Ординатура / Офтальмология / Английские материалы / Shields Textbook of Glaucoma, 6th edition_Allingham, Damji, Freedman_2010

glaucoma is less common than with blunt trauma in the early postinjury period because of the open wound. However, IOP elevation may follow closure of the wound, especially if meticulous care is not given to reconstruction of the anterior chamber and treatment of the associated inflammation in the early postoperative period (79).

Hyphemas Associated with Intraocular Surgery

Bleeding in the eye can be a serious complication of any intraocular procedure and may occur during the operation or in the early or even late postoperative period.

During Surgery

As an intraoperative complication, bleeding is usually associated with damage to the ciliary body, as can occur when a filtering procedure or iridectomy is performed. Intraoperative bleeding can usually be controlled by placing a large air bubble or viscoelastic agent in the anterior chamber for a few minutes, which raises the IOP and acts as a tamponade. Applying direct, gentle pressure with the tip of a sponge or Gel-Foam, or applying epinephrine (1:1000), to the ciliary body for 1 to 2 minutes can also help stop ciliary body bleeding. Cautery is generally avoided in these cases, although use of an intraocular, bipolar unit may be effective.

After Surgery

Bleeding in the early postoperative period is usually not associated with serious sequelae and should be managed conservatively with limited activity and elevation of the head. Small hyphemas after intraocular surgery normally clear rapidly, although the time may be considerably longer in eyes with preexisting glaucoma because of delayed passage of red blood cells through the trabecular meshwork. When a postoperative hyphema is associated with elevated IOP or excessive fibrin, conservative medical management should be instituted as required, by using drugs that lower aqueous production or hyperosmotics if necessary. Frequent topical steroid use can assist in clearing fibrin, and if this is unsuccessful, then intracameral use of tissue plasminogen activator (6.25 µg or 12.5 µg) can be helpfu l (80). Surgical intervention is reserved for critical cases, although the indications may be somewhat more liberal than with a traumatic hyphema if there is danger of rupturing a corneoscleral wound or causing further atrophy to an optic nerve that has previously been damaged by glaucoma.

Hemorrhage in the late postoperative period may result from the reopening of a uveal wound or from disruption of new vessels growing across a corneoscleral incision (81). In a study of 58 eyes 5 to 10 years after cataract extraction, 12% had vessels in the inner aspects of the incision site and nearly one half of these had evidence of mild intraocular hemorrhage (82). Direct argon laser therapy may be used to treat such vessels when they can be visualized gonioscopically (81), and use of transscleral Nd:YAG laser or diode photocoagulation may be effective if direct argon laser therapy is unsuccessful (83). Fortunately, postoperative hyphema is far less common because of the introduction of small incision and clear cornea cataract surgery.

Spontaneous Hyphemas

Hyphemas may also develop spontaneously in various conditions, most of which are considered in other chapters. In some cases, the hyphema may cause or contribute to an increase in the IOP.

Intraocular Tumors

A spontaneous hyphema may occur in a child with juvenile xanthogranuloma or retinoblastoma, and intraocular hemorrhage may be a manifestation of an ocular malignant melanoma or other intraocular neoplasm (see Chapter 21).

Neovascularization

New blood vessels in the anterior ocular segment, which may lead to a spontaneous hyphema, are seen in neovascular glaucoma (discussed in Chapter 19), Fuchs heterochromic cyclitis (Chapter 22), and other chronic uveitides.

Vascular Tufts at the Pupillary Margin

Vascular tufts at the pupillary margin, also called neovascular tufts or iris microhemangiomas, represent yet another source of spontaneous hyphema. Slitlamp biomicroscopy may reveal multiple vascular tufts along the pupillary margin, and fluorescein angiography of the iris has revealed small areas of staining and leakage from the lesions (84). One histopathologic study revealed thin-walled new vessels at the

pupillary margin of the iris with a mild inflammatory cell infiltration (85), and another report described the vascular abnormality as a hamartoma of the capillary hemangioma type (86). Although more common in older adults, this condition occurs in adults of all ages. Most patients have no systemic disease, although associations with diabetes mellitus and myotonic dystrophy have been reported (84, 87, 88). Spontaneous hyphemas occur in a few of these cases, occasionally causing transient IOP elevation (89, 90). Laser photocoagulation has been reported to successfully eradicate bleeding vascular tufts (85, 91). However, because having recurrent hyphemas or permanent damage related to the transiently elevated IOP is rare, it is best to withhold treatment until one or more recurrences of bleeding are documented.

Dilatation and Posterior Synechiae

Spontaneous hyphemas may result in individuals with posterior synechiae in whom dilation drops are used. As the iris pulls away from the synechiae, hemorrhage may occur (Fig. 24.3).

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Figure 24.3 Spontaneous hyphema in a patient with posterior synechiae whose eye has been dilated. Note the hemorrhage at the 12-o'clock position of the pupil.

GLAUCOMAS ASSOCIATED WITH DEGENERATED OCULAR BLOOD Ghost Cell Glaucoma

In 1976, Campbell and coworkers (92) described a form of glaucoma in which degenerated red blood cells (ghost cells) develop in the vitreous cavity and subsequently enter the anterior chamber, where they temporarily obstruct aqueous outflow.

Theories of Mechanism

Having entered the vitreous cavity by one of several mechanisms (trauma, surgery, or retinal disease), fresh erythrocytes are transformed from their typical biconcave, pliable nature to tanor khaki-colored, spherical, less-pliable structures, referred to as ghost cells (92). Histologically, these cells have thin walls and appear hollow except for clumps of denaturized hemoglobin, called Heinz bodies. Unlike fresh red blood cells, ghost cells do not pass readily through a 5-µm Millipore filter or human trabec ular meshwork. The ghost cells develop within 7 to 10 days and may remain in the vitreous cavity for many months, until a disruption of the anterior hyaloid allows them to enter the anterior chamber. Once in the anterior chamber, the abnormal cells accumulate in the trabecular meshwork, where they may cause a temporary, but occasionally marked, elevation of IOP.

Specific Causes

Several situations can lead to ghost cell glaucoma. Cataract Extraction

Cataract extraction may be associated with glaucoma due to ghost cells in one of three ways (93). First, a large hyphema with vitreous hemorrhage occurs in the early postoperative period. As the hyphema clears, ghost cells, which developed in the vitreous, come forward and obstruct aqueous outflow. Second, a vitreous hemorrhage is present before cataract surgery, and disruption of the anterior hyaloid due to the operation allows the ghost cells to enter the anterior chamber. Third, a vitreous hemorrhage develops at some point after cataract extraction because of retinal disease, and the ghost cells develop and come forward through previously made defects in the anterior hyaloid. Ghost cell glaucoma has also been associated with intraocular lens implantation, especially when anterior chamber or iris-fixation lenses were used (94).

Vitrectomy

Vitrectomy may lead to ghost cell glaucoma in eyes with preexisting vitreous hemorrhage if the anterior hyaloid is disrupted and the vitreous and cells are not completely removed (95).

Vitreous Hemorrhage without Surgery

Vitreous hemorrhage without surgery may also lead to ghost cell glaucoma. The vitreous hemorrhage may be caused by trauma or associated with a retinal disorder, such as diabetic retinopathy (96, 97). Bilateral vitreous hemorrhage and ghost cell glaucoma may occur after poisonous snakebites, especially those from crotalids, because proteolytic enzymes can disrupt vascular integrity and act as hemorrhagic factors (98). The traumatic cases may have associated hyphema, which may clear before the ghost cell glaucoma develops or may persist and mask the actual mechanism of the glaucoma. The route of ghost cells to the anterior chamber in these phakic eyes is presumed to be a defect in the anterior hyaloid face (96, 97).

Clinical Features

Depending on the number of ghost cells in the anterior chamber, the IOP ranges from normal to marked elevation with pain and corneal edema (92). Slitlamp biomicroscopy reveals characteristic khaki-colored cells in the aqueous and on the corneal endothelium (Fig. 24.4A,B). If present in large quantities, the ghost cells may layer out inferiorly, creating a pseudohypopyon, which is occasionally associated with a layer of fresher red blood cells (known as a “candy -stripe sign”) (Fig. 24.4C,D). On gonioscopy, the anterior chamber angle is typically open and may appear normal, or may be covered by scant to heavy amounts of khaki-colored cells.

Differential Diagnosis

Glaucoma due to ghost cells may be confused with the less common hemolytic and hemosiderotic glaucomas. Neovascular glaucoma and glaucoma due to inflammation must be ruled out. Although the diagnosis is usually made easily on the basis of history and clinical features, it may be confirmed by examination of an aqueous aspirate, which reveals the typical ghost cells. This examination may be performed with phase contrast microscopy or by routine light microscopy of a paraffinembedded specimen stained with hematoxylin and eosin (92, 99).

Management

Glaucoma due to ghost cells is not a permanent condition, but it may last for months before the

abnormal cells eventually clear from the anterior chamber angle. In the interim, the IOP can often be controlled with the use of standard antiglaucoma medications. Some cases, however, require surgical intervention, which usually involves removal of the ghost cells from the anterior chamber by irrigation or removal of all ocular ghost cells by vitrectomy (92, 100). After ghost cells are surgically removed, P.355

the IOP promptly returns to normal in most cases in the absence of preexisting glaucoma.

Figure 24.4 Eyes with ghost cell glaucoma. A,B: Khaki-colored cells fill the anterior chamber. C,D: Note the layering of ghost cells inferiorly, creating a pseudohypopyon. The eye in D shows a classic “ candy-stripe sign.”

Hemolytic Glaucoma

Fenton and Zimmerman (101) described a form of glaucoma associated with intraocular hemorrhage in which macrophages ingest contents of the red blood cells and then accumulate in the trabecular meshwork, where they temporarily obstruct aqueous outflow. Clinically, numerous red-tinted cells are seen floating in the aqueous, and the anterior chamber angle is typically open, with reddish-brown pigment covering the trabecular meshwork (102). Cytologic examination of the aqueous reveals macrophages containing golden-brown pigment (102). An ultrastructural study of seven eyes revealed red blood cells and macrophages with phagocytized blood and pigment in the trabecular spaces; the endothelial cells of the trabecular meshwork were degenerated and had phagocytized blood (103). The condition is self-limiting and should be managed medically, if possible. When surgical intervention is required, anterior chamber lavage has been recommended (102).

Hemosiderotic Glaucoma

Hemoglobin from lysed red blood cells in the anterior chamber is phagocytized by endothelial cells of the trabecular meshwork in this rare condition. Iron in the hemoglobin subsequently causes siderosis,

which is believed to produce tissue alterations in the trabecular meshwork, eventually resulting in obstruction to aqueous outflow (104). However, an association between iron staining of the trabecular meshwork and impairment of aqueous outflow has yet to be clearly established.

KEY POINTS

Red blood cells in a fresh or degenerated form in the anterior chamber may lead to elevated IOP by obstructing aqueous outflow through the trabecular meshwork.

The most common cause of a new hyphema is blunt trauma. Glaucoma may result from the initial hemorrhage, but more often from a rebleed, and initial therapy is directed toward accelerating resorption of the hyphema and minimizing rebleeding.

When glaucoma occurs, medical management may control the IOP until the hyphema clears, although some cases require surgical intervention, which includes removal of the blood. Hyphema in the setting of sickle cell hemoglobinopathies requires aggressive management, as even moderately elevated IOP can produce rapid damage to the optic nerve.

Other causes of new hyphemas include spontaneous bleeding from tumors; neovascularization; or, rarely, vascular tufts at the pupillary margin.

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The most common form of glaucoma associated with degenerated ocular blood is ghost cell glaucoma, in which degenerating erythrocytes obstruct aqueous outflow. This may follow cataract extraction, vitrectomy, or trauma.

Other situations in which degenerated blood may lead to glaucoma include hemolytic glaucoma and hemosiderotic glaucoma.

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Shields > SECTION II - The Clinical Forms of Glaucoma >

25 - Glaucomas Associated with Ocular Trauma

Authors: Allingham, R. Rand

Title: Shields Textbook of Glaucoma, 6th Edition Copyright ©2011 Lippincott Williams & Wilkins

> Table of Contents > SECTION II - The Clinical Forms of Glaucoma > 25 - Glaucomas Associated with Ocular Trauma

25

Glaucomas Associated with Ocular Trauma CONTUSION INJURIES

General Features

Blunt injuries involving the eye are not uncommon; fortunately, many can be prevented with the use of appropriate protective eyewear. A survey of data derived from hospital discharge abstracts in the United States between 1984 and 1987 revealed a rate of 13.2 cases per 100,000 for any ocular trauma as a principal diagnosis, of which approximately 40% were coded as contusion of the eyeball or adnexa or orbital blowout fracture (1). Young men appear to be most prone to such trauma. In a series of 205 patients with ocular contusion injuries, 85% were males and 75% were younger than 30 years (2). Sporting and domestic accidents accounted for almost two thirds of these injuries, with the remaining known causes divided between unintentional industrial injuries and malicious acts. Among 32 patients hospitalized for sport-related ocular contusion, ball games were the most common cause (3). Boxing is an especially high-risk sport for ocular trauma; in one series of 74 asymptomatic boxers, 66% of the men evaluated had one or more ocular injury (4). An increasingly common source of severe ocular trauma is air bag inflation in a motor vehicle accident (5).

Data from the U.S. Eye Injury Registry on 6021 patients with blunt ocular contusion suggest that the 6-

month incidence of posttraumatic glaucoma is 3.4% (6). The same study identified several independently predictive factors associated with the development of posttraumatic glaucoma, including poor initial visual acuity, advancing age, lens injury, angle recession, and hyphema. Another study compared 40 consecutive eyes with closed globe injury and a chronically elevated intraocular pressure (IOP) for a minimum of 3 months with 52 eyes that had closed globe injury and no evidence of glaucoma. Increased pigmentation at the angle, elevated baseline IOP, hyphema, lens displacement, and angle recession of more than 180 degrees were associated with the occurrence of chronic glaucoma after closed globe injury (7).

Figure 25.1 An eye with a traumatic hyphema. Slitlamp view reveals layered blood in the anterior chamber. (Courtesy of Joseph A. Halabis, OD.)

Clinical Findings

The anterior segment is the portion of the eye most frequently damaged by blunt trauma, and hyphema is the most common mode of clinical presentation (Fig. 25.1), occurring in 81% of the 212 eyes in one series (2). A late sign that is almost pathognomonic of hyphema is pigment clumps on the trabecular meshwork (Fig. 25.2). (The management of traumatic hyphema is discussed in Chapter 24.) As the blood clears, ruptures in various structures of the anterior segment may be found (Fig. 25.3). The most common of these is angle recession (Fig. 25.4A-C), which is seen by gonioscopy as an irregular widening of the ciliary body band. Histologically, this represents a tear between the longitudinal and circular muscles of the ciliary body. The reported prevalence of angle recession in eyes with traumatic hyphemas ranges from 60% to 94% (8, 9, 10, 11 and 12). Angle abnormalities occurred in more than one half of the 32 patients with sports-related ocular contusions and in 19% of the 74 boxers (3, 4). When gonioscopic examination was included in a population-based glaucoma survey, some degree of P.359

angle recession was found in 14.8% of the people studied, 5.5% of whom had glaucoma (13). Other associated injuries include iridodialysis, a tear in the root of the iris (Fig. 25.5), and cyclodialysis, which