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case report.This is a 60 years old female patient, a known Glaucoma patient:pptx
- 1. Unilateral acute granulomatous annterior uvitis + high IOP
- 2. OUTLINE • Introduction • Case Report • Discussion • Summary • References 2
- 3. Identification • Date of registration :3/9/15 EC • Name: • Age: 70 • Sex: m • Address: 3
- 4. • History – C/C : Itching sensetion of 1month duration (OU) – HPI : this is a 70 yrs old male pt presented with itching sensetion, foreign body sensetion and tearing of right eye for past 1 month – He also complains decreased vision for past 3yrs
- 5. Examination • VA OD 6/24 • IOP OD 44 • OS 6/18 • OS 12
- 6. SLE OD • Eelid /eye lash : no crusting ,no telangiectatic vessels over posterior lid • Conjunctiva : cilliary injection ,sub epithelial concretion • Cornea : whitish mutanfat kps,AS, • A/C: + 3 VH, No cell / flare,no atrophy OS • no crusting ,no telangiectatic vessels over posterior lid • Conjunctiva : cilliary injection ,sub epithelial concretion • Cornea : transparent, AS • A/C: + 3 VH, No cell / flare,no atrophy
- 7. OD • Lens : nuclear and psco OS • Lens : nuclear and psco
- 8. UVEITIS AND ELEVATED PRESSURE • Glaucomatocyclitic crisis • Fuchs heterochromic iridocyclitis • Herpes zoster or simplex-associated uveitis • Phacolytic and/or phacoantigenic glaucoma • Ciliary body inflammation and rotation with angle closure glaucoma
- 9. • Uveitis encompasses a large, diverse group of conditions, many of which are accompanied by IOP at some point in their clinical course. • In a particular patient with uveitis, the IOP may range from • quite low to very high, because inflammation decreases both – the rate of aqueous humor formation and – the ease of aqueous humor exit from the eye.
- 10. Cont… • The major causes of impaired outflow and thus elevated pressure are as follows: – Temporary blockage of trabecular meshwork by inflammatory debris – Peripheral anterior synechiae (PAS) formation related to organization of debris in – the angle and gradual incorporation of the iris – Appositional and then synechial angle closure caused by pupillary block from – posterior synechiae formation – Steroid-induced pressure elevation related to the treatment of ocular inflammation
- 11. • What is the goals of the evaluating of patients with uveitis and elevated pressure ? – Recognizing Particular Uveitis/Glaucoma Syndromes – to recognize those patients who have one of the chronic uveitis syndromes, most commonly • sarcoidosis or • juvenile idiopathic arthritis, so that their care can be planned for the long term from the outset.
- 12. Recognizing Particular Uveitis/Glaucoma Syndromes Glaucomatocyclitic Crisis • Typically presents as an acute unilateral pressure elevation associated with mild inflammation. • The patient's complaints relate to – corneal edema – either blurring or halo vision. – Pressures often reach the range of 40 to 55 mmHg, and – the anterior chamber has a modest cellular response with little or no flare. – The eye is not red. – Keratic precipitates may be absent initially but usually develop within a few days, • The usual error in diagnosis is to attribute the signs and symptoms to acute angle closure.
- 13. • Exam findings • The vision can vary from 20/20 to hand motion or light perception depending on the amount of corneal epithelial edema, although • the amount of edema is usually mild. • The pupil is often slightly dilated or sluggish. The conjunctiva is usually white and quiet, although a mild ciliary flush may be present. There may be small-to- medium, discrete, round, white keratic precipitates on the endothelium, usually in an inferior distribution (see Figure 2). The KPs usually resolve on their own or with anti-inflammatory treatment. The anterior chamber is deep with a mild iritis without significant cell or flare. In the past, iris atrophy or heterochromia has been noted in some cases, but it is not currently considered a characteristic finding for PSS. • Figure 2: Small, white, discrete keratic precipitates. • The IOP is often markedly elevated, usually 40-50 mmHg. Characteristically, IOP elevation is out of proportion to the amount of anterior chamber inflammation, and significant corneal epithelial edema may develop. IOP elevation may last from several hours to weeks and may precede or follow the anterior chamber reaction.
- 14. • An important criteria for diagnosis is an open angle on gonioscopy. Peripheral anterior synechiae are generally not present despite the presence of anterior chamber inflammation. • Early case series have noted the presence of angle abnormalities such as • an anteriorly displaced Schwalbe’s line, • prominent iris processes, or • a fine membrane covering the trabecular meshwork, but these are not considered typical diagnostic features.
- 15. • The optic nerve can demonstrate acute glaucomatous cupping during an acute attack, as well as decreased perfusion due to the sharp rise in IOP. • However, many patients present with normal appearing nerves in an active episode. • Cupping may reverse after the IOP returns to normal. • In cases of repeated attacks over a long period of time, persistent glaucomatous cupping may be observed indicating some degree of permanent damage to the optic nerve
- 17. • Ancillary testing – Iris angiograms performed during acute attacks demonstrate segmental iris ischemia, vascular congestion and vessel leakage. Interestingly in one case series, iris angiograms performed during the “prodromal phase” when IOP was not elevated also demonstrated focal iris ischemia.
- 18. • Associations • Primary open-angle glaucoma (POAG): Up to a 45% concomitance between PSS and POAG has been reported. Kass et al. described a case series of 11 PSS patients, some of whom demonstrated persistent elevated IOP in the affected eye between episodes, as well as fellow eyes with an elevated IOP.[15] Five patients demonstrated typical glaucomatous visual field loss, and four developed glaucoma optic nerve change on follow-up. • It has also been suggested, however, that persistent IOP elevation during frequent, recurrent attacks may lead to the same changes. • Non-arteritic ischemic optic neuropathy (NAION): 2 cases of NAION associated with PSS have been reported in the literature.[16][17] Both patients had a history of hypertension, and one had a “crowded disc” optic nerve morphology. The presumed mechanism is decreased optic disc perfusion due to an acute rise in IOP. Some have suggested that use of prophylactic IOP-lowering drops may decrease the chance of NAION in these patients, however rare it may be.
- 19. • Medical therapy • Initial treatment is directed towards controlling intraocular pressure and decreasing inflammation. Typical first-line therapeutics include topical beta- blockers such as timolol, alpha-agonists such as brimonidine, and carbonic anhydrase inhibitors such as dorzolamide. Apraclonidine has also been advocated as a first-line agent.[18][19] Prostaglandin analogs may also be used, and are effective for IOP control, however it is not firstline as there is evidence suggesting this class of medication might exacerbate inflammation. Oral carbonic anhydrase inhibitors are sometimes used acutely to quickly lower the IOP. • For control of inflammation a topical steroid drop is usually used, such as prednisolone acetate 1% QID, given the typically low level of inflammation. Topical NSAIDs may also be used. Oral NSAIDS such as indomethacin may also be used to avoid a possible steroid-induced glaucoma and for their anti-prostaglandin properties, as elevated prostaglandin levels in the aqueous have been associated with attacks.[20] • Miotics and mydriatic agents are rarely used. In particular, pilocarpine should be avoided as this is thought to exacerbate a possible trabeculitis
- 22. Fuchs’ Heterochromic Uveitis • Ernst Fuchs, 1906 • Anterior uveitis , heterochromia, cataract • 90% U/L • 3rd-4th decade, both sexes equally • Chronic
- 23. • Physical examination. • Patients with FHI are often asymptomatic for many years prior to presentation as, unlike with other anterior uveitides, they typically will have no pain, redness, or photophobia. • Presenting complaints are usually secondary to cataract or vitritis. Classically, patients will present with unilateral iris heterochromia and atrophy, KP, low-grade iridocyclitis, and cataract in the absence of posterior synechiae. • Only 5-10% of cases are bilateral.
- 24. • Conj • Cornea – Keratic precipitates are usually fine, stellate, and interconnected by fibrin bridges. In contrast to other types of anterior uveitides where KP tend to cluster inferiorly within Arlt’s triangle, KP in FHI tend to be diffuse, and involve the entire endothelial surface. • A/C
- 25. • Iris – heterochromia is seen in 75-90% of patients. – The lighter-colored iris usually, but not invariably, indicates the affected eye. – In patients with lightly colored irides, inverse heterochromia may be present, whereby loss of the pale anterior stroma leads to exposure of darker iris pigment epithelium. – Iris atrophy often precedes heterochromia. – The atrophic iris takes on a moth-eaten appearance, displaying smooth stromal architecture with loss of iris crypts
- 26. • Cataracts – are seen in all types of uveitis, however, they occur with particularly high frequency in FHI. – Three-quarters of lens opacities in FHI patients are posterior subcapsular. – FHI should be considered in the differential diagnosis of any unilateral cataract in a young patient in the absence of trauma or steroid use.
- 27. • Vitreous opacification – Patients with FHI can present with vitreous floaters from inflammatory debris, most often in the anterior vitreous. – If this floaters become visually significant, pars plana vitrectomy (PPV) has been shown to be exceedingly effective in improving vision in FHI. – In fact, PPV had better results in FHI patients than in those with other forms of uveitis, likely as a result of the less aggressive inflammatory course and lack of cystoid macular edema in FHI.
- 28. • chorioretinal scars seem to have a higher prevalence in patients with FHI versus other types of anterior uveitis, • though there is still no definitive link between toxoplasmosis and FHI, as previously mentioned
- 29. • Goneoscopy – Fine vessels crossing TM (~6-22% of patients) and are not – accompanied by PAS/fibrosis but may progress and may bleed spontaneously (hyphema) • Amsler sign: bleeding in AC after acute change in pressure in the eye (paracentesis)
- 30. • Management – Inflammation: Most cases of FHI do not require therapy, with patients generally having a good prognosis despite the persistent inflammation. – The expected sequelae of chronic uveitis (posterior synechiae, persistent cystoid macular edema) are usually not seen in FHI. – Since most of the inflammation is thought to be a result of blood aqueous barrier breakdown with resultant leakage of cells and protein, corticosteroids are generally ineffective in eliminating the low-grade anterior chamber reaction in FHI and should not be used aggressively. – Some advocate a short-course of topical steroids to differentiate FHI from Posner-Schlossman syndrome, but long-term steroids are not indicated.
- 31. Herpetic uveitis • HSV associated uveitis is a common cause of unilateral hypertensive anterior uveitis. • Herpetic anterior uveitis causes approximately 5-10% of uveitis cases • Secondary glaucoma 10%-54% • Acute rise in IOP, active iridocyclitis • U/L • Herpes simplex, Herpes Zoster, Varicella Zoster Karbassi M, Raizman MB, Schuman JS. Herpes zoster ophthalmicus. Surv Ophthalmol. 1992;36:395--410
- 32. 32 --Unilateral --Young to middle-aged adults --Inflammation is…mild --IOP elevation usually…severe --Is a recurrent condition --Good response to steroids --KP are ‘white and round ’ Posner-Schlossman syndrome Fuchs heterochromic iridocyclitis --Unilateral --Young to middle-aged adults --Inflammation is…mild --IOP elevation usually…mild (or absent) --Is a chronic condition --Poor response to steroids --KP are ‘white and stellate ’ --Associated with heterochromia iridis --Associated with NVI and NVA, but PAS and/or NVG rarely develop --Associated with PSC A Two forms of uveitic 2ndry OAG addressed in the Glaucoma book (aka glaucomatocyclitic crisis) Which has a strong association with cataract, and with what type of cataract is it associated?
- 33. Clinical features • Synechiae formation • Disciform keratitis, ulcer • Hypopyon / hyphaema / fibrin deposition • Diffuse / sectoral iris atrophy
- 34. • Cornea – epithelial and/or stromal edema, – stromal keratitis, keratic precipitates, endothelitis, and – anterior chamber cells and flare. – Keratic precipitates (KP) may take several forms. • They can be granulomatous, nongranulomatous, or stellate. • Often they may be present in a patch on the endothelial surface, underlying a localized patch of corneal edema. • They can be regional, in the inferior one-third of the cornea or diffuse. • When stellate KP are present, they are typically diffuse. [5]
- 35. • A/C • mild anterior chamber cell
- 36. • Iritis can also occur alone, without evidence of keratitis, and may present as an unilateral hypertensive anterior uveitis.
- 37. Management • Systemic antivirals • Topical steroids and cycloplegics • IOP- aqueous humour suppressants • Trabeculectomy with anti metabolites • Tube shunt surgery- active inflammation
- 38. Ciliary Body Rotation and Angle Closure Glaucoma • Inflammation of the ciliary body may cause the lens to move forward and close the angle by a posterior pushing mechanism • Symptoms include – blurred vision (from increased myopia, corneal edema, or both) and – photophobia.
- 39. Cont… • The central chamber has cells and flare. • It is shallow and asymmetric to the opposite eye. • Peripheral iridotomy does not resolve the angle closure, and • the condition is treated with – cycloplegia and – corticosteroids
Editor's Notes
- Hd/Nezif A/Jihad A/Gibe, +251921220518, Defakela, Dedo
- Most patients with nontraumatic uveitis and elevated pressure have either idiopathic inflammation or a recognized syndrome that is managed in largely the same manner as idiopathic uveitis.
- Posner-Schlossman Syndrome (PSS), also known as glaucomatocyclitic crisis, is a disease typified by acute, unilateral, recurrent attacks of elevated intraocular pressure (IOP) accompanied by mild anterior chamber inflammation. The pathophysiology is still unknown, although there are several theories proposed, ranging from autoimmune to infectious. Treatment management is focused on controlling the intraocular pressure and decreasing inflammation. While an attack usually resolves without sequelae, repeated attacks over time may lead to long-term glaucomatous damage (a secondary glaucoma). https://eyewiki.aao.org/Glaucomatocyclitic_Crisis_(Posner-Schlossman_Syndrome)#:~:text=Posner%20and%20Schlossman,and%20optic%20discs Posner and Schlossman first reported a series of 9 cases and coined the term “glaucomatocyclitic crisis” in 1948.[1] These patients suffered from recurrent unilateral attacks of ocular hypertension that shared the following characteristics:[2] Unilateral Recurrent Mild discomfort or blurring of vision Increased IOP with open angles Mild anterior chamber reaction or fine white keratic precipitates (KP) Crises lasting from several hours to weeks Normal IOP and no signs of uveitis between attacks Normal visual fields and optic discs
- Optic nerve topography and flowmetry demonstrate transient differences in morphology and blood flow during attacks compared to before/after attacks. Cup volume and area measured by Heidelberg Retinal Tomography increase during an attack, but pre- and post-attack measurements are comparable. Flowmetry may also demonstrate decreased optic nerve perfusion during an attack, particularly at the peripapillary temporal and nasal sectors, as well as at the level of the neuroretinal rim.[14] Visual fields performed during an attack may demonstrate non-specific changes, but in general, they remain normal following an attack. In patients whom repeated attacks occur, permanent glaucomatous optic nerve damage with accompanying visual field changes may occur[7] and may be an indication for surgical intervention.
- Surgical therapy In cases where the IOP cannot be controlled using maximal medical therapy, surgical therapy may be considered, especially when signs of glaucomatous optic nerve damage or visual field changes appear.[21] One case series reported 8 patients with PSS who underwent trabeculectomy with mitomycin-C for uncontrolled IOPs and visual field defects. At the end of follow-up, all patients did not require IOP-lowering drops, and although a recurrence of iritis was noted in 2 patients, the IOP remained stable during the episodes.[22] Follow up Patients should be followed daily until their IOP return to baseline, then weekly as anti-glaucoma drops and topical steroids are tapered. Well-educated and informed patients may also be able to initiate self-treatment with topical drops if they notice signs and symptoms of an impending or active attack, but should also be instructed to follow up immediately with an ophthalmologist. Prognosis Posner-Schlossman Syndrome has long thought to be a “benign” disease; most patients are treated for attacks and recover without long-term sequelae. However, a number of patients with repeated attacks, even if treated, may show long term glaucomatous changes in the optic nerve and on visual field testing. [7] It is thought that it is the total duration of elevated IOP, not the frequency of attacks, that contributes to the damage. These patients may be candidates for surgical therapy as discussed above.
- This syndrome classically involves unilateral heterochromia (lighter on the involved side), inflammation, and cataract formation. Approximately 10% of cases are bilateral and may be difficult to diagnose. Fuchs’ Heterochromic Iridocyclitis (FHI), also known as Fuchs’ uveitis syndrome (FUS), was first described in 1906 by Austrian ophthalmologist, Ernst Fuchs, who reported a series of 38 patients with iris heterochromia, cyclitis, and cataract.[1] Since then, FHI has been further characterized as a constellation of clinical findings, which classically includes low-grade unilateral anterior inflammation with stellate keratic precipitates (KP), iris heterochromia, and prominent iris and angle vessels that bleed after paracentesis (Amsler sign). Etiology Ernst Fuchs presumed that FHI was caused by a noxious stimulus of unknown origin.[1] The exact etiology of FHI is still unknown, and the disease process is likely multifactorial. Historical theories on the cause of FHI have associated it with sympathetic dysfunction, as well as multiple infectious etiologies such as toxoplasma, herpes simplex virus (HSV)[3] , chikungunya virus[4], cytomegalovirus (CMV), and rubella virus (RV). Sympathetic dysfunction resulting in decreased innervation to stromal melanocytes and iris hypopigmentation was an early proposed theory for the etiology of FHI.[5] [6] [7] The abnormal innervation was thought to account for not only the iris heterochromia, but also the breakdown of the blood-aqueous barrier and subsequent inflammation. However, this theory was dismissed after only 25 of 1746 (1.4%) FHI cases in a retrospective study were found to be associated with Horner’s syndrome.[8] The prevalence of peripheral chorioretinal scars in FHI varies from 7-65% of cases, with most studies noting a prevalence of 10%.[7] Multiple studies have reported toxoplasma-like chorioretinal scars in a significantly higher proportion of FHI patients compared to control groups.[9][10] For this reason, an etiologic association between toxoplasmosis and FHI has been investigated, however, no significant association between FHI and humoral or cellular immunity to toxoplasma has been found.[7] Both HSV and Chikungunya virus have been linked to FHI due to the isolation of viral DNA and RNA, respectively, from the aqueous humor of patients with FHI. Currently, however, these findings are limited only to case reports.[11][12] The strongest etiologic theories are those associating CMV and RV with FHI. CMV infection has been found to account for 16-42% of FHI in Asia, whereas in Western countries, FHI is predominantly associated with RV.[13][12][14][11] In one Chinese study, aqueous humor samples were obtained from 35 patients with presumed FHI, 15 of which were found to contain CMV DNA by PCR.[13] Aqueous humor and blood of 63 European patients with FHI were examined for RV antibodies in one of the largest series of FHI patients, all of whom were found to have intraocular antibody synthesis against RV.
- Iris nodules, particularly Koeppe and Busacca nodules, can be seen in FHI and may initially lead to a misdiagnosis of granulomatous uveitis. Iris crystals are small, refractile iris crystals called Russell bodies, which can be seen on the surface of the iris. Russell bodies are aggregations of spherical immunoglobulin. Figure 3: Gonioscopic view showing bridging vessels traversing across the angle in a patient with Fuchs' Heterochromic Iridocyclitis. Iris rubeosis can be seen in FHI. Gonioscopy should be performed in these eyes as some of these vessels may traverse over the trabecular meshwork (Figure 3). Furthermore, sclerosis of trabecular meshwork can result, and an inflammatory membrane can form over the angle. Although not pathognomonic for FHI, Amsler’s sign occurs when a hyphema results after paracentesis during cataract surgery, rupturing the vessels crossing the trabecular meshwork. These fragile vessels may also lead to hyphem
- Cataract: Patients with FHI have equivocal or better visual results following cataract extraction compared to other forms of chronic uveitis. Studies have shown phacoemulsification with posterior chamber intraocular lens implantation to be a safe and effective procedure in patients with FHI.[19] The peri-operative management of inflammation varies in FHI, with most surgeons placing patients on topical steroids.[6] Some clinicians even recommend pre-operative systemic steroids. Markers of severe disease, including severe iris atrophy with transillumination defects, glaucoma, and iris vasculature abnormalities, offer a more guarded post-operative prognosis.[17] Vitreous opacification: Patients with FHI can present with vitreous floaters from inflammatory debris, most often in the anterior vitreous. Should these floaters become visually significant, pars plana vitrectomy (PPV) has been shown to be exceedingly effective in improving vision in FHI.[20] In fact, PPV had better results in FHI patients than in those with other forms of uveitis, likely as a result of the less aggressive inflammatory course and lack of cystoid macular edema in FHI. Glaucoma Glaucoma is the most sight threatening and challenging complication of FHI. The prevalence of secondary glaucoma has been reported to be anywhere from 9-59% in FHI patients.[16][21] [22] [23] As is the case in primary open angle glaucoma (POAG), African Americans, as well as elderly patients may be at increased risk for developing secondary glaucoma from FHI.[24] In addition, time to diagnosis, male sex, presence of iris nodules at baseline, and the presence of a cataract (independent of age) have also been found to increase the risk for ocular hypertension and glaucoma in these patients.[25][26] In most cases of glaucoma secondary to FHI, the etiology is thought to be similar to that of chronic open-angle glaucoma. In some cases, inflammatory debris and nodules may play a role in aqueous outflow obstruction and secondary glaucoma. Other rare mechanisms include peripheral anterior synechiae and angle closure, lens-induced glaucoma such as phacolytic glaucoma, steroid induced glaucoma, and neovascular glaucoma from iris and angle rubeosis.[22] Glaucoma in the setting of FHI is particularly recalcitrant, with 73% failing to respond to maximal medical therapy.[7] These patients often require incisional surgery. In the management of uveitic glaucoma in general, laser therapy (trabeculoplasty, cyclophotocoagulation) is generally avoided due to inconsistent efficacy, as well as high risk for complications such as increased inflammatory response and hypotony. Incisional surgery is often more effective though surgical success rates are largely dependent upon the suppression of inflammation postoperatively. Patients with uveitic glaucoma undergoing incisional surgery often have lower rates of success compared to POAG patients due to a propensity for subconjunctival scarring, and higher rates of postoperative hypotony secondary to ciliary body dysfunction from recurrent inflammation.[27] Minimally invasive glaucoma surgeries (MIGS) are still being evaluated for use in uveitic glaucoma though preliminary data from studies treating these patients with canaloplasty and trabeculotomy, in particular, have yielded promising results. Notably, there is some concern that the narrow lumen of implantable devices such as the iStent and Xen may easily obstruct in uveitis patients due to the presence of inflammatory debris.[28] Trabeculectomy in uveitic glaucoma has been demonstrated to have limited success due to excessive scarring, with a 5 year success rate of 54% without adjuvant anti-metabolite therapy and 67% with a one-time does of 5-fluorouracil.[29][30] As such, glaucoma drainage implant devices (e.g. Ahmed, Baerveldt, Molteno) are generally the preferred initial surgical option in any uveitic glaucoma, with first year success rates ranging from 77-94%.[31][32][33] As mentioned, FHI is not typically characterized by severe inflammation[17][18], and outcomes for trabeculectomy and glaucoma drainage implants have been mixed. One retrospective review found that the success rate for patients with FHI-related glaucoma who underwent trabeculectomy with mitomycin C (MMC) was 90.9% and 62.3% at one and four years, respectively.[34] Success rates from a subsequent study was lower, however, reporting trabeculectomy success amongst FHI patients to be around 58% at one year.[35] This same study also showed that deep sclerectomy in FHI patients was equally efficacious compared to trabeculectomy, though did note that the rate of laser goniopuncture in this group was higher compared to other studies on deep sclerectomy.[35] Of note, in FHI-related glaucoma there appears to be no benefit to adding subconjunctival bevacizumab to the initial trabeculectomy with MMC.[36] Contrary to uveitic glaucoma in general, studies comparing Ahmed glaucoma valves and trabeculectomy in FHI-related glaucoma do not show a clear trend toward superiority. Two retrospective studies published within one year of each other offer differing conclusions, with Esfandiari et al[37] finding that Ahmed glaucoma valves had higher success rates than trabeculectomy (85.7% with AGV compared to 41.7% with trabeculectomy), and Nilforushan et al concluding the opposite (9% with AGV compared to 76% with trabeculectomy)[38]. Given the relative paucity of FHI cases within uveitic glaucoma, it is difficult to formulate conclusions to guide treatment based on small retrospective studies. Larger studies with a longer duration of follow-up will be necessary to gain a better understanding of outcomes between glaucoma drainage implant devices and glaucoma filtering surgery in this specific patient population.
- Due to inflammation of trabecular meshwork, swelling and obstruction of inflammatory cell and debris AHSV associated anterior uveitis is more common in patients in their 40-50's affecting both genders equallynterior uveitis is more common during reactivation vs primary disease.
- As stated previously, the presence of stellate KPs with mild anterior chamber cell, prominent iris and angle vessels, and iris heterochromia may be indicative of FHI. In addition, the potential diagnosis of Posner-Schlossman syndrome needs to be carefully considered, especially when clinical exam findings demonstrate episodes of anterior chamber cell with extremely elevated IOP, with quiescence and normal IOP in between episodes. Some studies have suggested HSV as a possible infectious etiology for Posner-Schlossman syndrome, although cytomegalovirus is also implicated.
- It is also important to note that fine, stellate KPs along with mild anterior chamber cell are also associated with Fuchs heterochromic iridocyclitis (FHI), and there has been evidence to suggest that HSV (and other infectious etiologies) may potentially cause FHI. In FHI, there may be prominent iris and angle vessels visible due to iris atrophy. High intraocular pressure is a common complication of HSV iritis and can serve as a diagnostic hallmark. The IOP can be very high, in the range of 50-60 mm Hg during an episode of acute iritis. High IOP is due to trabeculitis, as well as inflammatory cells clogging the trabecular meshwork. Although antiglaucoma therapy may be required in the acute setting, once the inflammation is controlled, typically the intraocular pressure will normalize and the patient will not require ongoing antiglaucoma treatment. By contrast, prolonged or recurrent inflammation may cause peripheral anterior synechiae (PAS), which can lead to secondary glaucoma. Other signs include posterior synechiae and iridoplegia. [2] Spontaneous hyphema can occur in HSV iritis, as well as layers of hyphema mixed with hypopyon, known as a “candy-cane hypopyon”. Although patchy iris atrophy may be present following an episode of HSV keratouveitis or iritis, inflammatory iris lesions are not typically seen. Disease is more common a unilateral process, but can be bilateral as well.
- Because of the high prevalence of positive HSV antibodies in most populations, serology is only helpful in the diagnosis in that a negative HSV antibody titer will rule out the possibility that iritis is due to HSV. Polymerase chain reaction for HSV DNA from an anterior chamber tap may be helpful in diagnosis with a high sensitivity (91.3%) and specificity (98.8).