Chapter 227 – Post-Traumatic Glaucoma

Chapter 227 – Post-Traumatic Glaucoma









• Elevated intraocular pressure secondary to ocular trauma.



• Hyphema.

• Angle recession.



• Rebleeding.

• Corneal blood staining.

• Ghost cell glaucoma.

• Gonioscopic angle deformities.





Elevated intraocular pressure (IOP) is a frequent occurrence after trauma to the eye. Following blunt trauma, glaucoma may occur early (acute), either with or without hemorrhage (hyphema). Glaucoma also may occur late (chronic), either with or without angle recession. In addition, glaucoma may occur after other types of ocular trauma, such as penetrating injuries, chemical burns, radiation therapy, and electrical injuries.


Blunt ocular trauma that results in hyphema is caused predominantly by blows (62%), although projectiles (34%) and explosions (4%) can cause it as well.[1] Most of the injuries are due to violent assaults or accidents. Only a small portion of hyphemas occurs from a lack of protective eyewear for sports or work.

A variety of ocular injuries can occur because of momentary anatomical deformation of the globe by blunt trauma. As the cornea and sclera are suddenly displaced posteriorly, a compensatory expansion occurs at the equator of the eye ( Fig. 227-1 ). The seven anterior ocular tissues that may tear, along with their resultant findings, are illustrated in Figure 227-2 .[2] A post-traumatic elevation in IOP may occur in association with any of these findings.

Acute glaucoma without hemorrhage may occur because of the presence of inflammatory cells and pigment in the anterior chamber, which causes blockage in the trabecular meshwork. This is treated with topical anti-inflammatory agents and usually subsides within 1–2 weeks. Occasionally, angle recession may occur without hemorrhage. The increased resistance to outflow associated with significant angle recession is the result of concomitant trabecular meshwork damage.[3]

The most frequent cause of hyphema is ocular trauma, but it should be kept in mind that hyphema also may occur perioperatively and spontaneously.[4] Blunt trauma causes distortion of the anterior chamber angle, which can result in vessel rupture in the iris or ciliary bodies and bleeding into the anterior chamber. As the IOP rises, bleeding diminishes and a clot forms. Clot lysis and



Figure 227-1 Equatorial expansion in eye at moment of blunt impact.

retraction occur 2–5 days after the injury, and the maximal risk of rebleeding from the injured vessels occurs at this time. Rebleeding has been reported in 0.4–35% of patients who did not receive oral medication for prophylaxis.[1] Factors that may increase the risk of rebleeding include large hyphemas, youth, and race, with a higher incidence of rebleeding in African-American and Hispanic patients. [4]

Late-onset glaucoma after a hyphema may result from angle recession, ghost cell glaucoma, peripheral anterior synechiae, or posterior synechiae with iris bombé. The incidence of glaucoma is related directly to the extent of angle recessed; it is approximately 4% if less than 180° of the angle is recessed, and approximately 10% if more than 180° is recessed.[5] The time of onset of angle-recession glaucoma is variable, ranging from 1–40 years after injury. It is likely that the trauma-related decrease in outflow facility occurs soon after the initial injury, and further loss in outflow facility occurs because of an underlying predisposition to the development of open-angle glaucoma. This is supported by a study of 18 patients who had angle-recession glaucoma; in these patients, the average time to diagnosis was 16.5 years, and the average IOP of the uninjured eye was 23.5?mmHg (3.13?kPa).[3] Corticosteroid-provocative testing of uninvolved eyes of patients who have traumatic glaucoma also confirms this theory.


The rebleed is often more severe than the initial episode and can lead to total hyphema (“eight-ball” hyphema). Usually, total hyphema is associated with sudden visual loss, high IOP, extreme





Figure 227-2 Seven areas of traumatic ocular tears (shown in yellow) with the resultant findings. (Adapted with permission from Campbell DG. Traumatic glaucoma. In: Shingleton BJ, Hersh PS, Kenyon KR, eds. Eye trauma. St. Louis: CV Mosby; 1991:117–25.)

pain, and nausea, as well as other symptoms related to acute glaucoma. The mechanism for the increase in IOP is mechanical obstruction of the trabecular meshwork by red blood cells and sometimes pupillary block from a clot.[6] Glaucoma and corneal blood staining are the two main complications of rebleeding.

Ghost cell (hemolytic) glaucoma can occur after vitreous hemorrhage associated with perforating or nonperforating ocular trauma. Approximately 2–3 weeks after the injury, normal red blood cells in the vitreous transform into rigid, khaki-colored ghost cells and migrate into the anterior chamber. These cells may create a high IOP because of trabecular meshwork obstruction.[2]


A careful history is taken, with emphasis on the existence and nature of prior ocular trauma. Lack of a positive history cannot rule out the existence of angle recession, because relatively mild blunt trauma can cause a tear in the ciliary body.

Gonioscopy can be performed carefully at the time of the initial injury and usually reveals the source of anterior chamber bleeding. However, because this manipulation may cause further bleeding, it is advisable to wait approximately 4 weeks before thorough gonioscopy is undertaken ( Fig. 227-3 ).

Gonioscopic findings of angle trauma include torn iris processes, trabecular meshwork tears, very white and distinct scleral spur, posteriorly displaced iris root, and exceptionally broad ciliary body band. The tear into the ciliary body, which splits the longitudinal and circular muscle fibers, begins to scar soon after injury. Some eyes show obliteration of the angle recess and peripheral anterior synechiae, which may obscure the angle recession. Gonioscopy is always performed on the normal, uninjured eye for comparative analysis. The pupils are dilated to look for subtle signs of lens trauma and zonular disruption, and the periphery of the retina is examined carefully.


Unilateral glaucoma may be caused by traumatic angle recession, as well as by primary open-angle glaucoma, angle-closure glaucoma,





Figure 227-3 Blunt injury from trauma with resultant hyphema and angle recession. A, Bleeding from the ciliary body (more common). B, Bleeding from the trabecular meshwork (less common).




Differential Diagnosis of Post-Traumatic Glaucoma




Epithelial ingrowth

Inflammation (iritis)

Sympathetic ophthalmia

Angle recession


Ghost cell glaucoma


Phacolytic glaucoma

Chemical injury

Lens block glaucoma

Radiation therapy

Peripheral anterior synechiae

Electrical injury






and any of the other causes of secondary glaucoma. The various causes of post-traumatic glaucoma are listed in Box 227-1 .


Hyphema in patients who have sickle cell disease or who are carriers of sickle cell traits presents unusual management difficulties. Red blood cells in these patients are more rigid in the sickled form and traverse the trabecular beams with difficulty. Even small amounts of blood in the anterior chamber may cause markedly elevated IOP. Sickle cell patients are prone to develop microvascular infarctions of the optic nerve, retina, and anterior segment, even when the IOP is elevated only moderately ( Fig. 227-4 ). [7]

At elevated IOPs, the acidity of the aqueous humor increases while the oxygen content decreases. These metabolic shifts cause further sickling and perpetuate the factors that lead to optic atrophy. Medical and surgical therapy needs to be more aggressive in sickle cell patients. If an oral carbonic anhydrase inhibitor is necessary, methazolamide is used rather than acetazolamide, because it is thought to produce less anterior chamber acidosis. Hyperosmotic agents are avoided, as they may cause vascular hyperviscosity with induced systemic sickling.



Figure 227-4 Total hyphema in an African-American patient. More aggressive treatment is necessary for patients who have sickle cell disease or trait.

If the IOP averages 24?mmHg (3.2?kPa) or greater for 24 hours, or if transient pressure elevations greater than 30?mmHg (4.0?kPa) occur, a paracentesis or anterior chamber washout is indicated.


Histologically, angle recession is characterized by a tear in the face of the ciliary body, which causes a posterior displacement of the iris root and inner pars plicata ( Fig. 227-5 ). In addition to a much widened ciliary body band, sclerosis and fibrosis of the trabecular meshwork are observed. Occasionally, an overgrowth of Descemet’s membrane (cuticular membrane) has been found to cover the trabecular meshwork. The formation of peripheral anterior synechiae may create a pseudoangle. Endothelial overgrowth of the pseudoangle may also occur.[8]





Figure 227-5 Angle recession. The ciliary body inserts into the scleral spur normally. The oblique and circular muscles of the ciliary body have atrophied, following a laceration into the anterior face of the ciliary body. The resulting scar tissue has contracted, pulling the angle recess, iris root, and ciliary process posteriorly. The anterior wedge shape of the ciliary body has been lost. The entire process results in a fusiform shape of the ciliary body. A number of mechanisms, such as trabecular damage and late scarring, peripheral anterior synechiae, and endothelialization of an open angle, can lead to secondary glaucoma that could result in optic nerve damage. (From Yanoff M, Fine BS. Ocular pathology, ed 5. St. Louis, Mosby; 2002.)



The goals of treatment of traumatic hyphema are to prevent a rebleed and to control IOP. Various medical treatments to reduce the risk of rebleeding are controversial, partly because conflicting results have been reported in the literature, and partly because the rate of secondary hemorrhage is so variable that there is debate about the necessity of treatment.

Most patients can be treated on an outpatient basis. Activity should be limited, but eye patching is not necessary. Drugs with antiplatelet activity, such as aspirin and nonsteroidal anti-inflammatory products, are avoided. Topical medications such as pilocarpine, atropine, and corticosteroids do not reduce the rate of rebleeding. The use of systemic corticosteroids has been recommended but is controversial. A well-controlled study found no difference in the rebleed rate in patients treated with either prednisone (40?mg/day) or aminocaproic acid. Both groups had rebleed rates of 7%, compared with a rebleed rate of 20–33% for patients treated with a placebo in other studies.[1]

Several studies have reported that aminocaproic acid reduces secondary hemorrhages in humans. It is an antifibrinolytic agent that inhibits the conversion of plasminogen to plasmin, thus preventing the blood clot from dissolving. The recommended dose of aminocaproic acid is 50?mg/kg every 4 hours, with a maximum dose of 30?g/day for 5 days. Common side effects are nausea, vomiting, diarrhea, and postural hypotension.[1] A topical preparation exists as well.

Termination of aminocaproic acid before completion of the 5-day course may result in a greater tendency to rebleed. Elevations in IOP have been noted 1–2 days after stopping aminocaproic acid, most likely because of a “wave” of clot lysis that liberates red blood cells and subsequently blocks the trabecular meshwork.[4]

Elevated IOP after hyphema may be treated medically with topical and oral agents. However, sympathomimetic and miotic agents typically are not used because of their inflammatory potential.

Prolonged elevated IOP is associated with an increased chance of optic nerve damage and corneal blood staining. The indications for surgical intervention are listed in Box 227-2 .

A multitude of surgical techniques have been advocated to treat hyphema. These include paracentesis, anterior chamber



Indications for Surgical Intervention After Hyphema

Intraocular pressure >50?mmHg (6.7?kPa) for 5 days


Intraocular pressure >35?mmHg (4.7?kPa) for 7 days


Total hyphema unresolved for 9 days


Microscopic corneal blood staining





washout, expression of the clot, automated removal of blood, and trabeculectomy. Although washout of free red blood cells is often helpful,[9] it is not necessary to completely remove the clot.

Angle-Recession Glaucoma

For chronic glaucoma that results from angle recession, standard glaucoma medications may be used. Miotics should be used cautiously, because they have been associated with an increase in IOP. Eyes that have angle-recession glaucoma have damaged trabecular meshwork and depend on uveoscleral outflow for drainage. [10] Whereas latanoprost and cycloplegic agents increase uveoscleral outflow, miotics cause a decrease.

Argon laser trabeculoplasty should be used cautiously, or not at all, because the results are poor. If medical treatment for angle-recession glaucoma fails, recalcitrant cases require surgical trabeculectomy, with adjunctive use of antimetabolites at the discretion of the surgeon.


An injury severe enough to cause hyphema also causes an angle recession in more than 60% of eyes. A hyphema that fills three fourths of the volume of the anterior chamber typically results in a traumatic cataract, and vitreous hemorrhage occurs in about 50% of such eyes. Glaucoma may develop in approximately 6% of eyes that have angle recession, most likely when the recession is 240° or greater. The initial injury may lead to cataract and phacolytic glaucoma. Approximately 25% of enucleated eyes with phacolytic glaucoma show angle recession.[7]

Patients who have angle recession and normal IOP should be examined annually for the rest of their lives because of the risk of developing late angle-recession glaucoma. Patients who have angle recession that exceeds 180° are followed particularly closely. In addition, the fellow eyes of patients who have angle-recession glaucoma have a 50% greater risk of developing open-angle glaucoma than do normal eyes. [11]





1. Farber MD, Fiscella R, Goldberg MF. Aminocaproic acid versus prednisone for the treatment of traumatic hyphema: a randomized clinical trail. Ophthalmology. 1991;98:279–86.


2. Campbell DG. Traumatic glaucoma. In: Shingleton BJ, Hersh PS, Kenyon KR, eds. Eye trauma. St. Louis: CV Mosby; 1991:117–25.


3. Herschler J. Trabecular damage due to blunt anterior segment injury and its relationship to traumatic glaucoma. Trans Am Acad Ophthalmol Otolaryngol. 1977; 83:239–44.


4. Sambursky DL, Azar DT. Corneal and anterior segment trauma and reconstruction. Ophthalmol Clin North Am. 1995;8(4):609–31.


5. Kaufman JH, Tolpin DW. Glaucoma after traumatic angle recession: a ten-year prospective study. Am J Ophthalmol. 1974;78:648–54.


6. Edwards WC, Layden WE. Traumatic hyphema: a report of 184 consecutive cases. Am J Ophthalmol. 1973;75:110–6.


7. Goldberg MF. Sickled erythrocytes, hyphema and secondary glaucoma. Ophthalmic Surg. 1979;10:17–23.


8. Yanoff M, Fine BS. Ocular pathology, 4th ed. London: Mosby Wolfe; 1996:132–4.


9. Herschler J, Cobo M. Trauma and elevated intraocular pressure. In: Ritch R, Shields MB, Krupin T, eds. The glaucomas. St Louis: CV Mosby; 1989:1225–37.


10. Fingeret M, Mathews TA, Fodera FA. Angle recession. Optom Clin. 1993;3(2): 41–8.


11. Tesluk G, Spaeth G. The occurrence of primary open-angle glaucoma in the fellow eye of patients with unilateral angle-cleavage glaucoma. Ophthalmology. 1985;92:904–11.

4 comments on “Chapter 227 – Post-Traumatic Glaucoma

  1. Great good sense assistance – unfortunately individuals which include fast treatments and frequently overlook the way the easy points are typically certainly much better

  2. we accustomed to believe often altering with the hair shampoo results in much more hairfall however ough stated everyone “should” change it available frequently

  3. Hi,

    Very nice article, but I think that the part talking about the chances to get a glaucoma in the fellow eye (“…In addition, the fellow eyes of patients who have angle-recession glaucoma have a 50% greater risk of developing open-angle glaucoma than do normal eyes…”) is wrong. In Tesluk G, Spaeth G research (11), it said that that “Patients with angle-cleavage glaucoma appear to have at least a 50% chance of developing open-angle glaucoma in the non-traumatized fellow eyes.” The meaning is different. One, out of every 2 patients with traumatic glaucoma, will have a glaucoma in the fellow eye, while from what you have written it might be understood that if the chances to have a glaucoma, in general, is 2%, in people with two healthy eyes, than people with traumatic glaucoma in one eye have 3% chance (2%*1.5) to get a glaucoma in the fellow eye.

    Correct me if i’m wrong…



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