Grand Rounds

Feburary 11, 1998
50 year old male with a dull ache around his left eye.

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.

He’s 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.

PMHx:  None
Drug Allergies: None
Meds: None.
FHx: Negative


Corrected Vision: OD: 20/20-, OS: 20/100

Pupils: OD 3mm RLA; OS 4mm RLA

EOM:  Full, no nystagmus, normal saccades
OD: Normal
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.
Press to enlarge: External examination: Press to enlarge:Left eye close up picture:

IOP: OD 16 mmHg;  OS: 58 mmHg

Gonioscopy: Angles open 360 degrees OU.  There is no synechiae or neo-vascularization present.

Fundi: normal OU.

Differential Diagnosis?

The differential diagnosis of acute open angle glaucoma is:

  • Pigment dispersion glaucoma
  • Posner-Schlossman syndrome (glaumatocyclitic crisis)
  • Angle recession glaucoma
  • Pseudoexfoliation glaucoma
  • Lens-induced glaucoma
  • Ocular inflammation and secondary open-angle glaucoma



Posner-Schlossman syndrome (glaumatocyclitic crisis):

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 the condition.

Clinical Features:
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 Duane’s 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.
3. Ophthalmology 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): 608-612.
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.

Feburary 1998

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