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Chapter 19: Ocular & Orbital Trauma
Authors:
Ocular & Orbital Trauma
Ocular trauma is a common cause of unilateral blindness in children and young adults; persons in these age groups sustain the majority of severe ocular injuries. Young adults-especially men-are the most likely victims of penetrating ocular injuries. Domestic accidents, violent assaults, exploding batteries, sports-related injuries, and motor vehicle accidents are the most common circumstances in which ocular trauma occurs. Increasingly, ocular injuries are the result of paintball air gun mishaps and air bag deployment in automobile accidents.
INITIAL EXAMINATION OF OCULAR TRAUMA
The history should include an estimate of visual acuity prior to and immediately following the injury. It should be noted whether any visual loss was slowly progressive or sudden in onset. An intraocular foreign body must be suspected if there is a history of hammering, grinding, or explosions. Injuries in a child with a history that is not appropriate for the injury sustained should raise a suspicion of child abuse (see Chapter 17).
Physical examination begins with the measurement and documentation of visual acuity. If visual loss is severe, check for light projection, two-point discrimination, and the presence of an afferent pupillary defect. Test ocular motility and periorbital skin sensation, and palpate for defects in the bony orbital rim. At the bedside, the presence of enophthalmos can be determined by viewing the profiles of the corneas from over the brow. If a slitlamp is not available in the emergency room, a penlight, loupe, or direct ophthalmoscope set on +10 (black numbers) can be used to examine the tarsal surfaces of the lids and the anterior segment for injury.
The corneal surface is examined for foreign bodies, wounds, and abrasions. The bulbar conjunctiva is inspected for hemorrhage, foreign material, or lacerations. The depth and clarity of the anterior chamber are noted. The size, shape, and light reaction of the pupil should be compared with the other eye to ascertain if an afferent pupillary defect is present in the injured eye. If the eyeball is undamaged, the lids, palpebral conjunctiva, and fornices can be more thoroughly examined, including inspection after eversion of the upper lid. The direct and indirect ophthalmoscopes are used to view the lens, vitreous, optic disk, and retina. Photographic documentation is useful for medicolegal purposes in all cases of external trauma. In all cases of ocular trauma, the apparently uninjured eye should also be carefully examined.
Immediate Management of Ocular Trauma
If there is obvious rupture of the globe, one should avoid further manipulation until the patient has been given general anesthesia. No cycloplegic agents or topical antibiotics should be applied prior to surgery because of potential toxicity to exposed intraocular tissues. A Fox shield (or the bottom third of a paper cup) is taped over the eye, and parenteral broad-spectrum antibiotics are started. Analgesics, antiemetics, and tetanus antitoxin are given as needed, with restriction of food and fluids. Induction of general anesthesia should not include the use of depolarizing neuromuscular blocking agents, because these transiently increase pressure on the globe and thus increase any tendency to herniation of intraocular contents. Small children may also be better examined initially with the aid of a short-acting general anesthetic.
In severe injuries, it is important for the nonophthalmologist to bear in mind the possibility of causing further damage by unnecessary manipulation while attempting to do a complete ocular examination.
Caution: Topical anesthetics, dyes, and other medications placed in an injured eye must be sterile. Both tetracaine and fluorescein are available in sterile, individual dose units.
ABRASIONS & LACERATIONS OF THE LIDS
Particulate matter should be removed from abrasions of the lids to reduce skin tattooing. The wound is then irrigated with saline and covered with an antibiotic ointment and sterile dressing. Avulsed tissue is cleaned and reattached. Because of the excellent vascularity of the lids, there is a good chance that ischemic necrosis will not occur.
Partial-thickness lacerations of the lids not involving the lid margin may be surgically repaired in the same way as other skin lacerations. Full-thickness lid lacerations involving the lid margin, however, must be repaired carefully to prevent marginal lid notching and trichiasis (Figure 19-1).
Correct lid repair requires precise approximation of the lacerated lid margin, tarsal plate, and skin (Figure 19-1A). This is initiated by placing a double-armed 6-0 silk or nylon suture in mattress fashion through the edge of the tarsal plate. The needle is first passed through corresponding edges of the tarsal plate before exiting the meibomian gland orifice on the opposing side. The other needle with 6-0 silk is then passed similarly with a 3-4 mm spacing (Figure 19-1B). A second 6-0 silk suture is preplaced through lash follicles 2 mm equidistant on either side of the laceration. These sutures are not tied until the tarsus has been repaired with interrupted absorbable 5-0 sutures (Figure 19-1C). Finally, the skin is closed with interrupted 6-0 nylon sutures (Figure 19-1D). Antibiotic ointment is then applied to the repaired lid tissue.
If primary repair is not effected within 24 hours, edema may necessitate delayed closure. The wound should be cleaned thoroughly and antibiotics administered. After swelling has subsided, repair may be performed. Debridement should be minimized, especially if the skin is not lax.
Lacerations near the inner canthus frequently involve the canaliculi. Early repair is desirable, since the tissue becomes more difficult to identify and repair when swollen. The value of direct repair of canalicular lacerations is debated. Simple apposition of the cut ends is often sufficient. Stenting or intubation may exacerbate the degree of canalicular damage and thus the risk of stenosis and may even result in damage to other parts of the canalicular system during surgical manipulation. Nevertheless, sharp lacerations through the distal canaliculus may benefit from repair with a Veirs rod or other form of stent. Similarly, avulsions or proximal canalicular lacerations may require silicone nasocanalicular intubation with Quickert probes. Various methods of intubating a single canaliculus have been described that serve to avoid the risky and traumatic use of pigtail probes, which are particularly likely to damage other parts of the canalicular system.
FOREIGN BODIES ON THE SURFACE OF THE EYE & CORNEAL ABRASIONS
Corneal foreign bodies and abrasion cause pain and irritation that can be felt during eye and lid movement, and corneal epithelial defects may cause a similar sensation. Fluorescein will stain the exposed basement membrane of an epithelial defect and can highlight aqueous leakage from penetrating wounds (positive Seidel test). A pattern of vertical scratch marks on the cornea indicates foreign bodies embedded on the tarsal conjunctival surface of the upper lid. Contact lens overwear produces corneal edema.
Simple corneal epithelial defects are treated with antibiotic ointment and a pressure patch to immobilize the lids. For removal of foreign matter, a topical anesthetic can be given and a spud or fine-gauge needle used to remove the material during slitlamp examination. A cotton-tipped applicator should not be used because it rubs off a large area of epithelium, often without removing the foreign body. Metallic rings surrounding copper or iron fragments (Figure 19-2) can be removed with a battery-operated drill with a burr tip. Deeply embedded inert materials (eg, glass, carbon) may be allowed to remain in the cornea. If removal of deeply embedded fragments is necessary or if there is an aqueous leak requiring sutures or cyanoacrylate glue, the procedure should be undertaken by microsurgical technique in an operating room, where the anterior chamber can be re-formed, if necessary, with or without viscoelastics under sterile conditions.
Following removal of a foreign body, antibiotic ointment should be instilled and the eye patched. The wound should be examined daily for evidence of infection until it is completely healed.
Never give a topical anesthetic solution to the patient for repeated use after a corneal injury, as this delays healing, masks further damage, and can lead to permanent corneal scarring. In addition, chronic anesthetic use can cause corneal infiltrates and ulceration which clinically can mimic the appearance of an infectious ulcer. Steroids should be avoided while an epithelial defect exists. Because corneal abrasions are a frequent complication of general anesthesia, care should be taken to avoid this injury during induction and throughout the procedure by taping the lids closed or instilling a lubricating ophthalmic ointment in the conjunctival fornices. Recurrent epithelial erosions sometimes follow corneal injuries and are treated with patching or a bandage contact lens.
PENETRATING INJURIES & CONTUSIONS OF THE EYEBALL
Rupture of the eyeball can occur as a result of sharp penetrating injury or blunt contusive force. Blunt trauma produces a rise in orbital and intraocular pressure, with deformation of the globe. Rapid decompression occurs when the eye wall ruptures or the orbital contents herniate into adjacent sinuses (blowout fracture; see below). The superonasal limbus is the most common site of globe rupture (contrecoup effect-the lower temporal quadrant being most exposed to trauma). Generally, blunt traumatic injuries have a worse prognosis than penetrating injuries because of the increased incidence of retinal detachment and intraocular tissue avulsion and herniation.
While most penetrating injuries cause a marked loss of vision, injuries due to small high-velocity particles generated by grinding or hammering might present with only mild pain and blurring. Other signs include hemorrhagic chemosis, conjunctival laceration, a shallow anterior chamber with or without an eccentrically placed pupil, hyphema, or vitreous hemorrhage. The intraocular pressure can be low, normal, or, rarely, slightly elevated.
In addition to rupture of the scleral wall, contusive forces to the eyeball can result in motility disorders, subconjunctival hemorrhage, corneal edema, iritis, hyphema, angle-recession glaucoma, traumatic mydriasis, rupture of the iris sphincter, iridodialysis, paralysis of accommodation, lens dislocation, and cataract. Injuries sustained by posterior structures include vitreal and retinal hemorrhages, retinal edema (commotio retinae, or Berlin's edema), retinal holes, vitreous base avulsions, retinal detachment, choroidal rupture, and optic nerve contusion or avulsion (Figures 19-3 and 19-4).
Many of these injuries cannot be seen upon external examination. Some, such as cataract, may not develop until days or weeks after the injury. The use of ultrasonic biomicroscopy has recently aided in diagnosing angle recession, iridodialysis, lens subluxation, and intraocular foreign bodies when visualization is limited by media opacities.
Treatment
Except for injuries involving rupture of the eyeball itself, most of the effects of contusion of the eye do not require immediate surgical treatment. However, any injury severe enough to cause intraocular hemorrhage increases the risk of delayed secondary hemorrhage and possible intractable glaucoma and permanent damage to the eyeball. The further management of these cases is described in the section below on hyphema.
In the closure of anterior segment wounds, microsurgical techniques should be used. Corneal lacerations are repaired with 10-0 nylon sutures to form a watertight closure. An incarcerated iris or ciliary body exposed for less than 24 hours can be reposited in the globe with viscoelastics or by introducing a cyclodialysis spatula through a limbal stab incision and sweeping the tissue out of the wound. If this cannot be achieved, if the tissue has been exposed for more than 24 hours, or if it is ischemic and severely damaged, then the prolapsing tissue should be excised at the level of the wound lip. Any excised tissue should be sent for pathologic examination. Cultures are taken for investigation of possible bacterial or fungal infection. Lens remnants and blood are removed with mechanical irrigation and aspiration or vitrectomy equipment. Anterior chamber reformation during repair is achieved with viscoelastics, air, or physiologic intraocular fluids.
Scleral wounds are closed with interrupted 8-0 or 9-0 nonabsorbable sutures. The rectus muscles may be temporarily disinserted to provide better exposure. Posterior scleral exit wounds in a double penetrating injury are self-sealing, and generally no attempt is made at closure.
The prognosis for traumatic retinal detachments is poor because of macular injury, giant retinal tears, and formation of intravitreal fibrovascular membranes that occur with penetrating injury. Such intravitreal membranes generate sufficient contractile force to detach the retina. Vitrectomy is effective in their treatment, but the timing of this procedure remains controversial. Early vitrectomy with intravitreal antibiotics is indicated for endophthalmitis. In noninfected cases, delaying surgery for 10-14 days may decrease the risk of intraoperative hemorrhage and permit a posterior vitreous detachment to develop, making surgery technically easier.
Vitreoretinal surgery in the presence of large corneal wounds can be done through a temporary Landers-Foulks keratoprosthesis prior to corneal grafting. Primary enucleation or evisceration should only be considered when the globe is completely disorganized. The fellow eye is susceptible to sympathetic ophthalmia whenever penetrating ocular trauma occurs, particularly if there has been damage to the uveal tissues; fortunately, this complication occurs very rarely.
INTRAOCULAR FOREIGN BODIES (Figure 19-5)
A complaint of discomfort or blurred vision in an eye with a history of striking metal upon metal, explosion, or high-velocity projectile injury should arouse a strong suspicion of intraocular foreign body. The anterior portion of the eye should be inspected with a loupe or slitlamp in an attempt to localize the wound of entry. Direct and indirect ophthalmoscopic visualization of an intraocular foreign body should be attempted. An orbital soft tissue x-ray or computed tomography (CT) scan must be taken to verify the presence of a radiopaque foreign body as well as for medicolegal reasons. Magnetic resonance imaging (MRI) is absolutely contraindicated in the identification and localization of intraocular foreign bodies because of the risk of movement of a metallic foreign body in the magnetic field.
Foreign bodies that have been identified and localized within the eye must be removed whenever possible. Particles of iron or copper must be removed to prevent later disorganization of ocular tissues from toxic degenerative changes (siderosis from iron and chalcosis from copper). Some of the newer alloys are more inert and may be tolerated. Other kinds of particles, such as glass or porcelain, may be tolerated indefinitely and are usually better left alone.
Localization of intraocular foreign bodies includes the geometric method of Sweet, the Comberg contact lens (containing a post and ring), ultrasonography, and coronal CT scan of the orbits. MRI is contraindicated in localizing intraocular metallic foreign bodies because the magnetic field produced during scanning can cause the foreign bodies to become high-velocity intraocular projectiles with catastrophic ocular effects.
Treatment
If the foreign body is anterior to the lens zonules, it should be removed through a limbal incision from the anterior chamber. If it is located behind the lens and anterior to the equator, it should be removed through the area of pars plana that is nearest to the foreign body because less retinal damage is caused in that manner. If the foreign body is posterior to the equator, it is best removed via the pars plana by vitrectomy and intraocular forceps, thus avoiding major cho-roidal hemorrhages from incisions of the posterior wall of the eyeball. This method is used for both magnetic and nonmagnetic foreign bodies. Special forceps are available for grasping spherical pellets.
Any damaged area of the retina must be treated with diathermy, photocoagulation, or endolaser coagulation to prevent retinal detachment.
HYPHEMA
Contusive forces will frequently tear the iris vessels and damage the anterior chamber angle. Blood in the aqueous may settle out in a visible layer (hyphema). Acute glaucoma occurs if the trabecular meshwork is blocked by fibrin and cells or if clot formation produces pupillary block.
Treatment
Patients with visible hyphema filling more than 5% of the anterior chamber should be placed at bed rest, and steroid drops should be instilled in the affected eye for 5 days. Pupillary dilation may increase the risk of rebleeding and thus is often deferred until the hyphema has resolved. Initial assessment for posterior segment damage may thus require ultrasound examination. The eye should be examined frequently for secondary bleeding, glaucoma, or corneal blood staining from iron pigment. Rebleeding occurs in 16-20% of cases within 2-3 days. This complication carries a high risk of glaucoma and corneal staining. Several studies indicate that the use of oral aminocaproic acid to stabilize clot formation reduces the risk of rebleeding. A dose of 100 mg/kg every 4 hours up to a maximum of 30 g/d for 5 days is a good regimen. If glaucoma occurs, management includes the use of ocular timolol 0.25% or 0.5.% applied twice a day; aceta- zolamide, 250 mg orally four times a day; and hyperosmotic agents (mannitol, glycerol, and sorbitol). Other ocular antihypertensives that may be used with timolol are dorzolamide applied three times a day and apraclonidine applied twice a day.
The hyphema must be surgically evacuated if the intraocular pressure remains elevated (> 35 mm Hg for 7 days or 50 mm Hg for 5 days) to avoid optic nerve damage and corneal staining. If the patient has a hemoglobinopathy, glaucomatous optic atrophy is likely to develop much more readily, and surgical evacuation of the clot should be considered much earlier. Vitrectomy instruments are used to remove the central clot and lavage the anterior chamber. The mechanized probe and irrigation port are introduced anterior to the limbus through clear cornea to avoid damage to the iris and lens. No attempt is made to extract the clot from the anterior chamber angle or from iris tissue. A peripheral iridectomy is then performed. Another means of clearing the anterior chamber is by viscoelastic evacuation. A small limbal incision is made to inject the viscoelastic, and a larger incision 180 degrees away allows the hyphema to be pushed out.
Late-onset glaucoma may follow months to years later as a result of angle recession. With rare exceptions, corneal blood staining clears slowly over a period of up to 1 year.
BURNS OF THE EYE
Chemical Burns
All chemical burns must be treated as ophthalmic emergencies. Immediate tap-water lavage should be started at the site of injury before the patient is transported. Any obvious foreign bodies should also be irrigated away if possible. In the emergency room, a brief history and examination precedes copious irrigation of the ocular surfaces, including the conjunctival fornices. Sterile isotonic saline (several liters per injured eye) is instilled with standard intravenous tubing. A lid speculum and local anesthetic infiltration of the lids may be necessary to overcome blephar-ospasm. Analgesics and topical anesthetic and cycloplegic agents are nearly always indicated. Use a moistened cotton-tipped applicator and jeweler's forceps to remove particulate matter from the fornices. Watch for respiratory distress due to soft tissue swelling of the upper airways. The pH of the ocular surface is checked by placing a strip of indicator paper in the fornix; resume irrigation if the pH is not between 7.3 and 7.7. After lavage, apply an antibiotic ointment and a pressure dressing.
Since alkali rapidly penetrates through ocular tissues and will continue to cause damage long after the injury is sustained, prolonged lavage and repeated pH checks are needed. Acids form a barrier of precipitated necrotic tissue that tends to limit further penetration and damage. Alkali burns cause an immediate rise in intraocular pressure owing to contraction of the sclera and trabecular meshwork damage. A secondary pressure rise occurs 2-4 hours later from the release of prostaglandins, which potentiate an intense uveitis. This is difficult to monitor through the opaque cornea. Treatment is with topical steroids, antiglaucoma agents, and cycloplegics during the first 2 weeks. Beyond 2 weeks, steroids must be used with caution because they inhibit reepithelialization. Corneal melting and possible perforation from continued collagenase activity can then occur. Ascorbate (vitamin C) and citrate drops are minimally effective for preventing corneal melting in patients with severe burns or persistent corneal epithelial defects. A trial with collagenase inhibitors (acetylcysteine) may prove beneficial. Corneal exposure and persistent epithelial defects are treated with artificial lubricants, tarsorrhaphy, or a bandage contact lens.
Long-term complications of chemical burns include angle-closure glaucoma, corneal scarring, symblepharon, entropion, and keratitis sicca. Competency of the conjunctival and scleral vasculature has been shown to be of prognostic value. A greater loss of perilimbal epithelium and conjunctival and scleral vasculature indicates a poorer prognosis.
Thermal Burns
Thermal burns of the lids are treated with topical antibiotics and sterile dressings. If corneal damage is sustained, the extensive lid swelling initially makes pressure patching unnecessary. After 2-3 days, ectropion and lid retraction begin. Tarsorrhaphies and moisture chambers fashioned from plastic wrap then protect the cornea. Full-thickness skin grafts are delayed until skin contraction is no longer progressing.
Ultraviolet irradiation, even in moderate doses, often produces a painful superficial keratitis. Pain often begins 6-12 hours after exposure. This keratitis follows exposure to an electric welding arc without the protection of a filter, short circuits in high-voltage lines, or exposure to the reflections from snow without protective sunglasses ("snow blindness").
In severe cases of "flash burn," instillation of a sterile topical anesthetic may be necessary for examination. Treatment consists of pressure patching with an antibiotic ointment. A mydriatic is instilled if there is iritis.
Infrared exposure rarely produces an ocular reaction. ("Glassblower's cataract" is rare today but once was common among workers who were required to watch the color changes in molten glass in furnaces without proper filters.) Radiant energy from viewing the sun or an eclipse of the sun without an adequate filter, however, may produce a serious burn of the macula, resulting in permanent impairment of vision.
Excessive exposure to radiation (x-ray) produces cataractous changes that may not appear for many months after the exposure. The same risk is inherent with exposure to nuclear radiation.
INJURIES INVOLVING THE ORBIT & ITS CONTENTS
Orbital Fractures (Figure 19-6)
Orbital fractures commonly occur with facial trauma. Fractures of the maxilla are classified by the Le Fort system: type I is below the orbital floor; type II passes through the nasal and lacrimal bones in addition to the maxilla forming the medial orbital floor; and type III involves the medial and lateral walls and the orbital floor in the presence of separation of the facial skeleton from the cranium. Orbital roof fractures are rare and are generally caused by penetrating injuries. If visual loss is progressing in the presence of an optic canal fracture, steroids and surgical decompression may be necessary. When visual loss is sudden and complete, however, recovery is less likely. Carotid-cavernous sinus fistulas are associated with orbital apex fractures, and the orbit should therefore be auscultated for bruits.
Tripod fractures of the zygoma involve the orbital floor but in the absence of dislocation may not need surgical repair. Zygomatic arch fractures do not involve the orbit. Telescoping fractures of the frontal process of the maxilla and the lacrimal and ethmoid bones produce a saddle-nose deformity with telecanthus and lacrimal system obstruction.
When the orbital entrance receives a blow, the compressive forces can fracture the thin medial and inferior walls, with prolapse and possible entrapment of soft tissues. There may be associated intraocular injury, including hyphema, angle recession, and retinal detachment. If the blowout is large, enophthalmos of the globe may develop immediately. Enophthalmos can occur later after the swelling subsides and atrophy or scarring of the soft tissues develops.
Diplopia can be caused by direct neuromuscular damage or swelling of orbital contents. This must be differentiated from entrapment of the inferior rectus and oblique muscle or adjacent tissue within the fracture. When entrapment is present, passive movement of the eye with forceps (forced ductions test) is restricted. Sufficient time should pass to allow for spontaneous improvement in eye movements with the resolution of swelling. Sensation is tested in the distribution of the infraorbital nerve. Hypesthesia is present with orbital floor fractures. CT scanning with axial and coronal views provides the best assessment of orbital trauma. Plain x-rays may be helpful in the initial identification of bony injury.
The indications for surgical repair of the blowout fracture are (1) persistent diplopia within 30 degrees of the primary position of gaze in the presence of entrapment; (2) enophthalmos of 2 mm or more; or (3) a large fracture (half the orbital floor), which is likely to cause late enophthalmos. Delaying surgery for 1-2 weeks helps the surgeon to assess whether the diplopia will resolve without intervention. Longer delays decrease the likelihood of successful repair of enophthalmos and strabismus because of progressive scarring.
Surgical repair is usually accomplished via an infraciliary or transconjunctival route, though trans-antral and infraorbital approaches are also done. The periorbita is incised and elevated to expose the fracture site in the floor and medial walls. Herniated tissue is pulled back into the orbit, and the defect is covered by an alloplastic implant, with care being taken not to damage the infraorbital neurovascular bundle. Complications include blindness, diplopia, extrusion of the implant, or migration of the implant to press against the lacrimal sac, causing obstruction and dacryocystitis. Other complications include hemorrhage, infection, lower eyelid retraction, and infraorbital anesthesia. Subsequent procedures for strabismus and ptosis may be needed.
Penetrating Injury of the Orbit
Penetrating injuries of the orbital tissue may be produced by high-velocity projectiles or sharp instruments. Radiopaque foreign bodies can be localized by methods similar to those used in locating intraocular foreign bodies within the eye.
Contusions of the Orbit
Contusion injuries to the orbital contents may result in hemorrhage or subsequent atrophy of the tissue, with enophthalmos. Traumatic paresis of the extraocular muscles occasionally occurs but is usually transient.
Pulsating Exophthalmos Following Orbital Injury
Pulsating exophthalmos occasionally follows a penetrating or contusion injury to the orbital contents due to the formation of an arteriovenous shunt. A common site of involvement is a bone fracture into the cavernous sinus. Spontaneous resolution is uncommon, and closure of the shunt, usually by embolization, is often required.
PREVENTION OF INJURIES TO THE EYE (See Also Chapter 21.)
Persons engaging in industrial or athletic activities while wearing prescription lenses made of glass or plastic are at increased risk from shattered lens fragments. The eyewear most effective in preventing injuries consists of polycarbonate lenses in polyamide frames with a posterior retention rim. Solid wraparound frames should be used (rather than hinged frames) because they better withstand lateral blows. In athletic or high-risk recreational activities (eg, air or paint-pellet gun "war games"), guards without lenses do not always protect the eye adequately. Proper eye protection is particularly indicated for those playing racquetball, handball, and squash. The sight of many eyes has been lost in these sports, particularly from ocular contusion trauma in the absence of adequate eye protection.
REFERENCESList of Figures
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Figure 19-1: Repair of full-thickness lid laceration. A: The defect shown. B: Initial vertical mattress suture through tarsal plate. C: Interrupted suture closure of tarsal plate. D: Interrupted suture closure of skin. (Reproduced, with permission, from Phelps C: Manual of Common Ophthalmic Surgical Procedures. Churchill Livingstone, 1986.) |
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Figure 19-2: Metallic corneal foreign body. (Courtesy of A Rosenberg.) |
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Figure 19-3: Hole in retina, macular area, posttraumatic. |
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Figure 19-4: Choroidal ruptures. (Photo by Diane Beeston.) |
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Figure 19-5: Ophthalmoscopic view of intraocular metallic (iron) foreign body in vitreous. |
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Figure 19-6: Right orbital blowout fracture in upgaze. |
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