1. Grand Rounds Raafay Sophie, M.D. 6/17/2016 University of Louisville
Department of Ophthalmology and Visual Sciences

2. Patient Presentation CC: Painful, Red eye OD x 2 days HPI:
42 yo AAF who presented to the VA ER with the following complaints
"pressure" type pain. About 6/10
photophobia
seeing halos
8/7/15

3. History
POHx/ PMHx:
Had a similar episode 10 yrs ago OD, and was told she had “traumatic glaucoma”.
She says she had told the Drs at that time that a rock had hit forehead and may have grazed her eye 5 years prior to that visit.
Was started on timolol but later this was discontinued

4. History
POHx/ PMHx:
Hx of mass lesion in hippocampus which required temporal brain surgery for seizures several years before- not sure of the lesion but says that it was benign
Hx of back pain for 16 years, told she had "degenerative back disease."
Asthma
Denies any recent trauma, autoimmune diseases, skin conditions recent travels or bug bites.

5. History FAMHx: Unremarkable, no uveitis or joint disease
MEDS: PRN albuterol inhaler
ALLERGIES: None
SOCIAL Hx:
Non-smoker
Occasional alcohol drinker
Worked on computers entering and analyzing data for the army

6. Exam 6→4 55,58 VACC TP P 5→3 15 CVF: Full OU EOM: 20/30 20/20
W sph
-1.00 sph
No RAPD
CVF: Full OU
EOM:

7. Slit Lamp Exam OD OS LIDS/LASHES WNL WNL
CONJ to +2 injection mild injection
CORNEA small NG KPs clear
A/C cell and flare deep and formed
Van Herick Grade 4
IRIS WNL WNL
LENS Clear Clear

8. DFE OD OS OPTIC DISC pink and sharp pink and sharp c/d 0.2 c/d 0.1
MACULA WNL WNL
VESSELS WNL WNL
PERIPHERY WNL WNL

9. Gonioscopy Spaeth Grading OU: D/30/f 0 (no pigment)
No PAS, angle recession or cyclodialysis cleft

10. Assessment
Acute rise in IOP with mild inflammation in anterior chamber with open angle:
Glaucoma 2/2 uveitis
Posner-Schlossmann
Intermittent Angle Closure Glaucoma

11. Course In ED: Alphagan and Cosopt Q 15-20 mins 500 mg of Diamox
IOP went down to 32
Sent home on PF 1% q2hr, Cosopt BID, Brimonidine TID, and Cyclopentolate BID

12. Course Seen next day over the weekend
Improvement in photophobia and “pressure”
VA 20/20, IOP 16
Trace KPs, 0.5+ cell and flare
Sent home on PF 1% QID, Cosopt BID, and Cyclopentolate BID
Plan for follow up/work up in clinic

13. 1 week visit VA 20/20 OU IOP 16/16 SLE:
OD: trace KPS, no cell or flare
OS : wnl
DFE:
OD: confirmed that there was no vitritis or pars planitis
OS: wnl

14. 1 week visit Plan Stopped Cosopt and Cyclopentolate Taper PF
Follow up in 2 weeks with OCT, Visual fields.
Told to get previous medical records

15. 3 weeks later VA 20/20 OU IOP 20/18 SLE:
OD: No KPs, trace pigment in AC
OS : wnl
Pachymetry: Central Corneal Thickness 582/593

16. Anterior segment OCT
OD:
D/30/f
No PAS

17. Anterior segment OCT
OS:
D/30/f
No PAS

18. OD

19. OS

20. HVF (12/15/2015)

21. HVF ( 10/04/2001)

22. HVF (07/10/2000)

23. Previous medical records:
Oct 1999
“OD red, with eye pain and headache x 1 wk”
“hit in eye by rock 5 years before” – She said it hit brow and not eye
IOP on that visit was ?16?. VA 20/20. Given glasses and told to f/up
Mar 2000
“Traumatic glaucoma on Timolol BID OD”
IOP 32, 34 with 20/50 VA
Added Xalatan QHS OD

24. Previous medical records:
Sep “Traumatic glaucoma OD”
IOP of 12,11 on timolol QAM and Xalatan QHS OD
Sep “Traumatic glaucoma OD”
IOP of 9 on timolol QAM and Xalatan QHS OD
July 04- “Traumatic glaucoma OD- stable”
“Stopped timolol 2003”, not on any drops. IOP of 11 OD
“Dry eyes due to periodic watery eyes OD>OS which lasted 5 minutes or so.”

25. Assessment
Acute intermittent rise in IOP with minimal inflammation in anterior chamber with open angle:
Posner-Schlossmann Syndrome

26. Posner–Schlossman Syndrome (PSS)
Also known as Glaucomatocyclitic Crisis
First described in 1948 by Posner and Schlossman
“The hallmark of PSS is the recurrent episodes of self-limited, mild, nongranulomatous
anterior uveitis with markedly elevated intraocular pressure (IOP)“

27. Etiologies Possible Infection Cytomegalovirus Herpes Simplex Virus
PCR studies of aqueous humor of PSS patients during the acute attack have been found to be positive for CMV
Herpes Simplex Virus
PCR and Southern blot hybridization studies of aqueous humor of patients during the acute attack of PSS have been found to be positive for HSV

28. Pathogenesis Abnormal Vascular process?
Patients with PSS have been shown to have significantly lower flow-mediated vasodilation (FMD) in their brachial artery compared to controls, indicating peripheral vascular endothelial dysfunction.
Impairment of outflow facility secondary to inflammatory changes in the trabecular meshwork?
Prostaglandins, particularly prostaglandin E, have been found in higher concentration in the aqueous humor of patients during acute attacks, but not in between PSS episodes

29. Pathogenesis Other Observations:
During the acute phase, optic nerve head configuration and retinal blood flow rates are temporarily altered, these changes are reversed without any permanent damage after resolution.
Transfer coefficients of fluorescein in aqueous in the anterior chamber, by flow and by diffusion, are elevated during attacks of glaucomatocyclitic crisis. Between attacks, both coefficients return to normal.

30. Clinical picture
Almost exclusively affects individuals aged 20–50 years
A unilateral condition of recurrent mild cyclitis, lasting for a few hours to several weeks
During the acute attack, minimal symptoms of ocular discomfort and blurred vision

31. Clinical picture
There is a trace cell and flare in the anterior chamber with mild ciliary flush, and fine nonpigmented keratic precipitates on the central and inferior cornea.
Lacking the development of posterior synechiae or peripheral anterior synechiae is a typical feature of PSS
A key feature of PSS is that the rise in IOP is typically out of proportion to the inflammatory process and reaches levels above 40 mmH
This rise in IOP precedes the identifiable inflammatory reaction, often by several days.

32. Clinical picture
Gonioscopy reveals an open angle and, rarely, fine keratic precipitates may be present on the trabecular meshwork.
Between attacks, both the anterior chamber and IOP return to normal, requiring no long- term treatment.
Some patients with glaucomatocyclitic crisis may also have an underlying primary open-angle glaucoma (POAG)
May have heterochromia with anisocoria, and a large pupil in the affected eye

33. Management Control the Inflammation Prednisolone acetate 1%
Alternatively, a topical NSAID such as Diclofenac 0.1%
Usually, elevated IOP normalizes with the control of inflammation
Control IOP elevation
Topical b-blockers and/or carbonic anhydrase inhibitors are the drugs of choice
Efficacy of prostaglandin analogs is not well established

34. Management
Patients often can sense an impending attack can institute appropriate self therapy to blunt IOP elevations associated with treatment delays.
In the absence of underlying POAG, antiglaucoma agents do not prevent recurrences of glaucomatocyclitic crisis
It is important to carefully observe patients periodically for recurrences of attacks and for development of POAG.

35. Management
If PSS attacks show increased frequency and IOP fluctuations are significant, surgical intervention may be indicated, especially if there is progressive optic nerve damage and visual field loss.
Glaucoma filtration surgery is not effective in preventing recurrences of the episodes of iritis but is for management of high IOP threatening vascular perfusion
There are no evidences that laser trabeculoplasty is useful in patients with PSS.

36. THANK YOU

37. References
Posner A, Schlossman A. Syndrome of unilateral recurrent attacks of glauucoma with cyclitic symptoms. Arch Ophthalmol. 1948;39:517.
Posner A, Schlossman A. Further observations on the syndrome of glaucomatocyclitic crisis. Trans Am Acad Ophthalmol Otolaryngol ;57:531
Teoh SB, Thean L, Koay E. Cytomegalovirus in aetiology of Posner-Schlossman syndrome: Evidence from quantitative polymerase chain reaction.
Eye. Dec 2005;19(12):1338–40.
Chee SP, Bacsal K, Jap A, Se-Thoe SY, Cheng CL, Tan BH. Clinical features of cytomegalovirus anterior uveitis in immunocompetent patients.
Am J Ophthalmol. May 2008;145(5):834–40.
Masuda K, Izawa Y, Mishima S. Prostaglandins and glaucomatocyclitic crisis. Jpn J Ophthalmol. 1975;19:368.
Neufeld AH, Sears ML. Prostaglandin and eye. Prostaglandins. Aug 1973;4(2):157–75.
Nagataki S, Mishima J. Aqueous humor dynamics in glaucomatocyclitic crisis. Invest Ophthalmol. 1976;15:365
Shazly TA, Aljajeh M, Latina MA. Posner-Schlossman glaucomatocyclitic crisis. Semin Ophthalmol Jul-Sep;26(4-5):282-4