disorders of the orbit
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DISORDERS OF THE ORBI
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--
Six P
s: pain, proptosis, progression, palpation, pulsation, .
Pain: inflammatory, infection, oribital hemorrhage,
ma gnan acn ma g an umors anProptosis--Hertel exophthalmometer
Axial proptosis-an intraconal space-occupying lesion,
Eccentric proptosis--- an ant.space-occupying lesion.
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RBI -- Pr r i n
Days to weeks--idiopathic orbital inflammatory dis.,
cellulitis, hemorrhage, thrombophlebitis, thyroid
, , ,
rhabdomyosarcoma, or granulocytic sarcoma.
ver mon s o years- ermo s, en gn m xe umors,
neurogenic tumors, cavernous hemanglomas, lymphoma,
fibrous histiocytoma, or osteomas.
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-- Superonasal quadrant--- mucoceles, mucopyoceles,
, ,, .
Superotemporal quadrant--- dermoids, prolapsed
lacrimal gland, lacrimal gland tumors, lymphoma,or idio athic orbital inflammation disease
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--
Without bruits-neurofibromatosis,meningoencep a oce es, or remova o t e
With or without bruits-carotid cavernous
fistulas, dural arteriovenous fistulas, and
.
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Clinical evaluation of orbital disease
1. History: (1)pain, (2)mode of onset of proptosis.
(1) large ipsilateral globe,,
(3) contralateral enophthalmos (blow-out fracture)
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3. Evaluation of ocular motility: restrictive
- ,
4. Visual acuity5. Dynamic properties -valsalva maneuver or jugular
,, ,6. Forced duction test
7. Differential IOP test
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thyroid function (T3,T4, TSH); antithyroglobulin,antimicrosomal antibodies(60%-70% of patients
antineutrophil cytoplasmic antibody (ANCAs),
serum assay, Wegener granulomatosis
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D sth roido hthalmo ath
Classification Eyelid retraction
involvement
Proptosis
Restrictive myopathy
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Hypertrophy of EOM Cellular infiltration
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Systemic steroids Radiotherapy
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Orbital infection and inflammations
Preseptal cellulitis: affects children. secondary tolid infection such as hordeolum, skin laceration or
an insect bite .
Examination: periorbital swelling, tenderness
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Orbital cellulitis: ethmoidal sinusitis, maxillarysinusitis, dacryocystitis, dental infection, post-trauma.
Most common causative organisms: streptococcus
pneumonia, streptococcus aurcus, streptococcuspyogenes;( age of 5 years--Haemophilus influenzae),
aspergillosis.
Examination--proptoisis, eyelids-swollen, erythematous,warm, tender. EOM--restricted and painful. CBC, CT,
oo an nasa cu ures.
Treatment--- bacteria-systemic antibiotics; fungus--iv
amp o er c n , w e exc s on.
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idiopathic, non-specific, inflammatory, orbital diseasePresentation--20-50 years of age. Painful lid edema,
EOM--limitation ro tosis. Children: 1 3 bilateral
involvement.--- .
Treatment--observation, systemic steroids, radiotherapy,
cy o ox c rugs.
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Unilateral ptosis, diplopia, redness and pain overthe involved muscle.
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field of action of the involved muscle.
: us orm en argemen o e nvo ve musc e.
Treatment-s stemic steroids or NSAID.
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Tolosa-Hunt syndrome involve the orbital apex, sup. Orbital fissure, such as
, , .Presentation-ipsilateral periorbital or hemicranial pain.
xam nat on--proptos s,ocu ar cran a nerve pa s es,pupillomotor dysfunction. Sensory loss of 1 and 2divisions of V nerve.
Treatment---s stemic steroids.
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Orbital tumors
Classificationascu ar capillary haemangioma
cavernous aemagn oma lymphagioma venous anoma es
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Lacrimal gland
pleomorphic adenoma
mixed-cell tumormailgnant
Rhabdomyosarcoma
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Cystic lesions dermoid cyst--the common benign tumor blood cyst
mucocele
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Neural optic nerve glioma optic nerve sheath meningioma
MetastaticTumor its vasion from ad acent structures
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Ca illar haeman nioma
the most common primary benign tumor of the orbit
Presentation-during the perinatal period with a
,combination of both.
---
lid.Superficial straw-berry naevi may also be.
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Natura course--- uring t e irst year o i e,
it starts to involute spontaneously Completeresolution
.
Association-subglottic haemangiomas,thrombocytopenia, high-output cardiac
failure.
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(1) most commonly secondary to induced
r .
(2) optic n. compression or
(3) exposure keratopathy.A v r m i l mi h
Severe necrosis of infection
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(1) Steroid injection,(2) Systemic steroids,
,
(4) Radiotherapy
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avernous aemangn omathe most common primarybenign orbital tumor in
.
Presentation--during middle age with a
s ow y progress ve un a era pro os s. n women e grow ra e
may be accelerated by pregnancy.
Examination--axial proptosis, may be
associated with optic disc edema and chorioretinal folds.Treatment --surgical excision.
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benign vascular tumor
tendency to recurrent hamorrhage, poorly
---
Presentation---in childhood or early adult life
xam na on-- n . umor: cys c
conjunctival component in the upper nasal quadrant.
Post. Tumor: sudden onset of painful protosis and spontanous
hamorrha e within the tumor--chocolate c sts.
Treatment---surgery is difficult. Chocolate
cys s- ra ne . ar on ox e aser--su o a y exc s on.
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Arteriovenous malformations (AVM): dilated .
Treatment-selective occlusion of the feeding vessels,.
Arteriovenous fistulas (AVF):- .
(2) degeneration--H/T. atheroselerosis.
Carotid cavernous fistula--AVF of the orbit andcavernous sinus.
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Orbital varices:Cause: dilation of preexisting venous channel.
Valsalva manuver--- ro tosis
Treatment---conservation
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most common epithelial turnor-benign mixed-cell tumor.
, , ,
slowly growth in the upper outer quadrant ) 1 year's duration.
Examination--most cases, arsing from the orbital portion ofthe lacrimal land. CT scan bon excavation of the lacrimal land
fossa.
--
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adenoid cystic carcinoma
mucoepidermoid carcinoma
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pleomorphic adenoma; rapidly growing lacrimal gland mass.
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Examination--CT MRI bio s nerolo icalassessment.
Radical surgery: orbital exenteration or-
the prognosis-extremely poor
Radiotherapy:
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most common primary malignant orbital tumor in
children. resen a on- e rs eca e o e w a rap y
progressive proptosis - .
Systernic investigations-evidence of metastatic spread:CT of the chest, abdomen, and pelvis; liver function tests; lumbarpuncture; bone marrow biopsy. and skeletal radiographs.
Treatment--radiotherapy and chemotherapy.
recurring or radiotherapyresistant tumor.The survival rate is90%--confined to the orbit and 65% in the presence of bonyes ruc on an ex ens on.
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most commn orbital tumors of childhood; benign
i r m h ri m . Lined by keratinized stratified squamous epith.,
such as sweat glands, sebaceous glands and hairo ic es.
Epidermoid cyst do not contain adnexal structures. Examination -upper temporal orbit.
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s ow-grow ng umor; young g r s; - opatients -associated neurofibromatosis type 1.
Presentation--visual loss in children, but this may not
- .
Examination---disc edema followed by pallor;
prop os s.
CT: fusiform enlargment of the optic nerve. MRI: demonstrating the post., extent of the
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Treatment-
for several year,
growing tumor,
ra iot erapy an c emot erapy: intracraniaextension.
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rare tumors; arise from the meningoendothelial cells of
-Presentation-slowly progressive, unliateral, visual loss.
xam na on- sc e ema, op coc ary s un vesse s
(capillaries connecting the central retinal vein with theperipapillary choroidal vessels), also seen in patients withoptic nerve glioma.
CT: tubular thichening and calcfication of the optic nerve.
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Treatment--
o serva on: m e-age pa en s w s ow
growing tumors because the prognosis is good.(2)radiotherapy: with slow-growing tumors and
.
(3)surgical excision: blind of eye in young patients
w grow ng umor.
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Childen: Neuroblastoma, Ewing's sarcomaacute myeloid leukemia
,
manifestation of the tumor. Breast
(Female), bronchus (Male), prostate (Male),
-, .
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maxillary carcinoma, ethmoidal carcinoma
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Craniofacial stenosesCrouzon syndrome-ptoptosis, corneal exposure,
hypertelorism, ET, optic atrophy.
' -anisometropic amblyopia, corneal exposureor optic atrophy.
a era ac a m cros om as
Treacher Collins syndrome-eyelid coloboma, strabismusand ambl o ia.
Goldenhar's syndrome--epibulbar dermoids,microphthalmos, anophthalmos, microcomea,
, . , .
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Hypertelorismexcessive bony tissue of the medial orbital
between the eyes.
-- , m crop t a mos, m crocomea an
optic atrophy.
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