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ChM > Oculoplastics > Flashcards

Oculoplastics Flashcards

1
Q

What etiologies should you consider for preseptal cellulitis?

A

sinus, dacryadenitis, skin, hematogenous

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2
Q

Most common cause of preseptal historically vs now?

A

h. influenza before. Now g+ cocci

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3
Q

choice of therapy for preseptal cellulitis

A

celaphalexin if anterior, augmentin if sinus source, bacterium if worried about MRSA, vans or ceftriaxone if refractory

also do warm compresses, nasal decongestants

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4
Q

hospital acquired MRSA are sensitive to what

A

vanc, linezolid

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5
Q

most common source of infection for orbital cellulitis

A

chronic bacterial sinusitis

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6
Q

signs of orbital cellulitis

A

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

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7
Q

what are the differences in organisms in adult and children with orbital cellulitis

A

adults usually mixed flora including G+C and anaerobes

Children usually one single organism and less likely need surgical intervention

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8
Q

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

A

medial wall

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9
Q

subperiosteal abscess may NOT be need to be drained in what circumstances?

A

isolated media/inferior abscess in children <9 years with isolated ethmoid sinusitis, intact vision, mild proptosis… can keep trying medical therapy

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10
Q

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

A

Clindamycin

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11
Q

signs of orbital TB

A

proptosis, EOM Abnl, bone destruction, draining fistulas

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12
Q

what stains is used for asperillus? whats the path finding

A

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

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13
Q

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

A

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

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14
Q

what are the forms of aspergillosis?

A

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.

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15
Q

what are the three most common parasitic orbital conditions?

A

trichinosis, ecchinococcosis, cysticerocosis (taenia solium)

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16
Q

what are the signs of TED?7

A

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

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17
Q

what is Von Graefe sign?

A

lid lag

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18
Q

most common sign of TED?

A

lid retraction.

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19
Q

is TED only seen in Graves?

A

no, it’s also in Hashimotos, or euthyroid circulating thyroid antibodies (TSHR ab, thyroid binding inhibitory abs, TSH Its, antimicrosomal)

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20
Q

what are the diagnostic criteria for TED?

A

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.

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21
Q

pathophys of TED?

A

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.

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22
Q

how to treat mild TED

A

life style education, AT’s, selenium

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23
Q

How to treat moderate TED

A

mod dose corticosteroids, cyclosporin, taping lids, moisture chambers

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24
Q

How to treat severe TED

A

high dose IV steroids, surgical decompression, radiotherapy

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25
Q

refractory TED treatment?

A

immunomodulators that are not steroids (rituxan)

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26
Q

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

A

elevated T3 and smokers

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27
Q

what are treatment strategies for hyperthyroid disease?

A

methimazole, radioactive iodine, orbital radiation therapy, thyroidectomy

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28
Q

How to treat TED flareups?

A

IV steroids (500 mg to 1g solumedrol; weekly for 6-12 weeks) –must check LFTs before

PO steroid 1 mg/kg prednisone

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29
Q

what is a risk of orbital radiation?

A

worsening (diabetic/ischemic) retinopathy

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30
Q

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

A

Older patients; male patients

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31
Q

whats a choristoma?

A

mature tissue found at abnormal site

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32
Q

what is IgG4 disease?

A

increased systemic IgG4 leading to increase in inflammatory T cells

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33
Q

symptoms of IgG4 disease

A

dacyradenitis, xanthogranulomas, orbital amyloidosis, orbital inflammation

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34
Q

treatment for IgG4 disease

A

steroids

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35
Q

vasculitis is what type of immune response?

A

type III hypersensitivity; circulating antibodies complexes depositing in vessels

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36
Q

mechanism of vision loss in GCA?

A

central artery occlusion OR ischemic optic neuropathy

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37
Q

symptoms of GCA

A

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

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38
Q

what antibody is associated with Wegener’s (GPA)

A

c ANCA ( anti proteinase 3)

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39
Q

triad path findings of GPA (wagerers)

A

vasculitis, granulomatous inflammation, necrosis

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40
Q

what are systemic findings of wegeners. GPA

A

glomerulonephritis, lung involvement, nasal/lacrimal extension

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41
Q

ocular manifestation of polyarteritis nodosa

A

retinal infarction; choroidal infarction.

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42
Q

path finding of polyarteritis nodosa

A

neutrophil and eosinophils in muscularis layer of vessels.

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43
Q

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

A

sarcoid; you can see the lacrimal gland with Gallium scan

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44
Q

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

A

EMO myositis, dacryadenitis, scleritis, orbital apex, diffuse

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45
Q

how is myositis in TED different than NSOI ?

A

TED spares the muscle insertion tendons

tendonitis in NSOI causes the “ring sign”

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46
Q

Features of infantile hemangioma?

A

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

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47
Q

Associations of infantile hemangioma?

A

premature, female, low birthweight, maternal chorionic villus sampling

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48
Q

How can you diagnose infantile hemangioma from other vascular lesions?

A

fine vascular channels and high blood flow on MRI

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49
Q

Where is the location intraorbitally of infantile capillary hemangioma usually? Extra orbitally?

A

Superonasal. can be on neck compromising airway or on organs leading to thrombocytopenia (Kasabach-Merritt Syndrome.

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50
Q

Treatment of infantile hemangioma?

A

observation, refraction/avoid amblyopia.

Can treat with topical timolol, oral propranolol, steroid, surgical excision, pulse dye laser

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51
Q

what is the most common benign intraorbital lesion?

A

cavernous hemangioma

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52
Q

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

A

cavernous hemangioma

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53
Q

Hemangiopericytoma MRI features

A

encapsulated hyper vascular/ hypercellular orbital lesion on MRI.

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54
Q

How are hemangiopericytoma different than cavernous hemangioma?

A

Hemangiopericytomas are blue colored intraoperatively

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55
Q

what is special about hemangiopericytomas on histo?

A

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

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56
Q

proptosis during URIs and/or sudden proptosis…what’s likely dx?

A

lymphangioma/lymphatic malformations

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57
Q

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

A

lymphangioma/ lymphatic malformation –fluid fluid is serum and RBC

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58
Q

lymphangioma/lymphatic malformation treatment?

A

observation vs sclerosis agents.

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59
Q

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

A

orbital venous malformations. CT while doing vaxsalva

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60
Q

treatment for venous malformation? should you biopsy?

A

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

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61
Q

whats the difference between AVMs and AV fistulas?

A

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

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62
Q

what are the two types of AV fistulas?

A

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)

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63
Q

clinical signs of CC fistulas?

A

pulsatile proptosis, pain, tortuous epibulbar vessels, elevated IOP, choroidal effusion, blood at angle, nongranulomatous uveitis, compression of CN VI, IV, or III

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64
Q

how to diagnose AV fistulas?

A

MRA (technically angiography is gold standard)

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65
Q

which of the two types of AV fistulas should be managed more aggressively? why?

A

Dural CC fisutula as it has arterialization of venous system leading to increase risk of intracranial hemorrhage.

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66
Q

CC fistulas treatment option?

A

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

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67
Q

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

A

superior subperiosteal space. observe unless there’s visual compromise

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68
Q

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

A

optic glioma

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69
Q

benign optic gliomas in children are called what?

A

pilocytic astrocytomas

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70
Q

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

A

neurofibromatosis

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71
Q

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

A

glioblastomas. adult males–painful progressive vision loss and proptosis

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72
Q

management of optic nerve gliomas?

A

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.

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73
Q

what are complications of radiation therapy of the orbit?

A

endocrinopathy, intellectual disability, groth retardation, secondary tumors

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74
Q

neurofibromas –what kind of cells are predminant?

A

Schwann cells within optic nerve sheath.

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75
Q

NF1 tumors of the orbit

A

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

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76
Q

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

A

S shaped lateral upper canthus associated NF1

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77
Q

what are the two types of neurofibromas?

A

plexiform and discrete. Discrete can be easily excised. plexiform are Schwann cells proliferating under nerve sheath…leading to difficult excision.

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78
Q

meningiomas –cells of origin? patient population?

A

arachnoid villi; women in third/fourth decade of life

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79
Q

what is a feature of spheroid wing meningiomas

A

hyperostosis of sphenoid bone.

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80
Q

tram tracking on CT head (tumor)

A

meningioma

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81
Q

management of meningiomas?

A

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

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82
Q

What is another name for schwannoma?

A

neurilemma

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83
Q

What are the two biphasic patterns on history of schwanoma?

A

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

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84
Q

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

A

Rhabdomyosarcoma. Supranasal.

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85
Q

management of rhabdomyosarcoma

A

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

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86
Q

rhabdomyosarcoma cells of origin?

A

undifferentiated mesenchymal cells

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87
Q

What are the 4 types of rhabdomyosarcoma? which one has best px?

A

embryonal (most undifferentiated; striations but not always on trichrome stain), alveolar(worst px, pleomorphic (best px; trichrome stain shows striations), and Botryoid

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88
Q

main management of rhabdomyosarcoma?

A

radiation/chemo, exenteration if needed only

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89
Q

fibroblastic and histolytic cells in storiform pattern?

A

fibrous histiocytoma

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90
Q

spindle cells with strong CD34 staining.

A

solitary fibrous tumor

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91
Q

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

A

hyperostotic bone on CT, MRI shows lack of dural enhancement

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92
Q

what syndrome is associated with fibrous dysplasia?

A

Albright syndrome.

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93
Q

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

A

Hx of Rb.

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94
Q

conjunctival MALTomas are associated with what? what’s the chance of systemic disease

A

chronic chalmydia. must follow up as systemic disease will develop in 50% of people in 10 years

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95
Q

What are the two low grade B cell lymphocytic tumors?

A

CLL and follicular center lymphoma

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96
Q

What are the 3 high grade lymphomas of the orbit

A

Burkitt, large cell, lymphoblastic

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97
Q

Clinical and imaging features of lymphoproliferative lesions

A

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

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98
Q

Lymphoproliferative lesions–how should you diagnose it?

A

open biopsy, send it fresh and fixed and plenty of tissue for PCR/immuno, flow cytometry, DNA hybridization.

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99
Q

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

A

conj, orbital, eyelid, lacrimal fossa.

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100
Q

Treatment of lymphoproliferative diseases–what is the treatment of choice for patients with local disease? what should you not give to patients?

A

radiation is therapy of choice. DO NOT give steroids

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101
Q

Langerhan cell histiocytosis–presenting features?

A

lytic lesions, super-temporal orbit/sphenoid wing

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102
Q

Langerhan cell histiocytosis prognosis based on age

A

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

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103
Q

treatment of hanger-on histiocytosis?

A

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

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104
Q

what are the 4 types of xanthogranulomas?

A

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

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105
Q

necrobiotic xanthogranuloma features? Associations?

A

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

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106
Q

Adult onset asthma with periocular xanthogranuloma features?

A

periocular xanthogranuloma, asthma, lymphadenopathy, increased Ig levels

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107
Q

Erdheim Chester disease

A

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

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108
Q

Adult onset xanthogranuloma features?

A

no systemic involvement.

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109
Q

how do epithelial tumors look different from inflammatory/lymphoproliferative tumors of the orbit on imaging?

A

lympho and inflammatory show molding without boney destruction. epithelial are globular and have boney destruction.

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110
Q

approxiamaly what percent of epithelial tumors are benign?

A

50% are benign mixed/pleomorphic andeomas

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111
Q

what are the malignant epithelial tumors?

A

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

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112
Q

management of benign mixed epithelial tumor/ pleomorphic epithelial tumor

A

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

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113
Q

Adenoid cystic carcinoma is also called what?

A

cylindroma

114
Q

what is the most common malignant tumor of the lacrimal gland?

A

adenoid cystic carcinoma. highly malignant and has perineurial invasion and bony destruction–therefore painful… this feature distinguishes from benign epithelial tumors.

115
Q

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

A

adenoid cystic carcinoma

116
Q

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

A

basaloid and cribriform. basaloid is worse

117
Q

what are features of malignant mixed epithelial tumors?

A

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
Q

mucoceles and mucopyoceles. what’s in them? location

A

mucus and pus. superonasal

119
Q

what is silent sinus syndrome?

A

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
Q

where do adenocarcinomas and squamous carcinomas come from usually?

A

maxillary, nasopharynx, oropharynx

121
Q

mets usually spread where in children

A

orbit

122
Q

mets usually spread where in adults?

A

choroid

123
Q

abrupt ecchymosis of periobital area

A

neuroblastoma

124
Q

neuroblastoma associations?

A

sudden periobrital ecchymosis, Horner’s

125
Q

neuroblastoma management?

A

chemo, radiation, look for primary source/mets

126
Q

neuroblastoma px based on age?

A

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

127
Q

which lymphoma is most likely to have mets to orbit?

A

ALL

128
Q

what is granulocytic sarcoma or chroma?

A

orbital mass of myelogenous leukemia

129
Q

when is leukemia in the orbit require emergent radiation?

A

subarachnoid spread causing nerve swelling

130
Q

what mets are most common in adults?

A

breast and lung

131
Q

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

A

EOMs, bone marrow if sphenoid

132
Q

features of breast CA mets to the orbit?

A

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

133
Q

prostate cancer mets are associated with what?

A

lytic lesions resembling acute nonspecific orbital inflammation

134
Q

Le Forte fractures by definition extends through what structure

A

pterygoid plate

135
Q

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

A

horizontally through low transverse maxillary. Guerin fracture

136
Q

Describe Le Forte II fracture

A

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

137
Q

Describe Le Forte III fracture

A

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

138
Q

Describe zygomaticomaxillary complex (ZMC) fx. what else is it called? tx indicated when?

A

tripod fx. involves inferior orbital rim, lat orbital rim, zygomatic arch, lat wall of maxillary sinus. displaced fx needs surgery

139
Q

orbital apex fx associated complications

A

optic nerve damage/TON, CSF leak, CCfistula

140
Q

orbital roof fractures are more common in children…why?

A

frontal sinuses have not developed

141
Q

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

A

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

142
Q

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

A

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

143
Q

Describe type I NOE

A

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

144
Q

Describe Type II NOE

A

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

145
Q

Describe Type III NOE

A

fx of maxillary,nasal, ethmoid (in direct medial orbital wall fx) resulting in comminuted canthal attachment site or if tendon is avulsed

146
Q

Complications of NOE fractures

A

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

147
Q

Indirect medial orbital wall fractures (medial wall blow out fractures). When is it indicated for surgery? which incisional approaches are good?

A

when entrapment is present, (or significant enophthalmos can be associated when there’s orbital floor fx). Incisional approaches include transconjunctival vs trancaruncle)

148
Q

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

A

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

149
Q

PEx signs of orbital floor fracture?

A

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
Q

When there’s no entrapment…when should you repair orbital floor fractures?

A

about 5-10 days s/p incident to allow decrease in swelling. Less than 2 weeks after injury to avoid fibrosis.

151
Q

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

A

PO steroids

152
Q

what are (loose guidelines) to surgical repair of orbital floor fractures when there’s no entrapment?

A

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
Q

what are incisional approaches for orbital floor repair? what are the general steps of surgery?

A

infraciliary approach, transconj approach w or w/o lateral canthotomy/cantholysis.
Steps: lift periorbita, free any adhesions from fracture, place implant.

154
Q

spontaneous orbital hemorrhage are associated with what conditions

A

lymphangioma and orbital varices

155
Q

What are three mechanisms of TON

A

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

156
Q

vision loss s/p trauma with normal appearing globe…what are the two most important exam findings for urgent intervention?

A

tight orbit–>orbital compartment syndrome

APD–>compartment vs TON

157
Q

What are three possible treatments for TON?

A

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
Q

what are the 5 surgical spaces of the orbit

A
  • subperiosteal
  • extraconal
  • intraconal
  • subtenon/episcleral
  • subarachnoid
159
Q

explain the superior transcutaneous incision process to access the superior orbit? what other space can it access/how?

A

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
Q

In superior transconjunctival incision approach to access superior/medial orbit what structure must you avoid…by doing what?

A

avoiding levator muscle by making incision medial to the levator

161
Q

What is the vertical eyelid splitting method of accessing the superior orbit?

A

vertically split lid, levator aponeurosis at medial 1/3 of superior lid. (must line up tarsal plate when closing)

162
Q

What are the 4 methods of accessing the superior orbit?

A

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

163
Q

inferior oblique inserts over what structure

A

macula

164
Q

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

A

infraciliary and inferior lid crease (larger scar)

165
Q

What are the methods of accessing the inferior orbit? 3

A

infraciliary, inferior lid, inferior transconj

166
Q

what is the Lynch incision? to access what space?

A

frontoethmoidal incision –vertically incised medial to medial canthal tendon. 9-10mm medial to medial canthal angle. to access subperiosteal space

167
Q

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

A

medial rectus

168
Q

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

A

superior oblique insertion site

169
Q

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

A

lacrimal system.

170
Q

what are the medial incisions to access the medial orbit?

A

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

171
Q

What is the Stallard-Wright incision? what space is it used for?

A

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
Q

orbital decompression involves doing what?

A

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

173
Q

orbital decompression: traditional approach? vs newer approach?

A

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

174
Q

what is sympathetic ophthalmia?

A

delayed hypersensitivity response to uveal antigens

175
Q

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

A

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

176
Q

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

A

retrobulbar ethanol injection

177
Q

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

A
  1. sufficient volume.
  2. lined with conj with adequate fornices
  3. lids with normal appearnce
  4. good motility
  5. comfortable and cosmetically pleasing
178
Q

what are advantages of eviseration?5

A
  1. simpler procedure
  2. preserved anatomy
  3. better motility
  4. treatment for endophthalmitis
  5. lower risk of migration/extrusion implant
179
Q

disadvantages of evisceration? 3

A

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

180
Q

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

A

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

181
Q

what are advantages and disadvantages of inert orbital implants

A

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

182
Q

porous bio integrated orbital implants allow for pegs to be placed. when should they be placed?

A

6-12 months after enucleation.

Pegs give better motility but associated with more inflammation post op

183
Q

What space does the orbital implant go after evisceration vs enucleation?

A

after evisceration it goes within or behind sclera. vs after enucleation it goes behind or within subtenons

184
Q

when is the prosthesis usually fitted after enucleation/evisceration?

A

4-8 weeks. removed once a month for cleaning

185
Q

what is a deep sulcus deformity? tx by ?

A

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
Q

giant fornix syndrome? what is it. complications. treatment

A

occurs when superior conj fornix is too deep. leads to retention of mucus and debris leading to infections.
Treat by superior conj resection

187
Q

what are two things you can do to prevent contracture of fornices?

A

placing EOMs where they should be and wearing conformers (do not remove for more than 24 hrs)

188
Q

Contracted socket is caused by what? 6

A 
radiation
severe alkali injury
poor surgical technique
multiple operations
removal of conformer
extrusion of implant
189
Q

what is contracted socket by definition?

A

when fornices are too small to hold prosthesis

190
Q

contracted socket can be expanded using what?

A

full thickness mucus membrane graft, amniotic membrane. (buccal graft with silicon sheet x2 weeks may be used if mild inferior socket contracture)

191
Q

when should you consider exenteration?

A
  1. destructive tumor
  2. intraocular tumors with extra ocular spread
  3. malignant epithelial lacrimal gland tumors
  4. sarcomas not responsive to therapy
  5. fungal infections
192
Q

what are the 3 types of exenteration?

A

subtotal, total, extended

193
Q

What is the SMAS

A

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

194
Q

What consists of SMAS

A

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

195
Q

what are the two major components of facial support?

A 
Osteocutaneous ligaments (orbitomalar, zygomatic, mandibular)
Fascial cutaneous ligaments *condensation of superficial and deep facia--paritodcutaneous and masseteric)
196
Q

what are the mimetic muscles of the lower face?

A

Superficial (neurovascularly suppllied posteriorly): platysma, zygomaticus major/minor, risorius
Deep (neurovascularly supplied anteriorly): buccinator, mentalist, elevator angle oris

197
Q

what are the mimetic muscles of the upper face?

A

frontalis, corrugator supercilii, procesrus muscles, orbicularis oculi,

198
Q

deep cervical fascia overlies what structure?

A

myohyaloid muscle and over the body of the mandible

199
Q

What facial plane is the temporal artery located? what other structure is here?

A

superficial to parotidomasseteric fascia (continuous to deep temporal fascia). temporal branch of facial nerve (CN VII) is here

200
Q

what are the 5 branches of the facial nerve?

A

Temporal, zygomatic, buccal, marginal manipular, cervical

201
Q

at what plane should you dissect when in the upper face to avoid the nerves? what about the lower face?

A

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
Q

What are the subdivisions of CNV1? 5

A

Supraorbital, supratrochlear, infratrochlear, external nasal, lacrimal

203
Q

What are the subdivisions of CNV2?

A

zygomaticotemporal, zygomaticofacial, infraorbital

204
Q

what are the subdivisions of CNV3?

A

auriculotemporal, buccal, mental

205
Q

7 structural layers of the eye lids

A

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

206
Q

the upper lid crease approximates what structure?

A

attachments of elevator panoenurosis to pretrial orbiculares bundles/skin.

207
Q

what makes lid crease differences in asian and caucasians?

A

caucasian levato aponeurosis inserts in to pretarsar orbicularis/ above tarsus
asians levator aponeursis inserts between top of tarsus and lid margin.

208
Q

what is the main protractor muscle?

A

orbicularis oculi

209
Q

what are the 3 parts of orbicularis oculi muscle?

A

pretrial, preseptal– for blinking

orbital- forced lid closure

210
Q

what is Horner muscle?

A

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

211
Q

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

A

from medial canthal tendon and inserts to lateral canthal raphae

212
Q

origin of orbital portions of orbicularis muscle?

A

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

213
Q

what creates the gray line. what does it do?

A

striate muscles called “muscle of riolan”–helps with blinking, meibomeian discharge, and position of lashes

214
Q

where does orbital fat lie?

A

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

215
Q

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

A

superior 2: nasal and central;

lower 3: nasal, central, temporal.

216
Q

why is central fat pad of the orbit important?

A

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

217
Q

what are the main retractors of the upper lid? lower lids?

A

levator superiororis, and muller muscle (superior tarsal muscle). Capsulopalpebral fascia and inferior tarsal muscle

218
Q

where does the levator originate? where does it insert?

A

apex of the orbit at the lesser wing of the sphenoid. inserts medially to lacrimal crest and laterally to lateral orbital tubercle

219
Q

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

A

muscle is 40 mm long. aponeurosis is 20 mm

220
Q

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

A

Whitnall ligament; Lockwood ligament

221
Q

what are the 7 layers of the eye lid?

A

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

222
Q

where in does the muller muscle originate? where does it lie? where does it insert?

A

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

223
Q

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

A

2mm. Horner’s syndrome

224
Q

between what two structures does the peripheral arcade run?

A

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

225
Q

what is the lower lid equivalent structure to levator superiors

A

capsulopalpebral fascia originating form inferior rectus. it fuses with inferior oblique and becomes Lockwood ligament

226
Q

what is the lower lid equivalent of muller muscle?

A

inferior tarsal muscle

227
Q

height of upper tarsal plate?

A

10-12 mm

228
Q

height of lower tarsal plate?

A

4mm

229
Q

how thick is tarsus

A

1mm

230
Q

what are the glands of Wolfring and glands of Krause?

A

Accessory lacrimal glands in subconj palpebral tissue. Wolfring is along non marginal tarsus and Krause is in fornices.

231
Q

origin of medial canthal tendon. describe it’s features

A

originates from ant and posterior lacrimal crest. anterior is strong and posterior is for positioning of lid allowing puncture to lie in tear lake

232
Q

what structure does the muscle of riolan overly?

A

it is pre tarsal portion of the orbicularis muscle

233
Q

size of horizontal palpebral fissure?

A

30 mm

234
Q

avg upper eye lash number? avg lower?

A

avg upper is 100. Lower is 50

235
Q

avg number of meibomian glands of upper lid? lower?

A

upper 25, lower 20.

236
Q

what are the two blood supplies of lids?

A

internal carotid–>ophthalmic–>supraorbital/lacrima

external carotid–>angular/temporal

237
Q

where does the marginal arcade locate?

A

2mm above margin anterior to the tarsus

238
Q

what are the two venous systems of the eye lids?

A

preseptal and postseptal venous systems.

239
Q

blepharophimosis ptosis epicanthus inversus syndrome (BPES) what gene is involved. What are the two types?

A

FOXL2 gene.
type I involves ovarian loss in women
type II involves hypoplastic nose bridge/superior orbit/ear deformity

240
Q

congenital ectropion. What’s the anatomical defect?

A

vertical insufficiency of anterior lamella
treat with horizontal tightening of lateral canthal tendon. and vertical lengthening of anterior lamella with skin graft.

241
Q

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

A

caused by conjunctivitis, inflammation, Downsyndrome.

treat with lubrication/patching or temporary tarshorrhaphy

242
Q

what is euryblepharon? tx?

A

vertical shortening and horizontal lengthening of lids.

tx with lateral tarsal strip/ lid margin resection

243
Q

what are the 4 types of epicanthus?

A
  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.
244
Q

epicanthus inverses is associated with what condition?

A

BPES (blepharophimosis, ptosis, epicanthus inversus syndrome.)

245
Q

what is epiblepharon?

A

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

246
Q

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

A

tarsal kink, absent lid retractors, absent tarsus

247
Q

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

A

electrolysis, cryoepilation, lid splitting to remove follicles.

248
Q

lid coloboma usually occurs upper or lower?

A

upper. If lower then think Goldenhar

249
Q

cryptophthalmos… what’s the mechanism? and what condition is the eye usually

A

fused anterior lid adnexa.

usually poor visual potential of eye due to severe defects

250
Q

chalazion…commonly associated conditions

A

blepharitis and rosacea and sebaceous gland ca

251
Q

options of chalazion treatment?

A 
WC/LH
topical abx/steroids
oral doxy
steroid injection --hypopigmented skin is risk
excision
252
Q

chalazion vs hordeolum?

A

chalazion is an internal posterior hordeolum (aka meibom)

hordeolum is acute infection of zeis OR meibom

253
Q

classic sx of floppy lid syndrome. finding

A

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

254
Q

floppy lid associations

A

obesity, OSA, DM, face sleepers, keratoeonus

255
Q

what is eyelid imbrication syndrome

A

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

256
Q

what type of lid lesion is associated with perineurial invasion

A

squamous cell CA

257
Q

how should you biopsy benign epithelial lesions

A

shave excision

258
Q

what is skin tag called

A

acrochordon

259
Q

what is pseudoepitheliomatous hyperplasia?

A

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

260
Q

epidermal inclusion cyst involves what structure. treatment?

A

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

261
Q

what are milia? tx

A

tiny epidermal inclusion cysts… treat with topical retinoid acid

262
Q

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

A

large epidermal inclusion cysts–usually in scalp or eye brows

263
Q

molluscum in adult…you think

A

AIDS

264
Q

molluscum treatment?

A

observation, cimetidine, excision, cry, curetage

265
Q

xanthelasma treatment

A

excision, laser ablation, topical trichloroacetic acid

266
Q

what are adnexa?

A

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

267
Q

many sebaceous gland hyperplasia is associated with what?

A

visceral malignancy. Muir-Torre syndrome

268
Q

what are the two types of hidrocystoma? where do they locate? what is the difference

A

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
Q

syringoma. what are they. what population

A

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

270
Q

trichoepithelioma. path feature

A

basasoid island and keratin cysts with immature hair follicles

271
Q

trichofolliculoma path feature

A

single umbilicate lesion.

squamous cyst with keratin and hair shaft

272
Q

trichilemmoma. path feature

A

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

273
Q

pilomatricoma

A

subQ mass attached to overlying skin.

Island of epithelial cells surrounded by basophilic cells with shadow cells

274
Q

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

A

papilloma, epidermal inclusion cysts, nevi

275
Q

characteristic of nevi.

A

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

276
Q

3 stages of nevi

A

junctional (basal layer of epiderm), compound, dermal

277
Q

ephelides. what is path

A

increased melanin but same number of melanocytes

278
Q

What are lentigo simplex. what is a condition it’s associated with

A

larger ephelides but increased number of melanocytes. NOT related sun exposure. Peutz-Jagher

279
Q

what are solar lentigo

A

sun exposure related increase in melanocytes

280
Q

what are blue nevi?

A

intra dermal nevi in children. usually excised

281
Q

nevus of Ota is what? what do you need to look out for in these patients?

A

blue dermal Nevis in V1 and V2 distribution. Need to monitor for glaucoma… and rarely uveal melanoma

282
Q

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

A

25% regression in 1 year.
0.25% malignant transformation of single lesion
15% of chance for squamous overall in pts with multiple lesions.

ChM (59 decks)

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