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Introduction
PEAR SHAPED CAVITIES CONTENTS.EYEBALLS ,MUSCLES,NERVES,MOST OF THE LACRIMAL APPRATUSFAT APEX DIRECTED POSTERIORLY,UPWARDS AND MEDIALLY MEDIAL WALL PARALLEL TO SAGITAL PLANE AND LATERAL WALL ANGLE OF 45
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ORBITAL WALLS
ROOF..Frontal and lesser wing FLOORmaxilla,zygomatic,palatine LATERAL WALLZygomatic,sphenoid MEDIAL WALLfrontal process of maxilla lacrimal,ethmoid, body of sphenoid
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ORBITAL DIMENSIONS
Height of orbital margin - 40 mm Width of orbital margin - 35 mm Depth of orbit - 40-50 mm Interorbital distance - 25 mm Volume of orbit - 30 cm3
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Superior orbital fissure Cranial nerves (CN) III, IV, and VI Lacrimal nerve Frontal nerve Nasociliary nerve Orbital branch of middle meningeal artery Recurrent branch of lacrimal artery Superior orbital vein Superior
OPTIC CANAL
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CLINICAL SIGNS
SOFT TISSUE INVOLVMENT PROPTOSIS DYSTOPIA ENOPHTHALMOS OPHTHALMOPLEGIA PULSATIONS FUNDUS CHANGES
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LID AND PERIORBITAL OEDEMA PTOSIS CHEMOSIS( OEDEMA OF CONJUNTIVA AND CARUNCLE) EPIBULBAR INJECTION
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Conjunctival injection
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PROPTOSIS
PSEUDOPROPTOSIS
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Muscle cone
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Bilateral proptosis
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Buphthalmos Myopia
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dystopia
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ophthalmoplegia
A Orbital mass Restrictive Myopathy(Thyroid Eye Disease, Orbital Myositis Ocular Motor Nerve involvement Tethering of EOM( Blow out fracture)
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Fundus changes
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Investigations
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ORBITAL DISEASES
(TED)
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TED
Thyrotoxicosis (Grave,s Disease), it is an autoimmune disorder 3rd and 4th deacades Women> men TED OCCURS IN 25-30% of Grave,s disease 5% have severe involvment TED may precede,coincide with OR follow hyperthyroidisim relation with severity of thyroid
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TED
RISK FACTORS
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LID RETRACTION
PATHOGENESIS(Fibrotic Contracture of Levator,Secondary over action of levator plus superior rectus, sympathetic overactivity causing Muller muscle SIGNS(Dalrymple,Kocher,vonGraefe MANAGEMENT(Observation,Mullerotomy, Recession of lower lid retractors,Botulinum Toxin Injection
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PROPTOSIS
Pathogenesis(Inflammation of EOM,Inflammatory cellular infilteration with lymphocytes,plasma cells,macrophages, mast cells of interstitial tissues and orbital fat Signs(Axial,uni/bilateral Management(systemic steroids,radiotherapy,surgical decompression
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Symptoms(Grittiness,Photophobia,Lacrim ation and retrobulbar discomfort Signs(Epibulbar hypremia,periorbital swelling,dry eyes Management(Lubricants, Head Elevation and Eyelid tapping
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Restrictive Myopathy
INDICATION,DIPLOPIA IN primary gaze or reading positions Surgical recessions of muscles Botulinum toxins
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Optic neuropathy
Presentations Signs (optic nerve functions i.e. va,visual fields,pupil, color vision Treatment I/V Steroids orbital decompression
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ORBITAL INFECTIONS
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PRESEPTAL CELLULITIS
Infection anterior to orbital septum Causes ..Skin trauma, spread of local infection i.e. sty,dacryocystitis From remote infection i.e. RTI SIGNS
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ORBITAL CELLULITIS
Life threatening infection of soft tissue of orbit behind the septum ANY AGE S,Pneumoniae, S.Aureus, S.Pyogenes and H.Influenzae
PATHOGENESIS
1) 2)
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ORBITAL CELLULITIS
Severe visual loss due to optic nerve involvement Painful Ophthalmoplegia FEVER RAISED LEUCOCYTE COUNT
COMPLICATIONS
OcularExposure,Glaucoma,CRAO, CRVO,
Enophthalmitis,Optic Neuropathy ORBITAL ABSCESS 4/17/12
PROPTOSIS OPHTHALMOPLEGIA SIGNS OF OPTIC NERVE INVOLVMENT SOFT TISSUE INVOLVMENT CORNRAL EXPOSURE KERATOPATHY
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RHINOMUCOR MYCOSIS
Gradual onset of facial and periorbital swelling Diplopia Ischemic infarction,Typical Black ESCHAR
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ORBITAL INFLAMMATIONS
1-IDIOPATHIC ORBITAL INFLAMMATORY DISEASE
(IOID)
Previously known as Orbital Pseudotumor 2-Acute dacryoadenitis 3-Orbital myositis 4-Wegner,s granulomatosis
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PSEUDOTUMOR
Very good response to systemic steroids is diagnostic of pseudotumour Oral NSAIDS Radiotherapy Antimetabolites Surgery is rarely needed
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VASCULAR MALFORMATIONS
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ORBITAL VARICES
Consists of weakened segments of the orbital venous system of variable length and complexity Enlarged with increased venous pressure Unilateral Early childhood to late middle life Intermittent proptosis Visible lesion in the eyelid
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ORBITAL VARICES
Conjuntival varices C.T Scan show Pheleboliths C.T Angiography Surgical excision if RECURRENT THROMBOSIS,PAIN, SEVERE PROPTOSIS and OPTIC NERVE COMPRESSION
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LYMPHANGIOMA
Are not neoplasms,but abortive non functional benign vascular malformations Haemodynamically isolated from the circulation PRESENTATION
Early childhood Anterior lesions several soft bluish mass in upper nasal quadrant with an associated cystic conjunctival component Posterior Lesions may cause sudden or 4/17/12
LYMPHANGIOMA
TREATMENT SURGICAL Excision is difficult because of friability and non-encapsulation easily bleed and may infiltrate normal orbital tissue Persistant sight threatening choclate cysts should be drained or removed sub-totally
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An A/V fistula is an abnormal communication between artery and vein. The blood within the affected vein becomes ARTERIALIZED
venous pressure rises and venous drainage may be altered in both rate and direction Arterial pressure and perfusion are also reduced IT IS COMMUNICATION BETWEEN CAROTID ARTERY AND CAVERNOUS SINUS
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CYSTIC LESIONS
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SINUS MUCOCOELE
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ENCEPHALOCOELE
FEATURES USUALLY SUPERONASAL ORBIT PULSATILE NON-REDUCIBLE SINCE BIRTH DUE TO DEFECTIVE ORBITAL ROOF FORMATION
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ORBITAL TUMORS
Capillary haemangioma Cavernous haemangioma Pleomorphic lacrimal gland adenoma Lacrimal gland carcinoma Optic nerve glioma Optic nerve sheath Meningioma Plexiform Neurofibroma Lymphoma sarcoma(Rhabdomyosarcoma
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CAPILLARY HAEMANGIOMA
Hamartoma(Abnormal tissue at normal place)
Most common tumour of the orbit and periorbital areas in childhood Girls>boys PRESENTATION First few weeks of life But 30% at birth
Capillary Haemangioma
1. 2. 3. 4.
Indications of treatment Amblyopia Optic nerve compression Exposure keratopathy A severe cosmetic blemish
steroids/hot water/almond
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CAVERNOUS HAEMANGIOMA
Most common benign orbital tumor in ADULTS MIDDLE AGED FEMALE 70% 4th to 5th decade AXIAL PROPTOSIS INTRACONAL LOCATION/Extra conal SURGERY is easy because of encapsulation/CRYOPROBE may be used
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Slowly growing astrocytoma 30% association with Neurofibromatosis ADOLOSCENT GIRLS PRESENTATION is first decade of life Visual loss is slowly progressive Intracranial spread may occur
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Arise from meningo-epithelial cells of arachnoid villi surrounding the intraorbital portion of optic nerve Typically affects middle aged women PRESENTATION Gradual decrease in visual impairment
CLASSICAL TRIAD
v v
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OBSERVATION if good vision and progress is slow SURGERY in youngs in aggressive cases if the eye is blind
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FRACTURES
BLOWOUT FRACTURES OF ORBIT Most common FLOOR then Medial Wall Fracture of Lateral Wall
SIGNS
ENOPHTHALMOS HYPOANESTHESIA OVER CHEEK DIPLOPIA PROPTOSIS? CHEMOSIS
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INDICATIONS OF TREATMENT
1- Diplopia in primary gaze/reading gaze 2- enophthalmos more than 2 mm
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THANKS
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