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Man referred for acute visual loss after being hit in the left eye
Nasal subconjunctival hemorrhage was present on slit lamp examination.
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A 54-year-old man was referred to the New England Eye Center with acute visual loss in his left eye after being hit by a golf ball.
 Jeffrey Chang |
 Vivek Chaturvedi |
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He initially presented to a local ophthalmologist with a hyphema and intraocular inflammation. Visual acuity in the left eye was reduced to hand motions at 1 foot. IOP in the injured eye was 17 mm Hg. The outside ophthalmologist started him on Pred Forte (prednisolone acetate, Allergan), atropine, Cosopt (dorzolamide HCI, timolol maleate ophthalmic solution, Merck) and Alphagan (brimonidine tartrate, Allergan) in the left eye and referred him 2 days later.
The patient’s review of systems was positive for chronic back pain. Ocular history was significant for a childhood corneal injury of his left eye due caused by a piece of glass. Medical problems included hypertension and degenerative disc disease. The patient denied alcohol and tobacco use. Medications included Lorcet (hydrocodone/acetaminophen, Forest Pharmaceuticals), In-docin (indomethacin, Merck), Protonix(pantoprazole sodium, Wyeth Pharmaceuticals) and an antihypertensive medication.
Examination
On our examination, visual acuity was 20/30 in the right eye and hand motions at 1 foot in the left eye. External exam revealed a left-sided periorbital hematoma. Extraocular motility was full in both eyes. The left pupil was dilated and nonreactive due to prior atropine use. There was no afferent pupillary defect noted in either eye. Applanation tonometry revealed pressures of 15 mm Hg in the right eye and 41 mm Hg in the left eye.
Slit lamp examination and dilated fundus examination of the right eye were unremarkable. Slit lamp exam of the left eye showed nasal subconjunctival hemorrhage and pinguecula. The cornea was edematous, and an epithelial defect and old scar were noted. The anterior chamber of the injured eye was deep and filled approximately one-third with blood and fibrin (Figure).
Due to the limited view of the posterior segment of the left eye, a B-scan was performed. No vitreous hemorrhage or retinal detachment was detected.
 Anterior segment photograph of the left eye showing nasal subconjunctival hemorrhage and pinguecula. The cornea is edematous and shows an epithelial defect and old scar. A hyphema fills approximately one-third of the anterior chamber. Image: Semela-Brenner L and Krishnan C
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What is your diagnosis?
Visual loss, high IOP
The patient was diagnosed with acute post-traumatic glaucoma associated with hyphema.
Post-traumatic glaucoma can be due to a variety of causes: blunt trauma, penetrating injuries, chemical burns or radiation. Blunt ocular trauma with hyphema is associated with blow injuries in 62% of cases, projectiles in 34% of cases and explosions in 4% of cases. Early post-traumatic glaucoma should be distinguished from a late-onset form with or without angle recession. In late-onset post-traumatic glaucoma, IOP rises only later.
Discussion and management
IOP elevation in early post-traumatic glaucoma is due to intraocular inflammation after contusion. If a hyphema is present, the erythrocytes obstruct the trabecular meshwork and inhibit aqueous outflow. IOPs of 35 mm Hg or higher, lasting longer than 5 to 7 days, are associated with increased risk of glaucomatous optic nerve damage. However, the patient’s susceptibility for optic neuropathy plays a key role.
When a hyphema is present, there is a critical period, 2 to 5 days after the injury, for re-bleeding due to clot lysis and retraction, which can further increase IOP or lead to blood staining of the cornea. The use of aminocaproic acid, an antifibrinolytic, to prevent re-bleeding is controversial given its side effects (nausea, vomiting, diarrhea and postural hypotension) and the tendency to re-bleed if the medication is stopped before its recommended 5-day course. Furthermore, IOP elevation has been described after stopping aminocaproic acid due to a sudden wave of clot lysis.
Management goals in traumatic hyphema are to prevent re-bleeding and control IOP. Physical activity should be limited, and head position should be elevated at night. Antiplatelet agents should be discontinued. Medical treatment options are topical or oral agents to lower IOP. The associated inflammation should be treated with topical steroids and cycloplegia. If the IOP is uncontrolled or prolonged, surgical interventions might be necessary, such as performing a paracentesis or anterior chamber washout to avoid corneal blood staining.
If a hyphema is present, the incidence of angle recession is between 50% to 100%. The incidence of glaucoma is directly related to the extent of angle involvement: 4% if the recession is less than 180·, 10% if the angle recession is larger than 180·.
The timing of IOP elevation is unpredictable. IOP can become elevated months to years after the trauma. Therefore, these patients need regular IOP checks. Angle recession is diagnosed by gonioscopy. Typical features include a broad ciliary body band and a white scleral spur.
A recent study looked at initial clinical and ultrasonographic biomicroscopy (UBM) features in eyes with closed globe injuries that would help predict the occurrence of chronic traumatic glaucoma during a 6-month follow-up.
The presence of increased angle pigmentation, elevated IOP at baseline, hyphema, lens displacement and angle recession greater than 180· were significantly associated with chronic glaucoma after closed globe injury. The UBM features that were significant predictors for development of traumatic glaucoma were a wider angle and the absence of cyclodialysis.
Our patient’s IOP was successfully controlled with topical and oral glaucoma medications and was lowered to 15 mm Hg. Given the post-traumatic intraocular inflammation, topical steroids and cycloplegia were continued. The hyphema slowly resolved. The patient’s visual acuity improved slightly from hand motion to counting fingers at 2 feet. He continues to follow up regularly at New England Eye Center to monitor IOP.
Conclusion
In summary, glaucoma must be considered as a possibility with every ocular injury, and it can occur by a variety of mechanisms at the time of the injury or anytime thereafter.
Treatment must be directed at the underlying injuries, with the suppression of inflammation, removal of foreign material and restoration of normal anatomy. Elevated IOP should be treated with aqueous suppressants. Miotics and prostaglandin analogues that have the potential for exacerbating inflammation should be avoided. Surgery may be necessary for IOP control if medical therapy fails, depending on the pressure level and the assessed risk for glaucomatous optic neuropathy.
References:
- Campbell DG. Traumatic glaucoma. In: Shingleton BJ, Hersh PS, Kenyon KR, eds. Eye Trauma. St. Louis: CV Mosby; 1991:117-125.
- Edwards WC, Layden WE. Traumatic hyphema. A report of 184 consecutive cases. Am J Ophthalmol. 1973;75(1):110-116.
- Farber MD, Fiscella R, Goldberg MF. Aminocaproic acid versus prednisone for the treatment of traumatic hyphema. A randomized clinical trial. Ophthalmology. 1991;98(3):279-286.
- Fingeret M, Mathews TA, Fodera FA. Angle recession. Optom Clin. 1993;3(2):41-48.
- Herschler J. Trabecular damage due to blunt anterior segment injury and its relationship to traumatic glaucoma. Trans Sect Ophthalmol Am Acad Ophthalmol Otolaryngol. 1977;83:239-248.
- Kaufman JH, Tolpin DW. Glaucoma after traumatic angle recession. A ten-year prospective study. Am J Ophthalmol. 1974;78(4):648-654.
- Sambursky DL, Azar DT. Corneal and anterior segment trauma and reconstruction. Ophthalmol Clin North Am. 1995;8(4):609-631.
- Sihota R, Kumar S, Gupta V, et al. Early predictors of traumatic glaucoma after closed globe injury: trabecular pigmentation, widened angle recess, and higher baseline intraocular pressure. Arch Ophthalmol. 2008;126(7):921-926.
- Tesluk G, Spaeth G. The occurrence of primary open-angle glaucoma in the fellow eye of patients with unilateral angle-cleavage glaucoma. Ophthalmology. 1985;92(7);904-911.
- Linda Semela-Brenner, MD, and Chandra-sekharan Krishnan, MD, can be reached at Tufts Medical Center, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com.
- Edited by Jeffrey Chang, MD, and Vivek Chaturvedi, MD. Drs. Chang and Chaturvedi can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com. Drs. Chang and Chaturvedi have no direct financial interest in the products mentioned in this article, nor are they paid consultants for any companies mentioned.
