Morbidity & Mortality

Conference

May 19, 2009

Michele Todman

20/20 OD, NLP OS

Photos 12/1/08

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AnatomyAnatomy Ophthalmic artery 1st branch of internal carotid within the skull

CRA, 2 posterior ciliary arteries, muscular branches - 7 anterior ciliary arteries

Mechanism of Vision Loss Mechanism of Vision Loss in GCA secondary to A-AIONin GCA secondary to A-AION

GCA almost always causes occlusion of the posterior ciliary arteries, occasionally of the central retinal artery, and rarely of the ophthalmic artery

PCA’s also supply cilioretinal artery so occlusion of PCA results in occlusion of cilioretinal artery too

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

 

6.5 505

37.8

135

3.5

103

23

11

0.9213

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

Laboratory DataLaboratory Data

FAFA

18s 21.3s

24.831.2s

36.5s 55.4s

6.06m1.24m

12/3/0812/3/08NLP OUNLP OU

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Right eye 7.7 seconds, 11.3 seconds, 13.4 seconds, 15.3 secondsRight 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 secondsRight eye 17 seconds, 18.8 seconds, 20.8 seconds, 23.2 seconds

Right eye 25.1 seconds, 30.7 seconds, 36 seconds, 39.8 secondsRight 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 minutesRight eye 47.8 seconds, 54.3 seconds, 57.2 seconds, 1.04 minutes

Right eye 1.16 minutesRight eye 1.16 minutesLeft eye 1.33 minutes, 1.41 minutes, 1.52 minutesLeft eye 1.33 minutes, 1.41 minutes, 1.52 minutes

Right eye 3.21 minutes, 6.11 minutesRight eye 3.21 minutes, 6.11 minutesLeft eye 3.47 minutes, 6.42 minutesLeft eye 3.47 minutes, 6.42 minutes

Right eye 9.35 minutesRight eye 9.35 minutesLeft eye 952 minutesLeft eye 952 minutes

““GCA ranks as the prime medical emergency in GCA ranks as the prime medical emergency in ophthalmology, there being no disease in which the ophthalmology, there being no disease in which the prevention of blindness depends so much on prompt prevention of blindness depends so much on prompt

recognition and early treatment”-Kearns, TPrecognition and early treatment”-Kearns, TP

How do we make an early diagnosis of GCA? What is the proper treatment to prevent blindness;

do IV vs. oral steroids make a difference? Why can vision continue to decrease even after

therapy has begun? Can blindness be reversed?

ROAD to recovery in A-AIONROAD to recovery in A-AION

Perfusion pressure=mean blood pressure-IOP Narrowing of PCA causes fall in perfusion

pressure in the optic nerve head circulation Nocturnal arterial hypotension may lead to further

fall in perfusion pressure and transient hypo-perfusion or non-perfusion of optic nerve head

Restoration of BP to normal when awakening could restore some circulation to optic nerve head

This may explain true neuronal recovery, resulting in visual improvement in a few eyes

Visual Improvement with corticosteroid Visual Improvement with corticosteroid therapy in giant cell arteritis. therapy in giant cell arteritis.

Report of a large study and review of the literatureReport of a large study and review of the literatureHayreh et al. 2002 Acta Ophthalmol. Scand.Hayreh et al. 2002 Acta Ophthalmol. Scand.

(84 patients with GCA confirmed by TAB over 25 years)(84 patients with GCA confirmed by TAB over 25 years)

4% of patients improved in both VA and central visual field within first 6 weeks after the acute visual loss

Goal of steroid therapy in GCA is to help prevent visual loss, not reverse it

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

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

21.2% of patients with visual loss and positive TAB for GCA had no systemic symptoms

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

ESR AND CRP together have the best specificity- 97% Thrombocytosis, 60.4% in this study AGE > 50 years old (Median 75.8 years, mean 77 years) Caucasian main racial group affected Amaurosis Fugax TAB considered definitive criterion for diagnosis of GCA

Visual Deterioration in Giant Cell Arteritis Patients while Visual Deterioration in Giant Cell Arteritis Patients while on High Doses of Corticosteroid Therapyon High Doses of Corticosteroid Therapy

Hayreh et al. 2003 OphthalmologyHayreh et al. 2003 Ophthalmology(144 Patients with GCA confirmed by (144 Patients with GCA confirmed by

TAB data collected over 25 years)TAB data collected over 25 years) 4% patients with visual loss in one or both eyes at presentation

developed further visual loss despite high doses of systemic corticosteroids

Visual deterioration on high dose corticosteroids when occurred happened within 5 days of the start of therapy, no loss if not within 5 days

No evidence that IV megadose therapy followed by 80mg-120mg oral prednisone is superior to high-dose oral steroid therapy alone

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.

Steroid taper should begin when BOTH ESR and CRP reach their lowest levels