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Flashcards in Oculoplastics Deck (282):
1

What etiologies should you consider for preseptal cellulitis?

sinus, dacryadenitis, skin, hematogenous

2

Most common cause of preseptal historically vs now?

h. influenza before. Now g+ cocci

3

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

4

hospital acquired MRSA are sensitive to what

vanc, linezolid

5

most common source of infection for orbital cellulitis

chronic bacterial sinusitis

6

signs of orbital cellulitis

leukocytosis, fever, erythema, proptosis, chemises, ptosis, restriction/pain with EOMs, decrease in vision, impaired color, restricted fields, pupil Abel

7

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

8

what kind of orbital wall fracture is at highest risk of subsequent orbital cellulitis

medial wall

9

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

10

what medicine is particularly good for nec fasc involving group A strep?

Clindamycin

11

signs of orbital TB

proptosis, EOM Abnl, bone destruction, draining fistulas

12

what stains is used for asperillus? whats the path finding

Grocott-Gomori methenamine-silver nitrate. shows septet branching hyphae with uniform width.

13

what stain is used for zygomycosis (mucor/rhizopus)? what's the finding?

stain is hematoxylin eosin. finding of nonseptated large branching hyphae.

14

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.

15

what are the three most common parasitic orbital conditions?

trichinosis, ecchinococcosis, cysticerocosis (taenia solium)

16

what are the signs of TED?7

proptosis, lid retraction, lid lag, restrictive extra ocular myopathy, compressive optic neuropathy, exposure keratopathy, conjunctival injection/chemosis.

17

what is Von Graefe sign?

lid lag

18

most common sign of TED?

lid retraction.

19

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)

20

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.

21

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.

22

how to treat mild TED

life style education, AT's, selenium

23

How to treat moderate TED

mod dose corticosteroids, cyclosporin, taping lids, moisture chambers

24

How to treat severe TED

high dose IV steroids, surgical decompression, radiotherapy

25

refractory TED treatment?

immunomodulators that are not steroids (rituxan)

26

which patients are at risk of worsened TED after radioactive iodine?

elevated T3 and smokers

27

what are treatment strategies for hyperthyroid disease?

methimazole, radioactive iodine, orbital radiation therapy, thyroidectomy

28

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

29

what is a risk of orbital radiation?

worsening (diabetic/ischemic) retinopathy

30

which patients are at highest risk for needing surgical intervention for TED?

Older patients; male patients

31

whats a choristoma?

mature tissue found at abnormal site

32

what is IgG4 disease?

increased systemic IgG4 leading to increase in inflammatory T cells

33

symptoms of IgG4 disease

dacyradenitis, xanthogranulomas, orbital amyloidosis, orbital inflammation

34

treatment for IgG4 disease

steroids

35

vasculitis is what type of immune response?

type III hypersensitivity; circulating antibodies complexes depositing in vessels

36

mechanism of vision loss in GCA?

central artery occlusion OR ischemic optic neuropathy

37

symptoms of GCA

CN defects, jaw claudication, scalp tenderness, HA, malaise

38

what antibody is associated with Wegener's (GPA)

c ANCA ( anti proteinase 3)

39

triad path findings of GPA (wagerers)

vasculitis, granulomatous inflammation, necrosis

40

what are systemic findings of wegeners. GPA

glomerulonephritis, lung involvement, nasal/lacrimal extension

41

ocular manifestation of polyarteritis nodosa

retinal infarction; choroidal infarction.

42

path finding of polyarteritis nodosa

neutrophil and eosinophils in muscularis layer of vessels.

43

noncaseating granulomatous inflammation of the lacrimal gland...what do you think of?

sarcoid; you can see the lacrimal gland with Gallium scan

44

what are the top 5 locations for nonspecific orbital inflammation to occur

EMO myositis, dacryadenitis, scleritis, orbital apex, diffuse

45

how is myositis in TED different than NSOI ?

TED spares the muscle insertion tendons
tendonitis in NSOI causes the "ring sign"

46

Features of infantile hemangioma?

dramatically enlarge over 6-12 months then regress between 3-7 years. (75%)

47

Associations of infantile hemangioma?

premature, female, low birthweight, maternal chorionic villus sampling

48

How can you diagnose infantile hemangioma from other vascular lesions?

fine vascular channels and high blood flow on MRI

49

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.

50

Treatment of infantile hemangioma?

observation, refraction/avoid amblyopia.
Can treat with topical timolol, oral propranolol, steroid, surgical excision, pulse dye laser

51

what is the most common benign intraorbital lesion?

cavernous hemangioma

52

well encapsulated, uniformity enhancing lesion on MRI with intralesional Chanels with low blood flow...in a woman. what is it?

cavernous hemangioma

53

Hemangiopericytoma MRI features

encapsulated hyper vascular/ hypercellular orbital lesion on MRI.

54

How are hemangiopericytoma different than cavernous hemangioma?

Hemangiopericytomas are blue colored intraoperatively

55

what is special about hemangiopericytomas on histo?

malignant appearing lesions can stay local and benign appearing ones can metastasize.

56

proptosis during URIs and/or sudden proptosis...what's likely dx?

lymphangioma/lymphatic malformations

57

multiple grape-like cystic lesions with fluid fluid layering on MRI...what's the dx?

lymphangioma/ lymphatic malformation --fluid fluid is serum and RBC

58

lymphangioma/lymphatic malformation treatment?

observation vs sclerosis agents.

59

exophthalmos at rest; proptosis with vaxsalva. what's the diagnosis? how to diagnose?

orbital venous malformations. CT while doing vaxsalva

60

treatment for venous malformation? should you biopsy?

surgery if painful lesion/significant proptosis. DO NOT do biopsy--it will bleed. can also endo coil

61

whats the difference between AVMs and AV fistulas?

AVMs are vascular dysgenesis vs AV fistulas are due to trauma or degemnative.

62

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)

63

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

64

how to diagnose AV fistulas?

MRA (technically angiography is gold standard)

65

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.

66

CC fistulas treatment option?

endo coil or glue; trans venous for dural cc fistulas; transarterial approach is for direct cc fistulas

67

Where do spontaneous orbital hemorrhages usually occur? how should you manage orbital bleeds in general?

superior subperiosteal space. observe unless there's visual compromise

68

smooth fusiform intradural lesion of the orbit with kinking of the optic nerve on imaging?

optic glioma

69

benign optic gliomas in children are called what?

pilocytic astrocytomas

70

optic gliomas spreading through subarachnoid space. Which population is this?

neurofibromatosis

71

malignant optic gliomas are called what? what patient population gets them?

glioblastomas. adult males--painful progressive vision loss and proptosis

72

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.

73

what are complications of radiation therapy of the orbit?

endocrinopathy, intellectual disability, groth retardation, secondary tumors

74

neurofibromas --what kind of cells are predminant?

Schwann cells within optic nerve sheath.

75

NF1 tumors of the orbit

optic gliomas, bilateral meningiomas, and neurofibromas-->pulsating proptosis due to sphenoid bone dysplasia

76

Plexiform neurofibromas? what does it look like and what is it associated with?

S shaped lateral upper canthus associated NF1

77

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.

78

meningiomas --cells of origin? patient population?

arachnoid villi; women in third/fourth decade of life

79

what is a feature of spheroid wing meningiomas

hyperostosis of sphenoid bone.

80

tram tracking on CT head (tumor)

meningioma

81

management of meningiomas?

can observe vs if there's vision compromise/proptosis surgery vs radiation.

82

What is another name for schwannoma?

neurilemma

83

What are the two biphasic patterns on history of schwanoma?

Antoni A patter(solid areas with nucleating plisaing) and Antoni B pattern (myxoid areas)

84

Which is the most common primary malignancy of the orbit in childhood? Common location?

Rhabdomyosarcoma. Supranasal.

85

management of rhabdomyosarcoma

image and excise. send for frozen, permanent, EM, and immunohisto

86

rhabdomyosarcoma cells of origin?

undifferentiated mesenchymal cells

87

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

88

main management of rhabdomyosarcoma?

radiation/chemo, exenteration if needed only

89

fibroblastic and histolytic cells in storiform pattern?

fibrous histiocytoma

90

spindle cells with strong CD34 staining.

solitary fibrous tumor

91

Fibrous dysplasia are similar to meningiomas. it can be distinguished how?

hyperostotic bone on CT, MRI shows lack of dural enhancement

92

what syndrome is associated with fibrous dysplasia?

Albright syndrome.

93

osteosarcoma, chondrosarcoma, fibrosarcomas are associated with what in children?

Hx of Rb.

94

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

95

What are the two low grade B cell lymphocytic tumors?

CLL and follicular center lymphoma

96

What are the 3 high grade lymphomas of the orbit

Burkitt, large cell, lymphoblastic

97

Clinical and imaging features of lymphoproliferative lesions

painLESS progressive mass, salmon patch, molding, EOM limitations. bone erosions are usually NOT seen

98

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.

99

lymphoproliferative tumors with lowest to highest risk of systemic disease based on anatomical location?

conj, orbital, eyelid, lacrimal fossa.

100

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

101

Langerhan cell histiocytosis--presenting features?

lytic lesions, super-temporal orbit/sphenoid wing

102

Langerhan cell histiocytosis prognosis based on age

<2 years old is <50%; and increases 87% when >2 years old

103

treatment of hanger-on histiocytosis?

aggressive chemo in children. low grade radiation/steroid can be done intralesional

104

what are the 4 types of xanthogranulomas?

necrobiotic xanthogranuloma
adult onset asthma with periocular xanthogranuloma
Erdheim-Chester disease
Adult onset xanthogranuloma

105

necrobiotic xanthogranuloma features? Associations?

fibrosis and ulceration. has subQ eyelid lesions and body lesions. multiple myeloma should be worked up

106

Adult onset asthma with periocular xanthogranuloma features?

periocular xanthogranuloma, asthma, lymphadenopathy, increased Ig levels

107

Erdheim Chester disease

worse px. dense recalcitrant fibrosclerosis of orbit and organs (mediastinal, pericardium, perinephric...VISION LOSS

108

Adult onset xanthogranuloma features?

no systemic involvement.

109

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.

110

approxiamaly what percent of epithelial tumors are benign?

50% are benign mixed/pleomorphic andeomas

111

what are the malignant epithelial tumors?

malignant mixed tumors, primary adenocarcinomas, mucoepidermoid carcinoma, squamous carcinomas

112

management of benign mixed epithelial tumor/ pleomorphic epithelial tumor

excision without distruption of pseudo capsule--therefore no biopsy. theres a chance of malignant degeneration

113

Adenoid cystic carcinoma is also called what?

cylindroma

114

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.

115

lacrimal fossa tumor with tubes, solid nests, and Swiss-cheese appearance.

adenoid cystic carcinoma

116

What are the two morphologies of adenoid cystic carcinomas? which is worse

basaloid and cribriform. basaloid is worse

117

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

118

mucoceles and mucopyoceles. what's in them? location

mucus and pus. superonasal

119

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

120

where do adenocarcinomas and squamous carcinomas come from usually?

maxillary, nasopharynx, oropharynx

121

mets usually spread where in children

orbit

122

mets usually spread where in adults?

choroid

123

abrupt ecchymosis of periobital area

neuroblastoma

124

neuroblastoma associations?

sudden periobrital ecchymosis, Horner's

125

neuroblastoma management?

chemo, radiation, look for primary source/mets

126

neuroblastoma px based on age?

<1 year is HIGH survival rate (90%); >1 is low (10%)

127

which lymphoma is most likely to have mets to orbit?

ALL

128

what is granulocytic sarcoma or chroma?

orbital mass of myelogenous leukemia

129

when is leukemia in the orbit require emergent radiation?

subarachnoid spread causing nerve swelling

130

what mets are most common in adults?

breast and lung

131

where in the orbits are most common for mets in adults?

EOMs, bone marrow if sphenoid

132

features of breast CA mets to the orbit?

fibrous restriction of EOMs, exophthalmos. --send fresh tissue for ER/PR testing.

133

prostate cancer mets are associated with what?

lytic lesions resembling acute nonspecific orbital inflammation

134

Le Forte fractures by definition extends through what structure

pterygoid plate

135

Describe Le Forte I fracture. Also called what other name?

horizontally through low transverse maxillary. Guerin fracture

136

Describe Le Forte II fracture

transverse maxillary, nasal, lacrimal bones, and medial orbital wall

137

Describe Le Forte III fracture

through medial, lateral orbital wall and orbital floor. craniofacial disjunction

138

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

139

orbital apex fx associated complications

optic nerve damage/TON, CSF leak, CCfistula

140

orbital roof fractures are more common in children...why?

frontal sinuses have not developed

141

potential complications associated orbital roof fx? when is surgery indicated?

pneumocephaly, CSF rhinorrhea, subperiosteal hematoma. Surgery is indicated when there's CNS involvement

142

Describe direct medial orbital wall fractures (NOE-naso orbital ethmoid)

maxillary frontal process, nasal bone, and ethmoid fracture. usually due to direct facial impact

143

Describe type I NOE

fx of maxillary,nasal, ethmoid (in direct medial orbital wall fx) resulting in central fragment attached to medial canthal tendons

144

Describe Type II NOE

fx of maxillary,nasal, ethmoid (in direct medial orbital wall fx) resulting in central fragment with commenuited central fragment

145

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

146

Complications of NOE fractures

severe epistaxis due to avulsion of ant ethmoid artery, lacrimal system damage , CSF rhinorrhea, orbital hematoma

147

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)

148

what's different with direct and indirect orbital floor fractures?

direct fx involves inferior orbital rim. indirect fx are blowout fractures.

149

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

150

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.

151

What can you do to decrease risk of diplopia s/p orbital floor fracture?

PO steroids

152

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

153

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.

154

spontaneous orbital hemorrhage are associated with what conditions

lymphangioma and orbital varices

155

What are three mechanisms of TON

direct injury, loss of perfusion, indirect trauma via stretching/shearing in the orbital apex

156

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

157

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.

158

what are the 5 surgical spaces of the orbit

-subperiosteal
-extraconal
-intraconal
-subtenon/episcleral
-subarachnoid

159

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.

160

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

161

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)

162

What are the 4 methods of accessing the superior orbit?

transcutaneous along superior eyelid crease, vertical eyelid splitting, superior transconjunctival, coronal

163

inferior oblique inserts over what structure

macula

164

what are the two transcutaneous inferior orbit incisional options to gain access to the inferior orbit

infraciliary and inferior lid crease (larger scar)

165

What are the methods of accessing the inferior orbit? 3

infraciliary, inferior lid, inferior transconj

166

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

167

using a medial transconjunctival approach what structure do you have to remove to access the intrazonal space?

medial rectus

168

Superomedial intraconal lesions can be accessed via medial eyelid crease incision. You must identify what structure?

superior oblique insertion site

169

transcaruncle incision is good to access the subperiosteal space with minimal scarring. What is a structure you must watch for?

lacrimal system.

170

what are the medial incisions to access the medial orbit?

Lynch (frontoethmoidal), upper medial lid crease, transcaruncle, transconjunctival

171

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.

172

orbital decompression involves doing what?

cutting through maxillary sinus/ethmoid sinus to give more space.

173

orbital decompression: traditional approach? vs newer approach?

Caldwell-Luc or transcutaneous anterior orbitotomy vs newer transconj +/- lat cathotomy

174

what is sympathetic ophthalmia?

delayed hypersensitivity response to uveal antigens

175

When enucleating eye for possible Rb. what should the surgeon do?

take a long piece of the optic nerve to ensure clear margins

176

what's an option for painful blind eyes unable to undergo enucleation?

retrobulbar ethanol injection

177

what are the 5 goals when creating an an ophthalmic socket?

1. sufficient volume.
2. lined with conj with adequate fornices
3. lids with normal appearnce
4. good motility
5. comfortable and cosmetically pleasing

178

what are advantages of eviseration?5

1. simpler procedure
2. preserved anatomy
3. better motility
4. treatment for endophthalmitis
5. lower risk of migration/extrusion implant

179

disadvantages of evisceration? 3

not for everyone (such as severe phthisis bulbs), less sent for pathology, theoretical risk of sympathetic ophthalmia

180

what are the two general type of lateral for orbital implants?

inert (glass, silicone, MMA) vs bio integrated (hydroxyapatite, porous polyethylene)

181

what are advantages and disadvantages of inert orbital implants

adv: cheaper, comfort, low extrusion
disadvantages: migration, decreased motility, may pinch conj

182

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

183

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

184

when is the prosthesis usually fitted after enucleation/evisceration?

4-8 weeks. removed once a month for cleaning

185

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

186

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

187

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)

188

Contracted socket is caused by what? 6

radiation
severe alkali injury
poor surgical technique
multiple operations
removal of conformer
extrusion of implant

189

what is contracted socket by definition?

when fornices are too small to hold prosthesis

190

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)

191

when should you consider exenteration?

1. destructive tumor
2. intraocular tumors with extra ocular spread
3. malignant epithelial lacrimal gland tumors
5. sarcomas not responsive to therapy
6. fungal infections

192

what are the 3 types of exenteration?

subtotal, total, extended

193

What is the SMAS

the superficial musculoaponeurotic system: consisting of facial memetic muscles and facial plane

194

What consists of SMAS

superficial neck facia, platysma, zygomaticus major, zygomaticus minor, orbicularis oculi

195

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)

196

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

197

what are the mimetic muscles of the upper face?

frontalis, corrugator supercilii, procesrus muscles, orbicularis oculi,

198

deep cervical fascia overlies what structure?

myohyaloid muscle and over the body of the mandible

199

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

200

what are the 5 branches of the facial nerve?

Temporal, zygomatic, buccal, marginal manipular, cervical

201

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

202

What are the subdivisions of CNV1? 5

Supraorbital, supratrochlear, infratrochlear, external nasal, lacrimal

203

What are the subdivisions of CNV2?

zygomaticotemporal, zygomaticofacial, infraorbital

204

what are the subdivisions of CNV3?

auriculotemporal, buccal, mental

205

7 structural layers of the eye lids

skin/subQ, muscles of protraction, orbital septum, orbital fat, muscles of retraction, tarsus, conj

206

the upper lid crease approximates what structure?

attachments of elevator panoenurosis to pretrial orbiculares bundles/skin.

207

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.

208

what is the main protractor muscle?

orbicularis oculi

209

what are the 3 parts of orbicularis oculi muscle?

pretrial, preseptal-- for blinking
orbital- forced lid closure

210

what is Horner muscle?

fused portion of pretrial orbicularis oculi muscle (originating from lacrimal crest and medial cants)

211

where does the preseptal portions of orbicularis oculi originate? where does it insert?

from medial canthal tendon and inserts to lateral canthal raphae

212

origin of orbital portions of orbicularis muscle?

anterior limb of medial canthal tendon, orbital process of frontal bone, and frontal process of maxillary bone

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what creates the gray line. what does it do?

striate muscles called "muscle of riolan"--helps with blinking, meibomeian discharge, and position of lashes

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where does orbital fat lie?

posterior to septum and anterior to levator aponeurosis./capsulopalpebral fascia

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how many fat pads are in superior lid? inferior lid?

superior 2: nasal and central;
lower 3: nasal, central, temporal.

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why is central fat pad of the orbit important?

it lies directly behind orbital septum and in front of levator aponeurosis

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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

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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

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how long is the the levator oculi superioris? how long is the aponeurosis?

muscle is 40 mm long. aponeurosis is 20 mm

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what is the superior transverse ligament around the elevator muscle? what's the inferior analogue?

Whitnall ligament; Lockwood ligament

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what are the 7 layers of the eye lid?

skin/subQ, muscles of protraction, septum, orbital fat, muscles of retraction, tarsus, conj

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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

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how much lift does muller muscle give. What condition gives muller muscle related ptosis?

2mm. Horner's syndrome

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between what two structures does the peripheral arcade run?

levator and muller muscles. This is the land mark for identifying muller muscle.

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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

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what is the lower lid equivalent of muller muscle?

inferior tarsal muscle

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height of upper tarsal plate?

10-12 mm

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height of lower tarsal plate?

4mm

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how thick is tarsus

1mm

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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.

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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

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what structure does the muscle of riolan overly?

it is pre tarsal portion of the orbicularis muscle

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size of horizontal palpebral fissure?

30 mm

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avg upper eye lash number? avg lower?

avg upper is 100. Lower is 50

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avg number of meibomian glands of upper lid? lower?

upper 25, lower 20.

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what are the two blood supplies of lids?

internal carotid-->ophthalmic-->supraorbital/lacrima
external carotid-->angular/temporal

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where does the marginal arcade locate?

2mm above margin anterior to the tarsus

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what are the two venous systems of the eye lids?

preseptal and postseptal venous systems.

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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

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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.

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complete eversion of upper eyelids in babies... causes? treatments?

caused by conjunctivitis, inflammation, Downsyndrome.
treat with lubrication/patching or temporary tarshorrhaphy

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what is euryblepharon? tx?

vertical shortening and horizontal lengthening of lids.
tx with lateral tarsal strip/ lid margin resection

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what are the 4 types of epicanthus?

1. epicanthus tarsal-most prominent upper fold
2. epicanthus inverses- most prominent lower lid
3. epicanthus palbebralis- equal upper and lower fold
4. epicanthus supraciliaris- starts from brow and comes down.

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epicanthus inverses is associated with what condition?

BPES (blepharophimosis, ptosis, epicanthus inversus syndrome.)

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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

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inward lashes can be seen in epiblepharon and congenital entropion in kids... what are mechanisms of entropion?

tarsal kink, absent lid retractors, absent tarsus

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congenital distichiasis results with improper differentiation of embryonic pilosebaceous units. How to treat?

electrolysis, cryoepilation, lid splitting to remove follicles.

248

lid coloboma usually occurs upper or lower?

upper. If lower then think Goldenhar

249

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

250

chalazion...commonly associated conditions

blepharitis and rosacea and sebaceous gland ca

251

options of chalazion treatment?

WC/LH
topical abx/steroids
oral doxy
steroid injection --hypopigmented skin is risk
excision

252

chalazion vs hordeolum?

chalazion is an internal posterior hordeolum (aka meibom)
hordeolum is acute infection of zeis OR meibom

253

classic sx of floppy lid syndrome. finding

irritation and mild mucus in AM. finding of chronic papillary conjunctivitis, lid eversion

254

floppy lid associations

obesity, OSA, DM, face sleepers, keratoeonus

255

what is eyelid imbrication syndrome

lax upper lid (with normal tarsal plate) overriding lower lid on closure. lubricate or tighten lid

256

what type of lid lesion is associated with perineurial invasion

squamous cell CA

257

how should you biopsy benign epithelial lesions

shave excision

258

what is skin tag called

acrochordon

259

what is pseudoepitheliomatous hyperplasia?

a pattern of reaction in epidermis that develops over areas of inflammation

260

epidermal inclusion cyst involves what structure. treatment?

infundibulum of hair follicle. filled with keratin. FB reaction if ruptures. Treatment: marsupialization

261

what are milia? tx

tiny epidermal inclusion cysts... treat with topical retinoid acid

262

pilar or trichilemmal cysts...what is it? where does it occur?

large epidermal inclusion cysts--usually in scalp or eye brows

263

molluscum in adult...you think

AIDS

264

molluscum treatment?

observation, cimetidine, excision, cry, curetage

265

xanthelasma treatment

excision, laser ablation, topical trichloroacetic acid

266

what are adnexa?

structures originating in dermis and passes to surface through epidermis. --hair, oil glands, sweat glands

267

many sebaceous gland hyperplasia is associated with what?

visceral malignancy. Muir-Torre syndrome

268

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

269

syringoma. what are they. what population

multiple eccrine benign sweat gland tumors. young females around puberty.

270

trichoepithelioma. path feature

basasoid island and keratin cysts with immature hair follicles

271

trichofolliculoma path feature

single umbilicate lesion.
squamous cyst with keratin and hair shaft

272

trichilemmoma. path feature

single lesion. resemble verrucae. glycogen rich cells oriented around hair follicles

273

pilomatricoma

subQ mass attached to overlying skin.
Island of epithelial cells surrounded by basophilic cells with shadow cells

274

what are the top 3 most common benign lesions in periocular area

papilloma, epidermal inclusion cysts, nevi

275

characteristic of nevi.

immature melanocytes in epidermis/dermis/ and junction zone. Not apparent at birth.
molds to ocular surface

276

3 stages of nevi

junctional (basal layer of epiderm), compound, dermal

277

ephelides. what is path

increased melanin but same number of melanocytes

278

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

279

what are solar lentigo

sun exposure related increase in melanocytes

280

what are blue nevi?

intra dermal nevi in children. usually excised

281

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

282

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.