TRAUMATIC GLAUCOMA

Guest author

IRAM JAHAN

Ajmal Khan Tibbiya College

Aligarh

India

INTRODUCTION

Blunt or penetrating ocular trauma can result in an elevated intra-ocular pressure (IOP). This elevation in IOP can cause early or late glaucoma, depending upon the nature of the injury.

Although glaucoma associated with trauma is a multifactorial disease process, the main feature is reduced aqueous humor outflow through the trabecular meshwork channels.

EPIDEMIOLOGY

Blunt ocular trauma commonly causes anterior segment damage as the cornea and sclera are displaced posteriorly. This compressive deformation causes posterior displacement of the iris-lens diaphragm with subsequent expansion at the equator of the eye. Such damage may cause various anterior and posterior ocular tissues to tear.

Penetrating ocular trauma can also cause an elevated IOP from intraocular inflammation, secondary angle closure, intraocular hemorrhage, lens injury or epithelial downgrowth.

DIAGNOSIS

A complete history of the nature and timing of the current injury, past ocular injury, any preexisting glaucoma and past medical history, including sickle cell disease, coagulation defects, tetanus, vaccination status and use of anticoagulants needs to be obtained. Next, a complete ophthalmologic examination including visual acuity, pupil examination, IOP measurement, slit lamp examination and fundus examination should be performed. Special attention should be taken to check for any lens damage, zonular injury and peripheral retinal lesions.

EARLY ONSET GLAUCOMA AFTER TRAUMA

Intraocular inflammation after trauma=

Anterior segment inflammation may be present after blunt or penetrating trauma. This inflammation may result in ocular hypotension with decreased aqueous production. However, it can also cause a rise in IOP with trabecular blockade with inflammatory cells and particulate debris.

Gerkin et al in a study of penetrating injuries found that baseline intraocular inflammation was highly associated with future development of glaucoma in a multivariate analysis.

Trabecular meshwork injury=

Direct damage to the trabecular meshwork outflow channels can cause an early rise in IOP. Gonioscopy findings include: focal hemorrhage in Schlemm’s canal, full thickness rupture of trabecular meshwork, trabecular flap or cyclodialysis.

Hyphema=

Traumatic hyphemas generally result from a tear in the ciliary body or iris.

The amount of blood in the anterior chamber determines the grade of hyphema.

GRADES OF HYPHEMA

GRADE 1	Blood fills <1/3rd of anterior chamber
GRADE 2	Blood fills <1/3rd to ½ of anterior chamber
GRADE 3	Blood fills ½ to <100% of anterior chamber
GRADE 4 (8-ball hyphema)	Blood or clot fills entire anterior chamber

Chemical injuries=

Alkaline injury is more likely to cause ocular hypertension and subsequent glaucoma than acid injury. Alkaline exposure causes an almost immediate shrinkage of the scleral collagen which can elevate IOP to 40-50 mmHg. Next, a second elevation of IOP is noted within a few hours as prostaglandins are released. This type of injury may also cause late onset glaucoma. In such cases peripheral anterior synechiae develop with possible trabecular meshwork scarring and pupillary block.

LATE ONSET GLAUCOMA AFTER TRAUMA

Angle recession=

Angle recession is the result of a tear between the longitudinal and circular muscles of the ciliary body. Studies report that 50-81% of post-traumatic eyes develop angle recession and 6-20% of these go on to develop glaucoma.

Gonioscopic appearance of angle recession

Ghost cell glaucoma=

The red blood cells of a vitreous hemorrhage can lose their pliable biconcave disc shape and hemoglobin. These then degenerate into tan/khaki spherical “ghost cells”. The ghost cell can fill the anterior chamber and form a tan hypopyon. As a result of their rigid spherical shape, ghost cells have difficulty crossing through the trabecular meshwork and clog the outflow pathway. This causes a rise in IOP and subsequent glaucoma.

Secondary angle closure=

Intraocular inflammation and blood, secondary to trauma are common clinical features. Persistent inflammation can lead to formation of peripheral anterior synechiae. If extensive enough the patient may develop angle closure glaucoma.

Lens injury=

There are four main types of traumatic lens injury that can ultimately lead to the development of secondary glaucoma:

Lens subluxation

Lens swelling

Phacolytic process

Phacoanaphylactic process

Lens subluxation can cause anterior or posterior displacement. Lens swelling can cause phacomorphic glaucoma. Phacolytic glaucoma results from the release of lens proteins through an intact capsule. Phacoanaphylactic glaucoma is a granulomatous reaction to the lens particles released from a disrupted lens capsule.

Cyclodialysis cleft closure=

Cyclodialysis is the separation of the ciliary body from the scleral spur. This creates a direct pathway for aqueous to flow into the suprachoroidal space. This separation may also cause a temporary or chronic hypotony.

Epithelial down-growth=

It is a potential complication of penetrating ocular injury and lens. Corneal or conjunctival epithelium invades the anterior chamber and covers other intraocular structures. Glaucoma is reportedly present in upto 43% of patients with epithelial downgrowth.

Retained intraocular foreign body=

Rarely, an iron containing retained intraocular foreign body can cause siderosis bulbi. The iron exposure can cause iris heterochromia and ocular hypertension as the toxic iron coats the trabecular meshwork impeding aqueous outflow.

Rhegmatogenous retinal detachment (RRD)=

RRD is more commonly associated with ocular hypotension with decreased aqueous production by the ciliary body. However, 5-10% of these patients may develop Schwartz-Matsuo syndrome. The pathogenesis of this condition is controversial. Schwartz hypothesized that iridocyclitis caused reduced aqueous outflow. Davidorf suggested pigment granules released from the retinal pigment epithelium could migrate anteriorly within the aqueous humor to block the trabecular meshwork. Matsuo and colleagues isolated photoreceptor outer segments and inflammatory cells in aqueous humor aspirates of patients with Schwartz syndrome. According to these researchers the photoreceptor outer segments pass through the retinal break and gain access to aqueous outflow pathways, leading to outflow obstruction. IOP typically returns to normal following surgical repair of the RD.

TREATMENT

General principles of medical & surgical management

• Management needs to be dictated by the status of the optic nerve.
• The management should be focused on the underlying etiology and at reducing IOP.
• Any inflammation should be treated with topical steroids.
• Cycloplegics should be considered to control ciliary spasm.
• Miotics are avoided as they worsen inflammation.
• Prostaglandin analogues can be tried in the absence of cystoid macular edema as a “final resort” prior to going for surgical options.
• If medical management fails then surgical intervention must be considered.

Hyphema treatment

• The two main goals in the treatment of traumatic hyphemas are: IOP control and prevention of rebleeding.
• All patients should be restricted to bed rest.
• The head of the bed should be elevated and treatment with cycloplegics and topical steroids initiated.
• Aspirin and NSAID medications should be avoided.
• IOP control should consist of topical beta blockers and alpha agonists.
• Carbonic anhydrase inhibitors can be used in non-sickle cell disease.

Indications for surgical intervention are:

• IOP more than 50 mmHg for five days
• IOP more than 35 mmHg for seven days
• Unresolved total hyphema for nine days
• Or corneal blood staining

Traumatic hyphemas have a 0.4-35% rate of rebleed, usually occurring within 2-5 days. For prevention of rebleeding aminocaproic acid or systemic steroids can be considered.

Angle recession glaucoma treatment

• It is often refractory to aqueous suppressant therapy.
• Miotics should be avoided.
• If medical therapy fails, the surgical options include trabeculectomy with or without antimetabolites and glaucoma drainage devices.
• Laser Trabeculoplasty is not effective in these cases.

Ghost cell glaucoma treatment

If medical management of IOP is inadequate, then surgical treatment options include anterior chamber wash-out or vitrectomy to remove as many red blood cells as possible.

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