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References

1.Musch DC, Gillespie BW, Lichter PR, Niziol LM, Janz NK: CIGTS study investigators. Visual field progression in the collaborative initial glaucoma treatment study the impact of treatment and other baseline factors, Ophthalmology

116:200–207, 2009.

2. Gedde SJ, Schiffman JC, Feuer WJ, Herndon LW, Brandt JD, Budenz DL: Tube versus trabeculectomy study group. Treatment outcomes in the tube versus.

3. Trabeculectomy (TVT) study after five years of follow-up. Am J Ophthalmol 153:789–803, 2012.

4. The Advanced Glaucoma Intervention Study (AGIS): 7: The relationship between control of intraocular pressure and visual field deterioration, Am J Ophthalmol 130:429–440, 2000.

5.Wilkins M, Indar A, Wormald R: Intraoperative Mitomycin C for glaucoma surgery, Cochrane Database Syst Rev, 2005. Issue 4. Art. No.: CD002897.

6.Vandewalle E, Abegão Pinto L, Van Bergen T, Spielberg L, Fieuws S, Moons L, Spileers W, Zeyen T, Stalmans I: Intracameral bevacizumab as an adjunct to trabeculectomy: a 1-year prospective, randomised study, Br J Ophthalmol 98:73–78, 2014.

7.Shetty RK, Warluft L, Moster MR: Slit-lamp needle revision of failed filtering blebs using high-dose mitomycin-C, J Glaucoma 14:52–56, 2005.

http://ophthalmologyebooks.com

1.What is a hyphema?

A hyphema is blood in the anterior chamber. The appearance of a hyphema may range from microscopic, seen only at the slit lamp as erythrocytes circulating in the aqueous, to a total hyphema that fills the entire anterior chamber.

2.List the causes of a hyphema.

There are three major causes of hyphema: trauma to the globe, intraocular surgery, or spontaneous anterior segment hemorrhage in association with ocular or systemic conditions, such as neovascularization of the iris or anterior chamber angle, intraocular tumors, or clotting disorders (Table 20-1).

3.What is the most common cause of a traumatic hyphema?

The most common cause of traumatic hyphema is blunt anterior segment trauma.

4.Describe the pathophysiology of a traumatic hyphema.

Blunt ocular trauma results in ocular indentation, which causes a sudden expansion of ocular tissues and an immediate rise in the intraocular pressure. The sudden forceful displacement of the cornea and limbus posteriorly and peripherally may result in splitting or tearing of these tissues. As the tissues tear, blood vessels in the vicinity may rupture, resulting in a hyphema.

5.List the anterior segment structures that may split or tear in response to blunt ocular injury.

•Central iris: Sphincter tear

•Peripheral iris: Iridodialysis

•Anterior ciliary body: Angle recession

•Separation of ciliary body from the scleral spur: Cyclodialysis

•Trabecular meshwork: Trabecular meshwork tear

•Zonules/lens: Zonular tears with possible lens subluxation

•Separation of the retina from the ora serrata: Retinal dialysis

6.When a patient presents with a hyphema due to blunt ocular trauma, which anterior segment structure is the most likely source of the hemorrhage?

Hyphema as a result of blunt ocular trauma most commonly occurs as a result of angle recession, a tear in the anterior face of the ciliary body between the longitudinal and the circular ciliary body muscles. Rupture of the blood vessels in the vicinity of the tear results in a hyphema. The most frequently ruptured blood vessels include the major arterial circle of the iris, the arterial branches to the ciliary body, and the recurrent choroidal arteries and vein crossing between the ciliary body and the episcleral venous plexus.

7.What ocular injuries may be associated with a traumatic hyphema?

•Ocular wall: Ruptured globe at the cornea, limbus, and/or sclera

•Cornea/conjunctiva: Epithelial abrasion, laceration, subconjunctival hemorrhage

•Iris: Sphincter tears, iridodialysis, mydriasis (long-term)

•Angle: Angle recession, iris dialysis, cyclodialysis cleft

•Lens: Traumatic cataract (acute, capsular rupture; chronic, direct injury), subluxation or total dislocation (damage of zonular attachments)

•Vitreous: Vitreous detachment, vitreous prolapse

•Retina: Retinal tear, detachment, and/or dialysis (vessel rupture, vascular occlusion)

•Retinal pigment epithelium and choroid: Choroidal rupture

•Optic nerve: Avulsion, optic nerve crush (chronic, glaucoma)

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8.Describe an appropriate approach to the workup of a patient with a hyphema.

The primary responsibility is to rule out a ruptured globe and search for an ocular foreign body in all patients who present with a traumatic hyphema. The color, character, and extent of the hyphema and associated ocular injuries, including corneal blood-staining status, should be documented. Gonioscopy is usually best deferred, but, if necessary, it may be performed gently, taking care to avoid a rebleed. Before a possible rebleed obscures the view, a dilated lens and fundus examination should be performed without scleral depression.

Table 20-1. Hyphema Classification by Etiology

I. Trauma

A.Blunt—rupture of iris or ciliary body blood vessels

B.Penetrating—direct severing of blood vessels II. Intraocular surgery

A.Intraoperative bleeding

1.Ciliary body or iris injury—most common when performing cyclodialysis, peripheral iridectomy, guarded filtration procedure, and cataract extraction

2.Laser peripheral iridectomy—bleeding is more common with the YAG laser than with the argon laser

3.Argon laser trabeculoplasty—rare

4.Selective laser trabeculoplasty—extremely rare

5.Cyclodestructive procedures—common, depending on the mechanism of elevated intraocular pressure (e.g., neovascular glaucoma)

B.Early postoperative bleeding

1.Dilation of a traumatized uveal vessel that was previously in spasm

2.Conjunctival bleeding that enters the anterior chamber through a corneoscleral wound or a sclerostomy

C.Late postoperative bleeding

1.Disruption of new vessels growing across the corneoscleral wound

2.Reopening of a uveal wound

3.Chronic iris erosion from an intraocular lens causing fibrovascular tissue growth

III.Spontaneous

A.Neovascularization of the iris secondary to (the conditions below cause the neovascularization):

1.Retinal detachment

2.Central retinal vein occlusion, central retinal artery occlusion, carotid occlusive disease

3.Proliferative diabetic retinopathy

4.Chronic uveitis

5.Fuchs’ heterochromic iridocyclitis

B.Intraocular tumors

1.Malignant melanoma

2.Juvenile xanthogranuloma

3.Retinoblastoma

4.Metastatic tumors

C.Iris microhemangiomas—may be associated with diabetes mellitus and myotonic dystrophy

D.Clotting factor disfunction

1.Leukemia

2.Hemophilia

3.Anemias

4.Aspirin

5.Coumadin

6.Ethanol

7.Nonsteroidal anti-inflammatory drugs

8.Vitamin C/gingko

IV.  Indirect: spillover from vitreous hemorrhage

Adapted from Gottsch JD: Hyphema: Diagnosis and management. Retina 10:S65–S71, 1990.

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Past medical and ocular history may identify risk factors for the bleeding episode and the chance of future complications. Sickle cell test and Hgb electrophoresis are suggested for all black and Hispanic patients and anyone with a positive family history. Establishing the exact nature of the trauma helps to estimate the likelihood of a possible ocular or orbital foreign body and/or ruptured globe. The exact timing of the injury is crucial in enabling one to predict when a patient will be at greatest risk for a rebleed and to help determine the expected time of clearing and the length of necessary treatment.

Four to six weeks after the injury, careful gonioscopy of the recovered eye may reveal an angle recession. At this time, one may also perform a dilated fundus examination with scleral depression to rule out peripheral retinal injury, such as described in Table 20-1.

KEY POINTS: TRAUMATIC HYPHEMA

1. All patients should be evaluated for systemic injuries (e.g., computed tomographic scans, x-rays). 2. All patients should be evaluated for intraocular foreign bodies and ruptured globes as well as other

ocular injuries.

3. Recurrent hemorrhages occur in 0.4 to 35% of patients, usually 2 to 5 days after trauma. 4. Corneal blood staining occurs in 5%.

9.What are pertinent questions to ask a patient who presents with a traumatic hyphema? Why?

1.When did your injury occur? Establishing the exact time of the injury is important because there is an increased rate of rebleed in patients who present more than 24 hours after trauma, and it will help to determine how soon a patient will be at greatest risk for a rebleed.

2.What type of injury did you sustain? The type and severity of an injury is important to help assess the likelihood of associated systemic injuries, an ocular or intraorbital foreign body, and the possibility of a ruptured globe.

3.Do you or any of your family members have a medical history of bleeding disorders or sickle cell disease? The answer to this question may help to establish a possible etiology for the hyphema and to determine what type and how aggressive the treatment should be.

4.What types of medications do you take (including alcohol intake)? Antiplatelet or anticoagulant effects of aspirin, nonsteroidal anti-inflammatory drugs, warfarin (Coumadin), and alcohol may predispose a patient to developing a hyphema or a rebleed after trauma and should be discontinued if possible.

10.How are hyphemas managed?

There is no consensus regarding the appropriate treatment for hyphema. Traditionally, most patients with a hyphema were admitted to the hospital for bed rest and sedation and were given a monocular or binocular patch for approximately 5 days. Today, compliant patients with a microhyphema and a low risk for rebleed are often followed as outpatients. It still appears prudent to hospitalize those patients who have a layered hyphema (Fig. 20-1), are at increased risk for rebleed, have a sickling hemoglobinopathy, or are noncompliant.

Figure 20-1.  Layered hyphema.

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2.Epinephrine compounds and α-agonists may cause vasoconstriction with subsequent deoxygenation and increased intravascular and intracameral sickling.

3.Hyperosmotics may cause hemoconcentration, which may lead to vascular sludging and sickling, which increases the risk of infarction in the eye as well as other organs.

4.Surgical interventions are used earlier and at lower intraocular pressures than in people who do not have sickle cell trait or disease (see question 15).

KEY POINTS: TRAUMATIC HYPHEMA AND SICKLE CELL DISEASE

1. More aggressive management is required to prevent optic nerve damage and central retinal artery occlusion.

2. β-Blockers and prostaglandin analogs should be used for intraocular pressure control.

3. Carbonic anhydrase inhibitors, epinephrine compounds, α-agonists, and hyperosmotics may increase sickling and are therefore contraindicated.

15.What level of intraocular pressure is considered medically uncontrolled?

An intraocular pressure that is considered uncontrolled depends upon the patient in question. (Some guidelines are included in subsequent discussions.) Surgery is generally not indicated in a patient with a healthy optic nerve unless the intraocular pressure is around 50 mm Hg for 5 days or greater than 35 mm Hg for a more prolonged period of time despite medical therapy. However, in the patient with previous glaucomatous optic nerve damage, the threshold for surgical intervention is lower and depends upon the level at which the intraocular pressure is likely to cause further optic nerve damage. In such patients, surgery may be appropriate within hours or days of the initial trauma. As previously discussed, aggressive therapy is required for patients with sickle cell disease, as these patients are predisposed to optic nerve damage and central retinal artery occlusion at minimally elevated intraocular pressures. Surgery is generally indicated in a patient with sickle cell disease if the intraocular pressure exceeds 24 mm Hg for more than 24 hours despite medical therapy.

16.List the indications for surgical intervention in the management of a hyphema.

As a rule, patients with true eight-ball hyphemas require prompt surgical intervention (see question 26); in contrast, approximately 5% of all traumatic hyphemas demand surgical management. Indications for surgical intervention include the following:

•A large hyphema that persists for more than 10 days

•A total hyphema that persists for more than 5 days (after which time peripheral anterior synechiae are more likely to develop)

•Early corneal blood staining

•An intraocular pressure that cannot be controlled medically and threatens to damage the optic nerve or cornea or result in retinal vascular occlusion, particularly in patients with sickle cell trait or disease.

The Read Criteria for surgical intervention include the following:

•Microscopic corneal blood staining

•Total hyphema with intraocular pressures of 50 mm Hg or more for 5 days (to prevent optic nerve damage)

•Hyphema that is initially total and does not resolve below 50% at 6 days with intraocular pressures of 25 mm Hg or more (to prevent corneal blood staining)

•Hyphema that remains unresolved for 9 days (to prevent peripheral anterior synechiae)

17.Name the major complications associated with a hyphema.

•Corneal blood staining

•Recurrent hemorrhage

•Secondary glaucoma

•In addition to the preceding complications, patients with sickle cell anemia or sickle cell trait have a predisposition to central retinal artery occlusion and optic nerve damage at only minimally elevated intraocular pressure owing to vascular sludging of the sickled cells, which leads to ischemia and vasoocclusion.

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202  OPHTHALMOLOGY SECRETS IN COLOR

Figure 20-2.  Clotted hyphema.

27.How is an eight-ball hyphema different from a total or 100% hyphema?

An eight-ball hyphema describes blood in the anterior chamber that has clotted and taken on a black or purple appearance. A total, or 100%, hyphema is one in which the blood filling the anterior chamber appears bright red. A hyphema that consists of bright red blood indicates that there is continuous aqueous circulation within the anterior chamber, which results in a significantly more favorable prognosis than an eight-ball hyphema.

28.What is the prognosis for an eight-ball hyphema?

Patients who develop an eight-ball hyphema carry a poor prognosis with respect to developing secondary glaucoma. Most, if not all, patients develop an elevated intraocular pressure that is usually severe and frequently difficult to control with medical therapy. Surgical intervention to evacuate the clot and/or decrease the intraocular pressure is generally required for most patients with an eight-ball hyphema.

29.When is the optimal time to remove a clotted or eight-ball hyphema? Why?

It is thought that the optimal time for evacuation of a clotted hyphema is 4 to 7 days after the hemorrhage, because it is at this time that there is maximal consolidation and retraction of a clot from adjacent structures and thus a decreased risk of causing new bleeding. However, extremely high intraocular pressures, with which vascular infarcts are a significant risk, are seen more commonly with eight-ball hyphema.

30.What types of surgical techniques can be used to evacuate a hyphema?

Surgical techniques in managing a hyphema include:

•Paracentesis and anterior-chamber washout alone or in association with a guarded filtration procedure (i.e., trabeculectomy)

•Clot expression with limbal delivery.

•Automated clot removal (hyphemectomy) with a vitrectomy instrument. (Take care to avoid lens and cornea; vasodilators can help maintain the chamber during removal of the clot. Keep the iris between the vitrectomy instrument and lens to minimize the risk of iatrogenic cataract).

•Peripheral iridectomy with or without a guarded filtration procedure to relieve pupillary block, which may be associated with an eight-ball hyphema.

Figure 20-3 provides an algorithm for the workup and management of a patient who presents with a hyphema.

•Trabecular gonioaspiration has been reported as a successful way of managing intraocular pressure elevation resulting from blood obstructing the trabecular meshwork in sickle cell patients.

31.List the types of secondary glaucoma associated with a traumatic hyphema.

An acute rise in intraocular pressure (IOP) is generally due to obstruction of the trabecular meshwork by erythrocytes or their breakdown products. The intraocular pressure at which medical or surgical therapy is initiated should be individualized and depends upon the presence of previous glaucomatous optic nerve damage, corneal endothelial dysfunction, or sickle cell disease.

Late secondary glaucoma may develop weeks to years after a hyphema. Causes of late secondary glaucoma are listed in Table 20-2. In one retrospective case–control study reviewing patients with open-globe injuries, 17% of patients developed ocular hypertension defined as IOP > 22 mm Hg at more than one visit or requiring treatment. A predictive risk factor includes the presence of hyphema, which reiterates the importance of monitoring IOP closely after trauma.

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Figure 20-3.  Treatment algorithm for ocular trauma and glaucoma. (From Higginbottom EJ, Lee DA: Clinical guide to glaucoma management. Woburn, MA, Butterworth-Heinemann, 2004.)

32.Is the chance of developing secondary glaucoma related to the size of the hyphema?

Although there are conflicting reports, the chance of developing a secondary glaucoma may be related to the size of the hyphema. Secondary glaucoma occurred in 13.5% of those eyes in which blood filled half of the anterior chamber, in 27% of those eyes in which blood filled greater than half of the

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Table 20-2.  Secondary Glaucomas Associated with Traumatic Hyphema

A.Early

1.Trabecular meshwork obstruction with fresh red blood cells and fibrin, resulting in secondary open-angle glaucoma

2.Pupillary block by the blood clot, resulting in secondary angle-closure glaucoma

3.Hemolytic glaucoma

4.Steroid-induced glaucoma from treatment

B.Late

1.Angle-recession glaucoma

2.Ghost-cell glaucoma

3.Peripheral anterior synechiae formation, resulting in secondary angle-closure glaucoma

4.Posterior synechiae formation with iris bombé, resulting in secondary angle-closure glaucoma

5.Hemosiderotic or hemolytic glaucoma

anterior chamber, and in 52% of those eyes in which there was a total hyphema. However, the amount of blood may simply be an indirect marker of the degree of trauma.

Recurrent hemorrhages are often larger than the initial hyphema and carry a greater risk for developing secondary glaucoma. Patients with eight-ball hyphemas develop glaucoma virtually 100% of the time.

33.Why and when is it important to perform gonioscopy on patients who have ­suffered a hyphema?

The gonioscopic appearance of angle recession may change with time. Immediately following blunt eye trauma, a hyphema may obscure adequate visualization of the angle. Thorough gonioscopic evaluation with indentation is recommended approximately 6 weeks after trauma, at which time the eye has recovered, the hyphema has resolved, and the risk of further injury has been minimized. Clues that may help the ophthalmologist diagnose an old angle recession include the presence of torn iris processes, depression or tears of the trabecular meshwork, and increased whitening of the scleral spur.

Up to 10% of patients with greater than 180 degrees of angle recession will eventually develop a chronic traumatic glaucoma. The term angle-recession glaucoma may also be used to describe the chronic traumatic glaucoma that occurs in association with an angle recession.

34.Given a history of ocular trauma, how can one make the diagnosis of angle ­recession on gonioscopic examination?

Angle recession can be diagnosed by careful gonioscopic examination of the injured eye and by comparing it with the fellow, nontraumatized eye. Gonioscopy may reveal an irregular widening of the ciliary body, indicating a tear between the longitudinal and the circular muscles of the ciliary body. A normal, nonrecessed ciliary body band is usually not as wide as the trabecular meshwork and should be roughly even in width throughout its entire circumference. Angle recession is found in 60 to 94% of patients with a traumatic hyphema (Fig. 20-4).

35.Explain the difference between a cyclodialysis and an angle recession

Although not as common as angle recession, cyclodialysis can occur secondary to blunt compressive trauma. An angle recession is a tear within the ciliary body itself, whereas a cyclodialysis is a tear between the ciliary body and the scleral spur. Disinsertion of the uvea from the sclera allows free passage of the anterior chamber aqueous fluid to the suprachoroidal space, thus permitting direct access to the uveoscleral outflow pathway. Temporary or permanent hypotony is usual. A cyclodialysis cleft should be suspected and carefully searched for when the intraocular pressure remains low after ocular trauma. Other causes for a low intraocular pressure following trauma are retinal detachment and an inflammatory-mediated decrease in ciliary body production.

36.Once a cyclodialysis cleft is suspected, how can it be diagnosed?

A traumatic cyclodialysis cleft can be diagnosed by careful gonioscopic examination. Although the wall of the cyclodialysis cleft is white (i.e., sclera), it appears shaded, owing to the fact that one is looking down into a hole. This is opposed to the gonioscopic appearance of angle recession, which appears simply as an enlarged ciliary body band secondary to a tear in the ciliary body itself. Treatment for a cyclodialysis cleft includes atropine, laser, and surgical repair. Ultrasound biomicroscopy provides high

CHAPTER 20  TRAUMATIC GLAUCOMA AND HYPHEMA  205

Figure 20-4.  Angle recession ultrasound biomicroscopy. Top, Normal angle. Bottom, Angle recession.

resolution (up to 50 μm) images of the anterior chamber angle, which can be particularly helpful if the cleft is small or as part of the preoperative evaluation to map the extent of a large cleft (see Fig. 20-4).

37.How long after a traumatic hyphema is a patient at risk for developing anglerecession glaucoma?

Angle-recession glaucoma may develop weeks to many years after blunt ocular trauma. Patients who develop traumatic or subsequent angle-recession glaucoma may have an underlying predisposition to primary open-angle glaucoma (POAG). It is believed that the infliction of trauma to a meshwork that is already predisposed to reduced aqueous outflow (POAG) may be just enough to push an already compromised trabecular meshwork over the edge, resulting in an angle-recession glaucoma. Evidence

to support this underlying predisposition to reduced aqueous outflow includes an unusually high incidence of POAG in the nontraumatized fellow eye and an increased tendency for the intraocular pressure to be increased by topical corticosteroids. Therefore, management of patients with angle recession includes long-term follow-up of both the injured and the uninjured eye.

38.Explain the pathophysiology of angle-recession glaucoma. Is it a direct result of injury to the ciliary body?

No. Angle recession is merely a marker for anterior segment contusion injury, specifically injury to the trabecular meshwork. Angle-recession glaucoma is thought not to be due to the angle recession itself (i.e., a tear in the ciliary body) but rather due to (1) direct trabecular meshwork damage and subsequent inflammation from the blunt trauma or (2) an extension of a Descemet’s-like membrane covering the trabecular meshwork. Both mechanisms may ultimately lead to chronic obstruction in the aqueous outflow pathway.

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