M&m may09f

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  • Morning after presentation
  • LEFT EYE 18seconds, 21.3 seconds, 24.8 seconds, 31.2 seconds
  • Left eye 36.5 seconds, 42.8 seconds, 55.4 seconds, 1.24 minutes
  • Right eye 7.7 seconds, 11.3 seconds, 13.4 seconds, 15.3 seconds
  • Right eye 17 seconds, 18.8 seconds, 20.8 seconds, 23.2 seconds
  • Right eye 25.1 seconds, 30.7 seconds, 36 seconds, 39.8 seconds
  • Right eye 47.8 seconds, 54.3 seconds, 57.2 seconds, 1.04 minutes
  • Right eye 1.16 minutes Left eye 1.33 minutes 1.41 minutes, 1.52 minutes
  • Right eye 3.21 minutes, 6.11 minutes Left eye 3.47 minutes , 6.42 minutes
  • Right eye 9.35 minutes Left eye 952 minutes
  • M&m may09f

    1. 1. Morbidity & Mortality Conference May 19, 2009 Michele Todman
    2. 2. 20/20 OD, NLP OS Photos 12/1/08
    3. 3. Red Free
    4. 4. Anatomy <ul><li>Ophthalmic artery 1 st branch of internal carotid within the skull </li></ul><ul><li>CRA, 2 posterior ciliary arteries, muscular branches - 7 anterior ciliary arteries </li></ul>
    5. 5. Mechanism of Vision Loss in GCA secondary to A-AION <ul><li>GCA almost always causes occlusion of the posterior ciliary arteries, occasionally of the central retinal artery, and rarely of the ophthalmic artery </li></ul><ul><li>PCA’s also supply cilioretinal artery so occlusion of PCA results in occlusion of cilioretinal artery too </li></ul><ul><li>Optic nerve head mainly supplied by posterior ciliary arteries and complete occlusion of PCA’s and no blood flow in optic nerve head results in infarction </li></ul>
    6. 6. Laboratory Data   6.5 505 37.8 135 3.5 103 23 11 0.9 213 12.8 ESR: 67 CRP: 92.9 (0-8 MG/L) Thrombocytosis in patients with biopsy-proven giant cell arteritis. Foroozan, Danesh-Mayer, Savino et al. Ophthalmology 2002
    7. 7. FA 18s 21.3s 24.8 31.2s
    8. 8. 36.5s 55.4s 6.06m 1.24m
    9. 9. 12/3/08 NLP OU
    10. 10. Red Free
    11. 11. Right eye 7.7 seconds, 11.3 seconds, 13.4 seconds, 15.3 seconds
    12. 12. Right eye 17 seconds, 18.8 seconds, 20.8 seconds, 23.2 seconds
    13. 13. Right eye 25.1 seconds, 30.7 seconds, 36 seconds, 39.8 seconds
    14. 14. Right eye 47.8 seconds, 54.3 seconds, 57.2 seconds, 1.04 minutes
    15. 15. Right eye 1.16 minutes Left eye 1.33 minutes, 1.41 minutes, 1.52 minutes
    16. 16. Right eye 3.21 minutes, 6.11 minutes Left eye 3.47 minutes, 6.42 minutes
    17. 17. Right eye 9.35 minutes Left eye 952 minutes
    18. 23. “ GCA ranks as the prime medical emergency in ophthalmology, there being no disease in which the prevention of blindness depends so much on prompt recognition and early treatment”-Kearns, TP <ul><li>How do we make an early diagnosis of GCA? </li></ul><ul><li>What is the proper treatment to prevent blindness; do IV vs. oral steroids make a difference? </li></ul><ul><li>Why can vision continue to decrease even after therapy has begun? </li></ul><ul><li>Can blindness be reversed? </li></ul>
    19. 24. ROAD to recovery in A-AION <ul><li>Perfusion pressure=mean blood pressure-IOP </li></ul><ul><li>Narrowing of PCA causes fall in perfusion pressure in the optic nerve head circulation </li></ul><ul><li>Nocturnal arterial hypotension may lead to further fall in perfusion pressure and transient hypo-perfusion or non-perfusion of optic nerve head </li></ul><ul><li>Restoration of BP to normal when awakening could restore some circulation to optic nerve head </li></ul><ul><li>This may explain true neuronal recovery, resulting in visual improvement in a few eyes </li></ul>
    20. 25. Visual Improvement with corticosteroid therapy in giant cell arteritis. Report of a large study and review of the literature Hayreh et al. 2002 Acta Ophthalmol. Scand. (84 patients with GCA confirmed by TAB over 25 years) <ul><li>4% of patients improved in both VA and central visual field within first 6 weeks after the acute visual loss </li></ul><ul><li>Goal of steroid therapy in GCA is to help prevent visual loss, not reverse it </li></ul><ul><li>If arterial supply to optic nerve head or retina is completely occluded, neither steroid therapy nor any other treatment can re-establish the circulation and reverse the ischemic damage </li></ul>
    21. 26. Giant cell arteritis: validity and reliability of various diagnostic criteria. Hayreh et al. Am J Ophthalmol 1997 363 patients with TAB- prospective study 22 years 106 positive TAB and 257 Negative TAB <ul><li>21.2% of patients with visual loss and positive TAB for GCA had no systemic symptoms </li></ul><ul><li>Odds of having TAB positive GCA were 9 times greater with jaw claudication, 3.4 x greater with neck pain, 3.2 x greater with CRP>2.45 mg/dl </li></ul><ul><li>ESR AND CRP together have the best specificity- 97% </li></ul><ul><li>Thrombocytosis, 60.4% in this study </li></ul><ul><li>AGE > 50 years old (Median 75.8 years, mean 77 years) </li></ul><ul><li>Caucasian main racial group affected </li></ul><ul><li>Amaurosis Fugax </li></ul><ul><li>TAB considered definitive criterion for diagnosis of GCA </li></ul>
    22. 27. Visual Deterioration in Giant Cell Arteritis Patients while on High Doses of Corticosteroid Therapy Hayreh et al. 2003 Ophthalmology (144 Patients with GCA confirmed by TAB data collected over 25 years) <ul><li>4% patients with visual loss in one or both eyes at presentation developed further visual loss despite high doses of systemic corticosteroids </li></ul><ul><li>Visual deterioration on high dose corticosteroids when occurred happened within 5 days of the start of therapy, no loss if not within 5 days </li></ul><ul><li>No evidence that IV megadose therapy followed by 80mg-120mg oral prednisone is superior to high-dose oral steroid therapy alone </li></ul><ul><li>Patients followed every 2-3 weeks until prednisone dose tapered to 40mg daily. Thereafter, patients are followed at 4-6 week intervals until a low stable dose achieved and they are then followed every 3 months. </li></ul><ul><li>Steroid taper should begin when BOTH ESR and CRP reach their lowest levels </li></ul>

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