Download A Case of Intermittently Raised IOP

Grand Rounds
Raafay Sophie, M.D.
6/17/2016
University of Louisville
Department of Ophthalmology and Visual Sciences
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
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
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.
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
Exam
20/30
VACC
55,58
TP
20/20
P
15
W -1.25 sph
-1.00 sph
CVF:
6→4
No RAPD
Full OU
EOM:
0
0
0
0
0
5→3
0
0
0
Slit Lamp Exam
LIDS/LASHES
OD
OS
WNL
WNL
CONJ
+1 to +2 injection
mild injection
CORNEA
small NG KPs
clear
A/C
+1 cell and flare
Van Herick Grade 4
IRIS
WNL
WNL
LENS
Clear
Clear
deep and formed
DFE
OD
OPTIC DISC
MACULA
VESSELS
PERIPHERY
pink and sharp
c/d 0.2
WNL
WNL
WNL
OS
pink and sharp
c/d 0.1
WNL
WNL
WNL
Gonioscopy
Spaeth Grading
OU:
D/30/f 0 (no pigment)
No PAS, angle recession or cyclodialysis cleft
Assessment

Acute rise in IOP with mild inflammation in anterior chamber with
open angle:
Glaucoma 2/2 uveitis
 Posner-Schlossmann
 Intermittent Angle Closure Glaucoma

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
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

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
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

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
Anterior
segment
OCT
OD:
D/30/f
No PAS
Anterior
segment
OCT
OS:
D/30/f
No PAS
OD
OS
HVF (12/15/2015)
HVF ( 10/04/2001)
HVF (07/10/2000)
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

Previous medical records:



Sep 2001 - “Traumatic glaucoma OD”
 IOP of 12,11 on timolol QAM and Xalatan QHS OD
Sep 2002- “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.”
Assessment

Acute intermittent rise in IOP with minimal inflammation in
anterior chamber with open angle:

Posner-Schlossmann Syndrome
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)“
Etiologies
• Possible Infection
• Cytomegalovirus
• 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
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
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.
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
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.
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 longterm 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
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
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.
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.
THANK YOU
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.
1953;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. 2011 Jul-Sep;26(4-5):282-4