Ocular trauma is a significant cause of visual impairment in the United States. Approximately 2.5 million injuries occur annually, 40,000 of which cause serious visual loss. Of the 900,000 people with trauma-induced visual impairment, 75% are monocularly blind (20/200 or less).¹ Vision is lost because of primary mechanical damage of vital ocular structures and secondary complications, such as infectious endophthalmitis and retinal detachment due to intraocular fibrous proliferation and contracture. Contemporary vitreoretinal surgical techniques play a vital role in the prevention and management of the secondary complications of ocular trauma.

SUBLUXATION OR DISLOCATION OF THE LENS

Minor degrees of subluxation should be suspected when phakodonesis or iridodonesis is noted. Zonular rupture is certain if there is vitreous prolapse into the anterior chamber. In the absence of cataractous changes and related visual impairment, treatment is not indicated. A subluxated, cataractous lens can be removed by aspiration-irrigation or phacofragmentation through a limbal incision, but complications may occur, including posterior dislocation of the lens or lens fragments, vitreous prolapse and incarceration, and vitreous aspiration with resultant vitreous base traction and retinal tear formation. Also, visualization of the anterior vitreous by coaxial illumination is poor compared with fiberoptic endoillumination. These problems make pars plana lensectomy an attractive alternative. Bimanual techniques permit fixation and simultaneous removal of the lens by the vitreous suction-cutter, if the lens is soft, or phacofragmentation if it is sclerotic (Fig. 1A). Posteriorly dislocated fragments can be removed safely, with minimal vitreous traction, using the same incisions and instruments (see Fig. 1B). With endoillumination, prolapsed and juxtalenticular vitreous is readily identified and excised with the vitrectomy probe.

Without question, pars plana lensectomy is the preferred method for removing a completely dislocated lens. The technical aspects of dislocated lens and lens fragment removal are described elsewhere in these volumes.

VITREOUS HEMORRHAGE

Blood in the vitreous may come from tears in the iris, ciliary body, choroid, or retina. Hemorrhage from choroidal ruptures accumulates beneath the neurosensory retina; it then passes through the retina into the vitreous without necessarily causing a retinal break. Regardless, it is important to assume that a retinal break is present until proved otherwise. Vitrectomy is indicated for vitreous hemorrhage caused by ocular contusion when a retinal detachment is suspected because of sudden additional loss of vision, when a retinal detachment is detected through a window in the hemorrhage, when a large retinal break or retinal detachment is diagnosed by ultrasound, or when there is no improvement after a reasonable period of observation.

Preoperative contact A-scan and B-scan ultrasonography is helpful for detecting posterior vitreous detachment and differentiating it from retinal detachment. It is dangerous, however, to rely completely upon the accuracy of ultrasound. The presumed posterior hyaloid should be approached with caution until it can be identified with certainty.

A standard three-port vitrectomy technique is preferred for nonclearing vitreous hemorrhage. Initially, a central core of opaque vitreous is removed, beginning sufficiently close to the lens that the tips of the cutter and endoilluminator can be visualized. The excision is carried posteriorly, removing successive layers of hemorrhagic and fibrinous vitreous, until the anticipated plane of the posterior hyaloid is approached. A constant surveillance is maintained for a gray membrane containing radially oriented vessels (undiagnosed detached retina). A small opening is made in the detached posterior hyaloid, through which unclotted blood is aspirated by use of active suction from a soft-tipped cannula. Once the retina has been visualized, it is best to remove as much retrohyaloid blood as possible to prevent dispersion into the vitreous cavity with consequent loss of visual control.

If the posterior vitreous cortex is not detached, it can be separated from the retina by gentle suction with a soft-tipped cannula at the edge of the optic disc. The elevated cortex is penetrated with a hooked needle or myringotomy blade, creating a window through which a pick is introduced to enlarge the area of cleavage. With the plane between hyaloid and retina established, the surgeon attempts to remove the entire cortical vitreous except for the firmly attached portion at the anterior vitreous base. Cortex that does not separate with gentle manipulation is isolated from surrounding vitreous to eliminate traction on the retina. It is important to remove the cortical vitreous from areas adjacent to retinal breaks. Failure to do so may result in subsequent tangential traction and retinal detachment. A scleral buckle should be considered if retinal breaks cannot be freed from surrounding vitreous cortex.

The placement of sclerotomies close to the 3 o'clock and 9 o'clock positions facilitates maximal excision of the hemorrhagic anterior vitreous skirt, thereby improving visualization of the peripheral retina and pars plana. With use of coaxial illumination and scleral depression, the peripheral vitreous on the temporal side of the globe is trimmed with the cutter placed in the temporal sclerotomy, reaching both the superior and inferior quadrants, after which it is transferred to the nasal sclerotomy, and the process is repeated. The fiberoptic endoilluminator may damage the lens if used internally to illuminate the peripheral vitreous on the opposite side of the globe. However, the cone of light from the probe may be directed through the cornea to augment or replace the coaxial light source. Hemorrhagic retrolenticular vitreous can be stripped from the posterior capsule of the lens by gentle aspiration into the cutting port followed by withdrawal of the probe and simultaneous activation of the cutting mode. This technique is dangerous in young children because the retrolenticular vitreous is adherent to the lens, which is sufficiently pliable for aspiration into the port with consequent cataract formation. When the lens is clear, the process of removing peripheral and retrolenticular vitreous is less important than preserving lens integrity in most cases.

It is important to expose the peripheral retina and vitreous base because most retinal breaks caused by ocular contusion are located in this area.² All retinal breaks should be treated. Endolaser is used for posterior breaks, whereas peripheral breaks are treated with indirect laser assisted by scleral depression or transscleral cryoretinopexy. Cryotherapy is preferred when residual opaque vitreous partially obscures the targeted break.

Encircling scleral buckles are not necessary after vitrectomy for nonclearing vitreous hemorrhage caused by ocular contusion when a clear view of the fundus periphery reveals no peripheral retinal tears or signs of traction, such as vitreous base avulsion. Similarly, the support of a buckle is usually not needed for treated retinal breaks without retinal detachment. A local scleral buckle should be used when there is residual traction on a posterior break. The peripheral retina should be supported by an encircling scleral buckle when traction on breaks in the oral zone persists or the periphery is poorly visualized because of residual opaque vitreous.

RETINAL BREAKS

Retinal breaks are created at the time of nonpenetrating blunt injuries³ in 10% to 20% of eyes.^3–6 Retinal dialyses are most frequent^2–6 and are most often found in the lower temporal (Fig. 2) and upper nasal periphery (Fig. 3).² Large irregular breaks at the point of impact of blunt trauma are less common but are equally characteristic of nonpenetrating injuries (see Fig. 3).^2,7,8 Horseshoe and opercular tears of the equatorial retina (see Fig. 3) are associated with the more characteristic breaks in 25% of eyes.² Small round holes in atrophic retina at the point of traumatic impact and macular holes (see Fig. 3) are infrequently observed after ocular contusion.^2,8

Prophylactic treatment of most traumatic retinal breaks is indicated. Breaks at the point of impact are one exception because they are frequently self-sealing. The surrounding necrotic retina and choroid often unite in a common scar without prophylaxis. It is wise, however, to treat these large tears when scleral depression reveals a slight elevation and movement of their edges and the surrounding retina. Traumatic macular holes also are not treated to prevent additional loss of central vision. They seldom cause retinal detachments when left alone.

RETINAL DETACHMENT

Although retinal breaks are produced at the time of injury, the retinal detachment may be delayed for months to years because the vitreous gel acts like a tamponade until liquefaction occurs.² The detachment is typically shallow and slowly progressive because the large volume of vitreous gel in younger eyes prevents bullous retinal elevation as commonly seen in older patients with nontraumatic retinal detachments.

Careful preoperative and intraoperative indirect ophthalmoscopy with scleral depression is the key to successful treatment of detachments caused by traumatic retinal dialyses. Small dialyses at the vitreous base borders are difficult to identify, particularly in the upper nasal quadrant where they frequently occur. Breaks of the pars plana epithelium, at the anterior vitreous base border, are less apparent than retinal tears at the posterior edge of the vitreous base. Small dialyses are closed by scleral depression, in which case they are more easily seen on the lateral slopes of the indentation than on its crest. Transscleral cryotherapy is diagnostically helpful. It is not unusual to discover breaks at the vitreous base border for the first time when the edges of the tear are whitened by freezing a suspicious area.

It is prudent to treat the entire zone of vitreous base pathology with cryotherapy under direct visual control (see Fig. 3). In this way, treatment of all retinal breaks is assured. The anterior, posterior, and lateral limits of the treated zone are carefully localized and supported by a broad scleral buckle to relieve traction on the entire area. The posterior edge of the dialysis should fall on the crest of the buckle, which must be sufficiently broad to support the anterior edge as well, thereby preventing a recurrent detachment due to anterior leakage. Segments of grooved solid silicone tires are used together with an encircling band, which is positioned on a great circle of the globe to minimize anterior or posterior migration of the buckle. The band is tightened to ensure permanent indentation of the tire segment, but a high encircling buckle is avoided because it promotes posterior gaping or “fish-mouthing” of the dialysis. The band is anchored by a nonabsorbable mattress suture or scleral belt loop in each of the quadrants not occupied by the tire segment.

The retinal detachment is often shallow. To avoid retinal perforation or incarceration, subretinal fluid is released through a sclerotomy in an area of sufficient retinal elevation determined by intraoperative indirect ophthalmoscopy with scleral depression. Viewed in profile, the scleral indentation helps gauge the distance between retina and retinal pigment epithelium. To avoid retinal incarceration and blowout, sclerotomies posterior to the buckle should be securely closed after the release of fluid, particularly if additional manipulation of the buckle or an intravitreal gas injection is anticipated.

Retinal dialyses in the lower temporal quadrant are often very large, with gaping posterior edges located well behind the equator (see Fig. 2). They are caused by injuries impacting the lower temporal portion of the globe that result in the dissolution and disappearance of retinal tissue.⁸ In contrast to nontraumatic giant retinal tears with rolled-over retina, they respond favorably to scleral buckling without vitrectomy. A scleral buckle is indicated for smaller dialyses that can be closed with an explant of reasonable size. Very large breaks, as illustrated in Figure 2, are best treated with vitrectomy, gas tamponade, and laser, as recommended for nontraumatic giant retinal tears, rather than with a very large scleral buckle.

Traumatic horseshoe and opercular tears are treated with scleral buckling surgery, as are similar nontraumatic retinal breaks. Likewise, traumatic macular holes in detached retina are managed by vitrectomy, internal drainage, and gas tamponade. The use of laser in such cases is controversial but is probably indicated for recurrent detachments and eyes with pre-existing poor central vision due to other traumatic macular damage.

TERMINOLOGY

To avoid confusion, penetration, in this chapter, is defined as a partial cut, tear, or passage through a structure. The term perforation implies complete cutting, tearing, or passage through the referenced structure. Therefore, a corneal laceration is a perforation of the cornea and a penetration of the globe. A foreign body that passes into and out of the eye perforates the globe, but such injures are frequently called double-penetrating, double-perforating, or through-and-through injuries.

PATHOGENESIS

The etiologies and, therefore, the mechanisms of damage of penetrating injuries are highly variable. They cause a wide spectrum of acute structural alterations and secondary complications that, consequently, call for multiple methods of repair.

Acute Effects of Ocular Contusion

Penetration of the eye by relatively blunt objects causes compression of the globe with resultant iridoparesis, iridodialysis, subluxation and dislocation of the lens, traumatic cataract, choroidal rupture, and retinal breaks at the vitreous base borders.^13,14 Ruptures of the uvea produce anterior chamber, choroidal, subretinal, and vitreous hemorrhage. Massive blunt trauma causes corneal and scleral ruptures and may avulse the optic nerve.

Acute Effects of Ocular Penetration

Penetrating objects cause lacerations of the cornea, iris, lens, sclera, ciliary body, choroid, retina, and optic nerve. Anterior chamber, choroidal, subretinal, and vitreous hemorrhages result from lacerations of uveal and retinal blood vessels. Perforation of the corneoscleral wall permits prolapse and incarceration of the lens, uvea, retina, and vitreous.

Early Secondary Complications of Ocular Penetration

The secondary complications of ocular penetration are important causes of the visual impairment that results from such injuries. Examples of early secondary complications include the toxic effects of intraocular foreign material, such as copper, and the introduction of bacteria and fungi with consequent infectious endophthalmitis. The chronic inflammation caused by the presence of lens material, hemorrhage, and the incarceration of vitreous and uvea, although less dramatic than infection or violent toxicity, plays an important role in the stimulation of intraocular fibrocellular proliferation.^15–17

Intermediate Secondary Complications of Ocular Penetration

Cleary and Ryan¹⁵ reported experimental evidence that blood and, to a lesser extent, lens material in the presence of a large scleral wound caused fibrocellular proliferation and membranes, the contraction of which produced tractional retinal detachments (Fig. 4). The clinical consequences of fibrocellular proliferation and membrane contraction are well established and include traction retinal detachments, retinal breaks, rhegmatogenous retinal detachments, proliferative vitreoretinopathy, cyclitic membranes, ciliary body detachments, hypotony, and phthisis bulbi.

Late Secondary Complications of Ocular Penetration

Recurrent fibrocellular proliferation causing tractional and rhegmatogenous retinal detachments and proliferative vitreoretinopathy is a common late complication of penetrating injuries. Macular pucker is a similar complication of lesser magnitude. Fungal endophthalmitis and sympathetic ophthalmia are infrequent late complications of ocular penetration that are important because of their potentially devastating consequences.

PRIMARY SURGICAL REPAIR

Exploration of the Globe

A careful exploration of the globe is indicated to determine the extent of the defects in the eye wall whenever ocular penetration is established or suspected. Although often the first step, exploration is deferred until obvious anterior lacerations or ruptures are repaired so that manipulations required to expose the posterior segment of the eye cause no additional prolapse of ocular contents. A complete conjunctival peritomy is performed and all quadrants of the globe inspected. Traction on temporary sutures, looped around the rectus muscles, combined with the retraction of conjunctiva and Tenon's fascia facilitates visualization of the sclera beneath the extraocular muscles and posteriorly. Care must be taken, when passing sutures or a muscle hook beneath rectus muscles, to avoid inadvertent penetration through an undetected defect in the sclera.

Wound Closure

Restoration of the structural integrity of the globe by careful anatomic reapposition and creation of a watertight wound closure is the main goal of the primary surgical repair of penetrating injuries. Corneal lacerations are closed with deeply placed interrupted 10-0 nylon sutures. Interrupted 7-0 or 8-0 nylon sutures are used to repair scleral wounds to withstand the stress of subsequent vitrectomy should a second operation become necessary. Homologous corneal or scleral grafts or glue may be used to close defects caused by the loss of tissue. Posterior exit wounds are usually self-sealing and not repaired unless they are large.¹⁸ Prolapsed lens material is removed and vitreous excised by use of Weck-cel spears (Weck) and scissors, or a vitreous suction-cutter. Unless necrotic and exposed for more than 24 hours, prolapsed uveal tissue is reposited. Extruded retina is also reposited taking care to avoid incarceration.

Reconstruction of the Anterior Chamber

Reconstruction of the anterior chamber and restoration of the pupil are important goals of the primary surgical repair. Iris and vitreous incarceration in a corneal laceration causes chronic inflammation, peripheral anterior synechiae, and closure of the anterior chamber angle. Incarcerated vitreous provides a scaffold for fibrous ingrowth that creates membranes, the contraction of which causes tractional retinal detachments and retinal tears. With use of a cyclodialysis spatula, iris is reposited through the wound or swept from it via a limbal incision on the opposite side of the globe. Alternatively, sodium hyaluronate may be used to reform the anterior chamber, protect a clear lens, if present, reposit tissues, and keep them out of the wound. An anteriorly displaced cataractous lens or lens fragments are removed with a vitrectomy probe through the limbus or, if large choroidal detachments have been excluded, the pars plana. Phacofragmentation may be needed to remove hard lens material from the eyes of elderly patients, in which case suction must be carefully monitored to avoid vitreous aspiration and consequent traction. An anterior vitrectomy is performed and air is placed in the anterior chamber to prevent recurrent iridocorneal adhesions and reincarceration of the vitreous.

Removal of Foreign Material

Foreign material should be removed from the eye during the primary repair of penetrating injuries. The management of intraocular foreign bodies will be discussed later. If infection is present, a vitrectomy is performed during the primary operation to remove organisms, exotoxins, and inflammatory debris.

In most cases, a traumatic cataract is removed during a second operation unless its presence interferes with wound closure. The removal of blood from the anterior chamber, should it become necessary to visualize the posterior segment of the eye, is also best deferred until a secondary repair is undertaken.

Prophylactic Cryopexy

The value of prophylactic cryopexy to surround the sutured wound is controversial. Although the retina is lacerated by all perforations of the eye wall that extend posterior to the ora serrata, many are self-sealed by incarcerated vitreous and subsequent surrounding chorioretinal scarring. Furthermore, experimental studies indicate that cryopexy breaks down the blood-retina barrier and stimulates cellular proliferation and migration, thereby causing membrane formation and tractional retinal detachment.¹⁹ On the other hand, retinal lacerations were responsible for 20% of the rhegmatogenous retinal detachments reported in one study of detachments caused by penetrating injuries.²⁰ We currently treat retinal lacerations with ophthalmoscopically monitored light cryoretinopexy, when possible, but not if blood in the vitreous prevents their visualization.

Prophylactic Antibiotics

Penetrating ocular injuries are complicated by infectious endophthalmitis in 2% to 7% of cases.²¹ Its presence is often masked by the pain and inflammation of the injury, resulting in a disastrous delay of the diagnosis. Approximately 25% of cases of endophthalmitis after penetrating injuries are caused by Bacillus species, the virulence of which results in a poor prognosis.^22,23 Systemic prophylaxis with intravenous antibiotics is the accepted standard of medical care, although the low drug level obtained within the vitreous cavity is of questionable value. For intravenous prophylaxis, we prefer vancomycin for the coverage of increasingly prevalent strains of penicillin- and cephalosporin-resistant gram-positive organisms. A third-generation cephalosporin (ceftazidime) is used for gram-negative coverage instead of parenteral aminoglycosides, which may cause renal complications. Intravenous prophylaxis is continued for 3 to 5 days depending on the level of concern generated by the nature of the penetrating injury. The recently introduced antibiotic ciprofloxacin may be of prophylactic value because of its reported penetrance of the eye with systemic administration.^24–26

Prophylactic antibiotics are injected into the vitreous cavity of eyes at high risk for infection during the primary surgical repair if the needle can be safely introduced and monitored. Foreign bodies contaminated by soil cause approximately 90% of cases of post-traumatic Bacillus endophthalmitis.²⁷ These virulent organisms are sensitive to vancomycin. Although gram-negative organisms are rarely the cause of post-traumatic endophthalmitis, they are covered more safely by ceftazidime than by gentamicin.^28,29 We recommend the intraocular injection of 1 mg of vancomycin as well as 250 or 400 μg of amikacin or 2.25 mg of ceftazidime when the history and clinical findings indicate a high risk of infection.

RETINAL BREAKS AND RHEGMATOGENOUS RETINAL DETACHMENT

Traction retinal detachments due to fibrocellular proliferation, membrane formation, and contracture are a characteristic feature of penetrating ocular trauma. Nevertheless, approximately 75% of retinal detachments after penetrating injuries are rhegmatogenous in origin.²⁰ Retinal breaks are produced at the time of the injury and occur later as sequelae of intraocular scarring.

Acute Retinal Breaks

The contusional component of penetrating injuries produces retinal breaks identical to those caused by blunt, nonperforating trauma to the eye. Retinal dialyses are found in 55% to 64% of eyes with retinal detachments caused by ocular penetration.^20,30 Horseshoe or opercular tears due to traction on the posterior edge of the vitreous base and on isolated vitreoretinal adhesions occur in approximately 30% of cases with detectable retinal breaks.²⁰ Atrophic holes are less frequent (18%).²⁰

Retinal lacerations are produced whenever the eye is penetrated posterior to the ora serrata. They occur at the site of scleral perforation and at the point of impact or exit of foreign bodies. Lacerations caused retinal detachments in 12 (20%) of 60 eyes reported by Cox and Freeman.²⁰ In 9 eyes, the lacerations occurred at foreign-body impact sites (Fig. 5). Faulty technique during magnet extraction caused iatrogenic retinal lacerations in 2 eyes. Only 1 eye developed a retinal detachment from a laceration at the point of scleral perforation because of the previously described self-sealing characteristics of these breaks.

Acute retinal breaks are treated during the primary repair of the injury, if possible, to prevent subsequent detachment of the retina. The detection of retinal tears is, therefore, a major goal of the preoperative and intraoperative examinations. Manipulation of the eye, including scleral depression, is deferred until all wounds have been securely closed. The fundus is then examined with the indirect ophthalmoscope by use of scleral depression, and particular attention is given to the region of the vitreous base. All discovered retinal breaks are treated with the same techniques previously described for tears caused by ocular contusion. Posterior breaks are treated with either the indirect laser or cryopexy if the breaks are accessible to the probe. Anterior breaks can be treated through clear media with the indirect laser by use of scleral depression. Cryopexy is preferred when breaks are partially obscured by opacities of the media or when the diagnostic capabilities of cryotherapy are used to freeze and thereby whiten the edges of an otherwise occult tear. As previously described, we apply light cryopexy to the edges of retinal lacerations at the site of scleral perforations only if such treatment can be monitored ophthalmoscopically. Lacerations caused by the impact of foreign bodies commonly cause detachments of the retina and are therefore treated with cryopexy or the indirect laser during the primary surgical repair.²⁰

Opacities of the media, such as cataract and hemorrhage, often prevent early diagnosis of breaks; this is a fact cited by advocates of early vitrectomy.³¹ In our experience, acute breaks in the retina seldom cause detachments immediately. The ocular media are cleared 7 to 14 days postinjury, during the secondary surgical repair, so previously undetected retinal breaks are discovered and treated at that time.

Retinal detachments caused by the contusional component of penetrating injuries are identical to those caused by blunt trauma. At this stage, they are not complicated by intraocular scarring and therefore respond favorably to conventional scleral buckling techniques. Detachments caused by lacerations in the posterior retina are treated by vitrectomy, internal drainage of subretinal fluid through the break with simultaneous fluid-air exchange, endolaser, and long-acting gas tamponade. Giant retinal tears and associated detachments require vitrectomy techniques and perfluorocarbon liquids.

Late Retinal Breaks Caused by Contracting Bands and Membranes

Retinal detachments caused by contracting membranes are characteristic of penetrating injuries.²⁰ Shrinking transvitreal membranes initially cause traction detachments of the retina opposite the site of scleral perforation (Fig. 6). In approximately 40% of cases, continued traction causes a dialysis at the vitreous base and consequent rhegmatogenous retinal detachment (Fig. 7).²⁰ Retinal incarceration in a scleral perforation produces a less common but equally characteristic traction retinal detachment (Fig. 8). Retinal folds radiate from the site of incarceration. Associated vitreous prolapse and entrapment cause traction on the adjacent vitreous base with consequent detachment of the underlying peripheral retina and pars plana epithelium. A retinal fold is created at the posterior border of the vitreous base, which becomes increasingly prominent because of the contracture of membranes interposed between the vitreous base and the incarceration site. Progressive traction by this membrane may cause breaks in the folded retina and consequent rhegmatogenous detachment (Fig. 9).

Although some retinal detachments with breaks caused by membranous contracture were successfully treated with broad, high, encircling scleral buckles before the advent of vitreous microsurgery, approximately 50% failed because of progressive postoperative traction.²⁰ These cases are best treated by vitrectomy techniques, often combined with scleral buckling, which are further discussed with other late complications of penetrating injuries.

GENERAL APPLICATIONS OF VITRECTOMY

The role of vitreous microsurgery in the treatment of penetrating eye injuries is not completely defined, but general principles and applications have emerged with the refinement of instruments and techniques and nearly two decades of experience. Although the value of these applications has not been established by controlled trial, there is agreement about the general principles of management.

Removal of Foreign Material and Substances That Stimulate Intraocular Fibrocellular Proliferation

Nonmagnetic foreign bodies, and magnetic foreign bodies that are difficult or dangerous to extract with an externally applied magnet, are removed by forceps after vitrectomy. Vitrectomy is used in cases of post-traumatic endophthalmitis to remove organisms, toxins, and inflammatory debris. Material is also obtained for microscopic identification and culture. Vitrectomy is used to remove blood and lens material from the vitreous of eyes with posterior segment wounds to reduce the stimulus of intraocular scarring.

Removal of Damaged Vitreous

To eliminate the scaffold for fibrocellular ingrowth, as much of the vitreous gel as possible, including the cortex posterior to the equator, is removed from eyes with severe posterior segment injuries.

Removal of Aberrant Tissue and Correction of Abnormal Tissue Relationships

Pars plana vitrectomy techniques effectively remove or reposit uveal tissue from anterior segment wounds. Incarcerated lens and vitreous is also excised. Relaxing retinotomies are performed to correct the distortion, folding, and tension caused by retinal incarceration in posterior segment wounds.

Clearance of Opacities From thedOcular Media

Cataractous lens and dense vitreous hemorrhage are removed to restore the optical pathway and re-establish visualization of the fundus. Vitrectomy thereby permits identification and treatment of retinal breaks.

INDICATIONS FOR VITRECTOMY

The selection of cases of ocular penetration for vitreous microsurgery correlates with the general principles and applications described above. Vitrectomy is performed when the risk of secondary complications is high and the prognosis for recovery without vitreous surgery is historically poor. Forceps extraction of reactive nonmagnetic foreign bodies exposed by vitrectomy is clearly the method of choice in such cases. The same approach is preferred over magnet extraction in some eyes with magnetic intraocular foreign bodies. Vitrectomy is performed on eyes with post-traumatic infectious endophthalmitis. Vitreous microsurgical instruments are used, through limbal or pars plana incisions, to restore the integrity of the anterior chamber when iris, lens, and vitreous are incarcerated in corneal wounds. The historically poor prognosis for eyes with large posterior wounds, vitreous prolapse, and vitreous hemorrhage, particularly in globes perforated by medium to large foreign bodies, indicates a need for vitreous surgery. Vitrectomy must be performed when a retinal detachment is obscured by vitreous hemorrhage of sufficient density to prevent repair by conventional techniques.

TIMING OF VITRECTOMY

Immediate Vitrectomy

Vitreous microsurgery is performed during the primary repair of eyes with reactive nonmagnetic intraocular foreign bodies. Immediate vitrectomy is also preferred over external magnet extraction when metallic objects are incarcerated in the retina and sclera or obscured by opaque media. An immediate vitrectomy is performed on eyes infected by penetrating injuries.

Delayed Vitrectomy

Vitrectomy is performed 7 to 14 days after the injury in cases where such surgery is indicated but not an essential part of the primary repair. The delay reduces the risk of recurrent hemorrhage from congested uvea, allows clearing of corneal edema and hyphema, provides time for additional evaluation and diagnostic testing, and permits complete prognostic discussion and disclosure with the patient and family. Serial ultrasonography during this interval provides a better preoperative understanding of structural relationships such as detachment of the choroid, retina, and vitreous. It is particularly helpful to identify the posterior separation of the vitreous from the retina, the occurrence of which greatly facilitates complete removal of the vitreous cortex posterior to the equator of the globe. Liquefaction of blood in the suprachoroidal space can be identified by ultrasound, thereby establishing the proper timing of evacuation.³²

Vitreous surgery is not delayed beyond 14 days. A timely enucleation can be performed to reduce the risk of sympathetic ophthalmia if exploratory vitrectomy discloses irreparable damage. The excision of damaged vitreous at this stage removes the scaffold for fibrocellular ingrowth before membranes form and traction begins. The maturation of membranes after 14 days can produce scars with a thickness and density that make their removal difficult or impossible.

Late Vitrectomy

Vitrectomies are performed after the 7- to 14-day window when secondary complications of ocular penetration develop. Traction or rhegmatogenous retinal detachment caused by contracting membranes requires vitreous microsurgical repair. Vitrectomy techniques are also needed if late or recurrent intraocular scarring leads to macular pucker or proliferative vitreoretinopathy.

MANAGEMENT OF POST-TRAUMATIC ENDOPHTHALMITIS

Epidemiology

Infection is a devastating complication of penetrating ocular trauma. It occurs in 1% to 10% of eyes and is more prevalent in cases with intraocular foreign bodies.^21,33,34 The visual prognosis of post-traumatic endophthalmitis is less favorable than that of other postoperative infections because of traumatic damage and the virulent profile of the organisms involved.^21,35,36 The diagnosis is frequently masked, and therefore delayed, by the inflammation of the injury itself. The relatively benign course of cases with Staphylococcus epidermidis endophthalmitis after surgery occurs less consistently in traumatized eyes infected with the same organism.³⁷

The prognosis is very poor when gram-negative organisms and Bacillus species are involved, which occurs in 10% to 20% of cases, respectively.^21,38 Bacillus species cause a rapid onset of panophthalmitis associated with severe pain, proptosis, fever, and leukocytosis. A characteristic ring corneal ulcer develops in 18 to 24 hours.³⁹ The virulence of this species results from the production of potent exotoxins--an enterotoxin and a hemolysin.⁴⁰ Once produced, these exotoxins may cause destruction of tissue, even after the eye is sterilized by antibiotics, and bacterialysis may result in their further release. Collagenase may enhance the diffusion of toxins and bacteria throughout the eye.³⁹

The production of destructive proteases and endotoxin causes the virulence of gram-negative organisms.⁴¹ Endotoxin is released after bacterial cell death and lysis. Removal of bacteria by vitrectomy may decrease endotoxin-mediated tissue destruction and further dilute and wash out exotoxins.

Treatment

After secure wound closure, undiluted aqueous and, if possible, vitreous samples are obtained for the identification of pathogenic organisms by microscopic inspection and culture. One tenth of a milliliter of aqueous is aspirated into a tuberculin syringe through a 27- or 30-gauge needle passed through the limbus. Prior to infusion, vitreous samples (0.3–0.5 mL) are obtained by manual aspiration after the vitrectomy probe is introduced into the vitreous cavity. If possible, vitreous sampling is deferred and infusion delayed until the suction-cutter and infusion cannula can be visualized. Aqueous and vitreous samples are immediately placed on slides for Gram and Giemsa stains, and plates of chocolate agar, blood agar, and Sabouraud's medium are inoculated. The possibility of anaerobic infection is investigated by inoculating chopped meat glucose broth or thioglycolate broth.

A vitrectomy is performed on all eyes with obvious infectious vitritis. In some cases, infection of the vitreous is not apparent until opacities of the media, such as cataractous lens and hemorrhage, are removed. A pars plana approach is delayed when the posterior segment of the eye cannot be visualized. Also, instruments cannot be safely passed into the vitreous cavity through the pars plana when ultrasound reveals large choroidal detachments. In such cases, the vitrectomy probe and infusion system (a 21-gauge needle or lighted infusion needle) are first introduced into the anterior chamber through limbal incisions. Opacities in the anterior segment are cleared. After the drainage of choroidal hemorrhage or the posterior reposition of detached retina, if present, by sodium hyaluronate, gas, or perfluorocarbon liquid, a standard infusion cannula is introduced into the vitreous cavity through the pars plana. The extent of the vitrectomy is determined by the clarity of the cornea. A generous core vitrectomy is performed when visibility permits such an undertaking. No effort is made to separate the cortex from the retina or remove the peripheral vitreous because infection-induced retinal necrosis increases the likelihood of retinal breaks. In one series, all eyes with retinal breaks and endophthalmitis were lost.²¹ Presumably, iatrogenic breaks would lead to the same outcome. A more complete vitrectomy is safely performed in eyes with posterior vitreous separation from the retina. When visibility is very limited, a small core is removed from the central vitreous cavity as long as detachment of the retina has been excluded by preoperative ultrasonography.

Intravitreal Antibiotics

Antibiotics are injected into the vitreous cavity after samples have been obtained for culture and the vitrectomy has been completed. Because of the recent emergence of gram-positive organisms resistant to penicillin and first-generation cephalosporins, particularly Bacillus species, we substitute vancomycin for the previously recommended combination of cefazolin and clindamycin.²³ We also use amikacin in place of gentamicin to reduce the likelihood of retinal toxicity. Our current regimen of intravitreal antibiotics, therefore, consists of vancomycin 1 mg/0.1 mL and amikacin 250 to 400 μg/0.1 mL, as recommended by the Endophthalmitis Vitrectomy Study Protocol for the treatment of postoperative endophthalmitis.⁴² Rarely, ceftazidime 2.25 mg/0.1 mL is substituted for amikacin.

Postoperative Antibiotics

We use regular-strength broad-spectrum topical antibiotics (trimethoprim sulfate-polymyxin B, bacitracin-polymyxin B, ciprofloxacin, or gentamicin) four to six times daily when corneal infection is absent. Infectious corneal infiltrates are treated more aggressively with frequent “fortified” gentamicin and vancomycin. Topical steroids (prednisolone 1%) are used four times daily, or more frequently, depending on the amount of intraocular inflammation.

As previously described, the value of systemic antibiotics is questionable because of poor penetrance of the blood-ocular barrier and the resultant low intravitreal concentration achieved. We continue to use intravenous vancomycin or cefazolin in combination with a third-generation cephalosporin effective for gram-negative organisms (ceftazidime). Postoperative intravenous antibiotics will remain the standard of medical care unless proved to be of no value by a controlled trial such as the Endophthalmitis Vitrectomy Study.⁴²

MANAGEMENT OF INTRAOCULAR FOREIGN BODIES

The prognosis for eyes with intraocular foreign bodies (IOFBs) is better than the prognosis for other types of serious penetrating trauma. A recent series reported a final visual outcome of 20/40 or better in 60% of eyes and 5/200 or better in 86% of eyes.⁴³ Before the advent of vitreous microsurgery, magnetic foreign bodies carried a more favorable prognosis than nonmagnetic ones because good results were obtained by electromagnetic extraction. With the introduction of foreign-body forceps, the controlled removal of all types of foreign material became possible.

Preoperative Evaluation

The case history often reveals the foreign-body composition and the relative risk of post-traumatic infection. Samples of the suspect material are obtained, if possible, to determine its toxicity and magnetic properties. In eyes with clear media, the exact composition, size, and location of an IOFB are revealed by ophthalmoscopy. Magnetic properties can be verified prior to extraction by observing movement in response to an electromagnet that is positioned increasingly closer to the eye until motion occurs or is excluded.

In eyes with cloudy media, ancillary tests are needed to determine the composition, size, shape, location, accessibility, and magnetic properties of an IOFB. Plain x-ray films, with Caldwell or Waters projections, may demonstrate the presence, but not the location, of radiopaque foreign objects, and will not detect radiolucent objects such as wood or glass. Ultrasound provides better foreign-body localization and is essential to determine other structural changes such as retinal and choroidal detachment. Care must be taken to avoid undue pressure on eyes with large wounds to prevent additional prolapse of ocular contents. Computed tomography (CT) scanning is the diagnostic study of choice because it detects and localizes radiolucent and radiopaque foreign objects in three dimensions.⁴⁴ A rough determination of IOFB composition is provided by its density, because wood is less dense than plastic, which is less dense than glass, which, in turn, is less dense than metal. Unfortunately, scatter from metallic foreign bodies can make localization difficult and erroneous. Magnetic resonance imaging (MRI) is contraindicated because the motion of a magnetic IOFB can cause significant intraocular damage.⁴⁵

Indications for Removal

All foreign bodies are removed during the primary repair of penetrating injuries because of their potential toxicity and relatively frequent association with post-traumatic endophthalmitis. Some IOFBs are inert, such as glass, gold, silver, platinum, and aluminum, and cause little continuing damage. Lead and zinc cause a mild nongranulomatous inflammation of the eye. The toxicity of copper-containing foreign bodies is determined by the concentration of copper. Metals with less than 70% copper are relatively inert, whereas those with 70% to 90% copper lead to ocular chalcosis. An acute suppurative inflammation is produced by pure copper foreign bodies. The chronic toxicity of iron-containing metals causes ocular siderosis.

To avoid the risk of operative complications, encapsulated IOFBs that have been present for a long time without causing ocular toxicity can be observed as an alternative to removal. Serial electroretinograms are obtained to monitor possible ocular siderosis in eyes with retained iron-containing foreign bodies.

Surgical Technique

Foreign bodies in the anterior segment of the eye are removed by diamond-coated foreign-body forceps through the wound before its repair or through a limbal incision of appropriate size. Small inert intralenticular IOFBs may be observed if the lens is clear. Toxic intralenticular foreign bodies and those that have caused a cataract are removed through the limbus by forceps or a rare earth magnet during extracapsular cataract extraction. A posterior chamber intraocular lens may be simultaneously inserted into an intact capsular bag or in the sulcus anterior to the capsule when the case is otherwise uncomplicated.

In eyes with clear media, small to medium-sized magnetic IOFBs in the vitreous cavity are removed by an electromagnet through the pars plana after closure of the entrance wound (Fig. 10). A full-thickness scleral incision, down to but not through the pars plana epithelium, is made 3.5 to 4 mm posterior and parallel to the limbus on the side of the globe opposite the IOFB. The length of the incision must permit an unobstructed exit of the foreign object from the eye so that it does not become trapped in the vitreous base. In some cases, the incision is extended anteriorly from its center to form a T-shaped exit wound for relatively large IOFBs. The exposed pars plana epithelium is treated with light diathermy to minimize subsequent hemorrhage and cause slight retraction of the edges of the incision. A nonabsorbable mattress suture is preplaced to permit prompt wound closure after the IOFB is removed, thereby minimizing vitreous loss. The magnet must be aligned with its long axis pointing directly at the foreign body because its power is focused at the base, not the tip, of the conical attachment. Misalignment will attract the IOFB toward tissues adjacent to the sclerotomy. With proper technique, the foreign body rapidly transits the vitreous cavity and works its way through the pars plana epithelium because of the pulsed attractions of the magnet. Failure to exit is usually due to a small incision rather than resistance of the uveal tissue. It is seldom necessary to penetrate the pars plana epithelium with a knife.

After extraction of the IOFB, the fundus is inspected and retinal breaks, if present, are treated by the methods previously described. With scleral depression, the exit site is visualized. No treatment is applied except in the rare instance where tractional elevation or breaks are detected in the adjacent retina or pars plana epithelium, in which case light cryopexy is used to surround the defects with chorioretinal or cilioretinal adhesions.

In eyes with clear media, small magnetic IOFBs embedded in the retina can be extracted through the underlying sclera by an externally applied magnet if they are anteriorly located and, therefore, accessible. The embedded foreign body is surrounded preoperatively by slit lamp-delivered argon laser or intraoperatively by indirect laser, after which its position is carefully localized ophthalmoscopically. A sclerotomy is performed where the IOFB is located after nonabsorbable sutures are positioned to create a localized scleral buckle. The magnetic extraction of the foreign body is immediately followed by placement of a silicone sponge explant. Traction on bridle sutures is simultaneously relaxed to reduce the intraocular pressure, thereby minimizing vitreous loss and the risk of retinal incarceration, which is the principal complication of this technique. Medium- to large-sized magnetic IOFBs embedded in the retina are removed by vitreous microsurgical techniques even from eyes with clear media. Posterior transscleral extraction of such objects creates large exit wounds with attending prolapse and incarceration of vitreous and retina.

Nonmagnetic foreign bodies and magnetic IOFBs in eyes with opaque media are removed by vitrectomy techniques. The integrity of the globe is first secured by watertight closure of entrance wounds. A three-port pars plana approach is used but must be deferred in severely disorganized eyes when blood or a cataractous lens in the anterior segment prevents visualization of instruments passed through the pars plana. In such cases, the anterior opacities are first cleared by a vitrectomy probe, and an infusion needle is placed through limbal incisions, after which the instruments are safely transferred to appropriate pars plana incisions. When ultrasound clearly demonstrates the absence of retinal or choroidal detachment, the removal of anterior opacities may begin primarily through pars plana incisions placed 3 to 3.5 mm posterior to the limbus. A lighted infusion needle can often be visualized through cloudy media and is, therefore, used to eliminate the possibility of subretinal or suprachoroidal infusion during the initial removal of the opaque anterior vitreous. It is replaced by a standard infusion cannula and separate endoilluminator when the anterior vitreous cavity has been cleared. In the eyes of young patients, soft cataracts are easily removed by the vitrectomy probe, but phacofragmentation may be needed when hard lenses are encountered in the eyes of older patients.

Proceeding posteriorly, opaque vitreous is removed until the IOFB is identified and exposed, after which it is grasped by foreign-body forceps. Surrounding adherent vitreous is removed by the vitrectomy probe before the foreign body is elevated to the midvitreous cavity; from there it is passed through a pars plana incision of appropriate size. The IOFB may be exchanged between forceps in the vitreous cavity to alter its alignment, thereby presenting the smallest diameter to the exit wound. Alternatively, large foreign bodies in aphakic eyes may be passed through a limbal incision. An open-sky technique may be the only possible means of removing very large foreign objects. The cornea is usually severely damaged by the entrance of such IOFBs and must be removed to visualize and facilitate their extraction. Eyes with very large foreign bodies are usually severely disorganized, are seldom salvaged, and generally come to enucleation.

Intraretinal nonmagnetic foreign bodies and embedded magnetic IOFBs unsuitable for posterior transscleral magnet extraction because of their large size, posterior location, or the presence of opaque media are removed by vitreous microsurgery. Intraretinal magnetic IOFBs are not removed by magnet through the pars plana because their passage through intervening retina can produce large lacerations and detachments (Fig. 11).²⁰ Approached and exposed in the same manner described above, they are gently dislodged, grasped with foreign-body forceps, and removed. A lighted pick can be used to manipulate the IOFB into a position or orientation favorable for a secure grip by diamond-coated forceps. Alternatively, magnetic intraretinal foreign bodies may be elevated to the midvitreous by a rare earth magnet, after which they are removed by forceps (Fig. 12) to avoid being dislodged in the vitreous base, as often occurs when extraction by the magnet itself is attempted. Intraretinal foreign bodies of 1 to 2 weeks' duration may become encapsulated (Fig. 13A), in which case the capsule is incised by a myringotomy knife or sharp needle before it can be grasped by forceps or dislodged by the rare earth magnet (see Fig. 13B).

The vitreous cortex posterior to the equator is removed, if possible, from eyes with intraretinal foreign bodies. If not detached spontaneously, it is separated with a retinal pick (Fig. 14) or by suction with a soft-tipped cannula. The retinal laceration at the site of foreign-body incarceration is surrounded by laser and supported by a localized scleral buckle when the surrounding cortical vitreous cannot be removed. If present, subretinal fluid surrounding the incarceration site is drained internally through the retinal laceration while a fluid-air exchange is performed. Endolaser is applied around the break and the air is replaced by a short-acting gas tamponade.

Although retinal lacerations at foreign-body impact and incarceration sites are frequently self-sealing, they lead to subsequent retinal detachments in some cases. Therefore, we treat these lacerations, and retinal breaks located elsewhere in the fundus, as previously described. An encircling scleral buckle is almost routinely used to support the residual peripheral vitreous, particularly in phakic eyes, where peripheral dissection is limited, and in cases where residual opacities interfere with visualization of the vitreous base.

SECONDARY SURGICAL REPAIR

After the primary closure of wounds, some eyes require vitreous microsurgery performed 7 to 14 days after the injury. The purpose of the vitrectomy is to prevent or minimize secondary complications of the ocular penetration. As previously described, iris, vitreous, and lens incarcerated in anterior segment wounds are removed to restore the anterior chamber, clear the pupil, and eliminate the scaffold for fibrous ingrowth. The vitrectomy is performed on eyes with large wounds of the posterior segment, vitreous prolapse, and vitreous hemorrhage to remove blood, disrupted lens, and damaged vitreous, thereby reducing the stimulus and eliminating the scaffold for fibrocellular ingrowth. As previously described, the anterior segment is cleared and all the vitreous, including the cortex, is removed posterior to the equator.

Globes perforated (double penetration) by medium to large foreign bodies, in particular, require a second operation (Fig. 15A). Although a complete vitrectomy is performed, the vitreous over a large self-sealed exit wound is isolated from adjacent structures and trimmed but not completely removed. A small vitreous plug is left behind to avoid reopening the wound (see Fig. 15B).

Retinal incarcerations causing fixed radiating folds are sometimes encountered during the secondary repair. Small incarcerations require no treatment unless they prevent retinal reattachment or the folds distort the macula. Peripheral retinal incarcerations, of medium size, can be supported by a scleral buckle if necessary. When successful, the radiating folds flatten with time. Scleral buckles fail when the peripheral incarceration is large and are less beneficial when incarcerations are posterior. Relaxing retinotomies are performed when fixed folds, unresponsive to scleral buckling, prevent retinal reattachment or distort the macula.⁴⁶

Focal incarcerations of the posterior retina are treated by a relaxing retinotomy that circles the site (Fig. 16). Endodiathermy is preplaced on the proposed path of the retinal incision to minimize bleeding. The retina is reattached by internal drainage of subretinal fluid through the retinotomy and simultaneous fluid-air exchange. The retinotomy is surrounded by two to three rows of endolaser, after which the air is replaced by an isoexpansive concentration of perfluoropropane gas.

The folds radiating from a peripheral incarceration of the retina are relaxed by an equatorial retinotomy placed posterior to the location of the incarceration, the two ends of which are carried anteriorly to eliminate all folds (Figs. 17A and B). For hemostasis, the incision is preceded by endodiathermy. If the retina is highly detached and mobile, 2 to 3 mL of perfluorocarbon liquid placed in the posterior vitreous cavity will stabilize the retina and thereby simplify the retinotomy. All traction on posterior retinal breaks, if present, should be eliminated before the infusion of perfluorocarbon so the material does not flow under the retina. When the retinotomy is small and the posterior edge does not roll over, the retina is reattached by fluid-air exchange with perfluorocarbon liquid removal. The flattened retinotomy is surrounded by laser, supported by an encircling scleral buckle, and the air is replaced by long-acting gas.

The retina is sometimes massively incarcerated in distant scleral ruptures (Fig. 18A). Such prolapse is encouraged by hemorrhage into the suprachoroidal space opposite the wound. It is necessary to perform a large retinotomy of 180° to 270° to release the retina, in which case a giant tear with a rolled posterior edge is created. Reattachment of the retina is accomplished by the injection of perfluorocarbon liquid into the posterior vitreous cavity as fluid is released anteriorly. The peripheral retina is supported by a broad scleral buckle of moderate height, and laser is applied 360° (see Fig. 18B). The perfluorocarbon is replaced by air, which in turn is replaced by silicone oil. An inferior iridectomy is performed in aphakic eyes (the lens is lost in virtually all of these cases) to prevent the prolapse of oil into the anterior chamber postoperatively.⁴⁷ We prefer silicone oil over long-acting gas in eyes with large retinotomies because a tamponade of long duration is achieved without the need for reinjection postoperatively. Postoperative positioning is also less restrictive with oil than with gas, and the transparency of oil permits early assessment of the visual acuity of the eye, which is helpful in determining the potential value of subsequent reoperations should they become necessary. In young patients, the long-term complications of silicone oil are significant, and therefore it is removed approximately 6 months postoperatively when the retina is secure.

Hemorrhage is sometimes encountered during the secondary repair. Temporary hemostasis is frequently achieved by raising the level of the infusion bottle, which increases the intraocular pressure and occludes both injured and normal vessels. Subsequent lowering of the infusate may reopen and thereby identify the injured vessel, which is cauterized with endodiathermy. Focal bleeding vessels in attached retina may be closed with endoargon laser, which has the added advantage of avoiding the adhesions that sometimes form between the target vessel and an endodiathermy probe.

Often, bleeding sites cannot be identified or are not accessible to focal cautery. In these cases, a fluid-air or fluid-silicone oil exchange may be helpful. Vascular compression and concentration of clotting factors have been proposed as possible explanations for the hemostatic effect of these agents.⁴⁸ The addition of thrombin to the infusate in a concentration of 100 U/mL may control occult or diffuse bleeding sites.^49,50 It should be washed out at the end of surgery to avoid postoperative inflammation and fibrin formation.

A damaged cornea may severely limit the visibility and, consequently, the secondary repair of pathology in the posterior segment of the eye. Edematous corneal epithelium is removed and the interference of striae reduced by the application of sodium hyaluronate to the endothelial surface. Nevertheless, it is sometimes necessary to use a temporary keratoprosthesis in difficult cases. The Eckardt device is preferred because it permits a good view of the fundus periphery.⁵¹ The prosthesis is replaced by donor cornea at the end of the operation.

Choroidal hemorrhage is commonly caused by penetrating trauma. Although usually small and self-limiting, massive bleeding into the suprachoroidal space can expel ocular contents through an open wound or force the apposition of inner retinal surfaces in the center of the vitreous cavity (kissing choroidal detachment). The untreated prognosis of small to medium-sized choroidal hemorrhages is good. Large choroidal hemorrhages must be treated during the secondary repair of penetrating injuries when they interfere with the correction of associated pathology such as retinal detachments. Uncontrollable elevation of the intraocular pressure is also an indication for drainage of large choroidal hemorrhages.

Hemorrhagic choroidal detachments are often first diagnosed by ultrasound, which is a good method of following their evolution and resolution. Liquefaction of clotted blood, which occurs between 7 and 14 days, can be demonstrated ultrasonographically. Thus, the optimal time for drainage, if necessary, is established. Drainage is accomplished through several sclerotomies placed to correspond to the major accumulations of suprachoroidal blood. Air is simultaneously infused into the restricted preretinal space by an air pump, which automatically controls the intraocular pressure. To avoid penetration of the retina, the infusion needle is first placed into the anterior chamber through the limbus. When sufficient drainage has been accomplished, infusion is transferred to a standard pars plana port, air is replaced by fluid, and the remaining repairs are performed. Alternatively, sodium hyaluronate or silicone oil may be used as the primary infusate to facilitate visualization of intraocular structures as the operation proceeds posteriorly. The cohesive quality of silicone oil, although limited, tends to maintain the integrity of the expanding preretinal space better than sodium hyaluronate, but the view is better through Healon (Kabi Pharmacia). The intraocular pressure is maintained throughout these maneuvers to avoid hypotony and consequent recurrent choroidal hemorrhaging.

Recently, we have treated choroidal hemorrhages by infusing perfluorocarbon liquid into the vitreous cavity instead of gas, sodium hyaluronate, or silicone oil. The heavy expanding mass of perfluorocarbon in the posterior vitreous cavity displaces the blood in the suprachoroidal space anteriorly toward the sclerotomies, thereby facilitating its removal. The same technique can be used advantageously to force subretinal blood from the posterior pole toward anterior retinal breaks or retinotomies, through which it is aspirated and eliminated.

LATE VITRECTOMY

Vitreous microsurgery can be performed whenever reparable late complications arise. These include complicated traction and rhegmatogenous retinal detachments caused by incarceration and contraction of intraocular scars, and the effects of reproliferation, such as macular pucker and proliferative vitreoretinopathy.

Complicated Traction and Rhegmatogenous Retinal Detachments

The detachments most characteristic of penetrating trauma are the traction elevations of the vitreous base and peripheral retina opposite a scleral wound (see Figs. 6 to 9). Progressive contracture of transvitreal membranes causes late dialyses at the vitreous base borders as previously described. These membranes are excised with a vitrectomy probe or, if mature and difficult to remove, by sharp dissection with a combination of scissors, knife, and forceps. The vitreous cortex posterior to the equator is removed. It has usually separated from the retina spontaneously, in which case the excision is accomplished without difficulty. When posterior vitreous detachment is absent, the cortex must be dissected from the retina. Epiretinal membranes, which may have formed after the injury, must also be removed. Traction detachments of the peripheral retina flatten after membrane removal and are additionally supported by a broad encircling scleral buckle of moderate height (Fig. 19). Rhegmatogenous detachments with large dialyses are reattached with perfluorocarbon liquid, as previously described, after the release of traction. A broad encircling scleral buckle is also used in these cases, but the height is limited to prevent radial folding of the retina.

Repair of retinal detachments complicated by incarceration and scar contracture requires relaxation by retinotomy and membrane dissection as described above. An encircling scleral buckle is used to support the peripheral retinotomy and the vitreous base. In cases of posterior incarceration and subsequent relaxing retinotomy, a circumferential scleral buckle is also routinely used to support the peripheral vitreous.

Cellular Reproliferation and Recurrent Intraocular Scarring Are Common After Ocular Penetration

The treatment of proliferative vitreoretinopathy and macular pucker, a minor manifestation of the same process, is described elsewhere in these volumes.

The prognosis for anterior segment injuries has consistently improved during the last half century. Approximately 40% of eyes with corneal or corneoscleral lacerations were lost before the end of World War II,^52,53 whereas 17% of eyes with similar injuries were lost according to reports covering the past two decades.^9,54 A final vision of 20/40 or better was achieved in 84% of eyes with corneal lacerations with or without lens damage.⁹ More recently, Lamkin and colleagues⁵⁵ reported a final visual acuity of 20/40 or better in seven out of seven eyes with simultaneous repair of corneal lacerations, extraction of cataracts, and posterior chamber lens implantation.

The outcome of eyes with severe posterior segment injuries was poor when they were treated by wound repair and antibiotics alone. Reports indicate a loss of approximately 40% to 70% of eyes with significant vitreous damage.^56–58 Eighty-four percent of eyes with rupture of the globe due to blunt trauma were lost after wound repair according to one study.⁵⁹ Only 13% of eyes with penetrating injuries of the posterior segment achieved a visual acuity of 20/40 or better according to two reports from the middle 1970s.^9,56 In comparison, the results of treating posterior penetrating injuries with vitreous surgery are encouraging. A synthesis of the results of available studies indicates that one third of eyes achieve vision of 20/100 or better, one third obtain ambulatory vision, and one third lose useful vision.^60–70

Good results are obtained by electromagnetic extraction of uncomplicated magnetic foreign bodies. Combined data report a final visual acuity of 20/40 or better in 62% of eyes with magnetic IOFBs in the lens or vitreous.^69,71,72 By comparison, reactive nonmagnetic foreign bodies do poorly without vitreous surgery. In one series, a final visual acuity of 20/50 or better was achieved in one third of eyes, whereas over 50% lost all useful vision or were enucleated. The results of vitreous surgery for foreign bodies, magnetic and nonmagnetic, are remarkably consistent and indicate a final visual acuity of 5/200 or better in two thirds of eyes.^{28,42,70,73,74}

Vitreoretinal microsurgery is of great value in the repair of penetrating injuries with retained nonmagnetic foreign bodies and selected cases of magnetic IOFBs that are difficult or dangerous to extract with an electromagnet. Vitrectomy may be helpful in the management of eyes with posttraumatic endophthalmitis. The restoration of the anterior chamber and pupil by the removal of incarcerated iris, lens, and vitreous with vitreous microsurgical techniques assists the repair of complicated anterior lacerations or ruptures. Secondary complications, including traction and rhegmatogenous retinal detachments, are minimized by the timely removal of hemorrhage, disrupted lens, and damaged vitreous that stimulate and provide the scaffold for fibrocellular ingrowth.

Otherwise irreparable traction and rhegmatogenous retinal detachments caused by contracting membranes and complicated by incarceration can be corrected by the proper application of vitreous surgery.

In conclusion, severely injured eyes can be salvaged and vision restored by vitreoretinal microsurgery unless the initial injury has irreversibly destroyed vital neurosensory elements.

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