Eyelids Flashcards

1
Q

What layers do the epidermis consist of?

A

Keratin Layer: Stratum corneum (horny layer) consists of flat cells devoid of nuclei

Granular cell layer (stratum granulosum) typically consists of 1-2 layers of flattened cells containing keratohyaline granules.

Prickle cell layer (stratum spinosum) is approximately
five cells deep. The cells are polygonal in cross-section and have abundant eosinophilic cytoplasm. Free borders have desmosomes

Basal cell layer (stratum basale) comprises a single row of columnar-shaped proliferating cells containing melanin derived from adjacent melanocytes.

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2
Q

Where are sebacious glands found?

A

located in the caruncle and within eyebrow hairs. Tiny sebaceous glands are associated with the
thin (vellus) hairs covering periocular skin.

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3
Q

Where are Meibomian glands found?

A

modified sebaceous glands found in the tarsal plates. They empty through a single row of 20–30 orifices on each lid.

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4
Q

Where are Glands of Zeis found?

A

modified sebaceous glands associated with lash follicles.

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5
Q

Where are Glands of Moll found?

A

modified apocrine sweat glands opening either into a lash follicle or directly onto the anterior lid margin between lashes. They are more numerous in the lower
lid.

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6
Q

Where are eccrine sweat glands found?

A

distributed throughout eyelid skin and are not confined to the lid margin, in contrast to glands of Moll.

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7
Q

What are pilosebacious units composed of?

A

comprise hair follicles and their sebaceous glands

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8
Q

What is an incisional biopsy

A

involves removal of a portion of a lesion for histopathology.

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9
Q

What is an excisional biopsy?

A

performed on small tumours and fulfils both diagnostic and treatment objectives.

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10
Q

What is Marsupialization?

A

involves the removal of the top of a cyst allowing drainage of its contents and subsequent epithelialization.

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11
Q

What is a chalazion?

A

a sterile chronic granulomatous inflammatory
lesion (lipogranuloma) of the meibomian, or sometimes Zeis, glands caused by retained sebaceous secretions.

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12
Q

What does chalazion histopathology show?

A

shows a lipogranulomatous chronic inflammatory picture with extracellular fat deposits surrounded by lipid-laden epithelioid cells, multinucleated giant cells and lymphocytes

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13
Q

Which drug predisposes the formation of chalazia within 3 months of initiation of treatment.

A

Bortezomib, a proteasome inhibitor used in the treatment of multiple myeloma,

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14
Q

How to manage Chalazia?

A

Oral antibiotics- for significant bacterial infection

Conservative- 1/3rd resolve spontaneously
Hot compress
Expression (between 2 sterile cotton buds)
Steroid injections shown to be equivocal resolution rates to I&C

If surgical approach with curretage, topical antibiotic 3x/day for 5 days should be used.

Marginal lesions managed by steroid injection or curretage of deeper chalazion, by I&C via horizontal incision on conj surface or through grey line

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15
Q

What is cyst of Zeis?

A

a small, non-translucent cyst on the anterior lid
margin arising from obstructed sebaceous glands associated with the eyelash follicle

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15
Q

What is cyst of Moll?

A

(apocrine hidrocystoma) is a small retention
cyst of the lid margin apocrine glands. It appears as a round, non-tender, translucent fluid-filled lesion on the anterior lid margin

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15
Q

What are comedones?

A

plugs of keratin and sebum within the dilated
orifice of hair follicles that often occur in patients with acne vulgaris. They may be either open (blackheads), containing a darkened plug of oxidized material or closed (whiteheads).

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16
Q

What are milia?

A

caused by occlusion of pilosebaceous units resulting
in retention of keratin. They are tiny, white, round, superficial papules that tend to occur in crops

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17
Q

What is an epidermoid cyst?

A

uncommon and usually developmental,
occurring along embryonic lines of closure. It is similar in
appearance to an epidermal inclusion cyst.

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18
Q

What is a dermoid cyst?

A

usually subcutaneous or deeper and is typically attached to the periosteum at the lateral end of the brow. It is caused by skin sequestered during embryonic development.

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19
Q

What is Xanthelasma?

A

yellowish subcutaneous plaques, usually in the
medial aspects of the eyelids, commonly bilateral and
are multiple

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20
Q

Chalazion vs Xanthelasma histology?

A

fat in xanthelasmata is mainly intracellular, with lipid-laden histiocytes (foam cells) in the dermis

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21
Q

Treatment for Xanthelasma?

A

principally for cosmesis. Recurrence occurs in up to 50% and is most common in patients with hypercholesterolaemia.

*Simple excision is commonly performed where adequate
excess skin is present.

*Microdissection. Larger lesions can be raised in a flap, the fatty deposits dissected from overlying skin under a surgical
microscope using micro scissors and the skin replaced.

*Good results can be obtained using chemical
peeling with bi- or trichloroacetic acid. Laser ablation and cryotherapy have advantages but may be more prone to scarring, including pigmentary changes.

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22
Q

What does histology show in squamous cell papilloma?

A

finger-like projections of fibrovascular connective tissue covered by irregular acanthotic and hyperkeratotic squamous epithelium

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23
Q

What are some treatments for squamous cell papilloma?

A

Treatment usually involves simple excision, but other
options include cryotherapy and laser or chemical ablation.

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24
Q

What does histology show in seborrhoeic keratosis?

A

Expansion of the squamous epithelium of the epidermis by proliferating basal cells, sometimes with keratin-filled horns or cystic inclusions

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25
Q

What are some treatments for Seborrhoeic keratosis?

A

Treatment involves shave biopsy (occasionally simple excision), electrodesiccation with curettage, laser ablation, cryotherapy with
liquid nitrogen and chemical peeling.

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26
Q

What does histology show in Actinic Keratosis?

A

irregular dysplastic epidermis with hyper-
keratosis, parakeratosis and cutaneous horn formation

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27
Q

What are some treatments for actinic keratosis?

A

Treatment involves biopsy followed by excision or cryotherapy.

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28
Q

What is a freckle?

A

(ephelis, plural ephelides) is a small (generally 1–5 mm)
brown macule due to increased melanin in the epidermal basal
layer, typically in sun-exposed skin

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29
Q

What does histopathology of a freckle show?

A

hyperpigmentation
of the basal layer of the epidermis, with a normal melanocyte population.

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30
Q

What is a congenital melanocytic naevus?

A

Congenital naevi are uncommon and histologically resemble their acquired counterparts

Rare variants include a ‘kissing’ or split naevus
that involves the upper and lower eyelid and may occasionally contain numerous hairs

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31
Q

What is a junctional naevus?

A

occurs in young individuals as a uniformly brown macule or plaque

The naevus cells are
located at the junction of the epidermis and dermis and have a low potential for malignant transformation

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32
Q

What is a compound naevus?

A

occurs in middle age as a raised papular lesion. The shade of pigment varies from light tan to dark brown but tends to be relatively uniform throughout

The naevus cells extend from the epidermis into the
dermis. It has a low malignant potential related to the junctional component.

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33
Q

What is an intradermal naevus?

A

most common, typically occurs in older patients. It is a papillomatous lesion, with little or no pigmentation.

Histologically, naevus cells are confined to the dermis and have no malignant potential

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34
Q

What is the margin for clearance of a suspicious pigmented lesion?

A

Excision should be
complete in most cases, with at least a 3 mm margin if melanoma is suspected.

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35
Q

What is a syringoma?

A

benign proliferations arising from eccrine sweat
glands. They are characterized by small papules that are often
multiple and bilateral

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36
Q

What is a pilomatricoma?

A

derived from the germinal matrix cells of the hair bulb affecting children and young adults and is more common
in females. Clinically it appears as amobile purplish dermal nodule that may have a hard consistency due to calcification

Malignant change is rare. The lesion is usually removed surgically.

Histopathology shows irregular epithelial islands
exhibiting viable basophilic cells at the periphery and degenerate ‘shadow’ cells centrally

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37
Q

What is a capillary haemangioma?

A

(strawberry naevus) is one of the most common tumours of infancy. It is three times as common in girls as boys

It presents shortly after birth as a unilateral, raised bright
red lesion usually in the upper lid. A deeper lesion appears purplish

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38
Q

What are some characteristics of a capillary haemangioma?

A

The lesion blanches on pressure and may swell on crying. Ptosis is frequent and there may be orbital extension

Occasionally the lesion may involve the skin of the face and some patients have strawberry naevi on other parts of the body.

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39
Q

How can capillary haemangioma be treated?

A

regular application of a topical beta-blocker to the
affected lesion.

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40
Q

What does histopathology of a capillary haemangioma show?

A

vascular channels of varying size within the dermis and
subcutaneous tissue

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41
Q

What is a port wine stain?

A

(naevus flammeus) is a congenital malformation of
vessels within the superficial dermis, consisting histopathologically of vascular spaces of varying calibre separated by thin fibrous septa

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42
Q

What percentage of children with port wine stain have associated ocular or CNS involvement?

A

About 10% including Sturge–Weber

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43
Q

What are some macroscopic features of a port wine stain?

A

manifests clinically as a sharply demarcated soft
pink patch that does not blanch with pressure, most frequently
located on the face.

It is usually unilateral and tends to be aligned with the skin area supplied by one or more divisions of the trigeminal nerve

Darkening to red or purple
takes place with age and there is commonly associated soft tissue hypertrophy

Bleeding may occur from focal overlying lobulations

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44
Q

How can port wine stains be treated?

A

Treatment with laser (e.g. pulsed-dye) is effective in decreasing skin discoloration, particularly if undertaken early. Topical preparations such as imiquimod and rapamycin, alone or with adjuvant laser, show promise.

Soft tissue debulking is used in a small number of cases. Screening for glaucoma should begin in infancy.

Systemic investigation is considered in some patients,
particularly those with a lesion of the lumbar area.

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45
Q

What is Sturge Weber syndrome?

A

(encephalotrigeminal angiomatosis) is a
congenital, sporadic phacomatosis.

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46
Q

What are some features of Sturge Weber syndrome?

A
  • Port-wine stain, extending over the area corresponding to the distribution of one or more branches of the trigeminal nerve.
  • Leptomeningeal haemangioma involving the ipsilateral parietal or occipital region may cause contralateral focal or generalized seizures,
    hemiparesis or hemianopia.
  • Ocular features may include ipsilateral glaucoma, episcleral
    haemangioma, iris heterochromia and diffuse choroidal haemangioma
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47
Q

What is a pyogenic granuloma?

A

a rapidly growing vascularized proliferation of granulation tissue that is usually antedated by surgery, trauma or infection, although some cases are idiopathic

Clinically there is a painful, rapidly growing, vascular granulating polypoidal
lesion that may bleed following relatively trivial trauma.
Cutaneous lesions should be excised

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48
Q

What is a Neurofibroma?

A

benign nerve tumours, usually
nodular or pedunculated, that can be found anywhere on the
skin

if multiple lesions are present, neurofibromatosis should be excluded

Plexiform neurofibromas typically present in childhood as a manifestation of neurofibromatosis
type 1 with a characteristic S-shaped deformity of the upper
eyelid

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49
Q

How can Neurofibromas be treated?

A

Treatment of solitary lesions involves simple excision, but removal of the more diffuse plexiform lesions may be
difficult.

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50
Q

Which systemic conditions may result in people developing eyelid malignancies

A

Xeroderma Pigmentosum
Gorlin- Goltz Syndrome
Muir- Torre syndrome
Bazex Syndrome

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51
Q

What is Xeroderma Pigmentosum?

A

characterized by skin damage
on exposure to sunlight, leading to progressive cutaneous
abnormalities.

More than 90% have ocular or
periocular involvement and 65% experience photophobia

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52
Q

What is the inheritance pattern for xeroderma pigmentosum?

A

AR

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53
Q

What are the facial features of Xeroderma Pigmentosum?

A

a bird-like facial appearance and a significant propensity to the development of basal cell carcinoma (BCC), squamous cell carcinoma (SCC) and melanoma

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54
Q

What is the inheritance pattern for Gorlin Goltz syndrome

A

AD

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55
Q

What are some features of Gorlin Goltz syndrome?

A

extensive congenital deformities of the eye, face, bone and central
nervous system. Many patients develop multiple small BCC
during the second decade of life

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56
Q

What tumours are Gorlin Goltz syndrome associated with?

A

Medulloblastoma,
Breast carcinoma
Hodgkin lymphoma.

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57
Q

What is the inheritance pattern for Muir-Torre syndrome?

A

AD

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58
Q

What are the tumours associated with Muir Torre syndrome?

A

Cutaneous tumours include BCC, sebaceous gland carcinoma and keratoacanthoma. Colorectal and genitourinary carcinomas are
the most common systemic tumours.

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59
Q

What are the 2 distinct conditions associated with Bazex syndrome?

A

1) Bazex–Dupré–Christol syndrome
2) Acrokeratosis paraneoplastica of Bazex

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60
Q

What is the most common human malignancy affecting older individuals?

A

BCC

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61
Q

What percentage of BCC’s occur in the head and neck vs the eyelid

A

90% head and neck
10% eyelid

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62
Q

Where do BCC’s tend to occur?

A

Lower eyelid followed in relative frequency by medial canthus, upper lid and lateral canthus

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63
Q

Where are BCC’s the riskiest and pose threats to invasion?

A

Medial canthus- prone to invading orbits and sinuses

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64
Q

What does BCC histopathology show?

A

The tumour arises from the cells that form the basal layer of the
epidermis. The cells proliferate downward and characteristically exhibit palisading at the periphery of a tumour lobule of cells

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65
Q

What are clinical features of Nodular BCC

A

a shiny, firm, pearly nodule with small overlying dilated blood vessels. Initially, growth is slow and it
may take the tumour 1–2 years to reach a diameter of 0.5 cm

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66
Q

What are clinical features of Nodulo-ulcerative BCC (Rodent Ulcer)?

A

is centrally ulcerated with pearly raised rolled edges and dilated and irregular blood vessels (telangiectasis) over its lateral margins

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67
Q

What are clinical features of Sclerosing (Morphoeic) BCC?

A

less common and may be
difficult to diagnose because it infiltrates laterally beneath
the epidermis as an indurated plaque

The margins of the tumour may be impossible to delineate
clinically and the lesion tends to be much more extensive on palpation than inspection.

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68
Q

What other condition can Sclerosing BCC mimic?

A

a localized area of unilateral
chronic blepharitis.

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69
Q

Which is commoner? SCC or BCC?

A

BCC

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70
Q

Where do SCC commonly metastasise to?

A

regional lymph nodes in about 20%
of cases.

The tumour may also exhibit perineural spread to the intracranial cavity via the orbit.

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71
Q

Who is SCC commonly seen in?

A

Immunocompromised individuals,
such as those with acquired immunodeficiency syndrome (AIDS)
or following renal transplantation are at increased risk, as are those
with a predisposing syndrome such as xeroderma pigmentosum.

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72
Q

Where do SCC’s tend to occur?

A

Lower eyelid and lid margin

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73
Q

What does histopathology of an SCC show?

A

The tumour arises from the squamous cell layer of the epidermis.
It is composed of variably sized groups of atypical epithelial cells with prominent nuclei and abundant eosinophilic cytoplasm within the dermis. Well-differentiated tumours may show characteristic keratin ‘pearls’ and intercellular bridges
(desmosomes)

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74
Q

What are clinical features of Nodular SCC

A

a hyperkeratotic nodule that
may develop crusting, erosions and fissures

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75
Q

What are clinical features of Ulcerating SCC?

A

a red base and sharply defined, indurated and everted borders, but pearly margins and telangiectasia are
not usually present

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76
Q

What are clinical features of cutaneous horn?

A

May have underlying invasive SCC

Ostensibly benign lesions such as keratoacanthoma and
cutaneous horn may reveal histological evidence of SCC in
deeper levels of sectioning.

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77
Q

What is a keratoacanthoma?

A

rare, rapidly growing but subsequently regressing tumour that usually occurs in fair-skinned individuals with a history of chronic sun exposure.

A pink dome-shaped hyperkeratotic lesion develops, often on
the lower lid and may double or treble in size within weeks.

Growth then ceases for 2–3 months, after which spontaneous involution occurs, when a keratin-filled crater may develop.

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78
Q

How to treat keratoacanthoma?

A

complete surgical excision with a margin of at least 3 mm or utilizing Mohs surgery. Radiotherapy, cryotherapy or local chemotherapy are sometimes used.

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79
Q

What are histological features of Keratoacanthoma?

A

irregular thickened
epidermis surrounded by acanthotic squamous epithelium. A
sharp transition from the thickened involved area to normal adjacent epidermis is referred to as shoulder formation and a keratin-filled crater may be seen.

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80
Q

What is a sebacious gland carcinoma?

A

rare, slowly growing
tumour that most frequently affects the elderly, with a predisposition for females

It usually arises from the meibomian glands, although on occasion it may arise from the glands of Zeis or
elsewhere.

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81
Q

What does histopathology of sebacious gland carcinoma show?

A

lobules of cells with pale
foamy vacuolated lipid-containing cytoplasm and large hyper-
chromatic nuclei

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82
Q

What is pagetoid spread of a tumour?

A

Pagetoid spread refers to extension
of a tumour within the epithelium and is not uncommon

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83
Q

What are some adverse prognostic factors of sebacious gland carcinoma?

A

Upper lid involvement, tumour size of 10 mm or more and duration of
symptoms of more than 6 months.

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84
Q

Where does Sebacious gland carcioma tend to occur compared to BCC/SCC?

A

Upper lid.

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85
Q

What does yellow material within a SGC suggest?

A

Yellowish material within the tumour is highly suggestive of SGC.

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86
Q

What SGC can be mistaken for a chalazion?

A

Nodular SGC

presents as a discrete, hard nodule, most commonly within the upper tarsal plate and may exhibit yellow discoloration due to the presence of lipid; it can be mistaken for a chalazion

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87
Q

What SGC can be mistaken for blepharitis?

A

Spreading SGC

infiltrates into the dermis and causes a diffuse thickening of the lid margin often with eyelash distortion and loss and can be mistaken for blepharitis.

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88
Q

Does melanoma develop on the lids?

A

Melanoma rarely develops on the eyelids but is potentially lethal.

Although pigmentation is a hallmark of skin melanomas, half of lid melanomas are non-pigmented and this may give rise to diagnostic difficulty.

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89
Q

What features are suggestive of melanoma?

A

recent onset of a pigmented lesion, change in an existing pigmented lesion, irregular margins, asymmetrical shape, colour change or
presence of multiple colours and diameter greater than 6 mm.

90
Q

What is lentigo maligna?

A

(melanoma in situ, intraepidermal melanoma,
Hutchinson freckle) is an uncommon condition that develops in sun-damaged skin in elderly individuals.

91
Q

What does histopathology of lentigo maligna show?

A

intraepidermal proliferation of spindle-shaped atypical melanocytes replacing the basal layer of the epidermis

92
Q

What are some clinical features of lentigo maligna?

A

presents as a slowly expanding pigmented macule with an irregular border

Treatment
is usually by excision.

93
Q

What features of lentigo maligna suggest malignant transformation?

A

Nodular thickening and areas of irregular
pigmentation are highly suggestive of malignant transformation

94
Q

What is the treatment of Melanoma?

A

Treatment is
usually by wide excision and may include local lymph node removal.

Radiotherapy and chemotherapy are of
limited efficacy, but new approaches using immunotherapy are
showing considerable promise.

95
Q

What is Merkel cell carcinoma?

A

Merkel cells are a form of sensory receptor concerned with light touch. Merkel cell carcinoma is a rapidly growing, highly malignant
tumour that typically affects older adults.

96
Q

Which lid does Merkel cell carcinoma typically affect?

A

Upper lid

97
Q

What is Kaposi sarcoma?

A

a vascular tumour that typically affects individuals with AIDS.

98
Q

What does histopathology of Kaposi Sarcoma show?

A

Histopathology shows proliferating spindle cells, vascular channels and inflammatory cells within the dermis

99
Q

What are some treatments for Kaposi Sarcoma?

A

Treatment is by radiotherapy or excision and by optimal control of AIDS.

100
Q

Treatments for malignant tumours?

A

1) Incisional Biopsy
2) Excisional Biopsy
3) Surgical excision
4) Laissex- Faire
5) Radiotherapy
6) Cryotherapy

101
Q

When is excisional biopsy used?

A

may consist of shave excision using a blade to remove shallow epithelial tumours, such as a papilloma and seborrhoeic keratosis, or full-
thickness skin excision for tumours that are not confined to the epidermis.

102
Q

When is surgical excision of tumours used?

A

aims to remove the entire tumour with preservation of as much normal tissue as possible. Smaller tumours can be removed via an excision biopsy and the defect closed directly

103
Q

What excision margin is preferred for BCC’s

A

2–4 mm margin of clinically normal tissue.

104
Q

When is conventional paraffin embedded specimen used?

A

Rapid processing can reduce the interval to confirmation of histological
clearance but still requires that reconstruction be performed as a separate procedure

105
Q

When is a standard frozen section used?

A

involves histological examination
of the margins of the excised specimen at the time of surgery
to ensure that they are tumour-free. If no tumour cells are
detected, the eyelid is reconstructed on the same day.

106
Q

When is mohs micrographic surgery used?

A

involves layered excision of the
tumour; specimens are usually examined frozen. Processing of each layer enables a map of the edges of the tumour to be developed. Further tissue is taken in any area where tumour is still present until clearance is achieved.

Good for diffusely growing tumours such as sclerosing BCC, SCC, recurrent tumours and those involving medial or lateral canthi.

107
Q

What techniques of eyelid reconstruction are used for small defects?

A

Small defects involving less than one-third of the eyelid can usually be closed directly, provided the surrounding tissue
is sufficiently elastic to allow approximation of the cut edges

108
Q

What techniques of eyelid reconstruction are used for moderate size defects?

A

involving up to half of the eyelid may require a flap (e.g. Tenzel semi-circular) for closure

109
Q

What techniques of eyelid reconstruction are used for large size defects?

A

involving over half of the eyelid may be closed by one of the following techniques:
1) Posterior lamellar reconstruction (Hughes flap from the upper lid)
2) Anterior lamellar reconstruction

110
Q

What is the Laissez- faire approach for eyelid reconstruction?

A

wound edges are approximated as far as possible and the defect is allowed
to granulate and heal by secondary intention. Even large defects can often achieve a satisfactory outcome with time.

111
Q

What are the indications for radiotherapy in Eyelid tumours?

A

○ Patients who are either unsuitable for, or refuse, surgery.

○ Highly radiosensitive tumours, such as Kaposi sarcoma.

○ Adjunctive therapy in some cases.

○ Palliative treatment.

112
Q

Complications of radiotherapy for treatment of eyelid tumours?

A

○Skin damage and madarosis (eyelash loss).

○Nasolacrimal duct stenosis following irradiation to the
medial canthal area.

○Conjunctival keratinization, dry eye, keratopathy and
cataract.

○Retinopathy and optic neuropathy.

113
Q

When is cryotherapy used for eyelid tumours?

A

may be considered for a small superficial BCC and can be a useful adjunct to surgery in some patients. Complications include skin depigmentation, madarosis and conjunctival
overgrowth.

114
Q

What is the normal anatomical appearance of the lid margin from anterior to posterior?

A

*Eyelashes (cilia).
*The grey line, by definition the border between the anterior
(lashes, skin and orbicularis) and posterior (tarsal plate and
conjunctiva) lamellae.
*The meibomian gland orifices are located just anterior to
the mucocutaneous junction. The edge of the tarsal plate is
deep to the gland orifices; the glands themselves run vertically
within the plate.
*The mucocutaneous junction is where keratinized epithelium
of the skin merges with conjunctival mucous membrane.
*Conjunctiva lines the posterior margin of the lid.

115
Q

What is trichiasis?

A

refers to misdirection of growth from individual follicles rather than a more extensive inversion of the lid or lid margin.

116
Q

What are some causes of trichiasis?

A

commonly due to inflammation such as chronic blepharitis or herpes zoster ophthalmicus, but can
also be caused by an injury or by surgery, such as incision and
curettage of a chalazion

117
Q

What is marginal entropion?

A

common cause of eyelash misdirection, secondary to subtle
cicatricial posterior lamellar shortening that rotates a segment
of the lid margin towards the eye.

The mucocutaneous junction migrates anteriorly and the posterior lid margin becomes rounded rather than physiologically square.

118
Q

What is congenital distichiasis?

A

rare condition that occurs when
a primary epithelial germ cell destined to differentiate into
a meibomian gland develops instead into a complete pilosebaceous unit.

The majority of patients also manifest primary lymphoedema of
the legs (lymphoedema–distichiasis syndrome). A partial or complete second row of lashes is seen to emerge at or slightly behind the meibomian gland orifices.

119
Q

What is acquired distichiasis?

A

caused by metaplasia of the meibo-
mian glands into hair follicles such that a variable number of lashes grow from meibomian gland openings.

The most important cause is intense conjunctival inflammation (e.g.
chemical injury, Stevens–Johnson syndrome, ocular cicatricial
pemphigoid

120
Q

Treatments for trichiasis?

A

1) Epilation with forceps
2) Electrolysis
3) Laser ablation
4) Surgery
5) Cryotherapy

121
Q

What are some surgical treatments for trichiasis?

A

Tarsal fracture (for marginal entropion)

A full thickness eyelid pentagon resection for a focal group of aberrant lashes after trauma/localised marginal entropion

Other options are lid splitting with follicle excision and anterior lamellar rotation surgery

122
Q

What is eyelash ptosis and what are the associated conditions?

A

refers to a downward sagging of the upper lid lashes

The condition may be idiopathic or associated with
floppy eyelid syndrome, dermatochalasis with anterior lamellar slip or long-standing facial palsy

123
Q

What is trichomegaly

A

excessive eyelash growth.

124
Q

What are some causes of Trichomegaly?

A

Drug-induced – topical prostaglandin analogues,
phenytoin and ciclosporin
Malnutrition
AIDS
Porphyria
Hypothyroidism
Familial
Congenital: Oliver–McFarlane, Cornelia de Lange,
Goldstein–Hutt, Hermansky–Pudlak syndromes

125
Q

What is madarosis?

A

term used for the loss of lashes

126
Q

What are some causes of madarosis?

A
  1. Local:
    a) Chronic anterior lid margin disease
    b) Infiltrating lid tumours
    c) Burns
    d) Radiotherapy or cryotherapy of lid tumours
  2. Skin disorders:
    a) Generalized alopecia
    b) Psoriasis
  3. Systemic diseases
    a) Myxoedema
    b) Systemic lupus erythematosus
    c) Acquired syphilis
    d) Lepromatous leprosy
  4. Following removal
    a) Procedures for trichiasis
    b) Trichotillomania – psychiatric disorder of hair removal
127
Q

What is poliosis?

A

premature localized whitening of hair, which may involve the lashes and eyebrows

128
Q

What are some causes of poliosis?

A
  1. Ocular:
    a) Chronic anterior blepharitis
    b) Sympathetic ophthalmitis
    c) Idiopathic uveitis
  2. Systemic
    a) Vogt–Koyanagi–Harada syndrome
    b) Waardenburg syndrome
    c) Vitiligo
    d) Marfan syndrome
    e) Tuberous sclerosis
129
Q

What is acute allergic oedema?

A

usually caused by exposure to pollen or by insect bites and manifests with the sudden onset of bilateral boggy periocular oedema often accompanied by conjunctival swelling.

130
Q

What is contact dermatitis?

A

an inflammatory response that usually follows exposure to a medication such as eye drops, cosmetics or metals.

The mediating reaction is
type IV (delayed type) hypersensitivity.

131
Q

What is atopic dermatitis?

A

Very common idiopathic condi-
tion, typically occurring in patients who also suffer from asthma
and hay fever. Eyelid involvement is relatively infrequent but when
present is invariably associated with generalized dermatitis.

Treatment of the lid features is with emollients to hydrate the skin and the judicious use of mild topical 1% hydrocortisone

132
Q

What is dermatomyositis and what are the clinical features seen?

A

a chronic inflammatory disorder of muscles which can present in an acute or chronic fashion with muscle weakness and a skin rash.

In children, about half develop eyelid swelling and a heliotrope rash

In adults it may be associated with ovarian, breast or lung cancer, as an autoimmune response. The
condition is treated with systemic steroids or immunosuppressive
medication (methotrexate, azathioprine).

133
Q

What is an external hordeolum and how is it treated?

A

(stye) is an acute staphylococcal abscess of a lash follicle and its associated gland of Zeis that is common.

A stye presents as a tender swelling in the lid margin pointing anteriorly through the skin, usually
with a lash at its apex

Treatment involves topical (occasionally oral) antibiotics, hot
compresses and epilation of the associated lash.

134
Q

What is impetigo and how is it treated?

A

a superficial skin infection caused by Staphylococcus
aureus or Streptococcus pyogenes, typically affecting children. Involvement of the eyelids is usually associated with infection of the face. Painful erythematous macules rapidly develop into thin-walled blisters, which develop golden-yellow crusts on rupturing.

Treatment is with topical and sometimes oral antibiotics (beta-lactamase resistant) and preventative measures
to reduce transmission as the condition is highly contagious. It is
particularly dangerous to neonates, contact with whom should be avoided.

135
Q

What is erysipelas?

A

an uncommon acute, potentially
severe, dermal and superficial lymphatic infection usually caused
by S. pyogenes. Diabetes, obesity and alcohol abuse are predisposing factors. An inflamed erythematous plaque develops.

A well-defined raised border distinguishes erysipelas from other forms of cellulitis. Complications such as metastatic infection are rare. Treatment is with oral antibiotics, but recurrence is common.

136
Q

What is Necrotizing fasciitis and how is it treated?

A

a rare but commonly very severe infection involving subcutaneous soft tissue and the skin, with associated rapidly progressive necrosis. It is usually caused by S. pyogenes and occasionally S. aureus.

The most frequent sites of involvement are the extremities, trunk and perineum, as well as postoperative wound sites. Unless early aggressive treatment is instituted, in the form of surgical debridement and high-dose intravenous antibiotics, death may result.

137
Q

What is molluscum contagiosum caused by?

A

a skin infection caused by a human- specific double-stranded DNA poxvirus that typically affects
otherwise healthy children, with a peak incidence between 2 and
4 years of age

Single or multiple pale, waxy, umbilicated nodules develop

138
Q

What does histopathology of molluscum contagiosum showing?

A

a central pit and lobules of hyperplastic epidermis with intracytoplasmic (Henderson–Patterson) inclusion bodies that displace the nuclear remnant to the edge of the cell. The bodies are small and eosinophilic near the surface and large and basophilic deeper down

139
Q

How is molluscum contagiosum treated?

A

Spontaneous resolution will usually occur within a few months,
so treatment may not be necessary, particularly in children, unless complications such as a significant secondary conjunctivitis are problematic.

Options include shave excision, curettage, cauterization, chemical ablation, cryotherapy and pulsed-dye laser.

140
Q

What are clinical features of Herpes Simplex virus infection?

A

results from either primary infection or reactivation of herpes simplex virus previously dormant in the trigeminal ganglion. Prodromal facial and lid tingling lasting about 24 hours is followed by the development of eyelid and periocular skin vesicles that breakdown over 48 hours.

Dendritic corneal ulcers can develop, especially in atopic patients, in whom skin involvement can be extensive and very severe
(eczema herpeticum)

141
Q

HSV vs HZO differentiating feature?

A

the distribution of the herpes simplex skin rash contrasts with the sharply delineated unilateral involvement in HZO

142
Q

How is HSV infection treated?

A

In many patients the inflammation will gradually settle without
treatment over about a week. If treatment is necessary, a topical
(aciclovir cream five times daily for 5 days) or oral (oral aciclovir,
famciclovir or valaciclovir) antiviral agent can be used.

Antibiotics (e.g. co-amoxiclav, erythromycin) may also be required in patients
with secondary bacterial infection. This is particularly common in
eczema herpeticum.

143
Q

What is anterior blepharitis?

A

affects the area surrounding the bases of the eyelashes and may be staphylococcal or seborrhoeic. It is sometimes regarded as related more to chronic infective elements and hence more amenable to treatment and remission than the posterior form

144
Q

What is posterior blepharitis?

A

caused by meibomian gland dysfunction and alterations in meibomian gland secretions. Bacterial lipases may result in the formation of free fatty acids. This increases the melting point of the meibum, preventing its expression from the glands, contributing to ocular surface irritation and possibly enabling growth of S. aureus.

there is an association with acne rosacea.

145
Q

What are the causes of chronic blepharitis?

A

1) Anterior blepharitis
2) Posterior blepharitis
3) A reaction to the extremely common hair follicle and sebaceous gland-dwelling mite Demodex

146
Q

What are symptoms of blepharitis?

A

Burning, grittiness, mild
photophobia and crusting and redness of the lid margins with remissions and exacerbations are characteristic. Symptoms
are usually worse in the mornings although in patients with associated dry eye they may increase during the day.

Contact lenses may be poorly tolerated.

147
Q

Seborrhoeic vs Staphylococcal blepharitis?

A

An aetiological factor in staphylococcal blepharitis may be an abnormal cell-mediated response to components of the cell wall of S. aureus, which may also be
responsible for the red eyes and peripheral corneal infiltrates seen in some patients

Seborrhoeic blepharitis is
strongly associated with generalized seborrhoeic dermatitis that characteristically involves the scalp, nasolabial folds, skin behind the ears and the sternum.

148
Q

Signs of staphylococcal blepharitis?

A

Hard scales and crusting are found, mainly located
around the bases of the lashes and are associated with collarettes.

Long-standing cases may develop scarring and notching ofthe lid margin, madarosis, trichiasis and poliosis.

Associated tear film instability and dry eye syndrome are
common.

Atopic keratoconjunctivitis may be present in patients
with atopic dermatitis.

149
Q

Signs of seborrhoeic blepharitis?

A

Hyperaemic and greasy anterior lid margins with soft
scales and adherence of lashes to each other

150
Q

Signs of posterior blepharitis?

A

Excessive and abnormal meibomian gland secretion,
manifesting as capping of meibomian gland orifices with
oil globules

Pouting, recession, or plugging of meibomian gland orifices

Hyperaemia and telangiectasis of the posterior lid margin.

Pressure on the lid margin results in expression of meibomian fluid that may be turbid or toothpaste-like

151
Q

Management for blepharitis

A

1) Lid hygiene with warm compress and lid cleaning to mechanically remove crusts/debris
2) Antibiotics- topical fusidic acid/erythromycin/chloramphenicol. Ointment rubbed onto anterior lid margin after cleaning
3) Oral antibiotics eg doxycycline (50-100mg) BD for 1 week then daily for 6-24 weeks.
Tetracyclines –> posterior disease, Azithromycin–> anterior disease.
4) Plant and fish oil supplements
5) Topical steroid eg FML 0.1% or loteprednol QDS for 1 week with papillary conjunctivitis is useful
6) Tear substitutes
7) Tea tree oil for demodex. Topical permethrin and topical cream or oral ivermectin have been used.
8) Novel therapies eg ciclosporin, pulsed light, Lipiflow in posterior disease

152
Q

What is Phthiriasis palpebrarum and how is it treated?

A

The crab louse Phthirus pubis is adapted to living in pubic hair, but is also commonly found in other hair-covered body areas.

Ova and their empty shells appear as oval, brownish, opalescent pearls adherent to the base of the cilia

Treatment–> mechanical removal of the lice and their attached lashes with fine forceps. If necessary, topical yellow mercuric
oxide 1% or petroleum jelly can be applied to the lashes and lids twice a day for 10 days. Consider family delousing

153
Q

What is tick infestation of the eyelid and how is it treated?

A

Ticks can attach themselves to the eyelid and should be removed at the earliest opportunity in order to minimize the risk of contract-
ing a tick-borne zoonosis such as Lyme disease, Rocky Mountain fever, African tick bite fever or tularaemia.

A scabies cream containing permethrim can be applied preventing the tick from injecting saliva.

154
Q

How long is Lyme disease transmission thought to occur after tick attachment?

A

Lyme disease transmission is thought to require
attachment of the tick for at least 36 hours.

155
Q

What is childhood BKC and how is it treated?

A

a poorly defined con-
dition that tends to be more severe in Asian and Middle Eastern populations. Presentation is usually at about 6 years of age with
recurrent episodes of anterior or posterior blepharitis, sometimes associated with recurrent styes or chalazia.

Conjunctival changes include diffuse hyperaemia, bulbar phlyctens and follicular or papillary hyperplasia.

Corneal changes include superficial punctate keratopathy, marginal keratitis, peripheral vascularization and axial subepithelial haze.

Treatment is with lid hygiene and topical antibiotic
ointment at bedtime. Topical low-dose steroids (prednisolone
0.1% or fluorometholone 0.1%)

156
Q

What is ptosis?

A

an abnormally low position of the upper lid, which may
be congenital or acquired.

157
Q

What is neurogenic ptosis?

A

caused by an innervational defect such as third nerve paresis and Horner syndrome

158
Q

What is myogenic ptosis?

A

caused by a myopathy of the levator muscle itself, or by impairment of transmission of impulses at the neuromuscular junction (neuromyopathic). Acquired myogenic ptosis occurs in myasthenia gravis, myotonic dystrophy and progressive external ophthalmoplegia

159
Q

What is aponeurotic ptosis?

A

involutional ptosis is caused by a defect in the levator aponeurosis

160
Q

What is mechanical ptosis?

A

caused by the gravitational effect of a mass or by scarring

161
Q

What are the causes of pseudoptosis?

A

Lack of support of the lids by the globe may be due to an
orbital volume deficit associated with an artificial eye

Contralateral lid retraction, which is detected by comparing the levels of the upper lids, remembering that the margin of the upper lid normally covers the superior 2 mm of the cornea

Ipsilateral hypotropia

Brow ptosis due to excessive skin on the brow, or seventh
nerve palsy

Dermatochalasis. Overhanging skin on the upper lids

162
Q

What is MRD?

A

Distance between the upper lid margin and the corneal reflection of a pen torch held by the examiner on which the patient fixates. The normal
measurement is 4–5 mm.

163
Q

What is palpebral fissure height?

A

distance between the upper and lower lid margins, measured in the pupillary plane
The upper lid margin normally rests about 2 mm below the
upper limbus and the lower 1 mm above the lower limbus.

164
Q

How is ptosis graded?

A

mild (up to 2 mm), moderate (3 mm) and severe (4 mm or more).

165
Q

What is levator function and how is it measured?

A

measured by placing
a thumb firmly against the patient’s brow to negate the action of the frontalis muscle, with the eyes in downgaze. The patient then looks up as far as possible and the amount of excursion is measured with a ruler.
Levator function is graded as normal (15 mm or more), good (12–14 mm), fair (5–11 mm) and poor (4 mm or less).

166
Q

Associated signs with ptosis?

A

1) Pupils- Horners/3rd Nerve palsy
2) Contralateral lid retraction which droops when ptotic lid elevated
3) Fatiguability
4) Ocular motility defects
5) Jaw winking
6) Bell phenomenon

167
Q

Why is the lid crease measurement important?

A

the vertical distance between the lid margin and the lid crease in downgaze. In females it measures about 10 mm and in males 8 mm. Absence of the crease
in a patient with congenital ptosis is evidence of poor levator function, whereas a high crease suggests an aponeurotic defect
(usually involutional).

168
Q

What is simple congenital ptosis and how is it treated?

A

Absent upper lid crease and poor levator function.
In downgaze the ptotic lid is higher than the normal
because of poor relaxation of the levator muscle. This
is in contrast to acquired ptosis, in which the affected
lid is either level with or lower than the normal lid on
downgaze.

Treatment should be carried out during the preschool years once accurate measurements can be obtained, but may be considered earlier in severe cases to prevent amblyopia. Levator resection is usually required.

169
Q

What is the pathophysiology of Marcus Gunn jaw-winking syndrome?

A

Most are unilateral.

it has been postulated that
a branch of the mandibular division of the fifth cranial nerve is misdirected to the levator muscle.

170
Q

Signs of Marcus Gunn jaw winking syndrome?

A

Retraction of the ptotic lid in conjunction with stimulation
of the ipsilateral pterygoid muscles by chewing, sucking,
opening the mouth or contralateral jaw
movement.

171
Q

Treatment for Marcus Gunn Jaw winking syndrome?

A

Surgery should be considered if jaw-winking or ptosis represents a
significant functional or cosmetic problem.
*Mild cases with reasonable levator function of 5 mm or better and little synkinetic movement may be treated with unilateral levator advancement.
* Moderate cases. Unilateral levator disinsertion can be performed to address the synkinetic winking component, with ipsilateral brow (frontalis) suspension so that lid elevation is
due solely to frontalis muscle elevation.

172
Q

What is third nerve misdirection and how is it treated?

A

Third nerve misdirection syndromes may be congenital, but more frequently follow acquired third nerve palsy

Ptosis may also occur following aberrant facial nerve
regeneration. Treatment is by levator disinsertion and brow
suspension.

173
Q

What is the pathophysiology of Involutional ptosis?

A

age-related condition
caused by dehiscence, disinsertion or stretching of the levator aponeurosis, limiting the transmission of force from a normal
levator muscle to the upper lid.

Due to fatigue of the Müller
muscle it frequently worsens towards the end of the day, so that it can sometimes be confused with ptosis secondary to myasthenia.

There is a variable, usually bilateral, ptosis with a high upper lid crease and good levator function. In severe cases the upper lid
crease may be absent.

174
Q

What are some treatments for involutional ptosis?

A

levator resection, advancement with reinsertion or anterior levator
repair.

175
Q

Where does the levator aponeurosis fuse with orbital septum?

A

about 4 mm above the superior border of the tarsal plate

176
Q

When is conjunctival Muller resection used?

A

This involves excision of Müller muscle and overlying conjunctiva with reattachment of the resected edges
The maximal elevation achievable is 2–3 mm, so it is used in cases of mild ptosis with good (at least 10 mm) levator function, which
includes most cases of Horner syndrome and mild congenital
ptosis.

177
Q

What is levator advancement (resection) and when is it done?

A

The levator complex is shortened through
either an anterior – skin or posterior – conjunctival approach.

Indications include ptosis of any cause, provided
residual levator function is at least 5 mm

The extent of resection is
determined by the severity of the ptosis and the amount of levator function.

The advantage of a posterior approach is the predictability of the lid contour.

178
Q

When is brow (frontalis) suspension performed and how is the surgery done?

A

Brow (frontalis) suspension is used for severe ptosis (>4 mm) with very poor levator function (<4 mm) from a variety of causes.
Typical indications include ptosis associated with third nerve palsy, blepharophimosis syndrome and following an unsatisfactory result from previous levator resection

The tarsal plate is
suspended from the frontalis muscle with a sling consisting of autologous fascia lata or non-absorbable material such
as prolene or silicone.

179
Q

What are the causes of involutional ectropion?

A

Horizontal lid laxity can be demonstrated by pulling the
central part of the lid 8 mm or more from the globe, with a
failure to snap back to its normal position on release without the patient first blinking.

Lateral canthal tendon laxity, characterized by a rounded
appearance of the lateral canthus and the ability to pull the lower lid medially more than 2 mm.

Medial canthal tendon laxity, demonstrated by pulling
the lower lid laterally and observing the position of the
inferior punctum. If the lid is normal the punctum should
not be displaced more than 1–2 mm. If laxity is mild the
punctum reaches the limbus and if severe it may reach the
pupil.

180
Q

What is the treatment for involutional ectropion?

A

Generalized ectropion is treated with repair of horizontal lid laxity. This is achieved with a lateral tarsal strip procedure, in which the lower canthal tendon is tightened by shortening
and reattachment to the lateral orbital rim

Excision of a tarsocon-
junctival pentagon

Medial ectropion, if mild, may be treated with a medial con-
junctival diamond excision (medial spindle procedure). It is often combined with a tarsal strip or lateral canthal sling (see or pentagon excision as significant horizontal laxity frequently co-exists.

181
Q

What is cicatricial ectropion?

A

caused by scarring or contracture of the
skin and underlying tissues, which pulls the eyelid away from the globe

If the skin is pushed up over the orbital margin with a finger the ectropion will be relieved. Opening the mouth
tends to accentuate the eversion.

182
Q

How is cicatricial ectropion treated?

A

Mild localized cases are
treated by excision of the offending scar tissue combined with a
procedure that lengthens vertical skin deficiency, such as Z-plasty.
Severe generalized cases require transposition flaps or free skin grafts. Sources of skin include the upper lids, posterior auricular,
preauricular and supraclavicular areas.

183
Q

What is paralytic ectropion?

A

caused by ipsilateral facial nerve palsy and is associated with retraction of the upper and lower lids and brow ptosis. The latter may mimic narrowing of the palpebral
aperture.

184
Q

What are some treatments for paralytic ectropion?

A

TEMPORARY MEASURES
1) Lubrications
2) Botox injection induce temporary ptosis
3) Temporary tarsorrhaphy in patients with poor Bell phenomenon with corneal exposure.

PERMANENT MEASURES
1) Medial canthoplasty if medial canthal tendon intact.
2) Lateral canthal sling or tarsal strip
3) Upper eyelid lowering by levator disinsertion

185
Q

What are some causes of involutional entropion?

A

Involutional (age-related) entropion affects mainly the lower lid.
* Horizontal lid laxity caused by stretching of the canthal
tendons and tarsal plate.
* Vertical lid instability caused by attenuation, dehiscence
or disinsertion of the lower lid retractors. Weakness of the
latter is recognized by decreased excursion of the lower lid in downgaze.
* Over-riding of the pretarsal by the preseptal orbicularis
during lid closure tends to move the lower border of the tarsal plate anteriorly, away from the globe and the upper border towards the globe, thus tipping the lid inwards
* Orbital septum laxity with prolapse of orbital fat into the
lower lid.

186
Q

What is the treatment of involutional entropion?

A

1) Transverse everting sutures prevent over-riding of the
preseptal orbicularis.

2) The Wies procedure gives a durable correction. It consists
of full-thickness horizontal lid splitting and insertion
of everting sutures

3) Lower lid retractor reinsertion. Involves direct
exposure and advancement of the retractors as opposed
to the less precise approach used in the Wies procedure.

4) Horizontal lid laxity is usually present and can be corrected with a lateral canthal sling (tarsal strip)

187
Q

What are the treatments for cicatricial entropion?

A

Causes include cicatrizing conjunctivitis, trachoma, trauma and chemical injuries.

Definitive surgical treatment of mild cases is by tarsal fracture (transverse tarsotomy) with anterior rotation of the lid margin,
as for marginal entropion of the lower lid. Treatment of severe cases is difficult and is directed at replacing deficient or keratinized conjunctiva and replacing the scarred and contracted tarsal plate
with composite grafts.

188
Q

What is an eyelid varix?

A

a common lesion that may be
mistaken for a naevus or haemangioma
A varix is commonly an
isolated lesion, but may be associated with orbital involvement.
Appears as a dark red/purple subcutaneous compressible lesion which in some cases may be visible only with a Valsalva manoeuvre

189
Q

What is Floppy Eyelid Syndrome?

A

It typically affects obese middle-aged
and older men who sleep with one or both eyelids against the pillow, which results in the lid pulling away from the globe.
Obstructive sleep apnoea (OSA) is strongly associated and is linked to significant morbidity, including cardiopulmonary disease and subtle but irreversible mental dysfunction

190
Q

Clinical findings with floppy eyelid syndrome?

A

The upper eyelid is typically extremely lax, often with
substantial excess loose upper lid skin

Papillary conjunctivitis of superior tarsal conjunctiva

Keratopathy-> punctate keratopathy, filamentary keratitis

Eyelash ptosis, lacrimal gland prolapse, ectropion and aponeurotic ptosis. Patients with FES increased risk of developing glaucoma

Investigations for OSA should be considered.

191
Q

How is Floppy eyelid syndrome treated?

A
  • Treatment of associated OSA is likely to be of benefit, and
    overweight patients should be encouraged to lose weight.
  • Mild cases may respond to lubrication together with nocturnal
    eye shield wear or taping of the lids.
  • Moderate–severe cases require horizontal shortening to stabilize the lid and ocular surface and prevent nocturnal
    lagophthalmos. A pentagonal excision of 10 mm or more is
    taken from the junction of the lateral third and medial two-
    thirds of the upper lid.
192
Q

What is blepharochalasis?

A

Uncommon condition characterized by
recurrent episodes of painless, non-pitting oedema of both upper lids that usually resolves spontaneously after a few days.

Presentation is usually around puberty, episodes becoming less frequent with time.

Severe cases may give rise to stretching of the canthal tendons and levator
aponeurosis resulting in ptosis and lacrimal gland prolapse

193
Q

What are the 2 forms of blepharochalasis?

A

A hypertrophic form with orbital fat herniation and an atrophic form with absorption of orbital fat have been
described.

194
Q

How is blepharochalasis treated?

A

blepharoplasty for redundant upper lid skin and correction of ptosis.

195
Q

What is eyelid imbrication syndrome?

A

an uncommon and frequently
unrecognized disorder in which the upper lid overlaps the lower on closure so that the lower lashes irritate the superior marginal tarsal conjunctiva.

Definitive treatment consists of upper lid pentagon resection and/or lateral canthal tightening.

196
Q

What is upper lid retraction?

A

when the upper lid margin is
either level with or above the superior limbus

197
Q

What are some causes of lid retraction?

A

1) TED
2) Neurogenic (third nerve misdirection, marcus gunn jaw winking, Parinaud syndrome, Parkinsonism, Sympathomimetic drops, Contralateral unilateral ptosis)
3) Mechanical (surgical overcorrection of ptosis, scarring of upper lid skin)
4) Congenital (isolated, Duane retraction syndrome, Down syndrome)
5) Prominent globe, severe liver disease (Summerskill sign), Idiopathic

198
Q

Which condition is the ‘setting sun’ sign seen in?

A

Infantile hydrocephalus

199
Q

What are some age related lid changes?

A

1) Reduced elasticity and wrinkled skin
2) Weakening of orbital septum leading to orbital fat prolapse
3) Thinning and stretching of canthal tendons, levator and lid retractors causing ptosis
4) Atrophy of orbital and eyebrow fat pads gives enophthalmos and eyebrow sagging
5) Weakening of frontalis cause descent of eyebrows and increased looseness of upper lid skin

200
Q

What are some non surgical techniques for age related lid changes?

A

Botox to periocular muscles (reduce wrinkling) at lateral canthus and glabellar frown lines. Complications include temporary ptosis/ lagophthalmos/ectropion/diplopia

Tissue fillers. Hyalouronic acid, autologous fat, others eg collagen, synthetic fillers

Skin resurfacing by chemical peels or laser can reduce wrinkling, removal of blemishes/

201
Q

What is upper lid blepharoplasty?

A

surplus upper eyelid skin (dermatochalasis) that leads to baggy lids with indistinct creases and pseudo- or mechanical ptosis.

effective for the removal of
surplus skin and can be combined with reduction of the superior orbital fat pads.

Complications include removal of excess skin leading to lagophthalmos and corneal drying and removal of excess orbital fat leading to an unattractive hollowed out upper eyelid sulcus.

202
Q

What are the 2 ways for brow ptosis correction?

A

Lifting of the brow needs to precede or occasionally be combined with upper lid blepharoplasty.
* Direct brow lift. An incision is made above the eyebrow hairs and an ellipse of skin is removed

  • Endoscopic brow lift. Small incisions within the hair-line
    enable endoscopic elevation of the whole forehead tissues
    and release at the eyebrow periosteum to allow lifting of the eyebrows through sutures supported on frontal bone anchors within the hair-line.
203
Q

What are epicanthic folds and how can they be treated?

A

bilateral vertical folds of skin that extend from the upper or lower lids towards the medial canthi. They may give rise to pseudoesotropia. Lower lid folds give rise to blepharophimosis syndrome

Treatment is by V–Y or Z-plasty.

204
Q

What is telecanthus and how is it treated?

A

an uncommon condition that may occur in isolation or in association with blepharophimosis and some systemic syndromes. It consists of increased distance between the medial canthi due to abnormally long medial canthal tendons

Treatment involves shorten-
ing and refixation of the medial canthal tendons to the anterior lacrimal crest, or insertion of a trans-nasal suture.

205
Q

Difference between hypertelorism and telecanthus?

A

hypertelorism is when there is wide bony separation of the orbits.

telecanthus is increased distance between the medial canthi due to abnormally long medial canthal tendons

206
Q

What is Blepharophimosis, ptosis and epicanthus inversus syndrome
(BPES)?

A

a complex of eyelid malformations consisting of
moderate–severe symmetrical ptosis with poor levator function, telecanthus, epicanthus inversus manifesting with small palpebral fissures

Inheritance is usually AD

207
Q

What are the 2 types of BPES and how is it treated?

A

Both BPES type
I (with premature ovarian failure) and BPES type II (without premature ovarian failure) are caused by mutations in the FOXL2 gene on chromosome 3.

Treatment initially involves correction of epicanthus and telecanthus, followed later by bilateral frontalis suspension. It is also important to treat amblyopia, which is
present in about 50%.

208
Q

What is an epiblepharon and how is it treated?

A

comprises an extra horizontal fold of skin stretching
across the anterior lid margin and is commonly found in individuals of Eastern Asian ethnicity. The lashes are directed vertically,
especially in the medial part of the lid

Treatment is not required in the majority of whites because
spontaneous resolution with age is usual. Persistent cases may be treated surgically.

209
Q

What is congenital entropion?

A

Upper lid entropion is usually secondary to the mechanical effects of microphthalmos, which cause variable degrees of upper lid inversion. Lower lid entropion is generally caused by maldevelopment of the inferior retractor aponeurosis.

Treatment involves the excision of a strip of skin and muscle and fixation of
the skin crease to the tarsal plate (Hotz procedure).

210
Q

What is a coloboma and how is it managed?

A

uncommon, unilateral or bilateral, partial- or full-thickness eyelid defect.

occurs when eyelid
development is incomplete, due to either failure of migration of lid ectoderm to fuse the lid folds or to mechanical forces such as amniotic bands.

The treatment of small defects involves primary closure, while large defects require skin grafts and rotation flaps.

211
Q

What is an upper lid coloboma and what are its associations?

A

occurs at the junction of the middle and inner thirds.

Relatively strong associations include cryptophthalmos, facial abnormalities and Goldenhar syndrome.

212
Q

What is a lower lid coloboma and what are its associations?

A

occurs at the junction of the middle and outer thirds and is frequently associated with
systemic conditions.

213
Q

What is Treacher Collins syndrome?

A

genetically heterogeneous condition characterized by
malformation of derivatives of the first and second branchial
arches, principally mandibular and ear anomalies.

Lower eyelid coloboma is a feature. Ocular anomalies also described include slanted palpebral apertures, cataract, microphthalmos and lacrimal atresia

214
Q

What is cryptophthalmos?

A

Cryptophthalmos is a rare congenital anomaly in which the eyelids are absent, replaced by a continuous layer of skin.

215
Q

What are the features of complete Cryptophthalmos?

A

A microphthalmic eye is covered by a fused layer of skin with no separation
between the lids.

216
Q

What are the features of incomplete Cryptophthalmos?

A

is characterized by rudimentary lids and microphthalmos

217
Q

What is Fraser syndrome?

A

a dominantly inherited condition in which cryptophthalmos is a common finding. Other features
can include syndactyly, urogenital and craniofacial anomalies.

218
Q

What is Euryblepharon?

A

horizontal enlargement of the palpebral fissure with associated lateral canthal malposition and lateral ectropion which may result in lagophthalmos and
exposure keratopathy

219
Q

What is microblepharon and what are its associations?

A

Microblepharon is characterized by small eyelids, often associated with anophthalmos

220
Q

What is Ablepharon and how is it treated?

A

deficiency of the anterior lamellae of the eyelids

Treatment involves reconstructive skin
grafting. Ablepharon-macrostomia syndrome is characterized
by an enlarged fish-like mouth ear, skin and genital
anomalies.

221
Q

What is congenital upper lid eversion and what are its associations?

A

a rare condition more frequently seen in infants of Afro-Caribbean origin, in Down syndrome and in congenital ichthyosis (collodion skin disease). It is
typically bilateral and symmetrical. It may resolve spontaneously with conservative treatment or require surgery.

222
Q

What is Ankyloblepharon Filiforme Adnatumand how is it treated?

A

the upper and lower
eyelids are joined by thin tags.
Most cases are sporadic.
Treatment involves transection with scissors, usually without anaesthesia.

223
Q
A