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Week 12 - Congenital Anomalies Flashcards

1
Q

List the aspects of a Full Paediatric Eye Examination

A

History
VA
Assessment of eye alignment (nystagmus, ability to fix and follow object)
Stereopsis
Motor fusion
Pupil evaluation (size, shape, symmetry, direct, consensual and afferent)
Red reflex
Visual inspection of the eye
Dilated fundus examination (may need to be done under sedation)

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2
Q

Which group of infants are at high risk of congenital anomalies?

A

Premature < 30 weeks’ gestational age (ROP)

Positive family history of:
* Retinoblastoma
* Congenital, infantile or juvenile cataracts
* Juvenile glaucoma
* Retinal abnormalities especially retinal dystrophies

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3
Q

Which conditions can manifest at birth or very early on?

A
  • Infantile cataract
  • Congenital glaucoma
  • Retinoblastoma
  • Lid abnormalities
  • Retinopathy of prematurity (ROP
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4
Q

What is equipment is required for screening in children?

A
  • Penlight
  • Transilluminator
  • Hand-held biomicroscope
  • Slit lamp (flying baby technique)
  • Burton lamp and NaFl
  • 20D lens with light source
  • Measuring IOP on indication
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5
Q

Describe the step of Bruckner Test

A

Direct ophthalmoscope on the large spot - arm lenght for px

Point light at px’s nose. Adjust lenght until both pupils have red reflex

Compare size, shape, colour, brightness

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6
Q

What are signs can be seen when looking at the ocular adenexae?

A

Strabismus

Inspect eyelids
* Erythematous eyelids, haemangiomas
* Trauma, infection, tumours, connective tissue disorders
* Ptosis
* Discharge
* Tearing
* Palpebral fissure
* Epicanthal folds

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7
Q

Consideration when prescribing drugs?

A

Dosage
Contraindictions/Precautions around kids

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8
Q

What do use for childrens dilation?

A

Cyclopentolate (preferred)
- 0.5% (>1year) - 1.0%
- 2.0% (AVOID - due to risk to toxicity)

Tropicamide
- less effect of hyperopes
- fast action and fast reversal (limited cyclo effect)
- 0.5 - 1.0%

may require 2 drops 5 minutes apart for either

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9
Q

Patient has Droopy upper eyelid. Present at birth or manifested in the first year of life. What condition?

A

Ptosis

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10
Q

What are complication of Ptosis?

A

Amblyopia
Astigmatism
Strabismys
Decrease VF

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11
Q

What are the 4 etiology for Congenital Ptosis?

A

Aponeurotic: trauma from forceps or through birth canal; lid low but generally
normal levator function and lid crease
* Myogenic: localized dystrophy of muscle tissue; the more fibrous tissue present, the
poorer the levator function
* Neurogenic: third nerve palsy or damage to sympathetic nerves of the orbit
* Marcus Gunn Jaw Winking Syndrome
* Type of congenital ptosis that includes an associated winking motion of the affected
eyelid on the movement of the jaw
* Branch of cranial nerve V misdirected during embryonic development and travels to the
lid when it innervates the levator
* When sucking or chewing muscles, activates the lid to flick open and gives appearance of
winking

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12
Q

What condition has these signs?
Droopy eyelid results from localized myogenic
dysgenesis

Unilateral or bilateral

Reduced visual acuity – amblyopia

Anisometropia – form deprivation myopia

A

Ptosis

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13
Q

What symptoms have this conditions?

Asymptomatic (most common)
Blurred vision (induced astigmatism)
Chin-up position (parental report)
Headache? Due to contraction of the frontalis
muscle to help elevate lid (compensation)

A

Ptosis

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14
Q

What features do you need to record for a Ptosis?

A

History: age at onse, congenital vs acquired, gestational age,
trauma at birth, other congenital anomalies, systemic illnesses

History of amblyopia or strabismus

Ocular motility

Iris heterochromia

Assess levator function

Any congenital malformations (possible due to lid anatomy)

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15
Q

What are DDx for Ptosis?

A

Anophthalmos
Microphthalmos
Corneal abrasion
Orbital cellulitis
Pseudoptosis

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16
Q

Management for Ptosis

A
  1. Observation only in mild cases (no strab, amblyopia or abnormal head movement) 3 - 12 monthly reviews
    - monitor for amblyopia, exclude other causes CN3 palsy, Horners
  2. Refer to Surgical correction (usually delayed until 3-4 years)
    - every 2-4 weeks for signs of exposure,
    keratopathy, infection, granuloma formation, and over/under correction
    - monitor VA, head posture, and refractive error
    - treat any residual amblyobia aggressively
  3. May require repeat surgery in 8 - 10 years later
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17
Q

Patient presents with a rare, bilateral, reduce volume of eye.

+/- coloboma and orbital cyst

+/- blindness and learnign disabilities.

What condition is this?

A

MICROPHTHALMIA

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18
Q

Risk factor for Microphthalmia?

A
  • Maternal age over 40,
  • Multiple births,
  • Infants of low birth weight and/or low gestational age,
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19
Q

Microphthalmia etiology?

A

Likely caused by disturbances of the morphogenetic
pathway that controls eye development

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20
Q

These symptoms are consistent this which condition?

Small or absent eyes noted at birth (maybe be
diagnosed during pregnancy ultrasound or CT
scan)
Nystagmus
Cataracts
Coloboma

A

Microphthalmia

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21
Q

What signs do you expect in Microphthalmia

A

Anatomical malformation and whose axial length is
two standard deviations below the mean for age

Associated Ocular abnormalities are microcornea, corneal
opacification, corectopia, ectopia lentis, aniridia,
cataract, persistent fetal vasculature and/or retinal
dysplasia

Good VA - if macular sparing.

High Ametropia (usually hyperopia)

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22
Q

DDx for MICROPHTHALMIA

A

Cryptophthalmos refers to completely
fused eyelid margins, without lashes.

Congenital cystic eye

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23
Q

Management for Micophthalmia?

A

1) Early examination and diagnosis (follow up any systemic conditions)
2) If there is retinal function - refraction, amblyopia treatment critical
3) Unilateral cases - protect fellow eye.
4) Socket expander for progressive growth (For 5 years) - 12 monthly review (monitor for pituitary abnormalities, and ACG)
4) Painted prosthesis if appropriate - 12 monthly review
5) Addition reconstruction if indication: primary orbital implant (in severe cases or anopthalmic or non seeing eyes)
6) Refer for developmental assessement by a paediatrician

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24
Q

Patient presents with the following: What condition is this?

Bilateral/Unilateral, common caused by a autosomal dominant genetic mutation, dense opacity of the crystalline len?

A

Congenital cataract

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25
What signs do you expect to see in congenital cataractz?
Diagnosis based on density and morphology and visual behaviour ( child will no be able to tell you symptoms) - based on red reflex and ophthalmoscopy -
26
MORPHOLOGY Congenital Cataracts
* Nuclear (confined to the embryonic or fetal nucleus are most common – can be dense or dust-like [pulverulent]) * Lamellar or Zonular (affect a particular lamella of the lens both anteriorly and posteriorly resulting in a central, circumscribed opacity around the nucleus; can be genetic, metabolic disorders, intrauterine infection) * Coronary (lies in the deep cortex and surrounds the nucleus like a crown – usually sporadic) * Blue dot (common and innocuous) * Sutural (opacities follow the anterior or posterior Y suture) * Polar (central opacity near the lens capsule) * Anterior polar (flat or conical [pyramidal] opacity – if flat, central, < 3mm in diameter, usually visually insignificant; pyramidal surrounded by cortical opacity may affect vision) * Posterior polar (occasionally associated with persistent hyaloid remnants (Mittendorf dots), posterior lenticonus and persistent anterior fetal vasculature) * Central ‘oil’ droplet (characteristic of galactosaemia) * Membranous (rare, associated with Hallermann-Streiff-Francois syndrome; lenticular material is reabsorbed, leaving a chalky-white residual between the anterior and posterior capsule
27
Possible Congenital Cataracts Associated Signs:
Anterior segment (corneal clouding, microphthalmos, glaucoma, persistent anterior fetal vasculature) * Posterior segment (chorioretinitis, Leber amaurosis, rubella retinopathy, foveal/optic nerve hypoplasia
28
Patient presents with the following: What condition is this? Absence of central fixation, nystagmus (poor visual prognosis), strabismus
Congenital Cataracts
29
What are the differential diagnosis of Congenital Cataracts?
Conditions associated with leukocoria: Retinoblastoma, persistent hyperplastic primary vitreous, Coat’s disease
30
Management for congenital cataracts
1. Refer for systemic investigation: if signs of intrauterine infection - urinalysis, fasting blood glucose 2. Refer to paediatrician for suspected genetic disease 3. May required cataract surgery (4-5 week old or later) ; partial cataract - surgery can be delayed. Unilateral cataract surgery (URGENT) followed by anti-amblyopia therapy (poor prognosis) >16 weeks age May or may not insert IOL
31
Possible post cataract surgery complications
* PCO * anterior vitreous opacification * secondayry membrane over pupil * proliferation of lens epithelium * ACG or SOAG * retinal detachment (uncommon(
32
Methods of visual rehab follow congential cataract surgery - aphakia
Spectacle - bilateral cases (risk of anisometropia and aniseikonia) CL - risk of compliance issues IOL - effective but risk of myopia due to developing eye (no guarantee on emmetropia in adulthood), risk of induced glaucoma Occlusion / Atropine - treat and prevent amblyopia
33
Management plan for congenital cataract surgery
1. Not causing amblyopia, glaucoma, uveitis - Observation only 2. Post surgery - monitor for complications, may need strabsmus surgery for EOM 3. Ametropic correction and amblyopia as vision develops
34
Patient presents with the following: What condition is this? * typically bilateral but asymmetrical * Angle anomaly (e.g. isolated trabeculodysgenesis) caused elevated IOP * Three variants * Newborn onset (0-1 month) * Infantile onset (>1-24 months) * Late onset or late recognized (>24 months) * visual loss occurs due to optic nerve damage, corneal opacities, cataracts and amblyopia
Childhood glaucoma
35
What condition is consistent with these symptoms? Classic triad: lacrimation, blepharospasm, photophobia (due to raised IOP and resulting corneal oedema) Hazy cornea Buphthalmos (unique to glaucoma in infancy due to corneal and scleral collagen immaturity; potential for corneal enlargement ceases at around 3 years of age)
Childhood glaucoma
36
What signs do you expect to see in childhood glaucoma?
Two or more required to make diagnosis * IOP > 21 mmHg * Optic disc cupping * progressive NRR narrowing – focal or diffuse * CD asymmetry of ≥0.2 when discs are same size * Corneal findings * Haab stria – pathognomonic for infantile glaucoma * ridge of Descemet’s membrane after rupture * Diffuse corneal oedema from influx of aqueous into stroma * Corneal diameter ≥11mm in newborn, > 12mm in child up to 12 months of age, > 13 mm in any age * Progressive myopia or myopic shift * Other refractive errors – astigmatism from Haab striae and corneal stretching, anisometropia in unilateral disease * Amblyopia * Reproducible visual field defect
37
DEFINITION OF A GLAUCOMA SUSPECT (CHILD)
At least one required IOP > 21 mmHg on two separate occasions Suspicious optic disc appearance e.g. increase CD ratio for size of optic disc Suspicious visual field Increased corneal diameter or axial length in setting of normal IOP
38
What are the differential diagnosis of DDx?
Cornea enlargement Corneal splits Corneal oedema/opacity Watering and red eye Congenital ON cupping
39
Management plan for childhood glaucoma
1. Mainstay treament is angle surgergy 2. IOP lowering medications can be used temporarily, may reduce corneal oedema (First line treatment in uveitis related, post cataract sx) - using minimum frequency and concentration to limit systemic absorption - brimonidine contraindicated 3. Consider tube implant if angle surgery unsuccessful or trabeculectomy or cryoablation 4. Review 1 month post surgery, ensure IOP is controlled and vision is rehabilitated (ametropic correction and amblyopia therapy) 5. Review 3 monthly - ensure target IOP is maintained and visual development is evaluated - risk of relapse later in life
40
Patient presents with the following: What condition is this? - anterior segment dysgenesis - corneal or iris defects - +/- glaucoma other body systems * Usually small teeth / fewer than normal teeth * Distinctive facial features * Umbilical abnormalities * Heart defects * sensory hearing loss
AXENFELD-RIEGER SYNDROME
41
Etiology for Axenfeld - Rieger Syndrome
Defects in differentiation, migration, or arrested development of neural crest cells in the Anterior chamber
42
What signs do you expect to see in AXENFELD-RIEGER SYNDROME
Most common ocular manifestations (80-95% of patients): - Corectopia/ iris atrophy - Posterior embryotoxon (in some patients only visible with gonioscopy Polycoria, ectropion uveae and increased IOP
43
What condition is consistent with these symptoms? Photophobia from iris atrophy/ pupil abnormalities Parents may notice middle craniofacial dysmorphism, dental abnormalities, redundant umbilical skin May have: widely spaced eyes, flattened midface, broad flat nasal bridge, prominent forehead
AXENFELD-RIEGER SYNDROME
44
What are the differential diagnosis of AXENFELD-RIEGER SYNDROME?
Iridocorneal Endothelial (ICE) Syndrome Peter’s Anomaly Aniridia
45
Management plan for AXENFELD-RIEGER SYNDROME
1. Mainstay treament is angle surgergy 2. IOP lowering medications can be used temporarily, may reduce corneal oedema (First line treatment in uveitis related, post cataract sx) - using minimum frequency and concentration to limit systemic absorption - brimonidine contraindicated 3. Consider tube implant if angle surgery unsuccessful or trabeculectomy or cryoablation 4. Consider tinted CL if there is glare and photophobia from iris atrophy, polycoria and correctopia 5. Review 1 month post surgery, ensure IOP is controlled and vision is rehabilitated (ametropic correction and amblyopia therapy) 6. Refer to multidisciplinary team to examined for possible associated facial, dental, periumbilical and other anomalies. Consider genetic analysis for other family members. 7. Regular review for glaucoma surveillance
46
Patient presents with the following: What condition is this? * severe and early visual impairment, sluggish or absent pupillary responses and severely subnormal or non-detectible ERG * congenital retinal dystrophies that results in severe vision loss at an early age * d fundus abnormalities usually present later in life * a.k.a. congenital retinitis pigmentosa (RP) * +/- keratoconus, cataracts
Leber's Congenital Amaurosis (LCA)
47
What signs do you expect to see in LCA?
Retinal appears almost normal at the start; later pigmentary disturbance develop Appearance varies from RP-like appearance to RPE changes, chorioretinal atrophy, macular coloboma, or a marbleized retinal appearance VA ranges from no light perception (~1/3 cases) to no better than 6/120, often with a hyperopic refraction (more than +5.00D) Electroretinography (ERG) responses are almost undetectable Up to 20% of children with LCA without associated anomalies develop intellectual disability
48
What condition is consistent with these symptoms? Photophobia Nystagmus Night blindness (RPE65 mutation) Severe visual impairment beginning in infancy Sluggish/ near absent pupil responses
Leber's Congenital Amaurosis (LCA)
49
What are the differential diagnosis of LCA?
Early-onset retinitis pigmentos Achromatopsia Ocular albinism Congenital stationary night blindness Intrauterine infection Autoimmune retinopathy
50
Management plan for LCA
1. Refer for genetic testing 2. Consider ophthalmic referral for gene therapy (if area within 100um of posterior role: - Luxturna Gene Therapy treat inherited retinal dystrophy involving the RPE65 gene - * Subretinal injection, adenoviral vector – delivers correct version of the mutated RPE65 gene to the retina
51
Patient presents with the following: What condition is this? * usually unilateral primary intraocular malignacy * usually in younger patients (<5 years)
RETINOBLASTOMA
52
What condition is consistent with these symptoms? Leukocoria (‘strange reflection in my child’s eye’ / loss of red reflex in photos) * Eye misalignment (strabismus – when central vision is lost) * Advanced disease may present with iris colour change, enlarged cornea and eye due to increased pressure, or noninfective orbital inflammation * Very late, the eye may bulge from the orbit, a common presentation where awareness and resources are inadequate
RETINOBLASTOMA
53
What signs do you expect to see in Retinoblastoma
* One/multiple nodular, white/cream masses often associated with increased vascularisation * Intraocular inflammation – similar appearance to cellulitis or endophthalmitis * Diagnosis of retinoblastoma does not rely on histopathologic examination since biopsy incurs risk of metastasis * Ocular ultrasonography (b-scan) – to detect size and calcification * MRI is used to assess invasion of the optic nerve
54
What are the differential diagnosis of Retinoblastoma?
Coats’ disease Persistent foetal vasculature Vitreous haemorrhage Cataract Toxocariasis (chorioretinitis) Retinopathy of prematurity
55
Management of Retinoblastoma
1. Check ICRB for best prognosis 2. Consider: Enculeation Radiotherapy (no longer preferred) Chemotherapy (+/- focal therapies e.g. cryotherapy: note no RCT to support/refute)
56
Follow up for Retinoblastoma px:
1. Regular review and monitor for secondary tumor (cancers) 2. Px with sparing treatment required more frequent review - 2 monthtly exam under GA until 3 years old, then extend interval beween follow ups as disease become inactive
57
Patient presents with the following: What condition is this? * disorganized growth of retinal blood vessels, which may lead to scarring and retinal detachment * risk: low birth weight, (<1.5kg) gestastional age <30 weeks
RETINOPATHY OF PREMATURITY
58
ROP Signs (early):
* No symptoms * Signs of strabismus or leukocoria in the more affected eye * Vision loss * Screening of retina begins around 31 weeks’ postmenstrual age or 4 weeks after birth (BIO with scleral indentation - by ophthalmologist)
59
What are the differential diagnosis of ROP?
Retinoblastoma Congenital cataract Persistent hyperplastic primary vitreous Retinal detachment Toxoplasmosis
60
Management plan for ROP?
1. Observation only - may resolve spontaneously (Stage 1/2) 2. Consider laser photocoagulation or cryotherapy. Aim to prevent RD and blindness. Treat within 72 hours (URGENT referral) 3. Follow up 307 day after treatment, monitor for regression. 4. Monitor for possible RD, strabismus, myopia, astigmatism, reduced visual acuity, reduced peripheral vision
61
Patient presents with the following: What condition is this? * imperfect closure of the edge of the embryonic fissure * Abnormal structure of the optic disc
Optic Disc Pits
62
What condition is consistent with these symptoms? * Asymptomatic unless complicated by secondary macular changes * When maculopathy is present, visual acuity is usually reduced to 6/18 to 6/60 or worse
Optic Disc Pits
63
What signs do you expect to see in optic disc pits?
- Small, hypopigmented, grayish, oval or round excavated depressions in the optic nerve head - Visual field defects, most commonly an enlarged blind spot, and a paracentral arcuate scotoma - Maculopathy: serous detachment and/or retinoschisis of the central macula; accumulation of intraretinal and subretinal fluid and RPE changes
64
What are the differential diagnosis of Optic Disc pits?
Optic disc anomalies (choroidal/ scleral crescent) Tilted disc syndrome Circumpapillary staphyloma Hypoplastic disc Glaucomatous optic neuropathy
65
Management plan for Optic Disc pits?
1. If Asymptomatic - 6-12 monthly monitoring for macular involvement, comprehensive eye exam including dilated retinal evaluations and threshold visual fields 2. Advise on home VA assessment + Amsler grid self monitoring for maculopathy 3. Symptomatic - referral for laser photocoagulation, Intravitreal gas injection, macula buckling, pars plana vitrectomy
66
Patient presents with the following: What condition is this? * usually in 2 years old * may be found in blind infants * decreased number of optic nerve axons *unilateral or bilateral * +/- midline cerebral structural defect * +/- coexistening CNS abnormalities on MRI
OPTIC NERVE HYPOPLASIA
67
What condition is consistent with these symptoms? * poor vision (normal - 6/60 or worse) * nystagmus * strabismus (typically esotropia) *systemic dysfunctions e.g. pituitary abnormalities, growth hormone deficiencies, hypothyroidism, endocrine dysfunction *Developmental delays such as motor and communication
OPTIC NERVE HYPOPLASIA
68
What signs do you expect to see in optic nerve hypoplasia?
Optic disc often pale or gray, and appears to be half the size of a normal optic disc or smaller Double ring sign – yellow to white ring around disc May also present with tortuous retinal vessels RAPD in unilateral or asymmetric cases
69
What are the differential diagnosis of Optic Nerve Hypoplasia?
Optic nerve atrophy Optic nerve coloboma Peripapillary staphyloma Morning glory disc anomaly Tilted disc syndrome Glaucoma
70
Management plan for Optic Nerve Hypoplasia?
1. Refer for neurological and developmental assessments 2. MRI scan in all cases of optic nerve hypoplasia 3. Strabsmus correction in case of symmetrical functional vision with potential for BV. Inilateral cases can be delayed 4. Refraction for any amblyopia from astigmatism 5. 3 monthly review for growth patterns, 12 monthly reveiw for assessment of visual function
71
Patient presents with the following: What condition is this? * nystagmus * melanin defiency *poor vision
ALBINISM
72
What condition is consistent with these symptoms? Photophobia Nystagmus Strabismus Poor vision
Ocular Albinism
73
What signs do you expect to see in Albinism?
Iris transillumination (diagnostic feature) Foveal hypoplasia Nystagmus Hypopigmented fundus Decreased visual acuity Poor vision High refractive error Photophobia Strabismus Nystagmus
74
What are the differential diagnosis of Albinism?
Chediak - Higashi Griscelli Elajalde
75
Management plan for Albinism
1. Refer for evaluation for systemic syndrome 2. Low vision aids, correct refractive errors/amblyopia. may need strab surgery 3. Consider Genetic testing and counselling 4. Regular review - monitor for SCC or BCC
76
Patient presents with the following: What condition is this? * ocular defect on an ocular structure *usually in the inferonasal quadrant of the affected structure * +/- cataracts , pigment deposits, subcapsular, cortical, anterior and posterior polar, and total opacification *+/- heart defects, choanal atresia, nervous system abnormalities, genital or urinary tract anomalies, or ear malformations (CHARGE syndrome)
COLOBOMA
77
What condition is consistent with these symptoms? -Depends on structure affected; may be asymptomatic - Coloboma of iris/ eyelid noticeable to parents - Typically seen at or soon after birth - Eyelid coloboma may be minimal at birth and not appreciated until later in childhood - Coloboma of macula or optic nerve can result in reduced vision - VF defect - photophobia
COLOBOMA
78
Read DDX and managment for Coloboma
Read DDX for Coloboma
79
What signs do you expect to see in Coloboma?
Eyelid coloboma are usually found in the upper eyelid Lens coloboma is seen as flattening of the equator of the lens in an area of absence of zonular fibres - Typically an incidental finding on DFE Iris coloboma is a defect in iris tissue, typically inferiorly Retinal coloboma is seen as an area of whitening often with pigment deposition at the junction of the coloboma and normal retina Optic nerve coloboma has a range of appearance from physiological cupping to extensive retinal involvement

Therapeutics (10 decks)

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