Aching left eye.
He complains of a dull ache around his left eye for three days.
The pain is slightly relieved by ice. Over the last day he has noticed haloes.
He has no nausea, and his appetite is normal.
Hes just arrived here 10 days ago
from a 6 year trip to Korea.
He has had 4 or five similar episodes of left eye pain over the last
three years all of which resolve spontaneously, each lasting about 5 days.
Drug Allergies: None
Corrected Vision: OD: 20/20-, OS: 20/100
Pupils: OD 3mm RLA; OS 4mm RLA
EOM: Full, no
nystagmus, normal saccades
OS: External examination is normal. The conjuntiva shows no
injection. The cornea is diffusely thickened and hazy, and there are fine keratic
precipitates on the central endothelium. The anterior chamber is deep and there are
rare cells and 1+ flare present. There is no iris heterchromia. The remainder of the
SLE is normal.
enlarge: External examination: Press to enlarge:Left eye close up
IOP: OD 16 mmHg; OS: 58 mmHg
Gonioscopy: Angles open 360 degrees
OU. There is no synechiae or neo-vascularization present.
Fundi: normal OU.
The differential diagnosis of acute open
angle glaucoma is:
- Pigment dispersion glaucoma
- Posner-Schlossman syndrome (glaumatocyclitic
- Angle recession glaucoma
- Pseudoexfoliation glaucoma
- Lens-induced glaucoma
- Ocular inflammation and secondary open-angle
Because of the small amount of inflammation
in the affected eye with open angles and absence of other pathologic findings, our patient
was diagnosed with Posner-Schlossman syndrome.
Glaumatocyclitic crisis was first described in 1948 by Posner and Schlossman. It is
characterized by recurrent episodes of mild unilateral inflammation associated with
markedly elevated intraocular pressure. This condition usually occurs between the
ages of 20 and 60. The affected pupil may be larger. No racial predilection
has been reported.
The exact etiology of this condition is unknown. Prostaglandin (PGE2
and PGFa) levels increase in the aqueous humor during acute attacks6. This may be
responsible for the decreased outflow facility and breakdown of the blood aqueous barrier
with release of proteins and cells into the anterior chamber. In one study, genomic
fragments of herpes simplex virus were found in the aqueous of patients during acute
attacks7 which could point towards HSV playing a role in the origin of
Posner-Schlossman syndrome,however it is argued that mild HSV keratitis may mimic
glaumatocyclitic crisis. In another study, phagocytic mononuclear cells were found
plugging the trabecular inter spaces of a patient with Posner-Schlossman syndrome, which
may lead to the raised IOP8. However, more work is needed to determine the cause of
Symptoms include mild discomfort and blurred vision and haloes if
corneal edema is present. The affected eye typically appears white and quiet on gross
inspection, but a small amount of inflammation can usually be detected. The anterior
chamber is deep. A common finding is that the pupil is slightly dilated in the affected
eye compared to the unaffected eye. Intraocular pressures may stay elevated for
several weeks and then return to normal. Between recurrences, no abnormality may be
noted. Posterior and anterior synechiae do not form in this condition. Although
episodes are self limited, glaucomatous cupping and field loss may occur10.
There is an association between
glaucomatocyclitic crisis and primary open angle glaucoma10. The endothelial cell
density is lower in effected eyes than in the contralateral healthy eye, an observation
that is thought to be due to the recurrent attacks of elevated pressure9.
Topical aqueous suppressants and oral carbonic anhydrase inhibitors
are useful to control the intraocular pressure. Topical corticosteroids are used to
decrease the inflammation. Given the possible role of prostaglandins in this condition,
prostaglandin inhibitors such as oral indomethacin have been tried with anecdotal success.
1. Godfrey, WA and Warren AW. Acute Anterior Uveitis in Duanes Clinical
Ophthalmology. (Lippincott-Raven: Philadelphia, 1996) (4) 40: 9.
2. American Academy of Ophthalmology . Glaucoma in Basic and Clinical Science
Course, 1996-97, (AAO: San Francisco, 1996) (10) 77.
Grand Rounds, The Digital Journal of Ophthalmology. MEEI (Boston) http://www.djo.harvard.
4. Raitta C, et al. Glaucomatocyclitic crisis. Arch Ophthalmol. 1977 Apr; 95(4):
5. Hung PT, et al. Treatment of glaucomatocyclitic crises. Am J Ophthalmol.
1974 Feb; 77(2): 169-172.
6. Masuda K, Izawa Y, Mishima S: Prostaglandings and glaumatocyclitic crisis. Jpn J
Ophthalmol 19:368 (1975)
7. Yamamoto S, et al. Possible role of herpes simplex virus in the origin of
Posner-Schlossman syndrome. Am J Ophthalmol. 1995 Jun; 119(6): 796-798.
8. Harstad HK, et al. Glaucomatocyclitic crises (Posner-Schlossman syndrome). A case
report. Acta Ophthalmol (Copenh). 1986 Apr; 64(2): 146-151.
9. Setala K, et al. Endothelial cells in the glaucomato-cyclitic crisis. Adv
Ophthalmol. 1978; 36: 218-224.
10. Kass MA, et al. Glaucomatocyclitic crisis and primary open-angle glaucoma. Am J
Ophthalmol. 1973 Apr; 75(4): 668-673.
Maintained by Frank
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