities throughout their lenses

glaucoma in 50% by age 6 but can be early on

corneal keloids

Hallerman Streif

Labs

especially to exclude Lowe's, galactosemia

consider TORCHS titers even in unilateral cases

Urine

reducing substances, aminoacids, blood/protein

copper, sediment

Blood

Ca+2/phos, glaucoma, amino acids, TORCHS serology, others

PHPV

wide spectrum of presentation

congenital, nonhereditary, usually unilateral

not associated with other defects except cataracts

retinoblastoma is rarely found in microphthalmic eyes


26/71

elongated ciliary processes

microphthalmos

shallow anterior chamber

radial iris vessels

retinal detachment

retrolental plaque

intraocular hemorrhage

angle closure glaucoma

US/CT very diagnostic

natural history of untreated eyes with moderately severe disease is progressive shallowing of anterior

chamber, cataract formation, and angle closure glaucoma

Pseudogliomas

benign neoplasm

astrocytic hamartoma

can mimic RB, involvement of disc, multifocal, bilateral

usually with tuberous sclerosis, rarely with neurofibromatosis

little postnatal growth

von Hippel angioma

medulloepithelioma

uveitis

nematode endophthalmitis

usually older boys, inflammation more

inactive lesions show more changes than RB (cataract, synechiae, etc)

ELISA + 90% with 1:8 dil


27/71

retinitis, old VH

Non-rhegmatogenous retinal detachment

Coats'

usually older boys age 8-10 years old

anomalous grapelike clusters of leaking blood vessels

serous RD with dilated vessels can look like retinoblastoma

aneurysmal dilation can look like angioma, but no feeder vessels

about one half of untreated patients will progress

treatment includes laser and cryotherapy

retinal dysplasia

juvenile retinoschisis

Misc

retinal hemorrhage

retinal folds

colobomas

Retinoblastoma

1:20,000 births, becoming more common

6% with FH, 25% have genetic mutation 13q14 with low esterase D levels

1-3 y.o., present older when unilateral

70% are unilateral with 30% bilateral

1/5 of unilateral on presentation get 2nd eye affected later

the differential dx of inflammation is the most difficult

leukocoria most commonstrabismusinflammation (pseudohypopyon)Ca2+vitreous seedingnormal size

globeglaucomahyphemaheterochromiafixed pupilserous RD with dilated vesselssigns different for

endophytic/exophytic

metastasis late with spinal cord, bone, skull, lymph nodes, abdomen

pineal gland trilateral tumor with very poor prognosis

up to 50% with secondary cancers especially osteogenic sarcoma, fibrosarcoma, rhabdomyosarcoma

many years later

Genetic risk

history

determine if germline or somatic

germline in multiplex and multifocal cases

simplex disease with unifocal RB has 12% risk for germline mutation

remember carrier status due to 80% penetrance


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unaffected parents with one child mutifocal RB have 6% risk for second child

examine family for regressed retinocytoma

Molecular genetic analysis

can find the specific gene mutation using Southern blotting

RFLPs to do linkage studies

Diffuse infiltrating RB

(1%) likely to be missed

occurs later (6 y.o.), unilateral, grows slower

RX

CT, MRI: look for calcification, pineal gland

U/S: A scan with high internal reflectivity and echo spikes from calcification, B scan with orbital

shadowing

bone scan, bone marrow, lumbar puncture as needed

with massive tumor, enucleation may be primary procedure

external beam radiation, Episcleral plaque, Photocoagulation, cryotherapy

systemic chemotherapy

regression

TI cottage cheeseTII fish fleshTIII combo of aboveTIV white sclera5 yr survival >90%, poorer with

metastasis

Histology

Flexner Wintersteiner rosettes -an attempt to make photoreceptors with clear lumen

fleurette with outer segs of photoreceptors

Homer Wright rosette- lumen with neurofibrillary material, also in medulloblastoma, neuroblastoma

pseudorosette-tumor around necrosis

viable tumor around vessels with areas of necrosis

ROP

85% of ROP is transient disease with spontaneous regression

examine all children born under 32 weeks or weighing less than 1,500 gm

CRYO-ROP study had 6% of children


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cryotherapy or indirect laser

6. Neuroophthalmology

CN palsies

congenital

IIIrd

maldevelopment, intrauterine injury, or birth trauma

1/2 of all IIIrd palsies in children

usually one eye and isolated with ptosis, ophthalmoplegia, and pupil involved

usually dilated but may be miotic with aberrant regeneration esp with adduction

other than birth trauma, most are permanent

IVth

common, compensated until later in life

VIth

unilateral isolated finding rare and usually due to birth trauma

most common congenital disorder with VI nerve is Mobius and Duanes syndromes

often is transient

acquired

VI

differential includes myasthenia gravis, myositis, and trauma

benign

usually recover by two months, otherwise image

can be recurrent and even in other eye

pseudotumor cerebri

pontine glioma

will develop other signs usually within two weeks of onset


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INO, gaze palsies, VII nerve dysfunction

posterior fossa tumors

Horners syndrome

in infantile cases, the third order neuron may degenerate transynaptically, so always investigate the

second order neurons

20% will have some pathology which will develop within the first 18 months

heterochromia is a soft sign for pathology

consult from pediatrics commonly with physiologic anisocoria, so test with cocaine to confirm diagnosis

true congenital

birth trauma from forceps or shoulder dystocia

aquired

almost always with ipsilateral sympathetic chain

chest lesions are always left sided since the right side sympathetic chain does not descend into the chest

most common cause is neuroblastoma

CNS tumorssyrinxinfiltrative lymphomavascular lesionspost ganglionic lesions are less common and

often with vascular etiology of ICA

workup

history, palpate abdomen, pharmocologic localization, CXR, urine levels of metanephrine, brain and neck

MRI

Hydrocephalus

nl LP in children is 180 mm water

+ venous pulsations means ICP is < 200 mm water

most common infantile causes include chiari malformation, dandy walker cyst, aqueductal stenosis,scarring due to meningitis

decreased upgazelight near dissociationabduction weaknessON atrophynystagmusXT with A

patternNystagmus


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warning signs for further workup include

vertical componantsintermittant naturenon conjugatenew onsetloss of visionRetractionOptic nerve

pallorInanitionCongenital

bilateral, conjugate, pedular horizontal nystagmus

fixation often makes it worse, may be better at near than far

head turn with null point is almost always evidence of congenital origin

differentiation is important since congenital nystagmus is a benign condition

disappears with sleep

Motor

No ocular abnormality, normal visual potential

decreased foveation time leads to decreased visual acuity

jerk with pedular component and null point

often have abnormal head positions to achieve null point

Latent

benign, never pathologic

only seen on monocular gaze

fast phase toward uncovered eye

in reality, most of these have a fine nystagmus at all times

test Va with +10 occluder

Manifest Latent

jerk nystagmus in patients with strabismus due to suppression

fast phase in direction of fixing eye

can become latent if eyes are aligned

if eyes are straight, then one must have visual loss

Sensory

pathology from cornea to optic nerve such as macular hypoplasia from albinism, aniridia, optic nerve

hypoplasia

nystagmus starts in the first few months

often develop nystagmus with severe sensory loss before age 2

can get nystagmus with visual loss up to age 4, and never after age 6


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pendular with occasional jerk movements, slow searching conjugate movements

carefully check media, refraction, foveal hypoplasia, and optic nerve atrophy/hypoplasia

Spasmus Nutans

onset 4-14 months rare to start after 3 years

vision good, but can have strabismus, amblyopia

nystagmus, torticollis, and head nodding (slow freq, 2-25 degrees)

dissociated assymetric high frequency (15 hz) small amplitude nystagmus

often have increased head bobbing when focusing on objects as this may suppress nystagmus and

improve vision

always check for optic atrophy, APD, decreased eating as associated signs of intracranial tumors

get MRI due to association with abnormal brain findings

usually goes away, often in less than one month, but can last 1-2 years

Diff dx:

CNS tumors especially chaismal gliomamonocular blindnesscongenital nystagmus

Downbeat

usually seen down/left or down/right more than straight down

lesion of cervicomedullary junction

Arnold-Chiari TII

multiple sclerosis

spinocerebellar degeneration

lithium, phenytoin

CVA (vertebral basiler system)

syringomyelia

neoplasm


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platybasia, basiler invagination

Vit B12, thiamine, magnesium def

paraneoplastic syndrome associated with Hodgkins lymphoma, breast, ovarian, and small cell

Upbeat

if seen in primary upgaze, usually pathologic

involving cerebellum or brainstem

if seen in eccentric gaze, may be gaze evoked

Gaze evoked

stabilized with fixation, increased with darkness, visual blur

posterior fossa or drugs

Periodic alternating nystagmus

horizontal, jerk changing direction from one side to other over a few minutes

often with changing head position

may have skew deviation, downbeat nystagmus

congenital

may be subset of congenital nystagmus (up to 5%)

Kestenbaum may not work due to changing AHP

consider four muscle recession

associated with albinism

acquired

cerebellar disease, bilateral visual loss, neurodegenerative conditions

check posterior fossa and craniocervical areas

MR to r/o Arnold Chiari

rx with baclofen

Superior oblique myokymia


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monocular episodic intorsion, oscillopsia or shimmering

brief, lasting seconds, but patients very aware of onset and end

can be induced by looking into field of action of SO or back to primary

can have intermittant SO OA and loss of elevation in adduction

can be the only symptom of midbrain tumor, consider imaging

natural hx of remission and relapses

INO

adduction lag with nystagmus in abducting eye

from interruption of MLF fibers

diff dx of myasthenia, MS, CVA, partial IIIrd, thyroid eye disease

See Saw

acquired form with intorting eye rises with extorting eye falling

often with INO

congenital form with either absent torsion or opposite

midbrain, chiasm, or otolith

craniopharygioma

pituitary tumors

CVA

trauma

septo optic dysplasia

Convergence-retraction

Vestibular nystagmus

Peripheral

unidirectional, rotary, uniplanar

greatest in gaze of fast componant


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usually vertigo, tinnitus, deafness

labrynthitis, ischemia, trauma, toxic

Central

unilateral or bidirect, may change direction

ear symptoms less severe

trauma, CVA, tumor, demylination

Optic neuritis

rare, more often bilateral with disc edema

may be less likely to develop MS

7. Phakomatoses

Ataxia Telangiectasia

AR, chromosome 11

ocular

nystagmus, strabismus

bulbar conjunctival telangiectasia especially at canthi, are venules, usually seen by 5 yo

oculomotor apraxia with head thrusts, loss of OKN, poor saccades

systemic

ataxia in infancy or soon after walking with subsequent neural deterioration

telangiectasia of ears, face, bridge of nose, extensor surfaces

many cancers including lymphomas and leukemias

immunocompromised with low IgA, increased ESR, CEA

mortality from sinopulmonary infections

carriers for the gene are more likely to develop malignancies and are more sensitive to radiation

Incontinentia Pigmenti


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patients often referred from dermatology after bx

Bloch-Sulzberger type F, congenital X-linked dominant (lethal to males)

systemic

dental defects (60%)

CNS (30%) includes mental retardation, seizures, hydrocephalus, cerebral ischemia and edema

ocular (30%)

can look like ROP

AV anastomoses/ peripheral neoavascular zones

exudates

VH

cataracts

optic atrophy

palpebral conjunctival nevi

patchy retinal mottling

foveal hypoplasia

peripheral colobomas

nystagmus

strabismus

skin lesions

S1 appears like viral exanthem with papules, macules, and bullae over trunk/limbs and bx revealing

intraepithelial vesicles filled with eosinophils

S2 are verrucous

S3 hyperpigmented whorls and streaks from 3-6 months of age and there is absence of pigment in basal

epithelium

JXG

usually diagnosed


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M=F, skin heals in 1-2 years without problems

in general, a benign condition

ocular

can occur without skin lesions

usually unilateral

spontaneous hyphema from rupture of tumor vessels

glaucoma secondary to direct trabecular obstruction

uveitis can be with minimal anterior chamber involvement only or may simulate posterior scleritis

heterochromia secondary to diffuse iris involvement

iris or ciliary body tumor with either nodular or diffuse infiltration

tumors can occur on eyelids (common), orbit (with bony destruction), cornea, and epibulbar tissues

generally without spontaneous involution in eye, so may need to excise, steroids

pathology

skin or iris biopsy and anterior chamber tap

classically with foamy histiocytes and Touton giant cells

Touton giant cells can be found in aqueous

Oil red O can be positive on frozen sections

immunohistochemistry can be useful

Neurofibromatosis Type I

AD, 1:3000, progressive with variable expression, chromosome 17

Cafe au lait spots

present by 1 yr, >6 over 0.5 cm, grow, anywhere on body

freckling develops later in intertriginous areas

Neurofibromas

nodular or diffuse (rare), benign but functional/cosmesis problems


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plexiform difficult to treat (see plastics)

histo neurons, Schwann cells, fibroblasts, mast cells, vessels

increasing superficial subcutaneous involvement is associated with less deep orbital involvement

Lisch nodules

indicates mutation at NF1 locus on long arm chromosome 17 affecting guanosine diphosphatase

activating protein

> 90% of pts over 6 y.o., increase in number

no correllation with severity or prognosis

usually bilateral, well defined dome shaped, gelatinous, elevated with smooth contour

typically less pigmented, yellow or tan, variable in size, height, and distribution

fleshy or velvety texture and often with glassy translucent character

Other findings

absence of sphenoid bonemeningiomasoptic nerve gliomaglaucoma especially on side of lid and facial

involvementthickened corneal nervesastrocytic harmartomasscoliosisIncreased incidence of JXGoptic

nerve glioma

aka Juvenile Pilocytic astrocytomas

PPLOV with APD, proptosis, increased ICP

most often in first decade (avg 3-4 yo)

usually more extensive ON and chiasmal involvement with NF1

if normal MRI scan by 2 yo, then unlikely to develop

up to 15% of NF1

increased mortality with chiasmal involvement

observe, radiation, surgery, biopsy

proliferating spindly astroglia or oligocytes, Rosenthal fibers

NF TII

Chromosome 22

acoustic neuromas

may have VII n involvement secondarily

ON glioma > 50%PSC and cortical cataractslagophthalmoscorneal hypesthesiadecreased lacrimal

secretionRetinal harmartomasSturge-Weber syndrome

no hereditary pattern

classic form includes facial hemangioma, ipsilateral intracranial hemangioma, ipsilateral choroidal

hemangioma, and congenital glaucoma

systemic

cutaneous

usually V1, V2 distribution not crossing midline

deep purple in adults with partial blanching

facial hemihypertrophy

if there is no supraorbital facial involvement, neurologic features are often absent

CNS

subarachnoid racemose angioma of venules with an associated maldevelopment of nearby cerebral

cortex


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calcifications of meninges, cortex as early as 1 y.o. and does not progress after age 20

these can form the railroad track sign of curvilinear doubled lines in the occipital and temporal lobes

decreased IQ in up to 50% of patients

localized seizures of the contralateral side and may become generalized

ocular

subconjunctival vessels

iris heterochromia, retinal tortousity

choroidal hemangioma

up to 50% of patients have a flat diffuse choroidal hemangioma

yellow-orange, minimal elevation, diffuse, most commonly in posterior pole but usually involves over

50% of the choroid

in children it may not be apparent except for the deep red coloring which has been labeled tomato

catsup fundus

slowly growretinal and choroidal degenerationgliosisSRNVMserous retinal detachmentfocal

calcificationmarked early hyperfluorescenceglaucoma

1/3 develop glaucoma with congenital > adult onset

most often when the eyelid is involved

angle abnormalities vs increased episcleral pressure

uncommonly bilateral, or bilateral glaucoma, visceral angiomas

Rx

skin lesions are treated with argon or dye laser, cosmetics

surgery risk of hemorrhagic expulsion/effusion

standard goniotomy, trabeculotomy have had poor success

some success with trabeculectomy with adjuvant MMC

associated syndromes

Klippel-Trenaunay-Weber syndrome

Tuberous Sclerosis

AD, chromosome 9 but new mutations are evident in 80% of new cases

systemic

neurologic

mental retardationepilepsyabnormal EEGlarge cortical massesintracranial calcifications of astrocytic

harmartomas especially in basal ganglia

skin lesions

ash leaf signcafe au lait spotsadenoma sebaceum

(80% ages 2-5 yo)shagreen patches (leathery, raised)peau d'orange in lumbosacral regionperiungal

fibromassubcutaneous nodulesdepigmented nevimisc

sclerosis of skullrenal cystsangiomyolipomasrhabdomyomas of heartWilms tumoraortic aneurysm

ocular

involved in 1/2 of patients

giant astrocytic hamartomaVF defectssmall flat gray white astrocytic hamartomas of


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NFLpoliosishypopigmented iris spotspapilledema

8. Plastics

hypertelorism is increased distance between medial orbital walls

telecanthus is increased distance between medial canthi

exorbitism is widely divergent lateral orbital walls (>90 deg)

Document palpebral fissure (PF)

Often with poor lid crease and levator function

Check tear function and corneal staining

PF increases on downgaze

Check for jaw winking and Bell's phenomenon

Occlusion amblyopia is rare, most often anisometropic amblyopia from induced astigmatism

Must carefully observe these infants for fixation preference

Rx

Indications for early surgery include occlusion and chin up head position

If levator function is present, then consider levator resection, aponeurotic surgery

Frontalis sling using a variety of suspension materials is commonly performed with poor levator function

1/2 of patients with banked fascia lata have late ptosis

Tearing

congenital dacryocele

refer to ENT to look for polyps, look up the nose as well

bluish cystic swelling medially with epiphora in first few wks of life

F>M, isolated finding, NLD obstruction with functional proximal obstructionDifferential dx

encephalocelemucoceledermoidcapillary hemangiomasudoriferous cystRx

conservative rx >50% will resolve (soaks, massage, topical antibiotics)

surgery (probing, DCR) if dacryocystitis, cellulitis, respiratory distress, no resolution in 1-2 wks

can recur with surgery

Congenital NLD obstruction

evident in 2-4% of babies stating at 1-2 wks after birth

1/3 bilateral, most systems become patent within 6 wks, 90% within one year

check puncta, causes for reflex tearing including conjunctivitis, epiblepharon, or congenital glaucomainspect medial canthus for distended sac or congenital defects

digital pressure over the sac revealing mucopurulent discharge is highly suggestive of NLD obstruction

usually at level of valve of Hasner

rx with observation and antibiotics, probing, repeat probing, intubation, and DCR


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Orbital Tumors

90% are benign usually cyts, most mal are rhabdo

Rhabdomyosarcoma

rapid proptosis with good Va, extraconal, often down

palpable often preseptal, 7 yo, M>F

CT shows irregular mass with uniform density

low to medium amplitude internal reflectivity with ultrasound

surgery

bone marrow bx, LP

fix in formalin and glutaradehyde for EM sections

pathology

embyonal most common, alveolar (worst, inferior), pleomorphic (best, least), botryoid (sinus invasion)

treatment

radiation 4-6000 cGys

adjuvent chemotherapy (vincristine/doxorubicin/cyclophosphomide) with good survival

Lymphangioma

50% present in preschool years

most commonly presents with gradual proptosis during the first few years of life

episodes of dark blue superonasal swelling, orbital hemorrhage or proptosis (avg 6 mm) during later

years

indolent growth with recurrent hemorrhage (can have N/V in children)

paindiplopiasudden enlargement with URIhemorrhage (chocolate cysts)conjunctival ectatic lymph

channelslid ecchymosisepistaxis (lesions in sinus/pharynx)ON edema/atrophyproptosis increases with

valsalva

1/3 of posterior lesions are intraconal

infiltrative, unencapsulated, large serum spaces, lymph follicles

CT lesions often appear as a solid mass with phleboliths (1/2)

Rx

conservative

some lesions arborize, bleed easily, and incorporate arteries

anterior lesions more easy to dissect out

may consider aspiration of hemorrhage, CO2 laser, debulking anterior lesions

Pseudotumor (pediatric)

In children, presents more like orbital cellulitis

nonspecific, idiopathic, benign inflammatory process with polymorphous lymphoid infiltrate with

varying amounts of fibrosis

up to 15% of all pseudotumor


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more recurrent in children

spontaneous orbital hemorrhage

peripheral eosinophilia in 1/3

CT ring sign of scleritis, tendons inflamed, diffuse infiltrate with streaky edges

Systemic steroids have dramatic effects

Fibrous Dysplasia

fibrous bone growth usually of multiple bones, 8 y.o.

rapid growth with stability after puberty

Albright's syndrome, systemic, skeletal bones, precocious puberty, abnormalities skin pigment

observe unless optic nerve compression

CT is best to image lesion, tumor has ground glass appearance

spicules of immature bone and osteoid with fibrous stroma

Ossifying Fibroma

only occur in facial bones

aggressive growth pattern needs total surgical excision

CT sclerotic margin with less radiodense center and foci of calcification

spicules of lamellar bone and osteoblasts present

Osteoma

slow growing along frontal/ethmoid sinus wall or others

extremely radiodense well circumscribed masses

usually subtotal resection for symptoms

Neuroblastoma

Mean age at diagnosis is 2 years old in orbital cases

prognosis depends on age of onset and bone metastasis

ocular

up to 1/2 have metastasis to orbit, but only 20% show clinical evidence

ecchymotic lids, unilateral or bilateral exophthalmos,Horner's syndrome, opsoclonus

bx extraperiosteally to avoid spread and fix in formalin/glutaraldehyde

Horner's syndrome may represent localized neuroblastoma in the neck or chest with a better prognosis

systemic

originates in adrenal glands or the sympathetic ganglion chain in the retroperitoneum or mediastinum

systemic metastasis to abdomen, thorax, bones

metastasis to lateral orbit with bone destruction and cranial metastasis

catecholamines in urine

pathology

sheets of round cells with neurosecretory granules

no Homer Wright rosettes in metastasis

Eosinophilic Granuloma


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superotemporal quadrant, M>F, F, Asia/African

Ectopic tissue masses

Choristoma

Growths of normal tissues in abnormal areas

Dermoid Cyst

preschool years

anterior to septum, smooth, painless, usually lateral superior rim, approximately 1 cm

progress slowly, can grow rapidly with trauma and inflammation

keratin filled cyst lined with epithelium, filled with adnexal structures

deeper cysts often underestimated in size; may extend intracranially after fossa formation and are

usually found in older patients

CT

image to r/o deeper intracranial involvement

focal defects of orbit bony wall, bone attenuation, or bone sclerosis

sharply defined margins with central low density, but often heterogenous densities

surgery

usually fibrous attachments to bone or suture

recurrence most often with remnants inside bone

may have to remove remnants off of lateral orbital rim

Teratomas

aberrant pluripotential germ cells with all three embryonic layers

may present with massive proptosis at birth

unilateral, cystic with rapid growth

CT heterogeneous cystic lesion with intracranial spread

surgical rx

poor vision due to optic nerve damage

most teratomas occur in the gonads or sacrococcygeal region


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Encephalocele

infancy or childhood with superomedial exophthalmos that may pulsate

often protrudes with valsalva or dependent position

cystic, fluctuant and reducible, and easily transilluminates

must have skull deformity of frontoethomoidal area or sphenoid dysplasia

other signs of CFA with hypertelorism, broad nasal bridge, and malar and orbital floor depression

common

may be associated with colobomas, optic nerve atrophy, microphthalmos, and optic nerve gliomas

r/o neurofibromatosis

may be ptotic with pulsating enophthalmos due to inferior floor loss

greater injury with mild trauma

imaging, neurosurgery

Limbal Dermoid

Inferotemporal with minimal postnatal growth

May contain hair follicles

Amblyopia due to astigmatism

Lipodermoid

Overlying epithelium is normal and hair follicles are absent

Can be extensive

Surgical excision should be conservative

Capillary hemangioma

1-2% of newborn children have it with 40% in head and neck, F>M

1-2 wks postnatal, blanch, invasive, swell with crying, compressible

grow up to 12 months and regress after age 2 (1/2 completely by 4 y.o. and 3/4 by 7 y.o.)

upper lid, supranasal orbit with proptosis

treat to prevent amblyopia secondary to occlusion, strabismus, and anisometropia

severe cases can cause thrombocytopenia with platelet entrapment, optic atrophy, exposure keratitis,

and skin ulceration

steroids

Oral:

1.5 - 2.5 mg/kg prednisone over weeks

Injection:

40 - 80 mg triamcinolone with 6 - 12 mg of betamethasone

minimal response in 10%

risks include emboli, lid necrosis, fat atrophy, pigmentary changes, adrenal suppression

Topical:

surgery

lid crease or transconjunctival, avoid entry into lobular mass which is usually encapsulated

cauterize feeder vessels

best for isolated orbital masses rather than large areas of skin


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risks include blood loss, scarring

9. Retina

Vitreoretinopathies

All AD exept Goldman Favre

Stickler's

high myopiacataractperipheral vitreal veilsstrabismusperivenous radial lattice with RDEctopia lentiscleft

palatePierre-Robin micrognathiahyperextensibilityArthritisCardiac defectsmid facial flattening

FEVR

AD with variable expression

dragged macula with temporal traction

abrupt end of vessels in a scalloped edge temporally

can look like ROP with neovascularization and RD in up to 30%

intraretinal hemorrhage/lipid in less then 10%, thus can mimic Coat's

rare nystagmus/strabismus

most RD occur before age 10 and then patients are stable

over 50% of patients will have normal vitreous

examine family members for subtle areas of peripheral avascular zones

Goldman Favre

AR

present between 10 and 20 years old with nyctolopia

often 20/200 in childhood

extensive peripheral retinoschisisbeaten copper maculapoor visionRPE changesbone spiculesvitrealstrandsPSC cataractsHVF similar to RP with ring scotomas

Albinism

See Retina

Leber's congenital amaurosis (rod cone dystrophy)

Hyperopia, sluggish pupils

AR

Most with normal posterior pole exam in infancy

Oculodigital reflexcataractskeratoconuskeratoglobuslate bone spicule pigmentblood vessel

attenuationretinal white dotsextensive chorioretinal atrophymarbelized retinadisc edemaMacular

"coloboma"nystagmusERG is reduced

Because of reported cases of Refsum disease and Bassen Kornzweig syndrome, consider blood lipid

profile, peripheral blood smear looking for acanthocytes, and serum phytanic acid levels

Achromatopsia

stable VA

complete (AR) and incomplete (AR and XL)


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better VA in the darkphotophobiahyperopic astigmatismparodoxic pupilsno color visionpoor central

visionnystagmuscone ERG reduced, rod normal

CSNB

XL, AR, AD

myopiastable but decreased VAnystagmusnyctalopiaparodoxic pupilsAttenuated B wave (never gets

back to baseline)

ERG similar to XL retinoschisis

10. Syndromes

Craniofacial syndromes

Craniosynostosis

simple cases are sporadic, syndromes are usually AD

Ocular

ON

ALL disk swelling should be evaluated

proptosis

shallow orbits can cause severe corneal exposure

strabismus

often extortion of orbits

may have absent SO, SR

treat refractive error and amblyopia

misc

variety of other malformations noted including coloboma, cataract, medullated NFL, keratoconus, iris TI

defectsfrequently have NLD obstruction with dacryocystitis

Apert

AD but most cases are sporadic

midfacial hypoplasia, syndactyly digits 2-4

coronal suture closed

Pfeiffer

similar, shallow orbits especially, short broad thumbs and toes

Carpenter

similar, extra thumb or big toe, obesity and shallow orbits

ARCrouzons

AD with 2/3 being familial

coronal suture most commonly affected

proptosis, ON swelling more frequently

plagiocephaly

unilateral coronal or lamboidal suture


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ocular problems generally with the coronal closure

head assymetry best viewed by looking down

ear and orbit elevated, nasal root deviated toward the side, the forehead is flattened

vertical strabismus common with desagitilization of the trochlea

usually without ON compromise

Treacher Collins

AD with variable expression

systemic

mandibular/malar hypoplasialarge mouthhighly arched palatedeformed downward earshairline

projection to cheekblind fistulas from ear to mouthpreauricular tagsnormal intelligenceocular

downward slanting PF (antimongoloid) with lower lid colobomas

variable amount of lower lid tissue can exist

tearing from punctal and lid abnormalities

minimal ocular problems

Hemifacial microsomia

sporadic

Goldenhars syndrome is a varient

systemic

unilateral facial involvement R>Lmandible usually greatly smallermalformed earspreauricular tags/pitsV

and VII nerve palsiescervical spine abnmacrostomiaheart/lung/kidney abnocular

epibulbar dermoidslipodermoidsstrabismusDuanes syndromelacrimal duct stenosiscolobomas of upper

lids

dermoids are usually small ( 6 drinks/ day

systemic

thin vermilion border of upper lipsmental retardationlow birth wt and htcardiac and skeletal

abnormalitiesCNS abnormalitieshyperactiveocular

primary telecanthus is characteristic

most commonly horizontal short PF, ptosis, and epicanthal folds

up to 1/2 with decreased Va

tortuous vesselsmild optic nerve hypoplasia (40%)high refractive error (+ and -)long eyelashesanterior


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segment dysgenesis

11. Uveitis

JRA

RF-, HLA B27-

Systemic (1/4)

60% male, 1/4 with destructive arthritis

systemic fever, exanthem, pericarditis, leukocytosis

ANA -

rarely have uveitis

Polyarticular (1/3)

3 yo, 80% female, >5 joints, symmetric arthritis of small and large joints

systemic malaise, anorexia, anemia

ANA+ 25%

infrequent uveitis

Pauciarticular Type I (1/4) early onset

< 4 y.o., 80% female,


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watch out for iris bombe, consider LPI

filters have poor prognosis

HLA B27+

early diagnosis difficult with spondylitis late and often peripheral arthritis

ankylosing spondylitis

90% are male, after age 8

FH of JRA, Reiters syndrome, iritis, or ankylosing spondylitis

Hip, sacroilitis, and Achilles tendonitis

20% have pauciarticular lower limb inflammation

only 2% present initially with iritis

Cervical spondylitis in females

mimics adult disease with polyarthritis symmetric with wrists and fingers

ANA+ can have chronic uveitis like JRA

Psoriatric arthritis

F>M, >10 yo, FH of psoriasis

at presentation, monoarticular arthritis affecting knees changing to asymmetric polyarthritis over time

skin disease and arthritis are correlated

iritis in 10% with 80% being ANA+

arthritis presents early 3-5 yo and the skin changes late 13 yo so often with diagnosis of JRA

Juvenile Reiters, IBD

Chronic iridocyclitis in young girls

like JRA without arthritis

can happen in boys

usually more severe

Acute iritis (1/4) with older children, symmetric, deforming polyarthritis.

Pars Planitis

Similar to adult uveitis

Tends to involve the optic nerve more frequently

Strabismus

I. Basic Science

Anatomy

rectus muscles

12 mm posterior to insertion the rectus muscles penetrate posterior Tenon's capsule which fuses with

the intramuscular septum to form muscle sheath

tendon length: 4-8 mm long

muscle length: 40 mm

muscle width: 10 mm

horseshoe shaped insertion so hook them posteriorly


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insertion from limbus is approximately:

5.5 mm (MR) 6.5 mm (IR) 7 mm (LR) 8 mm (SR)MR

easiest to lose without attachments to obliques

tendon is only 4 mm long, therefore resection is often bloody

LR

Faden procedure ineffective since it already has long arc of contact

easiest to expose

if lost, look at the inferior oblique insertion

tendon is 9 mm long

superior oblique

SO muscle is the shortest EOM, only32 mm long, but the tendon is the longest at 20 mm

As it passes underneath the SR, it becomes attached to the SR muscle sheath

insertion is variable, but usually at the lateral border of the SR

vortex vein is located posteriorly

inferior oblique

IO tendon 1 mm

inserts almost directly over macula about 12 mm posterior to the lower LR insertion

inferotemporal vortex vein very close

nerve enters as IO passes below IR

Blood supply

30% of anterior perfusion by 2 long posterior ciliary arteries at 3 and 9 oclock

70% by 7 anterior arteries in rectus muscles

LR only rectus muscle with one anterior ciliary artery, all others have two

after surgery, anterior ciliary arteries do NOT recannulate

because there are no posterior ciliary vessels superiorly and inferiorly, iris angiograms are more

disrupted when IR or SR are operated on

iris angiograms do not predict ischemia

older patients may be more prone to ischemia

perilimbal conjunctival vessels may play a role in circulation

CN nuclei

Remember IIIrd and VIth nuclei have ipsilateral innervation, whereas the IVth nerve nucleus has

contralateral innervation

Physiology

plane of rotation is13 mm behind cornea (slightly behind the equator)

The torque exerted by a muscle on the globe is where it becomes first tangent with the eye

The MR is tangent at or anterior to the equator while the LR is tangent just posterior to the equator

1 nerve fiber: 5 muscle fibers (highest in body)

Tension


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resting tension is 25g

saccades generate 50g

maximum isotonic contraction is 120g

ARC and suppression

Defense against diplopia

Acquired adult strabismus have minimal sensory adaptation, whereas children generally adapt

suppression

eliminates central diplopia

small scotoma with ET

hemiretinal with XT

ARC

eliminates peripheral diplopia

test with bagolini lenses

Exam

Stereo

20-50 arc seconds equals normal bifoveal fixation

80-3000 arc seconds is peripheral fusion

must have adequate illumination to test properly

Titmus

Fly is 3000 arc seconds

animals 400-200-100 arc seconds

circles 800-400-200-140-100-80-60-50-40 arc seconds

has monocular clues

If you rotate 90 deg, lose stereo (as a check)

Randot

less false positives, more false negatives

positive testing equals high grade stereopsis

Diplopia tests

Red filter

red filter over one eye, do they see a pink/red/white fixation light or double?

prism neutralization

if sees double with prism neutralization, then patient has ARC

W4D

can test strength of fusion by darkening the room and increasing the dissociation

dots are separated by 6 degrees at 1/3 m, and 1.25 degrees at 6 m, and 12 degrees at 1/6 m

alternating suppression can be confused with diplopia

Normal phorias

adults6 M2 pd E1/3 M6 pd Xchildren6 M8 pd E1/3 M8 pd EAngle Kappa

an abnormal angle kappa is different than eccentric fixation because the fovea is still used

positive= normal, nasal

negative= abnormal, temporal

Fusional amplitudes


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horizontalconvergenceD 14pddivergenceD 6pdN16pdvertical2.5pdBruckner test

direct ophthalmoscope at arms length, full brightness

perform Hirschbergs, then compare brightness of red reflex

assess fixation or hypoaccomodation

asymmetric red reflexes are due to strabismus, anisometropia, anisocoria, posterior pole abn/media

opacities

II. Amblyopia

not a defense against diplopia

2% of population

with neutral density filter, the difference between the eyes diminish

crowding phenomenon

eccentric fixation can be found with dense amblyopia

Strabismic

often with refractive componant

present earlier to doctor

density of amblyopia is not correlated with time of recovery during therapy

Refractive

meridional

> +3.00

ametropic

usually >+5.00

give correct Rx

may take a long time for vision to get better--be patient

anisometropia

very common

> 1.5 D difference in hyperope, >2 D in myopes

children with better initial vision will do better

anisekonia doesn't occur with correct rx

very small incidence of ET developing while patching

Organic

often a functional componant is also present

deprivation (amblyopia ex anopsia)

media opacity such as cataract or corneal opacity

structural

eg, optic atrophy, macular scar

small APD, abnormal PERG

Occlusion

less than 10%

usually reversible with cessation of patch or brief patching of other eye

Monofixation syndrome

< 8 pd of strabismus (cover/uncover or simultaneous prism and cover) and 1/3 have no deviation


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alt cover > cover-uncover, prism and cover

anisometropia common

small macular scotoma (debate about ARC and suppression)

usually good binocular vision, NRC, and abnl stereoacuity (


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asymmetric OKN

Rx

treat amblyopia and trial of glasses if > +3.00

surgery by 18 months to achieve single binocular vision (>90%)

if surgery after 2 yo, < 1/2 have binocularity

Diff Dx

accomodative ET

Duane's T1

Mobius syndrome

neurological abnormalities

nystagmus blockage

bilateral abducens palsy

sensory ET

Nystagmus blockage

manifest congenital nystagmus dampened by convergence

eyes straighten under general anesthesia

variable angles, but nystagmus often disappears with convergence

Accomodative ET

6 months to 7 yrs, avg 2.5 yrs, +FH

starts intermittent, precipitating illness, trauma

amblyopia frequent

no diplopia since suppression or ARC

Refractive


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+3.00 - +10.00 D, avg +4.00

hyperopia increases till age 7, then decreases

deviation same distance and near, 20 - 30 pd

If delayed RX, may not respond

If > +5.00 D, can get bilateral ammetropic amblyopia

RX

patch amblyopia, full time Rx

repeat refraction 2 months post glasses since ciliary relaxation

if overcorrected post surgery, try over minus therapy

High AC/A

near >10pd than distance is a rough clinical measurement

usually hyperopic (+2.25 D avg, but can be myopic or +10.00)

MUST BE ACCOMODATING TO GET FULL ET

can get nonaccommodative ET

measurement

normal AC/A 4:1

Gradient method:

(ET near with +3.00 lens - ET n)/3 (dioptric distance)

Heterophoria method:

(PD (cm) + ET near - ET distance)/ D (of near)

RX:

+3.00 large flattop bifocals with the segment splitting the pupils


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bring target close to child and if they reflexively assume chin up posture, then they are using bifocals

Diff dx

nonaccomodative (stress, cyclic

)paralytic

sensory deprivation

divergence insufficency (ET > dist than near)

Spasm of convergence

Incomitant ET

MR restriction

thyroid, blowout, post op

forced ductions are useful guide to surgical planning

VI nerve paresis

often with head turn for fusion

common in children

Check neurological exam, trauma, CT, MRI

patch, fresnel prisms, botulinum for diplopia short term

Post XT surgery

usually improves spontaneously

RX prisms, miotics, full CRx, patch, surgery

Surgery

chances for consecutive exotropia increase with anisometropia, high hyperopia, amblyopia, or cerebral

palsy

Tables

may do symmetrical surgery of weakening MR or strengthening LR by same amount OU


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in adults with >45pd of esotropia, consider three or four muscle surgery to avoid limitation of ductions

Note that these are a starting point and should be continuously monitored

ET angle (pd)recess MR in mmresect LR in mm6010

recess-resect

may weaken MR and strengthen LR of same eye by reading across table

used if one eye has much better vision

not as good for large deviations

Duane's syndrome

no VI nerve nucleus

innervation of LR by III nerve

sporadic usually, but AD in 1/10

F > M, OS > OD (slightly)

usually unilateral

children rarely complain, present usually with head turn

adults complain of asthenopia, intermittant diplopia, and vague discomfort

ocular

decreased ABduction

variable loss of ADduction

upshoots and downshoots on adduction

paresis of convergence

uveal colobomas

crocodile tears

amblyopia

On ADd, PF narrows, globe retracts secondary to activation of LR


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systemic

spinal defects

Goldenhar syndrome

Wildervanck syndrome

deafness, Klippel Feil anomaly (web neck), and Duanes syndrome

F>>M

Types

most commonly, patients have TI Duanes with ET in primary and minimal enophthalmos/leash, good

stereo

the less ET in primary position, the greater the enophthalmos

TI: decreased ABd, straight to ET in primary, bilateral 20%

TII: XT in primary and limit ADD

TIII: decreased ABD and ADD

Mobius syndrome

VI, VII nerve palsies, abn PPRF

some can also have III, IV, V, IX, X, and XII

may have variety of motility disturbances

limitation of adduction that improves with convergence

fissure changes

vertical muscle involvement

mask like facies

sporadic, although rare AD varients have been reported

systemic

Polands anomaly (absent pectoralis muscle)

limb, chest, and tongue defects

micrognathia, small mouth, hypodontia


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15% have MR

Convergence Spasm

Intermittent ET, miosis, and myopia (accommodation)

Symptoms include headache, asthenopia, diplopia, photophobia

May appear to have bilateral VI th nerve palsies, but will have miosis with abduction

Functional vs organic (posterior fossa, vestibulopathy, pituitary tumors, diffuse metabolic disease, MS,

and trauma)

Baclofen has been tried in MS

IV. Exotropia

Types

PseudoXT

+ angle kappa

ROP

dragged macula

Toxacara

telecanthus

Duanes TII

incomitant

Basic

same at distance and near

Divergence excess

distance > near by 15 pd

high AC/A

check post occlusion (break fusion)

simulated excess if becomes basic with +3.00D after patching for one hour


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most do not become ET at near post op if straight at distance

Convergence insufficiency

near > distance by 15 pd

near point of convergence (NPC) is remote

low AC/A

blurred near vision

often only with exophoria

traumatic

often resolve within one year (up to 2/3)

remaining are difficult to treat

usually prisms, orthoptics are ineffective

Rx

pencil pushups

reading or TV with BO prism to increase convergence amplitudes

chronically, can treat with BI prism

often have significant overcorrection early on, especially with bimedial resections

a recess/resect procedure provides some incomitance so the patient can fuse without diplopia

Exophoria

NPC may be remote

asthenopia if controlled by accommodative convergence

most commonly a problem with convergence insufficiency

NOT treatable by surgery, use convergence exercises

Intermitant XT


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most idiopathic, +FH, F>M

usually starts around age 2 close one eye in bright sunlight

ARCV pattern

only 1/4 improve or are stable

often complain about diplopia when driving or moving

must measure with accommodative target

bilateral temporal hemiretinal suppression

progressive with decrease tonic convergence, developed suppression, decreased accommodation, and

orbital divergence with age

most are pseudo-divergence excess, so patch 45min or check with +3.00d

Rx

give full myopic Rx

minus lenses, base in prisms work for small amounts

timing of surgery is determined by how often the eye is deviated, not by how much

Constant XT

older

Adults with monocular vision loss often with sensory XT

decompensated intermittant or sensory XT

often alternate freely

rare diplopia

congenital (infantile) XT

associated with organic disease, craniofacial abnormalities, or neurological problems.

If healthy, then commonly with X patterns, DVD

rx

bilateral LR recessions or unilateral recess/resect


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Consecutive XT

much check adduction to see if MR has slipped

Surgery

wait until 2 1/2 to 4 year old to promote fusion

if in lateral gaze measures10 pd < straight, then decrease recession by 1mm/muscle

BLRR should aim for 10 - 20 pd of ET early on

resect/recess should aim for a few pd overcorrected early on

for long standing cases, need to release contracted conjunctiva and Tenon's

Tables

may do symmetrical surgery of weakening LR or strengthening MR of both eyes

may weaken LR and strengthen MR of same eye by reading across table

at larger angles, may prefer to do four muscle surgery with the numbers in parenthesis

XT angle (pd)recess LR in mmresect MR in mm1543205425653076357.56.54087509 (6)7 (5)6010 (7)8

(6)7011 (7.5)9 (6.5)8012 (8)10 (7)

consecutive ET

usually resolve with time

may patch, prisms, full plus glasses, phospholine iodide

rare to have persistance, especially when ductions are full

if incomitant, after a resect/recess, may require reoperation

V. Vertical Deviation

DVD

updrift of nonfixating eye especially with cover-uncover


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deviated eye often aBDucts and EXtorts and almost bounces back into position

asymmetrical, spontaneous or with occlusion

equal deviation in gazes

etiology unknown, almost always bilateral

Usually NO hyPOtropia when hyPERtropic eye fixates

Herring's law does NOT apply

associated with latent nystagmus, congenital ET

measure with base down prism under occluder

often becomes evident after ET surgery

natural history with resolution in 15-25%

diff dx- IO overaction, hypertropia

SO palsy

Most common cause of vertical diplopia

Longstanding palsies with contraction of IO and vertical concomitance

pay careful attention to versions for the diagnosis

when fixating with paretic eye, can mimic a SR palsy of opposite side especially in ABDuction

(inhibitional paresis of the contralateral antagonist), ptosis

Three Step Test

patient prefers head tilt to OPPosite side with chin depression to minimize diplopia

HyPERtropia IPSIlaterally with elevation on ADDuction

+ Bielschowsky test: head tilt to IPSIlateral side with increased HYPER

Do Biechowsky head tilt supine and standing. Often, acute acquired IVth nerve will have normal exam in

supine position and hyperdeviation in standing.

Cyclotorsion

often worse in downgaze

double maddox rod


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often less than the true tropia due to sensory adaptation

pay attention only to the net torsion between the eyes

fundus exam

gives the true cyclotropia

Congenital

long standing head tilt

amblyopia uncommon, may indicate absent SO

facial asymmetry with affected side being more full

can decompensate at later age

often with subtle complaints of intermittant diplopia, asthenopia, neck ache with reading

no torsion on Maddox rod secondary to sensory compensation

may have mild decrease in stereo

forced ductions in OR show laxity and it is loose upon inspection

Acquired

traumatic, CVA, sinusitis, tumor

complain of tilting of objects

discrete hx of onset

can measure torsion with Maddox rod

usually < 20pd of hyperopia in primary

ischemic causes usually are in older patients with 5-10 pd of hypertropia

forced ductions in OR reveal normal SO of both sides

Bilateral

uncommon, associated with trauma

V-pattern ET downgaze often with chin down posture

Double Maddox rod > 10-15 degrees excylotorsion


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Head tilt shows either alternating hypertropia or is reduced to very little or none

can be masked

Double elevator Palsy

chin up position

decreased elevation

hypotropia worse on upgaze

ptosis or pseudoptosis

asymmetric Bell's

IR restriction

+forced ductions, normal forced generation, normal saccades superiorly

elevator weakness

-forced ductions, decreased force generation, decreased saccades superiorly

Monocular Supranuclear palsy

Rare acquired palsy due to lesions of the high midbrain interrupting supranuclear input to SR and IO of

one eye

Looks like double elevator palsy except normal Bell's and doll's eyes maneuver for upgaze

May have convergence weakness, pupil abnormalities, and decreased downgaze

R/O myasthenia

Brown's syndrome

congenital, tenosynovitis, IO abnormalities

Decreased elevation on ADDuc

usually DEPr on ADDuc

+ forced duction

V pattern, straight in primary

bilateral in 1/10


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r/o IO paresis

acquired

watch and wait often resolves

trochlear bursitis

JRA

adult RA

sinusitis/surgery

blepharoplasty

mets

orbital surgery

SLE

post partum

scleroderma

primary SO overaction

there is true muscular overcontraction, so tenotomy does not produce secondary SO palsy

be careful if patients have fusion

Congenital Fibrosis Syndrome

bilateral ptosis, static external ophthalmoplegia, and downward eye deviation

often incomplete with aberrant regeneration

may be familial

CPEO

bilateral asymmetric ptosis usually before adolescence

few yrs later, symmetric PEO with sparing of downgaze


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early on can have exotropia with convergence insufficiency pattern

may have diplopia

may have weakness of orbicularis, slow saccades, and nystagmus

serum CK may be elevated

mitochondrial cytopathy

classic ragged red muscle fibers on trichrome stain

may have increased sensitivity to induction agents and nondepolarizing muscle relaxants

Kearns-Sayre

post pole mottled RPE and may have spicules

ERG normal or mildy decreased

systemic

arrhythmias, congestive cardiomyopathy

deafness

intracranial calcifications

growth retardation

diabetes mellitis

thyroid abnormalities

dementia

endocrine dysfunction

CSF protein

skeletal muscle weakness

ataxia

Myotonic dystrophy

AD, onset in second decade presenting with blepharospasm


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ocular

ptosis

orbicularis weaknesss

low saccades

ophthalmoplegia

miotic pupils

light/near dissociation

christmas tree cataracts in all

systemic

cardiac disease

dysphagia

MR

incontinence

baldness

scoliosis

testicular atrophy

Oculopharygeal dystrophy

French Canadians with ptosis and dysphagia in third and fourth decade

increased risk of aspiration, starvation

ophthalmoplegia, orbicularis and facial weakness, limb girdle muscle weakness

palatal voice

Skew Deviation

Acquired supranuclear cause of a vertical deviation

May have torsional and horizontal componants

Classically described as comitant, skew deviation may present in many ways and can look like CN palsies


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Other signs of brainstem involvement

small degrees of incomitance if anynormal doll's eyes and Bell's reflex

Most commonly pontine lesion, but midbrain, cerebellum, and medulla can also be affected

Misc

it is less helpful in chronic paresis where vertical deviations are more comitant

fundus torsion can help to distinguish which vertical muscles are involved

clinically, vertical rectus muscles cause minimal complaints of tilting

forced ductions may help

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Differential diagnosis in eye