Dr.ANITHA S. MAIYA, Dr.RAVINDRA BANAKAR,Dr. MANJUNATH B.H.
Abstract:
Aim:This clinical study was undertaken to evaluate the profile, mechanisms and course of traumatic glaucoma in patients who have sustained blunt ocular trauma.
Methods: 100 consecutive patients who sustained ocular blunt trauma during the 1 year study period were enrolled in the study. All the patients underwent a comprehensive ophthalmic evaluation of the anterior and posterior segments along with relevant investigations. Patients with an IOP ≥ 21mm Hg with or without glaucomatous optic neuropathy were considered to have traumatic glaucoma and started on appropriate treatment.
RESULTS: 11 out of the 100 consecutive patients who sustained ocular blunt trauma developed traumatic glaucoma. The age of patients ranged between 11 – 65 years, 8 were males and 3 females; 6 patients were < 18 years of age and hyphaema (n = 6) was the most common cause of glaucoma followed by traumatic uveitis (n =2 ) and lens injuries (n = 1 ). Average IOP at presentation was 36 ± 9.6mmHg and patients required 1.636 ± 0.8 antiglaucoma medications for IOP control. 3 patients underwent surgical intervention for managing the complications of the ocular blunt trauma. Only one of the patients required glaucoma surgery. IOP at final follow up was 14.6 ± 2.73 mm Hg.
CONCLUSION: Traumatic glaucoma tends to occur more commonly in children. Certain markers the hyphaema, lens injuries and uveitis can predict the possibility of glaucoma. Traumatic glaucoma if detected early and treated energetically can improve visual outcomes in patients with ocular blunt trauma.
Keywords: hyphaema,ocular blunt trauma, traumatic glaucoma.
INTRODUCTION:
Ocular trauma is one of the common causes of ocular morbidity and uniocular blindness in the world [1] the reported incidence of ocular trauma in our country varies between 1% to 5% [2].
Ocular blunt trauma (OBT) causes rapid deformation and structural alternations of the ocular tissues [3] leading to a wide spectrum of ocular manifestations. One of the complications of such trauma is secondary glaucoma. The mechanisms of traumatic glaucoma (TG) is multifactorial and results from damage or obstruction of the trabecular meshwork causing decreased outflow of aqueous humour. In the acute stages, hyphaema, traumatic uveitis and lens induced mechanisms play a major role while angle recession causes glaucoma to develop several months or years later.
Few studies have attempted to identify the risk factors associated with glaucoma occuring following ocular trauma [4] [5]. A study involving a large cohort of patients who sustained blunt ocular trauma determined the predictive factors for the development of posttraumatic glaucoma to be poor initial visual acuity, advancing age, lens injury, angle recession and hyphaema [6].
In the management of patients with ocular blunt trauma, traumatic glaucoma is often overlooked. This can further worsen the visual prognosis leading to significant visual impairment. It is therefore important to identify and appropriately treat the secondary effects of OBT the TG in order to improve the visual outcomes in these patients.
We undertook this study to determine the clinical profile, mechanisms and course of TG in 100 consecutive patients of OBT in our institution.
METHODS:
Consecutive patients who had sustained ocular blunt trauma seeking treatment in the Ophthalmology OPD/casualty of our institution during a one year study period between May 2017 to April 2018 were included for evaluation. A detailed history for the details of the ocular injury – mode of OBT, duration between the trauma and visit and details of any prior treatment were recorded. Prior ocular history and demographic data was also noted. Informed consent was obtained from all patients in accordance with the declaration of Helsinki.
A comprehensive ocular examination of both eyes was performed which included best corrected visual acuity, slit lamp biomicroscopic examination, posterior segment examination with a +90D lens and indirect ophthalmoscopy (without scleral indentation). Intraocular pressure was measured on atleast 3 occasions using Goldman applanation tonometer/non-contact tonometer as appropriate. Gonioscopy was performed in all patients after 7 – 10 days of the injury after ruling out globe rupture.
Investigations line X-ray orbit and/or T scan and/or USG B scan was done as and when indicated. Exclusion criteria were patients with open globe injuries, orbital injuries, primary glaucoma or other pre-existing cause of secondary glaucoma and history of prior laser or ocular surgery.We also excluded patients having significantpolytrauma requiring interventions from other specialities. For the purpose of uniformity, we defined traumatic glaucoma (TG) as any raised IOP ≥ 21mm Hg post recent ocular blunt trauma with or without glaucomatous optic neuropathy.
The initial therapeutic regimen for all patients TG consisted of monotherapy or combination of antiglaucoma medications which included topical β-adrenergic blockers, topical – adrenergic agonists and topical and oral carbonic anhydrase inhibitors as and when needed. Topical steroids any cycloplegics were added according to the severity of inflammation. Surgical intervention for lens injuries or glaucoma was performed when necessary. All the patients were followed up to monitor the response to therapy.
RESULTS:
We studied 100 eyes of 100 consecutive patients who had a recent ocular blunt trauma. The demographic data of the patients are presented in table 1.
Table 1: Demographic data of the 100 patients included in the study
| Age wise distribution | No. of patients | Percentage |
| 0 – 9 | 9 | 9% |
| 10 – 19 | 12 | 12% |
| 20 – 29 | 25 | 25% |
| 30 – 39 | 19 | 19% |
| 40 – 49 | 12 | 12% |
| 50 – 59 | 15 | 15% |
| 60 – 69 | 7 | 7% |
| 70 – 79 | 1 | 1% |
| Gender wise distribution | No. of patients | Percentage |
| Male | 80 | 80% |
| Female | 20 | 20% |
| Mode of injury | No. of patients | Percentage |
| Agriculture related | 48 | 48% |
| RTA | 14 | 14% |
| Fall | 13 | 13% |
| Sports | 17 | 17% |
| Assault | 7 | 7% |
| Cracker burst | 2 | 1% |
11 patients (11%) were detected to have traumatic glaucoma. The clinical profile of cases with traumatic glaucoma are as follows:
- Age : The age of patients who developed TG ranged from 11 – 65 years with a mean (SD) of 26.272 (19.83) years.
- Gender : Of the 11 patients who developed TG, 8 were males (72.73%) and 3 (27.27%) were females.
- IOP : The IOP at presentation ranged from 26 – 60 mm Hg with mean (SD) of 36 (9.67) mm Hg. At the final follow up, the 10P ranged between 11 – 18 mm Hg with a mean (SD) of 14.63 (2.73) mm Hg.
The details of the 11 patients who developed TG with the possible mechanism is presented in Table 2.
Table 2. Details of the patients who developed traumatic glaucoma
| Patients | Age/Gender | Eye | Mode of OBT | BCVA @ presentation | Ocular manifestation | 10P @ presentation (mm Hg) | # of AGM | Mechanism of TG |
| Patient 1 | 12y/M | Right | Stick injury | 6/6P | Hyphaemmagrade II | 28 | 1 | SOAG dlthyphaema |
| Patient 2 | 17y/M | Left | Cricket ball | 1/60 | Traumatic uveitis, lens subluxation, vitreous nemorrhag | 38 | 2 | Ghost cell glaumcoma SOAG |
| Patient 3 | 12y/M | Left | Sports | 6/12 | Hyphaema grade II mild uveitis | 26 | 1 | SOAG dlthyphaema |
| Patient 4 | 13y/M | Left | Sports | 6/60 | Conjunetival tear hyphaema, zonular dehiscence, traumatic cataract, vitreous hemorrage, 2000 angel recession | 36 | 2 | SOAG dlthyphaema |
| Patient 5 | 11y/M | Right | Belt injury | 6/9 | Mild Hyphaematraumatic uveitis | 30 | 1 | SOAG dlt traumatic uveitis |
| Patient 6 | 65y/M | Right | Agricultural | HM | Corneal edema, posterior disclocation of cataractous lens severe uveitis | 60 | 3 | SOG dlt lens induce severe uveitis |
| Patient 7 | 22y/M | Right | Sport | 6/18 | Hyphaema grade I | 28 | 1 | SOAG dlthyphaema |
| Patient 8 | 28y/M | Right | RTA | 1/60 | Total hyphaema grade IV | 52 mm Hg | 3 | SOAG dlthyphaema |
| Patient 9 | 11y/M | Left | Cricket ball | 6/128 | Post cornea tear repair | 28 | 1 | SOAG dlt steroid induced |
| Patient 10 | 60y/F | Right | Agriculture | 6/12 | Anterior subluxation of lens | 30 | 1 | Secondary angle closure |
| Patient 11 | 38y/M | Right | RTA | 6/12 | Hyphaema grade III | 36 | 2 | SOAG dlthyphaema |
- Mechanism of TG : the postulated cause for raised 10P in our study is described in table 3.
Table 3: Mechanisms of TG in our study
| Sl. No. | Ocular complication of OBT | No. of eyes
(n = 100) |
No. of eyes developing TG
(n = 11) |
Mechanism of TG |
| 1. | Hyphaema | 16 | 6 | SOAG |
| 2. | Uveitis | 27 | 2 | SOAG |
| 3. | Subluxaion of lens | 3 | 1 | SACG |
| 4. | Vitreous haemorrhage | 3 | 1 | Ghost cell glaucoma
(SOAG) |
| 5. | Steroid induced ocular hypertension | – | 1 | SOAG |
| 6. | Angle recession | 18 | – |
Hyphaema was the most common cause of TG followed by traumatic uveitis.
- Treatment of TG the patients were treated as follows:
- Medical therapy: All the patients were started on medical therapy. Out of the 11 patients with TG, 6 required a single glaucoma medication for 10P control. 3 patients required 2 medications, while 2 patients required 3 medications for 10P control. The mean (SD) member of antiglaucoma medications required was 1.63 (0.8)
- Laser therapy:One patient (patient 10, table 2) had secondary angle closure glaucoma due to traumatic anterior subluxation of the lens. We performed Nd:YAG laser peripheral iridotomy after which her IOP was maintained with one AGM.
- Surgical therapy: Of the 11 patients who developed TG 3 required surgical intervention as follows:
Patient 2 initially underwent pars planavitrectomy with lensectomy which helped in controlling the Ghost cell glaucoma. 3 months later he underwent secondary scleral fixated intraocular lensimplantation.
Patient 4 underwent conjunctival tear repair with anterior cryopexy for giant retinal tear. His IOP was medically controlled.
Patient 8 who presented with total hyphaema underwent paracentesis with anterior chamber washout for uncontrolled IOP 8 days after the OBT. When the IOP remained uncontrolled with progressive worsening of the glaucomatous optic neuropathy, he underwent Trabeculectomy with Mitomycin C. His IOP stabilised at 16 mm Hg without any AGM after the surgery.
Patient 6 refused to undergo parsplanavitrectomy with lensectomy and was lost to followup subsequently.
DISCUSSION:
Ocular blunt trauma accounts for approximately 40% of the ocular injuries. [7] Traumatic glaucoma is a major concern because it may go unnoticed and get detected several years later with irreversible glaucomatous optic nerve damage. [4] The reported incidence of TG after ocular contusion has been stated to be around 3.4% within the first 6 months and upto 10% during the 10 years after trauma.[8]
Out of the 100 consecutive eyes who sustained OBT, 11 eyes were detected to have TG. The average age of the patients who developed TG was 26.272 ± 19.83 years and 6 of these patients were < 18 years of age. This may probably attributed to the fact that ocular trauma tends to occur more frequently in young adults and children and possible immaturity of the aqueous outflow system whichreduces the outflow facility further following the effects of the trauma.
Ocular blunt trauma and TG was more common in males (OBT – 80% of the patients were males ; TG – 91% of patients well males). This is consistent with other studies which have also found a male preponderance among patients experiencing OBT and TG. [6] [9]
The mechanisms of TG following OBT can be obstruction of the trabecular meshwork due to inflammatory cells and debris, red blood cells form hyphaema or senescent red blood cells from an old vitreous haemorrhage or lens particles. [10] [11] [12] Glaucoma may also be caused due to damage or scarring of the trabecular meshwork from the injury. [8] [13] In addition to the above anterior lens displacement may lead to pupillary block glaucoma.
The possible mechanisms for TG in our patients is outlined in table 3.Hyphaema was the most common cause attributable to TG among our patients. Although angle recession was detected in 18 patients none of them developed angle recession glaucoma(ARG). This is possible due to the fact that ARG develops as a late manifestation and our patients had only a short follow up of 3 months. In most of the previous studies hyphaema was the most frequent finding and is often seen in association with angle recession. [8] [15]The study by Girkin et as have found that hyphaema had the highest independent association with the development of glaucoma which is in agreement with our study.[6]
Most of our TG patients were controlled with medical therapy with 4 patients not requiring any AGM at the 3 months follow up visit. This shows that TG secondary to mild hyphaema and traumatic uveitis have a self limiting course and may resolve when treated appropriately. Only one of our patient who had total hyphaema ultimately required trabeculectomy for IOP control.
The limitations of our study are small number of patients, hospital based study and short term follow up of upto only 3 months. However we are following up all these patients and the long term effects of OBT in these patients would also be evaluated.
CONCLUSIONS:
Using the data obtained from 100 consecutive patients with OBT, we found that TG occurred in 11% of our patients this emphasises the importance of monitoring IOP in all patients with ocular trauma so that TG will not be missed. TG was found more frequently in children in our study and certain markers like hyphaema, severe traumatic uveitis and lens injury can predict the possibility of TG. Results of our study may be a useful starting point for future studies with larger sample size to determine the risk factors and outcomes of traumatic glaucoma. TG when detected early and treated energetically can improve visual outcomes in patients with ocular blunt trauma.
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