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Grand Rounds Conference Reema Syed, MBBS University of Louisville Department of Ophthalmology and Visual Sciences October 16, 2015.

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Presentation on theme: "Grand Rounds Conference Reema Syed, MBBS University of Louisville Department of Ophthalmology and Visual Sciences October 16, 2015."— Presentation transcript:

1 Grand Rounds Conference Reema Syed, MBBS University of Louisville Department of Ophthalmology and Visual Sciences October 16, 2015

2 History CC: “when will I see?” HPI: 56 yr old white male, unhelmeted motorcyclist, involved in MVA, sustained multiple injuries, intubated on arrival in ED. Ophthalmology consulted when patient extubated 10 days later and complained he couldn’t see Ophthalmology consulted when patient extubated 10 days later and complained he couldn’t see

3 History POH, PMH: unremarkable Medications: none Allergies: none

4 Hospital Course Extensive polytrauma: facial and orbital fractures, bilateral pubic and femur fractures, right humerus and sacral fractures Liver laceration, intraperitoneal bladder rupture Underwent exploratory laparotomy and coiling of left internal iliac artery, intramedullary nails for the femur fractures, open reduction and internal fixation for right humeral fracture

5 Exam ODOS BCVA:NLP20/200 Pupils: 3 mm non-reactive 3 to 2 mm + rAPD IOP:12 mmHg 11 mmHg

6 Exam

7 Exam PLE: ODOS E/L/Lproptosis complete ptosis Conj/scleratemporal chemosis OU Corneaclear OU ACformed OU Lenswnl OU Vitreousclear OU

8 Dilated fundus exam Optic nerves sharp and pink OU Small peri-papillary flame heme OU MVP wnl OUExam

9 CT Face without contrast

10

11

12 Assessment/Plan 56 year old male with no vision OD, low vision OS + CN III and CN VI palsy OS s/p motorcycle accident with multiple orbital and long bone fractures 56 year old male with no vision OD, low vision OS + CN III and CN VI palsy OS s/p motorcycle accident with multiple orbital and long bone fractures Differentials: Differentials: Traumatic orbital apex syndrome Traumatic orbital apex syndrome Carotid cavernous fistula Carotid cavernous fistula Traumatic optic neuropathy Orbital compartment syndrome Orbital compartment syndrome Posterior ischemic optic neuropathy Plan: CTA Plan: CTA

13 CTA

14 Angiogram Right ICALeft ICA

15 Treatment Coiling of bilateral ICA dissections and embolization of left CC fistula

16 1 month Follow-up BCVA: LP OD, 20/25 OS (-1.00+0.50x180) BCVA: LP OD, 20/25 OS (-1.00+0.50x180) IOP 13, 12 IOP 13, 12

17 CC Fistula Abnormal communication between venous cavernous sinus and carotid arterial system

18 Carotid Cavernous Sinus Fistula Classification: Classification: Etiology: traumatic vs spontaneous Etiology: traumatic vs spontaneous Hemodynamic: high vs low flow Hemodynamic: high vs low flow Arterial architecture: direct or indirect Arterial architecture: direct or indirect Barrow classification Barrow classification Type A: direct (80% trauma) Type A: direct (80% trauma) Type B-D: indirect (meningeal arteries) Type B-D: indirect (meningeal arteries)

19

20 CC Fistula Presentation: Presentation: Classic triad: exophthalmos, bruit, conjunctival chemosis Classic triad: exophthalmos, bruit, conjunctival chemosis venous congestion of eyelids/conj/episclera venous congestion of eyelids/conj/episclera CN palsies III, IV, VI CN palsies III, IV, VI elevated IOP (from increased episcleral venous pressure) elevated IOP (from increased episcleral venous pressure)

21 CC Fistula Treatment Treatment - endovascular approach coil embolization coil embolization transarterial transarterial transvenous (preferred tx for indirect) transvenous (preferred tx for indirect) anterior approach through superior ophthalmic vein anterior approach through superior ophthalmic vein

22 Retrospective review of 40 CCF patients Retrospective review of 40 CCF patients Most common presentations: proptosis (65%), binocular diplopia (60%), redness (57.5%), and chemosis (47.5%) Most common presentations: proptosis (65%), binocular diplopia (60%), redness (57.5%), and chemosis (47.5%) No radiologic evidence of enlarged SOV in 26% of patients on noninvasive imaging and in 8% on catheter angiography No radiologic evidence of enlarged SOV in 26% of patients on noninvasive imaging and in 8% on catheter angiography To avoid inappropriate interventions or delays in diagnosis and care, it is important to recognize that CCF can exist without SOV enlargement. To avoid inappropriate interventions or delays in diagnosis and care, it is important to recognize that CCF can exist without SOV enlargement.

23 Traumatic Optic Neuropathy Indirect: transmitted shock from an orbital impact to the intracanalicular portion of optic nerve Direct: penetrating injury, bony fragments in the optic canal, orbital hemorrhage and optic nerve sheath hematoma causing compression of optic nerve

24 Indirect Traumatic Optic Neuropathy High dose steroids – extrapolated from High dose steroids – extrapolated from the National Acute Spinal Cord Injury Study II CRASH study (Corticosteroid Randomization After Significant Head injury) - increased relative risk of death in patients given high dose steroids after significant head injury The International Optic Nerve Trauma Study – no difference in final visual acuity between patients that were observed compared with those given steroids

25 48 year M, unhelmeted motorcyclist involved in MVA Fracture of left sphenoid sinus involving the optic canal Vision improved from LP to 20/40 in 6 weeks

26 References BCSC Neuro-ophthalmology BCSC Neuro-ophthalmology BCSC orbit, eyelids and lacrimal system Moron F, Klucznik R, et al. Endovascular treatment of high-flow carotid cavernous fistulas by stent-assisted coil placement. AJNR Am J Neuroradiol 2005;26:1399-1404. Korkmazer B, Kocak B, et al. Endovascular treatment of carotid cavernous sinus fistula: A systematic review. World J Radiol 2013;5(4):143-155

27 Thank you


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