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Possner Schlossman
Syndrome (PSS)
• First described by Posner and Schlossman following case reports and coined the term in 1948
• Based on a group patients who suffered from recurrent unilateral attacks of ocular hypertension
and shared sx:
 Unilateral eye involvement
 Recurrent
 Mild discomfort and BOV
 Increased IOP with open angles
 Mild anterior chamber reaction /fine scattered keratoprecipitates
 Each attack can last several hours to weeks
 Normal IOP and no signs of uveitis in between attacks
 Normal VF and OD
1 Posner, Adolph, and ABRAHAM SCHLOSSMAN ‘’Syndrome of recurrent attacks of glaucoma with cyclitic symptoms.’’
Archives of Opthalmology 39.4 (1948): 517-535.
Epidemiology
• Typically affects between age 20 -50 yrs
• M > F (1.5:1)
• Generally, only one eye affected at one time
• Unilateral >>> Bilateral
Pathophysiology
• There are several proposed mechanism:
1 )Vascular endothelial dysfuntion
- Leads to local ischemia of iris and TM
- Ischemia of TM —> poor TM outflow
—> elevated IOP
3 Raitta C. Vannas A. ‘’Glaucomatocyclitic crisis’’. Arch Opthalmol. 1977;95:608
2) Inflammatory process
- Elevated level of PG found in AC samples of PSS patients
- PG —> breakdown of blood aqueous barrier —> increased production
of Aqueous fluid
- Inflammation —> cellular debris in TM —> decreased outflow,
elevated IOP
3) Infectious
- Infectious trabeculitis -> dysfunction of TM and WBC plugging of
damaged TM -> decreased aqueous outflow
- CMV, H. Pylori, HSV/VZV
- Based on retrospective case series (67 patients with clinical diagnosis
of Posner Schlossman Syndrome ,52.2% showed presence of CMV in
AC tap PCR)
• Diagnosis of exclusion
• Clinical diagnosis
• Exam findings:
Vision 6/6 to HM/PL
Conjunctiva Minimal to no ciliary flush
IOP Generally elevated and in the range of 40-60mmHg.
It is related to number of days of inflammation and not the
severity of inflammation.
IOP is elevated out of proportion to the amount of AC
inflammation
Cornea Depends on the degree of cornea edema, may be
odematous when IOP > 40mmHg
Fine Kps may be present. Usually appear after 2-3 days
AC Deep with AC cells present. The IOP is out of proportion to
the inflammation
Gonio: open angle
Iris Segmental ischemia may be present
PAS may be present.
Pupil Often slightly dilated/ sluggish
Optic nerve May demonstrate glaucomatous cupping during acute
attack
Management
• Initial treatment is directed towards controlling IOP and decreasin
inflammation
• Medical Therapy
1. First line Topical Beta Blockers, Alpha agonist and Carbonic anhy
inhibitors
2. PG analogue not first line as there is evidence suggesting that P
further exacerbate inflammation.
3. Oral carbonic anhydrase inhibitors are sometimes used acutely
IOP
4. Topical steroid may be used to control inflammation
5. Miotics and mydriatic agents are rarely used
Surgical Therapy
• In certain cases where IOP cannot be controlled using maximal
medical therapy —> surgical tx may be considered esp when signs of
glaucomatous optic nerve damage / VF changes appear
• One case series reported 8 patients with PSS who underwent
trabeculectomy with mitocin –C for uncontrolled IOP+ VF defects. At
the end of follow up, all 8 patients did not require IOP lowering
eyedrops and IOP remained stable during episodes of attacks.
Prognosis
• PSS has long thought to be ‘’benign’’ but is now recognized as
relatively rare cause of chronic secondary glaucoma
• Most patients are treated for attacks and most of them recover
without long term sequelae
• However, some patients with recurrent attacks, even treated may
show long term glaucomatous changes in ON and VF defects.
Quiz (True or False)
1. Patient with PSS often have extreme cell flare on exam out of
proportion to their degree of IOP elevation
2. Which infection has PSS been most commonly associated with
3. In patients with PSS, bilateral eye involvement is more common
with high IOP and marked AC inflammation
Thank you

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Posner Schlossman Syndrome

  • 2. • First described by Posner and Schlossman following case reports and coined the term in 1948 • Based on a group patients who suffered from recurrent unilateral attacks of ocular hypertension and shared sx:  Unilateral eye involvement  Recurrent  Mild discomfort and BOV  Increased IOP with open angles  Mild anterior chamber reaction /fine scattered keratoprecipitates  Each attack can last several hours to weeks  Normal IOP and no signs of uveitis in between attacks  Normal VF and OD 1 Posner, Adolph, and ABRAHAM SCHLOSSMAN ‘’Syndrome of recurrent attacks of glaucoma with cyclitic symptoms.’’ Archives of Opthalmology 39.4 (1948): 517-535.
  • 3. Epidemiology • Typically affects between age 20 -50 yrs • M > F (1.5:1) • Generally, only one eye affected at one time • Unilateral >>> Bilateral
  • 4. Pathophysiology • There are several proposed mechanism: 1 )Vascular endothelial dysfuntion - Leads to local ischemia of iris and TM - Ischemia of TM —> poor TM outflow —> elevated IOP 3 Raitta C. Vannas A. ‘’Glaucomatocyclitic crisis’’. Arch Opthalmol. 1977;95:608
  • 5. 2) Inflammatory process - Elevated level of PG found in AC samples of PSS patients - PG —> breakdown of blood aqueous barrier —> increased production of Aqueous fluid - Inflammation —> cellular debris in TM —> decreased outflow, elevated IOP
  • 6. 3) Infectious - Infectious trabeculitis -> dysfunction of TM and WBC plugging of damaged TM -> decreased aqueous outflow - CMV, H. Pylori, HSV/VZV - Based on retrospective case series (67 patients with clinical diagnosis of Posner Schlossman Syndrome ,52.2% showed presence of CMV in AC tap PCR)
  • 7. • Diagnosis of exclusion • Clinical diagnosis
  • 8. • Exam findings: Vision 6/6 to HM/PL Conjunctiva Minimal to no ciliary flush IOP Generally elevated and in the range of 40-60mmHg. It is related to number of days of inflammation and not the severity of inflammation. IOP is elevated out of proportion to the amount of AC inflammation Cornea Depends on the degree of cornea edema, may be odematous when IOP > 40mmHg Fine Kps may be present. Usually appear after 2-3 days AC Deep with AC cells present. The IOP is out of proportion to the inflammation Gonio: open angle Iris Segmental ischemia may be present PAS may be present. Pupil Often slightly dilated/ sluggish Optic nerve May demonstrate glaucomatous cupping during acute attack
  • 9.
  • 10. Management • Initial treatment is directed towards controlling IOP and decreasin inflammation • Medical Therapy 1. First line Topical Beta Blockers, Alpha agonist and Carbonic anhy inhibitors 2. PG analogue not first line as there is evidence suggesting that P further exacerbate inflammation. 3. Oral carbonic anhydrase inhibitors are sometimes used acutely IOP 4. Topical steroid may be used to control inflammation 5. Miotics and mydriatic agents are rarely used
  • 11. Surgical Therapy • In certain cases where IOP cannot be controlled using maximal medical therapy —> surgical tx may be considered esp when signs of glaucomatous optic nerve damage / VF changes appear • One case series reported 8 patients with PSS who underwent trabeculectomy with mitocin –C for uncontrolled IOP+ VF defects. At the end of follow up, all 8 patients did not require IOP lowering eyedrops and IOP remained stable during episodes of attacks.
  • 12. Prognosis • PSS has long thought to be ‘’benign’’ but is now recognized as relatively rare cause of chronic secondary glaucoma • Most patients are treated for attacks and most of them recover without long term sequelae • However, some patients with recurrent attacks, even treated may show long term glaucomatous changes in ON and VF defects.
  • 13. Quiz (True or False) 1. Patient with PSS often have extreme cell flare on exam out of proportion to their degree of IOP elevation 2. Which infection has PSS been most commonly associated with 3. In patients with PSS, bilateral eye involvement is more common with high IOP and marked AC inflammation