Orbital Apex conditions ophthalmology.pptx

Orbital apex and relevant conditions

1. Presentor : Dr Vishnu Prasad Rao Supervisor: Dr Lam Mun Wei ANATOMY OF ORBITAL APEX

2. APEX OF ORBIT Posterior most end of pyramid shaped orbit 4 orbital walls converge here at craniofacial junction Complex association b/w bony, neural, and vascular elements Has 2 orifices situated in the sphenoid bone Optic foramen Superior orbital fissure

3. SOF Bony cleft at orbital apex Lies b/w lateral wall and the roof of the orbit with optic strut at its superomedial margin bounded by greater and lesser wing of sphenoid the largest communication between orbit and middle cranial cavity It is situated lateral to optic foramen

4. pear-shaped with a broad base long axis extends upward at an angle of 45° from the base medially to the apex directed superotemporally . SOF is divided at the spina recti lateralis by the annulus of Zinn , the common tendinous origin of the recti muscles. DIMENSIONS Length: around 22 mm Width : 2-3 mm at the apex 7-8 mm at the base

5. Annulus of zinn encircles the optic foramen and central part of SOF,dividing it into upper,middle and lower part The superior part contains Trochlear nerve (IV) Frontal and lacrimal branches Of the ophthalmic division Of the trigeminal nerve (V1) Superior branch of ophthalmic vein Recurrent branch of the lacrimal artery(occasionally)

6. The middle part confined within the tendinous ring more susceptible to shearing injury during craniofacial trauma contains Superior and inferior branches of the oculomotor nerve (III) Nasociliary nerves (V1) Abducens nerve (VI) Fibers from the internal carotid sympathetic plexus

7. Lower part: • Inferior ophthalmic vein The inferior venous compartment is given by the confluence of the SOV and IOV which drain into the cavernous sinus

8. Located within the lesser wing of sphenoid It connects the orbit to the middle cranial fossa From an anterior view, the entrance to the optic canal is the most superior and medial structure in the apex. Attains adult dimensions by age 3 and is symmetric in most persons Optic Foramen

9. 2 bony roots that connect the lesser wing of the sphenoid with the body of the sphenoid form the optic canal. The inferior root separates the optic canal from SOF and also is referred to as the optic strut. The superior root forms the roof of the optic canal and separates it from the anterior cranial fossa. The body of the sphenoid forms the medial wall of the canal.

10. Optic canal Optic foramen: Vertically : 6-6.5mm horizontally: 4.5-5mm >7mm : Abnormal (enlarges in optic nerve gliomas, Meningiomas) Structures passing through it Optic nerve and its meningeal covering Ophthalmic artery Sympathetic nerves Optic canal: length : 8 to 10 mm width : 5 to 7 mm lateral wall is shortest medial wall is longest

11. Each optic canal passes posteromedially at an angle of approximately 35° to the sagittal opens posteriorly into the chiasmatic groove (which terminates posteriorly at the tuberculum sellae ). The canal has an intimate relationship to the sphenoid sinus , and with extensive sinus pneumatization, the optic canal may become completely surrounded by a posterior ethmoidal Onodi air cell, the sphenoid sinus, or an aerated anterior clinoid process.

12.   Throughout its intraorbital and intracanalicular course, the optic nerve is surrounded by pia mater, arachnoid, and dura mater, giving the nerve a sheath. Thus, optic nerve is a white matter tract of the brain and carries with it meningeal coverings. Within the orbit, the optic nerve is quite mobile however, within the canal, the optic nerve sheath remains adherent to the sphenoid periosteum and thus is fixed. Optic nerve glioma or Meningioma may lead to unilateral enlargement of Optic canal

13. Inferior orbital fissure 20-mm bony defect Lies between lateral wall and floor of the orbit bounded by the : • sphenoid • zygomatic • maxillary • palatine bones Communicates orbit with inf temporal fossa and pterygopalatine fossa

14. Structures passing through it: Zygomatic nerve (V2) Infraorbital nerve (V2) Infraorbital artery Infraorbital vein branch from Inferior ophthalmic vein leading to pterygoid plexus Max division of trigeminal Nerve Parasympathetics to lacrimal gland Orbital Br from pterygopalatine ganglion

15. Superior orbital fissure syndrome applies to lesions located immediately anterior to the orbital apex, including the structures exiting the annulus of Zinn and often those external to the annulus as multiple cranial nerve palsies may be seen in the absence of optic nerve pathology. Features ophthalmoplegia, upper eyelid ptosis nonreactive dilated pupil anesthesia over the ipsilateral forehead, loss of corneal sensation (and hence loss of corneal reflex orbital pain Axial proptosis. neurotrophic keratopathy

16. Syndrome Definition Orbital apex syndrome involves damage to oculomotor nerve (III) trochlear nerve (IV) abducens nerve (VI) ophthalmic branch of the trigeminal nerve (V1) with optic nerve (II) dysfunction The orbital apex syndrome is a SOF syndrome with loss of vision. Cavernous sinus syndrome (CSS) may include the features of an OAS with added involvement of the maxillary branch of the trigeminal nerve (V2) oculo -sympathetic fibers more commonly bilateral

17. Cavernous sinus syndrome  (involvement of cranial nerves III, IV, V1, V2, VI, and periarterial sympathetic plexus) sensory deficits in the maxillary branch of the trigeminal nerve orbital sympathetic innervation involvement Traumatic carotid-cavernous fistula may be present. vascular congestion proptosis Chemosis Ophthalmoplegia elevated intraocular pressure (IOP) vascular bruit CSF rhinorrhea  in fracture involving the sphenoid sinus, fovea ethmoidalis , or cribriform plate.

18. Traumatic optic neuropathy (involvement of cranial nerve II): The intracanalicular optic nerve may be damaged by sphenoid fractures The firm attachment of the dural sheath to the optic nerve may make the intracanalicular nerve particularly susceptible to acceleration or deceleration injuries.

19. The superior orbital fissure, orbital apex, and cavernous sinus are all contiguous, and although these terms define the precise anatomic locations of a disease process, the etiologies of these syndromes are similar. In some instances, patients who have features of a SOFS may subsequently develop orbital apex and cavernous sinus pathology.

20. Inflammatory (OID) 1. Thyroid orbitopathy 2. Sarcoidosis 3. Wegeners granulomatosis 4. Giant cell arteritis 5. Orbital inflammatory pseudo tumor 6. Tolosa hunt syndrome Vascular 1. Carotid cavernous aneurysm 2. Carotid cavernous fistula 3. Cavernous sinus thrombosis 4. Sickle cell anemia Etiology of Orbital Apex Syndrome

21. Infectious 1. Fungi: Aspergillosis, Mucormycosis 2. Bacteria: Streptococcus spp., Staphylococcus spp., Actinomyces spp., Gram-negative bacilli, anaerobes, Mycobacterium tuberculosis 3. Spirochetes: Treponema pallidum 4. Viruses: Herpes zoster Traumatic 1. Penetrating injury 2. Non penetrating injury 3. Orbital apex fracture 4. Retained foreign body Etiology of Orbital Apex Syndrome

22. Iatrogenic 1. Sinonasal surgery 2. Orbital/facial surgery Neoplastic 1. Head and neck tumors: nasopharyngeal carcinoma, adenoid cystic carcinoma, squamous cell carcinoma 2. Neural tumors: neurofibroma, meningioma, ciliary neurinoma, schwannoma, gliomas 3. Metastatic lesions: lung, breast, renal cell, malignant melanoma 4. Hematologic: Burkitt lymphoma, non-Hodgkin lymphoma, leukemia 5. Perineural invasion of cutaneous malignancy Etiology of Orbital Apex Syndrome

23. Clinical Presentation Vision Loss Diplopia Ophthalmoplegia Periorbital /Facial Pain Axial Proptosis Ptosis Ocular Deviation Headache Loss of sensations over the face

24. History taking h/o blunt orbital trauma h/o visual loss- whether at the time of injury or subsequently. Progressive decrease in vision suggests  optic neuropathy due to hemorrhage into the optic nerve sheath, retrobulbar hematoma, or compression by a bony fragment h/o diplopia    binocular misalignment. Diplopia will be worse in the field of gaze of the paretic muscle. h/o ptosis Past ophthalmic history- spectacles, amblyopia, strabismus, and previous ocular surgery. h/o Sensory disturbances in the distribution of V1 and V2

25. Examination Initial management in facial injuries assessing the airway security , hemodynamic stability, and cervical spine integrity. An assessment of neurologic status must be made, and head injuries must be excluded. Additional soft tissue and bony injuries of the head and neck must be sought. In patients with suspected orbital apex fractures, the examination should focus on an assessment for the presence of following that may demand acute intervention an optic neuropathy an evolving orbital compartment syndrome, or ruptured globe

26. Visual acuity : including pinhole vision and colour vision of each eye must be recorded. Confrontation visual fields may be performed at the bedside prior to more formal perimetric assessment. Assessment of pupil responses: The direct and consensual light responses An absolute or relative afferent pupil defect or an efferent pupil defect (as seen in third nerve palsy, ciliary ganglion injury, and traumatic mydriasis) is recorded.

27. Assessment of ocular motility : Volitional movements are examined at the bedside Forced ductions and force generation examinations are undertaken with appropriate topical anesthesia and patient cooperation. These assessments help differentiate between ocular motility disturbance caused by entrapped muscles, intramuscular hematoma, and nerve damage. Assessment of integrity of cranial nerve V : Sensory disturbances should be sought in the territories of branches of V1 and V2.

28. Orbital Inspection & palpation Periocular ecchymosis, edema, and proptosis in trauma Axial displacement of the globe should be assessed by exophthalmometry . Increased resistance to globe retropulsion is seen with orbital hemorrhage. Periorbital/facial pain and hypoesthesia of the forehead due to CNV involvement. Proptosis with or without orbital congestion Chemosis and/or conjunctival injection Subcutaneous emphysema Traumatic telecanthus

29. Ocular Slit lamp examination Exclude coexistent globe rupture Anterior segment examination to look for trauma related corneal injury, hyphema , iridodialysis , lens dislocation P osterior segment trauma including commotio retinae, retinal detachment, choroidal rupture, and scleral rupture. Raised IOP Assessment of optic nerve head perfusion, disc swelling, and peripapillary hemorrhages. In patients with head injuries, pharmacological pupil dilation should only be undertaken after neurosurgical consultation

30. Plain radiography The orbital apex may be visualized with 2 radiographic projections AP view for the superior orbital fissure oblique view for the optic foramen Water’s view ( occipitomental )

31. P A VI E W LATERAL VIEW Orbitoparietal oblique projection RHESE METHOD-OPTIC CANAL

32. CT scanning In facial trauma and suspected fractures, noncontrast CT scans - most appropriate initial imaging technique.   Associated intracranial injury, associated facial fractures, and intraorbital hematoma may be assessed. Axial and coronal views 3-mm cuts review the orbit, and 1-mm axial cuts may be used to assess the optic canal.

33. MRI The poor resolution of bone on MRI significantly limits its role in general orbital trauma. However, better soft tissue differentiation may be obtained. MRI reveals the abnormal signal indicative of recent hemorrhage in optic nerve sheath hematoma.   Associated neurological damage Wooden foreign bodies

34. The best resolution of orbital structures is presently obtained by MRI using standard T1w or T2w TSE pulse sequences . Fat appears hyperintense (bright) on T1w and T2w images, and other structures, such as vessels, nerves, and muscles, appear darker (hypointense) than orbital fat. Gd-DTPA enhances vascular structures, such as cavernous sinus or the venous plexus surrounding Meckel’s cave and the hypophysis. Fat suppression techniques like STIR with or without contrast enhancement are especially useful for the diagnosis of retrobulbar optic neuritis and intraorbital meningiomas.

35. Visual field assessment Automated static threshold perimetry (eg, Humphrey Visual Field analysis) or Kinetic perimetry (eg, Goldmann perimetry) used in patients with adequate cooperation and fixation to document visual field disturbance with optic neuropathy. No specific visual field loss pattern is pathognomonic for traumatic optic neuropathy.

36. Infections/DM/Tuberculosis/Syphilis/TAO/NSOI/GCA Vasculitis including SLE, RA, Wegners Granulomatosis, Sarcoidosis, Anemia Evaluation Infections, Tuberculosis, HSV, Sarcoidosis, LGBS, Invasive Aspergillosis, Lymphoproliferative disorders Granulomas, Mass Lesions, Fractures Confirmation of Diagnosis

37. Flowchart for OAS Assessment

38. Management of OAS Observation Medical Management Surgical Management Infectious: Antibiotics Antifungals Antivirals Non Infectious: Corticosteroids Immunosuppressant Spontaneous resolution under 4 weeks e.g.: OID, TO etc. Orbitotomies Endoscopic decompression Tumor removal/ debulking surgery

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