Friedman pediatrics Flashcards
DDx for photophobia and tearing in pediatric patient
nasolacrimal duct obstruction (NLDO)
cornea abrasion/FB
iritis
congenital glaucoma
Congenital glaucoma Rx
Topical meds: NOT brimonidine (assoc/w/death)
Surgical options:
1.5 yo, cloudy cornea, or two failed goniotomies)
Correct refractive error, amblyopia
Other options: trab w/MMC and glaucoma drainage implant, cycloablation.
Tests for watery eye in pediatric patient
Mucoid reflux with digital pressure over the lacrimal sac and conjunctivitis
dye disappearance test,
Jones I and II test
nasolacrimal irrigation
Dye disappearance test
POSITIVE when decreased clearance of fluorescein after 5 min
Jones I vs. II test
Jones I (physiologic)
POSITIVE when normal
NEGATIVE when no dye recovered on cotton tip at inferior meatus
1/3 false-negative rate in normal
Jones II (nonphysiologic)
POSITIVE when normal
NEGATIVE when no dye recovered after lacrimal irrigation with saline (through inferior punctum and canaliculus)
1) If dye is retrieved in the basin with no reflux, a partial nasolacrimal duct obstruction is suggested since dye can be irrigated through under nonphysiologic conditions.
2) If the irrigant retrieved is clear, no dye reached the lacrimal sac, and a punctal or canalicular obstruction is suspected.
3) If there is reflux from the upper punctum, there is an obstruction at or below the sac.
4) If there is reflux around the irrigating cannula, the obstruction is likely at the level of the common canaliculus.
Basic secretion test
Following topical anesthesia, measure filter paper at 5min
Normal?
>5mm
Schirmer I vs. II
Schirmer I No topical anesthesia Measures basic and reflex tearing Measure filter paper at 5min Normal? >10mm
Schirmer II No topical anesthesia Measures reflex tearing Use cotton tip to irritate nasal mucosa Measure filter paper at 5min Normal? >15mm
Valve at the beginning and end?
Valve at the beginning?
Rossenmuller
Valve at the end?
Hasner
Empties under which turbinate?
Inferior turbinate
DCR creates passage by?
Middle turbinate
Near cribiform plate
Most common organism for dacryocystitis?
Strep pneumo > Staph & H. flu
Most common organism for canaliculitis?
Actinomyces (Gram+ rods with sulfur granules)
Congenital NLDO location?
usually 2/2 membrane over valve of Hasner.
>usually spontaneously resolves with massage and warm compresses +/- abx gtts (like polytrim) if crusting
>if not resolved at 13 mo –> NLD probing
Questions to ask when evaluating strabismus:
Visual acuity +/- amblyopia? Refractive error AC/A ratio deviation measured at distance and near deviation: in/comitant? A or V pattern? oblique muscle overaction DVD? latent nystagmus? cross-fixate? suppression scotoma?
surgical Rx for DVD
bilateral superior rectus recession
inferior rectus resection
inferior oblique weakening or anterior transposition
congenital motor nystagmus
Horizontal, conjugate
Onset
congenital motor nystagmus Associated with?
Associated with? Ocular albinism Achromatopsia Leber’s Congenital Amaurosis Aniridia
Esotropia + Nystagmus?
Esotropia + Nystagmus?
Nystagmus Blockage Syndrome
(Esotropia that “eats up” prism)
Rx for congenital motor nystagmus
base-OUT prism glasses to stimulate convergence and therefore dampen the nystagmus.
If head turn > 50% of time to keep eyes in null point, then consider Kestenbaum procedure
Spasmus nutans
asymmetric typically horizontal “shimmering” nystagmus* = LOW-amplitude, HIGH-frequency nystagmus
Usually benign, typically resolves by age 6
TRIAD:
(1) head nodding
(2) monocular or ASYMMETRIC nystagmus
(3) torticollis (i.e. abnormal or stiff neck position).
*can also be vertical or rotary. It is typically of the pendular variety.
Spasmus nutans Associated with?
Associated with?
Chiasmal glioma
Tumors of the parasellar/hypothalamic area can present with a nearly indistinguishable nystagmus (Heimann-Bielschowsky phenomenon); therefore perform neuroimaging in all cases of spasmus nutans (controversial).
-nystagmus resembling spasmus nutans can occur in children with certain retinal disorders:
CSNB or rod/rod-cone dystrophy. Therefore, do ERG if patient has abnormal eye exam (pupils, DFE)
down syndrome associated eye disorders
refractive error (MC hyperopia) strabismus nystagmus amblyopia lid abnormalities (epicanthal folds, upward slanting of palpebral fissures, blepharitis, NLDO) keratoconus iris Brushfield spots cataracts glaucoma
Recommendations for down syndrome
route eye care and correct any associated disorders as a regular child
Head position for SO palsy
chin DOWN
face turned to OPPOSITE side and head tilted to OPPOSITE shoulder
Rx for SO palsy
For isolated palsy: observation and prism glasses or occlusion of one eye to alleviate the diplopia, which may improve with time
If it does not and is stable for at least 6 mo, can consider muscle surgery
Knapp classification
Harado Ito procedure (lateral transposition of SO tendon)
Prism Adaptation Test
In prism adaptation, the patient is fitted with prisms of sufficient magnitude to permit alignment of the visual axes. In many cases, this step provokes a restoration of sensory binocular cooperation in a form of fusion and even stereopsis. This technique simulates orthotropia and possibly offers some predictive value of whether fusion may be restored when the patient undergoes surgical alignment.
In some patients, however (especially those with acquired esotropia), placement of such prisms increases the deviation. In such cases, anomalous retinal correspondence based on the objective angle may drive the eyes to maintain this adaptive alignment even with prismatic correction. After wearing such prisms, the patient returns with a greater angle of deviation. Prism adaptation is used by some ophthalmologists in patients with acquired esotropia. The patient is reexamined every 1–2 weeks and given larger prism correction, if needed, until the deviation no longer increases. Surgery is then performed on the new, larger, prism-adapted angle. The Prism Adaptation Study demonstrated a smaller undercorrection rate when surgery was based on this deviation compared to standard surgery
V pattern XT Rx
1) correct any refractive error and Rx amblyopia present
2) over-minus spectacles to induce accmmodative convergence, fusional convergence training with progressive base-OUT prism or prism therapy with base-in prisms.
3) If ocular misalignment is present > 50% of the time, then surgery is necessary
V pattern XT Rx - surgery
1) prism adaptation test to uncover full amount of deviation
2) surgical correction: R & R or both eyes with bilateral lateral rectus recessions
3) V pattern corrected with horizontal rectus muscle transposition in direction of desired weakening
(MALE = medial recti moved towards the Apex of the pattern or lateral recti moved towards empty space of patter) or with Oblique muscle weakening.
VH DDx in baby
shaken baby
trauma
ROP
VH in baby = questions to ask
Duration of findings? birth history (premature, low birth weight, supplemental O2)? Other medical history? H/o trauma? baby - developing, sleeping, eating? situation at home? baby difficult/crying/colicky?
VH in baby work-up and Rx
Radiology studies to R/O other traumatic injuries
report case to protective services
monitor for amblyopia - may require vitrectomy for non-clearing VH
Systemic assoc/w/capillary hemangioma
Kassabach-Merrit syndrome: consumptive coagulopathy with platelet trapping that causes thrombocytopenia and cardiac failure.
Mortality failure of 30%
DDx for congenital cataracts
idiopathic
hereditary (usually AD)
metabolic
intrauterine infection (TORCH - toxoplasma, Other viruses, Rubella, CMV, Herpes virus)
Posterior polar criteria
posterior polar cataract = 3 mm and visually significant –> operate
avoid hydrodissection –> possible vitreous loss and/or retained lens material.
Who to screen for ROP?
Gestation 30wks if high risk or unstable clinical course
ROP staging
Stage 1: demarcation line Stage 2: elevated ridge Stage 3: extraretinal fibrovascular tissue Stage 4: subtotal RD Stage 5: total RD
Threshold ROP?
Stage 3 in zone 1 or 2 in 5 contiguous or 8 non-contiguous clock hours with plus disease
Defined by CRYO-ROP: Cryotherapy for threshold disease reduces vision loss
When to start screening for ROP?
at 4-6 wks of age or 31-33 wks post-conception (whichever later)
Needs >2 BIO exams
Screen weekly until zone II vascularized or ROP regressing
When do normal vessels complete vascularization? When is ROP likely to progress?
When do normal vessels complete vascularization?
36-40 weeks (nasal at 36wks, temporal at 40wks)
When is ROP likely to progress?
36-40 weeks
Plus disease
at least 2 quadrants of shunted blood –> produces engorged, tortuous vessels in the posterior pole, vitreous haze, and iris vascular congestion (poor Px sign)
ET-ROP
Early > conventional therapy of pre-threshold disease in reducing VA loss
Treat type 1 ROP early (
“Rush” disease
Aggressive posterior ROP or Rush disease (i.e. Plus disease in Zone 1 or posterior Zine 2) must be detected because it can rapidly progress to stage 5 ROP within a few days
potential complications of ROP
high myopia strabismus amblyopia macular dragging nystagmus glaucoma cataracts keratoconus band keratopathy RD phthisis bulbi
patching schedule
1 week per year of age before re-examination. Continue until vision in amblyopic eye has normalized or stabilized
Levels of anisometropia that require correction to prevent amblyopia?
Myopic ansimetropia > = 3D
hyperopic anismetropia > =1 D
astigmatic ansimoetropia > =1.5 D
Types of accommodative ET
refractive accommodative (normal AC/A ratio) nonrefractive accommodative (high AC/A ratio) mixed mechanism decompensated accommodative
Methods of determining Ac/A ratio
Heterophoria method (moving the fixation target)
AC/A = PD(cm) + [near Δ – distance Δ] divided by
[diopters of accomodation]
Gradient method (with + without lens)
AC/A = [Δ(with lens) – Δ(without lens)] divided by
[lens diopters]
Rx refractive accomodative ET
1) full cycoplegic refration
2) patch non-amblyopic eye until vision normalize/stabilize
3) surgery for any residual/non-accommodative component of ET (any deviation > 10 PD nor eliminated with glasses)
DDx of ptosis in a kid
congenital ptosis (MC = myopgenic)
neurogenic - congenital CN3 palsy or Horner’s
rarely: aponeurotic (birth trauma)
Ptosis examination
VA
levator function (poor in myogenic ptosis)
lid crease (loss in myogenic ptosis + eyelid lag)
pupil size and response
ocular motility
presence of jaw winking
iris color
Rx and Px of myogenic ptosis
Rx amblyopia, then surgical repair
Poor levator function: frontalis suspension with silicone rods, fascia lata or frontalis flap.
Maximal levator resection may be helpful in some cases but poor levator function is more difficult to treat
allergic conjunctivitis DDx
seasonal or perennial allergic conjunctivitis
giant papillary conjunctivitis (giant/large papillae)
vernal keratoconjunctivitis (giant/large papillae)
atopic kersatoconjunctivitis (may have symblepharon)
Ask about age of onsent, duration, preciptating factors, associated CL wear
history of atopy
Stargardt Disease - inheritance and fundus findings
Inheritance: AR (ABCA4)
Usually
Stargardt Disease FA findings?
Dark choroid + starry sky in >80% (flecks = block early stain late)
Due to increased lipofuscin
Can occur w/ argyrosis (silver, often from tanning agents)
Full-field ERG normal early, then worsens like rod-cone dystrophies
OCT - loss of photoreceptor layers corresponding to macular atrophic areas
abnml color vision
Bull’s Eye Maculopathy DDx
Stargardt’s disease
Cone dystrophy
Chloroquine/Hydroxychloroquine toxicity
AMD
Chronic macular hole
Also: central areolar choroidal dystrophy, pericentral RP
Stargardt Rx and Px
no validated approach, low vision aids
Px: poor with vision deteriorating to 20/200 or worse by 3rd decade.
AD - more benign course with milder color and night vision changes
Leukocoria DDx
cataract
retinoblastoma
ROP
Coat’s
Other etiologys: PHPV, toxocariasis, toxoplasmosis, coloboma, myelinated nerve fibers, RD
RB work-up
CT: to Dx extraocular extension and trilateral RB (with pineal blastoma or parasellar mass)
Oncology consult: bone scan, bone marrow aspiration and LP
Spontaneous hyphema in child Ddx?
JXG Retinoblastoma ROP PFV Coat’s disease Herpes simplex uveitis
Common secondary malignancies with RB?
Osteosarcoma, malignant melanoma
Reese-Ellsworth classification:
Predicts RB visual prognosis, NOT survival
RB Path?
Tumor grows around blood vessels
Flexner-Wintersteiner rosette (RB specific)
Homer Wright (also other neuroblastomas)
Fleurette (Photoreceptor differentiation)
RB Prognosis:
Good with early tx; spontaneous regression rare
Enucleation, radiation, chemo, cryo, laser
Px poor if ON or uveal invasion, extraocular extension, multifocal tumors, delay in Dx
(bilateral RB, degree of necrosis and calcifcation do not affect Px); RB fatal
RB Signs?
Leukocoria or strabismus usu. before age 3
Early tumor in macula, later in periphery
LDH aqueous:plasma ratio >1.0
Calcium on U/S or CT
Periorbital inflammation DDx
Periorbital cellulitis Ruptured dermoid cyst Rhabdomyosarcoma Orbital pseudotumor Leukemia Histiocytosis X (Eosinophilic granuloma) Infantile cortical hyperostosis
Orbital tumor in kids
Benign: capillary hemangioma dermoid cyst lymphangioma neurofibroma meningioma inflammatory psuedotumor
Malignant: rhabdomyosarcoma neuroblastoma teratoma ON glioma histiocytic tumors granulocytic sarcoma Burkitt's lymphoma
Rhabdomyosarcoma Pathology types?
Embryonal - Most common, Good survival
Alveolar - Worst prognosis, Honeycomb appearance
Pleomorphic - Least common, Best prognosis
Botryoid - Grapelike, Secondary tumor from paranasal sinuses or conj
Rhabdomyosarcoma Px
depends on type and extent of the malignancy
3 yr survival (with chemo, XRT) - 90% survival
localized orbital tumor - 95% survival
invasion of adjacent structures - 60% survival
Rhabdomyosarcoma Rx
Work-up Dx Bx with immunohistochemical staining and pediatric oncology consult (chest/abdomen CT, BM Bx, LP)
Treatment?
Chemo / radiation, NOT local excision
Exenteration if large
