Anterior segment ischaemia with giant cell arteritis

McKillop, Elisabeth; Tejwani, Deepak; Weir, Clifford R.; Jay, J L

doi:10.1139/i06-009

Cited by 17 publications

(14 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, choroidal ischemia was not observed (although fluoroscein angiography was not performed). Direct iris ischemia was one potential explanation for this patient's mydriasis, and could account for the absent response to dilute pilocarpine within the first ten days [7]. However, the absence of iris transillumination defects makes this explanation less likely.…”

Section: Discussionmentioning

confidence: 88%

“…We report the rare occurrence of GCA-related anisocoria without motility deficits, presumably due to microvascular ischemia of either the ciliary ganglion and post-ganglionic parasympathetic fibers or the iris sphincter itself [2][3][4][5][6][7]. Multiple recurrences of the patient's dilated pupil suggested ongoing microvascular insufficiency.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mydriatic pupil in giant cell arteritis

Prasad

Baccon

Galetta

2009

Journal of the Neurological Sciences

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Mydriatic pupil in giant cell arteritis

Prasad

Baccon

Galetta

2009

Journal of the Neurological Sciences

View full text Add to dashboard Cite

“…In GCA, up to 21% of cases present with no light perception vision. 3 Although GCA oftentimes presents with evidence of optic disc or retinal ischemia on clinical examination, GCA can less commonly present with anterior segment ischemia, 4 posterior ischemic optic neuropathy, cranial nerve palsies, or Horner's syndrome.…”

Section: Diagnosis and Discussionmentioning

confidence: 99%

A 71-year-old man with bilateral vision loss

2017

View full text Add to dashboard Cite

HistoryA 71-year-old white man presented to an outside hospital with acute bilateral vision loss of 1 week's duration. Five days prior to presentation he had been diagnosed with anterior uveitis by his primary ophthalmologist and was started on prednisolone acetate 1% and atropine eye drops. He reported a remote history of acute vision loss in the setting of a sinus infection with recovery of his vision following treatment of the infection.The patient's symptoms did not improve, and he was transferred to a tertiary care facility for additional workup. On further questioning, the patient endorsed new-onset headache of 2-3 weeks' duration, severe pain with chewing, scalp pain, and weight loss. He denied recent eye or head trauma. He denied recent illness, fevers, chills, night sweats, cough, and shortness of breath. He denied recent alcohol or drug use, and he denied any history of sexually transmitted diseases. ExaminationVisual acuity in each eye was no light perception, without saccades to optokinetic drum. Pupils were fixed and dilated (on atropine). Intraocular pressure was 4 mm Hg in the right eye and 5 mmHg in the left eye. The external examination was notable for right upper eyelid ptosis. The slit-lamp examination of the right eye showed significant opacification and edema of the right cornea, no keratic precipitates, and a hazy view to the anterior chamber without frank hypopyon or posterior synechiae (Figure 1). Slit-lamp examination of the left eye showed trace corneal edema, no keratic precipitates, and no cell or flare in the anterior chamber.Dilated fundus examination of the left eye was limited but showed 3+ optic nerve head edema. There was a cherry red spot. Arterioles were attenuated, and venules were dark and severely dilated (Figure 2). The peripheral retina was attached. There was no view posteriorly in the right eye. Ancillary TestingB-scan ultrasonography of the right eye showed no vitritis, posterior mass, or retinal detachment. In the left eye, optical coherence tomography (OCT) of the macula revealed diffuse macular thickening and enlarged venules (Figure 3). OCT of the retinal nerve fiber layer (RNFL) showed optic nerve head edema (Figure 4).Complete blood count was within normal limits with the exception of an elevated platelet count (484 ×10 3 /mm 3 ). Basic metabolic panel was remarkable for low sodium (132 mEq/L), potassium (2.3 mEq/L), chloride (95 mEq/L), and brain natriuretic peptide (6 mg/dL). Inflammatory markers were elevated: erythrocyte sedimentation rate (ESR) was 59 mm/hr, and C-reactive pro- Figure 1. Anterior segment photograph of the right eye demonstrating an edematous and opacified cornea without keratic precipitates.

show abstract

“…38 Acute extraocular muscle dysfunction in the elderly mandates consideration of GCA. Horner syndrome, 39 anterior segment ischemia, 40 and hypotony (likely secondary to decreased aqueous humor production) 41 have also been reported in patients with GCA.…”

Section: Ocular Manifestationsmentioning

confidence: 94%