Oculoplastics Flashcards
What etiologies should you consider for preseptal cellulitis?
sinus, dacryadenitis, skin, hematogenous
Most common cause of preseptal historically vs now?
h. influenza before. Now g+ cocci
choice of therapy for preseptal cellulitis
celaphalexin if anterior, augmentin if sinus source, bacterium if worried about MRSA, vans or ceftriaxone if refractory
also do warm compresses, nasal decongestants
hospital acquired MRSA are sensitive to what
vanc, linezolid
most common source of infection for orbital cellulitis
chronic bacterial sinusitis
signs of orbital cellulitis
leukocytosis, fever, erythema, proptosis, chemises, ptosis, restriction/pain with EOMs, decrease in vision, impaired color, restricted fields, pupil Abel
what are the differences in organisms in adult and children with orbital cellulitis
adults usually mixed flora including G+C and anaerobes
Children usually one single organism and less likely need surgical intervention
what kind of orbital wall fracture is at highest risk of subsequent orbital cellulitis
medial wall
subperiosteal abscess may NOT be need to be drained in what circumstances?
isolated media/inferior abscess in children <9 years with isolated ethmoid sinusitis, intact vision, mild proptosis… can keep trying medical therapy
what medicine is particularly good for nec fasc involving group A strep?
Clindamycin
signs of orbital TB
proptosis, EOM Abnl, bone destruction, draining fistulas
what stains is used for asperillus? whats the path finding
Grocott-Gomori methenamine-silver nitrate. shows septet branching hyphae with uniform width.
what stain is used for zygomycosis (mucor/rhizopus)? what’s the finding?
stain is hematoxylin eosin. finding of nonseptated large branching hyphae.
what are the forms of aspergillosis?
acute aspergillosis- fulminant sinus infection that invades the orbit
chronic aspergillosis-indolent infection with slow destruction of surrounding structures
Chronic localized noninvasive aspergillosis–fungal ball without destruction of bone/no inflammation
Allergic aspergillus sinusitis: immunocompetent patients with nasal polyposis and chronic sinusitis. –has elevated eosinophils/IgE bone remodeling and inflammation but no over invasion.
what are the three most common parasitic orbital conditions?
trichinosis, ecchinococcosis, cysticerocosis (taenia solium)
what are the signs of TED?7
proptosis, lid retraction, lid lag, restrictive extra ocular myopathy, compressive optic neuropathy, exposure keratopathy, conjunctival injection/chemosis.
what is Von Graefe sign?
lid lag
most common sign of TED?
lid retraction.
is TED only seen in Graves?
no, it’s also in Hashimotos, or euthyroid circulating thyroid antibodies (TSHR ab, thyroid binding inhibitory abs, TSH Its, antimicrosomal)
what are the diagnostic criteria for TED?
2/3 of the following:
current/recent thyroid dysfunction (graves, hash, or circulating abs), any eye findings consistent with TED, radiographic evidence of fusiform enlargement of any of these IR, MR, LR, SR/levator.
pathophys of TED?
orbital fibroblasts (from neurocrest cells, some become adipose and some fibroblast) have CD40 (usually seen on B cells) thats actively involved in inflammatory states up regulating glycosaminoglycan and can also be associated with fat hypertrophy. Insulin-like growth factor IgG’s may stimulate these receptors.
how to treat mild TED
life style education, AT’s, selenium
How to treat moderate TED
mod dose corticosteroids, cyclosporin, taping lids, moisture chambers
How to treat severe TED
high dose IV steroids, surgical decompression, radiotherapy
refractory TED treatment?
immunomodulators that are not steroids (rituxan)
which patients are at risk of worsened TED after radioactive iodine?
elevated T3 and smokers
what are treatment strategies for hyperthyroid disease?
methimazole, radioactive iodine, orbital radiation therapy, thyroidectomy
How to treat TED flareups?
IV steroids (500 mg to 1g solumedrol; weekly for 6-12 weeks) –must check LFTs before
PO steroid 1 mg/kg prednisone
what is a risk of orbital radiation?
worsening (diabetic/ischemic) retinopathy
which patients are at highest risk for needing surgical intervention for TED?
Older patients; male patients
whats a choristoma?
mature tissue found at abnormal site
what is IgG4 disease?
increased systemic IgG4 leading to increase in inflammatory T cells
symptoms of IgG4 disease
dacyradenitis, xanthogranulomas, orbital amyloidosis, orbital inflammation
treatment for IgG4 disease
steroids
vasculitis is what type of immune response?
type III hypersensitivity; circulating antibodies complexes depositing in vessels
mechanism of vision loss in GCA?
central artery occlusion OR ischemic optic neuropathy
symptoms of GCA
CN defects, jaw claudication, scalp tenderness, HA, malaise
what antibody is associated with Wegener’s (GPA)
c ANCA ( anti proteinase 3)
triad path findings of GPA (wagerers)
vasculitis, granulomatous inflammation, necrosis
what are systemic findings of wegeners. GPA
glomerulonephritis, lung involvement, nasal/lacrimal extension
ocular manifestation of polyarteritis nodosa
retinal infarction; choroidal infarction.
path finding of polyarteritis nodosa
neutrophil and eosinophils in muscularis layer of vessels.
noncaseating granulomatous inflammation of the lacrimal gland…what do you think of?
sarcoid; you can see the lacrimal gland with Gallium scan
what are the top 5 locations for nonspecific orbital inflammation to occur
EMO myositis, dacryadenitis, scleritis, orbital apex, diffuse
how is myositis in TED different than NSOI ?
TED spares the muscle insertion tendons
tendonitis in NSOI causes the “ring sign”
Features of infantile hemangioma?
dramatically enlarge over 6-12 months then regress between 3-7 years. (75%)
Associations of infantile hemangioma?
premature, female, low birthweight, maternal chorionic villus sampling
How can you diagnose infantile hemangioma from other vascular lesions?
fine vascular channels and high blood flow on MRI
Where is the location intraorbitally of infantile capillary hemangioma usually? Extra orbitally?
Superonasal. can be on neck compromising airway or on organs leading to thrombocytopenia (Kasabach-Merritt Syndrome.
Treatment of infantile hemangioma?
observation, refraction/avoid amblyopia.
Can treat with topical timolol, oral propranolol, steroid, surgical excision, pulse dye laser
what is the most common benign intraorbital lesion?
cavernous hemangioma
well encapsulated, uniformity enhancing lesion on MRI with intralesional Chanels with low blood flow…in a woman. what is it?
cavernous hemangioma
Hemangiopericytoma MRI features
encapsulated hyper vascular/ hypercellular orbital lesion on MRI.
How are hemangiopericytoma different than cavernous hemangioma?
Hemangiopericytomas are blue colored intraoperatively
what is special about hemangiopericytomas on histo?
malignant appearing lesions can stay local and benign appearing ones can metastasize.
proptosis during URIs and/or sudden proptosis…what’s likely dx?
lymphangioma/lymphatic malformations
multiple grape-like cystic lesions with fluid fluid layering on MRI…what’s the dx?
lymphangioma/ lymphatic malformation –fluid fluid is serum and RBC
lymphangioma/lymphatic malformation treatment?
observation vs sclerosis agents.
exophthalmos at rest; proptosis with vaxsalva. what’s the diagnosis? how to diagnose?
orbital venous malformations. CT while doing vaxsalva
treatment for venous malformation? should you biopsy?
surgery if painful lesion/significant proptosis. DO NOT do biopsy–it will bleed. can also endo coil
whats the difference between AVMs and AV fistulas?
AVMs are vascular dysgenesis vs AV fistulas are due to trauma or degemnative.
what are the two types of AV fistulas?
Direct carotid-cavernous fistulas (usually s/p trauma)
Indirect carotid-cavernous fistulas (Dural)-meningeal branches (of internal or external carotid) and the cavernous sinus. (degenerative; more insidious onset;iop elevation and glaucomatous damage)
clinical signs of CC fistulas?
pulsatile proptosis, pain, tortuous epibulbar vessels, elevated IOP, choroidal effusion, blood at angle, nongranulomatous uveitis, compression of CN VI, IV, or III
how to diagnose AV fistulas?
MRA (technically angiography is gold standard)
which of the two types of AV fistulas should be managed more aggressively? why?
Dural CC fisutula as it has arterialization of venous system leading to increase risk of intracranial hemorrhage.
CC fistulas treatment option?
endo coil or glue; trans venous for dural cc fistulas; transarterial approach is for direct cc fistulas
Where do spontaneous orbital hemorrhages usually occur? how should you manage orbital bleeds in general?
superior subperiosteal space. observe unless there’s visual compromise
smooth fusiform intradural lesion of the orbit with kinking of the optic nerve on imaging?
optic glioma
benign optic gliomas in children are called what?
pilocytic astrocytomas
optic gliomas spreading through subarachnoid space. Which population is this?
neurofibromatosis
malignant optic gliomas are called what? what patient population gets them?
glioblastomas. adult males–painful progressive vision loss and proptosis
management of optic nerve gliomas?
must be individualized. observe is confined to the orbit, remove if rapid growth or vision compromise, chemo therapy if progressive, and radiation if absolutely needed.
what are complications of radiation therapy of the orbit?
endocrinopathy, intellectual disability, groth retardation, secondary tumors
neurofibromas –what kind of cells are predminant?
Schwann cells within optic nerve sheath.
NF1 tumors of the orbit
optic gliomas, bilateral meningiomas, and neurofibromas–>pulsating proptosis due to sphenoid bone dysplasia
Plexiform neurofibromas? what does it look like and what is it associated with?
S shaped lateral upper canthus associated NF1
what are the two types of neurofibromas?
plexiform and discrete. Discrete can be easily excised. plexiform are Schwann cells proliferating under nerve sheath…leading to difficult excision.
meningiomas –cells of origin? patient population?
arachnoid villi; women in third/fourth decade of life
what is a feature of spheroid wing meningiomas
hyperostosis of sphenoid bone.
tram tracking on CT head (tumor)
meningioma
management of meningiomas?
can observe vs if there’s vision compromise/proptosis surgery vs radiation.
What is another name for schwannoma?
neurilemma
What are the two biphasic patterns on history of schwanoma?
Antoni A patter(solid areas with nucleating plisaing) and Antoni B pattern (myxoid areas)
Which is the most common primary malignancy of the orbit in childhood? Common location?
Rhabdomyosarcoma. Supranasal.
management of rhabdomyosarcoma
image and excise. send for frozen, permanent, EM, and immunohisto
rhabdomyosarcoma cells of origin?
undifferentiated mesenchymal cells
What are the 4 types of rhabdomyosarcoma? which one has best px?
embryonal (most undifferentiated; striations but not always on trichrome stain), alveolar(worst px, pleomorphic (best px; trichrome stain shows striations), and Botryoid
main management of rhabdomyosarcoma?
radiation/chemo, exenteration if needed only
fibroblastic and histolytic cells in storiform pattern?
fibrous histiocytoma
spindle cells with strong CD34 staining.
solitary fibrous tumor
Fibrous dysplasia are similar to meningiomas. it can be distinguished how?
hyperostotic bone on CT, MRI shows lack of dural enhancement
what syndrome is associated with fibrous dysplasia?
Albright syndrome.
osteosarcoma, chondrosarcoma, fibrosarcomas are associated with what in children?
Hx of Rb.
conjunctival MALTomas are associated with what? what’s the chance of systemic disease
chronic chalmydia. must follow up as systemic disease will develop in 50% of people in 10 years
What are the two low grade B cell lymphocytic tumors?
CLL and follicular center lymphoma
What are the 3 high grade lymphomas of the orbit
Burkitt, large cell, lymphoblastic
Clinical and imaging features of lymphoproliferative lesions
painLESS progressive mass, salmon patch, molding, EOM limitations. bone erosions are usually NOT seen
Lymphoproliferative lesions–how should you diagnose it?
open biopsy, send it fresh and fixed and plenty of tissue for PCR/immuno, flow cytometry, DNA hybridization.
lymphoproliferative tumors with lowest to highest risk of systemic disease based on anatomical location?
conj, orbital, eyelid, lacrimal fossa.
Treatment of lymphoproliferative diseases–what is the treatment of choice for patients with local disease? what should you not give to patients?
radiation is therapy of choice. DO NOT give steroids
Langerhan cell histiocytosis–presenting features?
lytic lesions, super-temporal orbit/sphenoid wing
Langerhan cell histiocytosis prognosis based on age
<2 years old is <50%; and increases 87% when >2 years old
treatment of hanger-on histiocytosis?
aggressive chemo in children. low grade radiation/steroid can be done intralesional
what are the 4 types of xanthogranulomas?
necrobiotic xanthogranuloma
adult onset asthma with periocular xanthogranuloma
Erdheim-Chester disease
Adult onset xanthogranuloma
necrobiotic xanthogranuloma features? Associations?
fibrosis and ulceration. has subQ eyelid lesions and body lesions. multiple myeloma should be worked up
Adult onset asthma with periocular xanthogranuloma features?
periocular xanthogranuloma, asthma, lymphadenopathy, increased Ig levels
Erdheim Chester disease
worse px. dense recalcitrant fibrosclerosis of orbit and organs (mediastinal, pericardium, perinephric…VISION LOSS
Adult onset xanthogranuloma features?
no systemic involvement.
how do epithelial tumors look different from inflammatory/lymphoproliferative tumors of the orbit on imaging?
lympho and inflammatory show molding without boney destruction. epithelial are globular and have boney destruction.
approxiamaly what percent of epithelial tumors are benign?
50% are benign mixed/pleomorphic andeomas
what are the malignant epithelial tumors?
malignant mixed tumors, primary adenocarcinomas, mucoepidermoid carcinoma, squamous carcinomas
management of benign mixed epithelial tumor/ pleomorphic epithelial tumor
excision without distruption of pseudo capsule–therefore no biopsy. theres a chance of malignant degeneration
Adenoid cystic carcinoma is also called what?
cylindroma
what is the most common malignant tumor of the lacrimal gland?
adenoid cystic carcinoma. highly malignant and has perineurial invasion and bony destruction–therefore painful… this feature distinguishes from benign epithelial tumors.
lacrimal fossa tumor with tubes, solid nests, and Swiss-cheese appearance.
adenoid cystic carcinoma
What are the two morphologies of adenoid cystic carcinomas? which is worse
basaloid and cribriform. basaloid is worse
what are features of malignant mixed epithelial tumors?
histologically they are the same as benign ones but has areas of malignancy…mostly come from long standing left behind being mixed from previous
mucoceles and mucopyoceles. what’s in them? location
mucus and pus. superonasal
what is silent sinus syndrome?
chronic subclinical sinusitis resulting in orbital floor thinning and compromise leading to enophthalmos and mild lid retraction–esp when associated with sudden changes in pressure
where do adenocarcinomas and squamous carcinomas come from usually?
maxillary, nasopharynx, oropharynx
mets usually spread where in children
orbit
mets usually spread where in adults?
choroid
abrupt ecchymosis of periobital area
neuroblastoma
neuroblastoma associations?
sudden periobrital ecchymosis, Horner’s
neuroblastoma management?
chemo, radiation, look for primary source/mets
neuroblastoma px based on age?
<1 year is HIGH survival rate (90%); >1 is low (10%)
which lymphoma is most likely to have mets to orbit?
ALL
what is granulocytic sarcoma or chroma?
orbital mass of myelogenous leukemia
when is leukemia in the orbit require emergent radiation?
subarachnoid spread causing nerve swelling
what mets are most common in adults?
breast and lung
where in the orbits are most common for mets in adults?
EOMs, bone marrow if sphenoid
features of breast CA mets to the orbit?
fibrous restriction of EOMs, exophthalmos. –send fresh tissue for ER/PR testing.
prostate cancer mets are associated with what?
lytic lesions resembling acute nonspecific orbital inflammation
Le Forte fractures by definition extends through what structure
pterygoid plate
Describe Le Forte I fracture. Also called what other name?
horizontally through low transverse maxillary. Guerin fracture
Describe Le Forte II fracture
transverse maxillary, nasal, lacrimal bones, and medial orbital wall
Describe Le Forte III fracture
through medial, lateral orbital wall and orbital floor. craniofacial disjunction
Describe zygomaticomaxillary complex (ZMC) fx. what else is it called? tx indicated when?
tripod fx. involves inferior orbital rim, lat orbital rim, zygomatic arch, lat wall of maxillary sinus. displaced fx needs surgery
orbital apex fx associated complications
optic nerve damage/TON, CSF leak, CCfistula
orbital roof fractures are more common in children…why?
frontal sinuses have not developed
potential complications associated orbital roof fx? when is surgery indicated?
pneumocephaly, CSF rhinorrhea, subperiosteal hematoma. Surgery is indicated when there’s CNS involvement
Describe direct medial orbital wall fractures (NOE-naso orbital ethmoid)
maxillary frontal process, nasal bone, and ethmoid fracture. usually due to direct facial impact
Describe type I NOE
fx of maxillary,nasal, ethmoid (in direct medial orbital wall fx) resulting in central fragment attached to medial canthal tendons
Describe Type II NOE
fx of maxillary,nasal, ethmoid (in direct medial orbital wall fx) resulting in central fragment with commenuited central fragment
Describe Type III NOE
fx of maxillary,nasal, ethmoid (in direct medial orbital wall fx) resulting in comminuted canthal attachment site or if tendon is avulsed
Complications of NOE fractures
severe epistaxis due to avulsion of ant ethmoid artery, lacrimal system damage , CSF rhinorrhea, orbital hematoma
Indirect medial orbital wall fractures (medial wall blow out fractures). When is it indicated for surgery? which incisional approaches are good?
when entrapment is present, (or significant enophthalmos can be associated when there’s orbital floor fx). Incisional approaches include transconjunctival vs trancaruncle)
what’s different with direct and indirect orbital floor fractures?
direct fx involves inferior orbital rim. indirect fx are blowout fractures.
PEx signs of orbital floor fracture?
eye lid signs (ecchymosis vs white eyed blowout)
Diplopia with up/down gaze
enophthalmos/globe ptosis
Hypoesthesia of inferior orbital nerve distribution
Orbital emphysema
When there’s no entrapment…when should you repair orbital floor fractures?
about 5-10 days s/p incident to allow decrease in swelling. Less than 2 weeks after injury to avoid fibrosis.
What can you do to decrease risk of diplopia s/p orbital floor fracture?
PO steroids
what are (loose guidelines) to surgical repair of orbital floor fractures when there’s no entrapment?
diplopia >30deg in up/down gaze. enophthalmos >2mm or cosmetically unacceptable to patient, fx >1/2 of orbital floor or involves large medial wall fx
what are incisional approaches for orbital floor repair? what are the general steps of surgery?
infraciliary approach, transconj approach w or w/o lateral canthotomy/cantholysis.
Steps: lift periorbita, free any adhesions from fracture, place implant.
spontaneous orbital hemorrhage are associated with what conditions
lymphangioma and orbital varices
What are three mechanisms of TON
direct injury, loss of perfusion, indirect trauma via stretching/shearing in the orbital apex
vision loss s/p trauma with normal appearing globe…what are the two most important exam findings for urgent intervention?
tight orbit–>orbital compartment syndrome
APD–>compartment vs TON
What are three possible treatments for TON?
observation, high dose steroids, and surgical decompression.
-national acute spinal cord injury study II (for spinal cords) showed improvement with 30mg/kg loading then 15 mg/kg Q6H steroids… due to antioxidant effects of steroids.
what are the 5 surgical spaces of the orbit
- subperiosteal
- extraconal
- intraconal
- subtenon/episcleral
- subarachnoid
explain the superior transcutaneous incision process to access the superior orbit? what other space can it access/how?
superior transcutaneous cut along the upper lid crease. dissect under orbicularis muscle and over septum to the superior orbital rim. Cut is made along arcus marginalis to access orbit.
Medial orbit can also be accessed this way by dissecting along intermuscular septum of superior and medial rectus.
In superior transconjunctival incision approach to access superior/medial orbit what structure must you avoid…by doing what?
avoiding levator muscle by making incision medial to the levator
What is the vertical eyelid splitting method of accessing the superior orbit?
vertically split lid, levator aponeurosis at medial 1/3 of superior lid. (must line up tarsal plate when closing)
What are the 4 methods of accessing the superior orbit?
transcutaneous along superior eyelid crease, vertical eyelid splitting, superior transconjunctival, coronal
inferior oblique inserts over what structure
macula
what are the two transcutaneous inferior orbit incisional options to gain access to the inferior orbit
infraciliary and inferior lid crease (larger scar)
What are the methods of accessing the inferior orbit? 3
infraciliary, inferior lid, inferior transconj
what is the Lynch incision? to access what space?
frontoethmoidal incision –vertically incised medial to medial canthal tendon. 9-10mm medial to medial canthal angle. to access subperiosteal space
using a medial transconjunctival approach what structure do you have to remove to access the intrazonal space?
medial rectus
Superomedial intraconal lesions can be accessed via medial eyelid crease incision. You must identify what structure?
superior oblique insertion site
transcaruncle incision is good to access the subperiosteal space with minimal scarring. What is a structure you must watch for?
lacrimal system.
what are the medial incisions to access the medial orbit?
Lynch (frontoethmoidal), upper medial lid crease, transcaruncle, transconjunctival
What is the Stallard-Wright incision? what space is it used for?
S shaped from lateral brow to zygomatic arch. Can be done with or without lateral cathotomy. To access lateral orbit/behind equator of globe
Leaves a scar.
orbital decompression involves doing what?
cutting through maxillary sinus/ethmoid sinus to give more space.
orbital decompression: traditional approach? vs newer approach?
Caldwell-Luc or transcutaneous anterior orbitotomy vs newer transconj +/- lat cathotomy
what is sympathetic ophthalmia?
delayed hypersensitivity response to uveal antigens
When enucleating eye for possible Rb. what should the surgeon do?
take a long piece of the optic nerve to ensure clear margins
what’s an option for painful blind eyes unable to undergo enucleation?
retrobulbar ethanol injection
what are the 5 goals when creating an an ophthalmic socket?
- sufficient volume.
- lined with conj with adequate fornices
- lids with normal appearnce
- good motility
- comfortable and cosmetically pleasing
what are advantages of eviseration?5
- simpler procedure
- preserved anatomy
- better motility
- treatment for endophthalmitis
- lower risk of migration/extrusion implant
disadvantages of evisceration? 3
not for everyone (such as severe phthisis bulbs), less sent for pathology, theoretical risk of sympathetic ophthalmia
what are the two general type of lateral for orbital implants?
inert (glass, silicone, MMA) vs bio integrated (hydroxyapatite, porous polyethylene)
what are advantages and disadvantages of inert orbital implants
adv: cheaper, comfort, low extrusion
disadvantages: migration, decreased motility, may pinch conj
porous bio integrated orbital implants allow for pegs to be placed. when should they be placed?
6-12 months after enucleation.
Pegs give better motility but associated with more inflammation post op
What space does the orbital implant go after evisceration vs enucleation?
after evisceration it goes within or behind sclera. vs after enucleation it goes behind or within subtenons
when is the prosthesis usually fitted after enucleation/evisceration?
4-8 weeks. removed once a month for cleaning
what is a deep sulcus deformity? tx by ?
large superior sulcus after enucleation/evisceration due to orbital volume loss. tx by placing subperiosteal implant on orbital floor +/- dermis fat grafts to upper orbit
giant fornix syndrome? what is it. complications. treatment
occurs when superior conj fornix is too deep. leads to retention of mucus and debris leading to infections.
Treat by superior conj resection
what are two things you can do to prevent contracture of fornices?
placing EOMs where they should be and wearing conformers (do not remove for more than 24 hrs)
Contracted socket is caused by what? 6
radiation severe alkali injury poor surgical technique multiple operations removal of conformer extrusion of implant
what is contracted socket by definition?
when fornices are too small to hold prosthesis
contracted socket can be expanded using what?
full thickness mucus membrane graft, amniotic membrane. (buccal graft with silicon sheet x2 weeks may be used if mild inferior socket contracture)
when should you consider exenteration?
- destructive tumor
- intraocular tumors with extra ocular spread
- malignant epithelial lacrimal gland tumors
- sarcomas not responsive to therapy
- fungal infections
what are the 3 types of exenteration?
subtotal, total, extended
What is the SMAS
the superficial musculoaponeurotic system: consisting of facial memetic muscles and facial plane
What consists of SMAS
superficial neck facia, platysma, zygomaticus major, zygomaticus minor, orbicularis oculi
what are the two major components of facial support?
Osteocutaneous ligaments (orbitomalar, zygomatic, mandibular) Fascial cutaneous ligaments *condensation of superficial and deep facia--paritodcutaneous and masseteric)
what are the mimetic muscles of the lower face?
Superficial (neurovascularly suppllied posteriorly): platysma, zygomaticus major/minor, risorius
Deep (neurovascularly supplied anteriorly): buccinator, mentalist, elevator angle oris
what are the mimetic muscles of the upper face?
frontalis, corrugator supercilii, procesrus muscles, orbicularis oculi,
deep cervical fascia overlies what structure?
myohyaloid muscle and over the body of the mandible
What facial plane is the temporal artery located? what other structure is here?
superficial to parotidomasseteric fascia (continuous to deep temporal fascia). temporal branch of facial nerve (CN VII) is here
what are the 5 branches of the facial nerve?
Temporal, zygomatic, buccal, marginal manipular, cervical
at what plane should you dissect when in the upper face to avoid the nerves? what about the lower face?
Upper: dissect deep to SMAS and CN VII (below temporoparietal fascia and superficial to deep temporal fascia)
lower face: dissect superficial to SMAS and CN VII
What are the subdivisions of CNV1? 5
Supraorbital, supratrochlear, infratrochlear, external nasal, lacrimal
What are the subdivisions of CNV2?
zygomaticotemporal, zygomaticofacial, infraorbital
what are the subdivisions of CNV3?
auriculotemporal, buccal, mental
7 structural layers of the eye lids
skin/subQ, muscles of protraction, orbital septum, orbital fat, muscles of retraction, tarsus, conj
the upper lid crease approximates what structure?
attachments of elevator panoenurosis to pretrial orbiculares bundles/skin.
what makes lid crease differences in asian and caucasians?
caucasian levato aponeurosis inserts in to pretarsar orbicularis/ above tarsus
asians levator aponeursis inserts between top of tarsus and lid margin.
what is the main protractor muscle?
orbicularis oculi
what are the 3 parts of orbicularis oculi muscle?
pretrial, preseptal– for blinking
orbital- forced lid closure
what is Horner muscle?
fused portion of pretrial orbicularis oculi muscle (originating from lacrimal crest and medial cants)
where does the preseptal portions of orbicularis oculi originate? where does it insert?
from medial canthal tendon and inserts to lateral canthal raphae
origin of orbital portions of orbicularis muscle?
anterior limb of medial canthal tendon, orbital process of frontal bone, and frontal process of maxillary bone
what creates the gray line. what does it do?
striate muscles called “muscle of riolan”–helps with blinking, meibomeian discharge, and position of lashes
where does orbital fat lie?
posterior to septum and anterior to levator aponeurosis./capsulopalpebral fascia
how many fat pads are in superior lid? inferior lid?
superior 2: nasal and central;
lower 3: nasal, central, temporal.
why is central fat pad of the orbit important?
it lies directly behind orbital septum and in front of levator aponeurosis
what are the main retractors of the upper lid? lower lids?
levator superiororis, and muller muscle (superior tarsal muscle). Capsulopalpebral fascia and inferior tarsal muscle
where does the levator originate? where does it insert?
apex of the orbit at the lesser wing of the sphenoid. inserts medially to lacrimal crest and laterally to lateral orbital tubercle
how long is the the levator oculi superioris? how long is the aponeurosis?
muscle is 40 mm long. aponeurosis is 20 mm
what is the superior transverse ligament around the elevator muscle? what’s the inferior analogue?
Whitnall ligament; Lockwood ligament
what are the 7 layers of the eye lid?
skin/subQ, muscles of protraction, septum, orbital fat, muscles of retraction, tarsus, conj
where in does the muller muscle originate? where does it lie? where does it insert?
muller muscle originates from the levator at the level of ligament of whitnall about 12 mm above tarsus. travels posterior to levator and tarsus. inserts in to conj
how much lift does muller muscle give. What condition gives muller muscle related ptosis?
2mm. Horner’s syndrome
between what two structures does the peripheral arcade run?
levator and muller muscles. This is the land mark for identifying muller muscle.
what is the lower lid equivalent structure to levator superiors
capsulopalpebral fascia originating form inferior rectus. it fuses with inferior oblique and becomes Lockwood ligament
what is the lower lid equivalent of muller muscle?
inferior tarsal muscle
height of upper tarsal plate?
10-12 mm
height of lower tarsal plate?
4mm
how thick is tarsus
1mm
what are the glands of Wolfring and glands of Krause?
Accessory lacrimal glands in subconj palpebral tissue. Wolfring is along non marginal tarsus and Krause is in fornices.
origin of medial canthal tendon. describe it’s features
originates from ant and posterior lacrimal crest. anterior is strong and posterior is for positioning of lid allowing puncture to lie in tear lake
what structure does the muscle of riolan overly?
it is pre tarsal portion of the orbicularis muscle
size of horizontal palpebral fissure?
30 mm
avg upper eye lash number? avg lower?
avg upper is 100. Lower is 50
avg number of meibomian glands of upper lid? lower?
upper 25, lower 20.
what are the two blood supplies of lids?
internal carotid–>ophthalmic–>supraorbital/lacrima
external carotid–>angular/temporal
where does the marginal arcade locate?
2mm above margin anterior to the tarsus
what are the two venous systems of the eye lids?
preseptal and postseptal venous systems.
blepharophimosis ptosis epicanthus inversus syndrome (BPES) what gene is involved. What are the two types?
FOXL2 gene.
type I involves ovarian loss in women
type II involves hypoplastic nose bridge/superior orbit/ear deformity
congenital ectropion. What’s the anatomical defect?
vertical insufficiency of anterior lamella
treat with horizontal tightening of lateral canthal tendon. and vertical lengthening of anterior lamella with skin graft.
complete eversion of upper eyelids in babies… causes? treatments?
caused by conjunctivitis, inflammation, Downsyndrome.
treat with lubrication/patching or temporary tarshorrhaphy
what is euryblepharon? tx?
vertical shortening and horizontal lengthening of lids.
tx with lateral tarsal strip/ lid margin resection
what are the 4 types of epicanthus?
- epicanthus tarsal-most prominent upper fold
- epicanthus inverses- most prominent lower lid
- epicanthus palbebralis- equal upper and lower fold
- epicanthus supraciliaris- starts from brow and comes down.
epicanthus inverses is associated with what condition?
BPES (blepharophimosis, ptosis, epicanthus inversus syndrome.)
what is epiblepharon?
horizontal lid fold of inferior lid forcing the eye lashes to straight position esp on down gaze causing keratitis. Usually gets better as facial bones mature
inward lashes can be seen in epiblepharon and congenital entropion in kids… what are mechanisms of entropion?
tarsal kink, absent lid retractors, absent tarsus
congenital distichiasis results with improper differentiation of embryonic pilosebaceous units. How to treat?
electrolysis, cryoepilation, lid splitting to remove follicles.
lid coloboma usually occurs upper or lower?
upper. If lower then think Goldenhar
cryptophthalmos… what’s the mechanism? and what condition is the eye usually
fused anterior lid adnexa.
usually poor visual potential of eye due to severe defects
chalazion…commonly associated conditions
blepharitis and rosacea and sebaceous gland ca
options of chalazion treatment?
WC/LH topical abx/steroids oral doxy steroid injection --hypopigmented skin is risk excision
chalazion vs hordeolum?
chalazion is an internal posterior hordeolum (aka meibom)
hordeolum is acute infection of zeis OR meibom
classic sx of floppy lid syndrome. finding
irritation and mild mucus in AM. finding of chronic papillary conjunctivitis, lid eversion
floppy lid associations
obesity, OSA, DM, face sleepers, keratoeonus
what is eyelid imbrication syndrome
lax upper lid (with normal tarsal plate) overriding lower lid on closure. lubricate or tighten lid
what type of lid lesion is associated with perineurial invasion
squamous cell CA
how should you biopsy benign epithelial lesions
shave excision
what is skin tag called
acrochordon
what is pseudoepitheliomatous hyperplasia?
a pattern of reaction in epidermis that develops over areas of inflammation
epidermal inclusion cyst involves what structure. treatment?
infundibulum of hair follicle. filled with keratin. FB reaction if ruptures. Treatment: marsupialization
what are milia? tx
tiny epidermal inclusion cysts… treat with topical retinoid acid
pilar or trichilemmal cysts…what is it? where does it occur?
large epidermal inclusion cysts–usually in scalp or eye brows
molluscum in adult…you think
AIDS
molluscum treatment?
observation, cimetidine, excision, cry, curetage
xanthelasma treatment
excision, laser ablation, topical trichloroacetic acid
what are adnexa?
structures originating in dermis and passes to surface through epidermis. –hair, oil glands, sweat glands
many sebaceous gland hyperplasia is associated with what?
visceral malignancy. Muir-Torre syndrome
what are the two types of hidrocystoma? where do they locate? what is the difference
eccrine vs apocrine.
Both are lower lid at canthi
Eccrine are ductal pretension cysts and enlarge with humidity/temp. tx excision
Apocrine are adenomas of hands of Moll, blue and transilluminate. tx: marsupialization
syringoma. what are they. what population
multiple eccrine benign sweat gland tumors. young females around puberty.
trichoepithelioma. path feature
basasoid island and keratin cysts with immature hair follicles
trichofolliculoma path feature
single umbilicate lesion.
squamous cyst with keratin and hair shaft
trichilemmoma. path feature
single lesion. resemble verrucae. glycogen rich cells oriented around hair follicles
pilomatricoma
subQ mass attached to overlying skin.
Island of epithelial cells surrounded by basophilic cells with shadow cells
what are the top 3 most common benign lesions in periocular area
papilloma, epidermal inclusion cysts, nevi
characteristic of nevi.
immature melanocytes in epidermis/dermis/ and junction zone. Not apparent at birth.
molds to ocular surface
3 stages of nevi
junctional (basal layer of epiderm), compound, dermal
ephelides. what is path
increased melanin but same number of melanocytes
What are lentigo simplex. what is a condition it’s associated with
larger ephelides but increased number of melanocytes. NOT related sun exposure. Peutz-Jagher
what are solar lentigo
sun exposure related increase in melanocytes
what are blue nevi?
intra dermal nevi in children. usually excised
nevus of Ota is what? what do you need to look out for in these patients?
blue dermal Nevis in V1 and V2 distribution. Need to monitor for glaucoma… and rarely uveal melanoma
Actinic keratosis. What % regress in 1 year. What’s the malignant transformation potential of a single lesion? What’s the overall incidence of squamous cell CA in its with multiple Ads
25% regression in 1 year.
0.25% malignant transformation of single lesion
15% of chance for squamous overall in pts with multiple lesions.
