Traumatic Glaucoma

Etiology

Closed-globe Trauma

• Early-onset
  • Traumatic hyphema
  • Traumatic iritis
  • Trabecular meshwork injury
  • Suprachoroidal hemorrhage
• Late-onset
  • Steroid response
  • Angle recession
  • Lens subluxation and dislocation +/- secondary pupil block
  • Phacomorphic glaucoma
  • Phacolytic glaucoma and lens particle glaucoma
  • Ghost cell glaucoma
  • Hemolytic glaucoma
  • Hemosiderotic glaucoma
  • Carotid-cavernous sinus fistula

Open-globe Trauma

• Epithelial downgrowth
• Fibrous downgrowth

Epidemiology

Eye trauma has been estimated to have an annual incidence of nearly 7 per 1000 populations in the United States, with the most common trauma being orbital fractures. Intraocular pressure elevation after repair of open-globe injuries is not uncommon, with one case series showing 23.3% of patients developed raised IOP (defined as ≥22 mm Hg at >1 visit). 6.2% of patients in the same study went on to develop glaucoma.[2] 

A 3.4% incidence of glaucoma following blunt globe trauma has been demonstrated at six months follow-up post-injury, but at ten years post-trauma, it is as high as 10%, highlighting the need for regular follow-up in this patient group.[3][4]

Pathophysiology

Closed-globe Trauma

Early-onset

Traumatic Hyphema

As a result of sudden compression-decompression forces onto the globe, the highly vascularized ciliary body and iris, most commonly at the angle, can be torn due to the sudden increase in IOP, limbal tissue stretching, posterior and peripheral flow of aqueous, and posterior displacement of the iris and lens, causing bleeding within the anterior chamber (AC). Depending on the extent of the blunt trauma, injury can occur to various angle structures. Commonly there is damage to the iris insertion manifesting as angle recession, followed by cyclodialysis and, very uncommonly, iridodialysis.[5] 

The associated injury to vascular structures leads to hemorrhage into the AC, causing a fluid level of blood called hyphema. If blood fills the entire volume of the AC, this is referred to as a total hyphema, also known colloquially as an “8-ball” hyphema.

Rebleeds, or secondary hemorrhages, can occur 2 to 5 days after the initial bleed and are estimated to have an incidence of 20 to 25% in traumatic hyphema.[5] This has been postulated to be a result of fibrinolysis and clot retraction.[6][7] Rebleeds are often associated with a higher risk of an increase in IOP and worse visual outcomes.[8]

The severity of hyphema can be graded according to the amount of blood within the AC, which correlates with an increased likelihood of IOP elevation. Grade I, II, III, and IV hyphemas correspond to less than one-third, one-third to one-half, more than half, and the entire AC being filled with blood, respectively.[5] Grade I and II are associated with a 13.5% risk of IOP elevation, while Grade III is associated with a 27% risk.[9] Grade IV and rebleeds are associated with a 50% risk. The mechanism of IOP elevation is thought to be secondary to the obstruction of the trabecular meshwork by red blood cells, fibrin, platelets, and other products of fibrinolysis.[10]

Traumatic Iritis

The mechanism of iritis (anterior uveitis) post-trauma is still poorly understood. It has been suggested that tissue damage from trauma triggers an innate immune response mediated by an increase in vascular permeability and an influx of inflammatory mediators.[11] It has also been theorized that traumatic iritis may be akin to similar inflammatory processes found elsewhere in other organ systems, such as the Koebner phenomenon, where a psoriasis flare is precipitated by a minor skin injury in about 25% of patients.[12]

Inflammatory cells and precipitates within the AC may block the trabecular meshwork, leading to reduced aqueous outflow and a secondary increase in IOP. Reduced outflow can also be due to inflammation of the trabecular meshwork itself (so-called “trabeculitis”) due to trauma, leading to trabecular meshwork congestion and resultant reduced outflow facility.[1]

Trabecular Meshwork Injury

Trauma to the eye can mechanically liberate pigments into the AC, which may block aqueous outflow through the trabecular meshwork, resulting in a rise in IOP.[1] An increase in trabecular meshwork pigmentation has been associated with an increased risk of the development of traumatic glaucoma.[13] The mechanism of IOP elevation is similar to conditions such as pigment dispersion syndrome and pseudoexfoliative glaucoma.[14][15]

Late-onset traumatic glaucoma can also occur due to trabecular meshwork injury, or more accurately, the tissue healing process following trabecular meshwork injury. Visible linear tear in the trabecular meshwork under gonioscopy with extension into the Schlemm’s Canal on ultrasound biomicroscopy had been reported after blunt trauma to the globe.[16] 

Superficial trauma tends to present as a flap at the scleral spur on the gonioscopy, while deeper tears may show shredded iris processes. Subsequent tissue remodeling from scarring along the angle structures can result in late-onset IOP elevation due to a gradual reduction in aqueous outflow.

Suprachoroidal Hemorrhage

Suprachoroidal hemorrhage is most commonly associated with intraocular surgery but can, of course, occur after blunt or penetrating trauma to the globe. The mechanism of hemorrhage in the suprachoroidal space is thought to be secondary to tearing forces on the long or short posterior ciliary arteries - either due to direct trauma or rapid decompression of the globe in the setting of intraocular surgery and globe penetration.[17] Traumatic glaucoma can occur following intraocular pressure elevation from secondary angle-closure due to the mass effect of the hemorrhage in the posterior segment, displacing the lens and iris forwards and causing angle narrowing.[18]

Late-onset

Steroid Response

Topical corticosteroid preparations are commonly used in an ocular trauma setting to reduce intraocular inflammation. Many patients develop an associated IOP elevation, most commonly 3 to 6 weeks following the initiation of topical corticosteroid treatment.[1] These patients are known as ‘steroid responders.’ So-called ‘high’ responders, which constitute 4 to 6% of the population, develop an IOP of more than 31 mmHg or an increase of more than 15 mmHg from their baseline IOP. ‘Moderate’ responders constitute about one-third of the population. They develop an IOP of between 25 and 31 mmHg or an increase of between 6-15 mmHg from baseline IOP. The remainder of the population is non-responders.[19]

The mechanism of steroid-induced IOP elevation was thought to be due to increased outflow resistance at the trabecular meshwork. This is secondary to the increased expression of glycosaminoglycans and extracellular matrix proteins.[20]

Angle Recession 

Angle recession is defined histologically as a rupture between the circular and longitudinal fibers of the ciliary muscles.[21] Gonioscopic examination shows a widened ciliary body band and sometimes a newly formed white hyaline membrane covering the trabecular meshwork, which often extends deep into the recessed angle, reducing aqueous outflow but often many years after the initial traumatic insult as the formation of the hyaline membrane is often a gradual process.[21] However, it has been shown to occur sooner in eyes that have sustained more than 270 degrees of angle recession.[22] 

Reduced outflow is also felt to be caused by the loss of tension of the ciliary muscle on the scleral spur due to the tearing of ciliary muscle fibers, leading to the narrowing of Schlemm’s canal.[22] As distinct from hyaline membrane formation, scarring and fibrosis over the angle can also lead to reduced aqueous outflow and subsequent IOP elevation. Very commonly, angle recession is also associated with hyphema, which had been reported in 71 to 100% of eyes with angle recession and is the main cause of the initial spike of IOP.

Lens Subluxation and Dislocation +/- Secondary Pupil Block

Ocular trauma can cause posterior displacement of the lens-iris diaphragm, subsequently rupturing the zonular fibers that hold the lens in place. A lens may be subluxated when greater than 25% of the zonules are torn, such that the lens is partially displaced from its normal centralized position. Lens dislocation occurs when there is a complete disruption of all or most of the zonules. The lens can then become dislocated into the anterior chamber through the pupil or into the vitreous cavity. IOP elevation can occur via several mechanisms, including pupil block with intermittent or acute angle-closure by a subluxated lens, the release of pigments from chafing of a subluxated or dislocated lens on the iris, and trabecular meshwork blockage from vitreous strands prolapsed into the AC, in the setting of a frankly dislocated lens into the vitreous cavity.[23]

Phacomorphic Glaucoma

Trauma, both blunt and globe-penetrating (in this scenario, without breaking the lens capsule), can lead to the rapid development of a large intumescent cataract. The now bulky lens can lead to secondary angle closure due to the forward displacement of the iris and subsequent pupillary block.[24]

Phacolytic Glaucoma and Lens Particle Glaucoma

Hypermature cataracts that occur after trauma may be associated with microscopic defects of the lens capsule due to the rapid stretching of the capsule at the time of injury. Soluble lens protein can leak through those defects into the anterior segment. As macrophages phagocytose these proteins, they can ultimately cause blockage of the trabecular meshwork, causing phacolytic glaucoma.[25] High-molecular-weight lens protein has also been suggested to play a role in directly obstructing the trabecular meshwork and impeding aqueous outflow.[26]

Although there are certain similarities between phacolytic and lens particle glaucoma, they are distinct entities. Pathophysiologically, lens particle glaucoma is caused by actual lens particles rather than soluble lens protein, depositing on the trabecular meshwork and obstructing outflow. These lens particles can come from the traumatic rupture of the lens capsule. These particles can also originate from the cataract itself during cataract surgery.[24] 

Rarely, Elsching pearls, which are an accumulation of clusters of proliferating lens epithelial cells formed in the equatorial region of the capsular bag, sometimes also migrating to the posterior capsule and contributing to posterior capsular opacification after cataract surgery, can be released into the aqueous by an Nd:YAG capsulotomy laser which will, in turn, cause an impedance to aqueous outflow.

Phacoantigenic Glaucoma

Phacoantigenic glaucoma, also known as phacoanaphylactic glaucoma, is a latent, chronic granulomatous reaction to retained lens material after trauma or cataract surgery.[1] Inflammation can occur in the affected or fellow eye after a latent period of immunological sensitization to antigens of the crystalline lens, previously enclosed by the lens capsule and hitherto unencountered by the body’s immune system. This is thought to be a type III hypersensitivity reaction.[27]

Ghost Cell Glaucoma

Ghost cells are old, spherical, degenerated, and depigmented red blood cells, which also contain clumps of degenerated residual hemoglobin binding onto the cell membrane called Heinz bodies.[28] They can occur after a longstanding vitreous hemorrhage following trauma, as well as in the context of other pathologies such as proliferative diabetic retinopathy.[29] 

Due to the trauma itself or previous surgery, the anterior hyaloid face of the vitreous may be disrupted, allowing passage of ghost cells within the vitreous cavity to the AC. As they are mechanically rigid, they can obstruct the pores of the trabecular meshwork and consequently reduce aqueous outflow. The formation of ghost cells occurs within 1 to 3 weeks after the initial vitreous hemorrhage, but the rise in IOP often occurs 1 to 3 months after.[30] 

It is uncommon for ghost cell glaucoma to occur in the setting of an isolated hyphema unless very longstanding, due to the high oxygen levels and high aqueous circulation rate within the AC allowing clearance of the hyphema before the red blood cells can degenerate into ghost cells.

Hemolytic Glaucoma

This may be confused with ghost cell glaucoma. In hemolytic glaucoma, red blood cells from either vitreous hemorrhage or anterior chamber hyphema are broken down into hemoglobin and hemosiderin. These, as well as hemoglobin-filled macrophages, in turn, block the aqueous outflow pathway.[31] On examination, cells in the AC in hemolytic glaucoma will have a red tinge, while in ghost cells, glaucoma cells are khaki colored.

Hemosiderotic Glaucoma

This is a rare entity caused by the direct toxic effect of intraocular iron on the trabecular meshwork, causing fibrosclerosis and subsequent obstruction of aqueous outflow. The source of intraocular iron can be introduced by trauma in the form of an intraocular foreign body or iron derived from blood in the AC. The hemoglobin in red blood cells is released after hemolysis and, in turn, is further degraded into hemosiderin which contains toxic granules of inorganic iron.[28]

Carotid-Cavernous Sinus Fistula

This type of fistula can develop after a trauma to the orbit. It can be subdivided into two subtypes: 1- direct high-flow shunt with communication between the internal carotid artery and cavernous sinus; and 2 -indirect low-flow dural shunt with communication between cavernous arterial branches and the cavernous sinus. Traumatic carotid-cavernous sinus fistula is more frequently high-flow in nature. Other causes of the high-flow fistula may include rupture of an internal carotid artery aneurysm within the cavernous sinus, Ehlers-Danlos syndrome type IV, and iatrogenic causes such as an internal carotid artery endarterectomy.[1] 

Low-flow fistula can be caused by hypertension, fibromuscular dysplasia, Ehlers-Danlos syndrome type IV, and dissection of the internal carotid artery. Carotid-cavernous sinus fistula can lead to a raised IOP via increased episcleral venous pressure, which can, in turn, cause angle closure due to edema of the ciliary body and choroid. Raised episcleral venous pressure can also lead to central retinal vein occlusion, leading to ischemia and subsequent iris neovascularization and neovascular glaucoma.[1][2]

Open-globe Trauma

Globe-penetrating injury can lead to secondary intraocular pressure elevation and glaucoma through any of the causes discussed above in the closed-globe trauma section. However, the following mechanisms are specific to eye injuries in which the corneoscleral envelope is breached through penetration or rupture.

Epithelial Downgrowth

Epithelial downgrowth occurs when non-keratinized stratified squamous epithelial cells, most commonly the conjunctiva and the cornea, are introduced through a wound into the AC. It comes in different forms, including epithelial pearls, cysts, and membranes. Epithelial pearls are small structures on the iris surface, often far from the original entry site of the trauma.[1] Epithelial cysts are often found closer to, or even in continuity with, the wound. The first two forms tend to be more benign in nature, but epithelial membranes proliferate aggressively and thus have the greatest potential to cause IOP elevation and glaucoma.[32]

Elevation of the IOP occurs due to epithelial membrane growth over the trabecular meshwork, causing aqueous outflow obstruction.[32] Peripheral anterior synechiae (PAS) may also form as the epithelial cells proliferate, which may also trigger an inflammatory response in the form of anterior uveitis, further speeding up the formation of PAS. These epithelial cells within the AC may also contain aberrant goblet cells, which can secrete mucin, in turn blocking the trabecular meshwork.[33] Membrane formation across the anterior lens and pupil may also lead to pupil block.

Fibrous Downgrowth

Fibrous downgrowth can appear similar to epithelial downgrowth, but it tends to be more common, benign, and indolent.[32] Fibrous downgrowth often presents as a thick fibrovascular membrane in the AC or as a retrocorneal membrane covering the corneal endothelium, trabecular meshwork, and iris, leading to IOP elevation due to reduced aqueous outflow.[32][34] The origin of the fibrous tissue is not well understood, but it may be related to subconjunctival connective tissue, stromal keratocytes, or metaplastic corneal endothelial cells.[1]

History and Physical

The remainder of this discussion will focus on managing elevated intraocular pressure as a sequel to the traumatic event and assumes the acute injury has been treated; management of ocular trauma in the acute setting will not be discussed further.

History

A thorough history of the trauma should be elicited and carefully documented. The specific details of the trauma should be noted, including the time, nature, and setting of the trauma (for example, an alleged assault or accidental injury at home, workplace, or during leisure activities), any possibility of foreign body involvement as well as the distance, trajectory, and speed of a foreign body if this is relevant. 

It is also important to record what treatment, and if applicable, what surgery has been carried out for the trauma. Determine the timing of the IOP elevation in relation to the injury and treatment given. Record any past ophthalmic and medical histories, such as a pre-existing history of glaucoma, previous eye surgery, bleeding disorders, sickle cell disease, the use of topical and systemic steroids, and the use of anticoagulation. A family history of sickle cell disease and blood dyscrasias should also be elicited.

Depending on the history, the possibility of traumatic optic neuropathy and traumatic brain injury needs to be considered as this may influence the interpretation of the physical examination and the results of visual field testing. Old correspondence from previous treating doctors, hospital discharge letters, and imaging reports (and the images themselves) may also require evaluation.

Physical

Visual acuity, intraocular pressure (ideally with Goldmann applanation tonometry), and pupillary reflexes (including for a relative afferent pupil defect) should be checked. Assessing for other features of optic nerve dysfunction with red and brightness desaturation, as well as for dyschromatopsia with color plate testing, may be helpful to determine whether a component of any optic nerve dysfunction can be attributed to non-glaucomatous causes such as traumatic optic neuropathy.

To make an appropriate adjustment for the intraocular pressure measurement, the central corneal thickness should be measured with ultrasound pachymetry, anterior segment optical coherence tomography, Schleimpflug (pentacam) tomography, or similar. 

Depending on how recent the injury occurred, the anterior chamber may show the presence of a hyphema, inflammatory cells or fibrin in cases of traumatic iritis, lens protein particles or lens material in cases of phacolytic, lens particle and phacoantigenic glaucoma, brownish-colored cells corresponding to red blood cells found in hemolytic glaucoma, as well as Khaki-colored cells corresponding to ghost cells in ghost cell glaucoma.

The corneal endothelium may show keratic precipitates from uveitis and corneal blood staining from previous longstanding hyphema. Iris examination may show iridodialysis, transillumination defects due to foreign body entry, and epithelial pearls from downgrowth. There may be signs of posterior synechiae at the pupil margin, indicating previous inflammation. The AC may be shallow in secondary narrow-angle or angle-closure glaucoma. It may also show signs of epithelial and fibrous downgrowth in the form of an epithelial membrane or fibrovascular membrane, respectively.

Gonioscopy may show signs of trauma to the angle, including hemorrhage, trabecular meshwork hyperpigmentation from trabecular meshwork injury, peripheral anterior synechiae, and angle recession.

The lens may show signs of subluxation (iridodonesis, phacodonesis, asymmetric AC depth, visibility of parts of the lens equator when pupil is dilated, strands of vitreous at the pupil margin, or frank prolapse of vitreous into the AC), dislocation, enlarged lens thickness, and disrupted capsule in phacolytic and lens particle glaucoma.

Posterior segment examination may reveal the presence of ghost cells, retained foreign body, vitreous hemorrhage, retinal hemorrhage, commotio retinae, retinal breaks with or without associated rhegmatogenous detachment, suprachoroidal hemorrhage, or choroidal rupture. If glaucoma has already evolved, then, of course, the optic discs may have a cupped appearance.

Evaluation

An ultrasound B-scan can be useful if the fundal view is blocked, for example, by dense longstanding vitreous hemorrhage.

In certain situations, more specific investigations may be necessary. An ultrasound biomicroscopy (UBM) may be useful in traumatic cataracts to detect and assess occult zonular defects.[35] UBM is also useful for evaluating angle structures and the anterior segment, including the ciliary body, in the settings of suspected angle recession, iridodialysis, and cyclodialysis cleft.[36] It aids diagnosis, especially when the view of the anterior segment is limited by media opacities and distortion of anatomy.[36]

Specular microscopy may be helpful in epithelial downgrowth. It may show a demarcation line between the epithelial membrane and the corneal endothelium in the setting of a retrocorneal epithelial membrane. However, its use requires a relatively clear cornea and will not be useful in the presence of corneal edema.[37] Anterior segment OCT may have utility in determining the origin of the epithelial downgrowth. However, an aqueous tap and cytology or a tissue biopsy of the membrane are required for definitive.

Treatment / Management

Closed-globe Trauma

Early-onset

Traumatic hyphema

Management of hyphema starts with medical treatment in the form of topical corticosteroids and cycloplegia. Strict bed rest with a 45 degrees head elevation is advised to allow the blood to settle inferiorly so that the visual axis can be cleared. Globe protection in the form of a rigid plastic eye shield may be useful to prevent further trauma to the eye. In conjunction with the patient’s physician, consider withholding any antiplatelet and anticoagulation agents, as well as non-steroidal anti-inflammatory drugs.

Certain cases deemed to be high-risk may require admission to the hospital for close observation. These include those who may be non-compliant with their treatment regime, children, rebleeding cases, Grade II hyphemas or worse, and those with sickle cell trait or disease. Rebleeds can occur 2 to 5 days after the initial injury, and patients should be closely monitored in the early stages.

If the IOP is raised and a decision is made to treat the IOP, having considered parameters such as the status of the optic disc, the presence of preexisting glaucoma, central corneal thickness, and the likelihood of IOP elevation settling, a stepwise approach should be taken starting with topical ocular antihypertensives. First-line treatment normally comprises a topical beta-blocker, alpha-2 agonist, carbonic anhydrase inhibitor, or a combination of these. There are variations amongst clinicians’ practice patterns, but some avoid using prostaglandin analogs as they are theoretically pro-inflammatory with the potential to further break down the blood-aqueous barrier, exacerbating intraocular inflammation and potentially causing a rise in the IOP.[38] 

Some clinics use prostaglandin analogs in these situations as well. If the IOP remains inadequately controlled with topical treatment alone, oral or intravenous acetazolamide may be considered. The use of both topical and systemic carbonic anhydrase inhibitors, as well as osmotic agents such as mannitol, should be avoided in patients with sickle cell trait or disease as it can promote sickling due to acidosis.[39] Sometimes if the IOP is acutely raised, one may consider treating with multiple agents simultaneously, expecting that one can withdraw treatment in a stepwise approach later.(B3)

Surgery in the form of AC paracentesis and/or AC washout to evacuate the hyphema may be needed in certain cases if medical treatment fails. A patient with high IOP that is resistant to maximum medical therapy should be a candidate for surgery. A general guide, as suggested by Wilson, indicates that those with IOP greater than 50 mmHg for over five days, IOP greater than 45 mmHg for over a week, or IOP greater than 35 mmHg for over two weeks should be considered for surgery. A more cautious approach should be taken in patients with sickle cell trait or disease, i.e., IOP greater than 24 mmHg for over a day.[39] (B3)

Other criteria include persistent grade IV hyphema (also called eight-ball hyphema) and early corneal blood staining. Despite an anticipated high failure rate and short duration of drainage function, trabeculectomy has been described in this context to maintain a safe level of IOP while the hyphema clears and aqueous outflow normalizes.[40][41] However, some prefer glaucoma drainage devices such as an Ahmed or Baerveldt Tube Shunt to achieve longer-term IOP control.[42](B3)

Traumatic Iritis

Topical corticosteroids and cycloplegia are the mainstays of treatment. Raised IOP is usually self-limiting in these cases, and topical ocular antihypertensives are generally sufficient to control raised IOP in most cases.

Trabecular Meshwork Injury

Topical ocular antihypertensives would be sufficient to counteract the initial IOP rise. The use of lasers such as argon laser trabeculoplasty (ALT) or selective laser trabeculoplasty (SLT) to the angle may also be considered. Kelman et al. and Akkin et al. previously reported using ALT directed to the traumatized Schlemm’s canal to treat recurrent hyphema due to laceration to the trabecular meshwork and Schlemm’s canal.[43][44] If the rise in IOP is late-onset, it may be due to scarring of the angle structures and will benefit from incisional glaucoma surgery.(B3)

Suprachoroidal Hemorrhage

Treatment of raised IOP in a well-established suprachoroidal hemorrhage is initially medical with topical and systemic ocular antihypertensives. Topical corticosteroids reduce intraocular inflammation and improve comfort. Cycloplegic agents rotate the ciliary body posteriorly and may help to maintain AC depth and minimize angle closure. Cycloplegia also reduces ciliary spasms and may help to relieve some of the ocular pain commonly associated with suprachoroidal hemorrhage. Surgical drainage should be considered if a high IOP or severe pain remains persistent. There is still no consensus regarding the decision and best timing of drainage, but in principle, it is preferable to wait 7 to 14 days for clot liquefaction to occur.[45] Indications for more urgent surgical drainage include kissing choroidal, retinal detachment, and persistently high IOP.

Late-onset

Steroid Response

Patients with previously known steroid response and predisposing risk factors, including those with high myopia, primary open-angle glaucoma or glaucoma suspects, first-degree relatives with primary open-angle glaucoma, type I diabetes, connective tissue disease (especially men with rheumatoid arthritis) and angle recession, should be closely monitored when started on corticosteroids.[46] The effect of a steroid-induced IOP elevation is normally temporary and reversible if it is used for less than 12 months. However, more than 18 months of corticosteroid use may lead to long-term IOP elevation that persists even after therapy withdrawal.[46] 

If corticosteroids are required in the setting of persistent inflammation, corticosteroids with lower potency and less ocular penetration should be considered. If periocular depot corticosteroids were used, they could be surgically excised.[20] If a steroid response occurs after intravitreal injection, such as triamcinolone acetonide, removal through vitrectomy can be helpful.[47] (B3)

The management of IOP elevation follows the same stepwise approach as in primary open-angle glaucoma. However, there is evidence that SLT in these patients is relatively more effective in lowering IOP.[48] Goniotomy and canaloplasty can be considered with two small case series showing encouraging results.[49][50](B2)

Angle Recession

In angle recession of more than 180 degrees, it has been suggested that a lifelong annual examination is required to detect glaucoma as it may develop several months to years after the initial traumatic insult.[22] Topical ocular antihypertensives will be the mainstay of treatment. Beta-blockers, alpha agonists, and carbonic anhydrase inhibitors work well in angle recession glaucoma. Some practitioners believe prostaglandin analogs should be used cautiously due to their theoretical pro-inflammatory effect. Other practitioners utilize them routinely but consider withdrawing or substituting with another drug class if intraocular inflammation is persistent or other considerations arise, such as cystoid macular edema. It also has a theoretical benefit as it reduces IOP via the uveoscleral pathway and hence would bypass the injured trabecular meshwork.(B3)

Argon laser trabeculoplasty, an outdated treatment modality, was found to have a minimal therapeutic effect in angle recession glaucoma.[51] Trabeculopuncture with an Nd: YAG laser has previously been described; one small study with a short follow-up showed some intraocular pressure lowering effect compared to ALT.[52] Non-enhanced trabeculectomies have been shown to have a high failure rate, with post-traumatic angle recession being an independent risk factor, while trabeculectomy with mitomycin-C has been shown to have favorable results in one study.[53][54](B2)

Lens Subluxation and Dislocation

If there is a pupil block, or there is suspicion that it is occurring intermittently, a laser peripheral iridotomy can be performed to relieve or prevent it.

Phacomorphic Glaucoma 

Initial treatment is with topical and systemic ocular antihypertensives. Laser iridotomy may be considered to treat any component of angle closure suspected to be secondary to relative pupil block. There is evidence showing that immediate argon laser peripheral iridoplasty (ALPI) is a safe and effective first-line treatment of acute phacomorphic angle-closure.[55] However, these patients often require surgical lens removal for definitive treatment of the phacomorphic component of their angle closure.(B3)

Phacolytic Glaucoma, Lens Particle Glaucoma, and Phacoantigenic Glaucoma

The management of phacolytic glaucoma will follow the same stepwise approach as initial medical management, including frequent topical steroids and cycloplegia. Ultimately lens extraction is required, ideally once intraocular inflammation has been controlled or stabilized, although this is not always achievable. Often, these patients develop peripheral anterior synechiae, and lens surgery may be combined with goniosynechialysis. Combined cataract surgery and trabeculectomy have been described, although we would advocate against this due to the high trabeculectomy failure rate. The management of lens particle glaucoma and phacoantigenic glaucoma is very similar.[56][57](B3)

Ghost Cell Glaucoma

Ghost cell glaucoma often responds to medical treatment. However, AC washout and pars plana vitrectomy may be considered in the setting of dense vitreous hemorrhage or recalcitrant high IOP.[30]

Hemolytic Glaucoma

Treatment is similar to that in ghost cell glaucoma, starting with conservative medical therapy, followed by AC washout and/or pars plana vitrectomy if needed.[58](B3)

Hemosiderotic Glaucoma

The principle in managing hemosiderotic glaucoma is the surgical removal of the iron-containing intraocular foreign body. The literature around hemosiderotic glaucoma is sparse; previous studies have primarily focused on the histological findings from enucleated eyes. There has been a case report where the IOP was normalized following the removal of the foreign body.[59]

Carotid-cavernous Sinus Fistula

Direct high-flow carotid-cavernous sinus fistula can be treated via endovascular interventional techniques utilizing embolic material such as detachable balloons, coils, and acrylic glue to occlude the fistulous connection. Indirect low-flow fistula can be managed by observation as it was shown that up to 70% of these fistulae close spontaneously.[3] Other options include intermittent compression of the ipsilateral internal carotid artery or superior ophthalmic vein, stereotactic radiosurgery, and endovascular surgery.[1] Raised IOP is managed temporarily by topical and systemic ocular antihypertensives as you would with other types of glaucoma.(B2)

Open-globe Trauma 

Epithelial Downgrowth

Different treatment modalities may be considered depending on the type of epithelial downgrowth. In general, epithelial pearls and cysts can be monitored if they are not otherwise causing elevation of the IOP. If they are growing in size and causing complications such as inflammation or IOP elevation, an en-bloc surgical resection can be considered.[60][61][62] (B3)

Short-term success has been reported for epithelial membranes with surgical resection, which can often be combined with cryotherapy and intraocular 5-fluorouracil injection.[63][64][65] However, these measures tend to have a high failure rate in the medium to long term.[66] Glaucoma drainage tube surgery will be the first-line surgical management of raised IOP despite maximum tolerated medical treatment.[67] (B3)

Filtering surgery tends to fail as the ostium will often become obstructed by epithelial cells.[68] If IOP remains uncontrolled following all these measures, cycloablation can be considered a last resort.(B2)

Fibrous Downgrowth

Similar to epithelial downgrowth, filtering surgery has high failure rates in fibrous downgrowth. Glaucoma drainage tube implantation in this setting may not work due to blockage of the tube lumen by fibrovascular tissue.[67] Surgical removal of the tissue can be attempted. Combined intracorneal and subconjunctival bevacizumab injection has been reported to arrest further vascularization of the fibrovascular membrane and may also control intraocular hemorrhage.[34](B3)

Differential Diagnosis

Since traumatic glaucoma is an umbrella term for all the different causes of IOP elevation secondary to trauma, one should consider all the various etiologies outlined within traumatic glaucoma as part of their differential diagnoses to target the treatment.

Prognosis

The prognosis varies depending on the underlying cause of traumatic glaucoma. Conditions such as traumatic hyphema, iritis, steroid-response, lens-related glaucoma, ghost cell glaucoma, hemolytic glaucoma, and hemosiderotic glaucoma tend to be associated with better prognosis as long as the underlying source of raised IOP is addressed.

Complications

Resistant IOP, despite multiple medical and surgical management, can rarely occur with certain etiologies within traumatic glaucoma. Ultimately, it will lead to severe, irreversible glaucomatous changes to the optic disc leading to irreversible blindness if the IOP cannot be controlled.