retinoid x receptor Turalba et al estimated a

Turalba et al. estimated a prevalence of 17% mainly due to ocular hypertension after OGI. According to Turalba’s criteria, cases of IOP⩾22mmHg at one visit treatment were included in the study, and this may have overestimated their prevalence.

Risk factors
It has been reported in a large study by Girkin et al. that several factors are significantly associated with the development of post-traumatic glaucoma, including advancing age, lens injury, poor presenting visual acuity, and intraocular inflammation. Turalba et al. presented risk factors for developing ocular hypertension after open-globe injury as: Increased age, hyphema, lens injury, and zone II injury. Osman et al. reported significant risk factors for glaucoma as: advancing age (p=0.05), poor visual acuity at presentation, perforating rather than penetrating ocular injury, vitreous hemorrhage, lens dislocation, presence of intraocular foreign body (IOFB) and undergoing cataract surgery following the primary repair.
Contrary to Girkin study, there was no significant association between the presence of retained IOFB and glaucoma, and this may be explained by their protocol of removing IOFB during the primary repair Table 1.

The causes of traumatic glaucoma are multifactorial depending on the amount and extent of the injured tissue. Numerous potential mechanisms have been raised; it can occur secondary to the disturbance of the trabecular meshwork or inflammatory scarring or stumbling block of the trabecular meshwork by direct inflammation, inflammatory debris, lens particles, coagulated blood components, red blood retinoid x receptor from a hyphema or from long-standing vitreous hemorrhage. Bai et al.divided the causes of ocular trauma related glaucoma into three stages, early, intermediate and late stage; they incorporated closed and open eye injuries of 103 cases. In the previous study at the early stage (1–4weeks) there were 33 cases retinoid x receptor due to inflammation, 36 due to hyphema and 22 due to lens dislocation; at the intermediate stage (1–6months) there were 3 cases due to pupillary block and 2 due to phacoanaphylactic glaucoma and at the advanced stage (more than 6months), 6 cases were due to angle recession and one case due to siderosis. Milder et al. postulated that the mechanism of traumatic glaucoma may be due to blockage of the trabecular meshwork with inflammatory debris and inflammation that can lead to peripheral anterior Synechiae or due to steroid use, epithelial/ stromal downgrowth and siderosis. De Leon and Girkin encountered an increase in the IOP to trabecular meshwork swelling without hyphema or angle recession. Osman et al. classified ocular trauma glaucoma after OGI into three stages namely early, intermediate, late stage, and contrary to Bai et al. they included open globe injuries cases only. In Osman study, the causes of glaucoma in the early stage are: un-removed lens particles in 11 patients, inflammation in 6 patients and hyphema in 3 patients. In the intermediate stage glaucoma was due to synechial angle closure in 9 patients, in 3 patients due to ghost cell glaucoma, and unremoved lens particles in another 2 patients. In the late stage, 4 patients were affected with glaucoma due to angle recession and 3 patients as a result of synechial angle closure.

Prevention still has a role in management of glaucoma after OGI. Viscoelastic material is advised during the repair of OGI to maintain the consistency of the angle of the anterior chamber and prevent the anterior Synechiae. Aggressive treatment is mandatory by frequent topical steroids to suppress the inflammation that can lead to peripheral anterior Synechiae. Bai et al., advised the use of 0.1% dexamethasone eye drop and dexamethasone 0.1–0.2mg/kg/d through intravenous route for 5–7days to eyes with inflammation. As regards medical treatment of glaucoma after OGI, Turalba et al. presented 65 patients with ocular hypertension, majority of patients were treated medically (74%) and this may be attributed to their criteria of definition of traumatic glaucoma as an elevation of IOP in one visit or more. Osman et al. had 10 cases (24%) that responded to medications by corticosteroid and cycloplegic and the IOP was controlled effectively in all these cases. Surgical intervention plays an important role in management of glaucoma post closed and open globe injuries that is not responding well to medical treatment. Mermuod et al. matched up the success of trabeculectomy in angle recession glaucoma to primary open angle glaucoma and concluded that posttraumatic angle recession is a risk factor for failure of trabeculectomy. Manners et al. study showed trabeculectomy with mitomycin C as an effective surgical procedure for medically uncontrolled post-traumatic angle recession glaucoma with the success rate at final follow up of 77% (33/43 eyes). Turalba et al. had 8 (12%) patients who underwent filtering or glaucoma drainage device surgery, while 4 (6%) required anterior chamber washout with no other glaucoma surgery. Osman et al. resulted in 5 patients with synechial angle closure, 2 cases with persistent hyphema and 2 with lens aspiration that underwent trabeculectomy with MMC surgery with an overall success rate of 100% as of the last follow-up visit assessment.