• Users Online: 355
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 32  |  Issue : 2  |  Page : 154-158

Traumatic glaucoma in 100 consecutive cases of ocular blunt trauma in a tertiary care center


Department of Ophthalmology, JJM Medical College, Davangere, Karnataka, India

Date of Submission07-Nov-2019
Date of Decision12-Jan-2020
Date of Acceptance26-Jan-2020
Date of Web Publication25-Aug-2020

Correspondence Address:
Dr. Anitha S Maiya
Department of Ophthalmology, JJM Medical College, Davangere - 577 004, Karnataka
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/kjo.kjo_75_19

Rights and Permissions
  Abstract 


Aim: This clinical study was undertaken to evaluate the profile, mechanisms, and course of traumatic glaucoma (TG) in patients who have sustained blunt ocular trauma.
Methods: One hundred consecutive patients who sustained ocular blunt trauma (OBT) during the 1-year were enrolled in the study. All the patients underwent a comprehensive ophthalmic evaluation of the anterior and posterior segments along with relevant investigations. Patients who were found to have an intraocular pressure (IOP) ≥21 mm Hg with or without glaucomatous optic neuropathy were considered to have TG and started on appropriate treatment.
Results: Eleven of the 100 consecutive patients who sustained OBT developed TG. The age of patients ranged between 8 and 65 years, 8 were male and 3 female; 6 patients were <18 years of age and hyphema (n = 4) was the most common cause of glaucoma followed by traumatic uveitis (n = 2) and lens injuries (n = 1). The average IOP at presentation was 36 ± 9.6 mm Hg and patients required 1.636 ± 0.8 antiglaucoma medications for IOP control. Three patients underwent surgical intervention for managing the complications of the OBT. Only one of the patients required glaucoma surgery. IOP at the final follow-up was 14.6 ± 2.73 mm Hg.
Conclusion: TG tends to occur more commonly in children. Certain markers such as hyphema, lens injuries, and uveitis can predict the possibility of glaucoma. TG if detected early and treated energetically can improve visual outcomes in patients with OBT.

Keywords: Hyphema, ocular blunt trauma, traumatic glaucoma


How to cite this article:
Maiya AS. Traumatic glaucoma in 100 consecutive cases of ocular blunt trauma in a tertiary care center. Kerala J Ophthalmol 2020;32:154-8

How to cite this URL:
Maiya AS. Traumatic glaucoma in 100 consecutive cases of ocular blunt trauma in a tertiary care center. Kerala J Ophthalmol [serial online] 2020 [cited 2020 Oct 24];32:154-8. Available from: http://www.kjophthal.com/text.asp?2020/32/2/154/293306




  Introduction Top


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% and 5%.[2]

Blunt ocular trauma cases rapid deformation and structural alternations of the ocular tissues leading to a wide spectrum of ocular manifestations.[3] One of the complications of such trauma is secondary glaucoma. The mechanisms of traumatic glaucoma (TG) are multifactorial and results from damage or obstruction of the trabecular meshwork causing a decreased outflow of aqueous humor. In the acute stages, hyphema, 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 occurring follow 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 post-TG to be poor initial visual acuity, advancing age, lens injury, angle recession, and hyphema.[6]

In the management of patients with ocular blunt trauma (OBT), TG 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 like TG 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 Top


This prospective study included 100 consecutive patients who had sustained recent OBT seeking treatment in the ophthalmology outpatient department/casualty of our institution during a 1-year study between May 2017 and April 2018. 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 were also noted. Informed consent was obtained from all patients in accordance with the tenets of the declaration of Helsinki. Patients with severe injuries involving other systems requiring surgical intervention, open globe injuries, orbital injuries, primary glaucoma, or other preexisting cause of secondary glaucoma were excluded from the study.

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 (IOP) was measured thrice using Goldmann applanation tonometer/non-contact tonometer as appropriate in each patient at the time of initial diagnosis (before initiation of antiglaucoma drugs). Each IOP reading was taken at least 1 h apart on the same day by a single examiner. At each subsequent follow-up visit, a single reading of IOP by GAT was taken into consideration. Since the duration between the OBT and day of presentation to the hospital varied among the patients, the IOP measurements could not be standardized according to the day/week/months posttrauma. Gonioscopy was performed in all patients after 7–10 days of the injury after ruling out the globe rupture. Central corneal thickness (CCT) was not taken into account in the present study.

Investigations such as X-ray orbit and/or computed tomography scan and/or USG B scan was done as and when indicated. We also excluded patients having significant polytrauma requiring interventions from other specialties. For uniformity, we defined TG as any raised IOP ≥21 mm Hg post recent OBT with or without glaucomatous optic neuropathy.

The initial therapeutic regimen for all patients with TG consisted of monotherapy or combination of antiglaucoma medications which included topical β-adrenergic blockers, topical α2– adrenergic agonists, and topical and oral carbonic anhydrase inhibitors as and when needed. Topical steroids and 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 Top


We studied 100 eyes of 100 consecutive patients who had a recent OBT. The demographic data of the patients are presented in [Table 1].
Table 1: Demographic data of the 100 patients included in the study

Click here to view


Majority of the patients (25%) were in the age group of 20–29 years and were males (80%). There was no difference in terms of the eye involved among our patients. Since our institution caters to the rural population with agricultural background, agriculture-related trauma was the most common mode of injury followed by sports-related trauma. Eleven patients (11%) were detected to have TG.

Clinical profile of cases with TG was as follows:

  1. Age: The age of patients who developed TG ranged from 11 to 65 years with a mean (standard deviation [SD]) of 26.272 (±19.83) years
  2. Gender: Of the 11 patients who developed TG, 8 were male (72.73%) and 3 (27.27%) were female
  3. IOP: The IOP at presentation ranged from 26 to 60 mm Hg with a mean (SD) of 36 (±9.67) mm Hg. All patients responded well to medical therapy and only one of the patients required trabeculectomy due to uncontrolled IOP despite maximum medical therapy with the progression of optic neuropathy. At the final follow-up, the IOP ranged between 11 and 18 mm Hg with a mean (SD) of 14.63 (2.73) mm Hg
  4. Antiglaucoma medications: our patients required 1.636 ± 0.8 antiglaucoma medications for IOP control
  5. The details of the 11 patients who developed TG with the possible mechanism are presented in [Table 2]
  6. Mechanism of TG: The postulated cause for raised IOP in our study is described in [Table 3].
Table 2: Description of patients who developed traumatic glaucoma

Click here to view
Table 3: Postulated mechanisms of traumatic glaucoma in our study

Click here to view


Hyphema was the most common cause of TG followed by traumatic uveitis. However, on statistical analysis, only hyphema had a significant association with TG (P = 0.000219).

  1. Treatment of TG: Patients with TG were treated as follows:


    1. Medical therapy: All the patients were started on medical therapy. Of the 11 patients with TG, 6 required a single glaucoma medication, 3 patients required 2 medications, whereas 2 patients required 3 medications for IOP control. The mean (SD) member of antiglaucoma medications required was 1.63 (0.8)
    2. Laser therapy: One patient [patient 10, [Table 2] had secondary angle-closure glaucoma due to the traumatic anterior subluxation of the lens. We performed Nd: YAG laser peripheral iridotomy after which her IOP was well controlled with one antiglaucoma medication (AGM)
    3. Surgical therapy: Patient 2 [Table 2] initially underwent pars plana vitrectomy with lensectomy, which helped in controlling the Ghost cell glaucoma. Three months later, he underwent secondary scleral fixated IOL implantation. Patient 4 [Table 2] underwent conjunctival tear repair with anterior cryopexy for giant retinal tear. Patient 8 [Table 2] who required trabeculectomy was a 28-year-old male who sustained OBT due to road traffic accident. He had total hyphema (RE) at presentation which led to raised IOP (52 mm Hg) at day 4 posttrauma. His IOP remained uncontrolled (>40 mm Hg) with the maximum tolerated medical therapy. He first underwent paracentesis and AC washout to evacuate the hyphema on day 8 posttrauma. His IOP remained uncontrolled on maximum tolerated medical therapy with the progression of optic disc changes. He complained of persistent pain (RE) with poor vision (best-corrected visual acuity 5/60). Hence, a trabeculectomy with mitomycin C was performed on day 15 posttrauma. His IOP on postoperative day 1 was 12 mmHg (by noncontact tonometer) and he maintained an IOP of 16 mm Hg without antiglaucoma medications 3 months follow-up visit. Patient 6 [Table 2] refused to undergo pars plana vitrectomy with lensectomy and was lost to follow-up subsequently.



  Discussion Top


OBT accounts for approximately 40% of the ocular injuries.[7] TG 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 up to 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 be attributed to the fact that ocular trauma tends to occur more frequently in young adults and children. The possible immaturity of the aqueous outflow system which reduces the outflow facility further following the effects of the trauma maybe the reason TG was more commonly seen in children who sustained OBT.

OBT and TG was more common in males (OBT– 80% of males; TG– 91% of patients were 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 from hyphema or senescent red cells form vitreous hemorrhage 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.[14] The possible mechanisms for TG in our patients are outlined in [Table 3]. Hyphaema was the most common cause attributable to TG among our patients. The study by Girkin et al. concluded that hyphema had the highest independent association with the development of glaucoma which is in agreement with this study.[6] Although angle recession was detected in 18 patients, none of them developed Angle recession glaucoma (ARG). This is possible because ARG develops as a late manifestation and our patients had only a short follow-up of 3 months. In most of the previous studies, hyphema was the most frequent finding and is often seen in association with angle recession.[8],[15]

Most of our TG patients achieved good IOP control on medical therapy with four patients not requiring any AGM at the 3 months follow-up visit. This shows that TG secondary to mild hyphema and traumatic uveitis have a self-limiting course and may resolve when treated appropriately. Only one of our patients who had total hyphema ultimately required trabeculectomy for IOP control.

The limitations of this study are small sample size, hospital-based study and short-term follow-up of 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. A prospective study with bigger sample size is being undertaken to include the 1-year follow-up data of the patients.


  Conclusions Top


Using the data obtained from 100 consecutive patients with OBT, we found that TG occurred in 11% of our patients. This emphasizes 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 such as hyphema, severe traumatic uveitis, and lens injury can predict the possibility of TG. The results of our study may be a useful starting point for future studies with a larger sample size to determine the risk factors and outcomes of TG. TG when detected early and treated energetically can be well controlled with medical management which prevents further deterioration of prognosis in patients with OBT.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Thylefors B. Epidemiological patterns of ocular trauma. Aust N Z J Ophthalmol 1992;20:95-8.  Back to cited text no. 1
    
2.
Shukla B. Epidemiology of ocular trauma. In: Shukla B. Natarajan S. editors. Management of Ocular Trauma 1st ed. Delhi: Meenakshi Printers; 2005. p. 3-4.  Back to cited text no. 2
    
3.
De Leon-Ortega JE, Girkin CA. Ocular trauma-related glaucoma. Ophthalmol Clin North Am 2002;15:215-23.  Back to cited text no. 3
    
4.
Sihota R, Sood NN, Agarwal HC. Traumatic glaucoma. Acta Ophthalmol Scand 1995;73:252-4.  Back to cited text no. 4
    
5.
Charfi Ben Ammar O, Chaker N, Soukah M, Asmi W, El Matri L. Posttraumatic glaucoma. J Fr Ophtalmol 2002;25:126-9.  Back to cited text no. 5
    
6.
Girkin CA, McGwin G Jr., Long C, Morris R, Kuhn F. Glaucoma after ocular contusion: A cohort study of the United States eye injury registry. J Glaucoma 2005;14:470-3.  Back to cited text no. 6
    
7.
Klopfer J, Tielsch JM, Vitale S, See LC, Canner JK. Ocular trauma in the United States. Eye injuries resulting in hospitalization, 1984 through 1987. Arch Ophthalmol 1992;110:838-42.  Back to cited text no. 7
    
8.
Kaufman JH, Tolpin DW. Glaucoma after traumatic angle recession. A ten-year prospective study. Am J Ophthalmol 1974;78:648-54.  Back to cited text no. 8
    
9.
Ozer PA, Yalvac IS, Satana B, Eksioglu U, Duman S. Incidence and risk factors in secondary glaucomas after blunt and penetrating ocular trauma. J Glaucoma 2007;16:685-90.  Back to cited text no. 9
    
10.
Coles WH. Traumatic hyphema: An analysis of 235 cases. South Med J 1968;61:813-6.  Back to cited text no. 10
    
11.
Campbell DG. Ghost cell glaucoma following trauma. Ophthalmology 1981;88:1151-8.  Back to cited text no. 11
    
12.
Epstein DL. Diagnosis and management of lens-induced glaucoma. Ophthalmology 1982;89:227-30.  Back to cited text no. 12
    
13.
Herschler J. Trabecular damage due to blunt anterior segment injury and its relationship to traumatic glaucoma. Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol 1977;83:239-48.  Back to cited text no. 13
    
14.
Netland KE, Martinez J, LaCour OJ 3rd, Netland PA. Traumatic anterior lens dislocation: A case report. J Emerg Med 1999;17:637-9.  Back to cited text no. 14
    
15.
Mooney D. Angle recession and secondary glaucoma. Br J Ophthalmol 1973;57:608-12.  Back to cited text no. 15
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Methods
Results
Discussion
Conclusions
References
Article Tables

 Article Access Statistics
    Viewed125    
    Printed16    
    Emailed0    
    PDF Downloaded19    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]