High IOP in Traumatic Hyphema
A review of the etiologies and management of elevated IOP after trauma to the crystalline lens.
Whether due to a blunt or penetrating injury, lens trauma can cause the IOP to rise. Mechanisms of lens-induced traumatic glaucoma include pupillary block, lens particle glaucoma, phacomorphic glaucoma, and phacolytic glaucoma. Blunt ocular injury is responsible for most cases of posttraumatic pupillary block and phacolytic glaucoma. Penetrating ocular injury typically results in lens particle glaucoma or phacomorphic glaucoma. Data from the Eye Injury Registry of Alabama have shown blunt, closed ocular injuries to be responsible for 77% of elevations in pressure after trauma versus 23% for open-globe injuries.1 Lens trauma and inflammation at the time of presentation are significant risk factors for patients’ developing glaucoma after penetrating ocular trauma.2
LENS PARTICLE GLAUCOMA
Lens particle glaucoma occurs when the immune system is sensitized to lens proteins released from a disrupted lens (Figure 1). The resultant zonular granulomatous inflammatory reaction impairs the function of the trabecular meshwork and can cause peripheral anterior synechiae to form.
If you suspect lens particle glaucoma after a penetrating injury, first focus on identifying the site and extent of ocular penetration. A computed tomography scan of the orbit is indicated to look for an intraocular or orbital foreign body and for gross deformity of the scleral wall. Vision may be severely decreased in an injured eye with extensive involvement of the lens and significant comorbidities, or it may be unaffected if the lens defect is more peripheral. A combination of anterior chamber cell, flare, and granulomatous keratic precipitates may be present starting several hours after the injury. A cortical cataract may be evident at the site of capsular disruption. If the eye is stable enough for gonioscopy to be performed, examine the angle for peripheral anterior synechiae, lens particles, and any other comorbid injuries. Peak pressure elevation typically occurs 1 to 2 weeks after the injury.
Self-sealing injuries may be observed without repair. Defects in the lens capsule usually spontaneously reepithelialize, and the resultant cataract may be focal enough to allow clear vision. In most cases of a large corneoscleral laceration, the focus of repair is to reestablish the integrity of the globe while leaving the removal of lenticular material for a subsequent surgery in the near future. If attempting to remove lenticular material after establishing control of the globe, you may find trypan blue helpful for identifying capsular tears. The inflammation must be managed with topical or oral steroids, and broad-spectrum antibiotics should be initiated to decrease the risk of endophthalmitis. Medications to lower the IOP may be necessary.
Blunt or penetrating lens trauma can cause hydration and thickening of the lens, resulting in phacomorphic glaucoma. Patients’ vision can be variable, but you will observe diffuse narrowing of the anterior chamber angle on gonioscopy. A laser peripheral iridotomy (LPI) to remove any component of pupillary block is recommended prior to the definitive treatment of cataract surgery.
Several mechanisms account for pupillary block after lens trauma. The rupture of zonules can result in anterior subluxation of the lens and thus cause pupillary block (Figure 2). Vitreous prolapse in an area of ruptured zonules can also cause pupillary block. Finally, patients seeking care several days to weeks after the injury may have significant posterior synechiae, resulting in a secluded pupil.
If you suspect pupillary-block glaucoma, gonioscopy is the crucial test, but it may not be possible secondary to a view compromised by corneal edema, inflammation, or hyphema. You may be able to improve microcystic edema by lowering the IOP, removing the corneal epithelium, or topically applying glycerin (off-label use). It is critical that you examine the eye for signs of zonular weakness, including phacodonesis, an asymmetrically deep sulcus, lens subluxation, and vitreous prolapse. Gonioscopy after pupillary dilation usually allows direct visualization of the zonules.
Cycloplegia is the initial approach to pupillary block attributed to zonular laxity. Pupillary dilation causes the ciliary body to rotate forward and the zonules to tighten, potentially resolving the blockage. Miotics constrict the ciliary muscle and aggravate preexisting zonular laxity.3 Furthermore, because aqueous misdirection is another part of the differential diagnosis, cycloplegia is essential. Initiate oral and topical aqueous suppressants and, if they are not effective, use hyperosmotics unless they are contraindicated. A paracentesis can be performed if you cannot lower the IOP. Be careful to avoid further traumatizing the subluxated lens by choosing a quadrant away from it. Perform an LPI as soon as possible in a location that is not prone to occlusion by the subluxated lens.
If you are sufficiently confident that you can perform a paracentesis without traumatizing the lens, you can use this intervention as the initial treatment, followed by an LPI. Then, titrate aqueous suppression to the level of residual IOP elevation.
Severe trauma can result in the complete dislocation of the lens into the vitreous (Figure 3). Phacolytic glaucoma may develop, as proteins from the hypermature cataract leak through the intact capsule. The symptoms of decreased vision, redness, and photophobia usually occur months to years after the initial injury. A significant inflammatory reaction is present. Although topical and oral steroids and glaucoma medications may temporize the situation, a pars plana lensectomy is indicated, since the eye is already functionally aphakic.
In severely traumatized eyes with elevated pressure, there is often more than one mechanism behind the increase. Bear in mind the differential diagnosis of elevated IOP after a traumatic injury to avoid overlooking contributing factors.
Johann G. Ohly, MD, is a glaucoma specialist at Mercy Clinic Eye Specialists in Springfield, Missouri. Dr. Ohly may be reached at (417) 820-9393; email@example.com.
- De Leon-Ortega JE, Girkin CA. Ocular trauma-related glaucoma. Ophthalmol Clin North Am. 2002;15:215-223.
- Girkin CA, McGwin G, Morris R, Kuhn F. Glaucoma following penetrating ocular trauma: a cohort study of the United States Eye Injury Registry. Am J Ophthalmol. 2005;139(1):100-105.
- Glaucomas associated with disorders of the lens. In: Allingham R, Damji K, Freedman S, et al, eds. Shields’ Textbook of Glaucoma. Philadelphia: Lippincott Williams & Wilkins; 2005:318-327.
TOP 5 ARTICLES FROM 2012
- Optic Disc Drusen
Practical implications and management.
By Tomas M. Grippo, MD; Spencer W. Rogers, MD; James C. Tsai, MD, MBA; and Richard A. Lewis, MD
- Laser Trabeculoplasty
By Hylton R. Mayer, MD; Brian A. Francis, MD, MS; Jeffrey A. Kammer, MD; and George R. Reiss, MD
- What’s New on the Tube?
Recent trends, updates, and controversy in aqueous shunt surgery.
By HERBERT P. FECHTER, MD, PE
- The Collaborative Initial Glaucoma Treatment Study—What We Have Learned so Far
By Jess T. Whitson, MD
- An Overview of Laser Iridoplasty
This procedure safely widens the angle, and it contributes to the success of other glaucoma procedures.
By Barbara A. Smythe, MD, and Yen Ngo, MD