A i.e. Cavernous sinus Abrupt (sudden/ very rapid) onset of marked systemic features (high grade fever) with proptosis, chemosis especially with prostration, sequential ophthalmoplegia (i.e. initial lateal gaze involvement), bilateral involvement and mastoid edemaQ strongly suggest the diagnosis of cavernous sinus thrombosis. - In cavernous sinus, the ophthmic division of trigeminal (Vi)nerve picks up sympathetic fibers from cavernous plexus. These are for dilator papillae muscle. Vi divides just posterior to superior orbital fissure into 3 branches (lacrimal nerve, frontal nerve, nasociliary nerve), which pass through superior orbital fissureQ - Lesions of cavernous sinus e.g. thrombosis, rupture of aneurysm of internal carotid aery at may lead to paralysis of 3rd 4th, 5th and 6th nerve Q Feature Cavernous Sinus Thrombosis Orbital Cellultis Orbital Apex Syndrome Arise from - Most septic CST arise from - Exension of inflammation - < 1% of orbital cellulitis result in sphenoid or ethmoid sinuses >> from neighbouring tissues esp OAS; howeve, >50% of these dental, facial & ear infection by gram positive bacteria sinuses (mc ethmoid); eyelid, eyeball, face etc or occur in patient with diabetes meltitus and most frequently - Aseptic thrombosis (rare) is penetrating injuries & d/t rhinocerebral caused by conditions that 1/t surgeries mucormycosis. venous thrombosis eg - Bacterial OC is more common - Ketoacidosis is most impoant polycythemia, sickle cell anemia, in children whereas, fungal risk factor b/o lack of inhibitory (vasculidities), trauma, neurosurgery, pregnancy & oral condraceptive use. (mucor or Aspergillus) affect diabetic (ketoacidosis) & immune compromised activity against Rhizopus in serum. Involve Cavernous sinus i.e. - All orbital contents may be - Superior orbital fissure - 6th CN & carotid plexus of involved and may evolve into transmitting 3rd,4th, 6th and Vi sympathetic nerves run through the substance orbital abscess cranial nerves - Optic canal transmitting optic - 3rd,4th,ophthalmic (Vi) and maxillary (V2) division of 5th (2nd) cranial nerve CN and trigeminal ganglion lie in lateral wall Onset & progression Abrupt / violent /Very RapidQ Slower (relatively) Slower (relatively) Systemic Features MarkedQ (fever, headache, nausea, vomiting) Mild (less prominent) Mild (less prominent) Mastoid edema DiagnosticQ (Present) Absent Absent Laterality Bilateral (in >50%), although initially unilateral Unilateral Unilateral Proptosis & Chemosis Marked (with eye pain) Marked (with severe eye pain) Mild to moderate (do not always complain of pain) Vision Not affected in early stagesQ May lost early if retrobulbar Lost in early stages d/t optic (2" CN) optic neuritis or compression develop nerve involvement (RAPD) present Ophthalmoplegia Sequential (beginning with 6th Concurrent & complete Concurrent & complete external (3,4,6 CN) nerve) and completeQ. Initial external ophthalmoplegia ophthalmoplegia involving 3rd,4th lateral rectus (gaze) palsyQ is d/ t early involvement of 6th nerve in substance of CS. involving 3rd,4th & 6th nerve & 6th nerve Irigeminal (V) nerve Opthalmic (V1) and maxillary - Opthalmic (V1) division involved (5 CN) (V2) division involved (= decreased corneal sensation) Clinical Features Abrupt onset marked periorbital Signs of anterior eye Visual loss (2" CN) and edema, orbital congestion (chemosis), proptosis, adnexal involvement (chemosis, edema) are usually out of ophthalmoplegia are out of propoion and often precede edema, eye pain, ptosis and ophthalmoplegia (involving 3rd, 4th, 6th cm CN) with involvement of VI & Vz. propoion to ophthalmoplegia at least initially signs of anterior eye involvement, such as proptosis periorbital (adnexel) edema, and orbital congestion